FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Wang, H
Smith, RN
Spooner, AE
Isselbacher, EM
Cambria, RP
MacGillivray, TE
Stone, JH
Stone, JR
AF Wang, He
Smith, R. Neal
Spooner, Amy E.
Isselbacher, Eric M.
Cambria, Richard P.
MacGillivray, Thomas E.
Stone, John H.
Stone, James R.
TI Giant cell aortitis of the ascending aorta without signs or symptoms of
systemic vasculitis is associated with elevated risk of distal aortic
events
SO ARTHRITIS AND RHEUMATISM
LA English
DT Editorial Material
C1 [Wang, He; Smith, R. Neal; Spooner, Amy E.; Isselbacher, Eric M.; Cambria, Richard P.; MacGillivray, Thomas E.; Stone, John H.; Stone, James R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Wang, H (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 5
TC 9
Z9 9
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD JAN
PY 2012
VL 64
IS 1
BP 317
EP 319
DI 10.1002/art.33343
PG 3
WC Rheumatology
SC Rheumatology
GA 869KZ
UT WOS:000298598100039
PM 21953530
ER
PT J
AU Bashyal, RK
Malchau, H
Nimkin, K
Holmes, LB
AF Bashyal, Ravi K.
Malchau, Henrik
Nimkin, Katherine
Holmes, Lewis B.
TI The association of a dysmorphic pelvis, absence of pubic rami, hip
dysplasia, and genitourinary anomalies
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Article
DE absent pubic rami; absent uterus; genitourinary; anomalies; dysmorphic
ID SUPPLY DISRUPTION SEQUENCE; POLAND; HYPOPLASIA
AB BACKGROUND There have been reports of children who had absence of the pubic rami, hip dysplasia, and genitourinary anomalies. CASE REPORT: We describe a 44-year-old woman with severe hip dysplasia, bilateral chronic congenital hip dislocations, abnormal development of the entire pelvis, and absence of the pubic rami in association with absence of the uterus. CONCLUSION: We present an individual who has abnormal development of the entire pelvis, including absence of the pubic rami, and genitourinary anomalies. We suggest that this is a rare pattern of associated anomalies confined to a localized region of the body. Potential underlying developmental abnormalities include somatic mutations which affected the mesodermal cells from which the pelvis and mullerian structures develop. Birth Defects Research (Part A) 94:57-60, 2012. (C) 2011 Wiley Periodicals, Inc.
C1 [Bashyal, Ravi K.; Malchau, Henrik] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Orthopaed, Boston, MA USA.
[Nimkin, Katherine] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Holmes, Lewis B.] Harvard Univ, Sch Med, Dept Pediat, Genet Unit,MassGen Hosp Children, Boston, MA 02115 USA.
RP Holmes, LB (reprint author), Mass Gen Hosp Children, Genet Unit, 175 Cambridge St, Boston, MA 02114 USA.
EM lewis@mgh.harvard.edu
NR 24
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD JAN
PY 2012
VL 94
IS 1
BP 57
EP 60
DI 10.1002/bdra.22873
PG 4
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 874JE
UT WOS:000298951600010
PM 22183795
ER
PT J
AU Xu, HS
Yi, BA
Wu, H
Bock, C
Gu, HC
Lui, KO
Park, JHC
Shao, Y
Riley, AK
Domian, IJ
Hu, E
Willette, R
Lepore, J
Meissner, A
Wang, Z
Chien, KR
AF Xu, Huansheng
Yi, B. Alexander
Wu, Hao
Bock, Christoph
Gu, Hongcang
Lui, Kathy O.
Park, Joo-Hye C.
Shao, Ying
Riley, Alyssa K.
Domian, Ibrahim J.
Hu, Erding
Willette, Robert
Lepore, John
Meissner, Alexander
Wang, Zhong
Chien, Kenneth R.
TI Highly efficient derivation of ventricular cardiomyocytes from induced
pluripotent stem cells with a distinct epigenetic signature
SO CELL RESEARCH
LA English
DT Article
DE induced pluripotent stem cells; ventricular cardiomyocyte; regenerative
medicine; epigenetic memory
ID CARDIOVASCULAR PROGENITORS; CARDIAC MYOCYTES; HEART-MUSCLE;
DIFFERENTIATION; MOUSE; MEMORY; REGENERATION; FIBROBLASTS; EXPRESSION;
GENERATION
AB Cardiomyocytes derived from pluripotent stem cells can be applied in drug testing, disease modeling and cell-based therapy. However, without procardiogenic growth factors, the efficiency of cardiomyogenesis from pluripotent stem cells is usually low and the resulting cardiomyocyte population is heterogeneous. Here, we demonstrate that induced pluripotent stem cells (iPSCs) can be derived from murine ventricular myocytes (VMs), and consistent with other reports of iPSCs derived from various somatic cell types, VM-derived iPSCs (ViPSCs) exhibit a markedly higher propensity to spontaneously differentiate into beating cardiomyocytes as compared to genetically matched embryonic stem cells (ESCs) or iPSCs derived from tail-tip fibroblasts. Strikingly, the majority of ViPSC-derived cardiomyocytes display a ventricular phenotype. The enhanced ventricular myogenesis in ViPSCs is mediated via increased numbers of cardiovascular progenitors at early stages of differentiation. In order to investigate the mechanism of enhanced ventricular myogenesis from ViPSCs, we performed global gene expression and DNA methylation analysis, which revealed a distinct epigenetic signature that may be involved in specifying the VM fate in pluripotent stem cells.
C1 [Xu, Huansheng; Yi, B. Alexander; Wu, Hao; Lui, Kathy O.; Park, Joo-Hye C.; Shao, Ying; Riley, Alyssa K.; Domian, Ibrahim J.; Wang, Zhong; Chien, Kenneth R.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Xu, Huansheng; Yi, B. Alexander; Wu, Hao; Bock, Christoph; Gu, Hongcang; Lui, Kathy O.; Domian, Ibrahim J.; Meissner, Alexander; Wang, Zhong; Chien, Kenneth R.] Harvard Univ, Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
[Xu, Huansheng; Yi, B. Alexander; Wu, Hao; Bock, Christoph; Gu, Hongcang; Lui, Kathy O.; Meissner, Alexander; Chien, Kenneth R.] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
[Bock, Christoph; Gu, Hongcang; Meissner, Alexander] Broad Inst, Cambridge, MA 02142 USA.
[Hu, Erding; Willette, Robert; Lepore, John] GlaxoSmithKline, Cardiac Biol, HF Discovery Performance Unit, Metab & Cardiovasc Therapeut Area Unit, King Of Prussia, PA 19406 USA.
RP Chien, KR (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charles River Plaza CPZN 3208,185 Cambridge St, Boston, MA 02114 USA.
EM krchien@partners.org
RI Wu, Hao/G-4145-2013; Lui, Kathy O./E-4883-2015;
OI Wu, Hao/0000-0002-1256-6891; Lui, Kathy O./0000-0002-1616-3643; Bock,
Christoph/0000-0001-6091-3088
FU Massachusetts General Hospital Executive Committee; NIH
[5T32HL007208-32]; MGH ECOR; Jane Coffin Childs postdoctoral fellowship;
Croucher Foundation; GlaxoSmithKline Pharmaceuticals
FX We would like to thank Laura Prickett-Rice, Kat Folz-Donahue, and
Sutanuka Lahiri of the Harvard Stem Cell Institute Flow Cytometry Core
Facility for assistance with FACS analysis, Chuang Du of the Tufts
Electrophysiology Core for assistance with electrophysiology recordings,
Jie Zhao and members of the Wellman Photopathology Core for assistance
with histology, Patricia Follett for assistance with blastocyst
injections, and Elizabeth Bearrick for assistance with experiments. We
would like to thank Konrad Hochedlinger (Massachusetts General Hospital,
Harvard University, USA) for sharing the Rosa26rtTA/rtTA
mouse line as well as the lentiviral constructs for iPSC derivation. We
would like to thank Lei Bu, Emil Hansson, members of the Chien
laboratory, and Konrad Hochedlinger for helpful discussion. HX is
supported by Massachusetts General Hospital Executive Committee of
Research Fund for Medical Discovery. BAY has received support under NIH
Training Grant (5T32HL007208-32) and the MGH ECOR Fund for Medical
Discovery. HW is supported by a Jane Coffin Childs postdoctoral
fellowship. KOL holds a Croucher Foundation Fellowship. This work is
partially funded by GlaxoSmithKline Pharmaceuticals.
NR 38
TC 40
Z9 43
U1 2
U2 15
PU INST BIOCHEMISTRY & CELL BIOLOGY
PI SHANGHAI
PA SIBS, CAS, 319 YUEYANG ROAD, SHANGHAI, 200031, PEOPLES R CHINA
SN 1001-0602
EI 1748-7838
J9 CELL RES
JI Cell Res.
PD JAN
PY 2012
VL 22
IS 1
BP 142
EP 154
DI 10.1038/cr.2011.171
PG 13
WC Cell Biology
SC Cell Biology
GA 879EQ
UT WOS:000299312900015
PM 22064699
ER
PT J
AU Roger, VL
O'Donnell, CJ
AF Roger, Veronique L.
O'Donnell, Christopher J.
TI Population Health, Outcomes Research, and Prevention Example of the
American Heart Association 2020 Goals
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Editorial Material
DE prevention; delivery of health care; outcomes assessment
ID CLINICAL-PRACTICE GUIDELINES; NEW-YORK-CITY; CARDIOVASCULAR-DISEASE;
CARE; BEHAVIOR; ERA
C1 [Roger, Veronique L.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN 55905 USA.
[Roger, Veronique L.] Mayo Clin, Div Cardiovasc Dis, Dept Internal Med, Rochester, MN 55905 USA.
[O'Donnell, Christopher J.] NHLBI, Framingham, MA USA.
[O'Donnell, Christopher J.] NHLBI Framingham Heart Study, Framingham, MA USA.
[O'Donnell, Christopher J.] Massachusetts Gen Hosp, Div Cardiol, Dept Internal Med, Boston, MA 02114 USA.
RP Roger, VL (reprint author), Mayo Clin, Dept Hlth Sci Res, 200 First St SW, Rochester, MN 55905 USA.
EM roger.veronique@mayo.edu
FU Intramural NIH HHS [Z99 HL999999]; NHLBI NIH HHS [R01 HL059205-13, R01
HL072435, R01 HL072435-08, R01 HL59205, R01 HL059205, R01 HL72435]
NR 25
TC 5
Z9 5
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7705
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD JAN
PY 2012
VL 5
IS 1
BP 6
EP 8
DI 10.1161/CIRCOUTCOMES.111.964734
PG 3
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 880ML
UT WOS:000299411100002
PM 22253367
ER
PT J
AU Arling, G
Reeves, M
Ross, J
Williams, LS
Keyhani, S
Chumbler, N
Phipps, MS
Roumie, C
Myers, LJ
Salanitro, AH
Ordin, DL
Myers, J
Bravata, DM
AF Arling, Greg
Reeves, Mathew
Ross, Joseph
Williams, Linda S.
Keyhani, Salomeh
Chumbler, Neale
Phipps, Michael S.
Roumie, Christianne
Myers, Laura J.
Salanitro, Amanda H.
Ordin, Diana L.
Myers, Jennifer
Bravata, Dawn M.
TI Estimating and Reporting on the Quality of Inpatient Stroke Care by
Veterans Health Administration Medical Centers
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE acute stroke; performance measurement; quality indicators; stroke
management; statistics
ID ACUTE ISCHEMIC-STROKE; PLASMINOGEN-ACTIVATOR; PERFORMANCE-MEASURES;
OF-CARE; OUTCOMES; MORTALITY; MODELS; IMPACT; INTERVENTION; IMPROVEMENT
AB Background-Reporting of quality indicators (QIs) in Veterans Health Administration Medical Centers is complicated by estimation error caused by small numbers of eligible patients per facility. We applied multilevel modeling and empirical Bayes (EB) estimation in addressing this issue in performance reporting of stroke care quality in the Medical Centers.
Methods and Results-We studied a retrospective cohort of 3812 veterans admitted to 106 Medical Centers with ischemic stroke during fiscal year 2007. The median number of study patients per facility was 34 (range, 12-105). Inpatient stroke care quality was measured with 13 evidence-based QIs. Eligible patients could either pass or fail each indicator. Multilevel modeling of a patient's pass/fail on individual QIs was used to produce facility-level EB-estimated QI pass rates and confidence intervals. The EB estimation reduced interfacility variation in QI rates. Small facilities and those with exceptionally high or low rates were most affected. We recommended 8 of the 13 QIs for performance reporting: dysphagia screening, National Institutes of Health Stroke Scale documentation, early ambulation, fall risk assessment, pressure ulcer risk assessment, Functional Independence Measure documentation, lipid management, and deep vein thrombosis prophylaxis. These QIs displayed sufficient variation across facilities, had room for improvement, and identified sites with performance that was significantly above or below the population average. The remaining 5 QIs were not recommended because of too few eligible patients or high pass rates with little variation.
Conclusions-Considerations of statistical uncertainty should inform the choice of QIs and their application to performance reporting. (Circ Cardiovasc Qual Outcomes. 2012;5:44-51.)
C1 [Arling, Greg; Williams, Linda S.; Chumbler, Neale; Bravata, Dawn M.] Regenstrief Inst Hlth Care, Indianapolis, IN 46202 USA.
[Arling, Greg; Reeves, Mathew; Williams, Linda S.; Chumbler, Neale; Myers, Laura J.; Ordin, Diana L.; Myers, Jennifer; Bravata, Dawn M.] Stroke Qual Enhancement Res Initiat QUERI, VHA Hlth Serv Res & Dev HSR& D, Indianapolis, IN USA.
[Ordin, Diana L.] VHA, Off Informat & Analyt, Washington, DC USA.
[Arling, Greg; Myers, Laura J.; Bravata, Dawn M.] Indiana Univ Sch Med, Dept Med, Indianapolis, IN USA.
[Reeves, Mathew] Michigan State Univ, Dept Epidemiol, E Lansing, MI 48824 USA.
[Ross, Joseph] Yale Univ, Sch Med, Dept Med, Gen Internal Med Sect, New Haven, CT 06510 USA.
[Ross, Joseph] Yale New Haven Med Ctr, Ctr Outcomes Res & Evaluat, New Haven, CT 06504 USA.
[Williams, Linda S.; Chumbler, Neale; Myers, Laura J.; Myers, Jennifer; Bravata, Dawn M.] Richard L Roudebush VHA Med Ctr, VHA HSR&D Ctr Excellence Implementing Evidence Ba, Indianapolis, IN USA.
[Williams, Linda S.] Indiana Univ Sch Med, Dept Neurol, Indianapolis, IN USA.
[Keyhani, Salomeh] Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA.
[Keyhani, Salomeh] San Francisco VA Med Ctr, HSR&D Res Enhancement Award Program, San Francisco, CA USA.
[Chumbler, Neale] Indiana Univ Purdue Univ, Indiana Univ, Sch Liberal Arts, Dept Sociol, Indianapolis, IN 46202 USA.
[Phipps, Michael S.] Yale Univ, Sch Med, Robert Wood Johnson Fdn, Clin Scholars Program, New Haven, CT USA.
[Phipps, Michael S.] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06510 USA.
[Roumie, Christianne] Vet Affairs Tennessee Valley Healthcare Syst, HSR&D Targeted Res Enhancement Program Ctr, GRECC, Nashville, TN USA.
[Roumie, Christianne] Vet Affairs Tennessee Valley Healthcare Syst, Clin Res Training Ctr Excellence, Nashville, TN USA.
[Roumie, Christianne; Salanitro, Amanda H.] Vanderbilt Univ, Med Ctr, Inst Med & Publ Hlth, Nashville, TN USA.
[Salanitro, Amanda H.] Vanderbilt Univ, Med Ctr, Sect Hosp Med, Nashville, TN USA.
RP Arling, G (reprint author), Regenstrief Inst Hlth Care, 410 W 10th St,Suite 2000, Indianapolis, IN 46202 USA.
EM GArling@IUPUI.edu
OI Phipps, Michael/0000-0001-8398-5404
FU Department of Veterans Affairs, Veterans Health Administration (VHA),
Office of Quality and Performance and Health Services Research, and
Development Service Quality Enhancement Research Initiative [RRP
09-184]; National Institute on Aging; American Federation of Aging
Research [K08 AG032886]; VA HSRD
FX The Department of Veterans Affairs, Veterans Health Administration
(VHA), Office of Quality and Performance and Health Services Research,
and Development Service Quality Enhancement Research Initiative (RRP
09-184) supported this project. Dr Ross is supported by the National
Institute on Aging and by the American Federation of Aging Research
through the Paul B. Beason Career Development Award Program (K08
AG032886). Dr Keyhani is supported by a VA HSR&D Career Development
Award.
NR 42
TC 18
Z9 19
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7705
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD JAN
PY 2012
VL 5
IS 1
BP 44
EP U102
DI 10.1161/CIRCOUTCOMES.111.961474
PG 23
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 880ML
UT WOS:000299411100009
PM 22147888
ER
PT J
AU Qian, F
Ling, FS
Deedwania, P
Hernandez, AF
Fonarow, GC
Cannon, CP
Peterson, ED
Peacock, WF
Kaltenbach, LA
Laskey, WK
Schwamm, LH
Bhatt, DL
AF Qian, Feng
Ling, Frederick S.
Deedwania, Prakash
Hernandez, Adrian F.
Fonarow, Gregg C.
Cannon, Christopher P.
Peterson, Eric D.
Peacock, W. Frank
Kaltenbach, Lisa A.
Laskey, Warren K.
Schwamm, Lee H.
Bhatt, Deepak L.
CA Get Guidelines Steering Comm
TI Care and Outcomes of Asian-American Acute Myocardial Infarction
Patients: Findings From the American Heart Association Get With The
Guidelines-Coronary Artery Disease Program
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE Asian-Americans; acute myocardial infarction; quality of care; outcomes
ID CARDIOVASCULAR RISK-FACTORS; RACIAL-DIFFERENCES; PERFORMANCE-MEASURES;
ETHNIC-DIFFERENCES; PACIFIC ISLANDERS; CARDIAC PATIENTS;
CLINICAL-TRIALS; UNSTABLE ANGINA; ST-ELEVATION; EVENT RATES
AB Background-Asian-Americans represent an important United States minority population, yet there are limited data regarding the clinical care and outcomes of Asian-Americans following acute myocardial infarction (AMI). Using data from the American Heart Association Get With The Guidelines-Coronary Artery Disease (GWTG-CAD) program, we compared use of and trends in evidence-based care AMI processes and outcome in Asian-American versus white patients.
Methods and Results-We analyzed 107 403 AMI patients (4412 Asian-Americans, 4.1%) from 382 United States centers participating in the Get With The Guidelines-Coronary Artery Disease program between 2003 and 2008. Use of 6 AMI performance measures, composite "defect-free" care (proportion receiving all eligible performance measures), door-to-balloon time, and in-hospital mortality were examined. Trends in care over this time period were explored. Compared with whites, Asian-American AMI patients were significantly older, more likely to be covered by Medicaid and recruited in the west region, and had a higher prevalence of diabetes, hypertension, heart failure, and smoking. In-hospital unadjusted mortality was higher among Asian-American patients. Overall, Asian-Americans were comparable with whites regarding the baseline quality of care, except that Asian-Americans were less likely to get smoking cessation counseling (65.6% versus 81.5%). Asian-American AMI patients experienced improvement in the 6 individual measures (P <= 0.048), defect-free care (P<0.001), and door-to-balloon time (P<0.001). The improvement rates were similar for both Asian-Americans and whites. Compared with whites, the adjusted in-hospital mortality rate was higher for Asian-Americans (adjusted relative risk: 1.16; 95% confidence interval: 1.00-1.35; P=0.04).
Conclusions-Evidence-based care for AMI processes improved significantly over the period of 2003 to 2008 for Asian-American and white patients in the Get With The Guidelines-Coronary Artery Disease program. Differences in care between Asian-Americans and whites, when present, were reduced over time. (Circ Cardiovasc Qual Outcomes. 2012;5:126-133.)
C1 [Qian, Feng] Univ Rochester, Med Ctr, Dept Anesthesiol, Rochester, NY 14642 USA.
[Deedwania, Prakash] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Hernandez, Adrian F.; Peterson, Eric D.; Kaltenbach, Lisa A.] Duke Univ, Durham, NC USA.
[Fonarow, Gregg C.] Ronald Reagan UCLA Med Ctr, Los Angeles, CA USA.
[Bhatt, Deepak L.] Brigham & Womens Hosp, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Fonarow, Gregg C.; Schwamm, Lee H.; Bhatt, Deepak L.] Harvard Univ, Sch Med, Boston, MA USA.
[Peacock, W. Frank] Cleveland Clin, Cleveland, OH 44106 USA.
[Laskey, Warren K.] Univ New Mexico, Albuquerque, NM 87131 USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Qian, F (reprint author), Univ Rochester, Med Ctr, Dept Anesthesiol, 601 Elmwood Ave,Box 604, Rochester, NY 14642 USA.
EM feng_qian@urmc.rochester.edu
RI Hernandez, Adrian F./A-7818-2016
OI Schwamm, Lee/0000-0003-0592-9145; Hernandez, Adrian
F./0000-0003-3387-9616
FU American Heart Association; Council on Clinical Cardiology of the
American Heart Association; NHLBI; Novartis; Pfizer; Accumetrics;
AstraZeneca; GlaxoSmithKline; Intekrin Therapeutics; Merck; Takeda;
Bristol-Myers Squibb/Sanofi; Alnylam; Abbott; BAS; Brahms;
Beckman-Coulter; Alere; Nanosphere; EKR; Medicines company; Amarin;
Bristol-Myers Squibb; Eisai; Sanofi Aventis; Medtronic
FX Dr Qian has received the American Heart Association Young Investigator
Database Seed Grant, which is sponsored by the Council on Clinical
Cardiology of the American Heart Association.; Dr Fonarow receives
research funding from the NHLBI (significant), and consulting fees from
Novartis (significant) and Pfizer (modest).; Dr Cannon receives research
grants/support from Accumetrics, AstraZeneca, GlaxoSmithKline, Intekrin
Therapeutics, Merck, and Takeda, and is on the advisory board (but funds
donated to charity) for Bristol-Myers Squibb/Sanofi, Novartis, and
Alnylam. He also receives an honorarium for development of independent
educational symposia for Pfizer and AstraZeneca, and is clinical advisor
for Automedics Medical Systems.; Dr Peacock has received research
funding from Abbott, BAS, Brahms, Beckman-Coulter, Alere, Nanosphere,
EKR, and The Medicines company. He has also served as a consultant for
these companies and Lily.; Dr Bhatt receives research funding from
Amarin, Astra Zeneca, Bristol-Myers Squibb, Eisai, Sanofi Aventis,
Medtronic, and The Medicines Company.
NR 43
TC 12
Z9 14
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7705
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD JAN
PY 2012
VL 5
IS 1
BP 126
EP 133
DI 10.1161/CIRCOUTCOMES.111.961987
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 880ML
UT WOS:000299411100019
PM 22235068
ER
PT J
AU Brennan, JM
Peterson, ED
Messenger, JC
Rumsfeld, JS
Weintraub, WS
Anstrom, KJ
Eisenstein, EL
Milford-Beland, S
Grau-Sepulveda, MV
Booth, ME
Dokholyan, RS
Douglas, PS
AF Brennan, J. Matthew
Peterson, Eric D.
Messenger, John C.
Rumsfeld, John S.
Weintraub, William S.
Anstrom, Kevin J.
Eisenstein, Eric L.
Milford-Beland, Sarah
Grau-Sepulveda, Maria V.
Booth, Michael E.
Dokholyan, Rachel S.
Douglas, Pamela S.
CA Duke Clinical Res Inst DEcIDE Team
TI Linking the National Cardiovascular Data Registry CathPCI Registry With
Medicare Claims Data Validation of a Longitudinal Cohort of Elderly
Patients Undergoing Cardiac Catheterization
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE catheterization; data linkage; outcomes
AB Background-The National Cardiovascular Data Registry CathPCI Registry was recently linked with longitudinal Centers for Medicare & Medicaid (CMS) claims data. The degree to which this linked cohort is representative of the overall CathPCI Registry and CMS PCI populations is unknown.
Methods and Results-CathPCI Registry records were linked to CMS inpatient claims using indirect identifiers. We examined the degree to which hospitals and patients in the linked cohort are representative of the elderly (>= 65 years) CathPCI Registry and CMS populations. From 2004 to 2006, 1492 hospitals filed CMS PCI claims and 663 contributed CathPCI Registry data. Of these hospitals, 643 (97%) were linked across data sources. Compared with all CMS PCI hospitals, the linked data set contained fewer governmental, northeastern, southern, and low-volume (<200 beds) sites. Among CMS beneficiaries, 993 351 PCI procedures were performed, including 398 508 (40.1%) at centers in the linked database. Of these, 341 916 (86%) were linked to CathPCI Registry records. Linked and unlinked CMS patients had similar demographic and clinical features. In the CathPCI Registry database, 477 456 elderly patients underwent PCI, with 359 077 (75%) linked to CMS claims. Linked and unlinked National Cardiovascular Data Registry patients were similar, except for less commercial or health maintenance organization insurance in the linked cohort.
Conclusions-By using deterministic matching strategies, a large and representative cohort with detailed clinical data from the CathPCI Registry and longitudinal follow-up from CMS claims has been created. (Circ Cardiovasc Qual Outcomes. 2012;5:134-140.)
C1 [Brennan, J. Matthew; Peterson, Eric D.; Eisenstein, Eric L.; Milford-Beland, Sarah; Grau-Sepulveda, Maria V.; Booth, Michael E.; Dokholyan, Rachel S.; Douglas, Pamela S.] Duke Univ, Duke Clin Res Inst, Med Ctr, Durham, NC 27705 USA.
[Messenger, John C.; Rumsfeld, John S.] Denver Vet Affairs Med Ctr, Denver, CO USA.
[Weintraub, William S.] Christiana Care Hlth Syst, Newark, DE USA.
RP Brennan, JM (reprint author), Duke Univ, Duke Clin Res Inst, Med Ctr, 2400 Pratt St, Durham, NC 27705 USA.
EM brenn009@mc.duke.edu
FU Agency for Healthcare Research and Quality, US Department of Health and
Human Services, Rockville, MD [24-EHC-1, HHSAA290-2005, 0032-TO4-WA2];
National Cardiovascular Data Registry, American College of Cardiology,
Washington, DC; BMS/Sanofi; Merck; Lilly; JJ; Society of Thoracic
Surgeons; ACC; Alexion; AstraZeneca; Bristol Myers Squibb; Innocoll
Pharmaceuticals; Medtronic; Pfizer; Proctor Gamble; Eli Lilly
FX This project was sponsored by the Agency for Healthcare Research and
Quality, US Department of Health and Human Services, Rockville, MD, as
part of the Cardiovascular Consortium and funded under Project ID:
24-EHC-1 and Work Assignment No. HHSAA290-2005 to 0032-TO4-WA2 as part
of the Developing Evidence to Inform Decisions about Effectiveness
(DEcIDE) program. Additional support was obtained from the National
Cardiovascular Data Registry, American College of Cardiology,
Washington, DC.; Dr Peterson reports receiving research funding from
BMS/Sanofi, Merck, Lilly, J&J, Society of Thoracic Surgeons, and ACC
(significant). Dr Messenger reports serving as the site principal
investigator for the Resolute Study and the EDUCATE study: Medtronic,
Inc (modest). Dr Rumsfeld is the Chief Science Officer for National
Cardiovascular Data Registry. Dr Anstrom reports receiving research and
salary support from Alexion, AstraZeneca, Bristol Myers Squibb, Lilly,
Innocoll Pharmaceuticals, Medtronic, Pfizer, and Proctor & Gamble
(modest); being on the data safety monitoring boards of Pfizer and
Vertex (modest); and providing consulting services to Pacific
Therapeutics, Bristol Myers Squibb, and AstraZeneca (modest). Dr
Eisenstein reports receiving research funding from Medtronic and Eli
Lilly (significant).
NR 6
TC 26
Z9 26
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7705
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD JAN
PY 2012
VL 5
IS 1
BP 134
EP 140
DI 10.1161/CIRCOUTCOMES.111.963280
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 880ML
UT WOS:000299411100020
PM 22253370
ER
PT J
AU Hashash, JG
Refaat, M
Abdulbaki, A
Aoun, EG
Baidoo, L
AF Hashash, Jana G.
Refaat, Marwan
Abdulbaki, Abdulrahman
Aoun, Elie G.
Baidoo, Leonard
TI The Clinical Picture Cytomegalovirus colitis
SO CLEVELAND CLINIC JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID INFLAMMATORY-BOWEL-DISEASE; PREVALENCE; INFECTION
C1 [Hashash, Jana G.; Aoun, Elie G.] Univ Pittsburgh, Div Gastroenterol Hepatol & Nutr, Dept Med, Pittsburgh, PA 15213 USA.
[Refaat, Marwan] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Refaat, Marwan] Harvard Univ, Sch Med, Boston, MA USA.
[Abdulbaki, Abdulrahman] Louisiana State Univ, Shreveport, LA 71105 USA.
[Abdulbaki, Abdulrahman] Hlth Sci Ctr, Shreveport, LA USA.
RP Hashash, JG (reprint author), Univ Pittsburgh, Div Gastroenterol Hepatol & Nutr, Dept Med, 200 Lothrop St, Pittsburgh, PA 15213 USA.
EM alhashashj@upmc.edu
NR 5
TC 3
Z9 3
U1 0
U2 2
PU CLEVELAND CLINIC
PI CLEVELAND
PA 9500 EUCLID AVE, CLEVELAND, OH 44106 USA
SN 0891-1150
J9 CLEV CLIN J MED
JI Clevel. Clin. J. Med.
PD JAN
PY 2012
VL 79
IS 1
BP 12
EP 13
DI 10.3949/ccjm.78a.11028
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 880XQ
UT WOS:000299444300002
PM 22219228
ER
PT J
AU Patil, SU
Shreffler, WG
AF Patil, S. U.
Shreffler, W. G.
TI Immunology in the Clinic Review Series; focus on allergies: basophils as
biomarkers for assessing immune modulation
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Review
DE basophil; desensitization; immunotherapy
ID FC-EPSILON-RI; GRASS-POLLEN IMMUNOTHERAPY; WASP VENOM ALLERGY; HUMAN
BLOOD BASOPHILS; HISTAMINE-RELEASE; IMMUNOGLOBULIN-G; GAMMA-RIIB; BEE
VENOM; ACTIVATION MARKERS; RUSH IMMUNOTHERAPY
AB Allergen-specific immunotherapy is an effective clinical treatment for hypersensitivity to many allergens. Studies of basophils during immunotherapy have provided insight into underlying immune mechanisms and support the potential use of basophil activation as a biomarker of clinical outcomes. This review examines the evidence for different pathways of basophil modulation associated with various forms of immunotherapy. Better understanding the molecular mechanisms of basophil activation and desensitization and the relationship between suppression of these effector cells to clinical outcomes holds promise for further development and improvement in potential therapies for allergic diseases.
C1 [Patil, S. U.; Shreffler, W. G.] Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Boston, MA 02114 USA.
RP Patil, SU (reprint author), 55 Fruit St,Cox 201, Boston, MA 02441 USA.
EM spatil35@partners.org
FU NIAID [R01 AI081845]
FX Studies on basophil activation by mouse allergen are supported by
funding from NIAID R01 AI081845.
NR 65
TC 10
Z9 12
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9104
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD JAN
PY 2012
VL 167
IS 1
BP 59
EP 66
DI 10.1111/j.1365-2249.2011.04503.x
PG 8
WC Immunology
SC Immunology
GA 855GL
UT WOS:000297551800008
PM 22132885
ER
PT J
AU Wesseling-Perry, K
Pereira, RC
Tseng, CH
Elashoff, R
Zaritsky, JJ
Yadin, O
Sahney, S
Gales, B
Juppner, H
Salusky, IB
AF Wesseling-Perry, Katherine
Pereira, Renata C.
Tseng, Chi-Hong
Elashoff, Robert
Zaritsky, Joshua J.
Yadin, Ora
Sahney, Shobha
Gales, Barbara
Jueppner, Harald
Salusky, Isidro B.
TI Early Skeletal and Biochemical Alterations in Pediatric Chronic Kidney
Disease
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID GROWTH-FACTOR 23; CHRONIC-RENAL-FAILURE; GLOMERULAR-FILTRATION-RATE;
PARATHYROID-HORMONE; LANTHANUM CARBONATE; HEALTHY-MEN; OSTEODYSTROPHY;
PHOSPHATE; CHILDREN; FGF23
AB Background and objectives The relationship between parathyroid hormone, fibroblast growth factor 23 (FGF-23), and indices of bone turnover and mineralization in children with early CKD is unknown; thus, this study characterizes the features of renal osteodystrophy and their relationship to biochemical markers of mineral metabolism.
Design, setting, participants, & measurements Fifty-two patients 2-21 years of age with predialysis CKD underwent tetracycline-labeled bone biopsy. Anthropomorphic measurements and biochemical values were obtained at the time of biopsy.
Results Serum phosphorus levels were increased in 4% of patients with stage 3 CKD and 43% of those with stage 4/5 CKD. Parathyroid hormone concentrations were elevated in 36% of patients with stage 2, 71% with stage 3, and 93% with stage 4/5 CKD, whereas FGF-23 values were elevated in 81% of all patients, regardless of CKD stage. Bone turnover was normal in all patients with stage 2, but was increased in 13% with stage 3 and 29% with stage 4/5 CKD. Defective mineralization was present in 29% of patients with stage 2, 42% with stage 3, and 79% with stage 4/5 CKD. Defective skeletal mineralization was associated with lower serum calcium levels and increased parathyroid hormone concentrations.
Conclusions Elevated circulating FGF-23 levels and defects in skeletal mineralization early in the course of CKD suggest that factors other than the traditional markers of mineral deficiency play a crucial role in the development of renal bone disease. Clin J Am Soc Nephrol 7: 146-152, 2012. doi: 10.2215/CJN.05940611
C1 [Wesseling-Perry, Katherine; Pereira, Renata C.; Zaritsky, Joshua J.; Yadin, Ora; Gales, Barbara; Salusky, Isidro B.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pediat, Los Angeles, CA 90095 USA.
[Tseng, Chi-Hong; Elashoff, Robert] Univ Calif Los Angeles, David Geffen Sch Med, Dept Biomath, Los Angeles, CA 90095 USA.
[Sahney, Shobha] Loma Linda Univ, Dept Pediat, Loma Linda, CA 92350 USA.
[Jueppner, Harald] Harvard Univ, Sch Med, Boston, MA USA.
[Jueppner, Harald] Massachusetts Gen Hosp, Pediat Nephrol Unit, Boston, MA 02114 USA.
[Jueppner, Harald] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
RP Wesseling-Perry, K (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Pediat, A2-383 MDCC,650 Charles Young Dr, Los Angeles, CA 90095 USA.
EM kwesseling@mednet.ucla.edu
FU US Public Health Service [DK-67563, DK-35423, DK-51081, DK-073039,
RR-00865]; Casey Lee Ball Foundation
FX This work was supported in part by grants from US Public Health Service
(DK-67563, DK-35423, DK-51081, DK-073039, and RR-00865) and funds from
the Casey Lee Ball Foundation.
NR 36
TC 47
Z9 47
U1 0
U2 14
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 JAN
PY 2012
VL 7
IS 1
BP 146
EP 152
DI 10.2215/CJN.05940611
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 877RD
UT WOS:000299198700023
PM 22052943
ER
PT J
AU Hashash, JG
Zakhary, L
Aoun, EG
Refaat, M
AF Hashash, J. G.
Zakhary, L.
Aoun, E. G.
Refaat, M.
TI Heterotopic mesenteric ossification
SO COLORECTAL DISEASE
LA English
DT Article
ID INTRAABDOMINAL MYOSITIS-OSSIFICANS
C1 [Hashash, J. G.] Univ Pittsburgh, Med Ctr, Div Gastroenterol Hepatol & Nutr, PUH, Pittsburgh, PA 15213 USA.
[Zakhary, L.; Refaat, M.] Massachusetts Gen Hosp, Dept Internal Med, Boston, MA 02114 USA.
RP Hashash, JG (reprint author), Univ Pittsburgh, Med Ctr, Div Gastroenterol Hepatol & Nutr, PUH, 200 Lothrop St,M2, Pittsburgh, PA 15213 USA.
EM alhashashj@upmc.edu
NR 5
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1462-8910
J9 COLORECTAL DIS
JI Colorectal Dis.
PD JAN
PY 2012
VL 14
IS 1
BP e29
EP e30
DI 10.1111/j.1463-1318.2011.02750.x
PG 2
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA 857SM
UT WOS:000297739500006
PM 21819525
ER
PT J
AU DeFronzo, RA
Davidson, JA
Del Prato, S
AF DeFronzo, R. A.
Davidson, J. A.
Del Prato, S.
TI The role of the kidneys in glucose homeostasis: a new path towards
normalizing glycaemia
SO DIABETES OBESITY & METABOLISM
LA English
DT Review
DE clinical trials; diabetes; glucose homeostasis; glycosuria;
hyperglycaemia; kidneys; renal glucose transport; SGLT2; SGLT2
inhibitors; sodium-glucose cotransporters
ID TYPE-2 DIABETES-MELLITUS; SELECTIVE SGLT2 INHIBITOR; JAPANESE
HEALTHY-VOLUNTEERS; RENAL PROXIMAL TUBULES; BETA-CELL DYSFUNCTION; FREE
FATTY-ACIDS; INSULIN-RESISTANCE; BLOOD-GLUCOSE; DOUBLE-BLIND;
BODY-WEIGHT
AB The maintenance of normal glucose homeostasis requires a complex, highly integrated interaction among the liver, muscle, adipocytes, pancreas and neuroendocrine system. Recent studies have showed that the kidneys also play a central role in glucose homeostasis by reabsorbing all the filtered glucose, an adaptive mechanism that ensures sufficient energy is available during fasting periods. This mechanism becomes maladaptive in diabetes, however, as hyperglycaemia augments the expression and activity of the sodiumglucose cotransporter (SGLT) 2 in the proximal tubule of the kidney. As a result, glucose reabsorption may be increased by as much as 20% in individuals with poorly controlled diabetes. SGLT2 is a low-affinity, high-capacity glucose transport protein that reabsorbs 90% of filtered glucose, while the high-affinity, low-capacity SGLT1 transporter reabsorbs the remaining 10%. SGLT2 represents a novel target for the treatment of diabetes. In animal studies, SGLT2 inhibition reduces plasma glucose levels, resulting in improved beta-cell function and enhanced insulin sensitivity in liver and muscle. Human studies have confirmed the efficacy of SLGT2 inhibitors in improving glucose control and reducing the A1c. Because the mechanism of SGLT2 inhibition is independent of circulating insulin levels or insulin sensitivity, these agents can be combined with all other antidiabetic classes, including exogenous insulin. Although the long-term efficacy and safety of SGLT2 inhibitors remain under study, the class represents a novel therapeutic approach with potential for the treatment of both type 2 and 1 diabetes.
C1 [DeFronzo, R. A.] Univ Texas Hlth Sci Ctr San Antonio, Diabet Div, Dept Med, San Antonio, TX 78229 USA.
[DeFronzo, R. A.] Audie L Murphy Mem Vet Adm Med Ctr, San Antonio, TX 78284 USA.
[Davidson, J. A.] Univ Texas SW Med Sch, Diabet Div, Dallas, TX USA.
[Del Prato, S.] Univ Pisa, Diabet Div, Pisa, Italy.
RP DeFronzo, RA (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Diabet Div, Dept Med, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM albarado@uthscsa.edu; davidsonmd@sbcglobal.net
RI Del Prato, Stefano/K-3405-2016
OI Del Prato, Stefano/0000-0002-5388-0270
FU AstraZeneca; Bayer Healthcare; Bristol-Myers Squibb; GlaxoSmithKline;
Johnson Johnson; Merck Sharp Dohme; Novartis; Novo Nordisk; Pfizer Inc;
Sanofi-Aventis
FX The authors have drafted this article on behalf of the Worldwide
Initiative for Diabetes Education (WorldWIDE). WorldWIDE had no input
into writing the initial version of the manuscript or into any revisions
of the manuscript. WorldWIDE is a charitable foundation that provides
training, education and information to healthcare providers. The mission
of WorldWIDE is to challenge and shape the future management of diabetes
in order to provide optimal treatment for all patients and to enhance
professional education for physicians and other diabetes professionals.
Publication of the article would help to achieve this goal. WorldWIDE
receives financial support from AstraZeneca, Bayer Healthcare,
Bristol-Myers Squibb, GlaxoSmithKline, Johnson & Johnson, Merck Sharp
&Dohme, Novartis, Novo Nordisk, Pfizer Inc and Sanofi-Aventis. The
authors acknowledge the editorial assistance of IntraMed Educational
Group in the styling of this manuscript.
NR 76
TC 151
Z9 163
U1 8
U2 36
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1462-8902
EI 1463-1326
J9 DIABETES OBES METAB
JI Diabetes Obes. Metab.
PD JAN
PY 2012
VL 14
IS 1
BP 5
EP 14
DI 10.1111/j.1463-1326.2011.01511.x
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 862AW
UT WOS:000298063200002
PM 21955459
ER
PT J
AU Henry, RR
Aroda, VR
Mudaliar, S
Garvey, WT
Chou, HS
Jones, MR
AF Henry, R. R.
Aroda, V. R.
Mudaliar, S.
Garvey, W. T.
Chou, H. S.
Jones, M. R.
TI Effects of colesevelam on glucose absorption and hepatic/peripheral
insulin sensitivity in patients with type 2 diabetes mellitus
SO DIABETES OBESITY & METABOLISM
LA English
DT Article
DE bile acid sequestrant; colesevelam; glucose; insulin sensitivity; type 2
diabetes mellitus
ID GLYCEMIC CONTROL; SECRETION; THERAPY; HYDROCHLORIDE
AB Aim: Colesevelam lowers glucose and low-density lipoprotein cholesterol levels in patients with type 2 diabetes mellitus. This study examined the mechanisms by which colesevelam might affect glucose control.
Methods: In this 12-week, randomized, double-blind, placebo-controlled study, subjects with type 2 diabetes and haemoglobin A(1c)(HbA(1c)) >= 7.5% on either stable diet and exercise or sulphonylurea therapy were randomized to colesevelam 3.75 g/day (n = 16) or placebo (n = 14). Hepatic/peripheral insulin sensitivity was evaluated at baseline and at week 12 by infusion of (3)H-labelled glucose followed by a 2-step hyperinsulinemic-euglycemic clamp. Two 75-g oral glucose tolerance tests (OGTTs) were conducted at baseline, one with and one without co-administration of colesevelam. A final OGTT was conducted at week 12. HbA(1c) and fasting plasma glucose (FPG) levels were evaluated pre- and post-treatment.
Results: Treatment with colesevelam, compared to placebo, had no significant effects on basal endogenous glucose output, response to insulin or on maximal steady-state glucose disposal rate. At baseline, co-administration of colesevelam with oral glucose reduced total area under the glucose curve (AUCg) but not incremental AUCg. At week 12, neither total AUCg nor incremental AUCg were changed from pre-treatment values in either group. Post-load insulin levels increased with colesevelam at 30 and 120 min, but these changes in total area under the insulin curve (AUCi) and incremental AUCi did not differ between groups. Both HbA(1c) and FPG improved with colesevelam, but treatment differences were not significant.
Conclusions: Colesevelam does not affect hepatic or peripheral insulin sensitivity and does not directly affect glucose absorption.
C1 [Henry, R. R.; Mudaliar, S.] VA San Diego Healthcare Syst, Sect Diabet Endocrinol & Metab, San Diego, CA 92161 USA.
[Henry, R. R.; Mudaliar, S.] Univ Calif San Diego, San Diego, CA 92161 USA.
[Aroda, V. R.] MedStar Hlth Res Inst, Hyattsville, MD USA.
[Garvey, W. T.] Univ Alabama, Dept Nutr Sci, Birmingham, AL 35294 USA.
[Garvey, W. T.] Birmingham VA Med Ctr, Birmingham, AL USA.
[Chou, H. S.] Daiichi Sankyo Prod Dev, Edison, NJ USA.
[Jones, M. R.] Daiichi Sankyo Inc, Parsippany, NJ USA.
RP Henry, RR (reprint author), VA San Diego Healthcare Syst, Sect Diabet Endocrinol & Metab, 3350 La Jolla Village Dr,111G, San Diego, CA 92161 USA.
EM rrhenry@vapop.ucsd.edu
FU Daiichi Sankyo Inc.; VA San Diego Healthcare System; Department of
Veteran Affairs; Veterans Medical Research Foundation; Diabetes
Education and Research Center [DK 063491]; General Clinical Research
Center [MO1 RR-00827]; University of Alabama Birmingham from the Center
for Clinical and Translational Science [UL1 RR02577]; Diabetes Research
and Training Center [P60 DK079626]
FX This study was sponsored by Daiichi Sankyo Inc. Editorial assistance was
provided by Karen Stauffer, PhD, of inScience Communications, a Wolters
Kluwer business. This assistance was performed in compliance with Good
Publication Practices outlined by the International Committee of Medical
Journal Editors and was funded by Daiichi Sankyo Inc. Support is
acknowledged in San Diego from the VA San Diego Healthcare System,
Department of Veteran Affairs, Veterans Medical Research Foundation, the
Diabetes Education and Research Center DK 063491, and the General
Clinical Research Center MO1 RR-00827. Support is acknowledged from the
University of Alabama Birmingham from the Center for Clinical and
Translational Science (UL1 RR02577) and the Diabetes Research and
Training Center (P60 DK079626).
NR 13
TC 12
Z9 12
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1462-8902
J9 DIABETES OBES METAB
JI Diabetes Obes. Metab.
PD JAN
PY 2012
VL 14
IS 1
BP 40
EP 46
DI 10.1111/j.1463-1326.2011.01486.x
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 862AW
UT WOS:000298063200006
PM 21831167
ER
PT J
AU Fang, JL
Wang, XL
Liu, HS
Wang, Y
Zhou, KH
Hong, Y
Liu, J
Wang, L
Xue, C
Song, M
Liu, BY
Zhu, B
AF Fang, Jiliang
Wang, Xiaoling
Liu, Hesheng
Wang, Yin
Zhou, Kehua
Hong, Yang
Liu, Jun
Wang, Lei
Xue, Chao
Song, Ming
Liu, Baoyan
Zhu, Bing
TI The Limbic-Prefrontal Network Modulated by Electroacupuncture at CV4 and
CV12
SO EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
LA English
DT Article
ID INTRINSIC FUNCTIONAL CONNECTIVITY; HUMAN BRAIN; ACUPUNCTURE STIMULATION;
IMPLICATED ACUPOINTS; CINGULATE CORTEX; HEALTHY-SUBJECTS; FMRI; MRI;
ACTIVATION; MECHANISM
AB fMRI studies showed that acupuncture could induce hemodynamic changes in brain networks. Many of these studies focused on whether specific acupoints could activate specific brain regions and were often limited to manual acupuncture at acupoints on the limbs. In this fMRI study, we investigated acupuncture's modulation effects on brain functional networks by electroacupuncture (EA) at acupoints on the midline of abdomen. Acupoints Guanyuan (CV4) and Zhongwan (CV12) were stimulated in 21 healthy volunteers. The needling sensations, brain activation, and functional connectivity were studied. We found that the limbic-prefrontal functional network was deactivated by EA at CV4 and CV12. More importantly, the local functional connectivity was significantly changed during EA stimulation, and the change persisted during the period after the stimulation. Although minor differences existed, both acupoints similarly modulated the limbic-prefrontal functional network, which is overlapped with the functional circuits associated with emotional and cognitive regulation.
C1 [Fang, Jiliang; Wang, Xiaoling; Zhou, Kehua; Hong, Yang; Wang, Lei; Xue, Chao] China Acad Chinese Med Sci, Funct Brain Imaging Lab, Dept Radiol, Guang An Men Hosp, Beijing 100053, Peoples R China.
[Fang, Jiliang; Liu, Hesheng] Harvard Univ, Sch Med, Athinoula A Martinos Ctr Biomed Imaging, Massachusetts Gen Hosp, Charlestown, MA 02129 USA.
[Wang, Yin; Liu, Jun] China Acad Chinese Med Sci, Dept Acupuncture & Moxibust, Guang An Men Hosp, Beijing 100053, Peoples R China.
[Zhou, Kehua] Daemen Coll, Dept Phys Therapy, Amherst, NY 14226 USA.
[Song, Ming] Chinese Acad Sci, Inst Automat, Beijing 100190, Peoples R China.
[Zhu, Bing] China Acad Chinese Med Sci, Inst Acupuncture & Moxibust, Beijing 100700, Peoples R China.
RP Fang, JL (reprint author), China Acad Chinese Med Sci, Funct Brain Imaging Lab, Dept Radiol, Guang An Men Hosp, Beijing 100053, Peoples R China.
EM fangjiliang@sohu.com
OI Liu, Hesheng/0000-0002-7233-1509
FU National Natural Science Foundation of China [30870668]; National
Institutes of Health, National Center for Complementary and Alternative
Medicine (NIH/NCCAM), USA [F05 AT003022-01-04]
FX This study was funded by the National Natural Science Foundation of
China (Grant Code no. 30870668) and National Institutes of Health,
National Center for Complementary and Alternative Medicine (NIH/NCCAM)
(F05 AT003022-01-04), USA.
NR 51
TC 10
Z9 11
U1 0
U2 7
PU HINDAWI PUBLISHING CORPORATION
PI NEW YORK
PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA
SN 1741-427X
J9 EVID-BASED COMPL ALT
JI Evid.-based Complement Altern. Med.
PY 2012
AR 515893
DI 10.1155/2012/515893
PG 11
WC Integrative & Complementary Medicine
SC Integrative & Complementary Medicine
GA 882AG
UT WOS:000299532900001
ER
PT J
AU Rajasuriar, R
Booth, DR
Gouillou, M
Spelman, T
James, I
Solomon, A
Chua, K
Stewart, G
Deeks, S
Bangsberg, DR
Muzoora, C
Cameron, PU
Hunt, P
Martin, J
Lewin, SR
AF Rajasuriar, R.
Booth, D. R.
Gouillou, M.
Spelman, T.
James, I.
Solomon, A.
Chua, K.
Stewart, G.
Deeks, S.
Bangsberg, D. R.
Muzoora, C.
Cameron, P. U.
Hunt, P.
Martin, J.
Lewin, S. R.
TI The role of SNPs in the alpha-chain of the IL-7R gene in CD4+T-cell
recovery in HIV-infected African patients receiving suppressive cART
SO GENES AND IMMUNITY
LA English
DT Article
DE HIV; IL-7R alpha; T cells; cART; Caucasian; African
ID POTENT ANTIRETROVIRAL THERAPY; INTERLEUKIN-7 RECEPTOR-ALPHA;
T-CELL-ACTIVATION; IMMUNE ACTIVATION; MULTIPLE-SCLEROSIS; MICROBIAL
TRANSLOCATION; PARKINSONS-DISEASE; VIRAL SUPPRESSION; DOWN-REGULATION;
CD4
AB We previously found an association between faster CD4+ T-cell recovery in HIV-infected patients receiving combination antiretroviral therapy (cART) and interleukin-7 receptor-alpha (IL-7R alpha) haplotype-2 in a predominantly Caucasian cohort. This study aims to determine whether this association was also significant in Africans. Patients were recruited from the Uganda AIDS Rural Treatment Outcomes (UARTO) cohort (n = 352). We used survival analysis and linear mixed modelling (LMM) to determine factors associated with CD4 T-cell recovery. Eight IL-7R alpha single-nucleotide polymorphisms (SNPs) were genotyped in both Africans and Caucasians (n = 57). Soluble (s)IL-7R alpha levels were measured by ELISA. In UARTO, IL-7R alpha haplotype-2 was associated with slower CD4 T-cell recovery following cART by using survival analysis (P = 0.020) and no association was found with LMM (P = 0.958). The tagging-SNP for IL-7R alpha haplotype-2 (rs6897932) was associated with decreased sIL-7R alpha (P < 0.001). The haplotypes for the IL-7R alpha. were significantly different in Africans and Caucasians. Using IL-7R alpha genotypes we found slower CD4 T-cell recovery in UARTO patients was still associated with rs6897932 (P = 0.009) and rs3194051 was associated with faster CD4 T-cell recovery (P = 0.006). Unlike Caucasians, we did not demonstrate a significant association between IL-7R alpha haplotype 2 and faster CD4 T-cell recovery in Africans. The IL-7R alpha SNPs associated with CD4 T-cell recovery following cART differ in African and Caucasian cohorts. Genes and Immunity (2012) 13, 83-93; doi:10.1038/gene.2011.65; published online 22 September 2011
C1 [Lewin, S. R.] Monash Univ, Infect Dis Unit, Dept Med, Floor Burnet Inst 2, Melbourne, Vic 3004, Australia.
[Rajasuriar, R.] Univ Malaya, Fac Med, Kuala Lumpur, Malaysia.
[Booth, D. R.; Stewart, G.] Univ Sydney, Westmead Millennium Inst, Sydney, NSW 2006, Australia.
[Gouillou, M.; Spelman, T.] Burnet Inst, Ctr Populat Hlth, Melbourne, Vic, Australia.
[James, I.] Murdoch Univ, Ctr Clin Immunol & Biomed Stat, Perth, WA, Australia.
[Deeks, S.; Hunt, P.; Martin, J.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Bangsberg, D. R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Global Hlth,Ragon Inst MGH MIT & Harvard, Boston, MA USA.
[Bangsberg, D. R.; Muzoora, C.] Mbarara Univ Sci & Technol, Mbarara, Uganda.
[Cameron, P. U.; Lewin, S. R.] Burnet Inst, Ctr Virol, Melbourne, Vic, Australia.
[Cameron, P. U.; Lewin, S. R.] The Alfred, Infect Dis Unit, Melbourne, Vic, Australia.
RP Lewin, SR (reprint author), Monash Univ, Infect Dis Unit, Dept Med, Floor Burnet Inst 2, 85 Commercial Rd, Melbourne, Vic 3004, Australia.
EM Sharon.Lewin@med.monash.edu.au
RI Rajasuriar, Reena/B-9569-2010
FU Malaysian Government; NHMRC; Alfred Foundation; Mark and Lisa Schwartz
Family Foundation; [MH54907]; [MH K-24 87227]
FX RR is a recipient of the Kings Scholarship from the Malaysian Government
and acknowledges the University of Malaya and the Ministry of Higher
Education. SRL is an Australian National Health and Medical Research
Council (NHMRC) practitioner fellow. SRL receives funding from the NHMRC
and the Alfred Foundation. The UARTO cohort was funded by MH54907 and
the Mark and Lisa Schwartz Family Foundation. DRB received additional
funding from MH K-24 87227.
NR 62
TC 8
Z9 8
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1466-4879
J9 GENES IMMUN
JI Genes Immun.
PD JAN
PY 2012
VL 13
IS 1
BP 83
EP 93
DI 10.1038/gene.2011.65
PG 11
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA 882XJ
UT WOS:000299596900010
PM 21938017
ER
PT J
AU Lapointe, J
Bouchard, K
Patenaude, AF
Maunsell, E
Simard, J
Dorval, M
AF Lapointe, Julie
Bouchard, Karine
Patenaude, Andrea Farkas
Maunsell, Elizabeth
Simard, Jacques
Dorval, Michel
CA INHERIT BRCAs Res Program
TI Incidence and predictors of positive and negative effects of BRCA1/2
genetic testing on familial relationships: a 3-year follow-up study
SO GENETICS IN MEDICINE
LA English
DT Article
DE BRCA genes; family communication; prospective study; psychosocial issues
ID OVARIAN-CANCER FAMILIES; AT-RISK RELATIVES; HEREDITARY BREAST;
PSYCHOLOGICAL IMPACT; MUTATION CARRIERS; SUSCEPTIBILITY; COMMUNICATION;
INFORMATION; DISTRESS; MODEL
AB Purpose: Little is known about the long-term impact of BRCA1/2 testing on the relationships between family members. We assessed the incidence of positive and negative family relationship effects of BRCA1/2 testing in the 3 years after result disclosure and identified predictors of these effects.
Methods: A total of 485 women and 67 men who had undergone BRCA1/2 testing were asked 3 years later whether having been tested had improved and/or disrupted relationships with their relatives. The associations with sociodemographic, medical, and psychosocial characteristics were assessed.
Results: Globally, 85.1% did not report any positive or negative effects of genetic testing on family relationships. Positive and negative effects were reported by 13.2% and 3.7% of participants, respectively. Reporting positive relationship effects was associated with older age, intolerance for uncertainty, cancer-specific distress, and more social support. Low education, positive attitude toward prophylactic mastectomy, and low social support increased the likelihood of negative effects.
Conclusion: Our findings do not support the belief that family relationships are frequently disrupted by BRCA1/2 testing. Understanding that most family relationships are unchanged long term by genetic testing may help genetic service providers encourage those considering testing to overcome hesitancy related to potential difficulties of communicating results to relatives.
C1 [Lapointe, Julie; Dorval, Michel] Univ Laval, Fac Pharm, Quebec City, PQ, Canada.
[Lapointe, Julie; Bouchard, Karine; Maunsell, Elizabeth; Dorval, Michel] Ctr Hosp Affilie Univ Quebec, Ctr Rech FRSQ, URESP, Quebec City, PQ, Canada.
[Patenaude, Andrea Farkas] Dana Farber Canc Inst, Dept Psychosocial Oncol & Palliat Care, Boston, MA 02115 USA.
[Patenaude, Andrea Farkas] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Maunsell, Elizabeth; Simard, Jacques] Univ Laval, Fac Med, Quebec City, PQ G1K 7P4, Canada.
[Maunsell, Elizabeth; Dorval, Michel] Hop St Sacrement, Ctr Malad Sein Deschenes Fabia, Quebec City, PQ, Canada.
[Simard, Jacques] CHUQ CHUL, Ctr Rech, Lab Genom Canc, Quebec City, PQ, Canada.
RP Dorval, M (reprint author), Univ Laval, Fac Pharm, Quebec City, PQ, Canada.
EM mdorval@uresp.ulaval.ca
FU Canadian Institutes of Health Research [CRT-43822, CRN-87521,
TGF-63285]; Canadian Breast Cancer Research Alliance [11383]; Fonds
d'Enseignement et de Recherche de la Faculte de Pharmacie de
l'Universite Laval; Fonds de la Recherche en Sante du Quebec
FX The INHERIT BRCAs research program was supported by the Canadian
Institutes of Health Research (grant nos. CRT-43822 and CRN-87521) and
the Canadian Breast Cancer Research Alliance (grant no. 11383). Julie
Lapointe is a CIHR Fellow in Psychosocial Oncology Research and Training
(PORT) and is funded through a CIHR Training Grant (no. TGF-63285) and
the Fonds d'Enseignement et de Recherche de la Faculte de Pharmacie de
l'Universite Laval; Jacques Simard is Chairholder of the Canada Research
Chair in Oncogenetics; and Michel Dorval holds a Fonds de la Recherche
en Sante du Quebec Investigator Award. The authors thank all the women
and their families who agreed to participate for their time and effort.
They also thank Claudia Cote for data management and quality insurance
and Richard Poulin for linguistic revision. Parts of these results were
presented in an oral session at the 12th World Congress of
Psycho-oncology of the International Psycho-oncology Society (IPOS) and
the Canadian Association of Psychosocial Oncology (CAPO) (25-29 May
2010).
NR 60
TC 4
Z9 4
U1 3
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
J9 GENET MED
JI Genet. Med.
PD JAN
PY 2012
VL 14
IS 1
BP 60
EP 68
DI 10.1038/gim.0b013e3182310a7f
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 873NI
UT WOS:000298889600006
PM 22237432
ER
PT J
AU Salvaris, M
Cinel, C
Citi, L
Poli, R
AF Salvaris, Mathew
Cinel, Caterina
Citi, Luca
Poli, Riccardo
TI Novel Protocols for P300-Based Brain-Computer Interfaces
SO IEEE TRANSACTIONS ON NEURAL SYSTEMS AND REHABILITATION ENGINEERING
LA English
DT Article
DE Brain-computer interfaces (BCIs); BCI mouse; event-related potentials;
oddball paradigm; P300
ID EVENT-RELATED POTENTIALS; P300; BCI; SPELLER
AB The oddball protocol is often used in brain-computer interfaces (BCIs) to induce P300 ERPs, although, recently, some issues have been shown to detrimentally effect its performance. In this paper, we study a new periodic protocol and explore whether it can compete with the standard oddball protocol within the context of a BCI mouse. We found that the new protocol consistently and significantly outperforms the standard oddball protocol in relation to information transfer rates (33 bits/min for the former and 22 bits/min for the latter, measured at 90% accuracy) as well as P300 amplitudes. Furthermore, we performed a comparison of two periodic protocols with two less conventional oddball-like protocols that reveals the importance of the interactions between task and sequence in determining the success of a protocol.
C1 [Salvaris, Mathew; Cinel, Caterina; Poli, Riccardo] Univ Essex, Brain Comp Interfaces Lab, Sch Comp Sci & Elect Engn, Colchester CO4 3SQ, Essex, England.
[Citi, Luca] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02117 USA.
[Citi, Luca] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
RP Salvaris, M (reprint author), Univ Essex, Brain Comp Interfaces Lab, Sch Comp Sci & Elect Engn, Colchester CO4 3SQ, Essex, England.
EM mssalv@essex.ac.uk; ccinel@essex.ac.uk; lciti@neurostat.mit.edu;
rpoli@essex.ac.uk
RI Citi, Luca/G-2270-2011;
OI Citi, Luca/0000-0001-8702-5654; Poli, Riccardo/0000-0003-4612-0780
FU U.K. Engineering and Physical Sciences Research Council [EP/F033818/1]
FX Manuscript received July 22, 2011; revised October 02, 2011; accepted
October 04, 2011. Date of publication December 12, 2011; date of current
version January 25, 2012. This work was supported by the U.K.
Engineering and Physical Sciences Research Council under Grant
EP/F033818/1.
NR 37
TC 13
Z9 14
U1 0
U2 7
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 1534-4320
EI 1558-0210
J9 IEEE T NEUR SYS REH
JI IEEE Trans. Neural Syst. Rehabil. Eng.
PD JAN
PY 2012
VL 20
IS 1
BP 8
EP 17
DI 10.1109/TNSRE.2011.2174463
PG 10
WC Engineering, Biomedical; Rehabilitation
SC Engineering; Rehabilitation
GA 881TN
UT WOS:000299512300003
PM 22180513
ER
PT J
AU Nicolau, DP
Carmeli, Y
Crank, CW
Goff, DA
Graber, CJ
Lima, ALL
Goldstein, EJC
AF Nicolau, David P.
Carmeli, Yehuda
Crank, Christopher W.
Goff, Debra A.
Graber, Christopher J.
Lima, Ana Lucia L.
Goldstein, Ellie J. C.
TI Carbapenem stewardship: does ertapenem affect Pseudomonas susceptibility
to other carbapenems? A review of the evidence
SO INTERNATIONAL JOURNAL OF ANTIMICROBIAL AGENTS
LA English
DT Review
DE Carbapenem; Ecology; Ertapenem; Pseudomonas; Stewardship; Susceptibility
ID 25 HOSPITALS; AERUGINOSA; IMIPENEM; THERAPY; IMPACT
AB The group 2 carbapenems (imipenem, meropenem and, more recently, doripenem) have been a mainstay of treatment for patients with serious hospital infections caused by Pseudomonas aeruginosa, Enterobacteriaceae and other difficult-to-treat Gram-negative pathogens as well as mixed aerobic/anaerobic infections. When ertapenem, a group 1 carbapenem, was introduced, questions were raised about the potential for ertapenem to select for imipenem-and meropenem-resistant Pseudomonas. Results from ten clinical studies evaluating the effect of ertapenem use on the susceptibility of Pseudomonas to carbapenems have uniformly shown that ertapenem use does not result in decreased Pseudomonas susceptibility to these antipseudomonal carbapenems. Here we review these studies evaluating the evidence of how ertapenem use affects P. aeruginosa as well as provide considerations for ertapenem use in the context of institutional stewardship initiatives. (C) 2011 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved.
C1 [Nicolau, David P.] Hartford Hosp, Ctr Anti Infect Res & Dev, Hartford, CT 06102 USA.
[Carmeli, Yehuda] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Div Epidemiol, IL-69978 Tel Aviv, Israel.
[Crank, Christopher W.] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Goff, Debra A.] Ohio State Univ, Med Ctr, Dept Pharm, Coll Pharm, Columbus, OH 43210 USA.
[Graber, Christopher J.; Goldstein, Ellie J. C.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Graber, Christopher J.] VA Greater Los Angeles Healthcare Syst, Infect Dis Sect, Los Angeles, CA USA.
[Lima, Ana Lucia L.] Univ Sao Paulo, Sch Med, Hosp Clin, Inst Orthopaed & Traumatol, Sao Paulo, Brazil.
[Goldstein, Ellie J. C.] St Johns Hlth Ctr, Dept Infect Dis, Santa Monica, CA USA.
RP Nicolau, DP (reprint author), Hartford Hosp, Ctr Anti Infect Res & Dev, 80 Seymour St, Hartford, CT 06102 USA.
EM dnicola@harthosp.org
OI Lima, Ana/0000-0002-1055-0554; Lima, Ana Lucia
Munhoz/0000-0002-2396-9880
FU Achaogen Inc.; Basilea Pharmaceutica; BioLine Therapeutics; Cempra
Pharmaceuticals Inc.; Intercell AG; Johnson and Johnson Pharmaceuticals;
Merck; Cubist; Ortho Pharmaceuticals; Schering-Plough Pharmaceuticals;
Optimer Pharmaceuticals; Theravance Inc.; Pfizer Inc.; Astellas Inc.;
Cerexa Inc.; Impex Pharmaceuticals; Novexel; Novartis; Clinical
Microbiology Institute; Genzyme; NanoPacific Holdings Inc.; Romark
Laboratories LC; ViroXis Corp.; Warner Chilcott; Avid-Biotics Corp.;
GLSynthesis Inc.; Immunome Inc.; Toltec Pharma LLC.;
Ortho-McNeil-Janssen; Sanofi-Aventis; Bayer-Schering Pharma;
AstraZeneca; Cerexa; Forest; Johnson Johnson; Pfizer
FX Competing interests: YC has served on speaker bureaus, scientific
advisory boards and/or received research grants from Achaogen Inc.,
Basilea Pharmaceutica, BioLine Therapeutics, Cempra Pharmaceuticals
Inc., Intercell AG, Johnson and Johnson Pharmaceuticals and Merck. DAG
has served on speaker bureaus and/or received research grants from
Cubist, Merck and Ortho Pharmaceuticals. EJCG has served on advisory
boards for Merck, Optimer Pharmaceuticals, Bayer Pharmaceuticals,
Theravance Inc., BioK+, ViroPharma and Kindred Healthcare Corp., on
speaker bureaus for Bayer Inc., Merck, Sanofi Pasteur and Forest Labs,
and has received research grants from Merck, Schering-Plough
Pharmaceuticals, Optimer Pharmaceuticals, Theravance Inc., Cubist,
Pfizer Inc., Astellas Inc., Cerexa Inc., Impex Pharmaceuticals, Novexel,
Novartis, Clinical Microbiology Institute, Genzyme, NanoPacific Holdings
Inc., Romark Laboratories LC, ViroXis Corp., Warner Chilcott,
Avid-Biotics Corp., GLSynthesis Inc., Immunome Inc. and Toltec Pharma
LLC. CJG has received a research grant from Merck and an unrestricted
educational grant from Ortho-McNeil-Janssen, and has served on an
advisory board for Pfizer. ALLL has served on speaker bureaus and/or
received research grants from Merck, Sanofi-Aventis and Bayer-Schering
Pharma. DPN has served on speaker bureaus and/or received research
grants from AstraZeneca, Cerexa, Cubist, Forest, Johnson & Johnson,
Merck and Pfizer. CWC declares no competing interests.
NR 19
TC 22
Z9 25
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-8579
J9 INT J ANTIMICROB AG
JI Int. J. Antimicrob. Agents
PD JAN
PY 2012
VL 39
IS 1
BP 11
EP 15
DI 10.1016/j.ijantimicag.2011.08.018
PG 5
WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
GA 863DO
UT WOS:000298143200002
PM 22047702
ER
PT J
AU Farr, SA
Price, TO
Dominguez, LJ
Motisi, A
Saiano, F
Niehoff, ML
Morley, JE
Banks, WA
Ercal, N
Barbagallo, M
AF Farr, Susan A.
Price, Tulin O.
Dominguez, Ligia J.
Motisi, Antonio
Saiano, Filippo
Niehoff, Michael L.
Morley, John E.
Banks, William A.
Ercal, Nuran
Barbagallo, Mario
TI Extra Virgin Olive Oil Improves Learning and Memory in SAMP8 Mice
SO JOURNAL OF ALZHEIMERS DISEASE
LA English
DT Article
DE Extra virgin olive oil; learning; memory; object recognition; oxidative
stress; SAMP8; T-maze
ID SENESCENCE-ACCELERATED MICE; ALPHA-LIPOIC ACID; ALZHEIMERS-DISEASE;
MEDITERRANEAN DIET; AMYLOID-BETA; GLUTATHIONE DISULFIDE; SENSORY
PROPERTIES; OXIDATIVE STRESS; FATTY-ACIDS; MOUSE MODEL
AB Polyphenols are potent antioxidants found in extra virgin olive oil (EVOO); antioxidants have been shown to reverse age-and disease-related learning and memory deficits. We examined the effects of EVOO on learning and memory in SAMP8 mice, an age-related learning/memory impairment model associated with increased amyloid-beta protein and brain oxidative damage. We administered EVOO, coconut oil, or butter to 11 month old SAMP8 mice for 6 weeks. Mice were tested in T-maze foot shock avoidance and one-trial novel object recognition with a 24 h delay. Mice which received EVOO had improved acquisition in the T-maze and spent more time with the novel object in one-trial novel object recognition versus mice which received coconut oil or butter. Mice that received EVOO had improve T-maze retention compared to the mice that received butter. EVOO increased brain glutathione levels suggesting reduced oxidative stress as a possible mechanism. These effects plus increased glutathione reductase activity, superoxide dismutase activity, and decreased tissue levels of 4-hydroxynoneal and 3-nitrotyrosine were enhanced with enriched EVOO (3x and 5x polyphenols concentration). Our findings suggest that EVOO has beneficial effects on learning and memory deficits found in aging and diseases, such as those related to the overproduction of amyloid-beta protein, by reversing oxidative damage in the brain, effects that are augmented with increasing concentrations of polyphenols in EVOO.
C1 [Farr, Susan A.] St Louis Univ, Sch Med, VA Med Ctr, Dept Internal Med,Div Geriatr Med, St Louis, MO 63106 USA.
[Farr, Susan A.; Morley, John E.] VA Med Ctr, GRECC, St Louis, MO USA.
[Price, Tulin O.] St Louis Univ, Sch Med, Div Endocrinol, Dept Internal Med, St Louis, MO 63106 USA.
[Dominguez, Ligia J.; Motisi, Antonio; Barbagallo, Mario] Univ Palermo, Div Geriatr Med, Palermo, Italy.
[Saiano, Filippo] Univ Palermo, Fac Agron, Dept DEMETRA, Palermo, Italy.
Univ Palermo, Dept Agroenvironm Syst, Palermo, Italy.
[Banks, William A.] Vet Affairs Puget Sound Hlth Care Syst, GRECC, Seattle, WA USA.
[Banks, William A.] Univ Washington, Sch Med, Div Gerontol & Geriatr Med, Dept Internal Med, Seattle, WA USA.
[Ercal, Nuran] Missouri Univ Sci & Technol, Dept Chem, Rolla, MO USA.
RP Farr, SA (reprint author), St Louis Univ, Sch Med, VA Med Ctr, Dept Internal Med,Div Geriatr Med, 915 N Grand Blvd,151-JC, St Louis, MO 63106 USA.
EM farrsa@slu.edu
OI BARBAGALLO, MARIO/0000-0002-1349-6530; dominguez, ligia
j/0000-0003-1466-8610
FU VA Medical Center, St. Louis, MO
FX This work was supported by VA Medical Center, St. Louis, MO.
NR 54
TC 51
Z9 52
U1 2
U2 14
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1387-2877
J9 J ALZHEIMERS DIS
JI J. Alzheimers Dis.
PY 2012
VL 28
IS 1
BP 81
EP 92
DI 10.3233/JAD-2011-110662
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 879EG
UT WOS:000299311900007
PM 21955812
ER
PT J
AU Baker, LD
Bayer-Carter, JL
Skinner, J
Montine, TJ
Cholerton, BA
Callaghan, M
Leverenz, JB
Walter, BK
Tsai, E
Postupna, N
Lampe, J
Craft, S
AF Baker, Laura D.
Bayer-Carter, Jennifer L.
Skinner, Jeannine
Montine, Thomas J.
Cholerton, Brenna A.
Callaghan, Maureen
Leverenz, James B.
Walter, Brooke K.
Tsai, Elaine
Postupna, Nadia
Lampe, Johanna
Craft, Suzanne
TI High-Intensity Physical Activity Modulates Diet Effects on Cerebrospinal
Amyloid-beta Levels in Normal Aging and Mild Cognitive Impairment
SO JOURNAL OF ALZHEIMERS DISEASE
LA English
DT Article
DE Aging; Alzheimer's disease; amyloid; biomarker; brain; diet; exercise;
interleukin; mild cognitive impairment; tau
ID TRANSGENIC MOUSE MODEL; ALZHEIMERS-DISEASE; OLDER-ADULTS; CALORIC
RESTRICTION; VOLUNTARY EXERCISE; MEDITERRANEAN DIET; RISK; BRAIN; MICE;
AGE
AB We previously showed that amyloid-beta 1-42 (A beta(42)) levels in cerebrospinal fluid (CSF) were markedly altered in response to a 4-week dietary intervention in normal aging and mild cognitive impairment (MCI). Here, we re-examined the data to assess whether diet-induced effects on CSF A beta(42) were modulated by high intensity physical activity (hi-PA). Normal older adults (n = 18, mean age = 68.6 +/- 7.4 y) and adults with amnestic MCI (n = 23, mean age = 68.0 +/- 6.5 y) received a low saturated fat/low glycemic index (LOW) diet or a high saturated fat/high glycemic index (HIGH) diet, and CSF levels of A beta(42), tau, and IL-8 were measured at baseline and week 4. Pre-study activity levels were assessed using a 7-d questionnaire, and weekly duration of hi-PA was quantified. At baseline, increased hi-PA in normals predicted lower CSF levels of tau (r = -0.54, p = 0.020) and IL-8 (r = -0.70, p = 0.025). Diet-induced effects on CSF A beta(42) during the intervention study were modulated by hi-PA, and the nature of this effect differed for normals and MCI (ANOVA, p = 0.039). That is, for normal adults, increased hi-PA attenuated the effects of the HIGH diet on CSF A beta(42) whereas in MCI, increased hi-PA potentiated the effects of the LOW diet. Our results suggest that normal adults who engage in hi-PA are less vulnerable to the pathological effects of an unhealthy diet, while in MCI, the benefit of a healthy diet on A beta modulation is greatest when paired with hi-PA. Exercise may thus interact with diet to alter pathological processes that ultimately modify risk of Alzheimer's disease.
C1 [Baker, Laura D.; Bayer-Carter, Jennifer L.; Skinner, Jeannine; Cholerton, Brenna A.; Callaghan, Maureen; Craft, Suzanne] Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Seattle, WA USA.
[Leverenz, James B.] Vet Affairs Puget Sound Hlth Care Syst, Mental Illness & Parkinson Dis Res Ctr, Seattle, WA USA.
[Baker, Laura D.; Skinner, Jeannine; Cholerton, Brenna A.; Walter, Brooke K.; Tsai, Elaine; Craft, Suzanne] Vet Affairs Puget Sound Hlth Care Syst, Dept Med, Seattle, WA USA.
Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Montine, Thomas J.; Postupna, Nadia] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA.
[Leverenz, James B.; Walter, Brooke K.] Univ Washington, Sch Med, Dept Neurol, Seattle, WA 98195 USA.
[Lampe, Johanna] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Leverenz, James B.] Vet Affairs Puget Sound Hlth Care Syst, Mental Illness & Parkinson Educ Ctr, Seattle, WA USA.
[Leverenz, James B.] Vet Affairs Puget Sound Hlth Care Syst, Mental Illness & Parkinson Clin Ctr, Seattle, WA USA.
RP Baker, LD (reprint author), S-182-GRECC,VAPSHCS 1660 S Columbian Way, Seattle, WA 98108 USA.
EM ldbaker@uw.edu
FU NIA [R37 AG-10880, P50 AG05136, 5T32 AG000258]; Nancy and Buster Alvord
Endowment; Office of Research and Development Medical Research Service;
Geriatric Research, Education and Clinical Center of the Department of
Veterans Affairs
FX This research was supported by NIA R37 AG-10880 (Craft), NIA P50 AG05136
Project 1 (Montine), NIA 5T32 AG000258 (Postupna), the Nancy and Buster
Alvord Endowment, and the Office of Research and Development Medical
Research Service and the Geriatric Research, Education and Clinical
Center of the Department of Veterans Affairs. Dr. Baker had full access
to all data and takes responsibility for its integrity and the accuracy
of the data analysis which was conducted without input from the funding
agencies.
NR 60
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Z9 13
U1 3
U2 24
PU IOS PRESS
PI AMSTERDAM
PA NIEUWE HEMWEG 6B, 1013 BG AMSTERDAM, NETHERLANDS
SN 1387-2877
J9 J ALZHEIMERS DIS
JI J. Alzheimers Dis.
PY 2012
VL 28
IS 1
BP 137
EP 146
DI 10.3233/JAD-2011-111076
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 879EG
UT WOS:000299311900012
PM 21971406
ER
PT J
AU Nielson, CM
Zmuda, JM
Carlos, AS
Wagoner, WJ
Larson, EA
Orwoll, ES
Klein, RF
AF Nielson, Carrie M.
Zmuda, Joseph M.
Carlos, Amy S.
Wagoner, Wendy J.
Larson, Emily A.
Orwoll, Eric S.
Klein, Robert F.
TI Rare coding variants in ALPL are associated with low serum alkaline
phosphatase and low bone mineral density
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Article
DE OSTEOPOROSIS; HEREDITY; GENETICS; ALKALINE PHOSPHATASE
ID QUANTITATIVE TRAIT LOCI; GENOME-WIDE ASSOCIATION; INFANTILE
HYPOPHOSPHATASIA; OSTEOPOROTIC FRACTURES; LINKAGE ANALYSIS; INBRED
STRAINS; PLASMA-LEVELS; MICE; C57BL/6J; GENES
AB Alkaline phosphatase (ALP) plays an essential role in the regulation of tissue mineralization, and its activity is highly heritable. Guided by genetic associations discovered in a murine model, we hypothesized a role for rare coding variants in determining serum ALP level and bone mineral density (BMD) in humans. We sequenced the coding regions of the ALP gene (ALPL) in men with low and normal serum ALP activity levels. Single-nucleotide ALPL variants, including 19 rare nonsynonymous variants (minor allele frequency <1%), were much more frequent among the low ALP group (33.8%) than the normal group (1.4%, p=1 x 10(-11)). Within the low ALP group, men with a rare, nonsynonymous variant had 11.2% lower mean serum ALP (p=3.9x 10(-4)), 6.7% lower BMD (p=0.03), and 11.1% higher serum phosphate (p=0.002) than those without. In contrast, common nonsynonymous variants had no association with serum ALP, phosphate, or BMD. Multiple rare ALPL coding variants are present in the general population, and nonsynonymous coding variants may be responsible for heritable differences in mineralization and thus BMD. (C) 2012 American Society for Bone and Mineral Research
C1 [Nielson, Carrie M.; Carlos, Amy S.; Wagoner, Wendy J.; Larson, Emily A.; Orwoll, Eric S.; Klein, Robert F.] Oregon Hlth & Sci Univ, Bone & Mineral Res Unit, Dept Med, Portland, OR 97239 USA.
[Zmuda, Joseph M.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Zmuda, Joseph M.] Univ Pittsburgh, Dept Human Genet, Pittsburgh, PA USA.
[Klein, Robert F.] Portland VA Med Ctr, Portland, OR USA.
RP Klein, RF (reprint author), Oregon Hlth & Sci Univ, Bone & Mineral Unit CR113, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM Kleinro@ohsu.edu
OI Orwoll, Eric/0000-0002-8520-7355
FU National Institutes of Health; National Institute of Arthritis and
Musculoskeletal and Skin Diseases (NIAMS) [AR44659, R01-AR051124];
National Institute on Aging (NIA) [R01-AG033618]; National Center for
Research Resources (NCRR); NIH Roadmap for Medical Research [U01
AR45580, U01 AR45614, U01 AR45632, U01 AR45647, U01 AR45654, U01
AR45583, U01 AG18197, U01-AG027810, UL1 RR024140]; Office of Research on
Women's Health; National Institute of Child Health and Human
Development, Building Interdisciplinary Research Careers in Women's
Health (BIRCWH) [HD043488-08]; VA Medical Research Service
FX The Osteoporotic Fractures in Men (MrOS) Study is supported by National
Institutes of Health funding; the following institutes provide support:
the National Institute of Arthritis and Musculoskeletal and Skin
Diseases (NIAMS), the National Institute on Aging (NIA), the National
Center for Research Resources (NCRR), and NIH Roadmap for Medical
Research under the following grant numbers: U01 AR45580, U01 AR45614,
U01 AR45632, U01 AR45647, U01 AR45654, U01 AR45583, U01 AG18197,
U01-AG027810, and UL1 RR024140. Dr. Nielson is also supported by the
Office of Research on Women's Health and the National Institute of Child
Health and Human Development, Building Interdisciplinary Research
Careers in Women's Health (BIRCWH) grant number HD043488-08. Dr. Klein's
research effort is supported by the National Institute of Arthritis,
Musculoskeletal and Skin Diseases (AR44659) and the VA Medical Research
Service. Dr. Zmuda's research effort is supported by the National
Institute of Arthritis and Musculoskeletal and Skin Diseases
(R01-AR051124) and by the National Institute on Aging (R01-AG033618).
NR 61
TC 10
Z9 10
U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD JAN
PY 2012
VL 27
IS 1
BP 93
EP 103
DI 10.1002/jbmr.527
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 867UA
UT WOS:000298479000009
PM 21956185
ER
PT J
AU Greendale, GA
Sowers, M
Han, WJ
Huang, MH
Finkelstein, JS
Crandall, CJ
Lee, JS
Karlamangla, AS
AF Greendale, Gail A.
Sowers, MaryFran
Han, Weijuan
Huang, Mei-Hua
Finkelstein, Joel S.
Crandall, Carolyn J.
Lee, Jennifer S.
Karlamangla, Arun S.
TI Bone mineral density loss in relation to the final menstrual period in a
multiethnic cohort: Results from the Study of Women's Health Across the
Nation (SWAN)
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Article
DE MENOPAUSE; PERIMENOPAUSE; BONE MINERAL DENSITY; ETHNIC DIFFERENCES;
LONGITUDINAL COHORT
ID HIP FRACTURE INCIDENCE; ESTROGEN DEFICIENCY; SEX-DIFFERENCES; SKELETAL
SITES; UNITARY MODEL; WHITE WOMEN; OSTEOPOROSIS; MENOPAUSE; GEOMETRY;
RISK
AB The objective of this study was to describe the time of onset and offset of bone mineral density (BMD) loss relative to the date of the final menstrual period (FMP); the rate and amount of BMD decline during the 5 years before and the 5 years after the FMP; and the independent associations between age at FMP, body mass index (BMI), and race/ethnicity with rates of BMD loss during this time interval. The sample included 242 African American, 384 white, 117 Chinese, and 119 Japanese women, pre- or early perimenopausal at baseline, who had experienced their FMP and for whom an FMP date could be determined. Loess-smoothed curves showed that BMD loss began 1 year before the FMP and decelerated (but did not cease) 2 years after the FMP, at both the lumbar spine (LS) and femoral neck (FN) sites. Piecewise, linear, mixed-effects regression models demonstrated that during the 10-year observation period, at each bone site, the rates and cumulative amounts of bone loss were greatest from 1 year before through 2 years after the FMP, termed the transmenopause. Postmenopausal loss rates, those occurring between 2 and 5 years after the FMP, were less than those observed during transmenopause. Cumulative, 10-year LS BMD loss was 10.6%; 7.38% was lost during the transmenopause. Cumulative FN loss was 9.1%; 5.8% was lost during the transmenopause. Greater BMI and African American heritage were related to slower loss rates, whereas the opposite was true of Japanese and Chinese ancestry. (C) 2012 American Society for Bone and Mineral Research
C1 [Greendale, Gail A.; Han, Weijuan; Huang, Mei-Hua; Karlamangla, Arun S.] Univ Calif Los Angeles, David Geffen Sch Med, Div Geriatr, Los Angeles, CA 90095 USA.
[Sowers, MaryFran] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Finkelstein, Joel S.] Massachusetts Gen Hosp, Dept Med, Endocrine Unit, Boston, MA 02114 USA.
[Crandall, Carolyn J.] Univ Calif Los Angeles, David Geffen Sch Med, Div Gen Internal Med, Los Angeles, CA 90095 USA.
[Lee, Jennifer S.] Univ Calif Davis, Dept Internal Med, Div Endocrinol, Davis, CA 95616 USA.
RP Greendale, GA (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Div Geriatr, 10945 Le Conte Ave,Suite 2339, Los Angeles, CA 90095 USA.
EM ggreenda@mednet.ucla.edu
FU National Institutes of Health (NIH); DHHS through National Institute on
Aging (NIA); National Institute of Nursing Research (NINR); NIH Office
of Research on Women's Health (ORWH) [NR004061, AG012505, AG012535,
AG012531, AG012539, AG012546, AG012553, AG012554, AG012495]
FX The Study of Women's Health Across the Nation (SWAN) has grant support
from the National Institutes of Health (NIH), DHHS, through the National
Institute on Aging (NIA), the National Institute of Nursing Research
(NINR), and the NIH Office of Research on Women's Health (ORWH) (grants
NR004061; AG012505, AG012535, AG012531, AG012539, AG012546, AG012553,
AG012554, AG012495). The content of this article is solely the
responsibility of the authors and does not necessarily represent the
official views of the NIA, NINR, ORWH, or the NIH.
NR 21
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U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD JAN
PY 2012
VL 27
IS 1
BP 111
EP 118
DI 10.1002/jbmr.534
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 867UA
UT WOS:000298479000011
PM 21976317
ER
PT J
AU Yu, EW
Thomas, BJ
Brown, JK
Finkelstein, JS
AF Yu, Elaine W.
Thomas, Bijoy J.
Brown, J. Keenan
Finkelstein, Joel S.
TI Simulated increases in body fat and errors in bone mineral density
measurements by DXA and QCT
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Article
DE BONE DENSITOMETRY; BONE QCT; BODY COMPOSITION
ID X-RAY ABSORPTIOMETRY; COMPUTED-TOMOGRAPHY QCT; GASTRIC BYPASS-SURGERY;
WEIGHT-LOSS; ACCURATE ASSESSMENT; MORBID-OBESITY; SOFT-TISSUE; SPINE;
PRECISION; MASS
AB Major alterations in body composition, such as with obesity and weight loss, have complex effects on the measurement of bone mineral density (BMD) by dual-energy X-ray absorptiometry (DXA). The effects of altered body fat on quantitative computed tomography (QCT) measurements are unknown. We scanned a spine phantom by DXA and QCT before and after surrounding with sequential fat layers (up to 12kg). In addition, we measured lumbar spine and proximal femur BMD by DXA and trabecular spine BMD by QCT in 13 adult volunteers before and after a simulated 7.5kg increase in body fat. With the spine phantom, DXA BMD increased linearly with sequential fat layering at the normal (P<0.01) and osteopenic (p<0.01) levels, but QCT BMD did not change significantly. In humans, fat layering significantly reduced DXA spine BMD values (mean +/- SD: -2.2 +/- 3.7%, p=0.05) and increased the variability of measurements. In contrast, fat layering increased QCT spine BMD in humans (mean +/- SD: 1.5 +/- 2.5%, p=0.05). Fat layering did not change mean DXA BMD of the femoral neck or total hip in humans significantly, but measurements became less precise. Associations between baseline and fat-simulation scans were stronger for QCT of the spine (r2=0.97) than for DXA of the spine (r2=0.87), total hip (r2=0.80), or femoral neck (r2=0.75). Bland-Altman plots revealed that fat-associated errors were greater for DXA spine and hip BMD than for QCT trabecular spine BMD. Fat layering introduces error and decreases the reproducibility of DXA spine and hip BMD measurements in human volunteers. Although overlying fat also affects QCT BMD measurements, the error is smaller and more uniform than with DXA BMD. Caution must be used when interpreting BMD changes in humans whose body composition is changing. (C) 2012 American Society for Bone and Mineral Research
C1 [Yu, Elaine W.; Finkelstein, Joel S.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Thomas, Bijoy J.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Brown, J. Keenan] Mindways Software, Austin, TX USA.
RP Yu, EW (reprint author), MGH Endocrine Unit, 50 Blossom St,Their 1051, Boston, MA 02114 USA.
EM ewyu@partners.org
FU NIDDK NIH HHS [T32 DK007028, K23 DK093713]
NR 27
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U1 0
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0884-0431
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD JAN
PY 2012
VL 27
IS 1
BP 119
EP 124
DI 10.1002/jbmr.506
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 867UA
UT WOS:000298479000012
PM 21915902
ER
PT J
AU Cooper, LT
Mather, PJ
Alexis, JD
Pauly, DF
Torre-Amione, G
Wittstein, IS
Dec, GW
Zucker, M
Narula, J
Kip, K
McNamara, DM
AF Cooper, Leslie T.
Mather, Paul J.
Alexis, Jeffrey D.
Pauly, Daniel F.
Torre-Amione, Guillermo
Wittstein, Ilan S.
Dec, G. William
Zucker, Mark
Narula, Jagat
Kip, Kevin
McNamara, Dennis M.
CA IMAC2 Investigators
TI Myocardial Recovery in Peripartum Cardiomyopathy: Prospective Comparison
With Recent Onset Cardiomyopathy in Men and Nonperipartum Women
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Article
DE Heart failure; pregnancy; dilated cardiomyopathy; myocardial recovery;
outcomes
ID POSTPARTUM CARDIOMYOPATHY; EUROPEAN-SOCIETY; PROLACTIN; HEART;
BROMOCRIPTINE; ASSOCIATION; MANAGEMENT; CARDIOLOGY; STATEMENT; DIAGNOSIS
AB Background: Whether myocardial recovery occurs more frequently in peripartum cardiomyopathy (PPCM) than in recent onset cardiomyopathies in men and nonperipartum women has not been prospectively evaluated. This was examined through an analysis of outcomes in the Intervention in Myocarditis and Acute Cardiomyopathy 2 (IMAC2) registry.
Methods and Results: IMAC2 enrolled 373 subjects with recent onset nonischemic dilated cardiomyopathy. Left ventricular ejection fraction (LVEF) was assessed at entry and 6 months, and subjects followed for up to 4 years. Myocardial recovery was compared between men (group 1), nonperipartum women (group 2) and subjects with PPCM (group 3). The cohort included 230 subjects in group 1, 104 in group 2, and 39 in group 3. The mean LVEF at baseline in groups 1, 2, and 3 was 0.23 +/- 0.08, 0.24 +/- 0.08, and 0.27 +/- 0.07 (P = .04), and at 6 months was 0.39 +/- 0.12, 0.42 +/- 0.11, and 0.45 +/- 0.14 (P = .007). Subjects in group 3 had a much greater likelihood of achieving an LVEF >0.50 at 6 months than groups 1 or 2 (19 %, 34%, and 48% respectively, P = .002).
Conclusions: Prospective evaluation confirms myocardial recovery is greatest in women with PPCM, poorest in men, and intermediate in nonperipartum women. On contemporary therapy, nearly half of women with PPCM normalize cardiac function by 6 months. (J Cardiac Fail 2012;18:28-33)
C1 [Cooper, Leslie T.] Mayo Clin, Rochester, MN USA.
[Mather, Paul J.] Thomas Jefferson Univ, Jefferson Med Coll, Philadelphia, PA 19107 USA.
[Alexis, Jeffrey D.] Univ Rochester, Rochester, NY USA.
[Pauly, Daniel F.] Univ Florida, Coll Med, Gainesville, FL USA.
[Torre-Amione, Guillermo] Methodist Hosp, Houston, TX 77030 USA.
[Wittstein, Ilan S.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Dec, G. William] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Zucker, Mark] Beth Israel Hosp, Newark, NJ USA.
[Narula, Jagat] Mt Sinai Sch Med, New York, NY USA.
[Kip, Kevin] Univ S Florida, Tampa, FL USA.
[McNamara, Dennis M.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
RP McNamara, DM (reprint author), Cardiovasc Inst, 200 Lothrop St, Pittsburgh, PA 15213 USA.
EM mcnamaradm@upmc.edu
FU NIH [HL75038, HL086918, HL102429, HL69912]
FX Supported by NIH contracts HL75038, HL086918, HL102429, HL69912.
NR 23
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U1 0
U2 5
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 1071-9164
J9 J CARD FAIL
JI J. Card. Fail.
PD JAN
PY 2012
VL 18
IS 1
BP 28
EP 33
DI 10.1016/j.cardfail.2011.09.009
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 878GE
UT WOS:000299242700004
PM 22196838
ER
PT J
AU Barber, JP
Barrett, MS
Gallop, R
Rynn, MA
Rickels, K
AF Barber, Jacques P.
Barrett, Marna S.
Gallop, Robert
Rynn, Moira A.
Rickels, Karl
TI Short-Term Dynamic Psychotherapy Versus Pharmacotherapy for Major
Depressive Disorder: A Randomized, Placebo-Controlled Trial
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID COLLABORATIVE RESEARCH-PROGRAM; MENTAL-HEALTH TREATMENT;
STAR-ASTERISK-D; CLINICAL-TRIALS; COGNITIVE THERAPY; PSYCHODYNAMIC
PSYCHOTHERAPY; NATIONAL-INSTITUTE; RATING-SCALE; CARE; CITALOPRAM
AB Objective: To determine whether supportive-expressive psychotherapy (SET), a form of dynamic psychotherapy, and pharmacotherapy + clinical management (MED) for major depressive disorder (MDD) are more effective than pill-placebo + clinical management (PBO).
Method:This National Institute of Mental Health (NIMH)-sponsored randomized controlled trial was conducted (from November 2001 through June 2007) at the University of Pennsylvania Medical School. The sample included 156 patients diagnosed with MDD (DSM-IV) and having a 17-item Hamilton Rating Scale for Depression (HRSD17) score >= 14 for at least 2 consecutive weeks. This was an underserved sample in which 41% were male, 52% were self-designated minorities, and 76% had an annual income under $30,000. Treatment lasted 16 weeks. Medication patients not responsive by week 8 (maximum dose 200 mg/d of sertraline) were switched to venlafaxine (maximum dose 375 mg/d). Nonresponsive placebo patients at week 8 were switched to a different placebo.
Results: Patients' depression improved over the 16 weeks (P<.0001), with no between-group differences (P=.95), even among severely (HRSD17 score >= 20) depressed patients (P=.45). Response rates did not differ between groups (P=.73). Gender and minority status moderated outcome (P=.014), with psychotherapy more efficacious for minority men than MED (P=.027, Cohen d=1.02) and PBO (P=.019, d=1.09). PBO was more efficacious for white men than MED (P=.03, d=0.62) and SET (P=.003, d=1.07). For white women, MED (P=.005, d=0.77) and SET (P=.033, d=0.71) were more efficacious than placebo. No differences among treatments were found for minority women.
Conclusions:This trial of urban MDD patients failed to confirm that either active treatment was better than placebo. Minority status and gender had significant and differential effects on outcome that warrant replication in future studies.
C1 [Barber, Jacques P.; Barrett, Marna S.; Gallop, Robert] Univ Penn, Sch Med, Dept Psychiat, Ctr Psychotherapy Res, Philadelphia, PA 19104 USA.
[Barber, Jacques P.] Philadelphia VA Med Ctr, CESATE, Philadelphia, PA USA.
[Barber, Jacques P.] Philadelphia VA Med Ctr, MIRECC, Philadelphia, PA USA.
[Barrett, Marna S.; Rynn, Moira A.; Rickels, Karl] Univ Penn, Sch Med, Dept Psychiat, Mood & Anxiety Disorders Sect, Philadelphia, PA 19104 USA.
[Rynn, Moira A.] Columbia Univ, Div Child & Adolescent Psychiat, New York, NY USA.
[Rynn, Moira A.] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
RP Barber, JP (reprint author), Adelphi Univ, Hy Weinberg Ctr, Derner Inst Adv Psychol Studies, Rm 301,1 South Ave,POB 701, Garden City, NY 11530 USA.
EM jbarber@adelphi.edu
FU National Institute of Mental Health (NIMH) [R01 MH 061410]; National
Institute on Drug Abuse (NIDA); Guilford Press; Basic Books; Cambridge
University Press; Boehringer Ingelheim Pharmaceuticals; Wyeth
Pharmaceuticals; Neuropharm; Astra Zeneca; Pfizer Pharmaceuticals; Eli
Lilly and Company; Forest Laboratories; Bristol-Myers Squibb; Organon;
Cephalon; Johnson & Johnson Pharmaceutical Research Development;
AstraZeneca; Bristol-Meyers Squibb; Epix Pharmaceuticals; Genaissance
Pharmaceuticals (PGxHealth); GlaxoSmithkline; Merck Co; Pamlab; Pfizer;
Somerset Pharmaceuticals; Wyeth Laboratory; Pfizer Corp.
FX Dr Barber has received funding from the National Institute of Mental
Health (NIMH) and the National Institute on Drug Abuse (NIDA); authors'
fees from Guilford Press, Basic Books, and Cambridge University Press;
and honoraria from Lundbeck. Dr Rynn has received research support from
NIMH, Boehringer Ingelheim Pharmaceuticals, Wyeth Pharmaceuticals,
Neuropharm, Astra Zeneca, Pfizer Pharmaceuticals, Eli Lilly and Company,
Forest Laboratories, Bristol-Myers Squibb, Organon, Cephalon, and
Johnson & Johnson Pharmaceutical Research & Development; has served as a
consultant for Wyeth Pharmaceuticals, Pfizer Pharmaceuticals, Astra
Zeneca, Pharmastar, Eli Lilly and Company, and Pepper Hamilton; has been
on speakers' bureaus for Pfizer Pharmaceuticals and Wyeth
Pharmaceuticals; has received royalties from APPI Press; and has
received honoraria from Post Graduate Institute for Medicine, American
Psychiatric Association, American Education Services, Oxford University
Press, Case Western Reserve University, and Pennsylvania Medical
Society. Please note that during this time period there are Grand Rounds
for which she does not have the documentation of the funding source. Dr
Rickels (from 2002 to 2009) has received honoraria and served as a
consultant or on advisory boards to Cephalon, DOV Pharmaceuticals, Eli
Lilly & Co, Hoffman-La Roche, Jazz Pharmaceuticals, Johnson & Johnson,
Novartis Pharmaceuticals, Pfizer Inc, Epix (PreDix) Pharmaceuticals,
PGxHealth, and Sanofi-Synthelabo Research; and has received research
grants (issued to the University of Pennsylvania) from AstraZeneca,
Bristol-Meyers Squibb, Cephalon, Epix Pharmaceuticals, Genaissance
Pharmaceuticals (PGxHealth), GlaxoSmithkline, Merck & Co, NIMH, Pamlab,
Pfizer, Somerset Pharmaceuticals, and Wyeth Laboratory. Drs Barrett and
Gallops have no potential conflict of interest to disclose.; Written
with support from NIMH grant R01 MH 061410 (Jacques P. Barber, PI). The
sertraline and placebo pills were provided by a grant from Pfizer Corp.
Neither sponsor had any role in the study besides funding the study
(NIMH) or supplying the sertraline and placebo pills (Pfizer).
NR 47
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U2 19
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 752870, MEMPHIS, TN 38175-2870 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD JAN
PY 2012
VL 73
IS 1
BP 66
EP 73
DI 10.4088/JCP.11m06831
PG 8
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 880LK
UT WOS:000299408400010
PM 22152401
ER
PT J
AU Sarris, J
Mischoulon, D
Schweitzer, I
AF Sarris, Jerome
Mischoulon, David
Schweitzer, Isaac
TI Omega-3 for Bipolar Disorder: Meta-Analyses of Use in Mania and Bipolar
Depression
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID FATTY-ACID SUPPLEMENTATION; PLACEBO-CONTROLLED TRIALS; DOUBLE-BLIND;
RATING-SCALE; OPEN-LABEL; MOOD DISORDERS; OMEGA-3-FATTY-ACIDS; EFFICACY;
BRAIN; ASSOCIATION
AB Objective: Studies using augmentation of pharmacotherapies with omega-3 in bipolar disorder have been conducted; however, to date a specific meta-analysis in this area has not been published. Thus, we present the significant findings from meta-analyses of omega-3 in the treatment of bipolar depression and bipolar mania.
Data Sources: Pub Med, CINAHL, Web of Science, and Cochrane Library databases were searched for clinical trials up to September 1, 2010, using the search terms bipolar disorder OR bipolar depression OR bipolar mania OR mania OR hypomania OR cyclothymia with the search terms omega 3 OR essential fatty acids OR polyunsaturated fatty acids OR DHA OR EPA OR fish oil OR flax oil. Clinical trial registries and gray literature (published or unpublished data not readily accessible via main databases) were also searched.
Data Selection: The analysis included randomized controlled studies 4 weeks or longer, with a sample size >10, written in English, using omega-3 for diagnosed bipolar depression or mania. No criteria were set for age, gender, or ethnicity.
Data Extraction: A random-effects model was used. The model analyzed the standard mean difference between treatment and placebo between baseline and endpoint, combining the effect size (Hedges g) data. Funnel plot and heterogeneity analyses (I-2) were also performed.
Data Synthesis:The findings of 5 pooled datasets (n=291) on the outcome of bipolar depression revealed a significant effect in favor of omega-3 (P=.029), with a moderate effect size of 0.34. On the outcome of mania, 5 pooled datasets (n=291) revealed a nonsignificant effect in favor of omega-3 (P=.099), with an effect size of 0.20. Minor heterogeneity between studies on the outcome of bipolar depression was found (I-2=30%; P=.213), which was not present on the outcome of bipolar mania (I-2=0%; P=.98). Funnel plot symmetry suggested no significant likelihood of publication bias. Meta-regression analysis between sample size and effect size, however, revealed that studies with smaller sample sizes had larger effect sizes (P=.05).
Conclusions: The meta-analytic findings provide strong evidence that bipolar depressive symptoms may be improved by adjunctive use of omega-3. The evidence, however, does not support its adjunctive use in attenuating mania. J an Psychiatry 2012;73(1):81-86 (C) Copyright 2011 Physicians Postgraduate Press, Inc.
C1 [Sarris, Jerome] Univ Melbourne, Melbourne Clin, Dept Psychiat, Fac Med, Richmond, Vic 3121, Australia.
[Sarris, Jerome] Swinburne Univ Technol, Ctr Human Psychopharmacol, Melbourne, Vic, Australia.
[Mischoulon, David] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Depress Clin & Res Program, Boston, MA USA.
RP Sarris, J (reprint author), Univ Melbourne, Melbourne Clin, Dept Psychiat, Fac Med, 2 Salisbury St, Richmond, Vic 3121, Australia.
EM jsarris@unimelb.edu.au
FU Integria Health and Society for Medicinal Plant; Natural Product
Research; Nordic Naturals; Fisher Wallace Laboratories; Ganeden; MGH
Psychiatry Academy; AstraZeneca; Eli Lilly; Lundbeck; Wyeth; Pfizer;
Bristol-Myers Squibb
FX Dr Sarris has received travel grant funding from Integria Health and
Society for Medicinal Plant and Natural Product Research and speaking
honoraria Dr Mischoulon has received research support from Nordic
Naturals, Fisher Wallace Laboratories, and Ganeden; been a consultant to
Bristol-Myers Squibb; has received writing honoraria from Pamlab; has
received royalties from Back Bay Scientific for PMS Escape and from
Lippincott Wilkins & Williams for the textbook Natural Medications for
Psychiatric Disorders: Considering the Alternatives; and has received
honoraria from Reed Medical Education (which is a logistics collaborator
for the MGH Psychiatry Academy). The education programs conducted by the
MGH Psychiatry Academy were supported through independent medical
education grants from pharmaceutical companies co-supporting programs
along with participant tuition. Commercial entities currently supporting
the MGH Psychiatry Academy are listed on the Academy's Web site,
www.mghcme.org. Dr Schweitzer has received speaking honoraria from
AstraZeneca, Eli Lilly, Lundbeck, Wyeth, Pfizer, Servier, and
Janssen-Cilag; consultancy fees from AstraZeneca, Eli Lilly, Lundbeck,
Wyeth, and Pfizer; and educational or research grants, sponsorships, or
donations from Wyeth, Lundbeck, and Bristol-Myers Squibb.
NR 42
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U1 1
U2 22
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 752870, MEMPHIS, TN 38175-2870 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD JAN
PY 2012
VL 73
IS 1
BP 81
EP 86
DI 10.4088/JCP.10r06710
PG 6
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 880LK
UT WOS:000299408400012
PM 21903025
ER
PT J
AU Weiner, E
Ball, MP
Buchholz, AS
Gold, JM
Evins, AE
McMahon, RP
Buchanan, RW
AF Weiner, Elaine
Ball, M. Patricia
Buchholz, Alison S.
Gold, James M.
Evins, A. Eden
McMahon, Robert P.
Buchanan, Robert W.
TI Bupropion Sustained Release Added to Group Support for Smoking Cessation
in Schizophrenia: A New Randomized Trial and a Meta-Analysis
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID PLACEBO-CONTROLLED TRIAL; MENTAL-HEALTH; DOUBLE-BLIND; NICOTINE;
CLOZAPINE; PHARMACOTHERAPIES; INTERVENTION; DISORDERS; ADDICTION;
BEHAVIORS
AB Objective: To clarify the efficacy and tolerability of bupropion sustained release (SR) for the treatment of cigarette smoking in people with schizophrenia.
Method:The first study is a double-blind, placebo-controlled clinical trial with 32 outpatients from the Maryland Psychiatric Research Center. From May 2003 to July 2007, clinically stable people with a DSM-IV diagnosis of schizophrenia or schizoaffective disorder who smoked at least 10 cigarettes per day and who were interested in quitting smoking or cutting down were recruited for participation. All participated in a 9-week support group and were randomly assigned to receive 12 weeks of bupropion SR or placebo. The primary outcome measure was 4 weeks' sustained abstinence over the last 4 study weeks. Secondary outcome measures included decrease in smoking behavior and change in symptoms, neuropsychological performance, and side effects. In the second study, we performed an electronic literature search of MEDLINE in September 2008. Articles in English published between 2003 and 2008 were searched for the terms schizophrenia, bupropion SR, and smoking. Bibliographies of studies identified through the MEDLINE search were also examined. Case reports, open-label studies, crossover studies, and studies using nonstandard dosing of bupropion SR were excluded. In this way, 4 studies similar in methodology to the currently presented clinical trial were identified and the individual data combined in a meta-analysis. A random effects meta-analysis using Comprehensive Meta-Analysis software was used to obtain a pooled estimate of the odds ratio for 4-week smoking abstinence between bupropion SR and placebo.
Results: There were no significant results on the primary or secondary smoking measures for the clinical trial, although a numeric advantage favored the bupropion SR group. There were no significant findings for secondary symptom or side effect measures and no significant change in neuropsychological performance. For the meta-analysis totaling 226 subjects, there were significant findings in favor of bupropion SR. The pooled estimate of the odds ratio for 4-week abstinence was 2.7 (95% Cl, 1.3 to 5.7; P=.009), and clinically significant greater smoking reduction in the bupropion SR group, with pooled difference estimates increasing over time between groups, became statistically significant by week 5 of study medication (P<.02).
Conclusions: New clinical trial data and a meta-analysis strongly support the tolerability and efficacy of bupropion SR for the treatment of cigarette smoking in people with schizophrenia.
C1 [Weiner, Elaine; Ball, M. Patricia; Buchholz, Alison S.; Gold, James M.; McMahon, Robert P.; Buchanan, Robert W.] Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Dept Psychiat, Baltimore, MD 21228 USA.
[Evins, A. Eden] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Addict Res Program, Boston, MA USA.
RP Weiner, E (reprint author), Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Dept Psychiat, POB 21247, Baltimore, MD 21228 USA.
EM eweiner@mprc.umaryland.edu
RI McMahon, Robert/C-5462-2009
FU GlaxoSmthKline; Pfizer; Novartis; Janssen; Bristol-Myers Squibb; Otsuka;
Cephalon; Veterans Affairs Capitol Network (VISN 5) Mental Illness
Research, Education, and Clinical Center; National Institute of Mental
Health, Advance Center for Intervention Services Research [MH068580-01]
FX Ms Ball has served as a consultant to ePharmaSolutions and Pfizer; Dr
Gold has served as a consultant to Merck, AstraZeneca, Solvay, Pfizer,
and GlaxoSmithKline. Dr Evins has served as a consultant to Pfizer,
Boehringer, and Schering Plough and has received grant/research support
from GlaxoSmthKline and Pfizer. Dr Buchanan has served as a consultant
to Abbott and GlaxoSmithKline; has received grant/research support from
Novartis and Janssen; has served on advisory boards for AstraZeneca,
Wyeth, Schering Plough, Solvay, and Pfizer; and has received other
material or financial support from Bristol-Myers Squibb, Otsuka, Pfizer,
and Cephalon. Drs Weiner and McMahon and Ms Buchholz report no financial
or other relationship relevant to the subject of this article.; Funded
in part by the Veterans Affairs Capitol Network (VISN 5) Mental Illness
Research, Education, and Clinical Center and National Institute of
Mental Health Grant MH068580-01, Advance Center for Intervention
Services Research.
NR 53
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PI MEMPHIS
PA P O BOX 240008, MEMPHIS, TN 38124 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD JAN
PY 2012
VL 73
IS 1
BP 95
EP 102
DI 10.4088/JCP.10m06143gre
PG 8
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 880LK
UT WOS:000299408400014
PM 21535998
ER
PT J
AU Mohamed, S
Rosenheck, R
Lyketsos, CG
Kaczynski, R
Sultzer, DL
Schneider, LS
AF Mohamed, Somaia
Rosenheck, Robert
Lyketsos, Constantine G.
Kaczynski, Richard
Sultzer, David L.
Schneider, Lon S.
TI Effect of Second-Generation Antipsychotics on Caregiver Burden in
Alzheimer's Disease
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID RATING-SCALE BPRS; FAMILY CAREGIVERS; BEHAVIORAL DISTURBANCES; DEMENTIA
VICTIMS; OLDER-ADULTS; CATIE-AD; HEALTH; PREDICTORS; TRIAL; DEPRESSION
AB Background: Alzheimer's disease (AD) imposes a severe burden upon patients and their caregivers. Severity of psychiatric symptoms and behavioral disturbances is an important determinant of caregivers' experience of burden. These symptoms may be improved with atypical antipsychotic treatment.
Objective: Data from the Clinical Antipsychotic Trials of Intervention Effectiveness-Alzheimer's Disease (CATIE-AD) trial were used to evaluate the effect of atypical antipsychotics versus placebo on the experiences of caregivers of outpatients with AD.
Method: We compared the effect of atypical antipsychotic drugs (olanzapine, risperidone, or quetiapine considered together as a group) versus placebo on the experiences of caregivers of AD outpatients (diagnosed according to DSM-IV-TR). We also evaluated whether improvement in patients' psychiatric and behavioral symptoms mediated the relationship between drug treatment and caregiver burden. The CATIE-AD trial, conducted from April 2001 through November 2004, included outpatients (mean age = 77.9 years [SD = 7.5 years]) in usual care settings and assessed treatment effectiveness over a 9-month period at 42 US sites. In a set of secondary analyses, data from CATIE-AD participants who had at least 1 postbaseline outcome assessment and data from their caregivers were examined in an intention-to-treat (ITT) analysis (N = 361). A phase 1-only analysis was conducted including only observations while patients were receiving the initially randomized drug (N = 153). The Burden Interview, the Beck Depression Inventory, and the Neuropsychiatric Inventory (NPI) Caregiver Distress Scale were used to evaluate caregiver burden.
Results: In both ITT and phase 1-only analyses, caregivers of patients treated with second-generation antipsychotics scored significantly lower than caregivers of patients receiving placebo on both the Burden Interview (P = .0090) and the NPI Caregiver Distress Scale (P = .0209). These differences appeared to have been mediated by lower levels of agitation, hostility, and psychotic distortions.
Conclusion: In AD patients with symptoms of psychosis, agitation, or aggressive behavior, medications can have a small but significant impact on caregiver burden. J Clin Psychiatry 2012;73(1):121-128 (C) Copyright 2011 Physicians Postgraduate Press, Inc.
C1 [Mohamed, Somaia; Rosenheck, Robert; Kaczynski, Richard] Vet Affairs New England Mental Illness Res Educ &, West Haven, CT USA.
[Mohamed, Somaia; Rosenheck, Robert; Kaczynski, Richard] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Lyketsos, Constantine G.] Johns Hopkins Univ, Dept Psychiat & Behav Sci, Baltimore, MD USA.
[Lyketsos, Constantine G.] Johns Hopkins Bayview Med Ctr, Baltimore, MD USA.
[Sultzer, David L.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Sultzer, David L.] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Schneider, Lon S.] Univ So Calif, Keck Sch Med, Dept Psychiat & Behav Sci, Los Angeles, CA 90033 USA.
RP Mohamed, S (reprint author), Vet Affairs Connecticut Hlth Care Syst, 950 Campbell Ave,182, West Haven, CT 06516 USA.
EM Somaia.Mohamed@yale.edu
FU Eli Lilly; Janssen; AstraZeneca; Pfizer; National Institute of Mental
Health (NIMH) [N01 MH9001]; National Institute on Aging; Associated
Jewish Federation of Baltimore; Harry and Jeanette Weinberg Foundation;
Forest; GlaxoSmithKline; Eisai; Ortho-McNeil; Bristol-Myers Squibb;
Novartis; National Football League (NFL); Elan; Supernus; Adlyfe;
Takeda; Lundbeck; Merz; Genentech; NFL Players Association; Forest
Research Institute; Johnson Johnson; National Institutes of Health (NIH)
[P50 AG05142, P01 AG05146]; Pfizer, Madison, New Jersey; Department of
Veterans Affairs
FX Dr Rosenheck has received research support from Eli Lilly, Janssen,
AstraZeneca, and Wyeth (currently Pfizer); has been a consultant to
GlaxoSmithKline, Bristol-Myers Squibb, Organon, and Janssen; and has
provided expert testimony in matters pertaining to Eli Lilly, Eli Lilly
Canada, Novapharm, Janssen-Ortho, and Janssen. Dr Lyketsos has received
grant support (for research or CME) from the National Institute of
Mental Health (NIMH), the National Institute on Aging, The Associated
Jewish Federation of Baltimore, The Harry and Jeanette Weinberg
Foundation, Forest, GlaxoSmithKline, Eisai, Pfizer, AstraZeneca, Eli
Lilly, Ortho-McNeil, Bristol-Myers Squibb, Novartis, National Football
League (NFL), and Elan; has received consulting fees from AstraZeneca,
GlaxoSmithKline, Eisai, Elan, Novartis, Forest, Supernus, Adlyfe,
Takeda, Wyeth (currently Pfizer), Lundbeck, Merz, Eli Lilly, Genentech,
Pfizer, NFL Players Association, and the NFL; and has received speaking
honoraria or travel support from Pfizer, Forest, GlaxoSmithKline, and
Health Monitor. Dr Sultzer has received research support from Eli Lilly
and Forest Research Institute. Dr Schneider has received consulting fees
from AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Forest,
GlaxoSmithKline, Novartis, Johnson & Johnson, and Pfizer and has
received research grant support from Novartis, Eli Lilly, and Pfizer.
Drs Mohamed and Kaczynski have no potential conflicts of interest with
regard to the subject of this article.; Conduct of the study was
supported by grant N01 MH9001 from NIMH, the National Institutes of
Health (NIH) (to Dr Schneider). Dr Schneider's efforts in writing the
manuscript were partially supported by grant P50 AG05142 from NIH to the
University of Southern California Alzheimer Disease Research Center, Los
Angeles, California. Dr Mohamed's efforts in writing the manuscript were
partially supported by a contract with Wyeth Pharmaceuticals (currently
Pfizer), Madison, New Jersey. Dr Lyketsos' efforts in writing the
manuscript were supported by grant P01 AG05146 from NIH to the Johns
Hopkins University Alzheimer's Disease Research Center, Baltimore,
Maryland. Dr Sultzer's efforts in writing the manuscript were partially
supported by the Department of Veterans Affairs (Merit Review Program).
NR 47
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PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 240008, MEMPHIS, TN 38124 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD JAN
PY 2012
VL 73
IS 1
BP 121
EP 128
DI 10.4088/JCP.10m06574
PG 8
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 880LK
UT WOS:000299408400018
PM 21939611
ER
PT J
AU Hoang, M
Mahalingam, M
AF Hoang, Mai
Mahalingam, Meera
TI Methodology matters, but...
SO JOURNAL OF CUTANEOUS PATHOLOGY
LA English
DT Letter
DE stem cell marker; nestin; scarring alopecia
C1 [Hoang, Mai] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Mahalingam, Meera] Harvard Univ, Sch Med, Dept Dermatol, Dermatopathol Sect, Boston, MA 02115 USA.
RP Hoang, M (reprint author), Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
EM mmahalin@bu.edu
OI Mahalingam, Meera/0000-0002-2800-9985
NR 2
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U1 2
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0303-6987
J9 J CUTAN PATHOL
JI J. Cutan. Pathol.
PD JAN
PY 2012
VL 39
IS 1
BP 78
EP 79
DI 10.1111/j.1600-0560.2011.01750.x
PG 2
WC Dermatology; Pathology
SC Dermatology; Pathology
GA 869HF
UT WOS:000298588100018
PM 21752058
ER
PT J
AU Ghandour, RM
Kogan, MD
Blumberg, SJ
Jones, JR
Perrin, JM
AF Ghandour, Reem M.
Kogan, Michael D.
Blumberg, Stephen J.
Jones, Jessica R.
Perrin, James M.
TI Mental Health Conditions Among School-Aged Children: Geographic and
Sociodemographic Patterns in Prevalence and Treatment
SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS
LA English
DT Article
DE mood disorders; conduct disorders; children; treatment; geographic
variation
ID COMORBIDITY SURVEY REPLICATION; SUPPLEMENT NCS-A; US CHILDREN;
PSYCHIATRIC-DISORDERS; LIFETIME PREVALENCE; SERVICE UTILIZATION; CONDUCT
PROBLEMS; RISK BEHAVIORS; ADOLESCENTS; STATE
AB Objective: To explore geographic differences in diagnosed emotional and behavioral mental health conditions and receipt of treatment. Methods: Data are from the 2007 National Survey of Children's Health, a nationally representative, parent-reported, cross-sectional survey. Pediatric mental health conditions were identified using parents' responses to 3 questions regarding whether a health care provider had ever told them that their child had depression, anxiety problems, or behavioral or conduct problems. Parents also reported on past-year treatment or counseling by a mental health professional. State-level differences in condition prevalence were identified using unadjusted and adjusted prevalence estimates. Multivariate logistic regression assessed the odds of not receiving treatment by state and diagnoses. Results: Nearly 8% of children aged 6 to 17 years have ever been diagnosed with depression or anxiety, and 5.4% have ever been diagnosed with behavioral or conduct problems. State-level estimates of parent-reported depression or anxiety varied from 4.8% in Georgia to 14.4% in Vermont, while prevalence of behavioral problems ranged from 3.2% in California to 9.2% in Louisiana. Nearly 10% of all school-aged children and 53.1% of those ever diagnosed with either condition type received past-year treatment. The odds of receiving past-year parent-reported treatment did not differ by state of residence with the exception of Louisiana and Nevada: children ever diagnosed had approximately 2.5 times the odds of not receiving past-year treatment in these states. Conclusion: The prevalence of parent-reported mental health disorders among children varies by geographic and sociodemographic factors, while receipt of treatment is generally dependent on sociodemographic and health-related factors.
C1 [Ghandour, Reem M.] US Hlth Resources & Serv Adm, Off Epidemiol Policy & Evaluat, Maternal & Child Hlth Bur, Rockville, MD 20857 USA.
[Blumberg, Stephen J.] Ctr Dis Control & Prevent, Natl Ctr Hlth Stat, Hyattsville, MD 20782 USA.
[Perrin, James M.] Massachusetts Gen Hosp, Ctr Child & Adolescent Hlth Policy, Boston, MA 02114 USA.
RP Ghandour, RM (reprint author), US Hlth Resources & Serv Adm, Off Epidemiol Policy & Evaluat, Maternal & Child Hlth Bur, 5600 Fishers Lane,Room 18-41, Rockville, MD 20857 USA.
EM rghandour@hrsa.gov
NR 48
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U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-206X
J9 J DEV BEHAV PEDIATR
JI J. Dev. Behav. Pediatr.
PD JAN
PY 2012
VL 33
IS 1
BP 42
EP 54
DI 10.1097/DBP.0b013e31823e18fd
PG 13
WC Behavioral Sciences; Psychology, Developmental; Pediatrics
SC Behavioral Sciences; Psychology; Pediatrics
GA 880FY
UT WOS:000299391700012
PM 22218014
ER
PT J
AU Carlson, KF
Meis, LA
Jensen, AC
Simon, AB
Gravely, AA
Taylor, BC
Bangerter, A
Schaaf, KW
Griffin, JM
AF Carlson, Kathleen F.
Meis, Laura A.
Jensen, Agnes C.
Simon, Alisha Baines
Gravely, Amy A.
Taylor, Brent C.
Bangerter, Ann
Schaaf, Katy Wilder
Griffin, Joan M.
TI Caregiver Reports of Subsequent Injuries Among Veterans With Traumatic
Brain Injury After Discharge From Inpatient Polytrauma Rehabilitation
Programs
SO JOURNAL OF HEAD TRAUMA REHABILITATION
LA English
DT Article
DE caregivers; health services; rehabilitation; traumatic brain injury;
trauma; injury
ID SPINAL-CORD-INJURY; RISK; MORTALITY; POPULATION; BEHAVIOR; DEATH; CARE;
INDIVIDUALS; POSTINJURY; CHILDREN
AB Objective: We examined prevalence of, and potential risk factors for, nonfatal injuries among Veterans with traumatic brain injury (TBI) postdischarge from Veterans Affairs inpatient polytrauma rehabilitation programs. Methods: We surveyed caregivers of patients who had military service anytime from 2001 to 2009, sustained polytrauma including TBI, received Veterans Affairs inpatient care from 2001 to 2009, were discharged at least 3 months before the study, and were alive when the study was fielded about caregiver and patient health, including patients' medically treated "accidents/new injuries" since discharge. We examined prevalence and source(s) of subsequent injuries and estimated patients' injury risk in reference to hypothesized risk factors. Odds ratios and 95% confidence intervals were calculated using multivariate logistic regression. Results: Caregivers reported that nearly one-third (32%) of patients incurred medically treated injuries after discharge; most were associated with falls (49%) and motor vehicles (37%). Odds of subsequent injury were associated with select demographics, initial injury characteristics, and postdischarge health and functioning. Characteristics of caregivers, including physical and mental health, were also associated with patients' odds of subsequent injury. Conclusions: A significant number of caregivers reported subsequent nonfatal injuries among patients treated for TBI/polytrauma in inpatient rehabilitation settings. Enhanced injury prevention efforts may be beneficial for this population.
