FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Hitosugi, T
Kang, SK
Heiden, MGV
Chung, TW
Elf, S
Lythgoe, K
Dong, SZ
Lonial, S
Wang, X
Chen, GZ
Xie, JX
Gu, TL
Polakiewicz, RD
Roesel, JL
Boggon, TJ
Khuri, FR
Gilliland, DG
Cantley, LC
Kaufman, J
Chen, J
AF Hitosugi, Taro
Kang, Sumin
Heiden, Matthew G. Vander
Chung, Tae-Wook
Elf, Shannon
Lythgoe, Katherine
Dong, Shaozhong
Lonial, Sagar
Wang, Xu
Chen, Georgia Z.
Xie, Jianxin
Gu, Ting-Lei
Polakiewicz, Roberto D.
Roesel, Johannes L.
Boggon, Titus J.
Khuri, Fadlo R.
Gilliland, D. Gary
Cantley, Lewis C.
Kaufman, Jonathan
Chen, Jing
TI Tyrosine Phosphorylation Inhibits PKM2 to Promote the Warburg Effect and
Tumor Growth
SO SCIENCE SIGNALING
LA English
DT Article
ID KINASE TYPE M2; PYRUVATE-KINASE; FACTOR RECEPTOR; HUMAN BREAST; CANCER;
EXPRESSION; FGFR1; METABOLISM; PROTEIN; ZNF198
AB The Warburg effect describes a pro-oncogenic metabolism switch such that cancer cells take up more glucose than normal tissue and favor incomplete oxidation of glucose even in the presence of oxygen. To better understand how tyrosine kinase signaling, which is commonly increased in tumors, regulates the Warburg effect, we performed phosphoproteomic studies. We found that oncogenic forms of fibroblast growth factor receptor type 1 inhibit the pyruvate kinase M2 (PKM2) isoform by direct phosphorylation of PKM2 tyrosine residue 105 (Y(105)). This inhibits the formation of active, tetrameric PKM2 by disrupting binding of the PKM2 cofactor fructose-1,6-bisphosphate. Furthermore, we found that phosphorylation of PKM2 Y(105) is common in human cancers. The presence of a PKM2 mutant in which phenylalanine is substituted for Y(105) (Y105F) in cancer cells leads to decreased cell proliferation under hypoxic conditions, increased oxidative phosphorylation with reduced lactate production, and reduced tumor growth in xenografts in nude mice. Our findings suggest that tyrosine phosphorylation regulates PKM2 to provide a metabolic advantage to tumor cells, thereby promoting tumor growth.
C1 [Hitosugi, Taro; Kang, Sumin; Chung, Tae-Wook; Elf, Shannon; Lythgoe, Katherine; Dong, Shaozhong; Lonial, Sagar; Wang, Xu; Chen, Georgia Z.; Khuri, Fadlo R.; Kaufman, Jonathan; Chen, Jing] Emory Univ, Sch Med, Winship Canc Inst, Atlanta, GA 30322 USA.
[Heiden, Matthew G. Vander; Cantley, Lewis C.] Beth Israel Deaconess Med Ctr, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Heiden, Matthew G. Vander; Gilliland, D. Gary; Cantley, Lewis C.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Xie, Jianxin; Gu, Ting-Lei; Polakiewicz, Roberto D.] Cell Signaling Technol Inc, Danvers, MA 01923 USA.
[Roesel, Johannes L.] Novartis Pharma AG, CH-4002 Basel, Switzerland.
[Boggon, Titus J.] Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06520 USA.
[Gilliland, D. Gary] Brigham & Womens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA.
RP Chen, J (reprint author), Emory Univ, Sch Med, Winship Canc Inst, Atlanta, GA 30322 USA.
EM jchen@emory.edu
RI Cantley, Lewis/D-1800-2014
OI Cantley, Lewis/0000-0002-1298-7653
FU NCI NIH HHS [R01 CA120272-03, CA120272, R01 CA120272, R01 CA120272-01,
R01 CA120272-02, R01 CA120272-04, R01 CA140515, T32 CA009172]; NIGMS NIH
HHS [R01 GM056203]
NR 25
TC 288
Z9 301
U1 9
U2 60
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1937-9145
J9 SCI SIGNAL
JI Sci. Signal.
PD NOV 17
PY 2009
VL 2
IS 97
AR ra73
DI 10.1126/scisignal.2000431
PG 8
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 570AZ
UT WOS:000275645300003
PM 19920251
ER
PT J
AU Susa, M
Iyer, AK
Ryu, K
Hornicek, FJ
Mankin, H
Amiji, MM
Duan, ZF
AF Susa, Michiro
Iyer, Arun K.
Ryu, Keinosuke
Hornicek, Francis J.
Mankin, Henry
Amiji, Mansoor M.
Duan, Zhenfeng
TI Doxorubicin loaded Polymeric Nanoparticulate Delivery System to overcome
drug resistance in osteosarcoma
SO BMC CANCER
LA English
DT Article
ID COPOLYMER-BOUND DOXORUBICIN; MULTIDRUG-RESISTANCE; OVARIAN-CARCINOMA;
CYCLOSPORINE-A; CANCER-CELLS; MDR1 GENE; TUMOR; DAUNOMYCIN; REVERSAL;
ACCUMULATION
AB Background: Drug resistance is a primary hindrance for the efficiency of chemotherapy against osteosarcoma. Although chemotherapy has improved the prognosis of osteosarcoma patients dramatically after introduction of neo-adjuvant therapy in the early 1980's, the outcome has since reached plateau at approximately 70% for 5 year survival. The remaining 30% of the patients eventually develop resistance to multiple types of chemotherapy. In order to overcome both the dose-limiting side effects of conventional chemotherapeutic agents and the therapeutic failure incurred from multidrug resistant (MDR) tumor cells, we explored the possibility of loading doxorubicin onto biocompatible, lipid-modified dextran-based polymeric nanoparticles and evaluated the efficacy.
Methods: Doxorubicin was loaded onto a lipid-modified dextran based polymeric nano-system. The effect of various concentrations of doxorubicin alone or nanoparticle loaded doxorubicin on KHOS, KHOS(R2), U-2OS, and U-2OS(R2) cells was analyzed. Effects on drug retention, immunofluorescence, Pgp expression, and induction of apoptosis were also analyzed.
Results: Dextran nanoparticles loaded with doxorubicin had a curative effect on multidrug resistant osteosarcoma cell lines by increasing the amount of drug accumulation in the nucleus via Pgp independent pathway. Nanoparticles loaded with doxorubicin also showed increased apoptosis in osteosarcoma cells as compared with doxorubicin alone.
Conclusion: Lipid-modified dextran nanoparticles loaded with doxorubicin showed pronounced anti-proliferative effects against osteosarcoma cell lines. These findings may lead to new treatment options for MDR osteosarcoma.
C1 [Susa, Michiro; Ryu, Keinosuke; Hornicek, Francis J.; Duan, Zhenfeng] Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA.
[Susa, Michiro; Ryu, Keinosuke; Hornicek, Francis J.; Mankin, Henry; Duan, Zhenfeng] Massachusetts Gen Hosp, Ctr Sarcoma & Connect Tissue Oncol, Sarcoma Biol Lab, Boston, MA 02114 USA.
[Iyer, Arun K.; Amiji, Mansoor M.] Northeastern Univ, Sch Pharm, Dept Pharmaceut Sci, Boston, MA 02115 USA.
RP Duan, ZF (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA.
EM msusa@partners.org; arun.iyer@radiology.ucsf.edu; kryu@partners.org;
fhornicek@partners.org; hmankin@partners.org; m.amiji@neu.edu;
zduan@partners.org
RI Susa, Michiro/L-2291-2013; Amiji, Mansoor/A-4365-2014;
OI Amiji, Mansoor/0000-0001-6170-881X; Iyer, Arun/0000-0002-4428-0222
FU National Cancer Institute, NIH [R01-CA119617]; Sarcoma Foundation of
America; Gattegno and Wechsler funds
FX This project was supported, in part, by a grant from the National Cancer
Institute, NIH (Nanotechnology Platform Partnership), R01-CA119617. Dr.
Duan is supported, in part, through a grant from Sarcoma Foundation of
America. Support has also been provided by the Gattegno and Wechsler
funds.
NR 45
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U1 8
U2 45
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD NOV 16
PY 2009
VL 9
AR 399
DI 10.1186/1471-2407-9-399
PG 12
WC Oncology
SC Oncology
GA 527AR
UT WOS:000272338700003
PM 19917123
ER
PT J
AU Ganz, DA
Yano, EM
Saliba, D
Shekelle, PG
AF Ganz, David A.
Yano, Elizabeth M.
Saliba, Debra
Shekelle, Paul G.
TI Design of a continuous quality improvement program to prevent falls
among community-dwelling older adults in an integrated healthcare system
SO BMC HEALTH SERVICES RESEARCH
LA English
DT Article
ID VULNERABLE ELDERS; MOBILITY PROBLEMS; CONTROLLED-TRIAL; METAANALYSIS;
MANAGEMENT; PEOPLE; RISK; IMPLEMENTATION; ORGANIZATIONS; INTERVENTIONS
AB Background: Implementing quality improvement programs that require behavior change on the part of health care professionals and patients has proven difficult in routine care. Significant randomized trial evidence supports creating fall prevention programs for community-dwelling older adults, but adoption in routine care has been limited. Nationally-collected data indicated that our local facility could improve its performance on fall prevention in community-dwelling older people. We sought to develop a sustainable local fall prevention program, using theory to guide program development.
Methods: We planned program development to include important stakeholders within our organization. The theory-derived plan consisted of 1) an initial leadership meeting to agree on whether creating a fall prevention program was a priority for the organization, 2) focus groups with patients and health care professionals to develop ideas for the program, 3) monthly workgroup meetings with representatives from key departments to develop a blueprint for the program, 4) a second leadership meeting to confirm that the blueprint developed by the workgroup was satisfactory, and also to solicit feedback on ideas for program refinement.
Results: The leadership and workgroup meetings occurred as planned and led to the development of a functional program. The focus groups did not occur as planned, mainly due to the complexity of obtaining research approval for focus groups. The fall prevention program uses an existing telephonic nurse advice line to 1) place outgoing calls to patients at high fall risk, 2) assess these patients' risk factors for falls, and 3) triage these patients to the appropriate services. The workgroup continues to meet monthly to monitor the progress of the program and improve it.
Conclusion: A theory-driven program development process has resulted in the successful initial implementation of a fall prevention program.
C1 [Ganz, David A.; Yano, Elizabeth M.; Saliba, Debra; Shekelle, Paul G.] VA Greater Los Angeles HSR&D Ctr Excellence, Sepulveda, CA 91343 USA.
[Ganz, David A.; Saliba, Debra] Vet Affairs Greater Los Angeles Healthcare Syst, Geriatr Res Educ & Clin Ctr, Los Angeles, CA 90073 USA.
[Ganz, David A.; Saliba, Debra; Shekelle, Paul G.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Yano, Elizabeth M.] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90095 USA.
[Saliba, Debra] Univ Calif Los Angeles, Borun Ctr Gerontol Res, Los Angeles, CA 90095 USA.
RP Ganz, DA (reprint author), VA Greater Los Angeles HSR&D Ctr Excellence, 16111 Plummer St, Sepulveda, CA 91343 USA.
EM David.Ganz@va.gov; Elizabeth.Yano@va.gov; Debra.Saliba@va.gov;
Paul.Shekelle@va.gov
FU U. S. Department of Veterans Affairs; U. S. Department of Veterans
Affairs, Veterans Health Administration; VA Health Services Research &
Development (HSR&D) Service through the VA Greater Los Angeles HSR&D
Center of Excellence [VA CD2 08-012-1]; UCLA Older Americans
Independence Center; NIH/NIA [P30-AG028748]; Greater Los Angeles VA
Health Services Research & Development Center of Excellence [LIP 65-150]
FX The views expressed in this article are those of the authors and do not
necessarily reflect the position or policy of the U. S. Department of
Veterans
NR 30
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U1 4
U2 13
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1472-6963
J9 BMC HEALTH SERV RES
JI BMC Health Serv. Res.
PD NOV 16
PY 2009
VL 9
AR 206
DI 10.1186/1472-6963-9-206
PG 11
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 521LA
UT WOS:000271921700001
PM 19917122
ER
PT J
AU Johnson, AS
Fisher, RJ
Weir, GC
Colton, CK
AF Johnson, Amy S.
Fisher, Robert J.
Weir, Gordon C.
Colton, Clark K.
TI Oxygen consumption and diffusion in assemblages of respiring spheres:
Performance enhancement of a bioartificial pancreas
SO CHEMICAL ENGINEERING SCIENCE
LA English
DT Article
DE Bioartificial pancreas; Islets; Oxygen consumption; Reaction-diffusion
models; Encapsulation; Biomedical engineering; Mathematical modeling;
Numerical analysis
ID ISLET CELLS; INSULIN RELEASE; MASS-TRANSFER; BLOOD-FLOW; BETA-CELLS;
RAT; TRANSPLANTATION; ENCAPSULATION; LANGERHANS; TENSION
AB Microencapsulation provides an immune barrier for transplanted islets of Langerhans to treat diabetes, but it imposes oxygen diffusional limitations that can result in loss of viability and function. We investigate two methods to reduce oxygen transport limitations: (1) enhancement of the encapsulant oxygen permeability, for example, by combination of a highly concentrated perfluorocarbon (PFC) emulsion with alginate (PFC alginate); and (2) reduction of islet tissue size, for example, by dispersing the islets into single cells followed by reaggregation into cell clusters smaller than the original islet. A theoretical reaction-diffusion model is used to predict the three-dimensional distribution of oxygen partial pressure in a spherical microcapsule and a planar slab containing islet tissue, from which the loss of cell viability and the reduction in insulin secretion rate is estimated. Numerical simulations are carried out for normal alginate and PFC alginate to examine the effect of surface oxygen partial pressure, capsule diameter, slab thickness, and the size and density of dispersed islet tissue. Results show that hypoxic conditions can be reduced, thereby enhancing islet viability and substantially maintaining insulin secretion rate when PFC emulsion is incorporated in the encapsulation material or when smaller islet cell aggregates are used in both types of geometries. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Johnson, Amy S.; Fisher, Robert J.; Colton, Clark K.] MIT, Dept Chem Engn, Cambridge, MA 02139 USA.
[Weir, Gordon C.] Joslin Diabet Ctr, Div Res, Sect Islet Transplantat & Cell Biol, Boston, MA 02215 USA.
RP Colton, CK (reprint author), MIT, Dept Chem Engn, Room 66-452,77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM amyl@mit.edu; rjfisher@mit.edu; gordon.weir@joslin.harvard.edu;
ckcolton@mit.edu
FU NIH [R01 DK50657, R01-DK063108-01A1]; NCRR ICR [U4Z 16606]; JDRF Center
for Islet Transplantation
FX This work was supported by grants from the NIH (R01 DK50657,
R01-DK063108-01A1, and NCRR ICR U4Z 16606) and the JDRF Center for Islet
Transplantation at Harvard Medical School.
NR 59
TC 25
Z9 25
U1 2
U2 25
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0009-2509
J9 CHEM ENG SCI
JI Chem. Eng. Sci.
PD NOV 16
PY 2009
VL 64
IS 22
SI SI
BP 4470
EP 4487
DI 10.1016/j.ces.2009.06.028
PG 18
WC Engineering, Chemical
SC Engineering
GA 513CG
UT WOS:000271299200003
ER
PT J
AU Merchant, FM
Noseworthy, PA
Weiner, RB
Singh, SM
Ruskin, JN
Reddy, VY
AF Merchant, Faisal M.
Noseworthy, Peter A.
Weiner, Rory B.
Singh, Sheldon M.
Ruskin, Jeremy N.
Reddy, Vivek Y.
TI Ability of Terminal QRS Notching to Distinguish Benign from Malignant
Electrocardiographic Forms of Early Repolarization
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID MONOMORPHIC VENTRICULAR-TACHYCARDIA; BRUGADA-SYNDROME;
CLINICAL-SIGNIFICANCE; CELLULAR BASIS
AB Recent studies have suggested that early repolarization (ER) might be associated with up to 1/3 of idiopathic ventricular tachycardia/ventricular fibrillation (VT/VF) cases ("malignant" ER). We sought to identify electrocardiographic features to distinguish benign from malignant variants of ER. We reviewed the medical records for implantable-cardioverter defibrillators implanted at a single institution (1988 to 2008) to identify cases of idiopathic VT/VF. The electrocardiograms were scored for ER, defined as a >= 0.1-mV elevation of the QRS-ST junction manifesting as J-point slurring or notching in 2 contiguous leads. We also identified a cohort of 200 healthy age- and gender-matched controls with electrocardiographic findings previously identified as normal ER ("benign" ER cohort). Of 1,224 consecutive implantable-cardioverter defibrillator implants, we identified 39 cases of idiopathic VT/VF. Of the 39 cases, 9 (23%) demonstrated ER. During a mean follow-up of 7.2 +/- 4.6 years, the combined end point of appropriate implantable-cardioverter defibrillator shocks or all-cause mortality occurred less frequently in cases of idiopathic VT/VF with ER than in those without ER (11% vs 30%, odds ratio 0.29, 95% confidence interval 0.03 to 2.69, p = 0.40). A comparison of the electrocardiograms between those with malignant ER and controls demonstrated that QRS notching was significantly more prevalent among cases when present in leads V4 (44% vs 5%, p = 0.001) and V5 (44% vs 8%, p = 0.006), with a similar trend in lead V6 (33% vs 5%, p = 0.013). In conclusion, left precordial terminal QRS notching is more prevalent in malignant variants of ER than in benign cases. These findings could have important implications for risk stratification of patients with ER. (c) 2009 Elsevier Inc. All rights reserved. (Am J Cardiol 2009;104:1402-1406)
C1 [Reddy, Vivek Y.] Mt Sinai Sch Med, Div Cardiol, New York, NY USA.
[Merchant, Faisal M.; Noseworthy, Peter A.; Weiner, Rory B.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Singh, Sheldon M.; Ruskin, Jeremy N.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Singh, Sheldon M.; Ruskin, Jeremy N.] Harvard Univ, Sch Med, Boston, MA USA.
RP Reddy, VY (reprint author), Mt Sinai Sch Med, Div Cardiol, New York, NY USA.
EM vivek.reddy@mountsinai.org
NR 14
TC 57
Z9 61
U1 0
U2 1
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 NOV 15
PY 2009
VL 104
IS 10
BP 1402
EP 1406
DI 10.1016/j.amjcard.2009.06.062
PG 5
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 522LE
UT WOS:000271998500015
PM 19892058
ER
PT J
AU Holmes, MD
Chen, WY
Hankinson, SE
Willett, WC
AF Holmes, Michelle D.
Chen, Wendy Y.
Hankinson, Susan E.
Willett, Walter C.
TI Physical Activity's Impact on the Association of Fat and Fiber Intake
With Survival After Breast Cancer
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE breast neoplasms; dietary fats; dietary fiber; exercise; survival
ID DIETARY-FAT; LIVING WHEL; WEIGHT-LOSS; DIAGNOSIS; WOMEN; MORTALITY;
FRUIT; QUESTIONNAIRE; RECURRENCE; VEGETABLES
AB This study examined whether, after a breast cancer diagnosis, high intake of animal fat was associated with increased breast cancer mortality and high intake of fiber was associated with decreased breast cancer mortality. Participants were 3,846 US female nurses diagnosed with stages I-III breast cancer between 1976 and 2001 and followed until death or May 2006. Breast cancer mortality was calculated according to dietary intake quintiles first assessed at least 12 months after diagnosis and was cumulatively averaged and updated. There were 446 breast cancer deaths. In simple models adjusted for time since diagnosis, age, and energy intake, animal fat intake was associated with increased breast cancer death, and cereal fiber intake was associated with reduced breast cancer death. However, no associations were found in fully adjusted models: for animal fat, the relative risks for increasing quintiles were 1.00, 0.89, 0.86, 0.85, and 0.89 (95% confidence interval: 0.61, 1.28), P = 0.68; for cereal fiber, they were 1.00, 0.95, 0.76, 0.81, and 1.00 (95% confidence interval: 0.71, 1.40), P = 0.59. Results of simple models adjusted additionally for physical activity were similar to those for full multivariate models. Results show that physical activity strongly confounds the association between diet and survival.
C1 [Holmes, Michelle D.; Chen, Wendy Y.; Hankinson, Susan E.; Willett, Walter C.] Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA.
[Holmes, Michelle D.; Chen, Wendy Y.; Hankinson, Susan E.; Willett, Walter C.] Harvard Univ, Sch Med, Boston, MA USA.
[Chen, Wendy Y.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Holmes, Michelle D.; Hankinson, Susan E.; Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
RP Holmes, MD (reprint author), Brigham & Womens Hosp, Channing Lab, Dept Med, 181 Longwood Ave, Boston, MA 02115 USA.
EM michelle.holmes@channing.harvard.edu
FU National Institutes of Health [CA87969]
FX This work was supported by the National Institutes of Health (grant
CA87969).
NR 36
TC 13
Z9 14
U1 1
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD NOV 15
PY 2009
VL 170
IS 10
BP 1250
EP 1256
DI 10.1093/aje/kwp291
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 514FN
UT WOS:000271379800007
PM 19850626
ER
PT J
AU Sadreyev, RI
Feramisco, JD
Tsao, H
Grishin, NV
AF Sadreyev, Ruslan I.
Feramisco, Jamison D.
Tsao, Hensin
Grishin, Nick V.
TI Phenotypic categorization of genetic skin diseases reveals new relations
between phenotypes, genes and pathways
SO BIOINFORMATICS
LA English
DT Article
ID MESANGIAL CELLS; OXIDATIVE STRESS; NADPH OXIDASE; HUMAN PHENOME; HIGH
GLUCOSE; GLUCOSE-6-PHOSPHATE-DEHYDROGENASE; ANGIOGENESIS; NETWORK;
DECREASES; MUTATIONS
AB Motivation: Systematic analysis of connection between proteins, their cellular function and phenotypic manifestations in disease is a central problem of biological and clinical research. The solution to this problem requires the development of new approaches to link the rapidly growing dataset of gene-disease associations with the many complex and overlapping phenotypes of human disease.
Results: We analyze genetic skin disorders and suggest a manually designed set of elementary phenotypes whose combinations define diseases as points in a multidimensional space, providing a basis for phenotypic disease clustering. Placing the known gene-disease associations in the context of this space reveals new patterns that suggest previously unknown functional links between proteins, signaling pathways and disease phenotypes. For example, analysis of telangiectasias (spider vein diseases) reveals a previously unrecognized interplay between the TGF-beta signaling pathway and pentose phosphate pathway. This interaction may mediate glucose-dependent regulation of TGF-beta signaling, providing a clue to the known association between angiopathies and diabetes and implying new gene candidates for mutational analysis and drug targeting.
C1 [Tsao, Hensin] Massachusetts Gen Hosp, Dept Dermatol, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Sadreyev, Ruslan I.; Grishin, Nick V.] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA.
[Feramisco, Jamison D.] Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94115 USA.
[Grishin, Nick V.] Univ Texas SW Med Ctr Dallas, Dept Biochem, Dallas, TX 75390 USA.
RP Tsao, H (reprint author), Massachusetts Gen Hosp, Dept Dermatol, Wellman Ctr Photomed, 55 Fruit St, Boston, MA 02114 USA.
EM grishin@chop.swmed.edu
FU National Institutes of Health [GM67165]; Welch Foundation [I1505];
American Cancer Society
FX National Institutes of Health ( GM67165 to N. V. G.); Welch Foundation (
I1505 to N. V. G.); American Cancer Society ( to H. T.).
NR 27
TC 3
Z9 3
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
J9 BIOINFORMATICS
JI Bioinformatics
PD NOV 15
PY 2009
VL 25
IS 22
BP 2891
EP 2896
DI 10.1093/bioinformatics/btp538
PG 6
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 516SY
UT WOS:000271564300001
PM 19744994
ER
PT J
AU Berriz, GF
Beaver, JE
Cenik, C
Tasan, M
Roth, FP
AF Berriz, Gabriel F.
Beaver, John E.
Cenik, Can
Tasan, Murat
Roth, Frederick P.
TI Next generation software for functional trend analysis
SO BIOINFORMATICS
LA English
DT Article
ID GENOME DATABASE; GENE; INFORMATION; RESOURCES; BIOLOGY
AB FuncAssociate is a web application that discovers properties enriched in lists of genes or proteins that emerge from large-scale experimentation. Here we describe an updated application with a new interface and several new features. For example, enrichment analysis can now be performed within multiple gene-and protein-naming systems. This feature avoids potentially serious translation artifacts to which other enrichment analysis strategies are subject.
C1 [Berriz, Gabriel F.; Beaver, John E.; Cenik, Can; Tasan, Murat; Roth, Frederick P.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Roth, Frederick P.] Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA.
RP Roth, FP (reprint author), Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, 250 Longwood Ave, Boston, MA 02115 USA.
EM fritz_roth@hms.harvard.edu
RI Roth, Frederick/H-6308-2011;
OI Cenik, Can/0000-0001-6370-0889; Roth, Frederick/0000-0002-6628-649X
FU US National Institutes of Health [NS054052, NS035611, HL081341,
HG0017115, HG004233, HG003224]; Canadian Institute for Advanced Research
Fellowship
FX US National Institutes of Health (grants NS054052, NS035611, HL081341,
HG0017115, HG004233 and HG003224, in part); Canadian Institute for
Advanced Research Fellowship (to F. P. R.).
NR 14
TC 145
Z9 146
U1 0
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
J9 BIOINFORMATICS
JI Bioinformatics
PD NOV 15
PY 2009
VL 25
IS 22
BP 3043
EP 3044
DI 10.1093/bioinformatics/btp498
PG 2
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 516SY
UT WOS:000271564300026
PM 19717575
ER
PT J
AU Peng, LF
Stanton, BZ
Maloof, N
Wang, X
Schreiber, SL
AF Peng, Lee F.
Stanton, Benjamin Z.
Maloof, Nicole
Wang, Xiang
Schreiber, Stuart L.
TI Syntheses of aminoalcohol-derived macrocycles leading to a
small-molecule binder to and inhibitor of Sonic Hedgehog
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE Sonic Hedgehog; Robotnikinin; Macrocycle; Small-molecule microarray;
Surface plasmon resonance; Shh-LIGHT2; Ptch1(-/-)
ID STOCK SOLUTION APPROACH; IMMUNOSUPPRESSANT FK506; CHEMICAL GENETICS;
ONE-BEAD; MICROARRAYS; DISCOVERY; SYNTHASE; PATHWAY
AB We report the synthesis and biological activity of a library of aminoalcohol-derived macrocycles from which robotnikinin (17), a binder to and inhibitor of Sonic Hedgehog, was derived. Using an asymmetric alkylation to set a key stereocenter and an RCM reaction to close the macrocycle, we were able to synthesize compounds for testing. High-throughput screening via small-molecule microarray (SMM) technology led to the discovery of a compound capable of binding ShhN. Follow-up chemistry led to a library of macrocycles with enhanced biological activity relative to the original hit compounds. Differences in ring size and stereochemistry, leading to alterations in the mode of binding, may account for differences in the degree of biological activity. These compounds are the first ones reported that inhibit Shh signaling at the ShhN level. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Peng, Lee F.] Massachusetts Gen Hosp, Dept Med, GI Unit, Boston, MA 02114 USA.
[Peng, Lee F.; Stanton, Benjamin Z.; Maloof, Nicole; Wang, Xiang; Schreiber, Stuart L.] Harvard Univ, Dept Chem & Biol Chem, Cambridge, MA 02138 USA.
[Peng, Lee F.; Stanton, Benjamin Z.; Maloof, Nicole; Wang, Xiang; Schreiber, Stuart L.] Broad Inst, Cambridge, MA 02142 USA.
[Schreiber, Stuart L.] Broad Inst Harvard & MIT, Howard Hughes Med Inst, Cambridge, MA 02142 USA.
RP Peng, LF (reprint author), Massachusetts Gen Hosp, Dept Med, GI Unit, 55 Fruit St, Boston, MA 02114 USA.
EM lpeng@partners.org
FU National Pancreas Foundation; American Gastroenterological Association;
American Liver Foundation; National Institute of General Medical
Sciences [GM-38627]
FX We thank Dr. Douglas M. Ho and Dr. Shao-Liang Zheng of the Center for
Crystallographic Studies at Harvard University for the X-ray
crystallographic analysis. We thank James K. Chen, Kazuo Nakai, Andrew
M. Stern, Gregory T. Copeland, Damian W. Young, and Timothy A. Lewis for
their helpful suggestions. L. F. P. is supported by grants from the
National Pancreas Foundation, the American Gastroenterological
Association, and the American Liver Foundation. This research was
supported by the National Institute of General Medical Sciences
(GM-38627, awarded to S. L. S.) S. L. S. is an investigator with the
Howard Hughes Medical Institute.
NR 21
TC 43
Z9 43
U1 1
U2 18
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD NOV 15
PY 2009
VL 19
IS 22
BP 6319
EP 6325
DI 10.1016/j.bmcl.2009.09.089
PG 7
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA 509PH
UT WOS:000271029600014
PM 19819139
ER
PT J
AU Phillips, KA
Marshall, DA
Haas, JS
Elkin, EB
Liang, SY
Hassett, M
Ferrusi, I
Brock, JE
Van Bebber, SL
AF Phillips, Kathryn A.
Marshall, Deborah A.
Haas, Jennifer S.
Elkin, Elena B.
Liang, Su-Ying
Hassett, MichaelJ.
Ferrusi, Ilia
Brock, Jane E.
Van Bebber, Stephanie L.
TI Clinical Practice Patterns and Cost Effectiveness of Human Epidermal
Growth Receptor 2 Testing Strategies in Breast Cancer Patients
SO CANCER
LA English
DT Article
DE personalized medicine; targeted therapies; genomics; HER2; trastuzumab;
breast cancer; utilization; cost effectiveness; clinical practice
patterns
ID ADJUVANT TRASTUZUMAB; CONCORDANCE; MEDICINE; THERAPY
AB BACKGROUND: Testing technologies are increasingly used to target cancer therapies. Human epidermal growth factor receptor 2 (HER2) testing to target trastuzumab for patients with breast cancer provides insights into the evidence needed for emerging testing technologies. METHODS: The authors reviewed literature on HER2 test utilization and cost effectiveness of HER2 testing for patients with breast cancer. They examined available evidence on: percentage of eligible patients tested for HER2; test methods used; concordance of test results between community and central/reference laboratories; use of trastuzumab by HER2 test result; and cost effectiveness of testing strategies. RESULTS: Little evidence was available to determine whether all eligible patients are tested, how many are retested to confirm results, and how many with negative HER2 test results still receive trastuzumab. Studies suggested that up to 66% of eligible patients had no documentation of testing in claims records, up to 20% of patients receiving trastuzumab were not tested or had no documentation of a positive test, and 20% of HER2 results may be incorrect. Few cost-effectiveness analyses of trastuzumab explicitly considered the economic implications of various testing strategies. CONCLUSIONS: There was little information about the actual use of HER2 testing in clinical practice, but evidence suggested important variations in testing practices and key gaps in knowledge exist. Given the increasing use of targeted therapies, it is critical to build an evidence base that supports informed decision making on emerging testing technologies in cancer care. Cancer 2009;115:5166-74. (C) 2009 American Cancer Society.
C1 [Phillips, Kathryn A.; Liang, Su-Ying; Van Bebber, Stephanie L.] Univ Calif San Francisco, Dept Clin Pharm, Ctr Translat & Policy Res Personalized Med TRANSP, San Francisco, CA 94143 USA.
[Marshall, Deborah A.; Ferrusi, Ilia] McMaster Univ, Dept Clin Epidemiol & Biostat, Hamilton, ON, Canada.
[Haas, Jennifer S.] Brigham & Womens Hosp, Div Gen Med, Boston, MA 02115 USA.
[Elkin, Elena B.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Hassett, MichaelJ.] Dana Farber Canc Inst, Ctr Outcomes & Policy Res, Boston, MA 02115 USA.
[Ferrusi, Ilia] St Josephs Healthcare, Ctr Evaluat Med, Hamilton, ON, Canada.
[Brock, Jane E.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Phillips, KA (reprint author), Univ Calif San Francisco, Dept Clin Pharm, Ctr Translat & Policy Res Personalized Med TRANSP, 3333 Calif St 420, San Francisco, CA 94143 USA.
EM PhillipsK@pharmacy.ucsf.edu
RI Marshall, Deborah/J-7248-2015
OI Marshall, Deborah/0000-0002-8467-8008
FU National Cancer Institute [R01CA101849, P01CA130818]; Blue Shield
Foundation of California
FX This Study was funded by, 2 grants to Dr. Phillips from the National
Cancer Institute (R01CA101849 and P01CA130818) and a grant from the Blue
Shield Foundation of California (oil restricted). Funding agencies had
no review of any portion of this work.
NR 28
TC 37
Z9 39
U1 0
U2 8
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2009
VL 115
IS 22
BP 5166
EP 5174
DI 10.1002/cncr.24574
PG 9
WC Oncology
SC Oncology
GA 516SW
UT WOS:000271564100009
PM 19753618
ER
PT J
AU Jayachandran, J
Banez, LL
Aronson, WJ
Terris, MK
Presti, JC
Amling, CL
Kane, CJ
Freedland, SJ
AF Jayachandran, Jayakrishnan
Banez, Lionel L.
Aronson, William J.
Terris, Martha K.
Presti, Joseph C., Jr.
Amling, Christopher L.
Kane, Christopher J.
Freedland, Stephen J.
CA SEARCH Database Study Grp
TI Obesity as a Predictor of Adverse Outcome Across Black and White Race
Results From the Shared Equal Access Regional Cancer Hospital (SEARCH)
Database
SO CANCER
LA English
DT Article
DE prostatic neoplasms; prostatectomy; recurrence; obesity; continental
population groups
ID PROSTATE-CANCER; RADICAL PROSTATECTOMY; STEROID-HORMONES; UNITED-STATES;
WEIGHT CHANGE; RISK; RECURRENCE; MORTALITY; MEN; IMPACT
AB BACKGROUND: Across multiple studies, obesity has been associated with an increased risk of higher grade disease and prostate-specific antigen (PSA) recurrence after radical prostatectomy (RP). Whether these associations vary by race is unknown. In the current study, the authors examined the association between obesity and outcome after RID stratified by race. METHODS: A retrospective analysis was performed on 1415 men in the Shared Equal Access Regional Cancer Hospital (SEARCH) database who underwent RID between 1989 and 2008. The association between increased body mass index (BMI) and adverse pathology and biochemical recurrence was examined using multivariate logistic regression and Cox models, respectively. Data were examined stratified by race. RESULTS: After adjusting for preoperative clinical characteristics, higher BMI was associated with higher tumor grade (P = .008) and positive surgical margins (P < .001) in white men, and similar but statistically nonsignificant trends were observed in black men. No significant interaction was noted between race and BMI for associations with adverse pathology (P(interaction)>=.12). After adjusting for preoperative clinical characteristics, higher BMI was associated with an increased risk of recurrence in both white men (P = .001) and black men (P = .03). After further adjusting for pathologic variables, higher BMI was associated with significantly increased risk of recurrence in white men (P = .002) and black men (P = .01). No significant interactions were observed between race and BMI for predicting biochemical progression adjusting either for preoperative factors (P(interaction) = .35) or for preoperative and pathologic features (P(interaction) = .47). CONCLUSIONS: Obesity was associated with a greater risk of recurrence among both black men and white men. Obesity did not appear to be more or less influential in 1 race than another but, rather, was identified as a risk factor for aggressive cancer regardless of race. Cancer 2009;115:5263-71. (C) 2009 American Cancer Society.
C1 [Jayachandran, Jayakrishnan; Banez, Lionel L.; Freedland, Stephen J.] Duke Univ, Sch Med, Dept Surg, Div Urol Surg, Durham, NC 27710 USA.
[Jayachandran, Jayakrishnan; Banez, Lionel L.; Freedland, Stephen J.] Duke Univ, Sch Med, Dept Pathol, Div Urol Surg, Durham, NC 27710 USA.
[Jayachandran, Jayakrishnan; Banez, Lionel L.; Freedland, Stephen J.] Duke Univ, Sch Med, Duke Prostate Ctr, Durham, NC 27710 USA.
[Jayachandran, Jayakrishnan; Banez, Lionel L.; Freedland, Stephen J.] Vet Affairs Med Ctr, Urol Sect, Durham, NC USA.
[Aronson, William J.] Vet Affairs Greater Los Angeles Healthcare Syst, Urol Sect, Los Angeles, CA USA.
[Aronson, William J.] Univ Calif Los Angeles, Sch Med, Dept Urol, Los Angeles, CA USA.
[Terris, Martha K.] Med Coll Georgia, Urol Sect, Augusta, GA 30912 USA.
[Presti, Joseph C., Jr.] Stanford Univ, Sch Med, Dept Urol, Palo Alto, CA 94304 USA.
[Presti, Joseph C., Jr.] Vet Affairs Med Ctr, Urol Sect, Palo Alto, CA 94304 USA.
[Amling, Christopher L.] Univ Alabama, Div Urol, Birmingham, AL USA.
[Amling, Christopher L.] Birmingham Vet Affairs Med Ctr, Urol Sect, Birmingham, AL USA.
[Kane, Christopher J.] Univ Calif San Diego, Sch Med, Div Urol, San Diego, CA 92103 USA.
RP Freedland, SJ (reprint author), Duke Univ, Sch Med, Med Ctr, Div Urol, Box 2626, Durham, NC 27710 USA.
EM steve.freedland@duke.edu
OI Terris, Martha/0000-0002-3843-7270
FU Department of Veterans Affairs, National Institutes of Health (NIH)
[RO1CA100938]; NIH Specialized Programs of Research Excellence [P50
CA92131-01A1]; Georgia Cancer Coalition; Department of Defense, Prostate
Cancer Research Program; American Urological Association
Foundation/Astellas Rising Star in Urology Award
FX Supported by the Department of Veterans Affairs, National Institutes of
Health (NIH) Grant RO1CA100938 (to W.J.A.); NIH Specialized Programs of
Research Excellence Grant P50 CA92131-01A1 (to W.J.A.); the Georgia
Cancer Coalition (to M.K.T.); the Department of Defense, Prostate Cancer
Research Program, (to S.J.F. and J.J.); and the American Urological
Association Foundation/Astellas Rising Star in Urology Award (to
S.J.F.).
NR 22
TC 38
Z9 38
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2009
VL 115
IS 22
BP 5263
EP 5271
DI 10.1002/cncr.24571
PG 9
WC Oncology
SC Oncology
GA 516SW
UT WOS:000271564100020
PM 19670453
ER
PT J
AU Chu, K
Lee, SW
AF Chu, Kiki
Lee, Sam W.
TI Revisiting calcein AM Alternative tool for identifying dye-effluxing
cancer stem cells?
SO CANCER BIOLOGY & THERAPY
LA English
DT Editorial Material
DE cancer stem cells; side-population; hoechst 33342; calcein AM; C(lo)P;
cell surface markers; cell sorting
ID SIDE-POPULATION PHENOTYPE; ACUTE MYELOID-LEUKEMIA; IDENTIFICATION;
LINES; MICE
C1 [Lee, Sam W.] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA.
Harvard Univ, Sch Med, Charlestown, MA USA.
RP Lee, SW (reprint author), Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA.
EM swlee@partners.org
NR 28
TC 0
Z9 0
U1 0
U2 3
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1002 WEST AVENUE, 2ND FLOOR, AUSTIN, TX 78701 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD NOV 15
PY 2009
VL 8
IS 22
BP 2205
EP 2207
DI 10.4161/cbt.8.22.10714
PG 3
WC Oncology
SC Oncology
GA 645PZ
UT WOS:000281477800025
ER
PT J
AU Chen, YF
Chou, CY
Wilkins, RJ
Ellory, JC
Mount, DB
Shen, MR
AF Chen, Yih-Fung
Chou, Cheng-Yang
Wilkins, Robert J.
Ellory, J. Clive
Mount, David B.
Shen, Meng-Ru
TI Motor Protein-Dependent Membrane Trafficking of KCl Cotransporter-4 Is
Important for Cancer Cell Invasion
SO CANCER RESEARCH
LA English
DT Article
ID K-CL COTRANSPORTER; EPITHELIAL-MESENCHYMAL TRANSITION; H EXCHANGER NHE1;
CERVICAL-CANCER; MATRIX METALLOPROTEINASES; OVARIAN-CANCER;
BREAST-CANCER; UP-REGULATION; GROWTH; RECEPTOR
AB The KCl cotransporter (KCC) is a major determinant of osmotic homeostasis and plays an emerging role in tumor biology. This study stresses the important role of KCC4 in tumor malignant behavior. Real-time reverse transcription-PCR on samples collected by laser microdissection and immunofluorescent stainings with different KCC isoform antibodies indicate that KCC4 is abundant in metastatic cervical and ovarian cancer tissues. Insulin-like growth factor I (IGF-I) and epidermal growth factor (EGF) stimulate KCC4 recruitment from a presumably inactive cytoplasmic pool of endoplasmic reticulum and Golgi to plasma membrane along actin cytoskeleton that is significantly inhibited by LY294002 and wortmannin. Throughout the trafficking process, KCC4 is incorporated into lipid rafts that function as a platform for the association between KCC4 and myosin Va, an actin-dependent motor protein. KCC4 and ezrin, a membrane cytoskeleton linker, colocalize at lamellipodia of migratory cancer cells. Interference with KCC activity by either an inhibitor or a dominant-negative loss-of-function mutant profoundly suppressed the IGF-I-induced membrane trafficking of KCC4 and the structural interaction between KCC4 and ezrin near the cell surface. Endogenous cancer cell invasiveness was significantly attenuated by small interfering RNA targeting KCC4, and the residual invasiveness was much less sensitive to IGF-I or EGF stimulation. In the metastatic cancer tissues, KCC4 colocalizes with IGF-I or EGF, indicating a likely in vivo stimulation of KCC4 function by growth factors. Thus, blockade of KCC4 trafficking and surface expression may provide a potential target for the prevention of IGF-I- or EGF-dependent cancer spread. [Cancer Res 2009;69(22):8585-93]
C1 [Chou, Cheng-Yang; Shen, Meng-Ru] Natl Cheng Kung Univ, Coll Med, Dept Obstet & Gynecol, Tainan 704, Taiwan.
[Chen, Yih-Fung] Natl Cheng Kung Univ, Coll Med, Inst Basic Med Sci, Tainan 704, Taiwan.
[Chen, Yih-Fung; Shen, Meng-Ru] Natl Cheng Kung Univ, Coll Med, Dept Pharmacol, Tainan 704, Taiwan.
[Wilkins, Robert J.; Ellory, J. Clive] Univ Oxford, Dept Physiol Anat & Genet, Oxford, England.
[Mount, David B.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Renal, Boston, MA 02115 USA.
[Mount, David B.] Harvard Univ, VA Boston Healthcare Syst, Sch Med, Div Renal, Boston, MA 02115 USA.
RP Shen, MR (reprint author), Natl Cheng Kung Univ, Coll Med, Dept Obstet & Gynecol, 138 Sheng Li Rd, Tainan 704, Taiwan.
EM mrshen@mail.ncku.edu.tw
FU National Science Council, Taiwan; Center of Excellence for Clinical
Trial and Research [DOH-TD-B-111-OG4]; Department of Health, Executive
Yuan, Taiwan; Center for Gene Regulation and Signal Transduction
Research and Center for Micro/Nano Science and Technology; National
Cheng Kong University, Taiwan; Medical Research Council [G0700759];
United Kingdom; NIH [DK57708]
FX National Science Council, Taiwan; Center of Excellence for Clinical
Trial and Research (DOH-TD-B-111-OG4), Department of Health, Executive
Yuan, Taiwan; Center for Gene Regulation and Signal Transduction
Research and Center for Micro/Nano Science and Technology, National
Cheng Kong University, Taiwan; Medical Research Council (MRC grant
G0700759). United Kingdom; and NIH grant (DK57708).
NR 42
TC 17
Z9 18
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2009
VL 69
IS 22
BP 8585
EP 8593
DI 10.1158/0008-5472.CAN-09-2284
PG 9
WC Oncology
SC Oncology
GA 520JC
UT WOS:000271839200009
PM 19887603
ER
PT J
AU Myers, AP
Meyerhardt, JA
Cantley, LC
AF Myers, Andrea P.
Meyerhardt, Jeffrey A.
Cantley, Lewis C.
TI Getting Knit-PI3Ky: PIK3CA Mutation Status to Direct Multimodality
Therapy?
SO CLINICAL CANCER RESEARCH
LA English
DT Editorial Material
ID RECTAL-CANCER; RANDOMIZED TRIAL; RADIOTHERAPY
AB There is high morbidity associated with local recurrence of rectal cancer. However, the adjuvant therapies given to prevent such recurrences also have significant side effects and associated risks. The ability to select patients with the highest risk of recurrence and greatest therapeutic response will improve rectal cancer care. (Clin Cancer Res 2009;15(22):6748-50)
C1 [Myers, Andrea P.; Cantley, Lewis C.] Beth Israel Deaconess Med Ctr, Div Signal Transduct, Boston, MA 02115 USA.
[Myers, Andrea P.; Meyerhardt, Jeffrey A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Cantley, Lewis C.] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA USA.
RP Cantley, LC (reprint author), Beth Israel Deaconess Med Ctr, Div Signal Transduct, Boston, MA 02115 USA.
EM lewis_cantley@hms.harvard.edu
RI Cantley, Lewis/D-1800-2014
OI Cantley, Lewis/0000-0002-1298-7653
FU NIGMS NIH HHS [R01 GM041890, R37 GM041890, R01 GM036624]
NR 11
TC 1
Z9 2
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2009
VL 15
IS 22
BP 6748
EP 6750
DI 10.1158/1078-0432.CCR-09-2305
PG 3
WC Oncology
SC Oncology
GA 520EJ
UT WOS:000271822600002
PM 19903790
ER
PT J
AU Yanagawa, J
Walser, TC
Zhu, LX
Hong, LS
Fishbein, MC
Mah, V
Chia, D
Goodglick, L
Elashoff, DA
Luo, J
Magyar, CE
Dohadwala, M
Lee, JM
St John, MA
Strieter, RM
Sharma, S
Dubinett, SM
AF Yanagawa, Jane
Walser, Tonya C.
Zhu, Li X.
Hong, Longsheng
Fishbein, Michael C.
Mah, Vei
Chia, David
Goodglick, Lee
Elashoff, David A.
Luo, Jie
Magyar, Clara E.
Dohadwala, Mariam
Lee, Jay M.
St John, Maie A.
Strieter, Robert M.
Sharma, Sherven
Dubinett, Steven M.
TI Snail Promotes CXCR2 Ligand-Dependent Tumor Progression in Non-Small
Cell Lung Carcinoma
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID EPITHELIAL-MESENCHYMAL TRANSITION; E-CADHERIN EXPRESSION; TRANSCRIPTION
FACTOR; CANCER-CELLS; COLON-CANCER; KAPPA-B; SURVIVAL; ANGIOGENESIS;
METASTASIS; INVASION
AB Purpose: As a transcriptional repressor of E-cadherin, Snail has predominantly been associated with epithelial-mesenchymal transition, invasion, and metastasis. However, other important Snail-dependent malignant phenotypes have not been fully explored. Here, we investigate the contributions of Snail to the progression of non-small cell lung cancer (NSCLC).
Experimental Design: Immunohistochemistry was done to quantify and localize Snail in human lung cancer tissues, and tissue microarray analysis was used to correlate these findings with survival. NSCLC cell lines gene-modified to stably overexpress Snail were evaluated in vivo in two severe combined immunodeficiency murine tumor models. Differential gene expression between Snail-overexpressing and control cell lines was evaluated using gene expression microarray analysis.
Results: Snail is upregulated in human NSCLC tissue, and high levels of Snail expression correlate with decreased survival (P < 0.026). In a heterotopic model, mice bearing Snail-overexpressing tumors developed increased primary tumor burden (P = 0.008). In an orthotopic model, mice bearing Snail-overexpressing tumors also showed a trend toward increased metastases. In addition, Snail overexpression led to increased angiogenesis in primary tumors as measured by MECA-32 (P < 0.05) positivity and CXCL8 (P = 0.002) and CXCL5 (P = 0.0003) concentrations in tumor homogenates. Demonstrating the importance of these proangiogenic chemokines, the Snail-mediated increase in tumor burden was abrogated with CXCR2 blockade. Gene expression analysis also revealed Snail-associated differential gene expression with the potential to affect angiogenesis and diverse aspects of lung cancer progression.
Conclusion: Snail upregulation plays a role in human NSCLC by promoting tumor progression mediated by CXCR2 ligands. (Clin Cancer Res 2009;15(22):6820-9)
C1 [Dubinett, Steven M.] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Lung Canc Res Program, Div Pulm & Crit Care Med, Los Angeles, CA 90095 USA.
[Yanagawa, Jane; Walser, Tonya C.; Elashoff, David A.; Luo, Jie; Dohadwala, Mariam; Dubinett, Steven M.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
[Hong, Longsheng; Fishbein, Michael C.; Mah, Vei; Chia, David; Goodglick, Lee; Magyar, Clara E.; Dubinett, Steven M.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
[Elashoff, David A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Biostat, Los Angeles, CA 90095 USA.
[Yanagawa, Jane; Lee, Jay M.; St John, Maie A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, Los Angeles, CA 90095 USA.
[Zhu, Li X.; Dohadwala, Mariam; Sharma, Sherven; Dubinett, Steven M.] VA Greater Los Angeles Hlth Care Ctr, Los Angeles, CA USA.
[Strieter, Robert M.] Univ Virginia, Dept Med, Charlottesville, VA USA.
RP Dubinett, SM (reprint author), Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Lung Canc Res Program, Div Pulm & Crit Care Med, 10833 Le Conte Ave,37-131 CHS, Los Angeles, CA 90095 USA.
EM sdubinett@mednet.ucla.edu
FU National Cancer Institute [CA90388]; University of California [NIH/NHLBI
T32 HL72752]; Reiss Family and Piansky Family Trust; Early Detection
Research Network [NCI CA-86366]
FX Specialized Programs of Research Excellence in Lung Cancer grant
P50-CA90388, National Cancer Institute, LUNGevity/Thoracic Surgery
Foundation for Research and Education Research Fellowship, University of
California at Los Angeles Pulmonary & Critical Care Training Grant,
NIH/NHLBI T32 HL72752, Department of Veteran Affairs Medical Research
Funds, Tobacco Related Disease Program Award Program of the University
of California, Reiss Family and Piansky Family Trust, and the Early
Detection Research Network, NCI CA-86366.
NR 50
TC 57
Z9 59
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2009
VL 15
IS 22
BP 6820
EP 6829
DI 10.1158/1078-0432.CCR-09-1558
PG 10
WC Oncology
SC Oncology
GA 520EJ
UT WOS:000271822600011
PM 19887480
ER
PT J
AU Zwicker, JI
Liebman, HA
Neuberg, D
Lacroix, R
Bauer, KA
Furie, BC
Furie, B
AF Zwicker, Jeffrey I.
Liebman, Howard A.
Neuberg, Donna
Lacroix, Romaric
Bauer, Kenneth A.
Furie, Barbara C.
Furie, Bruce
TI Tumor-Derived Tissue Factor-Bearing Microparticles Are Associated With
Venous Thromboembolic Events in Malignancy
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID FACTOR-POSITIVE MICROPARTICLES; CANCER-PATIENTS; HEMOSTATIC
ABNORMALITIES; PANCREATIC-CANCER; SOLID TUMORS; RISK-FACTORS;
ENDOTHELIAL MICROPARTICLES; COAGULATION ACTIVATION; DOUBLE-BLIND;
THROMBOSIS
AB Purpose: Despite the strong association between malignant disease and thromboembolic disorders, the molecular and cellular basis of this relationship remains uncertain. We evaluated the hypothesis that tumor-derived tissue factor-bearing microparticles in plasma contribute to cancer-associated thrombosis.
Experimental Design: We developed impedance-based flow cytometry to detect, quantitate, and size microparticles in platelet-poor plasma. We evaluated the number of tissue factor-bearing microparticles in a cohort of cancer patients of different histologies (N = 96) and conducted a case-control study of 30 cancer patients diagnosed with an acute venous thromboembolic event (VTE) compared with 60 cancer patients of similar age, stage, sex, and diagnosis without known VTE, as well as 22 patients with an idiopathic VTE.
Results: Tissue factor-bearing microparticles were detected in patients with advanced malignancy, including two thirds of patients with pancreatic carcinoma. Elevated levels of tissue factor-bearing microparticles were associated VTE in cancer patients (adjusted odds ratio, 3.72; 95% confidence interval, 1.18-11.76; P = 0.01). In cancer patients without VTE, a retrospective analysis revealed a 1-year cumulative incidence of VTE of 34.8% in patients with tissue factor-bearing microparticles versus 0% in those without detectable tissue factor-bearing microparticles (Gray test P = 0.002). The median number of tissue factor-bearing microparticles in the cancer VTE cohort (7.1 x 10(4) microparticles/mu L) was significantly greater than both the idiopathic VTE and cancer-no VTE groups (P = 0.002 and P = 0.03, respectively). Pancreatectomy in three patients eliminated or nearly eliminated these microparticles which coexpressed the epithelial tumor antigen, MUC-1.
Conclusion: We conclude that tumor-derived tissue factor-bearing microparticles are associated with VTE in cancer patients and may be central to the pathogenesis of cancer-associated thrombosis. (Clin Cancer Res 2009;15(22):6830-40)
C1 [Zwicker, Jeffrey I.; Lacroix, Romaric; Bauer, Kenneth A.; Furie, Barbara C.; Furie, Bruce] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Zwicker, Jeffrey I.; Lacroix, Romaric; Bauer, Kenneth A.; Furie, Barbara C.; Furie, Bruce] Harvard Univ, Sch Med, Boston, MA USA.
[Neuberg, Donna] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Liebman, Howard A.] Univ So Calif, Keck Sch Med, Div Hematol, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
RP Zwicker, JI (reprint author), Beth Israel Deaconess Med Ctr, Dept Med, 330 Brookline Ave, Boston, MA 02215 USA.
EM jzwicker@bidmc.harvard.edu
OI Zwicker, Jeffrey/0000-0001-5810-6893
FU NIH [K23 HL084052, HL095084]
FX NIH grants K23 HL084052 (J. Zwicker) and HL095084 (B.C. Furie, B.
Furie).
NR 45
TC 239
Z9 249
U1 2
U2 13
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2009
VL 15
IS 22
BP 6830
EP 6840
DI 10.1158/1078-0432.CCR-09-0371
PG 11
WC Oncology
SC Oncology
GA 520EJ
UT WOS:000271822600012
PM 19861441
ER
PT J
AU Al-Shakfa, F
Dulucq, S
Brukner, I
Milacic, I
Ansari, M
Beaulieu, P
Moghrabi, A
Laverdiere, C
Sallan, SE
Silverman, LB
Neuberg, D
Kutok, JL
Sinnett, D
Krajinovic, M
AF Al-Shakfa, Fidaa
Dulucq, Stephanie
Brukner, Ivan
Milacic, Iva
Ansari, Marc
Beaulieu, Patrick
Moghrabi, Albert
Laverdiere, Caroline
Sallan, Stephen E.
Silverman, Lewis B.
Neuberg, Donna
Kutok, Jeffery L.
Sinnett, Daniel
Krajinovic, Maja
TI DNA Variants in Region for Noncoding Interfering Transcript of
Dihydrofolate Reductase Gene and Outcome in Childhood Acute
Lymphoblastic Leukemia
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID METHOTREXATE RESISTANCE; HAPLOTYPE RECONSTRUCTION;
PROGNOSTIC-SIGNIFICANCE; ACQUIRED-RESISTANCE; INDUCED APOPTOSIS;
EXPRESSION; RNA; CHILDREN; P53; CHEMOTHERAPY
AB Purpose: Dihydrofolate reductase (DHFR) is the major target of methotrexate, a key component in childhood acute lymphoblastic leukemia (ALL) treatment. We recently reported an association of DHFR promoter polymorphisms with ALL outcome. Lower event-free survival correlated with haplotype *1, defined by A(-317) and C(-1610) alleles. Haplotype *1 was also associated higher DHFR expression.
Experimental Design: Here, we analyzed adjacent 400-bp region participating in DHFR regulation as both a major promoter and a noncoding minor transcript.
Results: Six polymorphisms were identified, of which five were single nucleotide polymorphisms and one was length polymorphism composed of variable number of 9-bp elements and 9-bp insertion/deletion. Haplotype analysis including all promoter polymorphisms revealed diversification of haplotype *1 into five subtypes (*1a-*1e). DNA variations of major promoter/noncoding transcript region and haplotype *1 subtypes were subsequently analyzed for the association with ALL outcome. Lower event-free survival was associated with an A allele of G(308)A polymorphism (P = 0.02) and with *1b haplotype (P = 0.01). This association was particularly striking in high-risk patients (P = 0.001) and was subsequently confirmed in independent patient cohort (P = 0.02). Haplotype *1b was the only haplotype *1 subtype associated with higher mRNA levels.
Conclusions: The study provides a new insight into DHFR regulatory variations predisposing to an event in ALL patients. (Clin Cancer Res 2009;15(22):6931-8)
C1 [Al-Shakfa, Fidaa; Dulucq, Stephanie; Brukner, Ivan; Milacic, Iva; Ansari, Marc; Beaulieu, Patrick; Moghrabi, Albert; Laverdiere, Caroline; Sinnett, Daniel; Krajinovic, Maja] CHU St Justine, Res Ctr, Montreal, PQ H3T 1C5, Canada.
[Moghrabi, Albert; Laverdiere, Caroline; Sinnett, Daniel; Krajinovic, Maja] Univ Montreal, Dept Pediat, Montreal, PQ H3C 3J7, Canada.
[Al-Shakfa, Fidaa; Krajinovic, Maja] Univ Montreal, Dept Pharmacol, Montreal, PQ H3C 3J7, Canada.
[Sallan, Stephen E.; Silverman, Lewis B.; Neuberg, Donna] Dana Farber Canc Inst, Dept Pediat Oncol Biostat & Computat Biol, Boston, MA 02115 USA.
[Sallan, Stephen E.; Silverman, Lewis B.] Childrens Hosp, Div Hematol Oncol, Boston, MA USA.
[Kutok, Jeffery L.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Krajinovic, M (reprint author), CHU St Justine, Res Ctr, 3175 Chemin Cote Ste Catherine, Montreal, PQ H3T 1C5, Canada.
EM maja.krajinovic@umontreal.ca
FU Canadian Institutes of Health Research; Leukemia Lymphoma Society of
Canada; CHU Sainte Justine; Charles Bruneau Foundation; Centre
d'excellence en Oncologie pediatrique et en soins palliatifs; National
Cancer Institute/NIH [P01 CA 68484]; Fonds de la Recherche en Sante du
Quebec
FX Canadian Institutes of Health Research, Leukemia Lymphoma Society of
Canada, Research Center of CHU Sainte Justine, Charles Bruneau
Foundation, and Centre d'excellence en Oncologie pediatrique et en soins
palliatifs. Dana-Farber Cancer Institute ALL treatment protocols are
supported by the National Cancer Institute/NIH grant P01 CA 68484. M.
Krajinovic and D. Sinnett are scholars of the Fonds de la Recherche en
Sante du Quebec.
NR 30
TC 18
Z9 22
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2009
VL 15
IS 22
BP 6931
EP 6938
DI 10.1158/1078-0432.CCR-09-0641
PG 8
WC Oncology
SC Oncology
GA 520EJ
UT WOS:000271822600022
PM 19861437
ER
PT J
AU Taplin, ME
Regan, MM
Ko, YJ
Bubley, GJ
Duggan, SE
Werner, L
Beer, TM
Ryan, CW
Mathew, P
Tu, SM
Denmeade, SR
Oh, WK
Sartor, O
Mantzoros, CS
Rittmaster, R
Kantoff, PW
Balk, SP
AF Taplin, Mary-Ellen
Regan, Meredith M.
Ko, Yoo-Joung
Bubley, Glenn J.
Duggan, Stephen E.
Werner, Lillian
Beer, Tomasz M.
Ryan, Christopher W.
Mathew, Paul
Tu, Shi-Ming
Denmeade, Samuel R.
Oh, William K.
Sartor, Oliver
Mantzoros, Christos S.
Rittmaster, Roger
Kantoff, Philip W.
Balk, Steven P.
TI Phase II Study of Androgen Synthesis Inhibition with Ketoconazole,
Hydrocortisone, and Dutasteride in Asymptomatic Castration-Resistant
Prostate Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID ANTIANDROGEN WITHDRAWAL; ABIRATERONE ACETATE; HORMONAL-THERAPY; RECEPTOR
GENE; PROGRESSION; EXPRESSION; MECHANISM; CYP17; TESTOSTERONE;
BICALUTAMIDE
AB Purpose: Increasing evidence indicates that enhanced intratumoral androgen synthesis contributes to prostate cancer progression after androgen deprivation therapy. This phase II study was designed to assess responses to blocking multiple steps in androgen synthesis with inhibitors of CYP17A1 (ketoconazole) and type I and II 5 alpha-reductases (dutasteride) in patients with castration-resistant prostate cancer (CRPC).
Experimental Design: Fifty-seven men with CRPC were continued on gonadal suppression and treated with ketoconazole (400 mg thrice daily), hydrocortisone (30 mg/AM, 10 mg/PM), and dutasteride (0.5 mg/d).
Results: Prostate-specific antigen response rate (>= 50% decline) was 56% (32 of 57; 95% confidence interval, 42.4-69.3%); the median duration of response was 20 months. In patients with measurable disease, 6 of 20 (30%) responded by the Response Evaluation Criteria in Solid Tumors. Median duration of treatment was 8 months; 9 patients remained on therapy with treatment durations censored at 18 to 32 months. Median time to progression was 14.5 months. Grade 3 toxicities occurred in 32% with only one reported grade 4 (thrombosis) toxicity. Dehydroepiandrosterone sulfate declined by 89%, androstenedione by 56%, and testosterone by 66%, and dihydrotestosterone declined to below detectable levels compared with baseline levels with testicular suppression alone. Median baseline levels and declines in dehydroepiandrosterone sulfate, androstenedione, testosterone, and dihydrotestosterone were not statistically different in the responders versus nonresponders, and hormone levels were not significantly increased from nadir levels at relapse.
Conclusion: The response proportion to ketoconazole, hydrocortisone, and dutasteride was at least comparable with previous studies of ketoconazole alone, whereas time to progression was substantially longer. Combination therapies targeting multiple steps in androgen synthesis warrant further investigation. (Clin Cancer Res 200915(22):7099-105)
C1 [Bubley, Glenn J.; Duggan, Stephen E.; Mantzoros, Christos S.; Balk, Steven P.] Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Taplin, Mary-Ellen; Regan, Meredith M.; Werner, Lillian; Oh, William K.; Sartor, Oliver; Kantoff, Philip W.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Taplin, Mary-Ellen; Regan, Meredith M.; Bubley, Glenn J.; Oh, William K.; Mantzoros, Christos S.; Kantoff, Philip W.; Balk, Steven P.] Harvard Univ, Sch Med, Boston, MA USA.
[Taplin, Mary-Ellen; Regan, Meredith M.; Bubley, Glenn J.; Werner, Lillian; Oh, William K.; Kantoff, Philip W.; Balk, Steven P.] Dana Farber Harvard Canc Ctr, Boston, MA USA.
[Taplin, Mary-Ellen; Bubley, Glenn J.; Beer, Tomasz M.; Ryan, Christopher W.; Mathew, Paul; Tu, Shi-Ming; Denmeade, Samuel R.; Oh, William K.; Kantoff, Philip W.; Balk, Steven P.] Dept Def Prostate Canc Clin Trials Consortium, New York, NY USA.
[Ko, Yoo-Joung] Sunnybrook Hlth Sci Ctr, Toronto, ON M4N 3M5, Canada.
[Beer, Tomasz M.; Ryan, Christopher W.] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97201 USA.
[Mathew, Paul; Tu, Shi-Ming] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Denmeade, Samuel R.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Sartor, Oliver] Tulane Canc Ctr, New Orleans, LA USA.
[Rittmaster, Roger] GlaxoSmithKline Inc, Res Triangle Pk, NC USA.
RP Balk, SP (reprint author), Beth Israel Deaconess Med Ctr, 330 Brookline Ave, Boston, MA 02115 USA.
EM sbalk@bidmc.harvard.edu
RI Oh, William/B-9163-2012
OI Oh, William/0000-0001-5113-8147
FU GlaxoSmithKline; Department of Defense Prostate Cancer Research Program
[PC060807]; NIH [R01CA111803, P01CA89021]; Prostate Cancer Foundation
Challenge
FX Grant support: GlaxoSmithKline, Department of Defense Prostate Cancer
Research Program grant PC060807, NIH grants R01CA111803 and P01CA89021,
and Prostate Cancer Foundation Challenge grant.
NR 30
TC 49
Z9 50
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2009
VL 15
IS 22
BP 7099
EP 7105
DI 10.1158/1078-0432.CCR-09-1722
PG 7
WC Oncology
SC Oncology
GA 520EJ
UT WOS:000271822600043
PM 19887483
ER
PT J
AU Weil, AA
Khan, AI
Chowdhury, F
LaRocque, RC
Faruque, ASG
Ryan, ET
Calderwood, SB
Qadri, F
Harris, JB
AF Weil, Ana A.
Khan, Ashraful I.
Chowdhury, Fahima
LaRocque, Regina C.
Faruque, A. S. G.
Ryan, Edward T.
Calderwood, Stephen B.
Qadri, Firdausi
Harris, Jason B.
TI Clinical Outcomes in Household Contacts of Patients with Cholera in
Bangladesh
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID ANTI-MICROBIAL AGENTS; EL-TOR STRAINS; VIBRIO-CHOLERAE; ENDEMIC CHOLERA;
FAMILY CONTACTS; RAPID DIAGNOSIS; SUSCEPTIBILITY; INFECTION; O1;
TETRACYCLINE
AB Background. Multiple Vibrio cholerae infections in the same household are common. The objective of this study was to examine the incidence of V. cholerae infection and associated clinical symptoms in household contacts of patients with cholera and to identify risk factors for development of severe dehydration in this cohort.
Methods. Household contacts of hospitalized patients with cholera were observed with frequent clinical assessments and collection of serum and rectal swab samples for culture for a period of 21 days after presentation of the index case.
Results. One-half (460 of 944) of all contacts reported diarrhea during the study period, and symptoms most frequently began 2 days after presentation of the index case. Antibiotics were used by 199 (43%) of 460 contacts with diarrhea. Results of rectal swab cultures for V. cholerae were positive for 202 (21%) of 944 contacts, and 148 (73%) infected contacts experienced diarrhea. Significant dehydration developed in 26 contacts; predictors of dehydration included vomiting, each additional day of diarrhea, and blood group O status.
Conclusions. In urban Bangladesh, the burden of diarrheal illness among household contacts of patients with cholera is higher than was previously estimated, and prophylactic intervention is feasible, because the majority of symptomatic cases of V. cholerae infection in contacts begin soon after presentation of the index case. Re-evaluation of targeted chemoprophylaxis for household contacts of patients with cholera may be warranted.
C1 [LaRocque, Regina C.; Ryan, Edward T.; Calderwood, Stephen B.; Harris, Jason B.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Weil, Ana A.; Khan, Ashraful I.; Chowdhury, Fahima; Faruque, A. S. G.; Qadri, Firdausi] Int Ctr Diarrhoeal Dis Res Dhaka, Dhaka, Bangladesh.
[LaRocque, Regina C.; Ryan, Edward T.; Calderwood, Stephen B.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Ryan, Edward T.] Harvard Univ, Sch Med, Dept Immunol & Infect Dis, Boston, MA USA.
[Calderwood, Stephen B.] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA.
[Harris, Jason B.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
RP Harris, JB (reprint author), Massachusetts Gen Hosp, Div Infect Dis, 55 Fruit St, Boston, MA 02114 USA.
EM jbharris@partners.org
FU International Centre for Diarrhoeal Disease Research, Bangladesh; Centre
for Health and Population Research [U01 AI058935, RO3 AI063079, U01
AI077883]; International Research Scientist Development Award [K01
TW07409]; National Institutes of Health; Fogarty International Center
through Vanderbilt University [R24 TW007988]
FX International Centre for Diarrhoeal Disease Research, Bangladesh, Centre
for Health and Population Research (U01 AI058935 to S. B. C., RO3
AI063079 to F. Q., U01 AI077883 to E. T. R., International Research
Scientist Development Award K01 TW07144 to R. C. L., and International
Research Scientist Development Award K01 TW07409 to J.B.H.); and
National Institutes of Health, Fogarty International Center through
Vanderbilt University (R24 TW007988 to S. B. C. and A. A. W.).
NR 27
TC 41
Z9 41
U1 3
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
EI 1537-6591
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2009
VL 49
IS 10
BP 1473
EP 1479
DI 10.1086/644779
PG 7
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 511EH
UT WOS:000271146200002
PM 19842974
ER
PT J
AU Lipsky, BA
Hoey, C
AF Lipsky, Benjamin A.
Hoey, Christopher
TI Topical Antimicrobial Therapy for Treating Chronic Wounds
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID ANTIBIOTIC-RESISTANT BACTERIA; DIABETIC FOOT ULCERS; VENOUS LEG ULCERS;
SKIN INFECTIONS; IN-VITRO; COLONIZATION; RETAPAMULIN; HONEY;
MICROBIOLOGY; MANAGEMENT
AB Various agents have been applied topically to treat infected wounds for millennia, but their proper role remains unclear. Topical therapy affords many potential advantages but also has disadvantages. Opinions differ on which clinical signs define wound infection and on whether quantitative microbiological studies are useful. Clinically infected wounds usually require systemic antibiotic therapy, whereas clinically uninfected wounds that are healing as expected do not require antimicrobials. There is controversy over how to treat poorly healing wounds with "secondary" signs suggesting infection; these may benefit from topical antimicrobial agents. Some evidence supports using topical agents for malodorous or burn wounds. Meta-analyses and systematic reviews suggest there are few proven indications for topical antimicrobials. Use of a newer, relatively nontoxic antiseptic (eg, cadexomer iodine or silver dressings) is preferable to use of topical antibiotics, especially agents that are available for systemic use. We provide clinically relevant information on currently available topical antimicrobial agents.
C1 [Lipsky, Benjamin A.; Hoey, Christopher] VA Puget Sound Hlth Care Syst, Seattle, WA 98108 USA.
[Lipsky, Benjamin A.] Univ Washington, Sch Med, Seattle, WA USA.
RP Lipsky, BA (reprint author), VA Puget Sound Hlth Care Syst, S-111-PCC 1660 S Columbian Way, Seattle, WA 98108 USA.
EM balipsky@u.washington.edu
OI Lipsky, Benjamin A./0000-0001-9886-5114
NR 53
TC 113
Z9 119
U1 6
U2 50
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
EI 1537-6591
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2009
VL 49
IS 10
BP 1541
EP 1549
DI 10.1086/644732
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 511EH
UT WOS:000271146200015
PM 19842981
ER
PT J
AU Carneiro, HA
Mylonakis, E
AF Carneiro, Herman Anthony
Mylonakis, Eleftherios
TI Google Trends: A Web-Based Tool for Real-Time Surveillance of Disease
Outbreaks
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID WEST-NILE-VIRUS; SYNDROMIC SURVEILLANCE; INFLUENZA SURVEILLANCE;
EPIDEMIC
AB Google Flu Trends can detect regional outbreaks of influenza 7-10 days before conventional Centers for Disease Control and Prevention surveillance systems. We describe the Google Trends tool, explain how the data are processed, present examples, and discuss its strengths and limitations. Google Trends shows great promise as a timely, robust, and sensitive surveillance system. It is best used for surveillance of epidemics and diseases with high prevalences and is currently better suited to track disease activity in developed countries, because to be most effective, it requires large populations of Web search users. Spikes in search volume are currently hard to interpret but have the benefit of increasing vigilance. Google should work with public health care practitioners to develop specialized tools, using Google Flu Trends as a blueprint, to track infectious diseases. Suitable Web search query proxies for diseases need to be established for specialized tools or syndromic surveillance. This unique and innovative technology takes us one step closer to true real-time outbreak surveillance.
C1 [Carneiro, Herman Anthony; Mylonakis, Eleftherios] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Carneiro, Herman Anthony] Univ London Imperial Coll Sci Technol & Med, Sch Med, London, England.
RP Mylonakis, E (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Infect Dis, 55 Fruit St,Gray Jackson 5,Rm GRJ-504, Boston, MA 02114 USA.
EM emylonakis@partners.org
NR 29
TC 166
Z9 178
U1 8
U2 69
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2009
VL 49
IS 10
BP 1557
EP 1564
DI 10.1086/630200
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 511EH
UT WOS:000271146200017
PM 19845471
ER
PT J
AU Losina, E
Schackman, BR
Sadownik, SN
Gebo, KA
Walensky, RP
Chiosi, JJ
Weinstein, MC
Hicks, PL
Aaronson, WH
Moore, RD
Paltiel, AD
Freedberg, KA
AF Losina, Elena
Schackman, Bruce R.
Sadownik, Sara N.
Gebo, Kelly A.
Walensky, Rochelle P.
Chiosi, John J.
Weinstein, Milton C.
Hicks, Perrin L.
Aaronson, Wendy H.
Moore, Richard D.
Paltiel, A. David
Freedberg, Kenneth A.
TI Racial and Sex Disparities in Life Expectancy Losses among HIV-Infected
Persons in the United States: Impact of Risk Behavior, Late Initiation,
and Early Discontinuation of Antiretroviral Therapy
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; INJECTING DRUG-USERS; COST-EFFECTIVENESS;
CONTROLLED-TRIAL; MEDICAL-CARE; TENOFOVIR DF; HEALTH-CARE; COHORT; AIDS;
MORTALITY
AB Background. Most persons with human immunodeficiency virus (HIV) infection in the United States present to care with advanced disease, and many patients discontinue therapy prematurely. We sought to evaluate sex and racial/ethnic disparities in life-years lost as a result of risk behavior, late presentation, and early discontinuation of HIV care, and we compared these survival losses for HIV-infected persons with losses attributable to high-risk behavior and HIV disease itself.
Methods. With use of a state-transition model of HIV disease, we simulated cohorts of HIV-infected persons and compared them with uninfected individuals who had similar demographic characteristics. We estimated non-HIV-related mortality with use of risk-adjusted standardized mortality ratios, as well as years of life lost because of late presentation and early discontinuation of antiretroviral therapy (ART) for HIV infection. Data from the national HIV Research Network, stratified by sex and race/ethnicity, were used for estimating CD4(+) cell counts at ART initiation.
Results. For HIV-uninfected persons in the United States who have risk profiles similar to those of individuals with HIV infection, the projected life expectancy, starting at 33 years of age, was 34.58 years, compared with 42.91 years for the general US population. Those with HIV infection lost an additional 11.92 years of life if they received HIV care concordant with guidelines; late treatment initiation resulted in 2.60 additional years of life lost, whereas premature ART discontinuation led to 0.70 more years of life lost. Losses from late initiation and early discontinuation were greatest for Hispanic individuals (3.90 years).
Conclusions. The high-risk profile of HIV-infected persons, HIV infection itself, as well as late initiation and early discontinuation of care, all lead to substantial decreases in life expectancy. Survival disparities resulting from late initiation and early discontinuation of therapy are most pronounced for Hispanic HIV-infected men and women. Interventions focused on risk behaviors, as well as on earlier linkage to and better retention in care, will lead to improved survival for HIV-infected persons in the United States.
C1 [Losina, Elena; Sadownik, Sara N.; Walensky, Rochelle P.; Chiosi, John J.; Aaronson, Wendy H.; Freedberg, Kenneth A.] Massachusetts Gen Hosp, Dept Med, Div Gen Med, Boston, MA 02114 USA.
[Walensky, Rochelle P.; Freedberg, Kenneth A.] Massachusetts Gen Hosp, Dept Med, Div Infect Dis, Boston, MA 02114 USA.
[Losina, Elena; Walensky, Rochelle P.; Freedberg, Kenneth A.] Harvard Univ, Sch Med, Ctr AIDS Res, Boston, MA USA.
[Losina, Elena] Brigham & Womens Hosp, Dept Orthoped Surg, Boston, MA 02115 USA.
[Walensky, Rochelle P.] Brigham & Womens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Sadownik, Sara N.; Weinstein, Milton C.; Freedberg, Kenneth A.] Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA.
[Losina, Elena; Freedberg, Kenneth A.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Losina, Elena; Freedberg, Kenneth A.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Schackman, Bruce R.] Weill Cornell Med Coll, Dept Publ Hlth, New York, NY USA.
[Gebo, Kelly A.; Hicks, Perrin L.; Moore, Richard D.] Johns Hopkins Univ, Dept Med, Sch Med, Baltimore, MD USA.
[Paltiel, A. David] Yale Univ, Dept Epidemiol & Publ Hlth, Sch Med, New Haven, CT 06520 USA.
RP Losina, E (reprint author), Massachusetts Gen Hosp, Dept Med, Div Gen Med, 50 Staniford St,9th Flr, Boston, MA 02114 USA.
EM elosina@partners.org
OI Walensky, Rochelle P./0000-0002-8795-379X
FU National Institute of Allergy and Infectious Diseases [K23 AI01794, K24
AI062476, K25 AI50436, R37 AI42006]; National Institute on Drug Abuse
[K23 DA000523, K01 DA017179, K24 DA00432]; National Institute of Mental
Health [MH065879]; Agency for Healthcare Research and Quality
[290-01-012]; Doris Duke Charitable Foundation; Johns Hopkins University
FX National Institute of Allergy and Infectious Diseases (K23 AI01794, K24
AI062476, K25 AI50436, and R37 AI42006), National Institute on Drug
Abuse (K23 DA000523, K01 DA017179, and K24 DA00432), National Institute
of Mental Health (MH065879), Agency for Healthcare Research and Quality
(290-01-012), Doris Duke Charitable Foundation (Clinical Scientist
Development Award to R.P.W.), and Johns Hopkins University (Richard S.
Ross Clinical Scientist Award to K.A.G.).
NR 67
TC 106
Z9 106
U1 2
U2 8
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2009
VL 49
IS 10
BP 1570
EP 1578
DI 10.1086/644772
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 511EH
UT WOS:000271146200019
PM 19845472
ER
PT J
AU Chen, TY
Ding, EL
Seage, GR
Kim, AY
AF Chen, Ting-Yi
Ding, Eric L.
Seage, George R., III
Kim, Arthur Y.
TI Meta-Analysis: Increased Mortality Associated with Hepatitis C in
HIV-Infected Persons Is Unrelated to HIV Disease Progression
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID ACTIVE ANTIRETROVIRAL THERAPY; HUMAN-IMMUNODEFICIENCY-VIRUS;
AIDS-DEFINING EVENTS; INJECTION-DRUG USERS; LIVER-DISEASE; CLINICAL
PROGRESSION; POSITIVE PATIENTS; FIBROSIS PROGRESSION; COINFECTED
PATIENTS; SURVIVAL
AB Background. It is unclear whether coinfection with hepatitis C virus (HCV) increases mortality in patients with human immunodeficiency virus (HIV) infection during the era of highly active antiretroviral therapy (HAART). With use of a meta-analysis, we estimated the effect of HCV infection on HIV disease progression and overall mortality in the pre-HAART and HAART eras.
Method. The PubMed and EMBASE databases were searched for studies published through 30 April 2008. Additional studies were identified from cited references. Studies reporting disease progression or mortality among HCV-HIV coinfected patients were selected. Cross-sectional studies, studies without HCV-negative control subjects, and studies involving children and/or patients who had undergone liver transplantation were excluded. Two authors reviewed articles and extracted data on the demographic characteristics of study populations and risk estimates. Meta-regression was used to explore heterogeneity.
Results. Ten studies from the pre-HAART era and 27 studies from the HAART era were selected. In the pre-HAART era, the risk ratio for overall mortality among patients with HCV-HIV coinfection, compared with that among patients with HIV infection alone, was 0.68 (95% confidence interval [CI], 0.53-0.87). In the HAART era, the risk ratio was 1.12 (95% CI, 0.82-1.51) for AIDS-defining events and 1.35 (95% CI, 1.11-1.63) for overall mortality among coinfected patients, compared with that among patients with HIV monoinfection.
Conclusions. HCV coinfection did not increase mortality among patients with HIV infection before the introduction of HAART. In contrast, in the HAART era, HCV coinfection, compared with HIV infection alone, increases the risk of mortality, but not the risk of AIDS-defining events. Future studies should determine whether successful treatment of HCV infection could reduce this excess risk of mortality in coinfected patients.
C1 [Chen, Ting-Yi] Wayne State Univ, Detroit Med Ctr, Detroit, MI 48201 USA.
[Ding, Eric L.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Seage, George R., III] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Kim, Arthur Y.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
RP Chen, TY (reprint author), Wayne State Univ, Detroit Med Ctr, 4201 St Antoine,2E, Detroit, MI 48201 USA.
EM tchen2@med.wayne.edu
RI Chen, Ting-Yi/B-3144-2013;
OI Ding, Eric/0000-0002-5881-8097
FU The Paul and Daisy Soros Foundation; National Institutes of
Health/National Institute of Allergy and Infectious Diseases [U19
AI066345, K23 AI054379]
FX The Paul and Daisy Soros Foundation (fellowship to E.L.D) and the
National Institutes of Health/National Institute of Allergy and
Infectious Diseases (grants U19 AI066345 and K23 AI054379 to A.Y.K.).
NR 73
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U1 0
U2 3
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2009
VL 49
IS 10
BP 1605
EP 1615
DI 10.1086/644771
PG 11
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 511EH
UT WOS:000271146200024
PM 19842982
ER
PT J
AU Aujesky, D
McCausland, JB
Whittle, J
Obrosky, DS
Yealy, DM
Fine, MJ
AF Aujesky, Drahomir
McCausland, Julie B.
Whittle, Jeff
Obrosky, D. Scott
Yealy, Donald M.
Fine, Michael J.
TI Reasons Why Emergency Department Providers Do Not Rely on the Pneumonia
Severity Index to Determine the Initial Site of Treatment for Patients
with Pneumonia
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID COMMUNITY-ACQUIRED PNEUMONIA; LOW-RISK PATIENTS; RESEARCH TEAM COHORT;
PREDICTION RULE; ADMISSION DECISION; CLINICAL JUDGMENT;
RANDOMIZED-TRIAL; HOSPITALIZATION; OUTCOMES; CARE
AB Background. Many emergency department (ED) providers do not follow guideline recommendations for the use of the pneumonia severity index (PSI) to determine the initial site of treatment for patients with community-acquired pneumonia (CAP). We identified the reasons why ED providers hospitalize low-risk patients or manage higher-risk patients as outpatients.
Methods. As a part of a trial to implement a PSI-based guideline for the initial site of treatment of patients with CAP, we analyzed data for patients managed at 12 EDs allocated to a high-intensity guideline implementation strategy study arm. The guideline recommended outpatient care for low-risk patients (nonhypoxemic patients with a PSI risk classification of I, II, or III) and hospitalization for higher-risk patients (hypoxemic patients or patients with a PSI risk classification of IV or V). We asked providers who made guideline-discordant decisions on site of treatment to detail the reasons for nonadherence to guideline recommendations.
Results. There were 1,306 patients with CAP (689 low-risk patients and 617 higher-risk patients). Among these patients, physicians admitted 258 (37.4%) of 689 low-risk patients and treated 20 (3.2%) of 617 higher-risk patients as outpatients. The most commonly reported reasons for admitting low-risk patients were the presence of a comorbid illness (178 [71.5%] of 249 patients); a laboratory value, vital sign, or symptom that precluded ED discharge (73 patients [29.3%]); or a recommendation from a primary care or a consulting physician (48 patients [19.3%]). Higher-risk patients were most often treated as outpatients because of a recommendation by a primary care or consulting physician (6 [40.0%] of 15 patients).
Conclusion. ED providers hospitalize many low-risk patients with CAP, most frequently for a comorbid illness. Although higher-risk patients are infrequently treated as outpatients, this decision is often based on the request of an involved physician.
C1 [Aujesky, Drahomir] Univ Lausanne, Dept Med, Div Gen Internal Med, Lausanne, Switzerland.
[McCausland, Julie B.; Yealy, Donald M.] Univ Pittsburgh, Dept Emergency Med, Pittsburgh, PA USA.
[Obrosky, D. Scott; Fine, Michael J.] Univ Pittsburgh, Dept Med, Div Gen Internal Med, Pittsburgh, PA USA.
[Obrosky, D. Scott; Fine, Michael J.] Vet Affairs Pittsburgh Healthcare Syst, Vet Affairs Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Whittle, Jeff] Med Coll Wisconsin, Clement J Zablocki Vet Affairs Med Ctr, Primary Care Div, Milwaukee, WI 53226 USA.
[Whittle, Jeff] Med Coll Wisconsin, Dept Med, Div Gen Internal Med, Milwaukee, WI 53226 USA.
RP Aujesky, D (reprint author), CHU Vaudois, Serv Med Interne, BH 10-622, CH-1011 Lausanne, Switzerland.
EM drahomir.aujesky@chuv.ch
FU Agency for Healthcare Research and Quality [R01 HS10049]; National
Institute of Allergy and Infectious Diseases [K24 AI001769]
FX Financial support. This research was conducted as part of the project
entitled "Guideline to Improve Quality of Initial Pneumonia Care,"
funded by the Agency for Healthcare Research and Quality (grant R01
HS10049). M.J.F. received support in part from a career development
award from the National Institute of Allergy and Infectious Diseases
(grant K24 AI001769).
NR 25
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U1 1
U2 3
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2009
VL 49
IS 10
BP E100
EP E108
DI 10.1086/644741
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 511EH
UT WOS:000271146200032
PM 19842971
ER
PT J
AU Lefebvre, L
Mar, L
Bogutz, A
Oh-McGinnis, R
Mandegar, MA
Paderova, J
Gertsenstein, M
Squire, JA
Nagy, A
AF Lefebvre, Louis
Mar, Lynn
Bogutz, Aaron
Oh-McGinnis, Rosemary
Mandegar, Mohammad A.
Paderova, Jana
Gertsenstein, Marina
Squire, Jeremy A.
Nagy, Andras
TI The interval between Ins2 and AscI2 is dispensable for imprinting centre
function in the murine Beckwith-Wiedemann region
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID MOUSE DISTAL CHROMOSOME-7; H19 GENE; TARGETED DISRUPTION; CRE
RECOMBINASE; MICE LACKING; IGF2 GENE; YOLK-SAC; DOMAIN; EXPRESSION;
METHYLATION
AB Imprinted genes are commonly clustered in domains across the mammalian genome, suggesting a degree of coregulation via long-range coordination of their monoallelic transcription. The distal end of mouse chromosome 7 (Chr 7) contains two clusters of imprinted genes within a similar to 1 Mb domain. This region is conserved on human 11p15.5 where it is implicated in the Beckwith-Wiedemann syndrome. In both species, imprinted regulation requires two critical cis-acting imprinting centres, carrying different germline epigenetic marks and mediating imprinted expression in the proximal and distal sub-domains. The clusters are separated by a region containing the gene for tyrosine hydroxylase (Th) as well as a high density of short repeats and retrotransposons in the mouse. We have used the Cre-loxP recombination system in vivo to engineer an interstitial deletion of this similar to 280-kb intervening region previously proposed to participate in the imprinting mechanism or to act as a boundary between the two sub-domains. The deletion allele, Del(7AI), is silent with respect to epigenetic marking at the two flanking imprinting centres. Reciprocal inheritance of Del(7AI) demonstrates that the deleted region, which represents more than a quarter of the previously defined imprinted domain, is associated with intrauterine growth restriction in maternal heterozygotes. In homozygotes, the deficiency behaves as a Th null allele and can be rescued pharmacologically by bypassing the metabolic requirement for TH in utero. Our results show that the deleted interval is not required for normal imprinting on distal Chr 7 and uncover a new imprinted growth phenotype.
C1 [Lefebvre, Louis; Bogutz, Aaron; Oh-McGinnis, Rosemary; Mandegar, Mohammad A.] Univ British Columbia, Dept Med Genet, Inst Life Sci, Vancouver, BC V6T 1Z3, Canada.
[Lefebvre, Louis; Bogutz, Aaron; Oh-McGinnis, Rosemary; Mandegar, Mohammad A.] Univ British Columbia, Mol Epigenet Grp, Inst Life Sci, Vancouver, BC V6T 1Z3, Canada.
[Mar, Lynn] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Paderova, Jana; Squire, Jeremy A.] Princess Margaret Hosp, Ontario Canc Inst, Toronto, ON M5G 2M9, Canada.
[Paderova, Jana; Squire, Jeremy A.] Univ Toronto, Dept Med Biophys, Toronto, ON M5G 2M9, Canada.
[Gertsenstein, Marina; Nagy, Andras] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
[Gertsenstein, Marina; Nagy, Andras] Univ Toronto, Dept Med Genet, Toronto, ON M5G 1X5, Canada.
RP Lefebvre, L (reprint author), Univ British Columbia, Dept Med Genet, Inst Life Sci, Vancouver, BC V6T 1Z3, Canada.
EM louis.lefebvre@ubc.ca
RI Nagy, Andras/G-6465-2013; Lefebvre, Louis/O-9309-2016
OI Lefebvre, Louis/0000-0001-5664-9480
FU Canadian Institutes of Health [MOP-82863, FRN 13687]; Canada Research
Chair; Michael Smith Foundation for Health Research (MSFHR)
FX This work was supported in part by the Canadian Institutes of Health
Research (MOP-82863 to L.L. and FRN 13687 to A.N.). L.L. holds a Canada
Research Chair and was also supported by a Michael Smith Foundation for
Health Research (MSFHR) Scholar Award.
NR 60
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U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 15
PY 2009
VL 18
IS 22
BP 4255
EP 4267
DI 10.1093/hmg/ddp379
PG 13
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 510RB
UT WOS:000271107300003
PM 19684026
ER
PT J
AU Berger, AK
Cortese, GP
Amodeo, KD
Weihofen, A
Letai, A
LaVoie, MJ
AF Berger, Alison K.
Cortese, Giuseppe P.
Amodeo, Katherine D.
Weihofen, Andreas
Letai, Anthony
LaVoie, Matthew J.
TI Parkin selectively alters the intrinsic threshold for mitochondrial
cytochrome c release
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID RECESSIVE JUVENILE PARKINSONISM; OXIDATIVE STRESS; CELL-DEATH; DISEASE;
MUTATIONS; APOPTOSIS; GENE; ACTIVATION; MUTANTS; BAX
AB Autosomal-recessive mutations in the Parkin gene are the second most common cause of familial Parkinson's disease (PD). Parkin deficiency leads to the premature demise of the catecholaminergic neurons of the ventral midbrain in familial PD. Thus, a better understanding of parkin function may elucidate molecular aspects of their selective vulnerability in idiopathic PD. Numerous lines of evidence suggest a mitochondrial function for parkin and a protective effect of ectopic parkin expression. Since mitochondria play a critical role in cell survival/cell death through regulated cytochrome c release and control of apoptosis, we sought direct evidence of parkin function in this pathway. Mitochondria were isolated from cells expressing either excess levels of human parkin or shRNA directed against endogenous parkin and then treated with peptides corresponding to the active Bcl-2 homology 3 (BH3) domains of pro-apoptotic proteins and the threshold for cytochrome c release was analyzed. Data obtained from both rodent and human neuroblastoma cell lines showed that the expression levels of parkin were inversely correlated with cytochrome c release. Parkin was found associated with isolated mitochondria, but its binding per se was not sufficient to inhibit cytochrome c release. In addition, pathogenic parkin mutants failed to influence cytochrome c release. Furthermore, PINK1 expression had no effect on cytochrome c release, suggesting a divergent function for this autosomal recessive PD-linked gene. In summary, these data demonstrate a specific autonomous effect of parkin on mitochondrial mechanisms governing cytochrome c release and apoptosis, which may be relevant to the selective vulnerability of certain neuronal populations in PD.
C1 [Berger, Alison K.; Cortese, Giuseppe P.; Amodeo, Katherine D.; Weihofen, Andreas; LaVoie, Matthew J.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Berger, Alison K.; Weihofen, Andreas; Letai, Anthony; LaVoie, Matthew J.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Weihofen, Andreas] Neurimmune Therapeut AG, Schlieren, Switzerland.
[Letai, Anthony] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP LaVoie, MJ (reprint author), Harvard Inst Med, Room 764,77 Ave Louis Pasteur, Boston, MA 02115 USA.
EM mlavoie@rics.bwh.harvard.edu
RI Weihofen, Andreas/A-1566-2011
FU National Institutes of Health [AG023094, AG00222]; The Smith Family
Foundation; Ludke Foundation; American Parkinson's Disease Association;
The Parkinson's Disease Foundation; Brigham and Women's Hospital [P50
NS03875]
FX This work was supported by the National Institutes of Health (AG023094
to M.J.L., AG00222 to A.K.B.); The Smith Family Foundation; the Ludke
Foundation to M.J.L and A.G.L.; the American Parkinson's Disease
Association to M.J.L.; and The Parkinson's Disease Foundation to M.J.L.
and the Brigham and Women's Hospital Udall Center of Excellence in
Parkinson's Disease Research (P50 NS03875).
NR 48
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U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 15
PY 2009
VL 18
IS 22
BP 4317
EP 4328
DI 10.1093/hmg/ddp384
PG 12
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 510RB
UT WOS:000271107300008
PM 19679562
ER
PT J
AU Won, JY
Gifford, E
Smith, RS
Yi, HQ
Ferreira, PA
Hicks, WL
Li, TS
Naggert, JK
Nishina, PM
AF Won, Jungyeon
Gifford, Elaine
Smith, Richard S.
Yi, Haiqing
Ferreira, Paulo A.
Hicks, Wanda L.
Li, Tiansen
Naggert, Juergen K.
Nishina, Patsy M.
TI RPGRIP1 is essential for normal rod photoreceptor outer segment
elaboration and morphogenesis
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID LEBER CONGENITAL AMAUROSIS; REGULATOR (RPGR)-INTERACTING PROTEIN; RDS
MUTANT MICE; RETINITIS-PIGMENTOSA; RETINAL DEGENERATION; MOUSE MODEL;
SUBCELLULAR-LOCALIZATION; GENE-EXPRESSION; IDENTIFICATION; MUTATIONS
AB The function of the retinitis pigmentosa GTPase regulator interacting protein 1 (RPGRIP1) gene is currently not known. However, mutations within the gene lead to Leber Congenital Amaurosis and autosomal recessive retinitis pigmentosa in human patients. In a previously described knockout mouse model of the long splice variant of Rpgrip1, herein referred to as Rpgrip1(tm1Tili) mice, mislocalization of key outer segment proteins and dysmorphogenesis of outer segment discs preceded subsequent photoreceptor degeneration. In this report, we describe a new mouse model carrying a splice acceptor site mutation in Rpgrip1, herein referred to as Rpgrip1(nmf247) that is phenotypically distinct from Rpgrip1(tm1Tili) mice. Photoreceptor degeneration in homozygous Rpgrip1(nmf247) mice is earlier in onset and more severe when compared with Rpgrip1(tm1Tili) mice. Also, ultrastructural studies reveal that whereas Rpgrip1(nmf247) mutants have a normal structure and number of connecting cilia, unlike Rpgrip1(tm1Tili) mice, they do not elaborate rod outer segments (OS). Therefore, in addition to its role in OS disc morphogenesis, RPGRIP1 is essential for rod OS formation. Our study indicates the absence of multiple Rpgrip1 isoforms in Rpgrip1(nmf247) mice, suggesting different isoforms may play different roles in photoreceptors and underscores the importance of considering splice variants when generating targeted null mutations.
C1 [Won, Jungyeon; Gifford, Elaine; Smith, Richard S.; Hicks, Wanda L.; Naggert, Juergen K.; Nishina, Patsy M.] Jackson Lab, Bar Harbor, ME 04609 USA.
[Yi, Haiqing; Ferreira, Paulo A.] Duke Univ, Med Ctr, Dept Ophthalmol, Durham, NC 27710 USA.
[Ferreira, Paulo A.] Duke Univ, Med Ctr, Dept Mol Genet & Microbiol, Durham, NC 27710 USA.
[Li, Tiansen] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
RP Nishina, PM (reprint author), Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA.
EM patsy.nishina@jax.org
RI Ferreira, Paulo/S-4209-2016
OI Ferreira, Paulo/0000-0003-4585-1717
FU National Institutes of Health [EY016501, 2P30-EY005722-21]; TJL
institutional core grant [CA34196]
FX This study was supported by National Institutes of Health grant,
EY016501 (P.M.N.), National Institutes of Health core grant,
2P30-EY005722-21 (P.A.F.), a TJL institutional core grant, CA34196, and
the Jules & Doris Stein Research to Prevent Blindness Professor
(P.A.F.).
NR 49
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U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 15
PY 2009
VL 18
IS 22
BP 4329
EP 4339
DI 10.1093/hmg/ddp385
PG 11
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 510RB
UT WOS:000271107300009
PM 19679561
ER
PT J
AU Antoniou, AC
Sinilnikova, OM
McGuffog, L
Healey, S
Nevanlinna, H
Heikkinen, T
Simard, J
Spurdle, AB
Beesley, J
Chen, XQ
Neuhausen, SL
Ding, YC
Couch, FJ
Wang, XS
Fredericksen, Z
Peterlongo, P
Peissel, B
Bonanni, B
Viel, A
Bernard, L
Radice, P
Szabo, CI
Foretova, L
Zikan, M
Claes, K
Greene, MH
Mai, PL
Rennert, G
Lejbkowicz, F
Andrulis, IL
Ozcelik, H
Glendon, G
Gerdes, AM
Thomassen, M
Sunde, L
Caligo, MA
Laitman, Y
Kontorovich, T
Cohen, S
Kaufman, B
Dagan, E
Baruch, RG
Friedman, E
Harbst, K
Barbany-Bustinza, G
Rantala, J
Ehrencrona, H
Karlsson, P
Domchek, SM
Nathanson, KL
Osorio, A
Blanco, I
Lasa, A
Benitez, J
Hamann, U
Hogervorst, FBL
Rookus, MA
Collee, JM
Devilee, P
Ligtenberg, MJ
van der Luijt, RB
Aalfs, CM
Waisfisz, Q
Wijnen, J
van Roozendaal, CEP
Peock, S
Cook, M
Frost, D
Oliver, C
Platte, R
Evans, DG
Lalloo, F
Eeles, R
Izatt, L
Davidson, R
Chu, C
Eccles, D
Cole, T
Hodgson, S
Godwin, AK
Stoppa-Lyonnet, D
Buecher, B
Leone, M
Bressac-de Paillerets, B
Remenieras, A
Caron, O
Lenoir, GM
Sevenet, N
Longy, M
Ferrer, SF
Prieur, F
Goldgar, D
Miron, A
John, EM
Buys, SS
Daly, MB
Hopper, JL
Terry, MB
Yassin, Y
Singer, C
Gschwantler-Kaulich, D
Staudigl, C
Hansen, TVO
Barkardottir, RB
Kirchhoff, T
Pal, P
Kosarin, K
Offit, K
Piedmonte, M
Rodriguez, GC
Wakeley, K
Boggess, JF
Basil, J
Schwartz, PE
Blank, SV
Toland, AE
Montagna, M
Casella, C
Imyanitov, EN
Allavena, A
Schmutzler, RK
Versmold, B
Engel, C
Meindl, A
Ditsch, N
Arnold, N
Niederacher, D
Deissler, H
Fiebig, B
Suttner, C
Schonbuchner, I
Gadzicki, D
Caldes, T
de la Hoya, M
Pooley, KA
Easton, DF
Chenevix-Trench, G
AF Antoniou, Antonis C.
Sinilnikova, Olga M.
McGuffog, Lesley
Healey, Sue
Nevanlinna, Heli
Heikkinen, Tuomas
Simard, Jacques
Spurdle, Amanda B.
Beesley, Jonathan
Chen, Xiaoqing
Neuhausen, Susan L.
Ding, Yuan C.
Couch, Fergus J.
Wang, Xianshu
Fredericksen, Zachary
Peterlongo, Paolo
Peissel, Bernard
Bonanni, Bernardo
Viel, Alessandra
Bernard, Loris
Radice, Paolo
Szabo, Csilla I.
Foretova, Lenka
Zikan, Michal
Claes, Kathleen
Greene, Mark H.
Mai, Phuong L.
Rennert, Gad
Lejbkowicz, Flavio
Andrulis, Irene L.
Ozcelik, Hilmi
Glendon, Gord
Gerdes, Anne-Marie
Thomassen, Mads
Sunde, Lone
Caligo, Maria A.
Laitman, Yael
Kontorovich, Tair
Cohen, Shimrit
Kaufman, Bella
Dagan, Efrat
Baruch, Ruth Gershoni
Friedman, Eitan
Harbst, Katja
Barbany-Bustinza, Gisela
Rantala, Johanna
Ehrencrona, Hans
Karlsson, Per
Domchek, Susan M.
Nathanson, Katherine L.
Osorio, Ana
Blanco, Ignacio
Lasa, Adriana
Benitez, Javier
Hamann, Ute
Hogervorst, Frans B. L.
Rookus, Matti A.
Collee, J. Margriet
Devilee, Peter
Ligtenberg, Marjolijn J.
van der Luijt, Rob B.
Aalfs, Cora M.
Waisfisz, Quinten
Wijnen, Juul
van Roozendaal, Cornelis E. P.
Peock, Susan
Cook, Margaret
Frost, Debra
Oliver, Clare
Platte, Radka
Evans, D. Gareth
Lalloo, Fiona
Eeles, Rosalind
Izatt, Louise
Davidson, Rosemarie
Chu, Carol
Eccles, Diana
Cole, Trevor
Hodgson, Shirley
Godwin, Andrew K.
Stoppa-Lyonnet, Dominique
Buecher, Bruno
Leone, Melanie
Bressac-de Paillerets, Brigitte
Remenieras, Audrey
Caron, Olivier
Lenoir, Gilbert M.
Sevenet, Nicolas
Longy, Michel
Ferrer, Sandra Fert
Prieur, Fabienne
Goldgar, David
Miron, Alexander
John, Esther M.
Buys, Saundra S.
Daly, Mary B.
Hopper, John L.
Terry, Mary Beth
Yassin, Yosuf
Singer, Christian
Gschwantler-Kaulich, Daphne
Staudigl, Christine
Hansen, Thomas V. O.
Barkardottir, Rosa Bjork
Kirchhoff, Tomas
Pal, Prodipto
Kosarin, Kristi
Offit, Kenneth
Piedmonte, Marion
Rodriguez, Gustavo C.
Wakeley, Katie
Boggess, John F.
Basil, Jack
Schwartz, Peter E.
Blank, Stephanie V.
Toland, Amanda E.
Montagna, Marco
Casella, Cinzia
Imyanitov, Evgeny N.
Allavena, Anna
Schmutzler, Rita K.
Versmold, Beatrix
Engel, Christoph
Meindl, Alfons
Ditsch, Nina
Arnold, Norbert
Niederacher, Dieter
Deissler, Helmut
Fiebig, Britta
Suttner, Christian
Schoenbuchner, Ines
Gadzicki, Dorothea
Caldes, Trinidad
de la Hoya, Miguel
Pooley, Karen A.
Easton, Douglas F.
Chenevix-Trench, Georgia
CA Kathleen Cuningham Fdn Consortium
OCGN
HEBON
EMBRACE
GEMO
Breast Canc Family Registry
CIMBA
TI Common variants in LSP1, 2q35 and 8q24 and breast cancer risk for BRCA1
and BRCA2 mutation carriers
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; ESTROGEN-RECEPTOR; OVARIAN-CANCER;
SUSCEPTIBILITY; GENE; POPULATION; EXPRESSION; ALLELES
AB Genome-wide association studies of breast cancer have identified multiple single nucleotide polymorphisms (SNPs) that are associated with increased breast cancer risks in the general population. In a previous study, we demonstrated that the minor alleles at three of these SNPs, in FGFR2, TNRC9 and MAP3K1, also confer increased risks of breast cancer for BRCA1 or BRCA2 mutation carriers. Three additional SNPs rs3817198 at LSP1, rs13387042 at 2q35 and rs13281615 at 8q24 have since been reported to be associated with breast cancer in the general population, and in this study we evaluated their association with breast cancer risk in 9442 BRCA1 and 5665 BRCA2 mutation carriers from 33 study centres. The minor allele of rs3817198 was associated with increased breast cancer risk only for BRCA2 mutation carriers [hazard ratio (HR) = 1.16, 95% CI: 1.07-1.25, P-trend = 2.8 x 10(-4)]. The best fit for the association of SNP rs13387042 at 2q35 with breast cancer risk was a dominant model for both BRCA1 and BRCA2 mutation carriers (BRCA1: HR = 1.14, 95% CI: 1.04-1.25, P = 0.0047; BRCA2: HR = 1.18 95% CI: 1.04-1.33, P = 0.0079). SNP rs13281615 at 8q24 was not associated with breast cancer for either BRCA1 or BRCA2 mutation carriers, but the estimated association for BRCA2 mutation carriers (per-allele HR = 1.06, 95% CI: 0.98-1.14) was consistent with odds ratio estimates derived from population-based case-control studies. The LSP1 and 2q35 SNPs appear to interact multiplicatively on breast cancer risk for BRCA2 mutation carriers. There was no evidence that the associations vary by mutation type depending on whether the mutated protein is predicted to be stable or not.
C1 [Antoniou, Antonis C.; McGuffog, Lesley; Peock, Susan; Cook, Margaret; Frost, Debra; Oliver, Clare; Platte, Radka; Pooley, Karen A.; Easton, Douglas F.; EMBRACE] Univ Cambridge, Dept Publ Hlth & Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England.
[Sinilnikova, Olga M.; Leone, Melanie] Univ Lyon, CNRS, Hosp Civils Lyon,Ctr Leon Berard,UMR5201, Unite Mixte Genet Constitut Canc Frequents, Lyon, France.
[Healey, Sue; Spurdle, Amanda B.; Beesley, Jonathan; Chen, Xiaoqing; Chenevix-Trench, Georgia] Queensland Inst Med Res, Brisbane, Qld 4029, Australia.
[Nevanlinna, Heli; Heikkinen, Tuomas] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, FIN-00290 Helsinki, Finland.
[Simard, Jacques] Univ Laval, Quebec City, PQ, Canada.
[Simard, Jacques] Univ Quebec, Ctr Hosp, Canada Res Chair Oncogenet, Canc Genom Lab, Quebec City, PQ, Canada.
[Kathleen Cuningham Fdn Consortium] Peter MacCallum Canc Inst, Melbourne, Vic 3002, Australia.
[Neuhausen, Susan L.; Ding, Yuan C.] Univ Calif Irvine, Dept Epidemiol, Irvine, CA USA.
[Couch, Fergus J.; Wang, Xianshu; Fredericksen, Zachary] Mayo Clin, Rochester, MN USA.
[Peterlongo, Paolo; Peissel, Bernard; Radice, Paolo] Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
[Peterlongo, Paolo; Radice, Paolo] Fdn Ist FIRC Oncol Molecolare, Milan, Italy.
[Bonanni, Bernardo; Bernard, Loris] Ist Europeo Oncol, Milan, Italy.
[Viel, Alessandra] IRCCS, Ctr Riferimento Oncol, Aviano, Italy.
[Bernard, Loris] Cogentech, Consortium Genom Technol, Milan, Italy.
[Szabo, Csilla I.] Mayo Clin, Coll Med, Dept Lab Med & Pathol, Rochester, MN USA.
[Foretova, Lenka] Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic.
[Zikan, Michal] Charles Univ Prague, Dept Biochem & Expt Oncol, Fac Med 1, Prague, Czech Republic.
[Claes, Kathleen] Ghent Univ Hosp, Ctr Med Genet, B-9000 Ghent, Belgium.
[Greene, Mark H.; Mai, Phuong L.] US Natl Canc Inst, Clin Genet Branch, Rockville, MD USA.
[Rennert, Gad; Lejbkowicz, Flavio] CHS Natl Canc Control Ctr, Haifa, Israel.
[Rennert, Gad; Lejbkowicz, Flavio] Carmel Hosp, Dept Community Med & Epidemiol, Haifa, Israel.
[Rennert, Gad; Lejbkowicz, Flavio] B Rappaport Fac Med, Haifa, Israel.
[Andrulis, Irene L.; Glendon, Gord; OCGN] Canc Care Ontario, Ontario Canc Genet Network, Toronto, ON M5G 2L7, Canada.
[Andrulis, Irene L.] Mt Sinai Hosp, Fred A Litwin Ctr Canc Genet, Samuel Lunenfeld Res Inst, Toronto, ON, Canada.
[Andrulis, Irene L.] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
[Gerdes, Anne-Marie; Thomassen, Mads] Odense Univ Hosp, Dept Biochem Pharmacol & Genet, DK-5000 Odense, Denmark.
[Sunde, Lone] Aarhus Univ Hosp, Dept Clin Genet, DK-8000 Aarhus, Denmark.
[Caligo, Maria A.] Univ Pisa, Div Surg Mol & Ultrastructural Pathol, Dept Oncol, Pisa, Italy.
[Caligo, Maria A.] Pisa Univ Hosp, Pisa, Italy.
[Laitman, Yael; Kontorovich, Tair; Cohen, Shimrit; Friedman, Eitan] Chaim Sheba Med Ctr, Susanne Levy Gertner Oncogenet Unit, IL-52621 Tel Hashomer, Israel.
[Kaufman, Bella] Chaim Sheba Med Ctr, Inst Oncol, IL-52621 Tel Hashomer, Israel.
[Kaufman, Bella; Friedman, Eitan] Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel.
[Dagan, Efrat; Baruch, Ruth Gershoni] Rambam Med Ctr, Genet Inst, Haifa, Israel.
[Harbst, Katja] Lund Univ, Dept Oncol, S-22100 Lund, Sweden.
[Barbany-Bustinza, Gisela; Rantala, Johanna] Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden.
[Ehrencrona, Hans] Uppsala Univ, Dept Genet & Pathol, Uppsala, Sweden.
[Karlsson, Per] Sahlgrenska Univ, Dept Oncol, Gothenburg, Sweden.
[Domchek, Susan M.; Nathanson, Katherine L.] Univ Penn, Philadelphia, PA 19104 USA.
[Osorio, Ana; Benitez, Javier] Ctr Invest Biomed Red Enfermedades Raras CIBERERE, Inst Salud Carlos III, Madrid, Spain.
[Osorio, Ana; Benitez, Javier] Spanish Natl Canc Ctr CNIO, Human Canc Genet Programme, Human Genet Grp, Madrid, Spain.
[Blanco, Ignacio] Catalan Inst Oncol ICO, Canc Genet Counseling Program, Barcelona, Spain.
[Lasa, Adriana] Hosp Santa Creu & Sant Pau, Genet Serv, Barcelona, Spain.
[Hamann, Ute] Deutsch Krebsforschungszentrum, Neuenheimer Feld 580 69120, D-6900 Heidelberg, Germany.
[Hogervorst, Frans B. L.] Netherlands Canc Inst, Dept Pathol, Family Canc Clin, NL-1066 CX Amsterdam, Netherlands.
[Rookus, Matti A.] Netherlands Canc Inst, Dept Epidemiol, Amsterdam, Netherlands.
[Collee, J. Margriet] Erasmus Univ, Dept Clin Genet, Rotterdam Family Canc Clin, Med Ctr, NL-3000 DR Rotterdam, Netherlands.
[Devilee, Peter] Dept Genet Epidemiol, Leiden, Netherlands.
[Wijnen, Juul] Leiden Univ, Med Ctr, Ctr Human & Clin Genet, Leiden, Netherlands.
[Ligtenberg, Marjolijn J.] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, NL-6525 ED Nijmegen, Netherlands.
[van der Luijt, Rob B.] Univ Utrecht, Med Ctr, Dept Clin Mol Genet, NL-3508 TC Utrecht, Netherlands.
[Aalfs, Cora M.] Univ Amsterdam, Acad Med Ctr, Dept Clin Genet, NL-1105 AZ Amsterdam, Netherlands.
[Waisfisz, Quinten] Vrije Univ Amsterdam, Med Ctr, Dept Clin Genet, Amsterdam, Netherlands.
[van Roozendaal, Cornelis E. P.] Univ Med Ctr, Dept Clin Genet, Maastricht, Netherlands.
[Evans, D. Gareth; Lalloo, Fiona] Cent Manchester Univ Hosp, NHS Fdn Trust, Manchester Acad Hlth Sci Ctr, Manchester, Lancs, England.
[Eeles, Rosalind] Inst Canc Res, Translat Canc Genet Team, London SW3 6JB, England.
[Eeles, Rosalind] Royal Marsden NHS Fdn Trust, London, England.
[Izatt, Louise] Guys Hosp, Clin Genet, London SE1 9RT, England.
[Davidson, Rosemarie] Ferguson Smith Ctr Clin Genet, Glasgow, Lanark, Scotland.
[Chu, Carol] Yorkshire Reg Genet Serv, Leeds, W Yorkshire, England.
[Eccles, Diana] Princess Anne Hosp, Wessex Clin Genet Serv, Southampton, Hants, England.
[Cole, Trevor] Birmingham Womens Hosp Healthcare, NHS Trust, W Midlands Reg Genet Serv, Birmingham, W Midlands, England.
[Hodgson, Shirley] Univ London, Dept Canc Genet, St Georges Hosp, London, England.
[Godwin, Andrew K.; Daly, Mary B.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Stoppa-Lyonnet, Dominique] Univ Paris 05, Paris, France.
[Stoppa-Lyonnet, Dominique; GEMO] Inst Curie, INSERM U509, Serv Genet Oncol, Paris, France.
[Buecher, Bruno] Inst Curie, Dept Genet, Paris, France.
[Bressac-de Paillerets, Brigitte; Remenieras, Audrey; Lenoir, Gilbert M.] Inst Cancrol Gustave Roussy, Dept Genet, Villejuif, France.
[Bressac-de Paillerets, Brigitte] Inst Cancerol Gustave Roussy, INSERM U946, Villejuif, France.
[Caron, Olivier] Inst Cancerol Gustave Roussy, Dept Med, Villejuif, France.
[Lenoir, Gilbert M.] Inst Cancerol Gustave Roussy, CNRS FRE2939, Villejuif, France.
[Sevenet, Nicolas; Longy, Michel] Inst Bergonie, Lab Genet Constitutionnelle, Bordeaux, France.
[Longy, Michel] Inst Bergonie, INSERM U916, Bordeaux, France.
[Ferrer, Sandra Fert] Hop Hotel Dieu, Ctr Hosp, Lab Genet Chromosom, Chambery, France.
[Prieur, Fabienne] CHU St Etienne, Serv Genet Clin Chromosom, St Etienne, France.
[Goldgar, David] Univ Utah, Dept Dermatol, Salt Lake City, UT 84112 USA.
[Miron, Alexander; Yassin, Yosuf] Dana Farber Canc Inst, Boston, MA 02115 USA.
[John, Esther M.] No Calif Canc Ctr, Fremont, CA USA.
[John, Esther M.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Buys, Saundra S.] Univ Utah, Hlth Sci Ctr, Huntsman Canc Inst, Salt Lake City, UT USA.
[Hopper, John L.] Univ Melbourne, Melbourne, Australia.
[Terry, Mary Beth] Columbia Univ, New York, NY USA.
[Singer, Christian; Gschwantler-Kaulich, Daphne; Staudigl, Christine] Med Univ Vienna, Div Special Gynecol, Dept OB GYN, Vienna, Austria.
[Hansen, Thomas V. O.] Univ Copenhagen, Rigshosp, Dept Clin Biochem, DK-2100 Copenhagen, Denmark.
[Barkardottir, Rosa Bjork] Landspitali Univ Hosp, Dept Pathol, Reykjavik, Iceland.
[Kirchhoff, Tomas; Pal, Prodipto; Kosarin, Kristi; Offit, Kenneth] Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, New York, NY 10021 USA.
[Piedmonte, Marion] Roswell Pk Canc Inst, GOG Stat & Data Ctr, Buffalo, NY 14263 USA.
[Rodriguez, Gustavo C.] Evanston NW Healthcare, NorthShore Univ Hlth Syst, Evanston, IL 60201 USA.
[Wakeley, Katie] Tufts Univ, New England Med Ctr, Boston, MA 02111 USA.
[Boggess, John F.] Univ N Carolina, Chapel Hill, NC 27599 USA.
[Basil, Jack] St Elizabeth Hosp, Edgewood, KY 41017 USA.
[Schwartz, Peter E.] Yale Univ, Sch Med, New Haven, CT 06510 USA.
[Blank, Stephanie V.] NYU, Sch Med, New York, NY 10016 USA.
[Toland, Amanda E.] Ohio State Univ, Dept Internal Med, Columbus, OH 43210 USA.
[Toland, Amanda E.] Ohio State Univ, Div Human Canc Genet, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Montagna, Marco; Casella, Cinzia] IRCCS, Ist Oncologico Veneto, Immunol & Mol Oncol Unit, Padua, Italy.
[Imyanitov, Evgeny N.] NN Petrov Inst Res Inst, St Petersburg, Russia.
[Allavena, Anna] Univ Turin, Dept Genet Biol & Biochem, Turin, Italy.
[Schmutzler, Rita K.; Versmold, Beatrix; Arnold, Norbert] Univ Cologne, Dept Obstet & Gynaecol, Div Mol Gynaeco Oncol, Cologne, Germany.
[Engel, Christoph] Univ Leipzig, Inst Med Informat Stat & Epidemiol, Leipzig, Germany.
[Meindl, Alfons] Tech Univ Munich, Dept Obstet & Gynaecol, Munich, Germany.
[Ditsch, Nina] Univ Munich, Dept Obstet & Gynecol, Munich, Germany.
Univ Schleswig Holstein, Dept Obstet & Gynaecol, Campus Kiel, Germany.
[Niederacher, Dieter] Univ Duesseldorf, Dept Obstet & Gynaecol, Mol Genet Lab, Dusseldorf, Germany.
[Deissler, Helmut] Univ Ulm, Dept Obstet & Gynaecol, Ulm, Germany.
[Fiebig, Britta] Univ Regensburg, Inst Human Genet, Regensburg, Germany.
[Suttner, Christian] Univ Heidelberg, Inst Human Genet, Heidelberg, Germany.
[Schoenbuchner, Ines] Univ Wurzburg, Inst Human Genet, D-8700 Wurzburg, Germany.
[Gadzicki, Dorothea] Med Univ, Inst Cellular & Mol Pathol, Hannover, Germany.
[Caldes, Trinidad; de la Hoya, Miguel] Hosp Clinico San Carlos 28040, Madrid, Spain.
RP Antoniou, AC (reprint author), Strangeways Res Lab, CR UK Genet Epidemiol, Cambridge CB1 8RN, England.
EM antonis@srl.cam.ac.uk
RI Spurdle, Amanda/A-4978-2011; Ehrencrona, Hans/M-5619-2014; Arnold,
Norbert/E-3012-2010; Toland, Amanda/E-4202-2011; montagna,
marco/E-2225-2012; Andrulis, Irene/E-7267-2013; Sunde, Lone/H-7402-2013;
Hoogerbrugge, Nicoline/O-1016-2013; Radice, Paolo/O-3119-2013; Blanco,
Ignacio/D-2565-2013; Ditsch, Nina/F-6267-2014; Osorio, Ana/I-4324-2014;
Bernard, Loris/K-5953-2014; GLADIEFF, Laurence/O-5129-2014; Ligtenberg,
Marjolijn/N-9666-2013; Peissel, Bernard/E-8187-2017;
OI Spurdle, Amanda/0000-0003-1337-7897; Ehrencrona,
Hans/0000-0002-5589-3622; Arnold, Norbert/0000-0003-4523-8808; montagna,
marco/0000-0002-4929-2150; Blanco, Ignacio/0000-0002-7414-7481; Osorio,
Ana/0000-0001-8124-3984; GLADIEFF, Laurence/0000-0002-6980-9719;
Ligtenberg, Marjolijn/0000-0003-1290-1474; Peissel,
Bernard/0000-0001-9233-3571; Nordling, Margareta/0000-0002-4047-4994;
Nathanson, Katherine/0000-0002-6740-0901; Eeles,
Rosalind/0000-0002-3698-6241; Sunde, Lone/0000-0002-8479-165X;
Nevanlinna, Heli/0000-0002-0916-2976; Kirchhoff,
Tomas/0000-0002-9055-2364; Evans, Gareth/0000-0002-8482-5784
FU Cancer Research UK; Associazione Italiana per la Ricerca sul Cancro
FX The CIMBA genotyping, data management and statistical analysis are
supported by Cancer Research UK. A.C.A. is a Cancer Research UK Senior
Cancer Research Fellow. We thank Ellen Goode for organizing the
distribution of the standard DNA plates.
NR 26
TC 72
Z9 74
U1 4
U2 22
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 15
PY 2009
VL 18
IS 22
BP 4442
EP 4456
DI 10.1093/hmg/ddp372
PG 15
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 510RB
UT WOS:000271107300019
PM 19656774
ER
PT J
AU Videtic, GMM
Gaspar, LE
Aref, AM
Germano, IM
Goldsmith, BJ
Imperato, JP
Marcus, KJ
McDermott, MW
McDonald, MW
Patchell, RA
Robins, HI
Rogers, CL
Suh, JH
Wolfson, AH
Wippold, FJ
AF Videtic, Gregory M. M.
Gaspar, Laurie E.
Aref, Amr M.
Germano, Isabelle M.
Goldsmith, Brian J.
Imperato, Joseph P.
Marcus, Karen J.
McDermott, Michael W.
McDonald, Mark W.
Patchell, Roy A.
Robins, H. Ian
Rogers, C. Leland
Suh, John H.
Wolfson, Aaron H.
Wippold, Franz J.
CA Expert Panel Radiation Oncology
TI AMERICAN COLLEGE OF RADIOLOGY APPROPRIATENESS CRITERIA ON MULTIPLE BRAIN
METASTASES
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Appropriateness criteria; Multiple brain metastases; Whole-brain
radiotherapy; Radiosurgery; Surgery
ID THERAPY ONCOLOGY GROUP; RANDOMIZED CLINICAL-TRIAL; RADIATION-THERAPY;
PHASE-III; STEREOTACTIC RADIOSURGERY; NEUROCOGNITIVE FUNCTION; MOTEXAFIN
GADOLINIUM; PROGNOSTIC-FACTORS; RADIOTHERAPY; RTOG
C1 [Videtic, Gregory M. M.] Cleveland Clin Fdn, Dept Radiat Oncol T28, Cleveland, OH 44195 USA.
[Gaspar, Laurie E.] Univ Colorado Denver, Aurora, CO USA.
[Aref, Amr M.] Van Elslander Canc Ctr, Grosse Point, MI USA.
[Germano, Isabelle M.] Mt Sinai Sch Med, New York, NY USA.
[Goldsmith, Brian J.] Radiol Associates Sacramento, Sacramento, CA USA.
[Imperato, Joseph P.] Lake Forest Hosp, Lake Forest, IL USA.
[Marcus, Karen J.] Harvard Univ, Childrens Hosp, Sch Med, Dana Farber Canc Ctr, Boston, MA 02115 USA.
[McDermott, Michael W.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[McDonald, Mark W.] Emory Univ, Atlanta, GA 30322 USA.
[Patchell, Roy A.] Barrow Neurol Inst, Phoenix, AZ 85013 USA.
[Robins, H. Ian] Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, Madison, WI USA.
[Rogers, C. Leland] GammaW Brachytherapy, Salt Lake City, UT USA.
[Wolfson, Aaron H.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Wippold, Franz J.] Washington Univ, Sch Med, St Louis, MO USA.
RP Videtic, GMM (reprint author), Cleveland Clin Fdn, Dept Radiat Oncol T28, 9500 Euclid Ave, Cleveland, OH 44195 USA.
EM videtig@ccf.org
NR 34
TC 19
Z9 20
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 15
PY 2009
VL 75
IS 4
BP 961
EP 965
DI 10.1016/j.ijrobp.2009.07.1720
PG 5
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 515RF
UT WOS:000271489600001
ER
PT J
AU Rodrigues, NA
Killion, L
Hickey, G
Silver, B
Martin, C
Stevenson, MA
Mauch, PM
Ng, AK
AF Rodrigues, Neesha A.
Killion, Leah
Hickey, Gail
Silver, Barbara
Martin, Chrystalla
Stevenson, Mary Ann
Mauch, Peter M.
Ng, Andrea K.
TI A PROSPECTIVE STUDY OF SALIVARY GLAND FUNCTION IN LYMPHOMA PATIENTS
RECEIVING HEAD AND NECK IRRADIATION
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Lymphoma; Head and neck; Quality of Life; Xerostomia; Amifostine
ID INTENSITY-MODULATED RADIOTHERAPY; STAGE NASOPHARYNGEAL CARCINOMA;
DOSE-RESPONSE RELATIONSHIPS; MANTLE FIELD RADIOTHERAPY;
RADIATION-THERAPY; PAROTID-GLAND; HODGKINS-DISEASE; PHASE-II; CANCER;
AMIFOSTINE
AB Purpose: To determine the radiation dose-response relationship on salivary dysfunction and quality of life (QOL) over time in patients With lymphoma receiving radiation therapy (RT) to the head and neck (H&N).
Methods and Materials: We conducted a prospective study on salivary-gland function in lymphoma patients jeceiving RT to the H&N. Fifteen patients were enrolled on the study. Dose-volume histograms and mean doses to the salivary glands were generated. Radiation-related toxicities and H&N-specific QOL were assessed before treatment and at prespecified time points posttreatment. Factors predicting a decrement in QOL were explored using Fisher's exact test.
Results: During RT, 47% of patients experienced Grade >= 2 acute toxicity of the salivary gland, mucous membrane, or both. QOL scores improved over time, but up to one third of patients continued to have persistent oral symptoms at 2 years. At 6 months, a mean dose to at least one of the parotids of > 31 Gy was significantly associated with persistent dry mouth (100% vs. 17%, p = 0.02) and sticky saliva (100% vs. 25 %, p = 0.04); a mean dose of > I I Gy to the minor salivary glands was significantly associated with persistent sticky saliva (100% vs. 25 %, p = 0.04), although the difference was no longer significant at 1 year.
Conclusions: Limiting the mean parotid dose to <= 31 Gy and mean minor salivary gland dose to <= 11 Gy in lymphoma patients treated to the H&N may help reduce the risk of subacute xerostomia. (C) 2009 Elsevier Inc.
C1 [Rodrigues, Neesha A.; Killion, Leah; Hickey, Gail; Silver, Barbara; Mauch, Peter M.; Ng, Andrea K.] Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
[Martin, Chrystalla; Stevenson, Mary Ann] Beth Israel Deaconess Med Ctr, Dept Radiat Oncol, Boston, MA 02215 USA.
RP Ng, AK (reprint author), 75 Francis St,ASB1-L2, Boston, MA 02115 USA.
EM ang@lroc.harvard.edu
FU MedImmune, Inc.
FX MedImmune, Inc., provided partial salary support for one of the research
nurses in this study (G.H.).
NR 23
TC 7
Z9 8
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 15
PY 2009
VL 75
IS 4
BP 1079
EP 1083
DI 10.1016/j.ijrobp.2008.12.053
PG 5
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 515RF
UT WOS:000271489600019
PM 19327910
ER
PT J
AU Sperduto, CM
Chakravarti, A
Aldape, K
Burger, P
Papermaster, GB
Sperduto, P
AF Sperduto, Christina Maria
Chakravarti, Arnab
Aldape, Ken
Burger, Peter
Papermaster, Gail Bender
Sperduto, Paul
TI TWENTY-YEAR SURVIVAL IN GLIOBLASTOMA: A CASE REPORT AND MOLECULAR
PROFILE
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Glioblastoma; Molecular Profile; Survival; Outcomes
ID LONG-TERM SURVIVORS; PROGNOSTIC-SIGNIFICANCE; MALIGNANT GLIOMA;
MULTIFORME; RADIOTHERAPY; TEMOZOLOMIDE
AB Background: The prognosis for patients with glioblastoma (GB) remains grim. Historically, the median survival has been 6 to 9 months. Recent research has improved the outcome slightly. A computer search of the literature reveals few long-term survivors.
Method: Presented here is a case report of a 20-year survivor of GB, with pathologic review to confirm the diagnosis. A battery of molecular studies was performed to develop a molecular profile of this unique patient.
Results: The results of the molecular genetic testing for this most unusual patient were as follows: (1) methylguanine methyl transferase (MGMT) was methylated, (2) p53 positive, (3) PTEN tumor suppressor gene positive, (4) protein kinase AKT (pAKT) negative, and (5) epidermal growth factor receptor negative.
Conclusion: To our knowledge, this is the longest survival of any patient in the literature whose initial diagnosis was GB. Triple-positive GBM patients (MGMT methylated, PTEN, and p53 positive) are uncommon but may be associated with a better prognosis. Further research is needed to confirm whether this molecular profile is prognostic of prolonged survival. Molecular genetics will determine future treatment and prognosis in GB. (C) 2009 Elsevier Inc.
C1 [Sperduto, Paul] Univ Minnesota, Gamma Knife Ctr, Dept Radiat Oncol, Med Ctr, Minneapolis, MN 55113 USA.
[Sperduto, Christina Maria] Minneapolis Radiat Oncol, Res Associate, Minneapolis, MN USA.
[Chakravarti, Arnab] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Aldape, Ken] UT MD Anderson Canc Ctr, Dept Pathol, Houston, TX USA.
[Burger, Peter] Johns Hopkins Sch Med, Div Neuropathol, Baltimore, MD USA.
[Papermaster, Gail Bender] Ridgeview Med Ctr, Dept Med Oncol, Waconia, MN USA.
RP Sperduto, P (reprint author), Univ Minnesota, Gamma Knife Ctr, Dept Radiat Oncol, Med Ctr, 420 Delaware St,MMC 494, Minneapolis, MN 55113 USA.
EM psperduto@mropa.com
NR 16
TC 9
Z9 9
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 15
PY 2009
VL 75
IS 4
BP 1162
EP 1165
DI 10.1016/j.ijrobp.2008.12.054
PG 4
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 515RF
UT WOS:000271489600031
PM 19327897
ER
PT J
AU Arvold, ND
Lessell, S
Bussiere, M
Beaudette, K
Rizzo, JF
Loeffler, JS
Shih, HA
AF Arvold, Nils D.
Lessell, Simmons
Bussiere, Marc
Beaudette, Kevin
Rizzo, Joseph F.
Loeffler, Jay S.
Shih, Helen A.
TI VISUAL OUTCOME AND TUMOR CONTROL AFTER CONFORMAL RADIOTHERAPY FOR
PATIENTS WITH OPTIC NERVE SHEATH MENINGIOMA
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Optic nerve sheath meningioma; Vision; Local control; Radiotherapy;
Proton
ID FRACTIONATED STEREOTACTIC RADIOTHERAPY; RADIATION-THERAPY; MANAGEMENT;
SURGERY; PROTON; BEAMS
AB Purpose: Optic nerve sheath meningioma (ONSM) is a rare tumor that almost uniformly leads to visual dysfunction and even blindness without intervention. Because surgical extirpation carries a high risk of postoperative blindness, vision-sparing treatment strategies are desirable.
Methods and Materials: We retrospectively reviewed the outcomes of 25 patients (25 optic nerves) with ONSM, treated at a single institution with conformal fractionated radiotherapy by either stereotactic photon or proton radiation. Primary endpoints were local control and visual acuity.
Results: The patients presented with symptoms of visual loss (21) or orbital pain (3) or were incidentally diagnosed by imaging (3). The mean age was 44 years, and 64% were female patients. The indication for treatment was the development or progression of symptoms. Of the patients, 13 were treated with photons, 9 were treated with protons, and 3 received a combination of photons and protons. The median dose delivered was 50.4 gray equivalents (range, 45-59.4 gray equivalents). Median follow-up after radiotherapy was 30 months (range, 3-168 months), with 3 patients lost to follow-up. At most recent follow-up, 21 of 22 patients (95%) had improved (14) or stable (7) visual acuity. One patient had worsened visual acuity after initial postirradiation improvement. Of the 22 patients, 20 (95%) had no radiographic progression. Three patients had evidence of asymptomatic, limited retinopathy on ophthalmologic examination, and one had recurrent ONSM 11 years after treatment.
Conclusions: Highly conformal, fractionated radiation therapy for symptomatic primary ONSM provides tumor control and improvement in visual function in most cases, with minimal treatment-induced morbidity. Longer follow-up is needed to assess the durability of tumor control and treatment-related late effects. (C) 2009 Elsevier Inc.
C1 [Arvold, Nils D.] Massachusetts Gen Hosp, Harvard Radiat Oncol Program, Boston, MA 02114 USA.
[Arvold, Nils D.; Bussiere, Marc; Beaudette, Kevin; Loeffler, Jay S.; Shih, Helen A.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Lessell, Simmons; Rizzo, Joseph F.] Massachusetts Eye & Ear Infirm, Dept Neuroophthalmol, Boston, MA 02114 USA.
[Arvold, Nils D.; Lessell, Simmons; Bussiere, Marc; Beaudette, Kevin; Rizzo, Joseph F.; Loeffler, Jay S.; Shih, Helen A.] Harvard Univ, Sch Med, Boston, MA USA.
RP Arvold, ND (reprint author), Massachusetts Gen Hosp, Harvard Radiat Oncol Program, 100 Blossom St,Cox 3, Boston, MA 02114 USA.
EM narvold@partners.org
NR 23
TC 28
Z9 28
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 15
PY 2009
VL 75
IS 4
BP 1166
EP 1172
DI 10.1016/j.ijrobp.2008.12.056
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 515RF
UT WOS:000271489600032
PM 19406585
ER
PT J
AU Dai, J
Kateneva, AV
Higgins, JMG
AF Dai, Jun
Kateneva, Anna V.
Higgins, Jonathan M. G.
TI Studies of haspin-depleted cells reveal that spindle-pole integrity in
mitosis requires chromosome cohesion
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE Chromosome cohesion; Centrosome; Mitosis; Gsg2 Spindle assembly;
Kinesin-5
ID SISTER-CHROMATID COHESION; XENOPUS EGG EXTRACTS; MAMMALIAN-CELLS;
MITOTIC SPINDLE; AURORA-A; CENTROMERIC COHESION; MOTOR PROTEINS;
GAMMA-TUBULIN; KINETOCHORE; MICROTUBULES
AB Cohesins and their regulators are vital for normal chromosome cohesion and segregation. A number of cohesion proteins have also been localized to centrosomes and proposed to function there. We show that RNAi-mediated depletion of factors required for cohesion, including haspin, Sgo1 and Scc1, leads to the generation of multiple acentriolar centrosome-like foci and disruption of spindle structure in mitosis. Live-cell imaging reveals that, in haspin-depleted cells, these effects occur only as defects in chromosome cohesion become manifest, and they require ongoing microtubule dynamics and kinesin-5 (also known as Eg5) activity. Inhibition of topoisomerase Pi in mitosis, which prevents decatenation and separation of chromatids, circumvents the loss of cohesion and restores integrity of the spindle poles. Although these results do not rule out roles for cohesin proteins at centrosomes, they suggest that when cohesion is compromised, spindle-pole integrity can be disrupted as an indirect consequence of the failure to properly integrate chromosome-and centrosome-initiated pathways for spindle formation.
C1 [Dai, Jun; Kateneva, Anna V.; Higgins, Jonathan M. G.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA.
RP Dai, J (reprint author), Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA.
EM jdai@partners.org; jhiggins@rics.bwh.harvard.edu
RI Dai, Jun/J-9718-2015
FU NIGMS NIH HHS [R01 GM074210, R01 GM074210-04]
NR 52
TC 27
Z9 27
U1 0
U2 4
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD NOV 15
PY 2009
VL 122
IS 22
BP 4168
EP 4176
DI 10.1242/jcs.054122
PG 9
WC Cell Biology
SC Cell Biology
GA 518HJ
UT WOS:000271681300018
PM 19910498
ER
PT J
AU Nguyen, DP
Wilson, MA
Brown, EN
Barbieri, R
AF Nguyen, David P.
Wilson, Matthew A.
Brown, Emery N.
Barbieri, Riccardo
TI Measuring instantaneous frequency of local field potential oscillations
using the Kalman smoother
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE Autoregressive model; Kalman smoother; Frequency modulation; Adaptive
filter; Hippocampus; Ripple oscillation
ID SLOW-WAVE SLEEP; TIME-SERIES; IN-VITRO; EEG; STATE; HIPPOCAMPUS; RAT;
NETWORKS; TRACKING; RIPPLES
AB Rhythmic local field potentials (LFPs) arise from coordinated neural activity. Inference of neural function based on the properties of brain rhythms remains a challenging data analysis problem. Algorithms that characterize non-stationary rhythms with high temporal and spectral resolution may be useful for interpreting LFP activity on the timescales in which they are generated. We propose a Kalman smoother based dynamic autoregressive model for tracking the instantaneous frequency (iFreq) and frequency modulation (FM) of noisy and non-stationary sinusoids such as those found in LFP data. We verify the performance of our algorithm using simulated data with broad spectral content, and demonstrate its application using real data recorded from behavioral learning experiments. In analyses of ripple oscillations (100-250 Hz) recorded from the rodent hippocampus, our algorithm identified novel repetitive, short timescale frequency dynamics. Our results suggest that iFreq and FM may be useful measures for the quantification of small timescale LFP dynamics. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Nguyen, David P.] MIT, Dept Brain & Cognit Sci, Picower Inst Learning & Memory, Cambridge, MA 02139 USA.
[Brown, Emery N.; Barbieri, Riccardo] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
[Brown, Emery N.; Barbieri, Riccardo] MIT, Dept Hlth & Sci Technol, Boston, MA 02139 USA.
RP Nguyen, DP (reprint author), MIT, Dept Brain & Cognit Sci, Picower Inst Learning & Memory, Bldg 46,Room 5233,43 Vassar St, Cambridge, MA 02139 USA.
EM dpnguyen@neurostat.mit.edu; mwilson@mit.edu; enb@neurostat.mit.edu;
barbieri@neurostat.mit.edu
OI Barbieri, Riccardo/0000-0001-9381-3833
FU NIH/NIMH [R01 MH59733]; NIH/NIHLB [R01 HL084502]; Singleton Graduate
Student Fellowship
FX This work was funded in part by the following grants: NIH/NIMH R01
MH59733, NIH/NIHLB R01 HL084502, and the Singleton Graduate Student
Fellowship. We thank members of the Wilson Lab, Brown Lab, and Tonegawa
Lab for helpful comments.
NR 47
TC 10
Z9 10
U1 0
U2 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0270
J9 J NEUROSCI METH
JI J. Neurosci. Methods
PD NOV 15
PY 2009
VL 184
IS 2
BP 365
EP 374
DI 10.1016/j.jneumeth.2009.08.012
PG 10
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 521IN
UT WOS:000271914400021
PM 19699763
ER
PT J
AU Li, XY
Standley, C
Sapp, E
Valencia, A
Qin, ZH
Kegel, KB
Yoder, J
Comer-Tierney, LA
Esteves, M
Chase, K
Alexander, J
Masso, N
Sobin, L
Bellve, K
Tuft, R
Lifshitz, L
Fogarty, K
Aronin, N
DiFiglia, M
AF Li, Xueyi
Standley, Clive
Sapp, Ellen
Valencia, Antonio
Qin, Zheng-Hong
Kegel, Kimberly B.
Yoder, Jennifer
Comer-Tierney, Laryssa A.
Esteves, Miguel
Chase, Kathryn
Alexander, Jonathan
Masso, Nicholas
Sobin, Lindsay
Bellve, Karl
Tuft, Richard
Lifshitz, Lawrence
Fogarty, Kevin
Aronin, Neil
DiFiglia, Marian
TI Mutant Huntingtin Impairs Vesicle Formation from Recycling Endosomes by
Interfering with Rab11 Activity
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID PERIPHERAL-BLOOD CELLS; PLASMA-MEMBRANE; AXONAL-TRANSPORT; INTRACELLULAR
TRAFFICKING; ENDOCYTIC PATHWAY; IN-VITRO; DISEASE; PROTEIN; NEURONS;
DROSOPHILA
AB Huntingtin (Htt) localizes to endosomes, but its role in the endocytic pathway is not established. Recently, we found that Htt is important for the activation of Rab11, a GTPase involved in endosomal recycling. Here we studied fibroblasts of healthy individuals and patients with Huntington's disease (HD), which is a movement disorder caused by polyglutamine expansion in Htt. The formation of endocytic vesicles containing transferrin at plasma membranes was the same in control and HD patient fibroblasts. However, HD fibroblasts were delayed in recycling biotin-transferrin back to the plasma membrane. Membranes of HD fibroblasts supported less nucleotide exchange on Rab11 than did control membranes. Rab11-positive vesicular and tubular structures in HD fibroblasts were abnormally large, suggesting that they were impaired in forming vesicles. We used total internal reflection fluorescence imaging of living fibroblasts to monitor fluorescence-labeled transferrin-carrying transport intermediates that emerged from recycling endosomes. HD fibroblasts had fewer small vesicles and more large vesicles and long tubules than did control fibroblasts. Dominant active Rab11 expressed in HD fibroblasts normalized the recycling of biotin-transferrin. We propose a novel mechanism for cellular dysfunction by the HD mutation arising from the inhibition of Rab11 activity and a deficit in vesicle formation at recycling endosomes.
C1 [Chase, Kathryn; Aronin, Neil] Univ Massachusetts, Sch Med, Dept Med & Cell Biol, Worcester, MA 01655 USA.
[Li, Xueyi; Sapp, Ellen; Valencia, Antonio; Qin, Zheng-Hong; Kegel, Kimberly B.; Yoder, Jennifer; Comer-Tierney, Laryssa A.; Esteves, Miguel; Alexander, Jonathan; Masso, Nicholas; Sobin, Lindsay; DiFiglia, Marian] Massachusetts Gen Hosp, Cellular Neurobiol Lab, Charlestown, MA 02129 USA.
[Li, Xueyi; Sapp, Ellen; Valencia, Antonio; Qin, Zheng-Hong; Kegel, Kimberly B.; Yoder, Jennifer; Comer-Tierney, Laryssa A.; Esteves, Miguel; Alexander, Jonathan; Masso, Nicholas; Sobin, Lindsay; DiFiglia, Marian] Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA 02129 USA.
[Li, Xueyi; Sapp, Ellen; Valencia, Antonio; Qin, Zheng-Hong; Kegel, Kimberly B.; Yoder, Jennifer; Comer-Tierney, Laryssa A.; Esteves, Miguel; Alexander, Jonathan; Masso, Nicholas; Sobin, Lindsay; DiFiglia, Marian] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Standley, Clive; Bellve, Karl; Tuft, Richard; Lifshitz, Lawrence; Fogarty, Kevin] Univ Massachusetts, Sch Med, Biomed Imaging Grp, Dept Physiol, Worcester, MA 01655 USA.
RP Aronin, N (reprint author), Univ Massachusetts, Sch Med, Dept Med & Cell Biol, Worcester, MA 01655 USA.
EM Neil.Aronin@umassmed.edu
FU NIH [NS R0138194]; DANA Foundation; High Q Foundation; Huntington's
Disease Society of America; Diabetes Endocrinology Research Center [DK
P3032520]; Hereditary Disease Foundation
FX This work was supported by grants from the NIH (grant NS R0138194 to N.
A., Philip D. Zamore, and M. D.), the DANA Foundation (to N. A. and M.
D.), the High Q Foundation (to M. D.), and the Huntington's Disease
Society of America (to M. D.). Core resources supported by Diabetes
Endocrinology Research Center grant DK P3032520 (University of
Massachusetts Medical School [UMMS]) were also used. X.-L. is supported
by a John J. Wasmuth postdoctoral fellowship from the Hereditary Disease
Foundation and DANA Foundation. We declare no conflict of interests.
NR 55
TC 34
Z9 35
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD NOV 15
PY 2009
VL 29
IS 22
BP 6106
EP 6116
DI 10.1128/MCB.00420-09
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 511ZB
UT WOS:000271209600012
PM 19752198
ER
PT J
AU Lovrecic, L
Kastrin, A
Kobal, J
Pirtosek, Z
Krainc, D
Peterlin, B
AF Lovrecic, Luca
Kastrin, Andrej
Kobal, Jan
Pirtosek, Zvezdan
Krainc, Dimitri
Peterlin, Borut
TI Gene Expression Changes in Blood as a Putative Biomarker for
Huntington's Disease
SO MOVEMENT DISORDERS
LA English
DT Article
DE biomarkers; gene expression; Huntington's disease; neurodegeneration;
transcriptomics
ID MICROARRAY
AB Several studies demonstrated alterations of gene expression in blood in various neurological disorders including Huntington's disease (HD). Using microarray technology, a recent study identified a large number of significantly altered mRNAs in HD blood, from which a 12-gene set was selected as classifier for discriminating controls and HD patients. The aim of our study was to validate expression changes of these 12 genes in an independent cohort of HD patients and evaluate their sensitivity and specificity. Four different subject groups were included-patients with HD, Parkinson's disease (PD), acute ischemic stroke (AS) and healthy controls. Although the previous results were successfully validated, gene expression changes in HD blood partly overlapped with those observed in blood from PD and AS patients. Predictive value of the selected biomarker set for HD group was 78%, with 82% sensitivity and 53% specificity. Further gene expression analyses in longitudinal studies are needed to validate and refine possible transcriptomic blood biomarkers in HD. (C) 2009 Movement Disorder Society
C1 [Lovrecic, Luca; Kastrin, Andrej; Peterlin, Borut] UMC, Inst Med Genet, Ljubljana 1000, Slovenia.
[Kobal, Jan; Pirtosek, Zvezdan] UMC, Dept Neurol, Ljubljana 1000, Slovenia.
[Krainc, Dimitri] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol,MassGen Inst Neurodegenerat, Charlestown, MA USA.
RP Peterlin, B (reprint author), UMC, Inst Med Genet, Slajmerjeva 3, Ljubljana 1000, Slovenia.
EM Borut.Peterlin@guest.arnes.si
RI peterlin, borut/C-6086-2011
OI peterlin, borut/0000-0001-7824-4978
FU Ministry of Science and Technology, Ljubljana [J3-7411]; Republic of
Slovenia
FX This research was supported by grant J3-7411 from the Ministry of
Science and Technology, Ljubljana, Republic of Slovenia. The authors
express special gratitude to the participants in this study.
NR 12
TC 17
Z9 17
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0885-3185
J9 MOVEMENT DISORD
JI Mov. Disord.
PD NOV 15
PY 2009
VL 24
IS 15
BP 2277
EP 2281
DI 10.1002/mds.22477
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA 530DU
UT WOS:000272570000015
PM 19844910
ER
PT J
AU Schwab, JH
Healey, JH
Rose, P
Casas-Ganem, J
Boland, PJ
AF Schwab, Joseph H.
Healey, John H.
Rose, Peter
Casas-Ganem, Jorge
Boland, Patrick J.
TI The Surgical Management of Sacral Chordomas
SO SPINE
LA English
DT Article
DE sacrum; chordoma
ID SACROCOCCYGEAL CHORDOMA; UNILATERAL SACRIFICE; MAJOR RESECTIONS;
BONE-TUMORS; CRYOSURGERY; SACRECTOMY; NERVES
AB Study Design. Retrospective case series.
Objective. The purpose of this study was to evaluate factors that contribute to improved local control and survival. In addition, we sought to define the expected morbidity associated with treatment.
Summary of Background Data. Sacral chordomas are rare tumors presumed to arise from notochordal cells. Local recurrence presents a major problem in the management of these tumors and it has been correlated with survival. Resection of sacral tumors is associated with significant morbidity.
Methods. Forty-two patients underwent resection for sacral chordoma between 1990 and 2005. Twelve patients had their initial surgery elsewhere. There were 12 female and 30 male patients. The proximal extent of the sacrectomy was at least S2 in 32 patients.
Results. Median survival was 84 months, and 5-year disease-free (DFS) and disease-specific survival (DSF) were 56% and 77%, respectively. Local recurrence (LR) and metastasis occurred in 17 (40%) and 13 (31%) patients, respectively. Local recurrence (P = 0.0001), metastasis (P = 0.0001), prior resection (P = 0.046), and higher grade (P = 0.05) were associated with a worse DSF. Prior resections (P = 0.0001) and intralesional resections (P = 0.01) were associated with a higher rate of LR. Intralesional resections were associated with a lower DSF (P = 0.0001). Wide contaminated margins treated with cryosurgery and/or radiation were not associated with a higher LR rate. Rectus abdominus flaps were associated with decreased wound complications (P = 0.01). Thirty-one (74%) patients reported that they self catheterize; and 16 (38%) patients required bowel training, while an additional twelve (29%) patients had a colostomy. Twenty-eight (67%) patients reported sexual dysfunction. Two (5%) patients died due to sepsis.
Conclusions. Intralesional resection should be avoided as it is associated with a higher LR rate and worse survival. Rectus abdominus flaps ought to be considered as they lower the wound complication rate. Sacral resection is associated with significant morbidity.
C1 [Schwab, Joseph H.; Healey, John H.; Rose, Peter; Casas-Ganem, Jorge; Boland, Patrick J.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RP Schwab, JH (reprint author), Massachusetts Gen Hosp, Dept Orthoped Surg, Yawkey 3,55 Fruit St, Boston, MA 02114 USA.
EM jhschwab@partners.org
NR 20
TC 51
Z9 53
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0362-2436
J9 SPINE
JI SPINE
PD NOV 15
PY 2009
VL 34
IS 24
BP 2700
EP 2704
PG 5
WC Clinical Neurology; Orthopedics
SC Neurosciences & Neurology; Orthopedics
GA 520YD
UT WOS:000271884700015
PM 19910774
ER
PT J
AU Tilney, NL
Delmonico, FL
Murray, JE
Thistlethwaite, R
Leichtman, AB
Hanto, DW
Shapiro, R
Danovitch, GM
Sayegh, MH
Brennan, DC
Harmon, WE
Salvatierra, O
Pomfret, EA
McDiarmid, SV
Stock, PG
Metzger, R
Bennett, WM
Conti, D
Norman, DJ
Sarwal, MM
Cosimi, BA
AF Tilney, Nicholas L.
Delmonico, Francis L.
Murray, Joseph E.
Thistlethwaite, Richard
Leichtman, Alan B.
Hanto, Douglas W.
Shapiro, Ronald
Danovitch, Gabriel M.
Sayegh, Mohamed H.
Brennan, Daniel C.
Harmon, William E.
Salvatierra, Oscar
Pomfret, Elizabeth A.
McDiarmid, Sue V.
Stock, Peter G.
Metzger, Robert
Bennett, William Michael
Conti, David
Norman, Douglas J.
Sarwal, Minnie M.
Cosimi, Benedict A.
TI Promotion of Altruistic Donation (vol 88, pg 847, 2009)
SO TRANSPLANTATION
LA English
DT Correction
C1 [Tilney, Nicholas L.; Murray, Joseph E.] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Delmonico, Francis L.; Cosimi, Benedict A.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Thistlethwaite, Richard] Univ Chicago, Dept Surg, Chicago, IL 60637 USA.
[Leichtman, Alan B.] Univ Michigan, Med Ctr, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Hanto, Douglas W.] Beth Israel Deaconess Med Ctr, Dept Surg, Boston, MA 02215 USA.
[Shapiro, Ronald] Thomas E Starzl Transplantat Inst, Pittsburgh, PA USA.
[Danovitch, Gabriel M.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Sayegh, Mohamed H.] Brigham & Womens Hosp, Transplantat Res Ctr, Boston, MA 02115 USA.
[Brennan, Daniel C.] Washington Univ, Sch Med, Renal Div Internal Med, St Louis, MO USA.
[Harmon, William E.] Childrens Hosp, Boston, MA 02115 USA.
[Salvatierra, Oscar] Stanford Univ, Sch Med, Dept Surg, Palo Alto, CA 94304 USA.
[Pomfret, Elizabeth A.] Lahey Clin Med Ctr, Burlington, MA 01803 USA.
[McDiarmid, Sue V.] Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA.
[McDiarmid, Sue V.] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA.
[Stock, Peter G.] Univ Calif San Francisco, Dept Surg, Div Transplantat, San Francisco, CA 94143 USA.
[Bennett, William Michael] Legacy Good Samaritan Hosp, Transplant Serv & NW Renal Clin, Portland, OR USA.
[Conti, David] Albany Med Ctr, Albany, NY USA.
[Norman, Douglas J.] Oregon Hlth & Sci Univ, Dept Transplantat Immunogenet, Portland, OR 97201 USA.
[Sarwal, Minnie M.] Stanford Univ, Dept Pediat, Palo Alto, CA 94304 USA.
RP Tilney, NL (reprint author), Brigham & Womens Hosp, Dept Surg, 75 Francis St, Boston, MA 02115 USA.
NR 1
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0041-1337
J9 TRANSPLANTATION
JI Transplantation
PD NOV 15
PY 2009
VL 88
IS 9
BP 1145
EP 1147
PG 3
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 519OM
UT WOS:000271776500017
ER
PT J
AU Bray, GA
Chatellier, A
Duncan, C
Greenway, FL
Levy, E
Ryan, DH
Polonsky, KS
Tobian, J
Ehrmann, D
Matulik, MJ
Clark, B
Czech, K
DeSandre, C
Hilbrich, R
McNabb, W
Semenske, AR
Goldstein, BJ
Smith, KA
Wildman, W
Pepe, C
Goldberg, RB
Calles, J
Ojito, J
Castillo-Florez, S
Florez, HJ
Giannella, A
Lara, O
Veciana, B
Haffner, SM
Montez, MG
Lorenzo, C
Martinez, A
Hamman, RF
Testaverde, L
Bouffard, A
Dabelea, D
Jenkins, T
Lenz, D
Perreault, L
Price, DW
Steinke, SC
Horton, ES
Poirier, CS
Swift, K
Caballero, E
Jackson, SD
Lambert, L
Lawton, KE
Ledbury, S
Kahn, SE
Montgomery, BK
Fujimoto, W
Knopp, RH
Lipkin, EW
Marr, M
Murillo, A
Trence, D
Kitabchi, AE
Murphy, ME
Applegate, WB
Bryer-Ash, M
Dagogo-Jack, S
Frieson, SL
Lambeth, H
Lichtermann, LC
Otkaei, H
Rutledge, LMK
Sherman, AR
Smith, CM
Soberman, JE
Williams-Cleaves, B
Metzger, BE
Molitch, ME
Johnson, MK
Giles, MM
Larsen, D
Niznik, C
Pen, SC
Schinleber, PA
Nathan, DM
McKitrick, C
Turgeon, H
Abbott, K
Altshuler, D
Anderson, E
Bissett, L
Cagliero, E
D'Anna, K
Delahanty, L
Florez, JC
Goldman, V
Poulos, A
Tseng, B
Barrett-Connor, E
Carrion-Petersen, ML
Horne, J
Leos, D
Mudaliar, S
Smith, J
Vejvoda, K
Pi-Sunyer, FX
Lee, JE
Foo, ST
Hagamen, S
Marrero, DG
Kelly, SM
Ackermann, RT
Fineberg, ES
Hadden, A
Jackson, MA
Kirkman, MS
Mather, KJ
Roach, PJ
Wheeler, ML
Ratner, RE
Aroda, V
Shapiro, S
Bavido-Arrage, C
Gibbs, P
Uwaifo, G
Wiggins, R
Saad, MF
Watson, K
Botrous, M
Jinagouda, S
Budget, M
Conzues, C
Magpuri, P
Ngo, K
Xapthalamous, K
White, NH
Das, S
Santiago, A
Brown, AL
Wernimont, C
Saudek, CD
Whittington, T
Clark, JM
Greene, A
Jiggetts, D
Mosley, H
Reusing, J
Rubin, RR
Stephen, S
Utsey, E
Schade, DS
Adams, KS
Hemphill, C
Hyde, P
Butler, L
Canady, JL
Colleran, K
Gonzales, Y
Hernandez-McGinnis, DA
Katz, P
King, C
Crandall, J
Brown-Friday, JO
Adorno, E
Duffy, H
Martinez, H
Pompi, D
Shamoon, H
Walker, EA
Wylie-Rosett, J
Orchard, T
Jeffries, S
Kramer, MK
Smith, M
Kriska, A
Pettigrew, J
Semler, L
Venditti, E
Weinzierl, V
Arakaki, RF
Baker-Ladao, NK
Isonaga, MK
Bermudez, NE
Mau, MK
Knowler, WC
Cooeyate, N
Hoskin, MA
Natewa, C
Percy, CA
Acton, KJ
Andre, VL
Begay, S
Bucca, BC
Cook, S
Doughty, MS
Glass, J
Glass, M
Hanson, RL
Hassenpflug, D
Ingraham, LE
Kobus, KM
Krakoff, J
Manus, C
McCabe, C
Michaels, S
Morgan, T
Nelson, JA
Roy, RJ
Smart, M
Tonemah, DP
Wilson, C
Fowler, S
Brenneman, T
Abebe, S
Bamdad, J
Callaghan, J
Christophi, CA
Edelstein, SL
Gao, Y
Gooding, R
Gottlieb, A
Grover, N
Hoffman, H
Jablonski, K
Katz, R
Kolinjivadi, P
Lachin, JM
Ma, Y
Reamer, S
Sapozhnikova, A
Sherif, H
Temprosa, M
Venditti, EM
Kriska, AM
Semler, L
Weinzierl, V
Marcovina, S
Strylewicz, G
Albers, J
Prineas, RJ
Alexander, T
Campbell, C
Hall, S
Hensley, S
Li, Y
Mills, M
Soliman, E
Zhang, Z
Fradkin, J
Garfield, S
Mayer-Davis, E
Moran, RR
Ganiats, T
Sarkin, AJ
AF Bray, G. A.
Chatellier, A.
Duncan, C.
Greenway, F. L.
Levy, E.
Ryan, D. H.
Polonsky, K. S.
Tobian, J.
Ehrmann, D.
Matulik, M. J.
Clark, B.
Czech, K.
DeSandre, C.
Hilbrich, R.
McNabb, W.
Semenske, A. R.
Goldstein, B. J.
Smith, K. A.
Wildman, W.
Pepe, C.
Goldberg, R. B.
Calles, J.
Ojito, J.
Castillo-Florez, S.
Florez, H. J.
Giannella, A.
Lara, O.
Veciana, B.
Haffner, S. M.
Montez, M. G.
Lorenzo, C.
Martinez, A.
Hamman, R. F.
Testaverde, L.
Bouffard, A.
Dabelea, D.
Jenkins, T.
Lenz, D.
Perreault, L.
Price, D. W.
Steinke, S. C.
Horton, E. S.
Poirier, C. S.
Swift, K.
Caballero, E.
Jackson, S. D.
Lambert, L.
Lawton, K. E.
Ledbury, S.
Kahn, S. E.
Montgomery, B. K.
Fujimoto, W.
Knopp, R. H.
Lipkin, E. W.
Marr, M.
Murillo, A.
Trence, D.
Kitabchi, A. E.
Murphy, M. E.
Applegate, W. B.
Bryer-Ash, M.
Dagogo-Jack, S.
Frieson, S. L.
Lambeth, H.
Lichtermann, L. C.
Otkaei, H.
Rutledge, L. M. K.
Sherman, A. R.
Smith, C. M.
Soberman, J. E.
Williams-Cleaves, B.
Metzger, B. E.
Molitch, M. E.
Johnson, M. K.
Giles, M. M.
Larsen, D.
Niznik, C.
Pen, S. C.
Schinleber, P. A.
Nathan, D. M.
McKitrick, C.
Turgeon, H.
Abbott, K.
Altshuler, D.
Anderson, E.
Bissett, L.
Cagliero, E.
D'Anna, K.
Delahanty, L.
Florez, J. C.
Goldman, V.
Poulos, A.
Tseng, B.
Barrett-Connor, E.
Carrion-Petersen, M. L.
Horne, J.
Leos, D.
Mudaliar, S.
Smith, J.
Vejvoda, K.
Pi-Sunyer, F. X.
Lee, J. E.
Foo, S. T.
Hagamen, S.
Marrero, D. G.
Kelly, S. M.
Ackermann, R. T.
Fineberg, E. S.
Hadden, A.
Jackson, M. A.
Kirkman, M. S.
Mather, K. J.
Roach, P. J.
Wheeler, M. L.
Ratner, R. E.
Aroda, V.
Shapiro, S.
Bavido-Arrage, C.
Gibbs, P.
Uwaifo, Gl
Wiggins, R.
Saad, M. F.
Watson, K.
Botrous, M.
Jinagouda, S.
Budget, M.
Conzues, C.
Magpuri, P.
Ngo, K.
Xapthalamous, K.
White, N. H.
Das, S.
Santiago, A.
Brown, A. L.
Wernimont, C.
Saudek, C. D.
Whittington, T.
Clark, J. M.
Greene, A.
Jiggetts, D.
Mosley, H.
Reusing, J.
Rubin, R. R.
Stephen, S.
Utsey, E.
Schade, D. S.
Adams, K. S.
Hemphill, C.
Hyde, P.
Butler, L.
Canady, J. L.
Colleran, K.
Gonzales, Y.
Hernandez-McGinnis, D. A.
Katz, P.
King, C.
Crandall, J.
Brown-Friday, J. O.
Adorno, E.
Duffy, H.
Martinez, H.
Pompi, D.
Shamoon, H.
Walker, E. A.
Wylie-Rosett, J.
Orchard, T.
Jeffries, S.
Kramer, M. K.
Smith, M.
Kriska, A.
Pettigrew, J.
Semler, L.
Venditti, E.
Weinzierl, V.
Arakaki, R. F.
Baker-Ladao, N. K.
Isonaga, M. K.
Bermudez, N. E.
Mau, M. K.
Knowler, W. C.
Cooeyate, N.
Hoskin, M. A.
Natewa, C.
Percy, C. A.
Acton, K. J.
Andre, V. L.
Begay, S.
Bucca, B. C.
Cook, S.
Doughty, M. S.
Glass, J.
Glass, M.
Hanson, R. L.
Hassenpflug, D.
Ingraham, L. E.
Kobus, K. M.
Krakoff, J.
Manus, C.
McCabe, C.
Michaels, S.
Morgan, T.
Nelson, J. A.
Roy, R. J.
Smart, M.
Tonemah, D. P.
Wilson, C.
Fowler, S.
Brenneman, T.
Abebe, S.
Bamdad, J.
Callaghan, J.
Christophi, C. A.
Edelstein, S. L.
Gao, Y.
Gooding, R.
Gottlieb, A.
Grover, N.
Hoffman, H.
Jablonski, K.
Katz, R.
Kolinjivadi, P.
Lachin, J. M.
Ma, Y.
Reamer, S.
Sapozhnikova, A.
Sherif, H.
Temprosa, M.
Venditti, E. M.
Kriska, A. M.
Semler, L.
Weinzierl, V.
Marcovina, S.
Strylewicz, G.
Albers, J.
Prineas, R. J.
Alexander, T.
Campbell, C.
Hall, S.
Hensley, S.
Li, Y.
Mills, M.
Soliman, E.
Zhang, Z.
Fradkin, J.
Garfield, S.
Mayer-Davis, E.
Moran, R. R.
Ganiats, T.
Sarkin, A. J.
CA Diabet Prevention Program Res Grp
TI 10-year follow-up of diabetes incidence and weight loss in the Diabetes
Prevention Program Outcomes Study
SO LANCET
LA English
DT Article
ID IMPAIRED GLUCOSE-TOLERANCE; LIFE-STYLE INTERVENTION; COST-EFFECTIVENESS;
RISK-FACTORS; METFORMIN; MELLITUS; PEOPLE; TRIAL; REDUCTION; DIAGNOSIS
AB Background In the 2.8 years of the Diabetes Prevention Program (DPP) randomised clinical trial, diabetes incidence in high-risk adults was reduced by 58% with intensive lifestyle intervention and by 31% with metformin, compared with placebo. We investigated the persistence of these effects in the long term.
Methods All active DPP participants were eligible for continued follow-up. 2766 of 3150 (88%) enrolled for a median additional follow-up of 5.7 years (IQR 5.5-5.8). 910 participants were from the lifestyle, 924 from the metformin, and 932 were from the original placebo groups. On the basis of the benefits from the intensive lifestyle intervention in the DPP, all three groups were offered group-implemented lifestyle intervention. Metformin treatment was continued in the original metformin group (850 mg twice daily as tolerated), with participants unmasked to assignment, and the original lifestyle intervention group was offered additional lifestyle support. The primary outcome was development of diabetes according to American Diabetes Association criteria. Analysis was by intention-to-treat. This study is registered with ClinicalTrials.gov, number NCT00038727.
Findings During the 10.0-year (IQR 9.0-10.5) follow-up since randomisation to DPP, the original lifestyle group lost, then partly regained weight. The modest weight loss with metformin was maintained. Diabetes incidence rates during the DPP were 4.8 cases per 100 person-years (95% CI 4.1-5.7) in the intensive lifestyle intervention group, 7.8 (6.8-8.8) in the metformin group, and 11.0 (9.8-12.3) in the placebo group. Diabetes incidence rates in this follow-up study were similar between treatment groups: 5.9 per 100 person-years (5.1-6.8) for lifestyle, 4.9 (4.2-5.7) for metformin, and 5.6 (4.8-6.5) for placebo. Diabetes incidence in the 10 years since DPP randomisation was reduced by 34% (24-42) in the lifestyle group and 18% (7-28) in the metformin group compared with placebo.
Interpretation During follow-up after DPP, incidences in the former placebo and metformin groups fell to equal those in the former lifestyle group, but the cumulative incidence of diabetes remained lowest in the lifestyle group. Prevention or delay of diabetes with lifestyle intervention or metformin can persist for at least 10 years.
C1 [Bray, G. A.; Fowler, S.; Brenneman, T.; Abebe, S.; Bamdad, J.; Callaghan, J.; Christophi, C. A.; Edelstein, S. L.; Gao, Y.; Gooding, R.; Gottlieb, A.; Grover, N.; Hoffman, H.; Jablonski, K.; Katz, R.; Kolinjivadi, P.; Lachin, J. M.; Ma, Y.; Reamer, S.; Sapozhnikova, A.; Sherif, H.; Temprosa, M.] George Washington Univ, Diabet Prevent Program Coordinating Ctr, Ctr Biostat, Rockville, MD 20852 USA.
[Bray, G. A.; Chatellier, A.; Duncan, C.; Greenway, F. L.; Levy, E.; Ryan, D. H.] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Polonsky, K. S.; Tobian, J.; Ehrmann, D.; Matulik, M. J.; Clark, B.; Czech, K.; DeSandre, C.; Hilbrich, R.; McNabb, W.; Semenske, A. R.] Univ Chicago, Chicago, IL 60637 USA.
[Goldstein, B. J.; Smith, K. A.; Wildman, W.; Pepe, C.] Thomas Jefferson Univ, Jefferson Med Coll, Philadelphia, PA 19107 USA.
[Goldberg, R. B.; Calles, J.; Ojito, J.; Castillo-Florez, S.; Florez, H. J.; Giannella, A.; Lara, O.; Veciana, B.] Univ Miami, Miami, FL USA.
[Haffner, S. M.; Montez, M. G.; Lorenzo, C.; Martinez, A.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Hamman, R. F.; Testaverde, L.; Bouffard, A.; Dabelea, D.; Jenkins, T.; Lenz, D.; Perreault, L.; Price, D. W.; Steinke, S. C.] Univ Colorado, Denver, CO 80202 USA.
[Horton, E. S.; Poirier, C. S.; Swift, K.; Caballero, E.; Jackson, S. D.; Lambert, L.; Lawton, K. E.; Ledbury, S.] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Kahn, S. E.; Montgomery, B. K.; Fujimoto, W.; Knopp, R. H.; Lipkin, E. W.; Marr, M.; Murillo, A.; Trence, D.] Univ Washington, Seattle, WA 98195 USA.
[Kitabchi, A. E.; Murphy, M. E.; Applegate, W. B.; Bryer-Ash, M.; Dagogo-Jack, S.; Frieson, S. L.; Lambeth, H.; Lichtermann, L. C.; Otkaei, H.; Rutledge, L. M. K.; Sherman, A. R.; Smith, C. M.; Soberman, J. E.; Williams-Cleaves, B.] Univ Tennessee, Memphis, TN USA.
[Metzger, B. E.; Molitch, M. E.; Johnson, M. K.; Giles, M. M.; Larsen, D.; Niznik, C.; Pen, S. C.; Schinleber, P. A.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Nathan, D. M.; McKitrick, C.; Turgeon, H.; Abbott, K.; Altshuler, D.; Anderson, E.; Bissett, L.; Cagliero, E.; D'Anna, K.; Delahanty, L.; Florez, J. C.; Goldman, V.; Poulos, A.; Tseng, B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Barrett-Connor, E.; Carrion-Petersen, M. L.; Horne, J.; Leos, D.; Mudaliar, S.; Smith, J.; Vejvoda, K.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Pi-Sunyer, F. X.; Lee, J. E.; Foo, S. T.; Hagamen, S.] St Lukes Roosevelt Hosp, New York, NY 10025 USA.
[Marrero, D. G.; Kelly, S. M.; Ackermann, R. T.; Fineberg, E. S.; Hadden, A.; Jackson, M. A.; Kirkman, M. S.; Mather, K. J.; Roach, P. J.; Wheeler, M. L.] Indiana Univ, Indianapolis, IN 46204 USA.
[Ratner, R. E.; Aroda, V.; Shapiro, S.; Bavido-Arrage, C.; Gibbs, P.; Uwaifo, Gl; Wiggins, R.] Medstar Res Inst, Washington, DC USA.
[Saad, M. F.; Watson, K.; Botrous, M.; Jinagouda, S.; Budget, M.; Conzues, C.; Magpuri, P.; Ngo, K.; Xapthalamous, K.] Univ Calif Los Angeles, Univ So Calif, Res Ctr, Alhambra, CA USA.
[White, N. H.; Das, S.; Santiago, A.; Brown, A. L.; Wernimont, C.] Washington Univ, St Louis, MO USA.
[Saudek, C. D.; Whittington, T.; Clark, J. M.; Greene, A.; Jiggetts, D.; Mosley, H.; Reusing, J.; Rubin, R. R.; Stephen, S.; Utsey, E.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Schade, D. S.; Adams, K. S.; Hemphill, C.; Hyde, P.; Butler, L.; Canady, J. L.; Colleran, K.; Gonzales, Y.; Hernandez-McGinnis, D. A.; Katz, P.; King, C.] Univ New Mexico, Albuquerque, NM 87131 USA.
[Crandall, J.; Brown-Friday, J. O.; Adorno, E.; Duffy, H.; Martinez, H.; Pompi, D.; Shamoon, H.; Walker, E. A.; Wylie-Rosett, J.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Orchard, T.; Jeffries, S.; Kramer, M. K.; Smith, M.; Kriska, A.; Pettigrew, J.; Semler, L.; Venditti, E.; Weinzierl, V.] Univ Pittsburgh, Pittsburgh, PA USA.
[Arakaki, R. F.; Baker-Ladao, N. K.; Isonaga, M. K.; Bermudez, N. E.; Mau, M. K.] Univ Hawaii, Honolulu, HI 96822 USA.
[Knowler, W. C.; Cooeyate, N.; Hoskin, M. A.; Natewa, C.; Percy, C. A.; Acton, K. J.; Andre, V. L.; Begay, S.; Bucca, B. C.; Cook, S.; Doughty, M. S.; Glass, J.; Glass, M.; Hanson, R. L.; Hassenpflug, D.; Ingraham, L. E.; Kobus, K. M.; Krakoff, J.; Manus, C.; McCabe, C.; Michaels, S.; Morgan, T.; Nelson, J. A.; Roy, R. J.; Smart, M.; Tonemah, D. P.; Wilson, C.] SW Amer Indian Ctr, Phoenix, AZ USA.
[Knowler, W. C.; Cooeyate, N.; Hoskin, M. A.; Natewa, C.; Percy, C. A.; Acton, K. J.; Andre, V. L.; Begay, S.; Bucca, B. C.; Cook, S.; Doughty, M. S.; Glass, J.; Glass, M.; Hanson, R. L.; Hassenpflug, D.; Ingraham, L. E.; Kobus, K. M.; Krakoff, J.; Manus, C.; McCabe, C.; Michaels, S.; Morgan, T.; Nelson, J. A.; Roy, R. J.; Smart, M.; Tonemah, D. P.; Wilson, C.] SW Amer Indian Ctr, Shiprock, NM USA.
[Knowler, W. C.; Cooeyate, N.; Hoskin, M. A.; Natewa, C.; Percy, C. A.; Acton, K. J.; Andre, V. L.; Begay, S.; Bucca, B. C.; Cook, S.; Doughty, M. S.; Glass, J.; Glass, M.; Hanson, R. L.; Hassenpflug, D.; Ingraham, L. E.; Kobus, K. M.; Krakoff, J.; Manus, C.; McCabe, C.; Michaels, S.; Morgan, T.; Nelson, J. A.; Roy, R. J.; Smart, M.; Tonemah, D. P.; Wilson, C.] SW Amer Indian Ctr, Zuni, NM USA.
[Marcovina, S.; Strylewicz, G.; Albers, J.] Cent Biochem Lab, Seattle, WA USA.
[Prineas, R. J.; Alexander, T.; Campbell, C.; Hall, S.; Hensley, S.; Li, Y.; Mills, M.; Soliman, E.; Zhang, Z.] Epidemiol Cardiol Res Ctr Epicare, Winston Salem, NC USA.
[Fradkin, J.; Garfield, S.] NIDDK, NIH, Bethesda, MD USA.
[Mayer-Davis, E.; Moran, R. R.] Nutr Coding Ctr, Columbia, SC USA.
[Ganiats, T.; Sarkin, A. J.] Qual Well Being Ctr, La Jolla, CA USA.
RP Bray, GA (reprint author), George Washington Univ, Diabet Prevent Program Coordinating Ctr, Ctr Biostat, 6110 Execut Blvd,Suite 750, Rockville, MD 20852 USA.
EM dppmail@biostat.bsc.gwu.edu
RI Altshuler, David/A-4476-2009; Uwaifo, Gabriel/M-2361-2016
OI Altshuler, David/0000-0002-7250-4107; Uwaifo,
Gabriel/0000-0002-6962-9304
FU National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK), National Institutes of Health
FX This study was funded by the National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK) as a cooperative agreement. We
thank the participants of the Diabetes Prevention Program and Diabetes
Prevention Program Outcomes Study for their commitment and dedication;
the National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK) of the National Institutes of Health for funding to the clinical
and coordinating centres that designed and undertook the study, and
collected, managed, analysed and interpreted the data; and the General
Clinical Research Center Program and the National Center for Research
Resources for support of data collection at many of the clinical
centres. The Southwestern American Indian Centers were supported
directly by the NIDDK, including its Intramural Research Program, and by
the Indian Health Service. Funding was also provided by the National
Institute of Child Health and Human Development, the National Institute
on Aging, the National Eye Institute, the National Heart Lung and Blood
Institute, the Office of Women's Health, the National Center for
Minority Health and Human Disease, the Centers for Disease Control and
Prevention, and the American Diabetes Association. Lipha (Merck-Sante)
provided medicines, and LifeScan donated materials. The opinions
expressed are those of the investigators and do not necessarily reflect
the views of the funding agencies.
NR 28
TC 800
Z9 806
U1 12
U2 82
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
J9 LANCET
JI Lancet
PD NOV 14
PY 2009
VL 374
IS 9702
BP 1677
EP 1686
DI 10.1016/S0140-6736(09)61457-4
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 522LP
UT WOS:000271999700023
ER
PT J
AU Eurich, K
Segawa, M
Toei-Shimizu, S
Mizoguchi, E
AF Eurich, Katrin
Segawa, Mayuko
Toei-Shimizu, Satoko
Mizoguchi, Emiko
TI Potential role of chitinase 3-like-1 in inflammation-associated
carcinogenic changes of epithelial cells
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Editorial Material
DE Mammals; Chitinase 3-like 1; Colon; Epithelial cells; Inflammation;
Colitis; Colon neoplasms; Inflammatory bowel disease
ID HUMAN CARTILAGE GLYCOPROTEIN-39; ACIDIC MAMMALIAN CHITINASE; SERUM
YKL-40 LEVEL; ADVANCED BREAST-CANCER; SMOOTH-MUSCLE-CELLS; FATTY
LIVER-DISEASE; HIGH-GRADE GLIOMAS; GENE-EXPRESSION; OVARIAN-CANCER;
BOWEL-DISEASE
AB The family of mammalian chitinases includes members both with and without glycohydrolase enzymatic activity against chitin, a polymer of N-acetylglucosamine. Chitin is the structural component of fungi, crustaceans, insects and parasitic nematodes, but is completely absent in mammals. Exposure to antigens containing chitin- or chitin-like structures sometimes induces strong T helper type-I responses in mammals, which may be associated with the induction of mammalian chitinases. Chitinase 3-like-1 (CHI3L1), a member of the mammalian chitinase family, is induced specifically during the course of inflammation in such disorders as inflammatory bowel disease, hepatitis and asthma In addition, CHI3L1 is expressed and secreted by several types of solid tumors including glioblastoma, colon cancer, breast cancer and malignant melanoma. Although the exact function of CHI3L1 in inflammation and cancer is still largely unknown, CHI3L1 plays a pivotal role in exacerbating the inflammatory processes and in promoting angiogenesis and remodeling of the extracellular matrix. CHI3L1 may be highly involved in the chronic engagement of inflammation which potentiates development of epithelial tumorigenesis presumably by activating the mitogen-activated protein kinase and the protein kinase B signaling pathways. Anti-CHI3L1 antibodies or pan-chitinase inhibitors may have the potential to suppress CHI3L1-mediated chronic inflammation and the subsequent carcinogenic change in epithelial cells. (C) 2009 The WJG Press and Baishideng. All rights reserved.
