FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Abu Habib, N
Wilcox, AJ
Daltveit, AK
Basso, O
Shao, J
Oneko, O
Lie, RT
AF Abu Habib, Ndema
Wilcox, Allen J.
Daltveit, Anne Kjersti
Basso, Olga
Shao, John
Oneko, Olola
Lie, Rolv Terje
TI Birthweight, preterm birth and perinatal mortality: a comparison of
black babies in Tanzania and the USA
SO ACTA OBSTETRICIA ET GYNECOLOGICA SCANDINAVICA
LA English
DT Article
DE Birthweight; developing country; fetal development; perinatal mortality;
preterm birth
ID UNITED-STATES; RURAL TANZANIA; BELGIUM; INFANTS
AB Objectives. Adverse conditions in Africa produce some of the highest rates of infant mortality in the world. Fetal growth restriction and preterm delivery are commonly regarded as major pathways through which conditions in the developing world affect infant survival. The aim of this article was to compare patterns of birthweight, preterm delivery, and perinatal mortality between black people in Tanzania and the USA. Design. Registry-based study. Settings. Referral hospital data from North Eastern Tanzania and US Vital Statistics. Sample. 14 444 singleton babies from a hospital-based registry (1999-2006) and 3 530 335 black singletons from US vital statistics (1995-2000). Main outcome measures. Birthweight, gestational age and perinatal mortality. Methods. Restricting our study to babies born at least 500g, we compared birthweight, gestational age, and perinatal mortality (stillbirths and deaths in the first week) in the two study populations. Results. Perinatal mortality in the Tanzanian sample was 41/1 000, compared with 10/1 000 among USA blacks. Tanzanian babies were slightly smaller on average (43g), but fewer were preterm (<37weeks) (10.0 vs. 16.2%). Applying the USA weight-specific mortality rates to Tanzanian babies born at term suggested that birthweight does not play a role in their increased mortality relative to USA blacks. Conclusions. Higher mortality independent of birthweight and preterm delivery for Tanzanian babies suggests the need to address the contribution of other pathways to further reduce the excess perinatal mortality.
C1 [Abu Habib, Ndema] Muhimbili Univ Hlth & Allied Sci, Dept Epidemiol & Biostat, Dar Es Salaam, Tanzania.
[Daltveit, Anne Kjersti; Lie, Rolv Terje] Univ Bergen, Dept Publ Hlth & Primary Hlth Care, N-5020 Bergen, Norway.
[Daltveit, Anne Kjersti; Lie, Rolv Terje] Norwegian Inst Publ Hlth, Div Epidemiol, Oslo, Norway.
[Wilcox, Allen J.; Basso, Olga] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Durham, NC USA.
[Shao, John; Oneko, Olola] Kilimanjaro Christian Med Ctr, Dept Obstet & Gynaecol, Moshi, Tanzania.
RP Abu Habib, N (reprint author), Muhimbili Univ Hlth & Allied Sci, Dept Epidemiol & Biostat, POB 65015, Dar Es Salaam, Tanzania.
EM ndema_h@yahoo.com
RI Basso, Olga/E-5384-2010;
OI Basso, Olga/0000-0001-9298-4921; Habib, Ndema/0000-0003-4882-1687;
Wilcox, Allen/0000-0002-3376-1311
FU Norwegian Council for Higher Education; NIH, National Institute of
Environmental Health Sciences
FX Funding for this work was provided by the Norwegian Council for Higher
Education's Program for Development Research (NUFU) with funds allocated
to the Centre for International Health at the University of Bergen under
the Health Systems Research and Health Promotion in relation to
Reproductive Health in Tanzania project, of which the Medical Birth
Registry at Kilimanjaro Christian Medical Center (KCMC) is one element.;
Partially supported by the Intramural Research Program of the NIH,
National Institute of Environmental Health Sciences.
NR 22
TC 2
Z9 2
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0001-6349
EI 1600-0412
J9 ACTA OBSTET GYN SCAN
JI Acta Obstet. Gynecol. Scand.
PD OCT
PY 2011
VL 90
IS 10
BP 1100
EP 1106
DI 10.1111/j.1600-0412.2011.01195.x
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 829PC
UT WOS:000295595100007
PM 21615361
ER
PT J
AU Andreasen, V
AF Andreasen, Viggo
TI The Final Size of an Epidemic and Its Relation to the Basic Reproduction
Number
SO BULLETIN OF MATHEMATICAL BIOLOGY
LA English
DT Article
DE Heterogeneous mixing; Final size relation
ID PANDEMIC INFLUENZA; TRANSMISSION DYNAMICS; MODELS; POPULATIONS;
NETWORKS; DISEASE; SPREAD; SUSCEPTIBLES; OUTBREAKS; SELECTION
AB We study the final size equation for an epidemic in a subdivided population with general mixing patterns among subgroups. The equation is determined by a matrix with the same spectrum as the next generation matrix and it exhibits a threshold controlled by the common dominant eigenvalue, the basic reproduction number R0: There is a unique positive solution giving the size of the epidemic if and only if R0 exceeds unity. When mixing heterogeneities arise only from variation in contact rates and proportionate mixing, the final size of the epidemic in a heterogeneously mixing population is always smaller than that in a homogeneously mixing population with the same basic reproduction number R0. For other mixing patterns, the relation may be reversed.
C1 [Andreasen, Viggo] Roskilde Univ Ctr, Dept Sci, DK-4000 Roskilde, Denmark.
[Andreasen, Viggo] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Andreasen, V (reprint author), Roskilde Univ Ctr, Dept Sci, DK-4000 Roskilde, Denmark.
EM viggo@ruc.dk
FU Danish Medical Research Council [271-07-0555]; Science & Technology
Directorate, Department of Homeland Security; Fogarty International
Center, National Institutes of Health
FX This research was supported in part by a grant 271-07-0555 from the
Danish Medical Research Council and by the RAPIDD programme of the
Science & Technology Directorate, Department of Homeland Security, and
the Fogarty International Center, National Institutes of Health. V.A.
thanks Bryan Grenfell for his hospitality during this project.
NR 41
TC 20
Z9 20
U1 2
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0092-8240
J9 B MATH BIOL
JI Bull. Math. Biol.
PD OCT
PY 2011
VL 73
IS 10
BP 2305
EP 2321
DI 10.1007/s11538-010-9623-3
PG 17
WC Biology; Mathematical & Computational Biology
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology
GA 844WY
UT WOS:000296783600003
PM 21210241
ER
PT J
AU Berhane, AM
Weil, EJ
Knowler, WC
Nelson, RG
Hanson, RL
AF Berhane, Abeba M.
Weil, E. Jennifer
Knowler, William C.
Nelson, Robert G.
Hanson, Robert L.
TI Albuminuria and Estimated Glomerular Filtration Rate as Predictors of
Diabetic End-Stage Renal Disease and Death
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID PIMA-INDIANS; COLLABORATIVE METAANALYSIS; POPULATION COHORTS;
KIDNEY-FUNCTION; HEART-DISEASE; ESTIMATED GFR; PROTEINURIA; RISK;
MORTALITY; MELLITUS
AB Background and objectives We investigated predictive value of albuminuria and estimated GFR (eGFR) for ESRD in Pima Indians with type 2 diabetes.
Design, setting, participants and measurements Beginning in 1982, 2420 diabetic Pima Indians >= 18 years old were followed until they developed ESRD or died or until December 31, 2005. Individuals were classified at baseline by urinary albumin-to-creatinirte ratio (ACR) and by eGFR, calculated by the Chronic Kidney Disease Epidemiology Collaboration equation. Predictors of ESRD and mortality were examined by proportional hazards regression.
Results During a mean follow-up of 10.2 years, 287 individuals developed ESRD. Incidence of ESRD among individuals with macroalbuminuria (ACR >= 300 mg/g) was 9.3 times that of those with normoalbuminuria (ACR < 30 mg/g), controlled for age, gender, and duration of diabetes. Incidence among individuals with eGFR 15 to 29 ml/min per 1.73 m(2) was 81.9 times that of those with eGFR 90 to 119 ml/min per 1.73 m(2). Models that combined albuminuria and eGFR added significant predictive information about risk of ESRD or death compared with models containing eGFR or albuminuria alone. The hazard ratio for ESRD associated with a 10-ml/min per 1.73 m(2) lower eGFR was 1.36, whereas that associated with an increase in albuminuria category was 2.69; corresponding hazard ratios for death were 1.15 and 1.37.
Conclusions These results suggest that incorporation of quantitative information about albuminuria into staging systems based on eGFR adds significant prognostic information about risk for diabetic ESRD and death. Clin J Am Soc Nephrol 6: 2444-2451, 2011. doi: 10.2215/CJN.00580111
C1 [Berhane, Abeba M.; Weil, E. Jennifer; Knowler, William C.; Nelson, Robert G.; Hanson, Robert L.] NIDDK, Diabet Epidemiol & Clin Res Sect, Phoenix Epidemiol & Clin Res Branch, NIH, Phoenix, AZ 85014 USA.
RP Hanson, RL (reprint author), NIDDK, Diabet Epidemiol & Clin Res Sect, Phoenix Epidemiol & Clin Res Branch, NIH, 1550 E Indian Sch Rd, Phoenix, AZ 85014 USA.
EM rhanson@phx.niddk.nih.gov
RI Nelson, Robert/B-1470-2012; Hanson, Robert/O-3238-2015
OI Hanson, Robert/0000-0002-4252-7068
FU National Institute of Diabetes and Digestive and Kidney Diseases
FX This research was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases. The
authors thank members of the Gila River Indian Community for
participating in this investigation and the staff involved in collecting
and processing data. Part of this material was presented at the 69th
Annual Scientific Meeting of the American Diabetes Association, June 7,
2009, New Orleans, LA.
NR 26
TC 35
Z9 35
U1 0
U2 1
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD OCT
PY 2011
VL 6
IS 10
BP 2444
EP 2451
DI 10.2215/CJN.00580111
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 830KX
UT WOS:000295657000018
PM 21852671
ER
PT J
AU Perrone, RD
Abebe, KZ
Schrier, RW
Chapman, AB
Torres, VE
Bost, J
Kaya, D
Miskulin, DC
Steinman, TI
Braun, W
Winklhofer, FT
Hogan, MC
Rahbari-Oskoui, F
Kelleher, C
Masoumi, A
Glockner, J
Halin, NJ
Martin, D
Remer, E
Patel, N
Pedrosa, I
Wetzel, LH
Thompson, PA
Miller, JP
Meyers, CM
Bae, KT
AF Perrone, Ronald D.
Abebe, Kaleab Z.
Schrier, Robert W.
Chapman, Arlene B.
Torres, Vicente E.
Bost, James
Kaya, Diana
Miskulin, Dana C.
Steinman, Theodore I.
Braun, William
Winklhofer, Franz T.
Hogan, Marie C.
Rahbari-Oskoui, Frederic
Kelleher, Cass
Masoumi, Amirali
Glockner, James
Halin, Neil J.
Martin, Diego
Remer, Erick
Patel, Nayana
Pedrosa, Ivan
Wetzel, Louis H.
Thompson, Paul A.
Miller, J. Philip
Meyers, Catherine M.
Bae, K. Ty
CA HALT PKD Study Grp
TI Cardiac Magnetic Resonance Assessment of Left Ventricular Mass in
Autosomal Dominant Polycystic Kidney Disease
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID GENDER-DIFFERENCES; YOUNG-ADULTS; BODY-SIZE; HYPERTROPHY; HYPERTENSION;
SURVIVAL; CHILDREN; MRI; AGE
AB Background and objectives Autosomal dominant polycystic kidney disease (ADPKD) is associated with a substantial cardiovascular disease burden including early onset hypertension, intracranial aneurysms, and left ventricular hypertrophy (LVH). A 41% prevalence of LVH has been reported in ADPKD, using echocardiographic assessment of LV mass (LVM). The HALT PKD study was designed to assess the effect of intensive angiotensin blockade on progression of total kidney volume and LVM. Measurements of LVM were performed using cardiac magnetic resonance (MR).
Design, setting, participants, & measurements Five hundred forty-three hypertensive patients with GFR >60 ml/min per 1.73 m(2) underwent MR assessment of LVM at baseline. LVM was adjusted for body surface area and expressed as LVM index (LVMI; g/m(2)).
Results Baseline BP was 125.1 +/- 14.5/79.3 +/- 11.6 mmHg. Average duration of hypertension was 5.79 years. Prior use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was present in 59.5% of patients. The prevalence of LVH assessed using nonindexed LVM (g) was 3.9% (n = 21, eight men and 13 women) and 0.93% (n = 5, one man and four women) using LVMI (g/m(2)). In exploratory analyses, the prevalence of LVH using LVM indexed to H-2.7, and the allometric index ppLVmass(HW), ranged from 0.74% to 2.23% (n = 4 to 12). Multivariate regression showed significant direct associations of LVMI with systolic BP, serum creatinine, and albuminuria; significant inverse associations with LVMI were found with age and female gender.
Conclusions The prevalence of LVH in hypertensive ADPKD patients <50 years of age with short duration of hypertension, and prior use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers is low. Early BP intervention in ADPKD may have decreased LVH and may potentially decrease cardiovascular mortality. Clin J Am Soc Nephrol 6: 2508-2515, 2011. doi: 10.2215/CJN.04610511
C1 [Perrone, Ronald D.] Tufts Med Ctr, Div Nephrol, Boston, MA 02111 USA.
[Torres, Vicente E.; Hogan, Marie C.; Glockner, James] Mayo Clin, Coll Med, Rochester, MN USA.
[Schrier, Robert W.; Patel, Nayana] Univ Colorado, Hlth Sci Ctr, Denver, CO USA.
[Chapman, Arlene B.; Rahbari-Oskoui, Frederic; Masoumi, Amirali; Martin, Diego] Emory Univ, Sch Med, Atlanta, GA USA.
[Abebe, Kaleab Z.; Bost, James; Kaya, Diana; Bae, K. Ty] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Winklhofer, Franz T.; Wetzel, Louis H.] Univ Kansas, Med Ctr, Kansas City, KS 66103 USA.
[Braun, William; Remer, Erick] Cleveland Clin, Cleveland, OH 44106 USA.
[Steinman, Theodore I.; Pedrosa, Ivan] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Miller, J. Philip] Washington Univ, St Louis, MO USA.
[Meyers, Catherine M.] NIDDK, NIH, Bethesda, MD USA.
[Kelleher, Cass] Amgen Inc, Thousand Oaks, CA USA.
[Thompson, Paul A.] Sanford Res USD Sioux Falls, Sioux Falls, SD USA.
RP Perrone, RD (reprint author), Tufts Med Ctr, Div Nephrol, 800 Washington St,Hosp Box 391, Boston, MA 02111 USA.
EM rperrone@tuftsmedicalcenter.org
OI Abebe, Kaleab/0000-0002-3644-8419
FU National Institutes of Health/National Institute of Diabetes and
Digestive and Kidney Diseases [DK62408, DK62401, DK62410, DK62402,
DK62411]; National Center for Research Resources [RR000039, RR000051,
RR00585, RR000054, RR23940, UL1 RR025008, UL1 RR025780, UL1 RR024150,
UL1 RR025752, UL1 RR024992]; Polycystic Kidney Disease Foundation
FX The HALT-PKD study is supported by cooperative agreements from the
National Institutes of Health/National Institute of Diabetes and
Digestive and Kidney Diseases (DK62408, DK62401, DK62410, DK62402, and
DK62411). The HALT-PKD study and this publication were also supported by
Grants from the National Center for Research Resources (RR000039 Emory,
RR000051 Colorado, RR00585 Mayo, RR000054 Tufts Medical Center, and
RR23940 Kansas and UL1 RR025008 Emory, UL1 RR025780 Colorado, UL1
RR024150 Mayo, UL1 RR025752 Tufts, and UL1 RR024992 Washington
University). Its contents are solely the responsibility of the authors
and do not necessarily represent the official views of the NCRR. Study
medication for both trials was provided by Boehringer-Ingelheim
Pharmaceuticals (telmisartan and matched placebo) and Merck & Co.
(lisinopril). The Polycystic Kidney Disease Foundation provided
financial support and recruitment assistance for the enrollment phase of
HALT PKD. The investigators thank Gigi Flynn and Robin Woltman and all
of the clinical coordinators at each clinical site for their
perseverance and hard work in implementing HALT PKD.
NR 21
TC 14
Z9 16
U1 0
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD OCT
PY 2011
VL 6
IS 10
BP 2508
EP 2515
DI 10.2215/CJN.04610511
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 830KX
UT WOS:000295657000026
PM 21903983
ER
PT J
AU Hanssen-Bauer, A
Solvang-Garten, K
Sundheim, O
Pena-Diaz, J
Andersen, S
Slupphaug, G
Krokan, HE
Wilson, DM
Akbari, M
Otterlei, M
AF Hanssen-Bauer, Audun
Solvang-Garten, Karin
Sundheim, Ottar
Pena-Diaz, Javier
Andersen, Sonja
Slupphaug, Geir
Krokan, Hans E.
Wilson, David M., III
Akbari, Mansour
Otterlei, Marit
TI XRCC1 Coordinates Disparate Responses and Multiprotein Repair Complexes
Depending on the Nature and Context of the DNA Damage
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE base excision repair; micro-irradiation; PARP inhibitors; PCNA; DNA
repair complexes
ID BASE EXCISION-REPAIR; STRAND BREAK REPAIR; POLY(ADP-RIBOSE) POLYMERASE;
MAMMALIAN-CELLS; LIGASE-III; IN-VITRO; PARP INHIBITION; LIVING CELLS;
PROTEIN; REPLICATION
AB XRCC1 is a scaffold protein capable of interacting with several DNA repair proteins. Here we provide evidence for the presence of XRCC1 in different complexes of sizes from 200 to 1500 kDa, and we show that immunoprecipitates using XRCC1 as bait are capable of complete repair of AP sites via both short patch (SP) and long patch (LP) base excision repair (BER). We show that POL beta and PNK colocalize with XRCC1 in replication foci and that POL beta and PNK, but not PCNA, colocalize with constitutively present XRCC1-foci as well as damage-induced foci when low doses of a DNA-damaging agent are applied. We demonstrate that the laser dose used for introducing DNA damage determines the repertoire of DNA repair proteins recruited. Furthermore, we demonstrate that recruitment of POL beta and PNK to regions irradiated with low laser dose requires XRCC1 and that inhibition of PARylation by PARP-inhibitors only slightly reduces the recruitment of XRCC1, PNK, or POL beta to sites of DNA damage. Recruitment of PCNA and FEN-1 requires higher doses of irradiation and is enhanced by XRCC1, as well as by accumulation of PARP-1 at the site of DNA damage. These data improve our understanding of recruitment of BER proteins to sites of DNA damage and provide evidence for a role of XRCC1 in the organization of BER into multiprotein complexes of different sizes. Environ. Mol. Mutagen. 52:623-635, 2011. (C) 2011 Wiley Periodicals, Inc.
C1 [Hanssen-Bauer, Audun; Solvang-Garten, Karin; Sundheim, Ottar; Pena-Diaz, Javier; Andersen, Sonja; Slupphaug, Geir; Krokan, Hans E.; Akbari, Mansour; Otterlei, Marit] Norwegian Univ Sci & Technol, Fac Med, Dept Canc Res & Mol Med, NO-7489 Trondheim, Norway.
[Wilson, David M., III] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Otterlei, M (reprint author), Norwegian Univ Sci & Technol, Fac Med, Dept Canc Res & Mol Med, NO-7489 Trondheim, Norway.
EM marit.otterlei@ntnu.no
RI Pena-Diaz, Javier/M-6232-2016;
OI Pena-Diaz, Javier/0000-0002-6316-6011; Akbari,
Mansour/0000-0002-6490-7766; Slupphaug, Geir/0000-0002-7498-3500
FU The Research Council of Norway; The National Programme for Research in
Functional Genomics in Norway (FUGE) in The Research Council of Norway;
St. Olavs. Hospital, Trondheim, Norway; The Norwegian Cancer Society;
The Svanhild and Arne Must Fund for Medical Research, Norway; NIH;
National Institute on Aging, USA; European Community
[LSHG-CT-2005-512113]
FX Grant sponsor: The Research Council of Norway; Grant sponsor: The
National Programme for Research in Functional Genomics in Norway (FUGE)
in The Research Council of Norway; Grant sponsor: The Cancer Fund at St.
Olavs. Hospital, Trondheim, Norway; Grant sponsor: The Norwegian Cancer
Society; Grant sponsor: The Svanhild and Arne Must Fund for Medical
Research, Norway; Grant sponsor: The Intramural Research Program of the
NIH; Grant sponsor: National Institute on Aging, USA; Grant sponsor:
Integrated Project on DNA Repair Supported by European Community; Grant
Number LSHG-CT-2005-512113.
NR 54
TC 32
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U1 2
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0893-6692
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PD OCT
PY 2011
VL 52
IS 8
BP 623
EP 635
DI 10.1002/em.20663
PG 13
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 845XQ
UT WOS:000296861100004
PM 21786338
ER
PT J
AU Chandler, RJ
Venditti, CP
AF Chandler, R. J.
Venditti, C. P.
TI Demonstration of pre-clinical efficacy of AAV gene therapy for
methylmalonic acidemia with a transgene suitable for human clinical
trials
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
C1 [Chandler, R. J.; Venditti, C. P.] NHGRI, NIH, Bethesda, MD 20892 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 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 2011
VL 22
IS 10
BP A47
EP A47
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 843WS
UT WOS:000296707900149
ER
PT J
AU Kaler, SG
Donsante, A
Haddad, MR
AF Kaler, Stephen G.
Donsante, Anthony
Haddad, Marie-Reine
TI AAV9 gene therapy rescues a murine model of Menkes disease
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
C1 [Kaler, Stephen G.; Donsante, Anthony; Haddad, Marie-Reine] NICHD, Program Mol Med, 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 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 2011
VL 22
IS 10
BP A77
EP A78
PG 2
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 843WS
UT WOS:000296707900248
ER
PT J
AU Leger, A
Le Guiner, C
Nickerson, ML
Ferry, N
Moullier, P
Snyder, RO
Penaud-Budloo, M
AF Leger, A.
Le Guiner, C.
Nickerson, M. L.
Ferry, N.
Moullier, P.
Snyder, R. O.
Penaud-Budloo, M.
TI Adeno-Associated Viral Vector DNA is insensitive to de novo CpG
methylation but rapidly associated with histone modifications in liver
and skeletal muscle
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
C1 [Leger, A.; Le Guiner, C.; Moullier, P.; Snyder, R. O.; Penaud-Budloo, M.] INSERM, UMR649, Nantes, France.
[Le Guiner, C.; Moullier, P.] GENETHON, Evry, France.
[Nickerson, M. L.] NCI, Canc & Inflammat Program, NIH, Frederick, MD 21701 USA.
[Ferry, N.] INSERM, UMR948, Nantes, France.
[Moullier, P.; Snyder, R. O.] Univ Florida, Coll Med, Dept Mol Genet & Microbiol, Gainesville, FL USA.
[Snyder, R. O.] Univ Florida, CERHB, Alachua, FL 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 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 2011
VL 22
IS 10
BP A103
EP A103
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 843WS
UT WOS:000296707900330
ER
PT J
AU Lynn, G
Laga, R
Fisher, K
Seder, R
Seymour, L
AF Lynn, G.
Laga, R.
Fisher, K.
Seder, R.
Seymour, L.
TI Polymer conjugates of toll-like receptor ligands as vaccine adjuvants
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
C1 [Lynn, G.; Laga, R.; Fisher, K.; Seymour, L.] Univ Oxford, Dept Oncol, Oxford OX3 7DQ, England.
[Seder, R.] NIH, Dept Cellular Immunol, Vaccine Res Ctr, Bethesda, MD 20814 USA.
RI Laga, Richard/G-3627-2014
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 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 2011
VL 22
IS 10
BP A70
EP A70
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 843WS
UT WOS:000296707900224
ER
PT J
AU Yu, DY
Jin, CJ
Leja, JL
Majdalani, NM
Nilsson, BN
Eriksson, FE
Essand, ME
AF Yu, D. Y.
Jin, C. J.
Leja, J. L.
Majdalani, N. M.
Nilsson, B. N.
Eriksson, F. E.
Essand, M. E.
TI Adenovirus with hexon Tat-PTD modification exhibits increased
therapeutic effect in experimental neuroblastoma and neuroendocrine
tumors
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
C1 [Yu, D. Y.; Jin, C. J.; Leja, J. L.; Nilsson, B. N.; Eriksson, F. E.; Essand, M. E.] Uppsala Univ, Uppsala, Sweden.
[Majdalani, N. M.] 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 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD OCT
PY 2011
VL 22
IS 10
BP A29
EP A29
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 843WS
UT WOS:000296707900095
ER
PT J
AU Katsounas, A
Schlaak, JF
Lempicki, RA
AF Katsounas, Antonios
Schlaak, Joerg F.
Lempicki, Richard A.
TI CCL5: A Double-Edged Sword in Host Defense Against the Hepatitis C Virus
SO INTERNATIONAL REVIEWS OF IMMUNOLOGY
LA English
DT Review
DE CCL5 (RANTES); Hepatitis C; Liver Fibrosis
ID CHEMOKINE GENE-EXPRESSION; T-LYMPHOCYTE RESPONSES; STELLATE CELLS;
INTERFERON-ALPHA; CYTOKINE PROFILES; IMMUNE-RESPONSES; CCR5 EXPRESSION;
LIVER-DISEASE; IFN-GAMMA; SEMIQUANTITATIVE ANALYSIS
AB C-C motif ligand 5 (CCL5) facilitates induction of chemotaxis in immune cells and activation of hepatic stellate cells (HSC) at sites of liver inflammation during chronic hepatitis C virus (HCV) infection. Importantly, CCL5 participates in the establishment of T-helper 1 responses crucial in controlling liver disease and HCV infection outcome and demonstrates distinct gene expression patterns between the blood and the liver, stressing the importance of immunoregulatory networks differentially functioning between these compartments. This review illustrates the significance of CCL5-dependent pathways in HCV-related immunopathogenesis by elaborating on biological mechanisms interconnecting peripheral and tissue immunology, liver pathology, HSC activation, and interferon-a immunotherapy.
C1 [Katsounas, Antonios; Schlaak, Joerg F.] Univ Hosp Essen, Dept Gastroenterol & Hepatol, D-45122 Essen, Germany.
[Katsounas, Antonios; Lempicki, Richard A.] NCI Frederick, Lab Immunopathogenesis & Bioinformat, SAIC Frederick Inc, Frederick, MD USA.
RP Katsounas, A (reprint author), Univ Hosp Essen, Dept Gastroenterol & Hepatol, Hufelandstr 55, D-45122 Essen, Germany.
EM antonios.katsounas@uk-essen.de
RI Lempicki, Richard/E-1844-2012;
OI Lempicki, Richard/0000-0002-7059-409X; Schlaak,
Joerg/0000-0002-9499-1014
FU Association for the Promotion of Scientific Research and Science of the
Clinic for Gastroenterology and Hepatology at the University Hospital
Essen (Essen, NRW, Germany); National Cancer Institute, National
Institutes of Health [HHSN261200800001E]
FX This research was funded in part with funds from the Association for the
Promotion of Scientific Research and Science of the Clinic for
Gastroenterology and Hepatology at the University Hospital Essen (Essen,
NRW, Germany) and in part with federal funds from the National Cancer
Institute, National Institutes of Health, under Contract No.
HHSN261200800001E. The illustration is the work of Jiro, Wada from the
Scientific Publications, Graphics & Media (SPGM), Information Systems
Program, SAIC-Frederick, Inc. National Cancer Institute at Frederick.
NR 105
TC 11
Z9 12
U1 0
U2 7
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0883-0185
J9 INT REV IMMUNOL
JI Int. Rev. Immunol.
PD OCT-DEC
PY 2011
VL 30
IS 5-6
BP 366
EP 378
DI 10.3109/08830185.2011.593105
PG 13
WC Immunology
SC Immunology
GA 843GY
UT WOS:000296661500008
PM 22053974
ER
PT J
AU Deater-Deckard, K
Lansford, JE
Malone, PS
Alampay, LP
Sorbring, E
Bacchini, D
Bombi, AS
Bornstein, MH
Chang, L
Di Giunta, L
Dodge, KA
Oburu, P
Pastorelli, C
Skinner, AT
Tapanya, S
Tirado, LMU
Zelli, A
Al-Hassan, SM
AF Deater-Deckard, Kirby
Lansford, Jennifer E.
Malone, Patrick S.
Pena Alampay, Liane
Sorbring, Emma
Bacchini, Dario
Bombi, Anna Silvia
Bornstein, Marc H.
Chang, Lei
Di Giunta, Laura
Dodge, Kenneth A.
Oburu, Paul
Pastorelli, Concetta
Skinner, Ann T.
Tapanya, Sombat
Uribe Tirado, Liliana Maria
Zelli, Arnaldo
Al-Hassan, Suha M.
TI The Association Between Parental Warmth and Control in Thirteen Cultural
Groups
SO JOURNAL OF FAMILY PSYCHOLOGY
LA English
DT Article
DE socialization; parenting; parent-child relations; culture
AB The goal of the current study was to investigate potential cross-cultural differences in the covariation between two of the major dimensions of parenting behavior: control and warmth. Participants included 1,421 (51% female) 7- to 10-year-old (M = 8.29, SD = .67 years) children and their mothers and fathers representing 13 cultural groups in nine countries in Africa, Asia, Europe, the Middle East, and North and South America. Children and parents completed questionnaires and interviews regarding mother and father control and warmth. Greater warmth was associated with more control, but this association varied widely between cultural groups.
C1 [Deater-Deckard, Kirby] Virginia Tech, Dept Psychol, Blacksburg, VA 24061 USA.
[Lansford, Jennifer E.; Dodge, Kenneth A.; Skinner, Ann T.] Duke Univ, Ctr Child & Family Policy, Durham, NC 27706 USA.
[Malone, Patrick S.] Univ S Carolina, Dept Psychol, Columbia, SC 29208 USA.
[Pena Alampay, Liane] Ateneo Manila Univ, Dept Psychol, Manila, Philippines.
[Bacchini, Dario] Univ Naples 2, Dept Psychol, Naples, Italy.
[Bombi, Anna Silvia; Di Giunta, Laura; Pastorelli, Concetta; Uribe Tirado, Liliana Maria] Sapienza Univ Rome, Dept Psychol, Rome, Italy.
[Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Child & Family Res, Eunice, LA USA.
[Chang, Lei] Chinese Univ Hong Kong, Dept Educ Psychol, Hong Kong, Hong Kong, Peoples R China.
[Oburu, Paul] Maseno Univ, Dept Educ Psychol, Maseno, Kenya.
[Tapanya, Sombat] Chiang Mai Univ, Dept Psychiat, Chiang Mai, Thailand.
[Zelli, Arnaldo] Univ Rome Foro Italico Italy, Dept Sports Psychol, Rome, Italy.
[Al-Hassan, Suha M.] Hashemite Univ, Dept Child Educ, Zarqa, Jordan.
RP Deater-Deckard, K (reprint author), Virginia Tech, Dept Psychol, 109 Williams Hall 0436, Blacksburg, VA 24061 USA.
EM kirbydd@vt.edu
RI Malone, Patrick/F-6851-2011; Eclevia, Marian/I-6486-2013; ZELLI,
ARNALDO/N-2333-2015;
OI Malone, Patrick/0000-0002-8364-6987; ZELLI, ARNALDO/0000-0003-4020-8159;
Bacchini, Dario/0000-0001-6140-9377
FU FIC NIH HHS [R03 TW008141, R03 TW008141-01]; NICHD NIH HHS [R01
HD054805, R01 HD054805-01A1]; NIDA NIH HHS [K01 DA024116, K01
DA024116-01A1, K05 DA015226, K05 DA015226-01]
NR 20
TC 24
Z9 24
U1 2
U2 119
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0893-3200
J9 J FAM PSYCHOL
JI J. Fam. Psychol.
PD OCT
PY 2011
VL 25
IS 5
BP 790
EP 794
DI 10.1037/a0025120
PG 5
WC Psychology, Clinical; Family Studies
SC Psychology; Family Studies
GA 836DA
UT WOS:000296087800019
PM 21875202
ER
PT J
AU Hansson, AC
Rimondini, R
Heilig, M
Mathe, AA
Sommer, WH
AF Hansson, Anita C.
Rimondini, Roberto
Heilig, Markus
Mathe, Aleksander A.
Sommer, Wolfgang H.
TI Dissociation of antidepressant-like activity of escitalopram and
nortriptyline on behaviour and hippocampal BDNF expression in female
rats
SO JOURNAL OF PSYCHOPHARMACOLOGY
LA English
DT Article
DE Depression; forced swim test; PCR; SSRI
ID NEUROTROPHIC FACTOR EXPRESSION; NERVE GROWTH-FACTOR; FLINDERS SENSITIVE
LINE; TREATMENT-RESISTANT DEPRESSION; MESSENGER-RNA; DIFFERENTIAL
REGULATION; ANIMAL-MODEL; ELECTROCONVULSIVE STIMULI; LEARNED
HELPLESSNESS; CELL-PROLIFERATION
AB A major hypothesis of depression postulates that a dysregulation of the neurotrophin systems is directly involved in the pathophysiology of depression, and that restoration of such deficits may underlie the therapeutic efficacy of antidepressant treatment. One key finding supporting this hypothesis is upregulation of brain derived neurotrophic factor (BDNF) in the hippocampus after antidepressant treatment. Here, we further test the hypothesis of BDNF involvement in antidepressant action in a genetic rat model of depression after chronic oral treatment with escitalopram, nortriptyline or placebo. Active treatments had significant behavioural antidepressant-like actions in female rats of the Flinders Sensitive Line (FSL) and non-selected Sprague Dawley (SD) rats, while Flinders Resistant Line (FRL) rats were unaffected. Escitalopram, but not norbiptyline, markedly reduced BDNF mRNA levels in the dentate gyrus of FSL rats. The BDNF downregulation was common to the four major promoters of the gene. Treatments did not affect BDNF expression in FRL or SD strains. We conclude that the antidepressant effects of escitalopram and nortriptyline, two common drugs with different pharmacological profiles, appear to be unrelated to the regulation of hippocampal BDNF expression in female rats. These results indicate that the tropic hypothesis of depression has limitations and emphasize the need for validated disease models of depression to assess potential treatment targets.
C1 [Hansson, Anita C.; Sommer, Wolfgang H.] Cent Inst Mental Hlth, Department Psychopharmacol, D-68159 Mannheim, Germany.
[Hansson, Anita C.; Heilig, Markus; Sommer, Wolfgang H.] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Rimondini, Roberto] Univ Bologna, Dept Pharmacol, Bologna, Italy.
[Mathe, Aleksander A.] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
RP Sommer, WH (reprint author), Cent Inst Mental Hlth, Department Psychopharmacol, Sq 35, D-68159 Mannheim, Germany.
EM aleksander.mathe@ki.se; wolfgang.sommer@zi-mannheim.de
OI roberto, rimondini/0000-0003-4099-513X
FU NIAAA; Swedish Medical Research Council [10414]; Karolinska Institute
FX This work was supported by the intramural research funds of NIAAA, the
Swedish Medical Research Council (grant number 10414 to AAM) and the
Karolinska Institute. The sponsors had no further role in study design:
in the collection, analysis and interpretation of data; in the writing
or the report; and in the decision to submit the paper for publication.
NR 78
TC 14
Z9 14
U1 0
U2 2
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0269-8811
J9 J PSYCHOPHARMACOL
JI J. Psychopharmacol.
PD OCT
PY 2011
VL 25
IS 10
BP 1378
EP 1387
DI 10.1177/0269881110393049
PG 10
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 846JH
UT WOS:000296892800014
PM 21262856
ER
PT J
AU Saubern, S
Guha, R
Baell, JB
AF Saubern, Simon
Guha, Rajarshi
Baell, Jonathan B.
TI KNIME Workflow to Assess PAINS Filters in SMARTS Format. Comparison of
RDKit and Indigo Cheminformatics Libraries
SO MOLECULAR INFORMATICS
LA English
DT Article
DE Chemoinformatics; Drug discovery; High-throughput screening; Virtual
screening
ID SOURCE JAVA LIBRARY; DEVELOPMENT KIT CDK; DRUG DISCOVERY
C1 [Saubern, Simon] CSIRO Mat Sci & Engn, Clayton, Vic 3169, Australia.
[Guha, Rajarshi] NIH, Ctr Translat Therapeut, Rockville, MD 20850 USA.
[Baell, Jonathan B.] Walter & Eliza Hall Inst Med Res, Parkville, Vic 3052, Australia.
[Baell, Jonathan B.] Univ Melbourne, Dept Med Biol, Parkville, Vic 3010, Australia.
RP Saubern, S (reprint author), CSIRO Mat Sci & Engn, Bag 10, Clayton, Vic 3169, Australia.
EM jbaell@wehi.edu.au
RI Saubern, Simon/F-7538-2012; Baell, Jonathan/E-5844-2017
OI Saubern, Simon/0000-0002-1989-4951; Baell, Jonathan/0000-0003-2114-8242
NR 20
TC 28
Z9 28
U1 2
U2 17
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1868-1743
J9 MOL INFORM
JI Mol. Inf.
PD OCT
PY 2011
VL 30
IS 10
BP 847
EP 850
DI 10.1002/minf.201100076
PG 4
WC Chemistry, Medicinal; Computer Science, Interdisciplinary Applications;
Mathematical & Computational Biology
SC Pharmacology & Pharmacy; Computer Science; Mathematical & Computational
Biology
GA 846LD
UT WOS:000296900100002
PM 27468104
ER
PT J
AU Nahab, FB
Wittevrongel, L
Ippolito, D
Toro, C
Grimes, GJ
Starling, J
Potti, G
Haubenberger, D
Bowen, D
Buchwald, P
Dong, CH
Kalowitz, D
Hallett, M
AF Nahab, Fatta B.
Wittevrongel, Loretta
Ippolito, Dominic
Toro, Camilo
Grimes, George J.
Starling, Judith
Potti, Gopal
Haubenberger, Dietrich
Bowen, Daniel
Buchwald, Peter
Dong, Chuanhui
Kalowitz, Daniel
Hallett, Mark
TI An Open-Label, Single-Dose, Crossover Study of the Pharmacokinetics and
Metabolism of Two Oral Formulations of 1-Octanol in Patients with
Essential Tremor
SO NEUROTHERAPEUTICS
LA English
DT Article
DE 1-Octanol; Octanoic acid; Essential tremor; Alcohol; Therapeutics;
Spirography
ID HARMALINE-INDUCED TREMOR; ALCOHOL-DEHYDROGENASE; OCTANOIC-ACID;
INTOXICATION
AB Existing therapeutic options for management of essential tremor are frequently limited by poor efficacy and adverse effects. Likely the most potent tremor suppressant used is ethanol, although its use is prohibitive due to a brief therapeutic window, and the obvious implications of excessive alcohol use. Longer-chain alcohols have been shown to suppress tremor in harmaline animal models, and appear to be safe and well tolerated in 2 prior studies in humans. Here we report on the findings of a phase I/II study of 1-octanol designed to explore pharmacokinetics, efficacy, and safety. The most significant finding was the identification of octanoic acid as the product of rapid 1-octanol metabolism. Furthermore, the temporal profile of efficacy closely matches the plasma concentration of octanoic acid. Therefore, these findings identify a novel class of compound (e.g., carboxylic acids) with tremor suppressive properties in ET. Administration of 1-octanol also appears to be safe based on various measures collected. Essential tremor (ET) is the most common tremor disorder, with tremors occurring during static posturing or movement. These tremors are known to briefly improve in many cases after alcohol (ethanol) consumption. Two previous studies of a longer chain alcohol, 1-octanol, have demonstrated longer duration tremor-suppressive effects without the occurrence of intoxication. The aim of this study was to characterize the pharmacokinetics of 1-octanol and its primary metabolite octanoic acid using two formulations, along with additional safety and efficacy measures. Participants with proven ethanol-responsive ET were recruited into 1 of 2 parts: (part A) a dose escalation study (1-64 mg/kg; n = 4), and (part B) a fixed dose (64 mg/kg; n = 10) balanced, open-label crossover design. Two participants in part B then completed an exploratory part C evaluating 128 mg/kg.Plasma samples were collected at 10 intervals during a 6-hour period postingestion. Efficacy was assessed using spirography, whereas safety was assessed with electrocardiograms, vital signs, adverse effects surveys, and an intoxication assessment. Plasma concentrations of 1-octanol were detectable at low levels whereas octanoic acid (OA) concentrations were approximately 100-fold higher. The half-life of OA was 87.6minutes. This was matched by a clinical reduction in tremor severity of 32% at 90 minutes, assessed using spirography. The safety profile was favorable, with the most commonly reported adverse effect being dysgeusia (38%). Early detection and higher plasma concentrations of OA are a product of rapid metabolism of 1-octanol.OA pharmacokinetics mirrored the timing of clinical improvement. These findings provide preliminary evidence for a new class of compound that may be effective in the treatment of ET.
C1 [Nahab, Fatta B.; Dong, Chuanhui] Univ Miami, Miller Sch Med, Dept Neurol, Miami, FL 33136 USA.
[Wittevrongel, Loretta; Ippolito, Dominic; Toro, Camilo; Haubenberger, Dietrich; Hallett, Mark] NINDS, Human Motor Control Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Grimes, George J.; Starling, Judith; Potti, Gopal] NIH, Pharmaceut Dev Sect, Bethesda, MD 20892 USA.
[Haubenberger, Dietrich] Med Univ Vienna, Dept Neurol, Vienna, Austria.
[Bowen, Daniel] Wake Forest Univ, Winston Salem, NC 27106 USA.
[Buchwald, Peter] Univ Miami, Miller Sch Med, Dept Mol & Cellular Pharmacol, Miami, FL 33136 USA.
[Kalowitz, Daniel] Albert Einstein Coll Med, Bronx, NY 10461 USA.
RP Nahab, FB (reprint author), Univ Miami, Miller Sch Med, Dept Neurol, Miami, FL 33136 USA.
EM fnahab@med.miami.edu
OI Buchwald, Peter/0000-0003-2732-8180
FU Intramural division of the National Institute of Neurological Disorders
and Stroke; Ariston PharmaceuticalsNational Institute of Neurological
Disorders and Stroke (NINDS); Austrian Science Fund FWF (Erwin
Schroedinger Fellowship) [J2783-B09]; Neurotoxin Institute; Blackwell
Publisher; Cambridge University Press; Springer Verlag; Taylor Francis
Group; Oxford University Press; John Wiley Sons; Elsevier; Ariston
Pharmaceuticals; National Institutes of Health (NIH)/NINDS; U.S.
Department of Defense (Army); NIH (from Brainsway); NIH; U.S. Army via
the Henry Jackson Foundation; Ariston Pharmaceutical Company via a
Cooperative Research and Development Agreement (CRADA); Kinetics
Foundation via a Clinical Trials Agreement (CTA)
FX This work was supported by the Intramural division of the National
Institute of Neurological Disorders and Stroke and a collaborative
research and development agreement with Ariston Pharmaceuticals; Dr.
Haubenberger received research support through the National Institute of
Neurological Disorders and Stroke (NINDS) Intramural Research Program
and the Austrian Science Fund FWF (Erwin Schroedinger Fellowship,
project no. J2783-B09); Dr. Hallett serves as Chair of the Medical
Advisory Board and receives funding for travel from the Neurotoxin
Institute; serves as Chair of the Medical Advisory Board of the Benign
Essential Blepharospasm Foundation and Chair of the Medical Advisory
Board of the International Essential Tremor Foundation; Dr. Hallett has
received honoraria and/or funding for travel for lectures or educational
activities not funded by industry; and serves on Editorial Advisory
Boards for Clinical Neurophysiology, Brain, Acta Neurologica
Scandinavica, Journal of Clinical Neurophysiology, Italian Journal of
Neurological Sciences, Medical Problems of Performing Artists, Annals of
Neurology, Neurology and Clinical Neurophysiology, The Cerebellum,
NeuroRx, Current Trends in Neurology, Faculty of 1000 Biology, Faculty
of 1000 Medicine, Brain Stimulation, Journal of Movement Disorders
(Korea), and World Neurology. Dr. Hallett may accrue revenue on U.S.
Patent #6,780,413 B2 (issued: August 24, 2004): immunotoxin (MAB-Ricin)
for the treatment of focal movement disorders; U. S. Patent #7,407,478
(issued: August 5, 2008): coil for magnetic stimulation and methods for
using the same; receives royalties from publishing from Blackwell
Publisher, Cambridge University Press, Springer Verlag, Taylor & Francis
Group, Oxford University Press, John Wiley & Sons, and Elsevier; Dr.
Hallett receives research support from Ariston Pharmaceuticals, National
Institutes of Health (NIH)/NINDS (Intramural Program) and the U.S.
Department of Defense (Army); Dr. Hallett has received license fee
payments from the NIH (from Brainsway) for licensing the patent for the
H-coil. Dr. Hallett's research at the NIH is largely supported by the
NIH Intramural Program. Supplemental research funds come from the U.S.
Army via the Henry Jackson Foundation, Ariston Pharmaceutical Company
via a Cooperative Research and Development Agreement (CRADA) with the
NIH, and the Kinetics Foundation via a Clinical Trials Agreement (CTA)
with the NIH. Dr. Hallett is an inventor for patent applications of
1-octanol and octanoic acid held by NINDS/NIH.
NR 21
TC 13
Z9 13
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1933-7213
J9 NEUROTHERAPEUTICS
JI Neurotherapeutics
PD OCT
PY 2011
VL 8
IS 4
BP 753
EP 762
DI 10.1007/s13311-011-0045-1
PG 10
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 844FS
UT WOS:000296733700019
PM 21594724
ER
PT J
AU Crocker, MK
Yanovski, JA
AF Crocker, Melissa K.
Yanovski, Jack A.
TI Pediatric Obesity: Etiology and Treatment
SO PEDIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Overweight; Differential diagnosis; Pharmacotherapy; Bariatric surgery;
Adiposity; Leptin
ID EARLY-ONSET OBESITY; BODY-MASS INDEX; GENOME-WIDE ASSOCIATION;
CONGENITAL LEPTIN DEFICIENCY; GASTRIC BYPASS-SURGERY; EXPERT COMMITTEE
RECOMMENDATIONS; RANDOMIZED CONTROLLED-TRIAL; TYPE-2 DIABETES-MELLITUS;
PLACEBO-CONTROLLED TRIAL; GLUCAGON-LIKE PEPTIDE-1
AB This article reviews factors that contribute to excessive weight gain in children and outlines current knowledge regarding approaches for treating pediatric obesity. Most of the known genetic causes of obesity primarily increase energy intake. Genes regulating the leptin signaling pathway are particularly important for human energy homeostasis. Obesity is a chronic disorder that requires long-term strategies for management. The foundation for all treatments for pediatric obesity remains restriction of energy intake with lifestyle modification. There are few long-term studies of pharmacotherapeutic interventions for pediatric obesity. Bariatric surgical approaches are the most efficacious treatment but, because of their potential risks, are reserved for those with the most significant complications of obesity.
C1 [Crocker, Melissa K.; Yanovski, Jack A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Growth & Obes, Program Dev Endocrinol & Genet, NIH,Dept Hlth & Human Serv,Hatfield Clin Res Ctr, Bethesda, MD USA.
RP Yanovski, JA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Growth & Obes, Program Dev Endocrinol & Genet, NIH,Dept Hlth & Human Serv,Hatfield Clin Res Ctr, Bethesda, MD USA.
EM jy15i@nih.gov
OI Yanovski, Jack/0000-0001-8542-1637
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development
FX This research was supported by the Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development. Dr Yanovski is a Commissioned Officer in the United States
Public Health Service, Department of Health and Human Services. Unit on
Growth and Obesity, Program in Developmental Endocrinology and Genetics,
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services, 9000 Rockville Pike, Hatfield Clinical Research Center,
Room 1-3330, MSC 1103, Bethesda, MD, 20892-1103, USA
NR 160
TC 20
Z9 21
U1 0
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0031-3955
EI 1557-8240
J9 PEDIATR CLIN N AM
JI Pediatr. Clin. N. Am.
PD OCT
PY 2011
VL 58
IS 5
BP 1217
EP +
DI 10.1016/j.pcl.2011.07.004
PG 25
WC Pediatrics
SC Pediatrics
GA 843NM
UT WOS:000296678700010
PM 21981957
ER
PT J
AU An, P
Li, RL
Wang, JM
Yoshimura, T
Takahashi, M
Samudralal, R
O'Brien, SJ
Phair, J
Goedert, JJ
Kirk, GD
Troyer, JL
Sezgin, E
Buchbinder, SP
Donfield, S
Nelson, GW
Winkler, CA
AF An, Ping
Li, Rongling
Wang, Ji Ming
Yoshimura, Teizo
Takahashi, Munehisa
Samudralal, Ram
O'Brien, Stephen J.
Phair, John
Goedert, James J.
Kirk, Gregory D.
Troyer, Jennifer L.
Sezgin, Efe
Buchbinder, Susan P.
Donfield, Sharyne
Nelson, George W.
Winkler, Cheryl A.
TI Role of Exonic Variation in Chemokine Receptor Genes on AIDS: CCRL2
F167Y Association with Pneumocystis Pneumonia
SO PLOS GENETICS
LA English
DT Article
ID HIV-1 DISEASE PROGRESSION; IMMUNODEFICIENCY-VIRUS TYPE-1; GENOME-WIDE
ASSOCIATION; INJECTION-DRUG USERS; AFRICAN-AMERICANS; CORECEPTOR USAGE;
INFECTION; CCR5; POLYMORPHISM; INDIVIDUALS
AB Chromosome 3p21-22 harbors two clusters of chemokine receptor genes, several of which serve as major or minor coreceptors of HIV-1. Although the genetic association of CCR5 and CCR2 variants with HIV-1 pathogenesis is well known, the role of variation in other nearby chemokine receptor genes remain unresolved. We genotyped exonic single nucleotide polymorphisms (SNPs) in chemokine receptor genes: CCR3, CCRL2, and CXCR6 (at 3p21) and CCR8 and CX3CR1 (at 3p22), the majority of which were non-synonymous. The individual SNPs were tested for their effects on disease progression and outcomes in five treatment-naive HIV-1/AIDS natural history cohorts. In addition to the known CCR5 and CCR2 associations, significant associations were identified for CCR3, CCR8, and CCRL2 on progression to AIDS. A multivariate survival analysis pointed to a previously undetected association of a non-conservative amino acid change F167Y in CCRL2 with AIDS progression: 167F is associated with accelerated progression to AIDS (RH = 1.90, P = 0.002, corrected). Further analysis indicated that CCRL2-167F was specifically associated with more rapid development of pneumocystis pneumonia (PCP) (RH = 2.84, 95% CI 1.28-6.31) among four major AIDS-defining conditions. Considering the newly defined role of CCRL2 in lung dendritic cell trafficking, this atypical chemokine receptor may affect PCP through immune regulation and inducing inflammation.
C1 [An, Ping; Winkler, Cheryl A.] NCI, Basic Res Lab, SAIC Frederick, Frederick, MD 21701 USA.
[Li, Rongling] NHGRI, Off Populat Genom, Bethesda, MD 20892 USA.
[Wang, Ji Ming; Yoshimura, Teizo; Takahashi, Munehisa] NCI, Mol Immunoregulat Lab, Frederick, MD 21701 USA.
[Samudralal, Ram] Univ Washington, Sch Med, Dept Microbiol, Seattle, WA 98195 USA.
[O'Brien, Stephen J.; Sezgin, Efe] NCI, Lab Genom Divers, Frederick, MD 21701 USA.
[Phair, John] Northwestern Univ, Div Infect Dis, Feinberg Sch Med, Sch Med, Chicago, IL USA.
[Goedert, James J.] NCI, Infect & Immunoepidemiol Branch, Bethesda, MD 20892 USA.
[Kirk, Gregory D.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Troyer, Jennifer L.; Nelson, George W.] NCI, BSP CCR Genet Core, SAIC Frederick, Frederick, MD 21701 USA.
[Buchbinder, Susan P.] San Francisco Dept Publ Hlth, San Francisco, CA USA.
[Donfield, Sharyne] Rho, Chapel Hill, NC USA.
RP An, P (reprint author), NCI, Basic Res Lab, SAIC Frederick, Frederick, MD 21701 USA.
EM pingan@nih.gov; winklerc@mail.nih.gov
RI Troyer, Jennifer/B-8415-2012; Sezgin, Efe/B-8418-2012;
OI Sezgin, Efe/0000-0002-8000-7485; O'Brien, Stephen J./0000-0001-7353-8301
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; NIH, National Cancer Institute, Center for Cancer
Research
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract HHSN261200800001E. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. Government.
This Research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 75
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PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD OCT
PY 2011
VL 7
IS 10
AR e1002328
DI 10.1371/journal.pgen.1002328
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 843IL
UT WOS:000296665400029
PM 22046140
ER
PT J
AU Avery, CL
He, QC
North, KE
Ambite, JL
Boerwinkle, E
Fornage, M
Hindorff, LA
Kooperberg, C
Meigs, JB
Pankow, JS
Pendergrass, SA
Psaty, BM
Ritchie, MD
Rotter, JI
Taylor, KD
Wilkens, LR
Heiss, G
Lin, DY
AF Avery, Christy L.
He, Qianchuan
North, Kari E.
Ambite, Jose L.
Boerwinkle, Eric
Fornage, Myriam
Hindorff, Lucia A.
Kooperberg, Charles
Meigs, James B.
Pankow, James S.
Pendergrass, Sarah A.
Psaty, Bruce M.
Ritchie, Marylyn D.
Rotter, Jerome I.
Taylor, Kent D.
Wilkens, Lynne R.
Heiss, Gerardo
Lin, Dan Yu
TI A Phenomics-Based Strategy Identifies Loci on APOC1, BRAP, and PLCG1
Associated with Metabolic Syndrome Phenotype Domains
SO PLOS GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; C-REACTIVE PROTEIN; PLASMINOGEN-ACTIVATOR
INHIBITOR-1; CORONARY-ARTERY-DISEASE; INSULIN-RESISTANCE; GENETIC-LOCI;
SIGNAL-TRANSDUCTION; DIABETES RISK; HEART; OBESITY
AB Despite evidence of the clustering of metabolic syndrome components, current approaches for identifying unifying genetic mechanisms typically evaluate clinical categories that do not provide adequate etiological information. Here, we used data from 19,486 European American and 6,287 African American Candidate Gene Association Resource Consortium participants to identify loci associated with the clustering of metabolic phenotypes. Six phenotype domains (atherogenic dyslipidemia, vascular dysfunction, vascular inflammation, pro-thrombotic state, central obesity, and elevated plasma glucose) encompassing 19 quantitative traits were examined. Principal components analysis was used to reduce the dimension of each domain such that >55% of the trait variance was represented within each domain. We then applied a statistically efficient and computational feasible multivariate approach that related eight principal components from the six domains to 250,000 imputed SNPs using an additive genetic model and including demographic covariates. In European Americans, we identified 606 genome-wide significant SNPs representing 19 loci. Many of these loci were associated with only one trait domain, were consistent with results in African Americans, and overlapped with published findings, for instance central obesity and FTO. However, our approach, which is applicable to any set of interval scale traits that is heritable and exhibits evidence of phenotypic clustering, identified three new loci in or near APOC1, BRAP, and PLCG1, which were associated with multiple phenotype domains. These pleiotropic loci may help characterize metabolic dysregulation and identify targets for intervention.
C1 [Avery, Christy L.; North, Kari E.; Heiss, Gerardo] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27515 USA.
[He, Qianchuan; Lin, Dan Yu] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
[Ambite, Jose L.] Univ So Calif, Inst Informat Sci, Los Angeles, CA USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr, Div Epidemiol, Houston, TX USA.
[Boerwinkle, Eric; Fornage, Myriam] Univ Texas Hlth Sci Ctr, Ctr Human Genet, Houston, TX USA.
[Hindorff, Lucia A.] NHGRI, Off Populat Gen, NIH, Bethesda, MD 20892 USA.
[Kooperberg, Charles] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Meigs, James B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Meigs, James B.] Harvard Univ, Sch Med, Boston, MA USA.
[Pankow, James S.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Pendergrass, Sarah A.; Ritchie, Marylyn D.] Vanderbilt Univ, Med Ctr, Ctr Human Genet Res, Nashville, TN USA.
[Psaty, Bruce M.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Psaty, Bruce M.] Univ Washington, Dept Epidemiol, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Psaty, Bruce M.] Grp Hlth Res Inst, Grp Hlth Cooperat, Seattle, WA USA.
[Rotter, Jerome I.; Taylor, Kent D.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
[Wilkens, Lynne R.] Univ Hawaii, Canc Res Ctr, Honolulu, HI 96813 USA.
RP Avery, CL (reprint author), Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27515 USA.
EM christy_avery@unc.edu
RI Ritchie, Marylyn/C-1114-2012;
OI Pankow, James/0000-0001-7076-483X
FU NIH/NHGRI [U01 HG004798]; NIH/NHLBI, U.S. Department of Health and Human
Services [N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115,
32118-32119, 32122, 42107-26, 42129-32, 44221, U01 HG004790]; National
Cancer Institute [R37CA54281, R01 CA63, P01CA33619, U01CA136792,
U01CA98758]; National Heart, Lung, and Blood Institute; NHLBI
[K99-HL-098458]; NIDDK [K24 DK080140, R01 DK078616]
FX PAGE: Support for the Genetic Epidemiology of Causal Variants Across the
Life Course (CALiCo) was provided through the National Human Genome
Research Institute's Population Architecture Using Genomics and
Epidemiology (PAGE) network (U01 HG004803). EAGLE work was funded by
NIH/NHGRI grant U01 HG004798. The WHI program is funded by NIH/NHLBI,
U.S. Department of Health and Human Services, through contracts
N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115,
32118-32119, 32122, 42107-26, 42129-32, 44221, and U01 HG004790. Funding
support for the Multiethnic Cohort study was provided through the
National Cancer Institute (R37CA54281, R01 CA63, P01CA33619,
U01CA136792, and U01CA98758) and NHGRI (U01 HG004802). CARe: The authors
wish to acknowledge the support of the National Heart, Lung, and Blood
Institute and the contributions of the research institutions, study
investigators, field staff, and study participants in creating this
resource for biomedical research. The following five parent studies
contributed parent study data, ancillary study data, and DNA samples
through the Broad Institute (N01-HC-65226) to create this
genotype/phenotype data base for wide dissemination to the biomedical
research community: Atherosclerosis Risk in Communities (ARIC):
University of North Carolina at Chapel Hill (N01-HC-55015), Baylor
Medical College (N01-HC55016), University of Mississippi Medical Center
(N01-HC-55021), University of Minnesota (N01-HC-55019), Johns Hopkins
University (N01-HC-55020), University of Texas, Houston (N01-HC-55017);
Cardiovascular Health Study (CHS): University of Washington
(N01-HC-85079), Wake Forest University (N01-HC-85080), Johns Hopkins
University (N01-HC-85081), University of Pittsburgh (N01-HC-85082),
University of California Davis (N01-HC-85083), University of California
Irvine (N01-HC85084), New England Medical Center (N01-HC-85085),
University of Vermont (N01-HC-85086), Georgetown University
(N01-HC-35129), Johns Hopkins University (N01 HC-15103), University of
Wisconsin (N01-HC-75150), Geisinger Clinic (N01-HC-45133), University of
Washington (N01 HC-55222, U01 HL080295); Coronary Artery Risk in Young
Adults (CARDIA): University of Alabama at Birmingham (N01-HC-48047),
University of Minnesota (N01-HC-48048), Northwestern University
(N01-HC-48049), Kaiser Foundation Research Institute (N01-HC-48050),
University of Alabama at Birmingham (N01-HC-95095), Tufts-New England
Medical Center (N01-HC-45204), Wake Forest University (N01-HC-45205),
Harbor-UCLA Research and Education Institute (N01-HC-05187), University
of California Irvine (N01-HC45134, N01-HC-95100); Framingham Heart Study
(FHS): Boston University (N01-HC-25195); Multi-Ethnic Study of
Atherosclerosis (MESA): University of Washington (N01-HC-95159), Regents
of the University of California (N01-HC-95160), Columbia University
(N01-HC-95161), Johns Hopkins University (N01-HC-95162), University of
Minnesota (N01-HC-95163), Northwestern University (N01-HC-95164), Wake
Forest University (N01-HC-95165), University of Vermont (N01-HC95166),
New England Medical Center (N01-HC-95167), Johns Hopkins University
(N01-HC-95168), Harbor-UCLA Research and Education Institute
(N01-HC-95169). CLA was supported by grant K99-HL-098458 from the NHLBI.
JBM was supported by grants K24 DK080140 and R01 DK078616 from the
NIDDK. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 61
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PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD OCT
PY 2011
VL 7
IS 10
AR e1002322
DI 10.1371/journal.pgen.1002322
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 843IL
UT WOS:000296665400023
PM 22022282
ER
PT J
AU Moore, LE
Nickerson, ML
Brennan, P
Toro, JR
Jaeger, E
Rinsky, J
Han, SS
Zaridze, D
Matveev, V
Janout, V
Kollarova, H
Bencko, V
Navratilova, M
Szeszenia-Dabrowska, N
Mates, D
Schmidt, LS
Lenz, P
Karami, S
Linehan, WM
Merino, M
Chanock, S
Boffetta, P
Chow, WH
Waldman, FM
Rothman, N
AF Moore, Lee E.
Nickerson, Michael L.
Brennan, Paul
Toro, Jorge R.
Jaeger, Erich
Rinsky, Jessica
Han, Summer S.
Zaridze, David
Matveev, Vsevolod
Janout, Vladimir
Kollarova, Hellena
Bencko, Vladimir
Navratilova, Marie
Szeszenia-Dabrowska, Neonilia
Mates, Dana
Schmidt, Laura S.
Lenz, Petra
Karami, Sara
Linehan, W. Marston
Merino, Maria
Chanock, Stephen
Boffetta, Paolo
Chow, Wong-Ho
Waldman, Frederic M.
Rothman, Nathaniel
TI Von Hippel-Lindau (VHL) Inactivation in Sporadic Clear Cell Renal
Cancer: Associations with Germline VHL Polymorphisms and Etiologic Risk
Factors
SO PLOS GENETICS
LA English
DT Article
ID TUMOR-SUPPRESSOR GENE; COMPARATIVE GENOMIC HYBRIDIZATION; KIDNEY CANCER;
TRICHLOROETHYLENE EXPOSURE; COLORECTAL-CANCER; SOMATIC MUTATIONS;
CENTRAL-EUROPE; POOR SURVIVAL; LINKAGE PHASE; CARCINOMA
AB Renal tumor heterogeneity studies have utilized the von Hippel-Lindau VHL gene to classify disease into molecularly defined subtypes to examine associations with etiologic risk factors and prognosis. The aim of this study was to provide a comprehensive analysis of VHL inactivation in clear cell renal tumors (ccRCC) and to evaluate relationships between VHL inactivation subgroups with renal cancer risk factors and VHL germline single nucleotide polymorphisms (SNPs). VHL genetic and epigenetic inactivation was examined among 507 sporadic RCC/470 ccRCC cases using endonuclease scanning and using bisulfite treatment and Sanger sequencing across 11 CpG sites within the VHL promoter. Case-only multivariate analyses were conducted to identify associations between alteration subtypes and risk factors. VHL inactivation, either through sequence alterations or promoter methylation in tumor DNA, was observed among 86.6% of ccRCC cases. Germline VHL SNPs and a haplotype were associated with promoter hypermethylation in tumor tissue (OR = 6.10; 95% CI: 2.28-16.35, p = 3.76E-4, p-global = 8E-5). Risk of having genetic VHL inactivation was inversely associated with smoking due to a higher proportion of wild-type ccRCC tumors [former: OR = 0.70 (0.20-1.31) and current: OR = 0.56 (0.32-0.99); P-trend = 0.04]. Alteration prevalence did not differ by histopathologic characteristics or occupational exposure to trichloroethylene. ccRCC cases with particular VHL germline polymorphisms were more likely to have VHL inactivation through promoter hypermethylation than through sequence alterations in tumor DNA, suggesting that the presence of these SNPs may represent an example of facilitated epigenetic variation (an inherited propensity towards epigenetic variation) in renal tissue. A proportion of tumors from current smokers lacked VHL alterations and may represent a biologically distinct clinical entity from inactivated cases.
C1 [Moore, Lee E.; Toro, Jorge R.; Rinsky, Jessica; Han, Summer S.; Karami, Sara; Chanock, Stephen; Chow, Wong-Ho; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Nickerson, Michael L.; Boffetta, Paolo] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Brennan, Paul] Int Agcy Res Canc, F-69372 Lyon, France.
[Jaeger, Erich; Waldman, Frederic M.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Zaridze, David; Matveev, Vsevolod] Russian Acad Med Sci, Canc Res Ctr, Inst Carcinogenesis, Moscow, Russia.
[Janout, Vladimir; Kollarova, Hellena] Palacky Univ, Fac Med, Dept Prevent Med, CR-77147 Olomouc, Czech Republic.
[Bencko, Vladimir] Charles Univ Prague, Inst Hyg & Epidemiol, Prague, Czech Republic.
[Navratilova, Marie] Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic.
[Szeszenia-Dabrowska, Neonilia] Inst Occupat Med, Dept Epidemiol, Lodz, Poland.
[Mates, Dana] Inst Publ Hlth, Bucharest, Romania.
[Schmidt, Laura S.] NCI, Basic Sci Program, SAIC Frederick, Frederick, MD 21701 USA.
[Schmidt, Laura S.; Linehan, W. Marston] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Lenz, Petra; Merino, Maria] NCI, Div Canc Epidemiol & Genet, SAIC Frederick, Frederick, MD 21701 USA.
[Chanock, Stephen] NCI, Core Genotyping Facil, Adv Technol Ctr, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Boffetta, Paolo] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
[Boffetta, Paolo] Int Canc Prevent Res Inst, Lyon, France.
RP Moore, LE (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM moorele@mail.nih.gov
RI Zaridze, David/K-5605-2013; Janout, Vladimir/M-5133-2014;
Szeszenia-Dabrowska, Neonila/F-7190-2010;
OI mates, dana/0000-0002-6219-9807
FU NIH, National Cancer Institute, Center for Cancer Research; National
Cancer Institute, National Institutes of Health [HHS261200800001E,
CA102600]; European Commission [IC15-CT96-0313]
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research, and
in part with federal funds from the National Cancer Institute, National
Institutes of Health, under contract HHS261200800001E (LS Schmidt, P
Lenz) and under contract CA102600 (FM Waldman), and by European
Commission INCO-COPERNICUS Grant IC15-CT96-0313. The funders had no role
in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 55
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PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD OCT
PY 2011
VL 7
IS 10
AR e1002312
DI 10.1371/journal.pgen.1002312
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 843IL
UT WOS:000296665400013
PM 22022277
ER
PT J
AU N'Diaye, A
Chen, GK
Palmer, CD
Ge, B
Tayo, B
Mathias, RA
Ding, JZ
Nalls, MA
Adeyemo, A
Adoue, V
Ambrosone, CB
Atwood, L
Bandera, EV
Becker, LC
Berndt, SI
Bernstein, L
Blot, WJ
Boerwinkle, E
Britton, A
Casey, G
Chanock, SJ
Demerath, E
Deming, SL
Diver, WR
Fox, C
Harris, TB
Hernandez, DG
Hu, JJ
Ingles, SA
John, EM
Johnson, C
Keating, B
Kittles, RA
Kolonel, LN
Kritchevsky, SB
Le Marchand, L
Lohman, K
Liu, JK
Millikan, RC
Murphy, A
Musani, S
Neslund-Dudas, C
North, KE
Nyante, S
Ogunniyi, A
Ostrander, EA
Papanicolaou, G
Patel, S
Pettaway, CA
Press, MF
Redline, S
Rodriguez-Gil, JL
Rotimi, C
Rybicki, BA
Salako, B
Schreiner, PJ
Signorello, LB
Singleton, AB
Stanford, JL
Stram, AH
Stram, DO
Strom, SS
Suktitipat, B
Thun, MJ
Witte, JS
Yanek, LR
Ziegler, RG
Zheng, W
Zhu, XF
Zmuda, JM
Zonderman, AB
Evans, MK
Liu, YM
Becker, DM
Cooper, RS
Pastinen, T
Henderson, BE
Hirschhorn, JN
Lettre, G
Haiman, CA
AF N'Diaye, Amidou
Chen, Gary K.
Palmer, Cameron D.
Ge, Bing
Tayo, Bamidele
Mathias, Rasika A.
Ding, Jingzhong
Nalls, Michael A.
Adeyemo, Adebowale
Adoue, Veronique
Ambrosone, Christine B.
Atwood, Larry
Bandera, Elisa V.
Becker, Lewis C.
Berndt, Sonja I.
Bernstein, Leslie
Blot, William J.
Boerwinkle, Eric
Britton, Angela
Casey, Graham
Chanock, Stephen J.
Demerath, Ellen
Deming, Sandra L.
Diver, W. Ryan
Fox, Caroline
Harris, Tamara B.
Hernandez, Dena G.
Hu, Jennifer J.
Ingles, Sue A.
John, Esther M.
Johnson, Craig
Keating, Brendan
Kittles, Rick A.
Kolonel, Laurence N.
Kritchevsky, Stephen B.
Le Marchand, Loic
Lohman, Kurt
Liu, Jiankang
Millikan, Robert C.
Murphy, Adam
Musani, Solomon
Neslund-Dudas, Christine
North, Kari E.
Nyante, Sarah
Ogunniyi, Adesola
Ostrander, Elaine A.
Papanicolaou, George
Patel, Sanjay
Pettaway, Curtis A.
Press, Michael F.
Redline, Susan
Rodriguez-Gil, Jorge L.
Rotimi, Charles
Rybicki, Benjamin A.
Salako, Babatunde
Schreiner, Pamela J.
Signorello, Lisa B.
Singleton, Andrew B.
Stanford, Janet L.
Stram, Alex H.
Stram, Daniel O.
Strom, Sara S.
Suktitipat, Bhoom
Thun, Michael J.
Witte, John S.
Yanek, Lisa R.
Ziegler, Regina G.
Zheng, Wei
Zhu, Xiaofeng
Zmuda, Joseph M.
Zonderman, Alan B.
Evans, Michele K.
Liu, Yongmei
Becker, Diane M.
Cooper, Richard S.
Pastinen, Tomi
Henderson, Brian E.
Hirschhorn, Joel N.
Lettre, Guillaume
Haiman, Christopher A.
TI Identification, Replication, and Fine-Mapping of Loci Associated with
Adult Height in Individuals of African Ancestry
SO PLOS GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; HUMAN-POPULATIONS; COMMON; VARIANTS; TRAITS
AB Adult height is a classic polygenic trait of high heritability (h(2) similar to 0.8). More than 180 single nucleotide polymorphisms (SNPs), identified mostly in populations of European descent, are associated with height. These variants convey modest effects and explain similar to 10% of the variance in height. Discovery efforts in other populations, while limited, have revealed loci for height not previously implicated in individuals of European ancestry. Here, we performed a meta-analysis of genome-wide association (GWA) results for adult height in 20,427 individuals of African ancestry with replication in up to 16,436 African Americans. We found two novel height loci (Xp22-rs12393627, P = 3.4x10(-12) and 2p14-rs4315565, P = 1.2x10(-8)). As a group, height associations discovered in European-ancestry samples replicate in individuals of African ancestry (P = 1.7x10(-4) for overall replication). Fine-mapping of the European height loci in African-ancestry individuals showed an enrichment of SNPs that are associated with expression of nearby genes when compared to the index European height SNPs (P<0.01). Our results highlight the utility of genetic studies in non-European populations to understand the etiology of complex human diseases and traits.
C1 [N'Diaye, Amidou; Lettre, Guillaume] Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada.
[Chen, Gary K.; Casey, Graham; Ingles, Sue A.; Stram, Alex H.; Stram, Daniel O.; Henderson, Brian E.; Haiman, Christopher A.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Chen, Gary K.; Casey, Graham; Ingles, Sue A.; Press, Michael F.; Stram, Alex H.; Stram, Daniel O.; Henderson, Brian E.; Haiman, Christopher A.] Univ So Calif, Norris Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Palmer, Cameron D.; Hirschhorn, Joel N.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Palmer, Cameron D.; Hirschhorn, Joel N.] Childrens Hosp, Div Genet, Boston, MA 02115 USA.
[Palmer, Cameron D.; Hirschhorn, Joel N.] Childrens Hosp, Div Endocrinol, Boston, MA 02115 USA.
[Palmer, Cameron D.; Hirschhorn, Joel N.] Childrens Hosp, Program Genom, Boston, MA 02115 USA.
[Ge, Bing; Adoue, Veronique; Pastinen, Tomi] McGill Univ, Dept Human Genet, Montreal, PQ, Canada.
[Ge, Bing; Adoue, Veronique; Pastinen, Tomi] Genome Quebec Innovat Ctr, Montreal, PQ, Canada.
[Tayo, Bamidele; Cooper, Richard S.] Loyola Univ, Chicago Stritch Sch Med, Dept Prevent Med & Epidemiol, Maywood, IL 60153 USA.
[Mathias, Rasika A.; Becker, Lewis C.; Suktitipat, Bhoom; Yanek, Lisa R.; Becker, Diane M.] Johns Hopkins Univ, Sch Med, Dept Med, Johns Hopkins GeneSTAR Res Program, Baltimore, MD 21205 USA.
[Ding, Jingzhong; Kritchevsky, Stephen B.; Lohman, Kurt; Liu, Yongmei] Wake Forest Univ, Bowman Gray Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Nalls, Michael A.; Britton, Angela; Hernandez, Dena G.; Singleton, Andrew B.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Adeyemo, Adebowale; Rotimi, Charles] NHGRI, NIH Intramural Ctr Res Genom & Global Hlth, NIH, Bethesda, MD 20892 USA.
[Ambrosone, Christine B.] Roswell Pk Canc Inst, Dept Canc Prevent & Control, Buffalo, NY 14263 USA.
[Atwood, Larry] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Bandera, Elisa V.] Canc Inst New Jersey, New Brunswick, NJ USA.
[Berndt, Sonja I.; Chanock, Stephen J.; Ziegler, Regina G.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Div Canc Etiol, Duarte, CA USA.
[Blot, William J.; Signorello, Lisa B.] Int Epidemiol Inst, Rockville, MD USA.
[Blot, William J.; Deming, Sandra L.; Signorello, Lisa B.; Zheng, Wei] Vanderbilt Univ, Dept Med, Div Epidemiol, Vanderbilt Epidemiol Ctr, Nashville, TN USA.
[Blot, William J.; Deming, Sandra L.; Signorello, Lisa B.; Zheng, Wei] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr, Div Epidemiol, Houston, TX USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr, Ctr Human Genet, Houston, TX USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr, Inst Mol Med, Houston, TX USA.
[Demerath, Ellen] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Diver, W. Ryan; Thun, Michael J.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Fox, Caroline] Univ Mississippi, Med Ctr, Dept Med, Jackson, MS 39216 USA.
[Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Hu, Jennifer J.; Rodriguez-Gil, Jorge L.] Univ Miami, Miller Sch Med, Dept Epidemiol & Publ Hlth, Miami, FL 33136 USA.
[Hu, Jennifer J.; Rodriguez-Gil, Jorge L.] Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA.
[John, Esther M.] Canc Prevent Inst Calif, Fremont, CA USA.
[John, Esther M.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[John, Esther M.] Stanford Univ, Stanford Canc Ctr, Stanford, CA 94305 USA.
[Johnson, Craig] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Keating, Brendan] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA.
[Kittles, Rick A.] Univ Illinois, Dept Med, Chicago, IL USA.
[Kolonel, Laurence N.; Le Marchand, Loic] Univ Hawaii, Canc Res Ctr, Program Epidemiol, Honolulu, HI 96813 USA.
[Liu, Jiankang] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Millikan, Robert C.; Nyante, Sarah] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
[Millikan, Robert C.; Nyante, Sarah] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Murphy, Adam] Northwestern Univ, Dept Urol, Chicago, IL 60611 USA.
[Musani, Solomon] Univ Mississippi, Med Ctr, Dept Med, Jackson Heart Study,Div Cardiovasc Dis, Jackson, MS 39216 USA.
[Neslund-Dudas, Christine; Rybicki, Benjamin A.] Henry Ford Hosp, Dept Biostat & Res Epidemiol, Detroit, MI 48202 USA.
[North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
[Ogunniyi, Adesola; Salako, Babatunde] Univ Ibadan, Dept Med, Ibadan, Nigeria.
[Ostrander, Elaine A.] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
[Papanicolaou, George] NHLBI, Div Cardiovasc Sci, NIH, Bethesda, MD 20892 USA.
[Patel, Sanjay; Redline, Susan] Brigham & Womens Hosp, Div Sleep Med, Boston, MA 02115 USA.
[Pettaway, Curtis A.] Univ Texas MD Anderson Canc Ctr, Dept Urol, Houston, TX 77030 USA.
[Press, Michael F.] Univ So Calif, Keck Sch Med, Dept Pathol, Los Angeles, CA 90033 USA.
[Stanford, Janet L.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Strom, Sara S.] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Suktitipat, Bhoom] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Witte, John S.] Univ Calif San Francisco, Dept Epidemiol & Biostat, Inst Human Genet, San Francisco, CA 94143 USA.
[Witte, John S.] Univ Calif San Francisco, Dept Urol, Inst Human Genet, San Francisco, CA USA.
[Zhu, Xiaofeng] Case Western Reserve Univ, Dept Biostat & Epidemiol, Cleveland, OH 44106 USA.
[Zmuda, Joseph M.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Zonderman, Alan B.] NIA, Lab Personal & Cognit, NIH, Baltimore, MD 21224 USA.
[Evans, Michele K.] NIA, Hlth Dispar Res Sect, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
[Hirschhorn, Joel N.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Lettre, Guillaume] Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada.
RP N'Diaye, A (reprint author), Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada.
EM joelh@broadinstitute.org; guillaume.lettre@umontreal.ca; haiman@usc.edu
RI Singleton, Andrew/C-3010-2009; Bandera, Elisa/M-4169-2014;
OI Bandera, Elisa/0000-0002-8789-2755; Suktitipat,
Bhoom/0000-0001-8034-7757; Kritchevsky, Stephen/0000-0003-3336-6781;
Adeyemo, Adebowale/0000-0002-3105-3231; Patel,
Sanjay/0000-0002-9142-5172; Zonderman, Alan B/0000-0002-6523-4778;
Ostrander, Elaine/0000-0001-6075-9738
FU Department of Defense Breast Cancer Research [BC075007]; NIH/NCI
[CA1326792, RC2 CA148085]; Fondation de l'Institut de Cardiologie de
Montreal; FRSQ; Canada Research Chair Program; CIHR; March of Dimes
[6-FY09-507]; NIH/NIDDK [R01DK075787]; MEC [R01-CA63464, R37-CA54281];
CARE (National Institute for Child Health and Development)
[NO1-HD-3-3175]; WCHS (U. S. Army Medical Research and Material Command
(USAMRMC) [DAMD-17-01-0-0334]; NIH [CA1326792, R01-CA100598, CA63464,
CA54281, CA148085, HG004726, R01 CA056678, R01 CA082664, R01 CA092579,
CA092447, HHSN268200782096C, R37-HL045508, R01-HL053353, R01-DK075787,
U01-HL054512, R01-HL074166, R01-HL086718, R01-HG003054, NR0224103];
Breast Cancer Research Foundation); SFBCS (NIH) [R01-CA77305]; United
States Army Medical Research [DAMD17-96-6071]; NC-BCFR (NIH)
[U01-CA69417]; CBCS (NIH) [P50-CA58223]; Center for Environmental Health
and Susceptibility, National Institute of Environmental Health Sciences,
NIH [P30-ES10126]; PLCO (National Cancer Institute, National Institutes
of Health); NHBS (National Institutes of Health) [R01-CA100374]; WFBC
(NIH) [R01-CA73629]; National Cancer Institute, NIH [RFA CA-95-011];
Division of Cancer Epidemiology and Genetics, NCI, NIH. LAAPC; Cancer
Research Fund [99-00524V-10258, 97-12013]; University of California
[98-00924V]; Department of Health Services; Fred Hutchinson Cancer
Research Center; National Human Genome Research Institute;
Vanderbilt-Ingram Cancer Center [P30 CA68485]; American Cancer Society;
NIH, NIA; National Center on Minority Health and Health Disparities
[Z01-AG000513, 2009-149]; National Heart, Lung, and Blood Institute,
NIH, U.S. Department of Health and Human Services [N01WH22110, 24152,
32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122,
42107-26, 42129-32, 44221]; NIA [N01AG62101, N01AG62103, N01AG62106,
1R01AG032098-01A1]; MISAIC Initiative; [R01CA68578]; [ES007784];
[DAMD W81XWH-07-1-0645]; [P50-CA140388]
FX The grants and contracts that have supported CARe are listed at
http://public.nhlbi.nih.gov/GeneticsGenomics/home/care.aspx, including
HHSN268200625226C (ADB No. N01-HC-65226). AABC was supported by a
Department of Defense Breast Cancer Research Program Era of Hope Scholar
Award to CA Haiman (BC075007) and AAPC was supported by NIH/NCI grants
(CA1326792 and RC2 CA148085). Additional support for this work was
provided by: the Fondation de l'Institut de Cardiologie de Montreal (G
Lettre), FRSQ (G Lettre and T Pastinen), Canada Research Chair Program
(G Lettre and T Pastinen), CIHR (T Pastinen), March of Dimes 6-FY09-507
(JN Hirschhorn), and NIH/NIDDK R01DK075787 (JN Hirschhorn). The grants
and contracts that have supported CARe are listed at
http://public.nhlbi.nih.gov/GeneticsGenomics/home/care.aspx, including
HHSN268200625226C (ADB No. N01-HC-65226). Each of the participating AABC
studies was supported by the following grants: MEC (NIH grants
R01-CA63464 and R37-CA54281), CARE (National Institute for Child Health
and Development grant NO1-HD-3-3175), WCHS (U. S. Army Medical Research
and Material Command (USAMRMC) grant DAMD-17-01-0-0334, NIH grant
R01-CA100598, and the Breast Cancer Research Foundation), SFBCS (NIH
grant R01-CA77305 and United States Army Medical Research Program grant
DAMD17-96-6071), NC-BCFR (NIH grant U01-CA69417), CBCS (NIH Specialized
Program of Research Excellence in Breast Cancer, grant number
P50-CA58223, and Center for Environmental Health and Susceptibility,
National Institute of Environmental Health Sciences, NIH, grant number
P30-ES10126), PLCO (Intramural Research Program, National Cancer
Institute, National Institutes of Health), NHBS (National Institutes of
Health grant R01-CA100374), and WFBC (NIH grant R01-CA73629). The Breast
Cancer Family Registry (BCFR) was supported by the National Cancer
Institute, NIH, under RFA CA-95-011 and through cooperative agreements
with members of the Breast Cancer Family Registry and Principal
Investigators. The content of this manuscript does not necessarily
reflect the views or policies of the National Cancer Institute or any of
the collaborating centers in the BCFR, nor does mention of trade names,
commercial products, or organizations imply endorsement by the U.S.
Government or the BCFR. AAPC was supported by NIH grants CA63464,
CA54281, CA1326792, CA148085, and HG004726. Genotyping of the PLCO
samples was funded by the Intramural Research Program of the Division of
Cancer Epidemiology and Genetics, NCI, NIH. LAAPC was funded by grant
99-00524V-10258 from the Cancer Research Fund, under Interagency
Agreement #97-12013 (University of California contract #98-00924V) with
the Department of Health Services Cancer Research Program. KCPCS was
supported by NIH grants R01 CA056678, R01 CA082664, R01 CA092579, with
additional support from the Fred Hutchinson Cancer Research Center and
the Intramural Program of the National Human Genome Research Institute.
MDA was support by grants R01CA68578, ES007784, DAMD W81XWH-07-1-0645,
and P50-CA140388. GECAP was supported by NIH grant ES011126. CaP Genes
was supported by CA88164 and CA127298. DCPC was supported by NIH grant
S06GM08016 and DOD grants DAMD W81XWH-07-1-0203 and DAMD
W81XWH-06-1-0066. SCCS is funded by NIH grant CA092447, and SCCS sample
preparation was conducted at the Epidemiology Biospecimen Core Lab that
is supported in part by the Vanderbilt-Ingram Cancer Center (P30
CA68485). CPS-II is supported by the American Cancer Society.; HANDLS
was supported by the Intramural Research Program of the NIH, NIA, and
the NationalCenter on Minority Health and Health Disparities (project
#Z01-AG000513 and human subjects protocol #2009-149). Data analyses for
the HANDLS study utilized the high-performance computational
capabilities of the Biowulf Linux cluster at the National Institutes of
Health, Bethesda, Md (http://biowulf.nih.gov). The WHI program is funded
by the National Heart, Lung, and Blood Institute, NIH, U. S. Department
of Health and Human Services through contracts N01WH22110, 24152,
32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122,
42107-26, 42129-32, and 44221. The authors thank the WHI investigators
and staff for their dedication, and the study participants for making
the program possible. A full listing of WHI investigators can be found
at:
http://www.whiscience.org/publications/WHI_investigators_shortlist.pdf.
HABC was supported by NIA contracts N01AG62101, N01AG62103, and
N01AG62106. The GWAS was funded by NIA grant 1R01AG032098-01A1 to Wake
Forest University Health Sciences and genotyping services were provided
by the Center for Inherited Disease Research (CIDR). CIDR is fully
funded through a federal contract from the NIH to The Johns Hopkins
University, contract number HHSN268200782096C. This research was
supported in part by the Intramural Research Program of the NIH, NIA.
The Nigerian cohort study was supported by NIH grant numbers
R37-HL045508, R01-HL053353, R01-DK075787 and U01-HL054512. The authors
acknowledge the assistance of the research staff and participants in
Igbo-Ora, Oyo State, Nigeria. Maywood cohort study was supported by the
NIH grant numbers R37-HL045508, R01-HL074166, R01-HL086718, and
R01-HG003054. GeneSTAR was supported by NIH grants NR0224103,
HL58625-01A1, HL59684, HL071025-01A1, U01HL72518, and HL087698 and by
M01-RR000052 to the Johns Hopkins General Clinical Research Center. RAM
was supported in part by the MISAIC Initiative Award at Johns Hopkins
University. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 22
TC 40
Z9 40
U1 0
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD OCT
PY 2011
VL 7
IS 10
AR e1002298
DI 10.1371/journal.pgen.1002298
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 843IL
UT WOS:000296665400007
PM 21998595
ER
PT J
AU Ohlsson, C
Wallaschofski, H
Lunetta, KL
Stolk, L
Perry, JRB
Koster, A
Petersen, AK
Eriksson, J
Lehtimaki, T
Huhtaniemi, IT
Hammond, GL
Maggio, M
Coviello, AD
Ferrucci, L
Heier, M
Hofman, A
Holliday, KL
Jansson, JO
Kahonen, M
Karasik, D
Karlsson, MK
Kiel, DP
Liu, YM
Ljunggren, O
Lorentzon, M
Lyytikainen, LP
Meitinger, T
Mellstrom, D
Melzer, D
Miljkovic, I
Nauck, M
Nilsson, M
Penninx, B
Pye, SR
Vasan, RS
Reincke, M
Rivadeneira, F
Tajar, A
Teumer, A
Uitterlinden, AG
Ulloor, J
Viikari, J
Volker, U
Volzke, H
Wichmann, HE
Wu, TS
Zhuang, WV
Ziv, E
Wu, FCW
Raitakari, O
Eriksson, A
Bidlingmaier, M
Harris, TB
Murray, A
De Jong, FH
Murabito, JM
Bhasin, S
Vandenput, L
Haring, R
AF Ohlsson, Claes
Wallaschofski, Henri
Lunetta, Kathryn L.
Stolk, Lisette
Perry, John R. B.
Koster, Annemarie
Petersen, Ann-Kristin
Eriksson, Joel
Lehtimaki, Terho
Huhtaniemi, Ilpo T.
Hammond, Geoffrey L.
Maggio, Marcello
Coviello, Andrea D.
Ferrucci, Luigi
Heier, Margit
Hofman, Albert
Holliday, Kate L.
Jansson, John-Olov
Kahonen, Mika
Karasik, David
Karlsson, Magnus K.
Kiel, Douglas P.
Liu, Yongmei
Ljunggren, Osten
Lorentzon, Mattias
Lyytikainen, Leo-Pekka
Meitinger, Thomas
Mellstrom, Dan
Melzer, David
Miljkovic, Iva
Nauck, Matthias
Nilsson, Maria
Penninx, Brenda
Pye, Stephen R.
Vasan, Ramachandran S.
Reincke, Martin
Rivadeneira, Fernando
Tajar, Abdelouahid
Teumer, Alexander
Uitterlinden, Andre G.
Ulloor, Jagadish
Viikari, Jorma
Voelker, Uwe
Voelzke, Henry
Wichmann, H. Erich
Wu, Tsung-Sheng
Zhuang, Wei Vivian
Ziv, Elad
Wu, Frederick C. W.
Raitakari, Olli
Eriksson, Anna
Bidlingmaier, Martin
Harris, Tamara B.
Murray, Anna
De Jong, Frank H.
Murabito, Joanne M.
Bhasin, Shalender
Vandenput, Liesbeth
Haring, Robin
CA EMAS Study Grp
TI Genetic Determinants of Serum Testosterone Concentrations in Men
SO PLOS GENETICS
LA English
DT Article
ID HORMONE-BINDING GLOBULIN; POPULATION-BASED COHORT; ELDERLY-MEN; OLDER
MEN; ANDROGEN DEFICIENCY; METABOLIC SYNDROME; RISK-FACTORS; SHBG GENE;
MORTALITY; HEALTH
AB Testosterone concentrations in men are associated with cardiovascular morbidity, osteoporosis, and mortality and are affected by age, smoking, and obesity. Because of serum testosterone's high heritability, we performed a meta-analysis of genome-wide association data in 8,938 men from seven cohorts and followed up the genome-wide significant findings in one in silico (n = 871) and two de novo replication cohorts (n = 4,620) to identify genetic loci significantly associated with serum testosterone concentration in men. All these loci were also associated with low serum testosterone concentration defined as,300 ng/dl. Two single-nucleotide polymorphisms at the sex hormone-binding globulin (SHBG) locus (17p13-p12) were identified as independently associated with serum testosterone concentration (rs12150660, p = 1.2x10(-41) and rs6258, p = 2.3x10(-22)). Subjects with >= 3 risk alleles of these variants had 6.5-fold higher risk of having low serum testosterone than subjects with no risk allele. The rs5934505 polymorphism near FAM9B on the X chromosome was also associated with testosterone concentrations (p = 5.6610216). The rs6258 polymorphism in exon 4 of SHBG affected SHBG's affinity for binding testosterone and the measured free testosterone fraction (p<0.01). Genetic variants in the SHBG locus and on the X chromosome are associated with a substantial variation in testosterone concentrations and increased risk of low testosterone. rs6258 is the first reported SHBG polymorphism, which affects testosterone binding to SHBG and the free testosterone fraction and could therefore influence the calculation of free testosterone using law-of-mass-action equation.
C1 [Ohlsson, Claes; Eriksson, Joel; Lorentzon, Mattias; Mellstrom, Dan; Nilsson, Maria; Eriksson, Anna; Vandenput, Liesbeth] Univ Gothenburg, Sahlgrenska Acad, Ctr Bone & Arthrit Res, Dept Internal Med,Inst Med, Gothenburg, Sweden.
[Wallaschofski, Henri; Nauck, Matthias; Haring, Robin] Ernst Moritz Arndt Univ Greifswald, Inst Clin Chem & Lab Med, Greifswald, Germany.
[Lunetta, Kathryn L.; Coviello, Andrea D.; Kiel, Douglas P.; Vasan, Ramachandran S.; De Jong, Frank H.; Murabito, Joanne M.; Bhasin, Shalender] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Lunetta, Kathryn L.; Zhuang, Wei Vivian] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Stolk, Lisette; Rivadeneira, Fernando; Uitterlinden, Andre G.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Perry, John R. B.; Murray, Anna] Univ Exeter, Peninsula Med Sch, Exeter, Devon, England.
[Stolk, Lisette; Hofman, Albert; Rivadeneira, Fernando; Uitterlinden, Andre G.] Netherlands Consortium Hlth Ageing, Rotterdam, Netherlands.
[Perry, John R. B.; Murray, Anna] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
[Koster, Annemarie; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Petersen, Ann-Kristin] Helmholtz Zentrum Munchen, Inst Genet Epidemiol, Neuherberg, Germany.
[Lehtimaki, Terho; Lyytikainen, Leo-Pekka] Univ Tampere, Dept Clin Chem, FIN-33101 Tampere, Finland.
[Lehtimaki, Terho; Kahonen, Mika; Lyytikainen, Leo-Pekka] Tampere Univ Hosp, Tampere, Finland.
[Huhtaniemi, Ilpo T.] Univ London Imperial Coll Sci Technol & Med, Dept Surg & Canc, London, England.
[Hammond, Geoffrey L.; Wu, Tsung-Sheng] Univ British Columbia, Dept Obstet & Gynecol, Vancouver, BC V5Z 1M9, Canada.
[Hammond, Geoffrey L.; Wu, Tsung-Sheng] Univ British Columbia, Child & Family Res Inst, Vancouver, BC V5Z 1M9, Canada.
[Maggio, Marcello] Univ Parma, Sect Geriatr, Dept Internal Med, I-43100 Parma, Italy.
[Maggio, Marcello] Univ Parma, Sect Geriatr, Dept Biomed Sci, I-43100 Parma, Italy.
[Coviello, Andrea D.; Vasan, Ramachandran S.; Ulloor, Jagadish; De Jong, Frank H.; Murabito, Joanne M.; Bhasin, Shalender] Boston Univ, Sch Med, Dept Med, Gen Internal Med Sect, Boston, MA 02118 USA.
[Coviello, Andrea D.; Vasan, Ramachandran S.; Ulloor, Jagadish; De Jong, Frank H.; Murabito, Joanne M.; Bhasin, Shalender] Boston Univ, Sch Med, Dept Med, Sect Prevent Med, Boston, MA 02118 USA.
[Coviello, Andrea D.; Vasan, Ramachandran S.; Ulloor, Jagadish; De Jong, Frank H.; Murabito, Joanne M.; Bhasin, Shalender] Boston Univ, Sch Med, Dept Med, Cardiol Sect, Boston, MA 02118 USA.
[Coviello, Andrea D.; Vasan, Ramachandran S.; Ulloor, Jagadish; De Jong, Frank H.; Murabito, Joanne M.; Bhasin, Shalender] Boston Univ, Sch Med, Dept Med, Sect Endocrinol Diabet & Nutr, Boston, MA 02118 USA.
[EMAS Study Grp] Univ Manchester, European Male Ageing Study, Manchester, Lancs, England.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
[Heier, Margit] Helmholtz Zentrum Munchen, Inst Epidemiol 2, Neuherberg, Germany.
[Hofman, Albert; Rivadeneira, Fernando; Uitterlinden, Andre G.] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Holliday, Kate L.; Pye, Stephen R.; Tajar, Abdelouahid] Univ Manchester, Arthrit Res UK Epidemiol Unit, Manchester Acad Hlth Sci Ctr, Manchester, Lancs, England.
[Jansson, John-Olov] Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Physiol, Gothenburg, Sweden.
[Kahonen, Mika] Univ Tampere, Dept Clin Physiol, FIN-33101 Tampere, Finland.
[Karasik, David; Kiel, Douglas P.] Harvard Univ, Sch Med, Boston, MA USA.
[Karasik, David; Kiel, Douglas P.] Hebrew SeniorLife Inst Aging Res, Boston, MA USA.
[Karlsson, Magnus K.] Lund Univ, Skane Univ Hosp, Dept Orthopaed, Malmo, Sweden.
[Karlsson, Magnus K.] Lund Univ, Dept Clin Sci, Clin & Mol Osteoporosis Res Unit, Malmo, Sweden.
[Liu, Yongmei] Wake Forest Univ Hlth Sci, Dept Epidemiol & Biostat, Winston Salem, NC USA.
[Ljunggren, Osten] Uppsala Univ, Dept Med Sci, Uppsala, Sweden.
[Meitinger, Thomas] Tech Univ Munich, Inst Human Genet, Munich, Germany.
[Meitinger, Thomas] Helmholtz Zentrum Munchen, Inst Human Genet, Neuherberg, Germany.
[Melzer, David] Univ Exeter, Peninsula Med Sch, Exeter, Devon, England.
[Miljkovic, Iva] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Penninx, Brenda] Vrije Univ Amsterdam Med Ctr, EMGO Inst Hlth & Care Res, Amsterdam, Netherlands.
[Penninx, Brenda] Vrije Univ Amsterdam Med Ctr, Dept Psychiat, Amsterdam, Netherlands.
[Reincke, Martin; Bidlingmaier, Martin] Univ Munich, Med Klin Innenstadt, D-8000 Munich, Germany.
[Teumer, Alexander; Voelker, Uwe] Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Genom, Greifswald, Germany.
[Viikari, Jorma] Univ Turku, Dept Med, Turku, Finland.
[Voelzke, Henry] Ernst Moritz Arndt Univ Greifswald, Inst Community Med, Greifswald, Germany.
[Wichmann, H. Erich] Univ Munich, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
[Wichmann, H. Erich] Univ Munich, Klinikum Grosshadern, D-8000 Munich, Germany.
[Wichmann, H. Erich] Helmholtz Zentrum Munchen, Inst Epidemiol 1, Neuherberg, Germany.
[Ziv, Elad] Univ Calif San Francisco, Dept Med, Div Gen Internal Med, San Francisco, CA USA.
[Ziv, Elad] Univ Calif San Francisco, Dept Epidemiol & Biostat, Inst Human Genet, San Francisco, CA 94143 USA.
[Wu, Frederick C. W.] Univ Manchester, Manchester Royal Infirm, Manchester Acad Hlth Sci Ctr, Androl Res Unit,Dev & Regenerat Biomed Res Grp, Manchester M13 9WL, Lancs, England.
[Raitakari, Olli] Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, SF-20500 Turku, Finland.
[Raitakari, Olli] Turku Univ Hosp, Dept Clin Physiol, FIN-20520 Turku, Finland.
RP Ohlsson, C (reprint author), Univ Gothenburg, Sahlgrenska Acad, Ctr Bone & Arthrit Res, Dept Internal Med,Inst Med, Gothenburg, Sweden.
EM claes.ohlsson@medic.gu.se
RI Koster, Annemarie/E-7438-2010; Pye, Stephen/D-9236-2011; Ziv,
Elad/L-5396-2014; Meitinger, Thomas/O-1318-2015; Rivadeneira,
Fernando/O-5385-2015; Lyytikainen, Leo-Pekka/C-8544-2016;
OI Ramachandran, Vasan/0000-0001-7357-5970; Kiel,
Douglas/0000-0001-8474-0310; Melzer, David/0000-0002-0170-3838; Karasik,
David/0000-0002-8826-0530; Vandenput, Liesbeth/0000-0002-1712-6131; Pye,
Stephen/0000-0002-7263-2897; Rivadeneira, Fernando/0000-0001-9435-9441;
Lyytikainen, Leo-Pekka/0000-0002-7200-5455; Murabito,
Joanne/0000-0002-0192-7516; Bidlingmaier, Martin/0000-0002-4681-6668;
Lunetta, Kathryn/0000-0002-9268-810X; Murray, Anna/0000-0002-2351-2522;
Miljkovic, Iva/0000-0002-3155-9777
FU National Institute of Aging (Genetics of Reproductive Life Period and
Health Outcomes) [R21AG032598]; National Heart, Lung, and Blood
Institute's Framingham Heart Study [N01-HC-25195, N02-HL-6-4278];
National Institute on Aging (NIA) [1RO1AG31206, N01-AG-6-2101,
N01-AG-6-2103, N01-AG-6-2106, 1R01AG032098-01A1]; Boston Claude D.
Pepper Older Americans Independence Center [5P30AG031679]; National
Institute on Aging and the National Institute of Arthritis
Musculoskeletal and Skin Diseases [R01 AR/AG 41398]; Robert Dawson Evans
Endowment of the Department of Medicine at Boston University School of
Medicine and Boston Medical Center; Leibniz Supercomputing Centre of the
Bavarian Academy of Sciences and Humanities [h1231]; Federal Ministry of
Education and Research [01ZZ9603, 01ZZ0103, 01ZZ0403, 03ZIK012];
Ministry of Cultural Affairs as well as the Social Ministry of the
Federal State of Mecklenburg - West Pomerania; Siemens Healthcare,
Erlangen, Germany; Federal State of Mecklenburg West Pomerania; Federal
Ministry of Education and Research and the Ministry of Cultural Affairs
of the Federal State of Mecklenburg - West Pomerania [03IS2061A];
Siemens Healthcare Diagnostics, Eschborn, formerly DPC Biermann GmbH,
Bad Nauheim, Germany; Swedish Research Council [K2010-54X-09894-19-3,
2006-3832, K2010-52X-20229-05-3]; Swedish Foundation for Strategic
Research [K2010-54X-09894-19-3, 2006-3832]; ALF/LUA in Gothenburg;
Lundberg Foundation; Torsten and Ragnar Soderberg's Foundation; Petrus
and Augusta Hedlunds Foundation; Vastra Gotaland Foundation; Goteborg
Medical Society; Novo Nordisk foundation; Canadian Institutes of Health
Research [MOP-15261]; European Commission [HEALTH-F2-2008-201865-GEFOS];
German Bundesministerium fuer Forschung und Technology [01 AK 803 A-H,
01 IG 07015]; Helmholtz Center Munich, German Research Center for
Environmental Health; German Federal Ministry of Education and Research
(BMBF); State of Bavaria; German National Genome Research Network
[NGFN-2, NGFNPlus:01GS0823]; Munich Center of Health Sciences (MC
Health) as part of LMUinnovativ; National Institutes of Health
[HHSN268200782096C]; NIH, National Institute on Aging; Netherlands
Organisation of Scientific Research NWO [175.010.2005.011, 911-03-012];
Institute for Diseases in the Elderly [014-93-015;RIDE2]; Netherlands
Genomics Initiative (NGI) - Netherlands Consortiumof Healthy Aging
(NCHA) [050-060-810]; European Commision [HEALTH-F2-2008-201865,
HEALTH-F2-2008-35627]; Erasmus Medical Center; Erasmus University
Rotterdam; Netherlands Organisation for Health Research and Development
(ZonMw); Research Institute for Diseases in the Elderly (RIDE); Ministry
of Education, Culture, and Science; Ministry for Health, Welfare, and
Sports; the European Commission (DG XII); Municipality of Rotterdam;
Italian Ministry of Health [ICS110.1/RF97.71]; U.S. National Institute
on Aging [263 MD 9164, 263 MD 821336, N.1-AG-1-1, N.1-AG-1-2111,
N01-AG-5-0002]; National Institute on Aging, National Institutes of
Health, Baltimore, Maryland; Commission of the European Community
[QLK6-CT-2001-00258]; UK Arthritis Research Campaign; University
Hospitals Leuven, Belgium; Academy of Finland [117797, 121584, 126925];
Social Insurance Institution of Finland; Turku University Foundation;
Tampere and Turku University Hospital; Emil Aaltonen Foundation; Juho
Vainio Foundation; Paavo Nurmi Foundation; Tampere Tubeculosis
Foundation; Orion-Farmos Research Foundation; Finnish Foundation of
Cardiovascular Research; Finnish Cultural Foundation
FX Framingham Heart Study (FHS): The FHS phenotype-genotype analyses for
this work were supported by the National Institute of Aging (Genetics of
Reproductive Life Period and Health Outcomes, R21AG032598; JM Murabito,
KL Lunetta, D Karasik, DP Kiel, WV Zhuang). The Framingham Heart Study
of the National Heart Lung and Blood Institute of the National
Institutes of Health and Boston University School of Medicine is
supported by the National Heart, Lung, and Blood Institute's Framingham
Heart Study Contract No. N01-HC-25195 and its contract with Affymetrix
for genotyping services (Contract No. N02-HL-6-4278). Sex hormone
measurements were funded primarily by National Institute on Aging grant
1RO1AG31206 (PIs: S Bhasin and RS Vasan); additional support was
provided by the Boston Claude D. Pepper Older Americans Independence
Center (5P30AG031679) and a grant from the National Institute on Aging
and the National Institute of Arthritis Musculoskeletal and Skin
Diseases to DP Kiel (R01 AR/AG 41398). Analyses reflect intellectual
input and resource development from the Framingham Heart Study
investigators participating in the SNP Health Association Resource
(SHARe) project. A portion of this research was conducted using the
Linux Cluster for Genetic Analysis (LinGA-II), funded by the Robert
Dawson Evans Endowment of the Department of Medicine at Boston
University School of Medicine and Boston Medical Center. Study of Health
in Pomerania (SHIP): Computing resources have been made available by the
Leibniz Supercomputing Centre of the Bavarian Academy of Sciences and
Humanities (HLRB project h1231). SHIP is part of the Community Medicine
Research net of the University of Greifswald, Germany, which is funded
by the Federal Ministry of Education and Research (grants no. 01ZZ9603,
01ZZ0103, and 01ZZ0403), the Ministry of Cultural Affairs as well as the
Social Ministry of the Federal State of Mecklenburg - West Pomerania.
Genome-wide data have been supported by the Federal Ministry of
Education and Research (grant no. 03ZIK012) and a joint grant from
Siemens Healthcare, Erlangen, Germany, and the Federal State of
Mecklenburg West Pomerania. The University of Greifswald is a member of
the "Center of Knowledge Interchange'' program of the Siemens AG. This
work is also part of the research project Greifswald Approach to
Individualized Medicine (GANI_MED). The GANI_MED consortium is funded by
the Federal Ministry of Education and Research and the Ministry of
Cultural Affairs of the Federal State of Mecklenburg - West Pomerania
(03IS2061A). The testosterone reagents used were sponsored by Siemens
Healthcare Diagnostics, Eschborn, formerly DPC Biermann GmbH, Bad
Nauheim, Germany. Novo Nordisc provided partial grant support for the
determination of serum samples and data analysis. Gothenburg
Osteoporosis and Obesity Determinants (GOOD) Study: Financial support
was received from the Swedish Research Council (K2010-54X-09894-19-3,
2006-3832, and K2010-52X-20229-05-3), the Swedish Foundation for
Strategic Research, the ALF/LUA research grant in Gothenburg, the
Lundberg Foundation, the Torsten and Ragnar Soderberg's Foundation,
Petrus and Augusta Hedlunds Foundation, the Vastra Gotaland Foundation,
the Goteborg Medical Society, the Novo Nordisk foundation, the Canadian
Institutes of Health Research (MOP-15261), and the European Commission
grant HEALTH-F2-2008-201865-GEFOS. We would like to acknowledge Maria
Nethander at the genomics core facility at University of Gothenburg for
statistical analyses. We would also like to thank Dr. Tobias A. Knoch,
Luc V.; de Zeeuw,Anis Abuseiris, and Rob de Graaf as well as their
institutions the Erasmus Computing Grid, Rotterdam, The Netherlands, and
especially the national German MediGRID and Services@MediGRID part of
the German D-Grid, both funded by the German Bundesministerium fuer
Forschung und Technology under grants #01 AK 803 A-H and #01 IG 07015 G
for access to their grid resources. Cooperative Research in the Region
of Augsburg (KORA): The KORA research platform was initiated and
financed by the Helmholtz Center Munich, German Research Center for
Environmental Health, which is funded by the German Federal Ministry of
Education and Research (BMBF) and by the State of Bavaria. Part of this
work was financed by the German National Genome Research Network (NGFN-2
and NGFNPlus:01GS0823). Our research was supported within the Munich
Center of Health Sciences (MC Health) as part of LMUinnovativ. This
study was in part supported by a grant from the German Federal Ministry
of Education and Research (BMBF) to the German Center for Diabetes
Research (DZD e. V.). Health, Aging, and Body Composition (Health ABC)
Study: This study was supported by National Institute on Aging contracts
N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106. The genome-wide
association study was funded by NIA grant 1R01AG032098-01A1 to Wake
Forest University Health Sciences and genotyping services were provided
by the Center for Inherited Disease Research (CIDR). CIDR is fully
funded through a federal contract from the National Institutes of Health
to The Johns Hopkins University, contract number HHSN268200782096C. This
research was supported (in part) by the Intramural Research Program of
the NIH, National Institute on Aging. Rotterdam study (RS1): The
generation and management of GWAS genotype data for the Rotterdam Study
is supported by the Netherlands Organisation of Scientific Research NWO
Investments (nr.175.010.2005.011, 911-03-012). This study is funded by
the Research Institute for Diseases in the Elderly (014-93-015;RIDE2),
the Netherlands Genomics Initiative (NGI) - Netherlands Consortiumof
Healthy Aging (NCHA) project nr.050-060-810, and funding from the
European Commision (HEALTH-F2-2008-201865, GEFOS; HEALTH-F2-2008-35627,
TREAT-OA). The Rotterdam Study is funded by Erasmus Medical Center and
Erasmus University Rotterdam; Netherlands Organisation for Health
Research and Development (ZonMw); the Research Institute for Diseases in
the Elderly (RIDE); the Ministry of Education, Culture, and Science; the
Ministry for Health, Welfare, and Sports; the European Commission (DG
XII); and the Municipality of Rotterdam. We thank Pascal Arp, Mila
Jhamai, Dr. Michael Moorhouse, Marijn Verkerk, and Sander Bervoets for
their help in creating the GWAS database. The authors are grateful to
the study participants, the staff from the Rotterdam Study, and the
participating general practioners and pharmacists. We would like to
thank Dr. Tobias A. Knoch, Luc V. de Zeeuw, Anis Abuseiris, and Rob de
Graaf as well as their institutions the Erasmus Computing Grid,
Rotterdam, The Netherlands, and especially the national German MediGRID
and Services@MediGRID part of the German D-Grid, both funded by the
German Bundesministerium fuer Forschung und Technology under grants # 01
AK 803 A-H and # 01 IG 07015 G for access to their grid resources.
Invecchiare in Chianti (InCHIANTI): The InCHIANTI study baseline
(1998-2000) was supported as a "targeted project'' (ICS110.1/RF97.71) by
the Italian Ministry of Health and in part by the U.S.; National
Institute on Aging (Contracts: 263 MD 9164 and 263 MD 82336); the
InCHIANTI Follow-up 1 (2001-2003) was funded by the U.S. National
Institute on Aging (Contracts: N.1-AG-1-1 and N.1-AG-1-2111); the
InCHIANTI Follow-ups 2 and 3 studies (2004-2010) were financed by the
U.S. National Institute on Aging (Contract: N01-AG-5-0002); supported in
part by the Intramural research program of the National Institute on
Aging, National Institutes of Health, Baltimore, Maryland. European Male
Ageing Study (EMAS): The EMAS is funded by the Commission of the
European Communities Fifth Framework Programme "Quality of Life and
Management of Living Resources'' Grant QLK6-CT-2001-00258 and supported
by funding from the UK Arthritis Research Campaign. The EMAS Principal
Investigator is Professor Frederick Wu, MD; Dept of Endocrinology,
Manchester Royal Infirmary, UK. The "EMAS Study Group'' consists of the
following people:Gyorgy Bartfai, Steven Boonen, Felipe Casanueva, Joseph
D Finn, Gianni Forti, Aleksander Giwercman, Thang S Han, Kate L
Holliday, Ilpo T Huhtaniemi, Krzysztof Kula, Michael EJ Lean, David M
Lee, Terence W O'Neill, Neil Pendleton, Margus Punab, Stephen R Pye,
Alan J Silman, Abdelouahid Tajar, Wendy Thomson, Dirk Vanderschueren,
and Frederick CW Wu. The authors wish to thank the men who participated
in the eight countries and the research/nursing staff in the eight
centres: C Pott, Manchester, E Wouters, Leuven, M Nilsson, Malmo, M del
Mar Fernandez, Santiago de Compostela, M Jedrzejowska, Lodz, H-M Tabo,
Tartu, A Heredi, Szeged for their data collection and C Moseley,
Manchester for data entry and project coordination. Dr. Vanderschueren
is a senior clinical investigator supported by the Clinical Research
Fund of the University Hospitals Leuven, Belgium. Dr. Boonen is a senior
clinical investigator of the Fund for Scientific Research-Flanders,
Belgium(F.W.O.-Vlaanderen). Dr. Boonen is holder of the Leuven
University Chair in Metabolic Bone Diseases. The Osteoporotic Fractures
in Men Study - Sweden (MrOS Sweden): Financial support was received from
the Swedish Research Council (K2010-54X-09894-19-3, 2006-3832), the
Swedish Foundation for Strategic Research, the ALF/LUA research grant in
Gothenburg, the Lundberg Foundation, the Torsten and Ragnar Soderberg's
Foundation, Petrus and Augusta Hedlunds Foundation, the Vastra Gotaland
Foundation, the Goteborg Medical Society, the Novo Nordisk Foundation,
and the European Commission grant HEALTH-F2-2008-201865-GEFOS. The
Cardiovascular Risk in Young Finns Study (YFS): YFS has been financially
supported by the Academy of Finland (grant no. 117797, 121584, and
126925), the Social Insurance Institution of Finland, Turku University
Foundation, Tampere and Turku University Hospital Medical Funds, Emil
Aaltonen Foundation (T. L), Juho Vainio Foundation, Paavo Nurmi
Foundation, the Tampere Tubeculosis Foundation, the Orion-Farmos
Research Foundation, Finnish Foundation of Cardiovascular Research, and
Finnish Cultural Foundation. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 34
TC 65
Z9 65
U1 0
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD OCT
PY 2011
VL 7
IS 10
AR e1002313
DI 10.1371/journal.pgen.1002313
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 843IL
UT WOS:000296665400014
PM 21998597
ER
PT J
AU Pierson, TM
Adams, D
Bonn, F
Martinelli, P
Cherukuri, PF
Teer, JK
Hansen, NF
Cruz, P
Mullikin, JC
Blakesley, RW
Golas, G
Kwan, J
Sandler, A
Fajardo, KF
Markello, T
Tifft, C
Blackstone, C
Rugarli, EI
Langer, T
Gahl, WA
Toro, C
AF Pierson, Tyler Mark
Adams, David
Bonn, Florian
Martinelli, Paola
Cherukuri, Praveen F.
Teer, Jamie K.
Hansen, Nancy F.
Cruz, Pedro
Mullikin, James C.
Blakesley, Robert W.
Golas, Gretchen
Kwan, Justin
Sandler, Anthony
Fajardo, Karin Fuentes
Markello, Thomas
Tifft, Cynthia
Blackstone, Craig
Rugarli, Elena I.
Langer, Thomas
Gahl, William A.
Toro, Camilo
CA NISC Comparative Sequencing
TI Whole-Exome Sequencing Identifies Homozygous AFG3L2 Mutations in a
Spastic Ataxia-Neuropathy Syndrome Linked to Mitochondrial m-AAA
Proteases
SO PLOS GENETICS
LA English
DT Article
ID DIMETHYLGLYCINE DEHYDROGENASE; INBORN ERROR; PARAPLEGIA; DEGENERATION;
SCA28; GENE; METALLOPROTEASE; IMPAIRMENT; DEFICIENCY; METABOLISM
AB We report an early onset spastic ataxia-neuropathy syndrome in two brothers of a consanguineous family characterized clinically by lower extremity spasticity, peripheral neuropathy, ptosis, oculomotor apraxia, dystonia, cerebellar atrophy, and progressive myoclonic epilepsy. Whole-exome sequencing identified a homozygous missense mutation (c.1847G>A; p.Y616C) in AFG3L2, encoding a subunit of an m-AAA protease. m-AAA proteases reside in the mitochondrial inner membrane and are responsible for removal of damaged or misfolded proteins and proteolytic activation of essential mitochondrial proteins. AFG3L2 forms either a homo-oligomeric isoenzyme or a hetero-oligomeric complex with paraplegin, a homologous protein mutated in hereditary spastic paraplegia type 7 (SPG7). Heterozygous loss-of-function mutations in AFG3L2 cause autosomal-dominant spinocerebellar ataxia type 28 (SCA28), a disorder whose phenotype is strikingly different from that of our patients. As defined in yeast complementation assays, the AFG3L2(Y616C) gene product is a hypomorphic variant that exhibited oligomerization defects in yeast as well as in patient fibroblasts. Specifically, the formation of AFG3L2(Y616C) complexes was impaired, both with itself and to a greater extent with paraplegin. This produced an early-onset clinical syndrome that combines the severe phenotypes of SPG7 and SCA28, in additional to other "mitochondrial'' features such as oculomotor apraxia, extrapyramidal dysfunction, and myoclonic epilepsy. These findings expand the phenotype associated with AFG3L2 mutations and suggest that AFG3L2-related disease should be considered in the differential diagnosis of spastic ataxias.
C1 [Pierson, Tyler Mark; Adams, David; Golas, Gretchen; Fajardo, Karin Fuentes; Markello, Thomas; Tifft, Cynthia; Gahl, William A.; Toro, Camilo] Natl Inst Hlth Off Rare Dis Res, NIH Undiagnosed Dis Program, Bethesda, MD USA.
[Adams, David; Golas, Gretchen; Markello, Thomas; Tifft, Cynthia; Gahl, William A.] NHGRI, Off Clin Director, NIH, Bethesda, MD 20892 USA.
[Pierson, Tyler Mark; Blackstone, Craig] Natl Inst Neurol Disorders & Stroke, Neurogenet Branch, NIH, Bethesda, MD USA.
[Martinelli, Paola; Rugarli, Elena I.] Univ Cologne, Bioctr, Cologne, Germany.
[Cherukuri, Praveen F.; Hansen, Nancy F.; Cruz, Pedro; Mullikin, James C.; Blakesley, Robert W.] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
[Teer, Jamie K.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Mullikin, James C.; NISC Comparative Sequencing] NHGRI, NIH Intramural Sequencing Ctr, NIH, Bethesda, MD 20892 USA.
[Kwan, Justin] Natl Inst Neurol Disorders & Stroke, EMG Sect, NIH, Bethesda, MD USA.
[Sandler, Anthony] Childrens Natl Med Ctr, Div Surg, Washington, DC 20010 USA.
[Langer, Thomas] Univ Cologne, Inst Genet, Ctr Mol Med CMMC, Cologne Excellence Cluster Cellular Stress Respon, D-5000 Cologne, Germany.
[Langer, Thomas] Max Planck Inst Biol Aging, Cologne, Germany.
RP Pierson, TM (reprint author), Natl Inst Hlth Off Rare Dis Res, NIH Undiagnosed Dis Program, Bethesda, MD USA.
EM piersonty@ninds.nih.gov
FU National Human Genome Research Institute or National Institutes of
Health; NIH, National Institutes of Health; Deutsche
Forschungsgemeinschaft [SFB635]; European Research Council
FX This work and D Adams, G Golas, K Fuentes Fajardo, T Markello, C Tifft,
WA Gahl, and C Toro were supported by the Intramural Research Program of
the National Human Genome Research Institute or National Institutes of
Health; this work and TM Pierson, D Adams, G Golas, K Fuente Fajardo, C
Tifft, WA Gahl, and C Toro were also supported by the NIH Undiagnosed
Diseases Program, National Institutes of Health. In addition, work was
also supported by grants from the Deutsche Forschungsgemeinschaft
(SFB635) and the European Research Council to T Langer. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 33
TC 73
Z9 75
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD OCT
PY 2011
VL 7
IS 10
AR e1002325
DI 10.1371/journal.pgen.1002325
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 843IL
UT WOS:000296665400026
PM 22022284
ER
PT J
AU Giannelli, SV
Graf, CE
Herrmann, FR
Michel, JP
Patel, KV
Pizzarelli, F
Ferrucci, L
Guralnik, J
AF Giannelli, Sandra V.
Graf, Christophe E.
Herrmann, Francois R.
Michel, Jean-Pierre
Patel, Kushang V.
Pizzarelli, Francesco
Ferrucci, Luigi
Guralnik, Jack
TI Natural History of Older Adults with Impaired Kidney Function: The
InCHIANTI Study
SO REJUVENATION RESEARCH
LA English
DT Article
ID GLOMERULAR-FILTRATION-RATE; NORMAL SERUM CREATININE; CHRONIC
RENAL-INSUFFICIENCY; CYSTATIN-C; FUNCTION DECLINE; UNITED-STATES;
DISEASE; PROGRESSION; AGE; POPULATION
AB The aim of this study was to assess the kidney function of an older community-dwelling population at baseline and appraise its evolution after 3 years of follow-up in terms of chronic kidney disease (CKD) stage progression, magnitude of glomerular filtration rate (GFR) changes, and value of serum creatinine. This was a prospective population-based study of 676 Italian participants, aged 65 years and older. GFR was estimated using the Cockcroft-Gault equation and the Modification of Diet in Renal Disease Study equation. Using the Cockcroft-Gault equation. A total of 33% of participants had criteria of CKD (GFR < 60 mL/min) at baseline; among them, the majority remained stable, 10% improved, and 7% progressed to more severe CKD stages at follow-up. Loss of GFR in participants with GFR < 60 mL/min was significantly lower (1.4 mL/min per year) than in participants with GFR >= 60 mL/min (3.3 mL/min per year) at baseline. Most participants classified with CKD stage 2 (GFR 60-89 mL/min) or stage 3 (GFR 30-59 mL/min) at baseline did not change stage, whereas 55% of people with CKD stage 1 (GFR > 90 mL/min) at baseline worsened to stage 2 and 10% worsened to stage 3. An abnormal high level of serum creatinine at baseline did not help to predict who might worsen at follow-up. Older people with CKD displayed a low progression of renal disease and therefore are at higher risk for comorbidities related to CKD than for progression to end-stage renal disease.
C1 [Giannelli, Sandra V.; Graf, Christophe E.; Herrmann, Francois R.; Michel, Jean-Pierre] Univ Hosp Geneva, Dept Internal Med Rehabil & Geriatr, Geneva, Switzerland.
[Patel, Kushang V.; Guralnik, Jack] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[Pizzarelli, Francesco] SM Annunziata Hosp, Div Nephrol, Florence, Italy.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
RP Giannelli, SV (reprint author), Univ Hosp Geneva, Dept Internal Med Rehabil & Geriatr, Rue Pont Bochet 3, CH-1226 Thonex, Switzerland.
EM sandra.giannelli@hcuge.ch
RI Giannelli, Sandra/E-8637-2011; HERRMANN, Francois/B-6710-2011; Graf,
Christophe/E-8635-2011
OI HERRMANN, Francois/0000-0003-1312-1517;
FU Italian Ministry of Health [ICS 100.1\RS97.71]; National Institute on
Aging, National Institutes of Health (NIH); Department of Rehabilitation
and Geriatrics, Geneva University Hospitals, Geneva, Switzerland
FX This study was supported as a "targeted project" (ICS 100.1\RS97.71) by
the Italian Ministry of Health, and in part by the Intramural Research
Program of the National Institute on Aging, National Institutes of
Health (NIH). Sandra V. Giannelli was supported by funds from the
Department of Rehabilitation and Geriatrics, Geneva University
Hospitals, Geneva, Switzerland. The granting institutions named did not
interfere in any way with the design, methods, subjects recruitment,
data collections, analysis, and preparation of paper.
NR 42
TC 7
Z9 7
U1 1
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1549-1684
J9 REJUV RES
JI Rejuv. Res.
PD OCT
PY 2011
VL 14
IS 5
BP 513
EP 523
DI 10.1089/rej.2011.1179
PG 11
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 839OA
UT WOS:000296375900006
PM 21954982
ER
PT J
AU Dutta, A
Henley, W
Lang, IA
Murray, A
Guralnik, J
Wallace, RB
Melzer, D
AF Dutta, Ambarish
Henley, William
Lang, Iain A.
Murray, Anna
Guralnik, Jack
Wallace, Robert B.
Melzer, David
TI The Coronary Artery Disease-Associated 9p21 Variant and Later Life
20-Year Survival to Cohort Extinction
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE coronary artery disease; genetic variation; myocardial infarction;
survival; Framingham Risk Score
ID CHROMOSOME 9P21.3; HEART-DISEASE; MYOCARDIAL-INFARCTION; ATHEROSCLEROSIS
RISK; GENETIC ASSOCIATION; ISCHEMIC-STROKE; LOCUS; POPULATION; DEATH;
SUSCEPTIBILITY
AB Background-Common variation at chromosome 9p21 (marked by rs10757278 or rs1333049) is associated with coronary artery disease (CAD) and peripheral vascular disease. A decreasing effect at older age was suggested, and effects on long-term mortality are unclear. We estimated 9p21 associations with CAD and all-cause mortality in a CAD diagnosis-free older population. We also estimated classification gains on adding the variant to the Framingham Risk Score (FRS) for CAD.
Methods and Results-DNA was from an Established Populations for Epidemiological Study of the Elderly-Iowa cohort from 1988 (participants >71 years), with death certificates obtained to 2008 for 92% of participants. Cox regression models were adjusted for confounders and CAD risk factors. Of 1095 CAD diagnosis-free participants, 52% were heterozygous (CG) and 22% were homozygous (CC) for the risk C allele rs1333049. Unadjusted CAD-attributed death rates in the CC group were 30 vs 22 per 1000 person-years for the GG group. The C allele was associated with all-cause (hazard ratio, 1.19; 95% CI, 1.08-1.30) and CAD (hazard ratio, 1.29; 95% CI, 1.08-1.56) mortality, independent of CAD risk factors. There was no association with stroke deaths. Variant associations with CAD mortality were attenuated after the age of 80 years (age-interaction term P = 0.05). In age group 71 to 80 years, FRS classified as high risk 21% of respondents who died of CAD within 10 years; adding 9p21 identified 27% of respondents.
Conclusions-In 71- to 80-year-old subjects free of CAD diagnoses, 9p21 is associated with excess mortality, mainly attributed to CAD mortality. Adding 9p21 to the FRS may improve the targeting of CAD prevention in older people, but validation in independent samples is needed for confirmation. (Circ Cardiovasc Genet. 2011; 4:542-548.)
C1 [Dutta, Ambarish; Henley, William; Lang, Iain A.; Melzer, David] Univ Exeter, Peninsula Med Sch, Epidemiol & Publ Hlth Grp, Exeter EX2 5DW, Devon, England.
[Wallace, Robert B.] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Ctr Aging, Iowa City, IA USA.
[Guralnik, Jack] NIA, NIH, Bethesda, MD 20892 USA.
RP Melzer, D (reprint author), Univ Exeter, Peninsula Med Sch, Epidemiol & Publ Hlth Grp, Barrack Rd, Exeter EX2 5DW, Devon, England.
EM david.melzer@pms.ac.uk
RI Lang, Iain/B-8255-2008;
OI Murray, Anna/0000-0002-2351-2522; Lang, Iain/0000-0002-8473-2350;
Melzer, David/0000-0002-0170-3838; Dutta, Ambarish/0000-0002-4019-7472
FU National Institutes of Health/National Institute on Aging [R01
AG024233]; Dunhill Trust UK; National Institute for Health Research;
Laboratory of Epidemiology, Demography and Biometry, National Institute
on Aging, Bethesda, MD
FX This study was supported by grant R01 AG024233 and the Intramural
Research Program, National Institutes of Health/National Institute on
Aging; an unrestricted research grant from the Dunhill Trust UK; and
funding from the National Institute for Health Research (Dr Henley).; We
thank the many people who contributed to the EPESE-Iowa study,
especially the respondents; and the support received from the Laboratory
of Epidemiology, Demography and Biometry, National Institute on Aging,
Bethesda, MD.
NR 33
TC 11
Z9 13
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1942-325X
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD OCT
PY 2011
VL 4
IS 5
BP 542
EP 548
DI 10.1161/CIRCGENETICS.111.960146
PG 7
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 841RB
UT WOS:000296529200015
PM 21852414
ER
PT J
AU Schnabel, RB
Kerr, KF
Lubitz, SA
Alkylbekova, EL
Marcus, GM
Sinner, MF
Magnani, JW
Wolf, PA
Deo, R
Lloyd-Jones, DM
Lunetta, KL
Mehra, R
Levy, D
Fox, ER
Arking, DE
Mosley, TH
Muller-Nurasyid, M
Young, TR
Wichmann, HE
Seshadri, S
Farlow, DN
Rotter, JI
Soliman, EZ
Glazer, NL
Wilson, JG
Breteler, MMB
Sotoodehnia, N
Newton-Cheh, C
Kaab, S
Ellinor, PT
Alonso, A
Benjamin, EJ
Heckbert, SR
AF Schnabel, Renate B.
Kerr, Kathleen F.
Lubitz, Steven A.
Alkylbekova, Ermeg L.
Marcus, Gregory M.
Sinner, Moritz F.
Magnani, Jared W.
Wolf, Philip A.
Deo, Rajat
Lloyd-Jones, Donald M.
Lunetta, Kathryn L.
Mehra, Reena
Levy, Daniel
Fox, Ervin R.
Arking, Dan E.
Mosley, Thomas H.
Mueller-Nurasyid, Martina
Young, Taylor R.
Wichmann, H. -Erich
Seshadri, Sudha
Farlow, Deborah N.
Rotter, Jerome I.
Soliman, Elsayed Z.
Glazer, Nicole L.
Wilson, James G.
Breteler, Monique M. B.
Sotoodehnia, Nona
Newton-Cheh, Christopher
Kaeaeb, Stefan
Ellinor, Patrick T.
Alonso, Alvaro
Benjamin, Emelia J.
Heckbert, Susan R.
CA Candidate Gene Assoc Resource CARe
TI Large-Scale Candidate Gene Analysis in Whites and African Americans
Identifies IL6R Polymorphism in Relation to Atrial Fibrillation The
National Heart, Lung, and Blood Institute's Candidate Gene Association
Resource (CARe) Project
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE atrial fibrillation; single nucleotide polymorphism; epidemiology;
cohort study; race/ethnicity
ID C-REACTIVE PROTEIN; CHROMOSOME 4Q25; ATHEROSCLEROSIS RISK; EUROPEAN
ANCESTRY; ISCHEMIC-STROKE; INFLAMMATION; VARIANTS; INTERLEUKIN-6;
DISEASE; DESIGN
AB Background-The genetic background of atrial fibrillation (AF) in whites and African Americans is largely unknown. Genes in cardiovascular pathways have not been systematically investigated.
Methods and Results-We examined a panel of approximately 50 000 common single-nucleotide polymorphisms (SNPs) in 2095 cardiovascular candidate genes and AF in 3 cohorts with participants of European (n = 18 524; 2260 cases) or African American descent (n = 3662; 263 cases) in the National Heart, Lung, and Blood Institute's Candidate Gene Association Resource. Results in whites were followed up in the German Competence Network for AF (n = 906, 468 cases). The top result was assessed in relation to incident ischemic stroke in the Cohorts for Heart and Aging Research in Genomic Epidemiology Stroke Consortium (n = 19 602 whites, 1544 incident strokes). SNP rs4845625 in the IL6R gene was associated with AF (relative risk [RR] C allele, 0.90; 95% confidence interval [CI], 0.85-0.95; P = 0.0005) in whites but did not reach statistical significance in African Americans (RR, 0.86; 95% CI, 0.72-1.03; P = 0.09). The results were comparable in the German AF Network replication, (RR, 0.71; 95% CI, 0.57-0.89; P = 0.003). No association between rs4845625 and stroke was observed in whites. The known chromosome 4 locus near PITX2 in whites also was associated with AF in African Americans (rs4611994; hazard ratio, 1.40; 95% CI, 1.16-1.69; P = 0.0005).
Conclusions-In a community-based cohort meta-analysis, we identified genetic association in IL6R with AF in whites. Additionally, we demonstrated that the chromosome 4 locus known from recent genome-wide association studies in whites is associated with AF in African Americans. (Circ Cardiovasc Genet. 2011; 4: 557-564.)
C1 [Heckbert, Susan R.] Univ Washington, Cardiovasc Hlth Res Unit, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98101 USA.
[Heckbert, Susan R.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
[Schnabel, Renate B.; Sinner, Moritz F.; Magnani, Jared W.; Wolf, Philip A.; Benjamin, Emelia J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Schnabel, Renate B.] Univ Med Ctr Hamburg Eppendorf, Dept Gen & Intervent Cardiol, Hamburg, Germany.
[Kerr, Kathleen F.] Univ Washington, Sch Publ Hlth, Dept Biostat, Seattle, WA 98101 USA.
[Lubitz, Steven A.; Sinner, Moritz F.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Alkylbekova, Ermeg L.; Fox, Ervin R.; Wilson, James G.] Univ Mississippi, Med Ctr, Dept Med, Jackson, MS 39216 USA.
[Marcus, Gregory M.] Univ Calif San Francisco, Div Cardiol, Electrophysiol Sect, San Francisco, CA USA.
[Sinner, Moritz F.; Mueller-Nurasyid, Martina; Kaeaeb, Stefan] Univ Munich, Univ Hosp Grosshadern, Dept Med 1, Munich, Germany.
[Magnani, Jared W.; Benjamin, Emelia J.] Boston Univ, Sch Med, Sect Cardiovasc Med, Boston, MA 02118 USA.
[Wolf, Philip A.; Seshadri, Sudha] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Wolf, Philip A.] Boston Univ, Sch Publ Hlth, Dept Neurol, Boston, MA USA.
[Deo, Rajat] Univ Penn, Div Cardiol, Electrophysiol Sect, Philadelphia, PA 19104 USA.
[Lloyd-Jones, Donald M.] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Lloyd-Jones, Donald M.] Northwestern Univ, Feinberg Sch Med, Bluhm Cardiovasc Inst, Chicago, IL 60611 USA.
[Lunetta, Kathryn L.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Mehra, Reena] Case Sch Med, Dept Med, Cleveland, OH USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
[Arking, Dan E.] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD USA.
[Mosley, Thomas H.] Univ Mississippi, Med Ctr, Dept Geriatr Med, Jackson, MS 39216 USA.
[Wichmann, H. -Erich] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol 1, Neuherberg, Germany.
[Mueller-Nurasyid, Martina; Wichmann, H. -Erich] Univ Munich, Chair Epidemiol, Inst Med Informat Biometry & Epidemiol, Munich, Germany.
[Young, Taylor R.; Farlow, Deborah N.; Newton-Cheh, Christopher] Broad Inst Harvard & Massachusetts Inst Technol, Cambridge, MA USA.
[Wichmann, H. -Erich] Univ Munich, Klinikum Grosshadern, D-8000 Munich, Germany.
[Rotter, Jerome I.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
[Soliman, Elsayed Z.] Wake Forest Univ, Bowman Gray Sch Med, Epidemiol Cardiol Res Ctr EPICARE, Winston Salem, NC USA.
[Glazer, Nicole L.] Boston Univ, Sch Med, Sect Prevent Med & Epidemiol, Boston, MA 02118 USA.
[Breteler, Monique M. B.] Univ Med Ctr, Erasmus MC, Rotterdam, Netherlands.
[Sotoodehnia, Nona; Heckbert, Susan R.] Univ Washington, Sch Med, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Sotoodehnia, Nona] Univ Washington, Sch Med, Dept Med, Div Cardiol, Seattle, WA 98195 USA.
[Newton-Cheh, Christopher] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiovasc Res Ctr,Ctr Human Genet Res, Boston, MA USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Alonso, Alvaro] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Benjamin, Emelia J.] Boston Univ, Dept Cardiol, Boston, MA 02215 USA.
[Benjamin, Emelia J.] Boston Univ, Dept Prevent Med, Boston, MA 02215 USA.
RP Heckbert, SR (reprint author), Univ Washington, Cardiovasc Hlth Res Unit, Sch Publ Hlth, Dept Epidemiol, 1730 Minor Ave,Suite 1360, Seattle, WA 98101 USA.
EM schnabelr@gmx.de; emelia@bu.edu; heckbert@u.washington.edu
RI Alonso, Alvaro/A-4917-2010; Lloyd-Jones, Donald/C-5899-2009; Kerr,
Kathleen/A-2893-2013; Schnabel, Renate/F-6527-2014; Breteler, Monique
/J-5058-2014;
OI Alonso, Alvaro/0000-0002-2225-8323; Lunetta,
Kathryn/0000-0002-9268-810X; Seshadri, Sudha/0000-0001-6135-2622; Mehra,
Reena/0000-0002-6222-2675; Benjamin, Emelia/0000-0003-4076-2336
FU NIH/NHLBI [RC1HL099452]; American Heart Association [09SDG2280087,
09FTF2190028]; CHS (Cardiovascular Health Study); National Heart, Lung,
and Blood Institute [N01-HC-85079, N01-HC-85086, N01-HC-35129,
N01-HC-15103, HHSN268200625226C, HHSN268200900055C, N01-HC-55015,
N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021,
N01-HC-55022 R01HL087641, R01HL59367, R01HL086694, R01HL093029]; FHS
(Framingham Heart Study) [R01-HL080295]; National Heart, Lung and Blood
Institute's Framingham Heart Study [N01-HC-25195]; Affymetrix, Inc
[N02-HL-6-4278]; Robert Dawson Evans Endowment of the Department of
Medicine at Boston University School of Medicine and Boston Medical
Center; NIH [HHSN268200625226C, 1R01HL092577, RC1HL101056, AG028321, T32
HL007575, DA027021, HL104156, HL105780]; Deutsche Forschungsgemeinschaft
(German Research Foundation) [SCHN 1149/1-1]; FHS [SCHN 1149/3-1];
German Federal Ministry of Education and Research (Bundesministerium fur
Bildung und Forschung); German National Genome Research Network (NGFN);
German National Competence Network on Atrial Fibrillation (AFNET);
Leducq Foundation [07-CVD 03]; German Heart Foundation; Helmholtz
Zentrum Munchen; State of Bavaria; German National Genome Research
Network; LMUinnovativ; National Human Genome Research Institute
[U01HG004402]; NIH Roadmap for Medical Research [UL1RR025005]; National
Institute on Aging [R01AG027002]; National Center for Research Resources
[M01RR00069]; National Institute of Diabetes and Digestive and Kidney
Diseases [DK063491]; Affymetrix [N02-HL-6-4278]; Robert Dawson Evans
Endowment of the Department of Medicine at Boston University School of
Medicine; Boston Medical Center; NINDS [NS17950]; National Institute of
Aging [AG08122, AG031287, AG033193]; Netherlands Organization of
Scientific Research [175.010.2005.011]; Netherlands Genomics Initiative
(NGI)/Netherlands Organization for Scientific Research (NWO) Netherlands
Consortium for Healthy Ageing [050-060-810]; Erasmus Medical Center and
Erasmus University, Rotterdam; Netherlands Organization for Health
Research and Development; Research Institute for Diseases in the
Elderly; Ministry of Education, Culture, and Science; Ministry for
Health, Welfare, and Sports; European Commission; Municipality of
Rotterdam to the Rotterdam Study; [01GS0499]; [01GI0204]; [01GS0838]
FX We acknowledge the support of the National Heart, Lung, and Blood
Institute and the contributions of the all research institutions, study
investigators, field staff, and study participants in creating the
Candidate Gene Association Resource for Biomedical Research (CARe). The
following 3 parent studies have specifically contributed phenotype data
and DNA samples through the Massachusetts Institute of Technology, Broad
Institute (N01-HC-65226) to create this genotype/phenotype database that
will become publically available: ARIC (Atherosclerosis Risk in
Communities), University of North Carolina at Chapel Hill
(N01-HC-55015), Baylor Medical College (N01-HC-55016), University of
Mississippi Medical Center (N01-HC-55021), University of Minnesota
(N01-HC-55019), Johns Hopkins University (N01-HC-55020), University of
Texas, Houston (N01-HC-55022), and University of North Carolina, Forsyth
County (N01-HC-55018). This study was additionally supported by grants
RC1HL099452 (NIH/NHLBI) and 09SDG2280087 (American Heart Association);
CHS (Cardiovascular Health Study). This research was supported by
contracts N01-HC-85079 through N01-HC-85086, N01-HC-35129, N01-HC-15103,
HHSN268200625226C, and HHSN268200900055C from the National Heart, Lung,
and Blood Institute, and by grant R01-HL080295; FHS (Framingham Heart
Study). This research was conducted using data and resources from the
Framingham Heart Study of the National Heart Lung and Blood Institute of
the National Institutes of Health and Boston University School of
Medicine based on analyses by Framingham Heart Study investigators
participating in the SNP Health Association Resource (SHARe) project.
This work was supported by the National Heart, Lung and Blood
Institute's Framingham Heart Study (contract No. N01-HC-25195) and its
contract with Affymetrix, Inc for genotyping services (contract No.
N02-HL-6-4278). A portion of this research utilized the Linux Cluster
for Genetic Analysis (LinGA-II) funded by the Robert Dawson Evans
Endowment of the Department of Medicine at Boston University School of
Medicine and Boston Medical Center. The Framingham Heart Study research
was supported by NIH grants 1R01HL092577 (P.T.E., E.J.B.); RC1HL101056
(E.J.B., A.A.); AG028321 (E.J.B.); T32 HL007575 (S.A.L.); DA027021,
HL104156, and HL105780 (P.T.E.); The Deutsche Forschungsgemeinschaft
(German Research Foundation) Research Fellowship SCHN 1149/1-1 and Emmy
Noether Program SCHN 1149/3-1 supported FHS research (R. B. S.). JWM was
supported by American Heart Association award No. 09FTF2190028;
AFNET/KORA S4: The study was also supported by the German Federal
Ministry of Education and Research (Bundesministerium fur Bildung und
Forschung) in the context of the German National Genome Research Network
(NGFN), the German National Competence Network on Atrial Fibrillation
(AFNET), the Leducq Foundation (07-CVD 03) by grants to Dr Kaab
(01GS0499, 01GI0204, and 01GS0838). Dr Sinner is supported by the German
Heart Foundation.; KORA S4: The KORA platform is funded by the Helmholtz
Zentrum Munchen, the BMBF partly in the context of the German National
Genome Research Network, and the State of Bavaria, and as part of
LMUinnovativ; CHARGE Stroke Consortium: Supported by grants or contracts
from the National Heart, Lung, and Blood Institute (N01-HC-55015,
N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021,
N01-HC-55022 R01HL087641, R01HL59367, and R01HL086694, R01HL093029), the
National Human Genome Research Institute (U01HG004402), and NIH
(HHSN268200625226C) and the NIH Roadmap for Medical Research
(UL1R025005) to the Atherosclerosis Risk in Communities study; contracts
and grants from the National Heart, Lung, and Blood Institute
(N01-HC-85079 through N01-HC-85086, N01-HC-35129, N01-HC-15103,
N01-HC-55222, N01-HC-75150, N01-HC-45133, U01HL080295, and R01HL087652),
the National Institute on Aging (R01AG027002), the National Center for
Research Resources (M01RR00069, that partially supported the
genotyping), and the National Institute of Diabetes and Digestive and
Kidney Diseases (DK063491) to the Cardiovascular Health Study; grants
from the National Heart, Lung, and Blood Institute (N01-HC-25195) and
its contract with Affymetrix for genotyping services (N02-HL-6-4278),
the Robert Dawson Evans Endowment of the Department of Medicine at
Boston University School of Medicine and Boston Medical Center for the
use of the Linux Cluster for Genetic Analysis; and by grants from the
NINDS (NS17950) and the National Institute of Aging (AG08122, AG031287,
and AG033193 to the Framingham Heart Study), the Netherlands
Organization of Scientific Research (175.010.2005.011), the Netherlands
Genomics Initiative (NGI)/Netherlands Organization for Scientific
Research (NWO) Netherlands Consortium for Healthy Ageing (050-060-810),
the Erasmus Medical Center and Erasmus University, Rotterdam, the
Netherlands Organization for Health Research and Development, the
Research Institute for Diseases in the Elderly, the Ministry of
Education, Culture, and Science, the Ministry for Health, Welfare, and
Sports, the European Commission, and the Municipality of Rotterdam to
the Rotterdam Study. We thank the staff and participants of the
above-mentioned studies for their important contributions.
NR 45
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1942-3268
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD OCT
PY 2011
VL 4
IS 5
BP 557
EP U188
DI 10.1161/CIRCGENETICS.110.959197
PG 28
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 841RB
UT WOS:000296529200017
PM 21846873
ER
PT J
AU Saunier, B
Triyatni, M
Berger, EA
AF Saunier, Bertrand
Triyatni, Miriam
Berger, Edward A.
TI Culturing HCV: challenges and progress
SO FUTURE VIROLOGY
LA English
DT Article
DE adaptive mutations; cell culture; deterministic approaches; HCV; human
hepatocytes; RNA replication
ID HEPATITIS-C-VIRUS; CELL-CULTURE; IN-VIVO; EFFICIENT REPLICATION;
STRUCTURAL PROTEINS; ACTING ANTIVIRALS; RNA REPLICATION; INFECTION;
PARTICLES; GENOTYPE
AB Hepatocellular carcinoma cell lines supporting HCV replication in culture produce infectious particles (cell culture-derived HCV) for only a limited number of strains. Mutations in the viral genome resulting from the combined effects of the error-prone HCV RNA polymerase coupled with selection of the best-adapted viral variants generate a drift in cell culture-derived HCV properties, which can result in a total loss of in vivo infectivity in the chimpanzee model. Other systems for producing HCV or HCV-related particles, some of which bypass HCV RNA replication, have been developed to study the biology of this virus, with limitations of their own. This review briefly analyzes the pros and cons of these in vitro models, focusing on recent advances.
C1 [Saunier, Bertrand] Inst Cochin, F-75014 Paris, France.
[Saunier, Bertrand] INSERM, U1016, Paris, France.
[Saunier, Bertrand] CNRS, UMR8104, Paris, France.
[Saunier, Bertrand] Univ Paris 05, Fac Med, F-75006 Paris, France.
[Triyatni, Miriam] Hoffmann La Roche Inc, Virol Discovery, Nutley, NJ 07110 USA.
[Berger, Edward A.] NIAID, Mol Struct Sect, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Saunier, B (reprint author), Inst Cochin, 27 Rue Fg St Jacques, F-75014 Paris, France.
EM bertrand.saunier@inserm.fr
NR 78
TC 0
Z9 0
U1 3
U2 3
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1746-0794
J9 FUTURE VIROL
JI Future Virol.
PD OCT
PY 2011
VL 6
IS 10
BP 1169
EP 1178
DI 10.2217/FVL.11.95
PG 10
WC Virology
SC Virology
GA 841FA
UT WOS:000296496700010
ER
PT J
AU Shriner, D
AF Shriner, D.
TI Investigating population stratification and admixture using
eigenanalysis of dense genotypes
SO HEREDITY
LA English
DT Article
DE admixture; population stratification; principal components; stopping
rule; vicariance
ID PRINCIPAL-COMPONENTS; NUMBER; ASSOCIATION; MAP
AB Principal components analysis of genetic data is used to avoid inflation in type I error rates in association testing due to population stratification by covariate adjustment using the top eigenvectors and to estimate cluster or group membership independent of self-reported or ethnic identities. Eigendecomposition transforms correlated variables into an equal number of uncorrelated variables. Numerous stopping rules have been developed to identify which principal components should be retained. Recent developments in random matrix theory have led to a formal hypothesis test of the top eigenvalue, providing another way to achieve dimension reduction. In this study, I compare Velicer's minimum average partial test to a test on the basis of Tracy-Widom distribution as implemented in EIGENSOFT, the most widely used implementation of principal components analysis in genome-wide association analysis. By computer simulation of vicariance on the basis of coalescent theory, EIGENSOFT systematically overestimates the number of significant principal components. Furthermore, this overestimation is larger for samples of admixed individuals than for samples of unadmixed individuals. Overestimating the number of significant principal components can potentially lead to a loss of power in association testing by adjusting for unnecessary covariates and may lead to incorrect inferences about group differentiation. Velicer's minimum average partial test is shown to have both smaller bias and smaller variance, often with a mean squared error of 0, in estimating the number of principal components to retain. Velicer's minimum average partial test is implemented in R code and is suitable for genome-wide genotype data with or without population labels. Heredity (2011) 107, 413-420; doi:10.1038/hdy.2011.26; published online 30 March 2011
C1 NHGRI, Ctr Res Genom & Global Hlth, Bethesda, MD 20892 USA.
RP Shriner, D (reprint author), NHGRI, Ctr Res Genom & Global Hlth, Bldg 12A,Room 4047,12 South Dr,MSC 5635, Bethesda, MD 20892 USA.
EM shrinerda@mail.nih.gov
FU National Institutes of Health [S06GM008016-320107, S06GM008016-380111,
2M01RR010284]; Center for Research on Genomics and Global Health
(CRGGH); National Human Genome Research Institute; National Institute of
Diabetes and Digestive and Kidney Diseases; Center for Information
Technology; Office of the Director at the National Institutes of Health
[Z01HG200362]
FX I thank Gil McVean for sharing R code to perform simulations of
coalescent vicariance for two populations. The contents of this
publication are solely the responsibility of the author and do not
necessarily represent the official view of the National Institutes of
Health. The Howard University Family Study was supported by National
Institutes of Health grants S06GM008016-320107 to Charles Rotimi and
S06GM008016-380111 to Adebowale Adeyemo. Participant enrollment was
carried out at the Howard University General Clinical Research Center,
supported by National Institutes of Health grant 2M01RR010284.
Genotyping support was provided by the Coriell Institute for Medical
Research. This research was supported by the Intramural Research Program
of the Center for Research on Genomics and Global Health (CRGGH). The
CRGGH is supported by the National Human Genome Research Institute, the
National Institute of Diabetes and Digestive and Kidney Diseases, the
Center for Information Technology, and the Office of the Director at the
National Institutes of Health (Z01HG200362).
NR 19
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U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0018-067X
J9 HEREDITY
JI Heredity
PD OCT
PY 2011
VL 107
IS 5
BP 413
EP 420
DI 10.1038/hdy.2011.26
PG 8
WC Ecology; Evolutionary Biology; Genetics & Heredity
SC Environmental Sciences & Ecology; Evolutionary Biology; Genetics &
Heredity
GA 842BE
UT WOS:000296560300005
PM 21448230
ER
PT J
AU Ji, HF
Ren, W
Wang, LY
Shi, P
Chen, XF
Wu, XQ
Yao, X
Lau, ST
Zhou, QF
Shung, KK
AF Ji, Hongfen
Ren, Wei
Wang, Lingyan
Shi, Peng
Chen, Xiaofeng
Wu, Xiaoqing
Yao, Xi
Lau, Sien-Ting
Zhou, Qifa
Shung, K. Kirk
TI Structure and Electrical Properties of Na0.5Bi0.5TiO3 Ferroelectric
Thick Films Derived From a Polymer Modified Sol-Gel Method
SO IEEE TRANSACTIONS ON ULTRASONICS FERROELECTRICS AND FREQUENCY CONTROL
LA English
DT Article
ID PULSED-LASER DEPOSITION; PIEZOELECTRIC PROPERTIES; MU-M; DEPENDENCE;
POLYVINYLPYRROLIDONE; FABRICATION; STRESS; MODEL
AB Lead-free Na0.5Bi0.5TiO3 (NBT) ferroelectric thick films were prepared by a poly(vinylpyrrolidone) (PVP) modified sol-gel method. The NBT thick films annealed from 500 degrees C to 750 degrees C exhibit a perovskite structure. The relationship between annealing temperature, thickness, and electrical properties of the thick films has been investigated. The dielectric constants and remnant polarizations of the thick films increase with annealing temperature. The electrical properties of the NBT films show strong thickness dependence. As thickness increases from 1.0 to 4.8 mu m, the dielectric constant of the NBT films increases from 620 to 848, whereas the dielectric loss is nearly independent of the thickness. The remnant polarization of the NBT thick films also increases with increasing thickness. The leakage current density first decreases and then increases with film thickness.
C1 [Ji, Hongfen; Ren, Wei; Wang, Lingyan; Shi, Peng; Chen, Xiaofeng; Wu, Xiaoqing; Yao, Xi] Xi An Jiao Tong Univ, Elect Mat Res Lab, Key Lab, Minist Educ, Xian, Peoples R China.
[Ji, Hongfen; Ren, Wei; Wang, Lingyan; Shi, Peng; Chen, Xiaofeng; Wu, Xiaoqing; Yao, Xi] Xi An Jiao Tong Univ, Int Ctr Dielect Res, Xian, Peoples R China.
[Lau, Sien-Ting; Zhou, Qifa; Shung, K. Kirk] Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA USA.
[Lau, Sien-Ting; Zhou, Qifa; Shung, K. Kirk] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
RP Ji, HF (reprint author), Xi An Jiao Tong Univ, Elect Mat Res Lab, Key Lab, Minist Educ, Xian, Peoples R China.
EM wren@mail.xtju.edu.cn
RI Lau, Sien-Ting/B-6091-2013; shi, peng/C-8551-2011
OI shi, peng/0000-0003-2217-8486
FU National Natural Science Foundation of China [90923001, U0634006];
International Science & Technology Cooperation Program of China
[2010DFB13640]; Shaanxi Province International Collaboration Program
[2009KW-12, 2010KW-09]; NIH [P41-EB2182]
FX Manuscript received December 31, 2010; accepted July 8, 2011. This work
was financially supported by the National Natural Science Foundation of
China (Grant Nos. 90923001 and U0634006), by the International Science &
Technology Cooperation Program of China (Grant No. 2010DFB13640), by the
Shaanxi Province International Collaboration Program (Grant Nos.
2009KW-12 and 2010KW-09), and by NIH Grant P41-EB2182.
NR 36
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U1 3
U2 25
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0885-3010
J9 IEEE T ULTRASON FERR
JI IEEE Trans. Ultrason. Ferroelectr. Freq. Control
PD OCT
PY 2011
VL 58
IS 10
BP 2042
EP 2049
DI 10.1109/TUFFC.2011.2054
PG 8
WC Acoustics; Engineering, Electrical & Electronic
SC Acoustics; Engineering
GA 847XI
UT WOS:000297007300003
PM 21989868
ER
PT J
AU Wang, E
Marincola, FM
AF Wang, Ena
Marincola, Francesco M.
TI Applying the uncertainty principle to immunology FOREWORD
SO IMMUNOTHERAPY
LA English
DT Editorial Material
ID CANCER PATIENTS; T-CELLS; TUMOR; IMMUNITY
C1 [Wang, Ena; Marincola, Francesco M.] NIH, Infect Dis Immunogenet Sect IDIS, Dept Transfus Med, Clin Ctr trans NIH Ctr Human Immunol CHI, Bethesda, MD 20892 USA.
RP Marincola, FM (reprint author), NIH, Infect Dis Immunogenet Sect IDIS, Dept Transfus Med, Clin Ctr trans NIH Ctr Human Immunol CHI, Bethesda, MD 20892 USA.
EM fmarincola@mail.cc.nih.gov
FU Intramural NIH HHS [ZIA CL002118-03]
NR 20
TC 1
Z9 1
U1 0
U2 1
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1750-743X
J9 IMMUNOTHERAPY-UK
JI Immunotherapy
PD OCT
PY 2011
VL 3
IS 10
BP 1127
EP 1128
DI 10.2217/IMT.11.125
PG 2
WC Immunology
SC Immunology
GA 843XX
UT WOS:000296711800001
PM 21995565
ER
PT J
AU Kotlan, B
Umansky, V
Malyguine, AM
Marincola, FM
Shurin, MR
AF Kotlan, Beatrix
Umansky, Viktor
Malyguine, Anatoli M.
Marincola, Francesco M.
Shurin, Michael R.
TI Immunotherapy reaches new milestones in cancer eradication
SO IMMUNOTHERAPY
LA English
DT News Item
ID ADOPTIVE IMMUNOTHERAPY; T-CELLS; THERAPY; LYMPHOCYTES
C1 [Kotlan, Beatrix] Natl Inst Oncol, Ctr Surg & Mol Tumor Pathol, Dept Mol Immunol & Toxicol, Budapest, Hungary.
[Umansky, Viktor] German Canc Res Ctr, Clin Cooperat Unit, D-69120 Heidelberg, Germany.
[Malyguine, Anatoli M.] NCI, Lab Cell Mediated Immun, SAIC Frederick, Frederick, MD 21702 USA.
[Marincola, Francesco M.] NIH, Infect Dis & Immunogenet Sect IDIS, Dept Translat Med, Ctr Clin, Bethesda, MD 20892 USA.
[Marincola, Francesco M.] NIH, Ctr Human Immunol, Bethesda, MD 20892 USA.
[Shurin, Michael R.] Univ Pittsburgh, Dept Pathol, Med Ctr, Pittsburgh, PA 15213 USA.
[Shurin, Michael R.] Univ Pittsburgh, Dept Immunol, Med Ctr, Pittsburgh, PA 15213 USA.
RP Kotlan, B (reprint author), Natl Inst Oncol, Ctr Surg & Mol Tumor Pathol, Dept Mol Immunol & Toxicol, 1122 Rath Gy St 7-9, Budapest, Hungary.
EM kotlanb@netscape.net
NR 21
TC 1
Z9 1
U1 0
U2 0
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1750-743X
J9 IMMUNOTHERAPY-UK
JI Immunotherapy
PD OCT
PY 2011
VL 3
IS 10
BP 1131
EP 1137
DI 10.2217/IMT.11.114
PG 7
WC Immunology
SC Immunology
GA 843XX
UT WOS:000296711800004
PM 21995567
ER
PT J
AU Subleski, JJ
Jiang, Q
Weiss, JM
Wiltrout, RH
AF Subleski, Jeff J.
Jiang, Qun
Weiss, Jonathan M.
Wiltrout, Robert H.
TI The split personality of NKT cells in malignancy, autoimmune and
allergic disorders
SO IMMUNOTHERAPY
LA English
DT Review
DE autoimmunity; cancer; inflammation; NAFLD; type I NKT cells; type II NKT
cells
ID KILLER T-CELLS; FATTY LIVER-DISEASE; INDUCED JOINT INFLAMMATION;
NONOBESE DIABETIC MICE; INNATE IMMUNE-SYSTEM; INDUCED AIRWAY
HYPERREACTIVITY; ANTIGEN-PRESENTING CELLS; PHASE I/II TRIAL;
NATURAL-KILLER; DENDRITIC CELLS
AB NKT cells are a heterogeneous subset of specialized, self-reactive T cells, with innate and adaptive immune properties, which allow them to bridge innate and adaptive immunity and profoundly influence autoimmune and malignant disease outcomes. NKT cells mediate these activities through their ability to rapidly express pro- and anti-inflammatory cytokines that influence the type and magnitude of the immune response. Not only do NKT cells regulate the functions of other cell types, but experimental evidence has found NKT cell subsets can modulate the functions of other NKT subsets. Depending on underlying mechanisms, NKT cells can inhibit or exacerbate autoimmunity and malignancy, making them potential targets for disease intervention. NKT cells can respond to foreign and endogenous antigenic glycolipid signals that are expressed during pathogenic invasion or ongoing inflammation, respectively, allowing them to rapidly react to and influence a broad array of diseases. In this article we review the unique development and activation pathways of NKT cells and focus on how these attributes augment or exacerbate autoimmune disorders and malignancy. We also examine the growing evidence that NKT cells are involved in liver inflammatory conditions that can contribute to the development of malignancy.
C1 [Subleski, Jeff J.; Jiang, Qun; Weiss, Jonathan M.; Wiltrout, Robert H.] NCI, Lab Expt Immunol, Canc & Inflammat Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
RP Wiltrout, RH (reprint author), NCI, Lab Expt Immunol, Canc & Inflammat Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
EM wiltrour@mail.nih.gov
RI Jiang, Qun/A-1358-2014
FU National Cancer Institute (NCI)/NIH
FX This work was supported by the Intramural Research Program of the
National Cancer Institute (NCI)/NIH. The authors have no other relevant
affiliations or financial involvement with any organization or entity
with a financial interest in or financial conflict with the subject
matter or materials discussed in the manuscript apart from those
disclosed.
NR 211
TC 17
Z9 20
U1 0
U2 2
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1750-743X
J9 IMMUNOTHERAPY-UK
JI Immunotherapy
PD OCT
PY 2011
VL 3
IS 10
BP 1167
EP 1184
DI 10.2217/IMT.11.117
PG 18
WC Immunology
SC Immunology
GA 843XX
UT WOS:000296711800007
PM 21995570
ER
PT J
AU Schauberger, EM
Ewart, SL
Arshad, SH
Huebner, M
Karmaus, W
Holloway, JW
Friderici, KH
Ziegler, JT
Zhang, HM
Rose-Zerilli, MJ
Barton, SJ
Holgate, ST
Kilpatrick, JR
Harley, JB
Lajoie-Kadoch, S
Harley, ITW
Hamid, Q
Kurukulaaratchy, RJ
Seibold, MA
Avila, PC
Rodriguez-Cintron, W
Rodriguez-Santana, JR
Hu, DL
Gignoux, C
Romieu, I
London, SJ
Burchard, EG
Langefeld, CD
Wills-Karp, M
AF Schauberger, Eric M.
Ewart, Susan L.
Arshad, Syed H.
Huebner, Marianne
Karmaus, Wilfried
Holloway, John W.
Friderici, Karen H.
Ziegler, Julie T.
Zhang, Hongmei
Rose-Zerilli, Matthew J.
Barton, Sheila J.
Holgate, Stephen T.
Kilpatrick, Jeffrey R.
Harley, John B.
Lajoie-Kadoch, Stephane
Harley, Isaac T. W.
Hamid, Qutayba
Kurukulaaratchy, Ramesh J.
Seibold, Max A.
Avila, Pedro C.
Rodriguez-Cintron, William
Rodriguez-Santana, Jose R.
Hu, Donglei
Gignoux, Christopher
Romieu, Isabelle
London, Stephanie J.
Burchard, Esteban G.
Langefeld, Carl D.
Wills-Karp, Marsha
TI Identification of ATPAF1 as a novel candidate gene for asthma in
children
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Asthma; ATPAF1; children; gene; genetic; genome-wide association;
purinergic; respiratory; single nucleotide polymorphism; SNP
ID GENOME-WIDE ASSOCIATION; CHILDHOOD ASTHMA; PUERTO-RICAN; SUSCEPTIBILITY
GENES; EXTRACELLULAR ATP; ASSEMBLY FACTORS; LINKAGE ANALYSES; DENDRITIC
CELLS; FRENCH EGEA; PHENOTYPES
AB Background: Asthma is a common disease of children with a complex genetic origin. Understanding the genetic basis of asthma susceptibility will allow disease prediction and risk stratification.
Objective: We sought to identify asthma susceptibility genes in children.
Methods: A nested case-control genetic association study of children of Caucasian European ancestry from a birth cohort was conducted. Single nucleotide polymorphisms (SNPs, n = 116,024) were genotyped in pools of DNA samples from cohort children with physician-diagnosed asthma (n = 112) and normal controls (n = 165). A genomic region containing the ATPAF1 gene was found to be significantly associated with asthma. Additional SNPs within this region were genotyped in individual samples from the same children and in 8 independent study populations of Caucasian, African American, Hispanic, or other ancestries. SNPs were also genotyped or imputed in 2 consortia control populations. ATPAF1 expression was measured in bronchial biopsies from asthmatic patients and controls.
Results: Asthma was found to be associated with a cluster of SNPs and SNP haplotypes containing the ATPAF1 gene, with 2 SNPs achieving significance at a genome-wide level (P = 2.26 x 10(-5) to 2.2 x 10(-8)). Asthma severity was also found to be associated with SNPs and SNP haplotypes in the primary population. SNP and/or gene-level associations were confirmed in the 4 non-Hispanic populations. Haplotype associations were also confirmed in the non-Hispanic populations (P = .045-.0009). ATPAF1 total RNA expression was significantly (P < .01) higher in bronchial biopsies from asthmatic patients than from controls.
Conclusion: Genetic variation in the ATPAF1 gene predisposes children of different ancestries to asthma. (J Allergy Clin Immunol 2011;128:753-60.)
C1 [Ewart, Susan L.] Michigan State Univ, Vet Med Ctr G100, E Lansing, MI 48824 USA.
[Arshad, Syed H.; Kurukulaaratchy, Ramesh J.] David Hide Asthma & Allergy Res Ctr, Isle Of Wight, England.
[Arshad, Syed H.; Holloway, John W.; Rose-Zerilli, Matthew J.; Barton, Sheila J.; Holgate, Stephen T.; Kurukulaaratchy, Ramesh J.] Univ Southampton, Sch Med, Southampton SO9 5NH, Hants, England.
[Karmaus, Wilfried; Zhang, Hongmei] Univ S Carolina, Columbia, SC 29208 USA.
[Ziegler, Julie T.; Langefeld, Carl D.] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
[Kilpatrick, Jeffrey R.; Harley, John B.] JKA Genom, Oklahoma City, OK USA.
[Harley, John B.] Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA.
[Lajoie-Kadoch, Stephane; Harley, Isaac T. W.; Wills-Karp, Marsha] Cincinnati Childrens Hosp, Med Ctr, Cincinnati, OH USA.
[Hamid, Qutayba] McGill Univ, Meakins Christie Lab, Montreal, PQ, Canada.
[Seibold, Max A.] Natl Jewish Hlth, Denver, CO USA.
[Avila, Pedro C.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Rodriguez-Cintron, William] Vet Affairs Med Ctr, San Juan, PR USA.
[Rodriguez-Santana, Jose R.] CSP, Ctr Neumol Pediatr, San Juan, PR USA.
[Hu, Donglei; Gignoux, Christopher; Burchard, Esteban G.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Romieu, Isabelle] Natl Inst Publ Hlth, Cuernevaca, Mexico.
[London, Stephanie J.] NIEHS, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Ewart, SL (reprint author), Michigan State Univ, Vet Med Ctr G100, E Lansing, MI 48824 USA.
EM ewart@cvm.msu.edu
RI Holloway, John/B-5424-2009; Schauberger, Eric/A-9213-2008;
OI Holloway, John/0000-0001-9998-0464; Schauberger,
Eric/0000-0001-5069-7190; Barton, Sheila/0000-0003-4963-4242; London,
Stephanie/0000-0003-4911-5290
FU National Institutes of Health [R01 AI061471, R01 HL67736, P01 HL076383,
T32GM063483]; Asthma UK [364]; Asthma, Allergy and Inflammation Research
Charity; Richard and Edith Strauss Foundation of Canada; Robert Wood
Johnson Foundation Amos Medical Faculty [HL078885, HL088133, AI077439,
ES015794]; Flight Attendant Medical Research Institute (FAMRI); National
Institutes of Health, National Institute of Environmental Health
Sciences [Z01 ES49019]; National Council of Science and Technology,
Mexico [26206-M]; National Center for Environmental Health at the
Centers for Disease Control and Prevention; National Heart, Lung, and
Blood Institute [NO1-HR-16044, NO1-HR-16045, NO1-HR-16046, NO1-HR-16047,
NO1-HR-16048, NO1-HR-16049, NO1-HR-16050, NO1-HR-16051, NO1-HR-16052,
HL071742-01, HL004519-04, 5U10HL064287, 5U10HL064288, 5U10HL064295,
5U10HL064307, 5U10HL064305, 5U10HL064313]; General Clinical Research
Center; National Center for Research Resources [M01RR00051,
M01RR0099718-24, M01RR02719-14, RR00036]; National Institutes of Health
and the National Jewish Medical and Research Center [M01 RR00036, M01
RR00051]
FX This study was funded by the National Institutes of Health, grants R01
AI061471, R01 HL67736, P01 HL076383, and T32GM063483, Asthma UK (364),
and the Asthma, Allergy and Inflammation Research Charity. The Wessex
Family Cohort was originally recruited in collaboration with Genome
Therapeutics Corporation and Schering-Plough. The Richard and Edith
Strauss Foundation of Canada and Dr Ron Olivenstein supported the severe
asthma program and collection of bronchial biopsies. The GALA studies
were supported by grants HL078885, HL088133, AI077439, and ES015794,
Robert Wood Johnson Foundation Amos Medical Faculty Development Program,
Flight Attendant Medical Research Institute (FAMRI). The Mexico
Childhood Asthma Study was supported by the Intramural Research Program
of the National Institutes of Health, National Institute of
Environmental Health Sciences (Z01 ES49019). Subject enrollment was also
supported in part by the National Council of Science and Technology
(grant 26206-M), Mexico. I. Romieu was supported in part by the National
Center for Environmental Health at the Centers for Disease Control and
Prevention. The CAMP study was supported by contracts with the National
Heart, Lung, and Blood Institute (NO1-HR-16044, NO1-HR-16045,
NO1-HR-16046, NO1-HR-16047, NO1-HR-16048, NO1-HR-16049, NO1-HR-16050,
NO1-HR-16051, and NO1-HR-16052) and by General Clinical Research Center
grants from the National Center for Research Resources (M01RR00051,
M01RR0099718-24, M01RR02719-14, and RR00036). The CARE study was
supported by grants (HL071742-01, HL004519-04, 5U10HL064287,
5U10HL064288, 5U10HL064295, 5U10HL064307, 5U10HL064305, and
5U10HL064313) from the National Heart, Lung, and Blood Institute. This
study was carried out in part in the General Clinical Research Centers
at Washington University School of Medicine (M01 RR00036) sponsored by
the National Institutes of Health and the National Jewish Medical and
Research Center (M01 RR00051). The data analyses for the CAMP, CARE,
Wellcome Trust Case Control Consortium, and the Consortium for Systemic
Lupus Erythematosus Genetics populations were supported by the Wake
Forest School of Medicine Center for Public Health Genomics.
NR 65
TC 14
Z9 14
U1 0
U2 4
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD OCT
PY 2011
VL 128
IS 4
BP 753
EP U415
DI 10.1016/j.jaci.2011.04.058
PG 19
WC Allergy; Immunology
SC Allergy; Immunology
GA 841UA
UT WOS:000296538100008
PM 21696813
ER
PT J
AU White, SS
Fenton, SE
Hines, EP
AF White, Sally S.
Fenton, Suzanne E.
Hines, Erin P.
TI Endocrine disrupting properties of perfluorooctanoic acid
SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Article
DE PFOA; Mammary gland; PPAR; Exposure; Developmental effects
ID MAMMARY-GLAND DEVELOPMENT; ACTIVATED RECEPTOR-ALPHA; NATIONAL BIRTH
COHORT; HUMAN BREAST-MILK; PERFLUORINATED COMPOUNDS; PEROXISOME
PROLIFERATOR; POLYFLUOROALKYL CHEMICALS; SULFONATE PFOS; AMMONIUM
PERFLUOROOCTANOATE; PRENATAL EXPOSURE
AB Perfluoroallcyl acids (PFAAs) have attracted attention in recent years for their environmental ubiquity, as well as their toxicity. Several PFAAs are found in human tissues globally, as humans are exposed on a daily basis through intake of contaminated food, water, and air, irrespective of proximity to industry. Perfluorooctanoic acid (PFOA) is a PFAA shown to be developmentally toxic in mice, with broad and varied health consequences that may include long-lasting effects in reproductive tissues and metabolic reprogramming. To date, the only demonstrated mode of action by which the health effects of PFOA are mediated is via the activation of the peroxisome proliferator-activated receptor alpha (PPAR alpha). The endogenous roles for this receptor, as well as the adverse outcomes of activation by exogenous agents during development, are currently under investigation. Recent studies suggest that PFOA may alter steroid hormone production or act indirectly, via ovarian effects, as a novel means of endocrine disruption. Here we review the existing literature on the known health effects of PFOA in animal models, focusing on sensitive developmental periods. To complement this, we also present epidemiologic health data, with the caveat that these studies largely address only associations between adult exposures and outcomes, rarely focusing on endocrine-specific endpoints, susceptible subpopulations, or windows of sensitivity. Further research in these areas is needed. Published by Elsevier
C1 [White, Sally S.; Fenton, Suzanne E.] NIEHS, Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
[Hines, Erin P.] US EPA, Natl Ctr Environm Assessment, Off Res & Dev, Res Triangle Pk, NC 27711 USA.
RP Fenton, SE (reprint author), NIEHS, Natl Toxicol Program, NIH, POB 12233,Bldg 101,MD E1-08, Res Triangle Pk, NC 27709 USA.
EM fentonse@niehs.nih.gov
OI Hines, Erin Pias/0000-0002-2458-6267
FU Intramural NIH HHS [ZIA ES102785-01, ZIA ES102785-02]
NR 99
TC 83
Z9 85
U1 6
U2 76
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-0760
J9 J STEROID BIOCHEM
JI J. Steroid Biochem. Mol. Biol.
PD OCT
PY 2011
VL 127
IS 1-2
SI SI
BP 16
EP 26
DI 10.1016/j.jsbmb.2011.03.011
PG 11
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 841WV
UT WOS:000296546800004
PM 21397692
ER
PT J
AU Liu, XD
Xu, LQ
Sun, LG
Liu, F
Wang, YH
Yan, H
Liu, Y
Luo, YH
Huang, J
AF Liu Xiaodong
Xu Liqiang
Sun Liguang
Liu Fei
Wang Yuhong
Yan Hong
Liu Yi
Luo Yuhan
Huang Jing
TI A 400-year record of black carbon flux in the Xisha archipelago, South
China Sea and its implication
SO MARINE POLLUTION BULLETIN
LA English
DT Article
DE Xisha Archipelago; Ornithogenic sediments; Black carbon; Deposition
flux; Energy structure
ID POLYCYCLIC AROMATIC-HYDROCARBONS; LAKE-SEDIMENTS; DONGDAO ISLAND;
GEOCHEMICAL EVIDENCE; SURFACE SEDIMENTS; ORGANIC-MATTER; SOILS;
EMISSIONS; RADIONUCLIDES; OXIDATION
AB We reconstructed the first long-term (similar to 400 years) records of black carbon (BC) deposition flux from three ornithogenic sediment profiles, which were collected from three remote, isolated islets of the Xisha archipelago, South China Sea. The significant correlations between black carbon, organic matter and excess Pb-210 suggested that black carbon was mainly derived from atmospheric deposition, and further enriched by plant-derived organic matter in sediments. During the past 400 years, the BC flux remained relatively low before the onset of 20th century; it started to increase from approximately 1900 AD, and peaked around the 1970s. In the recent 30 years, the BC flux seemed to display decreasing trend, very likely due to the change of energy structure and development of pollution control techniques. In comparison with marginal sea regions that are greatly impacted by anthropogenic activities, these pristine Xisha islands were not significantly influenced by black carbon of anthropogenic origin. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Liu Xiaodong; Xu Liqiang; Sun Liguang; Liu Fei; Yan Hong; Liu Yi; Luo Yuhan; Huang Jing] Univ Sci & Technol China, Inst Polar Environm, Sch Earth & Space Sci, Hefei 230026, Anhui, Peoples R China.
[Wang Yuhong] NIH, Bethesda, MD 20892 USA.
RP Liu, XD (reprint author), Univ Sci & Technol China, Inst Polar Environm, Sch Earth & Space Sci, Hefei 230026, Anhui, Peoples R China.
EM ycx@ustc.edu.cn; slg@ustc.edu.cn
RI Yan, Hong/I-8970-2014
FU National Natural Science Foundation of China [40730107]; National Basic
Research Program of China (973 Program) [2010CB428902]; CAS
[KZCX2-EW-QN50]; Ministry of Education of China's Ph.D. Programs
Foundation for the new teachers [20093402120004]; Fundamental Research
Funds for the Central Universities [WK2060190007]
FX This work was funded by the National Natural Science Foundation of China
(No. 40730107), the National Basic Research Program of China (973
Program, No. 2010CB428902), Knowledge Innovation Program of CAS
(KZCX2-EW-QN50), the Ministry of Education of China's Ph.D. Programs
Foundation for the new teachers (20093402120004) and the Fundamental
Research Funds for the Central Universities (No. WK2060190007). All
members of field study team, including the Chinese People's Liberation
Army, are acknowledged for their help in sample collection.
NR 52
TC 10
Z9 13
U1 5
U2 36
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0025-326X
EI 1879-3363
J9 MAR POLLUT BULL
JI Mar. Pollut. Bull.
PD OCT
PY 2011
VL 62
IS 10
BP 2205
EP 2212
DI 10.1016/j.marpolbul.2011.06.027
PG 8
WC Environmental Sciences; Marine & Freshwater Biology
SC Environmental Sciences & Ecology; Marine & Freshwater Biology
GA 834IX
UT WOS:000295954100033
PM 21840551
ER
PT J
AU Englund, EE
Neumann, S
Eliseeva, E
McCoy, JG
Titus, S
Zheng, W
Southall, N
Shinn, P
Leister, W
Thomas, CJ
Inglese, J
Austin, CP
Gershengorn, MC
Huang, WW
AF Englund, Erika E.
Neumann, Susanne
Eliseeva, Elena
McCoy, Joshua G.
Titus, Steven
Zheng, Wei
Southall, Noel
Shinn, Paul
Leister, William
Thomas, Craig J.
Inglese, James
Austin, Christopher P.
Gershengorn, Marvin C.
Huang, Wenwei
TI The synthesis and evaluation of dihydroquinazolin-4-ones and
quinazolin-4-ones as thyroid stimulating hormone receptor agonists
SO MEDCHEMCOMM
LA English
DT Article
ID HUMAN THYROTROPIN RECEPTOR; SMALL-MOLECULE AGONISTS; INVERSE AGONIST;
TSH RECEPTOR; BINDING; ANTAGONIST
AB We herein describe the rapid synthesis of a diverse set of dihydroquinazolin-4-ones and quinazolin-4-ones, their biological evaluation as thyroid stimulating hormone receptor (TSHR) agonists, and SAR analysis. Among the compounds screened, 8b was 60-fold more potent than the hit compound la, which was identified from a high throughput screen of over 73,000 compounds.
C1 [Englund, Erika E.; McCoy, Joshua G.; Titus, Steven; Zheng, Wei; Southall, Noel; Shinn, Paul; Leister, William; Thomas, Craig J.; Inglese, James; Austin, Christopher P.; Huang, Wenwei] NIH, Chem Genom Ctr, Bethesda, MD 20892 USA.
[Neumann, Susanne; Eliseeva, Elena; Gershengorn, Marvin C.] NIDDK, Bethesda, MD 20892 USA.
RP Huang, WW (reprint author), NIH, Chem Genom Ctr, 9800 Med Ctr Dr,Bldg B, Bethesda, MD 20892 USA.
RI Southall, Noel/H-8991-2012;
OI Southall, Noel/0000-0003-4500-880X; Zheng, Wei/0000-0003-1034-0757
FU National Institute of Diabetes and Digestive and Kidney Diseases;
Molecular Libraries Initiative of the Roadmap for Medical Research,
National Institutes of Health
FX This work was supported by the Intramural Research Programs of the
National Institute of Diabetes and Digestive and Kidney Diseases and the
Molecular Libraries Initiative of the Roadmap for Medical Research,
National Institutes of Health. We thank Chris LeClair, Jim Bougie,
Danielle VanLeer and Thomas Daniel for compound management and
analytical support.
NR 26
TC 5
Z9 5
U1 0
U2 5
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 2040-2503
J9 MEDCHEMCOMM
JI MedChemComm
PD OCT
PY 2011
VL 2
IS 10
BP 1016
EP 1020
DI 10.1039/c1md00145k
PG 5
WC Biochemistry & Molecular Biology; Chemistry, Medicinal
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 840AS
UT WOS:000296411200014
PM 22408719
ER
PT J
AU Devine, MJ
Gwinn, K
Singleton, A
Hardy, J
AF Devine, Michael J.
Gwinn, Katrina
Singleton, Andrew
Hardy, John
TI Parkinson's Disease and alpha-Synuclein Expression
SO MOVEMENT DISORDERS
LA English
DT Review
DE Parkinsonism; genetics; alpha-synuclein
ID MULTIPLE SYSTEM ATROPHY; LEWY BODY; IN-VIVO; SNCA DUPLICATION; GENE
DUPLICATION; MOUSE MODEL; NEURODEGENERATIVE DISEASE;
DOPAMINERGIC-NEURONS; LOCUS TRIPLICATION; MESSENGER-RNA
AB Genetic studies of Parkinson's disease over the last decade or more have revolutionized our understanding of this condition. alpha-Synuclein was the first gene to be linked to Parkinson's disease, and is arguably the most important: the protein is the principal constituent of Lewy bodies, and variation at its locus is the major genetic risk factor for sporadic disease. Intriguingly, duplications and triplications of the locus, as well as point mutations, cause familial disease. Therefore, subtle alterations of alpha-synuclein expression can manifest with a dramatic phenotype. We outline the clinical impact of alpha-synuclein locus multiplications, and the implications that this has for Parkinson's disease pathogenesis. Finally, we discuss potential strategies for disease-modifying therapies for this currently incurable disorder. (C) 2011 Movement Disorder Society
C1 [Devine, Michael J.; Hardy, John] UCL Inst Neurol, Dept Mol Neurosci, London WC1N 3BG, England.