C1 [Carlson, Kathleen F.] Portland VA Med Ctr, Portland Ctr Study Chron Comorbid Mental & Phys D, Portland, OR USA.
[Carlson, Kathleen F.] Oregon Hlth & Sci Univ, Dept Publ Hlth & Prevent Med, Portland, OR 97201 USA.
[Meis, Laura A.; Jensen, Agnes C.; Simon, Alisha Baines; Gravely, Amy A.; Taylor, Brent C.; Bangerter, Ann; Griffin, Joan M.] Minneapolis VA Hlth Care Syst, Ctr Chron Dis Outcomes Res, Minneapolis, MN USA.
[Taylor, Brent C.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Meis, Laura A.; Taylor, Brent C.; Griffin, Joan M.] Univ Minnesota, Sch Med, Dept Med, Minneapolis, MN 55455 USA.
[Schaaf, Katy Wilder] Virginia Commonwealth Univ, Dept Phys Med & Rehabil, Sch Med, Neuropsychol & Rehabil Psychol Serv, Richmond, VA USA.
[Schaaf, Katy Wilder] Hunter Holmes McGuire VA Med Ctr, Richmond, VA USA.
RP Carlson, KF (reprint author), Portland VA Med Ctr R&D 66, Portland Ctr Study Chron Comorbid Mental & Phys D, 3715 SW US Vet Hosp Rd, Portland, OR 97239 USA.
EM kathleen.carlson@va.gov
RI Taylor, Brent/A-8069-2009
OI Taylor, Brent/0000-0002-2140-8377
FU Veterans Health Administration Health Services Research and Development
Service [SDR 07-044, CDA 08-025]
FX This work was supported by grants from the Veterans Health
Administration Health Services Research and Development Service (SDR
07-044; CDA 08-025). The opinions expressed in this article are those of
the authors and do not necessarily reflect the position or policy of the
Department of Veterans Affairs or the United States government.
NR 50
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U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-9701
J9 J HEAD TRAUMA REHAB
JI J. Head Trauma Rehabil.
PD JAN-FEB
PY 2012
VL 27
IS 1
BP 14
EP 25
DI 10.1097/HTR.0b013e318236bd86
PG 12
WC Clinical Neurology; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA 879JV
UT WOS:000299326400002
PM 22218200
ER
PT J
AU Meterko, M
Baker, E
Stolzmann, KL
Hendricks, AM
Cicerone, KD
Lew, HL
AF Meterko, Mark
Baker, Errol
Stolzmann, Kelly L.
Hendricks, Ann M.
Cicerone, Keith D.
Lew, Henry L.
TI Psychometric Assessment of the Neurobehavioral Symptom Inventory-22: The
Structure of Persistent Postconcussive Symptoms Following
Deployment-Related Mild Traumatic Brain Injury Among Veterans
SO JOURNAL OF HEAD TRAUMA REHABILITATION
LA English
DT Article
ID POST-CONCUSSION SYNDROME; CONSTRUCT-VALIDITY
C1 [Meterko, Mark; Baker, Errol; Stolzmann, Kelly L.; Hendricks, Ann M.] VA Boston Healthcare Syst, Boston, MA 02130 USA.
[Meterko, Mark; Baker, Errol; Stolzmann, Kelly L.] VA Ctr Org Leadership & Management Res, Boston, MA USA.
[Meterko, Mark; Hendricks, Ann M.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Cicerone, Keith D.] JFK Johnson Rehabil Inst, Edison, NJ USA.
[Lew, Henry L.] Univ Hawaii Manoa, Def & Vet Brain Injury Ctr, Honolulu, HI 96822 USA.
[Lew, Henry L.] Univ Hawaii Manoa, John A Burns Sch Med, Honolulu, HI 96822 USA.
RP Meterko, M (reprint author), VA Boston Healthcare Syst, Mail Stop 152M,150 S Huntington Ave, Boston, MA 02130 USA.
EM mark.meterko@va.gov
FU VHA HSRD [SDR 08-405]
FX This research was supported by VHA HSR&D grant SDR 08-405. The views
expressed in this article are those of the authors and do not
necessarily reflect the position or policy of the Department of Veterans
Affairs.
NR 21
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U1 2
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-9701
J9 J HEAD TRAUMA REHAB
JI J. Head Trauma Rehabil.
PD JAN-FEB
PY 2012
VL 27
IS 1
BP 55
EP 62
DI 10.1097/HTR.0b013e318230fb17
PG 8
WC Clinical Neurology; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA 879JV
UT WOS:000299326400006
PM 22190009
ER
PT J
AU Brill, A
Fuchs, TA
Savchenko, AS
Thomas, GM
Martinod, K
De Meyer, SF
Bhandari, AA
Wagner, DD
AF Brill, A.
Fuchs, T. A.
Savchenko, A. S.
Thomas, G. M.
Martinod, K.
De Meyer, S. F.
Bhandari, A. A.
Wagner, D. D.
TI Neutrophil extracellular traps promote deep vein thrombosis in mice
SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
DE citrullination; deep vein thrombosis; histones; neutrophil extracellular
traps; von Willebrand factor
ID ACTIVATED PROTEIN-C; HISTONE DEIMINATION; INNATE IMMUNITY; P-SELECTIN;
CELL-DEATH; IN-VIVO; BLOOD; DNA; MICROPARTICLES; COAGULATION
AB . Background: Upon activation, neutrophils can release nuclear material known as neutrophil extracellular traps (NETs), which were initially described as a part of antimicrobial defense. Extracellular chromatin was recently reported to be prothrombotic in vitro and to accumulate in plasma and thrombi of baboons with experimental deep vein thrombosis (DVT). Objective: To explore the source and role of extracellular chromatin in DVT. Methods: We used an established murine model of DVT induced by flow restriction (stenosis) in the inferior vena cava (IVC). Results: We demonstrate that the levels of extracellular DNA increase in plasma after 6 h IVC stenosis, compared with sham-operated mice. Immunohistochemical staining revealed the presence of Gr-1-positive neutrophils in both red (RBC-rich) and white (platelet-rich) parts of thrombi. Citrullinated histone H3 (CitH3), an element of NETs structure, was present only in the red part of thrombi and was frequently associated with the Gr-1 antigen. Immunofluorescent staining of thrombi showed proximity of extracellular CitH3 and von Willebrand factor (VWF), a platelet adhesion molecule crucial for thrombus development in this model. Infusion of Deoxyribonuclease 1 (DNase 1) protected mice from DVT after 6 h and also 48 h IVC stenosis. Infusion of an unfractionated mixture of calf thymus histones increased plasma VWF and promoted DVT early after stenosis application. Conclusions: Extracellular chromatin, likely originating from neutrophils, is a structural part of a venous thrombus and both the DNA scaffold and histones appear to contribute to the pathogenesis of DVT in mice. NETs may provide new targets for DVT drug development.
C1 [Wagner, D. D.] Childrens Hosp, Immune Dis Inst, Program Cellular & Mol Med, Boston, MA 02115 USA.
[Brill, A.; Fuchs, T. A.; Savchenko, A. S.; Thomas, G. M.; De Meyer, S. F.; Wagner, D. D.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Martinod, K.] Harvard Univ, Sch Med, Grad Program Immunol, Div Med Sci, Boston, MA USA.
[De Meyer, S. F.] KULeuven Campus Kortrijk, Lab Thrombosis Res, Kortrijk, Belgium.
RP Wagner, DD (reprint author), Childrens Hosp, Immune Dis Inst, Program Cellular & Mol Med, 3 Blackfan Circle,3rd floor, Boston, MA 02115 USA.
EM wagner@idi.harvard.edu
RI Thomas, Grace/G-1020-2011; Fuchs, Tobias/F-1189-2013;
OI Thomas, Grace/0000-0003-4502-7154; Martinod,
Kimberly/0000-0002-1026-6107
FU National Heart, Lung, and Blood Institute of the National Institutes of
Health [R01 HL041002, R01 HL095091, R01 HL102101]
FX This work was supported by National Heart, Lung, and Blood Institute of
the National Institutes of Health grants R01 HL041002, R01 HL095091 and
R01 HL102101 (to D.D.W.). S. F. De Meyer is a postdoctoral fellow of the
'Fond voor Wetenschappelijk Onderzoek Vlaanderen' (FWO). We thank L.
Cowan for help in preparing the manuscript.
NR 42
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U2 31
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1538-7933
J9 J THROMB HAEMOST
JI J. Thromb. Haemost.
PD JAN
PY 2012
VL 10
IS 1
BP 136
EP 144
DI 10.1111/j.1538-7836.2011.04544.x
PG 9
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 872XD
UT WOS:000298843500018
PM 22044575
ER
PT J
AU Kloverpris, HN
Stryhn, A
Harndahl, M
van der Stok, M
Payne, RP
Matthews, PC
Chen, FB
Riddell, L
Walker, BD
Ndung'u, T
Buus, S
Goulder, P
AF Kloverpris, Henrik N.
Stryhn, Anette
Harndahl, Mikkel
van der Stok, Mary
Payne, Rebecca P.
Matthews, Philippa C.
Chen, Fabian
Riddell, Lynn
Walker, Bruce D.
Ndung'u, Thumbi
Buus, Soren
Goulder, Philip
TI HLA-B(star)57 Micropolymorphism Shapes HLA Allele-Specific Epitope
Immunogenicity, Selection Pressure, and HIV Immune Control
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; T-LYMPHOCYTE EPITOPES; DISEASE
PROGRESSION; CELL RESPONSES; INFECTED-CELLS; GAG; TRANSMISSION;
ASSOCIATIONS; REPERTOIRE; PROTEIN
AB The genetic polymorphism that has the greatest impact on immune control of human immunodeficiency virus (HIV) infection is expression of HLA-B(star)57. Understanding of the mechanism for this strong effect remains incomplete. HLA-B(star)57 alleles and the closely related HLA-B(star)5801 are often grouped together because of their similar peptide-binding motifs and HIV disease outcome associations. However, we show here that the apparently small differences between HLA-B(star)57 alleles, termed HLA-B(star)57 micropolymorphisms, have a significant impact on immune control of HIV. In a study cohort of >2,000 HIV C-clade-infected subjects from southern Africa, HLA-B(star)5703 is associated with a lower viral-load set point than HLA-B(star)5702 and HLA-B(star)5801 (medians, 5,980, 15,190, and 19,000 HIV copies/ml plasma; P = 0.24 and P = 0.0005). In order to better understand these observed differences in HLA-B(star)57/5801-mediated immune control of HIV, we undertook, in a study of >1,000 C-clade-infected subjects, a comprehensive analysis of the epitopes presented by these 3 alleles and of the selection pressure imposed on HIV by each response. In contrast to previous studies, we show that each of these three HLA alleles is characterized both by unique CD8(+) T-cell specificities and by clear-cut differences in selection pressure imposed on the virus by those responses. These studies comprehensively define for the first time the CD8(+) T-cell responses and immune selection pressures for which these protective alleles are responsible. These findings are consistent with HLA class I alleles mediating effective immune control of HIV through the number of p24 Gag-specific CD8(+) T-cell responses generated that can drive significant selection pressure on the virus.
C1 [Kloverpris, Henrik N.; Payne, Rebecca P.; Matthews, Philippa C.; Goulder, Philip] Univ Oxford, Dept Paediat, Oxford, England.
[Stryhn, Anette; Harndahl, Mikkel; Buus, Soren] Univ Copenhagen, Dept Int Hlth Immunol & Microbiol, Copenhagen, Denmark.
[van der Stok, Mary; Walker, Bruce D.; Ndung'u, Thumbi; Goulder, Philip] Univ KwaZulu Natal, Doris Duke Med Res Inst, HIV Pathogenesis Programme, Durban, South Africa.
[Walker, Bruce D.; Goulder, Philip] MIT, Ragon Inst Massachusetts Gen Hosp, Boston, MA USA.
[Chen, Fabian] Royal Berkshire Hosp, Dept Sexual Hlth, Reading RG1 5AN, Berks, England.
[Riddell, Lynn] Northhamptonshire Healthcare Natl Hlth Serv Trust, Northhampton Gen Hosp, Dept Genitourinary Med, Cliftonville, Northants, England.
[Walker, Bruce D.; Goulder, Philip] Harvard Univ, Boston, MA 02115 USA.
RP Kloverpris, HN (reprint author), Univ Oxford, Dept Paediat, Peter Medawar Bldg, Oxford, England.
EM henrik.kloverpris@paediatrics.ox.ac.uk
RI Buus, Soren/F-5446-2010;
OI Matthews, Philippa/0000-0002-4036-4269; Buus, Soren/0000-0001-8363-1999;
Ndung'u, Thumbi/0000-0003-2962-3992
FU Wellcome Trust; National Institutes of Health [RO1 AI46995]
FX This work was supported by the Wellcome Trust (P.G.) and the National
Institutes of Health, grant RO1 AI46995.
NR 59
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U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD JAN
PY 2012
VL 86
IS 2
BP 919
EP 929
DI 10.1128/JVI.06150-11
PG 11
WC Virology
SC Virology
GA 870MW
UT WOS:000298674600025
PM 22090105
ER
PT J
AU Ruhl, M
Chhatwal, P
Strathmann, H
Kuntzen, T
Bankwitz, D
Skibbe, K
Walker, A
Heinemann, FM
Horn, PA
Allen, TM
Hoffmann, D
Pietschmann, T
Timm, J
AF Ruhl, Marianne
Chhatwal, Patrick
Strathmann, Heiko
Kuntzen, Thomas
Bankwitz, Dorothea
Skibbe, Kathrin
Walker, Andreas
Heinemann, Falko M.
Horn, Peter A.
Allen, Todd M.
Hoffmann, Daniel
Pietschmann, Thomas
Timm, Joerg
TI Escape from a Dominant HLA-B*15-Restricted CD8(+) T Cell Response
against Hepatitis C Virus Requires Compensatory Mutations outside the
Epitope
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID REPLICATION CAPACITY; LYMPHOCYTE ESCAPE; CLASS-I; IMMUNE-RESPONSES;
INFECTION; EVOLUTION; HCV; TRANSMISSION; EXPRESSION; SELECTION
AB Antiviral CD8(+) T cells are a key component of the adaptive immune system against hepatitis C virus (HCV). For the development of immune therapies, it is essential to understand how CD8(+) T cells contribute to clearance of infection and why they fail so often. A mechanism for secondary failure is mutational escape of the virus. However, some substitutions in viral epitopes are associated with fitness costs and often require compensatory mutations. We hypothesized that compensatory mutations may point toward epitopes under particularly strong selection pressure that may be beneficial for vaccine design because of a higher genetic barrier to escape. We previously identified two HLA-B*15-restricted CD8(+) epitopes in NS5B (LLRHHNMVY2450-2458 and SQRQKKVTF(2466-2474)), based on sequence analysis of a large HCV genotype 1b outbreak. Both epitopes are targeted in about 70% of HLA-B*15-positive individuals exposed to HCV. Reproducible selection of escape mutations was confirmed in an independent multicenter cohort in the present study. Interestingly, mutations were also selected in the epitope flanking region, suggesting that compensatory evolution may play a role. Covariation analysis of sequences from the database confirmed a significant association between escape mutations inside one of the epitopes (H2454R and M2456L) and substitutions in the epitope flanking region (S2439T and K2440Q). Functional analysis with the subgenomic replicon Con1 confirmed that the primary escape mutations impaired viral replication, while fitness was restored by the additional substitutions in the epitope flanking region. We concluded that selection of escape mutations inside an HLA-B*15 epitope requires secondary substitutions in the epitope flanking region that compensate for fitness costs.
C1 [Ruhl, Marianne; Skibbe, Kathrin; Walker, Andreas; Timm, Joerg] Univ Duisburg Essen, Univ Hosp Essen, Inst Virol, Essen, Germany.
[Chhatwal, Patrick; Bankwitz, Dorothea; Pietschmann, Thomas] Ctr Expt & Clin Infect Res, Div Expt Virol, TWINCORE, Hannover, Germany.
[Strathmann, Heiko; Hoffmann, Daniel] Univ Duisburg Essen, Ctr Med Biotechnol, Essen, Germany.
[Kuntzen, Thomas] Univ Zurich Hosp, Dept Gastroenterol & Hepatol, CH-8091 Zurich, Switzerland.
[Heinemann, Falko M.; Horn, Peter A.] Univ Hosp Essen, Inst Transfus Med, Essen, Germany.
[Allen, Todd M.] Massachusetts Gen Hosp, Ragon Inst MGH MIT & Harvard, Charlestown, MA USA.
RP Timm, J (reprint author), Univ Duisburg Essen, Univ Hosp Essen, Inst Virol, Essen, Germany.
EM joerg.timm@uni-due.de
RI Allen, Todd/F-5473-2011; Pietschmann, Thomas/E-9241-2015;
OI Pietschmann, Thomas/0000-0001-5138-6239; Walker,
Andreas/0000-0002-8736-0863; Hoffmann, Daniel/0000-0003-2973-7869
FU Deutsche Forschungsgemeinschaft [DFG-TRR60, GK 1045]; National Institute
of Allergy and Infectious Diseases (NIAID) [R01-AI067926, U19-AI082630]
FX This work was supported by the Deutsche Forschungsgemeinschaft
(DFG-TRR60 and GK 1045) and by federal funds from the National Institute
of Allergy and Infectious Diseases (NIAID) under grants R01-AI067926
(T.M.A.) and U19-AI082630 (T.M.A.).
NR 55
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Z9 9
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD JAN
PY 2012
VL 86
IS 2
BP 991
EP 1000
DI 10.1128/JVI.05603-11
PG 10
WC Virology
SC Virology
GA 870MW
UT WOS:000298674600031
PM 22072759
ER
PT J
AU Wright, JK
Brumme, ZL
Julg, B
van der Stok, M
Mncube, Z
Gao, XJ
Carlson, JM
Goulder, PJR
Walker, BD
Brockman, MA
Ndung'u, T
AF Wright, Jaclyn K.
Brumme, Zabrina L.
Julg, Boris
van der Stok, Mary
Mncube, Zenele
Gao, Xiaojiang
Carlson, Jonathan M.
Goulder, Philip J. R.
Walker, Bruce D.
Brockman, Mark A.
Ndung'u, Thumbi
TI Lack of Association between HLA Class II Alleles and In Vitro
Replication Capacities of Recombinant Viruses Encoding HIV-1 Subtype C
Gag-Protease from Chronically Infected Individuals
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID T-CELL RESPONSES; TYPE-1; MUTATIONS; CONTROLLERS; SELECTION; PRESSURE;
IMMUNITY; FITNESS; ESCAPE; AIDS
AB It is unknown whether favorable HLA class II alleles may attenuate HIV-1 through selection pressure in a manner similar to that of protective HLA class I alleles. We investigated the relationship between HLA class II alleles and in vitro replication capacities of recombinant viruses encoding HIV-1 subtype C Gag-protease from chronically infected individuals. No associations were found between individual alleles and lower replication capacity, suggesting no significant HIV-1 attenuation by HLA class II-restricted Gag-specific CD4(+) T cell immune pressure.
C1 [Wright, Jaclyn K.; Julg, Boris; van der Stok, Mary; Mncube, Zenele; Goulder, Philip J. R.; Walker, Bruce D.; Ndung'u, Thumbi] Univ KwaZulu Natal, Doris Duke Med Res Inst, Nelson R Mandela Sch Med, HIV Pathogenesis Programme, Durban, South Africa.
[Brumme, Zabrina L.; Brockman, Mark A.] Simon Fraser Univ, Burnaby, BC V5A 1S6, Canada.
[Brumme, Zabrina L.; Brockman, Mark A.] BC Ctr Excellence HIV AIDS, Vancouver, BC, Canada.
[Julg, Boris; Goulder, Philip J. R.; Walker, Bruce D.; Ndung'u, Thumbi] MIT, Ragon Inst Massachusetts Gen Hosp, Boston, MA USA.
[Julg, Boris; Goulder, Philip J. R.; Walker, Bruce D.; Ndung'u, Thumbi] Harvard Univ, Boston, MA 02115 USA.
[Gao, Xiaojiang] NCI Frederick, SAIC Frederick, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MA USA.
[Carlson, Jonathan M.] Microsoft Res, eSci Grp, Redmond, WA USA.
[Goulder, Philip J. R.] Univ Oxford, Nuffield Dept Med, Dept Paediat, Oxford, England.
[Walker, Bruce D.] Howard Hughes Med Inst, Chevy Chase, MD USA.
RP Ndung'u, T (reprint author), Univ KwaZulu Natal, Doris Duke Med Res Inst, Nelson R Mandela Sch Med, HIV Pathogenesis Programme, Durban, South Africa.
EM ndungu@ukzn.ac
OI Ndung'u, Thumbi/0000-0003-2962-3992; Brockman, Mark/0000-0001-6432-1426
FU NIH [ROI-AI067073, NOI-AI-15422]; South African AIDS Vaccine Initiative;
Howard Hughes Medical Institute; Ragon Institute Fund for Innovation and
New International Initiatives; National Research Foundation; Ragon
Institute of Massachusetts General Hospital; Massachusetts Institute of
Technology; Harvard University; Canadian Institutes for Health Research
(CIHR); National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; NIH, National Cancer Institute, Center for Cancer
Research
FX This research was funded by NIH (grant ROI-AI067073, contract
NOI-AI-15422), the South African AIDS Vaccine Initiative, the Howard
Hughes Medical Institute International Program, and the Ragon Institute
Fund for Innovation and New International Initiatives. J.K.W. is funded
by the National Research Foundation and the Ragon Institute of
Massachusetts General Hospital, Massachusetts Institute of Technology
and Harvard University. Z.L.B. is supported by a New Investigator Award
from the Canadian Institutes for Health Research (CIHR). M. A. B. holds
a Canada Research Chair, Tier 2 in Viral Pathogenesis and Immunity. T.N.
holds the South African Department of Science and Technology/National
Research Foundation Research Chair in Systems Biology of HIV/AIDS. This
project has been funded in whole or in part with federal funds from the
National Cancer Institute, National Institutes of Health, under contract
no. HHSN261200800001E. This research was supported in part by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research.
NR 31
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U1 1
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD JAN
PY 2012
VL 86
IS 2
BP 1273
EP 1276
DI 10.1128/JVI.06533-11
PG 4
WC Virology
SC Virology
GA 870MW
UT WOS:000298674600060
PM 22090116
ER
PT J
AU Afzali, A
Berry, K
Ioannou, GN
AF Afzali, Anita
Berry, Kristin
Ioannou, George N.
TI Excellent posttransplant survival for patients with nonalcoholic
steatohepatitis in the United States
SO LIVER TRANSPLANTATION
LA English
DT Article
ID FATTY LIVER-DISEASE; CRYPTOGENIC CIRRHOSIS; NATURAL-HISTORY;
TRANSPLANTATION; POPULATION; PREVALENCE
AB Because of the ongoing epidemics of obesity and diabetes, nonalcoholic steatohepatitis (NASH) may become a leading indication for liver transplantation. There are concerns about the posttransplant survival of patients with NASH because of associated cardiovascular and metabolic risk factors. We aimed to determine recent trends in the proportion of patients undergoing transplantation for NASH-related cirrhosis in the United States and to estimate their posttransplant survival. We used data provided by the United Network for Organ Sharing for first-time adult cadaveric liver transplants performed in the United States between January 1, 1997 and October 31, 2010 (n = 53,738). The proportion of liver transplants performed for NASH-related cirrhosis increased dramatically from 1.2% in 1997-2003 to 7.4% in 2010 when NASH was the fourth most common indication for transplantation. The posttransplant survival of patients with NASH (n = 1810) at 1 (87.6%), 3 (82.2%), and 5 years (76.7%) was superior to the survival of patients with hepatocellular carcinoma, hepatitis C virus, alcoholic liver disease, acute hepatic necrosis, hemochromatosis, or cryptogenic liver disease and was inferior to the survival of only 4 groups of patients (those with primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis, or hepatitis B virus). In conclusion, NASH-related cirrhosis is increasing rapidly as an indication for liver transplantation in the United States and is associated with excellent posttransplant survival. Liver Transpl 18:2937, 2012. (C) 2011 AASLD.
C1 [Afzali, Anita; Ioannou, George N.] Univ Washington, Div Gastroenterol, Dept Med, Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Berry, Kristin] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Afzali, Anita; Ioannou, George N.] Vet Affairs Puget Sound Hlth Care Syst, Res Enhancement Award Program, Seattle, WA USA.
RP Afzali, A (reprint author), Univ Washington, Div Gastroenterol, Dept Med, Vet Affairs Puget Sound Hlth Care Syst, 1959 NE Pacific St,Suite AA103,Box 356424, Seattle, WA 98195 USA.
EM anitaa@medicine.washington.edu
FU Health Resources and Services Administration [234-2005-370011C]
FX This work was supported in part by the Health Resources and Services
Administration (contract 234-2005-370011C). The content is the
responsibility of the authors alone and does not necessarily reflect the
views or policies of the Department of Health and Human Services, nor
does mention of trade names, commercial products, or organizations imply
endorsement by the US Government.
NR 21
TC 49
Z9 50
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1527-6465
J9 LIVER TRANSPLANT
JI Liver Transplant.
PD JAN
PY 2012
VL 18
IS 1
BP 29
EP 37
DI 10.1002/lt.22435
PG 9
WC Gastroenterology & Hepatology; Surgery; Transplantation
SC Gastroenterology & Hepatology; Surgery; Transplantation
GA 867VO
UT WOS:000298483100005
PM 21932374
ER
PT J
AU Kontos, N
Querques, J
Freudenreich, O
AF Kontos, Nicholas
Querques, John
Freudenreich, Oliver
TI Fighting the Good Fight: Responsibility and Rationale in the
Confrontation of Patients
SO MAYO CLINIC PROCEEDINGS
LA English
DT Editorial Material
ID MEDICAL-ETHICS; CARE; CONSULTATION; DECISIONS; AUTONOMY; MODEL
C1 [Kontos, Nicholas] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Kontos, N (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 55 Fruit St, Boston, MA 02114 USA.
EM nkontos@partners.org
NR 29
TC 3
Z9 3
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0025-6196
J9 MAYO CLIN PROC
JI Mayo Clin. Proc.
PD JAN
PY 2012
VL 87
IS 1
BP 63
EP 66
DI 10.1016/j.mayocp.2011.07.002
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA 883XD
UT WOS:000299667300010
PM 22212970
ER
PT J
AU Tsai, A
Caprioli, J
Shen, LQ
AF Tsai, Andy
Caprioli, Joseph
Shen, Lucy Q.
TI Coupled parametric model for estimation of visual field tests based on
OCT macular thickness maps, and vice versa, in glaucoma care
SO MEDICAL IMAGE ANALYSIS
LA English
DT Article
DE OCT; Visual field testing; Glaucoma; PCA
ID OPTICAL COHERENCE TOMOGRAPHY; NERVE-FIBER LAYER; COMPONENT ANALYSIS;
REPRODUCIBILITY; PERIMETRY; EYES; PCA
AB The current standard of care for glaucoma patients consists of functional assessment of vision via visual field (VF) testing, which is sensitive but subjective, time-consuming, and often unreliable. A new imaging technology, Fourier domain optical coherence tomography (OCT), is being introduced to assess the structural characteristics of the macula. This new complementary exam is efficient, objective, and reliable. A complex, but consistent, relationship exists between the structural information provided by macular OCT and the functional information gathered by VF maps. We propose a learning-based framework with the ability to estimate the VF map based on OCT macular thickness measurements as input (and vice versa). Central to this algorithmic framework is a coupled parametric model that captures not only the individual variabilities of the OCT macular thickness measurements and the VF maps, but also their co-dependencies. This model is derived by applying principal component analysis (PCA) to a library consisting of various pairs of OCT and VF maps. The parameters of this coupled model are obtained by solving a linear least squares problem. Next, these estimated parameters are used, in conjunction with the eigenvectors derived from PCA, to compute the estimate. The accuracy of this coupled parametric estimation model was evaluated by performing multiple leave-one-out cross validation experiments. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Tsai, Andy] Childrens Hosp Boston, Dept Radiol, Boston, MA 02115 USA.
[Caprioli, Joseph] Jules Stein Eye Inst, Glaucoma Div, Los Angeles, CA 90095 USA.
[Shen, Lucy Q.] Massachusetts Eye & Ear Infirm, Glaucoma Serv, Boston, MA 02114 USA.
RP Tsai, A (reprint author), Childrens Hosp Boston, Dept Radiol, 300 Longwood Ave, Boston, MA 02115 USA.
EM andy.tsai@childrens.harvard.edu
OI Caprioli, Joseph/0000-0002-2383-7263
FU Department of Radiology, Children's Hospital Boston; American Glaucoma
Society; Research to Prevent Blindness; Pfizer Inc.; Harvard
Catalyst/the Harvard Clinical and Translational Science Center
FX This work was supported in part by Department of Radiology, Children's
Hospital Boston, American Glaucoma Society, unrestricted grants from
Research to Prevent Blindness and Pfizer Inc., and Harvard Catalyst/the
Harvard Clinical and Translational Science Center. The authors would
like to thank Optovue, Inc. for providing technical assistance with
RTVue, Dennis Mock for his role in data collection and processing, and
Nancy Drinan for her help in the preparation of this manuscript.
Finally, the authors would like to thank the anonymous reviewers for
their valuable comments and thoughtful suggestions.
NR 24
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Z9 3
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1361-8415
EI 1361-8423
J9 MED IMAGE ANAL
JI Med. Image Anal.
PD JAN
PY 2012
VL 16
IS 1
BP 101
EP 113
DI 10.1016/j.media.2011.05.012
PG 13
WC Computer Science, Artificial Intelligence; Computer Science,
Interdisciplinary Applications; Engineering, Biomedical; Radiology,
Nuclear Medicine & Medical Imaging
SC Computer Science; Engineering; Radiology, Nuclear Medicine & Medical
Imaging
GA 880KH
UT WOS:000299405500009
PM 21723180
ER
PT J
AU Ueno, K
Hirata, H
Majid, S
Yamamura, S
Shahryari, V
Tabatabai, ZL
Hinoda, Y
Dahiya, R
AF Ueno, Koji
Hirata, Hiroshi
Majid, Shahana
Yamamura, Soichiro
Shahryari, Varahram
Tabatabai, Z. Laura
Hinoda, Yuji
Dahiya, Rajvir
TI Tumor Suppressor MicroRNA-493 Decreases Cell Motility and Migration
Ability in Human Bladder Cancer Cells by Downregulating RhoC and FZD4
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID IN-VITRO; HEPATOCELLULAR-CARCINOMA; GENOMIC ANALYSIS; METASTASIS;
INVASION; PATHWAY; PROGRESSION; INHIBITION; BIOMARKERS; ACTIVATION
AB The purpose of this study was to identify new tumor suppressor microRNAs (miRNA; miR) in bladder cancer, conduct functional analysis of their suppressive role, and identify their specific target genes. To explore tumor suppressor miRs in bladder cancer, miR microarray was conducted using SV-HUC-1, T24, J82, and TCCSUP cells. Expression of miR-493 in bladder cancer (T24, J82, and TCCSUP) cells was downregulated compared with normal SV-HUC-1 cells. Also, the expression of miR-493 was significantly lower in bladder cancer tissues than in their corresponding noncancerous tissues. Transfection of miR-493 into T24 or J82 cells decreased their cell growth andmigration abilities. On the basis of this result, to identify potential miR-493 target genes, we used target scan algorithms to identify target oncogenes related to invasion and migration. miR-493 decreased 30-untranslated region luciferase activity and protein expression of FZD4 and RhoC. miR-493 also decreased binding of RhoC and Rock-1. miR-493 is a new tumor suppressor miRNA in bladder cancer and inhibits cell motility through downregulation of RhoC and FZD4. Mol Cancer Ther; 11(1); 244-53. (C) 2011 AACR.
C1 [Ueno, Koji; Hirata, Hiroshi; Majid, Shahana; Yamamura, Soichiro; Shahryari, Varahram; Dahiya, Rajvir] San Francisco VA Med Ctr, Dept Urol, San Francisco, CA USA.
[Tabatabai, Z. Laura] San Francisco VA Med Ctr, Dept Pathol, San Francisco, CA USA.
[Dahiya, Rajvir] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Hinoda, Yuji] Yamaguchi Univ, Grad Sch Med, Dept Oncol & Lab Med, Ube, Yamaguchi 755, Japan.
RP Dahiya, R (reprint author), Vet Affairs Med Ctr, Urol Res Ctr 112F, 4150 Clement St, San Francisco, CA 94121 USA.
EM rdahiya@urology.ucsf.edu
FU NIH [R01CA130860, R01CA138642, R01CA111470, T32DK007790]; VA
FX This study was supported by grants R01CA130860, R01CA138642,
R01CA111470, T32DK007790 from the NIH, VA Research Enhancement Award
Program (REAP), and Merit Review grants.
NR 30
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U1 2
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD JAN
PY 2012
VL 11
IS 1
BP 244
EP 253
DI 10.1158/1535-7163.MCT-11-0592
PG 10
WC Oncology
SC Oncology
GA 879CV
UT WOS:000299308200024
PM 22057916
ER
PT J
AU Yildirim, E
Sadreyev, RI
Pinter, SF
Lee, JT
AF Yildirim, Eda
Sadreyev, Ruslan I.
Pinter, Stefan F.
Lee, Jeannie T.
TI X-chromosome hyperactivation in mammals via nonlinear relationships
between chromatin states and transcription
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Article
ID DROSOPHILA DOSAGE COMPENSATION; EMBRYONIC STEM-CELLS; LINKED GENES;
PROXIMAL CHROMOSOME-7; ACETYL TRANSFERASE; UP-REGULATION; HISTONE H4;
RNA-SEQ; MOUSE; INACTIVATION
AB Dosage compensation in mammals occurs at two levels. In addition to balancing X-chromosome dosage between males and females via X inactivation, mammals also balance dosage of Xs and autosomes. It has been proposed that X-autosome equalization occurs by upregulation of Xa (active X). To investigate mechanism, we perform allele-specific ChIP-seq for chromatin epitopes and analyze RNA-seq data. The hypertranscribed Xa demonstrates enrichment of active chromatin marks relative to autosomes. We derive predictive models for relationships among Pol II occupancy, active mark densities and gene expression, and we suggest that Xa upregulation involves increased transcription initiation and elongation. Enrichment of active marks on Xa does not scale proportionally with transcription output, a disparity explained by nonlinear quantitative dependencies among active histone marks, Pol II occupancy and transcription. Notably, the trend of nonlinear upregulation also occurs on autosomes. Thus, Xa upregulation involves combined increases of active histone marks and Pol II occupancy, without invoking X-specific dependencies between chromatin states and transcription.
C1 [Yildirim, Eda; Sadreyev, Ruslan I.; Pinter, Stefan F.; Lee, Jeannie T.] Howard Hughes Med Inst, Boston, MA 02115 USA.
[Yildirim, Eda; Sadreyev, Ruslan I.; Pinter, Stefan F.; Lee, Jeannie T.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Yildirim, Eda; Sadreyev, Ruslan I.; Pinter, Stefan F.; Lee, Jeannie T.] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
RP Lee, JT (reprint author), Howard Hughes Med Inst, Boston, MA 02115 USA.
EM lee@molbio.mgh.harvard.edu
OI Yildirim, Eda/0000-0002-4796-3854; Pinter, Stefan/0000-0003-4750-1403
FU MGH ECOR; Deutsche Forschungsgemeinschaft; US National Institutes of
Health [RO1-GM090278]
FX We are thankful to members of Lee laboratory for valuable discussions,
to Y. Jeon for F1 mus/cast female MEFs and to B. Chapman, M.
Borowsky and T. Ohsumi of the Bioinformatics Core Facility (Department
of Molecular Biology, Massachusetts General Hospital (MGH)) for their
suggestions for ChIP-Seq analysis. This work was supported by the MGH
ECOR Medical Discovery Fund (E.Y.), the Deutsche Forschungsgemeinschaft
(S.F.P.) and the US National Institutes of Health (RO1-GM090278,
J.T.L.). J.T.L. is an investigator of the Howard Hughes Medical
Institute.
NR 53
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U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD JAN
PY 2012
VL 19
IS 1
BP 56
EP U72
DI 10.1038/nsmb.2195
PG 7
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 875PW
UT WOS:000299046000010
ER
PT J
AU Liu, WR
Xu, J
Wang, H
Xu, CS
Ji, C
Wang, Y
Feng, CS
Zhang, XN
Xu, ZP
Wu, AS
Xie, ZC
Yue, Y
AF Liu, Weiran
Xu, Jie
Wang, Hui
Xu, Chengshi
Ji, Chao
Wang, Yun
Feng, Chunsheng
Zhang, Xuena
Xu, Zhipeng
Wu, Anshi
Xie, Zhongcong
Yue, Yun
TI Isoflurane-induced spatial memory impairment by a mechanism independent
of amyloid-beta levels and tau protein phosphorylation changes in aged
rats
SO NEUROLOGICAL RESEARCH
LA English
DT Article
DE Amyloid-beta; Hippocampus; Isoflurane; Morris water maze; Tau
ID POSTOPERATIVE COGNITIVE DYSFUNCTION; NITROUS OXIDE ANESTHESIA;
GENERAL-ANESTHETICS; ALZHEIMERS-DISEASE; BRAIN; OLIGOMERIZATION;
ACQUISITION; APOPTOSIS
AB Objectives: The molecular mechanism of postoperative cognitive dysfunction is largely unknown. Isoflurane has been shown to promote Alzheimer's disease neuropathogenesis. We set out to determine whether the effect of isoflurane on spatial memory is associated with amyloid-beta (A-beta) levels and tau phosphorylation in aged rats.
Methods: Eighteen-month-old male Sprague-Dawley rats were randomly assigned as anesthesia group (n=31, received 1.4% isoflurane for 2 hours and had behavioral testing), training group (n=20, received no anesthesia but had behavioral testing), and control group (n=10, received no anesthesia and had no behavioral testing). Spatial memory was measured before and 2 days after the anesthesia by the Morris water maze. We divided the anesthesia group into an isoflurane-induced severe memory impairment group (SIG, n=6) and a no severe memory impairment group (NSIG, n=25), according to whether the escape latency was more than 1.96 stand deviation of that from the training group. Levels of A-beta and tau in the hippocampus were determined by enzyme-linked immunosorbent assay and quantitative western blot at the end of behavioral testing.
Results: We found that isoflurane increased the escape latency in the SIG as compared to that in the training group and NSIG without affecting swimming speed. However, there were no differences in the levels of A-beta and tau among SIG, NSIG, training, and control groups.
Conclusions: Isoflurane may induce spatial memory impairment through non-A-beta or tau neuropathogenesis mechanisms in aged rats.
C1 [Liu, Weiran; Xu, Jie; Wang, Hui; Xu, Chengshi; Wang, Yun; Feng, Chunsheng; Zhang, Xuena; Wu, Anshi; Yue, Yun] Capital Med Univ, Dept Anesthesia, Chaoyang Hosp, Beijing 100020, Peoples R China.
[Ji, Chao] Chinese Acad Med Sci, Dept Pharmacol, Sch Basic Med, Peking Union Med Coll, Beijing 100730, Peoples R China.
[Ji, Chao] Chinese Acad Med Sci, Inst Basic Med Sci, Beijing 100730, Peoples R China.
[Xu, Zhipeng; Xie, Zhongcong] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Charlestown, MA USA.
RP Yue, Y (reprint author), Capital Med Univ, Dept Anesthesia, Chaoyang Hosp, 8 Gongtinan Rd, Beijing 100020, Peoples R China.
EM yueyun@hotmail.com
FU National Nature Science Foundation of China [30872425]
FX Our study was supported by National Nature Science Foundation of China
(grant no. 30872425).
NR 25
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U1 0
U2 5
PU MANEY PUBLISHING
PI LEEDS
PA STE 1C, JOSEPHS WELL, HANOVER WALK, LEEDS LS3 1AB, W YORKS, ENGLAND
SN 0161-6412
J9 NEUROL RES
JI Neurol. Res.
PD JAN
PY 2012
VL 34
IS 1
BP 3
EP 10
DI 10.1179/1743132811Y.0000000047
PG 8
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 870KK
UT WOS:000298667900001
PM 22196855
ER
PT J
AU Li, YX
Berenji, GR
Shaba, WF
Tafti, B
Yevdayev, E
Dadparvar, S
AF Li, Yuxin
Berenji, Gholam R.
Shaba, Wisam F.
Tafti, Bashir
Yevdayev, Ella
Dadparvar, Simin
TI Association of vascular fluoride uptake with vascular calcification and
coronary artery disease
SO NUCLEAR MEDICINE COMMUNICATIONS
LA English
DT Article
DE atherosclerosis; bone scan; sodium [(18)F] fluoride; positron emission
tomography; vascular calcification
ID BEAM COMPUTED-TOMOGRAPHY; ATHEROSCLEROTIC PLAQUE; CARDIOVASCULAR EVENTS;
PET; CALCIUM; FEASIBILITY; RISK; FLUORODEOXYGLUCOSE; F-18-FLUORIDE;
INFLAMMATION
AB Objective The feasibility of a fluoride positron emission tomography/computed tomography (PET/CT) scan for imaging atherosclerosis has not been well documented. The purpose of this study was to assess fluoride uptake of vascular calcification in various major arteries, including coronary arteries.
Methods We retrospectively reviewed the imaging data and cardiovascular history of 61 patients who received whole-body sodium [(18)F] fluoride PET/CT studies at our institution from 2009 to 2010. Fluoride uptake and calcification in major arteries, including coronary arteries, were analyzed by both visual assessment and standardized uptake value measurement.
Results Fluoride uptake in vascular walls was demonstrated in 361 sites of 54 (96%) patients, whereas calcification was observed in 317 sites of 49 (88%) patients. Significant correlation between fluoride uptake and calcification was observed in most of the arterial walls, except in those of the abdominal aorta. Fluoride uptake in coronary arteries was demonstrated in 28 (46%) patients and coronary calcifications were observed in 34 (56%) patients. There was significant correlation between history of cardiovascular events and presence of fluoride uptake in coronary arteries. The coronary fluoride uptake value in patients with cardiovascular events was significantly higher than in patients without cardiovascular events.
Conclusion sodium [(18)F] fluoride PET/CT might be useful in the evaluation of the atherosclerotic process in major arteries, including coronary arteries. An increased fluoride uptake in coronary arteries may be associated with an increased cardiovascular risk. Nucl Med Commun 33:14-20 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Berenji, Gholam R.] VA Greater Los Angeles Healthcare Syst, Nucl Med Serv 115, Los Angeles, CA 90073 USA.
[Dadparvar, Simin] Univ PA Hlth Syst, Philadelphia, PA USA.
RP Berenji, GR (reprint author), VA Greater Los Angeles Healthcare Syst, Nucl Med Serv 115, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM Gholam.Berenji@va.gov
NR 33
TC 29
Z9 29
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0143-3636
J9 NUCL MED COMMUN
JI Nucl. Med. Commun.
PD JAN
PY 2012
VL 33
IS 1
BP 14
EP 20
DI 10.1097/MNM.0b013e32834c187e
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 872ZL
UT WOS:000298850000003
PM 21946616
ER
PT J
AU Pemberton, JD
Fay, A
AF Pemberton, John D.
Fay, Aaron
TI Idiopathic Sclerosing Orbital Inflammation: A Review of Demographics,
Clinical Presentation, Imaging, Pathology, Treatment, and Outcome
SO OPHTHALMIC PLASTIC AND RECONSTRUCTIVE SURGERY
LA English
DT Review
ID MULTIFOCAL FIBROSCLEROSIS; RETROPERITONEAL FIBROSIS; RIEDELS
THYROIDITIS; CASE SERIES; PSEUDOTUMOR; DISEASE; RITUXIMAB; PATIENT;
ENTITY
AB Purpose: To characterize clinical features, diagnostics studies, treatments, and outcomes of patients with histologically proven idiopathic sclerosing orbital inflammation (ISOI), to define optimal management for this recalcitrant disease, and to determine changes in characterization and management by comparing our results with the last significant literature review.
Methods: A search of the U. S. National Library of Medicine: National Institutes of Health's electronic database for cases and case series in the English literature of biopsy-proven ISOI published between March 1994 and September 2010 was conducted. A cross-literature review was performed to tabulate demographics, clinical findings, studies, treatments, and outcomes, which were compared with the ISOI data published by Rootman et al. (1994).
Results: Sixty-one cases, 71 eyes from 17 published reports, met inclusion criteria. No ethnic, sex, or comorbidity predilection was established. Patients typically presented in the fourth decade with proptosis (73%), pain (49%), and normal vision (44%). Orbital imaging and histopathology were sparsely reported. Most common treatments involved systemic corticosteroids either alone (34%) or combined with other modalities (51%).
Conclusions: Characteristics of the disease remain unchanged, and best management was not determined due to inconsistent reporting methods across the literature. Collaboration with established groups (i.e., European Group On Graves Orbitopathy (EUGOGO), International Thyroid Eye Disease Society (ITEDS)) or the formation of a new group of physicians and scientists to help develop a systematic approach for future reporting and evaluation was proposed. (Ophthal Plast Reconstr Surg 2012;28:79-83)
C1 [Pemberton, John D.; Fay, Aaron] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Pemberton, John D.; Fay, Aaron] Harvard Univ, Sch Med, Dept Ophthalmol, Cambridge, MA 02138 USA.
RP Fay, A (reprint author), Massachusetts Eye & Ear Infirm, 243 Charles St, Boston, MA 02114 USA.
EM aaron_fay@meei.harvard.edu
OI Pemberton, John/0000-0001-6305-4653
NR 33
TC 15
Z9 16
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0740-9303
J9 OPHTHAL PLAST RECONS
JI Ophthalmic Plast. Reconstr. Surg.
PD JAN-FEB
PY 2012
VL 28
IS 1
BP 79
EP 83
DI 10.1097/IOP.0b013e318238ecf7
PG 5
WC Ophthalmology; Surgery
SC Ophthalmology; Surgery
GA 880EO
UT WOS:000299387800042
PM 22262301
ER
PT J
AU Theodossiadis, PG
Theodoropoulou, S
Neamonitou, G
Grigoropoulo, V
Liarakos, V
Triantou, E
Theodossiadis, GP
Vlahakos, DV
AF Theodossiadis, Panagiotis G.
Theodoropoulou, Sofia
Neamonitou, Georgia
Grigoropoulo, Vlassis
Liarakos, Vasilios
Triantou, Eleni
Theodossiadis, George P.
Vlahakos, Demetrios V.
TI Hemodialysis-Induced Alterations in Macular Thickness Measured by
Optical Coherence Tomography in Diabetic Patients with End-Stage Renal
Disease
SO OPHTHALMOLOGICA
LA English
DT Article
DE Macular thickness; Hemodialysis; Optical coherence tomography; Retina
ID VISUAL-ACUITY; EDEMA; NEPHROPATHY; RETINOPATHY
AB Background/Aims: To evaluate changes in macular thickness measured by optical coherence tomography (OCT) during a hemodialysis (HD) session in diabetic patients with end-stage renal disease. Methods: 72 eyes of 36 diabetic patients with and without macular edema were evaluated before and immediately after an HD session. Average and maximum macular thicknesses in the central disk (6 mm in diameter) and total macular volume were measured. Results: In the eyes with diabetic macular edema, maximum macular thickness within the central disk of 6 mm, and mainly in its peripheral parts, was significantly reduced by 31.18 +/- 4.18 mu m after HD (p < 0.001). Average macular thickness and total macular volume were also significantly reduced (p = 0.003 and 0.015, respectively). In diabetic eyes without edema, maximum macular thickness decreased significantly by 11.21 +/- 1.98 mu m after HD (p < 0.001), while average macular thickness and total macular volume decreased slightly (p = 0.034, p = 0.043). Best-corrected visual acuity failed to change. We found a significant association of macular thickness changes with osmolality reduction and the presence of macular edema. Conclusion: HD decreases macular thickness in diabetic patients with macular edema, while there exists a less-pronounced effect in diabetic eyes without edema. Copyright (C) 2011 S. Karger AG, Basel
C1 [Theodossiadis, Panagiotis G.; Neamonitou, Georgia; Liarakos, Vasilios] Univ Athens, Attikon Univ Hosp, Dept Ophthalmol 2, GR-12462 Athens, Greece.
[Vlahakos, Demetrios V.] Univ Athens, Attikon Univ Hosp, Renal Unit, GR-12462 Athens, Greece.
[Grigoropoulo, Vlassis; Theodossiadis, George P.] Henry Dunant Hosp, Dept Ophthalmol 2, Athens, Greece.
[Triantou, Eleni] Henry Dunant Hosp, Renal Unit, Athens, Greece.
[Theodoropoulou, Sofia] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA.
RP Theodossiadis, PG (reprint author), Univ Athens, Attikon Univ Hosp, Dept Ophthalmol 2, 1 Rimini Str, GR-12462 Athens, Greece.
EM patheo@med.uoa.gr
NR 19
TC 11
Z9 11
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0030-3755
J9 OPHTHALMOLOGICA
JI Ophthalmologica
PY 2012
VL 227
IS 2
BP 90
EP 94
DI 10.1159/000331321
PG 5
WC Ophthalmology
SC Ophthalmology
GA 883WH
UT WOS:000299665100005
PM 21921588
ER
PT J
AU Celano, CM
Mastromauro, CA
Lenihan, EC
Januzzi, JL
Rollman, BL
Huffman, JC
AF Celano, Christopher M.
Mastromauro, Carol A.
Lenihan, Emma C.
Januzzi, James L.
Rollman, Bruce L.
Huffman, Jeff C.
TI Association of Baseline Anxiety With Depression Persistence at 6 Months
in Patients With Acute Cardiac Illness
SO PSYCHOSOMATIC MEDICINE
LA English
DT Article
DE anxiety; cardiac disease; heart failure; depression; myocardial
infarction
ID ACUTE MYOCARDIAL-INFARCTION; CORONARY-HEART-DISEASE;
RANDOMIZED-CONTROLLED-TRIAL; COMORBID MEDICAL ILLNESS; MAJOR DEPRESSION;
COLLABORATIVE CARE; ARTERY-DISEASE; ANTIDEPRESSANT TREATMENT; PROGNOSTIC
ASSOCIATION; ENHANCING RECOVERY
AB Objective: To assess the association of baseline anxiety with depression persistence and change in depressive symptoms 6 months after cardiac hospitalization. Methods: Data were analyzed from 137 depressed patients hospitalized on inpatient cardiac units for acute coronary syndrome, decompensated heart failure, or arrhythmia and who were enrolled in a randomized trial of collaborative care depression management. Subjects' demographic, medical, and psychiatric information at baseline was compiled. Measures of health-related quality of life, cardiac symptoms, and psychiatric symptoms, including the Hospital Anxiety and Depression Scale-anxiety subscale (HADS-A) for anxiety, were obtained at baseline and serially during a 6-month follow-up period. The association between baseline HADS-A score and depression persistence (<50% reduction in depressive symptoms on the Patient Health Questionnaire-9) at 6 months was assessed by multivariate logistic regression accounting for the effects of multiple relevant medical and psychological covariates. The association between baseline HADS-A score and improvement in depressive symptoms (Patient Health Questionnaire-9) from baseline at 6 months was assessed by linear regression accounting for the same covariates. Results: Baseline HADS-A score was independently associated with depression persistence at 6 months (odds ratio = 1.11, 95% confidence interval = 1.01-1.22, p = .03). Likewise, higher baseline HADS-A score was associated with less improvement in depressive symptoms at 6 months (A = -0.34, p = .01). Conclusions: Among a cohort of depressed cardiac patients, higher baseline anxiety score was linked with lesser improvement in depressive symptoms and increased likelihood of depression persistence at 6 months, independent of multiple relevant covariates. Trial Registration: clinicaltrials.gov Identifier: NCT00847132.
C1 [Celano, Christopher M.; Mastromauro, Carol A.; Lenihan, Emma C.; Huffman, Jeff C.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Celano, Christopher M.; Mastromauro, Carol A.; Lenihan, Emma C.; Januzzi, James L.; Huffman, Jeff C.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Januzzi, James L.] Massachusetts Gen Hosp, Dept Med, Div Cardiol, Boston, MA 02114 USA.
[Rollman, Bruce L.] Univ Pittsburgh, Dept Med, Div Gen Internal Med, Pittsburgh, PA USA.
RP Celano, CM (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Warren 605,55 Fruit St, Boston, MA 02114 USA.
EM ccelano@partners.org
FU American Heart Association [0735530T]
FX This study was supported by the American Heart Association Scientist
Development Grant 0735530T (Dr. Huffman).
NR 55
TC 14
Z9 14
U1 2
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0033-3174
J9 PSYCHOSOM MED
JI Psychosom. Med.
PD JAN
PY 2012
VL 74
IS 1
BP 93
EP 99
DI 10.1097/PSY.0b013e31823d3d38bc
PG 7
WC Psychiatry; Psychology; Psychology, Multidisciplinary
SC Psychiatry; Psychology
GA 880UW
UT WOS:000299434400013
PM 22210240
ER
PT J
AU Robertson, SM
Stanley, MA
Cully, JA
Naik, AD
AF Robertson, Suzanne M.
Stanley, Melinda A.
Cully, Jeffrey A.
Naik, Aanand D.
TI Positive Emotional Health and Diabetes Care: Concepts, Measurement, and
Clinical Implications
SO PSYCHOSOMATICS
LA English
DT Review
ID QUALITY-OF-LIFE; TREATMENT SATISFACTION; GLYCEMIC CONTROL; PSYCHOLOGICAL
ADJUSTMENT; CONTROLLED TRIAL; SELF-MANAGEMENT; NEGATIVE AFFECT; MOOD;
RESILIENCE; PEOPLE
AB Background: Numerous studies describe the effect of emotional problems, including diabetes-related distress and depression, on diabetes outcomes. Little attention has been devoted to positive emotional health and its potential role in facilitating patients' self-management and improved outcomes. Objective: This review describes the conceptualization and measurement of three empirically-tested aspects of positive emotional health (well-being, positive affect, resilience) in the diabetes literature and their relationship to diabetes outcomes. Method: A literature review was conducted using PubMed and the Cochrane Library databases from 1970 to January 2011 to identify studies focused on well-being, positive affect, and resilience in diabetes patients. Results: Twenty-two studies were identified based on our inclusion criteria. Well-being studies were least. likely to include conceptualizations and relied on two primary measurement instruments compared to more heterogeneous presentations found in positive affect and resilience studies. All three aspects of positive emotional health were linked to health-related outcomes and self-management. Conclusion: Positive emotional health may facilitate chronic care self-management and improved health outcomes. We present a model to guide future research and intervention development efforts designed to enhance positive emotional health. (Psychosomatics 2012; 53:1-12)
C1 [Robertson, Suzanne M.; Stanley, Melinda A.; Cully, Jeffrey A.; Naik, Aanand D.] Houston Hlth Serv Res & Dev Ctr Excellence, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX USA.
[Stanley, Melinda A.; Cully, Jeffrey A.; Naik, Aanand D.] Baylor Coll Med, Menninger Dept Psychiat & Behav Sci, Houston, TX 77030 USA.
[Stanley, Melinda A.; Cully, Jeffrey A.; Naik, Aanand D.] VA S Cent Mental Illness Res Educ & Clin Ctr, Houston, TX USA.
RP Robertson, SM (reprint author), Houston VA Hlth Serv Res & Dev Ctr Excellence, Michael E DeBakey VA Med Ctr, 2002 Holcombe Blvd,MEDVAMC 152, Houston, TX 77030 USA.
EM smr1@bcm.tmc.edu
FU Houston VA Health Services Research and Development Center of Excellence
[HFP90-020]; VA Office of Academic Affiliations; National Institute of
Aging [5K23AG027144]; Doris Duke Charitable Foundation
FX This review is supported with resources and the use of facilities at the
Houston VA Health Services Research and Development Center of Excellence
(HFP90-020) at the Michael E. DeBakey VA Medical Center, Houston, TX
Suzanne M. Robertson is a VA HSR post-doctoral fellow supported by VA
Office of Academic Affiliations. Aanand D. Naik receives support from a
National Institute of Aging Career Development Award (5K23AG027144) and
a Doris Duke Charitable Foundation Clinical Scientist Development Award.
The views expressed reflect those of the authors and not necessarily
those of the Department of Veterans Affairs or Baylor College of
Medicine.
NR 47
TC 9
Z9 9
U1 2
U2 10
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0033-3182
J9 PSYCHOSOMATICS
JI Psychosomatics
PD JAN-FEB
PY 2012
VL 53
IS 1
BP 1
EP 12
PG 12
WC Psychiatry; Psychology
SC Psychiatry; Psychology
GA 882TB
UT WOS:000299585700001
PM 22221716
ER
PT J
AU Silverman, BC
Stern, TW
Gross, AF
Rosenstein, DL
Stern, TA
AF Silverman, Benjamin C.
Stern, Thomas W.
Gross, Anne F.
Rosenstein, Donald L.
Stern, Theodore A.
TI Lewd, Crude, and Rude Behavior: The Impact of Manners and Etiquette in
the General Hospital
SO PSYCHOSOMATICS
LA English
DT Article
ID MEDICAL ETIQUETTE; DOCTORS; PSYCHIATRISTS; APPEARANCE; ATTITUDES;
PATIENT; ATTIRE; ETHICS; CARE
AB Background: Lewd, crude, and rude behaviors of patients and stall members have the potential to complicate care; unfortunately, the medical literature on manners and etiquette is sparse. Objective: We sought to understand the impact of lewd, crude, and rude behaviors in the general hospital and to provide a context in which to educate clinicians about the management of troublesome behaviors of patients and staff members. Method: We reviewed the history of etiquette in the general hospital, and discuss the ethical ramifications and clinical management of inappropriate behaviors. Results: Lewd, crude, and rude language and behaviors are often heard and seen in the general hospital: such behaviors can be understood in a biopsychosocial context. Conclusions: Teaching trainees about manners and etiquette can help them identify and manage offensive behaviors and can facilitate the provision of effective and ethical care. (Psychosomatics 2012; 53:13-20)
C1 [Silverman, Benjamin C.; Stern, Thomas W.; Gross, Anne F.; Stern, Theodore A.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Rosenstein, Donald L.] Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC USA.
RP Silverman, BC (reprint author), Adm Bldg,Rm G12D,115 Mill St, Boston, MA 02478 USA.
EM bcsilverman@partners.org
NR 43
TC 1
Z9 1
U1 1
U2 5
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0033-3182
J9 PSYCHOSOMATICS
JI Psychosomatics
PD JAN-FEB
PY 2012
VL 53
IS 1
BP 13
EP 20
PG 8
WC Psychiatry; Psychology
SC Psychiatry; Psychology
GA 882TB
UT WOS:000299585700002
PM 22221717
ER
PT J
AU Coleman, SM
Blashill, AJ
Gandhi, RT
Safren, SA
Freudenreich, O
AF Coleman, Shane M.
Blashill, Aaron J.
Gandhi, Rajesh T.
Safren, Steven A.
Freudenreich, Oliver
TI Impact of Integrated and Measurement-Based Depression Care: Clinical
Experience in an HIV Clinic
SO PSYCHOSOMATICS
LA English
DT Article
ID STAR-ASTERISK-D; ACTIVE ANTIRETROVIRAL THERAPY; CORONARY-HEART-DISEASE;
INFECTED PATIENTS; HEALTH-CARE; METAANALYSIS; OUTCOMES; EPIDEMIOLOGY;
OUTPATIENTS; DISORDERS
AB Background: Just as in heart disease and diabetes, depression in HIV/AIDS is associated with negative outcomes. While randomized trials have shown the efficacy of treatment for depression in HIV/AIDS, the implementation of evidence-based treatments in real-world settings remains a challenge. Objective: The objective of this study was to assess the effectiveness of a collaborative, measurement-based approach to depression care, including psychopharmacologic and ancillary psychological therapies in patients with HIV/AIDS and to examine whether or not effective depression treatment would also improve virologic and immunologic outcomes. Methods: This was a retrospective chart review of patients referred for depression to a co-located psychiatry consultation service embedded within an infectious diseases outpatient clinic at an urban tertiary hospital. Data extracted at initial assessment and at last appointment included: axis 1 diagnosis, whether the patient was on an antidepressant, whether the patient was on a stimulant, BDI-II score, HIV RNA level, and CD4 cell count. Results: One hundred twenty-four patient charts were included. Pre- vs. post-treatment analyses revealed significant reductions in depression (average BDI-II score of 23 to 15.7, p = 0.00001) and HIV RNA (14.1 K to 4 K copies/mL, p = 0.003), and significant increases in CD4 count (518 to 592 cells/mu L, p = 0.001). Additionally, more participants were prescribed antidepressants and stimulants at post- vs. pre-treatment. Conclusion: Taking a collaborative, measurement-based approach to depression care appears to be an effective method for improving depression, virologic, and immunologic outcomes in depressed patients with HIV/AIDS illness. (Psychosomatics 2012; 53:51-57)
C1 [Coleman, Shane M.] Univ Washington, Sch Med, Dept Psychiat, Seattle, WA 98195 USA.
[Coleman, Shane M.; Blashill, Aaron J.; Gandhi, Rajesh T.; Safren, Steven A.; Freudenreich, Oliver] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Coleman, Shane M.; Blashill, Aaron J.; Gandhi, Rajesh T.; Safren, Steven A.; Freudenreich, Oliver] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Coleman, SM (reprint author), Univ Washington, Sch Med, Dept Psychiat, 1959 NE Pacific St,Box 356560, Seattle, WA 98195 USA.
EM smc9@u.washington.edu
NR 33
TC 5
Z9 6
U1 0
U2 6
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0033-3182
J9 PSYCHOSOMATICS
JI Psychosomatics
PD JAN-FEB
PY 2012
VL 53
IS 1
BP 51
EP 57
PG 7
WC Psychiatry; Psychology
SC Psychiatry; Psychology
GA 882TB
UT WOS:000299585700007
PM 22221721
ER
PT J
AU Braun, IM
Rao, SR
Pirl, WF
AF Braun, Ilana M.
Rao, Sowmya R.
Pirl, William F.
TI Comparison of Self-reported Cognitive Difficulties in a National Sample
of Long-Term Cancer Survivors and Cancer-Naive Controls
SO PSYCHOSOMATICS
LA English
DT Article
ID COMORBIDITY SURVEY REPLICATION; MAJOR DEPRESSIVE DISORDER;
BREAST-CANCER; ADJUVANT CHEMOTHERAPY; MENOPAUSAL SYMPTOMS; NCS-R;
FATIGUE; WOMEN; DEFICITS
AB Background: Evidence that long-term cancer survivors (LTCS) experience greater cognitive dysfunction than individuals without cancer is mixed. This analysis of a population-based sample of United States residents compares self-reported cognitive difficulties in LTCS and cancer naive controls (CNC), controlling for psychiatric disorders. Methods: National Comorbidity Survey-Replication (NCS-R) interviews were conducted in a nationally-representative sample of 9282 people, of whom 5692 were assessed for cancer history. Long-term survivors of adult cancers were defined as individuals who were at least 18 years old at time of diagnosis; greater than 5 years following diagnosis; and with cancer reportedly in remission or cured. Cognitive dysfunction queries included two screening questions and five items drawn than the World Health Organization (WHO) Disability Assessment Schedule 2.0. Psychiatric disorders were identified using the WHO's Composite International Diagnostic Interview. Odds ratios and 95% confidence intervals were obtained from multi-variable logistic regression models fit to evaluate the relationship between cancer status (LTCS versus CNC) and cognitive symptoms. Results: Of NCS-R participants, 225 met criteria for LTCS and 3953 for CNC. Long-term cancer survivors and CNC screened positive for cognitive symptoms at a rate of 19.5% and 20.8%, respectively, for the first screen and 16.0% and 16.4%, respectively, for the second. Adjusting for demographic and psychiatric variables, LTCS did not carry increased odds of experiencing cognitive symptoms [(OR) 1.00 (95% CI, .59 to 1.68); (OR) .95 (95 %CI, .57 to 1.59)] Conclusions: Self-reported cognitive symptoms are common among LTCS and CNC. LTCS do not report cognitive symptoms with greater frequency. (Psychosomatics 2012; 53:68-74)
C1 [Braun, Ilana M.] Dana Farber Canc Inst, Dept Psychosocial Oncol & Palliat Care, Boston, MA 02215 USA.
[Rao, Sowmya R.] Univ Massachusetts, Sch Med, Worcester, MA USA.
[Rao, Sowmya R.] Vet Adm, Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA USA.
[Pirl, William F.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
RP Braun, IM (reprint author), Dana Farber Canc Inst, Dept Psychosocial Oncol & Palliat Care, Shields Warren 442B,450 Brookline Ave, Boston, MA 02215 USA.
EM ibraun@partners.org
NR 18
TC 3
Z9 3
U1 0
U2 2
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0033-3182
J9 PSYCHOSOMATICS
JI Psychosomatics
PD JAN-FEB
PY 2012
VL 53
IS 1
BP 68
EP 74
PG 7
WC Psychiatry; Psychology
SC Psychiatry; Psychology
GA 882TB
UT WOS:000299585700009
PM 22221723
ER
PT J
AU Pichurko
Ruppel
Kaminsky
Busse
Coates
Rundell, KW
Hess, DR
Hnatiuk
Enright
Salzman
AF Pichurko
Ruppel
Kaminsky
Busse
Coates
Rundell, Kenneth W.
Hess, Dean R.
Hnatiuk
Enright
Salzman
TI What Does Airway Resistance Tell Us About Lung Function? Discussion
SO RESPIRATORY CARE
LA English
DT Editorial Material
C1 [Rundell, Kenneth W.] Pharmaxis, Exton, PA USA.
[Hess, Dean R.] Massachusetts Gen Hosp, Resp Care Serv, Boston, MA 02114 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU DAEDALUS ENTERPRISES INC
PI IRVING
PA 9425 N MAC ARTHUR BLVD, STE 100, IRVING, TX 75063-4706 USA
SN 0020-1324
J9 RESP CARE
JI Respir. Care
PD JAN
PY 2012
VL 57
IS 1
SI SI
BP 96
EP 99
PG 4
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 880IA
UT WOS:000299399600015
ER
PT J
AU Saperstein, AM
Thysen, J
Medalia, A
AF Saperstein, Alice M.
Thysen, Julie
Medalia, Alice
TI The Measure of Insight into Cognition: Reliability and validity of
clinician-rated and self-report scales of neurocognitive insight for
schizophrenia
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Neurocognition; Insight
ID PSYCHOSIS; ILLNESS; CONSEQUENCES; PERFORMANCE; DEPRESSION; AWARENESS;
SYMPTOMS; DEFICITS
AB Poor insight into the neurocognitive deficits in schizophrenia-spectrum disorders may have significant clinical implications for treatment. The purpose of this study was to replicate and extend the psychometric findings initially reported on the Measure of Insight into Cognition Clinician-Rated (MIC-CR) and Self-Report (MIC-SR) which assess awareness, attribution, and frequency of neurocognitive deficits. Assessments conducted one week apart allowed for internal consistency, test-retest reliability, concurrent validity, and administration order effects to be determined. In this study sample (N = 80), 73 demonstrated significant neurocognitive impairment, yet on the MIC-CR, the average awareness and attribution scores indicated only partial awareness and attribution of neurocognitive deficits. The average MIC-SR score indicated rare frequency of cognitive difficulty in everyday life. Cronbach's alphas for the MIC-CR (0.83) and MIC-SR (0.93) were consistent with the initial validation study; test-retest reliability for both MIC assessments was significant (p < 0.001). In new analyses, concurrent validity was demonstrated by significant correlations between the MIC-CR and MIC-SR in the first validation sample: r=-0.75 (p < 0.001) and the current replication sample: r=-0.70 (p < 0.001). Effect sizes were large when frequencies of neurocognitive complaints (MIC-SR) were compared between subjects with good versus poor awareness on the MIC-CR. Reliability and concurrent validity results were similar and significant regardless of order of MIC-CR and MIC-SR administration. The MIC-CR and MIC-SR are thus reliable and valid complementary instruments to assess neurocognitive insight in people with schizophrenia spectrum disorders. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Saperstein, Alice M.; Medalia, Alice] Columbia Univ Coll Phys & Surg, Dept Psychiat, New York, NY 10032 USA.
[Thysen, Julie] James J Peters VA Med Ctr, Mt Sinai Sch Med, Bronx, NY 10468 USA.
RP Saperstein, AM (reprint author), Columbia Univ Coll Phys & Surg, Dept Psychiat, 1051 Riverside Dr, New York, NY 10032 USA.
EM saperst@nyspi.columbia.edu; am2938@columbia.edu
FU Eli Lilly [F1D-US-X310]
FX This research was supported by an Eli Lilly Investigator Initiated
Trial, Grant # F1D-US-X310, PI: Alice Medalia, PhD. This institution had
no further role in the study design, in the collection, analysis or
interpretation of data, in writing the report, or in the decision to
submit the paper for publication.
NR 24
TC 5
Z9 5
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD JAN
PY 2012
VL 134
IS 1
BP 54
EP 58
DI 10.1016/j.schres.2011.10.002
PG 5
WC Psychiatry
SC Psychiatry
GA 881NH
UT WOS:000299492900009
PM 22036020
ER
PT J
AU Kwiatkowski, N
Deng, XM
Wang, JH
Tan, L
Villa, F
Santaguida, S
Huang, HC
Mitchison, T
Musacchio, A
Gray, N
AF Kwiatkowski, Nicholas
Deng, Xianming
Wang, Jinhua
Tan, Li
Villa, Fabrizio
Santaguida, Stefano
Huang, Hsiao-Chun
Mitchison, Tim
Musacchio, Andrea
Gray, Nathanael
TI Selective Aurora Kinase Inhibitors Identified Using a Taxol-Induced
Checkpoint Sensitivity Screen
SO ACS CHEMICAL BIOLOGY
LA English
DT Article
ID SMALL-MOLECULE INHIBITOR; A KINASE; B KINASE; HUMAN-CELLS; SPINDLE
CHECKPOINT; PROTEIN-KINASE; TUMOR-GROWTH; IN-VIVO; ACTIVATION; COMPLEX
AB The members of the Aurora kinase family play critical roles in the regulation of the cell cycle and mitotic spindle assembly and have been intensively investigated as potential targets for a new class of anticancer drugs. We describe a new highly potent and selective class of Aurora kinase inhibitors discovered using a phenotypic cellular screen. Optimized inhibitors display many of the hallmarks of Aurora inhibition including endoreduplication, polyploidy, and loss of cell viability in cancer cells. Structure activity relationships with respect to kinome-wide selectivity and guided by an Aurora B co-crystal structure resulted in the identification of key selectivity determinants and discovery of a subseries with selectivity toward Aurora A. A direct comparison of biochemical and cellular profiles with respect to published Aurora inhibitors including VX-680, AZD1152, MLN8054, and a pyrimidine-based compound from Genentech demonstrates that compounds 1 and 3 will become valuable additional pharmacological probes of Aurora-dependent functions.
C1 [Kwiatkowski, Nicholas; Deng, Xianming; Wang, Jinhua; Tan, Li; Gray, Nathanael] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Kwiatkowski, Nicholas; Deng, Xianming; Wang, Jinhua; Tan, Li; Gray, Nathanael] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Huang, Hsiao-Chun; Mitchison, Tim] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
[Villa, Fabrizio; Santaguida, Stefano; Musacchio, Andrea] European Inst Oncol, Dept Expt Oncol, I-20139 Milan, Italy.
[Musacchio, Andrea] Max Planck Inst Mol Physiol, D-44227 Dortmund, Germany.
RP Gray, N (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, 44 Binney St, Boston, MA 02115 USA.
EM nathanael_gray@dfci.harvard.edu
RI villa, fabrizio/G-5757-2012;
OI Santaguida, Stefano/0000-0002-1501-6190; Musacchio,
Andrea/0000-0003-2362-8784
FU NIH [CA130876-03, HG005693-02, U54 HG006097-01, U54 HG006097,
IRC2HG005693]; Italian Association for Cancer Research; Italian
Foundation for Cancer Research
FX We thank DiscoveRx (Ambit Biosciences) for performing KINOMEscan, Life
Technologies Corporation for performing SelectScreen Kinase Profiling
and ActivX for performing KiNativ analysis, as well as the Nikon Imaging
Facility (HMS) and the Dana Farber Flow Cytometry Lab (DFCI) for
technical help and instrument use. Funding was provided by NIH grants
CA130876-03, HG005693-02, U54 HG006097-01. The HMS LINCS Center is
funded by NIH U54 HG006097, and NIH Grand Opportunities grant
IRC2HG005693. A.M. acknowledges generous funding from the Italian
Association for Cancer Research. S.S. is supported by a fellowship from
the Italian Foundation for Cancer Research.
NR 49
TC 11
Z9 11
U1 0
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1554-8929
J9 ACS CHEM BIOL
JI ACS Chem. Biol.
PD JAN
PY 2012
VL 7
IS 1
BP 185
EP 196
DI 10.1021/cb200305u
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 878FQ
UT WOS:000299241300020
PM 21992004
ER
PT J
AU Vendelbo, MH
Clasen, BFF
Treebak, JT
Moller, L
Krusenstjerna-Hafstrom, T
Madsen, M
Nielsen, TS
Stodkilde-Jorgensen, H
Pedersen, SB
Jorgensen, JOL
Goodyear, LJ
Wojtaszewski, JFP
Moller, N
Jessen, N
AF Vendelbo, M. H.
Clasen, B. F. F.
Treebak, J. T.
Moller, L.
Krusenstjerna-Hafstrom, T.
Madsen, M.
Nielsen, T. S.
Stodkilde-Jorgensen, H.
Pedersen, S. B.
Jorgensen, J. O. L.
Goodyear, L. J.
Wojtaszewski, J. F. P.
Moller, N.
Jessen, N.
TI Insulin resistance after a 72-h fast is associated with impaired AS160
phosphorylation and accumulation of lipid and glycogen in human skeletal
muscle
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE Akt substrate of 160 kDa; skeletal muscle metabolism; fasting; insulin
resistance in vivo; insulin signaling; TBC1D4
ID ACTIVATED PROTEIN-KINASE; FREE FATTY-ACIDS; SITE-SPECIFIC
PHOSPHORYLATION; GLUCOSE-TRANSPORT; TBC1D1 PHOSPHORYLATION;
GENE-EXPRESSION; POTENTIAL ROLE; 14-3-3 BINDING; EXERCISE; METABOLISM
AB Vendelbo MH, Clasen BF, Treebak JT, Moller L, Krusenstjerna-Hafstrom T, Madsen M, Nielsen TS, Stodkilde-Jorgensen H, Pedersen SB, Jorgensen JO, Goodyear LJ, Wojtaszewski JF, Moller N, Jessen N. Insulin resistance after a 72-h fast is associated with impaired AS160 phosphorylation and accumulation of lipid and glycogen in human skeletal muscle. Am J Physiol Endocrinol Metab 302: E190-E200, 2012. First published October 25, 2011; doi: 10.1152/ajpendo.00207.2011.-During fasting, human skeletal muscle depends on lipid oxidation for its energy substrate metabolism. This is associated with the development of insulin resistance and a subsequent reduction of insulin-stimulated glucose uptake. The underlying mechanisms controlling insulin action on skeletal muscle under these conditions are unresolved. In a randomized design, we investigated eight healthy subjects after a 72-h fast compared with a 10-h overnight fast. Insulin action on skeletal muscle was assessed by a hyperinsulinemic euglycemic clamp and by determining insulin signaling to glucose transport. In addition, substrate oxidation, skeletal muscle lipid content, regulation of glycogen synthesis, and AMPK signaling were assessed. Skeletal muscle insulin sensitivity was reduced profoundly in response to a 72-h fast and substrate oxidation shifted to predominantly lipid oxidation. This was associated with accumulation of both lipid and glycogen in skeletal muscle. Intracellular insulin signaling to glucose transport was impaired by regulation of phosphorylation at specific sites on AS160 but not TBC1D1, both key regulators of glucose uptake. In contrast, fasting did not impact phosphorylation of AMPK or insulin regulation of Akt, both of which are established upstream kinases of AS160. These findings show that insulin resistance in muscles from healthy individuals is associated with suppression of site-specific phosphorylation of AS160, without Akt or AMPK being affected. This impairment of AS160 phosphorylation, in combination with glycogen accumulation and increased intramuscular lipid content, may provide the underlying mechanisms for resistance to insulin in skeletal muscle after a prolonged fast.
C1 [Vendelbo, M. H.; Clasen, B. F. F.; Moller, L.; Krusenstjerna-Hafstrom, T.; Madsen, M.; Nielsen, T. S.; Pedersen, S. B.; Jorgensen, J. O. L.; Moller, N.; Jessen, N.] Aarhus Univ Hosp, Dept Internal Med & Endocrinol, DK-8000 Aarhus, Denmark.
[Clasen, B. F. F.; Nielsen, T. S.; Jessen, N.] Aarhus Univ Hosp, Dept Clin Pharmacol, DK-8000 Aarhus, Denmark.
[Treebak, J. T.; Wojtaszewski, J. F. P.] Univ Copenhagen, Dept Exercise & Sport Sci, Mol Physiol Grp, Copenhagen, Denmark.
[Stodkilde-Jorgensen, H.] Aarhus Univ Hosp, Magnet Resonance Res Ctr, DK-8000 Aarhus, Denmark.
[Goodyear, L. J.] Brigham & Womens Hosp, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Goodyear, L. J.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Goodyear, L. J.] Harvard Univ, Sch Med, Boston, MA USA.
RP Jessen, N (reprint author), Aarhus Univ Hosp NBG, Dept Clin Pharmacol, DK-8000 Aarhus C, Denmark.
EM Niels.Jessen@farm.au.dk
RI Wojtaszewski, Jorgen /P-6583-2014; Moller, Niels/E-5091-2011; Treebak,
Jonas/B-4521-2017;
OI Wojtaszewski, Jorgen /0000-0001-9785-6830; Moller,
Niels/0000-0001-5627-7322; Treebak, Jonas/0000-0003-1488-7012;
Stodkilde-Jorgensen, Hans/0000-0002-8649-4173; Pedersen, Steen
B./0000-0002-7838-8063; Jorgensen, Jens Otto Lunde/0000-0001-7408-1526;
Jessen, Niels/0000-0001-5613-7274
FU Danish Agency for Science Technology and Innovation [271-07-0719];
Lundbeck Foundation; Danish Medical Research Council; Danish Ministry of
Science, Technology, and Innovation; FOOD Study Group/Danish Ministry of
Food, Agriculture, and Fisheries; Ministry of Family and Consumer
Affairs [2101-05-0044]
FX This work was supported by Danish Agency for Science Technology and
Innovation Grant 271-07-0719 (to N. Jessen), the Lundbeck Foundation,
and the Danish Medical Research Council. The Molecular Physiology Group,
Department of Exercise and Sport Sciences, is part of the UNIK Project:
Food, Fitness, and Pharma for Health and Disease, which is supported by
the Danish Ministry of Science, Technology, and Innovation (to J. F. P.
Wojtaszewski); the FOOD Study Group/Danish Ministry of Food,
Agriculture, and Fisheries; and Ministry of Family and Consumer Affairs
Grant 2101-05-0044 (to N. Moller).
NR 55
TC 24
Z9 24
U1 3
U2 13
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 JAN
PY 2012
VL 302
IS 2
BP E190
EP E200
DI 10.1152/ajpendo.00207.2011
PG 11
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 876MX
UT WOS:000299112700004
PM 22028408
ER
PT J
AU Smith, GE
Camp, C
Cooley, S
Gonzalez, HM
Hartman-Stein, P
LaRue, A
Pachana, NA
Zeiss, A
AF Smith, Glenn E.
Camp, Cameron
Cooley, Susan
Gonzalez, Hector M.
Hartman-Stein, Paula
LaRue, Asenath
Pachana, Nancy A.
Zeiss, Antonette
CA Amer Psychological Assoc
TI Guidelines for the Evaluation of Dementia and Age-Related Cognitive
Change
SO AMERICAN PSYCHOLOGIST
LA English
DT Article
ID DIAGNOSTIC-CRITERIA; ALZHEIMERS-DISEASE; INFORMANT INTERVIEW;
IMPAIRMENT; PREVALENCE; MANAGEMENT; AGITATION; CONSENSUS
C1 [Smith, Glenn E.] Mayo Clin, Coll Med, Dept Psychiat & Psychol, Rochester, MN USA.
[Camp, Cameron] Hearthstone Alzheimer Care, Res & Prod Dev, Woburn, MA USA.
[Cooley, Susan] US Dept Vet Affairs, Off Geriatr & Extended Care, Geriatr Res & Dev & Dementia Initiat, Washington, DC USA.
[Gonzalez, Hector M.] Wayne State Univ, Inst Gerontol, Detroit, MI 48202 USA.
[Gonzalez, Hector M.] Wayne State Univ, Dept Family Med & Publ Hlth Sci, Detroit, MI 48202 USA.
[Hartman-Stein, Paula] Ctr Hlth Aging, Kent, OH USA.
[Hartman-Stein, Paula] Kent State Univ, E Liverpool, OH USA.
[LaRue, Asenath] Univ Wisconsin, Wisconsin Alzheimers Inst, Madison, WI 53706 USA.
[Pachana, Nancy A.] Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia.
[Pachana, Nancy A.] Univ Queensland, Ageing Mind Initiat, Brisbane, Qld 4072, Australia.
[Zeiss, Antonette] US Dept Vet Affairs, Off Patient Care Serv, Off Mental Hlth Serv, Washington, DC USA.
RP Smith, GE (reprint author), Amer Psychol Assoc, Publ Interest Directorate, Off Aging, 750 1st St,NE, Washington, DC 20002 USA.
NR 41
TC 13
Z9 13
U1 2
U2 7
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0003-066X
J9 AM PSYCHOL
JI Am. Psychol.
PD JAN
PY 2012
VL 67
IS 1
BP 1
EP 9
DI 10.1037/a0024643
PG 9
WC Psychology, Multidisciplinary
SC Psychology
GA 878BP
UT WOS:000299226800001
ER
PT J
AU Teixido, M
Kung, B
Rosowski, JJ
Merchant, SN
AF Teixido, Michael
Kung, Brian
Rosowski, John J.
Merchant, Saumil N.
TI Histopathology of the Temporal Bone in a Case of Superior Canal
Dehiscence Syndrome
SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY
LA English
DT Article
DE aural fullness; otopathology; superior canal dehiscence; temporal bone
histopathology; tinnitus
ID TULLIO PHENOMENON; HEARING; VERTIGO; SOUND
AB Objectives: We describe the histopathologic findings in the temporal bones of a patient who had, during life, received a diagnosis of superior canal dehiscence (SCD) syndrome.
Methods: The patient was found to have SCD syndrome at 59 years of age. She became a temporal bone donor, and died of unrelated causes at 62 years of age. Both temporal bones were prepared in celloidin and examined by light microscopy.
Results: The patient developed bilateral aural fullness, pulsatile tinnitus, and difficulty tolerating loud noises after minor head trauma at 53 years of age. The symptoms were worse on the right. She also had Valsalva-induced dizziness and eye movements, as well as sound-induced dizziness (more prominent on the right). Audiometry showed a small air-bone gap of 10 dB in the right ear. Vestibular evoked myogenic potential testing showed an abnormally low threshold of 66 dB on the right, and a computed tomography scan showed dehiscence of the superior canal on the right. Histopathologic examination of the right ear showed a 1.4 x 0.6-mm dehiscence of bone covering the superior canal. Dura was in direct contact with the endosteum and the membranous duct at the level of the dehiscence. No osteoclastic process was evident within the otic capsule bone surrounding the dehiscence. The left ear showed thin but intact bone over the superior canal. Both ears showed focal microdehiscences of the tegmen tympani and tegmen mastoideum. The auditory and vestibular sense organs on both sides appeared normal. No endolymphatic hydrops was observed.
Conclusions: The findings were consistent with the hypothesis put forth by Carey and colleagues that SCD may arise from a failure of postnatal bone development, and that minor trauma may disrupt thin bone or stable dura over the superior canal.
C1 [Rosowski, John J.; Merchant, Saumil N.] Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA.
[Rosowski, John J.; Merchant, Saumil N.] Harvard Univ, Sch Med, Boston, MA USA.
[Teixido, Michael; Kung, Brian] Christiana Care Hlth Syst, Dept Otolaryngol, Wilmington, DE USA.
RP Merchant, SN (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, 243 Charles St, Boston, MA 02114 USA.
FU NIH [U24 DC011943]
FX From the Department of Otolaryngology, Christiana Care Health System,
Wilmington, Delaware (Teixido, Kung), and the Department of
Otolaryngology, Massachusetts Eye and Ear Infirmary and Harvard Medical
School, Boston, Massachusetts (Rosowski, Merchant). This work was
supported by NIH grant U24 DC011943.
NR 14
TC 8
Z9 8
U1 0
U2 1
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 JAN
PY 2012
VL 121
IS 1
BP 7
EP 12
PG 6
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 879TS
UT WOS:000299355700002
PM 22312921
ER
PT J
AU Friedmann, DR
Eubig, J
Winata, LS
Pramanik, BK
Merchant, SN
Lalwani, AK
AF Friedmann, David R.
Eubig, Jan
Winata, Leon S.
Pramanik, Bidyut K.
Merchant, Saumil N.
Lalwani, Anil K.
TI A Clinical and Histopathologic Study of Jugular Bulb Abnormalities
SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY
LA English
DT Article
ID SEMICIRCULAR CANAL DEHISCENCE
AB Objective: To further define the spectrum of clinical presentation and explore the histologic sequelae of jugular bulb abnormalities (JBAs).
Design: Retrospective review.
Setting: Academic medical center.
Patients: Thirty patients with radiologic evidence of inner ear dehiscence by JBA.
Main Outcome Measure: Thirty patients with radiologic inner ear dehiscence by JBA and 1579 temporal bone specimens were evaluated for consequences from JBA.
Results: We found that JBA-associated inner ear dehiscence could be identified on computed tomography of the temporal bone but not on magnetic resonance imaging scan. Jugular bulb abnormalities eroded the vestibular aqueduct most often (in 25 patients), followed by the facial nerve (5 patients) and the posterior semicircular canal (4 patients). Half of the patients (15) were asymptomatic. Results from vestibular evoked myogenic potential (VEMP) tests were positive in 8 of 12 patients with inner ear dehiscence. Histologically, only 2 of 41 temporal bones with dehiscence of the vestibular aqueduct demonstrated endolymphatic hydrops.
Conclusions: Jugular bulb abnormalities can erode into the vestibular aqueduct, facial nerve, and the posterior semicircular canal. While symptoms may include pulsatile tinnitus, vertigo, or conductive hearing loss, in contrast to earlier reports, half of the patients were asymptomatic. Dehiscence of vestibular aqueduct rarely leads to clinical or histologic hydrops. The VEMP testing was useful in confirming the presence of inner ear dehiscence due to JBAs. Because the natural history of JBAs is unknown, these patients should be followed closely to evaluate for progression of the JBA or development of symptoms.
C1 [Friedmann, David R.; Lalwani, Anil K.] NYU, Sch Med, Dept Otolaryngol, New York, NY 10016 USA.
[Eubig, Jan; Pramanik, Bidyut K.] NYU, Sch Med, Dept Radiol, New York, NY 10016 USA.
[Lalwani, Anil K.] NYU, Sch Med, Dept Pediat, New York, NY 10016 USA.
[Lalwani, Anil K.] NYU, Sch Med, Dept Physiol & Neurosci, New York, NY 10016 USA.
[Winata, Leon S.; Merchant, Saumil N.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Massachusetts Eye & Ear Infirm, Boston, MA 02115 USA.
RP Lalwani, AK (reprint author), NYU, Sch Med, Dept Otolaryngol, 550 1st Ave,7Q, New York, NY 10016 USA.
EM anil.lalwani@nyumc.org
FU National Institutes of Health [U24DC011943]
FX This work was supported in part by National Institutes of Health grant
U24DC011943 to Dr Merchant.
NR 11
TC 16
Z9 16
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0886-4470
J9 ARCH OTOLARYNGOL
JI Arch. Otolaryngol. Head Neck Surg.
PD JAN
PY 2012
VL 138
IS 1
BP 66
EP 71
PG 6
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 876TT
UT WOS:000299131300012
PM 22249632
ER
PT J
AU Hill, CA
Gallagher, TQ
Maturo, S
Sadow, PM
Curtin, HD
Hartnick, CJ
AF Hill, Courtney A.
Gallagher, Thomas Q.
Maturo, Stephen
Sadow, Peter M.
Curtin, Hugh D.
Hartnick, Christopher J.
TI Radiology Quiz Case 1 Congenital cyst of the newborn
SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY
LA English
DT Editorial Material
ID LARYNGEAL CYSTS; CANCER
C1 [Hill, Courtney A.; Gallagher, Thomas Q.; Maturo, Stephen; Sadow, Peter M.; Curtin, Hugh D.; Hartnick, Christopher J.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA 02115 USA.
RP Hill, CA (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA 02115 USA.
NR 9
TC 0
Z9 0
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0886-4470
J9 ARCH OTOLARYNGOL
JI Arch. Otolaryngol. Head Neck Surg.
PD JAN
PY 2012
VL 138
IS 1
BP 87
EP 89
PG 3
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 876TT
UT WOS:000299131300017
PM 22249637
ER
PT J
AU Dwojak, SM
Hunt, JL
Cunningham, MJ
AF Dwojak, Sunshine M.
Hunt, Jennifer L.
Cunningham, Michael J.
TI Pathology Quiz Case 3: Neuroblastoma with cervical metastases
SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY
LA English
DT Editorial Material
ID PROGNOSIS; TUMORS
C1 [Dwojak, Sunshine M.; Cunningham, Michael J.] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Hunt, Jennifer L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Dwojak, Sunshine M.; Hunt, Jennifer L.; Cunningham, Michael J.] Harvard Univ, Sch Med, Boston, MA USA.
RP Dwojak, SM (reprint author), Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
NR 10
TC 0
Z9 0
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0886-4470
J9 ARCH OTOLARYNGOL
JI Arch. Otolaryngol. Head Neck Surg.
PD JAN
PY 2012
VL 138
IS 1
BP 99
EP 101
PG 3
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 876TT
UT WOS:000299131300022
PM 22249642
ER
PT J
AU Naeser, MA
Martin, PI
Ho, M
Treglia, E
Kaplan, E
Bashir, S
Pascual-Leone, A
AF Naeser, Margaret A.
Martin, Paula I.
Ho, Michael
Treglia, Ethan
Kaplan, Elina
Bashir, Shahid
Pascual-Leone, Alvaro
TI Transcranial Magnetic Stimulation and Aphasia Rehabilitation
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Aphasia; Rehabilitation; Stroke; Transcranial magnetic stimulation
ID HUMAN MOTOR CORTEX; PARADOXICAL FUNCTIONAL FACILITATION; INFERIOR
PREFRONTAL CORTEX; NONFLUENT APHASIA; POSTSTROKE APHASIA; IMPROVED
LANGUAGE; RIGHT-HEMISPHERE; PARS TRIANGULARIS; BRAIN PLASTICITY;
PREMOTOR CORTEX
AB Repetitive transcranial magnetic stimulation (rTMS) has been reported to improve naming in chronic stroke patients with nonfluent aphasia since 2005. In part 1, we review the rationale for applying slow, 1-Hz, rTMS to the undamaged right hemisphere in chronic nonfluent aphasia patients after a left hemisphere stroke; and we present a transcranial magnetic stimulation (TMS) protocol used with these patients that is associated with long-term, improved naming post-TMS. In part 2, we present results from a case study with chronic nonfluent aphasia where TMS treatments were followed immediately by speech therapy (constraint-induced language therapy). In part 3, some possible mechanisms associated with improvement after a series of TMS treatments in stroke patients with aphasia are discussed.
C1 [Naeser, Margaret A.; Martin, Paula I.; Ho, Michael; Treglia, Ethan; Kaplan, Elina] Boston Univ, Sch Med, Harold Goodglass Boston Univ, Aphasia Res Ctr,Dept Neurol, Boston, MA 02118 USA.
[Bashir, Shahid; Pascual-Leone, Alvaro] Harvard Univ, Sch Med, Berenson Allen Ctr Noninvas Brain Stimulat, Dept Neurol, Boston, MA USA.
[Bashir, Shahid; Pascual-Leone, Alvaro] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Pascual-Leone, Alvaro] Univ Autonoma Barcelona, Inst Guttman Neurorehabil, Inst Univ, Badalona, Spain.
RP Naeser, MA (reprint author), VA Boston Healthcare Syst, Aphasia Res Ctr 12 A, 150 S Huntington Ave, Boston, MA 02130 USA.
EM mnaeser@bu.edu
RI Bashir, Shahid/B-4203-2012; Bashir, Shahid/E-7212-2014
FU National Institutes of Health [ROI DC05672, RRO18875]; National
Institute on Deafness and Other Communication Disorders (NIDCD),
Bethesda, MD; Medical Research Service, Department of Veterans Affairs,
Washington, DC; Harvard-Thorndike General Clinical Research Center [NCRR
MO1 RR01032]; Harvard Clinical and Translational Science Center [UL1
RR025758]; NIDCD; Harold Goodglass BU Aphasia Research Center [P30
DC05207]
FX Supported by the National Institutes of Health (grant no. ROI DC05672)
from the National Institute on Deafness and Other Communication
Disorders (NIDCD), Bethesda, MD, and a grant from the Medical Research
Service, Department of Veterans Affairs, Washington, DC; a K24 National
Institutes of Health award (award no. RRO18875); the Harvard-Thorndike
General Clinical Research Center (grant no. NCRR MO1 RR01032); the
Harvard Clinical and Translational Science Center (grant no. UL1
RR025758); and a NIDCD grant to the Harold Goodglass BU Aphasia Research
Center (grant no. P30 DC05207).
NR 75
TC 24
Z9 27
U1 6
U2 27
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 JAN
PY 2012
VL 93
IS 1
SU 1
BP S26
EP S34
DI 10.1016/j.apmr.2011.04.026
PG 9
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 873SY
UT WOS:000298904500004
PM 22202188
ER
PT J
AU Rhee, EJ
Nallamshetty, S
Plutzky, J
AF Rhee, Eun-Jung
Nallamshetty, Shriram
Plutzky, Jorge
TI Retinoid metabolism and its effects on the vasculature
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
LA English
DT Review
DE Retinoid; Vascular smooth muscle cell; RXR; RAR; Inflammation;
Atherosclerosis
ID SMOOTH-MUSCLE-CELLS; VITAMIN-A-DEFICIENCY; C-REACTIVE PROTEIN;
MICROVASCULAR ENDOTHELIAL-CELLS; TRANSCRIPTION FACTOR KLF5/BTEB2;
NITRIC-OXIDE PRODUCTION; ACID RECEPTORS RARS; ALL-TRANS; X-RECEPTOR;
BETA-CAROTENE
AB Retinoids, the metabolically-active structural derivatives of vitamin A, are critical signaling molecules in many fundamental biological processes including cell survival, proliferation and differentiation. Emerging evidence, both clinical and molecular, implicates retinoids in atherosclerosis and other vasculoproliferative disorders such as restenosis. Although the data from clinical trials examining effect of vitamin A and vitamin precursors on cardiac events have been contradictory, this data does suggest that retinoids do influence fundamental processes relevant to atherosclerosis. Preclinical animal model and cellular studies support these concepts. Retinoids exhibit complex effects on proliferation, growth, differentiation and migration of vascular smooth muscle cells (VSMC), including responses to injury and atherosclerosis. Retinoids also appear to exert important inhibitory effects on thrombosis and inflammatory responses relevant to atherogenesis. Recent studies suggest retinoids may also be involved in vascular calcification and endothelial function, for example, by modulating nitric oxide pathways. In addition, established retinoid effects on lipid metabolism and adipogenesis may indirectly influence inflammation and atherosclerosis. Collectively, these observations underscore the scope and complexity of retinoid effects relevant to vascular disease. Additional studies are needed to elucidate how context and metabolite-specific retinoid effects affect atherosclerosis. This article is part of a Special Issue entitled: Retinoid and Lipid Metabolism. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Rhee, Eun-Jung; Nallamshetty, Shriram; Plutzky, Jorge] Harvard Univ, Brigham & Womens Hosp, Sch Med, Cardiovasc Div, Boston, MA 02115 USA.
[Nallamshetty, Shriram] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiovasc Div, Boston, MA USA.
[Rhee, Eun-Jung] Sungkyunkwan Univ, Sch Med, Kangbuk Samsung Hosp, Dept Endocrinol & Metab, Seoul, South Korea.
RP Plutzky, J (reprint author), 77 Ave Louis Pasteur,NRB 742, Boston, MA 02115 USA.
EM jplutzky@rics.bwh.harvard.edu
OI Rhee, Eun-Jung/0000-0002-6108-7758
NR 163
TC 17
Z9 17
U1 1
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1388-1981
J9 BBA-MOL CELL BIOL L
JI Biochim. Biophys. Acta Mol. Cell Biol. Lipids
PD JAN
PY 2012
VL 1821
IS 1
SI SI
BP 230
EP 240
DI 10.1016/j.bbalip.2011.07.001
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 877NX
UT WOS:000299190300021
PM 21810483
ER
PT J
AU Hook, V
Funkelstein, L
Wegrzyn, J
Bark, S
Kindy, M
Hook, G
AF Hook, Vivian
Funkelstein, Lydiane
Wegrzyn, Jill
Bark, Steven
Kindy, Mark
Hook, Gregory
TI Cysteine Cathepsins in the secretory vesicle produce active peptides:
Cathepsin L generates peptide neurotransmitters and cathepsin B produces
beta-amyloid of Alzheimer's disease
SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS
LA English
DT Review
DE Cathepsin L; Cathepsin B; Secretory vesicle; Peptide neurotransmitters;
beta-amyloid; Alzheimer's disease
ID PRECURSOR PROTEIN; TRANSGENIC MICE; IN-VIVO; CHROMOGRANIN-A; WILD-TYPE;
SELECTIVE INHIBITOR; CHROMAFFIN GRANULES; NEUROPEPTIDE-Y; FULL-LENGTH;
MOUSE-BRAIN
AB Recent new findings indicate significant biological roles of cysteine cathepsin proteases in secretory vesicles for production of biologically active peptides. Notably, cathepsin L in secretory vesicles functions as a key protease for proteolytic processing of proneuropeptides (and prohormones) into active neuropeptides that are released to mediate cell-cell communication in the nervous system for neurotransmission. Moreover, cathepsin B in secretory vesicles has been recently identified as a beta-secretase for production of neurotoxic beta-amyloid (A beta) peptides that accumulate in Alzheimer's disease (AD), participating as a notable factor in the severe memory loss in AD. These secretory vesicle functions of cathepsins L and B for production of biologically active peptides contrast with the well-known role of cathepsin proteases in lysosomes for the degradation of proteins to result in their inactivation. The unique secretory vesicle proteome indicates proteins of distinct functional categories that provide the intravesicular environment for support of cysteine cathepsin functions. Features of the secretory vesicle protein systems insure optimized intravesicular conditions that support the proteolytic activity of cathepsins. These new findings of recently discovered biological roles of cathepsins L and B indicate their significance in human health and disease. This article is part of a Special Issue entitled: Proteolysis 50 years after the discovery of lysosome. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Hook, Vivian; Funkelstein, Lydiane; Wegrzyn, Jill; Bark, Steven] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, Dept Neurosci, La Jolla, CA 92093 USA.
[Hook, Vivian; Funkelstein, Lydiane; Wegrzyn, Jill; Bark, Steven] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, Dept Pharmacol, La Jolla, CA 92093 USA.
[Hook, Vivian; Funkelstein, Lydiane; Wegrzyn, Jill; Bark, Steven] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, Dept Med, La Jolla, CA 92093 USA.
[Kindy, Mark] Med Univ S Carolina, Dept Neurosci, Charleston, SC 29425 USA.
[Kindy, Mark] Ralph H Johnson VA Med Ctr, Charleston, SC 29425 USA.
[Hook, Gregory] Amer Life Sci Pharmaceut Inc, San Diego, CA 92109 USA.
RP Hook, V (reprint author), Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, Dept Neurosci, 9500 Gilman Dr,MC 0744, La Jolla, CA 92093 USA.
EM vhook@ucsd.edu
OI Wegrzyn, Jill/0000-0001-5923-0888
FU National Institutes of Health [R01DA04271, R01NS24553, R01MH077305,
P01HL58120, K01DA023065]; Alzheimer's Association; NIA/NIH [AG027446,
1R44AG032784]; [P30NS047101]
FX The cathepsin L and proteomics research was supported by grants from the
National Institutes of Health to V. Hook consisting of R01DA04271,
R01NS24553, R01MH077305, P01HL58120 from the NIH, a grant from the
Alzheimer's Association, and a grant to J. Gleeson, P30NS047101, for the
microscopy core. S. Bark was supported by a NIH Mentored Scientist Award
(K01DA023065). The authors also appreciate scientific advice by Dr.
Shin-Rong Hwang, and technical assistance by Mr. Thomas Toneff, at the
Skaggs School of Pharmacy and Pharmaceutical Sciences, Univ. of Calif.,
San Diego, La Jolla, CA. The authors appreciate collaboration of these
studies with Dr. Thomas Reinheckel and Dr. Christoph Peters at the
Albert-Ludwigs University, Freiburg, Germany.; The cathepsin B and
Alzheimer's research was supported by the NIA/NIH R21 Grant AG027446 and
1R44AG032784 (to American Life Science Pharmaceuticals (ALSP)), and by
an award from the Alzheimer's Association to V. Hook. V.H. holds equity
in ALSP and serves on the Scientific Advisory Board of ALSP. The terms
of this agreement have been reviewed by the University of California,
San Diego, in accordance with its conflict of interest policies. G.H.
holds equity in and is employed by ALSP.
NR 121
TC 22
Z9 23
U1 0
U2 23
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1570-9639
J9 BBA-PROTEINS PROTEOM
JI BBA-Proteins Proteomics
PD JAN
PY 2012
VL 1824
IS 1
SI SI
BP 89
EP 104
DI 10.1016/j.bbapap.2011.08.015
PG 16
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 871CS
UT WOS:000298715900010
PM 21925292
ER
PT J
AU Li, Y
Schiepers, C
Lake, R
Dadparvar, S
Berenji, GR
AF Li, Yuxin
Schiepers, Christiaan
Lake, Ralph
Dadparvar, Simin
Berenji, Gholam R.
TI Clinical utility of F-18-fluoride PET/CT in benign and malignant bone
diseases
SO BONE
LA English
DT Review
DE F-18-sodium fluoride; Positron emission tomography, computed tomography,
PET-CT; Bone scan
ID POSITRON-EMISSION-TOMOGRAPHY; F-18 FLUORIDE-ION; BRAIN TRANSFER
CONSTANTS; CELL LUNG-CANCER; TIME UPTAKE DATA; WHOLE-BODY PET;
BREAST-CANCER; PROSTATE-CANCER; METABOLIC-ACTIVITY; SODIUM-FLUORIDE
AB F-18 labeled sodium fluoride is a positron-emitting, bone seeking agent with more favorable skeletal kinetics than conventional phosphate and diphosphonate compounds. With the expanding clinical usage of PET/CT', there is renewed interest in using F-18-fluoride PET/CT for imaging bone diseases. Growing evidence indicates that F-18 fluoride PET/CT offers increased sensitivity, specificity, and diagnostic accuracy in evaluating metastatic bone disease compared to Tc-99m based bone scintigraphy. National Oncologic PET Registry (NOPR) has expanded coverage for F-18 sodium fluoride PET scans since February 2011 for the evaluation of osseous metastatic disease. In this article, we reviewed the pharmacological characteristics of sodium fluoride, as well as the clinical utility of PET/CT' using F-18-fluoride in both benign and malignant bone disorders. Published by Elsevier Inc.
C1 [Berenji, Gholam R.] VA Greater Los Angeles Healthcare Syst, Nucl Med Serv 115, Los Angeles, CA 90073 USA.
[Schiepers, Christiaan] Univ Calif Los Angeles, Dept Mol & Med Pharmacol, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Dadparvar, Simin] Univ PA Hlth Syst, Philadelphia, PA USA.
RP Berenji, GR (reprint author), VA Greater Los Angeles Healthcare Syst, Nucl Med Serv 115, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM Gholam.Berenji@va.gov
NR 75
TC 33
Z9 33
U1 1
U2 13
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 8756-3282
J9 BONE
JI Bone
PD JAN
PY 2012
VL 50
IS 1
BP 128
EP 139
DI 10.1016/j.bone.2011.09.053
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 875VV
UT WOS:000299064200017
PM 22001678
ER
PT J
AU Reardon, DA
Cloughesy, T
Rich, J
Yung, WKA
Yung, LT
DiLea, C
Huang, JR
Dugan, M
Mietlowski, W
Maes, A
Conrad, C
AF Reardon, David A.
Cloughesy, Timothy
Rich, Jeremy
Yung, W. K. Alfred
Yung, Lotus
DiLea, Clifford
Huang, Jerry
Dugan, Margaret
Mietlowski, William
Maes, Andrea
Conrad, Charles
TI Pharmacokinetic drug interaction between AEE788 and RAD001 causing
thrombocytopenia in patients with glioblastoma
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Glioblastoma; AEE788; Tyrosine kinase inhibitor; RAD001; mTOR
ID PHASE-I; MAMMALIAN TARGET; INHIBITOR EVEROLIMUS; TUMOR-CELLS; CANCER;
COMBINATION; RESISTANCE; PATHWAY; TRIALS; GLIOMA
AB Treating glioblastoma through the simultaneous inhibition of multiple transduction pathways may prove more effective than single-pathway inhibition. We evaluated the safety, biologic activity, and pharmacokinetic profile of oral AEE788, a selective inhibitor of epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF), plus oral RAD001, a mammalian target of rapamycin inhibitor, in glioblastoma patients.
This phase IB/II, open-label, multicenter, 2-arm, dose-escalation study enrolled adult glioblastoma patients at first or second recurrence/relapse. Primary objective was to determine the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT) of AEE788 combined with RAD001. Secondary objectives included determining the safety/tolerability, pharmacokinetics, pharmacodynamics, and antitumor activity of the combination.
Sixteen patients were enrolled (AEE788 200 mg/day + RAD001 5 mg/day, 2 patients; AEE788 150 mg/day + RAD001 5 mg every other day [qod], 14); all patients discontinued the study most commonly because of disease progression. Four patients experienced DLT (AEE788 200 mg/day + RAD001 5 mg/day, 1 patient; AEE788 150 mg/day + RAD001 5 mg qod, 3). Both patients receiving AEE788 (200 mg/day) plus RAD001 (5 mg/day) experienced clinically significant thrombocytopenia requiring a dose reduction/interruption. AEE788 appeared to inhibit the metabolism of RAD001. The study was terminated prematurely before an MTD was determined because of safety findings in other studies evaluating AEE788 monotherapy.
The coadministration of AEE788 and RAD001 in glioblastoma patients caused a clinically significant thrombocytopenia and a higher-than-expected RAD001 area under the curve concentration when dosed at 200 and 5 mg/day, respectively. After a dose reduction to AEE788 (150 mg/day) and RAD001 (5 mg qod), the combination appeared to be better tolerated.
C1 [Reardon, David A.] Dana Farber Canc Inst, Ctr Neurooncol, Boston, MA 02215 USA.
[Cloughesy, Timothy] Univ Calif Los Angeles, Los Angeles, CA USA.
[Rich, Jeremy] Cleveland Clin, Lerner Res Inst, Cleveland, OH 44106 USA.
[Mietlowski, William; Conrad, Charles] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Yung, Lotus] Celgene Corp, Summit, NJ USA.
[DiLea, Clifford; Huang, Jerry; Dugan, Margaret; Mietlowski, William; Maes, Andrea] Novartis Pharmaceutical Corp, E Hanover, NJ USA.
RP Reardon, DA (reprint author), Dana Farber Canc Inst, Ctr Neurooncol, 450 Brookline Ave,SW 460F, Boston, MA 02215 USA.
EM David_Reardon@DFCI.harvard.edu
FU Novartis Pharmaceuticals Corporation, East Hanover, NJ
FX We are indebted to the patients who participated in this study and study
coordinators. We thank Syntaxx Communications, Inc. for assistance with
manuscript development and editing. Research support by Novartis
Pharmaceuticals Corporation, East Hanover, NJ.
NR 21
TC 5
Z9 5
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD JAN
PY 2012
VL 69
IS 1
BP 281
EP 287
DI 10.1007/s00280-011-1754-1
PG 7
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 870EO
UT WOS:000298652100032
PM 21984222
ER
PT J
AU Wolpin, BM
Ng, K
Bao, Y
Kraft, P
Stampfer, MJ
Michaud, DS
Ma, J
Buring, JE
Sesso, HD
Lee, IM
Rifai, N
Cochrane, BB
Wactawski-Wende, J
Chlebowski, RT
Willett, WC
Manson, JE
Giovannucci, EL
Fuchs, CS
AF Wolpin, Brian M.
Ng, Kimmie
Bao, Ying
Kraft, Peter
Stampfer, Meir J.
Michaud, Dominique S.
Ma, Jing
Buring, Julie E.
Sesso, Howard D.
Lee, I-Min
Rifai, Nader
Cochrane, Barbara B.
Wactawski-Wende, Jean
Chlebowski, Rowan T.
Willett, Walter C.
Manson, JoAnn E.
Giovannucci, Edward L.
Fuchs, Charles S.
TI Plasma 25-Hydroxyvitamin D and Risk of Pancreatic Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID VITAMIN-D STATUS; FOOD FREQUENCY QUESTIONNAIRE; PHYSICAL-ACTIVITY
QUESTIONNAIRE; MALE HEALTH-PROFESSIONALS; WOMENS HEALTH; PRIMARY
PREVENTION; REPRODUCIBILITY; VALIDITY; METAANALYSIS; ASPIRIN
AB Background: Laboratory studies suggest that vitamin D may inhibit pancreatic cancer cell growth. However, epidemiologic studies of vitamin D and pancreatic cancer risk have been conflicting.
Methods: To determine whether prediagnostic levels of plasma 25-hydroxyvitamin D (25[OH]D; IDS Inc.; enzyme immunoassay) were associated with risk of pancreatic cancer, we conducted a pooled analysis of nested case-control studies with 451 cases and 1,167 controls from five cohorts through 2008. Median follow-up among controls was 14.1 years in Health Professionals Follow-Up Study (HPFS), 18.3 years in Nurses' Health Study (NHS), 25.3 years in Physicians' Health Study (PHS), 12.2 years in Women's Health Initiative-Observational Study (WHI), and 14.4 years in Women's Health Study (WHS). Logistic regression was used to compare the odds of pancreatic cancer by plasma level of 25(OH) D.
Results: Mean plasma 25(OH) D was lower in cases versus controls (61.3 vs. 64.5 nmol/L, P = 0.005). In logistic regression models, plasma 25(OH) D was inversely associated with odds of pancreatic cancer. Participants in quintiles two through five had multivariable-adjusted ORs (95% confidence intervals) of 0.79 (0.56-1.10), 0.75 (0.53-1.06), 0.68 (0.48-0.97), and 0.67 (0.46-0.97; P(trend) = 0.03), respectively, compared with the bottom quintile. Compared with those with insufficient levels [25[OH] D, < 50 nmol/L], ORs were 0.75 (0.58-0.98) for subjects with relative insufficiency [25[OH] D, 50 to <75 nmol/L] and 0.71 (0.52-0.97) for those with sufficient levels [25[OH] D, >= 75 nmol/L]. No increased risk was noted in subjects with 25(OH) D >= 100 nmol/L, as suggested in a prior study. In subgroup analyses, ORs for the top versus bottom quartile of 25(OH) D were 0.72 (0.48-1.08) for women, 0.73 (0.40-1.31) for men, and 0.73 (0.51-1.03) for Whites.
Conclusions: Among participants in five large prospective cohorts, higher plasma levels of 25(OH) D were associated with a lower risk for pancreatic cancer.
Impact: Low circulating 25(OH) D may predispose individuals to the development of pancreatic cancer. Cancer Epidemiol Biomarkers Prev; 21(1); 82-91. (C) 2011 AACR.
C1 [Wolpin, Brian M.; Ng, Kimmie; Fuchs, Charles S.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Bao, Ying; Stampfer, Meir J.; Ma, Jing; Willett, Walter C.; Manson, JoAnn E.; Giovannucci, Edward L.; Fuchs, Charles S.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Buring, Julie E.; Sesso, Howard D.] Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MA 02115 USA.
[Buring, Julie E.; Sesso, Howard D.; Lee, I-Min; Manson, JoAnn E.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
[Buring, Julie E.] Harvard Univ, Sch Med, Dept Ambulatory Care & Prevent, Cambridge, MA 02138 USA.
[Kraft, Peter; Stampfer, Meir J.; Michaud, Dominique S.; Ma, Jing; Sesso, Howard D.; Lee, I-Min; Willett, Walter C.; Manson, JoAnn E.; Giovannucci, Edward L.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Cambridge, MA 02138 USA.
[Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Biostat, Cambridge, MA 02138 USA.
[Stampfer, Meir J.; Willett, Walter C.; Giovannucci, Edward L.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Cambridge, MA 02138 USA.
[Rifai, Nader] Childrens Hosp Boston, Dept Lab Med, Boston, MA USA.
[Michaud, Dominique S.] Brown Univ, Dept Publ Hlth Epidemiol, Providence, RI 02912 USA.
[Cochrane, Barbara B.] Univ Washington, Sch Nursing, Seattle, WA 98195 USA.
[Wactawski-Wende, Jean] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
[Chlebowski, Rowan T.] Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Torrance, CA 90509 USA.
RP Wolpin, BM (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM bwolpin@partners.org
RI Michaud, Dominique/I-5231-2014
FU National Cancer Institute, NIH [P01 CA87969, P01 CA55075, P50 CA127003,
R01 CA124908]; NCI [K07 CA140790]; American Society of Clinical
Oncology; Howard Hughes Medical Institute; NIH (Bethesda, MD) [CA97193,
CA34944, CA40360, HL26490, HL34595, CA047988, HL043851, HL080467];
National Heart, Lung, and Blood Institute, NIH; U.S. Department of
Health and Human Services [N01WH22110, 24152, 32100-2, 32105-6, 32108-9,
32111-13, 32115, 32118-32119, 32122, 42107-26, 42129-32, 44221]
FX The NHS and HPFS are supported by the National Cancer Institute, NIH
(grants no. P01 CA87969, P01 CA55075, P50 CA127003, and R01 CA124908).
B. M. Wolpin, MD, MPH, is supported by NCI K07 CA140790, an American
Society of Clinical Oncology Career Development award, and a Howard
Hughes Medical Institute Early Career Physician-Scientist award. The PHS
is supported by grants CA97193, CA34944, CA40360, HL26490, and HL34595
from the NIH (Bethesda, MD). The WHI program is funded by the National
Heart, Lung, and Blood Institute, NIH, U.S. Department of Health and
Human Services through contracts N01WH22110, 24152, 32100-2, 32105-6,
32108-9, 32111-13, 32115, 32118-32119, 32122, 42107-26, 42129-32, and
44221. The WHS is supported by grants CA047988, HL043851, and HL080467
from the NIH (Bethesda, MD).
NR 49
TC 48
Z9 48
U1 2
U2 12
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 JAN
PY 2012
VL 21
IS 1
BP 82
EP 91
DI 10.1158/1055-9965.EPI-11-0836
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 875RH
UT WOS:000299051500009
PM 22086883
ER
PT J
AU Mavaddat, N
Barrowdale, D
Andrulis, IL
Domchek, SM
Eccles, D
Nevanlinna, H
Ramus, SJ
Spurdle, A
Robson, M
Sherman, M
Mulligan, AM
Couch, FJ
Engel, C
McGuffog, L
Healey, S
Sinilnikova, OM
Southey, MC
Terry, MB
Goldgar, D
O'Malley, F
John, EM
Janavicius, R
Tihomirova, L
Hansen, TVO
Nielsen, FC
Osorio, A
Stavropoulou, A
Benitez, J
Manoukian, S
Peissel, B
Barile, M
Volorio, S
Pasini, B
Dolcetti, R
Putignano, AL
Ottini, L
Radice, P
Hamann, U
Rashid, MU
Hogervorst, FB
Kriege, M
van der Luijt, RB
Peock, S
Frost, D
Evans, DG
Brewer, C
Walker, L
Rogers, MT
Side, LE
Houghton, C
Weaver, J
Godwin, AK
Schmutzler, RK
Wappenschmidt, B
Meindl, A
Kast, K
Arnold, N
Niederacher, D
Sutter, C
Deissler, H
Gadzicki, D
Preisler-Adams, S
Varon-Mateeva, R
Schonbuchner, I
Gevensleben, H
Stoppa-Lyonnet, D
Belotti, M
Barjhoux, L
Isaacs, C
Peshkin, BN
Caldes, T
de la Hoya, M
Canadas, C
Heikkinen, T
Heikkila, P
Aittomaki, K
Blanco, I
Lazaro, C
Brunet, J
Agnarsson, BA
Arason, A
Barkardottir, RB
Dumont, M
Simard, J
Montagna, M
Agata, S
D'Andrea, E
Yan, M
Fox, S
Rebbeck, TR
Rubinstein, W
Tung, N
Garber, JE
Wang, XS
Fredericksen, Z
Pankratz, VS
Lindor, NM
Szabo, C
Offit, K
Sakr, R
Gaudet, MM
Singer, CF
Tea, MK
Rappaport, C
Mai, PL
Greene, MH
Sokolenko, A
Imyanitov, E
Toland, AE
Senter, L
Sweet, K
Thomassen, M
Gerdes, AM
Kruse, T
Caligo, M
Aretini, P
Rantala, J
von Wachenfeld, A
Henriksson, K
Steele, L
Neuhausen, SL
Nussbaum, R
Beattie, M
Odunsi, K
Sucheston, L
Gayther, SA
Nathanson, K
Gross, J
Walsh, C
Karlan, B
Chenevix-Trench, G
Easton, DF
Antoniou, AC
AF Mavaddat, Nasim
Barrowdale, Daniel
Andrulis, Irene L.
Domchek, Susan M.
Eccles, Diana
Nevanlinna, Heli
Ramus, Susan J.
Spurdle, Amanda
Robson, Mark
Sherman, Mark
Mulligan, Anna Marie
Couch, Fergus J.
Engel, Christoph
McGuffog, Lesley
Healey, Sue
Sinilnikova, Olga M.
Southey, Melissa C.
Terry, Mary Beth
Goldgar, David
O'Malley, Frances
John, Esther M.
Janavicius, Ramunas
Tihomirova, Laima
Hansen, Thomas V. O.
Nielsen, Finn C.
Osorio, Ana
Stavropoulou, Alexandra
Benitez, Javier
Manoukian, Siranoush
Peissel, Bernard
Barile, Monica
Volorio, Sara
Pasini, Barbara
Dolcetti, Riccardo
Putignano, Anna Laura
Ottini, Laura
Radice, Paolo
Hamann, Ute
Rashid, Muhammad U.
Hogervorst, Frans B.
Kriege, Mieke
van der Luijt, Rob B.
Peock, Susan
Frost, Debra
Evans, D. Gareth
Brewer, Carole
Walker, Lisa
Rogers, Mark T.
Side, Lucy E.
Houghton, Catherine
Weaver, JoEllen
Godwin, Andrew K.
Schmutzler, Rita K.
Wappenschmidt, Barbara
Meindl, Alfons
Kast, Karin
Arnold, Norbert
Niederacher, Dieter
Sutter, Christian
Deissler, Helmut
Gadzicki, Doroteha
Preisler-Adams, Sabine
Varon-Mateeva, Raymonda
Schoenbuchner, Ines
Gevensleben, Heidrun
Stoppa-Lyonnet, Dominique
Belotti, Muriel
Barjhoux, Laure
Isaacs, Claudine
Peshkin, Beth N.
Caldes, Trinidad
de la Hoya, Miguel
Canadas, Carmen
Heikkinen, Tuomas
Heikkila, Paivi
Aittomaki, Kristiina
Blanco, Ignacio
Lazaro, Conxi
Brunet, Joan
Agnarsson, Bjarni A.
Arason, Adalgeir
Barkardottir, Rosa B.
Dumont, Martine
Simard, Jacques
Montagna, Marco
Agata, Simona
D'Andrea, Emma
Yan, Max
Fox, Stephen
Rebbeck, Timothy R.
Rubinstein, Wendy
Tung, Nadine
Garber, Judy E.
Wang, Xianshu
Fredericksen, Zachary
Pankratz, Vernon S.
Lindor, Noralane M.
Szabo, Csilla
Offit, Kenneth
Sakr, Rita
Gaudet, Mia M.
Singer, Christian F.
Tea, Muy-Kheng
Rappaport, Christine
Mai, Phuong L.
Greene, Mark H.
Sokolenko, Anna
Imyanitov, Evgeny
Toland, Amanda Ewart
Senter, Leigha
Sweet, Kevin
Thomassen, Mads
Gerdes, Anne-Marie
Kruse, Torben
Caligo, Maria
Aretini, Paolo
Rantala, Johanna
von Wachenfeld, Anna
Henriksson, Karin
Steele, Linda
Neuhausen, Susan L.
Nussbaum, Robert
Beattie, Mary
Odunsi, Kunle
Sucheston, Lara
Gayther, Simon A.
Nathanson, Kate
Gross, Jenny
Walsh, Christine
Karlan, Beth
Chenevix-Trench, Georgia
Easton, Douglas F.
Antoniou, Antonis C.
CA HEBON
EMBRACE
GEMO Study Collaborators
kConFab Investigators
SWE-BRCA Collaborators
Consortium Investigators Modifiers
TI Pathology of Breast and Ovarian Cancers among BRCA1 and BRCA2 Mutation
Carriers: Results from the Consortium of Investigators of Modifiers of
BRCA1/2 (CIMBA)
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID ESTROGEN-RECEPTOR STATUS; IMMUNOHISTOCHEMICAL MARKERS; GERMLINE
MUTATIONS; TUMOR SUBTYPES; FEATURES; RISK; PHENOTYPE; WOMEN; PREDICTION;
CARCINOMA
AB Background: Previously, small studies have found that BRCA1 and BRCA2 breast tumors differ in their pathology. Analysis of larger datasets of mutation carriers should allow further tumor characterization.
Methods: We used data from 4,325 BRCA1 and 2,568 BRCA2 mutation carriers to analyze the pathology of invasive breast, ovarian, and contralateral breast cancers.
Results: There was strong evidence that the proportion of estrogen receptor (ER)-negative breast tumors decreased with age at diagnosis among BRCA1 (P-trend = 1.2 x 10(-5)), but increased with age at diagnosis among BRCA2, carriers (P-trend 6.8 x 10(-6)). The proportion of triple-negative tumors decreased with age at diagnosis in BRCA1 carriers but increased with age at diagnosis of BRCA2 carriers. In both BRCA1 and BRCA2 carriers, ER-negative tumors were of higher histologic grade than ER-positive tumors (grade 3 vs. grade 1; P = 1.2 x 10(-13) for BRCA1 and P = 0.001 for BRCA2). ER and progesterone receptor (PR) expression were independently associated with mutation carrier status [ER-positive odds ratio (OR) for BRCA2 = 9.4, 95% CI: 7.0-12.6 and PR-positive OR = 1.7, 95% CI: 1.3-2.3, under joint analysis]. Lobular tumors were more likely to be BRCA2-related (OR for BRCA2 = 3.3, 95% CI: 2.4-4.4; P = 4.4 x 10(-14)), and medullary tumors BRCA1-related (OR for BRCA2 = 0.25, 95% CI: 0.18-0.35; P = 2.3 x 10(-15)). ER-status of the first breast cancer was predictive of ER-status of asynchronous contralateral breast cancer (P = 0.0004 for BRCA1; P = 0.002 for BRCA2). There were no significant differences in ovarian cancer morphology between BRCA1 and BRCA2 carriers (serous: 67%; mucinous: 1%; endometrioid: 12%; clear-cell: 2%).