C1 [Eurich, Katrin; Segawa, Mayuko; Toei-Shimizu, Satoko; Mizoguchi, Emiko] Harvard Univ, Sch Med, Dept Med, Massachusetts Gen Hosp,Gastrointestinal Unit, Boston, MA 02114 USA.
[Mizoguchi, Emiko] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Study Inflammatory Bowel Dis, Boston, MA 02114 USA.
RP Mizoguchi, E (reprint author), Harvard Univ, Sch Med, Dept Med, Massachusetts Gen Hosp,Gastrointestinal Unit, GRJ 702,55 Fruit St, Boston, MA 02114 USA.
EM emizoguchi@partners.org
FU NIDDK NIH HHS [K08 DK064289-04, P30 DK043351, R01 DK080070, R01
DK080070-01A2, K08 DK064289, R01 DK080070-01A2S1, R03 DK074454, R03
DK074454-02, K08 DK064289-05]
NR 192
TC 41
Z9 41
U1 1
U2 4
PU W J G PRESS
PI BEIJING
PA APT 1066, YISHOU GARDEN, NO 58, NORTH LANGXINZHUANG RD, PO BOX 2345,
BEIJING 100023, PEOPLES R CHINA
SN 1007-9327
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 14
PY 2009
VL 15
IS 42
BP 5249
EP 5259
DI 10.3748/wjg.15.5249
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 520PI
UT WOS:000271857200001
PM 19908331
ER
PT J
AU Rossen, RD
Rubio, JA
Porter, WJ
Trial, J
Orson, FM
Rodriguez-Barradas, MC
Birdsall, HH
AF Rossen, Roger D.
Rubio, Jose A.
Porter, Wendy J.
Trial, JoAnn
Orson, Frank M.
Rodriguez-Barradas, Maria C.
Birdsall, Holly H.
TI Monocyte CD49e and 110-120 kDa fibronectin fragments: HIV prognostic
indicators independent of viral load and CD4 T-cell counts
SO AIDS
LA English
DT Article
DE cell-binding 110-120 kDa fibronectin fragments; inflammation; monocytes;
patient survival; protease-antiprotease balance
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TRANSENDOTHELIAL MIGRATION; PROTEASE
INHIBITORS; SECRETION; ALPHA(1)-ANTITRYPSIN; INFECTIVITY; ACTIVATION;
EXPRESSION; LEUKOCYTES; TYPE-1
AB Objective: To investigate the prognostic impact of chronic inflammation associated with HIV infections. Previously, we had observed that proteases, released in the course of HIV infections, cause 110-120 kDa fibronectin fragments (FNf) to appear in the blood of many patients. In vitro, at concentrations within the range found in patients' plasma, FNf stimulate monocytes to release proteolytic enzymes that remove CD49e from the cell surface and produce cytokines that suppress proliferation of activated T cells when stimulated by agents that crosslink their antigen receptors.
Design: A long-term observational study of patients whose plasma FNf and monocyte CD49e had been measured at 90-day intervals for 1.4 +/- 0.5 years.
Methods: Plasma FNf was measured by a quantitative western blot assay and monocyte CD49e expression by flow cytometry. Patients were monitored clinically for up to 5 years after enrollment.
Results: All-cause mortality was significantly higher in patients who had at least 5 mu g/ml FNf in more than 50% of plasma samples and/or persistent depletion of monocyte CD49e. Persistence of FNf and depletion of monocyte CD49e were not associated with changes in viral load or CD4 T-cell counts.
Conclusion: Persistently reduced expression of blood monocyte CD49e and/or the persistent presence of FNf in plasma are adverse prognostic markers in HIV-infected patients. (C) 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
C1 [Rossen, Roger D.; Rubio, Jose A.; Porter, Wendy J.; Trial, JoAnn; Orson, Frank M.; Rodriguez-Barradas, Maria C.; Birdsall, Holly H.] Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
[Rossen, Roger D.; Rubio, Jose A.; Porter, Wendy J.; Trial, JoAnn; Orson, Frank M.; Rodriguez-Barradas, Maria C.; Birdsall, Holly H.] Baylor Coll Med, Houston, TX 77030 USA.
RP Rossen, RD (reprint author), Michael E DeBakey Vet Affairs Med Ctr, Bldg 109,Room 228,2002 Holcombe Blvd, Houston, TX 77030 USA.
EM rrossen@bcm.tmc.edu
FU Department of Veterans Affairs Merit Review Program; National Institutes
of Health [RO1-AI46285, RO1-MH63035]
FX The support for this study was provided by the Department of Veterans
Affairs Merit Review Program and National Institutes of Health grants:
RO1-AI46285 and RO1-MH63035.
NR 30
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD NOV 13
PY 2009
VL 23
IS 17
BP 2247
EP 2253
DI 10.1097/QAD.0b013e3283318ff4
PG 7
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 517CF
UT WOS:000271589700002
PM 19710592
ER
PT J
AU Lo, J
Looby, SED
Wei, J
Adler, GK
Grinspoon, SK
AF Lo, Janet
Looby, Sara E. D.
Wei, Jeffrey
Adler, Gail K.
Grinspoon, Steven K.
TI Increased aldosterone among HIV-infected women with visceral fat
accumulation
SO AIDS
LA English
DT Article
ID CARDIOVASCULAR-DISEASE; METABOLIC SYNDROME; OBESITY
AB Increased aldosterone has been associated with obesity and the metabolic syndrome in non-HIV-infected individuals, but aldosterone has not been investigated among HIV-infected patients with increased visceral adipose tissue (VAT). Twenty-four-hour urine aldosterone was assessed among age and BMI-matched HIV-infected women with increased VAT, HIV-infected women without increased VAT and healthy controls. Twenty-four hour urine aldosterone was higher in HIV-infected women with increased VAT and was associated with SBP, VAT and hemoglobin A1c. Increased aldosterone may contribute to the detrimental effects of excess visceral adiposity on blood pressure and glucose homeostasis among HIV patients.
C1 [Lo, Janet; Looby, Sara E. D.; Wei, Jeffrey; Grinspoon, Steven K.] Massachusetts Gen Hosp, Program Nutr Metab, Boston, MA 02114 USA.
[Adler, Gail K.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA.
RP Lo, J (reprint author), Massachusetts Gen Hosp, Program Nutr Metab, Boston, MA 02114 USA.
FU National Institutes of Health (NIH) [K23 HL092792, NIH RO1 DK 59535, NIH
K24 DK064545, NIH M01 RR01066-2551]
FX This study is supported by National Institutes of Health (NIH) K23
HL092792, NIH RO1 DK 59535, NIH K24 DK064545 and NIH M01 RR01066-2551.
NR 14
TC 7
Z9 7
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD NOV 13
PY 2009
VL 23
IS 17
BP 2366
EP 2370
DI 10.1097/QAD.0b013e3283328d3b
PG 5
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 517CF
UT WOS:000271589700017
PM 19770620
ER
PT J
AU Sosnovik, DE
Wang, RP
Dai, GP
Reese, TG
Wedeen, VJ
AF Sosnovik, David E.
Wang, Ruopeng
Dai, Guangping
Reese, Timothy G.
Wedeen, Van J.
TI Diffusion MR tractography of the heart
SO JOURNAL OF CARDIOVASCULAR MAGNETIC RESONANCE
LA English
DT Review
ID MAGNETIC-RESONANCE; TENSOR MRI; IN-VIVO; LAMINAR STRUCTURE; CARDIAC
FIBER; HYPERTROPHIC CARDIOMYOPATHY; MYOCARDIAL MICROSTRUCTURE; TISSUE
ARCHITECTURE; WATER DIFFUSION; BOVINE TONGUE
AB Histological studies have shown that the myocardium consists of an array of crossing helical fiber tracts. Changes in myocardial fiber architecture occur in ischemic heart disease and heart failure, and can be imaged non-destructively with diffusion-encoded MR. Several diffusion- encoding schemes have been developed, ranging from scalar measurements of mean diffusivity to a 6-dimensional imaging technique known as diffusion spectrum imaging or DSI. The properties of DSI make it particularly suited to the generation of 3-dimensional tractograms of myofiber architecture. In this article we review the physical basis of diffusion-tractography in the myocardium and the attributes of the available techniques, placing particular emphasis on DSI. The application of DSI in ischemic heart disease is reviewed, and the requisites for widespread clinical translation of diffusion MR tractography in the heart are discussed.
C1 [Sosnovik, David E.; Wang, Ruopeng; Dai, Guangping; Reese, Timothy G.; Wedeen, Van J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Martinos Ctr Biomed Imaging, Boston, MA 02115 USA.
[Sosnovik, David E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[Sosnovik, David E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Boston, MA USA.
[Sosnovik, David E.; Wedeen, Van J.] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Sosnovik, DE (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Martinos Ctr Biomed Imaging, Boston, MA 02115 USA.
EM sosnovik@nmr.mgh.harvard.edu; rpwang@nmr.mgh.harvard.edu;
dai@nmr.mgh.harvard.edu; reese@nmr.mgh.harvard.edu;
van@nmr.mgh.harvard.edu
FU National Institutes of Health [R01 HL093038, K08 HL079984]; VJW [RO1
MH64044]; NCRR [P41RR14075]
FX This study was supported in part by the following grant from the
National Institutes of Health: DES (R01 HL093038 and K08 HL079984), VJW
( RO1 MH64044), and (NCRR P41RR14075) to the Martinos Center for
Biomedical Imaging.
NR 63
TC 69
Z9 70
U1 1
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1097-6647
J9 J CARDIOVASC MAGN R
JI J. Cardiov. Magn. Reson.
PD NOV 13
PY 2009
VL 11
AR 47
DI 10.1186/1532-429X-11-47
PG 15
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 525XF
UT WOS:000272250200001
PM 19912654
ER
PT J
AU Xiu, MH
Hui, L
Dang, YF
De Hou, T
Zhang, CX
Zheng, YL
Chen, DC
Kosten, TR
Zhang, XY
AF Xiu, Mei Hong
Hui, Li
Dang, Yu Feng
De Hou, Tian
Zhang, Chong Xi
Zheng, You Lan
Chen, Da Chun
Kosten, Thomas R.
Zhang, Xiang Yang
TI Decreased serum BDNF levels in chronic institutionalized schizophrenia
on long-term treatment with typical and atypical antipsychotics
SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
LA English
DT Review
DE Antipsychotic drug; Brain-derived neurotrophic factor; Neurotrophin;
Psychopathology; Schizophrenia
ID NEUROTROPHIC FACTOR; RAT HIPPOCAMPUS; MESSENGER-RNA; GROWTH-FACTOR;
PREFRONTAL CORTEX; BIPOLAR DISORDER; WEIGHT-GAIN; BRAIN; EXPRESSION;
PLASMA
AB Accumulating evidence showed that brain-derived neurotrophic factor (BDNF) may be involved in the pathophysiology of schizophrenia. Decreased BDNFlevels have been found in the serum of schizophrenic patients with mixed results. In the present study, we assessed serum BDNF levels in a large group of 364 schizophrenic patients (157 on clozapine, 89 on risperidone and 118 on typical antipsychotics), compared to 323 healthy control subjects matched for age and gender. The schizophrenia symptomatology was assessed by the Positive and Negative Syndrome Scale (PANSS), and serum BDNF levels were measured by sandwich ELISA. The results showed that BDNF levels were significantly lower in chronic patients with schizophrenia than in healthy control subjects (9.9 +/- 2.0 ng/ml vs. 11.9 +/- 23 ng/ml, p < 0.0001). Lower BDNF levels were observed in patients treated with risperidone (9.3 +/- 2.3 ng/ml) compared to those with clozapine (10.2 +/- 2.0 ng/ml, p < 0.001) and typical antipsychotics(10.0 +/- 2.1 ng/ml,p <0.01). Furthermore, a stepwise multiple regression analysis identified types of antipsychotic drugs (beta=-0.37, t=-3.15, p=0.001) and BDNF levels (beta=-0.26, t=-2.51, p = 0.014) as the influencing factor for the positive symptom subscore of PANSS. In addition, there was a sex difference in BDNF levels inpatients with schizophrenia (9.7 +/- 1.9 ng/ml for males vs. 10.4 +/- 2.1 ng/ml for female, p<0.005). but not in normal controls. Our findings indicated decreased BDNF serum levels in chronic patients with schizophrenia, which may be related to clinical phenotypes, including gender, antipsychotic treatment and the severity of psychotic symptoms. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Kosten, Thomas R.; Zhang, Xiang Yang] Baylor Coll Med, Menninger Dept Psychiat & Behav Sci, Houston, TX 77030 USA.
[Xiu, Mei Hong; Chen, Da Chun] Beijing HuiLongGuan Hosp, Ctr Biol Psychiat, Beijing, Peoples R China.
[Hui, Li; De Hou, Tian] NW Normal Univ Lanzhou, Coll Life Sci, Lanzhou, Gansu, Peoples R China.
[Dang, Yu Feng; Zheng, You Lan] Jilin Agr Univ, Coll Chinese Med Mat, Changchun, Peoples R China.
[Zhang, Chong Xi] Shandong Univ Weihai Shandong, Weihai 264209, Peoples R China.
RP Kosten, TR (reprint author), VA Med Ctr, Res Bldg 110,Room 229,2002 Holcombe Blvd, Houston, TX 77030 USA.
EM kosten@bcm.edu; xyzhang@bcm.edu
NR 34
TC 71
Z9 73
U1 0
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0278-5846
J9 PROG NEURO-PSYCHOPH
JI Prog. Neuro-Psychopharmacol. Biol. Psychiatry
PD NOV 13
PY 2009
VL 33
IS 8
BP 1508
EP 1512
DI 10.1016/j.pnpbp.2009.08.011
PG 5
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 532RL
UT WOS:000272767100030
PM 19720106
ER
PT J
AU Nemoto, T
Yamazawa, R
Kobayashi, H
Fujita, N
Chino, B
Fujii, C
Kashima, H
Rassovsky, Y
Green, MF
Mizuno, M
AF Nemoto, Takahiro
Yamazawa, Ryoko
Kobayashi, Hiroyuki
Fujita, Nobuharu
Chino, Bun
Fujii, Chiyo
Kashima, Haruo
Rassovsky, Yuri
Green, Michael F.
Mizuno, Masafumi
TI Cognitive training for divergent thinking in schizophrenia: A pilot
study
SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
LA English
DT Review
DE Cognitive training; Divergent thinking; Negative symptoms;
Schizophrenia; Social functioning
ID NEUROCOGNITIVE DEFICITS; REMEDIATION; SCALE
AB Individuals with schizophrenia demonstrate deficits in divergent thinking. This ability is indispensable for generating creative solutions and navigating the complexities of social interactions. In a pilot study, seventeen stable schizophrenia outpatients were randomly assigned to a training program for divergent thinking or a control program on convergent thinking. After eight weeks of training, participants in the divergent thinking program had significantly greater improvements on measures of idea fluency, negative symptoms, and interpersonal relations than did participants receiving the control program. These preliminary results suggest that interventions for divergent thinking in schizophrenia may lead to improvements in patients' social functioning. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Nemoto, Takahiro] Keio Univ, Sch Med, Dept Neuropsychiat, Shinjuku Ku, Tokyo 1608582, Japan.
[Nemoto, Takahiro] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Nemoto, Takahiro; Green, Michael F.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Fujii, Chiyo] Saitama Prefectural Univ, Dept Social Work, Saitama, Japan.
[Rassovsky, Yuri; Green, Michael F.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90024 USA.
[Mizuno, Masafumi] Toho Univ, Sch Med, Dept Neuropsychiat, Tokyo, Japan.
RP Nemoto, T (reprint author), Keio Univ, Sch Med, Dept Neuropsychiat, Shinjuku Ku, 35 Shinanomachi, Tokyo 1608582, Japan.
EM nemotaka@aol.com
FU Research Group for Schizophrenia, Japan
FX We thank Mr. Ryosuke Ito, who kindly consulted on the development of the
tasks in the study, and Dr. Jin Hwan Choi for help in interpretation of
the data. Funding for this study was provided by a grant to Takahiro
Nemoto from the Research Group for Schizophrenia, Japan.
NR 26
TC 7
Z9 7
U1 1
U2 17
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0278-5846
J9 PROG NEURO-PSYCHOPH
JI Prog. Neuro-Psychopharmacol. Biol. Psychiatry
PD NOV 13
PY 2009
VL 33
IS 8
BP 1533
EP 1536
DI 10.1016/j.pnpbp.2009.08.015
PG 4
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 532RL
UT WOS:000272767100035
PM 19733608
ER
PT J
AU Jacobsohn, DA
Gilman, AL
Rademaker, A
Browning, B
Grimley, M
Lehmann, L
Nemecek, ER
Thormann, K
Schultz, KR
Vogelsang, GB
AF Jacobsohn, David A.
Gilman, Andrew L.
Rademaker, Alfred
Browning, Brittan
Grimley, Michael
Lehmann, Leslie
Nemecek, Eneida R.
Thormann, Kimberly
Schultz, Kirk R.
Vogelsang, Georgia B.
TI Evaluation of pentostatin in corticosteroid-refractory chronic
graft-versus-host disease in children: a Pediatric Blood and Marrow
Transplant Consortium study
SO BLOOD
LA English
DT Article
ID CONSENSUS DEVELOPMENT PROJECT; STEM-CELL TRANSPLANTATION; WORKING
GROUP-REPORT; AUTOIMMUNE HEMOLYTIC-ANEMIA; CLINICAL-TRIALS; CHRONIC
GVHD; EXTRACORPOREAL PHOTOCHEMOTHERAPY; MYCOPHENOLATE-MOFETIL; CRITERIA;
THERAPY
AB There is no standard therapy for steroid-refractory chronic graft-versus-host disease (GVHD). This problem is particularly daunting in children with chronic GVHD, whereby the effects of the disease and its treatment may impair normal growth and development. Children are also particularly vulnerable to failure and/or toxicity of therapy; for example, joint contractures or joint damage may result in lifelong disability. The Pediatric Blood and Marrow Transplant Consortium performed a phase 2 trial of pentostatin for steroid-refractory chronic GVHD in 51 children (median age, 9.8 years) from 24 institutions. Overall response was 53% (95% confidence interval, 40%-64%), with a response of 59% (95% confidence interval, 42%-75%) in sclerosis. Thirteen subjects (25%) had toxicity requiring them to stop pentostatin. The drug had a significant steroid-sparing effect in those that responded. A trend was also observed toward increased survival at 3 years in responders versus nonresponders (69% vs 50%; P = .06). The intravenous administration of the drug ensures compliance in a patient group in which oral therapy is difficult to monitor. Pentostatin has activity in refractory chronic GVHD in children, and future studies, including treatment of children newly diagnosed with high-risk chronic GVHD, are warranted. The trial was registered at www.Clinicaltrials.gov as #NCT00144430. (Blood. 2009;114: 4354-4360)
C1 [Jacobsohn, David A.; Rademaker, Alfred; Thormann, Kimberly] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60614 USA.
[Gilman, Andrew L.] Levine Childrens Hosp, Charlotte, NC USA.
[Browning, Brittan] Univ Utah, Hlth Sci Ctr, Salt Lake City, UT USA.
[Grimley, Michael] Methodist Childrens Hosp, San Antonio, TX USA.
[Lehmann, Leslie] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Nemecek, Eneida R.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Schultz, Kirk R.] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
[Vogelsang, Georgia B.] Johns Hopkins Univ, Sidney Kimmel Canc Ctr, Baltimore, MD USA.
RP Jacobsohn, DA (reprint author), Northwestern Univ, Sch Med, Stem Cell Transplant Program, Childrens Mem Hosp, 2300 Childrens Plaza,Box 30, Chicago, IL 60614 USA.
EM djacobsohn@childrensmemorial.org
NR 36
TC 18
Z9 19
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD NOV 12
PY 2009
VL 114
IS 20
BP 4354
EP 4360
DI 10.1182/blood-2009-05-224840
PG 7
WC Hematology
SC Hematology
GA 518WW
UT WOS:000271727500006
PM 19745067
ER
PT J
AU Kubota, Y
Osawa, M
Jakt, LM
Yoshikawa, K
Nishikawa, SI
AF Kubota, Yasushi
Osawa, Masatake
Jakt, Lars Martin
Yoshikawa, Kazuaki
Nishikawa, Shin-Ichi
TI Necdin restricts proliferation of hematopoietic stem cells during
hematopoietic regeneration
SO BLOOD
LA English
DT Article
ID PRADER-WILLI-SYNDROME; NEURONAL GROWTH SUPPRESSOR; GENE-EXPRESSION;
IN-VIVO; DIFFERENTIATION; TRANSCRIPTION; PROTEIN; QUIESCENCE; INTERACTS;
APOPTOSIS
AB Hematopoietic stem cell (HSC) proliferation is tightly regulated by a poorly understood complex of positive and negative cell-cycle regulatory mechanisms. Necdin (Ndn) is an evolutionally conserved multifunctional protein that has been implicated in cell-cycle regulation of neuronal cells. Here, we provide evidence that necdin plays an important role in restricting excessive HSC proliferation during hematopoietic regeneration. We identify Ndn as being preferentially expressed in the HSC population on the basis of gene expression profiling and demonstrate that mice deficient in Ndn show accelerated recovery of the hematopoietic system after myelosuppressive injury, whereas no overt abnormality is seen in steady-state hematopoiesis. In parallel, after myelosuppression, Ndn-deficient mice exhibit an enhanced number of proliferating HSCs. Based on these findings, we propose that necdin functions in a negative feedback loop that prevents excessive proliferation of HSCs during hematopoietic regeneration. These data suggest that the inhibition of necdin after clinical myelosuppressive treatment (eg, chemotherapy, HSC transplantation) may provide therapeutic benefits by accelerating hematologic recovery. (Blood. 2009;114:4383-4392)
C1 [Kubota, Yasushi; Osawa, Masatake; Jakt, Lars Martin; Nishikawa, Shin-Ichi] RIKEN, Ctr Dev Biol, Lab Stem Cell Biol, Chuo Ku, Kobe, Hyogo 6500047, Japan.
[Osawa, Masatake] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA.
[Osawa, Masatake] Harvard Univ, Sch Med, Charlestown, MA USA.
[Yoshikawa, Kazuaki] Osaka Univ, Inst Prot Res, Osaka, Japan.
RP Kubota, Y (reprint author), RIKEN, Ctr Dev Biol, Lab Stem Cell Biol, Chuo Ku, Kobe, Hyogo 6500047, Japan.
EM kubotay@cdb.riken.jp
FU Grant-in-aid for Scientific Research Priority Areas [17045037]; Ministry
of Education, Culture, Sports, Science, and Technology of Japan
FX This work was supported by in part by a Grant-in-aid for Scientific
Research Priority Areas (17045037) (M.O.) and a grant for Regenerative
Medicine Realization Project (S.-I.N.) from Ministry of Education,
Culture, Sports, Science, and Technology of Japan.
NR 50
TC 26
Z9 26
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 12
PY 2009
VL 114
IS 20
BP 4383
EP 4392
DI 10.1182/blood-2009-07-230292
PG 10
WC Hematology
SC Hematology
GA 518WW
UT WOS:000271727500010
PM 19770359
ER
PT J
AU McGrath, CL
Glatt, SJ
Sklar, P
Le-Niculescu, H
Kuczenski, R
Doyle, AE
Biederman, J
Mick, E
Faraone, SV
Niculescu, AB
Tsuang, MT
AF McGrath, Casey L.
Glatt, Stephen J.
Sklar, Pamela
Le-Niculescu, Helen
Kuczenski, Ronald
Doyle, Alysa E.
Biederman, Joseph
Mick, Eric
Faraone, Stephen V.
Niculescu, Alexander B.
Tsuang, Ming T.
TI Evidence for genetic association of RORB with bipolar disorder
SO BMC PSYCHIATRY
LA English
DT Article
ID CONVERGENT FUNCTIONAL GENOMICS; DEFICIT HYPERACTIVITY DISORDER;
CIRCADIAN-RHYTHM; CANDIDATE GENES; WIDE ASSOCIATION; MOOD DISORDERS;
CLOCK GENES; STRESS; SYMPTOMS; ONSET
AB Background: Bipolar disorder, particularly in children, is characterized by rapid cycling and switching, making circadian clock genes plausible molecular underpinnings for bipolar disorder. We previously reported work establishing mice lacking the clock gene D-box binding protein (DBP) as a stress-reactive genetic animal model of bipolar disorder. Microarray studies revealed that expression of two closely related clock genes, RAR-related orphan receptors alpha (RORA) and beta (RORB), was altered in these mice. These retinoid-related receptors are involved in a number of pathways including neurogenesis, stress response, and modulation of circadian rhythms. Here we report association studies between bipolar disorder and single-nucleotide polymorphisms ( SNPs) in RORA and RORB.
Methods: We genotyped 355 RORA and RORB SNPs in a pediatric cohort consisting of a family-based sample of 153 trios and an independent, non-overlapping case-control sample of 152 cases and 140 controls. Bipolar disorder in children and adolescents is characterized by increased stress reactivity and frequent episodes of shorter duration; thus our cohort provides a potentially enriched sample for identifying genes involved in cycling and switching.
Results: We report that four intronic RORB SNPs showed positive associations with the pediatric bipolar phenotype that survived Bonferroni correction for multiple comparisons in the case-control sample. Three RORB haplotype blocks implicating an additional 11 SNPs were also associated with the disease in the case-control sample. However, these significant associations were not replicated in the sample of trios. There was no evidence for association between pediatric bipolar disorder and any RORA SNPs or haplotype blocks after multiple-test correction. In addition, we found no strong evidence for association between the age-at-onset of bipolar disorder with any RORA or RORB SNPs.
Conclusion: Our findings suggest that clock genes in general and RORB in particular may be important candidates for further investigation in the search for the molecular basis of bipolar disorder.
C1 [Le-Niculescu, Helen; Niculescu, Alexander B.] Indiana Univ, Sch Med, Dept Psychiat, Lab Neurophen, Indianapolis, IN 46202 USA.
[McGrath, Casey L.; Sklar, Pamela] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[McGrath, Casey L.] Indiana Univ, Dept Biol, Bloomington, IN USA.
[Glatt, Stephen J.; Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY USA.
[Kuczenski, Ronald; Tsuang, Ming T.] UC San Diego, Dept Psychiat, La Jolla, CA USA.
[Doyle, Alysa E.; Biederman, Joseph; Mick, Eric] Massachusetts Gen Hosp, Pediat Psychopharmacol Unit, Boston, MA 02114 USA.
[Doyle, Alysa E.; Biederman, Joseph; Mick, Eric] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Psychiat Psychopharmacol Unit, Boston, MA USA.
RP Niculescu, AB (reprint author), Indiana Univ, Sch Med, Dept Psychiat, Lab Neurophen, Indianapolis, IN 46202 USA.
EM mcgrath.casey@gmail.com; glatts@upstate.edu; sklar@broad.mit.edu;
hlenicul@iupui.edu; rkuczenski@ucsd.edu; doylea@helix.mgh.harvard.edu;
biederman@helix.mgh.harvard.edu; emick1@partners.org;
faraones@upstate.edu; anicules@iupui.edu; mtsuang@ucsd.edu
OI Glatt, Stephen/0000-0002-0360-7567; Mick, Eric/0000-0001-8505-8145;
Faraone, Stephen/0000-0002-9217-3982
FU U. S. National Institute of Mental Health [1 R01 MH 071912]; NARSAD
FX This work was supported by a grant ( 1 R01 MH 071912) from the U. S.
National Institute of Mental Health to MTT and NARSAD Mogens Schou Young
Investigator award to ABN.
NR 51
TC 53
Z9 53
U1 0
U2 8
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-244X
J9 BMC PSYCHIATRY
JI BMC Psychiatry
PD NOV 12
PY 2009
VL 9
AR 70
DI 10.1186/1471-244X-9-70
PG 8
WC Psychiatry
SC Psychiatry
GA 525MQ
UT WOS:000272220600001
PM 19909500
ER
PT J
AU Moellering, RE
Cornejo, M
Davis, TN
Del Bianco, C
Aster, JC
Blacklow, SC
Kung, AL
Gilliland, DG
Verdine, GL
Bradner, JE
AF Moellering, Raymond E.
Cornejo, Melanie
Davis, Tina N.
Del Bianco, Cristina
Aster, Jon C.
Blacklow, Stephen C.
Kung, Andrew L.
Gilliland, D. Gary
Verdine, Gregory L.
Bradner, James E.
TI Direct inhibition of the NOTCH transcription factor complex
SO NATURE
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; GAMMA-SECRETASE INHIBITORS; T-CELL
LEUKEMIA; PROGENITOR CELLS; HUMAN HOMOLOG; C-MYC; MUTATIONS; GENE;
MASTERMIND; ACTIVATION
AB Direct inhibition of transcription factor complexes remains a central challenge in the discipline of ligand discovery. In general, these proteins lack surface involutions suitable for high-affinity binding by small molecules. Here we report the design of synthetic, cell-permeable, stabilized alpha-helical peptides that target a critical protein-protein interface in the NOTCH transactivation complex. We demonstrate that direct, high-affinity binding of the hydrocarbon-stapled peptide SAHM1 prevents assembly of the active transcriptional complex. Inappropriate NOTCH activation is directly implicated in the pathogenesis of several disease states, including T-cell acute lymphoblastic leukaemia (T-ALL). The treatment of leukaemic cells with SAHM1 results in genome-wide suppression of NOTCH-activated genes. Direct antagonism of the NOTCH transcriptional program causes potent, NOTCH-specific anti-proliferative effects in cultured cells and in a mouse model of NOTCH1-driven T-ALL.
C1 [Moellering, Raymond E.; Bradner, James E.] Broad Inst Harvard & MIT, Chem Biol Program, Cambridge, MA 02142 USA.
[Moellering, Raymond E.; Verdine, Gregory L.] Harvard Univ, Dept Chem & Biol Chem, Cambridge, MA 02138 USA.
[Moellering, Raymond E.; Verdine, Gregory L.; Bradner, James E.] Dana Farber Canc Inst, Program Canc Chem Biol, Boston, MA 02115 USA.
[Cornejo, Melanie; Gilliland, D. Gary] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA.
[Del Bianco, Cristina; Aster, Jon C.; Blacklow, Stephen C.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Davis, Tina N.; Kung, Andrew L.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Davis, Tina N.; Kung, Andrew L.] Harvard Univ, Sch Med, Childrens Hosp, Boston, MA 02115 USA.
[Gilliland, D. Gary] Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA.
[Bradner, James E.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Div Hematol Neoplasia, Boston, MA 02115 USA.
RP Bradner, JE (reprint author), Broad Inst Harvard & MIT, Chem Biol Program, Cambridge, MA 02142 USA.
EM gregory_verdine@harvard.edu; james_bradner@dfci.harvard.edu
RI Del Bianco, Cristina/J-4665-2012;
OI Kung, Andrew/0000-0002-9091-488X
FU Leukaemia & Lymphoma Society; AACR Centennial Pre-doctoral Research
Fellowship in Cancer Research; American Society of Hematology; MCCB-NIH
[5T32GM007598]; Human Frontier Science Program; Harvard & Dana Farber
Program in Cancer Chemical Biology; National Cancer Institute's
Initiative for Chemical Genetics, National Institutes of Health
[N01-CO-12400]
FX We thank S. Schreiber and the Broad Institute Chemical Biology Program
for discussions and access to instrumentation; J. Rocnik for assistance
in the establishment of the T-ALL murine model; A. Ferrando for
providing GSI microarray data; M. Hancock and Invitrogen for providing
beta-lactamase HeLa reporter clones; K. Ross and A. Subramanian for
conversations and guidance about GSEA; and S. Gupta and the Broad
Institute Microarray Core. This work was supported by a Specialized
Center of Research grant from the Leukaemia & Lymphoma Society (to J. E.
B., J. C. A., S. C. B.), an AACR Centennial Pre-doctoral Research
Fellowship in Cancer Research (to R. E. M.), the American Society of
Hematology (to J. E. B.), MCCB-NIH Training Grant No. 5T32GM007598 (to
R. E. M.), the Human Frontier Science Program (to C. D.), and the
Harvard & Dana Farber Program in Cancer Chemical Biology (to J. E. B.,
R. E. M., G. L. V.). The project has been funded in part with Federal
funds from the National Cancer Institute's Initiative for Chemical
Genetics, National Institutes of Health, under Contract No.
N01-CO-12400. Histology and immunohistochemical staining was performed
in the Dana Farber/Harvard Cancer Center Specialized Histopathology
Services Core Laboratory.
NR 50
TC 410
Z9 419
U1 1
U2 72
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 12
PY 2009
VL 462
IS 7270
BP 182
EP U57
DI 10.1038/nature08543
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 517YM
UT WOS:000271655100035
PM 19907488
ER
PT J
AU Baden, LR
Digumarthy, SR
Guimaraes, ASR
Branda, JA
AF Baden, Lindsey R.
Digumarthy, Subba R.
Guimaraes, Alexander S. R.
Branda, John A.
TI Case 35-2009: A 60-Year-Old Male Renal-Transplant Recipient with Renal
Insufficiency, Diabetic Ketoacidosis, and Mental-Status Changes.
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID COCCIDIOIDES-IMMITIS; NECROSIS-FACTOR; INFECTION; SEROLOGY; DISEASE
C1 [Baden, Lindsey R.] Brigham & Womens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Digumarthy, Subba R.; Guimaraes, Alexander S. R.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Branda, John A.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Baden, Lindsey R.] Harvard Univ, Sch Med, Dept Med, Cambridge, MA 02138 USA.
[Digumarthy, Subba R.; Guimaraes, Alexander S. R.] Harvard Univ, Sch Med, Dept Radiol, Cambridge, MA 02138 USA.
[Branda, John A.] Harvard Univ, Sch Med, Dept Pathol, Cambridge, MA 02138 USA.
RP Baden, LR (reprint author), Brigham & Womens Hosp, Div Infect Dis, Boston, MA 02115 USA.
NR 23
TC 2
Z9 2
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 12
PY 2009
VL 361
IS 20
BP 1980
EP 1989
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 518AI
UT WOS:000271660500015
PM 19907046
ER
PT J
AU Kujawa, SG
Liberman, MC
AF Kujawa, Sharon G.
Liberman, M. Charles
TI Adding Insult to Injury: Cochlear Nerve Degeneration after "Temporary"
Noise-Induced Hearing Loss
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID KAINIC ACID EXCITOTOXICITY; GUINEA-PIG COCHLEA; CARBOPLATIN-TREATED
CHINCHILLAS; MAMMALIAN COCHLEA; CAT COCHLEA; SERIAL SECTIONS;
HAIR-CELLS; INNER-EAR; SYNAPSES; AFFERENT
AB Overexposure to intense sound can cause temporary or permanent hearing loss. Postexposure recovery of threshold sensitivity has been assumed to indicate reversal of damage to delicate mechano-sensory and neural structures of the inner ear and no persistent or delayed consequences for auditory function. Here, we show, using cochlear functional assays and confocal imaging of the inner ear in mouse, that acoustic overexposures causing moderate, but completely reversible, threshold elevation leave cochlear sensory cells intact, but cause acute loss of afferent nerve terminals and delayed degeneration of the cochlear nerve. Results suggest that noise-induced damage to the ear has progressive consequences that are considerably more widespread than are revealed by conventional threshold testing. This primary neurodegeneration should add to difficulties hearing in noisy environments, and could contribute to tinnitus, hyperacusis, and other perceptual anomalies commonly associated with inner ear damage.
C1 [Kujawa, Sharon G.; Liberman, M. Charles] Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA.
[Kujawa, Sharon G.; Liberman, M. Charles] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
[Kujawa, Sharon G.] Massachusetts Eye & Ear Infirm, Dept Audiol, Boston, MA 02114 USA.
[Kujawa, Sharon G.; Liberman, M. Charles] Harvard Massachusetts Inst Technol, Div Hlth Sci & Technol, Program Speech & Hearing Biosci & Technol, Cambridge, MA 02139 USA.
RP Kujawa, SG (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA.
EM sharon_kujawa@meei.harvard.edu
FU National Institute on Deafness and Other Communicative Disorders [R01
DC8577, RO1 DC0188, P30 DC5209]
FX Research was supported by grants from the National Institute on Deafness
and Other Communicative Disorders (R01 DC8577, RO1 DC0188, P30 DC5209)
and by a generous donation from Steve and Andrea Kaneb.
NR 56
TC 573
Z9 588
U1 10
U2 72
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 11
PY 2009
VL 29
IS 45
BP 14077
EP 14085
DI 10.1523/JNEUROSCI.2845-09.2009
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 518BD
UT WOS:000271664000003
PM 19906956
ER
PT J
AU Goebel, M
Stengel, A
Wang, LX
Tache, Y
AF Goebel, Miriam
Stengel, Andreas
Wang, Lixin
Tache, Yvette
TI Restraint stress activates nesfatin-1-immunoreactive brain nuclei in
rats
SO BRAIN RESEARCH
LA English
DT Article
DE Fos; Nesfatin-1; NUCB2; Restraint; Hypothalamus; Medulla
ID CORTICOTROPIN-RELEASING-FACTOR; DORSAL VAGAL COMPLEX; FOS EXPRESSION;
C-FOS; PARAVENTRICULAR NUCLEUS; NEUROENDOCRINE RESPONSES; EMOTIONAL
STRESSOR; SUPRAOPTIC NUCLEI; FACTOR RECEPTORS; CELL RESPONSES
AB Nesfatin-1 is a newly discovered peptide that was reported to reduce food intake when injected centrally. We recently described its wide distribution in rat brain autonomic nuclei which implies potential recruitment of nesfatin-1 by stress. We investigated whether restraint, a mixed psychological and physical stressor, activates nesfatin-1-immunoreactive (ir) neurons in the rat brain. Male Sprague-Dawley rats were either subjected to 30 min restraint or left undisturbed and 90 min later brains were processed for double immunohistochemical labeling of Fos and nesfatin-1. Restraint induced significant Fos expression in neurons of the supraoptic nucleus (SON), paraventricular nucleus (PVN), locus coeruleus (LC), rostral raphe pallidus (rRPa), nucleus of the solitary tract (NTS), and ventrolateral medulla (VLM). Double Fos/nesfatin-1 labeling revealed that Fos-ir neurons comprised 95% of nesfatin-1-ir cells in the SON, 90% in the VLM, 80% in the LC, 48% in the caudal NTS, 57% in the rRPa, 48% in the anterior parvicellular PVN, 27% in the medial magnocellular PVN, 18% in the lateral magnocellular PVN and 10% in the medial parvicellular PVN. These data demonstrate that nesfatin-1 neurons are part of the hypothalamic and hindbrain neuronal cell groups activated by restraint suggesting a possible role of nesfatin-1 in the response to stress. Published by Elsevier B.V.
C1 [Tache, Yvette] VA Greater Los Angeles Healthcare Syst, Ctr Neurovisceral Sci & Womens Hlth, Los Angeles, CA 90073 USA.
Univ Calif Los Angeles, David Geffen Sch Med, CURE Digest Dis Res Ctr,Ctr Neurobiol Stress, Digest Dis Div,Dept Med, Los Angeles, CA 90095 USA.
RP Tache, Y (reprint author), VA Greater Los Angeles Healthcare Syst, Ctr Neurovisceral Sci & Womens Hlth, CURE Bldg 115,Room 117, Los Angeles, CA 90073 USA.
EM ytache@mednet.ucla.edu
FU German Research Foundation fellowship [Go 1718/1-1, STE 1765/1-1]; VA
Research Career Scientist Award; Department of Veterans Affairs; NIHDK
[33061]; Center [DK41301]
FX This work was supported by German Research Foundation fellowship grants
Go 1718/1-1 (M.G.) and STE 1765/1-1 (A.S.), the VA Research Career
Scientist Award, Department of Veterans Affairs, NIHDK 33061 (Y.T.) and
Center grant DK41301 (Animal Core, Y.T.). We are grateful to Mrs.
Honghui Liang for her excellent technical support and Ms. Eugenia Hu for
reviewing the manuscript.
NR 53
TC 63
Z9 63
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 10
PY 2009
VL 1300
BP 114
EP 124
DI 10.1016/j.brainres.2009.08.082
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 520DC
UT WOS:000271819200012
PM 19733157
ER
PT J
AU Weiner, RB
Kiernan, TJ
Yan, BP
Rosenfield, K
Jaff, MR
AF Weiner, Rory B.
Kiernan, Thomas J.
Yan, Bryan P.
Rosenfield, Kenneth
Jaff, Michael R.
TI Adventitial Fibromuscular Dysplasia of the Renal Artery Management
Challenges of Nonatherosclerotic Renal Artery Stenosis
SO CIRCULATION
LA English
DT Editorial Material
ID RENOVASCULAR HYPERTENSION
C1 [Weiner, Rory B.; Kiernan, Thomas J.; Rosenfield, Kenneth; Jaff, Michael R.] Massachusetts Gen Hosp, Dept Med, Div Cardiol, Sect Vasc Med, Boston, MA 02114 USA.
[Yan, Bryan P.] Chinese Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China.
[Yan, Bryan P.] Prince Wales Hosp, Dept Med & Therapeut, Div Cardiol, Hong Kong, Hong Kong, Peoples R China.
[Yan, Bryan P.] Monash Univ, Dept Epidemiol & Prevent Med, Ctr Cardiovasc Res & Educ Therapeut, Melbourne, Vic 3004, Australia.
RP Weiner, RB (reprint author), Massachusetts Gen Hosp, Dept Med, Div Cardiol, Sect Vasc Med, Yawkey 5,55 Fruit St, Boston, MA 02114 USA.
EM rweiner@partners.org
RI Yan, Bryan/P-5928-2015
NR 4
TC 2
Z9 2
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 10
PY 2009
VL 120
IS 19
BP E157
EP E158
DI 10.1161/CIRCULATIONAHA.109.872853
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 516WS
UT WOS:000271574600016
PM 19901199
ER
PT J
AU Ligibel, JA
AF Ligibel, Jennifer A.
TI Could Modification of Lifestyle Factors Prevent Second Primary Breast
Cancers?
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Editorial Material
ID PHYSICAL-ACTIVITY; POOLED ANALYSIS; RISK-FACTORS; WOMEN; TAMOXIFEN;
DIAGNOSIS; PROGNOSIS; SURVIVAL; ALCOHOL; OBESITY
C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Ligibel, JA (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
NR 18
TC 4
Z9 4
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2009
VL 27
IS 32
BP 5301
EP 5302
DI 10.1200/JCO.2009.24.4517
PG 2
WC Oncology
SC Oncology
GA 516GT
UT WOS:000271530900001
PM 19738104
ER
PT J
AU Harris, JR
Morrow, M
AF Harris, Jay R.
Morrow, Monica
TI Clinical Dilemma of Ductal Carcinoma in Situ
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Editorial Material
ID BREAST-CANCER; LOCAL RECURRENCE; RADIOTHERAPY; SURGERY; WOMEN; EXCISION;
INSITU
C1 [Harris, Jay R.] Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Radiat Oncol,Med Sch, Boston, MA 02115 USA.
[Morrow, Monica] Mem Sloan Kettering Canc Ctr, Dept Surg, Breast Serv, New York, NY 10021 USA.
RP Harris, JR (reprint author), Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Radiat Oncol,Med Sch, Boston, MA 02115 USA.
NR 18
TC 6
Z9 6
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2009
VL 27
IS 32
BP 5303
EP 5305
DI 10.1200/JCO.2009.24.1489
PG 3
WC Oncology
SC Oncology
GA 516GT
UT WOS:000271530900002
PM 19826109
ER
PT J
AU Hughes, LL
Wang, ML
Page, DL
Gray, R
Solin, LJ
Davidson, NE
Lowen, MA
Ingle, JN
Recht, A
Wood, WC
AF Hughes, Lorie L.
Wang, Molin
Page, David L.
Gray, Robert
Solin, Lawrence J.
Davidson, Nancy E.
Lowen, Mary Ann
Ingle, James N.
Recht, Abram
Wood, William C.
TI Local Excision Alone Without Irradiation for Ductal Carcinoma In Situ of
the Breast: A Trial of the Eastern Cooperative Oncology Group
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID SURGICAL ADJUVANT BREAST; NUYS PROGNOSTIC INDEX; RANDOMIZED
CONTROLLED-TRIAL; CONSERVING TREATMENT; MARGIN WIDTH; CANCER;
RADIOTHERAPY; RECURRENCE; TAMOXIFEN; SURGERY
AB Purpose
To determine the risk of ipsilateral breast events in patients with ductal carcinoma in situ ( DCIS) treated with local excision without irradiation.
Patients and Methods
Patients with either low- or intermediate-grade DCIS measuring 2.5 cm or smaller, or high-grade DCIS measuring 1 cm or smaller who had microscopic margin widths of 3 mm or wider and no residual calcifications on postoperative mammograms were eligible for a prospective trial conducted from 1997 to 2002 by the Eastern Cooperative Oncology Group and North Central Cancer Treatment Group. Patients entered in 2000 and later could take tamoxifen if they wished. Median age at last surgery for the entire population was 60 years (range, 28 to 88 years), and median tumor sizes in the two strata were 6 mm and 5 mm, respectively.
Results
With a median follow-up of 6.2 years, the 5-year rate of ipsilateral breast events in the 565 eligible patients in the low/intermediate grade stratum was 6.1% (95% CI, 4.1% to 8.2%). With a median follow-up of 6.7 years, this incidence for the 105 eligible patients in the high-grade stratum was 15.3% (95% CI, 8.2% to 22.5%).
Conclusion
Rigorously evaluated and selected patients with low- to intermediate-grade DCIS with margins 3 mm or wider had an acceptably low rate of ipsilateral breast events at 5 years after excision without irradiation. Patients with high-grade lesions had a much higher rate, suggesting that excision alone is inadequate treatment. Further follow-up is necessary to document long-term results.
C1 N Georgia Radiat Therapy Hope Ctr, Cartersville, GA USA.
Emory Univ, Atlanta, GA 30322 USA.
Dana Farber Canc Inst, Boston, MA USA.
Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
Vanderbilt Univ, Nashville, TN USA.
Univ Penn, Philadelphia, PA 19104 USA.
Johns Hopkins Univ, Sch Med, Johns Hopkins Oncol Ctr, Baltimore, MD 21205 USA.
Baystate Med Ctr, Springfield, MA USA.
Mayo Clin, Rochester, MN USA.
RP Hughes, LL (reprint author), Hope Ctr, 100 Market Pl Blvd,Ste 102, Cartersville, GA 30121 USA.
EM lhughesmd@aol.com
FU National Cancer Institute, National Institutes of Health [CA23318,
CA66636, CA21115, CA40057, CA07190, CA25224, CA16116]; Department of
Health and Human Services
FX Supported in part by Public Health Service Grants No. CA23318, CA66636,
CA21115, CA40057, CA07190, CA25224, and CA16116 and from the National
Cancer Institute, National Institutes of Health, and the Department of
Health and Human Services.
NR 24
TC 164
Z9 176
U1 0
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2009
VL 27
IS 32
BP 5319
EP 5324
DI 10.1200/JCO.2009.21.8560
PG 6
WC Oncology
SC Oncology
GA 516GT
UT WOS:000271530900006
PM 19826126
ER
PT J
AU Kornblith, AB
Huang, HQ
Walker, JL
Spirtos, NM
Rotmensch, J
Cella, D
AF Kornblith, Alice B.
Huang, Helen Q.
Walker, Joan L.
Spirtos, Nick M.
Rotmensch, Jacob
Cella, David
TI Quality of Life of Patients With Endometrial Cancer Undergoing
Laparoscopic International Federation of Gynecology and Obstetrics
Staging Compared With Laparotomy: A Gynecologic Oncology Group Study
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID FUNCTIONAL ASSESSMENT; OPEN COLECTOMY; MANAGEMENT; CARCINOMA; WOMEN;
COST
AB Purpose
The study's objective was to compare the quality of life (QoL) of patients with endometrial cancer undergoing surgical staging via laparoscopy versus laparotomy.
Patients and Methods
The first 802 eligible patients (laparoscopy, n = 535; laparotomy, n = 267) participated in the QoL study in a Gynecologic Oncology Group (GOG) randomized trial of laparoscopy versus laparotomy (GOG 2222). Patients completed QoL assessments at baseline; at 1, 3, and 6 weeks; and at 6 months postsurgery.
Results
In an intent-to-treat analysis, laparoscopy patients reported significantly higher Functional Assessment of Cancer Therapy-General (FACT-G) scores (P = .001), better physical functioning (P = .006), better body image (BI; P < .001), less pain (P < .001) and its interference with QoL (P < .001), and an earlier resumption of normal activities (P = .003) and return to work (P = .04) over the 6-week postsurgery period, as compared with laparotomy patients. However, the differences in BI and return to work between groups were modest, and the adjusted FACT-G scores did not meet the minimally important difference ( MID) between the two surgical arms over 6 weeks. By 6 months, except for better BI in laparoscopy patients (P < .001), the difference in QoL between the two surgical techniques was not statistically significant.
Conclusion
Although the FACT-G did not show a MID between the two surgical groups, and only modest differences in return to work and BI were found between the two groups, statistically significantly better QoL across many parameters in the laparoscopy arm at 6 weeks provides modest support for the QoL advantage of using laparoscopy to stage patients with early endometrial cancer.
C1 [Kornblith, Alice B.] Dana Farber Canc Inst, Div Womens Cancers, Boston, MA 02115 USA.
Roswell Pk Canc Inst, Gynecol Oncol Grp Stat, Buffalo, NY 14263 USA.
Roswell Pk Canc Inst, Ctr Data, Buffalo, NY 14263 USA.
Univ Oklahoma, Hlth Sci Ctr, Dept Obstet & Gynecol, Oklahoma City, OK 73190 USA.
Univ Nevada, Sch Med, Womens Canc Ctr Nevada, Las Vegas, NV 89154 USA.
Rush Presbyterian St Lukes Med Ctr, Chicago, IL 60612 USA.
Ctr Outcomes Res & Educ, Evanston, IL USA.
RP Kornblith, AB (reprint author), Dana Farber Canc Inst, Div Womens Cancers, 44 Binney St,LW 231, Boston, MA 02115 USA.
EM alice_kornblith@dfci.harvard.edu
FU National Cancer Institute [CA 27469, CA 37517]; GOG
FX Supported by National Cancer Institute grants to the Gynecologic
Oncology Group (GOG) Administrative Office (Grant No. CA 27469) and the
GOG Statistical and Data Center (Grant No. CA 37517). J.L.W. was
supported by GOG.
NR 19
TC 114
Z9 121
U1 1
U2 4
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2009
VL 27
IS 32
BP 5337
EP 5342
DI 10.1200/JCO.2009.22.3529
PG 6
WC Oncology
SC Oncology
GA 516GT
UT WOS:000271530900009
PM 19805678
ER
PT J
AU Chen, AB
Punglia, RS
Kuntz, KM
Mauch, PM
Ng, AK
AF Chen, Aileen B.
Punglia, Rinaa S.
Kuntz, Karen M.
Mauch, Peter M.
Ng, Andrea K.
TI Cost Effectiveness and Screening Interval of Lipid Screening in
Hodgkin's Lymphoma Survivors
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID CORONARY-HEART-DISEASE; ACUTE MYOCARDIAL-INFARCTION; LONG-TERM
SURVIVORS; TREATMENT PANEL-III; ARTERY-DISEASE; MEDIASTINAL IRRADIATION;
RADIATION-THERAPY; DATA-BASE; MORTALITY; CHOLESTEROL
AB Purpose
Survivors of Hodgkin's lymphoma (HL) who received mediastinal irradiation have an increased risk of coronary heart disease. We evaluated the cost effectiveness of lipid screening in survivors of HL and compared different screening intervals.
Methods
We developed a decision-analytic model to evaluate lipid screening in a hypothetical cohort of 30-year-old survivors of HL who survived 5 years after mediastinal irradiation. We compared the following strategies: no screening, and screening at 1-, 3-, 5-, or 7-year intervals. Screen-positive patients were treated with statins. Markov models were used to calculate life expectancy, quality-adjusted life expectancy, and lifetime costs. Baseline probabilities, transition probabilities, and utilities were derived from published studies and US population data. Costs were estimated from Medicare fee schedules and the medical literature. Sensitivity analyses were performed.
Results
Using an incremental cost-effectiveness ratio (ICER) threshold of $100,000 per quality-adjusted life-year (QALY) saved, lipid screening at every interval was cost effective relative to a strategy of no screening. When comparing screening intervals, a 3- year interval was cost effective relative to a 5- year interval, but annual screening, relative to screening every 3 years, had an ICER of more than $100,000/QALY saved. Factors with the most influence on the results included risk of cardiac events/death after HL, efficacy of statins in reducing cardiac events/death, and costs of statins.
Conclusion
Lipid screening in survivors of HL, with statin therapy for screen-positive patients, improves survival and is cost effective. A screening interval of 3 years seems reasonable in the long-term follow-up of survivors of HL.
C1 [Chen, Aileen B.] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
Univ Minnesota, Sch Publ Hlth, Div Hlth Policy & Management, Minneapolis, MN USA.
RP Chen, AB (reprint author), Dana Farber Canc Inst, Dept Radiat Oncol, 44 Binney St,Smith 255, Boston, MA 02115 USA.
EM achen7@partners.org
OI Chen, Aileen/0000-0002-5385-3360
NR 53
TC 13
Z9 13
U1 1
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2009
VL 27
IS 32
BP 5383
EP 5389
DI 10.1200/JCO.2009.22.8460
PG 7
WC Oncology
SC Oncology
GA 516GT
UT WOS:000271530900016
PM 19752333
ER
PT J
AU Bilimoria, KY
Raval, MV
Bentrem, DJ
Wayne, JD
Balch, CM
Ko, CY
AF Bilimoria, Karl Y.
Raval, Mehul V.
Bentrem, David J.
Wayne, Jeffrey D.
Balch, Charles M.
Ko, Clifford Y.
TI National Assessment of Melanoma Care Using Formally Developed Quality
Indicators
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID CANCER DATA-BASE; COLORECTAL-CANCER; UNITED-STATES; APPROPRIATENESS
METHOD; PERFORMANCE-MEASURES; MALIGNANT-MELANOMA; ASSESSMENT TOOLS;
CARDIAC-SURGERY; SURGICAL CARE; HEALTH-CARE
AB Purpose
There is considerable variation in the quality of cancer care delivered in the United States. Assessing care by using quality indicators could help decrease this variability. The objectives of this study were to formally develop valid quality indicators for melanoma and to assess hospital-level adherence with these measures in the United States.
Methods
Quality indicators were identified from available literature, consensus guidelines, and melanoma experts. Thirteen experts ranked potential measures for validity on the basis of the RAND/University of California, Los Angeles Appropriateness Methodology. Adherence with individual valid indicators and a composite measure of all indicators were assessed at 1,249 Commission on Cancer hospitals by using the National Cancer Data Base (NCDB; 2004 through 2005).
Results
Of 55 proposed quality indicators, 26 measures (47%) were rated as valid. These indicators assessed structure (n = 1), process (n = 24), and outcome (n = 1). Of the 26 measures, 10 are readily assessable by using cancer registry data. Adherence with valid indicators ranged from 11.8% to 96.5% at the patient level and 3.7% to 83.0% at the hospital level. (Adherence required that > 90% of patients at a hospital receive concordant care.) Most hospitals were adherent with 50% or fewer of the individual indicators (median composite score, five; interquartile range, four to seven). Adherence was higher for diagnosis and staging measures and was lower for treatment indicators.
Conclusion
There is considerable variation in the quality of melanoma care in the United States. By using these formally developed quality indicators, hospitals can assess their adherence with current melanoma care guidelines through feedback mechanisms from the NCDB and can better direct quality improvement efforts.
C1 [Bilimoria, Karl Y.] Amer Coll Surg, Canc Programs, Chicago, IL 60611 USA.
Northwestern Univ, Dept Surg, Feinberg Sch Med, Chicago, IL 60611 USA.
Johns Hopkins Sch Med, Dept Surg, Baltimore, MD USA.
Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA.
Vet Affairs Greater Los Angeles Hlth Care Syst, Los Angeles, CA USA.
RP Bilimoria, KY (reprint author), Amer Coll Surg, Canc Programs, 633 N St Clair St,22nd Floor, Chicago, IL 60611 USA.
EM kbilimoria@facs.org
OI Raval, Mehul/0000-0002-1527-2661
FU American College of Surgeons Clinical Scholars in Residence program;
American College of Surgeons; Commission on Cancer; American Cancer
Society (National Cancer Data Base)
FX Supported by the American College of Surgeons Clinical Scholars in
Residence program (K.Y.B. and M.V.R.); and by the American College of
Surgeons, the Commission on Cancer, and the American Cancer Society
(National Cancer Data Base).
NR 51
TC 36
Z9 36
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2009
VL 27
IS 32
BP 5445
EP 5451
DI 10.1200/JCO.2008.20.9965
PG 7
WC Oncology
SC Oncology
GA 516GT
UT WOS:000271530900025
PM 19826131
ER
PT J
AU Lane, AA
Chabner, BA
AF Lane, Andrew A.
Chabner, Bruce A.
TI Histone Deacetylase Inhibitors in Cancer Therapy
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
ID T-CELL LYMPHOMA; SUBEROYLANILIDE HYDROXAMIC ACID; REFRACTORY SOLID
TUMORS; ACUTE MYELOID-LEUKEMIA; PHASE-II TRIAL; FRIEND ERYTHROLEUKEMIA
CELLS; HDAC INHIBITORS; MYELODYSPLASTIC SYNDROMES; HEMATOLOGIC
MALIGNANCIES; GENE-EXPRESSION
AB Purpose Epigenetic processes are implicated in cancer causation and progression. The acetylation status of histones regulates access of transcription factors to DNA and influences levels of gene expression. Histone deacetylase (HDAC) activity diminishes acetylation of histones, causing compaction of the DNA/histone complex. This compaction blocks gene transcription and inhibits differentiation, providing a rationale for developing HDAC inhibitors.
Methods In this review, we explore the biology of the HDAC enzymes, summarize the pharmacologic properties of HDAC inhibitors, and examine results of selected clinical trials. We consider the potential of these inhibitors in combination therapy with targeted drugs and with cytotoxic chemotherapy.
Results HDAC inhibitors promote growth arrest, differentiation, and apoptosis of tumor cells, with minimal effects on normal tissue. In addition to decompaction of the histone/DNA complex, HDAC inhibition also affects acetylation status and function of nonhistone proteins. HDAC inhibitors have demonstrated antitumor activity in clinical trials, and one drug of this class, vorinostat, is US Food and Drug Administration approved for the treatment of cutaneous T-cell lymphoma. Other inhibitors in advanced stages of clinical development, including depsipeptide and MGCD0103, differ from vorinostat in structure and isoenzyme specificity, and have shown activity against lymphoma, leukemia, and solid tumors. Promising preclinical activity in combination with cytotoxics, inhibitors of heat shock protein 90, and inhibitors of proteasome function have led to combination therapy trials.
Conclusion HDAC inhibitors are an important emerging therapy with single-agent activity against multiple cancers, and have significant potential in combination use.
C1 [Lane, Andrew A.; Chabner, Bruce A.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02214 USA.
RP Chabner, BA (reprint author), Massachusetts Gen Hosp, Ctr Canc, 55 Fruit St, Boston, MA 02214 USA.
EM bchabner@partners.org
RI qiao, zhixin/I-3408-2012
NR 130
TC 486
Z9 500
U1 6
U2 70
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2009
VL 27
IS 32
BP 5459
EP 5468
DI 10.1200/JCO.2009.22.1291
PG 10
WC Oncology
SC Oncology
GA 516GT
UT WOS:000271530900027
PM 19826124
ER
PT J
AU Marzocchetti, A
Tompkins, T
Clifford, DB
Gandhi, RT
Kesari, S
Berger, JR
Simpson, DM
Prosperi, M
De Luca, A
Koralnik, IJ
AF Marzocchetti, A.
Tompkins, T.
Clifford, D. B.
Gandhi, R. T.
Kesari, S.
Berger, J. R.
Simpson, D. M.
Prosperi, M.
De Luca, A.
Koralnik, I. J.
TI Determinants of survival in progressive multifocal leukoencephalopathy
SO NEUROLOGY
LA English
DT Article
ID ACTIVE ANTIRETROVIRAL THERAPY; CYTOTOXIC T-LYMPHOCYTES; JC VIRUS
EPITOPE; PROLONGED SURVIVAL; CLINICAL-COURSE; PML-IRIS; ASSOCIATION;
FREQUENCY; STEROIDS; HAART
AB Background: We sought to characterize the role of immunologic, virologic, and radiologic determinants of survival in patients with progressive multifocal leukoencephalopathy (PML).
Methods: We recorded the clinical outcome of 60 patients with PML (73% HIV+) who were prospectively evaluated between 2000 and 2007 for the presence of JC virus (JCV)-specific CD8+ cytotoxic T-lymphocytes (CTL) in blood.
Results: Estimated probability of survival at 1 year was 52% for HIV+/PML and 58% for HIV-patients with PML. Patients with PML with detectable CTL within 3 months of diagnosis had a 1-year estimated survival of 73% compared to 46% for those without CTL ( hazard ratio [HR] for death = 0.47, 95% confidence interval [CI] 0.13-1.75, p = 0.26). Patients with CTL response had an increased likelihood of having contrast enhancement of PML lesions and immune reconstitution inflammatory syndrome (odds ratio 3.7 and 7.8). Estimated 1-year survival was 48% in HIV-patients with PML with CD4 count <200/mu L at PML diagnosis compared to 67% in those with CD4 >200/mu L (HR for death 1.41, 95% CI 0.27-7.38, p = 0.68). JCV DNA was detected in the urine of 48% and in the blood of 56% of patients with PML, but viruria and viremia were not associated with survival.
Conclusions: The presence of JC virus (JCV)-specific cytotoxic T-lymphocytes ( CTL) was associated with a trend toward longer survival in patients with progressive multifocal leukoencephalopathy ( PML), which was more pronounced than the impact of CD4 count in HIV-patients with PML early after diagnosis. Despite the association of contrast enhancement and immune reconstitution inflammatory syndrome with JCV-specific CTL, these cannot be considered as surrogate markers for the prognostic value of the CTL. Strategies aiming at improving the cellular immune response may improve the course of PML. Neurology (R) 2009; 73: 1551-1558
C1 [Marzocchetti, A.; Tompkins, T.; Koralnik, I. J.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Viral Pathogenesis, Boston, MA 02215 USA.
[Koralnik, I. J.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Neurol, Boston, MA 02215 USA.
[Clifford, D. B.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
[Gandhi, R. T.] Harvard Univ, Sch Med, MGH, Dept Infect Dis, Boston, MA USA.
[Kesari, S.] Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Neurol,Med Sch, Boston, MA 02115 USA.
[Berger, J. R.] Univ Kentucky, Coll Med, Dept Neurol, Lexington, KY 40506 USA.
[Simpson, D. M.] Mt Sinai Sch Med, Dept Neurol, New York, NY USA.
[Prosperi, M.] Natl Inst Infect Dis L Spallanzani, Dept Virol, Rome, Italy.
[De Luca, A.] Catholic Univ, Div Infect Dis, Rome, Italy.
RP Koralnik, IJ (reprint author), Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Viral Pathogenesis, E CLS 1005,330 Brookline Ave, Boston, MA 02215 USA.
EM ikoralni@bidmc.harvard.edu
RI De Luca, Andrea/G-8810-2011; Kesari, Santosh/E-8461-2013
FU NIH [UO1 NS32228, UO1 AI69495, NIMH 22005, RO3 DA022137, NIMH MH058076,
R21 385753187, K08CA124804]; Gilead Sciences, Inc.; Tibotec
Therapeutics; Enzon Pharmaceuticals, Inc.; Sontag Foundation; EMD
Serono, Inc.; GlaxoSmithKline, Allergan, Inc.; Merz Pharmaceuticals,
LLC, and Torrey Pines Institute for Molecular Studies
FX Dr. Marzocchetti reports no disclosures. T. Tompkins holds stock options
in BioMarin Pharmaceutical, Inc. Dr. Clifford serves/has served on
scientific advisory boards for Biogen Idec, Elan Corporation, Roche,
Forest Laboratories, Inc., Genentech, Inc., GlaxoSmithKline, Millennium
Pharmaceuticals, Inc., Schering-Plough Corp., Bristol-Meyers Squibb, and
Genzyme Corporation; received speaker honorarium and funding for travel
from GlaxoSmithKline; has received research support from Pfizer Inc.,
Schering-Plough Corp., Bavarian Nordic, NeurogesX, GlaxoSmithKline,
Tibotec Therapeutics, Boehringer Ingelheim, and Gilead Sciences, Inc.;
and receives research support from the NIH [UO1 NS32228 ( PI), UO1
AI69495 ( PI), NIMH 22005 CHARTER Project ( Site PI), NIDA RO3 DA022137
(Co-I), NIMH MH058076 ( Site PI), and R21 385753187 ( PI)]. Dr. Gandhi
serves on the editorial board of Journal Watch Infectious Diseases,
received speaker honorarium from GlaxoSmithKline, received educational
support from Gilead Sciences, Inc. and Abbott, and receives research
support from Tibotec Therapeutics. Dr. Kesari serves on scientific
advisory boards for Bristol-Meyers Squibb and Genentech, Inc.; serves on
editorial boards for the Journal of Neuro-Oncology and the International
Journal of Biomedical Nanoscience and Nanotechnology; receives royalties
from publishing Cancer Neurology in Clinical Practice (Humana, 2008);
served on a speakers' bureau for Enzon Pharmaceuticals, Inc.; and
receives research support from GE Healthcare, the NIH [K08CA124804 (
PI)], and the Sontag Foundation. Dr. Berger serves/has served on
scientific advisory boards for Millennium Pharmaceuticals, Inc., Bayer
Schering Pharma, Merck Serono, Genentech, Inc., Astellas Pharma Inc.,
and Asphelia Pharmaceuticals; has received speaker honoraria from EMD
Serono, Inc., Teva Pharmaceutical Industries Ltd., and Bayer Schering
Pharma; and receives research support from Bayer Schering Pharma, EMD
Serono, Inc., Biogen Idec, Sanofi-Aventis, Genentech Inc., and UCB. Dr.
Simpson has served on scientific advisory boards for Boehringer
Ingelheim, Cephalon, Inc., Pfizer Inc., Endo Pharmaceuticals,
GlaxoSmithKline, Merz Pharmaceuticals, LLC, MEDA Pharmaceuticals Inc.,
Alpharma Pharmaceuticals LLC, and Biogen Idec; serves on the editorial
boards of the Clinical Journal of Pain and AIDS Patient Care; has served
as a consultant to NeurogesX, Eli Lilly and Company, Regeneron
Pharmaceuticals Inc., GlaxoSmithKline, Allergan, Inc., Merz
Pharmaceuticals, LLC, and Torrey Pines Institute for Molecular Studies;
served on speakers'
NR 22
TC 86
Z9 86
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD NOV 10
PY 2009
VL 73
IS 19
BP 1551
EP 1558
DI 10.1212/WNL.0b013e3181c0d4a1
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 517FO
UT WOS:000271598800007
PM 19901246
ER
PT J
AU Lopez, L
Weissman, JS
Schneider, EC
Weingart, SN
Cohen, AP
Epstein, AM
AF Lopez, Lenny
Weissman, Joel S.
Schneider, Eric C.
Weingart, Saul N.
Cohen, Amy P.
Epstein, Arnold M.
TI Disclosure of Hospital Adverse Events and Its Association With Patients'
Ratings of the Quality of Care
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID HARMFUL MEDICAL ERRORS; DRUG EVENTS; PHYSICIANS ATTITUDES; PATIENTS
WANT; EXPERIENCES; MISTAKES; MANAGEMENT; DOCTORS; SAFETY; VIEWS
AB Background: Little is known about how the characteristics of adverse events (AEs) affect the likelihood of disclosure or how the disclosure of an AE relates to patients' perception of quality of care.
Methods: The study included a random sample of medical and surgical acute care adult patients in Massachusetts hospitals between April I and October 1, 2003. The unit of analysis was the AE, and multivariable regression analyses accounted for clustering at the patient level.
Results: Overall, 603 patients reported 845 AEs, and 40% of AEs were disclosed. The AEs that required additional treatment (odds ratio [OR], 1.64; 95% confidence interval [CI], 1.16-2.32) or affected patients who reported good health (OR, 2.04; 95% CI, 1.29-3.24) were more likely to be disclosed. Disclosure was less likely if the events were preventable (OR, 0.58; 95% CI, 0.41-0.83) or if the patients were still affected by the AE at the time of survey (OR, 0.49; 95% CI, 0.31-0.78). Higher-quality ratings were associated with disclosure (OR, 2.04; 95% CI, 1.39-2.99) of preventable and nonpreventable events and with patients who felt that they were able to protect themselves from AEs (OR, 1.98; 95% CI, 1.21-3.24). Lower-quality ratings were associated with events that were preventable (OR, 0.55; 95% CI, 0.40-0.76), with events that caused increased discomfort (OR, 0.62; 95% CI, 0.46-0.86), or with events that still adversely affected the patient at the time of the survey (OR, 0.68; 95% CI, 0.46-0.98).
Conclusions: Rates of disclosure of AEs by medical personnel remain low in hospitalized patients. Disclosure of some of these events is associated with higher ratings of quality by patients.
C1 [Lopez, Lenny; Weissman, Joel S.] Massachusetts Gen Hosp, Inst Hlth Policy, Boston, MA 02114 USA.
[Lopez, Lenny; Weissman, Joel S.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Schneider, Eric C.; Epstein, Arnold M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Sect Hlth Serv & Policy Res,Div Gen Med, Boston, MA 02115 USA.
[Weissman, Joel S.; Epstein, Arnold M.] Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA.
[Cohen, Amy P.] Harvard Univ, Sch Publ Hlth, Dept Informat Technol, Boston, MA 02115 USA.
[Weingart, Saul N.] Dana Farber Canc Inst, Ctr Patient Safety, Boston, MA 02115 USA.
[Weissman, Joel S.] Massachusetts Execut Off Hlth & Human Serv, Boston, MA USA.
RP Lopez, L (reprint author), Massachusetts Gen Hosp, Inst Hlth Policy, 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM llopez1@partners.org
OI Schneider, Eric/0000-0002-1132-5084
FU Agency for Healthcare Research and Quality to the Massachusetts
Department of Public Health [U18 HS11928]; Institutional National
Research Service Award [5 T32 HP11001-19]
FX This work was supported by a Cooperative Agreement from the Agency for
Healthcare Research and Quality to the Massachusetts Department of
Public Health (U18 HS11928). Dr Lopez acknowledges the support of an
Institutional National Research Service Award (5 T32 HP11001-19).
NR 42
TC 36
Z9 36
U1 3
U2 5
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9926
J9 ARCH INTERN MED
JI Arch. Intern. Med.
PD NOV 9
PY 2009
VL 169
IS 20
BP 1888
EP 1894
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 516BX
UT WOS:000271517800010
PM 19901141
ER
PT J
AU Paik, JH
Ding, ZH
Narurkar, R
Ramkissoon, S
Muller, F
Kamoun, WS
Chae, SS
Zheng, HW
Ying, HQ
Mahoney, J
Hiller, D
Jiang, S
Protopopov, A
Wong, WH
Chin, L
Ligon, KL
DePinho, RA
AF Paik, Ji-hye
Ding, Zhihu
Narurkar, Rujuta
Ramkissoon, Shakti
Muller, Florian
Kamoun, Walid S.
Chae, Sung-Suk
Zheng, Hongwu
Ying, Haoqiang
Mahoney, Jed
Hiller, David
Jiang, Shan
Protopopov, Alexei
Wong, Wing H.
Chin, Lynda
Ligon, Keith L.
DePinho, Ronald A.
TI FoxOs Cooperatively Regulate Diverse Pathways Governing Neural Stem Cell
Homeostasis
SO CELL STEM CELL
LA English
DT Article
ID FORKHEAD TRANSCRIPTION FACTORS; SELF-RENEWAL; OXIDATIVE STRESS; ADULT
NEUROGENESIS; DOWN-REGULATION; IN-VIVO; DIFFERENTIATION; PROLIFERATION;
FOREBRAIN; BRAIN
AB The PI3K-AKT-FoxO pathway is integral to lifespan regulation in lower organisms and essential for the stability of long-lived cells in mammals. Here, we report the impact of combined FoxO1, 3, and 4 deficiencies on mammalian brain physiology with a particular emphasis on the study of the neural stem/progenitor cell (NSC) pool. We show that the FoxO family plays a prominent role in NSC proliferation and renewal. FoxO-deficient mice show initial increased brain size and proliferation of neural progenitor cells during early postnatal life, followed by precocious significant decline in the NSC pool and accompanying neurogenesis in adult brains. Mechanistically, integrated transcriptomic, promoter, and functional analyses of FoxO-deficient NSC cultures identified direct gene targets with known links to the regulation of human brain size and the control of cellular proliferation, differentiation, and oxidative defense. Thus, the FoxO family coordinately regulates diverse genes and pathways to govern key aspects of NSC homeostasis in the mammalian brain.
C1 [Paik, Ji-hye; Ding, Zhihu; Narurkar, Rujuta; Muller, Florian; Zheng, Hongwu; Ying, Haoqiang; Mahoney, Jed; Jiang, Shan; Protopopov, Alexei; Chin, Lynda; DePinho, Ronald A.] Dana Farber Canc Inst, Belfer Inst Appl Canc Sci, Dept Med Oncol, Boston, MA 02115 USA.
[Paik, Ji-hye; Ding, Zhihu; Narurkar, Rujuta; Muller, Florian; Zheng, Hongwu; Ying, Haoqiang; Mahoney, Jed; Jiang, Shan; Protopopov, Alexei; Chin, Lynda; DePinho, Ronald A.] Dana Farber Canc Inst, Belfer Inst Appl Canc Sci, Dept Med, Boston, MA 02115 USA.
[Paik, Ji-hye; Ding, Zhihu; Narurkar, Rujuta; Muller, Florian; Zheng, Hongwu; Ying, Haoqiang; Mahoney, Jed; Jiang, Shan; Protopopov, Alexei; Chin, Lynda; DePinho, Ronald A.] Dana Farber Canc Inst, Belfer Inst Appl Canc Sci, Dept Genet, Boston, MA 02115 USA.
[Ramkissoon, Shakti; Ligon, Keith L.] Dana Farber Canc Inst, Dept Med Oncol, Ctr Mol Oncol Pathol, Boston, MA 02115 USA.
[Ramkissoon, Shakti; Ligon, Keith L.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Kamoun, Walid S.; Chae, Sung-Suk] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Kamoun, Walid S.; Chae, Sung-Suk] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Hiller, David; Wong, Wing H.] Stanford Univ, Dept Stat, Stanford, CA 94305 USA.
RP DePinho, RA (reprint author), Dana Farber Canc Inst, Belfer Inst Appl Canc Sci, Dept Med Oncol, Boston, MA 02115 USA.
EM ron_depinho@dfci.harvard.edu
OI Zheng, Hongwu/0000-0002-5823-4913
FU Damon Runyon Cancer Research Foundation [DRG 1900-06]; Claudia Adam Barr
Foundation; ACS; ABTA; Ellison Medical Foundation; Robert A. and Renee
E. Belfer Foundation Institute for Applied Cancer Science;
[5P01CA95616]
FX J.-h.P. is Damon Runyon Fellow was supported by the Damon Runyon Cancer
Research Foundation (DRG 1900-06). Grant support includes the Claudia
Adam Barr Foundation (J.-h.P.), ACS fellowship (F.M.), ABTA fellowship
(H.Y.), Ellison Medical Foundation (R.A.D.), and 5P01CA95616 (R.A.D.,
K.L.L., L.C.). R.A.D. is an American Cancer Society Research Professor
and supported by the Robert A. and Renee E. Belfer Foundation Institute
for Applied Cancer Science. We thank D. Pellman and S. Yoshida for the
deconvolution microscope use and advice, R. Maser for MSCV-puro-v5
gateway vector, W. Hahn for shRNA constructs, and J. Ling for technical
assistance.
NR 50
TC 180
Z9 186
U1 2
U2 13
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1934-5909
J9 CELL STEM CELL
JI Cell Stem Cell
PD NOV 6
PY 2009
VL 5
IS 5
BP 540
EP 553
DI 10.1016/j.stem.2009.09.013
PG 14
WC Cell & Tissue Engineering; Cell Biology
SC Cell Biology
GA 522SR
UT WOS:000272019500015
PM 19896444
ER
PT J
AU Bujak, M
Dobaczewski, M
Gonzalez-Quesada, C
Xia, Y
Leucker, T
Zymek, P
Veeranna, V
Tager, AM
Luster, AD
Frangogiannis, NG
AF Bujak, Marcin
Dobaczewski, Marcin
Gonzalez-Quesada, Carlos
Xia, Ying
Leucker, Thorsten
Zymek, Pawel
Veeranna, Vikas
Tager, Andrew M.
Luster, Andrew D.
Frangogiannis, Nikolaos G.
TI Induction of the CXC Chemokine Interferon-gamma-Inducible Protein 10
Regulates the Reparative Response Following Myocardial Infarction
SO CIRCULATION RESEARCH
LA English
DT Article
DE infarction; remodeling; chemokines; fibrosis; wound healing
ID PULMONARY-FIBROSIS; IP-10 CHEMOKINE; RECEPTOR; MICE; ANGIOGENESIS;
REPERFUSION; EXPRESSION; INHIBITOR; ISCHEMIA; EFFECTOR
AB Rationale: Interferon-gamma-inducible protein (IP)-10/CXCL10, an angiostatic and antifibrotic chemokine with an important role in T-cell trafficking, is markedly induced in myocardial infarcts, and may regulate the reparative response.
Objective: To study the role of IP-10 in cardiac repair and remodeling.
Methods and Results: We studied cardiac repair in IP-10-null and wild-type (WT) mice undergoing reperfused infarction protocols and examined the effects of IP-10 on cardiac fibroblast function. IP-10-deficient and WT animals had comparable acute infarct size. However, the absence of IP-10 resulted in a hypercellular early reparative response and delayed contraction of the scar. Infarcted IP-10(-/-) hearts exhibited accentuated early dilation, followed by rapid wall thinning during infarct maturation associated with systolic dysfunction. Although IP-10-null and WT mice had comparable cytokine expression, the absence of IP-10 was associated with marked alterations in the cellular content of the infarct. IP-10(-/-) infarcts had more intense infiltration with CD45(+) leukocytes, Mac-2(+) macrophages, and alpha-smooth muscle actin (alpha-SMA)(+) myofibroblasts than WT infarcts but exhibited reduced recruitment of the subpopulations of leukocytes, T lymphocytes and alpha-SMA(+) cells that expressed CXCR3, the IP-10 receptor. IP-10 did not modulate cardiac fibroblast proliferation and apoptosis but significantly inhibited basic fibroblast growth factor-induced fibroblast migration. In addition, IP-10 enhanced growth factor-mediated wound contraction in fibroblast-populated collagen lattices.
Conclusions: Endogenous IP-10 is an essential inhibitory signal that regulates the cellular composition of the healing infarct and promotes wound contraction, attenuating adverse remodeling. IP-10-mediated actions may be due, at least in part, to direct effects on fibroblast migration and function. (Circ Res. 2009;105:973-983.)
C1 [Bujak, Marcin; Dobaczewski, Marcin; Gonzalez-Quesada, Carlos; Xia, Ying; Leucker, Thorsten; Zymek, Pawel; Veeranna, Vikas; Frangogiannis, Nikolaos G.] Baylor Coll Med, Dept Med, Cardiovasc Sci Sect, Houston, TX 77030 USA.
[Tager, Andrew M.; Luster, Andrew D.] Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Charlestown, MA USA.
[Tager, Andrew M.; Luster, Andrew D.] Harvard Univ, Sch Med, Charlestown, MA USA.
RP Frangogiannis, NG (reprint author), Baylor Coll Med, Dept Med, Cardiovasc Sci Sect, 1 Baylor Plaza BCM620, Houston, TX 77030 USA.
EM ngf@bcm.tmc.edu
FU NIH [R01 HL-76246, R01 HL-85440, R01 CA-69212]; Alkek Foundation;
Medallion Foundation
FX This work was supported by NIH grants R01 HL-76246 and R01 HL-85440, the
Alkek Foundation, and the Medallion Foundation (to N.G.F.); and NIH
grant R01 CA-69212 (to A.D.L.).
NR 27
TC 50
Z9 52
U1 2
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7330
J9 CIRC RES
JI Circ.Res.
PD NOV 6
PY 2009
VL 105
IS 10
BP 973
EP 983
DI 10.1161/CIRCRESAHA.109.199471
PG 11
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Hematology
GA 515XE
UT WOS:000271505400006
PM 19797174
ER
PT J
AU Finn, AV
John, M
Nakazawa, G
Polavarapu, R
Karmali, V
Xu, X
Cheng, Q
Davis, T
Raghunathan, C
Acampado, E
Ezell, T
Lajoie, S
Eppihimer, M
Kolodgie, FD
Virmani, R
Gold, HK
AF Finn, Aloke V.
John, Michael
Nakazawa, Gaku
Polavarapu, Rohini
Karmali, Vinit
Xu, Xin
Cheng, Qi
Davis, Talina
Raghunathan, Chitra
Acampado, Eduardo
Ezell, Tucker
Lajoie, Scott
Eppihimer, Michael
Kolodgie, Frank D.
Virmani, Renu
Gold, Herman Kalman
TI Differential Healing After Sirolimus, Paclitaxel, and Bare Metal Stent
Placement in Combination With Peroxisome Proliferator-Activator Receptor
gamma Agonists Requirement for mTOR/Akt2 in PPAR gamma Activation
SO CIRCULATION RESEARCH
LA English
DT Article
DE stents; thrombosis; endothelium; pharmacology
ID DRUG-ELUTING STENTS; ENDOTHELIAL-CELLS; PROTEIN-SYNTHESIS; MAMMALIAN
TARGET; RAPAMYCIN; EXPRESSION; GROWTH; MTOR; ROSIGLITAZONE; PGC-1-ALPHA
AB Rationale: Sirolimus-eluting coronary stents (SESs) and paclitaxel-eluting coronary stents (PESs) are used to reduce restenosis but have different sites of action. The molecular targets of sirolimus overlap with those of the peroxisome proliferator-activated receptor (PPAR)gamma agonist rosiglitazone (RSG) but the consequence of this interaction on endothelialization is unknown.
Objective: Using the New Zealand white rabbit iliac model of stenting, we examined the effects of RSG on SESs, PESs, and bare metal stents endothelialization.
Methods and Results: Animals receiving SESs, PESs, or bare metal stents and either RSG (3 mg/kg per day) or placebo were euthanized at 28 days, and arteries were evaluated by scanning electron microscopy. Fourteen-day organ culture and Western blotting of iliac arteries and tissue culture experiments were conducted. Endothelialization was significantly reduced by RSG in SESs but not in PESs or bare metal stents. Organ culture revealed reduced vascular endothelial growth factor in SESs receiving RSG compared to RSG animals receiving bare metal stent or PESs. Quantitative polymerase chain reaction in human aortic endothelial cells (HAECs) revealed that sirolimus (but not paclitaxel) inhibited RSG-induced vascular endothelial growth factor transcription. Western blotting demonstrated that inhibition of molecular signaling in SES+RSG-treated arteries was similar to findings in HAECs treated with RSG and small interfering RNA to PPAR gamma, suggesting that sirolimus inhibits PPAR gamma. Transfection of HAECs with mTOR (mammalian target of rapamycin) short hairpin RNA and with Akt2 small interfering RNA significantly inhibited RSG-mediated transcriptional upregulation of heme oxygenase-1, a PPAR gamma target gene. Chromatin immunoprecipitation assay demonstrated sirolimus interferes with binding of PPAR gamma to its response elements in heme oxygenase-1 promoter.
Conclusions: mTOR/Akt2 is required for optimal PPAR gamma activation. Patients who receive SESs during concomitant RSG treatment may be at risk for delayed stent healing. (Circ Res. 2009;105:1003-1012.)
C1 [Finn, Aloke V.; John, Michael; Polavarapu, Rohini; Karmali, Vinit; Davis, Talina; Raghunathan, Chitra; Ezell, Tucker; Lajoie, Scott] Emory Univ, Sch Med, Dept Med, Heart & Vasc Ctr, Atlanta, GA USA.
[Nakazawa, Gaku; Xu, Xin; Cheng, Qi; Acampado, Eduardo; Kolodgie, Frank D.; Virmani, Renu] CVPath Inst Inc, Gaithersburg, MD USA.
[Gold, Herman Kalman] Massachusetts Gen Hosp, Dept Med, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Eppihimer, Michael] Boston Sci, Natick, MA USA.
RP Finn, AV (reprint author), Emory Midtown Hosp, 550 Peachtree St NE, Atlanta, GA 30308 USA.
EM avfinn@emory.edu
FU Caryle Fraser Heart Center at Emory University
FX This study was supported in part by a grant from Boston Scientific. A.
V. F. is supported by the Caryle Fraser Heart Center at Emory
University.
NR 28
TC 21
Z9 21
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7330
J9 CIRC RES
JI Circ.Res.
PD NOV 6
PY 2009
VL 105
IS 10
BP 1003
EP 1012
DI 10.1161/CIRCRESAHA.109.200519
PG 10
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Hematology
GA 515XE
UT WOS:000271505400009
PM 19797172
ER
PT J
AU Liang, HY
Yoo, SE
Na, R
Walter, CA
Richardson, A
Ran, QT
AF Liang, Hanyu
Yoo, Si-Eun
Na, Ren
Walter, Christi A.
Richardson, Arlan
Ran, Qitao
TI Short Form Glutathione Peroxidase 4 Is the Essential Isoform Required
for Survival and Somatic Mitochondrial Functions
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID OXIDATIVE DAMAGE; LIPID-PEROXIDATION; CELLS; EXPRESSION; PHGPX; GPX4;
GLUTATHIONE-PEROXIDASE-4; APOPTOSIS; PROTECTS; SEQUENCE
AB Glutathione peroxidase 4 (Gpx4) is an essential antioxidant enzyme having multiple functions. A long form Gpx4 protein and a short form Gpx4 protein, which are distinguishable by the presence or lack of a mitochondrial signal peptide at the N terminus, are generated from the Gpx4 gene. In this study, we generated transgenic mice using mutated GPX4 genes encoding either the long form Gpx4 (lPX4 gene) or the short form Gpx4 (sGPX4 gene). Our results showed that transgenic mice with the sGPX4 gene had increased Gpx4 protein in all tissues and were protected against diquat-induced apoptosis in liver. Moreover, the sGPX4 gene was able to rescue the lethal phenotype of the mouse Gpx4-null mutation. In contrast, transgenic mice with the lGPX4 gene had increased Gpx4 protein only in the testes, and the lGPX4 gene failed to rescue the lethal phenotype of the mouse Gpx4-null mutation. In Gpx4-null mice rescued by the sGPX4 gene, the Gpx4 protein was present in mitochondria isolated from somatic tissues, and the submitochondrial distribution pattern of the Gpx4 protein in these mice was identical to that in wild-type mice. Interestingly, the male Gpx4-null mice rescued by the sGPX4 gene were infertile and exhibited sperm malformation. Together, our results demonstrated for the first time that the short form Gpx4 protein is present in somatic tissue mitochondria and is essential for survival and protection against apoptosis in mice, whereas the long form Gpx4 protein is important for male fertility.
C1 Univ Texas Hlth Sci Ctr San Antonio, Sam & Ann Barshop Inst Longev & Aging Studies, San Antonio, TX 78229 USA.
[Yoo, Si-Eun] Univ Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USA.
[Walter, Christi A.; Richardson, Arlan; Ran, Qitao] Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA.
[Walter, Christi A.; Richardson, Arlan; Ran, Qitao] S Texas Vet Hlth Care Syst, San Antonio, TX 78229 USA.
RP Ran, QT (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Sam & Ann Barshop Inst Longev & Aging Studies, 15355 Lambda Dr, San Antonio, TX 78245 USA.
EM ran@uthscsa.edu
RI Liang, Hanyu/A-1066-2010
FU National Institutes of Health [P01AG19316, R37 AG026557, AG021163]; San
Antonio Nathan Shock Aging Center [1P30-AG13319]; Veterans Affairs Merit
FX This work was supported, in whole or in part, by National Institutes of
Health Grants P01AG19316, R37 AG026557, and AG021163, San Antonio Nathan
Shock Aging Center Grant 1P30-AG13319, and Veterans Affairs Merit grants
(to A. R. and Q. R.).
NR 26
TC 34
Z9 35
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 6
PY 2009
VL 284
IS 45
BP 30836
EP 30844
DI 10.1074/jbc.M109.032839
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 514EZ
UT WOS:000271378400011
PM 19744930
ER
PT J
AU Kim, ST
Takeuchi, K
Sun, ZYJ
Touma, M
Castro, CE
Fahmy, A
Lang, MJ
Wagner, G
Reinherz, EL
AF Kim, Sun Taek
Takeuchi, Koh
Sun, Zhen-Yu J.
Touma, Maki
Castro, Carlos E.
Fahmy, Amr
Lang, Matthew J.
Wagner, Gerhard
Reinherz, Ellis L.
TI The alpha beta T Cell Receptor Is an Anisotropic Mechanosensor
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID THYMIC SELECTION; FG LOOP; CD3-EPSILON-GAMMA HETERODIMER; ECTODOMAIN
FRAGMENT; CRYSTAL-STRUCTURE; TCR; COMPLEX; ACTIVATION; THYMOCYTES; MODEL
AB Thymus-derived lymphocytes protect mammalian hosts against virus- or cancer-related cellular alterations through immune surveillance, eliminating diseased cells. In this process, T cell receptors (TCRs) mediate both recognition and T cell activation via their dimeric alpha beta, CD3 epsilon gamma, CD3 epsilon delta, and CD3 zeta zeta subunits using an unknown structural mechanism. Here, site-specific binding topology of anti-CD3 monoclonal antibodies (mAbs) and dynamic TCR quaternary change provide key clues. Agonist mAbs footprint to the membrane distal CD3 epsilon lobe that they approach diagonally, adjacent to the lever-like C beta FG loop that facilitates antigen (pMHC)-triggered activation. In contrast, a non-agonist mAb binds to the cleft between CD3 epsilon and CD3 gamma in a perpendicular mode and is stimulatory only subsequent to an external tangential but not a normal force (similar to 50 piconewtons) applied via optical tweezers. Specific pMHC but not irrelevant pMHC activates a T cell upon application of a similar force. These findings suggest that the TCR is an anisotropic mechanosensor, converting mechanical energy into a biochemical signal upon specific pMHC ligation during immune surveillance. Activating anti-CD3 mAbs mimic this force via their intrinsic binding mode. A common TCR quaternary change rather than conformational alterations can better facilitate structural signal initiation, given the vast array of TCRs and their specific pMHC ligands.
C1 [Kim, Sun Taek; Touma, Maki; Reinherz, Ellis L.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Lab Immunobiol, Boston, MA 02115 USA.
[Kim, Sun Taek; Touma, Maki; Reinherz, Ellis L.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Takeuchi, Koh; Sun, Zhen-Yu J.; Fahmy, Amr; Wagner, Gerhard] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Castro, Carlos E.; Lang, Matthew J.] MIT, Dept Mech Engn, Cambridge, MA 02139 USA.
[Lang, Matthew J.] MIT, Dept Biol Engn, Cambridge, MA 02139 USA.
RP Reinherz, EL (reprint author), 77 Ave Louis Pasteur,HIM 419, Boston, MA 02115 USA.
EM ellis_reinherz@dfci.harvard.edu
RI Takeuchi, Koh/B-4971-2010; Castro, Carlos/D-8756-2016
OI Castro, Carlos/0000-0001-7023-6105
FU National Institutes of Health [AI19807, AI37581, GM47467, EB002026]
FX This work was supported, in whole or in part, by National Institutes of
Health Grants AI19807 (to E. L. R.) and AI37581, GM47467, and EB002026
(to G. W.).
NR 46
TC 117
Z9 117
U1 1
U2 14
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 6
PY 2009
VL 284
IS 45
BP 31028
EP 31037
DI 10.1074/jbc.M109.052712
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 514EZ
UT WOS:000271378400032
PM 19755427
ER
PT J
AU Wade, CM
Giulotto, E
Sigurdsson, S
Zoli, M
Gnerre, S
Imsland, F
Lear, TL
Adelson, DL
Bailey, E
Bellone, RR
Blocker, H
Distl, O
Edgar, RC
Garber, M
Leeb, T
Mauceli, E
MacLeod, JN
Penedo, MCT
Raison, JM
Sharpe, T
Vogel, J
Andersson, L
Antczak, DF
Biagi, T
Binns, MM
Chowdhary, BP
Coleman, SJ
Della Valle, G
Fryc, S
Guerin, G
Hasegawa, T
Hill, EW
Jurka, J
Kiialainen, A
Lindgren, G
Liu, J
Magnani, E
Mickelson, JR
Murray, J
Nergadze, SG
Onofrio, R
Pedroni, S
Piras, MF
Raudsepp, T
Rocchi, M
Roed, KH
Ryder, OA
Searle, S
Skow, L
Swinburne, JE
Syvanen, AC
Tozaki, T
Valberg, SJ
Vaudin, M
White, JR
Zody, MC
Lander, ES
Lindblad-Toh, K
AF Wade, C. M.
Giulotto, E.
Sigurdsson, S.
Zoli, M.
Gnerre, S.
Imsland, F.
Lear, T. L.
Adelson, D. L.
Bailey, E.
Bellone, R. R.
Bloecker, H.
Distl, O.
Edgar, R. C.
Garber, M.
Leeb, T.
Mauceli, E.
MacLeod, J. N.
Penedo, M. C. T.
Raison, J. M.
Sharpe, T.
Vogel, J.
Andersson, L.
Antczak, D. F.
Biagi, T.
Binns, M. M.
Chowdhary, B. P.
Coleman, S. J.
Della Valle, G.
Fryc, S.
Guerin, G.
Hasegawa, T.
Hill, E. W.
Jurka, J.
Kiialainen, A.
Lindgren, G.
Liu, J.
Magnani, E.
Mickelson, J. R.
Murray, J.
Nergadze, S. G.
Onofrio, R.
Pedroni, S.
Piras, M. F.
Raudsepp, T.
Rocchi, M.
Roed, K. H.
Ryder, O. A.
Searle, S.
Skow, L.
Swinburne, J. E.
Syvanen, A. C.
Tozaki, T.
Valberg, S. J.
Vaudin, M.
White, J. R.
Zody, M. C.
Lander, E. S.
Lindblad-Toh, K.
CA Broad Inst Genome Sequencing Perfo
Broad Inst Whole Genome Assembly T
TI Genome Sequence, Comparative Analysis, and Population Genetics of the
Domestic Horse
SO SCIENCE
LA English
DT Article
ID STATIONARY NIGHT BLINDNESS; CENTROMERES; APPALOOSA; EVOLUTION; CATTLE
AB We report a high-quality draft sequence of the genome of the horse ( Equus caballus). The genome is relatively repetitive but has little segmental duplication. Chromosomes appear to have undergone few historical rearrangements: 53% of equine chromosomes show conserved synteny to a single human chromosome. Equine chromosome 11 is shown to have an evolutionary new centromere devoid of centromeric satellite DNA, suggesting that centromeric function may arise before satellite repeat accumulation. Linkage disequilibrium, showing the influences of early domestication of large herds of female horses, is intermediate in length between dog and human, and there is long-range haplotype sharing among breeds.
C1 [Wade, C. M.; Sigurdsson, S.; Gnerre, S.; Garber, M.; Mauceli, E.; Sharpe, T.; Biagi, T.; Fryc, S.; Onofrio, R.; White, J. R.; Zody, M. C.; Lander, E. S.; Lindblad-Toh, K.; Broad Inst Genome Sequencing Perfo; Broad Inst Whole Genome Assembly T] Broad Inst, Cambridge, MA 02142 USA.
[Wade, C. M.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Wade, C. M.] Univ Sydney, Fac Vet Sci, Sydney, NSW 2006, Australia.
[Giulotto, E.; Magnani, E.; Nergadze, S. G.; Piras, M. F.] Univ Pavia, Dipartimento Genet & Microbiol, I-27100 Pavia, Italy.
[Sigurdsson, S.; Imsland, F.; Andersson, L.; Zody, M. C.; Lindblad-Toh, K.] Uppsala Univ, Dept Med Biochem & Microbiol, SE-75124 Uppsala, Sweden.
[Zoli, M.; Della Valle, G.] Univ Bologna, Dipartimento Biol, I-40126 Bologna, Italy.
[Lear, T. L.; Bailey, E.; MacLeod, J. N.; Coleman, S. J.] Univ Kentucky, Dept Vet Sci, Maxwell H Gluck Equine Res Ctr, Lexington, KY 40546 USA.
[Adelson, D. L.; Raison, J. M.; Chowdhary, B. P.; Raudsepp, T.] Univ Adelaide, Adelaide, SA 5005, Australia.
[Bellone, R. R.; Roed, K. H.] Univ Tampa, Tampa, FL 33606 USA.
[Bloecker, H.] Helmholtz Ctr Infect Res, Braunschweig, Germany.
[Distl, O.; Leeb, T.] Univ Vet Med Hannover, Inst Genet & Anim Breeding, D-30559 Hannover, Germany.
[Leeb, T.] Univ Bern, Vetsuisse Fac, Inst Genet, CH-3001 Bern, Switzerland.
[Penedo, M. C. T.; Pedroni, S.] Univ Calif Davis, Vet Genet Lab, Davis, CA 95616 USA.
[Vogel, J.; Searle, S.] Wellcome Trust Sanger Inst, Cambridge CB10 1SA, England.
[Antczak, D. F.] Cornell Univ, Coll Vet Med, James A Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
[Binns, M. M.] Univ London Royal Vet Coll, London NW1 0TU, England.
[Skow, L.] Texas A&M Univ, Coll Vet Med, College Stn, TX 77843 USA.
[Guerin, G.] INRA, UMR 1313, F-44078350 Jouy En Josas, France.
[Hasegawa, T.] Japan Racing Assoc, Equine Res Inst, Utsunomiya, Tochigi 3200856, Japan.
[Hill, E. W.] Univ Coll Dublin, Sch Agr Food Sci & Vet Med, Anim Genom Lab, Dublin 4, Ireland.
[Jurka, J.] Genet Informat Res Inst, Mountain View, CA 94043 USA.
[Kiialainen, A.; Syvanen, A. C.] Uppsala Univ, Dept Med Sci, S-75185 Uppsala, Sweden.
[Lindgren, G.] Swedish Univ Agr Sci, Dept Anim Breeding & Genet, SE-75124 Uppsala, Sweden.
[Liu, J.] Univ Kentucky, Dept Comp Sci, Lexington, KY 40506 USA.
[Mickelson, J. R.; Valberg, S. J.] Univ Minnesota, Coll Vet Med, St Paul, MN 55108 USA.
[Murray, J.] Univ Calif Davis, Sch Vet Med, Davis, CA 95616 USA.
[Rocchi, M.] Univ Bari, Dept Genet & Microbiol, I-70126 Bari, Italy.
Norwegian Sch Vet Sci, Dept Basic Sci & Aquat Med, N-0033 Oslo, Norway.
[Ryder, O. A.] San Diego Zoos Inst Conservat Res, Escondido, CA 92029 USA.
[Swinburne, J. E.; Vaudin, M.] Anim Hlth Trust, Newmarket CB8 7UU, Suffolk, England.
[Tozaki, T.] Lab Racing Chem, Dept Mol Genet, Utsunomiya, Tochigi 3200851, Japan.
[Lander, E. S.] MIT, Dept Biol, Cambridge, MA 02142 USA.
RP Wade, CM (reprint author), Broad Inst, 7 Cambridge Ctr, Cambridge, MA 02142 USA.
EM c.wade@usyd.edu.au; kersli@broadinstitute.org
RI Leeb, Tosso/G-3187-2014; Adelson, David/E-5506-2011;
OI Leeb, Tosso/0000-0003-0553-4880; Adelson, David/0000-0003-2404-5636;
GIULOTTO, ELENA/0000-0002-4705-2049; Hill, Emmeline/0000-0002-1805-2250
FU National Human Genome Research Institute; Dorothy Russell Havemeyer
Foundation; Volkswagen Foundation; Morris Animal Foundation; Centro di
Eccellenza di Genomica in Campo Biomedico e Agrario; Programmi di
Ricerca Scientifica di Rilevante Interesse Nazionale [PRIN-2006];
European Science Foundation
FX We thank the Kentucky Horse Park and L. Chemnick for samples, L. Gaffney
for graphics, and M. Daly for useful discussions. Supported by the
National Human Genome Research Institute, the Dorothy Russell Havemeyer
Foundation, the Volkswagen Foundation, the Morris Animal Foundation, the
Centro di Eccellenza di Genomica in Campo Biomedico e Agrario, and the
Programmi di Ricerca Scientifica di Rilevante Interesse Nazionale
(PRIN-2006). K. L. T. is the recipient of a European Young Investigator
award funded by the European Science Foundation. Sequences have GenBank
accession numbers AAWR02000001 to AAWR02055316. 1,163,466 discovery SNPs
have accession numbers rs6844103 to rs69617090 in dbSNP 130.
NR 17
TC 301
Z9 324
U1 5
U2 110
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 6
PY 2009
VL 326
IS 5954
BP 865
EP 867
DI 10.1126/science.1178158
PG 3
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 515KG
UT WOS:000271468000047
PM 19892987
ER
PT J
AU Chirnomas, D
Smith, AL
Braunstein, J
Finkelstein, Y
Pereira, L
Bergmann, AK
Grant, FD
Paley, C
Shannon, M
Neufeld, EJ
AF Chirnomas, Deborah
Smith, Amber Lynn
Braunstein, Jennifer
Finkelstein, Yaron
Pereira, Luis
Bergmann, Anke K.
Grant, Frederick D.
Paley, Carole
Shannon, Michael
Neufeld, Ellis J.
TI Deferasirox pharmacokinetics in patients with adequate versus inadequate
response
SO BLOOD
LA English
DT Article
ID BETA-THALASSEMIA MAJOR; ORAL IRON CHELATOR; PHASE-II; ICL670;
TRANSFUSION; BIOAVAILABILITY; OVERLOAD; ANEMIA
AB Tens of thousands of transfusion-dependent (eg, thalassemia) patients worldwide suffer from chronic iron overload and its potentially fatal complications. The oral iron chelator deferasirox has become commercially available in many countries since 2006. Although this alternative to parenteral deferoxamine has been a major advance for patients with transfusional hemosiderosis, a proportion of patients have suboptimal response to the maximum approved doses (30 mg/kg per day), and do not achieve negative iron balance. We performed a prospective study of oral deferasirox pharmacokinetics (PK), comparing 10 transfused patients with inadequate deferasirox response (rising ferritin trend or rising liver iron on deferasirox doses >30 mg/kg per day) with control transfusion-dependent patients (n = 5) with adequate response. Subjects were admitted for 4 assessments: deferoxamine infusion and urinary iron measurement to assess readily chelatable iron; quantitative hepatobiliary scintigraphy to assess hepatic uptake and excretion of chelate; a 24-hour deferasirox PK study following a single 35-mg/kg dose of oral deferasirox; and pharmacogenomic analysis. Patients with inadequate response to deferasirox had significantly lower systemic drug exposure compared with control patients (P <.00001). Cmax, volume of distribution/bioavailability (Vd/F), and elimination half-life (t(1/2)) were not different between the groups, suggesting bioavailability as the likely discriminant. Effective dosing regimens for inadequately responding patients to deferasirox must be determined. This trial has been registered at http://www.clinicaltrials.gov under identifier NCT00749515. (Blood. 2009; 114: 4009-4013)
C1 [Neufeld, Ellis J.] Childrens Hosp, Div Hematol, Boston, MA 02115 USA.
[Chirnomas, Deborah; Finkelstein, Yaron; Bergmann, Anke K.; Grant, Frederick D.; Shannon, Michael; Neufeld, Ellis J.] Harvard Univ, Sch Med, Boston, MA USA.
[Chirnomas, Deborah; Neufeld, Ellis J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Finkelstein, Yaron; Pereira, Luis; Shannon, Michael] Childrens Hosp, Clin Pharmacol Unit, Boston, MA 02115 USA.
[Finkelstein, Yaron] Univ Toronto, Hosp Sick Children, Div Clin Pharmacol & Toxicol, Toronto, ON M5G 1X8, Canada.
[Grant, Frederick D.] Childrens Hosp, Div Nucl Med, Boston, MA 02115 USA.
[Paley, Carole] Novartis Pharmaceut, E Hanover, NJ USA.
RP Neufeld, EJ (reprint author), Childrens Hosp, Div Hematol, 300 Longwood Ave,Rm Karp 08210, Boston, MA 02115 USA.
EM ellis.neufeld@childrens.harvard.edu
RI Neufeld, Ellis/F-9331-2011
FU National Heart, Lung, and Blood Institute [NHLBI] [K12 HL087164, K24
HL004184]; Novartis; Harvard Catalyst Clinical and Translational Science
Center [UL1RR025758]; National Institutes of Health (NIH)
FX C. P. is a full-time employee of Novartis Pharmaceutical Corporation.
The remaining authors declare no competing financial interests. The
study was an investigator-initiated trial partially funded by Novartis,
which provided the study drug and paid for and conducted the
high-performance liquid chromatography analysis of deferasirox and
deferasirox-iron levels. The remainder of the study, including salary
support for D. C. and E. J. N., was provided by National Institutes of
Health (NIH) funding, K12 and K24 (see "Acknowledgements" for fund
numbers).
NR 17
TC 39
Z9 39
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 5
PY 2009
VL 114
IS 19
BP 4009
EP 4013
DI 10.1182/blood-2009-05-222729
PG 5
WC Hematology
SC Hematology
GA 515TJ
UT WOS:000271495500011
PM 19724055
ER
PT J
AU Giles, F
Vey, N
DeAngelo, D
Seiter, K
Stock, W
Stuart, R
Boskovic, D
Pigneux, A
Tallman, M
Brandwein, J
Kell, J
Robak, T
Staib, P
Thomas, X
Cahill, A
Albitar, M
O'Brien, S
AF Giles, Francis
Vey, Norbert
DeAngelo, Daniel
Seiter, Karen
Stock, Wendy
Stuart, Robert
Boskovic, Darinka
Pigneux, Arnaud
Tallman, Martin
Brandwein, Joseph
Kell, Jonathan
Robak, Tadeusz
Staib, Peter
Thomas, Xavier
Cahill, Ann
Albitar, Maher
O'Brien, Susan
TI Phase 3 randomized, placebo-controlled, double-blind study of high-dose
continuous infusion cytarabine alone or with laromustine (VNP40101M) in
patients with acute myeloid leukemia in first relapse
SO BLOOD
LA English
DT Article
ID SULFONYLHYDRAZINE ALKYLATING AGENT; O-6-ALKYLGUANINE-DNA
ALKYLTRANSFERASE; CLORETAZINE VNP40101M; REFRACTORY LEUKEMIA; PRODRUG
CLORETAZINE; INHIBITION; THERAPY; CANCER; TRIAL
AB Laromustine is a sulfonylhdrazine alkylator with significant antileukemia activity. An international, randomized (2: 1), double-blind, placebo-controlled study was conducted to compare complete remission (CR) rates and overall survival (OS) in patients with first relapse acute myeloid leukemia (AML) treated with laromustine and high-dose cytarabine (HDAC) versus HDAC/placebo. Patients received 1.5 g/m(2) per day cytarabine continuous infusion for 3 days and laromustine 600 mg/m(2) (n = 177) or placebo (n = 86) on day 2. Patients in CR received consolidation with laromustine/HDAC or HDAC/placebo as per initial randomization. After interim analysis at 50% enrollment, the Data Safety Monitoring Board (DSMB) expressed concern that any advantage in CR would be compromised by the observed on-study mortality, and enrollment was held. The CR rate was significantly higher for the laromustine/HDAC group (35% vs 19%, P = .005). However, the 30-day mortality rate and median progression-free survival were significantly worse in this group compared with HDAC/placebo (11% vs 2%; P = .016; 54 days vs 34; P = .002). OS and median response durations were similar in both groups. Laromustine/HDAC induced significantly more CR than HDAC/placebo, but OS was not improved due to mortality associated with myelosuppression and its sequelae. The DSMB subsequently approved a revised protocol with laromustine dose reduction and recombinant growth factor support. The study was registered as NCT00112554 at http://www.clinicaltrials.gov. (Blood. 2009; 114: 4027-4033)
C1 [Giles, Francis] Univ Texas Hlth Sci Ctr San Antonio, Canc Therapy & Res Ctr, San Antonio, TX 78229 USA.
[Vey, Norbert] Inst J Paoli I Calmettes, F-13009 Marseille, France.
[DeAngelo, Daniel] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Seiter, Karen] New York Med Coll, Valhalla, NY 10595 USA.
[Stock, Wendy] Univ Chicago, Chicago, IL 60637 USA.
[Stuart, Robert] Med Univ S Carolina, Hollings Canc Ctr, Charleston, SC 29425 USA.
[Boskovic, Darinka] Clin Ctr Serbia, Belgrade, Serbia.
[Pigneux, Arnaud] Hop Haut Leveque, Bordeaux, France.
[Tallman, Martin] Robert H Lurie Comprehens Canc Ctr, Chicago, IL USA.
[Brandwein, Joseph] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Kell, Jonathan] Univ Wales Hosp, Cardiff CF4 4XW, S Glam, Wales.
[Robak, Tadeusz] Med Univ Lodz, Lodz, Poland.
[Staib, Peter] Klinikum Univ Koln, Cologne, Germany.
[Thomas, Xavier] Hop Edouard Herriot, Lyon, France.
[Cahill, Ann] Vion Pharmaceut, New Haven, CT USA.
[Albitar, Maher] Quest Diagnost Nichols Inst, San Juan Capistrano, CA USA.
[O'Brien, Susan] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Giles, F (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Canc Therapy & Res Ctr, 7979 Wurzbach Rd,Mail Code 8026,Urschel Tower,Sui, San Antonio, TX 78229 USA.
EM frankgiles@aol.com
OI Stuart, Robert/0000-0001-7549-8008
NR 30
TC 25
Z9 25
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 5
PY 2009
VL 114
IS 19
BP 4027
EP 4033
DI 10.1182/blood-2009-06-229351
PG 7
WC Hematology
SC Hematology
GA 515TJ
UT WOS:000271495500014
PM 19710500
ER
PT J
AU Rodriguez, S
Chora, A
Goumnerov, B
Mumaw, C
Goebel, WS
Fernandez, L
Baydoun, H
HogenEsch, H
Dombkowski, DM
Karlewicz, CA
Rice, S
Rahme, LG
Carlesso, N
AF Rodriguez, Sonia
Chora, Angelo
Goumnerov, Boyan
Mumaw, Christen
Goebel, W. Scott
Fernandez, Luis
Baydoun, Hasan
HogenEsch, Harm
Dombkowski, David M.
Karlewicz, Carol A.
Rice, Susan
Rahme, Laurence G.
Carlesso, Nadia
TI Dysfunctional expansion of hematopoietic stem cells and block of myeloid
differentiation in lethal sepsis
SO BLOOD
LA English
DT Article
ID LINEAGE COMMITMENT; VIRULENCE FACTORS; GAMMA-INTERFERON; MECHANISMS;
MODEL; INFLAMMATION; NEUTROPHILS; QUIESCENCE; PROGENITOR; INFECTION
AB Severe sepsis is one of the leading causes of death worldwide. High mortality rates in sepsis are frequently associated with neutropenia. Despite the central role of neutrophils in innate immunity, the mechanisms causing neutropenia during sepsis remain elusive. Here, we show that neutropenia is caused in part by apoptosis and is sustained by a block of hematopoietic stem cell (HSC) differentiation. Using a sepsis murine model, we found that the human opportunistic bacterial pathogen Pseudomonas aeruginosa caused neutrophil depletion and expansion of the HSC pool in the bone marrow. "Septic" HSCs were significantly impaired in competitive repopulation assays and defective in generating common myeloid progenitors and granulocyte-monocyte progenitors, resulting in lower rates of myeloid differentiation in vitro and in vivo. Delayed myeloid-neutrophil differentiation was further mapped using a lysozyme-green fluorescent protein (GFP) reporter mouse. Pseudomonas's lipopolysaccharide was necessary and sufficient to induce myelosuppresion and required intact TLR4 signaling. Our results establish a previously unrecognized link between HSC regulation and host response in severe sepsis and demonstrate a novel role for TLR4. (Blood. 2009; 114: 4064-4076)
C1 [Rodriguez, Sonia; Mumaw, Christen; Goebel, W. Scott; Karlewicz, Carol A.; Rice, Susan; Carlesso, Nadia] Indiana Univ, Sch Med, Simon Canc Ctr, Herman B Wells Ctr, Indianapolis, IN 46202 USA.
[Chora, Angelo; Goumnerov, Boyan; Fernandez, Luis; Baydoun, Hasan; Dombkowski, David M.; Rahme, Laurence G.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Baydoun, Hasan; Rahme, Laurence G.] Shriners Burn Inst, Boston, MA 02114 USA.
[HogenEsch, Harm] Purdue Univ, Sch Vet Med, Dept Comparat Pathobiol, W Lafayette, IN 47907 USA.
RP Carlesso, N (reprint author), Indiana Univ, Sch Med, Herman B Wells Ctr Pediat Res, 1044 Walnut,Bldg R4,Rm 421, Indianapolis, IN 46202 USA.
EM ncarless@iupui.edu
OI Ferreira Chora, Angelo/0000-0002-7941-7196; HogenEsch,
Harm/0000-0002-2738-9189
FU National Institutes of Health [R01-HL068256-05A2]; Shawalter; Shriners
[8710]
FX This work was supported by the National Institutes of Health (grant no.
R01-HL068256-05A2 to N. C.), the Shawalter grant (N. C.), and Shriners
grant no. 8710 (to L. G. R.).
NR 39
TC 59
Z9 59
U1 1
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 5
PY 2009
VL 114
IS 19
BP 4064
EP 4076
DI 10.1182/blood-2009-04-214916
PG 13
WC Hematology
SC Hematology
GA 515TJ
UT WOS:000271495500018
PM 19696201
ER
PT J
AU Sharma, S
Lichtenstein, A
AF Sharma, Sanjai
Lichtenstein, Alan
TI Aberrant splicing of the E-cadherin transcript is a novel mechanism of
gene silencing in chronic lymphocytic leukemia cells
SO BLOOD
LA English
DT Article
ID MESSENGER-RNA DECAY; CANCER; EXPRESSION; MUTATIONS; TRANSACTIVATION;
SURVEILLANCE; INHIBITION; FAMILY; BRCA1; FORM
AB Premature termination codon (PTC) mutations are due to insertion or deletion of nucleotides causing a frameshift and premature termination codon in RNA. These transcripts are degraded by the nonsense-mediated decay pathway and have a very short half-life. We used a microarray technique to screen for genes that up-regulate their RNA signal upon nonsense-mediated decay pathway blockade in chronic lymphocytic leukemia (CLL) specimens and identified an Ecadherin transcript with PTC. Sequencing revealed an aberrant E-cadherin transcript lacking exon 11, resulting in a frameshift and PTC. The aberrant E-cadherin transcript was also identified in normal B cells, but occurred at a much lower level compared with CLL cells. In CLL specimens, E-cadherin expression was depressed more than 50% in 62% cases (relative to normal B cells). By real-time polymerase chain reaction analysis, the relative amounts of wild-type transcript inversely correlated with amounts of aberrant transcript (P = .018). Ectopic expression of E-cadherin in CLL specimens containing high amounts of aberrant transcript resulted in down-regulation of the wnt-beta-catenin pathway reporter, a pathway known to be up-regulated in CLL. Our data point to a novel mechanism of E-cadherin gene inactivation, with CLL cells displaying a higher proportion of aberrant nonfunctional transcripts and resulting up-regulation of the wnt-beta-catenin pathway. (Blood. 2009; 114: 4179-4185)
C1 [Sharma, Sanjai; Lichtenstein, Alan] Univ Calif Los Angeles, W Los Angeles Vet Affairs Med Ctr, Div Hematol Oncol, Los Angeles, CA 90073 USA.
RP Sharma, S (reprint author), Univ Calif Los Angeles, W Los Angeles Vet Affairs Med Ctr, Div Hematol Oncol, Bldg 304,Rm E1-115,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM sasharma@mednet.ucla.edu
FU American Society of Clinical Oncology (ASCO) Foundation [CA96920,
CA111448]; Veterans Administration
FX S.S. is a recipient of a grant from Flight Attendants Medical Research
Institute and an American Society of Clinical Oncology (ASCO) Foundation
Young Investigator Award. A. L. was supported by Grants CA96920 and
CA111448, and research funds from the Veterans Administration.
NR 33
TC 23
Z9 24
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 5
PY 2009
VL 114
IS 19
BP 4179
EP 4185
DI 10.1182/blood-2009-03-206482
PG 7
WC Hematology
SC Hematology
GA 515TJ
UT WOS:000271495500031
PM 19745069
ER
PT J
AU Huang, SC
Cho, A
Norton, S
Liu, ES
Park, J
Zhou, AY
Munagala, ID
Ou, AC
Yang, G
Wickrema, A
Tang, TK
Benz, EJ
AF Huang, Shu-Ching
Cho, Aeri
Norton, Stephanie
Liu, Eva S.
Park, Jennie
Zhou, Anyu
Munagala, Indira D.
Ou, Alexander C.
Yang, Guang
Wickrema, Amittha
Tang, Tang K.
Benz, Edward J., Jr.
TI Coupled transcription-splicing regulation of mutually exclusive splicing
events at the 5 ' exons of protein 4.1R gene
SO BLOOD
LA English
DT Article
ID PRE-MESSENGER-RNA; ALTERNATIVE 1ST EXONS; ERYTHROID-DIFFERENTIATION;
POLYMERASE-II; MAMMALIAN-CELLS; PROMOTER USAGE; SR PROTEINS; SITE AG;
IN-VIVO; EXPRESSION
AB The tightly regulated production of distinct erythrocyte protein 4.1R isoforms involves differential splicing of 3 mutually exclusive first exons (1A, 1B, 1C) to the alternative 3' splice sites (ss) of exon 2'/2. Here, we demonstrate that exon 1 and 2'/2 splicing diversity is regulated by a transcription-coupled splicing mechanism. We also implicate distinctive regulatory elements that promote the splicing of exon 1A to the distal 3' ss and exon 1B to the proximal 3' ss in murine erythroleukemia cells. A hybrid minigene driven by cytomegalovirus promoter mimicked 1B-promoter-driven splicing patterns but differed from 1A-promoter-driven splicing patterns, suggesting that promoter identity affects exon 2'/2 splicing. Furthermore, splicing factor SF2/ASF ultraviolet (UV) cross- linked to the exon 2'/2 junction CAGAGAA, a sequence that overlaps the distal U2AF35-binding 3'ss. Consequently, depletion of SF2/ASF allowed exon 1B to splice to the distal 3' ss but had no effect on exon 1A splicing. These findings identify for the first time that an SF2/ASF binding site also can serve as a 3' ss in a transcript-dependent manner. Taken together, our results suggest that 4.1R gene expression involves transcriptional regulation coupled with a complex splicing regulatory network. (Blood. 2009; 114:4233-4242)
C1 [Huang, Shu-Ching; Cho, Aeri; Norton, Stephanie; Liu, Eva S.; Park, Jennie; Zhou, Anyu; Munagala, Indira D.; Ou, Alexander C.; Yang, Guang; Benz, Edward J., Jr.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Huang, Shu-Ching; Zhou, Anyu; Yang, Guang; Benz, Edward J., Jr.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Wickrema, Amittha] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Tang, Tang K.] Acad Sinica, Inst Biomed Sci, Taipei, Taiwan.
[Benz, Edward J., Jr.] Dana Farber Harvard Canc Ctr, Boston, MA USA.
[Benz, Edward J., Jr.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Benz, Edward J., Jr.] Childrens Hosp, Dept Pediat, Boston, MA 02115 USA.
RP Huang, SC (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM shu-ching_huang@dfci.harvard.edu
FU National Institutes of Health [HL24385]
FX This study was supported by the National Institutes of Health grant
HL24385 (to E.J.B.) and Claudia BarrAward (to S.C.H.).
NR 49
TC 5
Z9 5
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 5
PY 2009
VL 114
IS 19
BP 4233
EP 4242
DI 10.1182/blood-2009-02-206219
PG 10
WC Hematology
SC Hematology
GA 515TJ
UT WOS:000271495500036
PM 19729518
ER
PT J
AU Barbie, DA
Tamayo, P
Boehm, JS
Kim, SY
Moody, SE
Dunn, IF
Schinzel, AC
Sandy, P
Meylan, E
Scholl, C
Frohling, S
Chan, EM
Sos, ML
Michel, K
Mermel, C
Silver, SJ
Weir, BA
Reiling, JH
Sheng, Q
Gupta, PB
Wadlow, RC
Le, H
Hoersch, S
Wittner, BS
Ramaswamy, S
Livingston, DM
Sabatini, DM
Meyerson, M
Thomas, RK
Lander, ES
Mesirov, JP
Root, DE
Gilliland, DG
Jacks, T
Hahn, WC
AF Barbie, David A.
Tamayo, Pablo
Boehm, Jesse S.
Kim, So Young
Moody, Susan E.
Dunn, Ian F.
Schinzel, Anna C.
Sandy, Peter
Meylan, Etienne
Scholl, Claudia
Froehling, Stefan
Chan, Edmond M.
Sos, Martin L.
Michel, Kathrin
Mermel, Craig
Silver, Serena J.
Weir, Barbara A.
Reiling, Jan H.
Sheng, Qing
Gupta, Piyush B.
Wadlow, Raymond C.
Le, Hanh
Hoersch, Sebastian
Wittner, Ben S.
Ramaswamy, Sridhar
Livingston, David M.
Sabatini, David M.
Meyerson, Matthew
Thomas, Roman K.
Lander, Eric S.
Mesirov, Jill P.
Root, David E.
Gilliland, D. Gary
Jacks, Tyler
Hahn, William C.
TI Systematic RNA interference reveals that oncogenic KRAS-driven cancers
require TBK1
SO NATURE
LA English
DT Article
ID NF-KAPPA-B; TUMOR-CELL SURVIVAL; LUNG ADENOCARCINOMA; ESSENTIAL GENES;
K-RAS; ACTIVATION; SCREEN; PHOSPHORYLATION; CLASSIFICATION; APOPTOSIS
AB The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. A complementary strategy for targeting KRAS is to identify gene products that, when inhibited, result in cell death only in the presence of an oncogenic allele(1,2). Here we have used systematic RNA interference to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical I kappa B kinase TBK1 was selectively essential in cells that contain mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappa B anti-apoptotic signals involving c-Rel and BCL-XL (also known as BCL2L1) that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations indicate that TBK1 and NF-kappa B signalling are essential in KRAS mutant tumours, and establish a general approach for the rational identification of co-dependent pathways in cancer.
C1 [Barbie, David A.; Kim, So Young; Moody, Susan E.; Dunn, Ian F.; Schinzel, Anna C.; Mermel, Craig; Sheng, Qing; Livingston, David M.; Meyerson, Matthew; Gilliland, D. Gary; Hahn, William C.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Kim, So Young; Meyerson, Matthew; Hahn, William C.] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Barbie, David A.; Tamayo, Pablo; Boehm, Jesse S.; Moody, Susan E.; Dunn, Ian F.; Schinzel, Anna C.; Chan, Edmond M.; Mermel, Craig; Silver, Serena J.; Weir, Barbara A.; Gupta, Piyush B.; Wadlow, Raymond C.; Le, Hanh; Wittner, Ben S.; Ramaswamy, Sridhar; Sabatini, David M.; Meyerson, Matthew; Lander, Eric S.; Mesirov, Jill P.; Root, David E.; Gilliland, D. Gary; Jacks, Tyler; Hahn, William C.] Broad Inst Harvard, Cambridge, MA 02142 USA.
[Barbie, David A.; Tamayo, Pablo; Boehm, Jesse S.; Moody, Susan E.; Dunn, Ian F.; Schinzel, Anna C.; Chan, Edmond M.; Mermel, Craig; Silver, Serena J.; Weir, Barbara A.; Gupta, Piyush B.; Wadlow, Raymond C.; Le, Hanh; Wittner, Ben S.; Ramaswamy, Sridhar; Sabatini, David M.; Meyerson, Matthew; Lander, Eric S.; Mesirov, Jill P.; Root, David E.; Gilliland, D. Gary; Jacks, Tyler; Hahn, William C.] MIT, Cambridge, MA 02142 USA.
[Barbie, David A.; Wadlow, Raymond C.; Wittner, Ben S.; Ramaswamy, Sridhar] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Dunn, Ian F.] Brigham & Womens Hosp, Dept Neurosurg, Boston, MA 02115 USA.
[Scholl, Claudia; Froehling, Stefan; Gilliland, D. Gary; Hahn, William C.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Sandy, Peter; Meylan, Etienne; Reiling, Jan H.; Sabatini, David M.; Lander, Eric S.; Jacks, Tyler] MIT, Dept Biol, Cambridge, MA 02139 USA.
[Sandy, Peter; Meylan, Etienne; Hoersch, Sebastian; Jacks, Tyler] Koch Inst Integrat Canc Res, Cambridge, MA 02142 USA.
[Sos, Martin L.; Michel, Kathrin; Thomas, Roman K.] Max Planck Soc, Max Planck Inst Neurol Res, Klaus Joachim Zulch Labs, D-50931 Cologne, Germany.
[Sos, Martin L.; Michel, Kathrin; Thomas, Roman K.] Univ Cologne, Fac Med, D-50931 Cologne, Germany.
[Reiling, Jan H.; Sabatini, David M.] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA.
[Sabatini, David M.; Gilliland, D. Gary; Jacks, Tyler] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA.
[Thomas, Roman K.] Univ Cologne, Ctr Integrated Oncol, D-50931 Cologne, Germany.
[Thomas, Roman K.] Univ Cologne, Dept Internal Med 1, D-50931 Cologne, Germany.
[Thomas, Roman K.] Max Planck Soc, Chem Genom Ctr, D-44227 Dortmund, Germany.
RP Hahn, WC (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM william_hahn@dfci.harvard.edu
RI Meyerson, Matthew/E-7123-2012;
OI Boehm, Jesse/0000-0002-6795-6336
FU US National Cancer Institute [R33 CA128625, R01 CA130988]; NIH [T32
CA09172-33]; Starr Cancer Consortium [I1-A11]; Susan Madden Fund; ASCO
YIA; Department of Defense Prostate Cancer Postdoctoral Fellowship;
Brain Science Foundation Fellowship; Deutsche Krebshilfe [107954];
Fritz-Thyssen-Stiftung [10.08.2.175]; German Ministry of Science and
Education [01GS08100]
FX This work was supported in part by grants from the US National Cancer
Institute (R33 CA128625, R01 CA130988) (W. C. H.) and NIH T32 CA09172-33
(D. A. B., S. E. M.), the Starr Cancer Consortium (I1-A11; W. C. H., D.
G. G.), the Susan Madden Fund and an ASCO YIA (D. A. B.), a Department
of Defense Prostate Cancer Postdoctoral Fellowship (S. Y. K.), a Brain
Science Foundation Fellowship (I. F. D.), the Deutsche Krebshilfe (grant
107954) (R. K. T.), the Fritz-Thyssen-Stiftung (grant 10.08.2.175; R. K.
T.) and the NGFNplus-program of the German Ministry of Science and
Education (BMBF, grant 01GS08100; R. K. T.). We thank C. Yu, G. Wei and
members of the Hahn laboratory for discussions. High-throughput RNAi
screening was conducted at the RNAi Platform of the Broad Institute of
MIT and Harvard.
NR 31
TC 531
Z9 542
U1 12
U2 37
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 5
PY 2009
VL 462
IS 7269
BP 108
EP U122
DI 10.1038/nature08460
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 514TT
UT WOS:000271419200042
PM 19847166
ER
PT J
AU Abate, JP
Blackwell, TK
AF Abate, Jess Porter
Blackwell, T. Keith
TI Life Is Short, if Sweet
SO CELL METABOLISM
LA English
DT Editorial Material
ID MECHANISMS; SPAN
AB Insulin is essential for glucose homeostasis, but reducing its activity delays the aging process in model organisms. In this issue of Cell Metabolism, Lee et al. (2009) show how these effects of insulin signaling intersect when glucose is fed to C. elegans.
C1 [Abate, Jess Porter; Blackwell, T. Keith] Harvard Univ, Sch Med, Harvard Stem Cell Inst, Joslin Diabet Ctr,Sect Dev & Stem Cell Biol,Dept, Boston, MA 02215 USA.
RP Blackwell, TK (reprint author), Harvard Univ, Sch Med, Harvard Stem Cell Inst, Joslin Diabet Ctr,Sect Dev & Stem Cell Biol,Dept, Boston, MA 02215 USA.
EM keith.blackwell@joslin.harvard.edu
NR 8
TC 8
Z9 8
U1 0
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
J9 CELL METAB
JI Cell Metab.
PD NOV 4
PY 2009
VL 10
IS 5
BP 338
EP 339
DI 10.1016/j.cmet.2009.10.006
PG 2
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 515UP
UT WOS:000271498700002
ER
PT J
AU O'Rourke, EJ
Soukas, AA
Carr, CE
Ruvkun, G
AF O'Rourke, Eyleen J.
Soukas, Alexander A.
Carr, Christopher E.
Ruvkun, Gary
TI C. elegans Major Fats Are Stored in Vesicles Distinct from
Lysosome-Related Organelles
SO CELL METABOLISM
LA English
DT Article
ID ABC TRANSPORTER PGP-2; CAENORHABDITIS-ELEGANS; NILE RED; LIPID DROPLETS;
LIFE-SPAN; BIOGENESIS; STORAGE; GENE; METABOLISM; LONGEVITY
AB Genetic conservation allows ancient features of fat storage endocrine pathways to be explored in C. elegans. Multiple studies have used Nile red or BODIPY-labeled fatty acids to identify regulators of fat mass. When mixed with their food, E coli bacteria, Nile red, and BODIPY-labeled fatty acids stain multiple spherical cellular structures in the C. elegans major fat storage organ, the intestine. However, here we demonstrate that, in the conditions previously reported, the lysosome-related organelles stained by Nile red and BODIPY-labeled fatty acids are not the C. elegans major fat storage compartment. We show that the major fat stores are contained in a distinct cellular compartment that is not stained by Nile red. Using biochemical assays, we validate oil red 0 staining as a method to assess major fat stores in C. elegans, allowing for efficient and accurate genetic and functional genomic screens for genes that control fat accumulation at the organismal level.
C1 [O'Rourke, Eyleen J.; Soukas, Alexander A.; Carr, Christopher E.; Ruvkun, Gary] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[O'Rourke, Eyleen J.; Soukas, Alexander A.; Carr, Christopher E.; Ruvkun, Gary] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA.
RP Ruvkun, G (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
EM ruvkun@molbio.mgh.harvard.edu
OI Carr, Christopher/0000-0002-7946-5622
FU National Institute of Diabetes and Digestive and Kidney Diseases
[R01DK070147, F32DK080607]; Human Frontiers Science Program
FX We would like to thank Sean Curran and Buck Samuel for creative input
and reading of the manuscript. We also thank other members of the
Ruvkun, Kaplan, and Ausubel labs for creative exchanges, and especially
Jihong Bai for taking confocal microscopy images. We thank Mason Freeman
for the use of his GCMS for lipid analysis. We want to thank Ho Yi Mak
and Marc Van-Gilst for sharing their experiences with lipid
histochemistry and biochemistry. Thanks to Kaveh Ashrafi and Kevin Jones
for sharing their experience with the neutral lipid dye LipidTOX. Thanks
to the Caenorhabditis Genome Center and Greg Hermann for providing
strains. This work was supported by Award Numbers R01DK070147 (to G.R.)
and F32DK080607 (to A.A.S.) from the National Institute of Diabetes and
Digestive and Kidney Diseases, and the Human Frontiers Science Program
(to E.J.O.).
NR 26
TC 152
Z9 157
U1 4
U2 24
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
J9 CELL METAB
JI Cell Metab.
PD NOV 4
PY 2009
VL 10
IS 5
BP 430
EP 435
DI 10.1016/j.cmet.2009.10.002
PG 6
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 515UP
UT WOS:000271498700011
PM 19883620
ER
PT J
AU Khan, M
Im, YB
Shunmugavel, A
Gilg, AG
Dhindsa, RK
Singh, AK
Singh, I
AF Khan, Mushfiquddin
Im, Yeong-Bin
Shunmugavel, Anandakumar
Gilg, Anne G.
Dhindsa, Ramanpreet K.
Singh, Avtar K.
Singh, Inderjit
TI Administration of S-nitrosoglutathione after traumatic brain injury
protects the neurovascular unit and reduces secondary injury in a rat
model of controlled cortical impact
SO JOURNAL OF NEUROINFLAMMATION
LA English
DT Article
ID NITRIC-OXIDE SYNTHASE; FOCAL CEREBRAL-ISCHEMIA; RECEPTOR AGONIST
8-OH-DPAT; ISCHEMIA/REPERFUSION INJURY; MATRIX METALLOPROTEINASES;
ENDOTHELIAL DYSFUNCTION; EXPERIMENTAL STROKE; COGNITIVE DEFICITS; FLAP
SURVIVAL; HEAD-INJURY
AB Background: Traumatic brain injury (TBI) is a major cause of preventable death and serious morbidity in young adults. This complex pathological condition is characterized by significant blood brain barrier (BBB) leakage that stems from cerebral ischemia, inflammation, and redox imbalances in the traumatic penumbra of the injured brain. Once trauma has occurred, combating these exacerbations is the keystone of an effective TBI therapy. Following other brain injuries, nitric oxide modulators such as S-nitrosoglutathione (GSNO) maintain not only redox balance but also inhibit the mechanisms of secondary injury. Therefore, we tested whether GSNO shows efficacy in a rat model of experimental TBI.
Methods: TBI was induced by controlled cortical impact (CCI) in adult male rats. GSNO (50 mu g/kg body weight) was administered at two hours after CCI. GSNO-treated injured animals (CCI+GSNO group) were compared with vehicle-treated injured animals (CCI+VEH group) in terms of tissue morphology, BBB leakage, edema, inflammation, cell death, and neurological deficit.
Results: Treatment of the TBI animals with GSNO reduced BBB disruption as evidenced by decreased Evan's blue extravasation across brain, infiltration/activation of macrophages (ED1 positive cells), and reduced expression of ICAM-1 and MMP-9. The GSNO treatment also restored CCI-mediated reduced expression of BBB integrity proteins ZO-1 and occludin. GSNO-mediated improvements in tissue histology shown by reduction of lesion size and decreased loss of both myelin (measured by LFB staining) and neurons (assayed by TUNEL) further support the efficacy of GSNO therapy. GSNO-mediated reduced expression of iNOS in macrophages as well as decreased neuronal cell death may be responsible for the histological improvement and reduced exacerbations. In addition to these biochemical and histological improvements, GSNO-treated injured animals recovered neurobehavioral functions as evaluated by the rotarod task and neurological score measurements.
Conclusion: GSNO is a promising candidate to be evaluated in humans after brain trauma because it not only protects the traumatic penumbra from secondary injury and improves overall tissue structure but also maintains the integrity of BBB and reduces neurologic deficits following CCI in a rat model of experimental TBI.
C1 [Khan, Mushfiquddin; Im, Yeong-Bin; Shunmugavel, Anandakumar; Gilg, Anne G.; Dhindsa, Ramanpreet K.; Singh, Inderjit] Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA.
[Singh, Avtar K.] Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA.
[Singh, Avtar K.] Ralph H Johnson VA Med Ctr, Charleston, SC 29401 USA.
RP Singh, I (reprint author), Med Univ S Carolina, Dept Pediat, 171 Ashley Ave, Charleston, SC 29425 USA.
EM khanm@musc.edu; imyb@musc.edu; anandak@musc.edu; gilg@musc.edu;
mushfiquddinkhan@gmail.com; singha@musc.edu; singhi@musc.edu
FU Betty and Guy Beatty Foundation; National Institutes of Health
[NS-22576, NS-34741, NS-37766]; Veteran Administration Merit; National
Center for Research Resources [C06 RR018823, C06 RR015455]
FX These studies were supported by grants from Betty and Guy Beatty
Foundation, National Institutes of Health (NS-22576, NS-34741 and
NS-37766) and Veteran Administration Merit Award. This work was also
supported by the NIH, Grants C06 RR018823 and No C06 RR015455 from the
Extramural Research Facilities Program of the National Center for
Research Resources. We thank Dr Md Nasrul Hoda and Dr Bilgen Mehmet for
their valuable technical assistance. We are grateful to Dr Tom Smith
from the MUSC Writing Center for his valuable editing and correction of
the manuscript. We would like to thank Ms. Joyce Bryan for procurement
of animals and chemicals and Chara Williams for secretarial assistance.
NR 77
TC 70
Z9 73
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-2094
J9 J NEUROINFLAMM
JI J. Neuroinflamm.
PD NOV 4
PY 2009
VL 6
AR 32
DI 10.1186/1742-2094-6-32
PG 12
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 525XX
UT WOS:000272252200001
PM 19889224
ER
PT J
AU Wen, B
Wang, GI
Dean, I
Delgutte, B
AF Wen, Bo
Wang, Grace I.
Dean, Isabel
Delgutte, Bertrand
TI Dynamic Range Adaptation to Sound Level Statistics in the Auditory Nerve
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID SHORT-TERM ADAPTATION; CELL AFFERENT SYNAPSE; INTENSITY DISCRIMINATION;
INFERIOR COLLICULUS; FIBER RESPONSES; RIBBON SYNAPSE; NOISE;
SUPPRESSION; STIMULI; NEURONS
AB The auditory system operates over a vast range of sound pressure levels (100-120 dB) with nearly constant discrimination ability across most of the range, well exceeding the dynamic range of most auditory neurons (20-40 dB). Dean et al. (2005) have reported that the dynamic range of midbrain auditory neurons adapts to the distribution of sound levels in a continuous, dynamic stimulus by shifting toward the most frequently occurring level. Here, we show that dynamic range adaptation, distinct from classic firing rate adaptation, also occurs in primary auditory neurons in anesthetized cats for tone and noise stimuli. Specifically, the range of sound levels over which firing rates of auditory nerve (AN) fibers grows rapidly with level shifts nearly linearly with the most probable levels in a dynamic sound stimulus. This dynamic range adaptation was observed for fibers with all characteristic frequencies and spontaneous discharge rates. As in the midbrain, dynamic range adaptation improved the precision of level coding by the AN fiber population for the prevailing sound levels in the stimulus. However, dynamic range adaptation in the AN was weaker than in the midbrain and not sufficient (0.25 dB/dB, on average, for broadband noise) to prevent a significant degradation of the precision of level coding by the AN population above 60 dB SPL. These findings suggest that adaptive processing of sound levels first occurs in the auditory periphery and is enhanced along the auditory pathway.
C1 [Wen, Bo; Wang, Grace I.; Delgutte, Bertrand] Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA.
[Wen, Bo; Wang, Grace I.; Delgutte, Bertrand] MIT, Elect Res Lab, Cambridge, MA 02139 USA.
[Wang, Grace I.] MIT, Dept Elect Engn & Comp Sci, Cambridge, MA 02139 USA.
[Dean, Isabel] UCL, Ear Inst, London WC1X 8EE, England.
RP Wen, B (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA.
EM bwen@mit.edu
OI , /0000-0003-1349-9608
FU National Institutes of Health [RO1 DC002258, P30 DC005209]; Royal
Society Dorothy Hodgkin Fellowship
FX This work was supported by National Institutes of Health Grants RO1
DC002258 and P30 DC005209 (B. D.) and a Royal Society Dorothy Hodgkin
Fellowship (I. D.). We thank K. Hancock for developing the experimental
software, C. Miller for expert surgical assistance, and N. Harper for
providing the code for computing the Fisher information. J. Guinan and
two anonymous reviewers made valuable comments on this manuscript.
NR 43
TC 68
Z9 71
U1 0
U2 9
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 4
PY 2009
VL 29
IS 44
BP 13797
EP 13808
DI 10.1523/JNEUROSCI.5610-08.2009
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 515LG
UT WOS:000271471400007
PM 19889991
ER
PT J
AU Panizzi, P
Nahrendorf, M
Wildgruber, M
Waterman, P
Figueiredo, JL
Aikawa, E
McCarthy, J
Weissleder, R
Hilderbrand, SA
AF Panizzi, Peter
Nahrendorf, Matthias
Wildgruber, Moritz
Waterman, Peter
Figueiredo, Jose-Luiz
Aikawa, Elena
McCarthy, Jason
Weissleder, Ralph
Hilderbrand, Scott A.
TI Oxazine Conjugated Nanoparticle Detects in Vivo Hypochlorous Acid and
Peroxynitrite Generation
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID ISCHEMIA-REPERFUSION INJURY; NITRIC-OXIDE; HYDROGEN-PEROXIDE;
FLUORESCENT-PROBE; MYELOPEROXIDASE ACTIVITY; REACTIVE NITROGEN; LIVING
CELLS; MYOCARDIAL-INFARCTION; OXIDATIVE STRESS; PROSTATE-CANCER
AB The current lack of suitable probes has limited the in vivo imaging of reactive oxygen/nitrogen species (ROS/RNS). ROS/RNS are often generated by ischemia-induced inflammation; defining the extent of tissue involvement or ROS/RNS-related damage would have a significant clinical impact. We present the preparation and demonstration of a fluorogenic sensor for monitoring peroxynitrite (ONOO(-)) and myeloperoxidase (MIPO) mediated hypochlorous acid (HOCl/OCl(-)) production. The sensor consists of a long circulating biocompatible nanoparticle that targets phagocytic cells in vivo and is coated with similar to 400 quenched oxazine fluorophores that are released by reaction with HOCl or ONOO(-) but are stable toward oxidants such as hydroxyl radical, hydrogen peroxide, and superoxide. MPO-dependent probe activation is chloride ion dependent and is negated in flow cytometry studies of MPO inhibitor treated neutrophils. Fluorescence reflectance imaging and microscopic fluorescence imaging in mouse hearts after myocardial infarction showed probe release into neutrophil-rich ischemic areas, making this ROS/RNS sensor a novel prognostic indicator.
C1 [Hilderbrand, Scott A.] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Hilderbrand, SA (reprint author), Massachusetts Gen Hosp, Ctr Syst Biol, Simches Res Bldg,185 Cambridge St, Boston, MA 02114 USA.
EM scoff_hilderbrand@hms.harvard.edu
OI Panizzi, Peter/0000-0003-0141-8807
FU NIH [R24-CA92782, U0114L080731]; American Heart Association [0835623D]
FX The authors acknowledge Cory Siegel, M.D. for help with image
acquisition; Vima Cortez-Retamozo, Ph.D. for help with FACS isolation of
neutrophils; Nikolai Sergeyev, Ph.D. for nanoparticle synthesis, Yoshiko
Iwamoto for help with histology; and Ned Keliher, Ph.D. for helpful
suggestions. This work was funded in part by NIH grants to R.W.
(R24-CA92782, U0114L080731), and an American Heart Association scientist
development grant to M.N. (0835623D).
NR 54
TC 101
Z9 101
U1 9
U2 64
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD NOV 4
PY 2009
VL 131
IS 43
BP 15739
EP 15744
DI 10.1021/ja903922u
PG 6
WC Chemistry, Multidisciplinary
SC Chemistry
GA 516AI
UT WOS:000271513600044
PM 19817443
ER
PT J
AU Ke, YG
Douglas, SM
Liu, MH
Sharma, J
Cheng, AC
Leung, A
Liu, Y
Shih, WM
Yan, H
AF Ke, Yonggang
Douglas, Shawn M.
Liu, Minghui
Sharma, Jaswinder
Cheng, Anchi
Leung, Albert
Liu, Yan
Shih, William M.
Yan, Hao
TI Multilayer DNA Origami Packed on a Square Lattice
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID DOUBLE-CROSSOVER MOLECULES; NANOSCALE SHAPES; FOLDING DNA;
NANOFABRICATION; INTEGRATION; ASSEMBLIES; OCTAHEDRON; PROTEINS; DESIGN
AB Molecular self-assembly using DNA as a structural building block has proven to be an efficient route to the construction of nanoscale objects and arrays of increasing complexity. Using the remarkable "scaffolded DNA origami" strategy, Rothemund demonstrated that a long single-stranded DNA from a viral genome (M13) can be folded into a variety of custom two-dimensional (2D) shapes using hundreds of short synthetic DNA molecules as staple strands. More recently, we generalized a strategy to build custom-shaped, three-dimensional (3D) objects formed as pleated layers of helices constrained to a honeycomb lattice, with precisely controlled dimensions ranging from 10 to 100 nm. Here we describe a more compact design for 3D origami, with layers of helices packed on a square lattice, that can be folded successfully into structures of designed dimensions in a one-step annealing process, despite the increased density of DNA helices. A square lattice provides a more natural framework for designing rectangular structures, the option for a more densely packed architecture, and the ability to create surfaces that are more flat than is possible with the honeycomb lattice. Thus enabling the design and construction of custom 3D shapes from helices packed on a square lattice provides a general foundational advance for increasing the versatility and scope of DNA nanotechnology.
C1 [Douglas, Shawn M.; Shih, William M.] Harvard Univ, Sch Med, Dept Canc Biol, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Douglas, Shawn M.; Shih, William M.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Douglas, Shawn M.; Shih, William M.] Wyss Inst Biologically Inspired Engn Harvard, Cambridge, MA 02138 USA.
[Ke, Yonggang; Liu, Minghui; Sharma, Jaswinder; Liu, Yan; Yan, Hao] Arizona State Univ, Dept Chem & Biochem, Tempe, AZ 85287 USA.
[Ke, Yonggang; Liu, Minghui; Sharma, Jaswinder; Liu, Yan; Yan, Hao] Arizona State Univ, Biodesign Inst, Tempe, AZ 85287 USA.
[Cheng, Anchi; Leung, Albert] Scripps Res Inst, Natl Resource Automated Mol Microscopy, La Jolla, CA 92037 USA.
RP Shih, WM (reprint author), Harvard Univ, Sch Med, Dept Canc Biol, Dana Farber Canc Inst, Boston, MA 02115 USA.
EM William_Shih@dfci.harvard.edu; hao.yan@asu.edu
RI Liu, Yan/K-1999-2014;
OI Liu, Yan/0000-0003-0906-2606; Douglas, Shawn/0000-0001-5398-9041
FU NSF; NIH [IDP2OD004641-01]; ONR; ARO; AFOSR; DOE; Sloan Research;
Claudia Adams Barr Program Investigator; Wyss Institute; National
Institutes of Health [RR17573]
FX This work was supported by grants from NSF, NIH, ONR, ARO, AFOSR, and
DOE and a Sloan Research Fellowship to H.Y. and grants from NSF, ARO,
and ONR to Y.L. This work was also supported by Claudia Adams Barr
Program Investigator, Wyss Institute for Biologically Inspired
Engineering, and NIH New Innovator (IDP2OD004641-01) grants to W.M.S.
National Resource for Automated Molecular Microscopy is supported by the
National Institutes of Health though the National Center for Research
Resources' P41 program (RR17573). We thank Erica Jacovetty for technical
assistance.
NR 31
TC 149
Z9 151
U1 11
U2 97
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD NOV 4
PY 2009
VL 131
IS 43
BP 15903
EP 15908
DI 10.1021/ja906381y
PG 6
WC Chemistry, Multidisciplinary
SC Chemistry
GA 516AI
UT WOS:000271513600062
PM 19807088
ER
PT J
AU Qaseem, A
Snow, V
Denberg, TD
Casey, DE
Forciea, MA
Owens, DK
Shekelle, P
AF Qaseem, Amir
Snow, Vincenza
Denberg, Thomas D.
Casey, Donald E., Jr.
Forciea, Mary Ann
Owens, Douglas K.
Shekelle, Paul
CA Amer Coll Phys
TI Hormonal Testing and Pharmacologic Treatment of Erectile Dysfunction: A
Clinical Practice Guideline From the American College of Physicians
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Article
ID PLACEBO-CONTROLLED TRIAL; SILDENAFIL CITRATE VIAGRA((R)); SPARING
RADICAL PROSTATECTOMY; RANDOMIZED CONTROLLED-TRIAL; URINARY-TRACT
SYMPTOMS; ON-DEMAND TADALAFIL; PHOSPHODIESTERASE TYPE-5 INHIBITOR;
BENIGN PROSTATIC HYPERPLASIA; EXTERNAL-BEAM RADIOTHERAPY; INCREASES
PENILE RIGIDITY
AB Description: The American College of Physicians developed this guideline to present the available evidence on hormonal testing in and pharmacologic management of erectile dysfunction. Current pharmacologic therapies include phosphodiesterase-5 (PDE-5) inhibitors, such as sildenafil, vardenafil, tadalafil, mirodenafil, and udenafil, and hormonal treatment.
Methods: Published literature on this topic was identified by using MEDLINE (1966 to May 2007), EMBASE (1980 to week 22 of 2007), Cochrane Central Register of Controlled Trials (second quarter of 2007), PsycINFO (1985 to June 2007), AMED (1985 to June 2007), and SCOPUS (2006). The literature search was updated by searching for articles in MEDLINE and EMBASE published between May 2007 and April 2009. Searches were limited to English-language publications. This guideline grades the evidence and recommendations by using the American College of Physicians' clinical practice guidelines grading system.
Recommendation 1: The American College of Physicians recommends that clinicians initiate therapy with a PDE-5 inhibitor in men who seek treatment for erectile dysfunction and who do not have a contraindication to PDE-5 inhibitor use (Grade: strong recommendation; high-quality evidence).
Recommendation 2: The American College of Physicians recommends that clinicians base the choice of a specific PDE-5 inhibitor on the individual preferences of men with erectile dysfunction, including ease of use, cost of medication, and adverse effects profile (Grade: weak recommendation; low-quality evidence).
Recommendation 3: The American College of Physicians does not recommend for or against routine use of hormonal blood tests or hormonal treatment in the management of patients with erectile dysfunction (Grade: insufficient evidence to determine net benefits and harms).
C1 [Qaseem, Amir] Amer Coll Physicians, Philadelphia, PA 19104 USA.
Univ Penn, Philadelphia, PA 19104 USA.
Univ Colorado, Aurora, CO USA.
Atlantic Hlth, Morristown, NJ USA.
Vet Affairs Palo Alto Hlth Care Syst, Stanford, CA USA.
Stanford Univ, Stanford, CA 94305 USA.
Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
RP Qaseem, A (reprint author), Amer Coll Physicians, 190 N Independence Mall W, Philadelphia, PA 19104 USA.
EM aqaseem@acponline.org
FU American College of Physicians' operating budget
FX Financial support for the development of this guideline comes
exclusively from the American College of Physicians' operating budget.
NR 211
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U1 2
U2 3
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA
SN 0003-4819
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD NOV 3
PY 2009
VL 151
IS 9
BP 639
EP W208
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 514IM
UT WOS:000271387700006
PM 19884625
ER
PT J
AU Sattler, M
Griffin, JD
AF Sattler, Martin
Griffin, James D.
TI JAK2 Gets Histone H3 Rolling
SO CANCER CELL
LA English
DT Editorial Material
ID FERM DOMAIN; TRANSCRIPTION; DISORDERS
AB Activation of JAK2 is implicated in normal hematopoiesis as well as oncogenic transformation. A paper in the recent issue of Nature demonstrates that phosphorylation of histone H3 by JAK2 releases the transcriptional repressor HP1 alpha from chromatin, resulting in gene transcription.
C1 [Sattler, Martin; Griffin, James D.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Sattler, Martin; Griffin, James D.] Harvard Univ, Dept Med, Boston, MA 02115 USA.
[Sattler, Martin] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Griffin, JD (reprint author), Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
EM james_griffin@dfci.harvard.edu
FU NCI NIH HHS [P01 CA066996]
NR 9
TC 6
Z9 6
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1535-6108
J9 CANCER CELL
JI Cancer Cell
PD NOV 3
PY 2009
VL 16
IS 5
BP 365
EP 366
DI 10.1016/j.ccr.2009.10.009
PG 2
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 519HG
UT WOS:000271755100004
PM 19878867
ER
PT J
AU Friedlander, SYG
Chu, GC
Snyder, EL
Girnius, N
Dibelius, G
Crowley, D
Vasile, E
DePinho, RA
Jacks, T
AF Friedlander, Sharon Y. Gidekel
Chu, Gerald C.
Snyder, Eric L.
Girnius, Nomeda
Dibelius, Gregory
Crowley, Denise
Vasile, Eliza
DePinho, Ronald A.
Jacks, Tyler
TI Context-Dependent Transformation of Adult Pancreatic Cells by Oncogenic
K-Ras
SO CANCER CELL
LA English
DT Article
ID INTRAEPITHELIAL NEOPLASIA; BETA-CELLS; MALIGNANT-TRANSFORMATION; DUCTAL
ADENOCARCINOMA; TRANSGENIC MICE; BREAST-CANCER; MOUSE MODEL; IN-VIVO;
EXPRESSION; LET-7
AB Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies. To investigate the cellular origin(s) of this cancer, we determined the effect of PDAC-relevant gene mutations in distinct cell types of the adult pancreas. We show that a subpopulation of Pdx1-expressing cells is susceptible to oncogenic K-Ras-induced transformation without tissue injury, whereas insulin-expressing endocrine cells are completely refractory to transformation under these conditions. However, chronic pancreatic injury can alter their endocrine fate and allow them to serve as the cell of origin for exocrine neoplasia. These results suggest that one mechanism by which inflammation and/or tissue damage can promote neoplasia is by altering the fate of differentiated cells that are normally refractory to oncogenic stimulation.
C1 [Friedlander, Sharon Y. Gidekel; Snyder, Eric L.; Girnius, Nomeda; Dibelius, Gregory; Crowley, Denise; Vasile, Eliza; Jacks, Tyler] MIT, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA.
[Jacks, Tyler] MIT, Dept Biol, Cambridge, MA 02139 USA.
[Crowley, Denise; Jacks, Tyler] MIT, Howard Hughes Med Inst, Cambridge, MA 02139 USA.
[Chu, Gerald C.; DePinho, Ronald A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Chu, Gerald C.; Snyder, Eric L.] Brigham & Womans Hosp, Dept Pathol, Boston, MA 02115 USA.
[Chu, Gerald C.; DePinho, Ronald A.] Belfer Fdn Inst Innovat Canc Sci, Ctr Appl Canc Sci, Boston, MA 02115 USA.
[DePinho, Ronald A.] Harvard Univ, Sch Med, Dept Med & Genet, Boston, MA 02115 USA.
RP Jacks, T (reprint author), MIT, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA.
EM tjacks@mit.edu
RI Vasile, Eugeniu/F-8276-2010
FU National Institutes of Health (NIH) [1-PO1-CA117969-01]; Cancer Center
Support; National Cancer Institute (NCI) [P30-CA14051]
FX We are grateful to D. Melton for gifts of the Pdx1CreER (TM),
proCPA1CreERT2, and RipCreER (TM) strains and stimulating
discussions. We thank A. Berns (Netherlands Cancer Institute) for
providing the Trp53flox mice; C. Wright for the anti-Pdx1
antibody; S. Hoersch for statistical analysis; and N. Bardeesy for
critical reading of the manuscript. T.J. is a Howard Hughes Medical
Institute Investigator and a Daniel K. Ludwig Scholar. S.Y.G.F. is an
Anna Fuller fund of New Haven Fellow. R.A.D. is an American Cancer
Society Research Professor. This work was supported by grant
1-PO1-CA117969-01 from the National Institutes of Health (NIH) and in
part by Cancer Center Support (core) grant P30-CA14051 from the National
Cancer Institute (NCI). The content is solely the responsibility of the
authors and does not necessarily represent the official views of the NCI
or the NIH.
NR 57
TC 108
Z9 108
U1 2
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1535-6108
J9 CANCER CELL
JI Cancer Cell
PD NOV 3
PY 2009
VL 16
IS 5
BP 379
EP 389
DI 10.1016/j.ccr.2009.09.027
PG 11
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 519HG
UT WOS:000271755100007
ER
PT J
AU Zhang, Q
Gu, JM
Li, LJ
Liu, JY
Luo, B
Cheung, HW
Boehm, JS
Ni, M
Geisen, C
Root, DE
Polyak, K
Brown, M
Richardson, AL
Hahn, WC
Kaelin, WG
Bommi-Reddy, A
AF Zhang, Qing
Gu, Jinming
Li, Lianjie
Liu, Jiayun
Luo, Biao
Cheung, Hiu-Wing
Boehm, Jesse S.
Ni, Min
Geisen, Christoph
Root, David E.
Polyak, Kornelia
Brown, Myles
Richardson, Andrea L.
Hahn, William C.
Kaelin, William G., Jr.
Bommi-Reddy, Archana
TI Control of Cyclin D1 and Breast Tumorigenesis by the EgIN2 Prolyl
Hydroxylase
SO CANCER CELL
LA English
DT Article
ID HYPOXIA-INDUCIBLE-FACTOR; TUMOR-SUPPRESSOR; ESTROGEN-RECEPTOR;
GENE-EXPRESSION; CANCER; HIF; PROTEIN; HIF-1-ALPHA; PATHWAY; GROWTH
AB 2-Oxoglutarate-dependent dioxygenases, including the EgIN prolyl hydroxylases that regulate HIF, can be inhibited with drug-like molecules. EgIN2 is estrogen inducible in breast carcinoma cells and the lone Drosophila EgIN interacts genetically with Cyclin D1. Although EgIN2 is a nonessential gene, we found that EgIN2 inactivation decreases Cyclin D1 levels and suppresses mammary gland proliferation in vivo. Regulation of Cyclin D1 is a specific attribute of EgIN2 among the EgIN proteins and is HIF independent. Loss of EgIN2 catalytic activity inhibits estrogen-dependent breast cancer tumorigenesis and can be rescued by exogenous Cyclin D1. EgIN2 depletion also impairs the fitness of lung, brain, and hematopoietic cancer lines. These findings support the exploration of EgIN2 inhibitors as therapeutics for estrogen-dependent breast cancer and other malignancies.
C1 [Zhang, Qing; Gu, Jinming; Li, Lianjie; Liu, Jiayun; Ni, Min; Geisen, Christoph; Polyak, Kornelia; Brown, Myles; Hahn, William C.; Kaelin, William G., Jr.; Bommi-Reddy, Archana] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Richardson, Andrea L.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Cell Biol, Boston, MA 02115 USA.
[Hahn, William C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Ctr Genome Discovery, Boston, MA 02115 USA.
[Richardson, Andrea L.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Luo, Biao; Cheung, Hiu-Wing; Boehm, Jesse S.; Root, David E.; Hahn, William C.] Broad Inst, Cambridge, MA 02142 USA.
[Li, Lianjie; Kaelin, William G., Jr.] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA.
RP Kaelin, WG (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM william_kaelin@dfci.harvard.edu
FU National Cancer Institute Dana-Farber/Harvard SPORE in Breast Cancer;
Breast Cancer Research Foundation; Terri Brodeur Breast Cancer
Foundation; Howard Hughes Medical Institute Investigator; Doris Duke
Distinguished Clinical Investigator; National Institutes of Health
[5R01CA068490-14]
FX We thank Regeneron Pharmaceuticals for the EgIN2-/- mice,
Oliver Hankinson for the ARNT-/- cells, Silvia Giordano for
the inducible shRNA vector, Yen Geng for help with mammary gland
analysis, Margaret McLaughlin-Drubin for help with E7 immunoblots,
Mariela Jaskelioff for help with xenograft studies, and members of the
Kaelin Laboratory for useful discussions. This work was supported by
National Cancer Institute Dana-Farber/Harvard SPORE in Breast Cancer
(A.L.R.) and the Breast Cancer Research Foundation (A.L.R. and W.G.K.).
QZ is supported by a postdoctoral fellowship from Terri Brodeur Breast
Cancer Foundation. W.G.K. is a Howard Hughes Medical Institute
Investigator and a Doris Duke Distinguished Clinical Investigator. This
work is supported in part by a National Institutes of Health grant
(5R01CA068490-14) to W.G.K. W.G.K. owns equity in Fibrogen, Inc., which
is developing prolyl hydroxylase inhibitors as potential therapeutics.
NR 52
TC 59
Z9 60
U1 0
U2 2
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1535-6108
J9 CANCER CELL
JI Cancer Cell
PD NOV 3
PY 2009
VL 16
IS 5
BP 413
EP 424
DI 10.1016/j.ccr.2009.09.029
PG 12
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 519HG
UT WOS:000271755100010
PM 19878873
ER
PT J
AU Zhou, DW
Conrad, C
Xia, F
Park, JS
Payer, B
Yin, Y
Lauwers, GY
Thasler, W
Lee, JT
Avruch, J
Bardeesy, N
AF Zhou, Dawang
Conrad, Claudius
Xia, Fan
Park, Ji-Sun
Payer, Bernhard
Yin, Yi
Lauwers, Gregory Y.
Thasler, Wolfgang
Lee, Jeannie T.
Avruch, Joseph
Bardeesy, Nabeel
TI Mst1 and Mst2 Maintain Hepatocyte Quiescence and Suppress Hepatocellular
Carcinoma Development through Inactivation of the Yap1 Oncogene
SO CANCER CELL
LA English
DT Article
ID NF2 TUMOR-SUPPRESSOR; CELL-PROLIFERATION; PROMOTES APOPTOSIS; KINASE
MST1; MUSCLE DIFFERENTIATION; CONTACT INHIBITION; CASPASE CLEAVAGE;
GROWTH-CONTROL; HIPPO PATHWAY; ORGAN SIZE
AB Hippo-Lats-Yorkie signaling regulates tissue overgrowth and tumorigenesis in Drosophila. We show that the Mst1 and Mst2 protein kinases, the mammalian Hippo orthologs, are cleaved and constitutively activated in the mouse liver. Combined Mst1/2 deficiency in the liver results in loss of inhibitory Ser127 phosphorylation of the Yorkie ortholog, Yap1, massive overgrowth, and hepatocellular carcinoma (HCC). Reexpression of Mst1 in HCC-derived cell lines promotes Yap1 Ser127 phosphorylation and inactivation and abrogates their tumorigenicity. Notably, Mst1/2 inactivates Yap1 in liver through an intermediary kinase distinct from Lats1/2. Approximately 30% of human HCCs show low Yap1 (Ser127) phosphorylation and a majority exhibit loss of cleaved, activated Mst1. Mst1/2 inhibition of Yap1 is an important pathway for tumor suppression in liver relevant to human HCC.
C1 [Zhou, Dawang; Xia, Fan; Payer, Bernhard; Yin, Yi; Lee, Jeannie T.; Avruch, Joseph] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Zhou, Dawang; Xia, Fan; Yin, Yi; Avruch, Joseph] Massachusetts Gen Hosp, Diabet Unit, Boston, MA 02114 USA.
[Conrad, Claudius; Park, Ji-Sun; Bardeesy, Nabeel] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Conrad, Claudius] Massachusetts Gen Hosp, Surg Serv, Boston, MA 02114 USA.
[Lauwers, Gregory Y.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Payer, Bernhard; Lee, Jeannie T.] Massachusetts Gen Hosp, Howard Hughes Med Inst, Boston, MA 02114 USA.
[Avruch, Joseph; Bardeesy, Nabeel] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Lauwers, Gregory Y.; Lee, Jeannie T.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Lee, Jeannie T.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Thasler, Wolfgang] LM Univ Munich, Hosp Grosshadern, Dept Surg, D-81377 Munich, Germany.
RP Avruch, J (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
EM avruch@molbio.mgh.harvard.edu; nelbardeesy@partners.org
RI Payer, Bernhard/F-7353-2010;
OI Payer, Bernhard/0000-0002-4694-2082; Zhou, Dawang/0000-0002-9053-5249
FU Sidney Kimmel Foundation for Cancer Research [DK17776, K01CA104647];
Linda J. Verville Cancer Research Foundation; [T32DK007028]
FX This work was supported in part by DK17776 (J.A.), K01CA104647, the
Sidney Kimmel Foundation for Cancer Research (N.B.), the Linda J.
Verville Cancer Research Foundation (NB), and institutional funds. D.Z.
is supported by T32DK007028. The study was designed by J.A., D.Z., and
N.B. and carried out by D.Z., with contributions from C.C., J.-S.P.,
F.X., Y.Y., B.P., and G.Y.L. N.B. and J.A. wrote the manuscript with
contributions by D.Z., C.C., B.P., and J.T.L. W.T. provided essential
materials. The authors thank S. Liebhaber for analysis of the human HCC
data, T. Weiss (University of Regensburg, Germany) for human liver
samples used in preliminary studies, and R.T. Bronson for histologic
analyses.
NR 43
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U1 3
U2 40
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1535-6108
J9 CANCER CELL
JI Cancer Cell
PD NOV 3
PY 2009
VL 16
IS 5
BP 425
EP 438
DI 10.1016/j.ccr.2009.09.026
PG 14
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 519HG
UT WOS:000271755100011
PM 19878874
ER
PT J
AU Patton, KK
Ellinor, PT
Heckbert, SR
Christenson, RH
DeFilippi, C
Gottdiener, JS
Kronmal, RA
AF Patton, Kristen K.
Ellinor, Patrick T.
Heckbert, Susan R.
Christenson, Robert H.
DeFilippi, Christopher
Gottdiener, John S.
Kronmal, Richard A.
TI N-Terminal Pro-B-Type Natriuretic Peptide Is a Major Predictor of the
Development of Atrial Fibrillation The Cardiovascular Health Study
SO CIRCULATION
LA English
DT Article
DE arrhythmia; atrial fibrillation; natriuretic peptides
ID RISK; DISEASE; SYSTEM
AB Background-Atrial fibrillation (AF), the most common cardiac rhythm abnormality, is associated with significant morbidity, mortality, and healthcare expenditures. Elevated B-type natriuretic peptide levels have been associated with the risk of heart failure, AF, and mortality.
Methods and Results-The relation between N-terminal pro-B-type natriuretic peptide (NT-proBNP) and AF was studied in 5445 Cardiovascular Health Study participants with the use of relative risk regression for predicting prevalent AF and Cox proportional hazards for predicting incident AF. NT-proBNP levels were strongly associated with prevalent AF, with an unadjusted prevalence ratio of 128 for the highest quintile (95% confidence interval, 17.9 to 913.3; P<0.001) and adjusted prevalence ratio of 147 for the highest quintile ( 95% confidence interval, 20.4 to 1064.3; P<0.001) compared with the lowest. After a median follow-up of 10 years (maximum of 16 years), there were 1126 cases of incident AF (a rate of 2.2 per 100 person-years). NT-proBNP was highly predictive of incident AF, with an unadjusted hazard ratio of 5.2 ( 95% confidence interval, 4.3 to 6.4; P<0.001) for the development of AF for the highest quintile compared with the lowest; for the same contrast, NT-proBNP remained the strongest predictor of incident AF after adjustment for an extensive number of covariates, including age, sex, medication use, blood pressure, echocardiographic parameters, diabetes mellitus, and heart failure, with an adjusted hazard ratio of 4.0 (95% confidence interval, 3.2 to 5.0; P<0.001).
Conclusions-In a community-based population of older adults, NT-proBNP was a remarkable predictor of incident AF, independent of any other previously described risk factor. (Circulation. 2009; 120: 1768-1774.)
C1 [Kronmal, Richard A.] Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Dept Biostat, Seattle, WA 98115 USA.
[Patton, Kristen K.] Univ Washington, Div Cardiol, Seattle, WA 98115 USA.
[Heckbert, Susan R.] Univ Washington, Dept Epidemiol, Seattle, WA 98115 USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Christenson, Robert H.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[DeFilippi, Christopher; Gottdiener, John S.] Univ Maryland, Med Ctr, Div Cardiol, Baltimore, MD 21201 USA.
RP Kronmal, RA (reprint author), Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Dept Biostat, Bldg 29,Suite 310,6200 NE 74th St, Seattle, WA 98115 USA.
EM kronmal@u.washington.edu
OI Patton, Kristen K./0000-0002-9034-6966
FU National Heart, Lung, and Blood Institute [HL080295]; National Institute
of Neurological Disorders and Stroke. Roche Diagnostics;
[N01-HC-85079]; [N01-HC-85086]; [N01-HC-35129]; [N01HC-15103]; [N01
HC-55222]; [N01-HC-75150]; [N01-HC-45133]
FX The research reported in this article was supported by contract numbers
N01-HC-85079 through N01-HC-85086, N01-HC-35129, N01HC-15103, N01
HC-55222, N01-HC-75150, N01-HC-45133, and grant number U01 HL080295 from
the National Heart, Lung, and Blood Institute, with additional
contribution from the National Institute of Neurological Disorders and
Stroke. Roche Diagnostics provided funding and laboratory reagents for
the NT pro-BNP assay.
NR 26
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U1 0
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
BP 1768
EP 1774
DI 10.1161/CIRCULATIONAHA.109.873265
PG 7
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 514YD
UT WOS:000271431800005
PM 19841297
ER
PT J
AU Tonelli, M
Curhan, G
Pfeffer, M
Sacks, F
Thadhani, R
Melamed, ML
Wiebe, N
Muntner, P
AF Tonelli, Marcello
Curhan, Gary
Pfeffer, Marc
Sacks, Frank
Thadhani, Ravi
Melamed, Michal L.
Wiebe, Natasha
Muntner, Paul
TI Relation Between Alkaline Phosphatase, Serum Phosphate, and All-Cause or
Cardiovascular Mortality
SO CIRCULATION
LA English
DT Article
DE kidney failure, chronic; cardiovascular diseases; myocardial infarction;
cohort studies; metabolism
ID CORONARY-ARTERY CALCIFICATION; CHRONIC KIDNEY-DISEASE;
HEMODIALYSIS-PATIENTS; VASCULAR CALCIFICATION; MYOCARDIAL-INFARCTION;
CHOLESTEROL LEVELS; EVENT RATE; PHOSPHORUS; CALCIUM; PEOPLE
AB Background-Higher levels of serum alkaline phosphatase (AlkP) are associated with excess mortality in dialysis patients, but whether AlkP is associated with adverse outcomes among people without kidney failure is unknown.
Methods and Results-We first analyzed the association between AlkP and cardiovascular outcomes among 4115 participants with a previous myocardial infarction (the Cholesterol And Recurrent Events [CARE] study). Results were validated by analyzing the association between AlkP and mortality in an independent sample of 14 716 adults from the general US population (the Third National Health and Nutrition Examination Survey). A graded, independent association was noted between baseline tertile of AlkP and the adjusted hazard ratio of all-cause mortality in CARE participants (P(trend)=0.02). After adjustment for serum phosphate, hepatic enzymes, and other potential confounders, participants with AlkP in the highest tertile had an adjusted hazard ratio of 1.43 (95% confidence interval 1.08 to 1.89) compared with those in the lowest tertile. Multivariable-adjusted associations between higher AlkP and all-cause and cardiovascular mortality were present in the Third National Health and Nutrition Examination Survey (P(trend) across tertiles of AlkP=0.006 and 0.038, respectively). Findings from both CARE and the Third National Health and Nutrition Examination Survey were similar among individuals with and without evidence of kidney disease, defined by estimated glomerular filtration rate <60 mL . min(-1) . 1.73 m(-2).
Conclusions-We found an independent relation between higher levels of AlkP and adverse outcomes among survivors of myocardial infarction and in a general population sample. The excess risk of death was present in people without evidence of kidney disease and was particularly high among people with higher levels of both AlkP and serum phosphate. (Circulation. 2009;120:1784-1792.)
C1 [Tonelli, Marcello; Wiebe, Natasha] Univ Alberta, Dept Med, Edmonton, AB T6B 2B7, Canada.
[Tonelli, Marcello] Univ Alberta, Dept Crit Care, Edmonton, AB T6B 2B7, Canada.
[Curhan, Gary] Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA.
[Pfeffer, Marc] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
[Sacks, Frank] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Thadhani, Ravi] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Melamed, Michal L.] Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA.
[Muntner, Paul] Mt Sinai Sch Med, Dept Community & Prevent Med, New York, NY USA.
RP Tonelli, M (reprint author), Univ Alberta, Dept Med, 7-129 Clinical Sci Bldg,8440 112 St, Edmonton, AB T6B 2B7, Canada.
EM mtonelli-admin@med.ualberta.ca
RI Tonelli, Marcello/B-3028-2009
FU Bristol-Myers Squibb; Alberta Heritage Foundation for Medical Research;
Canadian Institutes of Health Research; National Institute of Diabetes,
Digestive, and Kidney Diseases of the National Institutes of Health
[K23DK078774]; National Institutes of Health [HL093954]
FX The CARE study was an investigator-initiated study funded by
Bristol-Myers Squibb. This substudy on AlkP was not financially
supported by industry. Dr Tonelli was supported by a Population Health
Investigator Award from Alberta Heritage Foundation for Medical Research
and a New Investigator Award from the Canadian Institutes of Health
Research. Dr Melamed was supported by grant K23DK078774 from the
National Institute of Diabetes, Digestive, and Kidney Diseases of the
National Institutes of Health, and Dr Thadhani was supported by grant
HL093954 from the National Institutes of Health.
NR 31
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U1 0
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
BP 1784
EP 1792
DI 10.1161/CIRCULATIONAHA.109.851873
PG 9
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 514YD
UT WOS:000271431800007
PM 19841303
ER
PT J
AU Ahmed, H
Neuzil, P
d'Avila, A
Donaldson, DM
Laragy, M
Reddy, VY
AF Ahmed, Humera
Neuzil, Petr
d'Avila, Andre
Donaldson, David M.
Laragy, Margaret
Reddy, Vivek Y.
TI The Permanency of PV Isolation With a Cryoballoon Catheter During AF
Ablation
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Ahmed, Humera; d'Avila, Andre; Reddy, Vivek Y.] Mt Sinai Hosp, New York, NY 10029 USA.
[Neuzil, Petr] Homolka Hosp, Prague, Czech Republic.
[Donaldson, David M.; Laragy, Margaret] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RI d'Avila, Andre Luiz/F-8009-2010; d'Avila, Andre/A-7693-2009
OI d'Avila, Andre Luiz/0000-0001-8769-1411;
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S657
EP S657
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501658
ER
PT J
AU Atochin, D
Buys, E
Li, Q
Yuzawa, I
Rauwerdink, K
Ayata, C
Moskowitz, M
Brouckaert, P
Bloch, KD
Huang, P
AF Atochin, Dmitriy
Buys, Emmanuel
Li, Qian
Yuzawa, Izumi
Rauwerdink, Kristen
Ayata, Cenk
Moskowitz, Michael
Brouckaert, Peter
Bloch, Kenneth D.
Huang, Paul
TI Soluble Guanylate Cyclase Alpha 1 Beta 1 Limits Stroke Size and
Attenuates Neurological Injury in a Mouse Model of Cerebral
Ischemia-reperfusion
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Atochin, Dmitriy; Yuzawa, Izumi; Moskowitz, Michael; Huang, Paul] Massachusetts Gen Hosp, Charlestown, MA USA.
[Buys, Emmanuel; Rauwerdink, Kristen; Bloch, Kenneth D.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Li, Qian] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Brouckaert, Peter] Univ Ghent, B-9000 Ghent, Belgium.
[Brouckaert, Peter] Flanders Inst Biotechnol, Ghent, Belgium.
RI Atochin, Dmitriy/Q-3150-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1158
EP S1158
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504278
ER
PT J
AU Bangalore, S
Sawhney, S
Kinlay, S
Faxon, DP
AF Bangalore, Sripal
Sawhney, Sabrina
Kinlay, Scott
Faxon, David P.
TI Complete Revascularization versus Culprit-only Revascularization in
Patients With ST-Segment Elevation Myocardial Infarction and Multivessel
Disease: A Meta-Analysis
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Bangalore, Sripal; Kinlay, Scott; Faxon, David P.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Sawhney, Sabrina] St Raphaels Hasp, New Haven, CT USA.