[Gwinn, Katrina] Baylor Coll Med, Houston, TX 77030 USA.
[Singleton, Andrew] NIA, NIH, Bethesda, MD 20892 USA.
RP Devine, MJ (reprint author), UCL Inst Neurol, Dept Mol Neurosci, Queen Sq, London WC1N 3BG, England.
EM m.devine@ion.ucl.ac.uk
RI Hardy, John/C-2451-2009; Singleton, Andrew/C-3010-2009
FU Medical Research Council [G0800437, G0701075, MC_G1000735]; Parkinson's
UK [G-0907]; Wellcome Trust [089698]
NR 98
TC 64
Z9 65
U1 0
U2 9
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0885-3185
J9 MOVEMENT DISORD
JI Mov. Disord.
PD OCT
PY 2011
VL 26
IS 12
BP 2160
EP 2168
DI 10.1002/mds.23948
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 842PH
UT WOS:000296610900004
PM 21887711
ER
PT J
AU Bratslavsky, G
Linehan, WM
AF Bratslavsky, Gennady
Linehan, W. Marston
TI SURGERY Routine adrenalectomy in renal cancer-an antiquated practice
SO NATURE REVIEWS UROLOGY
LA English
DT Editorial Material
ID RADICAL NEPHRECTOMY; INSUFFICIENCY; COMPONENT; GLAND
AB For decades, complete removal of the kidney with all the contents of the Gerota's fascia (including the adrenal gland) has been a standard procedure for treating renal cell carcinoma (RCC). Two recent articles argue against routine adrenalectomy, and encourage adrenal preservation for the vast majority of patients with RCC.
C1 [Linehan, W. Marston] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Bratslavsky, Gennady] SUNY Upstate Med Univ, Dept Urol, Syracuse, NY 13210 USA.
RP Linehan, WM (reprint author), NCI, Urol Oncol Branch, NIH, 10 Ctr Dr,Room 1-5940, Bethesda, MD 20892 USA.
EM wml@nih.gov
FU Intramural NIH HHS [Z01 BC011023-01]; NCI NIH HHS [Z01 BC011092-01, Z01
BC011028-01, Z01 BC011023-01, Z01 BC011089-01]
NR 7
TC 1
Z9 1
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4812
J9 NAT REV UROL
JI Nat. Rev. Urol.
PD OCT
PY 2011
VL 8
IS 10
BP 534
EP 536
DI 10.1038/nrurol.2011.136
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA 838CT
UT WOS:000296265100002
PM 21931345
ER
PT J
AU Steeg, PS
Zollo, M
Wieland, T
AF Steeg, Patricia S.
Zollo, Massimo
Wieland, Thomas
TI A critical evaluation of biochemical activities reported for the
nucleoside diphosphate kinase/Nm23/Awd family proteins: opportunities
and missteps in understanding their biological functions
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Editorial Material
ID X-RAY-STRUCTURE; HETEROTRIMERIC G-PROTEINS; ENERGY PHOSPHATE TRANSFER;
SUPPRESS CELL-MIGRATION; GTP-BINDING-PROTEIN; BETA-GAMMA DIMERS;
ATP-CITRATE LYASE; KINASE NDPK B; TUMOR-METASTASIS; ESCHERICHIA-COLI
C1 [Wieland, Thomas] Univ Heidelberg, Mannheim Med Fac, Inst Expt & Clin Pharmacol & Toxicol, D-68169 Mannheim, Germany.
[Zollo, Massimo] Univ Naples Federico 2, Dipartimento Biochim & Biotecnol Avanzate, DBBM, Ctr Ingn Genet Biotecnol Avanzate,CEINGE, I-80131 Naples, Italy.
[Steeg, Patricia S.] NCI, Womens Canc Sect, Mol Pharmacol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Wieland, T (reprint author), Univ Heidelberg, Mannheim Med Fac, Inst Expt & Clin Pharmacol & Toxicol, Maybachstr 14, D-68169 Mannheim, Germany.
EM steegp@mail.nih.gov; massimo.zollo@unina.it;
thomas.wieland@urz.uni-heidelberg.de
RI Wieland, Thomas/G-1772-2012; Zollo, Massimo/K-5857-2016
OI Zollo, Massimo/0000-0002-0970-7243
NR 101
TC 20
Z9 20
U1 0
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0028-1298
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD OCT
PY 2011
VL 384
IS 4-5
BP 331
EP 339
DI 10.1007/s00210-011-0651-9
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 842YT
UT WOS:000296639000001
PM 21611737
ER
PT J
AU Marino, N
Marshall, JC
Steeg, PS
AF Marino, Natascia
Marshall, Jean-Claude
Steeg, Patricia S.
TI Protein-protein interactions: a mechanism regulating the anti-metastatic
properties of Nm23-H1
SO NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
LA English
DT Review
DE Nm23-H1; Protein interactions; Metastasis
ID NUCLEOSIDE DIPHOSPHATE KINASE; METASTASIS SUPPRESSOR NM23-H2;
BREAST-CARCINOMA CELLS; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE;
TUMOR-METASTASIS; ADHERENS JUNCTIONS; CANCER-CELLS; H-PRUNE;
SIGNAL-TRANSDUCTION; COMPLEX-FORMATION
AB Nm23-H1, also known as NDPK-A, was the first of a class of metastasis suppressor genes to be identified. Overexpression of Nm23-H1 in metastatic cell lines (melanoma, breast carcinoma, prostate, colon, hepatocellular, and oral squamous cell carcinoma) reduced cell motility in in vitro assays and metastatic potential in xenograft models, without a significant effect on primary tumor size. The mechanism of Nm23-H1 suppression of metastasis, however, is incompletely understood. Nm23-H1 has been reported to bind proteins, including those in small G-protein complexes, transcriptional complexes, the Map kinase, the TGF-beta signaling pathways and the cytoskeleton. Evidence supporting these associations is presented together with evidence of resultant biochemical and phenotypic consequences of association. Cumulatively, the data suggest that part of the anti-metastatic function of Nm23-H1 lies in pathways that it interrupts via binding and inactivation of proteins.
C1 [Marino, Natascia; Marshall, Jean-Claude] NIH, Bethesda, MD 20892 USA.
[Marino, Natascia; Marshall, Jean-Claude; Steeg, Patricia S.] NCI, Womens Canc Sect, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Marino, N (reprint author), NIH, Bldg 37,Room 1122, Bethesda, MD 20892 USA.
EM Marinon@mail.nih.gov; Marshallje@mail.nih.gov
FU National Cancer Institute
FX This research was supported by the Intramural program of the National
Cancer Institute.
NR 101
TC 22
Z9 26
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0028-1298
J9 N-S ARCH PHARMACOL
JI Naunyn-Schmiedebergs Arch. Pharmacol.
PD OCT
PY 2011
VL 384
IS 4-5
BP 351
EP 362
DI 10.1007/s00210-011-0646-6
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 842YT
UT WOS:000296639000003
PM 21713383
ER
PT J
AU Younes, SA
Punkosdy, G
Caucheteux, S
Chen, T
Grossman, Z
Paul, WE
AF Younes, Souheil-Antoine
Punkosdy, George
Caucheteux, Stephane
Chen, Tao
Grossman, Zvi
Paul, William E.
TI Memory Phenotype CD4 T Cells Undergoing Rapid, Nonburst-Like,
Cytokine-Driven Proliferation Can Be Distinguished from
Antigen-Experienced Memory Cells
SO PLOS BIOLOGY
LA English
DT Article
ID HOMEOSTATIC PROLIFERATION; NAIVE; LYMPHOCYTES; INFECTION; REPERTOIRE;
EXPANSION; EFFECTORS; SURVIVAL; OPINION
AB Memory phenotype (CD44(bright), CD25(negative)) CD4 spleen and lymph node T cells (MP cells) proliferate rapidly in normal or germ-free donors, with BrdU uptake rates of 6% to 10% per day and Ki-67 positivity of 18% to 35%. The rapid proliferation of MP cells stands in contrast to the much slower proliferation of lymphocytic choriomeningitis virus (LCMV)-specific memory cells that divide at rates ranging from <1% to 2% per day over the period from 15 to 60 days after LCMV infection. Anti-MHC class II antibodies fail to inhibit the in situ proliferation of MP cells, implying a non-T-cell receptor (TCR)-driven proliferation. Such proliferation is partially inhibited by anti-IL-7R alpha antibody. The sequence diversity of TCR beta CDR3 gene segments is comparable among the proliferating and quiescent MP cells from conventional and germ-free mice, implying that the majority of proliferating MP cells have not recently derived from a small cohort of cells that expand through multiple continuous rounds of cell division. We propose that MP cells constitute a diverse cell population, containing a subpopulation of slowly dividing authentic antigen-primed memory cells and a majority population of rapidly proliferating cells that did not arise from naive cells through conventional antigen-driven clonal expansion.
C1 [Younes, Souheil-Antoine; Punkosdy, George; Caucheteux, Stephane; Chen, Tao; Grossman, Zvi; Paul, William E.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Younes, SA (reprint author), NIAID, Immunol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM wpaul@niaid.nih.gov
RI younes, souheil-antoine/G-4503-2014
OI younes, souheil-antoine/0000-0003-2186-7140
FU Division of Intramural Research National Institute of Allergy and
Infectious Diseases
FX This research is funded by the Division of Intramural Research of the
National Institute of Allergy and Infectious Diseases. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 37
TC 18
Z9 18
U1 2
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1544-9173
J9 PLOS BIOL
JI PLoS. Biol.
PD OCT
PY 2011
VL 9
IS 10
AR e1001171
DI 10.1371/journal.pbio.1001171
PG 14
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics
GA 844GJ
UT WOS:000296735400004
PM 22022231
ER
PT J
AU Chi, BH
Yiannoutsos, CT
Westfall, AO
Newman, JE
Zhou, JL
Cesar, C
Brinkhof, MWG
Mwango, A
Balestre, E
Carriquiry, G
Sirisanthana, T
Mukumbi, H
Martin, JN
Grimsrud, A
Bacon, M
Thiebaut, R
AF Chi, Benjamin H.
Yiannoutsos, Constantin T.
Westfall, Andrew O.
Newman, Jamie E.
Zhou, Jialun
Cesar, Carina
Brinkhof, Martin W. G.
Mwango, Albert
Balestre, Eric
Carriquiry, Gabriela
Sirisanthana, Thira
Mukumbi, Henri
Martin, Jeffrey N.
Grimsrud, Anna
Bacon, Melanie
Thiebaut, Rodolphe
CA Int Epidemiologic Databases
TI Universal Definition of Loss to Follow-Up in HIV Treatment Programs: A
Statistical Analysis of 111 Facilities in Africa, Asia, and Latin
America
SO PLOS MEDICINE
LA English
DT Article
ID ANTIRETROVIRAL TREATMENT PROGRAMS; LOWER-INCOME COUNTRIES; SUB-SAHARAN
AFRICA; WESTERN KENYA; HIV-1-INFECTED PATIENTS; INFECTED PATIENTS;
THERAPY PROGRAMS; COHORT PROFILE; SCALE-UP; 1ST YEAR
AB Background: Although patient attrition is recognized as a threat to the long-term success of antiretroviral therapy programs worldwide, there is no universal definition for classifying patients as lost to follow-up (LTFU). We analyzed data from health facilities across Africa, Asia, and Latin America to empirically determine a standard LTFU definition.
Methods and Findings: At a set "status classification" date, patients were categorized as either "active" or "LTFU" according to different intervals from time of last clinic encounter. For each threshold, we looked forward 365 d to assess the performance and accuracy of this initial classification. The best-performing definition for LTFU had the lowest proportion of patients misclassified as active or LTFU. Observational data from 111 health facilities-representing 180,718 patients from 19 countries-were included in this study. In the primary analysis, for which data from all facilities were pooled, an interval of 180 d (95% confidence interval [CI]: 173-181 d) since last patient encounter resulted in the fewest misclassifications (7.7%, 95% CI: 7.6%-7.8%). A secondary analysis that gave equal weight to cohorts and to regions generated a similar result (175 d); however, an alternate approach that used inverse weighting for cohorts based on variance and equal weighting for regions produced a slightly lower summary measure (150 d). When examined at the facility level, the best-performing definition varied from 58 to 383 d (mean = 150 d), but when a standard definition of 180 d was applied to each facility, only slight increases in misclassification (mean = 1.2%, 95% CI: 1.0%-1.5%) were observed. Using this definition, the proportion of patients classified as LTFU by facility ranged from 3.1% to 45.1% (mean = 19.9%, 95% CI: 19.1%-21.7%).
Conclusions: Based on this evaluation, we recommend the adoption of >= 180 d since the last clinic visit as a standard LTFU definition. Such standardization is an important step to understanding the reasons that underlie patient attrition and establishing more reliable and comparable program evaluation worldwide.
C1 [Chi, Benjamin H.; Westfall, Andrew O.] Univ Alabama, Birmingham, AL USA.
[Chi, Benjamin H.; Westfall, Andrew O.] Ctr Infect Dis Res Zambia, Lusaka, Zambia.
[Yiannoutsos, Constantin T.] Indiana Univ, Indianapolis, IN 46204 USA.
[Newman, Jamie E.] RTI Int, Res Triangle Pk, NC USA.
[Zhou, Jialun] Univ New S Wales, Kirby Inst, Sydney, NSW, Australia.
[Cesar, Carina] Fdn Huesped, Buenos Aires, DF, Argentina.
[Brinkhof, Martin W. G.] Univ Bern, Bern, Switzerland.
[Mwango, Albert] Zambian Minist Hlth, Lusaka, Zambia.
[Balestre, Eric; Thiebaut, Rodolphe] Bordeaux Segalen Univ ISPED, INSERM, U897, Bordeaux, France.
[Carriquiry, Gabriela] Univ Peruana Cayetano Heredia, Inst Med Trop Alexander von Humboldt, Lima, Peru.
[Sirisanthana, Thira] Chiang Mai Univ, Chiang Mai 50000, Thailand.
[Martin, Jeffrey N.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Mukumbi, Henri] Amo Congo, Kinshasa, Zaire.
[Grimsrud, Anna] Univ Cape Town, ZA-7925 Cape Town, South Africa.
[Bacon, Melanie] NIH, Bethesda, MD 20892 USA.
RP Chi, BH (reprint author), Univ Alabama, Birmingham, AL USA.
EM bchi@cidrz.org
OI Westfall, Andrew/0000-0002-0468-4695; Brinkhof,
Martin/0000-0002-9319-665X; MASKEW, MHAIRI/0000-0003-4238-0200
FU National Institute of Allergy and Infectious Diseases; National Cancer
Institute; Eunice Kennedy Shriver National Institute of Child Health and
Human Development [U01AI069927, U01AI069919, U01AI069924, U01AI069907,
U01AI069923]; Foundation for AIDS Research (amfAR); Dutch Ministry of
Foreign Affairs; Stichting Aids Fonds; US National Institutes of Health
[D43-TW001035, P30-AI027767]; Doris Duke Charitable Foundation [2007061]
FX The International Epidemiologic Databases to Evaluate AIDS (IeDEA)
collaboration is funded jointly by the National Institute of Allergy and
Infectious Diseases, the National Cancer Institute, and the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
through the following grants: Central African region (U01AI069927),
Eastern African region (U01AI069919), Southern African region
(U01AI069924), Western African region (U01AI069919), Asia/Pacific region
(U01AI069907), and Caribbean, Central American, and South American
region (U01AI069923). The TREAT Asia HIV Observation Database, a
contributor to the Asia/Pacific IeDEA region, is jointly supported by
the Foundation for AIDS Research (amfAR), the Dutch Ministry of Foreign
Affairs, and Stichting Aids Fonds. Additional salary and trainee support
was provided by the US National Institutes of Health (D43-TW001035;
P30-AI027767) and the Doris Duke Charitable Foundation (2007061). No
funding bodies had any role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 30
TC 57
Z9 57
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1549-1277
J9 PLOS MED
JI PLos Med.
PD OCT
PY 2011
VL 8
IS 10
AR e1001111
DI 10.1371/journal.pmed.1001111
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 841YZ
UT WOS:000296552400012
PM 22039357
ER
PT J
AU Lessler, J
Metcalf, CJE
Grais, RF
Luquero, FJ
Cummings, DAT
Grenfell, BT
AF Lessler, Justin
Metcalf, C. Jessica E.
Grais, Rebecca F.
Luquero, Francisco J.
Cummings, Derek A. T.
Grenfell, Bryan T.
TI Measuring the Performance of Vaccination Programs Using Cross-Sectional
Surveys: A Likelihood Framework and Retrospective Analysis
SO PLOS MEDICINE
LA English
DT Article
ID COVERAGE
AB Background: The performance of routine and supplemental immunization activities is usually measured by the administrative method: dividing the number of doses distributed by the size of the target population. This method leads to coverage estimates that are sometimes impossible (e. g., vaccination of 102% of the target population), and are generally inconsistent with the proportion found to be vaccinated in Demographic and Health Surveys (DHS). We describe a method that estimates the fraction of the population accessible to vaccination activities, as well as within-campaign inefficiencies, thus providing a consistent estimate of vaccination coverage.
Methods and Findings: We developed a likelihood framework for estimating the effective coverage of vaccination programs using cross-sectional surveys of vaccine coverage combined with administrative data. We applied our method to measles vaccination in three African countries: Ghana, Madagascar, and Sierra Leone, using data from each country's most recent DHS survey and administrative coverage data reported to the World Health Organization. We estimate that 93% (95% CI: 91, 94) of the population in Ghana was ever covered by any measles vaccination activity, 77% (95% CI: 78, 81) in Madagascar, and 69% (95% CI: 67, 70) in Sierra Leone. "Within-activity" inefficiencies were estimated to be low in Ghana, and higher in Sierra Leone and Madagascar. Our model successfully fits age-specific vaccination coverage levels seen in DHS data, which differ markedly from those predicted by naive extrapolation from country-reported and World Health Organization-adjusted vaccination coverage.
Conclusions: Combining administrative data with survey data substantially improves estimates of vaccination coverage. Estimates of the inefficiency of past vaccination activities and the proportion not covered by any activity allow us to more accurately predict the results of future activities and provide insight into the ways in which vaccination programs are failing to meet their goals.
C1 [Lessler, Justin; Cummings, Derek A. T.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Metcalf, C. Jessica E.] Univ Oxford, Dept Zool, Oxford OX1 3PS, England.
[Grais, Rebecca F.] Harvard Univ, Harvard Humanitarian Initiat, Cambridge, MA 02138 USA.
[Grais, Rebecca F.; Luquero, Francisco J.] Epicentre, Paris, France.
[Grenfell, Bryan T.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Grenfell, Bryan T.] NIH, Forgarty Int Ctr, Bethesda, MD 20892 USA.
RP Lessler, J (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
EM jlessler@jhsph.edu
OI Lessler, Justin/0000-0002-9741-8109
FU Bill & Melinda Gates Foundation (Vaccine Modeling Initiative)
[705580-3]; Science & Technology Directorate, Department of Homeland
Security; Fogarty International Center, US National Institutes of
Health; Scientific Interface from the Burroughs Welcome Fund; Royal
Society; [NIH R01 GM083983-01]
FX The work of JL, CJEM, DATC, and BTG on this project was funded by a
grant from the Bill & Melinda Gates Foundation (Vaccine Modeling
Initiative, 705580-3). BTG and DATC were also supported by the RAPIDD
program of the Science & Technology Directorate, Department of Homeland
Security, and the Fogarty International Center, US National Institutes
of Health, and by grant NIH R01 GM083983-01. DATC holds a Career Award
at the Scientific Interface from the Burroughs Welcome Fund. CJEM is
funded by the Royal Society. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 16
TC 18
Z9 18
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1549-1277
J9 PLOS MED
JI PLos Med.
PD OCT
PY 2011
VL 8
IS 10
AR e1001110
DI 10.1371/journal.pmed.1001110
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 841YZ
UT WOS:000296552400011
PM 22039353
ER
PT J
AU Durbin, AP
Whitehead, SS
AF Durbin, Anna P.
Whitehead, Stephen S.
TI Next-Generation Dengue Vaccines: Novel Strategies Currently Under
Development
SO VIRUSES-BASEL
LA English
DT Review
DE Dengue vaccine; DNA vaccine; vectored-vaccine; sub-unit protein vaccine
ID NEUTRALIZING ANTIBODY-RESPONSE; GLYCOPROTEIN PROTECT MICE; TETRAVALENT
DNA VACCINE; FLAVIVIRUS-NAIVE ADULTS; VIRUS E-GLYCOPROTEIN;
IMMUNE-RESPONSES; MONOCLONAL-ANTIBODIES; NONHUMAN-PRIMATES; ADENOVIRUS
VECTOR; SUBUNIT VACCINE
AB Dengue has become the most important arboviral infection worldwide with more than 30 million cases of dengue fever estimated to occur each year. The need for a dengue vaccine is great and several live attenuated dengue candidate vaccines are proceeding through clinical evaluation. The need to induce a balanced immune response against all four DENV serotypes with a single vaccine has been a challenge for dengue vaccine developers. A live attenuated DENV chimeric vaccine produced by Sanofi Pasteur has recently entered Phase III evaluation in numerous dengue-endemic regions of the world. Viral interference between serotypes contained in live vaccines has required up to three doses of the vaccine be given over a 12-month period of time. For this reason, novel DENV candidate vaccines are being developed with the goal of achieving a protective immune response with an immunization schedule that can be given over the course of a few months. These next-generation candidates include DNA vaccines, recombinant adenovirus vectored vaccines, alphavirus replicons, and sub-unit protein vaccines. Several of these novel candidates will be discussed.
C1 [Durbin, Anna P.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Ctr Immunizat Res, Baltimore, MD 21205 USA.
[Whitehead, Stephen S.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Durbin, AP (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Ctr Immunizat Res, 624 N Broadway,Room 251, Baltimore, MD 21205 USA.
EM adurbin@jhsph.edu; swhitehead@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health, USA
FX Support for A. P. D. (in part) and S. S. W. is provided by the
Intramural Research Program of the National Institute of Allergy and
Infectious Diseases, National Institutes of Health, USA.
NR 65
TC 31
Z9 31
U1 0
U2 4
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD OCT
PY 2011
VL 3
IS 10
BP 1800
EP 1814
DI 10.3390/v3101800
PG 15
WC Virology
SC Virology
GA 842GY
UT WOS:000296585100001
PM 22069516
ER
PT J
AU Edwards, DC
McKinnon, KM
Fenizia, C
Jung, KJ
Brady, JN
Pise-Masison, CA
AF Edwards, Dustin C.
McKinnon, Katherine M.
Fenizia, Claudio
Jung, Kyung-Jin
Brady, John N.
Pise-Masison, Cynthia A.
TI Inhibition of Geranylgeranyl Transferase-I Decreases Cell Viability of
HTLV-1-Transformed Cells
SO VIRUSES-BASEL
LA English
DT Article
DE human T-cell leukemia virus type-1; HTLV-1; Tax; long terminal repeat;
LTR; geranylgeranyltransferase; GGTI-298; small GTPase; NF-kappa B; p53;
cell cycle
ID VIRUS TYPE-I; PROTEIN GERANYLGERANYLATION; LEUKEMIA-CELLS; HTLV-I;
1-TRANSFORMED CELLS; TUMOR-CELLS; TAX PROTEIN; RHO-GTPASES; KAPPA-B;
APOPTOSIS
AB Human T-cell leukemia virus type-1 (HTLV-1) is the etiological agent of adult T-cell leukemia (ATL), an aggressive and highly chemoresistant malignancy. Rho family GTPases regulate multiple signaling pathways in tumorigenesis: cytoskeletal organization, transcription, cell cycle progression, and cell proliferation. Geranylgeranylation of Rho family GTPases is essential for cell membrane localization and activation of these proteins. It is currently unknown whether HTLV-1-transformed cells are preferentially sensitive to geranylgeranylation inhibitors, such as GGTI-298. In this report, we demonstrate that GGTI-298 decreased cell viability and induced G(2)/M phase accumulation of HTLV-1-transformed cells, independent of p53 reactivation. HTLV-1-LTR transcriptional activity was inhibited and Tax protein levels decreased following treatment with GGTI-298. Furthermore, GGTI-298 decreased activation of NF-kappa B, a downstream target of Rho family GTPases. These studies suggest that protein geranylgeranylation contributes to dysregulation of cell survival pathways in HTLV-1-transformed cells.
C1 [Edwards, Dustin C.; Jung, Kyung-Jin; Brady, John N.; Pise-Masison, Cynthia A.] NCI, Virus Tumor Biol Sect, Cellular Oncol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[McKinnon, Katherine M.; Fenizia, Claudio] NCI, Vaccine Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Pise-Masison, CA (reprint author), NCI, Virus Tumor Biol Sect, Cellular Oncol Lab, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
EM edwardsd2@mail.nih.gov; mckinnonkm@mail.nih.gov; feniziac@mail.nih.gov;
jungk@kitox.re.kr; masisonc@mail.nih.gov
FU National Institute of Health, National Cancer Institute, Center for
Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institute of Health, National Cancer Institute, Center for
Cancer Research. We would like to thank the Brady lab for thoughtful
discussion.
NR 52
TC 2
Z9 2
U1 0
U2 0
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD OCT
PY 2011
VL 3
IS 10
BP 1815
EP 1835
DI 10.3390/v3101815
PG 21
WC Virology
SC Virology
GA 842GY
UT WOS:000296585100002
PM 22069517
ER
PT J
AU Parry, M
AF Parry, Manon
TI RETHINKING DR. SPOCK RESPONSE
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Letter
ID INFANT-DEATH-SYNDROME; SIDS RATES; POSITION
C1 Natl Lib Med, Exhibit Program, Bethesda, MD 20894 USA.
RP Parry, M (reprint author), Natl Lib Med, Exhibit Program, 8600 Rockville Pike,Bldg 38,Room 1E-21, Bethesda, MD 20894 USA.
EM parrym@mail.nlm.nih.gov
NR 7
TC 0
Z9 0
U1 0
U2 2
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 OCT
PY 2011
VL 101
IS 10
BP 1812
EP 1813
DI 10.2105/AJPH.2011.300337
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 830LB
UT WOS:000295657400002
ER
PT J
AU Frankel, LK
AF Frankel, Lee K.
TI The Relation of Life Insurance to Public Hygiene
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Editorial Material
C1 Natl Lib Med, Div Hist Med, Bethesda, MD 20894 USA.
RP Frankel, LK (reprint author), Natl Lib Med, Div Hist Med, Bethesda, MD 20894 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 OCT
PY 2011
VL 101
IS 10
BP 1868
EP 1869
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 830LB
UT WOS:000295657400020
PM 21917618
ER
PT J
AU Fee, E
AF Fee, Elizabeth
TI Lee K. Frankel (1867-1931): Public Health Leader and Life Insurance
Executive
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Biographical-Item
C1 NIH, Hist Med Div, Natl Lib Med, Bethesda, MD 20892 USA.
RP Fee, E (reprint author), NIH, Hist Med Div, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
EM feee@nlm.nih.gov
NR 1
TC 0
Z9 0
U1 0
U2 2
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 OCT
PY 2011
VL 101
IS 10
BP 1870
EP 1870
DI 10.2105/AJPH.2009.191072
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 830LB
UT WOS:000295657400021
ER
PT J
AU de Heer, HD
Koehly, L
Pederson, R
Morera, O
AF de Heer, Hendrik D.
Koehly, Laura
Pederson, Rockie
Morera, Osvaldo
TI Effectiveness and Spillover of an After-School Health Promotion Program
for Hispanic Elementary School Children
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID GEORGIA FITKID PROJECT; PHYSICAL-ACTIVITY PROGRAM; OBESITY PREVENTION;
MEDICAL-COLLEGE; CARDIOVASCULAR HEALTH; ADOLESCENT TRIAL; RISK BEHAVIOR;
INTERVENTION; YOUTH; CHILDHOOD
AB Objectives. We evaluated the effectiveness and spillover of an after-school health education and physical activity program among Hispanic elementary school children.
Methods. In fall 2008, students in third through fifth grades in 6 schools in El Paso, Texas (n=901), were randomized to intervention (n=292 participants) or control (n=354) classrooms (4 unknown). Intervention classrooms also contained a spillover group (n=251) that did not join the after-school program but that completed measurements and surveys. The intervention was a 12-week culturally tailored after-school program meeting twice a week. Four-month outcomes were body mass index, aerobic capacity, and dietary intentions and knowledge. We calculated intervention exposure as the proportion of after-school participants per classroom.
Results. Intervention exposure predicted lower body mass index (P=.045), higher aerobic capacity (P=.012), and greater intentions to eat healthy (P=.046) for the classroom at follow-up. Intervention effectiveness increased with increasing proportions of intervention participants in a classroom. Nonparticipants who had classroom contact with program participants experienced health improvements that could reduce their risk of obesity.
Conclusions. Spillover of beneficial intervention effects to nonparticipants is a valuable public health benefit and should be part of program impact assessments. (Am J Public Health. 2011;101:1907-1913. doi:10.2105/AJPH.2011.300177)
C1 [de Heer, Hendrik D.; Morera, Osvaldo] Univ Texas El Paso, Dept Psychol, El Paso, TX 79968 USA.
[Pederson, Rockie] Univ Texas El Paso, Dept Kinesiol, El Paso, TX 79968 USA.
[de Heer, Hendrik D.; Koehly, Laura] NHGRI, Social & Behav Res Branch, Bethesda, MD 20892 USA.
RP de Heer, HD (reprint author), No Arizona Univ, Dept Phys Therapy & Athlet Training, POB 15105,Bldg 66,Rm 102, Flagstaff, AZ 86011 USA.
EM dirkdeheer@hotmail.com
RI de Heer, Hendrik/D-3192-2013
OI de Heer, Hendrik/0000-0002-9241-5021
FU Center for Border Health Research through the Paso del Norte Health
Foundation; National Institutes of Health Hispanic Health Disparities
Research Center [P20MD002287-01]
FX This project was supported by pilot research grants from the Center for
Border Health Research through the Paso del Norte Health Foundation and
by the National Institutes of Health Hispanic Health Disparities
Research Center (grant P20MD002287-01).
NR 42
TC 12
Z9 12
U1 1
U2 14
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 OCT
PY 2011
VL 101
IS 10
BP 1907
EP 1913
DI 10.2105/AJPH.2011.300177
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 830LB
UT WOS:000295657400029
PM 21852659
ER
PT J
AU Wolf, R
Ruzicka, T
Yuspa, SH
AF Wolf, Ronald
Ruzicka, Thomas
Yuspa, Stuart H.
TI Novel S100A7 (psoriasin)/S100A15 (koebnerisin) subfamily: highly
homologous but distinct in regulation and function
SO AMINO ACIDS
LA English
DT Review
DE Calcium-binding protein; S100; Koebnerisin; Psoriasin; Evolution;
Paralogs; RAGE; Innate immunity; Inflammation; Cancer
ID GLYCATION END-PRODUCTS; EPIDERMAL DIFFERENTIATION COMPLEX;
HUMAN-CHROMOSOME 1Q21; PSORIASIN S100A7; CORNIFIED ENVELOPE;
ATOPIC-DERMATITIS; BREAST-CANCER; SUBCELLULAR-LOCALIZATION;
MOLECULAR-CLONING; PROTEIN PSORIASIN
AB S100A7 (psoriasin) and S100A15 (koebnerisin) were first identified in inflamed psoriatic skin. They are of major interest because of their putative functional roles in innate immunity, epidermal cell maturation, and epithelial tumorigenesis. Human S100A7 and S100A15 have lately evolved by gene duplications within the epidermal differentiation complex (chromosome 1q21) during primate evolution forming a novel S100 subfamily. Therefore, S100A7 and S100A15 are almost identical in sequence (> 90%) and are difficult to discriminate. Despite their high homology, S100A7 and S100A15 are distinct in tissue distribution, regulation, and function, and thus, exemplary for the diversity within the S100 family. Their different properties are compelling reasons to discriminate S100A7 (psoriasin) and S100A15 (koebnerisin) in epithelial homeostasis, inflammation, and cancer.
C1 [Wolf, Ronald; Ruzicka, Thomas] Univ Munich, Dept Dermatol, D-80337 Munich, Germany.
[Wolf, Ronald; Yuspa, Stuart H.] NCI, Lab Canc Biol & Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Wolf, R (reprint author), Univ Munich, Dept Dermatol, Frauenlobstr 9-11, D-80337 Munich, Germany.
EM Ronald.Wolf@med.uni-muenchen.de
FU NIH, National Cancer Institute, Center for Cancer Research; German
Research Foundation (DFG)
FX This work was supported by grants from the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research, and
the German Research Foundation (DFG).
NR 54
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U1 1
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0939-4451
J9 AMINO ACIDS
JI Amino Acids
PD OCT
PY 2011
VL 41
IS 4
BP 789
EP 796
DI 10.1007/s00726-010-0666-4
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 840VE
UT WOS:000296468600005
PM 20596736
ER
PT J
AU Gaitan, MI
Shea, CD
Evangelou, IE
Stone, RD
Fenton, KM
Bielekova, B
Massacesi, L
Reich, DS
AF Gaitan, Maria I.
Shea, Colin D.
Evangelou, Iordanis E.
Stone, Roger D.
Fenton, Kaylan M.
Bielekova, Bibiana
Massacesi, Luca
Reich, Daniel S.
TI Heterogeneity in Longitudinal Evolution of Ring-Enhancing Multiple
Sclerosis Lesions Reply
SO ANNALS OF NEUROLOGY
LA English
DT Letter
C1 [Gaitan, Maria I.; Shea, Colin D.; Evangelou, Iordanis E.; Stone, Roger D.; Fenton, Kaylan M.; Bielekova, Bibiana; Massacesi, Luca; Reich, Daniel S.] NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
[Massacesi, Luca] Univ Florence, Dept Neurol & Psychiat Sci, Florence, Italy.
RP Gaitan, MI (reprint author), NINDS, Neuroimmunol Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
NR 2
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2011
VL 70
IS 4
BP 669
EP 670
DI 10.1002/ana.22589
PG 3
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 839VD
UT WOS:000296396700026
ER
PT J
AU Hirtz, DG
AF Hirtz, D. G.
TI Effect of prenatal MgSO4 on head ultrasound imaging in preterm infants
SO ANNALS OF NEUROLOGY
LA English
DT Meeting Abstract
CT 136th Annual Meeting of the American-Neurological-Association (ANA)
CY SEP 25-27, 2011
CL San Diego, CA
SP Amer Neurol Assoc (ANA)
C1 [Hirtz, D. G.] Eunice Kennedy Shriver Natl Inst, Child Hlth & Human Dev Maternal Fetal Med Units N, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2011
VL 70
SU 15
BP S110
EP S111
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 840DW
UT WOS:000296419500357
ER
PT J
AU Han, Q
Robinson, H
Cai, T
Tagle, DA
Li, JY
AF Han, Qian
Robinson, Howard
Cai, Tao
Tagle, Danilo A.
Li, Jianyong
TI Biochemical and structural characterization of mouse mitochondrial
aspartate aminotransferase, a newly identified kynurenine
aminotransferase-IV
SO BIOSCIENCE REPORTS
LA English
DT Article
DE aspartate aminotransferase; crystal structure; oxo acid; kynurenic acid;
kynurenine; kynurenine aminotransferase
ID ACID-BINDING-PROTEIN; GLUTAMINE TRANSAMINASE-K; RAT-BRAIN ASTROCYTES;
SUBSTRATE-SPECIFICITY; CRYSTAL-STRUCTURE; ESCHERICHIA-COLI;
GLUTAMATERGIC NEURONS; SYNAPTIC-TRANSMISSION; OXIDATIVE-METABOLISM;
NICOTINIC RECEPTORS
AB Mammalian mAspAT (mitochondrial aspartate aminotransferase) is recently reported to have RAT (kynurenine aminotransferase) activity and plays a role in the biosynthesis of KYNA (kynurenic acid) in rat, mouse and human brains. This study concerns the biochemical and structural characterization of mouse mAspAT. In this study, mouse mAspAT cDNA was amplified from mouse brain first stand cDNA and its recombinant protein was expressed in an Escherichia coli expression system. Sixteen oxo acids were tested for the co-substrate specificity of mouse mAspAT and 14 of them were shown to be capable of serving as co-substrates for the enzyme. Structural analysis of mAspAT by macromolecular crystallography revealed that the cofactor-binding residues of mAspAT are similar to those of other KATs. The substrate-binding residues of mAspAT are slightly different from those of other KATs. Our results provide a biochemical and structural basis towards understanding the overall physiological role of mAspAT in vivo and insight into controlling the levels of endogenous KYNA through modulation of the enzyme in the mouse brain.
C1 [Han, Qian; Li, Jianyong] Virginia Tech, Dept Biochem, Blacksburg, VA 24061 USA.
[Robinson, Howard] Brookhaven Natl Lab, Dept Biol, Upton, NY 11973 USA.
[Cai, Tao] NIDCR, OIIB, NIH, Bethesda, MD 20892 USA.
[Tagle, Danilo A.] NINDS, Ctr Neurosci, NIH, Bethesda, MD USA.
RP Li, JY (reprint author), Virginia Tech, Dept Biochem, Blacksburg, VA 24061 USA.
EM lij@vt.edu
RI Han, Qian/J-8696-2014
OI Han, Qian/0000-0001-6245-5252
FU NINDS [NS062836]; NIDCR; NINDS at National Institutes of Health
FX This work was supported by a grant from NINDS [NS062836] and by
Intramural Research Programs of NIDCR and NINDS at National Institutes
of Health. The present study was carried out in part at the National
Synchrotron Light Source, Brookhaven National Laboratory.
NR 73
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Z9 13
U1 1
U2 11
PU PORTLAND PRESS LTD
PI LONDON
PA CHARLES DARWIN HOUSE, 12 ROGER STREET, LONDON WC1N 2JU, ENGLAND
SN 0144-8463
EI 1573-4935
J9 BIOSCIENCE REP
JI Biosci. Rep.
PD OCT
PY 2011
VL 31
IS 5
BP 323
EP 332
DI 10.1042/BSR20100117
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 841AA
UT WOS:000296482900004
PM 20977429
ER
PT J
AU Raju, TNK
AF Raju, Tonse N. K.
TI Breastfeeding Is a Dynamic Biological Process-Not Simply a Meal at the
Breast
SO BREASTFEEDING MEDICINE
LA English
DT Editorial Material
ID COGNITIVE-DEVELOPMENT; MILK FORMULA; BRAIN; INFANTS; VOICE; TRIAL; IQ
C1 [Raju, Tonse N. K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, Ctr Dev Biol & Perinatal Med, NIH, Bethesda, MD USA.
RP Raju, TNK (reprint author), NICHHD, NIH, 6100 Execut Blvd,Room 4B03, Bethesda, MD 20892 USA.
EM rajut@mail.nih.gov
NR 21
TC 6
Z9 7
U1 0
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1556-8253
J9 BREASTFEED MED
JI Breastfeed. Med.
PD OCT
PY 2011
VL 6
IS 5
BP 257
EP 259
DI 10.1089/bfm.2011.0081
PG 3
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 839QD
UT WOS:000296382300005
PM 22007804
ER
PT J
AU Parry, C
Kent, EE
Mariotto, AB
Alfano, CM
Rowland, JH
AF Parry, Carla
Kent, Erin E.
Mariotto, Angela B.
Alfano, Catherine M.
Rowland, Julia H.
TI Cancer Survivors: A Booming Population
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID BREAST-CANCER; OLDER-ADULTS; UNITED-STATES; PREVALENCE; CHALLENGES; AGE;
COMORBIDITY; REGISTRIES; CHILDHOOD; VARIANCE
AB Background: In this first article of what is planned to be an annual series, we examine the history of cancer prevalence reporting and the role that these annual figures play in guiding the direction of cancer control research, and specifically the science of cancer survivorship. For this inaugural year, we focus on the confluence of the growing number of survivors and population aging, and the impact these combined trends will have on cancer survivorship in the future.
Methods: State or metro area-level cancer incidence and prevalence data were collected from 9 registries via the Surveillance, Epidemiology, and End
Results Program. The complete prevalence method was used to estimate prevalence for 2008 and the Prevalence, Incidence Approach Model method was used to project prevalence data through 2020, assuming flat cancer incidence and survival trends but dynamic U. S. population projections. Results: As of January 2008, the number of cancer survivors is estimated at 11.9 million. Approximately 60% of cancer survivors are age 65 or older, and by the year 2020, it is estimated that 63% of cancer survivors will be age 65 or older.
Conclusions: Improved survival and population aging converge to generate a booming population of older adult cancer survivors, many of whom have multiple complex health conditions and unique survivorship needs. This demographic shift has important implications for future health care needs and costs of the U. S. population. Impact: The findings provide information critical for guiding cancer prevention and control research and service provision. Cancer Epidemiol Biomarkers Prev; 20(10); 1996-2005. (C) 2011 AACR.
C1 [Rowland, Julia H.] NCI, NIH, Off Canc Survivorship, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Kent, Erin E.] NCI, Canc Prevent Fellowship Program, Bethesda, MD 20892 USA.
[Mariotto, Angela B.] NCI, Surveillance Res Program, Bethesda, MD 20892 USA.
RP Rowland, JH (reprint author), NCI, NIH, Off Canc Survivorship, Div Canc Control & Populat Sci, 6116 Execut Blvd,Suite 404, Bethesda, MD 20892 USA.
EM rowlandj@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 43
TC 136
Z9 137
U1 2
U2 21
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 OCT
PY 2011
VL 20
IS 10
BP 1996
EP 2005
DI 10.1158/1055-9965.EPI-11-0729
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 831GR
UT WOS:000295717900002
PM 21980007
ER
PT J
AU Yabroff, KR
Lund, J
Kepka, D
Mariotto, A
AF Yabroff, K. Robin
Lund, Jennifer
Kepka, Deanna
Mariotto, Angela
TI Economic Burden of Cancer in the United States: Estimates, Projections,
and Future Research
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; POTENTIAL LIFE LOST; HEALTH-CARE COSTS;
BREAST-CANCER; LUNG-CANCER; PRODUCTIVITY COSTS; TUMOR-REGISTRY; MEDICAL
COSTS; TIME; SURVIVORS
AB The economic burden of cancer in the United States is substantial and expected to increase significantly in the future because of expected growth and aging of the population and improvements in survival as well as trends in treatment patterns and costs of care following cancer diagnosis. In this article, we describe measures of the economic burden of cancer and present current estimates and projections of the national burden of cancer in the United States. We discuss ongoing efforts to characterize the economic burden of cancer in the United States and identify key areas for future work including developing and enhancing research resources, improving estimates and projections of economic burden, evaluating targeted therapies, and assessing the financial burden for patients and their families. This work will inform efforts by health care policy makers, health care systems, providers, and employers to improve the cancer survivorship experience in the United States. Cancer Epidemiol Biomarkers Prev; 20(10); 2006-14. (C) 2011 AACR.
C1 [Yabroff, K. Robin] NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Lund, Jennifer] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
RP Yabroff, KR (reprint author), NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Execut Plaza N,Room 4005,6130 Execut Blvd,MSC 734, Bethesda, MD 20892 USA.
EM yabroffr@mail.nih.gov
RI Lund, Jennifer/G-9420-2012;
OI Yabroff, K. Robin/0000-0003-0644-5572
FU Intramural NIH HHS [Z99 CA999999]
NR 65
TC 68
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U1 1
U2 25
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 OCT
PY 2011
VL 20
IS 10
BP 2006
EP 2014
DI 10.1158/1055-9965.EPI-11-0650
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 831GR
UT WOS:000295717900003
PM 21980008
ER
PT J
AU Khoury, MJ
Clauser, SB
Freedman, AN
Gillanders, EM
Glasgow, RE
Klein, WMP
Schully, SD
AF Khoury, Muin J.
Clauser, Steven B.
Freedman, Andrew N.
Gillanders, Elizabeth M.
Glasgow, Russ E.
Klein, William M. P.
Schully, Sheri D.
TI Population Sciences, Translational Research, and the Opportunities and
Challenges for Genomics to Reduce the Burden of Cancer in the 21st
Century
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Review
ID EGAPP WORKING GROUP; GENETIC TESTING STRATEGIES; WIDE ASSOCIATION;
COLORECTAL-CANCER; BREAST-CANCER; LYNCH SYNDROME; MOLECULAR
EPIDEMIOLOGY; PERSONALIZED MEDICINE; MUTATION CARRIERS; RESEARCH AGENDA
AB Advances in genomics and related fields are promising tools for risk assessment, early detection, and targeted therapies across the entire cancer care continuum. In this commentary, we submit that this promise cannot be fulfilled without an enhanced translational genomics research agenda firmly rooted in the population sciences. Population sciences include multiple disciplines that are needed throughout the translational research continuum. For example, epidemiologic studies are needed not only to accelerate genomic discoveries and new biological insights into cancer etiology and pathogenesis, but to characterize and critically evaluate these discoveries in well-defined populations for their potential for cancer prediction, prevention and response to treatment. Behavioral, social, and communication sciences are needed to explore genomic-modulated responses to old and new behavioral interventions, adherence to therapies, decision making across the continuum, and effective use in health care. Implementation science, health services, outcomes research, comparative effectiveness research, and regulatory science are needed for moving validated genomic applications into practice and for measuring their effectiveness, cost-effectiveness, and unintended consequences. Knowledge synthesis, evidence reviews, and economic modeling of the effects of promising genomic applications will facilitate policy decisions and evidence-based recommendations. Several independent and multidisciplinary panels have recently made specific recommendations for enhanced research and policy infrastructure to inform clinical and population research for moving genomic innovations into the cancer care continuum. An enhanced translational genomics and population sciences agenda is urgently needed to fulfill the promise of genomics in reducing the burden of cancer. Cancer Epidemiol Biomarkers Prev; 20(10); 2105-14. (C)2011 AACR.
C1 [Khoury, Muin J.] Ctr Dis Control & Prevent, Office Publ Hlth Genom, Atlanta, GA USA.
[Khoury, Muin J.; Clauser, Steven B.; Freedman, Andrew N.; Gillanders, Elizabeth M.; Glasgow, Russ E.; Klein, William M. P.; Schully, Sheri D.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Khoury, MJ (reprint author), CDC, 1600 Clifton Rd, Atlanta, GA 30333 USA.
EM muk1@CDC.GOV
FU Intramural NIH HHS [Z99 CA999999]
NR 74
TC 23
Z9 23
U1 3
U2 21
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 OCT
PY 2011
VL 20
IS 10
BP 2105
EP 2114
DI 10.1158/1055-9965.EPI-11-0481
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 831GR
UT WOS:000295717900014
PM 21795499
ER
PT J
AU Milne, RL
Goode, EL
Garca-Closas, M
Couch, FJ
Severi, G
Hein, R
Fredericksen, Z
Malats, N
Zamora, MP
Perez, JIA
Benitez, J
Dork, T
Schurmann, P
Karstens, JH
Hillemanns, P
Cox, A
Brock, IW
Elliot, G
Cross, SS
Seal, S
Turnbull, C
Renwick, A
Rahman, N
Shen, CY
Yu, JC
Huang, CS
Hou, MF
Nordestgaard, BG
Bojesen, SE
Lanng, C
Alnaes, GG
Kristensen, V
Borrensen-Dale, AL
Hopper, JL
Dite, GS
Apicella, C
Southey, MC
Lambrechts, D
Yesilyurt, BT
Floris, G
Leunen, K
Sangrajrang, S
Gaborieau, V
Brennan, P
McKay, J
Chang-Claude, J
Wang-Gohrke, S
Radice, P
Peterlongo, P
Manoukian, S
Barile, M
Giles, GG
Baglietto, L
John, EM
Miron, A
Chanock, SJ
Lissowska, J
Sherman, ME
Figueroa, JD
Bogdanova, NV
Antonenkova, NN
Zalutsky, IV
Rogov, YI
Fasching, PA
Bayer, CM
Ekici, AB
Beckmann, MW
Brenner, H
Muller, H
Arndt, V
Stegmaier, C
Andrulis, IL
Knight, JA
Glendon, G
Mulligan, AM
Mannermaa, A
Kataja, V
Kosma, VM
Hartikainen, JM
Meindl, A
Heil, J
Bartram, CR
Schmutzler, RK
Thomas, GD
Hoover, RN
Fletcher, O
Gibson, LJ
Silva, ID
Peto, J
Nickels, S
Flesch-Janys, D
Anton-Culver, H
Ziogas, A
Sawyer, E
Tomlinson, I
Kerin, M
Miller, N
Schmidt, MK
Broeks, A
Van't Veer, LJ
Tollenaar, RAEM
Pharoah, PDP
Dunning, AM
Pooley, KA
Marme, F
Schneeweiss, A
Sohn, C
Burwinkel, B
Jakubowska, A
Lubinski, J
Jaworska, K
Durda, K
Kang, D
Yoo, KY
Noh, DY
Ahn, SH
Hunter, DJ
Hankinson, SE
Kraft, P
Lindstrom, S
Chen, XQ
Beesley, J
Hamann, U
Harth, V
Justenhoven, C
Winqvist, R
Pylkas, K
Jukkola-Vuorinen, A
Grip, M
Hooning, M
Hollestelle, A
Oldenburg, RA
Tilanus-Linthorst, M
Khusnutdinova, E
Bermisheva, M
Prokofieva, D
Farahtdinova, A
Olson, JE
Wang, XS
Humphreys, MK
Wang, Q
Chenevix-Trench, G
Easton, DF
AF Milne, Roger L.
Goode, Ellen L.
Garca-Closas, Montserrat
Couch, Fergus J.
Severi, Gianluca
Hein, Rebecca
Fredericksen, Zachary
Malats, Nuria
Pilar Zamora, M.
Arias Perez, Jose Ignacio
Benitez, Javier
Doerk, Thilo
Schuermann, Peter
Karstens, Johann H.
Hillemanns, Peter
Cox, Angela
Brock, Ian W.
Elliot, Graeme
Cross, Simon S.
Seal, Sheila
Turnbull, Clare
Renwick, Anthony
Rahman, Nazneen
Shen, Chen-Yang
Yu, Jyh-Cherng
Huang, Chiun-Sheng
Hou, Ming-Feng
Nordestgaard, Borge G.
Bojesen, Stig E.
Lanng, Charlotte
Alnaes, Grethe Grenaker
Kristensen, Vessela
Borrensen-Dale, Anne-Lise
Hopper, John L.
Dite, Gillian S.
Apicella, Carmel
Southey, Melissa C.
Lambrechts, Diether
Yesilyurt, Betul T.
Floris, Giuseppe
Leunen, Karin
Sangrajrang, Suleeporn
Gaborieau, Valerie
Brennan, Paul
McKay, James
Chang-Claude, Jenny
Wang-Gohrke, Shan
Radice, Paolo
Peterlongo, Paolo
Manoukian, Siranoush
Barile, Monica
Giles, Graham G.
Baglietto, Laura
John, Esther M.
Miron, Alexander
Chanock, Stephen J.
Lissowska, Jolanta
Sherman, Mark E.
Figueroa, Jonine D.
Bogdanova, Natalia V.
Antonenkova, Natalia N.
Zalutsky, Iosif V.
Rogov, Yuri I.
Fasching, Peter A.
Bayer, Christian M.
Ekici, Arif B.
Beckmann, Matthias W.
Brenner, Hermann
Mueller, Heiko
Arndt, Volker
Stegmaier, Christa
Andrulis, Irene L.
Knight, Julia A.
Glendon, Gord
Mulligan, Anna Marie
Mannermaa, Arto
Kataja, Vesa
Kosma, Veli-Matti
Hartikainen, Jaana M.
Meindl, Alfons
Heil, Joerg
Bartram, Claus R.
Schmutzler, Rita K.
Thomas, Gilles D.
Hoover, Robert N.
Fletcher, Olivia
Gibson, Lorna J.
Silva, Isabel dos Santos
Peto, Julian
Nickels, Stefan
Flesch-Janys, Dieter
Anton-Culver, Hoda
Ziogas, Argyrios
Sawyer, Elinor
Tomlinson, Ian
Kerin, Michael
Miller, Nicola
Schmidt, Marjanka K.
Broeks, Annegien
Van't Veer, Laura J.
Tollenaar, Rob A. E. M.
Pharoah, Paul D. P.
Dunning, Alison M.
Pooley, Karen A.
Marme, Frederik
Schneeweiss, Andreas
Sohn, Christof
Burwinkel, Barbara
Jakubowska, Anna
Lubinski, Jan
Jaworska, Katarzyna
Durda, Katarzyna
Kang, Daehee
Yoo, Keun-Young
Noh, Dong-Young
Ahn, Sei-Hyun
Hunter, David J.
Hankinson, Susan E.
Kraft, Peter
Lindstrom, Sara
Chen, Xiaoqing
Beesley, Jonathan
Hamann, Ute
Harth, Volker
Justenhoven, Christina
Winqvist, Robert
Pylkas, Katri
Jukkola-Vuorinen, Arja
Grip, Mervi
Hooning, Maartje
Hollestelle, Antoinette
Oldenburg, Rogier A.
Tilanus-Linthorst, Madeleine
Khusnutdinova, Elza
Bermisheva, Marina
Prokofieva, Darya
Farahtdinova, Albina
Olson, Janet E.
Wang, Xianshu
Humphreys, Manjeet K.
Wang, Qin
Chenevix-Trench, Georgia
Easton, Douglas F.
CA GENICA Network
KConFab Investigators
AOCS Grp
TI Confirmation of 5p12 As a Susceptibility Locus for
Progesterone-Receptor-Positive, Lower Grade Breast Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; CONFER SUSCEPTIBILITY; COMMON VARIANTS;
SUBTYPES; ALLELES; RISK
AB Background: The single-nucleotide polymorphism (SNP) 5p12-rs10941679 has been found to be associated with risk of breast cancer, particularly estrogen receptor (ER)-positive disease. We aimed to further explore this association overall, and by tumor histopathology, in the Breast Cancer Association Consortium.
Methods: Data were combined from 37 studies, including 40,972 invasive cases, 1,398 cases of ductal carcinoma in situ (DCIS), and 46,334 controls, all of white European ancestry, as well as 3,007 invasive cases and 2,337 controls of Asian ancestry. Associations overall and by tumor invasiveness and histopathology were assessed using logistic regression.
Results: For white Europeans, the per-allele OR associated with 5p12-rs10941679 was 1.11 (95% CI = 1.08-1.14, P = 7 x 10(-18)) for invasive breast cancer and 1.10 (95% CI = 1.01-1.21, P = 0.03) for DCIS. For Asian women, the estimated OR for invasive disease was similar (OR 1.07, 95% CI = 0.99-1.15, P = 0.09). Further analyses suggested that the association in white Europeans was largely limited to progesterone receptor (PR)positive disease (per-allele OR = 1.16, 95% CI = 1.12-1.20, P = 1 x 10(-18) vs. OR = 1.03, 95% CI = 0.99-1.07, P = 0.2 for PR-negative disease; P(heterogeneity) 2 x 10(-7)); heterogeneity by ER status was not observed (P = 0.2) once PR status was accounted for. The association was also stronger for lower grade tumors [per-allele OR (95% CI) 1.20 (1.14-1.25), 1.13 (1.09-1.16), and 1.04 (0.99-1.08) for grade 1, 2, and 3/4, respectively; Ptrend 5 x 10(-7)].
Conclusion: 5p12 is a breast cancer susceptibility locus for PR-positive, lower grade breast cancer.
Impact: Multicenter fine-mapping studies of this region are needed as a first step to identifying the causal variant or variants. Cancer Epidemiol Biomarkers Prev; 20(10); 2222-31. (C) 2011 AACR.
C1 [Milne, Roger L.; Malats, Nuria] Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid 28029, Spain.
[Benitez, Javier] Spanish Natl Canc Res Ctr CNIO, Human Genet Grp, Madrid 28029, Spain.
[Pilar Zamora, M.] Hosp Univ La Paz, Med Oncol Serv, Madrid, Spain.
[Milne, Roger L.; Severi, Gianluca; Hopper, John L.; Dite, Gillian S.; Apicella, Carmel; Giles, Graham G.; Baglietto, Laura] Univ Melbourne, Ctr Mol Environm Genet & Analyt Epidemiol, Melbourne, Vic 3010, Australia.
[Southey, Melissa C.] Univ Melbourne, Dept Pathol, Melbourne, Vic 3010, Australia.
[Severi, Gianluca; Giles, Graham G.; Baglietto, Laura] Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.
[Goode, Ellen L.; Fredericksen, Zachary; Olson, Janet E.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Couch, Fergus J.; Wang, Xianshu] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
[Gibson, Lorna J.; Silva, Isabel dos Santos; Peto, Julian] London Sch Hyg & Trop Med, London, England.
[Sawyer, Elinor] Guys & St Thomas NHS Fdn Trust Partnership Kings, Div Canc Studies, NIHR Comprehens Biomed Res Ctr, London, England.
[Hein, Rebecca; Chang-Claude, Jenny; Nickels, Stefan] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Brenner, Hermann; Mueller, Heiko; Arndt, Volker] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany.
[Burwinkel, Barbara] German Canc Res Ctr, Mol Epidemiol Unit, Heidelberg, Germany.
[Heil, Joerg; Marme, Frederik; Schneeweiss, Andreas; Sohn, Christof; Burwinkel, Barbara] Univ Heidelberg, Dept Obstet & Gynecol, Heidelberg, Germany.
[Bartram, Claus R.] Univ Heidelberg, Inst Human Genet, Heidelberg, Germany.
[Marme, Frederik; Schneeweiss, Andreas] Univ Heidelberg, Natl Ctr Tumor Dis, Heidelberg, Germany.
[Arias Perez, Jose Ignacio] Hosp Monte Naranco, Serv Cirugia Gen & Especialidades, Oviedo, Spain.
[Doerk, Thilo; Schuermann, Peter; Hillemanns, Peter; Bogdanova, Natalia V.] Hannover Med Sch, Dept Obstet & Gynaecol, D-3000 Hannover, Germany.
[Karstens, Johann H.; Bogdanova, Natalia V.] Hannover Med Sch, Dept Radiat Oncol, D-3000 Hannover, Germany.
[Cox, Angela; Brock, Ian W.; Elliot, Graeme] Univ Sheffield, Dept Oncol, Inst Canc Studies, Sheffield, S Yorkshire, England.
[Cross, Simon S.] Univ Sheffield, Acad Unit Pathol, Dept Neurosci, Sheffield, S Yorkshire, England.
[Elliot, Graeme] Univ Manchester, Manchester, Lancs, England.
[Seal, Sheila; Turnbull, Clare; Renwick, Anthony; Rahman, Nazneen] Inst Canc Res, Sect Canc Genet, Surrey, England.
[Shen, Chen-Yang] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
[Yu, Jyh-Cherng] Triserv Gen Hosp, Dept Surg, Taipei, Taiwan.
[Huang, Chiun-Sheng] Natl Taiwan Univ Hosp, Dept Surg, Taipei 100, Taiwan.
[Hou, Ming-Feng] Kaohsiung Med Univ Chung Ho Mem Hosp, Ctr Canc, Kaohsiung, Taiwan.
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[Nordestgaard, Borge G.; Bojesen, Stig E.] Copenhagen Univ Hosp, Herlev Hosp, Copenhagen Gen Populat Study, Copenhagen, Denmark.
[Nordestgaard, Borge G.; Bojesen, Stig E.] Copenhagen Univ Hosp, Herlev Hosp, Dept Clin Biochem, Copenhagen, Denmark.
[Lanng, Charlotte] Copenhagen Univ Hosp, Herlev Hosp, Dept Breast Surg, Copenhagen, Denmark.
[Alnaes, Grethe Grenaker; Kristensen, Vessela; Borrensen-Dale, Anne-Lise] Oslo Univ Hosp, Radiumhosp, Inst Canc Res, Dept Genet, Oslo, Norway.
[Kristensen, Vessela; Borrensen-Dale, Anne-Lise] Fac Med, Fac Div Ahus, Uio, Norway.
[Floris, Giuseppe; Leunen, Karin] Univ Hosp Gasthuisberg, Multidisciplinary Breast Ctr, B-3000 Louvain, Belgium.
[Sangrajrang, Suleeporn] Natl Canc Inst, Bangkok, Thailand.
[Gaborieau, Valerie; Brennan, Paul; McKay, James] Int Agcy Res Canc, F-69372 Lyon, France.
[Chang-Claude, Jenny; Wang-Gohrke, Shan] Univ Ulm, Dept Obstet & Gynecol, Ulm, Germany.
[Radice, Paolo; Peterlongo, Paolo] Fdn IRCCS Ist Nazl Tumori INT, Unit Mol Bases Genet Risk & Genet Testing, Dept Prevent & Predict Med, Tumori, Italy.
[Manoukian, Siranoush] Fdn IRCCS Ist Nazl Tumori INT, Unit Med Genet, Dept Prevent & Predict Med, Tumori, Italy.
[Barile, Monica] IEO, Div Canc Prevent & Genet, Milan, Italy.
[John, Esther M.] Fremont & Stanford Univ, Sch Med, Canc Prevent Inst Calif, Stanford, CA USA.
[Miron, Alexander] Dana Farber Canc Inst, Boston, MA USA.
[Hunter, David J.; Kraft, Peter; Lindstrom, Sara] Harvard Univ, Sch Publ Hlth, Program Mol & Genet Epidemiol, Cambridge, MA 02138 USA.
[Hunter, David J.; Hankinson, Susan E.; Kraft, Peter; Lindstrom, Sara] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Cambridge, MA 02138 USA.
[Hankinson, Susan E.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Hankinson, Susan E.] Harvard Univ, Sch Med, Boston, MA USA.
[Chanock, Stephen J.; Sherman, Mark E.; Figueroa, Jonine D.; Thomas, Gilles D.; Hoover, Robert N.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Jaworska, Katarzyna] Warsaw Med Univ, Postgrad Sch Mol Med, Warsaw, Poland.
[Antonenkova, Natalia N.; Zalutsky, Iosif V.; Rogov, Yuri I.] NN Alexandrov Res Inst Oncol & Med Radiol, Minsk, Byelarus.
[Fasching, Peter A.; Bayer, Christian M.; Beckmann, Matthias W.] Univ Hosp Erlangen, Comprehens Canc Ctr Erlangen Nuremberg, Dept Gynecol & Obstet, Univ Breast Ctr Franconia, Erlangen, Germany.
[Ekici, Arif B.] Univ Erlangen Nurnberg, Inst Human Genet, Erlangen, Germany.
[Fasching, Peter A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Hematol & Oncol, Los Angeles, CA 90095 USA.
[Stegmaier, Christa] Saarland Canc Registry, Saarbrucken, Germany.
[Andrulis, Irene L.; Glendon, Gord] Canc Care Ontario, Ontario Canc Genet Network, Toronto, ON, Canada.
[Andrulis, Irene L.] Mt Sinai Hosp, Fred A Litwin Ctr Canc Genet, New York, NY USA.
[Knight, Julia A.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, New York, NY USA.
[Andrulis, Irene L.] Univ Toronto, Dept Mol Genet, Dalla Lana Sch Publ Hlth, Toronto, ON M5S 1A1, Canada.
[Knight, Julia A.] Univ Toronto, Div Epidemiol, Dalla Lana Sch Publ Hlth, Toronto, ON M5S 1A1, Canada.
[Mulligan, Anna Marie] St Michaels Hosp, Dept Lab Med, Li Ka Shing Knowledge Inst, Toronto, ON M5B 1W8, Canada.
[Mulligan, Anna Marie] St Michaels Hosp, Keenan Res Ctr, Li Ka Shing Knowledge Inst, Toronto, ON M5B 1W8, Canada.
[Mannermaa, Arto; Kataja, Vesa; Kosma, Veli-Matti; Hartikainen, Jaana M.] Univ Eastern Finland, Sch Med, Inst Clin Med Pathol & Forens Med, Helsinki, Finland.
[Mannermaa, Arto; Kataja, Vesa; Kosma, Veli-Matti; Hartikainen, Jaana M.] Bioctr Kuopio, Kuopio, Finland.
[Mannermaa, Arto; Kosma, Veli-Matti; Hartikainen, Jaana M.] Kuopio Univ Hosp, Dept Clin Pathol, SF-70210 Kuopio, Finland.
[Kataja, Vesa] Kuopio Univ Hosp, Dept Oncol, SF-70210 Kuopio, Finland.
[Meindl, Alfons] Tech Univ Munich, Klinikum Rechts Isar, Div Obstet & Gynecol, D-8000 Munich, Germany.
[Schmutzler, Rita K.] Univ Hosp Cologne, CMMC, Dept Obstet & Gynaecol, Div Mol Gynecooncol, Cologne, Germany.
[Flesch-Janys, Dieter] Univ Clin Hamburg Eppendorf, Dept Canc Epidemiol, Clin Canc Registry, Hamburg, Germany.
[Flesch-Janys, Dieter] Univ Clin Hamburg Eppendorf, Inst Med Biometr & Epidemiol, Hamburg, Germany.
[Anton-Culver, Hoda; Ziogas, Argyrios] Univ Calif Irvine, Dept Epidemiol, Irvine, CA USA.
[Tomlinson, Ian] Univ Oxford, Welcome Trust Ctr Human Genet, Oxford OX1 2JD, England.
[Tomlinson, Ian] Univ Oxford, Oxford Biomed Res Ctr, Oxford OX1 2JD, England.
[Kerin, Michael; Miller, Nicola] Univ Hosp Galway, Inst Clin Sci, Galway, Ireland.
[Schmidt, Marjanka K.; Broeks, Annegien; Van't Veer, Laura J.] Antoni van Leeuwenhoek Hosp, Netherlands Canc Inst, Amsterdam, Netherlands.
[Tollenaar, Rob A. E. M.] Leiden Univ, Med Ctr, Leiden, Netherlands.
[Pharoah, Paul D. P.; Dunning, Alison M.] Univ Cambridge, Dept Oncol, Cambridge, England.
[Pharoah, Paul D. P.; Pooley, Karen A.; Easton, Douglas F.] Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England.
[Pharoah, Paul D. P.; Dunning, Alison M.; Pooley, Karen A.; Humphreys, Manjeet K.; Wang, Qin; Easton, Douglas F.] Univ Cambridge, Ctr Canc Genet Epidemiol, Cambridge, England.
[Jakubowska, Anna; Lubinski, Jan; Jaworska, Katarzyna; Durda, Katarzyna] Pomeranian Med Univ, Dept Genet & Pathol, Szczecin, Poland.
[Kang, Daehee; Yoo, Keun-Young; Noh, Dong-Young] Seoul Natl Univ, Coll Med, Seoul 151, South Korea.
[Ahn, Sei-Hyun] Univ Ulsan, Coll Med, Seoul, South Korea.
[Chen, Xiaoqing; Beesley, Jonathan; Chenevix-Trench, Georgia] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
[Harth, Volker] German Social Accid Insurance IPA, Inst Prevent & Occupat Med, Bochum, Germany.
[Justenhoven, Christina] Dr Margarete Fischer Bosch Inst Clin Pharmacol, Stuttgart, Germany.
[Justenhoven, Christina] Univ Tubingen, Tubingen, Germany.
[Winqvist, Robert; Pylkas, Katri] Univ Oulu, Oulu Univ Hosp, Canc Genet Lab, Dept Clin Genet, Oulu, Finland.
[Winqvist, Robert; Pylkas, Katri; GENICA Network] Univ Oulu, Oulu Univ Hosp, Bioctr Oulu, Oulu, Finland.
[Jukkola-Vuorinen, Arja] Univ Oulu, Oulu Univ Hosp, Dept Oncol, Oulu, Finland.
[Grip, Mervi] Univ Oulu, Dept Surg, Oulu Univ Hosp, Oulu, Finland.
[Hooning, Maartje] Family Canc Clin, Dept Med Oncol, Rotterdam, Netherlands.
[Oldenburg, Rogier A.] Family Canc Clin, Dept Clin Genet, Rotterdam, Netherlands.
[Tilanus-Linthorst, Madeleine] Family Canc Clin, Dept Surg Oncol, Rotterdam, Netherlands.
[Hollestelle, Antoinette] Erasmus Univ, Med Ctr, Dept Med Oncol, Josephine Nefkens Inst, Rotterdam, Netherlands.
[Khusnutdinova, Elza; Bermisheva, Marina; Prokofieva, Darya; Farahtdinova, Albina] Russian Acad Sci, Ufa Sci Ctr, Inst Biochem & Genet, Ufa 450001, Russia.
RP Milne, RL (reprint author), Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Melchor Fernandez Almagro 3, Madrid 28029, Spain.
EM rmilne@cnio.es
RI Jakubowska, Anna/O-8050-2014; Garcia-Closas, Montserrat /F-3871-2015;
Malats, Nuria/H-7041-2015; Hartikainen, Jaana/E-6256-2015; Bowtell,
David/H-1007-2016; Khusnutdinova, Elza/A-4810-2013; Brenner,
Hermann/B-4627-2017; manoukian, siranoush/E-7132-2017; Rahman,
Nazneen/D-2802-2013; Radice, Paolo/O-3119-2013; Rahman,
Nazneen/B-8890-2012; Dork, Thilo/J-8620-2012; Noh,
Dong-Young/G-5531-2011; Knight, Julia/A-6843-2012; Shen, CY/F-6271-2010;
Verdrengh, Evelien/H-4571-2012; Kang, Dae Hee/E-8631-2012; Yoo,
Keun-Young/J-5548-2012; Kerin, Michael/D-6748-2013; Ekici,
Arif/C-3971-2013; Andrulis, Irene/E-7267-2013
OI Lissowska, Jolanta/0000-0003-2695-5799; Dunning, Alison
Margaret/0000-0001-6651-7166; dos Santos Silva,
Isabel/0000-0002-6596-8798; Cox, Angela/0000-0002-5138-1099; Giles,
Graham/0000-0003-4946-9099; Arndt, Volker/0000-0001-9320-8684;
Garcia-Closas, Montserrat /0000-0003-1033-2650; Malats,
Nuria/0000-0003-2538-3784; Bowtell, David/0000-0001-9089-7525; Brenner,
Hermann/0000-0002-6129-1572; manoukian, siranoush/0000-0002-6034-7562;
Hollestelle, Antoinette/0000-0003-1166-1966; Rahman,
Nazneen/0000-0003-4376-0440; Dite, Gillian/0000-0002-2448-2548; Huang,
Chiun-Sheng/0000-0002-6557-211X; Cross, Simon/0000-0003-2044-1754;
FU European Community [223175, HEALTH-F2-2009-223175]; CR-UK [C1287/A10118,
C1287/A12014]; European Union COST [BM0606]; Dutch Cancer Society [NKI
2001-2423, 2007-3839, DDHK 2004-3124, DDHK 2009-4318]; Dutch National
Genomics Initiative; United States National Cancer Institute, NIH
[RFA-CA-06-503]; Breast Cancer Family Registry (BCFR); Cancer Care
Ontario [U01 CA69467]; Northern California Cancer Center [U01 CA69417];
University of Melbourne [U01 CA69638]; National Health and Medical
Research Council of Australia; New South Wales Cancer Council; Victorian
Health Promotion Foundation (Australia); Victorian Breast Cancer
Research Consortium; United States Army Medical Research and Materiel
Command [DAMD17-01-1-0729]; Cancer Council of Tasmania; Cancer
Foundation of Western Australia; NHMRC [199600, 145684, 288704, 454508];
ELAN-Fond of the University Hospital of Erlangen; Cancer Research UK
[C1287/A10118, C8620/A8372, C8620/A8857, C490/A10124, C8197/A10123];
Breakthrough Breast Cancer; NHS; Dietmar-Hopp Foundation; Helmholtz
Society; German Cancer Research Center (DKFZ); Chief Physician Johan
Boserup and Lise Boserup Fund; Danish Medical Research Council; Herlev
Hospital; Genome Spain Foundation; Red Tematica de Investigacion
Cooperativa en Cancer; Asociacion Espanola Contra el Cancer; Fondo de
Investigacion Sanitario [PI081583, PI081120]; Baden Wurttemberg Ministry
of Science, Research and Arts; German Cancer Aid (Deutsche Krebshilfe);
US Military Acquisition (ACQ)Activity, Era of Hope Award
[W81XWH-05-1-0204]; Institute of Cancer Research (UK); Medical Research
Council (UK); Deutsche Krebshilfe [107054]; German Cancer Research
Centre (DKFZ); Federal Ministry of Education and Research (BMBF) Germany
[01KW9975/5, 01KW9976/8, 01KW9977/0, 01KW0114]; Robert Bosch Foundation,
Stuttgart; Deutsches Krebsforschungszentrum (DKFZ), Heidelberg;
Institute for Prevention and Occupational Medicine of the German Social
Accident Insurance (IPA), Bochum; Department of Internal Medicine,
Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany;
Deutsche Krebshilfe e. V. [70492, 70-2892-BR I]; Hannover Medical
School; German Academic Exchange Program; German Federal Ministry of
Research and Education [RUS08/017]; Kuopio University Hospital; Cancer
Fund of North Savo; Finnish Cancer Organizations; Academy of Finland;
University of Eastern Finland; National Breast Cancer Foundation;
Queensland Cancer Fund; Cancer Councils of New South Wales; Cancer
Councils of Victoria; Cancer Councils of Tasmania; Cancer Councils of
South Australia; Stichting tegen Kanker [232-2008, 196-2010]; Hamburg
Cancer Society; German Cancer Research Center; Ministero della Salute;
Ministero dell'Universita' e Ricerca [RBLAO3-BETH]; Fondazione Italiana
per la Ricerca sul Cancro; Associazione Italiana per la Ricerca sul
Cancro [4017]; Fondazione IRCCS Istituto Nazionale Tumori [5 x 1000];
NIH [CA122340, CA128978, CA87969, CA58860, CA92044]; Specialized Program
of Research Excellence (SPORE) in Breast Cancer [CA116201]; VicHealth;
Cancer Council Victoria; Australian NHMRC [209057, 251553, 504711];
Norwegian Research council [155218/V40, 175240/S10]; Borrensen-Dale;
FUGE-NFR [181600/V11]; Swizz Bridge Award; Finnish Cancer Foundation;
Sigrid Juselius Foundation; University of Oulu; Oulu University
Hospital; National Cancer Institute, Department of Health and Human
Services, USA; Yorkshire Cancer Research; Breast Cancer Campaign;
Ministry of Health and Welfare, Republic of Korea [AO30001]; Polish
Foundation of Science; National Cancer Institute Thailand; Institute of
Biomedical Sciences, Academia Sinica, Taiwan; Lon V Smith Foundation
[LVS39420]; NIHR Comprehensive Biomedical Research Centre; Guy's & St.
Thomas' NHS Foundation; King's College London, United Kingdom; Oxford
Biomedical Research Centre; [PBZ_KBN_122/P05/2004]
FX Part of this work was supported by the European Community's Seventh
Framework Programme under grant agreement number 223175 (grant number
HEALTH-F2-2009-223175; COGS). The BCAC is funded by CR-UK (C1287/A10118
and C1287/A12014). Meetings of the BCAC have been funded by the European
Union COST Programme (BM0606). D.F. Easton is a Principal Research
Fellow of CR-UK. The ABCS was supported by the Dutch Cancer Society
(grants NKI 2001-2423, 2007-3839) and the Dutch National Genomics
Initiative. The ABCFS, NC-BCFR, and OFBCR work was supported by the
United States National Cancer Institute, NIH under RFA-CA-06-503 and
through cooperative agreements with members of the Breast Cancer Family
Registry (BCFR) and principal investigators, including Cancer Care
Ontario (U01 CA69467), Northern California Cancer Center (U01 CA69417),
University of Melbourne (U01 CA69638). The ABCFS was also supported by
the National Health and Medical Research Council of Australia, the New
South Wales Cancer Council, the Victorian Health Promotion Foundation
(Australia) and the Victorian Breast Cancer Research Consortium. J.L.
Hopper is a National Health and Medical Research Council (NHMRC)
Australia Fellow and a Victorian Breast Cancer Research Consortium Group
Leader. M.C. Southey is an NHMRC Senior Research Fellow and a Victorian
Breast Cancer Research Consortium Group Leader. Financial support for
the AOCS was provided by the United States Army Medical Research and
Materiel Command (DAMD17-01-1-0729), the Cancer Council of Tasmania and
Cancer Foundation of Western Australia and the NHMRC (199600). G.
Chenevix-Trench is supported by the NHMRC. The work of the BBCC was
partly funded by ELAN-Fond of the University Hospital of Erlangen. The
BBCS is funded by Cancer Research UK and Breakthrough Breast Cancer and
acknowledges NHS funding to the NIHR Biomedical Research Centre, and the
National Cancer Research Network (NCRN). The BSUCH study was supported
by the Dietmar-Hopp Foundation, the Helmholtz Society and the German
Cancer Research Center (DKFZ). The CGPS was supported by the Chief
Physician Johan Boserup and Lise Boserup Fund, the Danish Medical
Research Council, and Herlev Hospital. The CNIO-BCS was supported by the
Genome Spain Foundation, the Red Tematica de Investigacion Cooperativa
en Cancer, and grants from the Asociacion Espanola Contra el Cancer and
the Fondo de Investigacion Sanitario (PI081583 and PI081120). The ESTHER
study was supported by a grant from the Baden Wurttemberg Ministry of
Science, Research and Arts. Additional cases were recruited in the
context of the VERDI study, which was supported by a grant from the
German Cancer Aid (Deutsche Krebshilfe). The FBCS is supported by funds
from Cancer Research UK (C8620/A8372 and C8620/A8857), a US Military
Acquisition (ACQ) Activity, Era of Hope Award (W81XWH-05-1-0204), and
the Institute of Cancer Research (UK). C. Turnbull is funded by a
Medical Research Council (UK) Clinical Research Fellowship. The FBCS
acknowledges NHS funding to the Royal Marsden/Institute of Cancer
Research NIHR Specialist Cancer Biomedical Research Centre. The GC-HBOC
was supported by Deutsche Krebshilfe (107054), the Dietmar-Hopp
Foundation, the Helmholtz society, and the German Cancer Research Centre
(DKFZ).; The GENICA was funded by the Federal Ministry of Education and
Research (BMBF) Germany grants 01KW9975/5, 01KW9976/8, 01KW9977/0, and
01KW0114, the Robert Bosch Foundation, Stuttgart, Deutsches
Krebsforschungszentrum (DKFZ), Heidelberg, Institute for Prevention and
Occupational Medicine of the German Social Accident Isurance (IPA),
Bochum, as well as the Department of Internal Medicine, Evangelische
Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany. The GESBC
was supported by the Deutsche Krebshilfe e. V. (70492) and genotyping in
part by the state of Baden-Wurttemberg through the Medical Faculty of
the University of Ulm (P.685). The HABCS study was supported by an
intramural grant from Hannover Medical School. The HMBCS was supported
by short-term fellowships from the German Academic Exchange Program (to
N.V. Bogdanova), and the Friends of Hannover Medical School (to N.V.
Bogdanova). The HUBCS was supported by a grant from the German Federal
Ministry of Research and Education (RUS08/017). The KBCP was financially
supported by the special Government Funding (EVO) of Kuopio University
Hospital grants, Cancer Fund of North Savo, the Finnish Cancer
Organizations, The Academy of Finland, and by the strategic funding of
the University of Eastern Finland. kConFab is supported by grants from
the National Breast Cancer Foundation, the NHMRC, the Queensland Cancer
Fund, the Cancer Councils of New South Wales, Victoria, Tasmania, and
South Australia, and the Cancer Foundation of Western Australia. The
kConFab Clinical Follow Up Study was funded by the NHMRC (145684,
288704, 454508). LMBC is supported by the 'Stichting tegen Kanker'
(232-2008 and 196-2010). The MARIE study was supported by the Deutsche
Krebshilfe e. V. (70-2892-BR I), the Hamburg Cancer Society, the German
Cancer Research Center, and the genotype work in part by the Federal
Ministry of Education and Research (BMBF) Germany (01KH0402). MBCSG was
supported by grants from Ministero della Salute (Extraordinary National
Cancer Program 2006 "Alleanza contro il Cancro", and "Progetto Tumori
Femminili" to P. Radice), Ministero dell'Universita' e Ricerca
(RBLAO3-BETH to PR), Fondazione Italiana per la Ricerca sul Cancro
(Special Project "Hereditary tumors"), Associazione Italiana per la
Ricerca sul Cancro (4017 to P. Peterlongo), and by funds from Italian
citizens who allocated the 5/1000 share of their tax payment in support
of the Fondazione IRCCS Istituto Nazionale Tumori, according to Italian
laws (INT-Institutional strategic projects "5 x 1000"). The MCBCS was
supported by the NIH grants (CA122340, CA128978) and a Specialized
Program of Research Excellence (SPORE) in Breast Cancer (CA116201). MCCS
cohort recruitment was funded by VicHealth and Cancer Council Victoria.
The MCCS was further supported by Australian NHMRC grants 209057,
251553, and 504711 and by infrastructure provided by Cancer Council
Victoria. SEE ABCFS. The NBCS was supported by grants from the Norwegian
Research council, 155218/V40, 175240/S10 to A.-L. Borrensen-Dale,
FUGE-NFR 181600/V11 to V.-M. Kosma, and a Swizz Bridge Award to A.-L.
Borrensen-Dale. The NHS was funded by NIH grant CA87969. The OBCS was
supported by research grants from the Finnish Cancer Foundation, the
Sigrid Juselius Foundation, the Academy of Finland, the University of
Oulu, and the Oulu University Hospital. The PBCS was funded by
Intramural Research Funds of the National Cancer Institute, Department
of Health and Human Services, USA. The RBCS was funded by the Dutch
Cancer Society (DDHK 2004-3124, DDHK 2009-4318).; The SBCS was suppoted
by Yorkshire Cancer Research and the Breast Cancer Campaign. SEARCH is
funded by program grants from Cancer Research UK (C490/A10124,
C8197/A10123, C1287/A10118). The SEBCS was supported by the Korea Health
21 R&D Project (AO30001), Ministry of Health and Welfare, Republic of
Korea. The SZBCS was supported by Grant PBZ_KBN_122/P05/2004; K.
Jaworska is a fellow of International PhD program, Postgraduate School
of Molecular Medicine, Warsaw Medical University, supported by the
Polish Foundation of Science. The TBCS was funded by The National Cancer
Institute Thailand. The TWBCS is supported by the Taiwan Biobank project
of the Institute of Biomedical Sciences, Academia Sinica, Taiwan. The
UCIBCS component of this research was supported by the NIH (CA58860,
CA92044) and the Lon V Smith Foundation (LVS39420). E. Sawyer is
supported by NIHR Comprehensive Biomedical Research Centre, Guy's & St.
Thomas' NHS Foundation Trust in partnership with King's College London,
United Kingdom. I. Tomlinson is supported by the Oxford Biomedical
Research Centre.
NR 14
TC 23
Z9 23
U1 1
U2 13
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 OCT
PY 2011
VL 20
IS 10
BP 2222
EP 2231
DI 10.1158/1055-9965.EPI-11-0569
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 831GR
UT WOS:000295717900028
PM 21795498
ER
PT J
AU Shiels, MS
Chaturvedi, AK
Katki, HA
Gochuico, BR
Caporaso, NE
Engels, EA
AF Shiels, Meredith S.
Chaturvedi, Anil K.
Katki, Hormuzd A.
Gochuico, Bernadette R.
Caporaso, Neil E.
Engels, Eric A.
TI Circulating Markers of Interstitial Lung Disease and Subsequent Risk of
Lung Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SURFACTANT PROTEIN-D; IDIOPATHIC PULMONARY-FIBROSIS; EPIDEMIOLOGIC
EVIDENCE; SCREENING TRIAL; SERUM; TUBERCULOSIS; BIOMARKERS; CHINA; CELL;
ADENOCARCINOMA
AB Background: Inflammation and pulmonary diseases, including interstitial lung diseases, are associated with increased lung cancer risk. Circulating levels of surfactant protein-D (SP-D) and Krebs von Lungren-6 (KL-6) are elevated in interstitial lung disease patients and may be useful markers of processes contributing to lung cancer.
Methods: We conducted a nested case-control study, including 532 lung cancer cases, 582 matched controls, and 150 additional controls with chest X-ray (CXR) evidence of pulmonary scarring, in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Serum SP-D and KL-6 levels were measured using enzyme immunoassay. Logistic regression was used to estimate the associations of SP-D and KL-6 with lung cancer and CXR scarring.
Results: Cases had higher levels than controls for SP-D (median 118.7 vs. 105.4 ng/mL, P = 0.008) and KL-6 (372.0 vs. 325.8 mu g/mL, P = 0.001). Lung cancer risk increased with SP-D (P(trend) = 0.0003) and KL-6 levels (P(trend) = 0.005). Compared with the lowest quartile, lung cancer risk was elevated among those with the highest quartiles of SP-D (OR = 1.87, 95% CI: 1.32-2.64) or KL-6 (OR = 1.58, 95% CI: 1.11-2.25). Among controls, participants with CXR scarring were more likely than those without scarring to have elevated levels of SP-D (quartile 4 vs. quartile 1: OR = 1.67, 95% CI: 1.04-2.70, P(trend) = 0.05) but not of KL-6 (OR = 1.04, 95% CI: 0.64-1.68, P(trend) = 0.99).
Conclusion: Circulating levels of SP-D and KL-6 are associated with subsequent lung cancer risk.
Impact: Our findings support a potential role for interstitial lung disease in lung cancer etiology or early detection, but additional research is needed. Cancer Epidemiol Biomarkers Prev; 20(10); 2262-72. (C) 2011 AACR.
C1 [Shiels, Meredith S.] NCI, Infect & Immunoepidemiol Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Gochuico, Bernadette R.] NHGRI, Med Genet Branch, Bethesda, MD 20892 USA.
RP Shiels, MS (reprint author), NCI, Infect & Immunoepidemiol Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 7059, Rockville, MD 20852 USA.
EM shielsms@mail.nih.gov
RI Katki, Hormuzd/B-4003-2015; Chaturvedi, Anil/J-2024-2015
OI Chaturvedi, Anil/0000-0003-2696-8899
FU National Human Genome Research Institute; Division of Cancer
Epidemiology and Genetics; Division of Cancer Prevention, National
Cancer Institute, NIH, DHHS
FX This work was supported by the Intramural Research Program of the
National Human Genome Research Institute and of the Division of Cancer
Epidemiology and Genetics and by contracts from the Division of Cancer
Prevention, National Cancer Institute, NIH, DHHS.
NR 38
TC 15
Z9 15
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2011
VL 20
IS 10
BP 2262
EP 2272
DI 10.1158/1055-9965.EPI-11-0326
PG 11
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 831GR
UT WOS:000295717900032
PM 21828236
ER
PT J
AU Campo, RA
Rowland, JH
Irwin, ML
Nathan, PC
Gritz, ER
Kinney, AY
AF Campo, Rebecca A.
Rowland, Julia H.
Irwin, Melinda L.
Nathan, Paul C.
Gritz, Ellen R.
Kinney, Anita Y.
TI Cancer Prevention after Cancer: Changing the Paradigm-a Report from the
American Society of Preventive Oncology
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; LONG-TERM SURVIVORS; BREAST-CANCER;
CHILDHOOD-CANCER; PHYSICAL-ACTIVITY; 5-YEAR SURVIVORS; SUBSEQUENT
NEOPLASMS; TEACHABLE MOMENT; ADULT SURVIVORS; LATE MORTALITY
C1 [Kinney, Anita Y.] Univ Utah, Dept Internal Med, Salt Lake City, UT 84112 USA.
[Campo, Rebecca A.; Kinney, Anita Y.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[Rowland, Julia H.] NCI, Off Canc Survivorship, Div Canc Control & Populat Sci, NIH DHHS, Bethesda, MD 20892 USA.
[Irwin, Melinda L.] Yale Univ, Sch Publ Hlth, New Haven, CT USA.
[Nathan, Paul C.] Hosp Sick Children, Div Hematol Oncol, Toronto, ON M5G 1X8, Canada.
[Gritz, Ellen R.] Univ Texas MD Anderson Canc Ctr, Dept Behav Sci, Houston, TX 77030 USA.
RP Kinney, AY (reprint author), Univ Utah, Dept Internal Med, 2000 Circle Hope,Rm 4160, Salt Lake City, UT 84112 USA.
EM anita.kinney@hci.utah.edu
FU Office of Cancer Survivorship, Division of Cancer Control and Population
Sciences, National Cancer Institute
FX The 2011 annual American Society of Preventive Oncology Survivorship
Special Interest Group was partially supported by the Office of Cancer
Survivorship, Division of Cancer Control and Population Sciences,
National Cancer Institute.
NR 47
TC 10
Z9 10
U1 0
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2011
VL 20
IS 10
BP 2317
EP 2324
DI 10.1158/1055-9965.EPI-11-0728
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 831GR
UT WOS:000295717900039
PM 21908726
ER
PT J
AU Sissung, TM
Pressler, H
Price, DK
Figg, WD
AF Sissung, T. M.
Pressler, H.
Price, D. K.
Figg, W. D.
TI SLCO Transport Genes in Prostate Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Letter
ID TESTOSTERONE
C1 [Sissung, T. M.; Figg, W. D.] NCI, Clin Pharmacol Program, Bethesda, MD 20892 USA.
[Pressler, H.; Price, D. K.; Figg, W. D.] NCI, Mol Pharmacol Sect, Med Oncol Branch, Bethesda, MD 20892 USA.
[Pressler, H.] Johns Hopkins Univ, Baltimore, MD USA.
RP Figg, WD (reprint author), NCI, Clin Pharmacol Program, 9000 Rockville Pike,Bldg 10,Room 5A01, Bethesda, MD 20892 USA.
EM wf13e@nih.gov
RI Figg Sr, William/M-2411-2016
FU Intramural NIH HHS [Z01 BC010453-06]
NR 5
TC 0
Z9 0
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD OCT
PY 2011
VL 20
IS 10
BP 2325
EP 2325
DI 10.1158/1055-9965.EPI-11-0606
PG 1
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 831GR
UT WOS:000295717900040
PM 21896883
ER
PT J
AU Peters, JM
Gonzalez, FJ
AF Peters, Jeffrey M.
Gonzalez, Frank J.
TI Why Toxic Equivalency Factors Are Not Suitable for Perfluoroalkyl
Chemicals
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Article
ID ACTIVATED-RECEPTOR-ALPHA; ARYL-HYDROCARBON RECEPTOR; MAMMARY-GLAND
DEVELOPMENT; SPRAGUE-DAWLEY RATS; PPAR-ALPHA; PERFLUOROOCTANOIC ACID;
AMMONIUM PERFLUOROOCTANOATE; NUCLEAR RECEPTORS; HUMAN RELEVANCE;
IN-VITRO
AB The pervasive nature of perfluoroalkyl chemicals in the environment has generated considerable interest for developing new strategies for risk assessment. In experimental animal models, exposure to perfluoroalkyl chemicals can cause developmental toxicity and hepatotoxicity. Peroxisome proliferator-activated receptor-alpha (PPAR alpha) is required to mediate some but not all of these effects. Since PPARa has a role in mediating some of these effects, and there is some overlap in the type of toxicities elicited by perfluoroalkyl chemicals, it has been suggested that a scaling system analogous to the toxic equivalency factor (TEF) system used for polychlorinated dibenzo-p-dioxins (PCDD), polychlorinated dibenzofurans (PCDF), and polychlorinated biphenyls (PCB) could be used for perfluoroalkyl chemicals. However, evidence suggests that perfluoroalkyl chemicals can activate/interfere with other receptors, and there is reason to suggest the possibility of species differences in the response mediated by different receptors as well as qualitative differences in toxicities elicited by perfluoroalkyl chemicals. These differences and other data gaps preclude the development of a TEF approach for perfluoroalkyl chemicals.
C1 [Peters, Jeffrey M.] Penn State Univ, Dept Vet & Biomed Sci, University Pk, PA 16802 USA.
[Peters, Jeffrey M.] Penn State Univ, Ctr Mol Toxicol & Carcinogenesis, University Pk, PA 16802 USA.
[Gonzalez, Frank J.] NCI, Lab Metab, Bethesda, MD 20892 USA.
RP Peters, JM (reprint author), Penn State Univ, Dept Vet & Biomed Sci, University Pk, PA 16802 USA.
EM jmp21@psu.edu
NR 68
TC 20
Z9 21
U1 0
U2 12
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0893-228X
J9 CHEM RES TOXICOL
JI Chem. Res. Toxicol.
PD OCT
PY 2011
VL 24
IS 10
BP 1601
EP 1609
DI 10.1021/tx200316x
PG 9
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA 832PP
UT WOS:000295817800001
PM 21913657
ER
PT J
AU Mi, LX
Hood, BL
Stewart, NA
Xiao, Z
Govind, S
Wang, XT
Conrads, TP
Veenstra, TD
Chung, FL
AF Mi, Lixin
Hood, Brian L.
Stewart, Nicolas A.
Xiao, Zhen
Govind, Sudha
Wang, Xiantao
Conrads, Thomas P.
Veenstra, Timothy D.
Chung, Fung-Lung
TI Identification of Potential Protein Targets of Isothiocyanates by
Proteomics
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Article
ID PROSTATE-CANCER CELLS; PHENETHYL ISOTHIOCYANATE; INDUCED APOPTOSIS;
LUNG-CANCER; EXPRESSION LEVEL; PHASE-2 ENZYMES; S-NITROSYLATION; A/J
MICE; SULFORAPHANE; PHOSPHORYLATION
AB Isothiocyanates (ITCs), such as phenethyl isothiocyanate (PEITC) and sulforaphane (SFN), are effective cancer chemopreventive compounds. It is believed that the major mechanism for the cancer preventive activity of ITCs is through the induction of cell cycle arrest and apoptosis. However, the upstream molecular targets of ITCs have been underexplored until recently. To identify proteins that are covalently modified by ITCs, human non-small cell lung cancer A549 cells were treated with (14)C-PEITC and (14)C-SFN, and the cell lysates were extracted for analysis by 2-D gel electrophoresis and mass spectrometry. After superimposing the colloidal Coomassie blue protein staining pattern with the pattern of radioactivity obtained from X-ray films, it was clear that only a small fraction of cellular proteins contained radioactivity, presumably resulting from selective binding with PEITC or SFN via thiocarbamation. More than 30 proteins with a variety of biological functions were identified with high confidence. Here, we report the identities of these potential ITC target proteins and discuss their biological relevance. The discovery of the protein targets may facilitate studies of the mechanisms by which ITCs exert their cancer preventive activity and provide the molecular basis for designing more efficacious ITC compounds.
C1 [Mi, Lixin; Govind, Sudha; Wang, Xiantao; Chung, Fung-Lung] Georgetown Univ, Dept Oncol, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
[Hood, Brian L.; Stewart, Nicolas A.; Xiao, Zhen; Conrads, Thomas P.; Veenstra, Timothy D.] NCI, Lab Prote & Analyt Technol, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Chung, FL (reprint author), Georgetown Univ, Dept Oncol, Lombardi Comprehens Canc Ctr, 3800 Reservoir Rd,LL 128A,Box 571465, Washington, DC 20057 USA.
EM flc6@georgetown.edu
FU NIH [CA-100853]
FX This study was supported by NIH grant CA-100853.
NR 52
TC 37
Z9 38
U1 1
U2 12
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0893-228X
J9 CHEM RES TOXICOL
JI Chem. Res. Toxicol.
PD OCT
PY 2011
VL 24
IS 10
BP 1735
EP 1743
DI 10.1021/tx2002806
PG 9
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA 832PP
UT WOS:000295817800016
PM 21838287
ER
PT J
AU Hazard, M
Steele, S
Wang, DW
Pearson, T
Scheideler, M
Dewhurst, S
AF Hazard, Mike
Steele, Scott
Wang, Dongwen
Pearson, Thomas
Scheideler, Mark
Dewhurst, Steve
TI CTSA-IP: A Solution to Identifying and Aggregating Intellectual Property
across the NIH Clinical Translational Science Award (CTSA) Consortium of
Biomedical Research Institutes
SO CTS-CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Article
DE intellectual property; informatics; research partnerships
AB One of the objectives of the Consortium of Institutions with Clinical and Translational Science Awards (CTSAs) is to enhance technology transfer among the CTSAs and with public and private sector partners. Clinical and Translational Sciences Award Intellectual Property (CTSA-IP; http://www.CTSAIP.org) is a web-based, open access IP search tool that aggregates and promotes technologies from member institutions of the National Institutes of Health's (NIH) CTSAs consortium. Its ultimate aim is to stimulate collaborative research activity by encouraging the formation of public-private partnerships with CTSA institutions and the NIH. First launched in 2009, CTSA-IP has grown rapidly and met its first objectives of developing wide member institution participation and site usage. This communication will discuss the strategy employed in the initiative of aggregating IP across institutional boundaries, the promise that lies therein, as well as the challenges encountered and lessons learned in promoting CTSA-wide engagement. Clin Trans Sci 2011; Volume 4: 328-331
C1 [Steele, Scott] Univ Rochester, Med Ctr, Clin & Translat Sci Inst, Off Res Alliances & Publ Private Partnerships Key, Rochester, NY 14642 USA.
[Hazard, Mike; Wang, Dongwen] Univ Rochester, Sch Med & Dent, Dept Biostat & Computat Biol, Rochester, NY 14642 USA.
[Steele, Scott; Pearson, Thomas] Univ Rochester, Sch Med & Dent, Dept Community & Prevent Med, Rochester, NY 14642 USA.
[Scheideler, Mark] NINDS, Off Translat Res, NIH, Bethesda, MD 20892 USA.
[Dewhurst, Steve] Univ Rochester, Sch Med & Dent, Dept Microbiol & Immunol, Rochester, NY 14642 USA.
RP Steele, S (reprint author), Univ Rochester, Med Ctr, Clin & Translat Sci Inst, Off Res Alliances & Publ Private Partnerships Key, Rochester, NY 14642 USA.
EM scott.steele@rochester.edu
FU National Center for Research Resources, NIH, CTSA, part of the Roadmap
Initiative, Re-engineering the Clinical Research Enterprise
FX The authors gratefully thank Dr. Bonnie Harbinger of NIH for assistance
and advice throughout the development of this project. This project was
supported by a Supplement to Award Number UL1 RR024160 from the National
Center for Research Resources, NIH, CTSA program, part of the Roadmap
Initiative, Re-engineering the Clinical Research Enterprise. The content
is solely the responsibility of the authors and does not necessarily
represent the official views of the National Center for Research
Resources or the National Institutes of Health.
NR 8
TC 2
Z9 2
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1752-8054
J9 CTS-CLIN TRANSL SCI
JI CTS-Clin. Transl. Sci.
PD OCT
PY 2011
VL 4
IS 5
BP 328
EP 331
DI 10.1111/j.1752-8062.2011.00308.x
PG 4
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 840ER
UT WOS:000296421600010
PM 22029803
ER
PT J
AU Kunkel, TA
AF Kunkel, Thomas A.
TI Balancing eukaryotic replication asymmetry with replication fidelity
SO CURRENT OPINION IN CHEMICAL BIOLOGY
LA English
DT Review
ID DNA-POLYMERASE-DELTA; UNIQUE ERROR SIGNATURE; IMBALANCED DNTP POOLS;
MISMATCH REPAIR; SACCHAROMYCES-CEREVISIAE; RIBONUCLEOTIDE INCORPORATION;
S-PHASE; YEAST; EPSILON; FORK
AB Coordinated replication of eukaryotic nuclear genomes is asymmetric, with copying of a leading strand template preceding discontinuous copying of the lagging strand template. Replication is catalyzed by DNA polymerases alpha, delta and epsilon, enzymes that are related yet differ in physical and biochemical properties, including fidelity. Recent studies suggest that Pol epsilon is normally the primary leading strand replicase, whereas most synthesis by Pol delta occurs during lagging strand replication. New studies show that replication asymmetry can generate strand-specific genome instability resulting from biased deoxynucleotide pools and unrepaired ribonucleotides incorporated into DNA during replication, and that the eukaryotic replication machinery has evolved to most efficiently correct those replication errors that are made at the highest rates.
C1 [Kunkel, Thomas A.] NIEHS, Mol Genet Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Kunkel, Thomas A.] NIEHS, Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Kunkel, TA (reprint author), NIEHS, Mol Genet Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
EM kunkel@niehs.nih.gov
FU Division of Intramural Research, NIEHS, NIH [Z01 ES065070, Z01 ES065089]
FX To the many scientists whose work contributed to the topics considered
here but whose publications were not cited due to space limitations, I
thank them for their understanding. Interested readers arc encouraged to
consult the recent articles that are cited, where citations to many
other important studies can be found. I also thank Peter Burgers and
Andrei Chabes for thoughtful comments on this article. Research
performed in my laboratory is supported by Projects Z01 ES065070 and Z01
ES065089 from the Division of Intramural Research, NIEHS, NIH.
NR 51
TC 24
Z9 24
U1 3
U2 14
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1367-5931
J9 CURR OPIN CHEM BIOL
JI Curr. Opin. Chem. Biol.
PD OCT
PY 2011
VL 15
IS 5
BP 620
EP 626
DI 10.1016/j.cbpa.2011.07.025
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 840AL
UT WOS:000296410500007
PM 21862387
ER
PT J
AU Dainiak, N
Gent, RN
Carr, Z
Schneider, R
Bader, J
Buglova, E
Chao, N
Coleman, CN
Ganser, A
Gorin, C
Hauer-Jensen, M
Huff, LA
Lillis-Hearne, P
Maekawa, K
Nemhauser, J
Powles, R
Schunemann, H
Shapiro, A
Stenke, L
Valverde, N
Weinstock, D
White, D
Albanese, J
Meineke, V
AF Dainiak, Nicholas
Gent, Robert Nicolas
Carr, Zhanat
Schneider, Rita
Bader, Judith
Buglova, Elena
Chao, Nelson
Coleman, C. Norman
Ganser, Arnold
Gorin, Claude
Hauer-Jensen, Martin
Huff, L. Andrew
Lillis-Hearne, Patricia
Maekawa, Kazuhiko
Nemhauser, Jeffrey
Powles, Ray
Schuenemann, Holger
Shapiro, Alla
Stenke, Leif
Valverde, Nelson
Weinstock, David
White, Douglas
Albanese, Joseph
Meineke, Viktor
TI Literature Review and Global Consensus on Management of Acute Radiation
Syndrome Affecting Nonhematopoietic Organ Systems
SO DISASTER MEDICINE AND PUBLIC HEALTH PREPAREDNESS
LA English
DT Review
DE countermeasures for ARS; acute radiation syndrome management; treatment
of ARS; narrative review of countermeasures for ARS
ID MESENCHYMAL STEM-CELLS; RESPIRATORY-DISTRESS-SYNDROME;
MEDICAL-MANAGEMENT; CRITICALLY-ILL; GLUCOSE CONTROL; PUBLIC-HEALTH;
CRITICAL-CARE; SEPTIC SHOCK; DOUBLE-BLIND; LUNG INJURY
AB Objectives: The World Health Organization convened a panel of experts to rank the evidence for medical countermeasures for management of acute radiation syndrome (ARS) in a hypothetical scenario involving the hospitalization of 100 to 200 victims. The goal of this panel was to achieve consensus on optimal management of ARS affecting nonhematopoietic organ systems based upon evidence in the published literature.
Methods: English-language articles were identified in MEDLINE and PubMed. Reference lists of retrieved articles were distributed to conferees in advance of and updated during the meeting. Published case series and case reports of ARS, publications of randomized controlled trials of relevant interventions used to treat nonirradiated individuals, reports of studies in irradiated animals, and prior recommendations of subject matter experts were selected. Studies were extracted using the Grading of Recommendations Assessment Development and Evaluation system. In cases in which data were limited or incomplete, a narrative review of the observations was made.
Results: No randomized controlled trials of medical countermeasures have been completed for individuals with ARS. Reports of countermeasures were often incompletely described, making it necessary to rely on data generated in nonirradiated humans and in experimental animals. A strong recommendation is made for the administration of a serotonin-receptor antagonist prophylactically when the suspected exposure is >2 Gy and topical steroids, antibiotics, and antihistamines for radiation burns, ulcers, or blisters; excision and grafting of radiation ulcers or necrosis with intractable pain; provision of supportive care to individuals with neurovascular syndrome; and administration of electrolyte replacement therapy and sedatives to individuals with significant burns, hypovolemia, and/orshock. A strong recommendation is made against the use of systemic steroids in the absence of a specific indication. A weak recommendation is made for the use of fluoroquinolones, bowel decontamination, loperamide, and enteral nutrition, and for selective oropharyngeal/digestive decontamination, blood glucose maintenance, and stress ulcer prophylaxis in critically ill patients.
Conclusions: High-quality studies of therapeutic interventions in humans exposed to nontherapeutic radiation are not available, and because of ethical concerns regarding the conduct of controlled studies in humans, such studies are unlikely to emerge in the near future.
C1 [Meineke, Viktor] Bundeswehr Inst Radiobiol, D-80937 Munich, Germany.
[Dainiak, Nicholas] Yale Univ, Sch Med, New Haven, CT 06520 USA.
[Dainiak, Nicholas] Yale New Haven Hlth Bridgeport Hosp, New Haven, CT USA.
[Carr, Zhanat] World Hlth Org, Geneva, Switzerland.
[Schneider, Rita] Univ Wurzburg, Dept Nucl Med, D-97070 Wurzburg, Germany.
[Bader, Judith; Coleman, C. Norman] Natl Canc Inst, Bethesda, MD 20892 USA.
[Chao, Nelson] Duke Univ, Durham, NC 27706 USA.
[Ganser, Arnold] Hannover Med Sch, Dept Hematol Hemostasis Oncol & Stem Cell Transpl, Hannover, Germany.
[Gorin, Claude] Hosp St Antoine, St Antoine, France.
[Hauer-Jensen, Martin] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Huff, L. Andrew; Lillis-Hearne, Patricia] Armed Forces Radiobiol Res Inst, Bethesda, MD 20814 USA.
[Maekawa, Kazuhiko] Kanto Cent Hosp, Tokyo, Japan.
[Nemhauser, Jeffrey] Ctr Dis Control & Prevent, Atlanta, GA 30333 USA.
[Schuenemann, Holger] McMaster Univ, Hamilton, ON L8S 4L8, Canada.
[Shapiro, Alla] US FDA, Rockville, MD 20857 USA.
[Stenke, Leif] Karolinska Inst, S-10401 Stockholm, Sweden.
[Weinstock, David] Dana Farber Canc Inst, Boston, MA 02115 USA.
[White, Douglas] Univ Pittsburgh, Program Eth & Crit Care Med, Pittsburgh, PA 15260 USA.
[Albanese, Joseph] Yale New Haven Hlth Ctr Emergency Preparedness &, New Haven, CT USA.
RP Meineke, V (reprint author), Bundeswehr Inst Radiobiol, Neuherbergstr 11, D-80937 Munich, Germany.
EM ViktorMeineke@bundeswehr.org
FU National Institute of Allergy and Infectious Diseases
FX Owing to their seminal contributions in the field of radiation biology
and their pioneering approaches to treatment of victims of radiation
injury, this consultancy report is dedicated to Theodor M. Fliedner and
Angelina Guskova. The authors thank Makoto Akashi, Axel Bottger, Thierry
de Revel, Patrick Gourmelon, Richard Hatchett, Mikhail Konchalovski,
Ying Liu, Maria Julia Marinissen, Hilary Walker, Helmut Walerius, and
Wei Zhang for participating in the consultancy and contributing to
consensus building. The authors are grateful to Richard Hatchett and the
National Institute of Allergy and Infectious Diseases for providing
financial support for this consultancy.
NR 181
TC 28
Z9 28
U1 2
U2 10
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 1935-7893
J9 DISASTER MED PUBLIC
JI Dis. Med. Public Health Prep.
PD OCT
PY 2011
VL 5
IS 3
BP 183
EP 201
PG 19
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 839JU
UT WOS:000296362300007
PM 21986999
ER
PT J
AU Dainiak, N
Gent, RN
Carr, Z
Schneider, R
Bader, J
Buglova, E
Chao, N
Coleman, CN
Ganser, A
Gorin, C
Hauer-Jensen, M
Huff, LA
Lillis-Hearne, P
Maekawa, K
Nemhauser, J
Powles, R
Schunemann, H
Shapiro, A
Stenke, L
Valverde, N
Weinstock, D
White, D
Albanese, J
Meineke, V
AF Dainiak, Nicholas
Gent, Robert Nicolas
Carr, Zhanat
Schneider, Rita
Bader, Judith
Buglova, Elena
Chao, Nelson
Coleman, C. Norman
Ganser, Arnold
Gorin, Claude
Hauer-Jensen, Martin
Huff, L. Andrew
Lillis-Hearne, Patricia
Maekawa, Kazuhiko
Nemhauser, Jeffrey
Powles, Ray
Schuenemann, Holger
Shapiro, Alla
Stenke, Leif
Valverde, Nelson
Weinstock, David
White, Douglas
Albanese, Joseph
Meineke, Viktor
TI First Global Consensus for Evidence-Based Management of the
Hematopoietic Syndrome Resulting From Exposure to Ionizing Radiation
SO DISASTER MEDICINE AND PUBLIC HEALTH PREPAREDNESS
LA English
DT Review
DE countermeasures for ARS; cytokines and radiation injury; transplantation
for ARS; acute radiation syndrome management; hematopoietic syndrome
management
ID COLONY-STIMULATING FACTOR; MEDICAL-MANAGEMENT; PROGENITOR CELLS;
RHESUS-MONKEYS; RECOMMENDATIONS; ACCIDENT; MYELOSUPPRESSION;
RADIOSENSITIVITY; TRANSPLANTATION; GROWTH
AB Objective: Hematopoietic syndrome (HS) is a clinical diagnosis assigned to people who present with >1 new-onset cytopenias in the setting of acute radiation exposure. The World Health Organization convened a panel of experts to evaluate the evidence and develop recommendations for medical countermeasures for the management of HS in a hypothetical scenario involving the hospitalization of 100 to 200 individuals exposed to radiation. The objective of this consultancy was to develop recommendations for treatment of the HS based upon the quality of evidence.
Methods: English-language articles were identified in MEDLINE and PubMed. Reference lists of retrieved articles were distributed to panel members before the meeting and updated during the meeting. Published case series and case reports of individuals with HS, published randomized controlled trials of relevant interventions used to treat nonirradiated individuals, reports of studies in irradiated animals, and prior recommendations of subject matter experts were selected. Studies were extracted using the Grading of Recommendations Assessment Development and Evaluation (GRADE) system. In cases in which data were limited or incomplete, a narrative review of the observations was made. No randomized controlled trials of medical countermeasures have been completed for individuals with radiation-associated HS. The use of GRADE analysis of countermeasures for injury to hematopoietic tissue was restricted by the lack of comparator groups in humans. Reliance on data generated in nonirradiated humans and experimental animals was necessary.
Results: Based upon GRADE analysis and narrative review, a strong recommendation was made for the administration of granulocyte colony-stimulating factor or granulocyte macrophage colony-stimulating factor and a weak recommendation was made for the use of erythropoiesis-stimulating agents or hematopoietic stem cell transplantation.
Conclusions: Assessment of therapeutic interventions for HS in humans exposed to nontherapeutic radiation is difficult because of the limits of the evidence. (Disaster Med Public Health Preparedness. 2011;5:202-212)
C1 [Meineke, Viktor] Bundeswehr Inst Radiobiol, D-80937 Munich, Germany.
[Dainiak, Nicholas] Yale Univ, Sch Med, New Haven, CT 06520 USA.
[Dainiak, Nicholas] Yale New Haven Hlth Bridgeport Hosp, New Haven, CT USA.
[Carr, Zhanat] World Hlth Org, Geneva, Switzerland.
[Schneider, Rita] Univ Wurzburg, Dept Nucl Med, D-97070 Wurzburg, Germany.
[Bader, Judith; Coleman, C. Norman] Natl Canc Inst, Bethesda, MD 20892 USA.
[Chao, Nelson] Duke Univ, Durham, NC 27706 USA.
[Ganser, Arnold] Hannover Med Sch, Dept Hematol Hemostasis Oncol & Stem Cell Transpl, Hannover, Germany.
[Gorin, Claude] Hosp St Antoine, St Antoine, France.
[Hauer-Jensen, Martin] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Huff, L. Andrew; Lillis-Hearne, Patricia] Armed Forces Radiobiol Res Inst, Bethesda, MD 20814 USA.
[Maekawa, Kazuhiko] Kanto Cent Hosp, Tokyo, Japan.
[Nemhauser, Jeffrey] Ctr Dis Control & Prevent, Atlanta, GA 30333 USA.
[Schuenemann, Holger] McMaster Univ, Hamilton, ON L8S 4L8, Canada.
[Shapiro, Alla] US FDA, Rockville, MD 20857 USA.
[Stenke, Leif] Karolinska Inst, S-10401 Stockholm, Sweden.
[Weinstock, David] Dana Farber Canc Inst, Boston, MA 02115 USA.
[White, Douglas] Univ Pittsburgh, Program Eth & Crit Care Med, Pittsburgh, PA 15260 USA.
[Albanese, Joseph] Yale New Haven Hlth Ctr Emergency Preparedness &, New Haven, CT USA.
RP Meineke, V (reprint author), Bundeswehr Inst Radiobiol, Neuherbergstr 11, D-80937 Munich, Germany.
EM ViktorMeineke@bundeswehr.org
FU National Institute of Allergy and Infectious Diseases
FX Owing to their seminal contributions in the field of radiation biology
and their pioneering approaches to treatment of victims of radiation
injury, this consultancy report is dedicated to Theodor M. Fliedner and
Angelina Guskova. The authors thank Makoto Akashi, Axel Bottger, Thierry
de Revel, Patrick Gourmelon, Richard Hatchett, Mikhail Konchalovski,
Ying Liu, Maria Julia Marinissen, Hilary Walker, Helmut Walerius, and
Wei Zhang for participating in the consultancy and contributing to
consensus building. The authors are grateful to the National Institute
of Allergy and Infectious Diseases for providing financial support for
this consultancy.
NR 44
TC 32
Z9 34
U1 2
U2 6
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 1935-7893
J9 DISASTER MED PUBLIC
JI Dis. Med. Public Health Prep.
PD OCT
PY 2011
VL 5
IS 3
BP 202
EP 212
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 839JU
UT WOS:000296362300008
PM 21987000
ER
PT J
AU Davidson, TS
Shevach, EM
AF Davidson, Todd S.
Shevach, Ethan M.
TI Polyclonal Treg cells modulate T effector cell trafficking
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE EAE; Immunosuppression; Trafficking; Treg cells
ID DENDRITIC CELLS; AUTOIMMUNE-DISEASE; CUTTING EDGE; IN-VITRO; INHIBIT;
DIFFERENTIATION; RESPONSES; PREVENT; MICE; VIVO
AB In this study, we have analyzed the in vivo dynamics of the interaction between polyclonal Foxp3(+) Treg cells, effector T (Teff) cells, and DCs in order to further our understanding of the mechanisms of Treg cell-mediated suppression. Cotransfer of polyclonal activated Treg cells into healthy mice attenuated the induction of EAE. Suppression of disease strongly correlated with a reduced number of Teff cells in the spinal cord, but not with Treg cell-mediated inhibition of Th1/Th17 differentiation. Cotransfer of Treg cells with TCR-Tg Teff cells followed by immunization by multiple routes resulted in an enhanced number of Teff cells in the lymph nodes draining the site of immunization without an inhibition of Teff-cell differentiation. Fewer Teff cells could be detected in the blood in the presence of Treg cells and fewer T cells could access a site of antigen exposure in a modified delayed-type hypersensitivity assay. Teff cells recovered from LNs in the presence of Treg cells expressed decreased levels of CXCR4, syndecan, and the sphingosine phosphate receptor, S1P1 (sphingosine 1-phosphate receptor 1). Thus, polyclonal Treg cells influence Teff-cell responses by targeting trafficking pathways, thus allowing immunity to develop in lymphoid organs, but limiting the number of potentially auto-aggressive cells that are allowed to enter the tissues.
C1 [Davidson, Todd S.; Shevach, Ethan M.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Shevach, EM (reprint author), NIAID, Immunol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM eshevach@niaid.nih.gov
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases
FX These studies were supported by the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases.
NR 23
TC 25
Z9 25
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0014-2980
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD OCT
PY 2011
VL 41
IS 10
BP 2862
EP 2870
DI 10.1002/eji.201141503
PG 9
WC Immunology
SC Immunology
GA 837KB
UT WOS:000296199000009
PM 21728170
ER
PT J
AU Mkrtichyan, M
Najjar, YG
Raulfs, EC
Abdalla, MY
Samara, R
Rotem-Yehudar, R
Cook, L
Khleif, SN
AF Mkrtichyan, Mikayel
Najjar, Yana G.
Raulfs, Estella C.
Abdalla, Maher Y.
Samara, Raed
Rotem-Yehudar, Rinat
Cook, Larry
Khleif, Samir N.
TI Anti-PD-1 synergizes with cyclophosphamide to induce potent anti-tumor
vaccine effects through novel mechanisms
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE Cancer immunotherapy; Programmed death-1 receptor; Vaccine
ID REGULATORY T-CELLS; IMMUNOLOGICAL SELF-TOLERANCE; FACILITATED ADOPTIVE
IMMUNOTHERAPY; TUMOR-INFILTRATING LYMPHOCYTES; INCREASED POPULATIONS;
PERIPHERAL-BLOOD; CLINICAL-SIGNIFICANCE; CARCINOMA PATIENTS;
PROGNOSTIC-FACTORS; PANCREATIC-CANCER
AB Programmed death-1 receptor (PD-1) is expressed on T cells following TCR activation. Binding of this receptor to its cognate ligands, programmed death ligand (PDL)-1 and PDL-2, down-regulates signals by the TCR, promoting T-cell anergy and apoptosis, thus leading to immune suppression. Here, we find that using an anti-PD-1 antibody (CT-011) with Treg-cell depletion by low-dose cyclophosphamide (CPM), combined with a tumor vaccine, induces synergistic antigen-specific immune responses and reveals novel activities of each agent in this combination. This strategy led to complete regression of established tumors in a significant percentage of treated animals, with survival prolongation. We show for the first time that combining CT-011 and CPM significantly increases the number of vaccine-induced tumor-infiltrating CD8(+) T cells, with simultaneous decrease in infiltrating Treg cells. Interestingly, we find that CT-011 prolongs Treg-cell inhibition induced by CPM, leading to a sustainable significant synergistic decrease of splenic and tumor-infiltrated Treg cells. Surprisingly, we find that the anti-tumor effect elicited by the combination of CT-011 and CPM is dependent on both CD8(+) and CD4(+) T-cell responses, although the antigen we used is a class I MHC-restricted peptide. Thus, we describe a novel and effective therapeutic approach by combining multiple strategies to target several tumor-mediated immune inhibitory mechanisms.
C1 [Mkrtichyan, Mikayel; Najjar, Yana G.; Raulfs, Estella C.; Abdalla, Maher Y.; Samara, Raed; Khleif, Samir N.] NCI, Canc Vaccine Sect, NIH, Bethesda, MD 20892 USA.
[Rotem-Yehudar, Rinat] CureTech Ltd, Yavne, Israel.
[Cook, Larry] NIH, Lab Anim Sci Program, Bethesda, MD 20892 USA.
RP Khleif, SN (reprint author), NCI, Canc Vaccine Sect, NIH, Bldg 41,Room B900, Bethesda, MD 20892 USA.
EM khleif@nih.gov
FU Center for Cancer Research, NCI, NIH
FX The authors thank Daniel O'Mard, Ashley Reynolds and Gail McMullen from
the NIH animal facility for their technical assistance with animal
injections. This work was supported by the Intramural Research Program
of the Center for Cancer Research, NCI, NIH.
NR 46
TC 55
Z9 56
U1 0
U2 11
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0014-2980
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD OCT
PY 2011
VL 41
IS 10
BP 2977
EP 2986
DI 10.1002/eji.201141639
PG 10
WC Immunology
SC Immunology
GA 837KB
UT WOS:000296199000020
PM 21710477
ER
PT J
AU Faupel-Badger, JM
Staff, AC
Thadhani, R
Powe, CE
Potischman, N
Hoover, RN
Troisi, R
AF Faupel-Badger, Jessica M.
Staff, Anne Cathrine
Thadhani, Ravi
Powe, Camille E.
Potischman, Nancy
Hoover, Robert N.
Troisi, Rebecca
TI Maternal angiogenic profile in pregnancies that remain normotensive
SO EUROPEAN JOURNAL OF OBSTETRICS & GYNECOLOGY AND REPRODUCTIVE BIOLOGY
LA English
DT Article
DE Pregnancy; Angiogenic factors; sFlt1; PlGF; Soluble endoglin; Maternal
ID PLACENTAL GROWTH-FACTOR; SOLUBLE ENDOGLIN; HYPERTENSIVE DISORDERS;
ANTIANGIOGENIC FACTORS; TYROSINE KINASE-1; PREECLAMPSIA; RISK; SFLT1;
VASCULOGENESIS; PATHOGENESIS
AB Objective: We sought to determine if maternal characteristics are associated with angiogenic profile in the first and second trimester of normotensive pregnancies.
Study design: Circulating levels of maternal placental like growth factor (PIGF), soluble fms-like tyrosine kinase receptor (sFlt1), and soluble endoglin (sEng) were measured in serum samples collected during the first (median 11.3 weeks) and second trimester (median 17.1 weeks) of 182 normotensive pregnancies. Diastolic blood pressure (DBP), systolic blood pressure (SBP), and mean arterial pressure (MAP) were measured at the same visits when samples were collected to measure angiogenic factors. Linear regression analysis was used to examine associations of the angiogenic measures with maternal characteristics. The association between blood pressure measures and concentrations of angiogenic factors was evaluated using Spearman correlation and linear regression analysis.
Results: In adjusted analyses, nulliparous women had higher sFlt1 concentrations in both first (p = 0.06) and second (p = 0.001) trimester. Higher BMI was associated with greater sFlt1 concentrations in both the first (p = 0.004) and second trimester (p = 0.008), but significantly lower sEng concentrations in both trimesters (p = 0.002 for first trimester and p = 0.0009 for second). Nulliparity and higher BMI also were associated with higher sFlt1/PLGF anti-angiogenic ratios in both first (p = 0.05 and p = 0.007, respectively) and second trimesters (p = 0.003 and p = 0.02, respectively). First trimester sFlt1 levels were weakly correlated with first trimester SBP (r(s) = 0.18, p = 0.03) and MAP (r(s) = 0.16, p = 0.04). Second trimester sEng levels were inversely associated with second trimester MAP (r(s) = -0.17, p = 0.05). Including blood pressure measures in the linear regression models did not change the reported associations of angiogenic factors with maternal characteristics.
Conclusions: These results demonstrate that even early in normotensive pregnancies maternal characteristics are associated with variations in angiogenic profile across this population. Published by Elsevier Ireland Ltd.
C1 [Faupel-Badger, Jessica M.] NCI, Canc Prevent Fellowship Program, Ctr Canc Training, Rockville, MD USA.
[Faupel-Badger, Jessica M.; Hoover, Robert N.; Troisi, Rebecca] NCI, Epidemiol & Biostat Program, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Staff, Anne Cathrine] Oslo Univ Hosp, Dept Obstet & Gynaecol, Ulleval, Norway.
[Staff, Anne Cathrine] Univ Oslo, Fac Med, Oslo, Norway.
[Thadhani, Ravi; Powe, Camille E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Thadhani, Ravi; Powe, Camille E.] Harvard Univ, Sch Med, Boston, MA USA.
[Potischman, Nancy] NCI, Appl Res Program, Div Canc Control & Populat Sci, Rockville, MD USA.
[Troisi, Rebecca] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dept Community & Family Med, Hanover, NH 03756 USA.
RP Faupel-Badger, JM (reprint author), NIH, 6120 Execut Blvd,Suite 150E,MSC 7105, Bethesda, MD 20892 USA.
EM badgerje@mail.nih.gov
FU NIH; National Cancer Institute; Division of Cancer Epidemiology and
Genetics, National Cancer Institute, National Institutes of Health, U.S.
Department of Health and Human Services; Division Cancer Control and
Population Sciences, National Cancer Institute, National Institutes of
Health, U.S. Department of Health and Human Services; [HD 39223]
FX Funding support: This research was supported in part by the Intramural
Research Program of the NIH and the National Cancer Institute. The
Divisions of Cancer Epidemiology and Genetics and Cancer Control and
Population Sciences, National Cancer Institute, National Institutes of
Health, U.S. Department of Health and Human Services provided funding
for the data analysis and manuscript preparation. HD 39223 provided
funding for the collection of original data and laboratory assays.
NR 25
TC 10
Z9 10
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0301-2115
J9 EUR J OBSTET GYN R B
JI Eur. J. Obstet. Gynecol. Reprod. Biol.
PD OCT
PY 2011
VL 158
IS 2
BP 189
EP 193
DI 10.1016/j.ejogrb.2011.05.001
PG 5
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 838OK
UT WOS:000296301900012
PM 21641103
ER
PT J
AU Ko, SU
Stenholm, S
Chia, CW
Simonsick, EM
Ferrucci, L
AF Ko, Seung-uk
Stenholm, Sari
Chia, Chee W.
Simonsick, Eleanor M.
Ferrucci, Luigi
TI Gait pattern alterations in older adults associated with type 2 diabetes
in the absence of peripheral neuropathy-Results from the Baltimore
Longitudinal Study of Aging
SO GAIT & POSTURE
LA English
DT Article
DE Type 2 diabetes; Aging; Gait; Mobility limitation; Peripheral
neuropathy; Mechanical work expenditure
ID JOINT KINEMATICS; CENTER LOCATION; WALKING; MELLITUS; ACCURACY
AB Diabetes may impact gait mechanics before onset of frank neuropathies and other associated threats to mobility. This study aims to characterize gait pattern alterations of type 2 diabetic adults without peripheral neuropathy during walking at maximum speed (fast-walking) as well as at self-selected speed (usual-walking). One-hundred and eighty-six participants aged 60-87 from the Baltimore Longitudinal Study of Aging (BLSA) able to walk unassisted and without peripheral neuropathy were classified as nondiabetic (N = 160) or having type 2 diabetes (N = 26). Gait parameters from the fast-walking and usual-walking tests were compared between participants with and without type 2 diabetes. Participants with diabetes had a shorter stride length for fast-walking (p = 0.033) and a longer percentage of the gait cycle with the knee in 1st flexion for both fast- and usual-walking (p = 0.033, and 0.040, respectively) than non-diabetic participants. Participants with diabetes exhibited a smaller hip range of motion in the sagittal plane during usual-walking compared to non-diabetics (p = 0.049). During fast-walking, participants with diabetes used lower ankle generative mechanical work expenditure (MWE) and higher knee absorptive MWE compared to non-diabetic persons (p = 0.021, and 0.018, respectively). These findings suggest that individuals with type 2 diabetes without overt peripheral neuropathy exhibit altered and less efficient gait patterns than non-diabetic persons. These alterations are more apparent during walking at a maximum speed indicating that maximum gait testing may be useful for identifying early threats to mobility limitations in older adults with type 2 diabetes. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Ko, Seung-uk] Chonnam Natl Univ, Dept Mech Engn, Yeosu 550749, Jeonnam, South Korea.
[Chia, Chee W.; Simonsick, Eleanor M.; Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Stenholm, Sari] Natl Inst Hlth & Welf, Dept Hlth Funct Capac & Welf, Turku, Finland.
RP Ko, SU (reprint author), Chonnam Natl Univ, Dept Mech Engn, 50 Daehak Ro, Yeosu 550749, Jeonnam, South Korea.
EM seunguk.ko@gmail.com
RI Stenholm, Sari/G-6940-2011
FU NIH, National Institute on Aging
FX This research was supported entirely by the Intramural Research Program
of the NIH, National Institute on Aging. Data for these analyses were
obtained from the Baltimore Longitudinal Study of Aging, a study
performed by the National Institute on Aging.
NR 23
TC 26
Z9 27
U1 3
U2 6
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0966-6362
J9 GAIT POSTURE
JI Gait Posture
PD OCT
PY 2011
VL 34
IS 4
BP 548
EP 552
DI 10.1016/j.gaitpost.2011.07.014
PG 5
WC Neurosciences; Orthopedics; Sport Sciences
SC Neurosciences & Neurology; Orthopedics; Sport Sciences
GA 841AQ
UT WOS:000296484800020
PM 21873064
ER
PT J
AU Felizardo, T
Wang, JCM
McGray, RAJ
Evelegh, C
Spaner, DE
Fowler, DH
Bramson, JL
Medin, JA
AF Felizardo, T. C.
Wang, J. C. M.
McGray, R. A. J.
Evelegh, C.
Spaner, D. E.
Fowler, D. H.
Bramson, J. L.
Medin, J. A.
TI Differential immune responses mediated by adenovirus- and
lentivirus-transduced DCs in a HER-2/neu overexpressing tumor model
SO GENE THERAPY
LA English
DT Article
DE HER-2/neu; adenovirus; lentivirus; dendritic cells vaccine
ID PLASMACYTOID DENDRITIC CELLS; RECOMBINANT ADENOVIRUS; IN-VIVO; ANTITUMOR
IMMUNITY; CLINICAL-TRIALS; GENE DELIVERY; T-CELLS; ANTIGEN; VECTOR;
CANCER
AB Recent investigations have demonstrated that adenoviral and lentiviral vectors encoding HER-2 can be utilized in cancer immunotherapy. However, it is not known whether both viral systems elicit a similar immune response. Here, we compare the immune response in mice induced by dendritic cells (DCs) infected with either recombinant adenovirus or lentivirus encoding rat HER-2 (rHER-2). Both vaccine types yielded similar control of tumor growth, but we found clear differences in their immune responses 10 days after DC immunization. Adenovirus rHER-2-transduced DCs elicited locally and systemically high frequencies of CD4+ and CD8+ T cells, while lentivirus rHER-2-transduced DCs predominantly led to CD4+ T-cell infiltration at the tumor site. Splenocytes from mice immunized with lentivirus rHER-2-transduced DCs secreted higher levels of interferon (IFN)-gamma, mainly by CD4+ T cells, following stimulation by RM-1-mHER-2 tumors. In contrast, the adenovirus vaccinated group exhibited CD4+ and CD8+ T cells that both contributed to IFN-gamma production. Besides an established cellular immune response, the rHER-2/DC vaccine elicited a significant humoral response that was highest in the adenovirus group. DC subsets and regulatory T cells in the spleen were also differentially modulated in the two vaccine systems. Finally, adoptive transfer of splenocytes from both groups of immunized mice strongly inhibited in vivo tumor growth. Our results suggest that not only the target antigen but also the virus system may determine the nature and magnitude of antitumor immunity by DC vaccination. Gene Therapy (2011) 18, 986-995; doi:10.1038/gt.2011.53; published online 14 April 2011
C1 [Felizardo, T. C.; Medin, J. A.] Univ Hlth Network, Campbell Family Canc Res Inst, Toronto, ON M5G 2M1, Canada.
[Felizardo, T. C.; Medin, J. A.] Univ Hlth Network, Ontario Canc Inst, Toronto, ON M5G 2M1, Canada.
[Wang, J. C. M.; Medin, J. A.] Univ Toronto, Inst Med Sci, Toronto, ON M5S 1A1, Canada.
[Spaner, D. E.; Medin, J. A.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
[Spaner, D. E.] Sunnybrook Odette Canc Ctr, Dept Med Oncol, Toronto, ON, Canada.
[McGray, R. A. J.; Evelegh, C.; Bramson, J. L.] McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON, Canada.
[Fowler, D. H.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
RP Medin, JA (reprint author), Univ Hlth Network, Campbell Family Canc Res Inst, Room 456,67 Coll St, Toronto, ON M5G 2M1, Canada.
EM jmedin@uhnres.utoronto.ca
FU Ontario Ministry of Health and Long-Term Care; Terry Fox Foundation
Canada
FX We thank Cindy Guo and Kenneth Zhang for their technical assistance in
the preparation of plasmids and vectors used in these experiments. We
also would like to thank Dr Natalia Pacienza for helping with the
processing of samples. This research was funded in part by the Ontario
Ministry of Health and Long-Term Care. The views expressed do not
necessarily reflect those of the OMOHLTC. Funding was also provided in
part by a program project grant from The Terry Fox Foundation Canada to
JAM, JLB and DES.
NR 36
TC 6
Z9 8
U1 1
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0969-7128
J9 GENE THER
JI Gene Ther.
PD OCT
PY 2011
VL 18
IS 10
BP 986
EP 995
DI 10.1038/gt.2011.53
PG 10
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity; Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity; Research & Experimental Medicine
GA 836VS
UT WOS:000296145300007
PM 21490686
ER
PT J
AU Pagani, JH
Lee, HJ
Young, WS
AF Pagani, J. H.
Lee, H. -J.
Young, W. S., III
TI Postweaning, forebrain-specific perturbation of the oxytocin system
impairs fear conditioning
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Central amygdala; conditional knockout; oxytocin receptor; vasopressin
1a receptor
ID DIFFERENTIAL CONTRIBUTION; BASOLATERAL AMYGDALA; POTENTIATED STARTLE;
SOCIAL RECOGNITION; PERIRHINAL CORTEX; EXTENDED AMYGDALA; BINDING-SITES;
C57BL/6 MICE; RAT-BRAIN; VASOPRESSIN
AB Oxytocin (Oxt) and vasopressin (Avp) are important for a wide variety of behaviors and the use of transgenic mice lacking the peptides or their receptors, particularly when their loss is spatially and temporally manipulated, offers an opportunity to closely examine their role in a particular behavior. We used a cued fear conditioning paradigm to examine associative learning in three lines of transgenic mice: mice that constitutively lack vasopressin 1a (Avpr1a(-/-)) or Oxt receptors (Oxtr(-/-)) and mice that have Oxt receptor loss restricted to the forebrain that begins postweaning (OxtrFB/FB). Oxtr(-/-) and Avpr1a(-/-) mice have normal conditioned freezing. OxtrFB/FB mice have a reduction in freezing behavior during acquisition, as well as during context and cue retention. In addition to reduction of Oxtr in the central nucleus of the amygdala, in vitro receptor autoradiography showed that the OxtrFB/FB mice have significantly reduced levels of Avpr1a only in that structure. Our results show that postweaning alteration of the distribution of Oxtr receptors is critically important for fear behavior, an effect mirrored in the neural structures that mediate it. While constitutive knockouts of Oxtr and Avpr1a are useful for identifying the neural underpinnings of some behaviors, compensatory mechanisms within some circuits may obscure other behavioral roles.
C1 [Pagani, J. H.; Young, W. S., III] NIMH, Sect Neural Gene Express, NIH, DHHS, Bethesda, MD 20892 USA.
[Lee, H. -J.] Kyungpook Natl Univ, Sch Dent, Dept Dent Microbiol, Taegu, South Korea.
RP Young, WS (reprint author), NIMH, Sect Neural Gene Express, NIH, DHHS, 9000 Rockville Pike,Bldg 49,Room 5A56, Bethesda, MD 20892 USA.
EM wsy@mail.nih.gov
RI Young, W Scott/A-9333-2009;
OI Young, W Scott/0000-0001-6614-5112; , Heon-Jin/0000-0002-1911-5014
FU NIMH [Z01-MH-002498-22]
FX The authors would like to thank Kevin Brown, Michael Burman and Michael
Lehmann for their comments on the original document and Emily Shepard
and June Song for their technical assistance. This research was
supported by the NIMH Intramural Research Program (Z01-MH-002498-22).
The authors state that they have no conflicts of interest.
NR 57
TC 14
Z9 14
U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD OCT
PY 2011
VL 10
IS 7
BP 710
EP 719
DI 10.1111/j.1601-183X.2011.00709.x
PG 10
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 837WD
UT WOS:000296238100003
PM 21668734
ER
PT J
AU Cole, J
Weinberger, DR
Mattay, VS
Cheng, X
Toga, AW
Thompson, PM
Powell-Smith, G
Cohen-Woods, S
Simmons, A
McGuffin, P
Fu, CHY
AF Cole, J.
Weinberger, D. R.
Mattay, V. S.
Cheng, X.
Toga, A. W.
Thompson, P. M.
Powell-Smith, G.
Cohen-Woods, S.
Simmons, A.
McGuffin, P.
Fu, C. H. Y.
TI No effect of 5HTTLPR or BDNF Val66Met polymorphism on hippocampal
morphology in major depression
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE BDNF; 5HTTLPR; hippocampus; major depressive disorder; MRI; shape
mapping
ID SEROTONIN TRANSPORTER GENE; NEUROTROPHIC FACTOR; ALZHEIMERS-DISEASE;
5-HTTLPR POLYMORPHISM; BRAIN STRUCTURE; LONG VARIANT; VOLUME; DISORDER;
ASSOCIATION; MEMORY
AB Neuroimaging research implicates the hippocampus in the aetiology of major depressive disorder (MDD). Imaging genetics studies have investigated the influence of the serotonin transporter-linked polymorphic region (5HTTLPR) and brain-derived neurotrophic factor (BDNF) Val66Met polymorphism on the hippocampus in healthy individuals and patients with depression (MDD). However, conflicting results have led to inconclusive evidence about the effect of 5HTTLPR or BDNF on hippocampal volume (HCV). We hypothesized that analysis methods based on three-dimensional (3D) hippocampal shape mapping could offer improved sensitivity to clarify these effects. Magnetic resonance imaging data were collected in parallel samples of 111 healthy individuals and 84 MDD patients. Manual hippocampal segmentation was conducted and the resulting data used to investigate the influence of 5HTTLPR and BDNF Val66Met genotypes on HCV and 3D shape within each sample. Hippocampal volume normalized by intracranial volume (ICV) showed no significant difference between 5HTTLPR S allele carriers and L/L homozygotes or between BDNF Met allele carriers and Val/Val homozygotes in the group of healthy individuals. Moreover, there was no significant difference in normalized HCV between 5HTTLPR diallelic and triallelic classifications or between the BDNF Val66Met genotypes in MDD patients, although there was a relationship between BDNF Val66Met and ICV. Shape analysis detected dispersed between-group differences, but these effects did not survive multiple testing correction. In this study, there was no evidence of a genetic effect for 5HTTLPR or BDNF Val66Met on hippocampal morphology in either healthy individuals or MDD patients despite the relatively large sample sizes and sensitive methodology.
C1 [Cole, J.; Powell-Smith, G.; Cohen-Woods, S.; McGuffin, P.; Fu, C. H. Y.] Kings Coll London, Inst Psychiat, MRC Social Genet & Dev Psychiat Res Ctr, London SE5 8AF, England.
[Weinberger, D. R.; Mattay, V. S.; Cheng, X.] NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA.
[Toga, A. W.; Thompson, P. M.] Univ Calif Los Angeles, Dept Neurol, Lab Neuro Imaging, Los Angeles, CA 90024 USA.
[Simmons, A.; McGuffin, P.; Fu, C. H. Y.] Kings Coll London, S London & Maudsley NHS Fdn Trust, NIHR Biomed Res Ctr Mental Hlth, London WC2R 2LS, England.
[Simmons, A.] Kings Coll London, MRC Ctr Neurodegenerat Res, London WC2R 2LS, England.
[Simmons, A.] Kings Coll London, Inst Psychiat, Dept Neuroimaging, London WC2R 2LS, England.
RP Cole, J (reprint author), Kings Coll London, Inst Psychiat, MRC Social Genet & Dev Res Ctr, POB 80, London SE5 8AF, England.
EM james.h.cole@kcl.ac.uk
RI Cole, James/G-8045-2011; Simmons, Andrew/B-8848-2008; McGuffin,
Peter/A-1565-2012; Cohen-Woods, Sarah/F-8674-2014;
OI Simmons, Andrew/0000-0003-2306-5811; McGuffin,
Peter/0000-0002-9888-2907; Cohen-Woods, Sarah/0000-0003-2199-6129; Fu,
Cynthia/0000-0003-4313-3500
FU Medical Research Council; Wellcome Trust; GlaxoSmithKline, UK; National
Institute of Health Research Biomedical Research Centre for Mental
Health at the South London; Maudsley NHS Foundation Trust; Institute of
Psychiatry King's College London; NARSAD; NH [R01 EB008281, P41
RR013642]
FX J. C. was funded by a Medical Research Council studentship and a
Wellcome Trust Value in People award for the duration of this work. The
study was funded in part by GlaxoSmithKline, UK, and the National
Institute of Health Research Biomedical Research Centre for Mental
Health at the South London and Maudsley NHS Foundation Trust and
Institute of Psychiatry King's College London, as well as a NARSAD Young
Investigator Award to C. H. Y. F. Additional support for algorithm
development was provided by NH grants R01 EB008281 to P. M. T. and P41
RR013642 to A. W. T.
NR 58
TC 32
Z9 33
U1 2
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD OCT
PY 2011
VL 10
IS 7
BP 756
EP 764
DI 10.1111/j.1601-183X.2011.00714.x
PG 9
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 837WD
UT WOS:000296238100008
PM 21692988
ER
PT J
AU Pidala, J
Kurland, BF
Chai, XY
Vogelsang, G
Weisdorf, DJ
Pavletic, S
Cutler, C
Majhail, N
Lee, SJ
AF Pidala, Joseph
Kurland, Brenda F.
Chai, Xiaoyu
Vogelsang, Georgia
Weisdorf, Daniel J.
Pavletic, Steven
Cutler, Corey
Majhail, Navneet
Lee, Stephanie J.
TI Sensitivity of changes in chronic graft-versus-host disease activity to
changes in patient-reported quality of life: results from the Chronic
Graft-versus-Host Disease Consortium
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Article
DE chronic graft versus host disease; quality of life; sensitivity to
change
ID BONE-MARROW-TRANSPLANTATION; STEM-CELL TRANSPLANTATION; FORM HEALTH
SURVEY; RECOMMENDATIONS; RELIABILITY; SURVIVORS; RECOVERY; VALIDITY;
TRIALS; TESTS
AB Background
The 2005 National Institute of Health Chronic Graft-versus-Host Disease Consensus Conference recommended collection of patient-reported outcomes in clinical trials on chronic graft-versus-host disease. We assessed whether changes in chronic graft-versus-host disease severity, determined using National Institute of Health criteria, clinicians' assessment or patients' self-evaluation, correlated with patient-reported quality of life as measured by the Short Form-36 and Functional Assessment of Cancer Therapy - Bone Marrow Transplant (FACT-BMT) instruments.
Design and Methods
Three-hundred and thirty-six adult patients (median age 52 years; range, 19 - 79) with chronic graft-versus-host disease from six transplant centers contributed baseline and follow-up data (from 936 visits overall).
Results
While the majority of the patients had stable chronic graft-versus-host disease, improvement or worsening was noted in approximately 40% of follow-up visits. Multivariable analysis demonstrated no association between change in chronic graft-versus-host disease severity evaluated by National Institute of Health criteria and change in quality of life, while clinician-reported changes in severity were associated with changes in some quality of life measures. Patient-reported changes in the severity of chronic graft-versus-host disease were associated with changes in all quality of life measures. Comparison of the Short Form-36 and the FACT-BMT suggested that the data collected in the Functional Assessment of Cancer Therapy - General (FACT-G) core survey are sufficient without the need for the Short Form-36 or the FACT-BMT subscale.
Conclusions
We conclude that serial National Institute of Health and clinician-reported chronic graft-versus-host disease severity assessments cannot substitute for patient-reported outcomes in clinical trials. Collection of just the FACT-G instead of the Short Form-36 and the full FACT-BMT will decrease respondent burden without compromising quality of life assessment.
C1 [Pidala, Joseph] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Kurland, Brenda F.; Chai, Xiaoyu; Lee, Stephanie J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Vogelsang, Georgia] Johns Hopkins Univ, Baltimore, MD USA.
[Weisdorf, Daniel J.; Majhail, Navneet] Univ Minnesota, Minneapolis, MN USA.
[Pavletic, Steven] NCI, Bethesda, MD 20892 USA.
[Cutler, Corey] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Pidala, J (reprint author), H Lee Moffitt Canc Ctr & Res Inst, 12902 Magnolia Dr,FOB 3308, Tampa, FL 33612 USA.
EM joseph.pidala@moffitt.org
OI Kurland, Brenda/0000-0002-5669-0595
NR 26
TC 20
Z9 21
U1 0
U2 0
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOL-HEMATOL J
JI Haematol-Hematol. J.
PD OCT
PY 2011
VL 96
IS 10
BP 1528
EP 1535
DI 10.3324/haematol.2011.046367
PG 8
WC Hematology
SC Hematology
GA 837XR
UT WOS:000296245000020
PM 21685473
ER
PT J
AU Kelley, MW
Mann, ZF
AF Kelley, Matthew W.
Mann, Zoe F.
TI Response to a Letter to the Editor
SO HEARING RESEARCH
LA English
DT Letter
ID COCHLEAR HAIR-CELLS; MAMMALIAN COCHLEA; BASILAR PAPILLA; ONTOGENETIC
CHANGES; FREQUENCY MAP; EXPRESSION; CHICKEN; INNERVATION; PATTERN;
GERBIL
C1 [Kelley, Matthew W.; Mann, Zoe F.] Natl Inst Deafness & Commun Disorders, Lab Cochlear Dev, Porter Neurosci Res Ctr, Bethesda, MD 20892 USA.
RP Kelley, MW (reprint author), Natl Inst Deafness & Commun Disorders, Lab Cochlear Dev, Porter Neurosci Res Ctr, Bethesda, MD 20892 USA.
EM kelleymt@nidcd.nih.gov
NR 20
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-5955
J9 HEARING RES
JI Hear. Res.
PD OCT
PY 2011
VL 280
IS 1-2
BP 1
EP 2
DI 10.1016/j.heares.2011.04.009
PG 2
WC Audiology & Speech-Language Pathology; Neurosciences;
Otorhinolaryngology
SC Audiology & Speech-Language Pathology; Neurosciences & Neurology;
Otorhinolaryngology
GA 834XG
UT WOS:000295997200001
PM 21600274
ER
PT J
AU Bastian, H
Scheibler, F
Knelangen, M
Zschorlich, B
Nasser, M
Waltering, A
AF Bastian, Hilda
Scheibler, Fueloep
Knelangen, Marco
Zschorlich, Beate
Nasser, Mona
Waltering, Andreas
TI Choosing health technology assessment and systematic review topics: The
development of priority-setting criteria for patients' and consumers'
interests
SO INTERNATIONAL JOURNAL OF TECHNOLOGY ASSESSMENT IN HEALTH CARE
LA English
DT Article
DE `Priority setting; Disinvestments; Patient and consumer interests;
Patient participation
ID INVOLVEMENT; CARE
AB Background: The Institute for Quality and Efficiency in Health Care (IQWiG) was established in 2003 by the German parliament. Its legislative responsibilities are health technology assessment, mostly to support policy making and reimbursement decisions. It also has a mandate to serve patients' interests directly, by assessing and communicating evidence for the general public.
Objectives: To develop a priority-setting framework based on the interests of patients and the general public.
Methods: A theoretical framework for priority setting from a patient/consumer perspective was developed. The process of development began with a poll to determine level of lay and health professional interest in the conclusions of 124 systematic reviews (194 responses). Data sources to identify patients' and consumers' information needs and interests were identified.
Results: IQWiG's theoretical framework encompasses criteria for quality of evidence and interest, as well as being explicit about editorial considerations, including potential for harm. Dimensions of "patient interest" were identified, such as patients' concerns, information seeking, and use. Rather than being a single item capable of measurement by one means, the concept of "patients' interests" requires consideration of data and opinions from various sources.
Conclusions: The best evidence to communicate to patients/consumers is right, relevant and likely to be considered interesting and/or important to the people affected. What is likely to be interesting for the community generally is sufficient evidence for a concrete conclusion, in a common condition. More research is needed on characteristics of information that interest patients and consumers, methods of evaluating the effectiveness of priority setting, and methods to determine priorities for disinvestment.
C1 [Bastian, Hilda] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
[Scheibler, Fueloep; Knelangen, Marco; Zschorlich, Beate; Waltering, Andreas] Inst Qual & Efficiency Hlth Care, D-51105 Cologne, Germany.
[Nasser, Mona] Univ Exeter, Peninsula Coll Med & Dent, Plymouth PL6 8BU, Devon, England.
[Nasser, Mona] Univ Plymouth, Peninsula Coll Med & Dent, Plymouth PL6 8BU, Devon, England.
RP Bastian, H (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, 8600 Rockville Pike, Bethesda, MD 20894 USA.
EM hilda.bastian@nih.gov; fueloep.scheibler@iqwig.de;
beate.zschorlich@iqwig.de; andreas.waltering@iqwig.de
RI Nasser, Mona/J-3601-2013; Embrett, Mark/H-4466-2014;
OI Embrett, Mark/0000-0002-3969-0219; Bastian, Hilda/0000-0001-8544-7386
NR 20
TC 1
Z9 1
U1 0
U2 9
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0266-4623
J9 INT J TECHNOL ASSESS
JI Int. J. Technol. Assess. Health Care
PD OCT
PY 2011
VL 27
IS 4
BP 348
EP 356
DI 10.1017/S0266462311000547
PG 9
WC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Medical Informatics
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Medical Informatics
GA 840EH
UT WOS:000296420600013
PM 22004776
ER
PT J
AU Danner, M
Hummel, JM
Volz, F
van Manen, JG
Wiegard, B
Dintsios, CM
Bastian, H
Gerber, A
IJzerman, MJ
AF Danner, Marion
Hummel, J. Marjan
Volz, Fabian
van Manen, Jeannette G.
Wiegard, Beate
Dintsios, Charalabos-Markos
Bastian, Hilda
Gerber, Andreas
IJzerman, Maarten J.
TI Integrating patients' views into health technology assessment: Analytic
hierarchy process (AHP) as a method to elicit patient preferences
SO INTERNATIONAL JOURNAL OF TECHNOLOGY ASSESSMENT IN HEALTH CARE
LA English
DT Article
DE Patient involvement; Patient preferences; Analytic hierarchy process
(AHP); Health technology assessment (HTA); Medical decision making;
Multi-criteria decision analysis (MCDA)
ID DECISION-MAKING; CONJOINT-ANALYSIS; PRIORITIES; CARE
AB Background: Patient involvement is widely acknowledged to be a valuable component in health technology assessment (HTA) and healthcare decision making. However, quantitative approaches to ascertain patients' preferences for treatment endpoints are not yet established. The objective of this study is to introduce the analytic hierarchy process (AHP) as a preference elicitation method in HTA. Based on a systematic literature review on the use of AHP in health care in 2009, the German Institute for Quality and Efficiency in Health Care (IQWiG) initiated an AHP study related to its HTA work in 2010.
Methods: The AHP study included two AHP workshops, one with twelve patients and one with seven healthcare professionals. In these workshops, both patients and professionals rated their preferences with respect to the importance of different endpoints of antidepressant treatment by a pairwise comparison of individual endpoints. These comparisons were performed and evaluated by the AHP method and relative weights were generated for each endpoint.
Results: The AHP study indicates that AHP is a well-structured technique whose cognitive demands were well handled by patients and professionals. The two groups rated some of the included endpoints of antidepressant treatment differently. For both groups, however, the same six of the eleven endpoints analyzed accounted for more than 80 percent of the total weight.
Conclusions: AHP can be used in HTA to give a quantitative dimension to patients' preferences for treatment endpoints. Preference elicitation could provide important information at various stages of HTA and challenge opinions on the importance of endpoints.
C1 [Hummel, J. Marjan; van Manen, Jeannette G.; IJzerman, Maarten J.] Univ Twente, Dept Hlth Technol & Serv Res, NL-7500 AE Enschede, Netherlands.
[Bastian, Hilda] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Danner, M (reprint author), Inst Qual & Efficiency Hlth Care IQWiG, Hlth Econ Dept, D-51105 Cologne, Germany.
EM marion.danner@iqwig.de; j.m.hummel@utwente.nl; Fabian.volz@iqwig.de;
j.g.vanmanen@utwente.nl; beate.wiegard@iqwig.de;
charalabos-markos@iqwig.de; Hilda.bastian@nih.gov;
andreas.gerger@iqwig.de; m.j.ijzerman@utwente.nl
RI IJzerman, Maarten/Q-8963-2016;
OI IJzerman, Maarten/0000-0001-5788-5805; Bastian,
Hilda/0000-0001-8544-7386
FU IGWIG
FX The authors report that this work has been partly funded by IGWIG.
NR 25
TC 35
Z9 35
U1 1
U2 15
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0266-4623
J9 INT J TECHNOL ASSESS
JI Int. J. Technol. Assess. Health Care
PD OCT
PY 2011
VL 27
IS 4
BP 369
EP 375
DI 10.1017/S0266462311000523
PG 7
WC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Medical Informatics
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Medical Informatics
GA 840EH
UT WOS:000296420600016
PM 22004779
ER
PT J
AU Woo, JM
Gibbons, RD
Qin, P
Komarow, H
Kim, JB
Rogers, CA
Mann, JJ
Postolache, TT
AF Woo, Jong-Min
Gibbons, Robert D.
Qin, Ping
Komarow, Hirsh
Kim, Jong Bae
Rogers, Christine A.
Mann, J. John
Postolache, Teodor T.
TI Suicide and Prescription Rates of Intranasal Corticosteroids and
Nonsedating Antihistamines for Allergic Rhinitis: An Ecological Study
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID COMORBIDITY SURVEY REPLICATION; NASAL CORTICOSTEROIDS; CYTOKINE
EXPRESSION; MAJOR DEPRESSION; SLEEP; BEHAVIOR; BRAIN; DISTURBANCES;
NEUROBIOLOGY; INFLAMMATION
AB Objective: To estimate the relationship between antiallergy drug prescription rates and suicide across the United States and over time. The relationship between allergy, allergens, and suicidal behavior and suggestions of a possible immune mediation led us to hypothesize that intranasal corticosteroids, known to reduce local airway production of T-helper cell type 2 cytokines, may be associated with reduced risk of suicide relative to antihistamines, which only secondarily affect cytokine production.
Method: The authors evaluated the relationship of suicide rates at the county level in the United States (N=120,076 suicides) with prescriptions for intranasal corticosteroids and nonsedating antihistamines, in interaction with antidepressant prescriptions and other socioeconomic variables, for the period from 1999 to 2002. Suicide rate data were derived from state vital record systems based on local death certificate registries, and county-level allergy and antidepressant prescription data were obtained from IMS Health Incorporated (Plymouth Meeting, Pennsylvania).
Results: The prescription volume of intranasal corticosteroids was associated with a lower suicide risk (P=.0004), while that of antihistamines was associated with a modestly greater suicide risk (P=.0001). Adjustment for antidepressant prescriptions did not affect these relationships.
Conclusions:This is the first study, to our knowledge, to find a possible association between completed suicide and medications for allergic rhinitis and also the first report of an association of intranasal corticosteroid use with a lower suicide rate. This association should be considered preliminary and deserving of further investigation.
C1 [Woo, Jong-Min; Postolache, Teodor T.] Univ Maryland, Sch Med, Mood & Anxiety Program, Dept Psychiat, Baltimore, MD 21201 USA.
[Woo, Jong-Min] Seoul Paik Hosp, Dept Psychiat, Seoul, South Korea.
[Woo, Jong-Min] Inje Univ, Sch Med, Seoul, South Korea.
[Woo, Jong-Min] Inje Univ, Stress Res Inst, Seoul, South Korea.
[Gibbons, Robert D.; Kim, Jong Bae] Univ Illinois, Ctr Hlth Stat, Chicago, IL USA.
[Qin, Ping] Univ Aarhus, Natl Ctr Register Based Res, Aarhus, Denmark.
[Komarow, Hirsh] NIAID, Lab Allerg Dis, Bethesda, MD 20892 USA.
[Rogers, Christine A.] Univ Massachusetts, Amherst, MA 01003 USA.
[Mann, J. John] New York State Psychiat Inst & Hosp, Dept Mol Imaging & Neuropathol, New York, NY 10032 USA.
[Mann, J. John] Columbia Univ, New York, NY USA.
RP Postolache, TT (reprint author), Univ Maryland, Sch Med, Mood & Anxiety Program, Dept Psychiat, 685 W Baltimore St,MSTF Bldg,Room 930, Baltimore, MD 21201 USA.
EM teopostolache@gmail.com
RI Rogers, Christine/A-2189-2008
OI Rogers, Christine/0000-0003-0887-9606
FU National Institutes of Health [R01MH074891]; Inje Research and
Scholarship Foundation
FX Financial support was provided by the National Institutes of Health
(R01MH074891; principal investigator: Dr Postolache). Dr Woo was also
supported by the Inje Research and Scholarship Foundation from 2007 to
2009.
NR 47
TC 10
Z9 10
U1 1
U2 4
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 752870, MEMPHIS, TN 38175-2870 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD OCT
PY 2011
VL 72
IS 10
BP 1423
EP 1428
DI 10.4088/JCP.10m06765
PG 6
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 839XL
UT WOS:000296402700018
PM 22075102
ER
PT J
AU Corsini, E
Oukka, M
Pieters, R
Kerkvliet, NI
Ponce, R
Germolec, DR
AF Corsini, Emanuela
Oukka, Mohamed
Pieters, Raymond
Kerkvliet, Nancy I.
Ponce, Rafael
Germolec, Dori R.
TI Alterations in regulatory T-cells: Rediscovered pathways in
immunotoxicology
SO JOURNAL OF IMMUNOTOXICOLOGY
LA English
DT Review
DE Regulatory T-cells; immunosuppression; allergy; autoimmunity
ID ARYL-HYDROCARBON RECEPTOR; MERCURY-INDUCED AUTOIMMUNITY; BROWN-NORWAY
RATS; TRANSCRIPTION FACTOR; DENDRITIC CELLS; D-PENICILLAMINE; ORAL
TOLERANCE; CUTTING EDGE; TGF-BETA; IN-VIVO
AB In addition to the effector T-cells subsets, T-cells can also differentiate into cells that play a suppressive or regulatory role in adaptive immune responses. The cell types currently identified as regulatory T-cells (T-regs) include natural or thymic-derived T-regs, T-cells which express Foxp3(+)CD25(+)CD4(+) and can suppress immune responses to autoreactive T-cells, as well as inducible T-regs, that are generated from naive T-cells in the periphery after interaction with antigens presented by dendritic cells. Inducible T-regs include T(H)3 cells, T(r)1 cells, and Foxp3(+)-inducible T-regs. T-regs have been shown to be critical in the maintenance of immune responses and T-cell homeostasis. These cells play an important role in suppressing responses to self-antigens and in controlling inappropriate responses to non-self-antigens, such as commensal bacteria or food in the gut. For example, depletion of CD4(+)CD25(+) T-regs from mice resulted in the development of multi-organ autoimmune diseases. CD4(+)CD25(+) T-regs and/or IL-10-producing T(r)1 cells are capable of suppressing or attenuating T(H)2 responses to allergens. Moreover, adoptive transfer of CD4(+)CD25(+) T-regs from healthy to diseased animals resulted in the prevention or cure of certain autoimmune diseases, and was able to induce transplantation tolerance. Clinical improvement seen after allergen immunotherapy for allergic diseases such as rhinitis and asthma is associated with the induction of IL-10- and TGF beta-producing T(r)1 cells as well as FoxP3-expressing IL-10 T-cells, with resulting suppression of the T(H)2 cytokine milieu. Activation, expansion, or suppression of CD4(+)CD25(+) T-regs in vivo by xenobiotics, including drugs, may therefore represent a relevant mechanism underlying immunotoxicity, including immunosuppression, allergic asthma, and autoimmune diseases.
C1 [Corsini, Emanuela] Univ Milan, Dept Pharmacol Sci, Toxicol Lab, I-20133 Milan, Italy.
[Oukka, Mohamed] Harvard Univ, Sch Med, Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA USA.
[Pieters, Raymond] Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands.
[Pieters, Raymond] Utrecht Univ Appl Sci, Res Ctr Technol & Innovat, Utrecht, Netherlands.
[Kerkvliet, Nancy I.] Oregon State Univ, Dept Environm & Mol Toxicol, Corvallis, OR 97331 USA.
[Ponce, Rafael] Amgen Inc, Seattle, WA USA.
[Germolec, Dori R.] Natl Inst Environm Hlth Sci, Natl Toxicol Program, Res Triangle Pk, NC USA.
RP Corsini, E (reprint author), Univ Milan, Dept Pharmacol Sci, Toxicol Lab, Via Balzaretti 9, I-20133 Milan, Italy.
EM emanuela.corsini@unimi.it
FU Intramural NIH HHS [Z99 ES999999]
NR 67
TC 11
Z9 12
U1 0
U2 9
PU INFORMA HEALTHCARE
PI NEW YORK
PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA
SN 1547-691X
J9 J IMMUNOTOXICOL
JI J. Immunotoxicol.
PD OCT-DEC
PY 2011
VL 8
IS 4
BP 251
EP 257
DI 10.3109/1547691X.2011.598885
PG 7
WC Toxicology
SC Toxicology
GA 840SI
UT WOS:000296461200001
PM 21848365
ER
PT J
AU Guo, TL
Germolec, DR
Collins, BJ
Luebke, RW
Auttachoat, W
Smith, MJ
White, KL
AF Guo, Tai L.
Germolec, Dori R.
Collins, Bradley J.
Luebke, Robert W.
Auttachoat, Wimolnut
Smith, Matthew J.
White, Kimber L., Jr.
TI Immunotoxicological profile of chloramine in female B6C3F1 mice when
administered in the drinking water for 28 days
SO JOURNAL OF IMMUNOTOXICOLOGY
LA English
DT Article
DE Chloramine; monochloramine; immunotoxicity; drinking water disinfection
ID CHEMICAL-INDUCED IMMUNOTOXICITY; SWIMMING POOLS; EXPOSURE;
MONOCHLORAMINE; DISINFECTANT; PREVALENCE; RAT
AB Monochloramine has been used to provide a disinfecting residual in water distribution systems where it is difficult to maintain an adequate free-chlorine residual or where disinfection by-product formation is of concern. The goal of this study was to characterize the immunotoxic effects of chloramine in female B6C3F1 mice when administered via the drinking water. Mice were exposed to chloramine-containing deionized tap water at 2, 10, 20, 100, or 200 ppm for 28 days. No statistically significant differences in drinking water consumption, body weight, body weight gain, organ weights, or hematological parameters between the exposed and control animals were noted during the experimental period. There were no changes in the percentages and numbers of total B-lymphocytes, T-lymphocytes, CD4(+) and CD8(+) T-lymphocytes, natural killer (NK) cells, and macrophages in the spleen. Exposure to chloramine did not affect the IgM antibody-forming cell response to sheep red blood cells (SRBC) or anti-SRBC IgM antibody production. Minimal effects, judged to be biologically insignificant, were observed in the mixed-leukocyte response and NK activity. In conclusion, chloramine produced no toxicological and immunotoxic effects in female B6C3F1 mice when administered for 28 days in the drinking water at concentrations ranging from 2-200 ppm.
C1 [Guo, Tai L.; Auttachoat, Wimolnut; Smith, Matthew J.; White, Kimber L., Jr.] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA.
[Germolec, Dori R.; Collins, Bradley J.] NIEHS, Res Triangle Pk, NC 27709 USA.
[Luebke, Robert W.] US EPA, Cardiopulm & Immunotoxicol Branch, Environm Publ Hlth Div, NHEERL, Res Triangle Pk, NC USA.
RP White, KL (reprint author), Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, POB 980613, Richmond, VA 23298 USA.
EM klwhite@vcu.edu
FU EPA [DW75937992]; Division of Intramural Research at the NIEHS
[ES55538]; National Institute of Environmental Health Sciences [ES55538]
FX This work was supported in part by EPA Interagency Agreement DW75937992
and the Division of Intramural Research at the NIEHS through Contract
ES55538. The authors thank D. L. Musgrove and R. D. Brown for their
technical assistance, and Dr Michelle Hooth and Dr Marsha Ward for their
comments and review of the manuscript.; Dr Kimber L. White, Jr. is the
owner of a company, ImmunoTox (R), Inc., that conducts
immunotoxicological studies under Good Laboratory Practices (GLP). This
work was supported by the National Institute of Environmental Health
Sciences [ES55538]. This article may be the work product of an employee
or group of employees of the National Institute of Environmental Health
Sciences (NIEHS), National Institutes of Health (NIH), however, the
statements, opinions, or conclusions contained therein do not
necessarily represent the statements, opinions, or conclusions of NIEHS,
NIH, or the US government. This report has been reviewed by the
Environmental Protection Agency's Office of Research and Development and
approved for publication. Approval does not signify that the contents
necessarily reflect the views of the Agency nor does mention of trade
names or commercial products constitute endorsement or recommendation
for use.
NR 29
TC 0
Z9 0
U1 3
U2 6
PU INFORMA HEALTHCARE
PI NEW YORK
PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA
SN 1547-691X
J9 J IMMUNOTOXICOL
JI J. Immunotoxicol.
PD OCT-DEC
PY 2011
VL 8
IS 4
BP 381
EP 388
DI 10.3109/1547691X.2011.622317
PG 8
WC Toxicology
SC Toxicology
GA 840SI
UT WOS:000296461200015
PM 22017662
ER
PT J
AU Wang, C
Henkes, LM
Doughty, LB
He, M
Wang, DF
Meyer-Almes, FJ
Cheng, YQ
AF Wang, Cheng
Henkes, Leonhard M.
Doughty, Leah B.
He, Min
Wang, Difei
Meyer-Almes, Franz-Josef
Cheng, Yi-Qiang
TI Thailandepsins: Bacterial Products with Potent Histone Deacetylase
Inhibitory Activities and Broad-Spectrum Antiproliferative Activities
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID TUMOR-CELL-LINES; NATURAL-PRODUCTS; NONRIBOSOMAL PEPTIDES; ANTICANCER
AGENTS; BIOSYNTHESIS; DEPSIPEPTIDE; CANCER; FK228; POLYKETIDE;
MECHANISMS
AB Histone deacetylase (HDAC) inhibitors have emerged as a new class of anticancer drugs, with one synthetic compound, SAHA (vorinostat, Zolinza; 1), and one natural product, FK228 (depsipeptide, romidepsin, Istodax; 2), approved by FDA for clinical use. Our studies of FK228 biosynthesis in Chromobacterium violaceum no. 968 led to the identification of a cryptic biosynthetic gene cluster in the genome of Burkholderia thailandensis E264. Genome mining and genetic manipulation of this gene cluster further led to the discovery of two new products, thailandepsin A (6) and thailandepsin B (7). HDAC inhibition assays showed that thailandepsins have selective inhibition profiles different from that of FK228, with comparable inhibitory activities to those of FK228 toward human HDAC1, HDAC2, HDAC3, HDAC6, HDAC7, and HDAC9 but weaker inhibitory activities than FK228 toward HDAC4 and HDAC8, the latter of which could be beneficial. NCI-60 anticancer screening assays showed that thailandepsins possess broad-spectrum antiproliferative activities with GI(50) for over 90% of the tested cell lines at low nanomolar concentrations and potent cytotoxic activities toward certain types of cell lines, particularly for those derived from colon, melanoma, ovarian, and renal cancers. Thailandepsins thus represent new naturally produced HDAC inhibitors that are promising for anticancer drug development.
C1 [Wang, Cheng; Doughty, Leah B.; Cheng, Yi-Qiang] Univ Wisconsin, Dept Biol Sci, Milwaukee, WI 53201 USA.
[Henkes, Leonhard M.; Meyer-Almes, Franz-Josef] Univ Appl Sci Darmstadt, Dept Chem Engn & Biotechnol, D-64287 Darmstadt, Germany.
[He, Min] US Natl Canc Inst, Dev Therapeut Program, Frederick, MD 21701 USA.
[Wang, Difei] US Natl Canc Inst, Cell Biol Lab, Bethesda, MD 20892 USA.
[Cheng, Yi-Qiang] Wuhan Univ, Sch Pharmaceut Sci, MoE Key Lab Combinatorial Biosynth & Drug Dis, Wuhan 430071, Peoples R China.
RP Cheng, YQ (reprint author), Univ Wisconsin, Dept Biol Sci, POB 413, Milwaukee, WI 53201 USA.
EM ycheng@uwm.edu
RI Wang, Difei/E-7066-2010
FU Research Growth Initiative from University of Wisconsin-Milwaukee;
NIH/NCI [R01 CA152212]; NIH/NCI of the Center for Cancer Research
FX We thank D. DeShazer (Walter Reed Army Medical Center) and H. Schweizer
(Colorado State University) for providing vector tools, K. Nithipatikom
(Medical College of Wisconsin) for assistance with HR-MS analysis, H.
Foersterling (University of Wisconsin-Milwaukee) for assistance with NMR
analysis, the NCI Developmental Therapeutics Program for conducting
NCI-60 anticancer screening, M. Kunkel (NCI-DTP) for assistance with the
COMPARE analysis of NCI-60 data, and D. Newman (NCI-DTP) for critical
reading of this manuscript. This work was supported by a Research Growth
Initiative Award from the University of Wisconsin-Milwaukee and an
NIH/NCI grant R01 CA152212 (both to Y.-Q.C). D.W. also acknowledges the
NIH/NCI Intramural Research Program of the Center for Cancer Research
for a fellowship support.
NR 49
TC 43
Z9 44
U1 2
U2 19
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD OCT
PY 2011
VL 74
IS 10
BP 2031
EP 2038
DI 10.1021/np200324x
PG 8
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA 837LZ
UT WOS:000296206500001
PM 21793558
ER
PT J
AU Klausmeyer, P
Shipley, SM
Zuck, KM
McCloud, TG
AF Klausmeyer, Paul
Shipley, Suzanne M.
Zuck, Karina M.
McCloud, Thomas G.
TI Histone Deacetylase Inhibitors from Burkholderia thailandensis
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID CYSTEINE RESIDUES; DEPSIPEPTIDE; FR901228; GROWTH; CANCER; FK228;
PEPTIDES; CELLS
AB Bioactivity-guided fractionation of an extract of Burkholderia thailandensis led to the isolation and identification of a new cytotoxic depsipeptide and its dimer. Both compounds potently inhibited the function of histone deacetylases 1 and 4. The monomer, spiruchostatin C (2), was tested side by side with the clinical depsipeptide FK228 (1, Istodax, romidepsin) in a murine hollow fiber assay consisting of 12 implanted tumor cell lines. Spiruchostatin C (2) showed good activity toward LOX IMVI melanoma cells and NCI-H522 non small cell lung cancer cells. Overall, however, FK228 (1) showed a superior in vivo antitumor profile in comparison to the new compound.
C1 [Klausmeyer, Paul; Shipley, Suzanne M.; Zuck, Karina M.; McCloud, Thomas G.] NCI Frederick, Nat Prod Support Grp, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Klausmeyer, P (reprint author), NCI Frederick, Nat Prod Support Grp, SAIC Frederick Inc, Frederick, MD 21702 USA.
EM klausmeyerp@mail.nih.gov
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract HHSN261200800001E. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U.S. government.
This research was supported (in part) by the Developmental Therapeutics
Program in the Division of Cancer Treatment and Diagnosis of the
National Cancer Institute. We gratefully acknowledge Q Van for NMR
experiments, the NCI 60 team for in vitro biological assay results, M.
Hollingshead, M. Ahalt-Gottholm, and V. Brinsfield for the murine hollow
fiber assay results, and J. Britt for robotics and computer support.
NR 20
TC 13
Z9 13
U1 2
U2 11
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD OCT
PY 2011
VL 74
IS 10
BP 2039
EP 2044
DI 10.1021/np200532d
PG 6
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA 837LZ
UT WOS:000296206500002
PM 21967146
ER
PT J
AU Garg, PK
Liu, K
Ferrucci, L
Guralnik, JM
Criqui, MH
Tian, L
Sufit, R
Nishida, T
Tao, HM
Liao, YH
McDermott, MM
AF Garg, Parveen K.
Liu, Kiang
Ferrucci, Luigi
Guralnik, Jack M.
Criqui, Michael H.
Tian, Lu
Sufit, Robert
Nishida, Takashi
Tao, Huimin
Liao, Yihua
McDermott, Mary M.
TI Lower Extremity Nerve Function, Calf Skeletal Muscle Characteristics,
and Functional Performance in Peripheral Arterial Disease
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE claudication; muscles; peripheral nervous system; peripheral vascular
disease; physical functioning
ID ANKLE BRACHIAL INDEX; PHYSICAL-ACTIVITY; WOMENS HEALTH; 6-MINUTE WALK;
LEG SYMPTOMS; CLASSIFICATION; OSTEOARTHRITIS; ASSOCIATIONS; PREVALENCE;
DISABILITY
AB OBJECTIVES: To determine whether poor lower extremity nerve function is associated with less-favorable calf muscle characteristics and greater functional impairment in people with and without peripheral arterial disease (PAD).
DESIGN: Cross-sectional.
SETTING: Three Chicago-area medical centers.
PARTICIPANTS: Four hundred thirteen participants with PAD (ankle-brachial index (ABI) < 0.90) and 255 without.
MEASUREMENTS: Electrodiagnostic testing of the peroneal nerve was performed. Calf muscle cross-sectional area and percentage fat were measured using computed tomography at 66.7% of the distance between the distal and proximal tibia. Six-minute walk performance was measured.
RESULTS: Adjusting for age, sex, race, ABI, leg symptoms, smoking, physical activity, comorbidities, and other covariates, lower peroneal nerve conduction velocity (NCV) was associated with lower calf muscle area (first quartile 4,770.3 mm(2), fourth quartile 5,571 mm(2), P < .001) and poorer 6-minute walk distance (first quartile 989.2 feet, fourth quartile 1,210.8 feet, P < .001) in participants without diabetes mellitus with PAD. Lower peroneal NCV was associated with lower calf muscle area (first quartile 5,166.0 mm(2), fourth quartile 6,003.8 mm(2), P = .01) and poorer 6-minute walk distance (first quartile 866.4 feet, fourth quartile 1,082.5 feet, P = .01) in participants with diabetes mellitus and PAD as well. In participants without PAD, lower peroneal NCV was not associated with lower calf muscle area but was associated with poorer 6-minute walk distance only in participants without diabetes mellitus (first quartile 1,317.0 feet, fourth quartile 1,570.4 feet, P-trend < .001).
CONCLUSION: Lower peroneal nerve function is associated with smaller calf muscle area and greater functional impairment in individuals with PAD. Future study is needed to determine whether improving peroneal NCV prevents loss of calf muscle and functional decline in people with PAD. J Am Geriatr Soc 59:1855-1863, 2011.
C1 [Garg, Parveen K.; McDermott, Mary M.] Northwestern Univ, Dept Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Liu, Kiang; Tao, Huimin; Liao, Yihua; McDermott, Mary M.] Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Sufit, Robert; Nishida, Takashi] Northwestern Univ, Dept Neurol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Ferrucci, Luigi] NIA, Lab Clin Epidemiol, Bethesda, MD 20892 USA.
[Guralnik, Jack M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Tian, Lu] Stanford Univ, Palo Alto, CA 94304 USA.
[Criqui, Michael H.] Univ Calif San Diego, Dept Family & Prevent Med, San Diego, CA 92103 USA.
RP McDermott, MM (reprint author), 750 N Lake Shore Dr,10th Floor, Chicago, IL 60611 USA.
EM mdm608@northwestern.edu
FU National Heart Lung and Blood Institute [K12-HL083790, R01-HL58099,
R01-HL64739, R01-HL71223, R01-HL076298]; National Center for Research
Resources, National Institutes of Health [RR-00048]
FX Conflict of Interest: This study was supported by grants K12-HL083790,
R01-HL58099, R01-HL64739, and R01-HL71223, and R01-HL076298 from the
National Heart Lung and Blood Institute and grant RR-00048 from the
National Center for Research Resources, National Institutes of Health.
NR 28
TC 8
Z9 8
U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD OCT
PY 2011
VL 59
IS 10
BP 1855
EP 1863
DI 10.1111/j.1532-5415.2011.03600.x
PG 9
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 840OE
UT WOS:000296449300010
PM 22091499
ER
PT J
AU Hohman, TJ
Beason-Held, LL
Resnick, SM
AF Hohman, Timothy J.
Beason-Held, Lori L.
Resnick, Susan M.
TI Cognitive Complaints, Depressive Symptoms, and Cognitive Impairment: Are
They Related?
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE cognitive complaints; depression; aging
ID SUBJECTIVE MEMORY COMPLAINTS; OLDER-PEOPLE; ALZHEIMERS-DISEASE;
DEMENTIA; RISK; POPULATION; FAILURES; DECLINE; ADULTS
AB OBJECTIVES: To examine whether concurrent depressive symptoms and self-and informant-reported cognitive impairments are related to cognitive complaints.
DESIGN: Longitudinal aging study of the relationship between depressive symptoms, reported cognitive impairments, and cognitive complaints. Mixed-effects regression models were used to determine whether scores on the Center for Epidemiologic Studies Depression Scale (CES-D) and Clinical Dementia Rating Scale (CDR) predicted cognitive complaints. The Cognitive Failures Questionnaire (CFQ) assessed cognitive complaints.
SETTING: A community-dwelling sample in Baltimore, Maryland.
PARTICIPANTS: One hundred five cognitively normal older individuals with a mean baseline age of 75 followed for an average of 4 years.
MEASUREMENTS: The CES-D measured depressive symptoms. The CDR Sum of Boxes (CDR-SB) measured self-and informant-reported impairment, and the CFQ measured cognitive complaints.
RESULTS: Greater depressive symptoms and reported impairments are associated with higher CFQ scores. In addition, there was a significant interaction between depressive symptoms and reported impairment. Specifically, individuals without reported cognitive impairment had the strongest association between depressive symptoms and cognitive complaints. Finally, reported impairments interact with baseline age, suggesting that the relationship between reported impairments and cognitive complaints is strongest in individuals younger than 80.
CONCLUSION: These findings confirm a relationship between reported cognitive impairment and cognitive complaints in older individuals and highlight the extent to which age and depressive symptoms account for variation in complaints. These factors should be considered when interpreting cognitive complaints in a clinical setting. J Am Geriatr Soc 59:1908-1912, 2011.
C1 [Hohman, Timothy J.] American Univ, Dept Psychol, Washington, DC 20016 USA.
[Hohman, Timothy J.; Beason-Held, Lori L.; Resnick, Susan M.] NIA, Lab Behav Neurosci, NIH, Baltimore, MD 21224 USA.
RP Hohman, TJ (reprint author), American Univ, Dept Psychol, 4400 Massachusetts Ave NW, Washington, DC 20016 USA.
EM timothyjhohman@gmail.com
OI Hohman, Timothy/0000-0002-3377-7014
FU National Institutes of Health, NIA; [N01-AG-3-2124]
FX Conflict of Interest: The editor in chief has reviewed the conflict of
interest checklist provided by the authors and has determined that the
authors have no financial or any other kind of personal conflicts with
this paper. This research was supported in part by the Intramural
Research Program of the National Institutes of Health, NIA and by
Research and Development Contract N01-AG-3-2124.
NR 30
TC 12
Z9 12
U1 0
U2 18
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD OCT
PY 2011
VL 59
IS 10
BP 1908
EP 1912
DI 10.1111/j.1532-5415.2011.03589.x
PG 5
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 840OE
UT WOS:000296449300016
PM 22091504
ER
PT J
AU Clarke, JL
Ennis, MM
Yung, WKA
Chang, SM
Wen, PY
Cloughesy, TF
DeAngelis, LM
Robins, HI
Lieberman, FS
Fine, HA
Abrey, L
Gilbert, MR
Mehta, M
Kuhn, JG
Aldape, KD
Lamborn, KR
Prados, MD
AF Clarke, Jennifer L.
Ennis, Michele M.
Yung, W. K. Alfred
Chang, Susan M.
Wen, Patrick Y.
Cloughesy, Timothy F.
DeAngelis, Lisa M.
Robins, H. Ian
Lieberman, Frank S.
Fine, Howard A.
Abrey, Lauren
Gilbert, Mark R.
Mehta, Minesh
Kuhn, John G.
Aldape, Kenneth D.
Lamborn, Kathleen R.
Prados, Michael D.
CA N Amer Brain Tumor Consortium
TI Is surgery at progression a prognostic marker for improved 6-month
progression-free survival or overall survival for patients with
recurrent glioblastoma?