Conclusions/Impact: Pathologic characteristics of BRCA1 and BRCA2 tumors may be useful for improving risk-prediction algorithms and informing clinical strategies for screening and prophylaxis. Cancer Epidemiol Biomarkers Prev; 21(1); 134-47. (C) 2011 AACR.
C1 [Mavaddat, Nasim; Barrowdale, Daniel; McGuffog, Lesley; Peock, Susan; Frost, Debra; Easton, Douglas F.; Antoniou, Antonis C.; EMBRACE] Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
[Andrulis, Irene L.; O'Malley, Frances] Mt Sinai Hosp, Fred A Litwin Ctr Canc Genet, Samuel Lunenfeld Res Inst, Toronto, ON, Canada.
[Robson, Mark; Offit, Kenneth; Sakr, Rita] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY USA.
[Robson, Mark; Offit, Kenneth; Sakr, Rita] Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY USA.
[Robson, Mark; Offit, Kenneth; Sakr, Rita] Mem Sloan Kettering Canc Ctr, Dept Epidemiol Biostat, New York, NY USA.
[Terry, Mary Beth] Columbia Univ, Dept Epidemiol, New York, NY USA.
[Andrulis, Irene L.; O'Malley, Frances] Univ Toronto, Dept Mol Genet, Toronto, ON M5S 1A1, Canada.
[Mulligan, Anna Marie] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON M5S 1A1, Canada.
[Mulligan, Anna Marie] St Michaels Hosp, Toronto, ON M5B 1W8, Canada.
[Rebbeck, Timothy R.] Univ Penn, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Rebbeck, Timothy R.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Weaver, JoEllen] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Eccles, Diana] Univ Southampton, Fac Med, Southampton Univ Hosp, NHS Trust, Southampton SO9 5NH, Hants, England.
[Nevanlinna, Heli; Heikkinen, Tuomas] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, FIN-00290 Helsinki, Finland.
[Heikkila, Paivi] Univ Helsinki, Cent Hosp, Dept Pathol, Helsinki, Finland.
[Aittomaki, Kristiina] Univ Helsinki, Cent Hosp, Dept Clin Genet, Helsinki, Finland.
[Ramus, Susan J.; Gayther, Simon A.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90089 USA.
[Gross, Jenny; Walsh, Christine; Karlan, Beth] Cedars Sinai Med Ctr, Samuel Oschin Canc Inst, Womens Canc Program, Los Angeles, CA 90048 USA.
[Gross, Jenny; Walsh, Christine; Karlan, Beth] Cedars Sinai Med Ctr, Dept Obstet & Gynecol, Div Gynecol Oncol, Los Angeles, CA 90048 USA.
[Spurdle, Amanda; Healey, Sue; Chenevix-Trench, Georgia] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
[Sherman, Mark] NCI, Hormonal & Reprod Epidemiol Branch, Rockville, MD USA.
[Mai, Phuong L.; Greene, Mark H.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Couch, Fergus J.; Fredericksen, Zachary; Pankratz, Vernon S.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Lindor, Noralane M.] Mayo Clin, Dept Med Genet, Rochester, MN USA.
[Engel, Christoph] Univ Leipzig, Inst Med Informat Stat & Epidemiol, Leipzig, Germany.
[Sinilnikova, Olga M.] Ctr Hosp Univ Lyon, Ctr Leon Berard, Unite Mixte Genet Constitut Canc Frequents, Lyon, France.
[Sinilnikova, Olga M.; Barjhoux, Laure] Univ Lyon 1, Canc Res Ctr Lyon, CNRS, INSERM,U1052,UMR5286, F-69622 Villeurbanne, France.
[GEMO Study Collaborators] Federat Natl Ctr Lutte Canc, Canc Genet Network Grp Genet & Canc, Lyon, France.
[Southey, Melissa C.] Univ Melbourne, Dept Pathol, Genet Epidemiol Lab, Melbourne, Vic 3010, Australia.
[Fox, Stephen; kConFab Investigators] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
[Goldgar, David] Univ Utah, Sch Med, Dept Dermatol, Salt Lake City, UT USA.
[John, Esther M.] Canc Prevent Inst Calif, Dept Epidemiol, Fremont, CA USA.
[Janavicius, Ramunas] Vilnius Univ Hosp Santariskiu Clin, Dept Mol & Regenerat Med, Hematol Oncol & Transfus Med Ctr, Vilnius, Lithuania.
[Tihomirova, Laima] Latvian Biomed Res & Study Ctr, Riga, Latvia.
[Hansen, Thomas V. O.; Nielsen, Finn C.] Copenhagen Univ Hosp, Rigshosp, Dept Clin Biochem, Copenhagen, Denmark.
[Gerdes, Anne-Marie] Univ Copenhagen, Rigshosp, Dept Clin Genet, DK-1168 Copenhagen, Denmark.
[Caldes, Trinidad; de la Hoya, Miguel; Canadas, Carmen] Hosp Clin San Carlos, Mol Oncol Lab, Madrid, Spain.
[Stavropoulou, Alexandra] Natl Ctr Sci Res Demokritos, Mol Diagnost Lab, IRRP, Athens, Greece.
[Manoukian, Siranoush; Peissel, Bernard] Fdn IRCCS Ist Nazl Tumori INT, Dept Prevent & Predict Med, Unit Med Genet, San Giovanni Rotondo, Italy.
[Radice, Paolo] Fdn IRCCS Ist Nazl Tumori INT, Dept Prevent & Predict Med, Unit Mol Bases Genet Risk & Genet Testing, San Giovanni Rotondo, Italy.
[Volorio, Sara; Radice, Paolo] Fdn Ist FIRC Oncol Mol, IFOM, Milan, Italy.
[Pasini, Barbara] Univ Turin, Dept Genet Biol & Biochem, Turin, Italy.
[Dolcetti, Riccardo] IRCCS, Ctr Riferimento Oncol, Canc Bioimmunotherapy Unit, Aviano, PN, Italy.
[Putignano, Anna Laura] Univ Florence, Dept Clin Physiopathol, I-50121 Florence, Italy.
[Ottini, Laura] Univ Roma La Sapienza, Dept Mol Med, Rome, Italy.
[Sutter, Christian] Univ Heidelberg Hosp, Dept Human Genet, Inst Human Genet, Heidelberg, Germany.
[Rashid, Muhammad U.] Shaukat Khanum Mem Canc Hosp & Res Ctr, Dept Basic Sci, Lahore, Pakistan.
[Hogervorst, Frans B.] Family Canc Clin, Amsterdam, Netherlands.
[HEBON] Netherlands Canc Inst, Amsterdam, Netherlands.
[Kriege, Mieke] Erasmus Univ, Med Ctr, Family Canc Clin, Dept Med Oncol, Rotterdam, Netherlands.
[van der Luijt, Rob B.] Univ Med Ctr Utrecht, Dept Med Genet, Utrecht, Netherlands.
[Evans, D. Gareth] Cent Manchester Univ Hosp NHS Fdn Trust, Manchester Acad Hlth Sci Ctr, Manchester, Lancs, England.
[Brewer, Carole] Royal Devon & Exeter Hosp, Dept Clin Genet, Exeter EX2 5DW, Devon, England.
[Walker, Lisa] Churchill Hosp, Oxford Reg Genet Serv, Oxford OX3 7LJ, England.
[Rogers, Mark T.] Univ Wales Hosp, All Wales Med Genet Serv, Cardiff CF4 4XW, S Glam, Wales.
[Side, Lucy E.] Great Ormond St Hosp Sick Children, NE Thames Reg Genet Serv, London WC1N 3JH, England.
[Houghton, Catherine] Liverpool Womens NHS Fdn Trust, Cheshire & Merseyside Clin Genet Serv, Liverpool, Merseyside, England.
[Godwin, Andrew K.] Univ Kansas, Med Ctr, Dept Pathol & Lab Med, Kansas City, KS 66103 USA.
[Schmutzler, Rita K.; Wappenschmidt, Barbara] Univ Hosp Cologne, Ctr Familial Breast & Ovarian Canc, Dept Obstet & Gynaecol, Cologne, Germany.
[Schmutzler, Rita K.; Wappenschmidt, Barbara] Univ Hosp Cologne, Ctr Integrated Oncol, Cologne, Germany.
[Meindl, Alfons] Tech Univ Munich, Klinikum Rechts Isar, Dept Obstet & Gynaecol, Div Tumor Genet, D-8000 Munich, Germany.
[Kast, Karin] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dept Obstet & Gynaecol, D-01062 Dresden, Germany.
[Arnold, Norbert] Univ Kiel, Inst Human Genet, Univ Hosp Schleswig Holstein, Kiel, Germany.
[Niederacher, Dieter] Univ Dusseldorf, Dept Obstet & Gynaecol, Univ Hosp Dusseldorf, D-40225 Dusseldorf, Germany.
[Deissler, Helmut] Univ Hosp Ulm, Dept Obstet & Gynaecol, Ulm, Germany.
[Gadzicki, Doroteha] Hannover Med Sch, Inst Cell & Mol Pathol, D-3000 Hannover, Germany.
[Preisler-Adams, Sabine] Univ Munster, Inst Human Genet, D-4400 Munster, Germany.
[Varon-Mateeva, Raymonda] Charite, Inst Human Genet, Campus Virchov Klinikum, Berlin, Germany.
Univ Wurzburg, Dept Med Genet, Inst Human Genet, Ctr Familial Breast & Ovarian Canc, Wurzburg, Germany.
[Stoppa-Lyonnet, Dominique; Belotti, Muriel] Inst Curie, Serv Genet Oncol, F-75231 Paris, France.
[Stoppa-Lyonnet, Dominique] Inst Curie, INSERM, Unite U830, F-75231 Paris, France.
[Stoppa-Lyonnet, Dominique] Univ Paris 05, Fac Med, Paris, France.
[Isaacs, Claudine; Peshkin, Beth N.] Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC USA.
Germans Trias & Pujol Biopmed Res Inst IGTP, Inst Catala Oncol, Hereditary Canc Program, Badalona, Spain.
[Blanco, Ignacio; Lazaro, Conxi] Hosp Duran i Reynals, Inst Catala Oncol, Hereditary Canc Program, Bellvitge Biomed Res Inst IDIBELL, Barcelona, Spain.
[Brunet, Joan] Hosp Josp Trueta, Inst Catala Oncol, Hereditary Canc Program, Girona Biomed Res Inst IdiBGi, Girona, Spain.
[Agnarsson, Bjarni A.; Arason, Adalgeir; Barkardottir, Rosa B.] Univ Iceland, Univ Hosp, Dept Pathol, Reykjavik, Iceland.
[Agnarsson, Bjarni A.; Arason, Adalgeir; Barkardottir, Rosa B.] Univ Iceland, Fac Med, Reykjavik, Iceland.
[Simard, Jacques] Ctr Hosp Univ Quebec, Canc Genom Lab, Canada Res Chair Oncogenet, Quebec City, PQ, Canada.
[Simard, Jacques] Univ Laval, Quebec City, PQ, Canada.
[Montagna, Marco; Agata, Simona] IRCCS, Ist Oncol Veneto, Immunol & Mol Oncol Unit, Padua, Italy.
[D'Andrea, Emma] Univ Padua, Dept Oncol & Surg Sci, Padua, Italy.
[Yan, Max] Prince Wales Hosp, Dept Anat Pathol, Randwick, NSW 2031, Australia.
[Rubinstein, Wendy] N Shore Univ Hlth Syst, Ctr Med Genet, Evanston, IL USA.
[Tung, Nadine] Beth Israel Deaconess Med Ctr, Boston, MA USA.
[Garber, Judy E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Szabo, Csilla] Univ Delaware, Newark, DE USA.
[Gaudet, Mia M.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Singer, Christian F.; Tea, Muy-Kheng; Rappaport, Christine] Med Univ Vienna, Dept OB GYN, Vienna, Austria.
[Singer, Christian F.; Tea, Muy-Kheng; Rappaport, Christine] Med Univ Vienna, Ctr Comprehens Canc, Vienna, Austria.
[Sokolenko, Anna; Imyanitov, Evgeny] St Petersburg Pediat Med Acad, Mol Oncol Lab, NN Petrov Inst Oncol, St Petersburg, Russia.
[Sokolenko, Anna; Imyanitov, Evgeny] St Petersburg Pediat Med Acad, Dept Med Genet, St Petersburg, Russia.
[Toland, Amanda Ewart] Ohio State Univ, Med Ctr, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
[Senter, Leigha; Sweet, Kevin] Ohio State Univ, Med Ctr, Dept Internal Med, Div Human Genet,Comprehens Canc Ctr, Columbus, OH 43210 USA.
[Thomassen, Mads; Kruse, Torben] Odense Univ Hosp, Dept Clin Genet, DK-5000 Odense, Denmark.
[Caligo, Maria; Aretini, Paolo] Univ Pisa, Sect Genet Oncol, Dept Lab Med, Pisa, Italy.
[Caligo, Maria; Aretini, Paolo] Univ Hosp Pisa, Pisa, Italy.
[Rantala, Johanna] Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden.
[von Wachenfeld, Anna] Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
[SWE-BRCA Collaborators] Karolinska Univ, Stockholm, Sweden.
[Henriksson, Karin] Univ Lund Hosp, Ctr Oncol, S-22185 Lund, Sweden.
[Steele, Linda; Neuhausen, Susan L.] City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Duarte, CA USA.
[Nussbaum, Robert] Univ Calif San Francisco, Dept Med, Div Med Genet, San Francisco, CA USA.
[Beattie, Mary] Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA.
[Beattie, Mary] Univ Calif San Francisco, Dept Biostat, San Francisco, CA 94143 USA.
[Odunsi, Kunle] Roswell Pk Canc Inst, Dept Gynecol Oncol, Buffalo, NY 14263 USA.
[Sucheston, Lara] Roswell Pk Canc Inst, Dept Canc Prevent & Control, Buffalo, NY 14263 USA.
RP Antoniou, AC (reprint author), Strangeways Res Lab, Worts Causeway, Cambridge CB1 8RN, England.
EM antonis@srl.cam.ac.uk
RI Spurdle, Amanda/A-4978-2011; Ligtenberg, Marjolijn/N-9666-2013;
Sokolenko, Anna/G-3123-2013; manoukian, siranoush/E-7132-2017; Peissel,
Bernard/E-8187-2017; D'Andrea, Emma/B-4374-2013; Sweet,
Kevin/E-4172-2011; Andrulis, Irene/E-7267-2013; Hoogerbrugge,
Nicoline/O-1016-2013; Radice, Paolo/O-3119-2013; Oosterwijk, Jan
C./G-5770-2011; Osorio, Ana/I-4324-2014; GLADIEFF, Laurence/O-5129-2014;
Dolcetti, Riccardo/O-3832-2015; Lester, Jenny/B-5933-2012; Toland,
Amanda/E-4202-2011; Arnold, Norbert/E-3012-2010; montagna,
marco/E-2225-2012;
OI Blanco, Ignacio/0000-0002-7414-7481; Ramus, Susan/0000-0003-0005-7798;
Spurdle, Amanda/0000-0003-1337-7897; Barrowdale,
Daniel/0000-0003-1661-3939; PUTIGNANO, Anna Laura/0000-0001-9434-1612;
Brunet, Joan/0000-0003-1945-3512; Nevanlinna, Heli/0000-0002-0916-2976;
Fox, Stephen/0000-0002-7648-8896; Ligtenberg,
Marjolijn/0000-0003-1290-1474; manoukian, siranoush/0000-0002-6034-7562;
Peissel, Bernard/0000-0001-9233-3571; Janavicius,
Ramunas/0000-0002-3773-8485; Rappaport-Fuerhauser,
Christine/0000-0002-6820-0020; Robson, Mark/0000-0002-3109-1692; Eeles,
Rosalind/0000-0002-3698-6241; Nathanson, Katherine/0000-0002-6740-0901;
Osorio, Ana/0000-0001-8124-3984; GLADIEFF, Laurence/0000-0002-6980-9719;
Dolcetti, Riccardo/0000-0003-1625-9853; Arnold,
Norbert/0000-0003-4523-8808; montagna, marco/0000-0002-4929-2150;
Jacobs, Chris/0000-0002-9557-9080; Evans, Gareth/0000-0002-8482-5784
FU University of Kansas Cancer Center; Kansas Bioscience Authority Eminent
Scholar Program; Cancer Research UK [C12292/A11174, C1287/A10118,
C1287/A11990, C5047/A8385]; European Community [223175,
HEALTH-F2-2009-223175]; Medical Research Council; National Cancer
Institute, NIH, [RFA-CA-06-503]; Breast Cancer Family Registry and
Principal Investigators, including Cancer Care Ontario [U01 CA69467];
Columbia University [U01 CA69398]; Fox Chase Cancer Center [U01
CA69631]; Huntsman Cancer Institute [U01 CA69446]; Cancer Prevention
Institute of California [U01 CA69417]; University of Melbourne [U01
CA69638]; Research Triangle Institute Informatics Support Center (RFP)
[N02PC45022-46]; Cancer Care Ontario; U.S. National Cancer Institute,
NIH under RFA [CA-06-503]; Research Council of Lithuania [LIG-19/2010];
LSC [05.0023.04., 10.0010.08]; NEYE Foundation; Fundacion Mutua
Madrilena; Asociacion Espanola Contra el Cancer; Spanish Ministry of
Science and Innovation [FIS PI08 1120]; Basque Foundation for Health
Innovation and Research (BIOEF) [BIO07/CA/006]; DKFZ; Dutch Cancer
Society [NKI1998-1854, NKI2004-3088, NKI2007-3756]; ZonMW [91109024];
NIHR; Royal Marsden NHS Foundation Trust; Eileen Stein Jacoby Fund
[U01CA69631, 5U01CA113916]; Centre of Molecular Medicine Cologne (CMMC)
[109076]; Ligue National Contre le Cancer and The Association; National
Cancer Institute [NCI P30 CA51008-12]; Fisher Center for Familial Cancer
Research; Helsinki University Central Hospital; Academy of Finland
[132473]; Finnish Cancer Society; Sigrid Juselius Foundation; Icelandic
Association "Walking for Breast Cancer Research"; Landspitali University
Hospital; Canadian Breast Cancer Research [019511]; Ministero della
Salute [RFPS 2006-5-341353, ACC2/R6.9]; Progetto Tumori Femminili;
National Breast Cancer Foundation; National Health and Medical Research
Council (NHMRC) [145684, 288704, 454508]; Queensland Cancer Fund; Cancer
Councils of New South Wales, Victoria, Tasmania and South Australia;
Cancer Foundation of Western Australia; NIH [CA116167, CA128978,
CA74415]; Specialized Program of Research Excellence (SPORE) in Breast
Cancer [CA116201]; Komen Foundation for the Cure; Breast Cancer Research
Foundation; U.S. National Cancer Institute; Westat, Inc.
[NO2-CP-11019-50, N02-CP-65504]; Russian Federation for Basic Research
[10-04-92601, 11-04-00250, 11-04-00227]; Federal Agency for Science and
Innovations [02.740.11.0780]; Commission of the European Communities
[PITN-GA-2009-238132]; OSU Comprehensive Cancer Center; ITT (Tuscany
Institute for Tumors) [2010-2012]; NCI Bay Area Breast Cancer SPORE
[P50-CA058207]; Avon Foundation; UCSF Helen Diller Family Comprehensive
Cancer Center; CRUK; Cancer Genetics Network and Marjorie Cohen
Foundation; American Cancer Society [SIOP-06-258-01-CCE]
FX The author, A.K. Godwin, thanks the support from The University of
Kansas Cancer Center and the Kansas Bioscience Authority Eminent Scholar
Program. A.K. Godwin is the Chancellors Distinguished Chair in
Biomedical Sciences-endowed Professor.; This work was supported by
Cancer Research UK grants C12292/A11174 and C1287/A10118. The research
leading to these results has received funding from the European
Community's Seventh Framework Programme under grant agreement no 223175
(HEALTH-F2-2009-223175). NM was funded by a scholarship from the Medical
Research Council. ACA is a CR-UK Senior Cancer Research Fellow. DFE is a
CR-UK Principal Research Fellow.; This work was supported by the
National Cancer Institute, NIH, under RFA-CA-06-503 and through
cooperative agreements with members of the Breast Cancer Family Registry
and Principal Investigators, including Cancer Care Ontario (U01
CA69467), Columbia University (U01 CA69398), Fox Chase Cancer Center
(U01 CA69631), Huntsman Cancer Institute (U01 CA69446), Cancer
Prevention Institute of California (U01 CA69417), University of
Melbourne (U01 CA69638), and Research Triangle Institute Informatics
Support Center (RFP No. N02PC45022-46).; This work was supported by
Cancer Care Ontario and the U.S. National Cancer Institute, NIH, under
RFA # CA-06-503 and through cooperative agreements with members of the
Breast Cancer Family Registry (BCFR) and principal investigators.;
Lithuania: This work is financially supported by the Research Council of
Lithuania grant LIG-19/2010 to R. Janavicius.; Latvia: L. Tihomirova was
financially supported by LSC grants 05.0023.04. and 10.0010.08.; The
authors thank NEYE Foundation for financial support; This study was
partially supported financially by the Fundacion Mutua Madrilena,
Asociacion Espanola Contra el Cancer and the Spanish Ministry of Science
and Innovation (FIS PI08 1120). This was funded, in part, by the Basque
Foundation for Health Innovation and Research (BIOEF): BIO07/CA/006.;
The DKFZ study was supported by the DKFZ.; The HEBON study is supported
by the Dutch Cancer Society grants NKI1998-1854, NKI2004-3088, and
NKI2007-3756 and the ZonMW grant 91109024.; EMBRACE is financially
supported by Cancer Research UK Grants C1287/A10118 and C1287/A11990. D.
G. Evans and F. Lalloo are financially supported by an NIHR grant to the
Biomedical Research Centre, Manchester, UK. The investigators at The
Institute of Cancer Research and The Royal Marsden NHS Foundation Trust
are financially supported by an NIHR grant to the Biomedical Research
Centre at the Institute of Cancer Research and the Royal Marsden NHS
Foundation Trust. R. Eeles, E. Bancroft, and L. D'Mello are also
financially supported by a Cancer Research UK grant C5047/A8385.; A.K.
Godwinwas funded by U01CA69631, 5U01CA113916, and the Eileen Stein
Jacoby Fund.; GC-HBOC is financially supported by a grant of the German
Cancer Aid (grant 109076) the Centre of Molecular Medicine Cologne
(CMMC).; This study was supported by The Ligue National Contre le Cancer
and The Association "Le cancer du sein, parlons-en!" Award.; C. Isaacs
and B.N. Peshkin are supported by National Cancer Institute Grant (NCI
P30 CA51008-12) and by the Fisher Center for Familial Cancer Research.;
The HEBCS study has been financially supported by the Helsinki
University Central Hospital Research Fund, Academy of Finland (132473),
the Finnish Cancer Society, and the Sigrid Juselius Foundation.; The
ILUH group was supported by the Icelandic Association "Walking for
Breast Cancer Research" and by the Landspitali University Hospital
Research Fund.; This work was supported by the Canadian Institutes of
Health Research for the "CIHR Team in Familial Risks of Breast Cancer"
program and by the Canadian Breast Cancer Research Alliance-grant
#019511.; This study was supported by "Ministero della Salute" (grant
numbers RFPS 2006-5-341353, ACC2/R6.9 and "Progetto Tumori Femminili").;
kConFab is supported by grants from the National Breast Cancer
Foundation, the National Health and Medical Research Council (NHMRC) and
by the Queensland Cancer Fund, the Cancer Councils of New South Wales,
Victoria, Tasmania and South Australia, and the Cancer Foundation of
Western Australia (funded by NHMRC grants 145684, 288704, and 454508).;
The MAYO study was supported by NIH grants CA116167, CA128978, a
Specialized Program of Research Excellence (SPORE) in Breast Cancer
(CA116201), and awards from the Komen Foundation for the Cure and the
Breast Cancer Research Foundation.; The research of Drs. P. L. Mai and
M. H. Greene was supported by the Intramural Research Program of the
U.S. National Cancer Institute and by support services contracts
NO2-CP-11019-50 and N02-CP-65504 with Westat, Inc.; This work has been
supported by the Russian Federation for Basic Research (grants
10-04-92601, 11-04-00250, 11-04-00227), the Federal Agency for Science
and Innovations (contract 02.740.11.0780), and the Commission of the
European Communities (grant PITN-GA-2009-238132).; This work was
supported by the OSU Comprehensive Cancer Center. Caroline Craven and
Michelle O'Connor were responsible for patient accrual and data
management.; M. Caligo was supported by an ITT (Tuscany Institute for
Tumors) grant 2010-2012.; S. L. Neuhausen was partially supported by NIH
CA74415 and the Morris and Horowitz Families Endowed Professorship.; The
grant funding was obtained from the NIH, NCI Bay Area Breast Cancer
SPORE (P50-CA058207), and the Avon Foundation. Support was also provided
from the UCSF Helen Diller Family Comprehensive Cancer Center.; UKFOCR
was supported by a project grant from CRUK to Paul Pharoah.; The funding
was obtained from Breast Cancer Research Foundation (to K.L. Nathanson);
and Cancer Genetics Network and Marjorie Cohen Foundation (to S.M.
Domchek).; WCRI acknowledges support from the American Cancer Society,
SIOP-06-258-01-CCE.
NR 47
TC 110
Z9 112
U1 6
U2 43
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 JAN
PY 2012
VL 21
IS 1
BP 134
EP 147
DI 10.1158/1055-9965.EPI-11-0775
PG 14
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 875RH
UT WOS:000299051500014
PM 22144499
ER
PT J
AU Chan, AT
Hsu, M
Zauber, AG
Hawk, ET
Bertagnolli, MM
AF Chan, Andrew T.
Hsu, Meier
Zauber, Ann G.
Hawk, Ernest T.
Bertagnolli, Monica M.
TI The Influence of UGT1A6 Variants and Aspirin Use in a Randomized Trial
of Celecoxib for Prevention of Colorectal Adenoma
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID GENETIC-VARIANTS; RISK; CANCER; POLYMORPHISMS; RECURRENCE; POLYPS;
ENZYME; CYP2C9
AB Aspirin and celecoxib prevent colorectal adenoma recurrence. Genetic variants in the UGT1A6 enzyme are associated with delayed aspirin metabolism and greater chemopreventive efficacy. We examined the effect of combining aspirin and celecoxib in relation to UGT1A6 T181A and R184S variants among 1,647 patients in the Adenoma Prevention with Celecoxib (APC) trial who were stratified according to the use of low-dose aspirin after removal of adenomas and randomized to placebo, 200-mg twice daily, or 400-mg twice daily celecoxib for 3 years. Patients underwent follow-up colonoscopies at 1 and 3 years to assess on-treatment efficacy. At 5 years, 538 patients underwent a colonoscopy to assess risk of recurrence after treatment was discontinued for at least 1 year. During treatment, the relative risk (RR) of recurrent adenoma was 0.68 [95% confidence interval (CI), 0.59-0.79] for 200-mg twice daily celecoxib and 0.54 (95% CI, 0.46-0.64) for 400-mg twice daily celecoxib compared with placebo. Aspirin use was not independently associated with recurrent adenoma (RR, 0.98, 95% CI, 0.86-1.15). These results did not vary according to UGT1A6 genotype. However, among those with a variant UGT1A6 genotype on aspirin, the RR of adenoma was 1.60 (95% CI, 0.81-3.15) after withdrawal of 200-mg twice daily and 1.98 (95% CI, 1.06-3.70) after withdrawal of 400-mg twice daily celecoxib compared with withdrawal of placebo. In contrast, there was no increased risk associated with discontinuing celecoxib among any other groups. Concurrent use of low-dose aspirin does not influence the efficacy of celecoxib in adenoma prevention. However, discontinuing celecoxib among aspirin-using individuals who initially developed adenoma despite a UGT1A6 variant genotype resulted in rapid reemergence of disease. Cancer Prev Res; 5(1); 61-72. (C)2011 AACR.
C1 [Chan, Andrew T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Chan, Andrew T.; Bertagnolli, Monica M.] Harvard Univ, Sch Med, Boston, MA USA.
[Chan, Andrew T.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Bertagnolli, Monica M.] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Hsu, Meier; Zauber, Ann G.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Hawk, Ernest T.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Chan, AT (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, 55 Fruit St,GRJ-728A, Boston, MA 02114 USA.
EM achan@partners.org
FU Pfizer Inc.; National Cancer Institute at the NIH [R01 CA137178, N01
CN95015]
FX A. T. Chan has served as a consultant to Bayer HealthCare and Millennium
Pharmaceuticals. M. M. Bertagnolli is the recipient of research funding
from Pfizer Inc. E. T. Hawk has served as a consultant for Pozen
Pharmaceutical Development Company. The statistical analysis of the
entire data sets pertaining to efficacy and safety has been
independently confirmed by A. G. Zauber, who is not employed by any
corporate entity. A. T. Chan had full access to all of the data and
takes full responsibility for the veracity of the data and analysis. No
potential conflicts of interest were disclosed by other authors.; This
work was supported by the National Cancer Institute at the NIH (grant
number R01 CA137178 to A. T. Chan and N01 CN95015 to M. M. Bertagnolli).
A. T. Chan is a Damon Runyon Cancer Research Foundation Clinical
Investigator.
NR 21
TC 6
Z9 6
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD JAN
PY 2012
VL 5
IS 1
BP 61
EP 72
DI 10.1158/1940-6207.CAPR-11-0337
PG 12
WC Oncology
SC Oncology
GA 877RT
UT WOS:000299200500010
PM 22030088
ER
PT J
AU Joshu, CE
Parmigiani, G
Colditz, GA
Platz, EA
AF Joshu, Corinne E.
Parmigiani, Giovanni
Colditz, Graham A.
Platz, Elizabeth A.
TI Opportunities for the Primary Prevention of Colorectal Cancer in the
United States
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID CIGARETTE-SMOKING; BEHAVIOR-CHANGE; COLON-CANCER; RISK; INTERVENTIONS;
SOCIETY; HEALTH; TRENDS; MEN
AB Several studies indicate that screening in combination with lifestyle modification may produce a greater reduction in colorectal cancer rates than screening alone. To identify national opportunities for the primary prevention of colorectal cancer, we assessed the prevalence of modifiable lifestyle risk factors in the United States. We used nationally representative, cross-sectional data from 5 NHANES cycles (1999-2000, n = 2,753; 2001-2002, n = 3,169; 2003-2004, n = 2,872; 2005-2006, n = 2,993; 2007-2008, n = 3,438). We evaluated the 5 colorectal cancer risk factors deemed "convincing" by the World Cancer Research Fund (obesity, physical inactivity, intake of red meat, processed meat, alcohol), and cigarette smoking, a "suggestive" risk factor in the Surgeon General's report. We estimated the prevalence of each risk factor separately and jointly, and report it overall, and by sex, race/ethnicity, age, and year. In 2007 to 2008, 81% percent of U.S. adults, aged 20 to 69 years, had at least one modifiable risk factor for colorectal cancer. More than 15% of those younger than 50 years had 3 or more risk factors. There was no change in the prevalence of risk factors between 1999 and 2008. The most common risk factors were risk factors for other chronic diseases. Our findings provide additional support for the prioritization of preventive services in health care reform. Increasing awareness, especially among young adults, that lifestyle factors influence colorectal cancer risk, and other chronic diseases, may encourage lifestyle changes and adherence to screening guidelines. Complementary approaches of screening and lifestyle modification will likely provide the greatest reduction of colorectal cancer. Cancer Prev Res; 5(1); 138-45. (C)2011 AACR.
C1 [Joshu, Corinne E.; Platz, Elizabeth A.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
[Platz, Elizabeth A.] Johns Hopkins Med Inst, James Buchanan Brady Urol Inst, Baltimore, MD 21205 USA.
[Platz, Elizabeth A.] Johns Hopkins Med Inst, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21205 USA.
[Parmigiani, Giovanni] Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Parmigiani, Giovanni] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Colditz, Graham A.] Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA.
[Colditz, Graham A.] Washington Univ, Sch Med, Alvin J Siteman Canc Ctr, St Louis, MO USA.
RP Joshu, CE (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, 615 N Wolfe St,Rm E6137, Baltimore, MD 21205 USA.
EM cjoshu@jhsph.edu
RI Colditz, Graham/A-3963-2009
OI Colditz, Graham/0000-0002-7307-0291
FU National Cancer Institute at the NIH [T32 CA009314]; Seraph Foundation;
American Cancer Society
FX C. E. Joshu was supported by the National Cancer Institute at the NIH
(grant number T32 CA009314) and the Seraph Foundation. G. A. Colditz is
supported by the American Cancer Society (Clinical Research
Professorship).
NR 22
TC 8
Z9 8
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD JAN
PY 2012
VL 5
IS 1
BP 138
EP 145
DI 10.1158/1940-6207.CAPR-11-0322
PG 8
WC Oncology
SC Oncology
GA 877RT
UT WOS:000299200500017
PM 21955521
ER
PT J
AU Pang, PS
Hoffmann, U
Shah, SJ
AF Pang, Peter S.
Hoffmann, Udo
Shah, Sanjiv J.
TI Classification of Patients With Acute Heart Failure Syndromes in the
Emergency Department
SO CIRCULATION-HEART FAILURE
LA English
DT Editorial Material
DE Editorials; coronary artery disease; heart failure; ischemia; troponin
ID CORONARY-ARTERY-DISEASE; CLINICAL-TRIALS; MANAGEMENT; TROPONIN;
OUTCOMES; ASSOCIATION; GUIDELINES; DIAGNOSIS; SOCIETY; TRENDS
C1 [Pang, Peter S.] Northwestern Univ, Feinberg Sch Med, Dept Emergency Med, Chicago, IL 60611 USA.
[Pang, Peter S.] Northwestern Univ, Feinberg Sch Med, Ctr Cardiovasc Innovat, Chicago, IL 60611 USA.
[Shah, Sanjiv J.] Northwestern Univ, Feinberg Sch Med, Div Cardiol, Dept Med, Chicago, IL 60611 USA.
[Hoffmann, Udo] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Pang, PS (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Emergency Med, 211 E Ontario St,Ste 300, Chicago, IL 60611 USA.
EM ppang@northwestern.edu
NR 27
TC 1
Z9 1
U1 1
U2 3
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 JAN
PY 2012
VL 5
IS 1
BP 2
EP 5
DI 10.1161/CIRCHEARTFAILURE.111.965830
PG 4
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 879IY
UT WOS:000299324100007
PM 22253405
ER
PT J
AU Luke, JJ
Hodi, FS
AF Luke, Jason J.
Hodi, F. Stephen
TI Vemurafenib and BRAF Inhibition: A New Class of Treatment for Metastatic
Melanoma
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID PHASE-III; RAF; KINASE; PATHWAY; TRIAL; DACARBAZINE; RESISTANCE;
SORAFENIB; PLX4032; PLACEBO
AB The U.S. Food and Drug Administration recently approved vemurafenib for the treatment of BRAF valine in exon 15, at codon 600 (V600E) mutant metastatic melanoma. Vemurafenib is a competitive small-molecule serine-threonine kinase inhibitor that functions by binding to the ATP-binding domain of mutant BRAF. Compared with dacarbazine chemotherapy, vemurafenib significantly improved the 6-month overall survival of patients from 64% to 84% and exhibited a response rate of approximately 50%. Median progression-free survival was also significantly improved with vemurafenib as compared with dacarbazine (5.3 versus 1.6 months, respectively), and this was consistent among groups analyzed, including age, sex, geography, Eastern Cooperative Oncology Group status, disease stage, and serum lactate dehydrogenase. The success of targeting melanoma genomics has created a paradigm shift for future drug development. Currently, the elucidation of resistant mechanisms to vemurafenib therapy remains an important area of active investigation that will shape rational drug treatments for melanoma. The development of vemurafenib, the role of BRAF targeting, and the changing landscape of treatment for melanoma provide a new foundation for clinical investigation. Clin Cancer Res; 18(1); 9-14. (C) 2011 AACR.
C1 [Hodi, F. Stephen] Dana Farber Canc Inst, Melanoma Dis Ctr, Boston, MA 02215 USA.
[Hodi, F. Stephen] Harvard Univ, Sch Med, Boston, MA USA.
[Luke, Jason J.] Mem Sloan Kettering Canc Ctr, Melanoma & Sarcoma Serv, New York, NY 10021 USA.
[Luke, Jason J.] Weill Cornell Med Coll, New York, NY USA.
RP Hodi, FS (reprint author), Dana Farber Canc Inst, Melanoma Dis Ctr, 450 Brookline Ave, Boston, MA 02215 USA.
EM Stephen_hodi@dfci.harvard.edu
FU Genentech/Roche; Bristol-Myers Squibb; Novartis; Pfizer; Synta
FX F.S. Hodi, clinical trial research support, Genentech/Roche,
Bristol-Myers Squibb, Novartis, Pfizer, and Synta; nonpaid consultant,
Genentech, Roche, Novartis, and Bristol-Myers Squibb. J.J. Luke
disclosed no potential conflicts of interest.
NR 29
TC 34
Z9 37
U1 1
U2 7
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 JAN 1
PY 2012
VL 18
IS 1
BP 9
EP 14
DI 10.1158/1078-0432.CCR-11-2197
PG 6
WC Oncology
SC Oncology
GA 871SV
UT WOS:000298758900003
PM 22083257
ER
PT J
AU Alcala, AM
Flaherty, KT
AF Alcala, Alexander Marzuka
Flaherty, Keith T.
TI BRAF Inhibitors for the Treatment of Metastatic Melanoma: Clinical
Trials and Mechanisms of Resistance
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID MUTATIONS; SURVIVAL; EFFICACY; THERAPY; CRAF
AB The efficacy of selective BRAF inhibitors has now been established in the 50% of patients with metastatic melanoma whose tumors harbor activating mutations. However, for the vast majority of patients, responses persist for less than a year. In extensive preclinical investigations, researchers have focused on potential resistance mechanisms with the hope of identifying treatment strategies that can overcome resistance. Preliminary results suggest that reactivation of the mitogen-activated protein kinase (MAPK) pathway by several BRAF-independent mechanisms is the predominant pattern. However, MAPK pathway-independent mechanisms also seem to play a potential role. More definitive cataloging of resistance mechanisms in patients' tumor samples is needed as combination regimens are being readied for clinical evaluation. Clin Cancer Res; 18(1); 33-9. (C) 2012 AACR.
C1 [Flaherty, Keith T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, Boston, MA 02114 USA.
[Alcala, Alexander Marzuka] Yale Univ, Sch Med, New Haven, CT USA.
RP Flaherty, KT (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, 55 Fruit St,Yawkey 9E, Boston, MA 02114 USA.
EM kflaherty@partners.org
NR 28
TC 56
Z9 57
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
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD JAN 1
PY 2012
VL 18
IS 1
BP 33
EP 39
DI 10.1158/1078-0432.CCR-11-0997
PG 7
WC Oncology
SC Oncology
GA 871SV
UT WOS:000298758900007
PM 22215904
ER
PT J
AU Azab, F
Azab, AK
Maiso, P
Calimeri, T
Flores, L
Liu, Y
Quang, P
Roccaro, AM
Sacco, A
Ngo, HT
Zhang, Y
Morgan, BL
Carrasco, RD
Ghobrial, IM
AF Azab, Feda
Azab, Abdel Kareem
Maiso, Patricia
Calimeri, Teresa
Flores, Ludmila
Liu, Yang
Phong Quang
Roccaro, Aldo M.
Sacco, Antonio
Ngo, Hai T.
Zhang, Yong
Morgan, Brittany L.
Carrasco, Ruben D.
Ghobrial, Irene M.
TI Eph-B2/Ephrin-B2 Interaction Plays a Major Role in the Adhesion and
Proliferation of Waldenstrom's Macroglobulinemia
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID MULTIPLE-MYELOMA; TYROSINE KINASE; EPH RECEPTORS; TUMOR ANGIOGENESIS;
CELL-MIGRATION; CANCER; CHEMOTAXIS; REQUIRES; DISEASE; TARGET
AB Purpose: The ephrin receptors (Eph) are found in a wide range of cancers and correlate with metastasis. In this study, we characterized the role of Eph-B2 receptor in the interaction of Waldenstrom's macroglobulinemia (WM) cells with the bone marrow microenvironment.
Experimental Design: We screened the activity of different receptor tyrosine kinases in WM patients and found that Eph-B2 was overexpressed compared with control. Also, we tested the expression of ephrin-B2 ligand on endothelial cells and bone marrow stromal cells (BMSC) isolated from WM patients. We then tested the role of Eph-B2/Ephrin-B2 interaction in the adhesion of WM cells to endothelial cells and BMSCs; the cell signaling induced by the coculture in both the WM cells and the endothelial cells; WM cell proliferation, apoptosis, and cell cycle in vitro and tumor progression in vivo; and in angiogenesis.
Results: Eph-B2 receptor was found to be activated in WM patients compared with control, with a 5-fold increase in CD19(+) WM cells, and activated cell adhesion signaling, including focal adhesion kinase, Src, P130, paxillin, and cofilin, but decreased WM cell chemotaxis. Ephrin-B2 ligand was highly expressed on endothelial cells and BMSCs isolated from WM patients and on human umbilical vein endothelial cells and induced signaling in the endothelial cells promoting adhesion and angiogenesis. Blocking of ephrin-B2 or Eph-B2 inhibited adhesion, cytoskeletal signaling, proliferation, and cell cycle in WM cells, which was induced by coculture with endothelial cells and decreased WM tumor progression in vivo.
Conclusion: Ephrin-B2/Eph-B2 axis regulates adhesion, proliferation, cell cycle, and tumor progression in vivo through the interaction of WM with the cells in the bone marrow microenvironment. Clin Cancer Res; 18(1); 91-104. (C) 2011 AACR.
C1 [Azab, Feda; Azab, Abdel Kareem; Maiso, Patricia; Calimeri, Teresa; Flores, Ludmila; Liu, Yang; Phong Quang; Roccaro, Aldo M.; Sacco, Antonio; Ngo, Hai T.; Zhang, Yong; Morgan, Brittany L.; Carrasco, Ruben D.; Ghobrial, Irene M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Ghobrial, IM (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St,Mayer 548A, Boston, MA 02115 USA.
EM irene_ghobrial@dfci.harvard.edu
RI Sacco, Antonio/K-4681-2016;
OI Sacco, Antonio/0000-0003-2945-9416; Maiso, Patricia/0000-0003-3745-1924;
Roccaro, Aldo/0000-0002-1872-5128
FU Kirsch Laboratory for Waldenstrom's Macroglobulinemia; Heje fellowship;
International Waldenstrom's Macroglobulinemia Foundation (IWMF)
FX The work was supported by the Kirsch Laboratory for Waldenstrom's
Macroglobulinemia, the Heje fellowship for WM, and the International
Waldenstrom's Macroglobulinemia Foundation (IWMF).
NR 33
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U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD JAN 1
PY 2012
VL 18
IS 1
BP 91
EP 104
DI 10.1158/1078-0432.CCR-11-0111
PG 14
WC Oncology
SC Oncology
GA 871SV
UT WOS:000298758900012
PM 22010211
ER
PT J
AU Schroen, AT
Petroni, GR
Wang, HK
Thielen, MJ
Gray, R
Benedetti, J
Wang, XFF
Sargent, DJ
Wickerham, DL
Cronin, W
Djulbegovic, B
Slingluff, CL
AF Schroen, Anneke T.
Petroni, Gina R.
Wang, Hongkun
Thielen, Monika J.
Gray, Robert
Benedetti, Jacqueline
Wang, Xiaofei F.
Sargent, Daniel J.
Wickerham, Donald L.
Cronin, Walter
Djulbegovic, Benjamin
Slingluff, Craig L., Jr.
TI Achieving Sufficient Accrual to Address the Primary Endpoint in Phase
III Clinical Trials from US Cooperative Oncology Groups
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIALS; THERAPY EVALUATION PROGRAM; TIME;
RECRUITMENT
AB Purpose: Assessing impact of poor accrual on premature trial closure requires a relevant metric. We propose defining accrual sufficiency on apparent ability to address primary endpoints (PE) rather than attaining accrual targets.
Experimental Design: All phase III trials open January 1, 1993, to December 31, 2002, by five U.S. oncology Clinical Trials Cooperative Groups (CTCG) were evaluated for accrual sufficiency and scientific results. Sufficient accrual included meeting accrual target, CTCGs documentation attesting adequate accrual, or conclusive results at interim analysis; insufficient accrual included poor accrual as cited closure reason or other reasons rendering a trial unable to address its primary endpoints. Closure rates based on our accrual sufficiency definition are compared with rates of meeting accrual targets and addressing the primary endpoints. A percentage of target accrual above which trials commonly answer the intended scientific question was identified to serve as an alternative to meeting full target accrual in designating accrual success.
Results: Of 238 eligible trials, 158 (66%) closed with sufficient accrual. Among 80 trials with insufficient accrual, 70 (29%) closed specifically because of poor accrual. Inadequate accrual rates are overemphasized when defining accrual success solely by meeting accrual targets. Nearly 75% of trials conclusively addressed the primary endpoints with positive results in 39% of trials. Exceeding 80% of target accrual serves as a reliable proxy for answering the intended scientific question.
Conclusions: Approximately one third of phase III trials closed with insufficient accrual to address the primary endpoints, primarily due to poor accrual. Defining accrual sufficiency broader than meeting accrual targets represents a fairer account of trial closures. Clin Cancer Res; 18(1); 256-62. (C)2011 AACR.
C1 [Schroen, Anneke T.; Thielen, Monika J.; Slingluff, Craig L., Jr.] Univ Virginia, Dept Surg, Charlottesville, VA 22908 USA.
[Schroen, Anneke T.; Petroni, Gina R.; Wang, Hongkun] Univ Virginia, Dept Publ Hlth Sci, Charlottesville, VA 22908 USA.
[Gray, Robert] Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA.
[Benedetti, Jacqueline] SW Oncol Grp Stat Ctr, Seattle, WA USA.
[Wang, Xiaofei F.] Duke Univ, Dept Biostat & Bioinformat, Durham, NC USA.
[Sargent, Daniel J.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Wickerham, Donald L.; Cronin, Walter] Natl Surg Adjuvant Breast & Bowel Project Operati, Pittsburgh, PA USA.
[Djulbegovic, Benjamin] Univ S Florida, Dept Med, Tampa, FL USA.
RP Schroen, AT (reprint author), Univ Virginia, Dept Surg, POB 800709, Charlottesville, VA 22908 USA.
EM ats2x@virginia.edu
RI Djulbegovic, Benjamin/I-3661-2012;
OI Djulbegovic, Benjamin/0000-0003-0671-1447; Sargent,
Daniel/0000-0002-2684-4741
FU NIH [R01 CA118232]; Public Health Service from the National Cancer
Institute, Department of Health and Human Services [U10CA-12027,
U10CA-69974, U10CA-37377, U10CA-69651, U10CA-25224, U24CA-114732]
FX This work was supported by a grant from the NIH (R01 CA118232) to A.T.
Schroen and, in part, by Public Health Service grants U10CA-12027,
U10CA-69974, U10CA-37377, U10CA-69651, U10CA-25224, and U24CA-114732
from the National Cancer Institute, Department of Health and Human
Services.
NR 19
TC 17
Z9 17
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 JAN 1
PY 2012
VL 18
IS 1
BP 256
EP 262
DI 10.1158/1078-0432.CCR-11-1633
PG 7
WC Oncology
SC Oncology
GA 871SV
UT WOS:000298758900027
PM 21976533
ER
PT J
AU Desai, NR
Giugliano, RP
AF Desai, Nihar R.
Giugliano, Robert P.
TI Can We Predict Outcomes in Atrial Fibrillation?
SO CLINICAL CARDIOLOGY
LA English
DT Review
ID ACUTE MYOCARDIAL-INFARCTION; CONGESTIVE-HEART-FAILURE; SICK SINUS
SYNDROME; VENTRICULAR SYSTOLIC DYSFUNCTION; PARKINSON-WHITE SYNDROME;
PROGNOSTIC-SIGNIFICANCE; CARDIOVASCULAR EVENTS; RHYTHM CONTROL;
UNITED-STATES; RISK
AB Atrial fibrillation (AF) is the most common arrhythmia encountered by generalists and cardiologists alike. Much of the attendant morbidity from AF arises from systemic embolic complications which are effectively reduced with utilization of anti-platelet and/or anticoagulant therapy. The systemic embolic complications of AF and the medical therapy to attenuate these risks are very well established. Through the course of this review, we aim to highlight the complex relationship between AF and other, non-embolic outcomes. The presence of AF has been demonstrated to be associated with a 1.5 to 2-fold increase in mortality across numerous observational cohorts. Still further, AF frequently coexists with heart failure, whether as a causative factor or a consequence of underlying structural heart disease or neurohumoral derangement, where its presence is associated with worse clinical outcomes. Whether AF is an independent risk factor for acute coronary syndromes (ACS) remains controversial, though its occurrence in patients with ACS has been shown to be associated with adverse outcomes both in observational cohorts as well as clinical trial populations. Individuals with AF have a 1.5 to 3-fold increase in the rate of hospitalization and are at elevated risk for other arrhythmic disorders including both bradyarrhythmias as well as tachyarrhythmias. AF leads to considerable morbidity and mortality for patients and exacts a tremendous financial toll on the healthcare systemestimated to range from $6.0 to $26.0 billion. Given the current demographic transition in developed countries, the prevalence of AF will continue to increase and the need for refined approaches to risk stratification and pharmacotherapeutic interventions to attenuate the burden on patients will only become more important.
C1 [Desai, Nihar R.; Giugliano, Robert P.] Harvard Univ, Brigham & Womens Hosp, Div Cardiovasc Med, Dept Med,Med Sch, Boston, MA 02115 USA.
RP Giugliano, RP (reprint author), TIMI Study Grp, 350 Longwood Ave,1st Floor, Boston, MA 02115 USA.
EM rgiugliano@partners.org
FU Sanofi Aventis; Daiichi-Sankyo, Merck
FX N.R. Desai and R. P. Giugliano received an honorarium through an
educational grant from Sanofi Aventis for their time and expertise spent
writing this article. R. P. Giugliano has also received research grant
support and honoraria for CME lectures/consulting services from
Daiichi-Sankyo, Merck. He has also received honoraria for CME lectures
from Bristol Myers Squibb.
NR 36
TC 2
Z9 2
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0160-9289
J9 CLIN CARDIOL
JI Clin. Cardiol.
PD JAN
PY 2012
VL 35
SU 1
BP S10
EP S14
DI 10.1002/clc.20989
PG 5
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 875ZU
UT WOS:000299076800003
ER
PT J
AU Apple, FS
Blankenberg, S
Morrow, DA
AF Apple, Fred S.
Blankenberg, Stefan
Morrow, David A.
TI Impact of Biomarkers, Proteomics, and Genomics in Cardiovascular Disease
Introduction
SO CLINICAL CHEMISTRY
LA English
DT Editorial Material
C1 [Apple, Fred S.] Hennepin Cty Med Ctr, Minneapolis, MN 55415 USA.
[Apple, Fred S.] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
[Blankenberg, Stefan] Univ Med Ctr Hamburg Eppendorf, Univ Heart Ctr, Dept Gen & Intervent Cardiol, Hamburg, Germany.
[Morrow, David A.] Brigham & Womens Hosp, Dept Med, TIMI Study Grp, Boston, MA 02115 USA.
[Morrow, David A.] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, Boston, MA 02115 USA.
RP Apple, FS (reprint author), Hennepin Cty Med Ctr, Clin Labs P4,701 Pk Ave, Minneapolis, MN 55415 USA.
EM apple004@umn.edu
NR 28
TC 3
Z9 3
U1 0
U2 6
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 1
EP 2
DI 10.1373/clinchem.2011.175919
PG 2
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700001
PM 22125299
ER
PT J
AU Ho, JE
Wang, TJ
AF Ho, Jennifer E.
Wang, Thomas J.
TI Growth Differentiation Factor 15: A Canary in a Coal Mine?
SO CLINICAL CHEMISTRY
LA English
DT Editorial Material
ID CARDIOVASCULAR DYSFUNCTION; BETA SUPERFAMILY; DISEASE; ACTIVATION;
MARKER; MEMBER; HEART; RISK
C1 [Ho, Jennifer E.; Wang, Thomas J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP Wang, TJ (reprint author), Massachusetts Gen Hosp, Div Cardiol, GRB 800,55 Fruit St, Boston, MA 02114 USA.
EM tjwang@partners.org
OI Ho, Jennifer/0000-0002-7987-4768
FU NHLBI NIH HHS [R01-HL083197, R01-HL086875, R01-HL098283, R01-HL102780,
R01 HL102780, R01 HL083197, R01 HL086875, R01 HL098283]; NIDDK NIH HHS
[R01 DK081572, R01-DK081572]
NR 17
TC 6
Z9 6
U1 0
U2 1
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 3
EP 5
DI 10.1373/clinchem.2011.175406
PG 3
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700002
PM 22065154
ER
PT J
AU Apple, FS
Morrow, DA
AF Apple, Fred S.
Morrow, David A.
TI Delta Cardiac Troponin Values in Practice: Are We Ready to Move
Absolutely Forward to Clinical Routine?
SO CLINICAL CHEMISTRY
LA English
DT Editorial Material
ID ACUTE MYOCARDIAL-INFARCTION; I ASSAY; CORONARY SYNDROME;
EARLY-DIAGNOSIS; DEFINITION; ISCHEMIA; OUTCOMES; RISK
C1 [Apple, Fred S.] Hennepin Cty Med Ctr, Minneapolis, MN 55415 USA.
[Apple, Fred S.] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
[Morrow, David A.] Brigham & Womens Hosp, Dept Med, TIMI Study Grp, Boston, MA 02115 USA.
[Morrow, David A.] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, Boston, MA 02115 USA.
RP Apple, FS (reprint author), Hennepin Cty Med Ctr, Clinical Labs P4,701 Pk Ave, Minneapolis, MN 55415 USA.
EM apple004@umn.edu
NR 14
TC 14
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U1 0
U2 2
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 8
EP 10
DI 10.1373/clinchem.2011.175414
PG 3
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700004
PM 22125300
ER
PT J
AU Apple, FS
Morrow, D
Zaugg, C
Hickey, D
Zaharik, M
Blackwood, JJ
Jakobsen, K
AF Apple, Fred S.
Morrow, David
Zaugg, Christian
Hickey, David
Zaharik, Michelle
Blackwood, John J.
Jakobsen, Kirsten
TI The Challenges and Concerns Companies Face Pertaining to the US Food and
Drug Administration 510(k) Process for Cardiac Biomarkers
SO CLINICAL CHEMISTRY
LA English
DT Editorial Material
C1 [Apple, Fred S.] Hennepin Cty Med Ctr, Minneapolis, MN 55415 USA.
[Apple, Fred S.] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA.
[Morrow, David] Brigham & Womens Hosp, Dept Med, TIMI Study Grp, Boston, MA 02115 USA.
[Morrow, David] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, Boston, MA 02115 USA.
[Hickey, David] Roche Diagnost, Med & Sci Affairs, Rotkreuz, Switzerland.
[Hickey, David] Siemens Healthcare Diagnost, Chem Immunoassay & Automat Business Unit, Tarrytown, NY USA.
[Zaharik, Michelle] Response Biomed, Prod Dev, Vancouver, BC, Canada.
[Blackwood, John J.] Beckman Coulter, Prod Management, Chaska, MN USA.
[Jakobsen, Kirsten] Radiometer Med, Copenhagen, Denmark.
RP Apple, FS (reprint author), Hennepin Cty Med Ctr, Clinical Labs P4,701 Pk Ave, S Minneapolis, MN 55415 USA.
EM apple004@umn.edu
NR 0
TC 4
Z9 4
U1 0
U2 2
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 31
EP 38
DI 10.1373/clinchem.2011.165860
PG 8
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700009
PM 22096032
ER
PT J
AU Gilstrap, LG
Wang, TJ
AF Gilstrap, Lauren G.
Wang, Thomas J.
TI Biomarkers and Cardiovascular Risk Assessment for Primary Prevention: An
Update
SO CLINICAL CHEMISTRY
LA English
DT Review
ID C-REACTIVE PROTEIN; CORONARY-HEART-DISEASE; NATRIURETIC PEPTIDE LEVELS;
HIGHLY SENSITIVE ASSAY; PHOSPHOLIPASE A(2); ARTERY-DISEASE; INDEPENDENT
PREDICTOR; ATHEROSCLEROSIS RISK; MULTIPLE BIOMARKERS; ROC CURVE
AB BACKGROUND: Interest in cardiovascular biomarkers in primary prevention has increased dramatically in the past decade. This increase has been fueled by an improved understanding of cardiovascular pathophysiology, as well as novel technologies for biomarker identification.
CONTENT: In this review we provide a brief overview of recent concepts in the evaluation of screening biomarkers, because biomarkers may behave differently when used for screening as opposed to diagnosis or disease staging. The following specific biomarker examples are then discussed, with a focus on data from primary prevention studies: high-sensitivity C-reactive protein, B-type natriuretic peptide, lipoprotein-associated phospholipase A2, and high-sensitivity troponin T. The article concludes by addressing novel platforms for biomarker discovery, reviewing recent examples from the field of metabolomics.
SUMMARY: An ongoing challenge is to develop screening strategies that can identify individuals at risk for cardiovascular events well before symptoms appear. For this purpose, the measurement of soluble biomarkers could be an important adjunct to traditional cardiovascular risk assessment. Recent studies highlight both the strengths and limitations of "novel" circulating biomarkers, and suggest that substantial work is still needed to identify biomarkers that are sufficiently accurate and cost-effective for routine use in primary prevention. (C) 2011 American Association for Clinical Chemistry
C1 [Gilstrap, Lauren G.; Wang, Thomas J.] Harvard Univ, Div Cardiol, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
[Gilstrap, Lauren G.; Wang, Thomas J.] Harvard Univ, Dept Med, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
RP Wang, TJ (reprint author), Harvard Univ, Div Cardiol, Massachusetts Gen Hosp, Sch Med, GRB 800, Boston, MA 02114 USA.
EM tjwang@partners.org
FU NIH [R01-HL086875, R01-HL102780, R01-DK081572, R01-HL098283,
R01-HL083197]; Diasorin; Brahms; Critical Diagnostics; Singulex; Siemens
Healthcare Diagnostics; Roche Diagnostics
FX T.J. Wang, NIH R01-HL086875, R01-HL102780, R01-DK081572, R01-HL098283,
and R01-HL083197; Diasorin; Brahms; Critical Diagnostics; Singulex;
Siemens Healthcare Diagnostics; and Roche Diagnostics.
NR 77
TC 38
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U1 2
U2 16
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 72
EP 82
DI 10.1373/clinchem.2011.165712
PG 11
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700016
PM 22125305
ER
PT J
AU Schnabel, RB
Baccarelli, A
Lin, HH
Ellinor, PT
Benjamin, EJ
AF Schnabel, Renate B.
Baccarelli, Andrea
Lin, Honghuang
Ellinor, Patrick T.
Benjamin, Emelia J.
TI Next Steps in Cardiovascular Disease Genomic Research-Sequencing,
Epigenetics, and Transcriptomics
SO CLINICAL CHEMISTRY
LA English
DT Review
ID CORONARY-ARTERY-DISEASE; SINGLE-NUCLEOTIDE POLYMORPHISMS; COPY NUMBER
VARIANTS; DNA METHYLATION; GENE-EXPRESSION; MYOCARDIAL-INFARCTION; WIDE
ASSOCIATION; HEART-FAILURE; CHROMATIN MODIFICATIONS; CARDIAC-HYPERTROPHY
AB BACKGROUND: Genomic research in cardiovascular disease (CVD) has progressed rapidly over the last 5 years. In most cases, however, these groundbreaking observations have not yet been accompanied by clinically applicable tools for risk prediction, diagnosis, or therapeutic interventions.
CONTENT: We reviewed the scientific literature published in English for novel methods and promising genomic targets that would permit large-scale screening and follow-up of recent genomic findings for CVD. We anticipate that advances in 3 key areas will be critical for the success of these projects. First, exome-centered and whole-genome next-generation sequencing will identify rare and novel genetic variants associated with CVD and its risk factors. Improvements in methods will also greatly advance the field of epigenetics and gene expression in humans. Second, research is increasingly acknowledging that static DNA sequence variation explains only a fraction of the inherited phenotype. Therefore, we expect that multiple epigenetic and gene expression signatures will be related to CVD in experimental and clinical settings. Lever-aging existing large-scale consortia and clinical biobanks in combination with electronic health records holds promise for integrating epidemiological and clinical genomics data. Finally, a systems biology approach will be needed to integrate the accumulated multidimensional data.
SUMMARY: Novel methods in sequencing, epigenetics, and transcriptomics, plus unprecedented large-scale cooperative efforts, promise to generate insights into the complexity of CVD. The rapid accumulation and integration of knowledge will shed light on a considerable proportion of the missing heritability for CVD. (C) 2011 American Association for Clinical Chemistry
C1 [Schnabel, Renate B.] Univ Heart Ctr Hamburg, Dept Gen & Intervent Cardiol, Hamburg, Germany.
[Baccarelli, Andrea] Harvard Univ, Sch Publ Hlth, Lab Environm Epigenet, Exposure Epidemiol & Risk Program, Boston, MA 02115 USA.
[Lin, Honghuang; Benjamin, Emelia J.] NHLBI, Framingham, MA USA.
[Lin, Honghuang; Benjamin, Emelia J.] Boston Univ Framingham Heart Study, Framingham, MA USA.
[Lin, Honghuang] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Cardiol Sect, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Prevent Med Sect, Boston, MA 02118 USA.
RP Schnabel, RB (reprint author), Univ Heart Ctr Hamburg, Dept Gen & Intervent Cardiol, Hamburg, Germany.
EM schnabelr@gmx.de
RI Schnabel, Renate/F-6527-2014;
OI Lin, Honghuang/0000-0003-3043-3942; Baccarelli,
Andrea/0000-0002-3436-0640; Benjamin, Emelia/0000-0003-4076-2336
FU Evans Center for Interdisciplinary Biomedical Research ARC on "Atrial
Fibrillation at Boston University"; Deutsche Forschungsgemeinschaft
(German Research Foundation) [SCHN 1149/3-1]; National Institute of
Environmental Health Sciences [P30ES000002, R21ES019773, R01ES015172];
NIH [1R01HL092577, 5R21DA027021, 5R01HL104156, 1K24HL105780,
1RC1HL101056, 1R01HL102214, 1R01AG028321]
FX Evans Center for Interdisciplinary Biomedical Research ARC on "Atrial
Fibrillation at Boston University"
(http://www.bumc.bu.edu/evanscenteribr/). R. Schnabel, Deutsche
Forschungsgemeinschaft (German Research Foundation) Emmy Noether Program
SCHN 1149/3-1; A. Baccarelli, National Institute of Environmental Health
Sciences grants P30ES000002, R21ES019773, and R01ES015172; P. Ellinor,
NIH grants 1R01HL092577, 5R21DA027021, 5R01HL104156, and 1K24HL105780;
E. Benjamin, NIH grants 1R01HL092577, 1RC1HL101056, 1R01HL102214, and
1R01AG028321.
NR 100
TC 28
Z9 29
U1 1
U2 18
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 113
EP 126
DI 10.1373/clinchem.2011.170423
PG 14
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700020
PM 22100807
ER
PT J
AU van Kimmenade, RRJ
Januzzi, JL
AF van Kimmenade, Roland R. J.
Januzzi, James L., Jr.
TI Emerging Biomarkers in Heart Failure
SO CLINICAL CHEMISTRY
LA English
DT Review
ID BRAIN NATRIURETIC PEPTIDE; CELL DISTRIBUTION WIDTH;
GELATINASE-ASSOCIATED LIPOCALIN; GROWTH-DIFFERENTIATION FACTOR-15;
EXTRACELLULAR-MATRIX TURNOVER; ACUTE MYOCARDIAL-INFARCTION;
HIGH-SENSITIVITY TROPONIN; LONG PENTRAXIN PTX3; FAMILY-MEMBER ST2; RISK
STRATIFICATION
AB BACKGROUND: Until recently, biomarker testing in heart failure (HF) syndromes has been viewed as an elective supplement to diagnostic evaluation of patients suspected to suffer from this condition. This approach to the use of biomarker testing contrasts with other cardiovascular diagnoses such as acute myocardial infarction, for which biomarkers are integral to disease process definition, risk stratification, and in some cases treatment decision making.
CONTENT: In this review we consider various perspectives on the evaluation of biomarkers in HF. In addition, we examine recent advances in the understanding of established biomarkers in HF (such as the natriuretic peptides), the elucidation of novel biomarkers potentially useful for the evaluation and management of patients with HF, and the growing understanding of important and relevant comorbidities in HF. We also review candidate biomarkers from a number of classes: (a) myocyte stretch, (b) myocyte necrosis, (c) systemic inflammation, (d) oxidative stress, (e) extracellular matrix turnover, (f) neurohormones, and (g) biomarkers of extracardiac processes, such as renal function.
SUMMARY: Novel applications of established biomarkers of HF as well as elucidation and validation of emerging assays for HF syndromes have collectively led to a growing interest in the more widespread use of such testing in patients affected by the diagnosis. (C) 2011 American Association for Clinical Chemistry
C1 [Januzzi, James L., Jr.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[van Kimmenade, Roland R. J.] Maastricht Univ Med Ctr, Dept Cardiol, Maastricht, Netherlands.
RP Januzzi, JL (reprint author), Massachusetts Gen Hosp, Div Cardiol, Yawkey 5984,55 Fruit St, Boston, MA 02114 USA.
EM JJanuzzi@Partners.org
RI Kimmenade, R.R.J./L-4432-2015
FU Roche; Critical Diagnostics; Siemens
FX J.L. Januzzi, Roche, Critical Diagnostics, and Siemens.
NR 88
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U1 4
U2 16
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 127
EP 138
DI 10.1373/clinchem.2011.165720
PG 12
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700021
PM 22086968
ER
PT J
AU Rhee, EP
Gerszten, RE
AF Rhee, Eugene P.
Gerszten, Robert E.
TI Metabolomics and Cardiovascular Biomarker Discovery
SO CLINICAL CHEMISTRY
LA English
DT Review
ID CORONARY-ARTERY-DISEASE; HEART-DISEASE; RISK; REVEALS; MARKERS;
METABOLISM; EVENTS; PLASMA; BLOOD; TECHNOLOGIES
AB BACKGROUND: Metabolomics, the systematic analysis of low molecular weight biochemical compounds in a biological specimen, has been increasingly applied to biomarker discovery.
CONTENT: Because no single analytical method can accommodate the chemical diversity of the entire metabolome, various methods such as nuclear magnetic resonance spectroscopy (NMR) and mass spectrometry (MS) have been employed, with the latter coupled to an array of separation techniques including gas and liquid chromatography. Whereas NMR can provide structural information and absolute quantification for select metabolites without the use of exogenous standards, MS tends to have much higher analytical sensitivity, enabling broader surveys of the metabolome. Both NMR and MS can be used to characterize metabolite data either in a targeted manner or in a nontargeted, pattern-recognition manner. In addition to technical considerations, careful sample selection and study design are important to minimize potential confounding influences on the metabolome, including diet, medications, and comorbitidies. To this end, metabolite profiling has been applied to human biomarker discovery in small-scale interventions, in which individuals are extremely well phenotyped and able to serve as their own biological controls, as well as in larger epidemiological cohorts. Understanding how metabolites relate to each other and to established risk markers for diseases such as diabetes and renal failure will be important in evaluating the potential value of these metabolites as clinically useful biomarkers.
SUMMARY: Applied to both experimental and epidemiological study designs, metabolite profiling has begun to highlight the breadth metabolic disturbances that accompany human disease. Experimental work in model systems and integration with other functional genomic approaches will be required to establish a causal link between select biomarkers and disease pathogenesis. (C) 2011 American Association for Clinical Chemistry
C1 [Gerszten, Robert E.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Gerszten, Robert E.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Rhee, Eugene P.] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
[Rhee, Eugene P.; Gerszten, Robert E.] Broad Inst, Cambridge, MA USA.
RP Gerszten, RE (reprint author), Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
EM rgerszten@partners.org
FU NIDDK NIH HHS [K08 DK090142, K08 DK090142-02]
NR 36
TC 82
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U1 6
U2 58
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 139
EP 147
DI 10.1373/clinchem.2011.169573
PG 9
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700022
PM 22110018
ER
PT J
AU Kohli, P
Bonaca, MP
Kakkar, R
Kudinova, AY
Scirica, BM
Sabatine, MS
Murphy, SA
Braunwald, E
Lee, RT
Morrow, DA
AF Kohli, Payal
Bonaca, Marc P.
Kakkar, Rahul
Kudinova, Anastacia Y.
Scirica, Benjamin M.
Sabatine, Marc S.
Murphy, Sabina A.
Braunwald, Eugene
Lee, Richard T.
Morrow, David A.
TI Role of ST2 in Non-ST-Elevation Acute Coronary Syndrome in the
MERLIN-TIMI 36 Trial
SO CLINICAL CHEMISTRY
LA English
DT Article
ID FAMILY-MEMBER ST2; ACUTE MYOCARDIAL-INFARCTION; SERUM-SOLUBLE ST2;
HEART-FAILURE; NATRIURETIC PEPTIDE; BIOMARKER ST2; ACUTE DYSPNEA;
RECEPTOR; MORTALITY; PROTEIN
AB OBJECTIVE: We investigated the prognostic performance of ST2 with respect to cardiovascular death (CVD) and heart failure (HF) in patients with non-ST-elevation acute coronary syndrome (NSTE-ACS) in a large multinational trial.
BACKGROUND: Myocytes that are subjected to mechanical stress secrete ST2, a soluble interleukin-1 receptor family member that is associated with HF after STE-ACS.
METHODS: We measured ST2 with a high-sensitivity assay in all available baseline samples (N = 4426) in patients enrolled in the Metabolic Efficiency With Ranolazine for Less Ischemia in the Non-ST-Elevation Acute Coronary Syndrome Thrombolysis in Myocardial Infarction 36 (MERLIN-TIMI 36), a placebo-controlled trial of ranolazine in NSTE-ACS. All events, including cardiovascular death and new or worsening HF, were adjudicated by an independent events committee.
RESULTS: Patients with ST2 concentrations in the top quartile (> 35 mu g/L) were more likely to be older and male and have diabetes and renal dysfunction. ST2 was only weakly correlated with troponin and B-type natriuretic peptide. High ST2 was associated with increased risk for CVD/HF at 30 days (6.6% vs 1.6%, P < 0.0001) and 1 year (12.2% vs 5.2%, P < 0.0001). The risk associated with ST2 was significant after adjustment for clinical covariates and biomarkers (adjusted hazard ratio CVD/HF 1.90, 95% CI 1.15-3.13 at 30 days, P = 0.012; 1.51, 95% CI 1.15-1.98 at 1 year, P = 0.003), with a significant integrated discrimination improvement (P < 0.0001). No significant interaction was found between ST2 and ranolazine (P(interaction) = 0.15). CONCLUSIONS: ST2 correlates weakly with biomarkers of acute injury and hemodynamic stress but is strongly associated with the risk of HF after NSTE-ACS. This biomarker and related pathway merit further investigation as potential therapeutic targets for patients with ACS at risk for cardiac remodeling. (C) 2011 American Association for Clinical Chemistry
C1 [Kohli, Payal] Harvard Univ, Brigham & Womens Hosp, TIMI Study Grp, Cardiovasc Div,Sch Med, Boston, MA 02115 USA.
[Kohli, Payal; Bonaca, Marc P.; Kudinova, Anastacia Y.; Scirica, Benjamin M.; Sabatine, Marc S.; Braunwald, Eugene; Lee, Richard T.; Morrow, David A.] Harvard Univ, Brigham & Womens Hosp, Dept Med, Cardiovasc Div,Sch Med, Boston, MA 02115 USA.
[Kakkar, Rahul] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Kakkar, Rahul] Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Kohli, P (reprint author), Harvard Univ, Brigham & Womens Hosp, TIMI Study Grp, Cardiovasc Div,Sch Med, 75 Francis St, Boston, MA 02115 USA.
EM pkohli@partners.org
FU CV Therapeutics; NIH; Critical Diagnostics; National Heart, Lung, and
Blood Institute [RC1HL099692]
FX CV Therapeutics (acquired by Gilead Pharmaceuticals) provided research
grant support for the MERLIN-TIMI 36 trial. R.T. Lee, NIH; D.A. Morrow,
Critical Diagnostics and National Heart, Lung, and Blood Institute
(award number RC1HL099692); M.S. Sabatine, National Heart, Lung, and
Blood Institute (award number RC1HL099692). Critical Diagnostics
provided reagent for measurement of ST2.
NR 36
TC 46
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U1 2
U2 6
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 257
EP 266
DI 10.1373/clinchem.2011.173369
PG 10
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700039
PM 22096031
ER
PT J
AU Grandin, EW
Jarolim, P
Murphy, SA
Ritterova, L
Cannon, CP
Braunwald, E
Morrow, DA
AF Grandin, E. Wilson
Jarolim, Petr
Murphy, Sabina A.
Ritterova, Lea
Cannon, Christopher P.
Braunwald, Eugene
Morrow, David A.
TI Galectin-3 and the Development of Heart Failure after Acute Coronary
Syndrome: Pilot Experience from PROVE IT-TIMI 22
SO CLINICAL CHEMISTRY
LA English
DT Article
ID MYOCARDIAL-INFARCTION; PROGNOSTIC VALUE; FIBROSIS; MACROPHAGES;
DYSFUNCTION; PREDICTORS; EXPRESSION; MORTALITY; HF
AB BACKGROUND: Galectin-3 is a beta-galactoside-binding lectin that has been implicated in cardiac fibrosis and remodeling, is increased in models of failure-prone hearts, and has prognostic value in patients with heart failure (HF). The relationship between galectin-3 and the development of HF after acute coronary syndrome (ACS) is unknown.
METHODS: In a nested case-control study among patients with ACS in PROVE IT-TIMI 22, we identified 100 cases with a hospitalization for new or worsening HF. Controls were matched (1:1) for age, sex, ACS type, and randomized treatment. Serum galectin-3 was measured at baseline (within 7 days post-ACS).
RESULTS: Patients who developed HF had higher baseline galectin-3 [median 16.7 mu g/L (25th, 75th percentile 14.0, 20.6) vs 14.6 mu g/L (12.0, 17.6), P = 0.004]. Patients with baseline galectin-3 above the median had an odds ratio of 2.1 (95% CI 1.2-3.6) for developing HF, P = 0.010. Galectin-3 showed a graded relationship with risk of HF. Cases were more likely to have hypertension, diabetes, prior MI, and prior HF; after adjustment for these factors, this graded relationship with galectin-3 quartile and HF remained significant [adjusted OR 1.4 (95% CI 1.1-1.9), P = 0.020]. When BNP was added to the model, the relationship between galectin-3 and HF was attenuated [adjusted OR 1.3 (95% CI: 0.96 -1.9), P = 0.08].
CONCLUSIONS: The finding that galectin-3 is associated with the risk of developing HF following ACS adds to emerging evidence supporting galectin-3 as a biomarker of adverse remodeling contributing to HF as well as a potential therapeutic target. (C) 2011 American Association for Clinical Chemistry
C1 [Grandin, E. Wilson] Brigham & Womens Hosp, Dept Med, TIMI Study Grp, Boston, MA 02115 USA.
[Cannon, Christopher P.; Braunwald, Eugene; Morrow, David A.] Brigham & Womens Hosp, Dept Med, Cardiovasc Div, Boston, MA 02115 USA.
[Jarolim, Petr; Ritterova, Lea] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Grandin, EW (reprint author), Brigham & Womens Hosp, Dept Med, TIMI Study Grp, 75 Francis St, Boston, MA 02115 USA.
EM wgrandin1@partners.org
FU Bristol-Myers Squibb/Sankyo
FX The PROVE IT-TIMI 22 trial was supported by Bristol-Myers Squibb/Sankyo.
D.A. Morrow (principal investigator), BG Medicine.
NR 25
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U1 0
U2 5
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 267
EP 273
DI 10.1373/clinchem.2011.174359
PG 7
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700040
PM 22110019
ER
PT J
AU Karakas, M
Januzzi, JL
Hoffmann, U
Koenig, W
AF Karakas, Mahir
Januzzi, James L., Jr.
Hoffmann, Udo
Koenig, Wolfgang
TI Copeptin-A Novel Marker in Acute Myocardial Infarction In Reply
SO CLINICAL CHEMISTRY
LA English
DT Letter
ID SENSITIVITY TROPONIN-T; CHEST-PAIN; RAPID RULE; ELEVATION; ISCHEMIA
C1 [Karakas, Mahir; Koenig, Wolfgang] Univ Ulm, Med Ctr, Dept Internal Med Cardiol 3, D-89081 Ulm, Germany.
[Januzzi, James L., Jr.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Koenig, W (reprint author), Univ Ulm, Med Ctr, Dept Internal Med Cardiol 3, Albert Einstein Allee 23, D-89081 Ulm, Germany.
EM wolfgang.koenig@uniklinik-ulm.de
NR 10
TC 0
Z9 0
U1 1
U2 3
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
J9 CLIN CHEM
JI Clin. Chem.
PD JAN
PY 2012
VL 58
IS 1
BP 309
EP 311
DI 10.1373/clinchem.2011.175422
PG 4
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 875RQ
UT WOS:000299052700049
ER
PT J
AU Hendrickson, RG
McKeown, NJ
AF Hendrickson, Robert G.
McKeown, Nathanael J.
TI Is maternal opioid use hazardous to breast-fed infants?
SO CLINICAL TOXICOLOGY
LA English
DT Editorial Material
DE Opioids; Breast milk; Human milk; Breastfeeding; Analgesics
ID PATIENT-CONTROLLED ANALGESIA; HUMAN-MILK; HUMAN LIVER; CODEINE USE;
METHADONE-MAINTENANCE; NEONATAL-PERIOD; PREGNANT-WOMEN; DRUG-THERAPY;
IN-VITRO; MORPHINE
AB Over the last few decades, the rate of breastfeeding has increased steadily in the developed countries of the world. During this time, opioid use in the general population has steadily increased as well. Despite this, clinicians remain unclear whether opioid use is safe during breastfeeding. While the vast majority of medications used during breastfeeding occur without incident, case reports and studies have reported possible opioid toxicity in breast-fed infants. Multiple enzymes are involved in the metabolism of opioids. CYP2D6 catabolizes O-demethylation of codeine, tramadol, oxycodone, and hydrocodone to more potent metabolites. CYP3A4 inactivates methadone, meperidine, and buprenorphine. Glucoronide conjugation by the UGT enzyme family inactivates morphine and hydromorphone. Genetic polymorphisms and interfering medications affect the maternal metabolism, which in turn determines the exposure and risk to the breast-fed neonate. We review the production of breast milk, the transfer of xenobiotics from blood to milk, the characteristics that alter xenobiotic breast-milk concentrations, and we review the evidence of specific common opioids and infant toxicity. The short-term maternal use of prescription opioids is usually safe and infrequently presents a hazard to the newborn.
C1 [Hendrickson, Robert G.; McKeown, Nathanael J.] Oregon Hlth & Sci Univ, Portland, OR 97219 USA.
[Hendrickson, Robert G.; McKeown, Nathanael J.] Oregon Poison Ctr, Portland, OR USA.
[McKeown, Nathanael J.] Portland VA Med Ctr, Portland, OR USA.
RP Hendrickson, RG (reprint author), Oregon Hlth & Sci Univ, 3181 SW Sam Jackson Pk Rd,Mail Code CB550, Portland, OR 97219 USA.
EM hendriro@ohsu.edu
NR 110
TC 17
Z9 18
U1 3
U2 14
PU INFORMA HEALTHCARE
PI NEW YORK
PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA
SN 1556-3650
J9 CLIN TOXICOL
JI Clin. Toxicol.
PD JAN
PY 2012
VL 50
IS 1
BP 1
EP 14
DI 10.3109/15563650.2011.635147
PG 14
WC Toxicology
SC Toxicology
GA 876RZ
UT WOS:000299126700001
PM 22148986
ER
PT J
AU Marchiori, EJ
Torrente, J
del Blanco, A
Moreno-Ger, P
Sancho, P
Fernandez-Manjon, B
AF Marchiori, Eugenio J.
Torrente, Javier
del Blanco, Angel
Moreno-Ger, Pablo
Sancho, Pilar
Fernandez-Manjon, Baltasar
TI A narrative metaphor to facilitate educational game authoring
SO COMPUTERS & EDUCATION
LA English
DT Article
DE Authoring tools and methods; Serious games; Improving classroom teaching
ID END-USER DEVELOPMENT; DESIGN; COMPUTER
AB In this paper we present WEEV (Writing Environment for Educational Video games), a methodology for educational point-and-click adventure game authoring. Our approach aims to allow educators to actively collaborate in the educational game development process, using a narrative-based representation. WEEV is based on a pragmatic reinterpretation of previous works on narrativity and video games, enhanced by the use of a novel visual language to represent the flow of the story or narrative. The WEEV methodology has been implemented into an actual tool based on the already established < e-Adventure > platform for educational games. This tool was improved with feedback gathered from formative evaluation, end-users testing (i.e. educators), and actual use in the development of an educational game. The system, still under development, presents some user-interaction problems along with a need for the educational effectiveness of the resulting games to be further analyzed. However, this paper highlights that, according to the qualitative results of evaluations, WEEV can indeed be successfully applied to simplify the game creation process and that by using representations of games that educators can understand, WEEV can help provide educational value to games. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Marchiori, Eugenio J.; Torrente, Javier; del Blanco, Angel; Moreno-Ger, Pablo; Sancho, Pilar; Fernandez-Manjon, Baltasar] Univ Complutense, Dept Software Engn & Artificial Intelligence, E-28040 Madrid, Spain.
[Fernandez-Manjon, Baltasar] Harvard Univ, Massachusetts Gen Hosp, Comp Sci Lab, Boston, MA USA.
RP Marchiori, EJ (reprint author), Univ Complutense, Dept Software Engn & Artificial Intelligence, E-28040 Madrid, Spain.
EM emarchiori@fdi.ucm.es; jtorrente@fdi.ucm.es; angel.dba@fdi.ucm.es;
pablom@fdi.ucm.es; pilar@sip.ucm.es; balta@fdi.ucm.es
RI Fernandez-Manjon, Baltasar/A-5281-2011; Moreno-Ger, Pablo/B-5419-2009
OI Fernandez-Manjon, Baltasar/0000-0002-8200-6216; Moreno-Ger,
Pablo/0000-0003-4817-8150
FU Ministry of Education [Movilidad I-D+i PR2010-0070,
TIN2010-21735-C02-02]; Ministry of Industry [TSI-020110-2009-170,
TSI-020312-2009-27]; Complutense University of Madrid; Regional
Government of Madrid [GR35/10-A, S2009/TIC-1650]; PROACTIVE EU
[505469-2009-LLP-ES-KA3-KA3MP]; GALA EU Network of Excellence in serious
games [FP7-ICT-2009-5- 258169]
FX The Ministry of Education (grants Movilidad I-D+i PR2010-0070 and
TIN2010-21735-C02-02) and the Ministry of Industry (grants
TSI-020110-2009-170, TSI-020312-2009-27) have partially supported this
work, as well as the Complutense University of Madrid and the Regional
Government of Madrid (research group GR35/10-A and project e-Madrid
S2009/TIC-1650), and the PROACTIVE EU project
(505469-2009-LLP-ES-KA3-KA3MP) and the GALA EU Network of Excellence in
serious games (FP7-ICT-2009-5- 258169).
NR 36
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Z9 14
U1 5
U2 25
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0360-1315
J9 COMPUT EDUC
JI Comput. Educ.
PD JAN
PY 2012
VL 58
IS 1
BP 590
EP 599
DI 10.1016/j.compedu.2011.09.017
PG 10
WC Computer Science, Interdisciplinary Applications; Education &
Educational Research
SC Computer Science; Education & Educational Research
GA 868LH
UT WOS:000298524300052
ER
PT J
AU Fiedler, SE
Sisson, JH
Wyatt, TA
Pavlik, JA
Gambling, TM
Carson, JL
Carr, DW
AF Fiedler, Sarah E.
Sisson, Joseph H.
Wyatt, Todd A.
Pavlik, Jacqueline A.
Gambling, Todd M.
Carson, Johnny L.
Carr, Daniel W.
TI Loss of ASP but not ROPN1 reduces mammalian ciliary motility
SO CYTOSKELETON
LA English
DT Article
DE ROPN1L; ropporin; A-kinase anchoring protein; OmniBank (R)
ID KINASE ANCHORING PROTEIN; RADIAL SPOKE PROTEIN-3; AIRWAY
EPITHELIAL-CELLS; BEAT FREQUENCY; DEPENDENT PHOSPHORYLATION; FLAGELLAR
MOTILITY; REGULATORY SUBUNIT; BINDING-PROTEIN; FIBROUS SHEATH; CAMP
AB Protein kinase A (PKA) signaling is targeted by interactions with A-kinase anchoring proteins (AKAPs) via a dimerization/docking domain on the regulatory (R) subunit of PKA. Four other mammalian proteins [AKAP-associated sperm protein (ASP), ropporin (ROPN1), sperm protein 17 (SP17) and calcium binding tyrosine-(Y)-phosphorylation regulated protein (CABYR)] share this highly conserved RII dimerization/docking (R2D2) domain. ASP and ROPN1 are 41% identical in sequence, interact with a variety of AKAPs in a manner similar to PKA, and are expressed in ciliated and flagellated human cells. To test the hypothesis that these proteins regulate motility, we developed mutant mouse lines lacking ASP or ROPN1. Both mutant lines produced normal numbers of cilia with intact ciliary ultrastructure. Lack of ROPN1 had no effect on ciliary motility. However, the beat frequency of cilia from mice lacking ASP is significantly slower than wild type, indicating that ASP signaling may regulate ciliary motility. This is the first demonstration of in vivo function for ASP. Similar localization of ASP in mice and humans indicates that these findings may translate to human physiology, and that these mice will be an excellent model for future studies related to the pathogenesis of human disease. (C) 2011 Wiley Periodicals, Inc.
C1 [Fiedler, Sarah E.; Carr, Daniel W.] VA Med Ctr, Portland, OR USA.
[Fiedler, Sarah E.; Carr, Daniel W.] Oregon Hlth & Sci Univ, Dept Med, Portland, OR 97201 USA.
[Sisson, Joseph H.; Wyatt, Todd A.; Pavlik, Jacqueline A.] Univ Nebraska Med Ctr, Dept Internal Med, Pulm Crit Care Sleep & Allergy Div, Durham Res Ctr 2 1046, Omaha, NE USA.
[Gambling, Todd M.; Carson, Johnny L.] Univ N Carolina, Ctr Environm Med Asthma & Lung Biol, Chapel Hill, NC USA.
[Carson, Johnny L.] Univ N Carolina, Dept Pediat, Chapel Hill, NC USA.
RP Carr, DW (reprint author), Portland VA Med Ctr, Mail Code R&D8,3710 SW US Vet Hosp Rd, Portland, OR 97239 USA.
EM carrd@ohsu.edu
FU NIH [HD 36408, 5 R37AA008769-18]; VA Merit Award; Flight Attendant
Medical Research Institute; US Environmental Protection Agency
[CR833463-01]; Center for Environmental Medicine, Asthma, and Lung
Biology at the University of North Carolina at Chapel Hill
FX Funding for this project is provided by NIH Grant HD 36408 (DWC), VA
Merit Award (DWC), NIH Grant 5 R37AA008769-18 (JHS), a Clinical
Innovator Award (JLC) from the Flight Attendant Medical Research
Institute, and the US Environmental Protection Agency (JLC). Although
the research described in this article has been funded wholly or in part
by the US Environmental Protection Agency through cooperative agreement
CR833463-01 with the Center for Environmental Medicine, Asthma, and Lung
Biology at the University of North Carolina at Chapel Hill, it has not
been subjected to the agency's required peer and policy review, and
therefore does not necessarily reflect the views of the agency and no
official endorsement should be inferred. Mention of trade names or
commercial products does not constitute endorsement or recommendation
for use.
NR 39
TC 8
Z9 8
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1949-3584
J9 CYTOSKELETON
JI Cytoskeleton
PD JAN
PY 2012
VL 69
IS 1
BP 22
EP 32
DI 10.1002/cm.20539
PG 11
WC Cell Biology
SC Cell Biology
GA 877DG
UT WOS:000299156500002
PM 22021175
ER
PT J
AU Liu, E
McKeown, NM
Pittas, AG
Meigs, JB
Economos, CD
Booth, SL
Jacques, PF
AF Liu, E.
McKeown, N. M.
Pittas, A. G.
Meigs, J. B.
Economos, C. D.
Booth, S. L.
Jacques, P. F.
TI Predicted 25-hydroxyvitamin D score and change in fasting plasma glucose
in the Framingham offspring study
SO EUROPEAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
DE vitamin D; fasting plasma glucose; Framingham offspring cohort
ID VITAMIN-D SUPPLEMENTATION; PLACEBO-CONTROLLED TRIAL; SERUM
25-HYDROXYVITAMIN-D; INSULIN SENSITIVITY; WOMEN; CALCIUM; EXPRESSION;
RESISTANCE; RECEPTOR; ADULTS
AB Data on the association between vitamin D status and actual change in glycemic measures are limited. We examined the prospective association between a predicted 25-hydroxyvitamin D (25(OH)D) score and change in fasting plasma glucose concentration over a mean follow-up of 7 years, in 2571 men and women (mean age 54 years) without diabetes in the Framingham Offspring Study cohort. After adjustment for age, sex, body mass index and fasting plasma glucose at baseline, higher predicted 25(OH)D score at baseline was associated with a smaller 7-year increase in fasting plasma glucose concentrations (0.23 mmol/l versus 0.35 mmol/l for highest versus lowest tertile of 25(OH)D score, respectively, P-trend = 0.002). Vitamin D status may be an important determinant for change in fasting plasma glucose concentration among middle-aged and older adults without diabetes. European Journal of Clinical Nutrition (2012) 66, 139-141; doi:10.1038/ejcn.2011.181; published online 19 October 2011
C1 [Liu, E.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[McKeown, N. M.; Booth, S. L.; Jacques, P. F.] Tufts Univ, Jean Mayer USDA Human Nutr Res Ctr Aging, Boston, MA 02111 USA.
[McKeown, N. M.; Economos, C. D.; Booth, S. L.; Jacques, P. F.] Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
[Pittas, A. G.] Tufts Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA USA.
[Meigs, J. B.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Meigs, J. B.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Meigs, J. B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
RP Liu, E (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 1633 Tremont St, Boston, MA 02115 USA.
EM eliu@hsph.harvard.edu
FU US Department of Agriculture [58-1950-7-707]; National Heart Lung and
Blood Institute of the National Institutes of Health [N01-HC-25195];
American Diabetes Association; Career Development Award [NIDDK K24
DK080140, R01DK076092, R21DK078867, NIA AG14759]; Beverage Institute for
Health and Wellness
FX We are grateful to the Framingham Study participants and staff. We thank
Gail Rogers, from Jean Mayer USDA Human Nutrition Research Center, for
data management and statistical guidance. The present study was
supported in part by the US Department of Agriculture, under agreement
No. 58-1950-7-707, and the Framingham Heart Study of the National Heart
Lung and Blood Institute of the National Institutes of Health (Contract
No. N01-HC-25195), and by an American Diabetes Association Career
Development Award (JBM), NIDDK K24 DK080140 (JBM), R01DK076092 and
R21DK078867 (AGP), NIA AG14759 (SLB), and the Beverage Institute for
Health and Wellness (CDE).
NR 19
TC 10
Z9 10
U1 1
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0954-3007
J9 EUR J CLIN NUTR
JI Eur. J. Clin. Nutr.
PD JAN
PY 2012
VL 66
IS 1
BP 139
EP 141
DI 10.1038/ejcn.2011.181
PG 3
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 876GE
UT WOS:000299094800021
PM 22009071
ER
PT J
AU Hu, D
Liu, X
Zeng, WY
Weiner, HL
Ritz, J
AF Hu, Dan
Liu, Xia
Zeng, Wanyong
Weiner, Howard L.
Ritz, Jerome
TI A clonal model for human CD8(+) regulatory T cells: Unrestricted
contact-dependent killing of activated CD4(+) T cells
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE CD8+Treg cells; Suppression and cytotoxicity
ID IMMUNOLOGICAL SELF-TOLERANCE; MEDIATED APOPTOSIS; IMMUNE-RESPONSES;
SUPPRESSOR; FOXP3; ANTIGEN; LYMPHOCYTES; MECHANISMS; DISTINCT; DISEASE
AB Previous studies in murine systems have demonstrated that CD8+ Treg cells down-regulate immune responses in vivo through suppressing activated CD4+ T cells. Here we describe novel regulatory CD8+ T-cell clones isolated from healthy human peripheral blood following in vitro stimulation with autologous EpsteinBarr virus (EBV)-specific CD4+ T cells. TCR activation of CD4+ target T cells was required for CD8+ Treg cells to exert suppressive activity, which was mediated through lysis of CD4+ targets in a cell contact-dependent manner. Suppression was independent of Foxp3 expression in CD8+ Treg cells, HLA compatibility between CD8+ Treg cells and CD4+ target cells and antigen-specificity of CD4+ target T cells. CD8+ Treg clones expressed CD3 and a variety of TCR V beta chains as well as CD56, CD69, CD62L and CD95 but did not express CD16, CD161, CXCR4 and CCR7. When used together, antibodies specific for CD11a/CD18 and CD8 inhibited suppressive activity of CD8+ Treg clones. The ability to establish clonal CD8+ T cells that maintain regulatory function in vitro will facilitate further studies to define this population in vivo and to identify the mechanisms used for recognition and suppression of activated target cells.
C1 [Hu, Dan; Liu, Xia; Zeng, Wanyong; Ritz, Jerome] Dana Farber Canc Inst, Div Hematol Malignancies, Canc Vaccine Ctr, Boston, MA 02115 USA.
[Hu, Dan; Weiner, Howard L.; Ritz, Jerome] Harvard Univ, Sch Med, Boston, MA USA.
[Hu, Dan; Weiner, Howard L.] Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA.
RP Ritz, J (reprint author), Dana Farber Canc Inst, Div Hematol Malignancies, Canc Vaccine Ctr, 44 Binney St, Boston, MA 02115 USA.
EM Jerome_Ritz@dfci.harvard.edu
RI Hu, Dan/D-9642-2015;
OI Ritz, Jerome/0000-0001-5526-4669
FU National Institutes of Health [AI29530, CA142106]
FX The authors thank G. Freeman, G. Dranoff, U. von Andrian and H. von
Boehmer for helpful discussions; G. Freeman for reagents; D. Sese for
technical assistance; E. Zorn for technical advice. This research was
supported by grants from the National Institutes of Health (AI29530 and
CA142106 to J. R.).
NR 38
TC 4
Z9 4
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0014-2980
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD JAN
PY 2012
VL 42
IS 1
BP 69
EP 79
DI 10.1002/eji.201141618
PG 11
WC Immunology
SC Immunology
GA 869KK
UT WOS:000298596600009
PM 22002875
ER
PT J
AU Feuchtner, G
Loureiro, R
Bezerra, H
Rocha-Filho, JA
Sarwar, A
Pflederer, T
Marwan, M
Petranovic, M
Raffel, CO
Brady, TB
Jang, IK
Achenbach, S
Cury, RC
AF Feuchtner, Gudrun
Loureiro, Ricardo
Bezerra, Hiram
Rocha-Filho, Jose A.
Sarwar, Ammar
Pflederer, Tobias
Marwan, Mohamed
Petranovic, Milena
Raffel, Christopher O.
Brady, Thomas B.
Jang, Ik-Kyung
Achenbach, Stephan
Cury, Ricardo C.
TI Quantification of coronary stenosis by dual source computed tomography
in patients: A comparative study with intravascular ultrasound and
invasive angiography
SO EUROPEAN JOURNAL OF RADIOLOGY
LA English
DT Article
DE Computed tomography; Coronary stenosis; Quantification; Intravascular
ultrasound; Invasive coronary angiography
ID DIAGNOSTIC-ACCURACY; ARTERY STENOSIS; MULTIDETECTOR CT; DISEASE;
PERFORMANCE; NARROWINGS; LESIONS
AB Objective: To determine the accuracy of dual-source CT (DSCT) to quantify coronary stenosis compared to intravascular ultrasound (IVUS) and quantitative coronary angiography (QCA).
Methods: 21 patients (23 vessels) were examined with DSCT, IVUS and invasive coronary angiography. Coronary minimal luminal diameter (MLD) and area (MLA) were measured in cross-sectional multiplanar reformatted images perpendicular to the vessel long-axis. The vessel cross-sectional area stenosis (MLA/CSA ratio) was calculated. DSCT results were compared with IVUS and QCA.
Results: A good correlation between DSCT and IVUS was noted for diameter and area stenosis (r = 0.69 and r = 0.73), with an overestimation of MLD stenosis by DSCT (+9.1%) and an underestimation of MLA stenosis (-5.8%). For MLD and MLA, high correlation coefficients (r = 0.78 and r = 0.90, respectively) were found between DSCT and IVUS; and the bias was almost zero (-0.41 mm and +0.1 mm(2), respectively). The correlation between DSCT and QCA was moderate (r = 0.60) for MLD stenosis with minor overestimation by DSCT (+4.0%) and moderate (r = 0.59) for MLD (bias, +0.01 mm). The cross-sectional area stenosis showed a moderate correlation (r = 0.59) between DSCT and IVUS (+0.00).
Conclusions: DSCT allows accurate quantification of coronary stenosis as compared to IVUS. An excellent correlation was found for the MLA between DSCT and IVUS. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Feuchtner, Gudrun; Loureiro, Ricardo; Bezerra, Hiram; Rocha-Filho, Jose A.; Sarwar, Ammar; Petranovic, Milena; Brady, Thomas B.; Cury, Ricardo C.] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Feuchtner, Gudrun] Innsbruck Med Univ, Dept Radiol 2, Innsbruck, Austria.
[Pflederer, Tobias; Marwan, Mohamed; Achenbach, Stephan] Univ Erlangen Nurnberg, Div Cardiol, Erlangen, Germany.
[Raffel, Christopher O.; Jang, Ik-Kyung] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA 02115 USA.
[Feuchtner, Gudrun; Cury, Ricardo C.] Baptist Cardiac & Vasc Inst, Cardiovasc MR & CT Program, Miami, FL USA.
RP Cury, RC (reprint author), Baptist Cardiac Vasc Inst, Miami, FL 33156 USA.
EM rcury@baptisthealth.net
FU Pfizer Inc.; New York Cardiac Center
FX This research was partly supported from Pfizer Inc. and the New York
Cardiac Center.
NR 26
TC 15
Z9 18
U1 0
U2 0
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0720-048X
J9 EUR J RADIOL
JI Eur. J. Radiol.
PD JAN
PY 2012
VL 81
IS 1
BP 83
EP 88
DI 10.1016/j.ejrad.2010.12.008
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 876LU
UT WOS:000299109800027
PM 21227613
ER
PT J
AU Lampiris, HW
AF Lampiris, Harry W.
TI Elvitegravir: a once-daily, boosted, HIV-1 integrase inhibitor
SO EXPERT REVIEW OF ANTI-INFECTIVE THERAPY
LA English
DT Article
DE cobicistat; elvitegravir; HIV-1 integrase; integrase drug interactions;
integrase inhibitor; integrase pharmacokinetics; integrase resistance
ID ANTIRETROVIRAL THERAPY; EXPERIENCED PATIENTS; STRAND TRANSFER; IN-VITRO;
RESISTANCE; RALTEGRAVIR; PHARMACOKINETICS; INFECTION; FAILURE; EVOLUTION
AB The development of HIV-1 integrase strand transfer inhibitors (INSTIs) has been a major therapeutic breakthrough in the management of HIV-1 infection. The first HIV-1 integrase inhibitor, raltegravir, was licensed in 2007 and was subsequently approved for use in treatment-naive patients. Since then, newer members of the INSTI class have been developed, including elvitegravir (EVG), which is in advanced clinical development and is being developed for use in both treatment-naive and treatment-experienced patients. EVG utilizes pharmacokinetic boosting to achieve adequate serum levels with once-daily dosing. Boosting agents with which it is being studied include ritonavir and cobicistat. In addition, EVG is being studied as a once-daily INSTI in a coformulated fixed-dose combination pill with the agents tenofovir disoproxil fumarate, emtricitabine and cobicistat (QUAD pill), which has the additional potential benefit of convenient once-daily dosing. The in vitro activity, pharmacokinetic and pharmacodynamic properties, results of Phase I-III clinical trials, resistance profile and drug-drug interactions of EVG will be reviewed in this article.
C1 [Lampiris, Harry W.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Lampiris, Harry W.] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Lampiris, HW (reprint author), Univ Calif San Francisco, San Francisco, CA 94143 USA.
EM harry.lampiris@va.gov
NR 40
TC 11
Z9 12
U1 1
U2 2
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1478-7210
J9 EXPERT REV ANTI-INFE
JI Expert Rev. Anti-Infect. Ther.
PD JAN
PY 2012
VL 10
IS 1
BP 13
EP 20
DI 10.1586/ERI.11.157
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 875ES
UT WOS:000299013800007
PM 22149610
ER
PT J
AU Kang, K
Schmahl, J
Lee, JM
Garcia, K
Patil, K
Chen, A
Keene, M
Murphy, A
Sleeman, MW
AF Kang, Kihwa
Schmahl, Jennifer
Lee, Jong-Min
Garcia, Karen
Patil, Ketan
Chen, Amelia
Keene, Michelle
Murphy, Andrew
Sleeman, Mark W.
TI Mouse ghrelin-O-acyltransferase (GOAT) plays a critical role in bile
acid reabsorption
SO FASEB JOURNAL
LA English
DT Article
DE intestine; ISBT; metabolomics
ID STIMULATES INSULIN-SECRETION; DES-ACYL GHRELIN; BETA-CELLS; FOOD-INTAKE;
RAT ISLETS; ENDOCRINE; GLUCOSE; HORMONE; MICE; PANCREAS
AB Ghrelin is a unique peptide gut hormone that requires post-translational modification to stimulate both feeding and growth hormone release. Ghrelin O-acyltransferase (GOAT) was identified as a specific acyl-transferase for ghrelin, and recent genetic deletion studies of the Goat gene (Goat(-/-)) uncovered the role of ghrelin in the regulation of glucose homeostasis. To further understand the physiological functions of the GOAT/ghrelin system, we have conducted a metabolomic and microarray profile of Goat-null mice, as well as determined Goat expression in different tissues using the lacZ reporter gene. Serum metabolite profile analysis revealed that Goat(-/-) mice exhibited increased secondary bile acids > 2.5-fold. This was attributed to increased mRNA and protein expression of the ileal sodium-dependent bile acid transporter (ISBT) in the intestinal and biliary tract. Increased expression of additional solute carrier proteins, including Slc5a12 (> 10-fold) were also detected in the small intestine and bile duct. Goat staining was consistently observed in the pituitary glands, stomach, and intestines, and to a lesser extent in the gallbladder and pancreatic duct. This is the first report that the GOAT/ghrelin system regulates bile acid metabolism, and these findings suggest a novel function of GOAT in the regulation of intestinal bile acid reabsorption.-Kang, K., Schmahl, J., Lee, J. -M., Garcia, K., Patil, K., Chen, A., Keene, M., Murphy, A., Sleeman, M. W. Mouse ghrelin-O-acyltransferase (GOAT) plays a critical role in bile acid reabsorption. FASEB J. 26, 259-271 (2012). www.fasebj.org
C1 [Kang, Kihwa; Schmahl, Jennifer; Garcia, Karen; Patil, Ketan; Chen, Amelia; Keene, Michelle; Murphy, Andrew; Sleeman, Mark W.] Regeneron Pharmaceut, Tarrytown, NY USA.
[Lee, Jong-Min] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
RP Kang, K (reprint author), Regeneron Pharmaceut Inc, 777 Old Saw Mill River Rd, Tarrytown, NY 10591 USA.
EM kihwa.kang@regeneron.com; mark.sleeman@regeneron.com
NR 43
TC 16
Z9 18
U1 0
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 JAN
PY 2012
VL 26
IS 1
BP 259
EP 271
DI 10.1096/fj.11-191460
PG 13
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 877SF
UT WOS:000299202200027
PM 21965605
ER
PT J
AU Chattergoon, NN
Giraud, GD
Louey, S
Stork, P
Fowden, AL
Thornburg, KL
AF Chattergoon, Natasha N.
Giraud, George D.
Louey, Samantha
Stork, Philip
Fowden, Abigail L.
Thornburg, Kent L.
TI Thyroid hormone drives fetal cardiomyocyte maturation
SO FASEB JOURNAL
LA English
DT Article
DE proliferation; sheep fetus; p21
ID SIGNAL-REGULATED KINASE; CELL-CYCLE ACTIVITY; INTRAUTERINE GROWTH
RESTRICTION; ATRIAL-NATRIURETIC-FACTOR; ACTIVATED PROTEIN-KINASE;
CARDIAC-MUSCLE-CELLS; MEK-ERK PATHWAY; SARCOPLASMIC-RETICULUM;
POSTNATAL-DEVELOPMENT; SHEEP CARDIOMYOCYTES
AB Tri-iodo-L-thyronine (T-3) suppresses the proliferation of near-term serum-stimulated fetal ovine cardiomyocytes in vitro. Thus, we hypothesized that T-3 is a major stimulant of cardiomyocyte maturation in vivo. We studied 3 groups of sheep fetuses on gestational days 125-130 (term similar to 145 d): a T-3-infusion group, to mimic fetal term levels (plasma T-3 levels increased from similar to 0.1 to similar to 1.0 ng/ml; t(1/2) similar to 24 h); a thyroidectomized group, to produce low thyroid hormone levels; and a vehicle-infusion group, to serve as intact controls. At 130 d of gestation, sections of left ventricular freewall were harvested, and the remaining myocardium was enzymatically dissociated. Proteins involved in cell cycle regulation (p21, cyclin D1), proliferation (ERK), and hypertrophy (mTOR) were measured in left ventricular tissue. Evidence that elevated T-3 augmented the maturation rate of cardiomyocytes included 14% increased width, 31% increase in binucleation, 39% reduction in proliferation, 150% reduction in cyclin D1 protein, and 500% increase in p21 protein. Increased expression of phospho-mTOR, ANP, and SERCA2a also suggests that T-3 promotes maturation and hypertrophy of fetal cardiomyocytes. Thyroidectomized fetuses had reduced cell cycle activity and binucleation. These findings support the hypothesis that T-3 is a prime driver of prenatal cardiomyocyte maturation.-Chattergoon, N. N., Giraud, G. D., Louey, S., Stork, P., Fowden, A. L., Thornburg, K. L. Thyroid hormone drives fetal cardiomyocyte maturation FASEB J. 26, 397-408 (2012). www.fasebj.org
C1 [Chattergoon, Natasha N.; Giraud, George D.; Louey, Samantha; Thornburg, Kent L.] Oregon Hlth & Sci Univ, Heart Res Ctr, Portland, OR 97239 USA.
[Giraud, George D.; Thornburg, Kent L.] Oregon Hlth & Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97239 USA.
[Giraud, George D.; Louey, Samantha; Thornburg, Kent L.] Oregon Hlth & Sci Univ, Dept Med, Portland, OR 97239 USA.
[Stork, Philip] Oregon Hlth & Sci Univ, Vollum Inst, Portland, OR 97239 USA.
[Giraud, George D.] Portland VA Med Ctr, Portland, OR USA.
[Fowden, Abigail L.] Univ Cambridge, Physiol Lab, Dept Physiol Dev & Neurosci, Cambridge CB2 3EG, England.
RP Thornburg, KL (reprint author), Oregon Hlth & Sci Univ, Heart Res Ctr, 3303 SW Bond Ave,CH15H, Portland, OR 97239 USA.
EM thornbur@ohsu.edu
FU U.S. National Institute of Child Health and Human Development [P01 HD
34430]; National Heart, Lung, and Blood Institute (NHLBI) [R21 HL093617,
T32HL094294]; National Institutes of Health [R01 HL102763]
FX The authors thank Mr. Robert Webber and Ms. Loni Socha for excellent
technical assistance. The authors appreciate support from the M. Lowell
Edwards Endowment. This study was supported by funds from U.S. National
Institute of Child Health and Human Development grant P01 HD 34430,
National Heart, Lung, and Blood Institute (NHLBI) grant R21 HL093617,
and National Institutes of Health grant R01 HL102763. N.N.C. was
supported by NHLBI training grant T32HL094294.
NR 91
TC 37
Z9 38
U1 1
U2 10
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 JAN
PY 2012
VL 26
IS 1
BP 397
EP 408
DI 10.1096/fj.10-179895
PG 12
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 877SF
UT WOS:000299202200039
PM 21974928
ER
PT J
AU He, AB
Shen, XH
Ma, Q
Cao, JJ
von Gise, A
Zhou, PZ
Wang, G
Marquez, VE
Orkin, SH
Pu, WT
AF He, Aibin
Shen, Xiaohua
Ma, Qing
Cao, Jingjing
von Gise, Alexander
Zhou, Pingzhu
Wang, Gang
Marquez, Victor E.
Orkin, Stuart H.
Pu, William T.
TI PRC2 directly methylates GATA4 and represses its transcriptional
activity
SO GENES & DEVELOPMENT
LA English
DT Article
DE epigenetics; heart development; polycomb complex; transcriptional
regulation
ID HISTONE METHYLTRANSFERASE ACTIVITY; H3 LYSINE-27 METHYLATION;
STEM-CELLS; POLYCOMB; EZH2; DIFFERENTIATION; ACETYLATION; PROTEIN;
GENOME; HEART
AB Polycomb-repressive complex 2 (PRC2) promotes tissue-specific differentiation by depositing trimethylated histone H3 Lys 27 (H3K27me3) epigenetic marks to silence ectopic gene expression programs. Here, we show that EZH2, the catalytic subunit of PRC2, is required for cardiac morphogenesis. Both in vitro and in fetal hearts, EZH2 interacted with cardiac transcription factor GATA4 and directly methylated it at Lys 299. PRC2 methylation of GATA4 attenuated its transcriptional activity by reducing its interaction with and acetylation by p300. Our results reveal a new mechanism of PRC2-mediated transcriptional repression in which PRC2 methylates a transcription factor to inhibit its transcriptional activity.
C1 [He, Aibin; Ma, Qing; Cao, Jingjing; von Gise, Alexander; Zhou, Pingzhu; Wang, Gang; Pu, William T.] Harvard Univ, Sch Med, Dept Cardiol, Childrens Hosp Boston, Boston, MA 02115 USA.
[He, Aibin; Shen, Xiaohua; Ma, Qing; Cao, Jingjing; von Gise, Alexander; Zhou, Pingzhu; Wang, Gang; Orkin, Stuart H.; Pu, William T.] Harvard Univ, Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
[Shen, Xiaohua; Orkin, Stuart H.] Harvard Univ, Sch Med, Dept Pediat Oncol, Dana Farber Canc Inst,Childrens Hosp Boston, Boston, MA 02115 USA.
[Marquez, Victor E.] NCI, Biol Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA.
[Orkin, Stuart H.] Howard Hughes Med Inst, Boston, MA 02115 USA.
RP Pu, WT (reprint author), Harvard Univ, Sch Med, Dept Cardiol, Childrens Hosp Boston, Boston, MA 02115 USA.
EM wpu@enders.tch.harvard.edu
RI Zhou, Pingzhu/J-2809-2014
FU National Institutes of Health (NIH) [U01HL098166, R01HL095712]; American
Heart Association; NIDDK; NIH, National Cancer Institute, and Center for
Cancer Research
FX This work was supported by funding from the National Institutes of
Health (NIH) (U01HL098166 and R01HL095712 to W.T.P.) and the American
Heart Association (post-doctoral fellowship to A. H.); by charitable
donations from Edward Marram, Karen Carpenter, and Gail Federici Smith;
and by a Center of Excellence Award in Molecular Hematology from the
NIDDK to S.H.O., an Investigator of the HHMI. This research was
supported in part by the Intramural Research Program of the NIH,
National Cancer Institute, and Center for Cancer Research. Mass
spectrometry analysis was performed by the Proteomics Center at
Children's Hospital Boston.
NR 34
TC 72
Z9 78
U1 3
U2 23
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 0890-9369
J9 GENE DEV
JI Genes Dev.
PD JAN 1
PY 2012
VL 26
IS 1
BP 37
EP 42
DI 10.1101/gad.173930.111
PG 6
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 877RI
UT WOS:000299199200006
PM 22215809
ER
PT J
AU Calderwood, MS
Ma, A
Khan, YM
Olsen, MA
Bratzler, DW
Yokoe, DS
Hooper, DC
Stevenson, K
Fraser, VJ
Platt, R
Huang, SS
AF Calderwood, Michael S.
Ma, Allen
Khan, Yosef M.
Olsen, Margaret A.
Bratzler, Dale W.
Yokoe, Deborah S.
Hooper, David C.
Stevenson, Kurt
Fraser, Victoria J.
Platt, Richard
Huang, Susan S.
CA CDC Prevention Epictr Program
TI Use of Medicare Diagnosis and Procedure Codes to Improve Detection of
Surgical Site Infections following Hip Arthroplasty, Knee Arthroplasty,
and Vascular Surgery
SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY
LA English
DT Article
ID CARE-ASSOCIATED INFECTIONS; POSTOPERATIVE INFECTIONS; ENHANCED
IDENTIFICATION; ANTIBIOTIC EXPOSURE; SURVEILLANCE; INDICATORS;
HOSPITALS; DISCHARGE; CRITERIA; CLAIMS
AB OBJECTIVE. To evaluate the use of routinely collected electronic health data in Medicare claims to identify surgical site infections (SSIs) following hip arthroplasty, knee arthroplasty, and vascular surgery.
DESIGN. Retrospective cohort study.
SETTING. Four academic hospitals that perform prospective SSI surveillance.
METHODS. We developed lists of International Classification of Diseases, Ninth Revision, and Current Procedural Terminology diagnosis and procedure codes to identify potential SSIs. We then screened for these codes in Medicare claims submitted by each hospital on patients older than 65 years of age who had undergone 1 of the study procedures during 2007. Each site reviewed medical records of patients identified by either claims codes or traditional infection control surveillance to confirm SSI using Centers for Disease Control and Prevention/National Healthcare Safety Network criteria. We assessed the performance of both methods against all chart-confirmed SSIs identified by either method.
RESULTS. Claims-based surveillance detected 1.8-4.7-fold more SSIs than traditional surveillance, including detection of all previously identified cases. For hip and vascular surgery, there was a 5-fold and 1.6-fold increase in detection of deep and organ/space infections, respectively, with no increased detection of deep and organ/space infections following knee surgery. Use of claims to trigger chart review led to confirmation of SSI in 1 out of 3 charts for hip arthroplasty, 1 out of 5 charts for knee arthroplasty, and 1 out of 2 charts for vascular surgery.
CONCLUSION. Claims-based SSI surveillance markedly increased the number of SSIs detected following hip arthroplasty, knee arthroplasty, and vascular surgery. It deserves consideration as a more effective approach to target chart reviews for identifying SSIs. Infect Control Hosp Epidemiol 2012; 33(1):40-49
C1 [Calderwood, Michael S.] Harvard Univ, Sch Med, Dept Populat Med, Boston, MA 02115 USA.
[Calderwood, Michael S.; Platt, Richard] Harvard Pilgrim Healthcare Inst, Boston, MA 02115 USA.
[Ma, Allen; Bratzler, Dale W.] Oklahoma Fdn Med Qual, Oklahoma City, OK USA.
[Khan, Yosef M.; Stevenson, Kurt] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
[Khan, Yosef M.; Stevenson, Kurt] Ohio State Univ, Coll Med, Columbus, OH 43210 USA.
[Olsen, Margaret A.; Fraser, Victoria J.] Washington Univ, Sch Med, St Louis, MO USA.
[Bratzler, Dale W.] Univ Oklahoma, Hlth Sci Ctr, Coll Publ Hlth, Oklahoma City, OK USA.
[Yokoe, Deborah S.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Hooper, David C.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Huang, Susan S.] Univ Calif Irvine, Sch Med, Irvine, CA 92717 USA.
RP Calderwood, MS (reprint author), Harvard Univ, Sch Med, Dept Populat Med, 133 Brookline Ave,6th Floor, Boston, MA 02115 USA.
EM mcalderwood@partners.org
FU Centers for Disease Control and Prevention [1U01CI000344]; Agency for
Healthcare Research and Quality [F32HS018878]
FX Financial support. This study was funded in part by the Centers for
Disease Control and Prevention (Prevention Epicenter Program,
1U01CI000344 [R.P.]). This project was supported by grant F32HS018878
from the Agency for Healthcare Research and Quality (M.S.C.).
NR 23
TC 30
Z9 30
U1 2
U2 8
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0899-823X
J9 INFECT CONT HOSP EP
JI Infect. Control Hosp. Epidemiol.
PD JAN
PY 2012
VL 33
IS 1
BP 40
EP 49
DI 10.1086/663207
PG 10
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 876CP
UT WOS:000299085100008
PM 22173521
ER
PT J
AU Tan, WH
Goldstein, R
Gerrard, P
Ryan, CM
Niewczyk, P
Kowalske, K
Zafonte, R
Schneider, JC
AF Tan, Wei-Han
Goldstein, Richard
Gerrard, Paul
Ryan, Colleen M.
Niewczyk, Paulette
Kowalske, Karen
Zafonte, Ross
Schneider, Jeffrey C.
TI Outcomes and Predictors in Burn Rehabilitation
SO JOURNAL OF BURN CARE & RESEARCH
LA English
DT Article; Proceedings Paper
CT Canadian-Special-Interest-Group Meeting at the 43rd Annual Meeting of
the American-Burn-Association (ABA)
CY MAR 28-APR 01, 2011
CL Chicago, IL
SP Amer Burn Assoc (ABA), Canadian Special Interest Grp
ID SPINAL-CORD-INJURY; FUNCTIONAL INDEPENDENCE MEASURE; LENGTH-OF-STAY;
INPATIENT REHABILITATION; ENVIRONMENTAL-FACTORS; MULTIPLE IMPUTATION;
LIFE SATISFACTION; CLINICAL-RESEARCH; BRAIN-INJURY; HAND BURNS
AB Advances in burn care in recent decades have resulted in a growing population of burn survivors and an increased need for inpatient rehabilitation. Burn survivors who require inpatient rehabilitation typically experience severe and complicated injuries. The purpose of this study is to examine burn rehabilitation outcomes and their predictor variables. Data are obtained from the Uniform Data System for Medical Rehabilitation from 2002 to 2007. Inclusion criterion is primary diagnosis of burn injury. Predictor variables include demographic, medical, and facility data. Outcome measures are length of stay efficiency, FIM (R) gain, community discharge, and FIM (R) discharge of at least 78. Linear and logistic regression analyses are used to determine significant predictors of outcomes. There are 2920 patients who meet inclusion criteria. The mean age of the population is 51 years, 33% of the population is female, 73% is Caucasian, and 40% are married. The median TBSA decile is 20 to 29%. The population exhibits a mean FIM (R) gain of 28 and length of stay efficiency of 2.1. A majority of the population is discharged to the community (76%) and has a FIM (R) discharge of at least 78 (81%). Significant predictors of outcomes in burn rehabilitation include age, FIM (R) admission, onset days, employment status, and marital status. Inpatient rehabilitation is critical to community reintegration of burn survivors. Survivors who are young, married, employed, and higher functioning at the time of admission to rehabilitation demonstrate the best outcomes. This research will help assess the rehabilitation potential of burn survivors and inform resource allocation. (J Burn Care Res 2012;33:110-117)
C1 [Tan, Wei-Han; Goldstein, Richard; Gerrard, Paul; Zafonte, Ross; Schneider, Jeffrey C.] Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Spaulding Rehabil Hosp, Boston, MA 02114 USA.
[Ryan, Colleen M.] Harvard Univ, Sch Med, Sumner Redstone Burn Ctr, Surg Serv,Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Ryan, Colleen M.] Shriners Hosp Children, Boston, MA USA.
[Niewczyk, Paulette] Uniform Data Syst Med Rehabil, Amherst, NY USA.
[Niewczyk, Paulette] Daemen Coll, Hlth Care Studies Dept, Amherst, NY USA.
[Kowalske, Karen] Univ Texas SW Med Ctr Dallas, Dept Phys Med & Rehabil, Dallas, TX 75390 USA.
RP Schneider, JC (reprint author), Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Spaulding Rehabil Hosp, 125 Nashua St, Boston, MA 02114 USA.
OI Gerrard, Paul/0000-0003-0654-5354
NR 31
TC 19
Z9 19
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1559-047X
EI 1559-0488
J9 J BURN CARE RES
JI J. Burn Care Res.
PD JAN-FEB
PY 2012
VL 33
IS 1
BP 110
EP 117
DI 10.1097/BCR.0b013e318234d91a
PG 8
WC Emergency Medicine; Dermatology; Surgery
SC Emergency Medicine; Dermatology; Surgery
GA 877BQ
UT WOS:000299151900022
PM 21941195
ER
PT J
AU Li, WM
Rong, R
Zhao, S
Zhu, XM
Zhang, K
Xiong, X
Yu, XQ
Cui, QH
Li, SQ
Chen, L
Cai, J
Du, J
AF Li, Weiming
Rong, Rong
Zhao, Sheng
Zhu, Xiaoming
Zhang, Ke
Xiong, Xin
Yu, Xueqing
Cui, Qinghua
Li, Shuqiang
Chen, Li
Cai, Jun
Du, Jie
TI Proteomic analysis of metabolic, cytoskeletal and stress response
proteins in human heart failure
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE heart failure; proteomics; metabolism; cytoskeleton; heat shock protein
ID ALPHA-B-CRYSTALLIN; SPONTANEOUSLY HYPERTENSIVE-RATS; FAILING HUMAN
HEARTS; NF-KAPPA-B; DILATED CARDIOMYOPATHY; LIGHT-CHAIN; HYPERTROPHIC
CARDIOMYOPATHY; ISCHEMIA/REPERFUSION INJURY; SHOCK PROTEINS; BCL-2
HOMOLOG
AB Human heart failure is a complex syndrome and a primary cause of morbidity and mortality in the world. However, the molecular pathways involved in the remodelling process are poorly understood. In this study, we performed exhaustive global proteomic surveys of cardiac ventricle isolated from failing and non-failing human hearts, and determined the regulatory pathway to uncover the mechanism underlying heart failure. Two-dimensional gel electrophoresis (2-DE) coupled with tandem mass spectrometry was used to identify differentially expressed proteins in specimens from failing (n = 9) and non-failing (n = 6) human hearts. A total of 25 proteins with at least 1.5-fold change in the failing heart were identified; 15 proteins were up-regulated and 10 proteins were down-regulated. The altered proteins belong to three broad functional categories: (i) metabolic [e.g. NADH dehydrogenase (ubiquinone), dihydrolipoamide dehydrogenase, and the cytochrome c oxidase subunit]; (ii) cytoskeletal (e.g. myosin light chain proteins, troponin I type 3 and transthyretin) and (iii) stress response (e.g. aB-crystallin, HSP27 and HSP20). The marked differences in the expression of selected proteins, including HSP27 and HSP20, were further confirmed by Western blot. Thus, we carried out full-scale screening of the protein changes in human heart failure and profiled proteins that may be critical in cardiac dysfunction for future mapping.
C1 [Li, Weiming; Zhu, Xiaoming; Cai, Jun] Capital Med Univ, Chaoyang Hosp, Dept Cardiol, Minist Educ,Key Lab Remodelling Related Cardiovas, Beijing 100020, Peoples R China.