[Kinlay, Scott] VA Boston Healthcare Syst, Boston, MA USA.
RI Bangalore, Sripal/B-6246-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S987
EP S987
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503355
ER
PT J
AU Bangalore, S
Bhatt, DL
Rother, J
Thornton, J
Wolski, K
Goto, S
Cannon, CP
Steg, PG
AF Bangalore, Sripal
Bhatt, Deepak L.
Roether, Joachim
Thornton, Julie
Wolski, Kathy
Goto, Shinya
Cannon, Christopher P.
Steg, Philippe Gabriel
TI Carotid Endarterectomy versus Carotid Artery Stenting: Insights From a
Propensity Matched Analysis of the REduction of Atherothrombosis for
Continued Health (REACH) Registry
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Cannon, Christopher P.] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
[Bhatt, Deepak L.] VA Boston Healthcare Syst, Boston, MA USA.
[Roether, Joachim] Univ Hannover, Klinikum Minden, Minden, Germany.
[Thornton, Julie; Wolski, Kathy] Cleveland Clin, Cleveland, OH 44106 USA.
[Goto, Shinya] Tokai Univ, Kanagawa 2591100, Japan.
[Steg, Philippe Gabriel] Univ Paris 07, AP HP, Paris, France.
RI Bangalore, Sripal/B-6246-2013
NR 0
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S954
EP S955
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503226
ER
PT J
AU Bao, FP
Liang, YF
Kimball, WR
Zapol, WM
Kacmarek, RM
Jiang, YD
AF Bao, Fangping
Liang, Yafen
Kimball, William R.
Zapol, Warren M.
Kacmarek, Robert M.
Jiang, Yandong
TI Mouth-to-nose Breathing Provides more Effective Ventilation than
Mouth-to-mouth Breathing
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Bao, Fangping; Liang, Yafen; Kimball, William R.; Zapol, Warren M.; Kacmarek, Robert M.; Jiang, Yandong] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1476
EP S1476
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831505157
ER
PT J
AU Bautista, LE
Vera, L
Herrera, V
Casas, J
Orostegui, M
Miranda, J
Perel, P
Pichardo, R
Gonzalez, A
Sanchez, J
Ferreccio, C
Aguilera, X
Silva, E
Gomez, L
Chirinos, J
Medina-Lezama, J
Perez, C
Suarez, E
Ortiz, A
Rosero, L
Schapochnik, N
Ortiz, Z
Ferrante, D
AF Bautista, Leonelo E.
Vera, Lina
Herrera, Victor
Casas, Juan
Orostegui, Myriam
Miranda, Jaime
Perel, Pablo
Pichardo, Rafael
Gonzalez, Angel
Sanchez, Jose
Ferreccio, Catterina
Aguilera, Ximena
Silva, Egle
Gomez, Luis
Chirinos, Julio
Medina-Lezama, Josefina
Perez, Cynthia
Suarez, Erick
Ortiz, Ana
Rosero, Luis
Schapochnik, Norberto
Ortiz, Zulma
Ferrante, Daniel
TI Hypertension Awareness, Treatment and Control in Latin America
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Bautista, Leonelo E.; Vera, Lina; Herrera, Victor] Univ Wisconsin, Madison, WI USA.
[Casas, Juan; Miranda, Jaime; Perel, Pablo] London Sch Hyg & Trop Med, London WC1, England.
[Orostegui, Myriam] Univ Ind Santander, Bucaramanga, Colombia.
[Pichardo, Rafael; Gonzalez, Angel] Inst Dominicano Cardiol, Santo Domingo, Dominican Rep.
[Sanchez, Jose] Inst Nacl Salud, Ctr Nacl Alimentac & Nutr, Lima, Peru.
[Ferreccio, Catterina] Pontificia Univ Catolica Chile, Santiago, Chile.
[Aguilera, Ximena] Minist Salud Chile, Santiago, Chile.
[Silva, Egle] Univ Zulia, Maracaibo 4011, Venezuela.
[Gomez, Luis] Fdn FES Social, Bogota, Colombia.
[Chirinos, Julio] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Chirinos, Julio] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[Medina-Lezama, Josefina] Santa Maria Catholic Univ, Arequipa, Peru.
[Medina-Lezama, Josefina] Santa Maria Res Inst, Arequipa, Peru.
[Perez, Cynthia; Suarez, Erick; Ortiz, Ana] Univ Puerto Rico, San Juan, PR 00936 USA.
[Rosero, Luis] Univ Costa Rica, San Jose, Costa Rica.
[Schapochnik, Norberto] Minist Salud Prov Tierra del Fuego, Ushuaia, Argentina.
[Ortiz, Zulma] Acad Nacl med, Inst Invest Epidemiol, Buenos Aires, DF, Argentina.
[Ferrante, Daniel] Minist Salud & Ambiente, Buenos Aires, DF, Argentina.
RI Herrera, Victor/C-5602-2008; Miranda, J. Jaime/A-8482-2008
OI Miranda, J. Jaime/0000-0002-4738-5468
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S439
EP S440
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500555
ER
PT J
AU Beinart, R
Heist, K
Singh, S
Kabra, R
Blendea, D
Donaldson, D
Koruth, J
Barrett, C
Ruskin, J
Mansour, M
AF Beinart, Roy
Heist, Kevin
Singh, Sheldon
Kabra, Rajesh
Blendea, Dan
Donaldson, David
Koruth, Jacob
Barrett, Conor
Ruskin, Jeremy
Mansour, Moussa
TI Regional Differences in Left Atrial Wall Thickness in Patients With
Atrial Fibrillation
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Beinart, Roy; Heist, Kevin; Singh, Sheldon; Kabra, Rajesh; Blendea, Dan; Donaldson, David; Koruth, Jacob; Barrett, Conor; Ruskin, Jeremy; Mansour, Moussa] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S707
EP S707
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502033
ER
PT J
AU Buys, ES
Raher, MJ
Rauwerdink, KM
Sips, PY
Brouckaert, P
Bloch, KD
AF Buys, Emmanuel S.
Raher, Michael J.
Rauwerdink, Kristen M.
Sips, Patrick Y.
Brouckaert, Peter
Bloch, Kenneth D.
TI Hypertension in Soluble Guanylate Cyclase alpha(1)-Deficient Mice is
Associated With Hyperaldosteronism
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Buys, Emmanuel S.; Raher, Michael J.; Rauwerdink, Kristen M.; Sips, Patrick Y.; Bloch, Kenneth D.] Mass Gen Hosp, Boston, MA USA.
[Buys, Emmanuel S.; Raher, Michael J.; Rauwerdink, Kristen M.; Sips, Patrick Y.; Bloch, Kenneth D.] Harvard Univ, Sch Med, Boston, MA USA.
[Brouckaert, Peter] Flanders Inst Biotechnol, Ghent, Belgium.
[Brouckaert, Peter] Univ Ghent, B-9000 Ghent, Belgium.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1045
EP S1045
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503593
ER
PT J
AU Carson, P
Komajda, M
Zile, M
Johnson, RH
Hetzel, S
Mckelvie, R
McMurray, J
Staiger, C
Ptaszynska, A
Massie, B
AF Carson, Peter
Komajda, Michel
Zile, Michael
Johnson, Ralph H.
Hetzel, Scott
Mckelvie, Robert
McMurray, John
Staiger, Christoph
Ptaszynska, Agata
Massie, Barry
TI The Relation of Quality of Life Score to Outcome in Heart Failure With
Preserved Ejection Fraction: Findings From the Irbesartan in Heart
Failure With Preserved Ejection Fraction Trial (I-PRESERVE)
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Carson, Peter] Washington VA Med Ctr, Washington, DC USA.
[Komajda, Michel] Univ Paris 06, Paris, France.
[Komajda, Michel] Hosp Pitie Salpetriere, Paris, France.
[Zile, Michael; Johnson, Ralph H.] Vet Affairs Med Ctr, Charleston, SC 29403 USA.
[Zile, Michael; Johnson, Ralph H.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Hetzel, Scott] Univ Wisconsin, Madison, WI USA.
[Mckelvie, Robert] McMaster Univ, Hamilton, ON, Canada.
[McMurray, John] Univ Glasgow, British Heart Fdn, Glasgow Cardiovasc Rsch Ctr, Glasgow, Lanark, Scotland.
[Staiger, Christoph] Sanofi Aventis, Bridgewater, NJ USA.
[Ptaszynska, Agata] Bristol Myers Squibb Co, Princeton, NJ USA.
[Massie, Barry] San Francisco VA Med Ctr, San Francisco, CA USA.
[Massie, Barry] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S749
EP S749
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502208
ER
PT J
AU Chan, SY
Zhang, YY
Hemann, C
Zweier, JL
Loscalzo, J
AF Chan, Stephen Y.
Zhang, Ying-Yi
Hemann, Craig
Zweier, Jay L.
Loscalzo, Joseph
TI MicroRNA-210 Controls Metabolic Adaptation During Hypoxia in Pulmonary
Vascular Endothelium
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Chan, Stephen Y.] Brigham & Womens Hosp, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Zhang, Ying-Yi; Loscalzo, Joseph] Harvard Univ, Sch Med, Boston, MA USA.
[Hemann, Craig; Zweier, Jay L.] Ohio State Univ, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S743
EP S743
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502184
ER
PT J
AU Chiuve, SE
Korngold, EC
Januzzi, JJ
Gantzer, ML
Albert, CM
AF Chiuve, Stephanie E.
Korngold, Ethan C.
Januzzi, James J., Jr.
Gantzer, Mary Lou
Albert, Christine M.
TI Plasma Magnesium as a Predictor of Sudden Cardiac Death: Findings From
the Nurses' Health Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Chiuve, Stephanie E.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Korngold, Ethan C.; Januzzi, James J., Jr.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Gantzer, Mary Lou] Siemens Healthcare Diagnost Inc, Newark, DE USA.
[Albert, Christine M.] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S417
EP S417
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500469
ER
PT J
AU Christen, T
Rocha, V
Sheikine, Y
Goldfine, A
Di Carli, M
Libby, P
AF Christen, Thomas
Rocha, Viviane
Sheikine, Yuri
Goldfine, Allison
Di Carli, Marcelo
Libby, Peter
TI Increased Glucose Uptake in Visceral versus Subcutaneous Adipose Tissue
Revealed by PET Imaging
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Christen, Thomas; Rocha, Viviane; Sheikine, Yuri; Di Carli, Marcelo; Libby, Peter] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Goldfine, Allison] Joslin Diabet Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1051
EP S1051
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503615
ER
PT J
AU Das, S
Aiba, T
Xiao, CY
Hessler, K
Rosenberg, M
Tomaselli, G
Rosenzweig, A
AF Das, Saumya
Aiba, Takeshi
Xiao, Chunyang
Hessler, Katherine
Rosenberg, Michael
Tomaselli, Gordon
Rosenzweig, Anthony
TI SGK1 Activation in Cardiomyocytes Leads to Alteration of SCN5a Function,
Electrical Remodeling and Left Ventricular Dysfunction
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Das, Saumya] Mass Gen Hosp, Boston, MA USA.
[Aiba, Takeshi; Tomaselli, Gordon] Johns Hopkins Med Sch, Baltimore, MD USA.
[Xiao, Chunyang; Hessler, Katherine; Rosenberg, Michael; Rosenzweig, Anthony] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S693
EP S694
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501805
ER
PT J
AU Duval, S
Jaff, MR
Boden, WE
Alberts, MJ
Califf, RM
Eagle, KA
O'Agostino, RB
Massaro, JM
Pedley, A
Steg, PG
Bhatt, DL
Hirsch, AT
AF Duval, Susan
Jaff, Michael R.
Boden, William E.
Alberts, Mark J.
Califf, Robert M.
Eagle, Kim A.
O'Agostino, Ralph B., Sr.
Massaro, Joseph M.
Pedley, Alison
Steg, P. Gabriel
Bhatt, Deepak L.
Hirsch, Alan T.
TI A New Score to Improve the Detection of Peripheral Artery Disease
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Duval, Susan] Univ Minnesota, Minneapolis, MN USA.
[Jaff, Michael R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Boden, William E.] SUNY Buffalo, Sch Med, Buffalo, NY 14260 USA.
[Boden, William E.] SUNY Buffalo, Sch Publ Hlth, Buffalo, NY 14260 USA.
[Boden, William E.] SUNY Buffalo, Buffalo Gen Hosp, Buffalo, NY 14260 USA.
[Boden, William E.] SUNY Buffalo, Millard Fillmore Hosp, Buffalo, NY 14260 USA.
[Alberts, Mark J.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Alberts, Mark J.] Northwestern Univ, NW Mem Hosp, Chicago, IL 60611 USA.
[Califf, Robert M.] Duke Univ, Med Ctr, Durham, NC USA.
[Califf, Robert M.] Duke Univ, Duke Clin Rsch Inst, Durham, NC USA.
[Eagle, Kim A.] Univ Michigan, Cardiovasc Cntr, Ann Arbor, MI 48109 USA.
[O'Agostino, Ralph B., Sr.; Massaro, Joseph M.; Pedley, Alison] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[O'Agostino, Ralph B., Sr.; Massaro, Joseph M.; Pedley, Alison] Boston Univ, Harvard Clin Rsch Inst, Boston, MA USA.
[Steg, P. Gabriel] Univ Paris 07, INSERM, U698, Paris, France.
[Bhatt, Deepak L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Bhatt, Deepak L.] VA Boston Healthcare Syst, Boston, MA USA.
[Bhatt, Deepak L.] Harvard Univ, Sch Med, Boston, MA USA.
[Hirsch, Alan T.] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA.
[Hirsch, Alan T.] Minneapolis Heart Inst Fdn, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1149
EP S1149
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504238
ER
PT J
AU Eijgelsheim, M
Newton-Cheh, C
Sotoodehnia, N
de Bakker, PI
Muller, M
Morrison, AC
Smith, AV
Isaacs, A
Sanna, S
Dorr, M
Navarro, P
Fuchsberger, C
Wilson, JF
Pramstaller, PP
van Duijn, CM
Lakatta, EG
Felix, SB
Gudnason, V
Pfeufer, A
Heckbert, SR
Stricker, BH
Boerwinkle, E
O'Donnell, CJ
AF Eijgelsheim, Mark
Newton-Cheh, Christpher
Sotoodehnia, Nona
de Bakker, Paul I.
Mueller, Martina
Morrison, Alanna C.
Smith, Albert V.
Isaacs, Aaron
Sanna, Serena
Doerr, Marcus
Navarro, Pau
Fuchsberger, Christian
Wilson, James F.
Pramstaller, Peter P.
van Duijn, Cornelia M.
Lakatta, Edward G.
Felix, Stephan B.
Gudnason, Vilmundur
Pfeufer, Arne
Heckbert, Susan R.
Stricker, Bruno H.
Boerwinkle, Eric
O'Donnell, Christopher J.
TI Genome-wide Association Analysis of 25,330 Individuals Identifies
Multiple Loci Associated With Resting Heart Rate
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Eijgelsheim, Mark; Isaacs, Aaron; van Duijn, Cornelia M.; Stricker, Bruno H.] Erasmus MC, Rotterdam, Netherlands.
[Newton-Cheh, Christpher] Massachusetts Gen Hosp, Ctr Human Genet Res, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Sotoodehnia, Nona; Heckbert, Susan R.] Univ Washington, Seattle, WA 98195 USA.
[de Bakker, Paul I.] Broad Inst Harvard & MIT, Program Med Populat Genet, Boston, MA USA.
[Mueller, Martina] Helmholtz Ctr Munich, Munich, Germany.
[Morrison, Alanna C.; Boerwinkle, Eric] Univ Texas Houston, Houston, TX USA.
[Smith, Albert V.; Gudnason, Vilmundur] Iceland Heart Assoc Res Inst, Kopavagur, Iceland.
[Sanna, Serena] Ist Neurogenet & Neurofarmacol, Monserrato, Italy.
[Doerr, Marcus] Ernst Moritz Arndt Univ Greifswald, Greifswald, Germany.
[Navarro, Pau] Western Gen Hosp, Edinburgh EH4 2XU, Midlothian, Scotland.
[Fuchsberger, Christian; Pramstaller, Peter P.] European Acad Bozen, Bolzano, Italy.
[Wilson, James F.] Univ Edinburgh, Edinburgh, Midlothian, Scotland.
[Lakatta, Edward G.] NIA, Baltimore, MD 21224 USA.
[O'Donnell, Christopher J.] NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
RI Fuchsberger, Christian/C-9646-2010; Pfeufer, Arne/B-6634-2013;
Pramstaller, Peter/C-2357-2008; de Bakker, Paul/B-8730-2009; Gudnason,
Vilmundur/K-6885-2015
OI de Bakker, Paul/0000-0001-7735-7858; Gudnason,
Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S579
EP S579
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501330
ER
PT J
AU Faxon, DP
Kinlay, S
Hernandez, RK
Gaziano, JM
Lawler, E
AF Faxon, David P.
Kinlay, Scott
Hernandez, Rohini K.
Gaziano, J. Michael
Lawler, Elizabeth
TI Prolonged Use of Clopidogrel Reduces Death and Myocardial Infarction
Following Drug Eluting Stent but Not Bare Metal Stent Placement: The VA
DES Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Faxon, David P.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Kinlay, Scott; Hernandez, Rohini K.; Gaziano, J. Michael; Lawler, Elizabeth] VA Boston Healthcare Syst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S978
EP S979
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503322
ER
PT J
AU Feng, Y
Zou, L
Si, R
Nagasaka, Y
Shen, SQ
Chao, W
AF Feng, Yan
Zou, Lin
Si, Rui
Nagasaka, Yasuko
Shen, Shiqian
Chao, Wei
TI Bone Marrow MyD88 Contributes to Myocardial Infarction and Modulates
Neutrophil Function and Chemokine Receptor Expression
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Feng, Yan; Zou, Lin; Si, Rui; Nagasaka, Yasuko; Shen, Shiqian; Chao, Wei] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1489
EP S1489
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831505213
ER
PT J
AU Feng, Y
Zou, L
Si, R
Nagasaka, Y
Shen, SQ
Chao, W
AF Feng, Yan
Zou, Lin
Si, Ri
Nagasaka, Yasuko
Shen, Shiqian
Chao, Wei
TI Bone Marrow MyD88 Contributes to Ischemic Myocardial Infarction and
Modulates Neutrophil Function and Chemokine Receptor Expression
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Feng, Yan; Zou, Lin; Si, Ri; Nagasaka, Yasuko; Shen, Shiqian; Chao, Wei] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1041
EP S1041
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503574
ER
PT J
AU Ferencik, M
Schleft, CL
Nasir, K
Ghoshhajra, BB
Kriegel, MF
Joshi, SB
Rogers, I
Truong, QA
Banerji, D
Bamberg, F
Brady, TJ
Nagumey, JT
Hoffmann, U
AF Ferencik, Maros
Schleft, Christopher L.
Nasir, Khurram
Ghoshhajra, Brian B.
Kriegel, Matthias F.
Joshi, Subodh B.
Rogers, Ian
Truong, Quynh A.
Banerji, Dahlia
Bamberg, Fabian
Brady, Thomas J.
Nagumey, John T.
Hoffmann, Udo
TI A Computed Tomography Based Score to Identify Culprit Coronary Lesions
Among Patients With Acute Chest Pain and Low to Intermediate Likelihood
of Acute Coronary Syndrome
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Ferencik, Maros; Schleft, Christopher L.; Nasir, Khurram; Ghoshhajra, Brian B.; Kriegel, Matthias F.; Joshi, Subodh B.; Rogers, Ian; Truong, Quynh A.; Banerji, Dahlia; Bamberg, Fabian; Brady, Thomas J.; Nagumey, John T.; Hoffmann, Udo] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S317
EP S317
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500073
ER
PT J
AU Fernandez-Pereira, C
Rubilar, B
Mieres, J
Rodriguez-Pagani, C
Santaera, O
Rodriguez-Granillo, AM
Antoniucci, D
Palacios, IF
Serruys, PW
Rodriguez, AE
AF Fernandez-Pereira, Carlos
Rubilar, Bibiana
Mieres, Juan
Rodriguez-Pagani, Carlos
Santaera, Omar
Rodriguez-Granillo, Alfredo M.
Antoniucci, David
Palacios, Igor F.
Serruys, Patrick W.
Rodriguez, Alfredo E.
TI Percutaneous Coronary Intervention With Bare Metal Stents and Oral
Sirolimus Has Comparable Safety and Efficacy to Treatment With Drug
Eluting Stents but With Significant Lower Cost: 31 Months Cost Saving
and Clinical Events Analysis From the Randomized, Controlled ORAR III
(Oral Rapamycin in Argentina) Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Fernandez-Pereira, Carlos; Rubilar, Bibiana; Mieres, Juan; Rodriguez-Pagani, Carlos; Rodriguez, Alfredo E.] Otamendi Hosp, Buenos Aires, DF, Argentina.
[Santaera, Omar] Argentina Soc Cardiovasc Intervent CACI, Buenos Aires, DF, Argentina.
[Rodriguez-Granillo, Alfredo M.] Cardiovasc Res Ctr CECI, Buenos Aires, DF, Argentina.
[Palacios, Igor F.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Antoniucci, David] Careggi Hosp, Florence, Italy.
[Serruys, Patrick W.] Erasmus Thorax Ctr, Rotterdam, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S967
EP S967
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503275
ER
PT J
AU Figueroa, AL
Cury, RC
Hoffmann, U
Brady, TJ
Tawakol, A
AF Figueroa, Amparo L.
Cury, Ricardo C.
Hoffmann, Udo
Brady, Thomas J.
Tawakol, Ahmed
TI Characterization of Carotid Atherosclerosis: A Comparison Between PET
Activity, Plaque Morphology and Histopathology
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Figueroa, Amparo L.; Cury, Ricardo C.; Hoffmann, Udo; Brady, Thomas J.; Tawakol, Ahmed] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S349
EP S350
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500202
ER
PT J
AU Fonarow, GC
Smith, EE
Reeves, MJ
Pan, WQ
Olson, D
Hernandez, AF
Peterson, ED
Schwamm, LH
AF Fonarow, Gregg C.
Smith, Eric E.
Reeves, Matthew J.
Pan, Wenqin
Olson, DaiWai
Hernandez, Adrian F.
Peterson, Eric D.
Schwamm, Lee H.
CA Guidelines Steering Comm Hosps
TI Early Antithrombotic Therapy Performance Measure in Ischemic Stroke and
Clinical Outcomes
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Fonarow, Gregg C.] Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA.
[Smith, Eric E.] Univ Calgary, Calgary, AB, Canada.
[Reeves, Matthew J.] Michigan State Univ, E Lansing, MI 48824 USA.
[Pan, Wenqin; Olson, DaiWai; Hernandez, Adrian F.; Peterson, Eric D.] DCRI, Durham, NC USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RI Smith, Eric/C-5443-2012
OI Smith, Eric/0000-0003-3956-1668
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1129
EP S1129
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504155
ER
PT J
AU Fonarow, GC
Smith, EE
Reeves, MJ
Pan, WQ
Olson, D
Hernandez, AF
Peterson, ED
Schwamm, LH
AF Fonarow, Gregg C.
Smith, Eric E.
Reeves, Matthew J.
Pan, Wenqin
Olson, DaiWai
Hernandez, Adrian F.
Peterson, Eric D.
Schwamm, Lee H.
CA Get With Guidelines Steering Commi
TI Antithrombotic Therapy at Hospital Discharge Performance Measure in
Ischemic Stroke and Clinical Outcomes
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Fonarow, Gregg C.] Univ Calif Los Angeles, Ctr Med, Los Angeles, CA 90024 USA.
[Smith, Eric E.] Univ Calgary, Calgary, AB, Canada.
[Reeves, Matthew J.] Michigan State Univ, E Lansing, MI 48824 USA.
[Pan, Wenqin; Olson, DaiWai; Hernandez, Adrian F.; Peterson, Eric D.] DCRI, Durham, NC USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RI Smith, Eric/C-5443-2012
OI Smith, Eric/0000-0003-3956-1668
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S472
EP S473
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500692
ER
PT J
AU Fox, CS
Massaro, JM
Schlett, CL
Lehman, S
O'Donnell, CJ
Hoffmann, U
Murabito, JM
AF Fox, Caroline S.
Massaro, Joseph M.
Schlett, Christopher L.
Lehman, Sam
O'Donnell, Christopher J.
Hoffmann, Udo
Murabito, Joanne M.
TI Peri-vascular Fat Deposition is Associated With Peripheral Arterial
Disease: The Framingham Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Fox, Caroline S.; O'Donnell, Christopher J.] Framingham Heart Dis Epidemiol Study, Sch Med, Framingham, MA 02215 USA.
[Murabito, Joanne M.] Boston Univ, Boston, MA 02114 USA.
[Schlett, Christopher L.; Hoffmann, Udo] Massachusetts Gen Hosp, Boston, MA 5042 USA.
[Lehman, Sam] Flinders Univ S Australia, Bedford Pk, SA, Australia.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S509
EP S509
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501050
ER
PT J
AU Fukuda, D
Aikawa, E
Yamazaki, H
Yagita, H
Aikawa, M
AF Fukuda, Daiju
Aikawa, Elena
Yamazaki, Hiroyuki
Yagita, Hideo
Aikawa, Masanori
TI Blockade of the Notch Ligand Delta-like 4 (DII4) Prevents the
Cardiometabolic Syndrome
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Fukuda, Daiju; Yamazaki, Hiroyuki; Aikawa, Masanori] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Aikawa, Elena] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Charlestown, MA USA.
[Yagita, Hideo] Juntendo Univ, Sch Med, Tokyo 113, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1166
EP S1166
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504316
ER
PT J
AU Gibson, CM
Mega, JL
Jennings, LK
Mohanavelu, S
Misselwitz, F
Plotnikov, A
Sun, X
Zolynas, R
Braunwald, E
AF Gibson, C. Michael
Mega, Jessica L.
Jennings, Lisa K.
Mohanavelu, Satishkumar
Misselwitz, Frank
Plotnikov, Alexei
Sun, Xiang
Zolynas, Robert
Braunwald, Eugene
TI Effect of Rivaroxaban on Markers of Coagulation in Patients With Acute
Coronary Syndromes: An ATLAS ACS-TIMI 46 Substudy
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Gibson, C. Michael] Beth Israel Hosp, Boston, MA USA.
[Mega, Jessica L.; Braunwald, Eugene] Brigham & Womens Hosp, Boston, MA USA.
[Jennings, Lisa K.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Mohanavelu, Satishkumar] TIMI Study Grp, Boston, MA USA.
[Misselwitz, Frank] Bayer HealthCare, Wuppertal, Germany.
[Plotnikov, Alexei; Sun, Xiang; Zolynas, Robert] Johnson & Johnson, Raritan, NJ USA.
NR 0
TC 2
Z9 2
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1035
EP S1035
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503550
ER
PT J
AU Gleva, MJ
Holcomb, R
Uslan, D
Chung, M
Mela, T
Gottipaty, V
Borge, R
Dan, D
Shinn, T
AF Gleva, Marye J.
Holcomb, Richard
Uslan, Daniel
Chung, Mina
Mela, Theofanie
Gottipaty, Venkateshwar
Borge, Richard
Dan, Dan
Shinn, Timothy
TI Charlson Comorbidity Index and Risk of Cardiac Rhythm Device Generator
Replacement: Results From the REPLACE Registry
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Gleva, Marye J.] Washington Univ, St Louis, MO USA.
[Uslan, Daniel] Univ Calif Los Angeles, Los Angeles, CA USA.
[Chung, Mina] Cleveland Clin, Cleveland, OH 44106 USA.
[Mela, Theofanie] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Gottipaty, Venkateshwar] S Carolina Heart Cntr, Columbia, SC USA.
[Borge, Richard] Abington Med Specialists, Abington, PA USA.
[Dan, Dan] Piedmont Heart Inst, Atlanta, GA USA.
[Shinn, Timothy] Michigan Heart, Ypsilanti, MI USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S637
EP S637
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501572
ER
PT J
AU Goldman, A
Curtis, JP
Wang, YF
Maisel, WH
AF Goldman, Alena
Curtis, Jeptha P.
Wang, Yongfei
Maisel, William H.
TI Impact of Anticoagulation and Anti-platelet Therapy on ICD
Implant-Related Bleeding and Thromboembolic Events in Patients Enrolled
in the NCDR ICD Registry
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Goldman, Alena; Maisel, William H.] BIDMC, Boston, MA USA.
[Curtis, Jeptha P.; Wang, Yongfei] Yale Univ, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S638
EP S638
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501576
ER
PT J
AU Goyal, A
Bhatt, DL
Steg, PG
Gersh, BJ
Alberts, MJ
Ohman, EM
Corbalan, R
Eagle, KA
Gaxiola, E
Gao, RL
Goto, S
D'Agostino, RB
Califf, RM
Smith, SC
Wilson, PW
AF Goyal, Abhinav
Bhatt, Deepak L.
Steg, Ph. Gabriel
Gersh, Bernard J.
Alberts, Mark J.
Ohman, E. Magnus
Corbalan, Ramon
Eagle, Kim A.
Gaxiola, Efrain
Gao, Runlin
Goto, Shinya
D'Agostino, Ralph B.
Califf, Robert M.
Smith, Sidney C., Jr.
Wilson, Peter W.
TI The Impact Of Attained Educational Level On Incident Cardiovascular
Events Differs Between High-Income Countries and Low-and-Middle-Income
Countries
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Goyal, Abhinav] Emory Rollins Sch Publ Hlth, Atlanta, GA USA.
[Goyal, Abhinav; Wilson, Peter W.] Emory Sch Med, Atlanta, GA USA.
[Bhatt, Deepak L.] VA Boston Healthcare Syst, Boston, MA USA.
[Bhatt, Deepak L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Steg, Ph. Gabriel] Univ Paris 07, AP HP, INSERM, U698, Paris, France.
[Gersh, Bernard J.] Mayo Clin, Rochester, MN USA.
[Alberts, Mark J.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Ohman, E. Magnus; Califf, Robert M.] Duke Clin Rsch Inst, Durham, NC USA.
[Corbalan, Ramon] Pontificia Univ Catolica Chile, Santiago, Chile.
[Eagle, Kim A.] Univ Michigan, Med Ctr, Ann Arbor, MI 48109 USA.
[Gaxiola, Efrain] Jandines Hosp cle Especialidades, Cntr Especializado Terapia Endovasc, Guadalajara, Mexico.
[Gao, Runlin] Fuwai Hosp, Beijing, Peoples R China.
[Goto, Shinya] Tokai Univ, Sch Med, Kanagawa 2591100, Japan.
[D'Agostino, Ralph B.] Boston Univ, Boston, MA 02215 USA.
[Smith, Sidney C., Jr.] Univ N Carolina, UNC Cntr Cardiovasc Sci & Med, Chapel Hill, NC USA.
RI Goyal, Abhinav/J-5086-2012
OI Goyal, Abhinav/0000-0002-6286-2349
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S415
EP S415
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500463
ER
PT J
AU Grabowski, M
Szymanski, FM
Januzzi, JL
Wu, AH
Hrynkiewicz-Szymanska, A
Cacko, A
Filipiak, KJ
Kochman, J
Karpinski, G
Opolski, G
AF Grabowski, Marcin
Szymanski, Filip M.
Januzzi, James L.
Wu, Alan H.
Hrynkiewicz-Szymanska, Anna
Cacko, Andrzej
Filipiak, Krzysztof J.
Kochman, Janusz
Karpinski, Grzegorz
Opolski, Grzegorz
TI Prognostic Utility of Serial Measurements of a Novel Biomarker ST2 in
Stemi Patients Treated With Primary PCI
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Grabowski, Marcin; Szymanski, Filip M.; Hrynkiewicz-Szymanska, Anna; Cacko, Andrzej; Filipiak, Krzysztof J.; Kochman, Janusz; Karpinski, Grzegorz; Opolski, Grzegorz] Med Univ Warsaw, Warsaw, Poland.
[Januzzi, James L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Wu, Alan H.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S808
EP S808
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502449
ER
PT J
AU Greyson, C
Ahmad, H
Schwartz, GG
Lu, L
Ye, SY
Xu, Y
AF Greyson, Clifford
Ahmad, Hasan
Schwartz, Gregory G.
Lu, Li
Ye, Shuyu
Xu, Ya
TI Calpain Inhibition Attenuates Right Heart Failure and Prevents Talin
Degradation During Acute Pressure Overload
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Greyson, Clifford; Ahmad, Hasan; Schwartz, Gregory G.; Lu, Li; Ye, Shuyu; Xu, Ya] Denver VAMC, Denver, CO USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S805
EP S805
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502436
ER
PT J
AU Harkness, JR
Morrow, DA
Braunwald, E
Qin, J
Belardinelli, L
Wang, W
Karwatowska-Prokopczuk, E
Lopez-Sendon, J
Bode, C
Scirica, BM
AF Harkness, James R.
Morrow, David A.
Braunwald, Eugene
Qin, Jie
Belardinelli, Luiz
Wang, Whedy
Karwatowska-Prokopczuk, Ewa
Lopez-Sendon, Jose
Bode, Christophe
Scirica, Benjamin M.
TI Presence of Ischemia and Non-Sustained Ventricular Tachycardia is
Strongly Associated With the Risk of Cardiovascular Outcomes:
Observations From the MERLIN-TIMI 36 Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Harkness, James R.; Morrow, David A.; Braunwald, Eugene; Qin, Jie; Scirica, Benjamin M.] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
[Belardinelli, Luiz; Wang, Whedy; Karwatowska-Prokopczuk, Ewa] CV Therapeut Gilead, Palo Alto, CA USA.
[Lopez-Sendon, Jose] Hosp Univ La Paz, Madrid, Spain.
[Bode, Christophe] Univ Freiburg, Freiburg, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1086
EP S1087
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503773
ER
PT J
AU Januzzi, J
Bajwa, EK
Gong, MN
Thompson, T
Christiani, DC
AF Januzzi, James
Bajwa, Ednan K.
Gong, Michelle N.
Thompson, Taylor
Christiani, David C.
TI Plasma Levels of Interleukin Receptor Soluble ST2 Predict Disease
Severity and Mortality in Patients With Acute Respiratory Distress
Syndrome (ARDS)
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Januzzi, James; Bajwa, Ednan K.; Thompson, Taylor; Christiani, David C.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Gong, Michelle N.] Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1466
EP S1467
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831505114
ER
PT J
AU Januzzi, JL
Bamberg, F
Lee, H
Truong, QA
Nichols, J
Karakas, M
Mohammed, AA
Schlett, CL
Nagurney, JT
Hoffmann, U
Koenig, W
AF Januzzi, James L.
Bamberg, Fabian
Lee, Hang
Truong, Quynh A.
Nichols, John
Karakas, Mahir
Mohammed, Asim A.
Schlett, Christopher L.
Nagurney, John T.
Hoffmann, Udo
Koenig, Wolfgang
TI Correlates of High Sensitivity Troponin T Concentrations in Chest Pain
Patients With and Without Acute Coronary Syndrome
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Januzzi, James L.; Bamberg, Fabian; Lee, Hang; Truong, Quynh A.; Nichols, John; Mohammed, Asim A.; Schlett, Christopher L.; Nagurney, John T.; Hoffmann, Udo] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Karakas, Mahir; Koenig, Wolfgang] Univ Ulm, Ulm, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1036
EP S1036
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503553
ER
PT J
AU Johri, AM
Palacios, IF
Cubeddu, RJ
Inglessis, I
Passeri, J
AF Johri, Amer M.
Palacios, Igor F.
Cubeddu, Roberto J.
Inglessis, Ignacio
Passeri, Jonathan
TI Assessment of Atrial Septal Defect Anatomy by Real-Time
Three-dimensional Transesophageal Echocardiography and Residual Shunting
After Transcatheter Atrial Septal Defect Closure
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Johri, Amer M.; Palacios, Igor F.; Cubeddu, Roberto J.; Inglessis, Ignacio; Passeri, Jonathan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S392
EP S392
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500368
ER
PT J
AU Kadakia, MB
Fox, CS
Scirica, BM
Murphy, SA
Bonaca, MP
Morrow, DA
AF Kadakia, Mitul B.
Fox, Caroline S.
Scirica, Benjamin M.
Murphy, Sabina A.
Bonaca, Marc P.
Morrow, David A.
TI Central Obesity and Cardiovascular Outcomes in Patients With Acute
Coronary Syndromes: Observations From the MERLIN-TIMI 36 Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kadakia, Mitul B.; Scirica, Benjamin M.; Murphy, Sabina A.; Bonaca, Marc P.; Morrow, David A.] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
[Kadakia, Mitul B.; Scirica, Benjamin M.; Murphy, Sabina A.; Bonaca, Marc P.; Morrow, David A.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S510
EP S510
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501052
ER
PT J
AU Kaab, S
Lunetta, KL
Glazer, NL
Pfeufer, A
Alonso, A
Chung, MK
Sinner, MF
Darbar, D
von Noord, C
Smith, AV
Gudnason, V
Roden, DM
Witteman, JC
Barnard, J
Arking, DE
Benjamin, EJ
Heckbert, SR
Ellinor, PT
AF Kaeaeb, Stefan
Lunetta, Kathryn L.
Glazer, Nicole L.
Pfeufer, Arne
Alonso, Alvaro
Chung, Mina K.
Sinner, Moritz F.
Darbar, Dawood
von Noord, Charlotte
Smith, Albert V.
Gudnason, Vilmundur
Roden, Dan M.
Witteman, Jacqueline C.
Barnard, John
Arking, Dan E.
Benjamin, Emilia J.
Heckbert, Susan R.
Ellinor, Patrick T.
TI Common Variants in KCNN3 Are Associated With Early-Onset Atrial
Fibrillation
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kaeaeb, Stefan; Sinner, Moritz F.] Univ Munich, Klinikum Grosshadern, LMU Munich, D-8000 Munich, Germany.
[Lunetta, Kathryn L.; Benjamin, Emilia J.] Boston Univ, Boston, MA 02215 USA.
[Glazer, Nicole L.; Heckbert, Susan R.] Univ Washington, Seattle, WA 98195 USA.
[Pfeufer, Arne] Helmholtz Zentrum Munich, Neuherberg, Germany.
[Alonso, Alvaro] Univ Minnesota, Minneapolis, MN USA.
[Chung, Mina K.; Barnard, John] Cleveland Clin, Cleveland, OH 44106 USA.
[Darbar, Dawood; Roden, Dan M.] Vanderbilt Univ, Nashville, TN USA.
[von Noord, Charlotte; Witteman, Jacqueline C.] Erasmus MC, Rotterdam, Netherlands.
[Smith, Albert V.; Gudnason, Vilmundur] Icelandic Heart Assoc, Kopavogur, Iceland.
[Arking, Dan E.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Benjamin, Emilia J.] Boston Univ, Boston, MA 02215 USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RI Pfeufer, Arne/B-6634-2013; Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S578
EP S579
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501328
ER
PT J
AU Kalogeropoulos, AP
Georgiopoulou, VV
Psaty, BM
Rodondi, N
Smith, AL
Harrison, DG
Liu, YM
Hoffmann, U
Bauer, DC
Newman, AB
Kritchevsky, SB
Harris, TB
Butler, J
AF Kalogeropoulos, Andreas P.
Georgiopoulou, Vasiliki V.
Psaty, Bruce M.
Rodondi, Nicolas
Smith, Andreas L.
Harrison, David G.
Liu, Yongmei
Hoffmann, Udo
Bauer, Douglas C.
Newman, Anne B.
Kritchevsky, Stephen B.
Harris, Tamara B.
Butler, Javed
TI Inflammatory Markers and Incident Heart Failure Risk in Older Adults:
The Health, Aging, and Body Composition Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kalogeropoulos, Andreas P.; Georgiopoulou, Vasiliki V.; Smith, Andreas L.; Harrison, David G.; Butler, Javed] Emory Univ, Atlanta, GA 30322 USA.
[Psaty, Bruce M.] Univ Washington, Seattle, WA 98195 USA.
[Rodondi, Nicolas] Univ Lausanne, Lausanne, Switzerland.
[Liu, Yongmei; Kritchevsky, Stephen B.] Wake Forest Univ, Winston Salem, SC USA.
[Hoffmann, Udo] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Bauer, Douglas C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Newman, Anne B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, Tamara B.] NIA, Intramural Rsch Program, Bethesda, MD 20892 USA.
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S505
EP S505
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501036
ER
PT J
AU Kasahara, H
Briggs, L
Lu, JT
Chien, KR
Yang, TP
Bungert, J
AF Kasahara, Hideko
Briggs, Laura
Lu, Jonathan T.
Chien, Kenneth R.
Yang, Thomas P.
Bungert, Jorg
TI Nkx2-5-dependent Transcriptional Regulation of ANF and BNP Through a
Common Distal Enhancer
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kasahara, Hideko; Briggs, Laura; Yang, Thomas P.; Bungert, Jorg] Univ Florida, Gainesville, FL USA.
[Lu, Jonathan T.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Chien, Kenneth R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S571
EP S571
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501299
ER
PT J
AU Kathiresan, S
Voight, BF
AF Kathiresan, Sekar
Voight, Benjamin F.
CA Myocardial Infarction Genetics Con
TI DNA Sequence Variants Related to Plasma Triglycerides or High-Density
Lipoprotein Cholesterol and Risk of Myocardial Infarction
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kathiresan, Sekar; Voight, Benjamin F.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S559
EP S559
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501248
ER
PT J
AU Kim, DH
Seo, JS
Na, JO
Song, JM
Kang, DH
Song, JK
Handschumacher, MD
Levine, RA
AF Kim, Dae-Hee
Seo, Jung-Suk
Na, Jin-Oh
Song, Jong-Min
Kang, Duk-Hyun
Song, Jae-Kwan
Handschumacher, Mark D.
Levine, Robert A.
TI Determinants of Left Ventricular Outflow Tract Obstruction in Patients
With Asymmetric Septal Hypertrophy: Insights From Geometric Analysis
Using 3D Echocardiography
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kim, Dae-Hee; Seo, Jung-Suk; Na, Jin-Oh; Song, Jong-Min; Kang, Duk-Hyun; Song, Jae-Kwan] Asan Med Cntr, Seoul, South Korea.
[Handschumacher, Mark D.; Levine, Robert A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S315
EP S315
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500066
ER
PT J
AU Kim, S
Park, C
Han, JW
Kim, SW
Kim, H
Choi, YJ
Lee, E
Patel, R
Park, IH
Daley, GQ
Quyyumi, A
Yoon, YS
AF Kim, Sinae
Park, Changwon
Han, Ji Woong
Kim, Sung-Whan
Kim, Hyongbum
Choi, Yong Jin
Lee, Eugine
Patel, Riyaz
Park, In-Hyun
Daley, George Q.
Quyyumi, Arshed
Yoon, Young-sup
TI Generation of Induced Pluripotent Stem Cells From Peripheral Blood of
Coronary Artery Disease Patients
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kim, Sinae; Park, Changwon; Han, Ji Woong; Kim, Sung-Whan; Kim, Hyongbum; Choi, Yong Jin; Lee, Eugine; Patel, Riyaz; Quyyumi, Arshed; Yoon, Young-sup] Emory Univ, Decatur, GA USA.
[Park, In-Hyun; Daley, George Q.] Childrens Hosp, Boston, MA 02115 USA.
[Park, In-Hyun; Daley, George Q.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1091
EP S1091
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503794
ER
PT J
AU Kim, S
Park, C
Han, JW
Kim, SW
Kim, H
Choi, YJ
Lee, E
Patel, R
Park, IH
Daley, GQ
Quyyumi, A
Yoon, YS
AF Kim, Sinae
Park, Changwon
Han, Ji Woong
Kim, Sung-Whan
Kim, Hyongbum
Choi, Yong Jin
Lee, Eugine
Patel, Riyaz
Park, In-Hyun
Daley, George Q.
Quyyumi, Arshed
Yoon, Young-sup
TI Directed Differentiation of Endothelial Cells From Coronary Artery
Disease (CAD) Patients-derived iPS Cells
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kim, Sinae; Park, Changwon; Han, Ji Woong; Kim, Sung-Whan; Kim, Hyongbum; Choi, Yong Jin; Lee, Eugine; Patel, Riyaz; Quyyumi, Arshed; Yoon, Young-sup] Emory Univ, Decatur, GA USA.
[Park, In-Hyun; Daley, George Q.] Childrens Hosp, Boston, MA 02115 USA.
[Park, In-Hyun; Daley, George Q.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1092
EP S1092
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503796
ER
PT J
AU Kitzman, DW
Haas, MM
Carson, PE
Hetzel, S
Komajda, M
Zile, M
Mckelvie, R
Mcmurray, JJ
Demets, D
Staiger, C
Ptaszynska, A
Massie, B
AF Kitzman, Dalane W.
Haas, Marcus M.
Carson, Peter E.
Hetzel, Scott
Komajda, Michael
Zile, Michael
Mckelvie, Robert
Mcmurray, John J.
Demets, D.
Staiger, C.
Ptaszynska, Agata
Massie, Barry
TI Obesity and Its Relationship to Adverse Cardiovascular Outcomes in Older
Patients With Heart Failure and Preserved Ejection Fraction in the
I-PRESERVE Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kitzman, Dalane W.] Wake Forest Univ Hlth Sci, F-75634 Winston Salem, NC USA.
[Haas, Marcus M.] Theresienkrankenhaus, Mannheim, Germany.
[Carson, Peter E.] Washington VAMC, Washington, DC 29425 USA.
[Carson, Peter E.] Georgetown Univ, Washington, DC USA.
[Hetzel, Scott; Demets, D.] Univ Wisconsin, Madison, WI USA.
[Komajda, Michael] Univ Paris 06, Paris, France.
[Komajda, Michael] Grp Hosp Pitie Salpetriere, Paris, France.
[Zile, Michael] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
[Zile, Michael] Med Univ S Carolina, Charleston, SC 94143 USA.
[Mckelvie, Robert] McMaster Univ, Hamilton, ON, Canada.
[Mcmurray, John J.] British Heart Fdn, Glasgow Cardiovasc Rsch Cntr, Glasgow, Lanark, Scotland.
[Ptaszynska, Agata] Bristol Myers Squibb Co, Princeton, NJ USA.
[Staiger, C.] Sanofi Aventis, Bridgeport, CT USA.
[Massie, Barry] San Francisco VA Med Ctr, San Francisco, CA USA.
[Massie, Barry] Univ Calif San Francisco, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S757
EP S758
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502242
ER
PT J
AU Klein, L
Chae, CU
Greenland, P
Ning, HY
Kang, J
Limacher, MC
Margolis, KL
Howard, BV
Robinson, JG
Wong, ND
Gulati, M
Dupree, CS
LaCroix, AZ
Lloyd-Jones, DM
AF Klein, Liviu
Chae, Claudia U.
Greenland, Philip
Ning, Hongyan
Kang, Joseph
Limacher, Marian C.
Margolis, Karen L.
Howard, Barbara V.
Robinson, Jennifer G.
Wong, Nathan D.
Gulati, Martha
Dupree, Carla S.
LaCroix, Andrea Z.
Lloyd-Jones, Donald M.
TI Hormone Therapy and Heart Failure Incidence and Prognosis in
Post-Menopausal Women: The Women's Health Initiative Hormone Therapy
Randomized Trials
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Klein, Liviu; Greenland, Philip; Ning, Hongyan; Kang, Joseph; Gulati, Martha; Lloyd-Jones, Donald M.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Chae, Claudia U.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Limacher, Marian C.] Univ Florida, Gainesville, FL USA.
[Margolis, Karen L.] Hennepin Cty Med Ctr, Minneapolis, MN 55415 USA.
[Howard, Barbara V.] MedStar Rsch Inst, Washington, DC USA.
[Robinson, Jennifer G.] Univ Iowa, Iowa City, IA USA.
[Wong, Nathan D.] Univ Calif Irvine, Irvine, CA USA.
[Dupree, Carla S.] Univ N Carolina, Chapel Hill, NC USA.
[LaCroix, Andrea Z.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
RI Lloyd-Jones, Donald/C-5899-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S504
EP S504
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501031
ER
PT J
AU Klein, L
Lloyd-Jones, DM
Greenland, P
Ning, HY
Kang, J
Limacher, MC
Margolis, KL
Howard, BV
Robinson, JG
Wong, ND
Gulati, M
Dupree, CS
LaCroix, AZ
Chae, CU
AF Klein, Liviu
Lloyd-Jones, Donald M.
Greenland, Philip
Ning, Hongyan
Kang, Joseph
Limacher, Marian C.
Margolis, Karen L.
Howard, Barbara V.
Robinson, Jennifer G.
Wong, Nathan D.
Gulati, Martha
Dupree, Carla S.
LaCroix, Andrea Z.
Chae, Claudia U.
TI Heart Failure Incidence and Prognosis in Post-Menopausal Women According
to Different Diagnostic Criteria: The Women's Health Initiative Hormone
Therapy Randomized Trials
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Klein, Liviu; Lloyd-Jones, Donald M.; Greenland, Philip; Ning, Hongyan; Kang, Joseph; Gulati, Martha] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Limacher, Marian C.] Univ Florida, Gainesville, FL USA.
[Margolis, Karen L.] Hennepin Cty Med Ctr, Minneapolis, MN 55415 USA.
[Howard, Barbara V.] MedStar Rsch Inst, Washington, DC USA.
[Robinson, Jennifer G.] Univ Iowa, Iowa City, IA USA.
[Wong, Nathan D.] Univ Calif Irvine, Irvine, CA USA.
[Dupree, Carla S.] Univ N Carolina, Chapel Hill, NC USA.
[LaCroix, Andrea Z.] Fred Hutchinson Canc Res Ctr, Seattle, WA USA.
[Chae, Claudia U.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RI Lloyd-Jones, Donald/C-5899-2009
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S399
EP S399
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500395
ER
PT J
AU Lakdawala, N
Thune, JJ
Cirino, A
Havndrupm, O
Christiansen, M
Bundgaard, H
MacRae, CA
Carlsen, CM
Colan, SD
Kober, LV
Ho, CY
AF Lakdawala, Neal
Thune, Jens J.
Cirino, Allison
Havndrupm, Ole
Christiansen, Michael
Bundgaard, Henning
MacRae, Calum A.
Carlsen, Christian M.
Colan, Steven D.
Kober, Lars V.
Ho, Carolyn Y.
TI Electrocardiographic Manifestations of Sarcomere Mutations in
Hypertrophic Cardiomyopathy: Incremental Value in the Prediction Genetic
Risk
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Lakdawala, Neal; Cirino, Allison; Ho, Carolyn Y.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Thune, Jens J.; Havndrupm, Ole; Bundgaard, Henning; Kober, Lars V.] Copenhagen Univ Hosp, Copenhagen, Denmark.
[Christiansen, Michael] Statens Serum Inst, DK-2300 Copenhagen, Denmark.
[MacRae, Calum A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Carlsen, Christian M.] Bispebjerg Hosp, DK-2400 Copenhagen, Denmark.
[Colan, Steven D.] Childrens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S566
EP S566
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501276
ER
PT J
AU Leyton, P
Beppu, H
Yu, PB
Bloch, KD
AF Leyton, Patricio
Beppu, Hideyuki
Yu, Paul B.
Bloch, Kenneth D.
TI Heterozygous Mutation in the Carboxyl-Terminal Domain of the Type 2 Bone
Morphogenetic Protein Receptor Leads to Ligand-Specific Gain of Function
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Leyton, Patricio; Beppu, Hideyuki; Yu, Paul B.; Bloch, Kenneth D.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1135
EP S1136
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504182
ER
PT J
AU Li, Q
Atochin, D
Kashiwagi, S
Earle, J
Wang, A
Sessa, W
Huang, P
AF Li, Qian
Atochin, Dmitriy
Kashiwagi, Satoshi
Earle, John
Wang, Annie
Sessa, William
Huang, Paul
TI Phosphorylation of eNOS Corrects Diabetic Vascular Dysfunction and
Improves Outcome to Stroke
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Li, Qian; Atochin, Dmitriy; Kashiwagi, Satoshi; Earle, John; Wang, Annie; Huang, Paul] Massachusetts Gen Hosp, Charlestown, MA USA.
[Sessa, William] Yale Univ, Sch Med, New Haven, CT USA.
RI Atochin, Dmitriy/Q-3150-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1037
EP S1038
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503560
ER
PT J
AU Liu, YH
Rawnsley, D
Zeng, M
Yu, E
Pijnappels, D
Thibault, H
Scherrer-Crosbie, M
Wu, SM
AF Liu, Yuan-Hung
Rawnsley, David
Zeng, Ming
Yu, Esther
Pijnappels, Daniel
Thibault, Helene
Scherrer-Crosbie, Marielle
Wu, Sean M.
TI Myocardial Injury Induces the Expansion and Cardiomyogenic
Differentiation of Postnatal Nkx2.5 Progenitor Cells via Inflammatory
Signals
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Liu, Yuan-Hung] Far Eastern Mem Hosp, Taipei, Taiwan.
[Rawnsley, David] Massachusetts Gen Hosp, Taipei, MA, Taiwan.
[Zeng, Ming; Yu, Esther; Pijnappels, Daniel; Thibault, Helene; Scherrer-Crosbie, Marielle; Wu, Sean M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S756
EP S756
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502235
ER
PT J
AU Lo, J
Abbara, S
Shturman, L
Soni, A
Rocha, J
Wei, J
Grinspoon, S
AF Lo, Janet
Abbara, Suhny
Shturman, Leon
Soni, Anand
Rocha-Filho, Jose
Wei, Jeffrey
Grinspoon, Steven
TI Increased Prevalence of Subclinical Coronary Atherosclerosis Detected by
Coronary Computed Tomography Angiography in HIV-Infected Men
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Lo, Janet; Abbara, Suhny; Shturman, Leon; Soni, Anand; Rocha-Filho, Jose; Wei, Jeffrey; Grinspoon, Steven] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S463
EP S463
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500653
ER
PT J
AU Losordo, DW
Henry, T
Schatz, RA
Lee, JS
Costa, M
Bass, T
Schaer, G
Niederman, A
Mendelsohn, F
Davidson, C
Waksman, R
Soukas, PA
Simon, D
Chronos, N
Fortuin, FD
Huang, PP
Weintraub, N
Yeung, A
Rosenfield, K
Wong, SC
Taussig, A
Rava, AN
Sherman, W
Kereiakes, D
Strumpf, RK
Port, S
Pieper, K
Adams, PX
Harrington, R
AF Losordo, Douglas W.
Henry, Tim
Schatz, Richard A.
Lee, Joon Sup
Costa, Marco
Bass, Theodore
Schaer, Gary
Niederman, Alan
Mendelsohn, Farrell
Davidson, Charles
Waksman, Ron
Soukas, Peter A.
Simon, Daniel
Chronos, Nicolas
Fortuin, F. David
Huang, Paul P.
Weintraub, Neal
Yeung, Alan
Rosenfield, Kenneth
Wong, S. Chiu
Taussig, Andrew
Rava, Amish N.
Sherman, Warren
Kereiakes, Dean
Strumpf, Robert K.
Port, Steven
Pieper, Karen
Adams, Peter X.
Harrington, Robert
TI Autologous CD34+Cell Therapy for Refractory Angina: 12 Month Results of
the Phase II ACT34-CMI Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Losordo, Douglas W.; Davidson, Charles] Northwestern Univ, Chicago, IL 60611 USA.
[Henry, Tim] Minneapolis Heart Insitute, Minneapolis, MN USA.
[Schatz, Richard A.] Scripps Green Hosp, San Diego, CA USA.
[Lee, Joon Sup] UPMC, Pittsburgh, PA USA.
[Costa, Marco; Bass, Theodore; Simon, Daniel] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Schaer, Gary] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Niederman, Alan] Holy Cross Hosp, Ft Lauderdale, FL USA.
[Mendelsohn, Farrell] Cardiol PC, Birmingham, AL USA.
[Waksman, Ron] Washington Hosp Ctr, Washington, DC 20010 USA.
[Soukas, Peter A.] St Elizabeths, Boston, MA USA.
[Chronos, Nicolas] St Josephs Rsch Inst, Atlanta, GA USA.
[Fortuin, F. David] Mayo Clin, Scottsdale, AZ USA.
[Huang, Paul P.] Swedish Seattle Hosp, Seattle, WA USA.
[Weintraub, Neal] Univ Cincinnati, Med Ctr, Univ Iowa Healthcare, Cincinnati, OH 45267 USA.
[Yeung, Alan] Stanford Univ, Stanford, CA 94305 USA.
[Rosenfield, Kenneth] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Wong, S. Chiu] Cornell Univ, Ithaca, NY USA.
[Taussig, Andrew] Florida Hosp, Orlando, FL USA.
[Rava, Amish N.] Univ Wisconsin, Madison, WI USA.
[Sherman, Warren] Columbia Univ, New York, NY USA.
[Kereiakes, Dean] Lindner Clin Trial Ctr, Cincinnati, OH USA.
[Strumpf, Robert K.] Arizona Heart, Phoenix, AZ USA.
[Port, Steven] St Lukes, Kansas City, MO USA.
[Pieper, Karen; Harrington, Robert] Duke Clin Rsch Inst, Durham, NC USA.
[Adams, Peter X.] Baxter Healthcare Corp, Deerfield, IL 60015 USA.
NR 0
TC 4
Z9 4
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1132
EP S1132
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504167
ER
PT J
AU Lubitz, SA
Makino, S
Sinner, MF
Lunetta, KL
Pfeufer, A
Rahman, R
Danik, SP
Sonni, A
Shea, MA
del Monte, F
Perz, S
Peters, A
Greenberg, SM
Furie, KL
Benjamin, EJ
Rosand, J
Arking, DE
Alonso, A
Boerwinkle, E
Kaab, S
Ellinor, PT
AF Lubitz, Steven A.
Makino, Seiko
Sinner, Moritz F.
Lunetta, Kathryn L.
Pfeufer, Arne
Rahman, Rosanna
Danik, Stephan P.
Sonni, Akshata
Shea, Marisa A.
del Monte, Frederica
Perz, Siegfried
Peters, Annette
Greenberg, Steven M.
Furie, Karen L.
Benjamin, Emelia J.
Rosand, Jonathan
Arking, Dan E.
Alonso, Alvaro
Boerwinkle, Eric
Kaab, Stefan
Ellinor, Patrick T.
TI Additional Independent Susceptibility Markers for Atrial Fibrillation on
Chromosome 4q25
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Lubitz, Steven A.; Makino, Seiko; Ellinor, Patrick T.] Massachusetts Gen Hosp, Charlestown, MA USA.
[Sinner, Moritz F.; Kaab, Stefan] Univ Munich, Univ Hosp Grosshadern, Munich, Germany.
[Lunetta, Kathryn L.; Benjamin, Emelia J.] Boston Univ, Sch Med, Framingham, MA USA.
[Pfeufer, Arne] Tech Univ Munich, Munich, Germany.
[Rahman, Rosanna; Danik, Stephan P.; Sonni, Akshata; Shea, Marisa A.; del Monte, Frederica; Greenberg, Steven M.; Furie, Karen L.; Rosand, Jonathan] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Perz, Siegfried; Peters, Annette] German Res Ctr Environm Hlth, Neuherberg, Germany.
[Arking, Dan E.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Alonso, Alvaro] Univ Minnesota, Minneapolis, MN USA.
[Boerwinkle, Eric] Univ Texas Hlth Sci Ctr, Charlestown, TX USA.
RI Kaab, Stefan/H-3915-2012; Pfeufer, Arne/B-6634-2013; Peters,
Annette/A-6117-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S579
EP S579
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501329
ER
PT J
AU Mahoney, EM
Wang, KJ
Porath, A
Corbalan, R
Steg, PG
Bhatt, DL
AF Mahoney, Elizabeth M.
Wang, Kaijun
Porath, Avi
Corbalan, Ramon
Steg, Ph. G.
Bhatt, Deepak L.
TI Cholesterol Control in Patients With a History of Hyperlipidemia and
Established Vascular Disease Reflects National Economic/Health System
Characteristics
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Mahoney, Elizabeth M.; Wang, Kaijun] St Lukes Hosp, Mid Amer Heart Inst, Kansas City, MO 64111 USA.
[Porath, Avi] Ben Gurion Univ Negev, IL-84105 Beer Sheva, Israel.
[Corbalan, Ramon] Catholic Univ, Sch Med, Santiago, Chile.
[Steg, Ph. G.] Ctr Hosp Bichat Claude Bernard, Paris, France.
[Bhatt, Deepak L.] VA Boston Healthcare Syst, Boston, MA USA.
[Bhatt, Deepak L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S405
EP S406
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500423
ER
PT J
AU Maurovich-Horvat, P
Kriegel, ML
Schlett, CL
Nakazawa, G
Vorpahl, M
Nakano, M
Bamberg, F
Virmani, R
Hoffmann, U
AF Maurovich-Horvat, Pal
Kriegel, Matthias L.
Schlett, Christopher L.
Nakazawa, Gaku
Vorpahl, Marc
Nakano, Masataka
Bamberg, Fabian
Virmani, Renu
Hoffmann, Udo
TI Assessment of Coronary Atherosclerotic Plaque by High-Definition
Computed Tomography: An ex vivo Study in Human Hearts
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Maurovich-Horvat, Pal; Kriegel, Matthias L.; Schlett, Christopher L.; Bamberg, Fabian; Hoffmann, Udo] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Nakazawa, Gaku; Vorpahl, Marc; Nakano, Masataka; Virmani, Renu] CVPath Inst, Gaithersburg, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S303
EP S303
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500021
ER
PT J
AU Mega, JL
Iakoubova, OA
Devlin, JJ
Qin, J
Cannon, CP
Braunwald, E
Sabatine, MS
AF Mega, Jessica L.
Iakoubova, Olga A.
Devlin, James J.
Qin, Jie
Cannon, Christopher P.
Braunwald, Eugene
Sabatine, Marc S.
TI 9p21 Genetic Variant and Benefit From Intensive Statin Therapy After an
Acute Coronary Syndrome
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Mega, Jessica L.; Cannon, Christopher P.; Braunwald, Eugene; Sabatine, Marc S.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Iakoubova, Olga A.; Devlin, James J.] Celera, Alameda, CA USA.
[Qin, Jie] TIMI Study Grp, Boston, MA USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1144
EP S1144
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504218
ER
PT J
AU Mega, JL
Braunwald, E
Lee, M
Misselwitz, F
Mohanavelu, S
Notani, R
Peters, G
Gibson, CM
AF Mega, Jessica L.
Braunwald, Eugene
Lee, Mary
Misselwitz, Frank
Mohanavelu, Satishkumar
Notani, Ravi
Peters, Gary
Gibson, C. Michael
TI Cessation of Rivaroxaban in Post-ACS Patients is Not Associated With
Clinical Evidence of Rebound Hypercoagulability: An ATLAS ACS-TIMI 46
Substudy
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Mega, Jessica L.; Braunwald, Eugene] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Lee, Mary; Notani, Ravi; Peters, Gary] Johnson & Johnson, Raritan, NJ USA.
[Gibson, C. Michael] Beth Israel Hosp, Boston, MA USA.
[Mohanavelu, Satishkumar] TIMI Study Grp, Boston, MA USA.
[Misselwitz, Frank] Bayer HealthCare, Wuppertal, Germany.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1002
EP S1002
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503413
ER
PT J
AU Mehdi, H
Frangiskakis, JM
Grimley, S
Gutmann, R
Bloom, HL
Dudley, SC
Ellinor, PT
Shalaby, A
Weiss, R
Saba, S
McNamara, DM
London, B
AF Mehdi, Haider
Frangiskakis, J. M.
Grimley, Sara
Gutmann, Rebecca
Bloom, Heather L.
Dudley, Samuel C.
Ellinor, Patrick T.
Shalaby, Alaa
Weiss, Raul
Saba, Samir
McNamara, Dennis M.
London, Barry
TI NOS1AP is Associated With Arrhythmias in a Heart Failure Population With
Severe LV Dysfunction
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Mehdi, Haider; Frangiskakis, J. M.; Grimley, Sara; Gutmann, Rebecca; Saba, Samir; McNamara, Dennis M.; London, Barry] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
[Bloom, Heather L.] Emory Univ, Sch Med, Atlanta, GA USA.
[Dudley, Samuel C.] Univ Illinois, Chicago, IL USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Shalaby, Alaa] Vet Affairs Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Weiss, Raul] Ohio State Univ, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S571
EP S572
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501301
ER
PT J
AU Mela, T
Chung, M
Venkateshwar, G
Borge, R
Shinn, T
Dan, D
Uslan, D
Gleva, M
Holcomb, R
Mitchell, K
Poole, J
AF Mela, Theofanie
Chung, Mina
Venkateshwar, Gottipaty
Borge, Richard
Shinn, Timothy
Dan, Dan
Uslan, Daniel
Gleva, Marye
Holcomb, Richard
Mitchell, Kevin
Poole, Jeanne
TI Replacement of Cardiac Rhythm Devices: Is the Risk Different When
Performed by Trained Electrophysiologists, in Academic or Private
Practice? Results From the REPLACE Registry
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Mela, Theofanie] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Chung, Mina] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Venkateshwar, Gottipaty] S Carolina Heart Ctr, Columbia, SC USA.
[Borge, Richard] Abington Vied Specialists, Abington, PA USA.
[Shinn, Timothy] Michigan Heart, Ann Arbor, MI USA.
[Dan, Dan] Piedmont Heart Inst, Atlanta, GA USA.
[Uslan, Daniel] Univ Calif Los Angeles, Los Angeles, CA USA.
[Gleva, Marye; Poole, Jeanne] Washington Univ, Sch Med, St Louis, MO USA.
[Mitchell, Kevin] Biotronik, Lake Oswego, OR USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S637
EP S637
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501571
ER
PT J
AU Merchant, RM
Abotsi, EJ
Long, JA
Trudeau, ME
Groeneveld, PW
Becker, LB
Abella, BS
Asch, DA
AF Merchant, Raina M.
Abotsi, Edam J.
Long, Judith A.
Trudeau, Marti E.
Groeneveld, Peter W.
Becker, Lance B.
Abella, Benjamin S.
Asch, David A.
TI Real Time Cardiopulmonary Resuscitation Instructions via Cellular Phone
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Merchant, Raina M.; Abotsi, Edam J.; Long, Judith A.; Groeneveld, Peter W.; Becker, Lance B.; Abella, Benjamin S.; Asch, David A.] Univ Penn, Philadelphia, PA 19104 USA.
[Trudeau, Marti E.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1455
EP S1456
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831505066
ER
PT J
AU Miller, PS
Evangelista, LS
Giger, JN
Martinez-Maza, O
Corvera-Tindel, T
Esmailian, F
Doering, LV
AF Miller, Pamela S.
Evangelista, Lorraine S.
Giger, Joyce N.
Martinez-Maza, Otoniel
Corvera-Tindel, Teresita
Esmailian, Fardad
Doering, Lynn V.
TI Running on Exhaustion: Pathogen Burden, Immune Dysregulation, and
Endothelial Activation After Coronary Artery Bypass Graft Surgery
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Miller, Pamela S.; Evangelista, Lorraine S.; Giger, Joyce N.; Martinez-Maza, Otoniel; Esmailian, Fardad; Doering, Lynn V.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Corvera-Tindel, Teresita] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S416
EP S416
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500466
ER
PT J
AU Mitchell, K
Gupte, S
Wright, J
Minae, A
Sasson, J
Kehoe, K
Fiocchi, F
Oetgen, W
Rumsfeld, JS
AF Mitchell, Kristi
Gupte, Sunil
Wright, Janet
Minae, Ashley
Sasson, Joe
Kehoe, Katie
Fiocchi, Fran
Oetgen, William
Rumsfeld, John S.
TI Electronic Medical Record Adoption in Cardiology Practices: A 2009
Snapshot From the American College of Cardiology's IC3 (Improving
Continuous Cardiac Care) Program
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Mitchell, Kristi; Gupte, Sunil; Wright, Janet; Minae, Ashley; Kehoe, Katie; Fiocchi, Fran] Amer Coll Cardiol, Washington, DC USA.
[Sasson, Joe] MedAxiom, Tallahassee, FL USA.
[Oetgen, William] Georgetown Univ, Washington, DC USA.
[Rumsfeld, John S.] Univ Colorado, Denver, CO 80202 USA.
[Rumsfeld, John S.] Denver VA Med Ctr, Denver, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S438
EP S438
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500550
ER
PT J
AU Miyazaki, T
Yamazaki, H
Morishige, K
Aikawa, E
Aikawa, M
AF Miyazaki, Tetsuro
Yamazaki, Hiroyuki
Morishige, Kunio
Aikawa, Elena
Aikawa, Masanori
TI Notch3 Signaling in Macrophages Promotes Obesity and Atherosclerosis in
Hypercholesterolemic Mice
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Miyazaki, Tetsuro; Yamazaki, Hiroyuki; Morishige, Kunio; Aikawa, Masanori] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Aikawa, Elena] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1051
EP S1051
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503617
ER
PT J
AU Myrmel, T
Tsai, TT
Isselbacher, EM
Eagle, KA
Froehlich, JB
Montgomery, DG
Cooper, JV
Sundt, T
Pyeritz, RE
Hutchison, S
Bartnes, K
Ehrlich, M
Demertzis, S
Evangelista, A
Nienaber, CA
AF Myrmel, Truls
Tsai, Thomas T.
Isselbacher, Eric M.
Eagle, Kim A.
Froehlich, James B.
Montgomery, Daniel G.
Cooper, Jeanna V.
Sundt, Thoralf, III
Pyeritz, Reed E.
Hutchison, Stuart
Bartnes, Kristian
Ehrlich, Marek
Demertzis, Stefanos
Evangelista, Arturo
Nienaber, Christoph A.
CA IRAD Investigators
TI Partial Thrombosis of the False Lumen is Not a Predictor of Follow-up
Mortality in Patients With Acute Type A Aortic Dissection
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Myrmel, Truls; Bartnes, Kristian] Univ Hosp N Norway, Tromso, Norway.
[Tsai, Thomas T.] Univ Colorado, Denver, CO 80202 USA.
[Isselbacher, Eric M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Eagle, Kim A.; Froehlich, James B.; Montgomery, Daniel G.; Cooper, Jeanna V.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Sundt, Thoralf, III] Mayo Clin, Rochester, MN USA.
[Pyeritz, Reed E.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Hutchison, Stuart] Univ Calgary, Calgary, AB, Canada.
[Ehrlich, Marek] Univ Vienna, Vienna, Austria.
[Demertzis, Stefanos] Cardioctr Ticino, Lugano, Switzerland.
[Evangelista, Arturo] Hosp Gen Univ Vall Hebron, Barcelona, Spain.
[Nienaber, Christoph A.] Univ Hosp Rostock, Rostock, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S965
EP S965
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503267
ER
PT J
AU Nabavi, V
Ahmadi, N
Saeed, A
Hajsadeghi, F
Flores, F
Sourayanezhad, S
Mendoza, H
Ebrahimi, R
Ahmdi, A
Levenstein, S
Budoff, M
AF Nabavi, Vahid
Ahmadi, Naser
Saeed, Anila
Hajsadeghi, Fereshteh
Flores, Ferdinand
Sourayanezhad, Souraya
Mendoza, Helen
Ebrahimi, Ramin
Ahmdi, Ahmad
Levenstein, Susan
Budoff, Matthew
TI Association of the Extent of Perceived Mental Stress and Physical
Inactivity, and the Extent of Coronary Artery Disease Diagnosed by
Computed Tomography
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Nabavi, Vahid; Ahmadi, Naser; Saeed, Anila; Hajsadeghi, Fereshteh; Flores, Ferdinand; Sourayanezhad, Souraya; Mendoza, Helen; Ahmdi, Ahmad; Budoff, Matthew] Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Torrance, CA 90509 USA.
[Ebrahimi, Ramin] Univ Calif Los Angeles, Greater Los Angeles VA Healthcare Syst, Los Angeles, CA USA.
[Levenstein, Susan] Aventino Med Grp, Rome, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S494
EP S494
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500778
ER
PT J
AU Nazer, B
Ray, KK
Sloan, S
Scirica, BM
Morrow, DA
Cannon, CP
Braunwald, E
AF Nazer, Babak
Ray, Kausik K.
Sloan, Sarah
Scirica, Benjamin M.
Morrow, David A.
Cannon, Christopher P.
Braunwald, Eugene
TI Neopterin Levels Improve Risk Prediction for Heart Failure
Hospitalization Over and Above C-reactive Protein and B-type Natriuretic
Peptide in the PROVE IT-TIMI 22 Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Nazer, Babak] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Ray, Kausik K.] Univ Cambridge, Cambridge, England.
[Sloan, Sarah; Scirica, Benjamin M.; Morrow, David A.; Cannon, Christopher P.; Braunwald, Eugene] TIMI Study Grp, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S808
EP S808
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502448
ER
PT J
AU Okada, DR
Blankstein, R
Ghoshhajra, BB
Rocha, JA
Shturman, LD
Rogers, IS
Bezerra, HG
Sarwar, A
Gewirtz, H
Hoffmann, U
Mamuya, WS
Brady, TJ
Cury, RC
AF Okada, David R.
Blankstein, Ron
Ghoshhajra, Brian B.
Rocha-Filho, Jose A.
Shturman, Leonid D.
Rogers, Ian S.
Bezerra, Hiram G.
Sarwar, Ammar
Gewirtz, Henry
Hoffmann, Udo
Mamuya, Wilfred S.
Brady, Thomas J.
Cury, Ricardo C.
TI Direct Comparison of Rest and Adenosine Stress Myocardial Perfusion CT
With Rest and Stress SPECT
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Okada, David R.; Ghoshhajra, Brian B.; Rocha-Filho, Jose A.; Shturman, Leonid D.; Rogers, Ian S.; Sarwar, Ammar; Gewirtz, Henry; Hoffmann, Udo; Brady, Thomas J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Blankstein, Ron] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Bezerra, Hiram G.] Harrington McLaughlin Heart & Vasc Inst, Cleveland, OH USA.
[Mamuya, Wilfred S.] Lown Cardiovasc Grp, Brookline, MA USA.
[Cury, Ricardo C.] Baptist Cardiac & Vasc Inst, Miami, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S374
EP S374
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500297
ER
PT J
AU Peacock, JM
Keo, HH
Yu, XH
Oldenburg, N
Duval, S
Henry, TD
Jaff, MR
Baumgartner, I
Hirsch, AT
AF Peacock, James M.
Keo, Hong H.
Yu, Xinhua
Oldenburg, Niki
Duval, Sue
Henry, Timothy D.
Jaff, Michael R.
Baumgartner, Iris
Hirsch, Alan T.
TI The Incidence and Health Economic Burden of Critical Limb Ischemia and
Ischemic Amputation in Minnesota: 2005-2007
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Peacock, James M.; Yu, Xinhua; Oldenburg, Niki] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA.
[Keo, Hong H.; Duval, Sue; Hirsch, Alan T.] Univ Minnesota, Sch Publ Hlth, Abbott NW Hosp, Minneapolis Heart Inst Fdn, Minneapolis, MN USA.
[Jaff, Michael R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Baumgartner, Iris] Swiss Cardiovasc Cntr, Bern, Switzerland.
NR 0
TC 5
Z9 5
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1148
EP S1148
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504235
ER
PT J
AU Qadir, S
Brady, TJ
Tawakol, A
AF Qadir, Sadia
Brady, Thomas J.
Tawakol, Ahmed
TI F-18-FDG PET Imaging Predicts Progression of Carotid Stenosis: A
Prospective 2-Year Follow-up Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Qadir, Sadia; Brady, Thomas J.; Tawakol, Ahmed] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S388
EP S388
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500351
ER
PT J
AU Qi, S
van Dam, RM
Meigs, JB
Franco, OH
Mantzoros, CS
Hu, FB
AF Qi Sun
van Dam, Rob M.
Meigs, James B.
Franco, Oscar H.
Mantzoros, Christos S.
Hu, Frank B.
TI Leptin and Soluble Leptin Receptor Levels in Plasma and Risk of Type 2
Diabetes in US Women: A Prospective Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Qi Sun; van Dam, Rob M.; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Meigs, James B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Franco, Oscar H.] Univ Warwick, Coventry CV4 7AL, W Midlands, England.
[Mantzoros, Christos S.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S415
EP S415
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500461
ER
PT J
AU Riegel, B
Potashnik, S
Goldberg, L
Weaver, T
Weintraub, W
Fleck, D
Sayers, S
AF Riegel, Barbara
Potashnik, Sheryl
Goldberg, Lee
Weaver, Terri
Weintraub, William
Fleck, Desiree
Sayers, Steven
TI Is There a Better Way to Screen for Sleep Disordered Breathing in Adults
With Heart Failure?
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Riegel, Barbara; Potashnik, Sheryl; Goldberg, Lee; Weaver, Terri; Fleck, Desiree] Univ Penn, Philadelphia, PA 19104 USA.
[Weintraub, William] Christiana Care Hlth Syst, Newark, DE USA.
[Sayers, Steven] Philadelphia VA Med Ctr, Philadelphia, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S864
EP S864
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502678
ER
PT J
AU Rivera, JJ
Budoff, M
O'Leary, DH
Hoffman, U
Wasserman, B
Szklo, M
Burke, G
Blumenthal, RS
Nasir, K
AF Rivera, Juan J.
Budoff, Matthew
O'Leary, Daniel H.
Hoffman, Udo
Wasserman, Bruce
Szklo, Moyses
Burke, Gregory
Blumenthal, Roger S.
Nasir, Khurram
TI Relationship Between Carotid Intima Media Thickness and Coronary Artery
Calcium Progression in the Multi-ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Rivera, Juan J.; Wasserman, Bruce; Szklo, Moyses; Blumenthal, Roger S.] Johns Hopkins Univ, Baltimore, MD 02114 USA.
[Budoff, Matthew] Harbor UCLA Med Ctr, Los Angeles Biomed Rsch Inst, Los Angeles, CA USA.
[O'Leary, Daniel H.] Caritas Carney Hosp, Dorchester, MA USA.
[Hoffman, Udo] Massachusetts Gen Hosp, Boston, MA USA.
[Burke, Gregory] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Nasir, Khurram] Boston Univ Hosp, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S343
EP S343
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500179
ER
PT J
AU Rogers, IS
Joshi, SB
Johnson, JR
Ferencik, M
Shturman, LD
Abbara, S
Gaber, MS
Sciortino, N
Williams, J
Hachamovitch, R
Di Carli, MF
Hoffmann, U
AF Rogers, Ian S.
Joshi, Subodh B.
Johnson, James R.
Ferencik, Maros
Shturman, Leon D.
Abbara, Suhny
Gaber, Mariya S.
Sciortino, Nathan
Williams, Julie
Hachamovitch, Rory
Di Carli, Marcelo F.
Hoffmann, Udo
TI Reliability of Cardiac CT for the Detection of Significant Luminal
Narrowing: Results From the Study of Myocardial Perfusion and Coronary
Anatomy Imaging Roles in CAD (SPARC) Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Rogers, Ian S.; Joshi, Subodh B.; Ferencik, Maros; Shturman, Leon D.; Abbara, Suhny; Sciortino, Nathan; Hoffmann, Udo] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Johnson, James R.; Gaber, Mariya S.; Williams, Julie; Hachamovitch, Rory; Di Carli, Marcelo F.] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S301
EP S302
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500015
ER
PT J
AU Rusanescu, G
Aikawa, M
Weissleder, R
Aikawa, E
AF Rusanescu, Gabriel
Aikawa, Masanori
Weissleder, Ralph
Aikawa, Elena
TI Novel Roles of Notch2 and Notch3 in Differential Regulation of
Cardiovascular Calcification
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Rusanescu, Gabriel; Weissleder, Ralph; Aikawa, Elena] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Charlestown, MA USA.
[Aikawa, Masanori] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA USA.
NR 0
TC 1
Z9 1
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S307
EP S307
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500040
ER
PT J
AU Sakhuja, R
Rame, JE
Brown, C
Ordovas, K
Ursell, P
De Marco, T
AF Sakhuja, Rahul
Rame, J. Eduardo
Brown, Colleen
Ordovas, Karen
Ursell, Philip
De Marco, Teresa
TI A 22-Year-Old Female With Non-Hypertrophic Hypertrophic Cardiomyopathy
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Sakhuja, Rahul] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Rame, J. Eduardo; Brown, Colleen; Ordovas, Karen; Ursell, Philip; De Marco, Teresa] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S746
EP S747
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502196
ER
PT J
AU Schlett, CL
Banerji, D
Siegel, EL
Lehman, SJ
Bamberg, F
Ferencik, M
Rogers, IS
Brady, TJ
Nagumey, JT
Hoffmann, U
Truong, QA
AF Schlett, Christopher L.
Banerji, Dahlia
Siegel, Emily L.
Lehman, Sam J.
Bamberg, Fabian
Ferencik, Maros
Rogers, Ian S.
Brady, Thomas J.
Nagumey, John T.
Hoffmann, Udo
Truong, Quynh A.
TI Computed Tomography Angiography Results Predict Long-term Major Adverse
Cardiac Events in Patients With Chest Pain From the Emergency
Department: Two-year Outcome of the ROMICAT (Rule Out Myocardial
Infarction Using Computer Assisted Tomography) Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Schlett, Christopher L.; Banerji, Dahlia; Siegel, Emily L.; Lehman, Sam J.; Bamberg, Fabian; Ferencik, Maros; Rogers, Ian S.; Brady, Thomas J.; Nagumey, John T.; Hoffmann, Udo; Truong, Quynh A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S317
EP S317
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500072
ER
PT J
AU Schnabel, RB
Baumert, J
Barbalic, M
Dupuis, J
Ellinor, PT
Durda, P
Dehghan, A
Bis, JC
Witteman, JC
Hoogeveen, RC
Benjamin, EJ
Koenig, W
Tracy, RP
AF Schnabel, Renate B.
Baumert, Jens
Barbalic, Maja
Dupuis, Josee
Ellinor, Patrick T.
Durda, Peter
Dehghan, Abbas
Bis, Joshua C.
Witteman, Jacqueline C.
Hoogeveen, Ron C.
Benjamin, Emelia J.
Koenig, Wolfgang
Tracy, Russell P.
CA CHARGE Consortium
TI Duffy Antigen Receptor for Chemokines (Darc) Polymorphism Regulates
Circulating Concentrations of Monocyte Chemoattractant Protein-1 and
Other Circulating Inflammatory Mediators
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Schnabel, Renate B.] Johannes Gutenberg Univ Mainz, Mainz, 02114, Germany.
[Baumert, Jens] German Rsch Cntr Environm Hlth, Helmholtz Zentrum Munchen, Neuherberg, 05405, Germany.
[Barbalic, Maja; Hoogeveen, Ron C.] Univ Texas Hlth Sci Ctr, Human Genet Cntr, Houston, TX USA.
[Barbalic, Maja; Hoogeveen, Ron C.] Univ Texas Hlth Sci Ctr, Inst Mol Med, Houston, TX 98195 USA.
[Dupuis, Josee] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Rsch Cntr, Boston, MA USA.
[Durda, Peter] Univ Vermont, Coll Med, Dept Pathol, Burlington, VT USA.
[Dehghan, Abbas] Erasmus Med Cntr, Dept Epidemiol, D-7900 Rotterdam, Netherlands.
[Bis, Joshua C.] Univ Washington, Seattle, WA 05405 USA.
[Witteman, Jacqueline C.] Erasmus Med Cntr, Rotterdam, Netherlands.
[Benjamin, Emelia J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
[Koenig, Wolfgang] Univ Ulm, Dept Internal Med 2, Med Cntr, Ulm, Germany.
[Tracy, Russell P.] Univ Vermont, Coll Med, Dept Biochem, Burlington, VT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S559
EP S559
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501249
ER
PT J
AU Sibley, CT
Gottlieb, I
Cox, C
Godoy, G
Spooner, AE
Bluemke, DA
Lima, JA
AF Sibley, Christopher T.
Gottlieb, Ilan
Cox, Christopher
Godoy, Gustavo
Spooner, Amy E.
Bluemke, David A.
Lima, Joao A.
TI Comparative Effect of Statins vs Niacin on MRI Measured Regression of
Carotid Atherosclerosis in a Randomized Clinical Trial: The NIA Plaque
Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Sibley, Christopher T.; Godoy, Gustavo; Lima, Joao A.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Gottlieb, Ilan] Univ Fed Rio de Janeiro, Rio De Janeiro, Brazil.
[Cox, Christopher] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Spooner, Amy E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
RI Sibley, Christopher/C-9900-2013
NR 0
TC 9
Z9 9
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S376
EP S376
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500305
ER
PT J
AU Smith, EE
Reeves, MJ
Hernandez, AF
Saver, JL
Pan, WQ
Dai, D
Olson, DM
Fonarow, GC
Schwamm, LH
AF Smith, Eric E.
Reeves, Mathew J.
Hernandez, Adrian F.
Saver, Jeffrey L.
Pan, Wenqin
Dai, David
Olson, DaiWai M.
Fonarow, Gregg C.
Schwamm, Lee H.
TI Prediction of In-Hospital Mortality in Ischemic Stroke Using Data From
Get With the Guidelines Stroke
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Reeves, Mathew J.] Michigan State Univ, E Lansing, MI 48824 USA.
[Smith, Eric E.] Univ Calgary, Calgary, AB, Canada.
[Hernandez, Adrian F.; Pan, Wenqin; Dai, David; Olson, DaiWai M.] Duke Univ, Durham, NC USA.
[Saver, Jeffrey L.; Fonarow, Gregg C.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RI Smith, Eric/C-5443-2012
OI Smith, Eric/0000-0003-3956-1668
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S522
EP S522
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501101
ER
PT J
AU Sosnovik, DE
Garanger, E
Aikawa, E
Nahrendorf, M
Figueiredo, JL
Dai, GP
Reynolds, F
Rosenzweig, A
Weissleder, R
Josephson, L
AF Sosnovik, David E.
Garanger, Elisabeth
Aikawa, Elena
Nahrendorf, Matthias
Figueiredo, Jose-Luiz
Dai, Guangping
Reynolds, Fred
Rosenzweig, Anthony
Weissleder, Ralph
Josephson, Lee
TI Molecular MRI of Cardiomyocyte Apoptosis With Simultaneous Delayed
Enhancement MRI Distinguishes Apoptotic and Necrotic Myocytes in vivo:
Potential for Midmyocardial Salvage in Acute Ischemia
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Sosnovik, David E.; Garanger, Elisabeth; Aikawa, Elena; Nahrendorf, Matthias; Figueiredo, Jose-Luiz; Dai, Guangping; Reynolds, Fred; Rosenzweig, Anthony; Weissleder, Ralph; Josephson, Lee] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Charlestown, MA USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S367
EP S367
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500270
ER
PT J
AU Steinhaus, D
Moffatt, E
Vittinghoff, E
Whiteman, D
Tseng, ZH
AF Steinhaus, Daniel
Moffatt, Ellen
Vittinghoff, Eric
Whiteman, Dean
Tseng, Zian H.
TI Contemporary Burden of Sudden Cardiac Death in San Francisco County,
2007: Substantial Differences in Rates by Race and Gender
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Steinhaus, Daniel] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Moffatt, Ellen; Vittinghoff, Eric; Whiteman, Dean; Tseng, Zian H.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S417
EP S418
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500472
ER
PT J
AU Stolker, JM
McGuire, DK
Spertus, JA
Inzucchi, SE
Rathore, SS
Maddox, TM
Masoudi, FA
Tang, F
Jones, PG
Kosiborod, M
AF Stolker, Joshua M.
McGuire, Darren K.
Spertus, John A.
Inzucchi, Silvio E.
Rathore, Saif S.
Maddox, Thomas M.
Masoudi, Frederick A.
Tang, Fengming
Jones, Philip G.
Kosiborod, Mikhail
TI In-Hospital Assessment of Hemoglobin A(1c) in Patients With Diabetes
Treated for Myocardial Infarction: Variability Between Hospitals and
Relationship With Established Quality Indicators
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd National Conference and Exhibitions and Annual Scientific Session
of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Stolker, Joshua M.; Spertus, John A.; Tang, Fengming; Jones, Philip G.; Kosiborod, Mikhail] St Lukes Hosp, Mid Amer Heart Inst, Kansas City, MO 64111 USA.
[McGuire, Darren K.] Univ Texas Southwestern Sch Med, Dallas, TX USA.
[Inzucchi, Silvio E.; Rathore, Saif S.] Yale Univ, Sch Med, New Haven, CT USA.
[Maddox, Thomas M.; Masoudi, Frederick A.] Univ Colorado, Denver VAMC, Denver, CO 80202 USA.
[Masoudi, Frederick A.] Denver Hlth Med Ctr, Denver, CO 80202 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S485
EP S485
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500744
ER
PT J
AU Thanassoulis, G
Massaro, JM
O'Donnell, CJ
Levy, D
Hoffman, U
Ellinor, PT
Wang, TJ
Vasan, RS
Fox, CS
Benjamin, EJ
AF Thanassoulis, George
Massaro, Joseph M.
O'Donnell, Christopher J.
Levy, Daniel
Hoffman, Udo
Ellinor, Patrick T.
Wang, Thomas J.
Vasan, Ramachandran S.
Fox, Caroline S.
Benjamin, Emelia J.
TI Pericardial Fat is Associated With Prevalent AF - The Framingham Heart
Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Thanassoulis, George; O'Donnell, Christopher J.; Vasan, Ramachandran S.; Fox, Caroline S.; Benjamin, Emelia J.] NHLBI, NIH, Framingham Heart Study, Framingham, MA USA.
[Massaro, Joseph M.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Hoffman, Udo; Ellinor, Patrick T.; Wang, Thomas J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S519
EP S519
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501091
ER
PT J
AU Tofler, GH
Massaro, J
O'Donnell, CJ
Wilson, PW
Vasan, RS
Sutherland, PA
Lipinska, I
Meigs, JB
Levy, D
D'Agostino, RB
AF Tofler, Geoffrey H.
Massaro, Joseph
O'Donnell, Christopher J.
Wilson, Peter W.
Vasan, Ramachandran S.
Sutherland, Patrice A.
Lipinska, Izabela
Meigs, James B.
Levy, Daniel
D'Agostino, Ralph B.
TI Plasminogen Activator Inhibitor (PAI-1) and Risk of Cardiovascular
Disease: The Framingham Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Tofler, Geoffrey H.] Royal N Shore Hosp, Sydney, NSW 02215, Australia.
[Massaro, Joseph; Vasan, Ramachandran S.; Lipinska, Izabela; D'Agostino, Ralph B.] Boston Univ, Boston, MA USA.
[O'Donnell, Christopher J.; Levy, Daniel] NHLBI, Framingham, MA USA.
[O'Donnell, Christopher J.; Sutherland, Patrice A.; Levy, Daniel] Framingham Heart Dis Epidemiol Study, Framingham, MA 30322 USA.
[Wilson, Peter W.] Emory Univ, Atlanta, GA 02114 USA.
[Meigs, James B.] Massachusetts Gen Hosp, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S454
EP S454
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500614
ER
PT J
AU Tsai, TT
Maddox, TM
Roe, MT
Dai, D
Casserly, IP
Ho, PM
Messenger, JC
Nallamothu, BK
Peterson, ED
Rumsfeld, JS
AF Tsai, Thomas T.
Maddox, Thomas M.
Roe, Matthew T.
Dai, David
Casserly, Ivan P.
Ho, P. Michael
Messenger, John C.
Nallamothu, Brahmajee K.
Peterson, Eric D.
Rumsfeld, John S.
TI Contemporary Risk of In-Hospital Events in Dialysis Patients Undergoing
Percutaneous Coronary Interventions: Insights From the NCDR Cath-PCI
Registry
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Tsai, Thomas T.; Maddox, Thomas M.; Casserly, Ivan P.; Ho, P. Michael; Rumsfeld, John S.] Univ Colorado, Denver VAMC, Denver, CO 80202 USA.
[Roe, Matthew T.; Dai, David; Peterson, Eric D.] Duke Univ, Med Cntr, Durham, NC USA.
[Nallamothu, Brahmajee K.] Univ Michigan Hosp, Ann Arbor, MI 48109 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1101
EP S1101
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504029
ER
PT J
AU Tsang, ZH
Steinhaus, D
Vittinghoff, E
Whiteman, D
Moffatt, E
AF Tsang, Zian H.
Steinhaus, Daniel
Vittinghoff, Eric
Whiteman, Dean
Moffatt, Ellen
TI Sudden Cardiac Death in San Francisco County, 2007: Coronary Artery
Disease Accounts for Only 40% of SCDs but is Associated With a 3-Fold
Higher Risk
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Tsang, Zian H.; Vittinghoff, Eric; Whiteman, Dean; Moffatt, Ellen] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Steinhaus, Daniel] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S418
EP S418
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500473
ER
PT J
AU van der Giessen, AG
Toepker, MH
Donelly, PM
Bamberg, F
Raffle, C
Lee, H
Gijsen, FJ
Wentzel, JJ
Hoffmann, U
AF van der Giessen, Alina G.
Toepker, Michael H.
Donelly, Patrick M.
Bamberg, Fabian
Raffle, Christopher
Lee, Hang
Gijsen, Frank J.
Wentzel, Jolanda J.
Hoffmann, Udo
TI The Detection of Non-Calcified Coronary Plaques by Dual Source Computed
Tomography is Related to the Plaque Thickness
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [van der Giessen, Alina G.; Gijsen, Frank J.; Wentzel, Jolanda J.] ErasmusMC, Rotterdam, Netherlands.
[Toepker, Michael H.; Donelly, Patrick M.; Bamberg, Fabian; Raffle, Christopher; Lee, Hang; Hoffmann, Udo] Massachusetts Gen Hosp, Cardiac MRI PET CT Program, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S325
EP S325
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500107
ER
PT J
AU Vandenwijngaert, S
Pokreisz, P
Pellens, M
Gillijns, H
Veulemans, P
Liu, XS
Herijgers, P
D'hooge, J
Bloch, KD
Janssens, S
AF Vandenwijngaert, Sara
Pokreisz, Peter
Pellens, Marijke
Gillijns, Hilde
Veulemans, Paul
Liu, Xiaoshun
Herijgers, Paul
D'hooge, Jan
Bloch, Kenneth D.
Janssens, Stefan
TI Myocardial Phosphodiesterase 5 Expression Contributes to Left
Ventricular Dysfunction in the Pressure-Overloaded Heart
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Vandenwijngaert, Sara; Pokreisz, Peter; Veulemans, Paul; Liu, Xiaoshun; Herijgers, Paul; D'hooge, Jan; Janssens, Stefan] Katholieke Univ Leuven, Leuven, Belgium.
[Pellens, Marijke; Gillijns, Hilde] VIB, Leuven, Belgium.
[Bloch, Kenneth D.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RI Herijgers, Paul/B-8064-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S820
EP S820
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502498
ER
PT J
AU Velagaleti, RS
Gona, P
Chuang, ML
Yeon, SB
Salton, CJ
Fox, CS
Massaro, J
Hoffmann, U
Manning, WJ
O'Donnell, CJ
AF Velagaleti, Raghava S.
Gona, Philimon
Chuang, Michael L.
Yeon, Susan B.
Salton, Carol J.
Fox, Caroline S.
Massaro, Joseph
Hoffmann, Udo
Manning, Warren J.
O'Donnell, Christopher J.
TI Aortic Atherosclerosis and Left Ventricular Structure in the Community
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Velagaleti, Raghava S.; Gona, Philimon; Fox, Caroline S.; Massaro, Joseph; O'Donnell, Christopher J.] NHLBI, Framingham, MA USA.
[Chuang, Michael L.; Yeon, Susan B.; Salton, Carol J.; Manning, Warren J.] Beth Israel Deaconess Med Cntr, Boston, MA USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S380
EP S380
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500321
ER
PT J
AU Wang, CC
Lu, L
Xu, Y
Grayson, C
Jacobs, S
Reusch, JE
Gianani, R
Draznin, B
Schwartz, GG
AF Wang, Cecilia C.
Lu, Li
Xu, Ya
Grayson, Clifford
Jacobs, Susanna
Reusch, Jane E.
Gianani, Roberto
Draznin, Boris
Schwartz, Gregory G.
TI Diet-Induced Insulin Resistance Causes Isoform-Specific Abnormalities of
Akt Signaling in Arterial Wall of Pigs
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Wang, Cecilia C.; Lu, Li; Xu, Ya; Grayson, Clifford; Jacobs, Susanna; Reusch, Jane E.; Draznin, Boris; Schwartz, Gregory G.] Denver VA Med Ctr, Denver, CO USA.
[Wang, Cecilia C.; Lu, Li; Xu, Ya; Grayson, Clifford; Jacobs, Susanna; Reusch, Jane E.; Gianani, Roberto; Draznin, Boris; Schwartz, Gregory G.] Univ Colorado, Denver, CO 80202 USA.
[Gianani, Roberto] Childrens Hosp, Denver, CO 80218 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S443
EP S444
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500570
ER
PT J
AU Wann, LS
Thompson, RC
Allam, AH
Miyamoto, MI
Amer, HA
Badr, I
Abdel-maksoud, G
Nureldin, A
Thomas, JJ
Thomas, GS
AF Wann, L. S.
Thompson, Randall C.
Allam, Adel H.
Miyamoto, Michael I.
Amer, Hany A.
Badr, Ibrahem
Abdel-maksoud, Gomma
Nureldin, Abdelhalium
Thomas, Jennifer J.
Thomas, Gregory S.
TI Atherosclerosis: Not Just a Disease of Contemporary Humans
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Wann, L. S.] Wisconsin Heart Hosp, Milwaukee, WI USA.
[Thompson, Randall C.] St Lukes Hosp, Mid Amer Heart Inst, Kansas City, MO 64111 USA.
[Allam, Adel H.] Al Azhar Med Sch, Cairo, Egypt.
[Miyamoto, Michael I.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Amer, Hany A.] Natl Rsch Cntr, Giza, Egypt.
[Badr, Ibrahem; Abdel-maksoud, Gomma; Nureldin, Abdelhalium] Cairo Univ, Cairo, Egypt.
[Thomas, Jennifer J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Thomas, Gregory S.] Univ Calif Irvine, Orange, CA 92668 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S354
EP S354
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500220
ER
PT J
AU Weiner, RB
Kanayama, G
Hudson, JI
Hutter, AM
Picard, MH
Pope, HG
Baggish, AL
AF Weiner, Rory B.
Kanayama, Gen
Hudson, James I.
Hutter, Adolph M., Jr.
Picard, Michael H.
Pope, Harrison G., Jr.
Baggish, Aaron L.
TI Chronic Anabolic Androgenic Steroid Use is Associated With Left
Ventricular Systolic and Diastolic Dysfunction
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Weiner, Rory B.; Hutter, Adolph M., Jr.; Picard, Michael H.; Baggish, Aaron L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Kanayama, Gen; Hudson, James I.; Pope, Harrison G., Jr.] McLean Hosp, Belmont, MA 02178 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S741
EP S741
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502174
ER
PT J
AU Weiss, E
Merchant, F
Laferriere, S
Mela, T
Armoundas, A
AF Weiss, Eric
Merchant, Faisal
Laferriere, Shawna
Mela, Theofanie
Armoundas, Antonis
TI A Novel Intracardiac Pacing Method to Induce and Suppress Repolarization
Altemans
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Weiss, Eric; Merchant, Faisal; Laferriere, Shawna; Mela, Theofanie; Armoundas, Antonis] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S710
EP S710
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502046
ER
PT J
AU Wilson, SR
Angiolillo, DJ
Frelinger, AL
O'Donoghue, M
Neumann, FJ
Michelson, AD
Miller, DL
Luo, JX
McCabe, CH
Antman, EM
Braunwald, E
Wiviott, S
AF Wilson, Sean R.
Angiolillo, Dominick J.
Frelinger, Andrew L., III
O'Donoghue, Michelle
Neumann, Franz-Josef
Michelson, Alan D.
Miller, Debra L.
Luo, Junxiang
McCabe, Carolyn H.
Antman, Elliott M.
Braunwald, Eugene
Wiviott, Stephen
TI Platelet Function in Diabetes Mellitus: Observations From the
PRINCIPLE-TIMI 44 Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Wilson, Sean R.; O'Donoghue, Michelle; McCabe, Carolyn H.; Antman, Elliott M.; Braunwald, Eugene; Wiviott, Stephen] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
[Angiolillo, Dominick J.] Univ Florida, Jacksonville, FL USA.
[Frelinger, Andrew L., III; Michelson, Alan D.] Univ Massachusetts, Sch Med, Worcester, MA USA.
[Neumann, Franz-Josef] Herz Zentrum, Bad Krozingen, Germany.
[Miller, Debra L.; Luo, Junxiang] Eli Lilly & Co, Indianapolis, IN 46285 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S548
EP S549
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501207
ER
PT J
AU Winterfield, JR
Werdich, A
MacRae, CA
Milan, DJ
AF Winterfield, Jeffrey R.
Werdich, Andreas
MacRae, Calum A.
Milan, David J.
TI Stim1 Modulates Pacemaking and Contractility via Regulation of Calcium
Stores in the Embryonic Heart
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Winterfield, Jeffrey R.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Werdich, Andreas; MacRae, Calum A.; Milan, David J.] Massachusetts Gen Hosp, Charlestown, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S779
EP S779
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502328
ER
PT J
AU Yu, PB
Zamanian, RT
Malhotra, R
Schmidt, J
Deng, DY
Lai, CS
Parker, W
Bloch, KD
Elliott, CG
AF Yu, Paul B.
Zamanian, Roham T.
Malhotra, Rajeev
Schmidt, Jonathan
Deng, Donna Y.
Lai, Carol S.
Parker, William
Bloch, Kenneth D.
Elliott, C. Gregory
TI Circulating Soluble Endoglin is a Sensitive Predictor of Pulmonary
Arterial Hypertension and Exercise Function
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Yu, Paul B.; Malhotra, Rajeev; Deng, Donna Y.; Lai, Carol S.; Bloch, Kenneth D.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Zamanian, Roham T.] Stanford Univ, Stanford, CA 94305 USA.
[Schmidt, Jonathan; Elliott, C. Gregory] Univ Utah, Sch Med, Salt Lake City, UT USA.
[Parker, William] Duke Univ, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1137
EP S1137
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504187
ER
PT J
AU Zahid, M
Single, I
Good, C
Stone, RA
Kim, S
Fine, MJ
Sonel, AF
AF Zahid, Maliha
Single, Ish
Good, Chester
Stone, Roslyn A.
Kim, Sunghee
Fine, Michael J.
Sonel, Ali F.
TI Association Between Pneumococcal Vaccination and Fewer Adverse Outcomes
in Patients Hospitalized With Acute Coronary Syndromes
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Zahid, Maliha; Single, Ish; Good, Chester; Stone, Roslyn A.; Kim, Sunghee; Fine, Michael J.; Sonel, Ali F.] Univ Pittsburgh, Pittsburgh, PA USA.
[Good, Chester; Stone, Roslyn A.; Kim, Sunghee; Fine, Michael J.; Sonel, Ali F.] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Rsch & Promot, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1173
EP S1173
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504349
ER
PT J
AU Zou, L
Feng, Y
Chen, YJ
Si, R
Scherrer-Crosbie, M
Shen, SQ
Ichinose, F
Chao, W
AF Zou, Lin
Feng, Yen
Chen, Yu-Jung
Si, Rui
Scherrer-Crosbie, Marielle
Shen, Shiqian
Ichinose, Fumito
Chao, We
TI Toll-like Receptor 2 Signaling Contributes to Cardiac Dysfunction and
High Mortality During Experimental Sepsis
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1443
EP S1443
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831505010
ER
PT J
AU Dieplinger, B
Januzzi, JL
Steinmair, M
Gabriel, C
Poelz, W
Haltmayer, M
Mueller, T
AF Dieplinger, Benjamin
Januzzi, James L., Jr.
Steinmair, Martin
Gabriel, Christian
Poelz, Werner
Haltmayer, Meinhard
Mueller, Thomas
TI Analytical and clinical evaluation of a novel high-sensitivity assay for
measurement of soluble ST2 in human plasma - The Presage (TM) ST2 assay
SO CLINICA CHIMICA ACTA
LA English
DT Article
DE Heart failure; Inflammation; Interleukin-1 receptor family; Natriuretic
peptides; Pneumonia; Sepsis
ID RESPIRATORY-DISTRESS-SYNDROME; FAMILY-MEMBER ST2; HEART-FAILURE;
MYOCARDIAL-INFARCTION; BIOLOGICAL VARIATION; NATRIURETIC PEPTIDE; 1-YEAR
MORTALITY; BIOMARKER; RECEPTOR; PROTEIN
AB Background: The protein ST-2 is a member of the interleukin-1 receptor family. Blood concentrations of the soluble isoform of M (sST2) are increased in inflammatory diseases and in heart disease and are considered a prognostic marker in both. The aim of this study was the analytical and clinical evaluation of the novel Presage (TM) ST2 assay for the determination of sST2 in human plasma.
Methods: We evaluated precision and linearity of the assay, analyte stability, and biological variability, determined reference values, performed a method comparison with an established ELISA and quantified sST2 concentrations in various diseases.
Results: Within-run and total coefficients of variation were <2.5% and <4.0%. The method was linear across the whole measurement range of the assay. The analyte was stable for 48 h at room temperature, for 7 days at 4 degrees C, and for at least 2 months at -20 degrees C and -80 degrees C. The reference change value for healthy individuals was 30%. Age-independent reference values were 3-28 U/mL in males, and 2-16 U/mL in females. The method comparison revealed a high proportional bias. sST2 plasma concentrations were increased modestly in heart failure and moderately in pneumonia and chronic obstructive pulmonary disease. Patients with sepsis exhibited highly elevated sST2 values. In patients with chronic renal disease, however, there was no difference compared to healthy individuals.
Conclusion: The Presage (TM) ST2 assay meets the needs of quality specifications of laboratory medicine. The results of the clinical assay evaluation are novel with respect to sST2 in various diseases and should initiate further studies. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Dieplinger, Benjamin; Steinmair, Martin; Haltmayer, Meinhard; Mueller, Thomas] Konventhosp Barmherzige Brueder, Dept Lab Med, A-4020 Linz, Austria.
[Januzzi, James L., Jr.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Januzzi, James L., Jr.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Gabriel, Christian] Red Cross Transfus Serv Upper Austria, Linz, Austria.
[Poelz, Werner] Univ Linz, Inst Appl Syst Sci & Stat, A-4040 Linz, Austria.
RP Mueller, T (reprint author), Konventhosp Barmherzige Brueder, Dept Lab Med, Seilerstaette 2-A, A-4020 Linz, Austria.
EM thomas.mueller@bs-lab.at
RI Gabriel, Christian/A-1689-2014
OI Gabriel, Christian/0000-0003-2043-9320
FU Abbott Diagnostics; B.R.A.H.M.S AG; Roche Diagnostics; Presage(TM)
FX Funding: Critical Diagnostics, holder of the license for ST2 cardiac
testing, provided reagents for sST2 measurements with the Presage (TM)
ST2 assay and the MBL assay free of charge. The company did not play a
role in (1) the design of the study; (2) data collection, analysis and
interpretation; and (3) preparation of the manuscript.
NR 32
TC 101
Z9 106
U1 2
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0009-8981
J9 CLIN CHIM ACTA
JI Clin. Chim. Acta
PD NOV 3
PY 2009
VL 409
IS 1-2
BP 33
EP 40
DI 10.1016/j.cca.2009.08.010
PG 8
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 516SS
UT WOS:000271563600007
PM 19699192
ER
PT J
AU Maherali, N
Hochedlinger, K
AF Maherali, Nimet
Hochedlinger, Konrad
TI Tgf beta Signal Inhibition Cooperates in the Induction of iPSCs and
Replaces Sox2 and cMyc
SO CURRENT BIOLOGY
LA English
DT Article
ID PLURIPOTENT STEM-CELLS; HUMAN FIBROBLASTS; SOMATIC-CELLS;
DIFFERENTIATION; GENERATION; MOUSE; EXPRESSION; SYSTEM; OCT4
AB Ectopic expression of 004, Sox2, cMyc, and Klf4 confers a pluripotent state upon several differentiated cell types, generating induced pluripotent stem cells (IPSCs) [1-8]. iPSC derivation is highly inefficient, and the underlying mechanisms are largely unknown. This low efficiency suggests the existence of additional cooperative factors whose identification is critical for understanding reprogramming. In addition, the therapeutic use of iPSCs relies on the development of efficient nongenetic means of factor delivery, and although a handful of replacement molecules have been identified, their use yields a further reduction to the already low reprogramming efficiency [9-11]. Thus, the identification of compounds that enhance rather than solely replace the function of the reprogramming factors will be of great use. Here, we demonstrate that inhibition of Tgfb beta signaling cooperates in the reprogramming of murine fibroblasts by enabling faster, more efficient induction of iPSCs, whereas activation of Tgf beta signaling blocks reprogramming. In addition to exhibiting a strong cooperative effect, the Tgf beta receptor inhibitor bypasses the requirement for exogenous cMyc or Sox2, highlighting its dual role as a cooperative and replacement factor. The identification of a highly characterized pathway operating in iPSC induction will open new avenues for mechanistic dissection of the reprogramming process.
C1 [Maherali, Nimet; Hochedlinger, Konrad] Massachusetts Gen Hosp, Ctr Regenerat Med, Harvard Stem Cell Inst, Boston, MA 02114 USA.
[Maherali, Nimet; Hochedlinger, Konrad] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Maherali, Nimet] Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA.
[Maherali, Nimet; Hochedlinger, Konrad] Dept Stem Cell & Regenerat Biol, Boston, MA 02114 USA.
RP Hochedlinger, K (reprint author), Massachusetts Gen Hosp, Ctr Regenerat Med, Harvard Stem Cell Inst, 185 Cambridge St, Boston, MA 02114 USA.
EM khochedlinger@helix.mgh.harvard.edu
FU Natural Sciences and Engineering Research Council of Canada; Alberta
Scholarships Program; National Institutes of Health Director's Innovator
Award; Harvard Stem Cell Institute; Massachusetts General Hospital
FX We thank Matthias Stadtfeld for the pilot experiments that led to
conception of the study, as well as insightful discussion and critical
reading of the manuscript; we also thank Jose Polo for insightful
discussion. N.M. is supported by a graduate scholarship from the Natural
Sciences and Engineering Research Council of Canada and a Sir James
Lougheed Award from the Alberta Scholarships Program. K.H. is supported
by a National Institutes of Health Director's Innovator Award, the
Harvard Stem Cell Institute, and Massachusetts General Hospital.
NR 24
TC 197
Z9 203
U1 4
U2 13
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
J9 CURR BIOL
JI Curr. Biol.
PD NOV 3
PY 2009
VL 19
IS 20
BP 1718
EP 1723
DI 10.1016/j.cub.2009.08.025
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 515UM
UT WOS:000271498400027
PM 19765992
ER
PT J
AU Jaffer, FA
AF Jaffer, Farouc A.
TI Assessing Niacin as an Atherosclerosis Therapeutic Agent Valuable
Insights Provided by High-Resolution Vascular Magnetic Resonance Imaging
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Editorial Material
DE niacin; atherosclerosis; magnetic resonance imaging; high-density
lipoprotein; carotid
ID EXTENDED-RELEASE NIACIN; SIMVASTATIN; COMBINATION; PREVENTION; DISEASE;
MRI
C1 [Jaffer, Farouc A.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Jaffer, Farouc A.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP Jaffer, FA (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, Simches Res Bldg,Room 3206,185 Cambridge St, Boston, MA 02114 USA.
EM fjaffer@mgh.harvard.edu
OI Jaffer, Farouc/0000-0001-7980-384X
NR 15
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
EI 1558-3597
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 3
PY 2009
VL 54
IS 19
BP 1795
EP 1796
DI 10.1016/j.jacc.2009.07.026
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 512OO
UT WOS:000271259700007
PM 19874993
ER
PT J
AU Liao, SL
Luthra, M
Rogers, KM
AF Liao, Steve L.
Luthra, Munish
Rogers, Kevin M.
TI Leriche Syndrome
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Editorial Material
C1 [Liao, Steve L.; Luthra, Munish] James J Peters Vet Affairs Med Ctr, Dept Med, Bronx, NY USA.
[Rogers, Kevin M.] James J Peters Vet Affairs Med Ctr, Dept Radiol, Bronx, NY USA.
[Liao, Steve L.] Mt Sinai Sch Med, Dept Med Cardiol, New York, NY USA.
RP Liao, SL (reprint author), James J Peters Vet Affairs Med Ctr, Dept Med, Bronx, NY USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 3
PY 2009
VL 54
IS 19
BP E11
EP E11
DI 10.1016/j.jacc.2009.06.037
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 512OO
UT WOS:000271259700013
PM 19874987
ER
PT J
AU Uc, EY
McDermott, MP
Marder, KS
Anderson, SW
Litvan, I
Como, PG
Auinger, P
Chou, KL
Growdon, JC
AF Uc, E. Y.
McDermott, M. P.
Marder, K. S.
Anderson, S. W.
Litvan, I.
Como, P. G.
Auinger, P.
Chou, K. L.
Growdon, J. C.
CA Parkinson Study Grp DATATOP Invest
TI Incidence of and risk factors for cognitive impairment in an early
Parkinson disease clinical trial cohort
SO NEUROLOGY
LA English
DT Article
ID MENTAL-STATE-EXAMINATION; RATING-SCALE; DEMENTIA; LEVODOPA; DEPRENYL;
DYSFUNCTION; PROGRESSION; DISABILITY; TOCOPHEROL; MULTICENTER
AB Objective: To investigate the incidence of and risk factors for cognitive impairment in a large, well-defined clinical trial cohort of patients with early Parkinson disease (PD).
Methods: The Mini-Mental State Examination (MMSE) was administered periodically over a median follow-up period of 6.5 years to participants in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism trial and its extension studies. Cognitive impairment was defined as scoring 2 standard deviations below age-and education-adjusted MMSE norms.
Results: Cumulative incidence of cognitive impairment in the 740 participants with clinically confirmed PD (baseline age 61.0 +/- 9.6 years, Hoehn-Yahr stage 1-2.5) was 2.4% (95% confidence interval: 1.2%-3.5%) at 2 years and 5.8% (3.7%-7.7%) at 5 years. Subjects who developed cognitive impairment (n = 46) showed significant progressive decline on neuropsychological tests measuring verbal learning and memory, visuospatial working memory, visuomotor speed, and attention, while the performance of the nonimpaired subjects (n = 694) stayed stable. Cognitive impairment was associated with older age, hallucinations, male gender, increased symmetry of parkinsonism, increased severity of motor impairment (except for tremor), speech and swallowing impairments, dexterity loss, and presence of gastroenterologic/urologic disorders at baseline.
Conclusions: The relatively low incidence of cognitive impairment in the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism study may reflect recruitment bias inherent to clinical trial volunteers (e.g., younger age) or limitations of the Mini-Mental State Examination-based criterion. Besides confirming known risk factors for cognitive impairment, we identified potentially novel predictors such as bulbar dysfunction and gastroenterologic/urologic disorders (suggestive of autonomic dysfunction) early in the course of the disease. Neurology (R) 2009;73:1469-1477
C1 [Uc, E. Y.] Univ Iowa, Dept Neurol, Carver Coll Med, Iowa City, IA 52242 USA.
[Uc, E. Y.] Vet Affairs Med Ctr, Neurol Serv, Iowa City, IA 52242 USA.
[McDermott, M. P.] Univ Rochester, Dept Biostat & Computat Biol, Rochester, NY USA.
[McDermott, M. P.; Como, P. G.; Auinger, P.] Univ Rochester, Dept Neurol, Rochester, NY USA.
[Marder, K. S.] Columbia Univ, Dept Neurol, New York, NY USA.
[Litvan, I.] Univ Louisville, Dept Neurol, Louisville, KY 40292 USA.
[Chou, K. L.] Univ Michigan, Dept Neurol, Ann Arbor, MI USA.
[Growdon, J. C.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
RP Uc, EY (reprint author), Univ Iowa, Dept Neurol, Carver Coll Med, 200 Hawkins Dr 2RCP, Iowa City, IA 52242 USA.
EM ergun-uc@uiowa.edu
OI Chou, Kelvin/0000-0002-2597-7315; Litvan, Irene/0000-0002-3485-3445
FU Parkinson's Disease Foundation; US Public Health Service (National
Institute of Neurological Disorders and Stroke) [NS 24778]; Parkinson
Study Group; NIH [NINDS NS044930, NS42372, HD44430, DE16280, NS52619,
NS45686, NS46487, NS50095, NS49639, AR52274, NS50573, HL80107, RR24160,
NS58259, NS48843, NS36630, 1UL1 RR024156-01, PO412196-G, NIA 5 R01
PAS-03-092, 1 R13 NS062643-01, NINDS NPTUNE (Site PI)]; US Department of
Veterans Affairs [B6261R, 1 I01 RX000170]; Parkinson Disease Foundation;
Medivation, Inc.; Boehringer Ingelheim; NeuroSearch Sweden AB; Forest
Laboratories, Inc.; US Food and Drug Administration; Michael J. Fox
Foundation; Spinal Muscular Atrophy Foundation; Muscular Dystrophy
Association; Amarin Corporation; Huntington's Disease Society of
America; Kyowa Hakko Kirin Pharma, Inc.; University of Louisville;
Center for Environmental Genomics and Integrative Biology; Parkinson
Support Center of Kentuckiana; National Parkinson Foundation; Movement
Disorder Society; CurePSP
FX Growdon serves on a scientific advisory board for Neuroimmune
Therapeutics AG; serves on editorial boards for Archives of Neurology
and Neurodegenerative Diseases; receives royalties from publishing The
Dementias (Elsevier, 2007); and receives reserch support from the NIH
[NIA P50 AG05134 (Co-PI), NINDS P50 NS037372 (Co-PI), and NINDS R21
NS60310 (PI)] and from the Michael J. Fox Foundation.
NR 40
TC 69
Z9 71
U1 3
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD NOV 3
PY 2009
VL 73
IS 18
BP 1469
EP 1477
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 514XN
UT WOS:000271429900008
PM 19884574
ER
PT J
AU Gerstner, ER
Yip, S
Wang, DL
Louis, DN
Iafrate, AJ
Batchelor, TT
AF Gerstner, E. R.
Yip, S.
Wang, D. L.
Louis, D. N.
Iafrate, A. J.
Batchelor, T. T.
TI MGMT METHYLATION IS A PROGNOSTIC BIOMARKER IN ELDERLY PATIENTS WITH
NEWLY DIAGNOSED GLIOBLASTOMA
SO NEUROLOGY
LA English
DT Editorial Material
ID METHYLTRANSFERASE; TEMOZOLOMIDE; CELLS
C1 [Gerstner, E. R.; Wang, D. L.; Batchelor, T. T.] Massachusetts Gen Hosp, Ctr Canc, Dept Neurol, Boston, MA 02114 USA.
[Batchelor, T. T.] Massachusetts Gen Hosp, Ctr Canc, Dept Radiat Oncol, Boston, MA 02114 USA.
[Yip, S.; Louis, D. N.; Iafrate, A. J.] Massachusetts Gen Hosp, Ctr Canc, Dept Pathol, Boston, MA 02114 USA.
[Gerstner, E. R.; Batchelor, T. T.] Massachusetts Gen Hosp, Ctr Canc, Div Hematol & Oncol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Gerstner, ER (reprint author), Massachusetts Gen Hosp, Stephen E & Catherine Pappas Ctr Neurooncol, 55 Fruit St,Yawkey 9E, Boston, MA 02114 USA.
EM egerstner@partners.org
FU NCI NIH HHS [R01CA57683]
NR 6
TC 48
Z9 49
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD NOV 3
PY 2009
VL 73
IS 18
BP 1509
EP 1510
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 514XN
UT WOS:000271429900014
PM 19884580
ER
PT J
AU Lefkimmiatis, K
Moyer, MP
Curci, S
Hofer, AM
AF Lefkimmiatis, Konstantinos
Moyer, Mary Pat
Curci, Silvana
Hofer, Aldebaran M.
TI "cAMP Sponge": A Buffer for Cyclic Adenosine 3 ', 5 '-Monophosphate
SO PLOS ONE
LA English
DT Article
ID DEPENDENT PROTEIN-KINASE; CELLS; EPAC; PHOSPHORYLATION; COMMUNICATION;
INHIBITION; ACTIVATION; INDICATORS; DYNAMICS; CHANNELS
AB Background: While intracellular buffers are widely used to study calcium signaling, no such tool exists for the other major second messenger, cyclic AMP (cAMP).
Methods/Principal Findings: Here we describe a genetically encoded buffer for cAMP based on the high-affinity cAMP-binding carboxy-terminus of the regulatory subunit RI beta of protein kinase A (PKA). Addition of targeting sequences permitted localization of this fragment to the extra-nuclear compartment, while tagging with mCherry allowed quantification of its expression at the single cell level. This construct (named "cAMP sponge") was shown to selectively bind cAMP in vitro. Its expression significantly suppressed agonist-induced cAMP signals and the downstream activation of PKA within the cytosol as measured by FRET-based sensors in single living cells. Point mutations in the cAMP-binding domains of the construct rendered the chimera unable to bind cAMP in vitro or in situ. Cyclic AMP sponge was fruitfully applied to examine feedback regulation of gap junction-mediated transfer of cAMP in epithelial cell couplets.
Conclusions: This newest member of the cAMP toolbox has the potential to reveal unique biological functions of cAMP, including insight into the functional significance of compartmentalized signaling events.
RP Lefkimmiatis, K (reprint author), Brigham & Womens Hosp, VA Boston Healthcare Syst, W Roxbury, MA USA.
EM ahofer@rics.bwh.harvard.edu
RI Lefkimmiatis, Konstantinos/I-1239-2016
OI Lefkimmiatis, Konstantinos/0000-0001-7137-7866
NR 32
TC 12
Z9 12
U1 1
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 3
PY 2009
VL 4
IS 11
AR e7649
DI 10.1371/journal.pone.0007649
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 514RY
UT WOS:000271414500001
PM 19888343
ER
PT J
AU Lee, S
Verdine, GL
AF Lee, Seongmin
Verdine, Gregory L.
TI Atomic substitution reveals the structural basis for substrate adenine
recognition and removal by adenine DNA glycosylase
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE base-excision repair; general acid catalysis; substrate recognition
ID MISMATCH REPAIR ENZYME; ESCHERICHIA-COLI DNA; C-TERMINAL DOMAIN;
EXCISION-REPAIR; CRYSTAL-STRUCTURES; DUPLEX DNA; MUTY; 8-OXOGUANINE;
BASES; SPECIFICITY
AB Adenine DNA glycosylase catalyzes the glycolytic removal of adenine from the promutagenic A.oxoG base pair in DNA. The general features of DNA recognition by an adenine DNA glycosylase, Bacillus stearothermophilus MutY, have previously been revealed via the X-ray structure of a catalytically inactive mutant protein bound to an A: oxoG-containing DNA duplex. Although the structure revealed the substrate adenine to be, as expected, extruded from the DNA helix and inserted into an extrahelical active site pocket on the enzyme, the substrate adenine engaged in no direct contacts with active site residues. This feature was paradoxical, because other glycosylases have been observed to engage their substrates primarily through direct contacts. The lack of direct contacts in the case of MutY suggested that either MutY uses a distinctive logic for substrate recognition or that the X-ray structure had captured a noncatalytically competent state in lesion recognition. To gain further insight into this issue, we crystallized wild-type MutY bound to DNA containing a catalytically inactive analog of 2'-deoxyadenosine in which a single 2'-H atom was replaced by fluorine. The structure of this fluorinated lesion-recognition complex (FLRC) reveals the substrate adenine buried more deeply into the active site pocket than in the prior structure and now engaged in multiple direct hydrogen bonding and hydrophobic interactions. This structure appears to capture the catalytically competent state of adenine DNA glycosylases, and it suggests a catalytic mechanism for this class of enzymes, one in which general acid-catalyzed protonation of the nucleobase promotes glycosidic bond cleavage.
C1 [Lee, Seongmin; Verdine, Gregory L.] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
[Verdine, Gregory L.] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
[Verdine, Gregory L.] Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA.
[Verdine, Gregory L.] Dana Farber Canc Inst, Program Canc Chem Biol, Boston, MA 02115 USA.
RP Verdine, GL (reprint author), Harvard Univ, Dept Stem Cell & Regenerat Biol, 12 Oxford St, Cambridge, MA 02138 USA.
EM gregory_verdine@harvard.edu
FU NCI NIH HHS [CA100742, R01 CA100742]
NR 45
TC 37
Z9 39
U1 1
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 3
PY 2009
VL 106
IS 44
BP 18497
EP 18502
DI 10.1073/pnas.0902908106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 514XM
UT WOS:000271429800018
PM 19841264
ER
PT J
AU Rioux, JD
Goyette, P
Vyse, TJ
Hammarstrom, L
Fernando, MMA
Green, T
De Jager, PL
Foisy, S
Wang, J
de Bakker, PIW
Leslie, S
McVean, G
Padyukov, L
Alfredsson, L
Annese, V
Hafler, DA
Pan-Hammarstrom, Q
Matell, R
Sawcer, SJ
Compston, AD
Cree, BAC
Mirel, DB
Daly, MJ
Behrens, TW
Klareskog, L
Gregersen, PK
Oksenberg, JR
Hauser, SL
AF Rioux, John D.
Goyette, Philippe
Vyse, Timothy J.
Hammarstroem, Lennart
Fernando, Michelle M. A.
Green, Todd
De Jager, Philip L.
Foisy, Sylvain
Wang, Joanne
de Bakker, Paul I. W.
Leslie, Stephen
McVean, Gilean
Padyukov, Leonid
Alfredsson, Lars
Annese, Vito
Hafler, David A.
Pan-Hammarstroem, Qiang
Matell, Ritva
Sawcer, Stephen J.
Compston, Alastair D.
Cree, Bruce A. C.
Mirel, Daniel B.
Daly, Mark J.
Behrens, Tim W.
Klareskog, Lars
Gregersen, Peter K.
Oksenberg, Jorge R.
Hauser, Stephen L.
CA Int MHC Autoimmunity Genetics Netw
TI Mapping of multiple susceptibility variants within the MHC region for 7
immune-mediated diseases
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE autoimmunity; genes; genetics
ID MAJOR HISTOCOMPATIBILITY COMPLEX; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
GENOME-WIDE ASSOCIATION; INFLAMMATORY-BOWEL-DISEASE; SELECTIVE IGA
DEFICIENCY; CLASS-II REGION; RHEUMATOID-ARTHRITIS;
LINKAGE-DISEQUILIBRIUM; ULCERATIVE-COLITIS; MYASTHENIA-GRAVIS
AB The human MHC represents the strongest susceptibility locus for autoimmune diseases. However, the identification of the true predisposing gene(s) has been handicapped by the strong linkage disequilibrium across the region. Furthermore, most studies to date have been limited to the examination of a subset of the HLA and non-HLA genes with a marker density and sample size insufficient for mapping all independent association signals. We genotyped a panel of 1,472 SNPs to capture the common genomic variation across the 3.44 megabase (Mb) classic MHC region in 10,576 DNA samples derived from patients with systemic lupus erythematosus, Crohn's disease, ulcerative colitis, rheumatoid arthritis, myasthenia gravis, selective IgA deficiency, multiple sclerosis, and appropriate control samples. We identified the primary association signals for each disease and performed conditional regression to identify independent secondary signals. The data demonstrate that MHC associations with autoimmune diseases result from complex, multilocus effects that span the entire region.
C1 [Rioux, John D.; Goyette, Philippe; Foisy, Sylvain] Univ Montreal, Res Ctr, Montreal, PQ H1T 1C8, Canada.
[Rioux, John D.; Goyette, Philippe; Foisy, Sylvain] Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada.
[Vyse, Timothy J.; Fernando, Michelle M. A.] Hammersmith Hosp, Div Med, Rheumatol Sect, London W12 0NN, England.
[Vyse, Timothy J.; Fernando, Michelle M. A.] Univ London Imperial Coll Sci Technol & Med, London W12 0NN, England.
[Hammarstroem, Lennart; Pan-Hammarstroem, Qiang] Karolinska Inst, Div Clin Immunol, SE-14186 Huddinge, Sweden.
[Green, Todd; De Jager, Philip L.; Mirel, Daniel B.] Broad Inst, External Projects, Program Med & Populat Genet, Cambridge, MA 02142 USA.
[De Jager, Philip L.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Neurol,Program Translat Neuropsychiat Genom, Boston, MA 02115 USA.
[de Bakker, Paul I. W.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Div Genet, Boston, MA 02115 USA.
[Wang, Joanne; Cree, Bruce A. C.; Oksenberg, Jorge R.; Hauser, Stephen L.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
[Leslie, Stephen; McVean, Gilean] Univ Oxford, Dept Stat, Oxford OX1 3TG, England.
[Padyukov, Leonid] Karolinska Inst, Dept Med, Rheumatol Unit, S-17176 Stockholm, Sweden.
[Alfredsson, Lars] Karolinska Inst, Inst Environm Med, Cardiovasc Epidemiol Unit, SE-17177 Solna, Sweden.
[Annese, Vito] IRCCS CSS Hosp, Dept Med Sci, Ist Ricovero & Cura Carattere Sci Endoscopy & IBD, I-71013 San Giovanni Rotondo, Italy.
[Hafler, David A.] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06520 USA.
[Matell, Ritva] Karolinska Univ Hosp Solna, Dept Neurol, SE-17176 Stockholm, Sweden.
[Sawcer, Stephen J.; Compston, Alastair D.] Univ Cambridge, Addenbrookes Hosp, Dept Clin Neurosci, Cambridge CB2 2QQ, England.
[Daly, Mark J.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Behrens, Tim W.] Genentech Inc, Exploratory Clin Dev Immunol Tissue Growth & Repa, San Francisco, CA 94080 USA.
[Klareskog, Lars] Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, SE-17177 Solna, Sweden.
[Gregersen, Peter K.] N Shore Univ Hosp, Feinstein Inst Med Res, Robert S Boas Ctr Genom & Human Genet, Manhasset, NY 11030 USA.
RP Rioux, JD (reprint author), Univ Montreal, Res Ctr, Montreal, PQ H1T 1C8, Canada.
EM john.david.rioux@umontreal.ca; hausers@neurology.ucsf.edu
RI Fernando, Michelle/F-5554-2012; de Bakker, Paul/B-8730-2009; Rioux,
John/A-9599-2015; Hauser, Stephen/J-2978-2016;
OI de Bakker, Paul/0000-0001-7735-7858; Rioux, John/0000-0001-7560-8326;
Alfredsson, Lars/0000-0003-1688-6697; Klareskog,
Lars/0000-0001-9601-6186; Padyukov, Leonid/0000-0003-2950-5670
FU National Institutes of Allergy and Infectious Diseases [AI067152];
National Institute of Diabetes and Digestive and Kidney Diseases
[DK064869, DK062432]; National Institute of Neurological Disease and
Stroke [NS21799]; Swedish National Research Counci; Medical Research
Council [G0000934]; Wellcome Trust [068545/Z/02]; National Center for
Research Resources [U54 RR020278]
FX This work was supported primarily by Grant AI067152 from the National
Institutes of Allergy and Infectious Diseases. Additional support was
supplied by Grants DK064869 and DK062432 from the National Institute of
Diabetes and Digestive and Kidney Diseases (to J.D.R.), by Grant NS21799
from the National Institute of Neurological Disease and Stroke (to
SLH.), and by the Swedish National Research Council. We also thank the
disease-specific societies and foundations for support in DNA
collections. We acknowledge the use of DNA from the British 1958 Birth
Cohort collection (D. Strachan, S. Ring, W. McArdle, and M. Pembrey),
funded by the Medical Research Council Grant G0000934 and Wellcome Trust
Grant 068545/Z/02. The Broad Institute Center for Genotyping and
Analysis is supported by Grant U54 RR020278 from the National Center for
Research Resources.
NR 61
TC 122
Z9 127
U1 3
U2 14
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 3
PY 2009
VL 106
IS 44
BP 18680
EP 18685
DI 10.1073/pnas.0909307106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 514XM
UT WOS:000271429800049
ER
PT J
AU Siegrist, MS
Unnikrishnan, M
McConnell, MJ
Borowsky, M
Cheng, TY
Siddiqi, N
Fortune, SM
Moody, DB
Rubin, EJ
AF Siegrist, M. Sloan
Unnikrishnan, Meera
McConnell, Matthew J.
Borowsky, Mark
Cheng, Tan-Yun
Siddiqi, Noman
Fortune, Sarah M.
Moody, D. Branch
Rubin, Eric J.
TI Mycobacterial Esx-3 is required for mycobactin-mediated iron acquisition
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE secretion; siderophore
ID GENE-EXPRESSION; PATHOGENIC MYCOBACTERIA; SECRETION SYSTEM;
CALMETTE-GUERIN; DNA TRANSFER; TUBERCULOSIS; VIRULENCE; SMEGMATIS;
SIDEROPHORE; RD1
AB The Esx secretion pathway is conserved across Gram-positive bacteria. Esx-1, the best-characterized system, is required for virulence of Mycobacterium tuberculosis, although its precise function during infection remains unclear. Esx-3, a paralogous system present in all mycobacterial species, is required for growth in vitro. Here, we demonstrate that mycobacteria lacking Esx-3 are defective in acquiring iron. To compete for the limited iron available in the host and the environment, these organisms use mycobactin, high-affinity iron-binding molecules. In the absence of Esx-3, mycobacteria synthesize mycobactin but are unable to use the bound iron and are impaired severely for growth during macrophage infection. Mycobacteria thus require a specialized secretion system for acquiring iron from siderophores.
C1 [Siegrist, M. Sloan; Unnikrishnan, Meera; Siddiqi, Noman; Fortune, Sarah M.; Rubin, Eric J.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[McConnell, Matthew J.; Cheng, Tan-Yun; Moody, D. Branch] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy,Dept Med, Boston, MA 02115 USA.
[Borowsky, Mark] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
RP Rubin, EJ (reprint author), Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, 665 Huntington Ave, Boston, MA 02115 USA.
EM erubin@hsph.harvard.edu
OI Rubin, Eric/0000-0001-5120-962X
FU Burroughs Wellcome Fund; National Institutes of Health Grants [R01
AI48704, R0171155]
FX We gratefully acknowledge Dr. Colin Ratledge for helpful advice and for
providing ferri-mycobactin S and ferri-carboxymycobactin S. We also
thank Dr. Alfred Goldberg for providing the anti-ClpP1P2 antibody. This
work was supported by the Burroughs Wellcome Fund and the National
Institutes of Health Grants R01 AI48704 and R0171155.
NR 45
TC 113
Z9 123
U1 2
U2 11
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 3
PY 2009
VL 106
IS 44
BP 18792
EP 18797
DI 10.1073/pnas.0900589106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 514XM
UT WOS:000271429800068
PM 19846780
ER
PT J
AU Brunelle, JK
Ryan, J
Yecies, D
Opferman, JT
Letai, A
AF Brunelle, Joslyn K.
Ryan, Jeremy
Yecies, Derek
Opferman, Joseph T.
Letai, Anthony
TI MCL-1-dependent leukemia cells are more sensitive to chemotherapy than
BCL-2-dependent counterparts
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID MYC-INDUCED LYMPHOMAGENESIS; C-MYC; TRANSGENIC MICE; BH3 DOMAINS;
MEMBRANE PERMEABILIZATION; MITOCHONDRIAL APOPTOSIS; ANTIAPOPTOTIC BCL-2;
ANTAGONIST ABT-737; BH3-ONLY PROTEINS; IN-VIVO
AB Myeloid cell leukemia sequence 1 (MCL-1) and B cell leukemia/lymphoma 2 (BCL-2) are antiapoptotic proteins in the BCL-2 protein family often expressed in cancer. To compare the function of MCL-1 and BCL-2 in maintaining cancer survival, we constructed complementary mouse leukemia models based on E(mu)-Myc expression in which either BCL-2 or MCL-1 are required for leukemia maintenance. We show that the principal anti-apoptotic mechanism of both BCL-2 and MCL- 1 in these leukemias is to sequester pro-death BH3-only proteins rather than BAX and BAK. We find that the MCL-1-dependent leukemias are more sensitive to a wide range of chemotherapeutic agents acting by disparate mechanisms. In common across these varied treatments is that MCL-1 protein levels rapidly decrease in a proteosome-dependent fashion, whereas those of BCL-2 are stable. We demonstrate for the first time that two anti-apoptotic proteins can enable tumorigenesis equally well, but nonetheless differ in their influence on chemosensitivity.
C1 [Brunelle, Joslyn K.; Ryan, Jeremy; Yecies, Derek; Letai, Anthony] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02052 USA.
[Opferman, Joseph T.] St Jude Childrens Hosp, Dept Biochem, Memphis, TN 38105 USA.
RP Letai, A (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02052 USA.
EM Anthony_Letai@dfci.harvard.edu
FU National Institutes of Health [P01 CA068484, U01 CA105423, R01 CA129974]
FX The authors gratefully acknowledge financial support from National
Institutes of Health grants P01 CA068484, U01 CA105423, and R01
CA129974. A. Letai is a Leukemia and Lymphoma Society Scholar. A. Letai
is inventor on a patent application regarding BH3 profiling. A. Letai is
a founder and head of the scientific advisory board for Eutropics
Pharmaceuticals.
NR 38
TC 44
Z9 44
U1 0
U2 2
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
J9 J CELL BIOL
JI J. Cell Biol.
PD NOV 2
PY 2009
VL 187
IS 3
BP 429
EP 442
DI 10.1083/jcb.200904049
PG 14
WC Cell Biology
SC Cell Biology
GA 514DJ
UT WOS:000271374200013
PM 19948485
ER
PT J
AU Khan, AM
Janneck, LM
Bhatt, J
Panjabi, R
Marjoua, Y
Bharwani, A
AF Khan, Ali M.
Janneck, Laura M.
Bhatt, Jay
Panjabi, Rajesh
Marjoua, Youssra
Bharwani, Aleem
TI Building a Health-Peace Movement: Academic Medicine's Role in Generating
Solutions to Global Problems
SO ACADEMIC MEDICINE
LA English
DT Editorial Material
C1 [Khan, Ali M.] Virginia Commonwealth Univ, Off Student Affairs, Sch Med, Richmond, VA 23298 USA.
[Khan, Ali M.; Marjoua, Youssra; Bharwani, Aleem] Harvard Kennedy Sch, Cambridge, MA USA.
[Janneck, Laura M.] Case Western Reserve Univ, Sch Med, Cleveland, OH USA.
[Janneck, Laura M.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Bhatt, Jay; Panjabi, Rajesh] Harvard Univ, Sch Med, Boston, MA USA.
[Bhatt, Jay] Cambridge Hlth Alliance, Cambridge, MA USA.
[Panjabi, Rajesh] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Marjoua, Youssra] Yale Univ, Sch Med, New Haven, CT USA.
[Bharwani, Aleem] Univ Calgary, Dept Med, Calgary, AB, Canada.
RP Khan, AM (reprint author), Virginia Commonwealth Univ, Off Student Affairs, Sch Med, 1101 E Marshall St, Richmond, VA 23298 USA.
EM khanam@vcu.edu
NR 3
TC 3
Z9 3
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD NOV
PY 2009
VL 84
IS 11
BP 1486
EP 1486
DI 10.1097/ACM.0b013e3181bab2bf
PG 1
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA V15EV
UT WOS:000207786200013
PM 19858797
ER
PT J
AU Schlozman, SC
AF Schlozman, Steven C.
TI Using a Socratic Dialogue to Tackle Thorny Issues of Psychiatry
SO ACADEMIC MEDICINE
LA English
DT Article
AB Medical students often experience significant cognitive dissonance as they attempt to understand psychiatry. After the security of lab values and medical tests that characterize much of medical practice, the ambiguity of seemingly subjectively obtained information characteristic of psychiatry often leaves students somewhat uncomfortable with how psychiatric diagnoses are made and understood. This is, at its root, an issue of epistemology: How do we know what we say we know? Psychiatry can seem "fuzzy" to medical students, and it behooves psychiatry educators to explicitly address this discomfort but, at the same time, not apologize for the differences between psychiatry and "the rest of medicine." In this article, the author strives to emphasize that this kind of epistemological challenge is ancient and esteemed, represented to some extent in the writings of Plato (who believed that we measure the world by comparing our experience with our innate sense of what we know is true) and Aristotle (who insisted that what we know is based largely on what we can measurably experience). Using humor, an imagined conversation among these ancient philosophers and a modern psychiatrist-medical educator might help to dispel some of the discomfort that psychiatry education sometimes engenders among future physicians. The author presents an example of such a conversation. After a brief discussion of the epistemological differences characteristic of Platonic and Aristotelian views, students could be shown a script similar to the example script and then asked to discuss and debate the arguments elucidated. Perhaps even better, students could be asked to write their own debates based on how Plato or Aristotle would be expected to behave.
C1 [Schlozman, Steven C.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Schlozman, Steven C.] Harvard Univ, Sch Med, Boston, MA USA.
[Schlozman, Steven C.] MGH Hosp, Boston, MA USA.
[Schlozman, Steven C.] McLean Hosp, Boston, MA USA.
[Schlozman, Steven C.] Harvard Univ, Grad Sch Educ, Boston, MA 02115 USA.
RP Schlozman, SC (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Yawkey 6900,55 Fruit St, Boston, MA 02114 USA.
EM Sschlozman@partners.org
NR 24
TC 1
Z9 1
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD NOV
PY 2009
VL 84
IS 11
BP 1562
EP 1566
DI 10.1097/ACM.0b013e3181bb2593
PG 5
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA V15EV
UT WOS:000207786200033
PM 19858818
ER
PT J
AU Schlozman, SC
AF Schlozman, Steven C.
TI Using a Socratic Dialogue to Tackle Thorny Issues of Psychiatry
SO ACADEMIC MEDICINE
LA English
DT Article
AB Medical students often experience significant cognitive dissonance as they attempt to understand psychiatry. After the security of lab values and medical tests that characterize much of medical practice, the ambiguity of seemingly subjectively obtained information characteristic of psychiatry often leaves students somewhat uncomfortable with how psychiatric diagnoses are made and understood. This is, at its root, an issue of epistemology: How do we know what we say we know? Psychiatry can seem "fuzzy" to medical students, and it behooves psychiatry educators to explicitly address this discomfort but, at not apologize for the differences between psychiatry and "the rest of medicine." In this article, the author strives to emphasize that this kind of epistemological challenge is ancient and esteemed, represented to some extent in the writings of Plato (who believed that we measure the world by comparing our experience with our innate sense of what we know is true) and Aristotle (who insisted that what we know is based largely on what we can measurably experience). Using humor, an imagined conversation among these ancient philosophers and a modern psychiatrist-medical educator might help to dispel some of the discomfort that psychiatry education sometimes engenders among future physicians. The author presents an example of such a conversation. After a brief discussion of the epistemological differences characteristic of Platonic and Aristotelian views, students could be shown a script similar to the example script and then asked to discuss and debate the arguments elucidated. Perhaps even better, students could be asked to write their own debates based on how Plato or Aristotle would be expected to behave.
C1 [Schlozman, Steven C.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Schlozman, Steven C.] Harvard Univ, Sch Med, Boston, MA USA.
[Schlozman, Steven C.] MGH Hosp, Boston, MA USA.
[Schlozman, Steven C.] McLean Hosp, Boston, MA USA.
[Schlozman, Steven C.] Harvard Univ, Grad Sch Educ, Boston, MA 02115 USA.
RP Schlozman, SC (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Yawkey 6900,55 Fruit St, Boston, MA 02114 USA.
EM Sschlozman@partners.org
NR 24
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD NOV
PY 2009
VL 84
IS 11
PG 5
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA V15EV
UT WOS:000207786200034
ER
PT J
AU Abujudeh, HH
Kaewlai, R
Farsad, K
Orr, E
Gilman, M
Shepard, JAO
AF Abujudeh, Hani H.
Kaewlai, Rathachai
Farsad, Khashayar
Orr, Esther
Gilman, Matthew
Shepard, Jo-Anne O.
TI Computed Tomography Pulmonary Angiography: An Assessment of the
Radiology Report
SO ACADEMIC RADIOLOGY
LA English
DT Article
DE Quality of radiology report; limitations; computed tomographic pulmonary
angiography; pulmonary embolism
ID NEGATIVE SPIRAL CT; DIAGNOSTIC STRATEGY; CLINICAL-OUTCOMES;
THIN-COLLIMATION; PREDICTIVE VALUE; MULTISLICE CT; HELICAL CT; EMBOLISM;
OUTPATIENTS; MANAGEMENT
AB Rationale and Objective. The aim of this study was to evaluate the uncertainty in computed tomographic pulmonary angiography (CTPA) radiology reports, manifested by descriptions of report limitations and image quality.
Materials and Methods. CTPA reports between 2004 and 2006 were reviewed for patient demographic data (age, gender, pregnancy state), radiologist data (years of experience, subspecialty, final dictation by an attending radiologist vs a resident being present and dictating the report), the presence of pulmonary embolism (PE), and key words describing examination quality and limitations.
Results. There were 2151 CTPA reports. Patterns of reporting CTPA in the impression sections of radiology reports were as follows: (1) PE conclusively positive (10%), (2) PE conclusively negative (29%), (3) PE negative to segmental arteries (27%), (4) PE negative to central Pulmonary arteries (21%), (5) PE negative but suboptimal examination (8%), and (6) nondiagnostic examination (5%). Among the last three categories, seven PEs were not initially diagnosed but were found on subsequent imaging examinations. Limitations in image quality, respiratory motion artifact, and contrast enhancement were most frequently mentioned as limitations in image quality (62% and 28% of all reports, respectively). Radiologists tended to report limitations in image quality if they were thoracic radiology subspecialists, had >10 years of experience, or worked independently (P < .001).
Conclusion. Different patterns of reporting CTPA exist and vary on the basis of individual radiologists' subspecialties, experience, and whether they work independently or with residents. Certain wording regarding the presence of PE may falsely imply negativity of PE in a limited examination.
C1 [Abujudeh, Hani H.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Abujudeh, HH (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St, Boston, MA 02114 USA.
EM habujudeh@partners.org
NR 36
TC 8
Z9 8
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1076-6332
J9 ACAD RADIOL
JI Acad. Radiol.
PD NOV
PY 2009
VL 16
IS 11
BP 1309
EP 1315
DI 10.1016/j.acra.2009.06.012
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 513EA
UT WOS:000271304000002
PM 19692272
ER
PT J
AU Lee, JM
Halpern, EF
Rafferty, EA
Gazelle, GS
AF Lee, Janie M.
Halpern, Elkan F.
Rafferty, Elizabeth A.
Gazelle, G. Scott
TI Evaluating the Correlation between Film Mammography and MRI for
Screening Women with Increased Breast Cancer Risk
SO ACADEMIC RADIOLOGY
LA English
DT Article
DE Mammography; MRI; screening; technology assessment
ID HIGH FAMILIAL RISK; BRCA MUTATION CARRIERS; 2 DIAGNOSTIC-TESTS;
SURVEILLANCE; MASTECTOMY; ULTRASOUND
AB Rationale and Objectives. Breast magnetic resonance imaging (MRI) is increasingly being added to mammography for screening asymptomatic women at increased risk of breast cancer. Because the direction and extent of correlation between mammography and MRI could potentially result in over- or underestimation of the diagnostic gain related to using MRI as an adjunct to mammographic screening, we performed an analysis to evaluate the extent of correlation between mammography and MRI.
Materials and Methods. We reviewed the published literature to identify multimodality breast cancer screening studies reporting the sensitivity of mammography and MRi, alone and in combination, for breast cancer diagnosis. After calculating the expected sensitivity of combined mammography and MRI under conditions of test independence (no correlation), we compared the calculated and observed sensitivities for combined mammography and MRI. We then calculated correlation coefficients for mammography and MRI.
Results. Seven studies of multimodality screening in women at increased risk of developing breast cancer were included for analysis. Of these studies, the correlation between film mammography and MRI was positive in three studies, negative in two studies, and not identified in two studies. The calculated correlation coefficients ranged from -0.38 to 0.18. In six of seven studies, the 95% confidence interval for the correlation coefficient included 0.0, indicating no significant correlation.
Conclusions. Evidence from published trials of multimodality breast cancer screening identified no statistically significant correlation between film mammography and MRI. Using both tests for breast cancer screening is likely to improve the early detection of breast cancer in women at increased risk.
C1 [Lee, Janie M.; Halpern, Elkan F.; Rafferty, Elizabeth A.; Gazelle, G. Scott] Massachusetts Gen Hosp, Dept Radiol, Inst Technol Assessment, Boston, MA 02114 USA.
RP Lee, JM (reprint author), Massachusetts Gen Hosp, Dept Radiol, Inst Technol Assessment, 101 Merrimac St,10th Floor, Boston, MA 02114 USA.
EM jlee45@partners.org
FU National Cancer Institute [1K07CA128816]
FX Supported by grant funding from the National Cancer Institute (author
JML, 1K07CA128816). The authors thank Dr. Etta Pisano and Dr.
Constantine Gatsonis for their thoughtful comments on the draft
manuscript.
NR 24
TC 4
Z9 4
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1076-6332
J9 ACAD RADIOL
JI Acad. Radiol.
PD NOV
PY 2009
VL 16
IS 11
BP 1323
EP 1328
DI 10.1016/j.acra.2009.05.011
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 513EA
UT WOS:000271304000004
PM 19632865
ER
PT J
AU Nagata, K
Singh, AK
Sangwaiya, MJ
Nappi, J
Zalis, ME
Cai, WL
Yoshida, H
AF Nagata, Koichi
Singh, Anand Kumar
Sangwaiya, Minal Jagtiani
Naeppi, Janne
Zalis, Michael E.
Cai, Wenli
Yoshida, Hiroyuki
TI Comparative Evaluation of the Fecal-Tagging Quality in CT Colonography:
Barium vs. Iodinated Oral Contrast Agent
SO ACADEMIC RADIOLOGY
LA English
DT Article
DE Computed tomography; virtual colonoscopy; tagging; iodinated contrast;
barium
ID COMPUTED TOMOGRAPHIC COLONOGRAPHY; SMALL-BOWEL OBSTRUCTION; CONVENTIONAL
COLONOSCOPY; CATHARTIC PREPARATION; VIRTUAL COLONOSCOPY; PATIENT
ACCEPTANCE; PERFORMANCE; IOHEXOL; MEDIA; FEASIBILITY
AB Rationale and Objectives. The purpose of this evaluation was to compare the tagging quality of a barium-based regimen with that of iodine-based regimens for computed tomographic (CT) colonography.
Materials and Methods. Tagging quality was assessed retrospectively in three different types of fecal-tagging CT colonographic cases: 24 barium-based cases, 22 nonionic iodine-based cases, and 24 ionic iodine-based cases. For the purpose of evaluation, the large intestine was divided into six segments, and the tagging homogeneity of a total of 420 segments (70 patients) was graded by three blinded readers from 0 (heterogeneous) to 4 (homogeneous).
Results. For barium-based cases, the average score for the three readers was 2.4, whereas it was 3.4 for nonionic iodine and 3.6 for ionic iodine. The percentages of segments that were assigned scores of 4 (excellent tagging [100%]) were 11.6%, 61.9%, and 72.9% for the barium-based, nonionic iodine-based, and ionic iodine-based regimens, respectively. The homogeneity scores of iodine-based fecal-tagging regimens were significantly higher than those of the barium-based fecal-tagging regimen (P < .001). The CT attenuation values of tagging in the cases were also assessed: the minimum and maximum values were significantly higher for the iodine-based regimens than for the barium-based regimen (P < .001).
Conclusions. The iodine-based fecal-tagging regimens provide significantly greater homogeneity in oral-tagging fecal material than the barium-based fecal-tagging regimen. Iodine-based fecal-tagging regimens can provide an appropriate method for use in nonlaxative or minimum-laxative CT colonography.
C1 [Nagata, Koichi; Singh, Anand Kumar; Naeppi, Janne; Cai, Wenli; Yoshida, Hiroyuki] Massachusetts Gen Hosp, Imaging Lab 3D, Dept Radiol, Boston, MA 02114 USA.
[Sangwaiya, Minal Jagtiani; Zalis, Michael E.] Massachusetts Gen Hosp, Div Abdominal Imaging & Intervent Radiol, Dept Radiol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Nagata, K (reprint author), Massachusetts Gen Hosp, Imaging Lab 3D, Dept Radiol, 25 New Chardon St,Suite 400C, Boston, MA 02114 USA.
EM nagata7@aol.com
RI Nappi, Janne/B-9424-2008
OI Nappi, Janne/0000-0002-0108-0992
FU GE (Milwaukee, WI)
FX Dr Zalis received a research grant from GE (Milwaukee, WI).
NR 35
TC 11
Z9 11
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1076-6332
J9 ACAD RADIOL
JI Acad. Radiol.
PD NOV
PY 2009
VL 16
IS 11
BP 1393
EP 1399
DI 10.1016/j.acra.2009.05.003
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 513EA
UT WOS:000271304000013
PM 19596591
ER
PT J
AU Collinger, JL
Gagnon, D
Jacobson, J
Impink, BG
Boninger, ML
AF Collinger, Jennifer L.
Gagnon, Dany
Jacobson, Jon
Impink, Bradley G.
Boninger, Michael L.
TI Reliability of Quantitative Ultrasound Measures of the Biceps and
Supraspinatus Tendons
SO ACADEMIC RADIOLOGY
LA English
DT Article
DE Ultrasound; reliability; tendon; biceps; supraspinatus
ID ROTATOR CUFF; SONOGRAPHY; SHOULDER; TENDINOPATHY; CHILDREN; MUSCLES;
DISEASE; IMAGES; INDEX
AB Rationale and Objectives. Ultrasound is a proven method for examining soft tissue structures, including tendons, and recently quantitative ultrasound has become more prevalent in research settings. However, limited reliability data have been published for these new quantitative ultrasound measures. The main objective of this study was to quantify the reliability and measurement error of multiple quantitative ultrasound imaging protocols for the biceps and supraspinatus tendons.
Materials and Methods. Two examiners captured ultrasound images of the non-dominant long head of the biceps tendon and supraspinatus tendon from 15 able-bodied participants and five manual wheelchair users. Each examiner captured two images per subject under two different preparations, which included subject positioning and reference marker placement. Image processing (reading) was performed twice to compute nine quantitative ultrasound measures of grayscale tendon appearance using first-order statistics and texture analysis. Generalizability theory was applied to compute interrater and intrarater reliability using the coefficient of dependability (Phi) for multiple study design protocols.
Results. Interrater reliability was generally low (0.26 < Phi < 0.82), and it is recommended that a single evaluator capture all images for quantitative ultrasound protocols. Most of the quantitative ultrasound measures (n = 14 of 18) exhibited at least moderate (Phi > 0.50) intrarater reliability for a single image captured under one preparation and read once.
Conclusion. By following a protocol designed to minimize measurement error, one can increase the reliabdity of quantitative ultrasound measures. An appropriately designed protocol will allow quantitative ultrasound to be used as an outcome measure to identify structural changes within tendons.
C1 [Collinger, Jennifer L.; Gagnon, Dany; Impink, Bradley G.; Boninger, Michael L.] VA Pittsburgh Healthcare Syst, Human Engn Res Labs, Pittsburgh, PA 15206 USA.
[Collinger, Jennifer L.; Gagnon, Dany; Boninger, Michael L.] Univ Pittsburgh, Dept Phys Med & Rehabil, Pittsburgh, PA USA.
[Collinger, Jennifer L.; Impink, Bradley G.; Boninger, Michael L.] Univ Pittsburgh, Dept Bioengn, Pittsburgh, PA USA.
[Gagnon, Dany] Univ Montreal, Fac Med, Sch Rehabil, Montreal, PQ H3C 3J7, Canada.
[Jacobson, Jon] Univ Michigan, Dept Radiol, Ann Arbor, MI 48109 USA.
RP Boninger, ML (reprint author), VA Pittsburgh Healthcare Syst, Human Engn Res Labs, 7180 Highland Dr,Bldg 4,151R-1, Pittsburgh, PA 15206 USA.
EM boninger@pitt.edu
OI Jacobson, Jon/0000-0002-3676-6628; Boninger, Michael/0000-0001-6966-919X
FU Office of Research and Development, Rehabilitation Research &
Development Service, US Department of Veterans Affairs (Washington, DC)
[B3142C]; National Institutes of Health (Bethesda, MD) [R21HD054529];
National Institute on Disability and Rehabilitation Research's
Rehabilitation Engineering Research Center on Spinal Cord Injury
(Arlington, VA) [H133E070024]; National Science Foundation; Fonds de la
Recherche en Sante du Quebec (Montreal, QC, Canada)
FX This material is based on work supported by grant B3142C from the Office
of Research and Development, Rehabilitation Research & Development
Service, US Department of Veterans Affairs (Washington, DC); grant
R21HD054529 from the National Institutes of Health (Bethesda, MD); grant
H133E070024 the National Institute on Disability and Rehabilitation
Research's Rehabilitation Engineering Research Center on Spinal Cord
Injury (Arlington, VA); and a National Science Foundation graduate
research fellowship. D.G. held a postdoctoral scholarship from Fonds de
la Recherche en Sante du Quebec (Montreal, QC, Canada) at the time of
this study.
NR 22
TC 22
Z9 23
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1076-6332
J9 ACAD RADIOL
JI Acad. Radiol.
PD NOV
PY 2009
VL 16
IS 11
BP 1424
EP 1432
DI 10.1016/j.acra.2009.05.001
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 513EA
UT WOS:000271304000017
PM 19596592
ER
PT J
AU Johansen, KL
AF Johansen, Kirsten L.
TI Anabolic and Catabolic Mechanisms in End-Stage Renal Disease
SO ADVANCES IN CHRONIC KIDNEY DISEASE
LA English
DT Article
DE Muscle catabolism; End-Stage Renal Disease (ESRD); Catabolism
ID INTRADIALYTIC PARENTERAL-NUTRITION; MALNOURISHED HEMODIALYSIS-PATIENTS;
UBIQUITIN-PROTEASOME PATHWAY; SKELETAL-MUSCLE HYPERTROPHY; HUMAN
GROWTH-HORMONE; BODY PROTEIN-DEGRADATION; CHRONIC KIDNEY-DISEASE; P70 S6
KINASE; AMINO-ACID; WHOLE-BODY
AB Muscle wasting is a prominent feature of end-stage renal disease and is associated with muscle weakness and poor physical functioning. Potential reasons for muscle wasting include advancing age, sedentary behavior, inflammation, poor nutritional intake, androgen deficiency, oxidative stress, metabolic acidosis, and insulin resistance. Each of these conditions can be associated with decreased protein synthesis, increased protein degradation, or both. The primary muscle protein synthesis pathway is the insulin insulin-like growth factor-1/phosphatidyl inositol-3 kinase/Akt pathway, which results in the phosphorylation of the mammalian target of rapamycin and subsequent increased protein synthesis. The major protein degradation pathway is the ubiquitin-proteasome system. This review discusses the ways in which end-stage renal disease tips the balance of protein turnover towards catabolism and the mechanisms by which various interventions may work to mitigate wasting or even cause anabolism. (C) 2009 by the National Kidney Foundation, Inc. All rights reselved.
C1 [Johansen, Kirsten L.] San Francisco VA Med Ctr, Nephrol Sect, San Francisco, CA 94121 USA.
[Johansen, Kirsten L.] Univ Calif San Francisco, Div Nephrol, San Francisco, CA 94143 USA.
RP Johansen, KL (reprint author), San Francisco VA Med Ctr, Nephrol Sect, Box 111J,4150 Clement St, San Francisco, CA 94121 USA.
EM Kirsten.johansen@ucsf.edu
NR 68
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Z9 13
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 1548-5595
J9 ADV CHRONIC KIDNEY D
JI Adv. Chronic Kidney Dis.
PD NOV
PY 2009
VL 16
IS 6
BP 501
EP 510
DI 10.1053/j.ackd.2009.07.007
PG 10
WC Urology & Nephrology
SC Urology & Nephrology
GA 508LJ
UT WOS:000270932500010
PM 19801138
ER
PT J
AU Thomas, MA
Yaremchuk, MJ
AF Thomas, Mathew A.
Yaremchuk, Michael J.
TI Masseter Muscle Reattachment After Mandibular Angle Surgery
SO AESTHETIC SURGERY JOURNAL
LA English
DT Article
AB Background: Altering the dimensions of the mandibular angle by alloplastic augmentation or skeletal reduction requires elevation of the insertion of the masseter muscle, including the pterygomasseteric sling. Disruption of the pterygomasseteric sling during exposure of the inferior border of the mandible can cause the masseter muscle to retract superiorly, resulting in a loss of soft tissue volume over the angle of the mandible and a skeletonized appearance. Subsequent contraction of the masseter elevates the disinserted edge of the muscle and not only increases the skeletonized area, but also exaggerates the deficiency by causing a soft tissue bulge above it.
Objective: The authors describe the disinsertion of the masseter and the resulting deformity as a potential complication of mandibular angle surgery and review the technique for repair.
Methods: The records of 60 patients (44 primary, 16 secondary) who presented for alloplastic mandible augmentation between 2003 and 2008 were reviewed.
Results: Nine patients presented with clinical signs of disruption of the pterygomasseteric sling after mandibular angle surgery. Five patients had clinical signs consistent with complete disruption. Two of these patients requested reconstruction. The other four had signs consistent with partial disruption. Through a Risdon approach, the masseter was successfully reinserted using drill holes placed at the inferior border of the mandible.
Conclusions: Masseter disinsertion is a previously unreported sequelae after aesthetic surgery for the angle of the mandible. The resultant static and dynamic contour deformity can be corrected by reattaching the muscle to the inferior border of the mandible. (Aesthet Surg J; 29:473-476.)
C1 [Thomas, Mathew A.; Yaremchuk, Michael J.] Massachusetts Gen Hosp, Dept Surg, Div Plast Surg, Boston, MA 02114 USA.
[Thomas, Mathew A.; Yaremchuk, Michael J.] Harvard Univ, Sch Med, Boston, MA USA.
RP Yaremchuk, MJ (reprint author), Massachusetts Gen Hosp, Dept Surg, Div Plast Surg, 15 Parkman St,Wang 435, Boston, MA 02114 USA.
EM dr.y@dryaremchuk.com
NR 15
TC 3
Z9 3
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1090-820X
J9 AESTHET SURG J
JI Aesthet. Surg. J.
PD NOV
PY 2009
VL 29
IS 6
BP 473
EP 476
DI 10.1016/j.asj.2009.09.006
PG 4
WC Surgery
SC Surgery
GA V20LC
UT WOS:000208140500005
PM 19944991
ER
PT J
AU Lawrence, I
Moy, R
AF Lawrence, Ira
Moy, Ronald
TI An Evaluation of Neutralizing Antibody Induction During Treatment of
Glabellar Lines with a New US Formulation of Botulinum Neurotoxin Type A
SO AESTHETIC SURGERY JOURNAL
LA English
DT Article
AB BACKGROUND: The induction of neutralizing antibodies during the aesthetic application of botulinum neurotoxin type A is rare, but of potential clinical concern. Phase III studies of a new US formulation of botulinum neurotoxin type A, Dysport (BoNTA-ABO [abobotulinumtoxinA]; Medicis Aesthetics, Scottsdale, AZ), have not identified any cases of neutralizing antibody formation during the treatment of glabellar lines in patients who received up to nine treatments.
OBJECTIVE: To provide an in-depth analysis of the potential for induction of neutralizing antibodies in the study population enrolled in phase III trials of BoNTA-ABO in the treatment of glabellar lines.
METHODS: First and last available serum samples from patients in the BoNTA-ABO Glabellar Lines Development Program were screened for BoNTA-ABO antibodies with a radioimmunoprecipitation assay (RIPA), followed by a confirmatory competitive assay (RIPA-C). Confirmed RIPA-C-positive samples were further evaluated for the presence of neutralizing antibodies using a mouse protection assay (MPA), a highly specific bioassay for neutralizing antibodies. We conducted safety and efficacy evaluations, including day 30 responder rate (a rating of no or mild glabellar lines) and duration of response in the last treatment cycle.
RESULTS: Of 1554 patients who received at least one BoNTA-ABO treatment (10 units at five injection points, for a total dose of 50 units/treatment; range one to nine treatments), five (0.32%) were antibody positive on the RIPA-C assay-two at baseline and three at the last treatment cycle. None of the RIPA-C-positive samples tested positive for neutralizing antibodies upon further evaluation using the highly specific MPA. Of note, the RIPA-C-positive group had a responder rate of 100% and a mean response of 103.3 days, while the RIPA-C-negative group had a responder rate of 90% and a mean response of 89.4 days. The safety of BoNTA-ABO did not appear to be altered in the RIPA-C-positive group.
CONCLUSIONS: At the dose and treatment interval used in the correction of glabellar lines, induction of neutralizing antibodies to BoNTA-ABO was not observed. None of the five samples that initially gave positive results in a RIPA-C assay were positive when further evaluated using the MPA. Clinically, RIPA-C-positive status did not correlate with any reduction in efficacy or an altered safety profile, although the small numbers prevent definitive conclusions. These data suggest that the five RIPA-C-positive samples represented false positives. (Aesthetic Surg J 2009;29:S66-S71.)
C1 [Lawrence, Ira] Medicis Pharmaceut Corp, Res & Dev, Scottsdale, AZ USA.
[Moy, Ronald] W Los Angeles Vet Affairs Med Ctr, Fincher Med Grp, Los Angeles, CA 90073 USA.
[Moy, Ronald] Univ Calif Los Angeles, David Geffen Sch Med, Moy Fincher Med Grp, Los Angeles, CA 90024 USA.
RP Moy, R (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Moy Fincher Med Grp, 100 UCLA Med Plaza,Suite 590, Los Angeles, CA 90024 USA.
EM rmoy@ucla.edu
FU Medicis Aesthetics (Scottsdale, AZ)
FX The authors were compensated for their contributions in preparing this
manuscript and as investigators for this study. The writing of this
manuscript was funded by Medicis Aesthetics (Scottsdale, AZ). Dr.
Lawrence is employed by Medicis Pharmaceutical, the distributor of
Dysport for aesthetic use in the United States. Dr. Moy was a paid
investigator for Inamed (Santa Barbara, CA). He has no financial
arrangements with Medicis Aesthetics.
NR 22
TC 8
Z9 8
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1090-820X
J9 AESTHET SURG J
JI Aesthet. Surg. J.
PD NOV
PY 2009
VL 29
IS 6
SU S
BP S66
EP S71
DI 10.1016/j.asj.2009.09.009
PG 6
WC Surgery
SC Surgery
GA V20LB
UT WOS:000208140400007
PM 19945007
ER
PT J
AU Federman, AD
Cole, H
Sano, M
AF Federman, Alex D.
Cole, Helen
Sano, Mary
TI Cognitive performance in community-dwelling English- and
Spanish-speaking seniors
SO AGE AND AGEING
LA English
DT Article
DE elderly; cognition; language; Spanish
ID NEUROPSYCHOLOGICAL TEST-PERFORMANCE; MINI-MENTAL-STATE; VERBAL FLUENCY;
NORMATIVE DATA; EDUCATION; ELDERS; AGE; IMPAIRMENT; DISABILITY; AMERICAN
AB Design: cross-sectional.
Setting: community-based settings in New York City, including senior centres and residential complexes.
Subjects: four hundred and twenty independently living adults aged 60 or older (mean 73.8 years).
Methods: participants completed the Mini-Mental State Exam (MMSE), animal naming test (ANT) and Wechsler Memory Scale III (WMS) Story A immediate and delayed subtests. Scores were examined by strata of language, age or education and for different thresholds of the MMSE. We tested the association of language and cognitive test performance using multivariable linear regression.
Results: twenty-one per cent of subjects were interviewed in Spanish and 16.2% reported poor-fair English proficiency. The mean WMS scores were not statistically different between English and Spanish groups (immediate recall, 9.9 vs 9.5, P = 0.44; delayed recall, 8.0 vs 7.6, P = 0.36, respectively), whereas ANT scores did differ (16.6 vs 14.3, P < 0.0001). These associations were consistent across MMSE thresholds. The association of language and ANT score was not significant after accounting for education.
Conclusions: we found little difference in performance on the Story A subtests from the WMS suggesting that this test may be used for both English- and Spanish-speaking populations. Results suggest that variations in ANT performance may be accounted for by adjusting for the level of education. These results have important implications for the generalisability of test scores among diverse older populations.
C1 [Federman, Alex D.; Cole, Helen] Mt Sinai Sch Med, Div Gen Internal Med, New York, NY 10029 USA.
[Sano, Mary] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
[Sano, Mary] Bronx Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Bronx, NY USA.
RP Federman, AD (reprint author), Mt Sinai Sch Med, Div Gen Internal Med, 1 Gustave L Levy Pl,Box 1087, New York, NY 10029 USA.
EM alex.federman@mssm.edu
FU National Institute on Aging [1K23AG028955-01]; Mount Sinai School of
Medicine Alzheimer's Disease Research Center (NIH) [AG0051318]
FX This study was supported by a Paul B. Beeson Career Development Award in
Aging from the National Institute on Aging (Dr. Federman,
1K23AG028955-01). Additional support was provided by the Mount Sinai
School of Medicine Alzheimer's Disease Research Center (NIH AG0051318).
NR 29
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U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0002-0729
J9 AGE AGEING
JI Age Ageing
PD NOV
PY 2009
VL 38
IS 6
BP 669
EP 675
DI 10.1093/ageing/afp127
PG 7
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 510QQ
UT WOS:000271106000006
PM 19651699
ER
PT J
AU Thomas, B
Mimiaga, MJ
Mayer, KH
Johnson, CV
Menon, S
Chandrasekaran, V
Murugesan, P
Swaminathan, S
Safren, SA
AF Thomas, Beena
Mimiaga, Matthew J.
Mayer, Kenneth H.
Johnson, Carey V.
Menon, Sunil
Chandrasekaran, V.
Murugesan, P.
Swaminathan, Soumya
Safren, Steven A.
TI HIV Prevention Interventions in Chennai, India: Are Men Who Have Sex
with Men Being Reached?
SO AIDS PATIENT CARE AND STDS
LA English
DT Article
ID BASE-LINE DATA; RISK BEHAVIORS; PREVALENCE; INFECTION; EXPLORE; STATES
AB India has the greatest number of HIV infections in Asia and the third highest total number of infected persons globally. Men who have sex with men (MSM) are considered by the Government of India's National AIDS Control Organization (NACO) a "core risk group" for HIV in need of HIV prevention efforts. However there is a dearth of information on the frequency of participation in HIV prevention interventions and subsequent HIV risk and other correlates among MSM in India. Recruited through peer outreach workers, word of mouth and snowball sampling techniques, 210 MSM in Chennai completed an interviewer-administered assessment, including questions about participating in any HIV prevention interventions in the past year, sexual risk taking, demographics, MSM identities, and other psychosocial variables. Bivariate and multivariable logistic regression procedures were used to examine behavioral and demographic correlates with HIV prevention intervention participation. More than a quarter (26%) of the sample reported participating in an HIV prevention intervention in the year prior to study participation. Participants who reported engaging in unprotected anal sex (UAS; odds ratio [OR] = 0.28; p = 0.01) in the 3 months prior to study enrollment were less likely to have participated in an HIV prevention program in the past year. MSM who were older (OR = 1.04; p = 0.05), kothis (feminine acting/appearing and predominantly receptive partners in anal sex) compared to panthis (masculine appearing, predominantly insertive partners; OR = 5.52, p = 0.0004), those with higher educational attainment (OR = 1.48, p = 0.01), being "out" about having sex with other men (OR = 4.03, p = 0.0001), and MSM who reported ever having been paid in exchange for sex (OR = 2.92, p = 0.001) were more likely to have reported participation in an HIV prevention intervention in the preceding year. In a multivariable model, MSM reporting UAS in the prior 3 months were less likely to have participated in an HIV prevention intervention (AOR = 0.34, p = 0.04). MSM who were older (AOR = 1.05, p = 0.05), those with higher educational attainment (AOR = 1.92, p = 0.0009), and MSM who were "out" about having sex with other men (AOR = 2.71, p = 0.04) were more likely to have reported participating in an HIV prevention program. Findings suggest that exposure to HIV prevention interventions may be protective against engaging in UAS for some MSM in India. Understanding predictors of participation in an HIV prevention intervention is helpful for identifying Indian MSM who might have had no exposure to HIV prevention information and skills building, hence allowing researchers and prevention workers to focus efforts on individuals at greatest need.
C1 [Thomas, Beena; Chandrasekaran, V.; Murugesan, P.; Swaminathan, Soumya] Indian Council Med Res, TB Res Ctr, Madras, Tamil Nadu, India.
[Mimiaga, Matthew J.; Safren, Steven A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Mimiaga, Matthew J.; Mayer, Kenneth H.; Johnson, Carey V.; Safren, Steven A.] Fenway Inst, Boston, MA USA.
[Mayer, Kenneth H.] Miriam Hosp, Brown Med Sch, Providence, RI 02906 USA.
[Menon, Sunil] Sahodaran, Madras, Tamil Nadu, India.
RP Mimiaga, MJ (reprint author), Harvard MGH Behav Med, 1 Bowdoin Sq,7th Floor, Boston, MA 02114 USA.
EM mmimiaga@partners.org
FU [P30A1060354]; [MH085314]
FX Funding for data collection for this project was supported by a
supplement to grant P30A1060354 on which Bruce Walker, M. D. is the PI,
and Steven A. Safren, Ph. D. was the PI of the supplement. Support for
some staff time for analysis and manuscript preparation was from grant
MH085314 (Safren).
NR 35
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Z9 22
U1 1
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1087-2914
J9 AIDS PATIENT CARE ST
JI Aids Patient Care STDS
PD NOV
PY 2009
VL 23
IS 11
BP 981
EP 986
DI 10.1089/apc.2009.0092
PG 6
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 522KD
UT WOS:000271995700010
PM 19821722
ER
PT J
AU Marinkovic, K
Oscar-Berman, M
Urban, T
O'Reilly, CE
Howard, JA
Sawyer, K
Harris, GJ
AF Marinkovic, Ksenija
Oscar-Berman, Marlene
Urban, Trinity
O'Reilly, Cara E.
Howard, Julie A.
Sawyer, Kayle
Harris, Gordon J.
TI Alcoholism and Dampened Temporal Limbic Activation to Emotional Faces
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Review
DE Alcoholism; Emotion; Faces; Amygdala; Functional Magnetic Resonance
Imaging
ID FACIAL EXPRESSION RECOGNITION; AFFECTIVE PROSODY COMPREHENSION;
SURFACE-BASED ANALYSIS; PREFRONTAL CORTEX; CORTICAL SURFACE; FUNCTIONAL
MRI; HUMAN AMYGDALA; HIPPOCAMPAL VOLUME; COORDINATE SYSTEM; HUMAN BRAIN
AB Background:
Excessive chronic drinking is accompanied by a broad spectrum of emotional changes ranging from apathy and emotional flatness to deficits in comprehending emotional information, but their neural bases are poorly understood.
Methods:
Emotional abnormalities associated with alcoholism were examined with functional magnetic resonance imaging in abstinent long-term alcoholic men in comparison to healthy demographically matched controls. Participants were presented with emotionally valenced words and photographs of faces during deep (semantic) and shallow (perceptual) encoding tasks followed by recognition.
Results:
Overall, faces evoked stronger activation than words, with the expected material-specific laterality (left hemisphere for words, and right for faces) and depth of processing effects. However, whereas control participants showed stronger activation in the amygdala and hippocampus when viewing faces with emotional (relative to neutral) expressions, the alcoholics responded in an undifferentiated manner to all facial expressions. In the alcoholic participants, amygdala activity was inversely correlated with an increase in lateral prefrontal activity as a function of their behavioral deficits. Prefrontal modulation of emotional function as a compensation for the blunted amygdala activity during a socially relevant face appraisal task is in agreement with a distributed network engagement during emotional face processing.
Conclusions:
Deficient activation of amygdala and hippocampus may underlie impaired processing of emotional faces associated with long-term alcoholism and may be a part of the wide array of behavioral problems including disinhibition, concurring with previously documented interpersonal difficulties in this population. Furthermore, the results suggest that alcoholics may rely on prefrontal rather than temporal limbic areas in order to compensate for reduced limbic responsivity and to maintain behavioral adequacy when faced with emotionally or socially challenging situations.
C1 [Marinkovic, Ksenija] Univ Calif San Diego, Dept Radiol, La Jolla, CA 92093 USA.
[Urban, Trinity] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Oscar-Berman, Marlene] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02215 USA.
[Oscar-Berman, Marlene] Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02215 USA.
[Oscar-Berman, Marlene] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02215 USA.
[Oscar-Berman, Marlene; Howard, Julie A.; Sawyer, Kayle] VA Healthcare Syst, Psychol Res Serv, Boston, MA USA.
[Urban, Trinity; Harris, Gordon J.] Massachusetts Gen Hosp, Radiol Comp Aided Diagnost Lab, Boston, MA 02114 USA.