SO NEURO-ONCOLOGY
LA English
DT Article
DE glioblastoma; PFS6; prognosis; recurrence; surgery
ID II CLINICAL-TRIALS; PHASE-II; GLIOMA; THERAPY
AB Historically, the North American Brain Tumor Consortium used 6-month progression-free survival (PFS6) as the primary outcome for recurrent glioma phase II clinical trials. In some trials, a subset of patients received the trial treatment before surgery to assess tumor uptake and biological activity. We compared PFS6 and overall survival (OS) for patients with glioblastoma undergoing surgery at progression to results for those without surgery to evaluate the impact of surgical intervention on these outcomes. Two data sets were analyzed. The first included 511 patients enrolled during the period 1998-2005, 105 of whom had surgery (excluding biopsies) during the study or <= 30 days prior to registration. Analysis was stratified on the basis of whether temozolomide was part of the protocol treatment regimen. The second data set included 247 patients enrolled during 2005-2008, 103 of whom underwent surgery during the clinical trial or immediately prior to study registration. A combined data set consisting of all patients who did not receive temozolomide was also compiled. No statistically significant difference in PFS6 or OS was found between the surgery and nonsurgery groups in either data set alone or in the combined data set (P > .45). We conclude that PFS6 and OS results for patients with and without surgical intervention at the time of progression are similar, allowing data from these patients to be combined in assessing the benefit of new treatments without the need for stratification or other statistical adjustment.
C1 [Clarke, Jennifer L.; Chang, Susan M.; Lamborn, Kathleen R.; Prados, Michael D.] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA 94143 USA.
[Cloughesy, Timothy F.] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA.
[Yung, W. K. Alfred; Gilbert, Mark R.; Aldape, Kenneth D.] Univ Texas MD Anderson Canc Ctr, Dept Neurooncol, Houston, TX 77030 USA.
[Kuhn, John G.] Univ Texas Hlth Sci Ctr San Antonio, Dept Neurol, San Antonio, TX 78229 USA.
[Kuhn, John G.] Univ Texas Hlth Sci Ctr San Antonio, Pharmacotherapy Educ & Res Ctr, San Antonio, TX 78229 USA.
[Wen, Patrick Y.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[DeAngelis, Lisa M.; Abrey, Lauren] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Robins, H. Ian] Univ Wisconsin Hosp, Madison, WI USA.
[Lieberman, Frank S.] Univ Pittsburgh, Med Ctr Canc Pavil, Div Neurooncol, Pittsburgh, PA USA.
[Fine, Howard A.] NCI, Neurooncol Branch, NIH, Bethesda, MD 20892 USA.
[Mehta, Minesh] Northwestern Univ, Dept Radiat Oncol, Chicago, IL 60611 USA.
RP Clarke, JL (reprint author), Univ Calif San Francisco, Dept Neurol Surg, 400 Parnassus Ave,A-808, San Francisco, CA 94143 USA.
EM clarkej@neurosurg.ucsf.edu
RI Gilbert, Mark/J-7494-2016;
OI Gilbert, Mark/0000-0003-2556-9722; mehta, minesh/0000-0002-4812-5713
FU North American Brain Tumor Consortium [CA62399]
FX This work was supported by the North American Brain Tumor Consortium
[CA62399].
NR 5
TC 30
Z9 32
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2011
VL 13
IS 10
BP 1118
EP 1124
DI 10.1093/neuonc/nor110
PG 7
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 835YB
UT WOS:000296071900007
PM 21813511
ER
PT J
AU Kreisl, TN
Zhang, WT
Odia, Y
Shih, JH
Butman, JA
Hammoud, D
Iwamoto, FM
Sul, J
Fine, HA
AF Kreisl, Teri N.
Zhang, Weiting
Odia, Yazmin
Shih, Joanna H.
Butman, John A.
Hammoud, Dima
Iwamoto, Fabio M.
Sul, Joohee
Fine, Howard A.
TI A phase II trial of single-agent bevacizumab in patients with recurrent
anaplastic glioma
SO NEURO-ONCOLOGY
LA English
DT Article
DE anaplastic glioma; bevacizumab; FDG; perfusion MRI
ID HIGH-GRADE GLIOMAS; MALIGNANT BRAIN-TUMORS; PLUS IRINOTECAN;
GLIOBLASTOMA; SURVIVAL; CRITERIA; THERAPY; PROGRESSION
AB The purpose of this study was to evaluate the activity of single-agent bevacizumab in patients with recurrent anaplastic glioma and assess correlative advanced imaging parameters. Patients with recurrent anaplastic glioma were treated with bevacizumab 10 mg/kg every 2 weeks. Complete patient evaluations were repeated every 4 weeks. Correlative dynamic contrast-enhanced MR and (18)fluorodeoxyglucose PET imaging studies were obtained to evaluate physiologic changes in tumor and tumor vasculature at time points including baseline, 96 h after the first dose, and after the first 4 weeks of therapy. Median overall survival was 12 months (95% confidence interval [CI]: 6.08-22.8). Median progression-free survival was 2.93 months (95% CI: 2.01-4.93), and 6-month progression-free survival was 20.9% (95% CI: 10.3%-42.5%). Thirteen (43%) patients achieved a partial response. The most common grade >= 3 treatment-related toxicities were hypertension, hypophosphatemia, and thromboembolism. Single-agent bevacizumab produces significant radiographic response in patients with recurrent anaplastic glioma but did not meet the 6-month progression-free survival endpoint. Early change in enhancing tumor volume at 4 days after start of therapy was the most significant prognostic factor for overall and progression-free survival.
C1 [Kreisl, Teri N.; Zhang, Weiting; Odia, Yazmin; Iwamoto, Fabio M.; Sul, Joohee; Fine, Howard A.] NCI, Neurooncol Branch, Ctr Canc Res, Natl Inst Neurol Disorders & Stroke, Bethesda, MD 20892 USA.
[Shih, Joanna H.] NCI, Biometr Res Branch, Rockville, MD USA.
[Butman, John A.; Hammoud, Dima] NIH, Dept Radiol, Ctr Clin, Bethesda, MD 20892 USA.
RP Kreisl, TN (reprint author), NCI, Neurooncol Branch, Ctr Canc Res, Natl Inst Neurol Disorders & Stroke, 9030 Old Georgetown Rd,Rm 225, Bethesda, MD 20892 USA.
EM kreislt@mail.nih.gov
RI Hammoud, Dima/C-2286-2015; Butman, John/J-2780-2013
OI Butman, John/0000-0002-1547-9195
FU National Cancer Institute
FX National Cancer Institute Intramural Research Program.
NR 21
TC 48
Z9 53
U1 2
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD OCT
PY 2011
VL 13
IS 10
BP 1143
EP 1150
DI 10.1093/neuonc/nor091
PG 8
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 835YB
UT WOS:000296071900010
PM 21865400
ER
PT J
AU Dietz, J
Bradley, MM
Okun, MS
Bowers, D
AF Dietz, J.
Bradley, M. M.
Okun, M. S.
Bowers, D.
TI Emotion and ocular responses in Parkinson's disease
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE Emotion; Arousal; Parkinson's disease; Pupil; Eye movement
ID PUPILLARY LIGHT REFLEX; BASAL GANGLIA; DOPAMINERGIC MODULATION;
CLINICAL-DIAGNOSIS; APATHY; AMYGDALA; RECOGNITION; PATHOLOGY;
VOLUNTEERS; INSTRUMENT
AB Parkinson's disease (PD) is a neurodegenerative disease that affects motor, cognitive, and emotional functioning. Previous studies reported reduced skin conductance responses in PD patients, compared to healthy older adults when viewing emotionally arousing pictures. Attenuated skin conductance changes in PD may reflect peripheral autonomic dysfunction (e.g., reduced nerve endings at the sweat gland) or, alternatively, a more central emotional deficit. The aim of the current study was to investigate a second measure of sympathetic arousal-change in pupil dilation. Eye movements, a motor-based correlate of emotional processing, were also assessed. Results indicated that pupil dilation was significantly greater when viewing emotional, compared to neutral pictures for both PD patients and controls. On the other hand, PD patients made fewer fixations with shorter scan paths, particularly when viewing pleasant pictures. These results suggest that PD patients show normal sympathetic arousal to affective stimuli (indexed by pupil diameter), but differences in motor correlates of emotion (eye movements). (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Dietz, J.; Bowers, D.] Univ Florida, Dept Clin & Hlth Psychol, Gainesville, FL 32610 USA.
[Dietz, J.; Bradley, M. M.] Univ Florida, NIMH Ctr Study Emot & Attent, Gainesville, FL 32610 USA.
[Okun, M. S.] Univ Florida, Ctr Movement Disorders & Neurorestorat, Dept Neurol, Gainesville, FL 32610 USA.
[Okun, M. S.] Univ Florida, Ctr Movement Disorders & Neurorestorat, Dept Neurosurg, Gainesville, FL 32610 USA.
RP Dietz, J (reprint author), Univ Florida, Dept Clin & Hlth Psychol, POB 100165, Gainesville, FL 32610 USA.
EM jdietz@phhp.ufl.edu
OI Okun, Michael/0000-0002-6247-9358
FU National Institute of Mental Health [P50 MH72850]; Center for the Study
of Emotion and Attention (CSEA) at the University of Florida; National
Institute of Neurological Disorders and Stroke [RO1-NS05063,
K23-NS044997]; UF National Parkinson Foundation Center of Excellence
FX This project was completed as part of a master's thesis (J. Dietz) at
the University of Florida. The research was supported in part by a grant
from the National Institute of Mental Health (P50 MH72850) to PJ Lang &
MM Bradley at the Center for the Study of Emotion and Attention (CSEA)
at the University of Florida. Support was also provided by the National
Institute of Neurological Disorders and Stroke (RO1-NS05063 to D.
Bowers, K23-NS044997 to M.S. Okun) and the UF National Parkinson
Foundation Center of Excellence.
NR 54
TC 13
Z9 13
U1 2
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3932
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD OCT
PY 2011
VL 49
IS 12
BP 3247
EP 3253
DI 10.1016/j.neuropsychologia.2011.07.029
PG 7
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 839WP
UT WOS:000296400500009
PM 21839756
ER
PT J
AU Pitcher, D
Duchaine, B
Walsh, V
Yovel, G
Kanwisher, N
AF Pitcher, David
Duchaine, Bradley
Walsh, Vincent
Yovel, Galit
Kanwisher, Nancy
TI The role of lateral occipital face and object areas in the face
inversion effect
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE Face perception; Object recognition; Transcranial magnetic stimulation;
Occipital face area; Lateral occipital area
ID HUMAN OCCIPITOTEMPORAL CORTEX; SURFACE-BASED ANALYSIS; EXTRASTRIATE
CORTEX; FACIAL IDENTITY; PERCEPTION; RECOGNITION; PROSOPAGNOSIA;
DISSOCIATION; DISRUPTS; FEATURES
AB Stimulus inversion impairs face discrimination to a greater extent than discrimination of other non-face object categories. This finding has led to suggestions that upright faces are represented by mechanisms specialized for upright faces whereas inverted face representation depends on more general object recognition mechanisms. In the present study we tested the causal role of face-selective and object-selective cortical areas for upright and inverted face discrimination by transiently disrupting neural processing using transcranial magnetic stimulation (TMS). Participants matched upright and inverted faces while TMS was delivered over each participant's functionally localized right occipital face area (rOFA) or right lateral occipital area (rLO). TMS delivered over rOFA disrupted the discrimination of upright and inverted faces while TMS delivered over rLO impaired inverted face discrimination only. These results provide causal evidence that upright faces are represented by face-specific mechanisms whereas inverted faces are represented by both face-specific and object-specific mechanisms. The similar sensitivity of the OFA to upright and inverted faces is consistent with the hypothesis that the OFA processes facial features at an early stage of face processing. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Pitcher, David; Kanwisher, Nancy] MIT, McGovern Inst Brain Res, Cambridge, MA 02139 USA.
[Pitcher, David; Walsh, Vincent] UCL, Inst Cognit Neurosci, London WC1N 3AR, England.
[Duchaine, Bradley] Dartmouth Coll, Dept Psychol & Brain Sci, Hanover, NH 03755 USA.
[Yovel, Galit] Tel Aviv Univ, Dept Psychol, IL-69978 Tel Aviv, Israel.
RP Pitcher, D (reprint author), NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
EM pitcherdj@mail.nih.gov
FU BBSRC [BB/F022875/1]; [EY13455]
FX Thanks to Tanya Goldhaber. This work was partially supported by BBSRC
grant BB/F022875/1 to BD & VW and by EY13455 to NK.
NR 44
TC 22
Z9 22
U1 4
U2 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3932
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD OCT
PY 2011
VL 49
IS 12
BP 3448
EP 3453
DI 10.1016/j.neuropsychologia.2011.08.020
PG 6
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 839WP
UT WOS:000296400500032
PM 21896279
ER
PT J
AU Singh, CR
Watanabe, R
Zhou, DH
Jennings, MD
Fukao, A
Lee, B
Ikeda, Y
Chiorini, JA
Campbell, SG
Ashe, MP
Fujiwara, T
Wek, RC
Pavitt, GD
Asano, K
AF Singh, Chingakham Ranjit
Watanabe, Ryosuke
Zhou, Donghui
Jennings, Martin D.
Fukao, Akira
Lee, Bumjun
Ikeda, Yuka
Chiorini, John A.
Campbell, Susan G.
Ashe, Mark P.
Fujiwara, Toshinobu
Wek, Ronald C.
Pavitt, Graham D.
Asano, Katsura
TI Mechanisms of translational regulation by a human eIF5-mimic protein
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID GUANINE-NUCLEOTIDE EXCHANGE; IN-VIVO; SACCHAROMYCES-CEREVISIAE;
P-BODIES; INITIATION; EIF2; COMPLEX; DOMAIN; PHOSPHORYLATION; COMMON
AB The translation factor eIF5 is an important partner of eIF2, directly modulating its function in several critical steps. First, eIF5 binds eIF2/GTP/Met-tRNA(i)(Met) ternary complex (TC), promoting its recruitment to 40S ribosomal subunits. Secondly, its GTPase activating function promotes eIF2 dissociation for ribosomal subunit joining. Finally, eIF5 GDP dissociation inhibition (GDI) activity can antagonize eIF2 reactivation by competing with the eIF2 guanine exchange factor (GEF), eIF2B. The C-terminal domain (CTD) of eIF5, a W2-type HEAT domain, mediates its interaction with eIF2. Here, we characterize a related human protein containing MA3- and W2-type HEAT domains, previously termed BZW2 and renamed here as eIF5-mimic protein 1 (5MP1). Human 5MP1 interacts with eIF2 and eIF3 and inhibits general and gene-specific translation in mammalian systems. We further test whether 5MP1 is a mimic or competitor of the GEF catalytic subunit eIF2B epsilon or eIF5, using yeast as a model. Our results suggest that 5MP1 interacts with yeast eIF2 and promotes TC formation, but inhibits TC binding to the ribosome. Moreover, 5MP1 is not a GEF but a weak GDI for yeast eIF2. We propose that 5MP1 is a partial mimic and competitor of eIF5, interfering with the key steps by which eIF5 regulates eIF2 function.
C1 [Singh, Chingakham Ranjit; Watanabe, Ryosuke; Lee, Bumjun; Ikeda, Yuka; Asano, Katsura] Kansas State Univ, Div Biol, Mol Cellular & Dev Biol Program, Manhattan, KS 66506 USA.
[Zhou, Donghui; Wek, Ronald C.] Indiana Univ Sch Med, Dept Biochem & Mol Biol, Indianapolis, IN 46202 USA.
[Jennings, Martin D.; Campbell, Susan G.; Ashe, Mark P.; Pavitt, Graham D.] Univ Manchester, Fac Life Sci, Manchester M31 9PT, Lancs, England.
[Fukao, Akira; Fujiwara, Toshinobu] Kobe Univ, Grad Sch Engn, Dept Chem Sci & Engn, Kobe, Hyogo 6578501, Japan.
[Chiorini, John A.] NIDCR, NIH, Bethesda, MD 20892 USA.
RP Asano, K (reprint author), Kansas State Univ, Div Biol, Mol Cellular & Dev Biol Program, Ackert Hall, Manhattan, KS 66506 USA.
EM kasano@ksu.edu
RI Jennings, martin/E-5240-2010; Pavitt, Graham/A-1363-2010
OI Pavitt, Graham/0000-0002-8593-2418
FU National Institutes of Health [GM64781]; NCRR [P20 RR016475]; K-state
Terry Johnson Cancer Center; NIDCR; BBSRC [BB/E002005/1, BB/H010599/1];
[GM49164]
FX National Institutes of Health GM64781, NCRR K-INBRE Pilot Grant P20
RR016475; K-state Terry Johnson Cancer Center (to K. A.); NIDCR
intramural grant (to J.A.C.); GM49164 (to R.C.W.); BBSRC grants
BB/E002005/1 and BB/H010599/1 (to G.D.P.); and short-term fellowship for
his sabbatical to Manchester, UK in Feb-Mar, 2008 (to K. A.). Funding
for open access charge: K-state Terry Johnson Cancer Center.
NR 41
TC 9
Z9 11
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD OCT
PY 2011
VL 39
IS 19
BP 8314
EP 8328
DI 10.1093/nar/gkr339
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 839CB
UT WOS:000296341100012
PM 21745818
ER
PT J
AU Kodama, S
Hosseinpour, F
Goldstein, JA
Negishi, M
AF Kodama, Susumu
Hosseinpour, Fardin
Goldstein, Joyce A.
Negishi, Masahiko
TI Liganded pregnane X receptor represses the human sulfotransferase
SULT1E1 promoter through disrupting its chromatin structure
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID ESTROGEN SULFOTRANSFERASE; BREAST-CANCER; CROSS-TALK;
ANDROSTANE-RECEPTOR; GENE-EXPRESSION; ENHANCER MODULE; CYP2B6 GENE; CAR;
ACTIVATION; LIVER
AB Pregnane X receptor (PXR), acting as a xenobiotic-activated transcription factor, regulates the hepatic metabolism of therapeutics as well as endobiotics such as steroid hormones. Given our finding that PXR activation by rifampicin (RIF) represses the estrogen sulfotransferase (SULT1E1) gene in human primary hepatocytes and hepatocellular carcinoma Huh7 cells, here we have investigated the molecular mechanism of this repression. First the PXR-responsive enhancer was delineated to a 100 bp sequence (-1000/-901), which contains three half sites that constitute the overlapping direct repeat 1 (DR1) and direct repeat 2 (DR2) motifs and two forkhead factor binding sites. siRNA knockdown, chromatin immunoprecipitation and chromatin conformation capture assays were employed to demonstrate that hepatocyte nuclear factor 4 alpha (HNF4 alpha) bound to the PXR-responsive enhancer, and activated the enhancer by looping its position close to the proximal promoter. Upon activation by RIF, PXR indirectly interacted with the enhancer, decreasing the interaction with HNF4 alpha and dissolving the looped SULT1E1 promoter with deacetylation of histone 3. Removal of the DR sites from the enhancer hampers the ability of HNF4 alpha to loop the promoter and that of PXR to repress the promoter activity. Thus, PXR represses human SULT1E1, possibly attenuating the inactivation of estrogen.
C1 [Kodama, Susumu; Hosseinpour, Fardin; Negishi, Masahiko] NIEHS, Pharmacogenet Sect, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
[Goldstein, Joyce A.] NIEHS, Human Metab Sect, Lab Toxicol & Pharmacol, NIH, Res Triangle Pk, NC 27709 USA.
RP Negishi, M (reprint author), NIEHS, Pharmacogenet Sect, Lab Reprod & Dev Toxicol, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM negishi@niehs.nih.gov
RI Goldstein, Joyce/A-6681-2012
FU National Institutes of Health; National Institute of Environmental
Health Sciences [Z01ES1005-01]
FX Intramutal Research Program of the National Institutes of Health and
National Institute of Environmental Health Sciences: Z01ES1005-01.
Funding for open access charge: NIH.
NR 30
TC 16
Z9 18
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD OCT
PY 2011
VL 39
IS 19
BP 8392
EP 8403
DI 10.1093/nar/gkr458
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 839CB
UT WOS:000296341100018
PM 21764778
ER
PT J
AU Yu, TX
Wang, PY
Rao, JN
Zou, TT
Liu, L
Xiao, L
Gorospe, M
Wang, JY
AF Yu, Ting-Xi
Wang, Peng-Yuan
Rao, Jaladanki N.
Zou, Tongtong
Liu, Lan
Xiao, Lan
Gorospe, Myriam
Wang, Jian-Ying
TI Chk2-dependent HuR phosphorylation regulates occludin mRNA translation
and epithelial barrier function
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID BINDING PROTEIN HUR; POSTTRANSCRIPTIONAL GENE-REGULATION; TIGHT JUNCTION
PROTEIN; POLYAMINE DEPLETION; IN-VIVO; STABILIZATION; CELLS; STABILITY;
EXPRESSION; STRESS
AB Occludin is a transmembrane tight junction (TJ) protein that plays an important role in TJ assembly and regulation of the epithelial barrier function, but the mechanisms underlying its post-transcriptional regulation are unknown. The RNA-binding protein HuR modulates the stability and translation of many target mRNAs. Here, we investigated the role of HuR in the regulation of occludin expression and therefore in the intestinal epithelial barrier function. HuR bound the 3'-untranslated region of the occludin mRNA and enhanced occludin translation. HuR association with the occludin mRNA depended on Chk2-dependent HuR phosphorylation. Reduced HuR phosphorylation by Chk2 silencing or by reduction of Chk2 through polyamine depletion decreased HuR-binding to the occludin mRNA and repressed occludin translation, whereas Chk2 overexpression enhanced (HuR/occludin mRNA) association and stimulated occludin expression. In mice exposed to septic stress induced by cecal ligation and puncture, Chk2 levels in the intestinal mucosa decreased, associated with an inhibition of occludin expression and gut barrier dysfunction. These results indicate that HuR regulates occludin mRNA translation through Chk2-dependent HuR phosphorylation and that this influence is crucial for maintenance of the epithelial barrier integrity in the intestinal tract.
C1 [Yu, Ting-Xi; Wang, Peng-Yuan; Rao, Jaladanki N.; Zou, Tongtong; Liu, Lan; Xiao, Lan; Wang, Jian-Ying] Univ Maryland, Sch Med, Dept Surg, Cell Biol Grp, Baltimore, MD 21201 USA.
[Yu, Ting-Xi; Wang, Peng-Yuan; Rao, Jaladanki N.; Zou, Tongtong; Liu, Lan; Xiao, Lan; Wang, Jian-Ying] Baltimore Vet Affairs Med Ctr, Baltimore, MD 21201 USA.
[Gorospe, Myriam] Natl Inst Aging IRP, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
[Wang, Jian-Ying] Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA.
RP Wang, JY (reprint author), Univ Maryland, Sch Med, Dept Surg, Cell Biol Grp, Baltimore St, Baltimore, MD 21201 USA.
EM jwang@smail.umaryland.edu
FU US Department of Veterans Affairs; National Institutes of Health
[DK57819, DK61972, DK68491]; National Institute on Aging, National
Institutes of Health; National Institute of Diabetes and Digestive and
Kidney Diseases
FX Merit Review Grants to J.-Y.W. and J.N.R.) from US Department of
Veterans Affairs and by National Institutes of Health DK57819, DK61972,
DK68491 to J.-Y.W.). National Institute on Aging-Intramural Research
Program, National Institutes of Health to M.G.). Funding for open access
charge: National Institute of Diabetes and Digestive and Kidney
Diseases.
NR 64
TC 25
Z9 25
U1 1
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD OCT
PY 2011
VL 39
IS 19
BP 8472
EP 8487
DI 10.1093/nar/gkr567
PG 16
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 839CB
UT WOS:000296341100024
PM 21745814
ER
PT J
AU He, SS
Hickman, AB
Dyda, F
Johnson, NP
Chandler, M
Ton-Hoang, B
AF He, Susu
Hickman, Alison B.
Dyda, Fred
Johnson, Neil P.
Chandler, Michael
Ton-Hoang, Bao
TI Reconstitution of a functional IS608 single-strand transpososome: role
of non-canonical base pairing
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID DNA TRANSPOSASES; TRANSPOSITION; INSERTION; RECOGNITION; INTERMEDIATE;
REPLICATION; INTEGRATION; MECHANISM; CATALYSIS; COMPLEX
AB Single-stranded (ss) transposition, a recently identified mechanism adopted by members of the widespread IS200/IS605 family of insertion sequences (IS), is catalysed by the transposase, TnpA. The transposase of IS608, recognizes subterminal imperfect palindromes (IP) at both IS ends and cleaves at sites located at some distance. The cleavage sites, C, are not recognized directly by the protein but by short sequences 5' to the foot of each IP, guide (G) sequences, using a network of canonical ('Watson-Crick') base interactions. In addition a set of non-canonical base interactions similar to those found in RNA structures are also involved. We have reconstituted a biologically relevant complex, the transpososome, including both left and right ends and TnpA, which catalyses excision of a ss DNA circle intermediate. We provide a detailed picture of the way in which the IS608 transpososome is assembled and demonstrate that both C and G sequences are essential for forming a robust transpososome detectable by EMSA. We also address several questions central to the organization and function of the ss transpososome and demonstrate the essential role of non-canonical base interactions in the IS608 ends for its stability by using point mutations which destroy individual non-canonical base interactions.
C1 [He, Susu; Chandler, Michael; Ton-Hoang, Bao] CNRS, Lab Microbiol & Genet Mol, UMR 5100, F-31062 Toulouse, France.
[Hickman, Alison B.; Dyda, Fred] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Johnson, Neil P.] CNRS, Inst Pharmacol & Biol Struct, UMR 5089, F-31077 Toulouse, France.
RP Chandler, M (reprint author), CNRS, Lab Microbiol & Genet Mol, UMR 5100, 118 Rte Narbonne, F-31062 Toulouse, France.
EM mike@ibcg.biotoul.fr; tonhoang@ibcg.biotoul.fr
OI Chandler, Michael/0000-0002-0292-6662
FU Centre National de la Recherche Scientifique (France), by Agence
National de Recherche (France); National Institute of Diabetes and
Digestive and Kidney Diseases; Agence National de Recherche (France)
FX Centre National de la Recherche Scientifique (France), by Agence
National de Recherche (France) grant Mobigen (M.C. and N.P.J.); the
Intramural Program of the National Institute of Diabetes and Digestive
and Kidney Diseases (F.D.). Funding for open access charge: Agence
National de Recherche (France) (Grant MOBIGEN to M.C. and N.P.J.).
NR 27
TC 12
Z9 12
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD OCT
PY 2011
VL 39
IS 19
BP 8503
EP 8512
DI 10.1093/nar/gkr566
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 839CB
UT WOS:000296341100026
PM 21745812
ER
PT J
AU Abdelmohsen, K
Tominaga, K
Lee, EK
Srikantan, S
Kang, MJ
Kim, MM
Selimyan, R
Martindale, JL
Yang, XL
Carrier, F
Zhan, M
Becker, KG
Gorospe, M
AF Abdelmohsen, Kotb
Tominaga, Kumiko
Lee, Eun Kyung
Srikantan, Subramanya
Kang, Min-Ju
Kim, Mihee M.
Selimyan, Roza
Martindale, Jennifer L.
Yang, Xiaoling
Carrier, France
Zhan, Ming
Becker, Kevin G.
Gorospe, Myriam
TI Enhanced translation by Nucleolin via G-rich elements in coding and
non-coding regions of target mRNAs
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID POSTTRANSCRIPTIONAL GENE-REGULATION; SURFACE-EXPRESSED NUCLEOLIN;
INHIBITS HIV-INFECTION; PRE-RIBOSOMAL-RNA; BINDING-PROTEIN;
CELL-PROLIFERATION; GENOTOXIC STRESS; SIGNATURE MOTIF; HEAT-SHOCK;
IN-VIVO
AB RNA-binding proteins (RBPs) regulate gene expression at many post-transcriptional levels, including mRNA stability and translation. The RBP nucleolin, with four RNA-recognition motifs, has been implicated in cell proliferation, carcinogenesis and viral infection. However, the subset of nucleolin target mRNAs and the influence of nucleolin on their expression had not been studied at a transcriptome-wide level. Here, we globally identified nucleolin target transcripts, many of which encoded cell growth- and cancer-related proteins, and used them to find a signature motif on nucleolin target mRNAs. Surprisingly, this motif was very rich in G residues and was not only found in the 3'-untranslated region (UTR), but also in the coding region (CR) and 5'-UTR. Nucleolin enhanced the translation of mRNAs bearing the G-rich motif, since silencing nucleolin did not change target mRNA stability, but decreased the size of polysomes forming on target transcripts and lowered the abundance of the encoded proteins. In summary, nucleolin binds G-rich sequences in the CR and UTRs of target mRNAs, many of which encode cancer proteins, and enhances their translation.
C1 [Abdelmohsen, Kotb; Tominaga, Kumiko; Lee, Eun Kyung; Srikantan, Subramanya; Kang, Min-Ju; Kim, Mihee M.; Selimyan, Roza; Martindale, Jennifer L.; Yang, Xiaoling; Gorospe, Myriam] NIA, Lab Mol Biol & Immunol, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Carrier, France] Univ Maryland, Sch Med, Dept Radiat Oncol, Baltimore, MD 21201 USA.
[Zhan, Ming; Becker, Kevin G.] NIA, Res Resources Branch, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Abdelmohsen, K (reprint author), NIA, Lab Mol Biol & Immunol, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
EM abdelmohsenk@grc.nia.nih.gov
OI srikantan, subramanya/0000-0003-1810-6519; abdelmohsen,
Kotb/0000-0001-6240-5810; Becker, Kevin/0000-0002-6794-6656
FU National Institute on Aging of the National Institutes of Health; NIH
[RO1 1CA116491-01]
FX National Institute on Aging-Intramural Research Program of the National
Institutes of Health; NIH (RO1 1CA116491-01 to F.C.). Funding for open
access charge: National Institute on Aging-Intramural Research Program,
National Institutes of Health.
NR 71
TC 40
Z9 40
U1 3
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD OCT
PY 2011
VL 39
IS 19
BP 8513
EP 8530
DI 10.1093/nar/gkr488
PG 18
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 839CB
UT WOS:000296341100027
PM 21737422
ER
PT J
AU Huang, WC
Umbach, DM
Jordan, NV
Abell, AN
Johnson, GL
Li, LP
AF Huang, Weichun
Umbach, David M.
Jordan, Nicole Vincent
Abell, Amy N.
Johnson, Gary L.
Li, Leping
TI Efficiently identifying genome-wide changes with next-generation
sequencing data
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID CHIP-SEQ DATA; DIFFERENTIAL EXPRESSION ANALYSIS; FACTOR-BINDING SITES;
RNA-SEQ; TRANSCRIPTOMES; IDENTIFICATION; PACKAGE; MODEL; CELL; TOOL
AB We propose a new and effective statistical framework for identifying genome-wide differential changes in epigenetic marks with ChIP-seq data or gene expression with mRNA-seq data, and we develop a new software tool EpiCenter that can efficiently perform data analysis. The key features of our framework are: (i) providing multiple normalization methods to achieve appropriate normalization under different scenarios, (ii) using a sequence of three statistical tests to eliminate background regions and to account for different sources of variation and (iii) allowing adjustment for multiple testing to control false discovery rate (FDR) or family-wise type I error. Our software EpiCenter can perform multiple analytic tasks including: (i) identifying genome-wide epigenetic changes or differentially expressed genes, (ii) finding transcription factor binding sites and (iii) converting multiple-sample sequencing data into a single read-count data matrix. By simulation, we show that our framework achieves a low FDR consistently over a broad range of read coverage and biological variation. Through two real examples, we demonstrate the effectiveness of our framework and the usages of our tool. In particular, we show that our novel and robust 'parsimony' normalization method is superior to the widely-used 'tagRatio' method. Our software EpiCenter is freely available to the public.
C1 [Huang, Weichun; Umbach, David M.; Li, Leping] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Jordan, Nicole Vincent; Abell, Amy N.; Johnson, Gary L.] Univ N Carolina, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Jordan, Nicole Vincent; Abell, Amy N.; Johnson, Gary L.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
RP Huang, WC (reprint author), NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
EM weichun.huang@nih.gov; li3@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences [ES101765-05];
National Institutes of Health [GM30324, DK37871, GM007040]; UNC Cancer
Research Fund
FX Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences (ES101765-05); National Institutes of
Health (GM30324, DK37871 to G.L.J., GM007040 to N.V.J.); UNC Cancer
Research Fund (to G.L.J.). Funding for open access charge: Intramural
Research Program of the National Institutes of Health, the National
Institute of Environmental Health Sciences.
NR 35
TC 17
Z9 17
U1 0
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD OCT
PY 2011
VL 39
IS 19
AR e130
DI 10.1093/nar/gkr592
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 839CB
UT WOS:000296341100005
PM 21803788
ER
PT J
AU Saji, M
Narahara, K
McCarty, SK
Vasko, VV
La Perle, KM
Porter, K
Jarjoura, D
Lu, C
Cheng, SY
Ringel, MD
AF Saji, M.
Narahara, K.
McCarty, S. K.
Vasko, V. V.
La Perle, K. M.
Porter, K.
Jarjoura, D.
Lu, C.
Cheng, S-Y
Ringel, M. D.
TI Akt1 deficiency delays tumor progression, vascular invasion, and distant
metastasis in a murine model of thyroid cancer
SO ONCOGENE
LA English
DT Article
DE PI3 kinase; thyroid hormone receptor beta; thyrotropin; p27; gelsolin
ID EPITHELIAL-MESENCHYMAL TRANSITION; MOUSE MODEL; CELL-MIGRATION;
BREAST-CANCER; PHOSPHATIDYLINOSITOL 3-KINASE; DISTINCT ROLES;
BETA-RECEPTOR; P27(KIP1); GROWTH; MICE
AB Akt activation is common in progressive thyroid cancer. In breast cancer, Akt1 induces primary cancer growth, but is reported to inhibit metastasis in vivo in several model systems. In contrast, clinical and in vitro studies suggest a metastasis-promoting role for Akt1 in thyroid cancer. The goal of this study was to determine the functional role of Akt1 in thyroid cancer growth and metastatic progression in vivo using thyroid hormone receptor (TR) beta(PV/PV) knock-in (PV) mice, which develop metastatic thyroid cancer. We crossed Akt1(-/-) and PV mice and compared tumor development, local progression, metastasis and histology in TR beta(PV/PV)/Akt1(+/+) (PVPV-Akt1WT) and TR beta(PV/PV)/Akt1(-/-) (PVPV-Akt1KO) mice. Mice were killed at 3, 6, 9, 12 and 15 months; necropsy was performed and serum thyroid stimulating hormone (TSH) was measured. Thyroid hyperplasia occurred in both groups beginning at 3 months; the thyroid size was greater in the PVPV-Akt1WT mice (P<0.001). In comparison with PVPV-Akt1WT mice, thyroid cancer development was delayed in the PVPV-Akt1KO mice (P = 0.003) and the degree of tumor invasiveness was reduced. The PVPV-Akt1WT mice displayed pulmonary metastases at 12 and 15 months of age, by contrast PVPV-Akt1KO mice did not develop distant metastases at 15 months of age. Despite continued expression of Akt2 or Akt3, pAkt levels were decreased and there was evidence of reduced Akt effect on p27 in the PVPV-Akt1KO thyroids. TSH levels were similarly elevated in PV mice regardless of Akt1 expression. In conclusion, thyroid cancer development and progression in TR beta(PV/PV) mice are Akt1-dependent, consistent with a tumor progression-promoting role in this murine thyroid cancer model. Oncogene (2011) 30, 4307-4315; doi: 10.1038/onc.2011.136; published online 2 May 2011
C1 [Saji, M.; Narahara, K.; McCarty, S. K.; Ringel, M. D.] Ohio State Univ, Coll Med, Div Endocrinol, Columbus, OH 43210 USA.
[Saji, M.; Narahara, K.; McCarty, S. K.; Ringel, M. D.] Ohio State Univ, Coll Med, Div Diabet, Columbus, OH 43210 USA.
[Saji, M.; Narahara, K.; McCarty, S. K.; Ringel, M. D.] Ohio State Univ, Coll Med, Div Metab, Columbus, OH 43210 USA.
[Saji, M.; Narahara, K.; McCarty, S. K.; Porter, K.; Jarjoura, D.; Ringel, M. D.] Arthur G James Comprehens Canc Ctr, Columbus, OH USA.
[Ringel, M. D.] Ohio State Univ, Coll Med, Div Oncol, Columbus, OH 43210 USA.
[Porter, K.; Jarjoura, D.] Ohio State Univ, Coll Med, Ctr Biostat, Columbus, OH 43210 USA.
[Vasko, V. V.] Uniformed Serv Univ Hlth Sci, Dept Pediat, Bethesda, MD 20814 USA.
[La Perle, K. M.] Ohio State Univ, Coll Vet Med, Columbus, OH 43210 USA.
[Lu, C.; Cheng, S-Y] NCI, NIH, Bethesda, MD 20892 USA.
RP Ringel, MD (reprint author), Ohio State Univ, Coll Med, Div Endocrinol, 445D McCampbell Hall,1581 Dodd Dr, Columbus, OH 43210 USA.
EM matthew.ringel@osumc.edu
RI Saji, Motoyasu/E-4007-2011; La Perle, Krista/B-3099-2015
FU NIH [P01CA124570, R01CA102572]
FX Funding for the work is from NIH grants (P01CA124570 and R01CA102572) to
MDR. We appreciate the technical assistance of Michael Ostrowski, John
Thompson and Jun Liu.
NR 50
TC 24
Z9 24
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD OCT
PY 2011
VL 30
IS 42
BP 4307
EP 4315
DI 10.1038/onc.2011.136
PG 9
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 839HP
UT WOS:000296356400002
PM 21532616
ER
PT J
AU Liu, PC
Barb, J
Woodhouse, K
Taylor, JG
Munson, PJ
Raghavachari, N
AF Liu, Poching
Barb, Jennifer
Woodhouse, Kimberly
Taylor, James G.
Munson, Peter J.
Raghavachari, Nalini
TI Transcriptome profiling and sequencing of differentiated human
hematopoietic stem cells reveal lineage-specific expression and
alternative splicing of genes
SO PHYSIOLOGICAL GENOMICS
LA English
DT Article
DE hematopoiesis; differentiation; microarrays; gene expression; splicing;
qPCR; RNAseq
ID ERYTHROPOIESIS; LEUKEMOGENESIS; CATENIN; GTPASES; FAMILY; FATE
AB Liu P, Barb J, Woodhouse K, Taylor JG VI, Munson PJ, Raghavachari N. Transcriptome profiling and sequencing of differentiated human hematopoietic stem cells reveal lineage-specific expression and alternative splicing of genes. Physiol Genomics 43: 1117-1134, 2011. First published August 9, 2011; doi:10.1152/physiolgenomics.00099.2011.-Hematopoietic differentiation is strictly regulated by complex network of transcription factors that are controlled by ligands binding to cell surface receptors. Disruptions of the intricate sequences of transcriptional activation and suppression of multiple genes cause hematological diseases, such as leukemias, myelodysplastic syndromes, or myeloproliferative syndromes. From a clinical standpoint, deciphering the pattern of gene expression during hematopoiesis may help unravel disease-specific mechanisms in hematopoietic malignancies. Herein, we describe a human in vitro hematopoietic model system where lineage-specific differentiation of CD34(+) cells was accomplished using specific cytokines. Microarray and RNAseq-based whole transcriptome and exome analysis was performed on the differentiated erythropoietic, granulopoietic, and megakaryopoietic cells to delineate changes in expression of whole transcripts and exons. Analysis on the Human 1.0 ST exon arrays indicated differential expression of 172 genes (P < 0.0000001) and significant alternate splicing of 86 genes during differentiation. Pathway analysis identified these genes to be involved in Rac/RhoA signaling, Wnt/B-catenin signaling and alanine/aspartate metabolism. Comparison of the microarray data to next generation RNAseq analysis during erythroid differentiation demonstrated a high degree of correlation in gene (R = 0.72) and exon (R = 0.62) expression. Our data provide a molecular portrait of events that regulate differentiation of hematopoietic cells. Knowledge of molecular processes by which the cells acquire their cell-specific fate would be beneficial in developing cell-based therapies for human diseases.
C1 [Raghavachari, Nalini] NHLBI, Genom Core Facil, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Barb, Jennifer; Munson, Peter J.] NHLBI, Math & Stat Comp Lab, Ctr Informat Technol, NIH, Bethesda, MD 20892 USA.
[Taylor, James G.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
RP Raghavachari, N (reprint author), NHLBI, Genom Core Facil, Genet & Dev Biol Ctr, NIH, 10 Ctr Dr,Bldg 10,8C 103B, Bethesda, MD 20892 USA.
EM nraghavachari@nhlbi.nih.gov
OI Taylor, James/0000-0002-4421-1809
FU Intramural Research, NHLBI; CIT, NIH
FX We acknowledge Intramural Research, NHLBI, for the funding and Edge
Biosciences and Applied Biosystems for generous help in RNAseq analysis
using the SOLiD platform. We appreciate the help of Drs. Harry L. Malech
and Uimook Choi, in the Genetic Immunotherapy Section, Laboratory of
Host Defenses, National Institute of Allergy and Infectious Diseases,
NIH, for providing the CD34+ cells. We acknowledge Dr. Phil
Mccoy and Ms. Leigh Samsel in the NHLBI Flow Cytometry Core for help
with the flow characterization of cells. We gratefully acknowledge the
help of Dr. Zu Xi Yu in the Pathology Core Facility-NHLBI for help in
the staining of cells.; Funding by Intramural Research, NHLBI and CIT,
NIH.
NR 38
TC 7
Z9 7
U1 0
U2 12
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1094-8341
J9 PHYSIOL GENOMICS
JI Physiol. Genomics
PD OCT
PY 2011
VL 43
IS 20
BP 1117
EP 1134
DI 10.1152/physiolgenomics.00099.2011
PG 18
WC Cell Biology; Genetics & Heredity; Physiology
SC Cell Biology; Genetics & Heredity; Physiology
GA 841ZJ
UT WOS:000296553500001
PM 21828245
ER
PT J
AU Moore, RA
Timmes, AG
Wilmarth, PA
Safronetz, D
Priola, SA
AF Moore, Roger A.
Timmes, Andrew G.
Wilmarth, Phillip A.
Safronetz, David
Priola, Suzette A.
TI Identification and removal of proteins that co-purify with infectious
prion protein improves the analysis of its secondary structure
SO PROTEOMICS
LA English
DT Article
DE Animal proteomics; Apolipoprotein E; Ferritin; infrared spectroscopy;
Prion protein purification; Prion strains
ID TRANSFORM INFRARED-SPECTROSCOPY; TRANSMISSIBLE SPONGIFORM
ENCEPHALOPATHIES; SCRAPIE PRION; APOLIPOPROTEIN-E; DIFFERENT STRAINS;
MOUSE SCRAPIE; DISEASE; CONFORMATIONS; PURIFICATION; HAMSTERS
AB Prion diseases are neurodegenerative disorders associated with the accumulation of an abnormal isoform of the mammalian prion protein (PrP). Fourier transform infrared spectroscopy (FTIR) has previously been used to show that the conformation of aggregated, infectious PrP (PrP(Sc)) varies between prion strains and these unique conformations may determine strain-specific disease phenotypes. However, the relative amounts of alpha-helix, beta-sheet and other secondary structures have not always been consistent between studies, suggesting that other proteins might be confounding the analysis of PrP(Sc) secondary structure. We have used FTIR and LC-MS/MS to analyze enriched PrP(Sc) from mouse and hamster prion strains both before and after the removal of protein contaminants that commonly co-purify with PrP(Sc). Our data show that non-PrP proteins do contribute to absorbances that have been associated with alpha-helical, loop, turn and beta-sheet structures attributed to PrP(Sc). The major contaminant, the alpha-helical protein ferritin, absorbs strongly at 1652 cm(-1) in the FTIR spectrum associated with PrP(Sc). However, even the removal of more than 99% of the ferritin from PrP(Sc) did not completely abolish absorbance at 1652 cm(-1). Our results show that contaminating proteins alter the FTIR spectrum attributed to PrP(Sc) and suggest that the alpha-helical, loop/turn and beta-sheet secondary structure that remains following their removal are derived from PrP(Sc) itself.
C1 [Moore, Roger A.; Timmes, Andrew G.; Safronetz, David; Priola, Suzette A.] NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, NIH, Hamilton, MT 59840 USA.
[Wilmarth, Phillip A.] Oregon Hlth & Sci Univ, Dept Biochem & Mol Biol, Sch Med, Portland, OR 97201 USA.
RP Moore, RA (reprint author), NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, NIH, 903 S 4th Str, Hamilton, MT 59840 USA.
EM rmoore@niaid.nih.gov
FU National Institute of Allergy and Infectious Disease, National
Institutes of Health [AI000752-16]; National Institutes of Health
[EY007755]
FX The authors thank Dr. Bruce Chesebro, Dr. Gerald Baron and Dr. Byron
Caughey for critically evaluating the manuscript. Anita Mora and Austin
Athman provided technical assistance in preparation of the figures. The
authors thank Craig Martens, Kimmo Virtaneva and Steve Porcella from the
Rocky Mountain Research Technologies Branch for the extraction of tissue
used for obtaining hamster DNA sequencing data. The authors also thank
Brent Weatherly from NuSep, Inc. for helpful discussions with ProteoIQ
software. This research was supported by intramural research program of
the National Institute of Allergy and Infectious Disease, National
Institutes of Health (AI000752-16). P. A. W. was supported by National
Institutes of Health grant EY007755.
NR 55
TC 12
Z9 12
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1615-9853
J9 PROTEOMICS
JI Proteomics
PD OCT
PY 2011
VL 11
IS 19
SI SI
BP 3853
EP 3865
DI 10.1002/pmic.201100253
PG 13
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 836VF
UT WOS:000296142100012
PM 21805638
ER
PT J
AU Gundry, RL
Burridge, PW
Boheler, KR
AF Gundry, Rebekah L.
Burridge, Paul W.
Boheler, Kenneth R.
TI Pluripotent stem cell heterogeneity and the evolving role of proteomic
technologies in stem cell biology
SO PROTEOMICS
LA English
DT Review
DE Cell biology; Cell surface; Heterogeneity; Pluripotent stem cell
ID MOUSE EMBRYONIC STEM; PLASMA-MEMBRANE PROTEOMICS; TANDEM
MASS-SPECTROMETRY; HUMAN SOMATIC-CELLS; HEMATOPOIETIC STEM;
CARCINOMA-CELLS; HUMAN FIBROBLASTS; PROGENITOR CELLS; SURFACE MARKERS;
DEFINED FACTORS
AB Stem cells represent obvious choices for regenerative medicine and are invaluable for studies of human development and drug testing. The proteomic landscape of pluripotent stem cells (PSCs), in particular, is not yet clearly defined; consequently, this field of research would greatly benefit from concerted efforts designed to better characterize these cells. In this concise review, we provide an overview of stem cell potency, highlight the types and practical implications of heterogeneity in PSCs and provide a detailed analysis of the current view of the pluripotent proteome in a unique resource for this rapidly evolving field. Our goal in this review is to provide specific insights into the current status of the known proteome of both mouse and human PSCs. This has been accomplished by integrating published data into a unified PSC proteome to facilitate the identification of proteins, which may be informative for the stem cell state as well as to reveal areas where our current view is limited. These analyses provide insight into the challenges faced in the proteomic analysis of PSCs and reveal one area - the cell surface subproteome - that would especially benefit from enhanced research efforts.
C1 [Gundry, Rebekah L.] Med Coll Wisconsin, Dept Biochem, Milwaukee, WI 53226 USA.
[Gundry, Rebekah L.] Med Coll Wisconsin, Dept Biotechnol, Milwaukee, WI 53226 USA.
[Gundry, Rebekah L.] Med Coll Wisconsin, Ctr Bioengn, Milwaukee, WI 53226 USA.
[Burridge, Paul W.] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD USA.
[Boheler, Kenneth R.] NIA, Mol Cardiol & Stem Cell Unit, NIH, Baltimore, MD USA.
RP Gundry, RL (reprint author), Med Coll Wisconsin, Dept Biochem, 8701 Watertown Plank Rd, Milwaukee, WI 53226 USA.
EM rgundry@mcw.edu
FU Innovation Center at the Medical College of Wisconsin; Maryland Stem
Cell Research Fund; NIH, National Institute on Aging; NIH Induced
Pluripotent Stem Cell Center (NiPSCC); [4R00HL094708-03]
FX The authors are supported by 4R00HL094708-03 (R.L.G.), the Innovation
Center at the Medical College of Wisconsin (R.L.G.), Maryland Stem Cell
Research Fund Postdoctoral Fellowship (P.W.B.), the Intramural Research
Program of the NIH, National Institute on Aging (K.R.B.), and NIH
Induced Pluripotent Stem Cell Center (NiPSCC) Pilot Study Award
(K.R.B.).
NR 104
TC 11
Z9 11
U1 1
U2 22
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1615-9853
J9 PROTEOMICS
JI Proteomics
PD OCT
PY 2011
VL 11
IS 20
SI SI
BP 3947
EP 3961
DI 10.1002/pmic.201100100
PG 15
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 841DD
UT WOS:000296491800002
PM 21834136
ER
PT J
AU Mercer, BM
Spong, CY
AF Mercer, Brian M.
Spong, Catherine Y.
TI Indicated Late Preterm and Early-Term Births Introduction
SO SEMINARS IN PERINATOLOGY
LA English
DT Editorial Material
C1 [Mercer, Brian M.] Soc Maternal Fetal Med, Washington, DC 20024 USA.
[Mercer, Brian M.] Case Western Reserve Univ, Metrohlth Med Ctr, Cleveland, OH 44109 USA.
[Spong, Catherine Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, NIH, Bethesda, MD 20892 USA.
RP Mercer, BM (reprint author), Soc Maternal Fetal Med, Washington, DC 20024 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0146-0005
J9 SEMIN PERINATOL
JI Semin. Perinatol.
PD OCT
PY 2011
VL 35
IS 5
BP 245
EP 245
DI 10.1053/j.semperi.2011.05.001
PG 1
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 834KC
UT WOS:000295957200001
PM 21962620
ER
PT J
AU Acharya, P
Dogo-Isonagie, C
LaLonde, JM
Lam, SN
Leslie, GJ
Louder, MK
Frye, LL
Debnath, AK
Greenwood, JR
Luongo, TS
Martin, L
Watts, KS
Hoxie, JA
Mascola, JR
Bewley, CA
Kwong, PD
AF Acharya, Priyamvada
Dogo-Isonagie, Cajetan
LaLonde, Judith M.
Lam, Son N.
Leslie, George J.
Louder, Mark K.
Frye, Leah L.
Debnath, Asim K.
Greenwood, Jeremy R.
Luongo, Timothy S.
Martin, Loic
Watts, K. Shawn
Hoxie, James A.
Mascola, John R.
Bewley, Carole A.
Kwong, Peter D.
TI Structure-Based Identification and Neutralization Mechanism of Tyrosine
Sulfate Mimetics That Inhibit HIV-1 Entry
SO ACS CHEMICAL BIOLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; CORECEPTOR-BINDING-SITE; PROTEIN-PROTEIN
INTERACTIONS; GP120 ENVELOPE GLYCOPROTEIN; SMALL-MOLECULE INHIBITOR;
CCR5 N-TERMINUS; RECEPTOR-BINDING; LINKED GLYCAN; CD4; ANTIBODY
AB Tyrosine sulfate-mediated interactions play an important role in HIV-1 entry. After engaging the CD4 receptor at the cell surface, the HIV-1 gp120 glycoprotein binds to the CCR5 co-receptor via an interaction that requires two tyrosine sulfates, at positions 10 and 14 in the CCRS-N terminus. Building on previous structure determinations of this interaction, here we report the targeting of these tyrosine sulfate binding sites for drug design through in silica screening of Small molecule libraries, identification of lead compounds, and characterization of biological activity. A class of tyrosine sulfonate-mimicking small molecules containing a "phenyl sulfonate-linker-aromatic" motif was identified that specifically inhibited binding of gp120 to the CCRS-N terminus as well as to sulfated antibodies that recognize the co-receptor binding region on gp120. The most potent of these compounds bound gp120 with low micromolar affinity and its CD4-induced conformation with K(D)'s as tight as similar to 50 nM. Neutralization experiments suggested the targeted site to be conformationally inaccessible prior to CD4 engagement. Primary HIV-1 isolates were weakly neutralized, preincubation with soluble CD4 enhanced neutralization, and engineered isolates with increased dependence on the N terminus of CCR5 or with reduced, conformational barriers were neutralized with IC(50) values as low as similar to 1 mu M. These results reveal the potential of targeting the tyrosine sulfate interactions of HIV-1 and provide insight into how mechanistic barriers, evolved by HIV-1 to evade antibody recognition, also restrict small-molecule-mediated neutralization.
C1 [Dogo-Isonagie, Cajetan; Lam, Son N.; Bewley, Carole A.] NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Acharya, Priyamvada; Louder, Mark K.; Luongo, Timothy S.; Mascola, John R.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[LaLonde, Judith M.] Bryn Mawr Coll, Dept Chem, Bryn Mawr, PA 19010 USA.
[Leslie, George J.; Hoxie, James A.] Univ Penn, Dept Med, Div Hematol Oncol, Philadelphia, PA 19104 USA.
[Frye, Leah L.; Greenwood, Jeremy R.; Watts, K. Shawn] Schrodinger LLC, Portland, OR 97204 USA.
[Debnath, Asim K.] New York Blood Ctr, Lab Mol Modeling & Drug Design, Lindsley F Kimball Res Inst, New York, NY 10021 USA.
[Martin, Loic] CEA, iBiTecS, Serv Ingn Mol Prot, F-91191 Gif Sur Yvette, France.
RP Bewley, CA (reprint author), NIDDK, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM caroleb@mail.nih.gov; pdkwong@nih.gov
FU NIH (NIDDK); NIH (NIAID); European Community [LSHP-2003-503558]; French
National Agency of Research [ANR-07-EMPB-019-01]; NIH [GM 56550];
Intramural AIDS Research Fellowship
FX We thank J. Lloyd for HR-MS data, members of the Structural Biology
Section and Structural Bioinformatics Core at the NIH Vaccine Research
Center for comments on the manuscript, J. Stuckey for assistance with
figures, and I. Georgiev for discussions on statistical methods. sCD4
and Cf2Th cells stably expressing human CD4 and CCR5 were obtained
through the AIDS Research and Reference Reagent Program, Division of
AIDS, NIAID, NIH. Support for this work was provided by the Intramural
AIDS Targeted Antiviral Program (CAB. and P.D.K.), by the Intramural
Research Program of the NIH (NIDDK and NIAID), by grants from the
European Community's Sixth Framework programme (EMPRO) under grant
agreement no. LSHP-2003-503558, by a grant from the French National
Agency of Research (ANR-07-EMPB-019-01) (L.M.) and by a grant from the
NIH (GM 56550) (J.M.L.). C.D.-I. was supported by an Intramural AIDS
Research Fellowship.
NR 42
TC 20
Z9 20
U1 0
U2 8
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1554-8929
J9 ACS CHEM BIOL
JI ACS Chem. Biol.
PD OCT
PY 2011
VL 6
IS 10
BP 1069
EP 1077
DI 10.1021/cb200068b
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 837MO
UT WOS:000296208100013
PM 21793507
ER
PT J
AU Phan, VTM
Rabaa, MA
Vinh, H
Holmes, EC
Nguyen, VMH
Vinh, NT
Phuong, LT
Tham, NT
Phan, VBB
Campbell, JI
Farrar, J
Baker, S
AF Phan Vu Tra My
Rabaa, Maia A.
Ha Vinh
Holmes, Edward C.
Nguyen Van Minh Hoang
Nguyen Thanh Vinh
Lei Thi Phuong
Nguyen Thi Tham
Phan Van Be Bay
Campbell, James I.
Farrar, Jeremy
Baker, Stephen
TI The Emergence of Rotavirus G12 and the Prevalence of Enteric Viruses in
Hospitalized Pediatric Diarrheal Patients in Southern Vietnam
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID SPATIOTEMPORAL DYNAMICS; DEMOGRAPHIC-VARIABILITY; MOLECULAR
EPIDEMIOLOGY; ACUTE GASTROENTERITIS; SEQUENCE-ANALYSIS; CHILDREN;
SURVEILLANCE; HANOI; VACCINATION; INFECTIONS
AB Diarrhea is a major cause of childhood morbidity and mortality in developing countries, and the majority of infections are of viral etiology. We aimed to compare the etiological prevalence of the major enteric viruses in an urban and a rural setting in southern Vietnam. We simultaneously screened fecal specimens from 362 children in Ho Chi Minh City and Dong Thap province that were hospitalized with acute diarrhea over a 1-month-long period for four viral gastrointestinal pathogens. Rotavirus was the most common pathogen identified, but there was a differential prevalence of rotavirus and norovirus between the urban and rural locations. Furthermore, rotavirus genotyping and phylogenetic analysis again differentiated the genotypes by the sampling location. Our data show a disproportional distribution of enteric viral pathogens in urban and rural locations, and we provide evidence of continual importation of new rotavirus strains into southern Vietnam and report the emergence of rotavirus genotype G12.
C1 [Phan Vu Tra My; Nguyen Van Minh Hoang; Nguyen Thanh Vinh; Campbell, James I.; Farrar, Jeremy; Baker, Stephen] Univ Oxford, Enter Infect Grp, Wellcome Trust Major Overseas Programme, Hosp Trop Dis,Clin Res Unit, Ho Chi Minh City, Vietnam.
[Rabaa, Maia A.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Lei Thi Phuong; Nguyen Thi Tham; Phan Van Be Bay] Dong Thap Prov Hosp, Infect Ward, Dong Thap, Vietnam.
Univ Oxford, Ctr Trop Dis, Oxford, England.
[Ha Vinh] Hosp Trop Dis, Pediat Ward B, Ho Chi Minh City, Vietnam.
RP Baker, S (reprint author), Univ Oxford, Enter Infect Grp, Wellcome Trust Major Overseas Programme, Hosp Trop Dis,Clin Res Unit, 190 Ben Ham Tu,Dist 5, Ho Chi Minh City, Vietnam.
EM mypvt@oucru.org; maia.rabaa@gmail.com; vinhh@oucru.org; ech15@psu.edu;
hoangnvm@oucru.org; vinhnt@oucru.org; jcampbell@oucru.org;
jfarrar@oucru.org; sbaker@oucru.org
OI Rabaa, Maia/0000-0003-0529-2228; Farrar, Jeremy/0000-0002-2700-623X;
Holmes, Edward/0000-0001-9596-3552
FU Wellcome Trust, Euston Road, London, United Kingdom; Oak Foundation
through Oxford University; National Science Foundation
FX This work is supported by The Wellcome Trust, Euston Road, London,
United Kingdom. S.B. is supported by an Oak Foundation Fellowship
through Oxford University. M.A.R. is supported by a National Science
Foundation Graduate Research Fellowship.
NR 37
TC 0
Z9 0
U1 0
U2 4
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
EI 1476-1645
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD OCT
PY 2011
VL 85
IS 4
BP 768
EP 775
DI 10.4269/ajtmh.2011.11-0364
PG 8
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 833QB
UT WOS:000295898900033
ER
PT J
AU Kemp, CD
Ripley, RT
Mathur, A
Steinberg, SM
Nguyen, DM
Fojo, T
Schrump, DS
AF Kemp, Clinton D.
Ripley, R. Taylor
Mathur, Aarti
Steinberg, Seth M.
Nguyen, Dao M.
Fojo, Tito
Schrump, David S.
TI Pulmonary Resection for Metastatic Adrenocortical Carcinoma: The
National Cancer Institute Experience
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID ADRENAL-CORTICAL CARCINOMA; SERIES
AB Background. Adrenocortical carcinoma (ACC) is a rare neoplasm with a high propensity for locoregional recurrences and distant metastases for which there are no effective systemic therapies. This study was undertaken to determine outcomes of patients undergoing pulmonary metastasectomy for ACC.
Methods. A single-institution retrospective review was performed of patients undergoing pulmonary metastasectomy for ACC from 1979 to 2010.
Results. Twenty-six patients underwent 60 pulmonary metastasectomies. Fifteen patients (58%) underwent unilateral thoracotomy, 6 (23%) had staged thoracotomies, and 5 (19%) underwent median sternotomy as the initial thoracic procedure. Median number and size of lesions were 6 and 2 cm, respectively. Twenty-three patients (88%) were rendered free of disease in the lung, and 14 (54%) were rendered completely free of disease. Median overall and 5-year actuarial survivals from initial pulmonary metastasectomy were 40 months and 41%, respectively, with a median potential follow-up of 120 months. Median recurrence-free survival (RFS) and 5-year RFS for ipsilateral thoracic recurrences were 6 months, and 25%, respectively. The median RFS in the contralateral thorax was 5 months. Time to first recurrence after adrenalectomy and T stage of the primary tumor, but not adjuvant or neoadjuvant chemotherapy, were associated with increased overall survival after pulmonary metastasectomy.
Conclusions. This study represents the most comprehensive review of outcomes of patients undergoing pulmonary metastasectomy for ACC. Given the lack of effective systemic therapies, pulmonary metastasectomy may be beneficial in properly selected patients. (Ann Thorac Surg 2011;92:1195-201) (C) 2011 by The Society of Thoracic Surgeons
C1 [Schrump, David S.] NCI, Sect Thorac Oncol, Surg Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
NCI, Biostat & Data Management Sect, Off Clin Director, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Schrump, DS (reprint author), NCI, Sect Thorac Oncol, Surg Branch, Ctr Canc Res,NIH, 10 Ctr Dr,Rm 4-3942,MSC 1201, Bethesda, MD 20892 USA.
EM david_schrump@nih.gov
NR 17
TC 14
Z9 15
U1 0
U2 3
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 OCT
PY 2011
VL 92
IS 4
BP 1195
EP 1200
DI 10.1016/j.athoracsur.2011.05.013
PG 6
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 833ZI
UT WOS:000295924400016
PM 21958764
ER
PT J
AU Amirghofran, AA
Karimi, A
Emaminia, A
Sharifkazemi, MB
Salaminia, S
AF Amirghofran, Ahmad Ali
Karimi, Ashkan
Emaminia, Abbas
Sharifkazemi, Mohammad Bagher
Salaminia, Shirvan
TI Brucellosis Relapse Causing Prosthetic Valve Endocarditis and Aortic
Root Infective Pseudoaneurysm
SO ANNALS OF THORACIC SURGERY
LA English
DT Editorial Material
ID ABSCESS
AB We report a previously treated case of brucellosis and aortic root replacement, which became complicated by prosthetic valve endocarditis and a massive aortic root pseudoaneurysm. Preoperative blood and intraoperative pseudoaneurysm wall cultures were positive for Brucella, and the patient was managed successfully with a combination of surgical and medical treatment. Brucella endocarditis is further discussed. (Ann Thorac Surg 2011;92:e77-9) (C) 2011 by The Society of Thoracic Surgeons
C1 [Karimi, Ashkan] Univ Florida, Div Thorac & Cardiovasc Surg, Gainesville, FL 32610 USA.
Shiraz Univ Med Sci, Div Cardiothorac Surg, Shiraz, Iran.
NIH, Cardiothorac Surg Res Program, Ctr Heart, Bethesda, MD 20892 USA.
Shiraz Univ Med Sci, Div Cardiol, Dept Med, Shiraz, Iran.
RP Karimi, A (reprint author), Univ Florida, Div Thorac & Cardiovasc Surg, 1600 Archer Rd,Room NG-32, Gainesville, FL 32610 USA.
EM ashkan.karimi@surgery.ufl.edu
NR 10
TC 4
Z9 4
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 OCT
PY 2011
VL 92
IS 4
BP E77
EP E79
DI 10.1016/j.athoracsur.2011.03.144
PG 3
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 833ZI
UT WOS:000295924400004
PM 21958835
ER
PT J
AU Remaley, AT
AF Remaley, A. T.
TI "Who's on First": Determining the roster for the key players in the
reverse cholesterol transport pathway
SO ATHEROSCLEROSIS
LA English
DT Editorial Material
DE ABCA1; SR-BI; Atherosclerosis; Cholesterol efflux; High density
lipoproteins
ID DENSITY-LIPOPROTEIN CHOLESTEROL; SCAVENGER RECEPTOR BI; IN-VIVO; SR-BI;
ABCA1; HDL; DEFICIENT; SECRETION; DISEASE; ABCG1
C1 NHLBI, Lipoprot Metab Sect, Cardiopulm Branch, NIH, Bethesda, MD 20892 USA.
RP Remaley, AT (reprint author), NHLBI, Lipoprot Metab Sect, Cardiopulm Branch, NIH, Bldg 10,Room 2C-433,10 Ctr Dr, Bethesda, MD 20892 USA.
EM aremaley1@cc.nih.gov
FU Intramural NIH HHS [Z01 CL010303-07]
NR 18
TC 1
Z9 1
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0021-9150
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD OCT
PY 2011
VL 218
IS 2
BP 287
EP 289
DI 10.1016/j.atherosclerosis.2011.06.037
PG 3
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 836WJ
UT WOS:000296147600041
PM 21798543
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. Craig
Bluemke, David A.
Harrington, Anita
O'Leary, Daniel H.
Yanez, N. David
TI Associations of cardiovascular risk factors, carotid intima-media
thickness and left ventricular mass with inter-adventitial diameters of
the common carotid artery: The Multi-Ethnic Study of Atherosclerosis
(MESA)
SO ATHEROSCLEROSIS
LA English
DT Article
DE Carotid arteries; Ultrasonics; Hypertrophy; Magnetic resonance imaging;
Remodeling; Risk factors; Left ventricle
ID BLOOD-PRESSURE; OLDER-ADULTS; ENLARGEMENT; POPULATION; QUANTITATION;
COMMUNITIES; DISEASE; HEALTH
AB Background: Common carotid artery inter-adventitial diameter (IAD) and intima-media thickness (IMT) are measurable by ultrasound. IAD may be associated with left ventricular mass (LV mass) while IMT is a marker of subclinical atherosclerosis. It is not clear if IAD is associated with LV mass after accounting for IMT and traditional cardiovascular risk factors.
Methods: IAD and IMT were measured on participants of the Multi-Ethnic Study of Atherosclerosis ( MESA) IMT progression study. A total of 5641 of the originally enrolled 6814 MESA participants were studied. LV mass was measured by magnetic resonance imaging. Multivariable linear regression was used with IAD as the outcome and adjustment for risk factors, as well as IMT and LV mass.
Results: Traditional cardiovascular risk factors, height, weight and ethnicity were significantly associated with IAD. After adjustment for risk factors, a 1 mm difference in IMT was associated with a 1.802 mm (95% CI: 1.553, 2.051) higher mean IAD. A 1 g difference in LV mass was associated with a 0.006 mm (95% CI: 0.005, 0.007) higher mean IAD. After adjusting for cardiovascular risk factors and IMT, a 1 g difference in LV mass was associated with a 0.006 mm (95% CI: 0.005, 0.008) higher mean IAD for women and 0.004 mm (95% CI: 0.003, 0.005) higher IAD for men.
Conclusions: Inter-adventitial diameters are associated with left ventricular mass after adjusting for cardiovascular risk factors and IMT. IAD might serve as a surrogate for left ventricular mass and have predictive value for cardiovascular outcomes. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Polak, Joseph F.; Harrington, Anita; O'Leary, Daniel H.] Tufts Med Ctr, Dept Radiol, Boston, MA 02111 USA.
[Wong, Quenna; Johnson, W. Craig; Yanez, N. David] Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Seattle, WA 98115 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
RP Polak, JF (reprint author), Tufts Med Ctr, Dept Radiol, 800 Washington St,Box 299, Boston, MA 02111 USA.
EM jpolak@tuftsmedicalcenter.org
OI Bluemke, David/0000-0002-8323-8086
FU [N01-HC-95159]; [N01-HC-95165]; [N01-HC-95167]; [R01 HL069003]; [R01
HL081352]
FX The authors would like to thank the investigators, the staff, and the
participants of the Multi-Ethnic Study of Atherosclerosis, MESA for
their valuable contributions. This research was supported by Contracts
N01-HC-95159 through N01-HC-95165 and N01-HC-95167 as well as R01
HL069003 and R01 HL081352.
NR 22
TC 15
Z9 17
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0021-9150
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD OCT
PY 2011
VL 218
IS 2
BP 344
EP 349
DI 10.1016/j.atherosclerosis.2011.05.033
PG 6
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 836WJ
UT WOS:000296147600050
PM 21726862
ER
PT J
AU Xu, P
Alam, MM
Kalsy, A
Charles, RC
Calderwood, SB
Qadri, F
Ryan, ET
Kovac, P
AF Xu, Peng
Alam, Mohammad Murshid
Kalsy, Anuj
Charles, Richelle C.
Calderwood, Stephen B.
Qadri, Firdausi
Ryan, Edward T.
Kovac, Pavol
TI Simple, Direct Conjugation of Bacterial O-SP-Core Antigens to Proteins:
Development of Cholera Conjugate Vaccines
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID SQUARIC ACID DIESTER; VIBRIO-CHOLERAE; SEROTYPE INABA; DETOXIFIED
LIPOPOLYSACCHARIDE; ANTIBODY-RESPONSE; DIETHYL SQUARATE; SIDE-CHAIN;
POLYSACCHARIDE; INFECTION; CARRIER
AB Bacterial O-SP core antigens can be conjugated to proteins in the same, simple way as synthetic, linker-equipped carbohydrates by applying squaric acid chemistry. Introduction of spacers (linkers) to either O-SP core antigens or protein carriers, which is involved in commonly applied protocols, is not required. The newly developed method described here consists of preparation of a squaric acid monoester derivative of O-SP core antigen, utilizing the amino group inherent in the core, and reaction of the monoester with the carrier protein. The intermediate monoester can be easily purified; its conjugation can be monitored by SELDI-TOF mass spectrometry and, thus, readily controlled, since the conjugation can be terminated when the desired carbohydrate protein ratio is reached. Here, we describe production of conjugates containing the O-SP core antigen of Vibrio cholerae 01, the major cause of cholera, a severe dehydrating diarrheal disease of humans. The resultant products are recognized by convalescent phase sera from patients recovering from cholera in Bangladesh, and anti-O-SP-core-protein responses correlate with plasma antilipopolysaccharide and vibriocidal responses, which are the primary markers of protection from cholera. The results suggest that such conjugates have potential as vaccines for cholera and other bacterial diseases.
C1 [Alam, Mohammad Murshid; Kalsy, Anuj; Charles, Richelle C.; Calderwood, Stephen B.; Ryan, Edward T.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Xu, Peng; Kovac, Pavol] NIDDK, LBC, NIH, Bethesda, MD 20892 USA.
[Alam, Mohammad Murshid; Qadri, Firdausi] Int Ctr Diarrhoeal Dis Res, Dhaka 1000, Bangladesh.
[Calderwood, Stephen B.; Ryan, Edward T.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Ryan, Edward T.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Ryan, ET (reprint author), Massachusetts Gen Hosp, Div Infect Dis, 55 Fruit St, Boston, MA 02114 USA.
EM etryan@partners.org; kpn@helix.nih.gov
RI Xu, Peng/K-7036-2012; Kovac, Pavol/B-8813-2008
OI Kovac, Pavol/0000-0001-5044-3449
FU NIH, NIDDK; International Centre for Diarrhoeal Disease Research, Dhaka,
Bangladesh (ICDDR, B); Fogarty International Center (FIC) [TW05572]
FX This research was supported by the Intramural Research Program of the
NIH, NIDDK, as well the International Centre for Diarrhoeal Disease
Research, Dhaka, Bangladesh (ICDDR, B), and NIAID AI077883 (ETR),
AI058935 (SBC, FQ), AI089721 (RCC), and the Fogarty International Center
(FIC) TW05572 (MMA, FQ).
NR 35
TC 18
Z9 18
U1 0
U2 10
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 OCT
PY 2011
VL 22
IS 10
BP 2179
EP 2185
DI 10.1021/bc2001984
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 833WE
UT WOS:000295915100034
PM 21899371
ER
PT J
AU Hildebrandt, GC
Fazekas, T
Lawitschka, A
Bertz, H
Greinix, H
Halter, J
Pavletic, SZ
Holler, E
Wolff, D
AF Hildebrandt, G. C.
Fazekas, T.
Lawitschka, A.
Bertz, H.
Greinix, H.
Halter, J.
Pavletic, S. Z.
Holler, E.
Wolff, D.
TI Diagnosis and treatment of pulmonary chronic GVHD: report from the
consensus conference on clinical practice in chronic GVHD
SO BONE MARROW TRANSPLANTATION
LA English
DT Review
DE chronic GVHD; allo-SCT; lung; obliterative bronchiolitis; treatment
ID VERSUS-HOST-DISEASE; STEM-CELL TRANSPLANTATION;
BONE-MARROW-TRANSPLANTATION; BRONCHIOLITIS OBLITERANS SYNDROME; TOTAL
LYMPHOID IRRADIATION; HIGH-RESOLUTION CT; WORKING GROUP-REPORT;
LONG-TERM SURVIVORS; IDIOPATHIC PNEUMONIA SYNDROME; OBSTRUCTIVE AIRWAY
DISEASE
AB This consensus statement established under the auspices of the German working group on BM and blood stem cell transplantation (DAG-KBT), the German Society of Hematology and Oncology (DGHO), the Austrian Stem Cell Transplant Working Group, the Swiss Blood Stem Cell Transplantation Group (SBST) and the German-Austrian Pediatric Working Group on SCT (Pad-Ag-KBT) summarizes current evidence for diagnosis, immunosuppressive and supportive therapy to provide practical guidelines for the care and treatment of patients with pulmonary manifestations of chronic GVHD (cGVHD). Pulmonary cGVHD can present with obstructive and/or restrictive changes. Disease severity ranges from subclinical pulmonary function test (PFT) impairment to respiratory insufficiency with bronchiolitis obliterans being the only pulmonary complication currently considered diagnostic of cGVHD. Early diagnosis may improve clinical outcome, and regular post-transplant follow-up PFTs are recommended. Diagnostic work-up includes high-resolution computed tomography, bronchoalveolar lavage and histology. Topical treatment is based on inhalative steroids plus beta-agonists. Early addition of azithromycin is suggested. Systemic first-line treatment consists of corticosteroids plus, if any, continuation of other immunosuppressive therapy. Second-line therapy and beyond includes extracorporeal photopheresis, mammalian target of rapamycin inhibitors, mycophenolate, etanercept, imatinib and TLI, but efficacy is limited. Clinical trials are urgently needed to improve understanding and treatment of this deleterious complication. Bone Marrow Transplantation (2011) 46, 1283-1295; doi: 10.1038/bmt.2011.35; published online 28 March 2011
C1 [Hildebrandt, G. C.] LSUHSC Shreveport, Feist Weiller Canc Ctr, Blood & Marrow Transplant Program, Shreveport, LA 71130 USA.
[Hildebrandt, G. C.; Holler, E.; Wolff, D.] Univ Regensburg, Med Ctr, Dept Hematol & Oncol, Regensburg, Germany.
[Fazekas, T.; Lawitschka, A.] St Anna Childrens Hosp, Childrens Canc Res Inst, A-1090 Vienna, Austria.
[Bertz, H.] Univ Freiburg, Med Ctr, Dept Haematol & Oncol, D-7800 Freiburg, Germany.
[Greinix, H.] Med Univ Vienna, Dept Internal Med 1, Vienna, Austria.
[Halter, J.] Univ Basel Hosp, Dept Hematol, CH-4031 Basel, Switzerland.
[Pavletic, S. Z.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Hildebrandt, GC (reprint author), LSUHSC Shreveport, Feist Weiller Canc Ctr, Blood & Marrow Transplant Program, 1501 Kings Highway, Shreveport, LA 71130 USA.
EM ghilde@lsuhsc.edu
RI Halter, Joerg/C-9487-2012
FU Jose Carreras Foundation 'Competence center GVHD Regensburg'
FX We thank all participating centers of conferences and surveys, which
included participants from the transplant centers in Augsburg, Basel,
Berlin, Cologne, Dresden, Duesseldorf, Erlangen, Essen, Freiburg,
Greifswald, Hamburg, Hannover, Heidelberg, Jena, Kiel, Leipzig, Linz,
Mainz, Munster, Munich, Nantes, Nuernberg, Oldenburg, Paris, Regensburg,
Rostock, Tuebingen, Ulm, Vienna, Wiesbaden and Wuerzburg. We thank Anna
Hackl for evaluating the survey on treatment of cGVHD. The conference
was supported by the Jose Carreras Foundation project 'Competence center
GVHD Regensburg'. We convey our special thanks to Dr Nicolai Kittan for
his critical review of the manuscript and figure design.
NR 127
TC 62
Z9 63
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2011
VL 46
IS 10
BP 1283
EP 1295
DI 10.1038/bmt.2011.35
PG 13
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 838HR
UT WOS:000296279000001
PM 21441964
ER
PT J
AU Norman, BC
Jacobsohn, DA
Williams, KM
Au, BKC
Au, MA
Lee, SJ
Moravec, CK
Chien, JW
AF Norman, B. C.
Jacobsohn, D. A.
Williams, K. M.
Au, B. K. C.
Au, M. A.
Lee, S. J.
Moravec, C. K.
Chien, J. W.
TI Fluticasone, azithromycin and montelukast therapy in reducing
corticosteroid exposure in bronchiolitis obliterans syndrome after
allogeneic hematopoietic SCT: a case series of eight patients
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE bronchiolitis obliterans syndrome; corticosteroids; steroid sparing; FAM
ID STEM-CELL TRANSPLANTATION; VERSUS-HOST-DISEASE;
BONE-MARROW-TRANSPLANTATION; OBSTRUCTIVE LUNG-DISEASE; ADVERSE EVENTS;
RISK-FACTORS; EPIDEMIOLOGY; ADULTS
AB Bronchiolitis obliterans syndrome (BOS) is a devastating pulmonary complication affecting long-term survivors of allogeneic hematopoietic cell transplantation. Treatment of BOS with prolonged courses of high dose corticosteroids is often associated with significant morbidity. Reducing the exposure to corticosteroids may reduce treatment-related morbidity. Our institution has recently begun to treat patients with emerging therapies in an effort to diminish corticosteroid exposure. We retrospectively reviewed the 6-month corticosteroid exposure, lung function and failure rates in eight patients with newly diagnosed BOS who were treated with a combination of fluticasone, azithromycin and montelukast (FAM) and a rapid corticosteroid taper. These patients were compared with 14 matched historical patients who received high-dose corticosteroids, followed by a standard taper. The median 6-month prednisone exposure in FAM-treated patients was 1819 mg (0-4036 mg) compared with 7163 mg (6551-7829 mg) in the control group (P = 0.002). The median forced expiratory volume in 1s (FEV(1)) change in FAM-treated patients was 2% (-3 to 4%] compared with 1% (-4 to 5%) in the control group (P = 1.0). Prednisone exposure in FAM patients was one quarter that of a retrospective-matched group of patients, with minimal change in median FEV(1), suggesting that BOS may be spared of the morbidities associated with long-term corticosteroid use by using alternative agents with less side effects. Bone Marrow Transplantation (2011) 46, 1369-1373; doi: 10.1038/bmt.2010.311; published online 6 December 2010
C1 [Lee, S. J.; Moravec, C. K.; Chien, J. W.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98109 USA.
[Norman, B. C.] Univ Washington, Dept Med, Affiliated Hosp, Seattle, WA USA.
[Jacobsohn, D. A.] Northwestern Univ, Sch Med, Stem Cell Transplant Program, Chicago, IL USA.
[Williams, K. M.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Au, B. K. C.] Univ Hawaii, John A Burns Sch Med, Honolulu, HI 96822 USA.
[Au, M. A.] Univ Hawaii, Canc Res Ctr, Dept Epidemiol, Honolulu, HI 96813 USA.
RP Chien, JW (reprint author), Fred Hutchinson Canc Res Ctr, Div Clin Res, 1100 Fairview Ave N,D5-280, Seattle, WA 98109 USA.
EM jchien@fhcrc.org
FU National Institutes of Health [HL088201, AI083028]
FX Financial disclosure: This work was supported in part by the National
Institutes of Health Grants HL088201 and AI083028.
NR 23
TC 29
Z9 31
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD OCT
PY 2011
VL 46
IS 10
BP 1369
EP 1373
DI 10.1038/bmt.2010.311
PG 5
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 838HR
UT WOS:000296279000014
PM 21132024
ER
PT J
AU Ghanima, W
Junker, P
Hasselbalch, HC
Boiocchi, L
Geyer, JT
Feng, XM
Gudbrandsdottir, S
Orazi, A
Bussel, JB
AF Ghanima, Waleed
Junker, Peter
Hasselbalch, Hans Carl
Boiocchi, Leonardo
Geyer, Julia T.
Feng, Xingmin
Gudbrandsdottir, Sif
Orazi, Attilio
Bussel, James B.
TI Fibroproliferative activity in patients with immune thrombocytopenia
(ITP) treated with thrombopoietic agents
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE platelets; myelofibrosis; transforming growth factor beta (TGF-beta);
hepatocyte growth factor; procollagen
ID HEPATOCYTE GROWTH-FACTOR; BONE-MARROW RETICULIN; CHRONIC
MYELOPROLIFERATIVE DISORDERS; CONTROLLED-TRIAL; DOUBLE-BLIND;
FACTOR-BETA; PURPURA; ROMIPLOSTIM; ELTROMBOPAG; FIBROSIS
AB This study assessed the grade of bone marrow (BM) fibrosis and its association with a seromarker for collagen-III formation and fibrosis-related cytokines in 25 immune thrombocytopenia (ITP) patients treated with thrombopoietin receptor agonists (Tpo-RA) who had at least one BM biopsy. Assessment of 8 pre- and on-treatment BM biopsies revealed statistically significant increases in reticulin. Reticulin in biopsies performed after a median of 1.4 years of treatment was graded: MF-0 in 3 (12%), MF-1 in 19 (76%), MF-2 in 2 (8%) and MF-3 in 1 (4%). No cytogenetic or flow-cytometric abnormalities were detected. Median pretreatment Procollagen III N-propeptide (PIIINP) (6.6 mu g/l) was significantly higher than on-treatment levels (5.6 mu g/l); both were higher than controls (3.4 mu g/l; P < 0.001). PIIINP was negatively correlated with treatment duration (r = -0.49) suggesting a decelerated reticulin production over time. There was a trend towards an association between grade of reticulin and PIIINP. Transforming growth factor (GF)-beta and basic-Fibroblast GF were not different between patients and controls but Hepatocyte GF (HGF), an anti-fibrotic cytokine, was significantly elevated in patients. In conclusion, low-grade BM reticulin fibrosis is seen in most ITP patients on Tpo-RA. The novel findings of decreasing PIIINP and elevated HGF need further investigation to explore their significance in BM fibrogenesis.
C1 [Ghanima, Waleed; Bussel, James B.] Cornell Univ, Weill Med Coll, Dept Pediat Hematol Oncol, New York, NY 10065 USA.
[Ghanima, Waleed] Ostfold Hosp Trust Fredrikstad, Dept Med, Fredrikstad, Norway.
[Junker, Peter] Odense Univ Hosp, Dept Rheumatol C, DK-5000 Odense, Denmark.
[Hasselbalch, Hans Carl; Gudbrandsdottir, Sif] Roskilde Hosp, Dept Hematol Oncol, Roskilde, Denmark.
[Boiocchi, Leonardo; Geyer, Julia T.; Orazi, Attilio] Weill Cornell Med Coll, Dept Pathol & Lab Med, New York, NY USA.
[Boiocchi, Leonardo] Univ Milan, Sch Med, Dept Med,Pathol Unit, Fdn IRCCS Ca Granda Osped Maggiore Policlin, Milan, Italy.
[Feng, Xingmin] NHLBI, NIH, Bethesda, MD 20892 USA.
[Gudbrandsdottir, Sif] Rigshosp, Copenhagen Univ Hosp, Dept Rheumatol, Inst Inflammat Res, DK-2100 Copenhagen, Denmark.
RP Ghanima, W (reprint author), Cornell Univ, Weill Med Coll, Dept Pediat Hematol Oncol, New York, NY 10065 USA.
EM wghanima@c2i.net
OI Boiocchi, Leonardo/0000-0001-5188-6217
FU Amgen; GSK; Eisai; Shionogi
FX W.G has received research grants from Amgen, and received honorariums
for from Amgen and GlaxoSmithKline (GSK) whose products were studied in
the present report. S.G. has received research funding from GSK and
Amgen. J.B.B currently receives clinical research support from the
following companies: Amgen, GSK, Eisai, and Shionogi and has
participated in Advisory Boards for Amgen, GSK, and Eisai. His family
owns stock in Amgen and GSK.
NR 35
TC 15
Z9 15
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD OCT
PY 2011
VL 155
IS 2
BP 248
EP 255
DI 10.1111/j.1365-2141.2011.08845.x
PG 8
WC Hematology
SC Hematology
GA 835VD
UT WOS:000296063400011
PM 21902682
ER
PT J
AU Herrero, R
Wacholder, S
Rodriguez, AC
Solomon, D
Gonzalez, P
Kreimer, AR
Porras, C
Schussler, J
Jimenez, S
Sherman, ME
Quint, W
Schiller, JT
Lowy, DR
Schiffman, M
Hildesheim, A
AF Herrero, Rolando
Wacholder, Sholom
Rodriguez, Ana C.
Solomon, Diane
Gonzalez, Paula
Kreimer, Aimee R.
Porras, Carolina
Schussler, John
Jimenez, Silvia
Sherman, Mark E.
Quint, Wim
Schiller, John T.
Lowy, Douglas R.
Schiffman, Mark
Hildesheim, Allan
CA Costa Rica Vaccine Trial Grp
TI Prevention of Persistent Human Papillomavirus Infection by an HPV16/18
Vaccine: A Community-Based Randomized Clinical Trial in Guanacaste,
Costa Rica
SO CANCER DISCOVERY
LA English
DT Article
ID CERVICAL-CANCER VACCINE; YOUNG-WOMEN; PARTICLE VACCINE; HPV TYPES;
CROSS-PROTECTION; BROAD-SPECTRUM; DOUBLE-BLIND; RISK; PCR; IMPACT
AB Target groups for human papillomavirus (HPV) vaccination are controversial. We evaluated vaccine efficacy (VE) against 1-year persistent infection, stratified by age and sexual behavior, among young women in Costa Rica. We randomized 7,466 healthy women 18 to 25 years of age to HPV16/18 or hepatitis A vaccine (follow-up, 50.4 months). According-to-protocol (ATP) cohorts included compliant HPV-negative women; intention-to-treat (ITT) included all randomized women. ATP VE was 90.9% (95% CI, 82.0-95.9) against HPV16/18 infections, 44.5% against HPV31/33/45 (95% CI, 17.5-63.1), and 12.4% (95% CI, -3.2 to 25.6) against any oncogenic infection. Overall ITT VE against HPV16/18 infections was 49.0%, but ATP and ITT VE almost reached 100% in year 4 of follow-up. ATP efficacy against HPV16/18 was similar by age, but ITT VE was greatest among youngest women (68.9% among those 18-19 years of age; 21.8% among those 24-25 years of age) and 79.8% among virgins. Among previously unexposed women, vaccination is highly efficacious against HPV16/18 and partially against HPV31/33/45. Vaccination is most effective in women and girls before they initiate sexual activity, with programmatic and individual decision implications.
SIGNIFICANCE: In an independent trial of the bivalent ASO4-adjuvanted HPV16/18 vaccine (Cervarix) conducted among young women in Costa Rica, we confirmed the high efficacy against HPV16/18 persistent infection and partial cross-protection against HPV31/33/45. Furthermore, efficacy data suggest that the benefit of HPV vaccination is maximal when the vaccine is given to young women before they initiate sexual activity. Cancer Discovery;1(5):408-19. (C) 2011 AACR.
C1 [Herrero, Rolando] Int Agcy Res Canc, Early Detect & Prevent Sect, F-69372 Lyon, France.
[Herrero, Rolando; Rodriguez, Ana C.; Gonzalez, Paula; Porras, Carolina; Jimenez, Silvia] Fdn Inst Costarricense Invest & Ensenanza Nutr &, Proyecto Epidemiol Guanacaste, San Jose, Costa Rica.
[Wacholder, Sholom; Kreimer, Aimee R.; Sherman, Mark E.; Schiffman, Mark; Hildesheim, Allan] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Solomon, Diane] NCI, Div Canc Prevent & Control, Bethesda, MD 20892 USA.
[Schiller, John T.; Lowy, Douglas R.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Schussler, John] Informat Management Syst IMS, Beltsville, MD USA.
[Quint, Wim] DDL Diagnost Lab, Voorburg, Netherlands.
RP Herrero, R (reprint author), Int Agcy Res Canc, Early Detect & Prevent Sect, 150 Cours Albert Thomas, F-69372 Lyon, France.
EM herreror@iarc.fr
RI Hildesheim, Allan/B-9760-2015; Kreimer, Aimee/H-1687-2015
OI Hildesheim, Allan/0000-0003-0257-2363;
FU NCI [N01-CP-11005]; NIH Office of Research on Women's Health
FX The Costa Rican Vaccine Trial is a longstanding collaboration between
investigators in Costa Rica and NCI. The trial is sponsored and funded
by NCI (N01-CP-11005) with support from the NIH Office of Research on
Women's Health and conducted in agreement with the Ministry of Health of
Costa Rica. The NCI and Costa Rica investigators are responsible for the
design and conduct of the study; collection, management, analysis, and
interpretation of the data; and preparation of the manuscript. Vaccine
was provided for our trial by GSK Biologicals, under a Clinical Trials
Agreement with NCI. GSK also provided support for aspects of the trial
associated with regulatory submission needs of the company under FDA
BB-IND 7920. D. R. Lowy and J.T. Schiller are named inventors on U. S.
government-owned HPV vaccine patents that are licensed to GSK and Merck,
and so are entitled to limited royalties as specified by federal law.
None of the other coauthors have any potential conflicts of interest to
report.
NR 32
TC 59
Z9 61
U1 2
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
J9 CANCER DISCOV
JI Cancer Discov.
PD OCT
PY 2011
VL 1
IS 5
BP 408
EP 419
DI 10.1158/2159-8290.CD-11-0131
PG 12
WC Oncology
SC Oncology
GA 836UX
UT WOS:000296140600019
PM 22586631
ER
PT J
AU Hsiao, YH
Deng, CX
Mason, JT
Chou, MC
Man, YG
AF Hsiao, Yi-Hsuan
Deng, Chuxia
Mason, Jeffrey T.
Chou, Ming-Chih
Man, Yan-gao
TI Hidden malignant cells within leukocyte aggregates: Seeds for invasive
and metastatic cancer?
SO CANCER EPIDEMIOLOGY
LA English
DT Article
DE Leukocyte aggregate; Myoepithelial cell; Pregnancy-associated breast
cancer; Tumor invasion; Tumor metastasis
ID BREAST-TUMOR INVASION; MAMMARY-TUMORS; MACROPHAGES; PROGRESSION;
HYPOTHESIS; PREGNANCY; TRIGGER; LAYERS
AB Background: Our previous studies revealed that leukocyte infiltration into aged or injured myoepithelial cell layers is a key trigger for breast tumor invasion and metastasis. Our current study further assessed the possibility that leukocyte aggregates may harbor detached individual tumor cell or clusters of tumor cells. Materials and methods: Tissue sections from patients with pregnancy-associated breast cancer (PABC) and controls were subjected to morphological and immunohistochemical assessment with a panel of leukocyte and tumor cell related markers. Results: A total of 63 leukocyte aggregates were detected in the 20 PABC cases studied. Of these, 55 (87%) were distributed within normal or hyperplastic lobules adjacent to invasive lesions. Over 70% of these leukocyte aggregates harbored detached individual tumor cell or cell clusters with malignant properties, including strong p53 positivity, elevated proliferation, reduced cell surface adhesion molecules, and cytological resemblance to adjacent invasive cancer cells. A significant number of these tumor cells or condensed chromosomes of mitotic tumor cells were observed to conjoin with the plasma membrane of leukocytes. Similar alterations were seen in leukocyte aggregates within the inter-lobular space and in non-PABC with a lower frequency. Conclusions: These findings suggest that leukocyte infiltration may trigger dissemination of tumor cells from their primary site, and that leukocyte aggregates may serve as a reservoir for disseminated tumor cells that may be physically dragged to distant sites by leukocytes during their migration. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Hsiao, Yi-Hsuan; Chou, Ming-Chih] Chung Shan Med Univ, Inst Med, Taichung, Taiwan.
[Hsiao, Yi-Hsuan] Changhua Christian Hosp, Dept Obstet & Gynecol, Changhua, Taiwan.
[Deng, Chuxia] NIDDK, Mammalian Genet Sect, GDDB, NIH, Bethesda, MD USA.
[Mason, Jeffrey T.; Man, Yan-gao] Armed Forces Inst Pathol, Dept Infect & Parasit Dis Pathol, Amer Registry Pathol, Washington, DC 20306 USA.
[Man, Yan-gao] Armed Forces Inst Pathol, Dept Gynecol & Breast Pathol, Washington, DC 20306 USA.
RP Chou, MC (reprint author), Chung Shan Med Univ, Inst Med, Taichung, Taiwan.
EM graduate@csmu.edu.tw; man@afip.osd.mil
RI deng, chuxia/N-6713-2016
FU Susan G. Komen Breast Cancer Foundation [BCTR 0706983]; US Military
Cancer Institute [2008-02]; Henry M. Jackson Foundation; Ministry of
Chinese Science and Technology Department [2006CB910505]
FX This study was supported in part by research grants BCTR 0706983 from
The Susan G. Komen Breast Cancer Foundation, 2008-02 from the US
Military Cancer Institute and Henry M. Jackson Foundation, and
2006CB910505 from the Ministry of Chinese Science and Technology
Department to Dr. Yan-gao Man.
NR 20
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 OCT
PY 2011
VL 35
IS 5
BP 475
EP 479
DI 10.1016/j.canep.2010.11.010
PG 5
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 837CB
UT WOS:000296167600014
PM 21292584
ER
PT J
AU Yao, XL
Remaley, AT
Levine, SJ
AF Yao, Xianglan
Remaley, Alan T.
Levine, Stewart J.
TI New Kids on the Block The Emerging Role of Apolipoproteins in the
Pathogenesis and Treatment of Asthma
SO CHEST
LA English
DT Article
ID MIMETIC PEPTIDE; A-I; REDUCES ATHEROSCLEROSIS; AIRWAY INFLAMMATION;
DENSITY-LIPOPROTEIN; ALZHEIMERS-DISEASE; CHOLESTEROL EFFLUX; MOUSE
MODEL; APOA-I; MICE
AB New treatments are needed for patients with severe asthma. We hypothesized that a clinically relevant experimental model of house dust mite (HDM)-induced murine asthma could be used to discover new pathways that regulate disease severity. In HDM-challenged mice, genome-wide expression profiling of the asthmatic lung transcriptome identified apolipoprotein E (apoE) as a steroid-unresponsive gene with persistently upregulated expression despite dexamethasone treatment. ApoE and low-density lipoprotein receptor (LDLR) knockout mice were used to demonstrate that apoE, which is produced by lung macrophages, functions in a paracrine fashion by binding to LDLRs expressed on ciliated airway epithelial cells, to negatively modulate airway hyperreactivity, mucin gene expression, and goblet cell hyperplasia. Furthermore, administration of an apoE mimetic peptide, which corresponded to the LDLR-binding domain of apoE, prevented the induction of airway inflammation, airway hyperreactivity, and goblet cell hyperplasia in HDM-challenged apoE knockout mice. This suggests that therapeutic strategies that activate the apoE-LDLR pathway, such as apoE mimetic peptides, may represent a novel treatment approach for patients with asthma. Similarly, we showed that administration of a 5A apolipoprotein A-I mimetic peptide attenuated the induction of HDM-mediated asthma in mice. These preclinical data suggest that apoE and apoA-I mimetic peptides might be developed into alternative treatments for patients with severe asthma. Future clinical trials will be required to determine whether inhaled apolipoprotein E or apolipoprotein A-I mimetic peptides are effective for the treatment of severe asthma, including patients with phenotypes that lack effective therapeutic options. CHEST 2011; 140(4):1048-1054
C1 [Yao, Xianglan; Remaley, Alan T.; Levine, Stewart J.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RP Levine, SJ (reprint author), NHLBI, Cardiovasc & Pulm Branch, NIH, Bldg 10,Room 6D03,MSC 1590, Bethesda, MD 20892 USA.
EM levines@nhlbi.nih.gov
FU Division of Intramural Research, National Heart, Lung, and Blood
Institute, National Institutes of Health
FX This study was funded by the Division of Intramural Research, National
Heart, Lung, and Blood Institute, National Institutes of Health.
NR 50
TC 13
Z9 13
U1 0
U2 3
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD OCT
PY 2011
VL 140
IS 4
BP 1048
EP 1054
DI 10.1378/chest.11-0158
PG 7
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 833QP
UT WOS:000295900300032
PM 21972383
ER
PT J
AU Sheydina, A
Riordon, DR
Boheler, KR
AF Sheydina, Anna
Riordon, Daniel R.
Boheler, Kenneth R.
TI Molecular mechanisms of cardiomyocyte aging
SO CLINICAL SCIENCE
LA English
DT Article
DE aging; apoptosis; cardiomyocyte; cardiovascular disease
ID APOPTOSIS-INDUCING FACTOR; MITOCHONDRIAL-DNA MUTATIONS; PERMEABILITY
TRANSITION PORE; FAILING HUMAN HEART; AGE-RELATED-CHANGES; RAT
LEFT-VENTRICLE; MYOCYTE CELL LOSS; GENE-EXPRESSION; CARDIAC-HYPERTROPHY;
CARDIOVASCULAR-DISEASE
AB Western societies are rapidly aging, and cardiovascular diseases are the leading cause of death. In fact, age and cardiovascular diseases are positively correlated, and disease syndromes affecting the heart reach epidemic proportions in the very old. Genetic variations and molecular adaptations are the primary contributors to the onset of cardiovascular disease; however, molecular links between age and heart syndromes are complex and involve much more than the passage of time. Changes in CM (cardiomyocyte) structure and function occur with age and precede anatomical and functional changes in the heart. Concomitant with or preceding some of these cellular changes are alterations in gene expression often linked to signalling cascades that may lead to a loss of CMs or reduced function. An understanding of the intrinsic molecular mechanisms underlying these cascading events has been instrumental in forming our current understanding of how CMs adapt with age. In the present review, we describe the molecular mechanisms underlying CM aging and how these changes may contribute to the development of cardiovascular diseases.
C1 [Sheydina, Anna; Riordon, Daniel R.; Boheler, Kenneth R.] NIA, Cardiovasc Sci Lab, NIH, Gerontol Res Ctr, Baltimore, MD 21224 USA.
RP Boheler, KR (reprint author), NIA, Cardiovasc Sci Lab, NIH, Gerontol Res Ctr, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM bohelerk@grc.nia.nih.gov
FU National Institutes of Health National Institute on Aging
FX Our own work was supported entirely by the Intramural Research Program
of the National Institutes of Health National Institute on Aging.
NR 151
TC 19
Z9 22
U1 2
U2 6
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0143-5221
J9 CLIN SCI
JI Clin. Sci.
PD OCT
PY 2011
VL 121
IS 7-8
BP 315
EP 329
DI 10.1042/CS20110115
PG 15
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 836OG
UT WOS:000296120400005
PM 21699498
ER
PT J
AU Conlon, ASC
Taylor, JMG
Sargent, DJ
Yothers, G
AF Conlon, Anna S. C.
Taylor, Jeremy M. G.
Sargent, Daniel J.
Yothers, Greg
TI Using cure models and multiple imputation to utilize recurrence as an
auxiliary variable for overall survival
SO CLINICAL TRIALS
LA English
DT Article
ID INDIVIDUAL PATIENT DATA; SURROGATE END-POINTS; 18 RANDOMIZED-TRIALS;
CLINICAL-TRIALS; MIXTURE MODEL; COLON-CANCER; MARKER; TIME
AB Background Intermediate outcome variables can often be used as auxiliary variables for the true outcome of interest in randomized clinical trials. For many cancers, time to recurrence is an informative marker in predicting a patient's overall survival outcome and could provide auxiliary information for the analysis of survival times.
Purpose To investigate whether models linking recurrence and death combined with a multiple imputation procedure for censored observations can result in efficiency gains in the estimation of treatment effects and be used to shorten trial lengths.
Methods Recurrence and death times are modeled using data from 12 trials in colorectal cancer. Multiple imputation is used as a strategy for handling missing values arising from censoring. The imputation procedure uses a cure model for time to recurrence and a time-dependent Weibull proportional hazards model for time to death. Recurrence times are imputed, and then death times are imputed conditionally on recurrence times. To illustrate these methods, trials are artificially censored 2 years after the last accrual, the imputation procedure implemented, and a log-rank test and Cox model used to analyze and compare these new data with the original data.
Results The results show modest, but consistent gains in efficiency in the analysis using the auxiliary information in recurrence times. Comparison of analyses show the treatment effect estimates and log-rank test results from the 2-year censored imputed data to be in between the estimates from the original data and the artificially censored data, indicating that the procedure was able to recover some of the lost information due to censoring.
Limitations The models used are all fully parametric, requiring distributional assumptions of the data.
Conclusions The proposed models may be useful in improving the efficiency in estimation of treatment effects in cancer trials and shortening trial length. Clinical Trials 2011; 8: 581-590. http://ctj.sagepub.com
C1 [Conlon, Anna S. C.; Taylor, Jeremy M. G.] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA.
[Sargent, Daniel J.] Univ Minnesota, Sch Publ Hlth, Div Biostat, Mayo Clin, Rochester, MN USA.
[Yothers, Greg] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15261 USA.
[Yothers, Greg] Univ Pittsburgh, Natl Surg Adjuvant Breast & Bowel Project, Dept Biostat, Pittsburgh, PA 15261 USA.
RP Taylor, JMG (reprint author), Univ Michigan, Sch Publ Hlth, Dept Biostat, 1420 Washington Hts, Ann Arbor, MI 48109 USA.
EM jmgt@umich.edu
OI Yothers, Greg/0000-0002-7965-7333; Sargent, Daniel/0000-0002-2684-4741
FU NIH [CA129102, CA083654, GM74910]
FX This research was partially supported by NIH grants CA129102, CA083654
and GM74910.
NR 21
TC 4
Z9 4
U1 0
U2 7
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
J9 CLIN TRIALS
JI Clin. Trials
PD OCT
PY 2011
VL 8
IS 5
BP 581
EP 590
DI 10.1177/1740774511414741
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 835FI
UT WOS:000296020500004
PM 21921063
ER
PT J
AU Kernan, W
Viscoli, C
Brass, L
Amatangelo, M
Birch, A
Clark, W
Conwit, R
Furie, K
Gorman, M
Pesapane, B
Kleindorfer, D
Lovejoy, A
Osborne, J
Silliman, S
Zweifler, R
Horwitz, R
AF Kernan, W.
Viscoli, C.
Brass, L.
Amatangelo, M.
Birch, A.
Clark, W.
Conwit, R.
Furie, K.
Gorman, M.
Pesapane, B.
Kleindorfer, D.
Lovejoy, A.
Osborne, J.
Silliman, S.
Zweifler, R.
Horwitz, R.
TI Boosting enrolment in clinical trials: validation of a regional network
model
SO CLINICAL TRIALS
LA English
DT Article
ID STROKE; RECRUITMENT; SYSTEM
AB Background Clinical trials of stroke therapy have been hampered by slow rates of enrolment.
Purpose Our purpose is to validate a previously developed model for accelerating enrolment in clinical trials by replicating it at new locations. The model employs coordinators who travel from a host institution to enrol participants from a network of participating hospitals. Active surveillance assures identification of all eligible patients.
Methods Among 70 U. S. investigators participating in National Institutes of Health-funded trial of stroke prevention, five investigators were invited to develop local identification and outreach networks (LIONs). Each LION comprised a LION coordinating centre servicing multiple hospitals. Hospitals provided names of patients with stroke or transient ischaemic attack to researchers at the LION coordinating centre who initiated contact; patients were offered home visits for consent and randomization. Outcomes were feasibility, enrolment, data quality, and cost.
Results Five LIONs varied in size from two to eight hospitals. All 24 hospitals we approached agreed to participate. The average monthly rate of enrolment at the research sites increased from 1.4 participants to 3.5 after expanding from a single institution model to the LION format (mean change = 2.1, range 0.9-3.7). Monthly performance improved over time. Data quality was similar for LIONs and non-LION sites, except for drug adherence which was lower at LIONs. The average cost to randomize and follow one participant during the study interval was 2.4 times the cost under the per-patient, cost-reimbursement strategy at non-LION sites. The cost ratio declined from 3.4 in year one to 1.8 in year two.
Limitations The LION strategy requires unprecedented collaboration and trust among institutions. Applicability beyond stroke requires confirmation.
Conclusion LIONs are a practical, reproducible method to increase enrolment in trial research. Twelve months were required for the average site to reach its potential. The per-participant cost at LIONs was higher than conventional sites but declined over time. Clinical Trials 2011; 8: 645-653. http://ctj.sagepub.com
C1 [Kernan, W.] IRIS Coordinating Ctr, New Haven, CT USA.
[Viscoli, C.; Brass, L.; Pesapane, B.; Lovejoy, A.] Yale Univ, Sch Med, New Haven, CT USA.
[Amatangelo, M.; Birch, A.; Furie, K.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Clark, W.] Oregon Hlth & Sci Univ, Portland, OR USA.
[Conwit, R.] Natl Inst Neurol Disorders & Stroke, Bethesda, MD USA.
[Gorman, M.] Univ Vermont, Burlington, VT USA.
[Kleindorfer, D.; Osborne, J.] Univ Cinncinati, Cinncinati, OH USA.
[Silliman, S.] Univ Florida, Coll Medicine Jacksonville, Jacksonville, FL USA.
[Zweifler, R.] Eastern Virginia Med Sch, Norfolk, VA 23501 USA.
[Horwitz, R.] Glaxo Smithkline, Philadelphia, PA USA.
RP Kernan, W (reprint author), IRIS Coordinating Ctr, Suite 515 2 Church St S, New Haven, CT USA.
EM walter.kernan@yale.edu
RI Zweifler, Richard/K-1314-2015
FU National Institutes of Neurological Disorders and Stroke (NINDS) [U01
NS044876]
FX This work was supported by the National Institutes of Neurological
Disorders and Stroke (NINDS) (U01 NS044876). Placebo and pioglitazone
tablets were supplied by Takeda Pharmaceuticals North America, Inc.
NR 14
TC 2
Z9 2
U1 0
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
J9 CLIN TRIALS
JI Clin. Trials
PD OCT
PY 2011
VL 8
IS 5
BP 645
EP 653
DI 10.1177/1740774511414925
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 835FI
UT WOS:000296020500011
PM 21824978
ER
PT J
AU Jiang, CT
Qu, AJ
Matsubara, T
Chanturiya, T
Jou, W
Gavrilova, O
Shah, YM
Gonzalez, FJ
AF Jiang, Changtao
Qu, Aijuan
Matsubara, Tsutomu
Chanturiya, Tatyana
Jou, William
Gavrilova, Oksana
Shah, Yatrik M.
Gonzalez, Frank J.
TI Disruption of Hypoxia-Inducible Factor 1 in Adipocytes Improves Insulin
Sensitivity and Decreases Adiposity in High-Fat Diet-Fed Mice
SO DIABETES
LA English
DT Article
ID OBESE MICE; LIPID-METABOLISM; CYTOKINE SIGNALING-3; TISSUE HYPOXIA; ACID
OXIDATION; FACTOR 1-ALPHA; RESISTANCE; ADIPONECTIN; DIFFERENTIATION;
SUPPRESSOR
AB OBJECTIVE-Obesity, insulin resistance, and type 2 diabetes form a tightly correlated cluster of metabolic disorders in which adipose is one of the first affected tissues. The role of hypoxia and hypoxia-inducible factor 1 (HIF1) in the development of high-fat diet (HFD)-induced obesity and insulin resistance was investigated using animal models.
RESEARCH DESIGN AND METHODS-Mice with adipocyte-specific targeted disruption of the genes encoding the HIFI obligatory subunits Hif1 alpha or Arnt (Hif1 beta) were generated using an aP2-Cre transgene with the Cre/LoxP system. The mice were fed an HFD for 12 weeks and their metabolic phenotypes were determined. Gene expression patterns in adipose tissues were also determined by microarray and quantitative PCR.
RESULTS-On an HFD, adipocyte-specific ARNT knockout mice and adipocyte-specific HIF1 alpha knockout mice exhibit similar metabolic phenotypes, including reduced fat formation, protection from HFD-induced obesity, and insulin resistance compared with similarly fed wild-type controls. The cumulative food intake remained similar; however, the metabolic efficiency was lower in adipocyte-specific HIF1 alpha knockout mice. Moreover, indirect calorimetry revealed respiratory exchange ratios were reduced in adipocyte-specific HIF1 alpha knockout mice. Hyperinsulinemic-euglycemic clamp studies demonstrated that targeted disruption of HIF1 alpha in adipocytes enhanced whole-body insulin sensitivity. The improvement of insulin resistance is associated with decreased expression of Socs3 and induction of adiponectin.
CONCLUSIONS-Inhibition of HIF1 in adipose tissue ameliorates obesity and insulin resistance. This study reveals that HIF1 could provide a novel potential therapeutic target for obesity and type 2 diabetes. Diabetes 60:2484-2495, 2011
C1 [Jiang, Changtao; Qu, Aijuan; Matsubara, Tsutomu; Shah, Yatrik M.; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Chanturiya, Tatyana; Jou, William; Gavrilova, Oksana] Natl Inst Diabet & Digest & Kidney Dis, Mouse Metab Core Lab, NIH, Bethesda, MD USA.
[Shah, Yatrik M.] Univ Michigan, Sch Med, Dept Mol & Integrat Physiol & Internal Med, Div Gastroenterol, Ann Arbor, MI USA.
RP Gonzalez, FJ (reprint author), NCI, Lab Metab, Ctr Canc Res, Bethesda, MD 20892 USA.
EM gonzalef@mail.nih.gov
FU National Cancer Institute; National Institute of Diabetes; Digestive and
Kidney Diseases Intramural Research Programs; National Institutes of
Health [CA-148828]
FX This study was supported by the National Cancer Institute and National
Institute of Diabetes and Digestive and Kidney Diseases Intramural
Research Programs and National Institutes of Health Grant CA-148828 (to
Y.M.S.).
NR 41
TC 91
Z9 94
U1 2
U2 19
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD OCT
PY 2011
VL 60
IS 10
BP 2484
EP 2495
DI 10.2337/db11-0174
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 834XV
UT WOS:000295998700007
PM 21873554
ER
PT J
AU Faulhaber-Walter, R
Jou, W
Mizel, D
Li, LL
Zhang, JD
Kim, SM
Huang, YN
Chen, M
Briggs, JP
Gavrilova, O
Schnermann, JB
AF Faulhaber-Walter, Robert
Jou, William
Mizel, Diane
Li, Lingli
Zhang, Jiandi
Kim, Soo Mi
Huang, Yuning
Chen, Min
Briggs, Josephine P.
Gavrilova, Oksana
Schnermann, Jurgen B.
TI Impaired Glucose Tolerance in the Absence of Adenosine A1 Receptor
Signaling
SO DIABETES
LA English
DT Article
ID RAT SKELETAL-MUSCLE; IMPROVES INSULIN-RESISTANCE; A(1) ADENOSINE
RECEPTORS; A1 RECEPTOR; LATERAL HYPOTHALAMUS; SLEEP-WAKEFULNESS; WHITE
ADIPOCYTES; BODY-COMPOSITION; GROWTH-HORMONE; ADIPOSE-TISSUE
AB OBJECTIVE-The role of adenosine (ADO) in the regulation of glucose homeostasis is not clear. In the current study, we used A1-ADO receptor (A1AR)-deficient mice to investigate the role of ADO/A1AR signaling for glucose homeostasis.
RESEARCH DESIGN AND METHODS-After weaning, A1AR(-/-) and wild-type mice received either a standard diet (12 kcal% fat) or high-fat diet (HFD; 45 kcal% fat). Body weight, fasting plasma glucose, plasma insulin, and intraperitoneal glucose tolerance tests were performed in 8-week-old mice and again after 12-20 weeks of subsequent observation. Body composition was quantified by magnetic resonance imaging and epididymal fat-pad weights. Glucose metabolism was investigated by hyperinsulinemic-euglycemic clamp studies. To describe pathophysiological mechanisms, adipokines and Akt phosphorylation were measured.
RESULTS-A1AR(-/-) mice were significantly heavier than wild-type mice because of an increased fat mass. Fasting plasma glucose and insulin were significantly higher in A1AR(-/-) mice after weaning and remained higher in adulthood. An intraperitoneal glucose challenge disclosed a significantly slower glucose clearance in A1AR(-/-) mice. An HFD enhanced this phenotype in A1AR(-/-) mice and unmasked a dysfunctional insulin secretory mechanism. Insulin sensitivity was significantly impaired in A1AR(-/-) mice on the standard diet shortly after weaning. Clamp studies detected a significant decrease of net glucose uptake in A1AR(-/-) mice and a reduced glucose uptake in muscle and white adipose tissue. Effects were not triggered by leptin deficiency but involved a decreased Akt phosphorylation.
CONCLUSIONS-ADO/A1AR signaling contributes importantly to insulin-controlled glucose homeostasis and insulin sensitivity in C57BL/6 mice and is involved in the metabolic regulation of adipose tissue. Diabetes 60:2578-2587, 2011
C1 [Faulhaber-Walter, Robert; Jou, William; Mizel, Diane; Li, Lingli; Zhang, Jiandi; Kim, Soo Mi; Huang, Yuning; Chen, Min; Gavrilova, Oksana; Schnermann, Jurgen B.] Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD USA.
[Briggs, Josephine P.] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
RP Faulhaber-Walter, R (reprint author), Natl Inst Diabet & Digest & Kidney Dis, NIH, Bethesda, MD USA.
EM rofaulhaber@web.de
RI Briggs, Josephine/B-9394-2009;
OI Briggs, Josephine/0000-0003-0798-1190; Faulhaber-Walter,
Robert/0000-0002-7769-9652
FU National Institutes of Health (NIH)
FX This work was funded by a postdoctoral fellowship award of the National
Institutes of Health (NIH) (to R.F.-W.).
NR 47
TC 23
Z9 24
U1 0
U2 6
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD OCT
PY 2011
VL 60
IS 10
BP 2578
EP 2587
DI 10.2337/db11-0058
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 834XV
UT WOS:000295998700017
PM 21831968
ER
PT J
AU Strawbridge, RJ
Dupuis, J
Prokopenko, I
Barker, A
Ahlqvist, E
Rybin, D
Petrie, JR
Travers, ME
Bouatia-Naji, N
Dimas, AS
Nica, A
Wheeler, E
Chen, H
Voight, BF
Taneera, J
Kanoni, S
Peden, JF
Turrini, F
Gustafsson, S
Zabena, C
Almgren, P
Barker, DJP
Barnes, D
Dennison, EM
Eriksson, JG
Eriksson, P
Eury, E
Folkersen, L
Fox, CS
Frayling, TM
Goel, A
Gu, HF
Horikoshi, M
Isomaa, B
Jackson, AU
Jameson, KA
Kajantie, E
Kerr-Conte, J
Kuulasmaa, T
Kuusisto, J
Loos, RJF
Luan, JA
Makrilakis, K
Manning, AK
Martinez-Larrad, MT
Narisu, N
Mannila, MN
Ohrvik, J
Osmond, C
Pascoe, L
Payne, F
Sayer, AA
Sennblad, B
Silveira, A
Stancakova, A
Stirrups, K
Swift, AJ
Syvanen, AC
Tuomi, T
van 't Hooft, FM
Walker, M
Weedon, MN
Xie, WJ
Zethelius, B
Ongen, H
Malarstig, A
Hopewell, JC
Saleheen, D
Chambers, J
Parish, S
Danesh, J
Kooner, J
Ostenson, CG
Lind, L
Cooper, CC
Serrano-Rios, M
Ferrannini, E
Forsen, TJ
Clarke, R
Franzosi, MG
Seedorf, U
Watkins, H
Froguel, P
Johnson, P
Deloukas, P
Collins, FS
Laakso, M
Dermitzakis, ET
Boehnke, M
McCarthy, MI
Wareham, NJ
Groop, L
Pattou, F
Gloyn, AL
Dedoussis, GV
Lyssenko, V
Meigs, JB
Barroso, I
Watanabe, RM
Ingelsson, E
Langenberg, C
Hamsten, A
Florez, JC
AF Strawbridge, Rona J.
Dupuis, Josee
Prokopenko, Inga
Barker, Adam
Ahlqvist, Emma
Rybin, Denis
Petrie, John R.
Travers, Mary E.
Bouatia-Naji, Nabila
Dimas, Antigone S.
Nica, Alexandra
Wheeler, Eleanor
Chen, Han
Voight, Benjamin F.
Taneera, Jalal
Kanoni, Stavroula
Peden, John F.
Turrini, Fabiola
Gustafsson, Stefan
Zabena, Carina
Almgren, Peter
Barker, David J. P.
Barnes, Daniel
Dennison, Elaine M.
Eriksson, Johan G.
Eriksson, Per
Eury, Elodie
Folkersen, Lasse
Fox, Caroline S.
Frayling, Timothy M.
Goel, Anuj
Gu, Harvest F.
Horikoshi, Momoko
Isomaa, Bo
Jackson, Anne U.
Jameson, Karen A.
Kajantie, Eero
Kerr-Conte, Julie
Kuulasmaa, Teemu
Kuusisto, Johanna
Loos, Ruth J. F.
Luan, Jian'an
Makrilakis, Konstantinos
Manning, Alisa K.
Teresa Martinez-Larrad, Maria
Narisu, Narisu
Mannila, Maria Nastase
Ohrvik, John
Osmond, Clive
Pascoe, Laura
Payne, Felicity
Sayer, Avan A.
Sennblad, Bengt
Silveira, Angela
Stancakova, Alena
Stirrups, Kathy
Swift, Amy J.
Syvanen, Ann-Christine
Tuomi, Tiinamaija
van 't Hooft, Ferdinand M.
Walker, Mark
Weedon, Michael N.
Xie, Weijia
Zethelius, Bjorn
Ongen, Halit
Malarstig, Anders
Hopewell, Jemma C.
Saleheen, Danish
Chambers, John
Parish, Sarah
Danesh, John
Kooner, Jaspal
Ostenson, Claes-Goran
Lind, Lars
Cooper, Cyrus C.
Serrano-Rios, Manuel
Ferrannini, Ele
Forsen, Tom J.
Clarke, Robert
Franzosi, Maria Grazia
Seedorf, Udo
Watkins, Hugh
Froguel, Philippe
Johnson, Paul
Deloukas, Panos
Collins, Francis S.
Laakso, Markku
Dermitzakis, Emmanouil T.
Boehnke, Michael
McCarthy, Mark I.
Wareham, Nicholas J.
Groop, Leif
Pattou, Francois
Gloyn, Anna L.
Dedoussis, George V.
Lyssenko, Valeriya
Meigs, James B.
Barroso, Ines
Watanabe, Richard M.
Ingelsson, Erik
Langenberg, Claudia
Hamsten, Anders
Florez, Jose C.
CA DIAGRAM Consortium
GIANT Consortium
MuTHER Consortium
CARDIoGRAM Consortium
C4D Consortium
TI Genome-Wide Association Identifies Nine Common Variants Associated With
Fasting Proinsulin Levels and Provides New Insights Into the
Pathophysiology of Type 2 Diabetes
SO DIABETES
LA English
DT Article
ID CORONARY HEART-DISEASE; BETA-CELL FUNCTION; SUSCEPTIBILITY LOCI;
GLUCOSE-HOMEOSTASIS; INSULIN SENSITIVITY; POPULATION; TCF7L2; RISK;
OBESITY; METAANALYSIS
AB OBJECTIVE-Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired beta-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology.
RESEARCH DESIGN AND METHODS-We have conducted a meta-analysis of genome-wide association tests of similar to 2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates.
RESULTS-Nine SNPs at eight loci were associated with proinsulin levels (P < 5 x 10(-8)). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC3OA8, VPS13C/C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 x 10(-4)), improved beta-cell function (P = 1.1 x 10(-5)), and lower risk of T2D (odds ratio 0.88; P = 7.8 x 10(-6)). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets.
CONCLUSIONS-We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis. Diabetes 60:2624-2634, 2011
C1 [Voight, Benjamin F.; Florez, Jose C.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Strawbridge, Rona J.; Eriksson, Per; Mannila, Maria Nastase; Ohrvik, John; Sennblad, Bengt; Silveira, Angela; van 't Hooft, Ferdinand M.; Malarstig, Anders; Hamsten, Anders] Karolinska Inst, Karolinska Univ Hosp Solna, Dept Med Solna, Atherosclerosis Res Unit, Stockholm, Sweden.
[Dupuis, Josee; Chen, Han; Manning, Alisa K.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Dupuis, Josee; Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Prokopenko, Inga; Travers, Mary E.; Horikoshi, Momoko; Johnson, Paul; McCarthy, Mark I.; Gloyn, Anna L.] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford, England.
[Prokopenko, Inga; Dimas, Antigone S.; Peden, John F.; Goel, Anuj; Horikoshi, Momoko; Ongen, Halit; Watkins, Hugh; McCarthy, Mark I.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England.
[Barker, Adam; Barnes, Daniel; Loos, Ruth J. F.; Luan, Jian'an; Wareham, Nicholas J.; Langenberg, Claudia] Addenbrookes Hosp, Inst Metab Sci, MRC Epidemiol Unit, Cambridge, England.
[Ahlqvist, Emma; Taneera, Jalal; Turrini, Fabiola; Almgren, Peter; Groop, Leif; Lyssenko, Valeriya] Lund Univ, Dept Clin Sci Diabet & Endocrinol, Univ Hosp & Malmo, Malmo, Sweden.
[Rybin, Denis] Boston Univ, Data Coordinating Ctr, Boston, MA 02215 USA.
[Petrie, John R.] Univ Glasgow, BHF Cardiovasc Res Ctr, Glasgow, Lanark, Scotland.
[Bouatia-Naji, Nabila; Eury, Elodie; Kerr-Conte, Julie; Froguel, Philippe; Pattou, Francois] Univ Lille Nord France, Lille, France.
[Bouatia-Naji, Nabila; Eury, Elodie; Froguel, Philippe] Inst Pasteur, CNRS UMR 8199, Lille, France.
[Dimas, Antigone S.; Nica, Alexandra; Dermitzakis, Emmanouil T.] Univ Geneva, Sch Med, Dept Genet Med & Dev, CH-1211 Geneva, Switzerland.
[Wheeler, Eleanor; Payne, Felicity; Barroso, Ines] Wellcome Trust Sanger Inst, Metab Dis Grp, Hinxton, England.
[Voight, Benjamin F.; Florez, Jose C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Voight, Benjamin F.; Florez, Jose C.] Massachusetts Gen Hosp, Diabet Unit, Diabet Res Ctr, Boston, MA 02114 USA.
[Kanoni, Stavroula; Dedoussis, George V.] Harokopio Univ, Dept Dietet Nutr, Athens, Greece.
[Peden, John F.; Goel, Anuj; Ongen, Halit; Watkins, Hugh] Univ Oxford, Dept Cardiovasc Med, Oxford, England.
[Turrini, Fabiola] Univ Verona, Dept Med, I-37100 Verona, Italy.
[Gustafsson, Stefan; Ingelsson, Erik] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Zabena, Carina; Teresa Martinez-Larrad, Maria; Serrano-Rios, Manuel] CIBER Diabet & Enfermedades Metab Asociadas CIBER, Madrid, Spain.
[Zabena, Carina; Teresa Martinez-Larrad, Maria; Serrano-Rios, Manuel] Hosp Clin San Carlos, Fdn Invest Biomed, Madrid, Spain.
[Barker, David J. P.] Oregon Hlth & Sci Univ, Heart Res Ctr, Portland, OR 97201 USA.
[Dennison, Elaine M.; Jameson, Karen A.; Osmond, Clive; Sayer, Avan A.; Cooper, Cyrus C.] Univ Southampton, Southampton Gen Hosp, MRC Lifecourse Epidemiol Unit, Southampton, Hants, England.
[Eriksson, Johan G.; Kajantie, Eero] Natl Inst Hlth & Welf, Helsinki, Finland.
[Eriksson, Johan G.] Helsinki Univ Cent Hosp, Unit Gen Practice, Helsinki, Finland.
[Eriksson, Johan G.; Isomaa, Bo; Tuomi, Tiinamaija] Folkhalsan Res Ctr, Helsinki, Finland.
[Eriksson, Johan G.; Forsen, Tom J.] Univ Helsinki, Dept Gen Practice & Primary Hlth Care, Helsinki, Finland.
[Folkersen, Lasse] Karolinska Inst, Dept Med Solna, Expt Cardiovasc Res Unit, Stockholm, Sweden.
[Fox, Caroline S.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA.
[Frayling, Timothy M.; Weedon, Michael N.; Xie, Weijia] Univ Exeter, Peninsula Med Sch, Inst Biomed & Clin Sci, Exeter, Devon, England.
[Gu, Harvest F.; Ostenson, Claes-Goran] Karolinska Inst, Endocrinol & Diabet Unit, Dept Mol Med & Surg, Stockholm, Sweden.
[Isomaa, Bo] Malmska Municipal Hlth Care Ctr & Hosp, Pietarsaari, Finland.
[Jackson, Anne U.; Boehnke, Michael] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Kajantie, Eero] Helsinki Univ Cent Hosp, Hosp Children & Adolescents, Helsinki, Finland.
[Kerr-Conte, Julie; Pattou, Francois] INSERM, UMR 859, F-59045 Lille, France.
[Kuulasmaa, Teemu; Kuusisto, Johanna; Stancakova, Alena; Laakso, Markku] Univ Kuopio, Dept Med, SF-70210 Kuopio, Finland.
[Kuulasmaa, Teemu; Kuusisto, Johanna; Stancakova, Alena; Laakso, Markku] Kuopio Univ Hosp, SF-70210 Kuopio, Finland.
[Makrilakis, Konstantinos] Univ Athens, Sch Med, Laiko Gen Hosp, Dept Propaedeut Med 1, GR-11527 Athens, Greece.
[Narisu, Narisu; Swift, Amy J.] Natl Human Genome Res Inst, NIH, Bethesda, MD USA.
[Pascoe, Laura] Newcastle Univ, Inst Cell & Mol Biosci, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Syvanen, Ann-Christine; Lind, Lars] Uppsala Univ, Sci Life Lab, Dept Med Sci, Uppsala, Sweden.
[Tuomi, Tiinamaija] Helsinki Univ Cent Hosp, Dept Med, Helsinki, Finland.
[Tuomi, Tiinamaija] Univ Helsinki, Res Program Mol Med, Helsinki, Finland.
[Walker, Mark] Newcastle Univ, Inst Cellular Med, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Zethelius, Bjorn] Uppsala Univ, Dept Publ Hlth & Caring Sci, Uppsala, Sweden.
[Ongen, Halit] Univ Oxford, John Radcliffe Hosp, Dept Cardiovasc Med, Oxford OX3 9DU, England.
[Hopewell, Jemma C.; Parish, Sarah; Clarke, Robert] Univ Oxford, Clin Trial Serv Unit, Oxford, England.
[Saleheen, Danish; Danesh, John] Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England.
[Saleheen, Danish] Ctr Noncommunicable Dis Pakistan, Karachi, Pakistan.
[Kooner, Jaspal] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England.
[Chambers, John; Kooner, Jaspal] Ealing Hosp NHS Trust, Middlesex, England.
[Ferrannini, Ele] Univ Pisa, Sch Med, Dept Internal Med, I-56100 Pisa, Italy.
[Ferrannini, Ele] Univ Pisa, Sch Med, CNR Inst Clin Physiol, I-56100 Pisa, Italy.
[Forsen, Tom J.] Vaasa Hlth Care Ctr, Vaasa, Finland.
[Franzosi, Maria Grazia] Mario Negri Inst Pharmacol Res, Dept Cardiovasc Res, Milan, Italy.
[Seedorf, Udo] Univ Munster, Leibniz Inst Arteriosclerosis Res, Munster, Germany.
[Froguel, Philippe] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Hammersmith Hosp, Dept Genom Common Dis, London, England.
[Johnson, Paul] Univ Oxford, DRWF Human Islet Isolat Facil, Oxford, England.
[Johnson, Paul] Univ Oxford, Oxford Islet Transplant Programme, Oxford, England.
[McCarthy, Mark I.] Churchill Hosp, Oxford NIHR Biomed Res Ctr, Oxford OX3 7LJ, England.
[Meigs, James B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Meigs, James B.; Florez, Jose C.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Barroso, Ines] Univ Cambridge, Addenbrookes Hosp, Metab Res Labs, Inst Metab Sci, Cambridge CB2 2QQ, England.
[Watanabe, Richard M.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Watanabe, Richard M.] Univ So Calif, Keck Sch Med, Dept Physiol & Biophys, Los Angeles, CA 90033 USA.
RP Florez, JC (reprint author), Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
EM claudia.langenberg@mrc-epid.cam.ac.uk; anders.hamsten@ki.se;
jcflorez@partners.org
RI Smith, Albert Vernon/K-5150-2015; Erdmann, Jeanette/P-7513-2014;
Aulchenko, Yurii/M-8270-2013; Visvikis-Siest, Sophie/H-2324-2014;
Hayward, Caroline/M-8818-2016; BOUATIA-NAJI, NABILA/D-5863-2013;
Schwarz, Peter/B-5127-2013; Leander, Karin/C-7261-2017; Feitosa,
Mary/K-8044-2012; Zondervan, Krina/M-1143-2013; Cooper,
Matthew/J-4420-2014; Strawbridge, Rona/H-5422-2012; Palmer,
Lyle/K-3196-2014; Witte, Daniel/C-1722-2008; Boehm,
Bernhard/F-8750-2015; Gudnason, Vilmundur/K-6885-2015; Ripatti,
Samuli/H-9446-2014; Polasek, Ozren/B-6002-2011; Meitinger,
Thomas/O-1318-2015; Prokopenko, Inga/H-3241-2014; Aben,
Katja/G-9686-2016; Stark, Klaus/D-3813-2009; Kiemeney,
Lambertus/D-3357-2009; Aihie Sayer, Avan/A-4359-2012; Willenborg,
Christina/D-2668-2012; Ridderstrale, Martin/F-7678-2012; Elliott,
Amanda/G-5120-2012; Rudan, Igor/I-1467-2012; Barker, David/A-5671-2013;
Deloukas, Panos/B-2922-2013; Dermitzakis, Emmanouil/B-7687-2013; Tang,
Wai Hong/I-1238-2013; Cichon, Sven/H-8803-2013; Cichon, Sven/B-9618-2014
OI Kaprio, Jaakko/0000-0002-3716-2455; Lawlor, Debbie
A/0000-0002-6793-2262; Payne, Felicity/0000-0003-4228-581X; Pankow,
James/0000-0001-7076-483X; de Geus, Eco/0000-0001-6022-2666; Martin,
Nicholas/0000-0003-4069-8020; Dehghan, Abbas/0000-0001-6403-016X; Coin,
Lachlan/0000-0002-4300-455X; Chen, Han/0000-0002-9510-4923; Nothen,
Markus/0000-0002-8770-2464; Tuomi, Tiinamaija/0000-0002-8306-6202;
Karpe, Fredrik/0000-0002-2751-1770; Yang, Jian/0000-0003-2001-2474;
Jorgensen, Torben/0000-0001-9453-2830; Small,
Kerrin/0000-0003-4566-0005; Visscher, Peter/0000-0002-2143-8760;
Eriksson, Johan/0000-0002-2516-2060; Jones, Gregory
T/0000-0002-6950-4210; Ouwehand, Willem/0000-0002-7744-1790; Folkersen,
Lasse/0000-0003-0708-9530; Gieger, Christian/0000-0001-6986-9554;
Wijmenga, Cisca/0000-0002-5635-1614; Ziegler,
Andreas/0000-0002-8386-5397; Hide, Winston/0000-0002-8621-3271; Scherag,
Andre/0000-0002-9406-4704; Rivadeneira, Fernando/0000-0001-9435-9441;
Palmer, Colin/0000-0002-6415-6560; Jarvelin,
Marjo-Riitta/0000-0002-2149-0630; Aihie Sayer, Avan/0000-0003-1283-6457;
Esko, Tonu/0000-0003-1982-6569; Smith, Albert
Vernon/0000-0003-1942-5845; Stewart, Alexandre/0000-0003-2673-9164;
Manunta, Paolo/0000-0003-3976-9696; Zeggini,
Eleftheria/0000-0003-4238-659X; Erdmann, Jeanette/0000-0002-4486-6231;
Dupuis, Josee/0000-0003-2871-3603; Peyvandi, Flora/0000-0001-7423-9864;
Luben, Robert/0000-0002-5088-6343; van Dam, Rob/0000-0002-7354-8734;
Sijbrands, Eric/0000-0001-8857-7389; Goddard,
Michael/0000-0001-9917-7946; Griffin, Simon/0000-0002-2157-4797; Marre,
Michel/0000-0002-3071-1837; Barnes, Daniel/0000-0002-3781-7570; Johnson,
Toby/0000-0002-5998-3270; Cappuccio, Francesco
Paolo/0000-0002-7842-5493; Macciardi, Fabio/0000-0003-0537-4266; Lango
Allen, Hana/0000-0002-7803-8688; Bouatia-Naji,
Nabila/0000-0001-5424-2134; Magi, Reedik/0000-0002-2964-6011; Zgaga,
Lina/0000-0003-4089-9703; Rybin, Denis/0000-0002-3657-4829; Willer,
Cristen/0000-0001-5645-4966; Meisinger, Christa/0000-0002-9026-6544;
Beckmann, Jacques S /0000-0002-9741-1900; Pichler,
Irene/0000-0001-8251-0757; ELOSUA, ROBERTO/0000-0001-8235-0095;
Aulchenko, Yurii/0000-0002-7899-1575; Visvikis-Siest,
Sophie/0000-0001-8104-8425; Hayward, Caroline/0000-0002-9405-9550;
Schwarz, Peter/0000-0001-6317-7880; Leander, Karin/0000-0002-1404-9222;
Feitosa, Mary/0000-0002-0933-2410; Seedorf, Udo/0000-0003-4652-5358;
Thiering, Elisabeth/0000-0002-5429-9584; Kaakinen,
Marika/0000-0002-9228-0462; Zondervan, Krina/0000-0002-0275-9905;
Cooper, Matthew/0000-0003-1139-3682; Strawbridge,
Rona/0000-0001-8506-3585; Palmer, Lyle/0000-0002-1628-3055; Witte,
Daniel/0000-0002-0769-2922; Gudnason, Vilmundur/0000-0001-5696-0084;
Ripatti, Samuli/0000-0002-0504-1202; Polasek, Ozren/0000-0002-5765-1862;
Prokopenko, Inga/0000-0003-1624-7457; Aben, Katja/0000-0002-0214-2147;
Stark, Klaus/0000-0002-7832-1942; Kiemeney,
Lambertus/0000-0002-2368-1326; Willenborg,
Christina/0000-0001-5217-6882; Rudan, Igor/0000-0001-6993-6884;
Deloukas, Panos/0000-0001-9251-070X; Cichon, Sven/0000-0002-9475-086X;
Cichon, Sven/0000-0002-9475-086X
FU British Heart Foundation [RG/08/014/24067]; Diabetes UK [08/0003775];
Medical Research Council [MC_UP_A620_1014, 81696, G0601261, G0601966,
G0700222, G0700222(81696), G0700931, G0801056, MC_PC_U127561128,
MC_PC_U127592696, MC_U106188470, MC_U127561128, MC_U137686857,
MC_UP_A620_1015]; NHLBI NIH HHS [R01 HL087647, U01 HL054527]; NIDDK NIH
HHS [DK062370, K24 DK080140, R01 DK078616]; Wellcome Trust
[077016/Z/05/Z, 083270/Z/07/Z, 090532]
NR 47
TC 128
Z9 134
U1 3
U2 50
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD OCT
PY 2011
VL 60
IS 10
BP 2624
EP 2634
DI 10.2337/db11-0415
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 834XV
UT WOS:000295998700022
PM 21873549
ER
PT J
AU Park, BJ
Pappas, PG
Wannemuehler, KA
Alexander, BD
Anaissie, EJ
Andes, DR
Baddley, JW
Brown, JM
Brumble, LM
Freifeld, AG
Hadley, S
Herwaldt, L
Ito, JI
Kauffman, CA
Lyon, GM
Marr, KA
Morrison, VA
Papanicolaou, G
Patterson, TF
Perl, TM
Schuster, MG
Walker, R
Wingard, JR
Walsh, TJ
Kontoyiannis, DP
AF Park, Benjamin J.
Pappas, Peter G.
Wannemuehler, Kathleen A.
Alexander, Barbara D.
Anaissie, Elias J.
Andes, David R.
Baddley, John W.
Brown, Janice M.
Brumble, Lisa M.
Freifeld, Alison G.
Hadley, Susan
Herwaldt, Loreen
Ito, James I.
Kauffman, Carol A.
Lyon, G. Marshall
Marr, Kieren A.
Morrison, Vicki A.
Papanicolaou, Genovefa
Patterson, Thomas F.
Perl, Trish M.
Schuster, Mindy G.
Walker, Randall
Wingard, John R.
Walsh, Thomas J.
Kontoyiannis, Dimitrios P.
TI Invasive Non-Aspergillus Mold Infections in Transplant Recipients,
United States, 2001-2006
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID HEMATOPOIETIC STEM-CELL; CARE CANCER CENTER; SURVEILLANCE NETWORK
TRANSNET; FUNGAL-INFECTIONS; HEMATOLOGIC MALIGNANCIES; BREAKTHROUGH
ZYGOMYCOSIS; SCEDOSPORIUM-PROLIFICANS; RECEIVING VORICONAZOLE;
ANTIFUNGAL THERAPY; EPIDEMIOLOGY
AB Recent reports describe increasing incidence of non-Aspergillus mold infections in hematopoietic cell transplant (HCT) and solid organ transplant (SOT) recipients. To investigate the epidemiology of infections with Mucorales, Fusarium spp., and Scedosporium spp. molds, we analyzed data from the Transplant-Associated Infection Surveillance Network, 23 transplant centers that conducted prospective surveillance for invasive fungal infections during 2001-2006. We identified 169 infections (105 Mucorales, 37 Fusarium spp., and 27 Scedosporium spp.) in 169 patients; 124 (73.4%) were in HCT recipients, and 45 (26.6%) were in SOT recipients. The crude 90-day mortality rate was 56.6%. The 12-month mucormycosis cumulative incidence was 0.29% for HCT and 0.07% for SOT. Mucormycosis incidence among HCT recipients varied widely, from 0.08% to 0.69%, with higher incidence in cohorts receiving transplants during 2003 and 2004. Non-Aspergillus mold infections continue to be associated with high mortality rates. The incidence of mucormycosis in HOT recipients increased substantially during the surveillance period.
C1 [Park, Benjamin J.] Ctr Dis Control & Prevent, Mycot Dis Branch, Atlanta, GA 30333 USA.
[Pappas, Peter G.; Baddley, John W.] Univ Alabama, Med Ctr, Birmingham, AL 35294 USA.
[Alexander, Barbara D.] Duke Univ, Med Ctr, Durham, NC USA.
[Anaissie, Elias J.] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Andes, David R.] Univ Wisconsin, Madison, WI USA.
[Brown, Janice M.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Brumble, Lisa M.] Mayo Clin, Jacksonville, FL 32224 USA.
[Freifeld, Alison G.] Univ Nebraska Med Ctr, Omaha, NE USA.
[Hadley, Susan] Tufts Med Ctr, Boston, MA USA.
[Herwaldt, Loreen] Univ Iowa Hosp, Iowa City, IA USA.
[Ito, James I.] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Kauffman, Carol A.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Kauffman, Carol A.] Vet Affairs Ann Arbor Healthcare Syst Med, Ann Arbor, MI USA.
[Lyon, G. Marshall] Emory Univ, Sch Med, Atlanta, GA USA.
[Marr, Kieren A.; Perl, Trish M.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Marr, Kieren A.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Morrison, Vicki A.] Univ Minnesota, Minneapolis, MN USA.
[Morrison, Vicki A.] Vet Affairs Med Ctr, Minneapolis, MN USA.
[Papanicolaou, Genovefa] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Patterson, Thomas F.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Patterson, Thomas F.] S Texas Vet Healthcare Syst, San Antonio, TX USA.
[Schuster, Mindy G.] Hosp Univ Penn, Philadelphia, PA 19104 USA.
[Walker, Randall] Mayo Clin, Rochester, MN USA.
[Wingard, John R.] Univ Florida, Gainesville, FL USA.
[Walsh, Thomas J.] NIH, Bethesda, MD 20892 USA.
[Kontoyiannis, Dimitrios P.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Park, BJ (reprint author), Ctr Dis Control & Prevent, Mycot Dis Branch, 1600 Clifton Rd NE,Mailstop C09, Atlanta, GA 30333 USA.
EM bpark1@cdc.gov
OI Papanicolaou, Genovefa/0000-0002-2891-079X; Patterson, Thomas
/0000-0002-9513-7127
FU Centers for Disease Control and Prevention [5U01CI000286-05]; Merck Co.,
Inc.; Astellas U.S., Inc.; Pfizer, Inc.; Schering-Plough Research
Institute; Enzon Pharmaceuticals, Inc.
FX This study was supported through Centers for Disease Control and
Prevention Grant 5U01CI000286-05 and grants from Merck & Co., Inc.;
Astellas U.S., Inc.; Pfizer, Inc.; Schering-Plough Research Institute;
and Enzon Pharmaceuticals, Inc.
NR 35
TC 74
Z9 74
U1 0
U2 8
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD OCT
PY 2011
VL 17
IS 10
BP 1855
EP 1864
DI 10.3201/eid1710.110087
PG 10
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 833PL
UT WOS:000295897300009
PM 22000355
ER
PT J
AU Silbergleit, R
Lowenstein, D
Durkalski, V
Conwit, R
AF Silbergleit, Robert
Lowenstein, Daniel
Durkalski, Valerie
Conwit, Robin
CA Neurological Emergency Treatment
TI RAMPART (Rapid Anticonvulsant Medication Prior to Arrival Trial): A
double-blind randomized clinical trial of the efficacy of intramuscular
midazolam versus intravenous lorazepam in the prehospital treatment of
status epilepticus by paramedics
SO EPILEPSIA
LA English
DT Article
DE Binary outcome; Intravenous; Intramuscular; Lorazepam; Midazolam;
Placebo; Seizure termination
ID DIAZEPAM
AB Early treatment of prolonged seizures with benzodiazepines given intravenously by paramedics in the prehospital setting has been shown to be associated with improved outcomes. However, an increasing number of Emergency Medical System (EMS) protocols use an intramuscular (IM) route because it is faster and consistently achievable. RAMPART (Rapid Anticonvulsant Medication Prior to Arrival Trial) is a double-blind randomized clinical trial to determine if the efficacy of IM midazolam is noninferior by a margin of 10% to that of intravenous (IV) lorazepam in patients treated by paramedics for status epilepticus (SE). Children and adults with >5 min of convulsions who are still seizing after paramedic arrival are administered study medication by IM autoinjector or IV infusion. The primary efficacy outcome is absence of seizures at emergency department (ED) arrival, without EMS rescue therapy. Safety outcomes include acute endotracheal intubation and recurrent seizures. Secondary outcomes include timing of treatment and initial seizure cessation. At the time of writing this communication, enrollment of all subjects is near completion and the study data will soon be analyzed.
C1 [Lowenstein, Daniel] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
[Silbergleit, Robert] Univ Michigan Hlth Syst, Dept Emergency Med, Ann Arbor, MI USA.
[Durkalski, Valerie] Med Univ S Carolina, Div Biostat & Epidemiol, Charleston, SC 29425 USA.
[Conwit, Robin] NINDS, Div Extramural Res, Bethesda, MD 20892 USA.
RP Lowenstein, D (reprint author), Univ Calif San Francisco, Dept Neurol, 505 Parnussus Ave,Room M-794, San Francisco, CA 94143 USA.
EM lowenstein@medsch.ucsf.edu
FU National Institute of Neurological Disorders and Stroke (NINDS)
[5U01NS056975-04]; Office of the Director, National Institutes of Health
(OD); BARDA; NIH
FX This work is supported by award 5U01NS056975-04 from the National
Institute of Neurological Disorders and Stroke (NINDS), the Office of
the Director, National Institutes of Health (OD), BARDA, and the NIH
CounterACT program. This trial is registered with Clinical Trials.gov
(NCT00809146).
NR 4
TC 26
Z9 27
U1 0
U2 11
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD OCT
PY 2011
VL 52
SU 8
SI SI
BP 45
EP 47
DI 10.1111/j.1528-1167.2011.03235.x
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 835VR
UT WOS:000296065200015
PM 21967361
ER
PT J
AU Propst, AM
Hill, MJ
Bates, GW
Palumbo, M
Van Horne, AK
Retzloff, MG
AF Propst, Anthony M.
Hill, Micah J.
Bates, Gordon Wright
Palumbo, Michelle
Van Horne, Anne K.
Retzloff, Matthew G.
TI Low-dose human chorionic gonadotropin may improve in vitro fertilization
cycle outcomes in patients with low luteinizing hormone levels after
gonadotropin-releasing hormone antagonist administration
SO FERTILITY AND STERILITY
LA English
DT Article
DE GnRH antagonist; IVF; low-dose uhCG; luteinizing hormone
ID FOLLICLE-STIMULATING-HORMONE; CONTROLLED OVARIAN STIMULATION; HUMAN
MENOPAUSAL GONADOTROPIN; RECOMBINANT HUMAN FSH; HIGHLY PURIFIED HMG;
INTRACYTOPLASMIC SPERM INJECTION; HUMAN LH SUPPLEMENTATION;
EARLY-PREGNANCY LOSS; NORMOGONADOTROPHIC WOMEN; ASSISTED REPRODUCTION
AB Objective: To evaluate the effect of low levels of endogenous luteinizing hormone (LH) and low-dose human chorionic gonadotropin (hCG) supplementation on in vitro fertilization (IVF) cycle outcomes in a gonadotropin-releasing hormone (GnRH) antagonist protocol.
Design: Retrospective study.
Setting: Military medical center.
Patient(s): General in vitro fertilization/embryo transfer (IVF-ET) population.
Intervention(s): Addition of low-dose urinary hCG to IVF stimulations using a recombinant follicle-stimulating hormone (FSH) and GnRH antagonist protocol.
Main Outcome Measure(s): Implantation and live-birth rates.
Result(s): As part of a larger cohort of 239 patients, 42 patients with LH levels <= 0.5 mIU/mL were evaluated. In the larger cohort, there were no differences in implantation and pregnancy rates between the recombinant FSH only (n = 113) and the recombinant FSH with low-dose hCG supplementation (n = 126) groups. In the FSH-only group, patients with LH levels <= 0.5 mIU/mL had decreased implantation rates (19% vs. 42%) and live-birth rates (25% vs. 54%) as compared with patients with LH levels >0.5 mIU/mL. Low LH patients in the recombinant FSH with low-dose urinary hCG group had statistically significantly higher implantation rates (54% vs. 19%) and live-birth rates (64% vs. 25%) as compared with patients with similar low LH levels in the recombinant FSH-only group.
Conclusion(s): Endogenous LH levels <= 0.5 mIU/mL after GnRH antagonist treatment are associated with statistically significantly lower implantation and pregnancy rates in recombinant FSH-only cycles. The addition of low-dose urinary hCG results in improved implantation and live-birth rates in patients with low LH levels. (Fertil Steril (R) 2011; 96: 898-904. (C) 2011 by American Society for Reproductive Medicine.)
C1 [Propst, Anthony M.] Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, Bethesda, MD 20814 USA.
[Propst, Anthony M.; Hill, Micah J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Propst, Anthony M.; Bates, Gordon Wright; Palumbo, Michelle; Van Horne, Anne K.; Retzloff, Matthew G.] San Antonio Uniformed Serv Hlth Educ Consortium, Div Reprod Endocrinol, Wilford Hall Med Ctr, San Antonio, TX USA.
RP Propst, AM (reprint author), Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM anthony.propst@usuhs.mil
FU Ferring; Reproductive Biology and Medicine Branch, Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
National Institutes of Health
FX A.M.P. has received consulting fees from Ferring. M.J.H. has nothing to
disclose. G.W.B. has nothing to disclose. M.P. has nothing to disclose.
A.K.V.H. has nothing to disclose. M.G.R. has nothing to disclose.;
Supported in part by the Intramural research program of the Reproductive
Biology and Medicine Branch, Eunice Kennedy Shriver National Institute
of Child Health and Human Development, National Institutes of Health.
The opinions and conclusions in this paper are those of the authors and
are not intended to represent the official position of the Department of
Defense, United States Air Force, United States Army or any other
government agency.
NR 69
TC 5
Z9 7
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD OCT
PY 2011
VL 96
IS 4
BP 898
EP 904
DI 10.1016/j.fertnstert.2011.06.069
PG 7
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 834DF
UT WOS:000295938800030
PM 21839437
ER
PT J
AU Achyut, BR
Yang, L
AF Achyut, Bhagelu Ram
Yang, Li
TI Transforming Growth Factor-beta in the Gastrointestinal and Hepatic
Tumor Microenvironment
SO GASTROENTEROLOGY
LA English
DT Review
DE Cancer Cell Signaling; Proliferation; T beta R; Apoptosis
ID SQUAMOUS-CELL CARCINOMA; EPITHELIAL-MESENCHYMAL TRANSITION; GR-1+CD11B+
MYELOID CELLS; SMAD4 GENE-MUTATIONS; HUMAN BREAST-CANCER; AUTOCRINE
TGF-BETA; HEPATOCELLULAR-CARCINOMA; PANCREATIC-CANCER; COLON-CANCER;
IMMUNE CELLS
AB Transforming growth factor (TGF)-beta is a multifunctional cytokine that has important roles in tumor formation, progression, and metastasis. TGF-beta is overproduced, and its signaling is deregulated, in a variety of human tumors, including colorectal, gastric, pancreatic, and liver. Therapeutics are being developed to block TGF-beta signaling. However, TGF-beta also functions as a tumor suppressor in premalignant cells. It is not clear how its function changes from that of a tumor suppressor to a tumor promoter; improvements are needed in our understanding of TGF-beta functions in tumor development before we can design inhibitors for use as anticancer therapies. TGF-beta regulates not only different tumor-cell autonomous signaling pathways, but also interactions between tumor and host cells, through paracrine mechanisms. We review recent findings about how TGF-beta is regulated and its roles in the tumor microenvironment and metastasis, with a focus on gastrointestinal cancers. Improved understanding of TGF-beta regulation and how it mediates interaction between cancer epithelial cells, immune cells, and fibroblasts will provide important insights into tumor development and progression.
C1 [Yang, Li] NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bethesda, MD 20876 USA.
RP Yang, L (reprint author), NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bldg 37,Room 3134C,37 Convent Dr,MSC 4258, Bethesda, MD 20876 USA.
EM yangl3@mail.nih.gov
NR 147
TC 76
Z9 80
U1 1
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 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2011
VL 141
IS 4
BP 1167
EP 1178
DI 10.1053/j.gastro.2011.07.048
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829OQ
UT WOS:000295593700023
PM 21839702
ER
PT J
AU Sandler, NG
Koh, C
Roque, A
Eccleston, JL
Siegel, RB
Demino, M
Kleiner, DE
Deeks, SG
Liang, TJ
Heller, T
Douek, DC
AF Sandler, Netanya G.
Koh, Christopher
Roque, Annelys
Eccleston, Jason L.
Siegel, Rebecca B.
Demino, Mary
Kleiner, David E.
Deeks, Steven G.
Liang, T. Jake
Heller, Theo
Douek, Daniel C.
TI Host Response to Translocated Microbial Products Predicts Outcomes of
Patients With HBV or HCV Infection
SO GASTROENTEROLOGY
LA English
DT Article
DE Microbial Translocation; Soluble CD14; Hepatitis; Intestinal Fatty Acid
Binding Protein
ID ACID-BINDING-PROTEIN; C VIRUS-INFECTION; HEPATITIS-C; LIVER-DISEASE;
SOLUBLE CD14; BACTEROIDES-FRAGILIS; LIPOPOLYSACCHARIDE; CELLS;
EXPRESSION; ENDOTOXIN
AB BACKGROUND & AIMS: Chronic infection with hepatitis B or C virus (HBV or HCV) is a leading cause of cirrhosis by unknown mechanisms of pathogenesis. Translocation of gut microbial products into the systemic circulation might increase because of increased intestinal permeability, bacterial overgrowth, or impaired clearance of microbial products by Kupffer cells. We investigated whether the extent and progression of liver disease in patients with chronic HBV or HCV infection are associated with microbial translocation and subsequent activation of monocytes. METHODS: In a retrospective study, we analyzed data from 16 patients with minimal fibrosis, 68 with cirrhosis, and 67 uninfected volunteers. We analyzed plasma levels of soluble CD14 (sCD14), intestinal fatty acid binding protein, and interleukin-6 by enzyme-linked immunosorbent assay, and lipopolysaccharide (LPS) by the limulus amebocyte lysate assay, at presentation and after antiviral treatment. RESULTS: Compared with uninfected individuals, HCV- and HBV-infected individuals had higher plasma levels of LPS, intestinal fatty acid binding protein (indicating enterocyte death), sCD14 (produced upon LPS activation of monocytes), and interleukin-6. Portal hypertension, indicated by low platelet counts, was associated with enterocyte death (P = .045 at presentation, P < .0001 after therapy). Levels of sCD14 correlated with markers of hepatic inflammation (P = .02 for aspartate aminotransferase, P = .002 for ferritin) and fibrosis (P < .0001 for gamma-glutamyl transpeptidase, P = .01 for alkaline phosphatase, P < .0001 for alpha-fetoprotein). Compared to subjects with minimal fibrosis, subjects with severe fibrosis at presentation had higher plasma levels of sCD14 (P = .01) and more hepatic CD14(+) cells (P = .0002); each increased risk for disease progression (P = .0009 and P = .005, respectively). CONCLUSIONS: LPS-induced local and systemic inflammation is associated with cirrhosis and predicts progression to end-stage liver disease in patients with HBV or HCV infection.
C1 [Sandler, Netanya G.; Roque, Annelys; Siegel, Rebecca B.; Douek, Daniel C.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Koh, Christopher; Eccleston, Jason L.; Demino, Mary; Liang, T. Jake; Heller, Theo] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Deeks, Steven G.] Univ Calif San Francisco, San Francisco Gen Hosp, Div HIV AIDS, Dept Med, San Francisco, CA USA.
RP Douek, DC (reprint author), NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, 40 Convent Dr,Room 3509, Bethesda, MD 20892 USA.
EM theoh@intra.niddk.nih.gov; ddouek@mail.nih.gov
OI Utay, Netanya/0000-0002-6407-8670; Kleiner, David/0000-0003-3442-4453
FU National Institute of Allergy and Infectious Diseases; National
Institute of Diabetes and Digestive and Kidney Diseases; National Cancer
Institute (National Institutes of Health); National Institutes of Health
[AI-76174]
FX Grant support received from the intramural programs of National
Institute of Allergy and Infectious Diseases, National Institute of
Diabetes and Digestive and Kidney Diseases, and National Cancer
Institute (National Institutes of Health) and National Institutes of
Health grant AI-76174.
NR 56
TC 105
Z9 109
U1 1
U2 15
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2011
VL 141
IS 4
BP 1220
EP U640
DI 10.1053/j.gastro.2011.06.063
PG 14
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829OQ
UT WOS:000295593700029
PM 21726511
ER
PT J
AU Ahlenstiel, G
Edlich, B
Hogdal, LJ
Rotman, Y
Noureddin, M
Feld, JJ
Holz, LE
Titerence, RH
Liang, TJ
Rehermann, B
AF Ahlenstiel, Golo
Edlich, Birgit
Hogdal, Leah J.
Rotman, Yaron
Noureddin, Mazen
Feld, Jordan J.
Holz, Lauren E.
Titerence, Rachel H.
Liang, T. Jake
Rehermann, Barbara
TI Early Changes in Natural Killer Cell Function Indicate Virologic
Response to Interferon Therapy for Hepatitis C
SO GASTROENTEROLOGY
LA English
DT Article
DE Liver Disease; HCV Treatment; Response to Therapy; Cell Death
ID VIRUS-INFECTION; NK CELLS; RECEPTOR EXPRESSION; INNATE; HCV;
CYTOTOXICITY; CYTOKINES; SUBSET; ALPHA; RIBAVIRIN
AB BACKGROUND & AIMS: Mathematical modeling of hepatitis C virus (HCV) kinetics indicated that cellular immune responses contribute to interferon (IFN)-induced clearance of HCV. We investigated a potential role of natural killer (NK) cells in this process. METHODS: Phenotype and function of blood and liver NK cells were studied during the first 12 weeks of treatment with pegylated IFN-alfa and ribavirin, the time period used to define the early virological response. RESULTS: Within hours of treatment initiation, NK cells of patients that had an early virological response increased expression of activating receptors NKG2D, NKp30, and CD16 and decreased expression of NKG2C and 2B4, along with inhibitory receptors SIGLEC7 and NKG2A, resulting in NK cell activation. NK cell cytotoxicity, measured by degranulation and tumor necrosis factor-related apoptosis-inducing ligand production, peaked after 24 hours (P < .01), concomitant with an increase in alanine aminotransferase levels (P < .05), whereas IFN-gamma production decreased within 6 hours and did not recover for more than 4 weeks (P < .05). NK cells from liver biopsies taken 6 hours after treatment initiation had increased numbers of cytotoxic CD16(+)NK cells (P < .05) and a trend toward increased production of tumor necrosis factor-related apoptosis-inducing ligand. Degranulation of peripheral blood NK cells correlated with treatment-induced, first-phase decreases in viral load (P < .05) and remained higher in early virological responders than in nonresponders for weeks. CONCLUSIONS: IFN activates NK cells early after treatment is initiated. Their cytotoxic function, in particular, is strongly induced, which correlates to virologic response. Therefore, NK cell activation indicates responsiveness to IFN-alpha-based treatment and suggests the involvement of the innate immune cells in viral clearance.
C1 [Ahlenstiel, Golo; Edlich, Birgit; Hogdal, Leah J.; Holz, Lauren E.; Titerence, Rachel H.; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Rehermann, B (reprint author), NIDDK, Immunol Sect, Liver Dis Branch, NIH,Dept Hlth & Human Serv, 10 Ctr Dr,Bldg 10,Room 9B16, Bethesda, MD 20892 USA.
EM Rehermann@nih.gov
OI Rotman, Yaron/0000-0002-7549-8216; Ahlenstiel, Golo/0000-0003-0026-1457
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health
FX This study was supported by the National Institute of Diabetes and
Digestive and Kidney Diseases, National Institutes of Health intramural
research program.
NR 30
TC 82
Z9 85
U1 0
U2 11
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD OCT
PY 2011
VL 141
IS 4
BP 1231
EP U651
DI 10.1053/j.gastro.2011.06.069
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829OQ
UT WOS:000295593700030
PM 21741920
ER
PT J
AU Grandemange, S
Aksentijevich, I
Jeru, I
Gul, A
Touitou, I
AF Grandemange, S.
Aksentijevich, I.
Jeru, I.
Gul, A.
Touitou, I.
TI The regulation of MEFV expression and its role in health and familial
Mediterranean fever
SO GENES AND IMMUNITY
LA English
DT Review
DE expression; MEFV; FMF
ID NF-KAPPA-B; PRIMARY FIBROBLAST-CULTURES; MESSENGER-RNA;
SUBCELLULAR-LOCALIZATION; C5A INHIBITOR; PYRIN DOMAIN; SPRY DOMAIN;
GENE; PROTEIN; ASC
AB Familial Mediterranean fever (FMF) is a hereditary recurrent fever associated with mutations in the gene MEFV encoding pyrin. It is expressed mainly in neutrophils and macrophages, and modulates the production of the potent pro-inflammatory cytokine interleukin-1 beta through regulation of nuclear factor-kappa B and caspase-1. The MEFV gene expression depends on multiple levels of regulation. Sequence variants located in the promoter and at the 3'-untranslated region of the gene modulate this expression. Two studies demonstrated decreased mRNA levels in FMF patients compared with healthy subjects, whereas two others found no significant differences. The diverse experimental settings may have resulted in variable quantification of the 15 splice variants that have been identified recently. Some of these isoforms are regulated by nonsense-mediated decay in both cell-and transcript-specific manner, and may be differentially translated in THP1 cells. In addition, pyrin may be cleaved by caspase 1. The full-length pyrin was less abundant than the cleaved fragment in mononuclear cells from FMF patients than in controls, whereas the opposite was observed in granulocytes. Altogether, the regulation of MEFV expression is more complex than anticipated in both physiological and pathological conditions. Its deregulation is likely to alter the inflammasome function and subsequently result in uncontrolled inflammation as seen in FMF. Genes and Immunity (2011) 12, 497-503; doi:10.1038/gene.2011.53; published online 21 July 2011
C1 [Grandemange, S.; Touitou, I.] Hop Arnaud de Villeneuve, Unite Med Malad Autoinflammatoires, CHRU Montpellier, INSERM,U844,UM1, F-34295 Montpellier 5, France.
[Aksentijevich, I.] NHGRI, Bethesda, MD 20892 USA.
[Jeru, I.] Univ Paris 06, INSERM, U933, UMR S933, Paris, France.
[Gul, A.] Istanbul Univ, Istanbul Fac Med, Div Rheumatol, Dept Internal Med, Istanbul, Turkey.
RP Touitou, I (reprint author), Hop Arnaud de Villeneuve, Unite Med Malad Autoinflammatoires, CHRU Montpellier, INSERM,U844,UM1, 371 Ave Doyen Giraud, F-34295 Montpellier 5, France.
EM isabelle.touitou@inserm.fr
FU CHRU of Montpellier [PHRC2005]; National Human Genome Research
Institute; INSERM; Istanbul Faculty of Medicine
FX This work was supported by the CHRU of Montpellier (PHRC2005), the
National Human Genome Research Institute, INSERM and Istanbul Faculty of
Medicine. We thank the clinicians for providing patient samples, J Tazy
for helpful discussion and M Vittal for English editing of the
manuscript.
NR 39
TC 10
Z9 11
U1 0
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1466-4879
J9 GENES IMMUN
JI Genes Immun.
PD OCT
PY 2011
VL 12
IS 7
BP 497
EP 503
DI 10.1038/gene.2011.53
PG 7
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA 838ZI
UT WOS:000296332900001
PM 21776013
ER
PT J
AU Shakes, DC
Allen, AK
Albert, KM
Golden, A
AF Shakes, Diane C.
Allen, Anna K.
Albert, Kelsey M.
Golden, Andy
TI emb-1 Encodes the APC16 Subunit of the Caenorhabditis elegans
Anaphase-Promoting Complex
SO GENETICS
LA English
DT Article
ID CHROMOSOME SEGREGATION; SACCHAROMYCES-CEREVISIAE; DEVELOPMENTAL DEFECTS;
GENETIC INTERFERENCE; PROTEIN COMPLEXES; MEIOSIS-I; C-ELEGANS; YEAST;
COMPLEX/CYCLOSOME; MUTANTS
AB In the nematode Caenorhabditis elegans, temperature-sensitive mutants of emb-1 arrest as one-cell embryos in metaphase of meiosis I in a manner that is indistinguishable from embryos that have been depleted of known subunits of the anaphase-promoting complex or cyclosome (APC/C). Here we show that the emb-1 phenotype is enhanced in double mutant combinations with known APC/C subunits and suppressed in double mutant combinations with known APC/C suppressors. In addition to its meiotic function, emb-1 is required for mitotic proliferation of the germline. These studies reveal that emb-1 encodes K10D2.4, a homolog of the small, recently discovered APC/C subunit, APC16.
C1 [Allen, Anna K.; Golden, Andy] NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
[Shakes, Diane C.; Albert, Kelsey M.] Coll William & Mary, Dept Biol, Williamsburg, VA 23185 USA.
RP Golden, A (reprint author), 8 Ctr Dr,Bldg 8,Room 323, Bethesda, MD 20892 USA.
EM andyg@mail.nih.gov
FU National Institutes of Health (NIH) [R15GM60359]; Jeffress Memorial
Trust [J-840]; NIH, National Institute of Diabetes and Digestive and
Kidney Diseases
FX We acknowledge Yuji Kohara (National Institute of Genetics, Mishima,
Japan) for generously providing us with the cDNA clone for emb-1. We are
also grateful to Shohei Mitani (Tokyo Women's Medical University School
of Medicine) for generating the cid-1 deletion alleles, the C. elegans
Gene Knockout Consortium (Oklahoma Medical Research Foundation), and the
C. elegans Reverse Genetics Core Facility (Vancouver) for isolating the
ok2757 and ok2759 deletion alleles of emb-1. We thank Colin Thacker
(University of Utah) for generating our transgenic lines, the
Caenorhabditis Genetics Center for providing numerous strains for
mapping, James LaRue (College of William and Mary) for preliminary
studies of emb-1 doubles, and Kevin O'Connell for critical comments on
this manuscript. We are also grateful for the discussions and
suggestions from members of our laboratories and the Baltimore Worm
Club. This research was supported, in part, by National Institutes of
Health (NIH) grant R15GM60359 (D.C.S.), Jeffress Memorial Trust Grant
(J-840; D.C.S.), and the Intramural Research Program of the NIH,
National Institute of Diabetes and Digestive and Kidney Diseases (A.G.).
NR 55
TC 8
Z9 12
U1 0
U2 1
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 0016-6731
J9 GENETICS
JI Genetics
PD OCT
PY 2011
VL 189
IS 2
BP 549
EP 560
DI 10.1534/genetics.111.131714
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 836ZH
UT WOS:000296158500012
PM 21775471
ER
PT J
AU Saghir, SA
Ghanayem, BI
Schultz, IR
AF Saghir, Shakil A.
Ghanayem, Burhan I.
Schultz, Irvin R.
TI Kinetics of Trihalogenated Acetic Acid Metabolism and Isoform
Specificity in Liver Microsomes
SO INTERNATIONAL JOURNAL OF TOXICOLOGY
LA English
DT Article
DE bromodichloroacetic acid; chlorodibromoacetic acid; tribromoacetic acid;
microsomal metabolism; rat; mouse; human
ID B6C3F1 MICE; ORAL BIOAVAILABILITY; DIBROMOACETIC ACID; HALOACETIC ACIDS;
DRINKING-WATER; DEPLETED RATS; DICHLOROACETATE; TOXICOKINETICS;
BROMODICHLOROACETATE; TRICHLOROACETATE
AB This study determined the metabolism of 3 drinking water disinfection by-products (halogenated acetic acids [HAAs]), bromodichloroacetic acid (BDCAA), chlorodibromoacetic acid (CDBAA), and tribromoacetic acid (TBAA), using rat, mouse, human liver microsomes, and recombinant P450. Metabolism proceeded by reductive debromination forming a di-HAA; the highest under nitrogen >>2% oxygen > atmospheric headspaces. V(max) for the loss of tri-HAA was 4 to 5 times higher under nitrogen than atmospheric headspace. Intrinsic metabolic clearance was TBAA>CDBAA>>BDCAA. At the high substrate concentrations, tri-HAA consumption rate was 2 to 3 times higher than the formation of di-HAA. Liberation of Br(-) from TBAA corresponded to the expected amount produced after DBAA formation, indicating retention of Br(-) by additional metabolite/metabolites. Subsequent experiments with CDBAA detected negligible formation of chlorodibromomethane (CDBM) and failed to account for the missing tri-HAA. Carbon monoxide and especially diphenyleneiodonium ([DPI] P450 reductase inhibitor) blocked CDBAA metabolism. Other chemical inhibitors were only partially able to block CDBAA metabolism. Most effective were inhibitors of CYP 2E1 and CYP 3A4. Immunoinhibition studies using human liver microsomes and anti-human CYP 2E1 antibodies were successful in reducing CDBAA metabolism. However, CDBAA metabolism in wild-type (WT) and CYP 2E1 knockout (KO) mouse liver microsomes was similar, suggesting significant interspecies differences in CYP isoform in tri-HAA metabolism. Additional assessment of CYP isoform involvement was complicated by the finding that recombinantly expressed rat and human P450 reductase was able to metabolize CDBAA, which may be a contributing factor in interspecies differences in tri-HAA metabolism.
C1 [Saghir, Shakil A.] Dow Chem Co USA, Toxicol & Environm Res & Consulting, Midland, MI 48674 USA.
[Saghir, Shakil A.] Aga Khan Univ, Dept Biol & Biomed Sci, Karachi, Pakistan.
[Ghanayem, Burhan I.] NIEHS, Environm Toxicol Program, Pharmacol Lab, Res Triangle Pk, NC 27709 USA.
[Schultz, Irvin R.] Pacific NW Natl Lab, Sequim, WA USA.
RP Saghir, SA (reprint author), Dow Chem Co USA, Toxicol & Environm Res & Consulting, 1803 Bldg, Midland, MI 48674 USA.
EM ssaghir@dow.com
FU U.S. Environmental Protection Agency [R828044, R82594]
FX The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: U.S.
Environmental Protection Agency Grants R828044, R82594.
NR 30
TC 1
Z9 1
U1 1
U2 5
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1091-5818
J9 INT J TOXICOL
JI Int. J. Toxicol.
PD OCT
PY 2011
VL 30
IS 5
BP 551
EP 561
DI 10.1177/1091581811414213
PG 11
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 835GJ
UT WOS:000296023600011
PM 21933969
ER
PT J
AU Sun, HM
Veith, H
Xia, MH
Austin, CP
Huang, RL
AF Sun, Hongmao
Veith, Henrike
Xia, Menghang
Austin, Christopher P.
Huang, Ruili
TI Predictive Models for Cytochrome P450 Isozymes Based on Quantitative
High Throughput Screening Data
SO JOURNAL OF CHEMICAL INFORMATION AND MODELING
LA English
DT Article
ID MACHINE-LEARNING TECHNIQUES; CHEMICAL LIBRARIES; CRYSTAL-STRUCTURE;
DRUG-METABOLISM; CYP3A4; SELECTIVITY; BINDING; P450S; 3A4
AB The human cytochrome P450 (CYP450) isozymes are the most important enzymes in the body to metabolize many endogenous and exogenous substances including environmental toxins and therapeutic drugs. Any unnecessary interactions between a small molecule and CYP450 isozymes may raise a potential to disarm the integrity of the protection. Accurately predicting the potential interactions between a small molecule and CYP450 isozymes is highly desirable for assessing the metabolic stability and toxicity of the molecule. The National Institutes of Health Chemical Genomics Center (NCGC) has screened a collection of over 17,000 compounds against the five major isozymes of CYP450 (1A2, 2C9, 2C19, 2D6, and 3A4) in a quantitative high throughput screening (qHTS) format. In this study, we developed support vector classification (SVC) models for these five isozymes using a set of customized generic atom types. The CYP450 data sets were randomly split into equal-sized training and test sets. The optimized SVC models exhibited high predictive power against the test sets for all five CYP450 isozymes with accuracies of 0.93, 0.89, 0.89, 0.85, and 0.87 for 1A2, 2C9, 2C19, 2D6, and 3A4, respectively, as measured by the area under the receiver operating characteristic (ROC) curves. The important atom types and features extracted from the five models are consistent with the structural preferences for different CYP450 substrates reported in the literature. We also identified novel features with significant discerning power to separate CYP450 actives from inactives. These models can be useful in prioritizing compounds in a drug discovery pipeline or recognizing the toxic potential of environmental chemicals.
C1 [Sun, Hongmao; Veith, Henrike; Xia, Menghang; Austin, Christopher P.; Huang, Ruili] NIH, Chem Genom Ctr, Bethesda, MD 20892 USA.
RP Sun, HM (reprint author), NIH Chem Genom Ctr, NIH, 9800 Med Ctr Dr, Rockville, MD 20850 USA.
EM sunh7@mail.nih.gov
FU National Human Genome Research Institute, National Institutes of Health
FX This work was supported by the Intramural Research Programs of the
National Human Genome Research Institute, National Institutes of Health.
We thank in particular Rena Zheng for helpful comments and suggestions
during the preparation of this manuscript.
NR 35
TC 25
Z9 27
U1 2
U2 9
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1549-9596
J9 J CHEM INF MODEL
JI J. Chem Inf. Model.
PD OCT
PY 2011
VL 51
IS 10
BP 2474
EP 2481
DI 10.1021/ci200311w
PG 8
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Computer Science,
Information Systems; Computer Science, Interdisciplinary Applications
SC Pharmacology & Pharmacy; Chemistry; Computer Science
GA 835NX
UT WOS:000296044200004
PM 21905670
ER
PT J
AU da Silva, SP
Resnick, E
Lucas, M
Lortan, J
Patel, S
Cunningham-Rundles, C
Gatter, K
Liu, QY
Jaffe, ES
Chapel, H
AF da Silva, Sara Pereira
Resnick, Elena
Lucas, Mary
Lortan, Jennifer
Patel, Smita
Cunningham-Rundles, Charlotte
Gatter, Kevin
Liu, Qingyan
Jaffe, Elaine S.
Chapel, Helen
TI Lymphoid Proliferations of Indeterminate Malignant Potential arising in
Adults with Common Variable Immunodeficiency Disorders: Unusual Case
Studies and Immunohistological Review in the Light of Possible Causative
Events
SO JOURNAL OF CLINICAL IMMUNOLOGY
LA English
DT Article
DE Common variable immunodeficiency disorders; lymphoid proliferation;
lymphoma; infection
ID HELICOBACTER-PYLORI ERADICATION; T-CELL RESPONSE; ANTIBODY DEFICIENCY;
MALT LYMPHOMA; LONG-TERM; DISEASE; TISSUE; CLASSIFICATION;
ASPERGILLOSIS; INFECTION
AB Patients with common variable immunodeficiency disorders (CVIDs) who developed B cell lymphoproliferation of indeterminate malignant potential are described in order to raise a discussion of the relationship between infection and lymphoproliferation in infection prone patients. Those with CVID are at risk of developing either polyclonal or monoclonal lymphoproliferation in part due to the dysregulation of their adaptive immune systems. The aetiologies of the lymphoproliferations are unknown but intriguing; the relevance of infection being particularly problematic. The patients described here demonstrate variability in preceding infection, age at presentation, response to antibiotics and other types of therapy as well as outcome. The question of treatment is also controversial; issues include whether antibiotics or chemotherapy are the first line of therapy in all patients and whether transformation to aggressive B cell malignancy is inevitable or depends on other factors and if so, the length of time for such progression.
C1 [Lucas, Mary; Lortan, Jennifer; Patel, Smita; Chapel, Helen] Univ Oxford, John Radcliffe Hosp, Nuffield Dept Med, Clin Immunol Unit, Oxford OX3 9DU, England.
[da Silva, Sara Pereira] Hosp Santa Maria, Immunoallergol Dept, Lisbon, Portugal.
[Resnick, Elena; Cunningham-Rundles, Charlotte] Mt Sinai Med Ctr, Dept Med, New York, NY 10029 USA.
[Resnick, Elena; Cunningham-Rundles, Charlotte] Mt Sinai Med Ctr, Inst Immunol, New York, NY 10029 USA.
[Lortan, Jennifer; Gatter, Kevin] Univ Oxford, Nuffield Dept Clin Lab Sci, Oxford OX3 9DU, England.
[Liu, Qingyan; Jaffe, Elaine S.] NCI, Hematopathol Sect, Pathol Lab, Bethesda, MD 20892 USA.
RP Chapel, H (reprint author), Univ Oxford, John Radcliffe Hosp, Nuffield Dept Med, Clin Immunol Unit, Level 7,Headley Way, Oxford OX3 9DU, England.
EM helen.chapel@ndm.ox.ac.uk
OI Jaffe, Elaine/0000-0003-4632-0301
FU NIHR Oxford Biomedical Centre; EU; Primary Immunodeficiency Association;
Baxter Healthcare; Jeffrey Modell Foundation; Sociedade Portuguesa de
Alergologia e Imunologia Clinica; National Institutes of Health [AI
101093, AI-467320, AI-48693]; NIAID [03-22]; David S Gottesman
Immunology Chair
FX We are grateful to the following funding bodies for their financial
support: NIHR Oxford Biomedical Centre Programme, EU 7th Framework
Programme (PADnet), the Primary Immunodeficiency Association, Baxter
Healthcare, the Jeffrey Modell Foundation (HC, CCR) and to Sociedade
Portuguesa de Alergologia e Imunologia Clinica, for the scholarship
programme that allowed a training period in the Oxford Centre for
Clinical Immunology, Oxford Radcliffe Hospitals. This work was also
supported by grants from the National Institutes of Health, AI 101093,
AI-467320, AI-48693, NIAID contract 03-22 and the David S Gottesman
Immunology Chair (CCR.)
NR 34
TC 16
Z9 16
U1 0
U2 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0271-9142
J9 J CLIN IMMUNOL
JI J. Clin. Immunol.
PD OCT
PY 2011
VL 31
IS 5
BP 784
EP 791
DI 10.1007/s10875-011-9565-z
PG 8
WC Immunology
SC Immunology
GA 835CT
UT WOS:000296012300007
PM 21744182
ER
PT J
AU Woodson, SE
Holbrook, MR
AF Woodson, Sara E.
Holbrook, Michael R.
TI Infection of hepatocytes with 17-D vaccine-strain yellow fever virus
induces a strong pro-inflammatory host response
SO JOURNAL OF GENERAL VIROLOGY
LA English
DT Article
ID ACUTE-PHASE RESPONSE; IN-VIVO SYNTHESIS; VISCEROTROPIC DISEASE;
IMMUNE-RESPONSE; ADVERSE EVENTS; TGF-BETA; ACTIVATION; LIVER; APOPTOSIS;
PROTEIN
AB Yellow fever virus (YFV) causes serious disease in endemic areas of South America and Africa, even though a very well tolerated vaccine is available. YFV primarily targets the liver where as many as 80% of hepatocytes may be involved during infection. The objective of this project was to compare and contrast the cytokine response from hepatocytes infected with either wild-type (Asibi) or vaccine (17-D-204) strains of YFV, with the goal of identifying responses that might be correlated with disease severity or vaccine efficacy. We report here that PH5CH8 hepatocytes support a productive infection with both wild-type and vaccine-strain YFV. Infection with either virus resulted in elevated expression of several pro- and anti-inflammatory cytokines [interleukin (IL)-1 beta, IL-4, IL-6, IL-8, IL-10 and tumour necrosis factor-alpha) with a corresponding increase in transcription. Hepatocytes infected with vaccine virus had a more profound response than did cells infected with wild-type virus. Pre-stimulation of hepatocytes with IL-6 resulted in reduced viral titres, elevated concentrations of cytokines released from Asibi virus-infected cells and improved cell viability in cells infected with 17-D virus. Data reported here suggest that 17-D virus stimulates an appropriate antiviral inflammatory response in hepatocytes, while Asibi virus can attenuate the host response. These data identify potential mechanisms that are associated with increased virulence in wild-type virus infections and also provide clues towards potential immune-response limitations that may be associated with vaccine-related adverse events.
C1 Univ Texas Med Branch, Dept Pathol, Galveston, TX 77550 USA.
Univ Texas Med Branch, Inst Human Infect & Immun, Galveston, TX 77550 USA.
RP Holbrook, MR (reprint author), NIAID Integrated Res Facil, 8200 Res Plaza, Frederick, MD 21702 USA.
EM michael.holbrook@nih.gov
NR 45
TC 3
Z9 3
U1 0
U2 3
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-1317
J9 J GEN VIROL
JI J. Gen. Virol.
PD OCT
PY 2011
VL 92
BP 2262
EP 2271
DI 10.1099/vir.0.031617-0
PN 10
PG 10
WC Biotechnology & Applied Microbiology; Virology
SC Biotechnology & Applied Microbiology; Virology
GA 833BE
UT WOS:000295856000004
PM 21697351
ER
PT J
AU Cruz, AV
Mallet, N
Magill, PJ
Brown, P
Averbeck, BB
AF Cruz, Ana V.
Mallet, Nicolas
Magill, Peter J.
Brown, Peter
Averbeck, Bruno B.