[Rong, Rong; Yu, Xueqing] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Nephrol, Guangzhou 510275, Guangdong, Peoples R China.
[Zhao, Sheng] Nanjing Med Univ, Affiliated Hosp 1, Dept Cardiac Surg, Nanjing, Peoples R China.
[Zhang, Ke] Tech Univ Munich, German Res Ctr Environm Hlth, Munich, Germany.
[Xiong, Xin] Chongqing Med Univ, Affiliated Hosp 1, Chongqing, Peoples R China.
[Cui, Qinghua] Peking Univ, Hlth Sci Ctr, Dept Biomed Informat, Beijing 100871, Peoples R China.
[Li, Shuqiang] Harvard Univ, Sch Med, Dept Canc Immunol, Boston, MA 02115 USA.
[Li, Shuqiang] Harvard Univ, Sch Med, AIDS, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Chen, Li] Texas Heart Inst, Houston, TX 77025 USA.
[Du, Jie] Capital Med Univ, Beijing Anzhen Hosp, Key Lab Remodelling Related Cardiovasc Dis, Minist Educ, Beijing, Peoples R China.
RP Cai, J (reprint author), Capital Med Univ, Chaoyang Hosp, Dept Cardiol, Minist Educ,Key Lab Remodelling Related Cardiovas, Beijing 100020, Peoples R China.
EM caijun7879@yahoo.com.cn
FU National Science Foundation of China [81050012, 30888004, 30900590];
Beijing Nova Program [2009B39]; Beijing Natural Science Foundation
[7102057]; Scientific Research Foundation for the Returned Overseas
Chinese Scholars, Education Ministry of China
FX This work is supported by grants from the National Science Foundation of
China (Nos. 81050012, 30888004 and 30900590), Beijing Nova Program (No.
2009B39), Beijing Natural Science Foundation (No. 7102057) and the
Scientific Research Foundation for the Returned Overseas Chinese
Scholars, Education Ministry of China.
NR 46
TC 14
Z9 14
U1 0
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1582-1838
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD JAN
PY 2012
VL 16
IS 1
BP 59
EP 71
DI 10.1111/j.1582-4934.2011.01336.x
PG 13
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 869GT
UT WOS:000298586600006
PM 21545686
ER
PT J
AU DePaola, DP
AF DePaola, Dominick P.
TI The Evolution of Dental Education as a Profession, 1936-2011, and the
Role of the Journal of Dental Education
SO JOURNAL OF DENTAL EDUCATION
LA English
DT Article
DE dental education; research; access to care; educational milestones;
future of dental education as a profession; vision; assessment and
outcomes; transformational change
AB This article describes selected changes in dental education from 1936 to 2011 and describes how the Journal of Dental Education (JDE) has assisted in both reporting and, at times, championing change. The review provides a series of selective contextual milestones as a backdrop and running commentary for the changing profession of dental education. An assessment of the current state of knowledge in this field is articulated, as are some of the drivers of change. The article poses a series of questions in seven categories that define the extraordinary opportunities ahead. A vision of the future of the JDE and dental education is described including the use of the journal as a futurist forum to educate, cajole, and advocate for continuous movement toward realizing an enlightened destiny.
C1 [DePaola, Dominick P.] Nova SE Univ, Coll Dent Med, Ft Lauderdale, FL 33328 USA.
[DePaola, Dominick P.] Forsyth Inst, Cambridge, MA USA.
RP DePaola, DP (reprint author), Nova SE Univ, Coll Dent Med, 3200 S Univ Dr, Ft Lauderdale, FL 33328 USA.
EM ddominic@nova.edu
NR 33
TC 4
Z9 4
U1 1
U2 2
PU AMER DENTAL EDUCATION ASSOC
PI WASHINGTON
PA 1400 K STREET, NW, STE 1100, WASHINGTON, DC 20005 USA
SN 0022-0337
J9 J DENT EDUC
JI J. Dent. Educ.
PD JAN
PY 2012
VL 76
IS 1
SI SI
BP 14
EP 27
PG 14
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 876YS
UT WOS:000299144300003
PM 22262546
ER
PT J
AU Ibrahimi, OA
Campbell, T
Youker, S
Eisen, DB
AF Ibrahimi, Omar A.
Campbell, Tracy
Youker, Summer
Eisen, Daniel B.
TI Nonanatomic Free Cartilage Batten Grafting With Second Intention Healing
for Defects on the Distal Nose
SO JOURNAL OF DRUGS IN DERMATOLOGY
LA English
DT Article
ID NASAL ALA; SECONDARY INTENTION; TRANSPOSITION FLAP; RECONSTRUCTION;
REPAIR
AB Background: Defects of the distal nose, particularly the nasal ala, pose a reconstructive challenge due to the lack of loose adjacent tissue and proximity to a free margin.
Objective: We report our experience using nonanatomic free cartilage batten grafts in combination with second intention healing for nasal ala defects.
Methods: A retrospective study of distal nose defects repaired using nonanatomic free cartilage batten grafting with second intention healing was performed. Detailed data on the quality of the scar, post-operative complications, free margin distortion, functional impairments, and patient satisfaction were recorded. Digital images were also shown to an experienced fellowship-trained Mohs surgeon to assess the overall aesthetic outcome using a 5-point score ranging from poor to excellent.
Results: Sixteen subjects were included in the study. Complications were common, but minor. Five (similar to 31%) subjects had subtle contour depressions, three (similar to 18%) subjects had excessive granulation tissue, two (similar to 12%) subjects had post-operative ear pain at the donor site lasting up to 10 days, and one (similar to 6%) subject had a hypertrophic scar at the recipient site. There were two occurrences (similar to 12%) of mild alar notching but no occurrences of significant alar margin distortion or nasal valve dysfunction. In terms of aesthetic outcome, seven (similar to 43%) were assessed by an independent fellowship-trained Mohs surgeon as having excellent aesthetic outcomes, six (similar to 38%) were very good, and three (similar to 19%) were good. All sixteen subjects reported satisfaction on follow-up evaluation.
Conclusions: Nonanatomic free cartilage grafting with second intention healing allows for facile, single-step repair of nasal ala defects with high patient satisfaction and aesthetically pleasing results. This provides an attractive alternative to other flap techniques, skin grafting, and healing via secondary intention.
C1 [Ibrahimi, Omar A.] Univ Connecticut, Dept Dermatol, Farmington, CT USA.
[Ibrahimi, Omar A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Ctr Photomed, Boston, MA USA.
[Eisen, Daniel B.] Univ Calif Davis, Dept Dermatol, Sacramento, CA 95817 USA.
RP Ibrahimi, OA (reprint author), 21 South Rd,2nd Floor, Farmington, CT 06032 USA.
EM omar.ibrahimi@gmail.com
OI Eisen, Daniel/0000-0001-6741-3182
NR 21
TC 5
Z9 5
U1 0
U2 0
PU JOURNAL OF DRUGS IN DERMATOLOGY
PI NEW YORK
PA 377 PARK AVE SOUTH, 6TH FLOOR, NEW YORK, NY 10016 USA
SN 1545-9616
J9 J DRUGS DERMATOL
JI J. Drugs Dermatol.
PD JAN
PY 2012
VL 11
IS 1
BP 46
EP 50
PG 5
WC Dermatology
SC Dermatology
GA 875VE
UT WOS:000299062500006
PM 22206076
ER
PT J
AU Lenehan, G
AF Lenehan, Gail
TI ENA, SUPPORTING EMERGENCY NURSES ON THE FRONT LINES IN 2012
SO JOURNAL OF EMERGENCY NURSING
LA English
DT Editorial Material
C1 [Lenehan, Gail] Emergency Nurses Assoc, Boston, MA USA.
[Lenehan, Gail] Massachusetts Gen Hosp, Emergency Dept, Boston, MA 02114 USA.
RP Lenehan, G (reprint author), Emergency Nurses Assoc, Boston, MA USA.
EM gail.lenehan@gmail.com
NR 2
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 0099-1767
J9 J EMERG NURS
JI J. Emerg. Nurs.
PD JAN
PY 2012
VL 38
IS 1
BP 1
EP 2
DI 10.1016/j.jen.2011.12.003
PG 2
WC Emergency Medicine; Nursing
SC Emergency Medicine; Nursing
GA 878NJ
UT WOS:000299263500001
PM 22226130
ER
PT J
AU Rattner, DW
AF Rattner, David W.
TI Happy Mother's Day
SO JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Editorial Material
DE Women surgeons; SSAT presidential address; Gender and surgery
ID SURGERY; WOMEN
C1 Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
RP Rattner, DW (reprint author), Massachusetts Gen Hosp, Dept Surg, 15 Parkman St, Boston, MA 02114 USA.
EM drattner@partners.org
NR 7
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1091-255X
J9 J GASTROINTEST SURG
JI J. Gastrointest. Surg.
PD JAN
PY 2012
VL 16
IS 1
BP 1
EP 6
DI 10.1007/s11605-011-1656-x
PG 6
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA 873LJ
UT WOS:000298884500001
PM 22065314
ER
PT J
AU Cecchini, S
Correa-Gallego, C
Desphande, V
Ligorio, M
Dursun, A
Wargo, J
Fernandez-del Castillo, C
Warshaw, AL
Ferrone, CR
AF Cecchini, Stefano
Correa-Gallego, Camilo
Desphande, Vikram
Ligorio, Matteo
Dursun, Abdulmetin
Wargo, Jennifer
Fernandez-del Castillo, Carlos
Warshaw, Andrew Louis
Ferrone, Cristina Rosa
TI Superior Prognostic Importance of Perineural Invasion vs. Lymph Node
Involvement After Curative Resection of Duodenal Adenocarcinoma
SO JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Article
DE Duodenal adenocarcinoma; Duodenal cancer; Nodal metastases; Perineural
invasion; Prognosis; Survival; Predictor; Lymph node
ID INTERNATIONAL STUDY-GROUP; PERIAMPULLARY ADENOCARCINOMA; GASTRIC-CANCER;
AXON GUIDANCE; SURVIVAL; DEFINITION; MECHANISMS; CARCINOMA; AMPULLA;
GROWTH
AB Unlike other gastrointestinal tumors, lymph node involvement has not consistently been a negative prognostic factor for survival in patients with duodenal adenocarcinoma. Our aim is to examine prognostic factors in patients who underwent a curative resection of their duodenal adenocarcinoma.
A retrospective review of 169 patients diagnosed with primary duodenal lesions between 1982 and 2010 was performed, of whom 103 were treated with curative intent. Clinico-pathologic factors were evaluated.
A potentially curative resection was performed in 103 patients with a median age of 67 years (range, 22-91). Perineural and lympho-vascular invasion were identified in 30 (29.1%) and 39 patients (37.9%), respectively. Median follow-up was 26.5 months. The 5-year overall survival was 62% vs. 25% for patients with or without nodal metastases (p < 0.001) and 56% vs. 19% for patients with or without perineural invasion (p < 0.001), respectively. Lymph node ratio, type of resection, and size of tumor failed to stratify prognosis. By multivariate analysis, perineural invasion was the most powerful independent predictor of survival (HR, 2.520; CI, 1.361-4.664).
Perineural invasion is a stronger predictor for recurrence and survival than tumor size, depth of infiltration, lymph node involvement, and type of resection in patients with duodenal adenocarcinoma.
C1 [Ferrone, Cristina Rosa] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Gen Surg, Boston, MA 02114 USA.
[Cecchini, Stefano; Correa-Gallego, Camilo; Ligorio, Matteo; Dursun, Abdulmetin; Wargo, Jennifer; Fernandez-del Castillo, Carlos; Warshaw, Andrew Louis; Ferrone, Cristina Rosa] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Desphande, Vikram] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Ferrone, CR (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Gen Surg, 15 Parkman St,WAC 470F, Boston, MA 02114 USA.
EM cferrone@partners.org
RI Cecchini, Stefano/A-3084-2013
OI Cecchini, Stefano/0000-0002-7144-3154
NR 33
TC 13
Z9 14
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1091-255X
J9 J GASTROINTEST SURG
JI J. Gastrointest. Surg.
PD JAN
PY 2012
VL 16
IS 1
BP 113
EP 120
DI 10.1007/s11605-011-1704-6
PG 8
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA 873LJ
UT WOS:000298884500024
PM 22005894
ER
PT J
AU Cowan, J
Makanji, H
Mudgal, C
Jupiter, J
Ring, D
AF Cowan, James
Makanji, Heeren
Mudgal, Chaitanya
Jupiter, Jesse
Ring, David
TI Determinants of Return to Work After Carpal Tunnel Release
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Article
DE Carpal tunnel release; disability; pain anxiety; patient expectations;
work status
ID SURGERY; VALIDATION; PREDICTORS; SINCERITY; INCISION; TRIAL; SCALE; PAIN
AB Purpose The determinants of time to return to work a common measure of treatment effectiveness are incompletely defined. Our primary hypothesis was that employment circumstances are the strongest determinant of earlier return to work. Our secondary hypothesis was that return to work in patients with desk-based jobs is predicted by patient expectations and other psychosocial factors.
Methods We enrolled 65 employed patients with limited incision open carpal tunnel release in a prospective cohort study. Patients completed validated measures of depression, coping strategies, pain anxiety, and job burnout. Heavy lifting was not allowed for I month after surgery. Return to modified and full work duty was recorded in days. Although not specifically an exclusion criterion, none of the patients had a workers' compensation claim or other source of secondary gain.
Results Patients returned to modified duty an average of 11.8 days and full duty at an average of 18.9 days after surgery. Predictors of earlier return to modified duty in multivariate analyses included desk-based work and both the number of days patients expected to take off and the numbers of days they wanted to take off for the entire cohort, with an additional influence from catastrophic thinking in desk-based workers. Predictors of earlier return to full duty in multivariate analyses included desk-based work and number of days patients expected to take off before for the entire cohort, fewer days off desired in non-desk-based workers, fewer days off desired and change in work role in desk-based workers, and lower pain anxiety in part-time workers.
Conclusions The most important determinant of return to full duty work after limited incision open carpal tunnel release is job type, but psychological factors such as patient expectations, catastrophic wthinking, and anxiety in response to pain also have a role. (J Hand Surg 2012;37A:18-27. Copyright (C) 2012 by the American Society for Surgery of the Hand. All rights reserved.)
C1 [Ring, David] Harvard Univ, Sch Med, Massachusetts Gen Hosp,Yawkey Ctr, Hand & Upper Extrem Serv,Dept Orthopaed Surg, Boston, MA 02114 USA.
RP Ring, D (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp,Yawkey Ctr, Hand & Upper Extrem Serv,Dept Orthopaed Surg, Suite 2100,55 Fruit St, Boston, MA 02114 USA.
EM dring@partners.org
FU Wright Medical; AO Foundation; Smith and Nephew; Small Bone Innovations;
Joint Active Systems; Biomet
FX D.R. received support from Wright Medical, the AO Foundation, Smith and
Nephew, Small Bone Innovations, Joint Active Systems, and Biomet.
NR 23
TC 15
Z9 15
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 0363-5023
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD JAN
PY 2012
VL 37A
IS 1
BP 18
EP 27
DI 10.1016/j.jhsa.2011.10.033
PG 10
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 874OI
UT WOS:000298967500005
PM 22137062
ER
PT J
AU ten Berg, PWL
Ring, D
AF ten Berg, Paul W. L.
Ring, David
TI Patients Lost to Follow-Up After Metacarpal Fractures
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Article
DE Metacarpal fracture; non-attendance; follow-up; outpatient clinic
ID SOCIAL DEPRIVATION; NON-ATTENDANCE; HAND
AB Purpose To determine factors associated with non-attendance at scheduled follow-up visits for treatment of metacarpal fractures, to improve subject retention in prospective investigations.
Methods This study included adult patients with metacarpal fractures seen in an outpatient hand clinic between 2004 and 2009. We assessed a number of variables (demographic, social, and injury-specific) that might be associated with failure to return for follow-up. The statistical analysis included both bivariate and multivariable models.
Results In a cohort of 335 patients (228 men and 107 women) with a mean age of 40 years (range, 18-88 y), independent factors associated with non-attendance were unmarried status (single or divorced), having no insurance, having an unemployed or disabled status, having an unknown work status, and having a small finger metacarpal neck fracture.
Conclusions Patients who do not attend a scheduled 1-month follow-up after a single isolated metacarpal fracture are sociologically distinct from those who do attend. (J Hand Surg 2012;37A: 42-46. Copyright (C) 2012 by the American Society for Surgery of the Hand. All rights reserved.)
C1 [Ring, David] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv,Yawkey Ctr, Boston, MA 02114 USA.
RP Ring, D (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv,Yawkey Ctr, Suite 2100,55 Fruit St, Boston, MA 02114 USA.
EM dring@partners.org
NR 15
TC 8
Z9 8
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 0363-5023
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD JAN
PY 2012
VL 37A
IS 1
BP 42
EP 46
DI 10.1016/j.jhsa.2011.08.003
PG 5
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 874OI
UT WOS:000298967500008
PM 22015075
ER
PT J
AU Lichterfeld, M
Yu, XG
AF Lichterfeld, Mathias
Yu, Xu G.
TI The emerging role of leukocyte immunoglobulin-like receptors (LILRs) in
HIV-1 infection
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Review
DE regulatory cell surface molecules; innate cell-mediated immunity;
dendritic cell; immunodeficiency; retroviral/AIDS
ID CLASS-I MOLECULES; PLASMACYTOID DENDRITIC CELLS; INHIBITORY RECEPTOR;
MYELOMONOCYTIC CELLS; CUTTING EDGE; HLA-G; CRYSTAL-STRUCTURE;
T-LYMPHOCYTES; MYELOID CELLS; CTL ESCAPE
AB LILRs represent a group of immunomodulatory molecules that regulate the functional properties of professional APCs and influence immune activation in a variety of disease contexts. Many members of the LILR family recognize peptide/MHC class I complexes as their physiological ligands, and increasing evidence suggests that such interactions are prominently influenced by polymorphisms in HLA class I alleles or sequence variations in the presented antigenic peptides. Emerging data show that LILRs are involved in multiple, different aspects of HIV-1 disease pathogenesis and may critically influence spontaneous HIV-1 disease progression. Here, we review recent progress in understanding the role of LILR during HIV-1 infection by focusing on the dynamic interplay between LILR and HLA class I molecules in determining HIV-1 disease progression, the effects of HIV-1 mutational escape on LILR-mediated immune recognition, the contribution of LILR to HIV-1-associated immune dysfunction, and the unique expression patterns of LILR on circulating myeloid DCs from elite controllers, a small subset of HIV-1-infected patients with natural control of HIV-1 replication. Obtaining a more complete understanding of LILR-mediated immune regulation during HIV-1 infection may ultimately allow for improved strategies to treat or prevent HIV-1-associated disease manifestations. J. Leukoc. Biol. 91: 27-33; 2012.
C1 [Yu, Xu G.] Ragon Inst MGH MIT & Harvard, Boston, MA 02129 USA.
[Lichterfeld, Mathias] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
RP Yu, XG (reprint author), Ragon Inst MGH MIT & Harvard, 149 13th St, Boston, MA 02129 USA.
EM xyu@partners.org
FU Doris Duke Charitable Foundation; NIH [AI078799, AI089339, AI093203];
DDCF [2009034]
FX X.G.Y. and M.L. are recipients of the Clinical Scientist Development
Award from the Doris Duke Charitable Foundation. X.G.Y. is supported by
NIH grants AI078799 and AI089339, and M.L. is supported by NIH grant
AI093203 and DDCF grant 2009034. The authors thank Dr. Arman Bashirova
(NCI Frederick, Maryland, USA) and Mr. Jerome Rogich (Ragon Institute,
Boston, MA, USA) for helping with the preparation of the included table
and figure.
NR 66
TC 16
Z9 16
U1 0
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0741-5400
J9 J LEUKOCYTE BIOL
JI J. Leukoc. Biol.
PD JAN
PY 2012
VL 91
IS 1
BP 27
EP 33
DI 10.1189/jlb.0811442
PG 7
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 877HO
UT WOS:000299168600005
PM 22028331
ER
PT J
AU Penjweini, R
Loew, HG
Hamblin, MR
Kratky, KW
AF Penjweini, Rozhin
Loew, Hans G.
Hamblin, Michael R.
Kratky, Karl W.
TI Long-term monitoring of live cell proliferation in presence of
PVP-Hypericin: a new strategy using ms pulses of LED and the fluorescent
dye CFSE
SO JOURNAL OF MICROSCOPY
LA English
DT Article
DE CFSE; fluorescence; live cell imaging; photobleaching; phototoxicity;
pulsed LED excitation; PVP-Hypericin
ID LIGHT-EMITTING-DIODES; MICROSCOPY; PHOTOTOXICITY; ILLUMINATION
AB During fluorescent live cell imaging it is critical to keep excitation light dose as low as possible, especially in the presence of photosensitizer drugs, which generate free radicals upon photobleaching. During fluorescent imaging, stress by excitation and free radicals induces serious cell damages that may arrest the cell cycle. This limits the usefulness of the technique for drug discovery, when prolonged live cell imaging is necessary. This paper presents a strategy to provide gentle experimental conditions for dynamic monitoring of the proliferation of human lung epithelial carcinoma cells (A549) in the presence of the photosensitizer Polyvinylpyrrolidone-Hypericin. The distinctive strategy of this paper is based on the stringent environmental control and optimizing the excitation light dose by (i) using a low-power pulsed blue light-emitting diode with short pulse duration of 1.29 ms and (ii) adding a nontoxic fluorescent dye called carboxyfluorescein-diacetate-succinimidyl-ester (CFSE) to improve the fluorescence signals. To demonstrate the usefulness of the strategy, fluorescence signals and proliferation of dual-marked cells, during 5-h fluorescence imaging under pulsed excitation, were compared with those kept under continuous excitation and nonmarked reference cells. The results demonstrated 3% cell division and 2% apoptosis due to pulsed excitation compared to no division and 85% apoptosis under the continuous irradiation. Therefore, our strategy allows live cell imaging to be performed over longer time scales than with conventional continuous excitation.
C1 [Penjweini, Rozhin; Loew, Hans G.; Kratky, Karl W.] Univ Vienna, Fac Phys, A-1090 Vienna, Austria.
[Loew, Hans G.] Med Univ Vienna, Dept Therapeut Radiol, Vienna, Austria.
[Hamblin, Michael R.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Hamblin, Michael R.] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Hamblin, Michael R.] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Kratky, KW (reprint author), Univ Vienna, Fac Phys, Boltzmanng 5, A-1090 Vienna, Austria.
EM karl.kratky@univie.ac.at
RI Loew, Hans Gunter/L-2548-2013;
OI Hamblin, Michael/0000-0001-6431-4605
FU Austrian Economy Chamber; Hochschuljubilaumsfond [H1971-2006]
FX The new strategy and imaging setup used in this paper was supported by
the Austrian Economy Chamber (http://www.i2b.at) and developed by
RISCREEN, granted with First place i2B-Businessplan-2009 AWARD
(15.12.2009) and Hochschuljubilaumsfond-project H1971-2006. Authors
would like to thank Gottfried Koehler, Martin Knapp, Maria Eisenbauer
and Paul Breit for useful discussion.
NR 27
TC 9
Z9 10
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-2720
J9 J MICROSC-OXFORD
JI J. Microsc..
PD JAN
PY 2012
VL 245
IS 1
BP 100
EP 108
DI 10.1111/j.1365-2818.2011.03555.x
PG 9
WC Microscopy
SC Microscopy
GA 860LW
UT WOS:000297950800011
PM 21974829
ER
PT J
AU Osborne, C
Ecker, JL
Gauvreau, K
Lieberman, E
AF Osborne, Cara
Ecker, Jeffrey L.
Gauvreau, Kimberlee
Lieberman, Ellice
TI First Birth Cesarean and Risk of Antepartum Fetal Death in a Subsequent
Pregnancy
SO JOURNAL OF MIDWIFERY & WOMENS HEALTH
LA English
DT Article
DE antepartum care; cesarean birth; obstetric complications; primary
cesarean birth; quantitative research; stillbirth
ID UTERINE RUPTURE; STILLBIRTH; DELIVERY; WOMEN; OUTCOMES; WEIGHT; LABOR;
POPULATION; MORTALITY; SECTION
AB Introduction: To examine the relationship between first birth by cesarean and antepartum fetal death in a subsequent pregnancy in a large, hospital-based population.
Methods: Data for this retrospective cohort study were taken from a database of all women who gave birth at Brigham and Women's Hospital during 4 waves of data collection beginning in 1994 and ending in 2002. We calculated the risk of antepartum fetal death in the subsequent pregnancy for women whose first birth was by cesarean compared to women with a vaginal first birth. Survival analysis was used to examine the influence of gestational age at birth.
Results: Of 10,996 women who met inclusion criteria, 22% (n = 2450) had first births by cesarean, and 78% (n = 8546) had vaginal first births. The risk of antepartum fetal death in the subsequent pregnancy for women whose first birth was by cesarean was significantly greater than the risk for women whose first birth was vaginal (odds ratio 2.6; 95% confidence interval, 1.1-6.2). The relationship between first birth cesarean and antepartum fetal death in a subsequent pregnancy differed by gestational age at birth, with no excess risk among women with a previous cesarean birth who gave birth before 34 weeks' gestation but with a substantially increased risk for women who gave birth at 34 or more weeks' gestation (unadjusted hazard ratio = 5.6; 95% confidence interval, 1.6-19.8). Hazard ratio estimates for the association remained significant in bivariate models when adjusted for maternal height, weight, age, hypertension, and diabetes.
Discussion: In these data, first birth by cesarean was associated with an increased risk of antepartum fetal death in a subsequent pregnancy. Our findings suggest that antepartum fetal deaths in subsequent pregnancies might be prevented by avoiding primary cesarean birth. J MidwiferyWomens Health 2012; 57: 12-17 (C) 2011 by the American College of Nurse-Midwives.
C1 [Osborne, Cara] Univ Arkansas, Elenor Mann Sch Nursing, Fayetteville, AR 72701 USA.
[Ecker, Jeffrey L.; Gauvreau, Kimberlee; Lieberman, Ellice] Harvard Univ, Sch Med, Boston, MA USA.
[Ecker, Jeffrey L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Lieberman, Ellice] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Gauvreau, Kimberlee] Childrens Hosp Boston, Dept Cardiol, Boston, MA USA.
[Lieberman, Ellice] Brigham & Womens Hosp, Div Clin & Epidemiol Res, Boston, MA 02115 USA.
RP Osborne, C (reprint author), Univ Arkansas, Elenor Mann Sch Nursing, 216 F Ozark Hall, Fayetteville, AR 72701 USA.
EM cxo004@uark.edu
NR 24
TC 3
Z9 3
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1526-9523
J9 J MIDWIFERY WOM HEAL
JI J. Midwifery Women Health
PD JAN-FEB
PY 2012
VL 57
IS 1
BP 12
EP 17
DI 10.1111/j.1542-2011.2011.00142.x
PG 6
WC Nursing
SC Nursing
GA 877CZ
UT WOS:000299155800003
PM 22251907
ER
PT J
AU Spencer, R
Schorge, J
Del Carmen, M
Goodman, A
Growdon, W
Boruta, D
AF Spencer, Ryan
Schorge, John
Del Carmen, Marcela
Goodman, Annekathryn
Growdon, Whitfield
Boruta, David
TI Laparoscopic Surgery for Endometrial Cancer: Why Don't All Patients Go
Home the Day After Surgery?
SO JOURNAL OF MINIMALLY INVASIVE GYNECOLOGY
LA English
DT Article
DE Endometrial cancer; Hospital length of stay; Laparoscopy
ID CONTROLLED-TRIALS; HYSTERECTOMY; LYMPHADENECTOMY; SURVIVAL; COST
AB Study Objective: To identify risk factors for hospital length of stay (LOS) longer than 1 postoperative day in patients undergoing laparoscopic hysterectomy because of endometrial cancer.
Design: Retrospective observational study (Canadian Task Force classification II-2).
Setting: Tertiary-care university hospital.
Patients: One hundred thirty-three patients undergoing laparoscopic hysterectomy because of endometrial cancer between August 2006 and August 2010.
Interventions: One hundred thirty-three women underwent traditional laparoscopy. In 101 of these patients, lymph node sampling was performed.
Measurements and Main Outcomes: Seventy-four women (55%) were discharged on postoperative day 1. The percentage of women discharged on postoperative day 1 (POD1) vs after POD1 did not differ by extent of staging. Risk of perioperative complications was associated with hospital LOS longer than POD1 (odds ratio [OR], 11.45; 95% confidence interval [CI], 1.40-94.39). Procedure start time after 3:00 PM (OR, 3.20; 95% CI, 1.14-9.04) and procedure end time after 5:00 pm (OR, 2.47; 95% CI, 1.17-5.20) were independent factors associated with hospital LOS beyond POD1. There was a nonsignificant tendency toward later hospital discharge with administration of intravenous narcotic agents.
Conclusions: Laparoscopic surgery to treat endometrial cancer should be preferentially scheduled early in the day to facilitate discharge on POD1. The extent of staging lymphadenectomy performed does not increase hospital stay beyond POD1. Journal of Minimally Invasive Gynecology (2012) 19, 95-100 (C) 2012 AAGL. All rights reserved.
C1 [Spencer, Ryan] Harvard Univ, Div Gynecol Oncol, Dept Obstet & Gynecol, Massachusetts Gen Hosp,Med Sch,Yawkey Ctr, Boston, MA 02114 USA.
RP Spencer, R (reprint author), Harvard Univ, Div Gynecol Oncol, Dept Obstet & Gynecol, Massachusetts Gen Hosp,Med Sch,Yawkey Ctr, 32 Fruit St,Ste 4F, Boston, MA 02114 USA.
EM rjspencer@partners.org
NR 27
TC 5
Z9 5
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1553-4650
J9 J MINIM INVAS GYN
JI J. Mimim. Invasive Gynecol.
PD JAN-FEB
PY 2012
VL 19
IS 1
BP 95
EP 100
DI 10.1016/j.jmig.2011.10.007
PG 6
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 879BQ
UT WOS:000299305100017
PM 22196258
ER
PT J
AU Tuncel, N
Korkmaz, OT
Tekin, N
Sener, E
Akyuz, F
Inal, M
AF Tuncel, Nese
Korkmaz, Orhan Tansel
Tekin, Neslihan
Sener, Erol
Akyuz, Fahrettin
Inal, Mine
TI Antioxidant and Anti-Apoptotic Activity of Vasoactive Intestinal Peptide
(VIP) Against 6-Hydroxy Dopamine Toxicity in the Rat Corpus Striatum
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Article
DE Vasoactive intestinal peptide; Parkinson's disease; DNA fragmentation;
Oxidative damage; 6-OHDA; Nitric oxide
ID NITRIC-OXIDE SYNTHASE; PARKINSONS-DISEASE; OXIDATIVE STRESS; MAST-CELLS;
NEURODEGENERATIVE DISEASES; SUPEROXIDE-DISMUTASE; ISCHEMIA-REPERFUSION;
LIPID-PEROXIDATION; LUNG INJURY; PATHOGENESIS
AB 6-Hydroxydopamine (6-OHDA) is an oxidative stress neurotoxin, which is oxidized in neurons, causes respiratory inhibition, and induces free radical formation and oxidative stress. Therefore, a 6-OHDA-induced Parkinson's disease (PD) experimental model can be used to test a candidate molecule for use as an antioxidant that could be a promising therapeutic for treating Parkinson's disease. Recent studies have shown that vasoactive intestinal peptide (VIP) might be a good candidate agent for the treatment of PD. In this study, the anti-apoptotic and antioxidant actions of VIP were investigated using the 6-OHDA-lesioned rat model for PD. Twenty-four young adult Sprague-Dawley rats were used. The rats were separated into the following groups: group I (n = 8), sham operated; group II (n = 8), 6-OHDA lesioned; group III (n = 8), 6-OHDA lesioned + i.p. VIP-injected (25 ng/kg) every 2 days for 15 days. The first i.p. injection of VIP was made 1 h after the intrastriatal 6-OHDA microinjection. Antioxidant enzymatic activity [super oxide dismutase (SOD) and catalase (CAT)], lipid peroxidation, nitric oxide and DNA fragmentation were measured from homogenates isolated from the corpus striatum. SOD, CAT, malondialdehyde, and DNA fragmentation were measured using a spectrophotometer, and nitric oxide (NO) levels were measured by capillary electrophoresis. 6-OHDA significantly induced oxidative stress, lipid peroxidation, and DNA fragmentation in the corpus striatum of rats. VIP significantly protected neuronal tissue from oxidative stress and apoptosis by reducing lipid peroxidation and DNA fragmentation. 6-OHDA toxicity did not cause significant changes in NO production in the corpus striatum. However, VIP treatment significantly reduced NO levels in brain tissue.
C1 [Korkmaz, Orhan Tansel] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Korkmaz, Orhan Tansel] VA Boston Healthcare Syst, Dept Vet Affairs, Boston, MA 02130 USA.
[Korkmaz, Orhan Tansel; Tekin, Neslihan] Eskisehir Osmangazi Univ, Fac Med, Dept Physiol, TR-26480 Eskisehir, Turkey.
[Tekin, Neslihan; Akyuz, Fahrettin; Inal, Mine] Eskisehir Osmangazi Univ, Fac Med, Dept Biochem, TR-26480 Eskisehir, Turkey.
[Sener, Erol] Anadolu Univ, Fac Pharm, Dept Analyt Chem, TR-26470 Eskisehir, Turkey.
RP Korkmaz, OT (reprint author), Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
EM otk@bu.edu
NR 58
TC 18
Z9 19
U1 1
U2 16
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD JAN
PY 2012
VL 46
IS 1
BP 51
EP 57
DI 10.1007/s12031-011-9618-z
PG 7
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 879MA
UT WOS:000299332200006
PM 21850490
ER
PT J
AU Schmidt, HD
Sangrey, GR
Darnell, SB
Schassburger, RL
Cha, JHJ
Pierce, RC
Sadri-Vakili, G
AF Schmidt, Heath D.
Sangrey, Gavin R.
Darnell, Shayna B.
Schassburger, Rachel L.
Cha, Jang-Ho J.
Pierce, R. Christopher
Sadri-Vakili, Ghazeleh
TI Increased brain-derived neurotrophic factor (BDNF) expression in the
ventral tegmental area during cocaine abstinence is associated with
increased histone acetylation at BDNF exon I-containing promoters
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE addiction; chromatin remodeling; neurotrophic factor; psychostimulant;
self-administration; transcription
ID GLUTAMATE-RECEPTOR SUBUNITS; MESOLIMBIC DOPAMINE SYSTEM; MEDIAL
PREFRONTAL CORTEX; GENE-EXPRESSION; NUCLEUS-ACCUMBENS; PROTEIN-LEVELS;
D-3 RECEPTOR; TRANSCRIPTION; ADDICTION; INFUSION
AB Recent evidence suggests that the persistence of cocaine seeking during periods of protracted drug abstinence following chronic cocaine exposure is mediated, in part, by neuroadaptations in the mesolimbic dopamine system. Specifically, incubation of cocaine-seeking behavior coincides with increased brain-derived neurotrophic factor (BDNF) protein expression in the ventral tegmental area (VTA). However, the molecular mechanisms that regulate time-dependent changes in VTA BDNF protein expression during cocaine abstinence are unclear. The goal of these experiments was to determine whether VTA BDNF transcript levels are altered following cocaine abstinence and identify the molecular mechanisms regulating cocaine-induced changes in VTA BDNF transcription. Rats were allowed to self-administer cocaine (0.25 mg/infusion, i.v.) for 14 days on a fixed-ratio schedule of reinforcement followed by 7 days of forced drug abstinence. BDNF protein and exon I-containing transcripts were significantly increased in the VTA of cocaine-experienced rats following 7 days of forced drug abstinence compared to yoked saline controls. Cocaine-induced changes in BDNF mRNA were associated with increased acetylation of histone 3 and binding of CREB-binding protein to exon I-containing promoters in the VTA. Taken together, these results suggest that drug abstinence following cocaine self-administration remodels chromatin in the VTA resulting in increased expression of BDNF, which may contribute to neuroadaptations underlying cocaine craving and relapse.
C1 [Sangrey, Gavin R.; Darnell, Shayna B.; Cha, Jang-Ho J.; Sadri-Vakili, Ghazeleh] Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Boston, MA 02114 USA.
[Schmidt, Heath D.; Schassburger, Rachel L.; Pierce, R. Christopher] Univ Pennsylvania Sch, Perelman Sch Med, Dept Psychiat, Ctr Neurobiol & Behav, Philadelphia, PA USA.
RP Sadri-Vakili, G (reprint author), Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, 114 16th St, Charlestown, MA 02129 USA.
EM gsadrivakili@partners.org
FU NIDA [DA22339, DA18678]; K01 award [DA030445]
FX This work was supported by NIDA grants DA22339 (RCP and GSV) and DA18678
(RCP). HDS was supported by an individual K01 award (DA030445). The
authors declare no conflicts of interest.
NR 48
TC 34
Z9 37
U1 2
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3042
J9 J NEUROCHEM
JI J. Neurochem.
PD JAN
PY 2012
VL 120
IS 2
BP 202
EP 209
DI 10.1111/j.1471-4159.2011.07571.x
PG 8
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 869ME
UT WOS:000298601400002
PM 22043863
ER
PT J
AU Pinna, G
Rasmusson, AM
AF Pinna, Graziano
Rasmusson, Ann M.
TI Up-Regulation of Neurosteroid Biosynthesis as a Pharmacological Strategy
to Improve Behavioural Deficits in a Putative Mouse Model of
Post-Traumatic Stress Disorder
SO JOURNAL OF NEUROENDOCRINOLOGY
LA English
DT Review
DE allopregnanolone; 5a-reductase type I; selective brain steroidogenic
stimulants; aggressive behaviour; GABAA receptors; social isolation;
anxiety; post-traumatic stress disorder
ID GABA-A RECEPTOR; GAMMA-AMINOBUTYRIC-ACID; GENERALIZED ANXIETY DISORDER;
PROTRACTED SOCIAL-ISOLATION; RANDOMIZED CONTROLLED-TRIAL; NEURAL
PROGENITOR CELLS; VENTRAL TEGMENTAL AREA; PROTEIN 18 KDA; PREFRONTAL
CORTEX; NEUROACTIVE STEROIDS
AB Benzodiazepines remain the most frequently used psychotropic drugs for the treatment of anxiety spectrum disorders; however, their use is associated with the development of tolerance and dependence. Another major hindrance is represented by their lack of efficacy in many patients, including patients with post-traumatic stress disorder (PTSD). For these nonresponders, the use of selective serotonin reuptake inhibitors (SSRIs) has been the therapy of choice. In the past decade, clinical studies have suggested that the pharmacological action of SSRIs may include the ability of these drugs to normalise decreased brain levels of neurosteroids in patients with depression and PTSD; in particular, the progesterone derivative allopregnanolone, which potently, positively and allosterically modulates the action of GABA at GABAA receptors. Preclinical studies using the socially-isolated mouse as an animal model of PTSD have demonstrated that fluoxetine and congeners ameliorate anxiety-like behaviour, fear responses and aggressive behaviour expressed by such mice by increasing corticolimbic levels of allopregnanolone. This is a novel and more selective mechanism than serotonin reuptake inhibition, which, for half a century, has been considered to be the main molecular mechanism for the therapeutic action of SSRIs. Importantly, this finding may shed light on the high rates of SSRI resistance among patients with PTSD and depression, comprising disorders in which there appears to be a block in allopregnanolone synthesis. There are several different mechanisms by which such a block may occur, and SSRIs may only be corrective under some conditions. Thus, the up-regulation of allopregnanolone biosynthesis in corticolimbic neurones may offer a novel nontraditional pharmacological target for a new generation of potent nonsedating, anxiolytic medications for the treatment of anxiety, depression, and PTSD: selective brain steroidogenic stimulants.
C1 [Pinna, Graziano] Univ Illinois, Dept Psychiat, Inst Psychiat, Coll Med, Chicago, IL 60612 USA.
[Rasmusson, Ann M.] Boston Univ, Sch Med, Womens Hlth Sci Div,VA Boston Healthcare Syst, Natl Ctr Posttraumat Stress Disorder, Boston, MA 02118 USA.
RP Pinna, G (reprint author), Univ Illinois, Dept Psychiat, Inst Psychiat, Coll Med, 1601 W Taylor St, Chicago, IL 60612 USA.
EM gpinna@psych.uic.edu
FU National Institute of Mental Health [MH 085999, MH31113]; VA Boston
Healthcare System
FX This review was supported by the National Institute of Mental Health
Grant MH 085999 (to G. Pinna) and VA Boston Healthcare System and
National Institute of Mental Health Grant MH31113 (to A. Rasmusson).
NR 187
TC 32
Z9 34
U1 1
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-8194
J9 J NEUROENDOCRINOL
JI J. Neuroendocrinol.
PD JAN
PY 2012
VL 24
IS 1
BP 102
EP 116
DI 10.1111/j.1365-2826.2011.02234.x
PG 15
WC Endocrinology & Metabolism; Neurosciences
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA 869MI
UT WOS:000298601800010
PM 21981145
ER
PT J
AU Chen, M
Lee, G
Kwong, LN
Lamont, S
Chaves, C
AF Chen, Merry
Lee, Grace
Kwong, Lawrence N.
Lamont, Sharon
Chaves, Claudia
TI Cerebral White Matter Lesions in Patients with Crohn's Disease
SO JOURNAL OF NEUROIMAGING
LA English
DT Article
DE White matter abnormalities; Crohn's disease; MRI of the brain
ID INFLAMMATORY-BOWEL-DISEASE; DEFINITE MULTIPLE-SCLEROSIS; NEUROLOGICAL
COMPLICATIONS; PREDICT CONVERSION; BRAIN; ABNORMALITIES; CRITERIA; MR
AB BACKGROUND
To investigate the incidence, characteristics, and predisposing factors for cerebral white matter lesions in patients with Crohn's disease.
METHODS
We retrospectively evaluated the incidence and characteristics of cerebral T2 white matter abnormalities in 54 patients with Crohn's disease and compared to 100 age-matched controls. We also investigated potential co-morbidities known to be associated with white matter abnormalities in Crohn's patients with normal and abnormal Magnetic Resonance Imaging (MRI).
RESULTS
Seventy-two percent of patients with Crohn's disease had T2 white matter abnormalities, as compared with 34% of the age-matched controls (P < .001). Lesion severity and size were not significantly different between the two groups; however, periventricular distribution and fulfillment of the Barkhof MRI criteria were overrepresented in Crohn's population. History of hypertension, diabetes, and migraine; gender, duration of disease and prior exposure to anti-tumor necrosis factor were not significantly different between Crohn's patients with and without white matter abnormalities; however, patients with lesions were significantly older than those without.
CONCLUSIONS
Patients with Crohn's disease have a higher incidence of white matter T2 hyperintensities as compared with controls. Age was the only significant factor for the abnormalities within Crohn's group. White matter T2 hyperintensities are likely another extra-intestinal manifestation of Crohn's disease.
C1 [Chen, Merry; Lamont, Sharon; Chaves, Claudia] Lahey Clin Fdn, Dept Neurol, Lexington, MA 02421 USA.
[Lee, Grace] Lahey Clin Fdn, Dept Radiol, Burlington, MA USA.
[Kwong, Lawrence N.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Chaves, C (reprint author), Lahey Clin Fdn, Dept Neurol, 16 Hayden Ave, Lexington, MA 02421 USA.
EM Claudia.j.chaves@lahey.org
NR 17
TC 10
Z9 10
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1051-2284
J9 J NEUROIMAGING
JI J. Neuroimaging
PD JAN
PY 2012
VL 22
IS 1
BP 38
EP 41
DI 10.1111/j.1552-6569.2010.00538.x
PG 4
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 877DZ
UT WOS:000299158500007
PM 21091817
ER
PT J
AU Johnson, KA
Hartwell, K
LeMatty, T
Borckardt, J
Morgan, PS
Govindarajan, K
Brady, K
George, MS
AF Johnson, Kevin A.
Hartwell, Karen
LeMatty, Todd
Borckardt, Jeffrey
Morgan, Paul S.
Govindarajan, Koushik
Brady, Kathleen
George, Mark S.
TI Intermittent "Real-time" fMRI Feedback Is Superior to Continuous
Presentation for a Motor Imagery Task: A Pilot Study
SO JOURNAL OF NEUROIMAGING
LA English
DT Article
DE fMRI; neurofeedback; real-time fMRI; motor imagery
ID RESONANCE-IMAGING FMRI; CORTICAL ACTIVITY; BRAIN ACTIVATION;
SELF-REGULATION; FUNCTIONAL MRI; NEUROFEEDBACK
AB BACKGROUND
Real-time functional MRI feedback (RTfMRIf) is a developing technique, with unanswered methodological questions. Given a delay of seconds between neural activity and the measurable hemodynamic response, one issue is the optimal method for presentation of neurofeedback to subjects. The primary objective of this preliminary study was to compare the methods of continuous and intermittent presentation of neural feedback on targeted brain activity.
METHODS
Thirteen participants performed a motor imagery task and were instructed to increase activation in an individually defined region of left premotor cortex using RTfMRIf. The fMRI signal change was compared between real and false feedback for scans with either continuous or intermittent feedback presentation.
RESULTS
More individuals were able to increase their fMRI signal with intermittent feedback, while some individuals had decreased signal with continuous feedback. The evaluation of feedback itself activated an extensive amount of brain regions, and false feedback resulted in brain activation outside of the individually defined region of interest.
CONCLUSIONS
As implemented in this study, intermittent presentation of feedback is more effective than continuous presentation in promoting self-modulation of brain activity. Furthermore, it appears that the process of evaluating feedback involves many brain regions that can be isolated using intermittent presentation.
C1 [Johnson, Kevin A.] Stanford Univ, Dept Anesthesiol, Syst Neurosci & Pain Lab, Palo Alto, CA 94304 USA.
[Hartwell, Karen; LeMatty, Todd; Brady, Kathleen] Med Univ S Carolina, Dept Psychiat, CNS Div, Charleston, SC 29425 USA.
[Johnson, Kevin A.; Borckardt, Jeffrey; George, Mark S.] Med Univ S Carolina, Dept Psychiat, Brain Stimulat Lab, Charleston, SC 29425 USA.
[Johnson, Kevin A.; Morgan, Paul S.; Govindarajan, Koushik; George, Mark S.] Med Univ S Carolina, Ctr Adv Imaging Res, Charleston, SC 29425 USA.
[Morgan, Paul S.] Med Univ S Carolina, Dept Radiol, Charleston, SC 29425 USA.
[Hartwell, Karen; Brady, Kathleen; George, Mark S.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
RP Johnson, KA (reprint author), Stanford Univ, Dept Anesthesiol, Syst Neurosci & Pain Lab, 780 Welch Rd 208, Palo Alto, CA 94304 USA.
EM johnsk@stanford.edu
OI Morgan, Paul/0000-0002-5870-1446
FU NIH/NIDA (Brady, George) [1R21DA026085-01]
FX The authors have no conflicts of interest to disclose. This study is
supported in part by NIH/NIDA 1R21DA026085-01 (Brady, George).
NR 17
TC 37
Z9 39
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1051-2284
J9 J NEUROIMAGING
JI J. Neuroimaging
PD JAN
PY 2012
VL 22
IS 1
BP 58
EP 66
DI 10.1111/j.1552-6569.2010.00529.x
PG 9
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 877DZ
UT WOS:000299158500011
PM 20977537
ER
PT J
AU Pantilat, SZ
Kerr, KM
Billings, JA
Bruno, KA
O'Riordan, DL
AF Pantilat, Steven Z.
Kerr, Kathleen M.
Billings, J. Andrew
Bruno, Kelly A.
O'Riordan, David L.
TI Palliative Care Services in California Hospitals: Program Prevalence and
Hospital Characteristics
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Prevalence; structure; palliative care services; hospital
AB Context. In 2000, 17% of California hospitals offered palliative care (PC) services. Since then, hospital-based PC programs have become increasingly common, and preferred practices for these services have been proposed by expert consensus.
Objectives. We sought to examine the prevalence of PC programs in California, their structure, and the hospital characteristics associated with having a program.
Methods. A total of 351 acute care hospitals in California completed a survey that determined the presence of and described the structure of PC services. Logistic regression identified hospital characteristics associated with having a PC program.
Results. A total of 324 hospitals (92%) responded, of which 44% (n = 141) reported having a PC program. Hospitals most likely to have PC programs were large nonprofit facilities that belonged to a health system, had teaching programs, and had participated in a training program designed to promote development of PC services. Investor-owned sites (odds ratio [OR] = 0.08; 95% confidence interval [CI] = 0.03, 0.2) and city/county facilities (OR = 0.06; 95% CI = 0.01, 0.3) were less likely to have a PC program. The most common type of PC service was an inpatient consultation service (88%), staffed by a physician (87%), social worker (81%), chaplain (76%), and registered nurse (74%). Most programs (71%, n = 86) received funding from the hospital and were expected to meet goals set by the hospital or health system.
Conclusion. Although the number of hospital-based PC services in California has doubled since 2000, more than half of the acute care hospitals still do not provide PC services. Developing initiatives that target small, public, and investor-owned hospitals may lead to wider availability of PC services. J Pain Symptom Manage 2012; 43: 39-46. (C) 2012 U.S. Cancer Pain Relief Committee. Published by Elsevier Inc. All rights reserved.
C1 [Pantilat, Steven Z.; Kerr, Kathleen M.; O'Riordan, David L.] Univ Calif San Francisco, Palliat Care Program, Div Hosp Med, Dept Med, San Francisco, CA 94143 USA.
[Billings, J. Andrew] Massachusetts Gen Hosp, Palliat Care Serv, Boston, MA 02114 USA.
[Billings, J. Andrew] Harvard Univ, Sch Med, Ctr Palliat Care, Boston, MA USA.
[Bruno, Kelly A.] Natl Hlth Fdn, Los Angeles, CA USA.
RP Pantilat, SZ (reprint author), Univ Calif San Francisco, Palliat Care Program, Div Hosp Med, Dept Med, 521 Parnassus Ave,Suite C-126, San Francisco, CA 94143 USA.
EM stevep@medicine.ucsf.edu
FU California HealthCare Foundation; Hospital Council of Northern and
Central California; Hospital Council of Southern California; Hospital
Council of San Diego and Imperial Counties
FX The California HealthCare Foundation provided funding to support the
administration of the survey and analysis of findings, as well as
limited dissemination of results through the Foundation's communication
venues. The authors declare no competing interests.; The authors thank
the members of the advisory board for their input on the survey: Judy
Citko, Richard Della Penna, Betty Ferrell, James Hallenbeck, Andrew
Halpert, Karl Lorenz, Anna Schenck, Bradley Stuart, Mary Carol Todd, and
Charles von Gunten. They also thank the Hospital Council of Northern and
Central California, the Hospital Council of Southern California, and the
Hospital Council of San Diego and Imperial Counties for their support in
encouraging their members to participate. Finally, they thank all the
respondents for their diligence and care in responding to the survey.
NR 7
TC 12
Z9 12
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0885-3924
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD JAN
PY 2012
VL 43
IS 1
BP 39
EP 46
DI 10.1016/j.jpainsymman.2011.03.021
PG 8
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA 877WH
UT WOS:000299212900005
PM 21802898
ER
PT J
AU Lee, CN
Chang, YC
Adimorah, N
Belkora, JK
Moy, B
Partridge, AH
Ollila, DW
Sepucha, KR
AF Lee, Clara N.
Chang, Yuchiao
Adimorah, Nesochi
Belkora, Jeff K.
Moy, Beverly
Partridge, Ann H.
Ollila, David W.
Sepucha, Karen R.
TI Decision Making about Surgery for Early-Stage Breast Cancer
SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS
LA English
DT Article
ID PATIENT PARTICIPATION; SURGICAL-TREATMENT; INFORMED DECISION;
RANDOMIZED-TRIAL; LOCAL THERAPY; WOMEN; QUALITY; KNOWLEDGE; MASTECTOMY;
CARCINOMA
AB BACKGROUND: Practice variation in breast cancer surgery has raised concerns about the quality of treatment decisions. We sought to evaluate the quality of decisions about surgery for early-stage breast cancer by measuring patient knowledge, concordance between goals and treatments, and involvement in decisions.
STUDY DESIGN: A mailed survey of stage I/II breast cancer survivors was conducted at 4 sites. The Decision Quality Instrument measured knowledge, goals, and involvement in decisions. A multivariable logistic regression model of treatment was developed. The model-predicted probability of mastectomy was compared with treatment received for each patient. Concordance was defined as having mastectomy and predicted probability >0.5 or partial mastectomy and predicted probability <0.5. Frequency of discussion about partial mastectomy was compared with discussion about mastectomy using chi-square tests.
RESULTS: Four hundred and forty patients participated (59% response rate). Mean overall knowledge was 52.7%; 45.9% knew that local recurrence risk is higher after breast conservation and 55.7% knew that survival is equivalent for the 2 options. Most participants (89.0%) had treatment concordant with their goals. Participants preferring mastectomy had lower concordance (80.5%) than those preferring partial mastectomy (92.6%; p = 0.001). Participants reported more frequent discussion of partial mastectomy and its advantages than of mastectomy, and 48.6% reported being asked their preference.
CONCLUSIONS: Breast cancer survivors had major knowledge deficits, and those preferring mastectomy were less likely to have treatment concordant with goals. Patients perceived that discussions focused on partial mastectomy, and many were not asked their preference. Improvements in the quality of decisions about breast cancer surgery are needed. (J Am Coll Surg 2012; 214: 1-11. (C) 2012 by the American College of Surgeons)
C1 [Lee, Clara N.] Univ N Carolina, Div Plast & Reconstruct Surg, Lineberger Comprehens Canc Ctr, Sheps Ctr Hlth Serv Res, Chapel Hill, NC 27599 USA.
[Adimorah, Nesochi; Ollila, David W.] Univ N Carolina, Dept Surg, Chapel Hill, NC 27599 USA.
[Belkora, Jeff K.] Univ Calif San Francisco, Inst Hlth Policy Studies, San Francisco, CA 94143 USA.
[Chang, Yuchiao] Harvard Univ, Massachusetts Gen Hosp, Dept Gen Med, Sch Med, Boston, MA 02114 USA.
[Moy, Beverly] Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Sch Med, Boston, MA 02114 USA.
[Partridge, Ann H.] Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst, Sch Med, Boston, MA 02114 USA.
[Sepucha, Karen R.] Harvard Univ, Sch Med, Hlth Decis Sci Ctr, Boston, MA 02114 USA.
RP Lee, CN (reprint author), Univ N Carolina, Div Plast & Reconstruct Surg, Lineberger Comprehens Canc Ctr, Sheps Ctr Hlth Serv Res, CB 7195, Chapel Hill, NC 27599 USA.
EM cnlee@med.unc.edu
FU not-for-profit Foundation for Informed Medical Decision Making;
NIH/National Center for Resesarch Resources [1KL2RR025746]
FX Drs Belkora, Lee, and Sepucha were supported by a grant from the
not-for-profit Foundation for Informed Medical Decision Making. Dr Lee
was supported by NIH/National Center for Resesarch Resources
1KL2RR025746.
NR 38
TC 24
Z9 24
U1 2
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1072-7515
J9 J AM COLL SURGEONS
JI J. Am. Coll. Surg.
PD JAN
PY 2012
VL 214
IS 1
BP 1
EP 10
DI 10.1016/j.jamcollsurg.2011.09.017
PG 10
WC Surgery
SC Surgery
GA 875SF
UT WOS:000299054400003
PM 22056355
ER
PT J
AU Marcum, ZA
Amuan, ME
Hanlon, JT
Aspinall, SL
Handler, SM
Ruby, CM
Pugh, MJV
AF Marcum, Zachary A.
Amuan, Megan E.
Hanlon, Joseph T.
Aspinall, Sherrie L.
Handler, Steven M.
Ruby, Christine M.
Pugh, Mary Jo V.
TI Prevalence of Unplanned Hospitalizations Caused by Adverse Drug
Reactions in Older Veterans
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE adverse drug reactions; veterans; aged; pharmacoepidemiology
ID MEDICATION-USE; ELDERLY-PATIENTS; AMBULATORY-CARE; ADULTS; EVENTS;
ADMISSION; GUIDELINES; POLYPHARMACY; PATIENT; RATES
AB OBJECTIVES: To describe the prevalence of unplanned hospitalizations caused by adverse drug reactions (ADRs) in older veterans and to examine the association between this outcome and polypharmacy after controlling for comorbidities and other patient characteristics.
DESIGN: Retrospective cohort.
SETTING: Veterans Affairs Medical Centers.
PARTICIPANTS: Six hundred seventy-eight randomly selected unplanned hospitalizations of older (aged >= 65) veterans between October 1, 2003, and September 30, 2006.
MEASUREMENTS: Naranjo ADR algorithm, ADR preventability, and polypharmacy (0-4, 5-8, and >= 9 scheduled medications).
RESULTS: Seventy ADRs involving 113 drugs were found in 68 (10%) hospitalizations of older veterans, of which 25 (36.8%) were preventable. Extrapolating to the population of more than 2.4 million older veterans receiving care during the study period, 8,000 hospitalizations may have been unnecessary. The most common ADRs that occurred were bradycardia (n = 6; beta-blockers, digoxin), hypoglycemia (n = 6; sulfonylureas, insulin), falls (n = 6; antidepressants, angiotensin-converting enzyme inhibitors), and mental status changes (n = 6; anticonvulsants, benzodiazepines). Overall, 44.8% of veterans took nine or more outpatient medications and 35.4% took five to eight. Using multivariable logistic regression and controlling for demographic, health-status, and access-to-care variables, polypharmacy (>= 9 and 5-8) was associated with greater risk of ADR-related hospitalization (adjusted odds ratio (AOR) = 3.90, 95% confidence interval (CI) = 1.43-10.61 and AOR = 2.85, 95% CI = 1.03-7.85, respectively).
CONCLUSION: ADRs, determined using a validated causality algorithm, are a common cause of unplanned hospitalization in older veterans, are frequently preventable, and are associated with polypharmacy. J Am Geriatr Soc 60:34-41, 2012.
C1 [Marcum, Zachary A.; Hanlon, Joseph T.; Handler, Steven M.; Ruby, Christine M.] Univ Pittsburgh, Sch Med, Dept Geriatr, Pittsburgh, PA 15213 USA.
[Handler, Steven M.] Univ Pittsburgh, Sch Med, Dept Biomed Informat, Pittsburgh, PA 15213 USA.
[Hanlon, Joseph T.; Aspinall, Sherrie L.; Ruby, Christine M.] Univ Pittsburgh, Sch Pharm, Dept Pharm & Therapeut, Pittsburgh, PA 15213 USA.
[Amuan, Megan E.] Bedford Vet Affairs Med Ctr, Bedford, MA USA.
[Hanlon, Joseph T.; Handler, Steven M.] Vet Affairs Pittsburgh Healthcare Syst, Ctr Geriatr Res Educ & Clin, Pittsburgh, PA USA.
[Hanlon, Joseph T.; Aspinall, Sherrie L.] Vet Affairs Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Aspinall, Sherrie L.] Vet Affairs Ctr Medicat Safety, Hines, IL USA.
[Pugh, Mary Jo V.] S Texas Vet Hlth Care Syst, Vet Evidence Based Res Disseminat & Implementat C, San Antonio, TX USA.
[Pugh, Mary Jo V.] Univ Texas Hlth Sci Ctr San Antonio, Dept Epidemiol & Biostat, San Antonio, TX 78229 USA.
[Pugh, Mary Jo V.] Univ Texas Hlth Sci Ctr San Antonio, Div Geriatr & Gerontol, Dept Med, San Antonio, TX 78229 USA.
RP Marcum, ZA (reprint author), Univ Pittsburgh, Dept Geriatr Med, Kaufmann Med Bldg,Suite 500,3471 5th Ave, Pittsburgh, PA 15213 USA.
EM zam12@pitt.edu
OI Handler, Steven/0000-0002-3940-3224; Pugh, Mary Jo/0000-0003-4196-7763
FU National Institute on Aging (NIA) [R01AG027017, P30AG024827,
T32AG021885, K07AG033174, R01AG034056]; National Institute of Mental
Health [R34 MH082682]; National Institute of Nursing Research
[R01NR010135]; Agency for Healthcare Research and Quality [R01HS017695,
R01HS018721, R18HS018151, K12HS019461]; VA Health Services Research and
Development Service (HSR D) [IIR-06-062, DHI 09-237, IIR 02274, IIR
08-274, SDR-07-042, IIR-05-121, IAF-06-080, IIR-09335]; NIA
[K07AG033174, U01 AG012553]; Pennsylvania Department of Aging; Epilepsy
Foundation; SHP [08-140]
FX Dr. Hanlon has received research funding from National Institute on
Aging (NIA) Grants R01AG027017, P30AG024827, T32AG021885, K07AG033174,
and R01AG034056; National Institute of Mental Health Grant R34 MH082682,
National Institute of Nursing Research Grant R01NR010135, Agency for
Healthcare Research and Quality Grant R01HS017695, and VA Health
Services Research and Development Service (HSR& D) IIR-06-062. Dr.
Handler has received research funding from Agency for Healthcare
Research and Quality Grants R01HS018721 and R18HS018151; NIA Grant
K07AG033174, a Pennsylvania Department of Aging grant, and from VA HSR&
D IIR-06-062. Dr. Pugh has received research funding from VA HSR& D DHI
09-237 (PI); VA HSR& D IIR-06-062 (PI), Epilepsy Foundation (PI), VA
HSR& D PPO 09-295 PI, VA HSR& D IIR 02274 PI. Pugh as co-I: VA HSR& D
IIR 08-274, VA HSR& D SDR-07-042, IIR-05-121, IAF-06-080, IIR-09335, SHP
08-140, TRX 01-091 Department of Defense CDMRP 09090014, NIH
R01-NR010828, Pugh Speaker Honoraria: 2009 Kelsey Seybold Research
Foundation. The investigators received support from NIA Grant U01
AG012553 and Agency for Healthcare Research and Quality Grant
K12HS019461. The views expressed in this article are those of the
authors and do not necessarily represent the views of the Department of
Veterans Affairs.
NR 50
TC 45
Z9 47
U1 1
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD JAN
PY 2012
VL 60
IS 1
BP 34
EP 41
DI 10.1111/j.1532-5415.2011.03772.x
PG 8
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 875PN
UT WOS:000299044100005
PM 22150441
ER
PT J
AU Shega, JW
Dale, W
Andrew, M
Paice, J
Rockwood, K
Weiner, DK
AF Shega, Joseph W.
Dale, William
Andrew, Melissa
Paice, Judith
Rockwood, Kenneth
Weiner, Debra K.
TI Persistent Pain and Frailty: A Case for Homeostenosis
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE pain; frailty; older adults; homeostenosis
ID LOW-BACK-PAIN; OLDER-ADULTS; MORTALITY; PEOPLE; PREVALENCE; MANAGEMENT;
DEMENTIA; IMPACT; CARE; 3MS
AB OBJECTIVES: To compare the association between self-reported moderate to severe pain and frailty.
DESIGN: Cross-sectional analysis of the Canadian Study of Health and Aging Wave 2.
SETTING: Community.
PARTICIPANTS: Representative sample of persons aged 65 and older in Canada.
MEASUREMENTS: Pain (exposure) was categorized as no or very mild pain versus moderate or greater pain. Frailty (outcome) was operationalized as the accumulation of 33 possible self-reported health attitudes, illnesses, and functional abilities, subsequently divided into tertiles (not frail, prefrail, and frail). Multivariable logistic regression assessed for the association between pain and frailty.
RESULTS: Of participants who reported moderate or greater pain (35.5%, 1,765/4,968), 16.2% were not frail, 34.1% were prefrail, and 49.8% were frail. For persons with moderate or greater pain, the odds of being prefrail rather than not frail were higher by a factor of 2.52 (95% confidence interval (CI) = 2.13-2.99; P < .001). For persons with moderate or greater pain, the odds of being frail rather than not frail were higher by a factor of 5.52 (95% CI = 4.49-6.64 P < .001).
CONCLUSION: Moderate or higher pain was independently associated with frailty. Although causality cannot be ascertained in a cross-sectional analysis, interventions to improve pain management may help prevent or ameliorate frailty. J Am Geriatr Soc 60:113-117, 2012.
C1 [Shega, Joseph W.; Dale, William] Univ Chicago, Sect Geriatr & Palliat Med, Chicago, IL 60637 USA.
[Shega, Joseph W.] Univ Chicago, Sect Hematol & Oncol, Chicago, IL 60637 USA.
[Andrew, Melissa; Rockwood, Kenneth] Dalhousie Univ, Div Geriatr Med, Halifax, NS, Canada.
[Paice, Judith] Northwestern Univ, Feinberg Sch Med, Div Hematol Oncol, Chicago, IL 60611 USA.
[Weiner, Debra K.] Vet Affairs Pittsburgh Healthcare Syst, Ctr Geriatr Res Educ & Clin, Pittsburgh, PA USA.
[Weiner, Debra K.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Weiner, Debra K.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA.
[Weiner, Debra K.] Univ Pittsburgh, Dept Anesthesiol, Pittsburgh, PA USA.
RP Shega, JW (reprint author), Univ Chicago, Sect Geriatr & Palliat Med, MC 6098,5841 S Maryland Ave, Chicago, IL 60637 USA.
EM jshega@gmail.com
FU National Health Research Development Program; Seniors' Independence
Research program [6606-3954-MC(S)]; National Institute on Aging
[K23AG029815]; Canadian Institutes of Health Research [MOP-62823];
Dalhousie Medical Research Foundation; QEII Research Foundation
FX All the data reported here were gathered using public funding from the
National Health Research Development Program, which administrated a
grant from the Seniors' Independence Research program (6606-3954-MC(S)).
Funding for these analyses came from a career development award
K23AG029815 from the National Institute on Aging and from the Canadian
Institutes of Health Research through operating grant MOP-62823.
Additional support came from the Dalhousie Medical Research Foundation
(career support to KR as Kathryn Allen Weldon Professor of Alzheimer
Research) and the Fountain Innovation Fund of the QEII Research
Foundation.
NR 29
TC 22
Z9 22
U1 2
U2 9
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD JAN
PY 2012
VL 60
IS 1
BP 113
EP 117
DI 10.1111/j.1532-5415.2011.03769.x
PG 5
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 875PN
UT WOS:000299044100015
PM 22150394
ER
PT J
AU O'Hare, AM
AF O'Hare, Ann M.
TI Age and Access to Kidney Transplantation
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Editorial Material
ID OLDER-ADULTS; PROGNOSTIC INDEX; MORTALITY; VALIDATION
C1 [O'Hare, Ann M.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
[O'Hare, Ann M.] Vet Affairs Puget Sound Healthcare Syst, Dept Med, Seattle, WA USA.
[O'Hare, Ann M.] Grp Hlth Res Inst Seattle, Seattle, WA USA.
RP O'Hare, AM (reprint author), Univ Washington, Dept Med, Seattle, WA 98195 USA.
NR 15
TC 1
Z9 1
U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD JAN
PY 2012
VL 60
IS 1
BP 151
EP 153
DI 10.1111/j.1532-5415.2011.03790.x
PG 3
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 875PN
UT WOS:000299044100022
PM 22239294
ER
PT J
AU Jackson, ML
Wallis, J
Williams, K
Schoessow, K
Drohan, B
AF Jackson, Mary Lou
Wallis, Jennifer
Williams, Kristina
Schoessow, Kimberly
Drohan, Brian
TI Visual Function in the 'Oldest-Old' 1 Year After Comprehensive Vision
Rehabilitation
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Letter
ID QUALITY-OF-LIFE; IMPAIRMENT; OUTCOMES; ADULTS; IMPACT
C1 [Jackson, Mary Lou; Wallis, Jennifer; Williams, Kristina] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA.
[Schoessow, Kimberly] San Francisco Vet Affairs Hlth Care Syst, Frank Stein & Paul S May Ctr Low Vis Rehabil, Palo Alto, CA USA.
[Drohan, Brian] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Jackson, ML (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA.
NR 10
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD JAN
PY 2012
VL 60
IS 1
BP 183
EP 185
DI 10.1111/j.1532-5415.2011.03742.x
PG 3
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 875PN
UT WOS:000299044100043
PM 22239315
ER
PT J
AU Oklu, R
Habito, R
Mayr, M
Deipolyi, AR
Albadawi, H
Hesketh, R
Walker, TG
Linskey, KR
Long, CA
Wicky, S
Stoughton, J
Watkins, MT
AF Oklu, Rahmi
Habito, Roy
Mayr, Manuel
Deipolyi, Amy R.
Albadawi, Hassan
Hesketh, Robin
Walker, T. Gregory
Linskey, Katy R.
Long, Chandler A.
Wicky, Stephan
Stoughton, Julianne
Watkins, Michael T.
TI Pathogenesis of Varicose Veins
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Review
ID CHRONIC VENOUS INSUFFICIENCY; BETA BINDING PROTEIN-1;
EXTRACELLULAR-MATRIX; GENERAL-POPULATION; EDINBURGH VEIN; DISEASE; WALL;
PROTEOMICS; DISORDERS; MUTATIONS
AB Despite the high prevalence of varicose veins and the recent surge in research on the condition, the precise mechanisms underlying their development remain uncertain. In the past decade, there has been a shift from initial theories based on purely mechanical factors to hypotheses pointing to complex molecular changes causing histologic alterations in the vessel wall and extracellular matrix. Despite progress in understanding the molecular aspects of venous insufficiency, therapies for symptomatic varicose veins are directed toward anatomic and physical interventions. The present report reviews current evidence identifying the underlying biochemical alterations in the pathogenesis of varicose veins.
C1 [Oklu, Rahmi; Habito, Roy; Deipolyi, Amy R.; Walker, T. Gregory; Wicky, Stephan] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Vasc Imaging & Intervent, Boston, MA 02114 USA.
[Albadawi, Hassan; Long, Chandler A.; Stoughton, Julianne; Watkins, Michael T.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Vasc Surg, Boston, MA 02114 USA.
[Linskey, Katy R.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Hesketh, Robin] Univ Cambridge, Dept Biochem, Cambridge CB2 1QW, England.
[Mayr, Manuel] Kings Coll London, Dept Cardiol, London WC2R 2LS, England.
RP Oklu, R (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Vasc Imaging & Intervent, 55 Fruit St,290 Gray Bigelow, Boston, MA 02114 USA.
EM roklu@partners.org
OI Mayr, Manuel/0000-0002-0597-829X; Deipolyi, Amy/0000-0003-3144-386X
FU American College of Phlebology
FX R.O. is the recipient of the American College of Phlebology Investigator
Award. M.M. is a British Heart Foundation Senior Fellow. M.T.W. is the
Isenberg Scholar in Academic Surgery at Massachusetts General Hospital.
None of the authors have identified a conflict of interest.
NR 74
TC 15
Z9 17
U1 3
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD JAN
PY 2012
VL 23
IS 1
BP 33
EP 39
DI 10.1016/j.jvir.2011.09.010
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 877BL
UT WOS:000299151400005
PM 22030459
ER
PT J
AU Gervais, DA
AF Gervais, Debra A.
TI Preexisting Chronic Kidney Disease and Renal Tumor Ablation: Preliminary
Answers and Persistent Questions
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Gervais, DA (reprint author), Massachusetts Gen Hosp, Dept Radiol, White 270,55 Fruit St, Boston, MA 02114 USA.
EM dgervais@partners.org
NR 2
TC 1
Z9 1
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD JAN
PY 2012
VL 23
IS 1
BP 46
EP 47
DI 10.1016/j.jvir.2011.10.011
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 877BL
UT WOS:000299151400007
PM 22221472
ER
PT J
AU Krop, I
Winer, EP
AF Krop, Ian
Winer, Eric P.
TI Further progress in HER2-directed therapy
SO LANCET ONCOLOGY
LA English
DT Editorial Material
ID HER2-POSITIVE BREAST-CANCER; TRASTUZUMAB
C1 [Krop, Ian; Winer, Eric P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Krop, I (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA.
EM ikrop@partners.org
NR 9
TC 2
Z9 4
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
J9 LANCET ONCOL
JI Lancet Oncol.
PD JAN
PY 2012
VL 13
IS 1
BP 2
EP 3
PG 2
WC Oncology
SC Oncology
GA 875EZ
UT WOS:000299014500025
PM 22225715
ER
PT J
AU Kumar, SK
Lee, JH
Lahuerta, JJ
Morgan, G
Richardson, PG
Crowley, J
Haessler, J
Feather, J
Hoering, A
Moreau, P
Leleu, X
Hulin, C
Klein, SK
Sonneveld, P
Siegel, D
Blade, J
Goldschmidt, H
Jagannath, S
Miguel, JS
Orlowski, R
Palumbo, A
Sezer, O
Rajkumar, SV
Durie, BGM
AF Kumar, S. K.
Lee, J. H.
Lahuerta, J. J.
Morgan, G.
Richardson, P. G.
Crowley, J.
Haessler, J.
Feather, J.
Hoering, A.
Moreau, P.
LeLeu, X.
Hulin, C.
Klein, S. K.
Sonneveld, P.
Siegel, D.
Blade, J.
Goldschmidt, H.
Jagannath, S.
Miguel, J. S.
Orlowski, R.
Palumbo, A.
Sezer, O.
Rajkumar, S. V.
Durie, B. G. M.
CA Int Myeloma Working Grp
TI Risk of progression and survival in multiple myeloma relapsing after
therapy with IMiDs and bortezomib: A multicenter international myeloma
working group study
SO LEUKEMIA
LA English
DT Article
DE multiple myeloma; relapse; natural history; survival
ID LENALIDOMIDE PLUS DEXAMETHASONE; NEWLY-DIAGNOSED MYELOMA; COMBINATION
THERAPY; THALIDOMIDE; RETREATMENT; EXPERIENCE; IMPACT; TRIALS
AB Promising new drugs are being evaluated for treatment of multiple myeloma (MM), but their impact should be measured against the expected outcome in patients failing current therapies. However, the natural history of relapsed disease in the current era remains unclear. We studied 286 patients with relapsed MM, who were refractory to bortezomib and were relapsed following, refractory to or ineligible to receive, an IMiD (immunomodulatory drug), had measurable disease, and ECOG PS of 0, 1 or 2. The date patients satisfied the entry criteria was defined as time zero (T-0). The median age at diagnosis was 58 years, and time from diagnosis to T-0 was 3.3 years. Following T-0, 213 (74%) patients had a treatment recorded with one or more regimens (median = 1; range 0-8). The first regimen contained bortezomib in 55 (26%) patients and an IMiD in 70 (33%). A minor response or better was seen to at least one therapy after T0 in 94 patients (44%) including >= partial response in 69 (32%). The median overall survival and event-free survival from T-0 were 9 and 5 months, respectively. This study confirms the poor outcome, once patients become refractory to current treatments. The results provide context for interpreting ongoing trials of new drugs. Leukemia (2012) 26, 149-157; doi:10.1038/leu.2011.196; published online 29 July 2011
C1 [Kumar, S. K.; Rajkumar, S. V.] Mayo Clin, Div Hematol, Rochester, MN 55905 USA.
[Lee, J. H.] Gachon Univ, Gil Hosp, Div Hematooncol, Inchon, South Korea.
[Lahuerta, J. J.] Hosp Univ 12 Octubre, Dept Hematol, Madrid, Spain.
[Morgan, G.] Royal Marsden Hosp, Dept Hematol, Sutton, Surrey, England.
[Richardson, P. G.; Feather, J.] Dana Farber Canc Inst, Div Hematol Malignancies, Dept Med Oncol, Boston, MA 02115 USA.
[Crowley, J.; Haessler, J.; Hoering, A.] Canc Res & Biostat, Seattle, WA USA.
[Moreau, P.] Univ Hosp, Hotel Dieu, Div Hematol, Nantes, France.
[LeLeu, X.] CHU Lille, Hop Claude Huriez, Serv Malad Sang, Lille, France.
[Hulin, C.] CHU Nancy, Serv Dhematol, Nancy, France.
[Klein, S. K.; Sonneveld, P.] Erasmus MC, Dept Hematol, Rotterdam, Netherlands.
[Siegel, D.] Hackensack Univ Med Ctr, Ctr Canc, Hackensack, NJ USA.
[Blade, J.] Hosp Clin Barcelona, Barcelona, Spain.
[Goldschmidt, H.] Univ Heidelberg, Heidelberg, Germany.
[Jagannath, S.] Mt Sinai Canc Inst, New York, NY USA.
[Miguel, J. S.] Hosp Univ Salamanca, Serv Hematol, Salamanca, Spain.
[Orlowski, R.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Palumbo, A.] Univ Turin, Dept Hematol, Turin, Italy.
[Sezer, O.] Univ Hamburg, Dept Hematol, Hamburg, Germany.
[Durie, B. G. M.] Samuel Oschin Comprehens Canc Inst, Cedars Sinai Outpatient Canc Ctr, Los Angeles, CA USA.
RP Kumar, SK (reprint author), Mayo Clin, Div Hematol & Blood & Marrow Transplant, 200 1st St SW, Rochester, MN 55905 USA.
EM kumar.shaji@mayo.edu
RI Waage, Anders/D-7705-2013; Sangue, Inct/I-1919-2013; FACON,
THIERRY/M-9736-2014; Kumar, Shaji/A-9853-2008; richard,
chrystelle/K-8595-2015; Garcia-Sanz, Ramon/B-7986-2017;
OI FACON, THIERRY/0000-0001-7705-8460; Kumar, Shaji/0000-0001-5392-9284;
Garcia-Sanz, Ramon/0000-0003-4120-2787; Rajkumar, S.
Vincent/0000-0002-5862-1833; nahi, hareth/0000-0003-4711-5094
FU Celgene; Jansen-Cilag
FX JJL is on the Scientific advisory boards of Celgene and Janssen-Cilag.
PGR and JSM are Advisory board participants for Celgene, Millenium,
Johnson and Johnson. DS is on the Speakers Bureau and BD is an Advisory
board participant for Celgene and Millenium. AP is an Advisory Board
participant for Celgene, Johnson and Johnson. JB has received Honoraria
for lectures and advisory boards from Celgene, Jansen Cilag and Grant
support from Celgene and Jansen-Cilag. The remaining authors declare no
conflict of interest.
NR 31
TC 256
Z9 261
U1 3
U2 29
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD JAN
PY 2012
VL 26
IS 1
BP 149
EP 157
DI 10.1038/leu.2011.196
PG 9
WC Oncology; Hematology
SC Oncology; Hematology
GA 879GJ
UT WOS:000299317400015
PM 21799510
ER
PT J
AU Nelson, BD
Saltzman, A
Lee, PT
AF Nelson, Brett D.
Saltzman, Amy
Lee, Patrick T.
TI Bridging the global health training gap: Design and evaluation of a new
clinical global health course at Harvard Medical School
SO MEDICAL TEACHER
LA English
DT Article
ID NEGLECTED TROPICAL DISEASES; NEONATAL SURVIVAL; CHILD HEALTH; MATERNAL
MORTALITY; EXPERIENCES; ELECTIVES; DEATHS; CARE; INTERVENTIONS;
OPPORTUNITIES
AB Background: Medical student and resident interest in global health has been growing rapidly. Meanwhile, educational opportunities for trainees remain limited, and many trainees participate in global health experiences abroad without adequate preparation. Medical institutions are attempting to respond to this training gap by developing global health curricula.
Aims: We describe a novel clinical skills-based curriculum recently established among Harvard medical students and residents with the primary objective of providing essential clinical knowledge and skills to work effectively in resource-limited settings.
Methods: The course consisted of 10 evening sessions taught by a multidisciplinary faculty and focusing on practical management of the leading causes of the global burden of disease. Didactic discussions were reinforced by case studies and practical skills sessions, such as tropical microscopy, basic bedside ultrasound, simple dental extraction, and newborn resuscitation.
Results: Student mean knowledge scores increased significantly, from 64.5% (SD 8.9) before the course to 79.5% (SD 8.6) after the course (p < 0.001). Students also gave strongly positive evaluations and particularly valued the course's practical skills-building and the horizontal and vertical mentorship that developed among the diverse student, resident, and faculty participants.
Conclusions: This clinical course in global health may serve as one model for more effectively preparing trainees to work in developing countries.
C1 [Nelson, Brett D.; Lee, Patrick T.] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
[Nelson, Brett D.; Saltzman, Amy; Lee, Patrick T.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Nelson, BD (reprint author), Massachusetts Gen Hosp, Dept Pediat, 55 Fruit St, Boston, MA 02114 USA.
EM brett.d.nelson@gmail.com
RI yan, liu/A-1822-2015;
OI yan, liu/0000-0001-8517-1084; Nelson, Brett/0000-0002-5049-1798
NR 64
TC 9
Z9 9
U1 0
U2 3
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0142-159X
J9 MED TEACH
JI Med. Teach.
PY 2012
VL 34
IS 1
BP 45
EP 51
DI 10.3109/0142159X.2011.577122
PG 7
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA 877IQ
UT WOS:000299171600015
PM 21592020
ER
PT J
AU Zhan, W
Kang, GA
Glass, GA
Zhang, Y
Shirley, C
Millin, R
Possin, KL
Nezamzadeh, M
Weiner, MW
Marks, WJ
Schuff, N
AF Zhan, Wang
Kang, Gail A.
Glass, Graham A.
Zhang, Yu
Shirley, Cheryl
Millin, Rachel
Possin, Katherine L.
Nezamzadeh, Marzieh
Weiner, Michael W.
Marks, William J., Jr.
Schuff, Norbert
TI Regional Alterations of Brain Microstructure in Parkinson's Disease
Using Diffusion Tensor Imaging
SO MOVEMENT DISORDERS
LA English
DT Article
DE diffusion tensor imaging; magnetic resonance imaging; Parkinson's
disease; subtypes
ID SUBSTANTIA-NIGRA; BASAL GANGLIA; RAT MODEL; TRACT; SENSORIMOTOR;
DISORDERS; DEMENTIA; MRI
AB This study tested the hypothesis that diffusion tensor imaging can detect alteration in microscopic integrity of white matter and basal ganglia regions known to be involved in Parkinson's disease (PD) pathology. It was also hypothesized that there is an association between diffusion abnormality and PD severity and subtype. Diffusion tensor imaging at 4 Tesla was obtained in 12 PD and 20 control subjects, and measures of fractional anisotropy and mean diffusivity were evaluated using both region-of-interest and voxel-based methods. Movement deficits and subtypes in PD subjects were assessed using the Motor Subscale (Part III) of the Unified Parkinson's Disease Rating Scale. Reduced fractional anisotropy (P < .05, corrected) was found in PD subjects in regions related to the precentral gyrus, substantia nigra, putamen, posterior striatum, frontal lobe, and the supplementary motor areas. Reduced fractional anisotropy in the substantia nigra correlated (P < .05, corrected) with the increased rating scale motor scores. Significant spatial correlations between fractional anisotropy alterations in the putamen and other PD-affected regions were also found in the context of PD subtypes index analysis. Our data suggest that microstructural alterations detected with diffusion tensor might serve as a potential biomarker for PD. (C) 2011 Movement Disorder Society
C1 [Zhan, Wang; Zhang, Yu; Shirley, Cheryl; Millin, Rachel; Nezamzadeh, Marzieh; Weiner, Michael W.; Schuff, Norbert] Univ Calif San Francisco, Dept Radiol & Med Imaging, Ctr Imaging Neurodegenerat Dis, San Francisco, CA 94121 USA.
[Kang, Gail A.; Glass, Graham A.; Marks, William J., Jr.] San Francisco VA Med Ctr, Parkinsons Dis Res Educ & Clin Ctr, San Francisco, CA USA.
[Kang, Gail A.; Glass, Graham A.; Possin, Katherine L.; Marks, William J., Jr.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94121 USA.
RP Zhan, W (reprint author), Univ Calif San Francisco, Dept Radiol, VA Med Ctr 114M, 4150 Clement St, San Francisco, CA 94121 USA.
EM Wang.Zhan@gmail.com
FU Michael J. Fox Foundation [MJJF-BM2007]; NIH/NIRR "Research Resource for
MRI of Neurodegenerative Disorders" [1 P41RR023953]; Larry L. Hillblom
Foundation [2008-A-020-FEL]
FX This work was supported in part by the Michael J. Fox Foundation for
Parkinson's Research, "Multimodal MRI Markers for Parkinson's Disease"
(MJJF-BM2007); NIH/NIRR "Research Resource for MRI of Neurodegenerative
Disorders" (1 P41RR023953); and the Larry L. Hillblom Foundation, "Early
markers and brain bases of spatial impairment in alpha-synuclein
disorders" (2008-A-020-FEL).
NR 47
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U1 2
U2 13
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0885-3185
J9 MOVEMENT DISORD
JI Mov. Disord.
PD JAN
PY 2012
VL 27
IS 1
BP 90
EP 97
DI 10.1002/mds.23917
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 877DA
UT WOS:000299155900015
PM 21850668
ER
PT J
AU Chitnis, T
Tenembaum, S
Banwell, B
Krupp, L
Pohl, D
Rostasy, K
Yeh, EA
Bykova, O
Wassmer, E
Tardieu, M
Kornberg, A
Ghezzi, A
AF Chitnis, T.
Tenembaum, S.
Banwell, B.
Krupp, L.
Pohl, D.
Rostasy, K.
Yeh, E. A.
Bykova, O.
Wassmer, E.
Tardieu, M.
Kornberg, A.
Ghezzi, A.
CA Int Pediat Multiple Sclerosis
TI Consensus statement: evaluation of new and existing therapeutics for
pediatric multiple sclerosis
SO MULTIPLE SCLEROSIS JOURNAL
LA English
DT Article
DE disease-modifying therapies; multiple sclerosis
ID TECHNOLOGY-ASSESSMENT SUBCOMMITTEE; EARLY-ONSET MS; INTERFERON-BETA;
PSYCHOSOCIAL FEATURES; CLINICAL-FEATURES; AMERICAN-ACADEMY;
CHILDHOOD-ONSET; CELL REPERTOIRE; UNITED-STATES; JUVENILE MS
AB New therapies are being evaluated by clinical trials and, if efficacious, introduced for the treatment of adult MS. The role of these new and existing agents in the management of pediatric MS has yet to be defined. Pediatric investigation plans are now required by the Food and Drug Administration and European Medicines Agency for approval of new biological agents, providing an important opportunity to gather much-needed data for clinicians caring for children and adolescents with MS. However, challenges include the small number of patients, and the need for efficient yet comprehensive study designs incorporating factors necessary to inform the clinical care of children with MS. The elected Steering committee of the International Pediatric MS Study Group (IPMSSG) conducted a structured review of existing data on the disease-modifying therapies in pediatric MS and developed a consensus statement, which was further modified by the IPMSSG general membership, using an online survey tool. Fifty-one IPMSSG members from 21 countries responded to the survey, and 50 approved the final statement. Consensus recommendations regarding use of existing first-and second-line therapies, as well as a proposed definition for inadequate treatment response, are presented. Recommendations for the use and evaluation of emerging therapies (currently in phase III clinical trials or recently approved for adult MS) are discussed. The IPMSSG endorses the inclusion of pediatric MS patients in trials evaluating appropriate new and emerging therapies. Mechanisms for conducting high-impact, multicenter studies, including long-term follow-up in pediatric MS, are required to ensure that all MS patients, irrespective of age, benefit from advances in MS therapeutics.
C1 [Chitnis, T.] Massachusetts Gen Hosp, Partners Pediat Multiple Sclerosis Ctr, Boston, MA 02114 USA.
[Tenembaum, S.] Natl Pediat Hosp, Buenos Aires, DF, Argentina.
[Banwell, B.] Univ Toronto, Hosp Sick Children, Toronto, ON M5S 1A1, Canada.
[Krupp, L.] SUNY Stony Brook, Med Ctr, Stony Brook, NY USA.
[Pohl, D.] Univ Ottawa, Childrens Hosp Eastern Ontario, Ottawa, ON K1N 6N5, Canada.
[Rostasy, K.] Innsbruck Med Univ, Div Pediat Neurol & Inborn Errors Metab, Dept Pediat 4, Innsbruck, Austria.
[Yeh, E. A.] SUNY Buffalo, Dept Neurol, Buffalo, NY 14260 USA.
[Bykova, O.] Moscow Pediat Psychoneurol Hosp, Moscow, Russia.
[Wassmer, E.] Birmingham Childrens Hosp, Birmingham, W Midlands, England.
[Tardieu, M.] Hop Bicetre, AP HP, Paris, France.
[Tardieu, M.] Univ Paris 11, Paris, France.
[Kornberg, A.] Royal Childrens Hosp, Melbourne, Vic, Australia.
[Ghezzi, A.] Hosp Gallarate, Multiple Sclerosis Study Ctr, Gallarate, Italy.
RP Chitnis, T (reprint author), Massachusetts Gen Hosp, Partners Pediat Multiple Sclerosis Ctr, ACC-708,55 Fruit St, Boston, MA 02114 USA.
EM tchitnis@partners.org
OI amato, Maria Pia/0000-0003-3325-3760; Simone, Isabella
Laura/0000-0002-7429-3091; Jan, Mohammed/0000-0002-5188-8922
FU MS International Federation; National MS Society; Canadian MS Society
FX We would like to thank Professor Giancarlo Comi for valuable input
during the inaugural meeting. We would like to thank Professor Alan
Thompson and Professor Christopher Polman for critical reviewing of this
manuscript. The meeting of the IPMSSG Steering committee and invited
speakers on September 26, 2010 was funded by the MS International
Federation, National MS Society, and the Canadian MS Society.
NR 78
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U2 16
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1352-4585
J9 MULT SCLER J
JI Mult. Scler. J.
PD JAN
PY 2012
VL 18
IS 1
BP 116
EP 127
DI 10.1177/1352458511430704
PG 12
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 876CL
UT WOS:000299084600020
PM 22146610
ER
PT J
AU Hersher, R
DePinho, R
AF Hersher, Rebecca
DePinho, Ronald
TI Straight talk with ... Ronald DePinho
SO NATURE MEDICINE
LA English
DT Editorial Material
C1 [DePinho, Ronald] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[DePinho, Ronald] Dana Farber Canc Inst, Renowned Belfer Ctr Appl Canc Res, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD JAN
PY 2012
VL 18
IS 1
BP 9
EP 9
PG 1
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 875GO
UT WOS:000299018600011
ER
PT J
AU Garofalo, M
Romano, G
Di Leva, G
Nuovo, G
Jeon, YJ
Ngankeu, A
Sun, J
Lovat, F
Alder, H
Condorelli, G
Engelman, JA
Ono, M
Rho, JK
Cascione, L
Volinia, S
Nephew, KP
Croce, CM
AF Garofalo, Michela
Romano, Giulia
Di Leva, Gianpiero
Nuovo, Gerard
Jeon, Young-Jun
Ngankeu, Apollinaire
Sun, Jin
Lovat, Francesca
Alder, Hansjuerg
Condorelli, Gerolama
Engelman, Jeffrey A.
Ono, Mayumi
Rho, Jin Kyung
Cascione, Luciano
Volinia, Stefano
Nephew, Kenneth P.
Croce, Carlo M.
TI EGFR and MET receptor tyrosine kinase-altered microRNA expression
induces tumorigenesis and gefitinib resistance in lung cancers
SO NATURE MEDICINE
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; MESENCHYMAL TRANSITION; CELLS; AMPLIFICATION;
INHIBITORS; ADENOCARCINOMA; SENSITIVITY; METASTASIS; ACTIVATION; PTEN
AB The involvement of the MET oncogene in de novo and acquired resistance of non-small cell lung cancers (NSCLCs) to tyrosine kinase inhibitors (TKIs) has previously been reported, but the precise mechanism by which MET overexpression contributes to TKI-resistant NSCLC remains unclear. MicroRNAs (miRNAs) negatively regulate gene expression, and their dysregulation has been implicated in tumorigenesis. To understand their role in TKI-resistant NSCLCs, we examined changes in miRNA that are mediated by tyrosine kinase receptors. Here we report that miR-30b, miR-30c, miR-221 and miR-222 are modulated by both epidermal growth factor (EGF) and MET receptors, whereas miR-103 and miR-203 are controlled only by MET. We showed that these miRNAs have important roles in gefitinib-induced apoptosis and epithelial-mesenchymal transition of NSCLC cells in vitro and in vivo by inhibiting the expression of the genes encoding BCL2-like 11 (BIM), apoptotic peptidase activating factor 1 (APAF-1), protein kinase C epsilon (PKC-epsilon) and sarcoma viral oncogene homolog (SRC). These findings suggest that modulation of specific miRNAs may provide a therapeutic approach for the treatment of NSCLCs.
C1 [Garofalo, Michela; Di Leva, Gianpiero; Nuovo, Gerard; Jeon, Young-Jun; Ngankeu, Apollinaire; Sun, Jin; Lovat, Francesca; Alder, Hansjuerg; Cascione, Luciano; Volinia, Stefano; Croce, Carlo M.] Ohio State Univ, Ctr Comprehens Canc, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
[Romano, Giulia] Ist Ricovero & Cura Carattere Sci, Studio Diagnost Nucl SDN, Naples, Italy.
[Condorelli, Gerolama] Univ Naples Federico 2, Fac Biotechnol Sci, Inst Expt Endocrinol & Oncol, Dept Cellular & Mol Biol & Pathol,Consiglio Nazl, Naples, Italy.
[Engelman, Jeffrey A.] Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Engelman, Jeffrey A.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Ono, Mayumi] Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Pharmaceut Sci, Fukuoka 812, Japan.
[Rho, Jin Kyung] Univ Ulsan, Dept Pulm & Crit Care Med, Seoul, South Korea.
[Cascione, Luciano] Univ Catania, Dept Clin & Mol Biomed, Catania, Italy.
[Nephew, Kenneth P.] Indiana Univ, Simon Canc Ctr, Bloomington, IN USA.
[Nephew, Kenneth P.] Indiana Univ Sch Med, Med Sci Program, Dept Cellular & Integrated Physiol, Bloomington, IN USA.
RP Croce, CM (reprint author), Ohio State Univ, Ctr Comprehens Canc, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
EM carlo.croce@osumc.edu
RI Volinia, Stefano/A-3029-2010; Ngankeu, Apollinaire/J-8188-2012;
OI Volinia, Stefano/0000-0003-0910-3893; Cascione,
Luciano/0000-0002-4606-0637
FU Ohio State University; US National Institutes of Health [CA113001];
Kimmel Scholar Award
FX We thank K. Huebner and S. Lutz for revisions to the paper and P. Fadda
and S. Miller for qRT-PCR assistance. We also thank K. Sergott and
Ventana Medical Systems for supplying the immunohistochemistry reagents
used in this study. M. Nuovo (The Ohio State University Medical Center)
kindly provided the photomicroscopy work. We are grateful for research
support from The Ohio State University Targeted Investment in Excellence
Award, the US National Institutes of Health grant CA113001 and the
Kimmel Scholar Award (M.G.).
NR 31
TC 175
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U1 5
U2 56
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD JAN
PY 2012
VL 18
IS 1
BP 74
EP 82
DI 10.1038/nm.2577
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 875GO
UT WOS:000299018600032
PM 22157681
ER
PT J
AU Jeong, H
Cohen, DE
Cui, LB
Supinski, A
Savas, JN
Mazzulli, JR
Yates, JR
Bordone, L
Guarente, L
Krainc, D
AF Jeong, Hyunkyung
Cohen, Dena E.
Cui, Libin
Supinski, Andrea
Savas, Jeffrey N.
Mazzulli, Joseph R.
Yates, John R., III
Bordone, Laura
Guarente, Leonard
Krainc, Dimitri
TI Sirt1 mediates neuroprotection from mutant huntingtin by activation of
the TORC1 and CREB transcriptional pathway
SO NATURE MEDICINE
LA English
DT Article
ID DISEASE TRANSGENIC MICE; CALORIE RESTRICTION; GENE-TRANSCRIPTION;
NEURODEGENERATION; PGC-1-ALPHA; EXPRESSION; PROTEINS; NEURONS; REPEAT
AB Sirt1, a NAD-dependent protein deacetylase, has emerged as a key regulator of mammalian transcription in response to cellular metabolic status and stressl. Here we show that Sirt1 has a neuroprotective role in models of Huntington's disease, an inherited neurodegenerative disorder caused by a glutamine repeat expansion in huntingtin protein (HIT)2. Brain-specific knockout of Sirt1 results in exacerbation of brain pathology in a mouse model of Huntington's disease, whereas overexpression of Sirt1 improves survival, neuropathology and the expression of brain-derived neurotrophic factor (BDNF) in Huntington's disease mice. We show that Sirt1 deacetylase activity directly targets neurons to mediate neuroprotection from mutant HTT. The neuroprotective effect of Sirt1 requires the presence of CREB-regulated transcription coactivator 1 (TORC1), a brain-specific modulator of CREB activity3. We show that under normal conditions, Sirt1 deacetylates and activates TORC1 by promoting its dephosphorylation and its interaction with CREB. We identified BDNF as a key target of Sirt1 and TORC1 transcriptional activity in both normal and Huntington's disease neurons. Mutant HTT interferes with the TORC1-CREB interaction to repress BDNF transcription, and Sirt1 rescues this defect in vitro and in vivo. These studies suggest a key role for Sirt1 in transcriptional networks in both the normal and Huntington's disease brain and offer an opportunity for therapeutic development.
C1 [Jeong, Hyunkyung; Cui, Libin; Mazzulli, Joseph R.; Krainc, Dimitri] Harvard Univ, MassGen Inst Neurodegenerat Dis, Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA USA.
[Cohen, Dena E.; Supinski, Andrea; Guarente, Leonard] MIT, Dept Biol, Paul F Glenn Lab, Cambridge, MA USA.
[Savas, Jeffrey N.; Yates, John R., III] Scripps Res Inst, Dept Physiol Chem, La Jolla, CA 92037 USA.
[Bordone, Laura] Novartis Inst BioMed Res, Cardiovasc & Metab Dis Area, Cambridge, MA USA.
RP Krainc, D (reprint author), Harvard Univ, MassGen Inst Neurodegenerat Dis, Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA USA.
EM leng@mit.edu; krainc@helix.mgh.harvard.edu
FU US National Institutes of Health [R01NS051303, R01MH067880-08,
P41RR011823-15]; Cure Huntington's Disease Initiative (CHDI); Hereditary
Disease Foundation (FIDE); Glenn Foundation for Medical Research
FX We thank M. Montminy (Peptide Biology Laboratories (PBL), Salk
Institute) for the Flag-CREB, Flag-TORC1 and Flag-TORC1 S151A plasmids
and for antibody to TORC1 (#6937, PBL, Salk Institute) and helpful
discussions; M.E. Greenberg (Harvard Medical School) for the
pIII(170)Luc plasmid 15; T. Kouzarides (University of Cambridge) for
Sirt1 and Sift1 HY plasmids; Z. Wu (Novartis Institutes for Biomedical
Research) for the TORC1 plasmid; M. Difiglia (Massachusetts General
Hospital) for antibody to HTT (Ab1); E. Regulier (Novartis Institutes
for Biomedical Research) for lentiviral vectors expressing HTTEx1-25Q,
HTTEx1-72Q and Sirt1; and J.M. Park (Massachusetts General Hospital) for
the lentiviral vector used for CREB knockdown. We also acknowledge C.
Whitaker (Massachusetts Institute of Technology) for analysis of the
microarray data. This work was supported by grant R01NS051303 from the
US National Institutes of Health (D.K.); the Cure Huntington's Disease
Initiative (CHDI), Hereditary Disease Foundation (FIDE) (D.E.C.); US
National Institutes of Health, Glenn Foundation for Medical Research
(L.G.) and grants R01MH067880-08 and P41RR011823-15 from the US National
Institutes of Health (J.R.Y.).
NR 31
TC 127
Z9 133
U1 6
U2 18
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD JAN
PY 2012
VL 18
IS 1
BP 159
EP 165
DI 10.1038/nm.2559
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 875GO
UT WOS:000299018600043
PM 22179316
ER
PT J
AU Dickerson, BC
Wolk, DA
AF Dickerson, Bradford C.
Wolk, David A.
CA Alzheimers Dis Neuroimaging Initi
TI MRI cortical thickness biomarker predicts AD-like CSF and cognitive
decline in normal adults
SO NEUROLOGY
LA English
DT Article
ID PRECLINICAL ALZHEIMER-DISEASE; BRAIN ATROPHY RATES; TEMPORAL-LOBE;
DEMENTIA; MILD; IMPAIRMENT; SIGNATURE; NEUROPATHOLOGY; INDIVIDUALS;
PROGRESSION
AB Objective: New preclinical Alzheimer disease (AD) diagnostic criteria have been developed using biomarkers in cognitively normal (CN) adults. We implemented these criteria using an MRI biomarker previously associated with AD dementia, testing the hypothesis that individuals at high risk for preclinical AD would be at elevated risk for cognitive decline.
Methods: The Alzheimer's Disease Neuroimaging Initiative database was interrogated for CN individuals. MRI data were processed using a published set of a priori regions of interest to derive a single measure known as the AD signature (ADsig). Each individual was classified as ADsig-low (>= 1 SD below the mean: high risk for preclinical AD), ADsig-average (within 1 SD of mean), or ADsig-high (>= 1 SD above mean). A 3-year cognitive decline outcome was defined a priori using change in Clinical Dementia Rating sum of boxes and selected neuropsychological measures.
Results: Individuals at high risk for preclinical AD were more likely to experience cognitive decline, which developed in 21% compared with 7% of ADsig-average and 0% of ADsig-high groups (p = 0.03). Logistic regression demonstrated that every 1 SD of cortical thinning was associated with a nearly tripled risk of cognitive decline (p = 0.02). Of those for whom baseline CSF data were available, 60% of the high risk for preclinical AD group had CSF characteristics consistent with AD while 36% of the ADsig-average and 19% of the ADsig-high groups had such CSF characteristics (p = 0.1).
Conclusions: This approach to the detection of individuals at high risk for preclinical AD-identified in single CN individuals using this quantitative ADsig MRI biomarker-may provide investigators with a population enriched for AD pathobiology and with a relatively high likelihood of imminent cognitive decline consistent with prodromal AD. Neurology (R) 2012;78:84-90
C1 [Dickerson, Bradford C.] Massachusetts Gen Hosp, Dept Neurol, Frontotemporal Dementia Unit, Massachusetts Alzheimers Dis Res Ctr, Boston, MA 02114 USA.
[Dickerson, Bradford C.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Wolk, David A.] Univ Penn, Dept Neurol, Alzheimers Dis Core Ctr, Philadelphia, PA 19104 USA.
[Wolk, David A.] Univ Penn, Penn Memory Ctr, Philadelphia, PA 19104 USA.
RP Dickerson, BC (reprint author), Massachusetts Gen Hosp, Dept Neurol, Frontotemporal Dementia Unit, Massachusetts Alzheimers Dis Res Ctr, Boston, MA 02114 USA.
EM bradd@nmr.mgh.harvard.edu
RI Saykin, Andrew/A-1318-2007
OI Saykin, Andrew/0000-0002-1376-8532
FU Alzheimer's Disease Neuroimaging Initiative (ADNI) (NIH) [U01 AG024904];
National Institute on Aging; National Institute of Biomedical Imaging
and Bioengineering; Abbott; AstraZeneca AB; Bayer Schering Pharma AG;
Bristol-Myers Squibb; Eisai Global Clinical Development; Elan
Corporation; Genentech; GE Healthcare; GlaxoSmithKline; Innogenetics;
Johnson and Johnson; Eli Lilly and Co.; Medpace, Inc.; Merck and Co.,
Inc.; Novartis AG; Pfizer Inc; F. Hoffman-La Roche; Schering-Plough;
Synarc, Inc.; NIH [P30 AG010129, K01 AG030514]; Dana Foundation; NIA
[R01-AG29411, R21-AG29840, P50-AG005134, K23-AG028018, P30AG010124];
Alzheimer's Association; PA Department of Health
FX Data collection and sharing for this project was funded by the
Alzheimer's Disease Neuroimaging Initiative (ADNI) (NIH Grant U01
AG024904). ADNI is funded by the National Institute on Aging, the
National Institute of Biomedical Imaging and Bioengineering, and through
contributions from the following: Abbott, AstraZeneca AB, Bayer Schering
Pharma AG, Bristol-Myers Squibb, Eisai Global Clinical Development, Elan
Corporation, Genentech, GE Healthcare, GlaxoSmithKline, Innogenetics,
Johnson and Johnson, Eli Lilly and Co., Medpace, Inc., Merck and Co.,
Inc., Novartis AG, Pfizer Inc, F. Hoffman-La Roche, Schering-Plough,
Synarc, Inc., as well as nonprofit partners the Alzheimer's Association
and Alzheimer's Drug Discovery Foundation, with participation from the
U. S. Food and Drug Administration. Private sector contributions to ADNI
are facilitated by the Foundation for the NIH (www.fnih.org). The
grantee organization is the Northern California Institute for Research
and Education, and the study is coordinated by the Alzheimer's Disease
Cooperative Study at the University of California, San Diego. ADNI data
are disseminated by the Laboratory for Neuro Imaging at the University
of California, Los Angeles. This research was also supported by NIH
grants P30 AG010129, K01 AG030514, and the Dana Foundation. This
analysis was also supported by grants from the NIA R01-AG29411,
R21-AG29840, P50-AG005134, K23-AG028018, P30AG010124 and the Alzheimer's
Association.; Dr. Dickerson serves on the editorial board of
Hippocampus; serves as a consultant for Pfizer Inc; and receives
research support from the NIH and the Alzheimer's Association. Dr. Wolk
serves as a consultant for GE Healthcare and receives research support
from GE Healthcare, Pfizer Inc, the NIH, and the PA Department of
Health.
NR 33
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U1 2
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD JAN
PY 2012
VL 78
IS 2
BP 84
EP 90
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 877EL
UT WOS:000299159700007
PM 22189451
ER
PT J
AU Culhane, AC
Schroder, MS
Sultana, R
Picard, SC
Martinelli, EN
Kelly, C
Haibe-Kains, B
Kapushesky, M
St Pierre, AA
Flahive, W
Picard, KC
Gusenleitner, D
Papenhausen, G
O'Connor, N
Correll, M
Quackenbush, J
AF Culhane, Aedin C.
Schroeder, Markus S.
Sultana, Razvan
Picard, Shaita C.
Martinelli, Enzo N.
Kelly, Caroline
Haibe-Kains, Benjamin
Kapushesky, Misha
St Pierre, Anne-Alyssa
Flahive, William
Picard, Kermshlise C.
Gusenleitner, Daniel
Papenhausen, Gerald
O'Connor, Niall
Correll, Mick
Quackenbush, John
TI GeneSigDB: a manually curated database and resource for analysis of gene
expression signatures
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID CANCER; BIOINFORMATICS; ATLAS
AB GeneSigDB (http://www.genesigdb.org or http://compbio.dfci.harvard.edu/genesigdb/) is a database of gene signatures that have been extracted and manually curated from the published literature. It provides a standardized resource of published prognostic, diagnostic and other gene signatures of cancer and related disease to the community so they can compare the predictive power of gene signatures or use these in gene set enrichment analysis. Since GeneSigDB release 1.0, we have expanded from 575 to 3515 gene signatures, which were collected and transcribed from 1604 published articles largely focused on gene expression in cancer, stem cells, immune cells, development and lung disease. We have made substantial upgrades to the GeneSigDB website to improve accessibility and usability, including adding a tag cloud browse function, facetted navigation and a 'basket' feature to store genes or gene signatures of interest. Users can analyze GeneSigDB gene signatures, or upload their own gene list, to identify gene signatures with significant gene overlap and results can be viewed on a dynamic editable heatmap that can be downloaded as a publication quality image. All data in GeneSigDB can be downloaded in numerous formats including .gmt file format for gene set enrichment analysis or as a R/Bioconductor data file. GeneSigDB is available from http://www.genesigdb.org.
C1 [Culhane, Aedin C.; Schroeder, Markus S.; Sultana, Razvan; Picard, Shaita C.; Martinelli, Enzo N.; Kelly, Caroline; Haibe-Kains, Benjamin; St Pierre, Anne-Alyssa; Flahive, William; Picard, Kermshlise C.; Gusenleitner, Daniel; Papenhausen, Gerald; O'Connor, Niall; Correll, Mick; Quackenbush, John] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Culhane, Aedin C.; Haibe-Kains, Benjamin] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Kapushesky, Misha; Quackenbush, John] European Bioinformat Inst, EMBL Outstn Hinxton, Cambridge CB10 1SD, England.
RP Culhane, AC (reprint author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM aedin@jimmy.harvard.edu; johnq@jimmy.harvard.edu
RI Haibe-Kains, Benjamin/D-3702-2011
OI Haibe-Kains, Benjamin/0000-0002-7684-0079
FU National Institutes for Health National Library of Medicine [1R01
LM010129]; National Cancer Institute [1U19 CA148065]; Genome Research
Institute [1P50 HG004233]; Dana-Farber Cancer Institute Women; Claudia
Adams Barr foundation
FX This work was supported by National Institutes for Health National
Library of Medicine (1R01 LM010129), National Cancer Institute (1U19
CA148065), Genome Research Institute (1P50 HG004233); Dana-Farber Cancer
Institute Women's Cancers Program (to A. C. C); Claudia Adams Barr
foundation.
NR 24
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U1 1
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
EI 1362-4962
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2012
VL 40
IS D1
BP D1060
EP D1066
DI 10.1093/nar/gkr901
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 869MD
UT WOS:000298601300159
PM 22110038
ER
PT J
AU Haibe-Kains, B
Olsen, C
Djebbari, A
Bontempi, G
Correll, M
Bouton, C
Quackenbush, J
AF Haibe-Kains, Benjamin
Olsen, Catharina
Djebbari, Amira
Bontempi, Gianluca
Correll, Mick
Bouton, Christopher
Quackenbush, John
TI Predictive networks: a flexible, open source, web application for
integration and analysis of human gene networks
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID POSITIVE BREAST-CANCER; SOFTWARE ENVIRONMENT; INFERENCE; VISUALIZATION;
BIOCURATION; CYTOSCAPE; ALGORITHM; MODELS; SCALE; TOOL
AB Genomics provided us with an unprecedented quantity of data on the genes that are activated or repressed in a wide range of phenotypes. We have increasingly come to recognize that defining the networks and pathways underlying these phenotypes requires both the integration of multiple data types and the development of advanced computational methods to infer relationships between the genes and to estimate the predictive power of the networks through which they interact. To address these issues we have developed Predictive Networks (PN), a flexible, open-source, web-based application and data services framework that enables the integration, navigation, visualization and analysis of gene interaction networks. The primary goal of PN is to allow biomedical researchers to evaluate experimentally derived gene lists in the context of large-scale gene interaction networks. The PN analytical pipeline involves two key steps. The first is the collection of a comprehensive set of known gene interactions derived from a variety of publicly available sources. The second is to use these 'known' interactions together with gene expression data to infer robust gene networks. The PN web application is accessible from http://predictivenetworks.org. The PN code base is freely available at https://sourceforge.net/projects/predictivenets/.
C1 [Haibe-Kains, Benjamin; Quackenbush, John] Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02215 USA.
[Haibe-Kains, Benjamin; Quackenbush, John] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02215 USA.
[Olsen, Catharina; Bontempi, Gianluca] Univ Libre Bruxelles, Machine Learning Grp, Brussels, Belgium.
[Djebbari, Amira] Univ Toronto, Ontario Canc Inst, Princess Margaret Hosp UHN, Toronto, ON M5G 1L7, Canada.
[Djebbari, Amira] Univ Toronto, Campbell Family Inst Canc Res, Toronto, ON M5G 1L7, Canada.
[Correll, Mick; Quackenbush, John] Dana Farber Canc Inst, Ctr Canc Computat Biol, Boston, MA 02215 USA.
[Bouton, Christopher] Entagen, Newburyport, MA 01950 USA.
RP Haibe-Kains, B (reprint author), Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02215 USA.
EM bhaibeka@jimmy.harvard.edu; johnq@jimmy.harvard.edu
RI Haibe-Kains, Benjamin/D-3702-2011
OI Haibe-Kains, Benjamin/0000-0002-7684-0079
FU National Library of Medicine of the US National Institutes of Health
[1R01LM010129]
FX Funding for open access charge: National Library of Medicine of the US
National Institutes of Health (grant 1R01LM010129).
NR 49
TC 17
Z9 18
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2012
VL 40
IS D1
BP D866
EP D875
DI 10.1093/nar/gkr1050
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 869MD
UT WOS:000298601300130
PM 22096235
ER
PT J
AU Kapushesky, M
Adamusiak, T
Burdett, T
Culhane, A
Farne, A
Filippov, A
Holloway, E
Klebanov, A
Kryvych, N
Kurbatova, N
Kurnosov, P
Malone, J
Melnichuk, O
Petryszak, R
Pultsin, N
Rustici, G
Tikhonov, A
Travillian, RS
Williams, E
Zorin, A
Parkinson, H
Brazma, A
AF Kapushesky, Misha
Adamusiak, Tomasz
Burdett, Tony
Culhane, Aedin
Farne, Anna
Filippov, Alexey
Holloway, Ele
Klebanov, Andrey
Kryvych, Nataliya
Kurbatova, Natalja
Kurnosov, Pavel
Malone, James
Melnichuk, Olga
Petryszak, Robert
Pultsin, Nikolay
Rustici, Gabriella
Tikhonov, Andrew
Travillian, Ravensara S.
Williams, Eleanor
Zorin, Andrey
Parkinson, Helen
Brazma, Alvis
TI Gene Expression Atlas update-a value-added database of microarray and
sequencing-based functional genomics experiments
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID RNA-SEQ; ONTOLOGY; BIOINFORMATICS
AB Gene Expression Atlas (http://www.ebi.ac.uk/gxa) is an added-value database providing information about gene expression in different cell types, organism parts, developmental stages, disease states, sample treatments and other biological/experimental conditions. The content of this database derives from curation, re-annotation and statistical analysis of selected data from the ArrayExpress Archive and the European Nucleotide Archive. A simple interface allows the user to query for differential gene expression either by gene names or attributes or by biological conditions, e.g. diseases, organism parts or cell types. Since our previous report we made 20 monthly releases and, as of Release 11.08 (August 2011), the database supports 19 species, which contains expression data measured for 19 014 biological conditions in 136 551 assays from 5598 independent studies.
C1 [Kapushesky, Misha; Adamusiak, Tomasz; Burdett, Tony; Farne, Anna; Filippov, Alexey; Holloway, Ele; Klebanov, Andrey; Kryvych, Nataliya; Kurbatova, Natalja; Kurnosov, Pavel; Malone, James; Melnichuk, Olga; Petryszak, Robert; Pultsin, Nikolay; Rustici, Gabriella; Tikhonov, Andrew; Travillian, Ravensara S.; Williams, Eleanor; Zorin, Andrey; Parkinson, Helen; Brazma, Alvis] EMBL, European Bioinformat Inst, Hinxton, England.
[Culhane, Aedin] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Kapushesky, M (reprint author), EMBL, European Bioinformat Inst, Hinxton, England.
EM ostolop@ebi.ac.uk
OI Brazma, Alvis/0000-0001-5988-7409; Adamusiak,
Tomasz/0000-0002-0746-2916; Petryszak, Robert/0000-0001-6333-2182;
Burdett, Anthony/0000-0002-2513-5396; Parkinson,
Helen/0000-0003-3035-4195; Rustici, Gabriella/0000-0003-3085-1271;
Williams, Eleanor/0000-0002-0851-7990
FU European Molecular Biology Laboratory (EMBL); SLING; SYBARIS; GEUVADIS;
European Commission from the BBSRC [BB/G022755/1]; NHGRI; EMBL
FX The project was funded by the European Molecular Biology Laboratory
(EMBL), SLING, SYBARIS, GEUVADIS and GEN2PHEN grants from the European
Commission, grant #BB/G022755/1 from the BBSRC, and the MAGE grant from
the NHGRI. Funding for open access charge: EMBL.
NR 20
TC 74
Z9 77
U1 1
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
EI 1362-4962
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2012
VL 40
IS D1
BP D1077
EP D1081
DI 10.1093/nar/gkr913
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 869MD
UT WOS:000298601300161
PM 22064864
ER
PT J
AU Sui, SJH
Begley, K
Reilly, D
Chapman, B
McGovern, R
Rocca-Sera, P
Maguire, E
Altschuler, GM
Hansen, TAA
Sompallae, R
Krivtsov, A
Shivdasani, RA
Armstrong, SA
Culhane, AC
Correll, M
Sansone, SA
Hofmann, O
Hide, W
AF Sui, Shannan J. Ho
Begley, Kimberly
Reilly, Dorothy
Chapman, Brad
McGovern, Ray
Rocca-Sera, Philippe
Maguire, Eamonn
Altschuler, Gabriel M.
Hansen, Terah A. A.
Sompallae, Ramakrishna
Krivtsov, Andrei
Shivdasani, Ramesh A.
Armstrong, Scott A.
Culhane, Aedin C.
Correll, Mick
Sansone, Susanna-Assunta
Hofmann, Oliver
Hide, Winston
TI The Stem Cell Discovery Engine: an integrated repository and analysis
system for cancer stem cell comparisons
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID GENE-EXPRESSION; SIGNATURES; SURVIVAL; ONTOLOGY; DATABASE
AB Mounting evidence suggests that malignant tumors are initiated and maintained by a subpopulation of cancerous cells with biological properties similar to those of normal stem cells. However, descriptions of stem-like gene and pathway signatures in cancers are inconsistent across experimental systems. Driven by a need to improve our understanding of molecular processes that are common and unique across cancer stem cells (CSCs), we have developed the Stem Cell Discovery Engine (SCDE)-an online database of curated CSC experiments coupled to the Galaxy analytical framework. The SCDE allows users to consistently describe, share and compare CSC data at the gene and pathway level. Our initial focus has been on carefully curating tissue and cancer stem cell-related experiments from blood, intestine and brain to create a high quality resource containing 53 public studies and 1098 assays. The experimental information is captured and stored in the multi-omics Investigation/Study/Assay (ISA-Tab) format and can be queried in the data repository. A linked Galaxy framework provides a comprehensive, flexible environment populated with novel tools for gene list comparisons against molecular signatures in GeneSigDB and MSigDB, curated experiments in the SCDE and pathways in WikiPathways. The SCDE is available at http://discovery.hsci.harvard.edu.
C1 [Sui, Shannan J. Ho; Begley, Kimberly; Reilly, Dorothy; Chapman, Brad; McGovern, Ray; Altschuler, Gabriel M.; Hansen, Terah A. A.; Sompallae, Ramakrishna; Culhane, Aedin C.; Hofmann, Oliver; Hide, Winston] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Sui, Shannan J. Ho; Begley, Kimberly; Reilly, Dorothy; Chapman, Brad; McGovern, Ray; Hansen, Terah A. A.; Hofmann, Oliver; Hide, Winston] Harvard Univ, Sch Publ Hlth, HSPH Bioinformat Core, Boston, MA 02115 USA.
[Reilly, Dorothy; Sansone, Susanna-Assunta] Novartis Inst BioMed Res, Cambridge, MA USA.
[Rocca-Sera, Philippe; Maguire, Eamonn] Univ Oxford, Oxford E Res Ctr, Oxford OX1 2JD, England.
[Krivtsov, Andrei; Armstrong, Scott A.] Childrens Hosp, Dept Pediat Oncol, Boston, MA 02115 USA.
[Culhane, Aedin C.; Correll, Mick] Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA.
[Krivtsov, Andrei; Shivdasani, Ramesh A.; Armstrong, Scott A.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Shivdasani, Ramesh A.; Armstrong, Scott A.; Hide, Winston] Harvard Stem Cell Inst, Cambridge, MA USA.
[Correll, Mick] Dana Farber Canc Inst, Ctr Canc Computat Biol, Boston, MA 02115 USA.
RP Hide, W (reprint author), Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
EM shosui@hsph.harvard.edu; whide@hsph.harvard.edu
RI Hofmann, Oliver/F-1800-2013;
OI Hofmann, Oliver/0000-0002-7738-1513; Chapman, Brad/0000-0002-3026-1856;
Hide, Winston/0000-0002-8621-3271
FU National Institutes of Health [1RC2CA148222-01]; Harvard Stem Cell
Institute; Harvard School of Public Health
FX National Institutes of Health (1RC2CA148222-01 to R.S., S.A. and W.H.);
Harvard Stem Cell Institute. Funding for open access charge: Harvard
School of Public Health Dean's Fund; National Institutes of Health
Stimulus awards.
NR 25
TC 7
Z9 7
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2012
VL 40
IS D1
BP D984
EP D991
DI 10.1093/nar/gkr1051
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 869MD
UT WOS:000298601300148
ER
PT J
AU Wang, XW
Spandidos, A
Wang, HJ
Seed, B
AF Wang, Xiaowei
Spandidos, Athanasia
Wang, Huajun
Seed, Brian
TI PrimerBank: a PCR primer database for quantitative gene expression
analysis, 2012 update
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID REAL-TIME PCR; POLYMERASE-CHAIN-REACTION; CROSS-PLATFORM;
QUANTIFICATION; AMPLIFICATION; SEQUENCES; SELECTION; DESIGN; PROBES;
PAIRS
AB Optimization of primer sequences for polymerase chain reaction (PCR) and quantitative PCR (qPCR) and reaction conditions remains an experimental challenge. We have developed a resource, PrimerBank, which contains primers that can be used for PCR and qPCR under stringent and allele-invariant amplification conditions. A distinguishing feature of PrimerBank is the experimental validation of primer pairs covering most known mouse genes. Here, we describe a major update of PrimerBank that includes the design of new primers covering 17 076 and 18 086 genes for the human and mouse species, respectively. As a result of this update, PrimerBank contains 497 156 primers (an increase of 62% from the previous version) that cover 36 928 human and mouse genes, corresponding to around 94% of all known protein-coding gene sequences. An updated algorithm based on our previous approach was used to design new primers using current genomic information available from the National Center for Biotechnology Information (NCBI). PrimerBank primers work under uniform PCR conditions, and can be used for high-throughput or genome-wide qPCR. Because of their broader linear dynamic range and greater sensitivity, qPCR approaches are used to reanalyze changes in expression suggested by exploratory technologies such as microarrays and RNA-Seq. The primers and all experimental validation data can be freely accessed from the PrimerBank website, http://pga.mgh.harvard.edu/primerbank/.
C1 [Spandidos, Athanasia; Wang, Huajun; Seed, Brian] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
[Spandidos, Athanasia; Wang, Huajun; Seed, Brian] Harvard Univ, Dept Genet, Sch Med, Boston, MA 02115 USA.
[Wang, Xiaowei] Washington Univ, Sch Med, Dept Radiat Oncol, St Louis, MO 63108 USA.
RP Seed, B (reprint author), Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, 185 Cambridge St, Boston, MA 02114 USA.
EM bseed@ccib.mgh.harvard.edu
FU National Institutes of Health [U01 HL066678, R01 GM089784]; Center for
Computational and Integrative Biology, Massachusetts General Hospital
FX National Institutes of Health (U01 HL066678 and R01 GM089784). Funding
for open access charge: Center for Computational and Integrative
Biology, Massachusetts General Hospital.
NR 26
TC 115
Z9 119
U1 2
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2012
VL 40
IS D1
BP D1144
EP D1149
DI 10.1093/nar/gkr1013
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 869MD
UT WOS:000298601300171
PM 22086960
ER
PT J
AU Flaherty, P
Natsoulis, G
Muralidharan, O
Winters, M
Buenrostro, J
Bell, J
Brown, S
Holodniy, M
Zhang, N
Ji, HP
AF Flaherty, Patrick
Natsoulis, Georges
Muralidharan, Omkar
Winters, Mark
Buenrostro, Jason
Bell, John
Brown, Sheldon
Holodniy, Mark
Zhang, Nancy
Ji, Hanlee P.