[O'Reilly, Cara E.] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
RP Marinkovic, K (reprint author), Univ Calif San Diego, Dept Radiol, 9500 Gilman Dr 0841, La Jolla, CA 92093 USA.
EM xenia@ucsd.edu
OI Sawyer, Kayle/0000-0001-7767-5688
FU National Institute on Alcohol Abuse and Alcoholism (NIAAA) [R01-AA07112,
K05-AA00219, K01-AA13402, R01-AA016624]; Medical Research Service of the
US Department of Veterans Affairs; Alcoholic Beverage Medical Research
Foundation; MIND Institute; [P41RR14075]
FX This research was supported by funds from the National Institute on
Alcohol Abuse and Alcoholism (NIAAA), grants R01-AA07112 and
K05-AA00219, and Medical Research Service of the US Department of
Veterans Affairs to Dr. Marlene Oscar-Berman; NIAAA K01-AA13402,
R01-AA016624, and Alcoholic Beverage Medical Research Foundation to Dr.
Ksenija Marinkovic, by P41RR14075, and MIND Institute. We thank Diane
Merritt for recruitment assistance and Sheeva Azma and Susan Mosher for
help with data collection and analysis.
NR 113
TC 48
Z9 49
U1 6
U2 7
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD NOV
PY 2009
VL 33
IS 11
BP 1880
EP 1892
DI 10.1111/j.1530-0277.2009.01026.x
PG 13
WC Substance Abuse
SC Substance Abuse
GA 509YA
UT WOS:000271054000005
PM 19673745
ER
PT J
AU Griffin, WC
Lopez, MF
Becker, HC
AF Griffin, William C., III
Lopez, Marcelo F.
Becker, Howard C.
TI Intensity and Duration of Chronic Ethanol Exposure Is Critical for
Subsequent Escalation of Voluntary Ethanol Drinking in Mice
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Dependence; Excessive Drinking; Alcohol; Mouse
ID ALCOHOL-USE DISORDERS; C57BL/6J MICE; REPEATED CYCLES; ANIMAL-MODELS;
INTERMITTENT; DEPENDENCE; WITHDRAWAL; CONSUMPTION; ANTAGONIST;
ALLOSTASIS
AB Background:
Excessive alcohol drinking continues to be an important health problem. Recent studies from our laboratory and others have demonstrated that animal models of ethanol dependence and relapse can contribute to understanding factors that contribute to excessive drinking. In this study, we tested the hypothesis that the amount and duration of ethanol exposure is critical for promoting the escalation in drinking by mice given access to ethanol in a limited access paradigm.
Methods:
We used several methods of chronic intermittent ethanol exposure in male C57BL/6J mice that would vary in the amount and duration of exposure to ethanol as indicated by blood ethanol concentrations (BEC). After establishing baseline drinking in the mice using a 2 hours, 2 bottle choice drinking paradigm, each study involved alternating between periods of ethanol exposure and periods of limited access to ethanol (1 cycle) for a total of 3 cycles. In Study 1, mice were allowed extended access (16 hours) to ethanol for oral consumption or remained in the home cage. In Study 2, the ethanol exposure consisted of intragastric gavage of increasing doses of ethanol or isocaloric sucrose as the control. Study 3 compared intragastric gavage combined with pyrazole, an alcohol dehydrogenase inhibitor, with vapor inhalation of ethanol using procedures known to lead to increased drinking in mice. Finally, Study 4 was a retrospective review of several studies conducted in our laboratory using inhalation procedures. The retrospective review encompassed a range of postvapor chamber BEC values and ethanol intakes that would allow a relationship between increased drinking and BEC to be examined.
Results:
Allowing mice to drink for longer periods of time did not cause increased drinking in subsequent limited access sessions. Likewise, gastric intubation of ethanol which produced high BEC (> 300 mg/dl) with or without pyrazole did not increase drinking. Only the vapor inhalation procedure, which was associated with sustained BEC above 175 mg/dl for the entire exposure period resulted in increased drinking. The retrospective study provided further evidence that sustained BEC levels above 175 mg/dl was critical to the escalation in drinking.
Conclusions:
We found that the intensity (amount) and duration of ethanol exposure, indexed by BEC, is critical to produce increased drinking in mice. Specifically, BEC must regularly exceed 175 mg/dl for the escalation in drinking to occur. Future studies will examine neurobiological adaptations that may underlie the increased drinking behavior caused by chronic intermittent ethanol exposure.
C1 [Griffin, William C., III; Lopez, Marcelo F.; Becker, Howard C.] Med Univ S Carolina, Ctr Drug & Alcohol Programs, Dept Psychiat & Behav Sci, Charleston Alcohol Res Ctr, Charleston, SC 29425 USA.
[Becker, Howard C.] Med Univ S Carolina, Dept Neurosci, Charleston, SC 29425 USA.
[Becker, Howard C.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
RP Griffin, WC (reprint author), Med Univ S Carolina, Ctr Drug & Alcohol Programs, Dept Psychiat & Behav Sci, Charleston Alcohol Res Ctr, MSC 861, Charleston, SC 29425 USA.
EM griffinw@musc.edu
FU NIH [AA10716, AA14095, AA13885]
FX This work was supported by NIH grants AA10716, AA14095, and AA13885. The
authors acknowledge the expert technical assistance of Melissa
Overstreet, Laura Ralston, and Kay Fernandes in conducting these
studies.
NR 25
TC 60
Z9 61
U1 2
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD NOV
PY 2009
VL 33
IS 11
BP 1893
EP 1900
DI 10.1111/j.1530-0277.2009.01027.x
PG 8
WC Substance Abuse
SC Substance Abuse
GA 509YA
UT WOS:000271054000006
PM 19673744
ER
PT J
AU Thomas, D
Giugliano, RP
AF Thomas, Deepak
Giugliano, Robert P.
TI Management of ST-segment elevation myocardial infarction: Comparison of
the updated guidelines from North America and Europe
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID PERCUTANEOUS CORONARY INTERVENTION; CONVERTING-ENZYME INHIBITORS;
PLACEBO-CONTROLLED TRIAL; FIBRINOLYTIC THERAPY; RESCUE ANGIOPLASTY;
FOLLOW-UP; UNFRACTIONATED HEPARIN; THROMBUS ASPIRATION;
RANDOMIZED-TRIALS; MULTICENTER TRIAL
AB The American College of Cardiology/American Heart Association and the European Society of Cardiology each recently published updated guidelines for management of patients with acute ST elevation myocardial infarction. In this article, we highlight the most important new recommendations, review their supporting data, and describe differences between the guidelines.
Key aspects of these updates include detailed guidance regarding the selection of a reperfusion strategy and the incorporation of newer adjunctive antithrombotic agents. Both new guidelines suggest caution in the administration of intravenous beta-blockers, avoidance of nonsteroidal anti-inflammatory agents, and support a more aggressive approach to secondary risk factor management.
The 2 guidelines have some nuanced differences as well as some recommendations that are unique to each guideline. They present different levels of support for the 4 available adjunctive parenteral anticoagulants, vary in their endorsement of routine elective coronary angiography after fibrinolysis, and cite different targets for low density lipoprotein long-term. Major unique recommendations include the American College of Cardiology/American Heart Assocaition's emphasis of a stepped approach to analgesia in patients with musculoskeletal pain beginning with acetaminophen or aspirin and a lower target international normalized ratio in patients receiving warfarin, aspirin, and clopidogrel. Meanwhile, unique recommendations in the European Society of Cardiology guidelines include measures to prevent/treat microvascular obstruction and reperfusion injury associated with percutaneous coronary intervention and greater emphasis on maintaining eugylcemia.
As these guidelines represent an evidence based approach, health care providers should become familiar with the new data and the resultant updated recommendations to ensure optimal treatment of their patients with ST-elevation myocardial infarction. (Am Heart J 2009;158:695-705.)
C1 [Thomas, Deepak; Giugliano, Robert P.] Brigham & Womens Hosp, Div Cardiovasc Med, Boston, MA 02115 USA.
RP Giugliano, RP (reprint author), TIMI Study Off, 350 Longwood Ave,1st Floor Off, Boston, MA 02115 USA.
EM rgiugliano@partners.org
NR 51
TC 8
Z9 8
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD NOV
PY 2009
VL 158
IS 5
BP 695
EP 705
DI 10.1016/j.ahj.2009.08.023
PG 11
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 512UD
UT WOS:000271275400001
PM 19853685
ER
PT J
AU Bamberg, F
Truong, QA
Blankstein, R
Nasir, K
Lee, H
Rogers, IS
Achenbach, S
Brady, TJ
Nagurney, JT
Reiser, MF
Hoffmann, U
AF Bamberg, Fabian
Truong, Quynh A.
Blankstein, Ron
Nasir, Khurram
Lee, Hang
Rogers, Ian S.
Achenbach, Stephan
Brady, Thomas J.
Nagurney, John T.
Reiser, Maximilian F.
Hoffmann, Udo
TI Usefulness of Age and Gender in the Early Triage of Patients With Acute
Chest Pain Having Cardiac Computed Tomographic Angiography
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID CORONARY-ARTERY-DISEASE; ELEVATION MYOCARDIAL-INFARCTION; PRACTICE
GUIDELINES COMMITTEE; ASSOCIATION TASK-FORCE; EMERGENCY-DEPARTMENT;
PRACTICAL IMPLEMENTATION; SCIENTIFIC STATEMENT; CLINICAL CARDIOLOGY;
COST-EFFECTIVENESS; AMERICAN-COLLEGE
AB To identify the age- and gender-specific subpopulations of patients with acute chest pain in whom coronary computed tomograpbic angiography (CTA) will yield the greatest diagnostic benefit. Subjects with acute chest pain and an inconclusive initial evaluation (non-diagnostic electrocardiograhic findings, negative cardiac biomarkers) underwent contrast-enhanced 64-slice coronary CTA as a part of an observational cohort study. Independent investigators determined the presence of significant coronary stenosis (>50% luminal narrowing) and the occurrence of acute coronary syndrome (ACS) during the index hospitalization. We determined the diagnostic accuracy and effect on pretest probability of ACS using Bayes' theorem by age and gender. Of 368 patients (age 52.7 +/- 12 years, 61% men), 8% had ACS. The presence of significant coronary stenosis on CTA and the occurrence of ACS increased with age for both men and women (p < 0.001). Cardiac CTA was highly sensitive and specific in women <65 years of age (sensitivity 100% and specificity >87%) and men <55 years of age (sensitivity 100% for men <45 years and 80% for men 45 to 54 years old; specificity >88.2%). Moreover, in these patients, coronary CTA led to restratification from low to high risk (for positive findings on CTA) or from low to very low risk (for negative findings on CTA). In contrast, a negative result on CTA did not result in restratification to a low-risk category in women >65 years and men >55 years old. In conclusion, the present analysis provides initial evidence that men <55 years and women <65 years might benefit more from cardiac CTA than older patients. Thus, age and gender might serve as simple criteria to appropriately select patients who would derive the greatest diagnostic benefit from coronary CTA in the setting of acute chest pain. (C) 2009 Elsevier Inc. All rights reserved. (Am J Cardiol 2009;104:1165-1170)
C1 [Bamberg, Fabian; Truong, Quynh A.; Blankstein, Ron; Nasir, Khurram; Rogers, Ian S.; Brady, Thomas J.; Hoffmann, Udo] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
[Bamberg, Fabian; Blankstein, Ron; Brady, Thomas J.; Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Truong, Quynh A.; Rogers, Ian S.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Lee, Hang] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
[Nagurney, John T.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Bamberg, Fabian; Reiser, Maximilian F.] Univ Munich, Dept Clin Radiol, Munich, Germany.
[Achenbach, Stephan] Univ Erlangen Nurnberg, Dept Cardiol, Erlangen, Germany.
RP Bamberg, F (reprint author), Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
EM fbamberg@post.harvard.edu
FU NHLBI NIH HHS [R01 HL080053, R01 HL080053-03, T32 HL076136, T32
HL076136-05]
NR 28
TC 4
Z9 4
U1 0
U2 1
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 NOV 1
PY 2009
VL 104
IS 9
BP 1165
EP 1170
DI 10.1016/j.amjcard.2009.06.029
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 515QI
UT WOS:000271487100001
PM 19840556
ER
PT J
AU Depta, JP
Cannon, CP
Fonarow, GC
Zhao, X
Peacock, WF
Bhatt, DL
AF Depta, Jeremiah P.
Cannon, Christopher P.
Fonarow, Gregg C.
Zhao, Xin
Peacock, W. Frank
Bhatt, Deepak L.
CA Get Guidelines Steering Comm Inves
TI Patient Characteristics Associated With the Choice of Triple
Antithrombotic Therapy in Acute Coronary Syndromes
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID AMERICAN-HEART-ASSOCIATION; ATRIAL-FIBRILLATION; ANTIPLATELET THERAPY;
STROKE PREVENTION; BLEEDING RISK; WARFARIN; ANTICOAGULATION;
INTERVENTION; OUTCOMES; CLOPIDOGREL
AB Evidence regarding the use of dual antiplatelet therapy and oral anticoagulation (i.e., triple therapy) in acute coronary syndromes (ACS) is limited. We evaluated the characteristics associated with the choice of triple therapy in ACS. Using the Get With The Guidelines (GWTG) Coronary Artery Disease national registry, we studied patients with ACS at 361 sites in the United States from 2004 to 2007. Both univariate analysis and multivariate logistic regression analysis were used to assess the factors associated using triple therapy on discharge. The Generalized Estimating Equation method was used to account for within-hospital clustering in modeling. A total of 86,304 patients presented with ACS during the study period. At discharge, 3,933 patients (4.6%) were prescribed triple therapy, 60,716 patients (70.4%) received dual antiplatelet therapy, 2,348 patients (2.7%) received single antiplatelet therapy plus oral anticoagulation, 19,065 patients (22.1%) received antiplatelet monotherapy, and 242 patients (0.3%) received oral anticoagulation alone. Patients with a history of atrial fibrillation (odds ratio 7.01, 95% confidence interval 6.06 to 8.12; p<0.001), documented new-onset atrial fibrillation (odds ratio 3.76, 95% confidence interval 2.87 to 4.93; p<0.001), or history of atrial flutter (odds ratio 3.38, 95% confidence interval 2.15 to 5.32; p<0.001) were more frequently discharged with triple therapy. In conclusion, for patients with ACS, atrial fibrillation and atrial flutter were most strongly associated with the use of triple therapy; however, this therapy was used less often than dual or single antiplatelet therapy. Published by Elsevier Inc. (Am J Cardiol 2009;104:1171-1178)
C1 [Bhatt, Deepak L.] Vet Affairs Boston Healthcare Syst, Boston, MA USA.
[Cannon, Christopher P.] Brigham & Womens Hosp, Div Cardiovasc, TIMI Study Grp, Boston, MA 02115 USA.
[Depta, Jeremiah P.] Cleveland Clin, Inst Med, Dept Internal Med, Cleveland, OH 44106 USA.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA.
[Zhao, Xin] Duke Clin Res Inst, Durham, NC USA.
[Peacock, W. Frank] Cleveland Clin, Dept Emergency Med, Cleveland, OH 44106 USA.
RP Bhatt, DL (reprint author), Vet Affairs Boston Healthcare Syst, Boston, MA USA.
EM dlbhattmd@alum.mit.edu
NR 20
TC 12
Z9 12
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 NOV 1
PY 2009
VL 104
IS 9
BP 1171
EP 1178
DI 10.1016/j.amjcard.2009.06.027
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 515QI
UT WOS:000271487100002
PM 19840557
ER
PT J
AU Shea, MK
Gundberg, CM
Meigs, JB
Dallal, GE
Saltzman, E
Yoshida, M
Jacques, PF
Booth, SL
AF Shea, M. Kyla
Gundberg, Caren M.
Meigs, James B.
Dallal, Gerard E.
Saltzman, Edward
Yoshida, Makiko
Jacques, Paul F.
Booth, Sarah L.
TI gamma-Carboxylation of osteocalcin and insulin resistance in older men
and women
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID VITAMIN-K SUPPLEMENTATION; HOMEOSTASIS MODEL ASSESSMENT; BONE-MINERAL
DENSITY; PLASMA-GLUCOSE; BETA-CELL; ADIPONECTIN; METABOLISM
AB Background: The skeletal protein osteocalcin is gamma-carboxylated by vitamin K. High serum uncarboxylated osteocalcin reflects low vitamin K status. In vitro and animal studies indicate that high uncarboxylated osteocalcin is associated with reduced insulin resistance. However, associations between osteocalcin and measures of insulin resistance in humans are less clear.
Objective: Our aim was to examine cross-sectional and longitudinal associations between circulating forms of osteocalcin (total, uncarboxylated, and carboxylated) and insulin resistance in older men and women.
Design: Cross-sectional associations between serum measures of total osteocalcin, carboxylated osteocalcin, and uncarboxylated osteocalcin and insulin resistance were examined in 348 nondiabetic men and women (mean age: 68 y; 58% female) by using the homeostasis model assessment of insulin resistance (HOMA-IR). Associations between each form of osteocalcin at baseline and 3-y change in HOMA-IR were examined in 162 adults (mean age: 69 y; 63% female) who did not receive vitamin K supplementation.
Results: Lower circulating uncarboxylated osteocalcin was not associated with higher HOMA-IR at baseline or at 3-y follow-up. Those in the lowest tertiles of total osteocalcin and carboxylated osteocalcin at baseline had higher baseline HOMA-IR (P = 0.006 and P = 0.02, respectively). The concentration of carboxylated osteocalcin at baseline was inversely associated with a 3-y change in HOMA-IR (P = 0.002).
Conclusions: In older adults, circulating uncarboxylated osteocalcin was not associated with insulin resistance. In contrast, elevated carboxylated osteocalcin and total osteocalcin were associated with lower insulin resistance, which supports a potential link between skeletal physiology and insulin resistance in humans. The role of vitamin K status in this association remains unclear and merits further investigation. This trial is registered at clinicaltrials.gov as NCT00183001. Am J Clin Nutr 2009; 90: 1230-5.
C1 [Shea, M. Kyla; Dallal, Gerard E.; Saltzman, Edward; Yoshida, Makiko; Jacques, Paul F.; Booth, Sarah L.] Tufts Univ, USDA, Human Nutr Res Ctr Aging, Boston, MA 02111 USA.
[Gundberg, Caren M.] Yale Univ, Sch Med, Dept Orthopaed, New Haven, CT USA.
[Meigs, James B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Meigs, James B.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Meigs, James B.] Harvard Univ, Sch Med, Boston, MA USA.
RP Booth, SL (reprint author), Tufts Univ, USDA, Human Nutr Res Ctr Aging, 711 Washington St, Boston, MA 02111 USA.
EM sarah.booth@tufts.edu
FU GlaxoSmithKline; Sanofi-Aventis
FX The authors' responsibilities were as follows-SLB: designed the study
and contributed to the design of the analyses, the interpretation of the
data, and the writing of the manuscript; MKS: performed the statistical
analyses and drafted the manuscript; and CMG, JBM, GED, ES, MY, and PFJ:
contributed to the design of the analyses, the interpretation of the
data, and the writing of the manuscript. JBM currently has research
grants from GlaxoSmithKline and Sanofi-Aventis and serves on consultancy
boards for Eli Lilly, Interleukin Genetics, Kalypsis, and Outcomes
Sciences. MKS, CMG, ES, PFJ, MY, GED, and SLB had no conflicts of
interest.
NR 19
TC 102
Z9 105
U1 0
U2 3
PU AMER SOC CLINICAL NUTRITION
PI BETHESDA
PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998
USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD NOV 1
PY 2009
VL 90
IS 5
BP 1230
EP 1235
DI 10.3945/ajcn.2009.28151
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 508TO
UT WOS:000270959500017
PM 19776145
ER
PT J
AU Wilbur, DC
Black-Schaffer, WS
Luff, RD
Abraham, KP
Kemper, C
Molina, JT
Tench, WD
AF Wilbur, David C.
Black-Schaffer, W. Stephen
Luff, Ronald D.
Abraham, Kurian P.
Kemper, Cynthia
Molina, James T.
Tench, William D.
TI The Becton Dickinson FocalPoint GS Imaging System Clinical Trials
Demonstrate Significantly Improved Sensitivity for the Detection of
Important Cervical Lesions
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article; Proceedings Paper
CT 98th Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 07-13, 2009
CL Boston, MA
SP US & Canadian Acad Pathol
DE Cervical cytology; Computer-assisted screening; Cytology imaging system
ID PRIMARY SCREENING SYSTEM; QUALITY-CONTROL; AUTOPAP SYSTEM; INTENDED-USE;
CYTOLOGY; SMEARS; PERFORMANCE; NO; CLASSIFICATION; FEASIBILITY
AB Location-guided screening in cervical cytology offers a potentially significant advance over routine manual screening. A prospective, 2-armed, masked clinical trial of the BD FocalPoint GS Imaging System using SurePath slides (BD Diagnostics-TriPath, Burlington, NC) compared routine manual screening and quality control rescreening with computer-assisted, field-of-view screening and device-directed quality control rescreening. The results obtained in the 2 arms were compared with adjudicated reference diagnoses for each slide. Sensitivity, specificity, and negative predictive value were calculated for the detection of atypical squamous cells of undetermined significance and greater (ASC-US+), low-grade squamous intraepithelial lesion and greater (LSIL+), and high-grade squamous intraepithelial lesion and greater (HSIL+) groups. We evaluated 12,313 slides. The detection sensitivities for HSIL+ were increased by 19.6% (P < .0001) and for LSIL+ were increased by 9.8% (P < .0001) in the computer assisted arm, with small statistically significant decreases in specificity. For ASC-US+ sensitivity and specificity, the study arms were not statistically cl fferent. Use of this system might be expected to improve accuracy for clinically important entities without increasing equivocal case detection.
C1 [Wilbur, David C.; Black-Schaffer, W. Stephen] Massachusetts Gen Hosp, James Homer Wright Pathol Labs, Boston, MA 02114 USA.
[Wilbur, David C.; Black-Schaffer, W. Stephen] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Luff, Ronald D.] Quest Diagnost, Teterboro, NJ USA.
[Abraham, Kurian P.] Quest Diagnost, Schaumburg, IL USA.
[Kemper, Cynthia] Boyce & Bynum Pathol Labs PC, Columbia, MO USA.
[Tench, William D.] Palomar Med Ctr, Escondido, CA USA.
[Molina, James T.] Cyto Labs, San Antonio, TX USA.
RP Wilbur, DC (reprint author), Massachusetts Gen Hosp, James Homer Wright Pathol Labs, 55 Fruit St, Boston, MA 02114 USA.
NR 32
TC 34
Z9 34
U1 1
U2 3
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0002-9173
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD NOV
PY 2009
VL 132
IS 5
BP 767
EP 775
DI 10.1309/AJCP8VE7AWBZCVQT
PG 9
WC Pathology
SC Pathology
GA 509CA
UT WOS:000270988600017
PM 19846820
ER
PT J
AU Tsai, CL
Rowe, BH
Cydulka, RK
Camargo, CA
AF Tsai, Chu-Lin
Rowe, Brian H.
Cydulka, Rita K.
Camargo, Carlos A., Jr.
TI ED visit volume and quality of care in acute exacerbations of chronic
obstructive pulmonary disease
SO AMERICAN JOURNAL OF EMERGENCY MEDICINE
LA English
DT Article
ID EMERGENCY-DEPARTMENTS; MANAGEMENT; DIAGNOSIS; OUTCOMES
AB Objective: The purpose of this study is to determine whether emergency department (ED) visit volume is associated with ED quality of care in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD).
Methods: We performed a prospective multicenter cohort study involving 29 EDs in the United States and Canada. Using a standard protocol, we interviewed consecutive ED patients with COPD exacerbation, reviewed their charts, and completed a 2-week telephone follow-up. The associations between ED visit volume and quality of care (process and outcome measures) were examined at both the ED and patient levels.
Results: After adjustment for patient mix in the multivariable analyses, chest radiography was less frequent among patients with COPD exacerbations in the low-volume (odds ratio [OR], 0.2; 95% confidence interval [CI], 0.1-0.4) and high-volume EDs (OR, 0.1; 95% CI, 0.05-0.5), with medium-volume EDs as the reference. Arterial blood gas testing was less frequent in the low-volume EDs (OR, 0.1; 95% CI, 0.02-0.8). Medication use was similar across volume tertiles. With respect to outcome measures, patients in high-volume EDs were more likely to be discharged (OR, 4.2; 95% CI, 2.2-7.7) and to report ongoing exacerbation at a 2-week follow-up (OR, 1.9; 95% CI, 1.02-3.5).
Conclusions: Traditional positive volume-quality relationships did not apply to emergency care of COPD exacerbation. High-volume EDs used less guideline-recommended diagnostic procedures, had a higher admission threshold, and had a worse short-term patient-centered outcome. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Tsai, Chu-Lin] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med,EMNet Coordinating Ctr, Boston, MA 02114 USA.
[Tsai, Chu-Lin; Camargo, Carlos A., Jr.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Rowe, Brian H.] Univ Alberta, Dept Emergency Med, Edmonton, AB T6G 2B7, Canada.
[Cydulka, Rita K.] Case Western Reserve Univ, Metrohlth Med Ctr, Dept Emergency Med, Cleveland, OH 44109 USA.
RP Tsai, CL (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med,EMNet Coordinating Ctr, Boston, MA 02114 USA.
EM ctsai2@partners.org
OI TSAI, CHU-LIN/0000-0003-4639-1513
FU Boehringer Ingelheim
FX The present cohort studies were supported by an unrestricted grant from
Boehringer Ingelheim (Ridgefield, Conn, and Burlington, Ontario,
Canada).
NR 30
TC 2
Z9 2
U1 1
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0735-6757
J9 AM J EMERG MED
JI Am. J. Emerg. Med.
PD NOV
PY 2009
VL 27
IS 9
BP 1040
EP 1049
DI 10.1016/j.ajem.2008.07.034
PG 10
WC Emergency Medicine
SC Emergency Medicine
GA 527XB
UT WOS:000272403400003
PM 19931748
ER
PT J
AU Soremekun, OA
Shear, ML
Patel, S
Kim, GJ
Biddinger, PD
Parry, BA
Yialamas, MA
Thomas, SH
AF Soremekun, Olanrewaju A.
Shear, Melissa L.
Patel, Sagar
Kim, Gina J.
Biddinger, Paul D.
Parry, Blair A.
Yialamas, Maria A.
Thomas, Stephen H.
TI Rapid vascular glucose uptake via enzyme-assisted subcutaneous infusion:
Enzyme-Assisted Subcutaneous Infusion Access Study
SO AMERICAN JOURNAL OF EMERGENCY MEDICINE
LA English
DT Article
ID RECOMBINANT HUMAN HYALURONIDASE; RESUSCITATION; SKIN; VENIPUNCTURE
AB Background: Enzyme-assisted subcutaneous infusion (EASI), with subcutaneous human recombinant hyaluronidase pretreatment, may offer an alternative to standard intravenous (IV) access.
Objectives: This study's objectives were to assess paramedic (Emergency Medical Technician-Paramedic [EMTP])-placed EASI access in volunteers to determine (1) feasibility of EMTP EASI access placement; (2) subject/EMTP ratings of placement ease, discomfort, and overall EASI vs IV preference; and (3) speed of intravascular uptake of EASI infusate.
Methods: Twenty adults underwent 20-gauge IV placement by 4 EMTPs, receiving a 250-mL maximal-rate IV bolus of normal saline. Next, each subject received in the other arm a 20-gauge EASI access line (with 1-mL injection of 150 U of human recombinant hyaluronidase), through which was infused 250 mL D5NS (1 g glucose was labeled with stable tracer 13C). Blood draws enabled gas chromatography/mass spectrometry (GC/MS) assessment of 13C-glucose uptake. Intravenous access and EASI access were compared for time parameters and subject/EMTP ratings. Data were analyzed with median and interquartile range, Kruskal-Wallis testing, Fisher exact test, and regression (GC/MS data).
Results: Intravenous access and EASI access were successful in all 20 subjects. Compared with EASI access (all placed in <15 seconds), IV access took longer; but the 250-mL bolus was given more quickly via IV access. EMTPs rated EASI easier to place than IV; pain ratings were similar for Wand EASI. The GC/MS showed intravascular uptake at all time points.
C1 [Soremekun, Olanrewaju A.; Shear, Melissa L.; Patel, Sagar; Kim, Gina J.; Biddinger, Paul D.; Parry, Blair A.; Thomas, Stephen H.] Massachusetts Gen Hosp, Dept Emergency Serv, Boston, MA 02114 USA.
[Soremekun, Olanrewaju A.; Shear, Melissa L.; Patel, Sagar; Kim, Gina J.; Biddinger, Paul D.; Parry, Blair A.; Yialamas, Maria A.; Thomas, Stephen H.] Harvard Univ, Sch Med, Boston, MA USA.
[Yialamas, Maria A.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Soremekun, Olanrewaju A.] Brigham & Womens Hosp, Harvard Affiliated EM Residency Program, Boston, MA 02115 USA.
RP Thomas, SH (reprint author), Massachusetts Gen Hosp, Dept Emergency Serv, 0 Emerson Pl,Suite 3B, Boston, MA 02114 USA.
EM thomas.stephen@mgh.harvard.edu
FU Baxter
FX Project supported by an unrestricted grant from Baxter, the company that
markets the human recombinant hyaluronidase used in the study.
NR 27
TC 3
Z9 3
U1 0
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0735-6757
J9 AM J EMERG MED
JI Am. J. Emerg. Med.
PD NOV
PY 2009
VL 27
IS 9
BP 1072
EP 1080
DI 10.1016/j.ajem.2008.08.028
PG 9
WC Emergency Medicine
SC Emergency Medicine
GA 527XB
UT WOS:000272403400008
PM 19931753
ER
PT J
AU Friedman, LS
Gores, GJ
Vargo, JJ
Brandt, LJ
Katz, PO
Stolar, MH
Elta, GH
Kuemmerle, JF
Fitz, JG
Pardi, DS
AF Friedman, Lawrence S.
Gores, Gregory J.
Vargo, John J.
Brandt, Lawrence J.
Katz, Philip O.
Stolar, Michael H.
Elta, Grace H.
Kuemmerle, John F.
Fitz, J. Gregory
Pardi, Darrell S.
TI Report of the Multisociety Task Force on GI Training
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Editorial Material
C1 [Friedman, Lawrence S.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Friedman, Lawrence S.] Tufts Univ, Sch Med, Medford, MA 02155 USA.
[Friedman, Lawrence S.] Newton Wellesley Hosp, Newton, MA USA.
[Friedman, Lawrence S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Gores, Gregory J.; Pardi, Darrell S.] Mayo Clin, Coll Med Rochester, Rochester, MN 55905 USA.
[Vargo, John J.] Cleveland Clin, Lerner Coll Med, Cleveland, OH USA.
[Vargo, John J.] Cleveland Clin Fdn, Inst Digest Dis, Cleveland, OH USA.
[Brandt, Lawrence J.] Albert Einstein Coll Med, Montefiore Med Ctr, New York, NY USA.
[Katz, Philip O.] Thomas Jefferson Univ, Albert Einstein Med Ctr, Philadelphia, PA USA.
[Elta, Grace H.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Kuemmerle, John F.] Virginia Commonwealth Univ, Richmond, VA 23284 USA.
RP Friedman, LS (reprint author), Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
OI Vargo, John/0000-0001-7638-5283
NR 0
TC 3
Z9 3
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD NOV
PY 2009
VL 104
IS 11
BP 2659
EP 2663
DI 10.1038/ajg.2009.570
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 519YC
UT WOS:000271805100001
ER
PT J
AU Tukey, M
Pleskow, D
Legnani, P
Cheifetz, AS
Moss, AC
AF Tukey, Melissa
Pleskow, Doug
Legnani, Peter
Cheifetz, Adam S.
Moss, Alan C.
TI The Utility of Capsule Endoscopy in Patients With Suspected Crohn's
Disease
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID CHRONIC ABDOMINAL-PAIN; ENTEROCLYSIS; TRIAL; INDEX
AB OBJECTIVES: In patients with suspected Crohn's disease (CD), little is known about the test characteristics of capsule endoscopy (CE) in the diagnosis of this condition. We sought to determine the utility of CE for the subsequent diagnosis of CD in patients suspected to have this condition.
METHODS: All patients who underwent CE at a single tertiary-care center for investigation of suspected small bowel CD, and who had a 12-month follow-up, were included in the study. All patients had undergone other investigations that were normal or equivocal. The test characteristics of CE were determined on the basis of capsule findings of small bowel ulcers and a subsequent new diagnosis of CD within 12 months of CE.
RESULTS: The study included 102 patients with 12-month follow-up data. The majority (75%) met the established criteria to define "suspected Crohn's disease" as an indication for CE. Most had undergone computed tomography scan or small bowel follow-through (92%) and colonoscopy (99%) before CE. There were abnormal CE findings suggestive of CD in 39 patients. The prevalence rate of a new diagnosis of CD by 12 months in the study population was 13%. Using the presence of more than 3 ulcers as the criterion for an abnormal CE study, the sensitivity of CE for the diagnosis of CD was 77%, the specificity was 89%, the positive predictive value (PPV) was 50%, and the negative predictive value (NPV) was 96%.
CONCLUSIONS: In patients with suspected CD, CE has a high sensitivity and a NPV for this condition. The PPV varies depending on the patient population and the criteria for a CE diagnosis of CD.
C1 [Moss, Alan C.] Beth Israel Deaconess Med Ctr, Ctr Inflammatory Bowel Dis, Div Gastroenterol, Boston, MA 02215 USA.
[Tukey, Melissa; Pleskow, Doug; Cheifetz, Adam S.; Moss, Alan C.] Harvard Univ, Sch Med, Boston, MA USA.
[Legnani, Peter] Mt Sinai Sch Med, Div Gastroenterol, New York, NY USA.
RP Moss, AC (reprint author), Beth Israel Deaconess Med Ctr, Ctr Inflammatory Bowel Dis, Div Gastroenterol, Rose 1 E,BIDMC,330 Brookline Ave, Boston, MA 02215 USA.
EM amoss@bidmc.harvard.edu
OI Pleskow, Douglas/0000-0003-0092-9496
NR 22
TC 46
Z9 49
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD NOV
PY 2009
VL 104
IS 11
BP 2734
EP 2739
DI 10.1038/ajg.2009.404
PG 6
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 519YC
UT WOS:000271805100015
PM 19584828
ER
PT J
AU Mavandadi, S
Nazem, S
Ten Have, TR
Siderowf, AD
Duda, JE
Stern, MB
Weintraub, D
AF Mavandadi, Shahrzad
Nazem, Sarra
Ten Have, Thomas R.
Siderowf, Andrew D.
Duda, John E.
Stern, Matthew B.
Weintraub, Daniel
TI Use of Latent Variable Modeling to Delineate Psychiatric and Cognitive
Profiles in Parkinson Disease
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
DE Parkinson disease; neuropsychology; psychiatry; cognition; depression
ID QUALITY-OF-LIFE; NEUROPSYCHIATRIC DISTURBANCES; DEPRESSION; SYMPTOMS;
DEMENTIA; PREVALENCE; INVENTORY; SCALE; COMORBIDITY; DISORDERS
AB Objectives: A range of psychiatric symptoms and cognitive deficits occur in Parkinson disease (PD), and symptom overlap and comorbidity complicate the classification of nonmotor symptoms. The objective of this study was to use analytic-based approaches to classify psychiatric and cognitive symptoms in PD. Design: Cross-sectional evaluation of a convenience sample of patients in specialty care. Setting: Two outpatient movement disorders centers at the University of Pennsylvania and Philadelphia Veterans Affairs Medical Center. Participants: One hundred seventy-seven patients with mild-moderate idiopathic PD and without significant global cognitive impairment. Measurements: Subjects were assessed with an extensive psychiatric, neuropsychological, and neurological battery. Latent class analysis (LCA) was used to statistically delineate group-level symptom profiles across measures of psychiatric and cognitive functioning. Predictors of class membership were also examined. Results: Results from the LCA indicated that a four-class solution best fit the data. The 32.3% of the sample had good psychiatric and normal cognitive functioning, 17.5% had significant psychiatric comorbidity but normal cognition, 26.0% had few psychiatric symptoms but had poorer cognitive functioning across a range of cognitive domains, and 24.3% had both significant psychiatric comorbidity and poorer cognitive functioning. Age, disease severity, and medication use predicted class membership. Conclusions: LCA delineates four classes of patients in mild-moderate PD, three of which experience significant nonmotor impairments and comprise over two thirds of patients. Neuropsychiatric symptoms and cognitive deficits follow distinct patterns in PD, and further study is needed to determine whether these classes are generalizable, stable, predict function, quality of life, and long-term outcomes and are amenable to treatment at a class level. (Am J Geriatr Psychiatry 2009; 17:986-995)
C1 [Mavandadi, Shahrzad; Weintraub, Daniel] Philadelphia VA Med Ctr, Mental Illness Res Educ & Clin Ctr, Philadelphia, PA USA.
[Mavandadi, Shahrzad; Weintraub, Daniel] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA.
[Ten Have, Thomas R.] Univ Penn, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Siderowf, Andrew D.; Duda, John E.; Stern, Matthew B.; Weintraub, Daniel] Univ Penn, Dept Neurol, Philadelphia, PA 19104 USA.
[Duda, John E.; Stern, Matthew B.; Weintraub, Daniel] Philadelphia VA Med Ctr, Parkinsons Dis Res Educ & Clin Ctr, Philadelphia, PA USA.
RP Weintraub, D (reprint author), 3615 Chestnut St,Room 330, Philadelphia, PA 19104 USA.
EM daniel.weintraub@uphs.upenn.edu
FU National Institute of Mental Health (NIMH) [067894]
FX This work was supported by National Institute of Mental Health (NIMH)
grant no. 067894.
NR 42
TC 15
Z9 15
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1064-7481
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD NOV
PY 2009
VL 17
IS 11
BP 986
EP 995
PG 10
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA 517ZG
UT WOS:000271657200009
PM 19855199
ER
PT J
AU Harley, AE
Katz, ML
Heaney, CA
Duncan, DT
Buckworth, J
Odoms-Young, A
Willis, SK
AF Harley, Amy E.
Katz, Mira L.
Heaney, Catherine A.
Duncan, Dustin T.
Buckworth, Janet
Odoms-Young, Angela
Willis, Sharla K.
TI Social Support and Companionship Among Active African American Women
SO AMERICAN JOURNAL OF HEALTH BEHAVIOR
LA English
DT Article
DE physical activity; African Americans; women; qualitative research;
social support
ID PHYSICAL-ACTIVITY PARTICIPATION; ENVIRONMENTAL-INFLUENCES; SEDENTARY
WOMEN; UNITED-STATES; WALKING; COMMUNITY; EXERCISE; OUTCOMES; MEMBERS;
HEALTH
AB Objective: To examine the role of physical activity (PA) companions in supporting PA participation among African American women. Methods: Data were collected through in-depth interviews and focus groups. Fifteen physically active African American women participated in the study. Grounded theory data analysis techniques were used to develop a taxonomy depicting roles of PA companions for African American women. Results: PA companions functioned in 4 different roles: motivational, social, facilitative, and instructional. Supportive behaviors associated with each role were also elucidated. Conclusions: These findings provide an understanding for the function of companions in sustaining active lifestyle that can be used to inform intervention development.
C1 [Harley, Amy E.] Univ Wisconsin, Coll Hlth Sci, Ctr Urban Populat Hlth, Milwaukee, WI 53233 USA.
[Katz, Mira L.] Ohio State Univ, Coll Publ Hlth, Columbus, OH 43210 USA.
[Heaney, Catherine A.] Stanford Prevent Res Ctr, Stanford, CA USA.
[Duncan, Dustin T.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Buckworth, Janet] Ohio State Univ, Sch Phys Act & Educ Serv, Columbus, OH 43210 USA.
[Odoms-Young, Angela] Univ Illinois, Coll Appl Hlth Sci, Chicago, IL USA.
RP Harley, AE (reprint author), Univ Wisconsin, Coll Hlth Sci, Ctr Urban Populat Hlth, Milwaukee, WI 53233 USA.
EM harley@uwm.edu
RI Buckworth, Janet/B-5932-2012
NR 47
TC 12
Z9 12
U1 1
U2 7
PU PNG PUBLICATIONS
PI STAR CITY
PA PO BOX 4593, STAR CITY, WV 26504-4593 USA
SN 1087-3244
J9 AM J HEALTH BEHAV
JI Am. J. Health Behav.
PD NOV-DEC
PY 2009
VL 33
IS 6
BP 673
EP 685
PG 13
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 517FB
UT WOS:000271597500005
PM 19320616
ER
PT J
AU Romley, JA
Hussey, PS
de Vries, H
Wang, MC
Shekelle, PG
McGlynn, EA
AF Romley, John A.
Hussey, Peter S.
de Vries, Han
Wang, Margaret C.
Shekelle, Paul G.
McGlynn, Elizabeth A.
TI Efficiency and Its Measurement: What Practitioners Need to Know
SO AMERICAN JOURNAL OF MANAGED CARE
LA English
DT Article
ID HEALTH-CARE; QUALITY
AB Objective: To help health professionals understand and evaluate the concept of efficiency and its measurement in practice.
Study Design: We reviewed conceptual and practical analyses of healthcare efficiency and its measurement and describe our findings.
Methods: We searched the following 3 sources: the MEDLINE and EconLit databases for articles published from 1990 to 2008 using the keywords efficiency, inefficiency, productivity, and economic profiling; seminal economic studies of efficiency identified in MEDLINE or EconLit or in economics reference materials; and the "gray literature" on efficiency measures developed by private organizations.
Results: An essential element of efficiency is that healthcare outputs are as large as possible given their inputs. An efficiency measure specifies outputs and inputs appropriate to the goals of the assessment. Participants in the healthcare system have differing perspectives about the goals of efficiency assessments, relevant outputs and inputs, and validity of measures.
Conclusion: The broad meaning and the value of healthcare efficiency seem uncontroversial, yet any particular application may be confronted with conflicting perspectives and with practical challenges. (Am J Manag Care. 2009;15(11):842-845)
C1 [Romley, John A.; Hussey, Peter S.; Wang, Margaret C.; Shekelle, Paul G.; McGlynn, Elizabeth A.] RAND Corp, Santa Monica, CA 90407 USA.
[Romley, John A.] Occidental Coll, Dept Econ, Los Angeles, CA 90041 USA.
[de Vries, Han] RAND Europe, Cambridge, England.
[Shekelle, Paul G.] Greater Los Angeles Vet Affairs Healthcare Syst, Los Angeles, CA USA.
RP Romley, JA (reprint author), RAND Corp, 1776 Main St,POB 2138, Santa Monica, CA 90407 USA.
EM romley@rand.org
FU Agency for Healthcare research and Quality [282-00-0005-21]
FX This research was funded by the Agency for Healthcare research and
Quality, contract number 282-00-0005-21.
NR 13
TC 2
Z9 2
U1 0
U2 1
PU MANAGED CARE & HEALTHCARE COMMUNICATIONS LLC
PI PLAINSBORO
PA 666 PLAINSBORO RD, STE 300, PLAINSBORO, NJ 08536 USA
SN 1088-0224
J9 AM J MANAG CARE
JI Am. J. Manag. Care
PD NOV
PY 2009
VL 15
IS 11
BP 842
EP 845
PG 4
WC Health Care Sciences & Services; Health Policy & Services; Medicine,
General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 521QI
UT WOS:000271936800010
PM 19895189
ER
PT J
AU Chen, RC
Khorsandi, AS
Shatzkes, DR
Holliday, RA
AF Chen, R. C.
Khorsandi, A. S.
Shatzkes, D. R.
Holliday, R. A.
TI The Radiology of Referred Otalgia
SO AMERICAN JOURNAL OF NEURORADIOLOGY
LA English
DT Review
ID RHEUMATOID-ARTHRITIS; PAIN; EAR; NEURALGIA; VAGUS
AB Pain referred to the ear is a well-documented phenomenon, which can be due to a multitude of disease processes. With the recent and rapid progression of CT and MR imaging technology, radiologists have played an increasing role in solving this potentially difficult diagnostic dilemma. Essentially any pathology residing within the sensory net of cranial nerves V, VII, IX, and X and the upper cervical nerves C2 and C3 can potentially cause referred otalgia. This article will attempt to outline the various sensorineural pathways that dually innervate the ear and other sites within the head and neck, as well as discuss various disease processes that are known to result in referred otalgia.
C1 [Chen, R. C.; Khorsandi, A. S.] Beth Israel Deaconess Med Ctr, Dept Radiol, New York, NY 10003 USA.
[Shatzkes, D. R.] St Lukes Roosevelt Hosp, Dept Radiol, New York, NY USA.
[Holliday, R. A.] New York Eye & Ear Infirm, Dept Radiol, New York, NY 10003 USA.
RP Chen, RC (reprint author), Massachusetts Gen Hosp, Gray Bldg 273A,55 Fruit St, Boston, MA 02114 USA.
EM chenner23@gmail.com
NR 44
TC 4
Z9 4
U1 0
U2 1
PU AMER SOC NEURORADIOLOGY
PI OAK BROOK
PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA
SN 0195-6108
J9 AM J NEURORADIOL
JI Am. J. Neuroradiol.
PD NOV-DEC
PY 2009
VL 30
IS 10
BP 1817
EP 1823
DI 10.3174/ajnr.A1605
PG 7
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 527IV
UT WOS:000272361600005
PM 19797791
ER
PT J
AU Cuaron, JJ
Hirsch, JA
Medich, DC
Rosenstein, BS
Martel, CB
Hirsch, AE
AF Cuaron, J. J.
Hirsch, J. A.
Medich, D. C.
Rosenstein, B. S.
Martel, C. B.
Hirsch, A. E.
TI A Proposed Methodology to Select Radioisotopes for Use in Radionuclide
Therapy
SO AMERICAN JOURNAL OF NEURORADIOLOGY
LA English
DT Article
ID HEPATIC RADIOEMBOLIZATION; VERTEBRAL AUGMENTATION; COMPRESSION
FRACTURES; CANCER; BRACHYTHERAPY; RADIATION; AT-211; Y-90
AB The American Journal of Neuroradiology has played a seminal role in the history of vertebral augmentation (VA). Because VA is increasingly being included in the multidisciplinary management of malignant vertebral compression fractures (VCFs), combined therapeutic approaches that include strategies to treat metastatic disease along with the fracture have become appealing options for patients. To that end, we recently investigated the closimetric feasibility of treating malignant VCFs with radionuclide therapy. The goal would be to provide local control of the systemic disease beyond the pain relief and structural support provided by polymethylmethacrylate cement. The purpose of this article is to propose a methodology for evaluating radionuclides for use in radiation therapy that takes into account a number of factors including radiation characteristics, biochemical effects, production capacity, and safety, The goal of such a methodology is to introduce a systematic approach to selecting radionuclides in designing treatment regimens and future investigations and also to stimulate discussion and experimentation involving new radionuclides that may provide more effective treatments than the current isotopes in widespread use.
C1 [Cuaron, J. J.; Hirsch, A. E.] Boston Univ, Med Ctr, Dept Radiat Oncol, Sch Med, Boston, MA 02118 USA.
[Hirsch, J. A.] Massachusetts Gen Hosp, Dept Radiol, Div Intervent Neuroradiol, Boston, MA 02114 USA.
[Medich, D. C.] Univ Massachusetts, Radiat Lab, Lowell, MA USA.
[Rosenstein, B. S.] Mt Sinai Sch Med, Dept Radiat Oncol, New York, NY USA.
[Rosenstein, B. S.] Mt Sinai Sch Med, Dept Dermatol, New York, NY USA.
[Rosenstein, B. S.] Mt Sinai Sch Med, Dept Community & Prevent Med, New York, NY USA.
[Rosenstein, B. S.] NYU, Sch Med, Dept Radiat Oncol, New York, NY USA.
[Martel, C. B.] Brigham & Womens Hosp, Dept Hlth Phys, Boston, MA 02115 USA.
RP Hirsch, AE (reprint author), Boston Univ, Med Ctr, Dept Radiat Oncol, Massachusetts Gen Hosp, 830 Harrison Ave,Moakley Bldg LL, Boston, MA 02118 USA.
EM Ariel.hirsch@bmc.org
RI Medich, David/B-6006-2013
NR 34
TC 4
Z9 5
U1 0
U2 2
PU AMER SOC NEURORADIOLOGY
PI OAK BROOK
PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA
SN 0195-6108
J9 AM J NEURORADIOL
JI Am. J. Neuroradiol.
PD NOV-DEC
PY 2009
VL 30
IS 10
BP 1824
EP 1829
DI 10.3174/ajnr.A1773
PG 6
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 527IV
UT WOS:000272361600006
PM 19661172
ER
PT J
AU Eichler, F
Grodd, W
Grant, E
Sessa, M
Biffi, A
Bley, A
Kohlschuetter, A
Loes, DJ
Kraegeloh-Mann, I
AF Eichler, F.
Grodd, W.
Grant, E.
Sessa, M.
Biffi, A.
Bley, A.
Kohlschuetter, A.
Loes, D. J.
Kraegeloh-Mann, I.
TI Metachromatic Leukodystrophy: A Scoring System for Brain MR Imaging
Observations
SO AMERICAN JOURNAL OF NEURORADIOLOGY
LA English
DT Article
ID ADRENOLEUKODYSTROPHY; PHENOTYPE; MUTATION; ONSET
AB BACKGROUND AND PURPOSE: Metachromatic leukodystrophy (MLD) is a devastating demyelinating disease for which novel therapies are being tested. We hypothesized that MR imaging of brain lesion involvement in MLD could be quantified along a scale.
MATERIALS AND METHODS: Thirty-four brain MR images in 28 patients with proved biochemical and genetic defects for MLD were reviewed: 10 patients with late infantile, 16 patients with juvenile, and 2 patients with adult MLD. All MR images were reviewed by experienced neuroradiologists and neurologists (2 readers in Germany, 2 readers in the United States) for global disease burden, as seen on the T2 and fluid-attenuated inversion recovery images. A visual scoring method was based on a point system (range, 0-34) derived from the location of white matter involvement and the presence of global atrophy, aralogous to the scoring system developed for adrenoleukodystrophy. The readers were blinded to the neurologic findings.
RESULTS: Thirty-three of 34 MR images showed confluent T2 hyperintensities of white matter. The inter-rater reliability coefficient was 0.988. Scores between readers were within 2 points of each other. Serial MR imaging studies in 6 patients showed significant progressive disease in 3 patients (initial score average, 4; mean follow-up, 24.3) and no change or I point progression in 3 patients (initial score average, 12; mean follow-up, 12.66). Projection fibers and the cerebellum tended to be involved only in advanced stages of disease.
CONCLUSIONS: The MLD MR severity scoring method can be used to provide a measure of brain MR imaging involvement in MLD patients.
C1 [Eichler, F.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02114 USA.
[Eichler, F.; Grant, E.] AA Martinos Ctr Biomed Imaging, Charlestown, MA USA.
[Kraegeloh-Mann, I.] Univ Tubingen, Dept Pediat, Tubingen, Germany.
[Grodd, W.] Univ Tubingen, Dept Radiol, Tubingen, Germany.
[Sessa, M.; Biffi, A.] Ist Sci San Raffaele, San Raffaele Telethon Inst Gene Therapy, I-20132 Milan, Italy.
[Bley, A.; Kohlschuetter, A.] Univ Med Ctr Hamburg Eppendorf, Dept Pediat, Hamburg, Germany.
[Loes, D. J.] Suburban Radiol Consultants, Minneapolis, MN USA.
RP Eichler, F (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, 55 Fruit St,ACC 708, Boston, MA 02114 USA.
EM feichler@partners.org
FU National Institutes of Health [W08NS52550]; Fondazione Telethon
FX This work was supported by grant the National Institutes of Health grant
W08NS52550.
NR 13
TC 38
Z9 38
U1 0
U2 0
PU AMER SOC NEURORADIOLOGY
PI OAK BROOK
PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA
SN 0195-6108
J9 AM J NEURORADIOL
JI Am. J. Neuroradiol.
PD NOV-DEC
PY 2009
VL 30
IS 10
BP 1893
EP 1897
DI 10.3174/ajnr.A1739
PG 5
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 527IV
UT WOS:000272361600017
PM 19797797
ER
PT J
AU Bhat, PV
Jakobiec, FA
Kurbanyan, K
Zhao, TZ
Foster, CS
AF Bhat, Pooja V.
Jakobiec, Frederick A.
Kurbanyan, Kristina
Zhao, Tongzhen
Foster, C. Stephen
TI Chronic Herpes Simplex Scleritis: Characterization of 9 Cases of an
Underrecognized Clinical Entity
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID NECROTIZING SCLEROKERATITIS; WEGENERS-GRANULOMATOSIS; ACYCLOVIR;
DISEASE; EPISCLERITIS; INFECTION; KERATITIS; MANIFESTATIONS;
BLEPHARITIS; DIAGNOSIS
AB PURPOSE: To characterize in detail persistent and recalcitrant infectious scleritis resulting from herpes simplex virus (HSV).
DESIGN: Retrospective and interventional clinical and immunopathologic case series.
METHODS: Nine patients with chronic scleral redness, edema, and pain refractory to conventional therapy underwent a scleroconjunctival biopsy for routine histopathologic evaluation and definitive immunodiagnosis for the presence of HSV. Immunofluorescent probing for HSV was performed on the patient specimens. Negative controls for HSV included elimination of anti-HSV and anti-varicella zoster virus antibody in the probing process and the use of normal human conjunctiva and sclera as substrates. Response to therapy with acyclovir was monitored and recorded.
RESULTS: The average age of the affected patients was 50.2 years, and the average duration of symptoms before tissue diagnosis of herpetic scleritis was 3.2 years (me, dian, 4 years). Three histopathologic patterns were discovered: granulomatous inflammation (2 cases), plasma cell-rich pyogenic granuloma-like pattern (1 case), and reactive fibroinflammatory pattern (6 cases). Herpes antigen was demonstrated uniformly by immunofluorescence in a perivascular distribution and less commonly in the interstitium. Varicella zoster virus was not detected, and all controls for nonspecific antibody reagent binding to tissue showed negative results. Acyclovir caused a dramatic improvement in the chronic or recurrent ocular inflammation in all instances, with an average duration of improvement of inflammation of 15.3 months.
CONCLUSIONS: Unrecognized HSV infection can cause longstanding scleritis. Histopathologic features of HSV scleritis are varied and nonspecific; immunofluorescent demonstration of HSV protein can make a definitive diagnosis. Prolonged administration of acyclovir is required for effective therapy. (Am J Ophthalmol 2009;148:779-789. (C) 2009 by Elsevier Inc. All rights reserved.)
C1 [Bhat, Pooja V.; Jakobiec, Frederick A.] Massachusetts Eye & Ear Infirm, Dept Ophthalmol, David G Cogan Lab Ophthalm Pathol, Boston, MA 02114 USA.
[Bhat, Pooja V.; Jakobiec, Frederick A.; Kurbanyan, Kristina; Foster, C. Stephen] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA USA.
[Zhao, Tongzhen; Foster, C. Stephen] Ocular Immunol & Uveitis Fdn, Massachusetts Eye Res & Surg Inst, Cambridge, MA USA.
RP Jakobiec, FA (reprint author), Massachusetts Eye & Ear Infirm, Dept Ophthalmol, David G Cogan Lab Ophthalm Pathol, Suite 321,243 Charles St, Boston, MA 02114 USA.
EM Fred_Jakobiec@meei.harvard.edu
NR 49
TC 13
Z9 14
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD NOV
PY 2009
VL 148
IS 5
BP 779
EP 789
DI 10.1016/j.ajo.2009.06.025
PG 11
WC Ophthalmology
SC Ophthalmology
GA 518DA
UT WOS:000271669300021
PM 19674728
ER
PT J
AU Chung, ES
Chauhan, SK
Jin, YP
Nakao, S
Hafezi-Moghadam, A
van Rooijen, N
Zhang, Q
Chen, L
Dana, R
AF Chung, Eui-Sang
Chauhan, Sunil Kumar
Jin, Yiping
Nakao, Shintaro
Hafezi-Moghadam, Ali
van Rooijen, Nico
Zhang, Qiang
Chen, Lu
Dana, Reza
TI Contribution of Macrophages to Angiogenesis Induced by Vascular
Endothelial Growth Factor Receptor-3-Specific Ligands
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID VEGF-C; LYMPHATIC REGENERATION; TUMOR ANGIOGENESIS; FACTOR RECEPTOR-1;
TRANSGENIC MICE; EXPRESSION; LYMPHANGIOGENESIS; MOUSE; BLOOD; ACTIVATION
AB Vascular endothelial growth factor receptor (VEGFR)-2 is a major stimulator of hemangiogenesis (HA), whereas VEGFR-3 stimulates lymphangiogenesis (LA). Contrary to this understanding, we demonstrate that implantation of pellets containing VEGFR-3-specific ligands (VEGF-C156S and recombinant murine VEGF-D) into the corneal stroma induce not only LA but also robust HA characterized by blood vessels that are positive for VEGFR-3 expression. The implantation of pellets containing VEGFR-3-specific ligands also leads to the recruitment of VEGF-A-secreting macrophages. Depletion of these infiltrating macrophages using clodronate-liposome administration shows a significant reduction in HA as well as LA. Blockade of either VEGFR-2 or VEGFR-3 signaling reduces both HA and LA; however, the percent reduction of HA is greater in the VEGFR-2 blockade group. In addition, in the VEGFR-3 blockade group, the percent reduction of RA is significantly greater with VEGFR-3-specific ligands than that by VEGF-A or VEGF-C. Collectively, our data suggest that VEGFR-3-specific signaling can induce new blood vessels, to which macrophages contribute a major role, and signify its potential as an additional therapeutic target to the existing VEGF-A/VEGFR-2 signaling-based antiangiogenesis strategies. (Am J Pathol 2009, 175:1984-1992; DOI: 10.2353/ajpath.2009.080515)
C1 [Dana, Reza] Harvard Univ, Sch Med, Dept Ophthalmol, Schepens Eye Res Inst, Boston, MA 02114 USA.
[Chung, Eui-Sang] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Ophthalmol, Seoul, South Korea.
[Hafezi-Moghadam, Ali; Dana, Reza] Harvard Univ, Sch Med, Dept Ophthalmol, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[van Rooijen, Nico] Vrije Univ Amsterdam, Ctr Med, Dept Mol Cell Biol, Amsterdam, Netherlands.
RP Dana, R (reprint author), Harvard Univ, Sch Med, Dept Ophthalmol, Schepens Eye Res Inst, 20 Staniford St, Boston, MA 02114 USA.
EM reza.dana@schepens.harvard.edu
OI Hafezi-Moghadam, Ali/0000-0002-5336-0697
FU National Institutes of Health [NEI-RO1-12963]; U.S. Department of
Defense [W81XWH-07-2-0038]; New England Transplant Research Fund
FX Supported in part by National Institutes of Health grant NEI-RO1-12963,
U.S. Department of Defense grant W81XWH-07-2-0038, and New England
Transplant Research Fund (to R.D.).
NR 43
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U2 5
PU AMER SOC INVESTIGATIVE PATHOLOGY, INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3993 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD NOV
PY 2009
VL 175
IS 5
BP 1984
EP 1992
DI 10.2353/ajpath.2009.080515
PG 9
WC Pathology
SC Pathology
GA 515BH
UT WOS:000271440800020
PM 19808642
ER
PT J
AU Panda, D
Goltzman, D
Juppner, H
Karaplis, AC
AF Panda, Dibiyendu
Goltzman, David
Jueppner, Harald
Karaplis, Andrew C.
TI TIP39/parathyroid hormone type 2 receptor signaling is a potent
inhibitor of chondrocyte proliferation and differentiation
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE growth plate; cell cycle; osteoarthritis; secondary ossification center;
Sox9
ID OLIGOMERIC MATRIX PROTEIN; TRANSCRIPTION FACTOR SOX9; PTH-RELATED
PEPTIDE; PARATHYROID-HORMONE; TUBEROINFUNDIBULAR PEPTIDE; PTH/PTHRP
RECEPTOR; 39 RESIDUES; BLOMSTRAND-CHONDRODYSPLASIA; GROWTH-PLATE;
CATHEPSIN-D
AB Panda D, Goltzman D, Juppner H, Karaplis AC. TIP39/parathyroid hormone type 2 receptor signaling is a potent inhibitor of chondrocyte proliferation and differentiation. Am J Physiol Endocrinol Metab 297: E1125-E1136, 2009. First published August 25, 2009; doi: 10.1152/ajpendo.00254.2009.-Tuberoinfundibular peptide of 39 residues (TIP39) is a member of the parathyroid hormone (PTH) family of peptide hormones that exerts its function by interacting with the PTH type 2 receptor (PTH2R). Presently, no known function has been attributed to this signaling pathway in the developing skeleton. We observed that TIP39 and PTH2R were present in the newborn mouse growth plate, with the receptor localizing in the resting zone whereas ligand expression was restricted exclusively in prehypertrophic and hypertrophic chondrocytes. By 8 wk of life, PTH2R, and to a lesser degree TIP39, immunoreactivity was present in articular chondrocytes. We therefore sought to investigate the role of TIP39/PTH2R signaling in chondrocytes by generating stably transfected CFK2 chondrocytic cells overexpressing PTH2R (CFK2R). TIP39 treatment of CFK2R clones in culture inhibited their proliferation by restricting cells at the G(0)/G(1) phase of the cell cycle, coupled with decreased expression and activity of cyclin-dependent kinases Cdk2 and Cdk4, while p21, an inhibitor of Cdks, was upregulated. In addition, TIP39 treatment decreased expression of differentiation markers in these cells associated with marked alterations in extracellular matrix and metalloproteinase expression. Transcription of Sox9, the master regulator of cartilage differentiation, was reduced in TIP39-treated CFK2R clones. Moreover, Sox9 promoter activity, as measured by luciferase reporter assay, was markedly diminished after TIP39 treatment. In summary, our results show that TIP39/PTH2R signaling inhibits proliferation and alters differentiation of chondrocytes by modulating SOX9 expression, thereby substantiating the functional significance of this signaling pathway in chondrocyte biology.
C1 [Panda, Dibiyendu; Karaplis, Andrew C.] McGill Univ, Div Endocrinol, Dept Med, Sir Mortimer B Davis Jewish Gen Hosp, Montreal, PQ H3T 1E2, Canada.
[Panda, Dibiyendu; Karaplis, Andrew C.] McGill Univ, Lady Davis Inst Med Res, Sir Mortimer B Davis Jewish Gen Hosp, Montreal, PQ H3T 1E2, Canada.
[Goltzman, David] McGill Univ Hlth Ctr, Calcium Res Lab, Dept Med, Montreal, PQ, Canada.
[Jueppner, Harald] Massachusetts Gen Hosp, Dept Med, Endocrine Unit, Boston, MA 02114 USA.
[Jueppner, Harald] Harvard Univ, Sch Med, Boston, MA USA.
RP Karaplis, AC (reprint author), McGill Univ, Div Endocrinol, Dept Med, Sir Mortimer B Davis Jewish Gen Hosp, 3755 Cote Ste Catherine Rd, Montreal, PQ H3T 1E2, Canada.
EM akarapli@ldi.jgh.mcgill.ca
FU Canadian Institutes of Health Research (CIHR); National Institute of
Diabetes and Digestive and Kidney Diseases [DK-11794]; Fonds de la
Recherche en Sante du Quebec
FX This work was supported by grants from the Canadian Institutes of Health
Research (CIHR) (D. Goltzman and A. C. Karaplis) and National Institute
of Diabetes and Digestive and Kidney Diseases Grant DK-11794, project IV
(H. Juppner). A. C. Karaplis is recipient of a Bourse de Chercheurs
Nationaux from the Fonds de la Recherche en Sante du Quebec.
NR 43
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U1 0
U2 4
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1849
J9 AM J PHYSIOL-ENDOC M
JI Am. J. Physiol.-Endocrinol. Metab.
PD NOV
PY 2009
VL 297
IS 5
BP E1125
EP E1136
DI 10.1152/ajpendo.00254.2009
PG 12
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 509CL
UT WOS:000270990500018
PM 19706789
ER
PT J
AU Mani, SK
Balasubramanian, S
Zavadzkas, JA
Jeffords, LB
Rivers, WT
Zile, MR
Mukherjee, R
Spinale, FG
Kuppuswamy, D
AF Mani, Santhosh K.
Balasubramanian, Sundaravadivel
Zavadzkas, Juozas A.
Jeffords, Laura B.
Rivers, William T.
Zile, Michael R.
Mukherjee, Rupak
Spinale, Francis G.
Kuppuswamy, Dhandapani
TI Calpain inhibition preserves myocardial structure and function following
myocardial infarction
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE cardiomyocytes; cell death
ID ENDOPLASMIC-RETICULUM STRESS; CARDIAC MYOCYTE APOPTOSIS;
SMOOTH-MUSCLE-CELLS; HEART-FAILURE; DEGRADED COLLAGEN; CROSS-TALK;
ACTIVATION; DEATH; PATHOGENESIS; HYPERTROPHY
AB Mani SK, Balasubramanian S, Zavadzkas JA, Jeffords LB, Rivers WT, Zile MR, Mukherjee R, Spinale FG, Kuppuswamy D. Calpain inhibition preserves myocardial structure and function following myocardial infarction. Am J Physiol Heart Circ Physiol 297: H1744-H1751, 2009. First published September 4, 2009; doi:10.1152/ajpheart.00338.2009.-Cardiac pathology, such as myocardial infarction (MI), activates intracellular proteases that often trigger programmed cell death and contribute to maladaptive changes in myocardial structure and function. To test whether inhibition of calpain, a Ca(2+)-dependent cysteine protease, would prevent these changes, we used a mouse MI model. Calpeptin, an aldehydic inhibitor of calpain, was intravenously administered at 0.5 mg/kg body wt before MI induction and then at the same dose subcutaneously once per day. Both calpeptin-treated (n = 6) and untreated (n = 6) MI mice were used to study changes in myocardial structure and function after 4 days of MI, where end-diastolic volume (EDV) and left ventricular ejection fraction (EF) were measured by echocardiography. Calpain activation and programmed cell death were measured by immunohistochemistry, Western blotting, and TdT-mediated dUTP nick-end labeling (TUNEL). In MI mice, calpeptin treatment resulted in a significant improvement in EF [EF decreased from 67 +/- 2% pre-MI to 30 +/- 4% with MI only vs. 41 +/- 2% with MI + calpeptin] and attenuated the increase in EDV [EDV increased from 42 +/- 2 mu l pre-MI to 73 +/- 4 mu l with MI only vs. 55 +/- 4 mu l with MI + calpeptin]. Furthermore, calpeptin treatment resulted in marked reduction in calpain-and caspase-3-associated changes and TUNEL staining. These studies indicate that calpain contributes to MI-induced alterations in myocardial structure and function and that it could be a potential therapeutic target in treating MI patients.
C1 [Mani, Santhosh K.; Balasubramanian, Sundaravadivel; Zile, Michael R.; Kuppuswamy, Dhandapani] Med Univ S Carolina, Dept Med, Div Cardiol, Charleston, SC 29425 USA.
[Zavadzkas, Juozas A.; Jeffords, Laura B.; Rivers, William T.; Mukherjee, Rupak; Spinale, Francis G.] Med Univ S Carolina, Dept Surg, Div Cardiothorac Surg, Charleston, SC 29425 USA.
[Zile, Michael R.; Spinale, Francis G.; Kuppuswamy, Dhandapani] Ralph H Johnson Dept Vet Affairs Med Ctr, Charleston, SC USA.
RP Kuppuswamy, D (reprint author), Med Univ S Carolina, Gazes Cardiac Res Inst, 114 Doughty St, Charleston, SC 29425 USA.
EM kuppusd@musc.edu
FU National Heart, Lung, and Blood Institute (NHLBI) [PPG HL-48788, R01
HL-092124]; Research Service of the Department of Veterans Affairs
FX This study was supported by National Heart, Lung, and Blood Institute
(NHLBI) Grant PPG HL-48788, a Merit Award from the Research Service of
the Department of Veterans Affairs, and NHLBI Grant R01 HL-092124 (to D.
Kuppuswamy).
NR 59
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U1 0
U2 4
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD NOV
PY 2009
VL 297
IS 5
BP H1744
EP H1751
DI 10.1152/ajpheart.00338.2009
PG 8
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 511DF
UT WOS:000271143400024
PM 19734364
ER
PT J
AU Johnson, M
Allen, L
Dobbs, L
AF Johnson, Meshell
Allen, Lennell
Dobbs, Leland
TI Characteristics of Cl- uptake in rat alveolar type I cells
SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
LA English
DT Article
DE chloride transport; cystic fibrosis transmembrane regulator; CLC5
ID TRANSMEMBRANE CONDUCTANCE REGULATOR; POSTNATAL LUNG DEVELOPMENT; NASAL
EPITHELIAL-CELLS; CHLORIDE-CHANNEL; ION-TRANSPORT; TRACHEAL EPITHELIUM;
ANION-EXCHANGERS; SODIUM-CHANNELS; XENOPUS OOCYTES; FETAL LAMB
AB Johnson M, Allen L, Dobbs L. Characteristics of Cl- uptake in rat alveolar type I cells. Am J Physiol Lung Cell Mol Physiol 297: L816-L827, 2009. First published August 14, 2009; doi: 10.1152/ajplung.90466.2008. Although Cl- transport in fetal lung is important for fluid secretion and normal lung development, the role of Cl- transport in adult lung is not well understood. In physiological studies, the cystic fibrosis transmembrane regulator (CFTR) plays a role in fluid absorption in the distal air spaces of adult lung, and alveolar type II cells cultured for 5 days have the capacity to transport Cl-. Although both alveolar type I and type II cells express CFTR, it has previously not been known whether type I cells transport Cl-. We studied Cl- uptake in isolated type I cells directly, using either radioisotopic tracers or halide-sensitive fluorescent indicators. By both methods, type I cells take up Cl-. In the presence of beta-adrenergic agonist stimulation, Cl- uptake can be inhibited by CFTR antagonists. Type I cells express both the Cl-/HCO3- anion exchanger AE2 and the voltage-gated Cl- channels CLC5 and CLC2. Inhibitors of AE2 also block Cl- uptake in type I cells. Together, these results demonstrate that type I cells are capable of Cl- uptake and suggest that the effects seen in whole lung studies establishing the importance of Cl- movement in alveolar fluid clearance may be, in part, the result of Cl- transport across type I cells.
C1 [Johnson, Meshell; Dobbs, Leland] Univ Calif San Francisco, Dept Med, San Francisco, CA 94118 USA.
[Allen, Lennell; Dobbs, Leland] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94118 USA.
[Dobbs, Leland] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94118 USA.
[Johnson, Meshell] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Johnson, M (reprint author), Univ Calif San Francisco, Dept Med, 3333 Calif St,Suite 150,Box 1245, San Francisco, CA 94118 USA.
EM meshell.johnson@ucsf.edu
FU National Heart, Lung, and Blood Institute [HL-24075, HL-57426,
HL-088025]; Robert Wood Johnson Foundation Amos Medical Faculty
Development Program
FX This study was supported by National Heart, Lung, and Blood Institute
Grants HL-24075 and HL-57426 (L. Dobbs) and HL-088025 (M. Johnson) and
the Robert Wood Johnson Foundation Amos Medical Faculty Development
Program (M. Johnson).
NR 65
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U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1040-0605
J9 AM J PHYSIOL-LUNG C
JI Am. J. Physiol.-Lung Cell. Mol. Physiol.
PD NOV
PY 2009
VL 297
IS 5
BP L816
EP L827
DI 10.1152/ajplung.90466.2008
PG 12
WC Physiology; Respiratory System
SC Physiology; Respiratory System
GA 511CN
UT WOS:000271141600005
PM 19684200
ER
PT J
AU Williams, DL
Baskin, DG
Schwartz, MW
AF Williams, Diana L.
Baskin, Denis G.
Schwartz, Michael W.
TI Hindbrain leptin receptor stimulation enhances the anorexic response to
cholecystokinin
SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE
PHYSIOLOGY
LA English
DT Article
DE nucleus of the solitary tract; satiety signals; adiposity signals; food
intake
ID CENTRAL-NERVOUS-SYSTEM; CAUDAL BRAIN-STEM; FOOD-INTAKE; MEAL SIZE;
SOLITARY TRACT; GENE-EXPRESSION; BLOOD-GLUCOSE; OB PROTEIN; LEAN MICE;
C-FOS
AB Williams DL, Baskin DG, Schwartz MW. Hindbrain leptin receptor stimulation enhances the anorexic response to cholecystokinin. Am J Physiol Regul Integr Comp Physiol 297: R1238-R1246, 2009. First published September 2, 2009; doi: 10.1152/ajpregu.00182.2009.-Leptin is thought to reduce food intake, in part, by increasing sensitivity to satiation signals, including CCK. Leptin action in both forebrain and hindbrain reduces food intake, and forebrain leptin action augments both the anorexic and neuronal activation responses to CCK. Here, we asked whether leptin signaling in hindbrain also enhances these responses to CCK. We found that food intake was strongly inhibited at 30 min after a combination of 4th-intracerebroventricular (4th-icv) leptin injection and intraperitoneal CCK administration, whereas neither hormone affected intake during this period when given alone. Leptin injections targeted directly at the dorsal vagal complex (DVC) similarly enhanced the anorexic response to intraperitoneal CCK. Intra-DVC leptin injection also robustly increased the number of neurons positive for phospho-STAT3 staining in the area surrounding the site of injection, confirming local leptin receptor activation. Conversely, the anorexic response to 4th-icv leptin was completely blocked by IP devazepide, a CCKA-R antagonist, suggesting that hindbrain leptin reduces intake via a mechanism requiring endogenous CCK signaling. We then asked whether hindbrain leptin treatment enhances the dorsomedial hindbrain, hypothalamus, or amygdala c-Fos responses to IP CCK. We found that, in contrast to the effects of forebrain leptin administration, 4th-icv leptin injection had no effect on CCK-induced c-Fos in any structures examined. We conclude that leptin signaling in either forebrain or hindbrain areas can enhance the response to satiation signals and that multiple distinct neural circuits likely contribute to this interaction.
C1 [Williams, Diana L.] Florida State Univ, Dept Psychol, Tallahassee, FL 32306 USA.
[Williams, Diana L.] Florida State Univ, Program Neurosci, Tallahassee, FL 32306 USA.
[Baskin, Denis G.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Baskin, Denis G.; Schwartz, Michael W.] Univ Washington, Dept Med, Ctr Excellence, Seattle, WA USA.
[Baskin, Denis G.] Univ Washington, Dept Biol Struct, Ctr Excellence, Seattle, WA 98195 USA.
[Baskin, Denis G.; Schwartz, Michael W.] Univ Washington, Dept Diabet & Obes, Ctr Excellence, Seattle, WA 98195 USA.
RP Williams, DL (reprint author), Florida State Univ, Dept Psychol, POB 3064301, Tallahassee, FL 32306 USA.
EM williams@psy.fsu.edu
RI Schwartz, Michael/H-9950-2012; Williams, Diana/C-1699-2014
OI Williams, Diana/0000-0002-3548-7440
FU NIH [K99DK078779, DK52989, NS032273, DK68384, P30DK035816, P30DK17047];
Office of Research and Development Medical Research Service, Department
of Veterans Affairs
FX These studies were supported by NIH grants K99DK078779 to DLW and
DK52989, NS032273 and DK68384 to MWS. This material is also based upon
work supported in part by the Office of Research and Development Medical
Research Service, Department of Veterans Affairs. Dr. Baskin is Senior
Research Career Scientist, Research and Development Service, Department
of Veterans Affairs Puget Sound Health Care System, Seattle, WA. This
research was also supported by the Clinical Nutrition Research Unit at
the University of Washington, supported by NIH grant P30DK035816, and
the facilities of the Cellular and Molecular Imaging Core of the
University of Washington NIH Diabetes Endocrinology Research Center,
supported by NIH grant P30DK17047.
NR 30
TC 23
Z9 23
U1 0
U2 4
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6119
J9 AM J PHYSIOL-REG I
JI Am. J. Physiol.-Regul. Integr. Comp. Physiol.
PD NOV
PY 2009
VL 297
IS 5
BP R1238
EP R1246
DI 10.1152/ajpregu.00182.2009
PG 9
WC Physiology
SC Physiology
GA 514CR
UT WOS:000271371900003
PM 19726710
ER
PT J
AU Bauer, MS
Biswas, K
Kilbourne, AM
AF Bauer, Mark S.
Biswas, Kousick
Kilbourne, Amy M.
TI Enhancing Multiyear Guideline Concordance for Bipolar Disorder Through
Collaborative Care
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the VA-Health-Services-Research-and-Development
CY FEB 11-13, 2009
CL Baltimore, MD
SP VA Hlth Serv Res & Dev
ID IMPROVING PRIMARY-CARE; MEDICATION-ALGORITHM-PROJECT; CLINICAL-PRACTICE
GUIDELINES; RANDOMIZED CONTROLLED-TRIAL; LATE-LIFE DEPRESSION;
QUALITY-OF-CARE; MENTAL-HEALTH; THERAPEUTIC DRUG; CHRONIC ILLNESS; I
DISORDER
AB Objective: Implementation of evidence-based care for serious mental illnesses such as bipolar disorder has been suboptimal. Improving and sustaining concordance with clinical practice guidelines has been a cornerstone of efforts to enhance evidence-based care and improve outcomes. For bipolar disorder, however, there has been only one regional controlled trial reporting guideline concordance, and no data are available for time periods longer than 1 year. In a multiregion effectiveness trial in veterans with bipolar disorder, the authors assessed the effects of a collaborative care model for this disorder on guideline concordance in care over a 3-year period.
Method: A total of 306 participants with bipolar disorder were randomly assigned at hospital discharge to 3 years of follow-up treatment with a collaborative care model or to usual care. The collaborative care model included provider support through simplified practice guidelines, patient skills management enhancement through group psychoeducation, and facilitated access and continuity via nurse care management. Concordance with guideline-recommended antimanic pharmacotherapy was assessed at baseline and prospectively over six 6-month epochs. Group differences were assessed with generalized estimating equations that controlled for relevant covariates.
Results: The collaborative care model achieved significantly higher rates of guideline-concordant antimanic treatment than usual care over the entire follow-up period. Baseline guideline concordance, but not patient age or bipolar type, was associated with higher concordance.
Conclusions: Multicomponent collaborative care models, which include not only provider support for guideline implementation but also patient self-management skill enhancement and facilitated treatment access and continuity, can improve guideline concordance over the long term, even in severely impaired patients.
C1 Harvard Univ, Sch Med, Boston, MA USA.
Boston VA Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA USA.
Perry Point VA Cooperat Studies Coordinating Ctr, Perry Point, MD USA.
VA Natl Serious Mental Illness Treatment Res & Ev, Ann Arbor, MI USA.
Univ Michigan, Sch Med, Dept Psychiat, Ann Arbor, MI USA.
RP Bauer, MS (reprint author), VA Boston Healthcare Syst, Brockton Campus 116A7,940 Belmont St, Brockton, MA 02301 USA.
EM mark.bauer@va.gov
NR 37
TC 33
Z9 33
U1 2
U2 14
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD NOV
PY 2009
VL 166
IS 11
BP 1244
EP 1250
DI 10.1176/appi.ajp.2009.09030342
PG 7
WC Psychiatry
SC Psychiatry
GA 514XL
UT WOS:000271429600011
PM 19797436
ER
PT J
AU Rashid, JR
Spengler, RF
Wagner, RM
Melanson, C
Skillen, EL
Mays, RA
Heurtin-Roberts, S
Long, JA
AF Rashid, Jamila R.
Spengler, Robert F.
Wagner, Robin M.
Melanson, Cindi
Skillen, Elizabeth L.
Mays, Robert A., Jr.
Heurtin-Roberts, Suzanne
Long, Judith A.
TI Eliminating Health Disparities Through Transdisciplinary Research,
Cross-Agency Collaboration, and Public Participation
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Editorial Material
ID UNITED-STATES; TRENDS; SCIENCE; DISEASE
AB Despite efforts to the contrary, disparities in health and health care persist in the United States. To solve this problem, federal agencies representing different disciplines and perspectives are collaborating on a variety of transdisciplinary research initiatives. The most recent of these initiatives was launched in 2006 when the Centers for Disease Control and Prevention's Office of Public Health Research and the Department of Health and Human Services' Office of Minority Health brought together federal partners representing a variety of disciplines to form the Federal Collaboration on Health Disparities Research (FCHDR).
FCHDR collaborates with a wide variety of federal and nonfederal partners to support and disseminate research that aims to reduce or eliminate disparities in health and health care. Given the complexity involved in eliminating health disparities, there is a need for more transdisciplinary, collaborative research, and facilitating that research is FCHDR's mission. (Am J Public Health. 2009;99:1955-1961. doi:10.2105/AJPH.2009.167932)
C1 [Rashid, Jamila R.; Spengler, Robert F.; Wagner, Robin M.; Melanson, Cindi; Skillen, Elizabeth L.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Heurtin-Roberts, Suzanne] Off Minor Hlth, Dept Hlth & Human Serv, Rockville, MD USA.
[Mays, Robert A., Jr.] NIH, Bethesda, MD 20892 USA.
[Long, Judith A.] Philadelphia VA Ctr Hlth Equ Res & Promot, Dept Vet Affairs, Philadelphia, PA USA.
RP Rashid, JR (reprint author), HHS, Off Minor Hlth, 1101 Wootton Pkwy,Suite 600, Rockville, MD 20852 USA.
EM jamila.rashid@hhs.gov
RI Heurtin-Roberts, Suzanne/D-7274-2013
NR 31
TC 16
Z9 16
U1 0
U2 9
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
EI 1541-0048
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD NOV
PY 2009
VL 99
IS 11
BP 1955
EP 1961
DI 10.2105/AJPH.2009.167932
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 511ZD
UT WOS:000271209900012
PM 19762652
ER
PT J
AU Silverman, JB
Prasittivatechakool, K
Busaba, NY
AF Silverman, Joshua B.
Prasittivatechakool, Kajohnkiat
Busaba, Nicolas Y.
TI An evidence-based review of endoscopic frontal sinus surgery
SO AMERICAN JOURNAL OF RHINOLOGY & ALLERGY
LA English
DT Review
DE Draf procedure; endoscopic frontal surgery; evidence-based medicine;
frontal sinus; frontal sinusitis; Lothrop procedure; osteoplastic
frontal sinus obliteration
ID MODIFIED LOTHROP PROCEDURE; FOLLOW-UP; OSTEOPLASTIC FLAP; SURGICAL
OUTCOMES; EXPERIENCE; OBLITERATION; MANAGEMENT; REVISION; DRILLOUT;
SALVAGE
AB Background: Endoscopic approaches to treat frontal sinus disease gained in popularity over the past 20 years with a plethora of published studies that emphasize the high success rate of such surgeries. This study was designed to determine the levels of clinical evidence in the otolaryngology literature that address the efficacy of endoscopic approaches in the management of frontal sinus disease including frontal sinusitis.
Methods: Twenty-three publications that reported the surgical outcomes of endoscopic approaches to treat frontal sinus disease were reviewed. Data were collected regarding the study design, operative technique, number of patients, duration of follow-up, diagnostic method, surgical success rate, and method(s) used to assess surgical outcome.
Results: The study designs were a retrospective case series without control (16 articles), prospective case series without control (3 articles), and retrospective case series with internal control (4 articles). Eighty-three percent of the published articles provide an evidence level of IV, while the remaining 17% provide an evidence level of III. The surgical technique was described as frontal sinusotomy (n = 4), frontal sinusotomy or frontal sinus drillout (n = 1), frontal sinus drillout alone (n = 1), endoscopic modified Lothrop procedure (n = 9), Draf types I, II, or III (n = 6); trans-septal frontal sinusotomy (n = 1); and frontal sinus rescue procedure (n = 1). The mean number of subjects was 44, and the average follow-up period was 23.6 months. Surgical success rate ranged from 50 to 100%.
Conclusion: Despite the number of reports in the literature that address the surgical outcome of endoscopic approaches for treatment of frontal sinus disease, the majority of these studies have a small population size, short follow-up period, and provide a low clinical evidence level. (Am J Rhinol Allergy 23, e59-e62, 2009; doi: 10.2500/ajra.2009.23.3406)
C1 [Silverman, Joshua B.; Prasittivatechakool, Kajohnkiat; Busaba, Nicolas Y.] Massachusetts Eye & Ear Infirm, Dept Otolaryngol Head & Neck Surg, Boston, MA 02114 USA.
[Busaba, Nicolas Y.] VA Boston HealthCare Syst, Div Otolaryngol, Boston, MA USA.
[Silverman, Joshua B.; Busaba, Nicolas Y.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
[Prasittivatechakool, Kajohnkiat] Phramongkutklao Hosp, Dept Otorhinolaryngol, Bangkok, Thailand.
RP Busaba, NY (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol Head & Neck Surg, 243 Charles St, Boston, MA 02114 USA.
EM Nicolas_busaba@meei.harvard.edu
NR 28
TC 11
Z9 12
U1 0
U2 1
PU OCEAN SIDE PUBLICATIONS INC
PI PROVIDENCE
PA 95 PITMAN ST, PROVIDENCE, RI 02906 USA
SN 1945-8924
J9 AM J RHINOL ALLERGY
JI Am. J. Rhinol. Allergy
PD NOV-DEC
PY 2009
VL 23
IS 6
BP E59
EP E62
DI 10.2500/ajra.2009.23.3406
PG 4
WC Otorhinolaryngology
SC Otorhinolaryngology
GA V17NR
UT WOS:000207944400014
PM 19958599
ER
PT J
AU Kligerman, S
Digumarthy, S
AF Kligerman, Seth
Digumarthy, Subba
TI Staging of Non-Small Cell Lung Cancer Using Integrated PET/CT
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Review
DE non-small cell lung cancer; PET/CT
ID POSITRON-EMISSION-TOMOGRAPHY; CT; METASTASES
C1 [Kligerman, Seth; Digumarthy, Subba] Massachusetts Gen Hosp, Dept Thorac Radiol, Boston, MA 02111 USA.
[Kligerman, Seth; Digumarthy, Subba] Harvard Univ, Sch Med, Boston, MA 02111 USA.
RP Digumarthy, S (reprint author), Massachusetts Gen Hosp, Dept Thorac Radiol, 55 Fruit St,Founders 202, Boston, MA 02111 USA.
EM sdigumarthy@partners.org
NR 21
TC 29
Z9 33
U1 0
U2 2
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD NOV
PY 2009
VL 193
IS 5
BP 1203
EP 1211
DI 10.2214/AJR.09.3193
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 508ST
UT WOS:000270956700002
PM 19843732
ER
PT J
AU Argo, JL
Vick, CC
Graham, LA
Itani, KMF
Bishop, MJ
Hawn, MT
AF Argo, Joshua L.
Vick, Catherine C.
Graham, Laura A.
Itani, Kamal M. F.
Bishop, Michael J.
Hawn, Mary T.
TI Elective surgical case cancellation in the Veterans Health
Administration system: identifying areas for improvement
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
DE Surgery; Operating room efficiency; Case cancellation; Quality; Quality
improvement
ID OPERATING-ROOM EFFICIENCY; PREOPERATIVE EVALUATION; SURGERY; TIME
AB BACKGROUND: This study evaluated elective surgical case cancellation (CC) rates, reasons for these cancellations, and identified areas for improvement within the Veterans Health Administration (VA) system.
METHODS: CC data for 2006 were collected from the scheduling software for 123 VA facilities. Surveys were distributed to 40 facilities (10 highest and 10 lowest CC rates for high- and low-volume facilities). CC reasons were standardized and piloted at 5 facilities.
RESULTS: 017 329,784 cases scheduled by 9 surgical specialties, 40,988 (12.4%) were cancelled. CC reasons (9,528) were placed into 6 broad categories: patient (35%), work-up/medical condition change (28%), facility (20%), surgeon (8%), anesthesia (1%), and miscellaneous (8%). Survey results show areas for improvement at the facility level and a standardized list of 28 CC reasons was comprehensive.
CONCLUSIONS: Interventions that decrease cancellations caused by patient factors, inadequate work-Lip, and facility factors are needed to reduce overall elective surgical case cancellations. Published by Elsevier Inc.
C1 [Argo, Joshua L.; Vick, Catherine C.; Graham, Laura A.; Hawn, Mary T.] Birmingham Vet Adm Med Ctr, Ctr Surg Med Acute Care Res & Transit, Birmingham, AL USA.
[Argo, Joshua L.; Vick, Catherine C.; Hawn, Mary T.] Univ Alabama, Dept Surg, Birmingham, AL 35294 USA.
[Itani, Kamal M. F.] VA Boston Hlth Care Syst, Dept Surg, W Roxbury, MA USA.
[Itani, Kamal M. F.] Boston Univ, Dept Surg, Boston, MA 02215 USA.
[Bishop, Michael J.] Cent Off, Dept Vet Affairs, Washington, DC USA.
[Bishop, Michael J.] Puget Sound VA Hlth Care Syst, Seattle, WA USA.
[Bishop, Michael J.] Univ Washington, Dept Anesthesiol, Seattle, WA 98195 USA.
RP Hawn, MT (reprint author), Birmingham Vet Adm Med Ctr, Ctr Surg Med Acute Care Res & Transit, Birmingham, AL USA.
EM mary.hawn@ccc.uab.edu
FU Agency for Healthcare Research and Quality [5 T32 HS013852]; Office of
Patient Care Services of the Department of Veterans Affairs
FX This project was supported in part by grant number 5 T32 HS013852 from
the Agency for Healthcare Research and Quality and a contract from the
Office of Patient Care Services of the Department of Veterans Affairs.
NR 24
TC 33
Z9 34
U1 1
U2 4
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD NOV
PY 2009
VL 198
IS 5
BP 600
EP 606
DI 10.1016/j.amjsurg.2009.07.005
PG 7
WC Surgery
SC Surgery
GA 522KY
UT WOS:000271997900005
PM 19887185
ER
PT J
AU Dhaliwal, AS
Chu, D
Huh, J
Ghadir, M
Sansgiry, S
Atluri, P
LeMaire, SA
Coselli, JS
Bakaeen, FG
AF Dhaliwal, Amandeep S.
Chu, Danny
Huh, Joseph
Ghadir, Mued
Sansgiry, Shubhada
Atluri, Prasad
LeMaire, Scott A.
Coselli, Joseph S.
Bakaeen, Faisal G.
TI Prognostic impact of intra-aortic balloon pump insertion before versus
after cardiac surgical intervention in a veteran population
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
DE Intra-aortic balloon pump; Morbidity; Mortality; Cardiac surgery;
Outcomes
ID CORONARY-BYPASS SURGERY; GRAFT-SURGERY; RISK; OUTCOMES
AB BACKGROUND: The relative prognostic impact of intra-aortic balloon pump (IABP) placement before versus after cardiac surgery is not well defined.
METHODS: We reviewed data from all cardiac surgical patients who received perioperative IABP support at a veterans' hospital between April 1992 and April 2008. We compared outcomes between patients who received an IABP before surgery (BS, n = 36) and after surgery (AS, n = 28).
RESULTS: The AS group had higher operative morbidity (71% vs 42%) and mortality (43% vs 14%) rates than the BS aroup (P < .02 for both). Furthermore, survival rates were lower in the AS group than in the BS group at 1 year (50% vs 83%) and 3 years (46% vs 80%) (log-rank test, P < .004).
CONCLUSIONS: Patients who require IABP after cardiac surgery may have worse outcomes than patients who receive IABP support before surgery. In both groups, after an early peak in mortality, the midterm outcomes were characterized by a reassuring plateau in the survival rates. Published by Elsevier Inc.
C1 [Chu, Danny; Huh, Joseph; Ghadir, Mued; LeMaire, Scott A.; Coselli, Joseph S.; Bakaeen, Faisal G.] Baylor Coll Med, Michael E DeBakey Dept Surg, Div Cardiothorac Surg, Houston, TX 77030 USA.
[Dhaliwal, Amandeep S.] Baylor Coll Med, Dept Med, Div Cardiol, Houston, TX 77030 USA.
[Chu, Danny; Huh, Joseph; Sansgiry, Shubhada; Atluri, Prasad; Bakaeen, Faisal G.] Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
[Chu, Danny; Huh, Joseph; LeMaire, Scott A.; Coselli, Joseph S.; Bakaeen, Faisal G.] St Lukes Episcopal Hosp, Texas Heart Inst, Houston, TX USA.
RP Bakaeen, FG (reprint author), Baylor Coll Med, Michael E DeBakey Dept Surg, Div Cardiothorac Surg, Houston, TX 77030 USA.
EM fbakaeen@bcm.edu
NR 14
TC 6
Z9 8
U1 0
U2 0
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD NOV
PY 2009
VL 198
IS 5
BP 628
EP 632
DI 10.1016/j.amjsurg.2009.07.011
PG 5
WC Surgery
SC Surgery
GA 522KY
UT WOS:000271997900010
PM 19887190
ER
PT J
AU Kaafarani, HMA
Hur, K
Hirter, A
Kim, LT
Thomas, A
Berger, DH
Reda, D
Itani, KMF
AF Kaafarani, Haytham M. A.
Hur, Kwan
Hirter, Angie
Kim, Lawrence T.
Thomas, Anthony
Berger, David H.
Reda, Domenic
Itani, Kamal M. F.
TI Seroma in ventral incisional herniorrhaphy: incidence, predictors and
outcome
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
DE Seroma; Ventral hernia; Postoperative wound infection
ID HERNIA REPAIR; EXPANDED POLYTETRAFLUOROETHYLENE; LAPAROSCOPIC REPAIR;
TRIAL; MESH
AB BACKGROUND: Factors leading to seroma following ventral incisional herniorrhaphy (VIH) are poorly understood.
METHODS: Between 2004 and 2006, patients were prospectively randomized at 4 Veterans Affairs hospitals to undergo laparoscopic or open VIH. Patients who developed seromas within 8 weeks postoperatively were compared with those who did not. Multivariate analyses were per-formed to identify predictors of scroma.
RESULTS: Of 145 patients who underwent VIH, 24 (16.6%) developed seromas. Patients who underwent Open VIH had more seromas than those who underwent laparoscopic VIH (23.3% vs 6.8%, P = .011). Seroma patients had hernias that were never spontaneously reducible (0% vs 21%, P = .015), had more abdominal incisions preoperatively (mean, 2.4 vs 1.8; P = .037), and were less likely to have drain catheters placed than those without seromas (30.0% vs 63.1%, P = .011). In multivariate analyses, open VIH predicted seroma (odds ratio, 5.5; 95% confidence interval, 1.6-18.8), as well as the specific hospital at which the procedure was performed. Spontaneous resolution occurred in 71% of seromas; 29% required aspiration.
CONCLUSIONS: Procedural characteristics and hernia characteristics rather than patient comorbidities predicted seroma in VIH. Published by Elsevier Inc.
C1 [Kaafarani, Haytham M. A.; Itani, Kamal M. F.] VA Boston Healthcare Syst, W Roxbury, MA USA.
[Kaafarani, Haytham M. A.] Univ S Florida, Tampa, FL USA.
[Kaafarani, Haytham M. A.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Hur, Kwan; Hirter, Angie; Reda, Domenic] Coordinating Ctr, VA Cooperat Studies Program, Hines, IL USA.
[Kim, Lawrence T.] Cent Arkansas Vet Hlth Care Syst, Little Rock, AR USA.
[Kim, Lawrence T.] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Thomas, Anthony] N Texas VA Hlth Care Syst, Dallas, TX USA.
[Berger, David H.] Michael E DeBakey VA Med Ctr, Houston, TX USA.
[Thomas, Anthony] Southwestern Univ, Dallas, TX USA.
[Berger, David H.] Baylor Coll Med, Houston, TX 77030 USA.
[Itani, Kamal M. F.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Itani, Kamal M. F.] Harvard Univ, Sch Med, Boston, MA USA.
RP Itani, KMF (reprint author), VA Boston Healthcare Syst, W Roxbury, MA USA.
EM kitani@med.va.gov
OI Hirter, Angie/0000-0001-6616-2123
NR 18
TC 23
Z9 24
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 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD NOV
PY 2009
VL 198
IS 5
BP 639
EP 644
DI 10.1016/j.amjsurg.2009.07.019
PG 6
WC Surgery
SC Surgery
GA 522KY
UT WOS:000271997900012
PM 19887192
ER
PT J
AU Kougias, P
Chen, A
Cagiannos, C
Bechara, CF
Huynh, TT
Lin, PH
AF Kougias, Panagiotis
Chen, Aaron
Cagiannos, Catherine
Bechara, Carlos F.
Huynh, Tam T.
Lin, Peter H.
TI Subintimal placement of covered stent versus subintimal balloon
angioplasty in the treatment of long-segment superficial femoral artery
occlusion
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
DE Subintimal angioplasty; Covered stent; Superficial femoral artery;
Endovascular
ID PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY; FEMOROPOPLITEAL ARTERY; LIMB
ISCHEMIA; DISEASE; GRAFT; ENDOPROSTHESIS; OBSTRUCTIONS; MULTICENTER;
EXPERIENCE; BYPASS
AB BACKGROUND: Subintimal endovascular intervention has been used widely in the treatment of symptomatic superficial femoral artery (SFA) Occlusion. The relative effectiveness of subintimal placement of a covered stent (CS) versus balloon-only subintimal angioplasty (SIA) remains uncertain.
METHODS: We performed a retrospective cohort study of consecutive patients with symptomatic SFA occlusions (> 15 cm) who underwent subintimal endovascular intervention, either CS or SIA, in a single institution. Primary patency was the primary outcome. Secondary outcomes included complication rates, freedom from re-intervention, and limb salvage rates. Patency was ascertained with followup duplex or clinically.
RESULTS: We evaluated 57 patients in the SIA group and 31 patients in the CS group. At 1 year the SFA primary patency for the SIA and CS groups was 28% versus 75% (P < .001), whereas the primary assisted patency was 37% versus 84% (P < .001), respectively. Need for bypass was 13% versus 0% (P = .05) in the SIA and CS groups, respectively.
CONCLUSIONS: Placement of a covered stent improves patency after subintimal intervention for long SFA Occlusion. Published by Elsevier Inc.
C1 [Kougias, Panagiotis; Chen, Aaron; Cagiannos, Catherine; Bechara, Carlos F.; Huynh, Tam T.; Lin, Peter H.] Baylor Coll Med, Div Vasc Surg & Endovasc Therapy, Michael E DeBakey Dept Surg, Houston VAMC, Houston, TX 77030 USA.
RP Kougias, P (reprint author), Baylor Coll Med, Div Vasc Surg & Endovasc Therapy, Michael E DeBakey Dept Surg, Houston VAMC, 2002 Holcombe Blvd 112, Houston, TX 77030 USA.
EM pkougias@bcm.edu
NR 16
TC 18
Z9 20
U1 1
U2 1
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD NOV
PY 2009
VL 198
IS 5
BP 645
EP 649
DI 10.1016/j.amjsurg.2009.07.017
PG 5
WC Surgery
SC Surgery
GA 522KY
UT WOS:000271997900013
PM 19887193
ER
PT J
AU Leong, M
Chike-Obi, CJ
Basu, CB
Lee, EI
Albo, D
Netscher, DT
AF Leong, Mimi
Chike-Obi, Chuma J.
Basu, C. Bob
Lee, Edward I.
Albo, Daniel
Netscher, David T.
TI Effective breast reconstruction in female veterans
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
DE Breast reconstruction; Female veterans; Multidisciplinary teams
ID PATIENT SATISFACTION; CANCER; OUTCOMES; AFFAIRS; IMPACT; MASTECTOMY;
IMMEDIATE; CARE
AB BACKGROUND: Despite increasing female veteran numbers, literature regarding reconstruction after breast cancer is lacking. The purpose of this study was to examine breast reconstruction referral rates and reconstruction outcomes at a tertiary Veterans Affairs hospital.
METHODS: Female breast cancer patients (1997-2008) were identified. Demographics, tumor stage, oncologic therapies, reconstructive timings and procedures, and complications were noted.
RESULTS: Eighty-two women underwent mastectomy (46%) or breast conservation (43%). The referral rates to plastic surgery were 61% (mastectomy) and 32% (overall). Reconstruction rates were 42% (mastectomy) and 22% (overall). Sixty-nine percent were suitable candidates and chose immediate (67%) or delayed (33%) reconstruction, with implant-based (44%), autologous (39%), or autologous plus implants (17%). There were complications (28%) but no mortalities. Comorbidifies were not correlated with outcomes.
CONCLUSIONS: Breast reconstruction can be effectively delivered within the Veterans Affairs system. It is essential that sufficient Veterans Affairs resources be deployed to address the increasing reconstructive needs of female veterans. Published by Elsevier Inc.
C1 [Leong, Mimi; Netscher, David T.] Michael E DeBakey Vet Affairs Med Ctr, Sect Plast Surg, Houston, TX USA.
[Albo, Daniel] Michael E DeBakey Vet Affairs Med Ctr, Sect Gen Surg, Houston, TX USA.
[Leong, Mimi; Chike-Obi, Chuma J.; Lee, Edward I.; Netscher, David T.] Baylor Coll Med, Div Plast Surg, Houston, TX 77030 USA.
[Basu, C. Bob] Inst Adv Breast Reconstruct, Houston, TX USA.
RP Leong, M (reprint author), Michael E DeBakey Vet Affairs Med Ctr, Sect Plast Surg, Houston, TX USA.
EM mimi.leong@va.gov
NR 19
TC 1
Z9 1
U1 0
U2 0
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD NOV
PY 2009
VL 198
IS 5
BP 658
EP 663
DI 10.1016/j.amjsurg.2009.07.020
PG 6
WC Surgery
SC Surgery
GA 522KY
UT WOS:000271997900015
PM 19887195
ER
PT J
AU Wilks, JA
Balentine, CJ
Berger, DH
Anaya, D
Awad, S
Lee, L
Haderxhanaj, K
Albo, D
AF Wilks, Jonathan A.
Balentine, Courtney J.
Berger, David H.
Anaya, Daniel
Awad, Samir
Lee, Liz
Haderxhanaj, Kujtim
Albo, Daniel
TI Establishment of a minimally invasive program at a Veterans' Affairs
Medical Center leads to improved care in colorectal cancer patients
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
DE Colorectal cancer; Minimally invasive; Laparoscopic surgery; Veterans;
Clinical outcomes; Hand-assisted laparoscopic surgery
ID MRC CLASICC TRIAL; LAPAROSCOPIC-ASSISTED COLECTOMY; COST STUDY-GROUP;
RANDOMIZED-TRIAL; COLON-CANCER; LEARNING-CURVE; SURGERY; RESECTION;
OUTCOMES; METAANALYSIS
AB BACKGROUND: Despite significant advantages to patients, less than 5% of all colorectal Surgeries for cancer are performed laparoscopically. A minimally invasive colorectal cancer program was created in our Veterans' Affairs hospital with the intent of increasing access and improving quality of patient care while maintaining patient safety and oncologic standards.
METHODS: Sixty consecutive laparoscopic colorectal cancer resections and 60 age-matched open resections were identified. Our prospective database was queried for demographic, clinical outcomes, and oncologic data.
RESULTS: Patients undergoing laparoscopic resections experienced a shorter hospital stay and a quicker return of bowel function. Both groups had similar intraoperative blood loss and surgical times. Laparoscopic resections achieved equivalent lymph node retrieval and resection completeness compared with open resections. Laparoscopic resections resulted in fewer wounds and fewer complications requiring reoperation.
CONCLUSIONS: Establishment of a minimally invasive colorectal cancer program in a Veterans Affairs Medical Center leads to increased access to laparoscopic colorectal resections and improved patient care while maintaining patient safety. Published by Elsevier Inc.
C1 [Wilks, Jonathan A.; Balentine, Courtney J.; Berger, David H.; Anaya, Daniel; Awad, Samir; Lee, Liz; Haderxhanaj, Kujtim; Albo, Daniel] Michael E DeBakey Vet Affairs Med Ctr, Div Gen Surg & Surg Oncol, Houston, TX 77030 USA.
[Wilks, Jonathan A.; Balentine, Courtney J.; Berger, David H.; Anaya, Daniel; Awad, Samir; Lee, Liz; Albo, Daniel] Baylor Coll Med, Michael E DeBakey Dept Surg, Houston, TX 77030 USA.
RP Albo, D (reprint author), Michael E DeBakey Vet Affairs Med Ctr, Div Gen Surg & Surg Oncol, 2002 Holcombe Blvd,OCL 112-A, Houston, TX 77030 USA.
EM dalbo@bcm.edu
NR 27
TC 9
Z9 9
U1 0
U2 1
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD NOV
PY 2009
VL 198
IS 5
BP 685
EP 692
DI 10.1016/j.amjsurg.2009.07.016
PG 8
WC Surgery
SC Surgery
GA 522KY
UT WOS:000271997900020
PM 19887200
ER
PT J
AU Bush, RL
DePalma, RG
Itani, KMF
Henderson, WG
Smith, TS
Gunnar, WP
AF Bush, Ruth L.
DePalma, Ralph G.
Itani, Kamal M. F.
Henderson, William G.
Smith, Tracy S.
Gunnar, William P.
TI Outcomes of care of abdominal aortic aneurysm in Veterans Health
Administration facilities: results from the National Surgical Quality
Improvement Program
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
DE Abdominal aortic aneurysm; Endovascular aneurysm repair; EVAR; Veterans;
NSQIP; Ruptured abdominal aneurysm; Quality improvement
ID RANDOMIZED CONTROLLED-TRIAL; ENDOVASCULAR REPAIR; OPERATIVE MORTALITY;
PROVIDER VOLUME; LEARNING-CURVE; AAA REPAIRS; RISK; PERFORMANCE;
EXPERIENCE; SURVIVAL
AB This-report describes outcomes of care for abdominal aortic aneurysms (AAAs), along with methods used by the Veterans Affairs (VA) National Surgical Quality Improvement Program (NSQIP) in tracking, monitoring, and improving surgical results in VA facilities. Since the inception of NSQIP in 1994, a continual drop in overall surgical mortality, along with decreased morbidity, has occurred. A parallel improvement in results of vascular surgery and AAA repair was also observed. Soon after introduction of endovascular aneurysm repair (EVAR), with Food and Drug Administration device approval in 1999, robust electronic NSQIP records immediately began to capture individual facility performances and outcomes for both types of AAA repair. The NSQIP data center provided actual and risk-adjusted analyses for both procedures semiannually. These analyses have been used by its executive board to provide recommendations, often based on site visits, to improve outcomes. Requirements for reporting of facility-specific data and feedback, paper audits, and site visits appear to relate directly to improved AAA care. Veterans Health Administration (VHA) outcomes of AAA repair are comparable to those reported nationally and internationally and have continued to improve in recent years. National VHA initiatives, based on data feedback and active oversight, relate to some of the lowest AAA mortality rates available. This review describes past, present, and possible future NSQIP strategies to improve outcomes for AAA repair with general comments about recent alternative proposals. (C) 2009 Published by Elsevier Inc.
C1 [Bush, Ruth L.] Texas A&M Hlth Sci Ctr, Olin E Teague Vet Affairs Med Ctr, Temple, TX USA.
[DePalma, Ralph G.; Gunnar, William P.] Affairs Cent Off, Dept Vet, Washington, DC USA.
[Itani, Kamal M. F.] Boston Univ, Vet Affairs Boston Hlth Care Syst, Boston, MA 02215 USA.
[Itani, Kamal M. F.] Harvard Univ, Sch Med, Boston, MA USA.
[Henderson, William G.] Univ Colorado, Med Ctr, Denver, CO 80202 USA.
[Smith, Tracy S.] Denver Vet Affairs Med Ctr, Denver, CO USA.
RP Bush, RL (reprint author), Texas A&M Hlth Sci Ctr, Olin E Teague Vet Affairs Med Ctr, Temple, TX USA.
EM ruth.bush@va.gov
NR 31
TC 4
Z9 5
U1 0
U2 0
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD NOV
PY 2009
VL 198
IS 5A
BP S41
EP S48
DI 10.1016/j.amjsurg.2009.08.005
PG 8
WC Surgery
SC Surgery
GA 522KZ
UT WOS:000271998000007
PM 19874934
ER
PT J
AU Kaafarani, HMA
Rosen, AK
AF Kaafarani, Haytham M. A.
Rosen, Amy K.
TI Using administrative data to identify surgical adverse events: an
introduction to the Patient Safety Indicators
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article
DE Adverse events; Patient safety; Quality indicators; Patient safety
indicators; Quality improvement; Complications; Administrative data
ID QUALITY IMPROVEMENT PROGRAM; SURGERY REPORT CARDS; MORTALITY CONFERENCE;
COMPLICATIONS; MORBIDITY
AB BACKGROUND: The Patient Safety Indicators (PSIs) are algorithms based on the International Classification of Diseases, Ninth Revision, Clinical Modification, aimed at identifying potential safety-related adverse events through the automated screening of readily available administrative databases. Many of these indicators focus on surgical care, and a few have been endorsed by the National Quality Forum as performance measures. The aim of this report is to give a brief overview of the development and definitions of the PSIs as well as the current evidence for their validity, compared with the National Surgical Quality Improvement Program and chart abstraction designed for the. purpose of PSI validation.
METHODS: Several articles published in the past few years, in addition to primary data collected from an ongoing study of PSI validation in the Veterans Health Administration, were examined.
RESULTS: Selected surgical PSIs have positive predictive values ranging from 22% to 89%, depending on the nature of the PSI and the method of validation used.
CONCLUSIONS: With adequate coding revisions, PSI performance can be substantially improved. (C) 2009 Published by Elsevier Inc.
C1 [Kaafarani, Haytham M. A.; Rosen, Amy K.] Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA USA.
[Kaafarani, Haytham M. A.] VA Boston Healthcare Syst, Dept Surg, W Roxbury, MA USA.
[Rosen, Amy K.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
RP Rosen, AK (reprint author), Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA USA.
EM akrosen@bu.edu
NR 13
TC 22
Z9 22
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 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD NOV
PY 2009
VL 198
IS 5A
BP S63
EP S68
DI 10.1016/j.amjsurg.2009.08.008
PG 6
WC Surgery
SC Surgery
GA 522KZ
UT WOS:000271998000010
PM 19874937
ER
PT J
AU Graham, JA
Wilkinson, RA
Hirohashi, T
Chase, CM
Colvin, RB
Madsen, JC
Fishman, JA
Russell, PS
AF Graham, J. A.
Wilkinson, R. A.
Hirohashi, T.
Chase, C. M.
Colvin, R. B.
Madsen, J. C.
Fishman, J. A.
Russell, P. S.
TI Viral Infection Induces De Novo Lesions of Coronary Allograft
Vasculopathy Through a Natural Killer Cell-Dependent Pathway
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Article
DE Allograft arteriopathy; cardiac transplant; coronary artery disease;
graft rejection; NK-cells; viral; vasculopathy
ID MHC CLASS-I; DENDRITIC CELLS; NK CELLS; CARDIAC ALLOGRAFTS; T-CELLS;
VIRUS-INFECTION; MICE; REJECTION; ACTIVATION; IMMUNITY
AB Viral infections including those due to cytomegalovirus have been associated with accelerated cardiac allograft vasculopathy (CAV) in clinical trials and some animal models. Evidence demonstrating a direct causal relationship between such infections and de novo formation of coronary vascular lesions is lacking. Heterotopic murine cardiac transplants were performed in a parental to F1 combination in animals lacking both T- and B-lymphocytes (RAG-/-). Coronary vasculopathy developed almost exclusively in the presence of recipient infection with lymphocytic choriomeningitis virus but not in uninfected controls. This process was also dependent upon the presence of natural killer (NK) cells as depletion of NK cells abrogated the process. These data show that a viral infection in its native host, and not previously implicated in the production of CAV, can contribute to the development of advanced coronary vascular lesions in cardiac allotransplants in mice. These data also suggest that virus-induced CAV can develop via an NK-cell-dependent pathway in the absence of T- and B-lymphocytes.
C1 [Graham, J. A.; Hirohashi, T.; Chase, C. M.; Madsen, J. C.; Russell, P. S.] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp,Transplantat Res Div, Boston, MA 02115 USA.
[Graham, J. A.; Hirohashi, T.; Chase, C. M.; Madsen, J. C.; Russell, P. S.] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp,Cardiac Surg Div, Boston, MA 02115 USA.
[Wilkinson, R. A.; Fishman, J. A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Transplant Infect Dis Program,Infect Dis Div, Boston, MA USA.
[Colvin, R. B.] Harvard Univ, Sch Med, Dept Pathol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Graham, JA (reprint author), Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp,Transplantat Res Div, Boston, MA 02115 USA.
EM jfishman@partners.org
RI Graham, Jay/A-4896-2014
OI Graham, Jay/0000-0003-2054-1253
FU National Heart Blood and Lung Institute [NIH-NHLBI-RO1 HL071932];
National Institute of Allergy and Infectious Disease (NIH-NIAID)
[PO1-AI45897]; Roche Organ Transplant Research Foundation; American
Society of Transplantation
FX This work was funded in part by Public Health Services grants from the
National Heart Blood and Lung Institute (NIH-NHLBI-RO1 HL071932),
National Institute of Allergy and Infectious Disease (NIH-NIAID
PO1-AI45897) and a grant from the Roche Organ Transplant Research
Foundation. T.H. is the recipient of a Basic Science Grant from the
American Society of Transplantation. We thank Tricia DellaPelle for
expert preparation and staining of histological material.
NR 33
TC 21
Z9 21
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1600-6135
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD NOV
PY 2009
VL 9
IS 11
BP 2479
EP 2484
DI 10.1111/j.1600-6143.2009.02801.x
PG 6
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 508AT
UT WOS:000270899900009
PM 19843029
ER
PT J
AU Echeverria, GJ
McGrath, K
Bottino, R
Hara, H
Dons, EM
van der Windt, DJ
Ekser, B
Casu, A
Houser, S
Ezzelarab, M
Wagner, R
Trucco, M
Lakkis, FG
Cooper, DKC
AF Echeverria, G. J.
McGrath, K.
Bottino, R.
Hara, H.
Dons, E. M.
van der Windt, D. J.
Ekser, B.
Casu, A.
Houser, S.
Ezzelarab, M.
Wagner, R.
Trucco, M.
Lakkis, F. G.
Cooper, D. K. C.
TI Endoscopic Gastric Submucosal Transplantation of Islets (ENDO-STI):
Technique and Initial Results in Diabetic Pigs
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Article
DE Endoscopy; gastric submucosal space; pig; portal vein; transplantation;
islets
ID PANCREATIC-ISLETS; XENOTRANSPLANTATION; HYPOGLYCEMIA; IMPLANTATION;
STRATEGIES; CELLS; MODEL; SITE; AUTO
AB The results of transplantation of human donor islets into the portal vein (PV) in patients with diabetes are encouraging. However, there are complications, for example, hemorrhage, thrombosis and an immediate loss of islets through the 'instant blood-mediated inflammatory reaction' (IBMIR). The gastric submucosal space (GSMS) offers potential advantages. Islets were isolated from adult pigs. Recipient pigs were made diabetic by streptozotocin. Donor islets were injected into the GSMS through a laparotomy (Group 1A, n = 4) or endoscopically (Group 1B, n = 8) or into the PV through a laparotomy (Group 2, n = 3). The pigs were followed for a maximum of 28 days. Monitoring of C-peptide in Group 1 indicated that there was minimal immediate loss of islets whereas in Group 2 there was considerable loss from IBMIR. In Group 1, there were significant reductions in mean blood glucose and mean exogenous insulin requirement between pretransplantation and 20 days posttransplantation. In Group 2, there was no significant reduction in either parameter. Insulin-positive cells were seen in the GSMS in Group 1, but not in the liver in Group 2. Endoscopic gastric submucosal transplantation of islets (ENDO-STI) offers a minimally invasive and quick approach to islet transplantation, avoids IBMIR and warrants further exploration.
C1 [Echeverria, G. J.; Hara, H.; Dons, E. M.; van der Windt, D. J.; Ekser, B.; Ezzelarab, M.; Lakkis, F. G.; Cooper, D. K. C.] Univ Pittsburgh, Dept Surg, Thomas E Starzl Transplantat Inst, Pittsburgh, PA 15260 USA.
[Echeverria, G. J.] Fdn Clin Valle del Lili, Transplantat Unit, Cali, Colombia.
[McGrath, K.] Univ Pittsburgh, Div Gastroenterol Hepatol & Nutr, Pittsburgh, PA USA.
[Bottino, R.; van der Windt, D. J.; Casu, A.; Trucco, M.] Univ Pittsburgh, Dept Pediat, Div Immunogenet, Pittsburgh, PA 15260 USA.
[Dons, E. M.; van der Windt, D. J.] Erasmus MC, Dept Surg, Rotterdam, Netherlands.
[Houser, S.] Harvard Univ, Sch Med, Dept Pathol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Ekser, B.] Univ Padua, Dept Surg & Organ Transplantat, Padua, Italy.
[Wagner, R.] Univ Pittsburgh, Div Lab Anim Resources, Pittsburgh, PA USA.
RP Cooper, DKC (reprint author), Univ Pittsburgh, Dept Surg, Thomas E Starzl Transplantat Inst, Pittsburgh, PA 15260 USA.
EM cooperdk@upmc.edu
OI ECHEVERRI, GABRIEL/0000-0001-6432-0327; Ezzelarab,
Mohamed/0000-0002-3919-5250
FU Royal Netherlands Academy of Arts and Sciences; NIH [U01AI068642,
R21-A1074844]; US Department of Defense; University of Pittsburgh and
Revivicor, Inc., Blacksburg, VA; Thomas E. Starzl Transplantation
Institute, University of Pittsburgh
FX Funding source: Thomas E. Starzl Transplantation Institute, University
of Pittsburgh.
NR 32
TC 41
Z9 42
U1 0
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1600-6135
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD NOV
PY 2009
VL 9
IS 11
BP 2485
EP 2496
DI 10.1111/j.1600-6143.2009.02815.x
PG 12
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 508AT
UT WOS:000270899900010
PM 19775318
ER
PT J
AU Kelly, JX
O'Neil, M
Melendez, V
Harris, E
Ager, A
Smilkstein, M
Forquer, I
Dodean, R
Winter, R
Hinrichs, D
Riscoe, M
AF Kelly, Jane X.
O'Neil, Michael
Melendez, Victor
Harris, Erin
Ager, Arba
Smilkstein, Martin
Forquer, Isaac
Dodean, Rosie
Winter, Rolf
Hinrichs, Dave
Riscoe, Mike
TI A NOVEL ANTIMALARIAL CHEMOTYPE WITH EFFICACY AGAINST BOTH
EXOERYTHROCYTIC AND ERYTHROCYTIC STAGES
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Kelly, Jane X.; Forquer, Isaac; Dodean, Rosie; Winter, Rolf; Hinrichs, Dave; Riscoe, Mike] Portland VA Med Ctr, Portland, OR USA.
[O'Neil, Michael; Melendez, Victor; Harris, Erin] Walter Reed Army Inst Res, Div Expt Therapeut, Silver Spring, MD USA.
[Ager, Arba] Univ Miami, Sch Med, Miami, FL USA.
[Smilkstein, Martin] Oregon Translat Res & Drug Dev Inst, Portland, OR USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 295
BP 83
EP 83
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700295
ER
PT J
AU Weil, AA
Khan, AI
Chowdhury, F
LaRocque, RC
Faruque, AS
Ryan, ET
Calderwood, SB
Qadri, F
Harris, JB
AF Weil, Ana A.
Khan, Ashraful I.
Chowdhury, Fahima
LaRocque, Regina C.
Faruque, A. S.
Ryan, Edward T.
Calderwood, Stephen B.
Qadri, Firdausi
Harris, Jason B.
TI CLINICAL OUTCOMES IN HOUSEHOLD CONTACTS OF PATIENTS WITH CHOLERA IN
BANGLADESH
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Weil, Ana A.; Khan, Ashraful I.; Chowdhury, Fahima; Faruque, A. S.; Qadri, Firdausi] Int Ctr Diarrhoeal Dis Res, Dhaka 1000, Bangladesh.
[LaRocque, Regina C.; Ryan, Edward T.; Calderwood, Stephen B.; Harris, Jason B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 323
BP 92
EP 92
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700323
ER
PT J
AU Anstead, GM
Zhang, Q
Melby, PC
AF Anstead, Gregory M.
Zhang, Qiong
Melby, Peter C.
TI INSULIN-LIKE GROWTH FACTOR-1 ENHANCES THE INNATE IMMUNE RESPONSE OF
MACROPHAGES FROM WELL-NOURISHED MICE BUT CAN NOT RECTIFY THE DEFECTIVE
IMMUNE RESPONSE OF MACROPHAGES FROM MALNOURISHED MICE
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Anstead, Gregory M.; Zhang, Qiong; Melby, Peter C.] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 480
BP 137
EP 137
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700479
ER
PT J
AU Noah, JW
Citorik, R
Wallace, C
Lebrun, L
Nebane, M
McKellip, S
Sosa, M
Rasmussen, L
Ryan, E
White, EL
Jonsson, C
Harris, J
AF Noah, James W.
Citorik, Robert
Wallace, Carrie
Lebrun, Lauren
Nebane, Miranda
McKellip, Sara
Sosa, Melinda
Rasmussen, Lynn
Ryan, Edward
White, E. Lucile
Jonsson, Colleen
Harris, Jason
TI A COMPARATIVE HIGH-THROUGHPUT SCREEN OF 300,000 COMPOUNDS FOR REGULATORS
OF THE SALMONELLA ENTERICA PHOP REGULON BY THE MOLECULAR LIBRARIES PROBE
CENTERS NETWORK
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Noah, James W.; Wallace, Carrie; Nebane, Miranda; McKellip, Sara; Sosa, Melinda; Rasmussen, Lynn; White, E. Lucile; Jonsson, Colleen] So Res Inst, So Res Specialized Biocontainment Screening Ctr, Birmingham, AL 35255 USA.
[Citorik, Robert; Lebrun, Lauren; Ryan, Edward; Harris, Jason] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 610
BP 174
EP 174
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701026
ER
PT J
AU Osorio, EY
Zhao, WG
Espitia, CM
Saldarriaga, OA
Hawel, L
Byus, CV
Travi, BL
Melby, PC
AF Osorio, Elvia Y.
Zhao, Weiguo
Espitia, Claudia M.
Saldarriaga, Omar A.
Hawel, Leo
Byus, Craig V.
Travi, Bruno L.
Melby, Peter C.
TI DOMINANT ALTERNATIVE MACROPHAGE ACTIVATION IN PROGRESSIVE VISCERAL
LEISHMANIASIS IS MEDIATED BY PARASITE-INDUCED STAT6 ACTIVATION AND
ARGINASE EXPRESSION
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Osorio, Elvia Y.; Zhao, Weiguo; Espitia, Claudia M.; Saldarriaga, Omar A.; Travi, Bruno L.; Melby, Peter C.] Univ Texas Hlth Sci Ctr San Antonio, S Texas Vet Hlth Care Syst, San Antonio, TX 78229 USA.
[Hawel, Leo; Byus, Craig V.] Univ Calif Riverside, Riverside, CA 92521 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
BP 189
EP 189
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701077
ER
PT J
AU Singh, N
Singh, MP
Wylie, BJ
Shukla, MM
Hussain, M
Dash, AP
Yeboah-Antwi, K
Sabin, L
Udhayakumar, V
Desai, M
Hamer, DH
AF Singh, Neeru
Singh, Mrigendra P.
Wylie, Blair J.
Shukla, Manmohan M.
Hussain, Mobassir
Dash, Aditya P.
Yeboah-Antwi, Kojo
Sabin, Lora
Udhayakumar, Venkatachalam
Desai, Meghna
Hamer, Davidson H.
TI BURDEN OF MALARIA IN PREGNANCY IN WOMEN PRESENTING TO DELIVERY UNITS IN
AREAS WITH STABLE AND UNSTABLE MALARIA TRANSMISSION IN CHHATTISGARH,
INDIA
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Singh, Neeru] Reg Med Res Ctr ICMR, Jabalpur, India.
[Singh, Mrigendra P.; Shukla, Manmohan M.; Hussain, Mobassir] Natl Inst Malaria Res Field Stn, Jabalpur, India.
[Wylie, Blair J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Dash, Aditya P.] Natl Inst Malaria Res, Delhi, India.
[Yeboah-Antwi, Kojo; Sabin, Lora] Boston Univ, Ctr Int Hlth & Dev, Boston, MA 02215 USA.
[Udhayakumar, Venkatachalam; Desai, Meghna] Ctr Dis Control & Prevent, Malaria Branch, Atlanta, GA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
BP 191
EP 191
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701082
ER
PT J
AU Chowdhury, F
Begum, YA
Alam, M
Khan, AI
Ahmed, T
LaRocque, RC
Harris, JB
Faruque, ASG
Calderwood, SB
Ryan, ET
Svennerholm, AM
Qadri, F
AF Chowdhury, Fahima
Begum, Yasmin Ara
Alam, Murshid
Khan, Ashraful Islam
Ahmed, Tanvir
LaRocque, Regina C.
Harris, Jason B.
Faruque, A. S. G.
Calderwood, Stephen B.
Ryan, Edward T.
Svennerholm, Ann-Mari
Qadri, Firdausi
TI CONCOMITANT INFECTION WITH VIBRIO CHOLERAE O1 AND ENTEROTOXIGENIC
ESCHERICHIA COLI INDUCES A MORE ROBUST IMMUNE RESPONSE TO CHOLERA
ANTIGENS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Chowdhury, Fahima; Begum, Yasmin Ara; Alam, Murshid; Khan, Ashraful Islam; Ahmed, Tanvir; Faruque, A. S. G.; Qadri, Firdausi] Int Ctr Diarrhoeal Dis Res, Dhaka 1000, Bangladesh.
[LaRocque, Regina C.; Harris, Jason B.; Calderwood, Stephen B.; Ryan, Edward T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Svennerholm, Ann-Mari] Univ Gothenburg, Gothenburg, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 715
BP 206
EP 206
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701131
ER
PT J
AU LaRocque, RC
Sabeti, P
Duggal, P
Chowdhury, F
Khan, AI
Lebrun, LM
Harris, JB
Ryan, ET
Qadri, F
Calderwood, SB
AF LaRocque, Regina C.
Sabeti, Pardis
Duggal, Priya
Chowdhury, Fahima
Khan, Ashraful I.
Lebrun, Lauren M.
Harris, Jason B.
Ryan, Edward T.
Qadri, Firdausi
Calderwood, Stephen B.
TI A VARIANT IN LONG PALATE, LUNG AND NASAL EPITHELIUM CLONE 1 IS
ASSOCIATED WITH CHOLERA IN A BANGLADESHI POPULATION
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [LaRocque, Regina C.; Lebrun, Lauren M.; Harris, Jason B.; Ryan, Edward T.; Calderwood, Stephen B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Sabeti, Pardis] Broad Inst, Cambridge, MA USA.
[Duggal, Priya] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Chowdhury, Fahima; Khan, Ashraful I.; Qadri, Firdausi] Int Ctr Diarrhoeal Dis Res, Dhaka 1000, Bangladesh.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 716
BP 206
EP 206
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701132
ER
PT J
AU Dong, C
Urgaonkar, S
Cortese, J
Francisco, J
Garcia-Bustos, JF
Gomez-de-las-Heras, FM
Patel, V
Ross, L
Dvorin, JD
Duraisingh, MT
Wirth, D
Mazitschek, R
Clardy, J
AF Dong, Carolyn
Urgaonkar, Sameer
Cortese, Joe
Francisco, Javier
Garcia-Bustos, Jose F.
Gomez-de-las-Heras, Frederico M.
Patel, Vishal
Ross, Leila
Dvorin, Jeffrey D.
Duraisingh, Manoj T.
Wirth, Dyann
Mazitschek, Ralph
Clardy, Jon
TI TETRACYCLIC BENZOTHIAZEPINES: A NOVEL CLASS OF PLASMODIUM FALCIPARUM
CYTOCHROME BC1 INHIBITORS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Dong, Carolyn; Patel, Vishal; Duraisingh, Manoj T.; Wirth, Dyann] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Urgaonkar, Sameer; Cortese, Joe; Mazitschek, Ralph] Broad Inst Infect Dis Initiat, Boston, MA USA.
[Francisco, Javier; Garcia-Bustos, Jose F.; Gomez-de-las-Heras, Frederico M.] GlaxoSmithKline R&D, Dis Developing World Ctr, Drug Discovery Biol Grp, Madrid, Spain.
[Patel, Vishal; Ross, Leila; Mazitschek, Ralph; Clardy, Jon] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Dvorin, Jeffrey D.] Childrens Hosp Boston, Div Infect Dis, Boston, MA USA.
[Mazitschek, Ralph] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
RI Mazitschek, Ralph/E-3741-2013
OI Mazitschek, Ralph/0000-0002-1105-689X
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
BP 252
EP 253
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701293
ER
PT J
AU Singh, N
Singh, MP
Shukla, MM
Hussain, M
Dash, AP
Wylie, BJ
Yeboah-Antwi, K
Sabin, L
Udhayakumar, V
Desai, M
Hamer, DH
AF Singh, Neeru
Singh, Mrigendra P.
Shukla, Manmohan M.
Hussain, Mohassir
Dash, Aditya P.
Wylie, Blair J.
Yeboah-Antwi, Kojo
Sabin, Lora
Udhayakumar, Venkatachalam
Desai, Meghna
Hamer, Davidson H.
TI BURDEN OF MALARIA IN PREGNANCY IN AREAS OF STABLE AND UNSTABLE MALARIA
TRANSMISSION IN CHHATTISGARH, INDIA
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Singh, Neeru] Reg Med Res Ctr ICMR, Jabalpur, India.
[Singh, Mrigendra P.; Shukla, Manmohan M.; Hussain, Mohassir] Natl Inst Malaria Res Field Stn, Jabalpur, India.
[Dash, Aditya P.] Natl Inst Malaria Res, Delhi, India.
[Wylie, Blair J.] Massachusetts Gen Hosp, Dept Obstet, Boston, MA 02114 USA.
[Yeboah-Antwi, Kojo; Sabin, Lora; Hamer, Davidson H.] Ctr Int Hlth & Dev, Boston, MA USA.
[Udhayakumar, Venkatachalam; Desai, Meghna] Ctr Dis Control & Prevent, Malaria Branch, Atlanta, GA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 900
BP 259
EP 259
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701315
ER
PT J
AU Charles, RC
Sheikh, A
Rollins, S
Harris, JB
Bhuiyan, MS
Khanam, F
Bukka, A
Kalsy, A
Porwollik, S
Brooks, WA
LaRocque, R
McClelland, M
Logvinenko, T
Cravioto, A
Calderwood, SB
Graham, JE
Qadri, F
Ryan, ET
AF Charles, Richelle C.
Sheikh, Alaullah
Rollins, Sean
Harris, Jason B.
Bhuiyan, Md. Saruar
Khanam, Farhana
Bukka, Archana
Kalsy, Anuj
Porwollik, Steffen
Brooks, W. Abdullah
LaRocque, Regina
McClelland, Michael
Logvinenko, Tanya
Cravioto, Alejandro
Calderwood, Stephen B.
Graham, James E.
Qadri, Firdausi
Ryan, Edward T.
TI HIGH THROUGHPUT GENE EXPRESSION PROFILING OF SALMONELLA ENTERICA SEROVAR
PARATYPHI A IN THE BLOOD OF BACTEREMIC PATIENTS IN BANGLADESH
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Charles, Richelle C.; Rollins, Sean; Harris, Jason B.; Kalsy, Anuj; LaRocque, Regina; Calderwood, Stephen B.; Ryan, Edward T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Sheikh, Alaullah; Bhuiyan, Md. Saruar; Khanam, Farhana; Brooks, W. Abdullah; Cravioto, Alejandro; Qadri, Firdausi] Int Ctr Diarrhoeal Dis Res, Dhaka, Bangladesh.
[Bukka, Archana; Graham, James E.] Univ Louisville, Louisville, KY 40292 USA.
[Porwollik, Steffen; McClelland, Michael] Sidney Kimmel Canc Ctr, San Diego, CA USA.
[Logvinenko, Tanya] Tufts Univ, Med Ctr, Boston, MA 02111 USA.
RI McClelland, Michael/A-8583-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1145
BP 331
EP 331
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701559
ER
PT J
AU Sheikh, A
Khanam, F
Rahman, T
Pacek, M
Hu, YH
Baresch, A
Bhuiyan, MS
Rollins, S
Citorik, R
Kalsy, A
Charles, R
LaRocque, RC
LaBaer, J
Calderwood, SB
Harris, JB
Qadri, F
Ryan, ET
AF Sheikh, Alaullah
Khanam, Farhana
Rahman, Taibur
Pacek, Martin
Hu, Yanhui
Baresch, Andrea
Bhuiyan, Md. Saruar
Rollins, Sean
Citorik, Robert
Kalsy, Anuj
Charles, Richelle
LaRocque, Regina C.
LaBaer, Joshua
Calderwood, Stephen B.
Harris, Jason B.
Qadri, Firdausi
Ryan, Edward T.
TI EVALUATION OF INTERFERON-Gamma RESPONSES IN PATIENTS WITH SALMONELLA
ENTERICA SEROVAR TYPHI BACTEREMIA IN DHAKA, BANGLADESH
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Sheikh, Alaullah; Khanam, Farhana; Rahman, Taibur; Bhuiyan, Md. Saruar; Qadri, Firdausi] Int Ctr Diarrhoeal Dis Res, Dhaka, Bangladesh.
[Pacek, Martin; Hu, Yanhui; LaBaer, Joshua] Harvard Inst Prote, Boston, MA USA.
[Baresch, Andrea; Rollins, Sean; Citorik, Robert; Kalsy, Anuj; Charles, Richelle; LaRocque, Regina C.; Calderwood, Stephen B.; Harris, Jason B.; Ryan, Edward T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1144
BP 331
EP 331
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701558
ER
PT J
AU Moss, DR
Bartels, K
Peterfreund, GL
Lovich, MA
Sims, NM
Peterfreund, RA
AF Moss, David R.
Bartels, Karsten
Peterfreund, Gregory L.
Lovich, Mark A.
Sims, Nathaniel M.
Peterfreund, Robert A.
TI An In Vitro Analysis of Central Venous Drug Delivery by Continuous
Infusion: The Effect of Manifold Design and Port Selection
SO ANESTHESIA AND ANALGESIA
LA English
DT Article
ID DEAD-VOLUME; SYRINGE PUMPS; DYNAMICS; DELAYS; SET
AB BACKGROUND: Central venous catheters are used extensively in anesthesia and critical care. Multiport manifolds allow for simultaneous administration of multiple medication infusions into a common central venous catheter lumen. The structures of such manifolds vary considerably. In this study, we quantitatively compared, in a laboratory model of continuous drug infusion, the drug delivery dynamics of a traditional stopcock manifold and a microinfusion manifold constructed to minimize dead volume.
METHODS: A syringe pump infused a saline carrier solution at a low flow rate frequently used in an intensive care unit (10 mL/h) through a multiport manifold connected to the 16-gauge lumen of a standard 16-cm triple-lumen catheter. The model drug methylene blue (3 mL/h) joined the carrier flow at the first, second, or fourth stopcock of a traditional manifold or 1 of 2 positions in a microinfusion manifold, a new device designed to minimize dead volume. Effluent samples were collected every minute for quantitative spectrophotometric analysis of delivery onset and offset.
RESULTS: Onset and offset times differed significantly among individual ports of the traditional 4-stopcock manifold. There was also a significant difference between the 2 ports of the microinfusion manifold, but this was less pronounced. Both ports of the microinfusion manifold yielded delivery dynamics that were similar to the most downstream port of the 4-stopcock manifold. There was good correlation between dynamic data and dead volume for each of the manifolds.
CONCLUSIONS: Using a traditional stopcock manifold, port selection significantly affects drug delivery dynamics for continuous infusions. The findings provide quantitative support for the concept that the most critical infusion should join the system at the manifold port closest to the patient. Port selection was less important for the microinfusion manifold and dynamics were faster compared with the second and fourth ports of the stopcock manifold. The smaller dead volumes of the microinfusion manifold minimize unwanted delays in drug delivery onset and offset allowing more precise control over drug delivery by continuous infusion. (Anesth Analg 2009;109:1524-9)
C1 [Moss, David R.; Bartels, Karsten; Peterfreund, Gregory L.; Sims, Nathaniel M.; Peterfreund, Robert A.] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
[Lovich, Mark A.] Caritas St Elizabeths Med Ctr, Dept Anesthesiol & Pain Med, Boston, MA USA.
RP Peterfreund, RA (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Jackson 439,55 Fruit St, Boston, MA 02114 USA.
EM rpeterfreund@partners.org
FU Departments of Anesthesia and Critical Care, Massachusetts General
Hospital
FX Supported by Institutional funds from the Departments of Anesthesia and
Critical Care, Massachusetts General Hospital.
NR 10
TC 13
Z9 13
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-2999
J9 ANESTH ANALG
JI Anesth. Analg.
PD NOV
PY 2009
VL 109
IS 5
BP 1524
EP 1529
DI 10.1213/ANE.0b013e3181b7c359
PG 6
WC Anesthesiology
SC Anesthesiology
GA 509QF
UT WOS:000271032500030
PM 19843791
ER
PT J
AU Guan, ZH
Baker, K
Sandberg, WS
AF Guan, Zhonghui
Baker, Keith
Sandberg, Warren S.
TI Misalignment of Disposable Pulse Oximeter Probes Results in False
Saturation Readings That Influence Anesthetic Management
SO ANESTHESIA AND ANALGESIA
LA English
DT Article
AB We report a small case series in which misaligned disposable pulse oximeter sensors gave falsely low saturation readings. In each instance, the sensor performed well during preinduction oxygen administration and the early part of the case, most notably by producing a plethysmographic trace rated as high quality by the oximeter software. The reported pulse oximeter oxygen saturation eventually decreased to concerning levels in each instance, but the anesthesiologists, relying on the reported high-quality signal, initially sought other causes for apparent hypoxia. They undertook maneuvers and diagnostic procedures later deemed unnecessary. When the malpositioned sensors were discovered and repositioned, the apparent hypoxia was quickly relieved in each case. We then undertook a survey of disposable oximeter sensors as patients entered the recovery room, and discovered malposition of more than 1 cm in approximately 20% of all sensors, without apparent consequence. We conclude that the technology is quite robust, but that the diagnosis of apparent hypoxia should include a quick check of oximeter position early on. (Anesth Analg 2009;109:1530-3)
C1 [Guan, Zhonghui; Baker, Keith; Sandberg, Warren S.] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
[Guan, Zhonghui; Baker, Keith; Sandberg, Warren S.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Sandberg, WS (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, 55 Fruit St,Jackson 4, Boston, MA 02114 USA.
EM wsandberg@partners.org
OI Sandberg, Warren/0000-0002-9246-777X
FU Department of Anesthesia and Critical Care, Massachusetts General
Hospital
FX Supported by the Department of Anesthesia and Critical Care,
Massachusetts General Hospital.
NR 4
TC 7
Z9 7
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-2999
J9 ANESTH ANALG
JI Anesth. Analg.
PD NOV
PY 2009
VL 109
IS 5
BP 1530
EP 1533
DI 10.1213/ANE.0b013e3181b9a814
PG 4
WC Anesthesiology
SC Anesthesiology
GA 509QF
UT WOS:000271032500031
PM 19843792
ER
PT J
AU Costa, ELV
Melo, MFV
AF Costa, Eduardo L. V.
Melo, Marcos F. Vidal
TI Lung Water What You See (with Computed Tomography) and What You Get
(with a Bedside Device)
SO ANESTHESIOLOGY
LA English
DT Editorial Material
ID SINGLE TRANSPULMONARY THERMODILUTION; REGIONAL PULMONARY PERFUSION;
CRITICALLY-ILL; NITRIC-OXIDE; THERMAL-DYE; INJURY; VENTILATION;
INDICATOR; SEPSIS; MANAGEMENT
C1 [Costa, Eduardo L. V.; Melo, Marcos F. Vidal] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Costa, Eduardo L. V.; Melo, Marcos F. Vidal] Harvard Univ, Sch Med, Boston, MA USA.
[Costa, Eduardo L. V.] Univ Sao Paulo, Sch Med, Resp Intens Care Unit, Sao Paulo, Brazil.
RP Costa, ELV (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
EM mvidalmelo@partners.org
RI Costa, Eduardo/K-5841-2012
OI Costa, Eduardo/0000-0002-6941-3626
FU NHLBI NIH HHS [R01 HL086827, R01 HL086827-03]
NR 33
TC 4
Z9 4
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2009
VL 111
IS 5
BP 933
EP 935
PG 3
WC Anesthesiology
SC Anesthesiology
GA 511NN
UT WOS:000271172500002
PM 19858867
ER
PT J
AU Payne, SJ
Selb, J
Boas, DA
AF Payne, S. J.
Selb, J.
Boas, D. A.
TI Effects of Autoregulation and CO2 Reactivity on Cerebral Oxygen
Transport
SO ANNALS OF BIOMEDICAL ENGINEERING
LA English
DT Article
DE Autoregulation; Cerebral blood flow; CO2; Transfer function;
Mathematical model; Stroke
ID ACUTE ISCHEMIC-STROKE; NONLINEAR PHYSIOLOGICAL SYSTEMS; BLOOD-FLOW; SLOW
DYNAMICS; HEMODYNAMICS; HUMANS; FLUCTUATIONS; ARTERIAL; MODEL
AB Both autoregulation and CO2 reactivity are known to have significant effects on cerebral blood flow and thus on the transport of oxygen through the vasculature. In this paper, a previous model of the autoregulation of blood flow in the cerebral vasculature is expanded to include the dynamic behavior of oxygen transport through binding with hemoglobin. The model is used to predict the transfer functions for both oxyhemoglobin and deoxyhemoglobin in response to fluctuations in arterial blood pressure and arterial CO2 concentration. It is shown that only six additional nondimensional groups are required in addition to the five that were previously found to characterize the cerebral blood flow response. A resonant frequency in the pressure-oxyhemoglobin transfer function is found to occur in the region of 0.1 Hz, which is a frequency of considerable physiological interest. The model predictions are compared with results from the published literature of phase angle at this frequency, showing that the effects of changes in breathing rate can significantly alter the inferred phase dynamics between blood pressure and hemoglobin. The question of whether dynamic cerebral autoregulation is affected under conditions of stenosis or stroke is then examined.
C1 [Payne, S. J.] Univ Oxford, Dept Engn Sci, Inst Biomed Engn, Oxford OX1 3PJ, England.
[Selb, J.; Boas, D. A.] Massachusetts Gen Hosp, Photon Migrat Imaging Lab, Charlestown, MA USA.
RP Payne, SJ (reprint author), Univ Oxford, Dept Engn Sci, Inst Biomed Engn, Parks Rd, Oxford OX1 3PJ, England.
EM sjp@robots.ox.ac.uk
FU NCRR NIH HHS [P41 RR014075, P41 RR014075-075756]; NIBIB NIH HHS [R01
EB006385, R01 EB006385-03]
NR 24
TC 13
Z9 14
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0090-6964
J9 ANN BIOMED ENG
JI Ann. Biomed. Eng.
PD NOV
PY 2009
VL 37
IS 11
BP 2288
EP 2298
DI 10.1007/s10439-009-9763-5
PG 11
WC Engineering, Biomedical
SC Engineering
GA 502HL
UT WOS:000270448300010
PM 19629692
ER
PT J
AU Granpeesheh, D
Tarbox, J
Dixon, DB
Carr, E
Herbert, M
AF Granpeesheh, Doreen
Tarbox, Jonathan
Dixon, Dennis B.
Carr, Edward
Herbert, Martha
TI Retrospective analysis of clinical records in 38 cases of recovery from
autism
SO ANNALS OF CLINICAL PSYCHIATRY
LA English
DT Article
DE autism; ASD; recovery; EIBI; ABA
AB BACKGROUND: Twenty years of research on early intensive treatment using applied behavior analysis (ABA) for children with autism has consistently produced robust effects. There appears to be a subset of children whose response to intensive ABA treatments includes achieving a level of functioning that is indistinguishable from typically developing peers. The purpose of this study was to describe a subset of children who recovered from autism following intensive ABA interventions.
METHODS: We reviewed the clinical files of 38 children with autism who achieved an optimal outcome after receiving intensive ABA services.
RESULTS: The mean age at intake was 40 months. Average IQ was 83.6 at intake and 107.9 at discharge. Mean adaptive skills were 68.04 at intake and 88.87 at discharge.
CONCLUSIONS: Our study corroborates the finding that some children with autism who receive early intensive behavioral intervention achieve functioning in the average range.
C1 [Granpeesheh, Doreen; Tarbox, Jonathan; Dixon, Dennis B.] Ctr Autism & Related Disorders, Tarzana, CA 91356 USA.
[Carr, Edward] SUNY Stony Brook, Stony Brook, NY 11794 USA.
[Herbert, Martha] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cambridge, MA 02138 USA.
RP Granpeesheh, D (reprint author), Ctr Autism & Related Disorders, 19019 Ventura Blvd,3rd Floor, Tarzana, CA 91356 USA.
EM D.Granpeesheh@centerforautism.com
NR 28
TC 12
Z9 12
U1 4
U2 11
PU DOWDEN HEALTH MEDIA
PI MONTVALE
PA 110 SUMMIT AVE, MONTVALE, NJ 07645-1712 USA
SN 1040-1237
J9 ANN CLIN PSYCHIATRY
JI Ann. Clin. Psychiatry
PD NOV
PY 2009
VL 21
IS 4
BP 195
EP 204
PG 10
WC Psychiatry
SC Psychiatry
GA V16WR
UT WOS:000207900200002
PM 19917210
ER
PT J
AU Beslija, S
Bonneterre, J
Burstein, HJ
Cocquyt, V
Gnant, M
Heinemann, V
Jassem, J
Kostler, WJ
Krainer, M
Menard, S
Petit, T
Petruzelka, L
Possinger, K
Schmid, P
Stadtmauer, E
Stockler, M
Van Belle, S
Vogel, C
Wilcken, N
Wiltschke, C
Zielinski, CC
Zwierzina, H
AF Beslija, S.
Bonneterre, J.
Burstein, H. J.
Cocquyt, V.
Gnant, M.
Heinemann, V.
Jassem, J.
Koestler, W. J.
Krainer, M.
Menard, S.
Petit, T.
Petruzelka, L.
Possinger, K.
Schmid, P.
Stadtmauer, E.
Stockler, M.
Van Belle, S.
Vogel, C.
Wilcken, N.
Wiltschke, C.
Zielinski, C. C.
Zwierzina, H.
CA CECOG
TI Third consensus on medical treatment of metastatic breast cancer
SO ANNALS OF ONCOLOGY
LA English
DT Review
DE diagnosis; metastatic breast cancer; prognosis; treatment
ID PHASE-II TRIAL; PEGYLATED LIPOSOMAL DOXORUBICIN; HEAVILY PRETREATED
PATIENTS; IN-SITU HYBRIDIZATION; REPLACEMENT THERAPY WITHDRAWAL;
EVERY-2-WEEK DARBEPOETIN-ALPHA; CHEMOTHERAPY-INDUCED ANEMIA;
COLONY-STIMULATING FACTOR; PLACEBO-CONTROLLED TRIAL; WEEKLY
EPOETIN-ALPHA
AB Design: To provide timely and evidence-based recommendations for the diagnostic workup and treatment of patients with MBC, an international expert panel reviewed and discussed the evidence available from clinical trials regarding diagnostic, therapeutic and supportive measures with emphasis on their impact on the quality of life and overall survival of patients with MBC.
Results: Evidence-based recommendations for the diagnostic workup, endocrine therapy, chemotherapy, use of targeted therapies and bisphosphonates, surgical treatment and supportive care measures in the management of patients with MBC were formulated.
Conclusions: The present consensus manuscript updates evidence-based recommendations for state-of-the-art treatment of MBC depending on disease-associated and biological variables.
C1 [Koestler, W. J.; Krainer, M.; Wiltschke, C.; Zielinski, C. C.] Med Univ Vienna, Dept Med 1, Div Clin Oncol, A-1090 Vienna, Austria.
[Beslija, S.] Inst Oncol, Sarajevo, Bosnia & Herceg.
[Bonneterre, J.] Ctr Oscar Lambret, F-59020 Lille, France.
[Burstein, H. J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Cocquyt, V.; Van Belle, S.] Univ Ziekenhuis St Rafael, Oncolog Centrum, Ghent, Belgium.
[Gnant, M.] Med Univ Vienna, Dept Surg, Vienna, Austria.
[Heinemann, V.] Univ Munich, Klinikum Grosshadern, Med Klin & Poliklin 3, D-8000 Munich, Germany.
[Jassem, J.] Med Univ, Dept Radiotherapy & Oncol, Gdansk, Poland.
[Menard, S.] Ist Tumori, Milan, Italy.
[Petit, T.] Ctr Paul Strauss, Strasbourg, France.
[Petruzelka, L.] Charles Univ Prague, Dept Oncol, Prague, Czech Republic.
[Possinger, K.] Med Klin Charite, Berlin, Germany.
[Schmid, P.] Univ London Imperial Coll Sci Technol & Med, Charing Cross Hosp, London, England.
[Stadtmauer, E.] Univ Penn, Ctr Canc, Philadelphia, PA 19104 USA.
[Stockler, M.] Univ Sydney, Concord Hosp, Sydney, NSW 2006, Australia.
[Stockler, M.] Royal Prince Alfred Hosp, Sydney Canc Ctr, Sydney, NSW, Australia.
[Vogel, C.] Breast Canc Aptium Oncol Lynn Canc Inst W, Boca Raton, FL USA.
[Wilcken, N.] Westmead Hosp, Dept Med Oncol & Palliat Care, Sydney, NSW, Australia.
[Zielinski, C. C.] Cent European Cooperat Oncol Grp, Vienna, Austria.
[Zwierzina, H.] Med Univ Innsbruck, Dept Med 1, Innsbruck, Austria.
RP Zielinski, CC (reprint author), Med Univ Vienna, Dept Med 1, Div Clin Oncol, 18-20 Waehringer Guertel, A-1090 Vienna, Austria.
EM christoph.zielinski@meduniwien.ac.at
RI Stockler, Martin/N-3859-2016; Petruzelka, Lubos/A-2750-2017;
OI Stockler, Martin/0000-0003-3793-8724; Petruzelka,
Lubos/0000-0002-4397-0635; Gnant, Michael/0000-0003-1002-2118; Krainer,
Michael/0000-0002-7011-4957
FU Bristol Myers-Squibb; Eli Lilly; Roche
FX Bristol Myers-Squibb; Eli Lilly; Roche.
NR 193
TC 95
Z9 98
U1 1
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD NOV
PY 2009
VL 20
IS 11
BP 1771
EP 1785
DI 10.1093/annonc/mdp261
PG 15
WC Oncology
SC Oncology
GA 514GB
UT WOS:000271381300003
PM 19608616
ER
PT J
AU Sher, DJ
Mauch, PM
Van Den Abbeele, A
LaCasce, AS
Czerminski, J
Ng, AK
AF Sher, D. J.
Mauch, P. M.
Van Den Abbeele, A.
LaCasce, A. S.
Czerminski, J.
Ng, A. K.
TI Prognostic significance of mid- and post-ABVD PET imaging in Hodgkin's
lymphoma: the importance of involved-field radiotherapy
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE Hodgkin's lymphoma; involved-field radiotherapy; PET; radiotherapy;
response-adapted therapy
ID POSITRON-EMISSION-TOMOGRAPHY; DISEASE; RADIATION; CHEMOTHERAPY;
PROGRESSION; THERAPY; RELAPSE; INTERIM
AB Methods: Patients with HL treated with adriamycin, bleomycin, vinblastine and dacarbazine (ABVD)-based CT and radiotherapy (RT) at our institution from January 2000 to March 2007 were eligible. All patients had either a post-treatment PET or PET-CT before initiation of RT or a negative midtreatment PET or PET-CT. The primary end point was failure-free survival (FFS) for patients with and without residual FDG avidity after ABVD. The treatment outcome of patients with interim PET positivity during CT was also reported.
Results: Seventy-three patients were included in this study. Twenty patients (out of 46) were PET positive on interim PET, and 13 patients (out of 73) were PET positive at the conclusion of CT. At a median follow-up of 3.4 years for surviving patients, the 2-year FFSs for patients PET-negative versus PET-positive disease after ABVD were 95% and 69%, respectively (P < 0.01). On bivariable Cox regression, post-ABVD positivity (hazard ratio 4.8, P = 0.05) was predictive of disease recurrence after controlling for bulky disease. Of the 20 patients with interim PET positivity, three recurred, with a 2-year FFS of 85%. Among the 13 patients with interim PET positivity, but became PET negative at the completion of CT, the 2-year FFS was 92%.
Conclusion: Sixty-nine per cent of patients with residual FDG avidity after ABVD were free of disease after consolidative RT, indicating a majority of patients with persistent lymphoma can be cured by sterilizing this PET-positive disease.
C1 [Sher, D. J.; Mauch, P. M.; Czerminski, J.; Ng, A. K.] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
[Sher, D. J.; Mauch, P. M.; Czerminski, J.; Ng, A. K.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Van Den Abbeele, A.] Dana Farber Canc Inst, Dept Nucl Med, Boston, MA 02115 USA.
[LaCasce, A. S.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Sher, DJ (reprint author), Dana Farber Canc Inst, Dept Radiat Oncol, 44 Binney St, Boston, MA 02115 USA.
EM dsher@lroc.harvard.edu
NR 17
TC 41
Z9 42
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD NOV
PY 2009
VL 20
IS 11
BP 1848
EP 1853
DI 10.1093/annonc/mdp071
PG 6
WC Oncology
SC Oncology
GA 514GB
UT WOS:000271381300013
PM 19541793
ER
PT J
AU Mcgee, S
Mardirossian, V
Elackattu, A
Mirkovic, J
Pistey, R
Gallagher, G
Kabani, S
Yu, CC
Wang, Z
Badizadegan, K
Grillone, G
Feld, MS
AF McGee, Sasha
Mardirossian, Vartan
Elackattu, Alphi
Mirkovic, Jelena
Pistey, Robert
Gallagher, George
Kabani, Sadru
Yu, Chung-Chieh
Wang, Zimmern
Badizadegan, Kamran
Grillone, Gregory
Feld, Michael S.
TI Anatomy-Based Algorithms for Detecting Oral Cancer Using Reflectance and
Fluorescence Spectroscopy
SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY
LA English
DT Article
DE diagnosis; fluorescence; oral cancer; reflectance; spectroscopy
ID NATIVE CELLULAR FLUORESCENCE; AERODIGESTIVE TRACT CANCER; IN-VIVO;
AUTOFLUORESCENCE SPECTROSCOPY; EXCITATION WAVELENGTHS; OPTICAL
SPECTROSCOPY; INCISIONAL BIOPSY; LIGHT-SCATTERING; DIAGNOSIS; LESIONS
AB Objectives: We used reflectance and fluorescence spectroscopy to noninvasively and quantitatively distinguish benign from dysplastic/malignant oral lesions. We designed diagnostic algorithms to account for differences in the spectral properties among anatomic sites (gingiva, buccal mucosa, etc).
Methods: In vivo reflectance and fluorescence spectra were collected from 71 patients with oral lesions. The tissue was then biopsied and the specimen evaluated by histopathology. Quantitative parameters related to tissue morphology and biochemistry were extracted from the spectra. Diagnostic algorithms specific for combinations of sites with similar spectral properties were developed.
Results: Discrimination of benign from dysplastic/malignant lesions was most successful when algorithms were designed for individual sites (area under the receiver operator characteristic curve [ROC-AUC], 0.75 for the lateral surface of the tongue) and was least accurate when all sites were combined (ROC-AUC, 0.60). The combination of sites with similar spectral properties (floor of mouth and lateral surface of the ton-Lie) yielded an ROC-AUC of 0.71.
Conclusions: Accurate spectroscopic detection of oral disease must account for spectral variations among anatomic sites. Anatomy-based algorithms for single sites or combinations of sites demonstrated good diagnostic performance in distinguishing benign lesions from dysplastic/malignant lesions and consistently performed better than algorithms developed for all sites combined.
C1 [Mardirossian, Vartan; Elackattu, Alphi; Wang, Zimmern; Grillone, Gregory] Boston Med Ctr, Dept Otolaryngol Head & Neck Surg, Boston, MA USA.
[Pistey, Robert] Boston Med Ctr, Dept Anat Pathol, Boston, MA USA.
[McGee, Sasha; Mirkovic, Jelena; Yu, Chung-Chieh; Badizadegan, Kamran; Feld, Michael S.] MIT, GR Harrison Spect Lab, Boston, MA USA.
[Gallagher, George; Kabani, Sadru] Boston Univ, Goldman Sch Dent Med, Dept Oral & Maxillofacial Pathol, Boston, MA 02215 USA.
[Badizadegan, Kamran] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Badizadegan, Kamran] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Mcgee, S (reprint author), MIT, GR Harrison Spect Lab, Bldg 6-205,77 Massachusetts Ave, Cambridge, MA 02139 USA.
RI Mirkovic, Jelena/A-6253-2013
FU National Institutes of Health [R01-CA097966, P41-RR02594-21]
FX From the G. R. Harrison Spectroscopy Laboratory, Massachusetts Institute
of Technology (McGee, Mirkovic, Yu, Badizadegan, Feld), the Departments
of Otolaryngology-Head and Neck Surgery (Mardirossian, Elackattu, Wang,
Grillone) and Anatomic Pathology (Pistey), Boston Medical Center, the
Department of Oral and Maxillofacial Pathology, Boston University
Goldman School of Dental Medicine (Gallagher, Kabani), and the
Department of Pathology, Harvard Medical School and Massachusetts
General Hospital (Badizadegan), Boston. Massachusetts. This research was
supported by National Institutes of Health grants R01-CA097966 and
P41-RR02594-21.
NR 44
TC 20
Z9 20
U1 0
U2 0
PU ANNALS PUBL CO
PI ST LOUIS
PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 USA
SN 0003-4894
J9 ANN OTO RHINOL LARYN
JI Ann. Otol. Rhinol. Laryngol.
PD NOV
PY 2009
VL 118
IS 11
BP 817
EP 826
PG 10
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 523YX
UT WOS:000272112100012
PM 19999369
ER
PT J
AU Chambers, JA
Ray, PD
AF Chambers, James Alan
Ray, Peter Damian
TI Achieving Growth and Excellence in Medicine The Case History of Armed
Conflict and Modem Reconstructive Surgery
SO ANNALS OF PLASTIC SURGERY
LA English
DT Article
DE plastic surgery; reconstructive surgery; war; history; military; surgery
ID PLASTIC-SURGERY; HAND SURGERY; WAR; SPECIALTY; EVOLUTION; STORY
AB November 11, 2009 will mark over 90 years of commemorating Armistice Day, the end of World War I. Although conflict in the Middle East reminds us that WWI failed to end all wars, it did serve as both substrate and catalyst for the development of modem plastic and reconstructive surgery. This article will outline those ingredients most directly responsible for the growth of the specialty, tracing its development in response to armed conflict, and implications for continued excellence both in reconstructive Surgery and other fields in the future.
C1 [Chambers, James Alan] Massachusetts Gen Hosp, Hand & Upper Extrem Serv, Boston, MA 02114 USA.
[Ray, Peter Damian] Univ Alabama, Craniofacial Serv, Birmingham, AL USA.
RP Chambers, JA (reprint author), Massachusetts Gen Hosp, Hand & Upper Extrem Serv, 55 Fruit St,Yawkey 2100, Boston, MA 02114 USA.
EM j.alan.chambers@gmail.com
NR 58
TC 5
Z9 5
U1 3
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-7043
J9 ANN PLAS SURG
JI Ann. Plast. Surg.
PD NOV
PY 2009
VL 63
IS 5
BP 473
EP 478
DI 10.1097/SAP.0b013e3181bc327a
PG 6
WC Surgery
SC Surgery
GA 512QV
UT WOS:000271266100002
PM 20431512
ER
PT J
AU Zischek, C
Niess, H
Ischenko, I
Conrad, C
Huss, R
Jauch, KW
Nelson, PJ
Bruns, C
AF Zischek, Christoph
Niess, Hanno
Ischenko, Ivan
Conrad, Claudius
Huss, Ralf
Jauch, Karl-Walter
Nelson, Peter J.
Bruns, Christiane
TI Targeting Tumor Stroma Using Engineered Mesenchymal Stem Cells Reduces
the Growth of Pancreatic Carcinoma
SO ANNALS OF SURGERY
LA English
DT Article
AB Objective: To analyze the efficacy of engineered mesenchymal stem cell based therapy directed towards pancreatic tumor stroma.
Summary Background Data: Mesenchymal stem cells (MSC) are actively recruited to tumor stroma where they enhance tumor growth and metastases. Upregulation of chemotactic cytokine (CCL5) by MSCs within the tumor stroma has been shown to play a central role in this process. Murine MSCs were engineered to express reporter genes or therapeutic genes under control of the CCL5 promoter and adoptively transferred into mice with growing pancreatic tumors. The effect on tumor growth and metastases was then evaluated.
Methods: MSCs isolated from bone marrow of C57/Bl6 p53(-/-) mice were stably transfected with red fluorescent protein (RFP), enhanced green fluorescent protein (eGFP), or herpes simplex virus (HSV) thymidine kinase (Tk) gene driven by the RANTES promoter. MSCs were intravenously applied once per week over 3 weeks to mice carrying an orthotopic, syngeneic pancreatic Panc02 tumor.
Results: eGFP and RFP signals driven by the CCL5 promoter were detected by fluorescence in treated pancreatic tumor samples. The HSV-Tk therapy group treated intraperitoneal with the prodrug ganciclovir 5 to 7 days after stem cell application lead to a 50% reduction of primary pancreatic tumor growth (P < 0.0003, student t test) and reduced liver metastases (0% vs. 60%).
Conclusion: The active homing of MSCs into primary pancreatic tumor stroma and activation of the CCL5 promoter was verified using eGFP- and RFP-reporter genes. In the presence of ganciclovir, HSV-Tk transfected MSCs led to a significant reduction of primary pancreatic tumor growth and incidence of metastases. (Ann Surg 2009;250: 747-753)
C1 [Zischek, Christoph; Nelson, Peter J.] Univ Munich, Med Policlin, Clin Biochem Grp, Munich, Germany.
[Zischek, Christoph; Niess, Hanno; Ischenko, Ivan; Conrad, Claudius; Jauch, Karl-Walter; Bruns, Christiane] Univ Munich, Dept Surg, Munich, Germany.
[Conrad, Claudius] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Conrad, Claudius; Huss, Ralf] Harvard Stem Cell Inst, Cambridge, MA USA.
[Huss, Ralf] Univ Munich, Inst Pathol, D-80539 Munich, Germany.
[Conrad, Claudius; Huss, Ralf] Roche Diagnost GmbH, Pharma Res, Stem Cell Therapy Strategy Penzberg, Penzberg, Germany.
RP Bruns, C (reprint author), Univ Munich, Dept Surg, Munich, Germany.
EM christiane.bruns@med.uni-muenchen.de
FU Deutsche Forschungsgemeinschaft [SPP1190, SFB-TR36/B6]; EU
FX Supported by grants from the Deutsche Forschungsgemeinschaft, SPP1190
(to C.B. and P.J.N.); SFB-TR36/B6 (to P.J.N.); EU P6 "INNOCHEM" (to
P.J.N.).
NR 44
TC 65
Z9 71
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-4932
J9 ANN SURG
JI Ann. Surg.
PD NOV
PY 2009
VL 250
IS 5
BP 747
EP 753
DI 10.1097/SLA.0b013e3181bd62d0
PG 7
WC Surgery
SC Surgery
GA V28FT
UT WOS:000208667400012
PM 19826249
ER
PT J
AU Merritt, RE
Mathisen, DJ
Wain, JC
Gaissert, HA
Donahue, D
Lanuti, M
Allan, JS
Morse, CR
Wright, CD
AF Merritt, Robert E.
Mathisen, Douglas J.
Wain, John C.
Gaissert, Henning A.
Donahue, Dean
Lanuti, Michael
Allan, James S.
Morse, Christopher R.
Wright, Cameron D.
TI Long-Term Results of Sleeve Lobectomy in the Management of Non-Small
Cell Lung Carcinoma and Low-Grade Neoplasms
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID LYMPH-NODE INVOLVEMENT; BRONCHOPLASTIC PROCEDURES; INDUCTION THERAPY;
CANCER; SURVIVAL; PNEUMONECTOMY; MORBIDITY; MORTALITY; COMPLICATIONS;
CHEMOTHERAPY
AB Background. The objective of this study was to evaluate the operative mortality, morbidity, and long-term survival of sleeve lobectomy for non-small cell lung cancer and low-grade neoplasms. We evaluated the effects of neoadjuvant therapy on the bronchial anastomotic complication rate and determined whether sleeve lobectomy performed in patients with N1 disease resulted in decreased overall survival.
Methods. This study is a retrospective review of 196 patients who underwent sleeve lobectomy. One hundred twenty-five patients had non-small cell lung cancer. There were 117 men (59.7%) and 79 women (40.3%) with a mean age of 54 years. Sixteen patients (13%) received neoadjuvant therapy. Fifty-six patients with N1 disease underwent sleeve lobectomy.
Results. There were 4 (2.0%) postoperative deaths. The postoperative morbidity rate was 36.7%. Four patients (2.0%) experienced bronchopleural fistulas. Multivariate analysis demonstrated that age older than 70 years (p = 0.02) and the diagnosis of non-small cell lung cancer (p = 0.0002) were risk factors for postoperative complications. Multivariate analysis also demonstrated that neoadjuvant therapy predicted anastomotic complications (p = 0.01). For non-small cell lung cancer patients, the 5-year survival rate was 44%. The 5-year survival rates for patients with pathologic N0 disease and N1 disease were 52.6% versus 39.3%, respectively (p = 0.205).
Conclusions. Sleeve lobectomy can be performed with minimal bronchial anastomotic complications and low postoperative mortality. In our study, neoadjuvant therapy for non-small cell lung cancer adversely influenced the rate of anastomotic complications. Performing sleeve lobectomy for patients with N1 disease was not associated with decreased overall survival rates. (Ann Thorac Surg 2009;88:1574-82) (C) 2009 by The Society of Thoracic Surgeons
C1 [Wright, Cameron D.] Massachusetts Gen Hosp, Dept Thorac Surg, Gen Thorac Surg Div, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
RP Wright, CD (reprint author), Massachusetts Gen Hosp, Dept Thorac Surg, Gen Thorac Surg Div, 32 Fruit St,Blake 1570, Boston, MA 02114 USA.
EM cdwright@partners.org
NR 22
TC 19
Z9 20
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD NOV
PY 2009
VL 88
IS 5
BP 1574
EP 1582
DI 10.1016/j.athoracsur.2009.07.060
PG 9
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 512AZ
UT WOS:000271215700028
PM 19853115
ER
PT J
AU Armstrong, AW
Watson, AJ
Makredes, M
Frangos, JE
Kimball, AB
Kvedar, JC
AF Armstrong, April W.
Watson, Alice J.
Makredes, Maryanne
Frangos, Jason E.
Kimball, Alexandra B.
Kvedar, Joseph C.
TI Text-Message Reminders to Improve Sunscreen Use A Randomized, Controlled
Trial Using Electronic Monitoring
SO ARCHIVES OF DERMATOLOGY
LA English
DT Article
ID SKIN-CANCER PREVENTION; ULTRAVIOLET-RADIATION; REDUCING EXPOSURE; SUN
SAFETY; ADHERENCE; PROTECTION; POPULATION; MEDICATION; SCHOOLS; PATIENT
AB Objective: To evaluate the effectiveness of cellular telephone text messaging as a reminder tool for improving adherence to sunscreen application.
Design: We conducted a randomized, controlled trial of the effect of an electronic text- message reminder system on adherence to sunscreen application. Adherence to daily sunscreen use was evaluated using a novel electronic monitoring device.
Setting: Participants were recruited from the general community.
Participants: Seventy participants constituted a volunteer sample from the general community. The inclusion criteria required participants to be 18 years or older, to own a cellular telephone with text-message features, and to know how to retrieve text messages.
Intervention: Half of the participants received daily text-message reminders via cellular telephone for 6 weeks, and the other half did not receive reminders. The text-message reminders consisted of 2 components: a "hook" text detailing daily local weather information and a "prompt" text reminding users to apply sunscreen.
Main Outcome Measure: The primary end point of the study was adherence to sunscreen application measured by the number of days participants applied sunscreen during the 6-week study period.
Results: All 70 participants completed the 6-week study. There were no statistically significant differences in baseline characteristics between the 2 study groups. At the end of the study period, the 35 participants who did not receive reminders had a mean daily adherence rate of 30.0% (95% confidence interval, 23.1%-36.9%). In comparison, the 35 participants who received daily text-message reminders had a mean daily adherence rate of 56.1% (95% confidence interval, 48.1%-64.1%) (P<.001). Among the participants in the reminder group, 24 (69%) reported that they would keep using the text-message reminders after the study, and 31 (89%) reported that they would recommend the text-message reminder system to others. Subgroup analysis did not reveal any significant demographic factors that predicted adherence.
Conclusions: Despite awareness of the benefits of sunscreen, adherence is low, even in this population, for whom adherence was knowingly monitored. Shortterm data demonstrate that using existing cellular telephone text-message technology offers an innovative, low-cost, and effective method of improving adherence to sunscreen application. The use of ubiquitous communications technology, such as text messaging, may have implications for large-scale public health initiatives.
C1 [Armstrong, April W.] Univ Calif Davis Hlth Syst, Dept Dermatol, Teledermatol Program, Sacramento, CA 95816 USA.
[Watson, Alice J.] Massachusetts Gen Hosp, Ctr Connected Hlth, Boston, MA 02114 USA.
[Kimball, Alexandra B.] Massachusetts Gen Hosp, Clin Unit Res Trials Skin, Boston, MA 02114 USA.
[Watson, Alice J.; Kimball, Alexandra B.] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Makredes, Maryanne] Beth Israel Deaconess Med Ctr, Dept Internal Med, New York, NY 10003 USA.
[Frangos, Jason E.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Kimball, Alexandra B.; Kvedar, Joseph C.] Harvard Univ, Sch Med, Dept Dermatol, Cambridge, MA 02138 USA.
[Watson, Alice J.; Kvedar, Joseph C.] Partners HealthCare Syst, Ctr Connected Hlth, Boston, MA USA.
RP Armstrong, AW (reprint author), Univ Calif Davis Hlth Syst, Dept Dermatol, Teledermatol Program, 3301 C St,Ste 1400, Sacramento, CA 95816 USA.
FU Information Systems Council of Massachusetts General Hospital; Brigham
and Women's Hospital
FX Funding/Support: This study was supported by an institutional grant from
Information Systems Council of Massachusetts General Hospital and
Brigham and Women's Hospital. Study sunscreen was provided by
Neutrogena. Dr Makredes was a Doris Duke Clinical Research Fellow and Dr
Armstrong was a Stiefel/Connetics Research Fellow for Improving Access
to Dermatologic Care at the time of the study.
NR 40
TC 110
Z9 111
U1 3
U2 17
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-987X
J9 ARCH DERMATOL
JI Arch. Dermatol.
PD NOV
PY 2009
VL 145
IS 11
BP 1230
EP 1236
PG 7
WC Dermatology
SC Dermatology
GA 520ZS
UT WOS:000271889100003
PM 19917951
ER
PT J
AU Mollica, RF
Lyoo, IK
Chernoff, MC
Bui, HX
Lavelle, J
Yoon, SJ
Kim, JE
Renshaw, PF
AF Mollica, Richard F.
Lyoo, In Kyoon
Chernoff, Miriam C.
Bui, Hoan X.
Lavelle, James
Yoon, Sujung J.
Kim, Jieun E.
Renshaw, Perry F.
TI Brain Structural Abnormalities and Mental Health Sequelae in South
Vietnamese Ex-Political Detainees Who Survived Traumatic Head Injury and
Torture
SO ARCHIVES OF GENERAL PSYCHIATRY
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; HOPKINS SYMPTOM CHECKLIST-25;
CONCENTRATION CAMP SURVIVORS; COLLEGIATE FOOTBALL PLAYERS;
MAGNETIC-RESONANCE IMAGES; MAJOR DEPRESSIVE DISORDER; SURFACE-BASED
ANALYSIS; POW SURVIVORS; PREFRONTAL CORTEX; PSYCHOLOGICAL SEQUELAE
AB Context: A pilot study of South Vietnamese ex political detainees who had been incarcerated in Vietnamese reeducation camps and resettled in the United States disclosed significant mental health problems associated with torture and traumatic head injury (THI).
Objectives: To identify structural brain alterations associated with THI and to investigate whether these deficits are associated with posttraumatic stress disorder and depression.
Design: Cross-sectional neuroimaging study.
Setting: Massachusetts General Hospital and McLean Hospital.
Participants: A subsample of Vietnamese ex-political detainees (n=42) and comparison subjects (n=16) selected from a community study of 337 ex-political detainees and 82 comparison subjects.
Main Outcome Measures: Scores on the Vietnamese versions of the Hopkins Symptom Checklist-25 (HSCL) and Harvard Trauma Questionnaire for depression and posttraumatic stress disorder, respectively; cerebral regional cortical thickness; and manual volumetric morphometry of the amygdala, hippocampus, and thalamus.
Results: Ex-political detainees exposed to THI (n=16) showed a higher rate of depression (odds ratio, 10.2; 95% confidence interval, 1.2-90.0) than those without THI exposure (n=26). Ex-political detainees with THI had thinner prefrontotemporal cortices than those without THI exposure (P<.001 by the statistical difference brain map) in the left dorsolateral prefrontal and bilateral superior temporal cortices, controlling for age, handedness, and number of trauma/torture events (left superior frontal cortex [SFC], P=.006; left middle frontal cortex, P=.01; left superior temporal cortex [STC], P=.007; right STC, P=.01). Trauma/ torture events were associated with bilateral amygdala volume loss ( left, P=.045; right, P=.003). Cortical thinning associated with THI in the left SFC and bilateral STC was related to HSCL depression scores in THI-exposed (vs non THI-exposed) ex-political detainees (left SFC, P for interaction=.007; left STC, P for interaction=.03; right STC, P for interaction=.02).
Conclusions: Structural deficits in prefrontotemporal brain regions are linked to THI exposures. These brain lesions are associated with the symptom severity of depression in Vietnamese ex-political detainees.
C1 [Mollica, Richard F.; Lavelle, James] Massachusetts Gen Hosp, Harvard Program Refugee Trauma, Dept Psychiat, Cambridge, MA 02139 USA.
[Lyoo, In Kyoon; Kim, Jieun E.] Seoul Natl Univ, Dept Psychiat, Seoul, South Korea.
[Lyoo, In Kyoon] Seoul Natl Univ, Dept Neurosci, Seoul, South Korea.
[Lyoo, In Kyoon] Harvard Univ, McLean Hosp, Sch Med, Brain Imaging Ctr, Belmont, MA 02178 USA.
[Lyoo, In Kyoon] Harvard Univ, Sch Med, Dept Psychiat, Belmont, MA 02178 USA.
[Chernoff, Miriam C.] Harvard Univ, Sch Publ Hlth, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
[Bui, Hoan X.] Vietnamese Amer Civic Assoc, Dorchester, MA USA.
[Yoon, Sujung J.] Catholic Univ, Coll Med, Dept Psychiat, Seoul, South Korea.
[Renshaw, Perry F.] Univ Utah, Dept Psychiat, Salt Lake City, UT USA.
[Renshaw, Perry F.] Univ Utah, Inst Brain, Salt Lake City, UT USA.
[Renshaw, Perry F.] VISN 19 Mental Illness Res Educ & Clin Ctr, Dept Vet Affairs, Salt Lake City, UT USA.
RP Mollica, RF (reprint author), Massachusetts Gen Hosp, Harvard Program Refugee Trauma, Dept Psychiat, 22 Putnam Ave, Cambridge, MA 02139 USA.
EM rmollica@partners.org
FU National Institutes of Health [MH R01-059559-04]; Brain Research Center
of the 21st Century Frontier Research Program [2009K001272]; Ministry of
Education, Science, and Technology of South Korea
FX Research for this report was supported by grants MH R01-059559-04 from
the National Institutes of Health and 2009K001272 from the Brain
Research Center of the 21st Century Frontier Research Program, Ministry
of Education, Science, and Technology of South Korea.
NR 111
TC 32
Z9 33
U1 3
U2 13
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-990X
J9 ARCH GEN PSYCHIAT
JI Arch. Gen. Psychiatry
PD NOV
PY 2009
VL 66
IS 11
BP 1221
EP 1232
PG 12
WC Psychiatry
SC Psychiatry
GA 514WS
UT WOS:000271427500008
PM 19884610
ER
PT J
AU Hayden, KM
Zandi, PP
West, NA
Tschanz, JT
Norton, MC
Corcoran, C
Breitner, JCS
Welsh-Bohmer, KA
AF Hayden, Kathleen M.