TI Effects of dopamine depletion on information flow between the
subthalamic nucleus and external globus pallidus
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
DE maximum entropy; Parkinson's disease; coding capacity
ID TONICALLY ACTIVE NEURONS; PARKINSONS-DISEASE; BASAL GANGLIA;
BETA-OSCILLATIONS; CEREBRAL-CORTEX; NEURAL OSCILLATIONS; FIELD
POTENTIALS; SYNCHRONIZATION; NETWORK; MODEL
AB Cruz AV, Mallet N, Magill PJ, Brown P, Averbeck BB. Effects of dopamine depletion on information flow between the subthalamic nucleus and external globus pallidus. J Neurophysiol 106: 2012-2023, 2011. First published August 3, 2011; doi: 10.1152/jn.00094.2011.-Abnormal oscillatory synchrony is increasingly acknowledged as a pathophysiological hallmark of Parkinson's disease, but what promotes such activity remains unclear. We used novel, nonlinear time series analyses and information theory to capture the effects of dopamine depletion on directed information flow within and between the subthalamic nucleus (STN) and external globus pallidus (GPe). We compared neuronal activity recorded simultaneously from these nuclei in 6-hydroxydopamine-lesioned Parkinsonian rats with that in dopamine-intact control rats. After lesioning, both nuclei displayed pronounced augmentations of beta-frequency (similar to 20 Hz) oscillations and, critically, information transfer between STN and GPe neurons was increased. Furthermore, temporal profiles of the directed information transfer agreed with the neurochemistry of these nuclei, being "excitatory" from STN to GPe and "inhibitory" from GPe to STN. Separation of the GPe population in lesioned animals into "type-inactive" (GP-TI) and "type-active" (GP-TA) neurons, according to definitive firing preferences, revealed distinct temporal profiles of interaction with STN and each other. The profile of GP-TI neurons suggested their output is of greater causal significance than that of GP-TA neurons for the reduced activity that periodically punctuates the spiking of STN neurons during beta oscillations. Moreover, STN was identified as a key candidate driver for recruiting ensembles of GP-TI neurons but not GP-TA neurons. Short-latency interactions between GP-TI and GP-TA neurons suggested mutual inhibition, which could rhythmically dampen activity and promote anti-phase firing across the two subpopulations. Results thus indicate that information flow around the STN-GPe circuit is exaggerated in Parkinsonism and further define the temporal interactions underpinning this.
C1 [Cruz, Ana V.; Averbeck, Bruno B.] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
[Cruz, Ana V.; Brown, Peter; Averbeck, Bruno B.] UCL, Sobell Dept Motor Neurosci & Movement Disorders, Inst Neurol, London, England.
[Cruz, Ana V.] Inst Gulbenkian Ciencias, Oeiras, Portugal.
[Mallet, Nicolas; Magill, Peter J.] Univ Oxford, MRC, Anat Neuropharmacol Unit, Oxford, England.
[Mallet, Nicolas; Magill, Peter J.] Univ Oxford, Oxford Parkinsons Dis Ctr, Oxford, England.
[Brown, Peter] Univ Oxford, John Radcliffe Hosp, Dept Clin Neurol, Oxford OX3 9DU, England.
RP Averbeck, BB (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 49,Rm 1B-80, Bethesda, MD 20892 USA.
EM bruno.averbeck@nih.gov
RI Brown, Peter/J-4307-2016;
OI Brown, Peter/0000-0002-5201-3044; Magill, Peter/0000-0001-7141-7071
FU Fundacao para a Ciencia e Tecnologia [SFRH/BD/33201/2007]; Fundacao
Gulbenkian; Medical Research Council UK; Dana Foundation USA;
Parkinson's UK Grant [G-0806]; Oxford National Institute for Health
Research Biomedical Centre; Wellcome Trust; National Institute of Mental
Health
FX A. V. Cruz was supported by Fundacao para a Ciencia e Tecnologia Grant
SFRH/BD/33201/2007 and Fundacao Gulbenkian. N. Mallet and P. J. Magill
were supported by the Medical Research Council UK, The Dana Foundation
USA, and Parkinson's UK Grant G-0806. P. Brown was supported by the
Medical Research Council UK and the Oxford National Institute for Health
Research Biomedical Centre. B. B. Averbeck was supported by the Wellcome
Trust and the National Institute of Mental Health Intramural Research
Program.
NR 56
TC 23
Z9 24
U1 1
U2 13
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD OCT
PY 2011
VL 106
IS 4
BP 2012
EP 2023
DI 10.1152/jn.00094.2011
PG 12
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 836EJ
UT WOS:000296092000035
PM 21813748
ER
PT J
AU Zanarini, MC
Horwood, J
Wolke, D
Waylen, A
Fitzmaurice, G
Grant, BF
AF Zanarini, Mary C.
Horwood, Jeremy
Wolke, Dieter
Waylen, Andrea
Fitzmaurice, Garrett
Grant, Bridget F.
TI PREVALENCE OF DSM-IV BORDERLINE PERSONALITY DISORDER IN TWO COMMUNITY
SAMPLES: 6,330 ENGLISH 11-YEAR-OLDS AND 34,653 AMERICAN ADULTS
SO JOURNAL OF PERSONALITY DISORDERS
LA English
DT Article
ID NATIONAL EPIDEMIOLOGIC SURVEY; RANDOMIZED CONTROLLED-TRIAL;
RISK-FACTORS; FOLLOW-UP; AXIS-I; CHILDREN; RELIABILITY; PSYCHOPATHOLOGY;
ALCOHOL; ADOLESCENTS
AB This study had two main objectives. The first was to assess the prevalence of DSM-IV borderline personality disorder and its constituent symptoms in a community sample of late-latency children. The second was to compare these rates to those found in a community sample of American adults. A birth cohort of 6,330 11-year-old children in Bristol, England, was interviewed concerning borderline psychopathology in 2002-2004. A community sample of 34,653 American adults was interviewed about borderline psychopathology in 2004-2005. Rates of chronic emptiness, physically self-damaging acts, and stormy relationships were very similar in both samples (<2% difference). However, a significantly higher percentage of children than adults reported being angry and moody. In contrast, a significantly higher percentage of adults than children reported being paranoid/dissociated, having a serious identity disturbance, being impulsive, and making frantic efforts to avoid abandonment. In addition, a significantly higher percentage of adults than children met DSM-IV criteria for BPD (5.9% vs. 3.2%). Statistically significant but clinically minor gender differences were also found between girls and boys as well as men and women. Taken together, the results of this study suggest that late-latency children are about half as likely as adults to meet DSM-IV criteria for BPD. They also suggest that gender does not play a defining role in symptom expression.
C1 [Zanarini, Mary C.; Fitzmaurice, Garrett] McLean Hosp, Belmont, MA 02478 USA.
[Zanarini, Mary C.; Fitzmaurice, Garrett] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Horwood, Jeremy; Waylen, Andrea] Univ Bristol, Bristol BS8 1TH, Avon, England.
[Wolke, Dieter] Univ Warwick, Coventry CV4 7AL, W Midlands, England.
[Grant, Bridget F.] NIAAA, Bethesda, MD USA.
RP Zanarini, MC (reprint author), McLean Hosp, 115 Mill St, Belmont, MA 02478 USA.
EM zanarini@mclean.harvard.edu
RI Waylen, Andrea/H-7332-2014; Wolke, Dieter/C-5372-2008
OI Wolke, Dieter/0000-0003-0304-268X
FU Intramural NIH HHS [Z99 AA999999]; Wellcome Trust [092731]
NR 35
TC 35
Z9 35
U1 3
U2 16
PU GUILFORD PUBLICATIONS INC
PI NEW YORK
PA 72 SPRING STREET, NEW YORK, NY 10012 USA
SN 0885-579X
J9 J PERS DISORD
JI J. Pers. Disord.
PD OCT
PY 2011
VL 25
IS 5
BP 607
EP 619
PG 13
WC Psychiatry
SC Psychiatry
GA 836AB
UT WOS:000296077300004
PM 22023298
ER
PT J
AU Cao, XE
Pei, HR
Huo, LS
Hu, GH
Ito, Y
AF Cao, Xueli
Pei, Hairun
Huo, Liangsheng
Hu, Guanghui
Ito, Yoichiro
TI Development and evaluation of a spiral tube column for counter-current
chromatography
SO JOURNAL OF SEPARATION SCIENCE
LA English
DT Article
DE Anthocyanins; Counter-current chromatography; Peptides; Proteins; Spiral
tube column
ID STATIONARY-PHASE RETENTION; SPEED; SEPARATION; CCC
AB An improved type-J counter-current chromatography (CCC) planet centrifuge with two spiral tube columns (volume 2 x 15 mL, beta value 0.3-0.7, tubing 0.8 mm id) was developed and evaluated for its retention ability of four typical different solvent systems including heptane-methanol (1:1, v/v) (A), hexane-ethyl acetate-methanol-water (1:1:1:1, v/v) (B), n-butanol-acetic acid-water (4:1:5, v/v) (C), PEG1000-K(2)HPO(4)-water (12.5:12.5:75, w/w) (D) under eight different operation modes. The results indicated that the spiral tube column could significantly increase the retention of four typical solvent systems compared with a traditional multilayer coil column with similar parameters (volume 35 mL, beta value 0.3-0.7, tubing 0.8 mm id). The retention of stationary phase (S(f)) for the less polar system (A) and moderately polar solvent system (B) can be increased by about 10%, and for the polar system (C) and aqueous two-phase system (ATPS) (D) by 30-40%. The preliminary applications of this spiral tube column to the separation of small molecular compounds such as moderately polar theaflavins, polar anthocyanins and dipeptides were successful. Acceptable resolution can be obtained between cytochrome c and myoglobin, lysozyme and myoglobin when it was applied on protein separation; however, it still needs to be improved with regard to its column efficiency.
C1 [Cao, Xueli; Pei, Hairun; Huo, Liangsheng; Hu, Guanghui] Beijing Technol & Business Univ, Dept Bioengn, Beijing 100048, Peoples R China.
[Ito, Yoichiro] NHLBI, NIH, Biochem & Biophys Ctr, Bioseparat Technol Lab, Bethesda, MD 20892 USA.
RP Cao, XE (reprint author), Beijing Technol & Business Univ, Dept Bioengn, 33 Fucheng Rd, Beijing 100048, Peoples R China.
EM caoxl@th.btbu.edu.cn
FU National Natural Science Foundation of China [20877005]; National High
Technology Research and Development Program ("863" Program)
[2007AA061601]; Beijing Natural Science Foundation [2102016]
FX The authors acknowledge financial support of this work by the National
Natural Science Foundation of China (No. 20877005) the National High
Technology Research and Development Program ("863" Program No.
2007AA061601), and Beijing Natural Science Foundation (No. 2102016).
NR 14
TC 9
Z9 9
U1 0
U2 14
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1615-9306
J9 J SEP SCI
JI J. Sep. Sci.
PD OCT
PY 2011
VL 34
IS 19
BP 2611
EP 2617
DI 10.1002/jssc.201100205
PG 7
WC Chemistry, Analytical
SC Chemistry
GA 836VA
UT WOS:000296141200008
PM 21898798
ER
PT J
AU Ji, HF
Ren, W
Wang, LY
Shi, P
Chen, XF
Wu, XQ
Yao, X
Lau, ST
Zhou, QF
Shung, KK
AF Ji, Hongfen
Ren, Wei
Wang, Lingyan
Shi, Peng
Chen, Xiaofeng
Wu, Xiaoqing
Yao, Xi
Lau, Sien-Ting
Zhou, Qifa
Shung, K. Kirk
TI Enhanced Structures and Electrical Properties of Lead-Free
K0.5Na0.5NbO3-Bi0.5Na0.5TiO3 0-3 Composite Ferroelectric Thick Films
SO JOURNAL OF THE AMERICAN CERAMIC SOCIETY
LA English
DT Article
ID PIEZOELECTRIC PROPERTIES; DIELECTRIC-PROPERTIES; TRANSDUCERS;
FABRICATION
AB Lead-free K0.5Na0.5NbO3-Bi0.5Na0.5TiO3 (KNN-BNT) 0-3 composite ferroelectric thick films have been successfully prepared by a modified composite sol-gel process. The KNN fine ceramic powders were dispersed in the BNT precursor solution to form the uniform slurry that was spin coated on (111) Pt/TiO2/SiO2/Si substrates. The buffer layers and vacuum infiltration were used during the deposition process to improve the structure and density of the composite films. Influence of the annealing temperature and weight ratio of the powder-to-solution on the structures and electrical properties of KNN-BNT composite thick films has been investigated. X-ray diffraction analysis indicates that the composite thick films possess pure perovskite structures composed by KNN and BNT phases. The dielectric constant and remnant polarization of the composite thick films increase with increasing annealing temperature and decreasing powder-to-solution weight ratio due to reduction of pores and improvement of film density. The composite thick films with the powder-to-solution weight ratio of 0.40 and annealed at 750 degrees C have a dielectric constant of 848 and a remnant polarization of 23.6 mu C/cm(2). The KNN-BNT composite thick films obtained are a promising candidate for transducer applications.
C1 [Ji, Hongfen; Ren, Wei; Wang, Lingyan; Shi, Peng; Chen, Xiaofeng; Wu, Xiaoqing; Yao, Xi] Xi An Jiao Tong Univ, Elect Mat Res Lab, Key Lab, Minist Educ, Xian 710049, Peoples R China.
[Ji, Hongfen; Ren, Wei; Wang, Lingyan; Shi, Peng; Chen, Xiaofeng; Wu, Xiaoqing; Yao, Xi] Xi An Jiao Tong Univ, Int Ctr Dielect Res, Xian 710049, Peoples R China.
[Lau, Sien-Ting; Zhou, Qifa; Shung, K. Kirk] Univ So Calif, Dept Biomed Engn, NIH Transducer Resource Ctr, Los Angeles, CA 90089 USA.
RP Ren, W (reprint author), Xi An Jiao Tong Univ, Elect Mat Res Lab, Key Lab, Minist Educ, Xian 710049, Peoples R China.
EM wren@mail.xjtu.edu.cn
RI shi, peng/C-8551-2011; Lau, Sien-Ting/B-6091-2013; Wang,
Lingyan/K-7687-2013
OI shi, peng/0000-0003-2217-8486;
FU Natural Science Foundation of China [90923001]; International Science &
Technology Cooperation Program of China [2010DFB13640]; Shaanxi Province
International Collaboration Program [2009KW-12, 2010KW-09]; NIH
[P41-EB2182]
FX This work was financially supported by the Natural Science Foundation of
China (Grant No. 90923001), International Science & Technology
Cooperation Program of China (Grant No. 2010DFB13640), the Shaanxi
Province International Collaboration Program (Grant Nos. 2009KW-12 and
2010KW-09), and the NIH Grant P41-EB2182.
NR 26
TC 7
Z9 7
U1 3
U2 38
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-7820
EI 1551-2916
J9 J AM CERAM SOC
JI J. Am. Ceram. Soc.
PD OCT
PY 2011
VL 94
IS 10
BP 3425
EP 3430
DI 10.1111/j.1551-2916.2011.04524.x
PG 6
WC Materials Science, Ceramics
SC Materials Science
GA 828SY
UT WOS:000295524300050
ER
PT J
AU Yothers, G
Sargent, DJ
Wolmark, N
Goldberg, RM
O'Connell, MJ
Benedetti, JK
Saltz, LB
Dignam, JJ
Blackstock, AW
AF Yothers, Greg
Sargent, Daniel J.
Wolmark, Norman
Goldberg, Richard M.
O'Connell, Michael J.
Benedetti, Jacqueline K.
Saltz, Leonard B.
Dignam, James J.
Blackstock, A. William
CA ACCENT Collaborative Grp
TI Outcomes Among Black Patients With Stage II and III Colon Cancer
Receiving Chemotherapy: An Analysis of ACCENT Adjuvant Trials
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID RANDOMIZED CLINICAL-TRIAL; BOWEL PROJECT; RACIAL-DIFFERENCES;
AFRICAN-AMERICANS; COLORECTAL-CANCER; PLUS LEUCOVORIN; FLUOROURACIL;
BREAST; CARCINOMA; SURVIVAL
AB Background Among patients with resected colon cancer, black patients have worse survival than whites. We investigated whether disparities in survival and related endpoints would persist when patients were treated with identical therapies in controlled clinical trials.
Methods We assessed 14 611 patients (1218 black and 13 393 white) who received standardized adjuvant treatment in 12 randomized controlled clinical trials conducted in North America for resected stage II and stage III colon cancer between 1977 and 2002. Individual patient data on covariates and outcomes were extracted from the Adjuvant Colon Cancer ENdpoinTs (ACCENT) database. The endpoints examined in this meta-analysis were overall survival (time to death), recurrence-free survival (time to recurrence or death), and recurrence-free interval (time to recurrence). Cox models were stratified by study and controlled for sex, stage, age, and treatment to determine the effect of race. Kaplan-Meier estimates were adjusted for similar covariates to control for confounding. All statistical tests were two-sided.
Results Black patients were younger than whites (median age, 58 vs 61 years, respectively; P < .001) and more likely to be female (55% vs 45%, respectively; P < .001). Overall survival was worse in black patients than whites (hazard ratio [HR] of death = 1.22, 95% confidence interval [CI] = 1.11 to 1.34, P < .001). Five-year overall survival rates for blacks and whites were 68.2% and 72.8%, respectively. When subsets defined by sex, stage, and age were analyzed, overall survival was consistently worse in black patients. Recurrence-free survival was worse in black patients than whites (HR of recurrence or death = 1.14, 95% CI = 1.04 to 1.24, P = .0045). Three-year recurrence-free survival rates in blacks and whites were 68.4% and 72.1%, respectively. In contrast, recurrence-free interval was similar in black and white patients (HR of recurrence = 1.08, 95% CI = 0.97 to 1.19, P = .15). Three-year recurrence-free interval rates in blacks and whites were 71.3% and 74.2%, respectively.
Conclusions Black patients with resected stage II and stage III colon cancer who were treated with the same therapy as white patients experienced worse overall and recurrence-free survival, but similar recurrence-free interval, compared with white patients. The differences in survival may be mostly because of factors unrelated to the patients' adjuvant colon cancer treatment. J Natl Cancer Inst 2011; 103: 1498-1506
C1 [Yothers, Greg; Wolmark, Norman; O'Connell, Michael J.; Dignam, James J.] Natl Surg Adjuvant Breast & Bowel Project, Ctr Biostat, Pittsburgh, PA 15213 USA.
[Yothers, Greg; Wolmark, Norman; O'Connell, Michael J.; Dignam, James J.] Natl Surg Adjuvant Breast & Bowel Project, Operat Ctr, Pittsburgh, PA 15213 USA.
[Yothers, Greg] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15261 USA.
[Sargent, Daniel J.] Mayo Clin, Ctr Canc, Rochester, MN USA.
[Wolmark, Norman] Drexel Univ, Dept Human Oncol, Allegheny Gen Hosp, Coll Med, Pittsburgh, PA USA.
[Goldberg, Richard M.] Univ N Carolina, Chapel Hill Sch Med, Chapel Hill, NC USA.
[Benedetti, Jacqueline K.] Univ Washington, Seattle, WA 98195 USA.
[Benedetti, Jacqueline K.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Saltz, Leonard B.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Dignam, James J.] Univ Chicago, Chicago, IL 60637 USA.
[Blackstock, A. William] Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA.
[Goldberg, Richard M.; Saltz, Leonard B.; Blackstock, A. William] Canc & Leukemia Grp B, Chicago, IL USA.
[Benedetti, Jacqueline K.] SW Oncol Grp, Ann Arbor, MI USA.
[Dignam, James J.] Radiat Therapy Oncol Grp, Philadelphia, PA USA.
RP Yothers, G (reprint author), Natl Surg Adjuvant Breast & Bowel Project, Ctr Biostat, 1 Sterling Plaza,Ste 350,201 N Craig St, Pittsburgh, PA 15213 USA.
EM yothers@nsabp.pitt.edu
RI Goldberg , Richard/M-1311-2013;
OI Bot, Brian/0000-0002-2412-6826; Sargent, Daniel/0000-0002-2684-4741;
Yothers, Greg/0000-0002-7965-7333; Saltz, Leonard/0000-0001-8353-4670
FU National Surgical Adjuvant Breast and Bowel Project [U10CA-12027,
U10CA-69974, U10CA-37377, U10CA-69651, U24-CA-114732]; National Cancer
Institute, Department of Health and Human Services (North Central Cancer
Treatment Group) [CA 25224]; sanofi-aventis [C-07]
FX Public Health Service Grants U10CA-12027, U10CA-69974, U10CA-37377,
U10CA-69651, and U24-CA-114732 (National Surgical Adjuvant Breast and
Bowel Project); CA 25224 (North Central Cancer Treatment Group) from the
National Cancer Institute, Department of Health and Human Services.; NW
declares funding from sanofi-aventis to NSABP through a business
contract for C-07 only, for certain costs not covered by the NCI, for
non-standard-of-care procedures required for the study. Also,
consultancy from sanofi-aventis (C-07 only), honoraria to the NSABP for
NW's participation on the advisory board, and reasonable travel and
accommodations for the sanofi-aventis board meeting. There are no other
potential conflicts.
NR 30
TC 24
Z9 25
U1 1
U2 3
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 OCT
PY 2011
VL 103
IS 20
BP 1498
EP 1506
DI 10.1093/jnci/djr310
PG 9
WC Oncology
SC Oncology
GA 836JJ
UT WOS:000296107700007
PM 21997132
ER
PT J
AU Bedognetti, D
Sertoli, MR
Pronzato, P
Del Mastro, L
Venturini, M
Taveggia, P
Zanardi, E
Siffredi, G
Pastorino, S
Queirolo, P
Gardin, G
Wang, E
Monzeglio, C
Boccardo, F
Bruzzi, P
AF Bedognetti, Davide
Sertoli, Mario Roberto
Pronzato, Paolo
Del Mastro, Lucia
Venturini, Marco
Taveggia, Paola
Zanardi, Elisa
Siffredi, Guido
Pastorino, Simona
Queirolo, Paola
Gardin, Giovanni
Wang, Ena
Monzeglio, Clara
Boccardo, Francesco
Bruzzi, Paolo
TI Concurrent vs Sequential Adjuvant Chemotherapy and Hormone Therapy in
Breast Cancer: A Multicenter Randomized Phase III Trial
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID TAMOXIFEN; SURVIVAL; CELLS; WOMEN; 5-FLUOROURACIL; DISEASE; DRUGS
AB Background The most appropriate timing of chemotherapy and hormone therapy administration is a critical issue in early breast cancer patients. The purpose of our study was to compare the efficacy of concurrent vs sequential administration of adjuvant chemotherapy and tamoxifen.
Methods Women with node-positive primary breast cancer were randomly assigned to receive tamoxifen (20 mg/d for 5 years) during (concurrent arm) or after (sequential arm) adjuvant chemotherapy. Chemotherapy consisted of alternating regimens of cyclophosphamide, epidoxorubicin, and 5-fluorouracil and cyclophosphamide, methotrexate, and 5-fluorouracil every 21 days for a total of 12 cycles. The primary endpoint was overall survival (OS), and secondary endpoints were toxic effects and disease-free survival (DFS). No provision for interim analyses was made in the original study protocol. Survival curves were estimated by the Kaplan-Meier method. Multivariable Cox regression models, adjusted for age, menopausal status, tumor stage, and lymph node and hormone receptor status, were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). All statistical tests were two-sided.
Results From 1985 to 1992, 431 patients were randomly assigned and studied according to the intention-to-treat principle. After a maximum of 15.4 years of follow-up (median 12.3 years), the estimated actuarial 10-year OS was equivalent for the two study arms (concurrent arm: 111 patients, 66%, 95% CI = 59% to 72%; sequential arm: 114 patients, 65%, 95% CI = 59% to 72%, P = .86). No differences in DFS and toxic effects were evident. Four interim analyses were performed, but no alpha error adjustment was necessary because of the largely negative results of this final analysis (sequential vs concurrent arm: HR of death = 1.06, 95% CI = 0.78 to 1.44, P = .76; HR of relapse = 1.16, 95% CI = 0.88 to 1.52, P = .36).
Conclusions No statistically significant differences in OS, DFS, and toxic effects between concurrent and sequential adjuvant chemo-and hormone therapies were observed. Our study does not support the superiority of one schedule of chemo-and hormone-therapy administration over the other. However, because of the limited statistical power of the study, these results must be considered with caution. J Natl Cancer Inst 2011; 103: 1529-1539
C1 [Bedognetti, Davide; Wang, Ena] NIH, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Bedognetti, Davide; Wang, Ena] NIH, Trans NIH Ctr Human Immunol, Bethesda, MD 20892 USA.
[Bedognetti, Davide; Sertoli, Mario Roberto; Pronzato, Paolo; Del Mastro, Lucia; Venturini, Marco; Taveggia, Paola; Zanardi, Elisa; Pastorino, Simona; Queirolo, Paola; Gardin, Giovanni; Boccardo, Francesco] Natl Inst Canc Res, Dept Med Oncol, I-16132 Genoa, Italy.
[Bruzzi, Paolo] Natl Inst Canc Res, Dept Epidemiol, I-16132 Genoa, Italy.
[Bedognetti, Davide; Sertoli, Mario Roberto; Zanardi, Elisa; Siffredi, Guido; Boccardo, Francesco] Univ Genoa, Dept Oncol Biol & Genet, Genoa, Italy.
[Venturini, Marco] Sacro Cuore Don Calabria Hosp, Dept Oncol, Verona, Italy.
[Monzeglio, Clara] St Anna Univ Hosp, Dept Obstet & Gynecol, Turin, Italy.
RP Bedognetti, D (reprint author), NIH, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM bedodav@yahoo.it; marioroberto.sertoli@istge.it
RI Bedognetti, Davide/A-9090-2012; Queirolo, Paola/K-6778-2016;
OI Queirolo, Paola/0000-0002-9917-6633; Bedognetti,
Davide/0000-0002-5857-773X; Bruzzi, Paolo/0000-0002-7874-2077; Del
Mastro, Lucia/0000-0002-9546-5841
FU Italian National Research Council, Rome [8800601.44]; Conquer Cancer
Foundation of the American Society of Clinical Oncology
FX This study was supported by a grant from the Italian National Research
Council, Rome [Special Project Oncology (8800601.44)].; The funder had
no role in study design, data collection and analysis, decision to
publish, or preparation of the article. The random allocation sequence
was generated at the National Cancer Research Institute of Genoa under
the supervision of PB. The authors have no affiliations or financial
involvement with any organization or entity with a financial interest in
or financial conflict with the subject matter or materials discussed in
the article. The following centers and investigators also contributed to
patient accrual: Dr Pier Franco Conte (Department of Medical Oncology,
S. Chiara Hospital, Pisa), Dr Elio Paganini (Medical Oncology Unit,
Villa Scassi Hospital, Genoa, Italy); Dr Fulvio Brema (Department of
Oncology, S. Paolo Hospital, Savona, Italy), Dr Pietro Gallotti
(Clinical Oncology, Beato Matteo Clinical Institute, Vigevano, Italy).
DB thanks Dr Francesco Barone-Adesi (Cancer Epidemiology Unit, CeRMS and
CPO-Piemonte, University of Turin, Turin, Italy) and Dr Pietro Blandini
(U. C. Sampdoria, Genoa, Italy) for their useful statistical advice. The
authors thank Ms. Shari Lama (National Institutes of Health Library,
Bethesda, MD, USA) for help in editing for the English format. Davide
Bedognetti is a participant in the NIH Graduate Partnership Program and
a graduate student at University of Genoa. Davide Bedognetti's
scholarship is partially supported by the Conquer Cancer Foundation of
the American Society of Clinical Oncology (2011 Young Investigator
Award).
NR 38
TC 9
Z9 10
U1 0
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 OCT
PY 2011
VL 103
IS 20
BP 1529
EP 1539
DI 10.1093/jnci/djr351
PG 11
WC Oncology
SC Oncology
GA 836JJ
UT WOS:000296107700010
PM 21921285
ER
PT J
AU Simon, RM
Paik, S
Hayes, DF
AF Simon, Richard M.
Paik, Soonmyung
Hayes, Daniel F.
TI Re: Use of Archived Specimens in Evaluation of Prognostic and Predictive
Biomarkers Response
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Letter
C1 [Simon, Richard M.] NCI, Biometr Res Branch, Bethesda, MD 20892 USA.
[Paik, Soonmyung] Univ Pittsburgh, Natl Surg Adjuvant Breast & Bowel Project, Div Pathol, Pittsburgh, PA USA.
[Hayes, Daniel F.] Univ Michigan, Breast Oncol Program, Ctr Comprehens Canc, 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 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD OCT
PY 2011
VL 103
IS 20
BP 1559
EP U85
DI 10.1093/jnci/djr332
PG 2
WC Oncology
SC Oncology
GA 836JJ
UT WOS:000296107700016
ER
PT J
AU Shingai, M
Yoshida, T
Martin, MA
Strebel, K
AF Shingai, Masashi
Yoshida, Takeshi
Martin, Malcolm A.
Strebel, Klaus
TI Some Human Immunodeficiency Virus Type 1 Vpu Proteins Are Able To
Antagonize Macaque BST-2 In Vitro and In Vivo: Vpu-Negative Simian-Human
Immunodeficiency Viruses Are Attenuated In Vivo
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID RHESUS-MONKEYS; HIV-1 VPU; ENVELOPE GLYCOPROTEIN; PARTICLE RELEASE;
DOWN-MODULATION; BETA-TRCP; TRANSMEMBRANE DOMAIN; RESTRICTION FACTOR;
CLINICAL-OUTCOMES; MOLECULAR CLONE
AB Human immunodeficiency virus type 1 (HIV-1) Vpu enhances the release of viral particles from infected cells by targeting BST-2/tetherin, a cellular protein inhibiting virus release. The widely used HIV-1(NL4-3) Vpu functionally inactivates human BST-2 but not murine or monkey BST-2, leading to the notion that Vpu antagonism is species specific. Here we investigated the properties of the CXCR4-tropic simian-human immunodeficiency virus DH12 (SHIV(DH12)) and the CCR5-tropic SHIV(AD8), each of which carries vpu genes derived from different primary HIV-1 isolates. We found that virion release from infected rhesus peripheral blood mononuclear cells was enhanced to various degrees by the Vpu present in both SHIVs. Transfer of the SHIV(DH12) Vpu transmembrane domain to the HIV-1(NL4-3) Vpu conferred antagonizing activity against macaque BST-2. Inactivation of the SHIV(DH12) and SHIV(AD8) vpu genes impaired virus replication in 6 of 8 inoculated rhesus macaques, resulting in lower plasma viral RNA loads, slower losses of CD4(+) T cells, and delayed disease progression. The expanded host range of the SHIV(DH12) Vpu was not due to adaptation during passage in macaques but was an intrinsic property of the parental HIV-1(DH12) Vpu protein. These results demonstrate that the species-specific inhibition of BST-2 by HIV-1(NL4-3) Vpu is not characteristic of all HIV-1 Vpu proteins; some HIV-1 isolates encode a Vpu with a broader host range.
C1 [Shingai, Masashi; Yoshida, Takeshi; Martin, Malcolm A.; Strebel, Klaus] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
RP Martin, MA (reprint author), NIAID, Mol Microbiol Lab, NIH, Bldg 4,Room 310,4 Ctr Dr,MSC 0460, Bethesda, MD 20892 USA.
EM mmartin@nih.gov; kstrebel@nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 63
TC 17
Z9 17
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2011
VL 85
IS 19
BP 9708
EP 9715
DI 10.1128/JVI.00626-11
PG 8
WC Virology
SC Virology
GA 837ZH
UT WOS:000296253900006
PM 21775449
ER
PT J
AU Hogue, IB
Grover, JR
Soheilian, F
Nagashima, K
Ono, A
AF Hogue, Ian B.
Grover, Jonathan R.
Soheilian, Ferri
Nagashima, Kunio
Ono, Akira
TI Gag Induces the Coalescence of Clustered Lipid Rafts and
Tetraspanin-Enriched Microdomains at HIV-1 Assembly Sites on the Plasma
Membrane
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TYPE-1 MATRIX PROTEIN; TO-CELL
TRANSMISSION; MURINE LEUKEMIA-VIRUS; CAPSID PROTEIN;
ELECTRON-MICROSCOPY; PRIMARY MACROPHAGES; PARTICLE-PRODUCTION; ADHESION
RECEPTORS; INFECTIOUS HIV-1
AB The HIV-1 structural protein Gag associates with two types of plasma membrane microdomains, lipid rafts and tetraspanin-enriched microdomains (TEMs), both of which have been proposed to be platforms for HIV-1 assembly. However, a variety of studies have demonstrated that lipid rafts and TEMs are distinct microdomains in the absence of HIV-1 infection. To measure the impact of Gag on microdomain behaviors, we took advantage of two assays: an antibody-mediated copatching assay and a Forster resonance energy transfer (FRET) assay that measures the clustering of microdomain markers in live cells without antibody-mediated patching. We found that lipid rafts and TEMs copatched and clustered to a greater extent in the presence of membrane-bound Gag in both assays, suggesting that Gag induces the coalescence of lipid rafts and TEMs. Substitutions in membrane binding motifs of Gag revealed that, while Gag membrane binding is necessary to induce coalescence of lipid rafts and TEMs, either acylation of Gag or binding of phosphatidylinositol-(4,5)-bisphosphate is sufficient. Finally, a Gag derivative that is defective in inducing membrane curvature appeared less able to induce lipid raft and TEM coalescence. A higher-resolution analysis of assembly sites by correlative fluorescence and scanning electron microscopy showed that coalescence of clustered lipid rafts and TEMs occurs predominately at completed cell surface virus-like particles, whereas a transmembrane raft marker protein appeared to associate with punctate Gag fluorescence even in the absence of cell surface particles. Together, these results suggest that different membrane microdomain components are recruited in a stepwise manner during assembly.
C1 [Hogue, Ian B.; Grover, Jonathan R.; Ono, Akira] Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA.
[Soheilian, Ferri; Nagashima, Kunio] NCI, Electron Microscopy Lab, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP Ono, A (reprint author), Univ Michigan, Sch Med, Dept Microbiol & Immunol, 5736 Med Sci Bldg 2,1150 W Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM akiraono@umich.edu
OI Ono, Akira/0000-0001-7841-851X
FU NIH [R01 AI071727, R56 089282, T32 GM007544]; amfAR [107449-45-RGHF];
University of Michigan
FX This work was supported by NIH grant R01 AI071727 and R56 089282 (A.O.),
amfAR research grant 107449-45-RGHF (A.O.), NIH training grant T32
GM007544 (I.B.H.), and a University of Michigan Rackham Predoctoral
Fellowship (I.B.H.).
NR 146
TC 50
Z9 51
U1 0
U2 15
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 OCT
PY 2011
VL 85
IS 19
BP 9749
EP 9766
DI 10.1128/JVI.00743-11
PG 18
WC Virology
SC Virology
GA 837ZH
UT WOS:000296253900010
PM 21813604
ER
PT J
AU Yang, ZL
Reynolds, SE
Martens, CA
Bruno, DP
Porcella, SF
Moss, B
AF Yang, Zhilong
Reynolds, Sara E.
Martens, Craig A.
Bruno, Daniel P.
Porcella, Stephen F.
Moss, Bernard
TI Expression Profiling of the Intermediate and Late Stages of Poxvirus
Replication
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID VACCINIA VIRUS INTERMEDIATE; MUTATIONAL ANALYSIS; TEMPORAL REGULATION;
DNA-REPLICATION; LATE PROMOTERS; GENES; TRANSCRIPTION; COMPLEX; GENOME;
PROTEIN
AB The double-stranded DNA genome of vaccinia virus (VACV), the prototype poxvirus, contains approximately 200 open reading frames (ORFs) that are transcribed at early, intermediate, and late stages of infection. Previous high-throughput deep RNA sequencing allowed us to map 118 VACV early genes that are expressed before viral DNA replication and 93 postreplicative genes. However, the intermediate-and late-stage postreplicative genes could not be differentiated. Here, we synchronized infections with a reversible inhibitor of DNA replication and used a VACV mutant that conditionally transcribes late genes to sequence the two classes of mRNAs. In addition, each postreplicative ORF was individually expressed under conditions that distinguished intermediate and late classes. We identified 38 VACV genes that belong to the late class and 53 that belong to the intermediate class, with some of the latter continuing to be expressed late. These data allowed us to prepare a genome-wide early, intermediate, and late transcription map. Inspection of sequences upstream of these ORFs revealed distinctive characteristics of intermediate and late promoters and suggested that some promoters have intermediate and late elements. The intermediate genes encoded many DNA binding/packaging and core-associated proteins in addition to late transcription factors; the late genes encoded many morphogenesis and mature virion membrane proteins, including those involved in entry, in addition to early transcription factors. The top-ranked antigens for CD4(+) T cells and B cells were mainly intermediate rather than late gene products. The differentiation of intermediate and late genes may enhance understanding of poxvirus replication and lead to improvements in expression vectors and recombinant vaccines.
C1 [Yang, Zhilong; Reynolds, Sara E.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Reynolds, Sara E.] Univ Maryland, Dept Cell Biol & Mol Genet, College Pk, MD 20742 USA.
[Martens, Craig A.; Bruno, Daniel P.; Porcella, Stephen F.] NIAID, Res Technol Sect, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM bmoss@niaid.nih.gov
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX The study was supported by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health.
NR 25
TC 36
Z9 36
U1 1
U2 4
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 OCT
PY 2011
VL 85
IS 19
BP 9899
EP 9908
DI 10.1128/JVI.05446-11
PG 10
WC Virology
SC Virology
GA 837ZH
UT WOS:000296253900023
PM 21795349
ER
PT J
AU Lin, J
Cheng, NQ
Chow, M
Filman, DJ
Steven, AC
Hogle, JM
Belnap, DM
AF Lin, Jun
Cheng, Naiqian
Chow, Marie
Filman, David J.
Steven, Alasdair C.
Hogle, James M.
Belnap, David M.
TI An Externalized Polypeptide Partitions between Two Distinct Sites on
Genome-Released Poliovirus Particles
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HEPATITIS-B-VIRUS; CRYOELECTRON MICROSCOPY; CELLULAR RECEPTOR; CAPSID
PROTEIN; 3-DIMENSIONAL STRUCTURE; ENTRY-INTERMEDIATE;
STRUCTURAL-CHANGES; CRYSTAL-STRUCTURE; CORE ANTIGEN; VP1
AB During cell entry, native poliovirus (160S) converts to a cell-entry intermediate (135S) particle, resulting in the externalization of capsid proteins VP4 and the amino terminus of VP1 (residues 1 to 53). Externalization of these entities is followed by release of the RNA genome (uncoating), leaving an empty (80S) particle. The antigen-binding fragment (Fab) of a monospecific peptide 1 (P1) antibody, which was raised against a peptide corresponding to amino-terminal residues 24 to 40 of VP1, was utilized to track the location of the amino terminus of VP1 in the 135S and 80S states of poliovirus particles via cryogenic electron microscopy (cryo-EM) and three-dimensional image reconstruction. On 135S, P1 Fabs bind to a prominent feature on the external surface known as the "propeller tip." In contrast, our initial 80S-P1 reconstruction showed P1 Fabs also binding to a second site, at least 50 angstrom distant, at the icosahedral 2-fold axes. Further analysis showed that the overall population of 80S-P1 particles consisted of three kinds of capsids: those with P1 Fabs bound only at the propeller tips, P1 Fabs bound only at the 2-fold axes, or P1 Fabs simultaneously bound at both positions. Our results indicate that, in 80S particles, a significant fraction of VP1 can deviate from icosahedral symmetry. Hence, this portion of VP1 does not change conformation synchronously when switching from the 135S state. These conclusions are compatible with previous observations of multiple conformations of the 80S state and suggest that movement of the amino terminus of VP1 has a role in uncoating. Similar deviations from icosahedral symmetry may be biologically significant during other viral transitions.
C1 [Lin, Jun; Belnap, David M.] Brigham Young Univ, Dept Chem & Biochem, Provo, UT 84602 USA.
[Cheng, Naiqian; Steven, Alasdair C.; Belnap, David M.] NIAMSD, Struct Biol Res Lab, NIH, Bethesda, MD 20892 USA.
[Chow, Marie] Univ Arkansas Med Sci, Dept Microbiol & Immunol, Little Rock, AR 72205 USA.
[Filman, David J.; Hogle, James M.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
RP Belnap, DM (reprint author), Brigham Young Univ, Dept Chem & Biochem, C100 BNSN, Provo, UT 84602 USA.
EM David.Belnap@byu.edu
OI Hogle, James/0000-0002-3655-1504
FU BYU; National Institute of Arthritis and Musculoskeletal and Skin
Diseases of the National Institutes of Health; National Institute of
Allergy and Infectious Diseases [R15AI084085]; BYU Department of
Chemistry and Biochemistry; NIH [R01AI020566, R01 AI022627, AI042390]
FX This work was supported by BYU institutional funds (to D.M.B.) and by
the National Institute of Arthritis and Musculoskeletal and Skin
Diseases of the National Institutes of Health (to D.M.B., N.C., and
A.C.S.). Jun Lin was partially supported by grant R15AI084085 from the
National Institute of Allergy and Infectious Diseases (to D.M.B.) and a
fellowship from the BYU Department of Chemistry and Biochemistry. This
work was also supported by NIH grant R01AI020566 (to J.M.H.) and grants
R01 AI022627 and AI042390 (to M.C.).
NR 50
TC 24
Z9 26
U1 0
U2 4
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 OCT
PY 2011
VL 85
IS 19
BP 9974
EP 9983
DI 10.1128/JVI.05013-11
PG 10
WC Virology
SC Virology
GA 837ZH
UT WOS:000296253900030
PM 21775460
ER
PT J
AU Bonsignori, M
Hwang, KK
Chen, X
Tsao, CY
Morris, L
Gray, E
Marshall, DJ
Crump, JA
Kapiga, SH
Sam, NE
Sinangil, F
Pancera, M
Yang, YP
Zhang, BS
Zhu, J
Kwong, PD
O'Dell, S
Mascola, JR
Wu, L
Nabel, GJ
Phogat, S
Seaman, MS
Whitesides, JF
Moody, MA
Kelsoe, G
Yang, XZ
Sodroski, J
Shaw, GM
Montefiori, DC
Kepler, TB
Tomaras, GD
Alam, SM
Liao, HX
Haynes, BF
AF Bonsignori, Mattia
Hwang, Kwan-Ki
Chen, Xi
Tsao, Chun-Yen
Morris, Lynn
Gray, Elin
Marshall, Dawn J.
Crump, John A.
Kapiga, Saidi H.
Sam, Noel E.
Sinangil, Faruk
Pancera, Marie
Yang Yongping
Zhang, Baoshan
Zhu, Jiang
Kwong, Peter D.
O'Dell, Sijy
Mascola, John R.
Wu, Lan
Nabel, Gary J.
Phogat, Sanjay
Seaman, Michael S.
Whitesides, John F.
Moody, M. Anthony
Kelsoe, Garnett
Yang, Xinzhen
Sodroski, Joseph
Shaw, George M.
Montefiori, David C.
Kepler, Thomas B.
Tomaras, Georgia D.
Alam, S. Munir
Liao, Hua-Xin
Haynes, Barton F.
TI Analysis of a Clonal Lineage of HIV-1 Envelope V2/V3 Conformational
Epitope-Specific Broadly Neutralizing Antibodies and Their Inferred
Unmutated Common Ancestors
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HUMAN MONOCLONAL-ANTIBODIES;
EPSTEIN-BARR-VIRUS; B-CELL RESPONSES; CRYSTAL-STRUCTURE; PG16; PG9;
INDIVIDUALS; DIVERSITY; INFECTION
AB V2/V3 conformational epitope antibodies that broadly neutralize HIV-1 (PG9 and PG16) have been recently described. Since an elicitation of previously known broadly neutralizing antibodies has proven elusive, the induction of antibodies with such specificity is an important goal for HIV-1 vaccine development. A critical question is which immunogens and vaccine formulations might be used to trigger and drive the development of memory B cell precursors with V2/V3 conformational epitope specificity. In this paper we identified a clonal lineage of four V2/V3 conformational epitope broadly neutralizing antibodies (CH01 to CH04) from an African HIV-1-infected broad neutralizer and inferred their common reverted unmutated ancestor (RUA) antibodies. While conformational epitope antibodies rarely bind recombinant Env monomers, a screen of 32 recombinant envelopes for binding to the CH01 to CH04 antibodies showed monoclonal antibody (MAb) binding to the E.A244 gp120 Env and to chronic Env AE.CM243; MAbs CH01 and CH02 also bound to transmitted/founder Env B.9021. CH01 to CH04 neutralized 38% to 49% of a panel of 91 HIV-1 tier 2 pseudoviruses, while the RUAs neutralized only 16% of HIV-1 isolates. Although the reverted unmutated ancestors showed restricted neutralizing activity, they retained the ability to bind to the E.A244 gp120 HIV-1 envelope with an affinity predicted to trigger B cell development. Thus, E.A244, B. 9021, and AE.CM243 Envs are three potential immunogen candidates for studies aimed at defining strategies to induce V2/V3 conformational epitope-specific antibodies.
C1 [Bonsignori, Mattia; Haynes, Barton F.] Duke Univ, Med Ctr, Dept Med, Duke Human Vaccine Inst, Durham, NC 27710 USA.
[Crump, John A.] Duke Univ, Med Ctr, Dept Med, Div Infect Dis & Int Hlth, Durham, NC 27710 USA.
[Montefiori, David C.; Tomaras, Georgia D.] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA.
[Kelsoe, Garnett] Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA.
[Kepler, Thomas B.] Duke Univ, Med Ctr, Ctr Computat Immunol, Durham, NC 27710 USA.
[Morris, Lynn; Gray, Elin] Natl Inst Communicable Dis, Johannesburg, South Africa.
[Crump, John A.] Duke Univ, Duke Global Hlth Inst, Durham, NC 27710 USA.
[Crump, John A.; Sam, Noel E.] Kilimanjaro Christian Med Ctr, Moshi, Tanzania.
[Crump, John A.] Tumaini Univ, Kilimanjaro Christian Med Coll, Moshi, Tanzania.
[Kapiga, Saidi H.] London Sch Hyg & Trop Med, London WC1, England.
[Sinangil, Faruk] Global Solut Infect Dis, San Francisco, CA USA.
[Pancera, Marie; Yang Yongping; Zhang, Baoshan; Zhu, Jiang; Kwong, Peter D.; O'Dell, Sijy; Mascola, John R.; Wu, Lan; Nabel, Gary J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Phogat, Sanjay] IAVI, AIDS Vaccine Design & Dev Lab, Brooklyn, NY USA.
[Seaman, Michael S.; Yang, Xinzhen] Beth Israel Deaconess Med Ctr, Div Viral Pathogenesis, Boston, MA 02215 USA.
[Sodroski, Joseph] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Shaw, George M.] Univ Alabama, Dept Med, Birmingham, AL 35294 USA.
[Shaw, George M.] Univ Alabama, Dept Microbiol, Birmingham, AL 35294 USA.
RP Bonsignori, M (reprint author), Duke Univ, Med Ctr, Dept Med, Duke Human Vaccine Inst, MSRB 2,POB 103020,2 Genome Court, Durham, NC 27710 USA.
EM mattia.bonsignori@duke.edu; barton.haynes@duke.edu
RI Tomaras, Georgia/J-5041-2016;
OI Kepler, Thomas/0000-0002-1383-6865; Moody, Tony/0000-0002-3890-5855;
Gray, Elin/0000-0002-8613-3570
FU NIH [AI64518]; NIH, NIAID, the Division of AIDS with the Center for
HIV/AIDS Vaccine Immunology (CHAVI) [U19 AI067854]; Bill and Melinda
Gates Foundation; Vaccine Research Center, NIAID, NIH; International
AIDS Vaccine Initiative
FX Single-cell sorting was performed in the Research Flow Cytometry Core
Facility at the Duke Human Vaccine Institute, partly supported by the
NIH-funded Duke Center for AIDS Research (CFAR) (grant AI64518), and
directed by J.F.W. This work was supported by the NIH, NIAID, the
Division of AIDS with the Center for HIV/AIDS Vaccine Immunology (CHAVI)
(grant U19 AI067854); by a Collaboration for AIDS Vaccine Discovery
grant to B.F.H. from the Bill and Melinda Gates Foundation; in part by a
grant from the intramural research program of the Vaccine Research
Center, NIAID, NIH, to J.R.M., P.D.K., and G.J.N.; and by a grant from
the International AIDS Vaccine Initiative to J.R.M., P.D.K., and S.P.
NR 63
TC 216
Z9 219
U1 0
U2 20
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 OCT
PY 2011
VL 85
IS 19
BP 9998
EP 10009
DI 10.1128/JVI.05045-11
PG 12
WC Virology
SC Virology
GA 837ZH
UT WOS:000296253900032
PM 21795340
ER
PT J
AU Koh, Y
Aoki, M
Danish, ML
Aoki-Ogata, H
Amano, M
Das, D
Shafer, RW
Ghosh, AK
Mitsuya, H
AF Koh, Yasuhiro
Aoki, Manabu
Danish, Matthew L.
Aoki-Ogata, Hiromi
Amano, Masayuki
Das, Debananda
Shafer, Robert W.
Ghosh, Arun K.
Mitsuya, Hiroaki
TI Loss of Protease Dimerization Inhibition Activity of Darunavir Is
Associated with the Acquisition of Resistance to Darunavir by HIV-1
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TYPE-1 PROTEASE; IN-VITRO; ANTIRETROVIRAL
THERAPY; CRYSTAL-STRUCTURE; DRUG-RESISTANCE; ANTIVIRAL ACTIVITY; POTENT;
PI; SITE
AB Dimerization of HIV protease is essential for the acquisition of protease's proteolytic activity. We previously identified a group of HIV protease dimerization inhibitors, including darunavir (DRV). In the present work, we examine whether loss of DRV's protease dimerization inhibition activity is associated with HIV development of DRV resistance. Single amino acid substitutions, including I3A, L5A, R8A/Q, L24A, T26A, D29N, R87K, T96A, L97A, and F99A, disrupted protease dimerization, as examined using an intermolecular fluorescence resonance energy transfer (FRET)-based HIV expression assay. All recombinant HIV(NL4-3)-based clones with such a protease dimerization-disrupting substitution failed to replicate. A highly DRV-resistant in vitro-selected HIV variant and clinical HIV strains isolated from AIDS patients failing to respond to DRV-containing antiviral regimens typically had the V32I, L33F, I54M, and I84V substitutions in common in protease. None of up to 3 of the 4 substitutions affected DRV's protease dimerization inhibition, which was significantly compromised by the four combined substitutions. Recombinant infectious clones containing up to 3 of the 4 substitutions remained sensitive to DRV, while a clonal HIV variant with all 4 substitutions proved highly resistant to DRV with a 205-fold 50% effective concentration (EC(50)) difference compared to HIV(NL4-3). The present data suggest that the loss of DRV activity to inhibit protease dimerization represents a novel mechanism contributing to HIV resistance to DRV. The finding that 4 substitutions in PR are required for significant loss of DRV's protease dimerization inhibition should at least partially explain the reason DRV has a high genetic barrier against HIV's acquisition of DRV resistance.
C1 [Koh, Yasuhiro; Aoki, Manabu; Danish, Matthew L.; Aoki-Ogata, Hiromi; Amano, Masayuki; Mitsuya, Hiroaki] Kumamoto Univ, Grad Sch Med Sci, Dept Infect Dis, Kumamoto 8608556, Japan.
[Koh, Yasuhiro; Aoki, Manabu; Danish, Matthew L.; Aoki-Ogata, Hiromi; Amano, Masayuki; Mitsuya, Hiroaki] Kumamoto Univ, Grad Sch Med Sci, Dept Hematol, Kumamoto 8608556, Japan.
[Aoki, Manabu] Kumamoto Hlth Sci Univ, Dept Med Technol, Kumamoto 8615598, Japan.
[Das, Debananda; Mitsuya, Hiroaki] NCI, Expt Retrovirol Sect, HIV & AIDS Malignancy Branch, NIH, Bethesda, MD 20892 USA.
[Shafer, Robert W.] Stanford Univ, Med Ctr, Div Infect Dis, Stanford, CA 94305 USA.
[Ghosh, Arun K.] Purdue Univ, Dept Chem, W Lafayette, IN 47907 USA.
[Ghosh, Arun K.] Purdue Univ, Dept Med Chem, W Lafayette, IN 47907 USA.
RP Mitsuya, H (reprint author), Kumamoto Univ, Sch Med, Dept Infect Dis, 1-1-1 Honjo, Kumamoto 8608556, Japan.
EM hmitsuya@helix.nih.gov
RI Amano, Masayuki/N-7407-2016
OI Amano, Masayuki/0000-0003-0516-9502
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health; Ministry of Health, Welfare, and Labor of Japan;
Kumamoto University [78]; National Institutes of Health [GM53386]
FX This work was supported in part by the Intramural Research Program of
the Center for Cancer Research, National Cancer Institute, National
Institutes of Health, in part by a grant for global education and
research centers aimed at the control of AIDS (Global Center of
Excellence supported by Monbu-Kagakusho), Promotion of AIDS Research
from the Ministry of Health, Welfare, and Labor of Japan, by a grant to
the Cooperative Research Project on Clinical and Epidemiological Studies
of Emerging and Reemerging Infectious Diseases (Renkei Jigyo no. 78,
Kumamoto University) of Monbu-Kagakusho, and by a grant from the
National Institutes of Health (GM53386 to A.K.G.).
NR 42
TC 16
Z9 16
U1 1
U2 6
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 OCT
PY 2011
VL 85
IS 19
BP 10079
EP 10089
DI 10.1128/JVI.05121-11
PG 11
WC Virology
SC Virology
GA 837ZH
UT WOS:000296253900040
PM 21813613
ER
PT J
AU Lam, TTY
Zhu, HC
Wang, J
Smith, DK
Holmes, EC
Webster, RG
Webby, R
Peiris, JM
Guan, Y
AF Lam, Tommy Tsan-Yuk
Zhu, Huachen
Wang, Jia
Smith, David K.
Holmes, Edward C.
Webster, Robert G.
Webby, Richard
Peiris, Joseph M.
Guan, Yi
TI Reassortment Events among Swine Influenza A Viruses in China:
Implications for the Origin of the 2009 Influenza Pandemic
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID GENETIC REASSORTMENT; H1N1; PIGS; EVOLUTION; TRANSMISSION; MODELS
AB That pigs may play a pivotal role in the emergence of pandemic influenza was indicated by the recent H1N1/2009 human pandemic, likely caused by a reassortant between viruses of the American triple-reassortant (TR) and Eurasian avian-like (EA) swine influenza lineages. As China has the largest human and pig populations in the world and is the only place where both TR and EA viruses have been reported to cocirculate, it is potentially the source of the H1N1/2009 pandemic virus. To examine this, the genome sequences of 405 swine influenza viruses from China were analyzed. Thirty-six TR and EA reassortant viruses were identified before and after the occurrence of the pandemic. Several of these TR-EA reassortant viruses had genotypes with most segments having the same lineage origin as the segments of the H1N1/2009 pandemic virus. However, these viruses were generated from independent reassortment events throughout our survey period and were not associated with the current pandemic. One TR-EA reassortant, which is least similar to the pandemic virus, has persisted since 2007, while all the other variants appear to be transient. Despite frequent reassortment events between TR and EA lineage viruses in China, evidence for the genesis of the 2009 pandemic virus in pigs in this region is still absent.
C1 [Lam, Tommy Tsan-Yuk; Zhu, Huachen; Smith, David K.; Peiris, Joseph M.; Guan, Yi] Univ Hong Kong, State Key Lab Emerging Infect Dis, Li Ka Shing Fac Med, Pokfulam, Hong Kong, Peoples R China.
[Lam, Tommy Tsan-Yuk; Zhu, Huachen; Wang, Jia; Smith, David K.; Guan, Yi] Shantou Univ, Int Inst Infect & Immun, Coll Med, Shantou, Guangdong, Peoples R China.
[Holmes, Edward C.] Penn State Univ, Ctr Infect Dis Dynam, Dept Biol, Mueller Lab, University Pk, PA 16802 USA.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Webster, Robert G.; Webby, Richard] St Jude Childrens Hosp, Div Virol, Dept Infect Dis, Memphis, TN 38105 USA.
RP Guan, Y (reprint author), Univ Hong Kong, State Key Lab Emerging Infect Dis, Li Ka Shing Fac Med, 21 Sassoon Rd, Pokfulam, Hong Kong, Peoples R China.
EM yguan@hku.hk
RI Lam, Tommy Tsan-Yuk/D-4837-2012; Zhu, Huachen/A-8252-2017;
OI Zhu, Huachen/0000-0003-2711-0501; Holmes, Edward/0000-0001-9596-3552
FU National Institutes of Health (National Institute of Allergy and
Infectious Diseases) [HSN266200700005C]; Li Ka Shing Foundation; Area of
Excellence Scheme of the UGC of the Hong Kong SAR [AoE/M-12/06];
Computer Centre of The University of Hong Kong
FX We acknowledge the National Institutes of Health (National Institute of
Allergy and Infectious Diseases contract HSN266200700005C), the Li Ka
Shing Foundation, and the Area of Excellence Scheme of the UGC of the
Hong Kong SAR (grant AoE/M-12/06) for financial support.; We thank the
staff from the International Institute of Infection and Immunity
(Shantou, China) and the State Key Laboratory of Emerging Infectious
Diseases (Shenzhen and Hong Kong SAR, China) for technical assistance.
We acknowledge the support of HPCPower projects for bioinformatics and
computational services from the Computer Centre of The University of
Hong Kong. We also thank W. K. Kwan and Frankie Cheung for technical
assistance.
NR 27
TC 26
Z9 28
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 OCT
PY 2011
VL 85
IS 19
BP 10279
EP 10285
DI 10.1128/JVI.05262-11
PG 7
WC Virology
SC Virology
GA 837ZH
UT WOS:000296253900060
PM 21795347
ER
PT J
AU Yeh, WW
Rao, SS
Lim, SY
Zhang, JR
Hraber, PT
Brassard, LM
Luedemann, C
Todd, JP
Dodson, A
Shen, L
Buzby, AP
Whitney, JB
Korber, BT
Nabel, GJ
Mascola, JR
Letvin, NL
AF Yeh, Wendy W.
Rao, Srinivas S.
Lim, So-Yon
Zhang, Jinrong
Hraber, Peter T.
Brassard, Laura M.
Luedemann, Corinne
Todd, John Paul
Dodson, Alan
Shen, Ling
Buzby, Adam P.
Whitney, James B.
Korber, Bette T.
Nabel, Gary J.
Mascola, John R.
Letvin, Norman L.
TI The TRIM5 Gene Modulates Penile Mucosal Acquisition of Simian
Immunodeficiency Virus in Rhesus Monkeys
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID VIVO VIRAL REPLICATION; HIV-1 INFECTION; MALE CIRCUMCISION; TRIM5-ALPHA;
MACAQUES; CELLS; SIV; PROGRESSION; DETERMINANTS; RESTRICTION
AB There is considerable variability in host susceptibility to human immunodeficiency virus type 1 (HIV-1) infection, but the host genetic determinants of that variability are not well understood. In addition to serving as a block for cross-species retroviral infection, TRIM5 was recently shown to play a central role in limiting primate immunodeficiency virus replication. We hypothesized that TRIM5 may also contribute to susceptibility to mucosal acquisition of simian immunodeficiency virus (SIV) in rhesus monkeys. We explored this hypothesis by establishing 3 cohorts of Indian-origin rhesus monkeys with different TRIM5 genotypes: homozygous restrictive, heterozygous permissive, and homozygous permissive. We then evaluated the effect of TRIM5 genotype on the penile transmission of SIVsmE660. We observed a significant effect of TRIM5 genotype on mucosal SIVsmE660 acquisition in that no SIV transmission occurred in monkeys with only restrictive TRIM5 alleles. In contrast, systemic SIV infections were initiated after preputial pocket exposures in monkeys that had at least one permissive TRIM5 allele. These data demonstrate that host genetic factors can play a critical role in restricting mucosal transmission of a primate immunodeficiency virus. In addition, we used our understanding of TRIM5 to establish a novel nonhuman primate penile transmission model for AIDS mucosal pathogenesis and vaccine research.
C1 [Letvin, Norman L.] Beth Israel Deaconess Med Ctr, Div Viral Pathogensis, Boston, MA 02215 USA.
[Rao, Srinivas S.; Todd, John Paul; Nabel, Gary J.; Mascola, John R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Hraber, Peter T.; Korber, Bette T.] Los Alamos Natl Lab, Los Alamos, NM 87545 USA.
[Dodson, Alan] Bioqual, Rockville, MD 20850 USA.
RP Letvin, NL (reprint author), Beth Israel Deaconess Med Ctr, Div Viral Pathogensis, 330 Brookline Ave,E-CLS 1043, Boston, MA 02215 USA.
EM nletvin@bidmc.harvard.edu
RI Lujan Center, LANL/G-4896-2012;
OI Korber, Bette/0000-0002-2026-5757; Hraber, Peter/0000-0002-2920-4897
FU NIAID [K08 AI069995, R21 AI093199]; Vaccine Research Center, NIAID, NIH,
Center for HIV/AIDS Vaccine Immunology [U19 AI067854]; Harvard Clinical
and Translational Science Center [UL1 RR 025758]; Harvard Medical
School; Infectious Diseases Society of America; Harvard University
Center for AIDS Research [P30AI060354]
FX This work was supported by NIAID grants K08 AI069995 and R21 AI093199
(W.W.Y.), the intramural research program of the Vaccine Research
Center, NIAID, NIH, Center for HIV/AIDS Vaccine Immunology (grant U19
AI067854), Harvard Clinical and Translational Science Center grant UL1
RR 025758 (W.W.Y.), a Shore Fellowship from Harvard Medical School
(W.W.Y.), the Pfizer Young Investigator Award in Vaccine Development
from the Infectious Diseases Society of America (W.W.Y.), and Harvard
University Center for AIDS Research grant P30AI060354 (W.W.Y.).
NR 41
TC 30
Z9 30
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 OCT
PY 2011
VL 85
IS 19
BP 10389
EP 10398
DI 10.1128/JVI.00854-11
PG 10
WC Virology
SC Virology
GA 837ZH
UT WOS:000296253900070
PM 21775457
ER
PT J
AU Dilley, KA
Ni, N
Nikolaitchik, OA
Chen, JB
Galli, A
Hu, WS
AF Dilley, Kari A.
Ni, Na
Nikolaitchik, Olga A.
Chen, Jianbo
Galli, Andrea
Hu, Wei-Shau
TI Determining the Frequency and Mechanisms of HIV-1 and HIV-2 RNA
Copackaging by Single-Virion Analysis
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; MURINE LEUKEMIA-VIRUS; INTERSUBTYPE
RECOMBINATION; GENETIC-RECOMBINATION; INITIATION SIGNAL; COTE-DIVOIRE;
INFECTION; ORIGIN; GENOME; GAG
AB HIV-1 and HIV-2 are derived from two distinct primate viruses and share only limited sequence identity. Despite this, HIV-1 and HIV-2 Gag polyproteins can coassemble into the same particle and their genomes can undergo recombination, albeit at an extremely low frequency, implying that HIV-1 and HIV-2 RNA can be copackaged into the same particle. To determine the frequency of HIV-1 and HIV-2 RNA copackaging and to dissect the mechanisms that allow the heterologous RNA copackaging, we directly visualized the RNA content of each particle by using RNA-binding proteins tagged with fluorescent proteins to label the viral genomes. We found that when HIV-1 and HIV-2 RNA are present in viral particles at similar ratios, similar to 10% of the viral particles encapsidate both HIV-1 and HIV-2 RNAs. Furthermore, heterologous RNA copackaging can be promoted by mutating the 6-nucleotide (6-nt) dimer initiation signal (DIS) to discourage RNA homodimerization or to encourage RNA heterodimerization, indicating that HIV-1 and HIV-2 RNA can heterodimerize prior to packaging using the DIS sequences. We also observed that the coassembly of HIV-1 and HIV-2 Gag proteins is not required for the heterologous RNA copackaging; HIV-1 Gag proteins are capable of mediating HIV-1 and HIV-2 RNA copackaging. These results define the cis- and trans-acting elements required for and affecting the heterologous RNA copackaging, a prerequisite for the generation of chimeric viruses by recombination, and also shed light on the mechanisms of RNA-Gag recognition essential for RNA encapsidation.
C1 [Dilley, Kari A.; Ni, Na; Nikolaitchik, Olga A.; Chen, Jianbo; Galli, Andrea; Hu, Wei-Shau] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
RP Hu, WS (reprint author), NCI, HIV Drug Resistance Program, POB B,Bldg 535,Room 336, Frederick, MD 21702 USA.
EM Wei-Shau.Hu@nih.gov
RI Chen, Jianbo/N-3737-2014;
OI Chen, Jianbo/0000-0001-6491-6577; Galli, Andrea/0000-0002-4404-430X
FU NIH, National Cancer Institute, Center for Cancer Research; IATAP, NIH
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research; IATAP
funding, NIH.
NR 35
TC 11
Z9 11
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 OCT
PY 2011
VL 85
IS 20
BP 10499
EP 10508
DI 10.1128/JVI.05147-11
PG 10
WC Virology
SC Virology
GA 837ZJ
UT WOS:000296254100007
PM 21849448
ER
PT J
AU Khattar, SK
Samal, S
DeVico, AL
Collins, PL
Samal, SK
AF Khattar, Sunil K.
Samal, Sweety
DeVico, Anthony L.
Collins, Peter L.
Samal, Siba K.
TI Newcastle Disease Virus Expressing Human Immunodeficiency Virus Type 1
Envelope Glycoprotein Induces Strong Mucosal and Serum Antibody
Responses in Guinea Pigs
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID LYMPH-NODE IMMUNIZATION; NEUTRALIZING ANTIBODIES; VACCINE DEVELOPMENT;
IMMUNE-RESPONSES; INTRANASAL IMMUNIZATION; MONOCLONAL-ANTIBODIES;
OLIGOMERIC STRUCTURE; RESPIRATORY-TRACT; ATTENUATED SIV; HIV-1 VACCINE
AB Human immunodeficiency virus type 1 (HIV-1) is transmitted mainly through mucosal sites. Optimum strategies to elicit both systemic and mucosal immunity are critical for the development of vaccines against HIV-1. We therefore sought to evaluate the induction of systemic and mucosal immune responses by the use of Newcastle disease virus (NDV) as a vaccine vector. We generated a recombinant NDV, designated rLaSota/gp160, expressing the gp160 envelope (Env) protein of HIV-1 from an added gene. The gp160 protein expressed by rLaSota/gp160 virus was detected on an infected cell surface and was incorporated into the NDV virion. Biochemical studies showed that gp160 present in infected cells and in the virion formed a higher-order oligomer that retained recognition by conformationally sensitive monoclonal antibodies. Expression of gp160 did not increase the virulence of recombinant NDV (rNDV) strain LaSota. Guinea pigs were administered rLaSota/gp160 via the intranasal (i.n.) or intramuscular (i.m.) route in different prime-boost combinations. Systemic and mucosal antibody responses specific to the HIV-1 envelope protein were assessed in serum and vaginal washes, respectively. Two or three immunizations via the i.n. or i.m. route induced a more potent systemic and mucosal immune response than a single immunization by either route. Priming by the i.n. route was more immunogenic than by the i.m. route, and the same was true for the boosts. Furthermore, immunization with rLaSota/gp160 by any route or combination of routes induced a Th1-type response, as reflected by the induction of stronger antigen-specific IgG2a than IgG1 antibody responses. Additionally, i.n. immunization elicited a stronger neutralizing serum antibody response to laboratory-adapted HIV-1 strain MN.3. These data illustrate that it is feasible to use NDV as a vaccine vector to elicit potent humoral and mucosal responses to the HIV-1 envelope protein.
C1 [Khattar, Sunil K.; Samal, Sweety; Samal, Siba K.] Univ Maryland, Virginia Maryland Reg Coll Vet Med, College Pk, MD 20742 USA.
[DeVico, Anthony L.] Univ Maryland, Sch Med, Inst Human Virol, Div Basic Sci, Baltimore, MD 21201 USA.
[Collins, Peter L.] NIAID, Infect Dis Lab, Bethesda, MD 20892 USA.
RP Samal, SK (reprint author), Univ Maryland, Virginia Maryland Reg Coll Vet Med, College Pk, MD 20742 USA.
EM ssamal@umd.edu
FU NIAID [N01A060009]; NIAID, NIH
FX This research was supported in part by NIAID contract no. N01A060009. P.
L. C. was supported by the NIAID, NIH Intramural Research Program.
NR 73
TC 14
Z9 14
U1 0
U2 0
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 OCT
PY 2011
VL 85
IS 20
BP 10529
EP 10541
DI 10.1128/JVI.05050-11
PG 13
WC Virology
SC Virology
GA 837ZJ
UT WOS:000296254100010
PM 21849467
ER
PT J
AU Blaney, JE
Wirblich, C
Papaneri, AB
Johnson, RF
Myers, CJ
Juelich, TL
Holbrook, MR
Freiberg, AN
Bernbaum, JG
Jahrling, PB
Paragas, J
Schnell, MJ
AF Blaney, Joseph E.
Wirblich, Christoph
Papaneri, Amy B.
Johnson, Reed F.
Myers, Carey J.
Juelich, Terry L.
Holbrook, Michael R.
Freiberg, Alexander N.
Bernbaum, John G.
Jahrling, Peter B.
Paragas, Jason
Schnell, Matthias J.
TI Inactivated or Live-Attenuated Bivalent Vaccines That Confer Protection
against Rabies and Ebola Viruses
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NONHUMAN-PRIMATES; HEMORRHAGIC-FEVER; RESPIRATORY-TRACT; VECTORED
VACCINE; TYPE-1 GAG; SAD B19; GLYCOPROTEIN; RHABDOVIRUS; INFECTION;
PROTEIN
AB The search for a safe and efficacious vaccine for Ebola virus continues, as no current vaccine candidate is nearing licensure. We have developed (i) replication-competent, (ii) replication-deficient, and (iii) chemically inactivated rabies virus (RABV) vaccines expressing Zaire Ebola virus (ZEBOV) glycoprotein (GP) by a reverse genetics system based on the SAD B19 RABV wildlife vaccine. ZEBOV GP is efficiently expressed by these vaccine candidates and is incorporated into virions. The vaccine candidates were avirulent after inoculation of adult mice, and viruses with a deletion in the RABV glycoprotein had greatly reduced neurovirulence after intracerebral inoculation in suckling mice. Immunization with live or inactivated RABV vaccines expressing ZEBOV GP induced humoral immunity against each virus and conferred protection from both lethal RABV and EBOV challenge in mice. The bivalent RABV/ZEBOV vaccines described here have several distinct advantages that may speed the development of inactivated vaccines for use in humans and potentially live or inactivated vaccines for use in nonhuman primates at risk of EBOV infection in endemic areas.
C1 [Schnell, Matthias J.] Thomas Jefferson Univ, Jefferson Vaccine Ctr, Dept Microbiol & Immunol, Jefferson Med Coll, Philadelphia, PA 19107 USA.
[Blaney, Joseph E.; Papaneri, Amy B.; Johnson, Reed F.; Jahrling, Peter B.] NIAID, Emerging Viral Pathogens Sect, NIH, Bethesda, MD 20892 USA.
[Holbrook, Michael R.; Bernbaum, John G.; Jahrling, Peter B.; Paragas, Jason] NIAID, Integrated Res Facil, NIH, Ft Detrick, MD 21702 USA.
[Juelich, Terry L.; Holbrook, Michael R.; Freiberg, Alexander N.] Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA.
[Juelich, Terry L.; Freiberg, Alexander N.] Univ Texas Med Branch, Galveston Natl Lab, Galveston, TX 77555 USA.
RP Schnell, MJ (reprint author), Thomas Jefferson Univ, Jefferson Vaccine Ctr, Dept Microbiol & Immunol, Jefferson Med Coll, 531 BLSB,233 S 10th St, Philadelphia, PA 19107 USA.
EM jblaney@niaid.nih.gov; Matthias.schnell@jefferson.edu
OI Papaneri, Amy/0000-0003-2144-2441
FU NIAID Division of Intramural Research; Jefferson Vaccine Center, TJU
FX These studies were supported, in part, by the NIAID Division of
Intramural Research and internal funds of the Jefferson Vaccine Center,
TJU, to M.J.S.
NR 54
TC 33
Z9 38
U1 1
U2 15
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 OCT
PY 2011
VL 85
IS 20
BP 10605
EP 10616
DI 10.1128/JVI.00558-11
PG 12
WC Virology
SC Virology
GA 837ZJ
UT WOS:000296254100017
PM 21849459
ER
PT J
AU Nishimura, Y
Shingai, M
Lee, WR
Sadjadpour, R
Donau, OK
Willey, R
Brenchley, JM
Iyengar, R
Buckler-White, A
Igarashi, T
Martin, MA
AF Nishimura, Yoshiaki
Shingai, Masashi
Lee, Wendy R.
Sadjadpour, Reza
Donau, Olivia K.
Willey, Ronald
Brenchley, Jason M.
Iyengar, Ranjini
Buckler-White, Alicia
Igarashi, Tatsuhiko
Martin, Malcolm A.
TI Recombination-Mediated Changes in Coreceptor Usage Confer an Augmented
Pathogenic Phenotype in a Nonhuman Primate Model of HIV-1-Induced AIDS
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; SYNCYTIUM-INDUCING PHENOTYPE; HIV-1
INFECTION; T-CELL; RHESUS MACAQUE; DISEASE PROGRESSION; BIOLOGICAL
PHENOTYPE; CHEMOKINE RECEPTORS; CLINICAL-OUTCOMES; TYPE-1 INFECTION
AB Evolution of the env gene in transmitted R5-tropic human immunodeficiency virus type 1 (HIV-1) strains is the most widely accepted mechanism driving coreceptor switching. In some infected individuals, however, a shift in coreceptor utilization can occur as a result of the reemergence of a cotransmitted, but rapidly controlled, X4 virus. The latter possibility was studied by dually infecting rhesus macaques with X4 and R5 chimeric simian simian/human immunodeficiency viruses (SHIVs) and monitoring the replication status of each virus using specific primer pairs. In one of the infected monkeys, both SHIVs were potently suppressed by week 12 postinoculation, but a burst of viremia at week 51 was accompanied by an unrelenting loss of total CD4(+) T cells and the development of clinical disease. PCR analyses of plasma viral RNA indicated an env gene segment containing the V3 region from the inoculated X4 SHIV had been transferred into the genetic background of the input R5 SHIV by intergenomic recombination, creating an X4 virus with novel replicative, serological, and pathogenic properties. These results indicate that the effects of retrovirus recombination in vivo can be functionally profound and may even occur when one of the recombination participants is undetectable in the circulation as cell-free virus.
C1 [Nishimura, Yoshiaki; Shingai, Masashi; Lee, Wendy R.; Sadjadpour, Reza; Donau, Olivia K.; Willey, Ronald; Brenchley, Jason M.; Iyengar, Ranjini; Buckler-White, Alicia; Martin, Malcolm A.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Igarashi, Tatsuhiko] Kyoto Univ, Inst Virus Res, Lab Primate Models, Sakyo Ku, Kyoto 6068507, Japan.
RP Martin, MA (reprint author), NIAID, Mol Microbiol Lab, NIH, Bldg 4,Rm 315A,4 Ctr Dr,MSC 0460, Bethesda, MD 20892 USA.
EM malm@nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This study was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 60
TC 5
Z9 5
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD OCT
PY 2011
VL 85
IS 20
BP 10617
EP 10626
DI 10.1128/JVI.05010-11
PG 10
WC Virology
SC Virology
GA 837ZJ
UT WOS:000296254100018
PM 21813599
ER
PT J
AU Tosi, G
Forlani, G
Andresen, V
Turci, M
Bertazzoni, U
Franchini, G
Poli, G
Accolla, RS
AF Tosi, Giovanna
Forlani, Greta
Andresen, Vibeke
Turci, Marco
Bertazzoni, Umberto
Franchini, Genoveffa
Poli, Guido
Accolla, Roberto S.
TI Major Histocompatibility Complex Class II Transactivator CIITA Is a
Viral Restriction Factor That Targets Human T-Cell Lymphotropic Virus
Type 1 Tax-1 Function and Inhibits Viral Replication
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID BARE LYMPHOCYTE SYNDROME; ELEMENT-BINDING PROTEIN; COACTIVATOR CBP;
HIV-1 INFECTION; IN-VITRO; HTLV-I; LEUKEMIA; PROMOTERS; GENES; CREB
AB Human T-cell lymphotropic virus type 1 (HTLV-1) is the causative agent of an aggressive malignancy of CD4(+) T lymphocytes. Since the viral transactivator Tax-1 is a major player in T-cell transformation, targeting Tax-1 protein is regarded as a possible strategy to arrest viral replication and to counteract neoplastic transformation. We demonstrate that CIITA, the master regulator of major histocompatibility complex class II gene transcription, inhibits HTLV-1 replication by blocking the transactivating function of Tax-1 both when exogenously transfected in 293T cells and when endogenously expressed by a subset of U937 promonocytic cells. Tax-1 and CIITA physically interact in vivo via the first 108 amino acids of Tax-1 and two CIITA adjacent regions (amino acids 1 to 252 and 253 to 410). Interestingly, only CIITA 1-252 mediated Tax-1 inhibition, in agreement with the fact that CIITA residues from positions 64 to 124 were required to block Tax-1 transactivation. CIITA inhibitory action on Tax-1 correlated with the nuclear localization of CIITA and was independent of the transcription factor NF-YB, previously involved in CIITA-mediated inhibition of Tax-2 of HTLV-2. Instead, CIITA severely impaired the physical and functional interaction of Tax-1 with the cellular coactivators p300/CBP-associated factor (PCAF), cyclic AMP-responsive element binding protein (CREB), and activating transcription factor 1 (ATF1), which are required for the optimal activation of HTLV-1 promoter. Accordingly, the overexpression of PCAF, CREB, and ATF1 restored Tax-1-dependent transactivation of the viral long-terminal-repeat promoter inhibited by CIITA. These findings strongly support our original observation that CIITA, beside increasing the antigen-presenting function for pathogen antigens, acts as an endogenous restriction factor against human retroviruses by blocking virus replication and spreading.
C1 [Tosi, Giovanna; Forlani, Greta; Accolla, Roberto S.] Univ Insubria, Dept Expt Med, I-21100 Varese, Italy.
[Andresen, Vibeke; Franchini, Genoveffa] NCI, Anim Models & Retroviral Vaccines Sect, Bethesda, MD 20892 USA.
[Turci, Marco; Bertazzoni, Umberto] Univ Verona, Dept Life & Reprod Sci, Sect Biol & Genet, I-37100 Verona, Italy.
[Poli, Guido] Ist Sci San Raffaele, AIDS Immunopathogenesis Unit, Div Immunol Transplantat & Infect Dis, Milan, Italy.
RP Accolla, RS (reprint author), Univ Insubria, Dept Expt Med, Via O Rossi 9, I-21100 Varese, Italy.
EM roberto.accolla@uninsubria.it
OI Accolla, Roberto/0000-0003-2493-7378; FORLANI, GRETA/0000-0003-1987-7761
FU Fondazione Cariplo [A.I.R.C IG 8862]; MIUR [2008-WXF7KK]; University of
Insubria; Associazione Italiana per la Ricerca sul Cancro
FX This study was supported by the grants to R.S.A. (Fondazione Cariplo
2008-2230, Cellular and Molecular Basis of Human Retroviral-Dependent
Pathology; A.I.R.C IG 8862, New Strategies of Tumor Vaccination and
Immunotherapy Based on Optimized Triggering of Anti-Tumor
CD4+ T Cells; MIUR-PRIN project 2008-WXF7KK, New Strategies
of Immunointervention against Tumors), University of Insubria grants FAR
2009 and FAR 2010 to G. T., and grant Miur PRIN 2007 and AIRC 2008
regional grant to U. B.
NR 54
TC 9
Z9 9
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 OCT
PY 2011
VL 85
IS 20
BP 10719
EP 10729
DI 10.1128/JVI.00813-11
PG 11
WC Virology
SC Virology
GA 837ZJ
UT WOS:000296254100028
PM 21813598
ER
PT J
AU Kuniholm, MH
Gao, XJ
Xue, XN
Kovacs, A
Anastos, K
Marti, D
Greenblatt, RM
Cohen, MH
Minkoff, H
Gange, SJ
Fazzari, M
Young, MA
Strickler, HD
Carrington, M
AF Kuniholm, Mark H.
Gao, Xiaojiang
Xue, Xiaonan
Kovacs, Andrea
Anastos, Kathryn
Marti, Darlene
Greenblatt, Ruth M.
Cohen, Mardge H.
Minkoff, Howard
Gange, Stephen J.
Fazzari, Melissa
Young, Mary A.
Strickler, Howard D.
Carrington, Mary
TI Human Leukocyte Antigen Genotype and Risk of HIV Disease Progression
before and after Initiation of Antiretroviral Therapy
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; FEMALE GENITAL-TRACT; CLASS-I; HLA-BW4
HOMOZYGOSITY; DRUG-RESISTANCE; HLA-B; INFECTION; AIDS; WOMEN; RECOVERY
AB While the human leukocyte antigen (HLA) genotype has been associated with the rate of HIV disease progression in untreated patients, little is known regarding these relationships in patients using highly active antiretroviral therapy (HAART). The limited data reported to date identified few HLA-HIV disease associations in patients using HAART and even occasional associations that were opposite of those found in untreated patients. We conducted high-resolution HLA class I and II genotyping in a random sample (n = 860) of HIV-seropositive women enrolled in a long-term cohort initiated in 1994. HLA-HIV disease associations before and after initiation of HAART were examined using multivariate analyses. In untreated HIV-seropositive patients, we observed many of the predicted associations, consistent with prior studies. For example, HLA-B*57 (beta = -0.7; 95% confidence interval [CI] = -0.9 to -0.5; P = 5 x 10(-11)) and Bw4 (beta = -0.2; 95% CI = -0.4 to -0.1; P = 0.009) were inversely associated with baseline HIV viral load, and B*57 was associated with a low risk of rapid CD4(+) decline (odds ratio [OR] = 0.2; 95% CI = 0.1 to 0.6; P = 0.002). Conversely, in treated patients, the odds of a virological response to HAART were lower for B*57: 01 (OR = 0.2; 95% CI = 0.0 to 0.9; P = 0.03), and Bw4 (OR = 0.4; 95% CI = 0.1 to 1.0; P = 0.04) was associated with low odds of an immunological response. The associations of HLA genotype with HIV disease are different and sometimes even opposite in treated and untreated patients.
C1 [Kuniholm, Mark H.; Xue, Xiaonan; Anastos, Kathryn; Fazzari, Melissa; Strickler, Howard D.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10461 USA.
[Gao, Xiaojiang; Marti, Darlene; Carrington, Mary] SAIC Frederick Inc, NCI Frederick, Canc & Inflammat Program, Expt Immunol Lab, Frederick, MD USA.
[Gao, Xiaojiang; Marti, Darlene; Carrington, Mary] Ragon Inst MGH MIT & Harvard, Charlestown, MA USA.
[Kovacs, Andrea] Univ So Calif, Dept Pediat, Los Angeles, CA 90089 USA.
[Anastos, Kathryn] Montefiore Med Ctr, Dept Med, Bronx, NY 10467 USA.
[Greenblatt, Ruth M.] Univ Calif San Francisco, Dept Clin Pharm, San Francisco, CA 94143 USA.
[Cohen, Mardge H.] CORE Ctr, Cook Cty Bur Hlth Serv, Chicago, IL USA.
[Minkoff, Howard] Maimonides Hosp, Dept Obstet & Gynecol, Brooklyn, NY 11219 USA.
[Gange, Stephen J.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Young, Mary A.] Georgetown Univ, Med Ctr, Dept Med, Washington, DC 20007 USA.
RP Kuniholm, MH (reprint author), Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Belfer Bldg,Room 1308,1300 Morris Pk Ave, Bronx, NY 10461 USA.
EM mark.kuniholm@einstein.yu.edu
OI Gange, Stephen/0000-0001-7842-512X
FU National Institute of Allergy and Infectious Diseases [5R01AI057006,
R01A1052065, UO1-AI-35004, UO1-AI-31834, UO1-AI-34994, UO1-AI-34989,
UO1-AI-34993, UO1-AI-42590]; Eunice Kennedy Shriver National Institute
of Child Health and Human Development [UO1-HD-32632]; National Cancer
Institute; National Institute on Drug Abuse; National Institute on
Deafness and Other Communication Disorders; National Center for Research
Resources (UCSF-CTSI) [UL1 RR024131]; National Cancer Institute,
National Institutes of Health [HHSN261200800001E]; NIH; Center for
Cancer Research; Einstein-Montefiore Center for AIDS Research
[5P30AI051519-08]
FX Funding for this project was provided in part by grants from the
National Institute of Allergy and Infectious Diseases (5R01AI057006 to
H.D.S. and R01A1052065 to A.K.). The WIHS is funded by the National
Institute of Allergy and Infectious Diseases (grants UO1-AI-35004,
UO1-AI-31834, UO1-AI-34994, UO1-AI-34989, UO1-AI-34993, and
UO1-AI-42590) and by the Eunice Kennedy Shriver National Institute of
Child Health and Human Development (grant UO1-HD-32632). The study is
cofunded by the National Cancer Institute, the National Institute on
Drug Abuse, and the National Institute on Deafness and Other
Communication Disorders. Funding was also provided by the National
Center for Research Resources (UCSF-CTSI grant UL1 RR024131). This
project has also been funded in part with federal funds from the
National Cancer Institute, National Institutes of Health, under contract
HHSN261200800001E. This research was supported in part by the Intramural
Research Program of the NIH, National Cancer Institute, Center for
Cancer Research, and by the Einstein-Montefiore Center for AIDS Research
(grant 5P30AI051519-08).
NR 40
TC 12
Z9 12
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 OCT
PY 2011
VL 85
IS 20
BP 10826
EP 10833
DI 10.1128/JVI.00804-11
PG 8
WC Virology
SC Virology
GA 837ZJ
UT WOS:000296254100038
PM 21849458
ER
PT J
AU Nagel, JD
Rudick, J
AF Nagel, Joan Davis
Rudick, Joyce
TI Eighth Annual NIH Interdisciplinary Women's Health Research Symposium
November 17, 2011 Introduction
SO JOURNAL OF WOMENS HEALTH
LA English
DT Editorial Material
C1 [Rudick, Joyce] NIH, Programs & Management Off Res Womens Hlth, Bethesda, MD 20892 USA.
RP Rudick, J (reprint author), NIH, Programs & Management Off Res Womens Hlth, 6707 Democracy Blvd,Suite 400, Bethesda, MD 20892 USA.
EM orwh-research@od.nih.gov
NR 0
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U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT
PY 2011
VL 20
IS 10
BP 1384
EP 1385
PG 2
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 833IQ
UT WOS:000295877900001
ER
PT J
AU Alley, D
Yerges, L
Shardell, M
Metter, EJ
Simonsick, E
Snitker, S
Stenholm, S
Shuldiner, AR
Mitchell, B
Ferrucci, L
AF Alley, Dawn
Yerges, Laura
Shardell, Michelle
Metter, E. Jeffrey
Simonsick, Eleanor
Snitker, Soren
Stenholm, Sari
Shuldiner, Alan R.
Mitchell, Braxton
Ferrucci, Luigi
TI Cohort differences in Body Composition in Women: A Comparison of the
Baltimore Longitudinal Study of Aging and Old Order Amish
SO JOURNAL OF WOMENS HEALTH
LA English
DT Meeting Abstract
C1 [Alley, Dawn; Yerges, Laura; Shardell, Michelle; Snitker, Soren; Shuldiner, Alan R.; Mitchell, Braxton] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Metter, E. Jeffrey; Simonsick, Eleanor; Stenholm, Sari; Ferrucci, Luigi] NIA, Bethesda, MD 20892 USA.
RI Stenholm, Sari/G-6940-2011
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 1540-9996
EI 1931-843X
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT
PY 2011
VL 20
IS 10
BP 1387
EP 1387
PG 1
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 833IQ
UT WOS:000295877900005
ER
PT J
AU Foulkes, MA
Grady, C
Spong, CY
Bates, A
Clayton, JA
AF Foulkes, Mary A.
Grady, Christine
Spong, Catherine Y.
Bates, Angela
Clayton, Janine A.
TI Clinical Research Enrolling Pregnant Women: A Workshop Summary
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID DRUG-USE; PRESCRIPTION
AB Clinical research investigates mechanisms of human disease, interventions, or new technologies, but pregnant women are often excluded from clinical studies. Few studies, beyond research on pregnancy, are designed to address questions relevant to pregnant women. A recent National Institutes of Health workshop considered the barriers and opportunities in conducting clinical research studies enrolling pregnant women.
C1 [Foulkes, Mary A.] George Washington Univ, Ctr Biostat, Dept Hlth Policy, Rockville, MD 20852 USA.
[Foulkes, Mary A.] George Washington Univ, Ctr Biostat, Dept Epidemiol & Biostat, Rockville, MD 20852 USA.
[Grady, Christine] NIH, Ctr Clin, Dept Bioeth, Bethesda, MD 20892 USA.
[Spong, Catherine Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, Bethesda, MD USA.
[Bates, Angela; Clayton, Janine A.] NIH, Off Res Womens Hlth, Bethesda, MD 20892 USA.
RP Foulkes, MA (reprint author), George Washington Univ, Ctr Biostat, Dept Hlth Policy, 6110 Executive Blvd,Suite 750, Rockville, MD 20852 USA.
EM mfoulkes@bsc.gwu.edu
FU U.S. Public Health Service; NIH Office of Research on Women's Health;
Food and Drug Administration Office of Women's Health; Centers for
Disease Control and Prevention; Health Resources and Services
Administration; Eunice Kennedy Shriver National Institute of Child
Health and Development; National Institute of Allergy and Infectious
Diseases; National Institute of Drug Abuse; NIH Office of AIDS Research;
NIH Office of Behavioral and Social Sciences Research
FX The workshop summarized here was cosponsored by agencies of the U.S.
Public Health Service, including the NIH Office of Research on Women's
Health, the Food and Drug Administration Office of Women's Health, the
Centers for Disease Control and Prevention, the Health Resources and
Services Administration, the Eunice Kennedy Shriver National Institute
of Child Health and Development, the National Institute of Allergy and
Infectious Diseases, the National Institute of Drug Abuse, the NIH
Office of AIDS Research, and the NIH Office of Behavioral and Social
Sciences Research. The authors acknowledge the vision, support, and
encouragement of Dr. Vivian W. Pinn, Director, NIH Office of Research on
Women's Health, without whom this meeting and discussions would not have
occurred. A videocast of this meeting is available at
videocast.nih.gov/summary.asp?Live=9616.
NR 24
TC 8
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U1 0
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT
PY 2011
VL 20
IS 10
BP 1429
EP 1432
DI 10.1089/jwh.2011.3118
PG 4
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 833IQ
UT WOS:000295877900086
PM 21819233
ER
PT J
AU Espeland, MA
Miller, ME
Goveas, JS
Hogan, PE
Coker, LH
Williamson, J
Naughton, M
Resnick, SM
AF Espeland, Mark A.
Miller, Michael E.
Goveas, Joseph S.
Hogan, Patricia E.
Coker, Laura H.
Williamson, Jeff
Naughton, Michelle
Resnick, Susan M.
CA Whisca Study Grp
TI Cognitive Function and Fine Motor Speed in Older Women with Diabetes
Mellitus: Results from the Women's Health Initiative Study of Cognitive
Aging
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID ALZHEIMERS-DISEASE; INSULIN-RESISTANCE; POSTMENOPAUSAL WOMEN;
IMPAIRMENT; DECLINE; MEMORY; COHORT; ADULTS; RISK; HIPPOCAMPUS
AB Background: We sought to determine if type 2 diabetes mellitus (T2DM) was associated with accelerated decline in domain-specific measures of cognitive function and fine motor speed.
Methods: Women aged 65-80 years who were enrolled in a clinical trial of postmenopausal hormone therapy were grouped as having T2DM (n = 179) or not (n = 1984) and followed for an average of 5 years with annual standardized assessments of domain-specific cognitive function. Mean patterns of cognitive measures over time were contrasted between groups using general linear models and Wald tests, with varying levels of covariate adjustment. The influences of age at onset, use of oral medications, and use of insulin were also examined.
Results: T2DM was associated with mean deficits of 0.2-0.4 standard deviations (SD) across follow-up in most cognitive domains. Consistent evidence that rates of decline were accelerated among women with T2DM was evident only for verbal knowledge and verbal memory (p < 0.05). Decrements in fine motor speed, but no measure of cognitive function, were greater for women with earlier onset T2DM. Use of oral diabetes medications was associated with better relative cognitive function.
Conclusions: In these women, T2DM was associated with cognitive deficits in most domains. Relative deficits in verbal knowledge and verbal memory may continue to increase after deficits in other domains have stabilized. Relative deficits in fine motor speed may be greater among women with earlier onsets of T2DM. Use of insulin, which may reflect greater T2DM severity, was associated with relatively greater cognitive deficits.
C1 [Espeland, Mark A.; Miller, Michael E.; Hogan, Patricia E.] Wake Forest Sch Med, Dept Biostat Sci, Winston Salem, NC USA.
[Goveas, Joseph S.] Med Coll Wisconsin, Dept Psychiat & Behav Med, Milwaukee, WI 53226 USA.
[Coker, Laura H.; Naughton, Michelle] Wake Forest Sch Med, Dept Social Sci & Hlth Policy, Winston Salem, NC USA.
[Williamson, Jeff] Wake Forest Sch Med, Dept Internal Med, Winston Salem, NC USA.
[Resnick, Susan M.] NIH, Intramural Res Program, Natl Inst Aging, Baltimore, MD USA.
RP Espeland, MA (reprint author), Wake Forest Hlth Sci, Dept Biostat Sci, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM mespelan@wfubme.edu
FU Department of Health and Human Services; National Institute on Aging
[NO1-AG-1-2106]; National Heart, Lung, and Blood Institute; Wyeth
Pharmaceuticals; Wake Forest University; National Institutes of Health
FX The Women's Health Initiative Study of Cognitive Aging was supported by
the Department of Health and Human Services and the National Institute
on Aging (NO1-AG-1-2106). The Women's Health Initiative program is
funded by the National Heart, Lung, and Blood Institute. Wyeth
Pharmaceuticals provided the study drug and the placebo to the WHI
trial. The Women's Health Initiative Memory Study was funded by Wyeth
Pharmaceuticals, Wake Forest University, and the National Heart, Lung,
and Blood Institute. S. M. R. is supported by the Intramural Research
Program, National Institute on Aging, and National Institutes of Health.
NR 45
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U1 2
U2 9
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT
PY 2011
VL 20
IS 10
BP 1435
EP 1443
DI 10.1089/jwh.2011.2812
PG 9
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 833IQ
UT WOS:000295877900088
PM 21819251
ER
PT J
AU Benard, VB
Saraiya, MS
Soman, A
Roland, KB
Yabroff, KR
Miller, J
AF Benard, Vicki B.
Saraiya, Mona S.
Soman, Ashwini
Roland, Katherine B.
Yabroff, K. Robin
Miller, Jackie
TI Cancer Screening Practices Among Physicians in the National Breast and
Cervical Cancer Early Detection Program
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS; SOCIETY GUIDELINES; UNITED-STATES; MANAGEMENT;
WOMEN; AREAS; PAP
AB Background: The National Breast and Cervical Cancer Early Detection Program (NBCCEDP) provides low-income, uninsured women with screening and diagnostic services for breast and cervical cancer. Our study was conducted to describe the demographic and practice characteristics of participating and nonparticipating physicians, as well as their beliefs, adoption of new screening technologies, and recommendations for breast and cervical cancer screening.
Methods: From a 2006-2007 nationally representative survey, we identified 1,111 practicing primary care physicians who provide breast and cervical cancer screenings and assessed their recommendations using clinical vignettes related to screening initiation, frequency, and cessation. Responses of physicians participating in the NBCCEDP were compared with those from nonparticipating physicians.
Results: Of the physicians surveyed, 15% reported participation in the NBCCEDP, 65% were not participants, and 20% were not sure or did not respond to this question. Program physicians were significantly more likely to practice in multispecialty settings, in a rural location, and in a hospital or clinic setting and had more patients who were female and insured by Medicaid or uninsured compared with nonprogram physicians. Beliefs about the effectiveness of screening tools or procedures in reducing breast or cervical cancer mortality were similar by program participation. Adoption of new technologies, including digital mammography and human papillomavirus (HPV) testing, and making guideline-consistent recommendations for screening initiation, frequency, and cessation did not differ significantly by program participation.
Conclusions: Although there may be differences in physician characteristics and practice settings, the beliefs and screening practices for both breast and cervical cancer are similar between program and nonprogram providers.
C1 [Benard, Vicki B.] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Epidemiol & Appl Res Branch, Atlanta, GA 30341 USA.
[Yabroff, K. Robin] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Benard, VB (reprint author), Ctr Dis Control & Prevent, Div Canc Prevent & Control, Epidemiol & Appl Res Branch, 4770 Buford Highway,Mailstop K-55, Atlanta, GA 30341 USA.
EM vbenard@cdc.gov
OI Yabroff, K. Robin/0000-0003-0644-5572
FU NCI [N02-PC-51308]; CDC [Y3-PC-6017-01]; AHRQ [Y3-PC-5019-01,
Y3-PC-5019-02]
FX Funding for this study was provided by NCI (contract N02-PC-51308), CDC
(interagency agreement Y3-PC-6017-01) and AHRQ (interagency agreements
Y3-PC-5019-01 and Y3-PC-5019-02).
NR 21
TC 12
Z9 12
U1 0
U2 4
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT
PY 2011
VL 20
IS 10
BP 1479
EP 1484
DI 10.1089/jwh.2010.2530
PG 6
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 833IQ
UT WOS:000295877900092
PM 21774673
ER
PT J
AU Clark, C
AF Clark, Cindy
TI The 2011 Guide to Free or Nearly-Free e-Books
SO LEARNED PUBLISHING
LA English
DT Book Review
C1 [Clark, Cindy] Natl Inst Hlth Lib, Off Res Serv, NIH, Bethesda, MD 20892 USA.
RP Clark, C (reprint author), Natl Inst Hlth Lib, Off Res Serv, NIH, Bethesda, MD 20892 USA.
EM clarkc@ors.od.nih.gov
NR 1
TC 0
Z9 0
U1 0
U2 0
PU ASSOC LEARNED PROFESSIONAL SOC PUBL
PI W SUSSEX
PA SOUTH HOUSE, THE STREET WORTHING, W SUSSEX BN13 3UU, ENGLAND
SN 0953-1513
J9 LEARN PUBL
JI Learn. Publ.
PD OCT
PY 2011
VL 24
IS 4
BP 332
EP 334
PG 3
WC Information Science & Library Science
SC Information Science & Library Science
GA 833SU
UT WOS:000295906000013
ER
PT J
AU Clark, C
AF Clark, Cindy
TI E-books in Libraries: A Practical Guide
SO LEARNED PUBLISHING
LA English
DT Book Review
C1 [Clark, Cindy] Natl Inst Hlth Lib, Off Res Serv, NIH, Bethesda, MD 20892 USA.
RP Clark, C (reprint author), Natl Inst Hlth Lib, Off Res Serv, NIH, Bethesda, MD 20892 USA.
EM clarkc@ors.od.nih.gov
NR 1
TC 0
Z9 0
U1 0
U2 0
PU ASSOC LEARNED PROFESSIONAL SOC PUBL
PI W SUSSEX
PA SOUTH HOUSE, THE STREET WORTHING, W SUSSEX BN13 3UU, ENGLAND
SN 0953-1513
J9 LEARN PUBL
JI Learn. Publ.
PD OCT
PY 2011
VL 24
IS 4
BP 332
EP 334
PG 3
WC Information Science & Library Science
SC Information Science & Library Science
GA 833SU
UT WOS:000295906000012
ER
PT J
AU Kirschbaum, MH
Synold, T
Stein, AS
Tuscano, J
Zain, JM
Popplewell, L
Karanes, C
O'Donnell, MR
Pulone, B
Rincon, A
Wright, J
Frankel, P
Forman, SJ
Newman, EM
AF Kirschbaum, M. H.
Synold, T.
Stein, A. S.
Tuscano, J.
Zain, J. M.
Popplewell, L.
Karanes, C.
O'Donnell, M. R.
Pulone, B.
Rincon, A.
Wright, J.
Frankel, P.
Forman, S. J.
Newman, E. M.
TI A phase 1 trial dose-escalation study of tipifarnib on a week-on,
week-off schedule in relapsed, refractory or high-risk myeloid leukemia
SO LEUKEMIA
LA English
DT Article
DE farnesyltransferase; tipifarnib; Zarnestra; AML; acute myelogenous
leukemia; phase 1 trial
ID FARNESYLTRANSFERASE INHIBITOR TIPIFARNIB; ADVANCED CANCER; R115777; RAS
AB Inhibition of farnesyltransferase (FT) activity has been associated with in vitro and in vivo anti-leukemia activity. We report the results of a phase 1 dose-escalation study of tipifarnib, an oral FT inhibitor, in patients with relapsed, refractory or newly diagnosed (if over age 70) acute myelogenous leukemia (AML), on a week-on, week-off schedule. Forty-four patients were enrolled, two patients were newly diagnosed, and the rest were relapsed or refractory to previous treatment, with a median age of 61 (range 33-79). The maximum tolerated dose was determined to be 1200 mg given orally twice daily (b.i.d.) on this schedule. Cycle 1 dose-limiting toxicities were hepatic and renal. There were three complete remissions seen, two at the 1200 mg b.i.d. dose and one at the 1000 mg b.i.d. dose, with minor responses seen at the 1400 mg b.i.d. dose level. Pharmacokinetic studies performed at doses of 1400 mg b. i. d. showed linear behavior with minimal accumulation between days 1-5. Tipifarnib administered on a week-on, week-off schedule shows activity at higher doses, and represents an option for future clinical trials in AML. Leukemia (2011) 25, 1543-1547; doi: 10.1038/leu.2011.124; published online 31 May 2011
C1 [Kirschbaum, M. H.; Stein, A. S.; Zain, J. M.; Popplewell, L.; Karanes, C.; O'Donnell, M. R.; Pulone, B.; Forman, S. J.] City Hope Natl Med Ctr, HCT, Dept Hematol, Duarte, CA USA.
[Synold, T.; Newman, E. M.] City Hope Natl Med Ctr, Dept Mol Pharmacol, Duarte, CA USA.
[Tuscano, J.] Calif State Univ Sacramento, Div Hematol & Oncol, Davis Sch Med, Sacramento, CA 95819 USA.
[Rincon, A.; Frankel, P.] City Hope Natl Med Ctr, Dept Biostat, Duarte, CA USA.
[Wright, J.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Kirschbaum, MH (reprint author), Nevada Canc Inst, Dept Med Oncol, 1 Breakthrough Way, Las Vegas, NV 89135 USA.
EM mkirschb@yahoo.com
FU NCI Cancer Therapy Evaluation Program [U01-CA-62505, N01-CM-62209];
[P30-CA-033572]
FX We thank the City of Hope medical, nursing and administrative staff for
their dedication and support for this study. We also thank Sandra Thomas
for assistance with editing and review of the manuscript. This work was
supported by grant nos. U01-CA-62505 and N01-CM-62209 (NCI Cancer
Therapy Evaluation Program) and P30-CA-033572 (City of Hope).
NR 15
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U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD OCT
PY 2011
VL 25
IS 10
BP 1543
EP 1547
DI 10.1038/leu.2011.124
PG 5
WC Oncology; Hematology
SC Oncology; Hematology
GA 836WG
UT WOS:000296147300003
PM 21625235
ER
PT J
AU Jewett, MW
Jain, S
Linowski, AK
Sarkar, A
Rosa, PA
AF Jewett, Mollie W.
Jain, Sunny
Linowski, Angelika K.
Sarkar, Amit
Rosa, Patricia A.
TI Molecular characterization of the Borrelia burgdorferi in vivo-essential
protein PncA
SO MICROBIOLOGY-SGM
LA English
DT Article
ID LYME-DISEASE SPIROCHETE; LIFE-SPAN EXTENSION; ESCHERICHIA-COLI;
SACCHAROMYCES-CEREVISIAE; NICOTINAMIDASE PNCA; CALORIE RESTRICTION;
INITIATION CODON; INFECTIOUS CYCLE; GENE; IDENTIFICATION
AB The conversion of nicotinamide to nicotinic acid by nicotinamidase enzymes is a critical step in maintaining NAD(+) homeostasis and contributes to numerous important biological processes in diverse organisms. In Borrelia burgdorferi, the nicotinamidase enzyme, PncA, is required for spirochaete survival throughout the infectious cycle. Mammals lack nicotinamidases and therefore PncA may serve as a therapeutic target for Lyme disease. Contrary to the in vivo importance of PncA, the current annotation for the pncA ORF suggests that the encoded protein may be inactive due to the absence of an N-terminal aspartic acid residue that is a conserved member of the catalytic triad of characterized PncA proteins. Herein, we have used genetic and biochemical strategies to determine the N-terminal sequence of B. burgdorferi PncA. Our data demonstrate that the PncA protein is 24 aa longer than the currently annotated sequence and that pncA translation is initiated from the rare, non-canonical initiation codon AUU. These findings are an important first step in understanding the catalytic function of this in vivo-essential protein.
C1 [Jewett, Mollie W.; Sarkar, Amit; Rosa, Patricia A.] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Jewett, Mollie W.; Jain, Sunny; Linowski, Angelika K.] Univ Cent Florida, Coll Med, Burnett Sch Biomed Sci, Orlando, FL 32827 USA.
RP Jewett, MW (reprint author), NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
EM Mollie.Jewett@ucf.edu
FU NIH, NIAID [5K22AI081730]
FX Many thanks to S. J. Norris, University of Texas Health Science Center
at Houston, TX, USA, for giving us the Salmonella strains and to M. K.
Garfield in the Protein Chemistry Section of the Research Technologies
Branch, NIAID, NIH, Rockville, MD, USA, for N-terminal sequence
analysis. Thank you to T. J. Jewett for critical reading of this
manuscript. This research was supported, in part, by NIH, NIAID grant
5K22AI081730 to M. W. J. and the Intramural Research Program of the NIH,
NIAID.
NR 52
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U2 2
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 1350-0872
J9 MICROBIOL-SGM
JI Microbiology-(UK)
PD OCT
PY 2011
VL 157
BP 2831
EP 2840
DI 10.1099/mic.0.051706-0
PN 10
PG 10
WC Microbiology
SC Microbiology
GA 837FU
UT WOS:000296177300009
PM 21778210
ER
PT J
AU Gallin, JI
AF Gallin, John I.
TI The NIH Clinical Center and the future of clinical research
SO NATURE MEDICINE
LA English
DT Article
ID COMBINATION CHEMOTHERAPY; DOUBLE-BLIND; THERAPY; DISEASE; AIDS
C1 NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Gallin, JI (reprint author), NIH, Ctr Clin, Bethesda, MD 20892 USA.
EM jig@nih.gov
NR 24
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U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2011
VL 17
IS 10
BP 1221
EP 1223
DI 10.1038/nm.2466
PG 3
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 835FW
UT WOS:000296022100037
PM 21989014
ER
PT J
AU Bollee, G
Flamant, M
Schordan, S
Fligny, C
Rumpel, E
Milon, M
Schordan, E
Sabaa, N
Vandermeersch, S
Galaup, A
Rodenas, A
Casal, I
Sunnarborg, SW
Salant, DJ
Kopp, JB
Threadgill, DW
Quaggin, SE
Dussaule, JC
Germain, S
Mesnard, L
Endlich, K
Boucheix, C
Belenfant, X
Callard, P
Endlich, N
Tharaux, PL
AF Bollee, Guillaume
Flamant, Martin
Schordan, Sandra
Fligny, Cecile
Rumpel, Elisabeth
Milon, Marine
Schordan, Eric
Sabaa, Nathalie
Vandermeersch, Sophie
Galaup, Ariane
Rodenas, Anita
Casal, Ibrahim
Sunnarborg, Susan W.
Salant, David J.
Kopp, Jeffrey B.
Threadgill, David W.
Quaggin, Susan E.
Dussaule, Jean-Claude
Germain, Stephane
Mesnard, Laurent
Endlich, Karlhans
Boucheix, Claude
Belenfant, Xavier
Callard, Patrice
Endlich, Nicole
Tharaux, Pierre-Louis
TI Epidermal growth factor receptor promotes glomerular injury and renal
failure in rapidly progressive crescentic glomerulonephritis
SO NATURE MEDICINE
LA English
DT Article
ID PARIETAL EPITHELIAL-CELLS; GENE-EXPRESSION; CELLULAR CRESCENTS;
ENDOTHELIAL-CELLS; NEPHROTOXIC SERUM; MEDIATED-IMMUNITY; BOWMANS
CAPSULE; TRANSGENIC MICE; MESANGIAL CELLS; T-LYMPHOCYTES
AB Rapidly progressive glomerulonephritis (RPGN) is a life-threatening clinical syndrome and a morphological manifestation of severe glomerular injury that is marked by a proliferative histological pattern ('crescents') with accumulation of T cells and macrophages and proliferation of intrinsic glomerular cells. We show de novo induction of heparin-binding epidermal growth factor-like growth factor (HB-EGF) in intrinsic glomerular epithelial cells (podocytes) from both mice and humans with RPGN. HB-EGF induction increases phosphorylation of the epidermal growth factor receptor (EGFR, also known as ErbB1) in mice with RPGN. In HB-EGF-deficient mice, EGFR activation in glomeruli is absent and the course of RPGN is improved. Autocrine HB-EGF induces a phenotypic switch in podocytes in vitro. Conditional deletion of the Egfr gene from podocytes of mice alleviates the severity of RPGN. Likewise, pharmacological blockade of EGFR also improves the course of RPGN, even when started 4 d after the induction of experimental RPGN. This suggests that targeting the HB-EGF-EGFR pathway could also be beneficial in treatment of human RPGN.
C1 [Bollee, Guillaume; Fligny, Cecile; Milon, Marine; Tharaux, Pierre-Louis] INSERM, Unite Mixte Rech UMR 970, Paris Cardiovasc Res Ctr, Paris, France.
[Bollee, Guillaume; Fligny, Cecile; Milon, Marine; Tharaux, Pierre-Louis] Univ Paris 05, Paris, France.
[Flamant, Martin; Sabaa, Nathalie] Univ Paris Diderot, Paris, France.
[Flamant, Martin; Sabaa, Nathalie] Hop Bichat Claude Bernard, AP HP, Serv Physiol Explorat Fonct, F-75877 Paris, France.
[Schordan, Sandra; Rumpel, Elisabeth; Schordan, Eric; Endlich, Karlhans; Endlich, Nicole] Univ Med Greifswald, Inst Anat & Zellbiol, Greifswald, Germany.
[Vandermeersch, Sophie; Dussaule, Jean-Claude; Mesnard, Laurent] Hop Tenon, INSERM, UMR702, F-75970 Paris, France.
[Vandermeersch, Sophie; Dussaule, Jean-Claude; Mesnard, Laurent; Callard, Patrice] Sorbonne Univ, Univ Paris 06, Paris, France.
[Galaup, Ariane; Germain, Stephane] INSERM, Ctr Interdisciplinary Res Biol, Ctr Natl Rech Sci, UMR 7241,U1050, Paris, France.
[Galaup, Ariane; Germain, Stephane] Coll France, Chaire Med Expt, F-75231 Paris, France.
[Rodenas, Anita; Callard, Patrice] Hop Tenon, AP HP, Serv Anat & Cytol Pathol, F-75970 Paris, France.
[Casal, Ibrahim; Boucheix, Claude] Hop Paul Brousse, INSERM, UMR 1004, Inst Andre Lwoff, Villejuif, France.
[Casal, Ibrahim; Boucheix, Claude] Univ Paris 11, Villejuif, France.
[Sunnarborg, Susan W.] Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC USA.
[Salant, David J.] Boston Univ, Med Ctr, Renal Sect, Boston, MA USA.
[Kopp, Jeffrey B.] NIDDK, Kidney Dis Sect, Bethesda, MD USA.
[Threadgill, David W.] N Carolina State Univ, Dept Genet, Raleigh, NC 27695 USA.
[Quaggin, Susan E.] Univ Toronto, Mt Sinai Hosp, St Michaels Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
[Dussaule, Jean-Claude] Hop St Antoine, AP HP, Serv Physiol Explorat Fonct, F-75571 Paris, France.
[Belenfant, Xavier] Ctr Hosp Intercommunal Andre Gregoire, Serv Nephrol & Dialyse, Montreuil, France.
[Tharaux, Pierre-Louis] Hop Europeen Georges Pompidou, Assistance Publ Hop Paris, Serv Nephrol, Paris, France.
RP Tharaux, PL (reprint author), INSERM, Unite Mixte Rech UMR 970, Paris Cardiovasc Res Ctr, Paris, France.
EM pierre-louis.tharaux@inserm.fr
RI Endlich, Karlhans/G-5485-2013; Germain, Stephane/E-2301-2016; Tharaux,
Pierre-Louis/A-9155-2009; Threadgill, David/N-4425-2013;
OI Germain, Stephane/0000-0001-5992-1275; Tharaux,
Pierre-Louis/0000-0002-6062-5905; Threadgill, David/0000-0003-3538-1635;
Salant, David/0000-0002-3866-3120; Kopp, Jeffrey/0000-0001-9052-186X
FU INSERM; l'Agence Nationale de la Recherche of France [ANR-08-EBIO-003];
German Federal Ministry of Education and Research (BMBF) [01GN0805,
03IP612]; US National Institutes of Health [CA43793, DK30932]; la
Fondation pour la Recherche Medicale; la Fondation Lefoulon-Delalande
FX This work was supported by INSERM, grant ANR-08-EBIO-003 (P.-L. T.) from
l'Agence Nationale de la Recherche of France, grant 01GN0805 (K.E.) from
the German Federal Ministry of Education and Research (BMBF) and grants
CA43793 (S.W.S.) and DK30932 (D.S.) from the US National Institutes of
Health. We are grateful to la Fondation pour la Recherche Medicale and
la Fondation Lefoulon-Delalande for supporting G.B. and C.F.,
respectively. We thank L.B. Holzman (Perelman School of Medicine,
University of Pennsylvania) for the use of podocin-Cre mice crossed with
Z/EGFP mice. We also thank X. Biolchini, C. Kitou, C. Martin, E. Huc and
the ERI970 team for assistance in animal care and handling, H. Wegner,
R. Maciejewski and T. Felix for technical assistance and J. Peters for
help with fluorescence-activated cell sorting (FACS; supported by
InnoProfile grant 03IP612 of the BMBF). We acknowledge administrative
support from M.-C. Poeuf, V. Oberweiss, A. De Rueda, M. Autran and P.
Coudol.
NR 56
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2011
VL 17
IS 10
BP 1242
EP U272
DI 10.1038/nm.2491
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 835FW
UT WOS:000296022100042
PM 21946538
ER
PT J
AU Chang, SH
Wang, RH
Akagi, K
Kim, KA
Martin, BK
Cavallone, L
Haines, DC
Basik, M
Mai, P
Poggi, E
Isaacs, C
Looi, LM
Mun, KS
Greene, MH
Byers, SW
Teo, SH
Deng, CX
Sharan, SK
AF Chang, Suhwan
Wang, Rui-Hong
Akagi, Keiko
Kim, Kyung-Ae
Martin, Betty K.
Cavallone, Luca
Haines, Diana C.
Basik, Mark
Mai, Phuong
Poggi, Elizabeth
Isaacs, Claudine
Looi, Lai M.
Mun, Kein S.
Greene, Mark H.
Byers, Stephen W.
Teo, Soo H.
Deng, Chu-Xia
Sharan, Shyam K.
CA Kathleen Cuningham Fdn Consortium
TI Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155
SO NATURE MEDICINE
LA English
DT Article
ID CELL-CYCLE CHECKPOINT; DNA-DAMAGE RESPONSE; BREAST-CANCER; LIGASE
ACTIVITY; HIGH EXPRESSION; STEM-CELLS; IN-VIVO; C-MYC; PROTEIN; GENE
AB BRCA1, a well-known tumor suppressor with multiple interacting partners, is predicted to have diverse biological functions. However, so far its only well-established role is in the repair of damaged DNA and cell cycle regulation. In this regard, the etiopathological study of low-penetrant variants of BRCA1 provides an opportunity to uncover its other physiologically important functions. Using this rationale, we studied the R1699Q variant of BRCA1, a potentially moderate-risk variant, and found that it does not impair DNA damage repair but abrogates the repression of microRNA-155 (miR-155), a bona fide oncomir. Mechanistically, we found that BRCA1 epigenetically represses miR-155 expression via its association with HDAC2, which deacetylates histones H2A and H3 on the miR-155 promoter. We show that overexpression of miR-155 accelerates but the knockdown of miR-155 attenuates the growth of tumor cell lines in vivo. Our findings demonstrate a new mode of tumor suppression by BRCA1 and suggest that miR-155 is a potential therapeutic target for BRCA1-deficient tumors.
C1 [Sharan, Shyam K.; Kathleen Cuningham Fdn Consortium] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
[Chang, Suhwan; Kim, Kyung-Ae] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21701 USA.
[Wang, Rui-Hong; Deng, Chu-Xia] NIDDK, Genet Dev & Dis Branch, Bethesda, MD USA.
[Akagi, Keiko] Ohio State Univ, Human Canc Genet Program, Dept Mol Virol, Columbus, OH 43210 USA.
[Akagi, Keiko] Ohio State Univ, Human Canc Genet Program, Dept Immunol, Columbus, OH 43210 USA.
[Akagi, Keiko] Ohio State Univ, Human Canc Genet Program, Dept Med Genet, Columbus, OH 43210 USA.
[Martin, Betty K.] NCI, Sci Applicat Int Corp SAIC Frederick, Frederick, MD 21701 USA.
[Cavallone, Luca; Basik, Mark] McGill Univ, Jewish Gen Hosp, Lady Davis Inst, Montreal, PQ H3T 1E2, Canada.
[Cavallone, Luca] McGill Univ, Dept Oncol, Program Canc Genet, Montreal, PQ, Canada.
[Cavallone, Luca] McGill Univ, Dept Human Genet, Program Canc Genet, Montreal, PQ, Canada.
[Haines, Diana C.] NCI, Pathol Histotechnol Lab, SAIC Frederick, Frederick, MD 21701 USA.
[Mai, Phuong; Greene, Mark H.] NCI, Clin Genet Branch, Rockville, MD USA.
[Poggi, Elizabeth; Isaacs, Claudine; Byers, Stephen W.] Georgetown Univ, Georgetown Lombardi Comprehens Canc Ctr, Washington, DC USA.
[Looi, Lai M.; Mun, Kein S.] Univ Malaya, Dept Pathol, Med Ctr, Kuala Lumpur, Malaysia.
[Teo, Soo H.] Univ Malaya, Med Ctr, Dept Surg, Univ Malaya Canc Res Inst, Kuala Lumpur, Malaysia.
[Teo, Soo H.] Sime Darby Med Ctr, Canc Res Initiat Fdn, Kuala Lumpur, Malaysia.
RP Sharan, SK (reprint author), Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
EM sharans@mail.nih.gov
RI Mun, Kein Seong/E-4155-2010; Looi, Lai Meng/A-3382-2009; Teo,
Soo-hwang/H-2353-2014; deng, chuxia/N-6713-2016
OI Looi, Lai Meng/0000-0001-8325-0117;
FU Center for Cancer Research, US National Cancer Institute; US National
Institutes of Health
FX We thank J. Acharya, K. Biswas, R. Chittela, I. Daar, K. Reilly and A.
Spurdle for helpful discussions and critical review of the manuscript.
We also thank D. M. Livingston (Dana-Farber Cancer Institute) and D. L.
Turner (University of Michigan) for providing DNA constructs; D. Swing
for help with BAC transgenic mice and allograft experiment; W. D.
Foulkes, A. Spurdle, H. Thorne, Y.C. Har, P.S. Yee, A. Saleh, the
Georgetown-Lombardi Comprehensive Cancer Center, Familial Cancer and
Histopathology and Tissue Share Resources, who helped with the human
tumor samples; S. Burkett for cytogenetic analysis; C. H. Kim for
microarray analysis, and A. Kane and R. Frederickson for illustrations.
The research was sponsored by the Center for Cancer Research, US
National Cancer Institute and US National Institutes of Health.
NR 46
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PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2011
VL 17
IS 10
BP 1275
EP U308
DI 10.1038/nm.2459
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 835FW
UT WOS:000296022100046
PM 21946536
ER
PT J
AU Gattinoni, L
Lugli, E
Ji, Y
Pos, Z
Paulos, CM
Quigley, MF
Almeida, JR
Gostick, E
Yu, ZY
Carpenito, C
Wang, E
Douek, DC
Price, DA
June, CH
Marincola, FM
Roederer, M
Restifo, NP
AF Gattinoni, Luca
Lugli, Enrico
Ji, Yun
Pos, Zoltan
Paulos, Chrystal M.
Quigley, Maire F.
Almeida, Jorge R.
Gostick, Emma
Yu, Zhiya
Carpenito, Carmine
Wang, Ena
Douek, Daniel C.
Price, David A.
June, Carl H.
Marincola, Francesco M.
Roederer, Mario
Restifo, Nicholas P.
TI A human memory T cell subset with stem cell-like properties
SO NATURE MEDICINE
LA English
DT Article
ID SUPERIOR ANTITUMOR IMMUNITY; TRANSCRIPTION FACTOR; ADOPTIVE
IMMUNOTHERAPY; BETA-CATENIN; NAIVE RATHER; CANCER; DIFFERENTIATION;
LYMPHOCYTE; EXPRESSION; PHENOTYPE
AB Immunological memory is thought to depend on a stem cell-like, self-renewing population of lymphocytes capable of differentiating into effector cells in response to antigen re-exposure. Here we describe a long-lived human memory T cell population that has an enhanced capacity for self-renewal and a multipotent ability to derive central memory, effector memory and effector T cells. These cells, specific to multiple viral and self-tumor antigens, were found within a CD45RO(-), CCR7(+), CD45RA(+), CD62L(+), CD27(+), CD28(+) and IL-7R alpha(+) T cell compartment characteristic of naive T cells. However, they expressed large amounts of CD95, IL-2R beta, CXCR3, and LFA-1, and showed numerous functional attributes distinctive of memory cells. Compared with known memory populations, these lymphocytes had increased proliferative capacity and more efficiently reconstituted immunodeficient hosts, and they mediated superior antitumor responses in a humanized mouse model. The identification of a human stem cell-like memory T cell population is of direct relevance to the design of vaccines and T cell therapies.
C1 [Gattinoni, Luca; Ji, Yun; Yu, Zhiya; Restifo, Nicholas P.] NCI, Ctr Canc Res, US Natl Inst Hlth NIH, Bethesda, MD 20892 USA.
[Lugli, Enrico; Roederer, Mario] NIAID, ImmunoTechnol Sect, Vaccine Res Ctr, US Natl Inst Hlth, Bethesda, MD 20892 USA.
[Pos, Zoltan; Wang, Ena; Marincola, Francesco M.] US Natl Inst Hlth, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD USA.
[Pos, Zoltan; Wang, Ena; Marincola, Francesco M.] US Natl Inst Hlth, Ctr Human Immunol, Bethesda, MD USA.
[Paulos, Chrystal M.; Carpenito, Carmine; June, Carl H.] Univ Penn, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
[Paulos, Chrystal M.; Carpenito, Carmine; June, Carl H.] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
[Quigley, Maire F.; Gostick, Emma; Price, David A.] Cardiff Univ, Sch Med, Dept Infect Immun & Biochem, Cardiff, S Glam, Wales.
[Quigley, Maire F.; Almeida, Jorge R.; Douek, Daniel C.; Price, David A.] NIAID, Human Immunol Sect, Vaccine Res Ctr, US Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Gattinoni, L (reprint author), NCI, Ctr Canc Res, US Natl Inst Hlth NIH, Bethesda, MD 20892 USA.
EM gattinol@mail.nih.gov; restifo@nih.gov
RI Gattinoni, Luca/A-2281-2008; Ji, Yun/B-7245-2009; Restifo,
Nicholas/A-5713-2008; Pos, Zoltan/C-3623-2014; Price, David/C-7876-2013;
OI Gattinoni, Luca/0000-0003-2239-3282; Restifo, Nicholas
P./0000-0003-4229-4580; Ji, Yun/0000-0001-6340-7009; Pos,
Zoltan/0000-0002-2574-7616; Price, David/0000-0001-9416-2737; Ramos de
Almeida, Jorge/0000-0002-5009-8478
FU US National Institutes of Health, National Cancer Institute, Center for
Cancer Research; National Institute of Allergy and Infectious Diseases
FX This research was supported by the Intramural Research Programs of the
US National Institutes of Health, National Cancer Institute, Center for
Cancer Research and National Institute of Allergy and Infectious
Diseases. We thank S.A. Rosenberg and J.R. Wunderlich for providing
samples from HLA-A*0201 patients with melanoma; P. Scheinberg for
providing HLA-A*0201 samples; M. Sabatino for coordinating phereses;
B.J. Hill for assistance with the TREC assay; S. P. Perfetto, R. Nguyen,
D. A. Ambrozak, A. Mixon and S. Farid for help with cell sorting; P. K.
Chattopadhyay and J. Yu for antibody conjugation; and R. A. Seder and C.
A. Klebanoff for critical review of the manuscript.
NR 56
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U1 3
U2 47
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2011
VL 17
IS 10
BP 1290
EP U325
DI 10.1038/nm.2446
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 835FW
UT WOS:000296022100048
PM 21926977
ER
PT J
AU Diouf, B
Cheng, Q
Krynetskaia, NF
Yang, WJ
Cheok, M
Pei, DQ
Fan, YP
Cheng, C
Krynetskiy, EY
Geng, H
Chen, SY
Thierfelder, WE
Mullighan, CG
Downing, JR
Hsieh, P
Pui, CH
Relling, MV
Evans, WE
AF Diouf, Barthelemy
Cheng, Qing
Krynetskaia, Natalia F.
Yang, Wenjian
Cheok, Meyling
Pei, Deqing
Fan, Yiping
Cheng, Cheng
Krynetskiy, Evgeny Y.
Geng, Hui
Chen, Siying
Thierfelder, William E.
Mullighan, Charles G.
Downing, James R.
Hsieh, Peggy
Pui, Ching-Hon
Relling, Mary V.
Evans, William E.
TI Somatic deletions of genes regulating MSH2 protein stability cause DNA
mismatch repair deficiency and drug resistance in human leukemia cells
SO NATURE MEDICINE
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; COLORECTAL-CANCER; HMUTS-ALPHA;
EXPRESSION; MECHANISMS; DISEASE; BINDING; GROWTH; ADULT; TSC1
AB DNA mismatch repair enzymes (for example, MSH2) maintain genomic integrity, and their deficiency predisposes to several human cancers and to drug resistance. We found that leukemia cells from a substantial proportion of children (similar to 11%) with newly diagnosed acute lymphoblastic leukemia have low or undetectable MSH2 protein levels, despite abundant wild-type MSH2 mRNA. Leukemia cells with low levels of MSH2 contained partial or complete somatic deletions of one to four genes that regulate MSH2 degradation (FRAP1 (also known as MTOR), HERC1, PRKCZ and PIK3C2B); we also found these deletions in individuals with adult acute lymphoblastic leukemia (16%) and sporadic colorectal cancer (13.5%). Knockdown of these genes in human leukemia cells recapitulated the MSH2 protein deficiency by enhancing MSH2 degradation, leading to substantial reduction in DNA mismatch repair and increased resistance to thiopurines. These findings reveal a previously unrecognized mechanism whereby somatic deletions of genes regulating MSH2 degradation result in undetectable levels of MSH2 protein in leukemia cells, DNA mismatch repair deficiency and drug resistance.
C1 [Diouf, Barthelemy; Cheng, Qing; Krynetskaia, Natalia F.; Yang, Wenjian; Cheok, Meyling; Pei, Deqing; Cheng, Cheng; Krynetskiy, Evgeny Y.; Thierfelder, William E.; Mullighan, Charles G.; Downing, James R.; Pui, Ching-Hon; Relling, Mary V.; Evans, William E.] St Jude Childrens Hosp, Hematol Malignancies Program, Memphis, TN 38105 USA.
[Diouf, Barthelemy; Cheng, Qing; Krynetskaia, Natalia F.; Yang, Wenjian; Cheok, Meyling; Krynetskiy, Evgeny Y.; Thierfelder, William E.; Relling, Mary V.; Evans, William E.] St Jude Childrens Hosp, Dept Pharmaceut Sci, Memphis, TN 38105 USA.
[Pei, Deqing; Cheng, Cheng] St Jude Childrens Hosp, Dept Biostat, Memphis, TN 38105 USA.
[Fan, Yiping] St Jude Childrens Hosp, Hartwell Ctr Bioinformat & Biotechnol, Memphis, TN 38105 USA.
[Geng, Hui; Chen, Siying; Hsieh, Peggy] NIDDK, Genet & Biochem Branch, US Natl Inst Hlth NIH, Bethesda, MD USA.
[Mullighan, Charles G.; Downing, James R.; Pui, Ching-Hon] St Jude Childrens Hosp, Dept Pathol, Memphis, TN 38105 USA.
[Pui, Ching-Hon] St Jude Childrens Hosp, Dept Oncol, Memphis, TN 38105 USA.
RP Evans, WE (reprint author), St Jude Childrens Hosp, Hematol Malignancies Program, 332 N Lauderdale St, Memphis, TN 38105 USA.
EM william.evans@stjude.org
RI Cheok, Meyling/C-3822-2014;
OI Cheok, Meyling/0000-0002-7820-8026; Mullighan,
Charles/0000-0002-1871-1850
FU NIH National Institute of General Medical Sciences [U01 GM92666];
National Cancer Institute [CA 21765]; American Lebanese Syrian
Associated Charities (ALSAC); National Institute of Diabetes and
Digestive and Kidney Diseases of the NIH; [R37 CA36401]
FX We gratefully acknowledge the subjects and parents who participated in
this study and the outstanding technical support of the Hartwell Center
for Bioinformatics and Biotechnology at St. Jude Children's Research
Hospital. We also thank Y. Wang, T. Brooks, J. Smith, W. Du, S.
Mukatira, Y. Chu, M. Needham, P. Hargrove, G. Stocco and S. Paugh for
their advice and technical support; J. Groff for preparation of the
figures; K. Crews, N. Kornegay and M. Wilkinson for their research
database expertise; J. C. Panetta for his modeling expertise; J. Jenkins
for his immunohistochemistry expertise; T. Kunkel and A. B. Clark
(National Institute of Environmental Health Sciences) for providing the
E. coli strains, the wild-type and mutant M13mp2 phage and for their
contributions to our MMR experiments; and J. Luis Rosa (Universitat de
Barcelona) for providing us with antibodies to HERC1. We thank M. Kastan
and D. Green for their critical review and advice. This work was
supported in part by grant R37 CA36401 (W. E. E. and M. V. R.), NIH
National Institute of General Medical Sciences Pharmacogenomics Research
Network grant U01 GM92666 (M. V. R. and W. E. E.), CGM is a Pew Scholar
and a St. Baldrick's scholar, and St. Jude is supported by a Cancer
Center Support Grant CA 21765 from the National Cancer Institute and by
the American Lebanese Syrian Associated Charities (ALSAC). H. G., S. C.
and P. H. were funded by the Intramural Research Program of the National
Institute of Diabetes and Digestive and Kidney Diseases of the NIH.
NR 36
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PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD OCT
PY 2011
VL 17
IS 10
BP 1298
EP U332
DI 10.1038/nm.2430
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 835FW
UT WOS:000296022100049
PM 21946537
ER
PT J
AU Grunwald, L
Newcomb, CW
Daniel, E
Kacmaz, RO
Jabs, DA
Levy-Clarke, GA
Nussenblatt, RB
Rosenbaum, JT
Suhler, EB
Thorne, JE
Foster, CS
Kempen, JH
AF Grunwald, Lili
Newcomb, Craig W.
Daniel, Ebenezer
Kacmaz, R. Oktay
Jabs, Douglas A.
Levy-Clarke, Grace A.
Nussenblatt, Robert B.
Rosenbaum, James T.
Suhler, Eric B.
Thorne, Jennifer E.
Foster, C. Stephen
Kempen, John H.
CA Syst Immunosuppressive Therapy Eye
TI Risk of Relapse in Primary Acute Anterior Uveitis
SO OPHTHALMOLOGY
LA English
DT Article
ID OCULAR INFLAMMATION; CLINICAL-FEATURES; HLA-B27 UVEITIS; DISEASES;
OUTCOMES
AB Purpose: To evaluate the risk of and risk factors for a second episode (relapse) among patients with remitted primary anterior uveitis.
Design: Retrospective cohort study.
Participants: Patients with primary anterior uveitis presenting to 1 of 4 academic ocular inflammation subspecialty practices achieving remission of the primary episode within 90 days of initial uveitis diagnosis.
Methods: Data were obtained by standardized chart review.
Main Outcome Measures: Time to relapse of anterior uveitis and risk factors for relapse.
Results: We included 102 patients with a first episode of anterior uveitis who were seen within 90 days of first-ever uveitis onset and followed for 165 person-years after achieving remission of the initial episode. Most patients were female (60%) and white (78%). Forty patients had a recurrence of anterior uveitis. The incidence of relapse was 24% per person-year (95% confidence interval [CI], 17%-33%). At 1.5 years after remission, 61% (95% CI, 48%-71%) were still in remission. Younger adults had significantly higher relapse risk than middle-aged adults (hazard ratio [18-to 35-year-old persons vs. 35-to 55-year-old persons], 2.7; 95% CI, 1.3-6.0).
Conclusions: Our results suggest that many patients with remitted primary anterior uveitis presenting for tertiary uveitis care will relapse. Age in the young adult range was associated with higher risk of relapse. Given the high relapse risk, management of patients with primary anterior uveitis should include an explicit plan for detecting and managing relapses.
Financial Disclosure(s): Proprietary or commercial disclosure may be found after the references. Ophthalmology 2011;118: 1911-1915 (C) 2011 by the American Academy of Ophthalmology.
C1 [Kempen, John H.] Univ Penn, Dept Ophthalmol, Ctr Prevent Ophthalmol & Biostat, Philadelphia, PA 19104 USA.
[Newcomb, Craig W.; Kempen, John H.] Univ Penn, Univ Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Newcomb, Craig W.; Kempen, John H.] Univ Penn, Dept Biostat & Epidemiol & Ophthalmol, Philadelphia, PA 19104 USA.
[Kacmaz, R. Oktay; Foster, C. Stephen] Massachusetts Eye Res & Surg Inst, Cambridge, MA USA.
[Kacmaz, R. Oktay; Jabs, Douglas A.] Mt Sinai Sch Med, Dept Ophthalmol, New York, NY USA.
[Jabs, Douglas A.; Thorne, Jennifer E.] Johns Hopkins Univ, Dept Ophthalmol, Baltimore, MD USA.
[Jabs, Douglas A.; Thorne, Jennifer E.] Johns Hopkins Univ, Dept & Epidemiol, Baltimore, MD USA.
[Levy-Clarke, Grace A.] St Lukes Cataract & Laser Inst, Tarpon Springs, FL USA.
[Levy-Clarke, Grace A.; Nussenblatt, Robert B.] NEI, Immunol Lab, Bethesda, MD USA.
[Rosenbaum, James T.; Suhler, Eric B.] Oregon Hlth & Sci Univ, Dept Ophthalmol, Portland, OR 97201 USA.
[Rosenbaum, James T.] Oregon Hlth & Sci Univ, Dept Med, Portland, OR 97201 USA.
[Suhler, Eric B.] Portland VA Med Ctr, Portland, OR USA.
[Foster, C. Stephen] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA.
RP Kempen, JH (reprint author), Univ Penn, Dept Ophthalmol, Ctr Prevent Ophthalmol & Biostat, 3535 Market St,Suite 700, Philadelphia, PA 19104 USA.
EM john.kempen@uphs.upenn.edu
OI Daniel, Ebenezer/0000-0002-2027-2316
FU National Eye Institute [EY014943]; National Eye Institute; Department of
Veterans' Affairs
FX Supported primarily by National Eye Institute Grant EY014943 (Dr.
Kempen). Additional support was provided by Research to Prevent
Blindness and the Paul and Evanina Mackall Foundation. During part of
the conduct of this project, Dr Kempen was an RPB James S. Adams Special
Scholar Award recipient, Dr. Thorne was an RPB Harrington Special
Scholar Award recipient, and Drs. Jabs and Rosenbaum were Research to
Prevent Blindness Senior Scientific Investigator Award recipients. Dr.
Levy-Clarke was previously supported by and Dr. Nussenblatt continues to
be supported by intramural funds of the National Eye Institute. Dr.
Suhler receives support from the Department of Veterans' Affairs.
NR 23
TC 6
Z9 6
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0161-6420
J9 OPHTHALMOLOGY
JI Ophthalmology
PD OCT
PY 2011
VL 118
IS 10
BP 1911
EP 1915
DI 10.1016/j.ophtha.2011.02.044
PG 5
WC Ophthalmology
SC Ophthalmology
GA 835WG
UT WOS:000296066900004
PM 21680024
ER
PT J
AU Whiteman, DC
Pavan, WJ
Bastian, BC
AF Whiteman, David C.
Pavan, William J.
Bastian, Boris C.
TI The melanomas: a synthesis of epidemiological, clinical,
histopathological, genetic, and biological aspects, supporting distinct
subtypes, causal pathways, and cells of origin
SO PIGMENT CELL & MELANOMA RESEARCH
LA English
DT Review
DE Melanoma; melanocytes; risk factors; gene mutation; pathology
ID CUTANEOUS MALIGNANT-MELANOMA; SITE-SPECIFIC RISK; GENOME-WIDE
ASSOCIATION; MELANOCYTIC NEVI; SUN EXPOSURE; NEURAL CREST; BRAF
MUTATIONS; HUMAN-SKIN; UVEAL MELANOMA; EPIDERMAL MELANOCYTES
AB Converging lines of evidence from varied scientific disciplines suggest that cutaneous melanomas comprise biologically distinct subtypes that arise through multiple causal pathways. Understanding the respective relationships of each subtype with etiologic factors such as UV radiation and constitutional factors is the first necessary step toward developing refined prevention strategies for the specific forms of melanoma. Furthermore, classifying this disease precisely into biologically distinct subtypes is the key to developing mechanism-based treatments, as highlighted by recent discoveries. In this review, we outline the historical developments that underpin our understanding of melanoma heterogeneity, and we do this from the perspectives of clinical presentation, histopathology, epidemiology, molecular genetics, and developmental biology. We integrate the evidence from these separate trajectories to catalog the emerging major categories of melanomas and conclude with important unanswered questions relating to the development of melanoma and its cells of origin.
C1 [Whiteman, David C.] Queensland Inst Med Res, Canc Control Grp, Brisbane, Qld 4006, Australia.
[Pavan, William J.] NHGRI, Mouse Embryol Sect, Genet Dis Res Branch, Bethesda, MD 20892 USA.
[Bastian, Boris C.] Mem Sloan Kettering Canc Ctr, Dept Pathol & Member, Human Oncol & Pathogenesis Program, New York, NY 10021 USA.
RP Whiteman, DC (reprint author), Queensland Inst Med Res, Canc Control Grp, Brisbane, Qld 4006, Australia.
EM david.whiteman@qimr.edu.au; BastianB@mskcc.org
RI Whiteman, David/P-2728-2014
OI Whiteman, David/0000-0003-2563-9559
FU Australian Research Council; National Human Genome Research Institute;
National Cancer Institute [CA025874, CA142873, CA131524]
FX David C. Whiteman is supported by a Future Fellowship from the
Australian Research Council. William J. Pavan is supported by the
National Human Genome Research Institute's Intramural Research Program.
Boris C. Bastian is supported by grants from the National Cancer
Institute (CA025874, CA142873, CA131524).
NR 154
TC 92
Z9 94
U1 2
U2 27
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1755-1471
J9 PIGM CELL MELANOMA R
JI Pigment Cell Melanoma Res.
PD OCT
PY 2011
VL 24
IS 5
BP 879
EP 897
DI 10.1111/j.1755-148X.2011.00880.x
PG 19
WC Oncology; Cell Biology; Dermatology
SC Oncology; Cell Biology; Dermatology
GA 835SZ
UT WOS:000296057600005
PM 21707960
ER
PT J
AU Tock, CL
Turner, LR
Altiner, A
Batra, P
Booher, SL
Coelho, SG
Warner, JA
Therrien, JP
Turner, ML
Miller, SA
Beer, JZ
Kraemer, KH
Udey, MC
Vogel, JC
Terunuma, A
AF Tock, Christine L.
Turner, Lexa R.
Altiner, Ahmet
Batra, Priya
Booher, Susan L.
Coelho, Sergio G.
Warner, Jennifer A.
Therrien, Jean-Philippe
Turner, Maria L.
Miller, Sharon A.
Beer, Janusz Z.
Kraemer, Kenneth H.
Udey, Mark C.
Vogel, Jonathan C.
Terunuma, Atsushi
TI Transcriptional signatures of full-spectrum and non-UVB-spectrum solar
irradiation in human skin
SO PIGMENT CELL & MELANOMA RESEARCH
LA English
DT Letter
ID SUNSCREENS; PROTECTION
C1 [Tock, Christine L.; Turner, Lexa R.; Altiner, Ahmet; Batra, Priya; Booher, Susan L.; Warner, Jennifer A.; Therrien, Jean-Philippe; Turner, Maria L.; Kraemer, Kenneth H.; Udey, Mark C.; Vogel, Jonathan C.; Terunuma, Atsushi] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Coelho, Sergio G.; Miller, Sharon A.; Beer, Janusz Z.] US FDA, Ctr Devices & Radiol Hlth, Rockville, MD 20857 USA.
RP Terunuma, A (reprint author), NCI, Dermatol Branch, Ctr Canc Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM atsushi@mail.nih.gov
FU Intramural NIH HHS [ZIA BC004517-35]
NR 5
TC 2
Z9 2
U1 1
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1755-1471
J9 PIGM CELL MELANOMA R
JI Pigment Cell Melanoma Res.
PD OCT
PY 2011
VL 24
IS 5
BP 972
EP 974
DI 10.1111/j.1755-148X.2011.00899.x
PG 3
WC Oncology; Cell Biology; Dermatology
SC Oncology; Cell Biology; Dermatology
GA 835SZ
UT WOS:000296057600013
PM 21848663
ER
PT J
AU Terracciano, A
Lobina, M
Piras, MG
Mulas, A
Cannas, A
Meirelles, O
Sutin, AR
Zonderman, AB
Uda, M
Crisponi, L
Schlessinger, D
AF Terracciano, Antonio
Lobina, Monia
Piras, Maria Grazia
Mulas, Antonella
Cannas, Alessandra
Meirelles, Osorio
Sutin, Angelina R.
Zonderman, Alan B.
Uda, Manuela
Crisponi, Laura
Schlessinger, David
TI Neuroticism, Depressive Symptoms, and Serum BDNF
SO PSYCHOSOMATIC MEDICINE
LA English
DT Article
DE neuroticism; depression; brain-derived neurotrophic factor; serum;
plasma
ID NEUROTROPHIC FACTOR BDNF; POPULATION-BASED TWIN; PERSONALITY-TRAITS;
MAJOR DEPRESSION; BEHAVIORAL-MODELS; HUMAN PLATELETS; BRAIN; PLASMA;
AGE; STRESS
AB Objective: Animal models and clinical studies suggest that brain-derived neurotrophic factor (BDNF) is involved in the pathophysiology of depression. We test whether serum and plasma levels of BDNF are associated with trait neuroticism and its facets and with state measures of depressive symptoms. Methods: In a community-based cohort (N = 2099), we measured serum and plasma BDNF concentrations and administered the Revised NEO Personality Inventory and the Center for Epidemiological Studies Depression Scale. Covariates included age, sex, cigarette smoking, obesity, and antidepressant use. Results: Serum BDNF concentrations were inversely related to neuroticism (r = -0.074, p < .001), in particular the depression facet (r = -0.08, p < .001). Lower BDNF concentrations were also associated with severe depressive symptoms (Center for Epidemiological Studies Depression Scale >= 28; odds ratio - 0.906; 95% confidence interval - 0.851-0.965). The association of serum BDNF with neuroticism was independent of depressive symptoms, indicating that serum BDNF might represent a biological correlate of neuroticism and not just of transient depressive states. Plasma BDNF was not associated with measures of depression. Conclusions: Our study suggests that lower serum BDNF is associated with both a dispositional vulnerability to depression and acute depressive states in the general population.
C1 [Terracciano, Antonio; Meirelles, Osorio; Sutin, Angelina R.; Zonderman, Alan B.; Schlessinger, David] NIA, NIH, US Dept HHS, Baltimore, MD 21224 USA.
[Lobina, Monia; Piras, Maria Grazia; Mulas, Antonella; Cannas, Alessandra; Uda, Manuela; Crisponi, Laura] CNR, Ist Ric Genet & Biomed, Cagliari, Italy.
RP Terracciano, A (reprint author), NIA, NIH, US Dept HHS, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM Terraccianoa@mail.nih.gov
RI terracciano, antonio/B-1884-2008;
OI Mulas, Antonella/0000-0002-6856-1483; Lobina, Monia/0000-0003-3620-3160;
piras, maria grazia/0000-0001-9004-0900; Zonderman, Alan
B/0000-0002-6523-4778
FU National Institutes of Health, National Institute on Aging
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Institute on Aging.
NR 41
TC 24
Z9 24
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0033-3174
J9 PSYCHOSOM MED
JI Psychosom. Med.
PD OCT
PY 2011
VL 73
IS 8
BP 638
EP 642
DI 10.1097/PSY.0b013e3182306a4f
PG 5
WC Psychiatry; Psychology; Psychology, Multidisciplinary
SC Psychiatry; Psychology
GA 835QP
UT WOS:000296051200001
PM 21949427
ER
PT J
AU Pietrzak, RH
Goldstein, RB
Southwick, SM
Grant, BF
AF Pietrzak, Robert H.
Goldstein, Rise B.
Southwick, Steven M.
Grant, Bridget F.
TI Medical Comorbidity of Full and Partial Posttraumatic Stress Disorder in
US Adults: Results From Wave 2 of the National Epidemiologic Survey on
Alcohol and Related Conditions
SO PSYCHOSOMATIC MEDICINE
LA English
DT Article
DE comorbidity; epidemiology; posttraumatic stress disorder; medical
illness; cardiovascular
ID BORDERLINE PERSONALITY-DISORDER; PSYCHIATRIC DIAGNOSTIC MODULES;
INTERVIEW SCHEDULE AUDADIS; GENERAL-POPULATION SAMPLE;
CORONARY-HEART-DISEASE; DSM-IV ALCOHOL; UNITED-STATES; PRIMARY-CARE;
CARDIOVASCULAR-DISEASE; REENGINEERING SYSTEMS
AB Objective: This study examined associations between lifetime trauma exposures, PTSD and partial PTSD, and past-year medical conditions in a nationally representative sample of US adults. Methods: Face-to-face interviews were conducted with 34,653 participants in the Wave 2 National Epidemiologic Survey on Alcohol and Related Conditions. Logistic regression analyses evaluated associations of trauma exposure, PTSD, and partial PTSD with respondent-reported medical diagnoses. Results: After adjustment for sociodemographic characteristics and comorbid Axis I and II disorders, respondents with full PTSD were more likely than traumatized respondents without full or partial PTSD (comparison group) to report diagnoses of diabetes mellitus, noncirrhotic liver disease, angina pectoris, tachycardia, hypercholesterolemia, other heart disease, stomach ulcer, human immunodeficiency virus seropositivity, gastritis, and arthritis (odds ratios [ORs] = 1.2-2.5). Respondents with partial PTSD were more likely than the comparison group to report past-year diagnoses of stomach ulcer, angina pectoris, tachycardia, and arthritis (ORs = 1.3-1.6). Men with full and partial PTSD were more likely than controls to report diagnoses of hypertension (both ORs = 1.6), and both men and women with PTSD (OR = 1.8 and OR = 1.6, respectively) and men with partial PTSD (OR = 2.0) were more likely to report gastritis. The total number of lifetime traumatic event types was associated with many assessed medical conditions (ORs = 1.04-1.16), reducing the magnitudes and rendering some of the associations between PTSD status and medical conditions nonsignificant. Conclusions: Greater lifetime trauma exposure and PTSD are associated with numerous medical conditions, many of which are stress-related and chronic, in US adults. Partial PTSD is associated with intermediate odds of some of these conditions.
C1 [Pietrzak, Robert H.; Southwick, Steven M.] VA Connecticut Healthcare Syst, Natl Ctr Posttraumat Stress Disorder, West Haven, CT 06516 USA.
[Pietrzak, Robert H.; Southwick, Steven M.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Goldstein, Rise B.; Grant, Bridget F.] NIAAA, Lab Epidemiol & Biometry, Div Intramural Clin & Biol Res, NIH, Bethesda, MD USA.
RP Pietrzak, RH (reprint author), VA Connecticut Healthcare Syst, Natl Ctr Posttraumat Stress Disorder, 950 Campbell Ave 151-E, West Haven, CT 06516 USA.
EM robert.pietrzak@yale.edu
OI Goldstein, Rise/0000-0002-9603-9473
FU National Institute on Alcohol Abuse and Alcoholism; National Institute
on Drug Abuse; National Institutes of Health, National Institute on
Alcohol Abuse and Alcoholism; National Center for Posttraumatic Stress
Disorder; CogState, Inc
FX The National Epidemiologic Survey on Alcohol and Related Conditions is
funded by the National Institute on Alcohol Abuse and Alcoholism with
supplemental support from the National Institute on Drug Abuse. This
research was supported in part by the Intramural Program of the National
Institutes of Health, National Institute on Alcohol Abuse and
Alcoholism. Preparation of this article was also supported in part by
the National Center for Posttraumatic Stress Disorder and a private
donation. The funding agencies had no role in the design and conduct of
the study; analysis or interpretation of the data; or preparation,
review, or approval of the article.; Dr Pietrzak receives partial salary
support from CogState, Inc, for work that bears no relationship to the
present study. None of the authors have any financial conflict of
interest to report.
NR 86
TC 46
Z9 46
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0033-3174
J9 PSYCHOSOM MED
JI Psychosom. Med.
PD OCT
PY 2011
VL 73
IS 8
BP 697
EP 707
DI 10.1097/PSY.0b013e3182303775
PG 11
WC Psychiatry; Psychology; Psychology, Multidisciplinary
SC Psychiatry; Psychology
GA 835QP
UT WOS:000296051200010
PM 21949429
ER
PT J
AU Laditka, JN
Laditka, SB
Liu, R
Price, AE
Wu, B
Friedman, DB
Corwin, SJ
Sharkey, JR
Tseng, W
Hunter, R
Logsdon, RG
AF Laditka, James N.
Laditka, Sarah B.
Liu, Rui
Price, Anna E.
Wu, Bei
Friedman, Daniela B.
Corwin, Sara J.
Sharkey, Joseph R.
Tseng, Winston
Hunter, Rebecca
Logsdon, Rebecca G.
TI Older adults' concerns about cognitive health: commonalities and
differences among six United States ethnic groups
SO AGEING & SOCIETY
LA English
DT Article
DE cognition; ageing; Alzheimer's disease; dementia; memory; qualitative
research; focus groups; brain health
ID ALZHEIMERS-DISEASE; PHYSICAL-ACTIVITY; DEMENTIA; MEMORY; BRAIN;
PERCEPTIONS; AMERICANS; PERFORMANCE; POPULATION; IMPAIRMENT
AB We studied concerns about cognitive health among ethnically diverse groups of older adults. The study was grounded in theories of health behaviour and the representation of health and illness. We conducted 42 focus groups (N = 396, ages 50+) in four languages, with African Americans, American Indians, Chinese Americans, Latinos, Whites other than Latinos (hereafter, Whites) and Vietnamese Americans, in nine United States locations. Participants discussed concerns about keeping their memory or ability to think as they age. Audio recordings were transcribed verbatim. Constant comparison methods identified themes. In findings, all ethnic groups expressed concern and fear about memory loss, losing independence, and becoming 'a burden'. Knowing someone with Alzheimer's disease increased concern. American Indians, Chinese Americans, Latinos and Vietnamese Americans expected memory loss. American Indians, Chinese Americans and Vietnamese Americans were concerned about stigma associated with Alzheimer's disease. Only African Americans, Chinese and Whites expressed concern about genetic risks. Only African Americans and Whites expressed concern about behaviour changes. Although we asked participants for their thoughts about their ability to think as they age, they focused almost exclusively on memory. This suggests that health education promoting cognitive health should focus on memory, but should also educate the public about the importance of maintaining all aspects of cognitive health.
C1 [Laditka, James N.; Laditka, Sarah B.] Univ N Carolina, Dept Publ Hlth Sci, Charlotte, NC 28223 USA.
[Liu, Rui] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Price, Anna E.] Furman Univ, Dept Hlth & Exercise Sci, Greenville, SC 29613 USA.
[Wu, Bei] Univ N Carolina, Gerontol Program, Greensboro, NC 27412 USA.
[Friedman, Daniela B.; Corwin, Sara J.] Univ S Carolina, Dept Hlth Promot Educ & Behav, Columbia, SC 29208 USA.
[Sharkey, Joseph R.] Texas A&M Hlth Sci Ctr, Sch Rural Publ Hlth, Texas Hlth Aging Res Network Collaborating Ctr Tx, College Stn, TX USA.
[Tseng, Winston] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
[Hunter, Rebecca] Univ N Carolina, Carolina Geriatr Educ Ctr, Chapel Hill, NC USA.
[Hunter, Rebecca] Univ N Carolina, Ctr Ageing & Hlth, Chapel Hill, NC USA.
[Logsdon, Rebecca G.] Univ Washington, Sch Nursing, Seattle, WA 98195 USA.
RP Laditka, JN (reprint author), Univ N Carolina, Dept Publ Hlth Sci, 9201 Univ City Blvd, Charlotte, NC 28223 USA.
EM jladitka@uncc.edu
NR 51
TC 13
Z9 13
U1 4
U2 18
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0144-686X
J9 AGEING SOC
JI Ageing Soc.
PD OCT
PY 2011
VL 31
BP 1202
EP 1228
DI 10.1017/S0144686X10001273
PN 7
PG 27
WC Gerontology
SC Geriatrics & Gerontology
GA 829QE
UT WOS:000295598300008
ER
PT J
AU Alpert, MD
Harvey, JD
Lauer, WA
Reeves, RK
Piatak, M
Carville, A
Mansfield, KG
Lifson, JD
Li, W
Desrosiers, RC
Johnson, RP
Evans, DT
AF Alpert, M. D.
Harvey, J. D.
Lauer, W. A.
Reeves, R. K.
Piatak, M.
Carville, A.
Mansfield, K. G.
Lifson, J. D.
Li, W.
Desrosiers, R. C.
Johnson, R. P.
Evans, D. T.
TI Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) Is a Correlate of
Protection by Live-Attenuated SIV
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Alpert, M. D.; Harvey, J. D.; Lauer, W. A.; Desrosiers, R. C.; Evans, D. T.] Harvard Univ, Sch Med, New England Primate Res Ctr, Southborough, MA 01772 USA.
[Reeves, R. K.; Johnson, R. P.] Harvard Univ, Sch Med, Div Immunol, NEPRC, Southborough, MA 01772 USA.
[Piatak, M.; Lifson, J. D.] NCI, SAIC Frederick, Frederick, MD 21701 USA.
[Carville, A.; Mansfield, K. G.] Harvard Univ, Sch Med, Dept Pathol, NEPRC, Southborough, MA 01772 USA.
[Li, W.] Univ Massachusetts, Worcester, MA 01605 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A112
EP A112
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500289
ER
PT J
AU Amara, R
Kannanganat, S
Lai, L
Gangadhara, S
Kwa, S
Kozlowski, P
Hirsch, V
Wyatt, LS
Earl, PL
Moss, B
Robinson, HL
AF Amara, R.
Kannanganat, S.
Lai, L.
Gangadhara, S.
Kwa, S.
Kozlowski, P.
Hirsch, V.
Wyatt, L. S.
Earl, P. L.
Moss, B.
Robinson, H. L.
TI GM-CSF as an Adjuvant for MVA Vaccine: High Dose but Not Low Dose
Inhibits T Cell Responses and Rectal IgA by Modulating DC Activation and
Phenotype
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Amara, R.; Kannanganat, S.; Lai, L.; Gangadhara, S.; Kwa, S.] Emory Univ, Atlanta, GA 30322 USA.
[Kozlowski, P.] Louisiana State Univ, Hlth Sci Ctr, New Orleans, LA USA.
[Hirsch, V.; Wyatt, L. S.; Earl, P. L.; Moss, B.] NIAID, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A38
EP A38
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500088
ER
PT J
AU Baden, LR
Liu, J
Li, H
Walsh, S
Johnson, J
Milner, D
Seaman, M
Krause, K
Swan, E
Tucker, R
Weijtens, M
Pau, M
Dolin, R
Barouch, DH
AF Baden, L. R.
Liu, J.
Li, H.
Walsh, S.
Johnson, J.
Milner, D.
Seaman, M.
Krause, K.
Swan, E.
Tucker, R.
Weijtens, M.
Pau, M.
Dolin, R.
Barouch, D. H.
TI A Phase1 Clinical Trial to Evaluate the Safety, Mucosal and Innate
Immunity of Adenovirus Type 26 HIV-1 Vaccine in Healthy, HIV-1
Uninfected Adults
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Baden, L. R.; Walsh, S.; Johnson, J.; Milner, D.; Krause, K.; Tucker, R.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Liu, J.; Li, H.; Seaman, M.; Dolin, R.; Barouch, D. H.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Swan, E.] NIAID, DAIDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A124
EP A124
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500322
ER
PT J
AU Bonsignori, M
Wu, X
Moody, MA
Liao, H
Hwang, K
Crump, JA
Capiga, SH
Sam, NE
Tomaras, GD
Chen, X
Tsao, C
Alam, SM
Nabel, GJ
Kwong, PD
Morris, L
Montefiori, D
Mascola, JR
Haynes, BF
AF Bonsignori, M.
Wu, X.
Moody, M. A.
Liao, H.
Hwang, K.
Crump, J. A.
Capiga, S. H.
Sam, N. E.
Tomaras, G. D.
Chen, X.
Tsao, C.
Alam, S. M.
Nabel, G. J.
Kwong, P. D.
Morris, L.
Montefiori, D.
Mascola, J. R.
Haynes, B. F.
TI Isolation of CD4-Binding Site and V2/V3 Conformational (Quaternary)
Broadly Neutralizing Antibodies from the Same HIV-1 Infected African
Subject
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Bonsignori, M.; Moody, M. A.; Liao, H.; Hwang, K.; Tomaras, G. D.; Chen, X.; Tsao, C.; Alam, S. M.; Haynes, B. F.] Duke Univ, Med Ctr, Duke Human Vaccine Inst, Durham, NC USA.
[Wu, X.; Nabel, G. J.; Kwong, P. D.; Mascola, J. R.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Crump, J. A.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Capiga, S. H.] London Sch Hyg & Trop Med, London WC1, England.
[Sam, N. E.] Kilimanjaro Christian Med Ctr, Moshi, Tanzania.
[Morris, L.] Natl Inst Communicable Dis, Johannesburg, South Africa.
[Montefiori, D.] Duke Univ, Med Ctr, Dept Surg, Durham, NC 27710 USA.
RI Tomaras, Georgia/J-5041-2016
NR 0
TC 1
Z9 1
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 OCT
PY 2011
VL 27
IS 10
BP A120
EP A120
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500310
ER
PT J
AU Chen, W
Xiao, X
Zhang, C
Zhu, Z
Wang, Y
Goldstein, H
Dimitrov, DS
AF Chen, W.
Xiao, X.
Zhang, C.
Zhu, Z.
Wang, Y.
Goldstein, H.
Dimitrov, D. S.
TI Multifunctional Fusion Proteins of the Human Engineered Antibody Domain
m36.4 with Human Soluble CD4 and Fc as Potential Prophylactics
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Zhang, C.; Goldstein, H.] Albert Einstein Coll Med, New York, NY USA.
[Chen, W.; Xiao, X.; Zhu, Z.; Wang, Y.; Dimitrov, D. S.] NCI, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A73
EP A74
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500185
ER
PT J
AU Cheng, H
Moscoso, CG
Xing, L
Martin, L
Barnett, S
Srivastava, I
AF Cheng, H.
Moscoso, C. G.
Xing, L.
Martin, L.
Barnett, S.
Srivastava, I.
TI Role of Hypervariable Loops in Intersubunit Associations of Env:
Trimeric Gp140 Immunogen as a Platform for Novel Epitope Display
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Cheng, H.; Moscoso, C. G.; Xing, L.] Univ Calif Davis, Davis, CA 95616 USA.
[Martin, L.] CEA, Gif Sur Yvette, France.
[Barnett, S.] Novartis Inc, Cambridge, MA USA.
[Srivastava, I.] NIH, Gaithersburg, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A28
EP A29
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500068
ER
PT J
AU Cicala, C
Van Ryk, D
Nawaz, F
Pascuccio, M
Jelicic, K
Wei, D
Patel, N
Block, K
Arthos, J
Fauci, AS
AF Cicala, C.
Van Ryk, D.
Nawaz, F.
Pascuccio, M.
Jelicic, K.
Wei, D.
Patel, N.
Block, K.
Arthos, J.
Fauci, A. S.
TI The Removal of Transmission-linked Glycosylation Sites in HIV gp120
Promotes High a4b7-Reactivity
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Cicala, C.; Van Ryk, D.; Nawaz, F.; Pascuccio, M.; Jelicic, K.; Wei, D.; Patel, N.; Block, K.; Arthos, J.; Fauci, A. S.] Natl Inst Allergy & Infect Dis USA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A117
EP A117
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500304
ER
PT J
AU Currier, JR
Ratto-Kim, S
Ngauy, V
Ake, J
Lau, C
Doris, T
Herrera, E
David, WB
Sardesai, NY
Boyer, J
Khan, AS
Lee, J
Bagarazzi, M
Yan, J
Adams, E
Earl, P
Moss, B
Kim, J
Michael, N
Robb, M
Marovich, MA
AF Currier, J. R.
Ratto-Kim, S.
Ngauy, V.
Ake, J.
Lau, C.
Doris, T.
Herrera, E.
David, W. B.
Sardesai, N. Y.
Boyer, J.
Khan, A. S.
Lee, J.
Bagarazzi, M.
Yan, J.
Adams, E.
Earl, P.
Moss, B.
Kim, J.
Michael, N.
Robb, M.
Marovich, M. A.
TI Cell-Mediated Immune Responses After DNA Delivered by Either Biojector
or Electroporation and Boosted with a Heterologous Insert Recombinant
Poxvirus
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Currier, J. R.; Ratto-Kim, S.; Ake, J.; Lau, C.; Doris, T.; Herrera, E.; Kim, J.; Michael, N.; Robb, M.; Marovich, M. A.] Mil HIV Res Program, Rockville, MD USA.
[Ngauy, V.] Armed Forces Res Inst Med Sci, Bangkok 10400, Thailand.
[David, W. B.; Boyer, J.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Adams, E.] NIAID, Div Aids, Bethesda, MD 20892 USA.
[Earl, P.; Moss, B.] NIAID, Viral Dis Lab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A3
EP A4
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500003
ER
PT J
AU Doria-Rose, NA
Wu, X
Yang, Z
Louder, MK
Mckee, K
O'Dell, S
Schmidt, S
Koff, WC
Seaman, MS
Bailer, R
Burton, DR
Mascola, JR
AF Doria-Rose, N. A.
Wu, X.
Yang, Z.
Louder, M. K.
McKee, K.
O'Dell, S.
Schmidt, S.
Koff, W. C.
Seaman, M. S.
Bailer, R.
Burton, D. R.
Mascola, J. R.
TI Combined HIV-1 Neutralization Coverage by VRC01, PG9, and PG16
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Doria-Rose, N. A.; Wu, X.; Yang, Z.; Louder, M. K.; McKee, K.; O'Dell, S.; Schmidt, S.; Bailer, R.; Mascola, J. R.] NIH, Bethesda, MD 20892 USA.
[Koff, W. C.] Int AIDS Vaccine Initiat, New York, NY USA.
[Seaman, M. S.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Burton, D. R.] Scripps Res Inst, La Jolla, CA 92037 USA.
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 OCT
PY 2011
VL 27
IS 10
BP A48
EP A48
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500118
ER
PT J
AU Eller, L
Currier, J
Ratto-Kim, S
Robb, M
Kim, J
Eller, M
Barouch, D
Moss, B
Michael, N
Marovich, M
Earl, P
AF Eller, L.
Currier, J.
Ratto-Kim, S.
Robb, M.
Kim, J.
Eller, M.
Barouch, D.
Moss, B.
Michael, N.
Marovich, M.
Earl, P.
TI Construction and Characterization of HIV-1 Mosaic Modified Vaccinia
Ankara (MVA) Vaccines
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Eller, L.; Currier, J.; Ratto-Kim, S.; Robb, M.; Kim, J.; Eller, M.; Michael, N.; Marovich, M.] US Mil, HIV Res Program, Rockville, MD USA.
[Barouch, D.] Beth Israel Deaconess Med Ctr, Div Vaccine Res, Boston, MA 02215 USA.
[Moss, B.] Natl Inst Allergy & I, Viral Dis Lab, NIH, Bethesda, MD USA.
[Earl, P.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
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 OCT
PY 2011
VL 27
IS 10
BP A75
EP A75
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500188
ER
PT J
AU Falkowska, E
Burton, DR
Poignard, P
Mascola, J
Kwong, PD
Wu, X
AF Falkowska, E.
Burton, D. R.
Poignard, P.
Mascola, J.
Kwong, P. D.
Wu, X.
TI Potent and Broad Neutralization by a CD4 Binding Site Monoclonal
Antibody from an HIV-1 Infected Donor
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Falkowska, E.; Poignard, P.] Scripps Res Inst, La Jolla, CA 92037 USA.
[Falkowska, E.; Poignard, P.] IAVI Neutralizing Antibody Ctr, La Jolla, CA USA.
[Burton, D. R.] IAVI Ragon Inst MGH MIT & Harvard, Boston, MA USA.
[Mascola, J.; Kwong, P. D.; Wu, X.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
RI poignard, pascal/N-6678-2013
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 OCT
PY 2011
VL 27
IS 10
BP A8
EP A9
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500017
ER
PT J
AU Ferrari, G
Cox, J
Garcia, A
Rountree, W
DeCastro, C
Louzao, R
Liebl, B
Sambor, A
Sanchez, A
Sarzotti-Kelsoe, M
Lane, J
D'Souza, P
Koup, R
Denny, T
AF Ferrari, G.
Cox, J.
Garcia, A.
Rountree, W.
DeCastro, C.
Louzao, R.
Liebl, B.
Sambor, A.
Sanchez, A.
Sarzotti-Kelsoe, M.
Lane, J.
D'Souza, P.
Koup, R.
Denny, T.
TI Development of CAVD/EQAPOL Long-Term PBMC Repository ('07-'10) @ DUMC;
T-Cell Functionality as Measured by ELISpot and Flow Cytometry Is
Maintained Ov
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Garcia, A.; Rountree, W.; Louzao, R.; Liebl, B.; Sanchez, A.] Duke Univ, Duke Human Vaccine Inst, Durham, NC 27706 USA.
[Cox, J.] Int AIDS Vaccine Initiat, Rockville, MD USA.
[DeCastro, C.] Duke Univ, Duke Inst Genome Sci & Policy, Durham, NC 27706 USA.
[Sambor, A.] Fdn Natl Inst Hlth, Bethesda, MD USA.
[Sarzotti-Kelsoe, M.] Duke Univ, Ctr AIDS Res, Cent QA Unit, Durham, NC 27706 USA.
[Lane, J.; D'Souza, P.] Natl Inst All, Div AIDS, Bethesda, MD USA.
[Koup, R.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Denny, T.] Ctr HIV AIDS Vaccine Immunol, Duke Human Vaccine Inst, Durham, NC USA.
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 OCT
PY 2011
VL 27
IS 10
BP A55
EP A55
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500136
ER
PT J
AU Fletcher, J
Ridtitid, W
Marovich, M
Sereti, I
Rerknimitr, R
Schuetz, A
Pinyakorn, S
Suttichom, D
Rattanamanee, S
Trichavaroj, R
Nguay, V
Kim, JH
Ananworanich, J
AF Fletcher, J.
Ridtitid, W.
Marovich, M.
Sereti, I.
Rerknimitr, R.
Schuetz, A.
Pinyakorn, S.
Suttichom, D.
Rattanamanee, S.
Trichavaroj, R.
Nguay, V.
Kim, J. H.
Ananworanich, J.
TI Abnormal Liver Function During Acute HIV Infection Correlates with
Fiebig Stage and Systemic Inflammation
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Fletcher, J.; Pinyakorn, S.; Suttichom, D.; Rattanamanee, S.; Ananworanich, J.] Thai Red Cross AIDS Res Ctr, SEARCH, Bangkok, Thailand.
[Ridtitid, W.; Rerknimitr, R.] Chulalongkorn Univ, Fac Med, Bangkok 10330, Thailand.
[Marovich, M.] US Mil HIV Res Program, Rockville, MD USA.
[Sereti, I.] NIAID, Bethesda, MD 20892 USA.
[Schuetz, A.] Armed Forces Res Inst Med, Div Retrovirol, Bangkok, Thailand.
[Trichavaroj, R.; Nguay, V.; Kim, J. H.] AFRIMS, Div Retrovirol, Bangkok, Thailand.
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 OCT
PY 2011
VL 27
IS 10
BP A33
EP A33
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500075
ER
PT J
AU Franchini, G
Vaccari, M
Keele, B
Doster, M
Ma, Z
Hryniewicz, A
Morgan, T
Guan, Y
Ferrari, G
Montefiori, D
Venzon, D
Fenizia, C
Lifson, JD
Miller, C
Tartaglia, J
AF Franchini, G.
Vaccari, M.
Keele, B.
Doster, M.
Ma, Z.
Hryniewicz, A.
Morgan, T.
Guan, Y.
Ferrari, G.
Montefiori, D.
Venzon, D.
Fenizia, C.
Lifson, J. D.
Miller, C.
Tartaglia, J.
TI Efficacy of HIV Vaccine Candidate in Macaques Dependent on the Dose of
SIVmac251 Challenge Exposure: Immune Correlates of Vaccine Efficacy
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Franchini, G.; Vaccari, M.; Doster, M.; Hryniewicz, A.; Morgan, T.; Fenizia, C.] NCI, NIH, Bethesda, MD 20892 USA.
[Keele, B.] NCI, AIDS & Canc Virus Program, Frederick, MD 21701 USA.
[Guan, Y.] Univ Maryland, Human Monoclonal Antibody Core Lab, College Pk, MD 20742 USA.
[Ferrari, G.; Montefiori, D.] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Venzon, D.] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Lifson, J. D.] NCI Frederick, Human Retrovirus Sect, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A111
EP A111
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500287
ER
PT J
AU Franchini, G
Fenizia, C
Nichols, D
Cornara, S
Binello, N
Vaccari, M
Pegu, P
Robert-Guroff, M
Ma, Z
Miller, C
Keele, B
Venzon, D
Hirsch, V
AF Franchini, G.
Fenizia, C.
Nichols, D.
Cornara, S.
Binello, N.
Vaccari, M.
Pegu, P.
Robert-Guroff, M.
Ma, Z.
Miller, C.
Keele, B.
Venzon, D.
Hirsch, V.
TI TRIM5 alpha Does Not Affect SIVmac251 Replication in Vaccinated or
Unvaccinated Indian Rhesus Macaques
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Robert-Guroff, M.] NCI, Lab Immune Biol, Retroviral Infect Sect, NIH, Bethesda, MD 20892 USA.
[Keele, B.] NCI Frederick, Canc Virus Program, Frederick, MD USA.
[Venzon, D.] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Hirsch, V.] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A59
EP A59
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500147
ER
PT J
AU Franchini, G
Pegu, P
Vaccari, M
Gordon, S
Keele, B
Doster, M
Guan, Y
Ferrari, G
Montefiori, D
Venzon, D
Fenizia, C
Lifson, J
Michael, N
Kim, J
Tartaglia, J
AF Franchini, G.
Pegu, P.
Vaccari, M.
Gordon, S.
Keele, B.
Doster, M.
Guan, Y.
Ferrari, G.
Montefiori, D.
Venzon, D.
Fenizia, C.
Lifson, J.
Michael, N.
Kim, J.
Tartaglia, J.
TI Titered Mucosal Challenge of Rhesus Macaques with SIVmac251
Recapitulates HIV Vaccine Efficacy in Humans
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Venzon, D.] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Keele, B.] NCI Frederick, AIDS & Canc Virus Program, Frederick, MD USA.
[Guan, Y.] Univ Maryland, Human Monoclonal Antibody Core Lab, College Pk, MD 20742 USA.
[Ferrari, G.; Montefiori, D.] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Lifson, J.] NCI, Human Retrovirus Sect, NIH, Bethesda, MD 20892 USA.
[Michael, N.; Kim, J.] Walter Reed Army Inst Res, Silver Spring, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A4
EP A4
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500004
ER
PT J
AU Gordon, SN
Kines, RC
Kutsyna, G
Ma
Hryniewicz, A
Keele, BF
Roberts, JN
Fenizia, C
Hidajat
Cuburu, N
Buck, B
Bernardo, ML
Robert-Guroff, M
Miller, J
Graham, BS
Lowy, DR
Schiller, T
Franchini, G
AF Gordon, S. N.
Kines, R. C.
Kutsyna, G.
Ma
Hryniewicz, A.
Keele, B. F.
Roberts, J. N.
Fenizia, C.
Hidajat
Cuburu, N.
Buck, B.
Bernardo, M. L.
Robert-Guroff, M.
Miller, J.
Graham, B. S.
Lowy, D. R.
Schiller, T.
Franchini, G.
TI Targeting the Vaginal Mucosa with Human Papillomavirus Pseudovirion
Vaccines Delivering SIV DNA
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Gordon, S. N.; Kutsyna, G.; Hryniewicz, A.; Fenizia, C.; Franchini, G.] NCI, NIH, Bethesda, MD 20892 USA.
[Kines, R. C.; Roberts, J. N.; Cuburu, N.; Buck, B.; Bernardo, M. L.; Lowy, D. R.; Schiller, T.] NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA.
[Ma; Miller, J.] Univ Calif Davis, Calif Natl Primate Res Ctr, Davis, CA 95616 USA.
[Keele, B. F.] SAIC NCI Frederick, AIDS & Canc Virus Program, Frederick, MD USA.
[Hidajat; Robert-Guroff, M.] NCI, Immune Biol Retroviral Infect Sect, Bethesda, MD 20892 USA.
[Graham, B. S.] Natl Inst Allergy & Infect, Vaccine Res Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A26
EP A26
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500063
ER
PT J
AU Jalah, R
Patel, V
Kulkarni, V
Valentin, A
Alicea, C
Rosati, M
von Gegerfelt, A
Sardesai, NY
Bess, J
Lifson, JD
Keele, B
Amara, RR
Robinson, HL
Hirsch, VM
Guan, Y
Venzon, D
Montefiori, DC
Felber, BK
Pavlakis, GN
AF Jalah, R.
Patel, V.
Kulkarni, V.
Valentin, A.
Alicea, C.
Rosati, M.
von Gegerfelt, A.
Sardesai, N. Y.
Bess, J., Jr.
Lifson, J. D.
Keele, B.
Amara, R. R.
Robinson, H. L.
Hirsch, V. M.
Guan, Y.
Venzon, D.
Montefiori, D. C.
Felber, B. K.
Pavlakis, G. N.
TI DNA and Protein Vaccination Confers Protection Upon Mucosal Challenge
with Heterologous SIVsmE660
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Bess, J., Jr.; Lifson, J. D.; Keele, B.] NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Amara, R. R.] Yerkes Natl Primate Res Ctr, Atlanta, GA USA.
[Hirsch, V. M.] NIAID, Bethesda, MD 20892 USA.
[Guan, Y.] Univ Maryland, Sch Med, Inst Human Virol, Baltimore, MD 21201 USA.
[Venzon, D.] NCI, Bethesda, MD 20892 USA.
[Montefiori, D. C.] Duke Univ, Med Ctr, Durham, NC 27706 USA.
RI Bess, Jr., Julian/B-5343-2012
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 OCT
PY 2011
VL 27
IS 10
BP A24
EP A24
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500058
ER
PT J
AU Joyce, M
Zhou, T
Pancera, M
Moquin, S
Wu, X
Zhang, B
Lu, NJ
Zhu, J
Chen, X
Georgiev, I
Shapiro, L
Mascola, JR
Nabel, GJ
Kwong, PD
AF Joyce, M.
Zhou, T.
Pancera, M.
Moquin, S.
Wu, X.
Zhang, B.
Lu, N. J.
Zhu, J.
Chen, X.
Georgiev, I.
Shapiro, L.
Mascola, J. R.
Nabel, G. J.
Kwong, P. D.
TI Structures of Reverted and Mature VRC01-Like Antibodies Illustrate the
Evolution Required to Generate Effective HIV-1 Neutralizing Antibodies
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Joyce, M.; Zhou, T.; Pancera, M.; Moquin, S.; Wu, X.; Zhang, B.; Lu, N. J.; Zhu, J.; Chen, X.; Georgiev, I.; Shapiro, L.; Mascola, J. R.; Nabel, G. J.; Kwong, P. D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RI Zhou, Tongqing/A-6880-2010
OI Zhou, Tongqing/0000-0002-3935-4637
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 OCT
PY 2011
VL 27
IS 10
BP A119
EP A119
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500308
ER
PT J
AU Kalams, SA
Edupuganti, S
Elizaga, M
Metch, B
Eldridge, J
Sherwat, A
De Rosa, S
Khan, AS
Sardesai, N
Weiner, DB
AF Kalams, S. A.
Edupuganti, S.
Elizaga, M.
Metch, B.
Eldridge, J.
Sherwat, A.
De Rosa, S.
Khan, A. S.
Sardesai, N.
Weiner, D. B.
TI Robust Immunogenicity after HIV DNA Vaccination with IL-12 Plasmid
Cytokine Adjuvant Delivered via Electroporation in HIV Uninfected Adults
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Kalams, S. A.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Elizaga, M.; Metch, B.; De Rosa, S.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Edupuganti, S.] Emory Univ, Sch Med, Atlanta, GA USA.
[Eldridge, J.] Profectus BioSci Inc, Tarrytown, NY USA.
[Sherwat, A.] NIAID, Bethesda, MD 20892 USA.
[Khan, A. S.; Sardesai, N.] Inovio Pharmaceut, Blue Bell, PA USA.
[Weiner, D. B.] Univ Penn, Philadelphia, PA 19104 USA.
RI Weiner, David/H-8579-2014
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 OCT
PY 2011
VL 27
IS 10
BP A131
EP A131
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500340
ER
PT J
AU Klatt, NR
Vinton, CL
Ho, J
Darrah, PA
Lifson, JD
Moir, SL
Seder, RA
Brenchley, JM
AF Klatt, N. R.
Vinton, C. L.
Ho, J.
Darrah, P. A.
Lifson, J. D.
Moir, S. L.
Seder, R. A.
Brenchley, J. M.
TI SIV Infection of Rhesus Macaques Results in Dysfunctional T and B Cell
Responses to Neo and Recall Leishmania Major Vaccination
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Klatt, N. R.; Vinton, C. L.; Brenchley, J. M.] Natl Inst Allergy & Infect, NIH, Bethesda, MD USA.
[Ho, J.; Moir, S. L.] NIAID, NIH, LIR, Bethesda, MD 20892 USA.
[Darrah, P. A.; Seder, R. A.] NIAID, NIH, VRC, Bethesda, MD 20892 USA.
[Lifson, J. D.] NCI, ACVP, SAIC, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A93
EP A93
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500237
ER
PT J
AU Li, Y
O'Dell, S
Wu, X
Schmidt, S
Hogerkorp, C
Feng, Y
Chakrabarti, B
Wilson, R
Longo, N
Doria-Rose, N
Roederer, M
Connors, M
Wyatt, R
Mascola, J
AF Li, Y.
O'Dell, S.
Wu, X.
Schmidt, S.
Hogerkorp, C.
Feng, Y.
Chakrabarti, B.
Wilson, R.
Longo, N.
Doria-Rose, N.
Roederer, M.
Connors, M.
Wyatt, R.
Mascola, J.
TI Isolation of a Subset of Novel HIV-1 Broadly Neutralizing Antibodies
with Dual Specificity Overlapping the Env Receptor and Coreceptor
Binding Sites
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Li, Y.; Feng, Y.; Chakrabarti, B.; Wilson, R.; Wyatt, R.] Scripps Res Inst, IAVI, La Jolla, CA 92037 USA.