TI Ultrasensitive detection of rare mutations using next-generation
targeted resequencing
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID DNA; VARIANTS; PERFORMANCE; CANCER
AB With next-generation DNA sequencing technologies, one can interrogate a specific genomic region of interest at very high depth of coverage and identify less prevalent, rare mutations in heterogeneous clinical samples. However, the mutation detection levels are limited by the error rate of the sequencing technology as well as by the availability of variant-calling algorithms with high statistical power and low false positive rates. We demonstrate that we can robustly detect mutations at 0.1% fractional representation. This represents accurate detection of one mutant per every 1000 wild-type alleles. To achieve this sensitive level of mutation detection, we integrate a high accuracy indexing strategy and reference replication for estimating sequencing error variance. We employ a statistical model to estimate the error rate at each position of the reference and to quantify the fraction of variant base in the sample. Our method is highly specific (99%) and sensitive (100%) when applied to a known 0.1% sample fraction admixture of two synthetic DNA samples to validate our method. As a clinical application of this method, we analyzed nine clinical samples of H1N1 influenza A and detected an oseltamivir (antiviral therapy) resistance mutation in the H1N1 neuraminidase gene at a sample fraction of 0.18%.
C1 [Flaherty, Patrick; Natsoulis, Georges; Buenrostro, Jason; Bell, John; Ji, Hanlee P.] Stanford Univ, Stanford Genome Technol Ctr, Palo Alto, CA 94304 USA.
[Flaherty, Patrick] Stanford Univ, Dept Biochem, Stanford, CA 94305 USA.
[Muralidharan, Omkar; Zhang, Nancy] Stanford Univ, Dept Stat, Stanford, CA 94305 USA.
[Winters, Mark; Holodniy, Mark] Stanford Univ, Div Infect Dis, Dept Med, Stanford, CA 94305 USA.
[Brown, Sheldon] James J Peters VA Med Ctr, Bronx, NY 10468 USA.
[Holodniy, Mark] VA Palo Alto Hlth Care Syst, Palo Alto, CA 94304 USA.
[Ji, Hanlee P.] Stanford Univ, Div Oncol, Dept Med, Sch Med, Stanford, CA 94305 USA.
RP Ji, HP (reprint author), Stanford Univ, Stanford Genome Technol Ctr, Palo Alto, CA 94304 USA.
EM genomics_ji@stanford.edu
FU National Science Foundation, Division of Mathematical Sciences (NSF DMS)
DMS [1043204]; Department of Veterans Affairs; National Institutes of
Health (NIH) [5K08CA96879-6, DK56339, 2P01HG000205, R21CA140089]; Doris
Duke Clinical Foundation; Reddere Foundation; Liu Bie Ju Cha and Family
Fellowship in Cancer; Wang Family Foundation; Howard Hughes Medical
Foundation
FX National Science Foundation, Division of Mathematical Sciences (NSF DMS)
DMS (Grant #1043204 to N.Z. and H.P.J.); Department of Veterans Affairs
(in part, to M. H.); National Institutes of Health (NIH) (grants
5K08CA96879-6 to H.P.J., DK56339 to H.P.J, 2P01HG000205 to J.B., J.M.B.,
H.P.J. and P. F. and R21CA140089 to G.N. and H.P.J.); Doris Duke
Clinical Foundation (to H.P.J.); Reddere Foundation (to H.P.J.); Liu Bie
Ju Cha and Family Fellowship in Cancer (to H.P.J.); Wang Family
Foundation (to H.P.J.); Howard Hughes Medical Foundation (to H.P.J.).
Funding for open access charge: NIH (grant 2P01HG000205) and NSF DMS
(grant 1043204).
NR 21
TC 53
Z9 53
U1 1
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD JAN
PY 2012
VL 40
IS 1
AR e2
DI 10.1093/nar/gkr861
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 871JG
UT WOS:000298733500002
PM 22013163
ER
PT J
AU Livhits, M
Mercado, C
Yermilov, I
Parikh, JA
Dutson, E
Mehran, A
Ko, CY
Gibbons, MM
AF Livhits, Masha
Mercado, Cheryl
Yermilov, Irina
Parikh, Janak A.
Dutson, Erik
Mehran, Amir
Ko, Clifford Y.
Gibbons, Melinda Maggard
TI Preoperative Predictors of Weight Loss Following Bariatric Surgery:
Systematic Review
SO OBESITY SURGERY
LA English
DT Review
DE Bariatric surgery; Predictors; Weight loss; Preoperative; Outcomes
ID Y GASTRIC BYPASS; VERTICAL BANDED GASTROPLASTY; QUALITY-OF-LIFE;
MORBIDLY OBESE-PATIENTS; BODY-MASS INDEX; 12-MONTH POSTOPERATIVE
OUTCOMES; DUODENAL SWITCH OPERATION; CHILDHOOD SEXUAL-ABUSE;
BINGE-EATING DISORDER; RISKS VS. BENEFITS
AB Obesity affects 32% of adults in the USA. Surgery generates substantial weight loss, but 20-30% fails to achieve successful weight loss. Our objective was to identify preoperative psychosocial factors associated with weight loss following bariatric surgery.
We performed a literature search of PubMedA (R) and the Cochrane Database of Reviews of Effectiveness between 1988 and April 2010. Articles were screened for bariatric surgery and weight loss if they included a preoperative predictor of weight loss: body mass index (BMI), preoperative weight loss, eating disorders, or psychiatric disorder/substance abuse. One thousand seven titles were reviewed, 534 articles screened, and 115 included in the review.
Factors that may be positively associated with weight loss after surgery include mandatory preoperative weight loss (7 of 14 studies with positive association). Factors that may be negatively associated with weight loss include preoperative BMI (37 out of 62 studies with negative association), super-obesity (24 out of 33 studies), and personality disorders (7 out of 14 studies). Meta-analysis revealed a decrease of 10.1% excess weight loss (EWL) for super-obese patients (95% confidence interval (CI) [3.7-16.5%]), though there was significant heterogeneity in the meta-analysis, and an increase of 5.9% EWL for patients with binge eating at 12 months after surgery (95% CI [1.9-9.8%]).
Further studies are necessary to investigate whether preoperative factors can predict a clinically meaningful difference in weight loss after bariatric surgery. The identification of predictive factors may improve patient selection and help develop interventions targeting specific needs of patients.
C1 [Livhits, Masha; Yermilov, Irina; Parikh, Janak A.; Ko, Clifford Y.; Gibbons, Melinda Maggard] VA Greater Los Angeles Healthcare Syst, Dept Surg, Los Angeles, CA 90073 USA.
[Livhits, Masha; Mercado, Cheryl; Yermilov, Irina; Parikh, Janak A.; Dutson, Erik; Mehran, Amir; Ko, Clifford Y.; Gibbons, Melinda Maggard] Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, Los Angeles, CA 90095 USA.
[Gibbons, Melinda Maggard] Olive View UCLA, Dept Surg, Los Angeles, CA 91342 USA.
RP Livhits, M (reprint author), VA Greater Los Angeles Healthcare Syst, Dept Surg, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM mlivhits@mednet.ucla.edu
FU VA Department of Surgery; Robert Wood Johnson Physician Faculty
FX We would like to acknowledge the generous contribution of Paul G.
Shekelle to the design of our project and critical review of the
analysis. The VA Department of Surgery provided support for Dr. Livhits
and Dr. Gibbons. Dr. Gibbons's time was supported in part by a grant
from the Robert Wood Johnson Physician Faculty Scholars program.
NR 145
TC 153
Z9 153
U1 5
U2 44
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0960-8923
EI 1708-0428
J9 OBES SURG
JI Obes. Surg.
PD JAN
PY 2012
VL 22
IS 1
BP 70
EP 89
DI 10.1007/s11695-011-0472-4
PG 20
WC Surgery
SC Surgery
GA 876PU
UT WOS:000299120700013
PM 21833817
ER
PT J
AU Bourguignon, LYW
Earle, C
Wong, G
Spevak, CC
Krueger, K
AF Bourguignon, L. Y. W.
Earle, C.
Wong, G.
Spevak, C. C.
Krueger, K.
TI Stem cell marker (Nanog) and Stat-3 signaling promote MicroRNA-21
expression and chemoresistance in hyaluronan/CD44-activated head and
neck squamous cell carcinoma cells
SO ONCOGENE
LA English
DT Article
DE nanog; Stat-3; miR-21; hyaluronan; CD44; head & neck cancer
ID NF-KAPPA-B; CANCER STATISTICS; GENE-EXPRESSION; TUMOR-CELLS; RHO-KINASE;
HYALURONAN; BREAST; PROGRESSION; ACTIVATION; TRANSCRIPTION
AB MicroRNAs are often associated with the pathogenesis of many cancers, including head and neck squamous cell carcinoma (HNSCC). In particular, microRNA-21 (miR-21) appears to have a critical role in tumor cell survival, chemoresistance and HNSCC progression. In this study, we investigated matrix hyaluronan (HA)-induced CD44 (a primary HA receptor) interaction with the stem cell markers, Nanog and Stat-3, in HNSCC cells (HSC-3 cells). Our results indicate that HA binding to CD44 promotes Nanog-Stat-3 (also tyrosine phosphorylated Stat-3) complex formation, nuclear translocation and transcriptional activation. Further analyses reveal that miR-21 is controlled by an upstream promoter containing Stat-3 binding site(s), while chromatin immunoprecipitation assays demonstrate that stimulation of miR-21 expression by HA/CD44 signaling is Nanog/Stat-3-dependent in HNSCC cells. This process results in a decrease of a tumor suppressor protein (PDCD4), and an upregulation of i nhibitors of the apoptosis family of proteins (IAPs) as well as chemoresistance in HSC-3 cells. Treatment of HSC-3 cells with Nanog- and/or Stat-3-specific small interfering RNAs effectively blocks HA-mediated Nanog-Stat-3 signaling events, abrogates miR-21 production and increases PDCD4 expression. Subsequently, this Nanog-Stat-3 signaling inhibition causes downregulation of survival protein (IAP) expression and enhancement of chemosensitivity. To further evaluate the role of miR-21 in tumor cell-specific functions, HSC-3 cells were also transfected with a specific anti-miR-21 inhibitor in order to silence miR-21 expression and block its target functions. Our results demonstrate that anti-miR-21 inhibitor not only upregulates PDCD4 expression but also decreases IAP expression and enhances chemosensitivity in HA-treated HNSCC cells. Together, these findings indicate that the HA-induced CD44 interaction with Nanog and Stat-3 has a pivotal role in miR-21 production leading to PDCD4 reduction, IAP upregulation and chemoresistance in HNSCC cells. This novel Nanog/Stat-3 signaling pathway-specific mechanism involved in miR-21 production is significant for the formation of future intervention strategies in the treatment of HA/CD44-activated HNSCC. Oncogene (2012) 31, 149-160; doi:10.1038/onc.2011.222; published online 20 June 2011
C1 [Bourguignon, L. Y. W.] Univ Calif San Francisco, Dept Med, Endocrine Unit 111N, San Francisco, CA 94121 USA.
San Francisco VA Med Ctr, San Francisco, CA USA.
RP Bourguignon, LYW (reprint author), Univ Calif San Francisco, Dept Med, Endocrine Unit 111N, 4150 Clement St, San Francisco, CA 94121 USA.
EM lilly.bourguignon@ucsf.edu
FU Veterans Affairs (VA) Merit Review grant; United States Public Health
grants [R01 CA66163, R01 CA78633, P01 AR39448]
FX We gratefully acknowledge the assistance of Drs Gerard J Bourguignon and
Walter M Holleran in the preparation and review of this manuscript. We
are grateful for Ms Christina Camacho for her assistance in preparing
graphs and illustrations. We would also like to thank for Dr Shaomeng
Wang from the University of Michigan for providing us an IAP inhibitor,
SM164. This work was supported by Veterans Affairs (VA) Merit Review
grant and United States Public Health grants (R01 CA66163, R01 CA78633
and P01 AR39448). LYWB is a VA Senior Research Career Scientist.
NR 30
TC 89
Z9 93
U1 2
U2 12
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD JAN
PY 2012
VL 31
IS 2
BP 149
EP 160
DI 10.1038/onc.2011.222
PG 12
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 879CN
UT WOS:000299307400002
PM 21685938
ER
PT J
AU Uslan, DZ
Gleva, MJ
Warren, DK
Mela, T
Chung, MK
Gottipaty, V
Borge, R
Dan, D
Shinn, T
Mitchell, K
Holcomb, RG
Poole, JE
AF Uslan, Daniel Z.
Gleva, Marye J.
Warren, David K.
Mela, Theofanie
Chung, Mina K.
Gottipaty, Venkateshwar
Borge, Richard
Dan, Dan
Shinn, Timothy
Mitchell, Kevin
Holcomb, Richard G.
Poole, Jeanne E.
TI Cardiovascular Implantable Electronic Device Replacement Infections and
Prevention: Results from the REPLACE Registry
SO PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY
LA English
DT Article
DE pacemaker; defibrillator; infection
ID PERMANENT PACEMAKER IMPLANTATION; ANTIBIOTIC-PROPHYLAXIS; RISK-FACTORS;
CARDIOVERTER-DEFIBRILLATORS; TEMPORAL TRENDS; RATES; MANAGEMENT;
SURGERY; HEART
AB Background: Infection following cardiovascular implantable electronic device (CIED) replacement is a serious complication, and rates of infection have increased. Analysis of procedural and clinical data from device replacement procedures collected by the REPLACE Registry may provide insights into infection prevention strategies and outcomes.
Methods: We prospectively evaluated procedural complications in patients undergoing CIED replacement over 6 months from 72 U. S. sites. Major and minor infections were predefined and adjudicated by an independent blinded clinical events committee. Data regarding infection prevention strategies and infectious outcomes were analyzed for their potential relationships.
Results: A total of 1,744 patients were included in REPLACE. All patients received preoperative intravenous antibiotics and 68.7% received postoperative systemic antibiotic therapy. CIED infection developed in 22 patients (1.3%), of which 14 cases were major (0.8%, 95% confidence interval [CI] 0.4%-1.3%) and eight were minor (0.5%, 95% CI 0.2%-0.9%). Patients with infections were more likely to have had postoperative hematomas (five of 22 [22.7%] vs 17 of 1,722 [0.98%], P = 0.002). Participating sites experiencing infection rates >5% were more likely to use povidone-iodine for topical antisepsis, had lower implantation volume, and had patients with higher Charlson Comorbidity Index (2.79 vs 2.32, 95% CI for difference 0.08-0.86, P = 0.019).
Conclusions: In this multicenter prospective study with 6 months of follow-up, infections associated with CIED replacements were surprisingly infrequent, possibly due to the use of preoperative antibiotics. Patients with infections were more likely to have had a postoperative hematoma, and sites with higher infection rates had sicker patients and lower overall procedural volume. (PACE 2012; 35:81-87)
C1 [Uslan, Daniel Z.] Univ Calif Los Angeles, David Geffen Sch Med, Div Infect Dis, Los Angeles, CA 90095 USA.
[Gleva, Marye J.; Warren, David K.] Washington Univ, Sch Med, St Louis, MO USA.
[Mela, Theofanie] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Chung, Mina K.] Cleveland Clin, Inst Heart & Vasc, Cleveland, OH 44106 USA.
[Gottipaty, Venkateshwar] S Carolina Heart Ctr, 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.
[Mitchell, Kevin] Biotronik Inc, Lake Oswego, OR USA.
[Poole, Jeanne E.] Univ Washington, Seattle, WA 98195 USA.
RP Uslan, DZ (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Div Infect Dis, 10833 LeConte Ave,37-121 CHS, Los Angeles, CA 90095 USA.
EM duslan@mednet.ucla.edu
OI Warren, David/0000-0001-8679-8241
FU BIOTRONIK, Inc., Lake Oswego, Oregon; Biotronik
FX This study was supported by BIOTRONIK, Inc., Lake Oswego, Oregon.;
Disclosures have been made by all the authors, and details are on file.
All have received direct or indirect support from Biotronik. Most have
also received support from other CIED manufacturers and/or technology
companies and/ or pharmacologic companies.
NR 20
TC 43
Z9 44
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0147-8389
J9 PACE
JI PACE-Pacing Clin. Electrophysiol.
PD JAN
PY 2012
VL 35
IS 1
BP 81
EP 87
DI 10.1111/j.1540-8159.2011.03257.x
PG 7
WC Cardiac & Cardiovascular Systems; Engineering, Biomedical
SC Cardiovascular System & Cardiology; Engineering
GA 875MK
UT WOS:000299034400019
PM 22077194
ER
PT J
AU Meghani, SH
Polomano, RC
Tait, RC
Vallerand, AH
Anderson, KO
Gallagher, RM
AF Meghani, Salimah H.
Polomano, Rosemary C.
Tait, Raymond C.
Vallerand, April H.
Anderson, Karen O.
Gallagher, Rollin M.
TI Advancing a National Agenda to Eliminate Disparities in Pain Care:
Directions for Health Policy, Education, Practice, and Research
SO PAIN MEDICINE
LA English
DT Article
DE Pain; Disparities-Ethnic; Disparities-Racial; Pain Management; Pain
Treatment; Policy; Advocacy; Legislation; Ethnic Disparities; Opioids;
Analgesics; United States
ID LIMITED ENGLISH PROFICIENCY; PATIENT-PHYSICIAN RELATIONSHIP; RANDOMIZED
CONTROLLED-TRIAL; EMERGENCY-DEPARTMENT; UNITED-STATES; CULTURAL
COMPETENCE; ETHNIC DISPARITIES; WHITE AMERICANS; CANCER-PATIENTS;
MUSCULOSKELETAL PAIN
AB Background. Pain is strongly associated with significant personal and societal costs. A crucial element of any initiative on pain must focus on eliminating pain care disparities that are pervasive throughout the United States health care settings.
Objectives. This report focuses on macro-level factors related to pain care disparities in the United States that may be amenable to policy interventions.
Methods. We identify concrete opportunities for achieving equity in pain care, especially those occasioned by recent legislative changes in the United States health care system. An aggressive policy, advocacy, and research agenda is synthesized in five domains: 1) structural/system; 2) policy and advocacy; 3) workforce; 4) provider; and 5) research.
Results. Inequities in pain care remain an important and neglected health policy concern. Many direct and indirect provisions within the Affordable Care Act (ACA) and other national initiatives that leverage on ACA offer opportunities to achieve equity in pain care. These include changes in insurance, in public, provider, and legislative education, in primary care and pain specialist training, improving workforce diversity, achieving uniformity in race/ethnicity data collection, emphasizing patient-centered outcomes research, and encouraging focus on pain care disparities within the comparative effectiveness research paradigm.
Conclusions. Recent national legislative initiatives within ACA are expected to generate multilevel efforts that will impact the flow of funding to address the pervasive issue of disparities. It is an opportune time for the pain community to take a lead in implementing a concerted agenda on pain care disparities in order to leverage these national initiatives.
C1 [Meghani, Salimah H.] Univ Penn, Ctr Bioeth, NewCourtland Ctr Transit & Hlth, Dept Biobehav Hlth Sci,Sch Nursing, Philadelphia, PA 19104 USA.
[Tait, Raymond C.] St Louis Univ, St Louis, MO 63103 USA.
[Vallerand, April H.] Wayne State Univ, Detroit, MI USA.
[Anderson, Karen O.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Gallagher, Rollin M.] Univ Penn, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
RP Meghani, SH (reprint author), Univ Penn, Ctr Bioeth, NewCourtland Ctr Transit & Hlth, Dept Biobehav Hlth Sci,Sch Nursing, Claire M Fagin Hall,418 Curie Blvd,Room 337, Philadelphia, PA 19104 USA.
EM meghanis@nursing.upenn.edu
RI Vallerand, April/I-8150-2012
FU Pricara, Unit of Ortho-McNeil, Inc.
FX This work was supported by an unrestricted educational grant to the
Philadelphia Research and Education Foundation, Philadelphia VA Medical
Center, from Pricara, Unit of Ortho-McNeil, Inc., administered by
Ortho-McNeil Janssen Scientific Affairs.
NR 152
TC 34
Z9 34
U1 7
U2 22
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1526-2375
J9 PAIN MED
JI Pain Med.
PD JAN
PY 2012
VL 13
IS 1
BP 5
EP 28
DI 10.1111/j.1526-4637.2011.01289.x
PG 24
WC Medicine, General & Internal
SC General & Internal Medicine
GA 874KB
UT WOS:000298954200002
PM 22142450
ER
PT J
AU Ellenbogen, JM
Pace-Schott, EF
AF Ellenbogen, Jeffrey M.
Pace-Schott, Edward F.
TI Drug-induced sleep: theoretical and practical considerations
SO PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
LA English
DT Review
DE Sleep; Sleep disorders; Slow-wave sleep; Sleep-inducing drug;
Pharmacology; Sleep apnea; Receptor
ID SLOW-WAVE SLEEP; RESTLESS LEGS SYNDROME; DEPENDENT CORTICAL PLASTICITY;
SHORT-ACTING BENZODIAZEPINE; OREXIN RECEPTOR ANTAGONIST; GABA(A)
RECEPTOR; PRIMARY INSOMNIA; SODIUM OXYBATE; DOUBLE-BLIND; EXOGENOUS
MELATONIN
AB Faithful replication of normal sleep through medications-can it be achieved? Departure from normal sleep with the use of drugs-when is it desired? Answers to these questions depend on accurate understanding of sleep and on concrete criteria upon which to define it. Since these elements are evolving sciences, as yet incompletely known, one might take a nihilistic approach that we simply cannot judge whether we have successfully replicated sleep, since we do not fully grasp what sleep is or what it does. To address these potential obstacles, our article is written in two sections. The first addresses theoretical considerations for how medications might be seen in the larger framework of sleep. The purpose of this section is to inform readers about key issues in evaluating whether a drug has sufficient data to persuasively argue it is re-creating sleep. (We hope that researchers interested in conducting studies, or critical readers of the drug-study literature, might find this section particularly useful.) The second section of this article approaches exemplary, current concepts of pharmacologic manipulation of sleep, organized by disorders as articulated by the International Classification of Sleep Disorders (2005). This second section will combine practical knowledge of clinical sleep medicine, with emphasis on contemporary knowledge about molecular mechanisms that are felt to underlie some of these phenomena. We recognize that our collective knowledge about sleep will advance in the coming years. We hope that this article serves to facilitate that advance.
C1 [Ellenbogen, Jeffrey M.] Massachusetts Gen Hosp, Dept Neurol, Sleep Div, Boston, MA 02114 USA.
[Ellenbogen, Jeffrey M.] Harvard Univ, Sch Med, Boston, MA USA.
[Pace-Schott, Edward F.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Pace-Schott, Edward F.] Univ Massachusetts, Dept Psychol, Amherst, MA 01003 USA.
RP Ellenbogen, JM (reprint author), Massachusetts Gen Hosp, Dept Neurol, Sleep Div, 15 Blossom St,Wang 720, Boston, MA 02114 USA.
EM jeffrey_ellenbogen@hms.harvard.edu
NR 118
TC 1
Z9 1
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0031-6768
J9 PFLUG ARCH EUR J PHY
JI Pflugers Arch.
PD JAN
PY 2012
VL 463
IS 1
SI SI
BP 177
EP 186
DI 10.1007/s00424-011-1033-3
PG 10
WC Physiology
SC Physiology
GA 877BX
UT WOS:000299152600016
PM 21953011
ER
PT J
AU Zucker, DM
Choi, J
Gallagher, ER
AF Zucker, Donna M.
Choi, Jeungok
Gallagher, Emily R.
TI Mobile Outreach Strategies for Screening Hepatitis and HIV in High-Risk
Populations
SO PUBLIC HEALTH NURSING
LA English
DT Article
DE hepatitis; HIV; mobile strategies; risk factors
ID C VIRUS-INFECTION; HOMELESS ADULTS; PREDICTORS; PRISONERS; BEHAVIOR
AB Objectives: To screen, counsel and offer hepatitis A and B vaccination for subjects at high risk for hepatitis C virus (HCV) and HIV, and determine any relationship between risk factors and HCV positivity.
C1 [Zucker, Donna M.; Choi, Jeungok] Univ Massachusetts, Sch Nursing, Amherst, MA 01003 USA.
[Gallagher, Emily R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Zucker, DM (reprint author), Univ Massachusetts, Sch Nursing, 651 Pleasant St, Amherst, MA 01003 USA.
EM donna@acad.umass.edu
NR 17
TC 3
Z9 3
U1 0
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0737-1209
J9 PUBLIC HEALTH NURS
JI Public Health Nurs.
PD JAN-FEB
PY 2012
VL 29
IS 1
BP 27
EP 35
DI 10.1111/j.1525-1446.2011.00970.x
PG 9
WC Public, Environmental & Occupational Health; Nursing
SC Public, Environmental & Occupational Health; Nursing
GA 869IF
UT WOS:000298590900005
PM 22211749
ER
PT J
AU Martinez, F
Chung, JH
Digumarthy, SR
Kanne, JP
Abbott, GF
Shepard, JAO
Mark, EJ
Sharma, A
AF Martinez, Felipe
Chung, Jonathan H.
Digumarthy, Subba R.
Kanne, Jeffrey P.
Abbott, Gerald F.
Shepard, Jo-Anne O.
Mark, Eugene J.
Sharma, Amita
TI Common and Uncommon Manifestations of Wegener Granulomatosis at Chest
CT: Radiologic-Pathologic Correlation
SO RADIOGRAPHICS
LA English
DT Article
ID ANCA-ASSOCIATED VASCULITIDES; COMPLETE HEART-BLOCK; OPEN LUNG BIOPSIES;
THORACIC MANIFESTATIONS; COMPUTED-TOMOGRAPHY; PATHERGIC GRANULOMATOSIS;
PULMONARY VASCULITIS; SYSTEMIC VASCULITIS; EARLY DIAGNOSIS; DISEASE
AB Wegener granulomatosis is an uncommon necrotizing vasculitis that classically manifests as a clinical triad consisting of upper and lower airway involvement and glomerulonephritis. Other less frequently involved organ systems include the central and peripheral nervous system and large joints. The diagnosis is based on a combination of clinical and laboratory findings. Because thoracic involvement often predominates, chest radiographic findings are often the first to suggest the diagnosis. However, chest computed tomography (CT) has superior sensitivity and specificity for evaluation of the airways, lung parenchyma, and mediastinum, particularly with the use of multiplanar reformatted and three-dimensional images. Common pulmonary radiologic findings include waxing and waning nodules, masses, ground-glass opacities, and consolidation. Airway involvement is usually characterized by circumferential tracheobronchial thickening, which can be smooth or nodular. Pleural effusions are the most common manifestation of pleural disease and can result from primary involvement or be secondary to renal failure. Mediastinal lymphadenopathy is a nonspecific finding and is usually reactive. Uncommon thoracic radiologic manifestations include involvement of the heart and great vessels. CT is the imaging modality of choice for diagnosis, surveillance, and follow-up in patients with Wegener granulomatosis.
C1 [Martinez, Felipe; Chung, Jonathan H.; Digumarthy, Subba R.; Abbott, Gerald F.; Shepard, Jo-Anne O.; Sharma, Amita] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Mark, Eugene J.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Kanne, Jeffrey P.] Univ Wisconsin, Dept Radiol, Sch Med & Publ Hlth, Madison, WI 53706 USA.
RP Sharma, A (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,Founders 202, Boston, MA 02114 USA.
EM asharma2@partners.org
FU Amirsys; Norman; Hanson; DeTroy; Yale Cancer Center webinar; Wolter
Klewer
FX E.J.M.: Related financial activities: none. Other financial activities:
received payment for expert testimony in asbestos litigation. J.H.C.:
Related financial activities: none. Other financial activities: received
royalties from Amirsys. J.O.S.: Related financial activities: none.
Other financial activities: received payment for expert testimony from
Norman, Hanson, and DeTroy; received payment for lectures (including
service on speakers bureaus) from Yale Cancer Center webinar. J.P.K.:
Related financial activities: none. Other financial activities:
consultant for PTC Therapeutics and Perceptive Informatics, received
royalties from Wolter Klewer.
NR 68
TC 17
Z9 22
U1 0
U2 2
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0271-5333
J9 RADIOGRAPHICS
JI Radiographics
PD JAN-FEB
PY 2012
VL 32
IS 1
BP 51
EP 69
DI 10.1148/rg.321115060
PG 19
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 875TX
UT WOS:000299059200007
PM 22236893
ER
PT J
AU Drukteinis, JS
Gombos, EC
Raza, S
Chikarmane, SA
Swami, A
Birdwell, RL
AF Drukteinis, Jennifer S.
Gombos, Eva C.
Raza, Sughra
Chikarmane, Sona A.
Swami, Arpita
Birdwell, Robyn L.
TI MR Imaging Assessment of the Breast after Breast Conservation Therapy:
Distinguishing Benign from Malignant Lesions
SO RADIOGRAPHICS
LA English
DT Article
ID 20-YEAR FOLLOW-UP; COMPARING TOTAL MASTECTOMY; CONTRAST-ENHANCED MRI;
LOCAL RECURRENCE; CONSERVING SURGERY; FAT NECROSIS; RADICAL-MASTECTOMY;
RADIATION-THERAPY; TIME-COURSE; STAGE-I
AB Dynamic contrast material-enhanced magnetic resonance (MR) imaging has emerged as a valuable tool in evaluation of women who have undergone lumpectomy and whole-breast radiation therapy for breast cancer. Early diagnosis of local recurrence by means of close clinical and imaging follow-up is an important component of a breast-conserving strategy, as it may improve survival. In the post-breast conservation therapy (BCT) breast, resolving edema, fat necrosis, a small focal area of non-masslike enhancement (NMLE), and thin linear NMLE at the lumpectomy site can all be expected findings. In contrast, masslike enhancement or NMLE of ductal or segmental distribution can indicate recurrence. Therefore, at MR imaging of the post-BCT breast, it is important to identify lesions that are benign or appropriate for short-interval imaging surveillance to minimize unnecessary intervention, as well as to discern suspicious lesions and optimize the diagnosis of recurrence.
C1 [Drukteinis, Jennifer S.; Gombos, Eva C.; Raza, Sughra; Chikarmane, Sona A.; Swami, Arpita; Birdwell, Robyn L.] Brigham & Womens Hosp, Dept Radiol, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Drukteinis, JS (reprint author), Brigham & Womens Hosp, Dept Radiol, Dana Farber Canc Inst, 75 Francis St, Boston, MA 02115 USA.
EM jendruk@yahoo.com
FU GE Healthcare; Amirsys
FX E.C.G.: Related financial activities: grant from GE Healthcare. Other
financial activities: royalties from Amirsys. R. L. B.: Related
financial activities: none. Other financial activities: royalties from
Amirsys.
NR 33
TC 10
Z9 11
U1 0
U2 4
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0271-5333
J9 RADIOGRAPHICS
JI Radiographics
PD JAN-FEB
PY 2012
VL 32
IS 1
BP 219
EP 234
DI 10.1148/rg.321115016
PG 16
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 875TX
UT WOS:000299059200019
PM 22236903
ER
PT J
AU Thabet, A
Kalva, SP
Liu, B
Mueller, PR
Lee, SI
AF Thabet, Ashraf
Kalva, Sanjeeva P.
Liu, Bob
Mueller, Peter R.
Lee, Susanna I.
TI Interventional Radiology in Pregnancy Complications: Indications,
Technique, and Methods for Minimizing Radiation Exposure
SO RADIOGRAPHICS
LA English
DT Article
ID UTERINE ARTERY EMBOLIZATION; PRIMARY POSTPARTUM HEMORRHAGE;
TERM-FOLLOW-UP; ECTOPIC PREGNANCY; CESAREAN-SECTION; PLACENTA-ACCRETA;
PERCUTANEOUS NEPHROSTOMY; TRANSVAGINAL ASPIRATION; CERVICAL PREGNANCY;
FLUID COLLECTIONS
AB Complications of pregnancy, whether they occur during gestation or postpartum, often pose complex challenges because they affect two patients ( mother and fetus or infant) and because both short- and long-term outcomes must be considered in management decision making. Interventional radiologists play a critical role in treating complications such as ectopic implantation, postpartum hemorrhage, symptomatic ovarian cyst, post-cesarean section fluid collection, obstructive uropathy, and vesicouterine fistula. Interventional radiology offers therapeutic options that obviate surgery, thereby minimizing morbidity and mortality and maximizing the potential for fertility preservation. Such options include chemical injection of an ectopic gestational sac, uterine artery embolization, aspiration and drainage, percutaneous nephrostomy, and suprapubic cystostomy catheter placement. All these procedures are performed with the use of radiologic imaging for guidance. The levels of radiation to which the mother and fetus may be exposed during such procedures are of concern because of potential negative effects on long-term health. However, various methods can be used to lower maternal and fetal radiation dose levels to the minimum needed to accomplish the clinical objective.
C1 [Thabet, Ashraf; Liu, Bob; Mueller, Peter R.; Lee, Susanna I.] Massachusetts Gen Hosp, Div Abdominal Imaging & Intervent, Dept Radiol, Boston, MA 02114 USA.
[Kalva, Sanjeeva P.] Massachusetts Gen Hosp, Div Vasc Imaging & Intervent, Dept Radiol, Boston, MA 02114 USA.
RP Thabet, A (reprint author), Massachusetts Gen Hosp, Div Abdominal Imaging & Intervent, Dept Radiol, 55 Fruit St,White 270, Boston, MA 02114 USA.
EM athabet@partners.org
FU Amirsys
FX S.P.K.: Related financial activities: none. Other financial activities:
speaker for KMH Labs; royalties from Amirsys.
NR 73
TC 15
Z9 20
U1 0
U2 2
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0271-5333
J9 RADIOGRAPHICS
JI Radiographics
PD JAN-FEB
PY 2012
VL 32
IS 1
BP 255
EP 274
DI 10.1148/rg.321115064
PG 20
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 875TX
UT WOS:000299059200022
PM 22236906
ER
PT J
AU Wu, Y
Collier, L
Pan, J
Qin, W
Bauman, WA
Cardozo, CP
AF Wu, Y.
Collier, L.
Pan, J.
Qin, W.
Bauman, W. A.
Cardozo, C. P.
TI Testosterone reduced methylprednisolone-induced muscle atrophy in spinal
cord-injured rats
SO SPINAL CORD
LA English
DT Article
DE Spinal cord injury; methylprednisolone; muscle atrophy; atrogenes;
testosterone
ID HIGH-DOSE METHYLPREDNISOLONE; GROWTH-FACTOR-I; SKELETAL-MUSCLE; SERUM
TESTOSTERONE; CONTROLLED-TRIAL; GENE-EXPRESSION; UP-REGULATION;
MYOSTATIN; DIAPHRAGM; PROTEIN
AB Study design: Male rats with complete transections of the spinal cord were administered vehicle or methylprednisolone (MP) for 24 h, with or without infusion, for 7 days, of testosterone at either a replacement or low pharmacological doses. Muscles were collected at 7 days after SCI.
Objective: The objective of this study is to determine, in a rat model of complete spinal cord transection, whether testosterone reduces muscle atrophy or upregulates muscle atrophy-linked genes, induced by 24 h of MP administration at doses comparable to those prescribed in man during the period immediately following acute spinal cord injury (SCI) in an attempt to preserve neurological function.
Results: MP significantly reduced the mass of triceps, soleus and plantaris, and significantly increased expression of genes that promote atrophy. Testosterone significantly reduced muscle atrophy induced by MP, but did not prevent it; there was no difference between low-or high-dose testosterone in reducing MP-induced muscle loss. High-dose testosterone reduced expression of muscle atrophy genes more than did low dose. Testosterone-induced declines in mRNA levels for these atrophy-associated genes did not correlate well with protection against MP-induced muscle atrophy.
Conclusions: MP induces marked and lasting changes in the biology of muscle that persisted for at least 7 days, or 6 days after MP has been eliminated from the body. Testosterone partially protected against muscle atrophy and gene expression changes caused by 1 day of MP. Spinal Cord (2012) 50, 57-62; doi:10.1038/sc.2011.91; published online 20 September 2011
C1 [Wu, Y.; Collier, L.; Pan, J.; Qin, W.; Bauman, W. A.; Cardozo, C. P.] James J Peters VA Med Ctr, Ctr Excellence Med Consequences Spinal Cord Injur, Dept Vet Affairs, Bronx, NY 10468 USA.
[Qin, W.; Bauman, W. A.; Cardozo, C. P.] Mt Sinai Sch Med, Dept Med, New York, NY USA.
[Bauman, W. A.; Cardozo, C. P.] Mt Sinai Sch Med, Dept Rehabil Med, New York, NY USA.
RP Cardozo, CP (reprint author), James J Peters VA Med Ctr, Ctr Excellence Med Consequences Spinal Cord Injur, Dept Vet Affairs, Room 7A-13,130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM Chris.Cardozo@mssm.edu
FU Veterans Health Administration, Rehabilitation Research and Development
Service [B4162C, B3347 K]
FX This research was supported by the Veterans Health Administration,
Rehabilitation Research and Development Service (B4162C and B3347 K).
NR 33
TC 1
Z9 1
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1362-4393
EI 1476-5624
J9 SPINAL CORD
JI Spinal Cord
PD JAN
PY 2012
VL 50
IS 1
BP 57
EP 62
DI 10.1038/sc.2011.91
PG 6
WC Clinical Neurology; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA 879FB
UT WOS:000299314000011
PM 21931329
ER
PT J
AU Williams, RE
Bauman, WA
Spungen, AM
Vinnakota, RR
Farid, RZ
Galea, M
Korsten, MA
AF Williams, R. E., III
Bauman, W. A.
Spungen, A. M.
Vinnakota, R. R.
Farid, R. Z.
Galea, M.
Korsten, M. A.
TI SmartPill technology provides safe and effective assessment of
gastrointestinal function in persons with spinal cord injury
SO SPINAL CORD
LA English
DT Article
DE spinal cord injury; gastric emptying time; colonic transit time; whole
gut transit time; gastroesophageal reflux disease
ID CAPSULE
AB Study design: Spinal cord injury (SCI) results in gastrointestinal (GI) complications, including gastroesophageal reflux disease and constipation, but much of the data is based on older technology.
Objective: GI transit times were determined in subjects with SCI using a new device called a SmartPill. Our principal goal was to assess whether this new technology can be applied in persons with SCI.
Methods: SCI and age-and gender-matched able-bodied (AB) control subjects not taking proton pump inhibitors were studied. Following an 8-h overnight fast, subjects consumed 120 g EggBeaters (60 kcal), two slices of white bread (120 kcal) and 30g strawberry jam (74 kcal). A pH calibrated SmartPill capsule was swallowed with 8 ounces of water, after which subjects fasted for an additional 6 h prior to consuming an Ensure Plus nutrition shake (350kcal). Subjects remained fasted for an additional 2 h, after which time they resumed their regular diets.
Results: Twenty subjects with SCI and 10 AB control subjects were studied. Data are expressed as mean +/- s.d. Comparing the group with SCI to the AB control group, gastric emptying time (GET), colonic transit time (CTT) and whole gut transit time (WGTT) were prolonged (GET: 10.6 +/- 7.2 vs 3.5 +/- 1.0h, P < 0.01; CTT: 52.3 +/- 42.9 vs 14.2 +/- 7.6 h, P = 0.01; WGTT: 3.3 +/- 2.5 vs 1.0 +/- 0.7 days, P < 0.01). No complications or side effects were reported.
Conclusion: Our results indicate that the SmartPill technology is a safe, non-invasive assessment technique that provides valid diagnostic information in persons with SCI. Spinal Cord (2012) 50, 81-84; doi:10.1038/sc.2011.92; published online 30 August 2011
C1 [Korsten, M. A.] James J Peters Vet Affairs Med Ctr, Gastroenterol Serv, VA RR&D Ctr Excellence Med Consequences Spinal Co, Bronx, NY 10468 USA.
[Bauman, W. A.; Spungen, A. M.; Korsten, M. A.] James J Peters Vet Affairs Med Ctr, Med Serv, Bronx, NY 10468 USA.
[Bauman, W. A.; Spungen, A. M.; Korsten, M. A.] Mt Sinai Med Ctr, Dept Med, New York, NY 10029 USA.
[Bauman, W. A.; Spungen, A. M.; Korsten, M. A.] Mt Sinai Med Ctr, Dept Rehabil Med, New York, NY 10029 USA.
[Galea, M.] James J Peters Vet Affairs Med Ctr, Spinal Cord Injury Serv, Bronx, NY 10468 USA.
RP Korsten, MA (reprint author), James J Peters Vet Affairs Med Ctr, Gastroenterol Serv, VA RR&D Ctr Excellence Med Consequences Spinal Co, 130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM mark.korsten@va.gov
FU Department of Veteran Affairs Rehabilitation Research and Development
Service Center of Excellence for the Medical Consequences of Spinal Cord
Injury [B4162-C]; James J Peters VA Medical Center
FX The Department of Veteran Affairs Rehabilitation Research and
Development Service Center of Excellence for the Medical Consequences of
Spinal Cord Injury (#B4162-C) and the James J Peters VA Medical Center
have provided the support that made this work possible.
NR 11
TC 8
Z9 8
U1 1
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1362-4393
J9 SPINAL CORD
JI Spinal Cord
PD JAN
PY 2012
VL 50
IS 1
BP 81
EP 84
DI 10.1038/sc.2011.92
PG 4
WC Clinical Neurology; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA 879FB
UT WOS:000299314000016
PM 21876549
ER
PT J
AU Tomedi, LE
Bogen, DL
Hanusa, BH
Wisner, KL
Bodnar, LM
AF Tomedi, Laura Elizabeth
Bogen, Debra L.
Hanusa, Barbara H.
Wisner, Katherine L.
Bodnar, Lisa M.
TI A Pilot Study of the Nutritional Status of Opiate-Using Pregnant Women
on Methadone Maintenance Therapy
SO SUBSTANCE USE & MISUSE
LA English
DT Article
DE methadone; pregnancy; nutrition; obesity; dietary intake; nutritional
biomarkers
ID POSTNATAL DEPRESSION SCALE; NEURAL-TUBE DEFECTS; ILLICIT DRUG-USE;
HISTORY QUESTIONNAIRE; SUBSTANCE USE; BIRTH-WEIGHT; LIFE-STYLE; VITAMIN;
PREVALENCE; VALIDATION
AB Pregnant women in methadone maintenance therapy may have poor nutrition during pregnancy. In 2006-2008, methadone-treated pregnant women (n = 22) were recruited at an urban academic medical center and compared with nondrug-using pregnant women (n = 119) at 20-35 weeks' gestation. We measured adiposity using prepregnancy body mass index (BMI), dietary intake using a food frequency questionnaire, and micronutrient and essential fatty acid status using biomarkers. Methadone-treated women had lower BMI, consumed more calories, had lower serum carotenoid concentrations, and higher plasma homocysteine concentrations than controls. The study's limitations and implications for future research are discussed.
C1 [Tomedi, Laura Elizabeth; Wisner, Katherine L.; Bodnar, Lisa M.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15213 USA.
[Bogen, Debra L.] Univ Pittsburgh, Childrens Hosp Pittsburgh, Sch Med, Div Gen Acad Pediat, Pittsburgh, PA USA.
[Hanusa, Barbara H.] Vet Affairs Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Wisner, Katherine L.] Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Pittsburgh, PA USA.
[Wisner, Katherine L.] Univ Pittsburgh, Dept Obstet Gynecol & Reprod Sci, Sch Med, Pittsburgh, PA USA.
RP Tomedi, LE (reprint author), Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15213 USA.
EM let20@pitt.edu
FU Children's Hospital of Pittsburgh Research Advisory Committee; Gerber
Foundation; National Institutes of Health (NIH) [MO1RR00056]; Building
Interdisciplinary Research Careers in Women's Health (BIRCWH) Award [K12
HD043441]; NIH/NIMH (National Institute of Mental Health) [R01 MH060335,
K01 MH074092]; National Institute of Child Health and Human Development
(NICHD) [HD 055 162-03 NIH NRSA T32]
FX This study was funded by the Children's Hospital of Pittsburgh Research
Advisory Committee and the Gerber Foundation. Study visits were
conducted in the Magee-Womens Hospital Clinical and Translational
Research Center, which is funded by National Institutes of Health (NIH;
grant MO1RR00056). The authors' contributions to this work were
supported by K12 HD043441 [Building Interdisciplinary Research Careers
in Women's Health (BIRCWH) Award], NIH/NIMH (National Institute of
Mental Health) grants R01 MH060335 and K01 MH074092, and the
Reproductive, Perinatal and Pediatric Epidemiology grant HD 055 162-03
NIH NRSA T32 [National Institute of Child Health and Human Development
(NICHD)].
NR 52
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Z9 2
U1 4
U2 5
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1082-6084
EI 1532-2491
J9 SUBST USE MISUSE
JI Subst. Use Misuse
PY 2012
VL 47
IS 3
BP 286
EP 295
DI 10.3109/10826084.2011.635324
PG 10
WC Substance Abuse; Psychiatry; Psychology
SC Substance Abuse; Psychiatry; Psychology
GA 873BT
UT WOS:000298856500008
PM 22217127
ER
PT J
AU Shao, HL
Min, C
Issadore, D
Liong, M
Yoon, TJ
Weissleder, R
Lee, H
AF Shao, Huilin
Min, Changwook
Issadore, David
Liong, Monty
Yoon, Tae-Jong
Weissleder, Ralph
Lee, Hakho
TI Magnetic Nanoparticles and microNMR for Diagnostic Applications
SO THERANOSTICS
LA English
DT Review
DE biosensor; diagnostics; magnetic nanoparticle; microfluidics; nuclear
magnetic resonance
ID CORE-SHELL NANOPARTICLES; CANCER-CELLS; RELAXATION; RESONANCE;
BIOSENSOR; ASSAYS; PROTEIN; PROBES; ARRAYS; NANOCRYSTALS
AB Sensitive and quantitative measurements of clinically relevant protein biomarkers, pathogens and cells in biological samples would be invaluable for disease diagnosis, monitoring of malignancy, and for evaluating therapy efficacy. Biosensing strategies using magnetic nanoparticles (MNPs) have recently received considerable attention, since they offer unique advantages over traditional detection methods. Specifically, because biological samples have negligible magnetic background, MNPs can be used to obtain highly sensitive measurements in minimally processed samples. This review focuses on the use of MNPs for in vitro detection of cellular biomarkers based on nuclear magnetic resonance (NMR) effects. This detection platform, termed diagnostic magnetic resonance (DMR), exploits MNPs as proximity sensors to modulate the spin-spin relaxation time of water molecules surrounding the molecularly-targeted nanoparticles. With new developments such as more effective MNP biosensors, advanced conjugational strategies, and highly sensitive miniaturized NMR systems, the DMR detection capabilities have been considerably improved. These developments have also enabled parallel and rapid measurements from small sample volumes and on a wide range of targets, including whole cells, proteins, DNA/mRNA, metabolites, drugs, viruses and bacteria. The DMR platform thus makes a robust and easy-to-use sensor system with broad applications in biomedicine, as well as clinical utility in point-of-care settings.
C1 [Shao, Huilin; Min, Changwook; Issadore, David; Liong, Monty; Yoon, Tae-Jong; Weissleder, Ralph; Lee, Hakho] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Weissleder, Ralph] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
RP Weissleder, R (reprint author), Massachusetts Gen Hosp, Ctr Syst Biol, 185 Cambridge St,CPZN 5206, Boston, MA 02114 USA.
EM rweissleder@mgh.harvard.edu; hlee@mgh.harvard.edu
RI Issadore, David/L-8451-2014
FU Agency for Science, Technology and Research, Singapore; NIH
[2RO1EB004626, U01-HL080731, HHSN 268201000044C, U54-CA119349,
T32-CA79443]
FX The authors thank N. Sergeyev for providing cross-linked dextran-coated
iron oxide nanoparticles. H. Shao acknowledges financial support from
the B.S.-Ph.D. National Science Scholarship awarded by the Agency for
Science, Technology and Research, Singapore. This work was supported in
part by NIH Grants (2RO1EB004626, U01-HL080731, HHSN 268201000044C,
U54-CA119349 and T32-CA79443).
NR 59
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U1 15
U2 108
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1838-7640
J9 THERANOSTICS
JI Theranostics
PY 2012
VL 2
IS 1
BP 55
EP 65
DI 10.7150/thno.3465
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 876PZ
UT WOS:000299121200004
PM 22272219
ER
PT J
AU Perlstein, TS
Goldhaber, SZ
Nelson, K
Joshi, V
Morgan, TV
Lesko, LJ
Lee, JY
Gobburu, J
Schoenfeld, D
Kucherlapati, R
Freeman, MW
Creager, MA
AF Perlstein, Todd S.
Goldhaber, Samuel Z.
Nelson, Kerrie
Joshi, Victoria
Morgan, T. Vance
Lesko, Lawrence J.
Lee, Joo-Yeon
Gobburu, Jogarao
Schoenfeld, David
Kucherlapati, Raju
Freeman, Mason W.
Creager, Mark A.
TI The Creating an Optimal Warfarin Nomogram (CROWN) Study
SO THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
DE Pharmacogenetics; warfarin; clinical trial
ID ORAL ANTICOAGULATION; ATRIAL-FIBRILLATION; LABELING DECISIONS; VKORC1
HAPLOTYPES; DRUG APPLICATIONS; CLINICAL FACTORS; CHINESE PATIENTS;
CYP2C9 VARIANTS; IMPACT; GENOTYPE
AB A significant proportion of warfarin dose variability is explained by variation in the genotypes of the cytochrome P450 CYP2C9 and the vitamin K epoxide reductase complex, VKORC1, enzymes that influence warfarin metabolism and sensitivity, respectively. We sought to develop an optimal pharmacogenetic warfarin dosing algorithm that incorporated clinical and genetic information. We enroled patients initiating warfarin therapy. Genotyping was performed of the VKORC1, -1639G>A, the CYP2C9*2, 430C>T, and the CYP2C9*3,1075C>A genotypes. The initial warfarin dosing algorithm (Algorithm A) was based upon established clinical practice and published warfarin pharmacogenetic information. Subsequent dosing algorithms (Algorithms B and Algorithm C) were derived from pharmacokinetic / pharmacodynamic (PK/PD) modelling of warfarin dose, international normalised ratio (INR), clinical and genetic factors from patients treated by the preceding algorithm(s). The primary outcome was the time in the therapeutic range, considered an INR of 1.8 to 3.2.A total of 344 subjects are included in the study analyses. The mean percentage time within the therapeutic range for each subject increased progressively from Algorithm A toAlgorithm C from 58.9 (22.0), to 59.7 (23.0), to 65.8 (16.9) percent (p = 0.04). Improvement also occurred in most secondary endpoints, which included the per-patient percentage of INRs outside of the therapeutic range (p = 0.004), the time to the first therapeutic INR (p = 0.07), and the time to achieve stable therapeutic anticoagulation (p < 0.001). In conclusion, warfarin pharmacogenetic dosing can be optimised in real time utilising observed PK/PD information in an adaptive fashion.
C1 [Perlstein, Todd S.; Goldhaber, Samuel Z.; Creager, Mark A.] Brigham & Womens Hosp, Div Cardiovasc Med, Boston, MA 02115 USA.
[Nelson, Kerrie; Schoenfeld, David] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
[Schoenfeld, David] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Freeman, Mason W.] Massachusetts Gen Hosp, Lipid Metab Unit, Boston, MA 02114 USA.
[Freeman, Mason W.] Massachusetts Gen Hosp, Div Endocrine, Boston, MA 02114 USA.
[Joshi, Victoria] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Joshi, Victoria] Brigham & Womens Hosp, Partners Ctr Personalized Genet Med, Boston, MA 02115 USA.
[Morgan, T. Vance; Kucherlapati, Raju] Harvard Univ, Sch Med, Ctr Personalized Genet Med, Boston, MA USA.
[Lesko, Lawrence J.; Lee, Joo-Yeon; Gobburu, Jogarao] US FDA, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
RP Creager, MA (reprint author), Brigham & Womens Hosp, Div Cardiovasc, 75 Francis St, Boston, MA 02115 USA.
EM mcreager@partners.org
FU Partners HealthCare; National Heart, Lung, and Blood Institute
[K12-HL083786]
FX This work was funded by Partners HealthCare through a grant to the
Harvard Partners Center for Personalized Genetic Medicine. Dr Perlstein
received support from the National Heart, Lung, and Blood Institute
Research Career Development Award K12-HL083786. Dr. Creager is the Simon
C. Fireman Scholar in Cardiovascular Medicine at Brigham and Women's
Hospital.
NR 37
TC 7
Z9 7
U1 0
U2 8
PU SCHATTAUER GMBH-VERLAG MEDIZIN NATURWISSENSCHAFTEN
PI STUTTGART
PA HOLDERLINSTRASSE 3, D-70174 STUTTGART, GERMANY
SN 0340-6245
J9 THROMB HAEMOSTASIS
JI Thromb. Haemost.
PD JAN
PY 2012
VL 107
IS 1
BP 59
EP 68
DI 10.1160/TH11-08-0568
PG 10
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 879UO
UT WOS:000299357900012
PM 22116191
ER
PT J
AU Biederman, J
Petty, CR
Bhide, PG
Woodworth, KY
Faraone, S
AF Biederman, Joseph
Petty, Carter R.
Bhide, Pradeep G.
Woodworth, K. Yvonne
Faraone, Stephen
TI Does exposure to maternal smoking during pregnancy affect the clinical
features of ADHD? Results from a controlled study
SO WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE ADHD; smoking; children; brain development; childhood ADHD
ID DEFICIT HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY
DISORDER; DSM-III-R; FOLLOW-UP; RISK; GIRLS
AB Objectives. Exposure to maternal smoking during pregnancy may be a signifi cant risk factor for attention-deficit/hyperactivity disorder (ADHD) independently of family history of ADHD. The main aim of this study was to examine whether the clinical profile of ADHD differs between children with and without exposure to maternal smoking during pregnancy. Methods. This was a case-control study of boys and girls with and without ADHD ascertained from psychiatric and paediatric sources. Maternal smoking during pregnancy was defined by interviews with subjects' mothers. Main outcome measures were ADHD symptoms and associated clinical features in children with and without exposure to maternal smoking during pregnancy. Results. No signifi cant differences were found between ADHD children with and without exposure to maternal smoking during pregnancy on clinical characteristics. When these analyses were repeated in the subgroup of subjects without parental history of ADHD, there were also no statistically signifi cant differences found. Conclusions. Despite adequate statistical power, no signifi cant differences were found between ADHD children with and without exposure in the clinical features of ADHD and associated disorders. Results provide support for the notion that ADHD cases resulting from exposure to maternal smoking during pregnancy have similar clinical profiles as other ADHD cases.
C1 [Biederman, Joseph; Petty, Carter R.; Woodworth, K. Yvonne] Massachusetts Gen Hosp, Dept Psychiat, Clin Program Pediat Psychiat & Adult ADHD, Boston, MA 02114 USA.
[Biederman, Joseph; Petty, Carter R.; Woodworth, K. Yvonne] Massachusetts Gen Hosp, Dept Psychiat, Res Program Pediat Psychiat & Adult ADHD, Boston, MA 02114 USA.
[Biederman, Joseph; Bhide, Pradeep G.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Bhide, Pradeep G.] Massachusetts Gen Hosp, Neurosci Ctr, Boston, MA 02114 USA.
[Faraone, Stephen] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY USA.
RP Biederman, J (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Clin Program Pediat Psychiat & Adult ADHD, 55 Fruit St,Warren 705, Boston, MA 02114 USA.
EM jbiederman@partners.org
OI Bhide, Pradeep/0000-0003-4236-9415; Faraone, Stephen/0000-0002-9217-3982
FU Pediatric Psychopharmacology Philanthropy Fund; Elminda; Janssen;
McNeil; Shire; Fundacion Areces, Medice Pharmaceuticals; Spanish Child
Psychiatry Association; Abbott; Alza; AstraZeneca; Bristol Myers Squibb;
Celltech; Cephalon; Eli Lilly and Co.; Esai; Forest; Glaxo; Gliatech;
Merck; NARSAD; NIDA; New River; NICHD; NIMH; Novartis; Noven;
Neurosearch; Organon; Otsuka; Pfizer; Pharmacia; Prechter Foundation;
Stanley Foundation; UCB Pharma, Inc.; Wyeth.; National Institutes of
Health
FX This work was supported by the Pediatric Psychopharmacology Philanthropy
Fund. The funding organization did not play any role in the design and
conduct of the study, the collection, management analysis and
interpretation of the data, or in the preparation, review or approval of
the manuscript.; Dr Joseph Biederman is currently receiving research
support from the following sources: Elminda, Janssen, McNeil, and Shire.
In 2010, Dr Biederman did not receive any outside income. In 2009, Dr
Biederman received a speaker's fee from the following sources: Fundacion
Areces, Medice Pharmaceuticals, and the Spanish Child Psychiatry
Association. In previous years, Dr Biederman received research support,
consultation fees, or speaker's fees for/from the following additional
sources: Abbott, Alza, AstraZeneca, Bristol Myers Squibb, Celltech,
Cephalon, Eli Lilly and Co., Esai, Forest, Glaxo, Gliatech, Janssen,
McNeil, Merck, NARSAD, NIDA, New River, NICHD, NIMH, Novartis, Noven,
Neurosearch, Organon, Otsuka, Pfizer, Pharmacia, The Prechter
Foundation, Shire, The Stanley Foundation, UCB Pharma, Inc. and Wyeth.
In the past year, Dr Stephen Faraone has received consulting fees and
has been on Advisory Boards for Eli Lilly, Ortho-McNeil and Shire
Development and has received research support from Eli Lilly, Pfizer,
Shire and the National Institutes of Health. In previous years, Dr
Faraone has received consulting fees or has been on Advisory Boards or
has been a speaker for the following sources: Shire, McNeil, Janssen,
Novartis, Pfizer and Eli Lilly. In previous years he has received
research support from Eli Lilly, Shire, Pfi zer and the National
Institutes of Health. Dr Bhide, Mr Petty and Ms Woodworth have nothing
to disclose.
NR 21
TC 8
Z9 9
U1 0
U2 8
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1562-2975
J9 WORLD J BIOL PSYCHIA
JI World J. Biol. Psychiatry
PD JAN
PY 2012
VL 13
IS 1
BP 60
EP 64
DI 10.3109/15622975.2011.562243
PG 5
WC Psychiatry
SC Psychiatry
GA 878ZF
UT WOS:000299296100008
PM 21545244
ER
PT J
AU Mirzakhani, H
Welch, CA
Eikermann, M
Nozari, A
AF Mirzakhani, H.
Welch, C. A.
Eikermann, M.
Nozari, A.
TI Neuromuscular blocking agents for electroconvulsive therapy: a
systematic review
SO ACTA ANAESTHESIOLOGICA SCANDINAVICA
LA English
DT Review
ID NEUROLEPTIC MALIGNANT SYNDROME; POSTOPERATIVE RESIDUAL CURARIZATION;
POSTANESTHESIA CARE-UNIT; RELAXANT BINDING-AGENT; CONVULSIVE SHOCK
THERAPY; ANESTHETIC CONSIDERATIONS; SEVOFLURANE ANESTHESIA;
ELDERLY-PATIENTS; DOSE-RESPONSE; TRAUMATIC COMPLICATIONS
AB Electroconvulsive therapy (ECT) is the transcutaneous application of small electrical stimuli to the brain to induce generalised seizures for the treatment of selected psychiatric disorders. The clinical indications for ECT as an effective therapeutic modality have been considerably expanded since its introduction. Anaesthesia and neuromuscular blocking agents (NMBAs) are required to ensure patients safety during ECT. The optimal dose of muscle relaxant for ECT reduces muscle contractions without inducing complete paralysis. Slight residual motor convulsive activity is helpful in ascertaining that a seizure has occurred, while total paralysis prolongs the procedure unnecessarily. Suxamethonium is commonly used, but nondepolarising NMBAs are indicated in patients with certain comorbidities. In this review, we summarise current concepts of NMBA management for ECT.
C1 [Mirzakhani, H.; Eikermann, M.; Nozari, A.] Harvard Univ, Dept Anaesthesia Crit Care & Pain Med, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Welch, C. A.] Harvard Univ, Dept Psychiat, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Nozari, A (reprint author), Harvard Univ, Dept Anaesthesia Crit Care & Pain Med, Sch Med, Massachusetts Gen Hosp, GRJ 416, Boston, MA 02114 USA.
EM anozari@partners.org
NR 151
TC 14
Z9 14
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0001-5172
J9 ACTA ANAESTH SCAND
JI Acta Anaesthesiol. Scand.
PD JAN
PY 2012
VL 56
IS 1
BP 3
EP 16
DI 10.1111/j.1399-6576.2011.02520.x
PG 14
WC Anesthesiology
SC Anesthesiology
GA 860AS
UT WOS:000297918400002
PM 22092267
ER
PT J
AU Vallaster, M
Vallaster, CD
Wu, SM
AF Vallaster, Marcus
Vallaster, Caroline Dacwag
Wu, Sean M.
TI Epigenetic mechanisms in cardiac development and disease
SO ACTA BIOCHIMICA ET BIOPHYSICA SINICA
LA English
DT Review
DE epigenetics; histone modifications; DNA methylation; congenital heart
disease
ID HOLT-ORAM-SYNDROME; CONGENITAL HEART-DISEASE; EMBRYONIC STEM-CELLS;
CHROMATIN-REMODELING COMPLEX; TRANSCRIPTION FACTOR TBX5;
DIGEORGE-SYNDROME; SMOOTH-MUSCLE; PROGENITOR SPECIFICATION; HISTONE
ACETYLATION; MYOCARDIAL-CELLS
AB During mammalian development, cardiac specification and ultimately lineage commitment to a specific cardiac cell type is accomplished by the action of specific transcription factors (TFs) and their meticulous control on an epigenetic level. In this review, we detail how cardiac-specific TFs function in concert with nucleosome remodeling and histone-modifying enzymes to regulate a diverse network of genes required for processes such as cell growth and proliferation, or epithelial to mesenchymal transition (EMT), for instance. We provide examples of how several cardiac TFs, such as Nkx2.5, WHSC1, Tbx5, and Tbx1, which are associated with developmental and congenital heart defects, are required for the recruitment of histone modifiers, such as Jarid2, p300, and Ash2l, and components of ATP-dependent remodeling enzymes like Brg1, Baf60c, and Baf180. Binding of these TFs to their respective sites at cardiac genes coincides with a distinct pattern of histone marks, indicating that the precise regulation of cardiac gene networks is orchestrated by interactions between TFs and epigenetic modifiers. Furthermore, we speculate that an epigenetic signature, comprised of TF occupancy, histone modifications, and overall chromatin organization, is an underlying mechanism that governs cardiac morphogenesis and disease.
C1 [Vallaster, Marcus; Vallaster, Caroline Dacwag; Wu, Sean M.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Vallaster, Caroline Dacwag; Wu, Sean M.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Wu, Sean M.] Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
RP Wu, SM (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
EM SMWU@partners.org
FU NIH [OD004411, HL081086, HL100408, 5T32HL007208]
FX This work was supported by grants from the NIH (OD004411, HL081086,
HL100408 to S.M.W.; 5T32HL007208 to C.D.V.).
NR 103
TC 28
Z9 32
U1 2
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1672-9145
J9 ACTA BIOCH BIOPH SIN
JI Acta Biochim. Biophys. Sin.
PD JAN
PY 2012
VL 44
IS 1
SI SI
BP 92
EP 102
DI 10.1093/abbs/gmr090
PG 11
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 866NB
UT WOS:000298386700010
PM 22194017
ER
PT J
AU Montine, TJ
Phelps, CH
Beach, TG
Bigio, EH
Cairns, NJ
Dickson, DW
Duyckaerts, C
Frosch, MP
Masliah, E
Mirra, SS
Nelson, PT
Schneider, JA
Thal, DR
Trojanowski, JQ
Vinters, HV
Hyman, BT
AF Montine, Thomas J.
Phelps, Creighton H.
Beach, Thomas G.
Bigio, Eileen H.
Cairns, Nigel J.
Dickson, Dennis W.
Duyckaerts, Charles
Frosch, Matthew P.
Masliah, Eliezer
Mirra, Suzanne S.
Nelson, Peter T.
Schneider, Julie A.
Thal, Dietmar Rudolf
Trojanowski, John Q.
Vinters, Harry V.
Hyman, Bradley T.
TI National Institute on Aging-Alzheimer's Association guidelines for the
neuropathologic assessment of Alzheimer's disease: a practical approach
SO ACTA NEUROPATHOLOGICA
LA English
DT Article
ID BRAINNET EUROPE CONSORTIUM; LEWY BODY DISEASE; FRONTOTEMPORAL LOBAR
DEGENERATION; VASCULAR COGNITIVE IMPAIRMENT; CEREBRAL AMYLOID
ANGIOPATHY; HIPPOCAMPAL SCLEROSIS; DIAGNOSTIC GUIDELINES; SYNAPSE LOSS;
NEUROFIBRILLARY PATHOLOGY; CONSENSUS RECOMMENDATIONS
AB We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). Major revisions from previous consensus criteria are: (1) recognition that AD neuropathologic changes may occur in the apparent absence of cognitive impairment, (2) an "ABC" score for AD neuropathologic change that incorporates histopathologic assessments of amyloid beta deposits (A), staging of neurofibrillary tangles (B), and scoring of neuritic plaques (C), and (3) more detailed approaches for assessing commonly co-morbid conditions such as Lewy body disease, vascular brain injury, hippocampal sclerosis, and TAR DNA binding protein (TDP)-43 immunoreactive inclusions. Recommendations also are made for the minimum sampling of brain, preferred staining methods with acceptable alternatives, reporting of results, and clinico-pathologic correlations.
C1 [Montine, Thomas J.] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98104 USA.
[Phelps, Creighton H.] NIA, Bethesda, MD 20892 USA.
[Beach, Thomas G.] Banner Sun Hlth Res Inst, Civin Lab Neuropathol, Sun City, AZ USA.
[Bigio, Eileen H.] Northwestern Univ, Dept Pathol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Bigio, Eileen H.] Northwestern Univ, NW Alzheimer Dis Ctr, Feinberg Sch Med, Chicago, IL 60611 USA.
[Cairns, Nigel J.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
[Cairns, Nigel J.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA.
[Dickson, Dennis W.] Mayo Clin, Dept Neurosci, Jacksonville, FL 32224 USA.
[Duyckaerts, Charles] Hop La Pitie Salpetriere, Serv Neuropathol Raymond Escourolle, Paris, France.
[Frosch, Matthew P.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, CS Kubik Lab Neuropathol, Boston, MA USA.
[Masliah, Eliezer] Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA.
[Masliah, Eliezer] Univ Calif San Diego, Sch Med, Dept Pathol, La Jolla, CA 92093 USA.
[Mirra, Suzanne S.] Suny Downstate Med Ctr, Dept Pathol, Brooklyn, NY 11203 USA.
[Nelson, Peter T.] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40536 USA.
[Schneider, Julie A.] Rush Univ, Rush Alzheimers Dis Ctr, Med Ctr, Dept Pathol, Chicago, IL 60612 USA.
[Schneider, Julie A.] Rush Univ, Rush Alzheimers Dis Ctr, Med Ctr, Dept Neurol Sci, Chicago, IL 60612 USA.
[Thal, Dietmar Rudolf] Univ Ulm, Neuropathol Lab, Inst Pathol, Ulm, Germany.
[Trojanowski, John Q.] Univ Penn, Sch Med, Dept Pathol & Lab Med, Inst Aging,Ctr Neurodegenerat Dis Res, Philadelphia, PA 19104 USA.
[Vinters, Harry V.] Univ Calif Los Angeles, Dept Pathol & Lab Med Neuropathol, Los Angeles, CA USA.
[Vinters, Harry V.] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA.
[Hyman, Bradley T.] Harvard Univ, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Montine, TJ (reprint author), Univ Washington, Sch Med, Dept Pathol, Box 359791, Seattle, WA 98104 USA.
EM tmontine@uw.edu
OI Dickson, Dennis W/0000-0001-7189-7917
FU National Institute on Aging [AG05134, AG05136, AG03991, AG05681,
AG24904, AG28383, AG10161, AG17917, AG10124, AG13854, AG19610, NS62684,
AG15819, AG12435, AG05131, AG016976, AG16570, AG15866, AG18840];
Alzheimer's Association; Arizona Department of Health Services [211002];
Deutsche Forschungsgemeinschaft (DFG) [TH-624-4-1]; Alzheimer Forschung
Initiative (AFI) [10810]; Nancy and Buster Alvord Endowment; Charles and
Joanne Knight Alzheimer Research Initiative
FX Support was provided by the National Institute on Aging (AG05134,
AG05136, AG03991, AG05681, AG24904, AG28383, AG10161, AG17917, AG10124,
AG13854, AG19610, NS62684, AG16570, AG15819, AG12435, AG05131, AG016976,
AG16570, AG15866 and AG18840) as well as the Alzheimer's Association,
Arizona Department of Health Services (contract 211002, Arizona
Alzheimer's Consortium), Deutsche Forschungsgemeinschaft (DFG
TH-624-4-1) and Alzheimer Forschung Initiative (AFI #10810), the Nancy
and Buster Alvord Endowment, and the Charles and Joanne Knight Alzheimer
Research Initiative. We thank Dr. Joshua Sonnen for providing some
photomicrographs. The authors extend their deepest thanks to Dr. Heiko
Braak, Dr. Kelly Del Tredici, Dr. Nina Silverberg, Dr. Walter Kukull,
Dr. Kathleen Montine, Dr. Cerise Elliott, Dr. Bill Thies, Dr. Maria C.
Carrillo, and Ms. Sarah Monsell for their valuable input.
NR 64
TC 420
Z9 422
U1 6
U2 38
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-6322
J9 ACTA NEUROPATHOL
JI Acta Neuropathol.
PD JAN
PY 2012
VL 123
IS 1
BP 1
EP 11
DI 10.1007/s00401-011-0910-3
PG 11
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 870BF
UT WOS:000298643400001
PM 22101365
ER
PT J
AU Mufson, EJ
Binder, L
Counts, SE
DeKosky, ST
deToledo-Morrell, L
Ginsberg, SD
Ikonomovic, MD
Perez, SE
Scheff, SW
AF Mufson, Elliott J.
Binder, Lester
Counts, Scott E.
DeKosky, Steven T.
deToledo-Morrell, Leyla
Ginsberg, Stephen D.
Ikonomovic, Milos D.
Perez, Sylvia E.
Scheff, Stephen W.
TI Mild cognitive impairment: pathology and mechanisms
SO ACTA NEUROPATHOLOGICA
LA English
DT Review
DE Alzheimer's disease; Amyloid; Cholinergic; Dementia; MCI;
Neurofibrillary tangles; Neuropathology; Molecular; Neurotrophins;
Synapses
ID EARLY ALZHEIMERS-DISEASE; CHOLINERGIC BASAL FOREBRAIN; AMYLOID PRECURSOR
PROTEIN; NICOTINIC ACETYLCHOLINE-RECEPTOR; ENTORHINAL CORTEX NEURONS;
CENTRAL-NERVOUS-SYSTEM; PRIMARY VISUAL-CORTEX; E TYPE-4 ALLELE;
SUBSTANTIA INNOMINATA; NUCLEUS BASALIS
AB Mild cognitive impairment (MCI) is rapidly becoming one of the most common clinical manifestations affecting the elderly. The pathologic and molecular substrate of people diagnosed with MCI is not well established. Since MCI is a human specific disorder and neither the clinical nor the neuropathological course appears to follow a direct linear path, it is imperative to characterize neuropathology changes in the brains of people who came to autopsy with a well-characterized clinical diagnosis of MCI. Herein, we discuss findings derived from clinical pathologic studies of autopsy cases who died with a clinical diagnosis of MCI. The heterogeneity of clinical MCI imparts significant challenges to any review of this subject. The pathologic substrate of MCI is equally complex and must take into account not only conventional plaque and tangle pathology but also a wide range of cellular, biochemical and molecular deficits, many of which relate to cognitive decline as well as compensatory responses to the progressive disease process. The multifaceted nature of the neuronal disconnection syndrome associated with MCI suggests that there is no single event which precipitates this prodromal stage of AD. In fact, it can be argued that neuronal degeneration initiated at different levels of the central nervous system drives cognitive decline as a final common pathway at this stage of the dementing disease process.
C1 [Mufson, Elliott J.; Counts, Scott E.; deToledo-Morrell, Leyla; Perez, Sylvia E.] Rush Univ, Med Ctr, Dept Neurol Sci, Chicago, IL 60612 USA.
[Binder, Lester] Northwestern Univ, Dept Cell & Mol Biol, Feinberg Sch Med, Chicago, IL 60611 USA.
[DeKosky, Steven T.] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
[Ginsberg, Stephen D.] NYU, Langone Med Ctr, Ctr Dementia Res, Nathan Kline Inst,Dept Psychiat, Orangeburg, NY 10962 USA.
[Ginsberg, Stephen D.] NYU, Langone Med Ctr, Ctr Dementia Res, Nathan Kline Inst,Dept Physiol, Orangeburg, NY 10962 USA.
[Ginsberg, Stephen D.] NYU, Langone Med Ctr, Ctr Dementia Res, Nathan Kline Inst,Dept Neurosci, Orangeburg, NY 10962 USA.
[Ikonomovic, Milos D.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Ikonomovic, Milos D.] Univ Pittsburgh, Dept Neurol, Educ & Clin Ctr, Pittsburgh, PA 15260 USA.
[Ikonomovic, Milos D.] Univ Pittsburgh, Dept Psychiat, Educ & Clin Ctr, Pittsburgh, PA USA.
[Ikonomovic, Milos D.] Univ Pittsburgh, Dept Geriatr Res, Educ & Clin Ctr, Pittsburgh, PA USA.
[Scheff, Stephen W.] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40536 USA.
RP Mufson, EJ (reprint author), Rush Univ, Med Ctr, Dept Neurol Sci, 1735 W Harrison St,Suite 300, Chicago, IL 60612 USA.
EM emufson@rush.edu
OI Ginsberg, Stephen/0000-0002-1797-4288
FU NIA [PO1 AG14999, PO1 AG09466, AG10688, AG025204]
FX This study was supported by NIA grants PO1 AG14999, PO1 AG09466, AG10688
and AG025204. We thank all our collaborators and the participants in
each Alzheimer's Disease Center, institute and organization without whom
the information reviewed would not have been possible.
NR 188
TC 61
Z9 61
U1 5
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-6322
J9 ACTA NEUROPATHOL
JI Acta Neuropathol.
PD JAN
PY 2012
VL 123
IS 1
BP 13
EP 30
DI 10.1007/s00401-011-0884-1
PG 18
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 870BF
UT WOS:000298643400002
PM 22101321
ER
PT J
AU Augustinack, JC
Huber, KE
Postelnicu, GM
Kakunoori, S
Wang, RP
van der Kouwe, AJW
Wald, LL
Stein, TD
Frosch, MP
Fischl, B
AF Augustinack, Jean C.
Huber, Kristen E.
Postelnicu, Gheorghe M.
Kakunoori, Sita
Wang, Ruopeng
van der Kouwe, Andre J. W.
Wald, Lawrence L.
Stein, Thor D.
Frosch, Matthew P.
Fischl, Bruce
TI Entorhinal verrucae geometry is coincident and correlates with
Alzheimer's lesions: a combined neuropathology and high-resolution ex
vivo MRI analysis
SO ACTA NEUROPATHOLOGICA
LA English
DT Article
DE Neuroimaging; Modularity; Cortex; Ex vivo; Surface reconstruction
ID MILD COGNITIVE IMPAIRMENT; PROTEIN SYNTHETIC CAPABILITY;
AGE-RELATED-CHANGES; NEUROFIBRILLARY TANGLES; LAYER-II; PARAHIPPOCAMPAL
GYRUS; HIPPOCAMPAL-FORMATION; PATHOLOGICAL-CHANGES; CORTEX NEURONS;
SENILE PLAQUES
AB Entorhinal cortex displays a distinctive organization in layer II and forms small elevations on its surface called entorhinal verrucae. In Alzheimer's disease, the verrucae disappear due to neurofibrillary tangle formation and neuronal death. Isosurface models were reconstructed from high-resolution ex vivo MRI volumes scanned at 7.0 T and individual verruca were measured quantitatively for height, width, volume, and surface area on control and mild Alzheimer's cases. Mean verruca height was 0.13 +/- A 0.04 mm for our cognitively normal (controls) sample set whereas for mild AD samples mean height was 0.11 mm +/- A 0.05 mm (p < 0.001) in entorhinal cortex (n = 10 cases). These quantitative methods were validated by a significant correlation of verrucae height and volume with qualitative verrucae ratings (n = 36 cases). Entorhinal surfaces were significantly different from other cortical heights such as, cingulate, frontal, occipital, parietal and temporal cortices. Colocalization of verrucae with entorhinal islands was confirmed in ex vivo MRI and, moreover, verrucae ratings were negatively correlated to Braak and Braak pathological stage. This study characterizes novel methods to measure individual entorhinal verruca size, and shows that verrucae size correlates to Alzheimer's pathology. Taken together, these results suggest that verrucae may have the potential to serve as an early and specific morphological marker for mild cognitive impairment and Alzheimer's disease.
C1 [Augustinack, Jean C.; Huber, Kristen E.; Kakunoori, Sita; Wang, Ruopeng; van der Kouwe, Andre J. W.; Wald, Lawrence L.; Fischl, Bruce] Massachusetts Gen Hosp, Dept Pathol, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Postelnicu, Gheorghe M.] Google Inc, CH-8002 Zurich, Switzerland.
[Stein, Thor D.; Frosch, Matthew P.] Massachusetts Gen Hosp, Dept Neuropathol, Boston, MA 02115 USA.
[Fischl, Bruce] MIT, CSAIL, Cambridge, MA 02139 USA.
RP Augustinack, JC (reprint author), Massachusetts Gen Hosp, Dept Pathol, Athinoula A Martinos Ctr Biomed Imaging, Bldg 149,13th St,Room 2301, Charlestown, MA 02129 USA.
EM jean@nmr.mgh.harvard.edu
RI Wald, Lawrence/D-4151-2009;
OI Stein, Thor/0000-0001-6954-4477
FU National Center for Research Resources [P41-RR14075]; NCRR BIRN
[BIRN002, U24 RR021382]; National Institute for Biomedical Imaging and
Bioengineering [R01EB006758]; National Institute on Aging [AG022381,
AG028521]; National Center for Alternative Medicine [RC1AT005728-01];
National Institute for Neurological Disorders and Stroke [R01
NS052585-01, 1R21NS072652-01, 1R01NS070963]; Autism and Dyslexia
Project; Ellison Medical Foundation; NIH Blueprint for Neuro-science
Research [U01-MH093765]; [1S10RR023401]; [1S10RR019307];
[1S10RR023043]
FX We would like to thank those who donated tissue; their generous donation
made this work possible. We also thank David Salat for comments and
discussion. Support for this research was provided in part by the
National Center for Research Resources (P41-RR14075, and the NCRR BIRN
Morphometric Project BIRN002, U24 RR021382), the National Institute for
Biomedical Imaging and Bioengineering (R01EB006758), the National
Institute on Aging (AG022381) and (AG028521), the National Center for
Alternative Medicine (RC1AT005728-01), the National Institute for
Neurological Disorders and Stroke (R01 NS052585-01, 1R21NS072652-01,
1R01NS070963), and was made possible by the resources provided by Shared
Instrumentation Grants 1S10RR023401, 1S10RR019307, and 1S10RR023043.
Additional support was provided by The Autism and Dyslexia Project
funded by the Ellison Medical Foundation and by the NIH Blueprint for
Neuro-science Research (U01-MH093765, part of the multi-institutional
Human Connectome Project).
NR 56
TC 9
Z9 9
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-6322
J9 ACTA NEUROPATHOL
JI Acta Neuropathol.
PD JAN
PY 2012
VL 123
IS 1
BP 85
EP 96
DI 10.1007/s00401-011-0929-5
PG 12
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 870BF
UT WOS:000298643400007
PM 22160360
ER
PT J
AU Counter, SA
Buchanan, LH
Ortega, F
AF Counter, S. Allen
Buchanan, Leo H.
Ortega, Fernando
TI Acoustic stapedius muscle reflex in mercury-exposed Andean children and
adults
SO ACTA OTO-LARYNGOLOGICA
LA English
DT Article
DE Middle ear muscles; brainstem; facial nerve; methylmercury; elemental
mercury; neurotoxicity; environmental
ID BLOOD MERCURY; HEARING-LOSS; URINE; NEUROTOXICITY; TRANSPORT; RESPONSES;
HAIR; LEAD; AGE
AB Conclusion: The results suggested mercury (Hg)-induced anomalies in the brainstem-mediated acoustic stapedius muscle reflex in children. Objectives: Hg exposure has been associated with hearing impairment and brainstem anomalies. Acoustic stapedius reflex (ASR) thresholds, growth functions, decay/adaptation times, and behavioral auditory thresholds were used to screen Andean children and adults for Hg-induced auditory brainstem and facial nerve impairment. Methods: Fifty-one participants, which included 22 children (aged 6-17 years) and 29 adults (aged 19-83 years) living in gold mining areas of Ecuador where Hg is widely used in amalgamation, were screened using ASR immittance procedures. Results: Mean blood mercury (HgB) level in the children was 15.6 mu g/L (SD, 21.3; median, 7 mu g/L; range, 2.0-89 mu g/L), and in the adults 8.5 mu g/L (SD, 7.1; median, 6 mu g/L; range, 2.0-32 mu g/L). Mean contralateral ASR thresholds (ASRT) for the screening frequency of 2000 Hz in the children (39 ears) was 92.9 dB HL (SD, 6.1; range, 80-105 dB HL), and in the adults (53 ears) 90.0 dB HL (SD, 6.4; range, 65-105 dB HL). The ASRT in the children increased significantly with HgB level (rho = 0.433; p = 0.008).
C1 [Counter, S. Allen] Harvard Univ, Sch Med, Harvard Biol Labs, Dept Neurol, Cambridge, MA 02138 USA.
[Counter, S. Allen] Massachusetts Gen Hosp, Dept Neurophysiol, Boston, MA 02114 USA.
[Buchanan, Leo H.] Univ Massachusetts, Sch Med, Eunice Kennedy Shriver Ctr, Dept Pediat, Waltham, MA USA.
[Buchanan, Leo H.] Harvard Univ Hlth Serv, Dept Otolaryngol, Cambridge, MA USA.
[Ortega, Fernando] Univ San Francisco Quito, Coll Hlth Sci, Integrated Community Dev Dept, Quito, Ecuador.
RP Counter, SA (reprint author), Harvard Univ, Sch Med, Biol Labs, Dept Neurol, 16 Divin Ave, Cambridge, MA 02138 USA.
EM allen_counter@harvard.edu
FU Administration of Universidad San Francisco de Quito; Fundacion
Capacitar of Ecuador; Harvard Biological Laboratories; Harvard David
Rockefeller Center for Latin American Studies; Shriver Center/University
of Massachusetts Medical School; Harvard University
FX The authors thank the Administration of Universidad San Francisco de
Quito and the Fundacion Capacitar of Ecuador for support of this
project. The authors thank Anthony Bruce Jacobs for excellent technical
assistance, and the Mayo Medical Laboratories for laboratory support. We
are grateful to the Harvard Biological Laboratories, the Harvard David
Rockefeller Center for Latin American Studies, the Shriver
Center/University of Massachusetts Medical School, and Dr Jeremy Bloxham
of Harvard University for support.
NR 20
TC 4
Z9 5
U1 0
U2 2
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0001-6489
J9 ACTA OTO-LARYNGOL
JI Acta Oto-Laryngol.
PD JAN
PY 2012
VL 132
IS 1
BP 51
EP 63
DI 10.3109/00016489.2011.617778
PG 13
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 865FM
UT WOS:000298296400009
PM 22175530
ER
PT J
AU Rajasingham, R
Mimiaga, MJ
White, JM
Pinkston, MM
Baden, RP
Mitty, JA
AF Rajasingham, Radha
Mimiaga, Matthew J.
White, Jaclyn M.
Pinkston, Megan M.
Baden, Rachel P.
Mitty, Jennifer A.
TI A Systematic Review of Behavioral and Treatment Outcome Studies Among
HIV-Infected Men Who Have Sex with Men Who Abuse Crystal Methamphetamine
SO AIDS PATIENT CARE AND STDS
LA English
DT Review
ID ACTIVE ANTIRETROVIRAL THERAPY; PLACEBO-CONTROLLED TRIAL;
LOS-ANGELES-COUNTY; ILLICIT DRUG-USE; BISEXUAL MEN; RISK BEHAVIORS;
CONTINGENCY MANAGEMENT; POSITIVE MEN; SAN-FRANCISCO; MEDICATION
ADHERENCE
AB Men who have sex with men (MSM) have the highest incidence of HIV infection in the United States. One of the contributing factors to HIV spread among this group is the use of crystal methamphetamine ("meth''). The objective was to review the behavioral impact of crystal meth use in HIV-infected MSM and potential treatment options. A systematic review of MEDLINE identified studies that evaluated the clinical effects of crystal meth on the HIV-infected MSM population. Search terms included HIV, methamphetamine, MSM, antiretroviral therapy, adherence, resistance, and treatment. U. S. citations in the English language in peer-reviewed journals until December 2010 were included. The primary author reviewed eligible articles, and relevant data including study design, sample, and outcomes were entered into an electronic data table. The 61 included studies highlight that HIV-infected MSM who use crystal meth are more likely to report high-risk sexual behaviors, incident sexually transmitted infections, and serodiscordant unprotected anal intercourse, compared to HIV-infected MSM who do not use crystal meth. Medication adherence in this population is notably low, which may contribute to transmission of resistant virus. No medications have proven effective in the treatment of crystal meth addiction, and the role of behavioral therapies, such as contingency management are still in question. HIV-infected MSM who abuse crystal meth have worse HIV-related health outcomes. Behavioral interventions have shown variable results in treating crystal meth addiction, and more investigation into rehabilitation options are needed. The results presented support efforts to develop and implement novel interventions to reduce crystal meth use in HIV-infected MSM.
C1 [Rajasingham, Radha; Baden, Rachel P.; Mitty, Jennifer A.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Mimiaga, Matthew J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02215 USA.
[Mimiaga, Matthew J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA.
[Pinkston, Megan M.] Brown Med Sch, Dept Psychiat & Human Behav, Providence, RI USA.
[Mimiaga, Matthew J.; White, Jaclyn M.] Fenway Inst, Boston, MA USA.
RP Rajasingham, R (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Deaconess 311,330 Brookline Ave, Boston, MA 02215 USA.
EM radha.rajasingham@gmail.com
FU NIH [P30 AI060354]; NIAID; NCI; NICHD; NHLBI; NIDA; NIMH; NIA; NCCAM;
FIC; National Institute On Drug Abuse [R34DA031028]; National Institutes
of Mental Health [R01 (5R01MH084757-03)]; TNC-CDAAR [P30DA013868]
FX No competing financial interests exist. This publication was made
possible with help from the Harvard University Center for AIDS Research
(CFAR), an NIH funded program (P30 AI060354), which is supported by the
following NIH Co-Funding and Participating Institutes and Centers:
NIAID, NCI, NICHD, NHLBI, NIDA, NIMH, NIA, NCCAM, and FIC. This
publication was also supported in part by Award Number R34DA031028
(PI:Mimiaga) from the National Institute On Drug Abuse. The content is
solely the responsibility of the authors and does not necessarily
represent the official views of the National Institute On Drug Abuse or
the National Institutes of Health. MP was supported by National
Institutes of Mental Health R01 (5R01MH084757-03) and TNC-CDAAR
(P30DA013868).
NR 75
TC 28
Z9 30
U1 2
U2 17
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 JAN
PY 2012
VL 26
IS 1
BP 36
EP 52
DI 10.1089/apc.2011.0153
PG 17
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 866SL
UT WOS:000298402800006
PM 22070609
ER
PT J
AU Milloy, MJ
Kerr, T
Bangsberg, DR
Buxton, J
Parashar, S
Guillemi, S
Montaner, J
Wood, E
AF Milloy, M. -J.
Kerr, Thomas
Bangsberg, David R.
Buxton, Jane
Parashar, Surita
Guillemi, Silvia
Montaner, Julio
Wood, Evan
TI Homelessness as a Structural Barrier to Effective Antiretroviral Therapy
Among HIV-Seropositive Illicit Drug Users in a Canadian Setting
SO AIDS PATIENT CARE AND STDS
LA English
DT Article
ID MARGINALLY HOUSED ADULTS; SAN-FRANCISCO; MEDICATION ADHERENCE; VIRAL
LOAD; INFECTED INDIVIDUALS; PROTEASE INHIBITORS; FOOD INSECURITY;
HOUSING STATUS; LOS-ANGELES; CELL COUNT
AB Despite the advent of effective antiretroviral therapy (ART), HIV-seropositive injection drug users (IDU) continue to suffer from elevated levels of morbidity and mortality. Evidence is needed to identify social- and structural-level barriers to effective ART. We investigated the impact of homelessness on plasma HIV RNA response among illicit drug users initiating ART in a setting with free and universal access to HIV care. We accessed data from a long-running prospective cohort of community-recruited IDU linked to comprehensive HIV clinical monitoring and ART dispensation records. Using Cox proportional hazards with recurrent events modeling, we estimated the independent effect of homelessness on time to plasma HIV viral load suppression. Between May 1996 and September 2009, 247 antiretroviral naive individuals initiated ART and contributed 1755 person-years of follow-up. Among these individuals, the incidence density of plasma HIV RNA suppression less than 500 copies/mm(3) was 56.7 (95% confidence interval [CI]: 46.9-66.0) per 100 person-years. In unadjusted analyses, homelessness was strongly associated with lower rates suppression (hazard ratio = 0.56, 95% CI: 0.40-0.78, p = 0.001), however, after adjustment for adherence this association was no longer significant (adjusted hazard ratio = 0.79, 95% CI: 0.56-1.11, p = 0.177). Homelessness poses a significant structural barrier to effective HIV treatment. However, since this relationship appears to be mediated by lower levels of ART adherence, interventions to improve adherence among members of this vulnerable population are needed.
C1 [Milloy, M. -J.; Kerr, Thomas; Parashar, Surita; Guillemi, Silvia; Montaner, Julio; Wood, Evan] St Pauls Hosp, BC Ctr Excellence HIV AIDS, Vancouver, BC V6Z 1Y6, Canada.
[Kerr, Thomas; Montaner, Julio; Wood, Evan] Univ British Columbia, Dept Med, Vancouver, BC, Canada.
[Milloy, M. -J.; Buxton, Jane] Univ British Columbia, Sch Populat & Publ Hlth, Vancouver, BC V5Z 1M9, Canada.
[Bangsberg, David R.] Massachusetts Gen Hosp, Ctr Global Hlth, Boston, MA 02114 USA.
[Bangsberg, David R.] Harvard Univ, Sch Med, Boston, MA USA.
[Buxton, Jane] British Columbia Ctr Dis Control, Vancouver, BC, Canada.
RP Wood, E (reprint author), St Pauls Hosp, BC Ctr Excellence HIV AIDS, 608-1081 Burrard St, Vancouver, BC V6Z 1Y6, Canada.
EM uhri-ew@cfenet.ubc.ca
FU US National Institutes of Health [R01DA021525]; Canadian Institutes of
Health Research (CHIR) [MOP-79297, RAA-79918]; Michael Smith Foundation
for Health Research; Abbott Laboratories; Agouron Pharmaceuticals Inc.;
Boehringer Ingelheim Pharmaceuticals Inc.; Borean Pharma AS;
Bristol-Myers Squibb; DuPont Pharma; Gilead Sciences; GlaxoSmithKline;
Hoffmann-La Roche; Immune Response Corporation; Incyte; Janssen-Ortho
Inc.; Kucera Pharmaceutical Company; Merck Frosst Laboratories; Pfizer
Canada Inc.; Sanofi Pasteur; Shire Biochem Inc.; Tibotec Pharmaceuticals
Ltd.; Trimeris Inc.
FX The authors thank the study participants for their contribution to the
research as well as current and past researchers and staff. We would
specifically like to thank Deborah Graham, Tricia Collingham, Caitlin
Johnston, Steve Kain, and Calvin Lai for their research and
administrative assistance. The study was supported by the US National
Institutes of Health (R01DA021525) and the Canadian Institutes of Health
Research (MOP-79297, RAA-79918). Thomas Kerr is supported by the Michael
Smith Foundation for Health Research and the Canadian Institutes of
Health Research (CIHR). M.-J. Milloy is supported by a doctoral research
award from CIHR.; Dr. Montaner has received educational grants from,
served as an ad hoc adviser to or spoken at various events sponsored by
Abbott Laboratories, Agouron Pharmaceuticals Inc., Boehringer Ingelheim
Pharmaceuticals Inc., Borean Pharma AS, Bristol-Myers Squibb, DuPont
Pharma, Gilead Sciences, GlaxoSmithKline, Hoffmann-La Roche, Immune
Response Corporation, Incyte, Janssen-Ortho Inc., Kucera Pharmaceutical
Company, Merck Frosst Laboratories, Pfizer Canada Inc., Sanofi Pasteur,
Shire Biochem Inc., Tibotec Pharmaceuticals Ltd., and Trimeris Inc. Dr.
Bangsbergh receives research support from Abbott Laboratories, Gilead
Sciences, and Bristol-Myers Squibb.
NR 58
TC 41
Z9 41
U1 3
U2 8
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 JAN
PY 2012
VL 26
IS 1
BP 60
EP 67
DI 10.1089/apc.2011.0169
PG 8
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 866SL
UT WOS:000298402800008
PM 22107040
ER
PT J
AU Cullen, G
Kroshinsky, D
Cheifetz, AS
Korzenik, JR
AF Cullen, G.
Kroshinsky, D.
Cheifetz, A. S.
Korzenik, J. R.
TI Anti-TNF associated psoriasis: authors' reply
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Editorial Material
C1 [Cullen, G.; Korzenik, J. R.] Massachusetts Gen Hosp, Crohns & Colitis Ctr, Boston, MA 02114 USA.
[Kroshinsky, D.] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Cullen, G.; Cheifetz, A. S.] Beth Israel Deaconess Med Ctr, Div Gastroenterol, Boston, MA 02215 USA.
[Cullen, G.; Kroshinsky, D.; Cheifetz, A. S.; Korzenik, J. R.] Harvard Univ, Sch Med, Boston, MA USA.
RP Cullen, G (reprint author), Massachusetts Gen Hosp, Crohns & Colitis Ctr, Boston, MA 02114 USA.
EM gcullen@bidmc.harvard.edu
NR 2
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0269-2813
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD JAN
PY 2012
VL 35
IS 2
BP 309
EP 310
DI 10.1111/j.1365-2036.2011.04945.x
PG 2
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA 862JI
UT WOS:000298086600012
ER
PT J
AU White, WB
Grady, D
Giudice, LC
Berry, SM
Zborowski, J
Snabes, MC
AF White, William B.
Grady, Deborah
Giudice, Linda C.
Berry, Scott M.
Zborowski, Joanne
Snabes, Michael C.
TI A cardiovascular safety study of LibiGel (testosterone gel) in
postmenopausal women with elevated cardiovascular risk and hypoactive
sexual desire disordera
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID SURGICALLY MENOPAUSAL WOMEN; METABOLIC SYNDROME; BREAST-CANCER;
UNITED-STATES; HEALTH; DYSFUNCTION; PREVALENCE; EVENTS; MEN; ESTROGEN
AB Evaluation of the safety of hormonal preparations for the treatment of female sexual dysfunction is important to assess the benefit-to-risk profile of these drugs and has been strongly encouraged by the Food and Drug Administration. LibiGel (Biosante Pharmaceuticals, Inc., Lincolnshire, IL), a low-dose testosterone gel, is under development for the treatment of hypoactive sexual desire disorder (HSDD) in oophorectomized women. To evaluate the long-term effects of LibiGel on risk for cardiovascular (CV) events, breast cancer, and general safety, a randomized, placebo-controlled clinical study using a novel adaptive design to optimize sample size and power is being conducted. The primary end point of the BioSante LibiGel Safety Study (BLISS) is a composite of CV events including death, nonfatal myocardial infarction, nonfatal stroke, coronary revascularization, hospitalized unstable angina, and venous thromboembolic events. Breast cancer is a coprimary end point. Postmenopausal women (both surgically and naturally) with HSDD and increased risk for CV events will be followed up for up to 5 years postrandomization with an interim data analysis for regulatory approval after the last woman enrolled has been on therapy for at least 12 months. Determination of the number of subjects to enroll is based on an adaptive design that uses interim data to estimate the predictive probability of study success. In agreement with the Food and Drug Administration, LibiGel will be declared safe if the upper limit of the 97.2% CI of the hazard ratio is <= 2.0 or the upper bound of the 97.2% CI for the absolute difference between CV event rates per 100 person-years is <= 1% and the observed hazard ratio is <= 2.0. The BLISS study will define the CV safety profile of low-dose testosterone therapy in the formulation of LibiGel for postmenopausal women with HSDD, and the trial design may provide a paradigm for studies that aim to document long-term safety when the proposed outcome under study is an uncommon adverse event. (Am Heart J 2012;163:27-32.)
C1 [White, William B.] Univ Connecticut, Sch Med, Calhoun Cardiol Ctr, Div Hypertens & Clin Pharmacol, Farmington, CT 06030 USA.
[Grady, Deborah] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Grady, Deborah] Univ Calif San Francisco, San Francisco Vet Adm Med Ctr, San Francisco, CA 94143 USA.
[Giudice, Linda C.] Univ Calif San Francisco, Dept Obstet & Gynecol & Reprod Sci, San Francisco, CA 94143 USA.
[Berry, Scott M.] Berry Consultants, Austin, TX USA.
[Zborowski, Joanne; Snabes, Michael C.] Biosante Pharmaceut Inc, Lincolnshire, IL USA.
RP White, WB (reprint author), Univ Connecticut, Sch Med, Calhoun Cardiol Ctr, Div Hypertens & Clin Pharmacol, 263 Farmington Ave, Farmington, CT 06030 USA.
EM wwhite@nso1.uchc.edu
FU BioSante Pharmaceuticals, Inc, Lincolnshire, IL
FX The sponsor of this study is BioSante Pharmaceuticals, Inc,
Lincolnshire, IL.
NR 26
TC 23
Z9 25
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 JAN
PY 2012
VL 163
IS 1
BP 27
EP 32
DI 10.1016/j.ahj.2011.09.021
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 863HI
UT WOS:000298153000007
PM 22172433
ER
PT J
AU Diercks, DB
Peacock, WF
Hollander, JE
Singer, AJ
Birkhahn, R
Shapiro, N
Glynn, T
Nowack, R
Safdar, B
Miller, CD
Lewandrowski, E
Nagurney, JT
AF Diercks, Deborah B.
Peacock, W. Frank
Hollander, Judd E.
Singer, Adam J.
Birkhahn, Robert
Shapiro, Nathan
Glynn, Ted
Nowack, Richard
Safdar, Basmah
Miller, Chadwick D.
Lewandrowski, Elizabeth
Nagurney, John T.
CA MIDAS Investigators
TI Diagnostic accuracy of a point-of-care troponin I assay for acute
myocardial infarction within 3 hours after presentation in early
presenters to the emergency department with chest pain
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID ACUTE CORONARY SYNDROME; SYMPTOMS; BIOMARKERS; PROTOCOL; RISK
AB Background Guidelines recommend that serial cardiac marker testing to rule out acute myocardial infarction (AMI) be performed for 8 to 12 hours after symptom onset. We aim to determine the diagnostic accuracy of a contemporary point-of-care (POC) troponin I (TnI) assay within 3 hours for patients presenting within 8 hours of symptom onset.
Methods The MIDAS study collected blood from patients presenting with suspected acute coronary syndrome at presentation and at 90 minutes, 3 hours, and 6 hours in whom the emergency physician planned an objective cardiac ischemia evaluation. Criterion standard diagnoses were adjudicated by experienced clinicians using all available medical records per American Heart Association/American College of Cardiology criteria. Reviewers were blinded to the investigational marker, Cardio3 TnI POC. The Cardio3 TnI reference value was defined as >0.05 ng/mL. Measures of diagnostic accuracy are presented with 95% CI.
Results A total of 858 of 1107 patients met the inclusion criteria. The study cohort had 476 men (55.5%) with median age of 57.0 years (interquartile range 48.0-67.0 years). Median time from symptom onset to initial blood draw was 3.9 hours (interquartile range 2.7-5.2 hours). Acute myocardial infarction was diagnosed in 82 patients (9.6%). The sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio over 3 hours were 84.1, 93.4, 12.8, and 0.17, respectively. There was no significant improvement in diagnostic accuracy associated with adding 6-hour serial testing to the 3-hour sample.
Conclusion In suspected patients with acute coronary syndrome presenting to the emergency department within 8 hours of symptom onset, 3 hours of serial testing with the Cardio3 TnI POC platform provides similar diagnostic accuracy for AMI as longer periods. (Am Heart J 2012;163:74-80.e4.)
C1 [Diercks, Deborah B.] Univ Calif Davis, Sacramento, CA 95817 USA.
[Peacock, W. Frank] Cleveland Clin, Cleveland, OH 44106 USA.
[Hollander, Judd E.] Univ Penn, Philadelphia, PA 19104 USA.
[Singer, Adam J.] Stony Brook Univ & Med Ctr, Stony Brook, NY USA.
[Birkhahn, Robert] New York Methodist Hosp, Brooklyn, NY USA.
[Shapiro, Nathan] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Glynn, Ted] Ingham Reg Med Ctr, Lansing, MT USA.
[Diercks, Deborah B.; Peacock, W. Frank; Hollander, Judd E.; Singer, Adam J.; Birkhahn, Robert; Shapiro, Nathan; Glynn, Ted; Nowack, Richard; Safdar, Basmah; Miller, Chadwick D.; Lewandrowski, Elizabeth; Nagurney, John T.] Henry Ford Med Ctr, Detroit, MI USA.
[Nowack, Richard; Safdar, Basmah] Yale Univ, New Haven, CT USA.
[Miller, Chadwick D.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Lewandrowski, Elizabeth; Nagurney, John T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Diercks, DB (reprint author), UCMDC, 2315 Stockton Blvd,PSSB 2100, Sacramento, CA 95817 USA.
EM dbdiercks@ucdavis.edu
RI Shapiro, Nathan/F-1718-2016;
OI Hollander, Judd/0000-0002-1318-2785
FU Inverness Medical
FX This study was funded by Inverness Medical.
NR 17
TC 23
Z9 26
U1 0
U2 6
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 JAN
PY 2012
VL 163
IS 1
BP 74
EP U102
DI 10.1016/j.ahj.2011.09.028
PG 11
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 863HI
UT WOS:000298153000013
PM 22172439
ER
PT J
AU Rienstra, M
Sun, JX
Lubitz, SA
Frankel, DS
Vasan, RS
Levy, D
Magnani, JW
Sullivan, LM
Meigs, JB
Ellinor, PT
Benjamin, EJ
AF Rienstra, Michiel
Sun, Jenny X.
Lubitz, Steven A.
Frankel, David S.
Vasan, Ramachandran S.
Levy, Daniel
Magnani, Jared W.
Sullivan, Lisa M.
Meigs, James B.
Ellinor, Patrick T.
Benjamin, Emelia J.
TI Plasma resistin, adiponectin, and risk of incident atrial fibrillation:
The Framingham Offspring Study
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID CONGESTIVE-HEART-FAILURE; C-REACTIVE PROTEIN; MYOCARDIAL-INFARCTION;
OBESITY; ONSET; PIOGLITAZONE; HYPERTENSION; INFLAMMATION; INDIVIDUALS;
POPULATION
AB Background We sought to investigate whether higher concentrations of resistin and lower concentrations of adiponectin relate to incident atrial fibrillation (AF) and whether this association is mediated by AF risk factors and inflammation. Resistin and adiponectin are adipokines that have been associated with multiple known risk factors for AF including diabetes, obesity, inflammation, and heart failure.
Methods We studied the relations between circulating concentrations of both adipokines and incident AF in participants of the Framingham Offspring Study.
Results Participants (n = 2,487) had a mean age of 61 +/- 10 years, and 54% were women. During a mean follow-up of 7.6 +/- 2.0 years, 206 (8.3%) individuals (96 women) developed incident AF. Plasma resistin concentration was significantly associated with incident AF (multivariable-adjusted hazard ratio [HR] 1.17 per SD [0.41 ng/mL] of natural logarithmically transformed resistin, 95% CI 1.02-1.34, P =.028). The resistin-AF association was attenuated after further adjustment for C-reactive protein (HR per SD increase resistin 1.14, 95% CI 0.99-1.31, P =.073). Adiponectin concentrations were not significantly associated with incident AF (multivariable-adjusted HR of 0.95 per SD [0.62 mu g/mL] of logarithmically transformed adiponectin, 95% CI 0.81-1.10, P =.478).
Conclusion In our community-based longitudinal study, higher mean concentrations of resistin were associated with incident AF, but the relation was attenuated by adjustment for C-reactive protein. We did not detect a statistically significant association between adiponectin and incident AF. Additional studies are needed to clarify the potential role of adipokines in AF and mechanisms linking adiposity to AF. (Am Heart J 2012; 163: 119-124. e1.)
C1 [Rienstra, Michiel; Vasan, Ramachandran S.; Levy, Daniel; Magnani, Jared W.; Meigs, James B.; Ellinor, Patrick T.; Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA 01702 USA.
[Rienstra, Michiel] Univ Groningen, Univ Med Ctr Groningen, Dept Cardiol, Groningen, Netherlands.
[Rienstra, Michiel; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA USA.
[Rienstra, Michiel; Vasan, Ramachandran S.; Levy, Daniel; Magnani, Jared W.; Meigs, James B.; Benjamin, Emelia J.] NHLBI, Framingham, MA USA.
[Sun, Jenny X.; Sullivan, Lisa M.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Lubitz, Steven A.; Ellinor, Patrick T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiac Arrhythmia Serv, Boston, MA USA.
[Frankel, David S.] Hosp Univ Penn, Dept Med, Div Cardiovasc, Philadelphia, PA 19104 USA.
[Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Sch Med, Prevent Med Sect, Framingham, MA 01702 USA.
[Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Framingham, MA 01702 USA.
[Vasan, Ramachandran S.; Magnani, Jared W.; Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Cardiol Sect, Framingham, MA 01702 USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
[Meigs, James B.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Gen Med,Dept Med, Boston, MA USA.
RP Benjamin, EJ (reprint author), Boston Univ, Framingham Heart Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM emelia@bu.edu
OI Ramachandran, Vasan/0000-0001-7357-5970; Sullivan,
Lisa/0000-0003-0726-7149; Benjamin, Emelia/0000-0003-4076-2336;
Rienstra, Michiel/0000-0002-2581-070X
FU National Heart, Lung, and Blood Institute; NHLBI/NIH [N01-HC-25195];
Boston University School of Medicine; Netherlands Organization for
Scientific Research [825.09.020]; National Institutes of Health
[1R01HL092577, 1RC1HL101056, 1R01HL102214, R01AG028321, 6R01-NS17950,
5R21DA027021, 5RO1HL104156, 1K24HL105780, R01-DK-080739]; American Heart
Association [09FTF2190028]; Evans Center for Interdisciplinary
Biomedical Research ARC on "Atrial Fibrillation" at Boston University
FX The Framingham Heart Study is supported by National Heart, Lung, and
Blood Institute; Framingham Heart Study (NHLBI/NIH contract
N01-HC-25195); and the Boston University School of Medicine. Dr Rienstra
is supported by a grant from the Netherlands Organization for Scientific
Research (Rubicon grant 825.09.020). This work was supported by grants
from the National Institutes of Health to Drs Benjamin and Ellinor
(1R01HL092577); Dr Benjamin (1RC1HL101056, 1R01HL102214, R01AG028321;
and support via 6R01-NS17950) and Dr Ellinor (5R21DA027021,
5RO1HL104156, 1K24HL105780); and Dr Vasan (R01-DK-080739). Dr Magnani is
supported by American Heart Association Award 09FTF2190028. This work
was partially supported by the Evans Center for Interdisciplinary
Biomedical Research ARC on "Atrial Fibrillation" at Boston University
(http://www.bumc.bu.edu/evanscenteribr/).
NR 37
TC 26
Z9 26
U1 0
U2 5
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 JAN
PY 2012
VL 163
IS 1
BP 119
EP U151
DI 10.1016/j.ahj.2011.09.029
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 863HI
UT WOS:000298153000019
PM 22172445
ER
PT J
AU Steinhaus, DA
Vittinghoff, E
Moffatt, E
Hart, AP
Ursell, P
Tseng, ZH
AF Steinhaus, Daniel A.
Vittinghoff, Eric
Moffatt, Ellen
Hart, Amy P.
Ursell, Philip
Tseng, Zian H.
TI Characteristics of sudden arrhythmic death in a diverse, urban community
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID MULTIPLE SOURCE SURVEILLANCE; CARDIAC DEATH; MYOCARDIAL-INFARCTION;
TEMPORAL TRENDS; CORONARY DEATH; POPULATION; RISK; EPIDEMIOLOGY;
PREVENTION; ETIOLOGY
AB Background Sudden cardiac death (SCD) remains a major public health problem; however, its true burden remains unknown with widely variable estimates of its incidence. We aimed to examine the contemporary epidemiology and autopsy characteristics of SCD in an ethnically diverse community.
Methods Three physicians reviewed all deaths of individuals aged >= 20 years reported to the San Francisco medical examiner in 2007 for presentations fitting World Health Organization (WHO) SCD criteria-within 1 hour of symptom onset (witnessed) or within 24 hours of being observed alive and symptom free (unwitnessed). After comprehensive review of medical examiner investigation, WHO SCDs were classified as sudden arrhythmic death (SAD) or nonarrhythmic death. Coronary artery disease (CAD) and cardiac mass were evaluated in all SADs undergoing autopsy and compared with demographically similar accidental trauma control deaths.
Results We identified 252 WHO SCDs; 145 were SADs. Men had a 2.2-fold higher SAD rate (P < .0005). Blacks had a 3.15-fold higher SAD rate compared with whites (P = .003). Significant CAD was present in 38.9% of SADs and associated with higher SAD risk compared with control deaths (OR 2.58, 95% CI 1.12-5.97, P = .026). Mean cardiac mass was linearly associated with risk for SAD in cases without significant CAD (OR 2.06 per 100 g, 95% CI 1.43-2.98, P < .0005).
Conclusions In a diverse, urban population, SAD incidence varied substantially by gender and race. Significant CAD accounted for far fewer SADs than previous studies but remained associated with a 2.6-fold higher risk as compared with control deaths. These findings may reflect the evolving contemporary epidemiology of SCD. (Am Heart J 2012;163:125-31.)
C1 [Tseng, Zian H.] Univ Calif San Francisco, Sect Cardiac Electrophysiol, Dept Med, Div Cardiol, San Francisco, CA 94143 USA.
[Steinhaus, Daniel A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA USA.
[Vittinghoff, Eric] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Moffatt, Ellen; Hart, Amy P.] City & Cty San Francisco, Office Chief Med Examiner, San Francisco, CA USA.
[Ursell, Philip] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA.
RP Tseng, ZH (reprint author), Univ Calif San Francisco, Sect Cardiac Electrophysiol, Dept Med, Div Cardiol, 500 Parnassus Ave,Box 1354, San Francisco, CA 94143 USA.
EM zhtseng@medicine.ucsf.edu
FU National Center for Research Resources, a component of the National
Institutes of Health (NIH); NIH Roadmap for Medical Research [KL2
RR024130]; National Heart, Lung, and Blood Institute [R01 HL102090-01A1]
FX This research was funded by grants from the National Center for Research
Resources, a component of the National Institutes of Health (NIH) and
NIH Roadmap for Medical Research (KL2 RR024130) and the National Heart,
Lung, and Blood Institute (R01 HL102090-01A1), both to ZHT. There are no
relationships with industry.
NR 27
TC 13
Z9 13
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
EI 1097-5330
J9 AM HEART J
JI Am. Heart J.
PD JAN
PY 2012
VL 163
IS 1
BP 125
EP 131
DI 10.1016/j.ahj.2011.09.016
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 863HI
UT WOS:000298153000020
PM 22172446
ER
PT J
AU Berger, JS
Bhatt, DL
AF Berger, Jeffery S.
Bhatt, Deepak L.
TI Reply to the letter by Chatterjee et al "Bleeding, mortality, and
antiplatelet therapy: Results from the Clopidogrel for High
Atherothrombotic Risk and Ischemic Stabilization, Management, and
Avoidance (CHARISMA) trial"
SO AMERICAN HEART JOURNAL
LA English
DT Letter
C1 [Berger, Jeffery S.] NYU, Sch Med, New York, NY 10016 USA.
[Bhatt, Deepak L.] Brigham & Womens Hosp, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Bhatt, Deepak L.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Berger, JS (reprint author), NYU, Sch Med, 530 1st Ave,Skirball 9R, New York, NY 10016 USA.
EM Jeffrey.berger@nyumc.org; DLBHATTMD@post.harvard.edu
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN
PY 2012
VL 163
IS 1
BP E3
EP E3
DI 10.1016/j.ahj.2011.10.005
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 863HI
UT WOS:000298153000002
ER
PT J
AU Rosenblum, JL
Castro, VM
Moore, CE
Kaplan, LM
AF Rosenblum, Jennifer L.
Castro, Victor M.
Moore, Carolyn E.
Kaplan, Lee M.
TI Calcium and vitamin D supplementation is associated with decreased
abdominal visceral adipose tissue in overweight and obese adults
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID PLACEBO-CONTROLLED TRIAL; WEIGHT-LOSS; BODY-WEIGHT; FAT LOSS; DIETARY
CALCIUM; DAIRY; WOMEN; HEALTHY; RISK; ADOLESCENTS
AB Background: Several studies suggest that calcium and vitamin D (CaD) may play a role in the regulation of abdominal fat mass.
Objective: This study investigated the effect of CaD-supplemented orange juice (OJ) on weight loss and reduction of visceral adipose tissue (VAT) in overweight and obese adults (mean +/- SD age: 40.0 +/- 12.9 y).
Design: Two parallel, double-blind, placebo-controlled trials were conducted with either regular or reduced-energy (lite) orange juice. For each 16-wk trial, 171 participants were randomly assigned to 1 of 2 groups. The treatment groups consumed three 240-mL glasses of OJ (regular or lite) fortified with 350 mg Ca and 100 IU vitamin D per serving, and the control groups consumed either unfortified regular or lite OJ. Computed tomography scans of VAT and subcutaneous adipose tissue were performed by imaging a single cut at the lumbar 4 level.
Results: After 16 wk, the average weight loss (similar to 2.45 kg) did not differ significantly between groups. In the regular OJ trial, the reduction of VAT was significantly greater (P = 0.024) in the CaD group (-12.7 +/- 25.0 cm(2)) than in the control group (-1.3 +/- 13.6 cm(2)). In the lite OJ trial, the reduction of VAT was significantly greater (P = 0.039) in the CaD group (-13.1 +/- 18.4 cm(2)) than in the control group (-6.4 +/- 17.5 cm(2)) after control for baseline VAT. The effect of calcium and vitamin D on VAT remained highly significant when the results of the 2 trials were combined (P = 0.007).
Conclusions: The findings suggest that calcium and/or vitamin D supplementation contributes to a beneficial reduction of VAT. This trial is registered at clinicaltrial.gov as NCT00386672, NCT01363115. Am J Clin Nutr 2012;95:101-8.
C1 [Rosenblum, Jennifer L.; Castro, Victor M.; Kaplan, Lee M.] Massachusetts Gen Hosp, Weight Ctr, Boston, MA 02114 USA.
[Rosenblum, Jennifer L.; Castro, Victor M.; Kaplan, Lee M.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
RP Kaplan, LM (reprint author), Massachusetts Gen Hosp, Weight Ctr, 50 Staniford St,4th Floor, Boston, MA 02114 USA.
EM lmkaplan@partners.org
FU National Institute of Diabetes and Digestive and Kidney Diseases
[DK046200]; Beverage Institute for Health & Wellness of The Coca-Cola
Company; Massachusetts General Hospital Weight Center
FX Supported by the National Institute of Diabetes and Digestive and Kidney
Diseases (DK046200), Beverage Institute for Health & Wellness of The
Coca-Cola Company, and the Massachusetts General Hospital Weight Center.
NR 42
TC 47
Z9 50
U1 5
U2 24
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD JAN
PY 2012
VL 95
IS 1
BP 101
EP 108
DI 10.3945/ajcn.111.019489
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 866SF
UT WOS:000298402100014
PM 22170363
ER
PT J
AU Ryan, RJH
Sloan, JM
Collins, AB
Mansouri, J
Raje, NS
Zukerberg, LR
Ferry, JA
AF Ryan, Russell J. H.
Sloan, J. Mark
Collins, A. Bernard
Mansouri, Jaleh
Raje, Noopur S.
Zukerberg, Lawrence R.
Ferry, Judith A.
TI Extranodal Marginal Zone Lymphoma of Mucosa-Associated Lymphoid Tissue
With Amyloid Deposition A Clinicopathologic Case Series
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE Lymphoma; MALT lymphoma; Marginal zone lymphoma; Amyloid
ID B-CELL LYMPHOMA; OF-THE-LITERATURE; LOCALIZED PULMONARY AMYLOIDOSIS;
PRIMARY SJOGRENS-SYNDROME; ABDOMINAL FAT PAD; SYSTEMIC AMYLOIDOSIS;
MALT-LYMPHOMA; MALIGNANT-LYMPHOMA; PREDICTIVE-VALUE; NERVOUS-SYSTEM
AB Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT) lymphoma is a mature B-cell neoplasm that typically/follows an indolent clinical course. Amyloid deposition associated with MALT lymphoma is uncommon. We describe the clinical and pathologic features of 20 cases of MALT lymphoma and associated amyloid deposition across diverse primary sites. Frozen section immunofluorescence performed on 4 cases suggests that these deposits are a localized form of AL amyloid.
Clinical follow-up was available for 15 patients. Amyloid deposits distant from the initial site occurred in 5 cases, always at sites also involved by the underlying lymphoma. No definitive evidence of systemic amyloidosis affecting the heart, kidneys, or liver was present in any patient. Given the generally indolent clinical behavior of MALT lymphomas with associated amyloid, we do not recommend extensive follow-up testing for systemic amyloidosis or more aggressive therapy than would be indicated for other MALT lymphomas of similar clinical stage.
C1 [Ryan, Russell J. H.; Collins, A. Bernard; Zukerberg, Lawrence R.; Ferry, Judith A.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Raje, Noopur S.] Massachusetts Gen Hosp, Dept Med, Hematol Oncol Unit, Boston, MA 02114 USA.
[Sloan, J. Mark] Boston Univ, Amyloid Res & Treatment Program, Boston, MA 02215 USA.
[Mansouri, Jaleh] Lowell Gen Hosp, Dept Pathol, Lowell, MA USA.
RP Ryan, RJH (reprint author), Massachusetts Gen Hosp, Dept Pathol, 55 Fruit St,Warren 2, Boston, MA 02114 USA.
OI Sloan, John/0000-0001-7069-4528
FU Pathology Department, Massachusetts General Hospital
FX Supported by the Pathology Department, Massachusetts General Hospital.
NR 38
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U1 0
U2 5
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 JAN
PY 2012
VL 137
IS 1
BP 51
EP 64
DI 10.1309/AJCPI08WAKYVLHHA
PG 14
WC Pathology
SC Pathology
GA 865WC
UT WOS:000298340600008
PM 22180478
ER
PT J
AU Kim, JY
Dzik, WH
Dighe, AS
Lewandrowski, KB
AF Kim, Ji Yeon
Dzik, Walter H.
Dighe, Anand S.
Lewandrowski, Kent B.
TI Laboratory Test Utilization Reply
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Letter
C1 [Kim, Ji Yeon; Dzik, Walter H.; Dighe, Anand S.; Lewandrowski, Kent B.] Harvard Univ, Sch Med, Dept Pathol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Kim, JY (reprint author), Harvard Univ, Sch Med, Dept Pathol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0002-9173
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD JAN
PY 2012
VL 137
IS 1
BP 166
EP 166
PG 1
WC Pathology
SC Pathology
GA 865WC
UT WOS:000298340600025
ER
PT J
AU Ujkaj, M
Davidoff, DA
Seiner, SJ
Ellison, JM
Harper, DG
Forester, BP
AF Ujkaj, Manjola
Davidoff, Donald A.
Seiner, Stephen J.
Ellison, James M.
Harper, David G.
Forester, Brent P.
TI Safety and Efficacy of Electroconvulsive Therapy for the Treatment of
Agitation and Aggression in Patients With Dementia
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
DE agitation; aggression; BPSD; dementia; ECT; elderly; electroconvulsive
therapy
ID ILLNESS RATING-SCALE; DEPRESSED OLDER-ADULTS; ELDERLY-PATIENTS;
ALZHEIMERS-DISEASE; NEUROPSYCHIATRIC SYMPTOMS; CASE SERIES; ECT;
SCHIZOPHRENIA; PROPOFOL; DISORDER
AB Objectives: Noncognitive behavioral disturbances including agitation and aggression frequently accompany the cognitive symptoms of dementia accounting for much of dementia's morbidity, yet treatment options are currently limited. The authors examine the safety and efficacy of Electroconvulsive Therapy (ECT) for agitation and aggression in dementia patients. Design: Retrospective systematic chart review. Setting: McLean Hospital's geriatric neuropsychiatry unit. Participants: Sixteen patients with a diagnosis of dementia treated with ECT for agitation/aggression during 2004-2007. Measurements: Clinical charts were rated on the Pittsburgh Agitation Scale as the primary outcome, the Clinical Global Impression scale and the Global Assessment of Functioning pre- and post-ECT. Results: 16 patients of mean age 66.6 +/- 8.3 years were studied. Their average overall and pre-ECT lengths of stay were 59.7 +/- 39.7 days and 23 +/- 15.7 days, respectively. Patients received a mean of 9 ECT treatments, mostly bilateral. Patients showed significant reductions in their total Pittsburgh Agitation Scale scores from baseline after ECT (from 11.0 +/- 5.0 to 3.9 +/- 4.3 [F = 30.33, df = 1, 15, p < 0.001]). Clinical Global Impression scale decreased significantly (from 6.0 +/- 0.6 pre-ECT to 2.1 +/- 1.6 post-ECT [F = 112.97, df = 1, 15, p < 0.001]). Global Assessment of Functioning change was not significant (from 23.0 +/- 4.9 to 26.9 +/- 6.9 [F = 5.73, df = 1, 13, p = 0.32]). Only one patient, in whom ECT was discontinued following 11 bilateral treatments, showed no improvement. Eight patients showed transient postictal confusion, which typically resolved within 48 hours. Two patients showed more severe postictal confusion that required modification of treatment. Conclusions: These results suggest that ECT is an effective and safe treatment for agitation and aggression in dementia. Further prospective studies are warranted. (Am J Geriatr Psychiatry 2012; 20: 61-72)
C1 [Ujkaj, Manjola] Harvard Univ, VA Boston Healthcare Syst, Harvard S Shore Psychiat Residency Training Progr, Dept Psychiat,Sch Med,Brockton Div, Brockton, MA 02301 USA.
[Davidoff, Donald A.] Harvard Univ, McLean Hosp, Sch Med, Dept Neuropsychol, Belmont, MA 02178 USA.
[Davidoff, Donald A.; Seiner, Stephen J.; Ellison, James M.; Harper, David G.; Forester, Brent P.] Harvard Univ, McLean Hosp, Sch Med, Dept Psychiat, Belmont, MA 02178 USA.
RP Ujkaj, M (reprint author), Harvard Univ, VA Boston Healthcare Syst, Harvard S Shore Psychiat Residency Training Progr, Dept Psychiat,Sch Med,Brockton Div, Bldg 5,940 Belmont St, Brockton, MA 02301 USA.