Zandi, Peter P.
West, Nancy A.
Tschanz, JoAnn T.
Norton, Maria C.
Corcoran, Chris
Breitner, John C. S.
Welsh-Bohmer, Kathleen A.
CA Cache Cty Study Grp
TI Effects of Family History and Apolipoprotein E epsilon 4 Status on
Cognitive Decline in the Absence of Alzheimer Dementia The Cache County
Study
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID APOE GENOTYPE; DISEASE LOCUS; POPULATION-SAMPLE; TYPE-4 ALLELE; ONSET;
PERFORMANCE; MEMORY; RISK; AGE; APOE-EPSILON-4
AB Objective: To evaluate the influences of a family history of Alzheimer dementia (FHxAD) and the apolipoprotein E epsilon 4 genotype (APOE epsilon 4) on cognitive decline.
Design, Setting, and Participants: Residents of Cache County, Utah, aged 65 years or older, were invited to participate. At baseline, 2957 participants provided DNA for genotyping of APOE and a detailed FHxAD. They also completed the Modified Mini-Mental State Examination. Cognitive status was reexamined after 3 and 7 years. We used mixed-effects models to examine the association among FHxAD, APOE epsilon 4, and cognitive trajectories.
Main Outcome Measure: Modified Mini-Mental State Examination score trajectories over time.
Results: Compared with participants who did not have APOE epsilon 4 or an FHxAD, those with APOE epsilon 4 scored lower on the Modified Mini-Mental State Examination at base-line (-0.70 points; 95% confidence interval [CI], -1.15 to -0.24). Participants with an FHxAD and APOE epsilon 4 differed less, if at all, in baseline score (-0.46 points; 95% CI, -1.09 to 0.16) but declined faster during the 7-year study (-9.75 points [95% CI, -10.82 to -8.67] vs -2.91 points [95% CI, -3.37 to -2.44]). After exclusion of participants who developed prodromal AD or incident dementia, the group with an FHxAD and APOE epsilon 4 declined much less during the 7-year study (-1.54; 95% CI, -2.59 to -0.50).
Conclusions: Much of the association among FHxAD, APOE epsilon 4, and cognitive decline may be attributed to undetected incipient (latent) disease. In the absence of latent disease, the 2 factors do not appear individually to be associated with cognitive decline, although they may be additive.
C1 [Hayden, Kathleen M.; Welsh-Bohmer, Kathleen A.] Duke Univ, Med Ctr, Joseph & Kathleen Bryan Alzheimers Dis Res Ctr, Dept Med,Div Neurol, Durham, NC 27705 USA.
[Hayden, Kathleen M.; Welsh-Bohmer, Kathleen A.] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC 27705 USA.
[Zandi, Peter P.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Mental Hlth, Baltimore, MD USA.
[West, Nancy A.] Univ Colorado, Dept Epidemiol, Denver, CO 80202 USA.
[Norton, Maria C.] Utah State Univ, Dept Family Consumer & Human Dev, Logan, UT 84322 USA.
[Tschanz, JoAnn T.; Norton, Maria C.] Utah State Univ, Dept Psychol, Logan, UT 84322 USA.
[Corcoran, Chris] Utah State Univ, Dept Math & Stat, Logan, UT 84322 USA.
[Breitner, John C. S.] Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA USA.
[Breitner, John C. S.] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
RP Hayden, KM (reprint author), Duke Univ, Med Ctr, Joseph & Kathleen Bryan Alzheimers Dis Res Ctr, Dept Med,Div Neurol, 2200 W Main St,Ste A-200, Durham, NC 27705 USA.
EM khayden@duke.edu
RI Corcoran, Chris/F-2155-2010; Tschanz, JoAnn/E-5986-2010; Norton,
Maria/E-6994-2013
FU National Institutes of Health [R01-AG-11380, K01-AG-029336]
FX This work was supported by grants R01-AG-11380 (Dr Welsh-Bohmer) and
K01-AG-029336 (Dr Hayden) from the National Institutes of Health.
NR 49
TC 22
Z9 22
U1 4
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD NOV
PY 2009
VL 66
IS 11
BP 1378
EP 1383
PG 6
WC Clinical Neurology
SC Neurosciences & Neurology
GA 517AF
UT WOS:000271584400011
PM 19901170
ER
PT J
AU Crothers, BA
Tench, WD
Schwartz, MR
Bentz, JS
Moriarty, AT
Clayton, AC
Fatheree, LA
Chmara, BA
Wilbur, DC
AF Crothers, Barbara A.
Tench, William D.
Schwartz, Mary R.
Bentz, Joel S.
Moriarty, Ann T.
Clayton, Amy C.
Fatheree, Lisa A.
Chmara, Beth Anne
Wilbur, David C.
TI Guidelines for the Reporting of Nongynecologic Cytopathology Specimens
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID OF-AMERICAN-PATHOLOGISTS; SURGICAL PATHOLOGY; IMPROVE COMMUNICATION;
PAPANICOLAOU SOCIETY; CANCER; STANDARDIZATION; RECOMMENDATIONS;
CYTOLOGY; BREAST; IMMUNOHISTOCHEMISTRY
AB Context.-Gynecologic cytology terminology and report formatting have been nationally standardized since the implementation of The Bethesda System of 1988, but standard reporting for nongynecologic cytology has never been formally addressed on the same scale.
Objectives.-To promote patient safety through uniform reporting in nongynecologic cytology (including fine-needle aspiration cytology) and to improve communication between laboratories and health care providers.
Data Sources.-Sources include the College of American Pathologists Cytopathology Resource Committee; the College of American Pathologists Council on Scientific Affairs Ad Hoc Committee on Pathology Report Standardization; the College of American Pathologists Laboratory Accreditation Program inspection checklists; the Joint Commission for Accreditation of Healthcare Organizations; and the Clinical Laboratory Improvement Amendments of 1988.
Conclusions.-We describe the major elements of quality nongynecologic cytology reporting and discuss areas of controversy in cytology reporting. Standardized nongynecologic specimen reporting will expand the concept of common report elements already widely implemented in gynecologic cytology reporting. The intent is to improve communication with the health care team while remaining in compliance with federal mandates and accreditation guidelines. (Arch Pathol Lab Med. 2009; 133: 1743-1756)
C1 [Crothers, Barbara A.] Walter Reed Army Med Ctr, Dept Pathol, Washington, DC 20307 USA.
[Crothers, Barbara A.] Walter Reed Army Med Ctr, Area Lab Serv, Washington, DC 20307 USA.
[Tench, William D.] Palomar Med Ctr Lab, Escondido, CA USA.
[Schwartz, Mary R.] Methodist Hosp, Dept Pathol, Houston, TX 77030 USA.
[Bentz, Joel S.] Univ Utah, Dept Pathol, Salt Lake City, UT USA.
[Moriarty, Ann T.] AmeriPath Indiana, Dept Pathol, Indianapolis, IN USA.
[Clayton, Amy C.] Mayo Clin, Dept Anat Pathol, Rochester, MN USA.
[Fatheree, Lisa A.; Chmara, Beth Anne] Coll Amer Pathologists, Dept Cytol Surveys, Northfield, IL USA.
[Wilbur, David C.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Crothers, BA (reprint author), Walter Reed Army Med Ctr, Dept Pathol, MCHL UAP Ward 47,6900 Georgia Ave NW, Washington, DC 20307 USA.
EM barbara.crothers@us.army.mil
NR 43
TC 6
Z9 6
U1 0
U2 0
PU COLLEGE AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD NOV
PY 2009
VL 133
IS 11
BP 1743
EP 1756
PG 14
WC Medical Laboratory Technology; Medicine, Research & Experimental;
Pathology
SC Medical Laboratory Technology; Research & Experimental Medicine;
Pathology
GA 520WP
UT WOS:000271880500002
PM 19886707
ER
PT J
AU Moriarty, AT
Crothers, BA
Bentz, JS
Souers, RJ
Fatheree, LA
Wilbur, DC
AF Moriarty, Ann T.
Crothers, Barbara A.
Bentz, Joel S.
Souers, Rhona J.
Fatheree, Lisa A.
Wilbur, David C.
TI Automatic Failure in Gynecologic Cytology Proficiency Testing Results
From the College of American Pathologists Proficiency Testing Program
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID INTERLABORATORY COMPARISON PROGRAM; SQUAMOUS INTRAEPITHELIAL LESION;
CERVICOVAGINAL CYTOLOGY; VALIDATION CRITERIA; FEATURES; SLIDES; WELL
AB Context.-Automatic failure in gynecologic cytology proficiency testing occurs when a high-grade lesion or carcinoma (HSIL+, Category D) is misinterpreted as negative for intraepithelial lesion or malignancy (Category B).
Objectives.-To document the automatic failure rate in 2006 and 2007 from the College of American Pathologists proficiency testing program (PAP PT) and compare them to projected values from 2004.
Design.-Identify automatic failures from PAP PT in 2006 and 2007 and compare the rates of failure regarding participant and preparation type to validated slides in the College of American Pathologists Interlaboratory Comparison Program in 2004.
Results.-There were 65 264 participant responses for HSIL+ slides included in this analysis from 2006 and 2007. Overall, 1% (666 of 65 264) of the HSIL+ responses were classified as negative, resulting in automatic failure for the participant. There were significantly fewer automatic failures in 2007 as compared with either 2006 or projected from 2004 data (P<.001). Conventional preparations had a lower automatic failure rate than liquid-based preparations but only for 2006. Both pathologists and cytotechnologists interpreting liquid-based preparations faired better than projected from 2004 data.
Conclusions.-The automatic failure rate in PAP PT is lower than expected based on 2004 data from the College of American Pathologists Interlaboratory Comparison Program. Automatic failures are a relatively small component (1% or less) of proficiency testing failures. The rate of automatic failure decreased from 2006 to 2007 and may be due to loss of poor performers in the testing pool, the test-taking environment, or removal of less robust slides from the program. (Arch Pathol Lab Med. 2009; 133: 1757-1760)
C1 [Moriarty, Ann T.] AmeriPath Indiana, Dept Pathol, Indianapolis, IN 46219 USA.
[Crothers, Barbara A.] Walter Reed Army Med Ctr, Dept Pathol, Washington, DC 20307 USA.
[Crothers, Barbara A.] Walter Reed Army Med Ctr, Area Lab Serv, Washington, DC 20307 USA.
[Bentz, Joel S.] Univ Utah, Dept Pathol, Salt Lake City, UT USA.
[Souers, Rhona J.] Coll Amer Pathologists, Dept Stat, Northfield, IL USA.
[Wilbur, David C.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Moriarty, AT (reprint author), AmeriPath Indiana, Dept Pathol, 2560 N Shadeland Ave,Suite A, Indianapolis, IN 46219 USA.
EM amoriarty@ameripath.com
NR 13
TC 3
Z9 3
U1 0
U2 0
PU COLLEGE AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD NOV
PY 2009
VL 133
IS 11
BP 1757
EP 1760
PG 4
WC Medical Laboratory Technology; Medicine, Research & Experimental;
Pathology
SC Medical Laboratory Technology; Research & Experimental Medicine;
Pathology
GA 520WP
UT WOS:000271880500003
PM 19886708
ER
PT J
AU Kesselheim, JC
Lehmann, LE
Styron, NF
Joffe, S
AF Kesselheim, Jennifer C.
Lehmann, Leslie E.
Styron, Nancy Frumer
Joffe, Steven
TI The Ethics of Hematopoietic Stem Cell Donation by Minors Reply
SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE
LA English
DT Editorial Material
C1 [Kesselheim, Jennifer C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Kesselheim, JC (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM jennifer_kesselheim@dfci.harvard.edu
OI Joffe, Steven/0000-0002-0667-7384
NR 1
TC 0
Z9 0
U1 1
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 1072-4710
J9 ARCH PEDIAT ADOL MED
JI Arch. Pediatr. Adolesc. Med.
PD NOV
PY 2009
VL 163
IS 11
BP 1065
EP 1066
PG 2
WC Pediatrics
SC Pediatrics
GA 514WU
UT WOS:000271427700016
ER
PT J
AU De Jesus, M
Parast, L
Shelton, RC
Kokkinogenis, K
Othus, MKD
Li, Y
Allen, JD
AF De Jesus, Maria
Parast, Layla
Shelton, Rachel C.
Kokkinogenis, Kerry
Othus, Megan K. D.
Li, Yi
Allen, Jennifer D.
TI Actual vs Preferred Sources of Human Papillomavirus Information Among
Black, White, and Hispanic Parents
SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE
LA English
DT Editorial Material
C1 [De Jesus, Maria] Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA 02115 USA.
RP De Jesus, M (reprint author), Dana Farber Canc Inst, Ctr Community Based Res, 44 Binney St,LW 703, Boston, MA 02115 USA.
EM maria_dejesus@dfci.harvard.edu
RI Allen, Jennifer/M-2113-2015
FU NCI NIH HHS [P30 CA006516, P30 CA006516-44, T32 CA009337, P30CA006516]
NR 5
TC 2
Z9 2
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 1072-4710
J9 ARCH PEDIAT ADOL MED
JI Arch. Pediatr. Adolesc. Med.
PD NOV
PY 2009
VL 163
IS 11
BP 1066
EP 1067
PG 5
WC Pediatrics
SC Pediatrics
GA 514WU
UT WOS:000271427700017
PM 19884601
ER
PT J
AU Saunders, LL
Selassie, AW
Hill, EG
Horner, MD
Nicholas, JS
Lackland, DT
Corrigan, JD
AF Saunders, Lee L.
Selassie, Anbesaw W.
Hill, Elizabeth G.
Horner, Michael D.
Nicholas, Joyce S.
Lackland, Daniel T.
Corrigan, John D.
TI Pre-existing Health Conditions and Repeat Traumatic Brain Injury
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Brain injuries; Epilepsy; Rehabilitation; Seizures
ID PROFESSIONAL FOOTBALL PLAYERS; RECURRENT CONCUSSION;
SOCIOECONOMIC-STATUS; UNITED-STATES; HEAD-INJURY; ALCOHOL-USE;
POPULATION; EPILEPSY; SEIZURES; PREVALENCE
AB Objective: To assess and compare the effect of Pre-existing epilepsy/seizure disorder and drug/alcohol problem on the hazard of repeat traumatic brain injury (TBI) in persons with TBI who participated in a follow-up study.
Design: Retrospective cohort.
Setting: Acute care hospitals in South Carolina.
Participants: Participants were from the South Carolina Traumatic Brain Injury Follow-up Registry cohort of persons (N=2118) who were discharged from an acute care hospital in South Carolina and who participated in a year-1 follow-up interview.
Interventions: Not applicable.
Main Outcome Measures: Repeat TBI was defined by 2 isolated events of TBI in the same person at least 72 hours apart and recorded in hospital discharge or emergency department records from 1999 through 2005.
Results: A Cox proportional hazards model was used to assess the associations of Pre-existing epilepsy/seizure disorder and drug/alcohol problem with time to repeat TBI, controlling for other confounding factors. There were 2099 persons with information on both Pre-existing conditions. There were 147 (7%) persons who sustained repeat TBI after recruitment to the follow-up study, and 82 (3.9%) had a previous TBI before recruitment for which they were seen in the hospital discharge or emergency department since 1996. The hazard of repeat TBI for persons with Pre-existing epilepsy/seizure disorder was 2.3 times the hazard for those without (hazard ratio, 2.3; 95% confidence interval, 1.2-4.4; P=.011). Pre-existing drug/alcohol problem was not associated with repeat TBI. Other variables significantly associated with repeat TBI were having a prior TBI. being insured under Medicaid, and having no insurance.
Conclusions: Pre-existing epilepsy/seizure disorder predisposes to repeat TBI. Appropriate management of seizure control may be an important strategy to allay the occurrence of repeat TBI.
C1 [Saunders, Lee L.] Med Univ S Carolina, Dept Hlth Sci & Res, Charleston, SC 29425 USA.
[Selassie, Anbesaw W.; Hill, Elizabeth G.; Nicholas, Joyce S.; Lackland, Daniel T.] Med Univ S Carolina, Dept Biostat Bioinformat & Epidemiol, Charleston, SC 29425 USA.
[Horner, Michael D.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA.
[Horner, Michael D.] Ralph H Johnson Dept Vet Affairs, Med Ctr, Mental Hlth Serv, Charleston, SC USA.
[Corrigan, John D.] Ohio State Univ, Dept Phys Med & Rehabil, Columbus, OH 43210 USA.
RP Saunders, LL (reprint author), Med Univ S Carolina, Dept Rehabil Sci, 77 President St,Ste 117,MSC 700, Charleston, SC 29425 USA.
EM saundel@musc.edu
FU Division of Injury Response [U17/CCU421926]; National Center for Injury
Prevention and Control (NCIPC); Centers for Disease Control and
Prevention (CDC); Social Security Administration (SSA); Office of
Disability Income and Support Programs
FX Supported by the Division of Injury Response (grant no. U17/CCU421926),
National Center for Injury Prevention and Control (NCIPC), Centers for
Disease Control and Prevention (CDC). The study was performed pursuant
to a jointly financed cooperative arrangement between the NCIPC, the
National Center for Chronic Discase Prevention and Health Promotion,
CDC, and the Social Security Administration (SSA), Office of Disability
Income and Support Programs.
NR 39
TC 3
Z9 3
U1 4
U2 8
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0003-9993
J9 ARCH PHYS MED REHAB
JI Arch. Phys. Med. Rehabil.
PD NOV
PY 2009
VL 90
IS 11
BP 1853
EP 1859
DI 10.1016/j.apmr.2009.05.020
PG 7
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 520XC
UT WOS:000271881900006
PM 19887208
ER
PT J
AU Koontz, AM
Roche, BM
Collinger, JL
Cooper, RA
Boninger, ML
AF Koontz, Alicia M.
Roche, Bailey M.
Collinger, Jennifer L.
Cooper, Rory A.
Boninger, Michael L.
TI Manual Wheelchair Propulsion Patterns on Natural Surfaces During
Start-Up Propulsion
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Biomechanics; Kinetics; Rehabilitation; Wheelchairs
ID STROKE PATTERN; BIOMECHANICS; EFFICIENCY; SPEEDS
AB Objectives: To classify propulsion patterns over surfaces encountered in the natural environment during start-up and compare selected biomechanical variables between pattern types.
Design: Case series.
Setting: National Veterans Wheelchair Games, Minneapolis, MN, 2005.
Participants: Manual wheelchair users (N=29).
Intervention: Subjects pushed their wheelchairs from a resting position over high-pile carpet, over linoleum, and up a ramp with a 5 degrees incline while propulsion kinematics and kinetics were recorded with a motion capture system and an instrumented wheel.
Main Outcome Measures: Three raters classified the first 3 strokes as 1 of 4 types on each surf-ace: arc, semicircular (SC), single looping over propulsion (SC), and double looping over propulsion (DC). The Fisher exact test was used to assess pattern changes between strokes and surface type. A multiple analysis of variance test was used to compare peak and average resultant force and moment about the hub, average wheel velocity, stroke frequency, contact angle, and distance traveled between stroke patterns.
Results: SL was the most common pattern used during start-up propulsion (44.9%), followed by arc (35.9%), DL (14.1%), and SC (5.1%). Subjects who dropped their hands below the rim during recovery achieved faster velocities and covered greater distances (.016 <= P <=.075) during start-up on linoleum and carpet and applied more force during start-up on the ramp compared with those who used an arc pattern (P=.066).
Conclusions: Classifying propulsion patterns is a difficult task that should use multiple raters. In addition, propulsion patterns change during start-up, with an arc pattern most prevalent initially. The biomechanical findings in this study agree with current clinical guidelines that recommend training users to drop the hand below the pushrim during recovery.
C1 [Koontz, Alicia M.; Roche, Bailey M.; Collinger, Jennifer L.; Cooper, Rory A.; Boninger, Michael L.] Univ Pittsburgh, Dept Bioengn, Pittsburgh, PA USA.
[Collinger, Jennifer L.; Cooper, Rory A.; Boninger, Michael L.] Univ Pittsburgh, Dept Phys Med & Rehabil, Pittsburgh, PA USA.
[Koontz, Alicia M.; Cooper, Rory A.; Boninger, Michael L.] Univ Pittsburgh, Dept Rehabil Sci & Technol, Pittsburgh, PA USA.
[Koontz, Alicia M.; Roche, Bailey M.; Collinger, Jennifer L.; Cooper, Rory A.; Boninger, Michael L.] VA Pittsburgh Healthcare Syst, Human Engn Res Labs, Pittsburgh, PA 15206 USA.
RP Koontz, AM (reprint author), VA Pittsburgh Hlth Care Syst, Human Engn Res Labs 151R1 H, 7180 Highland Dr,151R1-H, Pittsburgh, PA 15206 USA.
EM akoontz@pitt.edu
OI Boninger, Michael/0000-0001-6966-919X
FU Department of Veterans Affairs Rehabilitation Research and Development
Service [B3142C]; National Science Foundation [EEC 0552351]; Paralyzed
veterans of America
FX Supported by the Department of Veterans Affairs Rehabilitation Research
and Development Service (project no. B3142C), the National Science
Foundation (project no. EEC 0552351), and the Paralyzed veterans of
America.
NR 22
TC 14
Z9 14
U1 3
U2 9
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0003-9993
J9 ARCH PHYS MED REHAB
JI Arch. Phys. Med. Rehabil.
PD NOV
PY 2009
VL 90
IS 11
BP 1916
EP 1923
DI 10.1016/j.apmr.2009.05.022
PG 8
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 520XC
UT WOS:000271881900015
PM 19887217
ER
PT J
AU Burnett, J
Dyer, CB
Naik, AA
AF Burnett, Jason
Dyer, Carmel B.
Naik, Aanand A.
TI Convergent Validation of the Kohlman Evaluation of Living Skills as a
Screening Tool of Older Adults' Ability to Live Safely and Independently
in the Community
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Activities of daily living; Comprehensive geriatric assessment; Older
persons or elders; Rehabilitation; Restorative care
ID COGNITIVE IMPAIRMENT; PHYSICAL-PERFORMANCE; SELF-NEGLECT; INSTRUMENTAL
ACTIVITIES; EXECUTIVE DYSFUNCTION; FUNCTIONAL DECLINE; DWELLING ELDERS;
FREEDOM HOUSE; FOLLOW-UP; DISABILITY
AB Objective: To evaluate the convergent validity of the Kohlman Evaluation of Living Skills (KELS) to screen older adults' ability to live safely and independently.
Design: Cross-sectional study correlating KELS with components of a Comprehensive Geriatric Assessment. Setting: Participants' homes.
Participants: Community-dwelling older adults (N=200) 65 years and older including 100 persons referred by Adult Protective Services (APS) and 100 ambulatory patients matched on age, race, sex, and socioeconomic status.
Interventions: In-home comprehensive assessment.
Main Outcome Measures: KELS, Geriatric Depression Scale (GDS), modified Physical Performance Test (mPPT), Mini-Mental State Examination (MMSE), Knee Extensor Break Test, Executive Cognitive Test (EXIT25). executive clock-drawing test (CLOX) 1 and 2, and an 8-foot walk test.
Results: Older adults with abnormal KELS scores performed significantly worse on all tests except for the Knee Extensor Break Test. Accordingly, among the entire group, the KELS correlated with measures of executive function (EXIT25, r=.705, P<.001; CLOX 1, r=-.629, P<.001), cognitive function (MMSE, r=-.508, P<.001), affect (GDS, r=.318, P<.001), and physical function (mPPT, r=-.472, P<.001) but did not correlate with the Knee Extensor Break Test (r=-.068, P=.456). Among those referred by APS, the KELS failed to correlate with only the 8-foot walk test (r=.175, P=.153) and GDS (r=.080, P=.450).
Conclusions: This study demonstrated the convergent validity of KELS with a battery of cognitive, affective, executive, and functional measures often used to determine older adults' ability to live safely and independently in the community. KELS may be a valid and pragmatic alternative to screen for the capacity to live safely and independently among older adults.
C1 [Naik, Aanand A.] Baylor Coll Med, Alkek Dept Med, Michael E DeBakey Vet Affairs Med Ctr, Houston Ctr Qual Care & Utilizat Studies, Houston, TX 77030 USA.
[Burnett, Jason; Dyer, Carmel B.] Univ Texas Hlth Sci Ctr Houston, Div Geriatr & Palliat Med, Dept Internal Med, Houston, TX USA.
[Burnett, Jason; Dyer, Carmel B.; Naik, Aanand A.] Consortium Res Elder Self Neglect Texas, Houston, TX USA.
[Burnett, Jason; Dyer, Carmel B.; Naik, Aanand A.] Harris Cty Hosp Dist, Houston, TX USA.
RP Naik, AA (reprint author), Michael E DeBakey VAMC 152, Houston Ctr Qual Care & Utilizat Studies, 2002 Holcombe, Houston, TX 77030 USA.
EM anaik@bcm.tmc.edu
FU Houston Center for Quality of Care & Utilization Studies [HFP90-020];
Michael E. DeBakey Veterans Affairs Medical Center; Consortium for
Research in Elder Self-Neglect of Texas [NIH P20-RR020626]; Greenwall
Foundation; National Institute of Aging [K23AG027144]; Doris Duke
Charitable Foundation
FX Supported by the Houston Center for Quality of Care & Utilization
Studies (grant no. HFP90-020) with resources and the use of facilities;
Michael E. DeBakey Veterans Affairs Medical Center, the Consortium for
Research in Elder Self-Neglect of Texas (grant no. NIH P20-RR020626): a
bioethics grant from the Greenwall Foundation: and the National
Institute of Aging (grant no. K23AG027144) and a Doris Duke Charitable
Foundation Clinical Scientist Development Award.
NR 30
TC 10
Z9 10
U1 4
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 NOV
PY 2009
VL 90
IS 11
BP 1948
EP 1952
DI 10.1016/j.apmr.2009.05.021
PG 5
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 520XC
UT WOS:000271881900020
PM 19887222
ER
PT J
AU Bentrem, DJ
Cohen, ME
Hynes, DM
Ko, CY
Bilimoria, KY
AF Bentrem, David J.
Cohen, Mark E.
Hynes, Denise M.
Ko, Clifford Y.
Bilimoria, Karl Y.
TI Identification of Specific Quality Improvement Opportunities for the
Elderly Undergoing Gastrointestinal Surgery
SO ARCHIVES OF SURGERY
LA English
DT Article
ID SURGICAL OUTCOMES; UNITED-STATES; COLORECTAL-CANCER; GASTRIC-CANCER;
POPULATION; RISK; CARE; RESECTION; OCTOGENARIANS; ESOPHAGUS
AB Hypothesis: Specific complications occur more frequently in elderly patients undergoing major gastrointestinal (GI) tract operations that may represent opportunities for quality improvement.
Design: Retrospective cohort study.
Setting: One hundred twenty-one hospitals participating in American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP).
Patients: Using the ACS-NSQIP participant use file (2005-2006), patients undergoing upper gastrointestinal tract (n=4115), hepatobiliary or pancreatic (n=3364), and colorectal (n=17 268) operations at 121 hospitals were examined.
Main Outcome Measures: Risk-adjusted 30-day outcomes were assessed using regression modeling adjusting for patient characteristics, comorbidities, and surgical procedures. The elderly were defined as those older than 75 years.
Results: Between January 1, 2005, and December 31, 2006, a total of 54 747 patients who underwent major GI tract operations were identified from the ACS-NSQIP data file. In the elderly, overall perioperative morbidity was 1.2 to 2 times higher and mortality was 2.9 to 6.7 times higher than in younger patients after adjusting for differences in preoperative comorbidities. Irrespective of procedure type, the elderly were significantly more likely to experience cardiac ( acute myocardial infarction and cardiac arrest), pulmonary ( pneumonia, pulmonary embolism, and respiratory failure), and urologic ( urinary tract infection and renal failure) complications. However, surgical site infections, postoperative bleeding events, deep venous thromboses, and rates of return to the operating room did not differ significantly by age.
Conclusions: Morbidity and mortality are markedly higher in older patients. Quality measures for the elderly currently address only myocardial infarction, surgical site infection, and deep venous thrombosis. If care for the elderly is to be improved, quality improvement initiatives need to be expanded to include postoperative pulmonary and renal complications.
C1 [Cohen, Mark E.; Ko, Clifford Y.; Bilimoria, Karl Y.] Amer Coll Surg, Div Res & Optimal Patient Care, Chicago, IL 60611 USA.
[Hynes, Denise M.] Univ Illinois, Coll Med, Dept Med, Sch Publ Hlth, Chicago, IL USA.
[Hynes, Denise M.] Univ Illinois, Sch Publ Hlth, Dept Hlth Policy Adm, Chicago, IL USA.
[Hynes, Denise M.] US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Ctr Management Complex Chron Care, Hines, IL 60141 USA.
[Ko, Clifford Y.] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA.
[Ko, Clifford Y.] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Bentrem, David J.; Bilimoria, Karl Y.] Northwestern Univ, Dept Surg, Sch Med, Chicago, IL 60611 USA.
RP Bilimoria, KY (reprint author), Amer Coll Surg, Div Res & Optimal Patient Care, 633 N St Clair St,22nd Floor, Chicago, IL 60611 USA.
EM k-bilimoria@northwestern.edu
FU American Cancer Society Illinois Division and by the Barnum Foundation
[ACSIRG 93-037-12]; Department of Veterans Affairs Health Services
Research and Development Service Research Career Scientist Award;
American College of Surgeons Clinical Scholars
FX This study was funded in part by grant ACSIRG 93-037-12 from the
American Cancer Society Illinois Division and by the Barnum Foundation (
Dr Bentrem). Dr Hynes is supported by the Department of Veterans Affairs
Health Services Research and Development Service Research Career
Scientist Award. Dr Bilimoria is supported by the American College of
Surgeons Clinical Scholars in Residence program.
NR 41
TC 48
Z9 52
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0004-0010
J9 ARCH SURG-CHICAGO
JI Arch. Surg.
PD NOV
PY 2009
VL 144
IS 11
BP 1013
EP 1020
PG 8
WC Surgery
SC Surgery
GA 521AG
UT WOS:000271890500007
PM 19917937
ER
PT J
AU Velmahos, GC
AF Velmahos, George C.
TI Patient Safety Systems: A Long Way to Go INVITED CRITIQUE
SO ARCHIVES OF SURGERY
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
RP Velmahos, GC (reprint author), Massachusetts Gen Hosp, Dept Surg, 165 Cambridge St,Ste 810, Boston, MA 02114 USA.
EM gvelmahos@partners.org
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0004-0010
J9 ARCH SURG-CHICAGO
JI Arch. Surg.
PD NOV
PY 2009
VL 144
IS 11
BP 1034
EP 1034
PG 1
WC Surgery
SC Surgery
GA 521AG
UT WOS:000271890500011
PM 19928295
ER
PT J
AU Paterson, AD
Lopes-Virella, MF
Waggott, D
Boright, AP
Hosseini, SM
Carter, RE
Shen, EQ
Mirea, L
Bharaj, B
Sun, L
Bull, SB
AF Paterson, Andrew D.
Lopes-Virella, Maria F.
Waggott, Daryl
Boright, Andrew P.
Hosseini, S. Mohsen
Carter, Rickey E.
Shen, Enqing
Mirea, Lucia
Bharaj, Bhupinder
Sun, Lei
Bull, Shelley B.
CA Diabet Control Complications Trial
TI Genome-Wide Association Identifies the ABO Blood Group as a Major Locus
Associated With Serum Levels of Soluble E-Selectin
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE E-selectin; ABO blood group; genome-wide association; SNP
ID PLASMODIUM-FALCIPARUM MALARIA; CELLULAR ADHESION MOLECULES;
LEUKOCYTE-ENDOTHELIAL ADHESION; VON-WILLEBRAND-FACTOR; RISK-FACTORS;
CARDIOVASCULAR-DISEASE; MACROVASCULAR COMPLICATIONS; DIABETES-MELLITUS;
VASCULAR-DISEASE; MARKERS
AB Background-Elevated serum soluble E-selectin levels have been associated with a number of diseases. Although E-selectin levels are heritable, little is known about the specific genetic factors involved. E-selectin levels have been associated with the ABO blood group phenotype.
Methods and Results-We performed a high-resolution genome-wide association study of serum soluble E-selectin levels in 685 white individuals with type 1 diabetes from the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Intervention and Complications (EDIC) study to identify major loci influencing levels. Highly significant evidence for association (P = 10(-29)) was observed for rs579459 near the ABO blood group gene, accounting for 19% of the variance in E-selectin levels. Levels of E-selectin were higher in O/O than O/A heterozygotes, which were likewise higher than A/A genotypes. Analysis of subgroups of A alleles reveals heterogeneity in the association, and even after this was accounted for, an intron 1 SNP remained significantly associated. We replicate the ABO association in nondiabetic individuals.
Conclusion-ABO is a major locus for serum soluble E-selectin levels. We excluded population stratification, fine-mapped the association to sub-A alleles, and also document association with additional variation in the ABO region. (Arterioscler Thromb Vasc Biol. 2009; 29: 1958-1967.)
C1 [Paterson, Andrew D.; Hosseini, S. Mohsen; Bharaj, Bhupinder] Hosp Sick Children, Program Genet & Genome Biol, Toronto, ON M5G 1L7, Canada.
[Waggott, Daryl; Shen, Enqing; Mirea, Lucia; Bull, Shelley B.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Prosserman Ctr Hlth Res, Toronto, ON M5G 1X5, Canada.
[Boright, Andrew P.] Univ Toronto, Dept Med, Univ Hlth Network, Toronto, ON M5S 1A1, Canada.
[Paterson, Andrew D.; Mirea, Lucia; Sun, Lei; Bull, Shelley B.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON M5S 1A1, Canada.
[Lopes-Virella, Maria F.] Med Univ S Carolina, Dept Med & Lab Serv, Charleston, SC USA.
Ralph H Johnson VA Med Ctr, Charleston, SC USA.
[Carter, Rickey E.] Med Univ S Carolina, Dept Biostat Bioinformat & Epidemiol, Charleston, SC USA.
RP Paterson, AD (reprint author), Hosp Sick Children, Program Genet & Genome Biol, TMDT Bldg E Tower,Rm 15-707,101 Coll St, Toronto, ON M5G 1L7, Canada.
EM andrew.paterson@utoronto.ca
RI Bull, Shelley/A-1920-2013; Hosseini, Mohsen/K-7133-2013; Paterson,
Andrew/A-4088-2011
OI Hosseini, Mohsen/0000-0003-3626-9928; Paterson,
Andrew/0000-0002-9169-118X
FU Department of Veterans Affairs; National Institutes of Health; Juvenile
Diabetes Research Foundation [PO1 HL55782]; National Institute of
Diabetes and Digestive and Kidney Diseases [N01-DK-6-2204,
R01-DK-077510]; Canadian Network of Centers of Excellence in
Mathematics; Canadian Institutes of Health Research (CIHR)
FX This research was supported by funding of the Merit Review Program of
the Department of Veterans Affairs, by joint funding of the National
Institutes of Health and Juvenile Diabetes Research Foundation (PO1
HL55782), National Institute of Diabetes and Digestive and Kidney
Diseases Contract N01-DK-6-2204, National Institute of Diabetes and
Digestive and Kidney Diseases Grant R01-DK-077510, and support from the
Canadian Network of Centers of Excellence in Mathematics. The DCCT/EDIC
Research Group is sponsored through research contracts from the National
Institute of Diabetes, Endocrinology, and Metabolic Diseases of the
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
and the National Institutes of Health. A. D. P. holds a Canada Research
Chair in the Genetics of Complex Diseases. S. B. B. was a recipient of a
Canadian Institutes of Health Research (CIHR) Senior Investigator award
(2002-7). L. M. is a recipient of a CIHR Research Scholarship.
NR 53
TC 77
Z9 78
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1079-5642
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD NOV
PY 2009
VL 29
IS 11
BP 1958
EP U609
DI 10.1161/ATVBAHA.109.192971
PG 26
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 509EE
UT WOS:000270996300039
PM 19729612
ER
PT J
AU Musunuru, K
Orho-Melander, M
Caulfield, MP
Li, SG
Salameh, WA
Reitz, RE
Berglund, G
Hedblad, B
Engstrom, G
Williams, PT
Kathiresan, S
Melander, O
Krauss, RM
AF Musunuru, Kiran
Orho-Melander, Marju
Caulfield, Michael P.
Li, Shuguang
Salameh, Wael A.
Reitz, Richard E.
Berglund, Goran
Hedblad, Bo
Engstrom, Gunnar
Williams, Paul T.
Kathiresan, Sekar
Melander, Olle
Krauss, Ronald M.
TI Ion Mobility Analysis of Lipoprotein Subfractions Identifies Three
Independent Axes of Cardiovascular Risk
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE lipids; lipoproteins; cardiovascular diseases; genetics
ID LOW-DENSITY-LIPOPROTEIN; CORONARY-HEART-DISEASE; LDL PARTICLE-SIZE;
MAGNETIC-RESONANCE-SPECTROSCOPY; FAMILIAL COMBINED HYPERLIPIDEMIA;
ARTERY-DISEASE; MYOCARDIAL-INFARCTION; GENETIC-DETERMINANTS;
INTERVENTION TRIAL; METABOLIC SYNDROME
AB Objective-Whereas epidemiological studies show that levels of low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) predict incident cardiovascular disease (CVD), there is limited evidence relating lipoprotein subfractions and composite measures of subfractions to risk for CVD in prospective cohort studies.
Methods and Results-We tested whether combinations of lipoprotein subfractions independently predict CVD in a prospective cohort of 4594 initially healthy men and women (the Malmo Diet and Cancer Study, mean follow-up 12.2 years, 377 incident cardiovascular events). Plasma lipoproteins and lipoprotein subfractions were measured at baseline with a novel high-resolution ion mobility technique. Principal component analysis (PCA) of subfraction concentrations identified 3 major independent (ie, zero correlation) components of CVD risk, one representing LDL-associated risk, a second representing HDL-associated protection, and the third representing a pattern of decreased large HDL, increased small/medium LDL, and increased triglycerides. The last corresponds to the previously described "atherogenic lipoprotein phenotype." Several genes that may underlie this phenotype-CETP, LIPC, GALNT2, MLXIPL, APOA1/A5, LPL-are suggested by SNPs associated with the combination of small/medium LDL and large HDL.
Conclusion-PCA on lipoprotein subfractions yielded three independent components of CVD risk. Genetic analyses suggest these components represent independent mechanistic pathways for development of CVD. (Arterioscler Thromb Vasc Biol. 2009; 29:1975-1980.)
C1 [Krauss, Ronald M.] Childrens Hosp Oakland, Res Inst, Oakland, CA 94609 USA.
[Musunuru, Kiran; Kathiresan, Sekar] Massachusetts Gen Hosp, Div Cardiol, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Musunuru, Kiran; Kathiresan, Sekar] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Musunuru, Kiran; Kathiresan, Sekar] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Orho-Melander, Marju; Berglund, Goran; Hedblad, Bo; Engstrom, Gunnar; Melander, Olle] Lund Univ, Malmo Univ Hosp, Malmo, Sweden.
[Caulfield, Michael P.; Li, Shuguang; Salameh, Wael A.; Reitz, Richard E.] Quest Diagnost Nichols Inst, San Juan Capistrano, CA USA.
[Williams, Paul T.] Ernest Orlando Lawrence Berkeley Natl Lab, Div Life Sci, Berkeley, CA USA.
RP Krauss, RM (reprint author), Childrens Hosp Oakland, Res Inst, 5700 Martin Luther King Jr Way, Oakland, CA 94609 USA.
EM rkrauss@chori.org
OI Engstrom, Gunnar/0000-0002-8618-9152
FU United States National Institutes of Health (NIH) [U01HL069757]; Swedish
Medical Research Council; Swedish Heart and Lung Foundation; Medical
Faculty of Lund University; Malmo University Hospital; Albert Pahlsson
Research Foundation; Crafoord foundation; Ernhold Lundstroms Research
Foundation; Region Skane; Hulda and Conrad Mossfelt Foundation; King
Gustaf V and Queen Victoria Foundation; Lennart Hanssons Memorial Fund;
Doris Duke Charitable Foundation; Fannie E. Rippel Foundation; Donovan
Family Foundation; Quest Diagnostics Inc
FX K. M. is supported by a T32 grant in Cell and Molecular Training for
Cardiovascular Biology from the United States National Institutes of
Health (NIH). M.O.-M. and O.M. are supported by the Swedish Medical
Research Council, the Swedish Heart and Lung Foundation, the Medical
Faculty of Lund University, Malmo University Hospital, the Albert
Pahlsson Research Foundation, the Crafoord foundation, the Ernhold
Lundstroms Research Foundation, the Region Skane, the Hulda and Conrad
Mossfelt Foundation, the King Gustaf V and Queen Victoria Foundation and
the Lennart Hanssons Memorial Fund. S. K. is supported by a Doris Duke
Charitable Foundation Clinical Scientist Development Award, a charitable
gift from the Fannie E. Rippel Foundation, the Donovan Family
Foundation, and a K23 career development award from the NIH. R. M. K. is
supported by U01HL069757 from the NIH and has received research support
from Quest Diagnostics Inc. For this study, ion mobility measurements of
study participants were provided free of charge by Quest Diagnostics,
which had no role in the analysis and interpretation of the data or in
the preparation, review, or approval of the manuscript.
NR 38
TC 76
Z9 78
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1079-5642
EI 1524-4636
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD NOV
PY 2009
VL 29
IS 11
BP 1975
EP U628
DI 10.1161/ATVBAHA.109.190405
PG 10
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 509EE
UT WOS:000270996300041
PM 19729614
ER
PT J
AU Elhassan, B
Ozbaydar, M
Diller, D
Massimini, D
Higgins, LD
Warner, JJP
AF Elhassan, Bassem
Ozbaydar, Mehmet
Diller, David
Massimini, Daniel
Higgins, Laurence D.
Warner, Jon J. P.
TI Open Versus Arthroscopic Acromioclavicular Joint Resection: A
Retrospective Comparison Study
SO ARTHROSCOPY-THE JOURNAL OF ARTHROSCOPIC AND RELATED SURGERY
LA English
DT Article
DE Acromioclavicular joint; Arthroscopic; Resection; Open; Comparison
ID DISTAL CLAVICLE RESECTION; CONCOMITANT SUBACROMIAL DECOMPRESSION;
CONSTANT SCORE; OSTEOLYSIS; SHOULDER; BURSAL
AB Purpose: The purpose was to compare open and arthroscopic acrormoclavicular joint (ACJ) resection. Methods: We retrospectively reviewed 103 patients (105 shoulders) who underwent ACJ resection between 2000 and 2005. There were 56 women and 47 men with a mean age of 48 years. The mean duration of follow-up was 51 months (range, 15 to 91 months). Arthroscopic ACJ resection by use of a direct approach was performed in 81 shoulders (group A), and open ACJ resection was performed in 24 shoulders (group 13). Results were graded according to pain relief both subjectively and objectively with cross-body adduction testing and direct palpation of the ACJ, subjective shoulder value, Constant score, and improved function. Results: The Constant scores increased from 50 (range, 34 to 65) to 89 (range, 39 to 100) in group A (P < .0001) and from 46 (range, 22 to 63) to 87 (range, 43 to 100) in group B (P < .0001). There was no statistical difference in the postoperative normalized Constant score between group A and group B (P = .47), Pain with cross-body adduction testing and palpation of the ACJ improved in 76 shoulders (94%) in group A and 22 shoulders (92%) in group B. No patients had signs or symptoms of ACJ anteroposterior instability. Revision ACJ resection was performed in 5 patients (5 shoulders [6.2%]) in group A and I shoulder (4.2%) in group B (P = .37). The radiographs of the patients who underwent revision showed that 3 patients (3.7%) from group A had regrowth of the distal clavicle; in addition, 2 patients (2.5%) from group A and 1 patient (4.3%) from group B had incomplete distal clavicle excision. Conclusions: This study did not show a significant difference in the outcome between arthroscopic and open ACJ resection. Incomplete excision and regrowth of the distal clavicle are the most common causes of revision. Although only the arthroscopic group showed a small percentage of patients (3.7%) with regrowth of the distal clavicle, the number is too small to assume that this complication is the result of the arthroscopic technique only. Level of Evidence: Level IV, therapeutic case series.
C1 [Elhassan, Bassem] Mayo Clin, Dept Orthoped, Rochester, MN USA.
[Higgins, Laurence D.] Harvard Univ, Sports Med & Shoulder Serv, Sch Med, Boston, MA 02493 USA.
[Warner, Jon J. P.] Harvard Univ, Dept Orthopaed Surg, Sch Med, Boston, MA 02493 USA.
[Higgins, Laurence D.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Ozbaydar, Mehmet; Diller, David; Massimini, Daniel; Higgins, Laurence D.; Warner, Jon J. P.] Harvard Univ, Harvard Shoulder Serv, Boston, MA 02493 USA.
RP Warner, JJP (reprint author), Harvard Univ, Harvard Shoulder Serv, Massachusetts Gen Hosp, Sch Med,Yawkey Ctr Outpatient Care, Suite 3G,55Fruit St, Boston, MA 02493 USA.
EM jwarner@partners.org
RI Ozbaydar, Mehmet/D-7391-2016
NR 28
TC 17
Z9 18
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 0749-8063
J9 ARTHROSCOPY
JI Arthroscopy
PD NOV
PY 2009
VL 25
IS 11
BP 1224
EP 1232
DI 10.1016/j.arthro.2009.06.010
PG 9
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 517NM
UT WOS:000271621700010
PM 19896043
ER
PT J
AU Seo, JH
Li, G
Shetty, GM
Kim, JH
Bae, JH
Jo, ML
Kim, JS
Lee, SJ
Nha, KW
AF Seo, Jeong-Hee
Li, Guoan
Shetty, Gautam M.
Kim, Ji-Hoon
Bae, Ji-Hoon
Jo, Myoung-Lae
Kim, Jung-Sung
Lee, Sung-Jae
Nha, Kyung-Wook
TI Effect of Repair of Radial Tears at the Root of the Posterior Horn of
the Medial Meniscus With the Pullout Suture Technique: A Biomechanical
Study Using Porcine Knees
SO ARTHROSCOPY-THE JOURNAL OF ARTHROSCOPIC AND RELATED SURGERY
LA English
DT Article
DE Medial meniscus; Posterior horn; Radial tear; Root tear; Contact area;
Contact pressure; Pullout suture
ID PRESSURE DISTRIBUTION; CONTACT AREA; MENISCECTOMY; CONSEQUENCES; JOINTS
AB Purpose: Our purpose was to evaluate the result of radial tears at the root of the posterior horn of the medial meniscus (PHMM) in terms of tibiofemoral contact mechanics and the effectiveness of pullout sutures for such tears. Methods: Eleven mature pig knees each underwent 15 different testing conditions with an intact, simulated (incised) radial tear at the root of the PHMM and placement of pullout sutures in the radial tears of the medial meniscus at 5 different angles of flexion (0 degrees, 15 degrees, 30 degrees, 60 degrees, and 90 degrees) under a 1,500-N axial load. A K-Scan pressure sensor (Tekscan, Boston, MA) was used to measure medial tibiofemoral contact area and peak tibiofemoral contact pressure. Data were analyzed to assess the difference in medial contact area and tibiofemoral peak contact pressure among the 3 meniscal conditions at various degrees of knee flexion. Results: The mean contact area was significantly lower, and the peak tibiofemoral contact pressure was significantly high in knees with simulated radial tears at all angles of knee flexion compared with knees with intact menisci (P < .0001). The peak tibiofemoral contact pressure after the pullout suture technique was significantly high at 0 degrees and 15 degrees of flexion (P < .0001) compared with intact knee specimens. Failure of sutures occurred in 45% of the specimens at 0 degrees of flexion. Conclusions: Radial tears at the root of the PHMM in a porcine model significantly increased medial tibiofemoral contact pressure and decreased contact area. Although repair of tears of the PHMM with the pullout suture technique aids in significantly reducing tibiofemoral peak contact pressure between 30 degrees and 90 degrees, it remains significantly high at 0 degrees and 15 degrees of flexion. Clinical Relevance: Pullout sutures for radial tears at the root of the PHMM may lead to an increase in peak medial tibiofemoral contact pressure and may be prone to mechanical failure, especially during the stance (loading) phase of gait (mean, 15 degrees of flexion).
C1 [Seo, Jeong-Hee; Shetty, Gautam M.; Kim, Ji-Hoon; Nha, Kyung-Wook] Inje Univ, Dept Orthopaed Surg, Ilsanpaik Hosp, Ilsan, South Korea.
[Li, Guoan] Massachusetts Gen Hosp, Dept Orthopaed Surg, Bioengn Lab, Boston, MA 02114 USA.
[Li, Guoan] Harvard Univ, Sch Med, Boston, MA USA.
[Bae, Ji-Hoon] Korea Univ, Dept Orthopaed Surg, Guro Hosp, Seoul, South Korea.
[Seo, Jeong-Hee; Jo, Myoung-Lae; Lee, Sung-Jae] Inje Univ, Dept Biomed Engn, Gimhae, South Korea.
[Kim, Jung-Sung] Corentec Co Ltd, Ctr Res & Dev, Cheonan, South Korea.
[Kim, Jung-Sung] Yonsei Univ, Coll Med, Dept Med Engn, Seoul, South Korea.
RP Nha, KW (reprint author), 2240 Daehwadong, Goyangsi 411706, Gyeonggido, South Korea.
EM Kwnhamj@hotmail.com
FU Ministry of Commerce, Industry and Energy South Korea [10025570]
FX Supported by a grant from the Materials & Components Technology R&D
Program funded by the Ministry of Commerce, Industry and Energy
(10025570), South Korea, and by a 2007 Inje University research grant.
NR 19
TC 25
Z9 26
U1 0
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 0749-8063
J9 ARTHROSCOPY
JI Arthroscopy
PD NOV
PY 2009
VL 25
IS 11
BP 1281
EP 1287
DI 10.1016/j.arthro.2009.05.014
PG 7
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 517NM
UT WOS:000271621700018
PM 19896051
ER
PT J
AU De Luca, G
Gibson, CM
Bellandi, F
Noc, M
Dudek, D
Zeymer, U
Arntz, HR
Cutlip, D
Maioli, M
Zorman, S
Gabriel, HM
Emre, A
Rakowski, T
Gyongyosi, M
Huber, K
van't Hof, AWJ
AF De Luca, Giuseppe
Gibson, C. Michael
Bellandi, Francesco
Noc, Marko
Dudek, Dariusz
Zeymer, Uwe
Arntz, Hans-Richard
Cutlip, Donald
Maioli, Mauro
Zorman, Simona
Gabriel, H. Mesquita
Emre, Ayse
Rakowski, Tomasz
Gyongyosi, Mariann
Huber, Kurt
van't Hof, Arnoud W. J.
TI Diabetes mellitus is associated with distal embolization, impaired
myocardial perfusion, and higher mortality in patients with ST-segment
elevation myocardial infarction treated with primary angioplasty and
glycoprotein IIb-IIIa inhibitors
SO ATHEROSCLEROSIS
LA English
DT Article
DE Primary angioplasty; Distal embolization; Diabetes; Myocardial perfusion
ID PERCUTANEOUS CORONARY INTERVENTION; NO-REFLOW PHENOMENON; THROMBOLYTIC
THERAPY; RANDOMIZED-TRIALS; REPERFUSION; HYPERGLYCEMIA; GLUCOSE;
ABCIXIMAB; VASODILATION; METAANALYSIS
AB Background: It has been shown that, among patients with ST-segment elevation myocardial infarction (STEMI), diabetes is associated with a significantly higher mortality. The aim of the current study was to investigate the impact of diabetes on myocardial perfusion and mortality among STEMI patients treated with primary angioplasty and glycoprotein IIb-IIIa inhibitors.
Methods: Our population is represented by a total of 1662 patients undergoing primary angioplasty for STEMI included in 11 randomized trials. Myocardial perfusion was evaluated by angiography (n = 1324) or postprocedural ECG ( n = 1371). Distal embolization was defined as an abrupt "cutoff" in the main vessel or one of the coronary branches of the infarct-related artery, distal to the angioplasty site ( data available in 1181 patients).
Results: Diabetes was observed in a total of 281 patients (16.9%). Diabetic patients were older, with a larger prevalence of female gender, hypertension, hypercholesterolemia, advanced killip class at presentation and multivessel disease. Diabetes was associated with impaired postprocedural TIMI 3 flow (82% vs 90%, p < 0.001), MBG 2-3 (60.1% vs 74.2%, p < 0.001), complete ST-segment resolution (43.2% vs 60%, p < 0.001) and more distal embolization (16.4% vs 10.1%, p < 0.0001). The association with impaired MBG and distal embolization was confirmed after correction for baseline confounding factors. Diabetes was associated with significantly impaired mortality (12.6% vs 3.9%, HR= 3.0 [1.84-4.89], p < 0.001), that persisted even after correction for baseline confounding factors (HR = 2.6 [1.52-4.45], p = 0.001).
Conclusion: This study showed that, among patients with STEMI undergoing primary angioplasty on the top of glycoprotein IIb-IIIa inhibitors, diabetes mellitus is independently associated with impaired perfusion and distal embolization, that contribute to explain the higher mortality observed in these patients. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
C1 [De Luca, Giuseppe] Eastern Piedmont Univ, Maggiore Carita Hosp, Div Cardiol, Novara, Italy.
[Gibson, C. Michael] Brigham & Womens Hosp, Div Cardiovasc, TIMI Study Grp, Boston, MA 02115 USA.
[Bellandi, Francesco; Maioli, Mauro] Prato Hosp, Div Cardiol, Prato, Italy.
[Noc, Marko; Zorman, Simona] Univ Med Ctr, Ctr Intens Internal Med, Ljubljana, Slovenia.
[Dudek, Dariusz; Rakowski, Tomasz] Jagiellonian Univ, Inst Cardiol, Dept Cardiol 2, Krakow, Poland.
[Zeymer, Uwe] Herzzentrum Ludwigshafen, Div Cardiol, Ludwigshafen, Germany.
[Arntz, Hans-Richard] Charite, Med Klin 2, Berlin, Germany.
[Cutlip, Donald] Beth Israel Deaconess Med Ctr, Intervent Cardiol Sect, Boston, MA 02215 USA.
[Gabriel, H. Mesquita] Hosp Santa Maria, Div Cardiol, Lisbon, Portugal.
[Emre, Ayse] Siyami Ersek Thorac & Cardiovasc Surg Ctr, Instabul, Turkey.
[Gyongyosi, Mariann] Med Univ Vienna, Dept Cardiol, Vienna, Austria.
[Huber, Kurt] Wilhelminen Hosp, Dept Med Cardiol & Emergency Med 3, Vienna, Austria.
[van't Hof, Arnoud W. J.] Hosp Weezenlanden, Div Cardiol, Zwolle, Netherlands.
RP De Luca, G (reprint author), Eastern Piedmont Univ, Maggiore Carita Hosp, Div Cardiol, Novara, Italy.
EM giuseppe.deluca@maggioreosp.novara.it
NR 38
TC 59
Z9 61
U1 1
U2 3
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 NOV
PY 2009
VL 207
IS 1
BP 181
EP 185
DI 10.1016/j.atherosclerosis.2009.03.042
PG 5
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 528QE
UT WOS:000272460700028
PM 19426981
ER
PT J
AU Cavusoglu, E
Marmur, JD
Chhabra, S
Chopra, V
Eng, C
Jiang, XC
AF Cavusoglu, Erdal
Marmur, Jonathan D.
Chhabra, Sandeep
Chopra, Vineet
Eng, Calvin
Jiang, Xian-Cheng
TI Relation of baseline plasma phospholipid transfer protein (PLTP)
activity to left ventricular systolic dysfunction in patients referred
for coronary angiography
SO ATHEROSCLEROSIS
LA English
DT Article
DE Phospholipid transfer protein; Inflammation; Left ventricular systolic
dysfunction; Atherosclerosis
ID CONGESTIVE-HEART-FAILURE; TYPE-2 DIABETES-MELLITUS; DENSITY-LIPOPROTEIN;
PROGNOSTIC PREDICTOR; INSULIN-RESISTANCE; RISK-FACTOR; VITAMIN-E;
DEFICIENCY; MICE; ATHEROSCLEROSIS
AB Phospholipid transfer protein (PLTP) is an important modulator of phospholipid transfer and exchange among proteins. It also plays a role in inflammation and oxidative stress. Accordingly, PLTP has been implicated in the development of atherosclerosis. Left ventricular (LV) systolic dysfunction is common in patients with atherosclerosis, and both inflammation and oxidative stress have also been implicated in its development and progression. The goal of the present study was to examine the relation between plasma PLTP activity and LV systolic function. Baseline plasma PLTP activity was measured in 389 male patients referred for coronary angiography for a variety of indications. Detailed clinical, angiographic and laboratory characteristics were available for the patients. Compared to those patients with normal LV function ( defined as an ejection fraction of >= 55% on ventriculography), patients with any degree of LV dysfunction had elevated PLTP activity ( median PLTP 17.8 pmol/mu l/h versus 15.9 pmol/mu l/h, p = 0.0038). Using multivariate analysis, and adjusting for a variety of confounding variables known to affect both LV function and PLTP activity, PLTP activity was an independent predictor of the presence of any left ventricular systolic dysfunction in the entire population (OR 1.47, 95% CI 1.12-1.93, p = 0.0052). Furthermore, PLTP activity was an independent predictor of the presence of LV dysfunction in both patients with and without myocardial infarction on presentation ( OR 2.39, 95% CI 1.18-4.86, p = 0.0161 and OR 1.41, 95% CI 1.05-1.89, p = 0.0206, respectively). In conclusion, PLTP activity may represent a novel marker of LV systolic dysfunction in patients with known or suspected coronary artery disease. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
C1 [Cavusoglu, Erdal; Marmur, Jonathan D.; Chhabra, Sandeep] Suny Downstate Med Ctr, Div Cardiol, Dept Med, Brooklyn, NY 11203 USA.
[Cavusoglu, Erdal; Chopra, Vineet; Eng, Calvin] Bronx Vet Affairs Med Ctr, Div Cardiol, Dept Med, Bronx, NY USA.
[Jiang, Xian-Cheng] Suny Downstate Med Ctr, Dept Anat & Cell Biol, Brooklyn, NY 11203 USA.
RP Cavusoglu, E (reprint author), SUNY Hlth Sci Ctr, 450 Clarkson Ave,Box 1199, Brooklyn, NY 11203 USA.
EM ECavusoglu@aol.com
FU National Institutes of Health ( Bethesda, Maryland) [HL-69817]
FX This study was supported in part by grant HL-69817 (XCJ) from the
National Institutes of Health ( Bethesda, Maryland).
NR 35
TC 11
Z9 15
U1 0
U2 0
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 NOV
PY 2009
VL 207
IS 1
BP 261
EP 265
DI 10.1016/j.atherosclerosis.2009.04.011
PG 5
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 528QE
UT WOS:000272460700042
PM 19446293
ER
PT J
AU Waldman, ID
Gizer, IR
Singh, AL
Harrington, KM
Rowe, DC
AF Waldman, I. D.
Gizer, I. R.
Singh, A. L.
Harrington, K. M.
Rowe, D. C.
TI Between- and within-study heterogeneity in the association of attention
deficit hyperactivity disorder with the 5HTTLPR
SO BEHAVIOR GENETICS
LA English
DT Meeting Abstract
CT 39th Annual Meeting of the Behavior-Genetics-Association
CY JUN 17-20, 2009
CL Mineapolis, MN
SP Behav Genet Assoc
C1 [Waldman, I. D.] Emory Univ, Dept Psychol, Atlanta, GA 30322 USA.
[Gizer, I. R.] Univ N Carolina, Dept Human Genet, Chapel Hill, NC 27599 USA.
[Singh, A. L.] Indiana Univ, Dept Psychol & Brain Sci, Bloomington, IN 47405 USA.
[Harrington, K. M.] VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA 02130 USA.
[Rowe, D. C.] Univ Arizona, Late Program Genet & Cell Biol, Tucson, AZ USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-8244
J9 BEHAV GENET
JI Behav. Genet.
PD NOV
PY 2009
VL 39
IS 6
BP 688
EP 688
PG 1
WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary
SC Behavioral Sciences; Genetics & Heredity; Psychology
GA 522VL
UT WOS:000272027300166
ER
PT J
AU Smith, RA
Yuan, HS
Weissleder, R
Cantley, LC
Josephson, L
AF Smith, R. Adam
Yuan, Hushan
Weissleder, Ralph
Cantley, Lewis C.
Josephson, Lee
TI A Wortmannin-Cetuximab as a Double Drug
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; DEPENDENT CELLULAR CYTOTOXICITY; LUNG-CANCER;
WILD-TYPE; CHEMOTHERAPY; COMBINATION; INHIBITION; THERAPY; PRODRUG;
CELLS
AB Double drugs are obtained when two pharmacologically active entities are covalently joined to improve potency. We conjugated the viridin Wm with a self-activating linkage to cetuximab and demonstrated the retention of immunoreactivity by the conjugate. Though cetuximab lacked a growth inhibitory activity against A549 cells, the Wm-cetuximab conjugate had an antiproliferative IC(50) of 155 nM in vitro. The chemistry of attaching a self-releasing Wm to clinically approved antibodies is general and, in selected instances, may yield antibody-based double drugs with improved efficacy.
C1 [Smith, R. Adam; Yuan, Hushan; Weissleder, Ralph; Josephson, Lee] Massachusetts Gen Hosp, Ctr Mol Imaging Res, Charlestown, MA 02129 USA.
[Smith, R. Adam; Yuan, Hushan; Weissleder, Ralph; Josephson, Lee] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Weissleder, Ralph] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Cantley, Lewis C.] Beth Israel Deaconess Med Ctr, Div Signal Transduct, Boston, MA 02115 USA.
[Cantley, Lewis C.] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
RP Josephson, L (reprint author), Massachusetts Gen Hosp, Ctr Mol Imaging Res, 149 13th St, Charlestown, MA 02129 USA.
EM ljosephson@mgh.harvard.edu
RI Cantley, Lewis/D-1800-2014
OI Cantley, Lewis/0000-0002-1298-7653
FU NCI NIH HHS [P50 CA086355]; NIBIB NIH HHS [R01 EB004472]; NIGMS NIH HHS
[R01 GM041890]
NR 27
TC 2
Z9 2
U1 0
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD NOV
PY 2009
VL 20
IS 11
BP 2185
EP 2189
DI 10.1021/bc900176a
PG 5
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 520FP
UT WOS:000271826600021
PM 19883074
ER
PT J
AU Koenigsberg, HW
Fan, J
Ochsner, KN
Liu, X
Guise, KG
Pizzarello, S
Dorantes, C
Guerreri, S
Tecuta, L
Goodman, M
New, A
Siever, LJ
AF Koenigsberg, Harold W.
Fan, Jin
Ochsner, Kevin N.
Liu, Xun
Guise, Kevin G.
Pizzarello, Scott
Dorantes, Christine
Guerreri, Stephanie
Tecuta, Lucia
Goodman, Marianne
New, Antonia
Siever, Larry J.
TI Neural Correlates of the Use of Psychological Distancing to Regulate
Responses to Negative Social Cues: A Study of Patients with Borderline
Personality Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Cognitive reappraisal; emotion; emotion regulation; fMRI; psychological
distancing; social cognitive neuroscience
ID EVENT-RELATED FMRI; ANTERIOR CINGULATE CORTEX; EMOTION REGULATION;
PREFRONTAL CORTEX; VOLUNTARY SUPPRESSION; AFFECTIVE INSTABILITY;
COGNITIVE CONTROL; PARIETAL CORTEX; FUNCTIONAL MRI; AMYGDALA
AB Background: Emotional instability is a defining feature of borderline personality disorder (BPD); yet, little is understood about its underlying neural correlates. One possible contributing factor to emotional instability is a failure to adequately employ adaptive cognitive regulatory strategies such as psychological distancing.
Methods: To determine whether there are differences in neural dynamics underlying this control strategy between BPD patients and healthy control (HC) subjects, blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging signals were acquired as 18 BPD and 16 HC subjects distanced from or simply looked at pictures depicting social interactions. Contrasts in signal between distance and look conditions were compared between groups.
Results: Borderline personality disorder patients showed a different pattern of activation compared with HC subjects when looking at negative versus neutral pictures. When distancing versus looking at negative pictures, both groups showed decreased negative affect ratings and increased activation of the dorsolateral prefrontal cortex, areas near/along the intraparietal sulcus (IPS), ventrolateral prefrontal cortex, and posterior cingulate/precuneus regions. However, the BPD group showed less BOLD signal change in dorsal anterior cingulate cortex and IPS, less deactivation in the amygdala, and greater activation in the superior temporal sulcus and superior frontal gyrus.
Conclusions: Borderline personality disorder and HC subjects display different neural dynamics while passively viewing social emotional stimuli. In addition, BPD patients do not engage the cognitive control regions to the extent that HCs do when employing a distancing strategy to regulate emotional reactions, which may be a factor contributing to the affective instability of BPD.
C1 [Koenigsberg, Harold W.] Mt Sinai Sch Med, James J Peters VA Med Ctr, Mental Hlth Patient Care Ctr, Bronx, NY 10468 USA.
[Koenigsberg, Harold W.; Fan, Jin; Liu, Xun; Guise, Kevin G.; Dorantes, Christine; Guerreri, Stephanie; Tecuta, Lucia; Goodman, Marianne; New, Antonia] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Ochsner, Kevin N.] Columbia Univ, Dept Psychol, New York, NY 10027 USA.
[Pizzarello, Scott] Florida State Univ, Dept Psychol, Tallahassee, FL 32306 USA.
RP Koenigsberg, HW (reprint author), Mt Sinai Sch Med, James J Peters VA Med Ctr, Mental Hlth Patient Care Ctr, 130 W Kingsbridge Rd,116A, Bronx, NY 10468 USA.
EM HWarrenK@nyc.rr.com
RI Fan, Jin/A-6716-2009; Frank, David/E-8213-2012; Liu, Xun/C-2400-2009;
OI Fan, Jin/0000-0001-9630-8330; Liu, Xun/0000-0003-1366-8926; TECUTA,
LUCIA/0000-0002-7984-3064
FU National Institute of Mental Health [RO1 MH077813]; HWK [MH076137];
National Center for Research Rasources, National institutes of Health
for the Mount Sinai General Clinical Research Center [5MO1 RR00071]
FX This work was supported in part by grants from, the National Institute
of Mental Health (RO1 MH077813, Principal Investigator: HWK; MH076137.
Principal Investigator: KNO) and from the National Center for Research
Rasources, National institutes of Health for the Mount Sinai General
Clinical Research Center (5MO1 RR00071).
NR 76
TC 97
Z9 98
U1 4
U2 17
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 NOV 1
PY 2009
VL 66
IS 9
BP 854
EP 863
DI 10.1016/j.biopsych.2009.06.010
PG 10
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 512BH
UT WOS:000271216800007
PM 19651401
ER
PT J
AU Pidala, J
Anasetti, C
Kharfan-Dabaja, MA
Cutler, C
Sheldon, A
Djulbegovic, B
AF Pidala, Joseph
Anasetti, Claudio
Kharfan-Dabaja, Mohamed A.
Cutler, Corey
Sheldon, Andy
Djulbegovic, Benjamin
TI Decision Analysis of Peripheral Blood versus Bone Marrow Hematopoietic
Stem Cells for Allogeneic Hematopoietic Cell Transplantation
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Peripheral blood mobilized stem cells; Bone marrow stem cells;
Allogeneic hematopoietic cell transplantation; Decision analysis; Markov
model
ID COLONY-STIMULATING FACTOR; VERSUS-HOST-DISEASE; HLA-IDENTICAL SIBLINGS;
HEMATOLOGICAL MALIGNANCIES; PROGENITOR CELLS; RANDOMIZED-TRIAL;
APLASTIC-ANEMIA; CD3(+) CELLS; LOW-RISK; G-CSF
AB Peripheral blood stem cells (PBSCs) and bone marrow (BM) hematopoietic stem cells represent therapeutic alternatives in allogeneic hematopoietic cell transplantation. Randomized controlled trials and an individual patient data meta-analysis (IPDMA) have demonstrated a decreased risk of disease relapse and an increased risk of acute and chronic graft-versus-host disease (aGVHD, cGVHD) in patients receiving PBSCs compared with those receiving BM stem cells. Decision modeling provides quantitative integration of the risks and benefits associated with these alternative treatments, incorporates survival discounts for lower quality of life in patients with aGVHD or cGVHD and post-transplantation relapse, and allows sensitivity analyses for all model assumptions. We have constructed an externally validated Markov model to represent and analyze the decision to use PBSC or BM, estimating post-transplantation state transition probabilities (eg, GVHD and relapse) and quality-of-life discounts from the IPDMA and relevant literature; importantly, this IPDMA synthesized data from primarily adult patients treated with myeloablative (MA) conditioning regimens with T cell-replete matched sibling donors. In this setting, the model demonstrates the superiority of PBSC over BM in both overall and quality-adjusted life expectancy, with a 7-month advantage for PBSC. Sensitivity analyses support this conclusion through a range of values for each variable supported by the IPDMA and quality-of-life discounts, as supported by the literature. However, BM is the optimal strategy in conditions in which the 1-year relapse probability is < 5%. PBSC is the optimal stem cell source in terms of both overall and quality-adjusted life expectancy, except in conditions with a very low relapse probability, in which BM provides optimal outcomes. Biol Blood Marrow Transplant 15: 1415-1421 (2009) (C) 2009 American Society for Blood and Marrow Transplantation
C1 [Pidala, Joseph; Anasetti, Claudio; Kharfan-Dabaja, Mohamed A.; Djulbegovic, Benjamin] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Blood, Tampa, FL 33612 USA.
[Pidala, Joseph; Anasetti, Claudio; Kharfan-Dabaja, Mohamed A.; Djulbegovic, Benjamin] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Dept Marrow Transplantat, Tampa, FL 33612 USA.
[Pidala, Joseph; Anasetti, Claudio; Kharfan-Dabaja, Mohamed A.; Djulbegovic, Benjamin] Univ S Florida, Dept Oncol Sci, Tampa, FL 33612 USA.
[Cutler, Corey] Dana Farber Canc Inst, Dept Blood & Marrow Transplantat, Boston, MA 02115 USA.
[Sheldon, Andy] TreeAge Software Inc, Williamstown, MA USA.
RP Pidala, J (reprint author), MCC GME, H Lee Moffitt Canc Ctr, 12902 Magnolia Dr, Tampa, FL 33612 USA.
EM joseph.pidala@moffitt.org
RI Djulbegovic, Benjamin/I-3661-2012
OI Djulbegovic, Benjamin/0000-0003-0671-1447
FU NCI NIH HHS [R01 CA133594]
NR 41
TC 30
Z9 35
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD NOV
PY 2009
VL 15
IS 11
BP 1415
EP 1421
DI 10.1016/j.bbmt.2009.07.009
PG 7
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 515UF
UT WOS:000271497700009
PM 19822301
ER
PT J
AU Ulrickson, M
Aldridge, J
Kim, HT
Hochberg, EP
Hammerman, P
Dube, C
Attar, E
Ballen, KK
Dey, BR
McAfee, SL
Spitzer, TR
Chen, YB
AF Ulrickson, Matthew
Aldridge, Julie
Kim, Haesook T.
Hochberg, Ephraim P.
Hammerman, Peter
Dube, Christine
Attar, Eyal
Ballen, Karen K.
Dey, Bimalangshu R.
McAfee, Steven L.
Spitzer, Thomas R.
Chen, Yi-Bin
TI Busulfan and Cyclophosphamide (Bu/Cy) as a Preparative Regimen for
Autologous Stem Cell Transplantation in Patients with Non-Hodgkin
Lymphoma: A Single-Institution Experience
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Lymphoma; Autologous transplant; Busulfan
ID BONE-MARROW-TRANSPLANTATION; HIGH-DOSE CHEMOTHERAPY; CONDITIONING
REGIMEN; MALIGNANT-LYMPHOMA; AGGRESSIVE LYMPHOMA; ETOPOSIDE; CARMUSTINE;
RECOVERY; SURVIVAL; THIOTEPA
AB High-dose chemotherapy with autologous stem cell transplantation (ASCT) has been established as a standard form of therapy for patients with non-Hodgkin lymphoma (NHL). While many high-dose chemotherapy combinations are used, no single regimen has proved superior over another. Here, we report our single center's experience in patients with NHL undergoing ASCT with the combination of busulfan and cyclophosphamide (Bu/Cy). This study is a retrospective analysis of 78 consecutive patients with NHL who underwent ASCT with Bu/Cy at Massachusetts General Hospital Cancer Center. Data were collected through review of electronic medical records. A total of 78 patients with NHL underwent ASCT with Bu/Cy preparative therapy between 1996 and 2006. Median follow-up for survivors was 5.0 years (range, 6 months to 12 years). Significant transplantation-associated complications included 9 documented bacterial infections, 4 cases of engraftment syndrome, 3 cases of hepatic veno-occlusive disease (VOID), 6 cases of cardiac complications, and 2 cases of pulmonary fibrosis. The 100-day treatment-related mortality (TRM) was 1%. At 3 years, progression-free survival (PFS) was 48% (95% confidence interval [CI] = 37% to 59%) and overall survival (OS) was 65% (95% CI = 53% to 74%). Our data indicate that in patients with NHL undergoing ASCT Bu/Cy has efficacy and toxicity comparable to that of other reported regimens. Biol Blood Marrow Transplant 15: 7447-1454 (2009) (C) 2009 American Society for Blood and Marrow Transplantation
C1 [Chen, Yi-Bin] Massachusetts Gen Hosp, Dept Hematol Oncol, Div Bone Marrow Transplantat, Boston, MA 02114 USA.
[Aldridge, Julie; Kim, Haesook T.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
RP Chen, YB (reprint author), Massachusetts Gen Hosp, Dept Hematol Oncol, Div Bone Marrow Transplantat, 55 Fruit St, Boston, MA 02114 USA.
EM ychen6@partners.org
FU Clinical Research of the Leukenna & Lymphoma Society
FX Y.C. is a Special Fellow in Clinical Research of the Leukenna & Lymphoma
Society. Author contributions: M.U. designed the research, collected
data, performed research, analyzed data, and wrote the manuscript; J.A.
analyzed data and reviewed the manuscript; H.T.K. analyzed data and
reviewed the manuscript;, E.P.H. designed the research and reviewed the
manuscript; P.H. collected data and reviewed the manuscript; C.D.
maintained the clinical database and reviewed the manuscript;, E.A.
provided clinical care and reviewed the manuscript; K.K.B. provided
clinical care and reviewed the manuscript; B.R.D. provided clinical care
and reviewed the manuscript;, S.L.M. provided clinical care and reviewed
the manuscript; T.R.S. provided clinical care and reviewed the
manuscript; Y.C. designed the research, performed research, collected
data, analyzed data, and wrote the manuscript.
NR 26
TC 16
Z9 16
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD NOV
PY 2009
VL 15
IS 11
BP 1447
EP 1454
DI 10.1016/j.bbmt.2009.07.014
PG 8
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 515UF
UT WOS:000271497700013
PM 19822305
ER
PT J
AU Fenske, TS
Hari, PN
Carreras, J
Zhang, MJ
Kamble, RT
Bolwell, BJ
Cairo, MS
Champlin, RE
Chen, YB
Freytes, CO
Gale, RP
Hale, GA
Ilhan, O
Khoury, HJ
Lister, J
Maharaj, D
Marks, DI
Munker, R
Pecora, AL
Rowlings, PA
Shea, TC
Stiff, P
Wiernik, PH
Winter, JN
Rizzo, JD
van Besien, K
Lazarus, HM
Vose, JM
AF Fenske, Timothy S.
Hari, Parameswaran N.
Carreras, Jeanette
Zhang, Mei-Jie
Kamble, Rammurti T.
Bolwell, Brian J.
Cairo, Mitchell S.
Champlin, Richard E.
Chen, Yi-Bin
Freytes, Cesar O.
Gale, Robert Peter
Hale, Gregory A.
Ilhan, Osman
Khoury, H. Jean
Lister, John
Maharaj, Dipnarine
Marks, David I.
Munker, Reinhold
Pecora, Andrew L.
Rowlings, Philip A.
Shea, Thomas C.
Stiff, Patrick
Wiernik, Peter H.
Winter, Jane N.
Rizzo, J. Douglas
van Besien, Koen
Lazarus, Hillard M.
Vose, Julie M.
TI Impact of Pre-transplant Rituximab on Survival after Autologous
Hematopoietic Stem Cell Transplantation for Diffuse Large B Cell
Lymphoma
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Autologous hematopoietic stem cell transplantation; Lymphoma; Rituximab
ID NON-HODGKINS-LYMPHOMA; R-CHOP; SALVAGE CHEMOTHERAPY; ELDERLY-PATIENTS;
PLUS RITUXIMAB; THERAPY; DLBCL
AB Incorporation of the anti-CD20 monoclonal antibody rituximab into front-line regimens to treat diffuse large B cell lymphoma (DLBCL) has resulted in improved survival. Despite this progress, however, many patients develop refractory or recurrent DLBCL and then undergo autologous hematopoietic stem cell transplantation (AuHCT). It is unclear to what extent pre-transplant exposure to rituximab affects outcomes after AuHCT Outcomes of 994 patients receiving AuHCT for DLBCL between 1996 and 2003 were analyzed according to whether rituximab was (n = 176; +R cohort) or was not (n = 818; -R cohort) administered with front-line or salvage therapy before AuHCT The +R cohort had superior progression-free survival (PFS; 50% vs 38%; P = .008) and overall survival (OS; 57% vs 45%; P = .006) at 3 years. Platelet and neutrophil engraftment were not affected by exposure to rituximab. Nonrelapse mortality (NRM) did not differ significantly between the 2 cohorts. In multivariate analysis, the +R cohort had improved PFS (relative risk of relapse/progression or death, 0.64; P < .001) and improved OS (relative risk of death, 0.74; P = .039). We conclude that pre-transplant rituximab is associated with a lower rate of progression and improved survival after AuHCT for DLBCL, with no evidence of impaired engraftment or increased NRM. Biol Blood Marrow Transplant 15: 1455-1464 (2009) (C) 2009 American Society for Blood and Marrow Transplantation
C1 [Fenske, Timothy S.] Med Coll Wisconsin, Div Neoplast Dis, Milwaukee, WI 53226 USA.
[Hari, Parameswaran N.; Carreras, Jeanette; Zhang, Mei-Jie; Rizzo, J. Douglas] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Kamble, Rammurti T.] Baylor Coll Med, Houston, TX 77030 USA.
[Bolwell, Brian J.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Cairo, Mitchell S.] New York Presbyterian Hosp, New York, NY USA.
[Champlin, Richard E.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Chen, Yi-Bin] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Freytes, Cesar O.] Univ Texas Hlth Sci Ctr San Antonio, S Texas Vet Hlth Care Syst, San Antonio, TX 78229 USA.
[Gale, Robert Peter] Celgene Corp, Summit, NJ USA.
[Hale, Gregory A.] Univ S Florida, All Childrens Hosp, St Petersburg, FL 33701 USA.
[Ilhan, Osman] Ibni Sina Hosp, Ankara, Turkey.
[Khoury, H. Jean] Emory Univ, Winship Canc Inst, Atlanta, GA 30322 USA.
[Lister, John] Western Penn Hosp, Pittsburgh, PA 15224 USA.
[Maharaj, Dipnarine] S Florida Bone Marrow Stem Cell Transplant Inst, Boynton Beach, FL USA.
[Marks, David I.] United Bristol Healthcare, Bristol, Avon, England.
[Munker, Reinhold] Louisiana State Univ, Med Ctr, Shreveport, LA USA.
[Pecora, Andrew L.] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
[Rowlings, Philip A.] Univ Newcastle, Calvary Mater Newcastle Hosp, Newcastle, NSW 2308, Australia.
[Shea, Thomas C.] Univ N Carolina, Chapel Hill, NC USA.
[Stiff, Patrick] Loyola Univ Hlth Syst, Maywood, IL USA.
[Wiernik, Peter H.] Montefiore Med Ctr, North Div, Bronx, NY 10467 USA.
[Wiernik, Peter H.] New York Med Coll, Bronx, NY USA.
[Winter, Jane N.] NW Mem Hosp, Chicago, IL 60611 USA.
[van Besien, Koen] Univ Chicago, Med Ctr, Chicago, IL 60637 USA.
[Lazarus, Hillard M.] Univ Hosp Case Med Ctr, Cleveland, OH USA.
[Vose, Julie M.] Univ Nebraska Med Ctr, Omaha, NE USA.
RP Fenske, TS (reprint author), Med Coll Wisconsin, Div Neoplast Dis, 9200 W Wisconsin Ave, Milwaukee, WI 53226 USA.
EM tfenske@mcw.edu
RI van Besien, Koen/G-4221-2012;
OI van Besien, Koen/0000-0002-8164-6211; Hari,
Parameswaran/0000-0002-8800-297X
FU National Cancer Institute (NICT) [U24-CA76518]; National Heart, Lung and
Blood Institute (NTHLBI); National Institute of Allergy and Infectious
Diseases (NIAID); NHLBI [5U01HL069294]; NCI; Health Resources and
Services Administration [HHSH234200637015C]; Office of Naval Research
[N0001406-1-0704, N00014-08-1-0058]; AABB; Aetna; American Society for
Blood and Marrow Transplantation; Amgen, Inc; Association of Medical
Microbiology; Infectious Disease Canada; Astellas Pharma US, Inc; Baxter
International, Inc; Bayer HealthCare Pharmaceuticals; BloodCenter of
Wisconsin; Blue Cross and Blue Shield Association; Bone Marrow
Foundation; Canadian Blood and Marrow Transplant Group; Celgene Corp;
CellGenix GmbH; Centers for Disease Control and Prevention; ClinImmune
Labs; CTI Clinical Trial and Consulting Services; Cubist
Pharmaceuticals; Cylex, Inc; CytoTherm; DOR BloPharma, Inc; Dynal
Biotech; Invitrogen Company; Enzon Pharmaceuticals, Inc; European Group
for Blood and Marrow Transplantation; Gambro BCT, Inc; Gamida Cell, Ltd;
Genzyme Corp; Histogenetics, Inc; HKS Medical Information Systems;
Hospira, Inc; Infectious Diseases Society of America; Kiadis Pharma;
Kirin Brewer, Co, Ltd; Merck Company; Medical College of Wisconsin; MGI
Pharma, Inc; Michigan Community Blood Centers; Millennium
Pharmaceuticals, Inc; Miller Pharmacal Group; Millinian USA, Inc;
Miltenyi Biotec, Inc; National Marrow Donor Program; Nature Publishing
Group; New York.Blood Center; Novartis Oncology; Oncology, Nursing
Society; Osiris Therapeutics, Inc; Otsuka Pharmaceutical Development &
Commercialization, Inc; Pall Life Sciences; PDL BioPharma, Inc; Pfizer
Inc; Pharmion Corp; Saladax Biomedical, Inc; Schering Plough Corp;
Society for Healthcare Epidemiology of America; StemCyte, Inc; StemSoft
Soft-ware, Inc; Sysmex; Teva Pharmaceutical Industries; Marrow
Foundation; THERAKOS, Inc; Vidacare Corp; Vion Pharmaceuticals, Inc;
VitaCorLaboratories; ViroPharma, Inc; Wellpoint, Inc
FX The CIBMR is supported by Public Health Service Grant/Cooperative
Agreement U24-CA76518 from the National Cancer Institute (NICT), the
National Heart, Lung and Blood Institute (NTHLBI), and the National
Institute of Allergy and Infectious Diseases (NIAID); Grant/Cooperative
Agreement 5U01HL069294 from NHLBI and NCI; Contract HHSH234200637015C
from the Health Resources and Services Administration, Grants
N0001406-1-0704 and N00014-08-1-0058 from the Office of Naval Research,
and grant. from AABB; Aetna; American Society for Blood and Marrow
Transplantation; Amgen, Inc, anonymous donation to the Medical College
of Wisconsin; Association of Medical Microbiology, and Infectious
Disease Canada; Astellas Pharma US, Inc; Baxter International, Inc;
Bayer HealthCare Pharmaceuticals; BloodCenter of Wisconsin, Blue Cross
and Blue Shield Association; Bone Marrow Foundation; Canadian Blood and
Marrow Transplant Group; Celgene Corp; CellGenix GmbH; Centers for
Disease Control and Prevention; ClinImmune Labs; CTI Clinical Trial and
Consulting Services; Cubist Pharmaceuticals; Cylex, Inc; CytoTherm; DOR
BloPharma, Inc, Dynal Biotech, an Invitrogen Company; Enzon
Pharmaceuticals, Inc; European Group for Blood and Marrow
Transplantation;, Gambro BCT, Inc; Gamida Cell, Ltd; Genzyme Corp;,
Histogenetics, Inc; HKS Medical Information Systems; Hospira, Inc;
Infectious Diseases Society of America; Kiadis Pharma; Kirin Brewer, Co,
Ltd; Merck & Company; Medical College of Wisconsin; MGI Pharma, Inc;
Michigan Community Blood Centers; Millennium Pharmaceuticals, Inc;
Miller Pharmacal Group; Millinian USA, Inc; Miltenyi Biotec, Inc;
National Marrow Donor Program; Nature Publishing Group; New York.Blood
Center; Novartis Oncology; Oncology, Nursing Society; Osiris
Therapeutics, Inc; Otsuka Pharmaceutical Development &
Commercialization, Inc; Pall Life Sciences; PDL BioPharma, Inc; Pfizer
Inc;, Pharmion Corp; Saladax Biomedical, Inc; Schering Plough Corp;
Society for Healthcare Epidemiology of America; StemCyte, Inc; StemSoft
Soft-ware, Inc; Sysmex; Teva Pharmaceutical Industries; The Marrow
Foundation; THERAKOS, Inc; Vidacare Corp; Vion Pharmaceuticals, Inc;
VitaCorLaboratories; ViroPharma, Inc; and Wellpoint, Inc.
NR 19
TC 31
Z9 35
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
EI 1523-6536
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD NOV
PY 2009
VL 15
IS 11
BP 1455
EP 1464
DI 10.1016/j.bbmt.2009.07.017
PG 10
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 515UF
UT WOS:000271497700014
PM 19822306
ER
PT J
AU Weisdorf, DJ
Nelson, G
Lee, SJ
Haagenson, M
Spellman, S
Antin, JH
Bolwell, B
Cahn, JY
Cervantes, F
Copelan, E
Gale, R
Gratwohl, A
Khoury, HJ
McCarthy, P
Marks, DI
Szer, J
Woolfrey, A
Cortes-Franco, J
Horowitz, MM
Arora, M
AF Weisdorf, Daniel J.
Nelson, Gene
Lee, Stephanie J.
Haagenson, Michael
Spellman, Stephen
Antin, Joseph H.
Bolwell, Brian
Cahn, Jean-Yves
Cervantes, Francisco
Copelan, Edward
Gale, Robert
Gratwohl, Alois
Khoury, H. Jean
McCarthy, Philip
Marks, David I.
Szer, Jeff
Woolfrey, Ann
Cortes-Franco, Jorge
Horowitz, Mary M.
Arora, Mukta
CA Chronic Leukemia Working Comm
TI Sibling versus Unrelated Donor Allogeneic Hematopoietic Cell
Transplantation for Chronic Myelogenous Leukemia: Refined HLA Matching
Reveals More Graft-versus-Host Disease but not Less Relapse
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Chronic myelogenous leukemia; HLA matching; Unrelated donor
allotransplantation; Graft versus leukemia; Graft-versus-host disease
ID BONE-MARROW-TRANSPLANTATION; CLASS-I; RECIPIENT; IMPACT
AB Unrelated donor (URD) hematopoietic cell transplantation (HCT) can eradicate chronic myelogenous leukemia (CML). It has been postulated that greater donor-recipient histoincompatibility can augment the graft-versus-leukemia (GVL) effect. We previously reported similar, but not equivalent, outcomes of URD versus sibling donor HCT for CML using an older, less precise classification of HLA matching. Here, we used our recently refined HLA-matching classification, which is suitable for interpretation when complete allele-level typing is unavailable, to reanalyze outcomes of previous HCT for CML. We found that using our new matching criteria identifies substantially more frequent mismatching than older, less precise "6 of 6 antigen-matched" URD-HCT Under the new criteria, only 37% of those previously deemed "HLA-matched" were HLA well matched, and 44% were partially matched. Using our refined matching criteria confirms the greater risk of graft failure in partially matched or mismatched URD-recipient pairs compared with either sibling or well-matched URID-recipient pairs. Acute and chronic graft-versus-host disease (aGVHD, cGVHD) are significantly more frequent with all levels of recategorized URD HLA matching. Importantly, overall survival (CS) and leukemia-free survival (LFS) remain significantly worse after URD-HCT at any matching level. No augmented GVL effect accompanied URD HLA mismatch. Compared with sibling donor transplants, we observed only marginally increased (not statistically significant) risks of relapse in well-matched, partially matched, and mismatched URD-HCT These data confirm the applicability of revised HILA-matching scheme in analyzing retrospective data sets when fully informative, allele-level typing is unavailable. In this analysis, greater histoincompatibility can augment GVHD, but does not improve protection against relapse; thus the best donor remains the most closely matched donor. Biol Blood Marrow Transplant 15: 1475-1478 (2009) (C) 2009 American Society for Blood and Marrow Transplantation
C1 [Weisdorf, Daniel J.; Arora, Mukta] Univ Minnesota, Minneapolis, MN 55455 USA.
[Weisdorf, Daniel J.; Nelson, Gene; Lee, Stephanie J.; Haagenson, Michael; Spellman, Stephen; Horowitz, Mary M.; Arora, Mukta] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
[Lee, Stephanie J.; Woolfrey, Ann] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Antin, Joseph H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bolwell, Brian; Copelan, Edward] Cleveland Clin, Cleveland, OH 44106 USA.
[Cahn, Jean-Yves] Besancon Univ Hosp, Besancon, France.
[Cervantes, Francisco] Univ Barcelona, IDIBAPS, Hosp Clin, Barcelona, Spain.
[Gale, Robert] Ctr Adv Studies Leukemia, Los Angeles, CA USA.
[Gratwohl, Alois] Univ Basel, Basel, Switzerland.
[Khoury, H. Jean] Emory Clin, Winship Canc Inst, Atlanta, GA 30322 USA.
[McCarthy, Philip] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Marks, David I.] United Bristol Healthcare Trust, Bristol, Avon, England.
[Szer, Jeff] Royal Melbourne & Western Hosp, Parkville, Vic, Australia.
[Cortes-Franco, Jorge] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Horowitz, Mary M.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
RP Weisdorf, DJ (reprint author), Univ Minnesota, MMC 480,480 Delaware St SE, Minneapolis, MN 55455 USA.
EM weisd001@umn.edu
RI Cahn, Jean-Yves/M-6493-2014;
OI Szer, Jeff/0000-0001-6783-2301
FU NCI NIH HHS [P01 CA111412, P01 CA111412-050001, U24 CA076518,
U24-CA76518]; NHLBI NIH HHS [U01 HL069290, U01 HL069290-10, U01
HL069294]; PHS HHS [5U01H L069294, HHSH234200637015C]
NR 8
TC 24
Z9 24
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD NOV
PY 2009
VL 15
IS 11
BP 1475
EP 1478
DI 10.1016/j.bbmt.2009.06.016
PG 4
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 515UF
UT WOS:000271497700016
PM 19822308
ER
PT J
AU Medarova, Z
AF Medarova, Z.
TI NONINVASIVE IMAGING OF BREAST CANCER
SO BIOTECHNOLOGY & BIOTECHNOLOGICAL EQUIPMENT
LA English
DT Review
DE breast cancer; imaging; magnetic resonance imaging; cancer staging;
muc-1
ID CARCINOMA IN-SITU; COMPARATIVE GENOMIC HYBRIDIZATION; LYMPH-NODE
METASTASES; POSITRON-EMISSION-TOMOGRAPHY; MONOCLONAL-ANTIBODIES;
TRANSFERRIN RECEPTOR; DUCTAL HYPERPLASIA; PROGNOSTIC-SIGNIFICANCE; TUMOR
CHARACTERISTICS; PULMONARY METASTASES
AB With the development of molecularly targeted cancer therapies, it is highly advantageous to be able to determine their efficacy, to improve overall patient survival, Non-invasive imaging techniques are currently available for visualizing different pathological conditions of the human body but their use for cancer monitoring is limited due to the lack of tumor-specific imaging probes. This review will attempt to summarize the current clinical diagnostic approaches for breast cancer detection, staging, and therapy assessment. In addition, I will present some novel concepts from the field of molecular imaging that form the basis of some of our research. We believe that this, general imaging strategy has the potential of significantly advancing our ability to diagnose breast cancer at the earliest stages of the pathology, before any overt clinical symptoms have developed as well as to better direct the development of molecularly-targeted individualized therapy protocols.
C1 Harvard Univ, Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Dept Radiol,MIT, Boston, MA 02115 USA.
RP Medarova, Z (reprint author), Harvard Univ, Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Dept Radiol,MIT, Boston, MA 02115 USA.
EM zmedarova@partners.org
NR 99
TC 2
Z9 2
U1 0
U2 2
PU DIAGNOSIS PRESS LTD
PI SOFIA
PA 67 DONDUKOV BLVD, 1504 SOFIA, BULGARIA
SN 1310-2818
J9 BIOTECHNOL BIOTEC EQ
JI Biotechnol. Biotechnol. Equip.
PD NOV
PY 2009
VL 23
IS 4
BP 1453
EP 1461
DI 10.2478/V10133-009-0001-Y
PG 9
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 525GA
UT WOS:000272201400011
ER
PT J
AU Roach, KL
King, KR
Uygun, BE
Kohane, IS
Yarmush, ML
Toner, M
AF Roach, Kenneth L.
King, Kevin R.
Uygun, Basak E.
Kohane, Isaac S.
Yarmush, Martin L.
Toner, Mehmet
TI High Throughput Single Cell Bioinformatics
SO BIOTECHNOLOGY PROGRESS
LA English
DT Article
DE cytometry; microfabrication; microwells; hepatocytes; mitochondria;
membrane potential; free radicals
ID GENE-EXPRESSION; NOISE; CYTOMETRY; PLATFORM; BIOLOGY; ARRAYS; CHIP
AB Advances in systems biology and bioinformatics have highlighted that no cell population is truly, uniform and that stochastic behavior is an inherent property of many biological systems. As a result, bulk measurements can be misleading even when particular care has been taken to isolate a single cell type. and measurements averaged over multiple cell populations in a tissue can be as misleading as the average height at an elementary school. There is a growing need for experimental techniques that can provide a combination of single cell resolution, large cell populations, and the ability to track cells over multiple time points. In this article, a microwell array cytometry platform was developed to meet this need and investigate the heterogeneity and stochasticity of cell behavior on a single cell basis. The platform consisted of a microfabricated device with high-density, arrays of cell-sized microwells and custom software for automated image processing and data analysis. As a model experimental system, we used primary hepatocytes labeled with fluorescent probes sensitive to mitochondrial membrane potential and free radical generation. The cells were exposed to oxidative stress and the responses were dynamically monitored for each cell. The resulting data was then analyzed using bioinformatics techniques such as hierarchical and k-means clustering to visualize the data and identify interesting features. The results showed that clustering of the dynamic data not only enhanced comparisons between the treatment groups but also revealed a number of distinct response patterns within each treatment group. Heat-maps with hierarchical clustering also provided a data-rich complement to survival curves in a dose response experiment. The microwell array cytometry platform was shown to be powerful easy to use, and able to provide a detailed picture of the heterogeneity, present in cell responses to oxidative stress. We believe that our microwell array cytometry platform will have general utility for a wide range of questions related to cell population heterogeneity, biological stochasticity, and cell behavior under stress conditions. (C) 2009 American Institute of Chemical Engineers Biotechnol. Prog., 25: 1772-1779, 2009
C1 [Roach, Kenneth L.; King, Kevin R.; Uygun, Basak E.; Yarmush, Martin L.; Toner, Mehmet] Harvard Univ, Massachusetts Gen Hosp, Shriners Hosp Children, Sch Med,BioMEMS Resource Ctr,Ctr Engn Med, Boston, MA 02115 USA.
[Roach, Kenneth L.; King, Kevin R.; Kohane, Isaac S.; Yarmush, Martin L.; Toner, Mehmet] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Kohane, Isaac S.] Childrens Hosp, Informat Program, Boston, MA 02115 USA.
RP Toner, M (reprint author), Harvard Univ, Massachusetts Gen Hosp, Shriners Hosp Children, Sch Med,BioMEMS Resource Ctr,Ctr Engn Med, Boston, MA 02115 USA.
EM mtoner@hms.harvard.edu
RI Kohane, Isaac Kohane/K-3716-2012; Uygun, Basak/I-1792-2012
OI Kohane, Isaac Kohane/0000-0003-2192-5160; Uygun,
Basak/0000-0002-2600-7900
FU NIDDK NIH HHS [P30 DK040561, P30 DK040561-14]
NR 36
TC 22
Z9 23
U1 0
U2 8
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 8756-7938
J9 BIOTECHNOL PROGR
JI Biotechnol. Prog.
PD NOV-DEC
PY 2009
VL 25
IS 6
BP 1772
EP 1779
DI 10.1002/btpr.289
PG 8
WC Biotechnology & Applied Microbiology; Food Science & Technology
SC Biotechnology & Applied Microbiology; Food Science & Technology
GA 537ZA
UT WOS:000273152000026
PM 19830811
ER
PT J
AU Mansour, HA
Talkowski, ME
Wood, J
Chowdari, K
McClain, L
Prasad, K
Montrose, D
Fagiolini, A
Friedman, ES
Allen, MH
Bowden, CL
Calabrese, J
El-Mallakh, RS
Escamilla, M
Faraone, SV
Fossey, MD
Gyulai, L
Loftis, JM
Hauser, P
Ketter, TA
Marangell, LB
Miklowitz, DJ
Nierenberg, AA
Patel, J
Sachs, GS
Sklar, P
Smoller, JW
Laird, N
Keshavan, M
Thase, ME
Axelson, D
Birmaher, B
Lewis, D
Monk, T
Frank, E
Kupfer, DJ
Devlin, B
Nimgaonkar, VL
AF Mansour, Hader A.
Talkowski, Michael E.
Wood, Joel
Chowdari, KodavaliV
McClain, Lora
Prasad, Konasale
Montrose, Debra
Fagiolini, Andrea
Friedman, Edward S.
Allen, Michael H.
Bowden, Charles L.
Calabrese, Joseph
El-Mallakh, Rif S.
Escamilla, Michael
Faraone, Stephen V.
Fossey, Mark D.
Gyulai, Laszlo
Loftis, Jennifer M.
Hauser, Peter
Ketter, Terence A.
Marangell, Lauren B.
Miklowitz, David J.
Nierenberg, Andrew A.
Patel, Jayendra
Sachs, Gary S.
Sklar, Pamela
Smoller, Jordan W.
Laird, Nan
Keshavan, Matcheri
Thase, Michael E.
Axelson, David
Birmaher, Boris
Lewis, David
Monk, Tim
Frank, Ellen
Kupfer, David J.
Devlin, Bernie
Nimgaonkar, Vishwajit L.
TI Association study of 21 circadian genes with bipolar I disorder,
schizoaffective disorder, and schizophrenia
SO BIPOLAR DISORDERS
LA English
DT Article
DE association; bipolar disorder; circadian; gene; schizoaffective
disorder; schizophrenia
ID GENOME-WIDE ASSOCIATION; SINGLE-NUCLEOTIDE-POLYMORPHISM;
GLYCOGEN-SYNTHASE; MUTATIONAL ANALYSIS; SUGGESTIVE EVIDENCE;
EUROPEAN-ANCESTRY; CANDIDATE GENES; CLOCK; LINKAGE; LITHIUM
AB Objective:
Published studies suggest associations between circadian gene polymorphisms and bipolar I disorder (BPI), as well as schizoaffective disorder (SZA) and schizophrenia (SZ). The results are plausible, based on prior studies of circadian abnormalities. As replications have not been attempted uniformly, we evaluated representative, common polymorphisms in all three disorders.
Methods:
We assayed 276 publicly available 'tag' single nucleotide polymorphisms (SNPs) at 21 circadian genes among 523 patients with BPI, 527 patients with SZ/SZA, and 477 screened adult controls. Detected associations were evaluated in relation to two published genome-wide association studies (GWAS).
Results:
Using gene-based tests, suggestive associations were noted between EGR3 and BPI (p = 0.017), and between NPAS2 and SZ/SZA (p = 0.034). Three SNPs were associated with both sets of disorders (NPAS2: rs13025524 and rs11123857; RORB: rs10491929; p < 0.05). None of the associations remained significant following corrections for multiple comparisons. Approximately 15% of the analyzed SNPs overlapped with an independent study that conducted GWAS for BPI; suggestive overlap between the GWAS analyses and ours was noted at ARNTL.
Conclusions:
Several suggestive, novel associations were detected with circadian genes and BPI and SZ/SZA, but the present analyses do not support associations with common polymorphisms that confer risk with odds ratios greater than 1.5. Additional analyses using adequately powered samples are warranted to further evaluate these results.
C1 [Mansour, Hader A.; Talkowski, Michael E.; Wood, Joel; Chowdari, KodavaliV; McClain, Lora; Prasad, Konasale; Montrose, Debra; Friedman, Edward S.; Keshavan, Matcheri; Axelson, David; Birmaher, Boris; Lewis, David; Monk, Tim; Frank, Ellen; Kupfer, David J.; Devlin, Bernie; Nimgaonkar, Vishwajit L.] Univ Pittsburgh, Western Psychiat Inst & Clin, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA.
[Talkowski, Michael E.; Nimgaonkar, Vishwajit L.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Human Genet, Pittsburgh, PA 15213 USA.
[Fagiolini, Andrea] Univ Siena, Sch Med, Dept Neurosci, I-53100 Siena, Italy.
[Allen, Michael H.] Univ Colorado, Depress Ctr, Dept Psychiat, Denver, CO 80202 USA.
[Bowden, Charles L.; Escamilla, Michael] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
[Calabrese, Joseph] Case Western Reserve Univ, Univ Hosp Cleveland, Sch Med, Dept Psychiat,Mood Disorders Program, Cleveland, OH 44106 USA.
[El-Mallakh, Rif S.] Univ Louisville, Sch Med, Dept Psychiat & Behav Sci, Louisville, KY 40292 USA.
[Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Psychiat & Human Behav, Syracuse, NY USA.
[Fossey, Mark D.; Hauser, Peter] Univ Oklahoma, Dept Psychiat, Tulsa, OK USA.
[Gyulai, Laszlo] Univ Penn, Med Ctr, Dept Psychiat, Philadelphia, PA 19104 USA.
[Loftis, Jennifer M.; Hauser, Peter] Oregon Hlth & Sci Univ, Behav Hlth & Clin Neurosci Div, Portland VA Med Ctr, Portland, OR 97201 USA.
[Loftis, Jennifer M.] Oregon Hlth & Sci Univ, Dept Psychiat, Portland, OR 97201 USA.
[Hauser, Peter] Oregon Hlth & Sci Univ, Dept Behav Neurosci, Portland, OR 97201 USA.
[Ketter, Terence A.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Bipolar Disorders Clin, Stanford, CA 94305 USA.
[Marangell, Lauren B.] Eli Lilly & Co, US Med Div, Indianapolis, IN 46285 USA.
[Miklowitz, David J.] Univ Colorado, Dept Psychol, Boulder, CO 80309 USA.
[Nierenberg, Andrew A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat,Clin Depress & Res Program, Boston, MA USA.
[Patel, Jayendra] Univ Massachusetts, Sch Med, Schizophrenia Res Program, Bipolar Disorder Program, Worcester, MA USA.
[Patel, Jayendra] Univ Massachusetts, Sch Med, Dept Psychiat, Ctr Psychopharmacol Res & Treatment, Worcester, MA 01655 USA.
[Sachs, Gary S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat,Bipolar Clin & Res Program, Boston, MA USA.
[Sklar, Pamela] Massachusetts Gen Hosp, Dept Psychiat, Ctr Human Genet Res, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA.
[Smoller, Jordan W.] Massachusetts Gen Hosp, Dept Psychiat, Psychiat Genet Program Mood & Anxiety Disorders, Boston, MA 02114 USA.
[Laird, Nan] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Thase, Michael E.] Univ Penn, Sch Med, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
RP Nimgaonkar, VL (reprint author), Univ Pittsburgh, Western Psychiat Inst & Clin, Grad Sch Publ Hlth, Dept Psychiat & Human Genet,Sch Med, 3811 Ohara St,Room 441, Pittsburgh, PA 15213 USA.
EM nimga+@pitt.edu
RI Allen, Michael/A-8776-2011; Lewis, David/G-4053-2014;
OI Lewis, David/0000-0002-3225-6778; FAGIOLINI, ANDREA/0000-0001-5827-0853;
Prasad, Konasale/0000-0003-0245-1393; Faraone,
Stephen/0000-0002-9217-3982
FU National Institutes of Health [MH63420, MH56242]; Mental Health
Intervention Research Center [MH30915, MH45156]; NIMH [MH56242, R01
MH060952-06]; NIH/NCRR/GCRC [M01 RR00056]; Calabrese NIMH [P20
MH-66054]; [UL1 RR024153]
FX We thank the research participants for their generous help. This
research was supported in part by grants from the National Institutes of
Health (MH63420, MH56242 to VLN, Mental Health Intervention Research
Center, MH30915 to DJK and MH45156). Recruitment of some of the
Pittsburgh controls was funded through NIMH grants (MH56242, R01
MH060952-06). This publication was also supported by funds received from
the c UL1 RR024153 and NIH/NCRR/GCRC Grant M01 RR00056 and Calabrese
NIMH P20 MH-66054. We thank Drs. Raymond Cho, Gordon Frankle, Gretchen
Haas, and the clinical core staff of the Center for the Neuroscience of
Mental Disorders (MH45156) for their assistance in diagnostic and
psychopathological assessments of some of the controls analyzed here.
NR 64
TC 82
Z9 83
U1 3
U2 10
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD NOV
PY 2009
VL 11
IS 7
BP 701
EP 710
PG 10
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 507BW
UT WOS:000270826100003
PM 19839995
ER
PT J
AU Ostacher, MJ
LeBeau, RT
Perlis, RH
Nierenberg, AA
Lund, HG
Moshier, SJ
Sachs, GS
Simon, NM
AF Ostacher, Michael J.
LeBeau, Richard T.
Perlis, Roy H.
Nierenberg, Andrew A.
Lund, Hannah G.
Moshier, Samantha J.
Sachs, Gary S.
Simon, Naomi M.
TI Cigarette smoking is associated with suicidality in bipolar disorder
SO BIPOLAR DISORDERS
LA English
DT Article
DE bipolar disorder; impulsivity; nicotine; smoking; substance abuse;
suicidality
ID TREATMENT ENHANCEMENT PROGRAM; SUBSTANCE USE DISORDERS; CLINICAL
PREDICTORS; MAJOR DEPRESSION; STEP-BD; IMPULSIVITY; AGGRESSION;
BEHAVIOR; ACTS; COMORBIDITY
AB Objectives:
Cigarette smoking in individuals with bipolar disorder has been associated with suicidal behavior, although the precise relationship between the two remains unclear.
Methods:
In this prospective observational study of 116 individuals with bipolar disorder, we examined the association between smoking and suicidality as measured by Linehan's Suicide Behaviors Questionnaire (SBQ) and prospective suicide attempts over a nine-month period. Impulsivity was measured by the Barratt Impulsiveness Scale.
Results:
Smoking was associated with higher baseline SBQ scores in univariate and adjusted analyses, but was not significant after statistical adjustment for impulsivity in a regression model. A higher proportion of smokers at baseline made a suicide attempt during the follow-up period (5/31, 16.1%) compared to nonsmokers (3/85, 3.5%); p = 0.031, odds ratio = 5.25 (95% confidence interval: 1.2-23.5). Smoking at baseline also significantly predicted higher SBQ score at nine months.
Conclusions:
In this study, current cigarette smoking was a predictor of current and nine-month suicidal ideation and behavior in bipolar disorder, and it is likely that impulsivity accounts for some of this relationship.
C1 [Ostacher, Michael J.] Massachusetts Gen Hosp, Bipolar Clin & Res Program, Boston, MA 02114 USA.
[Ostacher, Michael J.; Perlis, Roy H.; Nierenberg, Andrew A.; Sachs, Gary S.; Simon, Naomi M.] Harvard Univ, Sch Med, Boston, MA USA.
[Lund, Hannah G.] Virginia Commonwealth Univ, Dept Psychol, Richmond, VA 23284 USA.
RP Ostacher, MJ (reprint author), Massachusetts Gen Hosp, Bipolar Clin & Res Program, 50 Staniford St,Suite 580, Boston, MA 02114 USA.
EM mostacher@partners.org
OI Ostacher, Michael/0000-0003-0353-7535
FU MGH Claflin Distinguished Scholar Award (NMS) [N01MH-8001]; National
Institute of Mental Health (GSS); National Institute on Alcoholism and
Alcohol Abuse (MJO) [K23AA016340-01A1]
FX This study was supported by an MGH Claflin Distinguished Scholar Award
(NMS), grant N01MH-8001 from the National Institute of Mental Health
(GSS), and grant K23AA016340-01A1 from the National Institute on
Alcoholism and Alcohol Abuse (MJO).
NR 26
TC 34
Z9 34
U1 1
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD NOV
PY 2009
VL 11
IS 7
BP 766
EP 771
PG 6
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 507BW
UT WOS:000270826100010
PM 19840000
ER
PT J
AU Freytes, CO
Lazarus, HM
AF Freytes, C. O.
Lazarus, H. M.
TI Second hematopoietic SCT for lymphoma patients who relapse after
autotransplantation: another autograft or switch to allograft?
SO BONE MARROW TRANSPLANTATION
LA English
DT Review
DE second transplants; lymphoma; relapse
ID STEM-CELL TRANSPLANTATION; NON-HODGKINS-LYMPHOMA; BONE-MARROW
TRANSPLANTATION; MONOCLONAL-ANTIBODY THERAPY; PRIOR AUTOLOGOUS
TRANSPLANT; HIGH-DOSE CHEMOTHERAPY; ALLOGENEIC TRANSPLANTATION;
PROGRESSIVE DISEASE; FOLLICULAR LYMPHOMA; HEMATOLOGICAL MALIGNANCIES
AB Although autologous hematopoietic SCT (auto-HSCT) is the only potentially curative treatment for lymphoma that has relapsed after conventional chemotherapy, the prognosis of patients with disease recurrence after auto-HSCT is poor. Some highly selected patients can benefit from second transplants. One-third with late recurrence after initial auto-HSCT may attain a prolonged remission after second auto-HSCT. Non-myeloablative or reduced-intensity conditioning (RIC) allogeneic hematopoietic SCT (allo-HSCT) has been used successfully after auto-HSCT failures, especially in subjects who have an HLA-compatible donor, chemosensitive disease and good performance status. Patients with chemosenstive disease recurrence who have completed at least 1 year after their first auto-HSCT should be considered for a second auto-HSCT. Patients who have chemoresistant disease are best served by participation in a well-designed clinical trial examining novel antitumor agents. Bone Marrow Transplantation (2009) 44, 559-569; doi:10.1038/bmt.2009.214; published online 24 August 2009
C1 [Freytes, C. O.] Univ Texas Hlth Sci Ctr San Antonio, Dept Med Hematol & Med Oncol, BMTU 111, San Antonio, TX 78229 USA.
[Freytes, C. O.] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
[Lazarus, H. M.] Univ Hosp Case Med Ctr, Ireland Canc Ctr, Cleveland, OH USA.
[Lazarus, H. M.] Case Western Reserve Univ, Case Comprehens Canc Ctr, Cleveland, OH 44106 USA.
RP Freytes, CO (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Med Hematol & Med Oncol, BMTU 111, Mail Code 7880,7400 Merton Minter, San Antonio, TX 78229 USA.
EM Freytes@uthscsa.edu
NR 63
TC 6
Z9 8
U1 1
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 NOV
PY 2009
VL 44
IS 9
BP 559
EP 569
DI 10.1038/bmt.2009.214
PG 11
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 518AO
UT WOS:000271661700001
PM 19701250
ER
PT J
AU Ballen, K
AF Ballen, K.
TI Introduction to Cord Blood Special Issue
SO BONE MARROW TRANSPLANTATION
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 USA.
RP Ballen, K (reprint author), Massachusetts Gen Hosp, Div Hematol Oncol, Boston, MA 02114 USA.
EM kballen@partners.org
NR 0
TC 2
Z9 2
U1 0
U2 0
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 NOV
PY 2009
VL 44
IS 10
BP 619
EP 619
DI 10.1038/bmt.2009.279
PG 1
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 524XL
UT WOS:000272177600001
PM 19935808
ER
PT J
AU Cutler, C
Ballen, K
AF Cutler, C.
Ballen, K.
TI Reduced-intensity conditioning and umbilical cord blood transplantation
in adults
SO BONE MARROW TRANSPLANTATION
LA English
DT Review
DE reduced-intensity conditioning; umbilical cord blood; adults
ID BONE-MARROW; HEMATOLOGIC MALIGNANCIES; PREPARATIVE REGIMEN; UNRELATED
DONORS; SUCCESSFUL ENGRAFTMENT; LUNG INJURY; RECIPIENTS; LEUKEMIA;
FLUDARABINE; EXPERIENCE
AB Reduced-intensity conditioning (RIC) preparative regimens are now widely used in umbilical cord blood (UCB) transplantation. Developed to reduce the rate of transplant-related morbidity and mortality as in adult stem cell donor transplantation, they are becoming more widely accepted. Results from RIC UCB series show a shortened time to engraftment, ranging from 12 to 24 days, with rates of TRM that generally do not exceed the rates seen with myeloablative UCB transplantation. There does not seem to be a convincing trend toward an increase in the rate of malignant relapse after RIC UCB transplantation, despite the lower intensity of the conditioning regimen. In this review, the results from several RIC UCB series are reviewed, comparisons with myeloablative UCB experiences are made and hypotheses regarding the engraftment potential of UCB after RIC regimens are discussed. In addition, a strategy for the optimal use of RIC regimens and UCB transplantation is presented. Bone Marrow Transplantation (2009) 44, 667-671; doi: 10.1038/bmt.2009.283; published online 5 October 2009
C1 [Cutler, C.] Harvard Univ, Dept Med Oncol, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ballen, K.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Leukemia Program, Boston, MA 02115 USA.
RP Cutler, C (reprint author), Harvard Univ, Dept Med Oncol, Sch Med, Dana Farber Canc Inst, 44 Binney St,D1B13, Boston, MA 02115 USA.
EM corey_cutler@dfci.harvard.edu; kballen@partners.org
NR 30
TC 13
Z9 14
U1 0
U2 1
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 NOV
PY 2009
VL 44
IS 10
BP 667
EP 671
DI 10.1038/bmt.2009.283
PG 5
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 524XL
UT WOS:000272177600008
PM 19802028
ER
PT J
AU Thibert, RL
Burns, JD
Bhadelia, R
Takeoka, M
AF Thibert, Ronald L.
Burns, Joseph D.
Bhadelia, Rafeeque
Takeoka, Masanori
TI Reversible uncal herniation in a neonate with a large MCA infarct
SO BRAIN & DEVELOPMENT
LA English
DT Article
DE Neonate; Stroke; Uncal herniation
ID INTRACRANIAL-PRESSURE; CEREBRAL INFARCTION; SPACE
AB Uncal herniation due to a large cerebral infarct is well-described in adults, with high rates of morbidity and mortality. This phenomenon, however, has not been previously reported in neonates. We present a newborn male delivered via cesarean section with difficult extraction who presented with frequent seizures. He was found to have an acute left MCA territory infarct secondary to an M I occlusion detected on MRI/MRA. He became lethargic and developed a left uncal herniation on CT at 72 h of life. He was treated medically with osmolar agents and hemodynamic support, and had resolution of the herniation on CT at 120 h of life. At 19 months he had residual moderate right hemiparesis with only mild gait disturbance and mild speech delay. As seen in this case, uncal herniation, though rare, may occur in neonates. Also, the outcome for this neonate was much better than for typical adults with a similar disease course. (C) 2008 Elsevier B.V. All rights reserved.
C1 [Takeoka, Masanori] Childrens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Thibert, Ronald L.] Massachusetts Gen Hosp, Pediat Epilepsy Program, Boston, MA 02114 USA.
[Thibert, Ronald L.; Bhadelia, Rafeeque; Takeoka, Masanori] Harvard Univ, Sch Med, Boston, MA USA.
[Burns, Joseph D.] Mayo Clin, Dept Neurol, Rochester, MN USA.
[Bhadelia, Rafeeque] Beth Israel Deaconess Med Ctr, Dept Neuroradiol, Boston, MA 02215 USA.
[Thibert, Ronald L.; Burns, Joseph D.; Takeoka, Masanori] Floating Hosp Children, Div Pediat Neurol, Boston, MA USA.
[Bhadelia, Rafeeque] Tufts Univ New England Med Ctr, Dept Neuroradiol, Boston, MA USA.
RP Takeoka, M (reprint author), Childrens Hosp, Dept Neurol, Fegan 9,300 Longwood Ave, Boston, MA 02115 USA.
EM Masanori.Takeoka@childrens.harvard.edu
OI Burns, Joseph/0000-0003-4158-616X
NR 10
TC 2
Z9 2
U1 0
U2 0
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 NOV
PY 2009
VL 31
IS 10
BP 763
EP 765
DI 10.1016/j.braindev.2008.11.003
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 520CU
UT WOS:000271818400009
PM 19097834
ER
PT J
AU Ghosh-Choudhury, T
Mandal, CC
Woodruff, K
St Clair, P
Fernandes, G
Choudhury, GG
Ghosh-Choudhury, N
AF Ghosh-Choudhury, Triparna
Mandal, Chandi C.
Woodruff, Kathleen
St Clair, Patricia
Fernandes, Gabriel
Choudhury, Goutam G.
Ghosh-Choudhury, Nandini
TI Fish oil targets PTEN to regulate NF kappa B for downregulation of
anti-apoptotic genes in breast tumor growth
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Review
DE PTEN; NF kappa B; DHA; EPA; Breast tumor growth; Apoptotic signal
ID PROTEIN-KINASE B; PHOSPHATIDYLINOSITOL 3-KINASE/AKT PATHWAY; PROMOTES
CELL-SURVIVAL; CANCER-CELLS; PHOSPHOINOSITIDE 3-KINASE; SIGNALING
PATHWAY; PROSTATE-CANCER; BMP-2 GENE; OSTEOBLAST DIFFERENTIATION;
TRANSCRIPTION FACTOR
AB The molecular mechanism for the beneficial effect of fish oil on breast tumor growth is largely undefined. Using the xenograft model in nude mice, we for the first time report that the fish oil diet significantly increased the level of PTEN protein in the breast tumors. In addition, the fish oil diet attenuated the PI 3 kinase and Akt kinase activity in the tumors leading to significant inhibition of NF kappa B activation. Fish oil diet also prevented the expression of anti-apoptotic proteins Bcl-2 and Bcl-XL in the breast tumors with concomitant increase in caspase 3 activity. To extend these findings we tested the functional effects of DHA and EPA, the two active x-3 fatty acids of fish oil, on cultured MDA MB-231 cells. In agreement with our in vivo data, DHA and EPA treatment increased PTEN mRNA and protein expression and inhibited the phosphorylation of p65 subunit of NF kappa B in MDA MB-231 cells. Furthermore, DHA and EPA reduced expression of Bcl-2 and Bcl-XL. NF kappa B DNA binding activity and NF kappa B-dependent transcription of Bcl-2 and Bcl-XL genes were also prevented by DHA and EPA treatment. Finally, we showed that PTEN expression significantly inhibited NF kappa B-dependent transcription of Bcl-2 and Bcl-XL genes. Taken together, our data reveals a novel signaling pathway linking the fish oil diet to increased PTEN expression that attenuates the growth promoting signals and augments the apoptotic signals, resulting in breast tumor regression.
C1 [Ghosh-Choudhury, Triparna; Mandal, Chandi C.; Woodruff, Kathleen; St Clair, Patricia; Ghosh-Choudhury, Nandini] Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, San Antonio, TX 78229 USA.
[Choudhury, Goutam G.] Educ & Clin Ctr, San Antonio, TX USA.
[Choudhury, Goutam G.; Ghosh-Choudhury, Nandini] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
RP Ghosh-Choudhury, N (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, San Antonio, TX 78229 USA.
EM choudhury@uthscsa.edu
FU NIH [RO1 AR52425, RO1 DK 50190, RO1 AG023648]; DOD Breast cancer Concept
Award; Morrison Trust Fund; VA Merit Review grants; Juvenile Diabetes
Research Foundation; Department of Veterans Affairs
FX This work was supported by the NIH RO1 AR52425, DOD Breast cancer
Concept Award, Morrison Trust Fund and VA Merit Review grants to NGC.
GGC is supported by NIH RO1 DK 50190, VA Merit Review and Juvenile
Diabetes Research Foundation Regular Research Grants. GGC is recipient
of the Research Career Scientist Award from the Department of Veterans
Affairs. GF is supported by NIH RO1 AG023648.
NR 118
TC 45
Z9 46
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD NOV
PY 2009
VL 118
IS 1
BP 213
EP 228
DI 10.1007/s10549-008-0227-7
PG 16
WC Oncology
SC Oncology
GA 505YI
UT WOS:000270737800023
PM 18953692
ER
PT J
AU Vogl, DT
Stadtmauer, EA
Richardson, PG
Sonneveld, P
Schuster, MW
Irwin, D
Facon, T
Harousseau, JL
Boral, A
Neuwirth, R
Anderson, KC
AF Vogl, Dan T.
Stadtmauer, Edward A.
Richardson, Paul G.
Sonneveld, Pieter
Schuster, Michael W.
Irwin, David
Facon, Thierry
Harousseau, Jean-Luc
Boral, Anthony
Neuwirth, Rachel
Anderson, Kenneth C.
TI Impact of prior therapies on the relative efficacy of bortezomib
compared with dexamethasone in patients with relapsed/refractory
multiple myeloma
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE bortezomib; multiple myeloma; sequence; stem cell transplantation;
thalidomide
ID LENALIDOMIDE PLUS DEXAMETHASONE; CELL TRANSPLANTATION; RANDOMIZED-TRIAL;
THALIDOMIDE; CHEMOTHERAPY; MELPHALAN
AB This subgroup analysis of the phase III APEX (Assessment of Proteasome Inhibition for Extending Remissions) trial examined whether prior exposure to specific therapies affected the relative efficacy of bortezomib versus dexamethasone in relapsed/refractory myeloma. Time to progression and overall survival were superior with bortezomib in all subgroups, with no evidence of interaction between any prior therapies and assignment to study therapy. Patients with prior thalidomide exposure had worse outcomes overall, but neither prior thalidomide nor prior autologous stem cell transplantation affected the relative efficacy of bortezomib versus dexamethasone. These results confirm the superiority of bortezomib over dexamethasone, regardless of prior exposure to specific therapies (clinicaltrials. gov: NCT00048230).
C1 [Vogl, Dan T.; Stadtmauer, Edward A.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Richardson, Paul G.; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Sonneveld, Pieter] Univ Rotterdam Hosp, Rotterdam, Netherlands.
[Schuster, Michael W.] New York Presbyterian Hosp, New York, NY USA.
[Irwin, David] Alta Bates Canc Ctr, Berkeley, CA USA.
[Facon, Thierry] Hop Claude Huriez, Lille, France.
[Harousseau, Jean-Luc] Hop Hotel Dieu, Nantes, France.
[Boral, Anthony; Neuwirth, Rachel] Millennium Pharmaceut Inc, Cambridge, MA USA.
RP Vogl, DT (reprint author), Univ Penn, Abramson Canc Ctr, Perelman Ctr Room 2-189,3400 Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM Dan.Vogl@uphs.upenn.edu
RI FACON, THIERRY/M-9736-2014;
OI FACON, THIERRY/0000-0001-7705-8460; Vogl, Dan/0000-0002-2935-2566
NR 12
TC 20
Z9 21
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2009
VL 147
IS 4
BP 531
EP 534
DI 10.1111/j.1365-2141.2009.07875.x
PG 4
WC Hematology
SC Hematology
GA 512IN
UT WOS:000271240900012
PM 19725827
ER
PT J
AU Tammam, J
Ware, C
Efferson, C
O'Neil, J
Rao, S
Qu, X
Gorenstein, J
Angagaw, M
Kim, H
Kenific, C
Kunii, K
Leach, KJ
Nikov, G
Zhao, J
Dai, X
Hardwick, J
Scott, M
Winter, C
Bristow, L
Elbi, C
Reilly, JF
Look, T
Draetta, G
Van der Ploeg, LHT
Kohl, NE
Strack, PR
Majumder, PK
AF Tammam, J.
Ware, C.
Efferson, C.
O'Neil, J.
Rao, S.
Qu, X.
Gorenstein, J.
Angagaw, M.
Kim, H.
Kenific, C.
Kunii, K.
Leach, K. J.
Nikov, G.
Zhao, J.
Dai, X.
Hardwick, J.
Scott, M.
Winter, C.
Bristow, L.
Elbi, C.
Reilly, J. F.
Look, T.
Draetta, G.
Van der Ploeg, L. H. T.
Kohl, N. E.
Strack, P. R.
Majumder, P. K.
TI Down-regulation of the Notch pathway mediated by a gamma-secretase
inhibitor induces anti-tumour effects in mouse models of T-cell
leukaemia
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE gamma-secretase inhibitor; Notch; T-ALL; mitochondria; apoptosis
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; CHRONIC MYELOID-LEUKEMIA; C-MYC;
PROGNOSTIC-SIGNIFICANCE; TREATMENT RESPONSE; PROGENITOR CELLS;
APOPTOSIS; MUTATIONS; ACTIVATION; EXPRESSION
AB Background and purpose:
gamma-Secretase inhibitors (GSIs) block NOTCH receptor cleavage and pathway activation and have been under clinical evaluation for the treatment of malignancies such as T-cell acute lymphoblastic leukaemia (T-ALL). The ability of GSIs to decrease T-ALL cell viability in vitro is a slow process requiring > 8 days, however, such treatment durations are not well tolerated in vivo. Here we study GSI's effect on tumour and normal cellular processes to optimize dosing regimens for anti-tumour efficacy.
Experimental approach:
Inhibition of the Notch pathway in mouse intestinal epithelium was used to evaluate the effect of GSIs and guide the design of dosing regimens for xenograft models. Serum A beta(40) and Notch target gene modulation in tumours were used to evaluate the degree and duration of target inhibition. Pharmacokinetic and pharmacodynamic correlations with biochemical, immunohistochemical and profiling data were used to demonstrate GSI mechanism of action in xenograft tumours.
Key results:
Three days of > 70% Notch pathway inhibition was sufficient to provide an anti-tumour effect and was well tolerated. GSI-induced conversion of mouse epithelial cells to a secretory lineage was time- and dose-dependent. Anti-tumour efficacy was associated with cell cycle arrest and apoptosis that was in part due to Notch-dependent regulation of mitochondrial homeostasis.
Conclusions and implications:
Intermittent but potent inhibition of Notch signalling is sufficient for anti-tumour efficacy in these T-ALL models. These findings provide support for the use of GSI in Notch-dependent malignancies and that clinical benefits may be derived from transient but potent inhibition of Notch.
C1 [Tammam, J.; Efferson, C.; Kunii, K.; Scott, M.; Bristow, L.; Van der Ploeg, L. H. T.; Kohl, N. E.; Majumder, P. K.] Merck Res Labs, Dept Oncol Pharmacol, Boston, MA 02115 USA.
[Ware, C.; Qu, X.; Reilly, J. F.] Merck Res Labs, Dept Pharmacol, Boston, MA 02115 USA.
[Rao, S.; Gorenstein, J.; Kim, H.; Winter, C.; Elbi, C.; Draetta, G.; Van der Ploeg, L. H. T.; Majumder, P. K.] Merck Res Labs, Dept Canc Pathways Canc Biol & Therapeut, Boston, MA 02115 USA.
[Angagaw, M.] Merck Res Labs, Dept Lab Anim Res, Boston, MA 02115 USA.
[O'Neil, J.; Look, T.; Van der Ploeg, L. H. T.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Kenific, C.; Van der Ploeg, L. H. T.] Merck Res Labs, Dept Neuropharmacol, Boston, MA 02115 USA.
[Leach, K. J.; Nikov, G.; Zhao, J.] Merck Res Labs, Dept Drug Metab & Pharmacokinet, Boston, MA 02115 USA.
[Dai, X.; Hardwick, J.] Merck Res Labs, West Point, PA USA.
RP Majumder, PK (reprint author), Merck Res Labs, Dept Oncol Pharmacol, 33 Ave Louis Pasteur, Boston, MA 02115 USA.
EM Pradip_Majumder@merck.com
NR 53
TC 48
Z9 51
U1 0
U2 3
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1188
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD NOV
PY 2009
VL 158
IS 5
BP 1183
EP 1195
DI 10.1111/j.1476-5381.2009.00389.x
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 509FW
UT WOS:000271001400002
PM 19775282
ER
PT J
AU Pearson, KH
AF Pearson, Kimberly H.
TI Cognitive behavior therapy and eating disorders
SO BRITISH JOURNAL OF PSYCHOLOGY
LA English
DT Book Review
C1 [Pearson, Kimberly H.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Pearson, Kimberly H.] Massachusetts Gen Hosp, Eating Disorder Program, Boston, MA 02114 USA.
RP Pearson, KH (reprint author), Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU BRITISH PSYCHOLOGICAL SOC
PI LEICESTER
PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND
SN 0007-1269
J9 BRIT J PSYCHOL
JI Br. J. Psychol.
PD NOV
PY 2009
VL 100
BP 804
EP 806
DI 10.1348/000712609X464380
PG 4
WC Psychology, Multidisciplinary
SC Psychology
GA 509PY
UT WOS:000271031700013
ER
PT J
AU Horst, D
Budczies, J
Brabletz, T
Kirchner, T
Hlubek, F
AF Horst, David
Budczies, Jan
Brabletz, Thomas
Kirchner, Thomas
Hlubek, Falk
TI Invasion Associated Up-Regulation of Nuclear Factor kappa B Target Genes
in Colorectal Cancer
SO CANCER
LA English
DT Article
DE nuclear factor kappa B; target genes; colorectal cancer; invasion;
inflammation; up-regulation
ID MESSENGER-RNA EXPRESSION; BETA-CATENIN EXPRESSION; TRANSCRIPTION FACTOR;
INFLAMMATORY DISEASES; COLON-CARCINOMA; TENASCIN-C; MICROENVIRONMENT;
TRANSFORMATION; ACTIVATION; TUMORS
AB BACKGROUND: Colorectal cancer (CRC) displays intratumoral heterogeneity with less differentiated tumor cells at the invasive front (IF) than in the tumor center (TC). The authors previously observed that several genes were overexpressed at the IF of CRC with relations to inflammatory processes. Because nuclear factor kappa B (NF-kappa B), a dimeric transcription factor, is a major regulator of such processes, and because its target genes are involved in immune response, cell growth control, and cell survival, the expression of NF-kappa B target genes was investigated comparatively in CRC. METHODS: By using gene array profiling, NF-kappa B target gene expression was assessed in CRCs that expressed human mutL homolog 1 (hMLH1), hMSH2, and nuclear beta-catenin by comparing expression at the IF, in the TC, and in normal mucosa. In addition, 5 NF-kappa B target genes with high differential expression were validated by using immunohistochemistry. RESULTS: The expression of NF-kappa B target genes in the TC, at the IF, and in normal mucosa was distinct; whereas, specifically at the IF, most differentially expressed NF-kappa B targets were up-regulated. Moreover, the results indicated that the expression diverged between epithelial tumor cells and inflammatory stromal cells. CONCLUSIONS: Because the results demonstrated that inflammation and the activation of NF-kappa B signaling promoted CRC invasiveness, the current study provided further evidence that downstream targets of NF-kappa B signaling may be specifically relevant in invasion and progression of CRC. Finally, as has been suggested for colitis-associated cancer, the authors of this report concluded that the inhibition of NF-kappa B signaling also may be an additional option for the treatment of sporadic CRC. Cancer 2009;115:4946-58. (C) 2009 American Cancer Society.
C1 [Horst, David; Kirchner, Thomas; Hlubek, Falk] Univ Munich, Inst Pathol, D-8000 Munich, Germany.
[Budczies, Jan] Charite, Inst Pathol, D-13353 Berlin, Germany.
[Brabletz, Thomas] Univ Freiburg, Comprehens Canc Ctr & Visceral Surg, Freiburg, Germany.
RP Horst, D (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM DavidN_Horst@dfci.harvard.edu
NR 46
TC 29
Z9 32
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 1
PY 2009
VL 115
IS 21
BP 4946
EP 4958
DI 10.1002/cncr.24564
PG 13
WC Oncology
SC Oncology
GA 511LY
UT WOS:000271167900011
PM 19658179
ER
PT J
AU Carpenter, WR
Godley, PA
Clark, JA
Talcott, JA
Finnegan, T
Mishel, M
Bensen, J
Rayford, W
Su, LJ
Fontham, ETH
Mohler, JL
AF Carpenter, William R.
Godley, Paul A.
Clark, Jack A.
Talcott, James A.
Finnegan, Timothy
Mishel, Merle
Bensen, Jeannette
Rayford, Walter
Su, L. Joseph
Fontham, Elizabeth T. H.
Mohler, James L.
TI Racial Differences in Trust and Regular Source of Patient Care and the
Implications for Prostate Cancer Screening Use
SO CANCER
LA English
DT Article
DE African American; Caucasian American; continuity of care; prostate
cancer; screening; source of care; physician mistrust
ID CLINICAL PREVENTIVE SERVICES; EMERGENCY-DEPARTMENT; ETHNIC DISPARITIES;
AFRICAN-AMERICAN; UNITED-STATES; HEALTH; PHYSICIAN; MEDICINE;
SATISFACTION; EXPERIENCE
AB BACKGROUND: Nonmedical factors may modify the biological risk of prostate cancer (PCa) and contribute to the differential use of early detection; curative care; and, ultimately, greater racial disparities in PCa mortality. In this study, the authors examined patients' usual source of care, continuity of care, and mistrust of physicians and their association with racial differences in PCa screening. METHODS: Study nurses conducted in-home interviews of 1031 African-American men and Caucasian-American men aged >= 50 years in North Carolina and Louisiana within weeks of their PCa diagnosis. Medical records were abstracted, and the data were used to conduct bivariate and multivariate analyses. RESULTS: Compared with African Americans, Caucasian Americans exhibited higher physician trust scores and a greater likelihood of reporting a physician office as their usual source of care, seeing the same physician at regular medical encounters, and historically using any PCa screening. Seeing the same physician for regular care was associated with greater trust and screening use. Men who reported their usual source of care as a physician office, hospital clinic, or Veterans Administration facility were more likely to report prior PCa screening than other men. In multivariate regression analysis, seeing the same provider remained associated with prior screening use, whereas both race and trust lost their association with prior screening. CONCLUSIONS: The current results indicated that systems factors, including those that differ among different sources of care and those associated with the continuity of care, may provide tangible targets to address disparities in the use of PCa early detection, may attenuate racial differences in PCa screening use, and may contribute to reduced racial disparities in PCa mortality. Cancer 2009;115:5048-59. Published 2009 by the American Cancer Society*.
C1 [Carpenter, William R.] Univ N Carolina, Dept Hlth Policy & Management, Sch Publ Hlth, Chapel Hill, NC 27599 USA.
[Carpenter, William R.; Godley, Paul A.; Bensen, Jeannette; Mohler, James L.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Carpenter, William R.; Godley, Paul A.] Univ N Carolina, Cecil G Sheps Ctr Hlth Serv Res, Chapel Hill, NC 27599 USA.
[Carpenter, William R.] N Carolina Comprehens Canc Program, Raleigh, NC USA.
[Godley, Paul A.; Finnegan, Timothy] Univ N Carolina, Sch Med, Dept Med, Chapel Hill, NC 27599 USA.
[Godley, Paul A.; Bensen, Jeannette] Univ N Carolina, Sch Publ Hlth, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Clark, Jack A.] Boston Univ, Sch Publ Hlth, Edith Nourse Rogers Mem Vet Hosp, Ctr Hlth Qual Outcomes & Econ Res, Boston, MA USA.
[Talcott, James A.] Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Ctr Outcomes Res,Med Sch, Boston, MA 02114 USA.
[Mishel, Merle] Univ N Carolina, Sch Nursing, Chapel Hill, NC 27599 USA.
[Rayford, Walter] Univ Tennessee, Dept Prevent Med, Sch Med, Memphis, TN USA.
[Su, L. Joseph; Fontham, Elizabeth T. H.] Louisiana State Univ, Sch Publ Hlth, Hlth Sci Ctr, New Orleans, LA USA.
[Mohler, James L.] Roswell Pk Canc Inst, Dept Urol Oncol, Buffalo, NY 14263 USA.
[Mohler, James L.] SUNY Buffalo, Dept Urol, Buffalo, NY 14260 USA.
RP Carpenter, WR (reprint author), Univ N Carolina, Dept Hlth Policy & Management, Sch Publ Hlth, 1102 McGavran Greenberg Hall,CB 7411, Chapel Hill, NC 27599 USA.
EM wrc4@email.unc.edu
RI Carpenter, William/E-5125-2013;
OI Clark, Jack/0000-0002-7424-1670
FU Department of Defense [DAMD 17-03-2-0052]; National Cancer Institute
[R25T CA 57726]
FX The North Carolina-Louisiana Prostate Cancer Project is performed as a
collaborative study supported by the Department of Defense contract DAMD
17-03-2-0052. Dr. Carpenter was supported by a training grant from the
National Cancer Institute (R25T CA 57726).
NR 52
TC 47
Z9 48
U1 2
U2 6
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 1
PY 2009
VL 115
IS 21
BP 5048
EP 5059
DI 10.1002/cncr.24539
PG 12
WC Oncology
SC Oncology
GA 511LY
UT WOS:000271167900021
PM 19637357
ER
PT J
AU Chen, LL
Nolan, ME
Silverstein, MJ
Mihm, MC
Sober, AJ
Tanabe, KK
Smith, BL
Younger, J
Michaelson, JS
AF Chen, L. Leon
Nolan, Matthew E.
Silverstein, Melvin J.
Mihm, Martin C., Jr.
Sober, Arthur J.
Tanabe, Kenneth K.
Smith, Barbara L.
Younger, Jerry
Michaelson, James S.
TI The Impact of Primary Tumor Size, Lymph Node Status, and Other
Prognostic Factors on the Risk of Cancer Death
SO CANCER
LA English
DT Article
DE cancer death; risk; prediction; tumor size; lymph node status;
prognostic factors; breast cancer; melanoma
ID BREAST-CANCER; SURVIVAL
AB BACKGROUND: Although many prognostic factors are associated with differences in cancer lethality, it may not be obvious whether a factor truly makes an independent contribution to lethality or simply is correlated with tumor size. There is currently no method for integrating tumor size, lymph node status, and other prognostic information from a patient into a single risk of death estimate. METHODS: The SizeOnly equation, which captures the relation between tumor size and risk of death, makes it possible to determine whether a prognostic factor truly makes an independent contribution to cancer lethally or merely is associated with tumor size (SizeAssessment method). The magnitude of each factor's lethal contribution can be quantified by a parameter, g, inserted into the SizeOnly equation (PrognosticMeasurement method). A series of linked equations (the Size+Nodes+PrognosticFactors [SNAP] method) combines information on tumor size, lymph node status, and other prognostic factors from a patient into a single estimate of the risk of death, RESULTS: Nine prognostic factors were identified that made marked, independent contributions to breast carcinoma lethality: grade; mucinous, medullary, tubular, and scirrhous adenocarcinoma; male sex; inflammatory disease; Paget disease; and lymph node status. In addition, it was determined that lymph node status made an independent contribution to melanoma lethality. The SNAP method was able to accurately estimate the risk of death and to finely stratify patients by risk. CONCLUSIONS: The methods described provide a new framework for identifying and quantifying those factors that contribute to cancer lethality and provide a basis for web-based calculators (available at: http://www.CancerMath.net accessed July 29, 2009) that accurately estimate the risk of death for each patient. Cancer 2009;115:5071-83. (C) 2009 American Cancer Society.
C1 [Michaelson, James S.] Massachusetts Gen Hosp, Div Surg Oncol, Dept Surg, Boston, MA 02114 USA.
[Silverstein, Melvin J.] Hoag Mem Hosp, Breast Serv, Newport Beach, CA USA.
[Mihm, Martin C., Jr.; Michaelson, James S.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Mihm, Martin C., Jr.; Michaelson, James S.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Sober, Arthur J.] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Sober, Arthur J.] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Tanabe, Kenneth K.; Smith, Barbara L.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Younger, Jerry] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Younger, Jerry] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Michaelson, JS (reprint author), Massachusetts Gen Hosp, Div Surg Oncol, Dept Surg, Yawkey Bldg 7,32 Fruit St, Boston, MA 02114 USA.
EM michaelj@helix.mgh.harvard.edu
FU Massachusetts General Hospital
FX Supported by institutional funding to the Massachusetts General
Hospital.
NR 16
TC 12
Z9 12
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 1
PY 2009
VL 115
IS 21
BP 5071
EP 5083
DI 10.1002/cncr.24565
PG 13
WC Oncology
SC Oncology
GA 511LY
UT WOS:000271167900023
PM 19658184
ER
PT J
AU Michaelson, JS
Chen, LL
Silverstein, MJ
Cheongsiatmoy, JA
Mihm, MC
Sober, AJ
Tanabe, KK
Smith, BL
Younger, J
AF Michaelson, James S.
Chen, L. Leon
Silverstein, Melvin J.
Cheongsiatmoy, Justin A.
Mihm, Martin C., Jr.
Sober, Arthur J.
Tanabe, Kenneth K.
Smith, Barbara L.
Younger, Jerry
TI Why Cancer at the Primary Site and in the Lymph Nodes Contributes to the
Risk of Cancer Death
SO CANCER
LA English
DT Article
DE cancer death; risk; prediction; tumor size; lymph node status; breast
cancer; melanoma; metastasis
ID TUMOR SIZE; BREAST-CANCER; METASTASIS; CARCINOMA; GENES; PROGRESSION
AB BACKGROUND: Cancer at both the primary site and in the lymph nodes is associated with lethality, although the mechanism by which lethality arises from each site has been poorly understood. For breast carcinoma, each positive lymph node contributes an approximately 6% risk of death, and each millimeter of primary tumor greatest dimension contributes approximately 1%; whereas, for melanoma, each positive lymph node contributes an approximately 23% risk, and each millimeter of tumor thickness contributes approximately 8%: This is described by a pair of linked equations, the Size+Nodes method. METHODS: A simple expression, the ProbabilityEstimation equation, which was derived from the authors' binary-biologic model of cancer metastasis, was used to calculate the probabilities of spread of cancer cells from data on tumor size, lymph node status, and death rate. RESULTS: In this report, the authors demonstrated, that when similar masses of cancer are compared, the chance of lethal spread of a cancer cell to the periphery is approximately the same whether the spread emerges from a lymph node or from the primary site. The greater the number of cells at the primary site (tumor size) or the greater the number of cells in the lymph nodes (number of positive lymph nodes), the greater is the aggregate chance that 1 or more cells has undergone a lethal event of spread, a process captured by the Size+Nodes equations. CONCLUSIONS: The lethal contributions of cancer at the primary site and lymph nodes can be explained by a simple mechanical process of the spread of cancer cells occurring with definable probabilities per cell. The presence of cancer in the lymph nodes does not indicate an intrinsic change in a malignancy but, rather, an increased mass of cancer from which spread can emerge. Cancer 2009;115:5084-94. (C) 2009 American Cancer Society.
C1 [Michaelson, James S.] Massachusetts Gen Hosp, Div Surg Oncol, Dept Pathol, Boston, MA 02114 USA.
[Michaelson, James S.; Chen, L. Leon; Cheongsiatmoy, Justin A.; Tanabe, Kenneth K.; Smith, Barbara L.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Michaelson, James S.; Mihm, Martin C., Jr.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Silverstein, Melvin J.] Hoag Mem Hosp, Breast Serv, Newport Beach, CA USA.
[Sober, Arthur J.] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Sober, Arthur J.] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Tanabe, Kenneth K.; Smith, Barbara L.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Younger, Jerry] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Younger, Jerry] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Michaelson, JS (reprint author), Massachusetts Gen Hosp, Div Surg Oncol, Dept Pathol, Yawkey Bldg 7,32 Fruit St, Boston, MA 02114 USA.
EM michaelj@helix.mgh.harvard.edu
FU Massachusetts General Hospital
FX Supported by institutional funding of the Massachusetts General
Hospital.
NR 20
TC 11
Z9 11
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 1
PY 2009
VL 115
IS 21
BP 5084
EP 5094
DI 10.1002/cncr.24542
PG 11
WC Oncology
SC Oncology
GA 511LY
UT WOS:000271167900024
PM 19670457
ER
PT J
AU Michaelson, JS
Chen, LL
Silverstein, MJ
Mihm, MC
Sober, AJ
Tanabe, KK
Smith, BL
Younger, J
AF Michaelson, James S.
Chen, L. Leon
Silverstein, Melvin J.
Mihm, Martin C., Jr.
Sober, Arthur J.
Tanabe, Kenneth K.
Smith, Barbara L.
Younger, Jerry
TI How Cancer at the Primary Site and in the Lymph Nodes Contributes to the
Risk of Cancer Death
SO CANCER
LA English
DT Article
DE cancer death; risk; prediction; tumor size; lymph node status; breast
cancer; melanoma
ID RENAL-CELL CARCINOMA; BREAST-CANCER; TUMOR SIZE; SURVIVAL; MORPHOMETRY;
VALIDATION; RECURRENCE; MELANOMA; IMPACT
AB BACKGROUND: It has long been appreciated that tumor size, lymph node status, and patient survival are related qualities, although how to isolate their interactions has not been obvious, nor has it been obvious how to integrate tumor size and lymph node status into predictions of the risk of death for individual patients. METHODS: The authors describe a mathematical method, the binary-biological model of cancer metastasis, based on the spread of cancer cells, in which the equations capture the relations between tumor size, lymph node status, and cancer lethality. RESULTS: For melanoma, renal cell carcinoma, and breast carcinoma, the relation between tumor size and the risk of cancer death was captured by the SizeOnly equation. For melanoma and breast carcinoma, the relation between tumor size and the presence of cancer in the lymph nodes was captured by using the NodalSizeOnly equation. For lymph node-negative melanoma and breast carcinoma, the relation between tumor size and risk of death was captured by the PrimarySizeOnly equation. For breast carcinoma, the model indicated that each positive lymph node contributed similar to 6% extra risk of death, whereas each millimeter of greatest primary tumor dimension contributed similar to 1% risk of death. For melanoma, each positive lymph node contributed similar to 23% risk of death, whereas each millimeter of primary melanoma thickness contributed similar to 8% risk of death. This information was captured by a pair of linked equations, the Size+Nodes method. CONCLUSIONS: Both tumor size and the number of positive lymph nodes made independent contributions to the risk of cancer death, as estimated by using the Size+Nodes method. Cancer 2009;115:5095-107. (C) 2009 American Cancer Society.
C1 [Michaelson, James S.] Massachusetts Gen Hosp, Div Surg Oncol, Dept Pathol, Boston, MA 02114 USA.
[Michaelson, James S.; Chen, L. Leon; Tanabe, Kenneth K.; Smith, Barbara L.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Michaelson, James S.; Mihm, Martin C., Jr.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Silverstein, Melvin J.] Hoag Mem Hosp, Breast Serv, Newport Beach, CA USA.
[Sober, Arthur J.] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Sober, Arthur J.] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Tanabe, Kenneth K.; Smith, Barbara L.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Younger, Jerry] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Younger, Jerry] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
RP Michaelson, JS (reprint author), Massachusetts Gen Hosp, Div Surg Oncol, Dept Pathol, Yawkey Bldg 7,32 Fruit St, Boston, MA 02114 USA.
EM michaelj@helix.mgh.harvard.edu
FU Massachusetts General Hospital
FX Supported by institutional funding of the Massachusetts General
Hospital.
NR 20
TC 6
Z9 7
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 1
PY 2009
VL 115
IS 21
BP 5095
EP 5107
DI 10.1002/cncr.24592
PG 13
WC Oncology
SC Oncology
GA 511LY
UT WOS:000271167900025
PM 19670458
ER
PT J
AU Ramos, AH
Dutt, A
Mermel, C
Perner, S
Cho, J
Lafargue, CJ
Johnson, LA
Stiedl, AC
Tanaka, KE
Bass, AJ
Barretina, J
Weir, BA
Beroukhim, R
Thomas, RK
Minna, JD
Chirieac, LR
Lindeman, NI
Giordano, T
Beer, DG
Wagner, P
Wistuba, II
Rubin, MA
Meyerson, M
AF Ramos, Alex H.
Dutt, Amit
Mermel, Craig
Perner, Sven
Cho, Jeonghee
Lafargue, Christopher J.
Johnson, Laura A.
Stiedl, Ann-Cathrin
Tanaka, Kumiko E.
Bass, Adam J.
Barretina, Jordi
Weir, Barbara A.
Beroukhim, Rameen
Thomas, Roman K.
Minna, John D.
Chirieac, Lucian R.
Lindeman, Neal I.
Giordano, Thomas
Beer, David G.
Wagner, Patrick
Wistuba, Ignacio I.
Rubin, Mark A.
Meyerson, Matthew
TI Amplification of chromosomal segment 4q12 in non-small cell lung cancer
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE NSCLC; lung cancer; PDGFRA; KIT; sunitinib; imatinib; amplification;
4q12
ID GROWTH-FACTOR RECEPTOR; GASTROINTESTINAL STROMAL TUMORS;
GLIOBLASTOMA-MULTIFORME; KINASE INHIBITORS; SOMATIC MUTATIONS;
PDGFR-ALPHA; GENE; KIT; ADENOCARCINOMA; SUNITINIB
AB In cancer, proto-oncogenes are often altered by genomic amplification. Here we report recurrent focal amplifications of chromosomal segment 4q12 overlapping the proto-oncogenes PDGFRA and KIT in non-small cell lung cancer (NSCSCLC). Single nucleotide polymorphism (SNP) array and fluorescent in situ hybridization (FISH) analysis indicate that 4q12 is amplified in 3-7% of lung adenocarcinomas and 8-10% of lung squamous cell carcinomas. In addition, we demonstrate that the NSCLC cell line NCI-H1703 exhibits focal amplification of PDGFRA and is dependent on PDGFR alpha activity for cell growth. Treatment of NCI-H1703 cells with PDGFRA-specific shRNAs or with the PDGFR alpha/KIT small molecule inhibitors imatinib or sunitinib leads to cell growth inhibition. However, these observations do not extend to NSCLC cell lines with lower-amplitude and broader gains of chromosome 4q. Together these observations implicate PDGFRA and KIT as potential oncogenes in NSCLC, but further study is needed to define the specific characteristics of those tumors that could respond to PDGFR alpha/KIT inhibitors.
C1 [Ramos, Alex H.; Dutt, Amit; Mermel, Craig; Cho, Jeonghee; Johnson, Laura A.; Tanaka, Kumiko E.; Bass, Adam J.; Barretina, Jordi; Weir, Barbara A.; Beroukhim, Rameen; Meyerson, Matthew] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Ramos, Alex H.; Dutt, Amit; Mermel, Craig; Cho, Jeonghee; Johnson, Laura A.; Tanaka, Kumiko E.; Bass, Adam J.; Barretina, Jordi; Weir, Barbara A.; Beroukhim, Rameen; Meyerson, Matthew] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Ramos, Alex H.; Dutt, Amit; Mermel, Craig; Johnson, Laura A.; Tanaka, Kumiko E.; Bass, Adam J.; Barretina, Jordi; Weir, Barbara A.; Beroukhim, Rameen; Meyerson, Matthew] Harvard & MIT, Broad Inst, Canc Program, Cambridge, MA USA.
[Ramos, Alex H.; Mermel, Craig; Chirieac, Lucian R.; Lindeman, Neal I.; Meyerson, Matthew] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Perner, Sven; Stiedl, Ann-Cathrin] Univ Hosp Tubingen, Dept Pathol, Tubingen, Germany.
[Lafargue, Christopher J.; Wagner, Patrick; Rubin, Mark A.] Cornell Univ, Dept Pathol, Weill Med Coll, New York, NY 10021 USA.
[Thomas, Roman K.] Univ Cologne, Max Planck Inst Neurol Res, Klaus Joachim Zulch Labs, Max Planck Soc, Cologne, Germany.
[Thomas, Roman K.] Univ Cologne, Fac Med, Cologne, Germany.
[Thomas, Roman K.] Univ Cologne, Ctr Integrated Oncol, Cologne, Germany.
[Thomas, Roman K.] Univ Cologne, Dept Internal Med, Cologne, Germany.
[Minna, John D.] Univ Texas SW Med Ctr Dallas, Hamon Ctr Therapeut Oncol Res, Simmons Canc Ctr, Dallas, TX 75390 USA.
[Minna, John D.] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA.
[Minna, John D.] Univ Texas SW Med Ctr Dallas, Dept Pharmacol, Dallas, TX 75390 USA.
[Chirieac, Lucian R.; Lindeman, Neal I.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Giordano, Thomas] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
[Beer, David G.] Univ Michigan, Dept Surg, Thorac Surg Sect, Ann Arbor, MI 48109 USA.
[Wistuba, Ignacio I.] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Wistuba, Ignacio I.] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
RP Meyerson, M (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM Matthew_Meyerson@dfci.harvard.edu
RI Meyerson, Matthew/E-7123-2012; Dutt, Amit/I-1911-2013;
OI Dutt, Amit/0000-0002-1119-4774; Rubin, Mark/0000-0002-8321-9950;
Giordano, Thomas/0000-0003-0641-8873
FU Swiss National Science Foundation [PBZHB- 106297]; National Cancer
Institute [5R01CA109038, 5P20CA90578]
FX We thank Shantanu Banerji for critical reading of the manuscript and
Christopher A. French for providing microscopy support. A. D. is
supported by the Swiss National Science Foundation Fellowship # PBZHB-
106297. This work was supported by National Cancer Institute grants
5R01CA109038 and 5P20CA90578 (M. M.).
NR 45
TC 49
Z9 51
U1 0
U2 3
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD NOV 1
PY 2009
VL 8
IS 21
BP 2042
EP 2050
DI 10.4161/cbt.8.21.9764
PG 9
WC Oncology
SC Oncology
GA 533BF
UT WOS:000272796200013
PM 19755855
ER
PT J
AU Park, SM
Park, CT
Park, SY
Bae, DS
Nam, JH
Cho, CH
Lee, JM
Earle, CC
Yun, YH
AF Park, Sang Min
Park, Chong Taik
Park, Sang Yoon
Bae, Duk-Soo
Nam, Joo Hyun
Cho, Chi-Heum
Lee, Jong Min
Earle, Craig C.
Yun, Young Ho
TI Factors related to second cancer screening practice in disease-free
cervical cancer survivors
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Cancer screening; Cervical cancer survivor; Second cancer
ID RANDOMIZED CONTROLLED-TRIAL; BREAST-CANCER; PROSPECTIVE COHORT;
COLORECTAL-CANCER; RISK; CARCINOMA; QUALITY; WOMEN; MALIGNANCY;
INSURANCE
AB Background Although cancer survivors are at increased risk for developing cancers at other sites, little is known about the current status of second cancer (cancers other than the index cancer) screening practices and related factors in cervical cancer survivors.
Methods We enrolled 809 cervical cancer survivors aged >= 40 years who had been treated at six hospitals from 1983 to 2004. Subjects filled out a questionnaire that included the practices of second cancer screening (breast, stomach, and colorectum) and other sociodemographic variables.
Results Among subjects, 38.9% had been recommended to receive screening for other cancers from health care providers, and 27.4% reported that they thought they had lower risk of other cancer than general population. Older (age >= 65 years) and poor (family income < 1,000$/month) subjects were less likely to have second cancer screening. Those to whom health care providers had recommended screening for other cancers (aOR = 2.14; 95% CI, 1.542.98), and those who had an appropriate perception of second cancer risk (aOR = 1.64; 95% CI, 1.11-2.43) were more likely to undergo breast cancer screening.
Conclusion Lack of a recommendation for second cancer screening from health care providers and the misperception of second cancer risk might have negative impacts on the breast cancer screening behaviors in cervical cancer survivors.
C1 [Park, Sang Min; Yun, Young Ho] Natl Canc Ctr, Div Canc Control, Goyang Si 411769, Gyeonggi Do, South Korea.
[Park, Chong Taik] Pochon CHA Univ, Coll Med, Kangnam Cha Hosp, Dept Obstet & Gynecol, Seoul, South Korea.
[Park, Sang Yoon] Natl Canc Ctr, Ctr Uterine Canc, Goyang, Gyeonggi, South Korea.
[Bae, Duk-Soo] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Obstet & Gynecol, Seoul, South Korea.
[Nam, Joo Hyun] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Obstet & Gynecol, Seoul, South Korea.
[Cho, Chi-Heum] Keimyung Univ, Sch Med, Dept Obstet & Gynecol, Taegu, South Korea.
[Lee, Jong Min] Kyung Hee Univ, EW Neo Med Ctr, Dept Obstet & Gynecol, Seoul, South Korea.
[Earle, Craig C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol,Div Populat Sci, Boston, MA 02115 USA.
RP Yun, YH (reprint author), Natl Canc Ctr, Div Canc Control, 809 Madu Dong, Goyang Si 411769, Gyeonggi Do, South Korea.
EM lawyun08@ncc.re.kr
RI Yun, Young Ho/J-5560-2012; Park, Sang Min/J-5484-2012
FU National Cancer Center [04101502, 07104221]
FX This work was supported by National Cancer Center Grant No. 04101502 and
National Cancer Center Grant No. 07104221.
NR 29
TC 8
Z9 8
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD NOV
PY 2009
VL 20
IS 9
BP 1697
EP 1703
DI 10.1007/s10552-009-9421-0
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 511VF
UT WOS:000271198400017
PM 19688183
ER
PT J
AU Menes, TS
Kerlikowske, K
Jaffer, S
Seger, D
Miglioretti, DL
AF Menes, Tehillah S.
Kerlikowske, Karla
Jaffer, Shabnam
Seger, Deborah
Miglioretti, Diana L.
TI Rates of Atypical Ductal Hyperplasia Have Declined with Less Use of
Postmenopausal Hormone Treatment: Findings from the Breast Cancer
Surveillance Consortium
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID ESTROGEN PLUS PROGESTIN; SCREENING MAMMOGRAPHY; RISK-FACTORS; FOLLOW-UP;
DISEASE; FREQUENCY; THERAPY; WOMEN; POPULATION; BIOPSIES
AB Aim: To examine risk factors and rates of atypical ductal hyperplasia (ADH) with and without associated breast cancer over time and tumor characteristics of breast cancer with and without associated ADH in women previously screened with mammography.
Methods: Data on screening mammograms done between 1996 and 2005 were collected from mammography registries that participate in the Breast Cancer Surveillance Consortium. Associations between age, family history of breast cancer, postmenopausal hormone treatment (HT), and final pathology result (ADH or cancer with or without ADH in the same breast) were examined. Rates of different outcomes were calculated per exam year. Tumor characteristics of cancers with and without associated ADH were compared.
Results: A total of 2,453,483 screening mammograms were associated with 1,064 biopsies with ADH, 833 breast cancers with ADH, and 8,161 cancers with no ADH. Postmenopausal HT use decreased significantly from 35% to 11% during the study period. Rates of ADH decreased from a peak of 5.5/10,000 mammograms in 1999 to 2.4/10,000 in 2005. Rates of cancer with ADH decreased from a peak of 4.3/10,000 mammograms in 2003 to 3.3/10,000 in 2005. ADH and breast cancer were significantly associated with use of postmenopausal HT. Cancer associated with ADH was of lower grade and stage and more estrogen receptor positive than cancer with no ADH.
Summary: Postmenopausal HT is associated with an increased risk of ADH with or without cancer. Rates of ADH have decreased over the past decade, which may be partially explained by the significant reduction in use of postmenopausal HT. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2822-8)
C1 [Menes, Tehillah S.] Elmhurst Hosp Ctr, Dept Surg, Elmhurst, NY 11373 USA.
[Menes, Tehillah S.] Mt Sinai Sch Med, New York, NY USA.
[Kerlikowske, Karla] Univ Calif San Francisco, Dept Med, San Francisco Vet Affairs Med Ctr, Gen Internal Med Sect, San Francisco, CA 94143 USA.
[Kerlikowske, Karla] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco Vet Affairs Med Ctr, Gen Internal Med Sect, San Francisco, CA 94143 USA.
[Jaffer, Shabnam] Mt Sinai Med Ctr, Mt Sinai Sch Med, Dept Pathol, New York, NY 10029 USA.
[Miglioretti, Diana L.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
RP Menes, TS (reprint author), Elmhurst Hosp Ctr, Dept Surg, 79-01 Broadway, Elmhurst, NY 11373 USA.
EM menest@nychhc.org
FU National Cancer Institute [U01CA63740, U01CA86076, U01CA86082,
U01CA63736, U01CA70013, U01CA69976, U01CA63731, U01CA70040]
FX The National Cancer Institute-funded Breast Cancer Surveillance
Consortium co-operative agreement (U01CA63740, U01CA86076, U01CA86082,
U01CA63736, U01CA70013, U01CA69976, U01CA63731, and U01CA70040).
NR 27
TC 11
Z9 11
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 2822
EP 2828
DI 10.1158/1055-9965.EPI-09-0745
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600004
PM 19900937
ER
PT J
AU Pollitt, RA
Geller, AC
Brooks, DR
Johnson, TM
Park, ER
Swetter, SM
AF Pollitt, Ricardo A.
Geller, Alan C.
Brooks, Daniel R.
Johnson, Timothy M.
Park, Elyse R.
Swetter, Susan M.
TI Efficacy of Skin Self-Examination Practices for Early Melanoma Detection
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID MALIGNANT-MELANOMA; CUTANEOUS MELANOMA; INTERVENTION; 21ST-CENTURY;
PHOTOGRAPHS; POPULATION; PREVENTION; TRIAL; CHECK; RISK
AB Although skin self-examination (SSE) may increase rates of early melanoma detection, the efficacy of different SSE practices has not been thoroughly studied. We examined associations between SSE practices and tumor thickness in patients with recently diagnosed melanoma.
Methods: 321 melanoma patients at three hospitals completed questionnaires on demographics and SSE practices. Patient-reported SSE was measured by routine examination of 13 specific body areas, frequency of mole examination, and use of a melanoma picture aid to assist with SSE. Histologic diagnoses and Breslow depth were confirmed by dermatopathologists. Regression analyses were used to calculate ratios of geometric mean tumor thickness and odds ratios for having thicker versus thinner tumors for different SSE behaviors.
Results: Rates of SSE varied considerably by SSE item. Patients routinely examining at least some of their skin had thinner melanomas [adjusted geometric mean tumor ratio, 0.73; 95% confidence interval (95% CI), 0.50-0.94]. Frequency of mole examination did not predict tumor thickness. Using a melanoma picture as a SSE aid was strongly associated with reduced tumor thickness (adjusted ratio, 0.75; 95% Cl, 0.66-0.85 for ever versus never use). A composite measure of thoroughness of SSE was the best predictor of thickness (adjusted ratio, 0.58; 95% Cl, 0.36-0.75) for high versus low thoroughness.
Conclusions: SSE was associated with decreased tumor thickness by most measures. However, the diverse rates of SSE practices and the distinct associations between these practices and melanoma thickness suggest a complexity in SSE that should be addressed in future studies. SSE should be evaluated by more than one measure. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3018-23)
C1 [Pollitt, Ricardo A.; Swetter, Susan M.] Stanford Univ, Dept Dermatol, Pigmented Les & Melanoma Program, Sch Med, Stanford, CA 94305 USA.
[Geller, Alan C.] Harvard Univ, Sch Publ Hlth, Div Publ Hlth Practice, Boston, MA 02115 USA.
[Brooks, Daniel R.] Boston Univ, Dept Epidemiol, Sch Publ Hlth, Boston, MA 02215 USA.
[Johnson, Timothy M.] Univ Michigan, Sch Med, Dept Dermatol, Ann Arbor, MI USA.
[Johnson, Timothy M.] Univ Michigan, Sch Med, Dept Otolaryngol, Ann Arbor, MI USA.
[Johnson, Timothy M.] Univ Michigan, Sch Med, Dept Surg, Ann Arbor, MI USA.
[Park, Elyse R.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Park, Elyse R.] Massachusetts Gen Hosp, Inst Hlth Policy, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Swetter, Susan M.] Vet Affairs Palo Alto Hlth Care Syst, Dermatol Serv, Palo Alto, CA USA.
RP Swetter, SM (reprint author), Stanford Univ, Dept Dermatol, Med Ctr, 450 Broadway St,Pavil C,2nd Floor, Redwood City, CA 94063 USA.
EM sswetter@stanford.edu
OI Brooks, Daniel/0000-0001-6220-6889
FU Schering Plough
FX Grant support: Schering Plough. The sponsor had no role in the design
and conduct of the study, the collection, analysis, and interpretation
of data, or the preparation, review, or approval of the article.
NR 26
TC 36
Z9 36
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 3018
EP 3023
DI 10.1158/1055-9965.EPI-09-0310
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600031
PM 19861521
ER
PT J
AU Fejerman, L
Haiman, CA
Reich, D
Tandon, A
Deo, RC
John, EM
Ingles, SA
Ambrosone, CB
Bovbjerg, DH
Jandorf, LH
Davis, W
Ciupak, G
Whittemore, AS
Press, MF
Ursin, G
Bernstein, L
Huntsman, S
Henderson, BE
Ziv, E
Freedman, ML
AF Fejerman, Laura
Haiman, Christopher A.
Reich, David
Tandon, Arti
Deo, Rahul C.
John, Esther M.
Ingles, Sue A.
Ambrosone, Christine B.
Bovbjerg, Dana Howard
Jandorf, Lina H.
Davis, Warren
Ciupak, Gregory
Whittemore, Alice S.
Press, Michael F.
Ursin, Giske
Bernstein, Leslie
Huntsman, Scott
Henderson, Brian E.
Ziv, Elad
Freedman, Matthew L.
TI An Admixture Scan in 1,484 African American Women with Breast Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; LINKAGE DISEQUILIBRIUM; RACIAL-DIFFERENCES;
MULTIETHNIC POPULATION; CONFER SUSCEPTIBILITY; COMMON VARIANTS;
LOS-ANGELES; RISK LOCUS; SURVIVAL; ESTROGEN
AB African American women with breast cancer present more commonly with aggressive tumors that do not express the estrogen receptor (ER) and progesterone receptor (PR) compared with European American women. Whether this disparity is the result of inherited factors has not been established. We did an admixture-based genome-wide scan to search for risk alleles for breast cancer that are highly differentiated in frequency between African American and European American women, and may contribute to specific breast cancer phenotypes, such as ER-negative (ER-) disease. African American women with invasive breast cancer (n = 1,484) were pooled from six population-based studies and typed at similar to 1,500 ancestry-informative markers. We investigated global genetic ancestry and did a whole genome admixture scan searching for breast cancer-predisposing loci in association with disease phenotypes. We found a significant difference in ancestry between ER+PR+ and ER-PR- women, with higher European ancestry among ER+PR+ individuals, after controlling for possible confounders (odds ratios for a 0 to 1 change in European ancestry proportion, 2.84; 95% confidence interval, 1.13-7.14; P = 0.026). Women with localized tumors had higher European ancestry than women with non-localized tumors (odds ratios, 2.65; 95% confidence interval, 1.11-6.35; P = 0.029). No genome-wide statistically significant associations were observed between European or African ancestry at any specific locus and breast cancer, or in analyses stratified by ER/PR status, stage, or grade. In summary, in African American women, genetic ancestry is associated with ER/PR status and disease stage. However, we found little evidence that genetic ancestry at any one region contributes significantly to breast cancer risk or hormone receptor status. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3110-7)
C1 [Fejerman, Laura; Huntsman, Scott; Ziv, Elad] Univ Calif San Francisco, Div Gen Internal Med, Dept Med, Inst Human Genet, San Francisco, CA 94143 USA.
[Fejerman, Laura; Huntsman, Scott; Ziv, Elad] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
[Haiman, Christopher A.; Ingles, Sue A.; Ursin, Giske; Henderson, Brian E.] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Reich, David; Tandon, Arti; Deo, Rahul C.] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
[Deo, Rahul C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Cardiol Div, Boston, MA USA.
[Reich, David; Tandon, Arti; Freedman, Matthew L.] Broad Inst Harvard & Massachusetts Inst Technol, Program Med & Populat Genet, Boston, MA USA.
[John, Esther M.] No Calif Canc Ctr, Fremont, CA USA.
[John, Esther M.; Whittemore, Alice S.] Stanford Univ, Sch Med, Dept Hlth Res & Policy, Stanford, CA 94305 USA.
[Press, Michael F.] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Keck Sch Med, Dept Pathol, Los Angeles, CA 90033 USA.
[Ambrosone, Christine B.; Davis, Warren; Ciupak, Gregory] Roswell Pk Canc Inst, Dept Canc Prevent & Control, Buffalo, NY 14263 USA.
[Bovbjerg, Dana Howard] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
[Jandorf, Lina H.] Mt Sinai Sch Med, Dept Oncol Sci, New York, NY USA.
[Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Duarte, CA USA.
[Ursin, Giske] Univ Oslo, Dept Nutr, Oslo, Norway.
[Freedman, Matthew L.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Freedman, Matthew L.] Dana Farber Harvard Canc Ctr, Boston, MA USA.
RP Ziv, E (reprint author), Univ Calif San Francisco, Div Gen Internal Med, Dept Med, Inst Human Genet, Box 1732, San Francisco, CA 94143 USA.
EM elad.ziv@ucsf.edu; freedman@broad.mit.edu
OI Fejerman, Laura/0000-0003-3179-1151
FU Prevent Cancer Foundation; National Cancer Institute [CA63464, CA54281,
R01 CA63446, R01 CA77305]; Komen Foundation Investigator-Initiated
[KG080165]; Women's Circle of Health Study [NCI R01 CA100598,
DAMD17-01-1-0334]; U.S. Army Medical Research Program [DAMD17-96-6071];
Richard and Susan Smith Family Foundation, Chestnut Hill, MA; National
Institute of Child Health and Human Development [N01-HD-3-3175];
National Cancer Institute, NIH [RFA-CA-06-503]; Northern California
Cancer Center [U01 CA69417]
FX Grant support: Postdoctoral fellowship from the Prevent Cancer
Foundation (L. Fejerman). The Multiethnic Cohort Study was supported by
National Cancer Institute grants CA63464 and CA54281. Komen Foundation
Investigator-Initiated grant KG080165 (E. Ziv). The Women's Circle of
Health Study is supported by grants NCI R01 CA100598 and
DAMD17-01-1-0334. The San Francisco Bay Area Breast Cancer Study was
funded by grants from the National Cancer Institute (R01 CA63446 and R01
CA77305) and the U.S. Army Medical Research Program (DAMD17-96-6071;
E.M. John). Richard and Susan Smith Family Foundation, Chestnut Hill, MA
(M. Freedman). Burroughs Wellcome Career Development Award in the
Biomedical Sciences (D. Reich). The Los Angeles Component of the Women's
Contraceptive and Reproductive Experiences Study was supported by a
contract from the National Institute of Child Health and Human
Development (N01-HD-3-3175; L. Bernstein). The Breast Cancer Family
Registry (BCFR) is funded by the National Cancer Institute, NIH under
RFA-CA-06-503 and through cooperative agreements with members of the
BCFR and Principal Investigators. The registry contributing data to this
analysis was supported by U01 CA69417 (Northern California Cancer
Center). 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.
NR 47
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U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 3110
EP 3117
DI 10.1158/1055-9965.EPI-09-0464
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600045
PM 19843668
ER
PT J
AU Anderson, KC
AF Anderson, Kenneth C.
TI The Evolving Treatment Paradigm. in Multiple Myeloma
SO CANCER JOURNAL
LA English
DT Editorial Material
C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Div Hematol Neoplasia, Boston, MA 02115 USA.
RP Anderson, KC (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Div Hematol Neoplasia, 44 Binney St,Mayer Bldg,Room 557, Boston, MA 02115 USA.
EM kenneth_anderson@dfci.harvard.edu
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1528-9117
J9 CANCER J
JI Cancer J.
PD NOV-DEC
PY 2009
VL 15
IS 6
BP 456
EP 456
PG 1
WC Oncology
SC Oncology
GA 535EW
UT WOS:000272951000002
PM 20010163
ER
PT J
AU Cirstea, D
Vallet, S
Raje, N
AF Cirstea, Diana
Vallet, Sonia
Raje, Noopur
TI Future Novel Single Agent and Combination Therapies
SO CANCER JOURNAL
LA English
DT Review
DE multiple myeloma; novel agents; combination therapy; bone marrow
microenvironment
ID MULTIPLE-MYELOMA CELLS; LENALIDOMIDE PLUS DEXAMETHASONE; HISTONE
DEACETYLASE INHIBITOR; SUBEROYLANILIDE HYDROXAMIC ACID; ACTIVE
PROTEASOME INHIBITOR; DEPENDENT KINASE INHIBITOR; HIGH-DOSE
DEXAMETHASONE; IN-VIVO; SURVIVAL PATHWAYS; ANTICANCER AGENTS
AB Although multiple myeloma (MM) remains an incurable bone marrow cancer, survival rates have dramatically improved over the past decade, most notably in the younger patient population. An understanding of MM biology and improvement in stem-cell transplantation, better supportive care, and novel therapies with higher efficacy and lower toxicity are all responsible for this improvement. Despite these trends, improvements among older patients remain modest, underscoring the need for innovative approaches. The availability of a rich pipeline of novel agents undergoing early-phase clinical trials in MM is an exciting and active area of research. Current novel agents targeting tumor and stromal compartments can be conceptualized as those that target membrane-bound receptors (insulin-like growth factor-1, vascular endothelial growth factor, CD40, etc.), intracellular signaling kinases (Janus kinase/signal transducers and activators of transcription, phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin, mitogen-activated protein kinase pathways), cell cycle molecular machinery (cyclin-dependent kinases inhibitors), epigenetic abnormalities (DNA methyltransferase and histyone deacetylase), protein dynamics (heat-shock protein 90, ubiquitin-proteasome system), and tumor vasculature and microenvironment (angiogenesis, integrins). This review highlights some of these novel agents tested either alone or in combination for the treatment of MM.
C1 [Vallet, Sonia; Raje, Noopur] Harvard Univ, Sch Med, Massachusetts Gen Hosp, MGH Canc Ctr, Boston, MA 02114 USA.
[Cirstea, Diana; Raje, Noopur] Harvard Univ, Sch Med, Leebow Inst Myeloma Therapeut, Boston, MA 02114 USA.
[Cirstea, Diana; Raje, Noopur] Harvard Univ, Sch Med, Dana Farber Canc Inst, Jerome Lipper Multiple Myeloma Dis Ctr, Boston, MA 02114 USA.
RP Raje, N (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, MGH Canc Ctr, POB 216,55 Fruit St, Boston, MA 02114 USA.
EM nraje@partners.org
FU ASCO CDA; MMRF; LLS CDA
FX Supported by ASCO CDA, MMRF, and LLS CDA (to N.R.).
NR 95
TC 12
Z9 13
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1528-9117
EI 1540-336X
J9 CANCER J
JI Cancer J.
PD NOV-DEC
PY 2009
VL 15
IS 6
BP 511
EP 518
PG 8
WC Oncology
SC Oncology
GA 535EW
UT WOS:000272951000010
PM 20010171
ER
PT J
AU Xing, D
Scangas, G
Nitta, M
He, L
Xu, X
Ioffe, YJM
Aspuria, PJ
Hedvat, CY
Anderson, ML
Oliva, E
Karlan, BY
Mohapatra, G
Orsulic, S
AF Xing, Deyin
Scangas, George
Nitta, Mai
He, Lei
Xu, Xuan
Ioffe, Yevgeniya J. M.
Aspuria, Paul-Joseph
Hedvat, Cyrus Y.
Anderson, Matthew L.
Oliva, Esther
Karlan, Beth Y.