[O'Dell, S.; Wu, X.; Schmidt, S.; Hogerkorp, C.; Longo, N.; Roederer, M.; Mascola, J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Doria-Rose, N.; Connors, M.] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RI Feng, Yu/A-3396-2012
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 OCT
PY 2011
VL 27
IS 10
BP A16
EP A16
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500037
ER
PT J
AU Louder, RK
McLellan, J
Pancera, M
Schmidt, SD
Yang, Y
Zhang, B
Phogat, S
Bonsignori, M
Hwang, K
Liao, H
Chen, X
Moody, MA
Haynes, BF
Mascola, JR
Kwong, PD
AF Louder, R. K.
McLellan, J.
Pancera, M.
Schmidt, S. D.
Yang, Y.
Zhang, B.
Phogat, S.
Bonsignori, M.
Hwang, K.
Liao, H.
Chen, X.
Moody, M. A.
Haynes, B. F.
Mascola, J. R.
Kwong, P. D.
TI Structures of HIV-1 Quaternary-Structure-Preferring Antibodies, CH04 And
PG9, Show Conserved Structural Elements Within a Generallly Flexible CDR
H3
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Louder, R. K.; McLellan, J.; Pancera, M.; Schmidt, S. D.; Yang, Y.; Zhang, B.; Mascola, J. R.; Kwong, P. D.] NIH, Bethesda, MD 20892 USA.
[Phogat, S.] Int AIDS Vaccine Initiat, Brooklyn, NY USA.
[Bonsignori, M.; Hwang, K.; Liao, H.; Chen, X.; Moody, M. A.; Haynes, B. F.] Duke Univ, Sch Med, Durham, NC USA.
RI McLellan, Jason/A-6874-2010; Louder, Robert/F-4713-2014
OI Louder, Robert/0000-0002-6944-9346
NR 0
TC 0
Z9 0
U1 1
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A118
EP A119
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500307
ER
PT J
AU Lynch, RM
Louder, MK
Tran, L
Yang, Z
Tomaras, G
Cohen, M
Gray, ES
Sibeko, S
Karim, SA
Euler, Z
Nabel, GJ
Schuitemaker, H
Montefiori, DC
Morris, L
Haynes, BF
Mascola, J
AF Lynch, R. M.
Louder, M. K.
Tran, L.
Yang, Z.
Tomaras, G.
Cohen, M.
Gray, E. S.
Sibeko, S.
Karim, S. A.
Euler, Z.
Nabel, G. J.
Schuitemaker, H.
Montefiori, D. C.
Morris, L.
Haynes, B. F.
Mascola, J.
TI Detection of CD4-Binding Site Antibodies in Three HIV-1 Seroconverter
Cohorts
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Lynch, R. M.; Louder, M. K.; Tran, L.; Yang, Z.; Nabel, G. J.; Mascola, J.] NIH, Bethesda, MD 20892 USA.
[Tomaras, G.; Montefiori, D. C.; Haynes, B. F.] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Cohen, M.] Univ N Carolina, Sch Med, Chapel Hill, NC USA.
[Gray, E. S.; Morris, L.] Natl Inst Communicable Dis, Johannesburg, South Africa.
[Sibeko, S.; Karim, S. A.] Univ KwaZulu Natal, Durban, South Africa.
[Euler, Z.; Schuitemaker, H.] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands.
RI Tomaras, Georgia/J-5041-2016
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 OCT
PY 2011
VL 27
IS 10
BP A47
EP A47
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500115
ER
PT J
AU Madenwald, T
Fuchs, J
Sobieszczyk, M
Karuna, S
Sherwat, A
Koblin, B
Broder, G
Eaton, N
Andrasik, M
Hammer, S
AF Madenwald, T.
Fuchs, J.
Sobieszczyk, M.
Karuna, S.
Sherwat, A.
Koblin, B.
Broder, G.
Eaton, N.
Andrasik, M.
Hammer, S.
CA Div AIDS DAIDS HIV Vaccine Trials
TI Attitudes and Intent to Use PrEP Among Current Phase II Preventive HIV-1
Vaccine Trial Participants
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Madenwald, T.; Karuna, S.; Broder, G.; Eaton, N.; Andrasik, M.] Fred Hutchinson Canc Res, HIV Vaccine Trials Network, Seattle, WA USA.
[Fuchs, J.] San Francisco Dept Publ Hlth, San Francisco, CA USA.
[Sobieszczyk, M.; Hammer, S.] Columbia Univ, New York, NY USA.
[Sherwat, A.] NIAID, Div AID, Washington, DC USA.
[Koblin, B.] New York Blood Ctr, New York, NY 10021 USA.
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 OCT
PY 2011
VL 27
IS 10
BP A81
EP A81
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500205
ER
PT J
AU Mccoy, L
Forsman, A
Bulmer-Thomas, B
Strokappe, N
Verrips, T
Chen, L
Kwong, PD
Weiss, RA
AF McCoy, L.
Forsman, A.
Bulmer-Thomas, B.
Strokappe, N.
Verrips, T.
Chen, L.
Kwong, P. D.
Weiss, R. A.
TI Llama Antibody Fragments that Potently Neutralize HIV-1 at the CD4
Binding Site of HIV-1 Gp120
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [McCoy, L.; Forsman, A.; Bulmer-Thomas, B.; Weiss, R. A.] UCL, London, England.
[Strokappe, N.; Verrips, T.] Univ Utrecht, Utrecht, Netherlands.
[Chen, L.; Kwong, P. D.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
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 OCT
PY 2011
VL 27
IS 10
BP A44
EP A44
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500105
ER
PT J
AU McLellan, J
Pancera, M
Dai, K
Boyington, J
Yang, Z
Carrico, C
Shahzad-ul-Hussan, S
Sastry, M
Schmidt, S
Yang, Y
Bonsignori, M
Haynes, B
Phogat, S
Bewley, C
Mascola, J
Schief, W
Nabel, G
Kwong, P
AF McLellan, J.
Pancera, M.
Dai, K.
Boyington, J.
Yang, Z.
Carrico, C.
Shahzad-ul-Hussan, S.
Sastry, M.
Schmidt, S.
Yang, Y.
Bonsignori, M.
Haynes, B.
Phogat, S.
Bewley, C.
Mascola, J.
Schief, W.
Nabel, G.
Kwong, P.
TI HIV-1 gp120 V1V2-Scaffolds for Structural Analysis and Immunogen Design
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [McLellan, J.; Pancera, M.; Dai, K.; Boyington, J.; Yang, Z.; Shahzad-ul-Hussan, S.; Sastry, M.; Schmidt, S.; Yang, Y.; Mascola, J.; Nabel, G.; Kwong, P.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Carrico, C.; Schief, W.] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
[Bonsignori, M.; Haynes, B.] Duke Human Vaccine Inst, Durham, NC USA.
[Bonsignori, M.; Haynes, B.] Duke Ctr AIDS Res, Durham, NC USA.
[Phogat, S.] Int AIDS Vaccine Initiat, Brooklyn, NY USA.
[Bewley, C.] NIDDK, NIH, Bethesda, MD USA.
RI McLellan, Jason/A-6874-2010
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 OCT
PY 2011
VL 27
IS 10
BP A7
EP A8
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500014
ER
PT J
AU Mendoza, D
Johnson, S
Peterson, B
Doria-Rose, N
Franchini, G
Schneider, D
Trivett, MT
Trubey, CM
Coalter, V
Watkins, DI
Lifson, JD
Migueles, SA
Connors, M
AF Mendoza, D.
Johnson, S.
Peterson, B.
Doria-Rose, N.
Franchini, G.
Schneider, D.
Trivett, M. T.
Trubey, C. M.
Coalter, V.
Watkins, D. I.
Lifson, J. D.
Migueles, S. A.
Connors, M.
TI Cytotoxicity Capacity of SIV-Specific CD8+T Cells Against Primary
Autologous Targets Correlates with Immune Control in SIV-Infected Rhesus
Macaques
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Mendoza, D.; Johnson, S.; Peterson, B.; Doria-Rose, N.; Migueles, S. A.; Connors, M.] NIAID, NIH, Chevy Chase, MD USA.
[Franchini, G.] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Schneider, D.; Trivett, M. T.; Trubey, C. M.; Coalter, V.; Lifson, J. D.] SAIC Frederick Inc, AIDS & Canc Virus Program, Frederick, MD USA.
[Watkins, D. I.] Univ Wisconsin, Madison, WI 53706 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A19
EP A20
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500047
ER
PT J
AU Munier, S
Mercier, P
Calamel, A
Bosquet, N
Delair, T
Paul, S
Earl, P
Le Grand, R
Verrier, B
AF Munier, S.
Mercier, P.
Calamel, A.
Bosquet, N.
Delair, T.
Paul, S.
Earl, P.
Le Grand, R.
Verrier, B.
TI Priming with Synthetic Nanovaccine Followed by rMVA Boost Is the Best
Combination to Elicit Strong and Long-Lasting Gag or Env Immune
Responses
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Bosquet, N.; Le Grand, R.] CEA, Fontenay Aux Roses, France.
[Delair, T.] Univ Lyon, Lyon, France.
[Paul, S.] Univ St Etienne, St Etienne, France.
[Earl, P.] NIH, Bethesda, MD 20892 USA.
[Munier, S.; Mercier, P.; Calamel, A.; Verrier, B.] Ctr Natl Rech Sci, Lyon, France.
NR 0
TC 0
Z9 0
U1 0
U2 4
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 OCT
PY 2011
VL 27
IS 10
BP A108
EP A108
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500278
ER
PT J
AU Ortiz, A
Li, B
Klatt, NR
Lawson, B
Ryzhova, E
Carnathan, P
Paiardini, M
Else, J
Gonzalez-Scarano, F
Ratcliffe, SJ
Brenchley, J
Estes, J
Derdeyn, C
Silvestri, G
AF Ortiz, A.
Li, B.
Klatt, N. R.
Lawson, B.
Ryzhova, E.
Carnathan, P.
Paiardini, M.
Else, J.
Gonzalez-Scarano, F.
Ratcliffe, S. J.
Brenchley, J.
Estes, J.
Derdeyn, C.
Silvestri, G.
TI Evidence for CD4 T-Cell Mediated Immune Control of Macrophage Infection
in Rhesus Macaques Undergoing CD4+Lymphocyte Depletion Prior to SIV
Infection
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Ortiz, A.; Li, B.; Lawson, B.; Carnathan, P.; Paiardini, M.; Else, J.; Derdeyn, C.; Silvestri, G.] Emory Univ, Atlanta, GA 30322 USA.
[Klatt, N. R.; Brenchley, J.] NIH, Mol Microbiol Lab, Bethesda, MD 20892 USA.
[Ryzhova, E.] Univ Penn, Sch Med, Dept Neurol, Philadelphia, PA 19104 USA.
[Gonzalez-Scarano, F.] UT Hlth Sci Ctr San Antonio, Sch Med, San Antonio, TX USA.
[Ratcliffe, S. J.] Univ Penn, Dept Biostat, Philadelphia, PA 19104 USA.
[Estes, J.] NCI, AIDS & Canc Virus Program, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A17
EP A18
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500042
ER
PT J
AU Pancera, M
Zhu, J
O'Dell, S
Wu, X
Yang, Y
Zhang, B
Doria-Rose, N
Connors, M
Moore, P
Karim, S
Morris, L
Simek, M
Poignard, P
Burton, DR
Koff, W
Mascola, JR
Kwong, PD
AF Pancera, M.
Zhu, J.
O'Dell, S.
Wu, X.
Yang, Y.
Zhang, B.
Doria-Rose, N.
Connors, M.
Moore, P.
Karim, S.
Morris, L.
Simek, M.
Poignard, P.
Burton, D. R.
Koff, W.
Mascola, J. R.
Kwong, P. D.
TI 454 Pryosequencing of B Cells From HIV-1 Infected Donors With
Quaternary-Structure-Preferring Antibodies
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Pancera, M.; Zhu, J.; O'Dell, S.; Wu, X.; Yang, Y.; Zhang, B.; Mascola, J. R.; Kwong, P. D.] NIAID, VRC, NIH, Bethesda, MD 20892 USA.
[Moore, P.; Morris, L.] Natl Inst Communicable Dis, AIDS Virus Res Unit, Johannesburg, South Africa.
[Karim, S.] Univ KwaZulu Natal, CAPRISA, Durban, South Africa.
[Simek, M.; Koff, W.] Int AIDS Vaccine Initiat, New York, NY USA.
[Poignard, P.; Burton, D. R.] Scripps Res Inst, IAVI Neutralizing Antibody Ctr, La Jolla, CA 92037 USA.
RI poignard, pascal/N-6678-2013
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 OCT
PY 2011
VL 27
IS 10
BP A121
EP A121
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500313
ER
PT J
AU Pavlakis, GN
Rolland, M
Felber, BK
Kulkarni, V
Mothe, B
Brander, C
Termini, J
Stone, GW
Le Gall, S
Yan, J
Weiner, DB
Manocheewa, S
Swain, JV
Lanxon-Cookson, E
Mullins, JI
AF Pavlakis, G. N.
Rolland, M.
Felber, B. K.
Kulkarni, V.
Mothe, B.
Brander, C.
Termini, J.
Stone, G. W.
Le Gall, S.
Yan, J.
Weiner, D. B.
Manocheewa, S.
Swain, J. V.
Lanxon-Cookson, E.
Mullins, J. I.
TI Conserved Elements (CE) Vaccine
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Pavlakis, G. N.; Felber, B. K.; Kulkarni, V.] NCI, NIH, Frederick, MD 21701 USA.
[Mothe, B.; Brander, C.] Irsi Caixa HIVACAT, Barcelona, Spain.
[Termini, J.; Stone, G. W.] Univ Miami, Miami, FL USA.
[Le Gall, S.] Ragon Inst, Boston, MA USA.
[Yan, J.; Weiner, D. B.] Univ Penn, Philadelphia, PA 19104 USA.
[Rolland, M.; Manocheewa, S.; Swain, J. V.; Lanxon-Cookson, E.; Mullins, J. I.] Univ Washington, Seattle, WA 98195 USA.
RI Weiner, David/H-8579-2014
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 OCT
PY 2011
VL 27
IS 10
BP A110
EP A110
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500284
ER
PT J
AU Qureshi, H
Ma, Z
Huang, Y
Hodge, G
Thomas, M
DiPasquale, J
DeSilva, V
Fritts, L
Bett, AJ
Shiver, J
Robert-Guroff, M
Robertson, M
Casimiro, D
McChesney, M
Gilbert, P
Miller, C
AF Qureshi, H.
Ma, Z.
Huang, Y.
Hodge, G.
Thomas, M.
DiPasquale, J.
DeSilva, V.
Fritts, L.
Bett, A. J.
Shiver, J.
Robert-Guroff, M.
Robertson, M.
Casimiro, D.
McChesney, M.
Gilbert, P.
Miller, C.
TI Penile SIV Challenge of Ad5-Infected Macaques Immunized With an
Ad5-Based Vaccine Recapitulates the Enhanced Infection Rate Among STEP
Trial Vaccines
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Huang, Y.; Gilbert, P.] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98104 USA.
[Thomas, M.; DiPasquale, J.; Robert-Guroff, M.] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Bett, A. J.; Shiver, J.; Robertson, M.; Casimiro, D.] Merck Res Labs, West Point, PA USA.
[Qureshi, H.; Ma, Z.; Hodge, G.; DeSilva, V.; Fritts, L.; McChesney, M.; Miller, C.] UC Davis, Davis, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A126
EP A126
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500327
ER
PT J
AU Rerks-Ngarm, S
Paris, RM
Chunsutthiwat, S
Premsri, N
Namwat, C
Bowornwatanuwong, J
Li, S
Kaewkungkal, J
Trichavaroj, R
de Souza, M
Francis, D
Adams, E
Gurunathan, S
Tartaglia, J
O'Connell, R
Eamsila, C
Nitayaphan, S
Ngauy, V
Thongcharoen, P
Kunasol, P
Michael, N
Robb, M
Gilbert, P
Kim, J
AF Rerks-Ngarm, S.
Paris, R. M.
Chunsutthiwat, S.
Premsri, N.
Namwat, C.
Bowornwatanuwong, J.
Li, S.
Kaewkungkal, J.
Trichavaroj, R.
de Souza, M.
Francis, D.
Adams, E.
Gurunathan, S.
Tartaglia, J.
O'Connell, R.
Eamsila, C.
Nitayaphan, S.
Ngauy, V.
Thongcharoen, P.
Kunasol, P.
Michael, N.
Robb, M.
Gilbert, P.
Kim, J.
TI Extended Evaluation of Volunteers Who Become HIV-1 Infected During
Participation in a Phase III Vaccine Trial of ALVAC-HIV and AIDSVAX (R)
B/E
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Rerks-Ngarm, S.; Chunsutthiwat, S.; Premsri, N.; Namwat, C.; Kunasol, P.] Prime Boost HIV Vaccine Phase III Trial, Nonthaburi, Thailand.
[Paris, R. M.; O'Connell, R.; Robb, M.; Kim, J.] US Mil HIV Res Program, Rockville, MD USA.
[Bowornwatanuwong, J.] Chonburi Reg Hosp, Chon Buri, Thailand.
[Li, S.; Gilbert, P.] SCHARP, Seattle, WA USA.
[Kaewkungkal, J.] Mahidol Univ, Fac Trop Med, Bangkok, Thailand.
[Trichavaroj, R.] USAMC AFRIMS, Dept Retrovirol, Bangkok, Thailand.
[de Souza, M.; Ngauy, V.] MHRP AFRIMS, Bangkok, Thailand.
[Francis, D.] GSID, San Francisco, CA USA.
[Adams, E.] NIAID, NIH, Bethesda, MD 20892 USA.
[Gurunathan, S.; Tartaglia, J.] Sanofi Pasteur, Swiftwater, PA USA.
[Eamsila, C.; Nitayaphan, S.] Royal Thai Army, AFRIMS, Bangkok, Thailand.
[Thongcharoen, P.] Mahidol Univ, Fac Med, Siriraj Hosp, Bangkok 10700, Thailand.
[Michael, N.] US Mil HIV Res Program, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A28
EP A28
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500066
ER
PT J
AU Robinson, HL
Lai, L
Kwa, S
Kozlowski, PA
Hirsch, V
Felber, BK
Pavlakis, GN
Earl, PL
Moss, B
Amara, RR
AF Robinson, H. L.
Lai, L.
Kwa, S.
Kozlowski, P. A.
Hirsch, V.
Felber, B. K.
Pavlakis, G. N.
Earl, P. L.
Moss, B.
Amara, R. R.
TI Homologous Priming and Boosting with Recombinant MVA, Prevention of
Infection as Good as With the Heterologous Regimen of DNA Priming and
MVA Boosting
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Lai, L.; Kwa, S.] Yerkes Natl Primate Res Ctr, Atlanta, GA USA.
[Kozlowski, P. A.] Louisiana State Univ, Hlth Sci Ctr, New Orleans, LA USA.
[Hirsch, V.; Earl, P. L.; Moss, B.] NIAID, NIH, Bethesda, MD 20892 USA.
[Felber, B. K.; Pavlakis, G. N.] NCI, Frederick, MD 21701 USA.
[Amara, R. R.] Emory Univ, Vaccine Res Ctr, Atlanta, GA 30322 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A4
EP A5
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500006
ER
PT J
AU Simmons, RP
Groden, E
Chang, JJ
Lindsay, R
Fadda, L
Lifson, JD
Lane, K
Axten, K
Rosenberg, E
Allen, T
Altfeld, M
AF Simmons, R. P.
Groden, E.
Chang, J. J.
Lindsay, R.
Fadda, L.
Lifson, J. D.
Lane, K.
Axten, K.
Rosenberg, E.
Allen, T.
Altfeld, M.
TI Different Cytokine Profiles Induced by HIV-1 and HIV-1-Derived TLR
Ligands in Monocytes and mDCs
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Simmons, R. P.; Groden, E.; Chang, J. J.; Lindsay, R.; Fadda, L.; Lane, K.; Axten, K.; Allen, T.; Altfeld, M.] MIT & Harvard, Ragon Inst MGH, Charlestown, MA USA.
[Lifson, J. D.] NCI, AIDS & Canc Virus Program, Frederick, MD 21701 USA.
[Rosenberg, E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A63
EP A63
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500158
ER
PT J
AU Smith, LM
Parodi, LM
Hodara, VL
Pavlakis, G
Felber, B
Giavedoni, LD
AF Smith, L. M.
Parodi, L. M.
Hodara, V. L.
Pavlakis, G.
Felber, B.
Giavedoni, L. D.
TI Biologically Active Fusion Proteins of CD154 and SIVgp41 as Novel
Vaccine Components
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Pavlakis, G.; Felber, B.] NCI, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
[Smith, L. M.; Parodi, L. M.; Hodara, V. L.; Giavedoni, L. D.] Texas Biomed Res Inst, San Antonio, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A111
EP A112
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500288
ER
PT J
AU Sundling, C
Li, Y
Huynh, N
Wilson, R
O'Dell, S
Mascola, JR
Wyatt, RT
Hedestam, GBK
AF Sundling, C.
Li, Y.
Huynh, N.
Wilson, R.
O'Dell, S.
Mascola, J. R.
Wyatt, R. T.
Hedestam, G. B. Karlsson
TI Characterization of CD4-Binding Site Directed Monoclonal Antibodies
Isolated from HIV-1 gp140 Env Immunized Rhesus Macaques
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Sundling, C.; Huynh, N.; Hedestam, G. B. Karlsson] Karolinska Inst, Stockholm, Sweden.
[Li, Y.; Wilson, R.; Wyatt, R. T.] Dept Immunol & Microbial Sci, La Jolla, CA USA.
[O'Dell, S.; Mascola, J. R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A9
EP A10
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500020
ER
PT J
AU van Gils, MJ
Crooks, ET
Decker, JM
Gray, ES
Tumba, NL
Lynch, R
Mascola, JR
Morris, L
Binley, J
Schuitemaker, H
AF van Gils, M. J.
Crooks, E. T.
Decker, J. M.
Gray, E. S.
Tumba, N. L.
Lynch, R.
Mascola, J. R.
Morris, L.
Binley, J.
Schuitemaker, H.
TI Neutralizing Activity Against Both Gp120 and Gp41 in Patients with
HIV-Specific Cross-Reactive Neutralizing Humoral Immunity
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [van Gils, M. J.; Schuitemaker, H.] Univ Amsterdam, Acad Med Ctr, NL-1105 AZ Amsterdam, Netherlands.
[Crooks, E. T.; Binley, J.] Torrey Pines Inst Mol Studies, San Diego, CA USA.
[Decker, J. M.] Univ Alabama, Dept Med, Birmingham, AL 35294 USA.
[Gray, E. S.; Tumba, N. L.; Morris, L.] Natl Inst Communicable Dis, Johannesburg, South Africa.
[Lynch, R.] Natl Inst Allergy & Infect, Vaccine Res Ctr, NIH, Bethesda, MD USA.
[Mascola, J. R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A41
EP A41
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500098
ER
PT J
AU Wagner, D
Gaekwad, J
Narpala, S
Carpov, A
Pancera, M
Walker, LM
Hoffenberg, S
Kwong, PD
Mascola, JR
Burton, DR
Koff, WC
King, R
Wyatt, RT
Phogat, SK
AF Wagner, D.
Gaekwad, J.
Narpala, S.
Carpov, A.
Pancera, M.
Walker, L. M.
Hoffenberg, S.
Kwong, P. D.
Mascola, J. R.
Burton, D. R.
Koff, W. C.
King, R.
Wyatt, R. T.
Phogat, S. K.
TI PG16 Binding Early Transmitted HIV-1 Clade C Virus 16055 Soluble
Envelope Glycoprotein as Candidate Vaccine Immunogen
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Gaekwad, J.; Wyatt, R. T.] Scripps Res Inst, IAVI NAC Ctr, La Jolla, CA 92037 USA.
[Pancera, M.] NIAID, Vaccine Reserach Ctr, NIH, Bethesda, MD 20892 USA.
[Kwong, P. D.; Mascola, J. R.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Koff, W. C.; King, R.; Phogat, S. K.] Int AIDS Vaccine Initiat, Brooklyn, NY USA.
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 OCT
PY 2011
VL 27
IS 10
BP A53
EP A53
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500131
ER
PT J
AU Wang, YE
Oniangue-Nzda, C
Schneidewind, A
Kemper, M
Mellors, E
Qi, Y
Gladden, AD
Power, KA
Pereyra, F
Walker, BD
Carrington, M
Allen, TM
AF Wang, Y. E.
Oniangue-Nzda, C.
Schneidewind, A.
Kemper, M.
Mellors, E.
Qi, Y.
Gladden, A. D.
Power, K. A.
Pereyra, F.
Walker, B. D.
Carrington, M.
Allen, T. M.
TI Control of HIV Viral Replication Mediated by the Synergistic Effects of
Unique Combinations of HLA Class I Alleles
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Wang, Y. E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Oniangue-Nzda, C.; Kemper, M.; Mellors, E.; Gladden, A. D.; Power, K. A.; Pereyra, F.; Walker, B. D.; Allen, T. M.] Ragon Inst MGH MIT & Harvard, Boston, MA USA.
[Schneidewind, A.] Univ Regensburg, Regensburg, Germany.
[Carrington, M.] NCI Frederick, SAIC Frederick Inc, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A60
EP A60
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500150
ER
PT J
AU Whitney, JB
Rolland, M
Lacerda, M
Hraber, PT
DeCamp, A
Luedemann, C
Rao, SS
Mascola, JR
Korber, B
Nabel, GJ
Gilbert, P
Seoighe, C
Letvin, NL
AF Whitney, J. B.
Rolland, M.
Lacerda, M.
Hraber, P. T.
DeCamp, A.
Luedemann, C.
Rao, S. S.
Mascola, J. R.
Korber, B.
Nabel, G. J.
Gilbert, P.
Seoighe, C.
Letvin, N. L.
TI Reduction of Founder Virus in Vaccinated Monkeys After Mucosal SIV
Challenge
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Whitney, J. B.; Luedemann, C.; Letvin, N. L.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Whitney, J. B.; Luedemann, C.; Letvin, N. L.] Harvard Univ, Boston, MA 02115 USA.
[Rolland, M.] US Mil HIV Res Program MHRP, Rockville, MD USA.
[Lacerda, M.] NUI, Sch Math Stat & Appl Math, Galway, Ireland.
[Hraber, P. T.; Korber, B.] Los Alamos Natl Lab, Los Alamos, NM USA.
[DeCamp, A.; Gilbert, P.] Stat Ctr HIV AIDS Res & Prevent, Seattle, WA USA.
[Rao, S. S.] NIAID, Vaccine Res Ctr, Bethesda, MD USA.
[Mascola, J. R.; Nabel, G. J.] Vaccine Res Ctr NIAID, Bethesda, MD USA.
[Seoighe, C.] Sch Math Stat & Appl Math, Galway, Ireland.
NR 0
TC 0
Z9 0
U1 0
U2 5
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 OCT
PY 2011
VL 27
IS 10
BP A30
EP A30
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500071
ER
PT J
AU Wyatt, L
Xiao, W
Earl, P
Moss, B
AF Wyatt, L.
Xiao, W.
Earl, P.
Moss, B.
TI Optimizing the Immune Response to MVA/HIV Vaccine Candidates in Mice
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Wyatt, L.; Xiao, W.; Earl, P.; Moss, B.] NIAID, LVD, Natl In, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A105
EP A105
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500271
ER
PT J
AU Zeng, M
Duan, L
Li, Q
Smith, A
Wietgrefe, S
Southern, PJ
Reilly, CS
Pambuccian, S
Shang, L
Skinner, PJ
Zupancic, M
Piatak, M
Waterman, D
Reeves, K
Lifson, JD
Johnson, P
Haase, AT
AF Zeng, M.
Duan, L.
Li, Q.
Smith, A.
Wietgrefe, S.
Southern, P. J.
Reilly, C. S.
Pambuccian, S.
Shang, L.
Skinner, P. J.
Zupancic, M.
Piatak, M., Jr.
Waterman, D.
Reeves, K.
Lifson, J. D.
Johnson, P.
Haase, A. T.
TI SIV Attenuated Vaccine-Induced Plasma Cells and Antibodies Limit
Infection at the Portal of Entry and Systemically Following Vaginal
Challenge
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Zeng, M.; Duan, L.; Smith, A.; Wietgrefe, S.; Southern, P. J.; Reilly, C. S.; Pambuccian, S.; Shang, L.; Skinner, P. J.; Zupancic, M.; Haase, A. T.] Univ Minnesota, Minneapolis, MN USA.
[Li, Q.] Univ Nebraska, Lincoln, NE USA.
[Piatak, M., Jr.; Lifson, J. D.] NCI, Frederick, MD 21701 USA.
[Waterman, D.] ZeptoMetrix Corp, Buffalo, NY USA.
[Reeves, K.; Johnson, P.] Harvard Univ, Sch Med, Southborough, MA 01772 USA.
[Johnson, P.] Ragon Inst, Southborough, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A30
EP A30
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500072
ER
PT J
AU Zhang, M
Yuan, T
Li, J
Zhang, Y
Wang, Y
Streaker, E
Dimitrov, DS
AF Zhang, M.
Yuan, T.
Li, J.
Zhang, Y.
Wang, Y.
Streaker, E.
Dimitrov, D. S.
TI Putative Rhesus Macaque Germline Antibodies of Broadly HIV-Neutralizing
Antibodies: Similarities and Differences Compared with the Human
Counterparts
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Zhang, M.; Yuan, T.; Li, J.; Zhang, Y.] Univ Hong Kong, Pokfulam, Hong Kong, Peoples R China.
[Wang, Y.; Streaker, E.; Dimitrov, D. S.] NCI, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A39
EP A39
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500092
ER
PT J
AU Zhou, T
Wu, X
Zhang, B
Moquin, S
Zhu, J
Georgiev, I
Bonsignori, M
Crump, JA
Kapiga, SH
Noel, SE
Haynes, BF
Simek, M
Burton, DR
Koff, WC
Shapiro, L
Mascola, JR
Kwong, PD
AF Zhou, T.
Wu, X.
Zhang, B.
Moquin, S.
Zhu, J.
Georgiev, I.
Bonsignori, M.
Crump, J. A.
Kapiga, S. H.
Noel, S. E.
Haynes, B. F.
Simek, M.
Burton, D. R.
Koff, W. C.
Shapiro, L.
Mascola, J. R.
Kwong, P. D.
TI Structural Basis for VRC01-Like-Antibody Recognition of Variable Loops
that Surround the Site of CD4 Attachment on HIV-1 Gp120
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Zhou, T.; Wu, X.; Zhang, B.; Moquin, S.; Zhu, J.; Georgiev, I.; Mascola, J. R.; Kwong, P. D.] NIAID, NIH, Bethesda, MD 20892 USA.
[Bonsignori, M.; Haynes, B. F.] Duke Univ, Sch Med, Duke Human Vaccine Inst, Durham, NC USA.
[Crump, J. A.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Crump, J. A.] Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA.
[Kapiga, S. H.] Kilimanjaro Reprod Hlth Programme, Moshi, Tanzania.
[Noel, S. E.] Tumaini Univ, Moshi, Tanzania.
[Simek, M.; Koff, W. C.] Int AIDS Vaccine Initiat IAVI, New York, NY USA.
[Burton, D. R.] Scripps Res Inst, La Jolla, CA 92037 USA.
[Shapiro, L.] Columbia Univ, Dept Biochem & Mol Biophys, New York, NY USA.
RI Zhou, Tongqing/A-6880-2010
OI Zhou, Tongqing/0000-0002-3935-4637
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 OCT
PY 2011
VL 27
IS 10
BP A120
EP A120
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500311
ER
PT J
AU Zhu, Z
Qin, HR
Chen, W
Zhao, Q
Shen, X
Schutte, R
Wang, Y
Ofek, G
Streaker, E
Prabakaran, P
Fouda, GG
Liao, H
Owens, J
Louder, M
Yang, Y
Klaric, K
Moody, MA
Mascola, JR
Scott, JK
Kwong, PD
Montefiori, D
Haynes, BF
Tomaras, GD
Dimitrov, DS
AF Zhu, Z.
Qin, H. R.
Chen, W.
Zhao, Q.
Shen, X.
Schutte, R.
Wang, Y.
Ofek, G.
Streaker, E.
Prabakaran, P.
Fouda, G. G.
Liao, H.
Owens, J.
Louder, M.
Yang, Y.
Klaric, K.
Moody, M. A.
Mascola, J. R.
Scott, J. K.
Kwong, P. D.
Montefiori, D.
Haynes, B. F.
Tomaras, G. D.
Dimitrov, D. S.
TI 2F5-like Cross-Reactive HIV-1-Neutralizing Monoclonal Antibodies with
Low Number of Somatic Mutations
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT Conference on AIDS Vaccine
CY SEP 12-15, 2011
CL Bangkok, THAILAND
C1 [Shen, X.] Vaccine Inst, Durham, NC USA.
[Schutte, R.; Fouda, G. G.; Liao, H.; Moody, M. A.; Montefiori, D.; Haynes, B. F.; Tomaras, G. D.] Human Vaccine Inst, Durham, NC USA.
[Ofek, G.; Louder, M.; Yang, Y.; Mascola, J. R.; Kwong, P. D.] Vaccine Res Ctr, Bethesda, MD USA.
[Klaric, K.; Scott, J. K.] Simon Fraser Univ, Burnaby, BC V5A 1S6, Canada.
[Zhu, Z.; Qin, H. R.; Chen, W.; Zhao, Q.; Wang, Y.; Streaker, E.; Prabakaran, P.; Owens, J.; Dimitrov, D. S.] NCI, NIH, Frederick, MD 21701 USA.
RI Tomaras, Georgia/J-5041-2016
NR 0
TC 0
Z9 0
U1 1
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD OCT
PY 2011
VL 27
IS 10
BP A9
EP A9
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 832GD
UT WOS:000295790500019
ER
PT J
AU Chen, G
Carlson, VCC
Wang, J
Beck, A
Heinz, A
Ron, D
Lovinger, DM
Buck, KJ
AF Chen, Gang
Carlson, Verginia C. Cuzon
Wang, Jun
Beck, Anne
Heinz, Andreas
Ron, Dorit
Lovinger, David M.
Buck, Kari J.
TI Striatal Involvement in Human Alcoholism and Alcohol Consumption, and
Withdrawal in Animal Models
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE c-Fos; Electrophysiology; fMRI; Fyn Kinase; PET; Self-Administration
ID NR2B-CONTAINING NMDA RECEPTORS; ETHANOL WITHDRAWAL; PREFRONTAL CORTEX;
DORSAL STRIATUM; STRIATOPALLIDAL NEURONS; MACACA-FASCICULARIS;
CHROMOSOME-4 LOCUS; VENTRAL STRIATUM; BASAL GANGLIA; C57BL/6J MICE
AB Background: Different regions of the striatum may have distinct roles in acute intoxication, alcohol seeking, dependence, and withdrawal.
Methods: The recent advances are reviewed and discussed in our understanding of the role of the dorsolateral striatum (DLS), dorsomedial striatum (DMS), and ventral striatum in behavioral responses to alcohol, including alcohol craving in abstinent alcoholics, and alcohol consumption and withdrawal in rat, mouse, and nonhuman primate models.
Results: Reduced neuronal activity as well as dysfunctional connectivity between the ventral striatum and the dorsolateral prefrontal cortex is associated with alcohol craving and impairment of new learning processes in abstinent alcoholics. Within the DLS of mice and nonhuman primates withdrawn from alcohol after chronic exposure, glutamatergic transmission in striatal projection neurons is increased, while GABAergic transmission is decreased. Glutamatergic transmission in DMS projection neurons is also increased in ethanol withdrawn rats. Ex vivo or in vivo ethanol exposure and withdrawal causes a long-lasting increase in NR2B subunit-containing NMDA receptor activity in the DMS, contributing to ethanol drinking. Analyses of neuronal activation associated with alcohol withdrawal and site-directed lesions in mice implicate the rostroventral caudate putamen, a ventrolateral segment of the DMS, in genetically determined differences in risk for alcohol withdrawal involved in physical association of the multi-PDZ domain protein, MPDZ, with 5-HT(2C) receptors and/or NR2B.
Conclusions: Alterations of dopaminergic, glutamatergic, and GABAergic signaling within different regions of the striatum by alcohol is critical for alcohol craving, consumption, dependence, and withdrawal in humans and animal models.
C1 [Chen, Gang; Buck, Kari J.] Portland VA Med Ctr, Dept Behav Neurosci, Portland, OR USA.
[Chen, Gang; Buck, Kari J.] Portland VA Med Ctr, Portland Alcohol Res Ctr, Portland, OR USA.
[Chen, Gang; Buck, Kari J.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Carlson, Verginia C. Cuzon; Lovinger, David M.] NIAAA, Lab Integrat Neurosci, Rockville, MD 20852 USA.
[Wang, Jun; Ron, Dorit] Univ Calif San Francisco, Dept Neurol, Ernest Gallo Res Ctr, San Francisco, CA USA.
[Beck, Anne; Heinz, Andreas] Charite, Dept Psychiat & Psychotherapy, D-13353 Berlin, Germany.
RP Chen, G (reprint author), Univ Minnesota, Inst Translat Neurosci, RM 4-140,MBB 2101 6th SE,East Campus, Minneapolis, MN 55455 USA.
EM hdn_2001@yahoo.com
RI Wang, Jun/N-8472-2015; Wang, Jun/M-2337-2016
OI Wang, Jun/0000-0002-0085-4722; Wang, Jun/0000-0002-0085-4722
FU division of Intramural Clinical and Basic Research NIAAA [AA13510,
AA13641]; State of California for medical research on alcohol and
substance abuse through the University of California, San Francisco;
Department of Veterans Affairs; German Research Foundation (Deutsche
Forschungsgemeinschaft) [HE2597/4-3, 7-3]; Bernstein Center for
Computational Neuroscience Berlin [01GQ0411, 01GS08159]; [R01AA014366];
[MH13438]; [AA011114]; [AA10760]; [DA05228]
FX The work described in this review was supported by the division of
Intramural Clinical and Basic Research NIAAA, AA13510, AA13641 (VCCC,
DML); R01AA014366, MH13438, and funds provided by the State of
California for medical research on alcohol and substance abuse through
the University of California, San Francisco (DR); AA011114, AA10760,
DA05228, and the Department of Veterans Affairs (KJB); the German
Research Foundation (Deutsche Forschungsgemeinschaft, HE2597/4-3 and
7-3) and the Bernstein Center for Computational Neuroscience Berlin
(Bundesministerium fur Bildung und Forschung Grants 01GQ0411 and
01GS08159) (AH).
NR 80
TC 34
Z9 36
U1 1
U2 13
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2011
VL 35
IS 10
BP 1739
EP 1748
DI 10.1111/j.1530-0277.2011.01520.x
PG 10
WC Substance Abuse
SC Substance Abuse
GA 824QX
UT WOS:000295218200006
PM 21615425
ER
PT J
AU Schuckit, MA
Smith, TL
Heron, J
Hickman, M
Macleod, J
Lewis, G
Davis, JM
Hibbeln, JR
Brown, S
Zuccolo, L
Miller, LL
Davey-Smith, G
AF Schuckit, Marc A.
Smith, Tom L.
Heron, Jon
Hickman, Matthew
Macleod, John
Lewis, Glyn
Davis, John M.
Hibbeln, Joseph R.
Brown, Sandra
Zuccolo, Luisa
Miller, Laura L.
Davey-Smith, George
TI Testing a Level of Response to Alcohol-Based Model of Heavy Drinking and
Alcohol Problems in 1,905 17-year-olds
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Avon Longitudinal Study of Parents and Children; Alcohol; Level of
Response; Structural Equation Models; Adolescents
ID STRUCTURAL EQUATION MODELS; FAMILY-HISTORY; GENETIC RISK; FIT INDEXES;
QUESTIONNAIRE; PERFORMANCE; MEN; EXPECTANCIES; ADOLESCENTS; SENSITIVITY
AB Background: The low level of response (LR) to alcohol is one of several genetically influenced characteristics that increase the risk for heavy drinking and alcohol problems. Efforts to understand how LR operates through additional life influences have been carried out primarily in modest-sized U.S.-based samples with limited statistical power, raising questions about generalizability and about the importance of components with smaller effects. This study evaluates a full LR-based model of risk in a large sample of adolescents from the United Kingdom.
Methods: Cross-sectional structural equation models were used for the approximate first half of the age 17 subjects assessed by the Avon Longitudinal Study of Parents and Children, generating data on 1,905 adolescents (mean age 17.8 years, 44.2% boys). LR was measured with the Self-Rating of the Effects of Alcohol Questionnaire, outcomes were based on drinking quantities and problems, and standardized questionnaires were used to evaluate peer substance use, alcohol expectancies, and using alcohol to cope with stress.
Results: In this young and large U.K. sample, a low LR related to more adverse alcohol outcomes both directly and through partial mediation by all 3 additional key variables (peer substance use, expectancies, and coping). The models were similar in boys and girls.
Conclusions: These results confirm key elements of the hypothesized LR-based model in a large U.K. sample, supporting some generalizability beyond U.S. groups. They also indicate that with enough statistical power, multiple elements contribute to how LR relates to alcohol outcomes and reinforce the applicability of the model to both genders.
C1 [Schuckit, Marc A.; Smith, Tom L.; Brown, Sandra] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92037 USA.
[Heron, Jon; Hickman, Matthew; Macleod, John; Lewis, Glyn; Zuccolo, Luisa; Miller, Laura L.; Davey-Smith, George] Univ Bristol, Sch Social & Community Med, MRC Ctr Causal Anal Translat Epidemiol, Bristol, Avon, England.
[Davis, John M.] Univ Illinois, Dept Psychiat, Chicago, IL 60612 USA.
[Hibbeln, Joseph R.] NIAAA, LMBB, Bethesda, MD USA.
RP Schuckit, MA (reprint author), Univ Calif San Diego, Dept Psychiat, 8950 Villa La Jolla Dr,Suite B-218, La Jolla, CA 92037 USA.
EM mschuckit@ucsd.edu
RI Lewis, Glyn/E-9944-2012; Price, Katie/H-1931-2012; Heron,
Jon/D-5884-2011; Davey Smith, George/A-7407-2013;
OI Macleod, John/0000-0001-8202-1144; Lewis, Glyn/0000-0001-5205-8245;
Heron, Jon/0000-0001-6199-5644; Davey Smith, George/0000-0002-1407-8314;
Zuccolo, Luisa/0000-0002-7049-3037; Hickman, Matthew/0000-0001-9864-459X
FU U.K. Medical Research Council [74882, G0902144]; Wellcome Trust
[076467]; University of Bristol; NIAAA [AA00526]
FX We are extremely grateful to all the families who took part in this
study, the midwives for their help in recruiting them, and the whole
ALSPAC team, which includes interviewers, computer and laboratory
technicians, clerical workers, research scientists, volunteers,
managers, receptionists, and nurses. The U.K. Medical Research Council
(Grant ref: 74882), the Wellcome Trust (Grant ref: 076467), and the
University of Bristol provided core support for ALSPAC and for general
office, and statistical support was from NIAAA grant AA00526. LZ is
funded by a Population Health Scientist fellowship from the U.K. Medical
Research Council (Grant ref: G0902144). This publication is the work of
the authors and Dr. Marc A. Schuckit will serve as guarantor for the
contents of this paper.
NR 56
TC 14
Z9 14
U1 9
U2 17
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD OCT
PY 2011
VL 35
IS 10
BP 1897
EP 1904
DI 10.1111/j.1530-0277.2011.01536.x
PG 8
WC Substance Abuse
SC Substance Abuse
GA 824QX
UT WOS:000295218200022
PM 21762180
ER
PT J
AU Kroner, BL
Tolunay, HE
Basson, CT
Pyeritz, RE
Holmes, KW
Maslen, CL
Milewicz, DM
LeMaire, SA
Hendershot, T
Desvigne-Nickens, P
Devereux, RB
Dietz, HC
Song, HK
Ringer, D
Mitchell, M
Weinsaft, JW
Ravekes, W
Menashe, V
Eagle, KA
AF Kroner, Barbara L.
Tolunay, H. Eser
Basson, Craig T.
Pyeritz, Reed E.
Holmes, Kathryn W.
Maslen, Cheryl L.
Milewicz, Dianna M.
LeMaire, Scott A.
Hendershot, Tabitha
Desvigne-Nickens, Patrice
Devereux, Richard B.
Dietz, Harry C.
Song, Howard K.
Ringer, Danny
Mitchell, Megan
Weinsaft, Jonathan W.
Ravekes, William
Menashe, Victor
Eagle, Kim A.
CA GenTAC Registry Consortium
TI The National Registry of Genetically Triggered Thoracic Aortic Aneurysms
and Cardiovascular Conditions (GenTAC): Results from phase I and
scientific opportunities in phase II
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID MARFAN-SYNDROME
AB Background Genetically triggered thoracic aortic conditions (GenTACs) represent an important problem for patients and their families. Accordingly, the National Heart, Lung, and Blood Institute established the first phase of its national GenTAC Registry in 2006.
Enrollment and Diagnoses Between 2007 and 2010, 6 enrolling centers established the GenTAC I Registry consisting of 2,046 patients (Marfan syndrome 576 [28.2%], bicuspid aortic valve disease 504 [24.6%], aneurysm or dissection age <50 years 369 [18%], and others). Biologic samples for DNA analyses (white blood cells or saliva) are available in 97%, and stored plasma is available in 60% of enrollees.
Results Initial scientific inquiry using the GenTAC Registry has included validation studies of genetic causes for aortic syndromes, potential usefulness of transforming growth factor beta (TGFB) blood levels in Marfan subjects, and current surgical approaches to ascending aortic conditions.
Future Opportunity The second phase of GenTAC will allow biannual follow-up of GenTAC I enrollees for up to 9 years, enrollment of an additional 1,500 subjects, further integration of imaging findings with clinical and genetic data through utilization of an imaging core laboratory, important validation of phenotype-genotype correlations through a phenotyping core laboratory, and integration of a scientific advisory committee to help define the full range and depth of the Registry's scientific capabilities. The registry resources are available to the external scientific community through an application process accessible at https://gentac.rti.org. (Am Heart J 2011;162:627-632.e1.)
C1 [Kroner, Barbara L.; Hendershot, Tabitha; Ringer, Danny] RTI Int, Rockville, MD 20852 USA.
[Tolunay, H. Eser; Desvigne-Nickens, Patrice; Mitchell, Megan] NIH, Bethesda, MD 20892 USA.
[Basson, Craig T.; Devereux, Richard B.; Weinsaft, Jonathan W.; Ravekes, William] Weill Cornell Med Coll, New York, NY USA.
[Pyeritz, Reed E.] Univ Penn, Philadelphia, PA 19104 USA.
[Holmes, Kathryn W.; Dietz, Harry C.] Johns Hopkins Univ, Baltimore, MD USA.
[Maslen, Cheryl L.; Song, Howard K.; Menashe, Victor] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Milewicz, Dianna M.] Univ Texas Hlth Sci Ctr, Houston, TX USA.
[LeMaire, Scott A.] Baylor Coll Med, Houston, TX 77030 USA.
[Eagle, Kim A.] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Kroner, BL (reprint author), RTI Int, 6110 Execut Blvd,Suite 901, Rockville, MD 20852 USA.
EM byk@rti.org
FU NHLBI NIH HHS [N01 HV68199-3-0-0]
NR 9
TC 16
Z9 17
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD OCT
PY 2011
VL 162
IS 4
BP 627
EP U77
DI 10.1016/j.ahj.2011.07.002
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 833ZO
UT WOS:000295925100010
PM 21982653
ER
PT J
AU Pauly, DF
Johnson, BD
Anderson, RD
Handberg, EM
Smith, KM
Cooper-DeHoff, RM
Sopko, G
Sharaf, BM
Kelsey, SF
Merz, CNB
Pepine, CJ
AF Pauly, Daniel F.
Johnson, B. Delia
Anderson, R. David
Handberg, Eileen M.
Smith, Karen M.
Cooper-DeHoff, Rhonda M.
Sopko, George
Sharaf, Barry M.
Kelsey, Sheryl F.
Merz, C. Noel Bairey
Pepine, Carl J.
TI In women with symptoms of cardiac ischemia, nonobstructive coronary
arteries, and microvascular dysfunction, angiotensin-converting enzyme
inhibition is associated with improved microvascular function: A
double-blind randomized study from the National Heart, Lung and Blood
Institute Women's Ischemia Syndrome Evaluation (WISE)
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID ACUTE MYOCARDIAL-INFARCTION; LONG-TERM OUTCOMES; HYPERTENSIVE PATIENTS;
CHEST-PAIN; SYNDROME-X; GENDER-DIFFERENCES; VASCULAR-DISEASE; FLOW
VELOCITY; RESERVE; ANGINA
AB Background We investigated the role of the renin-angiotensin system in women with signs and symptoms of ischemia without obstructive coronary artery disease (CAD). Although microvascular dysfunction has been suggested to explain this syndrome and recently was found to predict adverse outcomes, the mechanisms and treatments remain unclear.
Methods In a substudy within the WISE, 78 women with microvascular dysfunction (coronary flow reserve [CFR] <3.0 following adenosine) and no obstructive CAD were randomly assigned to either an angiotensin-converting enzyme inhibition (ACE-I) with quinapril or a placebo treatment group. The primary efficacy parameter was CFR at 16 weeks adjusted for baseline characteristics and clinical site. The secondary response variable was freedom from angina symptoms assessed using the Seattle Angina Questionnaire.
Results A total of 61 women completed the 16-week treatment period with repeat CFR measurements, and treatment was well tolerated. For the primary outcome, at 16 weeks, CFR improved more with ACE-I than placebo (P < .02). For the secondary outcome of symptom improvement, ACE-I treatment (P = .037) and CFR increase (P = .008) both contributed.
Conclusions Microvascular function improves with ACE-I therapy in women with signs and symptoms of ischemia without obstructive CAD. This improvement is associated with reduction in angina. The beneficial response of the coronary microvasculature was limited to women with lower baseline CFR values, suggesting that the renin-angiotensin system may be more involved among women with more severe microvascular defects. (Am Heart J 2011;162:678-84.)
C1 [Pepine, Carl J.] Univ Florida, Coll Med, Div Cardiovasc Med, Gainesville, FL 32610 USA.
[Johnson, B. Delia; Kelsey, Sheryl F.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Cooper-DeHoff, Rhonda M.] Univ Florida, Dept Pharmacotherapy & Translat Res, Gainesville, FL 32610 USA.
[Sopko, George] NHLBI, NIH, Bethesda, MD 20892 USA.
[Sharaf, Barry M.] Rhode Isl Hosp, Div Cardiol, Providence, RI USA.
[Merz, C. Noel Bairey] Cedars Sinai Med Ctr, Inst Heart, Los Angeles, CA 90048 USA.
RP Pepine, CJ (reprint author), Univ Florida, Coll Med, Div Cardiovasc Med, POB 100277, Gainesville, FL 32610 USA.
EM pepincj@medicine.ufl.edu
FU National Heart, Lung and Blood Institute [N01-HV-68161, N01-HV-68162,
N01-HV-68163, N01-HV-68164]; National Center for Research Resources
[MO1-RR00425]; Gustavus and Louis Pfeiffer Research Foundation,
Denville, New Jersey; Women's Guild of Cedars-Sinai Medical Center, Los
Angeles, California; Ladies Hospital Aid Society of Western
Pennsylvania, Pittsburgh, Pennsylvania; Pfizer Labs; Edythe L. Broad
Endowment for Women's Heart Research, Los Angeles, California; Eminent
Scholar Research Chair, AHA Suncoast Chapter; NIH/NHLBI [5 U01
HL087366-04, 5 R01 HL091005-03, 5 R01 HL090957-03, 2 U01 GM074492-06];
NIH/AG [3 U01 AG022376-05A2S1]; NIH/NCRR [5 UL1 RR029890-02];
[U0164829]; [U01 HL649141]; [U01 HL649241]
FX This work was supported by contracts from the National Heart, Lung and
Blood Institute, nos. N01-HV-68161, N01-HV-68162, N01-HV-68163,
N01-HV-68164; grants U0164829, U01 HL649141, U01 HL649241; a GCRC grant
MO1-RR00425 from the National Center for Research Resources; and grants
from the Gustavus and Louis Pfeiffer Research Foundation, Denville, New
Jersey; Women's Guild of Cedars-Sinai Medical Center, Los Angeles,
California; Ladies Hospital Aid Society of Western Pennsylvania,
Pittsburgh, Pennsylvania; Pfizer Labs; and The Edythe L. Broad Endowment
for Women's Heart Research, Los Angeles, California. Dr Pepine was
funded, in part, by the Eminent Scholar Research Chair, AHA Suncoast
Chapter; by NIH/NHLBI grants 5 U01 HL087366-04, 5 R01 HL091005-03, 5 R01
HL090957-03, 2 U01 GM074492-06; NIH/AG grant 3 U01 AG022376-05A2S1;
NIH/NCRR grant 5 UL1 RR029890-02; and a research grant from Pfizer Labs.
NR 38
TC 38
Z9 40
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD OCT
PY 2011
VL 162
IS 4
BP 678
EP 684
DI 10.1016/j.ahj.2011.07.011
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 833ZO
UT WOS:000295925100017
PM 21982660
ER
PT J
AU Cheng, S
Fox, CS
Larson, MG
Massaro, JM
McCabe, EL
Khan, AM
Levy, D
Hoffmann, U
O'Donnell, CJ
Miller, KK
Newton-Cheh, C
Coviello, AD
Bhasin, S
Vasan, RS
Wang, TJ
AF Cheng, Susan
Fox, Caroline S.
Larson, Martin G.
Massaro, Joseph M.
McCabe, Elizabeth L.
Khan, Abigail May
Levy, Daniel
Hoffmann, Udo
O'Donnell, Christopher J.
Miller, Karen K.
Newton-Cheh, Christopher
Coviello, Andrea D.
Bhasin, Shalender
Vasan, Ramachandran S.
Wang, Thomas J.
TI Relation of Visceral Adiposity to Circulating Natriuretic Peptides in
Ambulatory Individuals
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID GLOMERULAR-FILTRATION-RATE; METABOLIC RISK-FACTORS; INSULIN-RESISTANCE;
BODY-MASS; ASSOCIATION; ATRIAL; SENSITIVITY; DIAGNOSIS; IMPACT; AGE
AB Natriuretic peptides have important roles in the regulation of vasomotor tone, salt homeostasis, and ventricular remodeling. Lower natriuretic peptide levels observed in obese individuals may underlie the greater cardiovascular risk associated with obesity. Thus the aim of this study was to determine whether lower natriuretic peptide levels in obesity are attributable to differences in regional fat distribution. We investigated the relation of plasma N-terminal pro B-type natriuretic peptide (NT pro-BNP) to regional adiposity in 1,873 community-based individuals (46% women, mean age 45 years). Subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) volumes were measured by multidetector computed tomography. In gender-specific multivariable analyses adjusting for age and blood pressure, log NT pro-BNP was inversely associated with VAT in men (beta -0.11 per standard deviation increment, p < 0.001) and women (beta -0.19, p < 0.001). Log NT pro-BNP was inversely associated with SAT in women only (beta -0.14, p < 0.001). In models containing VAT and SAT, only VAT was significantly associated with log NT pro-BNP (men, beta -0.137, p < 0.001; women, beta -0.184, p < 0.001). VAT remained associated with log NT pro-BNP even after adjustment for body mass index and waist circumference (beta -0.119, p < 0.001) and in analyses restricted to nonobese patients (beta -0.165, p < 0.001). Adjustment for insulin resistance attenuated the associations of NT pro-BNP with VAT and SAT. In conclusion, this study demonstrates that circulating NT pro-BNP is related to variations in regional and particularly visceral adiposity. These findings suggest that excess visceral adiposity and concomitant hyperinsulinemia may contribute to the natriuretic peptide "deficiency" observed in obesity. (C) 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;108:979-984)
C1 [Cheng, Susan; Fox, Caroline S.; Larson, Martin G.; Massaro, Joseph M.; McCabe, Elizabeth L.; Levy, Daniel; O'Donnell, Christopher J.; Newton-Cheh, Christopher; Coviello, Andrea D.; Vasan, Ramachandran S.; Wang, Thomas J.] Framingham Heart Dis Epidemiol Study, Framingham, MA 01702 USA.
[Cheng, Susan; McCabe, Elizabeth L.; Khan, Abigail May; O'Donnell, Christopher J.; Newton-Cheh, Christopher; Wang, Thomas J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[Hoffmann, Udo] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Miller, Karen K.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neuroendocrine Unit, Boston, MA 02115 USA.
[Newton-Cheh, Christopher] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Human Genet Res, Boston, MA 02115 USA.
[Cheng, Susan] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc Med,Dept Med, Boston, MA 02115 USA.
[Fox, Caroline S.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Endocrinol Metab & Diabet,Dept Med, Boston, MA 02115 USA.
[Levy, Daniel; O'Donnell, Christopher J.] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
[Larson, Martin G.; Massaro, Joseph M.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Levy, Daniel; Coviello, Andrea D.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Dept Med, Prevent Med Sect, Boston, MA 02118 USA.
[Levy, Daniel; Coviello, Andrea D.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Dept Med, Cardiol Sect, Boston, MA 02118 USA.
[Coviello, Andrea D.; Bhasin, Shalender] Boston Univ, Sch Med, Sect Endocrinol Diabet & Nutr, Boston, MA 02118 USA.
[Newton-Cheh, Christopher] Harvard Univ, Broad Inst, Program Med & Populat Genet, Cambridge, MA 02138 USA.
[Newton-Cheh, Christopher] MIT, Cambridge, MA 02139 USA.
RP Wang, TJ (reprint author), Framingham Heart Dis Epidemiol Study, Framingham, MA 01702 USA.
EM tjwang@partners.org
OI Massaro, Joseph/0000-0002-2682-4812; Larson, Martin/0000-0002-9631-1254;
Ramachandran, Vasan/0000-0001-7357-5970
FU National Heart, Lung, and Blood Institute of the National Institutes of
Health, Bethesda, Maryland [N01-HC-25195, R01-HL-086875]; Ellison
Foundation, Bethesda, Maryland
FX This work was supported in part by Contracts N01-HC-25195 and
R01-HL-086875 from the National Heart, Lung, and Blood Institute of the
National Institutes of Health, Bethesda, Maryland (Dr. Wang and Dr.
Newton-Cheh) and the Ellison Foundation, Bethesda, Maryland (Dr. Cheng).
NR 30
TC 23
Z9 23
U1 0
U2 2
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9149
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD OCT 1
PY 2011
VL 108
IS 7
BP 979
EP 984
DI 10.1016/j.amjcard.2011.05.033
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 833DY
UT WOS:000295863200014
PM 21813106
ER
PT J
AU Yasuda, M
Wilson, DR
Fugmann, SD
Moaddel, R
AF Yasuda, M.
Wilson, D. R.
Fugmann, S. D.
Moaddel, R.
TI Synthesis and Characterization of SIRT6 Protein Coated Magnetic Beads:
Identification of a Novel Inhibitor of SIRT6 Deacetylase from Medicinal
Plant Extracts
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID HISTONE-DEACETYLASE; ADP-RIBOSYLTRANSFERASE; GENE-EXPRESSION; CHROMATIN;
REGULATORS; GLUCOSE; LIGAND; CANCER; DRUGS
AB SIRT6 is a histone deacetylase that has been proposed as a potential therapeutic target for metabolic disorders and the prevention of age-associated diseases. Thus, the identification of compounds that modulate SIRT6 activity could be of great therapeutic importance. The aim of this study was to develop a screening method for the identification of novel modulators of SIRT6 from a natural plant extract. We immobilized SIRT6 onto the surface of magnetic beads, and assessed SIRT6 enzymatic activity on synthetic acetylated histone tails (H3K9Ac) by measuring products of the deacetylation process. The SIRT6 coated magnetic beads were then suspended in fenugreek seed extract (Trigonella foenum-graecum) as a bait to identify active ligands that suppress SIRT6 activity. While the entire extract also inhibited SIRT6 activity in a cell-based assay, the inhibitory effect of two flavonoids from this extract, quercetin and vitexin, was only detected in vitro. This is the first report on the use of protein-coated magnetic beads for the identification of an active ligand from a botanical matrix, and it sets the basis for the de novo identification of SIRT6 modulators from complex biological mixtures.
C1 [Moaddel, R.] NIA, Biomed Res Ctr, Bioanalyt & Drug Discovery Unit, Clin Invest Lab,NIH, Baltimore, MD 21224 USA.
RP Moaddel, R (reprint author), NIA, Biomed Res Ctr, Bioanalyt & Drug Discovery Unit, Clin Invest Lab,NIH, Suite 100,8B131 Biomed Res Ctr,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM moaddelru@grc.nia.nih.gov
FU NIH, National Institute on Aging
FX This research was supported by the Intramural Research Program of the
NIH, National Institute on Aging. There are no financial conflicts. We
would like to thank Dr. Michel Bernier for critical review of the
manuscript and Dr. Irving W. Wainer for his continued support.
NR 26
TC 30
Z9 31
U1 0
U2 35
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 OCT 1
PY 2011
VL 83
IS 19
BP 7400
EP 7407
DI 10.1021/ac201403y
PG 8
WC Chemistry, Analytical
SC Chemistry
GA 825SY
UT WOS:000295303600024
PM 21854049
ER
PT J
AU Cella, D
Nowinski, C
Peterman, A
Victorson, D
Miller, D
Lai, JS
Moy, C
AF Cella, David
Nowinski, Cindy
Peterman, Amy
Victorson, David
Miller, Deborah
Lai, Jin-Shei
Moy, Claudia
TI The Neurology Quality-of-Life Measurement Initiative
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Clinical research; Health-related quality of life; Neurology;
Patient-reported outcomes; Quality of life; Rehabilitation
AB Cella D, Nowinski C, Peterman A, Victorson D, Miller D, Lai J-S, Moy C. The neurology quality-of-life measurement initiative. Arch Phys Med Rehabil 2011;92 (10 Suppl 1):S28-S36.
Objective: To describe the development and calibration of the banks and scales of the Quality of Life in Neurological Disorders (Neuro-QOL) project, commissioned by the National Institute of Neurological Disorders and Stroke to develop a bilingual (English/Spanish), clinically relevant, and psychometrically robust health-related quality-of-life (HRQOL) assessment tool.
Design: Classic and modern test construction methods were used, including input from essential stakeholder groups.
Setting: An online patient panel testing service and 11 academic medical centers and clinics from across the United States and Puerto Rico that treat major neurologic disorders.
Participants: Adult and pediatric patients representing different neurologic disorders specified in this study, proxy respondents for select conditions (stroke, pediatric conditions), and English- and Spanish-speaking participants from the general population.
Interventions: Not applicable.
Main Outcome Measures: Multiple generic and condition-specific measures used to provide construct validity evidence for the new Neuro-QOL tool.
Results: Neuro-QOL has developed 14 generic item banks and 8 targeted scales to assess HRQOL in 5 adult (stroke, multiple sclerosis, Parkinson's disease, epilepsy, amyotrophic lateral sclerosis) and 2 pediatric conditions (epilepsy, muscular dystrophies).
Conclusions: The Neuro-QOL system will continue to evolve, with validation efforts in clinical populations and new bank development in health domains not presently included. The potential for Neuro-QOL measures in rehabilitation research and clinical settings is discussed.
C1 [Cella, David; Nowinski, Cindy; Victorson, David; Lai, Jin-Shei] Northwestern Univ, Dept Med Social Sci, Feinberg Sch Med, Chicago, IL 60611 USA.
[Peterman, Amy] Univ N Carolina, Dept Psychol, Charlotte, NC 28223 USA.
[Miller, Deborah] Cleveland Clin Fdn, Mellen Ctr Multiple Sclerosis Treatment & Res, Cleveland, OH 44195 USA.
[Moy, Claudia] NINDS, NIH, Bethesda, MD 20892 USA.
RP Cella, D (reprint author), Northwestern Univ, Dept Med Social Sci, Feinberg Sch Med, 710 N Lake Shore Dr,Ste 729, Chicago, IL 60611 USA.
EM d-cella@northwestern.edu
FU National Institute of Neurological Disorders and Stroke
[HHSN265200423601C]
FX Supported by the National Institute of Neurological Disorders and Stroke
(contract no. HHSN265200423601C).
NR 11
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U1 2
U2 11
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0003-9993
J9 ARCH PHYS MED REHAB
JI Arch. Phys. Med. Rehabil.
PD OCT
PY 2011
VL 92
IS 10
SU 1
BP S28
EP S36
DI 10.1016/j.apmr.2011.01.025
PG 9
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 833DG
UT WOS:000295861400005
PM 21958920
ER
PT J
AU Quatrano, LA
Cruz, TH
AF Quatrano, Louis A.
Cruz, Theresa H.
TI Future of Outcomes Measurement: Impact on Research in Medical
Rehabilitation and Neurologic Populations
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Outcome measures; Rehabilitation
ID QUALITY-OF-LIFE; HEALTH OUTCOMES; PARTICIPATION; INJURY
AB Quatrano LA, Cruz TH. Future of outcomes measurement: impact on research in medical rehabilitation and neurologic populations. Arch Phys Med Rehabil 2011;92 (10 Suppl 1):S7-11.
The National Institutes of Health (NIH) has embraced the investigation and development of health-related patient-reported outcomes (PROs) for their potential use in clinical trials, as well as in examining health care reimbursements and regulatory affairs. The NIH has 3 major programs to address this topic: the Patient-Reported Outcomes Measurement Information System (PROMIS), NIH Toolbox for Assessment of Neurological and Behavioral Function, and Quality of Life in Neurological Disorders (Neuro-QOL), a health-related quality-of-life assessment tool for adults and children with neurologic disorders. These initiatives are focused on developing, validating, and measuring aspects of health by using assessment tools that bridge disease type. Given that rehabilitation takes place across a variety of environments with differing levels of specialized equipment and skilled personnel, PROs may provide consistent measures over time and therefore are anticipated to have substantial impacts on the medical rehabilitation community. Despite their advantages, the widespread use of PROs in rehabilitation faces significant and diverse challenges. This article describes the background behind the NIH PRO initiatives and illustrates both potential benefits and challenges to PRO use in the medical rehabilitation setting.
C1 [Quatrano, Louis A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, BSRE, NCMRR, NIH, Bethesda, MD 20892 USA.
RP Quatrano, LA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, BSRE, NCMRR, NIH, 6100 Execut Blvd,Rm 2A03,MSC 7510, Bethesda, MD 20892 USA.
EM quatranol@mail.nih.gov
FU Northwestern University; technology center (Northwestern University);
network center (American Institutes for Research); State University of
New York
FX PROMIS II was funded by cooperative agreements with a statistical center
(Northwestern University, Principal Investigator [PI]: David Cella,
PhD), a technology center (Northwestern University, PI: Richard C.
Gershon, PhD), a network center (American Institutes for Research, PI:
Susan [San] D. Keller, PhD), and 13 primary research sites (State
University of New York, Stonybrook, PIs: Joan E. Broderick, PhD, and
Arthur A. Stone, PhD; University of Washington, Seattle, Pis: Heidi M.
Crane, MD, MPH, Paul K. Crane, MD, MPH, and Donald L. Patrick, PhD;
University of Washington, PI: Dagmar Amtmann, PhD; University of North
Carolina, Chapel Hill, PI: Darren A. DeWalt, MD; Children's Hospital of
Philadelphia, PI: Christopher Forrest, MD; Stanford University, PI:
James M. Fries, MD; Boston University, PI: Stephen M. Haley, PhD;
University of Michigan, Ann Arbor, PI: David Scott Tulsky, PhD;
University of California, Los Angeles, Pis: Dinesh Khanna, MD, and
Brennan Spiegel, MD, MSHS; University of Pittsburgh, PI: Paul A.
Pilkonis, PhD; Georgetown University, Washington, DC, Pis: Carol M.
Moinpour, PhD, and Arnold L. Pitosky, PhD; Children's Hospital Medical
Center, Cincinnati, PI: Esi M. Morgan Dewitt, MD; University of
Maryland, Baltimore, PI: Lisa M. Shulman, MD; and Duke University, PI:
Kevin P. Weinfurt, PhD). NIH Science Officers on this project have
included Vanessa Ameen, MD, Susan Czajkowski, PhD, Basil Eldadah, MD,
PhD, Lawrence Fox, MD, PhD, Lynne Haverkos, MD, MPH, Thomas Hilton, PhD,
Laura Lee Johnson, PhD, Michael Kozak, PhD, Peter Lyster, PhD, Donald
Mattison, MD, Claudia Moy, PhD, Louis Quatrano, PhD, Bryce Reeve, PhD,
Ellen Werner, PhD, and James Witter, MD, PhD.
NR 23
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U1 0
U2 6
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 OCT
PY 2011
VL 92
IS 10
SU 1
BP S7
EP S11
DI 10.1016/j.apmr.2010.08.032
PG 5
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 833DG
UT WOS:000295861400002
PM 21958925
ER
PT J
AU Young, K
Drevets, WC
Schulkin, J
Erickson, K
AF Young, Kymberly
Drevets, Wayne C.
Schulkin, Jay
Erickson, Kristine
TI Dose-Dependent Effects of Hydrocortisone Infusion on Autobiographical
Memory Recall
SO BEHAVIORAL NEUROSCIENCE
LA English
DT Article
DE cortisol; autobiographical memory; human; declarative memory; depression
ID GLUCOCORTICOID-INDUCED IMPAIRMENT; HEALTHY-YOUNG MEN; DECLARATIVE
MEMORY; EPISODIC MEMORY; CORTISOL-LEVELS; SEX-DIFFERENCES; HORMONAL
RESPONSES; MAJOR DEPRESSION; PLASMA-CORTISOL; ACUTE STRESS
AB The glucocorticoid hormone cortisol has been shown to impair episodic memory performance. The present study examined the effect of two doses of hydrocortisone (synthetic cortisol) administration on autobiographical memory retrieval. Healthy volunteers (n = 66) were studied on two separate visits, during which they received placebo and either moderate-dose (0.15 mg/kg IV; n = 33) or high-dose (0.45 mg/kg IV; n = 33) hydrocortisone infusion. From 75 to 150 min post-infusion subjects performed an Autobiographical Memory Test and the California Verbal Learning Test (CVLT). The high-dose hydrocortisone administration reduced the percent of specific memories recalled (p =.04), increased the percent of categorical (nonspecific) memories recalled (p <.001), and slowed response times for categorical memories (p <.001), compared with placebo performance. Under moderate-dose hydrocortisone the autobiographical memory performance did not change significantly with respect to percent of specific or categorical memories recalled or reaction times. Performance on the CVLT was not affected by hydrocortisone. These findings suggest that cortisol affects accessibility of autobiographical memories in a dose-dependent manner. Specifically, administration of hydrocortisone at doses analogous to those achieved under severe psychosocial stress impaired the specificity and speed of retrieval of autobiographical memories.
C1 [Young, Kymberly; Drevets, Wayne C.] Laureate Inst Brain Res, Tulsa, OK 74136 USA.
[Young, Kymberly; Drevets, Wayne C.; Erickson, Kristine] NIMH, Sect Neuroimaging Mood & Anxiety Disorders, NIH, Bethesda, MD 20892 USA.
[Young, Kymberly; Erickson, Kristine] American Univ, Dept Psychol, Washington, DC 20016 USA.
[Drevets, Wayne C.] Univ Oklahoma, Coll Med, Dept Psychiat, Norman, OK 73019 USA.
[Schulkin, Jay] Georgetown Univ, Dept Neurosci, Washington, DC 20057 USA.
RP Young, K (reprint author), Laureate Inst Brain Res, 6655 S Yale Ave, Tulsa, OK 74136 USA.
EM kyoung@laureateinstitute.org
OI Young, Kymberly/0000-0001-5133-2142
FU NIMH [Z01-MH002814]
FX We acknowledge the support of the NIMH Intramural Research Program, and
Joan Williams and Michele Drevets for assistance with recruitment and
clinical assessment of the participants. Funding for this study was
provided by NIMH Z01-MH002814. The DIRP within NIMH provided critical
peer review for the study design and approval of manuscript submission.
NIMH had no further role in the collection, analysis, and interpretation
of data, or in the writing of the report.
NR 49
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U1 2
U2 11
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0735-7044
J9 BEHAV NEUROSCI
JI Behav. Neurosci.
PD OCT
PY 2011
VL 125
IS 5
BP 735
EP 741
DI 10.1037/a0024764
PG 7
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 826GA
UT WOS:000295339400006
PM 21942435
ER
PT J
AU Stangl, B
Hirshman, E
Verbalis, J
AF Stangl, Bethany
Hirshman, Elliot
Verbalis, Joseph
TI Administration of Dehydroepiandrosterone (DHEA) Enhances Visual-Spatial
Performance in Postmenopausal Women
SO BEHAVIORAL NEUROSCIENCE
LA English
DT Article
DE dehydroepiadrosterone (DHEA); postmenopausal women; cognition;
visual-spatial tasks; androgens
ID TANDEM MASS-SPECTROMETRY; HEALTHY OLDER MEN; WORKING-MEMORY;
LIQUID-CHROMATOGRAPHY; REPLACEMENT THERAPY; HORMONE REPLACEMENT;
EXPLICIT MEMORY; ELDERLY-WOMEN; SEX STEROIDS; TESTOSTERONE
AB The current article examines the effect of administering dehydroepiandrosterone (DHEA) on visualspatial performance in postmenopausal women (N = 24, ages 55-80). The concurrent reduction of serum DHEA levels and visual-spatial performance in this population, coupled with the documented effects of DHEA's androgenic metabolites on visual-spatial performance, suggests that DHEA administration may enhance visual-spatial performance. The current experiment used a double-blind, placebo-controlled crossover design in which 50 mg of oral DHEA was administered daily in the drug condition to explore this hypothesis. Performance on the Mental Rotation, Subject-Ordered Pointing, Fragmented Picture Identification, Perceptual Identification, Same-Different Judgment, and Visual Search tasks and serum levels of DHEA, DHEAS, testosterone, estrone, and cortisol were measured in the DHEA and placebo conditions. In contrast to prior experiments using the current methodology that did not demonstrate effects of DHEA administration on episodic and short-term memory tasks, the current experiment demonstrated large beneficial effects of DHEA administration on Mental Rotation, Subject-Ordered Pointing, Fragmented Picture Identification, Perceptual Identification, and Same-Different Judgment. Moreover, DHEA administration enhanced serum levels of DHEA, DHEAS, testosterone, and estrone, and regression analyses demonstrated that levels of DHEA and its metabolites were positively related to cognitive performance on the visual-spatial tasks in the DHEA condition.
C1 [Hirshman, Elliot] San Diego State Univ, Off President, Dept Psychol, San Diego, CA 92182 USA.
[Stangl, Bethany] NIAAA, NIH, Bethesda, MD 20892 USA.
[Verbalis, Joseph] Georgetown Univ, Med Ctr, Dept Med, Washington, DC 20057 USA.
RP Hirshman, E (reprint author), San Diego State Univ, Off President, Dept Psychol, 5500 Campanile Dr, San Diego, CA 92182 USA.
EM ellioth@sdsu.edu
FU National Institute on Aging of the National Institutes of Health
[27675-1-CCLS-2035F, 5RO1AG020543]
FX The work presented here was supported by the National Institute on Aging
of the National Institutes of Health grant (27675-1-CCLS-2035F,
5RO1AG020543). Correspondence should be directed to the second author at
ellioth@sdsu.edu
NR 52
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Z9 9
U1 2
U2 7
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0735-7044
J9 BEHAV NEUROSCI
JI Behav. Neurosci.
PD OCT
PY 2011
VL 125
IS 5
BP 742
EP 752
DI 10.1037/a0025151
PG 11
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 826GA
UT WOS:000295339400007
PM 21942436
ER
PT J
AU Bond, LM
Brandstaetter, H
Sellers, JR
Kendrick-Jones, J
Buss, F
AF Bond, Lisa M.
Brandstaetter, Hemma
Sellers, James R.
Kendrick-Jones, John
Buss, Folma
TI Myosin motor proteins are involved in the final stages of the secretory
pathways
SO BIOCHEMICAL SOCIETY TRANSACTIONS
LA English
DT Article
DE actin; exocytosis; fusion; myosin; secretion; vesicle
ID CELL RIBBON SYNAPSES; F-ACTIN; PLASMA-MEMBRANE; FUSION PORE; CHROMAFFIN
CELLS; VESICLE DOCKING; GOLGI-COMPLEX; EXOCYTOSIS; VI; VA
AB In eukaryotes, the final steps in both the regulated and constitutive secretory pathways can be divided into four distinct stages: (i) the 'approach' of secretory vesicles/granules to the PM (plasma membrane), (ii) the 'docking' of these vesicles/granules at the membrane itself, (iii) the 'priming' of the secretory vesicles/granules for the fusion process, and, finally, (iv) the 'fusion' of vesicular/granular membranes with the PM to permit content release from the cell. Recent work indicates that non-muscle myosin II and the unconventional myosin motor proteins in classes 1c/1e, Va and VI are specifically involved in these final stages of secretion. In the present review, we examine the roles of these myosins in these stages of the secretory pathway and the implications of their roles for an enhanced understanding of secretion in general.
C1 [Bond, Lisa M.; Brandstaetter, Hemma; Buss, Folma] Univ Cambridge, Cambridge Inst Med Res, Cambridge CB2 0XY, England.
[Bond, Lisa M.; Sellers, James R.] NHLBI, Lab Mol Physiol, NIH, Bethesda, MD 20892 USA.
[Kendrick-Jones, John] MRC, Mol Biol Lab, Cambridge CB2 2QH, England.
RP Buss, F (reprint author), Univ Cambridge, Cambridge Inst Med Res, Wellcome Trust MRC Bldg,Hills Rd, Cambridge CB2 0XY, England.
EM fb1@mole.bio.cam.ac.uk
FU Wellcome Trust; Winston Churchill Foundation of the United States;
NIH-Oxford-Cambridge; Medical Research Council
FX This work was funded by the Wellcome Trust (to F.B. and H.B.), a
scholarship from the Winston Churchill Foundation of the United States
(to LB.) and an NIH-Oxford-Cambridge Ph.D. studentship (to LB.), and was
supported by the Medical Research Council (to J.K.J.). The Cambridge
Institute for Medical Research is in receipt of a strategic award from
the Wellcome Trust.
NR 50
TC 18
Z9 18
U1 3
U2 15
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0300-5127
J9 BIOCHEM SOC T
JI Biochem. Soc. Trans.
PD OCT
PY 2011
VL 39
BP 1115
EP 1119
DI 10.1042/BST0391115
PN 5
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 831QC
UT WOS:000295745200001
PM 21936774
ER
PT J
AU Wang, AB
Ma, XF
Conti, MA
Adelstein, RS
AF Wang, Aibing
Ma, Xuefei
Conti, Mary Anne
Adelstein, Robert S.
TI Distinct and redundant roles of the non-muscle myosin II isoforms and
functional domains
SO BIOCHEMICAL SOCIETY TRANSACTIONS
LA English
DT Article
DE cell-cell adhesion; cell migration; hydrocephalus; myosin; non-muscle
myosin II
ID HEAVY-CHAIN; MYH9-RELATED DISEASE; CELL-ADHESION; ABLATION; MUTATION;
MICE; DEFECTS; BRAIN
AB We propose that the in vivo functions of NM II (non-muscle myosin II) can be divided between those that depend on the N-terminal globular motor domain and those less dependent on motor activity but more dependent on the C-terminal domain. The former, being more dependent on the kinetic properties of NM II to translocate actin filaments, are less amenable to substitution by different NM II isoforms, whereas the in vivo functions of the latter, which involve the structural properties of NM II to cross-link actin filaments, are more amenable to substitution. In light of this hypothesis, we examine the ability of NM II-A, as well as a motor-compromised form of NM II-B, to replace NM II-B and rescue neuroepithelial cell-cell adhesion defects and hydrocephalus in the brain of NM II-B-depleted mice. We also examine the ability of NM II-B as well as chimaeric forms of NM II(II-A head and II-B tail and vice versa) to substitute for NM II-A in cell-cell adhesions in II-A-ablated mice. However, we also show that certain functions, such as neuronal cell migration in the developing brain and vascularization of the mouse embryo and placenta, specifically require NM II-B and II-A respectively.
C1 [Wang, Aibing; Ma, Xuefei; Conti, Mary Anne; Adelstein, Robert S.] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
RP Adelstein, RS (reprint author), NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
EM adelster@mail.nih.gov
OI Adelstein, Robert/0000-0002-8683-2144
FU National Heart, Lung, and Blood Institute/National Institutes of Health,
Division of Intramural Research
FX This work was funded by the National Heart, Lung, and Blood
Institute/National Institutes of Health, Division of Intramural
Research.
NR 19
TC 29
Z9 31
U1 2
U2 15
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0300-5127
J9 BIOCHEM SOC T
JI Biochem. Soc. Trans.
PD OCT
PY 2011
VL 39
BP 1131
EP 1135
DI 10.1042/BST0391131
PN 5
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 831QC
UT WOS:000295745200004
PM 21936777
ER
PT J
AU Siththanandan, VB
Sellers, JR
AF Siththanandan, Verl B.
Sellers, James R.
TI Regulation of myosin 5a and myosin 7a
SO BIOCHEMICAL SOCIETY TRANSACTIONS
LA English
DT Article
DE actin; ATPase activity; calcium; myosin
ID GLOBULAR TAIL DOMAIN; DUTY RATIO MOTOR; MELANOSOME TRANSPORT; PROCESSIVE
MOVEMENT; KINETIC MECHANISM; ATPASE ACTIVITY; V PROCESSIVITY;
DROSOPHILA; VIIA; CALMODULIN
AB The myosin superfamily is diverse in its structure, kinetic mechanisms and cellular function. The enzymatic activities of most myosins are regulated by some means such as Ca(2+) ion binding, phosphorylation or binding of other proteins. In the present review, we discuss the structural basis for the regulation of mammalian myosin Sa and Drosophila myosin 7a. We show that, although both myosins have a folded inactive state in which domains in the myosin tail interact with the motor domain, the details of the regulation of these two myosins differ greatly.
C1 [Siththanandan, Verl B.; Sellers, James R.] NHLBI, Lab Mol Physiol, NIH, Bethesda, MD 20892 USA.
RP Sellers, JR (reprint author), NHLBI, Lab Mol Physiol, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM sellersj@nhlbi.nih.gov
FU Intramural Research Division of the National Heart, Lung and Blood
Institute
FX This work was funded by the Intramural Research Division of the National
Heart, Lung and Blood Institute.
NR 48
TC 2
Z9 2
U1 1
U2 11
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0300-5127
J9 BIOCHEM SOC T
JI Biochem. Soc. Trans.
PD OCT
PY 2011
VL 39
BP 1136
EP 1141
DI 10.1042/BST0391136
PN 5
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 831QC
UT WOS:000295745200005
PM 21936778
ER
PT J
AU Lam, TK
Cross, AJ
Freedman, N
Park, Y
Hollenbeck, AR
Schatzkin, A
Abnet, C
AF Lam, Tram Kim
Cross, Amanda J.
Freedman, Neal
Park, Yikyung
Hollenbeck, Albert R.
Schatzkin, Arthur
Abnet, Christian
TI Dietary fiber and grain consumption in relation to head and neck cancer
in the NIH-AARP Diet and Health Study
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Diet; Fiber; Grains; Head and neck cancer; Prospective study
ID UPPER AERODIGESTIVE TRACT; RETIRED-PERSONS DIET; LARYNGEAL-CANCER;
RISK-FACTORS; AMERICAN-ASSOCIATION; NATIONAL-INSTITUTES; ESOPHAGEAL
CANCER; PHARYNGEAL CANCER; NUTRITION; ALCOHOL
AB Background Dietary fiber and grain consumption may reduce the risk of head and neck cancer; however, the epidemiological evidence is limited. We investigated this relationship in the National Institutes of Health (NIH)-AARP Diet and Health Study.
Methods Cox proportional hazards models were used to calculate multivariable hazard ratios (HR) and 95% confidence intervals (CI) to investigate dietary fiber and grain intake in relation to head and neck cancer.
Results During approximately 11 years of follow-up, 1,867 (401 women/1,466 men) cases of head and neck cancer were diagnosed. Our data indicated that the relationship between fiber and grain intake and head and neck cancer is modified by sex (p-interactions < 0.001 and 0.001, respectively). Women with higher intake of total fiber and total grains had a lower risk of head and neck cancer (HR(10g/day) = 0.77, 95% CI = 0.64-0.93; HR(serving/1,000kcal) = 0.89, 95% CI = 0.80-0.99, respectively); this inverse relation was consistent across subtypes of fiber and grains. Conversely in men, the inverse associations were weaker and nonsignificant.
Conclusions In the largest prospective cohort study to investigate this relation to date, intake of total fiber and grain foods was inversely associated with head and neck cancer incidence among women, but not among men.
C1 [Lam, Tram Kim] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet DCEG, NIH, Rockville, MD 20852 USA.
[Lam, Tram Kim] NCI, Canc Prevent Fellowship Program, Off Directors, NIH, Rockville, MD 20852 USA.
[Cross, Amanda J.; Freedman, Neal; Park, Yikyung; Schatzkin, Arthur; Abnet, Christian] NCI, Nutr Epidemiol Branch, DCEG, NIH, Rockville, MD 20852 USA.
[Hollenbeck, Albert R.] AARP, Washington, DC USA.
RP Lam, TK (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet DCEG, NIH, Rockville, MD 20852 USA.
EM lamt@mail.nih.gov
RI Abnet, Christian/C-4111-2015;
OI Abnet, Christian/0000-0002-3008-7843; Park, Yikyung/0000-0002-6281-489X
FU NIH, National Cancer Institute; Florida Department of Health (FDOH)
FX This research was supported [in part] by the Intramural Research Program
of the NIH, National Cancer Institute. Cancer incidence data from the
Atlanta metropolitan area were collected by the Georgia Center for
Cancer Statistics, Department of Epidemiology, Rollins School of Public
Health, Emory University. Cancer incidence data from California were
collected by the California Department of Health Services, Cancer
Surveillance Section. Cancer incidence data from the Detroit
metropolitan area were collected by the Michigan Cancer Surveillance
Program, Community Health Administration, State of Michigan. The Florida
cancer incidence data used in this report were collected by the Florida
Cancer Data System (FCDC) under contract with the Florida Department of
Health (FDOH). The views expressed herein are solely those of the
authors and do not necessarily reflect those of the FCDC or FDOH. Cancer
incidence data from Louisiana were collected by the Louisiana Tumor
Registry, Louisiana State University Medical Center in New Orleans.
Cancer incidence data from New Jersey were collected by the New Jersey
State Cancer Registry, Cancer Epidemiology Services, New Jersey State
Department of Health and Senior Services. Cancer incidence data from
North Carolina were collected by the North Carolina Central Cancer
Registry. Cancer incidence data from Pennsylvania were supplied by the
Division of Health Statistics and Research, Pennsylvania Department of
Health, Harrisburg, Pennsylvania. The Pennsylvania Department of Health
specifically disclaims responsibility for any analyses, interpretations,
or conclusions. Cancer incidence data from Arizona were collected by the
Arizona Cancer Registry, Division of Public Health Services, Arizona
Department of Health Services. Cancer incidence data from Texas were
collected by the Texas Cancer Registry, Cancer Epidemiology and
Surveillance Branch, Texas Department of State Health Services. We are
indebted to the participants in the NIH-AARP Diet and Health Study for
their outstanding cooperation. We also thank Sigurd Hermansen and Kerry
Grace Morrissey from Westat for study outcomes ascertainment and
management and Leslie Carroll at Information Management Services for
data support and analysis.
NR 50
TC 5
Z9 5
U1 0
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD OCT
PY 2011
VL 22
IS 10
BP 1405
EP 1414
DI 10.1007/s10552-011-9813-9
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 834VJ
UT WOS:000295992000006
PM 21785948
ER
PT J
AU Ben-Sasson, SZ
Caucheteux, S
Crank, M
Hu-Li, J
Paul, WE
AF Ben-Sasson, S. Z.
Caucheteux, Stephane
Crank, Michelle
Hu-Li, Jane
Paul, William E.
TI IL-1 acts on T cells to enhance the magnitude of in vivo immune
responses
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Ben-Sasson, S. Z.; Caucheteux, Stephane; Crank, Michelle; Hu-Li, Jane; Paul, William E.] NIAID, Immunol Lab, NIH, Bethesda, MD 20891 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 3
EP 3
DI 10.1016/j.cyto.2011.07.292
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800004
ER
PT J
AU Le Saout, C
Hasley, R
Tcheung, L
Imamichi, H
Park, JH
Sneller, M
Roby, G
Rehm, C
Lane, C
Catalfamo, M
AF Le Saout, Cecile
Hasley, Rebecca
Tcheung, Lueng
Imamichi, Hiromi
Park, Jung-Hyun
Sneller, Michael
Roby, Gregg
Rehm, Catherine
Lane, Clifford
Catalfamo, Marta
TI In vivo IL-7 exposure of CD4 T cells during HIV induced lymphopenia
leads to an enhanced Type-I IFN response
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 NIAID, CMRS, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 6
EP 6
DI 10.1016/j.cyto.2011.07.309
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800014
ER
PT J
AU Liao, W
Lin, JX
Wang, L
Li, P
Leonard, WJ
AF Liao, Wei
Lin, Jian-Xin
Wang, Lu
Li, Peng
Leonard, Warren J.
TI Modulation of cytokine receptors by IL-2 broadly regulates
differentiation into helper T cell lineages
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Liao, Wei; Lin, Jian-Xin; Wang, Lu; Li, Peng; Leonard, Warren J.] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 6
EP 6
DI 10.1016/j.cyto.2011.07.310
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800015
ER
PT J
AU Verthelyi, D
Pedras-Vasconcelos, J
Butts, C
Jones, Y
Puig, M
Wang, V
Trinchieri, G
Tami, C
AF Verthelyi, Daniela
Pedras-Vasconcelos, Joao
Butts, Cherie
Jones, Yava
Puig, Montserrat
Wang, Vivian
Trinchieri, Giorgio
Tami, Cecilia
TI Innate immune response modulators control inflammation and improve
survival in viral encephalitis
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Verthelyi, Daniela; Pedras-Vasconcelos, Joao; Butts, Cherie; Puig, Montserrat; Wang, Vivian; Tami, Cecilia] FDA, Div Therapeut Prot, Off Biotechnol, CDER, Jefferson, AR USA.
[Verthelyi, Daniela; Jones, Yava; Trinchieri, Giorgio] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 11
EP 11
DI 10.1016/j.cyto.2011.07.329
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800030
ER
PT J
AU Schmeisser, H
Fey, SB
Horowitz, J
Fischer, ER
Miyake, K
Balinsky, CA
Bekisz, J
Zoon, KC
AF Schmeisser, Hana
Fey, Samuel B.
Horowitz, Julie
Fischer, Elizabeth R.
Miyake, Kotaro
Balinsky, Corey A.
Bekisz, Joseph
Zoon, Kathryn C.
TI Human interferon-alpha2c induces autophagy in Daudi Burkitt's lymphoma
cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Schmeisser, Hana; Fey, Samuel B.; Horowitz, Julie; Miyake, Kotaro; Balinsky, Corey A.; Bekisz, Joseph; Zoon, Kathryn C.] NIAID, NIH, Cytokine Biol Sect, Bethesda, MD 20892 USA.
[Fischer, Elizabeth R.] NIAID, NIH, Rocky Mt Labs, Res Technol Sect, Hamilton, MT 59840 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 22
EP 22
DI 10.1016/j.cyto.2011.07.042
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800067
ER
PT J
AU Bekisz, J
Zhao, TM
Zoon, KC
AF Bekisz, Joseph
Zhao, Tongmao
Zoon, Kathryn C.
TI Pro-Inflammatory Cytokine Expression in Three Cell Types after Treatment
with IFN-alpha subtypes as Assessed by Multiplex Assays
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Bekisz, Joseph; Zhao, Tongmao; Zoon, Kathryn C.] NIAID, Cytokine Biol Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 29
EP 30
DI 10.1016/j.cyto.2011.07.080
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800094
ER
PT J
AU Thomas, E
Gonzalez, VD
Li, QS
Modi, AA
Uccellini, L
Thomas, JM
Chen, WP
Noureddin, M
Rotman, Y
Liang, TJ
AF Thomas, Emmanuel
Gonzalez, Veronica D.
Li, Qisheng
Modi, Ankit A.
Uccellini, Lorenzo
Thomas, Jaime M.
Chen, Weiping
Noureddin, Mazen
Rotman, Yaron
Liang, T. Jake
TI A robust induction of type III interferons and chemokines defines a
unique pattern of hepatic innate immunity in response to hepatitis C
virus infection
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Thomas, Emmanuel; Gonzalez, Veronica D.; Li, Qisheng; Modi, Ankit A.; Uccellini, Lorenzo; Thomas, Jaime M.; Chen, Weiping; Noureddin, Mazen; Rotman, Yaron; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
RI Li, Qisheng/K-1909-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 49
EP 49
DI 10.1016/j.cyto.2011.07.158
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800169
ER
PT J
AU Germain, RN
Meier-Schellersheim, M
Angermann, B
Klauschen, F
Zhang, FH
Brandes-Kuchen, M
Garcia, A
Prustel, T
Fraser, I
Li, N
Deng, L
Sun, J
Benet, Z
Nita-Lazar, A
Tsang, J
AF Germain, Ronald N.
Meier-Schellersheim, Martin
Angermann, Bastian
Klauschen, Frederick
Zhang, Fenghai
Brandes-Kuchen, Marlene
Garcia, Alex
Prustel, Thorsten
Fraser, Iain
Li, Ning
Deng, Li
Sun, Jing
Benet, Zachary
Nita-Lazar, Aleksandra
Tsang, John
TI Bottom-up and Top-Down Systems Biology Approaches to Understanding
Immunity
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Germain, Ronald N.; Meier-Schellersheim, Martin; Angermann, Bastian; Klauschen, Frederick; Zhang, Fenghai; Brandes-Kuchen, Marlene; Garcia, Alex; Prustel, Thorsten; Fraser, Iain; Li, Ning; Deng, Li; Sun, Jing; Benet, Zachary; Nita-Lazar, Aleksandra; Tsang, John] NIAID, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
[Germain, Ronald N.; Tsang, John] NIH, Ctr Human Immunol Autoimmun & Inflammat CHI, Bethesda, MD 20892 USA.
[Klauschen, Frederick] Charite, Inst Pathol, D-10117 Berlin, Germany.
RI Klauschen, Frederick/C-5637-2015
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 50
EP 50
DI 10.1016/j.cyto.2011.07.295
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800171
ER
PT J
AU Durum, SK
Li, WQ
Zenatti, P
Ribeiro, D
Zuurbier, L
Silva, MC
Paganin, M
Tritapoe, J
Hixon, JA
Silveira, AB
Cardoso, BA
Sarmento, LM
Correia, N
Toribio, ML
Kobarg, J
Horstmann, M
Pieters, R
Brandalise, SR
AF Durum, Soctt K.
Li, W. Q.
Zenatti, P.
Ribeiro, D.
Zuurbier, L.
Silva, M. C.
Paganin, M.
Tritapoe, J.
Hixon, J. A.
Silveira, A. B.
Cardoso, B. A.
Sarmento, L. M.
Correia, N.
Toribio, M. L.
Kobarg, J.
Horstmann, M.
Pieters, R.
Brandalise, S. R.
TI Oncogenic IL-7R gain-of-function mutations in childhood T-ALL
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Durum, Soctt K.; Li, W. Q.; Tritapoe, J.; Hixon, J. A.; Brandalise, S. R.] NCI, Bethesda, MD 20892 USA.
[Zenatti, P.; Silveira, A. B.; Brandalise, S. R.] Ctr Infantil Boldrini, Boldrini, Brazil.
[Ribeiro, D.; Silva, M. C.; Cardoso, B. A.; Sarmento, L. M.; Correia, N.] Univ Lisbon, P-1699 Lisbon, Portugal.
[Zuurbier, L.; Pieters, R.] Erasmus MC, Rotterdam, Netherlands.
[Durum, Soctt K.; Paganin, M.] Columbia Univ, New York, NY 10027 USA.
[Toribio, M. L.] Univ Autonoma Madrid, E-28049 Madrid, Spain.
[Horstmann, M.] Univ Med Ctr Hamburg Eppendorf, Hamburg, Germany.
[Durum, Soctt K.] Univ Estadual Campinas, BR-13081970 Campinas, SP, Brazil.
[Durum, Soctt K.] 12 Univ Estadual Campinas, Campinas, SP, Brazil.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 52
EP 53
DI 10.1016/j.cyto.2011.07.344
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800179
ER
PT J
AU Smith, M
Hurley, A
Karpova, T
Belkina, N
Shaw, S
Nickel, E
Packard, B
Imamichi, H
MacNally, J
Sneller, M
Lane, C
Catalfamo, M
AF Smith, Mindy
Hurley, Amanda
Karpova, Tatiana
Belkina, Natalya
Shaw, Steve
Nickel, Erin
Packard, Beverly
Imamichi, Hiromi
MacNally, James
Sneller, Michael
Lane, Clifford
Catalfamo, Marta
TI Thrombin mediates chemokinesis in human resting CD8 T cells through
specific interaction with thrombin receptor (PAR-1)
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Smith, Mindy; Hurley, Amanda; Nickel, Erin; Imamichi, Hiromi; Sneller, Michael; Lane, Clifford; Catalfamo, Marta] NIAID, CMRS Lab Immunoregulat, NIH, Bethesda, MD 20892 USA.
[Belkina, Natalya; Shaw, Steve] NCI, Expt Immunol Branch, Bethesda, MD 20892 USA.
[Packard, Beverly] Oncolmmunin Inc, Gaithersburg, MD 20877 USA.
[Karpova, Tatiana; MacNally, James] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 58
EP 58
DI 10.1016/j.cyto.2011.07.362
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800194
ER
PT J
AU Tewary, P
De, GD
Sharma, N
Rodriguez, L
Shirota, H
Steinhagen, F
Klinman, DM
Yang, D
Oppenheim, JJ
AF Tewary, Poonam
de la Rosa, Gonzalo
Sharma, Neeraj
Rodriguez, Luis
Shirota, Hidekatzu
Steinhagen, Folkert
Klinman, Dennis M.
Yang, De
Oppenheim, Joost J.
TI Effect of antimicrobial proteins/alarmins on DNA mediated activation of
pDC and inflammation
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Tewary, Poonam; de la Rosa, Gonzalo; Yang, De; Oppenheim, Joost J.] NCI, Lab Mol lmmunoregulat, Anal Lab, NCI SAIC Frederick,Ctr Canc Res, Frederick, MD 21702 USA.
[Sharma, Neeraj] NCI, Lab Expt Immunol, Anal Lab, NCI SAIC Frederick,Ctr Canc Res, Frederick, MD 21702 USA.
[Rodriguez, Luis] NCI, Opt Microscopy & Anal Lab, NCI SAIC Frederick, Ctr Canc Res, Frederick, MD 21702 USA.
[Shirota, Hidekatzu; Steinhagen, Folkert; Klinman, Dennis M.] NCI, Canc & Inflammat Programm, NCI SAIC Frederick, Ctr Canc Res,Anal Lab, Frederick, MD 21702 USA.
[Yang, De] NCI, Basic Sci Program, NCI SAIC Frederick, Ctr Canc Res,Anal Lab, Frederick, MD 21702 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 59
EP 59
DI 10.1016/j.cyto.2011.07.367
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800199
ER
PT J
AU Palmer, DC
Reger, RN
Garvin, LM
Frasheri, D
Ji, Y
Franco, ZJ
Gattinoni, CAKL
Restifo, L
AF Palmer, Douglas C.
Reger, Robert N.
Garvin, Lindsay M.
Frasheri, Donna
Ji, Yun
Franco, Zulmarie J.
Gattinoni, Christopher A. Klebanoff Luca
Restifo, Nicholas P.
TI Cish degradation of Htra1 regulates TGF-b signaling
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Palmer, Douglas C.; Reger, Robert N.; Garvin, Lindsay M.; Frasheri, Donna; Ji, Yun; Franco, Zulmarie J.; Gattinoni, Christopher A. Klebanoff Luca; Restifo, Nicholas P.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 60
EP 60
DI 10.1016/j.cyto.2011.07.372
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800203
ER
PT J
AU Murphy, PM
AF Murphy, Philip M.
TI Targeting CXCR4 in WHIM Syndrome
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Murphy, Philip M.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 62
EP 62
DI 10.1016/j.cyto.2011.07.377
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800207
ER
PT J
AU Miyake, K
Bekisz, J
Zhao, T
Clark, C
Zoon, KC
AF Miyake, Kotaro
Bekisz, Joseph
Zhao, Tongmao
Clark, Christopher
Zoon, Kathryn C.
TI Apoptosis-inducing factor (AIF) is targeted in IFN-alpha 2a-induced Bid
mediated apoptosis through Bak activation in ovarian cancer cells
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Miyake, Kotaro; Bekisz, Joseph; Zhao, Tongmao; Clark, Christopher; Zoon, Kathryn C.] NIAID, Cytokine Biol Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 97
EP 97
DI 10.1016/j.cyto.2011.07.286
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800330
ER
PT J
AU Ozato, K
Chang, TH
Xu, SX
Kubota, T
Matsuoka, M
AF Ozato, Keiko
Chang, Tsung-Hsien
Xu, Song Xiao
Kubota, Toru
Matsuoka, Mayumi
TI SUMO Modification of IRF Family Proteins and Regulation of Anti-Viral
Innate Immunity
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Ozato, Keiko; Chang, Tsung-Hsien; Xu, Song Xiao] NICHD, Program Genom Differentiat, NIH, Bethesda, MD USA.
[Kubota, Toru; Matsuoka, Mayumi] Natl Inst Infect Dis, Tokyo, Japan.
NR 3
TC 0
Z9 0
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 99
EP 99
DI 10.1016/j.cyto.2011.07.383
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800334
ER
PT J
AU Hodge, DL
Berthet, C
Coppola, V
Shirota, H
Reynolds, D
Klinman, DM
Young, HA
AF Hodge, Deborah L.
Berthet, Cyril
Coppola, Vincenzo
Shirota, Hidekazu
Reynolds, Della
Klinman, Dennis M.
Young, Howard A.
TI Loss of Ifn-g 3 ' Untranslated Region Au-rich Element Affects b220+b
Cell and Plasmacytoid Dendritic cell Populations in a Novel Murine Lupus
Model
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Hodge, Deborah L.; Shirota, Hidekazu; Reynolds, Della; Klinman, Dennis M.; Young, Howard A.] NCI, Expt Immunol Lab, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Coppola, Vincenzo] Ohio State Univ, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
[Berthet, Cyril] Oncodesign, Dijon, France.
RI Coppola, Vincenzo/E-2917-2011
OI Coppola, Vincenzo/0000-0001-6163-1779
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 100
EP 100
DI 10.1016/j.cyto.2011.07.389
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800340
ER
PT J
AU Zoon, KC
Nakashima, H
Miyake, K
Clark, C
Bekisz, J
Baron, S
Husain, SR
Puri, RK
AF Zoon, Kathryn C.
Nakashima, Hideyuki
Miyake, Kotaro
Clark, Christopher
Bekisz, Joseph
Baron, Samuel
Husain, Syed R.
Puri, Raj K.
TI Combination therapy with IFN-alpha plus IFN-gamma and monocytes mediates
synergistic antitumor effects against established human ovarian and
melanoma tumors in mouse models
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Zoon, Kathryn C.; Nakashima, Hideyuki; Husain, Syed R.; Puri, Raj K.] US FDA, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA.
[Zoon, Kathryn C.; Miyake, Kotaro; Clark, Christopher; Bekisz, Joseph; Baron, Samuel] NIAID, Cytokine Biol Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 102
EP 102
DI 10.1016/j.cyto.2011.07.397
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800347
ER
PT J
AU Sher, A
Mayer-Barber, K
Novikov, A
Andrade, B
Barber, D
Shenderov, K
Feng, C
AF Sher, A.
Mayer-Barber, K.
Novikov, A.
Andrade, B.
Barber, D.
Shenderov, K.
Feng, C.
TI Cytokine pathways regulating the innate immune response to mycobacteria
SO CYTOKINE
LA English
DT Meeting Abstract
CT 9th Joint Meeting of the
International-Cytokine-Society/International-Society-for-Interferon-and-
Cytokine-Research
CY OCT 09-12, 2011
CL Florence, ITALY
SP Int Cytokine Soc, Int Society Interferon & Cytokine Res
C1 [Sher, A.; Mayer-Barber, K.; Novikov, A.; Andrade, B.; Barber, D.; Shenderov, K.; Feng, C.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RI Andrade, Bruno/J-9111-2012
OI Andrade, Bruno/0000-0001-6833-3811
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 107
EP 107
DI 10.1016/j.cyto.2011.07.415
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800362
ER
PT J
AU Ben-Sasson, SZ
Caucheteux, S
Crank, M
Hu-Li, J
Paul, WE
AF Ben-Sasson, S. Z.
Caucheteux, Stephane
Crank, Michelle
Hu-Li, Jane
Paul, William E.
TI IL-1 acts on T cells to enhance the magnitude of in vivo immune
responses
SO CYTOKINE
LA English
DT Review
DE CD4; CD8; IL-1 receptor; Lipopolysaccharide; IL-1RA
ID EXPANSION; TH17
AB IL-1 strikingly enhances antigen-driven responses of CD4 and CD8 T cells. It is substantially more effective than LPS and when added to a priming regime of antigen plus LPS, it strikingly enhances cell expansion. The effect is mediated by direct action on CD4 and CD8 T cells; the response occurs when OT-I or OT-II cells are transferred to B6 IL-1R1-/- recipients and only cells that express IL-1 receptors can respond. The major mechanism through which IL-1 enhances responses is by increasing survival of responding cells. IL-1 enhances the proportion of responding CD4 T cells that differentiate into Th17 cells and increases the proportion of responding CD8 cells that express granzyme B. Of a wide range of cytokines tested, only IL-1 alpha and IL-1 beta mediate this function. The potency of IL-1 as an enhancer of T cell responses suggests that it could act to enhance responses to weak vaccines and that the pathway utilized by IL-1 might be considered in the design of new generations of adjuvants. Published by Elsevier Ltd.
C1 [Ben-Sasson, S. Z.; Caucheteux, Stephane; Crank, Michelle; Hu-Li, Jane; Paul, William E.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Paul, WE (reprint author), NIAID, Immunol Lab, NIH, Bldg 10,Rm 11N311, Bethesda, MD 20892 USA.
EM wpaul@niaid.nih.gov
FU NIAID Division of Intramural Research [1-Z01-AI000926-09-LI]
FX This work was supported by the NIAID Division of Intramural Research
through Project 1-Z01-AI000926-09-LI. The care and handling of the
animals used in our studies were in accordance with the guidelines of
the National Institutes of Health Animal Care and Use Committee. We
thank Shirley Starnes for excellent editorial assistance.
NR 11
TC 24
Z9 25
U1 0
U2 12
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2011
VL 56
IS 1
SI SI
BP 122
EP 125
DI 10.1016/j.cyto.2011.07.006
PG 4
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 827OM
UT WOS:000295437800378
PM 21843950
ER
PT J
AU Harris, PJ
Bible, KC
AF Harris, Pamela Jo
Bible, Keith C.
TI Emerging therapeutics for advanced thyroid malignancies: rationale and
targeted approaches
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Review
DE anaplastic thyroid cancer; differentiated thyroid cancer; medullary
thyroid cancer; taxanes; tyrosine kinase inhibitors
ID PHASE-II TRIAL; ADVANCED SOLID TUMORS; CANCER CELL-LINES;
PHOSPHATIDYLINOSITOL 3-KINASE/AKT; GENETIC ALTERATIONS; SIGNALING
PATHWAYS; RADIOIODINE UPTAKE; NA+/I-SYMPORTER; RETINOIC ACID;
UNITED-STATES
AB Introduction: Thyroid cancer is an emerging public health concern. In the USA, its incidence has doubled in the past decade, making it the eighth most commonly diagnosed neoplasmin 2010. Despite this alarming increase, most thyroid cancer patients benefit from conventional approaches (surgery, radioiodine, radiotherapy, TSH suppression with levothyroxine) and are often cured. Nevertheless, a minority have aggressive tumors resistant to cytotoxic and other historical therapies; these patients sorely need new treatment options.
Areas covered: Herein the biology and molecular characteristics of the common histological types of thyroid cancer are reviewed to provide context for subsequent discussion of recent developments and emerging therapeutics for advanced thyroid cancers.
Expert opinion: Several kinase inhibitors, especially those targeting VEGFR and/or RET, have already demonstrated promising activity in differentiated and medullary thyroid cancers (DTC, MTC). Although of minimal benefit in DTC and MTC, cytotoxic chemotherapy with anti-microtubule agents and/or anthracyclines in combination with intensity-modulated radiation therapy appears to extend survival for patients with locoregionally confined anaplastic thyroid cancer (ATC), but to have only modest benefit in metastatic ATC. Further discovery and development of novel agents and combinations of agents will be critical to further progress in treating advanced thyroid cancers of all histotypes.
C1 [Harris, Pamela Jo] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Bible, Keith C.] Mayo Clin, Div Med Oncol, Rochester, MN 55905 USA.
RP Harris, PJ (reprint author), NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
EM harrispj@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 97
TC 14
Z9 16
U1 0
U2 4
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1354-3784
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD OCT
PY 2011
VL 20
IS 10
BP 1357
EP 1375
DI 10.1517/13543784.2011.614230
PG 19
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 831GZ
UT WOS:000295718800005
PM 21910667
ER
PT J
AU Khoury, MJ
Gwinn, M
Dotson, D
Bowen, MS
AF Khoury, Muin J.
Gwinn, Marta
Dotson, David
Bowen, M. Scott
TI Is there a need for PGxceptionalism?
SO GENETICS IN MEDICINE
LA English
DT Editorial Material
C1 [Khoury, Muin J.; Gwinn, Marta; Dotson, David; Bowen, M. Scott] Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA USA.
[Khoury, Muin J.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Khoury, MJ (reprint author), CDC, Off Publ Hlth Genom, 1600 Clifton Rd, Atlanta, GA 30333 USA.
EM muk1@cdc.gov
OI Dotson, William David/0000-0002-9606-6594
NR 12
TC 5
Z9 7
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1098-3600
J9 GENET MED
JI Genet. Med.
PD OCT
PY 2011
VL 13
IS 10
BP 866
EP 867
DI 10.1097/GIM.0b013e3182265bed
PG 2
WC Genetics & Heredity
SC Genetics & Heredity
GA 833KN
UT WOS:000295884200003
PM 21799428
ER
PT J
AU Melis, M
Diaz, G
Mogavero, G
Tice, AB
Lam, JH
Brown, CR
Becker, S
Kabat, J
Hanson, J
Rodriguez-Canales, J
Emmert-Buck, MR
Kleiner, DE
Govindarajan, S
Zamboni, F
Farci, P
AF Melis, Marta
Diaz, Giacomo
Mogavero, Giulia
Tice, Ashley B.
Lam, Joyce H.
Brown, Charles R.
Becker, Steven
Kabat, Juraj
Hanson, Jeffrey
Rodriguez-Canales, Jaime
Emmert-Buck, Michael R.
Kleiner, David E.
Govindarajan, Sugantha
Zamboni, Fausto
Farci, Patrizia
TI GENE EXPRESSION PROFILING OF HEPATITIS B VIRUS (HBV)-ASSOCIATED
HEPATOCELLULAR CARCINOMA (HCC)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Melis, Marta; Tice, Ashley B.; Lam, Joyce H.; Farci, Patrizia] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Diaz, Giacomo] Univ Cagliari, Dept Biomed Sci & Technol, Cagliari, Italy.
[Mogavero, Giulia; Zamboni, Fausto] Brotzu Hosp, Liver Transplantat Ctr, Cagliari, Italy.
[Brown, Charles R.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Becker, Steven; Kabat, Juraj] NIAID, Biol Imaging Facil, NIH, Bethesda, MD 20892 USA.
[Hanson, Jeffrey; Rodriguez-Canales, Jaime; Emmert-Buck, Michael R.; Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Govindarajan, Sugantha] Univ So Calif, Rancho Los Amigos Hosp, Dept Pathol, Downey, CA 90242 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 371A
EP 372A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002025
ER
PT J
AU Shin, EC
Park, SH
Nascimbeni, M
Major, ME
Rice, CM
Rehermann, B
AF Shin, Eui-Cheol
Park, Su-Hyung
Nascimbeni, Michelina
Major, Marian E.
Rice, Charles M.
Rehermann, Barbara
TI THE PERCENTAGE OF HEPATITIS C VIRUS-SPECIFIC CD127+MEMORY T CELLS IN THE
ACUTE PHASE T CELL RESPONSE PREDICTS THE OUTCOME OF HCV INFECTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Shin, Eui-Cheol; Park, Su-Hyung; Nascimbeni, Michelina; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH, Bethesda, MD USA.
[Shin, Eui-Cheol] Korea Adv Inst Sci & Technol, Grad Sch Med Sci & Engn, Taejon 305701, South Korea.
[Major, Marian E.] US FDA, Lab Hepatitis Viruses, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA.
[Rice, Charles M.] Rockefeller Univ, Ctr Study Hepatitis C, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 380A
EP 380A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002040
ER
PT J
AU Wu, R
Lin, M
Lehil, M
Shen, H
Cozen, M
Gao, X
Martin, M
Lanier, LL
Yee, R
Duh, FM
Monto, A
Carrington, M
Ryan, JC
AF Wu, Richard
Lin, Monika
Lehil, Mandeep
Shen, Hui
Cozen, Myrna
Gao, Xiang
Martin, Maureen
Lanier, Lewis L.
Yee, Russell
Duh, Fuh-Mei
Monto, Alexander
Carrington, Mary
Ryan, James C.
TI INDEPENDENT INFLUENCES OF KILLER IMMUNOGLOBULIN RECEPTORS (KIR) AND THE
RS12979860 IL28B POLYMORPHISM ON SPONTANEOUS HCV RESOLUTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Wu, Richard; Lin, Monika; Lehil, Mandeep; Shen, Hui; Cozen, Myrna; Lanier, Lewis L.; Yee, Russell; Monto, Alexander; Ryan, James C.] UCSF, San Francisco, CA USA.
[Gao, Xiang; Martin, Maureen; Duh, Fuh-Mei; Carrington, Mary] NCI, SAIC, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 381A
EP 381A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002042
ER
PT J
AU Noureddin, M
Rotman, Y
Feld, JJ
Han, H
Park, YJ
Thomas, E
Koh, C
Abdalla, AA
Gara, N
Sarkar, S
Doo, E
Ghany, MG
Heller, T
Hoofnagle, JH
Liang, TJ
AF Noureddin, Mazen
Rotman, Yaron
Feld, Jordan J.
Han, Hwalih
Park, Yoon J.
Thomas, Emmanuel
Koh, Christopher
Abdalla, Adil A.
Gara, Naveen
Sarkar, Souvik
Doo, Edward
Ghany, Marc G.
Heller, Theo
Hoofnagle, Jay H.
Liang, T. Jake
TI DIFFERENTIAL HEPATIC EXPRESSION OF INTERFERON STIMULATED GENES BETWEEN
HCV GENOTYPES 1 AND 2/3 CORRELATES WITH RESPONSIVENESS TO PEGINTERFERON
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Noureddin, Mazen; Rotman, Yaron; Han, Hwalih; Park, Yoon J.; Thomas, Emmanuel; Koh, Christopher; Abdalla, Adil A.; Gara, Naveen; Sarkar, Souvik; Doo, Edward; Ghany, Marc G.; Heller, Theo; Hoofnagle, Jay H.; Liang, T. Jake] NIDDK, Bethesda, MD USA.
[Feld, Jordan J.] Univ Toronto, Toronto, ON, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 401A
EP 402A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002085
ER
PT J
AU Park, SH
Veerapu, NS
Rehermann, B
AF Park, Su-Hyung
Veerapu, Naga Suresh
Rehermann, Barbara
TI REPEATED EXPOSURE TO TRACE AMOUNTS OF HEPATITIS C VIRUS SUPPRESSES T
CELL RESPONSES TO SUBSEQUENT HIGH DOSE HCV CHALLENGE VIA INDUCTION OF
REGULATORY T CELLS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Park, Su-Hyung; Veerapu, Naga Suresh; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 403A
EP 403A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002087
ER
PT J
AU Hara, K
Koh, C
Sakiani, S
Rivera, M
Liang, TJ
Hoofnagle, JH
Heller, T
AF Hara, Koji
Koh, Christopher
Sakiani, Sasan
Rivera, Maria
Liang, T. Jake
Hoofnagle, Jay H.
Heller, Theo
TI IMPORTANT DETERMINANTS OF 5 ' UNTRANSLATED REGION (UTR) IN HEPATITIS C
VIRUS (HCV) GENOTYPING: CLINICAL IMPLICATIONS FOR TODAY AND THE FUTURE
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Hara, Koji; Koh, Christopher; Sakiani, Sasan; Rivera, Maria; Liang, T. Jake; Hoofnagle, Jay H.; Heller, Theo] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 404A
EP 405A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002090
ER
PT J
AU Li, QS
Krishnamurthy, S
El-Diwany, R
Liang, TJ
AF Li, Qisheng
Krishnamurthy, Siddharth
El-Diwany, Ramy
Liang, T. Jake
TI GENOME-WIDE FUNCTIONAL SCREEN DISCOVERS NOVEL HOST MICRORNAS THAT
MODULATE HEPATITIS C VIRUS INFECTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Li, Qisheng; Krishnamurthy, Siddharth; El-Diwany, Ramy; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
RI Li, Qisheng/K-1909-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 406A
EP 406A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002094
ER
PT J
AU Baghdasaryan, A
Claudel, T
Gumhold, J
Silbert, D
Adorini, L
Gonzalez, F
Schoonjans, K
Fickert, P
Trauner, M
AF Baghdasaryan, Anna
Claudel, Thierry
Gumhold, Judith
Silbert, Dagmar
Adorini, Luciano
Gonzalez, Frank
Schoonjans, Kristina
Fickert, Peter
Trauner, Michael
TI FXR BUT NOT TGR5 ACTIVATION STIMULATES HCO3-RICH BILE SECRETION AND
AMELIORATES LIVER DAMAGE IN MDR2-/- (ABCB4-/-) MOUSE MODEL OF CHRONIC
LIVER INJURY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Baghdasaryan, Anna; Claudel, Thierry; Gumhold, Judith; Silbert, Dagmar; Fickert, Peter; Trauner, Michael] Med Univ Graz, Dept Internal Med, Div Gastroenterol & Hepatol, Lab Expt & Mol Hepatol, Graz, Austria.
[Claudel, Thierry; Trauner, Michael] Med Univ Vienna, Dept Internal Med 3, Div Gastroenterol & Hepatol, Vienna, Austria.
[Adorini, Luciano] Intercept Pharmaceut, New York, NY USA.
[Gonzalez, Frank] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
[Schoonjans, Kristina] Ecole Polytech Fed Lausanne, Lab Integrat & Syst Physiol, Lausanne, Switzerland.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 425A
EP 425A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002133
ER
PT J
AU Kitade, M
Factor, VM
Akita, H
Holczbauer, A
Conner, EA
Lee, YH
Lee, SB
Thorgeirsson, SS
AF Kitade, Mitsuteru
Factor, Valentina M.
Akita, Hirofumi
Holczbauer, Agnes
Conner, Elizabeth A.
Lee, Yun-Han
Lee, Seung Bum
Thorgeirsson, Snorri S.
TI THE FUNCTIONS OF EGFR AND MET IN HEPATIC PROGENITOR CELL DIFFERENTIATION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Kitade, Mitsuteru; Factor, Valentina M.; Akita, Hirofumi; Holczbauer, Agnes; Conner, Elizabeth A.; Lee, Yun-Han; Lee, Seung Bum; Thorgeirsson, Snorri S.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 449A
EP 449A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002180
ER
PT J
AU Yamashita, T
Honda, M
Nakamoto, Y
Mizukoshi, E
Yamashita, T
Arai, K
Nio, K
Hara, Y
Wang, XW
Kaneko, S
AF Yamashita, Taro
Honda, Masao
Nakamoto, Yasunari
Mizukoshi, Eishiro
Yamashita, Tatsuya
Arai, Kuniaki
Nio, Kouki
Hara, Yasumasa
Wang, Xin W.
Kaneko, Shuichi
TI DISTINCT LIVER CANCER STEM CELLS DEFINED BY EPCAM AND CD90 IN HUMAN
HEPATOCELLULAR CARCINOMA
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Yamashita, Taro; Honda, Masao; Nakamoto, Yasunari; Mizukoshi, Eishiro; Yamashita, Tatsuya; Arai, Kuniaki; Nio, Kouki; Hara, Yasumasa; Kaneko, Shuichi] Kanazawa Univ, Grad Sch Med Sci, Dept Gastroenterol, Kanazawa, Ishikawa, Japan.
[Wang, Xin W.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 449A
EP 449A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002179
ER
PT J
AU Maldonado, EN
Sheldon, KL
Patnaik, JR
Rostovtseva, TK
Lemasters, JJ
AF Maldonado, Eduardo N.
Sheldon, Kely L.
Patnaik, Jyoti R.
Rostovtseva, Tatiana K.
Lemasters, John J.
TI ERASTIN ANTAGONIZES THE INHIBITORY EFFECT OF FREE TUBULIN ON VDAC AND
INCREASES MITOCHONDRIAL MEMBRANE POTENTIAL IN HEPG2 CELLS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Maldonado, Eduardo N.; Patnaik, Jyoti R.; Lemasters, John J.] Med Univ S Carolina, Ctr Cell Death Injury & Regenerat, Dept Pharmaceut & Biomed Sci, Charleston, SC 29425 USA.
[Maldonado, Eduardo N.; Patnaik, Jyoti R.; Lemasters, John J.] Med Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA.
[Sheldon, Kely L.; Rostovtseva, Tatiana K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Struct Biol, NIH, Bethesda, MD USA.
[Sheldon, Kely L.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, W Harry Feinstein Dept Mol Microbiol & Immunol, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 455A
EP 455A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002191
ER
PT J
AU Shneider, BL
Magee, JC
Karpen, SJ
Rand, E
Narkewicz, MR
Schwarz, KB
Whitington, PF
Bezerra, JA
Kerkar, N
Haber, B
Rosenthal, P
Turmelle, YP
Molleston, JP
Murray, KF
Ng, VL
Wang, KS
Romero, R
Moore, J
Robuck, PR
Sokol, RJ
AF Shneider, Benjamin L.
Magee, John C.
Karpen, Saul J.
Rand, Elizabeth
Narkewicz, Michael R.
Schwarz, Kathleen B.
Whitington, Peter F.
Bezerra, Jorge A.
Kerkar, Nanda
Haber, Barbara
Rosenthal, Philip
Turmelle, Yumirle P.
Molleston, Jean P.
Murray, Karen F.
Ng, Vicky L.
Wang, Kasper S.
Romero, Rene
Moore, Jeffrey
Robuck, Patricia R.
Sokol, Ronald J.
TI PROSPECTIVE MULTICENTER ANALYSIS OF POST-OPERATIVE TOTAL BILIRUBIN AS A
BIOMARKER FOR SHORT-TERM OUTCOME AFTER HEPATOPORTOENTEROSTOMY FOR
BILIARY ATRESIA
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Shneider, Benjamin L.] Univ Pittsburgh, Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA.
[Magee, John C.; Moore, Jeffrey] Univ Michigan, Ann Arbor, MI 48109 USA.
[Karpen, Saul J.] Texas Childrens Hosp, Houston, TX 77030 USA.
[Rand, Elizabeth; Haber, Barbara] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Narkewicz, Michael R.; Sokol, Ronald J.] Univ Colorado, Denver, CO 80202 USA.
[Schwarz, Kathleen B.] Johns Hopkins Univ, Baltimore, MD USA.
[Whitington, Peter F.] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Bezerra, Jorge A.] Cincinnati Childrens Med Ctr, Cincinnati, OH USA.
[Kerkar, Nanda] Mt Sinai Sch Med, New York, NY USA.
[Rosenthal, Philip] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Turmelle, Yumirle P.] Washington Univ, St Louis, MO USA.
[Molleston, Jean P.] Indiana Univ, Indianapolis, IN 46204 USA.
[Murray, Karen F.] Univ Washington, Seattle, WA 98195 USA.
[Ng, Vicky L.] Univ Toronto, Toronto, ON, Canada.
[Wang, Kasper S.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Romero, Rene] Childrens Hosp Atlanta, Atlanta, GA USA.
[Robuck, Patricia R.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 468A
EP 468A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002217
ER
PT J
AU Fried, MW
Navarro, VJ
Afdhal, NH
Wahed, AS
Hawke, RL
Belle, SH
Doo, E
Meyers, CM
Reddy, KR
AF Fried, Michael W.
Navarro, Victor J.
Afdhal, Nezam H.
Wahed, Abdus S.
Hawke, Roy L.
Belle, Steven H.
Doo, Edward
Meyers, Catherine M.
Reddy, K. Rajender
TI A RANDOMIZED, PLACEBO-CONTROLLED TRIAL OF ORAL SILYMARIN (MILK THISTLE)
FOR CHRONIC HEPATITIS C: FINAL RESULTS OF THE SYNCH MULTICENTER STUDY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Fried, Michael W.] Univ N Carolina, UNC Liver Ctr, Chapel Hill, NC USA.
[Navarro, Victor J.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Afdhal, Nezam H.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Wahed, Abdus S.; Belle, Steven H.] Univ Pittsburgh, Pittsburgh, PA USA.
[Hawke, Roy L.] Univ N Carolina, Eshelman Sch Pharm, Chapel Hill, NC USA.
[Doo, Edward] NIDDK, NIH, Bethesda, MD USA.
[Meyers, Catherine M.] NIH, NCCAM, Bethesda, MD 20892 USA.
[Reddy, K. Rajender] Univ Penn, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 475A
EP 475A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002228
ER
PT J
AU Gara, N
Ghany, MG
Zhao, XC
Collins, MT
Hoofnagle, JH
AF Gara, Naveen
Ghany, Marc G.
Zhao, Xiongce
Collins, Michael T.
Hoofnagle, Jay H.
TI PHOSPHATE WASTING NEPHROPATHY IN PATIENTS WITH CHRONIC HEPATITIS B
TREATED WITH LONG-TERM ADEFOVIR OR TENOFOVIR
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Gara, Naveen; Ghany, Marc G.; Hoofnagle, Jay H.] NIH, LDB, Bethesda, MD 20892 USA.
[Collins, Michael T.] NIDCR, Skeletal Clin Studies Unit, Bethesda, MD USA.
[Zhao, Xiongce] NIDDK, Bethesda, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 479A
EP 480A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002237
ER
PT J
AU Sarkar, M
French, A
Tien, P
Bacchetti, P
Glesby, M
Gange, SJ
Plankey, M
Sharp, G
Nowicki, MJ
Minkoff, H
Peters, MG
AF Sarkar, Monika
French, Audrey
Tien, Phyllis
Bacchetti, Peter
Glesby, Marshall
Gange, Stephen J.
Plankey, Michael
Sharp, Gerald
Nowicki, Marek J.
Minkoff, Howard
Peters, Marion G.
TI RACIAL/ETHNIC DIFFERENCES IN OVERALL AND LIVER-RELATED MORTALITY IN HIV
INFECTED WOMEN WITH CHRONIC HEPATITIS C
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Sarkar, Monika; Tien, Phyllis; Bacchetti, Peter; Peters, Marion G.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[French, Audrey] Rush Univ, Chicago, IL 60612 USA.
[Gange, Stephen J.] Johns Hopkins Univ, Baltimore, MD USA.
[Glesby, Marshall] Cornell Univ, New York, NY 10021 USA.
[Minkoff, Howard] SUNY Downstate, Brooklyn, NY USA.
[Nowicki, Marek J.] Univ So Calif, Los Angeles, CA USA.
[Plankey, Michael] Georgetown Univ, Washington, DC USA.
[Sharp, Gerald] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 483A
EP 484A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002244
ER
PT J
AU Odigie, M
Zhang, XZ
Masur, H
Polis, MA
Kottilil, S
Osinusi, A
AF Odigie, Madeline
Zhang, Xiaozhen
Masur, Henry
Polis, Michael A.
Kottilil, Shyam
Osinusi, Anu
TI IL23 PROMOTES INTERFERON RESPONSIVENESS IN HIV/HCV COINFECTED PATIENTS
TREATED WITH PEGYLATED INTERFERON AND RIBAVIRIN
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Odigie, Madeline; Zhang, Xiaozhen; Polis, Michael A.; Kottilil, Shyam; Osinusi, Anu] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
[Osinusi, Anu] NCI Frederick Inc, Clin Res Directorate, CMRP, SAIC Frederick, Frederick, MD USA.
[Masur, Henry] CC, CCMD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 488A
EP 488A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002252
ER
PT J
AU Thomas, E
Gonzalez, VD
Li, QS
Noureddin, M
Rotman, Y
Liang, TJ
AF Thomas, Emmanuel
Gonzalez, Veronica D.
Li, Qisheng
Noureddin, Mazen
Rotman, Yaron
Liang, T. Jake
TI ROBUST INDUCTION OF TYPE III INTERFERONS AND OTHER CYTOKINES DEFINES A
UNIQUE PATTERN OF INNATE IMMUNITY IN RESPONSE TO HEPATITIS C VIRUS
INFECTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Thomas, Emmanuel; Gonzalez, Veronica D.; Li, Qisheng; Noureddin, Mazen; Rotman, Yaron; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
RI Li, Qisheng/K-1909-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 493A
EP 493A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002262
ER
PT J
AU Nagata, T
Huang, YG
AF Nagata, Takako
Huang, Yuning G.
TI ROLE OF ADENOSINE A1 RECEPTORS IN EXACERBATION OF INFLAMMATION AND LIVER
DAMAGE UNDER EXCESSIVE ALCOHOL CONSUMPTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Nagata, Takako] Vet Affairs Med Ctr, Washington, DC 20422 USA.
[Huang, Yuning G.] NIDDK, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 512A
EP 512A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002305
ER
PT J
AU Alqahtani, S
Hoofnagle, JH
Ghabril, M
Chalasani, NP
Rockey, DC
AF Alqahtani, Saleh
Hoofnagle, Jay H.
Ghabril, Marwan
Chalasani, Naga P.
Rockey, Don C.
TI CEPHALOSPORIN INDUCED LIVER INJURY: CLINICAL AND BIOCHEMICAL FEATURES
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Alqahtani, Saleh; Rockey, Don C.] Univ Texas SW Med Ctr Dallas, Div Digest & Liver Dis, Dallas, TX 75390 USA.
[Hoofnagle, Jay H.] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD USA.
[Ghabril, Marwan; Chalasani, Naga P.] Indiana Univ, Div Gastroenterol & Hepatol, Indianapolis, IN 46204 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 516A
EP 516A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002314
ER
PT J
AU Kleiner, DE
Fontana, RJ
Rockey, DC
Chalasani, NP
Watkins, PB
Bonkovsky, HL
Davern, TJ
Navarro, VJ
Reddy, KR
Talwalkar, JA
Lee, WM
Stolz, A
Hoofnagle, JH
Gu, JZ
AF Kleiner, David E.
Fontana, Robert J.
Rockey, Don C.
Chalasani, Naga P.
Watkins, Paul B.
Bonkovsky, Herbert L.
Davern, Timothy J.
Navarro, Victor J.
Reddy, K. Rajender
Talwalkar, Jayant A.
Lee, William M.
Stolz, Andrew
Hoofnagle, Jay H.
Gu, Jiezhun
TI HISTOLOGIC ANALYSIS AND CORRELATION WITH CLINICAL OUTCOMES IN THE
DRUG-INDUCED LIVER INJURY NETWORK (DILIN)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Kleiner, David E.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Fontana, Robert J.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Rockey, Don C.; Lee, William M.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Chalasani, Naga P.] Indiana Univ, Indianapolis, IN 46204 USA.
[Watkins, Paul B.] Univ N Carolina, Chapel Hill, NC USA.
[Bonkovsky, Herbert L.] Carolinas Med Ctr, Charlotte, NC 28203 USA.
[Davern, Timothy J.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Navarro, Victor J.] Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA.
[Reddy, K. Rajender] Univ Penn, Philadelphia, PA 19104 USA.
[Talwalkar, Jayant A.] Mayo Clin, Coll Med, Rochester, MN USA.
[Hoofnagle, Jay H.] NIDDK, Bethesda, MD USA.
[Gu, Jiezhun] Duke Clin Res Inst, Durham, NC USA.
[Stolz, Andrew] Univ So Calif, Los Angeles, CA USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 518A
EP 519A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002320
ER
PT J
AU Bell, LN
Vuppalanchi, R
Watkins, PB
Bonkovsky, HL
Serrano, J
Fontana, RJ
Wang, M
Rochon, J
Chalasani, NP
AF Bell, Lauren N.
Vuppalanchi, Raj
Watkins, Paul B.
Bonkovsky, Herbert L.
Serrano, Jose
Fontana, Robert J.
Wang, Mu
Rochon, James
Chalasani, Naga P.
TI SERUM PROTEOMIC PROFILING IN PATIENTS WITH DRUG-INDUCED LIVER INJURY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Wang, Mu] Indiana Univ, Prot Anal Res Ctr, Indianapolis, IN 46204 USA.
[Watkins, Paul B.] Univ N Carolina, Chapel Hill, NC USA.
[Bonkovsky, Herbert L.] Carolinas Med Ctr, Cannon Res Ctr, Charlotte, NC 28203 USA.
[Bonkovsky, Herbert L.] Carolinas Med Ctr, Ctr Liver & Digest Dis, Charlotte, NC 28203 USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Farmington, CT USA.
[Serrano, Jose] NIDDK, Liver Dis Res Branch, NIH, Bethesda, MD USA.
[Fontana, Robert J.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Rochon, James] Duke Univ, Duke Clin Res Inst, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 521A
EP 522A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002326
ER
PT J
AU Vega, M
Vuppalanchi, R
Bonkovsky, HL
Reddy, KR
Talwalkar, JA
Seeff, LB
Serrano, J
Navarro, VJ
AF Vega, Maricruz
Vuppalanchi, Raj
Bonkovsky, Herbert L.
Reddy, K. Rajender
Talwalkar, Jayant A.
Seeff, Leonard B.
Serrano, Jose
Navarro, Victor J.
TI THE US DRUG INDUCED LIVER INJURY NETWORK: ESTABLISHMENT OF AN HERBAL AND
DIETARY SUPPLEMENT (HDS) REPOSITORY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Vega, Maricruz; Navarro, Victor J.] Thomas Jefferson Univ, Div Gastroenterol & Hepatol, Philadelphia, PA 19107 USA.
[Vuppalanchi, Raj] Indiana Univ, Indianapolis, IN 46204 USA.
[Bonkovsky, Herbert L.] Carolinas Med Ctr, Charlotte, NC 28203 USA.
[Reddy, K. Rajender] Univ Penn, Div Gastroenterol, Philadelphia, PA 19104 USA.
[Talwalkar, Jayant A.] Mayo Clin, Rochester, MN USA.
[Seeff, Leonard B.] US FDA, Bethesda, MD 20014 USA.
[Serrano, Jose] NIDDKD, Div Digest Dis & Nutr, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 528A
EP 529A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002341
ER
PT J
AU Steuerwald, N
Parsons, J
Norton, HJ
Saha, D
Chalasani, NP
Bell, LN
Fontana, RJ
Watkins, PB
Serrano, J
Bonkovsky, HL
AF Steuerwald, Nury
Parsons, Judith
Norton, Harry J.
Saha, Dhanonjoy
Chalasani, Naga P.
Bell, Lauren N.
Fontana, Robert J.
Watkins, Paul B.
Serrano, Jose
Bonkovsky, Herbert L.
TI CHEMOKINE/CYTOKINE PROFILES IN PATIENTS WITH ACUTE DILI: RESULTS FROM
THE US DRUG-INDUCED LIVER INJURY NETWORK
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Steuerwald, Nury; Parsons, Judith; Norton, Harry J.; Saha, Dhanonjoy; Bonkovsky, Herbert L.] Carolinas Med Ctr, Cannon Res Ctr, Charlotte, NC 28203 USA.
[Chalasani, Naga P.; Bell, Lauren N.] Indiana Univ, Indianapolis, IN 46204 USA.
[Fontana, Robert J.] Univ Michigan Hosp, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Watkins, Paul B.] Hamner Univ N Carolina, Inst Drug Safety Sci, Res Triangle Pk, NC USA.
[Serrano, Jose] NIDDK, Digest Dis Branch, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 529A
EP 529A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002342
ER
PT J
AU Werner, JM
Heller, T
Rehermann, B
AF Werner, Jens M.
Heller, Theo
Rehermann, Barbara
TI NATURAL KILLER CELL RESPONSES IN HEPATITIS C VIRUS EXPOSED HEALTHCARE
WORKERS WHO DO NOT DEVELOP ACUTE INFECTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Werner, Jens M.; Heller, Theo; Rehermann, Barbara] NIDDK, Liver Dis Branch, NIH, DHHS, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 557A
EP 557A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002399
ER
PT J
AU Noureddin, M
Wright, EC
Zhao, XC
Clark, S
Thomas, E
Alter, HJ
Kleiner, DE
Liang, TJ
Ghany, MG
AF Noureddin, Mazen
Wright, Elizabeth C.
Zhao, Xiongce
Clark, Shauna
Thomas, Emmanuel
Alter, Harvey J.
Kleiner, David E.
Liang, T. Jake
Ghany, Marc G.
TI RELATIONSHIP BETWEEN IL28B GENOTYPE AND HISTOLOGICAL PROGRESSION IN
PATIENTS WITH CHRONIC HEPATITIS C
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Noureddin, Mazen; Wright, Elizabeth C.; Zhao, Xiongce; Clark, Shauna; Thomas, Emmanuel; Liang, T. Jake; Ghany, Marc G.] NIDDK, Bethesda, MD USA.
[Alter, Harvey J.] NIH, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 562A
EP 562A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002409
ER
PT J
AU Gara, N
Kleiner, DE
Zhao, XC
Koh, C
Rotman, Y
Heller, T
Abdalla, AA
Sarkar, S
Noureddin, M
Wright, EC
Hoofnagle, JH
Liang, TJ
Ghany, MG
AF Gara, Naveen
Kleiner, David E.
Zhao, Xiongce
Koh, Christopher
Rotman, Yaron
Heller, Theo
Abdalla, Adil A.
Sarkar, Souvik
Noureddin, Mazen
Wright, Elizabeth C.
Hoofnagle, Jay H.
Liang, T. Jake
Ghany, Marc G.
TI PERFORMANCE OF TRANSIENT ELASTOGRAPHY AND APRI FOR PREDICTION OF
ADVANCED LIVER DISEASE IN A NORTH AMERICAN POPULATION WITH CHRONIC
HEPATITIS C
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Gara, Naveen; Koh, Christopher; Rotman, Yaron; Heller, Theo; Abdalla, Adil A.; Sarkar, Souvik; Noureddin, Mazen; Hoofnagle, Jay H.; Liang, T. Jake; Ghany, Marc G.] NIH, LDB, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, NIH, Bethesda, MD 20892 USA.
[Zhao, Xiongce; Wright, Elizabeth C.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 570A
EP 570A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002423
ER
PT J
AU Noureddin, M
Rotman, Y
Feld, JJ
Han, H
Park, YJ
Koh, C
Abdalla, AA
Sarkar, S
Gara, N
Thomas, E
Holz, L
Park, SH
Clark, S
Ghany, MG
Doo, E
Heller, T
Rehermann, B
Hoofnagle, JH
Liang, TJ
AF Noureddin, Mazen
Rotman, Yaron
Feld, Jordan J.
Han, Hwalih
Park, Yoon J.
Koh, Christopher
Abdalla, Adil A.
Sarkar, Souvik
Gara, Naveen
Thomas, Emmanuel
Holz, Lauren
Park, Su-Hyung
Clark, Shauna
Ghany, Marc G.
Doo, Edward
Heller, Theo
Rehermann, Barbara
Hoofnagle, Jay H.
Liang, T. Jake
TI THE IL28B POLYMORPHISM RS12979860 DOES NOT PREDICT RESPONSE TO RIBAVIRIN
MONOTHERAPY IN PATIENTS WITH CHRONIC HEPATITIS C
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Noureddin, Mazen; Rotman, Yaron; Han, Hwalih; Park, Yoon J.; Koh, Christopher; Abdalla, Adil A.; Sarkar, Souvik; Gara, Naveen; Thomas, Emmanuel; Holz, Lauren; Park, Su-Hyung; Clark, Shauna; Ghany, Marc G.; Doo, Edward; Heller, Theo; Rehermann, Barbara; Hoofnagle, Jay H.; Liang, T. Jake] NIDDK, Bethesda, MD USA.
[Feld, Jordan J.] Univ Toronto, Toronto, ON, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 576A
EP 577A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002437
ER
PT J
AU Han, H
Noureddin, M
Park, YJ
Hoofnagle, JH
Liang, TJ
Rotman, Y
AF Han, Hwalih
Noureddin, Mazen
Park, Yoon J.
Hoofnagle, Jay H.
Liang, T. Jake
Rotman, Yaron
TI CHANGES IN ORAL TEMPERATURE AFTER THE INITIAL INJECTION OF PEGINTERFERON
ALFA-2A IN PATIENTS WITH CHRONIC HEPATITIS C REFLECT HOST-INTERFERON
RESPONSIVENESS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Han, Hwalih; Noureddin, Mazen; Park, Yoon J.; Hoofnagle, Jay H.; Liang, T. Jake; Rotman, Yaron] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 600A
EP 601A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002486
ER
PT J
AU Mi, LJ
Rincon-Bejarano, LA
Babbar, R
Chiu, EK
Martell, M
Karsdon, J
Ghany, MG
AF Mi, Li-Jun
Rincon-Bejarano, Luz A.
Babbar, Rajeev
Chiu, Edward K.
Martell, Marialina
Karsdon, Jeffrey
Ghany, Marc G.
TI VITAMIN D DEFICIENCY IN ASIAN-AMERICAN PATIENTS WITH CHRONIC HEPATITIS B
IN NEW YORK DOWNTOWN HOSPITAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Mi, Li-Jun; Rincon-Bejarano, Luz A.; Babbar, Rajeev; Chiu, Edward K.; Martell, Marialina; Karsdon, Jeffrey] New York Downtown Hosp, New York, NY USA.
[Ghany, Marc G.] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 614A
EP 614A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002514
ER
PT J
AU Bell, LN
Molleston, JP
Lavine, JE
Schwimmer, JB
Murray, KF
Rosenthal, P
Abrams, SH
Sanyal, AJ
Brunt, EM
Kleiner, DE
Unalp, A
Wang, JX
Wilson, L
Chalasani, NP
AF Bell, Lauren N.
Molleston, Jean P.
Lavine, Joel E.
Schwimmer, Jeffrey B.
Murray, Karen F.
Rosenthal, Philip
Abrams, Stephanie H.
Sanyal, Arun J.
Brunt, Elizabeth M.
Kleiner, David E.
Unalp, Aynur
Wang, Jiangxia
Wilson, Laura
Chalasani, Naga P.
TI CHANGES IN ADIPOSE TISSUE INSULIN RESISTANCE CORRELATE WITH CHANGES IN
ALT AND LOBULAR INFLAMMATION IN CHILDREN ENROLLED IN THE TONIC TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Bell, Lauren N.; Molleston, Jean P.; Chalasani, Naga P.] Indiana Univ, Indianapolis, IN 46204 USA.
[Lavine, Joel E.] Columbia Univ, New York, NY USA.
[Schwimmer, Jeffrey B.] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Murray, Karen F.] Seattle Childrens Hosp, Seattle, WA USA.
[Rosenthal, Philip] Univ Calif San Francisco, Ctr Liver, San Francisco, CA 94143 USA.
[Abrams, Stephanie H.] Baylor Coll Med, Houston, TX 77030 USA.
[Sanyal, Arun J.] Virginia Commonwealth Univ, Richmond, VA USA.
[Brunt, Elizabeth M.] Washington Univ, Sch Med, St Louis, MO USA.
[Kleiner, David E.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Unalp, Aynur; Wang, Jiangxia; Wilson, Laura] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 711A
EP 711A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002724
ER
PT J
AU Liu, HX
Zhan, Q
Gonzalez, FJ
Wan, YJY
AF Liu, Hui-Xin
Zhan, Qi
Gonzalez, Frank J.
Wan, Yu-Jui Yvonne
TI PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR (PPAR) beta IS ESSENTIAL FOR
NORMAL PROGRESSION OF LIVER REGENERATION BY MODULATING LIPID HOMEOSTASIS
AND PHOSPHOINOSITIDE-DEPENDENT PROTEIN KINASE 1 (PDK1)/AKT-MEDIATED
SIGNALING
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Liu, Hui-Xin; Zhan, Qi; Wan, Yu-Jui Yvonne] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Kansas City, KS 66103 USA.
[Gonzalez, Frank J.] NCI, Natl Ilnstitutes Hlth, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 714A
EP 715A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002732
ER
PT J
AU Enriquez-Cortina, GC
Cornejo, MDDC
Lombarri, NN
Dominguez, M
Bucio, L
Souza, V
Thorgeirsson, SS
Factor, VM
Conner, EA
Dominguez, M
Gomez-Quiroz, LE
Gutierrez-Ruiz, MC
AF Enriquez-Cortina, Gloria C.
Clavijo Cornejo, Maria del Refugio Denise
Lombarri, Natalia Nuno
Dominguez, Mayra
Bucio, Leticia
Souza, Veronica
Thorgeirsson, Snorri S.
Factor, Valentina M.
Conner, Elizabeth A.
Dominguez, Marcela
Gomez-Quiroz, Luis E.
Gutierrez-Ruiz, Maria C.
TI HGF INDUCES THE ACTIVATION OF NRF2 IN MOUSE HEPATOCYTES BY A NADPH
OXIDASE AND PKC DEPENDENT MECHANISM
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Enriquez-Cortina, Gloria C.; Clavijo Cornejo, Maria del Refugio Denise; Lombarri, Natalia Nuno; Dominguez, Mayra; Bucio, Leticia; Souza, Veronica; Dominguez, Marcela; Gomez-Quiroz, Luis E.; Gutierrez-Ruiz, Maria C.] Univ Autonoma Metropolitana, Mexico City, DF, Mexico.
[Thorgeirsson, Snorri S.; Factor, Valentina M.; Conner, Elizabeth A.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RI Gomez-Quiroz, Luis/L-8415-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 717A
EP 718A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578002740
ER
PT J
AU Kong, XN
Feng, DC
Bertola, A
Park, O
Wang, H
Yin, S
Gao, B
AF Kong, Xiaoni
Feng, Dechun
Bertola, Adeline
Park, Ogyi
Wang, Hua
Yin, Shi
Gao, Bin
TI INTERLUKIN-22 INDUCES HEPATIC STELLATE CELL SENESCENCE AND RESTRICTS
LIVER FIBROSIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Kong, Xiaoni; Feng, Dechun; Bertola, Adeline; Park, Ogyi; Wang, Hua; Yin, Shi; Gao, Bin] NIAAA, Lab Liver Dis, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 733A
EP 733A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003013
ER
PT J
AU Marquardt, JU
Maass, T
Krupp, M
Staib, F
Andersen, JB
Galle, PR
Thorgeirsson, SS
Teufel, A
AF Marquardt, Jens U.
Maass, Thorsten
Krupp, Markus
Staib, Frank
Andersen, Jesper B.
Galle, Peter R.
Thorgeirsson, Snorri S.
Teufel, Andreas
TI DISSECTING THE ROLE OF PDGF-B DURING LIVER FIBROGENESIS: MECHANISTIC AND
THERAPEUTIC IMPLICATIONS FROM A TRANSGENIC MOUSE MODEL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Marquardt, Jens U.; Maass, Thorsten; Krupp, Markus; Staib, Frank; Galle, Peter R.; Teufel, Andreas] Johannes Gutenberg Univ Mainz, Dept Internal Med 1, D-6500 Mainz, Germany.
[Marquardt, Jens U.; Andersen, Jesper B.; Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 738A
EP 738A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003024
ER
PT J
AU Zhang, YX
Bonzo, JA
Gonzalez, FJ
Wang, L
AF Zhang, Yuxia
Bonzo, Jessica A.
Gonzalez, Frank J.
Wang, Li
TI DIURNAL REGULATION OF EGR-1 EXPRESSION BY HNF4 alpha AND SHP CROSSTALK
IN LIVER FIBROSIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Zhang, Yuxia; Wang, Li] Univ Utah, Sch Med, Dept Med, Salt Lake City, UT USA.
[Zhang, Yuxia; Wang, Li] Univ Utah, Sch Med, Dept Oncol Sci, Salt Lake City, UT USA.
[Bonzo, Jessica A.; Gonzalez, Frank J.] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 744A
EP 745A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003039
ER
PT J
AU Fu, D
Mitra, K
Lippincott-Schwartz, J
Arias, IM
AF Fu, Dong
Mitra, Kasturi
Lippincott-Schwartz, Jennifer
Arias, Irwin M.
TI HEPATOCYTE POLARIZATION REQUIRES MITOCHONDRIAL FUSION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Fu, Dong; Lippincott-Schwartz, Jennifer; Arias, Irwin M.] NICHD, NIH, Bethesda, MD USA.
[Mitra, Kasturi] NHLBI, NIH, Bethesda, MD 20892 USA.
RI Fu, Dong /J-1426-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 772A
EP 773A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003104
ER
PT J
AU Andersen, JB
Spee, B
Blechacz, B
Avital, I
Komuta, M
Barbour, A
Roskams, T
Roberts, LR
Factor, VM
Thorgeirsson, SS
AF Andersen, Jesper B.
Spee, Bart
Blechacz, Boris
Avital, Itzhak
Komuta, Mina
Barbour, Andrew
Roskams, Tania
Roberts, Lewis R.
Factor, Valentina M.
Thorgeirsson, Snorri S.
TI GENOMIC AND GENETIC CHARACTERIZATION OF HUMAN CHOLANGIOCARCINOMA
IDENTIFIES TREATMENT OPTIONS FOR TYROSINE KINASE INHIBITORS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Andersen, Jesper B.; Factor, Valentina M.; Thorgeirsson, Snorri S.] NCI, LEC, Bethesda, MD 20892 USA.
[Spee, Bart; Komuta, Mina; Roskams, Tania] Katholieke Univ Leuven, Louvain, Belgium.
[Blechacz, Boris; Roberts, Lewis R.] Mayo Clin, Rochester, MN USA.
[Avital, Itzhak] NCI, Surg Branch, Bethesda, MD 20892 USA.
[Barbour, Andrew] Univ Queensland, Brisbane, Qld, Australia.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 777A
EP 778A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003115
ER
PT J
AU Ahlenstiel, G
Edlich, B
Zabaleta, A
Rehermann, B
Noureddin, M
Feld, JJ
Liang, TJ
Rotman, Y
AF Ahlenstiel, Golo
Edlich, Birgit
Zabaleta, Aintzane
Rehermann, Barbara
Noureddin, Mazen
Feld, Jordan J.
Liang, T. Jake
Rotman, Yaron
TI EARLY CHANGES IN INTERFERON SIGNALING DEFINE NATURAL KILLER CELL
RESPONSE AND REFRACTORINESS DURING INTERFERON-BASED THERAPY OF HEPATITIS
C
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Ahlenstiel, Golo; Edlich, Birgit; Zabaleta, Aintzane; Rehermann, Barbara; Noureddin, Mazen; Feld, Jordan J.; Liang, T. Jake; Rotman, Yaron] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 796A
EP 796A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003157
ER
PT J
AU Thompson, AJ
Clark, PJ
Vock, DM
Pfeiffer, R
Tillmann, HL
Patel, K
Naggie, S
Poordad, FF
Nyberg, LM
Noviello, S
Pedicone, L
Brass, CA
Albrecht, JK
Goldstein, DB
McHutchison, JG
O'Brien, TR
Sulkowski, MS
Muir, AJ
AF Thompson, Alexander J.
Clark, Paul J.
Vock, David M.
Pfeiffer, Ruth
Tillmann, Hans L.
Patel, Keyur
Naggie, Susanna
Poordad, F. Fred
Nyberg, Lisa M.
Noviello, Stephanie
Pedicone, Lisa
Brass, Clifford A.
Albrecht, Janice K.
Goldstein, David B.
McHutchison, John G.
O'Brien, Thomas R.
Sulkowski, Mark S.
Muir, Andrew J.
TI PREDICTING PEGINTERFERON-alpha AND RIBAVIRIN TREATMENT RESPONSE IN
GENOTYPE 1 HCV PATIENTS - SIMPLE NOMOGRAMS TO SUPPORT CLINICIANS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Thompson, Alexander J.; Clark, Paul J.; Vock, David M.; Tillmann, Hans L.; Patel, Keyur; Naggie, Susanna; Muir, Andrew J.] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC USA.
[Thompson, Alexander J.] St Vincents Hosp, Fitzroy, Vic 3065, Australia.
[Goldstein, David B.] Duke Univ, Ctr Human Genome Variat, Durham, NC USA.
[Pfeiffer, Ruth; O'Brien, Thomas R.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Poordad, F. Fred] Cedars Sinai Med Ctr, Dept Gastroenterol, Los Angeles, CA 90048 USA.
[Nyberg, Lisa M.] Kaiser Permanente, San Diego, CA USA.
[Noviello, Stephanie; Pedicone, Lisa; Brass, Clifford A.; Albrecht, Janice K.] Merck & Co Inc, Whitehouse Stn, NJ USA.
[McHutchison, John G.] Gilead Sci Inc, Foster City, CA 94404 USA.
[Sulkowski, Mark S.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RI Clark, Paul/A-1480-2012
OI Clark, Paul/0000-0002-1821-4969
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 803A
EP 804A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003171
ER
PT J
AU Osinusi, A
Chary, A
Kottilil, S
Winters, MA
Naggie, S
Masur, H
Polis, MA
Holodniy, M
AF Osinusi, Anu
Chary, Aarthi
Kottilil, Shyam
Winters, Mark A.
Naggie, Susanna
Masur, Henry
Polis, Michael A.
Holodniy, Mark
TI IL28B POLYMORPHISM IS NOT ASSOCIATED WITH HCV PROTEASE DIVERSITY IN
HIV/HCV-COINFECTED PATIENTS TREATED WITH AN INTERFERON-BASED REGIMEN
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Osinusi, Anu; Kottilil, Shyam; Polis, Michael A.] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
[Osinusi, Anu] NCI Frederick Inc, SAIC Frederick, CMRP, Clin Res Directorate, Frederick, MD USA.
[Chary, Aarthi; Winters, Mark A.; Holodniy, Mark] Veterans Affairs Palo Alto Hlth Care Syst, Palo Alto, CA USA.
[Chary, Aarthi; Winters, Mark A.; Holodniy, Mark] Stanford Univ, Stanford, CA 94305 USA.
[Naggie, Susanna] Duke Clin Res Inst, Durham, NC USA.
[Masur, Henry] NIH, CCMD, CC, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 815A
EP 815A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003193
ER
PT J
AU Kohli, A
Naggie, S
Polis, MA
Masur, H
Kottilil, S
AF Kohli, Anita
Naggie, Susanna
Polis, Michael A.
Masur, Henry
Kottilil, Shyam
TI HIV/HCV-COINFECTED NATURAL VIRAL SUPPRESSORS HAVE BETTER VIROLOGIC
RESPONSES TO PEG-IFN AND RIBAVIRIN THAN ARV-TREATED HIV/HCV PATIENTS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Kohli, Anita; Polis, Michael A.; Masur, Henry; Kottilil, Shyam] NIH, Bethesda, MD 20892 USA.
[Naggie, Susanna] Duke, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 847A
EP 847A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003254
ER
PT J
AU Buckett, D
Shebl, FM
Pfeiffer, R
O'Brien, TR
AF Buckett, Dianna
Shebl, Fatma M.
Pfeiffer, Ruth
O'Brien, Thomas R.
TI IS ONE ALLELE BETTER THAN NONE? A META-ANALYSIS OF IL28B RS12979860
GENOTYPES AND CLEARANCE OF HEPATITIS C VIRUS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Buckett, Dianna; Shebl, Fatma M.; Pfeiffer, Ruth; O'Brien, Thomas R.] NIH, Dept Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 854A
EP 855A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003269
ER
PT J
AU Osinusi, A
Naggie, S
Poonia, S
Trippler, M
Hu, ZH
Funk, E
Schlaak, JF
Fishbein, D
Masur, H
Polis, MA
Kottilil, S
AF Osinusi, Anu
Naggie, Susanna
Poonia, Seerat
Trippler, Martin
Hu, Zonghui
Funk, Emily
Schlaak, Joerg F.
Fishbein, Dawn
Masur, Henry
Polis, Michael A.
Kottilil, Shyam
TI ITPA GENE POLYMORPHISMS SIGNIFICANTLY AFFECT HEMOGLOBIN DECLINE AND
TREATMENT OUTCOMES IN HIV/HCV CO-INFECTED PATIENTS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Osinusi, Anu; Poonia, Seerat; Funk, Emily; Polis, Michael A.; Kottilil, Shyam] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
[Osinusi, Anu; Fishbein, Dawn] NCI Frederick Inc, Clin Res Directorate, CMRP, SAIC Frederick, Frederick, MD USA.
[Naggie, Susanna] Duke Clin Res Inst, Durham, NC USA.
[Trippler, Martin; Schlaak, Joerg F.] Univ Hosp Essen, Essen, Germany.
[Hu, Zonghui] NIAID, BRB, NIH, Bethesda, MD 20892 USA.
[Masur, Henry] NIH, CCMD, CC, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 854A
EP 854A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003268
ER
PT J
AU Feld, JJ
Kleiner, DE
Haynes-Williams, V
Nichols, J
Hoofnagle, JH
Liang, TJ
Gladwin, M
Kato, GJ
Heller, T
AF Feld, Jordan J.
Kleiner, David E.
Haynes-Williams, Vanessa
Nichols, James
Hoofnagle, Jay H.
Liang, T. Jake
Gladwin, Mark
Kato, Gregory J.
Heller, Theo
TI DIRECT HYPERBILIRUBINEMIA IN SICKLE CELL DISEASE IS A MARKER OF
INTRINSIC LIVER PATHOLOGY AND A PREDICTOR OF MORTALITY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Feld, Jordan J.; Haynes-Williams, Vanessa; Hoofnagle, Jay H.; Liang, T. Jake; Heller, Theo] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Gladwin, Mark] Univ Pittsburgh, Pittsburgh, PA USA.
[Nichols, James; Kato, Gregory J.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, NIH, Bethesda, MD 20892 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 WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 923A
EP 923A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003410
ER
PT J
AU Feld, JJ
Kleiner, DE
Haynes-Williams, V
Nichols, J
Hoofnagle, JH
Liang, TJ
Gladwin, M
Kato, GJ
Heller, T
AF Feld, Jordan J.
Kleiner, David E.
Haynes-Williams, Vanessa
Nichols, James
Hoofnagle, Jay H.
Liang, T. Jake
Gladwin, Mark
Kato, Gregory J.
Heller, Theo
TI FERRITIN ELEVATION IS A MARKER OF TOTAL BODY IRON AND PREDICTOR OF
MORTALITY IN SICKLE CELL DISEASE
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Feld, Jordan J.; Haynes-Williams, Vanessa; Hoofnagle, Jay H.; Liang, T. Jake; Heller, Theo] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Gladwin, Mark] Univ Pittsburgh, Pittsburgh, PA USA.
[Nichols, James; Kato, Gregory J.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, NIH, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 929A
EP 930A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003424
ER
PT J
AU Yamazaki, Y
Kakizaki, S
Moore, R
Mori, M
Negishi, M
AF Yamazaki, Yuichi
Kakizaki, Satoru
Moore, Rick
Mori, Masatomo
Negishi, Masahiko
TI NUCLEAR RECEPTOR CAR (NR1I3) IS ESSENTIAL FOR DDC-INDUCED LIVER INJURY
AND OVAL CELL PROLIFERATION IN MOUSE LIVER
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Yamazaki, Yuichi; Moore, Rick; Negishi, Masahiko] NIEHS, Pharmacogenet Sect, LRDT, NIH, Res Triangle Pk, NC 27709 USA.
[Yamazaki, Yuichi; Kakizaki, Satoru; Mori, Masatomo] Gunma Univ, Grad Sch Med, Dept Med & Mol Sci, Gunma, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 956A
EP 956A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003485
ER
PT J
AU Li, Y
Wang, H
Wong, KA
Gao, B
Zang, MW
AF Li, Yu
Wang, Hua
Wong, Kimberly A.
Gao, Bin
Zang, Mengwei
TI MTORC1 IS AN IMPORTANT REGULATOR FOR INDUCTION OF ER STRESS AND
INFLAMMATORY RESPONSE DURING ALCOHOLIC LIVER INJURY IN MICE
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Li, Yu; Wong, Kimberly A.; Zang, Mengwei] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Wang, Hua; Gao, Bin] NIAAA, Lab Liver Dis, NIH, Bethesda, WA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 971A
EP 971A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003522
ER
PT J
AU Feng, DC
Kong, XN
Weng, HL
Park, O
Wang, H
Zheng, MQ
Dooley, S
Kolls, J
Young, HA
Gao, B
AF Feng, Dechun
Kong, Xiaoni
Weng, Honglei
Park, Ogyi
Wang, Hua
Zheng, Mingquan
Dooley, Steven
Kolls, Jay
Young, Howard A.
Gao, Bin
TI IL-22 PROMOTES LIVER PROGENITOR CELL PROLIFERATION IN MICE: A KEY LINKER
BETWEEN LIVER INFLAMMATION AND DUCTULAR REACTION IN PATIENTS WITH VIRAL
HEPATITIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Feng, Dechun; Kong, Xiaoni; Park, Ogyi; Wang, Hua; Gao, Bin] NIAAA, Lab Liver Dis, NIH, D-6800 Bethesda, MD USA.
[Weng, Honglei; Dooley, Steven] Univ Heidelberg, Med Clin Fac Med Mannheim, Mannheim, Germany.
[Zheng, Mingquan; Kolls, Jay] Louisiana State Univ, Hlth Sci Ctr, Dept Genet, New Orleans, LA 21701 USA.
[Young, Howard A.] NCI, Lab Expt Immunol, Canc & Inflammat Program, NIH, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 979A
EP 979A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578003539
ER
PT J
AU Trehanpati, N
Shrivastava, S
Kumar, B
Sukriti, S
Tripathi, DM
Singh, S
Gupta, S
Kottilil, S
Sarin, SK
AF Trehanpati, Nirupma
Shrivastava, Shikha
Kumar, Binayak
Sukriti, Sukriti
Tripathi, Dinesh M.
Singh, Shivender
Gupta, Subhash
Kottilil, Shyam
Sarin, Shiv K.
TI NOTCH 1 HELPS DIFFERENTIATE IMMUNE CELLS IN ACUTE HEPATITIS B AND WITH
TGF beta REGULATES FOXP3 EXPRESSION ON LIVER INFILTRATING LYMPHOCYTES IN
HBV RELATED CIRRHOSIS AND HCC
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Trehanpati, Nirupma; Shrivastava, Shikha; Kumar, Binayak; Sukriti, Sukriti; Tripathi, Dinesh M.; Singh, Shivender; Sarin, Shiv K.] Inst Liver & Biliary Sci, New Delhi, India.
[Kottilil, Shyam] NIAID, NIH, Bethesda, WA USA.
[Gupta, Subhash] Indraprastha Apollo Hosp, New Delhi, India.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1093A
EP 1094A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004007
ER
PT J
AU Noureddin, M
Vaughn, IA
Neuschwander-Tetri, BA
Sanyal, AJ
McCullough, AJ
Merriman, RB
Yates, KP
Tonascia, J
Unalp-Arida, A
Doo, E
Kleiner, DE
Behling, CA
Loomba, R
AF Noureddin, Mazen
Vaughn, Ivana A.
Neuschwander-Tetri, Brent A.
Sanyal, Arun J.
McCullough, Arthur J.
Merriman, Raphael B.
Yates, Katherine P.
Tonascia, James
Unalp-Arida, Aynur
Doo, Edward
Kleiner, David E.
Behling, Cynthia A.
Loomba, Rohit
TI CLINICAL AND HISTOLOGICAL DETERMINANTS OF NONALCOHOLIC STEATOHEPATITIS
(NASH) AND ADVANCED FIBROSIS IN THE ELDERLY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Noureddin, Mazen; Loomba, Rohit] UCSD, La Jolla, CA USA.
[Vaughn, Ivana A.; Yates, Katherine P.; Tonascia, James] Johns Hopkins Univ, Baltimore, MD USA.
[Neuschwander-Tetri, Brent A.; Unalp-Arida, Aynur] St Louis Univ, St Louis, MO 63103 USA.
[Sanyal, Arun J.] VCU, Div Gastroenterol Hepatol & Nutr, Richmond, VA USA.
[McCullough, Arthur J.] Cleveland Clin, Cleveland, OH 44106 USA.
[Merriman, Raphael B.] Calif Pacific Med Ctr & Res Inst, San Francisco, CA USA.
[Doo, Edward] NIDDK, Bethesda, MD USA.
[Kleiner, David E.] NCI, Bethesda, MD 20892 USA.
[Behling, Cynthia A.] Sharp Mem Hosp & Rehabil Ctr, San Diego, CA USA.
RI Vaughn, Ivana/B-6138-2016
OI Vaughn, Ivana/0000-0002-7201-0289
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1118A
EP 1118A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004062
ER
PT J
AU Rotman, Y
Gara, N
Koh, C
Han, H
Kleiner, DE
Liang, TJ
AF Rotman, Yaron
Gara, Naveen
Koh, Christopher
Han, Hwalih
Kleiner, David E.
Liang, T. Jake
TI SUCCESSFUL TREATMENT OF NON-ALCOHOLIC STEATOHEPATITIS DOES NOT IMPROVE
SERUM FGF-21 LEVELS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Rotman, Yaron; Gara, Naveen; Koh, Christopher; Han, Hwalih; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Kleiner, David E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1122A
EP 1123A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004072
ER
PT J
AU Ruh, CE
Matthews, CE
Freedman, ND
Everhart, JE
AF Ruh, Constance E.
Matthews, Charles E.
Freedman, Neal D.
Everhart, James E.
TI RELATIONSHIP OF LIVER INJURY WITH PHYSICAL ACTIVITY MEASURED BY
ACCELEROMETER IN THE UNITED STATES POPULATION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Ruh, Constance E.] Social & Sci Syst Inc, Silver Spring, MD USA.
[Matthews, Charles E.; Freedman, Neal D.] NCI, Rockville, MD USA.
[Everhart, James E.] NIDDK, Bethesda, MD USA.
RI Freedman, Neal/B-9741-2015
OI Freedman, Neal/0000-0003-0074-1098
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1133A
EP 1134A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004095
ER
PT J
AU Buetow, KH
Braun, R
Hu, Y
Sanyal, AJ
AF Buetow, Kenneth H.
Braun, Rosemary
Hu, Ying
Sanyal, Arun J.
TI ANALYSIS OF GENOME-WIDE VARIATION WITHIN NAFLD POPULATION IDENTIFIES
BIOLOGIC NETWORKS THAT ARE ASSOCIATED WITH DIFFERENT DISEASE PHENOTYPES
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Sanyal, Arun J.] Virginia Commonwealth Univ, Richmond, VA USA.
[Buetow, Kenneth H.; Braun, Rosemary; Hu, Ying] NCI, Lab Populat Genet, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1151A
EP 1151A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004133
ER
PT J
AU Holz, L
Yoon, JC
Raghuraman, S
Moir, S
Sneller, M
Rehermann, B
AF Holz, Lauren
Yoon, Joo Chun
Raghuraman, Sukanya
Moir, Susan
Sneller, Michael
Rehermann, Barbara
TI B CELL HOMEOSTASIS IN CHRONIC HEPATITIS C VIRUS-RELATED MIXED
CRYOGLOBULINEMIA
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Holz, Lauren; Yoon, Joo Chun; Raghuraman, Sukanya; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH,DHHS, Bethesda, MD USA.
[Moir, Susan; Sneller, Michael] NIAID, Immunoregulat Lab, NIH, DHHS, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1179A
EP 1179A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004197
ER
PT J
AU Silver, D
Karnik, G
Osinusi, A
Silk, R
Stabinski, L
Doonquah, L
Henn, S
Teferi, G
Masur, H
Kottilil, S
Fishbein, D
AF Silver, Dana
Karnik, Geeta
Osinusi, Anu
Silk, Rachel
Stabinski, Larissa
Doonquah, Leleka
Henn, Sarah
Teferi, Gebeyehu
Masur, Henry
Kottilil, Shyam
Fishbein, Dawn
TI LIVER FIBROSIS IN AFRICAN AMERICANS, COMPARING HCV MONO-INFECTION WITH
HIV-HCV COINFECTION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Silver, Dana; Masur, Henry] NIH CCMD, NIH, Bethesda, MD USA.
[Karnik, Geeta; Osinusi, Anu; Silk, Rachel; Fishbein, Dawn] NCI Frederic Inc, Support NIH CCMD, Clin Res Directorate CMRP, SAIC Frederick, Frederick, MD USA.
[Osinusi, Anu; Stabinski, Larissa; Kottilil, Shyam] NIH NIAID, NIH, Bethesda, MD USA.
[Doonquah, Leleka] Family & Med Counselling Serv Inc, Washington, DC USA.
[Teferi, Gebeyehu] Unity Healthcare Inc, Washington, DC USA.
[Henn, Sarah] Whitman Walker Hlth, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1186A
EP 1187A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004213
ER
PT J
AU Shebl, FM
Pfeiffer, R
Buckett, D
Muchmore, B
Chen, S
Dotrang, M
Prokunina-Olsson, L
Edlin, BR
O'Brien, TR
AF Shebl, Fatma M.
Pfeiffer, Ruth
Buckett, Dianna
Muchmore, Brian
Chen, Sabrina
Dotrang, Myhanh
Prokunina-Olsson, Ludmila
Edlin, Brian R.
O'Brien, Thomas R.
TI IL28B GENOTYPE AND SPONTANEOUS HCV CLEARANCE: IS A RECESSIVE GENETIC
MODEL BEST?
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Shebl, Fatma M.; Pfeiffer, Ruth; Buckett, Dianna; Muchmore, Brian; Prokunina-Olsson, Ludmila; O'Brien, Thomas R.] NCI, Rockville, MD USA.
[Chen, Sabrina] Informat Management Serv Inc, Silver Spring, MD USA.
[Edlin, Brian R.] SUNY Downstate Coll Med, Brooklyn, NY USA.
[Edlin, Brian R.] Urban Hlth Study, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1190A
EP 1190A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004221
ER
PT J
AU Sarkar, S
Jiang, Z
Evon, DM
Wahed, AS
Hoofnagle, JH
AF Sarkar, Souvik
Jiang, Zhen
Evon, Donna M.
Wahed, Abdus S.
Hoofnagle, Jay H.
TI FATIGUE BEFORE, DURING AND AFTER ANTIVIRAL THERAPY OF CHRONIC HEPATITIS
C: ANALYSIS OF THE VIRAHEP-C TRIAL
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Sarkar, Souvik; Hoofnagle, Jay H.] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Jiang, Zhen; Wahed, Abdus S.] Univ Pittsburgh, Dept Biostat, Pittsburgh, PA 15261 USA.
[Evon, Donna M.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1195A
EP 1195A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004231
ER
PT J
AU Noureddin, M
Woolridge, D
Zhao, XC
Noureddin, N
DeMino, M
Liang, TJ
Kleiner, DE
Heller, T
Hoofnagle, JH
AF Noureddin, Mazen
Woolridge, Daniel
Zhao, Xiongce
Noureddin, Nabil
DeMino, Mary
Liang, T. Jake
Kleiner, David E.
Heller, Theo
Hoofnagle, Jay H.
TI NON-INVASIVE PREDICTORS OF ADVANCED DISEASE IN PRIMARY BILIARY CIRRHOSIS
(PBC)
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Noureddin, Mazen; Woolridge, Daniel; Zhao, Xiongce; Noureddin, Nabil; DeMino, Mary; Liang, T. Jake; Heller, Theo; Hoofnagle, Jay H.] NIDDK, Bethesda, MD USA.
[Kleiner, David E.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1213A
EP 1213A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004269
ER
PT J
AU Noureddin, M
Matta, JR
Noureddin, N
Muldoon, N
Woolridge, D
Rotman, Y
Pettigrew, RI
Liang, TJ
Hoofnagle, JH
Heller, T
Gharib, AM
AF Noureddin, Mazen
Matta, Jatin R.
Noureddin, Nabil
Muldoon, Nancy
Woolridge, Daniel
Rotman, Yaron
Pettigrew, Roderic I.
Liang, T. Jake
Hoofnagle, Jay H.
Heller, Theo
Gharib, Ahmed M.
TI CORONARY ARTERY DISEASE IN PRIMARY BILIARY CIRRHOSIS (PBC) AS SHOWN BY
MULTI-DETECTOR CARDIAC COMPUTER TOMOGRAPHY (CT) SCAN
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Noureddin, Mazen; Matta, Jatin R.; Noureddin, Nabil; Woolridge, Daniel; Rotman, Yaron; Liang, T. Jake; Hoofnagle, Jay H.; Heller, Theo; Gharib, Ahmed M.] NIDDK, Bethesda, MD USA.
[Muldoon, Nancy] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
RI Gharib, Ahmed/O-2629-2016
OI Gharib, Ahmed/0000-0002-2476-481X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1213A
EP 1213A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004270
ER
PT J
AU Feld, JJ
Kleiner, DE
Sandler, NG
Haynes-Williams, V
Nichols, J
Hoofnagle, JH
Liang, TJ
Dovek, D
Gladwin, M
Kato, GJ
Heller, T
AF Feld, Jordan J.
Kleiner, David E.
Sandler, Netanya G.
Haynes-Williams, Vanessa
Nichols, James
Hoofnagle, Jay H.
Liang, T. Jake
Dovek, Daniel
Gladwin, Mark
Kato, Gregory J.
Heller, Theo
TI NON-CIRRHOTIC PORTAL HYPERTENSION IN SICKLE CELL DISEASE: AN
UNDERAPPRECIATED ENTITY
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Feld, Jordan J.; Haynes-Williams, Vanessa; Hoofnagle, Jay H.; Liang, T. Jake; Heller, Theo] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Gladwin, Mark] Univ Pittsburgh, Pittsburgh, PA USA.
[Nichols, James; Kato, Gregory J.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Kleiner, David E.] NCI, NIH, Bethesda, MD 20892 USA.
[Sandler, Netanya G.; Dovek, Daniel] NIAID, NIH, Bethesda, MD 20892 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 WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1236A
EP 1236A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004319
ER
PT J
AU Marquardt, JU
Fischer, K
Teufel, A
Thorgeirsson, SS
Galle, PR
Strand, S
AF Marquardt, Jens U.
Fischer, Kerstin
Teufel, Andreas
Thorgeirsson, Snorri S.
Galle, Peter R.
Strand, Susanne
TI PROGNOSTIC IMPLICATIONS OF SIRT6 IN HEPATOCELLULAR CARCINOMAS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Marquardt, Jens U.; Fischer, Kerstin; Teufel, Andreas; Galle, Peter R.; Strand, Susanne] Johannes Gutenberg Univ Mainz, Dept Internal Med, D-6500 Mainz, Germany.
[Marquardt, Jens U.; Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, CCR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1285A
EP 1285A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004424
ER
PT J
AU Maass, T
Westphal, H
Galle, PR
Teufel, A
AF Maass, Thorsten
Westphal, Heiner
Galle, Peter R.
Teufel, Andreas
TI DICKKOPF 2 (DKK2) DELETION RESULTS IN ENHANCED LIVER CANCER DEVELOPMENT
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Maass, Thorsten; Galle, Peter R.; Teufel, Andreas] Johannes Gutenberg Univ Mainz, Dept Med 1, D-6500 Mainz, Germany.
[Westphal, Heiner] NICHHD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1292A
EP 1292A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004438
ER
PT J
AU Zheng, X
Gai, XH
Hu, CL
Shire, AM
Elsawa, SF
Thorgeirsson, SS
Fernandez-Zapico, ME
Roberts, LR
AF Zheng, Xin
Gai, Xiaohong
Hu, Chunling
Shire, Abdirashid M.
Elsawa, Sherine F.
Thorgeirsson, Snorri S.
Fernandez-Zapico, Martin E.
Roberts, Lewis R.
TI GLI1 PROMOTES HCC RECURRENCE PARTLY VIA INDUCTION OF THE
EPITHELIAL-TO-MESENCHYMAL TRANSITION
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Zheng, Xin; Gai, Xiaohong; Hu, Chunling; Shire, Abdirashid M.; Roberts, Lewis R.] Mayo Clin, Coll Med, Rochester, MN USA.
[Zheng, Xin; Gai, Xiaohong; Hu, Chunling; Shire, Abdirashid M.; Elsawa, Sherine F.; Fernandez-Zapico, Martin E.; Roberts, Lewis R.] Mayo Clin, Schulze Ctr Novel Therapeut, Div Oncol Res, Rochester, MN USA.
[Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1298A
EP 1298A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004454
ER
PT J
AU Rotman, Y
Noureddin, M
Feld, JJ
Han, H
Park, YJ
Thomas, E
Abdalla, AA
Gara, N
Sarkar, S
Koh, C
Doo, E
Heller, T
Ghany, MG
Rehermann, B
Hoofnagle, JH
Liang, TJ
AF Rotman, Yaron
Noureddin, Mazen
Feld, Jordan J.
Han, Hwalih
Park, Yoon J.
Thomas, Emmanuel
Abdalla, Adil A.
Gara, Naveen
Sarkar, Souvik
Koh, Christopher
Doo, Edward
Heller, Theo
Ghany, Marc G.
Rehermann, Barbara
Hoofnagle, Jay H.
Liang, T. Jake
TI RIBAVIRIN EXERTS A WEAK INTERFERON-LIKE EFFECT ON GENE EXPRESSION IN THE
LIVER OF PATIENTS WITH CHRONIC HEPATITIS C
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Rotman, Yaron; Noureddin, Mazen; Feld, Jordan J.; Han, Hwalih; Park, Yoon J.; Thomas, Emmanuel; Abdalla, Adil A.; Gara, Naveen; Sarkar, Souvik; Koh, Christopher; Doo, Edward; Heller, Theo; Ghany, Marc G.; Rehermann, Barbara; Hoofnagle, Jay H.; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 1
U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1327A
EP 1328A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004521
ER
PT J
AU Kohli, A
Zhang, XZ
Funk, E
Polis, MA
Masur, H
Kottilil, S
AF Kohli, Anita
Zhang, Xiaozhen
Funk, Emily
Polis, Michael A.
Masur, Henry
Kottilil, Shyam
TI HCV INFECTION SELECTIVELY UPREGULATES IFN-lambda RA, ENHANCING
SUSCEPTIBILITY OF INFECTED HEPATOCYTES TO IFN-lambda OVER TIME
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Kohli, Anita; Zhang, Xiaozhen; Funk, Emily; Polis, Michael A.; Masur, Henry; Kottilil, Shyam] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1330A
EP 1330A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004527
ER
PT J
AU Aggarwal, R
Naik, A
Goel, A
Yu, CR
Goel, D
AF Aggarwal, Rakesh
Naik, Anshu
Goel, Amit
Yu, Claro
Goel, Divya
TI GENE EXPRESSION ANALYSIS IN PERIPHERAL BLOOD MONONUCLEAR CELLS IN
PATIENTS WITH ACUTE HEPATITIS E
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Aggarwal, Rakesh; Naik, Anshu; Goel, Amit; Goel, Divya] Sanjay Gandhi Postgrad Inst Med Sci, Lucknow, Uttar Pradesh, India.
[Yu, Claro] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1335A
EP 1335A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004539
ER
PT J
AU Dou, DR
Zhang, XZ
Kohli, A
Kottilil, S
AF Dou, Diana R.