EM manjola_ujkaj@hms.harvard.edu
NR 49
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Z9 14
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1064-7481
EI 1545-7214
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD JAN
PY 2012
VL 20
IS 1
BP 61
EP 72
DI 10.1097/JGP.0b013e3182051bbc
PG 12
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA 869ZQ
UT WOS:000298639300007
PM 22143072
ER
PT J
AU Goodfriend, T
AF Goodfriend, Theodore
TI Molecular Trafficking of Angiotensin Receptors
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Editorial Material
C1 William S Middleton Mem Vet Adm Med Ctr, Madison, WI 53705 USA.
RP Goodfriend, T (reprint author), William S Middleton Mem Vet Adm Med Ctr, Madison, WI 53705 USA.
EM tgoodfri@facstaff.wisc.edu
NR 2
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0895-7061
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD JAN
PY 2012
VL 25
IS 1
BP 23
EP 23
DI 10.1038/ajh.2011.222
PG 1
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 864UE
UT WOS:000298264800008
PM 22170076
ER
PT J
AU O'Seaghdha, CM
Yang, Q
Wu, HS
Hwang, SJ
Fox, CS
AF O'Seaghdha, Conall M.
Yang, Qiong
Wu, Hongsheng
Hwang, Shih-Jen
Fox, Caroline S.
TI Performance of a Genetic Risk Score for CKD Stage 3 in the General
Population
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Chronic kidney disease; genetics; risk prediction
ID CHRONIC KIDNEY-DISEASE; CORONARY-HEART-DISEASE;
GLOMERULAR-FILTRATION-RATE; DIABETIC-NEPHROPATHY; RENAL-INSUFFICIENCY;
UNITED-STATES; PREVALENCE; ADULTS; PREDICTION; FRAMINGHAM
AB Background: Recent genome-wide association studies have identified multiple genetic loci that increase the risk of chronic kidney disease (CKD) in the general population. We hypothesized that knowledge of these loci might permit improved CKD risk prediction beyond that provided by traditional phenotypic risk factors.
Study Design: Observational cohort study.
Setting & Participants: Participants who attended the 15th (1977-1979) and 24th (1995-1998) examination cycles of the original cohort or the 6th (1995-1998) and 8th cycles (2005-2008) of the offspring cohort of the Framingham Heart Study (n = 2,489).
Predictors: Single-nucleotide polymorphisms at 16 stage 3 CKD loci were genotyped and used to construct a genetic risk score. Standard clinical predictors of incident stage 3 CKD also were used.
Outcomes & Measurements: Incident stage 3 CKD was defined as estimated glomerular filtration rate <60 mL/min/1.73 m(2) at follow-up. Participants with baseline stage 3 CKD were excluded. Logistic regression was used to generate C statistics, which measured the power of the genetic risk score to discriminate risk of incident CKD stage 3 with and without traditional risk factors.
Results: There were 270 new stage 3 CKD cases during an average of 10.8 years of follow-up. Mean genetic risk score was 17.5 +/- 2.8 (SD) for those who developed stage 3 CKD and 17.3 +/- 2.6 for those who did not (P for genotype score difference = 0.2). The OR for stage 3 CKD was 1.06 (95% CI, 1.01-1.11; P = 0.03) per additional risk allele, adjusting for age and sex. In the age-and sex-adjusted model, the C statistic was 0.748 without the genotype score and 0.751 with the score (P difference = 0.3). The risk score was not statistically significant in a multivariable model adjusted for standard stage 3 CKD risk factors (P = 0.07).
Limitations: All participants were of European ancestry; the genotype score may not be valid in different ancestral groups.
Conclusions: A genetic score generated from 16 known CKD risk alleles did not predict new cases of stage 3 CKD in the community beyond knowledge of common clinical risk factors alone. Am J Kidney Dis. 59(1): 19-24. Published by Elsevier Inc. on behalf of the National Kidney Foundation, Inc. This is a US Government Work. There are no restrictions on its use.
C1 [O'Seaghdha, Conall M.; Hwang, Shih-Jen; Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA 01702 USA.
[O'Seaghdha, Conall M.; Hwang, Shih-Jen; Fox, Caroline S.] Ctr Populat Studies, Framingham, MA USA.
[O'Seaghdha, Conall M.] Massachusetts Gen Hosp, Div Renal, Brigham & Womens Hosp, Boston, MA 02114 USA.
[O'Seaghdha, Conall M.; Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
[Yang, Qiong; Wu, Hongsheng] Boston Univ, Dept Biostat, Boston, MA 02215 USA.
[Wu, Hongsheng] Wentworth Inst Technol, Dept Comp Sci, Boston, MA USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol, Boston, MA 02115 USA.
RP Fox, CS (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave,Ste 2, Framingham, MA 01702 USA.
EM foxca@nhlbi.nih.gov
RI Yang, Qiong/G-5438-2014
FU NHLBI's FHS [N01-HC-25195]
FX This research was conducted in part using data and resources from the
FHS of the National Heart, Lung, and Blood Institute (NHLBI) of the
National Institutes of Health and Boston University School of Medicine.
This work was partially supported by the NHLBI's FHS (Contract No.
N01-HC-25195). The sponsors had no role in the conduct or interpretation
of the study. The corresponding author had full access to all data in
the study and had final responsibility for the decision to submit for
publication.
NR 41
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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 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD JAN
PY 2012
VL 59
IS 1
BP 19
EP 24
DI 10.1053/j.ajkd.2011.08.030
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 863HO
UT WOS:000298153600008
PM 21995970
ER
PT J
AU Peralta, CA
Jacobs, DR
Katz, R
Ix, JH
Madero, M
Duprez, DA
Sarnak, MJ
Criqui, MH
Kramer, HJ
Palmas, W
Herrington, D
Shlipak, MG
AF Peralta, Carmen A.
Jacobs, David R., Jr.
Katz, Ronit
Ix, Joachim H.
Madero, Magdalena
Duprez, Daniel A.
Sarnak, Mark J.
Criqui, Michael H.
Kramer, Holly J.
Palmas, Walter
Herrington, David
Shlipak, Michael G.
TI Association of Pulse Pressure, Arterial Elasticity, and Endothelial
Function With Kidney Function Decline Among Adults With Estimated GFR >
60 mL/min/1.73 m(2): The Multi-Ethnic Study of Atherosclerosis (MESA)
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Kidney function; arterial elasticity; chronic kidney disease;
atherosclerosis
ID GLOMERULAR-FILTRATION-RATE; BLOOD-PRESSURE; HYPERTENSIVE PATIENTS;
CARDIOVASCULAR-DISEASE; RENAL-FUNCTION; WAVE VELOCITY; STIFFNESS; RISK;
DYSFUNCTION; POPULATION
AB Background: The association of subclinical vascular disease and early declines in kidney function has not been well studied.
Study Design: Prospective cohort study.
Setting & Participants: Multi-Ethnic Study of Atherosclerosis (MESA) participants with estimated glomerular filtration rate (eGFR) >= 60 mL/min/1.73 m(2) with follow-up of 5 years.
Predictors: Pulse pressure, small (SAE) and large arterial elasticity (LAE), and flow-mediated dilation.
Outcomes: Kidney function decline.
Measurements: SAE and LAE were measured by pulse contour analysis of the radial artery. Kidney function was assessed by eGFR based on serum creatinine (eGFR(SCr)) and cystatin C (eGFR(SCysC)).
Results: For 4,853 adults, higher pulse pressure and lower SAE and LAE had independent and linear associations with faster rates of kidney function decline. Compared with persons with pulse pressure of 40-50 mm Hg, eGFR(SCysC) declines were 0.29 (P = 0.006), 0.56 (P < 0.001), and 0.91 (P < 0.001) mL/min/1.73 m(2)/y faster in persons with pulse pressure of 50-60, 60-70, and >70 mm Hg, respectively. Compared with the highest quartile of SAE (most elastic), eGFR(SCysC) declines were 0.26 (P = 0.009), 0.35 (P = 0.001), and 0.70 (P < 0.001) mL/min/1.73 m(2)/y faster for the second, third, and fourth quartiles, respectively. For LAE, compared with the highest quartile, eGFR(SCysC) declines were 0.28 (P = 0.004), 0.58 (P < 0.001), and 0.83 (P < 0.001) mL/min/1.73 m(2)/y faster for each decreasing quartile of LAE. Findings were similar for eGFR(SCr). In contrast, for 2,997 adults with flow-mediated dilation and kidney function measures, flow-mediated dilation was not associated significantly with kidney function decline. For every 1-standard deviation greater flow-mediated dilation, eGFR(SCysC) and eGFR(SCr) changed by 0.05 (P = 0.3) and 0.06 mL/min/1.73 m(2)/y (P = 0.04), respectively.
Limitations: We had no direct measure of GFR, in common with nearly all large population-based studies.
Conclusions: Higher pulse pressure and lower arterial elasticity, but not flow-mediated dilation, were associated linearly and independently with faster kidney function decline in persons with eGFR >= 60 mL/min/1.73 m(2). Future studies should investigate whether treatments to decrease the stiffness of large and small arteries may slow the rate of kidney function loss. Am J Kidney Dis. 59(1):41-49. (C) 2011 by the National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
C1 [Peralta, Carmen A.; Shlipak, Michael G.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Peralta, Carmen A.; Shlipak, Michael G.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Jacobs, David R., Jr.] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA.
[Katz, Ronit] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Ix, Joachim H.] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
[Madero, Magdalena] Inst Nacl Cardiol Ignacio Chavez, Div Nephrol, Mexico City, DF, Mexico.
[Duprez, Daniel A.] Univ Minnesota, Div Cardiovasc, Sch Med, Minneapolis, MN 55455 USA.
[Sarnak, Mark J.] Tufts Med Ctr, Div Nephrol, Boston, MA USA.
[Criqui, Michael H.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
[Kramer, Holly J.] Loyola Univ, Med Ctr, Div Nephrol, Maywood, IL 60153 USA.
[Palmas, Walter] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
[Herrington, David] Wake Forest Univ, Sch Med, Internal Med Sect Cardiol, Winston Salem, NC 27109 USA.
RP Peralta, CA (reprint author), 4150 Clement St,111A1, San Francisco, CA 94121 USA.
EM carmenalicia.peralta@ucsf.edu
OI Kramer, Holly/0000-0002-6374-837X
FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95169];
National Institute of Diabetes and Digestive and Kidney Disease
[1K23DK082793-01]
FX This research was supported by contracts N01-HC-95159 through
N01-HC-95169 from the National Heart, Lung, and Blood Institute and by
the National Institute of Diabetes and Digestive and Kidney Disease
(grant 1K23DK082793-01, Dr Peralta). These funding sources had no
involvement in the design or execution of this study.
NR 44
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U1 1
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD JAN
PY 2012
VL 59
IS 1
BP 41
EP 49
DI 10.1053/j.ajkd.2011.08.015
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 863HO
UT WOS:000298153600011
PM 22000727
ER
PT J
AU Johansen, KL
Painter, P
AF Johansen, Kirsten L.
Painter, Patricia
TI Exercise in Individuals With CKD
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Review
DE Exercise; physical activity; chronic kidney disease
ID CHRONIC KIDNEY-DISEASE; CHRONIC-RENAL-FAILURE;
AMERICAN-HEART-ASSOCIATION; QUALITY-OF-LIFE; PHYSICAL-ACTIVITY;
CARDIOVASCULAR OUTCOMES; PREDIALYSIS PATIENTS; SPORTS-MEDICINE;
RISK-FACTOR; CAPACITY
AB There are few studies evaluating exercise in the nondialysis chronic kidney disease (CKD) population. This review covers the rationale for exercise in patients with CKD not requiring dialysis and the effects of exercise training on physical functioning, progression of kidney disease, and cardiovascular risk factors. In addition, we address the issue of the risk of exercise and make recommendations for implementation of exercise in this population. Evidence from uncontrolled studies and small randomized controlled trials shows that exercise training results in improved physical performance and functioning in patients with CKD. In addition, although there are no studies examining cardiovascular outcomes, several studies suggest that cardiovascular risk factors such as hypertension, inflammation, and oxidative stress may be improved with exercise training in this population. Although the current literature does not allow for definitive conclusions about whether exercise training slows the progression of kidney disease, no study has reported worsening of kidney function as a result of exercise training. In the absence of guidelines specific to the CKD population, recent guidelines developed for older individuals and patients with chronic disease should be applied to the CKD population. In sum, exercise appears to be safe in this patient population if begun at moderate intensity and increased gradually. The evidence suggests that the risk of remaining inactive is higher. Patients should be advised to increase their physical activity when possible and be referred to physical therapy or cardiac rehabilitation programs when appropriate. Am J Kidney Dis. 59(1):126-134. (C) 2011 by the National Kidney Foundation, Inc.
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.
[Painter, Patricia] Univ Minnesota, Sch Nursing, Div Hypertens & Renal Dis, Minneapolis, MN 55455 USA.
RP Johansen, KL (reprint author), San Francisco VA Med Ctr, Nephrol Sect, 4150 Clement St,111J, San Francisco, CA 94121 USA.
EM kirsten.johansen@ucsf.edu
FU NIDDK NIH HHS [K24 DK085153-02, K24 DK085153, K24 DK085153-03, K24
DK085153-01A1]
NR 52
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U1 1
U2 23
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD JAN
PY 2012
VL 59
IS 1
BP 126
EP 134
DI 10.1053/j.ajkd.2011.10.008
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 863HO
UT WOS:000298153600022
PM 22113127
ER
PT J
AU Weinberg, I
Jaff, MR
AF Weinberg, Ido
Jaff, Michael R.
TI Spontaneous Blue Finger Syndrome: A Benign Process
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Letter
C1 [Weinberg, Ido; Jaff, Michael R.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP Weinberg, I (reprint author), Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
NR 3
TC 3
Z9 3
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9343
J9 AM J MED
JI Am. J. Med.
PD JAN
PY 2012
VL 125
IS 1
BP E1
EP E2
DI 10.1016/j.amjmed.2011.05.007
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 866IF
UT WOS:000298373300001
PM 22195537
ER
PT J
AU Boatin, A
Wylie, B
Singh, MP
Singh, N
Yeboah-Antwi, K
Hamer, D
AF Boatin, Adeline
Wylie, Blair
Singh, Mrigendra Pal
Singh, Neeru
Yeboah-Antwi, Kojo
Hamer, Davidson
TI Prevalence of and risk factors for pica among pregnant women in
Chhattisgarh, India
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Boatin, Adeline] Massachusetts Gen Hosp, OB GYN, Boston, MA 02114 USA.
[Wylie, Blair] Massachusetts Gen Hosp, Dept Obstet & Gynecol, Boston, MA 02114 USA.
[Yeboah-Antwi, Kojo; Hamer, Davidson] Ctr Global Hlth & Dev, Boston, MA USA.
NR 0
TC 3
Z9 3
U1 2
U2 4
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 671
BP S299
EP S299
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900668
ER
PT J
AU Bryant, A
Madden, E
AF Bryant, Allison
Madden, Erin
TI Short interpregnancy intervals and maternal well-being: the association
with placental abruption
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Bryant, Allison] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Madden, Erin] NCIRE, Vet Hlth Res Inst, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 540
BP S245
EP S245
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900538
ER
PT J
AU Bryant, A
Madden, E
AF Bryant, Allison
Madden, Erin
TI Short interpregnancy intervals and health services utilization: is
neonatal hospital readmission associated with short intervals?
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of the
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Bryant, Allison] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Madden, Erin] NCIRE, Vet Res Inst, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 541
BP S246
EP S246
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900539
ER
PT J
AU Bryant, A
Madden, E
AF Bryant, Allison
Madden, Erin
TI Short interpregnancy intervals and health services utilization: is
maternal antepartum admission associated with short intervals?
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of the
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Bryant, Allison] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Madden, Erin] NCIRE, Vet Hlth Res Inst, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 542
BP S246
EP S246
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900540
ER
PT J
AU Caughey, AB
Nicholson, J
Kaimal, A
Dublin, S
Getahun, D
Cheng, YW
AF Caughey, Aaron B.
Nicholson, James
Kaimal, Anjali
Dublin, Sascha
Getahun, Darios
Cheng, Yvonne W.
TI Elective induction of labor and outcomes by gestational age
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Caughey, Aaron B.] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
[Nicholson, James] Univ Penn, Dept Family Med & Community Hlth, Philadelphia, PA 19104 USA.
[Kaimal, Anjali] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Kaimal, Anjali] Harvard Univ, Sch Med, Div Maternal Fetal Med, Boston, MA USA.
[Dublin, Sascha] Grp Hlth Res Inst, Grp Hlth, Seattle, WA USA.
[Getahun, Darios] Kaiser Permanente So Calif, Dept Res & Evaluat, Pasadena, CA USA.
[Cheng, Yvonne W.] Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 276
BP S134
EP S134
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900276
ER
PT J
AU Fuchs, K
Spitz, J
Toland, G
Bromley, B
Benacerraf, B
Platt, L
D'Alton, M
AF Fuchs, Karin
Spitz, Jean
Toland, Gregory
Bromley, Bryann
Benacerraf, Beryl
Platt, Lawrence
D'Alton, Mary
TI Impact of a required remediation program on nuchal translucency
measurements: experience of the Nuchal Translucency Quality Review
(NTQR) Program
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Fuchs, Karin; D'Alton, Mary] Columbia Univ, Med Ctr, Div Maternal Fetal Med, New York, NY USA.
[Spitz, Jean; Toland, Gregory] Maternal Fetal Med Fdn, Nuchal Translucency Qual Review Program, Washington, DC USA.
[Bromley, Bryann] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Benacerraf, Beryl] Harvard Univ, Dept Obstet Gynecol, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Benacerraf, Beryl] Harvard Univ, Dept Radiol, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Platt, Lawrence] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Platt, Lawrence] Ctr Fetal Med & Womens Ultrasound, Dept Obstet Gynecol, Los Angeles, CA USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 353
BP S166
EP S166
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900352
ER
PT J
AU Kaimal, A
Newman, K
Croft, D
Ecker, J
AF Kaimal, Anjali
Newman, Katharine
Croft, Damien
Ecker, Jeffrey
TI Cesarean birth after vaginal: risk factors for primary cesarean delivery
in multiparous women
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Kaimal, Anjali; Newman, Katharine; Croft, Damien; Ecker, Jeffrey] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 660
BP S295
EP S295
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900658
ER
PT J
AU Kaimal, A
Little, S
Caughey, AB
AF Kaimal, Anjali
Little, Sarah
Caughey, Aaron B.
TI Induction of labor for nulliparous women > 40: what is the optimal
gestational age?
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of the
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Kaimal, Anjali] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Little, Sarah] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Caughey, Aaron B.] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
[Little, Sarah] Harvard Univ, Sch Med, Div Maternal Fetal Med, Dept Ob Gyn, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 93
BP S56
EP S57
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900094
ER
PT J
AU Little, S
Sparks, TN
Pilliod, R
Shaffer, B
Caughey, AB
Kaimal, A
AF Little, Sarah
Sparks, Teresa N.
Pilliod, Rachel
Shaffer, Brian
Caughey, Aaron B.
Kaimal, Anjali
TI When is the optimal time to deliver dichorionic diamniotic twins?
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Little, Sarah] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Little, Sarah] Harvard Univ, Sch Med, Div Maternal Fetal Med, Dept Ob Gyn, Boston, MA USA.
[Sparks, Teresa N.] Brigham & Womens Massachusetts Gen Hosp, Boston, MA USA.
[Pilliod, Rachel; Shaffer, Brian; Caughey, Aaron B.] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
[Kaimal, Anjali] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 150
BP S78
EP S79
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900151
ER
PT J
AU Mohta, VJ
Caceres, I
Smith, L
Cohen, B
Declercq, G
Subramanian, SV
Ecker, J
AF Mohta, Vanitha Janakiraman
Caceres, Isabel
Smith, Lauren
Cohen, Bruce
Declercq, Gene
Subramanian, S. V.
Ecker, Jeffrey
TI Hospital variation in cesarean delivery rates among a very low risk
population in Massachusetts: an opportunity for quality improvement?
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Mohta, Vanitha Janakiraman; Ecker, Jeffrey] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Caceres, Isabel; Smith, Lauren; Cohen, Bruce] DPH, Massachusetts Dept Publ Hlth, Boston, MA USA.
[Declercq, Gene] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Subramanian, S. V.] Harvard Univ, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 638
BP S285
EP S286
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900636
ER
PT J
AU Panda, B
Panda, A
Abrahams, VM
Norwitz, E
Stanic, AK
Ecker, JL
Rueda, BR
AF Panda, Britta
Panda, Alexander
Abrahams, Vikki M.
Norwitz, Errol
Stanic, Aleksandar K.
Ecker, Jeffrey L.
Rueda, Bo R.
TI Increase in TLR protein in preeclamptic patients does not correlate with
a corresponding increase in TLR gene expression
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Panda, Britta; Stanic, Aleksandar K.; Ecker, Jeffrey L.; Rueda, Bo R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Panda, Alexander; Abrahams, Vikki M.] Yale Univ, New Haven, CT USA.
[Norwitz, Errol] Tufts Univ, Sch Med, Boston, MA 02111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 745
BP S330
EP S330
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889901011
ER
PT J
AU Panda, B
Young, B
Madden, E
Bryant, A
AF Panda, Britta
Young, Brett
Madden, Erin
Bryant, Allison
TI What happens after the puerperium? Analysis of late postpartum
admissions in California
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Panda, Britta; Young, Brett; Bryant, Allison] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Madden, Erin] NCIRE, Vet Res Inst, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 546
BP S248
EP S248
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900544
ER
PT J
AU Riley, L
Hutchings, Y
Lieberman, E
AF Riley, Laura
Hutchings, Yalonda
Lieberman, Ellice
TI The effect of doula support on epidural use among nulliparous women in
tertiary care centers
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Riley, Laura] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Maternal Fetal Med, Boston, MA USA.
[Hutchings, Yalonda; Lieberman, Ellice] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 2
Z9 2
U1 0
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 132
BP S70
EP S71
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900133
ER
PT J
AU Saxena, A
Seely, E
Rich-Edwards, J
Wilkins-Haug, L
Karumanchi, A
McElrath, T
AF Saxena, Aditi
Seely, Ellen
Rich-Edwards, Janet
Wilkins-Haug, Louise
Karumanchi, Ananth
McElrath, Thomas
TI First trimester PAPP-A levels correlate with sFlt-1 levels
longitudinally in pregnant women with and without preeclampsia
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Seely, Ellen] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Rich-Edwards, Janet] Brigham & Womens Hosp, Dept Dev Epidemiol, Boston, MA 02115 USA.
[Karumanchi, Ananth] Harvard Univ, Sch Med, BIDMC, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 732
BP S325
EP S325
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900727
ER
PT J
AU Sparks, TN
Burwick, R
Feinberg, B
AF Sparks, Teresa N.
Burwick, Richard
Feinberg, Bruce
TI Vitamin D deficiency is associated with increased mean arterial pressure
at term
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Sparks, Teresa N.; Burwick, Richard; Feinberg, Bruce] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Sparks, Teresa N.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
OI Sparks, Teresa/0000-0002-8593-2186
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 801
BP S352
EP S353
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889901067
ER
PT J
AU Sparks, TN
Little, S
Pilliod, R
Shaffer, B
Kaimal, A
Caughey, AB
AF Sparks, Teresa N.
Little, Sarah
Pilliod, Rachel
Shaffer, Brian
Kaimal, Anjali
Caughey, Aaron B.
TI When is the optimal time to deliver monochorionic diamniotic twins?
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Sparks, Teresa N.] Brigham & Womens Massachusetts Gen Hosp, Boston, MA USA.
[Little, Sarah] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Little, Sarah] Harvard Univ, Sch Med, Div Maternal Fetal Med, Dept Ob Gyn, Boston, MA USA.
[Pilliod, Rachel; Caughey, Aaron B.] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
[Kaimal, Anjali] Massachusetts Gen Hosp, Boston, MA 02114 USA.
OI Sparks, Teresa/0000-0002-8593-2186
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 155
BP S81
EP S82
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900156
ER
PT J
AU Yee, L
Nakagawa, S
Kaimal, A
Kuppermann, M
AF Yee, Lynn
Nakagawa, Sanae
Kaimal, Anjali
Kuppermann, Miriam
TI Postpartum sexual functioning and mode of delivery in a diverse
population of women
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Meeting Abstract
CT 32nd Annual Scientific Meeting/Pregnancy Meeting of
Society-for-Maternal-Fetal-Medicine
CY FEB 06-11, 2012
CL Dallas, TX
SP Soc Maternal Fetal Med
C1 [Yee, Lynn; Nakagawa, Sanae; Kuppermann, Miriam] Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA USA.
[Kaimal, Anjali] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD JAN
PY 2012
VL 206
IS 1
SU S
MA 329
BP S155
EP S155
PG 1
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 873NL
UT WOS:000298889900328
ER
PT J
AU New, DD
Block, K
Bhandhari, B
Gorin, Y
Abboud, HE
AF New, David D.
Block, Karen
Bhandhari, Basant
Gorin, Yves
Abboud, Hanna E.
TI IGF-I increases the expression of fibronectin by Nox4-dependent Akt
phosphorylation in renal tubular epithelial cells
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Article
DE extracellular matrix; growth factor signaling; kidney; reactive oxygen
species; redox signaling; NADPH oxidase 4; insulin-like growth factor
ID GROWTH-FACTOR-I; MESSENGER-RNA TRANSLATION; SMOOTH-MUSCLE-CELLS; NAD(P)H
OXIDASE; DIABETIC-NEPHROPATHY; NADPH OXIDASES; HIGH GLUCOSE;
PROTEIN-SYNTHESIS; MESANGIAL CELLS; ANGIOTENSIN-II
AB New DD, Block K, Bhandhari B, Gorin Y, Abboud HE. IGF-I increases the expression of fibronectin by Nox4-dependent Akt phosphorylation in renal tubular epithelial cells. Am J Physiol Cell Physiol 302: C122-C130, 2012. First published September 21, 2011; doi:10.1152/ajpcell.00141.2011.-Extracellular matrix accumulation contributes to the progression of chronic kidney disease. Many growth factors including insulin-like growth factor-I (IGF-I) enhance matrix protein accumulation. Proximal tubular epithelial cells (PTCs) synthesize matrix proteins. NADPH oxidases are major sources of reactive oxygen species (ROS), important signaling molecules that mediate biological responses in a variety of cells and tissue. We investigated the mechanism by which IGF-I regulates fibronectin accumulation in PTCs and the role of a potential redox-dependent signaling pathway. IGF-I induces an increase in NADPH-dependent superoxide generation, enhances the release of hydrogen peroxide, and increases the expression of NADPH oxidase 4 (Nox4) in PTCs. IGF-I also stimulates phosphorylation of Akt, and inhibition of Akt or its upstream activator phosphatidylinositol 3-kinase attenuates IGF-I-induced fibronectin accumulation. Expression of dominant negative Akt also inhibits IGF-I-induced expression of fibronectin, indicating a role for this kinase in fibronectin accumulation. Expression of dominant negative adenovirus Nox4 inhibits IGF-I-induced NADPH oxidase activity, Akt phosphorylation, and fibronectin protein expression. Moreover, transfection of small interfering RNA targeting Nox4 decreases Nox4 protein expression and blocks IGF-I-induced Akt phosphorylation and the increase in fibronectin, placing Nox4 and ROS upstream of Akt signaling pathway. To confirm the role of Nox4, PTCs were infected with adenovirus construct expressing wild-type Nox4. Ad-Nox4, but not control Ad-green fluorescent protein, upregulated Nox4 expression and increased NADPH oxidase activity as well as fibronectin expression. Taken together, these results provide the first evidence for a role of Nox4 in IGF-I-induced Akt phosphorylation and fibronectin expression in tubular epithelial cells.
C1 [Abboud, Hanna E.] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, Div Nephrol, San Antonio, TX 78229 USA.
[Block, Karen] Audie L Murphy Mem Hosp, S Texas Vet Healthcare Syst, San Antonio, TX USA.
RP Abboud, HE (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Med, Div Nephrol, MC 7882,7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM abboud@uthscsa.edu
OI Gorin, Yves/0000-0003-4048-6925
FU Veterans Administration; National Institutes of Health [DK-R01-078971,
CA131272, DK-079996]; Juvenile Diabetes Research Foundation; Career
Development Award
FX Support for these studies was provided by the following sources:
Veterans Administration Merit Review grant and National Institutes of
Health Grant DK-R01-078971 (H. E. Abboud) and Career Development Award
and National Institutes of Health Grant CA131272 (K. Block), Juvenile
Diabetes Research Foundation regular research grant, and National
Institutes of Health Grant DK-079996 (Y. Gorin).
NR 51
TC 28
Z9 28
U1 1
U2 3
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6143
J9 AM J PHYSIOL-CELL PH
JI Am. J. Physiol.-Cell Physiol.
PD JAN
PY 2012
VL 302
IS 1
BP C122
EP C130
DI 10.1152/ajpcell.00141.2011
PG 9
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA 866IN
UT WOS:000298374100015
PM 21940672
ER
PT J
AU Morton, GJ
Thatcher, BS
Reidelberger, RD
Ogimoto, K
Wolden-Hanson, T
Baskin, DG
Schwartz, MW
Blevins, JE
AF Morton, Gregory J.
Thatcher, Brendan S.
Reidelberger, Roger D.
Ogimoto, Kayoko
Wolden-Hanson, Tami
Baskin, Denis G.
Schwartz, Michael W.
Blevins, James E.
TI Peripheral oxytocin suppresses food intake and causes weight loss in
diet-induced obese rats
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE leptin; food intake
ID BRAIN-STEM NUCLEI; CENTRALLY ADMINISTERED OXYTOCIN; DEFICIENT MICE;
PARAVENTRICULAR NUCLEUS; ENERGY-EXPENDITURE; LEPTIN RESISTANCE;
SPINAL-CORD; SIM1 GENE; HYPERPHAGIC OBESITY; SOLITARY TRACT
AB Morton GJ, Thatcher BS, Reidelberger RD, Ogimoto K, Wolden-Hanson T, Baskin DG, Schwartz MW, Blevins JE. Peripheral oxytocin suppresses food intake and causes weight loss in diet-induced obese rats. Am J Physiol Endocrinol Metab 302: E134-E144, 2012. First published October 18, 2011; doi:10.1152/ajpendo.00296.2011.-Growing evidence suggests that oxytocin plays an important role in the regulation of energy balance and that central oxytocin administration induces weight loss in diet-induced obese (DIO) animals. To gain a better understanding of how oxytocin mediates these effects, we examined feeding and neuronal responses to oxytocin in animals rendered obese following exposure to either a high-fat (HFD) or low-fat diet (LFD). Our findings demonstrate that peripheral administration of oxytocin dose-dependently reduces food intake and body weight to a similar extent in rats maintained on either diet. Moreover, the effect of oxytocin to induce weight loss remained intact in leptin receptor-deficient Koletsky (fak/fak) rats relative to their lean littermates. To determine whether systemically administered oxytocin activates hindbrain areas that regulate meal size, we measured neuronal c-Fos induction in the nucleus of the solitary tract (NTS) and area postrema (AP). We observed a robust neuronal response to oxytocin in these hindbrain areas that was unexpectedly increased in rats rendered obese on a HFD relative to lean, LFD-fed controls. Finally, we report that repeated daily peripheral administration of oxytocin in DIO animals elicited a sustained reduction of food intake and body weight while preventing the reduction of energy expenditure characteristic of weight-reduced animals. These findings extend recent evidence suggesting that oxytocin circumvents leptin resistance and induces weight-loss in DIO animals through a mechanism involving activation of neurons in the NTS and AP, key hindbrain areas for processing satiety-related inputs.
C1 [Morton, Gregory J.; Ogimoto, Kayoko; Schwartz, Michael W.] Univ Washington, Dept Med, Diabet & Obes Ctr Excellence, Seattle, WA USA.
[Morton, Gregory J.; Baskin, Denis G.; Schwartz, Michael W.; Blevins, James E.] Univ Washington, Sch Med, Dept Med, Div Metab Endocrinol & Nutr, Seattle, WA 98195 USA.
[Thatcher, Brendan S.; Wolden-Hanson, Tami; Baskin, Denis G.; Blevins, James E.] Vet Affairs Puget Sound Hlth Care Syst, Dept Vet Affairs Med Ctr, Off Res & Dev, Med Res Serv, Seattle, WA USA.
[Reidelberger, Roger D.] Nebraska Western Iowa Hlth Care Syst, Dept Vet Affairs, Omaha, NE USA.
[Reidelberger, Roger D.] Creighton Univ, Dept Biomed Sci, Omaha, NE 68178 USA.
RP Morton, GJ (reprint author), Univ Washington S Lake Union, Dept Med, 815 Mercer St,N334,Box 358055, Seattle, WA 98109 USA.
EM gjmorton@u.washington.edu
RI Schwartz, Michael/H-9950-2012
FU Office of Research and Development, Medical Research Service, Department
of Veterans Affairs; Veterans Affairs Puget Sound Health Care System;
Department of Veterans Affairs; Department of Veterans Affairs Nebraska
Western Iowa Health Care System; NIH [DK-068304, DK-083042, DK-052989,
DK-089056]; American Heart Association; Cellular and Molecular Imaging
Core of the National Institutes of Health (NIH) Diabetes Endocrinology
Research Center (DERC) [P30 DK-17047]; NIH Nutrition Obesity Research
Unit Animal Studies Physiology Core at the University of Washington
(NORC) [P30 DK-035816]; NIH Mouse Metabolic Phenotyping Center Diabetes
and Energy Balance Core (MMPC) [U24 DK-076126]
FX This work was supported by resources from the Office of Research and
Development, Medical Research Service, Department of Veterans Affairs,
including the Department of Veterans Affairs Career Development Program,
Merit Review Research Program, and the Career Scientist Program. D. G.
Baskin is the recipient of a Department of Veterans Affairs Senior
Research Career Scientist Award at the Veterans Affairs Puget Sound
Health Care System. R. D. Reidelberger is the recipient of a Department
of Veterans Affairs Research Career Scientist Award at the Department of
Veterans Affairs Nebraska Western Iowa Health Care System. M. W.
Schwartz is supported by NIH grants (DK-068304, DK-083042, DK-052989).
G. J. Morton is supported by an NIH grant (DK-089056) and a Scientist
Development Grant from the American Heart Association. This research was
also supported by the Cellular and Molecular Imaging Core of the
National Institutes of Health (NIH) Diabetes Endocrinology Research
Center (DERC, P30 DK-17047), the NIH Nutrition Obesity Research Unit
Animal Studies Physiology Core at the University of Washington (NORC,
P30 DK-035816), and the NIH Mouse Metabolic Phenotyping Center Diabetes
and Energy Balance Core (MMPC, U24 DK-076126).
NR 64
TC 63
Z9 64
U1 1
U2 15
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 JAN
PY 2012
VL 302
IS 1
BP E134
EP E144
DI 10.1152/ajpendo.00296.2011
PG 11
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 866JU
UT WOS:000298377600015
PM 22008455
ER
PT J
AU Haegens, A
Schols, AM
Gorissen, SH
van Essen, AL
Snepvangers, F
Gray, DA
Shoelson, SE
Langen, RC
AF Haegens, Astrid
Schols, Annemie M.
Gorissen, Stefan H.
van Essen, Anon L.
Snepvangers, Frank
Gray, Douglas A.
Shoelson, Steven E.
Langen, Ramon C.
TI NF-kappa B activation and polyubiquitin conjugation are required for
pulmonary inflammation-induced diaphragm atrophy
SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
LA English
DT Article
DE inspiratory muscle; inflammation; protein degradation
ID SKELETAL-MUSCLE ATROPHY; SYSTEMIC INFLAMMATION; MUTANT UBIQUITIN;
DISEASE; DYSFUNCTION; MICE; LIPOPOLYSACCHARIDE; VENTILATION; EXPRESSION;
MORTALITY
AB Haegens A, Schols AM, Gorissen SH, van Essen AL, Snepvangers F, Gray DA, Shoelson SE, Langen RC. NF-kappa B activation and polyubiquitin conjugation are required for pulmonary inflammation-induced diaphragm atrophy. Am J Physiol Lung Cell Mol Physiol 302: L103-L110, 2012. First published October 14, 2011; doi: 10.1152/ajplung.00084.2011.-Loss of diaphragm muscle strength in inflammatory lung disease contributes to mortality and is associated with diaphragm fiber atrophy. Ubiquitin (Ub) 26S-proteasome system (UPS)-dependent protein breakdown, which mediates muscle atrophy in a number of physiological and pathological conditions, is elevated in diaphragm muscle of patients with chronic obstructive pulmonary disease. Nuclear factor kappa B (NF-kappa B), an essential regulator of many inflammatory processes, has been implicated in the regulation of poly-Ub conjugation of muscle proteins targeted for proteolysis by the UPS. Here, we test if NF-kappa B activation in diaphragm muscle and subsequent protein degradation by the UPS are required for pulmonary inflammation-induced diaphragm atrophy. Acute pulmonary inflammation was induced in mice by intratracheal lipopolysaccharide instillation. Fiber cross-sectional area, ex vivo tyrosine release, protein poly-Ub conjugation, and inflammatory signaling were determined in diaphragm muscle. The contribution of NF-kappa B or the UPS to diaphragm atrophy was assessed in mice with intact or genetically repressed NF-kappa B signaling or attenuated poly-Ub conjugation, respectively. Acute pulmonary inflammation resulted in diaphragm atrophy measured by reduced muscle fiber cross-sectional area. This was accompanied by diaphragm NF-kappa B activation, and proteolysis, measured by tyrosine release from the diaphragm. Poly-Ub conjugation was increased in diaphragm, as was the expression of muscle-specific E3 Ub ligases. Genetic suppression of poly-Ub conjugation prevented inflammation-induced diaphragm muscle atrophy, as did muscle-specific inhibition of NF-kappa B signaling. In conclusion, the present study is the first to demonstrate that diaphragm muscle atrophy, resulting from acute pulmonary inflammation, requires NF-kappa B activation and UPS-mediated protein degradation.
C1 [Haegens, Astrid; Schols, Annemie M.; Gorissen, Stefan H.; van Essen, Anon L.; Snepvangers, Frank; Langen, Ramon C.] Maastricht Univ Med Ctr, Dept Resp Med, NUTRIM Sch Nutr Toxicol & Metab, NL-6202 AZ Maastricht, Netherlands.
[Gray, Douglas A.] Ottawa Hosp Res Inst, Ottawa, ON, Canada.
[Shoelson, Steven E.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Shoelson, Steven E.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Schols, AM (reprint author), Maastricht Univ Med Ctr, Dept Resp Med, NUTRIM Sch Nutr Toxicol & Metab, POB 5800, NL-6202 AZ Maastricht, Netherlands.
EM a.schols@maastrichtuniv.nl
RI Gorissen, Stefan/H-5341-2016
OI Gorissen, Stefan/0000-0003-3737-9053
FU Dutch Top Institute Pharma [T1-201]; Organization for Scientific
Research NWO [VENI 91656112]
FX This work was supported by the Dutch Top Institute Pharma (project no.
T1-201) and the Organization for Scientific Research NWO (VENI
91656112).
NR 37
TC 20
Z9 23
U1 2
U2 2
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 JAN
PY 2012
VL 302
IS 1
BP L103
EP L110
DI 10.1152/ajplung.00084.2011
PG 8
WC Physiology; Respiratory System
SC Physiology; Respiratory System
GA 866VC
UT WOS:000298413000011
PM 22003096
ER
PT J
AU Zhao, KQ
Xiong, GX
Wilber, M
Cohen, NA
Kreindler, JL
AF Zhao, Ke-Qing
Xiong, Guoxiang
Wilber, Morgan
Cohen, Noam A.
Kreindler, James L.
TI A role for two-pore K+ channels in modulating Na+ absorption and Cl-
secretion in normal human bronchial epithelial cells
SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
LA English
DT Article
DE chloride secretion; cystic fibrosis; ion transport
ID CHLORIDE SECRETION; ANION SECRETION; POTASSIUM CHANNELS; AIRWAY
EPITHELIA; ION-TRANSPORT; LUNG-DISEASE; LINE CALU-3; CONDUCTANCE;
MEMBRANE; LIQUID
AB Zhao KQ, Xiong G, Wilber M, Cohen NA, Kreindler JL. A role for two-pore K+ channels in modulating Na+ absorption and Cl- secretion in normal human bronchial epithelial cells. Am J Physiol Lung Cell Mol Physiol 302: L4-L12, 2012. First published September 30, 2011; doi: 10.1152/ajplung.00102.2011.-Mucociliary clearance is the primary innate physical defense mechanism against inhaled pathogens and toxins. Vectorial ion transport, primarily sodium absorption and anion secretion, by airway epithelial cells supports mucociliary clearance. This is evidenced by diseases of abnormal ion transport such as cystic fibrosis and pseudohypoaldosteronism that are characterized by changes in mucociliary clearance. Sodium absorption and chloride secretion in human bronchial epithelial cells depend on potassium channel activity, which creates a favorable electrochemical gradient for both by hyperpolarizing the apical plasma membrane. Although the role of basolateral membrane potassium channels is firmly established and extensively studied, a role for apical membrane potassium channels has also been described. Here, we demonstrate that bupivacaine and quinidine, blockers of four-transmembrane domain, two-pore potassium (K2P) channels, inhibit both amiloride-sensitive sodium absorption and forskolin-stimulated anion secretion in polarized, normal human bronchial epithelial cells at lower concentrations when applied to the mucosal surface than when applied to the serosal surface. Transcripts from four genes, KCNK1 (TWIK-1), KCNK2 (TREK-1), KCNK5 (TASK-2), and KCNK6 (TWIK-2), encoding K2P channels were identified by RT-PCR. Protein expression at the apical membrane was confirmed by immunofluorescence. Our data provide further evidence that potassium channels, in particular K2P channels, are expressed and functional in the apical membrane of airway epithelial cells where they may be targets for therapeutic manipulation.
C1 [Zhao, Ke-Qing] Fudan Univ, Sch Shanghai Med, Dept Otorhinolaryngol Head & Neck Surg, Eye & Ear Nose & Throat Hosp, Shanghai 200433, Peoples R China.
[Zhao, Ke-Qing; Cohen, Noam A.] Univ Penn, Dept Otorhinolaryngol Head & Neck Surg, Philadelphia, PA 19104 USA.
[Xiong, Guoxiang] Childrens Hosp Philadelphia, Div Neurol, Philadelphia, PA 19104 USA.
[Cohen, Noam A.] Philadelphia Vet Affairs Med Ctr, Surg Serv, Philadelphia, PA USA.
[Kreindler, James L.] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.
RP Kreindler, JL (reprint author), Abramson Res Ctr, 3615 Civ Ctr Blvd,Rm 1016-D, Philadelphia, PA 19104 USA.
EM kreindler@email.chop.edu
OI Cohen, Noam/0000-0002-9462-3932
FU National Heart, Lung, and Blood Institute [K08-HL-081080]; Children's
Hospital of Philadelphia
FX This work was funded by National Heart, Lung, and Blood Institute Grant
K08-HL-081080 (to J. L. Kreindler) and by institutional funds from the
Children's Hospital of Philadelphia.
NR 33
TC 19
Z9 20
U1 0
U2 3
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 JAN
PY 2012
VL 302
IS 1
BP L4
EP L12
DI 10.1152/ajplung.00102.2011
PG 9
WC Physiology; Respiratory System
SC Physiology; Respiratory System
GA 866VC
UT WOS:000298413000002
PM 21964404
ER
PT J
AU Thomas, JJ
Weigel, TJ
Lawton, RK
Levendusky, PG
Becker, AE
AF Thomas, Jennifer J.
Weigel, Thomas J.
Lawton, Robert K.
Levendusky, Philip G.
Becker, Anne E.
TI Cognitive-Behavioral Treatment of Body Image Disturbance in a
Congenitally Blind Patient With Anorexia Nervosa
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Editorial Material
ID WOMAN TOTALLY BLIND; EATING-DISORDERS; DSM-V; AGE
C1 [Thomas, Jennifer J.] McLean Hosp, Klarman Eating Disorders Ctr, Belmont, MA 02178 USA.
Massachusetts Gen Hosp, Eating Disorders Clin & Res Program, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dept Global Hlth & Social Med, Boston, MA 02115 USA.
RP Thomas, JJ (reprint author), McLean Hosp, Klarman Eating Disorders Ctr, 115 Mill St, Belmont, MA 02178 USA.
EM jjthomas@partners.org
NR 19
TC 4
Z9 4
U1 2
U2 5
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 JAN
PY 2012
VL 169
IS 1
BP 16
EP 20
DI 10.1176/appi.ajp.2010.10040555
PG 5
WC Psychiatry
SC Psychiatry
GA 875UQ
UT WOS:000299061100006
PM 22223010
ER
PT J
AU Cannuscio, C
Bugos, E
Hersh, S
Asch, DA
Weiss, EE
AF Cannuscio, Carolyn
Bugos, Eva
Hersh, Shari
Asch, David A.
Weiss, Eve E.
TI Using ART to AMPLIFY Youth Voices on Housing Insecurity
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Editorial Material
C1 [Cannuscio, Carolyn; Asch, David A.] Univ Penn, Ctr Hlth Equi Res & Promot, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
[Cannuscio, Carolyn; Asch, David A.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Cannuscio, Carolyn] Univ Penn, Perelman Sch Med, Dept Family Med & Community Hlth, Philadelphia, PA 19104 USA.
[Cannuscio, Carolyn; Bugos, Eva; Weiss, Eve E.] Univ Penn, Mixed Methods Res Lab, Philadelphia, PA 19104 USA.
[Cannuscio, Carolyn; Bugos, Eva; Weiss, Eve E.] Univ Penn, Ctr Publ Hlth Initiat, Philadelphia, PA 19104 USA.
[Hersh, Shari] Mural Arts Program, Philadelphia, PA USA.
RP Cannuscio, C (reprint author), Univ Penn, Ctr Hlth Equi Res & Promot, Philadelphia VA Med Ctr, 3620 Hamilton Walk,Anat & Chem Bldg,Room 145, Philadelphia, PA 19104 USA.
EM carolyncannu@gmail.com
OI Asch, David/0000-0002-7970-286X
NR 4
TC 2
Z9 2
U1 2
U2 14
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD JAN
PY 2012
VL 102
IS 1
BP 10
EP 12
DI 10.2105/AJPH.2011.300494
PG 3
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 867IZ
UT WOS:000298449400005
PM 22095365
ER
PT J
AU Okechukwu, CA
El Ayadi, AM
Tamers, SL
Sabbath, EL
Berkman, L
AF Okechukwu, Cassandra A.
El Ayadi, Alison M.
Tamers, Sara L.
Sabbath, Erika L.
Berkman, Lisa
TI Household Food Insufficiency, Financial Strain, Work-Family Spillover,
and Depressive Symptoms in the Working Class: The Work, Family, and
Health Network Study
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID COMMON MENTAL-DISORDERS; JOB STRAIN; WELFARE RECIPIENTS; STAFF TURNOVER;
NURSING-HOMES; WOMEN; INCOME; INSECURITY; OVERWEIGHT; QUALITY
AB Objectives. We evaluated the association of household-level stressors with depressive symptoms among low-wage nursing home employees.
Methods. Data were collected in 2006 and 2007 from 452 multiethnic primary and nonprimary wage earners in 4 facilities in Massachusetts. We used logistic regression to estimate the association of depressive symptoms with household financial strain, food insufficiency, and work-family spillover (preoccupation with work-related concerns while at home and vice versa).
Results. Depressive symptoms were significantly associated with household financial strain (odds ratio [OR]=1.82; 95% confidence interval [CI]=1.03, 3.21) and food insufficiency (OR=2.10; 95% CI=1.10, 4.18). Among primary earners, stratified analyses showed that food insufficiency was associated with depressive symptoms (OR=3.60; 95% CI=1.42, 9.11) but financial strain was not. Among nonprimary wage earners, depressive symptoms correlated with financial strain (OR=3.65; 95% CI=1.48, 9.01) and work-family spillover (OR=3.22; 95% CI=1.11, 9.35).
Conclusions. Household financial strain, food insufficiency, and work-family spillover are pervasive problems for working populations, but associations vary by primary wage earner status. The prevalence of food insufficiency among full-time employees was striking and might have a detrimental influence on depressive symptoms and the health of working-class families. (Am J Public Health. 2012;102:126-133. doi:10.2105/AJPH.2011.300323)
C1 [Okechukwu, Cassandra A.; El Ayadi, Alison M.; Tamers, Sara L.; Sabbath, Erika L.; Berkman, Lisa] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Tamers, Sara L.] Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA 02115 USA.
[Berkman, Lisa] Harvard Univ, Ctr Populat & Dev Studies, Boston, MA USA.
RP Okechukwu, CA (reprint author), Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, 677 Huntington Ave,Kresge 7th Floor, Boston, MA 02115 USA.
EM cokechuk@hsph.harvard.edu
FU National Institute of Aging [3U01AG027669-06S1]; National Institute of
Child Health and Human Development [U01 5186989]; Maternal Child Health
(MCH) Bureau; MCH/School of Public Health Institute [5T76 MC 00001J,
T03MCO7648]; National Cancer Institute [5R25CA057711]
FX This study was conducted as part of the Work, Family, and Health
Network, which is funded by the National Institute of Aging and the
National Institute of Child Health and Human Development (grant U01
5186989). Cassandra A. Okechukwu was supported by a National Institute
of Aging supplement (grant 3U01AG027669-06S1). Alison M. El Ayadi was
supported by the Maternal Child Health (MCH) Bureau training grant and
an epidemiological MCH/School of Public Health Institute grant (5T76 MC
00001J [formerly MCJ201] and T03MCO7648). Sara L. Tamers was supported
by the National Cancer Institute Harvard Education Program in Cancer
Prevention Control (grant 5R25CA057711).
NR 52
TC 22
Z9 22
U1 1
U2 20
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD JAN
PY 2012
VL 102
IS 1
BP 126
EP 133
DI 10.2105/AJPH.2011.300323
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 867IZ
UT WOS:000298449400024
PM 22095360
ER
PT J
AU Walker, TG
Kalva, SP
Ganguli, S
Oklu, R
Salazar, GM
Waltman, AC
Wicky, S
AF Walker, T. Gregory
Kalva, Sanjeeva P.
Ganguli, Suvranu
Oeklue, Rahmi
Salazar, Gloria M.
Waltman, Arthur C.
Wicky, Stephan
TI Image Optimization During Endovascular Aneurysm Repair
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Review
DE endovascular aneurysm repair; image geometry; radiation safety
ID ABDOMINAL-AORTIC-ANEURYSM; RADIATION-EXPOSURE; PATIENT; RADIOLOGY;
INJURY; NEPHROTOXICITY; SUITABILITY; STRATEGIES; GUIDELINES; MANAGEMENT
AB OBJECTIVE. The purposes of this review are to examine various properties of the fluoroscopic imaging equipment used during endovascular aneurysm repair (EVAR) that can be modified to reduce radiation dose while optimizing image acquisition and display, to detail geometric aspects of EVAR intraprocedural imaging used to achieve consistently optimal EVAR results, and to describe acquisition parameters and strategies for minimizing contrast-induced nephropathy.
CONCLUSION. The outcome of EVAR is strongly linked to image acquisition and interpretation, including the preprocedural, intraprocedural, and postprocedural display of relevant vascular anatomy, positions and configurations of the endograft components, and documentation of successful aneurysm exclusion. Operator familiarity with the imaging equipment, radiation and contrast dose reduction strategies, and image optimization techniques strongly influence the outcome of EVAR.
C1 [Walker, T. Gregory; Kalva, Sanjeeva P.; Ganguli, Suvranu; Oeklue, Rahmi; Salazar, Gloria M.; Waltman, Arthur C.; Wicky, Stephan] Massachusetts Gen Hosp, Div Vasc Imaging & Intervent, Boston, MA 02116 USA.
RP Walker, TG (reprint author), Massachusetts Gen Hosp, Div Vasc Imaging & Intervent, 55 Fruit St,GRB 290A, Boston, MA 02116 USA.
EM TGWalker@partners.org
NR 34
TC 6
Z9 6
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 JAN
PY 2012
VL 198
IS 1
BP 200
EP 206
DI 10.2214/AJR.11.6608
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 873LF
UT WOS:000298884100057
PM 22194498
ER
PT J
AU Mc Auley, G
Jagannathan, J
O'Regan, K
Krajewski, KM
Hornick, JL
Butrynski, J
Ramaiya, N
AF Mc Auley, Grainne
Jagannathan, Jyothi
O'Regan, Kevin
Krajewski, Katherine M.
Hornick, Jason L.
Butrynski, James
Ramaiya, Nikhil
TI Extraskeletal Osteosarcoma: Spectrum of Imaging Findings
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE extraskeletal osteosarcoma; osteogenic osteosarcoma; soft-tissue sarcoma
ID OSTEOGENIC SARCOMA; SOFT TISSUES
AB OBJECTIVE. The purpose of this article is to present the spectrum of imaging findings of primary and metastatic extraskeletal osteosarcoma and highlight the differences from primary osteogenic osteosarcoma in bone.
CONCLUSION. Extraskeletal osteosarcoma is a rare mesenchymal malignancy of soft tissue, histologically indistinguishable from primary osteosarcoma of bone. However, there are distinct differences in demographics, imaging features, prognosis, and management compared with osteogenic osteosarcoma. Imaging characteristics reflect tumor morphology, with only 50% of primary tumors showing mineralization. Metastases may or may not show mineralization, even if present in the primary tumor. The overall prognosis is poor.
C1 [Mc Auley, Grainne; Jagannathan, Jyothi; O'Regan, Kevin; Krajewski, Katherine M.; Ramaiya, Nikhil] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiol, Boston, MA 02215 USA.
[Hornick, Jason L.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Butrynski, James] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
RP Mc Auley, G (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiol, 450 Brookline Ave, Boston, MA 02215 USA.
EM grainnemcauley@mac.com
NR 13
TC 13
Z9 14
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 JAN
PY 2012
VL 198
IS 1
BP W31
EP W37
DI 10.2214/AJR.11.6927
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 873LF
UT WOS:000298884100006
PM 22194512
ER
PT J
AU Dick, AA
Mercer, LD
Smith, JM
McDonald, RA
Young, B
Healey, PJ
AF Dick, Andre A.
Mercer, Laina D.
Smith, Jodi M.
McDonald, Ruth A.
Young, Bessie
Healey, Patrick J.
TI Living Donor Kidney Transplantation in Adolescents: Does Size Matter?
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Meeting Abstract
CT American-Society-of-Transplant-Surgeons (ASTS) 12th Annual State of the
Art Winter Symposium/North-American-Transplant-Coordinators-Organization
(NATCO) Symposium for Advanced Transplant Professionals
CY JAN 12-15, 2012
CL Miami, FL
SP Amer Soc Transplant Surg (ASTS), N Amer Transplant Coordinators Org (NATCO)
C1 [Dick, Andre A.; Healey, Patrick J.] Seattle Childrens Hosp, Div Pediat Transplantat, Seattle, WA USA.
[Mercer, Laina D.] Seattle Childrens Hosp, Seattle Childrens Res Inst, Seattle, WA USA.
[Smith, Jodi M.; McDonald, Ruth A.] Seattle Childrens Hosp, Div Nephrol, Dept Pediat, Seattle, WA USA.
[Young, Bessie] VA Puget Sound Hlth Care Syst, Div Nephrol, Seattle, WA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1600-6135
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD JAN
PY 2012
VL 12
SU 2
SI SI
BP 70
EP 70
PG 1
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 867UW
UT WOS:000298481300050
ER
PT J
AU Yeh, HD
Dong, N
Elizabeth, S
Schoenfeld, D
Markmann, J
AF Yeh, Heidi
Dong, Ning
Elizabeth, Smoot
Schoenfeld, David
Markmann, James
TI Listing Rates for Liver Transplantation Influence Mortality from Liver
Disease
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Meeting Abstract
CT American-Society-of-Transplant-Surgeons (ASTS) 12th Annual State of the
Art Winter Symposium/North-American-Transplant-Coordinators-Organization
(NATCO) Symposium for Advanced Transplant Professionals
CY JAN 12-15, 2012
CL Miami, FL
SP Amer Soc Transplant Surg (ASTS), N Amer Transplant Coordinators Org (NATCO)
C1 [Yeh, Heidi; Markmann, James] Massachusetts Gen Hosp, Dept Surg, Div Transplantat, Boston, MA 02114 USA.
[Dong, Ning; Elizabeth, Smoot; Schoenfeld, David] Massachusetts Gen Hosp, Dept Biostat, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1600-6135
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD JAN
PY 2012
VL 12
SU 2
SI SI
BP 90
EP 90
PG 1
WC Surgery; Transplantation
SC Surgery; Transplantation
GA 867UW
UT WOS:000298481300114
ER
PT J
AU Chunara, R
Andrews, JR
Brownstein, JS
AF Chunara, Rumi
Andrews, Jason R.
Brownstein, John S.
TI Social and News Media Enable Estimation of Epidemiological Patterns
Early in the 2010 Haitian Cholera Outbreak
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID WEB SEARCH; SURVEILLANCE; INFLUENZA; CONTACTS; NUMBER; MODEL; SARS
AB During infectious disease outbreaks, data collected through health institutions and official reporting structures may not be available for weeks, hindering early epidemiologic assessment. By contrast, data from informal media are typically available in near real-time and could provide earlier estimates of epidemic dynamics. We assessed correlation of volume of cholera-related HealthMap news media reports, Twitter postings, and government cholera cases reported in the first 100 days of the 2010 Haitian cholera outbreak. Trends in volume of informal sources significantly correlated in time with official case data and was available up to 2 weeks earlier. Estimates of the reproductive number ranged from 1..54 to 6.89 (informal sources) and 1.27 to 3.72 (official sources) during the initial outbreak growth period, and 1.04 to 1.51 (informal) and 1.06 to 1.73 (official) when Hurricane Tomas afflicted Haiti. Informal data can be used complementarily with official data in an outbreak setting to get timely estimates of disease dynamics.
C1 Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
Childrens Hosp Boston, Childrens Hosp Informat Program, Div Emergency Med, Boston, MA USA.
[Andrews, Jason R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, Boston, MA USA.
McGill Univ, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ, Canada.
RP Chunara, R (reprint author), 1 Autumn St,Suite 433, Boston, MA 02215 USA.
EM rumi@alum.mit.edu; jandrews6@partners.org;
john.brownstein@childrens.harvard.edu
OI Andrews, Jason/0000-0002-5967-251X
FU Google.org; National Library of Medicine [5G08LM9776-2]; National
Institutes of Health [1R01LM01812-01]; National institute of Allergy and
Infectious Diseases [T32AI007433-20]
FX Financial support for this study was provided by research grants from
Google.org, the National Library of Medicine (5G08LM9776-2), and
National Institutes of Health (1R01LM01812-01) to RC and JSB, and
National institute of Allergy and Infectious Diseases training grant
(T32AI007433-20) to JRA.
NR 29
TC 99
Z9 103
U1 7
U2 48
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 JAN
PY 2012
VL 86
IS 1
BP 39
EP 45
DI 10.4269/ajtmh.2012.11-0597
PG 7
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 875WF
UT WOS:000299065200013
PM 22232449
ER
PT J
AU Otto, M
Bowser, R
Turner, M
Berry, J
Brettschneider, J
Connor, J
Costa, J
Cudkowicz, M
Glass, J
Jahn, O
Lehnert, S
Malaspina, A
Parnetti, L
Petzold, A
Shaw, P
Sherman, A
Steinacker, P
Sussmuth, S
Teunissen, C
Tumani, H
Wuolikainen, A
Ludolph, A
AF Otto, Markus
Bowser, Robert
Turner, Martin
Berry, James
Brettschneider, Johannes
Connor, James
Costa, Julia
Cudkowicz, Merit
Glass, Jonathan
Jahn, Olaf
Lehnert, Stefan
Malaspina, Andrea
Parnetti, Lucilla
Petzold, Axel
Shaw, Pamela
Sherman, Alexander
Steinacker, Petra
Suessmuth, Sigurd
Teunissen, Charlotte
Tumani, Hayrettin
Wuolikainen, Anna
Ludolph, Albert
CA Volcano Grp
TI Roadmap and standard operating procedures for biobanking and discovery
of neurochemical markers in ALS
SO AMYOTROPHIC LATERAL SCLEROSIS
LA English
DT Review
DE Biomarker; biobank; proteomics; cerebrospinal fluid; brain bank
ID AMYOTROPHIC-LATERAL-SCLEROSIS; CREUTZFELDT-JAKOB-DISEASE;
CEREBROSPINAL-FLUID; QUANTITATIVE PROTEOMICS; MASS-SPECTROMETRY;
BRAINNET EUROPE; LIGAND LIBRARY; BIOMARKERS; DIAGNOSIS; BLOOD
AB Despite major advances in deciphering the neuropathological hallmarks of amyotrophic lateral sclerosis (ALS), validated neurochemical biomarkers for monitoring disease activity, earlier diagnosis, defining prognosis and unlocking key pathophysiological pathways are lacking. Although several candidate biomarkers exist, translation into clinical application is hindered by small sample numbers, especially longitudinal, for independent verification. This review considers the potential routes to the discovery of neurochemical markers in ALS, and provides a consensus statement on standard operating procedures that will facilitate multicenter collaboration, validation and ultimately clinical translation.
C1 [Otto, Markus; Brettschneider, Johannes; Lehnert, Stefan; Steinacker, Petra; Suessmuth, Sigurd; Tumani, Hayrettin; Ludolph, Albert] Univ Ulm, Dept Neurol, D-89081 Ulm, Germany.
[Bowser, Robert] St Josephs Hosp, Barrow Neurol Inst, Div Neurol, Phoenix, AZ USA.
[Turner, Martin] Univ Oxford, John Radcliffe Hosp, Nuffield Dept Clin Neurosci, Oxford OX3 9DU, England.
[Berry, James; Cudkowicz, Merit; Sherman, Alexander] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Connor, James] Penn State Univ, Coll Med, Dept Neurosurg, George M Leader Family Lab, Hershey, PA USA.
[Costa, Julia] Univ Nova Lisboa, Inst Tecnol Quim & Biol, Lab Glycobiol, Oeiras, Portugal.
[Glass, Jonathan] Emory Univ, Sch Med, Atlanta, GA USA.
[Jahn, Olaf] Max Planck Inst Expt Med, Gottingen, Germany.
[Malaspina, Andrea] Univ London, Queen Mary Hosp, Ctr Neurosci & Trauma, Blizard Inst Cell & Mol Sci, London WC1E 7HU, England.
[Parnetti, Lucilla] Univ Perugia, Neurol Sect, Lab Clin Neurochem, Ctr Memory Disturbances, I-06100 Perugia, Italy.
[Petzold, Axel] Natl Hosp Neurol & Neurosurg, UCL Inst Neurol, Dept Neuroimmunol, London WC1N 3BG, England.
[Petzold, Axel] Vrije Univ Amsterdam, Med Ctr, Dept Neurol, Amsterdam, Netherlands.
[Shaw, Pamela] Univ Sheffield, Sch Med, Acad Unit Neurol, Sheffield, S Yorkshire, England.
[Teunissen, Charlotte] Vrije Univ Amsterdam, Med Ctr, Dept Clin Chem, Neurol Lab, Amsterdam, Netherlands.
[Wuolikainen, Anna] Umea Univ, Dept Chem, Umea, Sweden.
RP Otto, M (reprint author), Univ Ulm, Dept Neurol, Oberer Eselsberg 34, D-89081 Ulm, Germany.
EM markus.otto@uni-ulm.de
RI Costa, Julia/B-7131-2008; Petzold, Axel/C-1090-2009; Otto,
Markus/F-4304-2015;
OI Costa, Julia/0000-0001-7782-6319; Petzold, Axel/0000-0002-0344-9749;
Otto, Markus/0000-0003-4273-4267; Turner, Martin/0000-0003-0267-3180;
Wuolikainen, Anna/0000-0003-0838-5526
FU World Federation of Neurology
FX This work was supported by World Federation of Neurology. The name
Volcano Group was chosen because the first meeting of the group had to
be postponed as several group members were stranded somewhere in the
world because of the eruption of the Eyjafjallajokull in Iceland in
April 2010.
NR 42
TC 40
Z9 40
U1 1
U2 11
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1748-2968
J9 AMYOTROPH LATERAL SC
JI Amyotroph. Lateral. Scler.
PD JAN
PY 2012
VL 13
IS 1
BP 1
EP 10
DI 10.3109/17482968.2011.627589
PG 10
WC Clinical Neurology
SC Neurosciences & Neurology
GA 871OF
UT WOS:000298746800001
PM 22214350
ER
PT J
AU Lawton, KA
Cudkowicz, ME
Brown, MV
Alexander, D
Caffrey, R
Wulff, JE
Bowser, R
Lawson, R
Jaffa, M
Milburn, MV
Ryals, JA
Berry, JD
AF Lawton, Kay A.
Cudkowicz, Merit E.
Brown, Meredith V.
Alexander, Danny
Caffrey, Rebecca
Wulff, Jacob E.
Bowser, Robert
Lawson, Robert
Jaffa, Matt
Milburn, Michael V.
Ryals, John A.
Berry, James D.
TI Biochemical alterations associated with ALS
SO AMYOTROPHIC LATERAL SCLEROSIS
LA English
DT Article
DE ALS; biomarker; metabolomics; pathophysiology
ID AMYOTROPHIC-LATERAL-SCLEROSIS; CREATINE; CANCER; TRIAL; DEGENERATION;
METABOLOME; MUTATIONS; NEURONS; MOUSE; DEATH
AB Our objective was to identify metabolic pathways affected by ALS using non-targeted metabolomics in plasma, comparing samples from healthy volunteers to those from ALS patients. This discovery could become the basis for the identification of therapeutic targets and diagnostic biomarkers of ALS. Two distinct cross-sectional studies were conducted. Plasma was collected from 62 (Study 1) and 99 (Study 2) participants meeting El Escorial criteria for possible, probable, or definite ALS; 69 (Study 1) and 48 (Study 2) healthy controls samples were collected. Global metabolic profiling was used to detect and evaluate biochemical signatures of ALS. Twenty-three metabolites were significantly altered in plasma from ALS patients in both studies. These metabolites include biochemicals in pathways associated with neuronal change, hypermetabolism, oxidative damage, and mitochondrial dysfunction, all of which are proposed disease mechanisms in ALS. The data also suggest possible hepatic dysfunction associated with ALS. In conclusion, the data presented here provide insight into the pathophysiology of ALS while suggesting promising areas of focus for future studies. The metabolomics approach can generate novel hypotheses regarding ALS disease mechanisms with the potential to identify therapeutic targets and novel diagnostic biomarkers.
C1 [Berry, James D.] Massachusetts Gen Hosp, Dept Neurol, Neurol Clin Trials Unit, Charlestown, MA 02129 USA.
[Lawton, Kay A.; Brown, Meredith V.; Alexander, Danny; Caffrey, Rebecca; Wulff, Jacob E.; Milburn, Michael V.; Ryals, John A.] Metabolon Inc, Durham, NC USA.
[Bowser, Robert] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
RP Berry, JD (reprint author), Massachusetts Gen Hosp, Dept Neurol, Neurol Clin Trials Unit, 149 13th St,Suite 2-2274, Charlestown, MA 02129 USA.
EM jdberry@partners.org
FU ALS Association; National Institutes of Health; National Institute of
Neurological Disorders and Stroke; National Institutes of
Health/National Center for Research Resources/General Clinical Research
Centers Program; North Carolina Biotechnology Center; Neuralstem Inc;
ISIS Pharmaceuticals Inc; Knopp Biosciences; Biogen Idec; NIH
FX The project was supported, in part, by support from the following: ALS
Association, National Institutes of Health, National Institute of
Neurological Disorders and Stroke, and National Institutes of
Health/National Center for Research Resources/General Clinical Research
Centers Program. The content of this publication is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Institute of Neurological Disorders and
Stroke, National Institutes of Health, or ALS Association. Support for
MVB was received from the North Carolina Biotechnology Center Industrial
Fellowship program. The authors would also like to acknowledge project
input and support from David Lacomis at the University of Pittsburgh
School of Medicine, the North-East ALS Consortium (NEALS), the NEALS
Biofluid Repository Committee and the committee co-Chairs, Robert Bowser
and Carol Milligan. The authors thank Lucie Bruijn and ALSA for
guidance; the NEALS Consortium for sample collection; Darlene Sawicki
for overseeing protocol development, informed consent design,
supervising clinical operations, and research coordination; Lisa Paige,
Bruce McCreedy and Jeff Shuster for contributions to preliminary
studies; and Matthew Mitchell, and the Metabolon Analytical Team for
contributing to statistical analyses and data acquisition. The analysis
for this paper was generated using Array Studio software. Array Studio,
Array Viewer and Array Server and all other Omicsoft products or service
names are registered trademarks or trademarks of Omicsoft Corporation.,
Research Triangle Park, NC, USA.; Kay Lawton, Meredith Brown, Danny
Alexander, Jacob Wulff, Rebecca Caffrey, Mike Milburn, and John Ryals
are employees of Metabolon, Inc. Merit Cudkowicz has worked as a
consultant for Shire, Trophos, and GlaxoSmithKline. She has received
industry-sponsored grants from Neuralstem Inc, ISIS Pharmaceuticals Inc,
Knopp Biosciences, and Biogen Idec. She has also received funding from
NIH grants. Robert Bowser is a cofounder of Knopp Neurosciences and
consultant to Cytonics Corporation. Robert Lawson and Matt Jaffa have no
disclosures. James Berry is on the editorial board of the Neurology
Resident and Fellow Section and is supported by an NIH training grant.
The authors have no other relevant affiliations or financial involvement
with any organization or entity with a financial interest in or
financial conflict with the subject matter or materials discussed in the
manuscript apart from those disclosed. No writing assistance was
utilized in the production of this manuscript.
NR 35
TC 33
Z9 33
U1 2
U2 13
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1748-2968
J9 AMYOTROPH LATERAL SC
JI Amyotroph. Lateral. Scler.
PD JAN
PY 2012
VL 13
IS 1
BP 110
EP 118
DI 10.3109/17482968.2011.619197
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 871OF
UT WOS:000298746800015
PM 22117131
ER
PT J
AU Karam, C
AF Karam, Chafic
TI IBP is a form of PLS and should be distinguished from PBP
SO AMYOTROPHIC LATERAL SCLEROSIS
LA English
DT Letter
ID AMYOTROPHIC-LATERAL-SCLEROSIS
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neuromuscular Div, Boston, MA 02215 USA.
RP Karam, C (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neuromuscular Div, Boston, MA 02215 USA.
NR 5
TC 0
Z9 0
U1 2
U2 3
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1748-2968
J9 AMYOTROPH LATERAL SC
JI Amyotroph. Lateral. Scler.
PD JAN
PY 2012
VL 13
IS 1
BP 158
EP 158
DI 10.3109/17482968.2011.610465
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 871OF
UT WOS:000298746800023
PM 22214358
ER
PT J
AU Troianos, CA
Hartman, GS
Glas, KE
Skubas, NJ
Eberhardt, RT
Walker, JD
Reeves, ST
AF Troianos, Christopher A.
Hartman, Gregg S.
Glas, Kathryn E.
Skubas, Nikolaos J.
Eberhardt, Robert T.
Walker, Jennifer D.
Reeves, Scott T.
CA Amer Soc Echocardiography
TI Guidelines for Performing Ultrasound Guided Vascular Cannulation:
Recommendations of the American Society of Echocardiography and the
Society of Cardiovascular Anesthesiologists
SO ANESTHESIA AND ANALGESIA
LA English
DT Article
ID INTERNAL JUGULAR-VEIN; CENTRAL VENOUS CATHETERIZATION; RADIAL ARTERY
CANNULATION; PERIPHERAL INTRAVENOUS ACCESS; RANDOMIZED CONTROLLED-TRIAL;
CONTROLLED CLINICAL-TRIAL; COMMON FEMORAL-ARTERY; CROSS-SECTIONAL AREA;
ANATOMIC RELATIONSHIP; HEAD ROTATION
C1 [Troianos, Christopher A.] W Penn Allegheny Hlth Syst, Dept Anesthesiol, Pittsburgh, PA USA.
[Hartman, Gregg S.] Dartmouth Hitchcock Med Ctr, Dept Anesthesiol, Lebanon, NH 03766 USA.
[Glas, Kathryn E.] Emory Univ, Dept Anesthesiol, Atlanta, GA 30322 USA.
[Skubas, Nikolaos J.] Weill Cornell Med Coll, Dept Anesthesiol, New York, NY USA.
[Eberhardt, Robert T.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Walker, Jennifer D.] Massachusetts Gen Hosp, Dept Cardiothorac Surg, Boston, MA 02114 USA.
[Reeves, Scott T.] Med Univ S Carolina, Dept Anesthesiol, Charleston, SC 29425 USA.
RP Troianos, CA (reprint author), W Penn Allegheny Hlth Syst, Dept Anesthesiol, Pittsburgh, PA USA.
NR 96
TC 88
Z9 95
U1 0
U2 8
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 JAN
PY 2012
VL 114
IS 1
BP 46
EP 72
DI 10.1213/ANE.0b013e3182407cd8
PG 27
WC Anesthesiology
SC Anesthesiology
GA 866UM
UT WOS:000298410400005
PM 22127816
ER
PT J
AU Frick, CG
Fink, H
Blobner, M
Martyn, J
AF Frick, Christiane G.
Fink, Heidrun
Blobner, Manfred
Martyn, Jeevendra
TI A Single Injection of Botulinum Toxin Decreases the Margin of Safety of
Neurotransmission at Local and Distant Sites
SO ANESTHESIA AND ANALGESIA
LA English
DT Article
ID MUSCULOSKELETAL-TISSUE ALLOGRAFTS; ACETYLCHOLINE-RECEPTORS;
D-TUBOCURARINE; RESISTANCE; NEUROTOXINS; MECHANISMS; MUSCLES
AB BACKGROUND: We tested the hypothesis that a single injection of botulinum toxin not only has local, but also distant effects on muscle function, biochemistry, and pharmacodynamics of atracurium.
METHODS: Botulinum toxin (2.5 U) was injected into the tibialis muscle of anesthetized rats (n = 26). The contralateral side with no injection served to study distant effects. Control animals (n = 25) received a saline injection. Neuromuscular function, pharmacology, and expression of acetylcholine receptors (nAChRs) were evaluated in the tibialis at 0, 4, and 16 days after injection and in comparison with saline-injected controls.
RESULTS: On day 4, botulinum toxin caused complete paralysis of the tibialis, while its contralateral side showed a decrease in absolute twitch tension (1.8 N [1.6; 1.9] vs 3.0 N [2.8; 3.1], Newton, P < 0.05). On day 16, muscle weakness was only present on the toxin-injected side where absolute twitch tension was decreased (0.6 N [0.6, 0.7] vs 3.4 N [3.1, 3.7], P < 0.05). Tibialis mass was decreased on the toxin-injected side at day 4 (1.46 mg/g [1.43, 1.48] vs 1.74 mg/g [1.72; 1.75], P < 0.05) and on day 16 (0.78 mg/g [0.76, 0.79] vs 1.73 mg/g [1.69; 1.77], P < 0.05). Effects distant from the site of injection were seen on day 16, when muscle atrophy was also present in the adjacent gastrocnemius and soleus muscles. Normalized to tibialis mass, specific twitch tension (tension/g muscle) was reduced on the contralateral side at day 4 and on the toxin-injected side at day 16 in relation to saline controls. At day 16, an increased sensitivity to atracurium was seen on the toxin-injected side, evidenced as a decreased ED(50) (0.23 mg/kg [0.13, 0.33] vs 0.72 mg/kg [0.63, 0.82], P < 0.05) and a lower infusion rate (38 mu L/kg/min [32, 43] vs135 mu L/kg/min [126, 144], P < 0.05), together with a reduced plasma concentration requirement of atracurium (0.5 mu g/mL [0.4, 0.7] vs 4.5 mu g/mL [3.8, 5.2], P < 0.05) to achieve a steady state 50% reduction in baseline (absolute) twitch tension. ED50 of atracurium was also decreased on the contralateral side at day 16 in relation to saline controls. The nAChRs in the tibialis were increased on the toxin-injected side to 123 fmol/mg [115, 131] vs 28 fmol/mg [25, 29] (P < 0.05) in time-matched saline-injected controls at day 4 and to 378 [341, 413] vs 27 fmol/mg [25, 29] (P < 0.05) at day 16.
CONCLUSIONS: Botulinum toxin has local and distant effects on muscle. The decrease in specific twitch tension indicates that the muscle atrophy alone cannot explain the functional changes; neuromuscular transmission is also impaired. An increased sensitivity to atracurium on the toxin-injected side, despite up-regulation of nAChRs, seems unique to botulinum toxin. (Anesth Analg 2012; 114: 102-9)
C1 [Frick, Christiane G.] TU Muenchen, Dept Anesthesia & Crit Care, Klin Anesthesiol, D-81675 Munich, Germany.
[Frick, Christiane G.; Martyn, Jeevendra] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
[Frick, Christiane G.; Martyn, Jeevendra] Harvard Univ, Sch Med, Shriners Hosp Children, Boston, MA USA.
RP Frick, CG (reprint author), TU Muenchen, Dept Anesthesia & Crit Care, Klin Anesthesiol, Ismaningerstr 22, D-81675 Munich, Germany.
EM c.frick@lrz.tu-muenchen.de
OI Lewald, Heidrun/0000-0002-5192-425X
FU National Institutes of Health, Bethesda, MD [GM 031569, GM 055082, GM
21500]; Shriners Hospital Research Philantrophy, Tampa, FL
FX Supported by grants (GM 031569, GM 055082, GM 21500-Project IV) from the
National Institutes of Health, Bethesda, MD, and Shriners Hospital
Research Philantrophy, Tampa, FL, to J.A.J. Martyn.
NR 22
TC 6
Z9 6
U1 0
U2 2
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 JAN
PY 2012
VL 114
IS 1
BP 102
EP 109
DI 10.1213/ANE.0b013e31823526bf
PG 8
WC Anesthesiology
SC Anesthesiology
GA 866UM
UT WOS:000298410400011
PM 22003222
ER
PT J
AU Lee, LA
Roth, S
Todd, MM
Posner, KL
Polissar, NL
Neradilek, MB
Torner, J
Newman, NJ
Domino, KB
Lauer, KK
Buddithi, R
Gollapudy, S
Pajewski, TN
Scalzo, DC
Avitsian, R
Brown, MJ
Buenvenida, S
Mashour, GA
Moore, LE
Samra, SK
Lieberman, J
Lane, RK
Ramani, R
Wagner, J
Tempelhoff, R
Monsey, CM
Robicsek, SA
Vu, MM
Weeks, J
Manninen, PH
Fu, ES
Sanchez-Yanes, GC
Peterfreund, RA
Albrecht, MA
Sapire, KJ
Baughman, VL
Caplan, RA
Cheney, FW
Metzner, J
AF Lee, Lorri A.
Roth, Steven
Todd, Michael M.
Posner, Karen L.
Polissar, Nayak L.
Neradilek, Moni B.
Torner, James
Newman, Nancy J.
Domino, Karen B.
Lauer, Kathryn K.
Buddithi, Rachel
Gollapudy, Suneeta
Pajewski, Thomas N.
Scalzo, David C.
Avitsian, Rafi
Brown, Michael J.
Buenvenida, Shonie
Mashour, George A.
Moore, Laurel E.
Samra, Satwant K.
Lieberman, Jeremy
Lane, Rondall K.
Ramani, Ramachandran
Wagner, Jessica
Tempelhoff, Rene
Monsey, Cynthia M.
Robicsek, Steven A.
Vu, Melissa M.
Weeks, Julie
Manninen, Pirjo H.
Fu, Eugene S.
Sanchez-Yanes, Greys C.
Peterfreund, Robert A.
Albrecht, Meredith A.
Sapire, Kenneth J.
Baughman, Verna L.
Caplan, Robert A.
Cheney, Frederick W.
Metzner, Julia
CA Postoperative Visual Loss Study Gr
TI Risk Factors Associated with Ischemic Optic Neuropathy after Spinal
Fusion Surgery
SO ANESTHESIOLOGY
LA English
DT Article
ID POSTOPERATIVE VISUAL-LOSS; RESUSCITATION; COMPLICATIONS
AB Background: Perioperative visual loss, a rare but dreaded complication of spinal fusion surgery, is most commonly caused by ischemic optic neuropathy (ION). The authors sought to determine risk factors for ION in this setting.
Methods: Using a multicenter case-control design, the authors compared 80 adult patients with ION from the American Society of Anesthesiologists Postoperative Visual Loss Registry with 315 adult control subjects without ION after spinal fusion surgery, randomly selected from 17 institutions, and matched by year of surgery. Preexisting medical conditions and perioperative factors were compared between patients and control subjects using stepwise multivariate analysis to assess factors that might predict ION.
Results: After multivariate analysis, risk factors for ION after spinal fusion surgery included male sex (odds ratio [OR] 2.53, 95% CI 1.35-4.91, P = 0.005), obesity (OR 2.83, 95% CI 1.52-5.39, P = 0.001), Wilson frame use (OR 4.30, 95% CI 2.13-8.75, P < 0.001), anesthesia duration (OR per 1 h = 1.39, 95% CI 1.22-1.58, P < 0.001), estimated blood loss (OR per 1 l = 1.34, 95% CI 1.13-1.61, P = 0.001), and colloid as percent of nonblood replacement (OR per 5% = 0.67, 95% CI 0.52-0.82, P < 0.001). After cross-validation, area under the curve = 0.85, sensitivity = 0.79, and specificity = 0.82.
Conclusions: This is the first study to assess ION risk factors in a large, multicenter case-control fashion with detailed perioperative data. Obesity, male sex, Wilson frame use, longer anesthetic duration, greater estimated blood loss, and decreased percent colloid administration were significantly and independently associated with ION after spinal fusion surgery.
C1 [Lee, Lorri A.; Posner, Karen L.; Domino, Karen B.] Univ Washington, Dept Anesthesiol & Pain Med, Sch Med, Seattle, WA 98195 USA.
[Roth, Steven] Univ Chicago, Dept Anesthesia & Crit Care, Chicago, IL 60637 USA.
[Todd, Michael M.; Weeks, Julie] Univ Iowa, Dept Anesthesia, Carver Coll Med, Iowa City, IA 52242 USA.
[Polissar, Nayak L.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Polissar, Nayak L.; Neradilek, Moni B.] Mt Whisper Light Stat, Seattle, WA USA.
[Torner, James] Univ Iowa, Dept Epidemiol, Carver Coll Med, Iowa City, IA USA.
[Newman, Nancy J.] Emory Univ, Dept Ophthalmol, Atlanta, GA 30322 USA.
[Newman, Nancy J.] Emory Univ, Dept Neurol, Atlanta, GA 30322 USA.
[Lauer, Kathryn K.; Buddithi, Rachel; Gollapudy, Suneeta] Med Coll Wisconsin, Dept Anesthesiol, Milwaukee, WI 53226 USA.
[Pajewski, Thomas N.; Scalzo, David C.] Univ Virginia Hlth Syst, Dept Anesthesiol & Neurol Surg, Charlottesville, VA USA.
[Avitsian, Rafi] Cleveland Clin, Inst Anesthesiol, Cleveland, OH 44106 USA.
[Brown, Michael J.] Mayo Clin, Coll Med, Dept Anesthesiol, Rochester, MN USA.
[Buenvenida, Shonie] Mayo Clin, Coll Med, Dept Anesthesiol, Rochester, MN USA.
[Mashour, George A.; Moore, Laurel E.; Samra, Satwant K.] Univ Michigan, Dept Anesthesiol, Sch Med, Ann Arbor, MI 48109 USA.
[Mashour, George A.] Univ Michigan, Sch Med, Dept Neurosurg, Ann Arbor, MI 48109 USA.
[Lieberman, Jeremy; Lane, Rondall K.] Univ Calif San Francisco, Dept Anesthesia & Perioperat Care, San Francisco, CA 94143 USA.
[Ramani, Ramachandran; Wagner, Jessica] Yale Univ, Sch Med, Dept Anesthesiol, New Haven, CT 06510 USA.
[Tempelhoff, Rene; Monsey, Cynthia M.] Washington Univ, Dept Anesthesiol, St Louis, MO USA.
[Robicsek, Steven A.; Vu, Melissa M.] Univ Florida, Dept Anesthesiol, Gainesville, FL USA.
[Manninen, Pirjo H.] Univ Toronto, Toronto Western Hosp, Dept Anesthesia, Univ Hlth Network, Toronto, ON M5T 2S8, Canada.
[Fu, Eugene S.; Sanchez-Yanes, Greys C.] Univ Miami, Sch Med, Dept Anesthesiol, Miami, FL USA.
[Peterfreund, Robert A.; Albrecht, Meredith A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, Boston, MA USA.
[Sapire, Kenneth J.] Univ Texas MD Anderson Canc Ctr, Dept Anesthesiol & Perioperat Med, Houston, TX 77030 USA.
[Baughman, Verna L.] Univ Illinois, Coll Med Chicago, Dept Anesthesiol, Chicago, IL USA.
[Caplan, Robert A.] Virginia Mason Med Ctr, Seattle, WA 98101 USA.
[Cheney, Frederick W.; Metzner, Julia] Univ Washington, Sch Med, Dept Anesthesiol & Pain Med, Seattle, WA USA.
RP Lee, LA (reprint author), Univ Washington, Dept Anesthesiol & Pain Med, Sch Med, Box 356540,1959 NE Pacific Ave, Seattle, WA 98195 USA.
EM lorlee@u.washington.edu
FU American Society of Anesthesiologists (ASA); ASA Closed Claims Project,
Park Ridge, Illinois; Washington State Society; Department of
Anesthesiology and Pain Medicine seed; University of Washington School
of Medicine, Seattle, Washington; Research to Prevent Blindness, Inc,
New York, New York; Lew Wasserman Award
FX Received from the Department of Anesthesiology and Pain Medicine,
University of Washington, Seattle, Washington. Submitted for publication
June 8, 2011. Accepted for publication September 27, 2011. Supported in
part by the American Society of Anesthesiologists (ASA) as part of the
ASA Closed Claims Project, Park Ridge, Illinois; the Washington State
Society of Anesthesiologists Seafair Grant; and the Department of
Anesthesiology and Pain Medicine seed funding grant, University of
Washington School of Medicine, Seattle, Washington. Dr. Newman reports
receiving partial research support from Research to Prevent Blindness,
Inc, New York, New York, via an unrestricted grant and the Lew Wasserman
Award to the Department of Ophthalmology, Emory University, Atlanta,
Georgia. The funding organizations 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, or approval of the manuscript.
Information on previous presentation of the information reported in this
manuscript: An abstract with preliminary data from a subset of the
control cases only (100 out of 315 controls) regarding range of
anesthetic management in spine surgery was presented at the American
Society of Anesthesiologists (ASA) annual meeting, on October 19, 2009,
in New Orleans, Louisiana, as Abstract #A1013. An abstract on the
predictive model for ischemic optic neuropathy was submitted to the ASA
annual meeting, held October 15-19, 2011, in Chicago, Illinois, for the
Late-Breaking Scientific Abstracts Session. No other presentations or
publications from this study have been made.The authors gratefully
acknowledge the following individuals for acquisition of data: Robin A.
Bruchas, M. S. W., Research Study Coordinator, and John Campos, M. A.,
Research Consultant, Department of Anesthesiology and Pain Medicine,
University of Washington School of Medicine, Seattle, Washington;
Melissa Passe, R. R. T., Study Coordinator, Department of
Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota;
Xing Fu, M. D., Resident in Anesthesiology, Department of
Anesthesiology, Yale University School of Medicine, New Haven,
Connecticut; Aki Honda, M. D., Research Assistant, Department of
Anesthesiology, Washington University, St. Louis, Missouri; Elaine
Hrinyo, B. S., C. P. C., Professional Fee Billing Manager, and Sharon
Jakubczyk, B.S.N., Research Nurse, Department of Anesthesia and Critical
Care, University of Chicago, Chicago, Illinois; Stephanie Davis, M. D.,
Resident, and John Klein, M. D., Resident, Department of Anesthesia,
University of Iowa Carver School of Medicine, Iowa City, Iowa; Yiqing
Yin, M. D., Anesthesia Fellow, and Qanwei Luo, M. D., Research
Assistant, Department of Anesthesia, Toronto Western Hospital,
University of Toronto, University Health Network University of Toronto,
Toronto, Ontario, Canada; Theresa A. Morris, R.N., Quality Assurance
Coordinator, Department of Anesthesia, Critical Care, and Pain Medicine,
Massachusetts General Hospital, Harvard Medical School, Boston,
Massachusetts; Sonya Meyers, M. D., Medical Student ( at time of data
collection), Department of Anesthesiology, University of Illinois
College of Medicine at Chicago, Chicago, Illinois. The authors
acknowledge Lynn Akerlund, Research Coordinator, Department of
Anesthesiology and Pain Medicine, University of Washington, Seattle,
Washington, for contributions to the project coordination and expert
secretarial assistance.
NR 23
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U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
J9 ANESTHESIOLOGY
JI Anesthesiology
PD JAN
PY 2012
VL 116
IS 1
BP 15
EP 24
DI 10.1097/ALN.0b013e31823d012a
PG 10
WC Anesthesiology
SC Anesthesiology
GA 869OU
UT WOS:000298608400006
ER
PT J
AU Eikermann, M
Grosse-Sundrup, M
Zaremba, S
Henry, ME
Bittner, EA
Hoffmann, U
Chamberlin, NL
AF Eikermann, Matthias
Grosse-Sundrup, Martina
Zaremba, Sebastian
Henry, Mark E.
Bittner, Edward A.
Hoffmann, Ulrike
Chamberlin, Nancy L.
TI Ketamine Activates Breathing and Abolishes the Coupling between Loss of
Consciousness and Upper Airway Dilator Muscle Dysfunction
SO ANESTHESIOLOGY
LA English
DT Article
ID GENIOGLOSSUS MUSCLE; NMDA RECEPTORS; NERVE ACTIVITY; SLEEP-WAKE;
IN-VIVO; ANESTHESIA; PROPOFOL; SEDATION; COLLAPSIBILITY; HYPOGLOSSAL
AB Background: Procedural sedation is frequently performed in spontaneously breathing patients, but hypnotics and opioids decrease respiratory drive and place the upper airway at risk for collapse.
Methods: In a randomized, controlled, cross-over, pharmaco-physiologic study in 12 rats, we conducted acute experiments to compare breathing and genioglossus electromyogram activity at equianesthetic concentrations of ketamine, a noncompetitive N-methyl-D-aspartate receptor antagonist that combines potent analgesic with hypnotic action effects, versus propofol. In 10 chronically instrumented rats resting in a plethysmograph, we measured these variables as well as electroencephalography during five conditions: quiet wakefulness, nonrapid-eye-movement sleep, rapid eye movement sleep, and low-dose (60 mg/kg intraperitoneally) and high-dose ketamine anesthesia (125 mg/kg intraperitoneally).
Results: Ketamine anesthesia was associated with markedly increased genioglossus activity (1.5 to fivefold higher values of genioglossus electromyogram) compared with sleep-and propofol-induced unconsciousness. Plethysmography revealed a respiratory stimulating effect: higher values of flow rate, respiratory rate, and duty-cycle (effective inspiratory time, 1.5-to-2-fold higher values). During wakefulness and normal sleep, the delta (f = 6.51, P = 0.04) electroencephalogram power spectrum was an independent predictor of genioglossus activity, indicating an association between electroencephalographic determinants of consciousness and genioglossus activity. Following ketamine administration, electroencephalogram power spectrum and genioglossus electroencephalogram was dissociated (P = 0.9 for the relationship between delta/theta power spectrum and genioglossus electromyogram).
Conclusions: Ketamine is a respiratory stimulant that abolishes the coupling between loss-of-consciousness and upper airway dilator muscle dysfunction in a wide dose-range. Ketamine compared with propofol might help stabilize airway patency during sedation and anesthesia.
C1 [Eikermann, Matthias] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Crit Care Div,Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
[Chamberlin, Nancy L.] Harvard Univ, Sch Med, Div Sleep Med, Boston, MA USA.
[Eikermann, Matthias] Univ Klinikum Essen, Klin Anasthesie & Intens Med, Essen, Germany.
[Grosse-Sundrup, Martina; Zaremba, Sebastian; Henry, Mark E.; Chamberlin, Nancy L.] Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA.
[Hoffmann, Ulrike] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Eikermann, M (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Crit Care Div,Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
EM meikermann@partners.org
FU National Institutes of Health, Bethesda, Maryland [HL095491, HL060292]
FX Received from the Department of Anesthesia and Critical Care,
Massachusetts General Hospital, and Harvard Medical School, Boston,
Massachusetts. Submitted for publication April 5, 2011. Accepted for
publication August 4, 2011. This work was performed by members of the
Respiratory and Anesthesia Translation Group, an interdisciplinary
cooperation between the Department of Anesthesia, Critical Care and Pain
Medicine, Massachusetts General Hospital, and the Department of
Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts.
Supported by grant Nos. HL095491 and HL060292 from the National
Institutes of Health, Bethesda, Maryland.
NR 56
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U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
J9 ANESTHESIOLOGY
JI Anesthesiology
PD JAN
PY 2012
VL 116
IS 1
BP 35
EP 46
DI 10.1097/ALN.0b013e31823d010a
PG 12
WC Anesthesiology
SC Anesthesiology
GA 869OU
UT WOS:000298608400008
PM 22108392
ER
PT J
AU Ruesch, D
Neumann, E
Wulf, H
Forman, SA
AF Ruesch, Dirk
Neumann, Elena
Wulf, Hinnerk
Forman, Stuart A.
TI An Allosteric Coagonist Model for Propofol Effects on alpha 1 beta 2
gamma 2L gamma-Aminobutyric Acid Type A Receptors
SO ANESTHESIOLOGY
LA English
DT Article
ID OPEN-CLOSE EQUILIBRIUM; GATED ION CHANNELS; GABA(A) RECEPTORS;
GENERAL-ANESTHETICS; AZI-ETOMIDATE; MODULATION; SUBUNIT; SITES;
EFFICACY; BINDING
AB Background: Propofol produces its major actions via gamma-aminobutyric acid type A (GABA(A)) receptors. At low concentrations, propofol enhances agonist-stimulated GABA(A) receptor activity, and high propofol concentrations directly activate receptors. Etomidate produces similar effects, and there is convincing evidence that a single class of etomidate sites mediate both agonist modulation and direct GABA(A) receptor activation. It is unknown if the propofol binding site(s) on GABA(A) receptors that modulate agonist-induced activity also mediate direct activation.
Methods: GABA(A) alpha 1 beta 2 gamma 2L receptors were heterologously expressed in Xenopus oocytes and activity was quantified using voltage clamp electrophysiology. We tested whether propofol and etomidate display the same linkage between agonist modulation and direct activation of GABA(A) receptors by identifying equiefficacious drug solutions for direct activation. We then determined whether these drug solutions produce equal modulation of GABA-induced receptor activity. We also measured propofol-dependent direct activation and modulation of low GABA responses. Allosteric coagonist models similar to that established for etomidate, but with variable numbers of propofol sites, were fitted to combined data.
Results: Solutions of 19 mu M propofol and 10 mu M etomidate were found to equally activate GABA(A) receptors. These two drug solutions also produced indistinguishable modulation of GABA-induced receptor activity. Combined electrophysiological data behaved in a manner consistent with allosteric coagonist models with more than one propofol site. The best fit was observed when the model assumed three equivalent propofol sites.
Conclusions: Our results support the hypothesis that propofol, like etomidate, acts at GABA(A) receptor sites mediating both GABA modulation and direct activation.
C1 [Forman, Stuart A.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Forman, Stuart A.] Harvard Univ, Sch Med, Boston, MA USA.
[Ruesch, Dirk; Wulf, Hinnerk] Univ Hosp Giessen Marburg, Dept Anesthesia & Intens Care, Marburg, Germany.
[Neumann, Elena] Univ Tubingen, Dept Anesthesiol, Sect Expt Anesthesiol, Tubingen, Germany.
RP Forman, SA (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Jackson 4,55 Fruit St, Boston, MA 02114 USA.
EM saforman@partners.org
FU National Institutes of Health, Bethesda, Maryland [P01 GM58448, R01
GM089745]; Department of Anesthesia, Critical Care and Pain Medicine,
Massachusetts General Hospital; Department of Anesthesia and Intensive
Care, University Hospital Giessen-Marburg, Marburg, Germany
FX Received from the Department of Anesthesia, Critical Care and Pain
Medicine, Massachusetts General Hospital, Boston, Massachusetts.
Submitted for publication May 12, 2011. Accepted for publication August
24, 2011. Supported by grant nos. P01 GM58448 and R01 GM089745 from the
National Institutes of Health, Bethesda, Maryland; the Department of
Anesthesia, Critical Care and Pain Medicine, Massachusetts General
Hospital; and the Department of Anesthesia and Intensive Care,
University Hospital Giessen-Marburg, Marburg, Germany.
NR 35
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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 JAN
PY 2012
VL 116
IS 1
BP 47
EP 55
DI 10.1097/ALN.0b013e31823d0c36
PG 9
WC Anesthesiology
SC Anesthesiology
GA 869OU
UT WOS:000298608400009
PM 22104494
ER
PT J
AU Agasti, SS
Liong, M
Tassa, C
Chung, HJ
Shaw, SY
Lee, H
Weissleder, R
AF Agasti, Sarit S.
Liong, Monty
Tassa, Carlos
Chung, Hyun Jung
Shaw, Stanley Y.
Lee, Hakho
Weissleder, Ralph
TI Supramolecular Host-Guest Interaction for Labeling and Detection of
Cellular Biomarkers
SO ANGEWANDTE CHEMIE-INTERNATIONAL EDITION
LA English
DT Article
DE antibodies; bioorthogonal labeling; host-guest systems; nanoparticles;
supramolecular chemistry
ID MESOPOROUS SILICA NANOPARTICLES; CIRCULATING TUMOR-CELLS; CHEMISTRY;
BINDING; SURFACE; RECOGNITION; COMPLEXES; PLATFORM; TARGETS; ASSAYS
C1 [Agasti, Sarit S.; Liong, Monty; Tassa, Carlos; Chung, Hyun Jung; Shaw, Stanley Y.; Lee, Hakho; Weissleder, Ralph] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Syst Biol, Boston, MA 02114 USA.
[Weissleder, Ralph] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
RP Lee, H (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Syst Biol, 185 Cambridge St, Boston, MA 02114 USA.
EM hlee@mgh.harvard.edu; rweissleder@mgh.harvard.edu
RI Chung, Hyun Jung/J-3205-2014
FU National Institutes of Health [R01-EB0044626, R01-EB010011, T32A79443,
P50A86355]; CCNE [U54A151884]; TPEN [HHSN268201000044C]
FX We thank M. Fernandez-Suarez, R. Mazitschek, T. Reiner, K. S. Yang, and
K. Tran for helpful discussions; I. Bagayev and E. Tiglao for assistance
in cell experiments; N. Sergeyev for providing the crosslinked iron
oxide particles; Y. Fisher-Jeffes for reviewing the manuscript. This
work was supported in part by National Institutes of Health Grants
R01-EB0044626, R01-EB010011, T32 grant T32A79443, P50 grant P50A86355,
CCNE contract U54A151884, and TPEN contract HHSN268201000044C.
NR 42
TC 29
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U1 9
U2 80
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1433-7851
J9 ANGEW CHEM INT EDIT
JI Angew. Chem.-Int. Edit.
PY 2012
VL 51
IS 2
BP 450
EP 454
DI 10.1002/anie.201105670
PG 5
WC Chemistry, Multidisciplinary
SC Chemistry
GA 872ER
UT WOS:000298792100019
PM 22113923
ER
PT J
AU Stone, MB
Nagdev, A
Tayal, VS
Noble, VE
AF Stone, Michael B.
Nagdev, Arun
Tayal, Vivek S.
Noble, Vicki E.
TI Ultrasonographic Infection Control Practices in the Emergency
Department: A Call for Evidence-Based Practice
SO ANNALS OF EMERGENCY MEDICINE
LA English
DT Letter
C1 [Stone, Michael B.; Nagdev, Arun] Highland Hosp, Dept Emergency Med, Alameda Cty Med Ctr, Oakland, CA USA.
[Tayal, Vivek S.] Carolinas Med Ctr, Dept Emergency Med, Charlotte, NC 28203 USA.
[Noble, Vicki E.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
RP Stone, MB (reprint author), Highland Hosp, Dept Emergency Med, Alameda Cty Med Ctr, Oakland, CA USA.
NR 3
TC 1
Z9 1
U1 0
U2 4
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0196-0644
J9 ANN EMERG MED
JI Ann. Emerg. Med.
PD JAN
PY 2012
VL 59
IS 1
BP 83
EP 84
DI 10.1016/j.annemergmed.2011.07.040
PG 2
WC Emergency Medicine
SC Emergency Medicine
GA 873OX
UT WOS:000298893800026
PM 22177685
ER
PT J
AU Sebro, R
Lange, C
Laird, NM
Rogus, JJ
Risch, NJ
AF Sebro, Ronnie
Lange, Christoph
Laird, Nan M.
Rogus, John J.
Risch, Neil J.
TI Differentiating Population Stratification from Genotyping Error Using
Family Data
SO ANNALS OF HUMAN GENETICS
LA English
DT Article
DE Genotyping error; population stratification; nonrandom mating
ID SINGLE NUCLEOTIDE POLYMORPHISMS; HARDY-WEINBERG EQUILIBRIUM;
TRANSMISSION/DISEQUILIBRIUM TEST; ASSOCIATION; DISEQUILIBRIUM
AB Identifying population stratification and genotyping error are important for candidate gene association studies using the Transmission Disequilibrium Test (TDT). Although the TDT retains the prespecified Type I error in the presence of population stratification, the test may have decreased power in the presence of population stratification. Genotyping error can also cause the TDT to have an elevated Type I error. Differentiating population stratification from genotyping error remains a challenge for geneticists. Both genotyping error and population stratification can result in an increase in the observed homozygosity of a sample relative to that expected assuming Hardy-Weinberg Equilibrium (HWE). We show that when family data are available, even if a limited number of markers are genotyped, evaluating the markers that show statistically significant deviation from HWE with the Mating Type Distortion Test (MTDT) a test based on the mating type distribution can reliably differentiate genotyping error from population stratification. We simulate data based on several models of genotyping error in previously published literature, and show how this method could be used in practice to assist in differentiating population stratification from systematic genotyping error.
C1 [Sebro, Ronnie; Risch, Neil J.] Univ Calif San Francisco, Inst Human Genet, San Francisco, CA 94143 USA.
[Sebro, Ronnie] Univ Calif San Francisco, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA.
[Lange, Christoph; Laird, Nan M.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Lange, Christoph] Univ Bonn, Inst Genom Math, Bonn, Germany.
[Lange, Christoph] German Ctr Neurodegenerat Dis DZNE, Bonn, Germany.
[Rogus, John J.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Sect Genet & Epidemiol, Boston, MA 02115 USA.
[Risch, Neil J.] Kaiser Permanente, Div Res, Oakland, CA 94612 USA.
[Risch, Neil J.] Univ Calif San Francisco, Dept Biostat & Epidemiol, San Francisco, CA 94143 USA.
RP Sebro, R (reprint author), Univ Calif San Francisco, Inst Human Genet, 513 Parnassus Ave,Suite S965, San Francisco, CA 94143 USA.
EM ronnie.sebro@radiology.ucsf.edu
FU Howard Hughes Medical Institute
FX Ronnie Sebro was supported by a Howard Hughes Medical Institute
Pre-Doctoral Fellowship. The authors thank Solandra Craig and the two
anonymous reviewers for their insightful comments that lead to
improvement of the manuscript.
NR 25
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U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0003-4800
J9 ANN HUM GENET
JI Ann. Hum. Genet.
PD JAN
PY 2012
VL 76
BP 42
EP 52
DI 10.1111/j.1469-1809.2011.00689.x
PN 1
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 864QJ
UT WOS:000298254600006
PM 22111716
ER
PT J
AU Olson, EM
Lin, NU
DiPiro, PJ
Najita, JS
Krop, IE
Winer, EP
Burstein, HJ
AF Olson, E. M.
Lin, N. U.
DiPiro, P. J.
Najita, J. S.
Krop, I. E.
Winer, E. P.
Burstein, H. J.
TI Responses to subsequent anti-HER2 therapy after treatment with
trastuzumab-DM1 in women with HER2-positive metastatic breast cancer
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE HER2/neu; lapatinib; metastatic breast cancer; trastuzumab;
trastuzumab-DM1
ID LAPATINIB
AB Background: Women with human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer (MBC) can respond to multiple lines of anti-HER2 therapy. It is unknown whether these patients will derive further clinical benefit following treatment with trastuzumab-MCC-DM1 (T-DM1).
Patients and methods: We retrospectively identified HER2-positive MBC patients treated with T-DM1 and characterized outcomes during subsequent lines of anti-HER2 therapy. Response was determined by a blinded radiology review. Time-dependent analyses were carried out using Kaplan-Meier estimates.
Results: We identified 23 patients treated with single-agent T-DM1 and report on the 20 patients who discontinued protocol therapy. All patients received trastuzumab-based metastatic therapy before initiation of T-DM1 [median 7 regimens (range 3-14)]. Of these 20 patients, 75% (15 of 20) received further therapy with or without anti-HER2 agents after discontinuing T-DM1. Partial response to either first-or second-subsequent line(s) of therapy was seen in 5 of 15 (33%) treated patients, including 33% (4 of 12) who received a regimen containing trastuzumab and/or lapatinib. Median durations of therapy to first- and second-subsequent regimens after T-DM1 were 5.5 and 6.4 months, respectively.
Conclusions: In heavily pretreated HER2-positive MBC patients, prior exposure to T-DM1 does not exhaust the potential benefit of ongoing anti-HER2 therapy with trastuzumab-and/or lapatinib-based regimens.
C1 [Olson, E. M.; Lin, N. U.; Krop, I. E.; Winer, E. P.; Burstein, H. J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[DiPiro, P. J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiol, Boston, MA 02215 USA.
[Najita, J. S.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02215 USA.
RP Burstein, HJ (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave,Yawkey 12, Boston, MA 02215 USA.
EM hburstein@partners.org
FU Canadian Cancer Society; Ontario Cancer Research Network; Ligue
Nationale Contre le Cancer; Sanofi-Aventis; USA National Cancer
Institute [CA 31946, 33601]; Alberta Heritage Foundation for Medical
Research; Alberta Cancer Foundation; Genentech Inc.
FX Canadian Cancer Society; Ontario Cancer Research Network; Ligue
Nationale Contre le Cancer; Sanofi-Aventis (unrestricted grants); USA
National Cancer Institute (CA 31946 and 33601); Alberta Heritage
Foundation for Medical Research; Alberta Cancer Foundation.; This work
was not supported by an outside source and thus there was no involvement
from an outside source in any part of this study. EMO, NUL, IEK, and EPW
receive research support for clinical trials from Genentech Inc. The
other authors declare no conflict of interest.
NR 12
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U1 1
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD JAN
PY 2012
VL 23
IS 1
BP 93
EP 97
DI 10.1093/annonc/mdr061
PG 5
WC Oncology
SC Oncology
GA 866MO
UT WOS:000298385300014
PM 21531783
ER
PT J
AU Prescott, JD
Parangi, S
AF Prescott, Jason D.
Parangi, Sareh
TI Bilaterality in Papillary Thyroid Carcinoma: Does It Influence
Prognosis?
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Editorial Material
ID CANCER DATA REGISTRY; RISING INCIDENCE; SURVEILLANCE; EPIDEMIOLOGY;
MUTATION
C1 [Prescott, Jason D.; Parangi, Sareh] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Thyroid Canc Res Lab,Dept Surg, Boston, MA 02114 USA.
RP Prescott, JD (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Thyroid Canc Res Lab,Dept Surg, Boston, MA 02114 USA.
EM sparangi@partners.org
FU NCI NIH HHS [R01 CA149738]
NR 10
TC 2
Z9 2
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD JAN
PY 2012
VL 19
IS 1
BP 1
EP 2
DI 10.1245/s10434-011-2098-0
PG 2
WC Oncology; Surgery
SC Oncology; Surgery
GA 873AL
UT WOS:000298852700001
PM 21956610
ER
PT J
AU Liu, R
Wolinsky, JB
Catalano, PJ
Chirieac, LR
Wagner, AJ
Grinstaff, MW
Colson, YL
Raut, CP
AF Liu, Rong
Wolinsky, Jesse B.
Catalano, Paul J.
Chirieac, Lucian R.
Wagner, Andrew J.
Grinstaff, Mark W.
Colson, Yolonda L.
Raut, Chandrajit P.
TI Paclitaxel-Eluting Polymer Film Reduces Locoregional Recurrence and
Improves Survival in a Recurrent Sarcoma Model: A Novel Investigational
Therapy
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article; Proceedings Paper
CT 63rd Annual Cancer Symposium of the Society-of-Surgical-Oncology
CY MAR 03-07, 2010
CL St Louis, MO
SP Soc Surg Oncol
ID SOFT-TISSUE SARCOMA; ELECTRON-BEAM RADIOTHERAPY; PLACEBO-CONTROLLED
TRIAL; RETROPERITONEAL SARCOMAS; RADIATION-THERAPY; PROGNOSTIC-FACTORS;
DRUG-DELIVERY; INTRAPERITONEAL CHEMOTHERAPY; CISPLATIN; RESECTION
AB Locoregional recurrences occur in up to 50% of patients after macroscopically complete (R0/R1) resections of abdominal, pelvic, and retroperitoneal sarcomas. Efficacy of a drug-eluting polymer film in reducing locoregional recurrence rates was assessed in a murine recurrent sarcoma model.
Poly(glycerol monostearate-co-caprolactone) polymer films were synthesized with and without 300 mu g paclitaxel (Pax-film and unloaded film). Cytotoxicity was assessed against CS-1 (human chondrosarcoma) cells in vitro and in vivo in nude mice. Following R0/R1 resection of primary subcutaneous tumors, mice were blindly randomized to: (1) Pax-film implant, (2) unloaded film implant, (3) paclitaxel 300 mu g IV (Pax IV), or (4) no other therapy ("untreated"). Locoregional recurrence, overall survival (OS), and tumor mitotic index were evaluated.
Pax-films, but not unloaded films, reduced CS-1 viability in vitro for > 50 days (P < 0.001). In vivo, locoregional recurrence was observed in 2 of 12 Pax-film mice (17%), 9 of 13 unloaded film mice (69%), 8 of 9 Pax IV mice (89%), and 7 of 8 untreated mice (88%) (P < 0.01). Median OS was 81, 64, 48, and 56 days, respectively. Paclitaxel levels in local tissues were 50- to 300-fold greater in Pax-film mice compared with Pax IV mice. Tumor mitotic index adjacent to Pax-films was significantly lower than adjacent to unloaded films.
Tumor bed implantation of Pax-films after R0/R1 resection is superior to Pax IV as evidenced by reduced locoregional recurrence and improved OS in a murine recurrent sarcoma model. Continuous local drug exposure via polymer films represents a potentially novel approach for treatment of locally aggressive sarcomas.
C1 [Liu, Rong; Colson, Yolonda L.; Raut, Chandrajit P.] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Wolinsky, Jesse B.; Grinstaff, Mark W.] Boston Univ, Dept Chem, Boston, MA 02215 USA.
[Wolinsky, Jesse B.; Grinstaff, Mark W.] Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA.
[Catalano, Paul J.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Chirieac, Lucian R.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Wagner, Andrew J.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Liu, R (reprint author), Brigham & Womens Hosp, Dept Surg, 75 Francis St, Boston, MA 02115 USA.
EM mgrin@bu.edu; ycolson@partners.org; craut@partners.org
OI Grinstaff, Mark/0000-0002-5453-3668
NR 42
TC 15
Z9 15
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD JAN
PY 2012
VL 19
IS 1
BP 199
EP 206
DI 10.1245/s10434-011-1871-4
PG 8
WC Oncology; Surgery
SC Oncology; Surgery
GA 873AL
UT WOS:000298852700034
PM 21769471
ER
PT J
AU Azadani, AN
Chitsaz, S
Matthews, PB
Jaussaud, N
Leung, J
Tsinman, T
Ge, L
Tseng, EE
AF Azadani, Ali N.
Chitsaz, Sam
Matthews, Peter B.
Jaussaud, Nicolas
Leung, James
Tsinman, Tonia
Ge, Liang
Tseng, Elaine E.
TI Comparison of Mechanical Properties of Human Ascending Aorta and Aortic
Sinuses
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID FINITE-ELEMENT; VALVE INCOMPETENCE; ROOT; ANEURYSM; ARTERIES; MODEL; AGE
AB Background. Computational finite element models of the aortic root have previously used material properties of the ascending aorta to describe both aortic sinuses and ascending aorta. We have previously demonstrated significant material property differences between ascending aorta and sinuses in pigs. However, it is unknown whether these regional material property differences exist in humans. The main objective of this study was to investigate biomechanics of fresh human ascending aorta and aortic sinuses and compare nonlinear material properties of these regions.
Methods. Fresh human aortic root specimens obtained from the California Transplant Donor Network (Oakland, CA) were subjected to displacement-controlled equibiaxial stretch testing within 24 hours of harvest. Stress-strain data recorded were used to derive strain energy functions for each region. Tissue behavior was quantified by tissue stiffness and a direct comparison was made between different regions of aortic root at physiologic stress levels.
Results. All regions demonstrated a nonlinear response to strain during stretch testing in both circumferential and longitudinal directions. No significant difference in tissue stiffness was found between anterior and posterior regions of the ascending aorta or among the three sinuses in both directions. However, our results demonstrated that human ascending aorta is significantly more compliant than aortic sinuses in both circumferential and longitudinal directions within the physiologic stress range.
Conclusions. Significant material and structural differences were observed between human ascending aorta and aortic sinuses. Regionally specific material properties should be employed in computational models used to assess treatments of structural aortic root disease. (Ann Thorac Surg 2012;93:87-94) (C) 2012 by The Society of Thoracic Surgeons
C1 [Tseng, Elaine E.] Univ Calif San Francisco, Med Ctr, Div Cardiothorac Surg, Dept Surg, San Francisco, CA 94143 USA.
San Francisco VA Med Ctr, San Francisco, CA USA.
RP Tseng, EE (reprint author), Univ Calif San Francisco, Med Ctr, Div Cardiothorac Surg, Dept Surg, 500 Parnassus Ave,Ste 405W,Box 0118, San Francisco, CA 94143 USA.
EM elaine.tseng@ucsfmedctr.org
RI Chitsaz, Sam/C-4586-2008
FU American Heart Association
FX We thank Dr Philip Ursell for his histologic characterization and the
California Transplant Donor Network for the hearts. This work was
supported by an American Heart Association Grant-in-Aid, which was
administered by the Northern California Institute for Research and
Education with resources of the Veterans Affairs Medical Center, San
Francisco, California.
NR 18
TC 19
Z9 19
U1 2
U2 13
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 JAN
PY 2012
VL 93
IS 1
BP 87
EP 94
DI 10.1016/j.athoracsur.2011.08.002
PG 8
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 864QR
UT WOS:000298255400019
PM 22075218
ER
PT J
AU Hynes, BG
Margey, RJ
Ruggiero, N
Kiernan, TJ
Rosenfield, K
Jaff, MR
AF Hynes, Brian G.
Margey, Ronan J.
Ruggiero, Nicholas, II
Kiernan, Thomas J.
Rosenfield, Kenneth
Jaff, Michael R.
TI Endovascular Management of Acute Limb Ischemia
SO ANNALS OF VASCULAR SURGERY
LA English
DT Review
ID TISSUE-PLASMINOGEN-ACTIVATOR; PROSPECTIVE RANDOMIZED TRIAL; PERIPHERAL
ARTERIAL-DISEASE; DIRECTED THROMBOLYTIC THERAPY; LOWER-EXTREMITY
ISCHEMIA; INTER-SOCIETY CONSENSUS; ACUTE LEG ISCHEMIA; SURGICAL
REVASCULARIZATION; INTRAOPERATIVE ANGIOGRAPHY; ANTITHROMBOTIC THERAPY
AB Despite major advances in pharmacologic and endovascular therapies, acute limb ischemia (ALI) continues to result in significant morbidity and mortality. The incidence of ALI may be as high as 13-17 cases per 100,000 people per year, with mortality rates approaching 18% in some series. This review will address the contemporary endovascular management of ALI encompassing pharmacologic and percutaneous interventional treatment strategies.
C1 [Hynes, Brian G.; Margey, Ronan J.; Rosenfield, Kenneth; Jaff, Michael R.] Massachusetts Gen Hosp, Div Cardiol, Sect Vasc Med, Boston, MA 02114 USA.
[Ruggiero, Nicholas, II] Thomas Jefferson Univ Hosp, Div Cardiol, Philadelphia, PA 19107 USA.
[Kiernan, Thomas J.] Cork Univ Hosp, Dept Cardiol, Cork, Ireland.
RP Jaff, MR (reprint author), Massachusetts Gen Hosp, Div Cardiol, Sect Vasc Med, 55 Fruit St, Boston, MA 02114 USA.
EM mrjaff@partners.org
NR 80
TC 6
Z9 9
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0890-5096
J9 ANN VASC SURG
JI Ann. Vasc. Surg.
PD JAN
PY 2012
VL 26
IS 1
BP 110
EP 124
DI 10.1016/j.avsg.2011.05.017
PG 15
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 865QR
UT WOS:000298325900020
PM 21920700
ER
PT J
AU Sizova, MV
Hohmann, T
Hazen, A
Paster, BJ
Halem, SR
Murphy, CM
Panikov, NS
Epstein, SS
AF Sizova, M. V.
Hohmann, T.
Hazen, A.
Paster, B. J.
Halem, S. R.
Murphy, C. M.
Panikov, N. S.
Epstein, S. S.
TI New Approaches for Isolation of Previously Uncultivated Oral Bacteria
SO APPLIED AND ENVIRONMENTAL MICROBIOLOGY
LA English
DT Article
ID IN-SITU CULTIVATION; SP-NOV.; UNCULTURABLE BACTERIA; DENTAL PLAQUE;
DIVERSITY; MICROORGANISMS; MICROBIOLOGY; CULTURE; METAGENOMICS;
CLOSTRIDIUM
AB A significant number of microorganisms from the human oral cavity remain uncultivated. This is a major impediment to the study of human health since some of the uncultivated species may be involved in a variety of systemic diseases. We used a range of innovations previously developed to cultivate microorganisms from the human oral cavity, focusing on anaerobic species. These innovations include (i) in vivo cultivation to specifically enrich for species actively growing in the oral cavity (the "minitrap" method), (ii) single-cell long-term cultivation to minimize the effect of fast-growing microorganisms, and (iii) modifications of conventional enrichment techniques, using media that did not contain sugar, including glucose. To enable cultivation of obligate anaerobes, we maintained strict anaerobic conditions in most of our cultivation experiments. We report that, on a per cell basis, the most successful recovery was achieved using minitrap enrichment (11%), followed by single-cell cultivation (3%) and conventional plating (1%). Taxonomically, the richest collection was obtained using the single-cell cultivation method, followed by minitrap and conventional enrichment, comprising representatives of 13, 9, and 4 genera, respectively. Interestingly, no single species was isolated by all three methods, indicating method complementarity. An important result is the isolation and maintenance in pure culture of 10 strains previously only known by their molecular signatures, as well as representatives of what are likely to be three new microbial genera. We conclude that the ensemble of new methods we introduced will likely help close the gap between cultivated and uncultivated species from the human oral cavity.
C1 [Sizova, M. V.; Hohmann, T.; Hazen, A.; Panikov, N. S.; Epstein, S. S.] Northeastern Univ, Dept Biol, Boston, MA 02115 USA.
[Paster, B. J.; Halem, S. R.; Murphy, C. M.] Forsyth Inst, Cambridge, MA USA.
[Paster, B. J.] Harvard Univ, Sch Dent Med, Dept Oral Med Infect & Immun, Boston, MA 02115 USA.
RP Epstein, SS (reprint author), Northeastern Univ, Dept Biol, Boston, MA 02115 USA.
EM s.epstein@neu.edu
FU NIH [1RC1DE020707-01, 3 R21 DE018026-02S1]
FX This work was supported by NIH grants 1RC1DE020707-01 and 3 R21
DE018026-02S1 to S.S.E.
NR 60
TC 31
Z9 31
U1 2
U2 36
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0099-2240
J9 APPL ENVIRON MICROB
JI Appl. Environ. Microbiol.
PD JAN
PY 2012
VL 78
IS 1
BP 194
EP 203
DI 10.1128/AEM.06813-11
PG 10
WC Biotechnology & Applied Microbiology; Microbiology
SC Biotechnology & Applied Microbiology; Microbiology
GA 866QR
UT WOS:000298396700025
PM 22057871
ER
PT J
AU Nakamura, Y
He, XJ
Kato, H
Wakitani, S
Kobayashi, T
Watanabe, S
Iida, A
Tahara, H
Warman, ML
Watanapokasin, R
Postlethwait, JH
AF Nakamura, Yukio
He, Xinjun
Kato, Hiroyuki
Wakitani, Shigeyuki
Kobayashi, Tatsuya
Watanabe, Sumiko
Iida, Atsumi
Tahara, Hideaki
Warman, Matthew L.
Watanapokasin, Ramida
Postlethwait, John H.
TI Sox9 Is Upstream of MicroRNA-140 in Cartilage
SO APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY
LA English
DT Article
DE MicroRNA-140 (miR-140); Sox9; Cartilage; Zebrafish; T/C-28; siRNA; In
situ hybridization; RT-PCR
ID SRY-RELATED GENE; AUTOSOMAL SEX REVERSAL; TRANSCRIPTIONAL REGULATION;
EMBRYONIC-DEVELOPMENT; CAMPOMELIC DYSPLASIA; EXPRESSION; ZEBRAFISH;
CHONDROGENESIS; PROTEIN; MUTATIONS
AB MicroRNA-140 (miR-140) is specifically expressed in developing cartilage tissues. We have previously reported that miR-140 plays an important role during palatal cartilage development by modulating platelet-derived growth factor receptor alpha (pdgfra) in zebrafish. However, the regulatory mechanism of miR-140 in cartilage is still unknown. Using developing zebrafish, sox9a mutant (sox9a-/-) and sox9b mutant (sox9b-/-) zebrafish and SOX9 small interfering RNA in human chondrocytes, T/C-28 cells, we found that miR-140 is regulated by the cartilage master transcription regulator Sox9 in zebrafish and mammalian cells.
C1 [Watanapokasin, Ramida] Srinakharinwirot Univ, Dept Biochem, Fac Med, Bangkok, Thailand.
[Warman, Matthew L.] Childrens Hosp Boston, Howard Hughes Med Inst, Dept Orthopaed Surg, Boston, MA 02115 USA.
[Warman, Matthew L.] Childrens Hosp Boston, Howard Hughes Med Inst, Dept Genet, Boston, MA 02115 USA.
[Warman, Matthew L.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Tahara, Hideaki] Univ Tokyo, Inst Med Sci, Adv Clin Res Ctr, Dept Surg & Bioengn, Tokyo 1088639, Japan.
[Watanabe, Sumiko; Iida, Atsumi] Univ Tokyo, Inst Med Sci, Dept Mol & Dev Biol, Tokyo 1088639, Japan.
[Kobayashi, Tatsuya] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Kobayashi, Tatsuya] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Wakitani, Shigeyuki] Osaka City Univ, Grad Sch Med, Dept Orthopaed Surg, Osaka 5458585, Japan.
[He, Xinjun; Postlethwait, John H.] Univ Oregon, Inst Neurosci, Eugene, OR 97403 USA.