Mohapatra, Gayatry
Orsulic, Sandra
TI A Role for BRCA1 in Uterine Leiomyosarcoma
SO CANCER RESEARCH
LA English
DT Article
ID SMOOTH-MUSCLE TUMORS; IMMUNOHISTOCHEMICAL ANALYSIS; MOUSE MODEL;
CELL-CYCLE; P53; EXPRESSION; LEIOMYOMAS; P16; RECEPTOR; MICE
AB Uterine leiomyosarcoma (ULMS) is a rare gynecologic malignancy with a low survival rate. Currently, there is no effective treatment for ULMS. Infrequent occurrences of human WAS hamper the understanding of the initiation and progression of the disease, thereby limiting the ability to develop efficient therapies. To elucidate the roles of the p53 and BRCA1 tumor suppressor genes in gynecologic malignancies, we generated mice in which p53 and/or BRCA1 can be conditionally deleted using anti-Mullerian hormone type II receptor (Anthr2)-driven Cre recombinase. We showed that conditional deletion of p53 in mice results in the development of uterine tumors that resemble human ULMS and that concurrent deletion of p53 and BRCA1 significantly accelerates the progression of these tumors. This finding led to our hypothesis that BRCA1 may play a role in human ULMS development. Consistent with this hypothesis, we showed that the BRCA1 protein is absent in 29% of human ULMS and that BRCA1 promoter methylation is the likely mechanism of BRCA1 downregulation. These data indicate that the loss of BRCA1 function may be an important step in the progression of ULMS. Our findings provide a rationale for investigating therapies that target BRCA1 deficiency in ULMS. [Cancer Res 2009;69(21):8231-5]
C1 [Xu, Xuan; Ioffe, Yevgeniya J. M.; Aspuria, Paul-Joseph; Karlan, Beth Y.; Orsulic, Sandra] Cedars Sinai Med Ctr, Womens Canc Res Inst, Los Angeles, CA 90048 USA.
[Xing, Deyin; Scangas, George; Nitta, Mai; He, Lei; Mohapatra, Gayatry; Orsulic, Sandra] Massachusetts Gen Hosp, Mol Pathol Unit, Charlestown, MA USA.
[Xing, Deyin; Scangas, George; Nitta, Mai; He, Lei; Mohapatra, Gayatry; Orsulic, Sandra] Massachusetts Gen Hosp, Ctr Canc Res, Charlestown, MA USA.
[Xing, Deyin; Scangas, George; Nitta, Mai; He, Lei; Oliva, Esther; Mohapatra, Gayatry; Orsulic, Sandra] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Oliva, Esther; Mohapatra, Gayatry; Orsulic, Sandra] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Hedvat, Cyrus Y.] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Anderson, Matthew L.] Baylor Coll Med, Div Gynecol Oncol, Houston, TX 77030 USA.
RP Orsulic, S (reprint author), Cedars Sinai Med Ctr, Womens Canc Res Inst, 8635 W 3rd St,Suite 290W, Los Angeles, CA 90048 USA.
EM orsulics@cshs.org
FU NIH [R01-CA103924]; Ovarian Cancer Research Fund; Liddy Shriver Sarcoma
Initiative; LMSarcoma Direct Research Foundation; Sarcoma Foundation of
America
FX Received 7/8/09; revised 9/8/09; accepted 9/14/09; published OnlineFirst
10/20/09.; Grant support: NIH (R01-CA103924), Ovarian Cancer Research
Fund, Liddy Shriver Sarcoma Initiative, LMSarcoma Direct Research
Foundation, and the Sarcoma Foundation of America (S. Orsulic).; The
costs of publication of this article were defrayed in part by the
payment. of page charges. This article must. therefore be hereby marked
advertisement in accordance with 18 U.S.C. Section 17,34 solely to
indicate this fact.; We thank Robert. Soslow (Memorial Sloan-Kettering
Cancer Center, New York, NY), Gian Franco Zannoni (Universita Cattolica.
Rome, Italy), Michele de Nictolis (Istituto di Anatomia e Istologia
Patologica, Ancona Italy), Philip Branton (Inova Fairfax Hospital, Falls
Church, VA), Christine Holschneider (Olive View Medical Center, Los
Angeles, CA), and jenny Gross (Cedars-Sinai Medical Center) for
contributing human specimens; Lejla Delic (Cedars-Sinai Medical Center)
for help with IIIC; Richard Behringer (University of Texas, M.D.
Anderson Cancer Center) for the Amhr2-Cre mice; members of the Women's
Cancer Research Institute at Cedars-Sinai Medical Center for insightful
suggestions; and Kristy J. Daniels for help in thepreparation of the
manuscript.
NR 20
TC 26
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U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2009
VL 69
IS 21
BP 8231
EP 8235
DI 10.1158/0008-5472.CAN-09-2543
PG 5
WC Oncology
SC Oncology
GA 514OA
UT WOS:000271403000003
PM 19843854
ER
PT J
AU Hubbard, SA
Friel, AM
Kumar, B
Zhang, L
Rueda, BR
Gargett, CE
AF Hubbard, Sonya A.
Friel, Anne M.
Kumar, Beena
Zhang, Ling
Rueda, Bo R.
Gargett, Caroline E.
TI Evidence for Cancer Stem Cells in Human Endometrial Carcinoma
SO CANCER RESEARCH
LA English
DT Article
ID SIDE-POPULATION CELLS; BETA-CATENIN EXPRESSION; PROSPECTIVE
IDENTIFICATION; E-CADHERIN; SCID MICE; IN-VITRO; TUMORS; CONTRIBUTE;
SIGNATURE; LINE
AB Emerging evidence indicates that the highly regenerative human endometrium harbors rare populations of epithelial progenitor cells. In tumors of other regenerative epithelial tissues, rare cancer stem cells (CSC) have been identified that may have originated from normal epithelial stem/progenitor cells. We hypothesized that CSC are responsible for epithelial neoplasia associated with endometrial carcinoma, the most common gynecologic malignancy in women. Stem cell characteristics of single cells isolated from endometrial carcinoma tissues from women ages 62 +/- 11.8 years (n = 34) were assessed. Twenty-five of 28 endometrial carcinoma samples contained a small population of clonogenic cells [0.24% (0-1.84%)], with no significant difference in cloning efficiency between the three grades of endometrial carcinoma or between endometrial carcinoma and normal endometrial epithelial samples. Isolated endometrial carcinoma cells transplanted under the kidney capsule of immunocompromised mice in serial dilution (2 x 10(6)-1 x 10(4) cells) generated tumors in 8 of 9 samples with morphologies similar to the parent tumors. These tumors recapitulated cytokeratin, vimentin, estrogen receptor-alpha, and progesterone receptor expression of the parent tumor, indicating that tumor-initiating cells likely differentiated into cells comprising the endometrial carcinoma tissue. Individual clones underwent serial clonal subculture 2.5 to 4 times, with a trend of increasing number of subclonings with increasing tumor grade, indicating increasing self-renewal with greater malignancy. Clonally derived endometrial carcinoma cells also expressed the self-renewal genes BMI-I, NANOG, and SOX-2. Isolated cells from primary tumors were serially transplanted 3 to 5 times in nonobese diabetic/severe combined immunodeficient mice, showing self-renewal in vivo. This evidence of cells with clonogenic, self-renewing, differentiating, and tumorigenic properties suggests that a CSC population may be responsible for production of endometrial carcinoma tumor cells. [Cancer Res 2009;69(21):8241-8]
C1 [Gargett, Caroline E.] Monash Univ, Dept Obstet & Gynaecol, Monash Med Ctr, Clayton, Vic 3168, Australia.
[Hubbard, Sonya A.; Gargett, Caroline E.] Monash Inst Med Res, Ctr Womens Hlth Res, Clayton, Vic, Australia.
[Friel, Anne M.; Zhang, Ling; Rueda, Bo R.] Massachusetts Gen Hosp, Vincent Obstet & Gynecol Serv, Vincent Ctr Reprod Biol, Boston, MA USA.
RP Gargett, CE (reprint author), Monash Univ, Dept Obstet & Gynaecol, Monash Med Ctr, 246 Clayton Rd, Clayton, Vic 3168, Australia.
EM Caroline.Gargett@med.monash.edu.au
OI Gargett, Caroline/0000-0002-3590-2077
FU Cancer Council Victoria [491079]; National Health and Medical Research
Council [465121]; Australian Postgraduate Award; Advanced Medical
Research Foundation; Harvard Stem Cell Institute; Victorian Government
FX Grant support: Cancer Council Victoria grant 491079 and National Health
and Medical Research Council R.D. Wright Career Development Award 465121
(C.E, Gargat); Australian Postgraduate Award (S.A. Hubbard); and
Advanced Medical Research Foundation and Harvard Stem Cell Institute
(B.R. Rueda). The endometrial cancer specimens used in this project were
provided by the Victorian Cancer Biobank which is supported by the
Victorian Government.; The costs of publication of this article were
defrayed in part by the payment of page charges. This article must
therefore be hereby marked advertisement in accordance with 18 U.S.C.
Section 1734 solely to indicate this fact.
NR 48
TC 51
Z9 55
U1 1
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2009
VL 69
IS 21
BP 8241
EP 8248
DI 10.1158/0008-5472.CAN-08-4808
PG 8
WC Oncology
SC Oncology
GA 514OA
UT WOS:000271403000005
PM 19843861
ER
PT J
AU Sholl, LM
Yeap, BY
Iafrate, AJ
Holmes-Tisch, AJ
Chou, YP
Wu, MT
Goan, YG
Su, L
Benedettini, E
Yu, J
Loda, M
Janne, PA
Christiani, DC
Chirieac, LR
AF Sholl, Lynette M.
Yeap, Beow Y.
Iafrate, A. John
Holmes-Tisch, Alison J.
Chou, Yi-Ping
Wu, Ming-Tsang
Goan, Yih-Gang
Su, Li
Benedettini, Elisa
Yu, Jian
Loda, Massimo
Jaenne, Pasi A.
Christiani, David C.
Chirieac, Lucian R.
TI Lung Adenocarcinoma with EGFR Amplification Has Distinct
Clinicopathologic and Molecular Features in Never-Smokers
SO CANCER RESEARCH
LA English
DT Article
ID GROWTH-FACTOR-RECEPTOR; IN-SITU-HYBRIDIZATION; GENE COPY NUMBER;
GEFITINIB SENSITIVITY; MUTATIONS; CANCER; EXPRESSION; CARCINOMA;
ERLOTINIB; RESPONSIVENESS
AB In a subset of lung adenocarcinomas, the epidermal growth factor receptor (EGFR) is activated by kinase domain mutations and/or gene amplification, but the interaction between the two types of abnormalities is complex and unclear. For this study, we selected 99 consecutive never-smoking women of East Asian origin with lung adenocarcinomas that were characterized by histologic subtype. We analyzed EGFR mutations by PCR-capillary sequencing, EGFR copy number abnormalities by fluorescence and chromogenic in situ hybridization and quantitative PCR, and EGFR expression by immunohistochemistry with both specific antibodies against exon 19 deletion-mutated EGFR and total EGFR. We compared molecular and clinicopathologic features with disease-free survival. Lung adenocarcinomas with EGFR amplification had significantly more EGFR exon 19 deletion mutations than adenocarcinomas with disomy, and low and high polysomy (100% versus 54%, P = 0.009). EGFR amplification occurred invariably on the mutated and not the mild-type allele (median mutated/wild-type ratios 14.0 versus 0.33, P = 0.003), was associated with solid histology (P = 0.008), and advanced clinical stage (P = 0.009). EGFR amplification was focally distributed in lung cancer specimens, mostly in regions with solid histology. Patients with EGFR amplification had a significantly worse outcome in univariate analysis (median disease-free survival, 16 versus 31 months, P = 0.01) and when adjusted for stage (P = 0.027). Lung adenocarcinomas with EGFR amplification have a unique association with exon 19 deletion mutations and show distinct clinicopathologic features associated with a significantly worsened prognosis. in these cases, EGFR amplification is heterogeneously distributed, mostly in areas with a solid histology. [Cancer Res 2009;69(21):8341-8]
C1 [Sholl, Lynette M.; Loda, Massimo; Chirieac, Lucian R.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Yeap, Beow Y.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Iafrate, A. John] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Christiani, David C.] Massachusetts Gen Hosp, Pulm & Crit Care Unit, Boston, MA 02114 USA.
[Holmes-Tisch, Alison J.; Benedettini, Elisa; Loda, Massimo; Jaenne, Pasi A.] Dana Farber Canc Inst, Dept Pathol, Boston, MA 02115 USA.
[Su, Li; Christiani, David C.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Chou, Yi-Ping] Kaohsiung Vet Gen Hosp, Dept Chest Surg, Kaohsiung, Taiwan.
[Wu, Ming-Tsang; Goan, Yih-Gang] Kaohsiung Med Univ Hosp, Dept Family Med, Kaohsiung, Taiwan.
[Wu, Ming-Tsang; Goan, Yih-Gang] Grad Inst Occupat Safety & Hlth, Kaohsiung, Taiwan.
[Chou, Yi-Ping] Natl Yang Ming Univ, Taipei, Taiwan.
[Yu, Jian] Cell Signaling Technol Inc, Danvers, MA USA.
RP Chirieac, LR (reprint author), Brigham & Womens Hosp, Dept Pathol, 75 Francis St, Boston, MA 02115 USA.
EM lchirieac@partners.org
RI Wu, Ming-Tsang/D-2385-2009
FU National Institutes of Health [CA074386, CA092824, ROI CA114465]
FX Grant support: CA074386, CA092824, and ROI CA114465 From the National
Institutes of Health.; The costs of publication of this article were
defrayed in part. by the payment of page charges. This article most
therefore be hereby marked advertisement in accordance with 18 U.S.C.
Section 1734 solely to indicate this fact. We thank Laura Kwan and
Brittany MacFarland for secretarial assistance, and Lilliam Z. Cruz for
laboratory support.
NR 33
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Z9 57
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2009
VL 69
IS 21
BP 8341
EP 8348
DI 10.1158/0008-5472.CAN-09-2477
PG 8
WC Oncology
SC Oncology
GA 514OA
UT WOS:000271403000017
PM 19826035
ER
PT J
AU Kikuchi, H
Pino, MS
Zeng, M
Shirasawa, S
Chung, DC
AF Kikuchi, Hirotoshi
Pino, Maria S.
Zeng, Min
Shirasawa, Senji
Chung, Daniel C.
TI Oncogenic KRAS and BRAF Differentially Regulate Hypoxia-inducible
Factor-1 alpha and-2 alpha in Colon Cancer
SO CANCER RESEARCH
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; TRANSCRIPTION FACTOR; FACTOR 1-ALPHA;
CELL-LINES; EXPRESSION; RAS; MUTATIONS; TUMORIGENESIS; VEGF;
ANGIOGENESIS
AB KRAS and BRAF mutations are frequently observed in human colon cancers. These mutations occur in a mutually exclusive manner, and each is associated with distinctive biological features. We showed previously that K-ras can interact with hypoxia to activate multiple signaling pathways. Many hypoxic responses are mediated by hypoxia-inducible factor (HIF)-1 alpha and HIF-2 alpha, and we sought to define the roles of mutant KRAS and BRAF in the induction of HIF-1 alpha and HIF-2 alpha in colon cancer cells. Ectopic expression of mutant K-ras in Caco2 cells enhanced the hypoxic induction of only HIF-1 alpha, whereas mutant BRAF enhanced both HIF-1 alpha and HIF-2 alpha. Knockout or knockdown of mutant KRAS in DLD-1 and HCT116 cells impaired the hypoxic induction of only HIF-1 alpha. HIF-1 alpha mRNA levels were comparable in cells with and without a KRAS mutation. However, the rate of HIF-1 alpha protein synthesis was higher in cells with a KRAS mutation, and this was suppressed by the phosphoinositide 3-kinase inhibitor LY294002. In contrast, knockdown of mutant BRAF in HT29 cells suppressed both HIF-1 alpha and HIF-2 alpha. Although BRAF regulated mRNA levels of both HIF-1 alpha and HIF-2 alpha, knockdown of BRAF or treatment with the MEK inhibitor PD98059 impaired the translation of only HIF-2 alpha. Our data reveal that oncogenic KRAS and BRAF mutations differentially regulate the hypoxic induction of HIF-1 alpha and HIF-2 alpha in colon cancer, and this may potentially contribute to the phenotypic differences of KRAS and BRAF mutations in colon tumors. [Cancer Res 2009;69(21):8499-506]
C1 [Kikuchi, Hirotoshi; Pino, Maria S.; Zeng, Min; Chung, Daniel C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit, Boston, MA 02114 USA.
[Chung, Daniel C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, Boston, MA 02114 USA.
[Shirasawa, Senji] Fukuoka Univ, Dept Cell Biol, Fac Med, Fukuoka 81401, Japan.
[Shirasawa, Senji] Fukuoka Univ, Dept Cell Biol, Fac Med, Fukuoka 81401, Japan.
RP Chung, DC (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit, 50 Blossom St, Boston, MA 02114 USA.
EM dchung@partners.org
FU NIH [CA92594]
FX NIH CA92594.
NR 41
TC 53
Z9 55
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2009
VL 69
IS 21
BP 8499
EP 8506
DI 10.1158/0008-5472.CAN-09-2213
PG 8
WC Oncology
SC Oncology
GA 514OA
UT WOS:000271403000035
PM 19843849
ER
PT J
AU Castorina, P
Carco, D
Guiot, C
Deisboeck, TS
AF Castorina, Paolo
Carco, Daniela
Guiot, Caterina
Deisboeck, Thomas S.
TI Tumor Growth Instability and Its Implications for Chemotherapy
SO CANCER RESEARCH
LA English
DT Article
ID NORTON-SIMON HYPOTHESIS; BREAST-CANCER; MODEL; RESISTANCE; THERAPY;
SENSITIVITY; EXPRESSION; DESIGN
AB Optimal delivery of chemotherapy intensity is dependent on host- and tumor-specific characteristics. In this article, the chemotherapy late intensity schedule is revised to account for tumor growth instability, where a small tumor cell fraction emerges that exhibits a higher proliferation rate than the parent strain. Modeling this instability as simplified two-population dynamics, we find that: (a) if this instability precedes the onset of treatment, the slope of the linear increase of the drug concentration for the standard "Norton-Simon late intensity schedule" changes and the initial value of the dose strongly depends on the ratio of the two tumor cell populations and on their distinct growth rates; and (b) if the instability trails the initial treatment, the effective chemotherapeutic drug concentration changes as well. Both cases point toward testable potential refinements of the Norton-Simon late intensity schedule. [Cancer Res 2009;69(21):8507-15]
C1 [Castorina, Paolo] Univ Catania, Dipartimento Fis, I-95100 Catania, Italy.
[Castorina, Paolo] Ist Nazl Fis Nucl, I-95129 Catania, Italy.
[Castorina, Paolo] Ctr Siciliano Fis Nucl & Struct Mat, Catania, Italy.
[Carco, Daniela] Ist Oncol Mediterraneo, Viagrande, Italy.
[Guiot, Caterina] Univ Turin, Dipartimento Neurosci, Turin, Italy.
[Guiot, Caterina] Univ Turin, CNISM, Turin, Italy.
[Guiot, Caterina] Politecn Torino, Turin, Italy.
[Deisboeck, Thomas S.] Massachusetts Gen Hosp, Harvard MIT HST, Athinoula A Martinos Ctr Biomed Imaging, Complex Biosyst Modeling Lab, Charlestown, MA USA.
RP Castorina, P (reprint author), Univ Catania, Dipartimento Fis, Via Santa Sofia 64, I-95100 Catania, Italy.
EM paolo.castorina@ct.infn.it
RI guiot, caterina/C-6708-2009;
OI guiot, caterina/0000-0001-8529-1625; Castorina,
Paolo/0000-0002-5617-8102
FU NIH [CA 113004]; Harvard-MIT Athinoula A. Martinos Center for Biomedical
Imaging; Department of Radiology at Massachusetts General Hospital;
Regione Piemonte; University of Torino
FX NIH grant CA 113004 (T.S. Deisboeck) and by the Harvard-MIT Athinoula A.
Martinos Center for Biomedical Imaging and the Department of Radiology
at Massachusetts General Hospital. C. Guiot was supported by Regione
Piemonte (PSF 2007, 2008) and University of Torino (60% 2007, 2008).
NR 25
TC 14
Z9 14
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2009
VL 69
IS 21
BP 8507
EP 8515
DI 10.1158/0008-5472.CAN-09-0653
PG 9
WC Oncology
SC Oncology
GA 514OA
UT WOS:000271403000036
PM 19861540
ER
PT J
AU Sugimoto, M
Ohno, T
Graham, DY
Yamaoka, Y
AF Sugimoto, Mitsushige
Ohno, Tomoyuki
Graham, David Y.
Yamaoka, Yoshio
TI Gastric mucosal interleukin-17 and-18 mRNA expression in Helicobacter
pylori-induced Mongolian gerbils
SO CANCER SCIENCE
LA English
DT Article
ID INTESTINAL METAPLASIA; INCREASED RISK; GENE POLYMORPHISMS; VIRULENCE
FACTORS; JAPANESE SUBJECTS; IMMUNE-RESPONSE; PEPTIC-ULCER; CANCER RISK;
INFECTION; INFLAMMATION
AB Helicobacter pylori infection causes characteristic mucosal infiltration of inflammatory cells, resulting in the development of peptic ulcers and gastric cancer in approximately 10% of cases. Different clinical expressions of the infection may reflect different patterns of cytokine expression. Interleukin (IL)-1 ss, tumor necrosis factor (TNF)-alpha, IL-17, and IL-18 have been reported to be involved in H. pylori-induced gastric mucosal inflammation, but the details and relation to different patterns of inflammation remain unclear. Moreover, the proinflammatory virulence factor outer inflammatory protein (OipA) was reported to be associated with gastric mucosal inflammatory cytokine levels. To clarify these findings, Mongolian gerbils were infected for up to 12 months with wild-type H. pylori 7.13 or with isogenic oipA mutants for 3 months, and mucosal cytokines (IL-1 ss, IL-17, IL-18, and TNF-alpha) mRNA levels were then assessed using real-time RT-PCR. Antral mucosal IL-1 beta and IL-18 mRNA levels peaked 1 month after infection, whereas the peak of TNF-alpha mRNA was at 6-12 months; IL-17 levels peaked at 12 months. The inflammatory cell infiltration and mRNA levels of all cytokines studied were significantly lower in oipA mutants than in wild-type-infected gerbils. Mucosal IL-1 ss, IL-17, and TNF-alpha expression, but not that of IL-18, were significantly associated with the grade of inflammatory cell infiltration. The pattern of increased inflammatory cytokines differed relative to the phase of the infection and pattern of inflammation. OipA appears to play a role in IL-1 ss, IL-17, and TNF-alpha expression and the resulting inflammation. (Cancer Sci 2009).
C1 [Sugimoto, Mitsushige; Ohno, Tomoyuki; Graham, David Y.; Yamaoka, Yoshio] Michael E DeBakey Vet Affairs Med Ctr, Dept Med Gastroenterol, Houston, TX USA.
[Sugimoto, Mitsushige; Ohno, Tomoyuki; Graham, David Y.; Yamaoka, Yoshio] Baylor Coll Med, Houston, TX 77030 USA.
[Yamaoka, Yoshio] Oita Univ, Fac Med, Dept Environm & Prevent Med, Oita 87011, Japan.
RP Yamaoka, Y (reprint author), Michael E DeBakey Vet Affairs Med Ctr, Dept Med Gastroenterol, Houston, TX USA.
EM yyamaoka@bcm.tmc.edu
FU NIH [DK62813]
FX This material is based upon work supported in part by the Office of
Research and Development Medical Research Service Department of Veterans
Affairs and by Public Health Service grant DK56338, which funds the
Texas Medical Center Digestive Diseases Center. Dr Yamaoka is supported
in part by a grant from the NIH (DK62813). The contents are solely the
responsibility of die authors and do not necessarily represent the
official views of the VA or NIH.
NR 46
TC 41
Z9 43
U1 0
U2 3
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1347-9032
J9 CANCER SCI
JI Cancer Sci.
PD NOV
PY 2009
VL 100
IS 11
BP 2152
EP 2159
DI 10.1111/j.1349-7006.2009.01291.x
PG 8
WC Oncology
SC Oncology
GA 505VV
UT WOS:000270728200021
PM 19694753
ER
PT J
AU Zhu, YJ
Hu, J
Hu, YD
Liu, WG
AF Zhu, Yongjian
Hu, Jue
Hu, Yiduo
Liu, Weiguo
TI Targeting DNA repair pathways: A novel approach to reduce cancer
therapeutic resistance
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE DNA repair; Cancer therapy; Chemotherapy and radiotherapy resistance;
Small molecule inhibitors
ID BASE EXCISION-REPAIR; DOUBLE-STRAND BREAKS; DEPENDENT PROTEIN-KINASE;
PHASE-II TRIAL; O-6-METHYLGUANINE-DNA METHYLTRANSFERASE; HOMOLOGOUS
RECOMBINATION; MOLECULAR-MECHANISMS; TOPOISOMERASE-II; MISMATCH REPAIR;
O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE
AB Increased chemo-resistance and radio-resistance of cancer cells is a major obstacle in the treatment and management of malignant cancers. An important mechanism that underlies the development of such therapeutic resistance is that cancer cells recognize DNA lesions induced by DNA-damaging agents and by ionizing radiation, and repair these lesions by activating various DNA repair pathways. Therefore, Use of pharmacological agents that can inhibit certain DNA repair pathways in cancer cells has the potential for enhancing the targeted cytotoxicity of anticancer treatments and reversing the associated therapeutic resistance associated with DNA repair; such agents, offering a promising opportunity to achieve better therapeutic efficacy. Here we review the major DNA repair pathways and discuss recent advances in the development of novel inhibitors of DNA repair pathways; many of these agents are under preclinical/clinical investigation. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Zhu, Yongjian; Liu, Weiguo] Zhejiang Univ, Dept Neurosurg, Affiliated Hosp 2, Sch Med, Hangzhou 310009, Zhejiang, Peoples R China.
[Hu, Jue] Zhejiang Med Coll, Dept Pharmacol, Hangzhou 310009, Zhejiang, Peoples R China.
[Hu, Yiduo] Harvard Univ, Sch Med, Dept Canc Biol, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hu, Yiduo] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
RP Liu, WG (reprint author), Zhejiang Univ, Dept Neurosurg, Affiliated Hosp 2, Sch Med, Hangzhou 310009, Zhejiang, Peoples R China.
EM yongjian_zhu@zju.edu.cn; hjmice@zjmc.net.cn; yiduo_hu@dfci.harvard.edu;
neurosurgery@zju.edu.cn
FU Zhejiang Provincial Administration of Traditional Chinese Medicine
[2009CA044]
FX We would like to thank Dr. Sonal Jhaveri for her comments on the
manuscript. This work is supported in part by grant from the Zhejiang
Provincial Administration of Traditional Chinese Medicine to J.H. (Grant
2009CA044).
NR 89
TC 31
Z9 31
U1 1
U2 10
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0305-7372
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD NOV
PY 2009
VL 35
IS 7
BP 590
EP 596
DI 10.1016/j.ctrv.2009.06.005
PG 7
WC Oncology
SC Oncology
GA 523TV
UT WOS:000272098400009
PM 19635647
ER
PT J
AU Sharma, SD
Meeran, SM
Katiyar, N
Tisdale, GB
Yusuf, N
Xu, H
Elmets, CA
Katiyar, SK
AF Sharma, Som D.
Meeran, Syed M.
Katiyar, Nandan
Tisdale, George B.
Yusuf, Nabiha
Xu, Hui
Elmets, Craig A.
Katiyar, Santosh K.
TI IL-12 deficiency suppresses 12-O-tetradecanoylphorbol-13-acetate-induced
skin tumor development in 7,12-dimethylbenz(a)anthracene-initiated mouse
skin through inhibition of inflammation
SO CARCINOGENESIS
LA English
DT Article
ID TEA POLYPHENOL (-)-EPIGALLOCATECHIN-3-GALLATE; NECROSIS-FACTOR-ALPHA;
IFN-GAMMA PRODUCTION; SKH-1 HAIRLESS MICE; OXIDATIVE STRESS; CELL
CARCINOMAS; HIGH-RISK; T-CELLS; IN-VIVO; INTERLEUKIN-12
AB Interleukin (IL)-12 deficiency exacerbates tumorigenesis in ultraviolet (UV) radiation-induced skin. Here, we assessed the effects of IL-12 deficiency on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tumor promotion in 7,12-dimethylbenz(a)anthracene (DMBA)-initiated mouse skin. Using this two-stage chemical carcinogenesis protocol, we found that the development of DMBA/TPA-induced skin tumors was diminished in IL-12p40-knockout mice than in their wild-type counterparts. At the termination of the experiment (at 24 weeks), the skin tumor incidence and tumor multiplicity were significantly lower (P < 0.005) in interleukin-12-knockout (IL-12 KO) mice than in their wild-type counterparts, as was the malignant transformation of DMBA/TPA-induced papillomas to carcinomas (P < 0.01). Analysis of samples collected at the termination of the experiments for biomarkers of inflammation by immunohistochemical analysis, western blotting, enzyme-linked immunosorbent assay and real-time polymerase chain reaction revealed significantly lower levels of cyclooxygenase-2 (COX-2), prostaglandin (PG) E(2), proliferating cell nuclear antigen, cyclin D1 and the proinflammatory cytokines (tumor necrosis factor-alpha, IL-1 beta and IL-6) in the DMBA/TPA-treated tumors and tumor-uninvolved skin of IL-12 KO mice than the skin and tumors of DMBA/TPA-treated wild-type mice. Analysis of the skin 6 h after TPA treatment showed that the TPA-induced promotion of skin edema, inflammatory leukocyte infiltration, COX-2 expression and PGE(2) production was significantly lower in the skin of the IL-12-KO mice than their wild-type counterparts. These results indicate that DMBA/TPA-induced skin tumor development differs from UVB-induced skin tumor development in that endogenous IL-12 acts to inhibit UVB-induced skin tumor development and malignant progression of the skin tumors to carcinoma. In the case of DMBA/TPA-induced skin tumor development, the endogenous IL-12 modulates the tumor promoter stimulation of inflammatory responses.
C1 [Sharma, Som D.; Meeran, Syed M.; Katiyar, Nandan; Tisdale, George B.; Yusuf, Nabiha; Xu, Hui; Elmets, Craig A.; Katiyar, Santosh K.] Univ Alabama, Dept Dermatol, Birmingham, AL 35294 USA.
[Yusuf, Nabiha; Xu, Hui; Elmets, Craig A.; Katiyar, Santosh K.] Univ Alabama, UAB Skin Dis Res Ctr, Birmingham, AL 35294 USA.
[Yusuf, Nabiha; Elmets, Craig A.; Katiyar, Santosh K.] Univ Alabama, UAB Comprehens Canc Ctr, Birmingham, AL 35294 USA.
[Elmets, Craig A.; Katiyar, Santosh K.] Birmingham Vet Affairs Med Ctr, Birmingham, AL 35294 USA.
RP Katiyar, SK (reprint author), Univ Alabama, Dept Dermatol, 1670 Univ Blvd,Volker Hall 557, Birmingham, AL 35294 USA.
EM skatiyar@uab.edu
RI Xu, Hui/A-8167-2009
FU Veterans Administration Merit Review Award; National Institutes of
Health [P30-AR050948, P30-CA013148]
FX Veterans Administration Merit Review Award to S. K. K. and C. A. E.;
National Institutes of Health (P30-AR050948, P30-CA013148).
NR 42
TC 11
Z9 11
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD NOV
PY 2009
VL 30
IS 11
BP 1970
EP 1977
DI 10.1093/carcin/bgp228
PG 8
WC Oncology
SC Oncology
GA 524YB
UT WOS:000272179200021
PM 19759192
ER
PT J
AU Joshi, SB
Blum, AR
Mansour, M
Abbara, S
AF Joshi, Subodh B.
Blum, Andrew R.
Mansour, Moussa
Abbara, Suhny
TI CT Applications in Electrophysiology
SO CARDIOLOGY CLINICS
LA English
DT Article
DE CT; Electrophysiology; Radiofrequency ablation; Cardiac
resynchronization therapy; Cardiac imaging
ID MULTIDETECTOR COMPUTED-TOMOGRAPHY; LEFT ATRIAL APPENDAGE; CARDIAC VENOUS
SYSTEM; RIGHT-VENTRICULAR DYSPLASIA/CARDIOMYOPATHY; ELECTROANATOMIC
MAPPING SYSTEM; PULMONARY VEIN ISOLATION; CHRONIC HEART-FAILURE;
CATHETER ABLATION; MAGNETIC-RESONANCE; IMAGE INTEGRATION
AB In recent years, extraordinary advances have been made in the management of cardiac arrhythmias. Increasingly complex procedures are being performed, and the breadth of conditions for which invasive arrhythmia therapy is indicated continues to grow. In addition to atrial and ventricular ablation procedures for treating arrhythmias, implantable defibrillators and biventricular pacemakers for cardiac resynchronization therapy have made electrophysiology an important part of heart failure management.
C1 [Joshi, Subodh B.; Blum, Andrew R.; Abbara, Suhny] Massachusetts Gen Hosp, Dept Radiol, Cardiac MR CT Program, Cardiovasc Imaging Sect, Boston, MA 02114 USA.
[Mansour, Moussa] Massachusetts Gen Hosp, Cardiol Sect, Dept Radiol, Boston, MA 02114 USA.
RP Abbara, S (reprint author), Massachusetts Gen Hosp, Dept Radiol, Cardiac MR CT Program, Cardiovasc Imaging Sect, 165 Cambridge St,Suite 400, Boston, MA 02114 USA.
EM sabbara@partners.org
NR 62
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 0733-8651
J9 CARDIOL CLIN
JI Cardiol. Clin.
PD NOV
PY 2009
VL 27
IS 4
BP 619
EP +
DI 10.1016/j.ccl.2009.06.012
PG 14
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 507RZ
UT WOS:000270873600010
PM 19766919
ER
PT J
AU Gould, D
Patel, A
Becker, G
Connors, B
Cardella, J
Dawson, S
Glaiberman, C
Kessel, D
Lee, M
Lewandowski, W
Phillips, R
Reekers, J
Sacks, D
Sapoval, M
Scerbo, M
AF Gould, Derek
Patel, Aalpen
Becker, Gary
Connors, Buddy
Cardella, John
Dawson, Steven
Glaiberman, Craig
Kessel, David
Lee, Mick
Lewandowski, William
Phillips, Roger
Reekers, Jim
Sacks, David
Sapoval, Marc
Scerbo, Mark
TI SIR/RSNA/CIRSE Joint Medical Simulation Task Force Strategic Plan:
Executive Summary (vol 30, pg 551, 2007)
SO CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Correction
C1 [Gould, Derek] Royal Liverpool Univ Trust, Dept Radiol, Liverpool, Merseyside, England.
[Patel, Aalpen] Univ Penn, Dept Radiol, Sch Med, Philadelphia, PA 19104 USA.
[Becker, Gary] Univ Arizona, Coll Med, Dept Radiol, Tucson, AZ 85724 USA.
[Connors, Buddy] Radiol Associates Sacramento, Sacramento, CA USA.
[Cardella, John] Baystate Hlth Syst Tufts Univ, Sch Med, Dept Radiol, Springfield, MA 01199 USA.
[Dawson, Steven] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA USA.
[Glaiberman, Craig] Washington Univ, Sch Med, Mallinckrodt Inst Radiol, St Louis, MO 63110 USA.
[Kessel, David] Leeds Teaching Hosp, Leeds, W Yorkshire, England.
[Lee, Mick] Beaumont Hosp, Dept Radiol, Royal Coll Surg Ireland, Dublin 9, Ireland.
[Lewandowski, William] William E Lewandowski Consulting, Daytona Beach, FL USA.
[Phillips, Roger] Univ Hull, Dept Comp Sci, Kingston Upon Hull HU6 7RX, N Humberside, England.
[Reekers, Jim] Univ Amsterdam, Acad Med Ctr, Dept Radiol, NL-1105 AZ Amsterdam, Netherlands.
[Sacks, David] Reading Hosp Med Ctr, Dept Radiol, Reading, PA USA.
[Sapoval, Marc] Hop Europeen G, Dept Radiol, Paris, France.
[Scerbo, Mark] Old Dominion Univ, Dept Psychol, Norfolk, VA USA.
RP Gould, D (reprint author), Royal Liverpool Univ Trust, Dept Radiol, Liverpool, Merseyside, England.
EM dgould@liv.ac.uk
NR 1
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0174-1551
J9 CARDIOVASC INTER RAD
JI Cardiovasc. Interv. Radiol.
PD NOV
PY 2009
VL 32
IS 6
BP 1320
EP 1320
DI 10.1007/s00270-009-9667-7
PG 1
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 515ON
UT WOS:000271481800036
ER
PT J
AU Chen, CY
Chai, H
Wang, XW
Lin, PH
Yao, QZ
AF Chen, Changyi
Chai, Hong
Wang, Xinwen
Lin, Peter H.
Yao, Qizhi
TI Chlamydia heat shock protein 60 decreases expression of endothelial
nitric oxide synthase in human and porcine coronary artery endothelial
cells (vol 83, pg 768, 2009)
SO CARDIOVASCULAR RESEARCH
LA English
DT Correction
C1 [Chen, Changyi; Chai, Hong; Wang, Xinwen; Lin, Peter H.; Yao, Qizhi] Baylor Coll Med, Div Vasc Surg & Endovasc Therapy, Michael E DeBakey Dept Surg R413, Mol Surg Res Ctr, Houston, TX 77030 USA.
[Chen, Changyi; Lin, Peter H.; Yao, Qizhi] Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
RP Chen, CY (reprint author), Baylor Coll Med, Div Vasc Surg & Endovasc Therapy, Michael E DeBakey Dept Surg R413, Mol Surg Res Ctr, 1 Baylor Plaza,Mail Stop BCM390, Houston, TX 77030 USA.
EM jchen@bcm.tmc.edu
RI Chai, Hong/H-5438-2011
NR 2
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0008-6363
J9 CARDIOVASC RES
JI Cardiovasc. Res.
PD NOV 1
PY 2009
VL 84
IS 2
BP 336
EP 336
DI 10.1093/cvr/cvp316
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 514VD
UT WOS:000271422900022
ER
PT J
AU Klein, AJ
Chen, SJ
Messenger, JC
Hansgen, AR
Plomondon, ME
Carroll, JD
Casserly, IP
AF Klein, Andrew J.
Chen, S. James
Messenger, John C.
Hansgen, Adam R.
Plomondon, Mary E.
Carroll, John D.
Casserly, Ivan P.
TI Quantitative Assessment of the Conformational Change in the
Femoropopliteal Artery with Leg Movement
SO CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE peripheral vascular disease; superficial femoral artery; popliteal
artery
ID SUPERFICIAL FEMORAL-ARTERY; SUBINTIMAL ANGIOPLASTY; STENT IMPLANTATION;
NATURAL-HISTORY; NITINOL STENTS; KNEE FLEXION; DISEASE; LESIONS; TRIAL;
LONG
AB Background: The unique physical forces exerted on the femoropopliteal (FP) artery during movement have been implicated in the high rates of restenosis and stent fracture in this artery. Conformational changes in the FP artery during movement are important surrogates of these forces. This study sought to quantify the conformational change in the FP artery between the straight-leg (SL) and crossed-leg (CL) positions. Methods: Using paired angiographic images of overlapping segments of the FP artery in SL and CL positions from patients with peripheral arterial disease, 3-D models of individual segments were generated and subsequently fused to create a 3-D model of the entire FP artery in both leg positions. Based on these 3-D models, the following parameters in the SL and CL positions were quantitatively assessed for the superficial femoral artery (SFA), popliteal artery (PA), and FP artery (i.e., SFA and PA): length, curvature, torsion, twist angle, and development of new flexion angles =15 degrees. Results: In nine male patients with a mean age of 57 +/- 10.2 years, anglography was performed in 10 FP arteries, with successful generation of 3-D models for all vessels. Movement from the SL to the CL position for the SFA, PA, and FP artery was associated with (a) a mean shortening of 18.2 mm (P = 0.002), 32.2 mm (P < 0.001), and 50.3 mm (P < 0.001), respectively; (b) a mean increase in curvature of 0.04 cm(-1) (P = 0.012), 0.2 cm(-1) (P < 0.001), and 0.11 cm(-1) (P < 0.001), respectively; (c) and small absolute changes in mean torsion of 0.034 cm(-1) (P = 0.48), 0.006 cm(-1) (P < 0.001), and 0.057 cm(-1) (P < 0.001), respectively. The same leg movement was associated with a mean twist angle of 45.6 degrees +/- 27.9 degrees (range of 17.4 degrees-103.4 degrees) and 61.1 degrees +/- 31.9 degrees (range of 20.5 degrees-101.1 degrees) for the SFA and PA, respectively. Compared to the SL position, the CL position induced a single flexion point (FxP) =15 degrees in the SFA in two patients, and a mean of 2.4 FxPs =15 degrees (range 1-5) in the PA. Conclusions: Significant changes in length, curvature, and twist occur in the PA and significant but more modest changes in length and twist occur in the SFA during movement from the SL to the CL position. This data has important implications for endovascular therapies that are used to treat disease in the FP artery. (C) 2009 Wiley-Liss, Inc.
C1 [Klein, Andrew J.; Chen, S. James; Messenger, John C.; Hansgen, Adam R.; Carroll, John D.; Casserly, Ivan P.] Univ Colorado Hosp, Aurora, CO USA.
[Plomondon, Mary E.] Denver VA Med Ctr, Denver, CO USA.
RP Casserly, IP (reprint author), Univ Colorado Denver, Anschutz Med Campus,Leprino Off Bldg,12401 E 17th, Aurora, CO 80045 USA.
EM ivan.casserly@ucdenver.edu
FU Boston Scientific
FX Grant sponsor: Boston Scientific.
NR 18
TC 39
Z9 41
U1 1
U2 7
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1522-1946
J9 CATHETER CARDIO INTE
JI Catheter. Cardiovasc. Interv.
PD NOV 1
PY 2009
VL 74
IS 5
BP 787
EP 798
DI 10.1002/ccd.22124
PG 12
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 515UD
UT WOS:000271497500018
PM 19521998
ER
PT J
AU Blackiston, DJ
McLaughlin, KA
Levin, M
AF Blackiston, Douglas J.
McLaughlin, Kelly A.
Levin, Michael
TI Bioelectric controls of cell proliferation Ion channels, membrane
voltage and the cell cycle
SO CELL CYCLE
LA English
DT Review
DE ion channel; ion pump; membrane voltage; electric potential; current;
mitosis; growth control
ID GATED POTASSIUM CHANNELS; EPIDERMAL-GROWTH-FACTOR; HUMAN
PROSTATE-CANCER; X-RAY-MICROANALYSIS; HUMAN T-LYMPHOCYTES; EAG K+
CHANNELS; PERIPHERAL-BLOOD LYMPHOCYTES; LEFT-RIGHT AXIS; A-GO-GO;
BREAST-CANCER
AB All cells possess long-term, steady-state voltage gradients across the plasma membrane. These transmembrane potentials arise from the combined activity of numerous ion channels, pumps and gap junction complexes. Increasing data from molecular physiology now reveal that the role of changes in membrane voltage controls, and is in turn controlled by, progression through the cell cycle. We review recent functional data on the regulation of mitosis by bioelectric signals, and the function of membrane voltage and specific potassium, sodium and chloride ion channels in the proliferation of embryonic, somatic and neoplastic cells. Its unique properties place this powerful, well-conserved, but still poorly-understood signaling system at the center of the coordinated cellular interactions required for complex pattern formation. Moreover, disregulation of ion channel expression and function is increasingly observed to be not only a useful marker but likely a functional element in oncogenesis. New advances in genomics and the development of in vivo biophysical techniques suggest exciting opportunities for molecular medicine, bioengineering and regenerative approaches to human health.
C1 [Blackiston, Douglas J.; McLaughlin, Kelly A.; Levin, Michael] Tufts Univ, Dept Biol, Dana Labs, Medford, MA 02155 USA.
[Blackiston, Douglas J.; Levin, Michael] Tufts Univ, Ctr Regenerat & Dev Biol, Medford, MA 02155 USA.
[Blackiston, Douglas J.] Forsyth Inst, Dept Regenerat & Dev Biol, Boston, MA USA.
RP Levin, M (reprint author), Tufts Univ, Dept Biol, Dana Labs, Medford, MA 02155 USA.
EM michael.levin@tufts.edu
FU NIH [R01-GM077425, R01-EY018168, R01-GM078484]; Forsyth Institute
[5T32DE007327-07]; NSF [IOS-0843355]
FX This paper is dedicated to C. D. Cone, who was one of the first to study
in detail the profound role of membrane voltage in proliferation
control. We are grateful to the members of the Levin lab and the
bioelectricity community for many useful discussions. We thank Dany
Adams for the photos in Figure 4, and Ai-Sun Tseng for her comments on
the manuscript. M. L. is supported by grants R01-GM077425, EY018168 and
GM078484 from the NIH. D. B. is supported by Forsyth Institute's T32
grant 5T32DE007327-07. Kelly McLaughlin is supported by NSF grant
IOS-0843355.
NR 176
TC 47
Z9 49
U1 0
U2 23
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD NOV 1
PY 2009
VL 8
IS 21
BP 3527
EP 3536
DI 10.4161/cc.8.21.9888
PG 10
WC Cell Biology
SC Cell Biology
GA 525LX
UT WOS:000272218600024
PM 19823012
ER
PT J
AU Hotokezaka, Y
van Leyen, K
Lo, EH
Beatrix, B
Katayama, I
Jin, G
Nakamura, T
AF Hotokezaka, Y.
van Leyen, K.
Lo, E. H.
Beatrix, B.
Katayama, I.
Jin, G.
Nakamura, T.
TI alpha NAC depletion as an initiator of ER stress-induced apoptosis in
hypoxia
SO CELL DEATH AND DIFFERENTIATION
LA English
DT Article
DE nascent polypeptide-associated complex; apoptosis; ER stress; glycogen
synthase kinase; hypoxia
ID POLYPEPTIDE-ASSOCIATED COMPLEX; ENDOPLASMIC-RETICULUM STRESS;
UBIQUITIN-PROTEASOME SYSTEM; NEURONAL CELL-DEATH; BETA-NAC; KINASE;
BRAIN; PHOSPHORYLATION; IDENTIFICATION; ACTIVATION
AB Accumulation of unfolded proteins triggers endoplasmic reticulum (ER) stress and is considered a part of the cellular responses to hypoxia. The nascent polypeptide-associated complex (NAC) participates in the proper maturation of newly synthesized proteins. However, thus far, there have been no comprehensive studies on NAC involvement in hypoxic stress. Here, we show that hypoxia activates glycogen synthase kinase-3 beta (GSK-3 beta) and that the activated GSK-3 beta destabilizes alpha NAC with the subsequent apoptosis of the cell. Hypoxia of various cell types and the mouse ischemic brain was associated with rapid downregulation of alpha NAC and ER stress responses involving PERK, ATF4, gamma-taxilin, elF2 alpha, Bip, and CHOP. Depletion of alpha NAC by RNA interference specifically activated ER stress responses and caused mitochondrial dysfunction, which resulted in apoptosis through caspase activation. Interestingly, we found that the hypoxic conditions activated GSK-3 beta, and that GSK-3 beta inhibition prevented alpha NAC protein downregulation in hypoxic cells and rescued the cells from apoptosis. In addition, alpha NAC overexpression increased the viability of hypoxic cells. Taken together, these results suggest that alpha NAC degradation triggers ER stress responses and initiates apoptotic processes in hypoxic cells, and that GSK-3 beta may participate upstream in this mechanism. Cell Death and Differentiation (2009) 16, 1505-1514; doi:10.1038/cdd.2009.90; published online 17 July 2009
C1 [Hotokezaka, Y.; Katayama, I.; Nakamura, T.] Nagasaki Univ, Sch Dent, Dept Radiol & Canc Biol, Nagasaki 8528588, Japan.
[van Leyen, K.; Lo, E. H.; Jin, G.] Massachusetts Gen Hosp, Dept Radiol, Neuroprotect Res Lab, Charlestown, MA 02129 USA.
[van Leyen, K.; Lo, E. H.; Jin, G.] Massachusetts Gen Hosp, Dept Neurol, Neuroprotect Res Lab, Charlestown, MA 02129 USA.
[van Leyen, K.; Lo, E. H.; Jin, G.] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Beatrix, B.] Univ Munich, Dept Chem & Biochem, Gene Ctr, LMU, D-81377 Munich, Germany.
RP Nakamura, T (reprint author), Nagasaki Univ, Sch Dent, Dept Radiol & Canc Biol, 1-7-1 Sakamoto, Nagasaki 8528588, Japan.
EM taku@nagasaki-u.ac.jp
RI van Leyen, Klaus/C-9126-2013
NR 46
TC 23
Z9 23
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1350-9047
J9 CELL DEATH DIFFER
JI Cell Death Differ.
PD NOV
PY 2009
VL 16
IS 11
BP 1505
EP 1514
DI 10.1038/cdd.2009.90
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 505GE
UT WOS:000270679000009
PM 19609276
ER
PT J
AU Schon, K
Quiroz, YT
Hasselmo, ME
Stern, CE
AF Schon, Karin
Quiroz, Yakeel T.
Hasselmo, Michael E.
Stern, Chantal E.
TI Greater Working Memory Load Results in Greater Medial Temporal Activity
at Retrieval
SO CEREBRAL CORTEX
LA English
DT Review
DE delayed match to sample; episodic memory; hippocampus; neuroimaging;
subiculum
ID SHORT-TERM-MEMORY; DORSOLATERAL PREFRONTAL CORTEX; MONKEY RETROSPLENIAL
CORTEX; GRADED PERSISTENT ACTIVITY; LATERAL FRONTAL-CORTEX;
EVENT-RELATED FMRI; ENTORHINAL CORTEX; EPISODIC MEMORY; RHESUS-MONKEY;
MACAQUE MONKEY
AB Most functional magnetic resonance imaging (fMRI) studies examining working memory (WM) load have focused on the prefrontal cortex (PFC) and have demonstrated increased prefrontal activity with increased load. Here we examined WM load effects in the medial temporal lobe (MTL) using an fMRI Sternberg task with novel complex visual scenes. Trials consisted of 3 sequential events: 1) sample presentation (encoding), 2) delay period (maintenance), and 3) probe period (retrieval). During sample encoding, subjects saw either 2 or 4 pictures consecutively. During retrieval, subjects indicated whether the probe picture matched one of the sample pictures. Results revealed that activity in the left anterior hippocampal formation, bilateral retrosplenial area, and left amygdala was greater at retrieval for trials with larger memory load, whereas activity in the PFC was greater at encoding for trials with larger memory load. There was no load effect during the delay. When encoding, maintenance, and retrieval periods were compared with fixation, activity was present in the hippocampal body/tail and fusiform gyrus bilaterally during encoding and retrieval, but not maintenance. Bilateral dorsolateral prefrontal activity was present during maintenance, but not during encoding or retrieval. The results support models of WM predicting that activity in the MTL should be modulated by WM load.
C1 [Schon, Karin; Quiroz, Yakeel T.; Hasselmo, Michael E.; Stern, Chantal E.] Boston Univ, Ctr Memory & Brain, Boston, MA 02215 USA.
[Schon, Karin; Quiroz, Yakeel T.; Hasselmo, Michael E.; Stern, Chantal E.] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
[Schon, Karin; Quiroz, Yakeel T.; Hasselmo, Michael E.; Stern, Chantal E.] Boston Univ, Ctr Excellence Learing Educ Sci & Technol, Boston, MA 02215 USA.
[Stern, Chantal E.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Dept Radiol, Charlestown, MA 02129 USA.
RP Schon, K (reprint author), Boston Univ, Ctr Memory & Brain, 2 Cummington St,Suite 109, Boston, MA 02215 USA.
EM kschon@bu.edu
OI Schon, Karin/0000-0003-2963-8449; Hasselmo, Michael/0000-0002-9925-6377
FU National Science Foundation [SBE-0354278]; National Institutes of Health
[P50 MH071702-01]; National Center for Research Resources [P41RR14075];
Mental Illness and Neuroscience Discovery Institute
FX National Science Foundation grant (SBE-0354278); National Institutes of
Health grants (P50 MH071702-01, National Center for Research Resources
P41RR14075); Mental Illness and Neuroscience Discovery Institute.
NR 111
TC 39
Z9 39
U1 2
U2 14
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
J9 CEREB CORTEX
JI Cereb. Cortex
PD NOV
PY 2009
VL 19
IS 11
BP 2561
EP 2571
DI 10.1093/cercor/bhp006
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 505IJ
UT WOS:000270685900006
PM 19224975
ER
PT J
AU Panizzon, MS
Fennema-Notestine, C
Eyler, LT
Jernigan, TL
Prom-Wormley, E
Neale, M
Jacobson, K
Lyons, MJ
Grant, MD
Franz, CE
Xian, H
Tsuang, M
Fischl, B
Seidman, L
Dale, A
Kremen, WS
AF Panizzon, Matthew S.
Fennema-Notestine, Christine
Eyler, Lisa T.
Jernigan, Terry L.
Prom-Wormley, Elizabeth
Neale, Michael
Jacobson, Kristen
Lyons, Michael J.
Grant, Michael D.
Franz, Carol E.
Xian, Hong
Tsuang, Ming
Fischl, Bruce
Seidman, Larry
Dale, Anders
Kremen, William S.
TI Distinct Genetic Influences on Cortical Surface Area and Cortical
Thickness
SO CEREBRAL CORTEX
LA English
DT Article
DE cortical volume; genetic correlation; heritability; magnetic resonance
imaging; twin study
ID VIETNAM ERA TWIN; REGIONAL BRAIN VOLUMES; HUMAN CEREBRAL-CORTEX;
SCHIZOPHRENIA; REGISTRY; METAANALYSIS; ZYGOSITY; AGE; INTELLIGENCE;
ORGANIZATION
AB Neuroimaging studies examining the effects of aging and neuropsychiatric disorders on the cerebral cortex have largely been based on measures of cortical volume. Given that cortical volume is a product of thickness and surface area, it is plausible that measures of volume capture at least 2 distinct sets of genetic influences. The present study aims to examine the genetic relationships between measures of cortical surface area and thickness. Participants were men in the Vietnam Era Twin Study of Aging (110 monozygotic pairs and 92 dizygotic pairs). Mean age was 55.8 years (range: 51-59). Bivariate twin analyses were utilized in order to estimate the heritability of cortical surface area and thickness, as well as their degree of genetic overlap. Total cortical surface area and average cortical thickness were both highly heritable (0.89 and 0.81, respectively) but were essentially unrelated genetically (genetic correlation = 0.08). This pattern was similar at the lobar and regional levels of analysis. These results demonstrate that cortical volume measures combine at least 2 distinct sources of genetic influences. We conclude that using volume in a genetically informative study, or as an endophenotype for a disorder, may confound the underlying genetic architecture of brain structure.
C1 [Panizzon, Matthew S.; Fennema-Notestine, Christine; Eyler, Lisa T.; Jernigan, Terry L.; Franz, Carol E.; Tsuang, Ming; Dale, Anders; Kremen, William S.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Fennema-Notestine, Christine; Jernigan, Terry L.] Univ Calif San Diego, Dept Radiol, La Jolla, CA 92093 USA.
[Eyler, Lisa T.; Kremen, William S.] San Diego Vet Adm Hlth Care Syst, San Diego, CA 92161 USA.
[Prom-Wormley, Elizabeth; Neale, Michael] Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Sch Med, Richmond, VA 23219 USA.
[Jacobson, Kristen] Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA.
[Lyons, Michael J.; Grant, Michael D.] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
[Xian, Hong] Washington Univ, Dept Psychiat, Sch Med, St Louis, MO 63130 USA.
[Tsuang, Ming; Kremen, William S.] Univ Calif San Diego, Ctr Behav Genom, La Jolla, CA 92093 USA.
[Tsuang, Ming] Harvard Univ, Sch Med, Harvard Inst Psychiat Epidemiol & Genet, Boston, MA 02115 USA.
[Fischl, Bruce] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02129 USA.
[Seidman, Larry] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Dale, Anders] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA.
[Tsuang, Ming] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
RP Panizzon, MS (reprint author), Univ Calif San Diego, Dept Psychiat, 9500 Gilman Dr MC 0738, La Jolla, CA 92093 USA.
EM mspanizz@ucsd.edu
RI Jacobson, Kristen/D-2064-2009; Dale, Anders/A-5180-2010; Lyons,
Michael/B-6119-2011;
OI Prom-Wormley, Elizabeth/0000-0001-9230-9723; Lyons,
Michael/0000-0001-6516-9219; Fennema-Notestine,
Christine/0000-0002-6527-6361
FU National Institutes of Health/National Institute on Aging [U24 RR021382,
R01 AG18386, RO1 AG18384, RO1 AG22381, RO1 AG 22982]; US Department of
Veterans Affairs; VA Cooperative Studies Program; Department of Defense;
National Personnel Records Center, National Archives, and Records
Administration; Internal Revenue Service; National Opinion Research
Center; National Research Council, National Academy of Sciences;
Institute for Survey Research, Temple University; Schulman, Ronca, and
Bucuvalas, Inc
FX National Institutes of Health/National Institute on Aging Grants U24
RR021382, R01 AG18386, RO1 AG18384, RO1 AG22381, RO1 AG 22982; US
Department of Veterans Affairs; VA Cooperative Studies Program;
Department of Defense; National Personnel Records Center, National
Archives, and Records Administration; Internal Revenue Service; National
Opinion Research Center; National Research Council, National Academy of
Sciences; Institute for Survey Research, Temple University; Schulman,
Ronca, and Bucuvalas, Inc.
NR 54
TC 371
Z9 374
U1 0
U2 22
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
J9 CEREB CORTEX
JI Cereb. Cortex
PD NOV
PY 2009
VL 19
IS 11
BP 2728
EP 2735
DI 10.1093/cercor/bhp026
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 505IJ
UT WOS:000270685900022
PM 19299253
ER
PT J
AU Solis, J
McCarty, D
Levine, RA
Handschumacher, MD
Fernandez-Friera, L
Chen-Tournoux, A
Mont, L
Vidal, B
Singh, JP
Brugada, J
Picard, MH
Sitges, M
Hung, J
AF Solis, Jorge
McCarty, David
Levine, Robert A.
Handschumacher, Mark D.
Fernandez-Friera, Leticia
Chen-Tournoux, Annabel
Mont, Luis
Vidal, Barbara
Singh, Jagmeet P.
Brugada, Josep
Picard, Michael H.
Sitges, Marta
Hung, Judy
TI Mechanism of Decrease in Mitral Regurgitation After Cardiac
Resynchronization Therapy Optimization of the Force-Balance Relationship
SO CIRCULATION-CARDIOVASCULAR IMAGING
LA English
DT Article
DE functional mitral regurgitation; 3D echocardiography; cardiac
resynchronization therapy
ID CHRONIC HEART-FAILURE; ORIFICE AREA; VENTRICULAR VOLUME; FLOW; INSIGHTS;
ECHOCARDIOGRAPHY; DYSSYNCHRONY; VALIDATION; PREDICTORS; SIZE
AB Background-Cardiac resynchronization therapy (CRT) has been shown to reduce functional mitral regurgitation (MR). It has been proposed that the mechanism of MR reduction relates to geometric change or, alternatively, changes in left ventricular (LV) contractile function. Normal mitral valve (MV) function relies on a balance between tethering and closing forces on the MV leaflets. Functional MR results from a derangement of this force-balance relationship, and CRT may be an important modulator of MV function by its ability to enhance the force-balance relationship on the MV. We hypothesized that CRT improves the comprehensive force balance acting on the valve, including favorable changes in both geometry and LV contractile function.
Methods and Results-We examined the effect of CRT on 34 patients with functional MR before and after CRT (209 +/- 81 days). MR regurgitant volume, closing forces on MV (derived from Doppler transmitral pressure gradients), including dP/dt and a factor (closing pressure ratio) expressing how long the peak closing gradient is maintained over systole (closing pressure ratio = velocity time integral/MR peak velocity x mitral regurgitation time), and dyssynchrony by tissue Doppler were measured. End-diastolic volume, end-systolic volume, mitral valve annular area (MAA) and contraction (percent change in MAA from end-diastole to midsystole), leaflet closing area (leaflet area during valve closure), and tenting volume (volume under leaflets to annular plane) were measured by 3D echocardiography. After CRT, end-diastolic volume (253 +/- 111 versus 221 +/- 110 mL, P < 0.001) and end-systolic volume (206 +/- 97 versus 167 +/- 91 mL, P < 0.001) decreased and ejection fraction (19 +/- 6 versus 27 +/- 9%, P < 0.001) increased. MR regurgitant volume decreased from 35 +/- 17 to 23 +/- 14 mL (P < 0.001), MAA from 11.6 +/- 3.5 to 10.5 +/- 3.1 cm(2) (P < 0.001), leaflet closing area from 15.4 +/- 5 to 13.7 +/- 3.8 cm(2) (P < 0.001), and tenting volume from 5.7 +/- 2.6 to 4.6 +/- 2.2 mL (P < 0.001). Peak velocity (and therefore transmitral closing pressure) was more sustained throughout systole, as reflected by the increase in the closing pressure ratio (0.77 +/- 0.1 versus 0.84 +/- 0.1 before CRT versus after CRT, P = 0.01); dP/dt also improved after CRT. There was no change in dyssynchrony or MAA contraction.
Conclusions-Reduction in MR after CRT is associated with favorable changes in MV geometry and closing forces on the MV. It does so by favorably affecting the force balance acting on the MV in 2 ways: reducing tethering through reversal of LV remodeling and increasing the systolic duration of peak transmitral closing pressures. (Circ Cardiovasc Imaging. 2009; 2: 444-450.)
C1 [Hung, Judy] Massachusetts Gen Hosp, Div Cardiol, Cardiac Ultrasound Lab, Boston, MA 02114 USA.
[Mont, Luis; Vidal, Barbara; Brugada, Josep; Sitges, Marta] Univ Barcelona, Dept Cardiol, Thorax Clin Inst, Hosp Clin IDIBAPS,IDIBAPS Inst Invest Biomed Augu, E-08007 Barcelona, Spain.
RP Hung, J (reprint author), Massachusetts Gen Hosp, Div Cardiol, Cardiac Ultrasound Lab, Blake 256,55 Fruit St, Boston, MA 02114 USA.
EM jhung@partners.org
RI Fernandez Friera, Leticia /E-9931-2015;
OI Fernandez Friera, Leticia /0000-0002-4237-2166; BRUGADA,
JOSEP/0000-0002-5662-8302; Picard, Michael/0000-0002-9264-3243
FU National Institutes of Health/National Institute for Biomedical Imaging
and Bioengineering [R21 EB005294]; American Society of Echocardiography
Career Development Award; Spanish Society of Cardiology; St Jude
Medical; Medtronic; Boston Scientific; Biotronix; Sorin; Philips Medical
Systems
FX Dr Singh is a consultant and recipient of research grants and speaking
fees for the following companies: St Jude Medical, Medtronic, Boston
Scientific, Biotronix, Sorin, and Philips Medical Systems.
NR 34
TC 27
Z9 29
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-9651
J9 CIRC-CARDIOVASC IMAG
JI Circ.-Cardiovasc. Imaging
PD NOV
PY 2009
VL 2
IS 6
BP 444
EP 450
DI 10.1161/CIRCIMAGING.108.823732
PG 7
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 521BX
UT WOS:000271895300004
PM 19920042
ER
PT J
AU Sosnovik, DE
Garanger, E
Aikawa, E
Nahrendorf, M
Figuiredo, JL
Dai, GP
Reynolds, F
Rosenzweig, A
Weissleder, R
Josephson, L
AF Sosnovik, David E.
Garanger, Elisabeth
Aikawa, Elena
Nahrendorf, Matthias
Figuiredo, Jose-Luiz
Dai, Guangping
Reynolds, Fred
Rosenzweig, Anthony
Weissleder, Ralph
Josephson, Lee
TI Molecular MRI of Cardiomyocyte Apoptosis With Simultaneous
Delayed-Enhancement MRI Distinguishes Apoptotic and Necrotic Myocytes In
Vivo Potential for Midmyocardial Salvage in Acute Ischemia
SO CIRCULATION-CARDIOVASCULAR IMAGING
LA English
DT Article
DE molecular imaging; MRI; apoptosis; myocardium; ischemia
ID ACUTE MYOCARDIAL-INFARCTION; IRON-OXIDE PARTICLES; MAGNETIC-RESONANCE;
CELL-DEATH; MICROVASCULAR OBSTRUCTION; CONTRAST AGENTS; FIELD-STRENGTH;
ANNEXIN-V; INJURY; VISUALIZATION
AB Background-A novel dual-contrast molecular MRI technique to image both cardiomyocyte apoptosis and necrosis in vivo within 4 to 6 hours of ischemia is presented. The technique uses the annexin-based nanoparticle AnxCLIO-Cy5.5 (apoptosis) and simultaneous delayed-enhancement imaging with a novel gadolinium chelate, Gd-DTPA-NBD (necrosis).
Methods and Results-Mice with transient coronary ligation were injected intravenously at the onset of reperfusion with AnxCLIO-Cy5.5 (n = 7) or the control probe Inact_CLIO-Cy5.5 (n = 6). T2*-weighted MR images (9.4 T) were acquired within 4 to 6 hours of reperfusion. The contrast-to-noise ratio between injured and uninjured myocardium was measured. The mice were then injected with Gd-DTPA-NBD, and delayed-enhancement imaging was performed within 10 to 30 minutes. Uptake of AnxCLIO-Cy5.5 was most prominent in the midmyocardium and was significantly greater than that of Inact_CLIO-Cy5.5 (contrast-to-noise ratio, 8.82 +/- 1.5 versus 3.78 +/- 1.1; P < 0.05). Only 21 +/- 3% of the myocardium with accumulation of AnxCLIO-Cy5.5 showed delayed-enhancement of Gd-DTPA-NBD. Wall thickening was significantly reduced in segments with delayed enhancement and/or transmural accumulation of AnxCLIO-Cy5.5 (P < 0.001). Fluorescence microscopy of AnxCLIO-Cy5.5 and immunohistochemistry of Gd-DTPA-NBD confirmed the presence of large numbers of apoptotic but potentially viable cardiomyocytes (AnxCLIO-Cy5.5 positive, Gd-DTPA-NBD negative) in the midmyocardium.
Conclusions-A novel technique to image cardiomyocyte apoptosis and necrosis in vivo within 4 to 6 hours of injury is presented and reveals large areas of apoptotic but viable myocardium in the midmyocardium. Strategies to salvage the numerous apoptotic but potentially viable cardiomyocytes in the midmyocardium in acute ischemia should be investigated. (Circ Cardiovasc Imaging. 2009; 2: 460-467.)
C1 [Sosnovik, David E.; Garanger, Elisabeth; Aikawa, Elena; Nahrendorf, Matthias; Figuiredo, Jose-Luiz; Reynolds, Fred; Weissleder, Ralph; Josephson, Lee] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Boston, MA USA.
[Sosnovik, David E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[Sosnovik, David E.; Dai, Guangping] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Martinos Ctr Biomed Imaging, Boston, MA USA.
[Nahrendorf, Matthias; Weissleder, Ralph] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Syst Biol, Boston, MA USA.
[Rosenzweig, Anthony] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Cardiovasc Inst, Boston, MA 02215 USA.
RP Sosnovik, DE (reprint author), 5416 CMIR,149 13th St, Charlestown, MA 02129 USA.
EM sosnovik@nmr.mgh.harvard.edu
FU National Institutes of Health [R01-HL093038, K08-HL079984, AHA 0835623D,
HL-080731, HL-078641, CA-92782, CA-86355, R01EB004472]
FX This study was supported in part by the following grants from the
National Institutes of Health: R01-HL093038 and K08-HL079984 (D. E. S.),
AHA 0835623D (M. N.), HL-080731, HL-078641, CA-92782, and CA-86355 (R.
W.), and R01EB004472 (L. J.).
NR 30
TC 49
Z9 53
U1 2
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-9651
J9 CIRC-CARDIOVASC IMAG
JI Circ.-Cardiovasc. Imaging
PD NOV
PY 2009
VL 2
IS 6
BP 460
EP 467
DI 10.1161/CIRCIMAGING.109.859678
PG 8
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 521BX
UT WOS:000271895300006
PM 19920044
ER
PT J
AU Sosnovik, DE
Nahrendorf, M
Panizzi, P
Matsui, T
Aikawa, E
Dai, GP
Li, L
Reynolds, F
Dorn, GW
Weissleder, R
Josephson, L
Rosenzweig, A
AF Sosnovik, David E.
Nahrendorf, Matthias
Panizzi, Peter
Matsui, Takashi
Aikawa, Elena
Dai, Guangping
Li, Ling
Reynolds, Fred
Dorn, Gerald W., II
Weissleder, Ralph
Josephson, Lee
Rosenzweig, Anthony
TI Molecular MRI Detects Low Levels of Cardiomyocyte Apoptosis in a
Transgenic Model of Chronic Heart Failure
SO CIRCULATION-CARDIOVASCULAR IMAGING
LA English
DT Article
DE apoptosis; heart failure; MRI; molecular imaging; cardiomyocyte
ID CARDIAC MYOCYTE APOPTOSIS; NONINVASIVE DETECTION; MEMBRANE
PHOSPHATIDYLSERINE; MYOCARDIAL-INFARCTION; ANNEXIN A5; IN-VIVO;
INHIBITION; ACTIVATION; DEATH; ATHEROSCLEROSIS
AB Background-The ability to image cardiomyocyte (CM) apoptosis in heart failure could facilitate more accurate diagnostics and optimize targeted therapeutics. We thus aimed to develop a platform to image CM apoptosis quantitatively and specifically in heart failure in vivo. The myocardium in heart failure, however, is characterized by very low levels of CM apoptosis and normal vascular permeability, factors thought to preclude the use of molecular MRI.
Methods and Results-Female mice with overexpression of Gaq were studied. Two weeks postpartum, these mice develop a cardiomyopathy characterized by low levels of CM apoptosis and minimal myocardial necrosis or inflammation. The mice were injected with the annexin-labeled nanoparticle (AnxCLIO-Cy5.5) or a control probe (CLIO-Cy5.5) and imaged in vivo at 9.4 T. Uptake of AnxCLIO-Cy5.5 occurred in isolated clusters, frequently in the subendocardium. Myocardial T2* was significantly lower (7.6 +/- 1.5 versus 16.8 +/- 2.7 ms, P < 0.05) in the mice injected with AnxCLIO-Cy5.5 versus CLIO-Cy5.5, consistent with the uptake of AnxCLIO-Cy5.5 by apoptotic CMs. A strong correlation (r(2) = 0.86, P < 0.05) was seen between in vivo T2* (AnxCLIO-Cy5.5 uptake) and myocardial caspase-3 activity.
Conclusions-The ability of molecular MRI to image sparsely expressed targets in the myocardium is demonstrated in this study. Moreover, a novel platform for high-resolution and specific imaging of CM apoptosis in heart failure is established. In addition to providing novel insights into the pathogenesis of CM apoptosis, the developed platform could facilitate the development of novel antiapoptotic therapies in heart failure. (Circ Cardiovasc Imaging. 2009; 2: 468-475.)
C1 [Sosnovik, David E.; Nahrendorf, Matthias; Panizzi, Peter; Aikawa, Elena; Reynolds, Fred; Weissleder, Ralph; Josephson, Lee] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Boston, MA USA.
[Sosnovik, David E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[Sosnovik, David E.; Dai, Guangping] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Martinos Ctr Biomed Imaging, Boston, MA USA.
[Matsui, Takashi; Li, Ling; Rosenzweig, Anthony] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Cardiovasc Inst, Boston, MA 02215 USA.
[Dorn, Gerald W., II] Washington Univ, Sch Med, Ctr Pharmacogenom, St Louis, MO USA.
RP Sosnovik, DE (reprint author), 5416,149 13th St, Charlestown, MA 02129 USA.
EM sosnovik@nmr.mgh.harvard.edu
OI Panizzi, Peter/0000-0003-0141-8807
FU National Institutes of Health [R01 HL093038, K08 HL079984, R01EB004472,
CA92782, CA86355, HL073363, HL077543, HL059521]; Leducq Network of
Research Excellence Award
FX This study was supported in part by the following grants from the
National Institutes of Health: R01 HL093038 and K08 HL079984 (Dr
Sosnovik); R01EB004472 (Dr Josephson); CA92782 and CA86355 (Dr
Weissleder); and HL073363, HL077543, and HL059521 (Dr Rosenzweig); and a
Leducq Network of Research Excellence Award (Dr Rosenzweig).
NR 37
TC 30
Z9 31
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-9651
J9 CIRC-CARDIOVASC IMAG
JI Circ.-Cardiovasc. Imaging
PD NOV
PY 2009
VL 2
IS 6
BP 468
EP 475
DI 10.1161/CIRCIMAGING.109.863779
PG 8
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 521BX
UT WOS:000271895300007
PM 19920045
ER
PT J
AU Bradley, SM
Levy, WC
Veenstra, DL
AF Bradley, Steven M.
Levy, Wayne C.
Veenstra, David L.
TI Cost-Consequences of Ultrafiltration for Acute Heart Failure A Decision
Model Analysis
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE heart failure; ultrafiltration; diuretics; costs and cost analysis
ID HEPARIN-INDUCED THROMBOCYTOPENIA; MOLECULAR-WEIGHT HEPARIN; CONTINUOUS
VENOVENOUS HEMOFILTRATION; DISEASE MANAGEMENT PROGRAMS; BLOOD-STREAM
INFECTIONS; UNFRACTIONATED HEPARIN; HOSPITALIZED-PATIENTS; READMISSION
RATES; CONTROLLED-TRIAL; OLDER PATIENTS
AB Background-Ultrafiltration for heart failure may reduce costs associated with acute heart failure by decreasing rehospitalization rates compared to intravenous diuretics.
Methods and Results-We developed a decision-analytic model to explore the clinical outcomes and associated costs of ultrafiltration compared to intravenous diuretics for index and subsequent acute heart failure hospitalizations to 90 days from index hospitalization. We evaluated the model from societal, Medicare, and hospital payer perspectives. Base-case probabilities and costs were derived from the Ultrafiltration versus Intravenous Diuretics for Patients Hospitalized for Acute Decompensated Congestive Heart Failure clinical trial, Medicare reimbursement schedules, and published data. From a societal perspective, treatment with ultrafiltration had an 86% probability of being more expensive than intravenous diuretics in probabilistic sensitivity analysis, with a base-case estimate of $13 469 per patient treated with ultrafiltration compared to $11 610 per patient treated with intravenous diuretics. Cost estimates were most influenced by length of index hospitalization, daily cost of rehospitalization, number of days rehospitalized, and number and cost of ultrafiltration filters. From a Medicare payer perspective, ultrafiltration had a >99% probability of being cost saving. From a hospital perspective, there was a 97% probability ultrafiltration was more expensive. Our model suggested similar 90-day mortality rates between treatment arms.
Conclusion-Despite a reduction in rehospitalization rates, it is unlikely ultrafiltration results in cost savings from a societal perspective. The discordance in cost between societal, Medicare, and hospital perspectives underscores the importance of payer perspective in formulating strategies and reimbursement structures to reduce heart failure hospitalizations. (Circ Cardiovasc Qual Outcomes. 2009; 2: 566-573.)
C1 [Bradley, Steven M.] VA Puget Sound Hlth Care Syst, Hlth Serv Res & Dev, Dept Vet Affairs, Seattle, WA 98101 USA.
[Bradley, Steven M.; Levy, Wayne C.] Univ Washington, Dept Med, Div Cardiol, Seattle, WA USA.
[Veenstra, David L.] Univ Washington, Dept Pharm, Pharmaceut Outcomes Res & Policy Program, Seattle, WA 98195 USA.
RP Bradley, SM (reprint author), VA Puget Sound Hlth Care Syst, Hlth Serv Res & Dev, Dept Vet Affairs, 1100 Olive Way,Suite 1400, Seattle, WA 98101 USA.
EM Steve.Bradley@va.gov
FU Department of Veterans Affairs; Veterans Health Administration; Office
of Research and Development; Health Services Research and Development
FX This material is based on work supported by the Department of Veterans
Affairs, the Veterans Health Administration, the Office of Research and
Development, and Health Services Research and Development.
NR 47
TC 22
Z9 23
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7713
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD NOV
PY 2009
VL 2
IS 6
BP 566
EP U99
DI 10.1161/CIRCOUTCOMES.109.853556
PG 13
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 575PD
UT WOS:000276078500009
PM 20031894
ER
PT J
AU Rose, AJ
Ozonoff, A
Grant, RW
Henault, LE
Hylek, EM
AF Rose, Adam J.
Ozonoff, Al
Grant, Richard W.
Henault, Lori E.
Hylek, Elaine M.
TI Epidemiology of Subtherapeutic Anticoagulation in the United States
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE warfarin; thromboembolism; anticoagulants; quality of health care;
medication therapy management
ID INTERNATIONAL NORMALIZED RATIO; ATRIAL-FIBRILLATION; BLEEDING
COMPLICATIONS; ORAL ANTICOAGULANT; WARFARIN THERAPY; RISK-FACTORS;
EXCESSIVE ANTICOAGULATION; HEMORRHAGE; THROMBOEMBOLISM; OUTPATIENTS
AB Background-Low international normalized ratio (INR; <= 1.5) increases risk for thromboembolism. However, little is known about the epidemiology of low INR.
Methods and Results-We prospectively collected data from 47 community-based clinics located throughout the United States from 2000 to 2002. We examined risk factors for low INR (<= 1.5), reasons given in the medical record for low INR, and proportion of thromboembolic events that occurred during periods of low INR. Of the 4489 patients in our database, 1540 (34%) had at least 1 low INR. Compared with men, women had an increased incidence of low INR (adjusted incidence rate ratio, 1.44; P<0.001). Compared with patients anticoagulated for atrial fibrillation, patients anticoagulated for venous thromboembolism had an increased incidence of low INR (adjusted incidence rate ratio, 1.48; P<0.001). The 5 most common reasons for low INR were nonadherence (17%), interruptions for procedures (16%), recent dose reductions (15%), no reason apparent after questioning (15%), and second or greater consecutive low INR (13%). A total of 21.8% of thromboembolic events (95% CI, 12.2 to 35.4%) occurred during periods of low INR; 58% of these events were related to an interruption of warfarin therapy.
Conclusions-In this cohort of patients receiving warfarin, more than 1 in 5 thromboembolic events occurred during a period of low INR. Women and patients anticoagulated for venous thromboembolism were particularly likely to experience low INR. Improving adherence, minimizing interruptions of therapy, and addressing low INR more promptly could reduce the risk of low INR. (Circ Cardiovasc Qual Outcomes. 2009;2:591-597.)
C1 [Rose, Adam J.; Ozonoff, Al] Bedford VA Med Ctr, Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA 01730 USA.
[Rose, Adam J.; Henault, Lori E.; Hylek, Elaine M.] Boston Univ, Sch Med, Dept Med, Gen Internal Med Sect, Boston, MA 02118 USA.
[Ozonoff, Al] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Grant, Richard W.] Massachusetts Gen Hosp, Dept Med, Clin Epidemiol Unit, Dept Med,Gen Med Div, Boston, MA 02114 USA.
RP Rose, AJ (reprint author), Bedford VA Med Ctr, Ctr Hlth Qual Outcomes & Econ Res, 200 Springs Rd,Bldg 70, Bedford, MA 01730 USA.
EM adamrose@bu.edu
OI Ozonoff, Al/0000-0003-4233-5899; Grant, Richard/0000-0002-6164-8025
FU Bristol-Myers Squibb; makers of Coumadin brand warfarin; Department of
Veterans Affairs Health Services Research and Development Service; NIDDK
[K23 DK067452]; Boehringer Ingelheim; Bayer
FX This study was funded by Bristol-Myers Squibb, the makers of Coumadin
brand warfarin. Bristol-Myers Squibb had no role in the design and
conduct of the study; in the collection, analysis, and interpretation of
the data; or in the preparation, review, and approval of the manuscript.
Dr Rose is supported by a career development award from the Department
of Veterans Affairs Health Services Research and Development Service. Dr
Grant is supported by an NIDDK career development award (K23 DK067452).
The opinions expressed in this manuscript do not necessarily represent
the views or policies of the Department of Veterans Affairs.; Dr Rose
has received research funding from Boehringer Ingelheim to study
warfarin utilization in the Veterans Affairs Health System. Dr Hylek has
served as an advisor to Boehringer Ingelheim, Bristol-Myers Squibb,
Sanofi-Aventis, and The Medicines Company and participated in a clinical
symposium sponsored by Bayer and Bristol-Myers Squibb.
NR 35
TC 30
Z9 31
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7713
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD NOV
PY 2009
VL 2
IS 6
BP 591
EP 597
DI 10.1161/CIRCOUTCOMES.109.862763
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 575PD
UT WOS:000276078500012
PM 20031897
ER
PT J
AU Lewis, WR
Ellrodt, AG
Peterson, E
Hernandez, AF
LaBresh, KA
Cannon, CP
Pan, WQ
Fonarow, GC
AF Lewis, William R.
Ellrodt, A. Gray
Peterson, Eric
Hernandez, Adrian F.
LaBresh, Kenneth A.
Cannon, Christopher P.
Pan, Wenqin
Fonarow, Gregg C.
TI Trends in the Use of Evidence-Based Treatments for Coronary Artery
Disease Among Women and the Elderly Findings From the Get With the
Guidelines Quality-Improvement Program
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE quality control; coronary artery disease; age factors; sex
ID ACUTE MYOCARDIAL-INFARCTION; LIPID-LOWERING THERAPY; RANDOMIZED TRIALS;
OLDER PATIENTS; UNITED-STATES; CARE; MORTALITY; AGE
AB Background-Significant disparities have been reported in the application of evidence-based guidelines in the treatment of coronary artery disease (CAD) in women and the elderly. We hypothesized that participation in a quality-improvement program could improve care for all patients and thus narrow treatment gaps over time.
Methods and Results-Treatment of 237 225 patients hospitalized with CAD was evaluated in the Get With the Guidelines-CAD program from 2002 to 2007. Six quality measures were evaluated in eligible patients without contraindications: aspirin on admission and discharge, beta-blockers use at discharge, angiotensin-converting enzyme inhibitor or angiotensin receptor antagonist use, lipid-lowering medication use, and tobacco cessation counseling along with other care metrics. Over time, composite adherence on these 6 measures increased from 86.5% to 97.4% (+10.9%) in men and 84.8% to 96.2% (+11.4%) in women. There was a slight difference in composite adherence by sex that remained significant over time (P<0.0001), but this was confined to patients <75 years. Composite adherence in younger patients (<75 years) increased from 87.1% to 97.7% (+10.6%) and from 83.0% to 95.1% (+12.1%) in the elderly (>= 75 years) over time.
Conclusions-Among hospitals participating in Get With the Guidelines-CAD, guideline adherence has improved substantially over time for both women and men and younger and older CAD patients, with only slight age and sex differences in some measures persisting. (Circ Cardiovasc Qual Outcomes. 2009;2:633-641.)
C1 [Lewis, William R.] Case Western Reserve Univ, Clin Cardiol Heart & Vasc Ctr, Cleveland, OH 44109 USA.
[Ellrodt, A. Gray] Berkshire Med Ctr, Pittsfield, MA USA.
[Peterson, Eric; Hernandez, Adrian F.; Pan, Wenqin] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC USA.
[LaBresh, Kenneth A.] Res Triangle Inst Int, Waltham, MA USA.
[Cannon, Christopher P.] Brigham & Womens Hosp, Div Cardiovasc, TIMI Study Grp, Boston, MA 02115 USA.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Los Angeles, CA USA.
RP Lewis, WR (reprint author), Case Western Reserve Univ, Clin Cardiol Heart & Vasc Ctr, MetroHlth Campus,2500 MetroHlth Dr,Hamman 350, Cleveland, OH 44109 USA.
EM wlewis@metrohealth.org
RI LaBresh, Kenneth/A-6995-2017; Hernandez, Adrian F./A-7818-2016
OI LaBresh, Kenneth/0000-0001-9040-1956; Hernandez, Adrian
F./0000-0003-3387-9616
FU American Heart Association; Schering Plough/Merck; BMS/Sanofi; Johnson
Johnson/Scios; GlaxoSmithKline; Medtronic; Novartis; AstraZeneca;
Accumetrics; Bristol-Myers Squibb/Sanofi; Merck; Merck/Schering Plough;
Pfizer; Schering
FX This study was funded by the American Heart Association.; Dr Lewis has
received speaker honoraria from Reliant Pharmaceuticals and has served
as a consultant for Medtronic. Dr Peterson has received research funding
from Schering Plough/Merck and BMS/Sanofi. Dr Hernandez has received
research funding and/or honoraria from Johnson & Johnson/Scios,
GlaxoSmithKline, Medtronic, Novartis, and AstraZeneca. Dr LaBresh is an
employee of Research Triangle Institute International. Dr Cannon has
received research funding from Accumetrics, AstraZeneca, Bristol-Myers
Squibb/Sanofi Partnership, GlaxoSmithKline, Merck, Merck/Schering Plough
Partnership and has ownership interest in Automedics Medical Systems. Dr
Fonarow has received research funding and honoraria from and served as a
consultant for Medtronic, GlaxoSmithKline, and Novartis; has received
other research support from Pfizer; and has served as a consultant for
and received honoraria from BMS/Sanofi, Merck, and Schering.
NR 21
TC 44
Z9 44
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7713
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD NOV
PY 2009
VL 2
IS 6
BP 633
EP U191
DI 10.1161/CIRCOUTCOMES.108.824763
PG 12
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 575PD
UT WOS:000276078500017
PM 20031902
ER
PT J
AU Spatz, ES
Ross, JS
AF Spatz, Erica S.
Ross, Joseph S.
TI Mis-SHAPEing Public Health Policy
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Editorial Material
DE atherosclerosis; imaging; prevention; legislative mandates
ID CARE; BENEFICIARIES; GUIDELINES; MEDICARE; SERVICES
C1 [Spatz, Erica S.] Yale Univ, Sch Med, Robert Wood Johnson Clin Scholars Program, New Haven, CT 06520 USA.
[Ross, Joseph S.] Mt Sinai Sch Med, Dept Geriatr & Adult Dev, New York, NY USA.
[Ross, Joseph S.] James J Peters VA Med Ctr, Hlth Serv Res & Dev Res Enhancement Award Program, Bronx, NY USA.
[Ross, Joseph S.] James J Peters VA Med Ctr, Ctr Geriatr Res Educ & Clin, Bronx, NY USA.
RP Spatz, ES (reprint author), Yale Univ, Sch Med, Robert Wood Johnson Clin Scholars Program, IE 61,333 Cedar St, New Haven, CT 06520 USA.
EM erica.spatz@yale.edu
FU NIA NIH HHS [K08 AG032886, K08 AG032886-01]
NR 15
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7713
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD NOV
PY 2009
VL 2
IS 6
BP 681
EP 683
DI 10.1161/CIRCOUTCOMES.109.890715
PG 3
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 575PD
UT WOS:000276078500024
PM 20031909
ER
PT J
AU Jensen, BC
Swigart, PM
De Marco, T
Hoopes, C
Simpson, PC
AF Jensen, Brian C.
Swigart, Philip M.
De Marco, Teresa
Hoopes, Charles
Simpson, Paul C.
TI alpha 1-Adrenergic Receptor Subtypes in Nonfailing and Failing Human
Myocardium
SO CIRCULATION-HEART FAILURE
LA English
DT Article
DE receptors, adrenergic, alpha; receptors, adrenergic, beta; heart
failure; myocardium
ID SUSTAINED-RELEASE MOXONIDINE; ARTERIAL BLOOD-PRESSURE;
ALPHA(1B)-ADRENERGIC RECEPTOR; HEART-FAILURE; ALPHA(1)-ADRENERGIC
RECEPTORS; DILATED CARDIOMYOPATHY; CARDIAC-HYPERTROPHY; TRANSGENIC MICE;
ADRENERGIC-RECEPTORS; GENE-EXPRESSION
AB Background-alpha 1-adrenergic receptors (alpha 1-ARs) play adaptive roles in the heart and protect against the development of heart failure. The 3 alpha 1-AR subtypes, alpha 1A, alpha 1B, and alpha 1D, have distinct physiological roles in mouse heart, but very little is known about alpha 1 subtypes in human heart. Here, we test the hypothesis that the alpha 1A and alpha 1B subtypes are present in human myocardium, similar to the mouse, and are not downregulated in heart failure.
Methods and Results-Hearts from transplant recipients and unused donors were failing (n = 12; mean ejection fraction, 24%) or nonfailing (n = 9; mean ejection fraction, 59%) and similar in age (approximate to 44 years) and sex (approximate to 70% male). We measured the alpha 1-AR subtypes in multiple regions of both ventricles by quantitative real-time reverse-transcription polymerase chain reaction and radioligand binding. All 3 alpha 1-AR subtype mRNAs were present, and alpha 1A mRNA was most abundant (approximate to 65% of total alpha 1-AR mRNA). However, only alpha 1A and alpha 1B binding were present, and the alpha 1B was most abundant (60% of total). In failing hearts, alpha 1A and alpha 1B binding was not downregulated, in contrast with beta 1-ARs.
Conclusions-Our data show for the first time that the alpha 1A and alpha 1B subtypes are both present in human myocardium, but alpha 1D binding is not, and the alpha 1 subtypes are not downregulated in heart failure. Because alpha 1 subtypes in the human heart are similar to those in the mouse, where adaptive and protective effects of alpha 1 subtypes are most convincing, it might become feasible to treat heart failure with a drug targeting the alpha 1A and/or alpha 1B. (Circ Heart Fail. 2009; 2: 654-663.)
C1 [Jensen, Brian C.; Swigart, Philip M.; Simpson, Paul C.] San Francisco VA Med Ctr, Cardiol Sect, San Francisco, CA USA.
[Jensen, Brian C.; Swigart, Philip M.; Simpson, Paul C.] San Francisco VA Med Ctr, Res Serv, San Francisco, CA USA.
[Jensen, Brian C.; De Marco, Teresa; Simpson, Paul C.] Univ Calif San Francisco, Div Cardiol, San Francisco, CA 94143 USA.
[Simpson, Paul C.] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA.
[Hoopes, Charles] Univ Calif San Francisco, Div Cardiothorac Surg, San Francisco, CA 94143 USA.
RP Simpson, PC (reprint author), VA Med Ctr 111C8, 4150 Clement St, San Francisco, CA 94121 USA.
EM paul.simpson@ucsf.edu
FU Department of Veterans Affairs; National Institutes of Health;
GlaxoSmithKline Research and Education Foundation; UCSF Foundation
FX This study was supported by the Department of Veterans Affairs and the
National Institutes of Health (P.C.S.), a Young Investigators Award from
the GlaxoSmithKline Research and Education Foundation for Cardiovascular
Disease (to B.C.J.), and the UCSF Foundation for Cardiac Research
(B.C.J.).
NR 50
TC 29
Z9 31
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-3289
J9 CIRC-HEART FAIL
JI Circ.-Heart Fail.
PD NOV
PY 2009
VL 2
IS 6
BP 654
EP 663
DI 10.1161/CIRCHEARTFAILURE.108.846212
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 521BD
UT WOS:000271893100017
PM 19919991
ER
PT J
AU Salloum, ML
Eberlin, KR
Sethna, N
Hamdan, US
AF Salloum, Mariah L.
Eberlin, Kyle R.
Sethna, Navil
Hamdan, Usama S.
TI Combined Use of Infraorbital and External Nasal Nerve Blocks for
Effective Perioperative Pain Control During and After Cleft Lip Repair
SO CLEFT PALATE-CRANIOFACIAL JOURNAL
LA English
DT Article
DE cleft lip repair; external nasal block; infraorbital block
ID CHILDREN; MALFORMATIONS; INFANTS; PALATE
AB Perioperative analgesia in patients undergoing cleft lip and palate repair is complicated by the risk of postoperative airway obstruction. We describe a technique of combined infraorbital and external nasal nerve blocks to reduce the need for opioid analgesia. Using this technique, we have successfully performed cleft lip repair under local anesthesia alone, without general anesthesia or intravenous sedation, in adolescents and adults. In children, this technique can reduce the need for postoperative opioids. We describe this novel analgesic approach to decrease opioid requirements and minimize perioperative risk.
C1 [Salloum, Mariah L.] Tufts Med Ctr, Dept Otolaryngol Head & Neck Surg, Boston, MA USA.
[Eberlin, Kyle R.] Massachusetts Gen Hosp, Harvard Plast Surg Training Program, Boston, MA 02114 USA.
[Sethna, Navil] Childrens Hosp Boston, Pain Treatment Serv, Boston, MA USA.
[Sethna, Navil; Hamdan, Usama S.] Harvard Univ, Sch Med, Boston, MA USA.
[Hamdan, Usama S.] Tufts Univ, Sch Med, Medford, MA 02155 USA.
[Hamdan, Usama S.] Boston Univ, Sch Med, Boston, MA 02118 USA.
RP Hamdan, US (reprint author), 28 Martingale Lane, Westwood, MA 02090 USA.
EM uh@hamdan.us
NR 24
TC 4
Z9 4
U1 0
U2 2
PU ALLIANCE COMMUNICATIONS GROUP DIVISION ALLEN PRESS
PI LAWRENCE
PA 810 EAST 10TH STREET, LAWRENCE, KS 66044 USA
SN 1055-6656
J9 CLEFT PALATE-CRAN J
JI Cleft Palate-Craniofac. J.
PD NOV
PY 2009
VL 46
IS 6
BP 629
EP 635
DI 10.1597/08-142.1
PG 7
WC Dentistry, Oral Surgery & Medicine; Surgery
SC Dentistry, Oral Surgery & Medicine; Surgery
GA 522JA
UT WOS:000271992500010
PM 19860508
ER
PT J
AU Schlesinger, N
Hassett, AL
Neustadter, L
Schumacher, HR
AF Schlesinger, N.
Hassett, A. L.
Neustadter, L.
Schumacher, H. R., Jr.
TI Does acute synovitis (pseudogout) occur in patients with chronic
pyrophosphate arthropathy (pseudo-osteoarthritis)?
SO CLINICAL AND EXPERIMENTAL RHEUMATOLOGY
LA English
DT Article
DE Pseudogout; pyrophosphate arthropathy
ID DIHYDRATE CRYSTAL DEPOSITION; OSTEO-ARTHRITIS; CALCIUM; KNEE;
CHONDROCALCINOSIS; DISEASE; PREVALENCE; JOINTS; SIZE
AB Objective
Pyrophosphate arthropathy has been linked to diverse clinical subtypes. The two most common are: acute synovitis (pseudogout) and chronic pyrophosphate arthropathy ("pseudo-osteoarthritis"). We have conducted a study to examine whether these are overlapping syndromes.
Methods
We reviewed all synovial fluid (SF) analyses performed in our laboratory from January 1988 to May 1997 to determine if patterns of SF leukocyte counts and Alizarin red stains in patients with repeated samples suggest that some patients were prone to acute attacks and some to chronic pyrophosphate arthropathy and whether acute attacks superimposed on chronic symptoms were common. Joint x-rays were screened for osteoarthritis (OA) and chondrocalcinosis.
Results
We identified 67 patients who had Calcium pyrophosphate dehydrate (CPPD) in their SF and had more than one SF examined (185 SF). We divided the patients into 2 groups. Group A (n=25) had at least one SF leukocyte count > than 2000 per mm(3) and group B (n=42) had SF leukocyte counts always < than 2000 per mm'. Chondrocalcinosis detected on x-ray was more common in group A versus group B, 48% versus 19% (p<0.05, Fisher's exact test). OA was mild (grades 0-1) in 39% of group A versus 12.5% of group B patients, but the difference between groups was not significant. CPPD crystals were not detected in 13.5% SFs previously having CPPD crystals. Alizarin red staining for suspected hydroxyapatite was more often 2+ to 3+ in group B (31.6%) compared to group A (15.5%; p<0.05, Fisher's exact test).
Conclusion
Acute synovitis and chronic pyrophosphate arthropathy are often two distinctive syndromes with some patients never having inflammatory attacks. Acute synovitis is more common in patients with chondrocalcinosis while chronic pyrophosphate arthropathy is associated with increased alizarin red staining and a trend suggestive of increased severity of OA.
C1 [Schlesinger, N.; Hassett, A. L.] UMDNJ, Robert Wood Johnson Med Sch, Div Rheumatol, Dept Med, New Brunswick, NJ 08903 USA.
[Neustadter, L.] S Jersey Healthcare Reg Med Ctr, Vineland, NJ USA.
[Schumacher, H. R., Jr.] Univ Penn, Sch Med, Div Rheumatol, Philadelphia, PA 19104 USA.
[Schumacher, H. R., Jr.] Vet Affairs Med Ctr, Director Arthrit Immunol Ctr, Philadelphia, PA USA.
RP Schlesinger, N (reprint author), UMDNJ, Robert Wood Johnson Med Sch, Div Rheumatol, Dept Med, MEB 468,POB 19, New Brunswick, NJ 08903 USA.
EM schlesna@umdnj.edu
NR 30
TC 4
Z9 5
U1 0
U2 0
PU CLINICAL & EXPER RHEUMATOLOGY
PI PISA
PA VIA SANTA MARIA 31, 56126 PISA, ITALY
SN 0392-856X
J9 CLIN EXP RHEUMATOL
JI Clin. Exp. Rheumatol.
PD NOV-DEC
PY 2009
VL 27
IS 6
BP 940
EP 944
PG 5
WC Rheumatology
SC Rheumatology
GA 552CO
UT WOS:000274264700008
PM 20149309
ER
PT J
AU Sheikh, A
Bhuiyan, MS
Khanam, F
Chowdhury, F
Saha, A
Ahmed, D
Jamil, KMA
LaRocque, RC
Harris, JB
Ahmad, MM
Charles, R
Brooks, WA
Calderwood, SB
Cravioto, A
Ryan, ET
Qadri, F
AF Sheikh, Alaullah
Bhuiyan, M. Saruar
Khanam, Farhana
Chowdhury, Fahima
Saha, Amit
Ahmed, Dilruba
Jamil, K. M. A.
LaRocque, Regina C.
Harris, Jason B.
Ahmad, Mian Mashhud
Charles, Richelle
Brooks, W. Abdullah
Calderwood, Stephen B.
Cravioto, Alejandro
Ryan, Edward T.
Qadri, Firdausi
TI Salmonella enterica Serovar Typhi-Specific Immunoglobulin A Antibody
Responses in Plasma and Antibody in Lymphocyte Supernatant Specimens in
Bangladeshi Patients with Suspected Typhoid Fever
SO CLINICAL AND VACCINE IMMUNOLOGY
LA English
DT Article
ID ENTEROTOXIGENIC ESCHERICHIA-COLI; INTESTINAL IMMUNE-RESPONSES;
VIBRIO-CHOLERAE O1; BONE-MARROW; WIDAL TEST; SECRETING CELLS; STOOL
SAMPLES; B-CELLS; VACCINE; BLOOD
AB Many currently available diagnostic tests for typhoid fever lack sensitivity and/or specificity, especially in areas of the world where the disease is endemic. In order to identify a diagnostic test that better correlates with typhoid fever, we evaluated immune responses to Salmonella enterica serovar Typhi (serovar Typhi) in individuals with suspected typhoid fever in Dhaka, Bangladesh. We enrolled 112 individuals with suspected typhoid fever, cultured day 0 blood for serovar Typhi organisms, and performed Widal assays on days 0, 5, and 20. We harvested peripheral blood lymphocytes and analyzed antibody levels in supernatants collected on days 0, 5, and 20 (using an antibody-in-lymphocyte-supernatant [ALS] assay), as well as in plasma on these days. We measured ALS reactivity to a serovar Typhi membrane preparation (MP), a formalin-inactivated whole-cell preparation, and serovar Typhi lipopolysaccharide. We measured responses in healthy Bangladeshi, as well as in Bangladeshi febrile patients with confirmed dengue fever or leptospirosis. We categorized suspected typhoid fever individuals into different groups (groups I to V) based on blood culture results, Widal titer, and clinical features. Responses to MP antigen in the immunoglobulin A isotype were detectable at the time of presentation in the plasma of 81% of patients. The ALS assay, however, tested positive in all patients with documented or highly suspicious typhoid, suggesting that such a response could be the basis of improved diagnostic point-of-care- assay for serovar Typhi infection. It can be important for use in epidemiological studies, as well as in difficult cases involving fevers of unknown origin.
C1 [Qadri, Firdausi] Int Ctr Diarrhoeal Dis Res, Div Sci Lab, Immunol Unit, Dhaka 1000, Bangladesh.
[Chowdhury, Fahima; LaRocque, Regina C.; Harris, Jason B.; Charles, Richelle; Calderwood, Stephen B.; Ryan, Edward T.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Ahmad, Mian Mashhud] Dhaka Med Coll Hosp, Dhaka, Bangladesh.
[Calderwood, Stephen B.; Ryan, Edward T.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Calderwood, Stephen B.] Harvard Univ, Sch Med, Dept Microbiol, Boston, MA USA.
[Calderwood, Stephen B.] Harvard Univ, Sch Med, Mol Ctr, Boston, MA USA.
[Ryan, Edward T.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Qadri, F (reprint author), Int Ctr Diarrhoeal Dis Res, Div Sci Lab, Immunol Unit, GPO Box 128, Dhaka 1000, Bangladesh.
EM fqadri@icddrb.org
FU National Institutes of Health [AI072599, AI058935]; Fogarty
International Center [TW05572, TW007409, TW07144]; Howard Hughes Medical
Institute
FX This study was supported by the ICDDR, B and grants from the National
Institutes of Health, including the National Institute of Allergy and
Infectious Diseases (AI072599 [E. T. R.] and AI058935 [R. C. C. and S.
B. C.]), a Training Grant in Vaccine Development from the Fogarty
International Center (TW05572 [A. S., M. S. B., and F. Q.]), and Career
Development Awards (K01) from the Fogarty International Center (TW007409
[J. B. H.] and TW07144 [R. C. L.]), and a Physician-Scientist Early
Career Award from the Howard Hughes Medical Institute (R. C. L.).
NR 39
TC 22
Z9 22
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1556-6811
J9 CLIN VACCINE IMMUNOL
JI Clin. Vaccine Immunol.
PD NOV
PY 2009
VL 16
IS 11
BP 1587
EP 1594
DI 10.1128/CVI.00311-09
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 514DE
UT WOS:000271373700008
PM 19741090
ER
PT J
AU Graham, DY
AF Graham, David Y.
TI Endoscopic Ulcers Are Neither Meaningful Nor Validated as a Surrogate
for Clinically Significant Upper Gastrointestinal Harm
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Editorial Material
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ANTI-INFLAMMATORY AGENTS; CORONARY
HEART-DISEASE; DOUBLE-BLIND; BLOOD-PRESSURE; END-POINTS; COMPLICATIONS;
ASPIRIN; RISK; MISOPROSTOL
C1 [Graham, David Y.] Michael E DeBakey Vet Affairs Med Ctr, Dept Med, Houston, TX USA.
[Graham, David Y.] Baylor Coll Med, Houston, TX 77030 USA.
RP Graham, DY (reprint author), Michael E DeBakey Vet Affairs Med Ctr, Dept Med, Houston, TX USA.
FU NCI NIH HHS [R01 CA116845]; NIDDK NIH HHS [P30 DK056338, P30
DK056338-07, DK56338]
NR 35
TC 15
Z9 15
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD NOV
PY 2009
VL 7
IS 11
BP 1147
EP 1150
DI 10.1016/j.cgh.2009.06.006
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 519GM
UT WOS:000271753000006
PM 19559818
ER
PT J
AU Chan, MY
Cohen, H
Spiegel, BMR
AF Chan, Michael Y.
Cohen, Hartley
Spiegel, Brennan M. R.
TI Fewer Polyps Detected by Colonoscopy as the Day Progresses at a
Veteran's Administration Teaching Hospital
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
ID COLORECTAL-CANCER; ADENOMA DETECTION; TECHNICAL PERFORMANCE; SCREENING
COLONOSCOPY; SLEEP-DEPRIVATION; COLONIC NEOPLASIA; ENDOSCOPY; QUALITY;
RATES; POLYPECTOMY
AB BACKGROUND & AIMS: One objective of colonoscopy is to identify and remove polyps-this process requires attention to detail and prolonged concentration. Providers are predisposed to cognitive errors because the procedure is often performed repetitively throughout the day. We measured the adjusted relationship between colonoscopy start time and polyp yield. METHODS: We performed a prospective Study of 477 patients that received screening, Surveillance, or diagnostic colonoscopies at a Veteran's Administration (VA) reaching hospital. The primary outcome measure was polyp yield. We collected data on colonoscopy start times, which were analyzed both as a dichotomous time period ("early-morning case" vs "later case") and as a continuous variable (start time). We identified significant risk factors using univariate analysis and performed Poisson multivariable regression to measure the independent effect of colonoscopy start time on polyp yield. We evaluated evidence of decreasing polyp yield as the day progressed throughout pre-specified time intervals. RESULTS: In univariate analysis, early-morning cases yielded 27% more polyps per patient than later cases (95% confidence interval, 11%-45%; P < .001). The total numbers of, hyperplastic and adenomatous polyps found decreased hour-by-hour as the day progressed. Multivariable analysis demonstrated that early-morning cases yielded 20% more polyps per patient than later cases (95% confidence interval, 5%-38%; P = .007). CONCLUSIONS: At a VA medical center, more polyps were detected in patients that received colonoscopies early in the morning compared with later in the day. Moreover, adenoma detection reduced as the day progressed. Providers might be most adept at detecting polyps at the beginning of the day; further validation in other practice settings is required.
C1 [Cohen, Hartley; Spiegel, Brennan M. R.] VA Greater Los Angeles Healthcare Syst, Dept Gastroenterol, Los Angeles, CA USA.
[Chan, Michael Y.; Spiegel, Brennan M. R.] Univ Calif Los Angeles, David Geffen Sch Med, Div Digest Dis, Los Angeles, CA 90095 USA.
[Spiegel, Brennan M. R.] Univ Calif Los Angeles, Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA 90024 USA.
[Spiegel, Brennan M. R.] CURE Digest Dis Res Ctr, Los Angeles, CA USA.
[Spiegel, Brennan M. R.] Univ Calif Los Angeles, VA Ctr Outcomes Res & Educ, Los Angeles, CA USA.
RP Spiegel, BMR (reprint author), 11301 Wilshire Blvd,Bldg 115,Room 215, Los Angeles, CA 90073 USA.
EM bspiegel@mednet.ucla.edu
FU Veteran's Affairs Health Services Research and Development (HSR&D)
Career Development Transition Award [RCD 03-179-2]
FX Dr Spiegel is supported by a Veteran's Affairs Health Services Research
and Development (HSR&D) Career Development Transition Award (RCD
03-179-2).
NR 28
TC 41
Z9 42
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD NOV
PY 2009
VL 7
IS 11
BP 1217
EP 1223
DI 10.1016/j.cgh.2009.07.013
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 519GM
UT WOS:000271753000019
PM 19631284
ER
PT J
AU Khalid, A
AF Khalid, Asif
TI Differentiating Neoplastic From Benign Lesions of the Pancreas:
Translational Techniques
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
CT 5th Joint Meeting of the
Japanese-Society-of-Gastroenterology/American-Gastroenterological-Associ
ation
CY MAY 07-08, 2009
CL Sapporo, JAPAN
SP Japanese Soc Gastroenterol, Amer Gastroenterol Assoc
ID FINE-NEEDLE-ASPIRATION; PAPILLARY-MUCINOUS TUMORS; CYSTIC NEOPLASMS;
BRUSH CYTOLOGY; TELOMERASE ACTIVITY; DIAGNOSTIC-ACCURACY; MOLECULAR
ANALYSIS; MALIGNANCY; STRICTURES; ADENOCARCINOMA
AB There has been substantial recent progress in our ability to image and sample the pancreas leading to the improved recognition of benign and premalignant conditions of the pancreas such as autoimmune pancreatitis (AIP) and mucinous lesions (mucinous cystic neoplasms [MCN] and intraductal papillary mucinous neoplasms [IPMN]), respectively. Clinically relevant and difficult situations that continue to be faced in this context include differentiating MCN and IPMN from nonmucinous pancreatic cysts, the early detection of malignant degeneration in MCN and IPMN, and accurate differentiation between pancreatic cancer and inflammatory masses, especially Alp. These challenges arise primarily due to the less than perfect sensitivity for malignancy utilizing cytological samples obtained via EUS and ERCP. Aspirates from pancreatic cysts are often paucicellular further limiting the accuracy of cytology. One approach to improve the diagnostic yield from these very small samples is through the use of molecular techniques. Because the development of pancreatic cancer and malignant degeneration in MCN and IPMN is associated with well studied genetic insults including oncogene activation (eg, k-ras), tumor suppressor gene losses (eg, p53, p16, and DPC4), and genome maintenance gene mutations (eg, BRCA2 and telomerase), detecting these molecular abnormalities may aid in improving our diagnostic accuracy. A number of studies have shown the utility of testing clinical samples from pancreatic lesions and bile duct strictures for these molecular markers of malignancy to differentiate between cancer and inflammation. The information from these studies will be discussed with emphasis on how to use this information in clinical practice.
C1 [Khalid, Asif] Univ Pittsburgh, Med Ctr, Pittsburgh, PA 15213 USA.
[Khalid, Asif] VA Pittsburgh Hlth Care Syst, Dept Med, Pittsburgh, PA USA.
RP Khalid, A (reprint author), Univ Pittsburgh, Med Ctr, M2,C Wing,PUH,200 Lothrop St, Pittsburgh, PA 15213 USA.
EM khalida@upmc.edu
NR 35
TC 3
Z9 3
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD NOV
PY 2009
VL 7
IS 11
BP S55
EP S58
DI 10.1016/j.cgh.2009.07.033
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 519GN
UT WOS:000271753100012
PM 19896100
ER
PT J
AU Pandol, S
Edderkaoui, M
Gukovsky, I
Lugea, A
Gukovskaya, A
AF Pandol, Stephen
Edderkaoui, Mouad
Gukovsky, Ilya
Lugea, Aurelia
Gukovskaya, Anna
TI Desmoplasia of Pancreatic Ductal Adenocarcinoma
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
CT 5th Joint Meeting of the
Japanese-Society-of-Gastroenterology/American-Gastroenterological-Associ
ation
CY MAY 07-08, 2009
CL Sapporo, JAPAN
SP Japanese Soc Gastroenterol, Amer Gastroenterol Assoc
ID CANCER CELL-SURVIVAL; STELLATE CELLS; NADPH OXIDASE;
EXTRACELLULAR-MATRIX; TUMOR PROGRESSION; MICROENVIRONMENT;
PROLIFERATION; EXPRESSION; PHENOTYPE; CARCINOMA
AB Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer and is characterized by remarkable desmoplasia. The desmoplasia is composed of extracellular matrix (ECM) proteins, myofibroblastic pancreatic stellate cells, and immune cells associated with a multitude of cytokines, growth factors, and ECM metabolizing enzymes. The mechanisms of participation of this complex matrix process in carcinogenesis are only starting to be appreciated. Recent studies showed key roles for stellate cells in the production of ECM proteins as well as cytokines and growth factors that promote the growth of the cancer cells all present in the desmoplastic parts of PDAC. In addition, interactions of ECM proteins and desmoplastic secreted growth factors with the cancer cells of PDAC activate intracellular signals including reactive oxygen species that act to make the cancer cells resistant to dying. These findings suggest that the desmoplasia of PDAC is a key factor in regulating carcinogenesis of PDAC as well as responses to therapies. A better understanding of the biology of desmoplasia in the mechanism of PDAC will likely provide significant opportunities for better treatments for this devastating cancer.
C1 [Pandol, Stephen] VA Greater Los Angeles Hlth Care Syst, Pancreat Res Grp, Dept Med, Los Angeles, CA 90073 USA.
Univ Calif Los Angeles, Los Angeles, CA USA.
RP Pandol, S (reprint author), VA Greater Los Angeles Hlth Care Syst, Pancreat Res Grp, Dept Med, Bldg 258,Room 340,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM stephen.pandol@va.gov
FU NCCIH NIH HHS [P01AT003960, P01 AT003960]; NCI NIH HHS [R01 CA119025,
R01CA119025]; NIAAA NIH HHS [P50 AA011999, P60 AA11999, R03 AA016008,
R21AA016840]
NR 32
TC 56
Z9 57
U1 1
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD NOV
PY 2009
VL 7
IS 11
BP S44
EP S47
DI 10.1016/j.cgh.2009.07.039
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 519GN
UT WOS:000271753100010
PM 19896098
ER
PT J
AU Levine, BS
Kleeman, CR
Felsenfeld, AJ
AF Levine, Barton S.
Kleeman, Charles R.
Felsenfeld, Arnold J.
TI The Journey From Vitamin D-Resistant Rickets to the Regulation of Renal
Phosphate Transport
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Review
ID FIBROBLAST GROWTH FACTOR-23; X-LINKED HYPOPHOSPHATEMIA; MATRIX
EXTRACELLULAR PHOSPHOGLYCOPROTEIN; CHRONIC KIDNEY-DISEASE;
25-HYDROXYVITAMIN D-1-ALPHA-HYDROXYLASE ACTIVITY; SERUM
PARATHYROID-HORMONE; HYP MOUSE PHENOTYPE; KLOTHO MUTANT MICE; D
METABOLISM; SECONDARY HYPERPARATHYROIDISM
AB In 1937, Fuller Albright first described two rare genetic disorders: Vitamin D resistant rickets and polyostotic fibrous dysplasia, now respectively known as X-linked hypophosphatemic rickets (XLH) and the McCune-Albright syndrome. Albright carefully characterized and meticulously analyzed one patient, W.M., with vitamin D-resistant rickets. Albright subsequently reported additional carefully performed balance studies on W.M. In this review, which evaluates the journey from the initial description of vitamin D-resistant rickets (XLH) to the regulation of renal phosphate transport, we (1) trace the timeline of important discoveries in unraveling the pathophysiology of XLH, (2) cite the recognized abnormalities in mineral metabolism in XLH, (3) evaluate factors that may affect parathyroid hormone values in XLH, (4) assess the potential interactions between the phosphate-regulating gene with homology to endopeptidase on the X chromosome and fibroblast growth factor 23 (FGF23) and their resultant effects on renal phosphate transport and vitamin D metabolism, (5) analyze the complex interplay between FGF23 and the factors that regulate FGF23, and (6) discuss the genetic and acquired disorders of hypophosphatemia and hyperphosphatemia in which FGF23 plays a role. Although Albright could not measure parathyroid hormone, he concluded on the basis of his studies that showed calcemic resistance to parathyroid extract in W.M. that hyperparathyroidism was present. Using a conceptual approach, we suggest that a defect in the skeletal response to parathyroid hormone contributes to hyperparathyroidism in XLH. Finally, at the end of the review, abnormalities in renal phosphate transport that are sometimes found in patients with polyostotic fibrous dysplasia are discussed. Clin J Am Soc Nephrol 4: 1866-1877, 2009. doi: 10.2215/CJN.03000509
C1 VA Greater Los Angeles Healthcare Syst, Dept Med, Los Angeles, CA USA.
Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
RP Felsenfeld, AJ (reprint author), W Los Angeles VA Med Ctr, Nephrol Sect 111L, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM arnold.felsenfeld@va.gov
NR 109
TC 9
Z9 11
U1 0
U2 8
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 NOV
PY 2009
VL 4
IS 11
BP 1866
EP 1877
DI 10.2215/CJN.03000509
PG 12
WC Urology & Nephrology
SC Urology & Nephrology
GA 517PN
UT WOS:000271628400025
PM 19808223
ER
PT J
AU Oreskovic, NM
Winickoff, JP
Kuhlthau, KA
Romm, D
Perrin, JM
AF Oreskovic, Nicolas M.
Winickoff, Jonathan P.
Kuhlthau, Karen A.
Romm, Diane
Perrin, James M.
TI Obesity and the Built Environment Among Massachusetts Children
SO CLINICAL PEDIATRICS
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the
Pediatric-Academic-Societies/Academic-Pediatric-Association/Society-for-
Pediatric-Research National Conference
CY MAY 02-06, 2008
CL Honolulu, HI
SP Pediat Acad Soc, Acad Pediat Assoc, Soc Pediat Res
DE obesity; pediatric; built environment; geographic information systems
(GIS)
ID FAST-FOOD RESTAURANTS; BODY-MASS INDEX; PHYSICAL-ACTIVITY;
UNITED-STATES; URBAN SPRAWL; OVERWEIGHT; WEIGHT; SCHOOL; ASSOCIATION;
PREVALENCE
AB Background: The built environment may influence weight status. Method: Using cross-sectional data for children aged 2 to 18 years, the authors linked clinical and spatial data using geographic information systems and analyzed for associations between body mass index (BMI) and density of and distance to nearest built environment variable (schools, sidewalks, subway stations, bicycle trails, open space, and fast-food restaurants) using bivariate and multilevel analyses. Results: The study sampled 21 008 children; 54% were white, 26% Hispanic, 37% overweight, and 20% obese. In bivariate analysis, distance to nearest fast-food restaurant was inversely associated with 13141, whereas density of fast-food restaurants was positively associated with BMI. Distance to school and subway station, amount of open space, and density of subway stations were inversely associated with BMI. Controlling for sociodemographic factors, only living near a greater density of subway stations was inversely associated with overweight (odds ratio, 0.87; 95% confidence interval, 0.81-0.94) and obesity (odds ratio. 0.90; 95% confidence interval, 0.82-0.99). Conclusion: Distance to nearest subway station is associated with BMI among Massachusetts children.
C1 [Oreskovic, Nicolas M.] Massachusetts Gen Hosp, Ctr Child & Adolescent Hlth Policy, Dept Internal Med, Boston, MA 02114 USA.
[Oreskovic, Nicolas M.; Winickoff, Jonathan P.; Perrin, James M.] Massachusetts Gen Hosp, Ctr Child & Adolescent Hlth Policy, Dept Pediat, Boston, MA 02114 USA.
RP Oreskovic, NM (reprint author), Massachusetts Gen Hosp, Ctr Child & Adolescent Hlth Policy, Dept Internal Med, 50 Staniford St,Suite 901, Boston, MA 02114 USA.
EM nicolas.oreskovic@gmail.com
OI Oreskovic, Nicolas/0000-0001-8702-8636
FU AHRQ HHS [T32 HS000063-13]
NR 39
TC 44
Z9 44
U1 2
U2 12
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0009-9228
J9 CLIN PEDIATR
JI Clin. Pediatr.
PD NOV
PY 2009
VL 48
IS 9
BP 904
EP 912
DI 10.1177/0009922809336073
PG 9
WC Pediatrics
SC Pediatrics
GA 506ZC
UT WOS:000270817400003
PM 19487763
ER
PT J
AU Sattelmair, JR
Pertman, JH
Forman, DE
AF Sattelmair, Jacob R.
Pertman, Jeremy H.
Forman, Daniel E.
TI Effects of Physical Activity on Cardiovascular and Noncardiovascular
Outcomes in Older Adults
SO CLINICS IN GERIATRIC MEDICINE
LA English
DT Article
DE Aging; Cardiovascular; Elderly; Exercise; Physical activity
ID RANDOMIZED CONTROLLED-TRIAL; CORONARY-HEART-DISEASE; QUALITY-OF-LIFE;
DEPENDENT DIABETES-MELLITUS; IMPAIRED GLUCOSE-TOLERANCE; BODY-MASS
INDEX; OXIDATIVE STRESS BIOMARKERS; LEUKOCYTE TELOMERE LENGTH;
HOME-BASED EXERCISE; GROWTH-FACTOR-I
AB Aging is associated with a cascade of morphologic and physiologic changes that naturally predispose older adults to progressive weakening, functional decline, morbidity. disability, poor quality of life, and increased mortality Physical activity moderates such insidious aging patterns and is a vital preventive and therapeutic strategy to optimize health throughout the aging process. Regular exercise provides many physiologic benefits, reduces risk of disease outcomes, and triggers important psychological gains Advanced age presents distinctive obstacles to maintaining a physically active lifestyle Individualized exercise strategies and regimens make it possible, however, for every elderly adult to benefit from physical activity
C1 [Forman, Daniel E.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
[Sattelmair, Jacob R.; Pertman, Jeremy H.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Forman, Daniel E.] VA Boston Healthcare Syst, Ctr Geriatr Res Educ & Clin, Boston, MA 02130 USA.
RP Forman, DE (reprint author), Brigham & Womens Hosp, Div Cardiovasc, 75 Francis St, Boston, MA 02115 USA.
NR 177
TC 35
Z9 39
U1 2
U2 13
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0749-0690
J9 CLIN GERIATR MED
JI Clin. Geriatr. Med.
PD NOV
PY 2009
VL 25
IS 4
BP 677
EP +
DI 10.1016/j.cger.2009.07.004
PG 28
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 596JD
UT WOS:000277680200008
PM 19944267
ER
PT J
AU Cusi, K
AF Cusi, Kenneth
TI Role of Insulin Resistance and Lipotoxicity in Non-Alcoholic
Steatohepatitis
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Insulin resistance; Lipotoxicity; NAFLD; NASH; Type 2 diabetes mellitus
ID FATTY LIVER-DISEASE; PLASMA ADIPONECTIN CONCENTRATIONS; INDUCED HEPATIC
LIPOTOXICITY; TYPE-2 DIABETIC-PATIENTS; HUMAN SKELETAL-MUSCLE; BODY-MASS
INDEX; FACTOR-KAPPA-B; GLUCOSE-TOLERANCE; ADIPOSE-TISSUE;
RESONANCE-SPECTROSCOPY
AB It is well established that the development of NAFLD and NASH are closely linked to an excess flow of free fatty acids (FFA) arising from dysfunctional/insulin resistant adipose tissue causing ectopic fat deposition in many organs. In the liver, when chronic lipid supply surpasses the metabolic ability to adapt it will induce hepatocellular damage as FFA are redirected into harmful pathways of non-oxidative metabolism with intracellular accumulation of toxic lipid-derived metabolites. Multiple mechanisms have been implicated including mitochondrial dysfunction, endoplasmic reticulum stress, and activation of multiple inflammatory pathways. Understanding the role of insulin resistance and lipotoxicity in NASH as part of a broader metabolic disorder is likely to assist practitioners in the successful management of these challenging patients.
C1 [Cusi, Kenneth] Univ Texas Hlth Sci Ctr San Antonio, Diabet Div, San Antonio, TX 78284 USA.
[Cusi, Kenneth] Audie L Murphy Vet Adm Med Ctr, San Antonio, TX 78284 USA.
RP Cusi, K (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Diabet Div, Room 3-390S,7703 Floyd Curl Dr, San Antonio, TX 78284 USA.
EM cusi@uthscsa.edu
NR 99
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U1 1
U2 13
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD NOV
PY 2009
VL 13
IS 4
BP 545
EP +
DI 10.1016/j.cld.2009.07.009
PG 20
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 514JJ
UT WOS:000271390100004
PM 19818304
ER
PT J
AU Chou, JCY
AF Chou, James C. -Y
TI MIXED EPISODES WITH PSYCHOTIC FEATURES
SO CNS SPECTRUMS
LA English
DT Article
ID BIPOLAR-I DISORDER; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; SUICIDAL
IDEATION; ACUTE MANIA; DEPRESSION; LITHIUM; DIVALPROEX; OLANZAPINE;
QUETIAPINE
C1 [Chou, James C. -Y] Mt Sinai Sch Med, New York, NY USA.
[Chou, James C. -Y] James J Peters VA Med Ctr, Bronx, NY USA.
RP Chou, JCY (reprint author), Mt Sinai Sch Med, New York, NY USA.
FU AstraZeneca; Bristol-Myers Squibb; Eli Lilly; GlaxoSmithKline; Janssen;
Pfizer
FX Dr. Chou has received honoraria from AstraZeneca, Bristol-Myers Squibb,
Eli Lilly, GlaxoSmithKline, Janssen, and Pfizer.
NR 16
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U1 0
U2 1
PU M B L COMMUNICATIONS, INC
PI NEW YORK
PA 333 HUDSON ST, 7TH FLOOR, NEW YORK, NY 10013 USA
SN 1092-8529
J9 CNS SPECTRUMS
JI CNS Spectr.
PD NOV
PY 2009
VL 14
IS 11
SU 11
BP 6
EP 8
PG 3
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 540TW
UT WOS:000273363500002
PM 20173694
ER
PT J
AU Nierenberg, AA
AF Nierenberg, Andrew A.
TI Failure to Integrate Brain and Mind (or Blaming Descartes to Understand
a Very Modern Dilemma about Explanatory Models, Psychiatric Treatment,
and Underfunding of Clinical Care and Research)
SO CNS SPECTRUMS
LA English
DT Editorial Material
ID MENTAL-DISORDERS; GLOBAL BURDEN
C1 [Nierenberg, Andrew A.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Nierenberg, Andrew A.] Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 02114 USA.
RP Nierenberg, AA (reprint author), Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
NR 9
TC 0
Z9 0
U1 0
U2 1
PU M B L COMMUNICATIONS, INC
PI NEW YORK
PA 333 HUDSON ST, 7TH FLOOR, NEW YORK, NY 10013 USA
SN 1092-8529
J9 CNS SPECTRUMS
JI CNS Spectr.
PD NOV
PY 2009
VL 14
IS 11
BP 599
EP 600
PG 2
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 529HV
UT WOS:000272507600001
PM 20173684
ER
PT J
AU Mendez, MF
AF Mendez, Mario F.
TI The Neurobiology of Moral Behavior: Review and Neuropsychiatric
Implications
SO CNS SPECTRUMS
LA English
DT Review
ID VENTROMEDIAL PREFRONTAL CORTEX; FRONTOTEMPORAL LOBAR DEGENERATION;
ANTISOCIAL PERSONALITY-DISORDER; POSITRON-EMISSION-TOMOGRAPHY; MIRROR
NEURON SYSTEM; SOCIAL COGNITION; DECISION-MAKING; ORBITOFRONTAL CORTEX;
ACQUIRED SOCIOPATHY; FRONTAL-CORTEX
AB Morality may be innate to the human brain. This review examines the neurobiological evidence from research involving functional magnetic resonance imaging of normal subjects, developmental sociopathy, acquired sociopathy from brain lesions, and frontotemporal dementia. These studies indicate a "neuromoral" network for responding to moral dilemmas centered in the ventromedial prefrontal cortex and its connections, particularly on the right. The neurobiological evidence indicates the existence of automatic "prosocial" mechanisms for identification with others that are part of the mora brain. Patients with disorders involving this moral network have attenuated emotional reactions to the possibility of harming others and may perform sociopathic acts. The existence of this neuromoral system has major clinical implications for the management of patients with dysmoral behavior from brain disorders and for forensic neuropsychiatry. CNS Spectr. 2009;14(11):608-620
C1 [Mendez, Mario F.] VA Greater Los Angeles Healthcare Ctr, Neurobehav Unit 691 116AF, Los Angeles, CA 90073 USA.
[Mendez, Mario F.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Mendez, Mario F.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
RP Mendez, MF (reprint author), VA Greater Los Angeles Healthcare Ctr, Neurobehav Unit 691 116AF, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM mmendez@UCLA.edu
FU [R01AG03449902]
FX This work was supported by grant # R01AG03449902.
NR 169
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U1 5
U2 32
PU M B L COMMUNICATIONS, INC
PI NEW YORK
PA 333 HUDSON ST, 7TH FLOOR, NEW YORK, NY 10013 USA
SN 1092-8529
J9 CNS SPECTRUMS
JI CNS Spectr.
PD NOV
PY 2009
VL 14
IS 11
BP 608
EP 620
PG 13
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 529HV
UT WOS:000272507600003
PM 20173686
ER
PT J
AU Marques, L
AF Marques, Luana
TI Interviewing Clients Across Cultures
SO COGNITIVE AND BEHAVIORAL PRACTICE
LA English
DT Book Review
C1 [Marques, Luana] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
RP Marques, L (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Simches Res Bldg,2nd Floor,185 Cambridge St, Boston, MA 02114 USA.
EM lmarques@partners.org
NR 4
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1077-7229
J9 COGN BEHAV PRACT
JI Cogn. Behav. Pract.
PD NOV
PY 2009
VL 16
IS 4
BP 480
EP 481
PG 2
WC Psychology, Clinical
SC Psychology
GA 521BJ
UT WOS:000271893800013
ER
PT J
AU Morland, LA
Greene, CJ
Rosen, C
Mauldin, PD
Frueh, BC
AF Morland, Leslie A.
Greene, Carolyn J.
Rosen, Craig
Mauldin, Patrick D.
Frueh, B. Christopher
TI Issues in the design of a randomized noninferiority clinical trial of
telemental health psychotherapy for rural combat veterans with PTSD
SO CONTEMPORARY CLINICAL TRIALS
LA English
DT Article
DE Posttraumatic stress disorder (PTSD); Rural; Military veterans;
Telemedicine; Noninferiority trial
ID POSTTRAUMATIC-STRESS-DISORDER; COGNITIVE-PROCESSING THERAPY;
QUALITY-OF-LIFE; URBAN DISPARITIES; EXPOSURE THERAPY; TELEPSYCHIATRY;
VALIDATION; INVENTORY; VICTIMS; SERVICE
AB This methodological article provides a description of the design, methods, and rationale of the first prospective, noninferiority designed randomized clinical trial evaluating the clinical and cost implications of delivering an evidence-based cognitive-behavioral group intervention specifically treating posttraumatic stress disorder (PTSD) with a trauma-focused intervention via video teleconferencing (VTC). PTSD is a prevalent mental health problem found among returning Operation Iraqi Freedom/Operation Enduring Freedom (OIF/OEF) military populations. These returning military personnel often live in rural areas and therefore have limited access to care and specialized psychological treatments. In the field of mental health, telemental health (TMH) technology has introduced a potential solution to the persistent problem of access to care in remote areas. This study is enrolling approximately 126 returning veterans with Current combat-related PTSD who are receiving services through the Veteran Administration (VA) mental health care clinics on 4 Hawaiian Islands. Cognitive Processing Therapy (CPT), an empirically supported manualized treatment for PTSD, is being delivered across 9 cohorts. Participants are assigned to either the experimental VTC condition or the in-person control condition. Assessments measuring clinical, process, and cost outcomes are being conducted at baseline, mid-treatment, post-treatment, and 3 and 6 months post-treatment. The study employs a noninferiority design to determine if the group treatment delivered via VTC is as good as the traditional in-person modality. In addition, a cost analysis will be performed in order to compare the cost of the 2 modalities. Novel aspects of this trial and specific challenges are discussed. (C) 2009 Published by Elsevier Inc.
C1 [Morland, Leslie A.] Natl Ctr PTSD, Pacific Isl Div, Dept Vet Affairs Pacific Isl Healthcare Syst, Honolulu, HI 96819 USA.
[Greene, Carolyn J.; Rosen, Craig] Natl Ctr PTSD, Disseminat & Training Div, Dept Vet Affairs Palo Alto Healthcare Syst, Palo Alto, CA USA.
[Greene, Carolyn J.; Rosen, Craig] Stanford Univ, Sch Med, Palo Alto, CA 94304 USA.
[Mauldin, Patrick D.] S Carolina Coll Pharm, Dept Clin Pharm & Outcome Sci, Charleston, SC USA.
[Mauldin, Patrick D.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
[Frueh, B. Christopher] Menninger Clin, Houston, TX USA.
[Frueh, B. Christopher] Baylor Coll Med, Houston, TX 77030 USA.
RP Morland, LA (reprint author), Natl Ctr PTSD, Pacific Isl Div, Dept Vet Affairs Pacific Isl Healthcare Syst, 3375 Koapaka St, Honolulu, HI 96819 USA.
EM Leslie.Morland@va.gova
FU Department of Defense [PT074516]; Office of Research and Development,
Medical Research Service, Department of Veterans Affairs
FX This work is partially supported by Grant PT074516 from the Department
of Defense. This work is also supported by the Office of Research and
Development, Medical Research Service, Department of Veterans Affairs.
All views and opinions expressed herein are those of the authors and do
not necessarily reflect those of our respective institutions or the
Department of Veterans Affairs.
NR 67
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U1 3
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1551-7144
J9 CONTEMP CLIN TRIALS
JI Contemp. Clin. Trials
PD NOV
PY 2009
VL 30
IS 6
BP 513
EP 522
DI 10.1016/j.cct.2009.06.006
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 523YM
UT WOS:000272111000003
PM 19576299
ER
PT J
AU Hahn, JO
Reisner, AT
Asada, HH
AF Hahn, Jin-Oh
Reisner, Andrew T.
Asada, H. Harry
TI Modeling and 2-sensor blind identification of human cardiovascular
system
SO CONTROL ENGINEERING PRACTICE
LA English
DT Article
DE Cardiovascular system; Blind system identification; Two-channel Wiener
system; Cardiovascular health monitoring; Aortic blood pressure
ID AORTIC PRESSURE; WAVE-FORM; DERIVATION
AB This paper presents modeling and blind identification of human cardiovascular system. In contrast to the population-based methods widespread in current practice, the proposed method does not require any a priori knowledge of the cardiovascular system. This paper develops a human cardiovascular system model, analyzes its identifiability, and identifies the model using two diametric blood pressure measurements. The aortic blood pressure reconstructed using the identified model can eliminate the use of invasive aortic blood pressure measurement for cardiovascular monitoring. Results based on the data from a realistic human cardiovascular system simulator demonstrate the validity of the proposed model and identification method. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Hahn, Jin-Oh; Asada, H. Harry] MIT, Dept Mech Engn, Arbeloff Lab Informat Syst & Technol, Cambridge, MA 02139 USA.
[Reisner, Andrew T.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
RP Hahn, JO (reprint author), MIT, Dept Mech Engn, Arbeloff Lab Informat Syst & Technol, 77 Massachusetts Ave 3-351, Cambridge, MA 02139 USA.
EM jinoh.hahn@alum.mit.edu
FU Sharp Corporation
FX This research was supported in part by the Sharp Corporation. We also
appreciate Professor Roger D. Kamm and Dr. Xinshu Xiao at Massachusetts
Institute of Technology for their kind assistance and suggestions in the
use of the human CV system simulator.
NR 22
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U1 0
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0967-0661
J9 CONTROL ENG PRACT
JI Control Eng. Practice
PD NOV
PY 2009
VL 17
IS 11
BP 1318
EP 1328
DI 10.1016/j.conengprac.2009.06.006
PG 11
WC Automation & Control Systems; Engineering, Electrical & Electronic
SC Automation & Control Systems; Engineering
GA 509TS
UT WOS:000271041900008
ER
PT J
AU Renaud, B
Santin, A
Coma, E
Camus, N
Van Pelt, D
Hayon, J
Gurgui, M
Roupie, E
Herve, J
Fine, MJ
Brun-Buisson, C
Labarere, J
AF Renaud, Bertrand
Santin, Aline
Coma, Eva
Camus, Nicolas
Van Pelt, Dave
Hayon, Jan
Gurgui, Merce
Roupie, Eric
Herve, Jerome
Fine, Michael J.
Brun-Buisson, Christian
Labarere, Jose
TI Association between timing of intensive care unit admission and outcomes
for emergency department patients with community-acquired pneumonia
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE pneumonia; community-acquired infection; emergency department; intensive
care; severity of illness index; time to admission
ID SYSTEMIC INFLAMMATORY RESPONSE; QUALITY-OF-LIFE; SEVERE SEPSIS; SEPTIC
SHOCK; PREDICTION RULE; SEVERITY-INDEX; GUIDELINES; MANAGEMENT;
DECISION; MULTICENTER
AB Objective: To compare the 28-day mortality and hospital length of stay of patients with community-acquired pneumonia who were transferred to an intensive care unit on the same day of emergency department presentation (direct-transfer patients) with those subsequently transferred within 3 days of presentation (delayed-transfer patients).
Design: Secondary analysis of the original data from two North American and two European prospective, multicenter, cohort studies of adult patients with community-acquired pneumonia. Patients: In all, 453 non-institutionalized patients transferred within 3 days of emergency department presentation to an intensive care unit were included in the analysis. Supplementary analysis was restricted to patients without an obvious indication for immediate transfer to an intensive care unit.
Interventions: None.
Measurements and Main Results: The sample consisted of 138 delayed-transfer and 315 direct-transfer patients, among whom 150 (33.1%) were considered to have an obvious indication for immediate intensive care unit admission. After adjusting for the quintile of propensity score, delayed intensive care unit transfer was associated with an increased odds ratio for 28-day mortality (2.07; 95% confidence interval, 1.12-3.85) and a decreased odds ratio for discharge from hospital for survivors (0.53; 95% confidence interval, 0.39-0.71). In a propensity-matched analysis, delayed-transfer patients had a higher 28-day mortality rate (23.4% vs. 11.7%; p = 0.02) and a longer median hospital length of stay (13 days vs. 7 days; p <.001) than direct-transfer patients. Similar results were found after excluding the 150 patients with an obvious indication for immediate intensive care unit admission.
Conclusions: Our findings suggest that some patients without major criteria for severe community-acquired pneumonia, according to the recent Infectious Diseases Society of America/American Thoracic Society consensus guideline, may benefit from direct transfer to the intensive care unit. Further studies are needed to prospectively identify patients who may benefit from direct intensive care unit admission despite a lack of major severity criteria for community-acquired pneumonia based on the current guidelines. (Crit Care Med 2009; 37:2867-2874)
C1 [Renaud, Bertrand; Santin, Aline; Camus, Nicolas; Hayon, Jan] Grp Hosp Henri Mondor Albert Chenevier, AP HP, Dept Emergency Med, Creteil, France.
[Coma, Eva] Hosp Duran & Reynals, Serv Atencio Continuada USAC, Inst Catala Oncol, Barcelona, Spain.
[Camus, Nicolas; Brun-Buisson, Christian] Univ Paris 12, Fac Med, Creteil, France.
[Van Pelt, Dave] Med Ctr, Dept Crit Care & Pulm Consultants, Aurora, CO USA.
[Hayon, Jan] Ctr Hosp Intercommunal Poissy St Germain, Dept Crit Care Med, St Germain En Laye, France.
[Gurgui, Merce] Hosp Santa Creu & Sant Pau, Dept Emergency Med, Barcelona, Spain.
[Roupie, Eric] Hop Cote Nacre, CHU Caen, Dept Emergency Med, Caen, France.
[Roupie, Eric] Univ Caen Basse Normandie, Fac Med, Caen, France.
[Fine, Michael J.] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Fine, Michael J.] Univ Pittsburgh, Dept Med, Div Gen Internal Med, Pittsburgh, PA USA.
[Labarere, Jose] CHU Grenoble, Qual Care Unit, F-38043 Grenoble, France.
RP Renaud, B (reprint author), Grp Hosp Henri Mondor Albert Chenevier, AP HP, Dept Emergency Med, Creteil, France.
EM bertrand.renaud@hmn.aphp.fr
RI Labarere, Jose/N-1688-2014;
OI Labarere, Jose/0000-0001-7621-6586
FU Departement de la Formation Continue des Medecins de I'Assistance
Publique des Hopitaux de Paris; ARMUR; AQUARE; GIaxoSmithKline France;
Direction de la Recherche Clinique d'lle de France [AOM 89-145]
FX Dr. Renaud has received grants from GIaxoSmithKline. Dr. Labarere was
supported by a grant from the Egide Foundation, Paris, France (Programme
Lavoisier) and from the Direction de la Recherche Clinique at Grenoble
University Hospital. The remaining authors have not disclosed any
potential conflicts of interest.
NR 36
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U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD NOV
PY 2009
VL 37
IS 11
BP 2867
EP 2874
DI 10.1097/CCM.0b013e3181b02dbb
PG 8
WC Critical Care Medicine
SC General & Internal Medicine
GA 517IP
UT WOS:000271607000001
PM 19770748
ER
PT J
AU Martin, PI
Naeser, MA
Ho, M
Treglia, E
Kaplan, E
Baker, EH
Pascual-Leone, A
AF Martin, Paula I.
Naeser, Margaret A.
Ho, Michael
Treglia, Ethan
Kaplan, Elina
Baker, Errol H.
Pascual-Leone, Alvaro
TI Research With Transcranial Magnetic Stimulation in the Treatment of
Aphasia
SO CURRENT NEUROLOGY AND NEUROSCIENCE REPORTS
LA English
DT Review
ID NONFLUENT APHASIA; POSTSTROKE APHASIA; RIGHT-HEMISPHERE; PREMOTOR
CORTEX; FUNCTIONAL MRI; SPEECH-PERCEPTION; LANGUAGE FUNCTION; BRAIN
PLASTICITY; FRONTAL-CORTEX; WORD RETRIEVAL
AB Repetitive transcranial magnetic stimulation (rTMS) has been used to improve language behavior, including naming, in stroke patients with chronic, nonfluent aphasia. Part 1 of this article reviews functional imaging studies related to language recovery in aphasia. Part 2 reviews the rationale for using rTMS to treat nonfluent aphasia (based on functional imaging) and presents our current rTMS protocol. We present language results from our rTMS studies as well as imaging results from overt naming functional MRI scans obtained before and after a series of rTMS treatments. Part 3 presents results from a pilot study in which rTMS treatments were followed immediately by constraint-induced language therapy. Part 4 reviews our diffusion tensor imaging study examining the possible connectivity of the arcuate fasciculus to different parts of Broca's area (pars triangularis, pars opercularis) and to the ventral premotor cortex. The potential role of mirror neurons in the right pars opercularis and ventral premotor cortex in aphasia recovery is discussed.
C1 [Martin, Paula I.] VA Boston Healthcare Syst, Aphasia Res Ctr 12A, Boston, MA 02130 USA.
RP Martin, PI (reprint author), VA Boston Healthcare Syst, Aphasia Res Ctr 12A, 150 S Huntington Ave, Boston, MA 02130 USA.
EM paulak@bu.edu
FU National Institutes of Health (NIH) [RO1 DC05672]; Medical Research
Service, Department of Veterans Affairs; NIH [RRO18875];
HarvardThorndike General Clinical Research Center [MO1 RR01032]; NIDCD
[P30 DC05207]
FX This research is supported by National Institutes of Health (NIH) grant
# RO1 DC05672 from the National Institute on Deafness and Other
Communication Disorders (NIDCD) and a grant from the Medical Research
Service, Department of Veterans Affairs (to Dr. Naeser); a K24 NIH award
(RRO18875; to Dr. Pascual-Leone) and the HarvardThorndike General
Clinical Research Center (NCRR MO1 RR01032); and a P30 DC05207 NIDCD
grant to the Harold Goodglass Boston University Aphasia Research Center.
NR 55
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U1 2
U2 18
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1528-4042
J9 CURR NEUROL NEUROSCI
JI Curr. Neurol. Neurosci. Rep.
PD NOV
PY 2009
VL 9
IS 6
BP 451
EP 458
PG 8
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 505XZ
UT WOS:000270736600006
PM 19818232
ER
PT J
AU Heath, RJ
Xavier, RJ
AF Heath, Robert J.
Xavier, Ramnik J.
TI Autophagy, immunity and human disease
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Article
DE adaptive immunity; autophagy; Crohn's disease; innate immunity
ID GENOME-WIDE ASSOCIATION; CROHNS-DISEASE; SUSCEPTIBILITY LOCI;
TUMOR-SUPPRESSOR; GENE ATG5; BECLIN 1; COMPLEX; LC3; MACROPHAGES;
ATG16L1
AB Purpose of review
To give an overview of autophagy and its effects on innate and adaptive immunity and touch on some of the roles of autophagy in disease.
Recent findings
Precise regulation of autophagy is necessary to maintain metabolic equilibrium, immune homeostasis, delineate cell fate and influence host cell responses to cytosolic pathogens. A growing number of studies have implicated that inactivation of autophagy-selective responses contributes to inflammatory disorders, neurodegeneration and cancer, but the precise steps at which disease-associated autophagy-related (ATG) genes affect autophagy pathways is unknown at present.
Summary
In eukaryotic cells autophagy is constitutively active at low levels, whereas significant up-regulation occurs in response to a multitude of stresses. Autophagy has achieved notoriety as a perturbed biological process in many disease states and an exponential increase of studies attribute roles for autophagy in innate and adaptive immunity. Understanding how individual disease-associated ATG genes function will lead to a better understanding of and potentially novel therapies for treating the diseases in which they are involved.
C1 [Xavier, Ramnik J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Computat & Integrat Biol,Richard B Simches Re, Boston, MA 02114 USA.
[Heath, Robert J.; Xavier, Ramnik J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit,Ctr Inflammatory Bowel Dis, Boston, MA 02114 USA.
[Xavier, Ramnik J.] Broad Inst MIT & Harvard, Cambridge, MA USA.
RP Xavier, RJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Computat & Integrat Biol,Richard B Simches Re, 185 Cambridge St,7th Floor, Boston, MA 02114 USA.
EM Xavier@molbiol.mgh.harvard.edu
FU NIH [A1062773, DK83756, DK043351]
FX R.J.X. and R.J.H. are supported by the following grants from the NIH:
A1062773, DK83756, DK043351.
NR 59
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U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0267-1379
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PD NOV
PY 2009
VL 25
IS 6
BP 512
EP 520
DI 10.1097/MOG.0b013e32833104f1
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 516SR
UT WOS:000271563500004
PM 19826372
ER
PT J
AU Lin, NH
Kuritzkes, DR
AF Lin, Nina H.
Kuritzkes, Daniel R.
TI Tropism testing in the clinical management of HIV-1 infection
SO CURRENT OPINION IN HIV AND AIDS
LA English
DT Article
DE CCR5; CXCR4; genotypic assay; phenotypic assay; viral tropism
AB Purpose of review
A variety of methods are available to determine HIV-1 co-receptor usage, commonly referred to as viral tropism. This article reviews recent data on phenotypic and genotypic assays of HIV-1 tropism.
Recent findings
Tropism assays are used to determine co-receptor usage of HIV-1 in patients who may be candidates for treatment with CCR5 antagonists. Phenotypic assays are used most often in the clinical trials of CCR5 antagonists, and are considered the 'gold standard' for comparison with other methods of tropism testing. Enhancements have allowed detection of a lower threshold of minor CXCR4-using species. When compared with phenotypic assays, genotypic methods have poor sensitivity but good specificity at detecting CXCR4-using HIV-1. Preliminary results from a recent comparative study suggest that some genotypic methods may perform as well as phenotypic tests in predicting virologic response to CCR5 antagonists. Several studies show that tropism testing may provide useful prognostic information regarding the risk of disease progression.
Summary
Understanding the characteristic of different tropism assays is important for their clinical use. Although phenotypic testing currently is favored, genotypic assays may be a suitable alternative in appropriate settings.
C1 [Lin, Nina H.] Massachusetts Gen Hosp, Infect Dis Unit, Boston, MA 02114 USA.
[Lin, Nina H.; Kuritzkes, Daniel R.] Harvard Univ, Sch Med, Boston, MA USA.
[Kuritzkes, Daniel R.] Brigham & Womens Hosp, Sect Retroviral Therapeut, Boston, MA 02115 USA.
RP Kuritzkes, DR (reprint author), Brigham & Womens Hosp, Sect Retroviral Therapeut, 65 Landsdowne St,Rm 449, Cambridge, MA 02139 USA.
EM dkuritzkes@partners.org
FU NIH [K24 RR016482, R37 AI055357, U01 AI068636]; Harvard Institute for
Global Health, Bristol-Myers Squibb; American Society for Tropical
Medicine and Hygiene
FX NIH grants K24 RR016482, R37 AI055357, and U01 AI068636 (to D.R.K) and
fellowship support from the Harvard Institute for Global Health,
Bristol-Myers Squibb, and the American Society for Tropical Medicine and
Hygiene (to N.H.L).
NR 46
TC 19
Z9 20
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1746-630X
J9 CURR OPIN HIV AIDS
JI Curr. Opin. HIV AIDS
PD NOV
PY 2009
VL 4
IS 6
BP 481
EP 487
DI 10.1097/COH.0b013e328331b929
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA V19PD
UT WOS:000208083400004
PM 20048714
ER
PT J
AU Herbstman, BJ
Pincus, HA
AF Herbstman, Benjamin J.
Pincus, Harold A.
TI Measuring mental healthcare quality in the United States: a review of
initiatives
SO CURRENT OPINION IN PSYCHIATRY
LA English
DT Review
DE indicators; measures; mental health; quality; United States
ID PERFORMANCE
AB Purpose of review
This review article aims to present a systematic overview of the current initiatives assessing mental and/or substance use (M/SU) healthcare quality in the United States.
Recent findings
The study found 36 initiatives incorporating M/SU indicators with efforts from the federal and state government, health plans, nongovernmental and professional organizations.
Summary
Although there has been much activity in recent years in the development of M/SU indicators, efforts have lacked coordination, have focused on limited areas of clinical activity, and have not been clearly linked to quality improvement activity. The study recommends that the United States government forms an entity to better coordinate efforts and address these concerns. Clinicians and provider organizations should also increase the use of already developed M/SU indicators to improve quality of care delivered.
C1 [Herbstman, Benjamin J.] Harvard Univ, Sch Med, Boston, MA USA.
[Herbstman, Benjamin J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Herbstman, Benjamin J.] McLean Hosp, Belmont, MA 02178 USA.
[Pincus, Harold A.] Columbia Univ, Dept Psychiat, New York, NY USA.
[Pincus, Harold A.] Columbia Univ, Irving Inst Clin & Translat Res, New York, NY USA.
[Pincus, Harold A.] New York Presbyterian Hosp, New York, NY USA.
[Pincus, Harold A.] RAND, Pittsburgh, PA USA.
RP Pincus, HA (reprint author), 1051 Riverside Dr,Room 5813,Unit Box 09, New York, NY 10032 USA.
EM pincush@pi.cpmc.columbia.edu
FU Center for Mental Health Services, Substance Abuse and Mental Health
Services Administration; U.S. Department of Health and Human Services,
Irving Institute for Clinical and Translational Research at Columbia
University [UL1 RR024156]; University of Pittsburgh [UL1 RR024153];
National Center for Research Resources (NCRR); National Institutes of
Health (NIH); Mental Heath Therapeutics CERT at Rutgers; Agency for
Healthcare Research and Quality (AHRQ) [5 U18 HS016097]
FX Funding for this work was received by the Center for Mental Health
Services, Substance Abuse and Mental Health Services Administration,
U.S. Department of Health and Human Services, Irving Institute for
Clinical and Translational Research at Columbia University (UL1
RR024156) and University of Pittsburgh (UL1 RR024153) both from the
National Center for Research Resources (NCRR), a component of the
National Institutes of Health (NIH), Mental Heath Therapeutics CERT at
Rutgers, the State University of New Jersey funded by the Agency for
Healthcare Research and Quality (AHRQ) (5 U18 HS016097).
NR 18
TC 10
Z9 10
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0951-7367
J9 CURR OPIN PSYCHIATR
JI Curr. Opin. Psychiatr.
PD NOV
PY 2009
VL 22
IS 6
BP 623
EP 630
DI 10.1097/YCO.0b013e3283318ece
PG 8
WC Psychiatry
SC Psychiatry
GA 513CW
UT WOS:000271301000021
PM 19745741
ER
PT J
AU Hulspas, R
Dombkowski, D
Preffer, F
Douglas, D
Kildew-Shah, B
Gilbert, J
AF Hulspas, Ruud
Dombkowski, David
Preffer, Frederic
Douglas, Derick
Kildew-Shah, Brian
Gilbert, John
TI Flow Cytometry and the Stability of Phycoerythrin-Tandem Dye Conjugates
SO CYTOMETRY PART A
LA English
DT Article
DE degradation; fluorochrome; stability; T-regulatory cells; CD4/CD8;
clinical; flow cytometry; compensation
ID ENERGY-TRANSFER; FLUORESCENCE COMPENSATION; QUALITY-CONTROL;
IMMUNOFLUORESCENCE; STANDARDS
AB Routine clinical flow cytometric procedures demand rigorous, simple, and reproducible procedures for spectral compensation. The current, often laborious, spectral compensation procedures are the result of variability in instrument settings, instrument performance, and variability in reagents. In particular, the use of tandem dye conjugates necessitates elaborate spectral compensation procedures that need to be applied frequently. Manufacturer, lot number, and handling procedures are considered the key aspects affecting the fluorescence characteristics of tandem dyes. A better understanding of how specific conditions affect the variability in emission spectra of tandem dyes can lead to a considerable increase in reliability of measurements and a potential simplification of setup procedures for routine, clinical flow cytometry. We investigated the effect of light exposure, handling, and storage conditions on the fluorescence characteristics of some common phycoerythrin tandem fluorochromes. in general, PE-Cy5 showed the lowest degradation rates, whereas PE-Cy7 showed the highest. During storage, long-term degradation rates were lowest for reagents packaged using an extra light protective approach. Under these conditions, a degradation rate of 0.9%/month of a PE-Cy7 conjugate decreased to 0.3%/month. As degradation rates were minimized, we studied the effect of slow degradation of a set of tandem dye conjugates on compensation matrix values over several months. Finally, we explored the effect of slow degradation on flow cytometric analysis using the same compensation settings for extended periods for an analysis template with preset regions and gating strategies. (C) 2009 International Society for Advancement of Cytometry
C1 [Hulspas, Ruud; Gilbert, John] Cytonome Inc, Boston, MA USA.
[Dombkowski, David; Preffer, Frederic] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Douglas, Derick; Kildew-Shah, Brian] Sperotech Inc, Lake Forest, IL USA.
RP Hulspas, R (reprint author), Cytonome ST LLC, 27 Drydock Ave, Boston, MA 02210 USA.
EM rhulspas@cytonomest.com
NR 20
TC 18
Z9 18
U1 1
U2 5
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4922
J9 CYTOM PART A
JI Cytom. Part A
PD NOV
PY 2009
VL 75A
IS 11
BP 966
EP 972
DI 10.1002/cyto.a.20799
PG 7
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 515UN
UT WOS:000271498500011
PM 19777547
ER
PT J
AU Cannizzo, E
Bellio, E
Ferry, JA
Hasserjian, RP
Sohani, AR
Dorn, ME
Sadowski, C
Bucci, JJ
Petrini, M
Carulli, G
Preffer, F
AF Cannizzo, Elisa
Bellio, Emanuele
Ferry, Judith A.
Hasserjian, Robert P.
Sohani, Aliyah R.
Dorn, Michelle E.
Sadowski, Craig
Bucci, Janessa J.
Petrini, Mario
Carulli, Giovanni
Preffer, Frederic
TI MULTIPARAMETER IMMUNOPHENOTYPING BY FLOW CYTOMETRY IN MULTIPLE MYELOMA:
DEFINING RANGES OF NORMAL EXPRESSION AND THEIR DIAGNOSTIC UTILITY
SO CYTOMETRY PART B-CLINICAL CYTOMETRY
LA English
DT Meeting Abstract
CT 24th Annual Meeting of the Clinical-Cytometry-Society
CY OCT 16-18, 2009
CL Jacksonville, FL
SP Clin Cytometry Soc
C1 [Cannizzo, Elisa; Ferry, Judith A.; Hasserjian, Robert P.; Sohani, Aliyah R.; Dorn, Michelle E.; Sadowski, Craig; Bucci, Janessa J.; Preffer, Frederic] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Cannizzo, Elisa; Ferry, Judith A.; Hasserjian, Robert P.; Sohani, Aliyah R.; Dorn, Michelle E.; Sadowski, Craig; Bucci, Janessa J.; Preffer, Frederic] Harvard Univ, Sch Med, Boston, MA USA.
[Cannizzo, Elisa; Bellio, Emanuele; Petrini, Mario; Carulli, Giovanni] Univ Pisa, Sect Hematol, Dept Oncol Transplants & Adv Med, Pisa, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4949
J9 CYTOM PART B-CLIN CY
JI Cytom. Part B-Clin. Cytom.
PD NOV
PY 2009
VL 76B
IS 6
BP 397
EP 397
PG 1
WC Medical Laboratory Technology; Pathology
SC Medical Laboratory Technology; Pathology
GA 508UK
UT WOS:000270962200013
ER
PT J
AU Cannizzo, E
Bellio, E
Sohani, AR
Hasserjian, RP
Ferry, JA
Dorn, ME
Sadowski, C
Bucci, JJ
Petrini, M
Carulli, G
Preffer, F
AF Cannizzo, Elisa
Bellio, Emanuele
Sohani, Aliyah R.
Hasserjian, Robert P.
Ferry, Judith A.
Dorn, Michelle E.
Sadowski, Craig
Bucci, Janessa J.
Petrini, Mario
Carulli, Giovanni
Preffer, Frederic
TI THE DIAGNOSTIC ROLE OF MULTIPARAMETER IMMUNOPHENOTYPING BY FLOW
CYTOMETRY IN MULTIPLE MYELOMA: A NEW MODEL
SO CYTOMETRY PART B-CLINICAL CYTOMETRY
LA English
DT Meeting Abstract
CT 24th Annual Meeting of the Clinical-Cytometry-Society
CY OCT 16-18, 2009
CL Jacksonville, FL
SP Clin Cytometry Soc
C1 [Cannizzo, Elisa; Sohani, Aliyah R.; Hasserjian, Robert P.; Ferry, Judith A.; Dorn, Michelle E.; Sadowski, Craig; Bucci, Janessa J.; Preffer, Frederic] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Cannizzo, Elisa; Sohani, Aliyah R.; Hasserjian, Robert P.; Ferry, Judith A.; Dorn, Michelle E.; Sadowski, Craig; Bucci, Janessa J.; Preffer, Frederic] Harvard Univ, Sch Med, Boston, MA USA.
[Cannizzo, Elisa; Bellio, Emanuele; Petrini, Mario; Carulli, Giovanni] Dept Oncol Transplants & Adv Med, Sect Hematol, Pisa, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4949
J9 CYTOM PART B-CLIN CY
JI Cytom. Part B-Clin. Cytom.
PD NOV
PY 2009
VL 76B
IS 6
BP 397
EP 397
PG 1
WC Medical Laboratory Technology; Pathology
SC Medical Laboratory Technology; Pathology
GA 508UK
UT WOS:000270962200012
ER
PT J
AU Mehta, NK
Chang, VW
AF Mehta, Neil K.
Chang, Virginia W.
TI MORTALITY ATTRIBUTABLE TO OBESITY AMONG MIDDLE-AGED ADULTS IN THE UNITED
STATES
SO DEMOGRAPHY
LA English
DT Article
ID BODY-MASS-INDEX; ALL-CAUSE MORTALITY; WAIST-HIP RATIO; US ADULTS; HEALTH
RESEARCH; EXCESS DEATHS; CONFIDENCE-INTERVALS; SOCIOECONOMIC-STATUS;
PROSPECTIVE COHORT; CIGARETTE-SMOKING
AB Obesity is considered a major cause of premature mortality and a potential threat to the long-standing secular decline in mortality in the United States. We measure relative and attributable risks associated with obesity among middle-aged adults using data from the Health and Retirement Study (1992-2004). Although class II/III obesity (BMI >= 35.0 kg/m(2)) increases mortality by 40% in females and 62% in males compared with normal BMI (BMI = 18.5-24.9), class I obesity (BMI = 30.0-34.9) and being overweight (BM] = 25.0-29.9) are not associated with excess mortality. With respect to attributable mortality, class II/III obesity (BMI >= 35.0) is responsible for approximately 4% of deaths among females and 3% of deaths among males. Obesity is often compared with cigarette smoking as a major source of avoidable mortality. Smoking-attributable mortality is much larger in this cohort: about 36% in females and 50% in males. Results are robust to confounding by preexisting diseases, multiple dimensions of socioeconomic status (SES), smoking, and other correlates. These findings challenge the viewpoint that obesity will stem the long-term secular decline in U.S. mortality
C1 [Mehta, Neil K.] Univ Michigan, Robert Wood Johnson Fdn Hlth & Soc, Sch Publ Hlth, Ann Arbor, MI 48109 USA.
[Chang, Virginia W.] Univ Penn, Sch Med, Dept Med, Philadelphia, PA 19104 USA.
[Chang, Virginia W.] Univ Penn, Dept Sociol, Philadelphia, PA 19104 USA.
[Chang, Virginia W.] Univ Penn, Ctr Populat Studies, Philadelphia, PA 19104 USA.
[Chang, Virginia W.] Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
RP Mehta, NK (reprint author), Univ Michigan, Robert Wood Johnson Fdn Hlth & Soc, Sch Publ Hlth, 3628 SPH Tower,1415 Washington Hts, Ann Arbor, MI 48109 USA.
EM nkmehta@umich.edu
FU NIA NIH HHS [T32 AG000177]; NICHD NIH HHS [K12 HD043459, K12HD043459]
NR 81
TC 49
Z9 49
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0070-3370
EI 1533-7790
J9 DEMOGRAPHY
JI Demography
PD NOV
PY 2009
VL 46
IS 4
BP 851
EP 872
PG 22
WC Demography
SC Demography
GA 526SE
UT WOS:000272312800010
PM 20084832
ER
PT J
AU Smoller, JW
Block, SR
Young, MM
AF Smoller, Jordan W.
Block, Stefanie R.
Young, Mirella M.
TI GENETICS OF ANXIETY DISORDERS: THE COMPLEX ROAD FROM DSM TO DNA
SO DEPRESSION AND ANXIETY
LA English
DT Review
DE genetics; anxiety; genomewide association study; heritability
ID OBSESSIVE-COMPULSIVE DISORDER; GENOME-WIDE ASSOCIATION; SEROTONIN
TRANSPORTER GENOTYPE; POSTTRAUMATIC-STRESS-DISORDER; HURRICANE-EXPOSED
ADULTS; PANIC DISORDER; SOCIAL PHOBIA; BEHAVIORAL-INHIBITION;
GENERALIZED ANXIETY; LINKAGE SCAN
AB Anxiety disorders are among the most common psychiatric disorders, affecting one in four individuals over a lifetime. Although our understanding of the etiology of these disorders is incomplete, familial and genetic factors are established risk factors. However, identifying the specific casual genes has been difficult. Within the past several years, advances in molecular and statistical genetic methods have made the genetic dissection of complex disorders a feasible project. Here we provide an overview of these developments, with a focus on their implications for genetic studies of anxiety disorders. Although the genetic and phenotypic complexity of the anxiety disorders present formidable challenges, advances in neuroimaging and experimental animal models of anxiety and fear offer important opportunities for discovery. Real progress in identifying the genetic basis of anxiety disorders will require integrative approaches that make use of these biologic tools as well as larger-scale genomic studies. If successful, such efforts may yield novel and more effective approaches for the prevention and treatment of these common and costly disorders. Depression and Anxiety 26:965-975, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Smoller, Jordan W.; Block, Stefanie R.; Young, Mirella M.] Massachusetts Gen Hosp, Dept Psychiat, Psychiat Genet Program Mood & Anxiety Disorders, Simches Res Bldg,185 Cambridge St, Boston, MA 02114 USA.
RP Smoller, JW (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Psychiat Genet Program Mood & Anxiety Disorders, Simches Res Bldg,185 Cambridge St, Boston, MA 02114 USA.
EM jsmoller@hms.harvard.edu
NR 113
TC 39
Z9 41
U1 6
U2 35
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1091-4269
EI 1520-6394
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PD NOV
PY 2009
VL 26
IS 11
BP 965
EP 975
DI 10.1002/da.20623
PG 11
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 515DV
UT WOS:000271447900002
PM 19885930
ER
PT J
AU Simon, NM
Herlands, NN
Marks, EH
Mancini, C
Letamendi, A
Li, ZH
Pollack, MH
Van Ameringen, M
Stein, MB
AF Simon, Naomi M.
Herlands, Nannette N.
Marks, Elizabeth H.
Mancini, Catherine
Letamendi, Andrea
Li, Zhonghe
Pollack, Mark H.
Van Ameringen, Michael
Stein, Murray B.
TI CHILDHOOD MALTREATMENT LINKED TO GREATER SYMPTOM SEVERITY AND POORER
QUALITY OF LIFE AND FUNCTION IN SOCIAL ANXIETY DISORDER
SO DEPRESSION AND ANXIETY
LA English
DT Article
DE social anxiety disorder; social phobia; anxiety; child abuse; abuse
ID NATIONAL COMORBIDITY SURVEY; INTERNATIONAL NEUROPSYCHIATRIC INTERVIEW;
SEXUAL-ABUSE; DSM-IV; PSYCHOMETRIC PROPERTIES; PHOBIA; RISK;
PSYCHOPATHOLOGY; SCALE; QUESTIONNAIRE
AB Background: There is a paucity of data examining the prevalence and impact of childhood maltreatment in patients presenting with a primary diagnosis of social anxiety disorder (SAD). We thus examined the presence of a broad spectrum of childhood maltreatment, including physical, sexual, and emotional abuse and neglect, in treatment-seeking individuals with the generalized subtype of SAD (GSAD). We hypothesized that a history of childhood maltreatment would be associated with greater SAD symptom severity and poorer associated function. Methods: One hundred and three participants with a primary diagnosis of GSAD (mean age 37+/-14, 70% male) completed the well-validated, self-related Childhood Trauma Questionnaire (CTQ), as well as measures of SAD symptom severity and quality of life. Results: Fully 70% (n = 72) of the GSAD sample met severity criteria for at least one type of childhood abuse or neglect as measured by the CTQ subscales using previously established thresholds CTQ total score adjusted for age and gender was associated with greater SAD severity, and poorer quality of life, Junction, and resilience. Further, the number of types of maltreatment present had an additive effect, with specific associations for emotional abuse and neglect with SAD severity. Conclusions: Despite the we of validated assessments, our findings are limited by the retrospective and subjective nature of self-report measures used to assess childhood maltreatment. Nonetheless, these data suggest a high rate of childhood maltreatment in individuals seeking treatment for GSAD, and the association of maltreatment with greater disorder severity suggests that screening is clinically prudent. Depression and Anxiety 26:1027-1032, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Simon, Naomi M.; Herlands, Nannette N.; Marks, Elizabeth H.; Li, Zhonghe; Pollack, Mark H.] Massachusetts Gen Hosp, Ctr Anxiety & Traumat Stress Disorders, Boston, MA 02114 USA.
[Mancini, Catherine; Van Ameringen, Michael] McMaster Univ, Med Ctr, Hamilton, ON, Canada.
[Letamendi, Andrea; Stein, Murray B.] Univ Calif San Diego, Anxiety & Traumat Stress Disorders Program, San Diego, CA 92103 USA.
RP Simon, NM (reprint author), Massachusetts Gen Hosp, Ctr Anxiety & Traumat Stress Disorders, Simches Res Bldg,2nd Floor,185 Cambridge St, Boston, MA 02114 USA.
EM nsimon@partners.org
FU NIMH NIH HHS [5R01MH070919, R01 MH070919, R01 MH070919-05]
NR 29
TC 44
Z9 45
U1 2
U2 17
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1091-4269
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PD NOV
PY 2009
VL 26
IS 11
BP 1027
EP 1032
DI 10.1002/da.20604
PG 6
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 515DV
UT WOS:000271447900010
PM 19750554
ER
PT J
AU Alquier, T
Peyot, ML
Latour, MG
Kebede, M
Sorensen, CM
Gesta, S
Kahn, CR
Smith, RD
Jetton, TL
Metz, TO
Prentki, M
Poitout, V
AF Alquier, Thierry
Peyot, Marie-Line
Latour, Martin G.
Kebede, Melkam
Sorensen, Christina M.
Gesta, Stephane
Kahn, C. Ronald
Smith, Richard D.
Jetton, Thomas L.
Metz, Thomas O.
Prentki, Marc
Poitout, Vincent
TI Deletion of GPR40 Impairs Glucose-Induced Insulin Secretion In Vivo in
Mice Without Affecting Intracellular Fuel Metabolism in Islets
SO DIABETES
LA English
DT Article
ID PROTEIN-COUPLED RECEPTOR; FATTY-ACID STIMULATION; PANCREATIC BETA-CELLS;
RAT ISLETS; EXPRESSION; PHOSPHOLIPASE-A(2); MODULATION; ACTIVATION;
STARVATION; CALCIUM
AB OBJECTIVE-The G-protein-coupled receptor GPR40 mediates fatty acid potentiation of glucose-stimulated insulin secretion, but its contribution to insulin secretion in vivo and mechanisms of action remain uncertain. This study was aimed to ascertain whether GPR40 controls insulin secretion in vivo and modulates intracellular fuel metabolism in islets.
RESEARCH DESIGN AND METHODS-Insulin secretion and sensitivity were assessed in GPR40 knockout mice and their wild-type littermates by hyperglycemic clamps and hyperinsulinemic euglycemic clamps, respectively. Transcriptomic analysis, metabolic studies, and lipid profiling were used to ascertain whether GPR40 modulates intracellular fuel metabolism in islets.
RESULTS-Both glucose- and arginine-stimulated insulin secretion in vivo were decreased by similar to 60% in GPR40 knockout fasted and fed mice, without changes in insulin sensitivity. Neither gene expression profiles nor intracellular metabolism of glucose and palmitate in isolated islets were affected by GPR40 deletion. Lipid profiling of isolated islets revealed that the increase in triglyceride and decrease in lyso-phosphatidylethanolamine species in response to palmitate in vitro was similar in wild-type and knockout islets. In contrast, the increase in intracellular inositol phosphate levels observed in wild-type islets in response to fatty acids in vitro was absent in knockout islets.
CONCLUSIONS-These results indicate that deletion of GPR40 impairs insulin secretion in vivo not only in response to fatty acids but also to glucose and arginine, without altering intracellular fuel metabolism in islets, via a mechanism that may involve the generation of inositol phosphates downstream of GPR40 activation. Diabetes 58:2607-2615, 2009
C1 [Alquier, Thierry; Peyot, Marie-Line; Latour, Martin G.; Kebede, Melkam; Prentki, Marc; Poitout, Vincent] Univ Montreal, Montreal Univ Hosp, Res Ctr, Montreal Diabet Res Ctr, Montreal, PQ, Canada.
[Alquier, Thierry; Kebede, Melkam; Poitout, Vincent] Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada.
[Sorensen, Christina M.; Smith, Richard D.; Metz, Thomas O.] Pacific NW Natl Lab, Div Biol Sci, Richland, WA 99352 USA.
[Gesta, Stephane; Kahn, C. Ronald] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Gesta, Stephane; Kahn, C. Ronald] Harvard Univ, Sch Med, Boston, MA USA.
[Jetton, Thomas L.] Univ Vermont, Coll Med, Div Endocrinol Diabet & Metab, Burlington, VT USA.
[Prentki, Marc] Univ Montreal, Dept Nutr, Montreal, PQ H3C 3J7, Canada.
RP Poitout, V (reprint author), Univ Montreal, Montreal Univ Hosp, Res Ctr, Montreal Diabet Res Ctr, Montreal, PQ, Canada.
EM vincent.poitout@umontreal.ca
OI Alquier, Thierry/0000-0001-8171-802X; Poitout,
Vincent/0000-0002-6555-5053; Metz, Tom/0000-0001-6049-3968
FU National Institutes of Health [R21-DK070598, R01-DK068329,
R33-DK070146]; Canadian Institutes of Health Research [MOP 177381];
Canadian Diabetes Association; DOE [DE-AC06-76LO-1830]
FX This work was supported by National Institutes of Health Grants
R21-DK070598 to V.P., R01-DK068329 to T.L.J., and R33-DK070146 to R.D.S.
and T.O.M. and the Canadian Institutes of Health Research (MOP 177381 to
V.P.). T.A. was supported by a postdoctoral fellowship from the Canadian
Diabetes Association. V.P. holds the Canada Research Chair in Diabetes
and Pancreatic P-Cell Function. M.P. holds the Canada Research Chair in
Diabetes and Metabolism. The Pacific Northwest National Laboratory
(PNNL) is operated by Battelle Memorial Institute for the DOE under
contract no. DE-AC06-76LO-1830.
NR 39
TC 67
Z9 68
U1 0
U2 5
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD NOV
PY 2009
VL 58
IS 11
BP 2607
EP 2615
DI 10.2337/db09-0362
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 515RQ
UT WOS:000271490900022
PM 19720802
ER
PT J
AU Pezzolesi, MG
Katavetin, P
Kure, M
Poznik, GD
Skupien, J
Mychaleckyj, JC
Rich, SS
Warram, JH
Krolewski, AS
AF Pezzolesi, Marcus G.
Katavetin, Pisut
Kure, Masahiko
Poznik, G. David
Skupien, Jan
Mychaleckyj, Josyf C.
Rich, Stephen S.
Warram, James H.
Krolewski, Andrzej S.
TI Confirmation of Genetic Associations at ELMO1 in the GoKinD Collection
Supports Its Role as a Susceptibility Gene in Diabetic Nephropathy
SO DIABETES
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; AFRICAN-AMERICANS; SCAN; COMPLICATIONS;
POPULATION; VARIANTS; MELLITUS; DISEASE
AB OBJECTIVE-To examine the association between single nucleotide polymorphisms (SNPs) in the engulftnent and cell motility 1 (ELMO1) gene, a locus previously shown to be associated with diabetic nephropathy in two ethnically distinct type 2 diabetic populations, and the risk of nephropathy in type 1 diabetes.
RESEARCH DESIGN AND METHODS-Genotypic data from a genome-wide association scan (GWAS) of the Genetics of Kidneys in Diabetes (GoKinD) study collection were analyzed for associations across the ELMO1 locus. In total, genetic associations were assessed using 118 SNPs and 1,705 individuals of European ancestry with type 1 diabetes (885 normoalbuminuric control subjects and 820 advanced diabetic nephropathy case subjects).
RESULTS-The strongest associations in ELMO1 occurred at rs11769038 (odds ratio [OR] 1.24; P = 1.7 X 10(-3)) and rs1882080 (OR 1.23; P = 3.2 X 10(-3)) located in intron 16. Two additional SNPs, located in introns 18 and 20, respectively, were also associated with diabetic nephropathy. No evidence of association for variants previously reported in type 2 diabetes was observed in our collection.
CONCLUSIONS-Using GWAS data from the GoKinD collection, we comprehensively examined evidence of association across the ELMO1 locus. Our investigation marks the third report of associations in ELMO1 with diabetic nephropathy, further establishing its role in the susceptibility of this disease. There is evidence of allelic heterogeneity, contributed by the diverse genetic backgrounds of the different ethnic groups examined. Further investigation of SNPs at this locus is necessary to fully understand the commonality of these associations and the mechanism(s) underlying their role in diabetic nephropathy. Diabetes 58:2698-2702, 2009
C1 [Pezzolesi, Marcus G.; Katavetin, Pisut; Kure, Masahiko; Poznik, G. David; Skupien, Jan; Warram, James H.; Krolewski, Andrzej S.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, Boston, MA 02115 USA.
[Pezzolesi, Marcus G.; Katavetin, Pisut; Kure, Masahiko; Poznik, G. David; Skupien, Jan; Warram, James H.; Krolewski, Andrzej S.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Mychaleckyj, Josyf C.; Rich, Stephen S.] Univ Virginia, Sch Med, Ctr Publ Hlth Genom, Charlottesville, VA 22908 USA.
RP Krolewski, AS (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, Boston, MA 02115 USA.
EM andrzej.krolewski@joslin.harvard.edu
FU National Institutes of Health (NIH) [DK77532]; Foundation for NIH (FNIH)
[06GAIN0]; Joslin Diabetes Center's NIH [DK007260-31]; Juvenile Diabetes
Research Foundation [3-2009-397]
FX No potential conflicts of interest relevant to this article were
reported.
NR 23
TC 56
Z9 56
U1 0
U2 0
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD NOV
PY 2009
VL 58
IS 11
BP 2698
EP 2702
DI 10.2337/db09-0641
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 515RQ
UT WOS:000271490900032
PM 19651817
ER
PT J
AU Li, RL
O'Sullivan, MJ
Robinson, J
Safford, MM
Curb, D
Johnson, KC
AF Li, Rongling
O'Sullivan, Mary J.
Robinson, Jennifer
Safford, Monika M.
Curb, David
Johnson, Karen C.
TI Family history of myocardial infarction predicts incident coronary heart
disease in postmenopausal women with diabetes: the Women's Health
Initiative Observational Study
SO DIABETES-METABOLISM RESEARCH AND REVIEWS
LA English
DT Article
DE family history; CHD; diabetes; women's health
ID CARDIOVASCULAR RISK-FACTORS; ATHEROSCLEROSIS RISK; PARENTAL HISTORY;
ARTERY DISEASE; MENOPAUSE; AGE; EPIDEMIOLOGY; FRAMINGHAM; COHORT
AB Background Diabetes is a risk factor for coronary heart disease (CHD) but CHD does not occur in all diabetic individuals. The goal of this study was to assess the relationship between family history of myocardial infarction (MI) and incident CHD in diabetic postmenopausal women.
Methods We conducted a prospective cohort study among 2642 diabetic postmenopausal women without CHD at baseline in the Women's Health Initiative Observational Study. Family history was defined as a proband report of MI in first-degree relatives. Incident CHD was defined as non-fatal MI, coronary revascularization, or CHD death.