Zhang, Xiaozhen
Kohli, Anita
Kottilil, Shyam
TI A NOVEL ANTIVIRAL MECHANISM OF INTERFERON-ALPHA: INTERFERON-ALPHA
INDUCED IFIT3 MEDIATES ANTI-HCV EFFECT
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Dou, Diana R.; Zhang, Xiaozhen; Kohli, Anita; Kottilil, Shyam] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1336A
EP 1337A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004542
ER
PT J
AU Kuntzen, T
Neumann-Haefelin, C
Lennon, N
Carlson, J
Berical, AC
Berlin, AM
Timm, J
Oniangue-Ndza, C
Young, S
Adams, S
Kleyman, M
Birch, CE
Ledlie, T
Roberts, AD
Rosen, HR
Bihl, FK
Cerny, A
Brander, C
Spengler, U
Galagan, J
Marincola, FM
Nusbaum, C
Walker, BD
Lake-Bakaar, G
Daari, ES
Jacobson, IM
Gomperts, ED
Edlin, BR
Thimme, R
Birren, BW
Donfield, SM
Chung, RT
Kim, AY
Lauer, GM
Talal, A
Marion, T
Carrington, M
Heckerman, D
Henn, MR
Allen, TM
AF Kuntzen, Thomas
Neumann-Haefelin, Christoph
Lennon, Niall
Carlson, Jonathan
Berical, Andrew C.
Berlin, Aaron M.
Timm, Joerg
Oniangue-Ndza, Cesar
Young, Sarah
Adams, Sharon
Kleyman, Marianna
Birch, Christopher E.
Ledlie, Timothy
Roberts, Andrew D.
Rosen, Hugo R.
Bihl, Florian K.
Cerny, Andreas
Brander, Christian
Spengler, Ulrich
Galagan, James
Marincola, Francesco M.
Nusbaum, Chad
Walker, Bruce D.
Lake-Bakaar, Gerond
Daari, Eric S.
Jacobson, Ira M.
Gomperts, Edward D.
Edlin, Brian R.
Thimme, Robert
Birren, Bruce W.
Donfield, Sharyne M.
Chung, Raymond T.
Kim, Arthur Y.
Lauer, Georg M.
Talal, Andrew
Marion, Tony
Carrington, Mary
Heckerman, David
Henn, Matthew R.
Allen, Todd M.
TI PROTECTIVE HLA CLASS I ALLELES IN HCV INFECTION: IMMUNE CONTROL LINKED
TO CLUSTERED CD8 ESCAPE MUTATIONS IN NS5B BY LARGE SCALE SEQUENCE
ANALYSIS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Kuntzen, Thomas] Univ Zurich Hosp, Dept Gastroenterol & Hepatol, CH-8091 Zurich, Switzerland.
[Kuntzen, Thomas; Neumann-Haefelin, Christoph; Berical, Andrew C.; Oniangue-Ndza, Cesar; Kleyman, Marianna; Birch, Christopher E.; Walker, Bruce D.; Kim, Arthur Y.; Lauer, Georg M.; Carrington, Mary; Allen, Todd M.] MIT & Harvard, Ragon Inst MGH, Boston, MA USA.
[Neumann-Haefelin, Christoph; Thimme, Robert] Univ Hosp Freiburg, Dept Med 2, Freiburg, Germany.
[Lennon, Niall; Berlin, Aaron M.; Young, Sarah; Ledlie, Timothy; Roberts, Andrew D.; Galagan, James; Nusbaum, Chad; Birren, Bruce W.; Henn, Matthew R.] Massachusetts Inst Technol & Harvard, Broad Inst, Cambridge, MA USA.
[Carlson, Jonathan; Heckerman, David] Microsoft Res, Redmond, WA USA.
[Timm, Joerg] Essen Univ Hosp, Dept Virol, Essen, Germany.
[Adams, Sharon; Marincola, Francesco M.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
[Adams, Sharon; Marincola, Francesco M.] NIH, Trans NIH Ctr Human Immunol, Bethesda, MD 20892 USA.
[Rosen, Hugo R.] Univ Colorado, Div Gastroenterol & Hepatol, Hlth Sci Ctr, Denver, CO USA.
[Bihl, Florian K.] Osped San Giovanni Bellinzona, Serv Gastroenterol, Bellinzona, Switzerland.
[Cerny, Andreas] Clin Moncucco, Lugano, Switzerland.
[Brander, Christian] Hosp Badalona Germans Trias & Pujol, AIDS Res Inst IrsiCaixa HIVACAT, Barcelona, Spain.
[Brander, Christian] Hosp Badalona Germans Trias & Pujol, Inst Catalana Recerca & Estudis Avancats ICREA, Barcelona, Spain.
[Spengler, Ulrich] Bonn Univ Hosp, Dept Internal Med 1, Bonn, Germany.
[Marion, Tony] Univ Tennessee, Ctr Hlth Sci, Hepatitis Cooperat C, Memphis, TN 38163 USA.
[Lake-Bakaar, Gerond; Jacobson, Ira M.; Edlin, Brian R.; Talal, Andrew] Weill Cornell Med Coll, Ctr Study Hepatitis C, New York, NY USA.
[Daari, Eric S.] Univ Calif Los Angeles, David Geffen Sch Med, Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Los Angeles, CA 90095 USA.
[Gomperts, Edward D.] Childrens Hosp Los Angeles, Saban Res Inst, Los Angeles, CA 90027 USA.
[Donfield, Sharyne M.] Rho Inc, Dept Biostat, Chapel Hill, NC USA.
[Chung, Raymond T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit, Boston, MA USA.
[Walker, Bruce D.] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Carrington, Mary] NCI, Expt Immunol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RI Neumann-Haefelin, Christoph/E-5550-2011
NR 0
TC 0
Z9 0
U1 0
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1341A
EP 1342A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004552
ER
PT J
AU Nara, K
Rivera, M
Raghuraman, S
Tsai, EH
Ko, MS
Saito, S
DeMino, M
Kirkland, H
Salehizadeh, Y
Auerbach, JS
Hoofnagle, JH
Liang, TJ
Rehermann, B
Heller, T
AF Nara, Koji
Rivera, Maria
Raghuraman, Sukanya
Tsai, Edward H.
Ko, Myung S.
Saito, Satoru
DeMino, Mary
Kirkland, Heather
Salehizadeh, Yasmin
Auerbach, Jonathan S.
Hoofnagle, Jay H.
Liang, T. Jake
Rehermann, Barbara
Heller, Theo
TI BREAKTHROUGH OF ACUTE HEPATITIS C WHILE ON INTERFERON IS ASSOCIATED WITH
CHANGES IN DIVERSITY IN HEPATITIS C VIRUS NONSTRUCTURAL PROTEINS BUT NOT
CHANGES IN T CELL RESPONSIVENESS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Nara, Koji; Rivera, Maria; Raghuraman, Sukanya; Tsai, Edward H.; Ko, Myung S.; Saito, Satoru; DeMino, Mary; Kirkland, Heather; Salehizadeh, Yasmin; Auerbach, Jonathan S.; Hoofnagle, Jay H.; Liang, T. Jake; Rehermann, Barbara; Heller, Theo] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1342A
EP 1342A
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004553
ER
PT J
AU Kawaguchi, K
Honda, M
Shirasaki, T
Emerson, SU
Purcell, RH
Kaneko, S
AF Kawaguchi, Kazunori
Honda, Masao
Shirasaki, Takayoshi
Emerson, Suzanne U.
Purcell, Robert H.
Kaneko, Shuichi
TI HCV INFECTIVITY VARIATION AND HVR1 QUASISPECIES SELECTION ARE ASSOCIATED
WITH THE DISTRIBUTION OF HCV E1/E2 SYNONYMOUS MUTATIONS
SO HEPATOLOGY
LA English
DT Meeting Abstract
CT 62nd Annual Meeting of the
American-Association-for-the-Study-of-Liver-Diseases (AASLD)
CY NOV 04-08, 2011
CL San Francisco, CA
SP Amer Assoc Study Liver Dis
C1 [Kawaguchi, Kazunori; Honda, Masao; Shirasaki, Takayoshi; Kaneko, Shuichi] Kanazawa Univ, Kanazawa, Ishikawa, Japan.
[Kawaguchi, Kazunori; Emerson, Suzanne U.; Purcell, Robert H.] NIAID, MHS, Bethesda, MD 20892 USA.
[Kawaguchi, Kazunori; Emerson, Suzanne U.; Purcell, Robert H.] NIAID, HVS, LID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
SU 1
BP 1352A
EP 1353A
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KG
UT WOS:000295578004575
ER
PT J
AU Iribarren, P
Wang, JM
AF Iribarren, Pablo
Wang, Ji Ming
TI Toll-like receptors and diseases
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Editorial Material
C1 [Iribarren, Pablo] Univ Nacl Cordoba, Fac Ciencias Quim, Dept Bioquim Clin, Ctr Invest Bioquim Clin & Inmunol CIBICI CONICET, RA-5000 Cordoba, Argentina.
[Wang, Ji Ming] NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.
RP Iribarren, P (reprint author), Univ Nacl Cordoba, Fac Ciencias Quim, Dept Bioquim Clin, CIBICI CONICET, Ciudad Univ,X5000HUA, RA-5000 Cordoba, Argentina.
EM piribarr@fcq.unc.edu.ar
FU FIC NIH HHS [1R01TW007621-01A2]
NR 9
TC 1
Z9 1
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD OCT
PY 2011
VL 11
IS 10
BP 1389
EP 1390
DI 10.1016/j.intimp.2011.08.010
PG 2
WC Immunology; Pharmacology & Pharmacy
SC Immunology; Pharmacology & Pharmacy
GA 834YI
UT WOS:000296000000001
PM 21884825
ER
PT J
AU Chen, KQ
Xiang, Y
Yao, XH
Liu, Y
Gong, WH
Yoshimura, T
Wang, JM
AF Chen, Keqiang
Xiang, Yi
Yao, Xiaohong
Liu, Ying
Gong, Wanghua
Yoshimura, Teizo
Wang, Ji Ming
TI The active contribution of Toll-like receptors to allergic airway
inflammation
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Allergic airway inflammation; Host response; TLRs
ID THYMIC STROMAL LYMPHOPOIETIN; DENDRITIC CELLS; MAST-CELLS; T-CELLS;
MEDIATED ACTIVATION; EPITHELIAL-CELLS; INNATE IMMUNITY; LUNG INJURY;
ASTHMA; DIFFERENTIATION
AB Epithelia lining the respiratory tract represent a major portal of entry for microorganisms and allergens and are equipped with innate and adaptive immune signaling receptors for host protection. These include Toll-like receptors (TLRs) that recognize microbial components and evoke diverse responses in cells of the respiratory system. TLR stimulation by microorganism-derived molecules activates antigen presenting cells, control T helper (Th) 1, Th2, and Th17 immune cell differentiation, cytokine production by mast cells, and activation of eosinophils. It is clear that TLR are involved in the pathophysiology of allergic airway diseases such as asthma. Dendritic cells (DCs), a kind of antigen presenting cells, which play a key role in the induction of allergic airway inflammation, are privileged targets for pathogen associated molecular patterns (PAMPs). During the allergic responses, engagement of TLRs on DCs determines the Th2 polarization of the T cells. TLR signaling in mast cells increases the release of IL-5, and TLR activation of airway epithelial cells forces the generation of proallergic Th2 type of cytokines. Although these responses aim to protect the host, they may also result in inflammatory tissue damage in the airway. Under certain conditions, stimulation of TLRs, in particular. TLR9, may reduce Th2-dependent allergic inflammation by induction of Th1 responses. Therefore, understanding the complex regulatory roles of TLRs in the pathogenesis of allergic airway inflammation should facilitate the development of preventive and therapeutic measures for asthmatic patients. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Chen, Keqiang; Liu, Ying; Yoshimura, Teizo; Wang, Ji Ming] NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.
[Xiang, Yi] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Respirat, Shanghai 200025, Peoples R China.
[Yao, Xiaohong] Third Mil Med Univ, Southwest Hosp, Inst Pathol, Chongqing 400038, Peoples R China.
[Yao, Xiaohong] Third Mil Med Univ, Southwest Hosp, SW Canc Ctr, Chongqing 400038, Peoples R China.
[Gong, Wanghua] SAIC Frederick, Frederick, MD 21702 USA.
RP Wang, JM (reprint author), NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Ctr Canc Res, Bldg 560,Room 31-76, Frederick, MD 21702 USA.
EM wangji@mail.nih.gov
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX This project has been funded in part with Federal funds from the
National Cancer Institute, National Institutes of Health, under Contract
No. HHSN261200800001E. The research was also supported in part by the
Intramural Research Program of the NCI, NIH.
NR 60
TC 29
Z9 33
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD OCT
PY 2011
VL 11
IS 10
BP 1391
EP 1398
DI 10.1016/j.intimp.2011.05.003
PG 8
WC Immunology; Pharmacology & Pharmacy
SC Immunology; Pharmacology & Pharmacy
GA 834YI
UT WOS:000296000000002
PM 21624504
ER
PT J
AU Chen, X
Oppenheim, JJ
AF Chen, Xin
Oppenheim, Joost J.
TI Resolving the identity myth: Key markers of functional CD4(+)FoxP3(+)
regulatory T cells
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE Regulatory T cells; Cellular markers; Immunosuppressive function
ID HUMAN PERIPHERAL-BLOOD; REMITTING MULTIPLE-SCLEROSIS; LATENT TGF-BETA;
FOXP3 EXPRESSION; RHEUMATOID-ARTHRITIS; SUPPRESSIVE FUNCTION; RECEPTOR
EXPRESSION; NEGATIVE REGULATION; CD127 EXPRESSION; WASTING DISEASE
AB Authenticating markers for the functional suppressive CD4(+)FoxP3(+) regulatory T cells (Tregs) are important for the quantitative identification and enrichment of viable Tregs for possible therapeutic use. CD25 as a surrogate marker of Tregs has some limitations, which prompted investigators to identify more specific marker(s) of Tregs. The search for a firm molecular definition of Tregs resulted in the identification of FoxP3 as a better marker of this subset of CD4 cells. Nevertheless, FoxP3(+) Tregs are phenotypically and functionally heterogeneous. Even in normal mice, only a minority of FoxP3(+) T cells are potent suppressor cells. Therefore, additional marker(s) are required for delineation of truly functional Tregs. In this review, the studies identifying markers of functional Tregs, both in mouse and in human, and their functional implications are discussed. Our finding that TNFR2, which mediates the effect of TNF on the activation of Tregs, is a superb marker of the most suppressive subset of mouse Tregs and its application in the identification of functional human Tregs will also be reviewed. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Chen, Xin] NCI Frederick, BSP, SAIC Frederick Inc, Mol Immunoregulat Lab,CIP, Frederick, MD 21702 USA.
[Oppenheim, Joost J.] NCI Frederick, Mol Immunoregulat Lab, Canc Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA.
RP Chen, X (reprint author), NCI Frederick, BSP, SAIC Frederick Inc, Mol Immunoregulat Lab,CIP, POB B,Bldg 560,Rm 31-19, Frederick, MD 21702 USA.
EM chenxin@mail.nih.gov
RI Chen, Xin/I-6601-2015
OI Chen, Xin/0000-0002-2628-4027
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; NIH, National Cancer Institute, Center for Cancer
Research
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract HHSN261200800001E. This Research was supported [in part] by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research.
NR 109
TC 25
Z9 30
U1 0
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD OCT
PY 2011
VL 11
IS 10
BP 1489
EP 1496
DI 10.1016/j.intimp.2011.05.018
PG 8
WC Immunology; Pharmacology & Pharmacy
SC Immunology; Pharmacology & Pharmacy
GA 834YI
UT WOS:000296000000012
PM 21635972
ER
PT J
AU Yilmaz, P
Gilbert, JA
Knight, R
Amaral-Zettler, L
Karsch-Mizrachi, I
Cochrane, G
Nakamura, Y
Sansone, SA
Glockner, FO
Field, D
AF Yilmaz, Pelin
Gilbert, Jack A.
Knight, Rob
Amaral-Zettler, Linda
Karsch-Mizrachi, Ilene
Cochrane, Guy
Nakamura, Yasukazu
Sansone, Susanna-Assunta
Gloeckner, Frank Oliver
Field, Dawn
TI The genomic standards consortium: bringing standards to life for
microbial ecology
SO ISME JOURNAL
LA English
DT Editorial Material
ID METAGENOMICS
C1 [Yilmaz, Pelin; Gloeckner, Frank Oliver] Max Planck Inst Marine Microbiol, Microbial Genom & Bioinformat Grp, Bremen, Germany.
[Yilmaz, Pelin; Gloeckner, Frank Oliver] Jacobs Univ Bremen gGmbH, Bremen, Germany.
[Gilbert, Jack A.] Argonne Natl Lab, Div Math & Comp Sci, Argonne, IL 60439 USA.
[Gilbert, Jack A.] Univ Chicago, Dept Ecol & Evolut, Chicago, IL 60637 USA.
[Knight, Rob] Univ Colorado, Howard Hughes Med Inst, Boulder, CO 80309 USA.
[Knight, Rob] Univ Colorado, Dept Chem & Biochem, Boulder, CO 80309 USA.
[Amaral-Zettler, Linda] Marine Biol Lab, Josephine Bay Paul Ctr Comparat Mol Biol & Evolut, Woods Hole, MA 02543 USA.
[Karsch-Mizrachi, Ilene] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Cochrane, Guy] European Bioinformat Inst, EMBL Outstn, Cambridge, England.
[Nakamura, Yasukazu] Res Org Informat & Syst, Ctr Informat Biol, Mishima, Shizuoka 4118540, Japan.
[Nakamura, Yasukazu] Res Org Informat & Syst, DNA Data Bank Japan, Natl Inst Genet, Mishima, Shizuoka 4118540, Japan.
[Sansone, Susanna-Assunta] Univ Oxford, Oxford E Res Ctr, Oxford, England.
[Field, Dawn] NERC Ctr Ecol & Hydrol, Oxford, England.
RP Yilmaz, P (reprint author), Max Planck Inst Marine Microbiol, Microbial Genom & Bioinformat Grp, Bremen, Germany.
EM fog@mpi-bremen.de
RI Knight, Rob/D-1299-2010;
OI Yilmaz, Pelin/0000-0003-4724-323X; Cochrane, Guy/0000-0001-7954-7057;
Sansone, Susanna-Assunta/0000-0001-5306-5690; Nakamura,
Yasukazu/0000-0002-6782-5715
FU Biotechnology and Biological Sciences Research Council [BB/E025080/1,
BB/I000771/1]
NR 13
TC 18
Z9 18
U1 2
U2 17
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1751-7362
EI 1751-7370
J9 ISME J
JI ISME J.
PD OCT
PY 2011
VL 5
IS 10
BP 1565
EP 1567
DI 10.1038/ismej.2011.39
PG 3
WC Ecology; Microbiology
SC Environmental Sciences & Ecology; Microbiology
GA 832DX
UT WOS:000295783200001
PM 21472015
ER
PT J
AU Shohreh, R
Sherafat-Kazemzadeh, R
Jee, YH
Blitz, A
Salvatori, R
AF Shohreh, Rugia
Sherafat-Kazemzadeh, Rosa
Jee, Youn Hee
Blitz, Ari
Salvatori, Roberto
TI A Novel Frame Shift Mutation in the GHRH Receptor Gene in Familial
Isolated GHD eficiency: Early Occurrence of Anterior Pituitary
Hypoplasia
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID GROWTH-HORMONE DEFICIENCY; MAGNETIC-RESONANCE; ENDOCRINE FUNCTION; SHORT
STATURE; GH-1 GENE; CHILDREN; GLAND; PREVALENCE; DWARFISM; MOUSE
AB Background: Mutations in the genes encoding for GHRH receptor (GHRHR) and GH (GH1) are the most common cause of familial isolated GH deficiency (IGHD). GHRHR mutations are often associated with anterior pituitary hypoplasia (APH), but this has been reported almost exclusively in children older than 8 yr. We analyzed the GHRHR and measured pituitary size in a consanguineous family with the father and three of the five siblings with IGHD.
Objective: The aim of the study was to find the mutated gene in a family with severe IGHD.
Methods: We sequenced the whole GHRHR coding regions and the intron-exon boundaries from peripheral DNA of the index patient. After identifying the novel mutation, we sequenced the region of interest in the other members of the family. We measured the anterior pituitary volume from magnetic resonance imaging (MRI).
Results: The father and the three affected children were homozygous for a new frame-shift mutation in the coding sequence of exon 4 (corresponding to the extracellular domain of the receptor) (c.391delG) that places the downstream sequence out of frame. The mother and two unaffected siblings were heterozygous for the mutation. Two of the affected children had MRI evidence of APH before reaching 6 yr of age.
Conclusions: We describe a new mutation in the GHRHR in a family with IGHD. The presence of frank APH before age 6 yr shows that MRI-evident reduced pituitary size can be present in GHRHR mutations even in children younger than 8 yr of age. (J Clin Endocrinol Metab 96: 2982-2986, 2011)
C1 [Shohreh, Rugia; Salvatori, Roberto] Johns Hopkins Univ, Dept Med, Div Endocrinol, Baltimore, MD 21287 USA.
[Blitz, Ari] Johns Hopkins Univ, Dept Radiol, Div Neuroradiol, Baltimore, MD 21287 USA.
[Sherafat-Kazemzadeh, Rosa] Georgetown Univ Hosp, Dept Pediat, Div Endocrinol, Washington, DC USA.
[Jee, Youn Hee] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD 20892 USA.
RP Salvatori, R (reprint author), Johns Hopkins Univ, Sch Med, Div Endocrinol & Metab, 1830 E Monument St,Suite 333, Baltimore, MD 21287 USA.
EM salvator@jhmi.edu
NR 30
TC 10
Z9 10
U1 0
U2 1
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD OCT
PY 2011
VL 96
IS 10
BP 2982
EP 2986
DI 10.1210/jc.2011-1031
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 833JC
UT WOS:000295879600030
PM 21816782
ER
PT J
AU Zemel, BS
Kalkwarf, HJ
Gilsanz, V
Lappe, JM
Oberfield, S
Shepherd, JA
Frederick, MM
Huang, XK
Lu, M
Mahboubi, S
Hangartner, T
Winer, KK
AF Zemel, Babette S.
Kalkwarf, Heidi J.
Gilsanz, Vicente
Lappe, Joan M.
Oberfield, Sharon
Shepherd, John A.
Frederick, Margaret M.
Huang, Xiangke
Lu, Ming
Mahboubi, Soroosh
Hangartner, Thomas
Winer, Karen K.
TI Revised Reference Curves for Bone Mineral Content and Areal Bone Mineral
Density According to Age and Sex for Black and Non-Black Children:
Results of the Bone Mineral Density in Childhood Study
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID PEDIATRIC OFFICIAL POSITIONS; BODY-COMPOSITION; FRACTURE RISK; US
ADULTS; ADOLESCENTS; GIRLS; PUBERTY; YOUNG; RACE; ASSOCIATION
AB Context: Deficits in bone acquisition during growth may increase fracture risk. Assessment of bone health during childhood requires appropriate reference values relative to age, sex, and population ancestry to identify bone deficits.
Objective: The objective of this study was to provide revised and extended reference curves for bone mineral content (BMC) and areal bone mineral density (aBMD) in children.
Design: The Bone Mineral Density in Childhood Study was a multicenter longitudinal study with annual assessments for up to 7 yr.
Setting: The study was conducted at five clinical centers in the United States.
Participants: Two thousand fourteen healthy children (992 males, 22% African-Americans) aged 5-23 yr participated in the study.
Intervention: There were no interventions.
Main Outcome Measures: Reference percentiles for BMC and aBMD of the total body, lumbar spine, hip, and forearm were obtained using dual-energy x-ray absorptiometry for Black and non-Black children. Adjustment factors for height status were also calculated.
Results: Extended reference curves for BMC and aBMD of the total body, total body less head, lumbar spine, total hip, femoral neck, and forearm for ages 5-20 yr were constructed relative to sex and age for Black and non-Black children. Curves are similar to those previously published for 7-17 year olds. BMC and aBMD values were greater for Black vs. non-Black children at all measurement sites.
Conclusions: We provide here dual-energy x-ray absorptiometry reference data on a well-characterized cohort of 2012 children and adolescents. These reference curves provide the most robust reference values for the assessment and monitoring of bone health in children and adolescents in the literature to date. (J Clin Endocrinol Metab 96: 3160-3169, 2011)
C1 [Zemel, Babette S.] Univ Penn, Childrens Hosp Philadelphia, Sch Med, Div Gastroenterol Hepatol & Nutr,Dept Pediat, Philadelphia, PA 19104 USA.
[Mahboubi, Soroosh] Childrens Hosp Philadelphia, Dept Radiol, Philadelphia, PA 19104 USA.
[Kalkwarf, Heidi J.] Cincinnati Childrens Hosp, Med Ctr, Dept Gen & Community Pediat, Cincinnati, OH 45229 USA.
[Gilsanz, Vicente] Childrens Hosp Los Angeles, Dept Radiol, Los Angeles, CA 90027 USA.
[Gilsanz, Vicente] Childrens Hosp Los Angeles, Dept Pediat, Los Angeles, CA 90027 USA.
[Lappe, Joan M.] Creighton Univ, Dept Med, Omaha, NE 68178 USA.
[Oberfield, Sharon] Columbia Univ, Dept Pediat, New York, NY 10032 USA.
[Shepherd, John A.] Univ Calif San Francisco, Dept Radiol, San Francisco, CA 94143 USA.
[Frederick, Margaret M.; Huang, Xiangke; Lu, Ming] Clin Trials & Surveys Corp, Owings Mills, MD 21117 USA.
[Hangartner, Thomas] Wright State Univ, Biomed Imaging Lab, Dayton, OH 45435 USA.
[Winer, Karen K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Endocrinol Nutr & Growth Branch, Ctr Res Mothers & Children, Bethesda, MD 20892 USA.
RP Zemel, BS (reprint author), Univ Penn, Childrens Hosp Philadelphia, Sch Med, Div Gastroenterol Hepatol & Nutr,Dept Pediat, 3535 Market St,Room 1560, Philadelphia, PA 19104 USA.
EM zemel@email.chop.edu
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [NO1-HD-1-3228, NO1-HD-1-3329, NO1-HD-1-3330, NO1-HD-1-3331,
NO1-HD-1-3332, NO1-HD-1-3333]; Clinical and Translational Research
Center [5-MO1-RR-000240, UL1 RR-026314]
FX This work was supported by Eunice Kennedy Shriver National Institute of
Child Health and Human Development Contracts NO1-HD-1-3228,
NO1-HD-1-3329, NO1-HD-1-3330, NO1-HD-1-3331, NO1-HD-1-3332 and
NO1-HD-1-3333 and the Clinical and Translational Research Center Grant
5-MO1-RR-000240 and UL1 RR-026314.
NR 32
TC 105
Z9 106
U1 0
U2 4
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD OCT
PY 2011
VL 96
IS 10
BP 3160
EP 3169
DI 10.1210/jc.2011-1111
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 833JC
UT WOS:000295879600052
PM 21917867
ER
PT J
AU Khan, AM
Cheng, S
Magnusson, M
Larson, MG
Newton-Cheh, C
McCabe, EL
Coviello, AD
Florez, JC
Fox, CS
Levy, D
Robins, SJ
Arora, P
Bhasin, S
Lam, CSP
Vasan, RS
Melander, O
Wang, TJ
AF Khan, Abigail May
Cheng, Susan
Magnusson, Martin
Larson, Martin G.
Newton-Cheh, Christopher
McCabe, Elizabeth L.
Coviello, Andrea D.
Florez, Jose C.
Fox, Caroline S.
Levy, Daniel
Robins, Sander J.
Arora, Pankaj
Bhasin, Shalender
Lam, Carolyn S. P.
Vasan, Ramachandran S.
Melander, Olle
Wang, Thomas J.
TI Cardiac Natriuretic Peptides, Obesity, and Insulin Resistance: Evidence
from Two Community-Based Studies
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID BODY-MASS INDEX; INCIDENT CARDIOVASCULAR EVENTS; EMERGENCY-DEPARTMENT
PRIDE; TERMINAL PRO-BNP; HEART-FAILURE; METABOLIC SYNDROME;
NORMAL-WEIGHT; MICE LACKING; ANGIOTENSIN-II; ADIPOSE-TISSUE
AB Background: The natriuretic peptides play an important role in salt homeostasis and blood pressure regulation. It has been suggested that obesity promotes a relative natriuretic peptide deficiency, but this has been a variable finding in prior studies and the cause is unknown.
Aim: The aim of this study was to examine the association between obesity and natriuretic peptide levels and evaluate the role of hyperinsulinemia and testosterone as mediators of this interaction.
Methods: We studied 7770 individuals from the Framingham Heart Study (n = 3833, 54% women) and the Malmo Diet and Cancer study (n = 3918, 60% women). We examined the relation of plasma N-terminal pro-B-type natriuretic peptide levels (N-BNP) with obesity, insulin resistance, and various metabolic subtypes.
Results: Obesity was associated with 6-20% lower levels of N-BNP (P < 0.001 in Framingham, P = 0.001 in Malmo), whereas insulin resistance was associated with 10-30% lower levels of N-BNP (P < 0.001 in both cohorts). Individuals with obesity who were insulin sensitive had only modest reductions in N-BNP compared with nonobese, insulin-sensitive individuals. On the other hand, individuals who were nonobese but insulin resistant had 26% lower N-BNP in Framingham (P < 0.001) and 10% lower N-BNP in Malmo (P < 0.001), compared with nonobese and insulin-sensitive individuals. Adjustment for serum-free testosterone did not alter these associations.
Conclusions: In both nonobese and obese individuals, insulin resistance is associated with lower natriuretic peptide levels. The relative natriuretic peptide deficiency seen in obesity could be partly attributable to insulin resistance, and could be one mechanism by which insulin resistance promotes hypertension. (J Clin Endocrinol Metab 96: 3242-3249, 2011)
C1 [Khan, Abigail May; Cheng, Susan; Newton-Cheh, Christopher; McCabe, Elizabeth L.; Arora, Pankaj; Wang, Thomas J.] Harvard Univ, Sch Med, Div Cardiol, Boston, MA 02114 USA.
[Newton-Cheh, Christopher; Florez, Jose C.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Florez, Jose C.] Harvard Univ, Sch Med, Diabet Res Ctr, Diabet Unit, Boston, MA 02114 USA.
[Khan, Abigail May] Univ Penn, Sch Med, Div Cardiovasc Med, Philadelphia, PA 19104 USA.
[Cheng, Susan; Larson, Martin G.; Newton-Cheh, Christopher; McCabe, Elizabeth L.; Fox, Caroline S.; Levy, Daniel; Robins, Sander J.; Vasan, Ramachandran S.; Wang, Thomas J.] Framingham Heart Dis Epidemiol Study, Framingham, MA 01702 USA.
[Cheng, Susan] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Cardiovasc Med,Dept Med, Boston, MA 02115 USA.
[Fox, Caroline S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Endocrinol Metab & Diabet,Dept Med, Boston, MA 02115 USA.
[Magnusson, Martin; Melander, Olle] Lund Univ, Dept Clin Sci, SE-20041 Malmo, Sweden.
Lund Univ, Dept Cardiol, Skanes Univ Hosp, SE-20502 Malmo, Sweden.
[Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Newton-Cheh, Christopher; Florez, Jose C.] Broad Inst Harvard & Massachusetts Inst Technol, Program Med & Populat Genet, Cambridge, MA 02142 USA.
[Fox, Caroline S.; Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20824 USA.
[Coviello, Andrea D.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Div Prevent Med, Dept Med, Boston, MA 02118 USA.
[Bhasin, Shalender] Boston Univ, Sch Med, Div Endocrinol Diabet & Nutr, Boston, MA 02118 USA.
[Lam, Carolyn S. P.] Natl Univ Hlth Syst, Singapore 119228, Singapore.
RP Wang, TJ (reprint author), Massachusetts Gen Hosp, Div Cardiol, GRB 800,55 Fruit St, Boston, MA 02114 USA.
EM tjwang@partners.org
RI Arora, Pankaj/F-3437-2011;
OI Arora, Pankaj/0000-0003-2420-3550; Larson, Martin/0000-0002-9631-1254;
Magnusson, Martin/0000-0003-1710-5936; Ramachandran,
Vasan/0000-0001-7357-5970
FU National Institutes of Health/National Heart, Lung, and Blood Institute
[N01-HC-25195, R01-HL-086875, R01-HL-094755]; Ellison Foundation
FX This work was supported by National Institutes of Health/National Heart,
Lung, and Blood Institute Contract N01-HC-25195 and Grants R01-HL-086875
and R01-HL-094755. S.C. is supported by a grant from the Ellison
Foundation.
NR 62
TC 60
Z9 64
U1 0
U2 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD OCT
PY 2011
VL 96
IS 10
BP 3242
EP 3249
DI 10.1210/jc.2011-1182
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 833JC
UT WOS:000295879600062
PM 21849523
ER
PT J
AU Abrams, JY
Schonberger, LB
Belay, ED
Maddox, RA
Leschek, EW
Mills, JL
Wysowski, DK
Fradkin, JE
AF Abrams, Joseph Y.
Schonberger, Lawrence B.
Belay, Ermias D.
Maddox, Ryan A.
Leschek, Ellen W.
Mills, James L.
Wysowski, Diane K.
Fradkin, Judith E.
TI Lower Risk of Creutzfeldt-Jakob Disease in Pituitary Growth Hormone
Recipients Initiating Treatment after 1977
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID UNITED-STATES; CONTAMINATION; THERAPY; TIME
AB Context: Creutzfeldt-Jakob disease (CJD) caused by contaminated cadaveric pituitary-derived human GH (hGH) has been responsible for hundreds of deaths worldwide. Studies of U. S. National Hormone and Pituitary Program (NHPP) hGH recipients have found CJD only in patients treated before 1977, when a new purification procedure with column chromatography was implemented for hGH extraction.
Objective: Our objective was to provide updated information on transmission of CJD to NHPP hGH recipients and determine whether recipients of hGH produced after 1977 had a significantly lower CJD risk than pre-1977 recipients.
Patients: A total of 5570 NHPP hGH recipients were included in the study: 2099 in the pre-1977 cohort and 3471 in the post-1977 cohort.
Main Outcome Measure: We used probability distribution functions to determine whether the observed number of CJD cases in the post-1977 cohort was significantly fewer than expected if the CJD risk was equal to that of the pre-1977 cohort, controlling for treatment duration and follow-up time.
Results: All 22 CJD cases (diagnosed from 1984-2009) occurred in the pre-1977 hGH recipients. Almost half (47.9%) of pre-1977 recipients had a treatment duration of at least 5 yr compared with only 13.8% for post-1977 recipients. Based on the rates present in the pre-1977 cohort, the probability of observing no cases in the post-1977 cohort by chance alone was low (P = 0.0019).
Conclusions: Risk of acquiring CJD was significantly lower for post-1977 NHPP hGH recipients than for pre-1977 recipients, suggesting that the new purification procedure in 1977 may have greatly reduced or eliminated CJD agent in hGH. (J Clin Endocrinol Metab 96: E1666-E1669, 2011)
C1 [Abrams, Joseph Y.; Schonberger, Lawrence B.; Belay, Ermias D.; Maddox, Ryan A.] Ctr Dis Control & Prevent, Natl Ctr Emerging & Zoonot Infect Dis, Atlanta, GA 30333 USA.
[Leschek, Ellen W.; Fradkin, Judith E.] NIDDK, Bethesda, MD 20817 USA.
[Mills, James L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
[Wysowski, Diane K.] US FDA, Silver Spring, MD 20993 USA.
RP Abrams, JY (reprint author), Ctr Dis Control & Prevent, Natl Ctr Emerging & Zoonot Infect Dis, 1600 Clifton Rd NE,CDC Mailstop A30, Atlanta, GA 30333 USA.
EM JAbrams@cdc.gov
RI Belay, Ermias/A-8829-2013
NR 12
TC 5
Z9 5
U1 0
U2 4
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD OCT
PY 2011
VL 96
IS 10
BP E1666
EP E1669
DI 10.1210/jc.2011-1357
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 833JC
UT WOS:000295879600016
PM 21816775
ER
PT J
AU Cizza, G
Bernardi, L
Smirne, N
Maletta, R
Tomaino, C
Costanzo, A
Gallo, M
Lewis, JG
Geracitano, S
Grasso, MB
Potenza, G
Monteleone, C
Brancati, G
Ho, JT
Torpy, DJ
Bruni, AC
AF Cizza, Giovanni
Bernardi, Livia
Smirne, Nicoletta
Maletta, Raffaele
Tomaino, Carmine
Costanzo, Angela
Gallo, Maura
Lewis, John G.
Geracitano, Silvana
Grasso, Maria Beatrice
Potenza, Giuseppe
Monteleone, Cosimo
Brancati, Giacomino
Ho, Jui T.
Torpy, David J.
Bruni, Amalia C.
TI Clinical Manifestations of Highly Prevalent Corticosteroid-Binding
Globulin Mutations in a Village in Southern Italy
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID GENETIC-VARIATION; FREE CORTISOL; DEFICIENCY; FATIGUE; AFFINITY;
GLUCOCORTICOIDS; SUBSTITUTION; ASSOCIATION; POPULATION; EPIFUND
AB Context: Corticosteroid-binding globulin (CBG) is the binding protein for cortisol. Rare kindreds with CBG mutations reducing CBG levels or altering binding affinity have been described, along with clinical manifestations encompassing fatigue, chronic pain, and hypotension. The largest kindred, exhibiting two mutations (null and Lyon) were Australian immigrants from Italy.
Objective: Our objective was to determine the prevalence of the null/Lyon mutations in the village where the original null/Lyon family emigrated and compare subjects with and without CBG mutations, without previous knowledge of their mutation status.
Design, Setting, and Participants: We conducted a survey field study that included 495 adult residents.
Main Outcomes: We assessed clinical history, CBG mutation analysis, plasma CBG, salivary cortisol, body mass index, waist circumference, blood pressure, and the Krupp fatigue scale.
Results: Eighteen of 495 participants (3.6%, seven males and 11 females) had one of two functionaltering CBG mutations. All were heterozygous for the null (n = 6) or Lyon mutations (n = 12). Of 12 Lyon participants (four males and eight females), eight (two males and six females) had chronic widespread pain and five osteoarthritis with associated pain (one male and four females). Of six null participants (three males and three females), three (one male and two females) had chronic pain and four osteoarthritis with associated pain (two males and two females).
Conclusions: A high combined prevalence (3.6%) of these two CBG mutations was detected. The presence of either mutation conferred a propensity to chronic pain. In other communities, individuals with the same genetic background complain more of fatigue than pain, suggesting an environmental effect on the phenotype. These findings, combined with animal CBG gene knockout and human CBG single-nucleotide polymorphism haplotype studies, suggest that CBG influences the endocrine and neurobehavioral response to stress, including the development of pain/fatigue syndromes. (J Clin Endocrinol Metab 96: E1684-E1693, 2011)
C1 [Cizza, Giovanni] NIDDK, Diabet Endocrine & Obes Branch, CRC, Bethesda, MD 20892 USA.
[Bernardi, Livia; Smirne, Nicoletta; Maletta, Raffaele; Tomaino, Carmine; Costanzo, Angela; Gallo, Maura; Geracitano, Silvana; Monteleone, Cosimo; Bruni, Amalia C.] Reg Neurogenet Ctr, I-88046 Catanzaro, Italy.
[Lewis, John G.] Canterbury Hlth Labs, Christchurch, New Zealand.
[Brancati, Giacomino] Dept Hlth, Epidemiol & Res Serv, I-88100 Catanzaro, Italy.
[Ho, Jui T.; Torpy, David J.] Royal Adelaide Hosp, Endocrine & Metab Unit, Adelaide, SA 5005, Australia.
RP Cizza, G (reprint author), NIDDK, Diabet Endocrine & Obes Branch, CRC, Bldg 10,Room 6-3940, Bethesda, MD 20892 USA.
EM cizzag@intra.niddk.nih.gov
RI , raffaele/K-4421-2016
OI Lewis, John/0000-0003-2757-4111; , raffaele/0000-0002-0758-1835
FU Assessorato alla Salute-Regione Calabria [772]; Italian Minister of
Health [42]; National Institutes of Health, National Institute of
Diabetes and Digestive and Kidney Diseases
FX This work was supported by a Project Grant (G. R. no. 772, August 6,
2002) of the Assessorato alla Salute-Regione Calabria; the Italian
Minister of Health (convention no. 42 of November 26, 2003, approved on
October 11, 2004), and by the National Institutes of Health, National
Institute of Diabetes and Digestive and Kidney Diseases Intramural
Program.
NR 35
TC 13
Z9 13
U1 0
U2 1
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD OCT
PY 2011
VL 96
IS 10
BP E1684
EP E1693
DI 10.1210/jc.2011-1321
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 833JC
UT WOS:000295879600020
PM 21795453
ER
PT J
AU Davidson, MH
Ballantyne, CM
Jacobson, TA
Bittner, VA
Braun, LT
Brown, AS
Brown, WV
Cromwell, WC
Goldberg, RB
McKenney, JM
Remaley, AT
Sniderman, AD
Toth, PP
Tsimikas, S
Ziajka, PE
Maki, KC
Dicklin, MR
AF Davidson, Michael H.
Ballantyne, Christie M.
Jacobson, Terry A.
Bittner, Vera A.
Braun, Lynne T.
Brown, Alan S.
Brown, W. Virgil
Cromwell, William C.
Goldberg, Ronald B.
McKenney, James M.
Remaley, Alan T.
Sniderman, Allan D.
Toth, Peter P.
Tsimikas, Sotirios
Ziajka, Paul E.
Maki, Kevin C.
Dicklin, Mary R.
TI Clinical utility of inflammatory markers and advanced lipoprotein
testing: Advice from an expert panel of lipid specialists
SO JOURNAL OF CLINICAL LIPIDOLOGY
LA English
DT Article
DE C-reactive protein; Lipoprotein-associated phospholipase A2;
Apolipoprotein B; Low-density lipoprotein particle concentration;
Lipoprotein(a); Lipoprotein subfractions
ID C-REACTIVE-PROTEIN; CORONARY-HEART-DISEASE; LOW-DENSITY-LIPOPROTEIN;
NUCLEAR-MAGNETIC-RESONANCE; NON-HDL CHOLESTEROL; FAMILIAL-COMBINED
HYPERLIPIDEMIA; MIDDLE-AGED MEN; ACTIVATING-FACTOR ACETYLHYDROLASE;
TRIAL EVALUATING ROSUVASTATIN; FUTURE CARDIOVASCULAR EVENTS
AB The National Cholesterol Education Program Adult Treatment Panel guidelines have established low-density lipoprotein cholesterol (LDL-C) treatment goals, and secondary non-high-density lipoprotein (HDL)-C treatment goals for persons with hypertriglyceridemia. The use of lipid-lowering therapies, particularly statins, to achieve these goals has reduced cardiovascular disease (CVD) morbidity and mortality; however, significant residual risk for events remains. This, combined with the rising prevalence of obesity, which has shifted the risk profile of the population toward patients in whom LDL-C is less predictive of CVD events (metabolic syndrome, low HDL-C, elevated triglycerides), has increased interest in the clinical use of inflammatory and lipid biomarker assessments. Furthermore, the cost effectiveness of pharmacological intervention for both the initiation of therapy and the intensification of therapy has been enhanced by the availability of a variety of generic statins. This report describes the consensus view of an expert panel convened by the National Lipid Association to evaluate the use of selected biomarkers [C-reactive protein, lipoprotein-associated phospholipase A(2), apolipoprotein B, LDL particle concentration, lipoprotein(a), and LDL and HDL subfractions] to improve risk assessment, or to adjust therapy. These panel recommendations are intended to provide practical advice to clinicians who wrestle with the challenges of identifying the patients who are most likely to benefit from therapy, or intensification of therapy, to provide the optimum protection from CV risk. (C) 2011 National Lipid Association. All rights reserved.
C1 [Davidson, Michael H.] Univ Chicago, Pritzker Sch Med, Chicago, IL 60610 USA.
[Maki, Kevin C.; Dicklin, Mary R.] Provident Clin Res, Glen Ellyn, IL USA.
[Goldberg, Ronald B.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Jacobson, Terry A.] Emory Univ, Lipoprot Biomarkers Sub Grp, Atlanta, GA 30322 USA.
[McKenney, James M.] Natl Clin Res Inc, Manakin Sabot, VA USA.
[McKenney, James M.] Virginia Commonwealth Univ, Manakin Sabot, VA USA.
[Remaley, Alan T.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Sniderman, Allan D.] McGill Univ, Montreal, PQ H3A 2T5, Canada.
[Toth, Peter P.] Univ Illinois, Coll Med, Sterling Rock Falls Clin Ltd, Peoria, IL 61656 USA.
[Tsimikas, Sotirios] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Ziajka, Paul E.] Florida Lipid Inst, Winter Pk, FL USA.
[Ballantyne, Christie M.] Baylor Coll Med, Inflammatory Biomarkers Sub Grp, Houston, TX 77030 USA.
[Bittner, Vera A.] Univ Alabama, Birmingham, AL USA.
[Braun, Lynne T.] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Brown, Alan S.] Loyola Univ, Stritch Sch Med, Maywood, IL 60153 USA.
[Brown, W. Virgil] Emory Univ, Sch Med, Atlanta, GA USA.
[Cromwell, William C.] Lipoprot & Metab Disorders Inst, Raleigh, NC USA.
[Cromwell, William C.] Wake Forest Univ, Sch Med, Winston Salem, NC 27109 USA.
RP Davidson, MH (reprint author), Univ Chicago, Pritzker Sch Med, 515 N State St,Suite 2700, Chicago, IL 60610 USA.
EM MDavidso@medicine.bsd.uchicago.edu
OI Cromwell, William/0000-0001-7610-4920; Jacobson,
Terry/0000-0002-9926-2179; Bittner, Vera/0000-0001-9456-850X
FU Abbott Laboratories; Atherotech Diagnostics Laboratory; Berkley Heart
Lab, Inc.; Boston Heart Diagnostics; diaDexus, Inc.; LipoScience; Merck
Co., Inc.; Spectracell Laboratories; Daiichi Sankyo; GlaxoSmithKline;
Merck Co.; Roche; Aegerion Pharmaceuticals; Amgen; AstraZeneca;
Atherotech Inc.; DTC MD; Esperion; Intelligent Medical Decisions;
Kinemed; Novo Nordisk; Sanofi-Aventis; Synarc; Takeda Pharmaceuticals;
Vindico Medical Education; Bristol-Myers Squibb; Kowa Pharmaceuticals;
Novartis Pharmaceuticals; Sanofi-Synthelabo; Adnexus; Amylin
Pharmaceuticals; Bristol Myers-Squibb; Genentech; Idera Pharmaceuticals;
Omthera; Resverlogix; Amarin Pharmaceuticals; National Institutes of
Health; Spirocor; Gilead; Pfizer Inc.; Anthera; Genzyme; Isis
Pharmaceuticals; LabCorp; Health Diagnostics Laboratory; Alpha-Core
Pharmaceuticals; VirxSys Inc.; ISIS; Genzyme/Sanofi; Quest; Atherotech;
Bio-Sante Pharmaceuticals; Cargill; Coca-Cola; Dairy Research Institute;
Fermenich; Kao Corporation; Kellogg Co.; Monsanto; National Starch/Corn
Products; Ocean Spray; PepsiCo; Pharmavite; Shaklee; Solae; Trygg
Pharmaceuticals; Welch's; General Mills; Biofortis
FX The January 2011 National Lipid Association (NLA) consensus conference
on inflammatory markers and advanced lipoprotein testing was supported
by unrestricted grant funding from the following companies: Abbott
Laboratories, Atherotech Diagnostics Laboratory, Berkley Heart Lab,
Inc., Boston Heart Diagnostics, diaDexus, Inc., LipoScience, Merck &
Co., Inc., and Spectracell Laboratories.; The NLA would like to thank
each company for its support of this endeavor. In accordance with the
National Lipid Association Code for Interactions with Companies, the NLA
maintained full control over the planning, content, quality, scientific
integrity, implementation, and evaluation of the consensus conference
and this inflammatory markers and advanced lipoprotein testing consensus
document. All related activities are free from commercial influence and
bias.; Dr. Davidson has received research grants from Abbott
Laboratories, Daiichi Sankyo, GlaxoSmithKline, Merck & Co. and Roche.
Dr. Davidson has received consulting fees from Abbott Laboratories,
Aegerion Pharmaceuticals, Amgen, AstraZeneca, Atherotech Inc., Daiichi
Sankyo, DTC MD, Esperion, GlaxoSmithKline, Intelligent Medical
Decisions, Kinemed, LipoScience, Merck & Co, Novo Nordisk, Roche,
Sanofi-Aventis, Synarc, Takeda Pharmaceuticals, and Vindico Medical
Education. Dr. Davidson has received honoraria related to speaking from
Abbott Laboratories, GlaxoSmithKline and Merck & Co. Dr. Davidson has
served on the Board of Directors of DTC MD, Omthera, Professional
Evaluation Inc., and Sonogene.; Dr. Ballantyne has received research
grants from Abbott Laboratories, AstraZeneca, Bristol-Myers Squibb,
diaDexus Inc., GlaxoSmithKline, Kowa Pharmaceuticals, Merck & Co.,
Novartis Pharmaceuticals, Roche, Sanofi-Synthelabo, and Takeda
Pharmaceuticals. Dr. Ballantyne has received consulting fees from Abbott
Laboratories, Adnexus, Amylin Pharmaceuticals, AstraZeneca, Bristol
Myers-Squibb, Esperion, Genentech, GlaxoSmithKline, Idera
Pharmaceuticals, Kowa Pharmaceuticals, Merck & Co., Novartis
Pharmaceuticals, Omthera, Resverlogix, Roche, Sanofi-Synthelabo, and
Takeda Pharmaceuticals. Dr. Ballantyne has received honoraria related to
speaking from Abbott Laboratories, AstraZeneca, GlaxoSmithKline, Merck &
Co., Sanofi-Synthelabo, and Takeda Pharmaceuticals.; Dr. Jacobson has
received consulting fees from Abbott Laboratories, Amarin
Pharmaceuticals, AstraZeneca, GlaxoSmithKline and Merck & Co.; Dr.
Bittner has received research grants from Abbott Laboratories, National
Institutes of Health, Spirocor, Roche, GlaxoSmithKline, Gilead, and
Pfizer Inc.; Dr. Braun has received honoraria related to speaking from
the American Heart Association and the Preventive Cardiovascular Nurses
Association. Dr. Braun has received salary support from the National
Institutes of Health.; Dr. Alan S. Brown has received honoraria related
to speaking from Abbott Laboratories, Forest Laboratories and Daiichi
Sankyo.; Dr. W. Virgil Brown has received consulting fees from Abbott
Laboratories, Amgen, Anthera, Genzyme, Pfizer Inc., LipoScience, and
Merck & Co. Dr. W. Virgil Brown has received honoraria related to
speaking from Abbott Laboratories, LipoScience, and Merck & Co.; Dr.
Cromwell has received consulting fees from Isis Pharmaceuticals,
LabCorp, and Health Diagnostics Laboratory. Dr. Cromwell has received
research grants from Isis Pharmaceuticals. Dr. Cromwell has received
honoraria related to speaking from Abbott Laboratories, LipoScience,
Merck & Co., and Merck Schering Plough.; Dr. Goldberg has received
research grants from Abbott Laboratories, GlaxoSmithKline and Roche. Dr.
Goldberg has received consulting fees from GlaxoSmithKline, Daiichi
Sankyo, and Pfizer Inc. Dr. Goldberg has received honoraria related to
speaking from Daiichi Sankyo, GlaxoSmithKline, and Merck & Co.; Dr.
McKenney has no relevant disclosures.; Dr. Remaley has received research
grants from Alpha-Core Pharmaceuticals, Kinemed, and VirxSys Inc.; Dr.
Sniderman has received research grants from AstraZeneca. A. D. S. has
received honoraria related to speaking from Merck & Co.; Dr. Toth has
received consulting fees from Abbott Laboratories, AstraZeneca,
GlaxoSmithKline, Kowa Pharmaceuticals, Pfizer Inc., and Merck & Co. Dr.
Toth has received honoraria related to speaking from Abbott
Laboratories, AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Pfizer
Inc., Merck & Co., and Takeda Pharmaceuticals.; Dr. Tsimikas has
received consulting fees from ISIS, Merck & Co., Genzyme/Sanofi and
Quest. Dr. Tsimikas has received honoraria related to speaking from
Merck & Co. Dr. Tsimikas has received research grants from Merck & Co.
and Pfizer Inc. Dr. Tsimikas has received equity interest from
Atherotope.; Dr. Ziajka has received honoraria related to speaking from
Abbott Laboratories, AstraZeneca and Merck & Co. Dr. Ziajka has received
research grants from Genzyme.; Dr. Maki has received research grants
from Abbott Laboratories, Amarin Pharmaceuticals, Atherotech, Bio-Sante
Pharmaceuticals, Cargill, Coca-Cola, Dairy Research Institute,
Fermenich, GlaxoSmithKline, Kao Corporation, Kellogg Co., Monsanto,
National Starch/Corn Products, Ocean Spray, Omthera, PepsiCo,
Pharmavite, Shaklee, Solae, Trygg Pharmaceuticals and Welch's. Dr. Maki
has received consulting fees from Abbott Laboratories, Cargill, Dairy
Research Institute, General Mills, GlaxoSmithKline, Omthera, PepsiCo,
Pharmavite and Trygg Pharmaceuticals. Dr. Maki has received salary
support from Biofortis.; Dr. Dicklin has received research grants from
Abbott Laboratories, Amarin Pharmaceuticals, Atherotech, Bio-Sante
Pharmaceuticals, Cargill, Coca-Cola, Dairy Research Institute,
Fermenich, GlaxoSmithKline, Kao Corporation, Kellogg Co., Monsanto,
National Starch/Corn Products, Ocean Spray, Omthera, PepsiCo,
Pharmavite, Shaklee, Solae, Trygg Pharmaceuticals and Welch's. Dr.
Dicklin has received consulting fees from Abbott Laboratories, Dairy
Research Institute, General Mills, GlaxoSmithKline, Omthera, PepsiCo,
Pharmavite, and Trygg Pharmaceuticals. Dr. Dicklin has received salary
support from Biofortis.
NR 219
TC 131
Z9 133
U1 0
U2 13
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1933-2874
J9 J CLIN LIPIDOL
JI J. Clin. Lipidol.
PD OCT
PY 2011
VL 5
IS 5
BP 338
EP 367
DI 10.1016/j.jacl.2011.07.005
PG 30
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 833QR
UT WOS:000295900500002
PM 21981835
ER
PT J
AU Horai, R
Caspi, RR
AF Horai, Reiko
Caspi, Rachel R.
TI Cytokines in Autoimmune Uveitis
SO JOURNAL OF INTERFERON AND CYTOKINE RESEARCH
LA English
DT Review
ID REGULATORY T-CELLS; GROWTH-FACTOR-BETA; KOYANAGI-HARADA-DISEASE;
NECROSIS-FACTOR-ALPHA; ROR-GAMMA-T; BEHCETS-DISEASE; IFN-GAMMA; TH17
CELLS; TGF-BETA; NONINFECTIOUS UVEITIS
AB Autoimmune uveitis is a complex group of sight-threatening diseases that arise without a known infectious trigger. The disorder is often associated with immunological responses to retinal proteins. Experimental models of autoimmune uveitis targeting retinal proteins have led to a better understanding of the basic immunological mechanisms involved in the pathogenesis of uveitis and have provided a template for the development of novel therapies. The disease in humans is believed to be T cell-dependent, as clinical uveitis is ameliorated by T cell-targeting therapies. The roles of T helper 1 (Th1) and Th17 cells have been major topics of interest in the past decade. Studies in uveitis patients and experiments in animal models have revealed that Th1 and Th17 cells can both be pathogenic effectors, although, paradoxically, some cytokines produced by these subsets can also be protective, depending on when and where they are produced. The major proinflammatory as well as regulatory cytokines in uveitis, the therapeutic approaches, and benefits of targeting these cytokines will be discussed in this review.
C1 [Horai, Reiko; Caspi, Rachel R.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Caspi, RR (reprint author), NEI, Immunol Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM rcaspi@helix.nih.gov
OI Caspi, Rachel/0000-0002-7140-7671
FU NIH/NEI
FX This work has been supported by NIH/NEI Intramural Funding.
NR 105
TC 54
Z9 60
U1 1
U2 10
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1079-9907
J9 J INTERF CYTOK RES
JI J. Interferon Cytokine Res.
PD OCT
PY 2011
VL 31
IS 10
BP 733
EP 744
DI 10.1089/jir.2011.0042
PG 12
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 834UJ
UT WOS:000295989300006
PM 21787221
ER
PT J
AU Buckley, PF
AF Buckley, Peter F.
TI Bromization The Truths We Know About the Psychopharmacology of
Schizophrenia
SO JOURNAL OF NERVOUS AND MENTAL DISEASE
LA English
DT Editorial Material
ID ANTIPSYCHOTIC POLYPHARMACY; OLANZAPINE
C1 [Buckley, Peter F.] Georgia Hlth Sci Univ, Sch Med, Augusta, GA 30912 USA.
[Buckley, Peter F.] NIMH, Bethesda, MD USA.
RP Buckley, PF (reprint author), Georgia Hlth Sci Univ, Sch Med, 1120 15th St, Augusta, GA 30912 USA.
EM pbuckley@georgiahealth.edu
NR 17
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3018
J9 J NERV MENT DIS
JI J. Nerv. Ment. Dis.
PD OCT
PY 2011
VL 199
IS 10
BP 736
EP 737
DI 10.1097/NMD.0b013e31822fc639
PG 2
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 827BD
UT WOS:000295399300002
PM 21964265
ER
PT J
AU Rovsing, L
Clokie, S
Bustos, DM
Rohde, K
Coon, SL
Litman, T
Rath, MF
Moller, M
Klein, DC
AF Rovsing, Louise
Clokie, Samuel
Bustos, Diego M.
Rohde, Kristian
Coon, Steven L.
Litman, Thomas
Rath, Martin F.
Moller, Morten
Klein, David C.
TI Crx broadly modulates the pineal transcriptome
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE Crx; gene expression; Hoxc4; microarray; pineal gland; transcriptome
profiling
ID ARYLALKYLAMINE N-ACETYLTRANSFERASE; OTX2 HOMEOBOX GENE; REV-ERB-ALPHA;
HOMEODOMAIN PROTEIN; CIRCADIAN CLOCK; MESSENGER-RNA; MOUSE PINEAL;
EXPRESSION; GLAND; MELATONIN
AB Cone-rod homeobox (Crx) encodes Crx, a transcription factor expressed selectively in retinal photoreceptors and pinealocytes, the major cell type of the pineal gland. In this study, the influence of Crx on the mammalian pineal gland was studied by light and electron microscopy and by use of microarray and qRTPCR technology, thereby extending previous studies on selected genes (Furukawa et al. 1999). Deletion of Crx was not found to alter pineal morphology, but was found to broadly modulate the mouse pineal transcriptome, characterized by a > 2-fold down-regulation of 543 genes and a > 2-fold up-regulation of 745 genes (p < 0.05). Of these, one of the most highly up-regulated (18-fold) was Hoxc4, a member of the Hox gene family, members of which are known to control gene expression cascades. During a 24-h period, a set of 51 genes exhibited differential day/night expression in pineal glands of wild-type animals; only eight of these were also day/night expressed in the Crx(-/-) pineal gland. However, in the Crx(-/-) pineal gland 41 genes exhibited differential night/day expression that was not seen in wild-type animals. These findings indicate that Crx broadly modulates the pineal transcriptome and also influences differential night/day gene expression in this tissue. Some effects of Crx deletion on the pineal transcriptome might be mediated by Hoxc4 up-regulation.
C1 [Rovsing, Louise; Clokie, Samuel; Bustos, Diego M.; Coon, Steven L.; Klein, David C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Neuroendocrinol, Program Dev Endocrinol & Genet, NIH, Bethesda, MD 20892 USA.
[Rovsing, Louise; Rohde, Kristian; Rath, Martin F.; Moller, Morten] Univ Copenhagen, Panum Inst, Dept Neurosci & Pharmacol, DK-2200 Copenhagen, Denmark.
[Litman, Thomas] Univ Copenhagen, Panum Inst, Dept Int Hlth Immunol & Microbiol, DK-2200 Copenhagen, Denmark.
[Bustos, Diego M.] INTECH, Chascomus, Argentina.
RP Klein, DC (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Neuroendocrinol, Program Dev Endocrinol & Genet, NIH, 49 Convent Dr,Room 6A82, Bethesda, MD 20892 USA.
EM kleind@mail.nih.gov
RI Rovsing, Louise/E-3225-2014;
OI Clokie, Samuel/0000-0002-0025-3652; Rath, Martin/0000-0002-4047-6324
FU Lundbeck Foundation; Danish Medical Research Council [271-07-0412]; Novo
Nordisk Foundation; Carlsberg Foundation; Fonden til Laegevidenskabens
Fremme; Simon Fougner Hartmanns Familiefond; Danish Eye Health Society;
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health
FX This study was supported by the Lundbeck Foundation, the Danish Medical
Research Council (grant no. 271-07-0412), the Novo Nordisk Foundation,
the Carlsberg Foundation, Fonden til Laegevidenskabens Fremme, Simon
Fougner Hartmanns Familiefond, the Danish Eye Health Society (Vaern om
Synet) and the Intramural Research Program of the The Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
National Institutes of Health. The authors wish to express their
appreciation to Dr. Connie Cepko for the generous gift of the
Crx-/- mice. The authors have no conflicts of interest.
NR 45
TC 15
Z9 15
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3042
J9 J NEUROCHEM
JI J. Neurochem.
PD OCT
PY 2011
VL 119
IS 2
BP 262
EP 274
DI 10.1111/j.1471-4159.2011.07405.x
PG 13
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 834PE
UT WOS:000295973900002
PM 21797868
ER
PT J
AU Torres-Altoro, MI
Mathur, BN
Drerup, JM
Thomas, R
Lovinger, DM
O'Callaghan, JP
Bibb, JA
AF Torres-Altoro, Melissa I.
Mathur, Brian N.
Drerup, Justin M.
Thomas, Rachel
Lovinger, David M.
O'Callaghan, James P.
Bibb, James A.
TI Organophosphates dysregulate dopamine signaling, glutamatergic
neurotransmission, and induce neuronal injury markers in striatum
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE chlorpyrifos; dopamine; Gulf War illness; insecticide; neurotoxicity;
organophosphate
ID CYCLIN-DEPENDENT KINASE-5; NEONATAL CHLORPYRIFOS EXPOSURE; ALPHA-7
NICOTINIC RECEPTORS; CENTRAL-NERVOUS-SYSTEM; GULF-WAR SYNDROME; SYNAPTIC
PLASTICITY; NEOSTRIATAL NEURONS; ALZHEIMERS-DISEASE; PESTICIDE EXPOSURE;
PRENATAL EXPOSURE
AB The neurological effects of organophosphate (OP) pesticides, commonly used on foods and in households, are an important public health concern. Furthermore, subclinical exposure to combinations of organophosphates is implicated in Gulf War illness. Here, we characterized the effects of the broadly used insecticide chlorpyrifos (CPF) on dopamine and glutamatergic neurotransmission effectors in corticostriatal motor/reward circuitry. CPF potentiated protein kinase A (PKA)-dependent phosphorylation of the striatal protein dopamine-and cAMP-regulated phosphoprotein of M(r) 32 kDa (DARPP-32) and the glutamate receptor 1 (GluR1) subunit of alpha-amino-3-hydroxy-5methyl- 4-isoxazolepropionic acid (AMPA) receptors in mouse brain slices. It also increased GluR1 phosphorylation by PKA when administered systemically. This correlated with enhanced glutamate release from cortical projections in rat striatum. Similar effects were induced by the sarin congener, diisopropyl fluorophosphate, alone or in combination with the putative neuroprotectant, pyridostigmine bromide and the pesticide N,N-diethyl-meta-toluamide (DEET). This combination, meant to mimic the neurotoxicant exposure encountered by veterans of the 1991 Persian Gulf War, also induced hyperphosphorylation of the neurofibrillary tangle-associated protein tau. Diisopropyl fluorophosphate and pyrodostigmine bromide, alone or in combination, also increased the aberrant activity of the protein kinase, Cdk5, as indicated by conversion of its activating cofactor p35 to p25. Thus, consistent with recent findings in humans and animals, organophosphate exposure causes dysregulation in the motor/reward circuitry and invokes mechanisms associated with neurological disorders and neurodegeneration.
C1 [Torres-Altoro, Melissa I.; Drerup, Justin M.; Thomas, Rachel; Bibb, James A.] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA.
[Mathur, Brian N.; Lovinger, David M.] NIAAA, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA.
[O'Callaghan, James P.] NIOSH, Ctr Dis Control & Prevent, Morgantown, WV USA.
[Bibb, James A.] Univ Texas SW Med Ctr Dallas, Dept Neurol & Neurotherapeut, Dallas, TX 75390 USA.
RP Bibb, JA (reprint author), Univ Texas SW Med Ctr Dallas, Dept Psychiat, 5323 Harry Hines Blvd,NC5-410, Dallas, TX 75390 USA.
EM james.bibb@utsouthwestern.edu
RI O'Callaghan, James/O-2958-2013
FU US National Institutes of Health [MH79710, MH083711, DA016672]; Centers
for Disease Control and Prevention-NIOSH; Division of Intramural
Clinical and Biological Research of NIAAA; IDIQ [VA549-P-0027];
Department of Veterans Affairs Medical Center, Dallas, TX
FX We thank Suzanne Saldanha, Brenda Billig, and Christopher Felton for
technical assistance. This work was supported by US National Institutes
of Health Grants to J.A.B (MH79710, MH083711, and DA016672), Intramural
funds from Centers for Disease Control and Prevention-NIOSH, and the
Division of Intramural Clinical and Biological Research of NIAAA.
Portions of this research were supported by IDIQ contract VA549-P-0027
(Robert W. Haley, M.D., PI), awarded and administered by the Department
of Veterans Affairs Medical Center, Dallas, TX. The content does not
necessarily reflect the position or the policy of the Federal government
or the sponsoring agency, and no official endorsement should be
inferred.
NR 54
TC 29
Z9 30
U1 1
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3042
J9 J NEUROCHEM
JI J. Neurochem.
PD OCT
PY 2011
VL 119
IS 2
BP 303
EP 313
DI 10.1111/j.1471-4159.2011.07428.x
PG 11
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 834PE
UT WOS:000295973900006
PM 21848865
ER
PT J
AU Cheon, Y
Park, JY
Modi, HR
Kim, HW
Lee, HJ
Chang, L
Rao, JS
Rapoport, SI
AF Cheon, Yewon
Park, Jee-Young
Modi, Hiren R.
Kim, Hyung-Wook
Lee, Ho-Joo
Chang, Lisa
Rao, Jagadeesh S.
Rapoport, Stanley I.
TI Chronic olanzapine treatment decreases arachidonic acid turnover and
prostaglandin E-2 concentration in rat brain
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE anti-psychotic; bipolar disorder; cyclooxygenase; phospholipid;
prostaglandin E-2; washout
ID CYTOSOLIC PHOSPHOLIPASE A(2); POLYUNSATURATED FATTY-ACIDS; THIN-LAYER
CHROMATOGRAPHY; GROUP-SPECIFIC ASSAYS; DOCOSAHEXAENOIC ACID; BIPOLAR
DISORDER; UNANESTHETIZED RAT; IN-VIVO; ANTIPSYCHOTIC MEDICATIONS;
ATYPICAL ANTIPSYCHOTICS
AB The atypical antipsychotic, olanzapine (OLZ), is used to treat bipolar disorder, but its therapeutic mechanism of action is not clear. Arachidonic acid (AA, 20:4n-6) plays a critical role in brain signaling and an up-regulated AA metabolic cascade was reported in postmortem brains from bipolar disorder patients. In this study, we tested whether, similar to the action of the mood stabilizers lithium, carbamazepine and valproate, chronic OLZ treatment would reduce AA turnover in rat brain. We administered OLZ (6 mg/kg/day) or vehicle i.p. to male rats once daily for 21 days. A washout group received 21 days of OLZ followed by vehicle on day 22. Two hours after the last injection, [1-C-14] AA was infused intravenously for 5 min, and timed arterial blood samples were taken. After the rat was killed at 5 min, its brain was microwaved, removed and analyzed. Chronic OLZ decreased plasma unesterified AA concentration, AA incorporation rates and AA turnover in brain phospholipids. These effects were absent after washout. Consistent with reduced AA turnover, OLZ decreased brain cyclooxygenase activity and the brain concentration of the proinflammatory AA-derived metabolite, prostaglandin E-2, In view of up-regulated brain AA metabolic markers in bipolar disorder, the abilities of OLZ and the mood stabilizers to commonly decrease prostaglandin E-2, and AA turnover in rat brain phospholipids, albeit by different mechanisms, may be related to their efficacy against the disease.
C1 [Cheon, Yewon; Park, Jee-Young; Modi, Hiren R.; Kim, Hyung-Wook; Lee, Ho-Joo; Chang, Lisa; Rao, Jagadeesh S.; Rapoport, Stanley I.] NIA, Brain Physiol & Metab Sect, NIH, Bethesda, MD 20892 USA.
RP Cheon, Y (reprint author), NIA, Brain Physiol & Metab Sect, NIH, 9000 Rockville Pike,Bldg 9,1S-126, Bethesda, MD 20892 USA.
EM cheony@mail.nih.gov
FU National Institute on Aging, NIH
FX This work was supported entirely by the Intramural Research Program of
the National Institute on Aging, NIH. Olanzapine was kindly provided by
Eli Lilly (Indianapolis, IN, USA). The authors thank, for their
editorial assistance, the NIH Fellows' Editorial Board.
NR 86
TC 28
Z9 28
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
J9 J NEUROCHEM
JI J. Neurochem.
PD OCT
PY 2011
VL 119
IS 2
BP 364
EP 376
DI 10.1111/j.1471-4159.2011.07410.x
PG 13
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 834PE
UT WOS:000295973900012
PM 21812779
ER
PT J
AU Rich, BA
Carver, FW
Holroyd, T
Rosen, HR
Mendoza, JK
Cornwell, BR
Fox, NA
Pine, DS
Coppola, R
Leibenluft, E
AF Rich, Brendan A.
Carver, Frederick W.
Holroyd, Tom
Rosen, Heather R.
Mendoza, Jennifer K.
Cornwell, Brian R.
Fox, Nathan A.
Pine, Daniel S.
Coppola, Richard
Leibenluft, Ellen
TI Different neural pathways to negative affect in youth with pediatric
bipolar disorder and severe mood dysregulation
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE Bipolar disorder; Pediatric; Mood dysregulation; Irritability;
Frustration; Magnetoencephalography
ID MAJOR DEPRESSIVE DISORDER; ANTERIOR CINGULATE CORTEX; SUBCORTICAL
BRAIN-REGIONS; MEDIAL PREFRONTAL CORTEX; FRONTAL MIDLINE THETA;
INDIVIDUAL-DIFFERENCES; BEHAVIORAL-RESPONSES; SOURCE LOCALIZATION;
AFFECTIVE PICTURES; BRODMANN AREA-6
AB Questions persist regarding the presentation of bipolar disorder (BD) in youth and the nosological significance of irritability. Of particular interest is whether severe mood dysregulation (SMD), characterized by severe non-episodic irritability, hyper-arousal, and hyper-reactivity to negative emotional stimuli, is a developmental presentation of pediatric BD and, therefore, whether the two conditions are pathophysiologically similar. We administered the affective Posner paradigm, an attentional task with a condition involving blocked goal attainment via rigged feedback. The sample included 60 youth (20 BD, 20 SMD, and 20 controls) ages 8-17. Magnetoencephalography (MEG) examined neuronal activity (4-50 Hz) following negative versus positive feedback. We also examined reaction time (RI), response accuracy, and self-reported affect. Both BD and SMD youth reported being less happy than controls during the rigged condition. Also, SMD youth reported greater arousal following negative feedback than both BD and controls, and they responded to negative feedback with significantly greater activation of the anterior cingulate cortex (ACC) and medial frontal gyrus (MFG) than controls. Compared to SMD and controls, BD youth displayed greater superior frontal gyrus (SFG) activation and decreased insula activation following negative feedback. Data suggest a greater negative affective response to blocked goal attainment in SMD versus BD and control youth. This occurs in tandem with hyperactivation of medial frontal regions in SMD youth, while BD youth show dysfunction in the SFG and insula. Data add to a growing empirical base that differentiates pediatric BD and SMD and begin to elucidate potential neural mechanisms of irritability. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Rich, Brendan A.; Rosen, Heather R.] Catholic Univ Amer, Dept Psychol, Washington, DC 20064 USA.
[Carver, Frederick W.; Holroyd, Tom; Coppola, Richard] MEG Core Facil, Bethesda, MD USA.
[Mendoza, Jennifer K.; Cornwell, Brian R.; Pine, Daniel S.; Leibenluft, Ellen] NIMH, Mood & Anxiety Disorders Program, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Fox, Nathan A.] Univ Maryland, Child Dev Lab, College Pk, MD 20742 USA.
RP Rich, BA (reprint author), Catholic Univ Amer, Dept Psychol, 620 Michigan Ave NE, Washington, DC 20064 USA.
EM richb@cua.edu
FU NIH, NIMH; NIMH [K22-MH078044]
FX This research was supported by the Intramural Research Program of the
NIH, NIMH. This funding organization was not involved in research
aspects such as study design and conduct; data collection, analysis, nor
interpretation. Dr. Rich is supported by NIMH grant K22-MH078044.
NR 108
TC 25
Z9 25
U1 5
U2 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD OCT
PY 2011
VL 45
IS 10
BP 1283
EP 1294
DI 10.1016/j.jpsychires.2011.04.006
PG 12
WC Psychiatry
SC Psychiatry
GA 834XT
UT WOS:000295998500002
PM 21561628
ER
PT J
AU Leibenluft, E
AF Leibenluft, Ellen
TI DSM-10: Coming Soon to a Psychiatric Practice Near You
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Editorial Material
ID ADOLESCENTS; CHILDREN
C1 [Leibenluft, Ellen] NIMH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch, Intramural Res Program,NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Leibenluft, E (reprint author), Bldg 15K,MSC-2670, Bethesda, MD 20892 USA.
EM leibs@mail.nih.gov
FU Intramural NIH HHS [Z99 MH999999]
NR 8
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD OCT
PY 2011
VL 50
IS 10
BP 972
EP 974
DI 10.1016/j.jaac.2011.07.008
PG 3
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 829EZ
UT WOS:000295562700004
PM 21961771
ER
PT J
AU Axelson, DA
Birmaher, B
Strober, MA
Goldstein, BI
Ha, W
Gill, MK
Goldstein, TR
Yen, SR
Hower, H
Hunt, JI
Liao, FZ
Iyengar, S
Dickstein, D
Kim, E
Ryan, ND
Frankel, E
Keller, MB
AF Axelson, David A.
Birmaher, Boris
Strober, Michael A.
Goldstein, Benjamin I.
Ha, Wonho
Gill, Mary Kay
Goldstein, Tina R.
Yen, Shirley
Hower, Heather
Hunt, Jeffrey I.
Liao, Fangzi
Iyengar, Satish
Dickstein, Daniel
Kim, Eunice
Ryan, Neal D.
Frankel, Erica
Keller, Martin B.
TI Course of Subthreshold Bipolar Disorder in Youth: Diagnostic Progression
From Bipolar Disorder Not Otherwise Specified
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE bipolar mood disorders; child psychiatry; diagnosis and classification
ID COMORBIDITY SURVEY REPLICATION; SCHOOL-AGE-CHILDREN; SPECTRUM DISORDERS;
MANIC SYMPTOMS; COMMUNITY SAMPLE; CLINICAL-COURSE; II DISORDER;
ADOLESCENTS; PREVALENCE; LIFETIME
AB Objective: To determine the rate of diagnostic conversion from an operationalized diagnosis of bipolar disorder not otherwise specified (BP-NOS) to bipolar I disorder (BP-I) or bipolar II disorder (BP-H) in youth over prospective follow-up and to identify factors associated with conversion. Method: Subjects were 140 children and adolescents recruited from clinical referrals or advertisement who met operationalized criteria for BP-NOS at intake and participated in at least one follow-up evaluation (91% of initial cohort). Diagnoses were assessed at follow-up interviews using the Longitudinal Interval Follow-Up Evaluation. The mean duration of follow-up was 5 years and the mean interval between assessments was 8.2 months. Results: Diagnostic conversion to BP-I or BP-II occurred in 63 subjects (45%): 32 (23%) to BP-I (nine of whom had initially converted to BP-II) and 31 to only BP-II (22%). Median time from intake to conversion was 58 weeks. First- or second-degree family history of mania or hypomania was the strongest baseline predictor of diagnostic conversion (p = .006). Over follow-up, conversion was associated with greater intensity of hypomanic symptoms and with greater exposure to specialized, intensive outpatient psychosocial treatments. There was no association between conversion and exposure to treatment with particular medication classes. Conclusions: Children and adolescents referred with mood symptoms that meet operationalized criteria for BP-NOS, particularly those with a family history of BP, frequently progress to BP-I or BP-H. Efforts to identify these youth and effectively intervene may have the potential to curtail the progression of mood disorders in this high-risk population. J. Am. Acad. Child Adolesc. Psychiatry, 2011;50(10):1001-1016.
C1 [Axelson, David A.; Birmaher, Boris; Ha, Wonho; Gill, Mary Kay; Goldstein, Tina R.; Liao, Fangzi; Iyengar, Satish; Ryan, Neal D.] Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Pittsburgh, PA 15213 USA.
[Goldstein, Benjamin I.] Univ Toronto, Sunnybrook Hlth Sci Ctr, Toronto, ON, Canada.
[Strober, Michael A.; Kim, Eunice] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Hunt, Jeffrey I.; Dickstein, Daniel] Brown Univ, Alpert Med Sch, Bradley Hosp, Providence, RI 02912 USA.
[Frankel, Erica] NIMH, Expt Therapeut Pathophysiol Branch, Bethesda, MD USA.
RP Axelson, DA (reprint author), Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, 3811 OHara St, Pittsburgh, PA 15213 USA.
EM axelsonda@upmc.edu
RI Dickstein, Daniel/L-3210-2016
OI Dickstein, Daniel/0000-0003-1647-5329
FU National Institute of Mental Health [MH59929, MH59977, MH59691, MH74945,
MH69904, MH074581]; Sunnybrook Foundation; Pfizer
FX This research was supported by National Institute of Mental Health
Grants MH59929 (B.B.), MH59977 (M.A.S.), and MH59691 (M.B.K.), MH74945
(D.D.), MH69904 (S.Y.), MH074581 (T.R.G.), and the Sunnybrook Foundation
(B.I.G.).; Dr. Birmaher has served as a consultant for Schering Plough,
and receives royalties Random House, Inc. and Lippincott Williams and
Wilkins. Dr. Hunt is a Senior Editor for the Brown Psychopharm
Newsletter published by Wiley Publishers. Dr. B. Goldstein has received
research grant support from Pfizer, and has received honoraria from
Purdue Pharma. Dr. Keller has received research grant support from
Pfizer. He has received honoraria from and/or served as a consultant for
Abbot, CENEREX, Cephalon, Cypress Bioscience, Cyberonics, Forest,
Janssen, JDS, Medtronic, Organon, Novartis, Pfizer, Roche, Solvay,
Wyeth, and Sierra Neuropharmaceuticals. He has served on the advisory
board for Abbott, Bristol-Myers Squibb, CENEREX, Cyberonics, Cypress
Bioscience, Forest, Janssen, Neuronetics, Novartis, Orgonon, and Pfizer.
Drs. Axelson, Strober, Ha, T. Goldstein, Dickstein, Yen, Kim, Iyengar,
and Ryan, and Ms. Frankel, Ms. Gill, Ms. Hower, and Ms. Liao report no
biomedical financial interests or potential conflicts of interest.
NR 47
TC 75
Z9 77
U1 2
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD OCT
PY 2011
VL 50
IS 10
BP 1001
EP 1016
DI 10.1016/j.jaac.2011.07.005
PG 16
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 829EZ
UT WOS:000295562700008
PM 21961775
ER
PT J
AU Choi, YY
Kim, J
Seo, D
Choi, D
Kim, MJ
Kim, JH
Lee, KJ
Hur, KY
AF Choi, Yoon Young
Kim, Jungman
Seo, Daekwan
Choi, Dongho
Kim, Min Joo
Kim, Jung Hoon
Lee, Kyung-Jae
Hur, Kyung Yul
TI Is routine nasogastric tube insertion necessary in
pancreaticoduodenectomy?
SO JOURNAL OF THE KOREAN SURGICAL SOCIETY
LA English
DT Article
DE Pancreaticoduodenectomy; Gastrointestinal intubation
ID PROSPECTIVE RANDOMIZED-TRIAL; ELECTIVE LAPAROTOMY; GASTRIC-CANCER;
DECOMPRESSION; SURGERY; GASTRECTOMY; INTUBATION; OPERATIONS; NEED
AB Purpose: The necessity of nasogastric decompression after abdominal surgical procedures has been increasingly questioned for several years. Traditionally,. nasogastric decompression is a mandatory procedure after classical pancreaticoduodenectomy (PD); however, we still do not know whether or not it is necessary for PD. The present study was designed to assess the clinical benefit of nasogastric decompression after PD. Methods: Between July 2004 and May 2007, 41 consecutive patients who underwent PD were enrolled in this study. Eighteen patients were enrolled in the nasogastric tube (NGT) group and 23 patients were enrolled in the no NGT group. Results: There were no differences in the demographics, pathology, co-morbid medical conditions, and pre-operative laboratory values between the two groups. In addition, the passage of flatus (P = 0.963) and starting time of oral intake (P = 0.951) were similar in both groups. In the NGT group, 61% of the patients complained of discomfort related to the NGT. Pleural effusions were frequent in the NGT group (P = 0.037); however, other post-operative complications, such as wound dehiscence and anastomotic leakage, occurred similarly in both groups. There was one case of NGT re-insertion in the NGT group. Conclusion: Routine nasogastric decompression in patients undergoing PD is not mandatory because it has no clinical advantages and increases patient discomfort.
C1 [Choi, Yoon Young; Kim, Jungman; Choi, Dongho; Kim, Min Joo; Hur, Kyung Yul] Soonchunhyang Univ, Coll Med, Dept Surg, Seoul 140743, South Korea.
[Seo, Daekwan] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kim, Jung Hoon] Seoul Natl Univ, Coll Med, Dept Radiol, Seoul, South Korea.
[Lee, Kyung-Jae] Soonchunhyang Univ, Coll Med, Dept Occupat Med, Seoul 140743, South Korea.
RP Choi, D (reprint author), Soonchunhyang Univ, Coll Med, Soonchunhyang Univ Hosp, Dept Surg, 657 Hannam Dong, Seoul 140743, South Korea.
EM dhchoi@schmc.ac.kr
NR 17
TC 5
Z9 5
U1 0
U2 2
PU KOREAN SURGICAL SOCIETY
PI SEOUL
PA 3304HO, 101 DONG, BROWNSTONE SEOUL, 335, JUNGMIN-DONG, JUNG-GU, SEOUL,
100-859, SOUTH KOREA
SN 2233-7903
J9 J KOREAN SURG SOC
JI J. Korean Surg. Soc.
PD OCT
PY 2011
VL 81
IS 4
BP 257
EP 262
DI 10.4174/jkss.2011.81.4.257
PG 6
WC Surgery
SC Surgery
GA 827JE
UT WOS:000295424000005
PM 22111081
ER
PT J
AU Barbash, IM
Schenke, WH
Halabi, M
Ratnayaka, K
Faranesh, AZ
Kocaturk, O
Lederman, RJ
AF Barbash, Israel M.
Schenke, William H.
Halabi, Majdi
Ratnayaka, Kanishka
Faranesh, Anthony Z.
Kocaturk, Ozgur
Lederman, Robert J.
TI Experimental Model of Large Pulmonary Embolism Employing Controlled
Release of Subacute Caval Thrombus in Swine
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
ID DEEP-VEIN THROMBOSIS; IN-VITRO; RHEOLYTIC THROMBECTOMY; PORCINE MODEL;
CATHETER; MANAGEMENT; HYPERTENSION; OUTCOMES; REGISTRY; ANGIOJET
AB Purpose: To develop a catheter-based model of large pulmonary embolism (PE) in swine based on in situ venous thrombus formation.
Materials and Methods: Ten Yorkshire swine underwent transjugular implantation of a retrievable inferior vena cava (IVC) filter. A thrombin and collagen mixture was injected into a confined space created by two balloons inflated proximal and distal to the IVC filter. Animals were left to survive for 7 days +/- 3 to allow thrombus to organize in situ. The caval thrombus was released on transcatheter retrieval of the IVC filter and embolized into the main and branch pulmonary arteries. The severity of PE was scored based on digital subtraction angiography with the Miller index. At necropsy, thrombi were recovered and analyzed histopathologically.
Results: Large PE was induced in all animals (Miller index score of 15 +/- 5). Two animals developed saddle embolus with bilateral pulmonary artery occlusion, and five developed proximal occlusion of the left or right pulmonary artery. Nevertheless, no animal exhibited significant hemodynamic compromise. Large tubular thrombi were explanted in the size range of 5-10 cm long and 0.5-1 cm wide. Histologic analysis indicated an organized thrombus with infiltration of white blood cells and fibrin deposition.
Conclusions: Large caval thrombi can be formed in vivo and released at a predetermined time to induce large PE in a large animal model. This may help in the development and testing of new therapeutic approaches for PE.
C1 [Barbash, Israel M.; Schenke, William H.; Halabi, Majdi; Ratnayaka, Kanishka; Faranesh, Anthony Z.; Kocaturk, Ozgur; Lederman, Robert J.] NHLBI, Cardiovasc & Pulm Branch, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Ratnayaka, Kanishka] Childrens Natl Med Ctr, Dept Cardiol, Washington, DC 20010 USA.
RP Lederman, RJ (reprint author), NHLBI, Cardiovasc & Pulm Branch, Div Intramural Res, NIH, Bldg 10,Room 2C713,MSC 1538, Bethesda, MD 20892 USA.
EM lederman@nih.gov
OI lederman, robert/0000-0003-1202-6673
FU Division of Intramural Research, National Heart Lung and Blood
Institute, National Institutes of Health [1ZIAHL005062-08,
Z01-HL006041-01]
FX This work was supported by Division of Intramural Research, National
Heart Lung and Blood Institute, National Institutes of Health Grants
1ZIAHL005062-08 and Z01-HL006041-01. None of the authors have identified
a conflict of interest.
NR 27
TC 4
Z9 4
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD OCT
PY 2011
VL 22
IS 10
BP 1471
EP 1477
DI 10.1016/j.jvir.2011.06.011
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 831DH
UT WOS:000295708400020
PM 21802315
ER
PT J
AU Singleton, AB
AF Singleton, Andrew B.
TI Exome sequencing: a transformative technology
SO LANCET NEUROLOGY
LA English
DT Review
ID DE-NOVO MUTATIONS; PARKINSONS-DISEASE; MENTAL-RETARDATION;
ALZHEIMERS-DISEASE; HEARING-LOSS; GENE; REVEALS; RISK; IDENTIFICATION;
DEFICIENCY
AB Background Much basic research into disease mechanisms has made use of genetic findings to model and understand aetiology. Broad success has been achieved in finding disease-linked mutations with traditional positional cloning approaches; however, because of the requirements of this method, these successes have been limited by the availability of large, well characterised families. Because of these and other restrictions the genetic basis of many diseases, and diseases in many families, remains unknown.
Recent developments Exome sequencing uses DNA-enrichment methods and massively parallel nucleotide sequencing to comprehensively identify and type protein-coding variants throughout the genome. Coupled with growing databases that contain known variants, exome sequencing makes identification of genetic mutations and risk factors possible in families and samples that were deemed insufficiently informative for previous genetic studies. Not only does exome sequencing enable identification of mutations in families that were undetectable with linkage and positional cloning methods, but compared with these methods, it is also much quicker and cheaper. Use of exome sequencing has so far been successful in many rare diseases.
Where next? Exome sequencing is being adopted widely and we can expect an abundance of mutation discovery, similar to the deluge of genome-wide-association findings reported over the past 5 years; it is expected to enable the discovery of not only rare causal variants, but also protein-coding risk variants. This method will have application in both the research and clinical arenas and sets the scene for the use of whole-genome sequencing.
C1 NIA, Neurogenet Lab, NIH, Poolesville, MD 20837 USA.
RP Singleton, AB (reprint author), NIA, Neurogenet Lab, NIH, Poolesville, MD 20837 USA.
EM singleta@mail.nih.gov
RI Singleton, Andrew/C-3010-2009
FU National Institute on Aging, US National Institutes of Health,
Department of Health and Human Services [Z01 AG000958-08]
FX This work was supported by the Intramural Research Program of the
National Institute on Aging, US National Institutes of Health,
Department of Health and Human Services; project Z01 AG000958-08.
NR 43
TC 59
Z9 66
U1 1
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1474-4422
J9 LANCET NEUROL
JI Lancet Neurol.
PD OCT
PY 2011
VL 10
IS 10
BP 942
EP 946
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA 832OP
UT WOS:000295814600015
PM 21939903
ER
PT J
AU Katki, HA
Kinney, WK
Fetterman, B
Lorey, T
Poitras, NE
Cheung, L
Demuth, F
Schiffman, M
Wacholder, S
Castle, PE
AF Katki, Hormuzd A.
Kinney, Walter K.
Fetterman, Barbara
Lorey, Thomas
Poitras, Nancy E.
Cheung, Li
Demuth, Franklin
Schiffman, Mark
Wacholder, Sholom
Castle, Philip E.
TI Premature conclusions on HPV-only testing Reply
SO LANCET ONCOLOGY
LA English
DT Letter
C1 [Katki, Hormuzd A.; Schiffman, Mark; Wacholder, Sholom] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Kinney, Walter K.] Kaiser Permanente Med Care Program, Div Gynecol Oncol, Oakland, CA USA.
[Fetterman, Barbara; Lorey, Thomas; Poitras, Nancy E.] Kaiser Permanente No Calif, Reg Lab, Berkeley, CA USA.
[Cheung, Li; Demuth, Franklin] Informat Management Serv Inc, Silver Spring, MD USA.
[Castle, Philip E.] Amer Soc Clin Pathologists, Washington, DC USA.
RP Katki, HA (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
EM katkih@mail.nih.gov
RI Katki, Hormuzd/B-4003-2015
NR 2
TC 1
Z9 1
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
J9 LANCET ONCOL
JI Lancet Oncol.
PD OCT
PY 2011
VL 12
IS 11
BP 993
EP 993
PG 1
WC Oncology
SC Oncology
GA 833KW
UT WOS:000295885200014
ER
PT J
AU Shen, J
AF Shen, Jun
TI Derivative encoding for parallel magnetic resonance imaging
SO MEDICAL PHYSICS
LA English
DT Article
DE parallel imaging; magnetic resonance imaging (MRI); derivative encoding;
image reconstruction; noise reduction
ID GRAPPA RECONSTRUCTION; MRI; REGULARIZATION; SENSE; COIL; MOTION
AB Purpose: To introduce a linear shift-invariant relationship between the partial derivatives of k space signals acquired using multichannel receive coils and to demonstrate that k space derivatives can be used for image unwrapping.
Methods: Fourier transform of k space derivatives contains information on the spatial origins of aliased pixels; therefore, images can be reconstructed by k space derivatives. Fully sampled phantom and brain images acquired at 3 T using a standard eight channel receive coil were used to validate the k space derivatives theorem by unwrapping aliased images.
Results: Derivative encoding leads to new methods for parallel imaging reconstruction in both k space and image domains. Noise amplification in sensitivity encoding image reconstruction, which is considered to produce the optimal SNR, can be further reduced using k space derivative encoding without making any assumptions on the characteristics of the images to be reconstructed.
Conclusions: This work demonstrated that the partial derivative of the k space signal acquired from one coil with respect to one direction can be expressed as a sum of partial derivatives of signals from multiple coils with respect to the perpendicular k space direction(s). This relationship between the partial derivatives of k space signals is linear and shift-invariant in the Cartesian coordinate system. (C) 2011 American Association of Physicists in Medicine. [DOI: 10.1118/1.3633908]
C1 NIMH, Mol Imaging Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Shen, J (reprint author), NIMH, Mol Imaging Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
EM shenj@intra.nimh.nih.gov
FU National Institute of Mental Health, National Institutes of Health,
Department of Health and Human Services (IRP-NIMH-NIH-DHHS)
FX The author gratefully acknowledges the support by the Intramural Program
of the National Institute of Mental Health, National Institutes of
Health, Department of Health and Human Services (IRP-NIMH-NIH-DHHS). The
author also thanks Dr. Fa-Hsuan Lin, MGH, and Dr. Yan Zhang, NIMH, for
valuable help.
NR 32
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD OCT
PY 2011
VL 38
IS 10
BP 5582
EP 5589
DI 10.1118/1.3633908
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 829WU
UT WOS:000295617400033
PM 21992376
ER
PT J
AU Freed, M
de Zwart, JA
Hariharan, P
Myers, MR
Badano, A
AF Freed, Melanie
de Zwart, Jacco A.
Hariharan, Prasanna
Myers, Matthew R.
Badano, Aldo
TI Development and characterization of a dynamic lesion phantom for the
quantitative evaluation of dynamic contrast-enhanced MRI
SO MEDICAL PHYSICS
LA English
DT Article
DE dynamic phantom; DCE-MRI; breast imaging
ID SPOILED GRADIENT-ECHO; MYOCARDIAL-PERFUSION; DIAGNOSTIC-ACCURACY; BREAST
MRI; PARAMETERS; SEQUENCES; RESONANCE; DTPA; STANDARDIZATION;
QUANTIFICATION
AB Purpose: To develop a dynamic lesion phantom that is capable of producing physiological kinetic curves representative of those seen in human dynamic contrast-enhanced MRI (DCE-MRI) data. The objective of this phantom is to provide a platform for the quantitative comparison of DCE-MRI protocols to aid in the standardization and optimization of breast DCE-MRI.
Methods: The dynamic lesion consists of a hollow, plastic mold with inlet and outlet tubes to allow flow of a contrast agent solution through the lesion over time. Border shape of the lesion can be controlled using the lesion mold production method. The configuration of the inlet and outlet tubes was determined using fluid transfer simulations. The total fluid flow rate was determined using x-ray images of the lesion for four different flow rates (0.25, 0.5, 1.0, and 1.5 ml/s) to evaluate the resultant kinetic curve shape and homogeneity of the contrast agent distribution in the dynamic lesion. High spatial and temporal resolution x-ray measurements were used to estimate the true kinetic curve behavior in the dynamic lesion for benign and malignant example curves. DCE-MRI example data were acquired of the dynamic phantom using a clinical protocol.
Results: The optimal inlet and outlet tube configuration for the lesion molds was two inlet molds separated by 30 degrees and a single outlet tube directly between the two inlet tubes. X-ray measurements indicated that 1.0 ml/s was an appropriate total fluid flow rate and provided truth for comparison with MRI data of kinetic curves representative of benign and malignant lesions. DCE-MRI data demonstrated the ability of the phantom to produce realistic kinetic curves.
Conclusions: The authors have constructed a dynamic lesion phantom, demonstrated its ability to produce physiological kinetic curves, and provided estimations of its true kinetic curve behavior. This lesion phantom provides a tool for the quantitative evaluation of DCE-MRI protocols, which may lead to improved discrimination of breast cancer lesions. (C) 2011 American Association of Physicists in Medicine. [DOI: 10.1118/1.3633911]
C1 [Freed, Melanie; Badano, Aldo] US FDA, Div Imaging & Appl Math, Off Sci & Engn Labs, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
[Freed, Melanie] Univ Maryland, Dept Bioengn, College Pk, MD 20742 USA.
[de Zwart, Jacco A.] Natl Inst Neurol Disorders & Stroke, Lab Funct & Mol Imaging, Adv MRI Sect, NIH, Bethesda, MD 20892 USA.
[Hariharan, Prasanna; Myers, Matthew R.] US FDA, Div Solid & Fluid Mech, Off Sci & Engn Labs, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
RP Freed, M (reprint author), US FDA, Div Imaging & Appl Math, Off Sci & Engn Labs, Ctr Devices & Radiol Hlth, 10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM melanie.freed@fda.hhs.gov
OI badano, aldo/0000-0003-3712-6670
FU FDA's Office of Women Health; Center for Devices and Radiological
Health; NINDS/NIH
FX The authors wish to thank Han Wen (NIH/NHLBI) for providing MRI scan
time, Hellmut Merkle (NIH/NINDS) for providing noise reduction filters
for the fluid pump, Eugene O'Bryan (FDA) for help with setting up the
timing circuit and his tireless material acquisition efforts, and Randy
Bidinger (FDA) and Bruce Fleharty (FDA) for machining of a variety of
experimental components. The authors also acknowledge funding from the
FDA's Office of Women Health. This project was supported in part by an
appointment to the Research Participation Program at the Center for
Devices and Radiological Health administered by the Oak Ridge Institute
for Science and Education through an interagency agreement between the
U.S. Department of Energy and the U.S. Food and Drug Administration.
This research was sponsored, in part, by the Intramural Research Program
of NINDS/NIH.
NR 33
TC 8
Z9 8
U1 0
U2 5
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD OCT
PY 2011
VL 38
IS 10
BP 5601
EP 5611
DI 10.1118/1.3633911
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 829WU
UT WOS:000295617400035
PM 21992378
ER
PT J
AU Linguraru, MG
Wang, SJ
Shah, F
Gautam, R
Peterson, J
Linehan, WM
Summers, RM
AF Linguraru, Marius George
Wang, Shijun
Shah, Furhawn
Gautam, Rabindra
Peterson, James
Linehan, W. Marston
Summers, Ronald M.
TI Automated noninvasive classification of renal cancer on multiphase CT
SO MEDICAL PHYSICS
LA English
DT Article
DE kidney; cancer; segmentation; classification; computer-aided diagnosis
ID COMPUTER-AIDED DIAGNOSIS; BRAIN-TUMOR SEGMENTATION; SUPPORT VECTOR
MACHINES; ENHANCED ABDOMINAL CT; KIDNEY CANCER; PULMONARY NODULES;
COLONIC POLYPS; IMAGES; SHAPE; TOMOGRAPHY
AB Purpose: To explore the added value of the shape of renal lesions for classifying renal neoplasms. To investigate the potential of computer-aided analysis of contrast-enhanced computed-tomography (CT) to quantify and classify renal lesions.
Methods: A computer-aided clinical tool based on adaptive level sets was employed to analyze 125 renal lesions from contrast-enhanced abdominal CT studies of 43 patients. There were 47 cysts and 78 neoplasms: 22 Von Hippel-Lindau (VHL), 16 Birt-Hogg-Dube (BHD), 19 hereditary papillary renal carcinomas (HPRC), and 21 hereditary leiomyomatosis and renal cell cancers (HLRCC). The technique quantified the three-dimensional size and enhancement of lesions. Intrapatient and interphase registration facilitated the study of lesion serial enhancement. The histograms of curvature-related features were used to classify the lesion types. The areas under the curve (AUC) were calculated for receiver operating characteristic curves.
Results: Tumors were robustly segmented with 0.80 overlap (0.98 correlation) between manual and semi-automated quantifications. The method further identified morphological discrepancies between the types of lesions. The classification based on lesion appearance, enhancement and morphology between cysts and cancers showed AUC = 0.98; for BHD + VHL (solid cancers) vs. HPRC + HLRCC AUC = 0.99; for VHL vs. BHD AUC = 0.82; and for HPRC vs. HLRCC AUC = 0.84. All semi-automated classifications were statistically significant (p < 0.05) and superior to the analyses based solely on serial enhancement.
Conclusions: The computer-aided clinical tool allowed the accurate quantification of cystic, solid, and mixed renal tumors. Cancer types were classified into four categories using their shape and enhancement. Comprehensive imaging biomarkers of renal neoplasms on abdominal CT may facilitate their noninvasive classification, guide clinical management, and monitor responses to drugs or interventions. (C) 2011 American Association of Physicists in Medicine. [DOI: 10.1118/1.3633898]
C1 [Linguraru, Marius George; Wang, Shijun; Shah, Furhawn; Summers, Ronald M.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Gautam, Rabindra; Peterson, James; Linehan, W. Marston] NCI, Urol Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Linguraru, MG (reprint author), NIH, Ctr Clin, 10 Ctr Dr, Bethesda, MD 20892 USA.
FU National Institutes of Health, Clinical Center; National Cancer
Institute, Center for Cancer Research
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, Clinical Center and National Cancer
Institute, Center for Cancer Research. The authors would like to thank
John A. Pura for helping with the data analysis.
NR 55
TC 6
Z9 6
U1 2
U2 5
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD OCT
PY 2011
VL 38
IS 10
BP 5738
EP 5746
DI 10.1118/1.3633898
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 829WU
UT WOS:000295617400045
PM 21992388
ER
PT J
AU Nash, TE
Garcia, HH
AF Nash, Theodore E.
Garcia, Hector H.
TI Diagnosis and treatment of neurocysticercosis
SO NATURE REVIEWS NEUROLOGY
LA English
DT Review
ID SOLITARY CYSTICERCUS GRANULOMA; HIGH-DOSE PRAZIQUANTEL; LINKED
IMMUNOELECTROTRANSFER BLOT; TAENIA-SOLIUM CYSTICERCOSIS;
DOUBLE-BLIND-TRIAL; CEREBRAL CYSTICERCOSIS; ALBENDAZOLE THERAPY;
FOLLOW-UP; EXTRAPARENCHYMAL NEUROCYSTICERCOSIS; CALCIFIED
NEUROCYSTICERCOSIS
AB Neurocysticercosis is a parasitic disease caused by the larval (cystic) form of the pork cestode tapeworm, Taenia solium, and is a major cause of acquired seizures and epilepsy worldwide. Development of sensitive and specific diagnostic methods, particularly CT and MRI, has revolutionized our knowledge of the burden of cysticercosis infection and disease, and has led to the development of effective antihelminthic treatments for neurocysticercosis. The importance of calcified granulomas with perilesional edema as foci of seizures and epilepsy in populations where neurocysticercosis is endemic is newly recognized, and indicates that treatment with anti-inflammatory agents could have a role in controlling or preventing epilepsy in these patients. Importantly, neurocysticercosis is one of the few diseases that could potentially be controlled or eliminated-an accomplishment that would prevent millions of cases of epilepsy. This Review examines the rationale for treatment of neurocysticercosis and highlights the essential role of inflammation in the pathogenesis of disease, the exacerbation of symptoms that occurs as a result of antihelminthic treatment, and the limitations of current antihelminthic and anti-inflammatory treatments. Nash, T. E. & Garcia, H. H. Nat. Rev. Neurol. 7, 584-594 (2011); published online 13 September 2011; doi:10.1038/nrneurol.2011.135
C1 [Garcia, Hector H.] Inst Nacl Ciencias Neurol, Cysticercosis Unit, Lima, Peru.
[Nash, Theodore E.] NIAID, Gastrointestinal Parasites Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Garcia, HH (reprint author), Inst Nacl Ciencias Neurol, Cysticercosis Unit, Jr Ancash 1271, Lima, Peru.
EM hgarcia@jhsph.edu
FU National Institutes of Health, National Institutes of Allergy and
Infection Diseases
FX This work was supported in part by the Intramural Research Program of
the National Institutes of Health, National Institutes of Allergy and
Infection Diseases. H. H. Garcia is a Wellcome Trust International
Senior Research Fellow.
NR 116
TC 68
Z9 71
U1 1
U2 17
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4758
J9 NAT REV NEUROL
JI Nat. Rev. Neurol.
PD OCT
PY 2011
VL 7
IS 10
BP 584
EP 594
DI 10.1038/nrneurol.2011.135
PG 11
WC Clinical Neurology
SC Neurosciences & Neurology
GA 834BU
UT WOS:000295933500008
PM 21912406
ER
PT J
AU Reyes-Turcu, FE
Zhang, K
Zofall, M
Chen, E
Grewal, SIS
AF Reyes-Turcu, Francisca E.
Zhang, Ke
Zofall, Martin
Chen, Eesin
Grewal, Shiv I. S.
TI Defects in RNA quality control factors reveal RNAi-independent
nucleation of heterochromatin
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID FISSION YEAST; POLYMERASE-II; EPIGENETIC CONTROL; TRIGGER RNAI; HP1
PROTEINS; TRANSCRIPTION; INTERFERENCE; ELONGATION; MECHANISMS; CHROMATIN
AB Heterochromatin assembly at Schizosaccharomyces pombe centromeres involves a self-reinforcing loop mechanism wherein chromatin-bound RNAi factors facilitate targeting of Clr4-Rik1 methyltransferase. However, the initial nucleation of heterochromatin has remained elusive. We show that cells lacking Mlo3, a protein involved in mRNP biogenesis and RNA quality control, assemble functional heterochromatin in RNAi-deficient cells. Heterochromatin restoration is linked to RNA surveillance because loss of Mlo3-associated TRAMP also rescues heterochromatin defects of RNAi mutants. mlo3 Delta, which causes accumulation of bidirectional repeat-transcripts, restores Rik1 enrichment at repeats and triggers de novo heterochromatin formation in the absence of RNAi. RNAi-independent heterochromatin nucleation occurs at selected euchromatic loci that show upregulation of antisense RNAs in mlo3 Delta cells. We find that the exosome RNA degradation machinery acts parallel to RNAi to promote heterochromatin formation at centromeres. These results suggest that RNAi-independent mechanisms exploit transcription and non-coding RNAs to nucleate heterochromatin.
C1 [Reyes-Turcu, Francisca E.; Zhang, Ke; Zofall, Martin; Chen, Eesin; Grewal, Shiv I. S.] NCI, Lab Biochem & Mol Biol, US Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Grewal, SIS (reprint author), NCI, Lab Biochem & Mol Biol, US Natl Inst Hlth, Bethesda, MD 20892 USA.
EM grewals@mail.nih.gov
FU US National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX We are thankful to D. Eick (Helmholtz Center Munich) for the gift of
phospho (Ser2) RNAPII antibody, R. Dhar and N. Krogan (University of
California, San Francisco) for strains, J. Dhakshnamoorthy, N.
Komissarova and S. Mehta for helpful contributions, and members of the
Grewal laboratory for discussions. This research was supported by the
Intramural Research Program of the US National Institutes of Health,
National Cancer Institute, Center for Cancer Research.
NR 60
TC 45
Z9 45
U1 0
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD OCT
PY 2011
VL 18
IS 10
BP 1132
EP U114
DI 10.1038/nsmb.2122
PG 8
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 834BF
UT WOS:000295931400007
PM 21892171
ER
PT J
AU Collins, J
Hu, S
Devarajan, P
Bonnemann, CG
Bennett, M
AF Collins, J.
Hu, S.
Devarajan, P.
Bonnemann, C. G.
Bennett, M.
TI Candidate biomarkers in merosin-deficient congenital muscular dystrophy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 16th International Congress of the World-Muscle-Society
CY OCT 18-22, 2011
CL Algarve, PORTUGAL
SP World Muscle Soc
C1 [Collins, J.; Hu, S.; Devarajan, P.; Bennett, M.] Cincinnati Childrens Hosp, Med Ctr, Cincinnati, OH USA.
[Bonnemann, C. G.] NINCDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2011
VL 21
IS 9-10
BP 660
EP 661
DI 10.1016/j.nmd.2011.06.824
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 834JP
UT WOS:000295955900073
ER
PT J
AU Foley, AR
Quijano-Roy, S
Collins, J
Straub, V
Deconinck, N
Mercuri, E
D'Amico, A
Bertini, E
North, K
Ryan, M
Rummey, C
Meier, T
Cole, T
Muntoni, F
Bonnemann, C
AF Foley, A. R.
Quijano-Roy, S.
Collins, J.
Straub, V.
Deconinck, N.
Mercuri, E.
D'Amico, A.
Bertini, E.
North, K.
Ryan, M.
Rummey, C.
Meier, T.
Cole, T.
Muntoni, F.
Boennemann, C.
TI The identification of a viable outcome measure in the collagen VI
myopathies promotes progress toward clinical trials
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 16th International Congress of the World-Muscle-Society
CY OCT 18-22, 2011
CL Algarve, PORTUGAL
SP World Muscle Soc
C1 [Foley, A. R.; Muntoni, F.] Dubowitz Neuromuscular Ctr, UCL Inst Child Hlth, London, England.
[Foley, A. R.; Muntoni, F.] Great Ormond St Hosp Sick Children, London WC1N 3JH, England.
[Quijano-Roy, S.] Hop Raymond Poincare, Neuromuscular Ctr, Garches, France.
[Collins, J.] Cincinnati Childrens Hosp, Med Ctr, Div Neurol, Cincinnati, OH USA.
[Straub, V.] Univ Newcastle, Int Ctr Life, Inst Human Genet, Newcastle, England.
[Deconinck, N.] Hop Univ Enfants Reine Fabiola, Dept Neurol, Brussels, Belgium.
[Mercuri, E.] Catholic Univ, Dept Paediat Neurol, Rome, Italy.
[D'Amico, A.; Bertini, E.] Bambino Gesu Pediat Hosp, Mol Med Unit, Rome, Italy.
[North, K.] Univ Sydney, Childrens Hosp Westmead, Inst Neuromuscular Res, Sydney, NSW 2006, Australia.
[Ryan, M.] Royal Childrens Hosp, Dept Neurol, Melbourne, Vic, Australia.
[Rummey, C.; Meier, T.] Santhera Pharmaceut, Liestal, Switzerland.
[Boennemann, C.] Natl Inst Neurol Disorders & Stroke NIH, Neuromuscular & Neurogenet Disorders Childhood Se, Bethesda, MD USA.
RI d'amico, adele/J-9203-2016
OI d'amico, adele/0000-0003-2438-2624
NR 0
TC 0
Z9 0
U1 1
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2011
VL 21
IS 9-10
BP 662
EP 662
DI 10.1016/j.nmd.2011.06.828
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 834JP
UT WOS:000295955900077
ER
PT J
AU Meilleur, KG
Medne, L
Hu, Y
Perkins, K
Powell-Hamilton, N
Finkel, R
Scavina, M
Bonnemann, C
AF Meilleur, K. G.
Medne, L.
Hu, Y.
Perkins, K.
Powell-Hamilton, N.
Finkel, R.
Scavina, M.
Bonnemann, C.
TI Further characterization of the clinical and mutational spectrum of
alpha-dystroglycanopathy caused by mutations in the LARGE gene
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 16th International Congress of the World-Muscle-Society
CY OCT 18-22, 2011
CL Algarve, PORTUGAL
SP World Muscle Soc
C1 [Meilleur, K. G.; Hu, Y.; Perkins, K.; Bonnemann, C.] Natl Inst Neurol Disorders & Stroke, Neurogenet Branch, Bethesda, MD USA.
[Medne, L.; Finkel, R.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Perkins, K.; Scavina, M.] AI Dupont Childrens Hosp, Wilmington, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2011
VL 21
IS 9-10
BP 664
EP 665
DI 10.1016/j.nmd.2011.06.836
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 834JP
UT WOS:000295955900085
ER
PT J
AU Perkins, KZ
Meilleur, K
Medne, L
Devoto, M
Tennekoon, G
Yum, S
Yang, M
Finkel, R
Johnson, J
Gibbs, JR
Ferguson, T
Zou, Y
Traynor, B
Bonnemann, C
AF Perkins, K. Z.
Meilleur, K.
Medne, L.
Devoto, M.
Tennekoon, G.
Yum, S.
Yang, M.
Finkel, R.
Johnson, J.
Gibbs, J. R.
Ferguson, T.
Zou, Y.
Traynor, B.
Bonnemann, C.
TI Exome sequencing with linkage analysis identifies a novel ACTA1 variant
in a large family with progressive muscle weakness
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 16th International Congress of the World-Muscle-Society
CY OCT 18-22, 2011
CL Algarve, PORTUGAL
SP World Muscle Soc
C1 [Perkins, K. Z.; Meilleur, K.; Zou, Y.; Bonnemann, C.] Natl Inst Neurol Disorders & Stroke, Bethesda, MD USA.
[Medne, L.; Devoto, M.; Tennekoon, G.; Yum, S.; Yang, M.; Finkel, R.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Johnson, J.; Gibbs, J. R.; Traynor, B.] NIA, Bethesda, MD 20892 USA.
[Ferguson, T.] Temple Univ, Philadelphia, PA 19122 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2011
VL 21
IS 9-10
BP 696
EP 697
DI 10.1016/j.nmd.2011.06.942
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 834JP
UT WOS:000295955900191
ER
PT J
AU Dowling, JJ
Arbogast, S
McEvoy, A
Nelson, DD
Brooks, SV
Kuwada, JY
Bonnemann, CG
Ferreiro, A
AF Dowling, J. J.
Arbogast, S.
McEvoy, A.
Nelson, D. D.
Brooks, S. V.
Kuwada, J. Y.
Bonnemann, C. G.
Ferreiro, A.
TI Increased oxidative stress and successful antioxidant treatment in a
vertebrate model of RYR1 related myopathy
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 16th International Congress of the World-Muscle-Society
CY OCT 18-22, 2011
CL Algarve, PORTUGAL
SP World Muscle Soc
C1 [Dowling, J. J.; McEvoy, A.; Nelson, D. D.; Brooks, S. V.; Kuwada, J. Y.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Arbogast, S.; Ferreiro, A.] INSERM, Inst Myol, Paris, France.
[Bonnemann, C. G.] NIH, Bethesda, MD 20892 USA.
RI Ferreiro, Ana/F-5371-2011
NR 0
TC 0
Z9 0
U1 1
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2011
VL 21
IS 9-10
BP 720
EP 721
DI 10.1016/j.nmd.2011.06.1019
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 834JP
UT WOS:000295955900268
ER
PT J
AU Vorgerd, M
Kley, RA
Serdaroglu-Oflazer, P
Odgerel, Z
Olive, M
Lee, HS
Hahn, Y
van der Ven, PFM
Hohfeld, J
Kirschner, J
Bilbao, JM
Goldfarb, LG
Furst, DO
AF Vorgerd, M.
Kley, R. A.
Serdaroglu-Oflazer, P.
Odgerel, Z.
Olive, M.
Lee, H. S.
Hahn, Y.
van der Ven, P. F. M.
Hoehfeld, J.
Kirschner, J.
Bilbao, J. M.
Goldfarb, L. G.
Fuerst, D. O.
TI Myofibrillar myopathy associated with filamin C mutations: Refining the
phenotype and new insights in pathogenesis
SO NEUROMUSCULAR DISORDERS
LA English
DT Meeting Abstract
CT 16th International Congress of the World-Muscle-Society
CY OCT 18-22, 2011
CL Algarve, PORTUGAL
SP World Muscle Soc
C1 [Vorgerd, M.; Kley, R. A.] Ruhr Univ Bochum, Univ Hosp Bergmannsheil, Dept Neurol, Bochum, Germany.
[Serdaroglu-Oflazer, P.] Istanbul Univ, Istanbul Fac Med, Dept Neurol, Istanbul, Turkey.
[Odgerel, Z.; Lee, H. S.; Goldfarb, L. G.] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD USA.
[Olive, M.] IDIBELL Hosp Univ Bellvitge, Inst Neuropatol, Barcelona, Spain.
[Hahn, Y.; van der Ven, P. F. M.; Hoehfeld, J.; Fuerst, D. O.] Univ Bonn, Inst Cell Biol, D-5300 Bonn, Germany.
[Kirschner, J.] Univ Childrens Hosp Freiburg, Div Neuropediat & Muscle Disorders, Freiburg, Germany.
RI Kirschner, Janbernd/H-7418-2016
OI Kirschner, Janbernd/0000-0003-1618-7386
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD OCT
PY 2011
VL 21
IS 9-10
BP 741
EP 741
DI 10.1016/j.nmd.2011.06.1085
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 834JP
UT WOS:000295955900334
ER
PT J
AU Munafo, MR
Johnstone, EC
Walther, D
Uhl, GR
Murphy, MFG
Aveyard, P
AF Munafo, Marcus R.
Johnstone, Elaine C.
Walther, Donna
Uhl, George R.
Murphy, Michael F. G.
Aveyard, Paul
TI CHRNA3 rs1051730 Genotype and Short-Term Smoking Cessation
SO NICOTINE & TOBACCO RESEARCH
LA English
DT Article
ID NICOTINE REPLACEMENT THERAPY; RANDOMIZED CONTROLLED-TRIAL; TOBACCO
DEPENDENCE; GENETIC-VARIATION; TRANSDERMAL NICOTINE; CLINICAL-TRIALS;
RECEPTOR DRD2; STOP SMOKING; FOLLOW-UP; ASSOCIATION
AB Introduction: The rs1051730 genetic variant within the CHRNA5-A3-B4 gene cluster is associated with heaviness of smoking and has recently been reported to be associated with likelihood of stopping smoking. We investigated the potential association of rs1051730 genotype with reduced likelihood of smoking cessation in 2 cohorts of treatment-seeking smokers in primary care in the United Kingdom.
Methods: Data were drawn from 2 clinical trials on which DNA was available. One sample was a randomized placebo-controlled trial of nicotine transdermal patch and the other sample an open-label trial where all participants received nicotine transdermal patch. Smoking status was biochemically verified. Logistic regression was used to assess evidence for association in each sample, and data were combined within a meta-analysis.
Results: There was evidence of association of rs1051730 genotype with short-term (4-week) cessation in our open-label trial sample but not our placebo-controlled trial sample. When combined in a meta-analysis, this effect remained. There was no evidence of association at later follow-up intervals. Adjustment for cigarette consumption and tobacco dependence did not alter these results substantially.
Conclusions: Our data, taken together with previous recent studies, provide some support for a weak association between this variant and short-term smoking cessation in treatment-seeking smokers, which does not seem to operate only among those receiving nicotine replacement therapy. Moreover, the rs1051730 variant may not merely operate as a marker for dependence or heaviness of smoking.
C1 [Munafo, Marcus R.] Univ Bristol, Sch Expt Psychol, Bristol BS8 1TU, Avon, England.
[Johnstone, Elaine C.] Univ Oxford, Dept Clin Pharmacol, Oxford, England.
[Walther, Donna; Uhl, George R.] Natl Inst Drug Abuse, Mol Neurobiol Branch, Natl Inst Hlth, Intramural Res Program, Baltimore, MD USA.
[Murphy, Michael F. G.] Univ Oxford, Childhood Canc Res Grp, Oxford, England.
[Aveyard, Paul] Univ Birmingham, Birmingham, W Midlands, England.
RP Munafo, MR (reprint author), Univ Bristol, Sch Expt Psychol, 12A Priory Rd, Bristol BS8 1TU, Avon, England.
EM marcus.munafo@bristol.ac.uk
OI Aveyard, Paul/0000-0002-1802-4217; Munafo, Marcus/0000-0002-4049-993X
FU Cancer Research UK [C53/A6281]; National Institutes of Health (National
Institute on Drug Abuse) Department of Health and Human Services, USA;
National Institute of Health Research; Economic and Social Research
Council; British Heart Foundation; Cancer Research UK; Department of
Health; Medical Research Council of the UK Clinical Research
FX This research was supported in part by a Cancer Research UK programme
grant (C53/A6281) and by the National Institutes of Health intramural
research program (National Institute on Drug Abuse) Department of Health
and Human Services, USA. PA is supported by the National Institute of
Health Research.; MRM and PA are members of the UK Centre for Tobacco
Control Studies, a U.K. Clinical Research Collaboration Public Health
Research Centre of Excellence. Funding from the Economic and Social
Research Council, the British Heart Foundation, Cancer Research UK, the
Department of Health, and the Medical Research Council, under the
auspices of the UK Clinical Research Collaboration, is gratefully
acknowledged. The authors are grateful for the support of the Patch
Study Team and the general practices which participated in the trial.
NR 35
TC 43
Z9 44
U1 1
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1462-2203
J9 NICOTINE TOB RES
JI Nicotine Tob. Res.
PD OCT
PY 2011
VL 13
IS 10
BP 982
EP 988
DI 10.1093/ntr/ntr106
PG 7
WC Substance Abuse; Public, Environmental & Occupational Health
SC Substance Abuse; Public, Environmental & Occupational Health
GA 828NL
UT WOS:000295508500012
PM 21690317
ER
PT J
AU Lee, YH
Judge, AD
Seo, D
Kitade, M
Gomez-Quiroz, LE
Ishikawa, T
Andersen, JB
Kim, BK
Marquardt, JU
Raggi, C
Avital, I
Conner, EA
MacLachlan, I
Factor, VM
Thorgeirsson, SS
AF Lee, Y-H
Judge, A. D.
Seo, D.
Kitade, M.
Gomez-Quiroz, L. E.
Ishikawa, T.
Andersen, J. B.
Kim, B-K
Marquardt, J. U.
Raggi, C.
Avital, I.
Conner, E. A.
MacLachlan, I.
Factor, V. M.
Thorgeirsson, S. S.
TI Molecular targeting of CSN5 in human hepatocellular carcinoma: a
mechanism of therapeutic response
SO ONCOGENE
LA English
DT Article
DE hepatocellular carcinoma; CSN5; targeted siRNA therapeutics; SNALP
ID BINDING PROTEIN-1 EXPRESSION; CYCLE INHIBITOR P27(KIP1); COP9
SIGNALOSOME; RNA INTERFERENCE; BREAST-CANCER; IN-VIVO;
PANCREATIC-CANCER; SYNTHETIC SIRNA; GENE-EXPRESSION; C-MYC
AB Development of targeted therapy for hepatocellular carcinoma (HCC) remains a major challenge. We have recently identified an elevated expression of the fifth subunit of COP9 signalosome (CSN5) in early HCC as compared with dysplastic stage. In the present study, we explored the possibility of CSN5 being a potential therapeutic target for HCC. Our results show that CSN5 knockdown by small-interfering (si) RNA caused a strong induction of apoptosis and inhibition of cell-cycle progression in HCC cells in vitro. The down-regulation of CSN5 was sufficient to interfere with CSN function as evidenced by the accumulation of neddylated Cullin 1 and changes in the protein levels of CSN-controlled substrates SKP2, p53, p27 and nuclear factor-kappa B, albeit to a different degree depending on the HCC cell line, which could account for the CSN5 knockdown phenotype. The transcriptomic analysis of CSN5 knockdown signature showed that the anti-proliferative effect was driven by a common subset of molecular alterations including down-regulation of cyclin-dependent kinase 6 (CDK6) and integrin beta 1 (ITGB1), which were functionally interconnected with key oncogenic regulators MYC and TGF beta 1 involved in the control of proliferation, apoptotic cell death and HCC progression. Consistent with microarray analysis, western blotting revealed that CSN5 depletion increased phosphorylation of Smad 2/3, key mediators of TGF beta 1 signaling, decreased the protein levels of ITGB1, CDK6 and cyclin D1 and caused reduced expression of anti-apoptotic Bcl-2, while elevating the levels of proapoptotic Bak. A chemically modified variant of CSN5 siRNA was then selected for in vivo application based on the growth inhibitory effect and minimal induction of unwanted immune response. Systemic delivery of the CSN5 3/8 variant by stable-nucleic-acid-lipid particles significantly suppressed the tumor growth in Huh7-luc(+) orthotopic xenograft model. Taken together, these results indicate that CSN5 has a pivotal role in HCC pathogenesis and maybe an attractive molecular target for systemic HCC therapy. Oncogene (2011) 30, 4175-4184; doi:10.1038/onc.2011.126; published online 18 April 2011
C1 [Lee, Y-H; Seo, D.; Kitade, M.; Gomez-Quiroz, L. E.; Ishikawa, T.; Andersen, J. B.; Kim, B-K; Marquardt, J. U.; Raggi, C.; Conner, E. A.; Factor, V. M.; Thorgeirsson, S. S.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Judge, A. D.; MacLachlan, I.] Tekmira Pharmaceut Corp, Burnaby, BC, Canada.
[Avital, I.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
RP Thorgeirsson, SS (reprint author), NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, 37 Convent Dr Dr MSC,Room 4146A, Bethesda, MD 20892 USA.
EM snorri_thorgeirsson@nih.gov
RI Gomez-Quiroz, Luis/L-8415-2013;
OI Andersen , Jesper B/0000-0003-1760-5244; RAGGI,
Chiara/0000-0003-2473-3535; Gomez-Quiroz, Luis
Enrique/0000-0002-5704-5985
FU Center for Cancer Research, NCI
FX This project was supported by the Intramural Research Program of the
Center for Cancer Research, NCI.
NR 53
TC 31
Z9 33
U1 0
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD OCT
PY 2011
VL 30
IS 40
BP 4175
EP 4184
DI 10.1038/onc.2011.126
PG 10
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 833ZK
UT WOS:000295924600004
PM 21499307
ER
PT J
AU Baladi, MG
Newman, AH
France, CP
AF Baladi, Michelle G.
Newman, Amy H.
France, Charles P.
TI Influence of body weight and type of chow on the sensitivity of rats to
the behavioral effects of the direct-acting dopamine-receptor agonist
quinpirole
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Direct-acting dopamine-receptor agonist; Quinpirole; Yawning; High-fat
chow; Body weight; Insulin; Dopamine; Rat; High fat
ID CHRONIC FOOD RESTRICTION; HIGH-FAT DIET; LOCOMOTOR SENSITIZATION;
DIFFERENTIALLY MODIFY; PARKINSONS-DISEASE; RHESUS-MONKEYS;
MESSENGER-RNA; D3 RECEPTOR; D-3; COCAINE
AB Rationale Amount and type of food can alter dopamine systems and sensitivity to drugs acting on those systems.
Objectives This study examined whether changes in body weight, food type, or both body weight and food type contribute to these effects.
Methods Rats had free or restricted access (increasing, decreasing, or maintaining body weight) to standard (5.7% fat) or high-fat (34.3%) chow.
Results In rats gaining weight with restricted or free access to high-fat chow, both limbs of the quinpirole yawning dose-response curve (0.0032-0.32 mg/kg) shifted leftward compared with rats eating standard chow. Restricting access to standard or high-fat chow (maintaining or decreasing body weight) decreased or eliminated quinpirole-induced yawning; within 1 week of resuming free feeding, sensitivity to quinpirole was restored, although the descending limb of the dose-response curve was shifted leftward in rats eating high-fat chow. These are not likely pharmacokinetic differences because quinpirole-induced hypothermia was not different among groups. PG01037 and L-741,626 antagonized the ascending and descending limbs of the quinpirole dose-response curve in rats eating high-fat chow, indicating D3 and D2 receptor mediation, respectively. Rats eating high-fat chow also developed insulin resistance.
Conclusions These results show that amount and type of chow alter sensitivity to a direct-acting dopamine-receptor agonist with the impact of each factor depending on whether body weight increases, decreases, or is maintained. These data demonstrate that feeding conditions, perhaps related to insulin and insulin sensitivity, profoundly impact the actions of drugs acting on dopamine systems.
C1 [Baladi, Michelle G.; France, Charles P.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA.
[France, Charles P.] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
[Newman, Amy H.] NIDA, Med Chem Sect AHN, Intramural Res Program, NIH, Baltimore, MD USA.
RP France, CP (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM france@uthscsa.edu
FU National Institute on Drug Abuse; Senior Scientist Award [KO5 DA17918]
FX AHN is supported by the National Institute on Drug Abuse, Intramural
Research Program. CPF is supported by a Senior Scientist Award (KO5
DA17918)
NR 50
TC 15
Z9 15
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 2011
VL 217
IS 4
BP 573
EP 585
DI 10.1007/s00213-011-2320-6
PG 13
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 833GI
UT WOS:000295870200011
PM 21544521
ER
PT J
AU Malayeri, AA
El Khouli, RH
Zaheer, A
Jacobs, MA
Corona-Villalobos, CP
Kamel, IR
Macura, KJ
AF Malayeri, Ashkan A.
El Khouli, Riham H.
Zaheer, Atif
Jacobs, Michael A.
Corona-Villalobos, Celia P.
Kamel, Ihab R.
Macura, Katarzyna J.
TI Principles and Applications of Diffusion-weighted Imaging in Cancer
Detection, Staging, and Treatment Follow-up
SO RADIOGRAPHICS
LA English
DT Article
ID PROSTATE-CANCER; HEPATOCELLULAR-CARCINOMA; BREAST-CANCER; NEOADJUVANT
CHEMOTHERAPY; DIAGNOSTIC-ACCURACY; COEFFICIENT VALUES; TREATMENT
RESPONSE; PERIPHERAL ZONES; TUMOR RESPONSE; LIVER FIBROSIS
AB Diffusion-weighted imaging relies on the detection of the random microscopic motion of free water molecules known as Brownian movement. With the development of new magnetic resonance (MR) imaging technologies and stronger diffusion gradients, recent applications of diffusion-weighted imaging in whole-body imaging have attracted considerable attention, especially in the field of oncology. Diffusion-weighted imaging is being established as a pivotal aspect of MR imaging in the evaluation of specific organs, including the breast, liver, kidney, and those in the pelvis. When used in conjunction with apparent diffusion coefficient mapping, diffusion-weighted imaging provides information about the functional environment of water in tissues, thereby augmenting the morphologic information provided by conventional MR imaging. Detected changes include shifts of water from extracellular to intracellular spaces, restriction of cellular membrane permeability, increased cellular density, and disruption of cellular membrane depolarization. These findings are commonly associated with malignancies; therefore, diffusion-weighted imaging has many applications in oncologic imaging and can aid in tumor detection and characterization and in the prediction and assessment of response to therapy. (C) RSNA, 2011 . radiographics.rsna.org
C1 [Malayeri, Ashkan A.; Zaheer, Atif; Jacobs, Michael A.; Corona-Villalobos, Celia P.; Kamel, Ihab R.; Macura, Katarzyna J.] Johns Hopkins Univ, Russell H Morgan Dept Radiol & Radiol Sci, Baltimore, MD 21287 USA.
[El Khouli, Riham H.] NIH, Dept Radiol, Bethesda, MD 20892 USA.
RP Malayeri, AA (reprint author), Johns Hopkins Univ, Russell H Morgan Dept Radiol & Radiol Sci, 600 N Wolfe St, Baltimore, MD 21287 USA.
EM amalayeri@jhmi.edu
RI Jacobs, Michael/G-2901-2010
FU Siemens Medical
FX I.R.K.: Related financial activities: patent with Siemens Medical. Other
financial activities: none. K.J.M.: Related financial activities: grant
from Siemens Medical. Other financial activities: consultant for ACR
ImageMetrix.
NR 51
TC 79
Z9 82
U1 3
U2 14
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0271-5333
J9 RADIOGRAPHICS
JI Radiographics
PD OCT
PY 2011
VL 31
IS 6
SI SI
BP 1773
EP 1791
DI 10.1148/rg.316115515
PG 19
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 834SU
UT WOS:000295985200020
PM 21997994
ER
PT J
AU Calado, RT
AF Calado, Rodrigo T.
TI Immunologic Aspects of Hypoplastic Myelodysplastic Syndrome
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA; BONE-MARROW FAILURE; SEVERE
APLASTIC-ANEMIA; NITRIC-OXIDE SYNTHASE; ANTITHYMOCYTE GLOBULIN;
CYCLOSPORINE-A; IMMUNOSUPPRESSIVE THERAPY; DYSKERATOSIS-CONGENITA;
REFRACTORY-ANEMIA; MUTATIONS
AB The pathophysiology of myelodysplastic syndromes (MDS) is multiple, complex, and poorly understood. In some cases of MDS, especially those in which the bone marrow is hypocellular, there is increasing experimental and clinical indication that an immune-mediated damage to hematopoietic precursors and changes in the hematopoiesis-supporting microenvironment contribute to disease development. Increased serum levels of type-1 cytokines, tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (INF-gamma), and oligoclonal expansion of cytotoxic T cells are observed in human MDS. In some cases, the immunologic attack to the marrow appears to be triggered by MDS-specific antigens, damaging the microenvironment and inducing cell apoptosis especially of normal progenitors. In murine models, dysregulation of osteoprogenitors leads to disrupted hematopoiesis of healthy hematopoietic progenitor and stem cells, eventually resulting in MDS and leukemia. In hypocellular MDS, marrow failure appears to be not only the result of ineffective erythropoiesis of abnormal clones, but also due to inhibition of normal progenitors. Immunosuppressive therapy with cyclosporine, anti-thymocyte globulin, or alemtuzumab may alleviate cytopenias and in some instances induce cytogenetic remission. However, not all patients respond to immunosuppression, and the identification of relevant biomarkers for an immune mechanism is necessary to identify those patients who may benefit from this treatment modality. Semin Oncol 38:667-672. Published by Elsevier Inc.
C1 [Calado, Rodrigo T.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Calado, RT (reprint author), 10 Ctr Dr,Bldg 10 CRC,Room 3E5140, Bethesda, MD 20892 USA.
EM calador@nhlbi.nih.gov
RI Calado, Rodrigo/G-2619-2011;
OI Calado, Rodrigo/0000-0002-7966-6029
FU NIH
FX This work was supported by the NIH Intramural Research Program.
NR 51
TC 20
Z9 23
U1 0
U2 7
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0093-7754
J9 SEMIN ONCOL
JI Semin. Oncol.
PD OCT
PY 2011
VL 38
IS 5
BP 667
EP 672
DI 10.1053/j.seminoncol.2011.04.006
PG 6
WC Oncology
SC Oncology
GA 833BT
UT WOS:000295857500009
PM 21943673
ER
PT J
AU Chason, RJ
Csokmay, J
Segars, JH
DeCherney, AH
Armant, DR
AF Chason, Rebecca J.
Csokmay, John
Segars, James H.
DeCherney, Alan H.
Armant, D. Randall
TI Environmental and epigenetic effects upon preimplantation embryo
metabolism and development
SO TRENDS IN ENDOCRINOLOGY AND METABOLISM
LA English
DT Review
ID ASSISTED REPRODUCTIVE TECHNOLOGY; X-CHROMOSOME INACTIVATION; EARLY MOUSE
EMBRYO; IN-VITRO; DNA METHYLATION; GENE-EXPRESSION; HISTONE
MODIFICATIONS; OXIDATIVE STRESS; IMPRINTED GENES; OXYGEN-TENSION
AB In vitro fertilization has provided a unique window into the metabolic processes that drive embryonic growth and development from a fertilized ovum to a competent blastocyst. Post-fertilization development is dependent upon a dramatic reshuffling of the parental genomes during meiosis, as well as epigenetic changes that provide a new and autonomous set of instructions to guide cellular differentiation both in the embryo and beyond. Although early literature focused simply on the substrates and culture conditions required for progress through embryonic development, more recent insights lead us to suggest that the surrounding environment can alter the epigenome, which can, in turn, impact upon embryonic metabolism and developmental competence.
C1 [Chason, Rebecca J.; Segars, James H.; DeCherney, Alan H.; Armant, D. Randall] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
[Csokmay, John] Walter Reed Army Med Ctr, Washington, DC 20307 USA.
[Armant, D. Randall] Wayne State Univ, Sch Med, CS Mott Ctr Human Growth & Dev, Detroit, MI 48201 USA.
[Armant, D. Randall] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Armant, D. Randall] Wayne State Univ, Sch Med, Dept Anat & Cell Biol, Detroit, MI 48201 USA.
RP Armant, DR (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
EM D.Armant@Wayne.edu
OI Armant, D. Randall/0000-0001-5904-9325
FU NIH [HD045966]; Eunice Kennedy Shriver National Institute of Child
Health and Human Development
FX This work was supported in part by the Intramural Research Program of
the NIH, the Eunice Kennedy Shriver National Institute of Child Health
and Human Development, and NIH grant HD045966 (to D.R.A.).
NR 108
TC 35
Z9 36
U1 2
U2 17
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1043-2760
J9 TRENDS ENDOCRIN MET
JI Trends Endocrinol. Metab.
PD OCT
PY 2011
VL 22
IS 10
BP 412
EP 420
DI 10.1016/j.tem.2011.05.005
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 835LI
UT WOS:000296037500004
PM 21741268
ER
PT J
AU Compton, P
AF Compton, P.
TI Acquisition of immunity against malaria: are we anywhere near
understanding it?
SO TROPICAL MEDICINE & INTERNATIONAL HEALTH
LA English
DT Meeting Abstract
C1 [Compton, P.] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1360-2276
J9 TROP MED INT HEALTH
JI Trop. Med. Int. Health
PD OCT
PY 2011
VL 16
SU 1
SI SI
BP 10
EP 10
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 828RC
UT WOS:000295519100010
ER
PT J
AU Doumbia, S
Lopera-Mesa, TM
Diakite, SAS
Konate, D
Traore, K
Doumbia, M
Tullo, G
Miura, K
Anderson, JM
Fay, MP
AF Doumbia, S.
Lopera-Mesa, T. M.
Diakite, S. A. S.
Konate, D.
Traore, K.
Doumbia, M.
Tullo, G.
Miura, K.
Anderson, J. M.
Fay, M. P.
TI The importance of hemoglobin level at enrollment on subsequent malaria
risk: results from a pediatric cohort in Mali, West Africa
SO TROPICAL MEDICINE & INTERNATIONAL HEALTH
LA English
DT Meeting Abstract
C1 [Doumbia, S.; Diakite, S. A. S.; Konate, D.; Traore, K.; Doumbia, M.] MRTC, Bamako, Mali.
[Lopera-Mesa, T. M.; Tullo, G.; Miura, K.; Anderson, J. M.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Fay, M. P.] NIAID, Biostat Res Branch, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1360-2276
J9 TROP MED INT HEALTH
JI Trop. Med. Int. Health
PD OCT
PY 2011
VL 16
SU 1
SI SI
BP 99
EP 99
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 828RC
UT WOS:000295519100279
ER
PT J
AU Pindolia, D
Wesolowski, A
Garcia, A
Eagle, N
Buckee, C
Smith, D
Tatem, A
AF Pindolia, D.
Wesolowski, A.
Garcia, A.
Eagle, N.
Buckee, C.
Smith, D.
Tatem, A.
TI Mapping communities in networks for malaria transmission and control in
Kenya
SO TROPICAL MEDICINE & INTERNATIONAL HEALTH
LA English
DT Meeting Abstract
C1 [Pindolia, D.; Garcia, A.; Tatem, A.] Univ Florida, Dept Geog, Gainesville, FL 32611 USA.
[Pindolia, D.; Garcia, A.; Smith, D.; Tatem, A.] Univ Florida, Emerging Pathogens Inst, Gainesville, FL USA.
[Pindolia, D.] Univ Oxford, Collaborat Programme, Malaria Publ Hlth & Epidemiol Grp, Ctr Geog Med,KEMRI Wellcome Trust, Nairobi, Kenya.
[Eagle, N.; Buckee, C.] Harvard Univ, Dept Epidemiol, Sch Publ Hlth, Cambridge, MA 02138 USA.
[Smith, D.] Ctr Dis Dynam Econ & policy, Washington, DC USA.
[Tatem, A.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RI Smith, David/L-8850-2013
OI Smith, David/0000-0003-4367-3849
NR 0
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1360-2276
J9 TROP MED INT HEALTH
JI Trop. Med. Int. Health
PD OCT
PY 2011
VL 16
SU 1
SI SI
BP 130
EP 130
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 828RC
UT WOS:000295519100371
ER
PT J
AU Kumar, R
Ansari, NA
Gautam, S
Nylen, S
Singh, OP
Sundar, S
Sacks, D
AF Kumar, R.
Ansari, N. A.
Gautam, S.
Nylen, S.
Singh, O. P.
Sundar, S.
Sacks, D.
TI IL-27 and IL-21 are associated with T cell IL-10 responses in human
visceral leishmaniasis
SO TROPICAL MEDICINE & INTERNATIONAL HEALTH
LA English
DT Meeting Abstract
C1 [Kumar, R.; Ansari, N. A.; Gautam, S.; Singh, O. P.; Sundar, S.] Banaras Hindu Univ, Varanasi 221005, Uttar Pradesh, India.
[Ansari, N. A.; Sacks, D.] NIAID, NIH, Bethesda, MD 20892 USA.
[Nylen, S.] Karolinska Inst, Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1360-2276
J9 TROP MED INT HEALTH
JI Trop. Med. Int. Health
PD OCT
PY 2011
VL 16
SU 1
SI SI
BP 188
EP 188
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 828RC
UT WOS:000295519100555
ER
PT J
AU Akhavan, AA
Yaghoobi-Ershadi, MR
Khamesipour, A
Mirhendi, H
Alimohammadian, MH
Rassi, Y
Bates, P
Kamhawi, S
Valenzuela, JG
Arandian, MH
Jafari, R
Abdoli, H
Shareghi, N
Ghanei, M
Jalali-Zand, N
AF Akhavan, A. A.
Yaghoobi-Ershadi, M. R.
Khamesipour, A.
Mirhendi, H.
Alimohammadian, M. H.
Rassi, Y.
Bates, P.
Kamhawi, S.
Valenzuela, J. G.
Arandian, M. H.
Jafari, R.
Abdoli, H.
Shareghi, N.
Ghanei, M.
Jalali-Zand, N.
TI Leishmania mixed infection in great gerbil populations of endemic areas
of zoonotic cutaneous leishmaniasis in central Iran
SO TROPICAL MEDICINE & INTERNATIONAL HEALTH
LA English
DT Meeting Abstract
C1 [Akhavan, A. A.; Yaghoobi-Ershadi, M. R.; Rassi, Y.] Univ Tehran Med Sci, Sch Publ Hlth, Dept Med Entomol & Vector Control, Tehran, Iran.
[Khamesipour, A.] Univ Tehran Med Sci, Ctr Res & Training Skin Dis & Leprosy, Tehran, Iran.
[Mirhendi, H.] Univ Tehran Med Sci, Sch Publ Hlth, Dept Med Parasitol & Mycol, Tehran, Iran.
[Alimohammadian, M. H.] Pasteur Inst Iran, Dept Immunol, Tehran, Iran.
[Bates, P.] Univ Lancaster, Sch Hlth & Med, Div Biomed & Life Sci, Lancaster, England.
[Kamhawi, S.; Valenzuela, J. G.; Jafari, R.; Abdoli, H.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
[Arandian, M. H.; Shareghi, N.] Univ Tehran Med Sci, Natl Inst Hlth Res, Esfahan Hlth Res Ctr, Tehran, Iran.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1360-2276
J9 TROP MED INT HEALTH
JI Trop. Med. Int. Health
PD OCT
PY 2011
VL 16
SU 1
SI SI
BP 212
EP 212
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 828RC
UT WOS:000295519100628
ER
PT J
AU Mishra, S
Undrovinas, NA
Maltsev, VA
Reznikov, V
Sabbah, HN
Undrovinas, A
AF Mishra, Sudhish
Undrovinas, Nidas A.
Maltsev, Victor A.
Reznikov, Vitaliy
Sabbah, Hani N.
Undrovinas, Albertas
TI Post-transcriptional silencing of SCN1B and SCN2B genes modulates late
sodium current in cardiac myocytes from normal dogs and dogs with
chronic heart failure
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE action potential; in silico simulation
ID RAT VENTRICULAR MYOCYTES; BETA-SUBUNITS; AUXILIARY SUBUNIT;
ACTION-POTENTIALS; CHANNEL BETA-4; FAILING HEART; CANINE MODEL;
CARDIOMYOCYTES; NA(V)1.5; CONTRACTION
AB Mishra S, Undrovinas NA, Maltsev VA, Reznikov V, Sabbah HN, Undrovinas A. Post-transcriptional silencing of SCN1B and SCN2B genes modulates late sodium current in cardiac myocytes from normal dogs and dogs with chronic heart failure. Am J Physiol Heart Circ Physiol 301: H1596-H1605, 2011. First published June 24, 2011; doi:10.1152/ajpheart.00948.2009.-The emerging paradigm for Na(+) current in heart failure (HF) is that its transient component (I(NaT)) responsible for the action potential (AP) upstroke is decreased, whereas the late component (I(NaL)) involved in AP plateau is augmented. Here we tested whether Na(v)beta(1)- and Na(v)beta(2)-subunits can modulate I(NaL) parameters in normal and failing ventricular cardiomyocytes (VCMs). Chronic HF was produced in nine dogs by multiple sequential coronary artery microembolizations, and six dogs served as a control. I(Na) and APs were measured by the whole cell and perforated patch-clamp in freshly isolated and cultured VCMs, respectively. I(NaL) was augmented with slower decay in HF VCMs compared with normal heart VCMs, and these properties remained unchanged within 5 days of culture. Posttranscriptional silencing SCN1B and SCN2B were achieved by virally delivered short interfering RNA (siRNA) specific to Na(v)beta(1)- and Na(v)beta(2). The delivery and efficiency of siRNA were evaluated by green fluorescent protein expression, by the real-time RT-PCR, and Western blots, respectively. Five days after infection, the levels of mRNA and protein for Na(v)beta(1) and Na(v)beta(2) were reduced by >80%, but mRNA and protein of Na(v)1.5, as well as I(NaT), remained unchanged in HF VCMs. Na(v)beta(1)-siRNA reduced I(NaL) density and accelerated I(NaL) two-exponential decay, whereas Na(v)beta(2)-siRNA produced an opposite effect in VCMs from both normal and failing hearts. Physiological importance of the discovered I(NaL) modulation to affect AP shape and duration was illustrated both experimentally and by numerical simulations of a VCM excitation-contraction coupling model. We conclude that in myocytes of normal and failing dog hearts Na(v)beta(1) and Na(v)beta(2) exhibit oppositely directed modulation of I(NaL).
C1 [Mishra, Sudhish; Undrovinas, Nidas A.; Reznikov, Vitaliy; Sabbah, Hani N.; Undrovinas, Albertas] Henry Ford Hosp, Dept Internal Med, Detroit, MI 48202 USA.
[Maltsev, Victor A.] NIA, Intramural Res Program, Baltimore, MD 21224 USA.
RP Undrovinas, A (reprint author), Henry Ford Hosp, Dept Internal Med, Cardiovasc Res Educ & Res Bldg,Rm 4015,2799 W Gra, Detroit, MI 48202 USA.
EM aundrov1@hfhs.org
FU National Heart, Lung, and Blood Institute [HL-53819, HL-074238];
American Heart Association [0350472Z]; National Institute on Aging
FX This study was supported by National Heart, Lung, and Blood Institute
Grants HL-53819 and HL-074238, by a grant-in-aid from the American Heart
Association (0350472Z; to A. Undrovinas), and, in part, by the
Intramural Research Program of the National Institute on Aging (to V. A.
Maltsev; the numerical modeling part).
NR 50
TC 17
Z9 17
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 OCT
PY 2011
VL 301
IS 4
BP H1596
EP H1605
DI 10.1152/ajpheart.00948.2009
PG 10
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 826NE
UT WOS:000295360100042
PM 21705762
ER
PT J
AU Zhao, H
Sun, JH
Deschamps, AM
Kim, G
Liu, CY
Murphy, E
Levine, RL
AF Zhao, Hang
Sun, Junhui
Deschamps, Anne M.
Kim, Geumsoo
Liu, Chengyu
Murphy, Elizabeth
Levine, Rodney L.
TI Myristoylated methionine sulfoxide reductase A protects the heart from
ischemia-reperfusion injury
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE myristoylation; oxidative stress; reactive oxygen species
ID OXIDATIVE STRESS; HYDROGEN-PEROXIDE; CARDIAC MYOCYTES; S-NITROSYLATION;
A MSRA; MITOCHONDRIAL; PROTEINS; PEPTIDE; CELLS; LOCALIZATION
AB Zhao H, Sun J, Deschamps AM, Kim G, Liu C, Murphy E, Levine RL. Myristoylated methionine sulfoxide reductase A protects the heart from ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol 301: H1513-H1518, 2011. First published August 12, 2011; doi:10.1152/ajpheart.00441.2011.-Methionine sulfoxide reductase A (MsrA) catalytically scavenges reactive oxygen species and also repairs oxidized methionines in proteins. Increasing MsrA protects cells and organs from a variety of oxidative stresses while decreasing MsrA enhances damage, but the mechanisms of action have not been elucidated. A single gene encodes MsrA of which similar to 25% is targeted to the mitochondria, a major site of reactive oxygen species production. The other similar to 75% is targeted to the cytosol and is posttranslationally modified by myristoylation. To determine the relative importance of MsrA in each compartment in protecting against ischemia-reperfusion damage, we created a series of transgenic mice overexpressing MsrA targeted to the mitochondria or the cytosol. We used a Langendorff model of ischemia-reperfusion and assayed both the rate pressure product and infarct size following ischemia and reperfusion as measures of injury. While the mitochondrially targeted MsrA was expected to be protective, it was not. Notably, the cytosolic form was protective but only if myristoylated. The nonmyristoylated, cytosolic form offered no protection against injury. We conclude that cytosolic MsrA protects the heart from ischemia-reperfusion damage. The requirement for myristoylation suggests that MsrA must interact with a hydrophobic domain to provide protection.
C1 [Zhao, Hang; Kim, Geumsoo; Levine, Rodney L.] NHLBI, Biochem Lab, NIH, Bethesda, MD 20892 USA.
[Sun, Junhui; Deschamps, Anne M.; Murphy, Elizabeth] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Liu, Chengyu] NHLBI, Transgen Mouse Facil, NIH, Bethesda, MD 20892 USA.
RP Levine, RL (reprint author), NHLBI, Biochem Lab, NIH, Bldg 50,Rm 2351,50 South Dr,MSC 8012, Bethesda, MD 20892 USA.
EM rlevine@nih.gov
RI Zhao, Hang/A-2558-2012; Sun, Junhui/C-3499-2011; Levine,
Rodney/D-9885-2011;
OI Deschamps, Anne/0000-0001-7415-1408
FU National Heart, Lung, and Blood Institute
FX This work was supported by the Intramural Research Program of the
National Heart, Lung, and Blood Institute.
NR 48
TC 20
Z9 20
U1 0
U2 3
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 OCT
PY 2011
VL 301
IS 4
BP H1513
EP H1518
DI 10.1152/ajpheart.00441.2011
PG 6
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 826NE
UT WOS:000295360100033
PM 21841012
ER
PT J
AU Mason, C
Foster-Schubert, KE
Imayama, I
Kong, A
Xiao, LR
Bain, C
Campbell, KL
Wang, CY
Duggan, CR
Ulrich, CM
Alfano, CM
Blackburn, GL
McTiernan, A
AF Mason, Caitlin
Foster-Schubert, Karen E.
Imayama, Ikuyo
Kong, Angela
Xiao, Liren
Bain, Carolyn
Campbell, Kristin L.
Wang, Ching-Yun
Duggan, Catherine R.
Ulrich, Cornelia M.
Alfano, Catherine M.
Blackburn, George L.
McTiernan, Anne
TI Dietary Weight Loss and Exercise Effects on Insulin Resistance in
Postmenopausal Women
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID DIABETES PREVENTION PROGRAM; IMPAIRED GLUCOSE-TOLERANCE; LIFE-STYLE
MODIFICATION; RANDOMIZED CONTROLLED-TRIAL; CARDIOVASCULAR-DISEASE;
PHYSICAL-ACTIVITIES; FASTING GLUCOSE; OLDER-ADULTS; FOLLOW-UP; OBESITY
AB Background: Comprehensive lifestyle interventions are effective in preventing diabetes and restoring glucose regulation; however, the key stimulus for change has not been identified and effects in older individuals are not established. The aim of the study was to investigate the independent and combined effects of dietary weight loss and exercise on insulin sensitivity and restoration of normal fasting glucose in middle-aged and older women.
Design: Four-arm RCT, conducted between 2005 and 2009 and data analyzed in 2010.
Setting/participants: 439 inactive, overweight/obese postmenopausal women.
Interventions: Women were assigned to: dietary weight loss (n=118); exercise (n=117); exercise + diet (n=117); or control (n=87). The diet intervention was a group-based reduced-calorie program with a 10% weight-loss goal. The exercise intervention was 45 min/day, 5 days/week of moderate-to-vigorous intensity aerobic activity.
Main outcome measures: 12-month change in serum insulin, C-peptide, fasting glucose, and whole body insulin resistance (HOMA-IR).
Results: A significant improvement in HOMA-IR was detected in the diet (-24%, p<0.001) and exercise + diet (-26%, p<0.001) groups but not in the exercise (-9%, p=0.22) group compared with controls (-2%); these effects were similar in middle-aged (50-60 years) and older women (aged 60-75 years). Among those with impaired fasting glucose (5.6-6.9 mmol/L) at baseline (n=143; 33%), the odds (95% CI) of regressing to normal fasting glucose after adjusting for weight loss and baseline levels were 2.5 (0.8, 8.4); 2.76 (0.8, 10.0); and 3.1 (1.0, 9.9) in the diet, exercise + diet, and exercise group, respectively, compared with controls.
Conclusions: Dietary weight loss, with or without exercise, significantly improved insulin resistance. Older women derived as much benefit as did the younger postmenopausal women.
C1 [McTiernan, Anne] Univ Washington, Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Prevent Ctr, Seattle, WA 98109 USA.
[Foster-Schubert, Karen E.; Wang, Ching-Yun; McTiernan, Anne] Univ Washington, Div Metab Endocrinol & Nutr, Sch Med, Seattle, WA 98109 USA.
[Alfano, Catherine M.] NCI, Off Canc Survivorship, Bethesda, MD USA.
[Blackburn, George L.] Harvard Univ, Sch Med, Div Nutr, Beth Israel Deaconess Med Ctr, Boston, MA USA.
[Campbell, Kristin L.] Univ British Columbia, Dept Physiotherapy, Vancouver, BC V5Z 1M9, Canada.
RP McTiernan, A (reprint author), Univ Washington, Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Prevent Ctr, M4-B874,POB 19024, Seattle, WA 98109 USA.
EM amctiern@fhcrc.org
RI Duggan, Catherine/F-9414-2015
OI Duggan, Catherine/0000-0001-7369-4021
FU National Cancer Institute at the NIH [R01 CA102504, U54-CA116847,
5KL2RR025015-03, R25 CA94880, 2R25CA057699-16]; Canadian Institutes of
Health Research
FX This work was supported by the National Cancer Institute at the NIH
(grant number: R01 CA102504, U54-CA116847, and 5KL2RR025015-03 to KFS,
R25 CA94880 and 2R25CA057699-16 to AK) and the Canadian Institutes of
Health Research (Fellowship to KLC and CM). None of the funding agencies
were involved in the trial design or conduct. While working on the
trial, CMA was employed at the Ohio State University, and located to NCI
following completion of her effort on the NEW trial.
NR 39
TC 44
Z9 44
U1 1
U2 20
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD OCT
PY 2011
VL 41
IS 4
BP 366
EP 375
DI 10.1016/j.amepre.2011.06.042
PG 10
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 832FV
UT WOS:000295789300004
PM 21961463
ER
PT J
AU Stange, KC
AF Stange, Kurt C.
TI Refocusing Knowledge Generation, Application, and Education Raising Our
Gaze to Promote Health Across Boundaries
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Editorial Material
ID PRIMARY-CARE RESEARCH; PARTICIPATORY RESEARCH; TRANSDISCIPLINARY
RESEARCH; COMPLEXITY SCIENCE; POPULATION HEALTH; RESEARCH NETWORKS; TEAM
SCIENCE; MULTIMETHOD RESEARCH; FAMILY-PRACTICE; MIXED METHODS
C1 [Stange, Kurt C.] Case Western Reserve Univ, Dept Family Med, Cleveland, OH 44106 USA.
[Stange, Kurt C.] Case Western Reserve Univ, Dept Epidemiol & Biostat, Cleveland, OH 44106 USA.
[Stange, Kurt C.] Case Western Reserve Univ, Dept Sociol, Cleveland, OH 44106 USA.
[Stange, Kurt C.] Cleveland Clin & Translat Sci Collaborat, Case Comprehens Canc Ctr, Cleveland, OH USA.
[Stange, Kurt C.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Stange, KC (reprint author), Case Western Reserve Univ, Dept Family Med, 10900 Euclid Ave, Cleveland, OH 44106 USA.
EM kcs@case.edu
FU NCRR NIH HHS [UL1 RR024989]; ODCDC CDC HHS [U36 CD319276, 5U36CD319276]
NR 99
TC 8
Z9 8
U1 0
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD OCT
PY 2011
VL 41
IS 4
SU 3
BP S164
EP S169
DI 10.1016/j.amepre.2011.06.022
PG 6
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 832SK
UT WOS:000295827300006
PM 21961659
ER
PT J
AU Zhang, W
Yang, HC
Wang, Q
Yang, ZJ
Chen, H
Wang, SM
Pan, ZM
Tang, BJ
Li, QQ
Li, L
AF Zhang, Wei
Yang, Hsin-Chih
Wang, Qi
Yang, Zhi-Jun
Chen, Hong
Wang, Su-Mei
Pan, Zhong-Mian
Tang, Bu-Jian
Li, Qingdi Quentin
Li, Li
TI Clinical Value of Combined Detection of Serum Matrix
Metalloproteinase-9, Heparanase, and Cathepsin for Determining Ovarian
Cancer Invasion and Metastasis
SO ANTICANCER RESEARCH
LA English
DT Article
DE Ovarian cancer; diagnosis; biomarkers; enzyme-linked immunosorbent
assay; cathepsin; matrix metalloproteinase-9; heparanase
ID MATRIX METALLOPROTEINASES; EXTRACELLULAR-MATRIX; BREAST-CANCER;
PROGNOSTIC-SIGNIFICANCE; CERVICAL-CANCER; CYSTATIN-C; EXPRESSION;
TUMORS; INHIBITORS; CARCINOMA
AB Aim: This study evaluated the clinical value of the combined detection of serum cathepsin L (CL), heparanase (Hpa), and matrix metalloproteinase-9 (MMP-9) for determining the degree of ovarian cancer invasion and metastasis before surgery. Patients and Methods: Enzyme-linked immunosorbent assays were used to measure the serum content of CL, Hpa, and MMP-9 in 217 patients with untreated ovarian cancer before surgery, 100 patients with benign ovarian tumors, and 101 healthy women as controls. In addition, the degrees of invasion and metastasis were assessed by the 'gold standard' of clinicopathological diagnosis. The associations of the preoperative serum CL, Hpa, and MMP-9 levels with the clinicopathological factors and metastatic status were analyzed. Receiver operating characteristic (ROC) curve analysis was used to evaluate the usefulness of these markers for determining the degree of ovarian cancer invasion before surgery. Results: The serum CL, Hpa, and MMP-9 levels were significantly higher (p=0.001) in patients with malignant ovarian cancer compared with patients with benign ovarian tumors and healthy controls. The serum CL level was significantly higher in patients with epithelial ovarian carcinoma compared with non-epithelial ovarian carcinoma (p=0.048), whereas the serum levels of Hpa (p=0.109) and MMP-9 (p=0.544) did not differ significantly between these two groups. The serum CL, Hpa, and MMP-9 levels correlated with the degree of differentiation and the FIGO staging (p>0.05). The serum CL (p=0.030) and MMP-9 (p=0.010) levels were significantly associated with peritoneal metastasis, and the serum Hpa level (p=0.042) was associated with distant metastasis. A ROC curve analysis revealed sensitivity of 60.9%, 69.6%, and 72.2%, and specificity of 57.4%, 67.2%, and 68.9% for the preoperative serum. levels of CL, Hpa, and MMP-9, respectively, as tumor markers for the degree of extra-pelvic metastasis. Conclusion: Elevated serum CL, Hpa, and MMP-9 levels are correlated with malignant invasion and progression in ovarian cancer. The combined detection of serum CL, Hpa, and MMP-9 may be useful for determining the extent of ovarian cancer metastasis before surgery.
C1 [Li, Qingdi Quentin] NIAID, NIH, Bethesda, MD 20892 USA.
[Zhang, Wei; Yang, Hsin-Chih; Wang, Qi; Yang, Zhi-Jun; Chen, Hong; Wang, Su-Mei; Pan, Zhong-Mian; Tang, Bu-Jian; Li, Li] Guangxi Med Univ, Canc Hosp, Dept Gynecol Oncol, Nanning 530021, Guangxi, Peoples R China.
RP Li, QQ (reprint author), NIAID, NIH, Bldg 10,Room 11N234, Bethesda, MD 20892 USA.
EM liquenti@mail.nih.gov; lili_temp@hotmail.com
FU Provincial Research Project Funding of Guangxi, China [GSR 9817101]
FX This study was supported by a grant from the Provincial Research Project
Funding of Guangxi, China (No. GSR 9817101).
NR 34
TC 25
Z9 29
U1 0
U2 3
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 OCT
PY 2011
VL 31
IS 10
BP 3423
EP 3428
PG 6
WC Oncology
SC Oncology
GA 830PA
UT WOS:000295667700041
PM 21965756
ER
PT J
AU Liang, HS
Zhong, YH
Luo, ZJ
Huang, Y
Lin, HD
Zhan, S
Xie, KQ
Li, QQ
AF Liang, Huasheng
Zhong, Yuhua
Luo, Zuojie
Huang, Yu
Lin, Huade
Zhan, Song
Xie, Kaiqing
Li, Qingdi Quentin
TI Diagnostic Value of 16 Cellular Tumor Markers for Metastatic Thyroid
Cancer: An Immunohistochemical Study
SO ANTICANCER RESEARCH
LA English
DT Article
DE Thyroid cancer; biomarker; diagnosis; sensitivity; specificity;
metastasis; immunohistochemistry
ID E-CADHERIN EXPRESSION; FOLLICULAR CARCINOMA; GROWTH-FACTOR; PAPILLARY;
CXCR4; METALLOPROTEINASE-9; ANGIOGENESIS; INDICATORS; INHIBITORS;
FEATURES
AB Background: The prognosis for thyroid cancer differs between metastatic and non-metastatic cases. To identify biomarkers useful for thyroid cancer diagnosis and to establish a marker panel for the early detection of metastatic thyroid carcinoma, this study compared histomorphological features and biomarker expression profiles in thyroid carcinomas according to pathological diagnoses. Patients and Methods: Thyroid carcinoma samples were obtained from 113 consecutive patients who underwent resection at multiple centers between 2001 and 2008. These cases included 63 metastatic thyroid tumors (34 papillary carcinomas, 20 follicular carcinomas, 9 undifferentiated carcinomas) and 50 non-metastatic thyroid tumors (36 papillary carcinomas, 14 follicular carcinomas). Tissue microarrays constructed using the 113 samples were analyzed by immunohistochemistry for the expression of 16 protein markers: MMP9, VEGF-C, E-cadherin, MMP2, PPAR gamma, PCNA, CXCR4, PTEN, C-myc, PTTG, HBME-1, p16, p53, FH1T, bFGF and hTERT. The clinicopathological variables with diagnostic significance were determined by multivariate analysis, and the predictive values of the identified biomarkers for metastasis in thyroid carcinoma were determined by receiver operating characteristic (ROC) curve analysis. Results: The expression of six proteins, VEGF-C, MMP2, CXCR4, PTTG, HBME-1 and bFGF, was up-regulated in metastatic compared to non-metastatic thyroid carcinoma. Multiple factor binary ordinal logistic regression analysis showed that MMP2, PTTG, VEGF-C, CXCR4 and bFGF were independent factors associated with the metastatic status of thyroid carcinoma. ROC curve analysis of these five proteins revealed that VEGF-C and bFGF were the most useful protein markers for the diagnosis of metastatic thyroid cancer. Conclusion: MMP2, PTTG, VEGF-C, CXCR4 and bFGF are potential cellular tumor markers for identifying thyroid cancer with greater risk for metastasis and the novel combination of VEGF-C and bFGF as biomarkers may improve the accuracy of early detection and the differential diagnosis between metastatic and non-metastatic thyroid carcinoma.
C1 [Liang, Huasheng; Zhong, Yuhua] Guangxi Med Univ, Affiliated Hosp 9, Beihai Inst Endocrine & Metab Dis, Beihai 536000, Peoples R China.
[Zhan, Song] Guangxi Med Univ, Affiliated Hosp 9, Dept Pathol, Beihai 536000, Peoples R China.
[Luo, Zuojie] Guangxi Med Univ, Hosp 1, Dept Endocrinol, Nanning 530021, Peoples R China.
[Huang, Yu] Guangxi Prov Hosp, Dept Hepatobiliary & Endocrine Surg, Nanning 530021, Peoples R China.
[Lin, Huade] Pingnan Peoples Hosp, Dept Hepatobiliary & Endocrine Surg, Pingnan 537300, Peoples R China.
[Xie, Kaiqing] So Med Univ, Nanfang Hosp, Guangzhou 510515, Guangdong, Peoples R China.
[Li, Qingdi Quentin] NIH, Bethesda, MD 20892 USA.
RP Zhong, YH (reprint author), Guangxi Med Univ, Affiliated Hosp 9, Beihai Inst Endocrine & Metab Dis, Beihai 536000, Peoples R China.
EM flowchaos@yahoo.com.cn; zhongyh111@163.com
FU Science and Technology Commission Foundation of Guangxi Province
[0339080]; Guangxi Provincial Science Foundation for Young Scientists
[0728108]
FX We are grateful to Xiujiu Liang for her technical assistance and to Su
Xuan for helping with the manuscript preparation. This study was
supported by grants from the Applied Basic Research Programs of Science
and Technology Commission Foundation of Guangxi Province (No. 0339080)
and Guangxi Provincial Science Foundation for Young Scientists (No.
0728108).
NR 24
TC 13
Z9 13
U1 0
U2 12
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 OCT
PY 2011
VL 31
IS 10
BP 3433
EP 3440
PG 8
WC Oncology
SC Oncology
GA 830PA
UT WOS:000295667700043
PM 21965758
ER
PT J
AU Iqbal, M
Naeem, MA
Riazuddin, SA
Ali, S
Farooq, T
Qazi, ZA
Khan, SN
Husnain, T
Riazuddin, S
Sieving, PA
Hejtmancik, JF
Riazuddin, S
AF Iqbal, Muhammad
Naeem, Muhammad Asif
Riazuddin, S. Amer
Ali, Shahbaz
Farooq, Tahir
Qazi, Zaheeruddin A.
Khan, Shaheen N.
Husnain, Tayyab
Riazuddin, Saima
Sieving, Paul A.
Hejtmancik, J. Fielding
Riazuddin, Sheikh
TI Association of Pathogenic Mutations in TULP1 With Retinitis Pigmentosa
in Consanguineous Pakistani Families
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Article
ID TUBBY-LIKE PROTEIN-1; GENE FAMILY; MEMBERS
AB Objective: To identify pathogenic mutations responsible for autosomal recessive retinitis pigmentosa in 5 consanguineous Pakistani families.
Methods: Affected individuals in the families underwent a detailed ophthalmological examination that consisted of fundus photography and electroretinography. Blood samples were collected from all participating family members, and genomic DNA was extracted. A genome-wide linkage scan was performed, followed by exclusion analyses among our cohort of nuclear consanguineous families with microsatellite markers spanning the TULP1 locus on chromosome 6p. Two-point logarithm of odds scores were calculated, and all coding exons of TULP1 were sequenced bidirectionally.
Results: The results of ophthalmological examinations among affected individuals in these 5 families were suggestive of retinitis pigmentosa. The genome-wide linkage scan localized the disease interval to chromosome 6p, harboring TULP1 in 1 of 5 families, and sequential analyses identified a single base pair substitution in TULP1 that results in threonine to alanine substitution (p.T380A). Subsequently, we investigated our entire cohort of families with autosomal recessive retinitis pigmentosa and identified 4 additional families with linkage to chromosome 6p, all of them harboring a single base pair substitution in TULP1 that results in lysine to arginine substitution (p.K489R). Results of single-nucleotide polymorphism haplotype analyses were suggestive of a common founder in these 4 families.
Conclusion: Pathogenic mutations in TULP1 are responsible for the autosomal recessive retinitis pigmentosa phenotype in these consanguineous Pakistani families, with a single ancestral mutation in TULP1 causing the disease phenotype in 4 of 5 families.
Clinical Relevance: Clinical and molecular characterization of pathogenic mutations in TULP1 will increase our understanding of retinitis pigmentosa at a molecular level. Arch Ophthalmol. 2011;129(10):1351-1357
C1 [Iqbal, Muhammad; Riazuddin, S. Amer; Ali, Shahbaz; Khan, Shaheen N.; Husnain, Tayyab; Riazuddin, Saima; Riazuddin, Sheikh] Univ Punjab, Natl Ctr Excellence Mol Biol, Lahore 53700, Pakistan.
[Riazuddin, Sheikh] Univ Hlth Sci, Allama Iqbal Med Coll, Lahore, Pakistan.
[Riazuddin, S. Amer] Johns Hopkins Univ, Sch Med, Wilmer Eye Inst Johns Hopkins, Baltimore, MD USA.
[Sieving, Paul A.; Hejtmancik, J. Fielding] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD USA.
[Riazuddin, Saima] Cincinnati Childrens Hosp Res Fdn, Div Pediat Otolaryngol Head & Neck Surg, Cincinnati, OH USA.
[Riazuddin, Saima] Cincinnati Childrens Hosp Res Fdn, Div Ophthalmol, Cincinnati, OH USA.
[Farooq, Tahir; Qazi, Zaheeruddin A.] Layton Rahmatulla Benevolent Trust Hosp, Lahore, Pakistan.
RP Riazuddin, S (reprint author), Univ Punjab, Natl Ctr Excellence Mol Biol, 87 W Canal Bank Rd, Lahore 53700, Pakistan.
EM riaz@aimrc.org; riaz@aimrc.org
RI Nasim Khan, Shaheen/F-2135-2015; Husnain, Tayyab/G-3805-2015
FU Higher Education Commission; Ministry of Science and Technology,
Islamabad, Pakistan
FX This study was supported in part by the Higher Education Commission and
the Ministry of Science and Technology, Islamabad, Pakistan.
NR 18
TC 6
Z9 6
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD OCT
PY 2011
VL 129
IS 10
BP 1351
EP 1357
PG 7
WC Ophthalmology
SC Ophthalmology
GA 830ZB
UT WOS:000295697300013
PM 21987678
ER
PT J
AU Tsai, CJ
Nussinov, R
AF Tsai, Chung-Jung
Nussinov, Ruth
TI Gene-specific transcription activation via long-range allosteric
shape-shifting
SO BIOCHEMICAL JOURNAL
LA English
DT Review
DE allosteric pathway; allosteric propagation; allostery; enhancer;
mediator; transcription initiation; transcription regulation;
transcription start site
ID RNA-POLYMERASE-II; MEDIATOR SUBUNIT MED1/TRAP220; TUMOR-SUPPRESSOR P53;
IN-VIVO; GLUCOCORTICOID-RECEPTOR; YEAST MEDIATOR;
FUNCTIONAL-ORGANIZATION; PREINITIATION COMPLEX; STRUCTURAL DISORDER;
ENERGY LANDSCAPES
AB How is specificity transmitted over long distances at the molecular level? REs (regulatory elements) are often far from transcription start sites. In the present review we discuss possible mechanisms to explain how information from specific REs is conveyed to the basal transcription machinery through TFs (transcription factors) and the Mediator complex. We hypothesize that this occurs through allosteric pathways: binding of a TF to a RE results in changes in the AD (activation domain) of the TF, which binds to Mediator and alters the distribution of the Mediator conformations, thereby affecting transcription initiation/activation. We argue that Mediator is formed by highly disordered proteins with large densely packed interfaces that make efficient long-range signal propagation possible. We suggest two possible general mechanisms for Mediator action: one in which Mediator influences PIC (pre-initiation complex) assembly and transcription initiation, and another in which Mediator exerts its effect on the already assembled but stalled transcription complex. We summarize (i) relevant information from the literature about Mediator composition, organization and structure; (ii) Mediator interaction partners and their effect on Mediator conformation, function and correlation to the RNA Pol II (polymerase II) CTD (C-terminal domain) phosphorylation; and (iii) propose that different allosteric signal propagation pathways in Mediator relate to PIC assembly and polymerase activation of the stalled transcription complex. The emerging picture provides for the first time a mechanistic view of allosteric signalling from the RE sequence to transcription activation, and an insight into how gene specificity and signal transmission can take place in transcription initiation.
C1 [Tsai, Chung-Jung; Nussinov, Ruth] NCI, Basic Sci Program, SAIC Frederick, Ctr Canc Res,Nanobiol Program, Frederick, MD 21702 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Inst Mol Med, Sackler Sch Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel.
RP Nussinov, R (reprint author), NCI, Basic Sci Program, SAIC Frederick, Ctr Canc Res,Nanobiol Program, Frederick, MD 21702 USA.
EM ruthnu@helix.nih.gov
FU National Cancer Institute [HHSN261200800001E]; National Cancer Institute
Center for Cancer Research
FX The work of the authors has been funded in whole or in part by the
National Cancer Institute under contract number HHSN261200800001E. This
research was supported (in part) by the Intramural Research Program of
the National Cancer Institute Center for Cancer Research.
NR 126
TC 22
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U1 0
U2 12
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD OCT 1
PY 2011
VL 439
BP 15
EP 25
DI 10.1042/BJ20110972
PN 1
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 831YN
UT WOS:000295767100002
PM 21916844
ER
PT J
AU Neddens, J
Fish, KN
Tricoire, L
Vullhorst, D
Shamir, A
Chung, W
Lewis, DA
McBain, CJ
Buonanno, A
AF Neddens, Joerg
Fish, Kenneth N.
Tricoire, Ludovic
Vullhorst, Detlef
Shamir, Alon
Chung, Wonjae
Lewis, David A.
McBain, Chris J.
Buonanno, Andres
TI Conserved Interneuron-Specific ErbB4 Expression in Frontal Cortex of
Rodents, Monkeys, and Humans: Implications for Schizophrenia
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Chandelier cell; gamma-aminobutyric acid (GABA); human; inhibition;
neuregulin; parvalbumin; primate; schizophrenia
ID PARVALBUMIN-POSITIVE INTERNEURONS; LONG-TERM POTENTIATION;
CENTRAL-NERVOUS-SYSTEM; CORTICAL GABA NEURONS; TYROSINE KINASE; NEURAL
DEVELOPMENT; PREFRONTAL CORTEX; KNOCKOUT MICE; NEUREGULIN-1; RECEPTORS
AB Background: Neuregulin-1 and ErbB4 are genetically associated with schizophrenia, and detailed knowledge of the cellular and subcellular localization of ErbB4 is important for understanding how neuregulin-1 regulates neuronal network activity and behavior. Expression of ErbB4 is restricted to interneurons in the rodent hippocampus and cortex. However, controversy remains about the cellular expression pattern in primate brain and its subcellular distribution in postsynaptic somatodendritic locations versus presynaptic terminals.
Methods: ErbB4 expression was analyzed in pyramidal cells and interneurons in the frontal cortex of five species: C57BL6 mice (n = 3), ErbB4-/- mice (n = 2), Sprague-Dawley rats (n = 3), two macaque species (n = 3 + 2), and humans (normal control subjects, n = 2). We investigated 1) messenger RNA in mice, macaques, and humans; 2) protein expression in all species using highly specific monoclonal antibodies; and 3) specificity tests of several ErbB4 antibodies on brain samples (mouse, macaque, human).
Results: ErbB4 RNA is restricted to interneurons in the frontal cortex of mice. ErbB4 protein is undetectable in pyramidal cells of rodents, macaques, and human frontal cortex, whereas most interneurons positive for parvalbumin, calretinin, or cholecystokinin, but only a minority of calbindin-positive cells, co-express ErbB4 in macaques. Importantly, no presynaptic ErbB4 expression was detected in any species.
Conclusions: The interneuron-selective somatodendritic expression of ErbB4 is consistent with a primary role of neuregulin-ErbB4 signaling in the postsynaptic modulation of gamma-aminobutyric acidergic function in rodents and primates. Our data validate the use of rodents to analyze effects of abnormal ErbB4 function as a means to model endophenotypes of psychiatric disorders.
C1 [Neddens, Joerg; Vullhorst, Detlef; Shamir, Alon; Buonanno, Andres] NICHHD, Mol Neurobiol Sect, NIH, Bethesda, MD 20892 USA.
[Tricoire, Ludovic; McBain, Chris J.] NICHHD, Program Dev Neurobiol, NIH, Bethesda, MD 20892 USA.
[Fish, Kenneth N.; Chung, Wonjae; Lewis, David A.] Univ Pittsburgh, Dept Psychiat, Translat Neurosci Program, Pittsburgh, PA USA.
[Lewis, David A.] Univ Pittsburgh, Dept Neurosci, Pittsburgh, PA USA.
RP Buonanno, A (reprint author), NICHHD, Mol Neurobiol Sect, NIH, 35 Lincoln Dr, Bethesda, MD 20892 USA.
EM buonanno@mail.nih.gov
RI Lewis, David/G-4053-2014
OI Lewis, David/0000-0002-3225-6778
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institutes of Health [MH085108, MH051234]
FX This research was supported by the Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health (AB, CJM), and National
Institutes of Health Grants MH085108 (KNF) and MH051234 (DAL). JN is
currently affiliated with the Department of Histology, JSW Life Sciences
GmbH, Graz-Grambach, Austria. LT is currently affiliated with the
Laboratoire de Neurobiologie des processus adaptatifs, Universite Pierre
et Marie Curie, Paris, France.
NR 48
TC 39
Z9 40
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
EI 1873-2402
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD OCT 1
PY 2011
VL 70
IS 7
BP 636
EP 645
DI 10.1016/j.biopsych.2011.04.016
PG 10
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 829PI
UT WOS:000295595800007
PM 21664604
ER
PT J
AU Sabichi, AL
Lee, JJ
Grossman, HB
Liu, SY
Richmond, E
Czerniak, BA
De la Cerda, J
Eagle, C
Viner, JL
Palmer, JL
Lerner, SP
AF Sabichi, Anita L.
Lee, J. Jack
Grossman, H. Barton
Liu, Suyu
Richmond, Ellen
Czerniak, Bogdan A.
De la Cerda, Jorge
Eagle, Craig
Viner, Jaye L.
Palmer, J. Lynn
Lerner, Seth P.
TI A Randomized Controlled Trial of Celecoxib to Prevent Recurrence of
Nonmuscle-Invasive Bladder Cancer
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID TRANSITIONAL-CELL CARCINOMA; BACILLUS-CALMETTE-GUERIN; NONSTEROIDAL
ANTIINFLAMMATORY DRUGS; URINARY-BLADDER; CLINICAL-TRIALS; IN-SITU;
CARDIOVASCULAR RISK; ADENOMA PREVENTION; COLORECTAL-CANCER; COX-2
INHIBITORS
AB Significant morbidity and expense result from frequent recurrences of nonmuscle-invasive bladder cancer (NMIBC) after standard treatment, and carcinoma in situ (Tis) is a poor prognostic factor. Predicated on observational and preclinical data strongly supporting cyclooxygenase-2 (COX-2) in the pathogenesis, and the activity of COX-2 inhibitors, in bladder cancer, we conducted a randomized, double-blind, placebo-controlled trial to determine whether celecoxib could reduce the time-to-recurrence (TTR) in NMIBC patients at high risk for recurrence. A total of 146 patients were randomized to celecoxib (200 mg) or placebo orally twice daily for at least 12 months. The average treatment duration was 1.25 years. Primary intent-to-treat analysis revealed celecoxib did not statistically significantly prolong TTR compared with placebo (P 0.17, log rank) with a median follow-up of 2.49 years. The recurrence-free rate at 12 months with celecoxib was 88% (95% CI: 0.81-0.96) versus 78% (95% CI: 0.69-0.89) with placebo. After controlling for covariates with Cox regression analysis, recurrence rates did not differ between the two study arms (HR 0.69; 95% CI: 0.37-1.29). However, celecoxib had a marginally significant effect on reducing meta-chronous recurrences (vs. placebo) with HR of 0.56 (95% CI: 0.3-1.06; P 0.075). Celecoxib was well tolerated, with similar adverse events and quality-of-life in both arms. Our clinical trial results do not show a clinical benefit for celecoxib in preventing NMIBC recurrence but further investigation of COX-2 inhibitors in this setting is warranted. Cancer Prev Res; 4(10); 1580-9. (C)2011 AACR.
C1 [Sabichi, Anita L.] Baylor Coll Med, Dept Med, Div Hematol Oncol, Houston, TX 77030 USA.
[Lerner, Seth P.] Baylor Coll Med, Dept Urol, Houston, TX 77030 USA.
[Lee, J. Jack; Liu, Suyu; Palmer, J. Lynn] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX USA.
[Grossman, H. Barton; De la Cerda, Jorge] Univ Texas MD Anderson Canc Ctr, Dept Urol, Houston, TX USA.
[Czerniak, Bogdan A.] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX USA.
[Richmond, Ellen; Viner, Jaye L.] NCI, Rockville, MD USA.
[Eagle, Craig] Pfizer Pharmaceut Inc, New York, NY USA.