[Nakamura, Yukio; Kato, Hiroyuki] Shinshu Univ, Sch Med, Dept Orthopaed Surg, Matsumoto, Nagano 3908621, Japan.
RP Watanapokasin, R (reprint author), Srinakharinwirot Univ, Dept Biochem, Fac Med, Bangkok, Thailand.
EM ramidawa@yahoo.com
RI He, Xinjun/F-9797-2011
FU NIH [HD22486, RR020833]
FX We thank Dr. Keiko Tamai at Case Western Reserve University, Cleveland,
OH for her valuable discussions and to NIH grants HD22486 and RR020833
to JHP.
NR 29
TC 26
Z9 32
U1 2
U2 7
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0273-2289
J9 APPL BIOCHEM BIOTECH
JI Appl. Biochem. Biotechnol.
PD JAN
PY 2012
VL 166
IS 1
BP 64
EP 71
DI 10.1007/s12010-011-9404-y
PG 8
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA 874XZ
UT WOS:000298992900007
PM 22052544
ER
PT J
AU Tanpowpong, P
Ingham, TR
Lampshire, PK
Kirchberg, FF
Epton, MJ
Crane, J
Camargo, CA
AF Tanpowpong, Pornthep
Ingham, Tristram R.
Lampshire, Phillipa K.
Kirchberg, Franca F.
Epton, Michael J.
Crane, Julian
Camargo, Carlos A., Jr.
CA New Zealand Asthma & Allergy Cohor
TI Coeliac disease and gluten avoidance in New Zealand children
SO ARCHIVES OF DISEASE IN CHILDHOOD
LA English
DT Article
ID IRRITABLE-BOWEL-SYNDROME; QUALITY-OF-LIFE; LACTOSE-INTOLERANCE; FREE
DIET; PREVALENCE; SYMPTOMS; DIAGNOSIS; RISK
AB Objectives Although gluten avoidance is thought to be common among New Zealanders, the prevalence of gluten avoidance and of actual coeliac disease (CD) in children is uncertain. Our aims were: (1) to determine the prevalence of doctor-diagnosed CD and of gluten avoidance in New Zealand children; and (2) among children without CD, to identify independent predictors of gluten avoidance.
Design The New Zealand Asthma and Allergy Cohort Study has detailed information on participants' demographic, pregnancy-related and neonatal factors. The authors surveyed parents regarding their child's history of lactose intolerance and gluten-related issues (eg, gluten avoidance, history of wheat or gluten allergy in first degree relatives, testing and doctor diagnosis of CD). After excluding children with doctor-diagnosed CD, the authors identified independent predictors of gluten avoidance.
Results Among 916 children, most (78%) were of European ethnicity. The authors identified nine (1.0%, 95% CI 0.5% to 1.9%) who had doctor-diagnosed CD, while 48 (5.2%, 95% CI 4.0% to 6.9%) avoided gluten. Among children without diagnosed CD, significant independent predictors for gluten avoidance were Christchurch site (OR 2.2, 95% CI 1.02 to 4.7), prior testing for CD (OR 9.0, 95% CI 4.1 to 19.5) and doctor-diagnosed lactose intolerance (OR 5.2, 95% CI 2.0 to 13.9).
Conclusions CD affected 1% of these New Zealand children, but 5% reported gluten avoidance. The predictors of gluten avoidance in children without doctor-diagnosed CD suggest important regional differences in community belief or medical practice regarding implementation of gluten avoidance and the contributory role of non-specific subjective abdominal complaints.
C1 [Kirchberg, Franca F.; Camargo, Carlos A., Jr.] Harvard Univ, Dept Emergency Med, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
[Tanpowpong, Pornthep] Harvard Univ, Div Pediat Gastroenterol Hepatol & Nutr, Sch Med, Massachusetts Gen Hosp Children,Dept Pediat, Boston, MA 02114 USA.
[Ingham, Tristram R.; Lampshire, Phillipa K.; Crane, Julian] Univ Otago, Wellington Asthma Res Grp, Dept Med, Wellington Sch Med & Hlth Sci, Wellington, New Zealand.
[Epton, Michael J.] Christchurch Hosp, Dept Resp Med, Christchurch, New Zealand.
RP Camargo, CA (reprint author), Harvard Univ, Dept Emergency Med, Massachusetts Gen Hosp, Sch Med, 326 Cambridge St,Suite 410, Boston, MA 02114 USA.
EM ccamargo@partners.org
OI Siebers, Robert/0000-0002-6359-3144; Kirchberg, Franca
Fabiana/0000-0001-6863-1202
FU Health Research Council of New Zealand; David and Cassie Anderson
Bequest (Wellington, New Zealand); Food Allergy & Anaphylaxis Network
(Fairfax, Virginia, USA)
FX This work was supported by grants from the Health Research Council of
New Zealand, the David and Cassie Anderson Bequest (Wellington, New
Zealand) and the Food Allergy & Anaphylaxis Network (Fairfax, Virginia,
USA).
NR 32
TC 38
Z9 39
U1 0
U2 14
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-9888
EI 1468-2044
J9 ARCH DIS CHILD
JI Arch. Dis. Child.
PD JAN
PY 2012
VL 97
IS 1
BP 12
EP 16
DI 10.1136/archdischild-2011-300248
PG 5
WC Pediatrics
SC Pediatrics
GA 865ZS
UT WOS:000298350000005
PM 22075107
ER
PT J
AU Roussos, P
Katsel, P
Davis, KL
Bitsios, P
Giakoumaki, SG
Jogia, J
Rozsnyai, K
Collier, D
Frangou, S
Siever, LJ
Haroutunian, V
AF Roussos, Panos
Katsel, Pavel
Davis, Kenneth L.
Bitsios, Panos
Giakoumaki, Stella G.
Jogia, Jigar
Rozsnyai, Kinga
Collier, David
Frangou, Sophia
Siever, Larry J.
Haroutunian, Vahram
TI Molecular and Genetic Evidence for Abnormalities in the Nodes of Ranvier
in Schizophrenia
SO ARCHIVES OF GENERAL PSYCHIATRY
LA English
DT Article
ID MULTIPLE BRAIN-REGIONS; ANTERIOR CINGULATE CORTEX; GENOME-WIDE
ASSOCIATION; MILD ALZHEIMER-DISEASE; BIPOLAR DISORDER; EXPRESSION;
MYELIN; HIPPOCAMPUS; DYSFUNCTION; PHENOTYPE
AB Context: Genetic, neuroimaging, and molecular neurobiological evidence support the hypothesis that the disconnectivity syndrome in schizophrenia (SZ) could arise from failures of saltatory conduction and abnormalities at the nodes of Ranvier (NOR) interface where myelin and axons interact.
Objective: To identify abnormalities in the expression of oligodendroglial genes and proteins that participate in the formation, maintenance, and integrity of the NOR in SZ.
Design: The messenger RNA (mRNA) expression levels of multiple NOR genes were quantified in 2 independent postmortem brain cohorts of individuals with SZ, and generalizability to protein expression was confirmed. The effect of the ANK3 genotype on the mRNA expression level was tested in postmortem human brain. Case-control analysis tested the association of the ANK3 genotype with SZ. The ANK3 genotype's influence on cognitive task performance and functional magnetic resonance imaging activation was tested in 2 independent cohorts of healthy individuals.
Setting: Research hospital.
Patients: Postmortem samples from patients with SZ and healthy controls were used for the brain expression study (n=46) and the case-control analysis (n=272). Healthy white men and women participated in the cognitive (n=513) and neuroimaging (n=52) studies.
Main Outcome Measures: The mRNA and protein levels in postmortem brain samples, genetic association with schizophrenia, cognitive performance, and blood oxygenation level-dependent functional magnetic resonance imaging.
Results: The mRNA expression of multiple NOR genes was decreased in schizophrenia. The ANK3 rs9804190 C allele was associated with lower ANK3 mRNA expression levels, higher risk for SZ in the case-control cohort, and poorer working memory and executive function performance and increased prefrontal activation during a working memory task in healthy individuals.
Conclusions: These results point to abnormalities in the expression of genes and protein associated with the integrity of the NOR and suggest them as substrates for the disconnectivity syndrome in SZ. The association of ANK3 with lower brain mRNA expression levels implicates a molecular mechanism for its genetic, clinical, and cognitive associations with SZ.
C1 [Roussos, Panos; Katsel, Pavel; Davis, Kenneth L.; Siever, Larry J.; Haroutunian, Vahram] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Roussos, Panos; Siever, Larry J.; Haroutunian, Vahram] James J Peters Vet Affairs Med Ctr, Bronx, NY USA.
[Roussos, Panos; Bitsios, Panos; Giakoumaki, Stella G.] Univ Crete, Dept Psychiat & Behav Sci, Fac Med, Iraklion, Crete, Greece.
[Jogia, Jigar; Frangou, Sophia] Kings Coll London, Sect Neurobiol Psychosis, Inst Psychiat, London, England.
[Rozsnyai, Kinga; Collier, David] Kings Coll London, Social Genet & Dev Psychiat Res Ctr, Inst Psychiat, London, England.
RP Haroutunian, V (reprint author), Mt Sinai Sch Med, Dept Psychiat, Room 4F-33,130 Kingsbridge Rd, Bronx, NY 10468 USA.
EM vahram.haroutunian@mssm.edu
RI Frangou, Sophia/A-2672-2013; Collier, David/D-1649-2011; Roussos,
Panos/J-7090-2013;
OI Collier, David/0000-0003-4087-1559; Roussos, Panos/0000-0002-4640-6239;
Jogia, Jigar/0000-0003-1799-1245
FU National Institutes of Health [MH066392, MH064673]; Veterans Affairs
Mental Illness Research Education and Clinical Center; Veterans Affairs
FX This work was supported by grants MH066392 and MH064673 from the
National Institutes of Health (Dr Haroutunian), a Veterans Affairs
Mental Illness Research Education and Clinical Center award (Dr Siever),
and a Veterans Affairs merit award (Dr Haroutunian).
NR 39
TC 45
Z9 48
U1 0
U2 12
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 JAN
PY 2012
VL 69
IS 1
BP 7
EP 15
DI 10.1001/archgenpsychiatry.2011.110
PG 9
WC Psychiatry
SC Psychiatry
GA 870NH
UT WOS:000298675700002
PM 21893642
ER
PT J
AU Olfson, M
Marcus, SC
Bridge, JA
AF Olfson, Mark
Marcus, Steven C.
Bridge, Jeffrey A.
TI Emergency Treatment of Deliberate Self-harm
SO ARCHIVES OF GENERAL PSYCHIATRY
LA English
DT Article
ID BORDERLINE PERSONALITY-DISORDER; ATTEMPTED-SUICIDE; FOLLOW-UP; COMPLETED
SUICIDE; DEPARTMENT VISITS; HEALTH-CARE; COHORT; ADULTS; RISK;
DEPRESSION
AB Context: Although concern exists over the quality of emergency mental health services, little is known about the mental health care of adults who are admitted to emergency departments for deliberately harming themselves and then discharged to the community.
Objective: To describe the predictors of emergency department discharge, the emergency mental health assessments, and the follow-up outpatient mental health care of adult Medicaid beneficiaries treated for deliberate self-harm.
Design: A retrospective longitudinal cohort analysis.
Setting: National Medicaid claims data supplemented with county-level sociodemographic variables and Medicaid state policy survey data.
Participants: Adults aged 21 to 64 years who were treated in emergency departments for 7355 episodes of deliberate self-harm, focusing on those who were discharged to the community (4595 episodes).
Main Outcome Measures: Rates and adjusted risk ratios (ARRs) of discharge to the community, mental health assessments in the emergency department, and outpatient mental health visits during the 30 days following the emergency department visit.
Results: Most patients (62.5%) were discharged to the community. Emergency department discharge was directly related to younger patient age (21-31 years vs 45-64 years) (ARR, 1.18 [99% confidence interval {CI}, 1.10-1.25]) and self-harm by cutting (ARR, 1.18 [99% CI, 1.12-1.24]) and inversely related to poisoning (ARR, 0.84 [99% CI, 0.80-0.89]) and recent psychiatric hospitalization (ARR, 0.74 [99% CI, 0.67-0.81]). Approximately one-half of discharged patients (47.5%) received a mental health assessment in the emergency department, and a similar percentage of discharged patients (52.4%) received a follow-up outpatient mental health visit within 30 days. Follow-up mental health care was directly related to recent outpatient mental health care (ARR, 2.30 [99% CI, 2.11-2.50]) and treatment in a state with Medicaid coverage of mental health clinic services (ARR, 1.13 [99% CI, 1.05-1.22]) and inversely related to African American (ARR, 0.86 [99% CI, 0.75-0.96]) and Hispanic (ARR, 0.86 [99% CI, 0.75-0.99]) race/ethnicity.
Conclusion: Most adult Medicaid beneficiaries who present for emergency care for deliberate self-harm are discharged to the community, and many do not receive emergency mental health assessments or follow-up outpatient mental health care.
C1 [Olfson, Mark] Columbia Univ, New York State Psychiat Inst, Dept Psychiat, Coll Phys & Surg, New York, NY 10032 USA.
[Marcus, Steven C.] Univ Penn, Ctr Hlth Equ Res & Promot, Philadelphia Vet Affairs Med Ctr, Philadelphia, PA 19104 USA.
[Marcus, Steven C.] Univ Penn, Sch Social Policy & Practice, Philadelphia, PA 19104 USA.
[Bridge, Jeffrey A.] Ohio State Univ, Res Inst, Nationwide Childrens Hosp, Ctr Innovat Pediat Practice, Columbus, OH USA.
[Bridge, Jeffrey A.] Ohio State Univ, Dept Pediat, Columbus, OH USA.
RP Olfson, M (reprint author), Columbia Univ, New York State Psychiat Inst, Dept Psychiat, Coll Phys & Surg, 1051 Riverside Dr, New York, NY 10032 USA.
EM mo49@columbia.edu
FU Eli Lilly; Bristol-Myers Squibb; AstraZeneca; Dainippon Sumitomo; Forest
Research Institute; Ortho-McNeil-Janssen; Pfizer Inc; Roche
Pharmaceuticals; sanofi-aventis; Schering-Plough; Sepracor; United
BioSource; Lundbeck; American Foundation for Suicide Prevention
FX Dr Olfson has received a research grant to Columbia University from Eli
Lilly and Bristol-Myers Squibb. Dr Bridge has received honoraria for
participation in a suicidality consensus conference supported by
independent educational or other unrestricted grant support from
AstraZeneca, Dainippon Sumitomo, Eli Lilly, Forest Research Institute,
Ortho-McNeil-Janssen, Pfizer Inc, Roche Pharmaceuticals, sanofi-aventis,
Schering-Plough, Sepracor, and United BioSource; and he has presented on
suicide prevention in children and adolescents at a conference supported
in part by Eli Lilly and Lundbeck.; This research was funded by a grant
to Columbia University from the American Foundation for Suicide
Prevention.
NR 60
TC 24
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U1 4
U2 9
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 JAN
PY 2012
VL 69
IS 1
BP 80
EP 88
DI 10.1001/archgenpsychiatry.2011.108
PG 9
WC Psychiatry
SC Psychiatry
GA 870NH
UT WOS:000298675700010
PM 21893643
ER
PT J
AU Craft, S
Baker, LD
Montine, TJ
Minoshima, S
Watson, GS
Claxton, A
Arbuckle, M
Callaghan, M
Tsai, E
Plymate, SR
Green, PS
Leverenz, J
Cross, D
Gerton, B
AF Craft, Suzanne
Baker, Laura D.
Montine, Thomas J.
Minoshima, Satoshi
Watson, G. Stennis
Claxton, Amy
Arbuckle, Matthew
Callaghan, Maureen
Tsai, Elaine
Plymate, Stephen R.
Green, Pattie S.
Leverenz, James
Cross, Donna
Gerton, Brooke
TI Intranasal Insulin Therapy for Alzheimer Disease and Amnestic Mild
Cognitive Impairment A Pilot Clinical Trial
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID AMYLOID-BETA; RATING-SCALE; OLDER-ADULTS; HUMAN BRAIN; IN-VIVO;
MECHANISMS; PLASTICITY; INCREASES; OLIGOMERS; SEVERITY
AB Objective: To examine the effects of intranasal insulin administration on cognition, function, cerebral glucose metabolism, and cerebrospinal fluid biomarkers in adults with amnestic mild cognitive impairment or Alzheimer disease (AD).
Design: Randomized, double-blind, placebo-controlled trial.
Setting: Clinical research unit of a Veterans Affairs medical center.
Participants: The intent-to-treat sample consisted of 104 adults with amnestic mild cognitive impairment (n=64) or mild to moderate AD (n=40).
Intervention: Participants received placebo (n=30), 20 IU of insulin (n=36), or 40 IU of insulin (n=38) for 4 months, administered with a nasal drug delivery device (Kurve Technology, Bothell, Washington).
Main Outcome Measures: Primary measures consisted of delayed story recall score and the Dementia Severity Rating Scale score, and secondary measures included the Alzheimer Disease's Assessment Scale-cognitive subscale (ADAS-cog) score and the Alzheimer's Disease Cooperative Study-activities of daily living (ADCS-ADL) scale. A subset of participants underwent lumbar puncture (n=23) and positron emission tomography with fludeoxyglucose F 18 (n=40) before and after treatment.
Results: Outcome measures were analyzed using repeated-measures analysis of covariance. Treatment with 20 IU of insulin improved delayedmemory(P <.05), and both doses of insulin (20 and 40 IU) preserved caregiver-rated functional ability (P <.01). Both insulin doses also preserved general cognition as assessed by the ADAS-cog score for younger participants and functional abilities as assessed by the ADCS-ADL scale for adults with AD (P <.05). Cerebrospinal fluid biomarkers did not change for insulin-treated participants as a group, but, in exploratory analyses, changes in memory and function were associated with changes in the A beta 42 level and in the tau protein-to-A beta 42 ratio in cerebrospinal fluid. Placebo-assigned participants showed decreased fludeoxyglucose F 18 uptake in the parietotemporal, frontal, precuneus, and cuneus regions and insulin-minimized progression. No treatment-related severe adverse events occurred.
Conclusions: These results support longer trials of intranasal insulin therapy for patients with amnestic mild cognitive impairment and patients with AD.
C1 [Craft, Suzanne; Baker, Laura D.; Watson, G. Stennis; Claxton, Amy; Arbuckle, Matthew; Callaghan, Maureen; Plymate, Stephen R.] Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Seattle, WA 98108 USA.
[Leverenz, James; Gerton, Brooke] Vet Affairs Puget Sound Hlth Care Syst, Mental Illness Res Educ & Clin Ctr, Seattle, WA 98108 USA.
[Craft, Suzanne; Baker, Laura D.; Watson, G. Stennis; Claxton, Amy; Leverenz, James] Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Montine, Thomas J.] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA.
[Minoshima, Satoshi; Cross, Donna] Univ Washington, Sch Med, Dept Radiol, Seattle, WA 98195 USA.
[Tsai, Elaine; Plymate, Stephen R.; Green, Pattie S.] Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA.
[Leverenz, James; Gerton, Brooke] Univ Washington, Sch Med, Dept Neurol, Seattle, WA USA.
RP Craft, S (reprint author), Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr, S-182,1660 S Columbian Way, Seattle, WA 98108 USA.
EM scraft@uw.edu
FU National Institute of Aging [AG027415, P50 AG05136, T32 AG000258]; Nancy
and Buster Alvord Endowment; Department of Veterans Affairs
FX This research was supported by National Institute of Aging grants
AG027415 (to Dr Craft), P50 AG05136 (to Dr Montine), and T32 AG000258
(to Dr Claxton), the Nancy and Buster Alvord Endowment, and the
Department of Veterans Affairs. This material is the result of work
supported in part by resources from the Veterans Affairs Puget Sound
Health Care System, Seattle, Washington.
NR 31
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U1 17
U2 82
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD JAN
PY 2012
VL 69
IS 1
BP 29
EP 38
DI 10.1001/archneurol.2011.233
PG 10
WC Clinical Neurology
SC Neurosciences & Neurology
GA 874GX
UT WOS:000298944500004
PM 21911655
ER
PT J
AU Gorman, MP
Tillema, JM
Ciliax, AM
Guttmann, CRG
Chitnis, T
AF Gorman, Mark P.
Tillema, Jan-Mendelt
Ciliax, Annika M.
Guttmann, Charles R. G.
Chitnis, Tanuja
TI Daclizumab Use in Patients With Pediatric Multiple Sclerosis
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID ANTIBODY; THERAPY; NATALIZUMAB
AB Background: Daclizumab, a humanized monoclonal antibody specific for the interleukin 2 receptor alpha chain, reduces clinical and magnetic resonance imaging disease activity in patients with adult-onset multiple sclerosis (MS) as monotherapy or add-on therapy with interferon.
Objective: To report the use of daclizumab in pediatric-onset MS.
Design: Case series.
Setting: Two comprehensive pediatric MS centers.
Patients: Seven patients with pediatric-onset MS with clinical and magnetic resonance imaging disease activity despite first-line disease-modifying therapy.
Intervention: Intravenous daclizumab, 1 mg/kg monthly.
Main Outcome Measures: Annualized relapse rates, Expanded Disability Status Scale scores, contrast-enhancing lesions, and adverse effects.
Results: Treatment with daclizumab, primarily combined with interferon, was associated with reductions in annualized relapse rates and contrast-enhancing lesions and with reduction or stabilization of Expanded Disability Status Scale scores in each patient. However, 4 patients had relapses and new contrast-enhancing lesions during daclizumab treatment. No significant adverse effects occurred.
Conclusion: Daclizumab may be a safe and at least partially effective treatment option for patients with pediatric-onset MS with disease activity despite first-line disease-modifying therapy.
C1 [Gorman, Mark P.; Chitnis, Tanuja] Massachusetts Gen Hosp, Partners Pediat Multiple Sclerosis Ctr, Boston, MA 02114 USA.
[Gorman, Mark P.] Childrens Hosp Boston, Pediat Multiple Sclerosis & Related Disorders Pro, Boston, MA USA.
[Ciliax, Annika M.; Guttmann, Charles R. G.] Brigham & Womens Hosp, Ctr Neurol Imaging, Boston, MA 02115 USA.
[Tillema, Jan-Mendelt] Cincinnati Childrens Hosp Med Ctr, Div Neurol, Cincinnati, OH USA.
RP Chitnis, T (reprint author), Massachusetts Gen Hosp, Partners Pediat Multiple Sclerosis Ctr, ACC 708,55 Fruit St, Boston, MA 02114 USA.
EM tchitnis@partners.org
FU Teva Neuroscience; Merck-Serono; EMD-Serono; Pediatric Multiple
Sclerosis Centers of Excellence from the National Multiple Sclerosis
Society
FX Dr Guttman has served as a consultant for Tibotec Therapeutics/Johnson &
Johnson and has received research support from Teva Neuroscience. Dr
Chitnis has served as a consultant for Biogen-Idec, EMD-Serono, Teva
Neuroscience, and Novartis and has received salary support from
Merck-Serono and EMD-Serono.; This work was supported by the Pediatric
Multiple Sclerosis Centers of Excellence Grant from the National
Multiple Sclerosis Society.
NR 18
TC 17
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U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD JAN
PY 2012
VL 69
IS 1
BP 78
EP 81
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA 874GX
UT WOS:000298944500011
PM 22232346
ER
PT J
AU Sperling, R
Johnson, K
AF Sperling, Reisa
Johnson, Keith
TI To Sleep, Perchance to Delay Dementia
SO ARCHIVES OF NEUROLOGY
LA English
DT Editorial Material
ID ALZHEIMERS-DISEASE; APNEA; HYPOXIA
C1 [Sperling, Reisa; Johnson, Keith] Brigham & Womens Hosp, Dept Neurol, Ctr Alzheimer Res & Treatment, Boston, MA 02115 USA.
[Sperling, Reisa; Johnson, Keith] Harvard Univ, Sch Med, Boston, MA USA.
[Sperling, Reisa; Johnson, Keith] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Johnson, Keith] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Sperling, R (reprint author), Brigham & Womens Hosp, Dept Neurol, Ctr Alzheimer Res & Treatment, 221 Longwood Ave, Boston, MA 02115 USA.
EM reisa@.rics.bwh.harvard.edu
NR 10
TC 5
Z9 5
U1 2
U2 6
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD JAN
PY 2012
VL 69
IS 1
BP 118
EP 120
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 874GX
UT WOS:000298944500018
PM 22232352
ER
PT J
AU Goyal, S
Chauhan, SK
Dana, R
AF Goyal, Sunali
Chauhan, Sunil K.
Dana, Reza
TI Blockade of Prolymphangiogenic Vascular Endothelial Growth Factor C in
Dry Eye Disease
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Article
ID SJOGRENS-SYNDROME; INFLAMMATORY LYMPHANGIOGENESIS; ANGIOGENESIS; CELLS;
KERATOCONJUNCTIVITIS; HEMANGIOGENESIS; MACROPHAGES; TH17
AB Objective: To determine whether blocking prolymphangiogenic factors such as vascular endothelial growth factor C (VEGF-C) would suppress alloimmunity in dry eye disease using a murine model.
Methods: The effects of intraperitoneal injections of 400 mu g of anti-VEGF-C antibody (treated group) and intraperitoneal normal saline (untreated group) were studied in murine dry eyes induced by exposing mice to high-flow desiccated air in a controlled-environment chamber. Growth of lymphatic vessels and infiltration of macrophages were evaluated by immunohistochemistry using CD31 (panendothelial marker), lymphatic vessel endothelial receptor 1 (lymphatic endothelial marker), and CD11b (monocyte and macrophage marker). Real-time polymerase chain reaction was performed to quantify expression of different inflammatory cytokine transcripts in the conjunctiva and lymph nodes as well as vascular endothelial growth factors and their receptors (VEGF-A, VEGF-C, VEGF-D, VEGFR-2, and VEGFR-3) in the cornea.
Results: Blocking VEGF-C led to significant reductions in lymphatic caliber (P=.02) and lymphatic area (P=.006) in the corneas of mice with dry eye disease. In addition to significantly decreasing CD11b(+) cells (P=.005), anti-VEGF-C treatment significantly decreased transcript levels of VEGF-C (P=.002), VEGF-D (P=.01), and VEGFR-3 (P=.02) in the corneas of the treated group. A significant decrease in expression of inflammatory cytokines in the conjunctiva (interleukin 1 alpha, P=.003; interleukin 1 beta, P=.02; interleukin 6, P=.005) and lymph nodes (interferon gamma, P=.008; interleukin 17, P=.003) was also seen with anti-VEGF-C treatment.
Conclusion: Treatment with anti-VEGF-C led to significant improvement in dry eye disease, reflected by a decrease in inflammation at the clinical, molecular, and cellular levels.
Clinical Relevance: Targeting prolymphangiogenic growth factors or their receptors could inhibit the trafficking of antigen-presenting cells to the draining lymph nodes and hence prove to be a potential therapeutic target for dry eye disease.
C1 [Dana, Reza] Harvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
RP Dana, R (reprint author), Harvard Univ, Sch Med, Schepens Eye Res Inst, 20 Staniford St, Boston, MA 02114 USA.
EM reza.dana@schepens.harvard.edu
FU National Institutes of Health [EY20889]; Vegenics (Circadian
Technologies); Research to Prevent Blindness; Sjogren's Syndrome
Foundation
FX This work was supported in part by grant EY20889 from the National
Institutes of Health and by grants from Vegenics (Circadian
Technologies), the Lew R. Wasserman Research Award of Research to
Prevent Blindness (Dr Dana), and Sjogren's Syndrome Foundation (Dr
Chauhan).
NR 33
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U1 1
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD JAN
PY 2012
VL 130
IS 1
BP 84
EP 89
DI 10.1001/archophthalmol.2011.266
PG 6
WC Ophthalmology
SC Ophthalmology
GA 874LE
UT WOS:000298957900009
PM 21911653
ER
PT J
AU Stevenson, W
Chauhan, SK
Dana, R
AF Stevenson, William
Chauhan, Sunil K.
Dana, Reza
TI Dry Eye Disease An Immune-Mediated Ocular Surface Disorder
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Article
ID PRIMARY SJOGRENS-SYNDROME; FLOW-CYTOMETRIC ANALYSIS; NONPRESERVED
METHYLPREDNISOLONE THERAPY; CYCLOSPORINE OPHTHALMIC EMULSION;
INFLAMMATORY CYTOKINE EXPRESSION; DYSFUNCTIONAL TEAR SYNDROME; CORNEAL
EPITHELIAL-CELLS; TUMOR-NECROSIS-FACTOR; VERSUS-HOST-DISEASE;
DESICCATING STRESS
AB Dry eye disease is a multifactorial disorder of the tears and ocular surface characterized by symptoms of dryness and irritation. Although the pathogenesis of dry eye disease is not fully understood, it is recognized that inflammation has a prominent role in the development and propagation of this debilitating condition. Factors that adversely affect tear film stability and osmolarity can induce ocular surface damage and initiate an inflammatory cascade that generates innate and adaptive immune responses. These immunoinflammatory responses lead to further ocular surface damage and the development of a self-perpetuating inflammatory cycle. Herein, we review the fundamental links between inflammation and dry eye disease and discuss the clinical implications of inflammation in disease management. Arch Ophthalmol. 2012; 130(1):90-100
C1 [Dana, Reza] Harvard Univ, Sch Med, Dept Ophthalmol, Schepens Eye Res Inst, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
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
FU Sjogren's Syndrome Foundation; National Institutes of Health [EY20889]
FX This work was supported in part by the Sjogren's Syndrome Foundation (Dr
Chauhan) and by grant EY20889 from the National Institutes of Health (Dr
Dana).
NR 133
TC 120
Z9 123
U1 3
U2 18
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD JAN
PY 2012
VL 130
IS 1
BP 90
EP 100
PG 11
WC Ophthalmology
SC Ophthalmology
GA 874LE
UT WOS:000298957900010
PM 22232476
ER
PT J
AU Takusagawa, HL
Hunter, RS
Jue, A
Pasquale, LR
Chen, TC
AF Takusagawa, Hana L.
Hunter, Rebecca S.
Jue, Andrea
Pasquale, Louis R.
Chen, Teresa C.
TI Bilateral Uveal Effusion and Angle-Closure Glaucoma Associated With
Bupropion Use
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Letter
ID VENLAFAXINE
C1 [Chen, Teresa C.] Massachusetts Eye & Ear Infirm, Glaucoma Serv, Boston, MA 02114 USA.
[Jue, Andrea] New York Eye & Ear Infirm, New York, NY 10003 USA.
RP Chen, TC (reprint author), Massachusetts Eye & Ear Infirm, Glaucoma Serv, 243 Charles St, Boston, MA 02114 USA.
EM teresa_chen@meei.harvard.edu
NR 6
TC 6
Z9 6
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD JAN
PY 2012
VL 130
IS 1
BP 120
EP 122
PG 4
WC Ophthalmology
SC Ophthalmology
GA 874LE
UT WOS:000298957900019
PM 22232485
ER
PT J
AU Grossman, JM
Ranganath, VK
Chen, WL
Furst, DE
McMahon, M
Volkmann, E
Gordon, R
Deal, C
Caplan, L
Curtis, JR
Patkar, NM
Saag, KG
AF Grossman, Jennifer M.
Ranganath, Veena K.
Chen, Weiling
Furst, Daniel E.
McMahon, Maureen
Volkmann, Elizabeth
Gordon, Rebecca
Deal, Chad
Caplan, Liron
Curtis, Jeffrey R.
Patkar, Nivedita M.
Saag, Kenneth G.
TI Fracture risk in glucocorticoid-induced osteoporosis: comment on the
article by Grossman et al
SO ARTHRITIS CARE & RESEARCH
LA English
DT Letter
C1 [Grossman, Jennifer M.; Ranganath, Veena K.; Chen, Weiling; Furst, Daniel E.; McMahon, Maureen; Volkmann, Elizabeth; Gordon, Rebecca] Univ Calif Los Angeles, Los Angeles, CA 90024 USA.
[Gordon, Rebecca] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Deal, Chad] Cleveland Clin, Cleveland, OH 44106 USA.
[Caplan, Liron] Univ Colorado, Denver, CO 80202 USA.
[Curtis, Jeffrey R.; Patkar, Nivedita M.; Saag, Kenneth G.] Univ Alabama, Birmingham, AL USA.
RP Grossman, JM (reprint author), Univ Calif Los Angeles, Los Angeles, CA 90024 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 2151-464X
J9 ARTHRIT CARE RES
JI Arthritis Care Res.
PD JAN
PY 2012
VL 64
IS 1
BP 157
EP 158
DI 10.1002/acr.20650
PG 2
WC Rheumatology
SC Rheumatology
GA 868QB
UT WOS:000298536700025
ER
PT J
AU Cheng, S
Wang, N
Larson, MG
Palmisano, JN
Mitchell, GF
Benjamin, EJ
Vasan, RS
Levy, D
McCabe, EL
Vita, JA
Wang, TJ
Shaw, SY
Cohen, KS
Hamburg, NM
AF Cheng, Susan
Wang, Na
Larson, Martin G.
Palmisano, Joseph N.
Mitchell, Gary F.
Benjamin, Emelia J.
Vasan, Ramachandran S.
Levy, Daniel
McCabe, Elizabeth L.
Vita, Joseph A.
Wang, Thomas J.
Shaw, Stanley Y.
Cohen, Kenneth S.
Hamburg, Naomi M.
TI Circulating angiogenic cell populations, vascular function, and arterial
stiffness
SO ATHEROSCLEROSIS
LA English
DT Article
DE Angiogenesis; Vascular function; Risk factors; Endothelium; Epidemiology
ID ENDOTHELIAL PROGENITOR CELLS; CORONARY-HEART-DISEASE;
COLONY-FORMING-UNITS; BONE-MARROW; CARDIOVASCULAR RISK;
MONONUCLEAR-CELLS; AORTIC STIFFNESS; ADVANCING AGE; DYSFUNCTION; NUMBER
AB Objective: Several bone marrow-derived cell populations have been identified that may possess angiogenic activity and contribute to vascular homeostasis in experimental studies. We examined the extent to which lower quantities of these circulating angiogenic cell phenotypes may be related to impaired vascular function and greater arterial stiffness.
Methods: We studied 1948 Framingham Heart Study participants (mean age, 66 +/- 9 years; 54% women) who were phenotyped for circulating angiogenic cells: CD34+, CD34+/KDR+, and early outgrowth colony forming units (CFU). Participants underwent non-invasive assessments of vascular function including peripheral arterial tone (PAT), arterial tonometry, and brachial reactivity testing.
Results: In unadjusted analyses, higher CD34+ and CD34+/KDR+ concentrations were modestly associated with lower PAT ratio (beta = -0.052 +/- 0.011, P < 0.001 and beta = -0.030 +/- 0.011, P = 0.008, respectively) and with higher carotid-brachial pulse wave velocity (beta = 0.144 +/- 0.043, P = 0.001 and beta = 0.112 +/- 0.043, P = 0.009), but not with flow-mediated dilation; higher CD34+ was also associated with lower carotid-femoral pulse wave velocity (beta = -0.229 +/- 0.094, P = 0.015). However, only the association of lower CD34+ concentration with higher PAT ratio persisted in multivariable analyses that adjusted for standard cardiovascular risk factors. In all analyses, CFU was not associated with measures of vascular function or arterial stiffness.
Conclusions: In our large, community-based sample of men and women, circulating angiogenic cell phenotypes largely were not associated with measures of vascular function or arterial stiffness in analyses adjusting for traditional risk factors. (c) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Hamburg, Naomi M.] Boston Univ, Sch Med, Dept Med, Whitaker Cardiovasc Inst, Boston, MA 02118 USA.
[Cheng, Susan; Larson, Martin G.; Benjamin, Emelia J.; Vasan, Ramachandran S.; Levy, Daniel; Wang, Thomas J.; Hamburg, Naomi M.] Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Cheng, Susan] Brigham & Womens Hosp, Div Cardiovasc Med, Boston, MA 02115 USA.
[Mitchell, Gary F.] Cardiovasc Engn Inc, Norwood, MA USA.
[Wang, Na; Palmisano, Joseph N.; Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02118 USA.
[Wang, Na; Palmisano, Joseph N.; Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Data Coordinating Ctr, Boston, MA 02118 USA.
[Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02118 USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
[Benjamin, Emelia J.; Vasan, Ramachandran S.; Vita, Joseph A.; Hamburg, Naomi M.] Boston Univ, Sch Med, Evans Dept Med, Boston, MA 02118 USA.
[Benjamin, Emelia J.; Vasan, Ramachandran S.; Vita, Joseph A.; Hamburg, Naomi M.] Boston Univ, Sch Med, Prevent Med Sect, Boston, MA 02118 USA.
[Benjamin, Emelia J.; Vasan, Ramachandran S.; Vita, Joseph A.; Hamburg, Naomi M.] Boston Univ, Sch Med, Cardiol Sect, Boston, MA 02118 USA.
[McCabe, Elizabeth L.; Wang, Thomas J.; Shaw, Stanley Y.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Shaw, Stanley Y.] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Cohen, Kenneth S.] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
[Cohen, Kenneth S.] Univ Chicago, Med Ctr, Hematol Oncol Sect, Chicago, IL 60637 USA.
RP Hamburg, NM (reprint author), Boston Univ, Sch Med, Dept Med, Whitaker Cardiovasc Inst, 88 E Newton St C818, Boston, MA 02118 USA.
EM naomi.hamburg@bmc.org
OI Benjamin, Emelia/0000-0003-4076-2336; Hamburg,
Naomi/0000-0001-5504-5589; Vita, Joseph/0000-0001-5607-1797; Larson,
Martin/0000-0002-9631-1254; Ramachandran, Vasan/0000-0001-7357-5970
FU NIH/NHLBI [N01-HC25195]; NIH [1R01HL60040, 1R01HL70100, R01AG028321,
HL083197, HL083781, HL102299]; Ellison Foundation; Itamar Medical
FX The Framingham Heart Study is funded by NIH/NHLBI contract N01-HC25195.
The project was supported NIH grants 1R01HL60040 (EJB), 1R01HL70100
(EJB), R01AG028321 (EJB), and HL083197 (TJW). Dr. Hamburg is supported
by NIH grants HL083781 and HL102299. Dr. Cheng is supported by a grant
from the Ellison Foundation. The work was supported by an unrestricted
research grant to Dr. Benjamin from Itamar Medical. The grant was used
to conduct statistical analyses following guidelines established by the
National Heart, Lung, and Blood Institute:
http://www.nhlbi.nih.gov/funding/policies/thirdparty.htm.
NR 36
TC 3
Z9 3
U1 0
U2 6
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 JAN
PY 2012
VL 220
IS 1
BP 145
EP 150
DI 10.1016/j.atherosclerosis.2011.10.015
PG 6
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 866IU
UT WOS:000298374800024
PM 22093724
ER
PT J
AU Ueland, T
Smedbakken, LM
Hallen, J
Atar, D
Januzzi, JL
Halvorsen, B
Jensen, JK
Aukrust, P
AF Ueland, T.
Smedbakken, L. M.
Hallen, J.
Atar, D.
Januzzi, J. L.
Halvorsen, B.
Jensen, J. K.
Aukrust, P.
TI Soluble CXCL16 and long-term outcome in acute ischemic stroke
SO ATHEROSCLEROSIS
LA English
DT Article
DE CXCL16; Acute ischemic stroke; Long-term prognosis; Mortality
ID CORONARY-ARTERY-DISEASE; SCAVENGER RECEPTOR; SR-PSOX; INFLAMMATION;
ATHEROSCLEROSIS; CHEMOKINE; CXCL16/SR-PSOX; LIPOPROTEIN; MARKER; RISK
AB Objective: CXCL16 is a chemokine involved in atherosclerosis by promoting inflammation, lipid accumulation and matrix degradation. The level of circulating CXCL16 has been proposed as a predictor of long-term mortality in acute coronary syndromes. We studied plasma CXCL16 in acute ischemic stroke and examined associations with long-term mortality following the acute event.
Methods: CXCL16 samples were obtained from 244 patients with acute ischemic stroke (age: 69 +/- 13 years) daily from presentation to day 5 and at half a year after the stroke. Patients with overt ischemic heart disease and atrial fibrillation were excluded. The patients were followed for 47 months, with all-cause and cardiovascular (CV) mortality as end-points.
Results: At follow-up, 72 patients had died with 43 due to CV causes. Plasma CXCL16 was stably elevated in the first days after the acute event followed by a marked decrease after 6 months. In patients who subsequently suffered an adverse outcome, CXCL16 levels at 4 days after the initial event were elevated and were moderately associated with mortality. The increase in CXCL16 from day 1 to 4 was a predictor for all-cause and, in particular, CV mortality even after adjustment in the multivariate analysis for established risk factors such as age, the presence of heart/renal failure, troponin, C-reactive protein and stroke severity.
Conclusions: An increase in plasma CXCL16 during the first days after the initial event is associated with an adverse outcome in patients with acute ischemic stroke, supporting the potential pathogenic role of CXCL16 in atherosclerosis and vascular remodelling as well as their major clinical consequences. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Ueland, T.; Smedbakken, L. M.; Halvorsen, B.; Aukrust, P.] Univ Oslo, Rikshosp, Internal Med Res Inst, Oslo Univ Hosp, N-0027 Oslo, Norway.
[Aukrust, P.] Univ Oslo, Rikshosp, Oslo Univ Hosp, Sect Clin Immunol & Infect Dis, N-0027 Oslo, Norway.
[Hallen, J.; Atar, D.] Univ Oslo, Ulleval Hosp, Div Cardiol, Oslo, Norway.
[Ueland, T.; Atar, D.; Aukrust, P.] Univ Oslo, Fac Med, N-0027 Oslo, Norway.
[Jensen, J. K.] Odense Univ Hosp, Dept Cardiol, DK-5000 Odense, Denmark.
[Januzzi, J. L.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP Ueland, T (reprint author), Univ Oslo, Rikshosp, Internal Med Res Inst, Oslo Univ Hosp, Room D1-2017,Sognsvannsveien 20, N-0027 Oslo, Norway.
EM thor.ueland@medisin.uio.no
NR 23
TC 11
Z9 12
U1 2
U2 4
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0021-9150
EI 1879-1484
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD JAN
PY 2012
VL 220
IS 1
BP 244
EP 249
DI 10.1016/j.atherosclerosis.2011.10.004
PG 6
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 866IU
UT WOS:000298374800041
PM 22055341
ER
PT J
AU Smolderen, KG
Spertus, JA
Reid, KJ
Buchanan, DM
Vaccarino, V
Lichtman, JH
Bekelman, DB
Chan, PS
AF Smolderen, Kim G.
Spertus, John A.
Reid, Kimberly J.
Buchanan, Donna M.
Vaccarino, Viola
Lichtman, Judith H.
Bekelman, David B.
Chan, Paul S.
TI Association of Somatic and Cognitive Depressive Symptoms and Biomarkers
in Acute Myocardial Infarction: Insights from the Translational Research
Investigating Underlying Disparities in Acute Myocardial Infarction
Patients' Health Status Registry
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Coagulation; depressive symptoms; inflammation; mechanisms; myocardial
infarction; neurohormones
ID C-REACTIVE PROTEIN; ACUTE CORONARY SYNDROMES; BRAIN NATRIURETIC PEPTIDE;
HEART-RATE-VARIABILITY; N-TERMINAL PROATRIAL; CARDIOVASCULAR-DISEASE;
INFLAMMATORY BIOMARKERS; SICKNESS BEHAVIOR; NATIONAL-HEART; PROGNOSIS
AB Background: Somatic depressive symptoms and certain biomarkers are each associated with worse acute myocardial infarction (AMI) prognosis, but the relationship between depressive symptom domains and inflammatory, neurohormonal, and coagulation markers is unknown.
Methods: We examined the relationship between depressive symptoms and 1-month biomarker levels (high-sensitivity C-reactive protein [hs-CRP], N-terminal pro-brain natriuretic peptide [NT-proBNP], white blood cell [WBC], platelet counts) in 1265 AMI patients. Depressive symptoms (9-item Patient Health Questionnaire) were assessed during index hospitalization and categorized as somatic or cognitive. Using median regression models, the upper quartile of somatic and cognitive depression scores and each biomarker were compared with the lower three quartiles, adjusting for site, demographics, and clinical characteristics.
Results: Although hs-CRP values were higher in patients with somatic symptoms, this association was attenuated after adjustment (B(per SD increase) = .02, 95% confidence interval: .00; .05, p = .07). WBC count was independently associated with somatic depressive symptoms (B(per SD increase) = .28, 95% confidence interval: .12; .44, p = .001). Cognitive depressive symptoms were not associated with hs-CRP or WBC count. Neither dimension was associated with NT-proBNP or platelet levels. For each biomarker, the depression dimensions explained <1% of their variation.
Conclusions: Neither somatic nor cognitive depressive symptoms were meaningfully associated with hs-CRP, NT-proBNP, WBC, or platelet counts 1 month after AMI, suggesting that the association between depression and long-term outcomes may be unrelated to these biomarkers. Future research should explore other biomarkers to better illuminate pathways by which depression adversely impacts AMI prognosis.
C1 [Smolderen, Kim G.; Spertus, John A.; Reid, Kimberly J.; Buchanan, Donna M.; Chan, Paul S.] St Lukes Mid Amer Heart & Vasc Inst, Kansas City, MO 64111 USA.
[Smolderen, Kim G.] Tilburg Univ, Dept Med Psychol, Ctr Res Psychol Somat Dis, NL-5000 LE Tilburg, Netherlands.
[Spertus, John A.; Chan, Paul S.] Univ Missouri, Dept Med, Kansas City, MO 64110 USA.
[Spertus, John A.; Chan, Paul S.] Univ Missouri, Dept Biomed & Hlth Informat, Kansas City, MO 64110 USA.
[Vaccarino, Viola] Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, Atlanta, GA 30322 USA.
[Lichtman, Judith H.] Yale Univ, Sch Publ Hlth, Div Chron Dis Epidemiol, New Haven, CT USA.
[Bekelman, David B.] Denver Vet Affairs Med Ctr, Res Sect, Denver, CO USA.
[Bekelman, David B.] Denver Vet Affairs Med Ctr, Geriatr Sect, Denver, CO USA.
[Vaccarino, Viola] Emory Univ, Sch Med, Div Cardiol, Atlanta, GA 30322 USA.
RP Smolderen, KG (reprint author), St Lukes Mid Amer Heart & Vasc Inst, 4401 Wornall Rd, Kansas City, MO 64111 USA.
EM k.g.e.smolderen@gmail.com
RI Smolderen, Kim/B-8078-2015
FU National Heart, Lung, and Blood Institute Specialized Center of
Clinically Oriented Research in Cardiac Dysfunction and Disease [P50
HL077113]; CV Therapeutics, Palo Alto, California; American Heart
Association [AHA: 0875149N]; Netherlands Organization for Scientific
Research [916.11.179]
FX Grant support was received from the National Heart, Lung, and Blood
Institute Specialized Center of Clinically Oriented Research in Cardiac
Dysfunction and Disease (Grant number P50 HL077113) and CV Therapeutics,
Palo Alto, California. Dr. Smolderen was supported by the Outcomes
Research postdoctoral fellowship awarded by the American Heart
Association Pharmaceutical Roundtable and David and Stevie Spina (Grant
number AHA: 0875149N) and by The Netherlands Organization for Scientific
Research (Veni Grant number: 916.11.179).
NR 50
TC 8
Z9 9
U1 2
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD JAN 1
PY 2012
VL 71
IS 1
BP 22
EP 29
DI 10.1016/j.biopsych.2011.07.029
PG 8
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 863BI
UT WOS:000298137400007
PM 21903199
ER
PT J
AU Roosen, A
Woodhouse, CRJ
Wood, DN
Stief, CG
McDougal, WS
Gerharz, EW
AF Roosen, Alexander
Woodhouse, Christopher R. J.
Wood, Daniel N.
Stief, Christian G.
McDougal, W. Scott
Gerharz, Elmar W.
TI Animal models in urinary diversion
SO BJU INTERNATIONAL
LA English
DT Review
DE urinary diversion; urinary reservoirs; continent; models; animal; rat;
dog
ID ANTIREFLUX URETEROILEAL ANASTOMOSIS; SEROSALIZED MUSCLE LAYER; FETAL
SHEEP BLADDER; CHRONIC UREMIC RATS; INTESTINAL SEGMENTS; AUGMENTATION
CYSTOPLASTY; PORCINE MODEL; ILEAL VALVE; URETEROINTESTINAL ANASTOMOSIS;
METABOLIC-ACIDOSIS
AB We set out to critically assess the value of animal experimentation in urinary diversion through intestinal segments, as some authors question the effectiveness of animal research, criticising the methodological quality, lack of standardization, inadequate reporting and the few systematic reviews in this fi eld. Based on a comprehensive MEDLINE literature search ( MeSH database; search terms: urinary diversion, urinary reservoirs, continent, rat, dog, animal models) we retrieved and evaluated all full- length papers published in English, German, French, and Spanish languages from 1966 to 2011 reporting the use of animal models in the setting of urinary diversion. Studies were stratifi ed according to the addressed research question. Within each category species, gender, number of animals, age at procedure, type of diversion, mortality, length of follow- up, experimental procedure and outcome were recorded and tabulated. In all, 159 articles were judged to be relevant and while there are numerous animal models only a few have been used in more than one study. Animals were used for the systematic study of new surgical techniques ( 93 articles) or metabolic and functional consequences of urinary reconstruction ( 66 articles). For the latter purpose, the most often used animal is the rat, whereas the dog model is preferred for technical experimentation. In many studies, the validity of the model is at least questionable. Animal experiments have repeatedly been conducted addressing the same question, often with striking discrepancies in outcome. Animal studies were even performed after a surgical technique had been pioneered in humans. The use of animal models in urinary diversion is far from standardized rendering the results less than ideal for comparison across studies. Due to differences in anatomy and physiology, the applicability of fi ndings in animal experiments to clinical urology is limited. Continued effort is needed to optimise the use of animal models in experimental urology.
C1 [Roosen, Alexander; Stief, Christian G.] Univ Munich, Dept Urol, Sch Med, D-81377 Munich, Germany.
[Woodhouse, Christopher R. J.; Wood, Daniel N.] UCL, Ctr Urol, London, England.
[McDougal, W. Scott] Massachusetts Gen Hosp, Urol Serv, Boston, MA 02114 USA.
[Gerharz, Elmar W.] Frankfurt Urol Associates, Frankfurt, Germany.
RP Roosen, A (reprint author), Univ Munich, Dept Urol, Sch Med, Marchioninistr 15, D-81377 Munich, Germany.
EM a_roosen@hotmail.com
NR 163
TC 3
Z9 3
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1464-4096
J9 BJU INT
JI BJU Int.
PD JAN
PY 2012
VL 109
IS 1
BP 6
EP 23
DI 10.1111/j.1464-410X.2011.10494.x
PG 18
WC Urology & Nephrology
SC Urology & Nephrology
GA 862AU
UT WOS:000298063000005
PM 21917109
ER
PT J
AU Singh, H
Giardina, TD
Petersen, LA
Smith, MW
Paul, LW
Dismukes, K
Bhagwath, G
Thomas, EJ
AF Singh, Hardeep
Giardina, Traber Davis
Petersen, Laura A.
Smith, Michael W.
Paul, Lindsey Wilson
Dismukes, Key
Bhagwath, Gayathri
Thomas, Eric J.
TI Exploring situational awareness in diagnostic errors in primary care
SO BMJ QUALITY & SAFETY
LA English
DT Article
ID PATIENT SAFETY; MALPRACTICE CLAIMS; DECISION-MAKING; MISSED
OPPORTUNITIES; CANCER DIAGNOSIS; DYNAMIC-SYSTEMS; ADVERSE EVENTS;
MEDICINE; STRATEGIES; COGNITION
AB Objective: Diagnostic errors in primary care are harmful but poorly studied. To facilitate the understanding of diagnostic errors in real-world primary care settings that use electronic health records (EHRs), this study explored the use of the situational awareness (SA) framework from aviation human factors research.
Methods: A mixed-methods study was conducted involving reviews of EHR data followed by semi-structured interviews of selected providers from two institutions in the USA. The study population included 380 consecutive patients with colorectal and lung cancers diagnosed between February 2008 and January 2009. Using a pre-tested data collection instrument, trained physicians identified diagnostic errors, defined as lack of timely action on one or more established indications for diagnostic work-up for lung and colorectal cancers. Twenty-six providers involved in cases with and without errors were interviewed. Interviews probed for providers' lack of SA and how this may have influenced the diagnostic process.
Results: Of 254 cases meeting inclusion criteria, errors were found in 30 of 92 (32.6%) lung cancer cases and 56 of 167 (33.5%) colorectal cancer cases. Analysis of interviews related to error cases revealed evidence of lack of one of four levels of SA applicable to primary care practice: information perception, information comprehension, forecasting future events, and choosing appropriate action based on the first three levels. In cases without error, application of the SA framework provided insight into processes involved in attention management.
Conclusions: A framework of SA can help analyse and understand diagnostic errors in primary care settings that use EHRs.
C1 [Singh, Hardeep; Giardina, Traber Davis; Petersen, Laura A.; Smith, Michael W.] Baylor Coll Med, Houston VA HSR&D Ctr Excellence, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
[Singh, Hardeep; Giardina, Traber Davis; Petersen, Laura A.; Smith, Michael W.] Baylor Coll Med, Dept Med, Sect Hlth Serv Res, Houston, TX 77030 USA.
[Paul, Lindsey Wilson] Univ Texas Austin, Sch Social Work, Austin, TX 78712 USA.
[Dismukes, Key] NASA, Ames Res Ctr, Moffett Field, CA 94035 USA.
[Bhagwath, Gayathri] Univ Texas Galveston, Med Branch, Dept Internal Med, Div Hematol Oncol, Galveston, TX 77550 USA.
[Thomas, Eric J.] Univ Texas Houston, Sch Med, Dept Med, Div Gen Med, Houston, TX 77030 USA.
[Thomas, Eric J.] Univ Texas Houston, Sch Med, Mem Hermann Ctr Healthcare Qual, Houston, TX USA.
RP Singh, H (reprint author), Med Ctr 152, 2002 Holcombe Blvd, Houston, TX 77030 USA.
EM hardeeps@bcm.edu
OI Davis Giardina, Traber/0000-0002-9184-6524
FU NIH [K23CA125585]; Houston VA HSR&D Center of Excellence [HFP90-020]
FX This study was supported by an NIH K23 career development award
(K23CA125585) to Dr Singh, and in part by the Houston VA HSR&D Center of
Excellence (HFP90-020). These sources had no role in the design and
conduct of the study; collection, management, analysis, and
interpretation of the data; and preparation, review, or approval of the
manuscript.
NR 77
TC 19
Z9 20
U1 4
U2 14
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 2044-5415
J9 BMJ QUAL SAF
JI BMJ Qual. Saf.
PD JAN
PY 2012
VL 21
IS 1
BP 30
EP 38
DI 10.1136/bmjqs-2011-000310
PG 9
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 862ZZ
UT WOS:000298133900005
PM 21890757
ER
PT J
AU Chirgwin, J
Sun, ZX
Smith, I
Price, KN
Thurlimann, B
Ejlertsen, B
Bonnefoi, H
Regan, MM
Goldhirsch, A
Coates, AS
AF Chirgwin, Jacquie
Sun, Zhuoxin
Smith, Ian
Price, Karen N.
Thuerlimann, Beat
Ejlertsen, Bent
Bonnefoi, Herve
Regan, Meredith M.
Goldhirsch, Aron
Coates, Alan S.
CA BIG 1-98 Collaborative Int Breast
TI The advantage of letrozole over tamoxifen in the BIG 1-98 trial is
consistent in younger postmenopausal women and in those with
chemotherapy-induced menopause
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Aromatase inhibitor; Menopause; Hormonal therapy; Letrozole; Tamoxifen;
Chemotherapy-induced amenorrhea
ID BREAST-CANCER PATIENTS; AROMATASE INHIBITORS; PREMENOPAUSAL WOMEN;
ADJUVANT CHEMOTHERAPY; INDUCED AMENORRHEA; THERAPY; DOCETAXEL; CAUTION;
TAXANE; IMPACT
AB Letrozole, an aromatase inhibitor, is ineffective in the presence of ovarian estrogen production. Two subpopulations of apparently postmenopausal women might derive reduced benefit from letrozole due to residual or returning ovarian activity: younger women (who have the potential for residual subclinical ovarian estrogen production), and those with chemotherapy-induced menopause who may experience return of ovarian function. In these situations tamoxifen may be preferable to an aromatase inhibitor. Among 4,922 patients allocated to the monotherapy arms (5 years of letrozole or tamoxifen) in the BIG 1-98 trial we identified two relevant subpopulations: patients with potential residual ovarian function, defined as having natural menopause, treated without adjuvant or neoadjuvant chemotherapy and age acurrency sign55 years (n = 641); and those with chemotherapy-induced menopause (n = 105). Neither of the subpopulations examined showed treatment effects differing from the trial population as a whole (interaction P values are 0.23 and 0.62, respectively). Indeed, both among the 641 patients aged acurrency sign55 years with natural menopause and no chemotherapy (HR 0.77 [0.51, 1.16]) and among the 105 patients with chemotherapy-induced menopause (HR 0.51 [0.19, 1.39]), the disease-free survival (DFS) point estimate favoring letrozole was marginally more beneficial than in the trial as a whole (HR 0.84 [0.74, 0.95]). Contrary to our initial concern, DFS results for young postmenopausal patients who did not receive chemotherapy and patients with chemotherapy-induced menopause parallel the letrozole benefit seen in the BIG 1-98 population as a whole. These data support the use of letrozole even in such patients.
C1 [Chirgwin, Jacquie] Australian New Zealand Breast Canc Trials Grp, Newcastle, NSW, Australia.
[Chirgwin, Jacquie] Monash Univ, Box Hill & Maroondah Hosp, Melbourne, Vic 3004, Australia.
[Sun, Zhuoxin] Dana Farber Canc Inst, Ctr Stat, Int Breast Canc Study Grp, Boston, MA 02115 USA.
[Smith, Ian] Royal Marsden Hosp, Inst Canc Res, London SW3 6JJ, England.
[Price, Karen N.] Frontier Sci & Technol Res Fdn Inc, Ctr Stat, Int Breast Canc Study Grp, Boston, MA USA.
[Thuerlimann, Beat] Kantonsspital St Gallen, Breast Ctr, St Gallen, Switzerland.
[Thuerlimann, Beat] Swiss Grp Clin Canc Res SAKK, Bern, Switzerland.
[Ejlertsen, Bent] Rigshosp, Danish Breast Canc Cooperat Grp DBCG, DK-2100 Copenhagen, Denmark.
[Bonnefoi, Herve] Univ Bordeaux, FNCLCC Unicancer, INSERM, Inst Bergonie,U916, Bordeaux, France.
[Regan, Meredith M.] Harvard Univ, Sch Med, Boston, MA USA.
[Regan, Meredith M.] Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Int Breast Canc Study Grp IBCSG,Stat Ctr,Dept Bio, Boston, MA 02115 USA.
RP Chirgwin, J (reprint author), Australian New Zealand Breast Canc Trials Grp, Newcastle, NSW, Australia.
EM chirgwin@tpg.com.au; zhuoxin@jimmy.harvard.edu; Ian.Smith@rmh.nhs.uk;
price@jimmy.harvard.edu; beat.thuerlimann@kssg.ch;
bent.ejlertsen@rh.regionh.dk; bonnefoi@bergonie.org;
mregan@jimmy.harvard.edu; aron.goldhirsch@ibcsg.org;
alan.coates@ibcsg.org
RI Munzone, Elisabetta/G-8848-2011; Cheuk, Robyn/H-1944-2013; Rimassa,
Lorenza/N-4884-2016; Sedlackova, Eva/B-9959-2017; GLADIEFF,
Laurence/O-5129-2014; Wardley, ANdrew/N-8135-2015; Wyld,
David/B-8893-2015; Gonzalez Larriba, Jose Luis/G-6177-2016; Petruzelka,
Lubos/A-2750-2017
OI Segelov, Eva/0000-0002-4410-6144; Cheuk, Robyn/0000-0001-9516-5526;
Rimassa, Lorenza/0000-0001-9957-3615; Sedlackova,
Eva/0000-0002-0089-1611; GLADIEFF, Laurence/0000-0002-6980-9719;
Wardley, ANdrew/0000-0002-9639-0888; Wyld, David/0000-0001-9523-4333;
Walpole, Euan/0000-0001-6105-9039; Gonzalez Larriba, Jose
Luis/0000-0003-2631-0309; Petruzelka, Lubos/0000-0002-4397-0635
FU Novartis; IBCSG: Swedish Cancer Society; Cancer Council Australia;
Australian New Zealand Breast Cancer Trials Group; Frontier Science and
Technology Research Foundation; Swiss Group for Clinical Cancer Research
(SAKK; National Cancer Institute [CA-75362]; Cancer Research
Switzerland/Oncosuisse; Foundation for Clinical Cancer Research of
Eastern Switzerland (OSKK)
FX We thank the patients, physicians, nurses, and data managers who
participated in the BIG 1-98 clinical trial. The BIG 1-98 trial was
financed by Novartis and coordinated by IBCSG. Support for the IBCSG:
Swedish Cancer Society, The Cancer Council Australia, Australian New
Zealand Breast Cancer Trials Group, Frontier Science and Technology
Research Foundation, Swiss Group for Clinical Cancer Research (SAKK),
National Cancer Institute Grant CA-75362, Cancer Research
Switzerland/Oncosuisse, and the Foundation for Clinical Cancer Research
of Eastern Switzerland (OSKK). Clinicaltrials.gov ID = NCT00004205.
NR 26
TC 7
Z9 7
U1 3
U2 14
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 JAN
PY 2012
VL 131
IS 1
BP 295
EP 306
DI 10.1007/s10549-011-1741-6
PG 12
WC Oncology
SC Oncology
GA 861GB
UT WOS:000298006300030
PM 21892704
ER
PT J
AU Ligibel, JA
O'Malley, AJ
Fisher, M
Daniel, GW
Winer, EP
Keating, NL
AF Ligibel, Jennifer A.
O'Malley, A. James
Fisher, Maxine
Daniel, Gregory W.
Winer, Eric P.
Keating, Nancy L.
TI Risk of myocardial infarction, stroke, and fracture in a cohort of
community-based breast cancer patients
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Aromatase inhibitor; Breast cancer; Fracture; Myocardial infarction;
Stroke; Tamoxifen
ID POSTMENOPAUSAL WOMEN; TAMOXIFEN THERAPY; RANDOMIZED-TRIAL; ADHERENCE;
ANASTROZOLE; MORTALITY; OUTCOMES; PROJECT; CARE
AB Clinical trials suggest that increased risk of osteoporosis and fracture are the only serious side effects of adjuvant aromatase inhibitors (AIs), but little is known regarding toxicities of AIs in non-trial populations. We evaluated whether use of AIs was associated with myocardial infarction, stroke, and fracture in a community-based population. Using data from the HealthCore Integrated Research Database, 44,463 women aged a parts per thousand yen50 years with a parts per thousand yen2 breast cancer diagnosis codes between 2001 and 2007 were followed through 2008. Of these, 44,026 were matched using propensity score methods to women aged a parts per thousand yen50 years with no breast cancer codes. We assessed whether treatment with AIs was associated with myocardial infarction, stroke, and fracture using Cox proportional hazards models with time-varying treatment variables. Among breast cancer patients, 68.7% received no hormonal therapy, 20.6% received AIs (15.8% received only AIs, 4.8% were also treated with tamoxifen), and 10.7% received tamoxifen only. Breast cancer patients on AIs had a higher risk of any fracture (AHR = 1.13, 95% CI = 1.02-1.25) than breast cancer patients not receiving hormonal therapy. Patients on tamoxifen had a lower risk of hip fracture (AHR = 0.51, 95% CI = 0.32-0.81) than breast cancer patients not receiving hormonal therapy. Rates of myocardial infarction and stroke for patients on AIs or tamoxifen did not differ significantly from breast cancer patients not on therapy. The side effect profile of AIs in this community-based population was similar to that seen in clinical trials. These findings provide reassurance that AIs appear to be associated with few serious side effects.
C1 [O'Malley, A. James; Keating, Nancy L.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Ligibel, Jennifer A.; Winer, Eric P.] Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA 02115 USA.
[Fisher, Maxine; Daniel, Gregory W.] HealthCore Inc, Wilmington, DE USA.
[Keating, Nancy L.] Brigham & Womens Hosp, Div Gen Internal Med, Boston, MA 02115 USA.
RP Keating, NL (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
EM keating@hcp.med.harvard.edu
FU National Institutes of Health [R01 CA127652]
FX This study was funded by the National Institutes of Health (R01 CA127652
to Dr. Keating).
NR 28
TC 8
Z9 8
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD JAN
PY 2012
VL 131
IS 2
BP 589
EP 597
DI 10.1007/s10549-011-1754-1
PG 9
WC Oncology
SC Oncology
GA 871QG
UT WOS:000298752200023
PM 21881937
ER
PT J
AU Beasley, JM
Kwan, ML
Chen, WY
Weltzien, EK
Kroenke, CH
Lu, W
Nechuta, SJ
Cadmus-Bertram, L
Patterson, RE
Sternfeld, B
Shu, XO
Pierce, JP
Caan, BJ
AF Beasley, Jeannette M.
Kwan, Marilyn L.
Chen, Wendy Y.
Weltzien, Erin K.
Kroenke, Candyce H.
Lu, Wei
Nechuta, Sarah J.
Cadmus-Bertram, Lisa
Patterson, Ruth E.
Sternfeld, Barbara
Shu, Xiao-Ou
Pierce, John P.
Caan, Bette J.
TI Meeting the physical activity guidelines and survival after breast
cancer: findings from the after breast cancer pooling project
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Physical activity guidelines; Breast cancer survival; Mortality;
Epidemiology
ID ACTIVITY QUESTIONNAIRE; WOMENS HEALTH; REPRODUCIBILITY; VALIDATION;
DIAGNOSIS; MORTALITY; VALIDITY; COHORT; DIET; LIFE
AB The 2008 Physical Activity (PA) Guidelines recommend engaging in at least 2.5 h (10 MET-hours/week) of moderate intensity PA per week (defined as 4 METs) to reduce risk of morbidity and mortality. This analysis was conducted to investigate whether this recommendation can be extended to breast cancer survivors. Data from four studies of breast cancer survivors measuring recreational PA from semi-quantitative questionnaires a median of 23 months post-diagnosis (interquartile range 18-32 months) were pooled in the After Breast Cancer Pooling Project (n = 13,302). Delayed entry Cox proportional hazards models were applied in data analysis with adjustment for age, post-diagnosis body mass index, race/ethnicity, menopausal status, TNM stage, cancer treatment, and smoking history. Engaging in at least 10 MET-hours/week of PA was associated with a 27% reduction in all-cause mortality (n = 1,468 events, Hazard Ratio (HR) = 0.73, 95% CI, 0.66-0.82) and a 25% reduction in breast cancer mortality (n = 971 events, HR = 0.75, 95% CI 0.65-0.85) compared with women who did not meet the PA Guidelines (< 10 MET-hours/week). Risk of breast cancer recurrence (n = 1,421 events) was not associated with meeting the PA Guidelines (HR = 0.96, 95% CI, 0.86-1.06). These data suggest that adhering to the PA guidelines may be an important intervention target for reducing mortality among breast cancer survivors.
C1 [Beasley, Jeannette M.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Kwan, Marilyn L.; Weltzien, Erin K.; Kroenke, Candyce H.; Sternfeld, Barbara; Caan, Bette J.] Kaiser Permanente Div Res, Oakland, CA 94612 USA.
[Chen, Wendy Y.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Chen, Wendy Y.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Lu, Wei] Shanghai Ctr Dis Control & Prevent, Shanghai, Peoples R China.
[Nechuta, Sarah J.; Shu, Xiao-Ou] Vanderbilt Univ, Nashville, TN 37203 USA.
[Cadmus-Bertram, Lisa; Patterson, Ruth E.; Pierce, John P.] Univ Calif San Diego, Moores UCSD Canc Ctr, Canc Prevent & Control Program, San Diego, CA 92093 USA.
RP Beasley, JM (reprint author), Fred Hutchinson Canc Res Ctr, 1000 Fairview Ave,N M3-A410, Seattle, WA 98109 USA.
EM jbeasley@whi.org
OI Beasley, Jeannette/0000-0002-9343-6895
FU National Cancer Institute [3R01CA118229-03S1]
FX Joan Schwalbe contributed substantively to the data analysis. This study
was supported by the National Cancer Institute (Grant number
3R01CA118229-03S1). The parent grants for each individual cohort
included in the After Breast Cancer Pooling Project are: LACE (National
Cancer Institute, R01 CA129059), NHS (P01 CA87969), SBCSS (Department of
Defense, DAMD 17-02-1-0607 and National Cancer Institute, R01 CA118229),
and WHEL (Susan G. Komen Foundation, #KG100988).
NR 28
TC 51
Z9 51
U1 0
U2 8
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 JAN
PY 2012
VL 131
IS 2
BP 637
EP 643
DI 10.1007/s10549-011-1770-1
PG 7
WC Oncology
SC Oncology
GA 871QG
UT WOS:000298752200028
PM 21935600
ER
PT J
AU Panageas, KS
Sima, CS
Liberman, L
Schrag, D
AF Panageas, K. S.
Sima, C. S.
Liberman, L.
Schrag, D.
TI Use of high technology imaging for surveillance of early stage breast
cancer
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Breast cancer surveillance; High technology imaging; SEER-Medicare
ID FOLLOW-UP; RANDOMIZED-TRIAL; SURVIVAL; UPDATE
AB Guidelines do not support utilization of high technology radiologic imaging (HTRI) for surveillance after curative treatment for early stage breast cancer. Surveillance, Epidemiology, and End Results (SEER)-Medicare linked data were used to identify 25,555 women diagnosed with stage I-II breast cancer between 1998 and 2003 who survived a parts per thousand yen48 months from diagnosis without evidence of second primary or recurrent cancer in this interval. HTRI utilization (computerized tomography scanning (CT), bone scan (BS), breast magnetic resonance imaging, and positron emission tomography scans) was measured in months 13-48 post-diagnosis. Cases were individually matched to 75,669 female Medicare enrollees without cancer. Factors associated with HTRI utilization were evaluated. Forty percent of women with stage I-II breast cancer and 25% of controls had a parts per thousand yen1 HTRI during the surveillance interval (P < 0.001). High utilization rates were observed for CT (30%) and BSs (19%). The proportion of women who had a CT during the surveillance period increased in both cancer survivors and controls. Among breast cancer cases age < 80, higher comorbidity index, stage II disease, and more recent diagnosis were independently associated with receipt of HTRI. Paralleling patterns observed in controls, HTRI utilization for surveillance following diagnosis of early stage breast cancer has steadily increased among Medicare beneficiaries. Strategies to foster judicious utilization of HTRI should be a priority.
C1 [Panageas, K. S.; Sima, C. S.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[Liberman, L.] Mem Sloan Kettering Canc Ctr, Dept Radiol, New York, NY 10021 USA.
[Schrag, D.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Panageas, KS (reprint author), Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, 307 E 63rd St,3rd Floor, New York, NY 10021 USA.
EM panageak@mskcc.org
NR 28
TC 11
Z9 13
U1 0
U2 0
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 JAN
PY 2012
VL 131
IS 2
BP 663
EP 670
DI 10.1007/s10549-011-1773-y
PG 8
WC Oncology
SC Oncology
GA 871QG
UT WOS:000298752200031
PM 21947679
ER
PT J
AU Moran, MS
Bai, HX
Harris, EER
Arthur, DW
Bailey, L
Bellon, JR
Carey, L
Goyal, S
Halyard, MY
Horst, KC
MacDonald, SM
Haffty, BG
AF Moran, Meena S.
Bai, Harrison X.
Harris, Eleanor E. R.
Arthur, Douglas W.
Bailey, Lisa
Bellon, Jennifer R.
Carey, Lisa
Goyal, Sharad
Halyard, Michele Y.
Horst, Kathleen C.
MacDonald, Shannon M.
Haffty, Bruce G.
TI ACR Appropriateness Criteria (R) Ductal Carcinoma in Situ
SO BREAST JOURNAL
LA English
DT Article
DE ACR appropriateness criteria; breast conservation therapy; ductal
carcinoma in situ; guidelines; radiation therapy
ID SURGICAL ADJUVANT BREAST; RADIOTHERAPY; TRIAL; CANCER; WOMEN
AB Ductal carcinoma in situ (DCIS) describes a wide spectrum of non-invasive tumors which carry a significant risk of invasive relapse, thus prevention of local recurrence is vital. For appropriate patients with limited disease, management with breast conserving surgery (BCS) followed by whole-breast radiation (RT) is supported by multiple Phase III studies, but mastectomy may be appropriate in selected patients. Omission of RT may also be reasonable in some patients, though which criteria are to be utilized remain unclear, and the existing data are contradictory with limited follow-up. Various RT techniques such as boost to the tumor bed, partial breast radiation or hypofractionated, whole-breast RT are increasingly utilized but the data to support their use specifically in DCIS is limited. Tamoxifen also increases local control for ER + DCIS, adding to the complexity of the local treatment management. This article reviews the existing scientific evidence, the controversies surrounding local management, and clinical guidelines for DCIS based on the group consensus by the ACR Breast Expert Panel. The American College of Radiology Appropriateness Criteria are evidence-based guidelines for specific clinical conditions that are reviewed every 2 years by a multidisciplinary expert panel. The guideline development and review include an extensive analysis of current medical literature from peer-reviewed journals and the application of a well established consensus methodology (modified Delphi) to rate the appropriateness of imaging and treatment procedures by the panel. In those instances where evidence is lacking or not definitive, expert opinion may be used to recommend imaging or treatment.
C1 [Moran, Meena S.; Bai, Harrison X.] Yale Univ, Sch Med, New Haven, CT USA.
[Harris, Eleanor E. R.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Arthur, Douglas W.] Virginia Commonwealth Univ, Med Coll Virginia, Richmond, VA 23298 USA.
[Bailey, Lisa] Alta Bates Summit Med Ctr, Oakland, CA USA.
[Bellon, Jennifer R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Carey, Lisa] Univ N Carolina Hlth Care Syst, Chapel Hill, NC USA.
[Goyal, Sharad; Haffty, Bruce G.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, New Brunswick, NJ USA.
[Halyard, Michele Y.] Mayo Clin, Scottsdale, AZ USA.
[Horst, Kathleen C.] Stanford Univ, Sch Med, Stanford, CA USA.
[MacDonald, Shannon M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Moran, MS (reprint author), Amer Coll Radiol, 1891 Preston White Dr, Reston, VA 20191 USA.
EM meena.moran@yale.edu
OI Harris, Eleanor/0000-0002-7529-7473
NR 11
TC 10
Z9 10
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1075-122X
J9 BREAST J
JI Breast J.
PD JAN-FEB
PY 2012
VL 18
IS 1
BP 8
EP 15
DI 10.1111/j.1524-4741.2011.01197.x
PG 8
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 873WX
UT WOS:000298916200003
PM 22107336
ER
PT J
AU Barkley, C
Burstein, H
Smith, B
Bellon, J
Wong, J
Gadd, M
Taghian, A
Winer, E
Iglehart, JD
Harris, J
Golshan, M
AF Barkley, Christina
Burstein, Harold
Smith, Barbara
Bellon, Jennifer
Wong, Julia
Gadd, Michele
Taghian, Alphonse
Winer, Eric
Iglehart, James Dirk
Harris, Jay
Golshan, Mehra
TI Can Axillary Node Dissection Be Omitted in a Subset of Patients with Low
Local and Regional Failure Rates?
SO BREAST JOURNAL
LA English
DT Article
DE axillary node dissection; breast cancer; sentinel node biopsy
ID SENTINEL LYMPH-NODE; BREAST-CANCER PATIENTS; BIOPSY; METASTASES;
RECURRENCE; NOMOGRAM; MICROMETASTASES; PREDICTION; LIKELIHOOD; SURGERY
AB Axillary node dissection (ALND) is the standard of care for patients who have a positive sentinel lymph node (SLN) on sentinel lymph node biopsy (SLNB). We sought to identify a low-risk patient population with positive SLN that may not need cALND. We analyzed SLNB for breast cancer at our institutions between 1999 and 2007. We identified 130 patients who had a positive SLN but did not undergo completion ALND. We evaluated clinical data, adjuvant treatment patterns and intermediate locoregional and distant events. The median patient age was 50; 19% had N0(i+) disease, 53% had micrometastatic (N1mi) disease, and 28% had macrometastasis. Eighty-eight percent of patients underwent radiation therapy; 66 patients (51%) had documented nodal radiation (of these 50 were treated with three fields and 14 with high tangents. Local recurrence in the breast occurred in two patients (2%) and nine patients (7%) developed distant metastases; there were no axillary/nodal recurrences. In this highly selected group of patients who had a positive SLNB but did not undergo cALND, we observed no axillary recurrences.
C1 [Barkley, Christina; Iglehart, James Dirk; Golshan, Mehra] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Burstein, Harold; Winer, Eric] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Smith, Barbara; Gadd, Michele] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Bellon, Jennifer; Wong, Julia; Harris, Jay] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
[Taghian, Alphonse] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
RP Golshan, M (reprint author), Brigham & Womens Hosp, Dept Surg, 75 Francis St, Boston, MA 02115 USA.
EM mgolshan@partners.org
NR 34
TC 5
Z9 5
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1075-122X
J9 BREAST J
JI Breast J.
PD JAN-FEB
PY 2012
VL 18
IS 1
BP 23
EP 27
DI 10.1111/j.1524-4741.2011.01178.x
PG 5
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 873WX
UT WOS:000298916200005
PM 22017599
ER
PT J
AU Warren, LE
Mendlinger, SE
Corso, KA
Greenberg, CC
AF Warren, Laura E.
Mendlinger, Sheryl E.
Corso, Katherine A.
Greenberg, Caprice C.
TI A Model of Knowledge Acquisition in Early Stage Breast Cancer Patients
SO BREAST JOURNAL
LA English
DT Article
DE breast cancer; decision-making; knowledge acquisition
ID DECISION-MAKING; RECONSTRUCTION; MASTECTOMY; SURGERY; WOMEN;
POSTMASTECTOMY; CONSERVATION; CHOICE; IMPACT
AB To meaningfully participate in the decision-making regarding a newly diagnosed breast cancer, a patient must acquire new knowledge. We describe a model of knowledge acquisition that can provide a framework for exploring the process and types of knowledge that breast cancer patients gain following their diagnosis. The four types of knowledge presented in this modelauthoritative, technical, embodied, and traditionalare described and potential sources discussed. An understanding of knowledge acquisition in early stage breast cancer patients can provide healthcare practitioners with an important framework for optimizing decision-making in this population.
C1 [Warren, Laura E.] Harvard Univ, Sch Med, Boston, MA USA.
[Mendlinger, Sheryl E.] Northeastern Univ, Inst Urban Hlth Res, Boston, MA 02115 USA.
[Corso, Katherine A.; Greenberg, Caprice C.] Brigham & Womens Hosp, Dept Surg, Ctr Surg & Publ Hlth, Boston, MA 02115 USA.
[Greenberg, Caprice C.] Dana Farber Canc Inst, Dept Med Oncol, Ctr Outcomes & Policy Res, Boston, MA 02115 USA.
RP Greenberg, CC (reprint author), Univ Wisconsin, Dept Surg, Wisconsin Surg Outcomes Res Program, Ctr Clin Sci, 600 Highland Ave H4-742, Madison, WI 53792 USA.
EM greenberg@sur-gery.wisc.edu
FU NCI NIH HHS [L30 CA123695]
NR 23
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1075-122X
J9 BREAST J
JI Breast J.
PD JAN-FEB
PY 2012
VL 18
IS 1
BP 69
EP 72
DI 10.1111/j.1524-4741.2011.01183.x
PG 4
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 873WX
UT WOS:000298916200012
PM 22226068
ER
PT J
AU Rudge, C
Matesanz, R
Delmonico, FL
Chapman, J
AF Rudge, C.
Matesanz, R.
Delmonico, F. L.
Chapman, J.
TI International practices of organ donation
SO BRITISH JOURNAL OF ANAESTHESIA
LA English
DT Review
DE living donors; organ transplantation; tissue and organ procurement;
transplantation
ID MEDICAL GUIDELINES; DONOR; FORUM; LIVER; CARE
AB Organ donation and transplant rates vary widely across the globe, but there remains an almost universal shortage of deceased donors. The unmet need for transplants has resulted in many systematic approaches to increase donor rates, but there have also been practices that have crossed the boundaries of legal and ethical acceptability. Recent years have seen intense interest from international political organizations, led by the World Health Organization, and professional bodies, led by The Transplantation Society. Their efforts have focused on the development of a series of legal and ethical frameworks, designed to encourage all countries to eradicate unacceptable practices while introducing programmes that strive to achieve national or regional self-sufficiency in meeting the need for organ transplants. These programmes should seek to reduce both the need for transplantation and also develop deceased donation to its maximum potential. Living donation remains the mainstay of transplantation in many parts of the world, and many of the controversial-and unacceptable-areas of practice are found in the exploitation of living donors. However, until lessons are learnt, and applied, from countries with highly developed deceased donor programmes, these abuses of human rights will be difficult to eradicate. A clear international framework is now in place to achieve this.
C1 [Rudge, C.] Dept Hlth, London SE1 8UG, England.
[Matesanz, R.] Natl Transplant Org ONT, Madrid 28029, Spain.
[Delmonico, F. L.] Massachusetts Gen Hosp, Transplantat Soc, Boston, MA 02114 USA.
[Delmonico, F. L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg, Boston, MA USA.
[Delmonico, F. L.] New England Organ Bank Inc, Waltham, MA USA.
[Chapman, J.] Univ Sydney, Westmead Hosp, Ctr Transplant & Renal Res, Westmead, NSW 2145, Australia.
RP Rudge, C (reprint author), Dept Hlth, Wellington House,Waterloo Rd, London SE1 8UG, England.
EM cjrudge@btinternet.com
NR 16
TC 37
Z9 38
U1 1
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0007-0912
J9 BRIT J ANAESTH
JI Br. J. Anaesth.
PD JAN
PY 2012
VL 108
SU 1
BP I48
EP I55
DI 10.1093/bja/aer399
PG 8
WC Anesthesiology
SC Anesthesiology
GA 866MG
UT WOS:000298384500008
PM 22194431
ER
PT J
AU Colpo, A
Boyer, D
Fathi, AT
AF Colpo, Anna
Boyer, Daniel
Fathi, Amir T.
TI Hypereosinophilia in relapsed acute myeloid leukaemia
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Editorial Material
C1 [Colpo, Anna] Univ Padua, Sch Med, Dept Clin & Expt Med Hematol & Clin Immunol, Padua, Italy.
[Boyer, Daniel] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA USA.
[Fathi, Amir T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Div Hematol Oncol, Boston, MA USA.
RP Colpo, A (reprint author), Univ Padua, Sch Med, Dept Clin & Expt Med Hematol & Clin Immunol, Padua, Italy.
EM afathi@partners.org
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD JAN
PY 2012
VL 156
IS 1
BP 2
EP 2
DI 10.1111/j.1365-2141.2011.08804.x
PG 1
WC Hematology
SC Hematology
GA 861YX
UT WOS:000298058100002
PM 21810088
ER
PT J
AU Cursiefen, C
Colin, J
Dana, R
Diaz-Llopis, M
Faraj, LA
Garcia-Delpech, S
Geerling, G
Price, FW
Remeijer, L
Rouse, BT
Seitz, B
Udaondo, P
Meller, D
Dua, H
AF Cursiefen, Claus
Colin, Joseph
Dana, Reza
Diaz-Llopis, Manuel
Faraj, Lana A.
Garcia-Delpech, Salvador
Geerling, Gerd
Price, Francis W.
Remeijer, Lies
Rouse, Barry T.
Seitz, Berthold
Udaondo, Patricia
Meller, Daniel
Dua, Harminder
TI Consensus statement on indications for anti-angiogenic therapy in the
management of corneal diseases associated with neovascularisation:
outcome of an expert roundtable
SO BRITISH JOURNAL OF OPHTHALMOLOGY
LA English
DT Review
ID ENDOTHELIAL GROWTH-FACTOR; STEM-CELL DEFICIENCY; HERPETIC STROMAL
KERATITIS; GRAFT-SURVIVAL; TOPICAL BEVACIZUMAB; RISK-FACTORS;
ARGON-LASER; PENETRATING KERATOPLASTY; ACANTHAMOEBA-KERATITIS; LYMPHATIC
VESSELS
AB The cornea is the clear window at the front of the eye and is the eye's main refractive medium. Its transparency is essential for vision. Corneal neovascularisation is a common clinical problem with serious consequences for vision; it can compromise corneal transparency and plays a major role in corneal graft rejection by breaching corneal immune privilege. In this review, we formulate a consensus on the unmet medical needs in the management of corneal neovascularisation and outline a framework for the clinical research that is needed to identify suitable agents to meet these needs.
C1 [Cursiefen, Claus] Univ Cologne, Dept Ophthalmol, Erlangen, Germany.
[Colin, Joseph] Ctr Hosp Univ Pellegrin, Bordeaux, France.
[Dana, Reza] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Schepens Eye Res Inst, Boston, MA USA.
[Diaz-Llopis, Manuel; Garcia-Delpech, Salvador; Udaondo, Patricia] La Fe Univ Hosp, Dept Ophthalmol, Valencia, Spain.
[Diaz-Llopis, Manuel; Garcia-Delpech, Salvador] Univ Valencia, Valencia, Spain.
[Diaz-Llopis, Manuel; Garcia-Delpech, Salvador; Udaondo, Patricia] Biomed Network Res Ctr Rare Dis CIBERER, Valencia, Spain.
[Faraj, Lana A.; Dua, Harminder] Univ Nottingham, Div Ophthalmol & Visual Sci, Nottingham NG7 2RD, England.
[Geerling, Gerd] Univ Wurzburg, Dept Ophthalmol, Wurzburg, Germany.
[Price, Francis W.] Price Vis Grp, Indianapolis, IN USA.
[Price, Francis W.] Cornea Res Fdn Amer, Indianapolis, IN USA.
[Remeijer, Lies] Rotterdam Eye Hosp, Cornea & External Dis Serv, Rotterdam, Netherlands.
[Rouse, Barry T.] Univ Tennessee, Coll Vet Med, Dept Pathobiol, Knoxville, TN 37901 USA.
[Seitz, Berthold] Univ Saarland, Dept Ophthalmol, D-6650 Homburg, Germany.
[Meller, Daniel] Univ Essen Gesamthsch, Dept Ophthalmol, Essen, Germany.
RP Cursiefen, C (reprint author), Univ Cologne, Dept Ophthalmol, Joseph Stelzmann Str 9, D-50924 Cologne, Germany.
EM claus.cursiefen@uk-koeln.de
OI Faraj, Lana/0000-0001-7060-166X
FU IZKF Erlangen (A9); Voisin Consulting Life Sciences, France
FX IZKF Erlangen (A9) and Voisin Consulting Life Sciences, France. The
planning of this study, interpretation of findings, writing and
conclusions of manuscript were undertaken entirely independently of the
company interests.
NR 84
TC 32
Z9 33
U1 0
U2 5
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0007-1161
J9 BRIT J OPHTHALMOL
JI Br. J. Ophthalmol.
PD JAN
PY 2012
VL 96
IS 1
BP 3
EP 9
DI 10.1136/bjo.2011.204701
PG 7
WC Ophthalmology
SC Ophthalmology
GA 866EZ
UT WOS:000298364600002
PM 21712359
ER
PT J
AU Gasperini, JL
Fawzi, AA
Khondkaryan, A
Lam, L
Chong, LP
Eliott, D
Walsh, AC
Hwang, J
Sadda, SR
AF Gasperini, Julie L.
Fawzi, Amani A.
Khondkaryan, Ani
Lam, Linda
Chong, Lawrence P.
Eliott, Dean
Walsh, Alexander C.
Hwang, John
Sadda, SriniVas R.
TI Bevacizumab and ranibizumab tachyphylaxis in the treatment of choroidal
neovascularisation
SO BRITISH JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID OPTICAL COHERENCE TOMOGRAPHY; RETINAL VEIN OCCLUSION; MACULAR
DEGENERATION; INTRAVITREAL BEVACIZUMAB; AVASTIN TREATMENT; ANTIBODIES;
REGRESSION; DISEASE; EDEMA
AB Aims To evaluate the effect of switching to bevacizumab or ranibizumab after developing tachyphylaxis during anti-vascular endothelial growth factor (VEGF) therapy for choroidal neovascularisation (CNV).
Methods The authors reviewed the records of all patients who received both ranibizumab and bevacizumab for treatment of CNV to identify those who developed tachyphylaxis, defined as optical coherence tomography evidence of initial decreased exudation followed by lack of further reduction or an increase in exudation. Signs of exudation included subreitnal fluid (SRF), pigment epithelial detachment (PED) and/or cystoid macular oedema (CMO).
Results 26 eyes were included. 10 were initially treated with bevacizumab and then changed to ranibizumab for persistent SRF, PED and/or CMO. Of these, seven had occult CNV and three had predominantly classic CNV. One eye in the occult CNV group did not respond after being switched to ranibizumab. Six eyes had a positive therapeutic response, after one injection in four eyes, and after two or three injections in one eye each. In the classic group, two responded to ranibizumab and one did not. Sixteen eyes were initially treated with ranibizumab before changing to bevacizumab. Of these, 15 had occult CNV and 1 was predominantly classic. Three of the 16 eyes failed to respond to bevacizumab; 6 improved after one injection and 5 after two injections.
Conclusions Patients with CNV who develop tachyphylaxis to ranibizumab or bevacizumab may respond to another anti-VEGF drug. The majority of cases (81%) in this series demonstrated at least some response after switching therapies.
C1 [Fawzi, Amani A.; Khondkaryan, Ani; Lam, Linda; Walsh, Alexander C.; Hwang, John; Sadda, SriniVas R.] Univ So Calif, Doheny Eye Inst, Doheny Retina Inst, Keck Sch Med,Dept Ophthalmol, Los Angeles, CA 90033 USA.
[Gasperini, Julie L.] S Coast Retina Ctr, Torrance, CA USA.
[Chong, Lawrence P.] VMR Inst, Huntington Beach, CA USA.
[Eliott, Dean] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
RP Sadda, SR (reprint author), Univ So Calif, Doheny Eye Inst, Doheny Retina Inst, Keck Sch Med,Dept Ophthalmol, 1450 San Pablo St,DEI 3623, Los Angeles, CA 90033 USA.
EM sadda@usc.edu
OI fawzi, amani/0000-0002-9568-3558
FU Research to Prevent Blindness Inc., New York, NY; Fletcher Jones
Foundation; Carl Zeiss Meditec; Optovue, Inc.
FX Supported in part by an unrestricted grant to the Department of
Ophthalmology from Research to Prevent Blindness Inc., New York, NY, and
a grant from the Fletcher Jones Foundation.; LPC: Allergan Consultant;
DE: Genentech Speaker; ACW: co-inventor of Doheny intellectual property
related to optical coherence tomography that has been licensed by Topcon
Medical Systems and receives research support from Carl Zeiss Meditec
and Optovue, Inc.; SVRS: co-inventor of Doheny intellectual property
related to optical coherence tomography that has been licensed by Topcon
Medical Systems, consultant for Heidelberg Engineering, Genentech and
Allergan, and receives research support from Carl Zeiss Meditec and
Optovue, Inc.
NR 26
TC 61
Z9 64
U1 0
U2 1
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0007-1161
J9 BRIT J OPHTHALMOL
JI Br. J. Ophthalmol.
PD JAN
PY 2012
VL 96
IS 1
BP 14
EP 20
DI 10.1136/bjo.2011.204685
PG 7
WC Ophthalmology
SC Ophthalmology
GA 866EZ
UT WOS:000298364600004
PM 21791509
ER
PT J
AU Lobo, AM
Rhee, DJ
AF Lobo, A-M
Rhee, D. J.
TI Delayed interval of involvement of the second eye in a male patient with
bilateral Chandler's syndrome
SO BRITISH JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID IRIDOCORNEAL ENDOTHELIAL SYNDROME; COGAN-REESE
C1 [Lobo, A-M; Rhee, D. 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
NR 16
TC 1
Z9 2
U1 1
U2 1
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0007-1161
J9 BRIT J OPHTHALMOL
JI Br. J. Ophthalmol.
PD JAN
PY 2012
VL 96
IS 1
BP 134
EP 147
DI 10.1136/bjo.2009.177931
PG 4
WC Ophthalmology
SC Ophthalmology
GA 866EZ
UT WOS:000298364600030
PM 20710048
ER
PT J
AU Saboo, SS
Krajewski, KM
O'Regan, KN
Giardino, A
Brown, JR
Ramaiya, N
Jagannathan, JP
AF Saboo, S. S.
Krajewski, K. M.
O'Regan, K. N.
Giardino, A.
Brown, J. R.
Ramaiya, N.
Jagannathan, J. P.
TI Spleen in haematological malignancies: spectrum of imaging findings
SO BRITISH JOURNAL OF RADIOLOGY
LA English
DT Review
ID NON-HODGKIN-LYMPHOMA; EXTRANODAL INVOLVEMENT; DIAGNOSTIC-ACCURACY;
F-18-FDG PET; DISEASE; CT; FEATURES; LEUKEMIA; MYELOMA
AB Imaging morphology and metabolic activity of splenic lesions is of paramount importance in patients with haematological malignancies; it can alter tumour staging, treatment protocols and overall prognosis. CT, MRI and positron emission tomography (PET)/CT have been shown to be powerful tools for the non-invasive assessment of splenic involvement in various haematological malignancies. Since many haematological malignancies and non-neoplastic conditions can involve the spleen and imaging manifestations can overlap, imaging and clinical findings outside of the spleen should be looked for to narrow the differential diagnosis; confirmation can be obtained by pathological findings. Radiologists should be familiar with the cross-sectional imaging patterns of haematological malignancies involving the spleen as well as non-neoplastic splenic findings common in these patients to facilitate their care and follow-up. This pictorial review provides the common and uncommon imaging appearances and complications of various haematological malignancies involving the spleen on CT, MRI and PET/CT, and common pitfalls in diagnosis.
C1 [Saboo, S. S.; Krajewski, K. M.; O'Regan, K. N.; Giardino, A.; Ramaiya, N.; Jagannathan, J. P.] Dana Farber Canc Inst, Dept Radiol, Boston, MA 02115 USA.
[Brown, J. R.] Dana Farber Canc Inst, Dept Hematol Oncol, Boston, MA 02115 USA.
[Saboo, S. S.; Brown, J. R.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Saboo, SS (reprint author), Dana Farber Canc Inst, Dept Radiol, 44 Binney St, Boston, MA 02115 USA.
EM ssaboo@partners.org
NR 26
TC 15
Z9 15
U1 0
U2 4
PU BRITISH INST RADIOLOGY
PI LONDON
PA 36 PORTLAND PLACE, LONDON W1N 4AT, ENGLAND
SN 0007-1285
J9 BRIT J RADIOL
JI Br. J. Radiol.
PD JAN
PY 2012
VL 85
IS 1009
BP 81
EP 92
DI 10.1259/bjr/31542964
PG 12
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 866RH
UT WOS:000298398900017
PM 22096219
ER
PT J
AU Rahbar, H
Tavakkol, Z
Bhargava, P
AF Rahbar, H.
Tavakkol, Z.
Bhargava, P.
TI Characteristic CT appearance of lung cysts prompting the diagnosis of a
rare genodermatosis
SO BRITISH JOURNAL OF RADIOLOGY
LA English
DT Editorial Material
ID HOGG-DUBE-SYNDROME; HEREDITARY
C1 [Rahbar, H.; Bhargava, P.] Univ Washington, Sch Med, Dept Radiol, Seattle, WA 98195 USA.
[Rahbar, H.; Bhargava, P.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Tavakkol, Z.] Univ Washington, Div Dermatol, Sch Med, Dept Med, Seattle, WA 98195 USA.
RP Bhargava, P (reprint author), VA Puget Sound Hlth Care Ctr, Mail Box 358280,1660 S Columbian Way, Seattle, WA 98108 USA.
EM bhargp@u.washington.edu
OI Bhargava, Puneet/0000-0002-3849-9666
NR 6
TC 0
Z9 0
U1 0
U2 0
PU BRITISH INST RADIOLOGY
PI LONDON
PA 36 PORTLAND PLACE, LONDON W1N 4AT, ENGLAND
SN 0007-1285
J9 BRIT J RADIOL
JI Br. J. Radiol.
PD JAN
PY 2012
VL 85
IS 1009
BP 93
EP 95
DI 10.1259/bjr/13687494
PG 3
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 866RH
UT WOS:000298398900018
PM 22190751
ER
PT J
AU Hoffman, KE
Neville, BA
Mamon, HJ
Kachnic, LA
Katz, MS
Earle, CC
Punglia, RS
AF Hoffman, Karen E.
Neville, Bridget A.
Mamon, Harvey J.
Kachnic, Lisa A.
Katz, Matthew S.
Earle, Craig C.
Punglia, Rinaa S.
TI Adjuvant therapy for elderly patients with resected gastric
adenocarcinoma Population-Based Practices and Treatment Effectiveness
SO CANCER
LA English
DT Article
DE gastric cancer; aged; SEER-Medicare; chemotherapy; radiotherapy
ID SEER-MEDICARE DATA; FEE-FOR-SERVICE; RADIATION-THERAPY; POSTOPERATIVE
CHEMORADIATION; INTERGROUP-0116 TRIAL; COMORBIDITY INDEX; CHEMOTHERAPY
USE; PROSTATE-CANCER; BREAST-CANCER; PATTERNS
AB BACKGROUND: A study was undertaken to determine the survival benefit of postoperative chemoradiation therapy for elderly patients with resected gastric adenocarcinoma. METHODS: The authors identified 1023 individuals aged 65 years and older (median 76) who underwent gastrectomy for nonmetastatic stage IB-IV gastric adenocarcinoma diagnosed between 2000 and 2002 in the linked Surveillance, Epidemiology, and End Results-Medicare database. They examined factors associated with receiving postoperative chemoradiation and analyzed the survival benefit associated with receiving postoperative chemoradiation. RESULTS: Thirty percent of patients received adjuvant chemoradiation. On multivariate analysis, younger age (P < .0001), lymph node involvement (P < .0001), and more recent diagnosis (P = .0284) were associated with receiving chemoradiation. There was a trend toward increased use among patients with less comorbidity (P = .0515). The median follow-up was 25.5 months, and 62% died. On multivariate survival analysis, older patients (P < .0001) and those with lymph node involvement (P < .0001), T3 or T4 disease (P = .0472), higher grade disease (P = .0355), and more comorbidity (P = .0411) were more likely to die. After adjustment for other factors, receipt of adjuvant chemoradiation therapy did not significantly increase survival (hazard ratio, 0.90; 95% confidence interval, 0.72-1.12; P = .3453) and did not increase survival in a multivariate analysis that included propensity scores (P = .2090). CONCLUSIONS: The authors did not detect a survival benefit, suggesting that some elderly patients with resected gastric adenocarcinoma may not gain a survival benefit from the administration of adjuvant chemoradiation. The analysis had limitations, and the results are hypothesis generating. Future gastric cancer trials should enroll more elderly patients and stratify patients by age to better understand the impact of treatment regimens on older patients. Cancer 2012;118:248-57. (C) 2011 American Cancer Society.
C1 [Hoffman, Karen E.; Mamon, Harvey J.; Punglia, Rinaa S.] Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02115 USA.
[Hoffman, Karen E.; Mamon, Harvey J.; Punglia, Rinaa S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hoffman, Karen E.] Harvard Univ, Sch Med, Harvard Radiat Oncol Program, Boston, MA USA.
[Neville, Bridget A.; Punglia, Rinaa S.] Dana Farber Canc Inst, Dept Med Oncol, Ctr Outcomes & Policy Res, Boston, MA 02115 USA.
[Kachnic, Lisa A.] Boston Med Ctr, Dept Radiat Oncol, Boston, MA USA.
[Katz, Matthew S.] Radiat Oncol Associates PA, Manchester, NH USA.
[Earle, Craig C.] Inst Clin Evaluat Sci, Toronto, ON, Canada.
RP Hoffman, KE (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Radiat Oncol, 1515 Holcombe Blvd,Unit 1202, Houston, TX 77030 USA.
EM khoffman1@mdanderson.org
FU National Institutes of Health [1K07CA118629]; J C R T Foundation
FX This work was supported by a National Institutes of Health grant
(1K07CA118629, R. S. P.) and a J C R T Foundation grant (K.E.H.).
NR 33
TC 9
Z9 9
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD JAN 1
PY 2012
VL 118
IS 1
BP 248
EP 257
DI 10.1002/cncr.26248
PG 10
WC Oncology
SC Oncology
GA 868TW
UT WOS:000298549700031
PM 21692071
ER
PT J
AU Parikh, R
Sher, DJ
AF Parikh, Ravi
Sher, David J.
TI Primary radiotherapy versus radical prostatectomy for high-risk prostate
cancer A Decision Analysis
SO CANCER
LA English
DT Article
DE decision analysis; radical prostatectomy; external beam radiation;
prostate cancer; high risk
ID QUALITY-OF-LIFE; ANDROGEN-DEPRIVATION THERAPY; 3-DIMENSIONAL CONFORMAL
RADIOTHERAPY; INTENSITY-MODULATED RADIOTHERAPY; GROUP PROTOCOL 92-02;
PHASE-III TRIAL; RADIATION-THERAPY; FOLLOW-UP; EUROPEAN-ORGANIZATION;
ONCOLOGY
AB BACKGROUND: Two evidence-based therapies exist for the treatment of high-risk prostate cancer (PCA): external-beam radiotherapy (RT) with hormone therapy (H) (RT + H) and radical prostatectomy (S) with adjuvant radiotherapy (S + RT). Each of these strategies is associated with different rates of local control, distant metastasis (DM), and toxicity. By using decision analysis, the authors of this report compared the quality-adjusted life expectancy (QALE) between men with high-risk PCA who received RT + H versus S + RT versus a hypothetical trimodality therapy (S + RT + H). METHODS: The authors developed a Markov model to describe lifetime health states after treatment for high-risk PCA. Probabilities and utilities were extrapolated from the literature. Toxicities after radiotherapy were based on intensity-modulated radiotherapy series, and patients were exposed to risks of diabetes, cardiovascular disease, and fracture for 5 years after completing H. Deterministic and probabilistic sensitivity analyses were performed to model uncertainty in outcome rates, toxicities, and utilities. RESULTS: RT + H resulted in a higher QALE compared with S + RT over a wide range of assumptions, nearly always resulting in an increase of >1 quality-adjusted life year with outcomes highly sensitive to the risk of increased all-cause mortality from H. S + RT + H typically was superior to RT + H, albeit by small margins (<0.5 quality-adjusted life year), with results sensitive to assumptions about toxicity and radiotherapy efficacy. CONCLUSIONS: For men with high-risk PCA, RT + H was superior to S + RT, and the result was sensitive to the risk of all-cause mortality from H. Moreover, trimodality therapy may offer local and distant control benefits that lead to optimal outcomes in a meaningful population of men. Cancer 2012;118:258-67. (C) 2011 American Cancer Society.
C1 [Sher, David J.] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
[Sher, David J.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Parikh, Ravi] Harvard Univ, Sch Med, Boston, MA USA.
[Sher, David J.] Dana Farber Canc Inst, Ctr Outcomes & Policy Res, 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 37
TC 3
Z9 3
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD JAN 1
PY 2012
VL 118
IS 1
BP 258
EP 267
DI 10.1002/cncr.26272
PG 10
WC Oncology
SC Oncology
GA 868TW
UT WOS:000298549700032
PM 21720990
ER
PT J
AU Dunn, JH
Ellis, LZ
Fujita, M
AF Dunn, Jeffrey H.
Ellis, Lixia Z.
Fujita, Mayumi
TI Inflammasomes as molecular mediators of inflammation and cancer:
Potential role in melanoma
SO CANCER LETTERS
LA English
DT Review
DE Inflammasome; Inflammation; Cancer; Melanoma; IL-1 beta; ASC
ID INTERLEUKIN-1 INDUCES INTERLEUKIN-1; CASPASE RECRUITMENT DOMAIN; INNATE
IMMUNE-RESPONSE; FAMILIAL MEDITERRANEAN FEVER; TUMOR-HOST INTERACTIONS;
TOLL-LIKE RECEPTORS; SPECK-LIKE PROTEIN; NF-KAPPA-B; NALP3 INFLAMMASOME;
IN-VITRO
AB The inflammasome is a multi-protein complex that mediates immune responses to microbial, host, and environmental signals. When active, inflammasomes regulate caspase-1 activation and IL-1 beta secretion. There is a strong link between inflammation and cancer, and IL-1 beta is one of the major molecules involved in both of these disease processes. Here we review the role of inflammasomes in regulating IL-1 beta secretion, and the impact of this pathway on cancer pathogenesis, with a focus on melanoma. This represents an exciting new area of research, and could potentially result in new targets for melanoma therapeutics in the future. Published by Elsevier Ireland Ltd.
C1 [Dunn, Jeffrey H.; Ellis, Lixia Z.; Fujita, Mayumi] Univ Colorado Denver, Dept Dermatol, Sch Med, Aurora, CO 80045 USA.
[Fujita, Mayumi] Denver Vet Affairs Med Ctr, Denver, CO 80220 USA.
RP Fujita, M (reprint author), Univ Colorado Denver, Dept Dermatol, Sch Med, Mail Stop 8127,12801 E 17th Ave,RC-1 S,Rm 4124, Aurora, CO 80045 USA.
EM mayumi.fujita@ucdenver.edu
FU Dermatology Foundation; Wendy Will Case Cancer Fund grant; Cancer League
of Colorado; Tadamitsu Cancer Research Fund
FX The authors thank Charles A Dinarello, MD, Miyako Okamoto, MD, PhD and
Weimin Liu, MD (University of Colorado Denver) for helpful discussions.
This work was supported, in whole or in part, by Dermatology Foundation
(to M.F.), Wendy Will Case Cancer Fund grant (to M.F.), Cancer League of
Colorado (to M.F.) and Tadamitsu Cancer Research Fund (to M.F.). The
funders had no role in study design, data collection, analysis and
interpretation, manuscript preparation and decision to submit the
manuscript.
NR 163
TC 28
Z9 28
U1 2
U2 9
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD JAN 1
PY 2012
VL 314
IS 1
BP 24
EP 33
DI 10.1016/j.canlet.2011.10.001
PG 10
WC Oncology
SC Oncology
GA 868OF
UT WOS:000298531900003
PM 22050907
ER
PT J
AU Judd, NP
Winkler, AE
Murillo-Sauca, O
Brotman, JJ
Law, JH
Lewis, JS
Dunn, GP
Bui, JD
Sunwoo, JB
Uppaluri, R
AF Judd, Nancy P.
Winkler, Ashley E.
Murillo-Sauca, Oihana
Brotman, Joshua J.
Law, Jonathan H.
Lewis, James S., Jr.
Dunn, Gavin P.
Bui, Jack D.
Sunwoo, John B.
Uppaluri, Ravindra
TI ERK1/2 Regulation of CD44 Modulates Oral Cancer Aggressiveness
SO CANCER RESEARCH
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; EPITHELIAL-MESENCHYMAL TRANSITION; NECK-CANCER;
RAS ACTIVATION; STEM-CELLS; HEAD; EXPRESSION; MODELS; GROWTH;
CARCINOGENESIS
AB Carcinogen-induced oral cavity squamous cell carcinoma (OSCC) incurs significant morbidity and mortality and constitutes a global health challenge. To gain further insight into this disease, we generated cell line models from 7,12-dimethylbenz(a) anthracene-induced murine primary OSCC capable of tumor formation upon transplantation into immunocompetent wild-type mice. Whereas several cell lines grew rapidly and were capable of metastasis, some grew slowly and did not metastasize. Aggressively growing cell lines displayed ERK1/2 activation, which stimulated expression of CD44, a marker associated with epithelial to mesenchymal transition and putative cancer stem cells. MEK (MAP/ERK kinase) inhibition upstream of ERK1/2 decreased CD44 expression and promoter activity and reduced cell migration and invasion. Conversely, MEK1 activation enhanced CD44 expression and promoter activity, whereas CD44 attenuation reduced in vitro migration and in vivo tumor formation. Extending these findings to freshly resected human OSCC, we confirmed a strict relationship between ERK1/2 phosphorylation and CD44 expression. In summary, our findings identify CD44 as a critical target of ERK1/2 in promoting tumor aggressiveness and offer a preclinical proof-of-concept to target this pathway as a strategy to treat head and neck cancer. Cancer Res; 72(1); 365-74. (C) 2011 AACR.
C1 [Judd, Nancy P.; Winkler, Ashley E.; Brotman, Joshua J.; Law, Jonathan H.; Lewis, James S., Jr.; Uppaluri, Ravindra] Washington Univ, Sch Med, Dept Otolaryngol, St Louis, MO 63110 USA.
[Uppaluri, Ravindra] Washington Univ, Sch Med, John Cochran VA Med Ctr, St Louis, MO 63110 USA.
[Lewis, James S., Jr.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
[Murillo-Sauca, Oihana; Sunwoo, John B.] Stanford Univ, Dept Otolaryngol, Stanford, CA 94305 USA.
[Dunn, Gavin P.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Bui, Jack D.] UCSD, Dept Pathol, La Jolla, CA USA.
RP Uppaluri, R (reprint author), Washington Univ, Sch Med, Dept Otolaryngol, 660 S Euclid Ave,Campus Box 8115, St Louis, MO 63110 USA.
EM uppalurr@wustl.edu
FU NCI [K08CA090403]; Veteran's Affairs Research Service; NIH [T32DC00022]
FX R. Uppaluri was supported by the NCI (K08CA090403) and the Veteran's
Affairs Research Service. N.P. Judd and J.H. Law were supported by
NIH-T32DC00022.
NR 50
TC 39
Z9 39
U1 1
U2 6
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 JAN 1
PY 2012
VL 72
IS 1
BP 365
EP 374
DI 10.1158/0008-5472.CAN-11-1831
PG 10
WC Oncology
SC Oncology
GA 871RO
UT WOS:000298755600036
PM 22086849
ER
PT J
AU Hirata, H
Hinoda, Y
Ueno, K
Shahryari, V
Tabatabai, ZL
Dahiya, R
AF Hirata, Hiroshi
Hinoda, Yuji
Ueno, Koji
Shahryari, Varahram
Tabatabai, Z. Laura
Dahiya, Rajvir
TI MicroRNA-1826 targets VEGFC, beta-catenin (CTNNB1) and MEK1 (MAP2K1) in
human bladder cancer
SO CARCINOGENESIS
LA English
DT Article
ID LYMPH-NODE METASTASIS; FACTOR-C EXPRESSION; SIGNAL-TRANSDUCTION; KINASE
CASCADE; CELL-LINES; TUMORS; LYMPHANGIOGENESIS; ACTIVATION; BIOMARKERS;
CARCINOMA
AB The Wnt/beta-catenin (CTNNB1) and Ras-Raf-MEK-ERK signaling pathway play an important role in bladder cancer (BC) progression. Tumor-suppressive microRNAs (miRNAs) targeting these cancer pathways may provide a new therapeutic approach for BC. We initially identified miRNA-1826 potentially targeting CTNNB1, VEGFC and MEK1 using several target scan algorithms. Also 3' untranslated region luciferase activity and protein expression of these target genes were significantly downregulated in miR-1826-transfected BC cells (J82 and T24). The expression of miR-1826 was lower in BC tissues and inverse correlation of miR-1826 with several clinical parameters (pT, grade) was observed. Also the expression of miR-1826 was much lower in three BC cell lines (J82, T24 and TCCSUP) compared with a normal bladder cell line (SV-HUC-1). We then performed analyses to look at miR-1826 function and found that miR-1826 inhibited BC cell viability, invasion and migration. We also found increased apoptosis and G(1) cell cycle arrest in miR-1826-transfected BC cells. To examine whether the effect of miR-1826 was through CTNNB1 (beta-catenin) or MEK1 knockdown, we knocked down CTNNB1/MEK1 messenger RNA using a small interfering RNA (siRNA) technique. We observed that CTNNB1 or MEK1 siRNA knockdown resulted in effects similar to those with miR-1826 in BC cells. In conclusion, our data suggest that the miR-1826 plays an important role as tumor suppressor via CTNNB1/MEK1/VEGFC downregulation in BC.
C1 [Hirata, Hiroshi; Ueno, Koji; Shahryari, Varahram; Dahiya, Rajvir] San Francisco VA Med Ctr, Dept Urol, San Francisco, CA 94121 USA.
[Hinoda, Yuji; Tabatabai, Z. Laura] Univ Calif San Francisco, San Francisco, CA 94121 USA.
[Hinoda, Yuji; Tabatabai, Z. Laura] Yamaguchi Univ, Grad Sch Med, Dept Oncol AnLab Med, Yamaguchi 7558505, Japan.
[Tabatabai, Z. Laura] San Francisco VA Med Ctr, Dept Pathol, San Francisco, CA 94121 USA.
RP Dahiya, R (reprint author), Vet Affairs Med Ctr, Urol Res Ctr 112F, San Francisco, CA 94121 USA.
EM rdahiya@urology.ucsf.edu
FU National Institutes of Health [RO1CA130860, RO1CA111470, RO1CA138642,
T32-DK07790]; VA Research Enhancement Award Program; Merit Review
grants; Yamada Science Foundation
FX RO1CA130860, RO1CA111470, RO1CA138642, T32-DK07790 from the National
Institutes of Health, VA Research Enhancement Award Program, Merit
Review grants and Yamada Science Foundation.
NR 36
TC 39
Z9 42
U1 2
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD JAN
PY 2012
VL 33
IS 1
BP 41
EP 48
DI 10.1093/carcin/bgr239
PG 8
WC Oncology
SC Oncology
GA 870HF
UT WOS:000298659200006
PM 22049531
ER
PT J
AU Stone, JR
Basso, C
Baandrup, UT
Bruneval, P
Butany, J
Gallagher, PJ
Halushka, MK
Miller, DV
Padera, RF
Radio, SJ
Sheppard, MN
Suvarna, K
Tan, CD
Thiene, G
van der Wal, AC
Veinot, JP
AF Stone, James R.
Basso, Cristina
Baandrup, Ulrik T.
Bruneval, Patrick
Butany, Jagdish
Gallagher, Patrick J.
Halushka, Marc K.
Miller, Dylan V.
Padera, Robert F.
Radio, Stanley J.
Sheppard, Mary N.
Suvarna, Kim
Tan, Carmela D.
Thiene, Gaetano
van der Wal, Allard C.
Veinot, John P.
TI Recommendations for processing cardiovascular surgical pathology
specimens: a consensus statement from the Standards and Definitions
Committee of the Society for Cardiovascular Pathology and the
Association for European Cardiovascular Pathology
SO CARDIOVASCULAR PATHOLOGY
LA English
DT Article
DE Cardiovascular disease; Cardiovascular surgical pathology specimens;
Patient care; Pathology standards
ID AMERICAN-HEART-ASSOCIATION; BIOPSY-PROVEN MYOCARDITIS; SUBAORTIC SEPTAL
MYECTOMY; HUMAN CARDIAC ALLOGRAFTS; TEMPORAL ARTERY BIOPSY;
ENDOMYOCARDIAL BIOPSY; HYPERTROPHIC CARDIOMYOPATHY; DILATED
CARDIOMYOPATHY; SCIENTIFIC STATEMENT; ATRIAL-FIBRILLATION
AB With the advent of molecular subclassification of diseases, much consideration should be given to the proper processing of cardiovascular surgical pathology specimens to maximize patient care. Such specimens include endomyocardial biopsies, cardiac myectomy specimens, cardiac apical core segments, resected cardiac valves, pericardial biopsies, resected segments of aorta, cardiac tumors, vascular stents, vascular grafts, cardiac devices, resected veins, arterial biopsies including temporal artery biopsies and hearts removed during cardiac transplantation. In this report, the Standards and Definitions Committee of the Society for Cardiovascular Pathology and the Association for European Cardiovascular Pathology present consensus guidelines for the gross description, sectioning, processing, and staining of these specimens. This report is presented to aid pathologists, pathology assistants, and clinicians in maximizing the diagnostic utility of cardiovascular surgical pathology specimens for enhanced patient care. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Stone, James R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Basso, Cristina] Univ Padua, Sch Med, Dept Med Diagnost Sci & Special Therapies, I-35121 Padua, Italy.
[Baandrup, Ulrik T.] Aalborg Univ, Vendsyssel Hosp, Aalborg, Denmark.
[Bruneval, Patrick] Univ Paris 05, Paris, France.
[Butany, Jagdish] Toronto Gen Hosp, Toronto, ON, Canada.
[Gallagher, Patrick J.] Southhampton Univ Hosp, Southampton, England.
[Halushka, Marc K.] Johns Hopkins Univ, Baltimore, MD USA.
[Miller, Dylan V.] Univ Utah, Salt Lake City, UT 84112 USA.
[Padera, Robert F.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Radio, Stanley J.] Univ Nebraska, Lincoln, NE 68583 USA.
[Sheppard, Mary N.] Univ London Imperial Coll Sci Technol & Med, London, England.
[Suvarna, Kim] No Gen Hosp, Sheffield, England.
[Tan, Carmela D.] Cleveland Clin, Cleveland, OH 44106 USA.
[van der Wal, Allard C.] Univ Amsterdam, Amsterdam, Netherlands.
[Veinot, John P.] Univ Ottawa, Ottawa, ON, Canada.
RP Stone, JR (reprint author), Massachusetts Gen Hosp, Simches Bldg,Room 8236, Boston, MA 02114 USA.
EM jrstone@partners.org; cristina.basso@unipd.it
OI Halushka, Marc/0000-0002-7112-7389
NR 85
TC 20
Z9 20
U1 2
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1054-8807
EI 1879-1336
J9 CARDIOVASC PATHOL
JI Cardiovasc. Pathol.
PD JAN-FEB
PY 2012
VL 21
IS 1
BP 2
EP 16
DI 10.1016/j.carpath.2011.01.001
PG 15
WC Cardiac & Cardiovascular Systems; Pathology
SC Cardiovascular System & Cardiology; Pathology
GA 867GT
UT WOS:000298443600002
PM 21353600
ER
PT J
AU Gordon, JA
AF Gordon, James A.
TI As Accessible as a Book on a Library Shelf The Imperative of Routine
Simulation in Modern Health Care
SO CHEST
LA English
DT Editorial Material
ID DELIBERATE PRACTICE; EXPERT PERFORMANCE; HOSPITAL LIBRARIES;
MEDICAL-EDUCATION; ACQUISITION; RESIDENTS
AB Technology-enhanced patient simulation has emerged as an important new modality for teaching and learning in medicine. In particular, immersive simulation platforms that replicate the clinical environment promise to revolutionize medical education by enabling an enhanced level of safety, standardization, and efficiency across health-care training. Such an experiential approach seems unique in reliably catalyzing a level of emotional engagement that fosters immediate and indelible learning and allows for increasingly reliable levels of performance evaluation-all in a completely risk-free environment. As such, medical simulation is poised to emerge as a critical component of training and certification throughout health care, promising to fundamentally enhance quality and safety across disciplines. To encourage routine simulation-based practice as part of its core quality and safety mission, Massachusetts General Hospital now incorporates simulation resources within its historic medical library (est. 1847), located at the center of the campus. In this new model, learners go to the library not only to read about a patient's illness, but also to take care of their "patient." Such an approach redefines and advances the central role of the library on the campus and ensures that simulation-based practice is centrally available as part of everyday hospital operations. This article describes the reasons for identifying simulation as an institutional priority leading up to the Massachusetts General Hospital Bicentennial Celebration (1811-2011) and for creating a simulation-based learning laboratory within a hospital library. CHEST 2012; 141(1):12-16
C1 Massachusetts Gen Hosp, MGH Learning Lab, Boston, MA 02114 USA.
[Gordon, James A.] Massachusetts Gen Hosp, Dept Emergency Med, Div Med Simulat, Boston, MA 02114 USA.
[Gordon, James A.] Harvard Univ, Sch Med, Gilbert Program Med Simulat, Boston, MA 02138 USA.
[Gordon, James A.] Ctr Integrat Med & Innovat Technol CIMIT, Boston, MA USA.
RP Gordon, JA (reprint author), Massachusetts Gen Hosp, MGH Learning Lab, 0 Emerson Pl,Ste 3B, Boston, MA 02114 USA.
EM jgordon3@partners.org
NR 27
TC 10
Z9 10
U1 0
U2 3
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD JAN
PY 2012
VL 141
IS 1
BP 12
EP 16
DI 10.1378/chest.11-0571
PG 5
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 874FW
UT WOS:000298941800006
PM 22215825
ER
PT J
AU Kerr, KM
Auger, WR
Marsh, JJ
Devendra, G
Spragg, RG
Kim, NH
Channick, RN
Jamieson, SW
Madani, MM
Manecke, GR
Roth, DM
Shragg, GP
Fedullo, PF
AF Kerr, Kim M.
Auger, William R.
Marsh, James J.
Devendra, Gehan
Spragg, Roger G.
Kim, Nick H.
Channick, Richard N.
Jamieson, Stuart W.
Madani, Michael M.
Manecke, Gerard R.
Roth, David M.
Shragg, Gordon P.
Fedullo, Peter F.
TI Efficacy of Methylprednisolone in Preventing Lung Injury Following
Pulmonary Thromboendarterectomy
SO CHEST
LA English
DT Article
ID CARDIOPULMONARY BYPASS; ENDARTERECTOMY; APROTININ; SURGERY
AB Background: We sought to determine the efficacy and safety of perioperative treatment with methylprednisolone on the development of lung injury after pulmonary thromboendarterectomy.
Methods: This was a randomized, prospective, double-blind, placebo-controlled study of 98 adult patients with chronic thromboembolic pulmonary hypertension who were undergoing pulmonary thromboendarterectomy at a single institution. The patients received either placebo (n = 47) or methylprednisolone (n = 51) (30 mg/kg in the cardiopulmonary bypass prime, 500 mg IV bolus following the final circulatory arrest, and 250 mg IV bolus 36 h after surgery). The primary end point was the presence of lung injury as determined by two independent, blinded physicians using prospectively defined criteria. The secondary end points included ventilator-free, ICU-free, and hospital-free days and selected levels of cytokines in the blood and in BAL fluid.
Results: The incidence of lung injury was similar in both treatment groups (45% placebo, 41% steroid; P = .72). There were no statistical differences in the secondary clinical end points between treatment groups. Treatment with methylprednisolone, compared with placebo, was associated with a statistically significant reduction in plasma IL-6 and IL-8, a significant increase in plasma IL-10, and a significant reduction in postoperative IL-Ira and IL-6, but not IL-8 in BAL fluid obtained 1 day after surgery.
Conclusions: Perioperative methylprednisolone does not reduce the incidence of lung injury following pulmonary thromboendarterectomy surgery despite having an antiinflammatory effect on plasma and lavage cytokine levels. CHEST 2012; 141(1):27-35
C1 [Kerr, Kim M.; Auger, William R.; Marsh, James J.; Spragg, Roger G.; Kim, Nick H.; Fedullo, Peter F.] Univ Calif San Diego, Div Pulm & Crit Care Med, San Diego, CA 92103 USA.
[Jamieson, Stuart W.; Madani, Michael M.] Univ Calif San Diego, Div Cardiothorac Surg, San Diego, CA 92103 USA.
[Manecke, Gerard R.; Roth, David M.] Univ Calif San Diego, Dept Anesthesiol, San Diego, CA 92103 USA.
[Shragg, Gordon P.] Univ Calif San Diego, Gen Clin Res Ctr, San Diego, CA 92103 USA.