Results During 7.3 (+/- 1.8) years of follow-up, 14.3% of the participants had incident CHD. The risk of incident CHD was 50% higher (HR = 1.50, 95% Cl: 1.20-1.87, p = 0.0003) in those with a family history of an MI in at least one first-degree relative, and 79% higher (HR = 1.79, 95% Cl: 1.36-2.35, P < 0.0001) if two or more first-degree relatives had an MI, compared to participants without a family history, after adjustment for covariates. The CHD risk increased with elevated systolic blood pressure (SBP) (HR = 1.01, 95% Cl: 1.003-1.02, p = 0.001) but decreased with elevated diastolic BP (HR = 0.98, 95% Cl: 0.97-0-999, p = 0.005) and with two or more episodes per week of physical activity (HR = 0.70, 95% Cl: 0.52-0.93, p = 0.02).
Conclusions The results suggest that a family history of MI predicts CHD in diabetic postmenopausal women. Close attention should be paid to BP control and physical activity in these women. Copyright (C) 2009 John Wiley & Sons Ltd,.
C1 [Li, Rongling; Johnson, Karen C.] Univ Tennessee, Ctr Hlth Sci, Dept Prevent Med, Memphis, TN 38163 USA.
[O'Sullivan, Mary J.] Univ Miami, Miller Sch Med, Dept Obstet & Gynecol, Miami, FL 33136 USA.
[Robinson, Jennifer] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA USA.
[Safford, Monika M.] Univ Alabama, Birmingham, AL USA.
[Safford, Monika M.] Birmingham VA Med Ctr, Deep S Ctr Effectiveness, Birmingham, AL USA.
[Curb, David] Pacific Hlth Res Inst, Honolulu, HI USA.
RP Li, RL (reprint author), NHGRI, OPG, NIH, 5635 Fishers Lane,Suite 4076,MSC 9305, Bethesda, MD 20892 USA.
EM lir2@mail.nih.gov
FU National Heart, Lung, and Blood Institute, NIH [NO1-WH-3-2100,
NO1-WH-3-2101, NO1-WH-3-2102, NO1-WH-3-2105, NO1-WH-3-2106,
NO1-WH-3-2108, NO1-WH-3-2109, NO1-WH-3-2110, NO1-WH-3-2111,
NO1-WH-3-2112, NO1-WH-3-2113, NO1-WH-3-2115, NO1-WH-3-2118,
NO1-WH-3-2119, NO1-WH-3-2120, NO1-WH-3-2122, NO1-WH-4-2107,
NO1-WH-4-2108]
FX We acknowledge all WHI-OS participants and NIH for making the funds
available for the study. The WHI program is funded by NIH Contracts:
NO1-WH-3-2100, NO1-WH-3-2101, NO1-WH-3-2102, NO1-WH-3-2105,
NO1-WH-3-2106, NO1-WH-3-2108, NO1-WH-3-2109, NO1-WH-3-2110,
NO1-WH-3-2111, NO1-WH-3-2112, NO1-WH-3-2113, NO1-WH-3-2115,
NO1-WH-3-2118, NO1-WH-3-2119, NO1-WH-3-2120, NO1-WH-3-2122,
NO1-WH-4-2107, NO1-WH-4-2108, NO1-WH-4-2109, NO1-WH-4-2110,
NO1-WH-4-2111, NO1-WH-4-2112, NO1-WH-4-2113, NO1-WH-4-2114,
NO1-WH-4-2115, NO1-WH-4-2116, NO1-WH-4-2117, NO1-WH-4-2118,
NO1-WH-4-2119, NO1-WH-4-2120, NO1-WH-4-2121, NO1-WH-4-2122,
NO1-WH-4-2123, NO1-WH-4-2124, NO1-WH-4-2125, NO1-WH-4-2126,
NO1-WH-4-2129, NO1-WH-4-2130, NO1-WH-4-2131, and NO1-WH-4-2132 from the
National Heart, Lung, and Blood Institute, NIH.
NR 26
TC 1
Z9 2
U1 0
U2 1
PU JOHN WILEY & SONS LTD
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND
SN 1520-7552
J9 DIABETES-METAB RES
JI Diabetes-Metab. Res. Rev.
PD NOV
PY 2009
VL 25
IS 8
BP 725
EP 732
DI 10.1002/dmrr.1010
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 522RP
UT WOS:000272016300005
PM 19780066
ER
PT J
AU Liew, CW
Holman, A
Kulkarni, RN
AF Liew, C. W.
Holman, A.
Kulkarni, R. N.
TI The roles of telomeres and telomerase in beta-cell regeneration
SO DIABETES OBESITY & METABOLISM
LA English
DT Article
DE beta-cells; diabetes; telomere; islets; ageing
ID PANCREATIC-ISLET CELLS; INSULIN-RESISTANCE; DIABETES-MELLITUS; MAMMALIAN
TELOMERES; MOUSE TELOMERASE; UNITED-STATES; BLOOD-CELLS; DNA-DAMAGE;
DYSFUNCTION; GROWTH
AB Telomerase is a specialized reverse transcriptase that is responsible for extending and preserving the end of the chromosomes (telomeres). Telomerase plays a key role in regulating the lifespan of mammalian cells and is involved in critical aspects of cellular ageing processes. In this review, we will briefly summarize our current understanding of the functions of telomeres, telomerase and their regulation. Considering that compensatory islet hyperplasia and beta-cell regeneration play important roles in the prevention and/or delay of the onset of overt diabetes, we will also examine current literature regarding the effects of diabetes on telomere shortening and provide insights from our own studies on the role of telomerase in beta-cell regeneration.
C1 [Kulkarni, R. N.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
RP Kulkarni, RN (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, Boston, MA 02115 USA.
EM Rohit.Kulkarni@joslin.harvard.edu
FU NIH [RO1 DK 67536, RO1 DK 68721, 1RL9EB008539-01]
FX We thank the organizers of the International Group on Insulin Secretion
(IGIS) for the opportunity to share these data, and Lindsay Huse for
excellent assistance with preparation of the manuscript. This work was
supported in part by RO1 DK 67536 (R. N. K.) and RO1 DK 68721 (R. N.
K.). An NIH training grant (1RL9EB008539-01) (SysCODE) supported C. W.
L.
NR 75
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Z9 11
U1 1
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1462-8902
J9 DIABETES OBES METAB
JI Diabetes Obes. Metab.
PD NOV
PY 2009
VL 11
BP 21
EP 29
DI 10.1111/j.1463-1326.2009.01103.x
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 504JS
UT WOS:000270613000004
PM 19817785
ER
PT J
AU Weir, GC
Marselli, L
Marchetti, P
Katsuta, H
Jung, MH
Bonner-Weir, S
AF Weir, G. C.
Marselli, L.
Marchetti, P.
Katsuta, H.
Jung, M. H.
Bonner-Weir, S.
TI Towards better understanding of the contributions of overwork and
glucotoxicity to the beta-cell inadequacy of type 2 diabetes
SO DIABETES OBESITY & METABOLISM
LA English
DT Article
DE beta-cell; endoplasmic reticulum (ER) stress; glucotoxicity; insulin
secretion; laser capture microdissection; type 2 diabetes
ID ENDOPLASMIC-RETICULUM STRESS; CHRONIC HYPERGLYCEMIA; INSULIN-SECRETION;
GENE-EXPRESSION; PARTIAL-PANCREATECTOMY; GLUCOSE-TOLERANCE; ISLETS; RAT;
REGENERATION; DYSFUNCTION
AB Type 2 diabetes (T2D) is characterized by reduction of beta-cell mass and dysfunctional insulin secretion. Understanding beta-cell phenotype changes as T2D progresses should help explain these abnormalities. The normal phenotype should differ from the state of overwork when beta-cells compensate for insulin resistance to keep glucose levels normal. When only mild hyperglycaemia develops, beta-cells are subjected to glucotoxicity. As hyperglycaemia becomes more severe, so does glucotoxicity. beta-Cells in all four of these situations should have separate phenotypes. When assessing phenotype with gene expression, isolated islets have artefacts resulting from the trauma of isolation and hypoxia of islet cores. An advantage comes from laser capture microdissection (LCM), which obtains beta-cell-rich tissue from pancreatic frozen sections. Valuable data can be obtained from animal models, but the real goal is human beta-cells. Our experience with LCM and gene arrays on frozen pancreatic sections from cadaver donors with T2D and controls is described. Although valuable data was obtained, we predict that the approach of taking fresh samples at the time of surgery is an even greater opportunity to markedly advance our understanding of how beta-cell phenotype evolves as T2D develops and progresses.
C1 [Weir, G. C.; Marselli, L.; Katsuta, H.; Jung, M. H.; Bonner-Weir, S.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Sect Islet Transplantat & Cell Biol, Boston, MA 02215 USA.
[Marchetti, P.] Univ Pisa, Dept Endocrinol & Metab, Metab Unit, Pisa, Italy.
RP Weir, GC (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Sect Islet Transplantat & Cell Biol, 1 Joslin Pl, Boston, MA 02215 USA.
EM gordon.weir@joslin.harvard.edu
RI Marchetti, Piero/J-7439-2013
OI Marchetti, Piero/0000-0003-4907-0635
FU American Diabetes Association; Juvenile Diabetes Research Foundation;
National Institutes of Health [DK66056, P30 DK36836]
FX This study was supported by grants from the American Diabetes
Association, the Juvenile Diabetes Research Foundation, the National
Institutes of Health (DK66056, P30 DK36836) including the Advanced
Microscopy Core of the Joslin Diabetes and Endocrinology Research Center
(DERC), the Diabetes Research and Wellness Foundation and an important
group of private donors.
NR 35
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Z9 50
U1 0
U2 9
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1462-8902
J9 DIABETES OBES METAB
JI Diabetes Obes. Metab.
PD NOV
PY 2009
VL 11
BP 82
EP 90
DI 10.1111/j.1463-1326.2009.01113.x
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 504JS
UT WOS:000270613000010
PM 19817791
ER
PT J
AU Markowitz, JT
Lowe, MR
Volkening, LK
Laffel, LMB
AF Markowitz, J. T.
Lowe, M. R.
Volkening, L. K.
Laffel, L. M. B.
TI Self-reported history of overweight and its relationship to disordered
eating in adolescent girls with Type 1 diabetes
SO DIABETIC MEDICINE
LA English
DT Article
DE adolescence; obesity; type 1 diabetes
ID QUESTIONNAIRE EDE-Q; DIETARY RESTRAINT; WOMEN; YOUNG; PREVALENCE;
MELLITUS; BEHAVIOR; FEMALES; WEIGHT; NORMS
AB Aims
Increased body weight and disordered eating attitudes/behaviours are common in adolescent girls with Type 1 diabetes (T1D). Disordered eating increases risks for diabetes-related complications. This study aimed to identify a rapid screening approach for disordered eating attitudes and behaviours in adolescent girls with T1D and to examine the relationship between disordered eating and body weight in this population.
Methods
Ninety adolescent girls, aged 12-19 years, provided a self-assessment of weight status. Participants also completed questionnaires to assess attitudes/behaviours toward food and eating, appetitive responsiveness to the food environment, disinhibition in eating and weight history.
Results
Forty-three per cent of participants reported a history of overweight. Compared with participants who reported never being overweight, those who reported ever being overweight were significantly older, scored significantly higher on all measures of disordered eating attitudes/behaviours (P < 0.009) and were 4.8 times more likely to be currently overweight or obese (P < 0.001). Glycated haemoglobin (HbA(1c)) was similar between those who did and did not report ever being overweight.
Conclusions
Because of the ill-health effects of disordered eating and the higher rate of overweight in adolescent girls with T1D, effective screening tools are warranted. The single question 'Have you ever been overweight?' may be sufficient as a first question to screen for those at high risk for disordered eating attitudes/behaviours and to provide early intervention and prevention.
C1 [Markowitz, J. T.; Volkening, L. K.; Laffel, L. M. B.] Joslin Diabet Ctr, Pediat Adolescent & Young Adult Sect, Boston, MA 02215 USA.
[Markowitz, J. T.; Volkening, L. K.; Laffel, L. M. B.] Joslin Diabet Ctr, Genet & Epidemiol Sect, Boston, MA 02215 USA.
[Lowe, M. R.] Drexel Univ, Dept Psychol, Philadelphia, PA 19104 USA.
RP Markowitz, JT (reprint author), Joslin Diabet Ctr, Pediat Adolescent & Young Adult Sect, 1 Joslin Pl, Boston, MA 02215 USA.
EM jessica.markowitz@joslin.harvard.edu
FU NIH [T32 DK007260]; Katherine Adler Astrove Youth Education Fund; Maria
Griffin Drury Pediatric Fund
FX The authors would like to thank Evan Forman PhD, Pamela Geller PhD,
Terri Lipman PhD and Nancy Silverman PhD for their support. In addition,
we would like to thank Yelena Chernyak MS and Graham Thomas MS for their
help with data collection and analysis. This study was supported in part
by NIH Training Grant No. T32 DK007260, the Charles H. Hood Foundation,
the Katherine Adler Astrove Youth Education Fund and the Maria Griffin
Drury Pediatric Fund.
NR 37
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Z9 5
U1 0
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0742-3071
J9 DIABETIC MED
JI Diabetic Med.
PD NOV
PY 2009
VL 26
IS 11
BP 1165
EP 1171
DI 10.1111/j.1464-5491.2009.02844.x
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 515ST
UT WOS:000271493900013
PM 19929996
ER
PT J
AU Grant, RW
Hivert, M
Pandiscio, JC
Florez, JC
Nathan, DM
Meigs, JB
AF Grant, R. W.
Hivert, M.
Pandiscio, J. C.
Florez, J. C.
Nathan, D. M.
Meigs, J. B.
TI The clinical application of genetic testing in type 2 diabetes: a
patient and physician survey
SO DIABETOLOGIA
LA English
DT Article
DE Diabetes prediction; Genetic risk; Genetic testing; Medication
adherence; Patient motivation; Type 2 diabetes
ID GENOME-WIDE ASSOCIATION; LIFE-STYLE MODIFICATION; PREVENTION PROGRAM;
RISK-FACTORS; VARIANT; ADULTS
AB Aims/hypothesis Advances in type 2 diabetes genetics have raised hopes that genetic testing will improve disease prediction, prevention and treatment. Little is known about current physician and patient views regarding type 2 diabetes genetic testing. We hypothesised that physician and patient views would differ regarding the impact of genetic testing on motivation and adherence.
Methods We surveyed a nationally representative sample of US primary care physicians and endocrinologists (n=304), a random sample of non-diabetic primary care patients (n=152) and patients enrolled in a diabetes pharmacogenetics study (n=89).
Results Physicians and patients favoured genetic testing for diabetes risk prediction (79% of physicians vs 80% of nondiabetic patients would be somewhat/very likely to order/request testing, p=0.7). More patients than physicians (71% vs 23%, p<0.01) indicated that a 'high risk' result would be very likely to improve motivation to adopt preventive lifestyle changes. Patients favoured genetic testing to guide therapy (78% of patients vs 48% of physicians very likely to request/recommend testing, p<0.01) and reported that genetic testing would make them 'much more motivated' to adhere to medications (72% vs 18% of physicians, p<0.01). Many physicians (39%) would be somewhat/very likely to order genetic testing before published evidence of clinical efficacy.
Conclusions/interpretation Despite the paucity of current data, physicians and patients reported high expectations that genetic testing would improve patient motivation to adopt key behaviours for the prevention or control of type 2 diabetes. This suggests the testable hypothesis that 'genetic' risk information might have greater value to motivate behaviour change compared with standard risk information.
C1 [Grant, R. W.; Hivert, M.; Pandiscio, J. C.; Meigs, J. B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Florez, J. C.; Nathan, D. M.] Massachusetts Gen Hosp, Diabet Res Ctr, Diabet Unit, Boston, MA 02114 USA.
[Grant, R. W.; Florez, J. C.; Nathan, D. M.; Meigs, J. B.] Harvard Univ, Sch Med, Boston, MA USA.
[Florez, J. C.] Broad Inst Harvard & MIT, Cambridge, MA USA.
RP Grant, RW (reprint author), Massachusetts Gen Hosp, Div Gen Med, 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM Rgrant@partners.org
OI Grant, Richard/0000-0002-6164-8025
FU National Institutes of Health [NIDDK K23 DK067452]; Charlton Family Fund
FX R. W. Grant is supported by a National Institutes of Health career
development award (NIDDK K23 DK067452). This study was funded in part by
the Charlton Family Fund.
NR 24
TC 47
Z9 47
U1 1
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD NOV
PY 2009
VL 52
IS 11
BP 2299
EP 2305
DI 10.1007/s00125-009-1512-7
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 504XE
UT WOS:000270650600007
PM 19727660
ER
PT J
AU Kaunitz, JD
AF Kaunitz, Jonathan D.
TI GRG Update: DDW 2009 and Upcoming GRG-Sponsored Meetings
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Editorial Material
C1 [Kaunitz, Jonathan D.] W Los Angeles Vet Affairs Med Ctr, Dept Med, Los Angeles, CA 90073 USA.
[Kaunitz, Jonathan D.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90073 USA.
RP Kaunitz, JD (reprint author), W Los Angeles Vet Affairs Med Ctr, Dept Med, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM jake@ucla.edu
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD NOV
PY 2009
VL 54
IS 11
BP 2301
EP 2302
DI 10.1007/s10620-009-0987-x
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 507FI
UT WOS:000270836900001
ER
PT J
AU Puli, SR
Reddy, JBK
Bechtold, ML
Antillon, MR
Brugge, WR
AF Puli, Srinivas R.
Reddy, Jyotsna B. K.
Bechtold, Matthew L.
Antillon, Mainor R.
Brugge, William R.
TI EUS-Guided Celiac Plexus Neurolysis for Pain due to Chronic Pancreatitis
or Pancreatic Cancer Pain: A Meta-Analysis and Systematic Review
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Review
DE Endoscopic ultrasound; Celiac plexus neurolysis; Pancreatic cancer;
Chronic pancreatitis; Meta-analysis; Systematic review
ID PROSPECTIVE RANDOMIZED-TRIAL; SHOCK-WAVE LITHOTRIPSY; ENDOSCOPIC
ULTRASOUND; ABDOMINAL-PAIN; CLINICAL-TRIALS; BLOCK; RESECTION; DRAINAGE;
THERAPY; QUALITY
AB The objective of this study was to evaluate the efficacy of EUS-guided CPN for pain relief in patients with chronic pancreatitis and pancreatic cancer. An initial search identified 1,439 reference articles, of which 130 relevant articles were selected and reviewed. Data was extracted from 8 studies (N = 283) for EUS-guided CPN for pain due to pancreatic cancer and nine studies for chronic pancreatitis (N = 376) which met the inclusion criteria. With EUS-guided CPN, the pooled proportion of patients with pancreatic cancer that showed pain relief was 80.12% (95% CI = 74.47-85.22). In patients with pain due to chronic pancreatitis, EUS-guided CPN provided pain relief in 59.45% (95% CI = 54.51-64.30). In conclusion, EUS-guided CPN offers a safe alternative technique for pain relief in patients with chronic pancreatitis or pancreatic cancer. In patients with pain due to chronic pancreatitis, better techniques or injected materials are needed to improve the response.
C1 [Puli, Srinivas R.; Reddy, Jyotsna B. K.; Bechtold, Matthew L.; Antillon, Mainor R.] Univ Missouri, Div Gastroenterol & Hepatol, Clin Support & Educ CE443, Columbia, MO 65212 USA.
[Brugge, William R.] Massachusetts Gen Hosp, GI Unit, Boston, MA 02114 USA.
RP Puli, SR (reprint author), Univ Missouri, Div Gastroenterol & Hepatol, Clin Support & Educ CE443, 5 Hosp Dr,DC043-00, Columbia, MO 65212 USA.
EM pulis@missouri.edu
NR 54
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Z9 103
U1 1
U2 8
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD NOV
PY 2009
VL 54
IS 11
BP 2330
EP 2337
DI 10.1007/s10620-008-0651-x
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 507FI
UT WOS:000270836900006
PM 19137428
ER
PT J
AU Sonnenberg, A
AF Sonnenberg, Amnon
TI Demographic Characteristics of Hospitalized IBD Patients
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Environmental risk factors; Epidemiology of IBD; Geographic variation;
Hospital statistics; Socio-economic status; Time trends
ID INFLAMMATORY-BOWEL-DISEASE; EPIDEMIOLOGY; AMERICANS; MORTALITY; VOLUME
AB The Nationwide Inpatient Sample of the Healthcare Cost and Utilization Project (HCUP) was used to study the recent demographic characteristics of patients with Crohn's disease (CD) or ulcerative colitis (UC).
HCUP data of the period 1997-2006 were extracted. The data were stratified by the categories pertaining to patient demographics, such as age-group, sex, race, insurance type, income group, residence in metropolitan area and region of the United States, as well as categories pertaining to hospital characteristics, such as type of ownership, teaching status, location, and bed-size. The distributions of inpatients among different categories were compared between CD or UC and all other diagnoses, using odds ratios and their 95% confidence intervals for comparison.
The data revealed a slight female predominance in CD (1.08, 1.09-1.09) and a slight male predominance in UC (1.15, 1.14-1.15). Compared to patients with other diagnoses, patients with inflammatory bowel disease tended to be white (CD: 2.47, 2.45-2.50; UC: 2.13, 2.10-2.15), more affluent (CD: 1.44, 1.43-1.45; UC: 1.59, 1.58-1.61), live in metropolitan areas (CD: 1.09, 1.08-1.10; UC: 1.26, 1.25-1.27) and in the Northeast of the United States (CD: 1.27, 1.27-1.28; UC: 1.44, 1.43-1.45).
These patterns confirm previously described characteristics of patients with inflammatory bowel disease and show that such characteristics still apply to present patient populations.
C1 Oregon Hlth & Sci Univ, Portland VA Med Ctr, Portland, OR 97239 USA.
RP Sonnenberg, A (reprint author), Oregon Hlth & Sci Univ, Portland VA Med Ctr, P3 GI,3710 SW US Vet Hosp Rd, Portland, OR 97239 USA.
EM sonnenbe@ohsu.edu
NR 22
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U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD NOV
PY 2009
VL 54
IS 11
BP 2449
EP 2455
DI 10.1007/s10620-009-0973-3
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 507FI
UT WOS:000270836900023
PM 19760158
ER
PT J
AU Nentwich, L
Ulrich, AS
AF Nentwich, Lauren
Ulrich, Andrew S.
TI High-Risk Chief Complaints II: Disorders of the Head and Neck
SO EMERGENCY MEDICINE CLINICS OF NORTH AMERICA
LA English
DT Article
DE Headache; Seizure; Acute neurologic deficits; Throat pain; Neck pain;
Ocular emergencies; Difficult airway
ID SPONTANEOUS INTRACEREBRAL HEMORRHAGE; PEDIATRIC EMERGENCY-DEPARTMENT;
DIFFICULT TRACHEAL INTUBATION; TISSUE-PLASMINOGEN ACTIVATOR; IMPOSSIBLE
MASK VENTILATION; ASSOCIATION STROKE COUNCIL; TRANSIENT ISCHEMIC ATTACK;
HEALTH-CARE PROFESSIONALS; OF-NEUROLOGY AFFIRMS; C-SPINE RULE
AB Of the many different complaints of patients presenting to the emergency department, some of the most difficult to diagnose and manage involve pathology of the head and neck. Often diagnoses of conditions affecting this part of the body are elusive, and occasionally, even once the diagnosis has been made, the management of these disorders remains challenging. This article addresses some of the high-risk chief complaints of the head and neck regarding diagnosis and management. These complaints include headache, seizure, acute focal neurologic deficits, throat and neck pain, ocular emergencies, and the difficult airway.
C1 [Nentwich, Lauren] Massachusetts Gen Hosp, Ctr Stroke Res, Dept Neurol, Boston, MA 02114 USA.
[Ulrich, Andrew S.] Boston Univ, Sch Med, Boston Med Ctr, Dept Emergency Med, Boston, MA 02118 USA.
RP Nentwich, L (reprint author), Massachusetts Gen Hosp, Ctr Stroke Res, Dept Neurol, 175 Cambridge St,Suite 300, Boston, MA 02114 USA.
EM lnentwich@partners.org
NR 99
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Z9 3
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 0733-8627
EI 1558-0539
J9 EMERG MED CLIN N AM
JI Emerg. Med. Clin. N. Am.
PD NOV
PY 2009
VL 27
IS 4
BP 713
EP +
DI 10.1016/j.emc.2009.08.002
PG 35
WC Emergency Medicine
SC Emergency Medicine
GA 602LK
UT WOS:000278140500014
PM 19932402
ER
PT J
AU Manini, AF
Ilgen, J
Noble, VE
Bamberg, F
Koenig, W
Bohan, JS
Hoffmann, U
AF Manini, A. F.
Ilgen, J.
Noble, V. E.
Bamberg, F.
Koenig, W.
Bohan, J. S.
Hoffmann, U.
TI Derivation and validation of a sensitive IMA cutpoint to predict cardiac
events in patients with chest pain
SO EMERGENCY MEDICINE JOURNAL
LA English
DT Article
ID ISCHEMIA-MODIFIED ALBUMIN; ACUTE CORONARY SYNDROMES;
EMERGENCY-DEPARTMENT; MYOCARDIAL-INFARCTION; BINDING ASSAY; LIMITATIONS;
TROPONIN; RULE
AB Objectives: In patients with acute chest pain, we derived a cutpoint for ischaemia-modified albumin (IMA) and prospectively validated this cutpoint to predict 30-day major adverse cardiac events (MACEs).
Methods: We prospectively recruited a derivation cohort (18-month period) to establish a serum IMA cutpoint targeting 80% sensitivity. This was followed by a prospective validation cohort study of emergency department patients with acute chest pain at two university hospitals over a 3-month period. A MACE was defined as myocardial infarction, revascularisation or death at 30-day follow-up.
Results: In the derivation cohort of 151 patients, the IMA cutpoint that achieved 80% sensitivity for MACEs was 75 KU/litre. The sensitivity was prospectively validated in 171 patients consecutively enrolled, of whom 106 underwent multiple-biomarker analysis (19.8% MACE rate, 81% sensitivity of IMA). Furthermore, IMA by itself (81%, p<0.01) and in combination with initial highly sensitive cardiac troponin T (hsTnT) (90%, p<0.001) had significantly higher sensitivity than initial hsTnT (29%) for prediction of MACEs.
Conclusions: We prospectively validated the sensitive IMA cutpoint of 75 KU/litre with 80% sensitivity for MACEs in patients with acute chest pain. Our data suggest that IMA alone and in combination with initial hsTnT are more sensitive than the initial hsTnT for MACEs.
C1 [Manini, A. F.] Mt Sinai Sch Med, Dept Emergency Med, New York, NY 10029 USA.
[Ilgen, J.] Harvard Univ, Sch Med, Harvard Affiliated Emergency Med Residency, Boston, MA USA.
[Noble, V. E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA USA.
[Bamberg, F.; Hoffmann, U.] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
[Koenig, W.] Univ Ulm, Div Cardiol, Ulm, Germany.
[Bohan, J. S.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Emergency Med, Boston, MA 02115 USA.
RP Manini, AF (reprint author), Mt Sinai Sch Med, Dept Emergency Med, 1 Gustrave L Levy Pl,Box 1620, New York, NY 10029 USA.
EM alex.manini@mountsinai.org
FU Dade Behring; Massachusetts General Hospital Departmental Award;
National Institutes of Health [HL080053]
FX Cardiac Diagnostics Grant from Dade Behring ( to JSB), Massachusetts
General Hospital Departmental Award ( to AFM) and in part by the
National Institutes of Health (HL080053 to UH).
NR 19
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Z9 5
U1 0
U2 3
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1472-0205
J9 EMERG MED J
JI Emerg. Med. J.
PD NOV
PY 2009
VL 26
IS 11
BP 791
EP 796
DI 10.1136/emj.2008.068130
PG 6
WC Emergency Medicine
SC Emergency Medicine
GA 509NB
UT WOS:000271023600010
PM 19850803
ER
PT J
AU Peluso, JJ
Gawkowska, A
Liu, XF
Shioda, T
Pru, JK
AF Peluso, John J.
Gawkowska, Anna
Liu, Xiufang
Shioda, Toshi
Pru, James K.
TI Progesterone Receptor Membrane Component-1 Regulates the Development and
Cisplatin Sensitivity of Human Ovarian Tumors in Athymic Nude Mice
SO ENDOCRINOLOGY
LA English
DT Article
ID CANCER-CELLS; MOLECULAR-MECHANISMS; BINDING-PROTEIN; EXPRESSION; MODELS;
XENOGRAFTS; RESISTANCE; INHIBITION; VIABILITY; APOPTOSIS
AB To determine whether progesterone receptor membrane component 1 (PGRMC1) regulates the development and cisplatin (CDDP)-sensitivity of human ovarian tumors, PGRMC1 was depleted from a human ovarian cancer cell line, dsRed-SKOV-3 cells, using a short hairpin RNA knockdown approach. Compared with parental dsRed-SKOV-3 cells, the PGRMC1-deplete cells grew slower in vitro and did not show progesterone's (P4) antiapoptotic effect. In fact, P4 induced apoptosis in PGRMC1-deplete cells in a dose-dependent manner. When transplanted into the peritoneum of athymic nude mice, parental dsRed-SKOV-3 cells developed numerous tumors, which were classified as either typical or oxyphilic clear cell tumors. CDDP increased the percentage of apoptotic nuclei in typical clear cell tumors and P4 attenuated CDDP-induced apoptosis. In contrast, the percentage of apoptotic nuclei in oxyphilic clear cell tumors was low (<= 1%) and was not significantly affected by CDDP and/or P4. Compared with tumors derived from parental dsRed SKOV-3 cells, PGRMC1-deplete tumors: 1) developed in fewer mice, 2) formed less frequently, 3) appeared smaller, and 4) resulted in fewer oxyphilic clear cell tumors. These PGRMC1-deplete tumors were not responsive to CDDP's apoptotic effects. The failure to respond to CDDP could be due to their poorly developed microvasculature system as judged by percentage of CD31-stained endothelial cells and/or their increased expression of ATP-binding cassette transporters, which are involved in drug resistance. Taken together, these findings indicate that PGRMC1 plays an essential role in the development and CDDP sensitivity of human ovarian tumors. (Endocrinology 150: 4846-4854, 2009)
C1 [Peluso, John J.; Gawkowska, Anna; Liu, Xiufang] Univ Connecticut, Ctr Hlth, Dept Cell Biol, Farmington, CT 06030 USA.
[Peluso, John J.] Univ Connecticut, Ctr Hlth, Dept Obstet & Gynecol, Farmington, CT 06030 USA.
[Shioda, Toshi] Harvard Univ, Dept Tumor Biol, Mol Profiling Lab, Massachusetts Gen Hosp Ctr Canc Res,Med Sch, Charlestown, MA 02129 USA.
[Pru, James K.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Vincent Obstet & Gynecol Serv, Boston, MA 02114 USA.
RP Peluso, JJ (reprint author), Univ Connecticut, Ctr Hlth, Dept Cell Biol, Farmington, CT 06030 USA.
EM peluso@nso2.uchc.edu
FU Connecticut Department of Public Health Biomedical Research
[BCH-2007-0918]; Vincent Memorial Research Funds
FX Disclosure Summary: The authors have nothing to disclose.
NR 35
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U1 0
U2 4
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD NOV
PY 2009
VL 150
IS 11
BP 4846
EP 4854
DI 10.1210/en.2009-0730
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 509ID
UT WOS:000271007700004
PM 19797399
ER
PT J
AU Hill, JW
Xu, Y
Preitner, F
Fukuda, M
Cho, YR
Luo, J
Balthasar, N
Coppari, R
Cantley, LC
Kahn, BB
Zhao, JJ
Elmquist, JK
AF Hill, Jennifer W.
Xu, Yong
Preitner, Frederic
Fukuda, Makota
Cho, You-Ree
Luo, Ji
Balthasar, Nina
Coppari, Roberto
Cantley, Lewis C.
Kahn, Barbara B.
Zhao, Jean J.
Elmquist, Joel K.
TI Phosphatidyl Inositol 3-Kinase Signaling in Hypothalamic
Proopiomelanocortin Neurons Contributes to the Regulation of Glucose
Homeostasis
SO ENDOCRINOLOGY
LA English
DT Article
ID INCREASED INSULIN SENSITIVITY; GLUCOCORTICOID-RECEPTOR ANTAGONISM;
POMC-EXPRESSING CELLS; PHOSPHOINOSITIDE 3-KINASE; MICE LACKING;
BODY-WEIGHT; ENERGY HOMEOSTASIS; P85-ALPHA SUBUNIT; ARCUATE NUCLEUS;
FOOD-INTAKE
AB Recent studies demonstrated a role for hypothalamic insulin and leptin action in the regulation of glucose homeostasis. This regulation involves proopiomelanocortin (POMC) neurons because suppression of phosphatidyl inositol 3-kinase (PI3K) signaling in these neurons blunts the acute effects of insulin and leptin on POMC neuronal activity. In the current study, we investigated whether disruption of PI3K signaling in POMC neurons alters normal glucose homeostasis using mouse models designed to both increase and decrease PI3K-mediated signaling in these neurons. We found that deleting p85 alpha alone induced resistance to diet-induced obesity. In contrast, deletion of the p110 alpha catalytic subunit of PI3K led to increased weight gain and adipose tissue along with reduced energy expenditure. Independent of these effects, increased PI3K activity in POMC neurons improved insulin sensitivity, whereas decreased PI3K signaling resulted in impaired glucose regulation. These studies show that activity of the PI3K pathway in POMC neurons is involved in not only normal energy regulation but also glucose homeostasis. (Endocrinology 150: 4874-4882, 2009)
C1 [Elmquist, Joel K.] Univ Texas SW Med Ctr Dallas, Div Hypothalam Res, Dept Internal Med, Touchstone Ctr Diabet Res, Dallas, TX 75390 USA.
[Cho, You-Ree] Univ Texas SW Med Ctr Dallas, Dept Internal Med & Pharmacol, Dept Internal Med & Cell Biol, Touchstone Ctr Diabet Res, Dallas, TX 75390 USA.
[Preitner, Frederic] Univ Lausanne, Cardiomet Mouse Metab Facil, Ctr Integrat Genom, CH-1015 Lausanne, Switzerland.
[Luo, Ji] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02215 USA.
[Cantley, Lewis C.] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02215 USA.
[Zhao, Jean J.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02215 USA.
[Luo, Ji] Brigham & Womens Hosp, Dept Med, Boston, MA 02215 USA.
[Cantley, Lewis C.] Beth Israel Deaconess Med Ctr, Div Signal Transduct, Boston, MA 02215 USA.
[Kahn, Barbara B.] Beth Israel Deaconess Med Ctr, Div Endocrinol, Boston, MA 02215 USA.
[Zhao, Jean J.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
[Balthasar, Nina] Univ Bristol, Div Physiol, Bristol BS8 1TD, Avon, England.
RP Elmquist, JK (reprint author), Univ Texas SW Med Ctr Dallas, Div Hypothalam Res, Dept Internal Med, Touchstone Ctr Diabet Res, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM jean_zhao@dfci.harvard.edu; joel.elmquist@utsouthwestern.edu
RI Fukuda, Makoto/C-9745-2009; Coppari, Roberto/B-4799-2014; Cantley,
Lewis/D-1800-2014; Fukuda, Makoto/I-7915-2014
OI Fukuda, Makoto/0000-0003-0112-9925; Cantley, Lewis/0000-0002-1298-7653;
Fukuda, Makoto/0000-0003-0112-9925
FU University of Texas Southwestern Medical Center at Dallas [PL1
DK081182-01]; National Institutes of Health [1F32DK066972, K99HD056491,
K99DK085330, PO1 DK56116, DK53301, GM41890, R01 DK53301-07S2, R01
CA134502-01]; V Foundation; Canadian Institute of Health Research;
American Diabetes Association Smith Family Foundation; Takeda
Pharmaceutical Co., Ltd., Japan
FX Disclosure Summary: The authors have nothing to declare.
NR 62
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Z9 48
U1 0
U2 2
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD NOV
PY 2009
VL 150
IS 11
BP 4874
EP 4882
DI 10.1210/en.2009-0454
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 509ID
UT WOS:000271007700007
PM 19819947
ER
PT J
AU Lessard, SJ
Rivas, DA
Chen, ZP
van Denderen, BJ
Watt, MJ
Koch, LG
Britton, SL
Kemp, BE
Hawley, JA
AF Lessard, Sarah J.
Rivas, Donato A.
Chen, Zhi-Ping
van denderen, Bryce J.
Watt, Matthew J.
Koch, Lauren G.
Britton, Steven L.
Kemp, Bruce E.
Hawley, John A.
TI Impaired Skeletal Muscle beta-Adrenergic Activation and Lipolysis Are
Associated with Whole-Body Insulin Resistance in Rats Bred for Low
Intrinsic Exercise Capacity
SO ENDOCRINOLOGY
LA English
DT Article
ID HORMONE-SENSITIVE LIPASE; ORPHAN NUCLEAR RECEPTORS; FATTY-ACID
OXIDATION; PROTEIN-KINASE; ARTIFICIAL SELECTION; AS160 PHOSPHORYLATION;
UNCOUPLING PROTEIN-3; ENDURANCE EXERCISE; GLUCOSE-TOLERANCE;
LIPID-CONTENT
AB Rats selectively bred for high endurance running capacity (HCR) have higher insulin sensitivity and improved metabolic health compared with those bred for low endurance capacity (LCR). We investigated several skeletal muscle characteristics, in vitro and in vivo, that could contribute to the metabolic phenotypes observed in sedentary LCR and HCR rats. After 16 generations of selective breeding, HCR had approximately 400% higher running capacity (P < 0.001), improved insulin sensitivity (P < 0.001), and lower fasting plasma glucose and triglycerides (P < 0.05) compared with LCR. Skeletal muscle ceramide and diacylglycerol content, basal AMP-activated protein kinase (AMPK) activity, and basal lipolysis were similar between LCR and HCR. However, the stimulation of lipolysis in response to 10 mu M isoproterenol was 70% higher in HCR (P = 0.004). Impaired isoproterenol sensitivity in LCR was associated with lower basal triacylglycerol lipase activity, Ser660 phosphorylation of HSL, and beta 2-adrenergic receptor protein content in skeletal muscle. Expression of the orphan nuclear receptor Nur77, which is induced by beta-adrenergic signaling and is associated with insulin sensitivity, was lower in LCR (P < 0.05). Muscle protein content of Nur77 target genes, including uncoupling protein 3, fatty acid translocase/CD36, and the AMPK gamma 3 subunit were also lower in LCR (P < 0.05). Our investigation associates whole-body insulin resistance with impaired beta-adrenergic response and reduced expression of genes that are critical regulators of glucose and lipid metabolism in skeletal muscle. We identify impaired beta-adrenergic signal transduction as a potential mechanism for impaired metabolic health after artificial selection for low intrinsic exercise capacity. (Endocrinology 150: 4883-4891, 2009)
C1 [Lessard, Sarah J.; Rivas, Donato A.; Hawley, John A.] Royal Melbourne Inst Technol, Sch Med Sci, Bundoora, Vic 3083, Australia.
[Chen, Zhi-Ping; van denderen, Bryce J.; Kemp, Bruce E.] Univ Melbourne, St Vincents Inst, Fitzroy, Vic 3065, Australia.
[Watt, Matthew J.] Monash Univ, Dept Physiol, Clayton, Vic 3800, Australia.
[Koch, Lauren G.; Britton, Steven L.] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Lessard, SJ (reprint author), Joslin Diabet Ctr, 1 Joslin Pl, Boston, MA 02215 USA.
EM sarah.lessard@joslin.harvard.edu
RI Koch, Lauren/D-1258-2010; Watt, Matthew/B-2089-2014; Kemp,
Bruce/L-2633-2014
OI Kemp, Bruce/0000-0001-6735-5082
FU National Center for Research Resources [R24 RR17718]; National
Institutes of Health; U.S. Public Health Service; Australian Research
Council
FX Disclosure Summary: The authors have nothing to disclose.
NR 56
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U1 0
U2 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD NOV
PY 2009
VL 150
IS 11
BP 4883
EP 4891
DI 10.1210/en.2009-0158
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 509ID
UT WOS:000271007700008
PM 19819977
ER
PT J
AU Stengel, A
Goebel, M
Wang, LX
Rivier, J
Kobelt, P
Monnikes, H
Lambrecht, NWG
Tache, Y
AF Stengel, Andreas
Goebel, Miriam
Wang, Lixin
Rivier, Jean
Kobelt, Peter
Moennikes, Hubert
Lambrecht, Nils W. G.
Tache, Yvette
TI Central Nesfatin-1 Reduces Dark-Phase Food Intake and Gastric Emptying
in Rats: Differential Role of Corticotropin-Releasing Factor(2) Receptor
SO ENDOCRINOLOGY
LA English
DT Article
ID CAUDAL BRAIN-STEM; BODY-WEIGHT; CRF; CHOLECYSTOKININ; NUCLEUS; NEURONS;
LEPTIN; IMMUNOREACTIVITY; HYPOTHALAMUS; INHIBITION
AB Nesfatin-1, derived from nucleobindin2, is expressed in the hypothalamus and reported in one study to reduce food intake (FI) in rats. To characterize the central anorexigenic action of nesfatin-1 and whether gastric emptying (GE) is altered, we injected nesfatin-1 into the lateral brain ventricle (intracerebroventricular, icv) or fourth ventricle (4v) in chronically cannulated rats or into the cisterna magna (intracisternal, ic) under short anesthesia and compared with ip injection. Nesfatin-1 (0.05 mu g/rat, icv) decreased 2-3 h and 3-6 h dark-phase FI by 87 and 45%, respectively, whereas ;ip administration (2 mu g/rat) had no effect. The corticotropin-releasing factor (CRF)(1)/CRF2 antagonist astressin-B or the CRF2 antagonist astressin(2)-B abolished icv nesfatin-1's anorexigenic action, whereas an astressin(2)-B analog, devoid of CRF-receptor binding affinity, did not. Nesfatin-1 icv induced a dose-dependent reduction of GE by 26 and 43% that was not modified by icv astressin(2)-B. Nesfatin-1 into the 4v (0.05 mu g/rat) or ic (0.5 mu g/rat) decreased cumulative dark-phase FI by 29 and 60% at 1 h and by 41 and 37% between 3 and 5 h, respectively. This effect was neither altered by ic astressin(2)-B nor associated with changes in GE. Cholecystokinin (ip) induced Fos expression in 43% of nesfatin-1 neurons in the paraventricular hypothalamic nucleus and 24% of those in the nucleus tractus solitarius. These data indicate that nesfatin-1 acts centrally to reduce dark phase FI through CRF2-receptor-dependent pathways after forebrain injection and CRF2-receptor-independent pathways after hindbrain injection. Activation of nesfatin-1 neurons by cholecystokinin at sites regulating food intake may suggest a role in gut peptide satiation effect. (Endocrinology 150: 4911-4919, 2009)
C1 [Stengel, Andreas; Goebel, Miriam; Wang, Lixin; Lambrecht, Nils W. G.; Tache, Yvette] Univ Calif Los Angeles, Vet Adm Greater Los Angeles Healthcare Syst, Dept Med, Ctr Neurobiol Stress,Digest Dis Div,CURE, Los Angeles, CA 90073 USA.
[Rivier, Jean] Salk Inst Biol Studies, Peptide Biol Labs, La Jolla, CA 92037 USA.
[Kobelt, Peter] Charite, Clin Psychosomat Med, D-10117 Berlin, Germany.
[Moennikes, Hubert] Martin Luther Hosp, Dept Med, D-14193 Berlin, Germany.
[Moennikes, Hubert] Martin Luther Hosp, Inst Neurogastroenterol, D-14193 Berlin, Germany.
RP Tache, Y (reprint author), Vet Adm Greater Los Angeles Healthcare Syst, Ctr Neurovisceral Sci & Womens Hlth CURE, Bldg 115,Room 117,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM ytache@mednet.ucla.edu
OI Lambrecht, Nils/0000-0002-1275-1384
FU German Research Foundation [STE 1765/1-1, GO1718/1-1]; Veterans
Administration Research Career Scientist Award; Veterans Administration
Merit Award [NIHDK 33061]; Center Grant [DK-41301]; [DK PO1-26741]
FX We thank Mrs. Honghui Liang for her excellent technical support, and we
thank Ms. Eugenia Hu for reviewing the manuscript.; Address all
correspondence and requests for reprints to: Yvette Tache, Ph.D., Center
for Neurovisceral Sciences and Women's Health CURE, Building 115, Room
117, Veterans Administration Greater Los Angeles Healthcare System,
11301 Wilshire Boulevard, Los Angeles, California 90073. E-mail:
ytache@mednet.ucla.edu.; This work was supported by German Research
Foundation Grants STE 1765/1-1 (A.S.), GO1718/1-1 (M.G.), Veterans
Administration Research Career Scientist Award, Veterans Administration
Merit Award, NIHDK 33061, Center Grant DK-41301 (Animal Core) (Y.T.),
and DK PO1-26741 (J.R.).; Disclosure Summary: A.S., M.G., L.W., P.K.,
H.M., N.W. G.L., and Y.T. have nothing to disclose. J.R. is Founder of
Sentia Medical Sciences, Inc. No conflicts of interest exist.
NR 49
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U1 0
U2 7
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD NOV
PY 2009
VL 150
IS 11
BP 4911
EP 4919
DI 10.1210/en.2009-0578
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 509ID
UT WOS:000271007700011
PM 19797401
ER
PT J
AU Mandal, CC
Choudhury, GG
Ghosh-Choudhury, N
AF Mandal, Chandi C.
Choudhury, Goutam Ghosh
Ghosh-Choudhury, Nandini
TI Phosphatidylinositol 3 Kinase/Akt Signal Relay Cooperates with Smad in
Bone Morphogenetic Protein-2-Induced Colony Stimulating Factor-1 (CSF-1)
Expression and Osteoclast Differentiation
SO ENDOCRINOLOGY
LA English
DT Article
ID TUMOR-SUPPRESSOR PTEN; INDUCED DNA-SYNTHESIS; TGF-BETA RECEPTOR; KAPPA-B
LIGAND; OSTEOBLAST DIFFERENTIATION; MESANGIAL CELLS; PROTEIN-KINASE;
C2C12 CELLS; BMP-2 GENE; C-FOS
AB Murine spleen cells produce mature osteoclasts when cocultured with osteoblastic cells. Colony-stimulating factor (CSF)-1 is the growth factor required for differentiating the monocyte-macrophage precursor cells into preosteoclasts. Bone morphogenic protein (BMP) signaling in osteoblasts regulates bone mass in mice, suggesting a role of BMP in osteoclastogenesis along with osteoblast activity. The intracellular signal transduction cross talk regulating the osteoblastic production of CSF-1 as a mechanism of BMP-induced osteoclastogenesis is described in this report. We have recently described the involvement of Smad 1/5 in BMP-2-induced CSF-1 expression and osteoclast formation. In this study, using the pharmacological inhibitors and the adenovirus (Ad) vectors expressing dominant-negative (DN) phosphatidylinositol 3 kinase (PI3K), the PI3K-signaling inhibitor, phosphatase and tensin homolog deleted in chromosome 10 (PTEN) or DN Akt kinase in the in vitro coculture assay, we show an essential role of the lipid kinase cascade in BMP-2-mediated multinucleated osteoclast formation and CSF-1 mRNA expression, transcription, and secretion. Inhibition of PI3K/Akt signaling blocked the binding of Smads 1/5 to the CSF-1 BMP-responsive element present in the CSF-1 promoter, resulting in attenuation of Smad-dependent CSF-1 transcription. Furthermore, PI3K inhibition and DN Akt prevented association of the transcriptional coactivator, CREB (cAMP response element binding protein) binding protein (CBP), with Smads 1/5. Together, these data for the first time demonstrate that PI3K-dependent Akt activation regulates BMP-2-induced CSF-1 expression and provides a mechanism for osteoblastic cell-assisted osteoclast differentiation. (Endocrinology 150: 4989-4998, 2009)
C1 [Mandal, Chandi C.; Ghosh-Choudhury, Nandini] Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, San Antonio, TX 78229 USA.
[Choudhury, Goutam Ghosh] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, San Antonio, TX 78229 USA.
[Choudhury, Goutam Ghosh; Ghosh-Choudhury, Nandini] S Texas Vet Hlth Care Syst, Dept Vet Affairs Res, San Antonio, TX USA.
[Choudhury, Goutam Ghosh] S Texas Vet Hlth Care Syst, Ctr Geriatr Res Educ & Clin, San Antonio, TX USA.
RP Ghosh-Choudhury, N (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM choudhury@uthscsa.edu
FU National Institutes of Health (NIH) [RO1AR52425, RO1 DK50190];
Department of Veterans Affairs (VA) Research Service Merit Review; VA
Merit Review; Juvenile Diabetes Research Foundation [1-2008-185]
FX Disclosure Summary: The authors have nothing to disclose.
NR 52
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Z9 28
U1 0
U2 3
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD NOV
PY 2009
VL 150
IS 11
BP 4989
EP 4998
DI 10.1210/en.2009-0026
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 509ID
UT WOS:000271007700019
PM 19819979
ER
PT J
AU Stengel, A
Keire, D
Goebel, M
Evilevitch, L
Wiggins, B
Tache, Y
Reeve, JR
AF Stengel, Andreas
Keire, David
Goebel, Miriam
Evilevitch, Lena
Wiggins, Brian
Tache, Yvette
Reeve, Joseph R., Jr.
TI The RAPID Method for Blood Processing Yields New Insight in Plasma
Concentrations and Molecular Forms of Circulating Gut Peptides
SO ENDOCRINOLOGY
LA English
DT Article
ID PANCREATIC-SECRETION; ENZYME-SECRETION; DESACYL GHRELIN; RATS;
CHOLECYSTOKININ; DEGRADATION; HORMONE; CCK-58; FOOD; STABILITY
AB The correct identification of circulating molecular forms and measurement of peptide levels in blood entails that the endocrine peptide being studied is stable and recovered in good yields during blood processing. However, it is not clear whether this is achieved in studies using standard blood processing. Therefore, we compared peptide concentration and form of 12 (125)I-labeled peptides using the standard procedure (EDTA-blood on ice) and a new method employing Reduced temperatures, Acidification, Protease inhibition, Isotopic exogenous controls, and Dilution (RAPID). During standard processing there was at least 80% loss for calcitonin-gene-related peptide and cholecystokinin-58 (CCK-58) and more than 35% loss for amylin, insulin, peptide YY forms (PYY((1-36)) and PYY((3-36))), and somatostatin-28. In contrast, the RAPID method significantly improved the recovery for 11 of 12 peptides (P < 0.05) and eliminated the breakdown of endocrine peptides occurring after standard processing as reflected in radically changed molecular forms for CCK-58, gastrin-releasing peptide, somatostatin-28, and ghrelin. For endogenous ghrelin, this led to an acyl/total ghrelin ratio of 1: 5 instead of 1: 19 by the standard method. These results show that the RAPID method enables accurate assessment of circulating gut peptide concentrations and forms such as CCK-58, acylated ghrelin, and somatostatin-28. Therefore, the RAPID method represents an efficacious means to detect circulating variations in peptide concentrations and form relevant to the understanding of physiological function of endocrine peptides. (Endocrinology 150: 5113-5118, 2009)
C1 Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Reeve, Joseph R., Jr.] Univ Calif Los Angeles, CURE Digest Dis Res Ctr, Los Angeles, CA 90073 USA.
RP Reeve, JR (reprint author), Univ Calif Los Angeles, CURE Digest Dis Res Ctr, Bldg 115,Room 117,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM JReeve@mednet.ucla.edu
FU German Research Foundation [STE 1765/1-1, GO 1718/1-1]; National
Institutes of Health Center [DK-41301, RO1 DK 33850, DK 56805]; Veterans
Administration Research Services
FX Disclosure Summary: The authors have nothing to disclose.
NR 30
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PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD NOV
PY 2009
VL 150
IS 11
BP 5113
EP 5118
DI 10.1210/en.2009-0697
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 509ID
UT WOS:000271007700032
PM 19819958
ER
PT J
AU Fassan, M
Castoro, C
Saenz, AJ
Cagol, M
Ninfo, V
Rugge, M
AF Fassan, M.
Castoro, C.
Saenz, A. J.
Cagol, M.
Ninfo, V.
Rugge, M.
TI Inflammatory myofibroblastic tumor as adverse outcome of eosinophilic
esophagitis
SO ENDOSCOPY
LA English
DT Editorial Material
C1 [Rugge, M.] Univ Padua, Cattedra Anat Patol 2, Dept Med Diagnost Sci & Special Therapies, Pathol Unit,Ist Oncol Veneto IRCCS, I-35121 Padua, Italy.
[Castoro, C.] IOV IRCCS, Surg Unit, Padua, Italy.
[Cagol, M.] Univ Padua, Dept Med & Surg Sci, Surg Unit, I-35121 Padua, Italy.
[Saenz, A. J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, James Homer Wright Pathol Labs, Boston, MA USA.
RP Rugge, M (reprint author), Univ Padua, Cattedra Anat Patol 2, Dept Med Diagnost Sci & Special Therapies, Pathol Unit,Ist Oncol Veneto IRCCS, Via Aristide Gabelli 61, I-35121 Padua, Italy.
EM massimo.rugge@unipd.it
RI Fassan, Matteo/F-5152-2012; Rugge, Massimo/K-7525-2016; Castoro,
Carlo/L-1046-2016
OI Fassan, Matteo/0000-0001-6515-5482; Castoro, Carlo/0000-0001-9601-9336
NR 5
TC 1
Z9 1
U1 0
U2 0
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0013-726X
J9 ENDOSCOPY
JI Endoscopy
PD NOV
PY 2009
VL 41
SU 2
BP E95
EP E96
DI 10.1055/s-2008-1077646
PG 2
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA V15DW
UT WOS:000207783700059
PM 19396747
ER
PT J
AU Hartnick, CJ
Zurakowski, D
Haver, K
AF Hartnick, Christopher J.
Zurakowski, David
Haver, Kenan
TI Validation of a pediatric cough questionnaire
SO ENT-EAR NOSE & THROAT JOURNAL
LA English
DT Article
ID QUALITY-OF-LIFE; PERSISTENT COUGH; CHILDREN; FREQUENCY; SPECTRUM;
THERAPY; SYMPTOM
AB We conducted a study to determine if a five-item pediatric cough questionnaire (PCQ) is a valid and reliable means of measuring cough-specific quality of life in children. The five questions, which are answered by the child's parent or caregiver, cover cough frequency (Q1), sleep disturbance of the child (Q2), sleep disturbance of the parent (Q3), cough severity (Q4), and the degree of bothersomeness to the child (Q5). Each of the five items was scored on a 6-point Likert scale. The PCQ was administered three times. The first occurred when the parent telephoned to schedule an appointment for the child at a pediatric pulmonology outpatient clinic for a chief complaint of cough. The second PCQ was administered within 2 weeks of the first but before any treatment had been instituted so that test-retest reliability could be assessed. Each child was then diagnosed and treated in accordance with standard care practices. The third PCQ was administered 3 weeks after the second to determine if it would accurately reflect the parent's perception of how the child's cough had changed following treatment. Also, at the second and third encounters, parents were asked to provide their global assessment of whether their child's cough had improved, worsened, or stayed the same since the previous encounter. The parents of 120 children (70 boys and 50 girls; mean age: 6.8 yr) completed all three PCQs. Test-retest reliability was established (p < 0.001) for each of the five PCQ questions by Spearman correlation analysis (Q1: r = 0.5; Q2: r = 0.38; Q3: r = 0.42; Q4: r = 0.53; Q5: r = 0.5). Other statistical analyses confirmed the PCQ's internal consistency, discriminant validity, and convergent validity. Based on our findings, we conclude that the PCQ is a valid and reliable instrument with which to follow children with chronic cough longitudinally.
C1 [Hartnick, Christopher J.] Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA.
[Zurakowski, David] Childrens Hosp, Dept Orthoped Surg, Boston, MA 02115 USA.
[Haver, Kenan] Massachusetts Gen Hosp Children, Div Pediat Pulm Med, Boston, MA USA.
RP Hartnick, CJ (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, 243 Charles St, Boston, MA 02114 USA.
EM Christopher_hartnick@meei.harvard.edu
NR 23
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U1 0
U2 0
PU VENDOME GROUP LLC
PI NEW YORK
PA 149 FIFTH AVE, 10TH FLOOR, NEW YORK, NY 10010 USA
SN 0145-5613
J9 ENT-EAR NOSE THROAT
JI ENT-Ear Nose Throat J.
PD NOV
PY 2009
VL 88
IS 11
BP 1213
EP 1217
PG 5
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 551JY
UT WOS:000274205400008
PM 19924664
ER
PT J
AU Hart, JE
Yanosky, JD
Puett, RC
Ryan, L
Dockery, DW
Smith, TJ
Garshick, E
Laden, F
AF Hart, Jaime E.
Yanosky, Jeff D.
Puett, Robin C.
Ryan, Louise
Dockery, Douglas W.
Smith, Thomas J.
Garshick, Eric
Laden, Francine
TI Spatial Modeling of PM10 and NO2 in the Continental United States,
1985-2000
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE GIS; nitrogen dioxide; outdoor air pollution; particulate matter
ID PARTICULATE AIR-POLLUTION; LAND-USE REGRESSION; LONG-TERM EXPOSURE;
RESPIRATORY SYMPTOMS; TRAFFIC EXPOSURE; TRUCKING INDUSTRY; LUNG-CANCER;
MORTALITY; COHORT; ADULTS
AB BACKGROUND: Epidemiologic studies of air pollution have demonstrated a link between long-term air pollution exposures and mortality. However, many have been limited to city-specific average pollution measures or spatial or land-use regression exposure models in small geographic areas.
OBJECTIVES: Our objective was to develop nationwide models of annual exposure to particulate matter < 10 mu m in diameter (PM10) and nitrogen dioxide during 1985-2000.
METHODS: We used generalized additive models (GAMS) to predict annual levels of the pollutants using smooth spatial surfaces of available monitoring data and geographic information system-derived covariates. Model performance was determined using a cross-validation (CV) procedure with 10% of the data. We also compared the results of these models with a commonly used spatial interpolation, inverse distance weighting.
RESULTS: For PM10, distance to road, elevation, proportion of low-intensity residential, high-intensity residential, and industrial, commercial, or transportation land use within 1 km were all statistically significant predictors of measured PM10 (model R-2 = 0.49, CV R-2 = 0.55). Distance to road, population density, elevation, land use, and distance to and emissions of the nearest nitrogen oxides-emitting power plant were all statistically significant predictors of measured NO2 (model R-2 = 0.88, CV R-2 = 0.90). The GAMS performed better overall than the inverse distance models, with higher CV R-2 and higher precision.
CONCLUSIONS: These models provide reasonably accurate and unbiased estimates of annual exposures for PM10 and NO2. This approach provides the spatial and temporal variability necessary to describe exposure in studies assessing the health effects of chronic air pollution.
C1 [Hart, Jaime E.; Yanosky, Jeff D.; Puett, Robin C.; Dockery, Douglas W.; Smith, Thomas J.; Laden, Francine] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Exposure Epidemiol & Risk Program, Boston, MA 02115 USA.
[Hart, Jaime E.; Garshick, Eric; Laden, Francine] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Hart, Jaime E.; Garshick, Eric; Laden, Francine] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Hart, Jaime E.; Dockery, Douglas W.; Laden, Francine] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Puett, Robin C.] Univ S Carolina, S Carolina Canc Prevent & Control Program, Columbia, SC 29208 USA.
[Puett, Robin C.] Univ S Carolina, Arnold Sch Publ Hlth, Dept Environm Hlth Sci, Columbia, SC 29208 USA.
[Puett, Robin C.] Univ S Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, Columbia, SC 29208 USA.
[Ryan, Louise] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Garshick, Eric] VA Boston Healthcare Syst, Med Serv, Pulm & Crit Care Med Sect, Boston, MA USA.
RP Hart, JE (reprint author), 181 Longwood Ave, Boston, MA 02115 USA.
EM Jaime.hart@channing.harvard.edu
RI Smith, Thomas/A-9640-2010; Ryan, Louise/A-4562-2009
OI Ryan, Louise/0000-0001-5957-2490
FU National Institutes of Health/National Cancer Institute [R01 CA90792];
National Institute of Environmental Health Sciences (NIEHS) Center
[ES00002]; NIEHS [T32 ES007069-29]
FX This study was supported by grant R01 CA90792 from the National
Institutes of Health/National Cancer Institute, National Institute of
Environmental Health Sciences (NIEHS) Center grant ES00002, and NIEHS
T32 ES007069-29 (J.E.H.).
NR 57
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U1 1
U2 24
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD NOV
PY 2009
VL 117
IS 11
BP 1690
EP 1696
DI 10.1289/ehp.0900840
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 514MQ
UT WOS:000271399300023
PM 20049118
ER
PT J
AU Myrskyla, M
Chang, VW
AF Myrskylae, Mikko
Chang, Virginia W.
TI Weight Change, Initial BMI, and Mortality Among Middle- and Older-aged
Adults
SO EPIDEMIOLOGY
LA English
DT Article
ID BODY-MASS INDEX; LONG-TERM MORTALITY; ALL-CAUSE MORTALITY; US ADULTS;
PROSPECTIVE COHORT; ELDERLY-MEN; LOSE WEIGHT; FOLLOW-UP; OVERWEIGHT;
OBESITY
AB Background: It is not known how the relationship between weight change and mortality is influenced by initial body mass index (BMI) or the magnitude of weight change.
Methods: We use the nationally representative Health and Retirement Study (n = 13,104; follow-up 1992-2006) and Cox regression analysis to estimate relative mortality risks for 2-year weight change by initial BMI among 50- to-70-year-old Americans. We defined small weight loss or gain as a change of 1-2.9 BMI units and large weight loss or gain as a change of 3-5 BMI units.
Results: Large and small weight losses were associated with excess mortality for all initial BMI levels below 32 kg/m(2) (eg, hazard ratio [HR] for large weight loss from BMI of 30 = 1.61 [95% confidence interval = 1.31-1.98]; HR for small : weight loss from BMI of 30 = 1.19 [1.06-1.28]). Large weight gains were associated with excess mortality only at high BMIs (eg, HR for large weight gain from BMI of 35 = 1.33 (1.00-1.77]). Small weight gains were not associated with excess mortality for any initial BMI level. The weight loss-mortality association was robust to adjustments for health status and to sensitivity analyses considering unobserved confounders.
Conclusions: Weight loss is associated with excess mortality among normal, overweight, and mildly obese middle- and older-aged adults. The excess risk increases for larger losses and lower initial BMI. These results suggest that the potential benefits of a lower BMI may be offset by the negative effects associated with weight loss. Weight gain may be associated with excess mortality only among obese people with an initial BMI over 35.
C1 [Myrskylae, Mikko] Max Planck Inst Demog Res, D-18057 Rostock, Germany.
[Chang, Virginia W.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
[Chang, Virginia W.] Univ Penn, Sch Med, Dept Med, Philadelphia, PA 19104 USA.
[Chang, Virginia W.] Univ Penn, Dept Sociol, Philadelphia, PA 19104 USA.
[Chang, Virginia W.] Univ Penn, Ctr Populat Studies, Philadelphia, PA 19104 USA.
RP Myrskyla, M (reprint author), Max Planck Inst Demog Res, Konrad Zuse Str 1, D-18057 Rostock, Germany.
EM myrskyla@demogr.mpg.de
FU National Institute of Child Health and Human Development [K12-HD043459]
FX Supported by National Institute of Child Health and Human Development,
K12-HD043459 (to VW.C.).
NR 40
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U1 1
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD NOV
PY 2009
VL 20
IS 6
BP 840
EP 848
DI 10.1097/EDE.0b013e3181b5f520
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 507SD
UT WOS:000270874000010
PM 19806061
ER
PT J
AU Bind, MA
Zanobetti, A
Schwartz, J
Suh, H
Vokonas, P
AF Bind, Marie-Abele
Zanobetti, Antonella
Schwartz, Joel
Suh, Helen
Vokonas, Pantel
TI Traffic-Related Pollutants and Inflammatory Markers in an Elderly
Cohort: Veterans Administration Normative Aging Study
SO EPIDEMIOLOGY
LA English
DT Meeting Abstract
CT 21st Annual Conference of the
International-Society-for-Environmental-Epidemiology
CY AUG 25-29, 2009
CL Dublin, IRELAND
C1 [Bind, Marie-Abele; Zanobetti, Antonella; Schwartz, Joel; Suh, Helen] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Harvard Exposure Epidemiol & Risk Program, Boston, MA 02115 USA.
[Vokonas, Pantel] VA Boston Healthcare Syst, VA Normat Aging Study, Boston, MA USA.
[Vokonas, Pantel] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD NOV
PY 2009
VL 20
IS 6
SU S
BP S144
EP S145
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 507SE
UT WOS:000270874101078
ER
PT J
AU Hart, J
Laden, F
Garshick, E
AF Hart, Jaime
Laden, Francine
Garshick, Eric
TI Biomakers of Inflammation and Short-Term Fine Particulate Exposures
SO EPIDEMIOLOGY
LA English
DT Meeting Abstract
CT 21st Annual Conference of the
International-Society-for-Environmental-Epidemiology
CY AUG 25-29, 2009
CL Dublin, IRELAND
C1 [Hart, Jaime; Laden, Francine; Garshick, Eric] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Hart, Jaime; Laden, Francine] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Hart, Jaime; Laden, Francine] Harvard Univ, Sch Med, Boston, MA USA.
[Garshick, Eric] VA Boston Healthcare Syst, Med Serv, Pulm & Crit Care Med Sect, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD NOV
PY 2009
VL 20
IS 6
SU S
BP S131
EP S132
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 507SE
UT WOS:000270874101035
ER
PT J
AU Hoffmann, B
Luttmann-Gibson, H
Cohen, A
Suh, H
Coull, B
Schwartz, J
Hamdy, O
Foley, C
Stone, P
Horton, E
Gold, D
AF Hoffmann, Barbara
Luttmann-Gibson, Heike
Cohen, Allison
Suh, Helen
Coull, Brent
Schwartz, Joel
Hamdy, Osama
Foley, Chris
Stone, Peter
Horton, Edward
Gold, Diane
TI Short-Term Fine Particulate Matter Air Pollution and Vascular Reactivity
in Diabetic Patients
SO EPIDEMIOLOGY
LA English
DT Meeting Abstract
CT 21st Annual Conference of the
International-Society-for-Environmental-Epidemiology
CY AUG 25-29, 2009
CL Dublin, IRELAND
C1 [Hoffmann, Barbara; Suh, Helen; Coull, Brent; Schwartz, Joel; Foley, Chris; Gold, Diane] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Hoffmann, Barbara; Luttmann-Gibson, Heike] Univ Duisburg Essen, Essen, Germany.
[Cohen, Allison; Hamdy, Osama; Horton, Edward] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Stone, Peter] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Gold, Diane] Harvard Univ, Sch Med, Channing Lab, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD NOV
PY 2009
VL 20
IS 6
SU S
BP S70
EP S71
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 507SE
UT WOS:000270874100180
ER
PT J
AU Luttmann-Gibson, H
Hoffmann, B
Cohen, A
Coull, B
de Souza, C
Horton, E
Schwartz, J
Suh, H
Gold, D
AF Luttmann-Gibson, Heike
Hoffmann, Barbara
Cohen, Allison
Coull, Brent
de Souza, Celine
Horton, Edward
Schwartz, Joel
Suh, Helen
Gold, Diane
TI Short-Term Effects of Air Pollution on Exhaled Nitric Oxide in Diabetic
Patients
SO EPIDEMIOLOGY
LA English
DT Meeting Abstract
CT 21st Annual Conference of the
International-Society-for-Environmental-Epidemiology
CY AUG 25-29, 2009
CL Dublin, IRELAND
C1 [Luttmann-Gibson, Heike; Hoffmann, Barbara; de Souza, Celine; Schwartz, Joel; Suh, Helen; Gold, Diane] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Hoffmann, Barbara] Univ Duisburg Essen, Inst Med Informat Biometry & Epidemiol, Essen, Germany.
[Cohen, Allison; Horton, Edward] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Coull, Brent] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Gold, Diane] Harvard Univ, Sch Med, Channing Lab, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD NOV
PY 2009
VL 20
IS 6
SU S
BP S144
EP S144
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 507SE
UT WOS:000270874101077
ER
PT J
AU Park, SK
Schwartz, J
Wright, R
Spiro, A
Vokonas, P
Hu, H
AF Park, Sung Kyun
Schwartz, Joel
Wright, Robert
Spiro, Avron, III
Vokonas, Pantel
Hu, Howard
TI Atherosclerosis-Related Genes, Low-Level Lead Exposure and Age-Related
Hearing Loss: The Normative Aging Study
SO EPIDEMIOLOGY
LA English
DT Meeting Abstract
CT 21st Annual Conference of the
International-Society-for-Environmental-Epidemiology
CY AUG 25-29, 2009
CL Dublin, IRELAND
C1 [Park, Sung Kyun; Hu, Howard] Univ Michigan, Sch Publ Hlth, Dept Environm Hlth Sci, Ann Arbor, MI 48109 USA.
[Schwartz, Joel; Wright, Robert] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Spiro, Avron, III; Vokonas, Pantel] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Spiro, Avron, III; Vokonas, Pantel] VA Boston Healthcare Syst, VA Normat Aging Study, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1044-3983
J9 EPIDEMIOLOGY
JI Epidemiology
PD NOV
PY 2009
VL 20
IS 6
SU S
BP S211
EP S211
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 507SE
UT WOS:000270874101291
ER
PT J
AU Maheshwari, A
Cash, S
AF Maheshwari, Atul
Cash, S.
TI THE BURST SUPPRESSION PATTERN OF SECONDARY GENERALIZED SEIZURES
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Maheshwari, Atul; Cash, S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 25
EP 25
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500046
ER
PT J
AU Frost, JD
Lee, CL
Hrachovy, RA
Swann, JW
AF Frost, James D.
Lee, C. L.
Hrachovy, R. A.
Swann, J. W.
TI HIGH FREQUENCY EEG ACTIVITY ASSOCIATED WITH ICTAL EVENTS IN THE TTX
MODEL OF INFANTILE SPASMS
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Lee, C. L.; Swann, J. W.] Baylor Coll Med, Cain Fdn Labs, Houston, TX 77030 USA.
[Hrachovy, R. A.] Michael E DeBakey Vet Affairs Med Ctr, Houston, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 28
EP 29
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500052
ER
PT J
AU Kinirons, P
Cash, S
Cole, A
AF Kinirons, Peter
Cash, S.
Cole, A.
TI RISK FACTORS FOR DRUG-RESISTANT IGE - A CLINICAL AND
ELECTROPHYSIOLOGICAL STUDY
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Kinirons, Peter; Cash, S.; Cole, A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 62
EP 63
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500128
ER
PT J
AU Valle, AC
Rodrigues, NE
Lima, MC
Chamma, MT
Jorge, MS
Neto, AR
Silva, DF
Fregni, F
AF Valle, A. C.
Rodrigues, N. E.
Lima, Moises C.
Chamma, M. T.
Jorge, M. S.
Neto, A. R.
Silva, D. F.
Fregni, F.
TI IDIOPATHIC GENERALIZED EPILEPSY IN ADULT CHARACTERIZED BY TYPICAL
ABSENCE SEIZURES VIDEO-EEG STUDIES
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Valle, A. C.; Rodrigues, N. E.; Lima, Moises C.; Chamma, M. T.] FMUSP, Sao Paulo, Brazil.
[Rodrigues, N. E.; Jorge, M. S.; Neto, A. R.; Silva, D. F.] Beneficencia Portuguesa, Sao Paulo, Brazil.
[Fregni, F.] BIDMC, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 67
EP 67
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500139
ER
PT J
AU Pugh, MJV
Copeland, LA
VanCott, AC
Mortensen, E
Zeber, J
Wang, C
Cramer, JA
AF Pugh, Mary Jo V.
Copeland, L. A.
VanCott, A. C.
Mortensen, E.
Zeber, J.
Wang, C.
Cramer, J. A.
TI SUICIDALITY AND NEW AED EXPOSURE IN OLDER PATIENTS: IS THE FDA WARNING
APPROPRIATE FOR ALL DRUGS IN ALL POPULATIONS?
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Pugh, Mary Jo V.; Copeland, L. A.; Mortensen, E.; Zeber, J.; Wang, C.] S Texas Vet Hlth Care Syst, VERDICT11C6, San Antonio, TX USA.
[VanCott, A. C.] Pittsburgh VA Hlth Care Syst, Pittsburgh, PA USA.
[Cramer, J. A.] Yale Univ, Sch Med, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 109
EP 109
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500222
ER
PT J
AU Van Cott, AC
Pugh, MJV
AF Van Cott, A. C.
Pugh, Mary Jo V.
TI TRENDS IN ANTIEPILEPTIC DRUG PRESCRIBING FOR OLDER PATIENTS WITH
NEW-ONSET EPILEPSY: 2004-2006
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Pugh, Mary Jo V.] S Texas Vet Hlth Care Syst, VERDICT 11C6, San Antonio, TX USA.
[Van Cott, A. C.] VA Pittsburgh Hlth Care Syst, Pittsburgh, PA USA.
[Van Cott, A. C.] Univ Pittsburgh, Pittsburgh, PA USA.
[Pugh, Mary Jo V.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 112
EP 112
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500227
ER
PT J
AU Pouliot, WA
Staley, KJ
Dudek, FE
AF Pouliot, Wendy A.
Staley, K. J.
Dudek, F. E.
TI THE EFFECTS OF THE CANNABINOID-RECEPTOR ANTAGONIST, SR141716A, ON THE
DEVELOPMENT OF SPONTANEOUS RECURRENT SEIZURES AFTER KAINATE-INDUCED
STATUS EPILEPTICUS
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Pouliot, Wendy A.; Dudek, F. E.] Univ Utah, Salt Lake City, UT USA.
[Staley, K. J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 119
EP 119
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500242
ER
PT J
AU Chu-Shore, C
Gallagher, A
Costello, D
Montenegro, M
Major, P
Thiele, EA
AF Chu-Shore, Catherine
Gallagher, A.
Costello, D.
Montenegro, M.
Major, P.
Thiele, E. A.
TI CO-REGISTRATION OF CYST-LIKE TUBERS AND EPILEPTIFORM ACTIVITY IN
TUBEROUS SCLEROSIS COMPLEX
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 168
EP 168
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500352
ER
PT J
AU Salinsky, MC
AF Salinsky, Martin C.
TI PSYCHOGENIC NON-EPILEPTIC SEIZURES AT A VETERANS ADMINISTRATION MEDICAL
CENTER
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Salinsky, Martin C.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Salinsky, Martin C.] Portland VA Med Ctr, Portland, OR USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 195
EP 195
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500413
ER
PT J
AU Gonzalez-Heydrich, J
Luna, LM
Rao, S
McClendon, J
Rotella, P
Waber, D
Boyer, K
Whitney, J
Faraone, SV
Guild, D
Hamoda, H
Biederman, J
AF Gonzalez-Heydrich, Joseph
Luna, L. M.
Rao, S.
McClendon, J.
Rotella, P.
Waber, D.
Boyer, K.
Whitney, J.
Faraone, S. V.
Guild, D.
Hamoda, H.
Biederman, J.
TI ELEVATED ADHD RATES IN MOTHERS OF CHILDREN WITH COMORBID ADHD AND
EPILEPSY
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Gonzalez-Heydrich, Joseph; Luna, L. M.; Rao, S.; McClendon, J.; Rotella, P.; Waber, D.; Boyer, K.; Whitney, J.; Guild, D.; Hamoda, H.] Harvard Univ, Sch Med, Dept Psychiat, Childrens Hosp, Boston, MA 02115 USA.
[Biederman, J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Psychopharmacol Unit, Boston, MA USA.
[Faraone, S. V.] SUNY Upstate Med Univ, Syracuse, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 236
EP 236
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500506
ER
PT J
AU Paolini, J
Chu-Shore, C
Macdonald, C
Bruno, P
Thibert, R
Thiele, E
AF Paolini, Jan
Chu-Shore, C.
Macdonald, C.
Bruno, P.
Thibert, R.
Thiele, E.
TI ADVERSE EVENTS ASSOCIATED WITH ANTICONVULSANT DRUG FORMULATION
SUBSTITUTION IN PEDIATRIC AND ADULT EPILEPSY PATIENTS
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Paolini, Jan; Chu-Shore, C.; Macdonald, C.; Bruno, P.; Thibert, R.; Thiele, E.] Mass Gen Hosp, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 259
EP 260
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500560
ER
PT J
AU Leeman, BA
Macklin, EA
Schomer, DL
O'Connor, MG
AF Leeman, Beth A.
Macklin, E. A.
Schomer, D. L.
O'Connor, M. G.
TI TRANSIENT NEWS EVENTS TEST: FEASIBILITY IN ASSESSMENT OF POST-TEMPORAL
LOBECTOMY REMOTE MEMORY DEFICITS
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Leeman, Beth A.; Schomer, D. L.; O'Connor, M. G.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Macklin, E. A.] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
[Leeman, Beth A.; Macklin, E. A.; Schomer, D. L.; O'Connor, M. G.] Harvard Univ, Sch Med, Boston, MA USA.
RI Macklin, Eric/E-2955-2013
OI Macklin, Eric/0000-0003-1618-3502
NR 1
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 266
EP 267
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500575
ER
PT J
AU Van Cott, AC
Pramuka, M
AF Van Cott, Anne C.
Pramuka, M.
TI SURVEY OF INTERNET AND COMPUTER USE IN VETERANS WITH EPILEPSY
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Van Cott, Anne C.] VA Pittsburgh Healthcare Syst, Div Neurol, Pittsburgh, PA USA.
[Van Cott, Anne C.; Pramuka, M.] Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 274
EP 275
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500590
ER
PT J
AU Staley, KJ
Coulter, D
Cossart, R
White, J
AF Staley, Kevin J.
Coulter, Douglas
Cossart, Rosa
White, John
TI IMAGING SYNCHRONY WITH ACTIVITY-DEPENDENT DYES: THE NUTS AND BOLTS
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Staley, Kevin J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Staley, Kevin J.] Harvard Univ, Sch Med, Boston, MA USA.
[Coulter, Douglas] Univ Penn, Philadelphia, PA 19104 USA.
[White, John] Univ Utah, Salt Lake City, UT USA.
[Cossart, Rosa] INSERM, U29, Luminy, France.
RI Cossart, Rosa/E-7674-2014
OI Cossart, Rosa/0000-0003-2111-6638
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 310
EP 310
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500677
ER
PT J
AU Dyhrfjeld-Johnsen, J
Swiercz, W
Sabolek, H
Berdichevsky, Y
Staley, K
AF Dyhrfjeld-Johnsen, Jonas
Swiercz, W.
Sabolek, H.
Berdichevsky, Y.
Staley, K.
TI INTERICTAL SPIKES APPEAR DURING THE LATENT PERIOD IN A MODEL OF
EPILEPTOGENESIS BASED ON ORGANOTYPIC HIPPOCAMPAL SLICE CULTURES
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Berdichevsky, Y.] Massachusetts Gen Hosp, Ctr Engn Med, Charlestown, MA USA.
[Dyhrfjeld-Johnsen, Jonas; Swiercz, W.; Sabolek, H.; Berdichevsky, Y.; Staley, K.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 348
EP 348
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500771
ER
PT J
AU Berdichevsky, Y
Swiercz, W
Yarmush, ML
Staley, KJ
AF Berdichevsky, Yevgeny
Swiercz, W.
Yarmush, M. L.
Staley, K. J.
TI PARTIAL VOLTAGE-GATED SODIUM CHANNEL INACTIVATION RESULTS IN SEIZURES IN
ORGANOTYPIC CULTURE MODEL OF EPILEPSY
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Berdichevsky, Yevgeny; Yarmush, M. L.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Swiercz, W.; Staley, K. J.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Berdichevsky, Yevgeny; Swiercz, W.; Yarmush, M. L.; Staley, K. J.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 356
EP 356
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500792
ER
PT J
AU Thibert, RL
Thiele, E
AF Thibert, Ronald L.
Thiele, E.
TI SEIZURES IN INDIVIDUALS WITH CHROMOSOME 15Q DUPLICATIONS
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Thibert, Ronald L.; Thiele, E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 400
EP 401
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500898
ER
PT J
AU Bruno, PL
Venna, P
Hirshberg, J
Paolini, J
Thibert, R
Thiele, E
AF Bruno, Patricia L.
Venna, P.
Hirshberg, J.
Paolini, J.
Thibert, R.
Thiele, E.
TI CLINICAL EXPERIENCE WITH RUFINAMIDE (BANZEL) IN PATIENTS WITH
INTRACTABLE EPILEPSY
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Bruno, Patricia L.; Venna, P.; Hirshberg, J.; Paolini, J.; Thibert, R.; Thiele, E.] Massachusetts Gen Hosp, Pediat Epilepsy Program, Boston, MA 02114 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 424
EP 424
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500949
ER
PT J
AU Camposano, SE
Dabora, S
Paolini, J
Thiele, EA
AF Camposano, S. E.
Dabora, S.
Paolini, J.
Thiele, E. A.
TI SIROLIMUS TREATMENT AND ITS EFFECT ON SEIZURES IN TSC: A CASE SERIES
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Camposano, S. E.; Paolini, J.; Thiele, E. A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Dabora, S.] Brigham & Womens Hosp, Translat Med Div, Boston, MA 02115 USA.
[Dabora, S.] Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 424
EP 424
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500950
ER
PT J
AU Kilbride, R
Costello, D
AF Kilbride, Ronan
Costello, D.
TI PREDICTORS OF SURVIVAL IN PROLONGED REFRACTORY STATUS EPILEPTICUS (PRSE)
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Kilbride, Ronan; Costello, D.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 426
EP 426
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500956
ER
PT J
AU Gallagher, A
Chu-Shore, CJ
Roche-Labarbe, N
Surova, A
Franceschini, MA
Thibert, RL
Cash, SS
Thiele, EA
Grant, PE
AF Gallagher, Anne
Chu-Shore, C. J.
Roche-Labarbe, N.
Surova, A.
Franceschini, M. A.
Thibert, R. L.
Cash, S. S.
Thiele, E. A.
Grant, P. E.
TI PRE AND POST-ANTICONVULSIVE TREATMENT CHANGES IN INTERICTAL CEREBRAL
OXYGENATION AND NEURONAL ACTIVITY IN INFANTS WITH INFANTILE SPASMS
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Gallagher, Anne; Chu-Shore, C. J.; Thibert, R. L.; Cash, S. S.; Thiele, E. A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Gallagher, Anne; Chu-Shore, C. J.; Roche-Labarbe, N.; Franceschini, M. A.; Thibert, R. L.; Cash, S. S.; Thiele, E. A.; Grant, P. E.] Harvard Univ, Sch Med, Boston, MA USA.
[Roche-Labarbe, N.; Surova, A.; Franceschini, M. A.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr, Charlestown, MA USA.
[Grant, P. E.] Childrens Hosp Boston, Fetal Neonatal Neuroimaging & Dev Sci Ctr, Boston, MA USA.
RI Roche-Labarbe, Nadege/N-9101-2015
OI Roche-Labarbe, Nadege/0000-0002-5010-0400
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 435
EP 435
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550500975
ER
PT J
AU Nakagawa, JA
Whittemore, VH
Cinkosky, M
Sparagana, S
Thiele, E
Brown, C
Frost, M
McClintock, W
Bebin, EM
Kohrman, M
Northrup, H
Wu, JY
Levisohn, P
Koh, S
Gupta, A
Ashwal, S
Duchowny, M
Miller, IO
LaJoie, J
Jansen, A
AF Nakagawa, Jo Anne
Whittemore, V. H.
Cinkosky, M.
Sparagana, S.
Thiele, E.
Brown, C.
Frost, M.
McClintock, W.
Bebin, E. M.
Kohrman, M.
Northrup, H.
Wu, J. Y.
Levisohn, P.
Koh, S.
Gupta, A.
Ashwal, S.
Duchowny, M.
Miller, I. O.
LaJoie, J.
Jansen, A.
TI THE TUBEROUS SCLEROSIS COMPLEX NATURAL HISTORY DATABASE PROJECT
SO EPILEPSIA
LA English
DT Meeting Abstract
CT 63rd Annual Meeting of the American-Epilepsy-Society
CY DEC 04-08, 2009
CL Boston, MA
SP Amer Epilepsy Soc
C1 [Nakagawa, Jo Anne; Whittemore, V. H.] Tuberous Sclerosis Alliance, Silver Spring, MD USA.
[Cinkosky, M.] Tesuji Inc, Denver, CO USA.
[Sparagana, S.] Texas Scottish Rite Hosp Children, Dallas, TX USA.
[Thiele, E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Brown, C.] Childrens Hosp Oakland, Oakland, CA USA.
[Frost, M.] Minnesota Epilepsy Grp PA, St Paul, MN USA.
[McClintock, W.] Childrens Natl Med Ctr, Fairfax, VA USA.
[Bebin, E. M.] Univ Alabama, Birmingham, AL USA.
[Kohrman, M.] Univ Chicago, Chicago, IL 60637 USA.
[Northrup, H.] Univ Texas Hlth Sci Ctr, Houston, TX USA.
[Wu, J. Y.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Levisohn, P.; Koh, S.] Univ Colorado, Denver, CO 80202 USA.
[Gupta, A.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Ashwal, S.] Loma Linda Univ, Med Ctr, Loma Linda, CA USA.
[Duchowny, M.; Miller, I. O.] Miami Childrens Hosp, New York, NY USA.
[LaJoie, J.] NYU, New York, NY USA.
[Jansen, A.] UZ Brussel Hosp, Brussels, Belgium.
RI Jansen, Anna/P-3121-2014
OI Jansen, Anna/0000-0002-3835-2824
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
BP 457
EP 458
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 503PP
UT WOS:000270550501027
ER
PT J
AU Thibert, RL
Conant, KD
Braun, EK
Bruno, P
Said, RR
Nespeca, MP
Thiele, EA
AF Thibert, Ronald L.
Conant, Kerry D.
Braun, Eileen K.
Bruno, Patricia
Said, Rana R.
Nespeca, Mark P.
Thiele, Elizabeth A.
TI Epilepsy in Angelman syndrome: A questionnaire-based assessment of the
natural history and current treatment options
SO EPILEPSIA
LA English
DT Article
DE Epilepsy; Angelman syndrome; Chromosome 15; Antiepileptic medications
ID EEG PATTERNS; DELETION; PHENOTYPES; DIAGNOSIS; EVOLUTION; 15Q11-13;
CRITERIA; CHILDREN; THERAPY
AB Purpose: Angelman syndrome (AS) commonly presents with epilepsy (>80%). The goal of this study was to examine the natural history and various treatments of epilepsy in AS in a large population.
Methods: A detailed electronic survey containing comprehensive questions regarding epilepsy in AS was conducted through the Angelman Syndrome Foundation.
Results: There were responses from 461 family members of individuals with AS, of whom 86% had epilepsy (60% with multiple seizure types), the most common being atonic, generalized tonic-clonic, absence, and complex partial. Partial-onset seizures only were reported in 11% of those with epilepsy. Epilepsy was most common among those with maternal deletions and unknown subtypes, with catastrophic epilepsies present in only these two subtypes. These epilepsies were refractory to medication, with only 15% responding to the first antiepileptic drug (AED). The most commonly prescribed AED were valproic acid and clonazepam, but lamotrigine and levetiracetam appeared to have similar efficacy and tolerability.
Discussion: This is the largest study to date assessing epilepsy in AS. Although epilepsy in AS is considered a generalized epilepsy, there was a high prevalence of partial seizures. There are few previous data regarding the use of newer AED in AS, and the results of this study suggest that these newer agents, specifically levetiracetam and lamotrigine, may have efficacy similar to that of valproic acid and clonazepam, and that they appear to have similar or better side-effect profiles. Non-pharmacologic therapies such as dietary therapy and vagus nerve stimulation (VNS) also suggest favorable efficacy and tolerability, although further studies are needed.
C1 [Thibert, Ronald L.; Conant, Kerry D.; Bruno, Patricia; Thiele, Elizabeth A.] Massachusetts Gen Hosp, Pediat Epilepsy Program, Dept Neurol, Boston, MA 02114 USA.
[Braun, Eileen K.] Angelman Syndrome Fdn, Aurora, IL USA.
[Said, Rana R.] Univ Texas SW Med Ctr Dallas, Div Pediat Neurol, Dept Pediat, Childrens Med Ctr, Dallas, TX 75390 USA.
[Nespeca, Mark P.] UCSD, Dept Neurosci, Div Neurol, Rady Childrens Hosp, San Diego, CA USA.
RP Thiele, EA (reprint author), Massachusetts Gen Hosp, Pediat Epilepsy Program, Dept Neurol, 175 Cambridge St 340, Boston, MA 02114 USA.
EM ethiele@partners.org
FU Angelman Syndrome Foundation
FX This study was supported by the Angelman Syndrome Foundation.
NR 37
TC 33
Z9 38
U1 2
U2 9
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
IS 11
BP 2369
EP 2376
DI 10.1111/j.1528-1167.2009.02108.x
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 509ZH
UT WOS:000271057300006
PM 19453717
ER
PT J
AU Conant, KD
Thibert, RL
Thiele, EA
AF Conant, Kerry D.
Thibert, Ronald L.
Thiele, Elizabeth A.
TI Epilepsy and the sleep-wake patterns found in Angelman syndrome
SO EPILEPSIA
LA English
DT Article
DE Epilepsy; Angelman syndrome; Sleep patterns; Behavioral Evaluation of
Disorders of Sleep
ID INDIVIDUALS
AB Sleep disturbances and epilepsy are common in Angelman syndrome (AS). This study examines seizure variables and sleep in a large AS cohort. Sleep disturbances and epilepsy were assessed in 290 individuals with AS using two questionnaires, including the Behavioral Evaluation of Disorders of Sleep (BEDS). Sensitivity to the sleeping environment, decreased nightly hours of sleep, and a difficulty initiating sleep were significantly correlated with the presence of epilepsy, particularly focal seizures. Use of multiple anticonvulsant drugs was shown to affect sleep. No significant associations were present between molecular sub-types of AS and individual sleep factors. Sleep problems appeared to be associated with epilepsy in individuals with AS, especially with focal and absence seizures and multiple seizure types. Results were consistent with those of prior studies assessing sleep in AS. Severity of epilepsy and use of anticonvulsant drugs may be related to a higher degree of sleep disturbance in this population.
C1 [Conant, Kerry D.; Thibert, Ronald L.; Thiele, Elizabeth A.] Massachusetts Gen Hosp, Dept Neurol, Pediat Epilepsy Program, Boston, MA 02114 USA.
RP Thiele, EA (reprint author), Massachusetts Gen Hosp, Dept Neurol, Pediat Epilepsy Program, 175 Cambridge St Suite 340, Boston, MA 02114 USA.
EM ethiele@partners.org
FU Angelman Syndrome Foundation (ASF)
FX This study was supported by the Angelman Syndrome Foundation (ASF).
NR 11
TC 26
Z9 26
U1 0
U2 3
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2009
VL 50
IS 11
BP 2497
EP 2500
DI 10.1111/j.1528-1167.2009.02109.x
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA 509ZH
UT WOS:000271057300020
PM 19453716
ER
PT J
AU Fuchs, BB
Mylonakis, E
AF Fuchs, Beth Burgwyn
Mylonakis, Eleftherios
TI Our Paths Might Cross: the Role of the Fungal Cell Wall Integrity
Pathway in Stress Response and Cross Talk with Other Stress Response
Pathways
SO EUKARYOTIC CELL
LA English
DT Review
ID PROTEIN-KINASE-C; YEAST SACCHAROMYCES-CEREVISIAE; GTP-BINDING PROTEIN;
SIGNAL-TRANSDUCTION PATHWAY; ACTIVATED MAP KINASE;
CRYPTOCOCCUS-NEOFORMANS; CANDIDA-ALBICANS; OXIDATIVE-STRESS; GENE
ENCODES; FISSION YEAST
AB Fungi occupy diverse environments and are subjected to many extreme conditions. Among the stressful conditions faced by fungi are pH changes, osmotic changes, thermal changes, oxide radicals, nutrient deprivation, and exposure to chemicals. These adversities can be found either in the environment or in animal and human hosts. The cell wall integrity (CWI) pathway provides a means to fortify and repair damages to the cell wall in order to withstand stressful environments. The CWI pathway in comprised of cell wall stress sensors that lead to activation of a mitogen-activated protein kinase (MAPK) cascade. Signaling through the MAPK cascade leads to expression of transcription factors that facilitate biosynthesis of cell wall components and actin organization. Given the relatively limited number of components of the CWI pathway and the very diverse stimuli, there must be a means of expanding the pathway. To manage the diverse stress conditions, the CWI pathway cross talks with other pathways or proteins, and these cross talk events enhance the signaling capabilities of the CWI pathway. Lateral influences that facilitate maintaining the cell wall under stress conditions are TOR signaling, calcineurin signaling, the high-osmolarity glycerol pathway, the cyclic AMP-protein kinase A pathway, and additional proteins. In this article, we highlight several of the cross talk events that have been described for Saccharomyces cerevisiae and several other fungi.
C1 [Fuchs, Beth Burgwyn; Mylonakis, Eleftherios] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
RP Mylonakis, E (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Infect Dis, Gray Jackson 504,55 Fruit St, Boston, MA 02114 USA.
EM emylonakis@partners.org
FU National Institutes of Health [R01 AI075286, R21 AI079569]
FX We acknowledge three anonymous reviewers for helpful feedback and
comments.
NR 83
TC 83
Z9 84
U1 2
U2 29
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1535-9778
J9 EUKARYOT CELL
JI Eukaryot. Cell
PD NOV
PY 2009
VL 8
IS 11
BP 1616
EP 1625
DI 10.1128/EC.00193-09
PG 10
WC Microbiology; Mycology
SC Microbiology; Mycology
GA 514BO
UT WOS:000271368700001
PM 19717745
ER
PT J
AU Pukkila-Worley, R
Peleg, AY
Tampakakis, E
Mylonakis, E
AF Pukkila-Worley, Read
Peleg, Anton Y.
Tampakakis, Emmanouil
Mylonakis, Eleftherios
TI Candida albicans Hyphal Formation and Virulence Assessed Using a
Caenorhabditis elegans Infection Model
SO EUKARYOTIC CELL
LA English
DT Article
ID HOST-PATHOGEN INTERACTIONS; ANTIFUNGAL DRUG-RESISTANCE;
SACCHAROMYCES-CEREVISIAE; TRANSCRIPTION FACTOR; FILAMENTOUS GROWTH;
INNATE IMMUNITY; AMPHOTERICIN-B; PH RESPONSES; YEAST; IDENTIFICATION
AB Candida albicans colonizes the human gastrointestinal tract and can cause life-threatening systemic infection in susceptible hosts. We study here C. albicans virulence determinants using the nematode Caenorhabditis elegans in a pathogenesis system that models candidiasis. The yeast form of C. albicans is ingested into the C. elegans digestive tract. In liquid media, the yeast cells then undergo morphological change to form hyphae, which results in aggressive tissue destruction and death of the nematode. Several lines of evidence demonstrate that hyphal formation is critical for C. albicans pathogenesis in C. elegans. First, two yeast species unable to form hyphae (Debaryomyces hansenii and Candida lusitaniae) were less virulent than C. albicans in the C. elegans assay. Second, three C. albicans mutant strains compromised in their ability to form hyphae (efg1 Delta/efg1 Delta, flo8 Delta/flo8 Delta, and cph1 Delta/cph1 Delta efg1 Delta/efg1 Delta) were dramatically attenuated for virulence. Third, the conditional tet-NRG1 strain, which enables the external manipulation of morphogenesis in vivo, was more virulent toward C. elegans when the assay was conducted under conditions that permit hyphal growth. Finally, we demonstrate the utility of the C. elegans assay in a screen for C. albicans virulence determinants, which identified several genes important for both hyphal formation in vivo and the killing of C. elegans, including the recently described CAS5 and ADA2 genes. These studies in a C. elegans-C. albicans infection model provide insights into the virulence mechanisms of an important human pathogen.
C1 [Pukkila-Worley, Read; Peleg, Anton Y.; Tampakakis, Emmanouil; Mylonakis, Eleftherios] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Peleg, Anton Y.] Beth Israel Deaconess Med Ctr, Div Infect Dis, Boston, MA 02215 USA.
[Pukkila-Worley, Read; Peleg, Anton Y.; Mylonakis, Eleftherios] Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Mylonakis, E (reprint author), Massachusetts Gen Hosp, Div Infect Dis, Gray Jackson 504,55 Fruit St, Boston, MA 02114 USA.
EM emylonakis@partners.org
OI Peleg, Anton/0000-0002-2296-2126
FU Cancer Research Institute; University of Queensland Postgraduate
Scholarship; National Institutes of Health [R01 AI075286]; Astellas
Pharma, Inc.; Pfizer, Inc.
FX E. M. received research support from Astellas Pharma, Inc., and is a
member of the Speaker's Bureau for Pfizer, Inc. A. Y. P. has served as
an advisor for Abbot Molecular, Inc. The other authors report no
potential conflicts of interest.
NR 52
TC 67
Z9 77
U1 1
U2 7
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1535-9778
J9 EUKARYOT CELL
JI Eukaryot. Cell
PD NOV
PY 2009
VL 8
IS 11
BP 1750
EP 1758
DI 10.1128/EC.00163-09
PG 9
WC Microbiology; Mycology
SC Microbiology; Mycology
GA 514BO
UT WOS:000271368700013
PM 19666778
ER
PT J
AU Matter, CM
Stuber, M
Nahrendorf, M
AF Matter, Christian M.
Stuber, Matthias
Nahrendorf, Matthias
TI Imaging of the unstable plaque: how far have we got?
SO EUROPEAN HEART JOURNAL
LA English
DT Review
DE Atherosclerosis; Molecular imaging; Vulnerable plaque
ID CORONARY-ARTERY-DISEASE; MAGNETIC-RESONANCE ANGIOGRAPHY; ACUTE
MYOCARDIAL-INFARCTION; ULTRASMALL SUPERPARAMAGNETIC PARTICLES; OPTICAL
COHERENCE TOMOGRAPHY; POSITRON-EMISSION-TOMOGRAPHY; WATER SUPPRESSION
IRON; IN-VIVO; INTRAVASCULAR ULTRASOUND; ATHEROSCLEROTIC PLAQUES
AB Rupture of unstable plaques may lead to myocardial infarction or stroke and is the leading cause of morbidity and mortality in western countries. Thus, there is a clear need for identifying these vulnerable plaques before the rupture occurs. Atherosclerotic plaques are a challenging imaging target as they are small and move rapidly, especially in the coronary tree. Many of the currently available imaging tools for clinical use still provide minimal information about the biological characteristics of plaques, because they are limited with respect to spatial and temporal resolution. Moreover, many of these imaging tools are invasive. The new generation of imaging modalities such as magnetic resonance imaging, nuclear imaging such as positron emission tomography and single photon emission computed tomography, computed tomography, fluorescence imaging, intravascular ultrasound, and optical coherence tomography offer opportunities to overcome some of these limitations. This review discusses the potential of these techniques for imaging the unstable plaque.
C1 [Matter, Christian M.] Univ Zurich, Inst Physiol, Zurich Ctr Integrat Human Physiol, CH-8057 Zurich, Switzerland.
[Matter, Christian M.] Univ Zurich Hosp, Ctr Cardiovasc, CH-8091 Zurich, Switzerland.
[Stuber, Matthias] Johns Hopkins Univ, Div Magnet Resonance Res, Dept Radiol, Sch Med, Baltimore, MD 21287 USA.
[Stuber, Matthias] CHU Vaudois, Dept Radiol, CH-1011 Lausanne, Switzerland.
[Stuber, Matthias] Univ Lausanne, CH-1011 Lausanne, Switzerland.
[Nahrendorf, Matthias] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Nahrendorf, Matthias] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Matter, CM (reprint author), Univ Zurich, Inst Physiol, Zurich Ctr Integrat Human Physiol, CH-8057 Zurich, Switzerland.
EM cmatter@physiol.uzh.ch
RI Stuber, Matthias/B-2949-2010; Centre d'imagerie Biomedicale,
CIBM/B-5740-2012
OI Stuber, Matthias/0000-0001-9843-2028;
FU Swiss National Science Foundation [31-114094/1]; AHA [0835623D]; NIH
[R01HL095629-01, R01HL096576-01, R01-HL084186, R01-HL61912]; Donald W.
Reynolds Foundation; MERCATOR Foundation Switzerland; Cardiovascular
Research Foundation Zurich
FX This work was supported by grants from the Swiss National Science
Foundation 31-114094/1 (C. M. M.), the URPP 'Integrative Human
Physiology' at the University of Zurich (C. M. M.), AHA SDG 0835623D (M.
N.), and in part by the NIH grants R01HL095629-01 (M. N.),
R01HL096576-01 (M. N.), R01-HL084186 (M. S.), R01-HL61912 (M. S.), and
the Donald W. Reynolds Foundation (M. S.). Further support was provided
by unrestricted grants from the MERCATOR Foundation Switzerland and a
strategic alliance with Pfizer, Inc. New York. Funding to pay the Open
Access publication charges for this article was provided by
Cardiovascular Research Foundation Zurich.
NR 76
TC 56
Z9 61
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0195-668X
J9 EUR HEART J
JI Eur. Heart J.
PD NOV
PY 2009
VL 30
IS 21
BP 2566
EP 2574
DI 10.1093/eurheartj/ehp419
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 516WE
UT WOS:000271573200009
PM 19833636
ER
PT J
AU Raut, CP
Nucci, MR
Wang, Q
Manola, J
Bertagnolli, MM
Demetri, GD
Morgan, JA
Muto, MG
Fletcher, CDM
George, S
AF Raut, Chandrajit P.
Nucci, Marisa R.
Wang, Qian
Manola, Judith
Bertagnolli, Monica M.
Demetri, George D.
Morgan, Jeffrey A.
Muto, Michael G.
Fletcher, Christopher D. M.
George, Suzanne
TI Predictive value of FIGO and AJCC staging systems in patients with
uterine leiomyosarcoma
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE Uterine sarcoma; Leiomyosarcoma; AJCC; FIGO; Staging system; Uterine
leiomyosarcoma; Predictive value
ID PROGNOSTIC-FACTORS; SARCOMAS; SURVIVAL; UTERUS; IMPACT; P53
AB Background: Cancer staging systems aim to identify patient cohorts with different outcomes based on clinically relevant prognostic factors. Uterine leiomyosarcoma (ULMS) is classified using the FIGO staging system developed for epithelial malignancies; other sarcomas use the AJCC staging system. Neither has been validated in ULMS. We critically evaluated both systems to determine if either identified patient groups with distinct outcomes.
Methods: We staged 230 ULMS patients by the FIGO and AJCC systems. Progression-free survival (PFS) and overall survival (OS) rates were calculated; statistical pairwise comparisons were performed.
Results: The number of stages I and III patients varied by staging system. There were few stage II patients by either system. Using the FIGO system, PFS was better in stage I patients versus stage III or IV patients, and OS was better in stage I patients versus stage IV patients. Using the AJCC system, PFS and OS were better in stage I patients (low grade) versus stage II, III or IV patients, and OS was better in stage III patients versus stage IV patients. Prognosis of patients with serosal involvement (FIGO IV) was similar to that of patients with metastases (FIGO IV).
Conclusion: Neither system classifies ULMS patients into four clinically meaningful, non-overlapping stages predictive of PFS and OS. This analysis highlights the relevance of certain factors (low grade, serosal involvement) and rarity of others (FIGO stage II, cervical invasion). Once identified, prognostic factors relevant to this malignancy should be incorporated into a new staging system in an effort to identify appropriate cohorts for different treatments. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Raut, Chandrajit P.; Bertagnolli, Monica M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Brigham & Womens Hosp,Dept Surg, Boston, MA 02115 USA.
[Nucci, Marisa R.; Fletcher, Christopher D. M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Brigham & Womens Hosp,Dept Pathol, Boston, MA 02115 USA.
[Wang, Qian; Manola, Judith] Harvard Univ, Sch Med, Dana Farber Canc Inst, Brigham & Womens Hosp,Dept Biostat, Boston, MA 02115 USA.
[Demetri, George D.; Morgan, Jeffrey A.; George, Suzanne] Harvard Univ, Sch Med, Dana Farber Canc Inst, Brigham & Womens Hosp,Dept Med Oncol, Boston, MA 02115 USA.
[Muto, Michael G.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Brigham & Womens Hosp,Dept Gynecol Oncol, Boston, MA 02115 USA.
RP Raut, CP (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Brigham & Womens Hosp,Dept Surg, 75 Francis St, Boston, MA 02115 USA.
EM craut@partners.org
NR 20
TC 23
Z9 24
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
J9 EUR J CANCER
JI Eur. J. Cancer
PD NOV
PY 2009
VL 45
IS 16
BP 2818
EP 2824
DI 10.1016/j.ejca.2009.06.030
PG 7
WC Oncology
SC Oncology
GA 526JL
UT WOS:000272284200017
PM 19647426
ER
PT J
AU Illigens, BM
Yamada, A
Anosova, N
Dong, VM
Sayegh, MH
Benichou, G
AF Illigens, Ben M.
Yamada, Akira
Anosova, Natalie
Dong, Victor M.
Sayegh, Mohamed H.
Benichou, Gilles
TI Dual effects of the alloresponse by Th1 and Th2 cells on acute and
chronic rejection of allotransplants
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE Chronic graft rejection; Heart transplantation; Skin graft; T-cell
allorecognition; Th1/Th2 cells
ID PERSISTENT ALLOPEPTIDE REACTIVITY; CARDIAC ALLOGRAFT VASCULOPATHY;
HLA-DR PEPTIDES; CD8(+) T-CELLS; INDIRECT RECOGNITION; IN-VIVO; INDIRECT
ALLORECOGNITION; GRAFT-REJECTION; MHC PEPTIDES; TRANSPLANT RECIPIENTS
AB The contribution of direct and indirect alloresponses by CD4(+) Th1 and Th2 cells in acute and chronic rejection of allogeneic transplants remains unclear. in the present study, we addressed this question using a transplant model in a single MHC class I-disparate donor-recipient mouse combination. BALB/c-dm2 (dm2) mutant mice do not express MHC class I L(d) molecules and reject acutely L(d+) skin grafts from BALB/c mice. In contrast, BALB/c hearts placed in dm2 mice are permanently accepted in the absence of chronic allograft vasculopathy. in this model, CD4(+) T cells are activated following recognition of a donor MHC class I determinant, L(d) 61-80, presented by MHC Class II A(d) molecules on donor and recipient APC. Pre-transplantation of recipients with L(d) 61-80 peptide emulsified in complete Freund's adjuvant induced a Th1 response, which accelerated the rejection of skin allografts, but it had no effect on cardiac transplants. In contrast, induction of a Th2 response to the same peptide abrogated the CD8(+) cytotoxic T cells response and markedly delayed the rejection of skin allografts while it induced de novo chronic rejection of heart transplants. This shows that Th2 cells activated via indirect allorecognition can exert dual effects on acute and chronic rejection of allogeneic transplants.
C1 [Illigens, Ben M.; Anosova, Natalie; Benichou, Gilles] Harvard Univ, Massachusetts Gen Hosp, Transplantat Unit, Cellular & Mol Immunol Lab,Dept Surg,Sch Med, Boston, MA 02114 USA.
[Yamada, Akira; Dong, Victor M.; Sayegh, Mohamed H.] Harvard Univ, Brigham & Womens Hosp, Transplantat Res Ctr, Sch Med, Boston, MA 02114 USA.
[Yamada, Akira; Dong, Victor M.; Sayegh, Mohamed H.] Harvard Univ, Childrens Hosp, Sch Med, Boston, MA 02114 USA.
RP Benichou, G (reprint author), Harvard Univ, Massachusetts Gen Hosp, Transplantat Unit, Cellular & Mol Immunol Lab,Dept Surg,Sch Med, 55 Fruit St,Thier 807, Boston, MA 02114 USA.
EM gbenichou@partners.org
FU NIH [KO2AI53103, R01 HD050484]
FX We would like to thank Ms. Karla Stenger, Colleen Doherty and Sarah
Connolly for their assistance in the preparation of the manuscript. We
also thank Drs. G. Tocco, A. Alessandrini and H. Winn for helpful
discussions. This work was supported by grants from the NIH (KO2AI53103
and R01 HD050484) to G. B.
NR 59
TC 18
Z9 20
U1 0
U2 3
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY
SN 0014-2980
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD NOV
PY 2009
VL 39
IS 11
BP 3000
EP 3009
DI 10.1002/eji.200838980
PG 10
WC Immunology
SC Immunology
GA 524EH
UT WOS:000272126100009
PM 19658090
ER
PT J
AU Iosifescu, DV
Greenwald, S
Devlin, P
Mischoulon, D
Denninger, JW
Alpert, JE
Fava, M
AF Iosifescu, Dan V.
Greenwald, Scott
Devlin, Philip
Mischoulon, David
Denninger, John W.
Alpert, Jonathan E.
Fava, Maurizio
TI Frontal EEG predictors of treatment outcome in major depressive disorder
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Major depressive disorder; Antidepressants; Treatment response;
Quantitative electroencephalography (QEEG)
ID BRAIN ELECTRICAL TOMOGRAPHY; TREATMENT RESPONSE; ANTIDEPRESSANT
TREATMENT; ASYMMETRY; SYMPTOMS; NONRESPONDERS; ONSET
AB Objective: To investigate the rote of frontal EEG as predictor of clinical response to SSRIs or venlafaxine in major depressive disorder (MDD). Method: 82 subjects (age 35.9 +/- 13.0; 47.6% female) meeting DSM-IV criteria for MDD entered an 8-week prospective treatment with SSRIs or venlafaxine. At baseline and week 1 we recorded serial, 4-channel EEGs (F7-Fpz, F8-Fpz, A1-Fpz, A2-Fpz). We evaluated prospectively the relative theta power as predictor of treatment outcome. We also developed an Antidepressant Treatment Response (ATR) index using EEG parameters assessed at baseline and week 1. Results: 45 subjects (54.9%) responded to treatment (HAM-D-17 reduction 50%). At baseline, frontal relative theta power (i.e., 4-8 Hz power/2-20 Hz power) was significantly (p=0.017) tower (21%) in treatment responders than in non-responders (24%). Baseline relative theta power predicted treatment response with 63% accuracy [64% sensitivity, 62% specificity, 66% area under the receiver operator curve (AUROC) (p=0.014)]. Relative theta power at week 1 predicted treatment response with 60% accuracy [62% sensitivity, 57% specificity, 61% AUROC (p=0.089)]. ATR predicted response with 70% accuracy [82% sensitivity, 54% specificity, 72% AURCC (p=0.001)]. Conclusion: Using automated analysis of frontal EEG collected during the first week of antidepressant treatment it may be possible to facilitate prediction of SSRI or venlafaxine efficacy in MDD. (C) 2009 Elsevier B.V. and ECNR All rights reserved.
C1 [Iosifescu, Dan V.; Mischoulon, David; Denninger, John W.; Alpert, Jonathan E.; Fava, Maurizio] Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 02114 USA.
[Iosifescu, Dan V.; Mischoulon, David; Denninger, John W.; Alpert, Jonathan E.; Fava, Maurizio] Harvard Univ, Sch Med, Boston, MA USA.
[Greenwald, Scott; Devlin, Philip] Aspect Med Syst Inc, Norwood, MA USA.
RP Iosifescu, DV (reprint author), Massachusetts Gen Hosp, Depress Clin & Res Program, 50 Staniford St,Suite 401, Boston, MA 02114 USA.
EM diosifescu@partners.org
OI Alpert, Jonathan/0000-0002-4332-908X
FU Aspect Medical Systems
FX This study was supported by a grant from Aspect Medical Systems. Aspect
Medical Systems had no further rote in the study design or data
collection. Dr. Greenwald and Mr. Devlin who are employees of Aspect
Medical Systems have contributed to the analysis of the EEG data and are
authors of this manuscript.
NR 28
TC 47
Z9 48
U1 3
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD NOV
PY 2009
VL 19
IS 11
BP 772
EP 777
DI 10.1016/j.euroneuro.2009.06.001
PG 6
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 511FX
UT WOS:000271150400002
PM 19574030
ER
PT J
AU Kassarjian, A
Llopis, E
Schwartz, RB
Bencardino, JT
AF Kassarjian, Ara
Llopis, Eva
Schwartz, Richard B.
Bencardino, Jenny T.
TI Obturator externus bursa: prevalence of communication with the hip joint
and associated intra-articular findings in 200 consecutive hip MR
arthrograms
SO EUROPEAN RADIOLOGY
LA English
DT Article
DE Hip; MRI; Arthrogram; Anatomy; Obturator externus; Bursa
ID FEMOROACETABULAR IMPINGEMENT; DIAGNOSIS
AB The purpose of the study was to demonstrate the prevalence of communication between the hip joint and the obturator externus bursa on hip MR arthrography. Following institutional review board approval, 200 hip MR arthrograms in 196 subjects were independently reviewed by two musculoskeletal radiologists. Discrepancies were resolved by adjudication. The presence or absence of communication between the hip joint and the obturator externus bursa was recorded. Associated lesions involving the acetabular labrum and articular cartilage were recorded. The obturator externus bursa was shown to communicate with the hip joint in 11 of the 200 (5.5%) hip MR arthrograms. Of these, six were in men and five were in women. The age range was 15-63 years with a mean age of 34 years. All 11 patients had labral tears. Eight of the 11 had cartilage lesions. The obturator externus bursa can be seen to communicate with the hip joint in 5.5% of hip MR arthrograms. Associated labral and cartilage lesions are common.
C1 [Kassarjian, Ara] Corades SL, Majadahonda Madrid 28220, Spain.
[Kassarjian, Ara] Massachusetts Gen Hosp, Div Musculoksleletal Radiol, Boston, MA 02114 USA.
[Llopis, Eva] Hosp Ribera, Dept Radiol, Valencia 46600, Spain.
[Schwartz, Richard B.] Longwood MRI Specialists, Brookline, MA 02446 USA.
[Bencardino, Jenny T.] NYU, Dept Radiol, New York, NY 10016 USA.
RP Kassarjian, A (reprint author), Corades SL, Calle Galeon 2, Majadahonda Madrid 28220, Spain.
EM Kassarjian@mac.com
NR 7
TC 6
Z9 6
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0938-7994
J9 EUR RADIOL
JI Eur. Radiol.
PD NOV
PY 2009
VL 19
IS 11
BP 2779
EP 2782
DI 10.1007/s00330-009-1476-5
PG 4
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 507FS
UT WOS:000270838000026
PM 19504101
ER
PT J
AU Smith, MR
AF Smith, Matthew R.
TI RANK Ligand-targeted Therapy: A Novel Approach to Prevent Bone Loss and
Fractures in Men with Prostate Cancer
SO EUROPEAN UROLOGY SUPPLEMENTS
LA English
DT Article
CT 24th Congress of the Annual European-Association-of-Urology
CY MAR 17-21, 2009
CL Stockholm, SWEDEN
SP European Assoc Urol
DE Bone; Bone metastases; Breast cancer; Denosumab; Prostate cancer; RANK;
RANK Ligand
ID ANDROGEN-DEPRIVATION THERAPY; CONTROLLED-TRIAL; ZOLEDRONIC ACID;
DENOSUMAB; RISK; BISPHOSPHONATES; WOMEN
AB Context: The importance of bone loss associated with both prostate cancer (PCa) and its treatment is being increasingly recognised, and new options to manage this complication are in development.
Objective: To assess the impact of androgen-deprivation therapy (ADT) on bone and to outline recently reported and ongoing phase 3 studies of agents designed to prevent bone loss and fractures in men with PCa.
Evidence acquisition: This article is based on a presentation at an Amgen-sponsored satellite symposium held at the European Association of Urology Congress in Stockholm, Sweden, in March 2009.
Evidence synthesis: ADT for PCa is associated with bone loss and an increased fracture risk. Several bisphosphonates have been shown to improve bone mineral density (BMD) during ADT, but their effects on treatment-related fractures are unknown. Denosumab, a fully human monoclonal antibody to RANK Ligand, is being investigated for the management of bone loss associated with PCa. The results of a phase 3 randomised, placebo-controlled trial of denosumab to prevent bone loss and fractures during ADT in men with PCa have recently been reported. Compared with placebo, denosumab (60 mg subcutaneously every 6 mo) significantly reduced the incidence of new vertebral fractures by 62% after 3 yr. Denosumab also increased BMD significantly at various skeletal sites, including the spine, hip, and wrist.
Conclusions: ADT decreases BMD and increases fracture risk in men with PCa. A recent phase 3 study has demonstrated that denosumab increases BMD and significantly reduces the risk of new vertebral fractures in men with PCa. Two ongoing phase 3 studies are evaluating denosumab for the prevention and treatment of bone metastases in men with castration-resistant prostate cancer. (C) 2009 European Association of Urology. Published by Elsevier B. V. All rights reserved.
C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
RP Smith, MR (reprint author), Massachusetts Gen Hosp, Ctr Canc, 55 Fruit St, Boston, MA 02114 USA.
EM smith.matthew@mgh.harvard.edu
NR 22
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1569-9056
J9 EUR UROL SUPPL
JI Eur. Urol. Suppl.
PD NOV
PY 2009
VL 8
IS 11
BP 834
EP 838
DI 10.1016/j.eursup.2009.08.006
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 512ZF
UT WOS:000271290500004
ER
PT J
AU Noda, K
Nakao, S
Zandi, S
Engelstadter, V
Mashima, Y
Hafezi-Moghadam, A
AF Noda, Kousuke
Nakao, Shintaro
Zandi, Souska
Engelstaedter, Verena
Mashima, Yukihiko
Hafezi-Moghadam, Ali
TI Vascular adhesion protein-1 regulates leukocyte transmigration rate in
the retina during diabetes
SO EXPERIMENTAL EYE RESEARCH
LA English
DT Article
DE diabetic retinopathy; leukocyte recruitment; adhesion molecules;
semicarbazide-sensitive amine oxidase
ID IN-VIVO; AMINE OXIDASES; P-SELECTIN; STREPTOZOTOCIN; LEUKOSTASIS;
RETINOPATHY; EXPRESSION; MOLECULE-1; CELLS; PERMEABILITY
AB Vascular adhesion protein-1 (VAP-1) is an endothelial adhesion molecule that possesses semicarbazide-sensitive amine oxidase (SSAO) activity and is involved in leukocyte recruitment. Leukocyte adhesion to retinal vessels is a predominant feature of experimentally induced diabetic retinopathy (DR). However, the role of VAP-1 in this process is unknown. Diabetes was induced by i.p. injection of Streptozotocin in Long-Evans rats. The specific inhibitor of VAP-1, UV-002, was administered by daily i.p. injections. The expression of VAP-1 mRNA in the retinal extracts of normal and diabetic animals was measured by real-time quantitative polymerase chain reaction (PCR). Firm leukocyte adhesion was quantified in retinal flatmounts after intravascular staining with concanavalin A (ConA). Leukocyte transmigration rate was quantified by in vivo acridine orange leukocyte staining (AOLS). In diabetic rats, the rate of leukocyte transmigration into the retinal tissues of live animals was significantly increased, as determined by AOLS. When diabetic animals were treated with daily injections of the VAP-1 inhibitor (0.3 mg/kg), leukocyte transmigration rate was significantly reduced (P < 0.05). However, firm adhesion of leukocytes in diabetic animals treated with the inhibitor did not differ significantly from vehicle-treated diabetic controls. This work provides evidence for an important role of VAP-1 in the recruitment of leukocyte to the retina in experimental DR. Our results reveal the critical contribution of VAP-1 to leukocyte transmigration, with little impact on firm leukocyte adhesion in the retinas of diabetic animals. VAP-1 inhibition might be beneficial in the treatment of DR. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Noda, Kousuke; Nakao, Shintaro; Zandi, Souska; Engelstaedter, Verena; Hafezi-Moghadam, Ali] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA.
[Noda, Kousuke; Nakao, Shintaro; Zandi, Souska; Engelstaedter, Verena; Hafezi-Moghadam, Ali] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA.
[Mashima, Yukihiko] R Tech Ueno Ltd, Tokyo, Japan.
RP Hafezi-Moghadam, A (reprint author), Angiogenesis Lab, 325 Cambridge St,3rd Floor, Boston, MA 02114 USA.
EM ahm@meei.harvard.edu
OI Hafezi-Moghadam, Ali/0000-0002-5336-0697
FU NIH [AI050775, HL086933]; R-TECH-UENO, Bausch & Lomb Fellowships; Japan
Eye Bank Association; NEI core [EY14104]; Massachusetts Lions Eye
Research Fund Inc.; Edward F. Knight AMD Fund; Research to Prevent
Blindness; American Health Assistance Foundation
FX We thank Alexander Schering for compiling the 3D confocal images. This
work was supported by NIH grants AI050775 (AHM) and HL086933 (Alan
Cross, University of Maryland), research funds from R-TECH-UENO, Bausch
& Lomb Fellowships (K.N. and S.N.), a Fellowship Award from the Japan
Eye Bank Association (K.N. and S.N.). and NEI core grant EY14104. We are
indebted to the Massachusetts Lions Eye Research Fund Inc. for generous
funds provided for laboratory equipment used in this project. We would
like to thank Marion W. and Edward F. Knight AMD Fund, Research to
Prevent Blindness, and American Health Assistance Foundation for their
support.
NR 41
TC 27
Z9 31
U1 0
U2 1
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0014-4835
J9 EXP EYE RES
JI Exp. Eye Res.
PD NOV
PY 2009
VL 89
IS 5
BP 774
EP 781
DI 10.1016/j.exer.2009.07.010
PG 8
WC Ophthalmology
SC Ophthalmology
GA 507KA
UT WOS:000270850800021
PM 19635478
ER
PT J
AU Yan, BP
Kiernan, TJ
Gonzales-Cruz, I
Lam, YY
AF Yan, Bryan P.
Kiernan, Thomas J.
Gonzales-Cruz, Ignacio
Lam, Yat-Yin
TI Left atrial appendage-occluding devices for stroke prevention in
patients with nonvalvular atrial fibrillation
SO EXPERT REVIEW OF MEDICAL DEVICES
LA English
DT Review
DE atrial fibrillation; left atrial appendage; oral anticoagulation; stroke
ID HIGH-RISK PATIENTS; TRANSCATHETER OCCLUSION; CARDIAC-SURGERY;
EXPERIENCE; REDUCTION; OBLITERATION; LIGATION; SYSTEM; TRIALS; PLAATO
AB Atrial fibrillation is associated with a fivefold increased risk for stroke, mostly secondary to thromboembolic events. Anticoagulation with a vitamin K antagonist is the standard medical therapy for these patients but is difficult to maintain within the therapeutic range and requires frequent monitoring and dose adjustments. Approximately 90% of thromboembolism occurs in the left atrial appendage (LAA) in patients with nonvalvular atrial fibrillation. Occlusion of flow into the LAA may prevent thrombus formation in the appendage and, hence, reduction of stroke. Recently, several percutaneous transcatheter techniques of LAA exclusion using the Percutaneous Left Atrial Appendage Transcatheter Occlusion device, the WATCHMAN(R) device, and AMPLATZER(R) septal occluder and cardiac plug have been employed, with encouraging results. Occlusion of the LAA may be an alternative to vitamin K antagonist therapy for selected patients.
C1 [Yan, Bryan P.; Lam, Yat-Yin] Chinese Univ Hong Kong, Dept Med & Therapeut, Hong Kong, Hong Kong, Peoples R China.
[Yan, Bryan P.] Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic 3004, Australia.
[Kiernan, Thomas J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Gonzales-Cruz, Ignacio] Univ Hosp Salamanca, Div Cardiol, Salamanca, Spain.
RP Yan, BP (reprint author), Chinese Univ Hong Kong, Dept Med & Therapeut, Hong Kong, Hong Kong, Peoples R China.
EM bryan.yan@cuhk.edu.hk
RI Hossain, Sarah /C-7332-2009; 2009, Secribsal/A-1266-2012; Yan,
Bryan/P-5928-2015
OI Hossain, Sarah /0000-0003-1355-0979;
NR 41
TC 4
Z9 4
U1 0
U2 2
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1743-4440
EI 1745-2422
J9 EXPERT REV MED DEVIC
JI Expert Rev. Med. Devices
PD NOV
PY 2009
VL 6
IS 6
BP 611
EP 620
DI 10.1586/ERD.09.45
PG 10
WC Engineering, Biomedical
SC Engineering
GA 528HC
UT WOS:000272432600010
PM 19911873
ER
PT J
AU Xu, DS
Sharma, C
Hemler, ME
AF Xu, Daosong
Sharma, Chandan
Hemler, Martin E.
TI Tetraspanin12 regulates ADAM10-dependent cleavage of amyloid precursor
protein
SO FASEB JOURNAL
LA English
DT Article
DE Alzheimer's disease; alpha-secretase; pericellular proteolysis
ID ALPHA-SECRETASE ADAM10; ALZHEIMERS-DISEASE; DISINTEGRIN-LIKE; TM4SF
PROTEINS; CELL-MIGRATION; GROWTH-FACTOR; INTEGRIN; COMPLEXES;
PALMITOYLATION; ASSOCIATION
AB Using mass spectrometry, we identified ADAM10 (a membrane-associated metalloproteinase) as a partner for TSPAN12, a tetraspanin protein. TSPAN12-ADAM10 interaction was confirmed by reciprocal coimmunoprecipitation in multiple tumor cell lines. TSPAN12, to a greater extent than other tetraspanins (CD81, CD151, CD9, and CD82), associated with ADAM10 but not with ADAM17. Overexpression of TSPAN12 enhanced ADAM10-dependent shedding of amyloid precursor protein (APP) in MCF7 (breast cancer) and SH-SY5Y (neuroblastoma) cell lines. Conversely, siRNA ablation of endogenous TSPAN12 markedly diminished APP proteolysis in both cell lines. Furthermore, TSPAN12 overexpression enhanced ADAM10 prodomain maturation, whereas TSPAN12 ablation diminished ADAM10 maturation. A palmitoylation-deficient TSPAN12 mutant failed to associate with ADAM10, inhibited ADAM10-dependent proteolysis of APP, and inhibited ADAM10 maturation, most likely by interfering with endogenous wild-type TSPAN12. In conclusion, TSPAN12 serves as a novel and robust partner for ADAM10 and promotes ADAM10 maturation, thereby facilitating ADAM10-dependent proteolysis of APP. This novel mode of regulating APP cleavage is of relevance to Alzheimer's disease therapy.-Xu, D., Sharma, C., Hemler, M. E. Tetraspanin12 regulates ADAM10-dependent cleavage of amyloid precursor protein. FASEB J. 23, 3674-3681 (2009). www.fasebj.org
C1 [Hemler, Martin E.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
RP Hemler, ME (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, 44 Binney St, Boston, MA 02115 USA.
EM martin_hemler@dfci.harvard.edu
FU National Institutes of Health [GM38903, CA102034]
FX This work was supported by National Institutes of Health grants GM38903
and CA102034 to M. E. H.
NR 50
TC 77
Z9 81
U1 1
U2 7
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 NOV
PY 2009
VL 23
IS 11
BP 3674
EP 3681
DI 10.1096/fj.09-133462
PG 8
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 512TC
UT WOS:000271272500005
PM 19587294
ER
PT J
AU Huttunen, HJ
Peach, C
Bhattacharyya, R
Barren, C
Pettingell, W
Hutter-Paier, B
Windisch, M
Berezovska, O
Kovacs, DM
AF Huttunen, Henri J.
Peach, Camilla
Bhattacharyya, Raja
Barren, Cory
Pettingell, Warren
Hutter-Paier, Birgit
Windisch, Manfred
Berezovska, Oksana
Kovacs, Dora M.
TI Inhibition of acyl-coenzyme A: cholesterol acyl transferase modulates
amyloid precursor protein trafficking in the early secretory pathway
SO FASEB JOURNAL
LA English
DT Article
DE Alzheimer's disease; cholesterol; endoplasmic reticulum; lipid; protein
maturation
ID ALZHEIMERS-DISEASE; ENDOPLASMIC-RETICULUM; BETA-PEPTIDE; QUALITY
CONTROL; APP; CLEAVAGE; METABOLISM; GENERATION; CELLS; MODEL
AB Amyloid beta-peptide (A beta) has a central role in the pathogenesis of Alzheimer's disease (AD). Cellular cholesterol homeostasis regulates endoproteolytic generation of A beta from the amyloid precursor protein (APP). Previous studies have identified acylcoenzyme A: cholesterol acyltransferase (ACAT), an enzyme that regulates subcellular cholesterol distribution, as a potential therapeutic target for AD. Inhibition of ACAT activity decreases A beta generation in cell-and animal-based models of AD through an unknown mechanism. Here we show that ACAT inhibition retains a fraction of APP molecules in the early secretory pathway, limiting the availability of APP for secretase-mediated proteolytic processing. ACAT inhibitors delayed the trafficking of immature APP molecules from the endoplasmic reticulum (ER) as shown by metabolic labeling and live-cell imaging. This resulted in partial ER retention of APP and enhanced ER-associated degradation of APP by the proteasome, without activation of the unfolded protein response pathway. The ratio of mature APP to immature APP was reduced in brains of mice treated with ACAT inhibitors, and strongly correlated with reduced brain APP-C99 and cerebrospinal fluid A beta levels in individual animals. Our results identify a novel ACAT-dependent mechanism that regulates secretory trafficking of APP, likely contributing to decreased A beta generation in vivo.-Huttunen, H. J., Peach, C., Bhattacharyya, R., Barren, C., Pettingell, W., Hutter-Paier, B., Windisch, M., Berezovska, O., Kovacs, D. M. Inhibition of acyl-coenzyme A: cholesterol acyl transferase modulates amyloid precursor protein trafficking in the early secretory pathway. FASEB J. 23, 3819-3828 (2009). www.fasebj.org
C1 [Huttunen, Henri J.; Peach, Camilla; Bhattacharyya, Raja; Barren, Cory; Pettingell, Warren; Kovacs, Dora M.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neurobiol Dis Lab,Genet & Aging Res Unit, Charlestown, MA 02129 USA.
[Huttunen, Henri J.; Peach, Camilla; Bhattacharyya, Raja; Barren, Cory; Pettingell, Warren; Berezovska, Oksana; Kovacs, Dora M.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Charlestown, MA 02129 USA.
[Huttunen, Henri J.; Peach, Camilla; Bhattacharyya, Raja; Barren, Cory; Pettingell, Warren; Hutter-Paier, Birgit; Windisch, Manfred; Berezovska, Oksana; Kovacs, Dora M.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA 02129 USA.
[Hutter-Paier, Birgit; Windisch, Manfred] Inst Expt Pharmacol, JSW Res Forsch Lab, Graz, Austria.
RP Kovacs, DM (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neurobiol Dis Lab,Genet & Aging Res Unit, 114 16th St, Charlestown, MA 02129 USA.
EM dora_kovacs@hms.harvard.edu
OI Huttunen, Henri/0000-0002-9867-4438
FU Cure Alzheimer's Fund; U.S. National Institutes of Health [R01 NS45860];
Helsingin Sanomat Centennial Foundation; Maud Kuistila Foundation
[CI-1011, CP-113,818]
FX This study was supported by grants from the Cure Alzheimer's Fund (D. M.
K.), the U.S. National Institutes of Health (R01 NS45860; D. M. K.), the
Helsingin Sanomat Centennial Foundation (H.J.H.), and the Maud Kuistila
Foundation (H.J.H.). CI-1011 and CP-113,818 were kind gifts from Lit-Fui
Lau and James Harwood (Pfizer, Groton, CT, USA), respectively.
NR 50
TC 29
Z9 30
U1 0
U2 0
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 NOV
PY 2009
VL 23
IS 11
BP 3819
EP 3828
DI 10.1096/fj.09-134999
PG 10
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 512TC
UT WOS:000271272500018
PM 19625658
ER
PT J
AU Brooks, TC
Burlingame, M
Burk, M
Tortorice, K
Dong, D
Glassman, PA
Lynch, JA
Good, CB
Rickman, HS
Claborn, M
Appleman, D
Jones, W
Shaverd, L
AF Brooks, Traci C.
Burlingame, Mark
Burk, Muriel
Tortorice, Kathy
Dong, Diane
Glassman, Peter A.
Lynch, Jennie A.
Good, Chester B.
Rickman, Holly S.
Claborn, Melanie
Appleman, Duva
Jones, William
Shaverd, Lanita
TI Travoprost A prostaglandin analogue for the treatment of glaucoma
SO FORMULARY
LA English
DT Article
ID OPEN-ANGLE GLAUCOMA; LATANOPROST
AB In August 2003, the US Department of Veterans Affairs (VA) awarded a contract for prostaglandin ophthalmic agents with travoprost as the agent of choice. Although there was no national mandate to switch patients from existing therapy, many VA facilities had agreements from their local ophthalmology and optometry departments to conduct a therapeutic interchange of patients from existing prostaglandins (eg, latanoprost) to travoprost. The primary purpose of this report is to describe the experience of conversion to travoprost after this contract. Medical records of converted patients were evaluated for change in intraocular pressure (IOP), change in visual field, adverse events, and whether or not a change back to the original therapy or alternative therapy was required. Of 578 patients evaluated, most (84%) had been using latanoprost before the conversion. After conversion, mean IOP was significantly reduced by 1.64 +/- 4.95 mm Hg (P<.0001). Of 188 patients with documented visual field assessment, 89.9% had no change or improvement in visual field after conversion. Adverse events occurred in 44 (7.6%) patients, with hyperemia occurring in 13 (2.2%) patients. Discontinuation of travoprost was attributed to an adverse event in 29 (5.0%) patients and attributed to ineffectiveness in 17 (2.9%) patients. Adverse drug event rates were significantly less than those reported in the literature. Travoprost was effective and well tolerated in most patients after therapeutic interchange. This evaluation provides additional information regarding outcomes associated with the therapeutic interchange. (Formulary. 2009; 44:322-328.)
C1 [Brooks, Traci C.] Womack Army Med Ctr, Ft Bragg, NC USA.
[Brooks, Traci C.; Burlingame, Mark] N Florida S Georgia Vet Hlth Syst, Gainesville, FL USA.
[Burk, Muriel; Dong, Diane] VA Ctr Medicat Safety, VACO PBM Serv, Hines, IL USA.
[Tortorice, Kathy] VACO Pharm Benefits Management Serv, Hines, IL USA.
[Glassman, Peter A.] Univ Calif Los Angeles, David Geffen Sch Med, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90095 USA.
[Lynch, Jennie A.] VISN 2 VA Healthcare Network Upstate New York, Syracuse, NY USA.
[Good, Chester B.] Univ Pittsburgh, Sch Med, VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Good, Chester B.] Univ Pittsburgh, Sch Pharm, Pittsburgh, PA USA.
[Rickman, Holly S.; Shaverd, Lanita] Cent Arkansas Vet Healthcare Syst, Little Rock, AR USA.
[Claborn, Melanie] Univ Arkansas Med Sci, Vet Healthcare Syst Ozarks, Fayetteville, AR USA.
[Appleman, Duva] Univ Calif, No Calif Vet Healthcare Syst, Davis Mather, CA USA.
[Jones, William] SW Consolidated Mail Outpatient Pharm, Tucson, AZ USA.
[Jones, William] VACO PBM Serv, Tucson, AZ USA.
RP Brooks, TC (reprint author), Womack Army Med Ctr, Ft Bragg, NC USA.
NR 8
TC 4
Z9 4
U1 0
U2 0
PU ADVANSTAR COMMUNICATIONS INC
PI WOODLAND HILLS
PA 6200 CANOGA AVE, 2ND FLR, WOODLAND HILLS, CA 91367 USA
SN 1082-801X
J9 FORMULARY
JI Formulary
PD NOV
PY 2009
VL 44
IS 11
BP 322
EP 328
PG 9
GA 521PK
UT WOS:000271934000001
ER
PT J
AU Bass, AJ
Meyerson, M
AF Bass, Adam J.
Meyerson, Matthew
TI Genome-Wide Association Study in Esophageal Squamous Cell Carcinoma
SO GASTROENTEROLOGY
LA English
DT Editorial Material
ID CANCER SUSCEPTIBILITY LOCUS; COLORECTAL-CANCER; GENETIC POLYMORPHISMS;
CHROMOSOME 8Q24; RISK; ALCOHOL; SCAN; CONSUMPTION; MUTATIONS; RS6983267
C1 [Bass, Adam J.; Meyerson, Matthew] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Bass, Adam J.; Meyerson, Matthew] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Bass, Adam J.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Meyerson, Matthew] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Bass, Adam J.; Meyerson, Matthew] Broad Inst, Cambridge, MA USA.
RP Bass, AJ (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM adam_bass@dfci.harvard.edu
RI Meyerson, Matthew/E-7123-2012
NR 21
TC 5
Z9 5
U1 0
U2 3
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 NOV
PY 2009
VL 137
IS 5
BP 1573
EP 1576
DI 10.1053/j.gastro.2009.09.026
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 515VJ
UT WOS:000271500700011
PM 19789091
ER
PT J
AU Nosho, K
Kure, S
Irahara, N
Shima, K
Baba, Y
Spiegelman, D
Meyerhardt, JA
Giovannucci, EL
Fuchs, CS
Ogino, S
AF Nosho, Katsuhiko
Kure, Shoko
Irahara, Natsumi
Shima, Kaori
Baba, Yoshifumi
Spiegelman, Donna
Meyerhardt, Jeffrey A.
Giovannucci, Edward L.
Fuchs, Charles S.
Ogino, Shuji
TI A Prospective Cohort Study Shows Unique Epigenetic, Genetic, and
Prognostic Features of Synchronous Colorectal Cancers
SO GASTROENTEROLOGY
LA English
DT Article
ID ISLAND METHYLATOR PHENOTYPE; POPULATION-BASED SAMPLE; MICROSATELLITE
INSTABILITY; DNA METHYLATION; LINE-1 HYPOMETHYLATION;
MOLECULAR-FEATURES; COLON CANCERS; BRAF MUTATION; CIMP-LOW; EXPRESSION
AB BACKGROUND & AIMS: Synchronous colorectal neoplasias (2 or more primary carcinomas identified in the same patient) are caused by common generic and environmental factors and can be used to study the field effect. Synchronous colon cancers have not been compared with control solitary cancers in a prospective study. METHODS: We analyzed data collected from 47 patients with synchronous colorectal cancers and 2021 solitary colorectal cancers (controls) in 2 prospective cohort studies. Tumors samples were analyzed for methylation in LINE-1 and 16 CpG islands (CACNA1G, CDKN2A [p16], CRABP1, IGF2, MLH1, NEUROG1, RUNX3, SOCS1, CHFR, HIC1, IGFBP3, MGMT, MINT1, MINT31, p14 [ARF], and WRN); microsatellite instability (MSI); the CpG island methylator phenotype (CIMP); 18q loss of heterozygosity; KRAS, BRAF, and PIK3CA mutations; and expression of beta-catenin, p53, p21, p27, cyclin D1, fatty acid synthase, and cyclooxygenase-2. RESULTS: Compared with patients with solitary colorectal cancer, synchronous colorectal cancer patients had reduced overall survival time (log-rank, P = .0048; hazard ratio [HR], 1.71; 95% confidence interval [CI]: 1.17-2.50; P = .0053; multivariate HR, 1.47; 9S% CI: 1.00-2.17; P = .049). Compared with solitary rumors, synchronous tumors more frequently contained BRAF mutations (P = .0041), CIMP-high (P = .013), and MSI-high (P = .037). Methylation levels of LINE-1 (Spearman r = 0.82; P = .0072) and CpG island methylation (P < .0001) correlated between synchronous cancer pairs from the same individuals. CONCLUSIONS: Synchronous colorectal cancers had more frequent mutations in BRAF, were more frequently CIMP- and MSI-high, and had a worse prognosis than solitary colorectal cancers. Similar epigenomic and epigenetic events were frequently observed within a synchronous cancer pair, suggesting the presence of a field defect.
C1 [Ogino, Shuji] Harvard Univ, Sch Med, Ctr Mol Oncol Pathol, Dana Farber Canc Inst,Dept Med Oncol, Boston, MA 02115 USA.
[Spiegelman, Donna; Giovannucci, Edward L.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Spiegelman, Donna] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Spiegelman, Donna; Giovannucci, Edward L.; Fuchs, Charles S.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Giovannucci, Edward L.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Ogino, Shuji] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Ogino, S (reprint author), Harvard Univ, Sch Med, Ctr Mol Oncol Pathol, Dana Farber Canc Inst,Dept Med Oncol, 44 Binney St,Room JF-215C, Boston, MA 02115 USA.
EM shuji_ogino@dfci.harvard.edu
FU NCI NIH HHS [K07 CA122826-02, K07 CA122826, K07 CA122826-01A1, K07
CA122826-03, P01 CA055075, P01 CA055075-15, P01 CA087969, P01
CA087969-10, P01 CA55075, P01 CA87969, P50 CA127003, P50 CA127003-03]
NR 50
TC 73
Z9 75
U1 0
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 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD NOV
PY 2009
VL 137
IS 5
BP 1609
EP 1620
DI 10.1053/j.gastro.2009.08.002
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 515VJ
UT WOS:000271500700018
PM 19686742
ER
PT J
AU Stoffel, E
Mukherjee, B
Raymond, VM
Tayob, N
Kastrinos, F
Sparr, J
Wang, F
Bandipalliam, P
Syngal, S
Gruber, SB
AF Stoffel, Elena
Mukherjee, Bhramar
Raymond, Victoria M.
Tayob, Nabihah
Kastrinos, Fay
Sparr, Jennifer
Wang, Fei
Bandipalliam, Prathap
Syngal, Sapna
Gruber, Stephen B.
TI Calculation of Risk of Colorectal and Endometrial Cancer Among Patients
With Lynch Syndrome
SO GASTROENTEROLOGY
LA English
DT Article
ID MSH2 MUTATION CARRIERS; FAMILY-HISTORY; HNPCC; GENE; ASCERTAINMENT;
INDIVIDUALS; ACCURACY; ONSET; MLH1
AB BACKGROUND & AIMS: Lynch syndrome is the most common hereditary colorectal cancer (CRC) syndrome. Some previous estimates of lifetime risk for CRC and endometrial cancer (EC) did not control for ascertainment and were susceptible to bias toward overestimated risk. METHODS: We studied 147 families with mismatch repair gene mutations (55 MLH1, 81 MSH2, and 11 MSH6) identified at 2 US cancer genetics clinics. Age-specific cumulative risks (penetrance) and hazard ratio (HR) estimates of CRC and EC risks were calculated and compared with the general population using modified segregation analysis. The likelihood for each pedigree was conditioned on the proband and first-degree relatives affected with CRC to reduce ascertainment bias and overestimation of penetrance. RESULTS: We analyzed 628 cases of CRC, diagnosed at the median ages of 42 and 47 years for men and women, respectively. The cumulative risk of CRC was 66.08% (95% confidence interval [CI], 59.47%-76.17%) for men and 42.71% (95% CI, 36.57%-52.83%) for women, with overall HRs of 148.4 and 51.1, respectively. CRC risk was highest for males with mutations in MLH1. There were 155 cases of EC, diagnosed at a median age of 47.5 years. The cumulative risk of EC was 39.39% (95% CI, 30.78%-46.94%) with an overall FIR of 39.0 (95% CI, 30.4-50.2). For women, the cumulative risk of CRC or EC was 73.42% (95% CI, 63.76%-80.54%). CONCLUSIONS: Lifetime risks of CRC and EC in mismatch repair gene mutation carriers are high even after adjusting for ascertainment. These estimates are valuable for patients and providers; specialized cancer surveillance is necessary.
C1 [Gruber, Stephen B.] Univ Michigan, Sch Publ Hlth, Div Epidemiol & Human Genet, Dept Epidemiol & Human Genet, Ann Arbor, MI 48105 USA.
[Gruber, Stephen B.] Univ Michigan, Sch Med, Dept Epidemiol & Human Genet, Ann Arbor, MI 48105 USA.
[Raymond, Victoria M.; Gruber, Stephen B.] Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48105 USA.
[Mukherjee, Bhramar; Tayob, Nabihah; Wang, Fei] Univ Michigan, Sch Med, Dept Biostat, Ann Arbor, MI 48105 USA.
[Mukherjee, Bhramar; Tayob, Nabihah; Wang, Fei] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48105 USA.
[Stoffel, Elena; Sparr, Jennifer; Bandipalliam, Prathap; Syngal, Sapna] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Stoffel, Elena; Kastrinos, Fay; Syngal, Sapna] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Gruber, SB (reprint author), Univ Michigan, Sch Publ Hlth, Div Epidemiol & Human Genet, Dept Epidemiol & Human Genet, 1524 BSRB, Ann Arbor, MI 48105 USA.
EM sgruber@med.umich.edu
FU National Cancer Institute [R01 CA81488, K07 CA 120448-01-A2, K24 CA
113433, R03 CA130045]; University of Michigan's Cancer Center [5 P30
CA46592]
FX This work was supported in part by the National Cancer Institute (R01
CA81488 to S.B.G., K07 CA 120448-01-A2 to E.S., and K24 CA 113433 to
S.S., R03 CA130045 to B.M.), the University of Michigan's Cancer Center
Support Grant (5 P30 CA46592).
NR 24
TC 152
Z9 158
U1 1
U2 10
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 NOV
PY 2009
VL 137
IS 5
BP 1621
EP 1627
DI 10.1053/j.gastro.2009.07.039
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 515VJ
UT WOS:000271500700019
PM 19622357
ER
PT J
AU Friedman, LS
Brandt, LJ
Elta, GH
Fitz, JG
Gores, GJ
Katz, PO
Kuemmerle, JF
Pardi, DS
Vargo, JJ
Stolar, MH
AF Friedman, Lawrence S.
Brandt, Lawrence J.
Elta, Grace H.
Fitz, J. Gregory
Gores, Gregory J.
Katz, Philip O.
Kuemmerle, John F.
Pardi, Darrell S.
Vargo, John J.
Stolar, Michael H.
TI Report of the Multisociety Task Force on GI Training
SO GASTROENTEROLOGY
LA English
DT Article
C1 [Friedman, Lawrence S.] Tufts Univ, Sch Med, Harvard Univ, Newton Wellesley Hosp,Massachusetts Gen Hosp, Medford, MA 02155 USA.
[Brandt, Lawrence J.] Albert Einstein Coll Med, Montefiore Med Ctr, Bronx, NY USA.
[Elta, Grace H.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Gores, Gregory J.; Pardi, Darrell S.] Mayo Clin, Coll Med Rochester, Rochester, MN USA.
[Katz, Philip O.] Thomas Jefferson Univ, Albert Einstein Med Ctr, Philadelphia, PA USA.
[Kuemmerle, John F.] Virginia Commonwealth Univ, Coll Med, Richmond, VA 23284 USA.
[Kuemmerle, John F.] Cleveland Clin Fdn, Inst Digest Dis, Cleveland Clin Lerner Coll Med, Cleveland, OH USA.
RP Friedman, LS (reprint author), Tufts Univ, Sch Med, Harvard Univ, Newton Wellesley Hosp,Massachusetts Gen Hosp, Medford, MA 02155 USA.
NR 0
TC 8
Z9 9
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD NOV
PY 2009
VL 137
IS 5
BP 1839
EP 1843
DI 10.1053/j.gastro.2009.07.003
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 515VJ
UT WOS:000271500700041
PM 19854349
ER
PT J
AU Friedman, LS
Brandt, LJ
Elta, GH
Fitz, JG
Gores, GJ
Katz, PO
Kuemmerle, JF
Pardi, DS
Vargo, JJ
Stolar, MH
AF Friedman, Lawrence S.
Brandt, Lawrence J.
Elta, Grace H.
Fitz, J. Gregory
Gores, Gregory J.
Katz, Philip O.
Kuemmerle, John F.
Pardi, Darrell S.
Vargo, John J.
Stolar, Michael H.
CA Multisoc Task Force GI Training
TI Report of the Multisociety Task Force on GI Training
SO GASTROINTESTINAL ENDOSCOPY
LA English
DT Article
C1 [Friedman, Lawrence S.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Brandt, Lawrence J.] Albert Einstein Coll Med, Montefiore Med Ctr, Bronx, NY 10461 USA.
[Elta, Grace H.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Gores, Gregory J.; Pardi, Darrell S.] Mayo Clin, Coll Med, Rochester, MN USA.
[Katz, Philip O.] Thomas Jefferson Univ, Albert Einstein Med Ctr, Philadelphia, PA 19107 USA.
[Kuemmerle, John F.] Virginia Commonwealth Univ, Med Coll Virginia Campus, Richmond, VA 23284 USA.
[Vargo, John J.] Cleveland Clin Fdn, Cleveland, OH USA.
[Vargo, John J.] Cleveland Clin, Lerner Coll Med, Inst Digest Dis, Cleveland, OH 44106 USA.
[Friedman, Lawrence S.] Tufts Univ, Sch Med, Medford, MA 02155 USA.
[Friedman, Lawrence S.] Newton Wellesley Hosp, Newton, MA USA.
[Friedman, Lawrence S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Friedman, LS (reprint author), Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
OI Vargo, John/0000-0001-7638-5283
NR 0
TC 7
Z9 7
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0016-5107
J9 GASTROINTEST ENDOSC
JI Gastrointest. Endosc.
PD NOV
PY 2009
VL 70
IS 5
BP 823
EP 827
DI 10.1016/j.gie.2009.08.018
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 521BK
UT WOS:000271893900001
ER
PT J
AU Jensen, DM
Machicado, GA
AF Jensen, Dennis M.
Machicado, Gustavo A.
TI Hemoclipping of chronic canine ulcers: a randomized, prospective study
of initial deployment success, clip retention rates, and ulcer healing
SO GASTROINTESTINAL ENDOSCOPY
LA English
DT Article
ID HEATER PROBE THERMOCOAGULATION; BLEEDING PEPTIC-ULCERS; ENDOSCOPIC
HEMOCLIP; GASTRIC-ULCERS; HIGH-RISK; HEMOSTASIS; INJECTION; HEMORRHAGE;
TRIAL
AB Background: Several different hemoclips are marketed for endoscopic hemostasis of nonvariceal upper GI (UGI) bleeding. No previous reports have compared Success rates of clip deployment onto bases of chronic gastric ulcers (GUs), clip retention rates, or their influence on ulcer healing.
Objectives: For the treatment of chronic GUs, to compare 3 different hemoclips with multipolar electrocoagulation (MPEC) and control.
Design: Randomized, controlled study
Subjects: Seven adult dogs with prehepatic portal hypertension had GUs created by rubber band ligation. Animals received oral proton pump inhibitors daily and underwent weekly endoscopies to quantitate clip retention and ulcer healing.
Interventions: One week after banding, 10 chronic ulcers were randomized in pairs to control (no endoscopic treatment), MPEC, or different hemoclips (QuickClip2 [QC], TriClip [TC], or Resolution Clip [RC]).
Main Outcome Measurements: Times and success of hemoclip deployment, clip retention rates, and ulcer healing rates on weekly endoscopies.
Results: Success rates of clip deployment were 100% for the RC, 93.1% for the TC, and 83.3% for the QC. Clip retention rates were significantly higher with the RC than the QC or TC at I to 3 weeks. Retained clips did not delay GU healing compared with MPEC or control.
Conclusions: Hemoclipping time was similar with all 3 clips; the RC was retained significantly longer than the QC or TC, hemoclips did not delay ulcer healing compared with control or MPEC, and all 3 hemoclips were safe and no complications Such as bleeding and weight loss were noted. (Gastrointest Endosc 2009;70:969-75.)
C1 [Jensen, Dennis M.] VA Greater Los Angeles Healthcare Syst, CURE Digest Dis Res Ctr, Hemostasis Res Grp, Los Angeles, CA 90073 USA.
Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
RP Jensen, DM (reprint author), VA Greater Los Angeles Healthcare Syst, CURE Digest Dis Res Ctr, Hemostasis Res Grp, Bldg 115,Room 318,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
FU Boston Scientific Corp; Olympus America Inc; Pentax Corp; NIH [K24
DK02650]
FX The following anthors received research support for this from Boston
Scientific Corp and Olympus America Inc (for the bemoclips, partial
funding for the animals, technical support, and supplies) and Pentax
Corp (for the endoscope): D. M. Jensen, G. A. Machicado. Supported by a
NIH grant (K24 DK02650) to D. M. Jensen.
NR 22
TC 18
Z9 18
U1 1
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0016-5107
J9 GASTROINTEST ENDOSC
JI Gastrointest. Endosc.
PD NOV
PY 2009
VL 70
IS 5
BP 969
EP 975
DI 10.1016/j.gie.2009.04.052
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 521BK
UT WOS:000271893900022
PM 19640519
ER
PT J
AU Boudreaux, ED
Allen, MH
Claassen, C
Currier, GW
Bertman, L
Glick, R
Park, J
Feifel, D
Camargo, CA
AF Boudreaux, Edwin D.
Allen, Michael H.
Claassen, Cindy
Currier, Glenn W.
Bertman, Louise
Glick, Rachel
Park, Jennifer
Feifel, David
Camargo, Carlos A., Jr.
CA PERC
TI The Psychiatric Emergency Research Collaboration-01: methods and results
SO GENERAL HOSPITAL PSYCHIATRY
LA English
DT Article
DE Psychiatric emergency; Emergency medicine; Psychiatry
ID SUBSTANCE USE; DEPARTMENT VISITS; INJURY; ROOM
AB Objective: To describe the Psychiatric Emergency Research Collaboration (PERC), the methods used to create a structured chart review tool and the results of our multicenter study.
Method: Members of the PERC Steering Committee created a structured chart review tool designed to provide a comprehensive picture of the assessment and management of psychiatric emergency patients. Ten primary indicators were chosen based on the Steering Committee's professional experience, the published literature and existing consensus panel guidelines. Eight emergency departments completed data abstraction of 50 randomly selected emergency psychiatric patients, with seven providing data from two independent raters. Inter-rater reliability (Kappas) and descriptive statistics were computed.
Results: Four hundred patient charts were abstracted. Initial concordance between raters was variable, with some sites achieving high agreement and others not. Reconciliation of discordant ratings through re-review of the original source documentation was necessary for four of the sites. Two hundred eighty-five (71%) subjects had some forth of laboratory test performed, including 212 (53%) who had urine toxicology screening and 163 (41%) who had blood alcohol levels drawn. Agitation was present in 220 (52%), with 98 (25%) receiving a medication to reduce agitation and 22 (6%) being physically restrained. Self-harm ideation was present in 226 (55%), while other-harm ideation was present in 82 (20%). One hundred seventy-nine (45%) were admitted to an inpatient or observation unit.
Conclusion: Creating a common standard for documenting, abstracting and reporting on the nature and management of psychiatric emergencies is feasible across a wide range of health care institutions. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Boudreaux, Edwin D.] Cooper Univ Hosp, Camden, NJ 08103 USA.
[Boudreaux, Edwin D.] UMDNJ RWJMS, Camden, NJ 08103 USA.
[Allen, Michael H.] Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA.
[Claassen, Cindy] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA.
[Currier, Glenn W.] Univ Rochester, Med Ctr, Dept Psychiat & Emergency Med, Rochester, NY 14642 USA.
[Currier, Glenn W.] Canandaigua VAMC, Ctr Excellence VISN2, Canandaigua, NY USA.
[Bertman, Louise] Calif Pacific Med Ctr, San Francisco, CA USA.
[Glick, Rachel] Univ Michigan, Sch Med, Dept Psychiat, Ann Arbor, MI USA.
[Park, Jennifer] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Feifel, David] Univ Calif San Diego, San Diego Med Ctr, Dept Psychiat, San Diego, CA 92103 USA.
[Camargo, Carlos A., Jr.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
RP Boudreaux, ED (reprint author), Cooper Univ Hosp, 1 Cooper Plaza, Camden, NJ 08103 USA.
EM edwin.boudreaux@umassmed.edu
RI Allen, Michael/A-8776-2011;
OI Boudreaux, Edwin/0000-0002-3223-6371
FU NIMH NIH HHS [K23 MH064517, K23 MH064517-05]
NR 22
TC 13
Z9 13
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0163-8343
EI 1873-7714
J9 GEN HOSP PSYCHIAT
JI Gen. Hosp. Psych.
PD NOV-DEC
PY 2009
VL 31
IS 6
BP 515
EP 522
DI 10.1016/j.genhosppsych.2009.04.009
PG 8
WC Psychiatry
SC Psychiatry
GA 523IN
UT WOS:000272066300004
PM 19892209
ER
PT J
AU Lamprecht, R
Dracheva, S
Assoun, S
LeDoux, JE
AF Lamprecht, R.
Dracheva, S.
Assoun, S.
LeDoux, J. E.
TI Fear conditioning induces distinct patterns of gene expression in
lateral amygdala
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Fear conditioning; gene expression; lateral amygdala; memory; microarray
ID LONG-TERM POTENTIATION; VISININ-LIKE PROTEIN-2; SYNAPTIC PLASTICITY;
MESSENGER-RNA; MEMORY CONSOLIDATION; CA(V)2.1 CHANNELS;
MEMBRANE-PROTEIN; GROWTH CONE; RECEPTOR; HIPPOCAMPUS
AB The lateral nucleus of the amygdala (LA) has been implicated in the formation of long-term associative memory (LTM) of stimuli associated with danger through fear conditioning. The current study aims to detect genes that are expressed in LA following associative fear conditioning. Using oligonucleotide microarrays, we monitored gene expression in rats subjected to paired training where a tone co-terminates with a footshock, or unpaired training where the tone and footshock are presented in a non-overlapping manner. The paired protocol consistently leads to auditory fear conditioning memory formation, whereas the unpaired protocol does not. When the paired group was compared with the unpaired group 5 h after training, the expression of genes coding for the limbic system-associated membrane protein (Lsamp), kinesin heavy chain member 2 (Kif2), N-ethylmaleimide-sensitive fusion protein (NSF) and Hippocalcin-like 4 protein (Hpcal4) was higher in the paired group. These genes encode proteins that regulate neuronal axonal morphology (Lsamp, Kif2), presynaptic vesicle cycling and release (Hpcal4 and NSF), and AMPA receptor maintenance in synapses (NSF). Quantitative real-time PCR (qPCR) showed that Kif2 and Lsamp are expressed hours following fear conditioning but minutes after unpaired training. Hpcal4 is induced by paired stimulation only 5 h after the training. These results show that fear conditioning induces a unique temporal activation of molecular pathways involved in regulating synaptic transmission and axonal morphology in LA, which is different from non-associative stimulation.
C1 [Lamprecht, R.] Univ Haifa, Dept Neurobiol & Ethol, Fac Sci & Sci Educ, IL-31905 Haifa, Israel.
[Lamprecht, R.; LeDoux, J. E.] Univ Haifa, Dept Biol, Fac Sci & Sci Educ, IL-31905 Haifa, Israel.
[Dracheva, S.] Bronx Vet Affairs Med Ctr, Bronx, NY USA.
[Dracheva, S.] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Assoun, S.] Univ Paris 06, Paris, France.
[LeDoux, J. E.] NYU, Ctr Neural Sci, New York, NY USA.
RP Lamprecht, R (reprint author), Univ Haifa, Dept Neurobiol & Ethol, Fac Sci & Sci Educ, IL-31905 Haifa, Israel.
EM rlamp@research.haifa.ac.il
FU National Institute of Health [P50 MH058911, R01 MH046516]; National
Science Foundation [IBN-0131433]; VISN3 Mental Illness Research and
Education Clinical Center
FX This research was supported by grants to J. E. L. (National Institute of
Health Grants P50 MH058911, R01 MH046516 and National Science Foundation
Grant IBN-0131433) and to S. D. (VISN3 Mental Illness Research and
Education Clinical Center). Wethank the Memorial Sloan-Kettering Cancer
Center Genomics Core laboratory for microarray assay and analysis.
NR 60
TC 20
Z9 20
U1 0
U2 4
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 NOV
PY 2009
VL 8
IS 8
BP 735
EP 743
DI 10.1111/j.1601-183X.2009.00515.x
PG 9
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 517QY
UT WOS:000271633300001
PM 19689454
ER
PT J
AU Leussis, MP
Frayne, ML
Saito, M
Berry, EM
Aldinger, KA
Rockwel, GN
Hammer, RP
Baskin-Hill, AE
Singer, JB
Nadeau, JH
Sklar, P
Petryshen, TL
AF Leussis, M. P.
Frayne, M. L.
Saito, M.
Berry, E. M.
Aldinger, K. A.
Rockwel, G. N.
Hammer, R. P., Jr.
Baskin-Hill, A. E.
Singer, J. B.
Nadeau, J. H.
Sklar, P.
Petryshen, T. L.
TI Genomic survey of prepulse inhibition in mouse chromosome substitution
strains
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Behavior; cognition; linkage; mouse genetics; psychiatric disorders;
psychopathology; quantitative trait locus; sensorimotor gating; startle
ID QUANTITATIVE TRAIT LOCI; ACOUSTIC STARTLE RESPONSE; OBSESSIVE-COMPULSIVE
DISORDER; SCHIZOTYPAL PERSONALITY-DISORDER; SENSORIMOTOR GATING
DEFICITS; BIPOLAR DISORDER; GENE-EXPRESSION; NEUROBIOLOGICAL MEASURES;
COGNITIVE DEFICITS; COMPLEX TRAITS
AB Prepulse inhibition (PPI) is a measure of sensorimotor gating, a pre-attentional inhibitory brain mechanism that filters extraneous stimuli. Prepulse inhibition is correlated with measures of cognition and executive functioning, and is considered an endophenotype of schizophrenia and other psychiatric illnesses in which patients show PPI impairments. As a first step toward identifying genes that regulate PPI, we performed a quantitative trait locus (QTL) screen of PPI phenotypes in a panel of mouse chromosome substitution strains (CSSs). We identified five CSSs with altered PPI compared with the host C57BL/6J strain: CSS-4 exhibited decreased PPI, whereas CSS-10, -11, -16 and -Y exhibited higher PPI compared with C57BL/6J. These data indicate that A/J chromosomes 4, 10, 11, 16 and Y harbor at least one QTL region that modulates PPI in these CSSs. Quantitative trait loci for the acoustic startle response were identified on seven chromosomes. Like PPI, habituation of the startle response is also disrupted in schizophrenia, and in the present study CSS-7 and -8 exhibited deficits in startle habituation. Linkage analysis of an F(2) intercross identified a highly significant QTL for PPI on chromosome 11 between positions 101.5 and 114.4 Mb (peak LOD = 4.54). Future studies will map the specific genes contributing to these QTLs using congenic strains and other genomic approaches. Identification of genes that modulate PPI will provide insight into the neural mechanisms underlying sensorimotor gating, as well as the psychopathology of disorders characterized by gating deficits.
C1 [Leussis, M. P.; Saito, M.; Berry, E. M.; Sklar, P.; Petryshen, T. L.] Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Ctr Human Genet Res, Boston, MA 02114 USA.
[Leussis, M. P.; Sklar, P.; Petryshen, T. L.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Leussis, M. P.; Sklar, P.; Petryshen, T. L.] Harvard Univ, Sch Med, Boston, MA USA.
[Leussis, M. P.; Frayne, M. L.; Saito, M.; Berry, E. M.; Aldinger, K. A.; Rockwel, G. N.; Sklar, P.; Petryshen, T. L.] Broad Inst Harvard, Stanley Ctr Psychiat Res, Cambridge, MA USA.
[Leussis, M. P.; Frayne, M. L.; Saito, M.; Berry, E. M.; Aldinger, K. A.; Rockwel, G. N.; Sklar, P.; Petryshen, T. L.] MIT, Cambridge, MA 02139 USA.
[Hammer, R. P., Jr.] Univ Arizona, Dept Basic Med Sci, Coll Med, Phoenix, AZ USA.
[Hammer, R. P., Jr.] Univ Arizona, Dept Pharmacol, Coll Med, Phoenix, AZ USA.
[Baskin-Hill, A. E.; Nadeau, J. H.] Case Western Reserve Univ, Sch Med, Dept Genet, Cleveland, OH 44106 USA.
[Singer, J. B.] Novartis Inst Biomed Res, Cambridge, MA USA.
RP Petryshen, TL (reprint author), Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Ctr Human Genet Res, 185 Cambridge St, Boston, MA 02114 USA.
EM petryshen@chgr.mgh.harvard.edu
FU National Institutes of Health [R21 MH071673, RR12305]; USPHS [R01
MH0703930]; Stanley Medical Research Institute; National Alliance for
Research on Schizophrenia and Depression; Canadian Institutes of Health
Research Postdoctoral Fellowship
FX This research was supported in whole or in part by National Institutes
of Health grants R21 MH071673 (PS) and RR12305 (JHN and AEBH), USPHS
Award R01 MH0703930 (RPH), the Stanley Medical Research Institute (TLP),
Young Investigator Awards from the National Alliance for Research on
Schizophrenia and Depression (TLP), and a Canadian Institutes of Health
Research Postdoctoral Fellowship (TLP). The authors wish to thank Dr.
Mark Daly and Andrew Kirby for analytical assistance and Skye Waggoner
for technical assistance.
NR 77
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U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD NOV
PY 2009
VL 8
IS 8
BP 806
EP 816
DI 10.1111/j.1601-183X.2009.00526.x
PG 11
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 517QY
UT WOS:000271633300008
PM 19694817
ER
PT J
AU Zhang, Y
Levin, M
AF Zhang, Ying
Levin, Michael
TI Left-Right Asymmetry in the Chick Embryo Requires Core Planar Cell
Polarity Protein Vangl2
SO GENESIS
LA English
DT Article
DE left-right asymmetry; planar cell polarity; embryogenesis; Vangl2; chick
ID LEFT-RIGHT AXIS; PRIMITIVE STREAK; EARLY STEP; SIGNALING PATHWAY;
CILIARY PROTEINS; TISSUE POLARITY; FROG EMBRYOS; HENSENS NODE;
STRABISMUS; MORPHOGENESIS
AB Consistent left-right patterning is a fascinating and biomedically important problem. In the chick embryo, it is not known how cells determine their position (left or right) relative to the primitive streak, which is required for subsequent asymmetric gene expression cascades. We show that the subcellular localization of Vangl2, a core planar cell polarity (PCP) protein, is consistently polarized, giving cells in the blastoderm a vector pointing toward the primitive streak. Moreover, morpholino-mediated loss-of-function of Vangl2 by electroporation into chicks at very early stages randomizes the normally left-sided expression of Sonic hedgehog. Strikingly, Vangl2 morpholinos also induce a desynchronization of asymmetric gene expression within the left and right domains of Hensen's node. These data reveal the existence of polarized planar cell polarity protein localization in gastrulating chick and demonstrate that the PCP pathway is functionally required for normal asymmetry in the chick upstream of Sonic hedgehog. These data suggest a new and widely applicable class of models for the spread and coordination of left-right patterning information in the embryonic blastoderm. genesis 47:719-728,2009. (C) 2009 Wiley-Liss, Inc.
C1 [Zhang, Ying; Levin, Michael] Forsyth Inst, Ctr Regenerat & Dev Biol, Boston, MA USA.
[Levin, Michael] Tufts Univ, Dept Biol, Medford, MA 02155 USA.
[Levin, Michael] Tufts Univ, Tufts Ctr Regenerat & Dev Biol, Medford, MA 02155 USA.
RP Levin, M (reprint author), Tufts Univ, Ctr Regenerat & Dev Biol, 200 Boston Ave, Medford, MA 02155 USA.
EM michael.levin@tufts.edu
RI Zhang, Ying/Q-6956-2016
OI Zhang, Ying/0000-0002-8045-3821
FU American Heart Association; NIH
FX Contract grant sponsors: American Heart Association and the NIH
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PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1526-954X
J9 GENESIS
JI Genesis
PD NOV
PY 2009
VL 47
IS 11
BP 719
EP 728
DI 10.1002/dvg.20551
PG 10
WC Developmental Biology; Genetics & Heredity
SC Developmental Biology; Genetics & Heredity
GA 525KS
UT WOS:000272215400001
PM 19621439
ER
PT J
AU Little, J
Higgins, JPT
Ioannidis, JPA
Moher, D
Gagnon, F
von Elm, E
Khoury, MJ
Cohen, B
Davey-Smith, G
Grimshaw, J
Scheet, P
Gwinn, M
Williamson, RE
Zou, GY
Hutchings, K
Johnson, CY
Tait, V
Wiens, M
Golding, J
van Duijn, C
McLaughlin, J
Paterson, A
Wells, G
Fortier, I
Freedman, M
Zecevic, M
King, R
Infante-Rivard, C
Stewart, A
Birkett, N
AF Little, Julian
Higgins, Julian P. T.
Ioannidis, John P. A.
Moher, David
Gagnon, France
von Elm, Erik
Khoury, Muin J.
Cohen, Barbara
Davey-Smith, George
Grimshaw, Jeremy
Scheet, Paul
Gwinn, Marta
Williamson, Robin E.
Zou, Guang Yong
Hutchings, Kim
Johnson, Candice Y.
Tait, Valerie
Wiens, Miriam
Golding, Jean
van Duijn, Cornelia
McLaughlin, John
Paterson, Andrew
Wells, George
Fortier, Isabel
Freedman, Matthew
Zecevic, Maja
King, Richard
Infante-Rivard, Claire
Stewart, Alex
Birkett, Nick
TI STrengthening the REporting of Genetic Association Studies (STREGA)-An
Extension of the STROBE Statement
SO GENETIC EPIDEMIOLOGY
LA English
DT Review
DE gene-disease associations; genetics; gene-environment interaction;
systematic review; meta-analysis; reporting recommendations;
epidemiology; genome-wide association
ID GENOME-WIDE ASSOCIATION; HARDY-WEINBERG EQUILIBRIUM; SINGLE-NUCLEOTIDE
POLYMORPHISMS; POPULATION STRATIFICATION; RANDOMIZED-TRIALS; DISEASE
ASSOCIATIONS; GENOTYPING ERRORS; COMPLEX DISEASES; PROSTATE-CANCER;
LINKAGE-DISEQUILIBRIUM
AB Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information in the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association studies (STREGA) initiative builds on the STrengthening the Reporting of OBservational Studies in Epidemiology (STROBE) Statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modelling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and the volume of data issues that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct, or analysis. Genet. Epidemiol. 33:581-598, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Little, Julian; Moher, David; Hutchings, Kim; Johnson, Candice Y.; Tait, Valerie; Wiens, Miriam; Birkett, Nick] Univ Ottawa, Dept Epidemiol & Community Med, Ottawa, ON K1H 8M5, Canada.
[Higgins, Julian P. T.] MRC, Biostat Unit, Cambridge CB2 2BW, England.
[Ioannidis, John P. A.] Univ Ioannina, Sch Med, Dept Hyg & Epidemiol, GR-45110 Ioannina, Greece.
[Ioannidis, John P. A.] Tufts Univ, Sch Med, Ctr Genet Epidemiol & Modeling, Boston, MA 02111 USA.
[Gagnon, France] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[von Elm, Erik] Univ Bern, Inst Social & Prevent Med, Bern, Switzerland.
[von Elm, Erik] Univ Med Ctr, Dept Med Biometry & Med Informat, German Cochrane Ctr, Freiburg, Germany.
[Khoury, Muin J.; Gwinn, Marta] Ctr Dis Control & Prevent, Natl Off Publ Hlth Genom, Atlanta, GA USA.
[Cohen, Barbara] Publ Lib Sci, San Francisco, CA USA.
[Davey-Smith, George] Univ Bristol, MRC, Ctr Causal Anal Translat Epidemiol, Dept Social Med, Bristol, Avon, England.
[Grimshaw, Jeremy] Univ Ottawa, Ottawa Hlth Res Inst, Clin Epidemiol Program, Dept Med, Ottawa, ON K1H 8M5, Canada.
[Scheet, Paul] Univ Texas Houston, MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Zou, Guang Yong] Univ Western Ontario, Dept Epidemiol & Biostat, London, ON, Canada.
[Zou, Guang Yong] Robarts Res Inst, London, ON N6A 5C1, Canada.
[McLaughlin, John] Canc Care Ontario, Toronto, ON, Canada.
[McLaughlin, John] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Prosserman Ctr Hlth Res, Toronto, ON M5G 1X5, Canada.
[Paterson, Andrew] Hosp Sick Children, Toronto, ON, Canada.
[Wells, George] Univ Ottawa, Cardiovasc Res Methods Ctr, Inst Heart, Ottawa, ON K1H 8M5, Canada.
[Fortier, Isabel] McGill Univ, Genome Quebec & P3G Observ, Montreal, PQ, Canada.
[Fortier, Isabel] Genome Quebec Innovat Ctr, Montreal, PQ, Canada.
[Freedman, Matthew] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Infante-Rivard, Claire] McGill Univ, Dept Epidemiol Biostat & Occupat Hlth, Fac Med, Montreal, PQ, Canada.
RP Little, J (reprint author), Univ Ottawa, Dept Epidemiol & Community Med, 451 Smyth Rd, Ottawa, ON K1H 8M5, Canada.
EM jlittle@uottawa.ca
RI Ioannidis, John/G-9836-2011; Higgins, Julian/H-4008-2011; Stewart,
Alexandre/A-5677-2011; Grimshaw, Jeremy/D-8726-2013; McLaughlin,
John/E-4577-2013; Zou, Guangyong/K-6408-2013; Paterson,
Andrew/A-4088-2011;
OI Moher , David /0000-0003-2434-4206; Higgins, Julian/0000-0002-8323-2514;
Paterson, Andrew/0000-0002-9169-118X; von Elm, Erik/0000-0002-7412-0406;
Stewart, Alexandre/0000-0003-2673-9164; Grimshaw,
Jeremy/0000-0001-8015-8243; Golding, Jean/0000-0003-2826-3307
FU Canadian Institutes of Health Research
NR 154
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U2 9
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0741-0395
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD NOV
PY 2009
VL 33
IS 7
BP 581
EP 598
DI 10.1002/gepi.20410
PG 18
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 514PB
UT WOS:000271406100003
PM 19278015
ER
PT J
AU Dupuis, J
Shi, JX
Manning, AK
Benjamin, EJ
Meigs, JB
Cupples, LA
Siegmund, D
AF Dupuis, Josee
Shi, Jianxin
Manning, Alisa K.
Benjamin, Emelia J.
Meigs, James B.
Cupples, L. Adrienne
Siegmund, David
TI Mapping Quantitative Traits in Unselected Families: Algorithms and
Examples
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE genetic linkage; quantitative trait locus; score test; extended
pedigrees; variance component analysis
ID BY-SEX INTERACTION; BODY-MASS INDEX; LINKAGE ANALYSIS;
VARIANCE-COMPONENTS; GENERAL PEDIGREES; GENETIC-LINKAGE; BLOOD-PRESSURE;
HEART-DISEASE; LOCI; REGRESSION
AB Linkage analysis has been widely used to identify from family data genetic variants influencing quantitative traits. Common approaches have both strengths and limitations. Likelihood ratio tests typically computed in variance component analysis can accommodate large families but are highly sensitive to departure from normality assumptions. Regression-based approaches are more robust but their use has primarily been restricted to nuclear families. In this paper, we develop methods for mapping quantitative traits in moderately large pedigrees. Our methods are based on the score statistic, which in contrast to the likelihood ratio statistic can use nonparametric estimators of variability to achieve robustness of the false-positive rate against departures from the hypothesized phenotypic model. Because the score statistic is easier to calculate than the likelihood ratio statistic, our basic mapping methods utilize relatively simple computer code that performs statistical analysis on output from any program that computes estimates of identity by descent. This simplicity also permits development and evaluation of methods to deal with multivariate and ordinal phenotypes, and with gene-gene and gene-environment interaction. We demonstrate our methods on simulated data and on fasting insulin, a quantitative trait measured in the Framingham Heart Study. Genet. Epidemiol. 33:617-627, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Dupuis, Josee] Boston Univ, Sch Publ Hlth, Dept Biostat, BUMC, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Evans Mem Dept Med,Whitaker Cardiovasc Inst, Boston, MA 02118 USA.
[Shi, Jianxin] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
[Benjamin, Emelia J.] NHLBIs Framingham Heart Study, Framingham, MA USA.
[Meigs, James B.] Massachusetts Gen Hosp, Dept Med, Div Gen Med, Boston, MA 02114 USA.
[Meigs, James B.] Harvard Univ, Sch Med, Boston, MA USA.
[Siegmund, David] Stanford Univ, Dept Stat, Stanford, CA 94305 USA.
RP Dupuis, J (reprint author), Boston Univ, Sch Publ Hlth, Dept Biostat, BUMC, 801 Mass Ave,3rd Floor, Boston, MA 02118 USA.