[Viner, Jaye L.] Medimmune Inc, Gaithersburg, MD 20878 USA.
RP Sabichi, AL (reprint author), Baylor Coll Med, Dept Med, Div Hematol Oncol, 1 Baylor Plaza,MS BCM 187, Houston, TX 77030 USA.
EM sabichi@bcm.edu; jjlee@mdanderson.org
FU Pfizer; NIH; NCI [N01-CN-85186]; Pfizer Pharmaceuticals; MD Anderson
Cancer Center [CA016672]
FX This work was funded for the conduct of the study at the satellite
accrual sites (but not at the parent site of MDACC or Baylor) by Pfizer.
NIH, NCI, N01-CN-85186, Pfizer Pharmaceuticals, MD Anderson Cancer
Center Support grant CA016672.
NR 54
TC 18
Z9 19
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD OCT
PY 2011
VL 4
IS 10
BP 1580
EP 1589
DI 10.1158/1940-6207.CAPR-11-0036
PG 10
WC Oncology
SC Oncology
GA 829XP
UT WOS:000295620000010
PM 21881030
ER
PT J
AU Rotunno, M
Hu, N
Su, H
Wang, CY
Goldstein, AM
Bergen, AW
Consonni, D
Pesatori, AC
Bertazzi, PA
Wacholder, S
Shih, J
Caporaso, NE
Taylor, PR
Landi, MT
AF Rotunno, Melissa
Hu, Nan
Su, Hua
Wang, Chaoyu
Goldstein, Alisa M.
Bergen, Andrew W.
Consonni, Dario
Pesatori, Angela C.
Bertazzi, Pier Alberto
Wacholder, Sholom
Shih, Joanna
Caporaso, Neil E.
Taylor, Phil R.
Landi, Maria Teresa
TI A Gene Expression Signature from Peripheral Whole Blood for Stage I Lung
Adenocarcinoma
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID MESSENGER-RNA EXPRESSION; PROSTATE-CANCER; MICROARRAY ANALYSIS; ETIOLOGY
EAGLE; CELL CARCINOMA; BREAST-CANCER; RUNX3 GENE; RT-PCR; RISK;
PROGRESSION
AB Affordable early screening in subjects with high risk of lung cancer has great potential to improve survival from this deadly disease. We measured gene expression from lung tissue and peripheral whole blood (PWB) from adenocarcinoma cases and controls to identify dysregulated lung cancer genes that could be tested in blood to improve identification of at-risk patients in the future. Genome-wide mRNA expression analysis was conducted in 153 subjects (73 adenocarcinoma cases, 80 controls) from the Environment And Genetics in Lung cancer Etiology study using PWB and paired snap-frozen tumor and noninvolved lung tissue samples. Analyses were conducted using unpaired t tests, linear mixed effects, and ANOVA models. The area under the receiver operating characteristic curve (AUC) was computed to assess the predictive accuracy of the identified biomarkers. We identified 50 dysregulated genes in stage I adenocarcinoma versus control PWB samples (false discovery rate <= 0.1, fold change >= 1.5 or <= 0.66). Among them, eight (TGFBR3, RUNX3, TRGC2, TRGV9, TARP, ACP1, VCAN, and TSTA3) differentiated paired tumor versus noninvolved lung tissue samples in stage I cases, suggesting a similar pattern of lung cancer-related changes in PWB and lung tissue. These results were confirmed in two independent gene expression analyses in a blood-based case-control study (n = 212) and a tumor-nontumor paired tissue study (n 54). The eight genes discriminated patients with lung cancer from healthy controls with high accuracy (AUC = 0.81, 95% CI = 0.74-0.87). Our finding suggests the use of gene expression from PWB for the identification of early detection markers of lung cancer in the future. Cancer Prev Res; 4(10); 1599-608. (C)2011 AACR.
C1 [Rotunno, Melissa; Hu, Nan; Su, Hua; Wang, Chaoyu; Goldstein, Alisa M.; Bergen, Andrew W.; Wacholder, Sholom; Caporaso, Neil E.; Taylor, Phil R.; Landi, Maria Teresa] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Shih, Joanna] NCI, Div Canc Treatment & Diag, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Bergen, Andrew W.] SRI Int, Ctr Hlth Sci, Menlo Pk, CA 94025 USA.
[Consonni, Dario; Pesatori, Angela C.; Bertazzi, Pier Alberto] Univ Milan, Fdn IRCCS Osped Maggiore Policlin, Epidemiol Unit, Milan, Italy.
[Consonni, Dario; Pesatori, Angela C.; Bertazzi, Pier Alberto] Univ Milan, Dept Occupat & Environm Hlth, Milan, Italy.
RP Landi, MT (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd,MSC 7114, Bethesda, MD 20892 USA.
EM landim@mail.nih.gov
RI bertazzi, pietro alberto/D-5039-2017;
OI bertazzi, pietro alberto/0000-0003-3475-2449; Bergen,
Andrew/0000-0002-1237-7644; pesatori, angela/0000-0002-0261-3252
FU Division of Cancer Epidemiology and Genetics, National Cancer Institute,
NIH, DHHS, Bethesda, MD
FX This research was supported by the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute,
NIH, DHHS, Bethesda, MD.
NR 47
TC 27
Z9 28
U1 1
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD OCT
PY 2011
VL 4
IS 10
BP 1599
EP 1608
DI 10.1158/1940-6207.CAPR-10-0170
PG 10
WC Oncology
SC Oncology
GA 829XP
UT WOS:000295620000012
PM 21742797
ER
PT J
AU Chandra, A
Latov, N
Wormser, GP
Marques, AR
Alaedini, A
AF Chandra, Abhishek
Latov, Norman
Wormser, Gary P.
Marques, Adriana R.
Alaedini, Armin
TI Epitope mapping of antibodies to VlsE protein of Borrelia burgdorferi in
post-Lyme disease syndrome
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE Lyme disease; Post-Lyme disease syndrome; Chronic Lyme disease; VlsE;
Epitope mapping; Antibody
ID IMMUNODOMINANT CONSERVED REGION; VARIABLE SURFACE-ANTIGEN;
ANTIBIOTIC-TREATMENT; PERSISTENT SYMPTOMS; DIAGNOSIS; HISTORY; PEPTIDE;
DOMAIN; VIRUS; TRIAL
AB The VlsE lipoprotein of Borrelia burgdorferi elicits a strong immune response during the course of Lyme disease. The present study was aimed at characterization of the epitopes of VlsE targeted by the antibody response in patients with post-Lyme disease syndrome, a condition characterized by persisting symptoms of pain, fatigue, and/or neurocognitive impairment despite antibiotic treatment of B. burgdorferi infection. Epitope mapping was carried out using microarrays that contained synthesized overlapping peptides covering the full sequence of VlsE from B. burgdorferi B31. In addition to the previously characterized IR6 region in the variable domain, specific sequences in the N- and C-terminal invariable domains of VlsE were found to be major B cell epitopes in affected patients. The crystal structure of VlsE indicated that the newly described epitopes form a contiguous region in the surface-exposed membrane-proximal part of the monomeric form of the protein. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Chandra, Abhishek; Latov, Norman; Alaedini, Armin] Cornell Univ, Weill Cornell Med Coll, Dept Neurol & Neurosci, New York, NY 10021 USA.
[Wormser, Gary P.] New York Med Coll, Dept Med, Div Infect Dis, Valhalla, NY 10595 USA.
[Marques, Adriana R.] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
RP Alaedini, A (reprint author), Columbia Univ, Med Ctr, Dept Med, 1130 St Nicholas Ave,Room 937, New York, NY 10032 USA.
EM aa819@columbia.edu
FU National Institutes of Health (NIH) [AI071180-02, N01-AI-65308]
FX This work was supported by the National Institutes of Health (NIH)
[grant number AI071180-02 to A. Alaedini] and involved the use of
specimens derived from an NIH-supported repository [contract number
N01-AI-65308]. It was also supported in part by the Intramural Research
Program of the NIH. We are indebted to Dr. Phillip J. Baker at NIH for
his invaluable support and guidance throughout this project. We thank
Ms. Diane Holmgren, Ms. Donna McKenna, and Ms. Susan Bittker for their
assistance with specimen collection and organization.
NR 28
TC 10
Z9 10
U1 0
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD OCT
PY 2011
VL 141
IS 1
BP 103
EP 110
DI 10.1016/j.clim.2011.06.005
PG 8
WC Immunology
SC Immunology
GA 829EC
UT WOS:000295558500012
PM 21778118
ER
PT J
AU Glasier, A
Cameron, ST
Blithe, D
Scherrer, B
Mathe, H
Levy, D
Gainer, E
Ulmann, A
AF Glasier, Anna
Cameron, Sharon T.
Blithe, Diana
Scherrer, Bruno
Mathe, Henri
Levy, Delphine
Gainer, Erin
Ulmann, Andre
TI Can we identify women at risk of pregnancy despite using emergency
contraception? Data from randomized trials of ulipristal acetate and
levonorgestrel
SO CONTRACEPTION
LA English
DT Article
DE Emergency contraception; Ulipristal acetate; Levonorgestrel; Risk
factors
ID CONCEPTION; RATES; PROBABILITY; INTERCOURSE; FAILURE; REGIMEN; OBESITY;
WEIGHT; PILL
AB Background: Emergency contraception (EC) does not always work. Clinicians should be aware of potential risk factors for EC failure.
Study Design: Data from a meta-analysis of two randomized controlled trials comparing the efficacy of ulipristal acetate (UPA) with levonorgestrel were analyzed to identify factors associated with EC failure.
Results: The risk of pregnancy was more than threefold greater for obese women compared with women with normal body mass index (odds ratio (OR), 3.60; 95% confidence interval (CI), 1.96-6.53; p<.0001), whichever EC was taken. However, for obese women, the risk was greater for those taking levonorgestrel (OR, 4.41; 95% CI, 2.05-9.44, p=.0002) than for UPA users (OR, 2.62; 95% CI, 0.89-7.00; ns). For both ECs, pregnancy risk was related to the cycle day of intercourse. Women who had intercourse the day before estimated day of ovulation had a fourfold increased risk of pregnancy (OR, 4.42; 95% CI, 2.33-8.20; p<.0001) compared with women having sex outside the fertile window. For both methods, women who had unprotected intercourse after using EC were more likely to get pregnant than those who did not (OR, 4.64; 95% CI, 2.22-8.96; p=.0002).
Conclusions: Women who have intercourse around ovulation should ideally be offered a copper intrauterine device. Women with body mass index >25 kg/m(2) should be offered an intrauterine device or UPA. All women should be advised to start effective contraception immediately after EC. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Glasier, Anna; Cameron, Sharon T.] Univ Edinburgh, Edinburgh EH8 9YL, Midlothian, Scotland.
[Blithe, Diana] NICHHD, Bethesda, MD 20892 USA.
[Scherrer, Bruno; Mathe, Henri; Levy, Delphine; Gainer, Erin; Ulmann, Andre] HRA Phrama, Paris, France.
RP Glasier, A (reprint author), Univ Edinburgh, Edinburgh EH8 9YL, Midlothian, Scotland.
EM anna.glasier@ed.ac.uk
NR 32
TC 97
Z9 97
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0010-7824
J9 CONTRACEPTION
JI Contraception
PD OCT
PY 2011
VL 84
IS 4
BP 363
EP 367
DI 10.1016/j.contraception.2011.02.009
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 829DY
UT WOS:000295557900004
PM 21920190
ER
PT J
AU Frush, S
Li, ZW
Potts, EN
Du, WL
Eu, JP
Garantziotis, S
He, YW
Foster, WM
Hollingsworth, JW
AF Frush, Sarah
Li, Zhuowei
Potts, Erin N.
Du, Wanglei
Eu, Jerry P.
Garantziotis, Stavros
He, You-Wen
Foster, W. Michael
Hollingsworth, John W.
TI The Role of the Extracellular Matrix Protein Mindin in Airway Response
to Environmental Airways Injury (Retracted article. See vol. 124, pg.
A69, 2016)
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article; Retracted Publication
DE airway smooth muscle; endotoxin; innate immunity; lipopolysaccharide;
LPS; lung; mindin; ozone; Tlr4; toll-like receptor
ID INDUCED LUNG INFLAMMATION; TOLL-LIKE RECEPTOR-4; OZONE EXPOSURE; GRAIN
DUST; FLOW OBSTRUCTION; DAILY MORTALITY; CUTTING EDGE; GUINEA-PIG; MOUSE
LUNG; TLR4
AB Background: Our previous work demonstrated that the extracellular matrix protein mindin contributes to allergic airways disease. However, the role of mindin in non-allergic airways disease has not previously been explored.
Objectives: We hypothesized that mindin would contribute to airways disease after inhalation of either lipopolysaccharide (LPS) or ozone.
Methods: We exposed C57BL/6J and mindin-deficient ((-/-)) mice to aerosolized LPS (0.9 mu g/m(3) for 2.5 hr), saline, ozone (1 ppm for 3 hr), or filtered air (FA). All mice were evaluated 4 hr after LPS/saline exposure or 24 hr after ozone/FA exposure. We characterized the physiological and biological responses by analysis of airway hyperresponsiveness (AHR) with a computer-controlled small-animal ventilator (FlexiVent), inflammatory cellular recruitment, total protein in bronchoalveolar lavage fluid (BALF), pro-inflammatory cytokine profiling, and ex vivo bronchial ring studies.
Results: After inhalation of LPS, mindin(-/-) mice demonstrated significantly reduced total cell and neutrophil recruitment into the airspace compared with their wild-type counter-parts. Mindin(-/-) mice also exhibited reduced pro-inflammatory cytokine production and lower AHR to methacholine challenge by FlexiVent. After inhalation of ozone, mice had no detectible differences in cellular inflammation or total BALF protein dependent on mindin. However, mindin(-/-) mice were protected from increased pro-inflammatory cytokine production and AHR compared with their C57BL/6J counter-parts. After ozone exposure, bronchial rings derived from mindin(-/-) mice demonstrated reduced constriction in response to carbachol.
Conclusions: These data demonstrate that the extracellular matrix protein mindin modifies the airway response to both LPS and ozone. Our data support a conserved role of mindin in production of pro-inflammatory cytokines and the development of AHR in two divergent models of reactive airways disease, as well as a role of mindin in airway smooth muscle contractility after exposure to ozone.
C1 [Frush, Sarah; Li, Zhuowei; Potts, Erin N.; Du, Wanglei; Eu, Jerry P.; Foster, W. Michael; Hollingsworth, John W.] Duke Univ, Med Ctr, Div Pulm Allergy & Crit Care Med, Dept Med, Durham, NC 27710 USA.
[Garantziotis, Stavros] NIEHS, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[He, You-Wen; Hollingsworth, John W.] Duke Univ, Dept Immunol, Durham, NC 27710 USA.
RP Hollingsworth, JW (reprint author), Duke Univ, Med Ctr, Div Pulm Allergy & Crit Care Med, Dept Med, Box 103004, Durham, NC 27710 USA.
EM john.hollingsworth@duke.edu
RI Garantziotis, Stavros/A-6903-2009
OI Garantziotis, Stavros/0000-0003-4007-375X
FU National Institutes of Health [ES016126, ES02046, ES016347, HL081825]
FX This work was supported by National Institutes of Health grants to
J.W.H. (ES016126, ES02046), W.M.F. (ES016347), and J.P.E. (HL081825).
NR 45
TC 6
Z9 7
U1 0
U2 3
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2011
VL 119
IS 10
BP 1403
EP 1408
DI 10.1289/ehp.1003339
PG 6
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 827CA
UT WOS:000295402400024
PM 21684833
ER
PT J
AU Barth, H
Rybczynska, J
Patient, R
Choi, Y
Sapp, RK
Baumert, TF
Krawczynski, K
Liang, TJ
AF Barth, Heidi
Rybczynska, Jolanta
Patient, Romuald
Choi, Youkyung
Sapp, Ronda K.
Baumert, Thomas F.
Krawczynski, Kris
Liang, T. Jake
TI Both Innate and Adaptive Immunity Mediate Protective Immunity Against
Hepatitis C Virus Infection in Chimpanzees
SO HEPATOLOGY
LA English
DT Article
ID RECOVERED CHIMPANZEES; DENDRITIC CELLS; RESPONSES; REINFECTION;
RECHALLENGE; INTERFERON; GENOTYPE; PERSISTENCE; CLEARANCE; KINETICS
AB Understanding the immunological correlates associated with protective immunity following hepatitis C virus (HCV) reexposure is a prerequisite for the design of effective HCV vaccines and immunotherapeutics. In this study we performed a comprehensive analysis of innate and adaptive immunity following HCV reexposure of two chimpanzees that had previously recovered from HCV-JFH1 infection. One of the chimpanzees, CH10274, became protected from active viremia by repeated challenges with homologous HCV-JFH1 and developed neutralizing antibodies, but was later infected with high-level viremia by a heterologous challenge with the HCV H77 virus that persisted for more than 1 year. The other chimpanzee, CH10273, was protected from a similar, heterologous H77 challenge without any evidence of neutralizing antibodies. Peripheral HCV-specific T-cell responses were present in both chimpanzees after challenges and, interestingly, the overall magnitude of response was lower in uninfected CH10273, which, however, exhibited a more robust CD8+ T-cell response. CH10273 showed higher hepatic expression of CD8 and CD56 (natural killer) markers than CH10274 did shortly after inoculation with H77. The heightened T-cell response was associated with an enhanced hepatic production of interferons (both type I and II) and interferon-stimulated genes (ISGs) in CH10273. Therefore, protection or clearance of HCV reinfection upon heterologous rechallenge depends on the activation of both intrahepatic innate and cellular immune responses. Furthermore, our results suggest that serum neutralizing antibodies may contribute to early control of viral replication and spread after homologous HCV rechallenges but may not be sufficient for a long-term protective immunity. Conclusion: Our study shows that protective immunity against HCV reinfection is orchestrated by a complex network of innate and adaptive immune responses. (HEPATOLOGY 2011;54:1135-1148)
C1 [Barth, Heidi; Patient, Romuald; Sapp, Ronda K.; Liang, T. Jake] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Barth, Heidi; Baumert, Thomas F.] INSERM, U748, Strasbourg, France.
[Barth, Heidi; Baumert, Thomas F.] Univ Strasbourg, Strasbourg, France.
[Rybczynska, Jolanta; Choi, Youkyung; Krawczynski, Kris] Ctr Dis Control & Prevent, Div Viral Hepatitis, Atlanta, GA USA.
[Patient, Romuald] INSERM, Dept Biol Cellulaire, U966, Tours, France.
[Baumert, Thomas F.] Hop Univ Strasbourg, Strasbourg, France.
RP Liang, TJ (reprint author), NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
EM kzk1@cdc.gov; JakeL@bdg10.niddk.nih.gov
FU Deutsche Forschungsgemeinschaft, Bonn, Germany [BA 3643/1-1]; National
Institute of Diabetes and Digestive and Kidney Diseases; NIH; Division
of Viral Hepatitis; NCHHSTP; CDC; Agence Nationale de Recherche sur le
SIDA et les Hepatites Virales [2010-106, 2010-242]; Inserm, France
FX Supported by the Deutsche Forschungsgemeinschaft, Bonn, Germany (BA
3643/1-1 to H.B.), the Intramural Research Program of the National
Institute of Diabetes and Digestive and Kidney Diseases, NIH, and
programmatic support of Division of Viral Hepatitis, NCHHSTP, CDC, and
the Agence Nationale de Recherche sur le SIDA et les Hepatites Virales
(2010-106; 2010-242 to H.B.), and Inserm, France.
NR 30
TC 29
Z9 31
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
IS 4
BP 1135
EP 1148
DI 10.1002/hep.24489
PG 14
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KA
UT WOS:000295577200006
PM 21674561
ER
PT J
AU Baghdasaryan, A
Claudel, T
Gumhold, J
Silbert, D
Adorini, L
Roda, A
Vecchiotti, S
Gonzalez, FJ
Schoonjans, K
Strazzabosco, M
Fickert, P
Trauner, M
AF Baghdasaryan, Anna
Claudel, Thierry
Gumhold, Judith
Silbert, Dagmar
Adorini, Luciano
Roda, Aldo
Vecchiotti, Stefania
Gonzalez, Frank J.
Schoonjans, Kristina
Strazzabosco, Mario
Fickert, Peter
Trauner, Michael
TI Dual Farnesoid X Receptor/TGR5 Agonist INT-767 Reduces Liver Injury in
the Mdr2(-/-) (Abcb4(-/-)) Mouse Cholangiopathy Model by Promoting
Biliary HCO3- Output
SO HEPATOLOGY
LA English
DT Article
ID TRANSMEMBRANE CARBONIC-ANHYDRASE; HUMAN GALLBLADDER EPITHELIUM;
BILE-ACID-HOMEOSTASIS; NUCLEAR RECEPTOR; SCLEROSING CHOLANGITIS;
CL-/HCO3-EXCHANGER; URSODEOXYCHOLIC ACID; TRANSPORT METABOLON; RAT
HEPATOCYTES; KNOCKOUT MICE
AB Chronic cholangiopathies have limited therapeutic options and represent an important indication for liver transplantation. The nuclear farnesoid X receptor (FXR) and the membrane G protein-coupled receptor, TGR5, regulate bile acid (BA) homeostasis and inflammation. Therefore, we hypothesized that activation of FXR and/or TGR5 could ameliorate liver injury in Mdr2(-/-) (Abcb4(-/-)) mice, a model of chronic cholangiopathy. Hepatic inflammation, fibrosis, as well as bile secretion and key genes of BA homeostasis were addressed in Mdr2(-/-) mice fed either a chow diet or a diet supplemented with the FXR agonist, INT-747, the TGR5 agonist, INT-777, or the dual FXR/TGR5 agonist, INT-767 (0.03% w/w). Only the dual FXR/TGR5 agonist, INT-767, significantly improved serum liver enzymes, hepatic inflammation, and biliary fibrosis in Mdr2(-/-) mice, whereas INT-747 and INT-777 had no hepatoprotective effects. In line with this, INT-767 significantly induced bile flow and biliary HCO3- output, as well as gene expression of carbonic anhydrase 14, an important enzyme able to enhance HCO3- transport, in an Fxr-dependent manner. In addition, INT-767 dramatically reduced bile acid synthesis via the induction of ileal Fgf15 and hepatic Shp gene expression, thus resulting in significantly reduced biliary bile acid output in Mdr2(-/-) mice. Conclusion: This study shows that FXR activation improves liver injury in a mouse model of chronic cholangiopathy by reduction of biliary BA output and promotion of HCO3- -rich bile secretion. (HEPATOLOGY 2011;54:1303-1312)
C1 [Claudel, Thierry; Trauner, Michael] Med Univ Vienna, Div Gastroenterol & Hepatol, Dept Internal Med 3, A-1090 Vienna, Austria.
[Baghdasaryan, Anna; Claudel, Thierry; Gumhold, Judith; Silbert, Dagmar; Fickert, Peter; Trauner, Michael] Med Univ Graz, Lab Expt & Mol Hepatol, Div Gastroenterol & Hepatol, Dept Internal Med, Graz, Austria.
[Adorini, Luciano] Intercept Pharmaceut, New York, NY USA.
[Roda, Aldo; Vecchiotti, Stefania] Univ Bologna, Dept Pharmaceut Sci, Lab Bioanalyt & Analyt Chem, I-40126 Bologna, Italy.
[Gonzalez, Frank J.] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
[Schoonjans, Kristina] Ecole Polytech Fed Lausanne, Lab Integrat & Syst Physiol, Lausanne, Switzerland.
[Strazzabosco, Mario] Yale Univ, Sch Med, Dept Internal Med, Sect Digest Dis, New Haven, CT 06510 USA.
[Strazzabosco, Mario] Univ Milano Bicocca, Dept Clin Med & Prevent, Milan, Italy.
RP Trauner, M (reprint author), Med Univ Vienna, Div Gastroenterol & Hepatol, Dept Internal Med 3, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
EM michael.trauner@meduniwien.ac.at
OI Fickert, Peter/0000-0003-0906-4636
FU Austrian Science Foundation [P18613-B05, P19118, SFB 3008]; Swiss
National Science Foundation [SNF 31003A-125487/1]; Medical University of
Graz; Intercept
FX This work was supported by the Austrian Science Foundation (grant nos.
P18613-B05, P19118, and SFB 3008; to M.T.), the Swiss National Science
Foundation (grant no. SNF 31003A-125487/1; to K.S.), and by the PhD
Program of the Medical University of Graz (to A.B.).; Dr. Adornini owns
stock in Intercept. Dr. Trauner is a consultant for Phenex. He is on the
speakers' bureau of Falk and received grants from Intercept.
NR 65
TC 71
Z9 72
U1 0
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
IS 4
BP 1303
EP 1312
DI 10.1002/hep.24537
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KA
UT WOS:000295577200022
PM 22006858
ER
PT J
AU Berg, CL
Merion, RM
Shearon, TH
Olthoff, KM
Brown, RS
Baker, TB
Everson, GT
Hong, JC
Terrault, N
Hayashi, PH
Fisher, RA
Everhart, JE
AF Berg, Carl L.
Merion, Robert M.
Shearon, Tempie H.
Olthoff, Kim M.
Brown, Robert S., Jr.
Baker, Talia B.
Everson, Gregory T.
Hong, Johnny C.
Terrault, Norah
Hayashi, Paul H.
Fisher, Robert A.
Everhart, James E.
TI Liver Transplant Recipient Survival Benefit with Living Donation in the
Model for Endstage Liver Disease Allocation Era
SO HEPATOLOGY
LA English
DT Article
ID HEPATOCELLULAR-CARCINOMA; DONOR; MELD
AB Receipt of a living donor liver transplant (LDLT) has been associated with improved survival compared with waiting for a deceased donor liver transplant (DDLT). However, the survival benefit of liver transplant has been questioned for candidates with Model for Endstage Liver Disease (MELD) scores <15, and the survival advantage of LDLT has not been demonstrated during the MELD allocation era, especially for low MELD patients. Transplant candidates enrolled in the Adult-to-Adult Living Donor Liver Transplantation Cohort Study after February 28, 2002 were followed for a median of 4.6 years. Starting at the time of presentation of the first potential living donor, mortality for LDLT recipients was compared to mortality for patients who remained on the waiting list or received DDLT (no LDLT group) according to categories of MELD score (<15 or >= 15) and diagnosis of hepatocellular carcinoma (HCC). Of 868 potential LDLT recipients (453 with MELD <15; 415 with MELD >= 15 at entry), 712 underwent transplantation (406 LDLT; 306 DDLT), 83 died without transplant, and 73 were alive without transplant at last follow-up. Overall, LDLT recipients had 56% lower mortality (hazard ratio [HR] = 0.44, 95% confidence interval [CI] 0.32-0.60; P < 0.0001). Among candidates without HCC, mortality benefit was seen both with MELD <15 (HR = 0.39; P = 0.0003) and MELD >= 15 (HR = 0.42; P = 0.0006). Among candidates with HCC, a benefit of LDLT was not seen for MELD <15 (HR = 0.82, P = 0.65) but was seen for MELD >= 15 (HR = 0.29, P = 0.043). Conclusion: Across the range of MELD scores, patients without HCC derived a significant survival benefit when undergoing LDLT rather than waiting for DDLT in the MELD liver allocation era. Low MELD candidates with HCC may not benefit from LDLT. (HEPATOLOGY 2011;54:1313-1321)
C1 [Berg, Carl L.] Univ Virginia Hlth Syst, Dept Med, Charlottesville, VA 22908 USA.
[Merion, Robert M.] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA.
[Merion, Robert M.] Arbor Res Collaborat Hlth, Ann Arbor, MI USA.
[Shearon, Tempie H.] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Olthoff, Kim M.] Univ Penn, Dept Surg, Philadelphia, PA 19104 USA.
[Brown, Robert S., Jr.] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
[Baker, Talia B.] Northwestern Univ, Dept Surg, Chicago, IL 60611 USA.
[Everson, Gregory T.] Univ Colorado, Dept Med, Aurora, CO USA.
[Hong, Johnny C.] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA.
[Terrault, Norah] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Hayashi, Paul H.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Fisher, Robert A.] Virginia Commonwealth Univ, Med Coll Virginia Hosp, Dept Surg, Richmond, VA USA.
[Everhart, James E.] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD USA.
RP Berg, CL (reprint author), Univ Virginia Hlth Syst, Dept Med, POB 800708, Charlottesville, VA 22908 USA.
EM CLB7D@hscmail.mcc.virginia.edu
FU National Institutes of Health (NIDDK) [U01-DK62536, U01-DK62444,
U01-DK62467, U01-DK62483, U01-DK62484, U01-DK62494, U01-DK62496,
U01-DK62498, U01-DK62505, U01-DK62531]; American Society of Transplant
Surgeons; U.S. Department of Health and Human Services, Health Resources
and Services Administration
FX Supported in part by the National Institutes of Health (NIDDK grant
numbers U01-DK62536, U01-DK62444, U01-DK62467, U01-DK62483, U01-DK62484,
U01-DK62494, U01-DK62496, U01-DK62498, U01-DK62505, U01-DK62531), the
American Society of Transplant Surgeons, and the U.S. Department of
Health and Human Services, Health Resources and Services Administration.
NR 12
TC 46
Z9 46
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
IS 4
BP 1313
EP 1321
DI 10.1002/hep.24494
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KA
UT WOS:000295577200023
PM 21688284
ER
PT J
AU Ghany, MG
Nelson, DR
Strader, DB
Thomas, DL
Seeff, LB
AF Ghany, Marc G.
Nelson, David R.
Strader, Doris B.
Thomas, David L.
Seeff, Leonard B.
TI An Update on Treatment of Genotype 1 Chronic Hepatitis C Virus
Infection: 2011 Practice Guideline by the American Association for the
Study of Liver Diseases
SO HEPATOLOGY
LA English
DT Editorial Material
ID SUSTAINED VIROLOGICAL RESPONSE; PEGINTERFERON ALPHA-2A;
GENETIC-VARIATION; PLUS RIBAVIRIN; VIRAL RESPONSE; HCV INFECTION;
FOLLOW-UP; TELAPREVIR; COMBINATION; IL28B
C1 [Ghany, Marc G.] NIDDK, Liver Dis Branch, NIH, Bethesda, MD 20892 USA.
[Nelson, David R.] Univ Florida, Sect Hepatobiliary Dis, Gainesville, FL USA.
[Strader, Doris B.] Univ Vermont, Coll Med, Div Gastroenterol & Hepatol, Burlington, VT USA.
[Thomas, David L.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Seeff, Leonard B.] Hill Grp, Bethesda, MD USA.
RP Ghany, MG (reprint author), NIDDK, Liver Dis Branch, NIH, Bldg 10,Room 9B-16,10 Ctr Dr,MSC 1800, Bethesda, MD 20892 USA.
EM marcg@intra.niddk.nih.gov
FU NCI NIH HHS [K24 CA139570]
NR 33
TC 728
Z9 768
U1 2
U2 25
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD OCT
PY 2011
VL 54
IS 4
BP 1433
EP 1444
DI 10.1002/hep.24641
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 829KA
UT WOS:000295577200035
PM 21898493
ER
PT J
AU Soekadar, SR
Witkowski, M
Mellinger, J
Ramos, A
Birbaumer, N
Cohen, LG
AF Soekadar, Surjo R.
Witkowski, Matthias
Mellinger, Juergen
Ramos, Ander
Birbaumer, Niels
Cohen, Leonardo G.
TI ERD-Based Online Brain-Machine Interfaces (BMI) in the Context of
Neurorehabilitation: Optimizing BMI Learning and Performance
SO IEEE TRANSACTIONS ON NEURAL SYSTEMS AND REHABILITATION ENGINEERING
LA English
DT Article
DE Brain-machine interface; event-related desynchronization;
neurorehabilitation; stroke
ID COMPUTER INTERFACE; CHRONIC STROKE; BCI SYSTEM; EEG; MOVEMENT; RECOVERY;
COMMUNICATION; FMRI; ARM
AB Event-related desynchronization (ERD) of sensori-motor rhythms (SMR) can be used for online brain-machine interface (BMI) control, but yields challenges related to the stability of ERD and feedback strategy to optimize BMI learning. Here, we compared two approaches to this challenge in 20 right-handed healthy subjects (HS, five sessions each, S1-S5) and four stroke patients (SP, 15 sessions each, S1-S15). ERD was recorded from a 275-sensor MEG system. During daily training, motor imagery-induced ERD led to visual and proprioceptive feedback delivered through an orthotic device attached to the subjects' hand and fingers. Group A trained with a heterogeneous reference value (RV) for ERD detection with binary feedback and Group B with a homogenous RV and graded feedback (10 HS and 2 SP in each group). HS in Group B showed better BMI performance than Group A and improved BMI control from S1 to S5 while Group A did not. In spite of the small n, SP in Group B showed a trend for a higher BMI performance and learning was significantly better. Using a homogeneous RV and graded feedback led to improved modulation of ipsilesional activity resulting in superior BMI learning relative to use of a heterogeneous RV and binary feedback.
C1 [Soekadar, Surjo R.; Witkowski, Matthias; Cohen, Leonardo G.] NINDS, Human Cort Physiol & Stroke Neurorehabilitat Sec, NIH, Bethesda, MD 20892 USA.
[Mellinger, Juergen; Ramos, Ander; Birbaumer, Niels] Univ Tubingen, Inst Med Psychol & Behav Neurobiol IMP, D-72076 Tubingen, Germany.
RP Soekadar, SR (reprint author), NINDS, Human Cort Physiol & Stroke Neurorehabilitat Sec, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM surjo@soekadar.com; matthias.witkowski@gmx.de;
juergen.mellinger@uni-tuebingen.de; ramos@gmail.com;
niels.birbaumer@uni-tuebingen.de; cohenl@ninds.nih.gov
OI Soekadar, Surjo R./0000-0003-1280-5538; Ramos-Murguialday,
Ander/0000-0002-1549-4029
FU Intramural Research Program (IRP) of the National Institute of
Neurological Disorders and Stroke (NINDS), National Institues of Health
(NIH); German Federal Ministry of Education and Research (BMBF)
[01GQ0831]; Deutsche Forschungsgemeinschaft (DFG); IRP of the NINDS/NIH;
Center for Neuroscience and Regenerative Medicine, Uniformed Services
University of Health Sciences, Bethesda, MD
FX Manuscript received February 01, 2011; revised April 20, 2011; accepted
August 06, 2011. Date of current version October 07, 2011. The work of
S. Soekadar was supported by the Intramural Research Program (IRP) of
the National Institute of Neurological Disorders and Stroke (NINDS),
National Institues of Health (NIH), the German Federal Ministry of
Education and Research (BMBF # 01GQ0831) and the Deutsche
Forschungsgemeinschaft (DFG). The work of M. Witkowski was supported by
the IRP of the NINDS/NIH, the DFG and the BMBF (01GQ0831). The work of
N. Birbaumer was supported by the BMBF (01GQ0831) and the DFG. The work
of L. G. Cohen is supported by the IRP of the NINDS/NIH and the Center
for Neuroscience and Regenerative Medicine, Uniformed Services
University of Health Sciences, Bethesda, MD.
NR 41
TC 25
Z9 25
U1 0
U2 16
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 1534-4320
J9 IEEE T NEUR SYS REH
JI IEEE Trans. Neural Syst. Rehabil. Eng.
PD OCT
PY 2011
VL 19
IS 5
BP 542
EP 549
DI 10.1109/TNSRE.2011.2166809
PG 8
WC Engineering, Biomedical; Rehabilitation
SC Engineering; Rehabilitation
GA 832GW
UT WOS:000295792900010
PM 21984519
ER
PT J
AU Mezey, E
AF Mezey, Eva
TI The Therapeutic Potential of Bone Marrow-Derived Stromal Cells
SO JOURNAL OF CELLULAR BIOCHEMISTRY
LA English
DT Article
DE BONE MARROW STROMAL CELLS; TISSUE REPAIR; IMMUNE REGULATION
ID MESENCHYMAL STEM-CELLS; SUPPRESS T-LYMPHOCYTE; IN-VIVO; TISSUE-REPAIR;
RESPONSES; SECRETION; MIGRATION; EXPRESS; VITRO; TRANSDIFFERENTIATION
AB Since the replacement of the hematopoietic system became feasible through bone marrow (BM) transplantation, the idea of how to replace other organs of the body has been in the forefront of medical research. Scientists have been searching for the ideal stem cell that could be manipulated to differentiate into any tissue. Although the embryonal stem cells seemed to have the ability to do this, the difficulties surrounding their use prevented them from becoming therapeutically useful. Thus, the field turned to adult stem cells, particularly stem cells of BM origin. We have learnt a lot during the last decade about the potential of the BM-derived stromal (also called mesenchymal stem) cells (BMSCs). The first studies suggested them as cell replacement tools, but later it turned out that their usefulness is more likely due to paracrine effects due to a large variety of secreted factors that induce growth and differentiation of the tissue-specific stem cells as well as prevent injured cells from apoptotic death. Finally, a whole new field emerged when many groups confirmed that these cells are also capable of regulating immune function in a so far unknown, dynamic manner. When BMSCs are injected they seem to be able to sense the environment and respond according to the actual need of the organism in order to survive. This plasticity can never be done by the use of any drugs and such a "live" cell therapy could open a whole new chapter in clinical care in the future. J. Cell. Biochem. 112: 2683-2687, 2011. (C) 2011 Wiley-Liss, Inc.
C1 NIDCR, NIH, Adult Stem Cell Unit, Bethesda, MD 20892 USA.
RP Mezey, E (reprint author), NIDCR, NIH, Adult Stem Cell Unit, Bldg 49,5A76,49 Convent Dr, Bethesda, MD 20892 USA.
EM mezeye@mail.nih.gov
FU NIH, DHHS
FX This research was supported by the Division of Intramural Research
program of NIDCR, in the Intramural Research Program, NIH, DHHS.
NR 43
TC 22
Z9 33
U1 0
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0730-2312
J9 J CELL BIOCHEM
JI J. Cell. Biochem.
PD OCT
PY 2011
VL 112
IS 10
BP 2683
EP 2687
DI 10.1002/jcb.23216
PG 5
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 829YP
UT WOS:000295623300005
PM 21678464
ER
PT J
AU Osada, T
Gu, YH
Kanazawa, M
Tsubota, Y
Hawkins, BT
Spatz, M
Milner, R
del Zoppo, GJ
AF Osada, Takashi
Gu, Yu-Huan
Kanazawa, Masato
Tsubota, Yoshiaki
Hawkins, Brian T.
Spatz, Maria
Milner, Richard
del Zoppo, Gregory J.
TI Interendothelial claudin-5 expression depends on cerebral endothelial
cell-matrix adhesion by beta(1)-integrins
SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
LA English
DT Article
DE beta(1)-integrins; cerebral endothelial cells; claudin-5; extracellular
matrix; matrix adhesion receptors; microvessel permeability
ID BLOOD-BRAIN-BARRIER; TIGHT JUNCTION PROTEINS; IN-VITRO; RAT-BRAIN;
TYROSINE PHOSPHORYLATION; GLIOBLASTOMA-MULTIFORME; EXTRACELLULAR-MATRIX;
BASEMENT-MEMBRANE; ISCHEMIA; PERMEABILITY
AB The hypothesis tested by these studies states that in addition to interendothelial cell tight junction proteins, matrix adhesion by beta(1)-integrin receptors expressed by endothelial cells have an important role in maintaining the cerebral microvessel permeability barrier. Primary brain endothelial cells from C57 BL/6 mice were incubated with beta(1)-integrin function-blocking antibody (Ha2/5) or isotype control and the impacts on claudin-5 expression and microvessel permeability were quantified. Both flow cytometry and immunofluorescence studies demonstrated that the interendothelial claudin-5 expression by confluent endothelial cells was significantly decreased in a time-dependent manner by Ha2/5 exposure relative to isotype. Furthermore, to assess the barrier properties, transendothelial electrical resistance and permeability measurements of the monolayer, and stereotaxic injection into the striatum of mice were performed. Ha2/5 incubation reduced the resistance of endothelial cell monolayers significantly, and significantly increased permeability to 40 and 150 kDa dextrans. Ha2/5 injection into mouse striatum produced significantly greater IgG extravasation than the isotype or the control injections. This study demonstrates that blockade of beta(1)-integrin function changes interendothelial claudin-5 expression and increases microvessel permeability. Hence, endothelial cell-matrix interactions via beta(1)-integrin directly affect interendothelial cell tight junction claudin-5 expression and brain microvascular permeability. Journal of Cerebral Blood Flow & Metabolism (2011) 31, 1972-1985; doi:10.1038/jcbfm.2011.99; published online 20 July 2011
C1 [Osada, Takashi; Gu, Yu-Huan; Kanazawa, Masato; Hawkins, Brian T.; del Zoppo, Gregory J.] Univ Washington, Sch Med, Div Hematol, Dept Med,Harborview Med Ctr, Seattle, WA 98104 USA.
[Osada, Takashi; Gu, Yu-Huan; Kanazawa, Masato; Hawkins, Brian T.; del Zoppo, Gregory J.] Univ Washington, Sch Med, Dept Neurol, Seattle, WA 98104 USA.
[Tsubota, Yoshiaki] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98104 USA.
[Spatz, Maria] NINDS, Stroke Branch, Bethesda, MD 20892 USA.
[Milner, Richard; del Zoppo, Gregory J.] Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA.
RP del Zoppo, GJ (reprint author), Univ Washington, Sch Med, Div Hematol, Dept Med,Harborview Med Ctr, Box 359756,325 9th Ave, Seattle, WA 98104 USA.
EM grgdlzop@u.washington.edu
RI Osada, Takashi/B-2060-2015
FU NIH [NS 053716, NS 038710, NS 036945]; Kanae Foundation for the
Promotion of Medical Science
FX This study was supported in part by NIH Grants NS 053716, NS 038710, and
NS 036945 to Dr del Zoppo. Dr Osada also received funding from the Kanae
Foundation for the Promotion of Medical Science.
NR 41
TC 42
Z9 44
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0271-678X
J9 J CEREBR BLOOD F MET
JI J. Cereb. Blood Flow Metab.
PD OCT
PY 2011
VL 31
IS 10
BP 1972
EP 1985
DI 10.1038/jcbfm.2011.99
PG 14
WC Endocrinology & Metabolism; Hematology; Neurosciences
SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology
GA 829YB
UT WOS:000295621600003
PM 21772312
ER
PT J
AU Zanotti-Fregonara, P
Chen, K
Liow, JS
Fujita, M
Innis, RB
AF Zanotti-Fregonara, Paolo
Chen, Kewei
Liow, Jeih-San
Fujita, Masahiro
Innis, Robert B.
TI Image-derived input function for brain PET studies: many challenges and
few opportunities
SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
LA English
DT Review
DE image-derived input function; kinetic modeling; neuroreceptor tracers;
PET
ID POSITRON-EMISSION-TOMOGRAPHY; INDEPENDENT COMPONENT ANALYSIS; CEREBRAL
METABOLIC-RATE; NONINVASIVE QUANTIFICATION; DYNAMIC PET;
KINETIC-PARAMETERS; QUANTITATIVE PET; PROSTATE-CANCER; FDG-PET; GLUCOSE
AB Quantitative positron emission tomography (PET) brain studies often require that the input function be measured, typically via arterial cannulation. Image-derived input function (IDIF) is an elegant and attractive noninvasive alternative to arterial sampling. However, IDIF is also a very challenging technique associated with several problems that must be overcome before it can be successfully implemented in clinical practice. As a result, IDIF is rarely used as a tool to reduce invasiveness in patients. The aim of the present review was to identify the methodological problems that hinder widespread use of IDIF in PET brain studies. We conclude that IDIF can be successfully implemented only with a minority of PET tracers. Even in those cases, it only rarely translates into a less-invasive procedure for the patient. Finally, we discuss some possible alternative methods for obtaining less-invasive input function. Journal of Cerebral Blood Flow & Metabolism (2011) 31, 1986-1998; doi:10.1038/jcbfm.2011.107; published online 3 August 2011
C1 [Zanotti-Fregonara, Paolo; Liow, Jeih-San; Fujita, Masahiro; Innis, Robert B.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Chen, Kewei] Banner Alzheimers Inst, Phoenix, AZ USA.
[Chen, Kewei] Banner Good Samaritan PET Ctr, Phoenix, AZ USA.
[Chen, Kewei] Arizona State Univ, Dept Math & Stat, Tempe, AZ USA.
RP Innis, RB (reprint author), NIMH, Mol Imaging Branch, NIH, Bldg 10,Room B1D43,31 Ctr Dr,MSC 1026, Bethesda, MD 20892 USA.
EM innisr@mail.nih.gov
RI Chen, kewei/P-6304-2015
OI Chen, kewei/0000-0001-8497-3069
FU National Institute of Mental Health, National Institutes of Health,
Department of Health and Human Services (IRP-NIMH-NIH-DHHS); National
Institute of Mental Health, US [RO1 MH57899]; National Institute on
Aging, US [R01AG031581-10, P30 AG19610]; state of Arizona
FX This study was supported by the Intramural Research Program of the
National Institute of Mental Health, National Institutes of Health,
Department of Health and Human Services (IRP-NIMH-NIH-DHHS), by the
National Institute of Mental Health, US (RO1 MH57899), the National
Institute on Aging, US (R01AG031581-10 and P30 AG19610), and the state
of Arizona.
NR 93
TC 43
Z9 43
U1 0
U2 12
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0271-678X
J9 J CEREBR BLOOD F MET
JI J. Cereb. Blood Flow Metab.
PD OCT
PY 2011
VL 31
IS 10
BP 1986
EP 1998
DI 10.1038/jcbfm.2011.107
PG 13
WC Endocrinology & Metabolism; Hematology; Neurosciences
SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology
GA 829YB
UT WOS:000295621600004
PM 21811289
ER
PT J
AU Onojafe, IF
Adams, DR
Simeonov, DR
Zhang, J
Chan, CC
Bernardini, IM
Sergeev, YV
Dolinska, MB
Alur, RP
Brilliant, MH
Gahl, WA
Brooks, BP
AF Onojafe, Ighovie F.
Adams, David R.
Simeonov, Dimitre R.
Zhang, Jun
Chan, Chi-Chao
Bernardini, Isa M.
Sergeev, Yuri V.
Dolinska, Monika B.
Alur, Ramakrishna P.
Brilliant, Murray H.
Gahl, William A.
Brooks, Brian P.
TI Nitisinone improves eye and skin pigmentation defects in a mouse model
of oculocutaneous albinism
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID TYROSINASE GENE-MUTATIONS; HIMALAYAN MOUSE;
2-(2-NITRO-4-TRIFLUOROMETHYLBENZOYL)-CYCLOHEXANE-1,3-DIONE NTBC;
MAMMALIAN TYROSINASE; TISSUE DISTRIBUTION; P GENE; IDENTIFICATION;
CATABOLISM; EXPRESSION; PROTEINS
AB Mutation of the tyrosinase gene (TYR) causes oculocutaneous albinism, type 1 (OCA1), a condition characterized by reduced skin and eye melanin pigmentation and by vision loss. The retinal pigment epithelium influences postnatal visual development. Therefore, increasing ocular pigmentation in patients with OCA1 might enhance visual function. There are 2 forms of OCA1, OCA-1A and OCA-1B. Individuals with the former lack functional tyrosinase and therefore lack melanin, while individuals with the latter produce some melanin. We hypothesized that increasing plasma tyrosine concentrations using nitisinone, an FDA-approved inhibitor of tyrosine degradation, could stabilize tyrosinase and improve pigmentation in individuals with OCA1. Here, we tested this hypothesis in mice homozygous for either the Tyr(c-2J) null allele or the Tyr(c-h) allele, which model OCA-1A and OCA-1B, respectively. Only nitisinone-treated Tyr(c-h/c-h) mice manifested increased pigmentation in their fur and irides and had more pigmented melanosomes. High levels of tyrosine improved the stability and enzymatic function of the Tyr(c-h) protein and also increased overall melanin levels in melanocytes from a human with OCA-1B. These results suggest that the use of nitisinone in OCA-1B patients could improve their pigmentation and potentially ameliorate vision loss.
C1 [Onojafe, Ighovie F.; Sergeev, Yuri V.; Dolinska, Monika B.; Alur, Ramakrishna P.; Brooks, Brian P.] NEI, Unit Pediat Dev & Genet Eye Dis, NIH, Bethesda, MD 20892 USA.
[Adams, David R.; Simeonov, Dimitre R.; Bernardini, Isa M.; Gahl, William A.] NHGRI, Sect Human Biochem Genet, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Zhang, Jun; Chan, Chi-Chao] NEI, Immunopathol Sect, NIH, Bethesda, MD 20892 USA.
[Brilliant, Murray H.] Marshfield Clin Fdn Med Res & Educ, Ctr Human Genet, Marshfield, WI USA.
RP Brooks, BP (reprint author), Bldg 10,Room 10N226,MSC 1860,10 Ctr Dr, Bethesda, MD 20892 USA.
EM brooksb@mail.nih.gov
RI Zhang, Jun/K-2424-2012
FU National Eye Institute; National Human Genome Research Institute;
National Human Genome Research Institute, NIH; Blind Children's Center
FX The authors thank V. Hearing for the gift of alpha PEP7 antiserum and
review of the manuscript, J.T. Wroblewski for the gift of CHO cells, and
C. Olivares for the gift of the mouse tyrosinase expression construct.
We thank the intramural programs of the National Eye Institute and the
National Human Genome Research Institute, NIH, for funding this
research. B.P. Brooks's lab was partially funded by a 1-year seed grant
from the Blind Children's Center.
NR 72
TC 10
Z9 10
U1 2
U2 16
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 2011
VL 121
IS 10
BP 3914
EP 3923
DI 10.1172/JCI59372
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 829RC
UT WOS:000295601000020
PM 21968110
ER
PT J
AU Akilesh, S
Suleiman, H
Yu, HY
Stander, MC
Lavin, P
Gbadegesin, R
Antignac, C
Pollak, M
Kopp, JB
Winn, MP
Shaw, AS
AF Akilesh, Shreeram
Suleiman, Hani
Yu, Haiyang
Stander, M. Christine
Lavin, Peter
Gbadegesin, Rasheed
Antignac, Corinne
Pollak, Martin
Kopp, Jeffrey B.
Winn, Michelle P.
Shaw, Andrey S.
TI Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is
associated with familial focal segmental glomerulosclerosis
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID ACTIN CYTOSKELETON; FILAMIN-A; KIDNEY PODOCYTES; CELL MOTILITY; RHO;
DISEASE; PROTEINURIA; DYNAMICS; NEF; REARRANGEMENTS
AB The specialized epithelial cell of the kidney, the podocyte, has a complex actin-based cytoskeleton. Dynamic regulation of this cytoskeleton is required for efficient barrier function of the kidney. Podocytes are a useful cell type to study the control of the actin cytoskeleton in vivo, because disruption of components of the cytoskeleton results in podocyte damage, cell loss, and a prototypic injury response called focal segmental glomerulosclerosis (FSGS). Searching for actin regulatory proteins that are expressed in podocytes, we identified a RhoA-activated Rac1 GTPase-activating protein (Rac1-GAP), Arhgap24, that was upregulated in podocytes as they differentiated, both in vitro and in vivo. Increased levels of active Rac1 and Cdc42 were measured in Arhgap24 knockdown experiments, which influenced podocyte cell shape and membrane dynamics. Consistent with a role for Arhgap24 in normal podocyte functioning in vivo, sequencing of the ARHGAP24 gene in patients with FSGS identified a mutation that impaired its Rac1-GAP activity and was associated with disease in a family with FSGS. Thus, Arhgap24 contributes to the careful balancing of RhoA and Rac1 signaling in podocytes, the disruption of which may lead to kidney disease.
C1 [Suleiman, Hani; Yu, Haiyang; Stander, M. Christine; Shaw, Andrey S.] Washington Univ, Howard Hughes Med Inst, Div Immunobiol, Dept Pathol & Immunol,Sch Med, St Louis, MO 63110 USA.
[Akilesh, Shreeram] Barnes Jewish Hosp, Dept Pathol, St Louis, MO 63110 USA.
[Lavin, Peter; Winn, Michelle P.] Duke Univ, Med Ctr, Div Nephrol, Dept Med, Durham, NC USA.
[Lavin, Peter; Gbadegesin, Rasheed; Winn, Michelle P.] Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC USA.
[Gbadegesin, Rasheed] Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA.
[Antignac, Corinne] Hop Necker Enfants Malades Tour Lavoisier, INSERM, U423, Paris, France.
[Pollak, Martin] Brigham & Womens Hosp, Div Renal, Dept Med, Boston, MA 02115 USA.
[Pollak, Martin] Harvard Univ, Sch Med, Boston, MA USA.
[Kopp, Jeffrey B.] NIH, Kidney Dis Sect, Bethesda, MD 20892 USA.
RP Shaw, AS (reprint author), Washington Univ, Howard Hughes Med Inst, Div Immunobiol, Dept Pathol & Immunol,Sch Med, Campus Box 8118,660 S Euclid Ave, St Louis, MO 63110 USA.
EM shaw@pathology.wustl.edu
RI Yu, Haiyang/J-2810-2013;
OI Akilesh, Shreeram/0000-0003-3152-7991; Yu, Haiyang/0000-0003-3460-6716;
Kopp, Jeffrey/0000-0001-9052-186X
FU Washington University George M. O'Brien Center for Kidney Disease
Research [P30 DK079333]; NIDDK [RO1DK058366]; Howard Hughes Medical
Institute; Medical Scientist Training Program
FX We are grateful for the support of Washington University George M.
O'Brien Center for Kidney Disease Research (P30 DK079333) for some of
the patient specimens. We would like to thank Jeffrey Miner for helpful
discussions and Jiancheng Hu for technical assistance and reagents for
the GTPase activity pull-down assays. This work was supported in part by
the NIDDK Intramural (to J.B. Kopp) and Extramural Research Programs
(RO1DK058366, to A.S. Shaw), Howard Hughes Medical Institute, and the
Medical Scientist Training Program Grant to Washington University School
of Medicine.
NR 33
TC 84
Z9 87
U1 0
U2 5
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD OCT
PY 2011
VL 121
IS 10
BP 4127
EP 4137
DI 10.1172/JCI46458
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 829RC
UT WOS:000295601000038
PM 21911940
ER
PT J
AU Xiang, Y
Shen, J
AF Xiang, Yun
Shen, Jun
TI Windowed Stochastic Proton Decoupling for In Vivo C-13 Magnetic
Resonance Spectroscopy with Reduced RF Power Deposition
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE in vivo C-13 MRS; carboxylic/amide carbons; stochastic decoupling
scheme; RF power deposition
ID HUMAN BRAIN; 11.7 TESLA; RAT-BRAIN; METABOLISM; HUMANS; CYCLE; NMR; MRS
AB Purpose: To propose a strategy for reducing radiofrequency (RF) power deposition by stochastic proton decoupiing based on Rayleigh's theorem.
Materials and Methods: Rayleigh's theorem was used to remove frequency components of stochastic decoupling over the 3.90-6.83 ppm range. (2-C-13] or [2,5-C-13(2)]glucose was infused intravenously to anesthetized rats. C-13 labeling of brain metabolites was detected in the carboxylic/amide spectral region at 11.7 T using either the original stochastic decoupling method developed by Ernst or the proposed windowed stochastic decoupling method.
Results: By restricting frequency components of stochastic decoupling to 1.91-3.90 ppm and 6.83-7.60 ppm spectral regions decoupling power deposition was reduced by approximate to 50%. The proposed windowed stochastic decoupling scheme is experimentally demonstrated for in vivo C-13 MRS of rat brain at 11.7 T.
Conclusion: The large reduction in decoupling power deposition makes it feasible to perform stochastic proton decoupling at very high magnetic fields for human brain C-13 MRS studies.
C1 [Xiang, Yun; Shen, Jun] NIMH, Mol Imaging Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Shen, J (reprint author), NIMH, Mol Imaging Branch, Intramural Res Program, NIH, Bldg 10,Rm 2D51A,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM shenj@intra.nimh.nih.gov
FU NIH, NIMH
FX Contract grant sponsor: Intramural Research Program of the NIH, NIMH.
NR 18
TC 5
Z9 5
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1053-1807
J9 J MAGN RESON IMAGING
JI J. Magn. Reson. Imaging
PD OCT
PY 2011
VL 34
IS 4
BP 968
EP 972
DI 10.1002/jmri.22667
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 826ZP
UT WOS:000295394400031
PM 21769967
ER
PT J
AU Bang, H
Park, S
Hwang, J
Jin, H
Cho, E
Kim, DY
Song, T
Shamputa, IC
Via, LE
Barry, CE
Cho, SN
Lee, H
AF Bang, Hyeeun
Park, Sangjung
Hwang, Joohwan
Jin, Hyunwoo
Cho, Eunjin
Kim, Dae Yoon
Song, Taeksun
Shamputa, Isdore Chola
Via, Laura E.
Barry, Clifton E., III
Cho, Sang-Nae
Lee, Hyeyoung
TI Improved rapid molecular diagnosis of multidrug-resistant tuberculosis
using a new reverse hybridization assay, REBA MTB-MDR
SO JOURNAL OF MEDICAL MICROBIOLOGY
LA English
DT Article
ID LINE PROBE ASSAY; MYCOBACTERIUM-TUBERCULOSIS; ISONIAZID RESISTANCE; RPOB
GENE; RIFAMPIN RESISTANCE; MUTATIONS; STRAINS; BEACONS; LEVEL; KATG
AB Rapid diagnosis of multidrug-resistant tuberculosis (MDR-TB) is essential for the prompt initiation of effective second-line therapy to improve treatment outcome and limit transmission of this obstinate disease. A variety of molecular methods that enable the rapid detection of mutations implicated in MDR-TB have been developed. The sensitivity of the methods is dependent, in principle, on the repertoire of mutations being detected, which is typically limited to mutations in the genes rpoB, katG and the promoter region of inhA. In this study, a new reverse hybridization assay, REBA MTB-MDR (M&D), that probes mutations in the oxyR-ahpC intergenic region, in addition to those in rpoB, katG and the inhA promoter region, was evaluated. A set of 240 Mycobacterium tuberculosis clinical isolates from patients receiving retreatment regimens was subjected to conventional phenotypic drug-susceptibility testing (DST) and the REBA MTB-MDR assay. The nucleotide sequences of the loci known to be involved in drug resistance were determined for comparison. In brief, the results showed that the REBA MTB-MDR assay efficiently recognized nucleotide changes in the oxyR-ahpC intergenic region as well as those in rpoB, katG and the inhA promoter region with higher sensitivity, resulting in an 81.0% detection rate for isoniazid resistance. Inclusion of the oxyR-ahpC intergenic region in the REBA MTB-MDR assay improved the overall sensitivity of molecular DST for MDR-TB from 73.1 to 79.9%.
C1 [Bang, Hyeeun; Park, Sangjung; Hwang, Joohwan; Jin, Hyunwoo; Lee, Hyeyoung] Yonsei Univ, Coll Hlth Sci, Dept Biomed Lab Sci, Wonju 220710, South Korea.
[Cho, Eunjin; Song, Taeksun] Int TB Res Ctr, Chang Won 631710, South Korea.
[Kim, Dae Yoon] Mokpo Natl Hosp, Mokpo 530828, South Korea.
[Shamputa, Isdore Chola; Via, Laura E.; Barry, Clifton E., III] NIAID, TB Res Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20852 USA.
[Cho, Sang-Nae] Yonsei Univ, Genome Res Ctr Resp Pathogens, Coll Med, Seoul 120752, South Korea.
RP Lee, H (reprint author), Yonsei Univ, Coll Hlth Sci, Dept Biomed Lab Sci, Wonju 220710, South Korea.
EM hyelee@yonsei.ac.kr
RI Barry, III, Clifton/H-3839-2012;
OI Via, Laura/0000-0001-6074-9521
FU National Institutes of Health, National Institute of Allergy and
Infectious Disease
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Disease.
NR 22
TC 10
Z9 11
U1 0
U2 2
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-2615
J9 J MED MICROBIOL
JI J. Med. Microbiol.
PD OCT
PY 2011
VL 60
IS 10
BP 1447
EP 1454
DI 10.1099/jmm.0.032292-0
PG 8
WC Microbiology
SC Microbiology
GA 833CW
UT WOS:000295860400005
PM 21596910
ER
PT J
AU Kimura, Y
Fujita, M
Hong, JS
Lohith, TG
Gladding, RL
Zoghbi, SS
Tauscher, JA
Goebl, N
Rash, KS
Chen, ZG
Pedregal, C
Barth, VN
Pike, VW
Innis, RB
AF Kimura, Yasuyuki
Fujita, Masahiro
Hong, Jinsoo
Lohith, Talakad G.
Gladding, Robert L.
Zoghbi, Sami S.
Tauscher, Johannes A.
Goebl, Nancy
Rash, Karen S.
Chen, Zhaogen
Pedregal, Concepcion
Barth, Vanessa N.
Pike, Victor W.
Innis, Robert B.
TI Brain and Whole-Body Imaging in Rhesus Monkeys of C-11-NOP-1A, a
Promising PET Radioligand for Nociceptin/Orphanin FQ Peptide Receptors
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE molecular imaging; positron emission tomography; nociceptin/orphanin
peptide
ID POSITRON-EMISSION-TOMOGRAPHY; ANTI-OPIOID PEPTIDE; IN-VIVO;
PHARMACOLOGICAL CHARACTERIZATION; ANTAGONIST SB-612111; ORPHANIN FQ;
BINDING; LOCALIZATION; EXPRESSION; MODEL
AB Our laboratory developed (S)-3-(2'-fluoro-6',7'-dihydrospiro [piperidine-4,4'-thieno[3,2-c]pyran]-1-yl)-2-(2-fluorobenzyl)-N-methylpropanamide (C-11-NOP-1A), a new radioligand for the nociceptin/orphanin FQ peptide (NOP) receptor, with high affinity (K-i, 0.15 nM) and appropriate lipophilicity (measured logD, 3.4) for PET brain imaging. Here, we assessed the utility of C-11-NOP-1A for quantifying NOP receptors in the monkey brain and estimated the radiation safety profile of this radioligand based on its biodistribution in monkeys. Methods: Baseline and blocking PET scans were acquired from head to thigh for 3 rhesus monkeys for approximately 120 min after C-11-NOP-1A injection. These 6 PET scans were used to quantify NOP receptors in the brain and to estimate radiation exposure to organs of the body. In the blocked scans, a selective nonradioactive NOP receptor antagonist (SB-612111; 1 mg/kg intravenously) was administered before C-11-NOP-1A. In all scans, arterial blood was sampled to measure the parent radioligand C-11-NOP-1A. Distribution volume (V-T; a measure of receptor density) was calculated with a compartment model using brain and arterial plasma data. Radiation-absorbed doses were calculated using the MIRD Committee scheme. Results: After C-11-NOP-1A injection, peak uptake of radioactivity in the brain had a high concentration (similar to 5 standardized uptake value), occurred early (similar to 12 min), and thereafter washed out quickly. V-T (mL . cm(-3)) was highest in the neocortex (similar to 20) and lowest in hypothalamus and cerebellum (similar to 13). SB-612111 blocked approximately 50%-70% of uptake and reduced V-T in all brain regions to approximately 7 mL . cm(-3). Distribution was well identified within 60 min of injection and stable for the remaining 60 min, consistent with only parent radioligand and not radiometabolites entering the brain. Whole-body scans confirmed that the brain had specific (i.e., displaceable) binding but could not detect specific binding in peripheral organs. The effective dose for humans estimated from the baseline scans in monkeys was 5.0 mSv/MBq. Conclusion: C-11-NOP-1A is a useful radioligand for quantifying NOP receptors in the monkey brain, and its radiation dose is similar to that of other C-11-labeled ligands for neuroreceptors. C-11-NOP-1A appears to be a promising candidate for measuring NOP receptors in the human brain.
C1 [Kimura, Yasuyuki; Fujita, Masahiro; Hong, Jinsoo; Lohith, Talakad G.; Gladding, Robert L.; Zoghbi, Sami S.; Pike, Victor W.; Innis, Robert B.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Kimura, Yasuyuki] Natl Inst Radiol Sci, Dept Mol Neuroimaging, Mol Imaging Ctr, Chiba 260, Japan.
[Tauscher, Johannes A.; Goebl, Nancy; Rash, Karen S.; Chen, Zhaogen; Pedregal, Concepcion; Barth, Vanessa N.] Eli Lilly & Co, Indianapolis, IN 46285 USA.
RP Innis, RB (reprint author), NIMH, Mol Imaging Branch, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM robert.innis@nih.gov
RI Kimura, Yasuyuki/D-4459-2016; Tauscher, Johannes/M-5976-2016
OI Kimura, Yasuyuki/0000-0002-7927-9483;
FU National Institute of Mental Health, National Institutes of Health; Eli
Lilly
FX We thank Kacey Anderson, Leah P. Dickstein, Kimberly Jenko, Nobuyo
Kimura, Cheryl L. Wallisch, Jeih-San Liow, Harushige Ozaki, and the
staff of the PET Department for assistance in completing these studies
and PMOD Technologies (Zurich, Switzerland) for providing its image
analysis and modeling software. Ioline Henter provided invaluable
editorial assistance. Garth Terry created the table for scaling factors
for organs in monkey and man. This study was supported by the Intramural
Research Program of the National Institute of Mental Health, National
Institutes of Health, and by a Cooperative Research and Development
Agreement with Eli Lilly. No other potential conflict of interest
relevant to this article was reported.
NR 27
TC 19
Z9 19
U1 0
U2 2
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD OCT 1
PY 2011
VL 52
IS 10
BP 1638
EP 1645
DI 10.2967/jnumed.111.091181
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 828XM
UT WOS:000295537800024
PM 21880575
ER
PT J
AU Sutin, AR
Stockdale, GD
AF Sutin, Angelina R.
Stockdale, Gary D.
TI Trait Dissociation and the Subjective Affective, Motivational, and
Phenomenological Experience of Self-Defining Memories
SO JOURNAL OF PERSONALITY
LA English
DT Article
ID AUTOBIOGRAPHICAL MEMORIES; NONCLINICAL POPULATION;
INDIVIDUAL-DIFFERENCES; COGNITIVE-PROCESSES; PERSONAL STRIVINGS; SCALE;
RELIABILITY; VALIDITY; DISTURBANCES; TENDENCIES
AB The present research reports 2 studies that examine the relation between nonpathological trait dissociation and the subjective affect, motivation, and phenomenology of self-defining memories. In Study 1 (N = 293), participants retrieved and rated the emotional and motivational experience of a general and a positive and negative achievement-related memory. Study 2 (N = 449) extended these ratings to relationship-related memories and the phenomenological experience of the memory. Dissociation was associated with incongruent affect in valenced memories (e. g., positive affect in a negative memory) and memories that were visually incoherent and saturated with power motivation, hubristic pride, and shame, regardless of valence or domain. The present findings demonstrate that autobiographical memories, which integrate emotional, motivational, and phenomenological components, reflect the emotional and motivational processes inherent to dissociation.
C1 [Sutin, Angelina R.] NIA, Lab Personal & Cognit, NIH, DHHS, Baltimore, MD 21224 USA.
[Stockdale, Gary D.] Univ Calif Davis, Davis, CA 95616 USA.
RP Sutin, AR (reprint author), NIA, Lab Personal & Cognit, NIH, DHHS, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM sutina@mail.nih.gov
FU Intramural NIH HHS [Z99 AG999999]
NR 51
TC 5
Z9 5
U1 0
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3506
J9 J PERS
JI J. Pers.
PD OCT
PY 2011
VL 79
IS 5
BP 939
EP 963
DI 10.1111/j.1467-6494.2010.00708.x
PG 25
WC Psychology, Social
SC Psychology
GA 824UN
UT WOS:000295227800003
PM 21204840
ER
PT J
AU Yadav, PN
Kroeze, WK
Farrell, MS
Roth, BL
AF Yadav, Prem N.
Kroeze, Wesley K.
Farrell, Martilias S.
Roth, Bryan L.
TI Antagonist Functional Selectivity: 5-HT2A Serotonin Receptor Antagonists
Differentially Regulate 5-HT2A Receptor Protein Level In Vivo
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID 5-HYDROXYTRYPTAMINE(2A) RECEPTOR; NEUROLEPTIC AGENTS; DRUG DISCOVERY;
RAT-BRAIN; BINDING; VITRO; MIANSERIN; AGONIST; INTERNALIZATION;
SCHIZOPHRENIA
AB Dysregulation of the 5-HT2A receptor is implicated in both the etiology and treatment of schizophrenia. Although the essential role of 5-HT2A receptors in atypical antipsychotic drug actions is widely accepted, the contribution of 5-HT2A down-regulation to their efficacy is not known. We hypothesized that down-regulation of cortical 5-HT2A receptors contributes to the therapeutic action of atypical antipsychotic drugs. To test this hypothesis, we assessed the effect of chronically administered antipsychotics (clozapine, olanzapine, and haloperidol) and several 5-HT2A antagonists [ketanserin, altanserin, alpha-(2,3-dimethoxyphenyl)-1-[ 2-(4-fluorophenylethyl)]-4-piperidinemethanol (M100907), alpha-phenyl-1-(2-phenylethyl)-4-piperidinemethano (M11939), 4-[(2Z)-3-{[2-(dimethylamino)ethoxy]amino}-3-(2-fluorophenyl)prop-2-en-1-ylidene]cyclohexa-2,5-dien-1-one (SR46349B), and pimavanserin], on the phencyclidine (PCP)-induced hyperlocomotor response and cortical 5-HT2A receptor levels in C57BL/6J mice. Clozapine and olanzapine, but not haloperidol, induced receptor down-regulation and attenuated PCP-induced locomotor responses. Of the selective 5-HT2A antagonists tested, only ketanserin caused significant receptor protein down-regulation, whereas SR46349B up-regulated 5-HT2A receptors and potentiated PCP-hyperlocomotion; the other 5-HT2A receptor antagonists were without effect. The significance of these findings with respect to atypical antipsychotic drug action is discussed.
C1 [Yadav, Prem N.; Kroeze, Wesley K.; Farrell, Martilias S.; Roth, Bryan L.] Univ N Carolina, Chapel Hill Med Sch, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] Univ N Carolina, Chapel Hill Med Sch, Dept Med Chem, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] Univ N Carolina, Chapel Hill Med Sch, Dept Psychiat, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] Univ N Carolina, Chapel Hill Med Sch, Program Neurosci, Chapel Hill, NC 27599 USA.
[Roth, Bryan L.] Univ N Carolina, Chapel Hill Med Sch, Natl Inst Mental Hlth, Psychoact Drug Screening Program, Chapel Hill, NC 27599 USA.
RP Roth, BL (reprint author), Univ N Carolina, Chapel Hill Med Sch, Dept Pharmacol, 4072 Genet Med Bldg,120 Mason Farm Rd, Chapel Hill, NC 27599 USA.
EM bryan_roth@med.unc.edu
RI Roth, Bryan/F-3928-2010
FU National Institutes of Health National Institute of Mental Health
[U19-MH82441, R01-MH61887]; Michael Hooker Chair
FX This work was supported by the National Institutes of Health National
Institute of Mental Health [Grants U19-MH82441, R01-MH61887] (to B.L.R.)
and the Michael Hooker Chair.
NR 39
TC 28
Z9 29
U1 1
U2 6
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 2011
VL 339
IS 1
BP 99
EP 105
DI 10.1124/jpet.111.183780
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 821UC
UT WOS:000294998900011
PM 21737536
ER
PT J
AU Jutkiewicz, EM
Brooks, EA
Kynaston, AD
Rice, KC
Woods, JH
AF Jutkiewicz, Emily M.
Brooks, Emily A.
Kynaston, Adam D.
Rice, Kenner C.
Woods, James H.
TI Patterns of Nicotinic Receptor Antagonism: Nicotine Discrimination
Studies
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID DIHYDRO-BETA-ERYTHROIDINE; APPARENT PA(2) ANALYSIS; DRUG DISCRIMINATION;
STIMULUS PROPERTIES; SMOKING-CESSATION; ACETYLCHOLINE-RECEPTORS;
SUBSTITUTION PATTERNS; LABORATORY-ANIMALS; INTRINSIC EFFICACY; DEPOT
NALTREXONE
AB Evaluation of the discriminative stimulus effects of drugs is a useful procedure for identification of receptor mediation of in vivo drug effects. This assay can be enhanced when the stimulus effects of different doses of agonist are evaluated. In the present study, rats were trained to discriminate small or large doses of nicotine from saline, and interactions of these effects with nicotinic receptor antagonists and partial agonists were determined. The insurmountable nicotine antagonist mecamylamine blocked both the discriminative stimulus and response rate-reducing effects of nicotine but was less effective against the large dose of nicotine. The alpha 4 beta 2*-selective, competitive antagonist dihydro-beta-erythrodine (DH beta E) antagonized the discriminative stimulus effects of both doses but was less effective against the larger training dose of nicotine. Schild analyses of DH beta E suggested that different nicotinic receptor populations may be mediating the stimulus effects of large and small doses of nicotine. This suggestion was supported by observations that the discriminative stimulus effects of the partial agonist cytisine were more like those of the large dose than of the small dose of nicotine and that cytisine antagonized the effects of only the small nicotine dose. Varenicline produced nicotine-like effects in both training dose groups but reduced the discriminative stimulus effects of intermediate doses of nicotine in the group trained to the small dose of nicotine. Overall, these results suggest that small doses of nicotine produce their stimulus effects via alpha 4 beta 2* nicotine receptors, whereas larger doses of nicotine recruit additional nicotine receptor subtypes, as revealed by drug discrimination assays in rats.
C1 [Jutkiewicz, Emily M.; Brooks, Emily A.; Kynaston, Adam D.; Woods, James H.] Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48109 USA.
[Woods, James H.] Univ Michigan, Dept Psychol, Ann Arbor, MI 48109 USA.
[Rice, Kenner C.] NIDA, Chem Biol Res Branch, Bethesda, MD 20892 USA.
[Rice, Kenner C.] NIAAA, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
RP Woods, JH (reprint author), Univ Michigan, Dept Pharmacol, 1301 MSRB III,1150 W Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM jhwoods@umich.edu
FU National Institutes of Health National Institute on Drug Abuse
[T32-DA007268]; National Institute on Alcohol Abuse and Alcoholism;
University of Michigan Tobacco Research Network
FX This work was supported in part by the Intramural Research Programs of
the National Institutes of Health National Institute on Drug Abuse and
the National Institute on Alcohol Abuse and Alcoholism; the National
Institutes of Health National Institute on Drug Abuse [Grant
T32-DA007268]; and the University of Michigan Tobacco Research Network.
NR 56
TC 23
Z9 23
U1 1
U2 3
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD OCT
PY 2011
VL 339
IS 1
BP 194
EP 202
DI 10.1124/jpet.111.182170
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 821UC
UT WOS:000294998900021
PM 21730011
ER
PT J
AU Kulyyassov, A
Shoaib, M
Pichugin, A
Kannouche, P
Ramanculov, E
Lipinski, M
Ogryzko, V
AF Kulyyassov, Arman
Shoaib, Muhammad
Pichugin, Andrei
Kannouche, Patricia
Ramanculov, Erlan
Lipinski, Marc
Ogryzko, Vasily
TI PUB-MS: A Mass Spectrometry-based Method to Monitor Protein-Protein
Proximity in vivo
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE protein-protein interactions; biotinylation; proximity; multiplexing;
pulse-chase; SILAC
ID RESONANCE ENERGY-TRANSFER; INACTIVE X-CHROMOSOME; FRAGMENT
COMPLEMENTATION ASSAYS; CHROMATIN IMMUNOPRECIPITATION;
SELF-ORGANIZATION; HISTONE H2A; BIOTINYLATION; COMPLEX; CELLS; DNA
AB The common techniques to study protein-protein proximity in vivo are not well adapted to the capabilities and the expertise of a standard proteomics laboratory, typically based on the use of mass spectrometry. With the aim of closing this gap, we have developed PUB-MS (for proximity utilizing biotinylation and mass spectrometry), an approach to monitor protein-protein proximity, based on biotinylation of a protein fused to a biotin-acceptor peptide (BAP) by a biotin-ligase, BirA, fused to its interaction partner. The biotinylation status of the BAP can be further detected by either Western analysis or mass spectrometry. The BAP sequence was redesigned for easy monitoring of the biotinylation status by LC-MS/MS. In several experimental models, we demonstrate that the biotinylation in vivo is specifically enhanced when the BAP- and BirA-fused proteins are in proximity to each other. The advantage of mass spectrometry is demonstrated by using BAPs with different sequences in a single experiment (allowing multiplex analysis) and by the use of stable isotopes. Finally, we show that our methodology can be also used to study a specific subfraction of a protein of interest that was in proximity with another protein at a predefined time before the analysis.
C1 [Kulyyassov, Arman; Shoaib, Muhammad; Pichugin, Andrei; Kannouche, Patricia; Lipinski, Marc; Ogryzko, Vasily] Inst Gustave Roussy, F-94805 Villejuif, France.
[Kulyyassov, Arman; Ramanculov, Erlan] Natl Biotechnol Ctr, Astana 01000, Kazakhstan.
RP Ogryzko, V (reprint author), Inst Gustave Roussy, 39 Rue Camilles Desmoulin, F-94805 Villejuif, France.
EM vogryzko@gmail.com
RI Ramanculov, Erlan/E-2823-2013; Ogryzko, Vasily/M-6665-2015;
OI Ogryzko, Vasily/0000-0002-8548-1389; Kulyyassov,
Arman/0000-0002-7932-5689
FU La Ligue Contre le Cancer [9ADO1217/1B1-BIOCE]; Institut National du
Cancer [247343/1B1-BIOCE]; Centre National de la Recherche Scientifique
[CNRS-INCA-MSHE] [3037987]; NCB Kazakhstan [0103_00404]
FX We thank Dr. M. Lechner (Drexel University, Philadelphia) for the
KAP1-HP1BDwt and KAP1-HP1BDwt plasmids, Drs H. Willard and M. Chadwick
(Case Western Reserve University, Cleveland) for the ORFs of the H2A.BBD
and macroH2A, and Dr. L. L. Pritchard for critical reading of the
manuscript. We also thank Chloe Robin for the Figure 2C. This work was
supported by grants from "La Ligue Contre le Cancer"
(9ADO1217/1B1-BIOCE), the "Institut National du Cancer"
(247343/1B1-BIOCE) and Centre National de la Recherche Scientifique
[CNRS-INCA-MSHE Franco-Pologne #3037987) to VO, by NCB Kazakhstan
(0103_00404) to AK and by a travel grant to AK. from the Cooperation
Universitaire et Scientifique Department of the French Embassy in
Astana, Kazakhstan.
NR 37
TC 7
Z9 8
U1 1
U2 14
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
J9 J PROTEOME RES
JI J. Proteome Res.
PD OCT
PY 2011
VL 10
IS 10
BP 4416
EP 4427
DI 10.1021/pr200189p
PG 12
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 829RT
UT WOS:000295602700006
PM 21842862
ER
PT J
AU Avital, I
AF Avital, Itzhak
TI Regional Chemotherapy for Pancreatic Cancer
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Editorial Material
ID STATISTICS
C1 NCI, USUHS, Head GI & Hepatobiliary Malignancies Sect, Surg Branch,NIH, Bethesda, MD 20892 USA.
RP Avital, I (reprint author), NCI, USUHS, Head GI & Hepatobiliary Malignancies Sect, Surg Branch,NIH, 10 Ctr Dr,CRC Room 4-3961, Bethesda, MD 20892 USA.
EM avitali@mail.nih.gov
NR 4
TC 1
Z9 3
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-4790
J9 J SURG ONCOL
JI J. Surg. Oncol.
PD OCT
PY 2011
VL 104
IS 5
BP 453
EP 453
DI 10.1002/jso.21975
PG 1
WC Oncology; Surgery
SC Oncology; Surgery
GA 828WR
UT WOS:000295535400001
PM 21618244
ER
PT J
AU Kreimer, AR
Rodriguez, AC
Hildesheim, A
Herrero, R
Porras, C
Schiffman, M
Gonzalez, P
Solomon, D
Jimenez, S
Schiller, JT
Lowy, DR
Quint, W
Sherman, ME
Schussler, J
Wacholder, S
AF Kreimer, Aimee R.
Cecilia Rodriguez, Ana
Hildesheim, Allan
Herrero, Rolando
Porras, Carolina
Schiffman, Mark
Gonzalez, Paula
Solomon, Diane
Jimenez, Silvia
Schiller, John T.
Lowy, Douglas R.
Quint, Wim
Sherman, Mark E.
Schussler, John
Wacholder, Sholom
CA CVT Vaccine Grp
TI Proof-of-Principle Evaluation of the Efficacy of Fewer Than Three Doses
of a Bivalent HPV16/18 Vaccine
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS; BROAD-SPECTRUM; PCR; INFECTION; TRIAL; ASSAY
AB Background Three-dose regimens for human papillomavirus (HPV) vaccines are expensive and difficult to complete, especially in settings where the need for cervical cancer prevention is greatest.
Methods We evaluated the vaccine efficacy of fewer than three doses of the HPV16/18 vaccine Cervarix in our Costa Rica Vaccine Trial. Women were randomly assigned to receive three doses of the HPV16/18 vaccine or to a control vaccine and were followed for incident HPV16 or HPV18 infection that persisted in visits that were 10 or more months apart (median follow-up 4.2 years). After excluding women who had no follow-up or who were HPV16 and HPV18 DNA positive at enrollment, 5967 women received three vaccine doses (2957 HPV vaccine vs 3010 control vaccine), 802 received two doses (422 HPV vs 380 control), and 384 received one dose (196 HPV vs 188 control). Reasons for receiving fewer doses and other pre- and post-randomization characteristics were balanced within each dosage group between women receiving the HPV and control vaccines.
Results Incident HPV16 or HPV18 infections that persisted for 1 year were unrelated to dosage of the control vaccine. Vaccine efficacy was 80.9% for three doses of the HPV vaccine (95% confidence interval [CI] = 71.1% to 87.7%; 25 and 133 events in the HPV and control arms, respectively), 84.1% for two doses (95% CI = 50.2% to 96.3%; 3 and 17 events), and 100% for one dose (95% CI = 66.5% to 100%; 0 and 10 events).
Conclusion Four years after vaccination of women who appeared to be uninfected, this nonrandomized analysis suggests that two doses of the HPV16/18 vaccine, and maybe even one dose, are as protective as three doses.
C1 [Kreimer, Aimee R.; Hildesheim, Allan] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Sherman, Mark E.] NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Wacholder, Sholom] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Schiffman, Mark] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Solomon, Diane] NCI, Breast & Gynecol Canc Res Grp, Canc Prevent Div, NIH, Rockville, MD 20852 USA.
[Schiller, John T.; Lowy, Douglas R.] NCI, Cellular Oncol Lab, Ctr Canc Res, NIH, Rockville, MD 20852 USA.
[Cecilia Rodriguez, Ana; Herrero, Rolando; Porras, Carolina; Gonzalez, Paula; Jimenez, Silvia] Fdn INCIENSA, Proyecto Epidemiol Guanacaste, San Jose, Costa Rica.
[Quint, Wim] DDL Diagnost Lab, Voorburg, Netherlands.
[Schussler, John] Informat Management Syst, Rockville, MD USA.
[Herrero, Rolando] Int Agcy Res Canc, Early Detect & Prevent Sect, F-69372 Lyon, France.
RP Kreimer, AR (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS 7084, Rockville, MD 20852 USA.
EM kreimera@mail.nih.gov
RI Hildesheim, Allan/B-9760-2015; Kreimer, Aimee/H-1687-2015
OI Hildesheim, Allan/0000-0003-0257-2363;
FU NCI [N01-CP-11005]; National Institutes of Health Office of Research on
Women's Health; Ministry of Health of Costa Rica
FX The Costa Rica HPV Vaccine Trial is a long-standing collaboration
between investigators in Costa Rica and the US National Cancer Institute
(NCI). The trial is sponsored and funded by the NCI (contract
N01-CP-11005), with funding support from the National Institutes of
Health Office of Research on Women's Health.; This study was conducted
with the support from the Ministry of Health of Costa Rica. Vaccine was
provided for our trial by GlaxoSmithKline Biologicals (GSK), under a
Clinical Trials Agreement with the NCI. GSK also provided support for
aspects of the trial associated with regulatory submission needs of the
company under FDA BB-IND 7920. SchillerJ. T. Schiller and D. R. Lowy
report that they are named inventors on US government-owned HPV vaccine
patents that are licensed to GSK and Merck and for which the NCI
receives licensing fees. J. T. Schiller and D. R. Lowy are entitled to
limited royalties as specified by federal law. No other financial
disclosures were reported.
NR 19
TC 170
Z9 170
U1 2
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 OCT
PY 2011
VL 103
IS 19
BP 1444
EP 1451
DI 10.1093/jnci/djr319
PG 8
WC Oncology
SC Oncology
GA 830UX
UT WOS:000295683800008
PM 21908768
ER
PT J
AU Schiffman, M
Wentzensen, N
Wacholder, S
Kinney, W
Gage, JC
Castle, PE
AF Schiffman, Mark
Wentzensen, Nicolas
Wacholder, Sholom
Kinney, Walter
Gage, Julia C.
Castle, Philip E.
TI Re: Human Papillomavirus Testing in the Prevention of Cervical Cancer
Response
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Letter
C1 [Schiffman, Mark; Wentzensen, Nicolas; Wacholder, Sholom; Gage, Julia C.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Kinney, Walter] Kaiser Permanente Med Care Program, Div Gynecol Oncol, Oakland, CA USA.
[Castle, Philip E.] Amer Soc Clin Pathologists, Washington, DC USA.
RP Schiffman, M (reprint author), Rm 7012,6120 Execut Blvd, Rockville, MD 20852 USA.
EM schiffmm@mail.nih.gov
NR 7
TC 1
Z9 1
U1 0
U2 1
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 OCT
PY 2011
VL 103
IS 19
BP 1483
EP U73
DI 10.1093/jnci/djr309
PG 2
WC Oncology
SC Oncology
GA 830UX
UT WOS:000295683800016
ER
PT J
AU Brewinski, M
Megazzini, K
Hance, LF
Cruz, MC
Pavia-Ruz, N
Della Negra, M
Ferreira, FGF
Marques, H
Hazra, R
AF Brewinski, Margaret
Megazzini, Karen
Hance, Laura Freimanis
Cashat Cruz, Miguel
Pavia-Ruz, Noris
Della Negra, Marinella
Faleiro Ferreira, Flavia Gomes
Marques, Heloisa
Hazra, Rohan
CA NISDI Pediat Study Grp 2010
TI Dyslipidemia in a Cohort of HIV-infected Latin American Children
Receiving Highly Active Antiretroviral Therapy*
SO JOURNAL OF TROPICAL PEDIATRICS
LA English
DT Article
DE HIV; cholesterol; triglycerides; pediatric
ID CARDIOVASCULAR RISK-FACTORS; PROTEASE INHIBITORS; YOUNG; ASSOCIATION;
CHILDHOOD; ATHEROSCLEROSIS; DISEASE; OBESITY
AB In order to describe the prevalence of hypercholesterolemia and hypertriglyceridemia in a cohort of HIV-infected children and adolescents in Latin America and to determine associations with highly active antiretroviral therapy (HAART), we performed this cross-sectional analysis within the NICHD International Site Development Initiative pediatric cohort study. Eligible children had to be at least 2 years of age and be on HAART. Among the 477 eligible HIV-infected youth, 98 (20.5%) had hypercholesterolemia and 140 (29.4%) had hypertriglyceridemia. In multivariable analyses, children receiving protease inhibitor (PI)-containing HAART were at increased risk for hypercholesterolemia [adjusted odds ratio (AOR) = 2.7, 95% confidence interval (CI) 1.3-5.6] and hypertriglyceridemia (AOR = 3.5, 95% CI 1.9-6.4) compared with children receiving non-nucleoside reverse transcriptase inhibitor (NNRTI)-containing HAART. In conclusion, HIV-infected youth receiving PI-containing HAART in this Latin American cohort were at increased risk for hypercholesterolemia and hypertriglyceridemia compared with those receiving NNRTI-containing HAART.
C1 [Hazra, Rohan] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Adolescent & Maternal AIDS Branch, Ctr Res Mothers & Children, NIH, Bethesda, MD 20892 USA.
[Brewinski, Margaret] US Agcy Int Dev, Off HIV AIDS, Washington, DC 20005 USA.
[Megazzini, Karen; Hance, Laura Freimanis] Westat Corp, Rockville, MD 20850 USA.
[Cashat Cruz, Miguel; Pavia-Ruz, Noris] Hosp Infantil Mexico Dr Federico Gomez, Dept Infectol, Clin Inmunodeficiencias, Federico Gomez 06720, Mexico.
[Della Negra, Marinella] Inst Infectol Emilio Ribas, BR-02146900 Sao Paulo, Brazil.
[Faleiro Ferreira, Flavia Gomes] Univ Fed Minas Gerais, Sch Med, BR-30130100 Belo Horizonte, MG, Brazil.
[Marques, Heloisa] Univ Sao Paulo, Inst Crianca HCFM, BR-05403900 Sao Paulo, Brazil.
RP Hazra, R (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Adolescent & Maternal AIDS Branch, Ctr Res Mothers & Children, NIH, 6100 Execut Blvd,Room 4B11, Bethesda, MD 20892 USA.
EM hazrar@mail.nih.gov
RI Mussi-Pinhata, Marisa/G-6568-2012
FU National Institutes of Health (NICHD) [HHSN2672008 00001C,
N01-HD-3-3345, N01-HD-8-0001]
FX This work was supported by the National Institutes of Health (NICHD
Contract # HHSN2672008 00001C [NICHD Control #: N01-HD-3-3345 and
N01-HD-8-0001]).
NR 26
TC 7
Z9 7
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0142-6338
J9 J TROP PEDIATRICS
JI J. Trop. Pediatr.
PD OCT
PY 2011
VL 57
IS 5
BP 324
EP 332
DI 10.1093/tropej/fmq089
PG 9
WC Pediatrics; Tropical Medicine
SC Pediatrics; Tropical Medicine
GA 828VU
UT WOS:000295532600003
PM 20889625
ER
PT J
AU Ballyns, JJ
Shah, JP
Hammond, J
Gebreab, T
Gerber, LH
Sikdar, S
AF Ballyns, Jeffrey J.
Shah, Jay P.
Hammond, Jennifer
Gebreab, Tadesse
Gerber, Lynn H.
Sikdar, Siddhartha
TI Objective Sonographic Measures for Characterizing Myofascial Trigger
Points Associated With Cervical Pain
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Article
DE color Doppler imaging; elastography; myofascial trigger points;
sonography
ID SKELETAL-MUSCLE; BLOOD-FLOW; SOFT-TISSUE; ANGIOGENESIS; INFLAMMATION;
PRESSURE; REMOTE; MTRPS
AB Objectives-The purpose of this study was to determine whether the physical properties and vascular environment of active myofascial trigger points associated with acute spontaneous cervical pain, asymptomatic latent trigger points, and palpably normal muscle differ in terms of the trigger point area, pulsatility index, and resistivity index, as measured by sonoelastography and Doppler imaging.
Methods-Sonoelastography was performed with an external 92-Hz vibration in the upper trapezius muscles in patients with acute cervical pain and at least 1 palpable trigger point (n = 44). The area of reduced vibration amplitude was measured as an estimate of the size of the stiff myofascial trigger points. Patients also underwent triplex Doppler imaging of the same region to analyze blood flow waveforms and calculate the pulsatility index of blood flow in vessels at or near the trigger points.
Results On sonoelastography, active sites (spontaneously painful with palpable myofascial trigger points) had larger trigger points (mean +/- SD, 0.57 +/- 0.20 cm(2)) compared to latent sites (palpable trigger points painful on palpation; 0.36 +/- 0.16 cm(2)) and palpably normal sites (0.17 +/- 0.22 cm(2); P <.01). Analysis of receiver operating characteristic curves showed that area measurements could robustly distinguish between active, latent, and normal sites (areas under the curve, 0.9 for active versus latent, 0.8 for active versus normal, and 0.8 for latent versus normal, respectively). Doppler spectral waveform data showed that vessels near active sites had a significantly higher pulsatility index (median, 8.3) compared to normal sites (median, 3.0; P <.05).
Conclusions-The results presented in this study show that myofascial trigger points may be classified by area using sonoelastography. Furthermore, monitoring the trigger point area and pulsatility index may be useful in evaluating the natural history of myofascial pain syndrome.
C1 [Ballyns, Jeffrey J.; Sikdar, Siddhartha] George Mason Univ, Dept Elect & Comp Engn, Fairfax, VA 22030 USA.
[Gerber, Lynn H.] George Mason Univ, Coll Hlth & Human Serv, Fairfax, VA 22030 USA.
[Shah, Jay P.; Hammond, Jennifer; Gebreab, Tadesse] 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
FU National Institutes of Health (NIH); Clinical Center and Office of the
Director, NIH [1R01-AR057348]; National Institutes of Arthritis and
Musculoskeletal and Skin Diseases, NIH
FX This research was supported in part by the Intramural Research Program,
National Institutes of Health (NIH), the Clinical Center and Office of
the Director, NIH, and grant 1R01-AR057348 from the National Institutes
of Arthritis and Musculoskeletal and Skin Diseases, NIH.
NR 36
TC 36
Z9 37
U1 0
U2 4
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
USA
SN 0278-4297
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD OCT
PY 2011
VL 30
IS 10
BP 1331
EP 1340
PG 10
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 829BW
UT WOS:000295551300003
PM 21968483
ER
PT J
AU Brown, P
Gipson, C
AF Brown, Patricia
Gipson, Chester
TI A word from OLAW and USDA
SO LAB ANIMAL
LA English
DT Editorial Material
C1 [Brown, Patricia] NIH, OLAW, OER, OD,HHS, Bethesda, MD 20892 USA.
[Gipson, Chester] USDA, APHIS, AC, Washington, DC USA.
RP Brown, P (reprint author), NIH, OLAW, OER, OD,HHS, Bethesda, MD 20892 USA.
NR 5
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0093-7355
J9 LAB ANIMAL
JI Lab Anim.
PD OCT
PY 2011
VL 40
IS 10
BP 297
EP 297
PG 1
WC Veterinary Sciences
SC Veterinary Sciences
GA 830ZQ
UT WOS:000295698800016
PM 22358204
ER
PT J
AU Guardiani, E
Zalewski, C
Brewer, C
Merideth, M
Introne, W
Smith, ACM
Gordon, L
Gahl, W
Kim, HJ
AF Guardiani, Elizabeth
Zalewski, Christopher
Brewer, Carmen
Merideth, Melissa
Introne, Wendy
Smith, Ann C. M.
Gordon, Leslie
Gahl, William
Kim, H. Jeffrey
TI Otologic and Audiologic Manifestations of Hutchinson-Gilford Progeria
Syndrome
SO LARYNGOSCOPE
LA English
DT Article
DE Hutchinson-Gilford Progeria syndrome; hearing loss; progeria; middle
ear; external ear
ID SENSORINEURAL HEARING-LOSS; PHENOTYPE; RECURRENT; CHILDREN
AB Objectives/Hypothesis: To define the audiologic and otologic phenotype of Hutchinson-Gilford progeria syndrome (HGPS).
Study Design: Prospective case series.
Methods: Fifteen patients with HGPS were enrolled in a prospective natural history study; 14 were evaluated in the neurotology clinic, and 11 received audiologic evaluations. The physical exam and audiologic findings of these patients were reviewed to define an otologic and audiologic phenotype for HGPS in the largest series of subjects in the literature.
Results: All patients were noted to have stiff auricular cartilages, small or absent lobules, and hypoplasia of the lateral soft-tissue portion of the external ear canal leading to a shortened canal. Ten of 14 patients (71%) had dry cerumen impaction, and four of 14 patients (29%) reported a history of recurrent otitis media. Nineteen of 22 ears (86.4%) demonstrated low-frequency conductive hearing loss in the 250 to 500 Hz range. Sixteen of 22 ears (73%) had type A tympanograms; three of 22 ears (14%) displayed bimodal or "W" peaked tympanograms; two of 22 ears (9%) had type B tympanograms; one of 22 ears (4%) had a type C tympanogram. Nine of 10 patients had distortion product otoacoustic emissions consistent with normal peripheral hearing sensitivity.
Conclusions: HGPS is caused by a mutation in the LMNA gene resulting in the production of an abnormal nuclear protein; this in turn affects nuclear structure and function. Patients with HGPS have characteristic otologic features due to cartilaginous and subcutaneous tissue abnormalities and typically demonstrate low-frequency conductive hearing loss despite largely normal tympanometry. It is important to be aware of these conditions in managing these patients.
C1 [Guardiani, Elizabeth; Kim, H. Jeffrey] Georgetown Univ Hosp, Dept Otolaryngol Head & Neck Surg, Washington, DC 20007 USA.
[Zalewski, Christopher; Brewer, Carmen; Kim, H. Jeffrey] Natl Inst Deafness & Other Commun Disorders, Bethesda, MD USA.
[Merideth, Melissa; Introne, Wendy; Smith, Ann C. M.; Gahl, William] NHGRI, Bethesda, MD 20892 USA.
[Gordon, Leslie] Brown Univ, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Gordon, Leslie] Hasbro Childrens Hosp, Dept Pediat, Providence, RI USA.
[Gordon, Leslie] Harvard Univ, Sch Med, Dept Anesthesia, Childrens Hosp Boston, Boston, MA 02115 USA.
RP Kim, HJ (reprint author), Georgetown Univ Hosp, Dept Otolaryngol Head & Neck Surg, 1st Floor Gorman Bldg,3800 Reservoir Rd NW, Washington, DC 20007 USA.
EM hk7@georgetown.edu
RI SMITH, ANN C.M./C-1122-2008
FU National Human Genome Research Institute; National Institute on Deafness
and Other Communication Disorders
FX This work was supported by the intramural research programs of the
National Human Genome Research Institute and the National Institute on
Deafness and Other Communication Disorders. The authors have no other
funding, financial relationships, or conflicts of interest to disclose.
NR 25
TC 4
Z9 4
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0023-852X
J9 LARYNGOSCOPE
JI Laryngoscope
PD OCT
PY 2011
VL 121
IS 10
BP 2250
EP 2255
DI 10.1002/lary.22151
PG 6
WC Medicine, Research & Experimental; Otorhinolaryngology
SC Research & Experimental Medicine; Otorhinolaryngology
GA 824UX
UT WOS:000295228800036
PM 21898437
ER
PT J
AU Shevtsov, AB
Kushugulova, AR
Tynybaeva, IK
Kozhakhmetov, SS
Abzhalelov, AB
Momynaliev, KT
Stoyanova, LG
AF Shevtsov, A. B.
Kushugulova, A. R.
Tynybaeva, I. K.
Kozhakhmetov, S. S.
Abzhalelov, A. B.
Momynaliev, K. T.
Stoyanova, L. G.
TI Identification of phenotypically and genotypically related Lactobacillus
strains based on nucleotide sequence analysis of the groEL, rpoB, rplB,
and 16S rRNA genes
SO MICROBIOLOGY
LA English
DT Article
DE national fermented milk drinks; identification; genotyping;
Lactobacillus; 16S rRNA genes; groEL; rplB; rpoB genes
ID ALIGNMENT; BACTERIA; PRODUCTS
AB Sixty-eight cultures of lactic acid bacteria were isolated and identified from national fermented milk drinks (airan, koumiss, kurunga, shubat) home-made in different regions of the Republic of Kazakhstan and the Buryat Republic of Russia. The cultures of lactic acid bacteria of the genus Lactobacillus were identified as L. paracasei and L. rhamnosus related to the L. casei group and as L. brevis, L. buchneri, L. diolivorans, and L. parabuchneri (the L. buchneri group) using the classical microbiological methods and on the basis of the 16S rRNA gene sequence analysis. The polymorphism of the nucleotide sequences of the genes groEL, rpoB, and rplB encoding specific proteins was studied for intraspecific differentiation of the lactobacilli. The analysis of these genes allowed a more accurate identification of the lactobacilli that are genetically and phenotypically related to the L. casei group as L. paracasei subsp. paracasei and L. paracasei subsp. tolerans. The gene nucleotide sequences of all the genotyped strains were deposited in the GenBank database.
C1 [Stoyanova, L. G.] Moscow MV Lomonosov State Univ, Fac Biol, Dept Microbiol, Moscow 119992, Russia.
[Shevtsov, A. B.; Momynaliev, K. T.] Republ Kazakhstan Natl Ctr Biotechnol, Astana, Kazakhstan.
[Kushugulova, A. R.; Tynybaeva, I. K.; Kozhakhmetov, S. S.; Abzhalelov, A. B.] Republican Collect Microorganisms, Astana, Kazakhstan.
RP Stoyanova, LG (reprint author), Moscow MV Lomonosov State Univ, Fac Biol, Dept Microbiol, Moscow 119992, Russia.
EM stoyanovamsu@mail.ru
RI Kushugulova, Almagul/C-7185-2012;
OI Kushugulova, Almagul/0000-0001-9479-0899; Shevtsov,
Alexandr/0000-0002-7576-2750
NR 23
TC 2
Z9 2
U1 2
U2 23
PU MAIK NAUKA/INTERPERIODICA/SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA
SN 0026-2617
EI 1608-3237
J9 MICROBIOLOGY+
JI Microbiology
PD OCT
PY 2011
VL 80
IS 5
BP 672
EP 681
DI 10.1134/S0026261711050134
PG 10
WC Microbiology
SC Microbiology
GA 830UI
UT WOS:000295682300010
ER
PT J
AU Enewold, L
Zhou, J
Devesa, SS
Erickson, RL
Zhu, KM
McGlynn, KA
AF Enewold, Lindsey
Zhou, Jing
Devesa, Susan S.
Erickson, Ralph L.
Zhu, Kangmin
McGlynn, Katherine A.
TI Trends in Testicular Germ Cell Tumors Among US Military Servicemen,
1990-2003
SO MILITARY MEDICINE
LA English
DT Article
ID UNITED-STATES; CANCER; RATES
AB Objective: To determine the incidence of testicular germ cell tumors among active duty males and compare it with the incidence in the general U.S. population. Methods: The Automated Cancer Tumor Registry and the Surveillance, Epidemiology, and End Results Program data from 1990 to 2003 were analyzed for men aged between 20 and 59 years by histology and stage at diagnosis. Rates were age adjusted using the male active duty military population as the standard. Results: Nonseminoma incidence was significantly lower in the military than in the general population (incidence rate ratio = 0.90, 95% confidence interval = 0.82-0.98). Trends in incidence tended to be similar in both the populations. Increases were observed for both histologic types but were only significant for seminoma (Automated Cancer Tumor Registry: 21% and Surveillance, Epidemiology, and End Results program: 16%; p < 0.05). Increases in incidence were only observed for localized tumors of both histologic types. Conclusions: The lower incidence of non-seminoma in the military and the increased incidence of localized tumors in both populations remain unexplained.
C1 [Enewold, Lindsey; Zhou, Jing; Zhu, Kangmin] Walter Reed Army Med Ctr, US Mil Canc Inst, Washington, DC 20307 USA.
[Devesa, Susan S.; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Erickson, Ralph L.] Walter Reed Army Inst Res, Silver Spring, MD 20910 USA.
[Zhu, Kangmin] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
RP Enewold, L (reprint author), Walter Reed Army Med Ctr, US Mil Canc Inst, 6900 Georgia Ave NW,Bldg 1,Suite A 109, Washington, DC 20307 USA.
FU Division of Cancer Epidemiology and Genetics, National Cancer Institute,
National Institutes of Health, Department of Health and Human Services;
United States Military Cancer Institute via the Uniformed Services
University of the Health Sciences under Henry M. Jackson Foundation for
the Advancement of Military Medicine
FX This study was partly supported by 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, and by the United States Military Cancer Institute via the
Uniformed Services University of the Health Sciences under the auspices
of the Henry M. Jackson Foundation for the Advancement of Military
Medicine.
NR 15
TC 4
Z9 5
U1 0
U2 3
PU ASSOC MILITARY SURG US
PI BETHESDA
PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 USA
SN 0026-4075
J9 MIL MED
JI Milit. Med.
PD OCT
PY 2011
VL 176
IS 10
BP 1184
EP 1187
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA 831EK
UT WOS:000295711300019
PM 22128656
ER
PT J
AU Dozmorov, IM
Jarvis, J
Saban, R
Benbrook, DM
Wakeland, E
Aksentijevich, I
Ryan, J
Chiorazzi, N
Guthridge, JM
Drewe, E
Tighe, PJ
Centola, M
Lefkovits, I
AF Dozmorov, Igor M.
Jarvis, James
Saban, Ricardo
Benbrook, Doris M.
Wakeland, Edward
Aksentijevich, Ivona
Ryan, John
Chiorazzi, Nicholas
Guthridge, Joel M.
Drewe, Elizabeth
Tighe, Patrick J.
Centola, Michael
Lefkovits, Ivan
TI Internal standard-based analysis of microarray data2-Analysis of
functional associations between HVE-genes
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; JUVENILE RHEUMATOID-ARTHRITIS; LNCAP
CELL-PROLIFERATION; EXPRESSION; PATHWAYS; CANCER;
5-ALPHA-ANDROSTANE-3-ALPHA; SUSCEPTIBILITY; INFLAMMATION; RECEPTORS
AB In this work we apply the Internal Standard-based analytical approach that we described in an earlier communication and here we demonstrate experimental results on functional associations among the hypervariably-expressed genes (HVE-genes). Our working assumption was that those genetic components, which initiate the disease, involve HVE-genes for which the level of expression is un-distinguishable among healthy individuals and individuals with pathology. We show that analysis of the functional associations of the HVE-genes is indeed suitable to revealing disease-specific differences. We show also that another possible exploit of HVE-genes for characterization of pathological alterations is by using multivariate classification methods. This in turn offers important clues on naturally occurring dynamic processes in the organism and is further used for dynamic discrimination of groups of compared samples. We conclude that our approach can uncover principally new collective differences that cannot be discerned by individual gene analysis.
C1 [Dozmorov, Igor M.; Guthridge, Joel M.; Centola, Michael] Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA.
[Jarvis, James; Saban, Ricardo; Benbrook, Doris M.] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK 73104 USA.
[Wakeland, Edward] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Aksentijevich, Ivona; Ryan, John] NIAMSD, Bethesda, MD 20892 USA.
[Chiorazzi, Nicholas] N Shore Univ Hosp, Feinstein Inst Med Res, Manhasset, NY USA.
[Chiorazzi, Nicholas] N Shore Univ Hosp, Dept Med, Manhasset, NY USA.
[Chiorazzi, Nicholas] N Shore Univ Hosp, Dept Cell Biol, Manhasset, NY USA.
[Chiorazzi, Nicholas] Albert Einstein Coll Med, Manhasset, NY USA.
[Drewe, Elizabeth; Tighe, Patrick J.] Univ Nottingham, Nottingham NG7 2RD, England.
[Lefkovits, Ivan] Univ Clin Basel, Dept Biomed, CH-4051 Basel, Switzerland.
RP Dozmorov, IM (reprint author), Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA.
EM igor-dozmorov@omrf.org
RI Lefkovits, Ivan/B-9777-2009
OI Lefkovits, Ivan/0000-0003-1783-8881
FU National Institutes of Health [P20 RR020143, R01 AI045050, P30 AR053483,
P20RR016478, R01 AI084200, CA106713]; Royal College of Pathology UK;
Journal of Experimental Pathology; Jones Charitable Trust
FX The National Institutes of Health (P20 RR020143 to I. D., R01 AI045050
to I. D., P30 AR053483 to I. D. and J.G., P20RR016478 to I. D., R01
AI084200 to I. D. and J.J., CA106713 to D. B.); The Royal College of
Pathology UK and The Journal of Experimental Pathology (to E. D. and
P.J.T.); and The Jones Charitable Trust (to E. D. and P.J.T.). Funding
for open access charge: P20RR016478.
NR 35
TC 4
Z9 4
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD OCT
PY 2011
VL 39
IS 18
BP 7881
EP 7899
DI 10.1093/nar/gkr503
PG 19
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 830WC
UT WOS:000295687700009
PM 21715372
ER
PT J
AU McNeill, DR
Lin, PC
Miller, MG
Pistell, PJ
de Souza-Pinto, NC
Fishbein, KW
Spencer, RG
Liu, Y
Pettan-Brewer, C
Ladiges, WC
Wilson, DM
AF McNeill, Daniel R.
Lin, Ping-Chang
Miller, Marshall G.
Pistell, Paul J.
de Souza-Pinto, Nadja C.
Fishbein, Kenneth W.
Spencer, Richard G.
Liu, Yie
Pettan-Brewer, Christina
Ladiges, Warren C.
Wilson, David M., III
TI XRCC1 haploinsufficiency in mice has little effect on aging, but
adversely modifies exposure-dependent susceptibility
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID BASE EXCISION-REPAIR; STRAND BREAK REPAIR; DNA-LIGASE-III; DAMAGE;
DISEASE; PROTEIN; CANCER; MOUSE; GENE; POLYMORPHISMS
AB Oxidative DNA damage plays a role in disease development and the aging process. A prominent participant in orchestrating the repair of oxidative DNA damage, particularly single-strand breaks, is the scaffold protein XRCC1. A series of chronological and biological aging parameters in XRCC1 heterozygous (HZ) mice were examined. HZ and wild-type (WT) C57BL/6 mice exhibit a similar median lifespan of similar to 26 months and a nearly identical maximal life expectancy of similar to 37 months. However, a number of HZ animals (7 of 92) showed a propensity for abdominal organ rupture, which may stem from developmental abnormalities given the prominent role of XRCC1 in endoderm and mesoderm formation. For other end-points evaluated-weight, fat composition, blood chemistries, condition of major organs, tissues and relevant cell types, behavior, brain volume and function, and chromosome and telomere integrity-HZ mice exhibited by-and-large a normal phenotype. Treatment of animals with the alkylating agent azoxymethane resulted in both liver toxicity and an increased incidence of precancerous lesions in the colon of HZ mice. Our study indicates that XRCC1 haploinsufficiency in mammals has little effect on chronological longevity and many key biological markers of aging in the absence of environmental challenges, but may adversely affect normal animal development or increase disease susceptibility to a relevant genotoxic exposure.
C1 [McNeill, Daniel R.; Liu, Yie; Wilson, David M., III] NIA, Lab Mol Gerontol, NIH, IRP,Biomed Res Ctr, Baltimore, MD 21224 USA.
[Lin, Ping-Chang; Fishbein, Kenneth W.; Spencer, Richard G.] NIA, Clin Invest Lab, NIH, IRP,Biomed Res Ctr, Baltimore, MD 21224 USA.
[Miller, Marshall G.] Tufts Univ, Human Nutr Res Ctr Aging, Boston, MA 02111 USA.
[Pistell, Paul J.] Towson Univ, Dept Psychol, Towson, MD 21252 USA.
[de Souza-Pinto, Nadja C.] Univ Sao Paulo, Dept Bioquim, Inst Quim, BR-05508000 Sao Paulo, Brazil.
[Pettan-Brewer, Christina; Ladiges, Warren C.] Univ Washington, Dept Comparat Med, Seattle, WA 98195 USA.
RP Wilson, DM (reprint author), NIA, Lab Mol Gerontol, NIH, IRP,Biomed Res Ctr, Baltimore, MD 21224 USA.
EM wladiges@u.washington.edu; wilsonda@mail.nih.gov
RI Souza-Pinto, Nadja/C-3462-2013; 3, INCT/H-4497-2013; Redoxoma,
Inct/H-9962-2013;
OI Souza-Pinto, Nadja/0000-0003-4206-964X; Lin,
Ping-Chang/0000-0003-0918-4072; Fishbein, Kenneth/0000-0002-6353-4603
FU National Institute on Aging; National Institute of Environmental Health
Sciences [R21ES016572]
FX Funding for open access charge: Intramural Research Program of the
National Institute on Aging and National Institute of Environmental
Health Sciences grant R21ES016572 (to W.L.).
NR 35
TC 13
Z9 14
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD OCT
PY 2011
VL 39
IS 18
BP 7992
EP 8004
DI 10.1093/nar/gkr280
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 830WC
UT WOS:000295687700017
PM 21737425
ER
PT J
AU Molino-Lova, R
Macchi, C
Gori, AM
Marcucci, R
Polcaro, P
Cecchi, F
Lauretani, F
Bandinelli, S
Abbate, R
Beghi, E
Guralnik, JM
Ferrucci, L
AF Molino-Lova, R.
Macchi, C.
Gori, A. M.
Marcucci, R.
Polcaro, P.
Cecchi, F.
Lauretani, F.
Bandinelli, S.
Abbate, R.
Beghi, E.
Guralnik, J. M.
Ferrucci, L.
TI High sensitivity C-reactive protein predicts the development of new
carotid artery plaques in older persons
SO NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES
LA English
DT Article
DE C-reactive protein; Atherosclerosis; Carotid arteries; Risk factors;
Older persons
ID INTIMA-MEDIA THICKNESS; GLOBAL CARDIOVASCULAR RISK; ATHEROSCLEROSIS
PROGRESSION; MONOCYTE COUNT; INFLAMMATION; CORONARY; ROTTERDAM;
POPULATION; MEN; INTERLEUKIN-6
AB Background and Aim: Previous studies have shown that increased levels of C-reactive protein (CRP) predict cardiovascular events, including stroke, myocardial infarction and death from cardiovascular causes. Previous studies have also shown that increased levels of CRP are strong predictors of the progression of pre-existing carotid artery plaques. However, whether CRP is involved in the development of new plaques, that may or may not be associated with clinical events, in subjects with clean carotid arteries has been scarcely investigated.
Methods and Results: 486 "InCHIANTI'' Study participants (200 men and 286 women, 72% aged 65 years and over) free from carotid artery plaques at baseline, also underwent carotid artery scan three years later. We tested the association of baseline characteristics, cardiovascular risk factors and inflammatory markers with the development of new carotid artery plaques. Older participants were significantly more likely to develop new plaques. Independent of age, the relative risks of developing new plaques associated with heavy smoking and family history of atherosclerosis were 1.7 (95% CI 1.5-1.9) and 1.9 (95% CI 1.2-3.1), respectively.Participants with high (> 3 mu g/mL) and moderate (>= 1 and <= 3 mu g/mL) CRP levels had a relative risk of 2.2 (95% CI 1.9-2.6) and 1.9 (95% CI 1.6-2.3) respectively, when compared with subjects with low (<1 mu g/mL) CRP levels. Surprisingly, risk factors such as hypertension, diabetes, dyslipidemia and overweight/obesity were not significant predictors of the development of new carotid artery plaques.
Conclusions: High CRP levels independently predict the development of new plaques in older persons with carotid arteries free from atherosclerotic lesions. (C) 2010 Elsevier B.V. All rights reserved.
C1 [Molino-Lova, R.; Macchi, C.; Gori, A. M.; Polcaro, P.; Cecchi, F.] Fdn Don C Gnocchi, Dept Cardiovasc Rehabil, I-50020 Florence, Italy.
[Molino-Lova, R.] Fdn Don C Gnocchi, Dept Cardiopulm Rehabil, Massa, Italy.
[Gori, A. M.; Marcucci, R.] Univ Florence, Dept Med & Surg Crit Care, Ctr Study Mol & Clin Level Chron Degenerat & Neop, Florence, Italy.
[Lauretani, F.] Tuscany Hlth Reg Agcy, Florence, Italy.
[Bandinelli, S.] ASF, Geriatr Rehabil Unit, Florence, Italy.
[Beghi, E.] Mario Negri Inst Pharmacol Res, Lab Neurol Disorders, Milan, Italy.
[Guralnik, J. M.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, Bethesda, MD 20892 USA.
RP Molino-Lova, R (reprint author), Fdn Don C Gnocchi, Dept Cardiovasc Rehabil, Via Imprunetana 124, I-50020 Florence, Italy.
EM rmolino@dongnocchi.it
RI Lauretani, Fulvio/K-5115-2016;
OI Gori, annamaria.gori@unifi.it/0000-0001-6857-5861; Marcucci,
Rossella/0000-0001-9549-7176; Lauretani, Fulvio/0000-0002-5287-9972;
Cecchi, Franco/0000-0002-2035-5621
FU NIA NIH HHS [N01 AG916413]
NR 39
TC 9
Z9 11
U1 1
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0939-4753
J9 NUTR METAB CARDIOVAS
JI Nutr. Metab. Carbiovasc. Dis.
PD OCT
PY 2011
VL 21
IS 10
BP 776
EP 782
DI 10.1016/j.numecd.2010.02.003
PG 7
WC Cardiac & Cardiovascular Systems; Endocrinology & Metabolism; Nutrition
& Dietetics
SC Cardiovascular System & Cardiology; Endocrinology & Metabolism;
Nutrition & Dietetics
GA 830DS
UT WOS:000295638100004
PM 20554169
ER
PT J
AU Apud, JA
AF Apud, Jose A.
TI The extraction, isolation and purification of an endogenous regulator
for the 5-HT2 receptor
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Endocoids; 5-HT2 receptor; H-3-Ketanserin; PI turnover; 293 cells
AB Early studies indicated that serotonin, a primary transmitter in the central nervous system, may not represent the primary endogenous regulator for the 5-HT2 receptor labeled by [H-3]-ketanserin. Instead, an endogenous ligand may be responsible for modulating the [H-3]-ketanserin site. Through different isolation and purification procedures, a pronase-sensitive peptide with activity on [H-3]-ketanserin binding was identified in the rat brain. This peptide seems specific for the 5-HT2 receptor since it does not displace the binding of [H-3]-mipramine or [H-3]-mianserin from rat cortical membranes and is able to stimulate PI turnover in a ketanserin sensitive fashion. Given the role of 5-HT2 receptors in the action of antidepressants, this finding may help understand some of the molecular mechanisms involved in antidepressant effect. Published by Elsevier Ltd.
C1 NIMH, Clin Brain Disorders Branch, GCAP, NIH, Bethesda, MD 20892 USA.
RP Apud, JA (reprint author), NIMH, Clin Brain Disorders Branch, GCAP, NIH, Bldg 10,CRC 7-3342,10 Ctr Dr, Bethesda, MD 20892 USA.
EM apudj@mail.nih.gov
NR 4
TC 1
Z9 1
U1 1
U2 6
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
J9 PHARMACOL RES
JI Pharmacol. Res.
PD OCT
PY 2011
VL 64
IS 4
BP 312
EP 313
DI 10.1016/j.phrs.2011.05.022
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 831YO
UT WOS:000295767200003
PM 21683793
ER
PT J
AU Armstrong, D
AF Armstrong, David
TI Age- and disease-related neuroplasticity of chemically identified
neuronal circuits: A tribute to Professor Erminio Costa
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Alzheimer's disease; NMDA; Hippocampus; AMPA; Glutamate
ID RECEPTOR SUBTYPE IMMUNOREACTIVITY; ALZHEIMERS-DISEASE;
HIPPOCAMPAL-FORMATION; ENTORHINAL CORTEX; PLAQUES
AB The following review highlights a small portion of the research ongoing in my laboratory at the Fidia Georgetown Institute of Neuroscience (FGIN) during the years 1989-1994. Specifically, this work focused on the selective vulnerability of neurons in Alzheimer's disease. At the time, it was known that alpha-amino3-hydroxy-5-methyl-4-isoaxolepropionate (AMPA) receptors were composed of one or more subunits (GluR1-4). Furthermore, the presence of the GluR2 subunit was known to substantially reduce Ca(2+) through AMPA receptors in response to ligand binding. This finding led us to hypothesize that the presence or absence of the GluR2 subunit in the AMPA receptor may have a profound influence on the ability of the cell to gate extracellular Ca(2+) and maintain intracellular calcium homeostasis. Furthermore, in Alzheimer's disease we hypothesized that cells at risk for developing AD neuropathology will express certain combinations of glutamate receptor subunits that form channels with increased permeability to Ca(2+). In turn, these cells may become more vulnerable to the pathologic consequences of increased intracellular Ca(2+) and destabilized intracellular Ca(2+) homeostasis. To test this hypothesis we employed anatomical techniques and examined post mortem materials from patients with AD. The results of these studies are summarized in this review.
Notably, this review also highlights the valuable collaborations established during my five years at FGIN and pays tribute to the intellectually rich and supportive environment provided by Dr. Costa and colleagues. (C) 2011 Published by Elsevier Ltd.
C1 NIMH, NIH, Bethesda, MD 20892 USA.
RP Armstrong, D (reprint author), NIMH, NIH, Neurosci Bldg,Room 6138,6001 Execut Blvd,MSC 9606, Bethesda, MD 20892 USA.
EM armstrda@mail.nih.gov
NR 7
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
J9 PHARMACOL RES
JI Pharmacol. Res.
PD OCT
PY 2011
VL 64
IS 4
BP 336
EP 338
DI 10.1016/j.phrs.2011.05.023
PG 3
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 831YO
UT WOS:000295767200012
PM 21704164
ER
PT J
AU Schwandt, ML
Lindell, SG
Higley, JD
Suomi, SJ
Heilig, M
Barr, CS
AF Schwandt, Melanie L.
Lindell, Stephen G.
Higley, James D.
Suomi, Stephen J.
Heilig, Markus
Barr, Christina S.
TI OPRM1 gene variation influences hypothalamic-pituitary-adrenal axis
function in response to a variety of stressors in rhesus macaques
SO PSYCHONEUROENDOCRINOLOGY
LA English
DT Article
DE Opioids; Hypothalamic-pituitary-adrenal (HPA) axis; Cortisol; Stress;
Nonhuman primate; Separation; Alcohol; Postpartum depression
ID MU-OPIOID-RECEPTOR; SINGLE NUCLEOTIDE POLYMORPHISM; ENDOGENOUS OPIOIDS;
HPA AXIS; PHYSIOLOGICAL-RESPONSES; MORPHINE CONSUMPTION; ALCOHOL
DEPENDENCE; A118G POLYMORPHISM; PLASMA-CORTISOL; RESPIRATORY DEPRESSION
AB The endogenous opioid system is involved in modulating a number of behavioral and physiological systems, including the hypothalamic pituitary adrenal (HPA) axis. In humans, a functional variant in the OPRM1 gene (OPRM1 A118G) is associated with a number of outcomes, including attenuated HPA axis responses to stress. A nonsynonymous variant (OPRM1 C77G) in the rhesus macaque has been shown to have similar effects in vivo to the human variant. The current study investigated whether OPRM1 C77G influences HPA axis response to stress in rhesus macaques. We analyzed plasma adrenocorticotropic hormone (ACTH) and cortisol levels measured in response to three different stressors: (1) maternal separation in infant subjects at 6 months of age, (2) acute ethanol administration in adolescent subjects at 4 years of age, and (3) postpartum HPA axis function in adult rhesus macaque females. For the maternal separation paradigm, ACTH and cortisol levels were determined at baseline as well as peak levels during each of 4 consecutive separation episodes. For the acute ethanol administration paradigm, hormone levels were determined at baseline and again at 5 min, 10 min, and 60 min following the ethanol infusion. For postpartum sampling, hormone levels were determined at postpartum days 7, 14, 21, 30, 60, 90, 120, and 150. Infants carrying the 77G allele exhibited lower levels of cortisol across all 4 separation episodes. Furthermore, adolescents carrying the 77G allele exhibited lower cortisol levels at 5 and 10 min following acute ethanol administration. Adult females with prior reproductive experience and who carry the 77G allele exhibited lower cortisol levels across the postpartum period. No significant genotype effects were found for ACTH, although there were some trends for lower ACTH levels in 77G allele carriers. These data are consistent with human studies that have demonstrated attenuated cortisol responses to stress among carriers of the OPRM1 118G allele, lending further support to the argument that the rhesus and human allelic variants are functionally similar. Our results also suggest that OPRM1 variation may influence coping style, as well as alcohol-induced and postpartum levels of HPA axis activity and, as such, may modify vulnerability to alcohol use disorders and postpartum depression. Published by Elsevier Ltd.
C1 [Schwandt, Melanie L.; Lindell, Stephen G.; Heilig, Markus; Barr, Christina S.] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Lindell, Stephen G.; Barr, Christina S.] NIAAA, Sect Comparat Behav Genom, LNG, NIH, Rockville, MD 20852 USA.
[Higley, James D.] Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA.
[Suomi, Stephen J.] NICHD, Comparat Ethol Lab, NIH, Poolesville, MD USA.
RP Schwandt, ML (reprint author), 10 Ctr Dr,10CRC 1-5330, Bethesda, MD 20892 USA.
EM melanies@mail.nih.gov
RI Schwandt, Melanie/L-9866-2016;
OI Heilig, Markus/0000-0003-2706-2482
FU National Institute on Alcohol Abuse and Alcoholism (NIAAA); National
Institute of Child Health and Human Development (NICHD)
FX Funding for this study was provided by the intramural programs of the
National Institute on Alcohol Abuse and Alcoholism (NIAAA) and the
National Institute of Child Health and Human Development (NICHD). The
NIAAA and NICHD had no further role in study design; in the collection,
analysis, and interpretation of data; in the writing of the report; and
in the decision to submit the paper for publication.
NR 88
TC 18
Z9 18
U1 1
U2 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4530
J9 PSYCHONEUROENDOCRINO
JI Psychoneuroendocrinology
PD OCT
PY 2011
VL 36
IS 9
BP 1303
EP 1311
DI 10.1016/j.psyneuen.2011.03.002
PG 9
WC Endocrinology & Metabolism; Neurosciences; Psychiatry
SC Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry
GA 829TZ
UT WOS:000295608500005
PM 21459516
ER
PT J
AU de Gonzalez, AB
Brenner, A
Hartge, P
Lee, C
Morton, L
Rajaraman, P
AF de Gonzalez, Amy Berrington
Brenner, Alina
Hartge, Patricia
Lee, Choonsik
Morton, Lindsay
Rajaraman, Preetha
TI Evolving Strategies in Epidemiologic Research on Radiation and Cancer
SO RADIATION RESEARCH
LA English
DT Editorial Material
ID US RADIOLOGIC TECHNOLOGISTS; ATOMIC-BOMB SURVIVORS; BREAST-CANCER;
IONIZING-RADIATION; CHILDHOOD-CANCER; LUNG-CANCER; HODGKINS-LYMPHOMA;
POOLED ANALYSIS; THYROID-CANCER; RISK
C1 [de Gonzalez, Amy Berrington; Brenner, Alina; Hartge, Patricia; Lee, Choonsik; Morton, Lindsay; Rajaraman, Preetha] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP de Gonzalez, AB (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM berringtona@mail.nih.gov
RI Morton, Lindsay/B-5234-2015; Lee, Choonsik/C-9023-2015
OI Morton, Lindsay/0000-0001-9767-2310; Lee, Choonsik/0000-0003-4289-9870
NR 35
TC 1
Z9 1
U1 1
U2 3
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD OCT
PY 2011
VL 176
IS 4
BP 527
EP 532
DI 10.1667/RRXX37.1
PG 6
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
Nuclear Medicine & Medical Imaging
GA 829SV
UT WOS:000295605500011
PM 21823973
ER
PT J
AU Linet, M
Kleinerman, R
Mabuchi, K
AF Linet, Martha
Kleinerman, Ruth
Mabuchi, Kiyohiko
TI IN MEMORIAM Elaine Ron 1943-2010
SO RADIATION RESEARCH
LA English
DT Biographical-Item
C1 [Linet, Martha; Kleinerman, Ruth; Mabuchi, Kiyohiko] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Linet, M (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD OCT
PY 2011
VL 176
IS 4
BP 533
EP 534
DI 10.1667/RRXX36.1
PG 2
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
Nuclear Medicine & Medical Imaging
GA 829SV
UT WOS:000295605500012
ER
PT J
AU Abdel-Rahman, A
Anyangwe, N
Carlacci, L
Casper, S
Danam, RP
Enongene, E
Erives, G
Fabricant, D
Gudi, R
Hilmas, CJ
Hines, F
Howard, P
Levy, D
Lin, Y
Moore, RJ
Pfeiler, E
Thurmond, TS
Turujman, S
Walker, NJ
AF Abdel-Rahman, Ali
Anyangwe, Njwen
Carlacci, Louis
Casper, Steve
Danam, Rebecca P.
Enongene, Evaristus
Erives, Gladys
Fabricant, Daniel
Gudi, Ramadevi
Hilmas, Corey J.
Hines, Fred
Howard, Paul
Levy, Dan
Lin, Ying
Moore, Robert J.
Pfeiler, Erika
Thurmond, T. Scott
Turujman, Saleh
Walker, Nigel J.
TI The Safety and Regulation of Natural Products Used as Foods and Food
Ingredients
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE botanicals; dietary supplements; food; food ingredients; safety;
regulation
ID CHINESE HERBS NEPHROPATHY; GREEN TEA; STEVIA-REBAUDIANA; ARISTOLOCHIC
ACID; REBAUDIOSIDE-A; EPIGALLOCATECHIN GALLATE; DIETARY-SUPPLEMENTS;
RATS; STEVIOSIDE; EXTRACT
AB The use of botanicals and dietary supplements derived from natural substances as an adjunct to an improved quality of life or for their purported medical benefits has become increasingly common in the United States. This review addresses the safety assessment and regulation of food products containing these substances by the U.S. Food and Drug Administration (FDA). The issue of safety is particularly critical given how little information is available on the toxicity of some of these products. The first section uses case studies for stevia and green tea extracts as examples of how FDA evaluates the safety of botanical and herbal products submitted for consideration as Generally Recognized as Safe under the Federal Food, Drug, and Cosmetics Act. The 1994 Dietary Supplement Health Education Act (DSHEA) created a regulatory framework for dietary supplements. The article also discusses the regulation of this class of dietary supplements under DSHEA and addresses the FDA experience in analyzing the safety of natural ingredients described in pre-market safety submissions. Lastly, we discuss an ongoing interagency collaboration to conduct safety testing of nominated dietary supplements.
C1 [Danam, Rebecca P.; Erives, Gladys; Thurmond, T. Scott] US FDA, Off Food Addit Safety, Ctr Food Safety & Appl Nutr, College Pk, MD 21029 USA.
[Abdel-Rahman, Ali; Anyangwe, Njwen; Carlacci, Louis; Casper, Steve; Enongene, Evaristus; Fabricant, Daniel; Gudi, Ramadevi; Hilmas, Corey J.; Hines, Fred; Levy, Dan; Lin, Ying; Moore, Robert J.; Turujman, Saleh] US FDA, Div Dietary Supplement Programs, Off Nutr Labeling & Dietary Supplements, College Pk, MD 21029 USA.
[Howard, Paul] US FDA, Off Sci Coordinat, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
[Pfeiler, Erika] US FDA, Off Commissioner, Off Chief Scientist, Laurel, MD 20708 USA.
[Walker, Nigel J.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
RP Thurmond, TS (reprint author), US FDA, Off Food Addit Safety, Ctr Food Safety & Appl Nutr, 5100 Paint Branch Pkwy,HFS 265, College Pk, MD 21029 USA.
EM scott.thurmond@fda.hhs.gov
RI Walker, Nigel/D-6583-2012
OI Walker, Nigel/0000-0002-9111-6855
NR 55
TC 38
Z9 43
U1 2
U2 62
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD OCT
PY 2011
VL 123
IS 2
BP 333
EP 348
DI 10.1093/toxsci/kfr198
PG 16
WC Toxicology
SC Toxicology
GA 828VW
UT WOS:000295532900002
PM 21821733
ER
PT J
AU Shpyleva, SI
Muskhelishvili, L
Tryndyak, VP
Koturbash, I
Tokar, EJ
Waalkes, MP
Beland, FA
Pogribny, IP
AF Shpyleva, Svitlana I.
Muskhelishvili, Levan
Tryndyak, Volodymyr P.
Koturbash, Igor
Tokar, Erik J.
Waalkes, Michael P.
Beland, Frederick A.
Pogribny, Igor P.
TI Chronic Administration of 2-Acetylaminofluorene Alters the Cellular Iron
Metabolism in Rat Liver
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE 2-acetylaminofluorene; carcinogenesis; iron metabolism; liver; rat
ID HEPATOCELLULAR-CARCINOMA; HEPATIC IRON; REGULATORY GENES; TRANSFERASE-P;
CANCER; HEPCIDIN; HEPATOCARCINOGENESIS; CARCINOGENESIS; EXPRESSION;
DISEASE
AB Dysregulated intracellular iron homeostasis has been found not only in rodent and human hepatocellular carcinomas but also in several preneoplastic pathological states associated with hepatocarcinogenesis; however, the precise underlying mechanisms of metabolic iron disturbances in preneoplastic liver and the role of these disturbances remain unexplored. In the present study, using an in vivo model of rat hepatocarcinogenesis induced by 2-acetylaminofluorene, we found extensive alterations in cellular iron metabolism at preneoplastic stages of liver carcinogenesis. These were characterized by a substantial decrease in the levels of cytoplasmic non-heme iron in foci of initiated hepatocytes and altered expression of the major genes responsible for the proper maintenance of intracellular iron homeostasis. Gene expression analysis revealed that the decreased intracellular levels of iron in preneoplastic foci might be attributed to increased iron export from the cells, driven by upregulation of ferroportin (Fpn1), the only known non-heme iron exporter. Likewise, increased Fpn1 gene expression was found in vitro in TRL1215 rat liver cells with an acquired malignant phenotype, suggesting that upregulation of Fpn1 might be a specific feature of neoplastically transformed cells. Other changes observed in vivo included the downregulation of hepcidin (Hamp) gene, a key regulator of Fpn1, and this was accompanied by decreased levels of CCAAT/enhancer binding proteins alpha and beta, especially at the Hamp promoter. In conclusion, our results demonstrate the significance of altered intracellular iron metabolism in the progression of liver carcinogenesis and suggest that correction of these alterations could possibly affect liver cancer development.
C1 [Shpyleva, Svitlana I.; Tryndyak, Volodymyr P.; Koturbash, Igor; Beland, Frederick A.; Pogribny, Igor P.] Natl Ctr Toxicol Res, Div Biochem Toxicol, Jefferson, AR 72079 USA.
[Shpyleva, Svitlana I.; Tryndyak, Volodymyr P.] RE Kavetsky Inst Expt Pathol Oncol & Radiobiol, Dept Mech Anticanc Therapy, UA-03022 Kiev, Ukraine.
[Muskhelishvili, Levan] Natl Ctr Toxicol Res, Toxicol Pathol Associates, Jefferson, AR 72079 USA.
[Waalkes, Michael P.] NIEHS, Inorgan Toxicol Grp, Natl Toxicol Program, Res Triangle Pk, NC 27713 USA.
RP Pogribny, IP (reprint author), Natl Ctr Toxicol Res, Div Biochem Toxicol, Bldg 14C,Off 101, Jefferson, AR 72079 USA.
EM igor.pogribny@fda.hhs.gov
FU National Institute of Environmental Health Sciences (NIEHS), National
Institutes of Health (NIH)
FX National Toxicology Program, National Institute of Environmental Health
Sciences (NIEHS), National Institutes of Health (NIH).
NR 42
TC 3
Z9 3
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD OCT
PY 2011
VL 123
IS 2
BP 433
EP 440
DI 10.1093/toxsci/kfr193
PG 8
WC Toxicology
SC Toxicology
GA 828VW
UT WOS:000295532900011
PM 21785164
ER
PT J
AU La Maestra, S
Kisby, GE
Micale, RT
Johnson, J
Kow, YW
Bao, GB
Sheppard, C
Stanfield, S
Tran, H
Woltjer, RL
D'Agostini, F
Steele, VE
De Flora, S
AF La Maestra, Sebastiano
Kisby, Glen E.
Micale, Rosanna T.
Johnson, Jessica
Kow, Yoke W.
Bao, Gaobin
Sheppard, Clayton
Stanfield, Sarah
Huong Tran
Woltjer, Randall L.
D'Agostini, Francesco
Steele, Vernon E.
De Flora, Silvio
TI Cigarette Smoke Induces DNA Damage and Alters Base-Excision Repair and
Tau Levels in the Brain of Neonatal Mice
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE cigarette smoke; brain; neonatal mice; DNA damage; base-excision repair;
tau; neurodegenerative disorders
ID OXIDATIVE STRESS; ALZHEIMERS-DISEASE; N-ACETYLCYSTEINE; BIRTH OUTCOMES;
TOBACCO-SMOKE; PROTEIN-TAU; CANCER; MOUSE; SCLEROSIS; EXPOSURE
AB The prenatal and perinatal periods of brain development are especially vulnerable to insults by environmental agents. Early life exposure to cigarette smoke (CS), which contains both genotoxicants and oxidants, is considered an important risk factor for both neurodevelopmental and neurodegenerative disorders. Yet, little is known regarding the underlying pathogenetic mechanisms. In the present study, neonatal Swiss ICR (CD-1) albino mice were exposed to various concentrations of CS for 4 weeks and the brain examined for lipid peroxides, DNA damage, base-excision repair (BER) enzymes, apoptosis, and levels of the microtubule protein tau. CS induced a dose-dependent increase in both malondialdehyde and various types of DNA damage, including single-strand breaks, double-strand breaks, and DNA-protein cross-links. However, the CS-induced DNA damage in the brain returned to basal levels 1 week after smoking cessation. CS also modulated the activity and distribution of the BER enzymes 8-oxoguanine-DNA-glycosylase (OGG1) and apyrimidinic/apurinic endonuclease (APE1) in several brain regions. Normal tau (i.e., three-repeat tau, 3R tau) and various pathological forms of tau were also measured in the brain of CS-exposed neonatal mice, but only 3R tau and tau phosphorylated at serine 199 were significantly elevated. The oxidative stress, genomic dysregulation, and alterations in tau metabolism caused by CS during a critical period of brain development could explain why CS is an important risk factor for both neurodevelopmental and neurodegenerative disorders appearing in later life.
C1 [La Maestra, Sebastiano; Micale, Rosanna T.; D'Agostini, Francesco; De Flora, Silvio] Univ Genoa, Dept Hlth Sci, I-16132 Genoa, Italy.
[Kisby, Glen E.; Johnson, Jessica] Oregon Hlth & Sci Univ, CROET, Portland, OR 97239 USA.
[Kow, Yoke W.; Bao, Gaobin; Sheppard, Clayton] Emory Univ, Dept Radiat Oncol, Sch Med, Atlanta, GA 30322 USA.
[Stanfield, Sarah; Huong Tran; Woltjer, Randall L.] Oregon Hlth & Sci Univ, Dept Pathol, Portland, OR 97239 USA.
[Steele, Vernon E.] NCI, Canc Prevent Div, Rockville, MD 20892 USA.
RP De Flora, S (reprint author), Univ Genoa, Dept Hlth Sci, I-16132 Genoa, Italy.
EM sdf@unige.it
FU U.S. National Cancer Institute [NO1-CN53301, CA90860]; Department of
Defense [DAMD17-98-1-8625]
FX U.S. National Cancer Institute (NO1-CN53301, CA90860); Department of
Defense (DAMD17-98-1-8625).
NR 49
TC 11
Z9 12
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD OCT
PY 2011
VL 123
IS 2
BP 471
EP 479
DI 10.1093/toxsci/kfr187
PG 9
WC Toxicology
SC Toxicology
GA 828VW
UT WOS:000295532900014
PM 21778470
ER
PT J
AU Oakley, MS
Gerald, N
McCutchan, TF
Aravind, L
Kumar, S
AF Oakley, Miranda S.
Gerald, Noel
McCutchan, Thomas F.
Aravind, L.
Kumar, Sanjai
TI Clinical and molecular aspects of malaria fever
SO TRENDS IN PARASITOLOGY
LA English
DT Review
ID PLASMODIUM-FALCIPARUM; FEBRILE TEMPERATURES; HOST ERYTHROCYTE; CEREBRAL
MALARIA; PARASITES; GLYCOSYLPHOSPHATIDYLINOSITOL; RESPONSES; PIGMENT;
RECEPTORS; INFECTION
AB Although clinically benign, malaria fever is thought to have significant relevance in terms of parasite growth and survival and its virulence which in turn may alter the clinical course of illness. In this article, the historical literature is reviewed, providing some evolutionary perspective on the genesis and biological relevance of malaria fever, and the available molecular data on the febrile-temperature-inducible parasite factors that may contribute towards the regulation of parasite density and alteration of virulence in the host is also discussed. The potential molecular mechanisms that could be responsible for the induction and regulation of cyclical malaria fevers caused by different species of Plasmodiurn are also discussed.
C1 [Gerald, Noel; McCutchan, Thomas F.; Kumar, Sanjai] US FDA, Div Emerging Transfus Transmitted Dis, CBER, Rockville, MD 20857 USA.
[Oakley, Miranda S.] US FDA, Div Bacterial Parasit & Allergen Prod, Ctr Biol Evaluat & Res, Rockville, MD 20857 USA.
[Aravind, L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Kumar, S (reprint author), US FDA, Div Emerging Transfus Transmitted Dis, CBER, Rockville, MD 20857 USA.
EM sanjai.kumar@fda.hhs.gov
NR 49
TC 12
Z9 12
U1 2
U2 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4922
J9 TRENDS PARASITOL
JI Trends Parasitol.
PD OCT
PY 2011
VL 27
IS 10
BP 442
EP 449
DI 10.1016/j.pt.2011.06.004
PG 8
WC Parasitology
SC Parasitology
GA 831RN
UT WOS:000295748900005
PM 21795115
ER
PT J
AU Chen, M
Wang, YR
Hou, TT
Zhang, HL
Qu, AJ
Wang, XH
AF Chen, Min
Wang, Yanru
Hou, Tingting
Zhang, Huiliang
Qu, Aijuan
Wang, Xianhua
TI Differential mitochondrial calcium responses in different cell types
detected with a mitochondrial calcium fluorescent indicator, mito-GCaMP2
SO ACTA BIOCHIMICA ET BIOPHYSICA SINICA
LA English
DT Article
DE fluorescent indicator; mitochondria; calcium; cardiomyocyte
ID RABBIT CARDIAC MYOCYTES; IN-VIVO; CA2+ SIGNALS; TRANSIENTS; PROTEINS;
MECHANISMS
AB Mitochondrial calcium plays a crucial role in mitochondrial metabolism, cell calcium handling, and cell death. However, some mechanisms concerning mitochondrial calcium regulation are still unknown, especially how mitochondrial calcium couples with cytosolic calcium. In this work, we constructed a novel mitochondrial calcium fluorescent indicator (mito-GCaMP2) by genetic manipulation. Mito-GCaMP2 was imported into mitochondria with high efficiency and the fluorescent signals co-localized with that of tetramethyl rhodamine methyl ester, a mitochondrial membrane potential indicator. The mitochondrial inhibitors specifically decreased the signals of mito-GCaMP2. The apparent K(d) of mito-GCaMP2 was 195.0 nmol/L at pH 8.0 in adult rat cardiomyocytes. Furthermore, we observed that mito-GCaMP2 preferred the alkaline pH surrounding of mitochondria. In HeLa cells, we found that mitochondrial calcium ([Ca(2+)](mito)) responded to the changes of cytosolic calcium ([Ca(2+)](cyto)) induced by histamine or thapasigargin. Moreover, external Ca(2+) (100 mu mol/L) directly induced an increase of [Ca(2+)](mito) in permeabilized HeLa cells. However, in rat cardiomyocytes [Ca(2+)](mito) did not respond to cytosolic calcium transients stimulated by electric pacing or caffeine. In permeabilized cardiomyocytes, 600 nmol/L free Ca(2+) repeatedly increased the fluorescent signals of mito-GCaMP2, which excluded the possibility that mito-GCaMP2 lost its function in cardiomyocytes mitochondria. These results showed that the response of mitochondrial calcium is diverse in different cell lineages and suggested that mitochondria in cardiomyocytes may have a special defense mechanism to control calcium flux.
C1 [Chen, Min] Yunnan Ctr Dis Prevent & Control, Kunming 650022, Peoples R China.
[Chen, Min; Wang, Yanru; Hou, Tingting; Zhang, Huiliang; Wang, Xianhua] Peking Univ, Inst Mol Med, Beijing 100871, Peoples R China.
[Qu, Aijuan] NCI, Lab Metab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Chen, M (reprint author), Yunnan Ctr Dis Prevent & Control, Kunming 650022, Peoples R China.
EM chenminyx@gmail.com; xianhua@pku.edu.cn
FU National Natural Science Foundation of China [30800371]
FX This work was supported by a grant from the National Natural Science
Foundation of China (30800371).
NR 36
TC 10
Z9 10
U1 2
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1672-9145
J9 ACTA BIOCH BIOPH SIN
JI Acta Biochim. Biophys. Sin.
PD OCT
PY 2011
VL 43
IS 10
BP 822
EP 830
DI 10.1093/abbs/gmr075
PG 9
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 827EU
UT WOS:000295411300010
PM 21880604
ER
PT J
AU Aue, G
Lozier, JN
Tian, X
Cullinane, AM
Soto, S
Samsel, L
Mccoy, P
Wiestner, A
AF Aue, Georg
Lozier, Jay Nelson
Tian, Xin
Cullinane, Ann M.
Soto, Susan
Samsel, Leigh
McCoy, Philip
Wiestner, Adrian
TI Inflammation, TNF alpha and endothelial dysfunction link lenalidomide to
venous thrombosis in chronic lymphocytic leukemia
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID MULTIPLE-MYELOMA; THALIDOMIDE; THROMBOEMBOLISM; RISK; COMPLICATIONS;
ASPIRIN; MALIGNANCIES; PREVENTION; CANCER; CELLS
AB Patients receiving lenalidomide are at an increased risk for deep venous thrombosis (DVT). Here, we prospectively investigated the DVT risk in patients with relapsed chronic lymphocytic leukemia (CLL) treated with lenalidomide (n = 32). Five patients developed six incidents of DVT over 1 year for an annual incidence of 16%. Three of these were considered drug-related. Median time to DVT was 105 days (range 56-259 days). No pulmonary embolism was detected. Hypercoagulability screen before study entry was negative in all patients who subsequently developed DVTs. Compared to normal volunteers CLL patients had increased baseline levels of D-dimer, thrombin-antithrombin, soluble vascular endothelial adhesion molecule 1 (sVCAM-1), and thrombomodulin (p < 0.001). After 1 week on lenalidomide D-dimer, thrombomodulin, sVCAM-1, factor VIII, TNF alpha, and C-reactive protein were significantly increased while protein C was decreased (p < 0.001). In patients with lenalidomide-related DVTs, TNF alpha, and sVCAM-1 were more strongly upregulated than in all other patients (p < 0.05) and TNF alpha and sVCAM-1 levels were significantly correlated (r = 0.65, p < 0.001). These data link lenalidomide associated DVTs with TNF alpha upregulation and endothelial cell dysfunction and suggest that aspirin may have a role for DVT prophylaxis in these patients. Am. J. Hematol. 86: 835-840, 2011. (C) 2011 Wiley-Liss, Inc.
C1 [Aue, Georg; Soto, Susan; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Lozier, Jay Nelson; Cullinane, Ann M.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Tian, Xin] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
[Samsel, Leigh; McCoy, Philip] NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA.
RP Wiestner, A (reprint author), NHLBI, Hematol Branch, NIH, Bld 10,CRC 3-5140,10 Ctr Dr, Bethesda, MD 20892 USA.
EM wiestnera@mail.nih.gov
FU NIH
FX This research was supported by NIH Intramural Research program.
NR 30
TC 14
Z9 15
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
EI 1096-8652
J9 AM J HEMATOL
JI Am. J. Hematol.
PD OCT
PY 2011
VL 86
IS 10
BP 835
EP 840
DI 10.1002/ajh.22114
PG 6
WC Hematology
SC Hematology
GA 824WB
UT WOS:000295231800003
PM 21812019
ER
PT J
AU Rabkin, CS
Engels, EA
Landgren, O
Schuurman, R
Camargo, MC
Pfeiffer, R
Goedert, JJ
AF Rabkin, Charles S.
Engels, Eric A.
Landgren, Ola
Schuurman, Rob
Camargo, M. Constanza
Pfeiffer, Ruth
Goedert, James J.
TI Circulating cytokine levels, Epstein-Barr viremia, and risk of acquired
immunodeficiency syndrome-related non-Hodgkin lymphoma
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID ELEVATED SERUM-LEVELS; B-CELL LYMPHOMA; HOMOSEXUAL-MEN; AIDS;
EXPRESSION; INTERLEUKIN-5; INFECTION; SEQUENCE; CANCER
AB Cytokine dysregulation and decontrol of Epstein-Barr virus (EBV) latency by human immunodeficiency virus (HIV) infection are potential mechanisms for acquired immunodeficiency syndrome (AIDS)-related non-Hodgkin lymphoma (NHL). We therefore assessed circulating blood levels in pre-diagnosis plasma or serum from 63 AIDS-related NHL cases 0.1-2.0 (median 1.0) years pre-NHL and 181 controls matched for CD4+ T-cell count. Cytokines were measured by Millipore 30-plex Luminex assays and cell-free EBV DNA detected by polymerase chain reaction (PCR). Correlations in multiplex cytokine levels were summarized by factor analysis. Individual cytokines and their principal factors were analyzed for associations with NHL by conditional logistic regression. Cases had higher levels for 25 of the 30 cytokines. In analyses of cytokine profiles, cases had significantly higher scores for a principal factor primarily reflecting levels of interleukin (IL)-4, IL-5, IL-13, and granulocyte-macrophage colony stimulating factor (four gene products with coordinated transcription in vitro), as well as IL-1alpha. Epstein-Barr viremia was not significantly associated based on 113 evaluable samples without PCR inhibition. We found increases of T-helper Type 2 interleukins and generalized elevations of other inflammatory cytokines and growth factors up to 2 years before AIDS-NHL. Cytokine-mediated hyperstimulation of B-cell proliferation may play a role in AIDS-related lymphomagenesis.
C1 [Rabkin, Charles S.; Engels, Eric A.; Camargo, M. Constanza; Pfeiffer, Ruth; Goedert, James J.] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Landgren, Ola] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Schuurman, Rob] Univ Med Ctr Utrecht, Dept Virol, Utrecht, Netherlands.
RP Rabkin, CS (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Suite 7082, Rockville, MD 20852 USA.
EM rabkinc@mail.nih.gov
RI Camargo, M. Constanza/R-9891-2016
FU Intramural NIH HHS [ZIA CP010212-01]
NR 24
TC 10
Z9 10
U1 0
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD OCT
PY 2011
VL 86
IS 10
BP 875
EP 878
DI 10.1002/ajh.22119
PG 4
WC Hematology
SC Hematology
GA 824WB
UT WOS:000295231800014
PM 22022727
ER
PT J
AU O'Seaghdha, CM
Fox, CS
AF O'Seaghdha, Conall M.
Fox, Caroline S.
TI In Reply to 'Does High or Low Urinary Connective Tissue Growth Factor
Predict CKD?'
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Letter
C1 [O'Seaghdha, Conall M.; Fox, Caroline S.] Brigham & Womens Hosp, NHLBI, Boston, MA 02115 USA.
RP O'Seaghdha, CM (reprint author), Brigham & Womens Hosp, NHLBI, 75 Francis St, Boston, MA 02115 USA.
NR 8
TC 0
Z9 0
U1 1
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD OCT
PY 2011
VL 58
IS 4
BP 681
EP 682
DI 10.1053/j.ajkd.2011.08.007
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA 826UE
UT WOS:000295379600030
ER
PT J
AU Gripp, KW
Hopkins, E
Johnston, JJ
Krause, C
Dobyns, WB
Biesecker, LG
AF Gripp, Karen W.
Hopkins, Elizabeth
Johnston, Jennifer J.
Krause, Caitlin
Dobyns, William B.
Biesecker, Leslie G.
TI Long-Term Survival in TARP Syndrome and Confirmation of RBM10 as the
Disease-Causing Gene
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE ASD; cryptorchidism; persistent left superior vena cava; Pierre-Robin
sequence; RBM10; talipes equinovarus; X-linked
AB TARP syndrome, comprising Talipes equinovarus, atrial septal defect (ASD), Robin sequence (micrognathia, glossoptosis, and cleft palate), and persistence of the left superior vena cava, is an X-linked condition with pre- or postnatal lethality in affected males. Based on linkage studies and massively parallel sequencing of X-chromosome exons in two families, the disease-causing gene was identified as RBM10. We identified a maternally inherited frameshift mutation in an unrelated patient, confirming RBM10 as the disease gene. This is the first reported individual with TARP syndrome who survived past early infancy, thus expanding the phenotypic spectrum of this disorder. In addition to the characteristic cleft palate, ASD, and persistent superior vena cava, he had low-set and posteriorly angulated ears, upslanting palpebral fissures, cryptorchidism, and structural brain abnormalities including partial agenesis of the corpus callosum, dysplastic enlarged caudate, and cerebellar hypoplasia with megacisterna magna. Preterm delivery, suspected pulmonary hypoplasia, and pulmonary hypertension resulted in chronic lung disease. At the age of 3 7/12 years, he remained ventilator-dependent at night, and he was fed exclusively through a gastro-jejunal tube. Sensorineural hearing loss required a hearing aid. Optic atrophy and cortical visual impairment were noted. He was unable to sit independently, was non-communicative and he had severe intellectual disability. Atrial flutter required recurrent ablation of intra-atrial re-entry pathways. The mother's hetero-zygosity for the RBM10 mutation underscored the importance of accurate diagnosis and counseling for TARP syndrome. (C) 2011 Wiley-Liss, Inc.
C1 [Gripp, Karen W.; Hopkins, Elizabeth] Alfred I DuPont Hosp Children, Div Med Genet, Wilmington, DE 19803 USA.
[Johnston, Jennifer J.; Krause, Caitlin; Biesecker, Leslie G.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Dobyns, William B.] Seattle Childrens Res Inst, Seattle, WA USA.
RP Gripp, KW (reprint author), Alfred I DuPont Hosp Children, Div Med Genet, Wilmington, DE 19803 USA.
EM kgripp@nemours.org
OI Dobyns, William/0000-0002-7681-2844
FU National Human Genome Research Institute of the National Institutes of
Health
FX Grant sponsor: Intramural Program of the National Human Genome Research
Institute of the National Institutes of Health.; We appreciate the
family's generosity in allowing us to share this information. This work
was supported in part by funding from the Intramural Program of the
National Human Genome Research Institute of the National Institutes of
Health.
NR 3
TC 14
Z9 14
U1 0
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2011
VL 155A
IS 10
BP 2516
EP 2520
DI 10.1002/ajmg.a.34190
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 826BL
UT WOS:000295326300029
PM 21910224
ER
PT J
AU Lieu, TA
Au, D
Krishnan, JA
Moss, M
Selker, H
Harabin, A
Taggart, V
Connors, A
AF Lieu, Tracy A.
Au, David
Krishnan, Jerry A.
Moss, Marc
Selker, Harry
Harabin, Andrea
Taggart, Virginia
Connors, Alfred
CA Comparative Effectiveness Res Lung
TI Comparative Effectiveness Research in Lung Diseases and Sleep Disorders
Recommendations from the National Heart, Lung, and Blood Institute
Workshop
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE randomized controlled trials; observational studies; implementation;
study designs; methodology
ID UNITED-STATES; TIME-SERIES; CARE; SAFETY; NETWORK; ASTHMA; TRIAL
AB The Division of Lung Diseases of the National Heart, Lung, and Blood Institute (NHLBI) held a workshop to develop recommendations on topics, methodologies, and resources for comparative effectiveness research (CER) that will guide clinical decision making about available treatment options for lung diseases and sleep disorders. A multidisciplinary group of experts with experience in efficacy, effectiveness, implementation, and economic research identified (a) what types of studies the domain of CER in lung diseases and sleep disorders should include, (b) the criteria and process for setting priorities, and (c) current resources for and barriers to CER in lung diseases. Key recommendations were to (1) increase efforts to engage stakeholders in developing CER questions and study designs; (2) invest in further development of databases and other infrastructure, including efficient methods for data sharing; (3) make full use of a broad range of study designs; (4) increase the appropriate use of observational designs and the support of methodologic research; (5) ensure that committees that review CER grant applications include persons with appropriate perspective and expertise; and (6) further develop the workforce for CER by supporting training opportunities that focus on the methodologic and practical skills needed.
C1 [Harabin, Andrea; Taggart, Virginia] NHLBI, Div Lung Dis, NIH, Bethesda, MD 20892 USA.
[Connors, Alfred] Case Western Reserve Univ, Sch Med, Metrohlth Med Ctr, Cleveland, OH USA.
[Lieu, Tracy A.] Harvard Univ, Sch Med, Dept Populat Med, Boston, MA USA.
[Lieu, Tracy A.] Harvard Pilgrim Hlth Care Inst, Boston, MA USA.
[Lieu, Tracy A.] Childrens Hosp, Div Gen Pediat, Boston, MA 02115 USA.
[Au, David] VA Puget Sound Hlth Care Syst, Hlth Serv Res & Dev, Seattle, WA USA.
[Au, David] Univ Washington, Div Pulm & Crit Care Med, Seattle, WA 98195 USA.
[Au, David] Dept Vet Affairs, Seattle, WA USA.
[Krishnan, Jerry A.] Univ Chicago, Dept Med, Asthma & COPD Ctr, Chicago, IL 60637 USA.
[Krishnan, Jerry A.] Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA.
[Moss, Marc] Univ Colorado, Sch Med, Dept Med, Denver, CO USA.
[Selker, Harry] Tufts Univ, Tufts Med Ctr, Inst Clin Res & Hlth Policy Studies, Clin & Translat Sci Inst, Boston, MA 02111 USA.
RP Taggart, V (reprint author), NHLBI, Div Lung Dis, NIH, 6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM taggartv@nih.gov
FU Division of Lung Diseases, National Heart, Lung, and Blood Institute,
National Institutes of Health; HSR&D, VA Puget Sound Health Care System
FX Supported by the Division of Lung Diseases, National Heart, Lung, and
Blood Institute, National Institutes of Health.; D.A. was funded by
HSR&D, VA Puget Sound Health Care System. The views expressed in this
manuscript are those of the authors and do not necessarily represent the
opinions of the Department of Veterans Affairs.
NR 42
TC 23
Z9 24
U1 1
U2 4
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD OCT 1
PY 2011
VL 184
IS 7
BP 848
EP 856
DI 10.1164/rccm.201104-0634WS
PG 9
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 827DM
UT WOS:000295407300020
PM 21965016
ER
PT J
AU Miller, FG
AF Miller, Franklin G.
TI Dispensing With Equipoise
SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES
LA English
DT Article
DE Clinical equipoise; Informed consent; Clinical research; Research ethics
ID RANDOMIZED CLINICAL-TRIALS; PLACEBO-CONTROLLED TRIALS; ETHICS;
HYPERPLASIA; DISORDER; CRITIQUE; BENEFIT; CANCER
AB Equipoise is widely endorsed as a necessary requirement for ethical design and conduct of randomized controlled trials. Nevertheless, I argue in this article that the equipoise principle suffers from fundamental defects. In particular, equipoise provides flawed ethical guidance for placebo-controlled trials and for decisions to terminate trials early based on interim data relating to benefit. The problems with equipoise are traced to a "therapeutic orientation to clinical trials," which conflates the ethics of clinical research with the ethics of medical care. Because of this mistaken therapeutic orientation, equipoise fails to adequately account for the central purpose of randomized trials in providing evidence sufficient to guide health policy decisions relating to licensing new treatments and insurance coverage. I conclude that it is time to dispense with equipoise. The principles of research ethics are sufficient to provide adequate guidance to protect subjects and to promote socially valuable research without any appeal to equipoise.
C1 NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
RP Miller, FG (reprint author), NIH, Dept Bioeth, Ctr Clin, Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM fmiller@nih.gov
NR 26
TC 2
Z9 2
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0002-9629
J9 AM J MED SCI
JI Am. J. Med. Sci.
PD OCT
PY 2011
VL 342
IS 4
BP 276
EP 281
DI 10.1097/MAJ.0b013e318227e871
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA 825ZN
UT WOS:000295321000004
PM 21804362
ER
PT J
AU Colbert, RA
Cronstein, BN
AF Colbert, Robert A.
Cronstein, Bruce N.
TI Biosimilars: The Debate Continues
SO ARTHRITIS AND RHEUMATISM
LA English
DT Editorial Material
C1 [Colbert, Robert A.] NIAMSD, Pediat Translat Res Branch, NIH, CRC, Bethesda, MD 20892 USA.
[Cronstein, Bruce N.] NYU, Sch Med, New York, NY USA.
RP Colbert, RA (reprint author), NIAMSD, Pediat Translat Res Branch, NIH, CRC, 10 Ctr Dr,Room 1-5142,MSC 1102, Bethesda, MD 20892 USA.
EM colbertr@mail.nih.gov
FU Intramural NIH HHS [ZIA AR041184-02]; NCRR NIH HHS [UL1 RR029893,
UL1-RR-029893]; NIAMS NIH HHS [AR-54897, AR-56672, AR-56672S1, R01
AR054897, R56 AR056672, R01 AR056672]
NR 6
TC 10
Z9 11
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2011
VL 63
IS 10
BP 2848
EP 2850
DI 10.1002/art.30505
PG 3
WC Rheumatology
SC Rheumatology
GA 825PN
UT WOS:000295293000002
PM 21702015
ER
PT J
AU Greenwell-Wild, T
Moutsopoulos, NM
Gliozzi, M
Kapsogeorgou, E
Rangel, Z
Munson, PJ
Moutsopoulos, HM
Wahl, SM
AF Greenwell-Wild, Teresa
Moutsopoulos, Niki M.
Gliozzi, Maria
Kapsogeorgou, Efstathia
Rangel, Zoila
Munson, Peter J.
Moutsopoulos, Haralampos M.
Wahl, Sharon M.
TI Chitinases in the Salivary Glands and Circulation of Patients With
Sjogren's Syndrome Macrophage Harbingers of Disease Severity
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID COLONY-STIMULATING FACTOR; NECROSIS-FACTOR-ALPHA; T-CELLS; IN-VIVO;
EXPRESSION; STAT4; INTERLEUKIN-17; ACTIVATION; INTERFERON; INVOLVEMENT
AB Objective. Sjogren's syndrome (SS) is a chronic autoimmune disease of unknown etiology that targets salivary and lacrimal glands and may be accompanied by multiorgan systemic manifestations. To further the understanding of immunopathology associated with SS and identify potential therapeutic targets, we undertook the present study comparing the gene expression profiles of salivary glands with severe inflammation versus those of salivary glands with mild or no disease.
Methods. Using microarray profiling of salivary gland tissue from patients with SS and control subjects, we identified target genes, which were further characterized in tissue, serum, and cultured cell populations by real-time polymerase chain reaction and protein analysis.
Results. Among the most highly expressed SS genes were those associated with myeloid cells, including members of the mammalian chitinase family, which had not previously been shown to be associated with exocrinopathies. Both chitinase 3-like protein 1 and chitinase 1, highly conserved chitinase-like glycoproteins (one with enzymatic activity and one lacking enzymatic activity), were evident at the transcriptome level and were detected within inflamed tissue. Chitinases were expressed during monocyte-to-macrophage differentiation and their levels augmented by stimulation with cytokines, including interferon-alpha (IFN alpha).
Conclusion. Because elevated expression of these and other macrophage-derived molecules corresponded with more severe SS, the present observations suggest that macrophages have potential immunopathologic involvement in SS and that the tissue macrophage transcription profile reflects multiple genes induced by IFN alpha.
C1 [Wahl, Sharon M.] Natl Inst Dent & Craniofacial Res, NIH, Oral Infect & Immun Branch, Bethesda, MD 20892 USA.
[Kapsogeorgou, Efstathia; Moutsopoulos, Haralampos M.] Natl Univ Athens, Sch Med, Athens, Greece.
[Rangel, Zoila; Munson, Peter J.] NIH, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Wahl, SM (reprint author), Natl Inst Dent & Craniofacial Res, NIH, Oral Infect & Immun Branch, Bldg 30,Room 320,30 Convent Dr,MSC 4352, Bethesda, MD 20892 USA.
EM SMWahl@mail.nih.gov
FU NIH, National Institute of Dental and Craniofacial Research
FX Supported in part by the Intramural Research Program of the NIH,
National Institute of Dental and Craniofacial Research.
NR 55
TC 15
Z9 15
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD OCT
PY 2011
VL 63
IS 10
BP 3103
EP 3115
DI 10.1002/art.30465
PG 13
WC Rheumatology
SC Rheumatology
GA 825PN
UT WOS:000295293000032
PM 21618203
ER
PT J
AU Xu, MY
Weinberg, CR
Umbach, DM
Li, LP
AF Xu, Mengyuan
Weinberg, Clarice R.
Umbach, David M.
Li, Leping
TI coMOTIF: a mixture framework for identifying transcription factor and a
coregulator motif in ChIP-seq Data
SO BIOINFORMATICS
LA English
DT Article
ID FACTOR-BINDING SITES; EXPECTATION MAXIMIZATION; EM ALGORITHM; BAYESIAN
MODELS; DISCOVERY; GIBBS; SEQUENCE; ALIGNMENT; ELEMENTS; IDENTIFICATION
AB Motivation: ChIP-seq data are enriched in binding sites for the protein immunoprecipitated. Some sequences may also contain binding sites for a coregulator. Biologists are interested in knowing which coregulatory factor motifs may be present in the sequences bound by the protein ChIP'ed.
Results: We present a finite mixture framework with an expectation-maximization algorithm that considers two motifs jointly and simultaneously determines which sequences contain both motifs, either one or neither of them. Tested on 10 simulated ChIP-seq datasets, our method performed better than repeated application of MEME in predicting sequences containing both motifs. When applied to a mouse liver Foxa2 ChIP-seq dataset involving similar to 12 000 400-bp sequences, coMOTIF identified co-occurrence of Foxa2 with Hnf4a, Cebpa, E-box, Ap1/Maf or Sp1 motifs in similar to 6-33% of these sequences. These motifs are either known as liver-specific transcription factors or have an important role in liver function.
C1 [Xu, Mengyuan; Weinberg, Clarice R.; Umbach, David M.; Li, Leping] Natl Inst Environm Hlth Sci, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
RP Li, LP (reprint author), Natl Inst Environm Hlth Sci, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
FU National Institutes of Health; National Institute of Environmental
Health Sciences [ES101765-05]
FX Funding: Intramural Research Program of the National Institutes of
Health; National Institute of Environmental Health Sciences
(ES101765-05).
NR 37
TC 4
Z9 5
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
J9 BIOINFORMATICS
JI Bioinformatics
PD OCT 1
PY 2011
VL 27
IS 19
BP 2625
EP 2632
DI 10.1093/bioinformatics/btr397
PG 8
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA 827FC
UT WOS:000295412200002
PM 21775309
ER
PT J
AU Han, HY
Qiu, L
Wang, XH
Qiu, F
Wong, YC
Yao, XS
AF Han, Huiying
Qiu, Li
Wang, Xianghong
Qiu, Feng
Wong, Yongchuan
Yao, Xinsheng
TI Physalins A and B Inhibit Androgen-Independent Prostate Cancer Cell
Growth through Activation of Cell Apoptosis and Downregulation of
Androgen Receptor Expression
SO BIOLOGICAL & PHARMACEUTICAL BULLETIN
LA English
DT Article
DE physalin A; physalin B; androgen-independent prostate cancer; apoptosis;
androgen receptor
ID SIGNAL-TRANSDUCTION PATHWAYS; PROTEIN-KINASE; DEATH; GENE; P38;
PROGRESSION; CARCINOMA; ANTIGEN
AB Androgen deprivation therapy is a common treatment strategy for advanced prostate cancer. Though effective initially, the tumor often progresses to androgen independent stage in most patients eventually after a period of remission. One of the key factors of development of resistance is reflected in expression of androgen receptor (AR). In this study, we showed that two natural compounds, physalins A and B, both secosteriods from Physalisalkekengi var. franchetii, significantly inhibited the growth of two androgen-independent cell lines CWR22Rv1 and C42B, induced apoptosis via c-Jun N-terminal kinase (JNK) and/or extracellular signal-regulated kinase (ERK) activation, and decreased AR expression. In addition, physalins A and B down-regulated the expression of prostate specific antigen (PSA) in C42B cells which is a target gene of AR. Our results suggest that physalin A and B might be useful agents in preventing the growth of androgen-independent prostate cancer (AI-PCa).
C1 [Wang, Xianghong; Wong, Yongchuan] Univ Hong Kong, Fac Med, Dept Anat, Canc Biol Grp, Hong Kong, Hong Kong, Peoples R China.
[Han, Huiying] NCI, Extracellular Matrix Pathol Sect, Radiat Oncol Branch, Ctr Canc Res,NIH,Adv Technol Ctr, Bethesda, MD 20892 USA.
[Qiu, Li] Guangxi Inst Med Plant, Nanning 530023, Guangxi, Peoples R China.
[Qiu, Feng; Yao, Xinsheng] Shenyang Pharmaceut Univ, Coll Tradit Chinese Mat Med, Shenyang 110015, Peoples R China.
[Yao, Xinsheng] Jinan Univ, Inst Tradit Chinese Med & Nat Prod, Guangzhou 510632, Guangdong, Peoples R China.
RP Wong, YC (reprint author), Univ Hong Kong, Fac Med, Dept Anat, Canc Biol Grp, 21 Sassoon Rd, Hong Kong, Hong Kong, Peoples R China.
EM ycwong@hkucc.hku.hk; tyaoxs@jnu.edu.cn
NR 33
TC 7
Z9 7
U1 0
U2 4
PU PHARMACEUTICAL SOC JAPAN
PI TOKYO
PA 2-12-15 SHIBUYA, SHIBUYA-KU, TOKYO, 150-0002, JAPAN
SN 0918-6158
J9 BIOL PHARM BULL
JI Biol. Pharm. Bull.
PD OCT
PY 2011
VL 34
IS 10
BP 1584
EP 1588
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 826YI
UT WOS:000295391100010
PM 21963499
ER
PT J
AU Pearl, PL
Shukla, L
Theodore, WH
Jakobs, C
Gibson, KM
AF Pearl, Phillip L.
Shukla, Lovy
Theodore, William H.
Jakobs, Cornelis
Gibson, K. Michael
TI Epilepsy in succinic semialdehyde dehydrogenase deficiency, a disorder
of GABA metabolism
SO BRAIN & DEVELOPMENT
LA English
DT Article; Proceedings Paper
CT 13th Annual Meeting of the Infantile-Seizure-Society/International
Symposium on Epilepsy in Neurometabolic Diseases (ISENMD)
CY MAR 26-28, 2010
CL Taipei, TAIWAN
SP Infantile Seizure Soc
ID GAMMA-HYDROXYBUTYRIC ACID; SSADH DEFICIENCY; MICE DEFICIENT; ABSENCE
SEIZURES; VIGABATRIN; CHILDREN; MECHANISMS; DISEASE; PATIENT; ADULTS
AB Objectives: Succinic semialdehyde dehydrogenase (SSADH) deficiency is a gamma-aminobutyric acid (GABA) degradative defect. Epilepsy affects half of patients. The murine model is associated with a transition from absence to convulsive seizures in the third week, with fatal status epilepticus.
Methods: The clinical phenotype is reported from a patient database. Flumazenil-Positron Emission Topography (FMZ-PET) and Transcranial Magnetic Stimulation (TMS) were used to study GABA neurotransmission. Electrocorticography, single cell electrophysiology, and radioligand binding studies are reported from animal studies.
Results: Generalized seizures predominate, including tonic clonic, atypical absence, and myoclonic. EEG discharges are typically generalized spike-wave. MRI shows a dentatopallidoluysian pattern. Sudden Unexpected Death in Epilepsy Patients (SUDEP) has occurred and the associated neuropathology reveals chronic excitotoxic injury in gloubus pallidus. Investigations using FMZ-PET and TMS support downregulation of GABA(A) and GABA(B) activity, respectively, in patients. Gamma-hydroxybutyrate (GHB) induces spike-wave discharges in homozygous null mice via GHB and GABA(B)-mediated mechanisms. These resemble absence seizures and are abolished by a GABA(B) receptor antagonist. Decreased binding of GABA(A) and GABA(B) receptor antagonists has been demonstrated in P19 and P14 null mice, respectively. Downregulation of GABA(A) and GABA(B) receptor subunits is observed by P14. GABA(A) and GABA(B) mediated potentials are reduced from P8-P14.
Conclusion: Generalized epilepsy and epileptiform discharges are characteristic of SSADH deficiency. Spontaneous absence seizures appear in null mice by the third week, which may be induced by GHB or GABA(B) activity. Subsequent overuse dependent downregulation of GABA(A) and GABA(B) receptor activity may be associated with hyperexcitability concomitant with the transition to generalized seizures. (C) 2011 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
C1 [Pearl, Phillip L.; Shukla, Lovy] George Washington Univ, Sch Med, Childrens Natl Med Ctr, Dept Neurol, Washington, DC 20010 USA.
[Pearl, Phillip L.; Theodore, William H.] Natl Inst Neurol Disorders & Stroke, Clin Epilepsy Branch, NIH, Bethesda, MD USA.
[Jakobs, Cornelis] Vrije Univ Amsterdam, Med Ctr, Dept Clin Chem, Metab Unit, Amsterdam, Netherlands.
[Gibson, K. Michael] Michigan Technol Univ, Dept Biol Sci, Houghton, MI 49931 USA.
RP Pearl, PL (reprint author), George Washington Univ, Sch Med, Childrens Natl Med Ctr, Dept Neurol, 111 Michigan Ave NW, Washington, DC 20010 USA.
EM ppearl@cnmc.org
FU NICHD NIH HHS [NS 40270/HD58553, R01 HD058553]; NINDS NIH HHS [R01
NS040270]
NR 35
TC 20
Z9 20
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0387-7604
J9 BRAIN DEV-JPN
JI Brain Dev.
PD OCT
PY 2011
VL 33
IS 9
BP 796
EP 805
DI 10.1016/j.braindev.2011.04.013
PG 10
WC Clinical Neurology
SC Neurosciences & Neurology
GA 827QN
UT WOS:000295443100013
PM 21664777
ER
PT J
AU Amodio, E
Goedert, JJ
Barozzi, P
Riva, G
Firenze, A
Bonura, F
Viviano, E
Romano, N
Luppi, M
AF Amodio, Emanuele
Goedert, James J.
Barozzi, Patrizia
Riva, Giovanni
Firenze, Alberto
Bonura, Filippa
Viviano, Enza
Romano, Nino
Luppi, Mario
TI Differences in Kaposi sarcoma-associated herpesvirus-specific and
herpesvirus-non-specific immune responses in classic Kaposi sarcoma
cases and matched controls in Sicily
SO CANCER SCIENCE
LA English
DT Article
ID ACTIVE ANTIRETROVIRAL THERAPY; MULTICENTRIC CASTLEMANS-DISEASE; PRIMARY
EFFUSION LYMPHOMA; SWISS HIV COHORT; T-CELL RESPONSES; PERIPHERAL-BLOOD;
INFECTED INDIVIDUALS; RISK-FACTORS; HUMAN-HERPESVIRUS-8; VIRUS
AB Kaposi sarcoma (KS) might develop because of incompetent immune responses, both non-specifically and specifically against the KS-associated herpesvirus (KSHV). Peripheral blood mononuclear cells from 15 classic (non-AIDS) KS cases, 13 KSHV seropositives (without KS) and 15 KSHV-seronegative controls were tested for interferon-c T-cell (enzyme-linked immunospot [Elispot]) responses to KSHV-latency-associated nuclear antigen (LANA), KSHV-K8.1 and CMV/Epstein-Barr virus (EBV) peptide pools. The forearm and thigh of each participant was also tested for delayed-type hypersensitivity (DTH) against common recall antigens. Groups were compared with Fisher exact test and multinomial logistic regression to calculate odds ratios (OR) and 95% confidence intervals (CI). A KSHV Elispot response was detected in 10 (67%) classic KS cases, 11 (85%) KSHV seropositives (without KS) and two (13%) seronegative controls. All four cases with KSHV-LANA responses had current KS lesions, whereas five of six cases with KSHV-K8.1 responses had no lesions (P = 0.048). No case responded to both LANA and K8.1. Compared with the seronegative controls, the risk for classic KS was inversely related to DTH in the thigh (OR 0.71, 95% CI 0.55-0.94, P = 0.01), directly associated with DTH in the forearm (OR 1.35, 95% CI 1.02-1.80, P = 0.04) and tended to be increased fivefold per KSHV Elispot response (OR 5.13, 95% CI 0.86-30.77, P = 0.07). Compared with KSHV seropositives (without KS), the risk for classic KS was reduced fivefold (OR 0.20, CI 0.03-0.77, P = 0.04) per KSHV response. The CMV/EBV Elispot responses were irrelevant. Deficiency of both KSHV-specific and KSHV-non-specific immunity is associated with classic KS. This might clarify why Kaposi sarcoma responds to immune reconstitution. (Cancer Sci 2011; 102: 1769-1773)
C1 [Goedert, James J.] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Amodio, Emanuele; Firenze, Alberto; Bonura, Filippa; Viviano, Enza; Romano, Nino] Univ Palermo, Dept Sci Hlth Promot G DAlessandro, Sect Hyg, Palermo, Italy.
[Barozzi, Patrizia; Riva, Giovanni; Luppi, Mario] Univ Modena & Reggio Emilia, Dept Oncol, Modena, Italy.
[Barozzi, Patrizia; Riva, Giovanni; Luppi, Mario] Univ Modena & Reggio Emilia, Dept Hematol, Modena, Italy.
[Barozzi, Patrizia; Riva, Giovanni; Luppi, Mario] Univ Modena & Reggio Emilia, Dept Resp Dis, Modena, Italy.
RP Goedert, JJ (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
EM goedertj@mail.nih.gov
RI Luppi, Mario/J-3668-2016; Barozzi, Patrizia/Q-2638-2016
OI Luppi, Mario/0000-0002-0373-1154; Barozzi, Patrizia/0000-0002-8936-1114
FU National Cancer Institute, National Institutes of Health; Associazione
Italiana per la Ricerca sul Cancro (AIRC), Milan, Italy; Programma di
ricerca Regione-Universita (PRU), Regione Emilia Romagna; European
Commission [LSHC-CT-2005-018704]; Associazione Italiana Lotta alle
Leucemie, Linfoma e Mieloma (AIL)-Sezione "Luciano
Pavarotti"-Modena-ONLUS
FX The authors thank Liliana Preiss, RTI International, for computer
programming and analysis, as well as the study participants. This study
was supported in part by: the Intramural Research Program of the
National Cancer Institute, National Institutes of Health (J. J. G.); the
Associazione Italiana per la Ricerca sul Cancro (AIRC), Milan, Italy (M.
L.); the Programma di ricerca Regione-Universita (PRU) 2007-2009,
Regione Emilia Romagna (M. L.); the European Commission's FP6
Life-Science-Health Programme (INCA project; LSHC-CT-2005-018704) (M.
L.); and the Associazione Italiana Lotta alle Leucemie, Linfoma e
Mieloma (AIL)-Sezione "Luciano Pavarotti"-Modena-ONLUS (M. L.).
NR 30
TC 6
Z9 6
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1347-9032
J9 CANCER SCI
JI Cancer Sci.
PD OCT
PY 2011
VL 102
IS 10
BP 1769
EP 1773
DI 10.1111/j.1349-7006.2011.02032.x
PG 5
WC Oncology
SC Oncology
GA 826CK
UT WOS:000295328800001
PM 21740480
ER
PT J
AU Wong, HL
Rabkin, CS
Shu, XO
Pfeiffer, RM
Cai, Q
Ji, BT
Yang, G
Li, HL
Rothman, N
Gao, YT
Zheng, W
Chow, WH
AF Wong, Hui-Lee
Rabkin, Charles S.
Shu, Xiao-Ou
Pfeiffer, Ruth M.
Cai, Qiuyin
Ji, Bu-Tian
Yang, Gong
Li, Hong-Lan
Rothman, Nathaniel
Gao, Yu-Tang
Zheng, Wei
Chow, Wong-Ho
TI Systemic cytokine levels and subsequent risk of gastric cancer in
Chinese Women
SO CANCER SCIENCE
LA English
DT Article
ID HELICOBACTER-PYLORI INFECTION; NECROSIS-FACTOR-ALPHA; ELEVATED LEVELS;
INTERLEUKIN-6; HEALTH; POPULATION; REPRODUCIBILITY; POLYMORPHISMS;
INFLAMMATION; METASTASIS
AB Although control of the host cytokine network is known to influence gastric cancer susceptibility, the specific inflammatory responses in gastric carcinogenesis remain unclear. We prospectively examined the relationships between gastric cancer risk and plasma levels of interleukin (IL)-1 beta, IL-6, IL-8 and tumor necrosis factor (TNF)-alpha in a nested case control study within The Shanghai Women's Health Study. Two controls were matched to each case on the basis of age, menopausal status, and sample collection parameters. The associations between gastric cancer risk and tertiles of cytokine levels were estimated by odds ratios (OR) and 95% confidence intervals (CI) from conditional logistic regression, adjusting for education. During a median follow-up period of 4 years (range 0.1-8 years), 141 women developed gastric cancer and were matched to 282 cancer-free study participants. Elevated levels of plasma IL-6 were associated with an increased risk of gastric cancer (P-trend = 0.04). Risk increased 70% (OR = 1.7; 95% CI 1.0, 3.0) for women in the highest tertile (>4 pg/mL) of IL-6 compared with those in the lowest tertile (<1.8 pg/mL). The association between gastric cancer risk and IL-6 was stronger after 4 years of follow-up (OR = 2.6 [95% CI 1.0, 6.7] for highest versus lowest tertile) compared with an OR of 1.4 (95% CI 0.7, 2.9) for those diagnosed within 1-4 years of follow-up. No associations were observed with the other pro-inflammatory cytokines examined, namely IL-1 beta, IL-8, and TNF-alpha. Systemic plasma IL-6 levels may inform long-term gastric cancer risk. This novel finding awaits confirmation in future studies with sequential plasma collection. (Cancer Sci 2011; 102: 1911-1915)
C1 [Wong, Hui-Lee] US FDA, Silver Spring, MD USA.
[Rabkin, Charles S.; Pfeiffer, Ruth M.; Ji, Bu-Tian; Rothman, Nathaniel; Chow, Wong-Ho] NCI, US NIH, Rockville, MD USA.
[Shu, Xiao-Ou; Cai, Qiuyin; Yang, Gong; Zheng, Wei] Vanderbilt Univ, Nashville, TN USA.
[Li, Hong-Lan; Gao, Yu-Tang] Shanghai Canc Inst, Shanghai, Peoples R China.
RP Wong, HL (reprint author), US FDA, Silver Spring, MD USA.
EM huilee.wong@fda.hhs.gov
FU National Institutes of Health [R37 CA70867]; Intramural Research Program
[N02 CP1101066]; Vanderbilt-Ingram Cancer Center [P30 CA68485]
FX The work was supported by a grant from the National Institutes of Health
(R37 CA70867) and an Intramural Research Program contract (N02
CP1101066). The authors thank the Shanghai residents who participated in
the study and the research staff of the Shanghai Women's Health Study.
The authors also thank Regina Courtney for plasma sample preparation at
the Survey and Biospecimen Shared Resources supported, in part, by the
Vanderbilt-Ingram Cancer Center (P30 CA68485).
NR 31
TC 10
Z9 11
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1347-9032
J9 CANCER SCI
JI Cancer Sci.
PD OCT
PY 2011
VL 102
IS 10
BP 1911
EP 1915
DI 10.1111/j.1349-7006.2011.02033.x
PG 5
WC Oncology
SC Oncology
GA 826CK
UT WOS:000295328800010
PM 21740481
ER
PT J
AU Liu, F
Hsing, AW
Wang, X
Shao, Q
Qi, J
Ye, Y
Wang, ZY
Chen, HY
Gao, X
Wang, GZ
Chu, LW
Ding, Q
OuYang, J
Gao, X
Huang, YC
Chen, YB
Gao, YT
Zhang, ZF
Rao, J
Shi, R
Wu, QJ
Wang, ML
Zhang, ZD
Zhang, YY
Jiang, HW
Zheng, J
Hu, YL
Guo, L
Lin, XL
Tao, S
Jin, GF
Sun, JL
Lu, DR
Zheng, SL
Sun, YH
Mo, ZN
Xu, JF
AF Liu, Fang
Hsing, Ann W.
Wang, Xiang
Shao, Qiang
Qi, Jun
Ye, Yu
Wang, Zhong
Chen, Hongyan
Gao, Xin
Wang, Guozeng
Chu, Lisa W.
Ding, Qiang
OuYang, Jun
Gao, Xu
Huang, Yichen
Chen, Yanbo
Gao, Yu Tang
Zhang, Zuo-Feng
Rao, Jianyu
Shi, Rong
Wu, Qijun
Wang, Meilin
Zhang, Zhengdong
Zhang, Yuanyuan
Jiang, Haowen
Zheng, Jie
Hu, Yanlin
Guo, Ling
Lin, Xiaoling
Tao, Sha
Jin, Guangfu
Sun, Jielin
Lu, Daru
Zheng, S. Lilly
Sun, Yinghao
Mo, Zengnan
Xu, Jianfeng
TI Systematic confirmation study of reported prostate cancer
risk-associated single nucleotide polymorphisms in Chinese men
SO CANCER SCIENCE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; SUSCEPTIBILITY LOCI; VARIANTS; MULTIPLE;
IDENTIFICATION; REPLICATION; POPULATIONS; 8Q24
AB More than 30 prostate cancer (PCa) risk-associated loci have been identified in populations of European descent by genome-wide association studies. We hypothesized that a subset of these loci might be associated with PCa risk in Chinese men. To test this hypothesis, 33 single nucleotide polymorphisms (SNP), one each from the 33 independent PCa risk-associated loci reported in populations of European descent, were investigated for their associations with PCa risk in a case-control study of Chinese men (1108 cases and 1525 controls). We found that 11 of the 33 SNP were significantly associated with PCa risk in Chinese men (P < 0.05). The reported risk alleles were associated with increased risk for PCa, with allelic odds ratios ranging from 1.12 to 1.44. The most significant locus was located on 8q24 region 2 (rs16901979, P = 5.14 x 10(-9)) with a genome-wide significance (P < 10(-8)), and three loci reached the Bonferroni correction significance level (P < 1.52 x 10(-3)), including 8q24 region 1 (rs1447295, P = 7.04 x 10(-6)), 8q24 region 5 (rs10086908, P = 9.24 x 10(-4)) and 8p21 (rs1512268, P = 9.39 x 10(-4)). Our results suggest that a subset of the PCa risk-associated SNP discovered by genome-wide association studies among men of European descent is also associated with PCa risk in Chinese men. This finding provides evidence of ethnic differences and similarity in genetic susceptibility to PCa. Genome-wide association studies in Chinese men are needed to identify Chinese-specific PCa risk-associated SNP. (Cancer Sci 2011; 102: 1916-1920)
C1 [Gao, Xu; Sun, Yinghao] Second Mil Med Univ, Changhai Hosp, Dept Urol, Shanghai, Peoples R China.
[Liu, Fang; Chen, Hongyan; Lin, Xiaoling; Sun, Jielin; Lu, Daru; Zheng, S. Lilly; Xu, Jianfeng] Fudan Univ, Sch Life Sci, Fudan VARI Ctr Genet Epidemiol, Shanghai 200433, Peoples R China.
[Hsing, Ann W.; Chu, Lisa W.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Wang, Xiang; Ding, Qiang; Jiang, Haowen; Zheng, Jie; Xu, Jianfeng] Fudan Univ, Huashan Hosp, Dept Urol, Shanghai 200433, Peoples R China.
[Shao, Qiang] Suchow Univ, Affiliated Hosp 1, Suzhou Municipal Hosp, Dept Urol, Suzhou, Peoples R China.
[Qi, Jun; Huang, Yichen] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Urol, Shanghai 200030, Peoples R China.
[Ye, Yu; Hu, Yanlin; Mo, Zengnan] Guangxi Med Univ, Affiliated Hosp 1, Dept Urol, Guangxi, Peoples R China.
[Wang, Zhong; Chen, Yanbo] Shanghai Jiao Tong Univ, Sch Med, Peoples Hosp 9, Dept Urol, Shanghai 200030, Peoples R China.
[Chen, Hongyan; Lu, Daru; Xu, Jianfeng] Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Key Lab Contemporary Anthropol, Shanghai 200433, Peoples R China.
[Gao, Xin] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Urol, Guangzhou 510275, Guangdong, Peoples R China.
[Wang, Guozeng] Pudong Gongli Hosp, Dept Urol, Shanghai, Peoples R China.
[OuYang, Jun] Suzhou Univ, Peoples Hosp 1, Dept Urol, Suzhou 215006, Peoples R China.
[Gao, Yu Tang] Shanghai Canc Inst, Shanghai, Peoples R China.
[Zhang, Zuo-Feng] Univ Calif Los Angeles, Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA 90024 USA.
[Rao, Jianyu] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90024 USA.
[Shi, Rong; Wu, Qijun] Shanghai Jiao Tong Univ, Sch Publ Hlth, Shanghai 200030, Peoples R China.
[Wang, Meilin; Zhang, Zhengdong] Nanjing Med Univ, Sch Publ Hlth, Ctr Canc, Dept Mol & Genet Toxicol, Nanjing, Peoples R China.
[Zhang, Yuanyuan] Wake Forest Univ, Bowman Gray Sch Med, Dept Urol, Winston Salem, NC 27103 USA.
[Jin, Guangfu; Sun, Jielin; Zheng, S. Lilly; Xu, Jianfeng] Wake Forest Univ, Bowman Gray Sch Med, Ctr Canc Genom, Winston Salem, NC 27103 USA.
[Guo, Ling; Tao, Sha; Xu, Jianfeng] Van Andel Res Inst, Grand Rapids, MI USA.
RP Sun, YH (reprint author), Second Mil Med Univ, Changhai Hosp, Dept Urol, Shanghai, Peoples R China.
EM sunyh@medmail.com.cn; mozengnan@gmail.com; jxu@wfubmc.edu
RI tao, sha/B-7750-2012
FU National Cancer Institute [R01CA129684]
FX This study was partially funded by the National Cancer Institute
(R01CA129684 to J. X.).
NR 25
TC 26
Z9 31
U1 1
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1349-7006
J9 CANCER SCI
JI Cancer Sci.
PD OCT
PY 2011
VL 102
IS 10
BP 1916
EP 1920
DI 10.1111/j.1349-7006.2011.02036.x
PG 5
WC Oncology
SC Oncology
GA 826CK
UT WOS:000295328800011
PM 21756274
ER
PT J
AU Srikantan, S
Gorospe, M
Abdelmohsen, K
AF Srikantan, Subramanya
Gorospe, Myriam
Abdelmohsen, Kotb
TI Senescence-associated microRNAs linked to tumorigenesis
SO CELL CYCLE
LA English
DT Editorial Material
ID APOPTOSIS
C1 [Srikantan, Subramanya; Gorospe, Myriam; Abdelmohsen, Kotb] NIA IRP, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
RP Abdelmohsen, K (reprint author), NIA IRP, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
EM abdelmohsenk@grc.nia.nih.gov
OI srikantan, subramanya/0000-0003-1810-6519; abdelmohsen,
Kotb/0000-0001-6240-5810
NR 10
TC 5
Z9 5
U1 0
U2 9
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD OCT 1
PY 2011
VL 10
IS 19
BP 3211
EP 3212
DI 10.4161/cc.10.19.17050
PG 2
WC Cell Biology
SC Cell Biology
GA 827FB
UT WOS:000295412100001
PM 21941082
ER
PT J
AU Bai, YW
Zhou, Z
Feng, HQ
Zhou, BR
AF Bai, Yawen
Zhou, Zheng
Feng, Hanqiao
Zhou, Bing-Rui
TI Recognition of centromeric histone variant CenH3s by their chaperones
Structurally conserved or not
SO CELL CYCLE
LA English
DT Editorial Material
C1 [Bai, Yawen; Zhou, Zheng; Feng, Hanqiao; Zhou, Bing-Rui] NCI, Biochem & Mol Biol Lab, Bethesda, MD 20892 USA.
RP Bai, YW (reprint author), NCI, Biochem & Mol Biol Lab, Bethesda, MD 20892 USA.
EM yawen@helix.nih.gov
RI Zhou, Bing-Rui/D-4766-2009
NR 11
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 OCT 1
PY 2011
VL 10
IS 19
BP 3217
EP 3218
DI 10.4161/cc.10.19.17077
PG 2
WC Cell Biology
SC Cell Biology
GA 827FB
UT WOS:000295412100004
PM 21926476
ER
PT J
AU Fer, N
Melillo, G
AF Fer, Nicole
Melillo, Giovanni
TI The HIF-1 alpha-c-Myc pathway and tumorigenesis: Evading the apoptotic
gatekeeper
SO CELL CYCLE
LA English
DT Editorial Material
ID HYPOXIA; CANCER; CELLS; MYC
C1 [Fer, Nicole; Melillo, Giovanni] NCI, Frederick, MD 21701 USA.
RP Fer, N (reprint author), NCI, Frederick, MD 21701 USA.
EM melillog@mail.nih.gov
NR 8
TC 5
Z9 5
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 OCT 1
PY 2011
VL 10
IS 19
BP 3228
EP 3228
DI 10.4161/cc.10.19.17049
PG 1
WC Cell Biology
SC Cell Biology
GA 827FB
UT WOS:000295412100010
PM 21971179
ER
PT J
AU Sackett, DL
Fojo, T
AF Sackett, Dan L.
Fojo, Tito
TI Taccalonolides: A microtubule stabilizer poses a new puzzle with old
pieces
SO CELL CYCLE
LA English
DT Editorial Material
ID PACLITAXEL; TUBULIN; AGENTS
C1 [Sackett, Dan L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
[Fojo, Tito] NCI, NIH, Bethesda, MD 20892 USA.
RP Sackett, DL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
EM ds1k@nih.gov; fojot@mail.nih.gov
NR 6
TC 4
Z9 4
U1 0
U2 4
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD OCT 1
PY 2011
VL 10
IS 19
BP 3233
EP 3234
DI 10.4161/cc.10.19.17126
PG 2
WC Cell Biology
SC Cell Biology
GA 827FB
UT WOS:000295412100015
PM 21946521
ER
PT J
AU Cui, CY
Kunisada, M
Childress, V
Michel, M
Schlessinger, D
AF Cui, Chang-Yi
Kunisada, Makoto
Childress, Victoria
Michel, Marc
Schlessinger, David
TI Shh is required for Tabby hair follicle development
SO CELL CYCLE
LA English
DT Article
DE Eda; Shh; Wnt; hair follicle subtypes; Tabby
ID HEDGEHOG SIGNALING PATHWAY; SWEAT GLAND DEVELOPMENT; SONIC-HEDGEHOG;
ECTODERMAL DYSPLASIA; SALIVARY-GLANDS; INDUCTION; ECTODYSPLASIN; MICE;
EDA; EXPRESSION
AB In embryonic Eda mutant ("Tabby") mice, the development of one of the two major types of hair, "primary" hair fails, but other "secondary" hairs develop in normal numbers, though shorter and slightly aberrant. In Tabby mice, Shh is undetectable in skin early on, but is activated during secondary hair formation. We inferred that Shh may be involved in primary hair formation, activated normally by Eda, and also possibly in secondary hair formation, activated by an Eda-independent pathway. Varying the dosage of Shh now supports these inferences. In Shh knockout mice, mice were totally hairless: primary and secondary hair follicle germs were formed, but further progression failed. Consistent with these findings, when Shh loss was restricted to the skin, secondary hair follicle germs were initiated on time in Tabby mice, but their subsequent development (down-growth) failed. An Shh transgene expressed in Tabby skin could not restore induction of primary hair follicles, but restored normal length to the somewhat aberrant secondary hair that was formed and prolonged the anagen phase of hair cycling. Thus, Shh is required for primary and secondary hair down-growth and full secondary hair length, but is not itself sufficient to replace Eda or make fully normal secondary hair.
C1 [Cui, Chang-Yi; Childress, Victoria; Michel, Marc; Schlessinger, David] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
[Kunisada, Makoto] Kobe Univ, Div Dermatol, Dept Internal Med Related, Grad Sch Med, Kobe, Hyogo 657, Japan.
RP Cui, CY (reprint author), NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
EM CuiC@mail.nih.gov
FU National Institute on Aging, National Institutes of Health
FX The authors thank David Richardson and Anna Butler for helping with
animal management. This work was entirely supported by the Intramural
Research Program of National Institute on Aging, National Institutes of
Health.
NR 32
TC 9
Z9 9
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 OCT 1
PY 2011
VL 10
IS 19
BP 3379
EP 3386
DI 10.4161/cc.10.19.17669
PG 8
WC Cell Biology
SC Cell Biology
GA 827FB
UT WOS:000295412100036
PM 21926481
ER
PT J
AU Begaye, A
Trostel, S
Zhao, ZM
Taylor, RE
Schriemer, DC
Sackett, DL
AF Begaye, Adrian
Trostel, Shana
Zhao, Zhiming
Taylor, Richard E.
Schriemer, David C.
Sackett, Dan L.
TI Mutations in the beta-tubulin binding site for peloruside A confer
resistance by targeting a cleft significant in side chain binding
SO CELL CYCLE
LA English
DT Article
DE peloruside A; laulimalide; paclitaxel; drug resistance; mitotic arrest;
binding site; beta-tubulin
ID MICROTUBULE-STABILIZING AGENTS; TAXOID SITE; CELLS RESISTANT;
ALPHA-TUBULIN; LAULIMALIDE; PACLITAXEL; DRUGS; COLCHICINE; MUTANTS;
MITOSIS
AB Peloruside A is a microtubule-stabilizing macrolide that binds to beta-tubulin at a site distinct from the taxol site. The site was previously identified by H-D exchange mapping and molecular docking as a region close to the outer surface of the microtubule and confined in a cavity surrounded by a continuous loop of protein folded so as to center on Y340. We have isolated a series of peloruside A-resistant lines of the human ovarian carcinoma cell line A2780( 1A9) to better characterize this binding site and the consequences of altering residues in it. Four resistant lines (Pel A-D) are described with singlebase mutations in class I beta-tubulin that result in the following substitutions: R306H, Y340S, N337D and A296S in various combinations. The mutations are localized to peptides previously identified by Hydrogen-Deuterium exchange mapping, and center on a cleft in which the drug side chain appears to dock. The Pel lines are 10-15-fold resistant to peloruside A and show cross resistance to laulimalide but not to any other microtubule stabilizers. They show no cross-sensitivity to any microtubule destabilizers, nor to two drugs with targets unrelated to microtubules. Peloruside A induces G(2)/M arrest in the Pel cell lines at concentrations 10-15 times that required in the parental line. The cells show notable changes in morphology compared with the parental line.
C1 [Begaye, Adrian; Sackett, Dan L.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, Bethesda, MD 20892 USA.
[Trostel, Shana] NCI, NIH, Bethesda, MD 20892 USA.
[Zhao, Zhiming; Taylor, Richard E.] Univ Notre Dame, Dept Chem & Biochem, Notre Dame, IN 46556 USA.
[Schriemer, David C.] Univ Calgary, Dept Biochem & Mol Biol, Calgary, AB, Canada.
RP Sackett, DL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, Bethesda, MD 20892 USA.
EM sackettd@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health; Human
Development, NIH
FX This work was supported in part by funding from the Intramural Research
Program of the Eunice Kennedy Shriver National Institute of Child Health
and Human Development, NIH.
NR 35
TC 18
Z9 18
U1 0
U2 13
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD OCT 1
PY 2011
VL 10
IS 19
BP 3387
EP 3396
DI 10.4161/cc.10.19.17706
PG 10
WC Cell Biology
SC Cell Biology
GA 827FB
UT WOS:000295412100037
PM 21926482
ER
PT J
AU Hawkins, RD
Hon, GC
Yang, CH
Antosiewicz-Bourget, JE
Lee, LK
Ngo, QM
Klugman, S
Ching, KA
Edsall, LE
Ye, Z
Kuan, S
Yu, PZ
Liu, H
Zhang, XM
Green, RD
Lobanenkov, VV
Stewart, R
Thomson, JA
Ren, B
AF Hawkins, R. David
Hon, Gary C.
Yang, Chuhu
Antosiewicz-Bourget, Jessica E.
Lee, Leonard K.
Ngo, Que-Minh
Klugman, Sarit
Ching, Keith A.
Edsall, Lee E.
Ye, Zhen
Kuan, Samantha
Yu, Pengzhi
Liu, Hui
Zhang, Xinmin
Green, Roland D.
Lobanenkov, Victor V.
Stewart, Ron
Thomson, James A.
Ren, Bing
TI Dynamic chromatin states in human ES cells reveal potential regulatory
sequences and genes involved in pluripotency
SO CELL RESEARCH
LA English
DT Article
DE hESCs; epigenomics; histone modifications; enhancers
ID EMBRYONIC STEM-CELLS; HUMAN SOMATIC-CELLS; HUMAN GENOME; HISTONE
MODIFICATIONS; TRANSCRIPTION FACTORS; SELF-RENEWAL; DEVELOPMENTAL
REGULATORS; DEFINED FACTORS; PROTEIN CTCF; ENHANCERS
AB Pluripotency, the ability of a cell to differentiate and give rise to all embryonic lineages, defines a small number of mammalian cell types such as embryonic stem (ES) cells. While it has been generally held that pluripotency is the product of a transcriptional regulatory network that activates and maintains the expression of key stem cell genes, accumulating evidence is pointing to a critical role for epigenetic processes in establishing and safeguarding the pluripotency of ES cells, as well as maintaining the identity of differentiated cell types. In order to better understand the role of epigenetic mechanisms in pluripotency, we have examined the dynamics of chromatin modifications genome-wide in human ES cells (hESCs) undergoing differentiation into a mesendodermal lineage. We found that chromatin modifications at promoters remain largely invariant during differentiation, except at a small number of promoters where a dynamic switch between acetylation and methylation at H3K27 marks the transition between activation and silencing of gene expression, suggesting a hierarchy in cell fate commitment over most differentially expressed genes. We also mapped over 50 000 potential enhancers, and observed much greater dynamics in chromatin modifications, especially H3K4me1 and H3K27ac, which correlate with expression of their potential target genes. Further analysis of these enhancers revealed potentially key transcriptional regulators of pluripotency and a chromatin signature indicative of a poised state that may confer developmental competence in hESCs. Our results provide new evidence supporting the role of chromatin modifications in defining enhancers and pluripotency.
C1 [Antosiewicz-Bourget, Jessica E.; Yu, Pengzhi; Thomson, James A.] Univ Wisconsin, Genome Ctr Wisconsin, Madison, WI 53706 USA.
[Hawkins, R. David; Hon, Gary C.; Lee, Leonard K.; Ngo, Que-Minh; Klugman, Sarit; Ching, Keith A.; Edsall, Lee E.; Ye, Zhen; Kuan, Samantha; Ren, Bing] Univ Calif San Diego, Sch Med, Ludwig Inst Canc Res, Dept Cellular & Mol Med, La Jolla, CA 92093 USA.
[Yang, Chuhu; Stewart, Ron] Morgridge Inst Res, Madison, WI 53707 USA.
[Liu, Hui; Zhang, Xinmin; Green, Roland D.] Roche NimbleGen, Madison, WI 53719 USA.
[Lobanenkov, Victor V.] NIAID, Rockville, MD 20892 USA.
RP Thomson, JA (reprint author), Univ Wisconsin, Genome Ctr Wisconsin, Madison, WI 53706 USA.
EM thomson@primate.wisc.edu; biren@ucsd.edu
RI Yu, Pengzhi/I-3182-2016;
OI Yu, Pengzhi/0000-0001-7637-404X; Lobanenkov, Victor/0000-0001-6665-3635;
Edsall, Lee Elizabeth/0000-0002-0326-2829
FU California Institute of Regenerative Medicine [RS1-00292-1,
RN2-00905-1]; NIH [U01 ES017166-01]; Ludwig Institute for Cancer
Research
FX This work is supported, in part, by funding from the California
Institute of Regenerative Medicine (to BR; RS1-00292-1 and RN2-00905-1),
the NIH (U01 ES017166-01) and the Ludwig Institute for Cancer Research.
NR 78
TC 50
Z9 53
U1 0
U2 12
PU INST BIOCHEMISTRY & CELL BIOLOGY
PI SHANGHAI
PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
SN 1001-0602
J9 CELL RES
JI Cell Res.
PD OCT
PY 2011
VL 21
IS 10
BP 1393
EP 1409
DI 10.1038/cr.2011.146
PG 17
WC Cell Biology
SC Cell Biology
GA 827VN
UT WOS:000295457400005
PM 21876557
ER
PT J
AU Pezzolo, A
Parodi, F
Marimpietri, D
Raffaghello, L
Cocco, C
Pistorio, A
Mosconi, M
Gambini, C
Cilli, M
Deaglio, S
Malavasi, F
Pistoia, V
AF Pezzolo, Annalisa
Parodi, Federica
Marimpietri, Danilo
Raffaghello, Lizzia
Cocco, Claudia
Pistorio, Angela
Mosconi, Manuela
Gambini, Claudio
Cilli, Michele
Deaglio, Silvia
Malavasi, Fabio
Pistoia, Vito
TI Oct-4(+)/Tenascin C+ neuroblastoma cells serve as progenitors of
tumor-derived endothelial cells
SO CELL RESEARCH
LA English
DT Article
DE neuroblastoma; vascular mimicry; tumor-derived endothelium; progenitor
cells; Tenascin C
ID STEM-LIKE CELLS; TENASCIN-C; SELF-RENEWAL; DIFFERENTIAL-DIAGNOSIS;
STEM/PROGENITOR CELLS; PERIVASCULAR NICHE; INITIATING CELLS; GANGLIOSIDE
GD2; CANCER; EXPRESSION
AB Neuroblastoma (NB)-associated endothelial microvessels (EMs) may be lined by tumor-derived endothelial cells (TECs), that are genetically unstable and chemoresistant. Here we have addressed the identification of TEC progenitors in NB by focusing on Octamer-binding transcription factor 4 (Oct-4) as a putative marker. Oct-4(+) cells were detected in primary NB samples (n = 23), metastatic bone marrow aspirates (n = 10), NB cell lines (n = 4), and orthotopic tumors (n = 10) formed by the HTLA-230 NB cell line in immunodeficient mice. Most Oct-4(+) cells showed a perivascular distribution, with 5% of them homing in perinecrotic areas. All Oct-4(+) cells were tumor-derived since they shared amplification of MYCN oncogene with malignant cells. Perivascular Oct-4(+) cells expressed stem cell-related, neural progenitor-related and NB-related markers, including surface Tenascin C (TNC), that was absent from perinecrotic Oct-4(+) cells and bulk tumor cells. TNC+ but not TNC-HTLA-230 cells differentiated in vitro into endothelial-like cells expressing vascular-endothelial-cadherin, prostate-specific membrane antigen and CD31 upon culture in medium containing vascular endothelial growth factor (VEGF). TNC+ but not TNC-HTLA-230 cells formed neurospheres when cultured in serum-free medium. Both cell fractions were tumorigenic, but only tumors formed by TNC+ cells contained EMs lined by TECs. In conclusion, we have identified in NB tumors two putative niches containing Oct-4(+) tumor cells. Oct-4(+)/TNC+ perivascular NB cells displayed a high degree of plasticity and served as progenitors of TECs. Therapeutic targeting of Oct4(+)/TNC+ progenitors may counteract the contribution of NB-derived ECs to tumor relapse and chemoresistance.
C1 [Pezzolo, Annalisa; Parodi, Federica; Marimpietri, Danilo; Raffaghello, Lizzia; Pistoia, Vito] Ist Giannina Gaslini, Lab Oncol, I-16147 Genoa, Italy.
[Cocco, Claudia] Ist Giannina Gaslini, AIRC Tumor Immunol Unit, I-16147 Genoa, Italy.
[Pistorio, Angela] Ist Giannina Gaslini, Epidemiol & Biostat Unit, I-16147 Genoa, Italy.
[Mosconi, Manuela; Gambini, Claudio] IRCCS G Gaslini Hosp, Dept Expt & Lab Med, Pathol Lab, Genoa, Italy.
[Cilli, Michele] Natl Canc Inst, Anim Res Facil, Genoa, Italy.
[Deaglio, Silvia; Malavasi, Fabio] Univ Turin, Dept Genet Biol & Biochem, Turin, Italy.
RP Pezzolo, A (reprint author), Ist Giannina Gaslini, Lab Oncol, Largo G Gaslini 5, I-16147 Genoa, Italy.
EM annalisapezzolo@ospedale-gaslini.ge.it
RI Deaglio, Silvia/G-4814-2011;
OI Raffaghello, Lizzia/0000-0003-2357-0607
FU Fondazione Italiana Neuroblastoma, Fondazione; Ministero della Salute
Progetto Strategico Oncologico; Associazione Italiana per la Ricerca sul
Cancro (AIRC)
FX We thank the late Dr Giorgio Corte for reading the manuscript. Special
thanks go to Dr Paolo Bianco for discussion and suggestions. This work
was supported by Fondazione Italiana Neuroblastoma, Fondazione "Guido
Berlucchi", Fondazione "Bianca e Wilma Querci", Progetto di Ricerca
Regione Liguria "Endotelio di derivazione tumorale: caratterizzazione e
targeting immunologico a fini terapeutici" and Ministero della Salute
Progetto Strategico Oncologico 2006 "Microambiente tumorale: ruolo nella
progressione neoplastica sulle difese dell'ospite. Identificazione di
nuovi bersagli per lo sviluppo di terapie innovative". CC was supported
by Associazione Italiana per la Ricerca sul Cancro (AIRC).
NR 78
TC 22
Z9 24
U1 0
U2 5
PU INST BIOCHEMISTRY & CELL BIOLOGY
PI SHANGHAI
PA SIBS, CAS, 319 YUEYAND ROAD, SHANGHAI, 200031, PEOPLES R CHINA
SN 1001-0602
J9 CELL RES
JI Cell Res.
PD OCT
PY 2011
VL 21
IS 10
BP 1470
EP 1486
DI 10.1038/cr.2011.38
PG 17
WC Cell Biology
SC Cell Biology
GA 827VN
UT WOS:000295457400010
PM 21403679
ER
PT J
AU Roberts, DD
AF Roberts, David D.
TI Emerging functions of matricellular proteins
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Review
ID EXTRACELLULAR-MATRIX; THROMBOSPONDIN-1; INTEGRIN; DISEASE; MICE;
ABNORMALITIES; COLLAGEN
C1 NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Roberts, DD (reprint author), NCI, Pathol Lab, Ctr Canc Res, NIH, Bldg 10,Room 2A33,10 Ctr Dr MSC1500, Bethesda, MD 20892 USA.
EM droberts@helix.nih.gov
RI Roberts, David/A-9699-2008
OI Roberts, David/0000-0002-2481-2981
FU Center for Cancer Research, National Cancer Institute, NIH
FX Cited work in the author's laboratory was supported by the Intramural
Research Program of the Center for Cancer Research, National Cancer
Institute, NIH. Conference support was provided by DK089753-01, the
Center for Cancer Research, and the NIH Office of Rare Diseases
Research.
NR 26
TC 15
Z9 15
U1 0
U2 2
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 OCT
PY 2011
VL 68
IS 19
BP 3133
EP 3136
DI 10.1007/s00018-011-0779-2
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 826BX
UT WOS:000295327500001
PM 21833584
ER
PT J
AU Gemoll, T
Roblick, UJ
Szymczak, S
Braunschweig, T
Becker, S
Igl, BW
Bruch, HP
Ziegler, A
Hellman, U
Difilippantonio, MJ
Ried, T
Jornvall, H
Auer, G
Habermann, JK
AF Gemoll, Timo
Roblick, Uwe J.
Szymczak, Silke
Braunschweig, Till
Becker, Susanne
Igl, Bernd-Wolfgang
Bruch, Hans-Peter
Ziegler, Andreas
Hellman, Ulf
Difilippantonio, Michael J.
Ried, Thomas
Jornvall, Hans
Auer, Gert
Habermann, Jens K.
TI HDAC2 and TXNL1 distinguish aneuploid from diploid colorectal cancers
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Article
DE Colon cancer; Genomic instability; Two-dimensional gel electrophoresis;
Mass spectrometry; Aneuploidy; HDAC2
ID COMPARATIVE GENOMIC HYBRIDIZATION; CHROMOSOMAL INSTABILITY;
COLON-CANCER; GEL-ELECTROPHORESIS; TISSUE MICROARRAYS; CELL-LINES;
EXPRESSION; CARCINOMA; THIOREDOXIN; BINDING
AB DNA aneuploidy has been identified as a prognostic factor for epithelial malignancies. Further understanding of the translation of DNA aneuploidy into protein expression will help to define novel biomarkers to improve therapies and prognosis. DNA ploidy was assessed by image cytometry. Comparison of gel-electrophoresis-based protein expression patterns of three diploid and four aneuploid colorectal cancer cell lines detected 64 ploidy-associated proteins. Proteins were identified by mass spectrometry and subjected to Ingenuity Pathway Analysis resulting in two overlapping high-ranked networks maintaining Cellular Assembly and Organization, Cell Cycle, and Cellular Growth and Proliferation. CAPZA1, TXNL1, and HDAC2 were significantly validated by Western blotting in cell lines and the latter two showed expression differences also in clinical samples using a tissue microarray of normal mucosa (n = 19), diploid (n = 31), and aneuploid (n = 47) carcinomas. The results suggest that distinct protein expression patterns, affecting TXNL1 and HDAC2, distinguish aneuploid with poor prognosis from diploid colorectal cancers.
C1 [Gemoll, Timo; Roblick, Uwe J.; Bruch, Hans-Peter; Habermann, Jens K.] Med Univ Lubeck, Surg Res Lab, Dept Surg, D-23538 Lubeck, Germany.
[Gemoll, Timo; Roblick, Uwe J.; Jornvall, Hans; Habermann, Jens K.] Karolinska Inst, Dept Med Biochem & Biophys, S-17177 Stockholm, Sweden.
[Gemoll, Timo; Becker, Susanne; Auer, Gert] Karolinska Inst, Karolinska Biom Ctr, S-17176 Stockholm, Sweden.
[Braunschweig, Till] Univ Clin RWTH Aachen, Inst Pathol, D-52074 Aachen, Germany.
[Szymczak, Silke; Igl, Bernd-Wolfgang; Ziegler, Andreas] Med Univ Lubeck, Inst Med Biometry & Stat, D-23538 Lubeck, Germany.
[Hellman, Ulf] Canc Res Ltd, Ludwig Inst, S-75124 Uppsala, Sweden.
[Difilippantonio, Michael J.; Ried, Thomas] NCI, Dept Genet, Ctr Canc Res, NIH, Bethesda, MD 20814 USA.
RP Habermann, JK (reprint author), Med Univ Lubeck, Surg Res Lab, Dept Surg, Ratzeburger Allee 160, D-23538 Lubeck, Germany.
EM Jens.Habermann@gmail.com
RI Szymczak, Silke/C-6625-2013; Habermann, Jens/E-2968-2010;
OI Ziegler, Andreas/0000-0002-8386-5397
FU Swedish Cancer Society (Cancerfonden); Cancer Society Stockholm
(Cancerforeningen); Swedish Research Council; Wallenberg Consortium
North; Knut and Alice Wallenberg Foundation; Ad Infinitum Foundation;
Werner and Clara Kreitz Foundation
FX Grants from the Swedish Cancer Society (Cancerfonden), the Cancer
Society Stockholm (Cancerforeningen), the Swedish Research Council, the
Wallenberg Consortium North, the Knut and Alice Wallenberg Foundation,
the Ad Infinitum Foundation, and the Werner and Clara Kreitz Foundation
are gratefully acknowledged. We thank Elke Gheribi and Regina Kaatz for
assistance with clinical sample collection, Gisela Grosser-Pape for
support with ploidy assessment, and Claudia Killaitis for clinical data
administration. This study was performed in collaboration with the North
German Tumor Bank of Colorectal Cancer (DKH #108446) and the Surgical
Center for Translational Oncology-Lubeck (SCTO-L).
NR 41
TC 4
Z9 4
U1 0
U2 6
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 OCT
PY 2011
VL 68
IS 19
BP 3261
EP 3274
DI 10.1007/s00018-011-0628-3
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 826BX
UT WOS:000295327500011
PM 21290163
ER
PT J
AU Pan, Q
Qiao, F
Gao, C
Norman, B
Optican, L
Zelenka, PS
AF Pan, Q.
Qiao, F.
Gao, C.
Norman, B.
Optican, L.
Zelenka, Peggy S.
TI Cdk5 targets active Src for ubiquitin-dependent degradation by
phosphorylating Src(S75)
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Article
DE Cdk5; Src; Signal transduction; Ubiquitination; Kinase activity
ID TYROSINE KINASE; C-SRC; CELL-MATRIX; ACTIVATION; MITOSIS; SITE;
PP60(C-SRC); MORPHOLOGY; PP60C-SRC; ADHESION
AB The non-receptor tyrosine kinase Src is a critical regulator of cytoskeletal contraction, cell adhesion, and migration. In normal cells, Src activity is stringently controlled by Csk-dependent phosphorylation of Src(Y530), and by Cullin-5-dependent ubiquitinylation, which affects active Src(pY419) exclusively, leading to its degradation by the proteosome. Previous work has shown that Src activity is also limited by Cdk5, a proline-directed kinase, which has been shown to phosphorylate Src(S75). Here we show that this phosphorylation promotes the ubiquitin-dependent degradation of Src, thus restricting the availability of active Src. We demonstrate that Src(S75) phosphorylation occurs in vivo in epithelial cells, and like ubiquitinylation, is associated only with active Src. Preventing Cdk5-dependent phosphorylation of Src(S75), by site-specific mutation of S75 or by Cdk5 inhibition or suppression, increases Src(Y419) phosphorylation and kinase activity, resulting in Src-dependent cytoskeletal changes. In transfected cells, ubiquitinylation of Src(S75A) is about 35% that of wild-type Src-V5, and its half-life is approximately 2.5-fold greater. Cdk5 suppression leads to a comparable decrease in the ubiquitinylation of endogenous Src and a similar increase in Src stability. Together, these findings demonstrate that Cdk5-dependent phosphorylation of Src(S75) is a physiologically significant mechanism of regulating intracellular Src activity.
C1 [Pan, Q.; Qiao, F.; Gao, C.; Norman, B.; Zelenka, Peggy S.] NEI, Lab Mol & Dev Biol, NIH, Bethesda, MD 20892 USA.
[Optican, L.] NEI, Sensorimotor Res Lab, NIH, Bethesda, MD 20892 USA.
RP Zelenka, PS (reprint author), NEI, Lab Mol & Dev Biol, NIH, 5635 Fishers Lane,Room 1127, Bethesda, MD 20892 USA.
EM zelenkap@nei.nih.gov
FU National Eye Institute [Z01-EY000238-25]
FX We thank Dr. John Reddan of Oakland University for the human lens
epithelial cell line (FHL124), Drs. Xiao Dong Jiao and J. Fielding
Hejtmancik for generously sequencing DNA clones, and Ms. Andrea Elfstrom
for technical assistance. This work was supported by the National Eye
Institute Intramural Research Program Z01-EY000238-25.
NR 30
TC 17
Z9 19
U1 0
U2 7
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 OCT
PY 2011
VL 68
IS 20
BP 3425
EP 3436
DI 10.1007/s00018-011-0638-1
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 826BS
UT WOS:000295327000010
PM 21442427
ER
PT J
AU Zaidi, MR
Merlino, G
AF Zaidi, M. Raza
Merlino, Glenn
TI The Two Faces of Interferon-gamma in Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID METASTATIC MALIGNANT-MELANOMA; MAJOR HISTOCOMPATIBILITY ANTIGENS;
CHRONIC MYELOGENOUS LEUKEMIA; IFN-GAMMA; T-CELLS; IN-VIVO; INDOLEAMINE
2,3-DIOXYGENASE; CUTANEOUS MELANOMA; INDUCED ARTHRITIS; IMMUNE ESCAPE
AB Interferon-gamma is a cytokine whose biological activity is conventionally associated with cytostatic/cytotoxic and antitumor mechanisms during cell-mediated adaptive immune response. It has been used clinically to treat a variety of malignancies, albeit with mixed results and side effects that can be severe. Despite ample evidence implicating a role for IFN-gamma in tumor immune surveillance, a steady flow of reports has suggested that it may also have protumorigenic effects under certain circumstances. We propose that, in fact, IFN-gamma treatment is a double-edged sword whose anti-and protumorigenic activities are dependent on the cellular, microenvironmental, and/or molecular context. As such, inhibition of the IFN-gamma/IFN-gamma receptor pathway may prove to be a viable new therapeutic target for a subset of malignancies. Clin Cancer Res; 17(19); 6118-24. (C) 2011 AACR.
C1 [Zaidi, M. Raza; Merlino, Glenn] NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Zaidi, MR (reprint author), 37 Convent Dr,5002, Bethesda, MD 20892 USA.
EM zaidir@mail.nih.gov
RI Zaidi, M. Raza/H-1386-2016
OI Zaidi, M. Raza/0000-0003-0480-3188
FU Center for Cancer Research, NCI, NIH
FX This work was supported in part by the Intramural Research Program of
the Center for Cancer Research, NCI, NIH.
NR 85
TC 139
Z9 144
U1 0
U2 21
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 OCT 1
PY 2011
VL 17
IS 19
BP 6118
EP 6124
DI 10.1158/1078-0432.CCR-11-0482
PG 7
WC Oncology
SC Oncology
GA 827VR
UT WOS:000295457900003
PM 21705455
ER
PT J
AU Parkhurst, MR
Riley, JP
Dudley, ME
Rosenberg, SA
AF Parkhurst, Maria R.
Riley, John P.
Dudley, Mark E.
Rosenberg, Steven A.
TI Adoptive Transfer of Autologous Natural Killer Cells Leads to High
Levels of Circulating Natural Killer Cells but Does Not Mediate Tumor
Regression
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID KIR LIGAND INCOMPATIBILITY; NK CELLS; INHIBITORY RECEPTORS; METASTATIC
MELANOMA; CANCER REGRESSION; SELF-TOLERANCE; BREAST-CANCER;
IMMUNOTHERAPY; TRANSPLANTATION; THERAPY
AB Purpose: Adoptive transfer of tumor-infiltrating lymphocytes (TIL) can mediate regression of metastatic melanoma. However, many patients with cancer are ineligible for such treatment because their TIL do not expand sufficiently or because their tumors have lost expression of antigens and/or MHC molecules. Natural killer (NK) cells are large granular lymphocytes that lyse tumor cells in a non-MHC-restricted manner. Therefore, we initiated in a clinical trial to evaluate the efficacy of adoptively transferred autologous NK cells to treat patients with cancers who were ineligible for treatment with TIL.
Experimental Design: Patients with metastatic melanoma or renal cell carcinoma were treated with adoptively transferred in vitro activated autologous NK cells after the patients received a lymphodepleting but nonmyeloablative chemotherapy regimen. Clinical responses and persistence of the adoptively transferred cells were evaluated.
Results: Eight patients were treated with an average of 4.7 x 10(10) (+/- 2.1 x 10(10)) NK cells. The infused cells exhibited high levels of lytic activity in vitro. Although no clinical responses were observed, the adoptively transferred NK cells seemed to persist in the peripheral circulation of patients for at least one week posttransfer and, in some patients, for several months. However, the persistent NK cells in the circulation expressed significantly lower levels of the key activating receptor NKG2D and could not lyse tumor cell targets in vitro unless reactivated with IL-2.
Conclusions: The persistent NK cells could mediate antibody-dependent cell-mediated cytotoxicity without cytokine reactivation in vitro, which suggests that coupling adoptive NK cell transfer with monoclonal antibody administration deserves evaluation. Clin Cancer Res; 17(19); 6287-97. (C) 2011 AACR.
C1 [Parkhurst, Maria R.; Riley, John P.; Dudley, Mark E.; Rosenberg, Steven A.] NCI, NIH, Surg Branch, Bethesda, MD 20892 USA.
RP Parkhurst, MR (reprint author), NCI, NIH, Surg Branch, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM Maria_Parkhurst@nih.gov
FU NCI
FX This work was funded through the NCI intramural program.
NR 34
TC 98
Z9 104
U1 3
U2 8
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 OCT 1
PY 2011
VL 17
IS 19
BP 6287
EP 6297
DI 10.1158/1078-0432.CCR-11-1347
PG 11
WC Oncology
SC Oncology
GA 827VR
UT WOS:000295457900019
PM 21844012
ER
PT J
AU Hoofnagle, AN
Aebersold, R
Anderson, NL
Felsenfeld, A
Liebler, DC
AF Hoofnagle, Andrew N.
Aebersold, Ruedi
Anderson, N. Leigh
Felsenfeld, Adam
Liebler, Daniel C.
TI Painting a Moving Picture: Large-Scale Proteomics Efforts and Their
Potential for Changing Patient Care
SO CLINICAL CHEMISTRY
LA English
DT Editorial Material
C1 [Hoofnagle, Andrew N.] Univ Washington, Dept Lab Med, Seattle, WA 98195 USA.
[Aebersold, Ruedi] Swiss Fed Inst Technol, Inst Mol Syst Biol, Dept Biol, Zurich, Switzerland.
[Anderson, N. Leigh] Plasma Proteome Inst, Washington, DC USA.
[Felsenfeld, Adam] NHGRI, Bethesda, MD 20892 USA.
[Liebler, Daniel C.] Vanderbilt Univ, Jim Ayers Inst Precance Detect & Diag, Nashville, TN USA.
[Hoofnagle, Andrew N.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
RP Hoofnagle, AN (reprint author), Univ Washington, Dept Lab Med, 1959 NE Pacific,Campus Box 357110, Seattle, WA 98195 USA.
EM ahoof@u.washington.edu
OI Liebler, Daniel/0000-0002-7873-3031
NR 0
TC 1
Z9 1
U1 0
U2 2
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD OCT
PY 2011
VL 57
IS 10
BP 1357
EP 1360
DI 10.1373/clinchem.2010.158311
PG 4
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 825ZX
UT WOS:000295322000004
PM 21540400
ER
PT J
AU Hutchison, CA
Landgren, O
AF Hutchison, Colin A.
Landgren, Ola
TI Polyclonal Immunoglobulin Free Light Chains as a Potential Biomarker of
Immune Stimulation and Inflammation
SO CLINICAL CHEMISTRY
LA English
DT Article
ID C-REACTIVE PROTEIN; SERUM; CATABOLISM; DISORDERS; DISEASE; RISK
C1 [Hutchison, Colin A.] Univ Hosp Birmingham, Dept Nephrol, Birmingham B15 2TH, W Midlands, England.
[Hutchison, Colin A.] Univ Birmingham, Dept Nephrol, Renal Inst Birmingham, Birmingham, W Midlands, England.
[Landgren, Ola] NCI, Multiple Myeloma Sect, Med Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Hutchison, CA (reprint author), Univ Hosp Birmingham, Dept Nephrol, Birmingham B15 2TH, W Midlands, England.
EM c.a.hutchison@bham.ac.uk
NR 18
TC 30
Z9 31
U1 0
U2 4
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD OCT
PY 2011
VL 57
IS 10
BP 1387
EP 1389
DI 10.1373/clinchem.2011.169433
PG 3
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 825ZX
UT WOS:000295322000010
PM 21836076
ER
PT J
AU Schwope, DM
Karschner, EL
Gorelick, DA
Huestis, MA
AF Schwope, David M.
Karschner, Erin L.
Gorelick, David A.
Huestis, Marilyn A.
TI Identification of Recent Cannabis Use: Whole-Blood and Plasma Free and
Glucuronidated Cannabinoid Pharmacokinetics following Controlled Smoked
Cannabis Administration
SO CLINICAL CHEMISTRY
LA English
DT Article
ID TANDEM MASS-SPECTROMETRY; ORAL FLUID; DELTA-9-TETRAHYDROCANNABINOL THC;
TEMPORAL INDICATION; HEPATIC MICROSOMES; HUMAN-URINE; METABOLISM;
DELTA(9)-TETRAHYDROCANNABINOL; MARIJUANA; TETRAHYDROCANNABINOL
AB BACKGROUND: Delta(9)-Tetrahydrocannabinol (THC) is the most frequently observed illicit drug in investigations of accidents and driving under the influence of drugs. THC-glucuronide has been suggested as a marker of recent cannabis use, but there are no blood data following controlled THC administration to test this hypothesis. Furthermore, there are no studies directly examining whole-blood cannabinoid pharmacokinetics, although this matrix is often the only available specimen.
METHODS: Participants (9 men, 1 woman) resided on a closed research unit and smoked one 6.8% THC cannabis cigarette ad libitum. We quantified THC, 11-hydroxy-THC (11-OH-THC), 11-nor-9-carboxy-THC (THCCOOH), cannabidiol (CBD), cannabinol (CBN), THC-glucuronide and THCCOOH-glucuronide directly in whole blood and plasma by liquid chromatography/tandem mass spectrometry within 24 h of collection to obviate stability issues.
RESULTS: Median whole blood (plasma) observed maximum concentrations (C(max)) were 50 (76), 6.4 (10), 41 (67), 1.3 (2.0), 2.4 (3.6), 89 (190), and 0.7 (1.4) mu g/L 0.25 h after starting smoking for THC, 11-OH-THC, THCCOOH, CBD, CBN, and THCCOOH-glucuronide, respectively, and 0.5 h for THCglucuronide. At observed C(max), whole-blood (plasma) detection rates were 60% (80%), 80% (90%), and 50% (80%) for CBD, CBN, and THC-glucuronide, respectively. CBD and CBN were not detectable after 1 h in either matrix (LOQ 1.0 mu g/L).
CONCLUSIONS: Human whole-blood cannabinoid data following cannabis smoking will assist whole blood and plasma cannabinoid interpretation, while furthering identification of recent cannabis intake. (C) 2011 American Association for Clinical Chemistry
C1 [Schwope, David M.; Karschner, Erin L.; Gorelick, David A.; Huestis, Marilyn A.] NIDA, Chem & Drug Metab Intramural Res Program, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Huestis, MA (reprint author), NIDA, Chem & Drug Metab Intramural Res Program, NIH, Biomed Res Ctr, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU National Institute on Drug Abuse, NIH
FX D.M. Schwope, Intramural Research Program, National Institute on Drug
Abuse, NIH; M.A. Huestis, Intramural Research Program, National
Institute on Drug Abuse, NIH.
NR 37
TC 49
Z9 50
U1 6
U2 26
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD OCT
PY 2011
VL 57
IS 10
BP 1406
EP 1414
DI 10.1373/clinchem.2011.171777
PG 9
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 825ZX
UT WOS:000295322000013
PM 21836075
ER
PT J
AU Matsumoto, RR
Li, SM
Katz, JL
Fantegrossi, WE
Coop, A
AF Matsumoto, Rae R.
Li, Su-Min
Katz, Jonathan L.
Fantegrossi, William E.
Coop, Andrew
TI Effects of the selective sigma receptor ligand,
1-(2-phenethyl)piperidine oxalate (AC927), on the behavioral and toxic
effects of cocaine
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE Cocaine; Conditioned place preference; Drug discrimination; Locomotor
activity; Self-administration; Sigma receptors
ID CONDITIONED PLACE PREFERENCE; PHEOCHROMOCYTOMA PC12 CELLS;
RHESUS-MONKEYS; PROTEIN EXPRESSION; GUINEA-PIG; IN-VIVO; RAT; DOPAMINE;
INVOLVEMENT; BINDING
AB Background: Sigma receptors represent a unique structural class of proteins and they have become increasingly studied as viable medication development targets for neurological and psychiatric disorders, including drug abuse. Earlier studies have shown that cocaine and many other abused substances interact with sigma receptors and that antagonism of these proteins can mitigate their actions.
Methods: In the present study, AC927 (1-(2-phenethyl)piperidine oxalate), a selective sigma receptor ligand, was tested against the behavioral and toxic effects of cocaine in laboratory animals.
Results: Acute administration of AC927 in male, Swiss Webster mice significantly attenuated cocaine-induced convulsions, lethality, and locomotor activity, at doses that alone had no significant effects on behavior. Subchronic administration of AC927 also attenuated cocaine-induced conditioned place preference in mice, at doses that alone had no effects on place conditioning. In drug discrimination studies in male, Sprague-Dawley rats, AC927 partially substituted for the discriminative stimulus effects of cocaine. When it was administered with cocaine, AC927 shifted the cocaine dose-response curve to the left, suggesting an enhancement of the discriminative stimulus effects of cocaine. In non-human primates, AC927 was self-administered, maintaining responding that was intermediate between contingent saline and a maintenance dose of cocaine.
Conclusion: The ability of AC927 to elicit some cocaine-like appetitive properties and to also reduce many cocaine-induced behaviors suggests that it is a promising lead for the development of a medication to treat cocaine abuse. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Matsumoto, Rae R.] W Virginia Univ, Sch Pharm, Dept Basic Pharmaceut Sci, Morgantown, WV 26506 USA.
[Matsumoto, Rae R.] Univ Oklahoma, Hlth Sci Ctr, Dept Pharmaceut Sci, Coll Pharm, Norman, OK 73019 USA.
[Li, Su-Min; Katz, Jonathan L.] Natl Inst Drug Abuse, Psychobiol Sect, Lexington, KY USA.
[Fantegrossi, William E.] Univ Michigan, Sch Med, Dept Pharmacol, Ann Arbor, MI 48109 USA.
[Fantegrossi, William E.] Univ Arkansas Med Sci, Dept Pharmacol & Toxicol, Little Rock, AR 72205 USA.
[Coop, Andrew] Univ Maryland, Sch Pharm, Dept Pharmaceut Sci, College Pk, MD 20742 USA.
RP Matsumoto, RR (reprint author), W Virginia Univ, Sch Pharm, Dept Basic Pharmaceut Sci, Morgantown, WV 26506 USA.
EM rmatsumoto@hsc.wvu.edu
OI Katz, Jonathan/0000-0002-1068-1159
FU National Institute on Drug Abuse (NIDA) [DA11979, DA13978, DA05018,
DA19634]; College on Problems of Drug Dependence (CPDD)
FX Funding for this study was provided by the National Institute on Drug
Abuse (NIDA, DA11979, DA13978, and DA05018) and the College on Problems
of Drug Dependence (CPDD). Andrew Coop is the recipient of a K02 award
from NIDA (DA19634). The NIDA and CPDD had no further role in study
design; in the collection, analysis and interpretation of the data; in
the writing of the report; or in the decision to submit the paper for
publication.
NR 52
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U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0376-8716
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD OCT 1
PY 2011
VL 118
IS 1
BP 40
EP 47
DI 10.1016/j.drugalcdep.2011.02.017
PG 8
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 826ZN
UT WOS:000295394200007
PM 21420799
ER
PT J
AU Edin, ML
Wang, ZJ
Bradbury, JA
Graves, JP
Lih, FB
DeGraff, LM
Foley, JF
Torphy, R
Ronnekleiv, OK
Tomer, KB
Lee, CR
Zeldin, DC
AF Edin, Matthew L.
Wang, ZhongJing
Bradbury, J. Alyce
Graves, Joan P.
Lih, Fred B.
DeGraff, Laura M.
Foley, Julie F.
Torphy, Robert
Ronnekleiv, Oline K.
Tomer, Kenneth B.
Lee, Craig R.
Zeldin, Darryl C.
TI Endothelial expression of human cytochrome P450 epoxygenase CYP2C8
increases susceptibility to ischemia-reperfusion injury in isolated
mouse heart
SO FASEB JOURNAL
LA English
DT Article
DE CYP2J2; EETs; reactive oxygen species; leukotoxin; Langendorff
ID SOLUBLE EPOXIDE HYDROLASE; EPOXYEICOSATRIENOIC ACIDS; ARACHIDONIC-ACID;
LINOLEIC-ACID; MYOCARDIAL-INFARCTION; POSTISCHEMIC RECOVERY;
ATHEROSCLEROSIS RISK; CONTRACTILE FUNCTION; GENETIC-VARIATION; DISEASE
RISK
AB Cytochrome P450 (CYP) epoxygenases CYP2C8 and CYP2J2 generate epoxyeicosatrienoic acids (EETs) from arachidonic acid. Mice with expression of CYP2J2 in cardiomyocytes (alpha MHC-CYP2J2 Tr) or treated with synthetic EETs have increased functional recovery after ischemia/reperfusion (I/R); however, no studies have examined the role of cardiomyocyte-vs. endothelial-derived EETs or compared the effects of different CYP epoxygenase isoforms in the ischemic heart. We generated transgenic mice with increased endothelial EET biosynthesis (Tie2-CYP2C8 Tr and Tie2-CYP2J2 Tr) or EET hydrolysis (Tie2-sEH Tr). Compared to wild-type (WT), alpha MHC-CYP2J2 Tr hearts showed increased recovery of left ventricular developed pressure (LVDP) and decreased infarct size after I/R. In contrast, LVDP recovery and infarct size were unchanged in Tie2-CYP2J2 Tr and Tie2-sEH Tr hearts. Surprisingly, compared to WT, Tie2-CYP2C8 Tr hearts had significantly reduced LVDP recovery (from 21 to 14%) and increased infarct size after I/R (from 51 to 61%). Tie2-CYP2C8 Tr hearts also exhibited increased reactive oxygen species (ROS) generation, dihydroxyoctadecenoic acid (DiHOME) formation, and coronary resistance after I/R. ROS scavengers and CYP2C8 inhibition reversed the detrimental effects of CYP2C8 expression in Tie2-CYP2C8 Tr hearts. Treatment of WT hearts with 250 nM 9,10-DiHOME decreased LVDP recovery compared to vehicle (16 vs. 31%, respectively) and increased coronary resistance after I/R. These data demonstrate that increased ROS generation and enhanced DiHOME synthesis by endothelial CYP2C8 impair functional recovery and mask the beneficial effects of increased EET production following I/R.-Edin, M. L., Wang, Z. J., Bradbury, J. A., Graves, J. P., Lih, F. B., DeGraff, L. M., Foley, J. F., Torphy, R., Ronnekleiv, O. K., Tomer, K. B., Lee, C. R., Zeldin, D. C. Endothelial expression of human cytochrome P450 epoxygenase CYP2C8 increases susceptibility to ischemia-reperfusion injury in isolated mouse heart. FASEB J. 25, 3436-3447 (2011). www.fasebj.org
C1 [Edin, Matthew L.; Wang, ZhongJing; Bradbury, J. Alyce; Graves, Joan P.; Lih, Fred B.; DeGraff, Laura M.; Foley, Julie F.; Torphy, Robert; Tomer, Kenneth B.; Zeldin, Darryl C.] NIEHS, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
[Ronnekleiv, Oline K.] Oregon Hlth & Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97201 USA.
[Ronnekleiv, Oline K.] Oregon Hlth & Sci Univ, Dept Anesthesiol & Perioperat Med, Portland, OR 97201 USA.
[Lee, Craig R.] Univ N Carolina, Eshelman Sch Pharm, Div Pharmacotherapy & Expt Therapeut, Chapel Hill, NC USA.
RP Zeldin, DC (reprint author), 111 TW Alexander Dr,Bldg 101,Rm A222, Res Triangle Pk, NC 27709 USA.
EM zeldin@niehs.nih.gov
RI Tomer, Kenneth/E-8018-2013;
OI Edin, Matthew/0000-0002-7042-500X; Lee, Craig/0000-0003-3595-5301
FU NIH, NIEHS [Z01 ES050167, Z01 ES025034, R01 GM088199]
FX The authors thank Dr. Bruce Hammock (University of California, Davis,
CA, USA) for providing the sEH antibody, Dr. Joyce Goldstein [U.S.
National Institutes of Health (NIH)/National Institute for Environmental
Health Sciences (NIEHS), Research Triangle Park, NC, USA] for providing
the CYP2C8 antibody, and Dr. Tom Sato (University of Texas Southwestern
Medical Center, Dallas, TX, USA) for providing the Tie2 promoter
construct. The authors also thank staff at Xenogen Biosciences
(Cranberry, NJ, USA) for assistance with pronuclear injections and staff
in the NIEHS Laboratory of Experimental Pathology (Natasha Clayton and
Tiwanda Masinde) for assistance with immunohistochemistry. This work was
supported with funds from the Intramural Research Program of the NIH,
NIEHS, to K.B.T. (Z01 ES050167), D.C.Z. (Z01 ES025034), and C.R.L. (R01
GM088199).
NR 56
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U1 1
U2 6
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD OCT
PY 2011
VL 25
IS 10
BP 3436
EP 3447
DI 10.1096/fj.11-188300
PG 12
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 826LU
UT WOS:000295356400015
PM 21697548
ER
PT J
AU Kashimada, K
Svingen, T
Feng, CW
Pelosi, E
Bagheri-Fam, S
Harley, VR
Schlessinger, D
Bowles, J
Koopman, P
AF Kashimada, Kenichi
Svingen, Terje
Feng, Chun-Wei
Pelosi, Emanuele
Bagheri-Fam, Stefan
Harley, Vincent R.
Schlessinger, David
Bowles, Josephine
Koopman, Peter
TI Antagonistic regulation of Cyp26b1 by transcription factors SOX9/SF1 and
FOXL2 during gonadal development in mice
SO FASEB JOURNAL
LA English
DT Article
DE Forkhead box protein L2; germ cells; meiosis; retinoic acid; sex
determination
ID STEROIDOGENIC FACTOR-I; GERM-CELL FATE; SEX DETERMINATION;
RETINOIC-ACID; GENE-TRANSCRIPTION; TESTIS DEVELOPMENT; NUCLEAR RECEPTOR;
MOUSE; DIFFERENTIATION; EXPRESSION
AB Sex determination in fetal germ cells depends on a balance between exposure to retinoic acid (RA) and the degradation of RA achieved by the testis-specific expression of the catabolic cytochrome P450 enzyme, CYP26B1. Therefore, identification of factors regulating the expression of the Cyp26b1 gene is an important goal in reproductive biology. We used in situ hybridization to demonstrate that Cyp26b1 and transcription factor genes steroidogenic factor-1 (Sf1) and Sry-related HMG box 9 (Sox9) are coexpressed in Sertoli cells, whereas Cyp26b1 and Sf1 are coexpressed in Leydig cells in mouse fetal testes. In the mouse gonadal somatic cell line TM3, transfection of constructs expressing SOX9 and SF1 activated Cyp26b1 expression, independently of the positive regulator RA. In embryonic gonads deficient in SOX9 or SF1, Cyp26b1 expression was decreased relative to wild-type (WT) controls, as measured by quantitative RT-PCR (qRT-PCR). Furthermore, qRT-PCR showed that Cyp26b1 up-regulation by SOX9/SF1 was attenuated by the ovarian transcription factor Forkhead box L2 (FOXL2) in TM3 cells, whereas in Foxl2-null mice, Cyp26b1 expression in XX gonads was increased similar to 20-fold relative to WT controls. These data support the hypothesis that SOX9 and SF1 ensure the male fate of germ cells by up-regulating Cyp26b1 and that FOXL2 acts to antagonize Cyp26b1 expression in ovaries.-Kashimada, K., Svingen, T., Feng, C.-W., Pelosi, E., Bagheri-Fam, S., Harley, V. R., Schlessinger, D., Bowles, J., Koopman, P. Antagonistic regulation of Cyp26b1 by transcription factors SOX9/SF1 and FOXL2 during gonadal development in mice. FASEB J. 25, 3561-3569 (2011). www.fasebj.org
C1 [Kashimada, Kenichi; Svingen, Terje; Feng, Chun-Wei; Bowles, Josephine; Koopman, Peter] Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia.
[Pelosi, Emanuele; Schlessinger, David] NIA, NIH, Biomed Res Ctr, Intramural Res Program,Lab Genet, Baltimore, MD 21224 USA.
[Bagheri-Fam, Stefan; Harley, Vincent R.] Prince Henrys Inst Med Res, Clayton, Vic, Australia.
RP Koopman, P (reprint author), Univ Queensland, Inst Mol Biosci, Brisbane, Qld 4072, Australia.
EM p.koopman@imb.uq.edu.au
RI Svingen, Terje/A-5283-2010; Koopman, Peter /C-9416-2009; Bowles,
Josephine/B-6583-2013;
OI Svingen, Terje/0000-0003-4650-7651; Koopman, Peter /0000-0001-6939-0914;
Bowles, Josephine/0000-0003-2867-7438; Harley,
Vincent/0000-0002-2405-1262; Pelosi, Emanuele/0000-0003-1890-9821;
Kashimada, Kenichi/0000-0003-2505-5932
FU Australian Research Council (ARC); National Health and Medical Research
Council of Australia; U.S. National Institutes of Health, National
Institute on Aging
FX The authors thank R. Chandraratna and K. Yin Tsang (Vitae
Pharmaceuticals, Fort Washington, PA, USA) for providing AGN193109,
Ken-Ichirou Morohashi (Kyushu University, Fukuoka, Japan) for providing
SF1 antibody, and Sally L. Dunwoodie (Victor Chang Cardiac Research
Institute, Sydney, NSW, Australia) for providing Cited2-knockout mice.
The authors also thank C. Spiller and C. Harris for technical support.
This work was supported by research grants from the Australian Research
Council (ARC), the National Health and Medical Research Council of
Australia, and the Intramural Research Program of the U.S. National
Institutes of Health, National Institute on Aging. P.K. is a Federation
Fellow of the ARC.
NR 56
TC 36
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U1 0
U2 6
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD OCT
PY 2011
VL 25
IS 10
BP 3561
EP 3569
DI 10.1096/fj.11-184333
PG 9
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 826LU
UT WOS:000295356400026
PM 21757499
ER
PT J
AU An, J
Golech, S
Klaewsongkram, J
Zhang, YQ
Subedi, K
Huston, GE
Wood, WH
Wersto, RP
Becker, KG
Swain, SL
Weng, NP
AF An, Jie
Golech, Susanne
Klaewsongkram, Jettanong
Zhang, Yongqing
Subedi, Kalpana
Huston, Gail E.
Wood, William H., III
Wersto, Robert P.
Becker, Kevin G.
Swain, Susan L.
Weng, Nanping
TI Kruppel-like factor 4 (KLF4) directly regulates proliferation in
thymocyte development and IL-17 expression during Th17 differentiation
SO FASEB JOURNAL
LA English
DT Article
DE transcription factor; T-cell homeostasis; autoimmune disease
ID T-CELL DEVELOPMENT; ROR-GAMMA-T; EMBRYONIC STEM-CELLS; TRANSCRIPTION
FACTOR; DOWN-REGULATION; T-H-17 CELLS; TGF-BETA; LINEAGE; SURVIVAL;
ALPHA
AB Kruppel-like factor 4 (KLF4), a transcription factor, plays a key role in the pluripotency of stem cells. We sought to determine the function of KLF4 in T-cell development and differentiation by using T-cell-specific Klf4-knockout (KO) mice. We found that KLF4 was highly expressed in thymocytes and mature T cells and was rapidly down-regulated in mature T cells after activation. In Klf4-KO mice, we observed a modest reduction of thymocytes (27%) due to the reduced proliferation of double-negative (DN) thymocytes. We demonstrated that a direct repression of Cdkn1b by KLF4 was a cause of decreased DN proliferation. During in vitro T-cell differentiation, we observed significant reduction of IL-17-expressing CD4(+) T cells (Th17; 24%) but not in other types of Th differentiation. The reduction of Th17 cells resulted in a significant attenuation of the severity (35%) of experimental autoimmune encephalomyelitis in vivo in Klf4-KO mice as compared with the Klf4 wild-type littermates. Finally, we demonstrated that KLF4 directly binds to the promoter of Il17a and positively regulates its expression. In summary, these findings identify KLF4 as a critical regulator in T-cell development and Th17 differentiation.-An, J., Golech, S., Klaewsongkram, J., Zhang, Y., Subedi, K., Huston, G. E., Wood, W. H., III, Wersto, R. P., Becker, K. G., Swain, S. L., Weng, N. Kruppel-like factor 4 (KLF4) directly regulates proliferation in thymocyte development and IL-17 expression during Th17 differentiation. FASEB J. 25, 3634-3645 (2011). www.fasebj.org
C1 [An, Jie; Golech, Susanne; Klaewsongkram, Jettanong; Subedi, Kalpana; Weng, Nanping] NIA, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
[Zhang, Yongqing; Wood, William H., III; Becker, Kevin G.] NIA, DNA Array Unit, NIH, Baltimore, MD 21224 USA.
[Wersto, Robert P.] NIA, Flow Cytometry Unit, NIH, Baltimore, MD 21224 USA.
[Huston, Gail E.] Trudeau Inst, New York, NY USA.
[Swain, Susan L.] Univ Massachusetts, Sch Med, Dept Pathol, Worcester, MA 01605 USA.
RP Weng, NP (reprint author), 251 Bayview Blvd,Ste 100, Baltimore, MD 21224 USA.
EM wengn@mail.nih.gov
OI Klaewsongkram, Jettanong/0000-0001-6063-2403; Becker,
Kevin/0000-0002-6794-6656
FU National Institute on Aging; National Institute on Aging, National
Institutes of Health
FX The authors thank Drs. Richard Hodes and Joyti Sen for critical reading
of the manuscript, Andrea Wurster and Qing Yu for help with Th2- and
Th17-cell differentiation, Jun Ho Lee for help with the EAE mouse model,
Cuong Nguyen and Tonya Wolf of the Flow Cytometry Unit for cell sorting,
the staff of the National Institute on Aging animal facility for support
and assistance, and Ana Lustig for proofreading the manuscript. This
research was supported by the Intramural Research Program of the
National Institute on Aging, National Institutes of Health. J.A and S.
G. designed and performed experiments, analyzed the data, and
contributed to the writing of the manuscript. J.K., Y.Z., K.S., G.E.H.,
W.H.W., R.P.W., and K.G.B. contributed to some of the experiments and
data analysis. S.L.S and N.W. directed the experiments and wrote the
manuscript. N.W. conceived the research, designed the experiments, and
funded the research. The authors declare no competing financial
interests.
NR 51
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U2 6
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD OCT
PY 2011
VL 25
IS 10
BP 3634
EP 3645
PG 12
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 826LU
UT WOS:000295356400033
PM 21685331
ER
PT J
AU Allen, MD
Neumann, S
Gershengorn, MC
AF Allen, Michael D.
Neumann, Susanne
Gershengorn, Marvin C.
TI Occupancy of both sites on the thyrotropin (TSH) receptor dimer is
necessary for phosphoinositide signaling
SO FASEB JOURNAL
LA English
DT Article
DE GPCR; inositolphosphates; IP1; G(q/11) coupling
ID PHOSPHOLIPASE-C; FLUORESCENT PROTEIN; CYTOSOLIC CA-2+; PHARMACOLOGY;
DIMERIZATION; TRANSDUCIN; MUTATIONS; RHODOPSIN; FAMILIES; PEPTIDE
AB The thyroid-stimulating hormone (TSH) receptor signals via Gs to produce cAMP and via G(q/11) to produce inositol-1,4,5-trisphosphate, which is degraded to inositol monophosphate (IP1; phosphoinositide signaling). The potency of TSH for cAMP signaling is higher than for phosphoinositide signaling, and it was suggested that there are "spare receptors" for cAMP signaling. In a human embryonic kidney macrophage scavenger receptor-expressing (HEK-EM) 293 model system, there are no spare receptors, but the cells still exhibited 100-fold differences in potencies. Dose responses for TSH-stimulated dissociation of prebound 125I-TSH (negative cooperativity; EC50 = 70 mU/ml), which requires TSH binding to both sites of the TSH receptor (TSHR) homodimer, and TSH-stimulated IP1 production (EC50 = 50 mU/ml) were indistinguishable. Fluorescence resonance energy transfer (FRET) using tagged receptors showed that TSHR formed homodimers and heterodimers with two binding-deficient mutant TSHRs, L252P and C41S. When L252P or C41S was expressed with TSHR, that is, when TSHR/L252P or TSHR/C41S heterodimers could only bind one TSH, TSH-stimulated IP1 production was decreased relative to cAMP production. The slopes of linear regression analyses comparing fold stimulation by TSH of IP1 vs. cAMP production were 0.044 +/- 0.0047, 0.0043 +/- 0.0041, and 0.0059 +/- 0.0014 for cells expressing TSHR alone, TSHR and L252P, or TSHR and C41S, respectively. We suggest that TSHR coupling to phosphoinositide signaling is dependent on binding 2 molecules of TSH to TSHR homodimer, causing a conformational change allowing coupling to G(q/11).Allen, M. D., Neumann, S., Gershengorn, M. C. Occupancy of both sites on the thyrotropin (TSH) receptor dimer is necessary for phosphoinositide signaling. FASEB J. 25, 3687-3694 (2011). www.fasebj.org
C1 [Allen, Michael D.; Neumann, Susanne; Gershengorn, Marvin C.] NIDDK, CEB, NIH, Bethesda, MD 20892 USA.
RP Gershengorn, MC (reprint author), NIDDK, CEB, NIH, 50 South Dr, Bethesda, MD 20892 USA.
EM marving@intra.niddk.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases, U.S.
National Institutes of Health [Z01-DK011006]
FX The authors thank Stefano Costanzi and Jurgen Wess for helpful comments.
This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases
(Z01-DK011006), U.S. National Institutes of Health.
NR 27
TC 18
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U1 0
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD OCT
PY 2011
VL 25
IS 10
BP 3687
EP 3694
DI 10.1096/fj.11-188961
PG 8
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 826LU
UT WOS:000295356400037
PM 21705666
ER
PT J
AU Appella, E
Johansson, J
AF Appella, Ettore
Johansson, Jan
TI Special Issue: Protein Structure and Proteomics Introduction
SO FEBS JOURNAL
LA English
DT Editorial Material
C1 [Appella, Ettore] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
[Johansson, Jan] Karolinska Inst, KI Alzheimers Dis Res Ctr, NVS Dept, Stockholm, Sweden.
RP Appella, E (reprint author), NCI, Cell Biol Lab, NIH, Bldg 37, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1742-464X
J9 FEBS J
JI FEBS J.
PD OCT
PY 2011
VL 278
IS 20
SI SI
BP 3795
EP 3795
DI 10.1111/j.1742-4658.2011.08313.x
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 826EW
UT WOS:000295335500001
PM 21883927
ER
PT J
AU Auttachoat, W
Germolec, DR
Smith, MJ
White, KL
Guo, TL
AF Auttachoat, Wimolnut
Germolec, Dori R.
Smith, Matthew J.
White, Kimber L., Jr.
Guo, Tai L.
TI Contact sensitizing potential of annatto extract and its two primary
color components, cis-bixin and norbixin, in female BALB/c mice
SO FOOD AND CHEMICAL TOXICOLOGY
LA English
DT Article
DE Annatto; Bixin; Norbixin; LLNA; MEST
ID LOCAL LYMPH-NODE; ASSAY; ALLERGENS; HYPERSENSITIVITY; IRRITANTS;
CHEMICALS; IDENTIFICATION; DISCRIMINATE; URTICARIA; RESPONSES
AB The present studies were performed to examine the contact allergenic effects of an annatto extract (ANT) in female BALB/c mice. ANT at 5-10% induced a greater than threefold increase in lymph node cell proliferation when compared to the control in the LLNA. Moreover, a significant increase in the percent ear swelling at 24 h after ANT challenge was observed in the MEST. A significant increase in the percentage of B cells was also observed. To determine which of the two predominant coloring components (norbixin and bixin) in ANT was responsible for the sensitizing effects of ANT, norbixin was subsequently examined, with negative results being observed in both the LLNA and MEST following treatment with norbixin (1-20%). These findings suggested that perhaps bixin was responsible for the positive responses in both the LLNA and MEST following exposure to ANT. Therefore, further studies using a partially purified cis-bixin extract were conducted. Positive responses in both the LLNA and MEST were observed in mice treated with cis-bixin at the concentrations as low as 0.1-0.5%. These results have demonstrated that cis-bixin, but not norbixin, is likely a contact sensitizer and contributes to the contact hypersensitivity effects observed following dermal exposure to ANT in mice. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Auttachoat, Wimolnut; Smith, Matthew J.; White, Kimber L., Jr.; Guo, Tai L.] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA.
[Germolec, Dori R.] NIEHS, Res Triangle Pk, NC 27709 USA.
RP White, KL (reprint author), Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, POB 980613, Richmond, VA 23298 USA.
EM klwhite@vcu.edu
FU NIEHS [ES 55538]
FX This work was supported by the NIEHS Contract ES 55538. "This article
may be the work product of an employee or group of employees of the
National Institute of Environmental Health Sciences (NIEHS), National
Institutes of Health (NIH). however, the statements, opinions or
conclusions contained therein do not necessarily represent the
statements, opinions or conclusions of NIEHS, NIH or the United States
government".
NR 46
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U1 0
U2 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0278-6915
EI 1873-6351
J9 FOOD CHEM TOXICOL
JI Food Chem. Toxicol.
PD OCT
PY 2011
VL 49
IS 10
BP 2638
EP 2644
DI 10.1016/j.fct.2011.07.009
PG 7
WC Food Science & Technology; Toxicology
SC Food Science & Technology; Toxicology
GA 824ZW
UT WOS:000295241700021
PM 21777644
ER
PT J
AU Hu, GQ
Schones, DE
Cui, KR
Ybarra, R
Northrup, D
Tang, QS
Gattinoni, L
Restifo, NP
Huang, SM
Zhao, KJ
AF Hu, Gangqing
Schones, Dustin E.
Cui, Kairong
Ybarra, River
Northrup, Daniel
Tang, Qingsong
Gattinoni, Luca
Restifo, Nicholas P.
Huang, Suming
Zhao, Keji
TI Regulation of nucleosome landscape and transcription factor targeting at
tissue-specific enhancers by BRG1
SO GENOME RESEARCH
LA English
DT Article
ID CHROMATIN REMODELING COMPLEXES; GENOME-WIDE ANALYSIS; BAF COMPLEX;
GENE-EXPRESSION; DNA; PROMOTER; PROTEIN; CELLS; OCCUPANCY; INDUCTION
AB Enhancers of transcription activate transcription via binding of sequence-specific transcription factors to their target sites in chromatin. In this report, we identify GATA1-bound distal sites genome-wide and find a global reorganization of the nucleosomes at these potential enhancers during differentiation of hematopoietic stem cells (HSCs) to erythrocytes. We show that the catalytic subunit BRG1 of BAF complexes localizes to these distal sites during differentiation and generates a longer nucleosome linker region surrounding the GATA1 sites by shifting the flanking nucleosomes away. Intriguingly, we find that the nucleosome shifting specifically facilitates binding of TAL1 but not GATA1 and is linked to subsequent transcriptional regulation of target genes.
C1 [Hu, Gangqing; Schones, Dustin E.; Cui, Kairong; Northrup, Daniel; Tang, Qingsong; Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Ybarra, River; Huang, Suming] Univ Florida, Coll Med, Dept Biochem & Mol Biol, Gainesville, FL 32611 USA.
[Gattinoni, Luca; Restifo, Nicholas P.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Zhao, KJ (reprint author), NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
EM zhaok@nhlbi.nih.gov
RI HU, GANGQING/K-5849-2012; Restifo, Nicholas/A-5713-2008; cheng,
yong/I-4270-2012; Gattinoni, Luca/A-2281-2008
OI Restifo, Nicholas P./0000-0003-4229-4580; Gattinoni,
Luca/0000-0003-2239-3282
FU Division of Intramural Research Program of the National Heart, Lung and
Blood Institute, NIH [R01HL090589, R01HL091929, K22HL101950]
FX This work was supported by the Division of Intramural Research Program
of the National Heart, Lung and Blood Institute, NIH (K.Z.), R01HL090589
and R01HL091929 (S.H.), and K22HL101950 (D.E.S.).
NR 53
TC 80
Z9 80
U1 0
U2 6
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
J9 GENOME RES
JI Genome Res.
PD OCT
PY 2011
VL 21
IS 10
BP 1650
EP 1658
DI 10.1101/gr.121145.111
PG 9
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 827DQ
UT WOS:000295407800009
PM 21795385
ER
PT J
AU Cox, S
Kuo, C
Jamieson, DJ
Kourtis, AP
McPheeters, ML
Meikle, SF
Posner, SF
AF Cox, Shanna
Kuo, Cassie
Jamieson, Denise J.
Kourtis, Athena P.
McPheeters, Melissa L.
Meikle, Susan F.
Posner, Samuel F.
TI Poisoning hospitalisations among reproductive-aged women in the USA,
1998-2006
SO INJURY PREVENTION
LA English
DT Article
ID EMERGENCY-DEPARTMENT VISITS; ATTEMPTED-SUICIDE; NONMEDICAL USE;
UNITED-STATES; INJURY; ASSOCIATION; DRUGS
AB Objective To describe poisoning hospitalisations among reproductive-aged women from 1998 to 2006.
Methods 1998-2006 data from the Nationwide Inpatient Sample of the Healthcare Cost and Utilisation Project were used to identify hospitalisations for poisonings among US women aged 15-44 years. Differences in hospitalisation characteristics were compared by intent using chi(2) statistics. Trends in poisoning hospitalisation rates were calculated overall and by subgroup.
Results There were approximately 636 000 poisoning hospitalisations in women aged 15-44 years during 1998-2006. Hospitalisations for intentionally self-inflicted poisonings had a higher proportion of women aged 15-24 years and privately insured women than did unintentional poisonings (p<0.001). Poisoning hospitalisations in rural areas and those that resulted in death were more likely to be of undetermined intent than those for which intent was specified (p<0.001). Co-diagnoses of substance abuse (34.5%) or mental disorders (66.5%) were high. The rate of poisoning hospitalisations overall and unintentional poisoning hospitalisations increased 6% and 22%, respectively, during this period (p<0.001). The most frequently diagnosed poisoning agent was acetaminophen. Poisonings attributable to acetaminophen, opioids, central nervous system stimulants and benzodiazepines increased, while poisonings attributable to antidepressants decreased (p<0.05).
Conclusions The increase in unintentional poisoning hospitalisations among women aged 15-44 years and the changing profile of poisoning agents should inform the healthcare community's poisoning prevention strategies. Poisoning prevention strategies should include a component to address substance abuse and mental health disorders among reproductive-age women.
C1 [Cox, Shanna; Kuo, Cassie; Jamieson, Denise J.; Kourtis, Athena P.; Posner, Samuel F.] Ctr Dis Control & Prevent, Div Reprod Hlth, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA 30341 USA.
[McPheeters, Melissa L.] Vanderbilt Univ, Med Ctr, Dept Obstet & Gynecol, Nashville, TN 37232 USA.
[Meikle, Susan F.] NIH, Off Res Womens Hlth, Bethesda, MD 20892 USA.
RP Cox, S (reprint author), Ctr Dis Control & Prevent, Div Reprod Hlth, Natl Ctr Chron Dis Prevent & Hlth Promot, 4770 Buford Highway MS K-20, Atlanta, GA 30341 USA.
EM shanna.cox@cdc.hhs.gov
OI Posner, Samuel/0000-0003-1574-585X
NR 36
TC 8
Z9 8
U1 0
U2 2
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1353-8047
J9 INJURY PREV
JI Inj. Prev.
PD OCT
PY 2011
VL 17
IS 5
BP 332
EP 337
DI 10.1136/ip.2010.029793
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 823MB
UT WOS:000295125300010
PM 21296799
ER
PT J
AU Twardoski, B
Feldmann, H
Bloom, ME
Ward, J
AF Twardoski, Barri
Feldmann, Heinz
Bloom, Marshall E.
Ward, Joe
TI Modern dosimetric tools for Co-60 irradiation at high containment
laboratories
SO INTERNATIONAL JOURNAL OF RADIATION BIOLOGY
LA English
DT Article
DE Microbiology; radiation chemistry; radiation physics; dose-response
curve; dosimetry; radiation
ID FLUORESCENT FILM DOSIMETER
AB Purpose: To evaluate an innovative photo-fluorescent film as a routine dosimetric tool during 1.0 SD on each test) was analyzed with logistic regression.
Results: Older adults with high pentosidine level had worse baseline DSST score (p = 0.05) but not different 3MS score (p = 0.32). On both tests, there was a more pronounced 9-year decline in those with high and mid pentosidine level compared to those in the lowest tertile (3MS 7.0, 5.4, and 2.5 point decline, p overall < 0.001; DSST 5.9, 7.4, and 4.5 point decline, p = 0.03). Incident cognitive impairment was higher in those with high or mid pentosidine level than those in the lowest tertile (3MS: 24% vs 17%, odds ratio = 1.55; 95% confidence interval 1.07-2.26; DSST: 31% vs 22%, odds ratio = 1.62; 95% confidence interval 1.13-2.33). There was no interaction between pentosidine level, diabetes status, and cognitive decline. Multivariate adjustment for age, sex, race, education, hypertension, cardiovascular disease, estimated glomerular filtration rate, and diabetes diminished results somewhat but overall patterns remained similar.
Conclusion: High peripheral AGE level is associated with greater cognitive decline in older adults with and without diabetes. Neurology (R) 2011;77:1351-1356
C1 [Yaffe, K.; Vitartas, C.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94121 USA.
[Yaffe, K.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94121 USA.
[Yaffe, K.; Schwartz, A. V.; Vittinghoff, E.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94121 USA.
[Lindquist, K.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94121 USA.
[Yaffe, K.; Vitartas, C.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Satterfield, S.] Univ Tennessee, Hlth Sci Ctr, Dept Prevent Med, Memphis, TN USA.
[Simonsick, E. M.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Launer, L.; Harris, T.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Baltimore, MD 21224 USA.
[Rosano, C.; Cauley, J. A.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
RP Yaffe, K (reprint author), Univ Calif San Francisco, Dept Psychiat, Box 181,4150 Clement St, San Francisco, CA 94121 USA.
EM kristine.yaffe@ucsf.edu
OI Rosano, Caterina/0000-0002-0909-1506; Rosano,
Caterina/0000-0002-4271-6010; Cauley, Jane A/0000-0003-0752-4408
FU NIH, National Institute of Aging; American Health Assistance Foundation
[A201-0029]; Amgen; Merck Serono; GlaxoSmithKline; Anonymous Foundation;
Alzheimer Association; NIH (NIA, NIDDK, NIMH); Department of Defense;
NIH (NIDDK, NIA); Medtronic, Inc.; Zoll Medical Corporation; NIH (NIA,
NIDDK, NHLBI, NIAID, NIMH); NIH/NIA; Novartis; NIH; NIA [N01-AG-6-2101,
N01-AG-6-2103, N01-AG-6-2106]
FX NIA contract nos. N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106. This
research was supported in part by the Intramural Research Program of the
NIH, National Institute of Aging, and by a grant from the American
Health Assistance Foundation, grant no. A201-0029.; Dr. Yaffe has served
on data safety monitoring boards for Pfizer Inc, Medivation, Inc. and
the NIH (NIMH and NIA trials); and has received research support from
the NIH (NIA, NIDDK, NIMH), the Department of Defense, American Health
Assistance Foundation, Anonymous Foundation, and the Alzheimer
Association. K. Lindquist reports no disclosures. Dr. Schwartz serves on
a scientific advisory board for GlaxoSmithKline; has received speaker
honoraria from Amgen and Merck Serono; has received funding for travel
from Amgen; and receives research support from Merck Serono,
GlaxoSmithKline, the NIH (NIDDK, NIA). C. Vitartas reports no
disclosures. Dr. Vittinghoff receives publishing royalties for
Regression Methods in Biostatistics: Linear, Logistic, Survival and
Repeated Measures Models (Springer Verlag, 2005); and receives research
support from Medtronic, Inc., Zoll Medical Corporation, Amgen, and the
NIH (NIA, NIDDK, NHLBI, NIAID, NIMH). Dr. Satterfield receives research
support from the NIH/NIA. Dr. Simonsick serves as an Associate Editor
for the Journal of Gerontology Medical Sciences and on the editorial
board of the Journal of Aging and Health. Dr. Launer receives research
support from the NIH/NIA Intramural Research Program. Dr. Rosano reports
no disclosures. Dr. Cauley receives research support from Novartis. Dr.
Harris receives research support from the NIH.
NR 31
TC 48
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U1 1
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD OCT
PY 2011
VL 77
IS 14
BP 1351
EP 1356
DI 10.1212/WNL.0b013e3182315a56
PG 6
WC Clinical Neurology
SC Neurosciences & Neurology
GA 828XV
UT WOS:000295539000010
PM 21900628
ER
PT J
AU Zheng, CY
Seabold, GK
Horak, M
Petralia, RS
AF Zheng, Chan-Ying
Seabold, Gail K.
Horak, Martin
Petralia, Ronald S.
TI MAGUKs, Synaptic Development, and Synaptic Plasticity
SO NEUROSCIENTIST
LA English
DT Review
DE SAP97; MAGI; CASK; PSD-95; SAP102
ID ADHESION-LIKE MOLECULES; DENDRITIC SPINE MORPHOGENESIS; RECEPTOR SURFACE
EXPRESSION; DENSITY PROTEIN PSD-95; D-ASPARTATE RECEPTORS; NMDA
RECEPTOR; POSTSYNAPTIC DENSITY; AMPA RECEPTORS; EXCITATORY SYNAPSES;
IN-VIVO
AB MAGUKs are proteins that act as key scaffolds in surface complexes containing receptors, adhesion proteins, and various signaling molecules. These complexes evolved prior to the appearance of multicellular animals and play key roles in cell-cell intercommunication. A major example of this is the neuronal synapse, which contains several presynaptic and postsynaptic MAGUKs including PSD-95, SAP102, SAP97, PSD-93, CASK, and MAGIs. Here, they play roles in both synaptic development and in later synaptic plasticity events. During development, MAGUKs help to organize the postsynaptic density via associations with other scaffolding proteins, such as Shank, and the actin cytoskeleton. They affect the clustering of glutamate receptors and other receptors, and these associations change with development. MAGUKs are involved in long-term potentiation and depression (e.g., via their phosphorylation by kinases and phosphorylation of other proteins associated with MAGUKs). Importantly, synapse development and function are dependent on the kind of MAGUK present. For example, SAP102 shows high mobility and is present in early synaptic development. Later, much of SAP102 is replaced by PSD-95, a more stable synaptic MAGUK; this is associated with changes in glutamate receptor types that are characteristic of synaptic maturation.
C1 [Zheng, Chan-Ying; Seabold, Gail K.; Horak, Martin; Petralia, Ronald S.] Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD USA.
RP Petralia, RS (reprint author), NIDCD, NIH, 50-4142,50 S Dr,MSC 8027, Bethesda, MD 20892 USA.
EM petralia@nidcd.nih.gov
RI Horak, Martin/F-9819-2010
FU National Institute on Deafness and Other Communication Disorders (NIDCD)
at the National Institutes of Health (NIH)
FX The authors thank Drs. Katherine W. Roche and Elizabeth Webber for
critical review of the article. This work was supported by the
Intramural Program of the National Institute on Deafness and Other
Communication Disorders (NIDCD) at the National Institutes of Health
(NIH).
NR 119
TC 72
Z9 77
U1 8
U2 24
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-8584
J9 NEUROSCIENTIST
JI Neuroscientist
PD OCT
PY 2011
VL 17
IS 5
BP 493
EP 512
DI 10.1177/1073858410386384
PG 20
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 827HR
UT WOS:000295420100009
PM 21498811
ER
PT J
AU Wadden, TA
Neiberg, RH
Wing, RR
Clark, JM
Delahanty, LM
Hill, JO
Krakoff, J
Otto, A
Ryan, DH
Vitolins, MZ
AF Wadden, Thomas A.
Neiberg, Rebecca H.
Wing, Rena R.
Clark, Jeanne M.
Delahanty, Linda M.
Hill, James O.
Krakoff, Jonathan
Otto, Amy
Ryan, Donna H.
Vitolins, Mara Z.
CA Look AHEAD Res Grp
TI Four-Year Weight Losses in the Look AHEAD Study: Factors Associated With
Long-Term Success
SO OBESITY
LA English
DT Article
ID LIFE-STYLE INTERVENTION; DIABETES-PREVENTION-PROGRAM; LOSS MAINTENANCE;
CARDIOVASCULAR-DISEASE; BEHAVIORAL TREATMENT; PHYSICAL-ACTIVITY;
OBESE-PATIENTS; ACTIVITY GOALS; RISK-FACTORS; MANAGEMENT
AB This report provides a further analysis of the year 4 weight losses in the Look AHEAD (Action for Health in Diabetes) study and identifies factors associated with long-term success. A total of 5,145 overweight/obese men and women with type 2 diabetes were randomly assigned to an intensive lifestyle intervention (ILI) or a usual care group, referred to as Diabetes Support and Education (DSE). ILI participants were provided approximately weekly group or individual treatment in year 1; continued but less frequent contact was provided in years 2-4. DSE participants received three group educational sessions in all years. As reported previously, at year 4, ILI participants lost an average of 4.7% of initial weight, compared with 1.1% for DSE (P < 0.0001). More ILI than DSE participants lost >= 5% (46% vs. 25%, P < 0.0001) and >= 10% (23% vs. 10%, P < 0.0001) of initial weight. Within the ILI, achievement of both the 5% and 10% categorical weight losses at year 4 was strongly related to meeting these goals at year 1. A total of 887 participants in ILI lost >= 10% at year 1, of whom 374 (42.2%) achieved this loss at year 4. Participants who maintained the loss, compared with those who did not, attended more treatment sessions and reported more favorable physical activity and food intake at year 4. These results provide critical evidence that a comprehensive lifestyle intervention can induce clinically significant weight loss (i.e., >= 5%) in overweight/obese participants with type 2 diabetes and maintain this loss in more than 45% of patients at 4 years.
C1 [Wadden, Thomas A.] Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
[Neiberg, Rebecca H.] Wake Forest Univ, Dept Biostatist Sci, Winston Salem, NC 27109 USA.
[Wing, Rena R.] Miriam Hosp, Dept Psychiat & Human Behav, Brown Med Sch, Providence, RI USA.
[Clark, Jeanne M.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Delahanty, Linda M.] Harvard Univ, Sch Med, Boston, MA USA.
[Delahanty, Linda M.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Hill, James O.] Univ Colorado, Hlth Sci Ctr, Dept Pediat, Denver, CO 80262 USA.
[Krakoff, Jonathan] NIDDK, NIH, Phoenix, AZ USA.
[Otto, Amy] Univ Pittsburgh, Dept Hlth & Phys Act, Pittsburgh, PA USA.
[Ryan, Donna H.] Pennington Biomed Res Ctr, Dept Clin Res, Baton Rouge, LA USA.
[Vitolins, Mara Z.] Wake Forest Univ, Dept Epidemiol & Prevent, Winston Salem, NC 27109 USA.
RP Wadden, TA (reprint author), Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
EM Wadden@mail.med.upenn.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases;
National Heart, Lung, and Blood Institute; Centers for Disease Control
and Prevention; Department of Health and Human Services; National
Institutes of Health [DK57136, DK57149, DK56990, DK57177, DK57171,
DK57151, DK57182, DK57131, DK57002, DK57078, DK57154, DK57178, DK57219,
DK57008, DK57135, DK56992]; National Institute of Nursing Research;
National Center on Minority Health and Health Disparities; Office of
Research on Women's Health; Department of Veterans Affairs
FX Federal sponsors; National Institute of Diabetes and Digestive and
Kidney Diseases. Mary Evans, PhD; Barbara Harrison, MS; Van S. Hubbard,
MD, PhD; Susan Z. Yanovski, MD; Robert Kuczmarski, PhD; National Heart,
Lung, and Blood Institute. Lawton S. Cooper, MD, MPH; Peter Kaufman,
PhD, FABMR; Centers for Disease Control and Prevention. Edward W. Gregg,
PhD; David F. Williamson, PhD; Ping Zhang, PhD; This study is supported
by the Department of Health and Human Services through the following
cooperative agreements from the National Institutes of Health: DK57136,
DK57149, DK56990, DK57177, DK57171, DK57151, DK57182, DK57131, DK57002,
DK57078, DK57154, DK57178, DK57219, DK57008, DK57135, and DK56992. The
following federal agencies have contributed support: National Institute
of Diabetes and Digestive and Kidney Diseases; National Heart, Lung, and
Blood Institute; National Institute of Nursing Research; National Center
on Minority Health and Health Disparities; Office of Research on Women's
Health; the Centers for Disease Control and Prevention; and the
Department of Veterans Affairs. This research was supported in part by
the Intramural Research Program of the National Institute of Diabetes
and Digestive and Kidney Diseases. The Indian Health Service (IHS)
provided personnel, medical oversight, and use of facilities. The
opinions expressed in this paper are those of the authors and do not
necessarily reflect the views of the IHS or other funding sources.
NR 53
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Z9 154
U1 1
U2 18
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD OCT
PY 2011
VL 19
IS 10
BP 1987
EP 1998
DI 10.1038/oby.2011.230
PG 12
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 825IX
UT WOS:000295266700010
PM 21779086
ER
PT J
AU Cohen, SS
Gammon, MD
North, KE
Millikan, RC
Lange, EM
Williams, SM
Zheng, W
Cai, QY
Long, JR
Smith, JR
Signorello, LB
Blot, WJ
Matthews, CE
AF Cohen, Sarah S.
Gammon, Marilie D.
North, Kari E.
Millikan, Robert C.
Lange, Ethan M.
Williams, Scott M.
Zheng, Wei
Cai, Qiuyin
Long, Jirong
Smith, Jeffrey R.
Signorello, Lisa B.
Blot, William J.
Matthews, Charles E.
TI ADIPOQ, ADIPOR1, and ADIPOR2 Polymorphisms in Relation to Serum
Adiponectin Levels and BMI in Black and White Women
SO OBESITY
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; APM1 GENE; CARDIOVASCULAR-DISEASE; QUANTITATIVE
TRAITS; INSULIN-RESISTANCE; HEALTHY CAUCASIANS; METABOLIC SYNDROME;
HERITAGE FAMILY; IRAS FAMILY; OBESITY
AB Adiponectin is an adipose-secreted protein with influence on several physiologic pathways including those related to insulin sensitivity, inflammation, and atherogenesis. Adiponectin levels are highly heritable and several single-nucleotide polymorphisms (SNPs) in adiponectin-related genes (ADIPOQ, ADIPOR1, ADIPOR2) have been examined in relation to circulating adiponectin levels and obesity phenotypes, but despite differences in adiponectin levels and obesity prevalence by race, few studies have included black participants. Using cross-sectional interview data and blood samples collected from 990 black and 977 white women enrolled in the Southern Community Cohort Study (SCCS) from 2002 to 2006, we examined 25 SNPs in ADIPOQ, 19 in ADIPOR1, and 27 in ADIPOR2 in relation to serum adiponectin levels and BMI using race-stratified linear regression models adjusted for age and percentage African ancestry. SNP rs17366568 in ADIPOQ was significantly associated with serum adiponectin levels in white women only (adjusted mean adiponectin levels = 15.9 for G/G genotype, 13.7 for A/G, and 9.3 for A/A, P = 0.00036). No other SNPs were associated with adiponectin or BMI among blacks or whites. Because adiponectin levels as well as obesity are highly heritable and vary by race but associations with polymorphisms in the ADIPOQ, ADIPOR1, and ADIPOR2 genes have been few in this and other studies, future work including large populations from diverse racial groups is needed to detect additional genetic variants that influence adiponectin and BMI.
C1 [Cohen, Sarah S.; Gammon, Marilie D.; North, Kari E.; Millikan, Robert C.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27515 USA.
[Cohen, Sarah S.; Signorello, Lisa B.; Blot, William J.] Int Epidemiol Inst, Rockville, MD USA.
[North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
[Lange, Ethan M.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Lange, Ethan M.] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Williams, Scott M.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Sch Med, Nashville, TN 37232 USA.
[Zheng, Wei; Cai, Qiuyin; Long, Jirong; Signorello, Lisa B.; Blot, William J.] Vanderbilt Univ, Dept Med, Div Epidemiol,Vanderbilt Ingram Cancer Ctr, Vanderbilt Epidemiol Ctr,Sch Med, Nashville, TN USA.
[Smith, Jeffrey R.] Vanderbilt Univ, Dept Med, Sch Med, Nashville, TN USA.
[Matthews, Charles E.] NCI, Nutr Epidemiol Branch, Rockville, MD USA.
RP Cohen, SS (reprint author), Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27515 USA.
EM sarah@ieixmail.com
RI Williams, Scott/B-9491-2012; Smith, Jeff/C-3484-2012; matthews,
Charles/E-8073-2015
OI matthews, Charles/0000-0001-8037-3103
FU Susan G. Komen for the Cure [OP05-0927-DR1]; National Cancer Institute
(NCI) [R01 CA092447, T32 CA09330-26, 5-R25-CA057726]; National Institute
of Environmental Health Sciences [P30ES10126]; Vanderbilt-Ingram Cancer
Center [P30 CA68485]
FX This project was funded in part by grant OP05-0927-DR1 from Susan G.
Komen for the Cure. The Southern Community Cohort Study is funded by
grant R01 CA092447 from the National Cancer Institute (NCI). S. S. C.
also received support from NCI Training Grants T32 CA09330-26 and
5-R25-CA057726. M. D. G. is supported in part from P30ES10126 from the
National Institute of Environmental Health Sciences. Sample preparation
was conducted at the Survey and Biospecimen Shared Resource that is
supported in part by the Vanderbilt-Ingram Cancer Center (P30 CA68485).
We thank Regina Courtney and the late Qing Wang for serum and DNA sample
preparation, and Kevin Bradley and Joan Breyer for genotyping
assistance, including contributing to the design of gene targets. We
also thank Heather Munro at the International Epidemiology Institute for
her statistical review.
NR 42
TC 14
Z9 16
U1 1
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD OCT
PY 2011
VL 19
IS 10
BP 2053
EP 2062
DI 10.1038/oby.2010.346
PG 10
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 825IX
UT WOS:000295266700019
PM 21273992
ER
PT J
AU Malhotra, A
Kobes, S
Knowler, WC
Baier, LJ
Bogardus, C
Hanson, RL
AF Malhotra, Alka
Kobes, Sayuko
Knowler, William C.
Baier, Leslie J.
Bogardus, Clifton
Hanson, Robert L.
TI A Genome-Wide Association Study of BMI in American Indians
SO OBESITY
LA English
DT Article
ID BODY-MASS INDEX; PIMA-INDIANS; OBESITY; VARIANTS; LOCI; POPULATIONS;
EXTREME; FAMILY; ONSET; RISK
AB Numerous studies have been done to understand genetic contributors to BMI, but only a limited number of studies have been done in nonwhite groups such as American Indians. A genome-wide association study (GWAS) for BMI was therefore performed in Pima Indians. BMI measurements from a longitudinal study of 1,120 Pima Indians and 454,194 single-nucleotide polymorphisms (SNPs) from the 1 million Affymetrix SNP panel were used (35% of SNPs were excluded due to minor allele frequency < 0.05). Data included BMI measured at multiple examinations collected from 1965 to 2004, as well as the maximum BMI at one of these visits. General and within-family tests were performed using a maximum-likelihood based mixed model procedure. No SNP reached a genome-wide significance level (estimated at P < 4.94 x 10(-7)). For repeated measures analyses, the strongest associations for general and within-family tests mapped to two different regions on chromosome 6 (rs9342220 (P = 1.39 x 10(-6)) and rs7758764 (P = 2.51 x 10(-6)), respectively). For maximum BMI, the strongest association for the general tests mapped to chromosome 4 (rs17612333; P = 1.98 x 10(-6)) and to chromosome 3 (rs11127958; P = 1.53 x 10(-6)) for the within-family tests. Further analysis is important because only a few of these regions have been previously implicated in a GWAS and genetic susceptibility may differ by ethnicity.
C1 [Malhotra, Alka; Kobes, Sayuko; Knowler, William C.; Baier, Leslie J.; Bogardus, Clifton; Hanson, Robert L.] NIDDK, Phoenix Epidemiol & Clin Res Branch, Phoenix, AZ USA.
RP Malhotra, A (reprint author), NIDDK, Phoenix Epidemiol & Clin Res Branch, Phoenix, AZ USA.
EM alka@niddk.nih.gov
RI Hanson, Robert/O-3238-2015
OI Hanson, Robert/0000-0002-4252-7068
FU National Institute of Diabetes and Digestive and Kidney Diseases
FX The authors thank the study participants and staff of the Diabetes
Epidemiology and Clinical Research Section and of the Diabetes Molecular
Genetics Section for performing the studies generating these data. This
research was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases.
NR 21
TC 20
Z9 21
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD OCT
PY 2011
VL 19
IS 10
BP 2102
EP 2106
DI 10.1038/oby.2011.178
PG 5
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 825IX
UT WOS:000295266700027
PM 21701565
ER
PT J
AU Sekine, Y
Osei-Hwedieh, D
Matsuda, K
Raghavachari, N
Liu, DL
Furuya, Y
Koike, H
Suzuki, K
Remaley, AT
AF Sekine, Yoshitaka
Osei-Hwedieh, David
Matsuda, Kant
Raghavachari, Nalini
Liu, Delong
Furuya, Yosuke
Koike, Hidekazu
Suzuki, Kazuhiro
Remaley, Alan T.
TI High Fat Diet Reduces the Expression of Glutathione Peroxidase 3 in
Mouse Prostate
SO PROSTATE
LA English
DT Article
DE high fat diet; prostate; GPx3; cholesterol; mouse
ID CANCER CELL-LINES; OXIDATIVE STRESS; NUDE-MICE; GROWTH;
GLUTATHIONE-PEROXIDASE-3; CARCINOGENESIS; INFLAMMATION; CHOLESTEROL;
CARCINOMA; LNCAP
AB BACKGROUND. High fat diets are known to be a risk factor for prostate cancer. In this study, we investigated the effect of high fat diet on mouse prostate gene expression.
METHODS. C57BL/6J mice were fed either a control or high fat diet for 12 weeks. Microarray analyses were performed on mouse ventral prostate (VP) and dorsolateral prostate (DLP), followed by canonical pathway analysis and regulatory network identification. mRNA changes were confirmed by real time PCR.
RESULTS. Approximately 2,125, and 1,194 genes responded significantly to the high fat diet in VP, DLP, respectively. Pathways and networks related to oxidative stress, glutathione metabolism, NRF-mediated oxidative stress response and NF-kappaB were all differentially regulated by high fat diet. Glutathione peroxidase 3 (GPx3) mRNA levels were decreased by approximately twofold by high fat diet in all three prostate lobes. In human non-transformed prostate cells (PrSC, PrEC, and BPH-1), cholesterol loading decreased GPx3 expression, and increased H(2)O(2) levels of culture medium. Troglitazone increased GPx3 expression in three normal prostate cells, and decreased H(2)O(2) levels. In addition, troglitazone attenuated cholesterol-induced H(2)O(2) increase. Tissue from prostate cancer biopsies had decreased GPx3 mRNA and its level was inversely related to the Gleason score.
CONCLUSIONS. High fat diet alters pathways related to many genes concerned with oxidative stress. GPx3, a gene identified by this analysis, was found to be down-regulated by high fat diet and appears be decreased in human prostate cancers, suggesting that GPx3 may have a possible role in modulating carcinogenesis. Prostate 71: 1499-1509, 2011. (C) 2011 Wiley-Liss, Inc.
C1 [Sekine, Yoshitaka; Osei-Hwedieh, David; Remaley, Alan T.] NHLBI, Lipoprot Metab Sect, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Matsuda, Kant] NCI, Tissue Array Res Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Raghavachari, Nalini] NHLBI, Genom Core Facil, NIH, Bethesda, MD 20892 USA.
[Liu, Delong] NHLBI, Math & Stat Comp Lab, CIT, NIH, Bethesda, MD 20892 USA.
[Liu, Delong] NHLBI, Genom Core Facil, NIH, Bethesda, MD 20892 USA.
[Sekine, Yoshitaka; Furuya, Yosuke; Koike, Hidekazu; Suzuki, Kazuhiro] Gunma Univ, Grad Sch Med, Dept Urol, Gunma, Japan.
RP Sekine, Y (reprint author), NHLBI, Lipoprot Metab Sect, Pulm & Vasc Med Branch, NIH, Bldg 10,Room 8N224,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM ysekine@showa.gunma-u.ac.jp
FU Intramural NHBLI National Institutes of Health
FX Grant sponsor: Intramural NHBLI National Institutes of Health.
NR 40
TC 8
Z9 8
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-4137
J9 PROSTATE
JI Prostate
PD OCT 1
PY 2011
VL 71
IS 14
BP 1499
EP 1509
DI 10.1002/pros.21365
PG 11
WC Endocrinology & Metabolism; Urology & Nephrology
SC Endocrinology & Metabolism; Urology & Nephrology
GA 827CR
UT WOS:000295404400003
PM 21374652
ER
PT J
AU Fesinmeyer, MD
Kwon, EM
Fu, R
Ostrander, EA
Stanford, JL
AF Fesinmeyer, Megan D.
Kwon, Erika M.
Fu, Rong
Ostrander, Elaine A.
Stanford, Janet L.
TI Genetic Variation in RNASEL and Risk for Prostate Cancer in a
Population-Based Case-Control Study
SO PROSTATE
LA English
DT Article
DE prostate cancer; RNASEL; Gleason grade; prostatitis
ID RIBONUCLEASE-L; ASSOCIATION; VARIANTS; POLYMORPHISMS; INFLAMMATION;
MUTATIONS; FAMILIES; GENOME; HPC1
AB BACKGROUND. Linkage studies have implicated chromosome 1q24 as a putative locus for hereditary prostate cancer. The RNASEL gene maps to 1q24 and has been associated with prostate cancer risk in multiple family-based linkage studies. The RNASEL gene product combats viral infection by degrading viral RNA and inducing apoptosis of infected cells. Few studies have evaluated the role of RNASEL variants in unselected or sporadic prostate cancer, or have considered the potential interaction between RNASEL variants and patient characteristics associated with past infection.
METHODS. Ten SNPs in the RNASEL gene were genotyped in 1,308 prostate cancer cases and 1,267 age-matched controls from prior population-based, case-control studies. The association between each SNP and haplotype with prostate cancer risk was calculated using logistic regression. Associations stratified by Gleason score were evaluated using polytomous regression. The likelihood ratio test was used to investigate effect modification.
RESULTS. Two RNASEL SNPs were associated with overall increases in prostate cancer risk (OR = 1.13 for each variant allele of rs12723593; OR = 1.88 for any variant allele of rs56250729). Risk estimates did not vary substantially by Gleason score, but there was effect modification for the variant allele of rs635261 by history of prostatitis (P = 0.02).
CONCLUSIONS. This study identified three RNASEL variants that are associated with risk for prostate cancer. Further research is required to confirm these results and to better understand the potential role RNASEL variants may play in the etiology of sporadic prostate cancer. Prostate 71: 1538-1547, 2011. (C) 2011 Wiley-Liss, Inc.
C1 [Fesinmeyer, Megan D.; Fu, Rong; Stanford, Janet L.] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Kwon, Erika M.; Ostrander, Elaine A.] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
[Fu, Rong] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Stanford, Janet L.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
RP Stanford, JL (reprint author), Fred Hutchinson Canc Res Ctr, Program Epidemiol, Div Publ Hlth Sci, 1100 Fairview Ave N,M4-B874, Seattle, WA 98109 USA.
EM jstanfor@fhcrc.org
OI Ostrander, Elaine/0000-0001-6075-9738
FU NIH [RO1 CA056678, RO1 CA092579, P50 CA097186]
FX Grant sponsor: NIH; Grant numbers: RO1 CA056678; RO1 CA092579; P50
CA097186; Additional support provided by the Fred Hutchinson Cancer
Research Center and the Intramural Program of the National Human Genome
Research Institute.
NR 34
TC 3
Z9 5
U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-4137
J9 PROSTATE
JI Prostate
PD OCT 1
PY 2011
VL 71
IS 14
BP 1538
EP 1547
DI 10.1002/pros.21370
PG 10
WC Endocrinology & Metabolism; Urology & Nephrology
SC Endocrinology & Metabolism; Urology & Nephrology
GA 827CR
UT WOS:000295404400007
PM 21360564
ER
PT J
AU Hari, D
Xin, HW
Jaiswal, K
Wiegand, G
Kim, BK
Ambe, C
Burka, D
Koizumi, T
Ray, S
Garfield, S
Thorgeirsson, S
Avital, I
AF Hari, Danielle
Xin, Hong-Wu
Jaiswal, Kshama
Wiegand, Gordon
Kim, Bo-Kyu
Ambe, Che
Burka, Douglas
Koizumi, Tomotake
Ray, Satyajit
Garfield, Susan
Thorgeirsson, Snorri
Avital, Itzhak
TI Isolation of Live Label-Retaining Cells and Cells Undergoing Asymmetric
Cell Division via Nonrandom Chromosomal Cosegregation from Human Cancers
SO STEM CELLS AND DEVELOPMENT
LA English
DT Article
ID IMMORTAL STRAND HYPOTHESIS; HEMATOPOIETIC STEM-CELLS; TEMPLATE DNA
STRANDS; SELECTIVE SEGREGATION; IN-VITRO; IDENTIFICATION; GENOME; VIVO;
SKIN
AB The ability to retain DNA labels over time is a property proposed to be associated with adult stem cells. Recently, label retaining cells (LRC) were indentified in cancer. LRC were suggested to be the result of either slow-cycling or asymmetric-cell-division with nonrandom-chromosomal-cosegregation (ACD-NRCC). ACD-NRCC is proposed to segregate the older template DNA strands into daughter stem cells and newly synthesized DNA into daughter cells destined for differentiation. The existence of cells undergoing ACD-NRCC and the stem-like nature of LRC remain controversial. Currently, to detect LRC and ACD-NRCC, cells need to undergo fixation. Therefore, testing the stem-cell nature and other functional traits of LRC and cells undergoing ACD-NRCC has been limited. Here, we show a method for labeling DNA with single and dual-color nucleotides in live human liver cancer cells avoiding the need for fixation. We describe a novel methodology for both the isolation of live LRC and cells undergoing ACD-NRCC via fluorescence-activated cell sorting with confocal microscopy validation. This has the potential to be a powerful adjunct to stem-cell and cancer research.
C1 [Hari, Danielle; Xin, Hong-Wu; Jaiswal, Kshama; Wiegand, Gordon; Kim, Bo-Kyu; Ambe, Che; Burka, Douglas; Koizumi, Tomotake; Ray, Satyajit; Avital, Itzhak] NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Hari, Danielle] Hosp Univ Penn, Dept Surg, Philadelphia, PA 19104 USA.
[Garfield, Susan; Thorgeirsson, Snorri] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Avital, I (reprint author), NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM avitali@mail.nih.gov
FU NCI [1ZIABC011005-02]
FX We thank L. Liam and P. Mannan for the confocal microscopy and surface
rendering work. A. Mixon and S. Farid for help with the FACS analysis
experiments. This work was supported by an NCI intramural grant
(1ZIABC011005-02).
NR 32
TC 19
Z9 19
U1 0
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1547-3287
J9 STEM CELLS DEV
JI Stem Cells Dev.
PD OCT
PY 2011
VL 20
IS 10
BP 1649
EP 1658
DI 10.1089/scd.2010.0455
PG 10
WC Cell & Tissue Engineering; Hematology; Medicine, Research &
Experimental; Transplantation
SC Cell Biology; Hematology; Research & Experimental Medicine;
Transplantation
GA 826AX
UT WOS:000295324900001
PM 21294632
ER
PT J
AU Casson, PR
Krawetz, SA
Diamond, MP
Zhang, HP
Legro, RS
Schlaff, WD
Coutifaris, C
Brzyski, RG
Christman, GM
Santoro, N
Eisenberg, E
AF Casson, Peter R.
Krawetz, Stephen A.
Diamond, Michael P.
Zhang, Heping
Legro, Richard S.
Schlaff, William D.
Coutifaris, Christos
Brzyski, Robert G.
Christman, Gregory M.
Santoro, Nanette
Eisenberg, Esther
CA Reprod Med Network
TI Proactively Establishing a Biologic Specimens Repository for Large
Clinical Trials: An Idea Whose Time has Come
SO SYSTEMS BIOLOGY IN REPRODUCTIVE MEDICINE
LA English
DT Article
DE biorepository; repository; Reproductive Medicine Network
AB Large randomized clinical trials are becoming more costly, and resources to support them increasingly scarce. Biologic materials, such as blood, DNA, body fluids, or tissue samples collected and stored as a component of these studies represent an invaluable resource, to answer immediate secondary hypotheses, but also as archived material, linked to the study data, for the use of investigators long into the future. The regulatory climate surrounding the storage and future unconstrained utilization of biologic materials is evolving quickly. It is no longer acceptable simply to store samples and use them in an unbridled and unregulated fashion. Thus, to fully utilize the tremendous potential of biologic samples generated from large clinical trials and their related databases, investigators should consider proactively creating a biologic specimen repository, or biorepository. A repository likely assures appropriate subject consent, sample provenance, secure storage, and codified procedures for sample and data retrieval and sharing that protect the subject's confidentiality, the investigator's need for accurate data, and the limited resource. Importantly, the biorepository specimens/samples are typically collected in addition to local and core specimens obtained for the parent study that provide baseline assessments for safety and efficacy outcomes.
C1 [Casson, Peter R.] Univ Vermont, Dept Med & Obstet & Gynecol, Burlington, VT 05401 USA.
[Krawetz, Stephen A.; Diamond, Michael P.] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
[Zhang, Heping] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[Legro, Richard S.] Penn State Univ, Dept Obstet & Gynecol, Hershey, PA USA.
[Schlaff, William D.; Santoro, Nanette] Univ Colorado, Dept Obstet & Gynecol, Denver, CO 80202 USA.
[Coutifaris, Christos] Univ Penn, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
[Brzyski, Robert G.] Univ Texas Hlth Sci Ctr San Antonio, Dept Obstet & Gynecol, San Antonio, TX 78229 USA.
[Christman, Gregory M.] Univ Michigan, Dept Obstet & Gynecol, Reprod Sci Program, Ann Arbor, MI 48109 USA.
[Eisenberg, Esther] NICHHD, Reprod Sci Branch, Bethesda, MD 20892 USA.
RP Casson, PR (reprint author), Univ Vermont, Div Reprod Endocrinol & Infertil, Dept Obstet Gynecol & Reprod Sci, MCHV Fletcher Allen Hlth Care, Smith 401,111 Colchester Ave, Burlington, VT 05401 USA.
EM Peter.casson@vtmednet.org
OI Diamond, Michael/0000-0001-6353-4489
FU NICHD NIH HHS [U10 HD055936, U10 HD055942, U10 HD038992]
NR 8
TC 5
Z9 5
U1 0
U2 1
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1939-6368
J9 SYST BIOL REPROD MED
JI Syst. Biol. Reprod. Med.
PD OCT
PY 2011
VL 57
IS 5
BP 217
EP 221
DI 10.3109/19396368.2011.604818
PG 5
WC Andrology; Reproductive Biology
SC Endocrinology & Metabolism; Reproductive Biology
GA 825KT
UT WOS:000295273900002
PM 21951166
ER
PT J
AU Krawetz, SA
Casson, PR
Diamond, MP
Zhang, HP
Legro, RS
Schlaff, WD
Coutifaris, C
Brzyski, RG
Christman, GM
Santoro, N
Eisenberg, E
AF Krawetz, Stephen A.
Casson, Peter R.
Diamond, Michael P.
Zhang, Heping
Legro, Richard S.
Schlaff, William D.
Coutifaris, Christos
Brzyski, Robert G.
Christman, Gregory M.
Santoro, Nanette
Eisenberg, Esther
CA Reprod Med Network
TI Establishing a Biologic Specimens Repository for Reproductive Clinical
Trials: Technical Aspects
SO SYSTEMS BIOLOGY IN REPRODUCTIVE MEDICINE
LA English
DT Article
DE biorepository; protocol; Reproductive Medicine Network; sample
collection
ID HUMAN-SPERMATOZOA; BUFFER SYSTEMS; BLOOD-CLOTS; BIOMARKERS; COLLECTION;
GENOME; FROZEN; RNA; DNA
AB The individual research group or independent investigator often requires access to samples from a unique well characterized subject population. Cohorts of such samples from a well-defined comparative population are rare and limited access can impede progress. This bottleneck can be removed by accessing the samples provided by biorepositories such as the NIH/NICHD Cooperative Reproductive Medicine Network (RMN) Biorepository (detailed in the preceeding manuscript in this issue. In those cases where the individual research group or independent investigator already has access to a unique population, comparisons between well-defined groups are often sought to contextualize the data. In both cases seamless integration of data resources associated with the samples is required to ensure optimal comparisons. At the most basic level this requires standardization of sample collection and storage, as well as a de-identified data base containing demographic, clinical, and laboratory values. To facilitate such interoperability, the reagents and protocols that have been adopted by the RMN Biorepository for the collection and storage of serum, blood, saliva and sperm are described.
C1 [Krawetz, Stephen A.; Diamond, Michael P.] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
[Casson, Peter R.] Univ Vermont, Dept Med & Obstet & Gynecol, Burlington, VT USA.
[Zhang, Heping] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[Legro, Richard S.] Penn State Univ, Dept Obstet & Gynecol, Hershey, PA USA.
[Schlaff, William D.; Santoro, Nanette] Univ Colorado, Dept Obstet & Gynecol, Denver, CO 80202 USA.
[Coutifaris, Christos] Univ Penn, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
[Brzyski, Robert G.] Univ Texas Hlth Sci Ctr San Antonio, Dept Obstet & Gynecol, San Antonio, TX 78229 USA.
[Christman, Gregory M.] Univ Michigan, Dept Obstet & Gynecol, Reprod Sci Program, Ann Arbor, MI 48109 USA.
[Eisenberg, Esther] NICHHD, Reprod Sci Branch, Bethesda, MD 20892 USA.
RP Krawetz, SA (reprint author), Ctr Mol Med & Genet, Dept Obstet & Gynecol, CS Mott Ctr Human Grwoth & Dev, 275 E Hancock, Detroit, MI 48201 USA.
EM steve@compbio.med.wayne.edu
OI Diamond, Michael/0000-0001-6353-4489
FU NIH/NICHD [U10HD055925, U10 HD038992, U10 HD038998, U10 HD027049, U10
HD039005, U10 HD055936, U10 HD055942, H10 HD055944]
FX This work was supported in part by NIH/NICHD grants U10HD055925 (HZ),
U10 HD038992 (RL), U10 HD038998 (WS), U10 HD027049 (CC), U10 HD039005
(MD), U10 HD055936 (GC), U10 HD055942 (RB), and H10 HD055944 (PC). The
authors would like to thank the other members of the RMN for their
invaluable assistance in developing the RMN biorepository.
NR 33
TC 5
Z9 5
U1 0
U2 1
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1939-6368
J9 SYST BIOL REPROD MED
JI Syst. Biol. Reprod. Med.
PD OCT
PY 2011
VL 57
IS 5
BP 222
EP 227
DI 10.3109/19396368.2011.604819
PG 6
WC Andrology; Reproductive Biology
SC Endocrinology & Metabolism; Reproductive Biology
GA 825KT
UT WOS:000295273900003
PM 21899384
ER
PT J
AU Goldstein, AM
AF Goldstein, Alisa M.
TI Germline BAP1 mutations and tumor susceptibility
SO NATURE GENETICS
LA English
DT Editorial Material
ID SOMATIC MUTATIONS; CANCER; LOSSES; BREAST
C1 NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Goldstein, AM (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM goldstea@mail.nih.gov
FU Intramural NIH HHS [Z01 CP004410-31]
NR 15
TC 21
Z9 21
U1 2
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2011
VL 43
IS 10
BP 925
EP 926
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 825XT
UT WOS:000295316200003
PM 21956388
ER
PT J
AU Hyde, RK
Liu, PP
AF Hyde, R. Katherine
Liu, P. Paul
TI GATA2 mutations lead to MDS and AML
SO NATURE GENETICS
LA English
DT Editorial Material
ID SPORADIC MONOCYTOPENIA; AUTOSOMAL-DOMINANT; MYELOID-LEUKEMIA;
MYELODYSPLASIA
C1 [Hyde, R. Katherine; Liu, P. Paul] NHGRI, Oncogenesis & Dev Sect, NIH, Bethesda, MD 20892 USA.
RP Hyde, RK (reprint author), NHGRI, Oncogenesis & Dev Sect, NIH, Bethesda, MD 20892 USA.
EM pliu@mail.nih.gov
RI Liu, Paul/A-7976-2012;
OI Liu, Paul/0000-0002-6779-025X; Hyde, R. Katherine/0000-0003-2808-1749
NR 14
TC 14
Z9 14
U1 1
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2011
VL 43
IS 10
BP 926
EP 927
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 825XT
UT WOS:000295316200004
PM 21956389
ER
PT J
AU Zenatti, PP
Ribeiro, D
Li, WQ
Zuurbier, L
Silva, MC
Paganin, M
Tritapoe, J
Hixon, JA
Silveira, AB
Cardoso, BA
Sarmento, LM
Correia, N
Toribio, ML
Kobarg, J
Horstmann, M
Pieters, R
Brandalise, SR
Ferrando, AA
Meijerink, JP
Durum, SK
Yunes, JA
Barata, JT
AF Zenatti, Priscila P.
Ribeiro, Daniel
Li, Wenqing
Zuurbier, Linda
Silva, Milene C.
Paganin, Maddalena
Tritapoe, Julia
Hixon, Julie A.
Silveira, Andre B.
Cardoso, Bruno A.
Sarmento, Leonor M.
Correia, Nadia
Toribio, Maria L.
Kobarg, Joerg
Horstmann, Martin
Pieters, Rob
Brandalise, Silvia R.
Ferrando, Adolfo A.
Meijerink, Jules P.
Durum, Scott K.
Yunes, J. Andres
Barata, Joao T.
TI Oncogenic IL7R gain-of-function mutations in childhood T-cell acute
lymphoblastic leukemia
SO NATURE GENETICS
LA English
DT Article
ID SEVERE COMBINED IMMUNODEFICIENCY; INTERLEUKIN-7 RECEPTOR;
MULTIPLE-SCLEROSIS; GENE-EXPRESSION; PRECURSOR-B; ACTIVATION; NOTCH1;
PTEN; IL-7; MICE
AB Interleukin 7 (IL-7) and its receptor, formed by IL-7R alpha (encoded by IL7R) and gamma c, are essential for normal T-cell development and homeostasis. Here we show that IL7R is an oncogene mutated in T-cell acute lymphoblastic leukemia (T-ALL). We find that 9% of individuals with T-ALL have somatic gain-of-function IL7R exon 6 mutations. In most cases, these IL7R mutations introduce an unpaired cysteine in the extracellular juxtamembrane-transmembrane region and promote de novo formation of intermolecular disulfide bonds between mutant IL-7Ra subunits, thereby driving constitutive signaling via JAK1 and independently of IL-7, gamma c or JAK3. IL7R mutations induce a gene expression profile partially resembling that provoked by IL-7 and are enriched in the T-ALL subgroup comprising TLX3 rearranged and HOXA deregulated cases. Notably, IL7R mutations promote cell transformation and tumor formation. Overall, our findings indicate that IL7R mutational activation is involved in human T-cell leukemogenesis, paving the way for therapeutic targeting of IL-7R-mediated signaling in T-ALL.
C1 [Ribeiro, Daniel; Silva, Milene C.; Cardoso, Bruno A.; Sarmento, Leonor M.; Correia, Nadia; Barata, Joao T.] Univ Lisbon, Fac Med, Inst Med Mol, Canc Biol Unit, P-1699 Lisbon, Portugal.
[Zenatti, Priscila P.; Silveira, Andre B.; Brandalise, Silvia R.; Yunes, J. Andres] Ctr Infantil Boldrini, Lab Biol Mol, Campinas, SP, Brazil.
[Li, Wenqing; Tritapoe, Julia; Hixon, Julie A.; Durum, Scott K.] NCI, Immunol Cytokine Grp, Mol Immunoregulat Lab, Ctr Canc Res, Frederick, MD 21701 USA.
[Zuurbier, Linda; Meijerink, Jules P.] Erasmus Med Ctr MC Sophia Childrens Hosp, Dept Pediat Oncol Hematol, Rotterdam, Netherlands.
[Paganin, Maddalena; Ferrando, Adolfo A.] Columbia Univ Med Ctr, Inst Canc Genet, New York, NY USA.
[Toribio, Maria L.] Univ Autonoma Madrid, Ctr Biol Mol Severo Ochoa, CSIC, Madrid, Spain.
[Kobarg, Joerg] CNPEM, LNBio, Campinas, SP, Brazil.
[Horstmann, Martin] German Cooperat Study Grp Childhood Acute Lymphob, Hamburg, Germany.
[Horstmann, Martin] Univ Med Ctr Hamburg Eppendorf, Clin Pediat Hematol & Oncol, Childrens Canc Ctr Hamburg, Res Inst, Hamburg, Germany.
[Brandalise, Silvia R.] Univ Estadual Campinas, Serv Hematol Oncol Pediat, Campinas, SP, Brazil.
[Ferrando, Adolfo A.] Columbia Univ Med Ctr, Dept Pathol, New York, NY USA.
[Yunes, J. Andres] Univ Estadual Campinas, Fac Ciencias Med, Dept Genet Med, Campinas, SP, Brazil.
RP Barata, JT (reprint author), Univ Lisbon, Fac Med, Inst Med Mol, Canc Biol Unit, P-1699 Lisbon, Portugal.
EM joao_barata@fm.ul.pt
RI Barata, Joao/D-9181-2015; Toribio, Maria L/C-2039-2017; Meijerink,
Jules/D-4393-2017; Silveira, Andre/I-8859-2012;
OI Barata, Joao/0000-0002-4826-8976; Toribio, Maria L/0000-0002-8637-0373;
Meijerink, Jules/0000-0002-6860-798X; Silveira,
Andre/0000-0003-3375-1081; Cardoso, Bruno/0000-0002-6521-7257; Sarmento,
Leonor/0000-0002-3692-0592
FU Fundacao para a Ciencia e a Tecnologia (FCT) [PTDC/SAU-OBD/104816/2008];
Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
[08/10034-1]; National Cancer Institute, US National Institutes of
Health (NIH); Conselho Nacional de Desenvolvimento Cientifico e
Tecnologico (CNPq); Bolsa de Investigacao (BI); FCT; foundation Children
Cancer-Free (Stichting Kinderen Kankervrij; KiKa) [2007-012]
FX We are grateful to the subjects and their families for providing the
specimens for this study. We thank S. Walsh (University of Maryland) for
helpful discussions on the IL7R transmembrane domain; K. Czarra and M.
Karwan for animal technical assistance; A. Silva, I. Antunes, A. Melao
and J. Buijs-Gladdines for experimental support; P. Vandenabeele for
kindly providing the WEHI3B cell line; and J. O'Shea for providing
Jak3-/- bone marrow and CP-690550. This work was supported by
grants from Fundacao para a Ciencia e a Tecnologia (FCT;
PTDC/SAU-OBD/104816/2008, J. T. B.), Fundacao de Amparo a Pesquisa do
Estado de Sao Paulo (FAPESP; 08/10034-1, J.A.Y.) and the intramural
program of the National Cancer Institute, US National Institutes of
Health (NIH) (S. K. D.). P.P.Z. and A. B. S. have Conselho Nacional de
Desenvolvimento Cientifico e Tecnologico (CNPq) PhD scholarships. L. M.
S. has a postdoctoral fellowship; D. R., B. A. C. and N.C. have PhD
scholarships, and M. C. S. had a Bolsa de Investigacao (BI) fellowship,
all from the FCT. L.Z. was supported by a grant (2007-012) from the
foundation Children Cancer-Free (Stichting Kinderen Kankervrij; KiKa).
NR 51
TC 132
Z9 136
U1 3
U2 26
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2011
VL 43
IS 10
BP 932
EP U31
DI 10.1038/ng.924
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 825XT
UT WOS:000295316200006
PM 21892159
ER
PT J
AU Bis, JC
Kavousi, M
Franceschini, N
Isaacs, A
Abecasis, GR
Schminke, U
Post, WS
Smith, AV
Cupples, LA
Markus, HS
Schmidt, R
Huffman, JE
Lehtimaki, T
Baumert, J
Munzel, T
Heckbert, SR
Dehghan, A
North, K
Oostra, B
Bevan, S
Stoegerer, EM
Hayward, C
Raitakari, O
Meisinger, C
Schillert, A
Sanna, S
Volzke, H
Cheng, YC
Thorsson, B
Fox, CS
Rice, K
Rivadeneira, F
Nambi, V
Halperin, E
Petrovic, KE
Peltonen, L
Wichmann, HE
Schnabel, RB
Dorr, M
Parsa, A
Aspelund, T
Demissie, S
Kathiresan, S
Reilly, MP
Taylor, K
Uitterlinden, A
Couper, DJ
Sitzer, M
Kahonen, M
Illig, T
Wild, PS
Orru, M
Ludemann, J
Shuldiner, AR
Eiriksdottir, G
White, CC
Rotter, JI
Hofman, A
Seissler, J
Zeller, T
Usala, G
Ernst, F
Launer, LJ
D'Agostino, RB
O'Leary, DH
Ballantyne, C
Thiery, J
Ziegler, A
Lakatta, EG
Chilukoti, RK
Harris, TB
Wolf, PA
Psaty, BM
Polak, JF
Li, X
Rathmann, W
Uda, M
Boerwinkle, E
Klopp, N
Schmidt, H
Wilson, JF
Viikari, J
Koenig, W
Blankenberg, S
Newman, AB
Witteman, J
Heiss, G
van Duijn, C
Scuteri, A
Homuth, G
Mitchell, BD
Gudnason, V
O'Donnell, CJ
AF Bis, Joshua C.
Kavousi, Maryam
Franceschini, Nora
Isaacs, Aaron
Abecasis, Goncalo R.
Schminke, Ulf
Post, Wendy S.
Smith, Albert V.
Cupples, L. Adrienne
Markus, Hugh S.
Schmidt, Reinhold
Huffman, Jennifer E.
Lehtimaki, Terho
Baumert, Jens
Muenzel, Thomas
Heckbert, Susan R.
Dehghan, Abbas
North, Kari
Oostra, Ben
Bevan, Steve
Stoegerer, Eva-Maria
Hayward, Caroline
Raitakari, Olli
Meisinger, Christa
Schillert, Arne
Sanna, Serena
Voelzke, Henry
Cheng, Yu-Ching
Thorsson, Bolli
Fox, Caroline S.
Rice, Kenneth
Rivadeneira, Fernando
Nambi, Vijay
Halperin, Eran
Petrovic, Katja E.
Peltonen, Leena
Wichmann, H. Erich
Schnabel, Renate B.
Doerr, Marcus
Parsa, Afshin
Aspelund, Thor
Demissie, Serkalem
Kathiresan, Sekar
Reilly, Muredach P.
Taylor, Kent
Uitterlinden, Andre
Couper, David J.
Sitzer, Matthias
Kahonen, Mika
Illig, Thomas
Wild, Philipp S.
Orru, Marco
Luedemann, Jan
Shuldiner, Alan R.
Eiriksdottir, Gudny
White, Charles C.
Rotter, Jerome I.
Hofman, Albert
Seissler, Jochen
Zeller, Tanja
Usala, Gianluca
Ernst, Florian
Launer, Lenore J.
D'Agostino, Ralph B., Sr.
O'Leary, Daniel H.
Ballantyne, Christie
Thiery, Joachim
Ziegler, Andreas
Lakatta, Edward G.
Chilukoti, Ravi Kumar
Harris, Tamara B.
Wolf, Philip A.
Psaty, Bruce M.
Polak, Joseph F.
Li, Xia
Rathmann, Wolfgang
Uda, Manuela
Boerwinkle, Eric
Klopp, Norman
Schmidt, Helena
Wilson, James F.
Viikari, Jorma
Koenig, Wolfgang
Blankenberg, Stefan
Newman, Anne B.
Witteman, Jacqueline
Heiss, Gerardo
van Duijn, Cornelia
Scuteri, Angelo
Homuth, Georg
Mitchell, Braxton D.
Gudnason, Vilmundur
O'Donnell, Christopher J.
CA CARDIoGRAM Consortium
TI Meta-analysis of genome-wide association studies from the CHARGE
consortium identifies common variants associated with carotid intima
media thickness and plaque
SO NATURE GENETICS
LA English
DT Article
ID CORONARY-ARTERY-DISEASE; SINGLE NUCLEOTIDE POLYMORPHISMS; URIC-ACID
LEVELS; HEART-DISEASE; MYOCARDIAL-INFARCTION; GENETIC-LOCI;
LIPID-LEVELS; ATHEROSCLEROSIS; RISK; POPULATION
AB Carotid intima media thickness (cIMT) and plaque determined by ultrasonography are established measures of subclinical atherosclerosis that each predicts future cardiovascular disease events. We conducted a meta-analysis of genome-wide association data in 31,211 participants of European ancestry from nine large studies in the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. We then sought additional evidence to support our findings among 11,273 individuals using data from seven additional studies. In the combined meta-analysis, we identified three genomic regions associated with common carotid intima media thickness and two different regions associated with the presence of carotid plaque (P < 5 x 10(-8)). The associated SNPs mapped in or near genes related to cellular signaling, lipid metabolism and blood pressure homeostasis, and two of the regions were associated with coronary artery disease (P < 0.006) in the Coronary Artery Disease Genome-Wide Replication and Meta-Analysis (CARDIoGRAM) consortium. Our findings may provide new insight into pathways leading to subclinical atherosclerosis and subsequent cardiovascular events.
C1 [Bis, Joshua C.; Heckbert, Susan R.; Psaty, Bruce M.] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Bis, Joshua C.; Psaty, Bruce M.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
[Kavousi, Maryam; Dehghan, Abbas; Uitterlinden, Andre; Hofman, Albert; Witteman, Jacqueline] Erasmus MC, Dept Epidemiol, Rotterdam, Netherlands.
[Kavousi, Maryam; Dehghan, Abbas; Rivadeneira, Fernando; Uitterlinden, Andre; Hofman, Albert; Witteman, Jacqueline; van Duijn, Cornelia] Sponsored Netherlands Consortium Healthy Aging NC, NGI, Rotterdam, Netherlands.
[Franceschini, Nora; Li, Xia; Heiss, Gerardo] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Isaacs, Aaron; van Duijn, Cornelia] Erasmus MC, Dept Epidemiol, Genet Epidemiol Unit, Rotterdam, Netherlands.
[Isaacs, Aaron; Oostra, Ben; van Duijn, Cornelia] Ctr Med Syst Biol, Leiden, Netherlands.
[Abecasis, Goncalo R.] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Schminke, Ulf] Ernst Moritz Arndt Univ Greifswald, Dept Neurol, Greifswald, Germany.
[Post, Wendy S.] Johns Hopkins Univ, Dept Med, Div Cardiol, Baltimore, MD USA.
[Smith, Albert V.; Thorsson, Bolli; Aspelund, Thor; Eiriksdottir, Gudny; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Cupples, L. Adrienne; Demissie, Serkalem; White, Charles C.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Cupples, L. Adrienne; Fox, Caroline S.; Wolf, Philip A.; O'Donnell, Christopher J.] Natl Heart Lung & Blood Inst Framingham Heart Stu, Framingham, MA USA.
[Markus, Hugh S.; Bevan, Steve] St Georges Univ London, Ctr Clin Neurosci, London, England.
[Schmidt, Reinhold; Stoegerer, Eva-Maria] Med Univ Graz, Dept Neurol, Graz, Austria.
[Huffman, Jennifer E.; Hayward, Caroline] Western Gen Hosp, Human Genet Unit, Inst Genet & Mol Med, MRC, Edinburgh EH4 2XU, Midlothian, Scotland.
[Lehtimaki, Terho] Univ Tampere, Dept Clin Chem, FIN-33101 Tampere, Finland.
[Lehtimaki, Terho; Kahonen, Mika] Tampere Univ Hosp, Tampere, Finland.
[Baumert, Jens; Meisinger, Christa] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol 2, Neuherberg, Germany.
[Muenzel, Thomas; Schnabel, Renate B.; Wild, Philipp S.; Zeller, Tanja; Blankenberg, Stefan] Univ Med Ctr Mainz, Dept Med 2, Mainz, Germany.
[Heckbert, Susan R.; Psaty, Bruce M.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Heckbert, Susan R.; Psaty, Bruce M.] Grp Hlth, Grp Hlth Res Inst, Seattle, WA USA.
[North, Kari] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
[Oostra, Ben] Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands.
[Raitakari, Olli] Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland.
[Raitakari, Olli] Turku Univ Hosp, Dept Clin Physiol, FIN-20520 Turku, Finland.
[Schillert, Arne; Ziegler, Andreas] Univ Lubeck, Univ Klinikum Schleswig Holstein, Inst Med Biometry & Stat, Lubeck, Germany.
[Sanna, Serena; Orru, Marco; Usala, Gianluca; Uda, Manuela] CNR, IRGB, Cagliari, Italy.
[Voelzke, Henry] Ernst Moritz Arndt Univ Greifswald, Inst Community Med, Greifswald, Germany.
[Cheng, Yu-Ching] Univ Maryland, Sch Med, Div Endocrinol Diabet & Nutr, Baltimore, MD 21201 USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol Metab & Diabet, Boston, MA 02115 USA.
[Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
[Rice, Kenneth] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Rivadeneira, Fernando; Uitterlinden, Andre] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Nambi, Vijay; Ballantyne, Christie] Baylor Coll Med, Houston, TX 77030 USA.
[Nambi, Vijay] Methodist DeBakey Heart & Vasc Ctr, Ctr Cardiovasc Prevent, Houston, TX USA.
[Nambi, Vijay] Ben Taub Gen Hosp, Houston, TX 77030 USA.
[Halperin, Eran] Tel Aviv Univ, Blavatnik Sch Comp Sci, IL-69978 Tel Aviv, Israel.
[Halperin, Eran] Int Comp Sci Inst, Berkeley, CA 94704 USA.
[Petrovic, Katja E.] Med Univ Graz, Graz, Austria.
[Petrovic, Katja E.] Gen Hosp, Dept Neurol, Graz, Austria.
[Peltonen, Leena] Wellcome Trust Sanger Inst, Cambridge, England.
[Peltonen, Leena] Univ Helsinki, Biomedicum, Inst Mol Med Finland, Helsinki, Finland.
[Peltonen, Leena] Natl Inst Hlth & Welf, Helsinki, Finland.
[Wichmann, H. Erich] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol 1, Neuherberg, Germany.
[Doerr, Marcus] Ernst Moritz Arndt Univ Greifswald, Dept Internal Med B, Greifswald, Germany.
[Parsa, Afshin; Shuldiner, Alan R.; Mitchell, Braxton D.] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA.
[Aspelund, Thor; Gudnason, Vilmundur] Univ Iceland, Reykjavik, Iceland.
[Kathiresan, Sekar] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Kathiresan, Sekar] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Kathiresan, Sekar] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Kathiresan, Sekar] Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA USA.
[Reilly, Muredach P.] Univ Penn, Cardiovasc Inst, Philadelphia, PA 19104 USA.
[Taylor, Kent; Rotter, Jerome I.] Cedars Sinai Med Ctr, Med Genet Inst, Los Angeles, CA 90048 USA.
[Couper, David J.] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Sitzer, Matthias] Klinikum Herford, Dept Neurol, Herford, Germany.
[Kahonen, Mika] Univ Tampere, Dept Clin Physiol, FIN-33101 Tampere, Finland.
[Illig, Thomas; Klopp, Norman] German Res Ctr Environm Hlth, Res Unit Mol Epidemiol, Helmholtz Zentrum Muenchen, Neuherberg, Germany.
[Illig, Thomas] Hannover Med Sch, Biobank Hannover Med Sch, D-3000 Hannover, Germany.
[Orru, Marco] Santa Barbara Hosp, Div Med, Cardiol Operating Unit, Santa Barbara, CA, Italy.
[Luedemann, Jan] Ernst Moritz Arndt Univ Greifswald, Inst Clin Chem & Lab Med, Greifswald, Germany.
[Shuldiner, Alan R.] Vet Adm Med Ctr, Geriatr Res & Educ Clin Ctr, Baltimore, MD 21218 USA.
[Seissler, Jochen] Univ Munich, Med Clin Innenstadt, Ctr Diabet, Munich, Germany.
[Ernst, Florian; Chilukoti, Ravi Kumar; Homuth, Georg] Ernst Moritz Arndt Univ Greifswald, Interfac Inst Genet & Funct Gen, Greifswald, Germany.
[Launer, Lenore J.; Harris, Tamara B.] NIA, Intramural Res Program, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
[D'Agostino, Ralph B., Sr.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[O'Leary, Daniel H.] Tufts Univ, Sch Med, St Elizabeths Med Ctr, Boston, MA 02111 USA.
[Thiery, Joachim] Univ Hosp Leipzig, Inst Lab Med Clin Chem & Mol Diagnost, Leipzig, Germany.
[Thiery, Joachim] Univ Leipzig, Fac Med, Leipzig Res Ctr Civilizat Dis, Leipzig, Germany.
[Lakatta, Edward G.; Scuteri, Angelo] NIA, Gerontol Res Ctr, Baltimore, MD 21224 USA.
[Wolf, Philip A.] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
[Polak, Joseph F.] Tufts Univ, Sch Med, Dept Radiol, Boston, MA 02111 USA.
[Rathmann, Wolfgang] Univ Dusseldorf, Inst Biometr & Epidemiol, German Diabet Ctr, Leibniz Ctr Diabet Res, Dusseldorf, Germany.
[Boerwinkle, Eric] Univ Texas Houston, Sch Publ Hlth, Ctr Human Genet, Houston, TX USA.
[Schmidt, Helena] Med Univ Graz, Inst Mol Biol & Biochem, Graz, Austria.
[Wilson, James F.] Univ Edinburgh, Ctr Populat Hlth Sci, Edinburgh, Midlothian, Scotland.
[Viikari, Jorma] Univ Turku, Dept Med, Turku, Finland.
[Koenig, Wolfgang] Univ Ulm, Med Ctr, Dept Internal Med Cardiol 2, Ulm, Germany.
[Newman, Anne B.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA USA.
[Mitchell, Braxton D.] Univ Maryland, Sch Med, Dept Epidemiol & Publ Hlth, Baltimore, MD 21201 USA.
[O'Donnell, Christopher J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiol Div,Dept Med, Boston, MA USA.
RP Bis, JC (reprint author), Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
EM joshbis@uw.edu; odonnellc@nhlbi.nih.gov
RI Rivadeneira, Fernando/O-5385-2015; Smith, Albert/K-5150-2015; Hayward,
Caroline/M-8818-2016; Aspelund, Thor/C-5983-2008; Abecasis,
Goncalo/B-7840-2010; Rice, Kenneth/A-4150-2013; Newman,
Anne/C-6408-2013; Meisinger, Christine/B-5358-2014; Schnabel,
Renate/F-6527-2014; Gudnason, Vilmundur/K-6885-2015; Wilson, James
F/A-5704-2009;
OI Meisinger, Christa/0000-0002-9026-6544; sanna,
serena/0000-0002-3768-1749; Abecasis, Goncalo/0000-0003-1509-1825;
Ziegler, Andreas/0000-0002-8386-5397; Bevan, Steve/0000-0003-0490-6830;
Mitchell, Braxton/0000-0003-4920-4744; Rivadeneira,
Fernando/0000-0001-9435-9441; Smith, Albert/0000-0003-1942-5845;
Hayward, Caroline/0000-0002-9405-9550; Cupples, L.
Adrienne/0000-0003-0273-7965; Aspelund, Thor/0000-0002-7998-5433; Rice,
Kenneth/0000-0001-5779-4495; Newman, Anne/0000-0002-0106-1150; Gudnason,
Vilmundur/0000-0001-5696-0084; Wilson, James F/0000-0001-5751-9178;
Dehghan, Abbas/0000-0001-6403-016X
FU US National Institutes of Health (NIH) [N01-AG-12100]; National
Institute on Aging (NIA) Intramural Research Program; Hjartavernd (the
Icelandic Heart Association); Althingi (the Icelandic Parliament); NIH
[R01 AG18728, R01 HL088119, U01 GM074518-04, U01 HL072515-06];
University of Maryland General Clinical Research Center [M01 RR 16500];
Baltimore Veterans Administration Medical Center Geriatrics Research and
Education Clinical Center; Paul Beeson Physician Faculty Scholars in
Aging Program; National Heart, Lung, and Blood Institute [N01-HC-55015,
N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021,
N01-HC-55022, R01HL087641, R01HL59367, R01HL086694]; National Human
Genome Research Institute [U01HG004402]; US National Institutes of
Health [HHSN268200625226C, UL1RR025005]; NIH Roadmap for Medical
Research; Netherlands Organisation for Scientific Research; Erasmus
Medical Center; Centre for Medical Systems Biology (CMSB); National
Heart, Lung, and Blood Institute (NHLBI) [N01-HC-85239, N01-HC-85079,
N01-HC-85086, N01-HC-35129, N01 HC-15103, N01 HC-55222, N01-HC-75150,
N01-HC-45133, HL080295, HL075366, HL087652, HL105756]; National
Institute of Neurological Disorders and Stroke (NINDS); National
Institute of Aging [AG-023629, AG-15928, AG-20098, AG-027058, AG08122,
AG16495, AG033193]; National Center for Research Resources [M01RR00069];
National Institute of Diabetes and Digestive and Kidney Diseases
[DK063491]; National Heart, Lung, and Blood Institute's Framingham Heart
Study [N01-HC-25195]; Affymetrix, Inc. [N02-HL-6-4278]; National
Institute of Neurological Disorders and Stroke [NS17950]; Robert Dawson
Evans Endowment of the Department of Medicine at Boston University
School of Medicine and Boston Medical Center; Netherlands Organisation
of Scientific Research (NWO, De Nederlandse Organisatie voor
Wetenschappelijk Onderzoek) [175.010.2005.011, 911-03-012]; Research
Institute for Diseases in the Elderly [014-93-015, RIDE2]; Netherlands
Genomics Initiative (NGI)/Netherlands Consortium for Healthy Aging
(NCHA) [050-060-810]; NWO [918-76-619]; Erasmus Medical Center and
Erasmus University; Rotterdam; Netherlands Organization for the Health
Research and Development (ZonMw); Research Institute for Diseases in the
Elderly (RIDE); Ministry of Education, Culture and Science; Ministry for
Health, Welfare and Sports; European Commission (DG XII); Municipality
of Rotterdam; German Bundesministeriumfuer Forschung und Technology [01
AK 803 A-H, 01 IG 07015 G]; National Institute on Aging, NIH; National
Institute on Aging [NO1-AG-1-2109]; National Institute on Aging to the
University of Michigan [263-MA-410953]; National Institutes of Health
[HG005581, HL084729]; Federal Ministry of Education and Research
[01ZZ9603, 01ZZ0103, 01ZZ0403, 03ZIK012]; Ministry of Cultural Affairs
as well as the Social Ministry of the Federal State of Mecklenburg-West
Pomerania; Siemens Healthcare, Erlangen, Germany; Federal State of
Mecklenburg-West Pomerania; Austrian Science Fond (FWF) [P20545-P05,
P13180]; Medical University of Graz; European Community [201668];
government of Rheinland-Pfalz ('Stiftung Rheinland Pfalzfur Innovation')
[AZ 961-386261/733]; Wissenschafft Zukunft; 'Schwerpunkt Vaskulare
Pravention' of the Johannes Gutenberg-University of Mainz;
BoehringerIngelheim; Philips Medical Systems; Gutenberg Heart Study;
National Genome Network 'NGFNplus' [A3 01GS0833]; Federal Ministry of
Education and Research, Germany; Helmholtz Zentrum Munchen; German
Research Center for Environmental Health, Neuherberg, Germany; German
Federal Ministry of Education and Research (BMBF); German National
Genome Research Network (NGFNplus) [01GS0834]; University of Ulm; Munich
Center of Health Sciences (MC Health); Karl-Wilder Foundation; German
Diabetes Center; German Federal Ministry of Health; Ministry of
Innovation, Science, Research and Technology of the State of North Rhine
Westphalia; Office of the Scottish Government; Royal Society; European
Union [LSHG-CT-2006-018947]; Academy of Finland [117797, 121584,
126925]; Social Insurance Institution of Finland; University Hospital
Medical funds to Tampere; Turku University Hospitals; Finnish Foundation
of Cardiovascular Research
FX The Age, Gene/Environment Susceptibility (AGES) Reykjavik Study was
funded by US National Institutes of Health (NIH) contract N01-AG-12100,
the National Institute on Aging (NIA) Intramural Research Program,
Hjartavernd (the Icelandic Heart Association) and the Althingi (the
Icelandic Parliament).; The Old Order Amish Studies were supported by
grants and contracts from the NIH including R01 AG18728 (Amish Longevity
Study), R01 HL088119 (Amish Calcification Study), U01 GM074518-04 (The
Amish Pharmacogenomics of Anti-Platelet Intervention (PAPI) study) and
U01 HL072515-06 (the Heredity and Phenotype Intervention (HAPI) heart
study), the University of Maryland General Clinical Research Center
grant M01 RR 16500, the Baltimore Veterans Administration Medical Center
Geriatrics Research and Education Clinical Center and the Paul Beeson
Physician Faculty Scholars in Aging Program. We thank our Amish research
volunteers for their long-standing partnership in research and the
research staff at the Amish Research Clinic for their hard work and
dedication.; The Atherosclerosis Risk in Communities Study (ARIC) was
carried out as a collaborative study supported by National Heart, Lung,
and Blood Institute contracts N01-HC-55015, N01-HC-55016, N01-HC-55018,
N01-HC-55019, N01-HC-55020, N01-HC-55021, N01-HC-55022, R01HL087641,
R01HL59367 and R01HL086694; National Human Genome Research Institute
contract U01HG004402; and US National Institutes of Health contract
HHSN268200625226C. The authors thank the staff and participants of the
ARIC study for their important contributions. Study infrastructure was
partly supported by grant number UL1RR025005, a component of the US
National Institutes of Health and NIH Roadmap for Medical Research.; The
Erasmus Rucphen Family Study was supported by grants from The
Netherlands Organisation for Scientific Research, Erasmus Medical Center
and the Centre for Medical Systems Biology (CMSB). We are grateful to
all study participants and their relatives, the general practitioners
and neurologists for their contributions and to P. Veraart for her help
in genealogy, J. Vergeer for the supervision of the laboratory work and
P. Snijders for his help in data collection.; The Cardiovascular Health
Study research reported in this article was supported by National Heart,
Lung, and Blood Institute (NHLBI) contracts N01-HC-85239, N01-HC-85079
through N01-HC-85086; N01-HC-35129, N01 HC-15103, N01 HC-55222,
N01-HC-75150, N01-HC-45133 and NHLBI grants HL080295, HL075366,
HL087652, HL105756 with additional contribution from National Institute
of Neurological Disorders and Stroke (NINDS). Additional support was
provided through AG-023629, AG-15928, AG-20098 and AG-027058 from the
National Institute of Aging. See also http://www.chs-nhlbi.org/pi.htm.
DNA handling and genotyping was supported in part by National Center for
Research Resources grant M01RR00069 to the Cedars-Sinai General Clinical
Research Center Genotyping core and National Institute of Diabetes and
Digestive and Kidney Diseases grant DK063491 to the Southern California
Diabetes Endocrinology Research Center.; The Framingham Heart Study of
the National Heart, Lung, and Blood Institute of the US National
Institutes of Health and Boston University School of Medicine was
supported by the National Heart, Lung, and Blood Institute's Framingham
Heart Study (Contract No. N01-HC-25195) and its contract with
Affymetrix, Inc. for genotyping services (Contract No. N02-HL-6-4278)
and by grants from the National Institute of Neurological Disorders and
Stroke (NS17950, P. A. W.) and the National Institute of Aging (AG08122,
AG16495, P. A. W. and AG033193, S. S.). A portion of this research used
the Linux Cluster for Genetic Analysis (LinGA-II) funded by the Robert
Dawson Evans Endowment of the Department of Medicine at Boston
University School of Medicine and Boston Medical Center. Analyses
reflect intellectual input and resource development from the Framingham
Heart Study investigators participating in the SNP Health Association
Resource (SHARe) project.; Rotterdam Study I and II (RS I and RS II):
The Rotterdam GWAS was funded by the Netherlands Organisation of
Scientific Research (NWO, De Nederlandse Organisatie voor
Wetenschappelijk Onderzoek) Investments (number 175.010.2005.011,
911-03-012), the Research Institute for Diseases in the Elderly
(014-93-015; RIDE2), the Netherlands Genomics Initiative
(NGI)/Netherlands Consortium for Healthy Aging (NCHA) project number
050-060-810. This study was further supported by an NWO grant (vici,
918-76-619). The Rotterdam Study was funded by the Erasmus Medical
Center and Erasmus University, Rotterdam, Netherlands Organization for
the Health Research and Development (ZonMw), the Research Institute for
Diseases in the Elderly (RIDE), the Ministry of Education, Culture and
Science, the Ministry for Health, Welfare and Sports, the European
Commission (DG XII), and the Municipality of Rotterdam. The authors are
very grateful to the participants and staff from the Rotterdam Study,
the participating general practioners and the pharmacists. We thank P.
Arp, M. Jhamai, M. Moorhouse, M. Verkerk and S. Bervoets for their help
in creating the GWAS database. We would like to thank T. A. Knoch, L. V.
de Zeeuw, A. Abuseiris and R. de Graaf as well as their institutions the
Erasmus Computing Grid, Rotterdam, The Netherlands, and especially the
National German MediGRID and Services@MediGRID part of the German
D-Grid, both funded by the German Bundesministeriumfuer Forschung und
Technology under grants #01 AK 803 A-H and #01 IG 07015 G, for access to
their grid resources.; The SardiNIA Study: This work was supported by
the Intramural Research Program of the National Institute on Aging, NIH.
The SardiNIA ('Progenia') team was supported by Contract NO1-AG-1-2109
from the National Institute on Aging. The efforts of G. R. A. were
supported in part by contract 263-MA-410953 from the National Institute
on Aging to the University of Michigan and by research grants HG005581
and HL084729 from the National Institutes of Health (to G.R.A.).; The
Study of Health in Pomerania (SHIP) is part of the Community Medicine
Research net of the University of Greifswald, Germany, which is funded
by the Federal Ministry of Education and Research (grants number
01ZZ9603, 01ZZ0103 and 01ZZ0403), and the Ministry of Cultural Affairs
as well as the Social Ministry of the Federal State of Mecklenburg-West
Pomerania. Genome-wide data have been supported by the Federal Ministry
of Education and Research (grant no. 03ZIK012) and a joint grant from
Siemens Healthcare, Erlangen, Germany, and the Federal State of
Mecklenburg-West Pomerania. The SHIP authors are grateful to the
contribution of A. Teumer, A. Hoffmann and A. Petersmann in generating
the SNP data. The University of Greifswald is a member of the 'Center of
Knowledge Interchange' program of the Siemens AG.; The Austrian Stroke
Prevention Study (ASPS): The research reported in this article was
funded by the Austrian Science Fond (FWF) grant number P20545-P05 and
P13180. The Medical University of Graz supports the databank of the
ASPS.; The Coronary Artery Progression Study: Research leading these
results has received funding from the European Community's Seventh
Framework Programme (FP7/2007-2013) under grant agreement no. 201668;
AtheroRemo.; The Gutenberg Heart Study was funded through the government
of Rheinland-Pfalz ('Stiftung Rheinland Pfalzfur Innovation', contract
number AZ 961-386261/733), the research programs 'Wissenschafft Zukunft'
and 'Schwerpunkt Vaskulare Pravention' of the Johannes
Gutenberg-University of Mainz and its contract with BoehringerIngelheim
and Philips Medical Systems, including an unrestricted grant for the
Gutenberg Heart Study. Specifically, the research reported in this
article was supported by the National Genome Network 'NGFNplus'
(contract number project A3 01GS0833) by the Federal Ministry of
Education and Research, Germany.; Monitoring of Trends and Determinants
in Cardiovascular Disease (MONICA)/Cooperative Health Research in the
Region of Augsburg (KORA) studies were financed by the Helmholtz Zentrum
Munchen, German Research Center for Environmental Health, Neuherberg,
Germany, and supported by grants from the German Federal Ministry of
Education and Research (BMBF). Part of this work was financed by the
German National Genome Research Network (NGFNplus, project number
01GS0834) and through additional funds from the University of Ulm.
Furthermore, the research was supported within the Munich Center of
Health Sciences (MC Health) as part of Ludwig-Maximilians-Universitat
Munich (LMU) innovative. IMT measurement of the KORA cohort was funded
by a grant of the Karl-Wilder Foundation. Finally, part of this work was
financed by the German Diabetes Center, which is funded by the German
Federal Ministry of Health and the Ministry of Innovation, Science,
Research and Technology of the State of North Rhine Westphalia.; The
Orkney Complex Disease Study (ORCADES) was supported by the Chief
Scientist Office of the Scottish Government, the Royal Society and the
European Union framework program 6 EUROSPAN project (contract no.
LSHG-CT-2006-018947). DNA extractions were performed at the Wellcome
Trust Clinical Research Facility in Edinburgh. We would like to
acknowledge the invaluable contributions of L. Anderson and the research
nurses in Orkney, the administrative team in Edinburgh and the people of
Orkney.; The Cardiovascular Risk in Young Finns Study was supported by
the Academy of Finland (grant numbers 117797, 121584 and 126925), the
Social Insurance Institution of Finland, University Hospital Medical
funds to Tampere, and Turku University Hospitals, the Finnish Foundation
of Cardiovascular Research.
NR 37
TC 92
Z9 92
U1 0
U2 11
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2011
VL 43
IS 10
BP 940
EP U40
DI 10.1038/ng.920
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 825XT
UT WOS:000295316200007
PM 21909108
ER
PT J
AU Ripke, S
Sanders, AR
Kendler, KS
Levinson, DF
Sklar, P
Holmans, PA
Lin, DY
Duan, J
Ophoff, RA
Andreassen, OA
Scolnick, E
Cichon, S
Clair, DS
Corvin, A
Gurling, H
Werge, T
Rujescu, D
Blackwood, DHR
Pato, CN
Malhotra, AK
Purcell, S
Dudbridge, F
Neale, BM
Rossin, L
Visscher, PM
Posthuma, D
Ruderfer, DM
Fanous, A
Stefansson, H
Steinberg, S
Mowry, BJ
Golimbet, V
De Hert, M
Jonsson, EG
Bitter, I
Pietilainen, OPH
Collier, DA
Tosato, S
Agartz, I
Albus, M
Alexander, M
Amdur, RL
Amin, F
Bass, N
Bergen, SE
Black, DW
Borglum, AD
Brown, MA
Bruggeman, R
Buccola, NG
Byerley, WF
Cahn, W
Cantor, RM
Carr, VJ
Catts, SV
Choudhury, K
Cloninger, CR
Cormican, P
Craddock, N
Danoy, PA
Datta, S
De Haan, L
Demontis, D
Dikeos, D
Djurovic, S
Donnelly, P
Donohoe, G
Duong, L
Dwyer, S
Fink-Jensen, A
Freedman, R
Freimer, NB
Friedl, M
Georgieva, L
Giegling, I
Gill, M
Glenthoj, B
Godard, S
Hamshere, M
Hansen, M
Hansen, T
Hartmann, AM
Henskens, FA
Hougaard, DM
Hultman, CM
Ingason, A
Jablensky, AV
Jakobsen, KD
Jay, M
Jurgens, G
Kahn, R
Keller, MC
Kenis, G
Kenny, E
Kim, Y
Kirov, GK
Konnerth, H
Konte, B
Krabbendam, L
Krasucki, R
Lasseter, VK
Laurent, C
Lawrence, J
Lencz, T
Lerer, FB
Liang, KY
Lichtenstein, P
Lieberman, JA
Linszen, DH
Lonnqvist, J
Loughland, CM
Maclean, AW
Maher, BS
Maier, W
Mallet, J
Malloy, P
Mattheisen, M
Mattingsdal, M
McGhee, KA
McGrath, JJ
McIntosh, A
McLean, DE
McQuillin, A
Melle, I
Michie, PT
Milanova, V
Morris, DW
Mors, O
Mortensen, PB
Moskvina, V
Muglia, P
Myin-Germeys, I
Nertney, DA
Nestadt, G
Nielsen, J
Nikolov, I
Nordentoft, M
Norton, N
Nothen, MM
O'Dushlaine, CT
Olincy, A
Olsen, L
O'Neill, FA
Orntoft, TF
Owen, MJ
Pantelis, C
Papadimitriou, G
Pato, MT
Peltonen, L
Petursson, H
Pickard, B
Pimm, J
Pulver, AE
Puri, V
Quested, D
Quinn, EM
Rasmussen, HB
Rethelyi, JM
Ribble, R
Rietschel, M
Riley, BP
Ruggeri, M
Schall, U
Schulze, TG
Schwab, SG
Scott, RJ
Shi, JX
Sigurdsson, E
Silverman, JM
Spencer, CCA
Stefansson, K
Strange, A
Strengman, E
Stroup, TS
Suvisaari, J
Terenius, L
Thirumalai, S
Thygesen, JH
Timm, S
Toncheva, D
van den Oord, E
van Os, J
van Winkel, R
Veldink, J
Walsh, D
Wang, AG
Wiersma, D
Wildenauer, DB
Williams, HJ
Williams, NM
Wormley, B
Zammit, S
Sullivan, PF
O'Donovan, MC
Daly, MJ
Gejman, PV
AF Ripke, Stephan
Sanders, Alan R.
Kendler, Kenneth S.
Levinson, Douglas F.
Sklar, Pamela
Holmans, Peter A.
Lin, Dan-Yu
Duan, Jubao
Ophoff, Roel A.
Andreassen, Ole A.
Scolnick, Edward
Cichon, Sven
Clair, David St.
Corvin, Aiden
Gurling, Hugh
Werge, Thomas
Rujescu, Dan
Blackwood, Douglas H. R.
Pato, Carlos N.
Malhotra, Anil K.
Purcell, Shaun
Dudbridge, Frank
Neale, Benjamin M.
Rossin, Lizzy
Visscher, Peter M.
Posthuma, Danielle
Ruderfer, Douglas M.
Fanous, Ayman
Stefansson, Hreinn
Steinberg, Stacy
Mowry, Bryan J.
Golimbet, Vera
De Hert, Marc
Jonsson, Erik G.
Bitter, Istvan
Pietilainen, Olli P. H.
Collier, David A.
Tosato, Sarah
Agartz, Ingrid
Albus, Margot
Alexander, Madeline
Amdur, Richard L.
Amin, Farooq
Bass, Nicholas
Bergen, Sarah E.
Black, Donald W.
Borglum, Anders D.
Brown, Matthew A.
Bruggeman, Richard
Buccola, Nancy G.
Byerley, William F.
Cahn, Wiepke
Cantor, Rita M.
Carr, Vaughan J.
Catts, Stanley V.
Choudhury, Khalid
Cloninger, C. Robert
Cormican, Paul
Craddock, Nicholas
Danoy, Patrick A.
Datta, Susmita
De Haan, Lieuwe
Demontis, Ditte
Dikeos, Dimitris
Djurovic, Srdjan
Donnelly, Peter
Donohoe, Gary
Duong, Linh
Dwyer, Sarah
Fink-Jensen, Anders
Freedman, Robert
Freimer, Nelson B.
Friedl, Marion
Georgieva, Lyudmila
Giegling, Ina
Gill, Michael
Glenthoj, Birte
Godard, Stephanie
Hamshere, Marian
Hansen, Mark
Hansen, Thomas
Hartmann, Annette M.
Henskens, Frans A.
Hougaard, David M.
Hultman, Christina M.
Ingason, Andres
Jablensky, Assen V.
Jakobsen, Klaus D.
Jay, Maurice
Juergens, Gesche
Kahn, Renes
Keller, Matthew C.
Kenis, Gunter
Kenny, Elaine
Kim, Yunjung
Kirov, George K.
Konnerth, Heike
Konte, Bettina
Krabbendam, Lydia
Krasucki, Robert
Lasseter, Virginia K.
Laurent, Claudine
Lawrence, Jacob
Lencz, Todd
Lerer, F. Bernard
Liang, Kung-Yee
Lichtenstein, Paul
Lieberman, Jeffrey A.
Linszen, Don H.
Lonnqvist, Jouko
Loughland, Carmel M.
Maclean, Alan W.
Maher, Brion S.
Maier, Wolfgang
Mallet, Jacques
Malloy, Pat
Mattheisen, Manuel
Mattingsdal, Morten
McGhee, Kevin A.
McGrath, John J.
McIntosh, Andrew
McLean, Duncan E.
McQuillin, Andrew
Melle, Ingrid
Michie, Patricia T.
Milanova, Vihra
Morris, Derek W.
Mors, Ole
Mortensen, Preben B.
Moskvina, Valentina
Muglia, Pierandrea
Myin-Germeys, Inez
Nertney, Deborah A.
Nestadt, Gerald
Nielsen, Jimmi
Nikolov, Ivan
Nordentoft, Merete
Norton, Nadine
Noethen, Markus M.
O'Dushlaine, Colm T.
Olincy, Ann
Olsen, Line
O'Neill, F. Anthony
Orntoft, Torben F.
Owen, Michael J.
Pantelis, Christos
Papadimitriou, George
Pato, Michele T.
Peltonen, Leena
Petursson, Hannes
Pickard, Ben
Pimm, Jonathan
Pulver, Ann E.
Puri, Vinay
Quested, Digby
Quinn, Emma M.
Rasmussen, Henrik B.
Rethelyi, Janos M.
Ribble, Robert
Rietschel, Marcella
Riley, Brien P.
Ruggeri, Mirella
Schall, Ulrich
Schulze, Thomas G.
Schwab, Sibylle G.
Scott, Rodney J.
Shi, Jianxin
Sigurdsson, Engilbert
Silverman, Jeremy M.
Spencer, Chris C. A.
Stefansson, Kari
Strange, Amy
Strengman, Eric
Stroup, T. Scott
Suvisaari, Jaana
Terenius, Lars
Thirumalai, Srinivasa
Thygesen, Johan H.
Timm, Sally
Toncheva, Draga
van den Oord, Edwin
van Os, Jim
van Winkel, Ruud
Veldink, Jan
Walsh, Dermot
Wang, August G.
Wiersma, Durk
Wildenauer, Dieter B.
Williams, Hywel J.
Williams, Nigel M.
Wormley, Brandon
Zammit, Stan
Sullivan, Patrick F.
O'Donovan, Michael C.
Daly, Mark J.
Gejman, Pablo V.
CA Schizophrenia Psychiat Genome-Wide
TI Genome-wide association study identifies five new schizophrenia loci
SO NATURE GENETICS
LA English
DT Article
ID COMMON SNPS EXPLAIN; BIPOLAR DISORDER; HUMAN HEIGHT; LARGE PROPORTION;
MICRORNA; VARIANTS; SUSCEPTIBILITY; HERITABILITY; INDIVIDUALS; ANCESTRY
AB We examined the role of common genetic variation in schizophrenia in a genome-wide association study of substantial size: a stage 1 discovery sample of 21,856 individuals of European ancestry and a stage 2 replication sample of 29,839 independent subjects. The combined stage 1 and 2 analysis yielded genome-wide significant associations with schizophrenia for seven loci, five of which are new (1p21.3, 2q32.3, 8p23.2, 8q21.3 and 10q24.32-q24.33) and two of which have been previously implicated (6p21.32-p22.1 and 18q21.2). The strongest new finding (P = 1.6 x 10(-11)) was with rs1625579 within an intron of a putative primary transcript for MIR137 (microRNA 137), a known regulator of neuronal development. Four other schizophrenia loci achieving genome-wide significance contain predicted targets of MIR137, suggesting MIR137-mediated dysregulation as a previously unknown etiologic mechanism in schizophrenia. In a joint analysis with a bipolar disorder sample (16,374 affected individuals and 14,044 controls), three loci reached genome-wide significance: CACNA1C (rs4765905, P = 7.0 x 10(-9)), ANK3 (rs10994359, P = 2.5 x 10(-8)) and the ITIH3-ITIH4 region (rs2239547, P = 7.8 x 10(-9)).
C1 [Sanders, Alan R.; Duan, Jubao; Gejman, Pablo V.] NorthShore Univ HealthSyst, Dept Psychiat & Behav Sci, Evanston, IL USA.
[Ripke, Stephan; Sklar, Pamela; Rossin, Lizzy; Ruderfer, Douglas M.; Bergen, Sarah E.; Daly, Mark J.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Sanders, Alan R.; Duan, Jubao; Gejman, Pablo V.] Univ Chicago, Dept Psychiat & Behav Sci, Chicago, IL 60637 USA.
[Kendler, Kenneth S.; Maher, Brion S.; Ribble, Robert; Riley, Brien P.; Wormley, Brandon] Virginia Commonwealth Univ, Sch Med, Virginia Inst Psychiat & Behav Genet, Richmond, VA USA.
[Kendler, Kenneth S.; Fanous, Ayman; Maher, Brion S.; Ribble, Robert; Riley, Brien P.; Wormley, Brandon] Virginia Commonwealth Univ, Sch Med, Dept Psychiat, Richmond, VA USA.
[Kendler, Kenneth S.; Maher, Brion S.; Ribble, Robert; Riley, Brien P.; Wormley, Brandon] Virginia Commonwealth Univ, Sch Med, Dept Human & Mol Genet, Richmond, VA USA.
[Levinson, Douglas F.; Alexander, Madeline] Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
[Sklar, Pamela; Silverman, Jeremy M.] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Holmans, Peter A.; Craddock, Nicholas; Dwyer, Sarah; Georgieva, Lyudmila; Hamshere, Marian; Kirov, George K.; Moskvina, Valentina; Nikolov, Ivan; Norton, Nadine; Owen, Michael J.; Williams, Hywel J.; Williams, Nigel M.; Zammit, Stan; O'Donovan, Michael C.] Cardiff Univ, MRC, Ctr Neuropsychiat Genet & Gen, Sch Med, Cardiff, S Glam, Wales.
[Holmans, Peter A.; Craddock, Nicholas; Dwyer, Sarah; Georgieva, Lyudmila; Hamshere, Marian; Kirov, George K.; Moskvina, Valentina; Nikolov, Ivan; Norton, Nadine; Owen, Michael J.; Williams, Hywel J.; Williams, Nigel M.; Zammit, Stan; O'Donovan, Michael C.] Cardiff Univ, Dept Psychol Med & Neurol, Sch Med, Cardiff, S Glam, Wales.
[Lin, Dan-Yu] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Ophoff, Roel A.; Strengman, Eric] Univ Med Ctr Utrecht, Dept Med Genet, Utrecht, Netherlands.
[Ophoff, Roel A.; Strengman, Eric] Univ Med Ctr Utrecht, Rudolf Magnus Inst Neurosci, Utrecht, Netherlands.
[Ophoff, Roel A.; Cantor, Rita M.; Freimer, Nelson B.] Univ Calif Los Angeles, Ctr Neurobehav Genet, Los Angeles, CA USA.
[Ophoff, Roel A.; Cantor, Rita M.] Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA.
[Andreassen, Ole A.; Agartz, Ingrid; Djurovic, Srdjan; Mattingsdal, Morten; Melle, Ingrid] Univ Oslo, Inst Clin Med, Psychiat Sect, Oslo, Norway.
[Andreassen, Ole A.; Melle, Ingrid] Oslo Univ Hosp, Dept Psychiat, Oslo, Norway.
[Scolnick, Edward; Purcell, Shaun; Neale, Benjamin M.] Broad Inst, Cambridge, MA USA.
[Cichon, Sven; Mattheisen, Manuel; Noethen, Markus M.] Univ Bonn, Dept Genom, Life & Brain Ctr, D-5300 Bonn, Germany.
[Cichon, Sven] Res Ctr Juelich, Inst Neurosci & Med INM 1, Julich, Germany.
[Cichon, Sven; Mattheisen, Manuel; Noethen, Markus M.] Univ Bonn, Inst Human Genet, D-5300 Bonn, Germany.
[Clair, David St.] Univ Aberdeen, Inst Med Sci, Aberdeen, Scotland.
[Corvin, Aiden; Cormican, Paul; Donohoe, Gary; Gill, Michael; Kenny, Elaine; Morris, Derek W.; O'Dushlaine, Colm T.; Quinn, Emma M.] Trinity Coll Dublin, Neuropsychiat Genet Res Grp, Dublin, Ireland.
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[Hansen, Mark] Illumina Inc, La Jolla, CA USA.
[Henskens, Frans A.] Univ Newcastle, School Elect Engn & Comp Sci, Newcastle, NSW 2300, Australia.
[Hougaard, David M.] State Serum Inst, Dept Clin Chem & Immunol, Sect Neonatal Screening & Hormones, Copenhagen, Denmark.
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RP Gejman, PV (reprint author), NorthShore Univ HealthSyst, Dept Psychiat & Behav Sci, Evanston, IL USA.
EM pgejman@gmail.com
RI Melle, Ingrid /B-4858-2011; Ruderfer, Douglas/M-5795-2016; Lencz,
Todd/J-3418-2014; McQuillin, Andrew/C-1623-2008; Stroup,
Thomas/F-9188-2014; Demontis, Ditte/M-4515-2013; Cichon,
Sven/H-8803-2013; Cichon, Sven/B-9618-2014; Sigurdsson,
Engilbert/D-2486-2014; Myin-Germeys, Inez /L-5106-2014; Jablensky,
Assen/H-5116-2014; Pickard, Benjamin/K-3923-2014; Hansen,
Thomas/O-5965-2014; Holmans, Peter/F-4518-2015; Mortensen,
Preben/D-2358-2015; SCHALL, ULRICH/G-7452-2013; Mattheisen,
Manuel/B-4949-2012; Pantelis, Christos/H-7722-2014; Liang,
Kung-Yee/F-8299-2011; Tosato, Sarah /E-6045-2010; Cloninger,
Claude/F-5357-2012; Ingason, Andres/G-6817-2012; Bergen,
Sarah/I-8313-2012; McIntosh, Andrew/B-9379-2008; McGrath,
John/G-5493-2010; Cahn , Wiepke /B-5743-2013; Catts,
Stanley/G-6917-2013; Schulze, Thomas/H-2157-2013; Gurling,
Hugh/A-5029-2010; Maher, Brion/F-9185-2010; Nielsen, Jimmi /G-2990-2010
OI Andreassen, Ole A./0000-0002-4461-3568; Henskens,
Frans/0000-0003-2358-5630; Visscher, Peter/0000-0002-2143-8760;
Suvisaari, Jaana/0000-0001-7167-0990; Bruggeman,
Richard/0000-0002-3238-8471; O'Neill, Francis
Anthony/0000-0002-7531-7657; Stefansson, Hreinn/0000-0002-9331-6666;
Escott-Price, Valentina/0000-0003-1784-5483; Golimbet,
Vera/0000-0002-9960-7114; Agartz, Ingrid/0000-0002-9839-5391; Jonsson,
Erik/0000-0001-8368-6332; Nothen, Markus/0000-0002-8770-2464; Donohoe,
Gary/0000-0003-3037-7426; Morris, Derek/0000-0002-3413-570X; Rethelyi,
Janos/0000-0002-3641-012X; Myin-Germeys, Inez/0000-0002-3731-4930;
KELLER, MATTHEW/0000-0002-6075-9882; Gill, Michael/0000-0003-0206-5337;
Buccola, Nancy/0000-0003-1378-4636; lichtenstein,
paul/0000-0003-3037-5287; Thygesen, Johan H/0000-0002-7479-3459; Melle,
Ingrid /0000-0002-9783-548X; Ruderfer, Douglas/0000-0002-2365-386X;
Lencz, Todd/0000-0001-8586-338X; McQuillin, Andrew/0000-0003-1567-2240;
Bergen, Sarah/0000-0002-5888-0034; Corvin, Aiden/0000-0001-6717-4089;
O'Donovan, Michael/0000-0001-7073-2379; Zammit,
Stanley/0000-0002-2647-9211; Stroup, Thomas/0000-0002-3123-0672; Cichon,
Sven/0000-0002-9475-086X; Cichon, Sven/0000-0002-9475-086X; Sigurdsson,
Engilbert/0000-0001-9404-7982; Pickard, Benjamin/0000-0002-2374-6329;
Hansen, Thomas/0000-0001-6703-7762; Holmans, Peter/0000-0003-0870-9412;
Mortensen, Preben/0000-0002-5230-9865; Mattheisen,
Manuel/0000-0002-8442-493X; Pantelis, Christos/0000-0002-9565-0238;
Cloninger, Claude/0000-0003-3096-4807; McIntosh,
Andrew/0000-0002-0198-4588; McGrath, John/0000-0002-4792-6068;
FU US National Institutes of Health
FX We thank the study participants and the research staff at the many study
sites. Over 40 US National Institutes of Health grants and similar
numbers of government grants from other countries, along with
substantial private and foundation support, enabled this work. We
greatly appreciate the sustained efforts of T. Lehner (National
Institute of Mental Health) on behalf of the Schizophrenia Psychiatric
Genome-Wide Association Study (GWAS) Consortium (PGC). Detailed
acknowledgments, including grant support, are listed in the
Supplementary Note.
NR 32
TC 535
Z9 547
U1 11
U2 155
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD OCT
PY 2011
VL 43
IS 10
BP 969
EP U77
DI 10.1038/ng.940
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 825XT
UT WOS:000295316200011
ER
EF