EM dupuis@bu.edu
OI Cupples, L. Adrienne/0000-0003-0273-7965; Dupuis,
Josee/0000-0003-2871-3603; Benjamin, Emelia/0000-0003-4076-2336
FU National Institute of Health [R01 HG000848, R21 DK65732, K24 DK080140];
American Diabetes Association Career Development [RO1 HL076784, 1R01
AG028321, RO1 HL064753]; National Heart, Lung, and Blood Institute's
Framingham Heart Study [N01-HC-25195]; Boston University Linux Cluster
for Genetic Analysis (LinGA); NIH NCRR [1S10RR163736-01A1]
FX Supported by the National Institute of Health R01 HG000848 (D.S.; J.D.),
R21 DK65732, K24 DK080140 (J.B.M.), an American Diabetes Association
Career Development Award (J.B.M.), RO1 HL076784 (E.J.B.), 1801 AG028321
(E.J.B.), RO1 HL064753 (E.J.B.), the National Heart, Lung, and Blood
Institute's Framingham Heart Study (Contract No. N01-HC-25195), and the
Boston University Linux Cluster for Genetic Analysis (LinGA) funded by
the NIH NCRR Shared Instrumentation grant (1S10RR163736-01A1).
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PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0741-0395
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD NOV
PY 2009
VL 33
IS 7
BP 617
EP 627
DI 10.1002/gepi.20413
PG 11
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 514PB
UT WOS:000271406100006
PM 19278016
ER
PT J
AU Boros, J
Donaldson, IJ
O'Donnell, A
Odrowaz, ZA
Zeef, L
Lupien, M
Meyer, CA
Liu, XS
Brown, M
Sharrocks, AD
AF Boros, Joanna
Donaldson, Ian J.
O'Donnell, Amanda
Odrowaz, Zaneta A.
Zeef, Leo
Lupien, Mathieu
Meyer, Clifford A.
Liu, X. Shirley
Brown, Myles
Sharrocks, Andrew D.
TI Elucidation of the ELK1 target gene network reveals a role in the
coordinate regulation of core components of the gene regulation
machinery
SO GENOME RESEARCH
LA English
DT Article
ID TRANSCRIPTION FACTORS ELK-1; TERNARY COMPLEX FACTORS; SERUM RESPONSE
FACTOR; RNA-POLYMERASE-II; EXPRESSION; PROMOTER; FAMILY; SAP-1; CHIP;
SRF
AB Transcription factors play an important role in orchestrating the activation of specific networks of genes through targeting their proximal promoter and distal enhancer regions. However, it is unclear how the specificity of downstream responses is maintained by individual members of transcription-factor families and, in most cases, what their target repertoire is. We have used ChIP-chip analysis to identify the target genes of the ETS-domain transcription factor ELK1. Two distinct modes of ELK1 target gene selection are identified; the first involves redundant promoter binding with other ETS-domain family members; the second occurs through combinatorial binding with a second transcription factor SRF, which specifies a unique group of target genes. One of the most prominent groups of genes forming the ELK1 target network includes classes involved in core gene expression control, namely, components of the basal transcriptional machinery, the spliceosome and the ribosome. Amongst the set of genes encoding the basal transcription machinery components, are a functionally linked subset of GTFs and TAFs. Our study, therefore, reveals an unsuspected level of coordinate regulation of components of the core gene expression control machinery and also identifies two different modes of promoter targeting through binding with a second transcription factor or redundant binding with other ETS-domain family members.
C1 [Boros, Joanna; Donaldson, Ian J.; O'Donnell, Amanda; Odrowaz, Zaneta A.; Zeef, Leo; Sharrocks, Andrew D.] Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England.
[Lupien, Mathieu; Brown, Myles] Dana Farber Canc Inst, Dept Med Oncol, Div Mol & Cellular Oncol, Boston, MA 02115 USA.
[Lupien, Mathieu; Brown, Myles] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Lupien, Mathieu; Brown, Myles] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Meyer, Clifford A.; Liu, X. Shirley] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Meyer, Clifford A.; Liu, X. Shirley] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
RP Sharrocks, AD (reprint author), Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England.
EM a.d.sharrocks@manchester.ac.uk
RI Sharrocks, Andrew/J-6756-2013;
OI Brown, Myles/0000-0002-8213-1658; O'Donnell, Amanda/0000-0003-3655-6126
FU Wellcome Trust; AICR; Cancer Research UK and a Royal Society-Wolfson
award
FX We thank Anne Clancy, Karren Palmer, and Leanne Wardleworth for
excellent technical assistance; Andy Hayes in the core microarray
facility; Casey Bergman and Stefan Roberts and members of our laboratory
for comments on the manuscript and stimulating discussions; Richard
Treisman for reagents; Andrew Smith ( Cold Spring Harbor Laboratory) for
help, advice, and access to DME2; and Takashi Kondo and Takeshi Hori for
access to anisomycin microarray cluster analysis gene lists. This work
was supported by grants from the Wellcome Trust, the AICR, Cancer
Research UK and a Royal Society-Wolfson award to A. D. S.
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PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI WOODBURY
PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
SN 1088-9051
J9 GENOME RES
JI Genome Res.
PD NOV
PY 2009
VL 19
IS 11
BP 1963
EP 1973
DI 10.1101/gr.093047.109
PG 11
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 514WK
UT WOS:000271426600005
PM 19687146
ER
PT J
AU Longas, MO
Mrabat, H
Hales, C
Garg, H
AF Longas, Maria O.
Mrabat, Hicham
Hales, Charles
Garg, Hari
TI N-Desulfonation of Low Molecular Weight 3-O-Acylated Heparin Decreases
Its Growth Inhibition of Pulmonary Artery Smooth Muscle Cells
SO GLYCOBIOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Glycobiology
CY NOV 12-15, 2009
CL San Diego, CA
SP Soc* Glycobiol
C1 [Longas, Maria O.] Purdue Univ Calumet, Hammond, IN USA.
[Mrabat, Hicham; Hales, Charles; Garg, Hari] Harvard Univ, Massachusetts Gen Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0959-6658
J9 GLYCOBIOLOGY
JI Glycobiology
PD NOV
PY 2009
VL 19
IS 11
MA 124
BP 1324
EP 1324
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 505PX
UT WOS:000270707700135
ER
PT J
AU Jacobson, BC
Chan, AT
Giovannucci, EL
Fuchs, CS
AF Jacobson, B. C.
Chan, A. T.
Giovannucci, E. L.
Fuchs, C. S.
TI Body mass index and Barrett's oesophagus in women
SO GUT
LA English
DT Article
ID GASTROESOPHAGEAL-REFLUX DISEASE; GASTRIC CARDIA; ABDOMINAL OBESITY;
RISK-FACTORS; INCREASING INCIDENCE; PROSPECTIVE COHORT; UNITED-STATES;
FOLLOW-UP; ADENOCARCINOMA; ASSOCIATION
AB Objective: Excess body mass is associated with symptoms of gastro-oesophageal reflux disease, and cross-sectional studies suggest an association between body mass index (BMI) and Barrett's oesophagus. The present study sought prospectively to examine the influence of BMI and other anthropomorphic measures on the risk for Barrett's oesophagus among women.
Methods: This was a prospective study of 15 861 women who participated in the Nurses' Health Study, without a history of cancer, who underwent upper gastrointestinal endoscopy for any reason between 1986 and 2004. The main outcome measures were 261 cases of pathologically confirmed specialised intestinal metaplasia within the oesophagus (Barrett's oesophagus). Self-reported data on weight were collected from biennial questionnaires. Self-reported height was collected in 1976, and self-reported waist and hip circumferences were collected in 1986.
Results: Compared with women with a BMI of 20-24.9 kg/m(2), women with a BMI of 25-29.9 had a multivariate OR for Barrett's oesophagus of 0.92 (95% CI 0.66 to 1.27), women with a BMI >= 30 had a multivariate OR of 1.52 (95% CI 1.02 to 2.28) and women with a BMI,20 had a multivariate OR of 0.92 (95% CI 0.65 to 1.31). Results were similar when controlling for symptoms of gastro-oesophageal reflux, and among the entire Nurses' Health Study cohort (n = 93 609) regardless of a history of endoscopy. In contrast, waist-to-hip ratio, waist circumference and height did not appear to be associated with Barrett's oesophagus.
Conclusions: Obese, but not overweight, women appear to be at increased risk for Barrett's oesophagus.
C1 [Jacobson, B. C.] Boston Med Ctr, Dept Med, Gastroenterol Sect, Boston, MA USA.
[Chan, A. T.] Massachusetts Gen Hosp, Dept Med, Gastrointestinal Unit, Boston, MA 02114 USA.
[Giovannucci, E. L.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Giovannucci, E. L.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Fuchs, C. S.] Dana Farber & Harvard Canc Ctr, Canc Epidemiol Program, Boston, MA USA.
RP Jacobson, BC (reprint author), Boston Univ, Med Ctr, 88 E Concord St,Room 7721, Boston, MA 02118 USA.
EM brian.jacobson@bmc.org
OI Jacobson, Brian/0000-0001-7064-2357
FU National Cancer Institute [CA087969, CA107412]; National Institutes of
Diabetes and Digestive and Kidney Diseases [DK070706]; Damon Runyon
Cancer Research Foundation Clinical Investigator Award
FX This work was supported by the National Cancer Institute (CA087969;
CA107412 to ATC) and the National Institutes of Diabetes and Digestive
and Kidney Diseases (DK070706 to BCJ). ATC is a recipient of the Damon
Runyon Cancer Research Foundation Clinical Investigator Award. The
sponsors had no role in the design and conduct of the study; collection,
management, analyses and interpretation of the data; or preparation,
review or approval of the manuscript.
NR 68
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U1 0
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PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD NOV
PY 2009
VL 58
IS 11
BP 1460
EP 1466
DI 10.1136/gut.2008.174508
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 507JG
UT WOS:000270848700008
PM 19336423
ER
PT J
AU Zinner, DE
Bolcic-Jankovic, D
Clarridge, B
Blumenthal, D
Campbell, EG
AF Zinner, Darren E.
Bolcic-Jankovic, Dragana
Clarridge, Brian
Blumenthal, David
Campbell, Eric G.
TI Participation Of Academic Scientists In Relationships With Industry
SO HEALTH AFFAIRS
LA English
DT Article
ID CONFLICTS-OF-INTEREST; NATIONAL-SURVEY; BIOMEDICAL-RESEARCH; UNIVERSITY;
POLICIES; FACULTY
AB Relationships between academic researchers and industry have received considerable attention in the past twenty years. However, current data on the prevalence, magnitude, and trends in such relationships are rare. In a mailed survey of 3,080 academic life science researchers conducted in 2007, we found that 52.8 percent have some form of relationship with industry. Life science faculty with industry research support were more productive than faculty without such support on virtually every measure. However, we also found a significant decrease in industry support of university research, which could have major consequences for the academic life science research sector. [Health Aff (Millwood). 2009; 28(6): 1814-25]
C1 [Zinner, Darren E.] Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA 02254 USA.
[Blumenthal, David] Massachusetts Gen Hosp Partners Healthcare, Inst Hlth Policy, Boston, MA USA.
RP Zinner, DE (reprint author), Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA 02254 USA.
EM ecampbell@partners.org
FU National Human Genome Research Institute of the National Institutes of
Health [1R01GM074915-01]; Brandeis University's Health Industry Forum
FX This research was supported by the National Human Genome Research
Institute of the National Institutes of Health (Grant no.
1R01GM074915-01, EricG. Campbell, principal investigator). Darren Zinner
is partially supported by Brandeis University's Health Industry Forum,
an independent policy consortium of major health care insurers, delivery
systems, and biopharmacuetical and medical device firms. However, the
research for this paper was conducted before he became part of the
group. The authors acknowledge the contributions of Sandra Feibelmann,
Steffanie Bristol, and Sowmya Rao of the Institute for Health Policy at
Massachusetts General Hospital. The views expressed herein do not
necessarily represent the views of the U.S. Department of Health and
Human Services.
NR 21
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PU PROJECT HOPE
PI BETHESDA
PA 7500 OLD GEORGETOWN RD, STE 600, BETHESDA, MD 20814-6133 USA
SN 0278-2715
J9 HEALTH AFFAIR
JI Health Aff.
PD NOV-DEC
PY 2009
VL 28
IS 6
BP 1814
EP 1825
DI 10.1377/hlthaff.28.6.1814
PG 12
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 517NR
UT WOS:000271622300026
PM 19887423
ER
PT J
AU Blumenthal, D
AF Blumenthal, David
TI PERSPECTIVE Portrait Of A Policy And Political Entrepreneur
SO HEALTH AFFAIRS
LA English
DT Article
C1 [Blumenthal, David] Massachusetts Gen Hosp Partners HealthCare Syst, Boston, MA USA.
[Blumenthal, David] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Blumenthal, David] Harvard Univ, Interfac Program Hlth Syst Improvement, Cambridge, MA 02138 USA.
EM David.Blumenthal@hhs.gov
NR 0
TC 1
Z9 1
U1 0
U2 3
PU PROJECT HOPE
PI BETHESDA
PA 7500 OLD GEORGETOWN RD, STE 600, BETHESDA, MD 20814-6133 USA
SN 0278-2715
J9 HEALTH AFFAIR
JI Health Aff.
PD NOV-DEC
PY 2009
VL 28
IS 6
BP W1037
EP W1039
DI 10.1377/hlthaff.28.6.w1037
PG 3
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 517NR
UT WOS:000271622300049
PM 19762356
ER
PT J
AU Jha, AK
DesRoches, CM
Shields, AE
Miralles, PD
Zheng, J
Rosenbaum, S
Campbell, EG
AF Jha, Ashish K.
DesRoches, Catherine M.
Shields, Alexandra E.
Miralles, Paola D.
Zheng, Jie
Rosenbaum, Sara
Campbell, Eric G.
TI Evidence Of An Emerging Digital Divide Among Hospitals That Care For The
Poor
SO HEALTH AFFAIRS
LA English
DT Article
ID ELECTRONIC HEALTH RECORDS; INFORMATION-TECHNOLOGY; AMBULATORY-CARE;
NATIONAL-SURVEY; UNITED-STATES; COSTS; BENEFITS; QUALITY; PHYSICIANS;
EFFICIENCY
AB Some hospitals that disproportionately care for poor patients are falling behind in adopting electronic health records (EHRs). Data from a national survey indicate early evidence of an emerging digital divide: U. S. hospitals that provide care to large numbers of poor patients also had minimal use of EHRs. These same hospitals lagged others in quality performance as well, but those with EHR systems seemed to have eliminated the quality gap. These findings suggest that adopting EHRs should be a major policy goal of health reform measures targeting hospitals that serve large populations of poor patients. [Health Aff (Millwood). 2009; 28(6): w1160-70 (published online 26 October 2009; 10.1377/hlthaff.28.6.w1160)]
C1 [Jha, Ashish K.; Zheng, Jie] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[DesRoches, Catherine M.; Campbell, Eric G.] Massachusetts Gen Hosp, Inst Hlth Policy, Boston, MA 02114 USA.
[Rosenbaum, Sara] George Washington Univ, Sch Publ Hlth & Hlth Serv, Washington, DC USA.
RP Jha, AK (reprint author), Harvard Univ, Sch Publ Hlth, 665 Huntington Ave, Boston, MA 02115 USA.
EM ajha@hsph.harvard.edu
FU Office of the National Coordinator for Health Information Technology in
the U.S. Department of Health and Human Services; Robert Wood Johnson
Foundation
FX This work was supported by the Office of the National Coordinator for
Health Information Technology in the U.S. Department of Health and Human
Services and by the Robert Wood Johnson Foundation. Ashish Jha provides
consulting support for UpToDate Inc. The authors report no other
potential conflicts of interest relevant to this work.
NR 23
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PI BETHESDA
PA 7500 OLD GEORGETOWN RD, STE 600, BETHESDA, MD 20814-6133 USA
SN 0278-2715
J9 HEALTH AFFAIR
JI Health Aff.
PD NOV-DEC
PY 2009
VL 28
IS 6
BP W1160
EP W1170
DI 10.1377/hlthaff.28.6.w1160
PG 11
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 517NR
UT WOS:000271622300062
PM 19858142
ER
PT J
AU Pizer, SD
Frakt, AB
Iezzoni, LI
AF Pizer, Steven D.
Frakt, Austin B.
Iezzoni, Lisa I.
TI Uninsured Adults With Chronic Conditions Or Disabilities: Gaps In Public
Insurance Programs
SO HEALTH AFFAIRS
LA English
DT Article
ID HEALTH-INSURANCE; US ADULTS; COVERAGE; ACCESS; CARE; PROSPECTS; RISK
AB Among nonelderly U. S. adults (ages 25-61), uninsurance rates increased from 13.7 percent in 2000 to 16.0 percent in 2005. Despite the existence of public insurance programs, rates remained high for low-income people reporting serious health conditions (25 percent across years) or disabilities (15 percent). Residents of southern states had even higher rates (32 percent with health conditions, 22 percent with disabilities). Those who did not belong to a federally mandated Medicaid eligibility category were about twice as likely as others to be uninsured overall, and uninsurance among this group increased more rapidly over time. These regional and categorical differences reflect gaps in current policy that pose challenges for incremental health reform. [Health Aff (Millwood). 2009; 28(6): w1141-50 (published online 20 October 2009; 10.1377/hlthaffairs.28.6.w1141)]
C1 [Pizer, Steven D.; Frakt, Austin B.] US Dept Vet Affairs, Boston, MA USA.
[Iezzoni, Lisa I.] Harvard Univ, Sch Med, Inst Hlth Policy, Boston, MA USA.
[Iezzoni, Lisa I.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Pizer, SD (reprint author), US Dept Vet Affairs, Boston, MA USA.
EM Pizer@bu.edu
FU Agency for Healthcare Research and Quality (AHRQ) [R01 HS01594-1-01];
Health Services Research and Development Service of the U.S. Department
of Veterans Affairs [IIR 06-238]
FX Preliminary results from this research were presented at the Academy
Health Annual Research Meeting, 29 June 2009, in Chicago, Illinois. The
authors gratefully acknowledge financial support from the Agency for
Healthcare Research and Quality (AHRQ) (R01 HS01594-1-01) and from the
Health Services Research and Development Service of the U.S. Department
of Veterans Affairs (VA) (IIR 06-238). They thank Mari-Lynn Drainoni as
well as the editors and two anonymous reviewers for helpful comments on
previous drafts. The opinions expressed in this paper are those of the
authors and do not necessarily reflect the official positions of AHRQ,
the VA, Boston University, or Harvard University.
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U1 0
U2 3
PU PROJECT HOPE
PI BETHESDA
PA 7500 OLD GEORGETOWN RD, STE 600, BETHESDA, MD 20814-6133 USA
SN 0278-2715
J9 HEALTH AFFAIR
JI Health Aff.
PD NOV-DEC
PY 2009
VL 28
IS 6
BP W1141
EP W1150
DI 10.1377/hlthaff.28.6.w1141
PG 10
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 517NR
UT WOS:000271622300060
PM 19843552
ER
PT J
AU Melcher, JR
Levine, RA
Bergevin, C
Norris, B
AF Melcher, Jennifer R.
Levine, Robert A.
Bergevin, Christopher
Norris, Barbara
TI The auditory midbrain of people with tinnitus: Abnormal sound-evoked
activity revisited
SO HEARING RESEARCH
LA English
DT Article
DE Hyperacusis; Midbrain; Phantom sensation; fMRI; Neuroimaging
ID HUMAN BRAIN-STEM; FMRI ACTIVATION; PSYCHOMETRIC PROPERTIES; LATERALIZED
TINNITUS; INFERIOR COLLICULUS; NOISE EXPOSURE; ACOUSTIC NOISE; SCANNER
NOISE; LOUDNESS; PLASTICITY
AB Sound-evoked fMRI activation of the inferior colliculi (IC) was compared between tinnitus and non-tinnitus subjects matched in threshold (normal), age, depression, and anxiety. Subjects were stimulated with broadband sound in an "on/off" fMRI paradigm with and without on-going sound from the scanner coolant pump.
(1) With pump sounds off. the tinnitus; group showed greater stimulus-evoked activation of the IC than the non-tinnitus group, suggesting abnormal gain within the auditory pathway of tinnitus subjects.
(2) Having pump sounds on reduced activation in the tinnitus, but not the non-tinnitus; group. This result suggests response saturation in tinnitus subjects, possibly occurring because abnormal gain increased response amplitude to an upper limit.
(3) In contrast to Melcher et al. (2000), the ratio of activation between right and left IC did not differ significantly between tinnitus and non-tinnitus subjects or in a manner dependent on tinnitus laterality. However, new data from subjects imaged previously by Melcher et al. suggest a possible tinnitus subgroup with abnormally asymmetric function of the IC.
The present and previous data together suggest elevated responses to sound in the IC are common among those with tinnitus and normal thresholds, while abnormally asymmetric activation is not, even among those with lateralized tinnitus. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Melcher, Jennifer R.; Levine, Robert A.; Bergevin, Christopher; Norris, Barbara] Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA.
[Melcher, Jennifer R.; Bergevin, Christopher] MIT, Harvard Mit Div Hlth Sci & Technol, Speech & Hearing Biosci & Technol Program, Cambridge, MA 02139 USA.
[Melcher, Jennifer R.; Levine, Robert A.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
[Levine, Robert A.] Massachusetts Gen Hosp, Neurol Serv, Boston, MA 02114 USA.
RP Melcher, JR (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA.
EM jennifer_melcher@meei.harvard.edu
FU Tinnitus Research Consortium; American Tinnitus Association; Royal
National Institute for Deaf People; Tinnitus Research Initiative; Jack
and Shelley Blais; Kenneth Griffin; NIH/NIDCD [P30DC005209]; National
Center for Research Resources [P41RR14075]; Mental Illness and
Neuroscience Discovery (MIND) Institute
FX We thank Irina Sigalovsky for her assistance in performing some of the
experiments and Inge Knudson, Jianwen Gu and Christopher Shera for their
comments on an earlier version of this manuscript. Support was provided
by the Tinnitus Research Consortium, American Tinnitus Association,
Royal National Institute for Deaf People, Tinnitus Research Initiative,
Jack and Shelley Blais, Kenneth Griffin, and NIH/NIDCD P30DC005209.
Partial support was also provided by the National Center for Research
Resources (P41RR14075) and the Mental Illness and Neuroscience Discovery
(MIND) Institute.
NR 47
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U1 1
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-5955
J9 HEARING RES
JI Hear. Res.
PD NOV
PY 2009
VL 257
IS 1-2
BP 63
EP 74
DI 10.1016/j.heares.2009.08.005
PG 12
WC Audiology & Speech-Language Pathology; Neurosciences;
Otorhinolaryngology
SC Audiology & Speech-Language Pathology; Neurosciences & Neurology;
Otorhinolaryngology
GA 511QB
UT WOS:000271180200007
PM 19699287
ER
PT J
AU Friedman, LS
Brandt, LJ
Elta, GH
Fitz, JG
Gores, GJ
Katz, PO
Kuemmerle, JF
Pardi, DS
Vargo, JJ
Stolar, MH
AF Friedman, Lawrence S.
Brandt, Lawrence J.
Elta, Grace H.
Fitz, J. Gregory
Gores, Gregory J.
Katz, Philip O.
Kuemmerle, John F.
Pardi, Darrell S.
Vargo, John J.
Stolar, Michael H.
CA Task Force
TI Report of the Multisociety Task Force on GI Training
SO HEPATOLOGY
LA English
DT Article
C1 [Friedman, Lawrence S.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Friedman, Lawrence S.] Tufts Univ, Sch Med, Medford, MA 02155 USA.
[Friedman, Lawrence S.] Newton Wellesley Hosp, Newton, MA USA.
[Friedman, Lawrence S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Brandt, Lawrence J.] Montefiore Med Ctr, New York, NY USA.
[Brandt, Lawrence J.] Albert Einstein Coll Med, Bronx, NY USA.
[Elta, Grace H.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Fitz, J. Gregory] Univ Texas SW Med Sch, Dallas, TX USA.
[Gores, Gregory J.; Pardi, Darrell S.] Mayo Clin, Coll Med Rochester, Rochester, MN USA.
[Katz, Philip O.] Albert Einstein Med Ctr, Philadelphia, PA 19141 USA.
[Katz, Philip O.] Thomas Jefferson Univ, Philadelphia, PA USA.
[Kuemmerle, John F.] Virginia Commonwealth Univ, Richmond, VA 23284 USA.
[Vargo, John J.] Cleveland Clin, Lerner Coll Med, Cleveland, OH USA.
[Vargo, John J.] Cleveland Clin Fdn, Cleveland, OH USA.
RP Friedman, LS (reprint author), Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
NR 0
TC 4
Z9 4
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD NOV
PY 2009
VL 50
IS 5
BP 1325
EP 1329
DI 10.1002/hep.23257
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 516TK
UT WOS:000271565600001
ER
PT J
AU Freedman, ND
Everhart, JE
Lindsay, KL
Ghany, MG
Curto, TM
Shiffman, ML
Lee, WM
Lok, AS
Di Bisceglie, AM
Bonkovsky, HL
Hoefs, JC
Dienstag, JL
Morishima, C
Abnet, CC
Sinha, R
AF Freedman, Neal D.
Everhart, James E.
Lindsay, Karen L.
Ghany, Marc G.
Curto, Teresa M.
Shiffman, Mitchell L.
Lee, William M.
Lok, Anna S.
Di Bisceglie, Adrian M.
Bonkovsky, Herbert L.
Hoefs, John C.
Dienstag, Jules L.
Morishima, Chihiro
Abnet, Christian C.
Sinha, Rashmi
CA HALT-C Trial Grp
TI Coffee Intake Is Associated with Lower Rates of Liver Disease
Progression in Chronic Hepatitis C
SO HEPATOLOGY
LA English
DT Article
ID ALANINE AMINOTRANSFERASE ACTIVITY; GAMMA-GLUTAMYL-TRANSFERASE; TEA
CONSUMPTION; HEPATOCELLULAR-CARCINOMA; UNITED-STATES; RISK; CAFFEINE;
INHIBITION; CIRRHOSIS; PEGINTERFERON
AB Higher coffee consumption has been associated inversely with the incidence of chronic liver disease in population studies. We examined the relationship of coffee consumption with liver disease progression in individuals with advanced hepatitis C-related liver disease. Baseline coffee and tea intake were assessed in 766 participants of the Hepatitis C Antiviral Long-Term Treatment against Cirrhosis (HALT-C) trial who had hepatitis C-related bridging fibrosis or cirrhosis on liver biopsy and failed to achieve a sustained virological response to peginterferon plus ribavirin treatment. Participants were followed for 3.8 years for clinical outcomes and, for those without cirrhosis, a 2-point increase in Ishak fibrosis score on protocol biopsies. At baseline, higher coffee consumption was associated with less severe steatosis on biopsy, lower serum aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio, alpha-fetoprotein, insulin, and homeostatic model assessment (HOMA2) score, and higher albumin (P < 0.05 for all). Two hundred thirty patients had outcomes. Outcome rates declined with increasing coffee intake: 11.1/100 person-years for none, 12.1 for less than 1 cup/day, 8.2 for 1 to fewer than 3 cups/day, and 6.3 for 3 or more cups/day (P-trend = 0.0011). Relative risks (95% confidence intervals) were 1.11 (0.76-1.61) for less than I cup/day; 0.70 (0.48-1.02) for I to fewer than 3 cups/day; and 0.47 (0.27-0.85) for 3 or more cups/day (P-trend = 0.0003) versus not drinking. Risk estimates did not vary by treatment assignment or cirrhosis status at baseline. Tea intake was not associated with outcomes. Conclusion: In a large prospective study of participants with advanced hepatitis C-related liver disease, regular coffee consumption was associated with lower rates of disease progression. (HEPATOLOGY 2009;50:1360-1369.)
C1 [Freedman, Neal D.; Abnet, Christian C.; Sinha, Rashmi] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Everhart, James E.] NIDDK, Div Digest Dis & Nutr, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Lindsay, Karen L.] Univ So Calif, Keck Sch Med, Div Gastrointestinal & Liver Dis, Los Angeles, CA 90033 USA.
[Ghany, Marc G.] NIDDK, Liver Dis Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Curto, Teresa M.] New England Res Inst, Watertown, MA 02172 USA.
[Shiffman, Mitchell L.] Virginia Commonwealth Univ, Med Ctr, Hepatol Sect, Richmond, VA USA.
[Lee, William M.] Univ Texas SW Med Ctr Dallas, Div Digest & Liver Dis, Dallas, TX 75390 USA.
[Lok, Anna S.] Univ Michigan, Med Ctr, Div Gastroenterol, Ann Arbor, MI USA.
[Di Bisceglie, Adrian M.] St Louis Univ, Sch Med, Div Gastroenterol & Hepatol, St Louis, MO USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Med, Farmington, CT USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Dept Mol & Struct Biol, Farmington, CT USA.
[Bonkovsky, Herbert L.] Univ Connecticut, Ctr Hlth, Liver Biliary Pancreat Ctr, Farmington, CT USA.
[Hoefs, John C.] Univ Calif Irvine, Div Gastroenterol, Irvine, CA USA.
[Dienstag, Jules L.] Massachusetts Gen Hosp, Gastrointestinal Unit, Med Serv, Boston, MA 02114 USA.
[Dienstag, Jules L.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Morishima, Chihiro] Univ Washington, Dept Lab Med, Div Virol, Seattle, WA 98195 USA.
RP Freedman, ND (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, 6120 Execut Blvd,EPS-320,MSC 7232, Rockville, MD 20852 USA.
EM freedmanne@mail.nih.gov
RI Abnet, Christian/C-4111-2015; Sinha, Rashmi/G-7446-2015; Freedman,
Neal/B-9741-2015;
OI Abnet, Christian/0000-0002-3008-7843; Sinha, Rashmi/0000-0002-2466-7462;
Freedman, Neal/0000-0003-0074-1098; Yang, Shuman/0000-0002-9638-0890
FU National Institute of Diabetes and Digestive and Kidney Diseases;
National Institute of Allergy and Infectious Diseases; National Cancer
Institute; National Center for Minority Health and Health Disparities;
General Clinical Research Center; National Center for Research
Resources, National Institutes of Health
FX Supported by the National Institute of Diabetes and Digestive and Kidney
Diseases. Additional support was provided by the National Institute of
Allergy and Infectious Diseases, the National Cancer Institute, the
National Center for Minority Health and Health Disparities and by
General Clinical Research Center grants from the National Center for
Research Resources, National Institutes of Health. This research was
also supported in part by the Intramural Research Program of the
National Cancer Institute. Additional funding to conduct this study was
supplied by Hoffmann-La Roche, Inc., through a Cooperative Research and
Development Agreement with the National Institutes of Health. The
funding organizations bad no role in the design and conduct of the
study; the collection, analysis, and interpretation of the data; or the
preparation, review, or approval of the manuscript.
NR 42
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U1 0
U2 5
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD NOV
PY 2009
VL 50
IS 5
BP 1360
EP 1369
DI 10.1002/hep.23162
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 516TK
UT WOS:000271565600008
PM 19676128
ER
PT J
AU Kim, DI
Manoach, DS
Mathalon, DH
Turner, JA
Mannell, M
Brown, GG
Ford, JM
Gollub, RL
White, T
Wible, C
Belger, A
Bockholt, HJ
Clark, VP
Lauriello, J
O'Leary, D
Mueller, BA
Lim, KO
Andreasen, N
Potkin, SG
Calhoun, VD
AF Kim, Dae Il
Manoach, Dara S.
Mathalon, Daniel H.
Turner, Jessica A.
Mannell, Maggie
Brown, Greg G.
Ford, Judith M.
Gollub, Randy L.
White, Tonya
Wible, Cynthia
Belger, Aysenil
Bockholt, H. Jeremy
Clark, Vince P.
Lauriello, John
O'Leary, Daniel
Mueller, Bryon A.
Lim, Kelvin O.
Andreasen, Nancy
Potkin, Steve G.
Calhoun, Vince D.
TI Dysregulation of Working Memory and Default-Mode Networks in
Schizophrenia Using Independent Component Analysis, an fBIRN and MCIC
Study
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE ICA; schizophrenia; working memory; functional connectivity; fBIRN;
MCIC; auditory oddball; Sternberg
ID DORSOLATERAL PREFRONTAL CORTEX; TASK-INDUCED DEACTIVATION; RESTING-STATE
NETWORKS; FUNCTIONAL MRI DATA; COGNITIVE CONTROL; BLIND SEPARATION;
MENTAL-DISORDERS; CORTICAL REGIONS; TIME-SERIES; HUMAN BRAIN
AB Deficits in working memory (WM) are a consistent neurocognitive marker for schizophrenia. Previous studies have suggested that WM is the product of coordinated activity in distributed functionally connected brain regions. Independent component analysis (ICA) is a data-driven approach that can identify temporally coherent networks that underlie fMRI activity. We applied ICA to an fMRI dataset for 115 patients with chronic schizophrenia and 130 healthy controls by performing the Sternberg Item Recognition Paradigm. Here, we describe the first results using ICA to identify differences in the function of WM networks in schizophrenia compared to controls. ICA revealed six networks that showed significant differences between patients with schizophrenia and healthy controls. Four of these networks were negatively task-correlated and showed deactivation across the posterior cingulate, precuneus, medial prefrontal cortex, anterior cingulate, inferior parietal lobules, and parahippocampus. These networks comprise brain regions known as the default-mode network (DMN), a well-characterized set of regions shown to be active during internal modes of cognition and implicated in schizophrenia. Two networks were positively task-correlated, with one network engaging WM regions such as bilateral DLPFC and inferior parietal lobules while the other network engaged primarily the cerebellum Our results Suggest that DLPFC dysfunction in schizophrenia might be lateralized to the left and intrinsically tied to other regions such as the inferior parietal lobule and cingulate gyrus. Furthermore, we found that DMN dysfunction in schizophrenia exists across multiple subnetworks of the DMN and that these subnetworks are individually relevant to the pathophysiology of schizophrenia. In summary, this large multsite study identified multiple temporally coherent networks, which are aberrant in schizophrenia versus healthy controls and suggests that both task-correlated and task-anticorrelated networks may serve as potential biomarkers. Himi Brain Mapp 30:3795-3811, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Kim, Dae Il; Mannell, Maggie; Bockholt, H. Jeremy; Clark, Vince P.; Calhoun, Vince D.] Mind Res Network, Albuquerque, NM 87131 USA.
[Manoach, Dara S.; Gollub, Randy L.] Massachusetts Gen Hosp, Dept Psychiat, Neuroimaging Div, Charlestown, MA USA.
[Manoach, Dara S.; Gollub, Randy L.] Harvard Univ, Sch Med, Athinoula Martinos Ctr Biomed Imaging, Boston, MA USA.
[Mathalon, Daniel H.; Ford, Judith M.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
[Turner, Jessica A.; Potkin, Steve G.] Univ Calif Irvine, Dept Psychiat & Human Behav, Irvine, CA 92717 USA.
[Brown, Greg G.] Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA.
[White, Tonya; Mueller, Bryon A.; Lim, Kelvin O.] Univ Minnesota, Dept Psychiat, Med Ctr, Minneapolis, MN 55455 USA.
[Wible, Cynthia] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Belger, Aysenil] Duke Univ, Med Ctr, Brain Imaging & Anal Ctr, Durham, NC USA.
[Clark, Vince P.; Lauriello, John] Univ New Mexico, Dept Psychiat, Albuquerque, NM 87131 USA.
[O'Leary, Daniel; Andreasen, Nancy] Univ Iowa, Dept Psychiat, Iowa City, IA 52242 USA.
[Calhoun, Vince D.] Univ New Mexico, Dept Elect & Comp Engn, Albuquerque, NM 87131 USA.
[Clark, Vince P.] Univ New Mexico, Dept Psychol, Albuquerque, NM 87131 USA.
[Belger, Aysenil] Univ N Carolina, Chapel Hill, NC USA.
RP Kim, DI (reprint author), Mind Res Network, 1101 Yale Blvd NE, Albuquerque, NM 87131 USA.
EM dkim@mm.org; vcalhoun@unm.edu
RI Clark, Vincent/B-3343-2010; Potkin, Steven/A-2021-2013; Calhoun,
Vince/H-7146-2013; Turner, Jessica/H-7282-2015;
OI Clark, Vincent/0000-0002-9151-2102; Calhoun, Vince/0000-0001-9058-0747;
Turner, Jessica/0000-0003-0076-8434; Mathalon,
Daniel/0000-0001-6090-4974; Gollub, Randy L./0000-0002-9434-4044;
Potkin, Steven/0000-0003-1028-1013; Belger, Aysenil/0000-0003-2687-1966
FU National Institutes of Health [1 R01 EB 000840]; NCRR [U24-RR021992];
DOE [DE-FG02-99ER62764]
FX National Institutes of Health; Contract grant number: 1 R01 EB 000840;
Contract grant sponsor: NCRR; Contract grant number: U24-RR021992;
Contract grant sponsor: DOE; Contract grant number: DE-FG02-99ER62764.
NR 63
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U1 4
U2 14
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1065-9471
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD NOV
PY 2009
VL 30
IS 11
BP 3795
EP 3811
DI 10.1002/hbm.20807
PG 17
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 516TH
UT WOS:000271565300028
PM 19434601
ER
PT J
AU Oh, JS
Kubicki, M
Rosenberger, G
Bouix, S
Levitt, JJ
McCarley, RW
Westin, CF
Shenton, ME
AF Oh, Jungsu S.
Kubicki, Marek
Rosenberger, Gudrun
Bouix, Sylvain
Levitt, James J.
McCarley, Robert W.
Westin, Carl-Fredrik
Shenton, Martha E.
TI Thalamo-Frontal White Matter Alterations in Chronic Schizophrenia: A
Quantitative Diffusion Tractography Study
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE diffusion tensor imaging (DTI); Brodmann area (BA); internal capsule
(IC); parameterization; chronic schizophrenia
ID ASSOCIATION FIBER PATHWAYS; HUMAN BRAIN; COORDINATE SYSTEM;
CORPUS-CALLOSUM; WORKING-MEMORY; TENSOR MRI; CORTEX; INTEGRITY;
ABNORMALITIES; CONNECTIONS
AB Diffusion tensor imaging (DTI) and fiber tractography are useful tools for reconstructing white matter tracts (WMT) in the brain. Previous tractography studies have sought to segment reconstructed WMT into anatomical structures using several approaches, but quantification has been limited to extracting mean values of diffusion indices. Delineating WMT in schizophrenia is of particular interest because schizophrenia has been hypothesized to be a disorder of disrupted connectivity, especially between frontal and temporal regions of the brain. In this study, we aim to differentiate diffusion properties of thalamo-frontal pathways in schizophrenia from normal controls. We present a quantitative group comparison method, which combines the strengths of both tractography-based and voxel-based studies. Our algorithm extracts white matter pathways using whole brain tractography. Functionally relevant bundles are selected and parsed from the resulting set of tracts, using an internal capsule (IC) region of interest (ROI) as "source", and different Brodmann area (BA) ROIs as "targets". The resulting bundles are then longitudinally parameterized so that diffusion properties can be measured and compared along the WMT. Using this processing pipeline, we were able to find altered diffusion properties in male patients with chronic schizophrenia in terms of fractional anisotropy (FA) decreases and mean diffusivity (MD) increases in precise and functionally relevant locations. These findings suggest that our method can enhance the regional and functional specificity of DTI group studies, thus improving our understanding of brain function. Hum Brain Mapp 30:3812-3825, 2009. (C) 2009 Wiley-Liss. Inc.
C1 [Oh, Jungsu S.; Kubicki, Marek; Rosenberger, Gudrun; Bouix, Sylvain; Levitt, James J.; Shenton, Martha E.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Psychiat,Psychiat Neuroimaging Lab, Boston, MA 02215 USA.
[Oh, Jungsu S.] Seoul Natl Univ, Brain Korea Div Human Life Sci 21, Seoul, South Korea.
[Kubicki, Marek; Levitt, James J.; McCarley, Robert W.; Shenton, Martha E.] VA Boston Healthcare Syst, Clin Neurosci Div, Neurosci Lab, Brockton, MA USA.
[Rosenberger, Gudrun] Med Univ Innsbruck, Dept Gen Psychiat, Innsbruck, Austria.
[Westin, Carl-Fredrik] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Radiol,Lab Math Imaging, Boston, MA 02215 USA.
[Shenton, Martha E.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Radiol,MRI Div,Surg Planning Lab, Boston, MA 02215 USA.
RP Shenton, ME (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Psychiat,Psychiat Neuroimaging Lab, 1249 Boylston St, Boston, MA 02215 USA.
EM shenton@bwh.harvard.edu
RI McCarley, Robert/N-5562-2014;
OI McCarley, Robert/0000-0001-5705-7495; Bouix,
Sylvain/0000-0003-1326-6054; Oh, Jungsu/0000-0002-1925-8103
FU Korea Research Foundation; Korean Government [MOEHRD
KRF2006-352-D00220]; Second Stage Brain Korea 21 Project in 2008
(Division of Human Life Science), National Institute of Health [K05
MH070047, R01 MH 50740, P50 MH080272-01]; National Alliance for Medical
Image Computing; NIH Roadmap for Medical Research Award [U54 EB005149];
Department of Veterans Affairs Merit Awards; VA Schizophrenia Center
FX Contract grant sponsors: Korea Research Foundation by the Korean
Government; Contract grant number: MOEHRD KRF2006-352-D00220; Contract
grant sponsors: Second Stage Brain Korea 21 Project in 2008 (Division of
Human Life Science), National Institute of Health; Contract grant
numbers: K05 MH070047, R01 MH 50740, P50 MH080272-01; Contract grant
sponsor: National Alliance for Medical Image Computing, and NIH Roadmap
for Medical Research Award; Contract grant number: U54 EB005149;
Contract grant sponsors: Department of Veterans Affairs Merit Awards; VA
Schizophrenia Center.
NR 67
TC 53
Z9 54
U1 2
U2 8
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1065-9471
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD NOV
PY 2009
VL 30
IS 11
BP 3812
EP 3825
DI 10.1002/hbm.20809
PG 14
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 516TH
UT WOS:000271565300029
PM 19449328
ER
PT J
AU Saran, N
Lyszkiewicz, M
Pommerencke, J
Witzlau, K
Vakilzadeh, R
von Boehmer, H
Krueger, A
AF Saran, Namita
Lyszkiewicz, Marcin
Pommerencke, Jens
Witzlau, Katrin
Vakilzadeh, Ramin
von Boehmer, Harald
Krueger, Andreas
TI Multiple extra-thymic precursors contribute to T cell development with
different kinetics
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
CT Combined Meeting of the 17th
European-Society-of-Gene-and-Cell-Therapy/16th
German-Society-for-Gene-Therapy/4th
German-Society-for-Stem-Cell-Research
CY NOV 21-25, 2009
CL Hannover, GERMANY
SP Int Soc Cellular Therapy, European Branch, European Soc Gene & Cell Therapy, German Soc Gene Therapy, German Soc Stem Cell Res, BD Biosci, Biotech GmbH, Genethon, Cellectis, EUFETS, Lonza, Oxford BioMedica, Peprotech, Plasmidfactory, Regenx Biosci, Rentschler, Sartorius Stedim, StemCell Technologies
C1 [Saran, Namita; Lyszkiewicz, Marcin; Pommerencke, Jens; Witzlau, Katrin; Vakilzadeh, Ramin; Krueger, Andreas] Hannover Med Sch, Hannover, Germany.
[von Boehmer, Harald] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
EM krueger.andreas@mh-hannover.de
RI Krueger, Andreas/B-9427-2009
OI Krueger, Andreas/0000-0001-7873-7334
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 NOV
PY 2009
VL 20
IS 11
BP 1466
EP 1466
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 515BJ
UT WOS:000271441000336
ER
PT J
AU Dirice, E
Sanlioglu, A
Kahraman, S
Ozturk, S
Balci, M
Omer, A
Griffith, T
Sanlioglu, S
AF Dirice, Ercument
Sanlioglu, Ahter
Kahraman, Sevim
Ozturk, Saffet
Balci, Mustafa
Omer, Abdulkadir
Griffith, Thomas
Sanlioglu, Salih
TI Adenovirus mediated TRAIL gene therapy approach provides sustained
insulin expression in STZ-induced diabetic rats
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
CT Combined Meeting of the 17th
European-Society-of-Gene-and-Cell-Therapy/16th
German-Society-for-Gene-Therapy/4th
German-Society-for-Stem-Cell-Research
CY NOV 21-25, 2009
CL Hannover, GERMANY
SP Int Soc Cellular Therapy, European Branch, European Soc Gene & Cell Therapy, German Soc Gene Therapy, German Soc Stem Cell Res, BD Biosci, Biotech GmbH, Genethon, Cellectis, EUFETS, Lonza, Oxford BioMedica, Peprotech, Plasmidfactory, Regenx Biosci, Rentschler, Sartorius Stedim, StemCell Technologies
ID PROSTATE CARCINOMA-CELLS; APOPTOSIS; SIRNA
C1 [Ozturk, Saffet] Akdeniz Univ, Fac Med, Dept Histol & Embryol, Antalya, Turkey.
[Balci, Mustafa] Akdeniz Univ, Fac Med, Div Endocrinol & Metab Dis, Antalya, Turkey.
[Omer, Abdulkadir] Harvard Univ, Sch Med, Joslin Diabet Ctr, Cambridge, MA 02138 USA.
[Griffith, Thomas] Univ Iowa, Dept Urol, Iowa City, IA 52242 USA.
[Griffith, Thomas] Univ Iowa, Dept Urol, Iowa City, IA 52242 USA.
EM sanlioglu@akdeniz.edu.tr
RI Ozturk, Saffet/C-1239-2016; Sanlioglu, Salih/F-9305-2016
NR 4
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 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD NOV
PY 2009
VL 20
IS 11
BP 1471
EP 1472
PG 2
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 515BJ
UT WOS:000271441000351
ER
PT J
AU Kahraman, S
Hapil, FZ
Aydin, C
Bisgin, A
Dirice, E
Griffith, TS
Sanlioglu, AD
Sanlioglu, S
AF Kahraman, Sevim
Hapil, Fatma Zehra
Aydin, Cigdem
Bisgin, Atil
Dirice, Ercument
Griffith, Thomas S.
Sanlioglu, Ahter Dilsad
Sanlioglu, Salih
TI Tracing of the fate of allogeneic islet grafts via CCD camera
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
CT Combined Meeting of the 17th
European-Society-of-Gene-and-Cell-Therapy/16th
German-Society-for-Gene-Therapy/4th
German-Society-for-Stem-Cell-Research
CY NOV 21-25, 2009
CL Hannover, GERMANY
SP Int Soc Cellular Therapy, European Branch, European Soc Gene & Cell Therapy, German Soc Gene Therapy, German Soc Stem Cell Res, BD Biosci, Biotech GmbH, Genethon, Cellectis, EUFETS, Lonza, Oxford BioMedica, Peprotech, Plasmidfactory, Regenx Biosci, Rentschler, Sartorius Stedim, StemCell Technologies
C1 [Kahraman, Sevim; Hapil, Fatma Zehra; Aydin, Cigdem; Bisgin, Atil; Sanlioglu, Ahter Dilsad; Sanlioglu, Salih] Akdeniz Univ, Fac Med, Human Gene Therapy Div Med Genet, Antalya, Turkey.
[Dirice, Ercument] Harvard Univ, Sch Med, Joslin Diabet Ctr, Cambridge, MA 02138 USA.
[Griffith, Thomas S.] Univ Iowa, Dept Urol, Iowa City, IA 52242 USA.
EM sanlioglu@akdeniz.edu.tr
RI Sanlioglu, Salih/F-9305-2016
NR 2
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 NOV
PY 2009
VL 20
IS 11
BP 1479
EP 1479
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 515BJ
UT WOS:000271441000371
ER
PT J
AU Kahraman, S
Hapil, FZ
Ertosun, MG
Dirice, E
Sanlioglu, AD
Sanlioglu, S
AF Kahraman, Sevim
Hapil, Fatma Zehra
Ertosun, Mustafa Gokhan
Dirice, Ercument
Sanlioglu, Ahter Dilsad
Sanlioglu, Salih
TI In vivo fluorescence imaging as a method to assess pancreatic islet
xenograft failure
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
CT Combined Meeting of the 17th
European-Society-of-Gene-and-Cell-Therapy/16th
German-Society-for-Gene-Therapy/4th
German-Society-for-Stem-Cell-Research
CY NOV 21-25, 2009
CL Hannover, GERMANY
SP Int Soc Cellular Therapy, European Branch, European Soc Gene & Cell Therapy, German Soc Gene Therapy, German Soc Stem Cell Res, BD Biosci, Biotech GmbH, Genethon, Cellectis, EUFETS, Lonza, Oxford BioMedica, Peprotech, Plasmidfactory, Regenx Biosci, Rentschler, Sartorius Stedim, StemCell Technologies
C1 [Kahraman, Sevim; Hapil, Fatma Zehra; Ertosun, Mustafa Gokhan; Sanlioglu, Ahter Dilsad; Sanlioglu, Salih] Akdeniz Univ, Fac Med, Human Gene Therapy Div Med Genet, Antalya, Turkey.
[Dirice, Ercument] Harvard Univ, Sch Med, Joslin Diabet Ctr, Cambridge, MA 02138 USA.
EM sanlioglu@akdeniz.edu.tr
RI Sanlioglu, Salih/F-9305-2016
NR 2
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 NOV
PY 2009
VL 20
IS 11
BP 1479
EP 1479
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 515BJ
UT WOS:000271441000370
ER
PT J
AU Kahraman, S
Dirice, E
Sanlioglu, A
Yoldas, B
Bagci, H
Erkilic, M
Griffith, T
Sanlioglu, S
AF Kahraman, Sevim
Dirice, Ercument
Sanlioglu, Ahter
Yoldas, Burcak
Bagci, Huseyin
Erkilic, Metin
Griffith, Thomas
Sanlioglu, Salih
TI Monitoring of systemic delivery of adenovirus mediated EGFP transgene
expression in mice using fluorescence imaging
SO HUMAN GENE THERAPY
LA English
DT Meeting Abstract
CT Combined Meeting of the 17th
European-Society-of-Gene-and-Cell-Therapy/16th
German-Society-for-Gene-Therapy/4th
German-Society-for-Stem-Cell-Research
CY NOV 21-25, 2009
CL Hannover, GERMANY
SP Int Soc Cellular Therapy, European Branch, European Soc Gene & Cell Therapy, German Soc Gene Therapy, German Soc Stem Cell Res, BD Biosci, Biotech GmbH, Genethon, Cellectis, EUFETS, Lonza, Oxford BioMedica, Peprotech, Plasmidfactory, Regenx Biosci, Rentschler, Sartorius Stedim, StemCell Technologies
C1 [Kahraman, Sevim; Sanlioglu, Ahter; Yoldas, Burcak; Bagci, Huseyin; Sanlioglu, Salih] Akdeniz Univ, Fac Med, Human Gene Therapy Unit, Antalya, Turkey.
[Dirice, Ercument] Harvard Univ, Sch Med, Joslin Diabet Ctr, Cambridge, MA 02138 USA.
[Erkilic, Metin] Akdeniz Univ, Dept Nucl Med, Fac Med, Antalya, Turkey.
[Griffith, Thomas] Univ Iowa, Dept Urol, Iowa City, IA 52242 USA.
EM sanlioglu@akdeniz.edu.tr
RI yoldas, burcak/C-3522-2016; Erkilic, Metin/C-8748-2016; Sanlioglu,
Salih/F-9305-2016
NR 3
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 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD NOV
PY 2009
VL 20
IS 11
BP 1507
EP 1507
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 515BJ
UT WOS:000271441000447
ER
PT J
AU Eijgelsheim, M
Newton-Cheh, C
Aarnoudse, ALHJ
van Noord, C
Witteman, JCM
Hofman, A
Uitterlinden, AG
Stricker, BHC
AF Eijgelsheim, Mark
Newton-Cheh, Christopher
Aarnoudse, Adrianus L. H. J.
van Noord, Charlotte
Witteman, Jacqueline C. M.
Hofman, Albert
Uitterlinden, Andre G.
Stricker, Bruno H. C.
TI Genetic variation in NOS1AP is associated with sudden cardiac death:
evidence from the Rotterdam Study
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID QT-INTERVAL DURATION; GENOME-WIDE ASSOCIATION; ANALYSIS SYSTEM MEANS;
MYOCARDIAL-INFARCTION; GENERAL-POPULATION; REGULATOR NOS1AP; COMMON
VARIANTS; FAMILY-HISTORY; HEART-FAILURE; RISK
AB Common variation within the nitric oxide-1 synthase activator protein (NOS1AP) locus is strongly related to QT interval, a sudden cardiac death (SCD) risk factor. A recent report describes common variation in NOS1AP associated with SCD in a US population of European ancestry. The objective of the current study was to obtain additional evidence by investigating the association between NOS1AP variants and SCD in the prospective population-based Rotterdam Study. The study population consisted of 5974 European ancestry subjects, aged 55 years and older, genotyped on Illumina arrays. SCD was defined according to European Society of Cardiology guidelines. Smoking, body mass index, diabetes mellitus, hypertension, heart failure and myocardial infarction were used as covariates in Cox proportional hazard models. Results were combined with reported evidence using inverse-variance weighted meta-analysis. Two hundred and eight (109 witnessed) cases of SCD occurred during a mean follow-up of 10.4 years. Within the Rotterdam Study alone, no significant associations were observed. Upon pooling of results with existing data, we observed strengthening of existing evidence for rs16847549 (US data HR = 1.31, P = 0.0024; Rotterdam Study HR = 1.18, P = 0.16; joint HR = 1.26, P = 0.0011). When the case definition in the Rotterdam Study was restricted to witnessed SCD, association of rs16847549 with SCD became stronger (joint P = 0.00019) and additionally the association between rs12567209 and SCD gained significance (US data HR = 0.57, P = 0.0035; Rotterdam Study HR = 0.69, P = 0.23; joint HR = 0.60, P = 0.0018). In conclusion, this study provided additional evidence for association between genetic variation within NOS1AP and SCD. The mechanism by which this effect is exerted remains to be elucidated.
C1 [Eijgelsheim, Mark; Aarnoudse, Adrianus L. H. J.; van Noord, Charlotte; Witteman, Jacqueline C. M.; Hofman, Albert; Uitterlinden, Andre G.; Stricker, Bruno H. C.] Erasmus MC, Dept Epidemiol, NL-3000 CA Rotterdam, Netherlands.
[Uitterlinden, Andre G.; Stricker, Bruno H. C.] Erasmus MC, Dept Internal Med, NL-3000 CA Rotterdam, Netherlands.
[Newton-Cheh, Christopher] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Ctr Human Genet Res, Boston, MA 02114 USA.
[van Noord, Charlotte] Dutch Med Evaluat Board, NL-2500 BE The Hague, Netherlands.
[Witteman, Jacqueline C. M.; Hofman, Albert; Uitterlinden, Andre G.; Stricker, Bruno H. C.] Netherlands Genom Initiat, Netherlands Consortium Healthy Ageing, Rotterdam, Netherlands.
[Stricker, Bruno H. C.] Inspectorate Hlth Care, NL-2500 BC The Hague, Netherlands.
RP Stricker, BHC (reprint author), Erasmus MC, Dept Epidemiol, POB 2040, NL-3000 CA Rotterdam, Netherlands.
EM b.stricker@erasmusmc.nl
FU National Genomic Initiative/Netherlands Organization for Scientific
Research [050.060.810]; Netherlands Organization for Scientific Research
[175.010.2005.011]; Netherlands Heart Foundation [2007B221]; NIH
[HL080025]; Doris Duke Charitable Foundation Clinical Scientist
Development Award; Burroughs Wellcome Fund Career Award for Medical
Scientists
FX This work was supported by the National Genomic Initiative/Netherlands
Organization for Scientific Research [050.060.810]; the Netherlands
Organization for Scientific Research [175.010.2005.011]; the Netherlands
Heart Foundation [2007B221 to M. E.]; NIH [HL080025 to C.N.-C.]; the
Doris Duke Charitable Foundation Clinical Scientist Development Award
[to C.N.-C.]; and the Burroughs Wellcome Fund Career Award for Medical
Scientists [to C.N.-C.].
NR 34
TC 38
Z9 39
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 1
PY 2009
VL 18
IS 21
BP 4213
EP 4218
DI 10.1093/hmg/ddp356
PG 6
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 505QD
UT WOS:000270708300019
PM 19643915
ER
PT J
AU Li, J
Milbury, CA
Li, C
Makrigiorgos, GM
AF Li, Jin
Milbury, Coren A.
Li, Cheng
Makrigiorgos, G. Mike
TI Two-Round Coamplification at Lower Denaturation Temperature-PCR
(COLD-PCR)-Based Sanger Sequencing Identifies a Novel Spectrum of
Low-Level Mutations in Lung Adenocarcinoma
SO HUMAN MUTATION
LA English
DT Article
DE lung cancer; TP53; low-level mutation; intratumor heterogeneity;
COLD-PCR
ID P53 MUTATIONS; CELL CARCINOMA; COLD-PCR; CANCER; DNA; ABNORMALITIES;
SURVIVAL; SAMPLES; ASSAY; CURVE
AB Reliable identification of cancer-related mutations in TP53 is often problematic, as these mutations can be randomly distributed throughout numerous codons and their relative abundance in clinical samples can fall below the sensitivity limits of conventional sequencing. To ensure the highest sensitivity in mutation detection, we adapted the recently described coamplification at lower denaturation temperature-PCR (COLD-PCR) method to employ two consecutive rounds of COLD-PCR followed by Sanger sequencing. Using this highly sensitive approach we screened 48 nonmicrodissected lung adenocarcinoma samples for TP53 mutations. Twenty-four missense/frameshift TP53 mutations throughout exons 5 to 8 were identified in 23 out of 48 (48%) lung adenocarcinoma samples examined, including eight low-level mutations at an abundance of similar to 1 to 17%, most of which would have been missed using conventional methodologies. The identified alterations include two rare lung adenocarcinoma mutations, one of which is a "disruptive" mutation currently undocumented in the lung cancer mutation databases. A sample harboring a low-level mutation (similar to 2% abundance) con, currently with a clonal mutation (80% abundance) revealed intratumoral TP53 mutation heterogeneity. The ability to identify and sequence low-level mutations in the absence of elaborate microdissection, via COLD-PCR-based Sanger sequencing, provides a platform for accurate mutation profiling in clinical specimens and the use of TP53 as a prognostic/predictive biomarker, evaluation of cancer risk, recurrence, and further under standing of cancer biology. Hum Mutat 30:1583-1590, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Li, Jin; Milbury, Coren A.; Makrigiorgos, G. Mike] Harvard Univ, Sch Med, Dana Farber Brigham & Womens Canc Ctr, Div DNA Repair & Genome Stabil,Dept Radiat Oncol, Boston, MA USA.
[Makrigiorgos, G. Mike] Harvard Univ, Sch Med, Dana Farber Brigham & Womens Canc Ctr, Div Med Phys & Biophys,Dept Radiat Oncol, Boston, MA USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Li, Cheng] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Makrigiorgos, GM (reprint author), Brigham & Womens Hosp, Dana Farber Brigham & Womens Canc Ctr, Level L2,75 Francis St, Boston, MA 02115 USA.
EM mmakrigiorgos@partners.org
FU JCRT Foundation; NIH [5 T32 CA09078, CA-138280, CA-111994]
FX J.L. was supported by the JCRT Foundation and C.M. was supported by NIH
training grant 5 T32 CA09078. This work was supported in part by NIH
grants CA-138280 and CA-111994.
NR 41
TC 33
Z9 36
U1 0
U2 6
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1059-7794
J9 HUM MUTAT
JI Hum. Mutat.
PD NOV
PY 2009
VL 30
IS 11
BP 1583
EP 1590
DI 10.1002/humu.21112
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 516XL
UT WOS:000271576600011
PM 19760750
ER
PT J
AU Glasser, SP
Basile, JN
Lackland, DT
AF Glasser, Stephen P.
Basile, Jan N.
Lackland, Daniel T.
TI Does Prehypertension Represent an Increased Risk for Incident
Hypertension and Adverse Cardiovascular Outcome?
SO HYPERTENSION
LA English
DT Editorial Material
ID BLOOD-PRESSURE; FOLLOW-UP; MORTALITY; COHORT; ADULTS; HEALTH
C1 [Glasser, Stephen P.] Univ Alabama, Div Prevent Med, Birmingham, AL 35205 USA.
[Basile, Jan N.] Med Univ S Carolina, Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC 29425 USA.
[Lackland, Daniel T.] Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA.
RP Glasser, SP (reprint author), Univ Alabama, Div Prevent Med, 1717 11th Ave S MT 638, Birmingham, AL 35205 USA.
EM sglasser@uab.edu
OI Glasser, Stephen/0000-0001-9620-6406
FU NHLBI NIH HHS [K30 HL004104]
NR 13
TC 4
Z9 4
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD NOV
PY 2009
VL 54
IS 5
BP 954
EP 955
DI 10.1161/HYPERTENSIONAHA.109.138545
PG 2
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 509CW
UT WOS:000270992100004
PM 19720951
ER
PT J
AU Granado, NS
Smith, TC
Swanson, GM
Harris, RB
Shahar, E
Smith, B
Boyko, EJ
Wells, TS
Ryan, MAK
AF Granado, Nisara S.
Smith, Tyler C.
Swanson, G. Marie
Harris, Robin B.
Shahar, Eyal
Smith, Besa
Boyko, Edward J.
Wells, Timothy S.
Ryan, Margaret A. K.
CA Millennium Cohort Study Team
TI Newly Reported Hypertension After Military Combat Deployment in a Large
Population-Based Study
SO HYPERTENSION
LA English
DT Article
DE hypertension; incidence; stressful events; cohort studies; military
personnel
ID AMERICAN-HEART-ASSOCIATION; BLOOD-PRESSURE CONTROL; GULF-WAR VETERANS;
BODY-MASS INDEX; MILLENNIUM COHORT; CARDIOVASCULAR-DISEASE; RESISTANCE
EXERCISE; US MILITARY; ARTERIAL STIFFNESS; CIGARETTE-SMOKING
AB High-stress situations, such as combat deployments, are a potential risk factor for hypertension. Although stress is postulated to increase blood pressure, the underlying role of stress on hypertension is not well established. We sought to determine the relations between combat deployment-induced stress and hypertension. The Millennium Cohort baseline questionnaire (2001-2003) was completed by 77 047 US active-duty and Reserve/National Guard members. Follow-up was completed by 55 021 responders approximate to 3 years later (2004-2006). Multivariable logistic regression was used to estimate the 3-year risk of newly reported hypertension, adjusting for general and mental health, demographics, and occupational and behavioral characteristics. After applying exclusion criteria, our analyses included 36 061 service members. Subanalyses of deployers included 8829 participants. Newly reported hypertension was identified in 6.9% of the cohort between baseline and follow-up, many of whom had deployed on military operations in support of the conflicts in Iraq and Afghanistan. After adjusting, deployers who experienced no combat exposures were less likely to report hypertension than nondeployers (odds ratio: 0.77; 95% CI: 0.67 to 0.89). Among deployers, those reporting multiple combat exposures were 1.33 times more likely to report hypertension compared with noncombat deployers (95% CI: 1.07 to 1.65). Although military deployers, in general, had a lower incidence of hypertension than nondeployers, deployment with multiple stressful combat exposures appeared to be a unique risk factor for newly reported hypertension. (Hypertension. 2009; 54: 966-973.)
C1 [Granado, Nisara S.; Smith, Tyler C.; Smith, Besa] USN, Hlth Res Ctr, Dept Def Ctr Deployment Hlth Res, San Diego, CA 92106 USA.
[Swanson, G. Marie] Indiana Univ, Sch Med, Dept Publ Hlth, Indianapolis, IN USA.
[Harris, Robin B.; Shahar, Eyal] Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Tucson, AZ USA.
[Boyko, Edward J.] Vet Affairs Puget Sound Hlth Care Syst, Seattle Epidemiol Res & Informat Ctr, Seattle, WA USA.
[Smith, Tyler C.] USAF, Res Lab, Dayton, OH USA.
[Ryan, Margaret A. K.] USN, Hosp Camp Pendleton, Dept Occupat Hlth, Camp Pendleton, CA USA.
RP Granado, NS (reprint author), USN, Hlth Res Ctr, Dept Def Ctr Deployment Hlth Res, 140 Sylvester Rd, San Diego, CA 92106 USA.
EM nisara.granado@med.navy.mil
FU Military Operational Medicine Research Program; United States Army
Medical Research and Material Command
FX The Millennium Cohort Study is funded through the Military Operational
Medicine Research Program, United States Army Medical Research and
Material Command (Fort Detrick, MD).
NR 43
TC 36
Z9 37
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD NOV
PY 2009
VL 54
IS 5
BP 966
EP 973
DI 10.1161/HYPERTENSIONAHA.109.132555
PG 8
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 509CW
UT WOS:000270992100010
PM 19752293
ER
PT J
AU Decaluwe, K
Nimmegeers, S
Thoonen, R
Buys, E
Brouckaert, P
Van de Voorde, J
AF Decaluwe, K.
Nimmegeers, S.
Thoonen, R.
Buys, E.
Brouckaert, P.
Van de Voorde, J.
TI IN VITRO AND IN VIVO STUDIES ON THE IMPORTANCE OF THE SOLUBLE GUANYLYL
CYCLASE ALPHA 1 SUBUNIT IN PENILE ERECTION
SO HYPERTENSION
LA English
DT Meeting Abstract
CT 14th Annual Meeting of the European-Council-for-Cardiovascular-Research
CY OCT 09-11, 2009
CL Nice, FRANCE
SP European Council Cardiovasc Res
C1 [Decaluwe, K.; Nimmegeers, S.; Van de Voorde, J.] Univ Ghent, Dept Pharmacol, B-9000 Ghent, Belgium.
[Thoonen, R.; Brouckaert, P.] VIB, Dept Mol Biomed Res, Ghent, Belgium.
[Buys, E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Anesthesia Ctr Crit Care Res,Dept Anesthesia & Cr, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD NOV
PY 2009
VL 54
IS 5
BP 1181
EP 1181
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 509CW
UT WOS:000270992100121
ER
PT J
AU Patel, S
Lorincz, K
Hughes, R
Huggins, N
Growdon, J
Standaert, D
Akay, M
Dy, J
Welsh, M
Bonato, P
AF Patel, Shyamal
Lorincz, Konrad
Hughes, Richard
Huggins, Nancy
Growdon, John
Standaert, David
Akay, Metin
Dy, Jennifer
Welsh, Matt
Bonato, Paolo
TI Monitoring Motor Fluctuations in Patients With Parkinson's Disease Using
Wearable Sensors
SO IEEE TRANSACTIONS ON INFORMATION TECHNOLOGY IN BIOMEDICINE
LA English
DT Article
DE Body sensor networks; Parkinson's disease; support vector machines
(SVMs); wearable sensors
ID LEVODOPA-INDUCED DYSKINESIAS; NEURAL-NETWORKS; 2 PARTS
AB This paper presents the results of a pilot study to assess the feasibility of using accelerometer data to estimate the severity of symptoms and motor complications in patients with Parkinson's disease. A support vector machine (SVM) classifier was implemented to estimate the severity of tremor, bradykinesia and dyskinesia from accelerometer data features. SVM-based estimates were compared with clinical scores derived via visual inspection of video recordings taken while patients performed a series of standardized motor tasks. The analysis of the video recordings was performed by clinicians trained in the use of scales for the assessment of the severity of Parkinsonian symptoms and motor complications. Results derived from the accelerometer time series were analyzed to assess the effect on the estimation of clinical scores of the duration of the window utilized to derive segments (to eventually compute data features) from the accelerometer data, the use of different SVM kernels and misclassification cost values, and the use of data features derived from different motor tasks. Results were also analyzed to assess which combinations of data features carried enough information to reliably assess the severity of symptoms and motor complications. Combinations of data features were compared taking into consideration the computational cost associated with estimating each data feature on the nodes of a body sensor network and the effect of using such data features on the reliability of SVM-based estimates of the severity of Parkinsonian symptoms and motor complications.
C1 [Patel, Shyamal; Hughes, Richard; Bonato, Paolo] Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Spaulding Rehabil Hosp, Boston, MA 02114 USA.
[Lorincz, Konrad; Welsh, Matt] Harvard Univ, Sch Engn & Appl Sci, Cambridge, MA 02138 USA.
[Huggins, Nancy; Growdon, John] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Movement Disorders Unit, Boston, MA 02114 USA.
[Standaert, David] Univ Alabama, Birmingham, AL 35294 USA.
[Akay, Metin] Arizona State Univ, Sch Biol & Hlth Syst Engn, Tempe, AZ 85287 USA.
[Dy, Jennifer] Northeastern Univ, Dept Elect & Comp Engn, Boston, MA 02115 USA.
[Bonato, Paolo] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Patel, S (reprint author), Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Spaulding Rehabil Hosp, Boston, MA 02114 USA.
EM spatel19@partners.org; konrad@eecs.harvard.edu; rhughes1@partners.org;
huggins.nancy@gmail.com; growdon@helix.mgh.harvard.edu;
dstandaert@uab.edu; metin.akay@asu.edu; jdy.ece@gmail.com;
mdw@eecs.harvard.edu; pbonato@partners.org
RI Patel, Shyamal/K-3176-2012;
OI Standaert, David/0000-0003-2921-8348
FU National Institute of Neurological Disorders and Stroke
[R21NS045401-02]; National Science Foundation [CNS-0546338]; Michael J.
Fox Foundation for Parkinson's Research
FX This work was supported in part by the National Institute of
Neurological Disorders and Stroke under Grant R21NS045401-02, by the
National Science Foundation under Grant CNS-0546338, by the Michael J.
Fox Foundation for Parkinson's Research, and by gifts from Intel
Corporation, Siemens, Microsoft, and Sun Microsystems.
NR 24
TC 149
Z9 151
U1 2
U2 24
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA
SN 1089-7771
J9 IEEE T INF TECHNOL B
JI IEEE T. Inf. Technol. Biomed.
PD NOV
PY 2009
VL 13
IS 6
BP 864
EP 873
DI 10.1109/TITB.2009.2033471
PG 10
WC Computer Science, Information Systems; Computer Science,
Interdisciplinary Applications; Mathematical & Computational Biology;
Medical Informatics
SC Computer Science; Mathematical & Computational Biology; Medical
Informatics
GA 515OI
UT WOS:000271481300002
PM 19846382
ER
PT J
AU Sharma, G
Rege, K
Budil, DE
Yarmush, M
Mavroidis, C
AF Sharma, Gaurav
Rege, Kaushal
Budil, David E.
Yarmush, Martin
Mavroidis, Constantinos
TI Biological Force Measurement in a Protein-Based Nanoactuator
SO IEEE TRANSACTIONS ON NANOTECHNOLOGY
LA English
DT Article
DE Biomolecular devices; coiled-coil protein; force measurement;
nanotechnology
ID MOLECULAR-DYNAMICS SIMULATIONS; SINGLE KINESIN MOLECULES; FREE-ENERGY
CALCULATION; LEUCINE-ZIPPER; DNA; ALGORITHMS; GENERATION; KINETICS;
SYSTEMS
AB The mechanical force exerted by a nanoactuator due to pH actuation is discussed from a statistical mechanics and free energy of conformational change viewpoint. We use molecular dynamics to show that the nanoactuator, based on the coiled-coil leucine zipper portion of a yeast transcriptional activator protein, can generate mechanical forces of the order of 20-40 pN upon pH modulation. The forces are generated due to the electrostatic repulsions at low pH between His-tag handles and other charged residues engineered into the protein sequence. The biological force output of the nanoactuator is comparable to that generated by adenosine triphosphate (ATP)-based molecular motors such as myosin and kinesin even though the nanoactuator is smaller in size to these molecular motors. The force calculation technique can readily be applied to other biomolecular systems and has implications in the area of bionanotechnology and in particular to study and characterize the properties of novel protein and DNA-based nanodevices.
C1 [Sharma, Gaurav; Mavroidis, Constantinos] Northeastern Univ, Mech & Ind Engn Dept, Boston, MA 02115 USA.
[Rege, Kaushal] Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Budil, David E.] Northeastern Univ, Dept Chem & Chem Biol, Boston, MA 02115 USA.
[Yarmush, Martin] Massachusetts Gen Hosp, Ctr Engn Med, Boston, MA 02114 USA.
RP Sharma, G (reprint author), Burnham Inst Med Res, La Jolla, CA 92037 USA.
EM gsharma@burnham.org; kaushal.rege@asu.edu; d.budil@neu.edu;
ireis@sbi.org; mavro@coe.neu.edu
RI Budil, David/A-9931-2012
OI Budil, David/0000-0003-2384-7928
NR 46
TC 1
Z9 1
U1 0
U2 6
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA
SN 1536-125X
J9 IEEE T NANOTECHNOL
JI IEEE Trans. Nanotechnol.
PD NOV
PY 2009
VL 8
IS 6
BP 684
EP 691
DI 10.1109/TNANO.2009.2023517
PG 8
WC Engineering, Electrical & Electronic; Nanoscience & Nanotechnology;
Materials Science, Multidisciplinary; Physics, Applied
SC Engineering; Science & Technology - Other Topics; Materials Science;
Physics
GA 523BW
UT WOS:000272047300004
ER
PT J
AU Weil, AA
Arifuzzaman, M
Bhuiyan, TR
LaRocque, RC
Harris, AM
Kendall, EA
Hossain, A
Tarique, AA
Sheikh, A
Chowdhury, F
Khan, AI
Murshed, F
Parker, KC
Banerjee, KK
Ryan, ET
Harris, JB
Qadri, F
Calderwood, SB
AF Weil, Ana A.
Arifuzzaman, Mohammad
Bhuiyan, Taufiqur R.
LaRocque, Regina C.
Harris, Aaron M.
Kendall, Emily A.
Hossain, Azim
Tarique, Abdullah A.
Sheikh, Alaullah
Chowdhury, Fahima
Khan, Ashraful I.
Murshed, Farhan
Parker, Kenneth C.
Banerjee, Kalyan K.
Ryan, Edward T.
Harris, Jason B.
Qadri, Firdausi
Calderwood, Stephen B.
TI Memory T-Cell Responses to Vibrio cholerae O1 Infection
SO INFECTION AND IMMUNITY
LA English
DT Article
ID RURAL EAST PAKISTAN; VACCINE CVD 103-HGR; FIELD-TRIAL AREA;
BIOTYPE-EL-TOR; INFLAMMATORY MEDIATORS; COAGGLUTINATION TEST;
SEROLOGICAL SURVEY; IMMUNE-RESPONSES; ENDEMIC CHOLERA; SYNONYM BENGAL
AB Vibrio cholerae O1 can cause diarrheal disease that may be life-threatening without treatment. Natural infection results in long-lasting protective immunity, but the role of T cells in this immune response has not been well characterized. In contrast, robust B-cell responses to V. cholerae infection have been observed. In particular, memory B-cell responses to T-cell-dependent antigens persist for at least 1 year, whereas responses to lipopolysaccharide, a T-cell-independent antigen, wane more rapidly after infection. We hypothesize that protective immunity is mediated by anamnestic responses of memory B cells in the gut-associated lymphoid tissue, and T-cell responses may be required to generate and maintain durable memory B-cell responses. In this study, we examined B- and T-cell responses in patients with severe V. cholerae infection. Using the flow cytometric assay of the specific cell-mediated immune response in activated whole blood, we measured antigen-specific T-cell responses using V. cholerae antigens, including the toxin-coregulated pilus (TcpA), a V. cholerae membrane preparation, and the V. cholerae cytolysin/hemolysin (VCC) protein. Our results show that memory T-cell responses develop by day 7 after infection, a time prior to and concurrent with the development of B- cell responses. This suggests that T-cell responses to V. cholerae antigens may be important for the generation and stability of memory B- cell responses. The T-cell proliferative response to VCC was of a higher magnitude than responses observed to other V. cholerae antigens.
C1 [LaRocque, Regina C.; Murshed, Farhan; Ryan, Edward T.; Harris, Jason B.; Calderwood, Stephen B.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Weil, Ana A.; Arifuzzaman, Mohammad; Bhuiyan, Taufiqur R.; Harris, Aaron M.; Kendall, Emily A.; Hossain, Azim; Tarique, Abdullah A.; Sheikh, Alaullah; Chowdhury, Fahima; Khan, Ashraful I.; Qadri, Firdausi] Int Ctr Diarrheal Dis Res, Dhaka, Bangladesh.
[LaRocque, Regina C.; Ryan, Edward T.; Calderwood, Stephen B.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Parker, Kenneth C.] Virgin Instruments, Sudbury, MA USA.
[Banerjee, Kalyan K.] Natl Inst Cholera & Enter Dis, Div Biochem, Kolkata, India.
[Ryan, Edward T.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Harris, Jason B.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Calderwood, Stephen B.] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA.
RP Calderwood, SB (reprint author), Massachusetts Gen Hosp, Div Infect Dis, 55 Fruit St, Boston, MA 02114 USA.
EM scalderwood@partners.org
RI Tarique, Abdullah/M-2860-2013;
OI Tarique, Abdullah/0000-0003-3782-345X; Parker,
Kenneth/0000-0002-6282-2478; Kendall, Emily/0000-0002-0083-422X
FU Centre for Health and Population Research [U01 AI058935, RO3 AI063079,
U01 AI077883]; International Research Scientist Development Award [KO1
TW07144]; Howard Hughes Medical Institute Physician Scientist Early
Career Award; Fogarty International Center Global Infectious Disease
Research Training Program Award in Vaccine Development [D43 TW05572];
Fogarty International Center at the National Institutes of Health [D43
TW005572, R24 TW007988]; Swedish Agency for International Development
and Corp. (SIDA/ SAREC)
FX This research was supported by the ICDDR, B Centre for Health and
Population Research and by the following grants: U01 AI058935 (S. B.
C.), RO3 AI063079 (F. Q.), U01 AI077883 (E. T. R.), International
Research Scientist Development Award KO1 TW07144 (R. C. L.), Howard
Hughes Medical Institute Physician Scientist Early Career Award (R. C.
L.), International Research Scientist Development Award KO1 TW07409 (J.
B. H.), and a Fogarty International Center Global Infectious Disease
Research Training Program Award in Vaccine Development D43 TW05572 (M.
A., A. A. T., and A. S.). A. A. W., A. M. H., E. A. K., F. C., and A. I.
K. are recipients of a Fogarty International Clinical Research Scholars
award from the Fogarty International Center at the National Institutes
of Health (D43 TW005572 and R24 TW007988). F. M. is a recipient of a
Harvard Initiative for Global Health SURF Award. F. Q. and T. R. B. are
recipients of funds from the Swedish Agency for International
Development and Corp. (SIDA/ SAREC).; We are grateful for the
participation of patients and the work of the field staff at the ICDDR,
B. We also thank Mohammad Rasheduzzaman at the ICDDR, B and Richelle
Charles at Massachusetts General Hospital for laboratory and technical
assistance.
NR 50
TC 23
Z9 23
U1 2
U2 4
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
EI 1098-5522
J9 INFECT IMMUN
JI Infect. Immun.
PD NOV
PY 2009
VL 77
IS 11
BP 5090
EP 5096
DI 10.1128/IAI.00793-09
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 507WH
UT WOS:000270885800043
PM 19703973
ER
PT J
AU Smith, RM
Conn, AKT
AF Smith, R. Malcolm
Conn, Alasdair K. T.
TI Prehospital care - Scoop and run or stay and play?
SO INJURY-INTERNATIONAL JOURNAL OF THE CARE OF THE INJURED
LA English
DT Article
DE Prehospital Care; "Scoop and run"; "Stay and play"
ID TRAUMATIC BRAIN-INJURY; LIFE-SUPPORT; HEAD-INJURY; INTUBATION
AB Improved training and expertise has enabled emergency medical personnel to provide advanced levels of care at the scene of trauma. While this could be expected to improve the outcome from major injury, current data does not support this. Indeed, prehospital interventions beyond the BLS level have not been shown to be effective and in many cases have proven to be detrimental to patient outcome. It is better to "scoop and run" than "stay and play". Current data relates to the urban environment where transport times to trauma centres are short and where it appears better to simply rapidly transport the patient to hospital than attempt major interventions at the scene. There may be more need for advanced techniques in the rural environment or where transport times are prolonged and certainly a need for more studies into subsets of patients who may benefit from interventions in the field.
C1 [Smith, R. Malcolm] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Orthopaed Trauma Serv, Boston, MA 02114 USA.
RP Smith, RM (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Orthopaed Trauma Serv, 55 Fruit St,WACC 5-525, Boston, MA 02114 USA.
EM rmsmith@partners.org
NR 9
TC 24
Z9 26
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0020-1383
J9 INJURY
JI Injury-Int. J. Care Inj.
PD NOV
PY 2009
VL 40
BP S23
EP S26
DI 10.1016/j.injury.2009.10.033
PG 4
WC Critical Care Medicine; Emergency Medicine; Orthopedics; Surgery
SC General & Internal Medicine; Emergency Medicine; Orthopedics; Surgery
GA 534YI
UT WOS:000272933100004
PM 19895949
ER
PT J
AU Montgomery, SA
Fava, M
Padmanabhan, SK
Guico-Pabia, CJ
Tourian, KA
AF Montgomery, Stuart A.
Fava, Maurizio
Padmanabhan, Sudharshan K.
Guico-Pabia, Christine J.
Tourian, Karen A.
TI Discontinuation symptoms and taper/poststudy-emergent adverse events
with desvenlafaxine treatment for major depressive disorder
SO INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Article
DE Discontinuation-Emergent Signs and Symptoms; discontinuation symptoms;
major depressive disorder; selective serotonin reuptake inhibitors;
serotonin-norepinephrine reuptake inhibitors; taper/poststudy-emergent
adverse events
ID PLACEBO-CONTROLLED TRIAL; SEROTONIN REUPTAKE INHIBITORS; DOUBLE-BLIND;
ANTIDEPRESSANT DISCONTINUATION; ABRUPT DISCONTINUATION; VENLAFAXINE XR;
100 MG/DAY; EFFICACY; SAFETY; WITHDRAWAL
AB The objective of this study was to assess discontinuation symptoms with desvenlafaxine (administered as desvenlafaxine succinate) treatment for major depressive disorder. Data were analyzed from nine 8-week, double-blind (DB), placebo-controlled studies of desvenlafaxine (50, 100, 200, or 400 mg/day; placebo, n = 319; desvenlafaxine, n = 578) and a relapse-prevention study [12-week, open-label (OL) 200 or 400 mg/day desvenlafaxine (n = 373); 6-month 1313 placebo (n = 73) or desvenlafaxine (n = 118)]. Rates of taper/poststudy-emergent adverse events were summarized. Discontinuation-Emergent Signs and Symptoms (DESS) checklist scores were analyzed in treatment completers at the end of OL and DB treatment. The most common (>= 5%) taper/poststudy-emergent adverse events among desvenlafaxine patients were dizziness, nausea, headache, irritability, diarrhea, anxiety, abnormal dreams, fatigue, and hyperhidrosis. In the short-term studies, the highest DESS scores observed for desvenlafaxine groups occurred at first assessment after discontinuation of all active treatment (1.9-5.7). Desvenlafaxine 50- and 100-mg/day groups had significantly increased scores versus placebo (P values <= 0.028). DESS scores increased significantly for patients discontinuing 12-week, OL desvenlafaxine 200 and 400 mg/day doses compared with those continuing desvenlafaxine (P values <= 0.022). After the 6-month DB phase, DESS scores increased significantly compared with placebo for patients discontinuing 400 mg/day only (P = 0.029). In conclusion, cessation of desvenlafaxine use is associated with discontinuation symptoms after both short-term and long-term treatment. Int Clin Psychopharmacol 24:296-305 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Montgomery, Stuart A.] Univ London Imperial Coll Sci Technol & Med, Sch Med, London, England.
[Fava, Maurizio] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Padmanabhan, Sudharshan K.; Guico-Pabia, Christine J.; Tourian, Karen A.] Wyeth Res, Collegeville, PA USA.
RP Montgomery, SA (reprint author), POB 8751, London W13 8WH, England.
EM Stuart@samontgomery.co.uk
FU Wyeth Research, Collegeville, P.A.
FX Medical writing support for the preparation of this article was provided
by Kathleen Dorries, PhD, of Advogent, and this assistance was funded by
Wyeth Research, Collegeville, P.A.
NR 42
TC 7
Z9 7
U1 1
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0268-1315
J9 INT CLIN PSYCHOPHARM
JI Int. Clin. Psychopharmacol.
PD NOV
PY 2009
VL 24
IS 6
BP 296
EP 305
DI 10.1097/YIC.0b013e32832fbb5a
PG 10
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA 516RP
UT WOS:000271560400003
PM 19779354
ER
PT J
AU Dougherty, DD
Jameson, M
Deckersbach, T
Loh, R
Thompson-Hollands, J
Jenike, M
Keuthen, NJ
AF Dougherty, Darin D.
Jameson, Mariko
Deckersbach, Thilo
Loh, Rebecca
Thompson-Hollands, Johanna
Jenike, Michael
Keuthen, Nancy J.
TI Open-label study of high (30 mg) and moderate (20 mg) dose escitalopram
for the treatment of obsessive-compulsive disorder
SO INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Article
DE compulsions; escitalopram; obsessions; obsessive-compulsive disorder;
selective serotonin reuptake inhibitors
ID DEPRESSION; INVENTORY; PLACEBO; SCALE
AB This study sought to investigate the efficacy of escitalopram at different dosages for the treatment of obsessive-compulsive disorder (OCD). Thirty individuals were enrolled in a 16-week, open-label trial of escitalopram and randomly assigned to the 20 or 30 mg study arm. Study measures assessing OCD symptoms, anxiety, depression, and quality of life were administered at baseline and weeks 2, 4, 8, 12, and 16. For the 23 study completers, pretreatment and posttreatment analyses revealed significant improvements (P<0.05) on clinician-rated and self-rated measures of OCD symptoms, quality of life, anxiety, and depression. Approximately half of the sample (n=12) satisfied full medication response criteria and less than one-quarter (n=5) were partial medication responders. Intention-to-treat analyses showed similar improvements (P<0.05) on all study measures. At study completion, a superior responder rate and more improvement on the Yale-Brown Obsessive Compulsive Scale (P<0.05) was reported for those in the 30 versus 20 mg study arm. The difference between the two groups, however, disappeared when initial differences in baseline depression and anxiety scores were used as analysis covariates. These results suggest that the 30 mg (vs. 20 mg) dose of escitalopram may provide a superior reduction in OCD symptoms for those sufferers with comorbid depression and/or anxiety. Int Clin Psychopharmacol 24:306-311 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Dougherty, Darin D.; Jameson, Mariko; Deckersbach, Thilo; Thompson-Hollands, Johanna; Jenike, Michael; Keuthen, Nancy J.] Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Loh, Rebecca] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
RP Dougherty, DD (reprint author), MGH E, Massachusetts Gen Hosp, OCD Clin, Neurotherapeut Div, Fl 2,149 13th St, Charlestown, MA 02129 USA.
EM ddougherty@partners.org
FU Forest Laboratories Inc.
FX This study was supported by a research grant from Forest Laboratories
Inc.
NR 17
TC 11
Z9 11
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0268-1315
J9 INT CLIN PSYCHOPHARM
JI Int. Clin. Psychopharmacol.
PD NOV
PY 2009
VL 24
IS 6
BP 306
EP 311
DI 10.1097/YIC.0b013e32833119d8
PG 6
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA 516RP
UT WOS:000271560400004
PM 19730388
ER
PT J
AU Calil, C
Liberato, FL
Pereira, AC
Meneghim, MD
Goodson, JM
Groppo, FC
AF Calil, C.
Liberato, F. L.
Pereira, A. C.
de Castro Meneghim, M.
Goodson, J. M.
Groppo, F. C.
TI The relationship between volatile sulphur compounds, tongue coating and
periodontal disease
SO INTERNATIONAL JOURNAL OF DENTAL HYGIENE
LA English
DT Article
DE halitosis; periodontal disease; tongue coating
AB The purpose of the present study was to observe the casual levels of volatile sulphur compounds (VSC) in volunteers with different clinical scores of tongue coating, periodontal pockets depth and Gingival Bleeding Index. Seventy-two subjects who attended for the first time at the dental clinic of the University were randomly selected for intra-oral and periodontal examinations. Systemic and dental histories were also obtained. The subjects were unaware of all procedures. The level of VSC was assessed by using a portable sulphide monitor (Halimeter (R); Interscan Co., Chatsworth, CA, USA). High tongue coating levels were related with more VSC counts (multivariate anova, P = 0.01). No statistically significant relation (multiple linear regression, P > 0.05) was observed among the VSC levels considering age, bleeding and periodontal pockets sites (depth > 4 mm). We concluded that the tongue coating was one of the main factors influencing the VSC levels.
C1 [Calil, C.; Groppo, F. C.] Univ Estadual Campinas, Dept Physiol Sci, Piracicaba Dent Sch, BR-13414903 Piracicaba, SP, Brazil.
[Calil, C.] Univ Sao Paulo, Discipline Periodont, Dept Stomatol, Sch Dent, Sao Paulo, Brazil.
[Liberato, F. L.; Pereira, A. C.; de Castro Meneghim, M.] Univ Estadual Campinas, Dept Social & Prevent Dent, Piracicaba Dent Sch, BR-13414903 Piracicaba, SP, Brazil.
[Goodson, J. M.] Forsyth Inst, Dept Periodontol, Boston, MA USA.
RP Groppo, FC (reprint author), Univ Estadual Campinas, Dept Physiol Sci, Piracicaba Dent Sch, CP 52, BR-13414903 Piracicaba, SP, Brazil.
EM fcgroppo@fop.unicamp.br
RI Groppo, Francisco/C-3516-2012; Meneghim, Marcelo/D-8940-2012
OI Groppo, Francisco/0000-0002-8513-773X;
NR 29
TC 13
Z9 13
U1 1
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1601-5029
J9 INT J DENT HYG
JI Int. J. Dent. Hyg.
PD NOV
PY 2009
VL 7
IS 4
BP 251
EP 255
DI 10.1111/j.1601-5037.2009.00366.x
PG 5
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA V16UT
UT WOS:000207895200004
PM 19832911
ER
PT J
AU Kimball, AB
Wu, Y
AF Kimball, Alexa Boer
Wu, Ying
TI Cardiovascular disease and classic cardiovascular risk factors in
patients with psoriasis
SO INTERNATIONAL JOURNAL OF DERMATOLOGY
LA English
DT Review
ID C-REACTIVE PROTEIN; CORONARY-ARTERY-DISEASE; IMPAIRED GLUCOSE-TOLERANCE;
OCCLUSIVE VASCULAR-DISEASE; BETA-CELL DYSFUNCTION; MIDDLE-AGED MEN;
MYOCARDIAL-INFARCTION; INSULIN-RESISTANCE; ALCOHOL-CONSUMPTION;
METABOLIC SYNDROME
C1 Harvard Univ, Sch Med, Boston, MA 02114 USA.
Centocor Inc, Res & Dev, Malvern, PA 19355 USA.
RP Kimball, AB (reprint author), Harvard Univ, Sch Med, CURTIS, Massachusetts Gen Hosp, 50 Staniford St 246, Boston, MA 02114 USA.
EM harvardskinstudies@partners.org
FU Centocor, Inc
FX Editorial support for the writing of the manuscript was provided by
Jason McDonough, phd, and was funded by Centocor, Inc. The authors were
not compensated and retained full editorial control.Dr Kimball is a
consultant/investigator for Centocor, Abbott, and Amgen. Dr Wu is an
employee of Centocor.
NR 84
TC 15
Z9 15
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0011-9059
J9 INT J DERMATOL
JI Int. J. Dermatol.
PD NOV
PY 2009
VL 48
IS 11
BP 1147
EP 1156
PG 10
WC Dermatology
SC Dermatology
GA 509WK
UT WOS:000271049800001
PM 20064165
ER
PT J
AU Becker, AE
Eddy, KT
Perloe, A
AF Becker, Anne E.
Eddy, Kamryn T.
Perloe, Alexandra
TI Clarifying Criteria for Cognitive Signs and Symptoms for Eating
Disorders in DSM-V
SO INTERNATIONAL JOURNAL OF EATING DISORDERS
LA English
DT Review
DE diagnostic criteria; anorexia nervosa; bulimia nervosa; clinical
inference; refusal
ID ANOREXIA-NERVOSA; GASTROINTESTINAL PRACTICE; CLINICAL JUDGMENT;
SELF-REPORT; BODY-IMAGE; HONG-KONG; CULTURE; ADOLESCENCE; ILLNESS;
STIGMATIZATION
AB Objective: This article reviews literature relevant to challenges in clinical ascertainment of cognitively-based diagnostic criteria of anorexia nervosa (AN) and bulimia nervosa (BN) to examine whether revision might enhance their clinical utility.
Method: We performed a systematic literature search to identify publications relevant to clinical evaluation of cognitive symptoms of AN and BN.
Results: The literature supports several reasons that individuals with an eating disorder may not endorse cognitive symptoms, despite their presence. These include limited insight, minimization, or denial, as well as intentional concealment related to perceived stigma, social desirability, or investment in maintaining behavioral symptoms. We also identified reasons that the word "refusal" in AN criterion A may render its application problematic.
Discussion: We conclude that specific guidance for ascertainment of cognitive signs for AN and BN in the absence of patient disclosure or endorsement, longitudinal evaluation, and/or collateral data may improve clinical utility of these diagnostic criteria. (C) 2009 American Psychiatric Association.
C1 [Becker, Anne E.] Harvard Univ, Sch Med, Dept Global Hlth & Social Med, Boston, MA 02115 USA.
[Eddy, Kamryn T.] Massachusetts Gen Hosp, Dept Psychiat, Harris Ctr Educ & Advocacy Eating Disorders, Boston, MA 02114 USA.
RP Becker, AE (reprint author), Harvard Univ, Sch Med, Dept Global Hlth & Social Med, 641 Huntington Ave, Boston, MA 02115 USA.
EM anne_becker@hms.harvard.edu
NR 74
TC 37
Z9 38
U1 2
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0276-3478
EI 1098-108X
J9 INT J EAT DISORDER
JI Int. J. Eating Disord.
PD NOV
PY 2009
VL 42
IS 7
BP 611
EP 619
DI 10.1002/eat.20723
PG 9
WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology
SC Psychology; Nutrition & Dietetics; Psychiatry
GA 518QO
UT WOS:000271708400006
PM 19650082
ER
PT J
AU Becker, AE
Thomas, JJ
Pike, KM
AF Becker, Anne E.
Thomas, Jennifer J.
Pike, Kathleen M.
TI Should Non-Fat-Phobic Anorexia Nervosa Be Included in DSM-V?
SO INTERNATIONAL JOURNAL OF EATING DISORDERS
LA English
DT Review
DE anorexia nervosa; fat phobia; non-fal-phobic AN; low drive for thinness
AN
ID EATING-DISORDER INVENTORY; ENVIRONMENTAL RISK-FACTORS; HONG-KONG;
CHINESE PATIENTS; SELF-STARVATION; ATTITUDES TEST; WEIGHT PHOBIA;
BODY-IMAGE; BULIMIA-NERVOSA; UNDUE INFLUENCE
AB Objective: Cross-cultural data suggest that rationales for food refusal vary in anorexia nervosa (AN), and a variant, termed non-fat-phobic AN (NFP-AN), has been described. This review evaluates whether data support modification of the requirement for intense fear of weight gain to meet AN criterion B in DSM-V.
Method: We performed a systematic search of the Medline and Psychinfo literature and evaluated the relevant publications by Robins and Guze's (Am J Psychiatry 126, 983-987, 1970) criteria as a standard for diagnostic validity. We also performed a meta-analysis comparing the severity of eating pathology in AN to (a) NFP-AN and (b) AN with low drive for thinness (low-DT-AN).
Results: A modest literature indicates that NFP-AN has wide geographic distribution and occurs in both Western and non-Western populations alongside cases of typical AN. Aggregating across eligible studies, patients with NFP-AN or low-DT-AN score at least 2/3 of a standard deviation lower on measures of eating pathology than patients with conventional AN. Transcultural comparison of drive for thinness suggests significantly lower norms in non-Western cultures.
Discussion: NFP-AN occurs with wide distribution. Further research is necessary on the course and outcomes of NFP-AN to characterize its congruence with, or distinction from, conventional AN. We discuss several options for including a description of NFP-AN in DSM-V. (C) 2009 American Psychiatric Association.
C1 [Becker, Anne E.] Harvard Univ, Sch Med, Dept Global Hlth & Social Med, Boston, MA 02115 USA.
[Becker, Anne E.; Thomas, Jennifer J.] Massachusetts Gen Hosp, Dept Psychiat, Eating Disorders Clin & Res Program, Boston, MA 02114 USA.
[Thomas, Jennifer J.] McLean Hosp, Klarman Eating Disorders Ctr, Belmont, MA 02178 USA.
[Pike, Kathleen M.] Temple Univ Japan, Coll Liberal Arts, Tokyo, Japan.
RP Becker, AE (reprint author), Harvard Univ, Sch Med, Dept Global Hlth & Social Med, 641 Huntington Ave, Boston, MA 02115 USA.
EM anne_becker@hms.harvard.edu
NR 74
TC 54
Z9 56
U1 3
U2 15
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0276-3478
J9 INT J EAT DISORDER
JI Int. J. Eating Disord.
PD NOV
PY 2009
VL 42
IS 7
BP 620
EP 635
DI 10.1002/eat.20727
PG 16
WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology
SC Psychology; Nutrition & Dietetics; Psychiatry
GA 518QO
UT WOS:000271708400007
PM 19655370
ER
PT J
AU Viswanathan, AN
Cormack, R
Rawal, B
Lee, H
AF Viswanathan, Akila N.
Cormack, Robert
Rawal, Bhupendra
Lee, Hang
TI Increasing Brachytherapy Dose Predicts Survival for Interstitial and
Tandem-Based Radiation for Stage IIIB Cervical Cancer
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
LA English
DT Article
DE Cervical cancer; Brachytherapy; Interstitial; Tandem; Stage IIIB
ID GYNECOLOGICAL MALIGNANCIES; CARCINOMA; INTRACAVITARY; IRRADIATION;
THERAPY; TEMPLATE; PATTERNS; TRIAL
AB Purpose: To evaluate factors affecting survival and toxicity in patients with stage IIIB cervical cancer treated with external-beam radiotherapy and low-dose-rate brachytherapy.
Materials and Methods: Seventy patients with stage IIIB cervical cancer treated between 1980 and 2000 were identified. A total of 51 patients had a tandem placed; 19 had interstitial brachytherapy only with no tandem placed. Univariate and multivariate analyses assessed factors potentially associated with survival and long-term complications.
Results: Kaplan-Meier estimates for overall survival (OS) for the entire population at 2, 3, and 4 years were 43%, 29%, and 27%, respectively. Overall survival differed significantly between those treated with a tandem versus those treated without (log rank P < 0.0001). Significant predictors of OS on univariate Cox regression were presence of a tandem (hazards ratio [HR], 0.31; P = 0.0001) and cumulative dose to point A (HR, 0.95; P = 0.0001). Multivariate regression showed that the presence of a tandem was the only significant predictor of OS (HR, 0.46; P = 0.04). There were no significant predictors of complications.
Conclusions: The dose to point A of approximately 85 Gy as associated with tandem use was a significant predictor of survival in patients with stage IIIB cervical carcinoma, indicating the significance of the central location of the high dose provided by the tandem. Patients selected for interstitial brachytherapy alone must receive sufficient dose, and a tandem should be placed whenever feasible for all patients with an intact uterus treated for locally advanced cervical cancer.
C1 [Viswanathan, Akila N.; Cormack, Robert] Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02115 USA.
[Viswanathan, Akila N.; Cormack, Robert] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Rawal, Bhupendra; Lee, Hang] Massachusetts Gen Hosp, Dept Biostat Sci, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Viswanathan, AN (reprint author), Brigham & Womens Hosp, Dept Radiat Oncol, 75 Francis St L2, Boston, MA 02115 USA.
EM aviswanathan@lroc.harvard.edu
OI Cormack, Robert/0000-0001-5553-9984
NR 24
TC 15
Z9 17
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1048-891X
J9 INT J GYNECOL CANCER
JI Int. J. Gynecol. Cancer
PD NOV
PY 2009
VL 19
IS 8
BP 1402
EP 1406
DI 10.1111/IGC.0b013e3181b62e73
PG 5
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 522YJ
UT WOS:000272035900020
PM 20009897
ER
PT J
AU Seemayer, TA
Arseneau, J
Young, RH
AF Seemayer, Thomas A.
Arseneau, Jocelyne
Young, Robert H.
TI History of Gynecological Pathology XXIII. Jean-Paul Andre Latour, MD, CM
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY
LA English
DT Biographical-Item
DE History of gynecological pathology; Jean-Paul Andre Latour
C1 [Arseneau, Jocelyne] McGill Univ, Dept Pathol, Fac Med, Montreal, PQ H3A 2B4, Canada.
[Seemayer, Thomas A.] Univ Nebraska, Med Ctr, Omaha, NE USA.
[Arseneau, Jocelyne] Royal Victoria Hosp, Montreal, PQ H3A 1A1, Canada.
[Young, Robert H.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, James Homer Wright Pathol Labs, Boston, MA USA.
RP Arseneau, J (reprint author), McGill Univ, Dept Pathol, Fac Med, Lyman Duff Med Sci Bldg,3775 Univ Ave, Montreal, PQ H3A 2B4, Canada.
EM jocelyne.arseneau@mcgill.ca
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-1691
J9 INT J GYNECOL PATHOL
JI Int. J. Gynecol. Pathol.
PD NOV
PY 2009
VL 28
IS 6
BP 505
EP 513
DI 10.1097/PGP.0b013e3181a9ea34
PG 9
WC Obstetrics & Gynecology; Pathology
SC Obstetrics & Gynecology; Pathology
GA 512JP
UT WOS:000271244700001
PM 19851196
ER
PT J
AU Kawakami, T
Urakami, S
Hirata, H
Tanaka, Y
Nakajima, K
Enokida, H
Shiina, H
Ogishima, T
Tokizane, T
Kawamoto, K
Miura, K
Ishii, N
Dahiya, R
AF Kawakami, T.
Urakami, S.
Hirata, H.
Tanaka, Y.
Nakajima, K.
Enokida, H.
Shiina, H.
Ogishima, T.
Tokizane, T.
Kawamoto, K.
Miura, K.
Ishii, N.
Dahiya, R.
TI Superoxide dismutase analog (Tempol: 4-hydroxy-2, 2, 6,
6-tetramethylpiperidine 1-oxyl) treatment restores erectile function in
diabetes-induced impotence
SO INTERNATIONAL JOURNAL OF IMPOTENCE RESEARCH
LA English
DT Article
DE oxidative stress; nitric oxide; superoxide; diabetes; erectile
dysfunction
ID NITRIC-OXIDE; ENDOTHELIAL DYSFUNCTION; ANTIOXIDANT THERAPY; PENILE
CRURA; RATS; STREPTOZOTOCIN; APOPTOSIS; COMPLICATIONS; EXPRESSION;
DAMAGE
AB We hypothesized that the administration of the superoxide dismutase (SOD) mimetic Tempol (4-hydroxy-2, 2, 6, 6-tetramethylpiperidine 1-oxyl) may reverse diabetes-induced erectile dysfunction. To test this hypothesis, reactive oxygen species-related genes (SOD1, SOD2, GP x 1, CAT, NOS2, NOS3) were tested, erectile functional studies and immunohistochemical analysis were carried out in diabetic rats treated with or without Tempol. Thirty Sprague-Dawley (3-4months old) rats were divided into three groups (n = 10 each), 20 with diabetes (diabetic control and Tempol treatment) and 10 healthy controls. At 12 weeks after the induction of diabetes by streptozotocin and Tempol treatment, all groups underwent in vivo cavernous nerve stimulation. Rat crura were harvested and the expression of antioxidative defense enzymes were examined by semi-quantitative reverse transcriptase PCR (RT-PCR). To confirm the RT-PCR results, we carried out immunohistochemistry (IHC) for catalase (CAT) and iNOS (NOS2). Nitration of tyrosine groups in proteins was also examined by IHC. Mean intracavernous pressure in the diabetic group was significantly lower than in the healthy controls (P < 0.001) and was reversed by Tempol treatment (P < 0.0108). NOS2 protein expression was significantly increased in diabetic animals compared with healthy controls and Tempol restored NOS2 protein level. Nitrotyrosine was also higher in diabetic animals and although Tempol treatment decreased its formation, it remained higher than that found in healthy controls. This study suggests that Tempol treatment increased erectile function through modulating oxidative stress-related genes in diabetic rats. This is the first report about the relationship between diabetes-induced erectile dysfunction and oxidative stress, and antioxidative therapy using the superoxide dismutase mimetic, Tempol, to restore erectile function. International Journal of Impotence Research (2009) 21, 348-355; doi:10.1038/ijir.2009.28; published online 25 June 2009
C1 [Kawakami, T.; Urakami, S.; Hirata, H.; Tanaka, Y.; Enokida, H.; Shiina, H.; Ogishima, T.; Tokizane, T.; Kawamoto, K.; Dahiya, R.] San Francisco VA Med Ctr, Dept Urol, San Francisco, CA USA.
[Kawakami, T.; Urakami, S.; Hirata, H.; Tanaka, Y.; Enokida, H.; Shiina, H.; Ogishima, T.; Tokizane, T.; Kawamoto, K.; Dahiya, R.] Univ Calif San Francisco, San Francisco, CA 94121 USA.
[Kawakami, T.; Nakajima, K.; Miura, K.; Ishii, N.] Toho Univ, Fac Med, Dept Urol, Tokyo, Japan.
RP Dahiya, R (reprint author), Vet Affairs Med Ctr, Dept Urol, Urol Res Ctr 112F, 4150 Clement St, San Francisco, CA 94121 USA.
EM rdahiya@urology.ucsf.edu
FU NIH [RO1DK075524, T32DK007790]
FX We thank Dr Roger Erickson for his support and assistance with the
preparation of the paper. This study was supported by Grants
RO1DK075524, T32DK007790 from the NIH.
NR 29
TC 9
Z9 12
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0955-9930
J9 INT J IMPOT RES
JI Int. J. Impot. Res.
PD NOV-DEC
PY 2009
VL 21
IS 6
BP 348
EP 355
DI 10.1038/ijir.2009.28
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 517OV
UT WOS:000271626400004
PM 19554009
ER
PT J
AU Salama, JK
Haddad, RI
Kies, MS
Busse, PM
Dong, L
Brizel, DM
Eisbruch, A
Tishler, RB
Trotti, AM
Garden, AS
AF Salama, Joseph K.
Haddad, Robert I.
Kies, Merril S.
Busse, Paul M.
Dong, Lei
Brizel, David M.
Eisbruch, Avraham
Tishler, Roy B.
Trotti, Andy M.
Garden, Adam S.
TI CLINICAL PRACTICE GUIDANCE FOR RADIOTHERAPY PLANNING AFTER INDUCTION
CHEMOTHERAPY IN LOCOREGIONALLY ADVANCED HEAD-AND-NECK CANCER
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Induction chemotherapy; Intensity-modulated radiotherapy; Radiotherapy
planning; Head-and-neck cancer
ID INTENSITY-MODULATED RADIOTHERAPY; LOCALLY ADVANCED HEAD; SQUAMOUS-CELL
CARCINOMA; STAGE NASOPHARYNGEAL CARCINOMA; RADIATION-THERAPY; CONCURRENT
CHEMORADIOTHERAPY; SALIVARY FUNCTION; EXPERIENCE; FLUOROURACIL;
IRRADIATION
AB Purpose: The use of induction chemotherapy (IC) for locoregionally advanced head-and-neck cancer is increasing. The response to IC often causes significant alterations in tumor volume and location and shifts in normal anatomy. Proper determination of the radiotherapy (RT) targets after IC becomes challenging, especially with the use of conformal and precision RT techniques. Therefore, a consensus conference was convened to discuss issues related to RT planning and coordination of care for patients receiving IC.
Methods and Materials: Ten participants with special expertise in the various aspects of integration of IC and RT for the treatment of locoregionally advanced head-and-neck cancer, including radiation oncologists, medical oncologists, and a medical physicist, participated. The individual members were assigned topics for focused, didactic presentations. Discussion was encouraged after each presentation, and recommendations were formulated.
Results: Recommendations and guidelines emerged that emphasize up-front evaluation by all members of the head-and-neck management team, high-quality baseline and postinduction planning scans with the patient in the treatment position, the use of preinduction target volumes, and the use of full-dose RT, even in the face of a complete response.
Conclusion: A multidisciplinary approach is strongly encouraged. Although these recommendations were provided primarily for patients treated with IC, many of these same principles apply to concurrent chemoradiotherapy without IC. A rapid response during RT is quite common, requiring the development of two or more plans in a sizeable fraction of patients, and suggesting the need for similar guidance in the rapidly evolving area of adaptive RT. (C) 2009 Elsevier Inc.
C1 [Salama, Joseph K.] Univ Chicago, Dept Radiat & Cellular Oncol, Chicago, IL 60637 USA.
[Haddad, Robert I.; Tishler, Roy B.] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kies, Merril S.; Dong, Lei; Garden, Adam S.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Busse, Paul M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Brizel, David M.] Duke Univ, Med Ctr, Duke Comprehens Canc Ctr, Durham, NC 27710 USA.
[Eisbruch, Avraham] Univ Michigan, Ann Arbor, MI 48109 USA.
[Trotti, Andy M.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
RP Salama, JK (reprint author), Univ Chicago, Dept Radiat & Cellular Oncol, 5758 S Maryland Ave,MC 9006, Chicago, IL 60637 USA.
EM jsalama@radonc.uchicago.edu
OI Dong, Lei/0000-0003-2623-3198
NR 53
TC 36
Z9 42
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 1
PY 2009
VL 75
IS 3
BP 725
EP 733
DI 10.1016/j.ijrobp.2008.11.059
PG 9
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 503WR
UT WOS:000270573100013
PM 19362781
ER
PT J
AU Lee, LJ
Sadow, CA
Russell, A
Viswanathan, AN
AF Lee, Larissa J.
Sadow, Cheryl A.
Russell, Anthony
Viswanathan, Akila N.
TI CORRELATION OF POINT B AND LYMPH NODE DOSE IN 3D-PLANNED HIGH-DOSE-RATE
CERVICAL CANCER BRACHYTHERAPY
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE HDR brachytherapy; cervical cancer; pelvic lymph nodes; point B
ID PELVIC RADIOTHERAPY; RADIATION-THERAPY; UTERINE CERVIX; CARCINOMA;
RECOMMENDATIONS; GUIDELINES; VOLUME; DELINEATION; TERMS
AB Purpose: To compare high dose rate (HDR) point B to pelvic lymph node dose using three-dimensional-planned brachytherapy for cervical cancer.
Methods and Materials: Patients with FIGO Stage IB-IIIB cervical cancer received 70 tandem HDR applications using CT-based treatment planning. The obturator, external, and internal iliac lymph nodes (LN) were contoured. Per fraction (PF) and combined fraction (CF) right (R), left (L), and bilateral (Bil) nodal doses were analyzed. Point B dose was compared with LN dose-volume histogram (DVH) parameters by paired t test and Pearson correlation coefficients.
Results: Mean PF and CF doses to point B were R 1.40 Gy +/- 0.14 (CF: 7 Gy), L 1.43 +/- 0.15 (CF: 7.15 Gy), and Bil 1.41 +/- 0.15 (CF: 7.05 Gy). The correlation coefficients between point B and the D100, D90, D50, D2cc, D1cc, and D0.1cc LN were all less than 0.7. Only the D2cc to the obturator and the D0.1cc to the external iliac nodes were not significantly different from the point B dose. Significant differences between R and L nodal DVHs were seen, likely related to tandem deviation from irregular tumor anatomy.
Conclusions: With HDR brachytherapy for cervical cancer, per fraction nodal dose approximates a dose equivalent to teletherapy. Point B is a poor surrogate for dose to specific nodal groups. Three-dimensional defined nodal contours during brachytherapy provide a more accurate reflection of delivered dose and should be part of comprehensive planning of the total dose to the pelvic nodes, particularly when there is evidence of pathologic involvement. (C) 2009 Elsevier Inc.
C1 [Viswanathan, Akila N.] Harvard Univ, Brigham & Womens Hosp, Dept Radiat Oncol, Dana Farber Canc Inst,Sch Med, Boston, MA 02115 USA.
[Lee, Larissa J.] Harvard Univ, Sch Med, Harvard Radiat Oncol Program, Boston, MA 02115 USA.
[Sadow, Cheryl A.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Russell, Anthony] Harvard Univ, Sch Med, Dept Radiat Oncol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Viswanathan, AN (reprint author), Harvard Univ, Brigham & Womens Hosp, Dept Radiat Oncol, Dana Farber Canc Inst,Sch Med, 75 Francis St L2, Boston, MA 02115 USA.
EM aviswanathan@lroc.harvard.edu
OI Viswanathan, Akila/0000-0002-2003-0392
FU NCI NIH HHS [K07 CA117979, K07 CA117979-02, K07 CA117979-01, K07
CA117979-04, K07 CA117979-03]
NR 16
TC 13
Z9 14
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 1
PY 2009
VL 75
IS 3
BP 803
EP 809
DI 10.1016/j.ijrobp.2008.11.052
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 503WR
UT WOS:000270573100024
PM 19286328
ER
PT J
AU Rosenstein, BS
Held, KD
Rockwell, S
Williams, JP
Zeman, EM
AF Rosenstein, Barry S.
Held, Kathryn D.
Rockwell, Sara
Williams, Jacqueline P.
Zeman, Elainie M.
TI AMERICAN SOCIETY FOR RADIATION ONCOLOGY (ASTRO) SURVEY OF RADIATION
BIOLOGY EDUCATORS IN US AND CANADIAN RADIATION ONCOLOGY RESIDENCY
PROGRAMS
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Radiation biology; Teaching; Radiation oncology residents
ID RADIOBIOLOGY; CONSENSUS
AB Purpose: To obtain, in a survey-based study, detailed information on the faculty currently responsible for teaching radiation biology courses to radiation oncology residents in the United States and Canada.
Methods and Materials: In March-December 2007 a survey questionnaire was sent to faculty having primary responsibility for teaching radiation biology to residents in 93 radiation oncology residency programs in the United States and Canada.
Results: The responses to this survey document the aging of the faculty who have primary responsibility for teaching radiation biology to radiation oncology residents. The survey found a dramatic decline with time in the percentage of educators whose graduate training was in radiation biology. A significant number of the educators responsible for teaching radiation biology were not fully acquainted with the radiation sciences, either through training or practical application. In addition, many were unfamiliar with some of the organizations setting policies and requirements for resident education. Freely available tools, such as the American Society for Radiation Oncology (ASTRO) Radiation and Cancer Biology Practice Examination and Study Guides, were widely used by residents and educators. Consolidation of resident courses or use of a national radiation biology review course was viewed as unlikely by most programs.
Conclusions: A high priority should be given to the development of comprehensive teaching tools to assist those individuals who have responsibility for teaching radiation biology courses but who do not have an extensive background in critical areas of radiobiology related to radiation oncology. These findings also suggest a need for new graduate programs in radiobiology. (C) 2009 Elsevier Inc.
C1 [Rosenstein, Barry S.] Mt Sinai Sch Med, Dept Radiat Oncol, New York, NY 10029 USA.
[Rosenstein, Barry S.] NYU, Sch Med, Dept Radiat Oncol, New York, NY USA.
[Held, Kathryn D.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, Boston, MA USA.
[Rockwell, Sara] Yale Univ, Sch Med, Yale Comprehens Canc Ctr, Dept Radiat Therapy, New Haven, CT USA.
[Rockwell, Sara] Yale Univ, Sch Med, Dept Pharmacol, Yale Comprehens Canc Ctr, New Haven, CT 06510 USA.
[Williams, Jacqueline P.] Univ Rochester, James P Wilmot Canc Ctr, Dept Radiat Oncol, Rochester, NY USA.
[Zeman, Elainie M.] Univ N Carolina, Sch Med, Dept Radiat Oncol, Chapel Hill, NC 27599 USA.
RP Rosenstein, BS (reprint author), Mt Sinai Sch Med, Dept Radiat Oncol, 1 Gustave Levy Pl, New York, NY 10029 USA.
EM bany.rosenstein@mssm.edu
RI Rockwell, Sara/B-8458-2009
FU National Institutes of Health/National Institute of Allergy and
Infectious Diseases [5U19 AI067733-03]
FX Supported in part by Education Core Grant 5U19 AI067733-03 from the
National Institutes of Health/National Institute of Allergy and
Infectious Diseases (to J.W.).
NR 11
TC 7
Z9 8
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0360-3016
J9 INT J RADIAT ONCOL
JI Int. J. Radiat. Oncol. Biol. Phys.
PD NOV 1
PY 2009
VL 75
IS 3
BP 896
EP 905
DI 10.1016/j.ijrobp.2009.05.009
PG 10
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 503WR
UT WOS:000270573100036
PM 19733012
ER
PT J
AU Ooi, YH
Oh, DJ
Rhee, DJ
AF Ooi, Yen Hoong
Oh, Dong-Jin
Rhee, Douglas J.
TI Effect of Bimatoprost, Latanoprost, and Unoprostone on Matrix
Metalloproteinases and Their Inhibitors in Human Ciliary Body Smooth
Muscle Cells
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID OPEN-ANGLE GLAUCOMA; ELEVATED INTRAOCULAR-PRESSURE; RANDOMIZED
CLINICAL-TRIAL; FP PROSTAGLANDIN RECEPTOR; NORMAL-TENSION GLAUCOMA;
OCULAR HYPERTENSION; TISSUE INHIBITORS; TRABECULAR MESHWORK; LOWERING
EFFICACY; AQUEOUS-HUMOR
AB PURPOSE. Matrix metalloproteinase (MMP)-mediated turnover of extracellular matrix (ECM) affects outflow resistance in the uveoscleral pathway. The balance of MMPs and tissue inhibitors of metalloproteinases (TIMPs) governs the rate of ECM turnover in many tissues. The hypothesis was that a differential effect on MMPs and TIMPs in ciliary body smooth muscle (CBSM) cells would relate to the relative intraocular pressure-lowering effectiveness of the prostaglandin analogues (PGAs) bimatoprost, latanoprost, and unoprostone.
METHODS. Human CBSM cells isolated from donor corneoscleral rims were incubated for 24 hours with control (0.015% ethanol in DMEM) or the free acid forms of bimatoprost (0.01 or 0.1 mu g/mL), latanoprost (0.03 or 0.3 mu g/mL), or unoprostone (0.145 or 1.45 mu g/mL). Western blot analysis determined the relative protein concentrations of MMP-1, -2, -3, -9, and -24 as well as TIMP-1 through -4. Zymography measured the relative activity levels of MMP-1, -2, -3, and -9.
RESULTS. All PGAs increased MMP-1, -3, and -9. Bimatoprost and latanoprost did not change MMP-2. Unoprostone decreased MMP-2 (21% +/- 3%). On zymography, MMP-1 and -2 did not change. Bimatoprost and latanoprost increased MMP-9 activity by 75% +/- 27% and 75% +/- 24%, respectively. MMP-3 activity was not detected on zymography. All PGAs increased TIMP-3, but only unoprostone increased TIMPs1 and -4 by 100% +/- 20% and 61% +/- 11%, respectively. TIMP-2 was unchanged by bimatoprost and latanoprost, but decreased by unoprostone (35% +/- 8%).
CONCLUSIONS. Decreased MMP-2 with concurrent increases of TIMP-1 and -4 by unoprostone may explain the lower clinical efficacy of unoprostone. The MMP/TIMP balance relates to the observed intraocular pressure-lowering effectiveness in clinical studies with PGAs. (Invest Ophthalmol Vis Sci. 2009;50:5259-5265) DOI:10.1167/iovs.08-3356
C1 [Ooi, Yen Hoong; Oh, Dong-Jin; Rhee, Douglas J.] Massachusetts Eye & Ear Infirm, Dept Ophthalmol, Boston, MA 02114 USA.
RP Rhee, DJ (reprint author), Massachusetts Eye & Ear Infirm, Dept Ophthalmol, 243 Charles St, Boston, MA 02114 USA.
EM dougrhee@aol.com
FU Allergan; American Glaucoma Society Clinician-Scientist Fellowship;
Massachusetts Lions Eye Research Foundation; Pfizer Ophthalmics; [EY
14104]
FX Supported by Allergan, American Glaucoma Society Clinician-Scientist
Fellowship, Massachusetts Lions Eye Research Foundation, Pfizer
Ophthalmics, and EY 14104 (MEEI Vision-Core Grant).
NR 74
TC 13
Z9 13
U1 1
U2 1
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD NOV
PY 2009
VL 50
IS 11
BP 5259
EP 5265
DI 10.1167/iovs.08-3356
PG 7
WC Ophthalmology
SC Ophthalmology
GA 514XH
UT WOS:000271429200032
PM 19443729
ER
PT J
AU Vymazal, J
Spuentrup, E
Cardenas-Molina, G
Wiethoff, AJ
Hartmann, MG
Caravan, P
Parsons, EC
AF Vymazal, Josef
Spuentrup, Elmar
Cardenas-Molina, Gerardo
Wiethoff, Andrea J.
Hartmann, Michael G.
Caravan, Peter
Parsons, Edward C., Jr.
TI Thrombus Imaging With Fibrin-Specific Gadolinium-Based MR Contrast Agent
EP-2104R Results of a Phase II Clinical Study of Feasibility
SO INVESTIGATIVE RADIOLOGY
LA English
DT Article
DE contrast media; fibrin; magnetic resonance imaging; thrombosis; thrombus
ID STATE FREE PRECESSION; DEEP VENOUS THROMBOSIS; MAGNETIC-RESONANCE;
PULMONARY-EMBOLISM; COMPUTED-TOMOGRAPHY; CORONARY-THROMBOSIS;
INITIAL-EXPERIENCE; VEIN THROMBOSIS; THORACIC AORTA; SWINE MODEL
AB Purpose: To determine the feasibility of detecting thrombi using a fibrin-specific gadolinium-based magnetic resonance imaging contrast agent, EP-2104R.
Methods: Subjects with confirmed thrombus in the venous system (n = 14), or in the heart, or arterial system (n = 38) were enrolled. Patients were imaged before and at various times following a 4 mu mol/kg intravenous bolus injection of EP-2104R: < 1 hour (N = 16), 2 to 6 hours (N = 36), and/or 20 to 36 hours (N = 33). Images were assessed by investigators at each site and by a single reader not affiliated with the sites to determine whether thrombi were visible, not visible, or further enhanced with EP-2104R. A subset of data was analyzed quantitatively by measuring a signal intensity relative to background tissue.
Results: Overall, 29 thrombi were visible before contrast administration, 3 of 14 in the venous system, and 26 of 38 in the arteries and heart. Thrombi generally enhanced in signal after EP-2104R injection, and an additional 7 were visualized. After contrast, 4 of 14 thrombi were visible in the venous system, and 32 of 38 in the arteries and heart. Thrombi were more conspicuous when imaged at 2 to 6 hours post EP-2104R compared with within I hour, because of lower blood background. Quantitatively, the post: pre signal intensity ratio was 1.90 at 2 to 6 hours post injection (standard deviation = 1.08, N = 20, P < 0.001); and 2.04 (standard deviation = 1.29, N = 19, P < 0.0025) for the 20 to 36 hours time point. There were no serious adverse events considered related to study drug.
Conclusion: EP-2104R enhanced magnetic resonance imaging detects thrombi not readily visible in precontrast screening and gives additional enhancement of thrombi that are visible in precontrast imaging.
C1 [Vymazal, Josef] Hosp Homolce, Dept Radiodiagnost, Prague, Czech Republic.
[Spuentrup, Elmar] Univ Cologne, Dept Radiol, Cologne, Germany.
[Cardenas-Molina, Gerardo] Hosp & Clin OCA, Monterrey, NL, Mexico.
[Wiethoff, Andrea J.] Philips Healthcare, Best, Netherlands.
[Hartmann, Michael G.] VP Diagnost Inc, Seattle, WA USA.
[Caravan, Peter] Massachusetts Gen Hosp, AA Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Parsons, Edward C., Jr.] EPIX Pharmaceut Inc, Lexington, MA USA.
RP Parsons, EC (reprint author), 30 Wheatland St, Burlington, MA 01803 USA.
EM edward.parsons@aya.yale.edu
FU EPIX Pharmaceuticals, Inc
FX Supported by EPIX Pharmaceuticals, Inc.
NR 30
TC 70
Z9 74
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0020-9996
J9 INVEST RADIOL
JI Invest. Radiol.
PD NOV
PY 2009
VL 44
IS 11
BP 697
EP 704
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 515SN
UT WOS:000271493300002
PM 19809344
ER
PT J
AU Rukstalis, JM
Habener, JF
AF Rukstalis, J. Michael
Habener, Joel F.
TI Neurogenin3 A master regulator of pancreatic islet differentiation and
regeneration
SO ISLETS
LA English
DT Review
DE beta-cells; stem/progenitor cells; pancreas regeneration; diabetes;
islets; ducts
AB The basic helix-loop-helix transcription factor neurogenin-3 (Ngn3, Neurog3) is critical for the development of the endocrine cells of the islets. Either disrupted or forced expression of Ngn3 early in mouse pancreas development abrogates the formation of islets. The successive waves of Ngn3 expression that occur during the primary and secondary transitions of endocrine cell development temporally determine the four distinct endocrine cell lineages, alpha, beta, PP and delta cells that express glucagon, insulin, pancreatic polypeptide and somatostatin, respectively. During islet regeneration after injury of the adult mouse pancreas, such as by duct ligation or streptozotocin, Ngn3 is activated in duct-associated stem/progenitor cells that transform into alpha and/or beta-cells (Xu et al., Collombat et al.). The important role of Ngn3 as a master regulator of endocrine pancreas development directs attention to finding therapeutic approaches to enhance Ngn3 expression in diabetes as a means to increase beta-cell mass and functions.
C1 [Rukstalis, J. Michael; Habener, Joel F.] Massachusetts Gen Hosp, Mol Endocrinol Lab, Boston, MA 02114 USA.
RP Habener, JF (reprint author), Massachusetts Gen Hosp, Mol Endocrinol Lab, Boston, MA 02114 USA.
EM jhabener@partners.org
FU USPHS
FX We thank William Hillmann for helpful contributions in the laboratory.
Supported in part by a USPHS Research Career Development Award to J.M.R.
NR 80
TC 48
Z9 51
U1 0
U2 3
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1938-2014
J9 ISLETS
JI Islets
PD NOV-DEC
PY 2009
VL 1
IS 3
BP 177
EP 184
DI 10.4161/isl.1.3.9877
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA V16WV
UT WOS:000207900600002
PM 21099270
ER
PT J
AU Kawamori, D
Kulkarni, RN
AF Kawamori, Dan
Kulkarni, Rohit N.
TI Insulin modulation of glucagon secretion The role of insulin and other
factors in the regulation of glucagon secretion
SO ISLETS
LA English
DT Article
DE glucagon; insulin; insulin receptor; hypoglycemia; somatostatin
C1 [Kulkarni, Rohit N.] Harvard Univ, Sch Med, Dept Cellular & Mol Physiol, Joslin Diabet Ctr, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Kulkarni, RN (reprint author), Harvard Univ, Sch Med, Dept Cellular & Mol Physiol, Joslin Diabet Ctr, Boston, MA 02115 USA.
EM Rohit.Kulkarni@joslin.harvard.edu
NR 35
TC 12
Z9 13
U1 0
U2 3
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1938-2014
J9 ISLETS
JI Islets
PD NOV-DEC
PY 2009
VL 1
IS 3
BP 276
EP 279
DI 10.4161/isl.1.3.9967
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA V16WV
UT WOS:000207900600017
PM 21099284
ER
PT J
AU Lehman, SJ
Schlett, CL
Bamberg, F
Lee, H
Donnelly, P
Shturman, L
Kriegel, MF
Brady, TJ
Hoffmann, U
AF Lehman, Sam J.
Schlett, Christopher L.
Bamberg, Fabian
Lee, Hang
Donnelly, Patrick
Shturman, Leon
Kriegel, Matthias F.
Brady, Thomas J.
Hoffmann, Udo
TI Assessment of Coronary Plaque Progression in Coronary Computed
Tomography Angiography Using a Semiquantitative Score
SO JACC-CARDIOVASCULAR IMAGING
LA English
DT Article
DE atherosclerosis; computed tomography; coronary artery disease; risk
factors; progression
ID RANDOMIZED CONTROLLED-TRIAL; INTRAVASCULAR ULTRASOUND; ATHEROSCLEROTIC
PLAQUE; ARTERY CALCIFICATION; CARDIOVASCULAR RISK; LEFT MAIN; DISEASE;
ASSOCIATION; REGRESSION; ACCURACY
AB OBJECTIVES We sought to describe the progression of coronary atherosclerotic plaque over time by computed tomography (CT) angiography stratified by plaque composition and its association with cardiovascular risk profiles.
BACKGROUND Data on the progression of atherosclerosis stratified by plaque composition with the use of noninvasive assessment by CT are limited and hampered by high measurement variability.
METHODS This analysis included patients who presented with acute chest pain to the emergency department but initially showed no evidence of acute coronary syndromes. All patients underwent contrast-enhanced 64-slice CT at baseline and after 2 years with the use of a similar protocol. CT datasets were coregistered and assessed for the presence of calcified and noncalcified plaque at 1 mm cross sections of the proximal 40 mm of each major coronary artery. Plaque progression over time and its association with risk factors were determined. Measurement reproducibility and correlation to plaque volume was performed in a subset of patients.
RESULTS We included 69 patients (mean age 55 +/- 12 years, 59% male patients) and compared 8,311 coregistered cross sections at baseline and follow-up. At baseline, any plaque, calcified plaque, and noncalcified were detected in 12.5%, 10.1%, and 2.4% of cross sections per patient, respectively. There was significant progression in the mean number of cross sections containing any plaque (16.5 +/- 25.3 vs. 18.6 +/- 25.5, p = 0.01) and noncalcified plaque (3.1 +/- 5.8 vs. 4.4 +/- 7.0, p = 0.04) but not calcified plaque (13.3 +/- 23.1 vs. 14.2 +/- 22.0, p = 0.2). In longitudinal regression analysis, the presence of baseline plaque, number of cardiovascular risk factors, and smoking were independently associated with plaque progression after adjustment for age, sex, and follow-up time interval. The semiquantitative score based on cross sections correlated closely with plaque volume progression (r = 0.75, p < 0.0001) and demonstrated an excellent intraobserver and interobserver agreement (kappa = 0.95 and kappa = 0.93, respectively).
CONCLUSIONS Coronary plaque burden of patients with acute chest pain significantly increases during the course of 2 years. Progression over time is dependent on plaque composition and cardiovascular risk profile. Larger studies are needed to confirm these results and to determine the effect of medical treatment on progression. (J Am Coll Cardiol Img 2009; 2: 1262-70) (C) 2009 by the American College of Cardiology Foundation
C1 [Bamberg, Fabian; Brady, Thomas J.; Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Cardiac MR PET CT Program, Boston, MA 02114 USA.
[Lee, Hang] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Hoffmann, U (reprint author), Massachusetts Gen Hosp, Dept Radiol, Cardiac MR PET CT Program, 165 Charles River Plaza,Suite 400, Boston, MA 02114 USA.
EM uhoffmann@partners.org
FU NIH [RO1 HL080053, T32HL076136]; Siemens Medical Solutions; General
Electric Healthcare; National Heart Foundation of Australia; Royal
Australian and New Zealand College of Physicians; German Federal
Ministry of Education and Research; Foundation of German Business,
Berlin Germany
FX This work was supported by the NIH (RO1 HL080053) and in part supported
by Siemens Medical Solutions and General Electric Healthcare. Dr. Lehman
was supported by grants from the National Heart Foundation of Australia
and the Royal Australian and New Zealand College of Physicians, Dr.
Schlett in part by grants from the German Federal Ministry of Education
and Research and the Foundation of German Business, Berlin Germany, and
Dr. Shturman in part by the National Institutes of Health grant
T32HL076136. Drs. Lehman and Schlett contributed equally to this work.
NR 27
TC 39
Z9 40
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-878X
J9 JACC-CARDIOVASC IMAG
JI JACC-Cardiovasc. Imag.
PD NOV
PY 2009
VL 2
IS 11
BP 1262
EP 1270
DI 10.1016/j.jcmg.2009.07.007
PG 9
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 725OX
UT WOS:000287656200003
PM 19909929
ER
PT J
AU Weiser, SD
Fernandes, KA
Brandson, EK
Lima, VD
Anema, A
Bangsberg, DR
Montaner, JS
Hogg, RS
AF Weiser, Sheri D.
Fernandes, Kimberly A.
Brandson, Eirikka K.
Lima, Viviane D.
Anema, Aranka
Bangsberg, David R.
Montaner, Julio S.
Hogg, Robert S.
TI The Association Between Food Insecurity and Mortality Among HIV-Infected
Individuals on HAART
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE food insecurity; HIV/AIDS; mortality; Vancouver
ID ACTIVE ANTIRETROVIRAL THERAPY; INJECTION-DRUG USERS;
IMMUNODEFICIENCY-VIRUS-INFECTION; CHRONIC ENERGY DEFICIENCY; BODY-MASS
INDEX; CD4 CELL COUNT; DISEASE PROGRESSION; MENTAL-HEALTH; WEIGHT-LOSS;
EPIDEMIOLOGY RESEARCH
AB Background: Food insecurity is increasingly recognized as a barrier to optimal treatment outcomes, but there is little data on this issue. We assessed associations between food insecurity and mortality among HIV-infected antiretroviral therapy-treated individuals in Vancouver, British Columbia, and whether body max index (BMI) modified associations.
Methods: Individuals were recruited from the British Columbia HIV/AIDS drug treatment program in 1998 and 1999 and were followed until June 2007 for outcomes. Food insecurity was measured with the Radimer/Cornell questionnaire. Cox proportional hazard models were used to determine associations between food insecurity, BMI, and nonaccidental deaths when controlling for confounders.
Results: Among 1119 participants, 536 (48%) were categorized as food insecure and 160 (14%) were categorized as underweight (BMI < 18.5). After a median follow-up time of 8.2 years, 153 individuals (14%) had died from nonaccidental deaths. After controlling for adherence, CD4 counts, and socioeconomic variables, people who were food insecure and underweight were nearly 2 times more likely to die (adjusted hazard ratio = 1.94, 95% confidence interval = 1.10 to 3.40) compared with people who were not food insecure or underweight. There was also a trend toward increased risk of mortality among people who were food insecure and not underweight (adjusted hazard ratio = 1.40, 95% confidence interval = 0.91 to 2.05). In contrast, people who were underweight but food secure were not more likely to die.
Conclusions: Food insecurity is a risk factor for mortality among antiretroviral therapy-treated individuals in British Columbia, particularly among individuals who are underweight. Innovative approaches to address food insecurity should be incorporated into HIV treatment programs.
C1 [Weiser, Sheri D.] Univ Calif San Francisco, Posit Hlth Program, Dept Med, San Francisco Gen Hosp, San Francisco, CA 94143 USA.
[Weiser, Sheri D.] Univ Calif San Francisco, Dept Med, Ctr AIDS Prevent Studies, San Francisco, CA 94143 USA.
[Fernandes, Kimberly A.; Brandson, Eirikka K.; Lima, Viviane D.; Anema, Aranka; Montaner, Julio S.; Hogg, Robert S.] British Columbia Ctr Excellence HIV AIDS, Vancouver, BC, Canada.
[Lima, Viviane D.; Montaner, Julio S.] Univ British Columbia, Dept Med, Vancouver, BC V5Z 1M9, Canada.
[Bangsberg, David R.] Harvard Univ, Massachusetts Gen Hosp, Harvard Initiat Global Hlth, Ctr Global Hlth,Ragon Inst,Sch Med, Boston, MA USA.
[Hogg, Robert S.] Simon Fraser Univ, Fac Hlth Sci, Burnaby, BC V5A 1S6, Canada.
RP Weiser, SD (reprint author), Univ Calif San Francisco, Posit Hlth Program, POB 0874, San Francisco, CA 94143 USA.
EM sheri.weiser@ucsf.edu
RI Hogg, Robert/B-2783-2012;
OI Hogg, Robert/0000-0003-3463-5488
FU Canadian Institute of Health Research; NIMH [79713-01]; Hellman Family
Foundation
FX Supported by funding from the Canadian Institute of Health Research. Dr.
Sheri D. Weiser received additional funding from NIMH 79713-01 and the
Hellman Family Foundation.
NR 68
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U1 3
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD NOV 1
PY 2009
VL 52
IS 3
BP 342
EP 349
PG 8
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 511WR
UT WOS:000271202900007
PM 19675463
ER
PT J
AU Allen, JD
Fantasia, HC
Fontenot, H
Flaherty, S
Santana, J
AF Allen, Jennifer D.
Fantasia, Heidi Collins
Fontenot, Holly
Flaherty, Stephen
Santana, Jeans
TI College Men's Knowledge, Attitudes, and Beliefs about the Human
Papillomavirus Infection and Vaccine
SO JOURNAL OF ADOLESCENT HEALTH
LA English
DT Article
DE Human papillomavirus; HPV; College health; Men's health
ID BURDEN
AB Men enrolled in an urban university participated in focus groups (k = 6; n = 45) to explore knowledge about human papillomavirus and attitudes toward prophylactic vaccine. Results suggest that regardless of whether vaccines become available to men, educational efforts should include them, as men tend to have many misconceptions and do not perceive themselves to be vulnerable. (C) 2009 Society for Adolescent Medicine. All rights reserved.
C1 [Allen, Jennifer D.; Fantasia, Heidi Collins; Fontenot, Holly; Santana, Jeans] Boston Coll, William Connell Sch Nursing, Chestnut Hill, MA 02167 USA.
[Allen, Jennifer D.; Flaherty, Stephen] Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA 02115 USA.
RP Allen, JD (reprint author), Boston Coll, William Connell Sch Nursing, 140 Commonwealth Ave, Boston, MA 02167 USA.
EM Jennifer.allen.5@bc.edu
RI Allen, Jennifer/M-2113-2015
NR 10
TC 19
Z9 19
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1054-139X
J9 J ADOLESCENT HEALTH
JI J. Adolesc. Health
PD NOV
PY 2009
VL 45
IS 5
BP 535
EP 537
DI 10.1016/j.jadohealth.2009.05.014
PG 3
WC Psychology, Developmental; Public, Environmental & Occupational Health;
Pediatrics
SC Psychology; Public, Environmental & Occupational Health; Pediatrics
GA 513HR
UT WOS:000271313800017
PM 19837363
ER
PT J
AU Soutullo, CA
Escamilla-Canales, I
Wozniak, J
Gamazo-Garran, P
Figueroa-Quintana, A
Biederman, J
AF Soutullo, Cesar A.
Escamilla-Canales, Inmaculada
Wozniak, Janet
Gamazo-Garran, Pilar
Figueroa-Quintana, Ana
Biederman, Joseph
TI Pediatric bipolar disorder in a Spanish sample: Features before and at
the time of diagnosis
SO JOURNAL OF AFFECTIVE DISORDERS
LA English
DT Article
DE Mania; Bipolar; Children; Adolescents; Phenomenology; Europe
ID AGE-CHILDREN-PRESENT; K-SADS-PL; PREPUBERTAL CHILDREN;
AFFECTIVE-ILLNESS; MOOD DISORDERS; MANIA SYMPTOMS; ADOLESCENTS;
PHENOMENOLOGY; ONSET; ADHD
AB Introduction: Bipolar disorder (BD) often starts in childhood or adolescence. Diagnostic delay is common and may have a negative impact on treatment response and outcome.
Objectives: To describe the clinical characteristics and symptoms of children with BD prior to their diagnosis and at the time of diagnosis in a sample in Spain.
Methods: We retrospectively reviewed the medical records of all children and adolescents (N = 38) with a DSM-IV diagnosis of BD evaluated in the Child & Adolescent Psychiatry Unit, University of Navarra, over a 6-year period. We collected the DSM-lV symptoms of BD prior and at the time of diagnosis using the K-SADS-PL interview template.
Results: BID was diagnosed in close to 4% of clinic patients. Thirty (79%) were boys and 8 (21%) were girls; 17 (44.7%) had BD-1, 2 (5.3%) BD-2, and 19 (49.9%) BD-NOS. Median age at diagnosis was 13.9 (10.6; 15.9). Delay of diagnosis was 1.5 (0.7;3.4) years. Symptoms of BD were similar to those reported in U.S. samples with high rates of severe irritability (94.6%) and psychiatric comorbidity: 92.1% of the BD children had at least one comorbid disorder and 18.4% had three comorbidities, most frequently ADHD (21%) and substance abuse (18.4%).
Conclusions: Clinical findings in this Spanish sample of children with BD closely resembles those described in U.S. clinics. Diagnostic delay, as in the U.S., and frequent misdiagnosis may explain low prevalence estimates found outside the U.S. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Soutullo, Cesar A.; Figueroa-Quintana, Ana] Univ Navarra, Child & Adolescent Psychiat Unit, Dept Psychiat & Med Psychol, Clin Univ, Pamplona 31008, Spain.
[Escamilla-Canales, Inmaculada; Gamazo-Garran, Pilar] Univ Navarra, Child & Adolescent Psychiat Unit, Dept Psychiat & Med Psychol, Clin Univ, Madrid, Spain.
[Wozniak, Janet; Biederman, Joseph] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Pediat Psychopharmacol Res Unit, Boston, MA USA.
RP Soutullo, CA (reprint author), Univ Navarra, Child & Adolescent Psychiat Unit, Dept Psychiat & Med Psychol, Clin Univ, Apartado 4209, Pamplona 31008, Spain.
EM csoutullo@unav.es
FU Alicia Koplowitz Foundation
FX The authors thank the Alicia Koplowitz Foundation for a Teaching Grant
that made possible a rotation of one of the authors (Dra. Inmaculada
Escamilla-Canales) at the MCH Pediatric Psycho pharmacology Unit,
Harvard University, Boston, MA, USA.
NR 55
TC 16
Z9 19
U1 4
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0327
J9 J AFFECT DISORDERS
JI J. Affect. Disord.
PD NOV
PY 2009
VL 118
IS 1-3
BP 39
EP 47
DI 10.1016/j.jad.2009.02.010
PG 9
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 506CI
UT WOS:000270750500005
PM 19285348
ER
PT J
AU Yong, PL
Werner, RM
AF Yong, Pierre L.
Werner, Rachel M.
TI Process quality measures and asthma exacerbations in the Medicaid
population
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Asthma; quality of care; Healthcare Effectiveness Data and Information
Set; Medicaid
ID PLAN EMPLOYER DATA; INHALED CORTICOSTEROIDS; OF-CARE; ADMINISTRATIVE
DATA; PERSISTENT ASTHMA; INFORMATION SET; RISK; VALIDATION; PREVENTION;
OUTCOMES
AB Background: Asthma quality assessment often focuses on controller medication use, yet claims-based studies find conflicting associations between this care process and clinical outcomes.
Objective: We sought to compare the association between 3 controller-based quality measures and asthma exacerbations to gain better understanding of how processes of care are related to clinical outcomes.
Methods: Identifying a cohort of Medicaid beneficiaries with persistent asthma by using Healthcare Effectiveness Data and Information Set (HEDIS) criteria for asthma in 2001-2002 in California and New York, we assessed 3 asthma quality metrics in 2002: (1) the current HEDIS measure of at least I controller medication filling; (2) at least 4 controller medication prescription fillings; and (3) a controller-to-total asthma medication ratio of at least 0.5. We calculated the odds of having an asthma exacerbation in 2003 as a function of performance on each quality metric, adjusting for race, sex, age, and prior outpatient and acute care use for asthma.
Results: Of 90,909 subjects with persistent asthma in California (48.1%) and New York (51.9%), those who obtained at least I or at least 4 controller medications had increased likelihood of poor outcomes (adjusted odds ratios, 1.80 [95% CI, 1.73-1.87] and 1.44 [95% CI 1.40-1.48], respectively). Beneficiaries meeting the controller-to-total asthma medication ratio measure were 23.0% less likely to have exacerbations (adjusted odds ratio, 0.77 [95% CI, 0.75-0.80]).
Conclusions: A higher controller medication ratio indicated a lower likelihood of asthma exacerbations, whereas assessing the number of controller medication-dispensing events was associated with a higher odds of exacerbation. (J Allergy Clin Immunol 2009;124:961-6.)
C1 [Yong, Pierre L.] Univ Penn, Robert Wood Johnson Clin Scholars Program, Sch Med, Philadelphia, PA 19106 USA.
[Yong, Pierre L.; Werner, Rachel M.] Philadelphia Vet Affairs Med Ctr, Dept Med, Philadelphia, PA USA.
[Yong, Pierre L.] Hosp Univ Penn, Dept Pulm Allergy & Crit Care, Philadelphia, PA 19104 USA.
[Yong, Pierre L.; Werner, Rachel M.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19106 USA.
[Yong, Pierre L.] Univ Penn, Ctr Publ Hlth Initiat, Philadelphia, PA 19106 USA.
RP Yong, PL (reprint author), Univ Penn, Robert Wood Johnson Clin Scholars Program, Sch Med, 1303A Blockley Hall,423 Guardian Dr, Philadelphia, PA 19106 USA.
EM pyong@nas.edu
FU Philadelphia Veterans Affairs Medical Center; Robert Wood Johnson
Clinical Scholars; Veterans Affairs HSR&D Career Development; Clinical
and Translational Science [UL1-RR024134]
FX P. L. Y. is supported by a training grant from the Philadelphia Veterans
Affairs Medical Center and the Robert Wood Johnson Clinical Scholars
Program. R. M. W is supported in part by a Veterans Affairs HSR&D Career
Development Award. The study was supported by pilot grant funding from
the Leonard Davis Institute of Health Economics and resources supported
by the Clinical and Translational Science Awards (UL1-RR024134).
NR 26
TC 20
Z9 20
U1 1
U2 5
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 NOV
PY 2009
VL 124
IS 5
BP 961
EP 966
DI 10.1016/j.jaci.2009.07.027
PG 6
WC Allergy; Immunology
SC Allergy; Immunology
GA 523XI
UT WOS:000272108000013
PM 19748660
ER
PT J
AU Patel, NC
Chinen, J
Rosenblatt, HM
Hanson, IC
Krance, RA
Paul, ME
Abramson, SL
Noroski, LM
Davis, CM
Seeborg, FO
Foster, SB
Leung, KS
Brown, BS
Ritz, J
Shearer, WT
AF Patel, Niraj C.
Chinen, Javier
Rosenblatt, Howard M.
Hanson, I. Celine
Krance, Robert A.
Paul, Mary E.
Abramson, Stuart L.
Noroski, Lenora M.
Davis, Carla M.
Seeborg, Filiz O.
Foster, Samuel B.
Leung, Kathryn S.
Brown, Betty S.
Ritz, Jerome
Shearer, William T.
TI Outcomes of patients with severe combined immunodeficiency treated with
hematopoietic stem cell transplantation with and without preconditioning
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Hematopoietic stem cell transplantation; graft-versus-host disease;
severe combined immunodeficiency; immune reconstitution; primary
immunodeficiency; conditioning
ID BONE-MARROW-TRANSPLANTATION; IMMUNE RECONSTITUTION; SINGLE-CENTER;
DEFICIENCY; BMT
AB Background: The effect of pretransplantation conditioning on the long-term outcomes of patients receiving hematopoietic stem cell transplantation for severe combined immunodeficiency (SCID) has not been completely determined.
Objective: We sought to assess the outcomes of 23 mostly conditioned patients with SCID and compare their outcomes with those of 25 previously reported nonconditioned patients with SCID who underwent transplantation.
Methods: In the present study we reviewed the medical records of these 23 consecutive, mostly conditioned patients with SCID who underwent transplantation between 1998 and 2007.
Results: Eighteen patients (median age at transplantation, 10 months; range, 0.8-108 months) received haploidentical mismatched related donor, matched unrelated donor, or mismatched unrelated donor transplants, 17 of whom received pretransplantation conditioning (with I not conditioned); 13 (72%) patients engrafted with donor cells and survive at a median of 3.8 years (range, 1.8-9.8 year); 5 (38%) of 13 patients require intravenous immunoglobulin; and 6 of 6 age-eligible children attend school. Of 5 recipients (median age at transplantation, 7 months; range, 2-23 months) of matched related donor transplants, all 5 engrafted and survive at a median of 7.5 years (range, 1.5-9.5 year), I recipient requires intravenous immunoglobulin, and 3 of 3 age-eligible children attend school. Gene mutations were known in 16 cases: mutation in the common gamma chain of the IL-2 receptor (IL2RG) in 7 patients, mutation in the alpha chain of the IL-7 receptor (IL7RA) in 4 patients, mutation in the recombinase-activating gene (RAG1) in 2 patients, adenosine deaminase deficiency (ADA) in 2 patients, and adenylate kinase 2 (AK2) in I patient. Early outcomes and quality of life of the previous nonconditioned versus the present conditioned cohorts were not statistically different, but longer-term follow-up is necessary for confirmation.
Conclusions: Hematopoietic stem cell transplantation in patients with SCED results in engraftment, long-term survival, and a good quality of life for the majority of patients with or without pretransplantation conditioning. (J Allergy Clin Immunol 2009;124:1062-9.)
C1 [Patel, Niraj C.; Chinen, Javier; Hanson, I. Celine; Paul, Mary E.; Abramson, Stuart L.; Noroski, Lenora M.; Davis, Carla M.; Seeborg, Filiz O.; Foster, Samuel B.; Brown, Betty S.; Shearer, William T.] Texas Childrens Hosp, Dept Pediat, Sect Allergy & Immunol, Baylor Coll Med, Houston, TX 77039 USA.
[Rosenblatt, Howard M.] Dell Childrens Med Ctr Cent Texas, Austin, TX USA.
[Krance, Robert A.; Leung, Kathryn S.] Texas Childrens Hosp, Sect Hematol & Oncol, Baylor Coll Med, Houston, TX 77039 USA.
[Ritz, Jerome] Harvard Univ, Sch Med, Div Hematol Malignancies, Boston, MA USA.
[Ritz, Jerome] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Ritz, Jerome] Harvard Univ, Sch Med, Harvard Stem Cell Inst, Boston, MA USA.
RP Shearer, WT (reprint author), Texas Childrens Hosp, Dept Pediat, Sect Allergy & Immunol, Baylor Coll Med, 6621 Fannin,FC 330-01, Houston, TX 77039 USA.
EM wtsheare@texaschildrenshospital.org
FU Pfizer; Astella; Novartis; CSL Behring; Food Allergy and Anaphylaxis
Network
FX R. A. Krance has received research support from Pfizer and Astella. S.
L. Abramson has received research support from Novartis and CSL Behring.
C. M. Davis has received research support from the Food Allergy and
Anaphylaxis Network.
NR 17
TC 26
Z9 27
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 NOV
PY 2009
VL 124
IS 5
BP 1062
EP 1069
DI 10.1016/j.jaci.2009.08.041
PG 8
WC Allergy; Immunology
SC Allergy; Immunology
GA 523XI
UT WOS:000272108000029
PM 19895994
ER
PT J
AU Leissner, KB
Mahmood, FU
AF Leissner, Kay B.
Mahmood, Feroze U.
TI Physiology and pathophysiology at high altitude: considerations for the
anesthesiologist
SO JOURNAL OF ANESTHESIA
LA English
DT Review
DE High altitude; High altitude illness; Hypoxia; Hypoxic pulmonary
vasoconstriction
ID ACUTE MOUNTAIN-SICKNESS; HYPOXIC PULMONARY VASOCONSTRICTION; OPERATION
EVEREST-II; INHALED NITRIC-OXIDE; PATENT FORAMEN OVALE; SEA-LEVEL;
MODERATE ALTITUDE; CEREBRAL EDEMA; VENTILATORY RESPONSE; SIMULATED
ALTITUDE
AB Millions of people live in, work in, and travel to areas of high altitude (HA). Skiers, trekkers, and mountaineers reach altitudes of 2500 m to more than 8000 m for recreation, and sudden ascents to high altitude without the benefits of acclimatization are increasingly common. HA significantly affects the human body, especially the cardiovascular and pulmonary systems, because of oxygen deprivation due to decreased ambient barometric pressure. Rapid ascents may lead to high-altitude diseases that sometimes have fatal consequences. Other factors, such as severe cold, dehydration, high winds, and intense solar radiation, increase the morbidity of patients at HA. Anesthesiologists working in or visiting areas of higher elevations should become familiar with the human physiology, altered pharmacology, and disease pattern of HA.
C1 [Leissner, Kay B.] VA Boston Healthcare Syst, Dept Anesthesia, Boston, MA USA.
[Leissner, Kay B.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Mahmood, Feroze U.] Harvard Univ, Beth Israel Deaconess Med Ctr, Dept Anesthesia, Sch Med, Boston, MA 02215 USA.
RP Leissner, KB (reprint author), VA Boston Healthcare Serv, Anesthesiol Serv, 1400 VFW Pkwy, W Roxbury, MA 02132 USA.
RI Mahmood, Feroze/B-1383-2008
OI Mahmood, Feroze/0000-0002-7071-0476
NR 114
TC 12
Z9 13
U1 2
U2 18
PU SPRINGER TOKYO
PI TOKYO
PA 1-11-11 KUDAN-KITA, CHIYODA-KU, TOKYO, 102-0073, JAPAN
SN 0913-8668
J9 J ANESTH
JI J. Anesth.
PD NOV
PY 2009
VL 23
IS 4
BP 543
EP 553
DI 10.1007/s00540-009-0787-7
PG 11
WC Anesthesiology
SC Anesthesiology
GA 521QP
UT WOS:000271938000013
PM 19921365
ER
PT J
AU Kellogg, DL
Zhao, JL
Wu, YB
AF Kellogg, Dean L., Jr.
Zhao, Joan L.
Wu, Yubo
TI Roles of nitric oxide synthase isoforms in cutaneous vasodilation
induced by local warming of the skin and whole body heat stress in
humans
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE skin; nitric oxide; nitric oxide synthase 1; nitric oxide synthase 3;
microdialysis
ID HUMAN CARDIOVASCULAR ADJUSTMENTS; FEMALE REPRODUCTIVE HORMONES;
BLOOD-FLOW; REFLEX CONTROL; SELECTIVE-INHIBITION; ACTIVE VASODILATION;
CONTROL MECHANISMS; CORE TEMPERATURE; L-ARGININE; IN-VIVO
AB Kellogg DL, Jr, Zhao JL, Wu Y. Roles of nitric oxide synthase isoforms in cutaneous vasodilation induced by local warming of the skin and whole body heat stress in humans. J Appl Physiol 107: 1438-1444, 2009. First published September 10, 2009; doi: 10.1152/japplphysiol.00690.2009.Nitric oxide (NO) participates in the cutaneous vasodilation caused by increased local skin temperature (Tloc) and whole body heat stress in humans. In forearm skin, endothelial NO synthase (eNOS) participates in vasodilation due to elevated Tloc and neuronal NO synthase (nNOS) participates in vasodilation due to heat stress. To explore the relative roles and interactions of these isoforms, we examined the effects of a relatively specific eNOS inhibitor, N(omega)-amino-L-arginine (LNAA), and a specific nNOS inhibitor, N(omega)-propyl-L-arginine (NPLA), both separately and in combination, on skin blood flow (SkBF) responses to increased Tloc and heat stress in two protocols. In each protocol, SkBF was monitored by laser-Doppler flowmetry (LDF) and mean arterial pressure (MAP) by Finapres. Cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). Intradermal microdialysis was used to treat one site with 5 mM LNAA, another with 5 mM NPLA, a third with combined 5 mM LNAA and 5 mM NPLA (Mix), and a fourth site with Ringer only. In protocol 1, Tloc was controlled with combined LDF/local heating units. Tloc was increased from 34 degrees C to 41.5 degrees C to cause local vasodilation. In protocol 2, after a period of normothermia, whole body heat stress was induced (water-perfused suits). At the end of each protocol, all sites were perfused with 58 mM nitroprusside to effect maximal vasodilation for data normalization. In protocol 1, at Tloc = 34 degrees C, CVC did not differ between sites (P > 0.05). LNAA and Mix attenuated CVC increases at Tloc = 41.5 degrees C to similar extents (P < 0.05, LNAA or Mix vs. untreated or NPLA). In protocol 2, in normothermia, CVC did not differ between sites (P > 0.05). During heat stress, NPLA and Mix attenuated CVC increases to similar extents, but no significant attenuation occurred with LNAA (P > 0.05, NPLA or Mix vs. untreated or LNAA). In forearm skin, eNOS mediates the vasodilator response to increased Tloc and nNOS mediates the vasodilator response to heat stress. The two isoforms do not appear to interact during either response.
C1 [Kellogg, Dean L., Jr.] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, Div Geriatr & Gerontol, San Antonio, TX 78229 USA.
Audie L Murphy Mem Vet Hosp Div, Geriatr Res Educ & Clin Ctr, Dept Vet Affairs, San Antonio, TX USA.
RP Kellogg, DL (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Med, Div Geriatr & Gerontol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM kelloggd@uthscsa.edu
FU National Heart, Lung, and Blood Institute [HL-065599]
FX This work was supported in part by National Heart, Lung, and Blood
Institute Grant HL-065599.
NR 60
TC 61
Z9 64
U1 3
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD NOV
PY 2009
VL 107
IS 5
BP 1438
EP 1444
DI 10.1152/japplphysiol.00690.2009
PG 7
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 515KO
UT WOS:000271468900011
PM 19745188
ER
PT J
AU Mayhew, DL
Kim, JS
Cross, JM
Ferrando, AA
Bamman, MM
AF Mayhew, David L.
Kim, Jeong-su
Cross, James M.
Ferrando, Arny A.
Bamman, Marcas M.
TI Translational signaling responses preceding resistance training-mediated
myofiber hypertrophy in young and old humans
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE translation initiation; protein synthesis; muscle fiber; aging
ID MUSCLE PROTEIN-SYNTHESIS; HUMAN SKELETAL-MUSCLE; EXERCISE-INDUCED
INCREASE; P70 S6 KINASE; CLUSTER-ANALYSIS; MIXED MUSCLE; MYONUCLEAR
ADDITION; GENE-EXPRESSION; MEN; PHOSPHORYLATION
AB Mayhew DL, Kim J-S, Cross JM, Ferrando AA, Bamman MM. Translational signaling responses preceding resistance training-mediated myofiber hypertrophy in young and old humans. J Appl Physiol 107: 1655-1662, 2009. First published July 9, 2009; doi:10.1152/japplphysiol.91234.2008.-While skeletal muscle protein accretion during resistance training (RT)-mediated myofiber hypertrophy is thought to result from upregulated translation initiation signaling, this concept is based on responses to a single bout of unaccustomed resistance exercise (RE) with no measure of hypertrophy across RT. Further, aging appears to affect acute responses to RE, but whether age differences in responsiveness persist during RT leading to impaired RT adaptation is unclear. We therefore tested whether muscle protein fractional synthesis rate (FSR) and Akt/mammalian target of rapamycin (mTOR) signaling in response to unaccustomed RE differed in old vs. young adults, and whether age differences in acute responsiveness were associated with differences in muscle hypertrophy after 16 wk of RT. Fifteen old and 21 young adult subjects completed the 16-wk study. The phosphorylation states of Akt, S6K1, ribosomal protein S6 (RPS6), eukaryotic initiation factor 4E (eIF4E) binding protein (4EBP1), eIF4E, and eIF4G were all elevated (23-199%) 24 h after a bout of unaccustomed RE. A concomitant 62% increase in FSR was found in a subset (6 old, 8 young). Age x time interaction was found only for RPS6 phosphorylation (+335% in old subjects only), while there was an interaction trend (P = 0.084) for FSR (+96% in young subjects only). After 16 wk of RT, gains in muscle mass, type II myofiber size, and voluntary strength were similar in young and old subjects. In conclusion, at the level of translational signaling, we found no evidence of impaired responsiveness among older adults, and for the first time, we show that changes in translational signaling after unaccustomed RE were associated with substantial muscle protein accretion (hypertrophy) during continued RT.
C1 [Bamman, Marcas M.] Univ Alabama, Dept Physiol & Biophys, Core Muscle Res Lab, Birmingham, AL 35294 USA.
[Cross, James M.] Univ Alabama, Dept Surg, Birmingham, AL 35294 USA.
[Mayhew, David L.] Univ Alabama, Med Scientist Training Program, Birmingham, AL 35294 USA.
[Mayhew, David L.; Kim, Jeong-su; Bamman, Marcas M.] Birmingham Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Birmingham, AL USA.
[Ferrando, Arny A.] Univ Arkansas Med Sci, Ctr Translat Res Aging & Longev, Little Rock, AR 72205 USA.
[Ferrando, Arny A.] Univ Arkansas Med Sci, Dept Geriatr, Little Rock, AR 72205 USA.
RP Bamman, MM (reprint author), Univ Alabama, Dept Physiol & Biophys, Core Muscle Res Lab, 966 McCallum Basic Hlth Sci Bldg,1530 3rd Ave S, Birmingham, AL 35294 USA.
EM mbamman@uab.edu
RI Ferrando, Adolfo /Q-7026-2016
FU National Institute on Aging [R01-AG-017896, F30-AG-031623]; Veterans
Affairs Merit Grant; General Clinical Research Center [M01-RR-00032]
FX Funding for this work was provided by National Institute on Aging Grants
R01-AG-017896 (M. M. Bamman) and F30-AG-031623 (D. L. Mayhew), a
Veterans Affairs Merit Grant (M. M. Bamman), and General Clinical
Research Center Grant M01-RR-00032.
NR 47
TC 86
Z9 88
U1 0
U2 5
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD NOV
PY 2009
VL 107
IS 5
BP 1655
EP 1662
DI 10.1152/japplphysiol.91234.2008
PG 8
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 515KO
UT WOS:000271468900036
PM 19589955
ER
PT J
AU Sillanpaa, J
Nallapareddy, SR
Qin, X
Singh, KV
Muzny, DM
Kovar, CL
Nazareth, LV
Gibbs, RA
Ferraro, MJ
Steckelberg, JM
Weinstock, GM
Murray, BE
AF Sillanpaa, Jouko
Nallapareddy, Sreedhar R.
Qin, Xiang
Singh, Kavindra V.
Muzny, Donna M.
Kovar, Christie L.
Nazareth, Lynne V.
Gibbs, Richard A.
Ferraro, Mary J.
Steckelberg, James M.
Weinstock, George M.
Murray, Barbara E.
TI A Collagen-Binding Adhesin, Acb, and Ten Other Putative MSCRAMM and
Pilus Family Proteins of Streptococcus gallolyticus subsp gallolyticus
(Streptococcus bovis Group, Biotype I)
SO JOURNAL OF BACTERIOLOGY
LA English
DT Article
ID EXTRACELLULAR-MATRIX PROTEINS; URINARY-TRACT-INFECTION; GROUP-A
STREPTOCOCCI; ENTEROCOCCUS-FAECALIS; STAPHYLOCOCCUS-AUREUS; BIOFILM
FORMATION; ANTIGEN-I/II; CELL-WALL; SURFACE-PROTEINS; HUG MODEL
AB Members of the Streptococcus bovis group are important causes of endocarditis. However, factors associated with their pathogenicity, such as adhesins, remain uncharacterized. We recently demonstrated that endocarditis-derived Streptococcus gallolyticus subsp. gallolyticus isolates frequently adhere to extracellular matrix (ECM) proteins. Here, we generated a draft genome sequence of an ECM protein-adherent S. gallolyticus subsp. gallolyticus strain and found, by genome-wide analyses, 11 predicted LPXTG-type cell wall-anchored proteins with characteristics of MSCRAMMs, including a modular architecture of domains predicted to adopt immunoglobulin (Ig)-like folding. A recombinant segment of one of these, Acb, showed high-affinity binding to immobilized collagen, and cell surface expression of Acb correlated with the presence of acb and collagen adherence of isolates. Three of the 11 proteins have similarities to major pilus subunits and are organized in separate clusters, each including a second Ig-fold-containing MSCRAMM and a class C sortase, suggesting that the sequenced strain encodes three distinct types of pili. Reverse transcription-PCR demonstrated that all three genes of one cluster, acb-sbs7-srtC1, are cotranscribed, consistent with pilus operons of other gram-positive bacteria. Further analysis detected expression of all 11 genes in cells grown to mid to late exponential growth phases. Wide distribution of 9 of the 11 genes was observed among S. gallolyticus subsp. gallolyticus isolates with fewer genes present in other S. bovis group species/subspecies. The high prevalence of genes encoding putative MSCRAMMs and pili, including a collagen-binding MSCRAMM, among S. gallolyticus subsp. gallolyticus isolates may play an important role in the predominance of this subspecies in S. bovis endocarditis.
C1 [Sillanpaa, Jouko; Nallapareddy, Sreedhar R.; Singh, Kavindra V.; Murray, Barbara E.] Univ Texas Houston, Sch Med, Dept Internal Med, Div Infect Dis, Houston, TX 77030 USA.
[Sillanpaa, Jouko; Nallapareddy, Sreedhar R.; Singh, Kavindra V.; Murray, Barbara E.] Univ Texas Houston, Sch Med, Ctr Study Emerging & Reemerging Pathogens, Houston, TX 77030 USA.
[Murray, Barbara E.] Univ Texas Houston, Sch Med, Dept Microbiol & Mol Genet, Houston, TX 77030 USA.
[Qin, Xiang; Muzny, Donna M.; Kovar, Christie L.; Nazareth, Lynne V.; Gibbs, Richard A.; Weinstock, George M.] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
[Ferraro, Mary J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Steckelberg, James M.] Mayo Clin, Coll Med, Dept Internal Med, Div Infect Dis, Rochester, MN 55905 USA.
RP Murray, BE (reprint author), Univ Texas Houston, Sch Med, Dept Internal Med, Div Infect Dis, 6431 Fannin St,MSB 2-112, Houston, TX 77030 USA.
EM bem.asst@uth.tmc.edu
RI Weinstock, George/C-6314-2013
OI Weinstock, George/0000-0002-2997-4592
FU J. Ralph Meadows Professorship in the Department of Internal Medicine,
University of Texas Medical School
FX This work was supported by the J. Ralph Meadows Professorship in the
Department of Internal Medicine, University of Texas Medical School, to
Barbara E. Murray.
NR 73
TC 40
Z9 40
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0021-9193
J9 J BACTERIOL
JI J. Bacteriol.
PD NOV
PY 2009
VL 191
IS 21
BP 6643
EP 6653
DI 10.1128/JB.00909-09
PG 11
WC Microbiology
SC Microbiology
GA 505UQ
UT WOS:000270723700017
PM 19717590
ER
PT J
AU George, PM
Saigal, R
Lawlor, MW
Moore, MJ
Lavan, DA
Marini, RP
Selig, M
Makhni, M
Burdick, JA
Langer, R
Kohane, DS
AF George, Paul M.
Saigal, Rajiv
Lawlor, Michael W.
Moore, Michael J.
LaVan, David A.
Marini, Robert P.
Selig, Martin
Makhni, Melvin
Burdick, Jason A.
Langer, Robert
Kohane, Daniel S.
TI Three-dimensional conductive constructs for nerve regeneration
SO JOURNAL OF BIOMEDICAL MATERIALS RESEARCH PART A
LA English
DT Article
DE biocompatibility; electroactive polymer; nerve guide; nerve
regeneration; polypyrrole
ID NEURITE OUTGROWTH; AXON REGENERATION; DRUG-DELIVERY; GROWTH-FACTOR;
POLYMER; BIOCOMPATIBILITY; STIMULATION; COMPOSITE; SCAFFOLDS; BEHAVIOR
AB The unique electrochemical properties of conductive polymers can be utilized to form stand-alone polymeric tubes and arrays of tubes that are suitable for guides to promote peripheral nerve regeneration. Noncomposite, polypyrrole (PPy) tubes ranging in inner diameter from 25 mu m to 1.6 mm as well as multichannel tubes were fabricated by electrodeposition. While oxidation of the pyrrole monomer causes growth of the film, brief Subsequent reduction allowed mechanical dissociation from the electrode mold, creating a stand-alone, conductive PPy tube. Conductive polymer nerve guides made in this manner were placed in transected rat sciatic nerves and shown to support nerve regeneration over an 8-week time period. (C) 2008 Wiley Periodicals, Inc. J Biomed Mater Res 91A: 519-527, 2009
C1 [Kohane, Daniel S.] Harvard Univ, Sch Med, Childrens Hosp,Lab Biomat & Drug Delivery, Div Crit Care Med,Dept Anesthesiol, Boston, MA 02115 USA.
[George, Paul M.; Saigal, Rajiv] MIT, Div Hlth Sci & Technol, Cambridge, MA 02142 USA.
[Lawlor, Michael W.; Selig, Martin] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Lawlor, Michael W.; Makhni, Melvin; Langer, Robert] MIT, Dept Chem Engn, Cambridge, MA 02142 USA.
[Moore, Michael J.] Tulane Univ, Dept Biomed Engn, New Orleans, LA 70118 USA.
[LaVan, David A.] Yale Univ, Dept Mech Engn, New Haven, CT 06511 USA.
[Marini, Robert P.] MIT, Div Comparat Med, Cambridge, MA 02142 USA.
[Burdick, Jason A.] Univ Penn, Dept Bioengn, Philadelphia, PA 19104 USA.
RP Kohane, DS (reprint author), Harvard Univ, Sch Med, Childrens Hosp,Lab Biomat & Drug Delivery, Div Crit Care Med,Dept Anesthesiol, Boston, MA 02115 USA.
EM daniel.kohane@childrens.harvard.edu
RI Moore, Michael/E-9107-2011; LaVan, David/C-3943-2012
OI Moore, Michael/0000-0002-7853-5756; LaVan, David/0000-0002-1952-0028
FU NIH [GM073626, DE13023]
FX Contract grant sponsor: NIH; contract grant numbers: GM073626, DE13023
NR 20
TC 19
Z9 20
U1 1
U2 22
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1549-3296
J9 J BIOMED MATER RES A
JI J. Biomed. Mater. Res. Part A
PD NOV
PY 2009
VL 91A
IS 2
BP 519
EP 527
DI 10.1002/jbm.a.32226
PG 9
WC Engineering, Biomedical; Materials Science, Biomaterials
SC Engineering; Materials Science
GA 506BA
UT WOS:000270746200022
PM 18985787
ER
PT J
AU Sheth, RA
Josephson, L
Mahmood, U
AF Sheth, Rahul A.
Josephson, Lee
Mahmood, Umar
TI Evaluation and clinically relevant applications of a fluorescent imaging
analog to fluorodeoxyglucose positron emission tomography
SO JOURNAL OF BIOMEDICAL OPTICS
LA English
DT Article
DE optical molecular imaging; fluorescence biomarkers; FDG-PET; minimally
invasive imaging; metabolic imaging; fluorescence endoscopy;
quantitative imaging; intraoperative imaging
ID GLUCOSE-UPTAKE; IN-VIVO; DEOXYGLUCOSE ANALOG; CELLS; 2-NBDG; MICE;
SINGLE; PROBE; MODEL
AB A fluorescent analog to 2-deoxy-2 [(18)F] fluoro-D-glucose position emission tomography (FDG-PET) would allow for the introduction of metabolic imaging into intraoperative and minimally invasive settings. We present through in vitro and in vivo experimentation an evaluation of 2-(N-(7-nitrobenz-2-oxa-1,3-diazol- 4-yl)amino)-2-deoxyglucose (2-NBDG), a fluorescently labeled glucose molecule, as a molecular beacon of glucose utilization. The competitive inhibition of 2-NBDG uptake by excess free glucose is directly compared against FDG uptake inhibition in cultured cells. 2-NBDG uptake in the brain of a mouse experiencing a generalized seizure is measured, as well as in subcutaneously implanted tumors in mice during fed and fasting states. Localization of 2-NBDG into malignant tissues is studied by laser scanning microscopy. The clinical relevance of 2-NBDG imaging is examined by performing fluorescence colonoscopy, and by correlating preoperative FDG-PET with intraoperative fluorescence imaging. 2-NBDG exhibits a similar uptake inhibition to FDG by excess glucose in the growth media. Uptake is significantly increased in the brain of an animal experiencing seizures versus control, and in subcutaneous tumors after the animals are kept nil per os (NPO) for 24 h versus ad libidum feeding. The clinical utility of 2-NBDG is confirmed by the demonstration of very high target-to-background ratios in minimally invasive and intraoperative imaging of malignant lesions. We present an optical analog of FDGPET to extend the applicability of metabolic imaging to minimally invasive and intraoperative settings. (C) 2009 Society of Photo-Optical Instrumentation Engineers. [DOI: 10.1117/1.3259364]
C1 [Sheth, Rahul A.; Josephson, Lee; Mahmood, Umar] Massachusetts Gen Hosp, Div Nucl Med & Mol Imaging, Dept Radiol, Boston, MA 02114 USA.
RP Mahmood, U (reprint author), Massachusetts Gen Hosp, Div Nucl Med & Mol Imaging, Dept Radiol, 55 Fruit St,White 427, Boston, MA 02114 USA.
EM umahmood@mgh.harvard.edu
FU NIH [P50CA127003, R01-EB001872]
FX The authors wish to express their appreciation to Brett Marinelli for
his assistance with the PET/CT imaging, and to Shena Hembrador for her
assistance with the FDG cell uptake experiments. This research was
supported in part by the Susan G. Komen for the Cure Foundation, as well
as NIH grants P50CA127003 and R01-EB001872.
NR 21
TC 23
Z9 24
U1 0
U2 4
PU SPIE-SOC PHOTOPTICAL INSTRUMENTATION ENGINEERS
PI BELLINGHAM
PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98225 USA
SN 1083-3668
J9 J BIOMED OPT
JI J. Biomed. Opt.
PD NOV-DEC
PY 2009
VL 14
IS 6
AR 064014
DI 10.1117/1.3259364
PG 8
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
Medical Imaging
GA 552DO
UT WOS:000274267900021
PM 20059252
ER
PT J
AU Lo Celso, C
Wu, JW
Lin, CP
AF Lo Celso, Cristina
Wu, Juwell W.
Lin, Charles P.
TI In vivo imaging of hematopoietic stem cells and their microenvironment
SO JOURNAL OF BIOPHOTONICS
LA English
DT Review
DE hematopoietic stem cell transplantation; in vivo imaging; intravital
microscopy; cell tracking
ID BONE-MARROW NICHES; PROGENITOR CELLS; PENETRATING PEPTIDES;
MYELOID-LEUKEMIA; DENDRITIC CELLS; B-CELLS; QUIESCENCE; REPAIR; TISSUE;
MICE
AB In this review we provide a description of the basic concepts and paradigms currently constituting the foundations of adult stem cell biology, and discuss the role that live imaging techniques have in the development of the field. We focus on live imaging of hematopoietic stein cells (HSCs) as the basic biology and clinical applications of HSCs have historically been at the forefront of the stem cell field, and HSC are the first mammalian tissue stem cells to be visualized in vivo using advanced light microscopy techniques. We outline the current technical challenges that remain to be overcome before stein cells and their niche can be more fully characterized using the live imaging technology.
[GRAPHICS]
.
hi vivo imaging of HSCs (white) 1 day after injection into an irradiated recipient, showing a single cell on the left and a cluster of 4 cells on the right that have undergone cell division. Blue, bone; green, osteoblasts; red, vasculature. Bar = 50 mu m. (C) 2009 by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
C1 [Lo Celso, Cristina; Lin, Charles P.] Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
[Lo Celso, Cristina] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
[Wu, Juwell W.] Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02145 USA.
[Wu, Juwell W.; Lin, Charles P.] Massachusetts Gen Hosp, Adv Microscopy Program, Ctr Syst Biol, Boston, MA 02114 USA.
[Wu, Juwell W.; Lin, Charles P.] Massachusetts Gen Hosp, Adv Microscopy Program, Wellman Ctr Photomed, Boston, MA 02114 USA.
RP Lin, CP (reprint author), Harvard Stem Cell Inst, 42 Church St, Cambridge, MA 02138 USA.
EM lin@helix.mgh.harvard.edu
OI Lo Celso, Cristina/0000-0002-1163-4207
FU EMBO; HFSP; Wellman Center; National Institutes of Health; Harvard Stem
Cell Institute; M.O
FX Cristina Lo Celso was funded by EMBO and HFSP. Juwell Wu was supported
by Wellman Center for Photomedicine Graduate Student Fellowship. The
project was funded by the National Institutes of Health, the Harvard
Stem Cell Institute (to CPL) and by a personal anonymous donation to
NIGH from M.O.
NR 72
TC 27
Z9 27
U1 0
U2 11
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PO BOX 10 11 61, D-69451 WEINHEIM, GERMANY
SN 1864-063X
J9 J BIOPHOTONICS
JI J. Biophotonics
PD NOV
PY 2009
VL 2
IS 11
BP 619
EP 631
DI 10.1002/jbio.200910072
PG 13
WC Biochemical Research Methods; Biophysics; Optics
SC Biochemistry & Molecular Biology; Biophysics; Optics
GA 524EN
UT WOS:000272126700007
PM 19847800
ER
EF