[Devendra, Gehan] Kaiser Permanente, Sacramento, CA USA.
[Channick, Richard N.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Kerr, KM (reprint author), Univ Calif San Diego, Med Ctr, Pulm & Crit Care Med Div, 9300 Campus Point Dr,M-C 7381, La Jolla, CA 92037 USA.
EM kmkerr@ucsd.edu
FU National Institutes of Health, National Center for Research Resources
for the University of California, San Diego, General Clinical Research
Center [NHLBI HL23584, MO1-RR0827]
FX This study was supported by the National Institutes of Health [Grants
NHLBI HL23584 and MO1-RR0827 from the National Center for Research
Resources for the University of California, San Diego, General Clinical
Research Center].
NR 20
TC 9
Z9 10
U1 0
U2 5
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
EI 1931-3543
J9 CHEST
JI Chest
PD JAN
PY 2012
VL 141
IS 1
BP 27
EP 35
DI 10.1378/chest.10-2639
PG 9
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 874FW
UT WOS:000298941800009
PM 21835900
ER
PT J
AU Zemans, RL
Stream, AR
Musani, AI
Dhaliwal, G
AF Zemans, Rachel L.
Stream, Amanda R.
Musani, Ali I.
Dhaliwal, Gurpreet
TI A 46-Year-Old Man With Seizures, Brain Lesions, and Pulmonary
Infiltrates
SO CHEST
LA English
DT Editorial Material
ID ALVEOLAR PROTEINOSIS; THERAPY
C1 [Zemans, Rachel L.; Musani, Ali I.] Natl Jewish Hlth, Dept Med, Denver, CO 80206 USA.
[Zemans, Rachel L.; Stream, Amanda R.; Musani, Ali I.] Univ Colorado Denver, Dept Med, Aurora, CO USA.
[Dhaliwal, Gurpreet] San Francisco VA Med Ctr, Dept Med, San Francisco, CA USA.
[Dhaliwal, Gurpreet] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
RP Zemans, RL (reprint author), Natl Jewish Hlth, Dept Med, 1400 Jackson St,A555, Denver, CO 80206 USA.
EM ZemansR@NJHealth.org
FU NHLBI NIH HHS [K08 HL103772, HL103772]
NR 10
TC 0
Z9 0
U1 1
U2 2
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD JAN
PY 2012
VL 141
IS 1
BP 265
EP 269
DI 10.1378/chest.11-1397
PG 5
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 874FW
UT WOS:000298941800041
PM 22215837
ER
PT J
AU Mavros, MN
Velmahos, GC
Falagas, ME
AF Mavros, Michael N.
Velmahos, George C.
Falagas, Matthew E.
TI Edict of Postoperative Fever and Atelectasis Response
SO CHEST
LA English
DT Letter
C1 [Mavros, Michael N.; Falagas, Matthew E.] Alfa Inst Biomed Sci, Athens 15123, Greece.
[Velmahos, George C.] Massachusetts Gen Hosp, Div Trauma Emergency Surg & Surg Crit Care, Boston, MA 02114 USA.
[Velmahos, George C.] Harvard Univ, Sch Med, Boston, MA USA.
[Falagas, Matthew E.] Henry Dunant Hosp, Dept Med, Athens, Greece.
[Falagas, Matthew E.] Tufts Univ, Sch Med, Dept Med, Athens, Greece.
RP Falagas, ME (reprint author), Alfa Inst Biomed Sci, 9 Neapoleos St, Athens 15123, Greece.
EM m.falagas@aibs.gr
NR 4
TC 0
Z9 0
U1 0
U2 1
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD JAN
PY 2012
VL 141
IS 1
BP 275
EP 275
DI 10.1378/chest.11-2206
PG 1
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 874FW
UT WOS:000298941800046
ER
PT J
AU Bostic, JQ
Bagnell, AL
AF Bostic, Jeffrey Q.
Bagnell, Alexa L.
TI Evidence-Based School Psychiatry Preface
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Editorial Material
C1 [Bostic, Jeffrey Q.] Massachusetts Gen Hosp, Sch Psychiat, Boston, MA 02114 USA.
[Bagnell, Alexa L.] Dalhousie Univ, Dept Psychiat, IWK Maritime Psychiat, Halifax, NS B3K 6R8, Canada.
RP Bostic, JQ (reprint author), Massachusetts Gen Hosp, Sch Psychiat, 55 Fruit St, Boston, MA 02114 USA.
EM JBOSTIC@PARTNERS.ORG; Alexa.Bagnell@iwk.nshealth.ca
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1056-4993
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD JAN
PY 2012
VL 21
IS 1
BP XIII
EP XVI
DI 10.1016/j.chc.2011.10.001
PG 4
WC Psychiatry
SC Psychiatry
GA 865JY
UT WOS:000298308400001
PM 22137822
ER
PT J
AU Brunt, C
Bostic, JQ
AF Brunt, Colby
Bostic, Jeffrey Q.
TI School Law for the Child Psychiatrist: Legal Principles and Case
Implications
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE School; Mental health; Legal; School law psychiatry; Special education
AB Schools are evolving to support all students, including those with mental health issues. Clinicians can help patients and schools by providing diagnostic clarity about a child's condition, how that condition interferes with school progress, and what interventions are needed in the school setting. State and Federal legislation supports timely response by schools to mental health issues emerging in students through special education laws and general education accommodations, such as Response To Intervention (RTI), which encourages schools to implement evidence-based interventions for students exhibiting mental health conditions. Case examples illuminate important legal considerations when clinicians are faced with issues such as therapeutic placements, home hospital forms, and substance abuse, and student misconduct.
C1 [Bostic, Jeffrey Q.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02114 USA.
[Bostic, Jeffrey Q.] Massachusetts Gen Hosp, Sch Psychiat, Boston, MA 02114 USA.
RP Bostic, JQ (reprint author), Harvard Univ, Sch Med, Dept Psychiat, 6900 Yawkey Bldg,55 Fruit St, Boston, MA 02114 USA.
EM jbostic@partners.org
NR 4
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 1056-4993
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD JAN
PY 2012
VL 21
IS 1
BP 29
EP +
DI 10.1016/j.chc.2011.09.001
PG 15
WC Psychiatry
SC Psychiatry
GA 865JY
UT WOS:000298308400005
PM 22137809
ER
PT J
AU Jellinek, MS
Okoli, UD
AF Jellinek, Mike S.
Okoli, Uchenwa D.
TI When a Student Dies: Organizing the School's Response
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Crisis counseling; Death; Grief; School
ID SHOOTINGS; SUICIDE
AB Principals, teachers, and guidance counselors feel ill-prepared to address a student's death. Often the death is not anticipated, comes as a shock, and has many reverberations in the school itself and in the broader community. The principal and others in the school may be called upon to serve as leaders in this sudden crisis and have broad responsibilities to their school community that may seem overwhelming in the face of their own grief and reactions to the loss. These guidelines present a meaningful response to an event that can profoundly affect the school and community.
C1 [Jellinek, Mike S.; Okoli, Uchenwa D.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Newton, MA USA.
RP Jellinek, MS (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Newton, MA USA.
EM mjellinek@partners.org
NR 21
TC 1
Z9 1
U1 2
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1056-4993
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD JAN
PY 2012
VL 21
IS 1
BP 57
EP +
DI 10.1016/j.chc.2011.08.008
PG 12
WC Psychiatry
SC Psychiatry
GA 865JY
UT WOS:000298308400007
PM 22137811
ER
PT J
AU Bostic, JQ
Hart, LJ
AF Bostic, Jeffrey Q.
Hart, Lauren J.
TI Building Better Brains: Evidence-Based Interventions to Enhance
Contemporary Schooling
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE School; Mental health; Academic success
ID PHYSICAL-ACTIVITY; ADOLESCENT SLEEP; START TIME; CHILDREN; FITNESS;
IMPACT; YOUTH; CONSUMPTION; EFFICACY; BEHAVIOR
AB School is a rich environment for cultivating academic skills, but also for developing metacognitive skills such as executive functioning and emotional regulation. However, the hours students spend in school are often guided by familiar practices rather than contemporary findings about how the brain best learns and grows. This article describes biological conditions favorable to brain development, psychological skills associated with effective school functioning, and school practices associated with academic and interpersonal success. The aim is that schooling might be shaped with regard to children's and adolescents' brain development needs rather than social custom.
C1 [Bostic, Jeffrey Q.; Hart, Lauren J.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02114 USA.
[Bostic, Jeffrey Q.] Massachusetts Gen Hosp, Sch Psychiat, Boston, MA 02114 USA.
[Hart, Lauren J.] Northeastern Univ, Dept Publ Hlth, Boston, MA USA.
RP Bostic, JQ (reprint author), Dept Child Psychiat, 6900 Yawkey Bldg,55 Fruit St, Boston, MA 02114 USA.
EM jbostic@partners.org
NR 34
TC 0
Z9 0
U1 0
U2 7
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1056-4993
EI 1558-0490
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD JAN
PY 2012
VL 21
IS 1
BP 69
EP +
DI 10.1016/j.chc.2011.09.006
PG 14
WC Psychiatry
SC Psychiatry
GA 865JY
UT WOS:000298308400008
PM 22137812
ER
PT J
AU Yule, AM
Prince, JB
AF Yule, Amy M.
Prince, Jefferson B.
TI Adolescent Substance Use Disorders in the School Setting
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Substance abuse; Adolescents; Prevention programs; School; Treatment
ID ABUSE RESISTANCE EDUCATION; CLUSTER-RANDOMIZED-TRIAL; DRUG-ABUSE;
PROJECT ALERT; FOLLOW-UP; ALCOHOL-USE; PREVENTION; TOBACCO; MIDDLE; DARE
AB Adolescent substance use is a major public health problem that concerns parents, schools, clinicians, and policy makers. The authors review school-based prevention programs, school drug policies, clinical signs and symptoms of substance impairment, recommendations for referral and engaging adolescents who are using substances, and treatment interventions for adolescent substance use disorders.
C1 [Yule, Amy M.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Prince, Jefferson B.] MassGen Children N Shore Med Ctr, Salem, MA 01970 USA.
[Prince, Jefferson B.] Massachusetts Gen Hosp, Pediat Psychopharmacol Clin, Boston, MA 02114 USA.
[Prince, Jefferson B.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Yule, AM (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 55 Fruit St, Boston, MA 02114 USA.
EM ayule@partners.org
NR 63
TC 0
Z9 0
U1 1
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1056-4993
EI 1558-0490
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD JAN
PY 2012
VL 21
IS 1
BP 175
EP +
DI 10.1016/j.chc.2011.09.003
PG 13
WC Psychiatry
SC Psychiatry
GA 865JY
UT WOS:000298308400016
PM 22137820
ER
PT J
AU Stevens, JR
Prince, JB
AF Stevens, Jonathan R.
Prince, Jefferson B.
TI Schooling Students with Psychotic Disorders
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Psychosis; Childhood-onset schizophrenia; Hallucinations; School
interventions
ID CHILDHOOD-ONSET SCHIZOPHRENIA; SYMPTOMS; THERAPY
AB The term psychosis is generally used to describe the abnormal behaviors of children and adolescents with grossly impaired reality testing. This article discusses evaluation of psychotic symptoms in students and psychosocial school interventions for students with psychosis, including the roles of teachers and school administrators. Psychoeducation provided by clinicians and school staff to enhance coping and cognitive strategies is described.
C1 [Stevens, Jonathan R.] Med Ctr, Pediat Inpatient Psychiat Unit, Lynn, MA 01904 USA.
[Prince, Jefferson B.] MassGen Children N Shore Med Ctr, Salem, MA USA.
[Prince, Jefferson B.] Massachusetts Gen Hosp, Pediat Psychopharmacol Clin, Boston, MA 02114 USA.
RP Stevens, JR (reprint author), Med Ctr, Pediat Inpatient Psychiat Unit, 500 Lynnfield St, Lynn, MA 01904 USA.
EM jstevens@partners.org
NR 18
TC 1
Z9 1
U1 2
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1056-4993
EI 1558-0490
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD JAN
PY 2012
VL 21
IS 1
BP 187
EP +
DI 10.1016/j.chc.2011.09.008
PG 15
WC Psychiatry
SC Psychiatry
GA 865JY
UT WOS:000298308400017
PM 22137821
ER
PT J
AU Gray, SW
Hornik, RC
Schwartz, JS
Armstrong, K
AF Gray, S. W.
Hornik, R. C.
Schwartz, J. S.
Armstrong, K.
TI The impact of risk information exposure on women's beliefs about
direct-to-consumer genetic testing for BRCA mutations
SO CLINICAL GENETICS
LA English
DT Article
DE BRCA; cancer; communication; direct-to-consumer; informed consent
ID POLICY STATEMENT UPDATE; CANCER SUSCEPTIBILITY; GENOMIC MEDICINE;
AMERICAN-SOCIETY; OVARIAN-CANCER; UNITED-STATES; INTERNET; SERVICES;
BREAST; VIEWS
AB Despite an increase in direct-to-consumer (DTC) genetic testing, little is known about how variations in website content might alter consumer behavior. We evaluated the impact of risk information provision on women's attitudes about DTC BRCA testing. We conducted a randomized experiment; women viewed a 'mock' BRCA testing website without [control group (CG)] or with information on the potential risks of DTC testing [RG; framed two ways: unattributed risk (UR) information and risk information presented by experts (ER)]. Seven hundred and sixty-seven women participated; mean age was 37 years, mean education was 15 years, and 79% of subjects were white. Women in the RG had less positive beliefs about DTC testing (mean RG = 23.8, CG = 25.2; p = 0.001), lower intentions to get tested (RG = 2.8, CG = 3.1; p = 0.03), were more likely to prefer clinic-based testing (RG = 5.1, CG = 4.8; p = 0.03) and to report that they had seen enough risk information (RG = 5.3, CG = 4.7; p < 0.001). UR and ER exposure produced similar effects. Effects did not differ for women with or without a personal/family history of breast/ovarian cancer. Exposing women to the potential risks of DTC BRCA testing altered their beliefs, preferences, and intentions. Risk messages appear to be salient to women irrespective of their chance of having a BRCA mutation.
C1 [Gray, S. W.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Gray, S. W.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Hornik, R. C.] Univ Penn, Annenberg Sch Commun, Ctr Excellence Canc Commun Res, Philadelphia, PA 19104 USA.
[Schwartz, J. S.; Armstrong, K.] Univ Penn, Sect Gen Internal Med, Philadelphia, PA 19104 USA.
[Schwartz, J. S.] Univ Penn, Wharton Sch, Philadelphia, PA 19104 USA.
[Armstrong, K.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
RP Gray, SW (reprint author), Dana Farber Canc Inst, 450 Brookline Ave,LW 633, Boston, MA 02215 USA.
EM stacyw_gray@dfci.harvard.edu
OI Hornik, Robert/0000-0002-2148-8805
FU Robert Wood Johnson Foundation; NCI [5P50CA095856-05, R25 CA092203];
American Society for Clinical Oncology
FX Funding/Support for this study was provided by Robert Wood Johnson
Foundation, NCI 5P50CA095856-05, The American Society for Clinical
Oncology, and NCI R25 CA092203.
NR 57
TC 4
Z9 4
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9163
J9 CLIN GENET
JI Clin. Genet.
PD JAN
PY 2012
VL 81
IS 1
BP 29
EP 37
DI 10.1111/j.1399-0004.2011.01797.x
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 860CP
UT WOS:000297925600005
PM 21992449
ER
PT J
AU Hermos, JA
Young, MM
Fonda, JR
Gagnon, DR
Fiore, LD
Lawler, EV
AF Hermos, John A.
Young, Melissa M.
Fonda, Jennifer R.
Gagnon, David R.
Fiore, Louis D.
Lawler, Elizabeth V.
TI Risk of Community-Acquired Pneumonia in Veteran Patients to Whom Proton
Pump Inhibitors Were Dispensed
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID SPONTANEOUS BACTERIAL PERITONITIS; ACID SUPPRESSION;
GASTROESOPHAGEAL-REFLUX; ASSOCIATION; DISEASE; INFECTIONS; OVERGROWTH;
THERAPY; ADULTS; OLDER
AB Background. Observational studies linking proton pump inhibitor (PPI) exposure with community-acquired pneumonia (CAP) have reported either modest or no associations. Accordingly, we studied PPI exposure and CAP in veteran patients, using a retrospective, nested case-control design.
Methods. From linked pharmacy and administrative databases of the New England Veterans Healthcare System, we identified 71 985 outpatients newly prescribed PPIs between 1998 and 2007; 1544 patients met criteria for CAP subsequent to PPI initiation; 15 440 controls were matched through risk-set sampling by age and time under observation. Crude and adjusted odds ratios comparing current with past PPI exposures, as well as tests for interactions, were conducted for the entire and stratified samples.
Results. Current PPI use associated with CAP (adjusted odds ratio [OR], 1.29 [95% confidence interval {CI}, 1.15-1.45]). Risks were not substantially altered by age or year of diagnosis. Dementia (n = 85; P = .062 for interaction) and sedative/tranquilizer use (n = 224; P = .049 for interaction) were likely effect modifiers increasing a PPI-CAP association; conversely, for some chronic medical conditions, PPI-associated CAP risks were reversed. PPI exposures between 1 and 15 days increased CAP risks, compared with longer exposures, but PPI initiation also frequently occurred shortly after CAP diagnoses. Prescribed PPI doses.1 dose/day also increased PPI-associated CAP risks.
Conclusions. Among the veterans studied, current compared with past PPI exposures associated modestly with increased risks of CAP. However, our observations that recent treatment initiation and higher PPI doses were associated with greater risks, and the inconsistent PPI-CAP associations between patient subgroups, indicate that further inquiries are needed to separate out coincidental patterns of associations.
C1 [Hermos, John A.; Young, Melissa M.; Fonda, Jennifer R.; Gagnon, David R.; Fiore, Louis D.; Lawler, Elizabeth V.] VA Boston Healthcare Syst, VA Cooperat Studies Program, Massachusetts Vet Epidemiol Res & Informat Ctr, Pharmacoepidemiol Grp, Boston, MA USA.
[Hermos, John A.; Fiore, Louis D.] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Gagnon, David R.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Lawler, Elizabeth V.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Hermos, JA (reprint author), VA Boston Healthcare Syst 151MAV, 150 S Huntington Ave, Boston, MA 02130 USA.
EM john.hermos@va.gov
OI Gagnon, David/0000-0002-6367-3179
FU Core Funds Massachusetts Veterans Epidemiology Research and Information
Center; VA Cooperative Studies Program, VA Boston Healthcare System
FX This work was supported by Core Funds Massachusetts Veterans
Epidemiology Research and Information Center, VA Cooperative Studies
Program, VA Boston Healthcare System.
NR 34
TC 25
Z9 28
U1 0
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD JAN 1
PY 2012
VL 54
IS 1
BP 33
EP 42
DI 10.1093/cid/cir767
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 866LX
UT WOS:000298383500008
PM 22100573
ER
PT J
AU Butt, AA
Kanwal, F
AF Butt, Adeel A.
Kanwal, Fasiha
TI Boceprevir and Telaprevir in the Management of Hepatitis C
Virus-Infected Patients
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Review
ID GENOTYPE 1 INFECTION; PROTEASE INHIBITOR; ANTIVIRAL THERAPY; PLUS
RIBAVIRIN; INTERFERON; RESISTANCE
AB Recent approval of direct-acting antiviral agents (DAAs) against hepatitis C virus (HCV) offers a major advance in the management of HCV infection. These DAAs, boceprevir and telaprevir, when given with pegylated interferon alfa (Peg-IFN) and ribavirin (RBV), result in a much higher sustained virologic response rate compared with Peg-IFN and RBV. The DAA-containing regimens are approved for HCV genotype 1 infection in HCV treatment-naive and HCV treatment-experienced patients. In this review, we present an overview of pharmacology, efficacy, adverse events, and emergence of resistance-associated variants with the use of these agents. As with all drugs, especially newly approved drugs, clinicians must consult the package insert for detailed prescribing information, list of all reported adverse events, contraindications, and drug interactions.
C1 [Butt, Adeel A.] Univ Pittsburgh, Sch Med, Div Infect Dis, Dept Med, Pittsburgh, PA 15213 USA.
[Butt, Adeel A.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Butt, Adeel A.] Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Kanwal, Fasiha] St Louis Univ, Sch Med, St Louis Vet Affairs Med Ctr, St Louis, MO 63103 USA.
[Kanwal, Fasiha] St Louis Univ, Sch Med, Dept Med, Div Gastroenterol & Hepatol, St Louis, MO 63103 USA.
RP Butt, AA (reprint author), Univ Pittsburgh, Sch Med, Dept Med & Infect Dis, 3601 5th Ave,Ste 3A, Pittsburgh, PA 15213 USA.
EM aabutt@pitt.edu
FU Merck Sharp Dohme Corp.
FX A. A. B. has received investigator-initiated grant support (to
University of Pittsburgh) from Merck Sharp & Dohme Corp.
NR 21
TC 45
Z9 48
U1 1
U2 10
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD JAN 1
PY 2012
VL 54
IS 1
BP 96
EP 104
DI 10.1093/cid/cir774
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 866LX
UT WOS:000298383500020
PM 22156853
ER
PT J
AU Vorhies, JS
Wang, Y
Herndon, JH
Maloney, WJ
Huddleston, JI
AF Vorhies, John S.
Wang, Yun
Herndon, James H.
Maloney, William J.
Huddleston, James I.
TI Decreased Length of Stay After TKA Is Not Associated With Increased
Readmission Rates in a National Medicare Sample
SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH
LA English
DT Article
ID KNEE REPLACEMENT SURGERY; TOTAL HIP-REPLACEMENT; UNITED-STATES; SURGICAL
CARE; ARTHROPLASTY; OUTCOMES; QUALITY
AB Background There is a trend toward decreasing length of hospital stay (LOS) after TKA although it is unclear whether this trend is detrimental to the overall postoperative course. Such information is important for future decisions related to cost containment.
Questions/purposes We determined whether decreases in LOS after TKA are associated with increases in readmission rates.
Patients and Methods We retrospectively reviewed the rates and reasons for readmission and LOS for 4057 Medicare TKA patients from 2002 to 2007. We abstracted data from the Medicare Patient Safety Monitoring System. Hierarchical generalized linear modeling was used to assess the odds of changing readmission rates and LOS over time, controlling for changes in patient demographic and clinical variables.
Results The overall readmission rate in the 30 days after discharge was 228/4057 (5.6%). The 10 most common reasons for readmission were congestive heart failure (20.4%), chronic ischemic heart disease (13.9%), cardiac dysrhythmias (12.5%), pneumonia (10.8%), osteoarthrosis (9.4%), general symptoms (7.4%), acute myocardial infarction (7.0%), care involving other specified rehabilitation procedure (6.3%), diabetes mellitus (6.3%), and disorders of fluid, electrolyte, and acid-base balance (5.9%); the top 10 causes did not include venous thromboembolism syndromes. We found no difference in the readmission rate between the periods 2002-2004 (5.5%) and 2005-2007 (5.8%) but a reduction in LOS between the periods 2002-2004 (4.1 +/- A 2.0 days) and 2005-2007 (3.8 +/- A 1.7 days).
Conclusions The most common causes for readmission were cardiac-related. A reduction in LOS was not associated with an increase in the readmission rate in this sample. Optimization of cardiac status before discharge and routine primary care physician followup may lead to lower readmission rates.
C1 [Vorhies, John S.; Maloney, William J.; Huddleston, James I.] Stanford Med Outpatient Ctr, Dept Orthopaed Surg, Redwood City, CA 94063 USA.
[Wang, Yun] Qualidigm Inc, Middletown, CT USA.
[Wang, Yun] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Herndon, James H.] Harvard Univ, Sch Med, Dept Orthopaed Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Huddleston, JI (reprint author), Stanford Med Outpatient Ctr, Dept Orthopaed Surg, 450 Broadway St,Mailcode 6324, Redwood City, CA 94063 USA.
EM jhuddleston@stanford.edu
NR 22
TC 32
Z9 33
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0009-921X
J9 CLIN ORTHOP RELAT R
JI Clin. Orthop. Rel. Res.
PD JAN
PY 2012
VL 470
IS 1
BP 166
EP 171
DI 10.1007/s11999-011-1957-0
PG 6
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 862OR
UT WOS:000298103100021
PM 21720934
ER
PT J
AU Lambers, K
Ootes, D
Ring, D
AF Lambers, Kaj
Ootes, Daan
Ring, David
TI Incidence of Patients with Lower Extremity Injuries Presenting to US
Emergency Departments by Anatomic Region, Disease Category, and Age
SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH
LA English
DT Article
ID ANKLE INJURIES; HIP-FRACTURES; UNITED-STATES; EPIDEMIOLOGY; SPRAINS;
POPULATION; PREDICTORS; ACCIDENT; RULES
AB Background The incidence of patients with lower extremity injuries presenting to emergency departments in the United States with respect to specific anatomic regions and disease categories is unknown. Such information might be used for injury prevention, resource allocation, and training priorities.
Questions/purposes We determined the anatomic regions, disease categories, and circumstances that account for the highest incidence of leg problems among patients presenting to emergency departments in the United States.
Methods We used the National Electronic Injury Surveillance System (NEISS) to obtain a probability sample of all lower extremity injuries treated at emergency departments during 2009. A total of 119,815 patients who presented to emergency departments with lower extremity injuries in 2009 were entered in the NEISS database. Patient and injury characteristics were analyzed. Incidence rates for various regions, disease categories, injuries, and age groups were calculated using US census data.
Results We identified 112 unique combinations of disease categories and anatomic regions. Strains and sprains accounted for 36% of all lower extremity injuries. The injury with the greatest incidence was an ankle sprain (206 per 100,000; 95% confidence interval, 181-230). Younger patients were more likely to have ankle sprains, foot contusions/abrasions, and foot strains/sprains. Older patients were more likely to have lower trunk fractures and lower trunk contusions/abrasions. The most common incidence for injury was at home (45%).
Conclusions Given relatively low-acuity leg problems such as strains and sprains account for a substantial number of emergency department visits pertaining to leg problems, use of telephone triage, scheduled same or next-day urgent care appointments, and other alternatives to the traditional emergency room might result in better use of emergency healthcare resources.
C1 [Ring, David] Yawkey Ctr, Boston, MA 02114 USA.
[Lambers, Kaj; Ootes, Daan; Ring, David] Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA.
RP Ring, D (reprint author), Yawkey Ctr, 55 Fruit St,Suite 2100, Boston, MA 02114 USA.
EM dring@partners.org
NR 24
TC 27
Z9 28
U1 1
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0009-921X
J9 CLIN ORTHOP RELAT R
JI Clin. Orthop. Rel. Res.
PD JAN
PY 2012
VL 470
IS 1
BP 284
EP 290
DI 10.1007/s11999-011-1982-z
PG 7
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 862OR
UT WOS:000298103100036
PM 21785896
ER
PT J
AU Isong, IA
Luff, D
Perrin, JM
Winickoff, JP
Ng, MW
AF Isong, Inyang A.
Luff, Donna
Perrin, James M.
Winickoff, Jonathan P.
Man Wai Ng
TI Parental Perspectives of Early Childhood Caries
SO CLINICAL PEDIATRICS
LA English
DT Article
DE children; parents; caries; qualitative interviews
ID CHILDRENS ORAL-HEALTH; HEAD-START CHILDREN; YOUNG-CHILDREN; QUALITATIVE
RESEARCH; MEDICAL LITERATURE; USERS GUIDES; CARE; IMPACT; LITERACY;
OUTCOMES
AB Background. Parental perspectives of children with early childhood caries may help inform the development and improvement of caries prevention strategies. Objectives. This study aimed to explore parents' experiences, perceptions, and expectations regarding prevention and management of early childhood caries. Methods. The authors conducted semistructured interviews with 25 parents of children aged 2 to 5 years, with a known history of caries. All interviews were transcribed and coded, and iterative analyses were conducted to identify key emergent themes within the data. Results. Parents had limited knowledge of behaviors contributing to early childhood caries and when to first seek regular dental care. Parents expected pediatricians to provide education on how to prevent childhood caries, conduct preliminary oral health assessments, and help establish early linkages between medical and dental care. Conclusion. The findings make a strong case for pediatricians to take responsibility for engaging and educating parents on fostering optimal oral health and helping to access early childhood dental care.
C1 [Isong, Inyang A.] MassGen Hosp Children, Ctr Child & Adolescent Hlth Policy, Boston, MA 02114 USA.
[Luff, Donna] Harvard Pediat Hlth Serv Res Program, Boston, MA USA.
[Man Wai Ng] Childrens Hosp Boston, Boston, MA USA.
RP Isong, IA (reprint author), MassGen Hosp Children, Ctr Child & Adolescent Hlth Policy, 50 Staniford St,Suite 901, Boston, MA 02114 USA.
EM iisong@partners.org
FU DentaQuest Institute; Health Resources and Services Administration,
Department of Health and Human Services [T32 HP10018]
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This study
was supported by DentaQuest Institute. Dr Isong's work is supported by a
National Research Service Award (T32 HP10018) from the Health Resources
and Services Administration, Department of Health and Human Services. We
thank Odeviz Soto (OS), Gay Torresyap and Dr. Peter Maramaldi for
support and contributions to the study.
NR 31
TC 9
Z9 9
U1 1
U2 23
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 JAN
PY 2012
VL 51
IS 1
BP 77
EP 85
DI 10.1177/0009922811417856
PG 9
WC Pediatrics
SC Pediatrics
GA 870GC
UT WOS:000298656200010
PM 21903623
ER
PT J
AU Daniel, BS
Hertl, M
Werth, VP
Eming, R
Murrell, DF
AF Daniel, Benjamin S.
Hertl, Michael
Werth, Victoria P.
Eming, Ruediger
Murrell, Dedee F.
TI Severity score indexes for blistering diseases
SO CLINICS IN DERMATOLOGY
LA English
DT Article
ID PEMPHIGUS-VULGARIS; ORAL PEMPHIGUS; IMMUNOADSORPTION; AUTOANTIBODIES;
PROGRESSION; ANTIBODIES; RITUXIMAB
AB Scoring systems are used to assess the severity of a disease and the response to treatment. The main severity scoring indexes are the Autoimmune Bullous Skin Disorder Intensity Score (ABSIS) and the Pemphigus Disease Area Index (PDAI). They have been validated and are already used in the evaluation of pemphigus and in clinical trials. They quantify disease severity by performing a global assessment of all lesions. In recent years, other severity scoring systems have been developed for pemphigus and other autoimmune blistering diseases. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Daniel, Benjamin S.; Murrell, Dedee F.] St George Hosp, Dept Dermatol, Sydney, NSW, Australia.
[Daniel, Benjamin S.; Murrell, Dedee F.] Univ New S Wales, Dept Dermatol, Sydney, NSW, Australia.
[Hertl, Michael; Eming, Ruediger] Univ Marburg, Dept Dermatol, Marburg, Germany.
[Werth, Victoria P.] Philadelphia VA Med Ctr, Dept Dermatol, Philadelphia, PA USA.
[Werth, Victoria P.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
RP Murrell, DF (reprint author), St George Hosp, Dept Dermatol, Sydney, NSW, Australia.
EM d.murrell@unsw.edu.au
FU National Institutes of Health [NIH K24-AR 02207]
FX This work was supported in part by the National Institutes of Health
(grant number NIH K24-AR 02207) to VPW.
NR 28
TC 26
Z9 28
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0738-081X
J9 CLIN DERMATOL
JI Clin. Dermatol.
PD JAN-FEB
PY 2012
VL 30
IS 1
BP 108
EP 113
DI 10.1016/j.clindermatol.2011.03.017
PG 6
WC Dermatology
SC Dermatology
GA 864BS
UT WOS:000298212600014
PM 22137234
ER
PT J
AU Schalock, PC
Menne, T
Johansen, JD
Taylor, JS
Maibach, HI
Liden, C
Bruze, M
Thyssen, JP
AF Schalock, Peter C.
Menne, Torkil
Johansen, Jeanne D.
Taylor, James S.
Maibach, Howard I.
Liden, Carola
Bruze, Magnus
Thyssen, Jacob P.
TI Hypersensitivity reactions to metallic implants - diagnostic algorithm
and suggested patch test series for clinical use
SO CONTACT DERMATITIS
LA English
DT Review
DE allergic contact dermatitis; implant reactions; metals; patch tests
ID TOTAL JOINT REPLACEMENT; TOTAL HIP-ARTHROPLASTY; IN-STENT RESTENOSIS;
ORTHOPEDIC IMPLANTS; CONTACT SENSITIVITY; BONE-CEMENT; T-CELL; HUMAN
OSTEOCLASTS; ION RELEASE; ALLERGY
AB Cutaneous and systemic hypersensitivity reactions to implanted metals are challenging to evaluate and treat. Although they are uncommon, they do exist, and require appropriate and complete evaluation. This review summarizes the evidence regarding evaluation tools, especially patch and lymphocyte transformation tests, for hypersensitivity reactions to implanted metal devices. Patch test evaluation is the gold standard for metal hypersensitivity, although the results may be subjective. Regarding pre-implant testing, those patients with a reported history of metal dermatitis should be evaluated by patch testing. Those without a history of dermatitis should not be tested unless considerable concern exists. Regarding post-implant testing, a subset of patients with metal hypersensitivity may develop cutaneous or systemic reactions to implanted metals following implant. For symptomatic patients, a diagnostic algorithm to guide the selection of screening allergen series for patch testing is provided. At a minimum, an extended baseline screening series and metal screening is necessary. Static and dynamic orthopaedic implants, intravascular stent devices, implanted defibrillators and dental and gynaecological devices are considered. Basic management suggestions are provided. Our goal is to provide a comprehensive reference for use by those evaluating suspected cutaneous and systemic metal hypersensitivity reactions.
C1 [Schalock, Peter C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol, Boston, MA 02114 USA.
[Menne, Torkil; Johansen, Jeanne D.; Thyssen, Jacob P.] Univ Copenhagen, Gentofte Hosp, Dept Dermatoallergol, Natl Allergy Res Ctr, DK-2820 Copenhagen, Denmark.
[Taylor, James S.] Cleveland Clin, Dept Dermatol, Cleveland, OH 44195 USA.
[Maibach, Howard I.] Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94115 USA.
[Liden, Carola] Karolinska Inst, Inst Environm Med, S-10462 Stockholm, Sweden.
[Bruze, Magnus] Lund Univ, Dept Occupat & Environm Dermatol, Skane Univ Hosp, S-20502 Malmo, Sweden.
RP Schalock, PC (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol, 55 Fruit St, Boston, MA 02114 USA.
EM schalock.prof@gmail.com
OI Schalock, Peter/0000-0001-8953-4639; Liden, Carola/0000-0001-9951-5896
NR 91
TC 40
Z9 41
U1 2
U2 20
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0105-1873
EI 1600-0536
J9 CONTACT DERMATITIS
JI Contact Dermatitis
PD JAN
PY 2012
VL 66
IS 1
BP 4
EP 19
DI 10.1111/j.1600-0536.2011.01971.x
PG 16
WC Allergy; Dermatology
SC Allergy; Dermatology
GA 860CX
UT WOS:000297926500002
PM 21957996
ER
PT J
AU Braun, AB
Gibbons, FK
Litonjua, AA
Giovannucci, E
Christopher, KB
AF Braun, Andrea B.
Gibbons, Fiona K.
Litonjua, Augusto A.
Giovannucci, Edward
Christopher, Kenneth B.
TI Low serum 25-hydroxyvitamin D at critical care initiation is associated
with increased mortality
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE 25-hydroxyvitamin D; mortality; epidemiology; vitamin D
ID CHRONIC KIDNEY-DISEASE; REGULATORY T-CELLS; DISPARITIES GEOCODING
PROJECT; VITAMIN-D DEFICIENCY; NUTRITION EXAMINATION SURVEY; PROLONGED
CRITICAL ILLNESS; 3RD NATIONAL-HEALTH; ILL PATIENTS; NEIGHBORHOOD
POVERTY; INTENSIVE-CARE
AB Objective: We hypothesized that deficiency in 25-hydroxyvitamin D at critical care initiation would be associated with all-cause mortalities.
Design: Two-center observational study.
Setting: Two teaching hospitals in Boston, MA.
Patients: The study included 1,325 patients, age >= 18 yrs, in whom 25-hydroxyvitamin D was measured 7 days before or after critical care initiation between 1998 and 2009.
Measurements: 25-hydroxyvitamin D was categorized as deficiency in 25-hydroxyvitamin D (<= 15 ng/mL), insufficiency (16-29 ng/mL), and sufficiency (>= 30 ng/mL). Logistic regression examined death by days 30, 90, and 365 postcritical care initiation and in-hospital mortality. Adjusted odds ratios were estimated by multivariable logistic regression models.
Interventions: None.
Key Results: 25-hydroxyvitamin D deficiency is predictive for short-term and long-term mortality. Thirty days following critical care initiation, patients with 25-hydroxyvitamin D deficiency have an odds ratio for mortality of 1.85 (95% confidence interval 1.15-2.98; p = .01) relative to patients with 25-hydroxyvitamin D sufficiency. 25-hydroxyvitamin D deficiency remains a significant predictor of mortality at 30 days following critical care initiation following multivariable adjustment for age, gender, race, Deyo-Charlson index, sepsis, season, and surgical vs. medical patient type (adjusted odds ratio 1.94; 95% confidence interval 1.18-3.20; p = .01). Results were similarly significant at 90 and 365 days following critical care initiation and for in-hospital mortality. The association between vitamin D and mortality was not modified by sepsis, race, or neighborhood poverty rate, a proxy for socioeconomic status.
Conclusion: Deficiency of 25-hydroxyvitamin D at the time of critical care initiation is a significant predictor of all-cause patient mortality in a critically ill patient population. (Crit Care Med 2012; 40:63-72)
C1 [Braun, Andrea B.; Christopher, Kenneth B.] Brigham & Womens Hosp, Div Renal, Boston, MA 02115 USA.
[Litonjua, Augusto A.] Brigham & Womens Hosp, Pulm & Crit Care Div, Boston, MA 02115 USA.
[Christopher, Kenneth B.] Brigham & Womens Hosp, Nathan E Hellman Mem Lab, Boston, MA 02115 USA.
[Gibbons, Fiona K.] Massachusetts Gen Hosp, Div Pulm, Boston, MA 02114 USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
RP Christopher, KB (reprint author), Brigham & Womens Hosp, Div Renal, Boston, MA 02115 USA.
EM kbchristopher@partners.org
OI Litonjua, Augusto/0000-0003-0422-5875
FU NIH [K08AI060881]
FX Supported, in part, by NIH K08AI060881 (KBC).
NR 105
TC 79
Z9 92
U1 2
U2 6
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 JAN
PY 2012
VL 40
IS 1
BP 63
EP 72
DI 10.1097/CCM.0b013e31822d74f3
PG 10
WC Critical Care Medicine
SC General & Internal Medicine
GA 866KO
UT WOS:000298379800010
PM 21926604
ER
PT J
AU Berra, L
Coppadoro, A
Bittner, EA
Kolobow, T
Laquerriere, P
Pohlmann, JR
Bramati, S
Moss, J
Pesenti, A
AF Berra, Lorenzo
Coppadoro, Andrea
Bittner, Edward A.
Kolobow, Theodor
Laquerriere, Patrice
Pohlmann, Joshua R.
Bramati, Simone
Moss, Joel
Pesenti, Antonio
TI A clinical assessment of the Mucus Shaver: A device to keep the
endotracheal tube free from secretions
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE bacterial biofilm; endotracheal tube; endotracheal tube occlusion;
endotracheal tube suctioning; mechanical ventilation; Mucus Shaver;
secretion removal; ventilator-associated pneumonia
ID VENTILATOR-ASSOCIATED PNEUMONIA; PSEUDOMONAS-AERUGINOSA BIOFILMS;
MECHANICAL VENTILATION; BACTERIAL-COLONIZATION; TRACHEAL TUBE;
INTUBATION; PREVENTION; RESISTANCE; INFECTION; DIAMETER
AB Objective: We evaluated a new device designed to clean the endotracheal tube in mechanically ventilated patients, the Mucus Shaver.
Design: Prospective, randomized trial.
Setting: University hospital intensive care unit.
Patients: We enrolled 24 patients expected to remain ventilated for >72 hrs.
Interventions: The Mucus Shaver is a concentric inflatable catheter for the removal of mucus and secretions from the interior surface of the endotracheal tube. The Mucus Shaver is advanced to the distal endotracheal tube tip, inflated, and subsequently withdrawn over a period of 3-5 secs. Patients were prospectively randomized within 2 hrs of intubation to receive standard endotracheal tube suctioning treatment or standard suctioning plus Mucus Shaver use until extubation.
Measurements and Main Results: During the study period, demographic data, recent medical history, adverse events, and staff evaluation of the Mucus Shaver were recorded. At extubation, each endotracheal tube was removed, cultured, and analyzed by scanning electron microscopy. Twelve patients were assigned to the study group and 12 were assigned to the control group. No adverse events related to the use of the Mucus Shaver were observed. At extubation, only one endotracheal tube from the Mucus Shaver group was colonized, whereas in the control group ten endotracheal tubes were colonized (8% vs. 83%; p < .001). Scanning electron microscopy showed little secretions on the endotracheal tubes from the study group, whereas thick bacterial deposits were present on all the endotracheal tubes from the control group (p < .001 by Fisher exact test, using a maximum biofilm thickness of 30 mu m as cut-off). The nursing staff was satisfied by the overall safety, feasibility, and efficacy of the Mucus Shaver.
Conclusions: The Mucus Shaver is a safe, feasible, and efficient device for endotracheal tube cleaning in the clinical setting. The Mucus Shaver is helpful in preventing endotracheal tube colonization by potentially harmful microorganisms. (Crit Care Med 2012; 40:119-124)
C1 [Berra, Lorenzo; Coppadoro, Andrea; Bittner, Edward A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02115 USA.
[Coppadoro, Andrea; Pesenti, Antonio] Univ Milano Bicocca, Dept Expt Med, Milan, Italy.
[Kolobow, Theodor] NHLBI, Sect Pulm & Cardiac Assist Devices, Pulm Crit Care Med Branch, NIH, Bethesda, MD 20892 USA.
[Laquerriere, Patrice] Univ Reims, INSERM, Electron Microscopy Lab, Reims, France.
[Pohlmann, Joshua R.] Univ Michigan, Dept Gen Surg, Ann Arbor, MI 48109 USA.
[Bramati, Simone] San Gerardo Hosp, Microbiol & Virol Dept, Monza, Italy.
[Moss, Joel] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Pesenti, Antonio] San Gerardo Hosp, Dept Perioperat Med & Intens Care, Monza, Italy.
RP Berra, L (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02115 USA.
EM lberra@partners.org
RI Pesenti, Antonio/H-7483-2012; Laquerriere, Patrice/P-1025-2016
OI Laquerriere, Patrice/0000-0001-7637-9094
FU National Heart, Lung, and Blood Institute, Division of International
Research, National Institutes of Health, Department of Health and Human
Services, Bethesda, Maryland; Department of Perioperative Medicine and
Intensive Care, San Gerardo Hospital, Monza, Italy; National Institutes
of Health, National Heart, Lung, and Blood Institute, Bethesda, Maryland
FX Supported, in part, by the National Heart, Lung, and Blood Institute,
Division of International Research, National Institutes of Health,
Department of Health and Human Services, Bethesda, Maryland, and by the
Department of Perioperative Medicine and Intensive Care, San Gerardo
Hospital, Monza, Italy. Dr. Moss and Dr. Kolobow were supported by the
Intramural Research Program, National Institutes of Health, National
Heart, Lung, and Blood Institute, Bethesda, Maryland.
NR 30
TC 37
Z9 38
U1 2
U2 5
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 JAN
PY 2012
VL 40
IS 1
BP 119
EP 124
DI 10.1097/CCM.0b013e31822e9fe3
PG 6
WC Critical Care Medicine
SC General & Internal Medicine
GA 866KO
UT WOS:000298379800017
PM 21926595
ER
PT J
AU Pejo, E
Feng, Y
Chao, W
Cotten, JF
Ge, RL
Raines, DE
AF Pejo, Ervin
Feng, Yan
Chao, Wei
Cotten, Joseph F.
Ge, Ri Le
Raines, Douglas E.
TI Differential effects of etomidate and its pyrrole analogue
carboetomidate on the adrenocortical and cytokine responses to
endotoxemia
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE anesthesia; corticosteroine; cytokines; endotoxemia;
lipopolysaccharides; sepsis
ID RAPID-SEQUENCE INTUBATION; LOW-DOSE HYDROCORTISONE; SEPTIC SHOCK;
NITROUS-OXIDE; ADRENAL INSUFFICIENCY; EMERGENCY-DEPARTMENT;
CRITICALLY-ILL; ANIMAL-MODELS; INDUCTION; SEPSIS
AB Objective: We developed a novel pyrrole analog of etomidate, (R)-ethyl 1-(1-phenylethyl)-1H-pyrrole-2-carboxylate (carboetomidate), which retains etomidate's desirable anesthetic and hemodynamic properties but lacks its potent inhibitory affect on adrenocorticotropic hormone-stimulated steroid synthesis. The objective of this study was to test the hypothesis that in contrast to etomidate, carboetomidate neither suppresses the adrenocortical response to endotoxemia nor enhances the accompanying production of proinflammatory cytokines.
Design: Animal study.
Setting: University research laboratory.
Subjects: Male Sprague-Dawley rats.
Interventions: For both single and multiple anesthetic dose studies, rats were injected with Escherichia coli lipopolysaccharide immediately followed by a hypnotic dose of etomidate, carboetomidate, or vehicle alone (dimethyl sulfoxide) as a control. For single-dose studies, no additional anesthetic (or vehicle) was administered. For multiple anesthetic dose studies, additional doses of anesthetic (or vehicle) were administered every 15 mins for a total of eight anesthetic (or vehicle) doses.
Measurements and Main Results: Plasma adrenocorticotropic hormone, corticosterone, and cytokine concentrations were measured before lipopolysaccharide administration and intermittently throughout the 5-hr experiment. In single anesthetic dose studies, plasma adrenocorticotropic hormone and cytokine concentrations were not different at any time point among the etomidate, carboetomidate, and vehicle groups, whereas plasma corticosterone concentrations were briefly (60-120 mins) reduced in the etomidate group. In multiple anesthetic dose studies, plasma corticosterone concentrations were persistently lower and peak plasma interleukin-1 beta and interleukin-6 concentrations were higher in the etomidate group vs. the carboetomidate and control groups. Peak plasma interleukin-10 concentrations were similarly elevated in the etomidate and carboetomidate groups vs. the control group.
Conclusions: Compared with etomidate, carboetomidate produces less suppression of adrenocortical function and smaller increases in proinflammatory cytokine production in an endotoxemia model of sepsis. These findings suggest that carboetomidate could be a useful alternative to etomidate for maintaining anesthesia for a prolonged period of time in patients with sepsis. (Crit Care Med 2012; 40: 187-192)
C1 [Pejo, Ervin; Feng, Yan; Chao, Wei; Cotten, Joseph F.; Ge, Ri Le; Raines, Douglas E.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
RP Pejo, E (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
EM draines@partners.org
RI Feng, Yan/H-5808-2012
FU National Institutes of Health, Bethesda, MD [R01-GM087316, R21-DA029253,
K08-GM083216]; Department of Anesthesia, Critical Care, and Pain
Medicine, Massachusetts General Hospital, Boston, MA; National
Institutes of Health
FX Supported by grants R01-GM087316, R21-DA029253, and K08-GM083216 from
the National Institutes of Health, Bethesda, MD, and the Department of
Anesthesia, Critical Care, and Pain Medicine, Massachusetts General
Hospital, Boston, MA.; The Massachusetts General Hospital has submitted
patent applications for carboetomidate and related analogues. Two
authors (Drs. Raines and Cotten), and their respective laboratories,
departments, and institutions, could receive compensation related to the
development or sale of these drugs. Dr. Raines is the cofounder of
Annovation Biopharma and has an equity interest in Annovation BioPharma,
Inc., which has an option to license this technology for development.
Dr. Raines is also the lead inventor of Carboetomidate and received
royalties as an inventor. Dr. Cotten received patents and royalties from
the National Institutes of Health. The remaining authors have not
disclosed any potential conflicts of interest.
NR 54
TC 10
Z9 12
U1 0
U2 6
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 JAN
PY 2012
VL 40
IS 1
BP 187
EP 192
DI 10.1097/CCM.0b013e31822d7924
PG 6
WC Critical Care Medicine
SC General & Internal Medicine
GA 866KO
UT WOS:000298379800027
PM 21926608
ER
PT J
AU Kabra, R
Singh, JP
AF Kabra, Rajesh
Singh, Jagmeet P.
TI Catheter ablation targeting complex fractionated atrial electrograms for
the control of atrial fibrillation
SO CURRENT OPINION IN CARDIOLOGY
LA English
DT Review
DE ablation; atrial fibrillation; complex fractionated atrial electrograms
ID MAGNETIC-RESONANCE; SUBSTRATE ABLATION; PERSISTENT; HUMANS; PREVALENCE;
MECHANISMS; AF
AB Purpose of review
Catheter ablation of persistent atrial fibrillation has a lower success rate than for paroxysmal atrial fibrillation, due to structural, electrical and anatomical remodeling of the left atrium. Ablation strategies targeting complex fractionated atrial electrograms (CFAEs) are commonly employed to identify and eliminate the substrate responsible for atrial fibrillation maintenance in persistent cases. This review discusses the pathophysiology as well as the role of targeting CFAEs in catheter ablation of atrial fibrillation.
Recent findings
As our understanding regarding the origin and role of CFAEs in atrial fibrillation continues to evolve, there have been multiple recent studies looking at pathophysiology, distribution and significance of CFAEs in atrial fibrillation. In addition, different ablation strategies targeting CFAEs have been compared with the standard pulmonary vein isolation in persistent as well as paroxysmal atrial fibrillation. Recent meta-analysis studies have striven to identify atrial fibrillation patients who would benefit from CFAE ablation.
Summary
Whereas CFAE ablation in addition to standard pulmonary vein isolation improves outcomes in patients with persistent atrial fibrillation, there is no benefit of CFAE ablation in paroxysmal atrial fibrillation. Further studies are required to define and identify CFAEs more accurately, in a standardized manner, to enhance the success of catheter ablation and freedom from atrial fibrillation.
C1 [Singh, Jagmeet P.] Harvard Univ, Sch Med, Cardiac Arrhythmia Serv, Massachusetts Gen Hosp,Heart Ctr, Boston, MA 02114 USA.
[Singh, Jagmeet P.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Kabra, Rajesh] Univ Tennessee, Ctr Hlth Sci, Dept Med & Cardiac Electrophysiol, Memphis, TN 38163 USA.
RP Singh, JP (reprint author), Harvard Univ, Sch Med, Cardiac Arrhythmia Serv, Massachusetts Gen Hosp,Heart Ctr, Boston, MA 02114 USA.
EM jsingh@partners.org
FU St Jude Medical; Medtronic, Inc.; Boston Scientific Corp.; Biotronik;
Guidant Corp.; Sorin Group
FX J.P.S. received grant supports from St Jude Medical, Medtronic, Inc.,
Boston Scientific Corp., and Biotronik; served on advisory boards or as
a consultant for Boston Scientific Corp., St Jude Medical, and
Medtronic; and received honoraria or speaker fees from Medtronic, Inc.,
Biotronik, Guidant Corp., St Jude Medical, and Sorin Group.
NR 33
TC 5
Z9 5
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0268-4705
J9 CURR OPIN CARDIOL
JI Curr. Opin. Cardiol.
PD JAN
PY 2012
VL 27
IS 1
BP 49
EP 54
DI 10.1097/HCO.0b013e32834dc3bc
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 863EF
UT WOS:000298144900009
PM 22123605
ER
PT J
AU Haining, WN
Barnitz, RA
AF Haining, W. Nicholas
Barnitz, R. Anthony
TI Deconvolving heterogeneity in the CD8(+) T-cell response to HIV
SO CURRENT OPINION IN HIV AND AIDS
LA English
DT Review
DE genomics; heterogeneity; HIV; single-cell
ID DISEASE PROGRESSION; LUNG ADENOCARCINOMA; MELANOMA PATIENTS; EXPRESSION;
INFECTION; DIFFERENTIATION; EXHAUSTION; IMMUNE; DISCOVERY; ANTIGEN
AB Purpose of review
This review will discuss the use of systems biology approaches to dissect the heterogeneity of the HIV-specific CD8(+) T-cell response.
Recent findings
New experimental approaches have allowed complex phenotypes of individual cells present in the human antigen-specific CD8(+) T-cell response to be characterized. Genome-wide measurements of gene expression in antigen-specific T cells have created broad molecular phenotypes of the T-cell response to HIV. Pattern recognition algorithms to discover new subclasses of samples in microarray datasets are becoming increasingly sophisticated. Together, these advances now allow the heterogeneity of the T-cell response to HIV to be unraveled.
Summary
The phenotype of antigen-specific T cells responding to pathogens like HIV in humans is seen as much 'noisier' than in animal models of infection. However, applying new systems biology tools may provide an opportunity to identify the sources of this 'noise' as novel, biologically distinct subclasses of the CD8(+) T-cell response to HIV.
C1 [Haining, W. Nicholas; Barnitz, R. Anthony] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Haining, W. Nicholas] Harvard Univ, Sch Med, Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
RP Haining, WN (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, 44 Binney St,Dana 640, Boston, MA 02115 USA.
EM nicholas_haining@dfci.harvard.edu
OI Barnitz, Tony/0000-0002-9634-4558
FU National Institutes of Health [NIAID R01AI091493]
FX The work was supported by the National Institutes of Health (NIAID
R01AI091493 to W.N.H.).
NR 48
TC 1
Z9 1
U1 0
U2 2
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 JAN
PY 2012
VL 7
IS 1
BP 38
EP 43
DI 10.1097/COH.0b013e32834dde1c
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 863GS
UT WOS:000298151400007
PM 22156844
ER
PT J
AU Yonekawa, Y
Kim, IK
AF Yonekawa, Yoshihiro
Kim, Ivana K.
TI Pseudophakic cystoid macular edema
SO CURRENT OPINION IN OPHTHALMOLOGY
LA English
DT Review
DE anti-vascular endothelial growth factor; corticosteroids; Irvine-Gass
syndrome; nonsteroidal anti-inflammatory drugs; pseudophakic cystoid
macular edema
ID OPTICAL COHERENCE TOMOGRAPHY; NONSTEROIDAL ANTIINFLAMMATORY DRUGS;
INTRAOCULAR-LENS IMPLANTATION; CATARACT-SURGERY; INTRAVITREAL
BEVACIZUMAB; PHACOEMULSIFICATION SURGERY; TRIAMCINOLONE ACETONIDE;
COMBINATION THERAPY; TOPICAL DICLOFENAC; EFFICACY
AB Purpose of review
Pseudophakic cystoid macular edema (PCME) is a common cause of visual impairment after cataract surgery. This article systematically reviews and discusses the epidemiology, risk factors, diagnosis, and treatment of PCME, with a focus on advances in the past 1-2 years.
Recent findings
The incidence of PCME has declined with the advent of modern surgical techniques. Optical coherence tomography (OCT) has become an important adjunct to biomicroscopy and fluorescein angiography. PCME prophylaxis with topical nonsteroidal anti-inflammatory drugs remains unproven because long-term visual outcomes and comparative effectiveness studies are lacking. Chronic, refractory CME remains a therapeutic challenge, but investigational therapies with potential include corticosteroid intravitreal injections and implants, and intravitreal anti-vascular endothelial growth factor treatments. Few studies have assessed surgical options.
Summary
There is currently a lack of well designed randomized clinical trials to guide the treatment of PCME.
C1 [Yonekawa, Yoshihiro; Kim, Ivana K.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Retina Serv,Dept Ophthalmol, Boston, MA 02114 USA.
RP Kim, IK (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Retina Serv,Dept Ophthalmol, 243 Charles St, Boston, MA 02114 USA.
EM ivana_kim@meei.harvard.edu
FU Genentech, Inc.
FX I.K.K. has received research support from Genentech, Inc. and has served
as a consultant for Genentech and Novartis.
NR 54
TC 36
Z9 39
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8738
J9 CURR OPIN OPHTHALMOL
JI Curr. Opin. Ophthalmol.
PD JAN
PY 2012
VL 23
IS 1
BP 26
EP 32
DI 10.1097/ICU.0b013e32834cd5f8
PG 7
WC Ophthalmology
SC Ophthalmology
GA 863GL
UT WOS:000298150700006
PM 22134362
ER
PT J
AU Sahin, A
Hamrah, P
AF Sahin, Afsun
Hamrah, Pedram
TI Clinically relevant biometry
SO CURRENT OPINION IN OPHTHALMOLOGY
LA English
DT Review
DE biometry; cataract surgery; intraocular lens calculation; keratometry;
refractive surgery
ID INTRAOCULAR-LENS POWER; PARTIAL COHERENCE INTERFEROMETRY; CORNEAL
REFRACTIVE SURGERY; CHAMBER DEPTH MEASUREMENTS; CATARACT-SURGERY; OCULAR
BIOMETRY; ORBSCAN II; EYES; FORMULA; ACCURACY
AB Purpose of review
Obtaining precise postoperative target refraction is of utmost importance in today's modern cataract and refractive surgery. Given the growing number of patients undergoing premium intraocular lens (IOL) implantations, patient expectation continues to rise. In order to meet heightened patient expectations, it is crucial to pay utmost attention to patient selection, accurate keratometry and biometry readings, as well as to the application of correct IOL power formula with optimized lens constants. This article reviews recent advances in the field of clinical biometry and IOL power calculations.
Recent findings
Recently developed low-coherence reflectometry optical biometry is comparable to older ultrasonic biometric and keratometric techniques. In addition, the new IOLMaster software upgrade has improved reproducibility and enhanced signal acquisition. Further, the modern lens power formulas currently determine the effective lens position and the shape of the intraocular lens power prediction curve more accurately.
Summary
In order to reach target refraction, precise biometric measurements are imperative. Understanding the strengths and limitations of the currently available biometry devices allows prevention of high variability and inaccuracy, ultimately determining the refractive outcomes.
C1 [Sahin, Afsun; Hamrah, Pedram] Massachusetts Eye & Ear Infirm, Cornea & Refract Surg Serv, Ocular Surface Imaging Ctr, Boston, MA 02114 USA.
[Sahin, Afsun; Hamrah, Pedram] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02114 USA.
[Sahin, Afsun] Eskisehir Osmangazi Univ, Sch Med, Dept Ophthalmol, Eskisehir, Turkey.
RP Hamrah, P (reprint author), Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Cornea Serv, 243 Charles St, Boston, MA 02114 USA.
EM pedram_hamrah@meei.harvard.edu
FU National Institutes of Health, Bethesda, Maryland, USA [K08-EY020575];
Research to Prevent Blindness
FX The research was supported by a career development grant K08-EY020575
(P.H.) from the National Institutes of Health, Bethesda, Maryland, USA.
P. H. is also the recipient of a Career Development Award from Research
to Prevent Blindness.
NR 41
TC 14
Z9 14
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8738
J9 CURR OPIN OPHTHALMOL
JI Curr. Opin. Ophthalmol.
PD JAN
PY 2012
VL 23
IS 1
BP 47
EP 53
DI 10.1097/ICU.0b013e32834cd63e
PG 7
WC Ophthalmology
SC Ophthalmology
GA 863GL
UT WOS:000298150700009
PM 22081032
ER
PT J
AU Ripoll, LH
AF Ripoll, Luis H.
TI Clinical psychopharmacology of borderline personality disorder: an
update on the available evidence in light of the Diagnostic and
Statistical Manual of Mental Disorders-5
SO CURRENT OPINION IN PSYCHIATRY
LA English
DT Review
DE Borderline personality disorder; Diagnostic and Statistical Manual of
Mental Disorders-5; psychopharmacology
ID 18-MONTH FOLLOW-UP; POSITRON-EMISSION-TOMOGRAPHY; DIALECTICAL
BEHAVIOR-THERAPY; SELF-INJURIOUS-BEHAVIOR; DOUBLE-BLIND; TOPIRAMATE
TREATMENT; 10-YEAR COURSE; PART II; PHARMACOLOGICAL-TREATMENT; AFFECTIVE
INSTABILITY
AB Purpose of review
Clinical considerations for evidence-based treatment of borderline personality disorder (BPD) are outlined in the context of the best available evidence, discussed with reference to BPD traits currently identified in the upcoming Diagnostic and Statistical Manual of Mental Disorders - 5 (DSM-5) revision. The DSM-5 will highlight refractory affective, interpersonal, and identity symptoms in BPD as potential treatment targets. In addition to providing a framework for clinical decision-making, future research strategies will also focus on neurotransmitter systems of greater relevance to understanding overall personality functioning.
Recent findings
Although only a few randomized controlled trials of psychopharmacological treatments for BPD have been published recently, several meta-analyses and systematic reviews converge on the consensus effectiveness of lamotrigine, topiramate, valproate, aripiprazole, olanzapine, and omega-3 fatty acid supplementation. Stronger evidence exists for treating disinhibition and antagonism than negative affectivity, particularly interpersonal facets of such traits. In addition, basic research suggests a future role for modifying glutamatergic, opioid, and oxytocinergic neurotransmitter systems to treat BPD.
Summary
Clinicians should utilize omega-3, anticonvulsants, and atypical antipsychotic agents in treating specific DSM-5 BPD traits, notably disinhibition, antagonism, and some aspects of negative affectivity. Future research will focus on normalizing opioid and oxytocin dysregulation, as an adjunct to evidence-based psychotherapy, in an effort to improve interpersonal functioning.
C1 [Ripoll, Luis H.] MIRECC, James J Peters VA Med Ctr, Bronx, NY 10468 USA.
[Ripoll, Luis H.] Mt Sinai Sch Med, Mood & Personal Res Program, New York, NY USA.
RP Ripoll, LH (reprint author), MIRECC, James J Peters VA Med Ctr, 130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM luis.ripoll@mssm.edu
FU US Department of Veteran Affairs via a MIRECC
FX The author has nothing to disclose, in terms of private funding relevant
to this research. At present, he is funded entirely through US
Department of Veteran Affairs via a MIRECC Fellowship.
NR 91
TC 7
Z9 7
U1 1
U2 25
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 JAN
PY 2012
VL 25
IS 1
BP 52
EP 58
DI 10.1097/YCO.0b013e32834c3f19
PG 7
WC Psychiatry
SC Psychiatry
GA 863CS
UT WOS:000298141000009
PM 22037092
ER
PT J
AU Carruthers, MN
Stone, JH
Khosroshahi, A
AF Carruthers, Mollie N.
Stone, John H.
Khosroshahi, Arezou
TI The latest on IgG4-RD: a rapidly emerging disease
SO CURRENT OPINION IN RHEUMATOLOGY
LA English
DT Review
DE autoimmune pancreatitis; IgG4; IgG4 related disease; IgG4 related
systemic disease
ID IGG4-RELATED SYSTEMIC-DISEASE; ANGIOMATOID-NODULAR-TRANSFORMATION;
EOSINOPHILIC ANGIOCENTRIC FIBROSIS; INFLAMMATORY MYOFIBROBLASTIC TUMOR;
PLASMA-CELLS; TUBULOINTERSTITIAL NEPHRITIS; AUTOIMMUNE PANCREATITIS;
MEMBRANOUS NEPHROPATHY; SCLEROSING MESENTERITIS; MULTIFOCAL
FIBROSCLEROSIS
AB Purpose of review
Provide an update of the developments in IgG4 related disease within the last year in terms of nomenclature, diagnostic criteria and clinical features.
Recent findings
The number of diseases associated with IgG4 related disease continues to grow. The entities of idiopathic orbital inflammation, idiopathic cervical fibrosis, eosinophilic angiocentric fibrosis, reactive nodular fibrous pseudotumor, sclerosing mesenteritis, and membranous glomerulonephritis should all be added to the list of diseases associated with the IgG4 related disease spectrum. The issues of nomenclature and diagnostic criteria for IgG4 related disease have important recent developments as well.
Summary
The diagnosis of IgG4 related disease continues to be challenging. Increasing recognition of IgG4 related disease has led to a large body of literature on organ sites of involvement. Understanding how the disease manifests itself is critical to diagnosis and ultimately treatment.
C1 [Carruthers, Mollie N.; Stone, John H.; Khosroshahi, Arezou] Massachusetts Gen Hosp, Rheumatol Unit, Div Rheumatol, Dept Med, Boston, MA 02114 USA.
RP Stone, JH (reprint author), Massachusetts Gen Hosp, Rheumatol Unit, Div Rheumatol, Dept Med, 55 Fruit St, Boston, MA 02114 USA.
EM jhstone@partners.org
NR 45
TC 57
Z9 68
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8711
J9 CURR OPIN RHEUMATOL
JI Curr. Opin. Rheumatol.
PD JAN
PY 2012
VL 24
IS 1
BP 60
EP 69
DI 10.1097/BOR.0b013e32834ddb4a
PG 10
WC Rheumatology
SC Rheumatology
GA 863DG
UT WOS:000298142400009
PM 22157413
ER
PT J
AU Stathatos, N
Daniels, GH
AF Stathatos, Nikolaos
Daniels, Gilbert H.
TI Autoimmune thyroid disease
SO CURRENT OPINION IN RHEUMATOLOGY
LA English
DT Review
DE autoimmune; rheumatologic disorders; thyroid disorders
ID GRAVES-DISEASE; RHEUMATOID-ARTHRITIS; HASHIMOTOS-THYROIDITIS;
STIMULATING HORMONE; PRETIBIAL MYXEDEMA; NA+/I-SYMPORTER; THYROGLOBULIN;
ANTIBODY; GENE; AUTOANTIBODIES
AB Purpose of review
Autoimmune thyroid disorders (AITDs) are the most common organ-specific autoimmune disorders. The genetics as well as clinical and laboratory manifestations of AITDs are reviewed.
Recent findings
We discuss the association between specific rheumatologic disorders and AITDs and manifestations of AITDs that mimic rheumatologic disorders. The recently discovered common molecular pathways involved in these processes are discussed.
Summary
AITDs and rheumatologic disorders have significant commonalities both clinically and etiologically. This information is important for rheumatologists and primary care physicians who care for patients with these disorders.
C1 [Stathatos, Nikolaos; Daniels, Gilbert H.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
RP Stathatos, N (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, 15 Parkman St,WACC 730S, Boston, MA 02114 USA.
EM nstathatos@partners.org
NR 64
TC 16
Z9 16
U1 3
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1040-8711
EI 1531-6963
J9 CURR OPIN RHEUMATOL
JI Curr. Opin. Rheumatol.
PD JAN
PY 2012
VL 24
IS 1
BP 70
EP 75
DI 10.1097/BOR.0b013e32834ddb27
PG 6
WC Rheumatology
SC Rheumatology
GA 863DG
UT WOS:000298142400010
PM 22157414
ER
PT J
AU Schaefer, EAK
Pratt, DS
AF Schaefer, Esperance A. K.
Pratt, Daniel S.
TI Autoimmune hepatitis: current challenges in diagnosis and management in
a chronic progressive liver disease
SO CURRENT OPINION IN RHEUMATOLOGY
LA English
DT Review
DE autoimmune; hepatitis; iimunosuppression; liver disease; treatment
ID EPIDEMIOLOGY
AB Purpose of review
The understanding of autoimmune hepatitis (AIH) has evolved in the past two decades since diagnostic criteria were developed. Now with long-term experience with well characterized cohorts, strides have been gained in understanding the true epidemiology and natural history of the disease. Therapeutic trials have also added new tools to the armamentarium in managing this challenging disease.
Recent findings
AIH has been demonstrated to be a disease of middle-aged women, with a disease course that frequently progresses to cirrhosis, transplant or death. Despite its rare prevalence, AIH is one of the most common indications for transplantation. Diagnosis remains challenging, and the most recently adopted criteria prove very specific but lack sensitivity in the diagnosis of AIH, particularly when presenting atypically. Recently, drug-induced AIH and IgG4(+)-associated AIH have been proposed as distinct clinicopathological entities. Clinical trials for alternate therapeutics have long been needed, and recently two agents, budesonide and mycophenolate mofeteil, show promise in treating AIH.
Summary
Increasing evidence has mounted to suggest that AIH is a disease that often requires long-term treatment, and frequently progresses to end-stage liver disease. Further research identifying predictors of poor outcome, optimal therapeutic regimens and duration of treatment is much needed.
C1 [Schaefer, Esperance A. K.; Pratt, Daniel S.] Massachusetts Gen Hosp, Dept Med, Gastroenterol Unit, Boston, MA 02114 USA.
RP Pratt, DS (reprint author), Massachusetts Gen Hosp, Dept Med, Gastroenterol Unit, Boston, MA 02114 USA.
EM dspratt@partners.org
NR 28
TC 0
Z9 1
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8711
J9 CURR OPIN RHEUMATOL
JI Curr. Opin. Rheumatol.
PD JAN
PY 2012
VL 24
IS 1
BP 84
EP 89
DI 10.1097/BOR.0b013e32834de5d9
PG 6
WC Rheumatology
SC Rheumatology
GA 863DG
UT WOS:000298142400012
PM 22089102
ER
PT J
AU Carvello, M
Petrelli, A
Vergani, A
Lee, KM
Tezza, S
Chin, M
Orsenigo, E
Staudacher, C
Secchi, A
Dunussi-Joannopoulos, K
Sayegh, MH
Markmann, JF
Fiorina, P
AF Carvello, Michele
Petrelli, Alessandra
Vergani, Andrea
Lee, Kang Mi
Tezza, Sara
Chin, Melissa
Orsenigo, Elena
Staudacher, Carlo
Secchi, Antonio
Dunussi-Joannopoulos, Kyri
Sayegh, Mohamed H.
Markmann, James F.
Fiorina, Paolo
TI Inotuzumab Ozogamicin Murine Analog Mediated B-Cell Depletion Reduces
Anti-islet ABo- and Autoimmune Responses
SO DIABETES
LA English
DT Article
ID ISLET ALLOGRAFT SURVIVAL; COSTIMULATION BLOCKADE; NOD MICE; PHASE-I;
REJECTION; TRANSPLANTATION; TOLERANCE; LYMPHOCYTES; RITUXIMAB; LYMPHOMA
AB B cells participate in the priming of the allo- and autoimmune responses, and their depletion can thus be advantageous for islet transplantation. Herein, we provide an extensive study of the effect of B-cell depletion in murine models of islet transplantation. Islet transplantation was performed in hyperglycemic B-cell-deficient (mu MT) mice, in a purely alloimmune setting (BALB/c into hyperglycemic C57BL/6), in a purely autoimmune setting (NOD.SCID into hyperglycemic NOD), anti in a mixed allo-/autoimmune setting (BALB/c into hyperglycemic NOD). Inotuzumab ozogarnicin murine analog (anti-CD22 monoclonal antibody conjugated with calicheamicin [anti-CD22/cal]) efficiently depleted B cells in all three models of islet transplantation examined. Islet graft survival was significantly prolonged in B-cell-depleted mice compared with control groups in transplants of islets from BALB/c into C57BL/6 (mean survival time [MST]: 16.5 vs. 12.0 days; P = 0.004), from NOD.SCID into NOD (MST: 23.5 vs. 14.0 days; P = 0.03), and from BALB/c into NOD (MST: 12.0 vs. 5.5 days; P = 0.003). In the BALB/c into B-cell-deficient mice model, islet survival was prolonged as well (MST: mu MT = 32.5 vs. WT = 14 days; P = 0.002). Pathology revealed reduced CD3(+) cell islet infiltration and confirmed the absence of B cells in treated mice. Mechanistically, effector T cells were reduced in number, concomitant with a peripheral Th2 profile skewing and ex vivo recipient hyporesponsiveness toward donor-derived antigen as well as islet autoantigens. Finally, an anti-CD22/cal and CTLA4-Ig-based combination therapy displayed remarkable prolongation of graft survival in the stringent model of islet transplantation (BALB/c into NOD). And-CD22/cal-mediated B-cell depletion promotes the reduction of the anti-islet immune response in various models of islet transplantation. Diabetes 61:155-165,2012
C1 [Petrelli, Alessandra; Vergani, Andrea; Tezza, Sara; Chin, Melissa; Sayegh, Mohamed H.; Fiorina, Paolo] Harvard Univ, Childrens Hosp, Sch Med, Transplantat Res Ctr,Nephrol Div, Boston, MA 02115 USA.
[Carvello, Michele; Lee, Kang Mi; Markmann, James F.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02115 USA.
[Carvello, Michele; Orsenigo, Elena; Staudacher, Carlo] Ist Sci San Raffaele, Dept Surg, I-20132 Milan, Italy.
[Petrelli, Alessandra; Secchi, Antonio; Fiorina, Paolo] Ist Sci San Raffaele, Dept Med, I-20132 Milan, Italy.
[Dunussi-Joannopoulos, Kyri] Pfizer Res, Cambridge, MA USA.
RP Fiorina, P (reprint author), Harvard Univ, Childrens Hosp, Sch Med, Transplantat Res Ctr,Nephrol Div, Boston, MA 02115 USA.
EM paolo.florina@childrens.harvard.edu
RI Petrelli, Alessandra/M-7004-2015
OI Petrelli, Alessandra/0000-0002-5639-9415
FU Juvenile Diabetes Research Foundation; American Society of Nephrology;
American Diabetes Association; Italian Ministero dell'Istruzione,
dell'Universita e della Ricerca [Staminali RF-FSR-2008-1213704]; Pfizer
FX P.F. is the recipient of a Juvenile Diabetes Research Foundation Career
Development Award, an American Society of Nephrology Career Development
Award, an American Diabetes Association mentor-based fellowship, and a
grant from the Italian Ministero dell'Istruzione, dell'Universita e
della Ricerca (Staminali RF-FSR-2008-1213704). K.D.J. is a paid employee
of Pfizer. Pfizer provided anti-CD22/cal and control antibody compounds.
No other potential conflicts of interest relevant to this article were
reported.
NR 42
TC 9
Z9 9
U1 0
U2 3
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD JAN
PY 2012
VL 61
IS 1
BP 155
EP 165
DI 10.2337/db11-0684
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 871XZ
UT WOS:000298772300019
PM 22076927
ER
PT J
AU Nicolau, JC
Serrano, CV
Giraldez, RR
Baracioli, LM
Moreira, HG
Lima, F
Franken, M
Kalil, R
Ramires, JAF
Giugliano, RP
AF Nicolau, Jose Carlos
Serrano, Carlos Vicente, Jr.
Giraldez, Roberto Rocha
Baracioli, Luciano Moreira
Moreira, Humberto Graner
Lima, Felipe
Franken, Marcelo
Kalil, Roberto
Franchini Ramires, Jose Antonio
Giugliano, Robert P.
TI In Patients With Acute Myocardial Infarction, the Impact of
Hyperglycemia as a Risk Factor for Mortality Is Not Homogeneous Across
Age-Groups
SO DIABETES CARE
LA English
DT Article
ID ACUTE CORONARY SYNDROME; DIABETES-MELLITUS; GLYCEMIC CONTROL; INSULIN;
INFLAMMATION; ASSOCIATION; THERAPY; GLUCOSE
AB OBJECTIVE To assess the impact of hyperglycemia in different age-groups of patients with acute myocardial infarction (AM I).
RESEARCH DESIGN AND METHODS A total of 2,027 patients with AMI were categorized into one of five age-groups: <50 years (n = 301), >= 50 and <60 (n = 477),>= 60 and <70 (n = 545), >= 70 and <80 (n = 495), and years (n = 209). Hyperglycemia was defined as initial glucose >= 115 mg/dL.
RESULTS The adjusted odds ratios for hyperglycemia predicting hospital mortality in groups 1-5 were, respectively, 7.57 (P = 0.004), 3.21 (P 0.046), 3.50 (P = 0.003), 3.20 (P < 0.001.), and 2.16 (P = 0.021). The adjusted P values for correlation between glucose level (as a continuous variable) and mortality were 0.007, <0.001, 0.043, <0.001, and 0.064. The areas under the ROC curves (AUCs) were 0.785, 0.709, 0.657, 0.648, and 0.613. The AUC in group 1 was significantly higher than those in groups 3-5.
CONCLUSIONS The impact of hyperglycemia as a risk factor for hospital mortality in AMI is more pronounced in younger patients.
C1 [Nicolau, Jose Carlos; Serrano, Carlos Vicente, Jr.; Giraldez, Roberto Rocha; Baracioli, Luciano Moreira; Moreira, Humberto Graner; Lima, Felipe; Franken, Marcelo; Kalil, Roberto; Franchini Ramires, Jose Antonio] Univ Sao Paulo, Sch Med, Heart Inst InCor, Sao Paulo, Brazil.
[Giugliano, Robert P.] Brigham & Womens Hosp, Thrombolysis Myocardial Infarct TIMI Study Grp, Boston, MA 02115 USA.
RP Nicolau, JC (reprint author), Univ Sao Paulo, Sch Med, Heart Inst InCor, Sao Paulo, Brazil.
EM corjnicolau@incor.usp.br
RI Moreira, Humberto/D-2001-2012; Nicolau, Jose/E-1487-2012; Giraldez,
Roberto/E-2498-2012; Serrano Junior, Carlos Vicente/I-2729-2013; Kalil
Filho, Roberto/D-4994-2014
NR 15
TC 6
Z9 7
U1 0
U2 1
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD JAN
PY 2012
VL 35
IS 1
BP 150
EP 152
DI 10.2337/dc11-1170
PG 3
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 871XV
UT WOS:000298771900026
PM 22028280
ER
PT J
AU Funnell, MM
Brown, TL
Childs, BP
Haas, LB
Hosey, GM
Jensen, B
Maryniuk, M
Peyrot, M
Piette, JD
Reader, D
Siminerio, LM
Weinger, K
Weiss, MA
AF Funnell, Martha M.
Brown, Tammy L.
Childs, Belinda P.
Haas, Linda B.
Hosey, Gwen M.
Jensen, Brian
Maryniuk, Melinda
Peyrot, Mark
Piette, John D.
Reader, Diane
Siminerio, Linda M.
Weinger, Katie
Weiss, Michael A.
TI National Standards for Diabetes Self-Management Education
SO DIABETES CARE
LA English
DT Review
ID RANDOMIZED CONTROLLED-TRIAL; CHRONIC DISEASE MANAGEMENT; IMPROVE
GLYCEMIC CONTROL; PRIMARY-CARE PATIENTS; HEALTH-CARE; COMPLICATIONS
TRIAL; PATIENT EDUCATION; AFRICAN-AMERICAN; COMMUNITY-HEALTH; CHRONIC
ILLNESS
C1 [Funnell, Martha M.] Univ Michigan, Dept Med Educ, Ctr Diabet Res & Training, Ann Arbor, MI 48109 USA.
[Brown, Tammy L.] Indian Hlth Serv, Albuquerque, NM USA.
[Childs, Belinda P.] MidAmer Diabet Associates, Wichita, KS USA.
[Haas, Linda B.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Hosey, Gwen M.] Ctr Dis Control & Prevent, Div Diabet Translat, Natl Ctr Chron Dis Prevent & Hlth Promot, Atlanta, GA USA.
[Jensen, Brian] Lakeshore Apothacare, Two Rivers, WI USA.
[Maryniuk, Melinda; Weinger, Katie] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Peyrot, Mark] Loyola Coll, Baltimore, MD 21210 USA.
[Piette, John D.] VA Ann Arbor Hlth Care Syst, Ann Arbor, MI USA.
[Piette, John D.] Univ Michigan, Dept Internal Med, Ctr Diabet Res & Training, Ann Arbor, MI 48109 USA.
[Reader, Diane] Int Diabet Ctr, Minneapolis, MN USA.
[Siminerio, Linda M.] Univ Pittsburgh, Med Ctr, Inst Diabet, Pittsburgh, PA USA.
[Weiss, Michael A.] Patient Ctr Solut, Pittsburgh, PA USA.
RP Funnell, MM (reprint author), Univ Michigan, Dept Med Educ, Ctr Diabet Res & Training, Ann Arbor, MI 48109 USA.
EM mfunnell@umich.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases of the
National Institutes of Health [NIH5P60 DK20572, 1 R18 0K062323];
American Diabetes Association; American Association of Diabetes
Educators
FX Work on this article was supported in part by grant nos. NIH5P60 DK20572
and 1 R18 0K062323 from the National Institute of Diabetes and Digestive
and Kidney Diseases of the National Institutes of Health.; The Task
Force gratefully acknowledges the assistance and support of Paulina
Duker, MPH, APRN-BC, CDE, and Nathanial Clark, MD, CDE, of the American
Diabetes Association; Lori Porter, MBA, RD, CAE, of the American
Association of Diabetes Educators; and Karmeen Kulkami, MS, RD, BC-ADM,
Past President, Health Care and Education of the American Diabetes
Association; Malincla Peeples, MS, RN, CDE, Past President of the
American Association of Diabetes Educators; and Carole' Mensing, RN, MA,
CDE, for their insights and helpful suggestions.
NR 164
TC 78
Z9 78
U1 3
U2 19
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD JAN
PY 2012
VL 35
IS 1
SU 1
BP S101
EP S108
DI 10.2337/dc12-S089
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 871XY
UT WOS:000298772200010
PM 22187467
ER
PT J
AU Fan, Y
Liu, Y
Oklu, R
He, NS
Li, P
Wu, Q
Deipolyi, A
Wicky, S
Song, HY
AF Fan, Yong
Liu, Yang
Oklu, Rahmi
He, Neng-Shu
Li, Ping
Wu, Qi
Deipolyi, Amy
Wicky, Stephan
Song, Ho-Young
TI Balloon occlusion of the right main bronchus in an ovine model provides
sufficient time for emergent interventions in massive pulmonary embolism
SO DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
DE pulmonary embolism; ventilation-perfusion ratio; balloon
catheterization; animal experimentation
ID AUTOLOGOUS BLOOD; PORCINE MODEL; THROMBOLYSIS
AB PURPOSE
Massive pulmonary embolism (PE) causes hemodynamic compromise and is associated with a high rate of mortality. We sought to create a model of massive PE and to determine whether occlusion of the right main bronchus could mitigate the physiological effects of massive PE in this model.
MATERIALS AND METHODS
We used 27 female sheep to generate a model of massive PE by either autologous blood clot injection (n=18) or detachable balloon release (n=9) into the right main pulmonary artery. Four sheep were excluded after blood clot injection, as they did not exhibit adequate declines in blood oxygen saturation (SaO(2)). Nine of the sheep that received autologous blood clot and nine that received detachable balloons went on to treatment with right main bronchus occlusion. The control group (n=5) received the autologous blood clot, but no occlusion of the right main bronchus. All sheep underwent continuous monitoring of pulmonary arterial mean pressure (PAMP), SaO(2), arterial partial pressure of oxygen (PaO(2)), and arterial partial pressure of carbon dioxide.
RESULTS
Twenty-three sheep (85%) subjected to PE demonstrated immediate tachycardia, tachypnea, and decline in SaO(2) of at least 25% within 30 min. After right main bronchus occlusion, 18 sheep (100%) survived for the length of the experiment and exhibited persistently higher SaO(2) and PaO(2) levels, as well as decreased PAMP compared with the controls. In the control group, two out of five sheep died within 30 min, and the three surviving subjects demonstrated significantly decreased SaO(2) and PaO(2) levels.
CONCLUSION
Occlusion of the right main bronchus in an ovine model of massive PE effectively extends life and provides favorable physiological parameters to allow emergent interventions.
C1 [Oklu, Rahmi; Deipolyi, Amy; Wicky, Stephan] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Vasc Imaging & Intervent, Cambridge, MA 02138 USA.
[Fan, Yong] Tianjin Med Univ, Grad Sch, Tianjin, Peoples R China.
[Liu, Yang] Childrens Hosp, Dept Radiol, Tianjin, Peoples R China.
[He, Neng-Shu] Tianjin Med Univ, Gen Hosp, Dept Radiol, Tianjin, Peoples R China.
[Li, Ping] Haihe Hosp, Dept Radiol, Tianjin, Peoples R China.
[Wu, Qi] Haihe Hosp, Dept Pulmonol, Tianjin, Peoples R China.
[Song, Ho-Young] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Radiol, Seoul, South Korea.
RP Oklu, R (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Vasc Imaging & Intervent, Cambridge, MA 02138 USA.
EM rahmioklu@gmail.com
OI Deipolyi, Amy/0000-0003-3144-386X
NR 19
TC 0
Z9 0
U1 0
U2 1
PU TURKISH SOC RADIOLOGY
PI ANKARA
PA HOSDERE CAD, GUZELKENT SOK, CANKAYA EVLERI, F-2, ANKARA, 06540, TURKEY
SN 1305-3825
J9 DIAGN INTERV RADIOL
JI Diagn. Interv. Radiol.
PD JAN-FEB
PY 2012
VL 18
IS 1
BP 127
EP 131
DI 10.4261/1305-3825.DIR.4069-10.2
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 872RZ
UT WOS:000298828300017
PM 22020948
ER
PT J
AU Deipolyi, A
Karaosmanoglu, A
Habito, C
Brannan, S
Wicky, S
Hirsch, J
Oklu, R
AF Deipolyi, Amy
Karaosmanoglu, Ali
Habito, Cicero
Brannan, Scott
Wicky, Stephan
Hirsch, Joshua
Oklu, Rahmi
TI The role of bilateral inferior petrosal sinus sampling in the diagnostic
evaluation of Cushing syndrome
SO DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY
LA English
DT Review
DE ACTH-secreting pituitary adenoma; inferior petrosal sinus sampling;
Cushing syndrome
ID CORTICOTROPIN-RELEASING-FACTOR; DIFFERENTIAL-DIAGNOSIS;
ADRENOCORTICOTROPIC HORMONE; TRANSSPHENOIDAL SURGERY; VENOUS DRAINAGE;
DISEASE; ADENOMAS; COMPLICATIONS; POPULATION; ACTH
AB Bilateral inferior petrosal sinus sampling is the gold standard diagnostic assay in identifying the pituitary source of adrenocorticotropic hormone secretion in Cushing syndrome. The noninvasive assays used in the workup of Cushing syndrome are often misleading or ambiguous, yielding sensitivities of up to only 80%. Inferior petrosal sinus sampling, however, is highly accurate and safe when performed in experienced centers. We review here the historical and technical details of the procedure, with emphasis on the relevant anatomy and a discussion of possible rare complications.
C1 [Deipolyi, Amy; Karaosmanoglu, Ali; Habito, Cicero; Brannan, Scott; Wicky, Stephan; Oklu, Rahmi] Massachusetts Gen Hosp, Dept Vasc Imaging & Intervent, Boston, MA 02114 USA.
[Hirsch, Joshua] Massachusetts Gen Hosp, Dept Neurointervent Radiol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Oklu, R (reprint author), Massachusetts Gen Hosp, Dept Vasc Imaging & Intervent, Boston, MA 02114 USA.
EM roklu@partners.org
RI Karaosmanoglu, Ali/D-8624-2015;
OI Karaosmanoglu, Ali/0000-0003-0027-9593; Deipolyi,
Amy/0000-0003-3144-386X
FU American College of Phlebology
FX Dr. Oklu is the recipient of the Junior Faculty Investigator Award from
the American College of Phlebology.
NR 55
TC 7
Z9 7
U1 0
U2 1
PU TURKISH SOC RADIOLOGY
PI ANKARA
PA HOSDERE CAD, GUZELKENT SOK, CANKAYA EVLERI, F-2, ANKARA, 06540, TURKEY
SN 1305-3825
EI 1305-3612
J9 DIAGN INTERV RADIOL
JI Diagn. Interv. Radiol.
PD JAN-FEB
PY 2012
VL 18
IS 1
BP 132
EP 138
DI 10.4261/1305-3825.DIR.4279-11.0
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 872RZ
UT WOS:000298828300018
PM 21348009
ER
PT J
AU Sikanderkhel, S
Luthra, M
Chavalitdhamrong, D
AF Sikanderkhel, Saad
Luthra, Munish
Chavalitdhamrong, Disaya
TI SNAKESKIN-LIKE PATTERN MIMICKING PORTAL HYPERTENSIVE GASTROPATHY IN
PATIENT WITH EOSINOPHILIC GASTRITIS
SO DIGESTIVE ENDOSCOPY
LA English
DT Editorial Material
C1 [Sikanderkhel, Saad; Luthra, Munish; Chavalitdhamrong, Disaya] Mt Sinai Sch Med, James J Peters Vet Affairs Med Ctr, Bronx, NY USA.
RP Sikanderkhel, S (reprint author), Mt Sinai Sch Med, James J Peters Vet Affairs Med Ctr, Bronx, NY USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0915-5635
J9 DIGEST ENDOSC
JI Dig. Endosc.
PD JAN
PY 2012
VL 24
IS 1
BP 53
EP 53
DI 10.1111/j.1443-1661.2011.01155.x
PG 1
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA 869KT
UT WOS:000298597500013
PM 22211417
ER
PT J
AU Levack, MM
Savitt, LR
Berger, DL
Shellito, PC
Hodin, RA
Rattner, DW
Goldberg, SM
Bordeianou, L
AF Levack, Melissa M.
Savitt, Lieba R.
Berger, David L.
Shellito, Paul C.
Hodin, Richard A.
Rattner, David W.
Goldberg, Stanley M.
Bordeianou, Liliana
TI Sigmoidectomy Syndrome? Patients' Perspectives on the Functional
Outcomes Following Surgery for Diverticulitis
SO DISEASES OF THE COLON & RECTUM
LA English
DT Article
DE Diverticulitis; Quality of life; Fecal incontinence; Colectomy
ID QUALITY-OF-LIFE; FECAL INCONTINENCE; COMORBIDITY; PREVALENCE;
INSTRUMENT; PARAMETERS; DIAGNOSIS; COLOSTOMY; RESECTION; SYMPTOMS
AB BACKGROUND: Bowel function following surgery for diverticulitis has not previously been systematically described.
OBJECTIVE: This study aimed to document the frequency, severity, and predictors of suboptimal bowel function in patients who have undergone sigmoid colectomy for diverticulitis.
DESIGN: This study is a retrospective analysis.
SETTING: This study was conducted at a large, academic medical center.
PATIENTS: Three hundred twenty-five patients who underwent laparoscopic or open sigmoid colectomy with restoration of intestinal continuity for diverticulitis were included in the study population. Of these, 249 patients (76.6%) returned a 70-question survey incorporating the Fecal Incontinence Severity Index, the Fecal Incontinence Quality of Life Scale, and the Memorial Bowel Function Instrument.
MAIN OUTCOME MEASURES: Survey responders and nonresponders were compared with the use of chi(2) and t tests. Responders with suboptimal bowel function (fecal incontinence, urgency and/or incomplete emptying) were then compared with those with good outcomes by the use of logistic regression analysis to determine the predictors of poor function.
RESULTS: Of the responders, 24.8% reported clinically relevant fecal incontinence (Fecal Incontinence Severity Index >= 24), 19.6% reported fecal urgency (Memorial Bowel Function Instrument Urgency Subscale >= 4), and 20.8% reported incomplete emptying (Memorial Bowel Function Instrument Emptying Subscale >= 4). On logistic regression analysis, fecal incontinence was predicted by female sex (OR = 2.3, p = 0.008) and the presence of a preoperative abscess (OR = 1.4, p < 0.05). Fecal urgency was associated with female sex (OR = 1.3, p < 0.05) and a diverting ileostomy (OR = 2.1, p < 0.001). Incomplete emptying was associated with female sex (OR = 1.4, p < 0.05) and postoperative sepsis (OR = 1.9, p < 0.05).
LIMITATIONS: This study was limited by the fact that we did not use a nondiverticulitis control group and we had limited preoperative data on the history of bowel impairment symptoms.
CONCLUSION: One-fifth of patients reported fecal urgency, fecal incontinence, or incomplete emptying after surgery for diverticulitis. Despite the limitations of our study, these results are concerning and should be investigated further prospectively.
C1 [Levack, Melissa M.; Savitt, Lieba R.; Berger, David L.; Shellito, Paul C.; Hodin, Richard A.; Rattner, David W.; Bordeianou, Liliana] Massachusetts Gen Hosp, Div Gastrointestinal Surg, Colon & Rectal Surg Program, Boston, MA 02114 USA.
[Levack, Melissa M.; Savitt, Lieba R.; Berger, David L.; Shellito, Paul C.; Hodin, Richard A.; Rattner, David W.; Bordeianou, Liliana] Harvard Univ, Sch Med, Boston, MA USA.
[Goldberg, Stanley M.] Univ Minnesota, Dept Colon & Rectal Surg, Minneapolis, MN USA.
RP Bordeianou, L (reprint author), Massachusetts Gen Hosp, Div Gastrointestinal Surg, Colon & Rectal Surg Program, 15 Parkman St,ACC 460, Boston, MA 02114 USA.
EM lbordeianou@partners.org
NR 23
TC 22
Z9 22
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0012-3706
J9 DIS COLON RECTUM
JI Dis. Colon Rectum
PD JAN
PY 2012
VL 55
IS 1
BP 10
EP 17
DI 10.1097/DCR.0b013e31823907a9
PG 8
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA 863GK
UT WOS:000298150600007
PM 22156862
ER
PT J
AU Rosowski, JJ
Nakajima, HH
Hamade, MA
Mahfoud, L
Merchant, GR
Halpin, CF
Merchant, SN
AF Rosowski, John J.
Nakajima, Hideko H.
Hamade, Mohamad A.
Mahfoud, Lorice
Merchant, Gabrielle R.
Halpin, Christopher F.
Merchant, Saumil N.
TI Ear-Canal Reflectance, Umbo Velocity, and Tympanometry in Normal-Hearing
Adults
SO EAR AND HEARING
LA English
DT Article
ID HUMAN MIDDLE-EAR; LASER-DOPPLER VIBROMETRY; TYMPANIC MEMBRANE; ENERGY
REFLECTANCE; MULTIFREQUENCY TYMPANOMETRY; ACOUSTIC-IMPEDANCE;
OTOSCLEROTIC EARS; INPUT IMPEDANCE; SOUND PRESSURE; FREQUENCY
AB Objective: This study compares measurements of ear-canal reflectance (ECR) to other objective measurements of middle ear function including audiometry, umbo velocity (V(U)), and tympanometry in a population of strictly defined normal-hearing ears.
Design: Data were prospectively gathered from 58 ears of 29 normal-hearing subjects, 16 females and 13 males, aged 22 to 64 yr. Subjects met all of the following criteria to be considered as having normal hearing: (1) no history of significant middle ear disease; (2) no history of otologic surgery; (3) normal tympanic membrane on otoscopy; (4) pure-tone audiometric thresholds of 20 dB HL or better for 0.25 to 8 kHz; (5) air-bone gaps no greater than 15 dB at 0.25 kHz and 10 dB for 0.5 to 4 kHz; (6) normal, type-A peaked tympanograms; and (7) all subjects had two "normal" ears (as defined by these criteria). Measurements included pure-tone audiometry for 0.25 to 8 kHz, standard 226 Hz tympanometry, ECR for 0.2 to 6 kHz at 60 dB SPL using the Mimosa Acoustics HearID system, and umbo velocity (V(U)) for 0.3 to 6 kHz at 70 to 90 dB SPL using the HLV-1000 laser Doppler vibrometer (Polytec Inc).
Results: Mean power reflectance (vertical bar ECR vertical bar(2)) was near 1.0 at 0.2 to 0.3 kHz, decreased to a broad minimum of 0.3 to 0.4 between 1 and 4 kHz, and then sharply increased to almost 0.8 by 6 kHz. The mean pressure reflectance phase angle (angle ECR) plotted on a linear frequency scale showed a group delay of approximately 0.1 msec for 0.2 to 6 kHz. Small significant differences were observed in vertical bar ECR vertical bar(2) at the lowest frequencies between right and left ears and between males and females at 4 kHz. vertical bar ECR vertical bar(2) decreased with age but reached significance only at 1 kHz. Our ECR measurements were generally similar to previous published reports. Highly significant negative correlations were found between vertical bar ECR vertical bar(2) and V(U) for frequencies below 1 kHz. Significant correlations were also found between the tympanometrically determined peak total compliance and vertical bar ECR vertical bar(2) and V(U) at frequencies below 1 kHz. The results suggest that middle ear compliance contributes significantly to the measured power reflectance and umbo velocity at frequencies below 1 kHz but not at higher frequencies.
Conclusions: This study has established a database of objective measurements of middle ear function (ECR, umbo velocity, tympanometry) in a population of strictly defined normal-hearing ears. These data will promote our understanding of normal middle ear function and will serve as a control for comparison to similar measurements made in pathological ears.
C1 [Rosowski, John J.; Nakajima, Hideko H.; Hamade, Mohamad A.; Mahfoud, Lorice; Merchant, Gabrielle R.; Merchant, Saumil N.] Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA.
[Rosowski, John J.; Nakajima, Hideko H.; Hamade, Mohamad A.; Mahfoud, Lorice; Merchant, Saumil N.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
[Rosowski, John J.; Nakajima, Hideko H.; Merchant, Gabrielle R.; Merchant, Saumil N.] MIT, Harvard Mit Div Hlth Sci & Technol, Speech & Hearing Biosci & Technol Program, Cambridge, MA 02139 USA.
[Halpin, Christopher F.] Massachusetts Eye & Ear Infirm, Dept Audiol, Boston, MA 02114 USA.
RP Rosowski, JJ (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA.
EM john_rosowski@meei.harvard.edu
OI Merchant, Gabrielle/0000-0001-7251-1879
FU NIH/NIDCD [R01-DC004798]
FX This work was supported by NIH/NIDCD Grant R01-DC004798.
NR 70
TC 29
Z9 30
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-0202
J9 EAR HEARING
JI Ear Hear.
PD JAN-FEB
PY 2012
VL 33
IS 1
BP 19
EP 34
DI 10.1097/AUD.0b013e31822ccb76
PG 16
WC Audiology & Speech-Language Pathology; Otorhinolaryngology
SC Audiology & Speech-Language Pathology; Otorhinolaryngology
GA 869WS
UT WOS:000298630200003
PM 21857517
ER
PT J
AU Nakajima, HH
Pisano, DV
Roosli, C
Hamade, MA
Merchant, GR
Mahfoud, L
Halpin, CF
Rosowski, JJ
Merchant, SN
AF Nakajima, Hideko H.
Pisano, Dominic V.
Roosli, Christof
Hamade, Mohamad A.
Merchant, Gabrielle R.
Mahfoud, Lorice
Halpin, Christopher F.
Rosowski, John J.
Merchant, Saumil N.
TI Comparison of Ear-Canal Reflectance and Umbo Velocity in Patients With
Conductive Hearing Loss: A Preliminary Study
SO EAR AND HEARING
LA English
DT Article
ID HUMAN MIDDLE-EAR; ENERGY REFLECTANCE; TYMPANIC MEMBRANE; OSSICULAR
CHAIN; DEHISCENCE; ADULTS; ADMITTANCE; VIBROMETRY; IMPEDANCE; INFANTS
AB Objective: The goal of the present study was to investigate the clinical utility of measurements of ear-canal reflectance (ECR) in a population of patients with conductive hearing loss in the presence of an intact, healthy tympanic membrane and an aerated middle ear. We also sought to compare the diagnostic accuracy of umbo velocity (V(U)) measurements and measurements of ECR in the same group of patients.
Design: This prospective study comprised 31 adult patients with conductive hearing loss, of which 14 had surgically confirmed stapes fixation due to otosclerosis, 6 had surgically confirmed ossicular discontinuity, and 11 had computed tomography and vestibular evoked myogenic potential confirmed superior semicircular canal dehiscence (SCD). Measurements on all 31 ears included pure-tone audiometry for 0.25 to 8 kHz, ECR for 0.2 to 6 kHz using the Mimosa Acoustics HearID system, and V(U) for 0.3 to 6 kHz using the HLV-1000 laser Doppler vibrometer (Polytec Inc, Waldbronn, Germany). We analyzed power reflectance vertical bar ECR vertical bar(2) as well as the absorbance level = 10 x log(10)(1 - vertical bar ECR vertical bar(2)). All measurements were made before any surgical intervention. The V(U) and ECR data were plotted against normative data obtained in a companion study of 58 strictly defined normal ears (Rosowski et al., 2011).
Results: Small increases in vertical bar ECR vertical bar(2) at low-to-mid frequencies (400-1000 Hz) were observed in cases with stapes fixation, while narrowband decreases were seen for both SCD and ossicular discontinuity. The SCD and ossicular discontinuity differed in that the SCD had smaller decreases at mid-frequency (similar to 1000 Hz), whereas ossicular discontinuity had larger decreases at lower frequencies (500-800 Hz). SCD tended to have less air-bone gap at high frequencies (1-4 kHz) compared with stapes fixation and ossicular discontinuity. The vertical bar ECR vertical bar(2) measurements, in conjunction with audiometry, could successfully separate 28 of the 31 cases into the three pathologies. By comparison, VU measurements, in conjunction with audiometry, could successfully separate various pathologies in 29 of 31 cases.
Conclusions: The combination of vertical bar ECR vertical bar(2) with audiometry showed clinical utility in the differential diagnosis of conductive hearing loss in the presence of an intact tympanic membrane and an aerated middle ear and seems to be of similar sensitivity and specificity to measurements of V(U) plus audiometry. Additional research is needed to expand upon these promising preliminary results.
C1 [Nakajima, Hideko H.; Pisano, Dominic V.; Roosli, Christof; Hamade, Mohamad A.; Merchant, Gabrielle R.; Mahfoud, Lorice; Rosowski, John J.; Merchant, Saumil N.] Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, Boston, MA 02114 USA.
[Nakajima, Hideko H.; Roosli, Christof; Hamade, Mohamad A.; Mahfoud, Lorice; Halpin, Christopher F.; Rosowski, John J.; Merchant, Saumil N.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
[Nakajima, Hideko H.; Merchant, Gabrielle R.; Rosowski, John J.; Merchant, Saumil N.] MIT, Harvard Mit Div Hlth Sci & Technol, Speech & Hearing Biosci & Technol Program, Cambridge, MA 02139 USA.
[Halpin, Christopher F.] Massachusetts Eye & Ear Infirm, Dept Audiol, Boston, MA 02114 USA.
RP Nakajima, HH (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA.
EM heidi_nakajima@meei.harvard.edu
OI Merchant, Gabrielle/0000-0001-7251-1879
FU NIH [R01 DC004798]
FX This work was supported by NIH Grant R01 DC004798 and a donation from
Mr. Lakshmi Mittal.
NR 34
TC 23
Z9 24
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-0202
J9 EAR HEARING
JI Ear Hear.
PD JAN-FEB
PY 2012
VL 33
IS 1
BP 35
EP 43
DI 10.1097/AUD.0b013e31822ccba0
PG 9
WC Audiology & Speech-Language Pathology; Otorhinolaryngology
SC Audiology & Speech-Language Pathology; Otorhinolaryngology
GA 869WS
UT WOS:000298630200004
PM 21857516
ER
PT J
AU Jones, JA
Freyman, RL
AF Jones, J. Ackland
Freyman, Richard L.
TI Effect of Priming on Energetic and Informational Masking in a
Same-Different Task
SO EAR AND HEARING
LA English
DT Article
ID ON-SPEECH MASKING; IMPLICIT MEMORY; OLDER-ADULTS; WORD RECOGNITION;
RELEASE; CONTEXT; YOUNGER; PERCEPTION; HEARING; RECALL
AB Objectives: The primary goal of this study was to investigate how speech perception is altered by the provision of a preview or "prime" of a sample of speech just before it is presented in masking. A same-different test paradigm was developed which enabled the effect of priming to be measured with energetic maskers in addition to those that most likely produced both energetic and informational masking. Using this paradigm, the benefit of priming in overcoming energetic and informational masking was compared.
Design: Twenty-four normal-hearing subjects listened to nonsense sentences presented in a background of competing speech (two-talker babble) or one of two types of speech-shaped noise. Both target and masker were presented via loudspeaker directly in front of the listeners. In the baseline condition, the listeners were then shown a sentence on a computer screen that either matched the auditory target sentence exactly or contained a replacement for one of the three target key words. Their task was to judge whether the printed sentence matched the auditory target and respond via computer keyboard. In the first experimental condition, the printed sentence preceded rather than followed the auditory presentation (the priming condition). In the second experimental condition, the perception of spatial separation was created between target and masker by presenting the masker from two loudspeakers (front and 60 to the right) and imposing a 4-msec delay in the masker coming from the front loudspeaker. This resulted in the target being heard from the front while, because of the precedence effect, the masker was heard well to the right (the spatial condition). In a third experimental condition, spatial separation and priming were combined. A total of five signal-to-noise ratios were tested for each masker.
Results: The competing speech masker produced more masking than noise, consistent with previous findings. For the competing speech masker, the signal-to-noise ratio for 80% correct performance was approximately 6.7 dB lower when the listeners read the sentences first (the priming condition) than in the baseline condition. This priming effect was similar to the improvement obtained when the target and masker were separated spatially. Significant priming effects were also observed with speech-shaped noise maskers, and when there was perceived spatial separation between target and masker, conditions in which informational masking was believed to have been minimal. There seemed to be an additive effect of spatial separation and priming in the two-talker babble condition.
Conclusions: (1) Priming was effective in improving speech perception in all conditions, including those consisting of primarily energetic masking. (2) It is not clear how much benefit from priming could be attributed to release from informational masking. (3) Performance on the same-different task was linearly related to performance on an open-set speech recognition task using the same target and masker.
C1 [Jones, J. Ackland] Massachusetts Eye & Ear Infirm, Dept Audiol, Boston, MA 02114 USA.
[Jones, J. Ackland; Freyman, Richard L.] Univ Massachusetts, Dept Commun Disorders, Amherst, MA 01003 USA.
RP Jones, JA (reprint author), Massachusetts Eye & Ear Infirm, Dept Audiol, 243 Charles St,2nd Floor, Boston, MA 02114 USA.
EM ackland_jones@meei.harvard.edu
FU NIDCD [01625]
FX This work was supported by NIDCD Grant No. 01625.
NR 33
TC 3
Z9 3
U1 3
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-0202
J9 EAR HEARING
JI Ear Hear.
PD JAN-FEB
PY 2012
VL 33
IS 1
BP 124
EP 133
DI 10.1097/AUD.0b013e31822b5bee
PG 10
WC Audiology & Speech-Language Pathology; Otorhinolaryngology
SC Audiology & Speech-Language Pathology; Otorhinolaryngology
GA 869WS
UT WOS:000298630200013
PM 21841488
ER
PT J
AU Tanaka, Y
Park, JH
Tanwar, PS
Kaneko-Tarui, T
Mittal, S
Lee, HJ
Teixeira, JM
AF Tanaka, Yoshihiro
Park, Joo Hyun
Tanwar, Pradeep S.
Kaneko-Tarui, Tomoko
Mittal, Shilpi
Lee, Ho-Joon
Teixeira, Jose M.
TI Deletion of Tuberous Sclerosis 1 in Somatic Cells of the Murine
Reproductive Tract Causes Female Infertility
SO ENDOCRINOLOGY
LA English
DT Article
ID ANTI-MULLERIAN HORMONE; REGULATE MUC1 EXPRESSION; BABOON PAPIO-ANUBIS;
UTERINE EPITHELIUM; PRIMORDIAL FOLLICLES; LIFE-SPAN; INHIBITING
SUBSTANCE; ENDOMETRIAL CANCER; BETA-CATENIN; MOUSE UTERUS
AB Tumors develop with dysregulated activation of mammalian target of rapamycin (mTOR), the kinase activity of which is kept in an inactive state by a tumor suppressor dimer containing tuberous sclerosis 1 (TSC1) and TSC2. We examined whether conditional deletion of TSC1 by a knock-in allele of the anti-Mullerian hormone type 2 receptor (Amhr2) driving Cre expression and subsequent activation of mTOR in granulosa cells and in oviductal and uterine stromal cells affects fertility in female mice. Increased phosphorylation of ribosomal protein S6, a downstream target of activated mTOR, was observed in all AMHR2-expressing tissues examined, indicating loss of TSC1 activity. TSC1 deletion in granulosa cells led to the detection of significantly fewer primordial follicles in mutant mice at 12 wk, suggesting premature ovarian insufficiency, which might be related to the significantly increased time mutant mice spent in estrus. Although the number of good-quality ovulated oocytes was not significantly different compared with controls, there was a significantly higher number of degenerated oocytes after normal and superovulation, suggesting compromised oocyte quality, as well. Natural mating also showed severalfold higher numbers of degenerate bodies in the mutants that collected in bilateral swellings resembling hydrosalpinges that formed in all mice examined because of occlusion of the proximal oviduct. Attempts to transfer control embryos into mutant uteri also failed, indicating that implantation was compromised. Endometrial epithelial cells continued to proliferate, and quantitative RT-PCR showed that mucin 1 expression persisted during the window of implantation in mutantuteri, without any changes in progesterone receptor mRNA expression, suggesting a mechanism that does not involve disrupted estradiol-regulated progesterone receptor expression. Homozygous deletion of TSC1 in reproductive tract somatic tissues of mice rendered females completely infertile, which is likely due to these pleiotropic effects on follicle recruitment, oviductal development, and blastocyst implantation. (Endocrinology 153: 404-416, 2012)
C1 Massachusetts Gen Hosp, Vincent Ctr Reprod Biol, Dept Obstet Gynecol & Reprod Biol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Teixeira, JM (reprint author), Massachusetts Gen Hosp, Vincent Ctr Reprod Biol Thier 931, 55 Fruit St, Boston, MA 02114 USA.
EM teixeira@helix.mgh.harvard.edu
OI Teixeira, Jose/0000-0002-6438-5064
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD) [HD052701]; Vincent Memorial Research Funds; NICHD
(Specialized Cooperative Centers) [U54-HD28934]
FX This work was supported by funding from the Eunice Kennedy Shriver
National Institute of Child Health and Human Development (NICHD)
(HD052701) and by Vincent Memorial Research Funds to J.M.T. The
University of Virginia Center for Research in Reproduction Ligand Core
Laboratory is supported by NICHD (Specialized Cooperative Centers
Program in Reproduction and Infertility Research) Grant U54-HD28934.
NR 61
TC 20
Z9 21
U1 0
U2 3
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD JAN
PY 2012
VL 153
IS 1
BP 404
EP 416
DI 10.1210/en.2011-1191
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 869XC
UT WOS:000298631500038
PM 22128018
ER
PT J
AU Sonnenberg, A
AF Sonnenberg, A.
TI Test sequence in the management of gastrointestinal bleeding
SO ENDOSCOPY
LA English
DT Article
ID EPIDEMIOLOGY; DIAGNOSIS
AB Background and study aim: A large variety of test procedures is available to diagnose and treat patients with suspected gastrointestinal bleeding. The aim of the study was to investigate which test sequence should be utilized in managing gastrointestinal bleeding.
Methods: For each endoscopic, radiologic, or laboratory test procedure, professional fees and facility costs were estimated based on payments allowed by the US Centers for Medicare and Medicaid Services during the fiscal year 2010. A threshold analysis was used to compare the costs associated with different test sequences of varying clinical scenarios.
Results: A threshold represents the lowest expected probability of success, for which a test would still be indicated. In a work-up including all possible management options, the threshold associated with laboratory tests and gastric lavage was 1%, esophagogastroduodenoscopy (EGD) 8%, colonoscopy 9%, nuclear scan 9%, enteroscopy 11%, computed tomography (CT) angiography 14%, capsule endoscopy 23%, and angiography with transcatheter embolization 25%. Varying sets of thresholds were calculated for different clinical scenarios. The thresholds of EGD and colonoscopy remained low in most scenarios. In sensitivity analysis, rising risk of complications or costs of a procedure also lead to rising threshold values for it, potentially rendering the particular procedure untenable.
Conclusions: A low threshold indicated a preferred management option that should be used early rather than late in a sequence of multiple possible test procedures to work up instances of gastrointestinal bleeding.
C1 [Sonnenberg, A.] Portland VA Med Ctr, Portland, OR 97239 USA.
[Sonnenberg, A.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
RP Sonnenberg, A (reprint author), Portland VA Med Ctr, P3-GI 3710 SW US Vet Hosp Rd, Portland, OR 97239 USA.
EM sonnenbe@ohsu.edu
NR 8
TC 5
Z9 5
U1 2
U2 2
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0013-726X
J9 ENDOSCOPY
JI Endoscopy
PD JAN
PY 2012
VL 44
IS 1
BP 43
EP 47
DI 10.1055/s-0031-1291536
PG 5
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA 866TF
UT WOS:000298405400008
PM 22198774
ER
PT J
AU Connorton, E
Perry, MJ
Hemenway, D
Miller, M
AF Connorton, Ellen
Perry, Melissa J.
Hemenway, David
Miller, Matthew
TI Humanitarian Relief Workers and Trauma-related Mental Illness
SO EPIDEMIOLOGIC REVIEWS
LA English
DT Article
DE anxiety; depression; mental health; relief work; stress disorders;
post-traumatic; stress disorders; traumatic; acute; stress;
psychological; substance-related disorders
ID POSTTRAUMATIC-STRESS-DISORDER; NATIONAL COMORBIDITY SURVEY;
RISK-FACTORS; AID WORKERS; VICARIOUS TRAUMA; UN-SOLDIERS; HEALTH;
SYMPTOMS; PEACEKEEPERS; EXPOSURE
AB Humanitarian relief work is a growing field characterized by ongoing exposure to primary and secondary trauma, which has implications for workers' occupational mental health. This paper reviews and summarizes research to date on mental health effects of relief work. Twelve studies on relief workers and 5 studies on organizations that employ relief workers are examined to determine whether relief work is a risk factor for trauma-related mental illness. Although studies are inconsistent regarding methods and outcomes documenting trauma-related mental illness among relief workers, it appears that relief workers, compared with the general population, experience elevated trauma rates and suffer from more posttraumatic stress disorder, depression, and anxiety. Organizations that employ relief workers have varying approaches to train for these risks, and more support in the field is needed.
C1 [Connorton, Ellen; Hemenway, David; Miller, Matthew] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02215 USA.
[Connorton, Ellen; Hemenway, David; Miller, Matthew] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Perry, Melissa J.] George Washington Univ, Univ Sch Publ Hlth & Hlth Serv, Dept Environm & Occupat Hlth, Washington, DC USA.
RP Connorton, E (reprint author), Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, 450 Brookline Ave,LW 750, Boston, MA 02215 USA.
EM econnort@hsph.harvard.edu
NR 51
TC 14
Z9 14
U1 4
U2 23
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0193-936X
J9 EPIDEMIOL REV
JI Epidemiol. Rev.
PD JAN
PY 2012
VL 34
IS 1
BP 145
EP 155
DI 10.1093/epirev/mxr026
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 873NN
UT WOS:000298890100013
PM 22180469
ER
PT J
AU Power, MC
Weuve, J
Gagne, JJ
McQueen, MB
Viswanathan, A
Blacker, D
AF Power, Melinda C.
Weuve, Jennifer
Gagne, Joshua J.
McQueen, Matthew B.
Viswanathan, Anand
Blacker, Deborah
TI Hypertension and Alzheimer Disease Is There a Link? response
SO EPIDEMIOLOGY
LA English
DT Letter
C1 [Power, Melinda C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Power, Melinda C.; Weuve, Jennifer] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Weuve, Jennifer] Rush Univ, Med Ctr, Inst Healthy Aging, Chicago, IL 60612 USA.
[Weuve, Jennifer] Rush Univ, Med Ctr, Dept Internal Med, Chicago, IL 60612 USA.
[Gagne, Joshua J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Gagne, Joshua J.] Harvard Univ, Sch Med, Boston, MA USA.
[Gagne, Joshua J.] Brigham & Womens Hosp, Div Pharmacoepidemiol & Pharmacoecon, Boston, MA 02115 USA.
[McQueen, Matthew B.] Univ Colorado, Dept Psychol, Boulder, CO 80309 USA.
[McQueen, Matthew B.] Univ Colorado, Inst Behav Genet, Boulder, CO 80309 USA.
[Viswanathan, Anand] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol,Hemorrhag Stroke Res Program, Boston, MA USA.
[Blacker, Deborah] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Blacker, Deborah] Harvard Univ, Sch Med, Dept Psychiat, Gerontol Res Unit, Boston, MA 02115 USA.
RP Power, MC (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, 665 Huntington Ave, Boston, MA 02115 USA.
EM mcpower@hsph.harvard.edu
NR 2
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 JAN
PY 2012
VL 23
IS 1
BP 177
EP 178
DI 10.1097/EDE.0b013e31823b6513
PG 3
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 863IU
UT WOS:000298156800029
ER
PT J
AU Graber, CJ
Hutchings, C
Dong, F
Lee, W
Chung, JK
Tran, T
AF Graber, C. J.
Hutchings, C.
Dong, F.
Lee, W.
Chung, J. K.
Tran, T.
TI Changes in antibiotic usage and susceptibility in nosocomial
Enterobacteriaceae and Pseudomonas isolates following the introduction
of ertapenem to hospital formulary
SO EPIDEMIOLOGY AND INFECTION
LA English
DT Article
DE Antibiotic resistance; antibiotics; hospital-acquired (nosocomial)
infections; hospital microbiology; Pseudomonas
ID TIME-SERIES ANALYSIS; RESISTANT; AERUGINOSA; IMIPENEM; THERAPY; RATES
AB There is concern that widespread usage of ertapenem may promote cross-resistance to other carbapenems. To analyse the impact that adding ertapenem to our hospital formulary had on usage of other broad-spectrum agents and on susceptibilities of nosocomial Enterobacteriaceae and Pseudomonas isolates, we performed interrupted time-series analyses to determine the change in linear trend in antibiotic usage and change in mean proportion and linear trend of susceptibility pre-(March 2004-June 2005) and post-(July 2005-December 2008) ertapenem introduction. Usage of piperacillin-tazobactam (P = 0.0013) and ampicillin-sulbactam (P = 0.035) declined post-ertapenem introduction. For Enterobacteriaceae, the mean proportion susceptible to ciprofloxacin (P = 0.016) and piperacillin-tazobactam (P = 0.038) increased, while the linear trend in susceptibility significantly increased for cefepime (P = 0.012) but declined for ceftriaxone (P = 0.0032). For Pseudomonas, the mean proportion susceptible to cefepime (P = 0.011) and piperacillin-tazobactam (P = 0.028) increased, as did the linear trend in susceptibility to ciprofloxacin (P = 0.028). Notably, no significant changes in carbapenem susceptibility were observed.
C1 [Graber, C. J.] Univ Calif Los Angeles, David Geffen Sch Med, UCLA Infect Dis Sect, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Graber, C. J.; Tran, T.] VA Greater Los Angeles Healthcare Syst, Infect Dis Sect, Los Angeles, CA USA.
[Hutchings, C.; Dong, F.; Tran, T.] VA Greater Los Angeles Healthcare Syst, Serv Pharm, Los Angeles, CA USA.
[Lee, W.] Univ So Calif, Keck Sch Med, Dept Biostat, Los Angeles, CA 90033 USA.
[Chung, J. K.] Univ So Calif, Sch Pharm, Los Angeles, CA USA.
RP Graber, CJ (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, UCLA Infect Dis Sect, VA Greater Los Angeles Healthcare Syst, 11301 Wilshire Blvd,111-F, Los Angeles, CA 90073 USA.
EM cgraber@ucla.edu
FU Merck Pharmaceuticals; Ortho-McNeil-Janssen
FX This project was supported by a grant from Merck Pharmaceuticals.;
C.J.G. has received an unrestricted educational grant from
Ortho-McNeil-Janssen and has served on an advisory board for Pfizer.
NR 13
TC 3
Z9 3
U1 0
U2 2
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0950-2688
J9 EPIDEMIOL INFECT
JI Epidemiol. Infect.
PD JAN
PY 2012
VL 140
IS 1
BP 115
EP 125
DI 10.1017/S0950268811000082
PG 11
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 868TC
UT WOS:000298547400015
PM 21303590
ER
PT J
AU Ahasic, AM
Zhai, RH
Su, L
Zhao, Y
Aronis, KN
Thompson, BT
Mantzoros, CS
Christiani, DC
AF Ahasic, Amy M.
Zhai, Rihong
Su, Li
Zhao, Yang
Aronis, Konstantinos N.
Thompson, B. Taylor
Mantzoros, Christos S.
Christiani, David C.
TI IGF1 and IGFBP3 in acute respiratory distress syndrome
SO EUROPEAN JOURNAL OF ENDOCRINOLOGY
LA English
DT Article
ID GROWTH-FACTOR-I; IDIOPATHIC PULMONARY-FIBROSIS; FACTOR-BINDING
PROTEIN-3; ACUTE LUNG INJURY; BRONCHOALVEOLAR LAVAGE FLUID; MORTALITY;
ADULTS; PREDICTORS; HORMONE; DISEASE
AB Objective: IGF1 and its most abundant binding protein, IGF-binding protein 3 (IGFBP3), have been implicated in fibrotic lung diseases and persistent acute respiratory distress syndrome (ARDS) due to profibrogenic and antiapoptotic activity. Whether circulating levels of IGF1 and IGFBP3 are altered in ARDS and whether they predict progression of and survival from ARDS remains unknown. This study aims to characterize the circulating levels of IGF1 and IGFBP3 in patients at risk for ARDS in relation to i) development of ARDS and ii) mortality among ARDS cases.
Design: In this case-cohort study, consecutive patients with risk factors for ARDS admitted to the intensive care unit were enrolled and followed prospectively for the development of ARDS. Cases were followed for all-cause mortality through day 60. Of the 2397 patients enrolled in the parent study, plasma samples were available in 531 (22%) patients (356 controls and 175 cases) from early in presentation. Total plasma IGF1 and IGFBP3 levels were measured.
Results: After adjusting for relevant clinical covariates including severity of illness, IGF1 and IGFBP3 levels were significantly lower in ARDS cases than in controls (odds ratio (OR), 0.58; P=0.006; OR, 0.57; P=0.0015 respectively). Among the ARDS cases, IGF1 and IGFBP3 levels were significantly lower in the 78 (45%) non-survivors (hazard ratio (HR), 0.70; P=0.024; HR, 0.69; P=0.021 respectively).
Conclusions: Lower circulating levels of IGF1 and IGFBP3 were independently associated with ARDS case status. Furthermore, lower levels were associated with mortality among the ARDS cases. These data support the role of the IGF pathway in ARDS.
C1 [Ahasic, Amy M.] Yale Univ, Sch Med, Dept Med, Sect Pulm & Crit Care Med, New Haven, CT 06520 USA.
[Ahasic, Amy M.; Zhai, Rihong; Su, Li; Zhao, Yang; Mantzoros, Christos S.; Christiani, David C.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Aronis, Konstantinos N.; Mantzoros, Christos S.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab,Dept Med, Boston, MA 02215 USA.
[Thompson, B. Taylor; Christiani, David C.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Pulm & Crit Care Unit,Dept Med, Boston, MA 02114 USA.
RP Ahasic, AM (reprint author), Yale Univ, Sch Med, Dept Med, Sect Pulm & Crit Care Med, 300 Cedar St,POB 208057, New Haven, CT 06520 USA.
EM amy.ahasic@yale.edu
RI Aronis, Konstantinos/F-3586-2012; Aronis, Konstantinos/J-6582-2014
OI Aronis, Konstantinos/0000-0001-7189-8434;
FU National Institutes of Health [R01-HL60710 (NHLBI), ES00002 (NIEHS),
T32-HL07874 (NHLBI)]; American Heart Association [10FTF3440007]
FX This work was supported by the National Institutes of Health
(R01-HL60710 (NHLBI), ES00002 (NIEHS), T32-HL07874 (NHLBI)) and by the
American Heart Association (10FTF3440007).
NR 31
TC 7
Z9 8
U1 0
U2 3
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 0804-4643
J9 EUR J ENDOCRINOL
JI Eur. J. Endocrinol.
PD JAN
PY 2012
VL 166
IS 1
BP 121
EP 129
DI 10.1530/EJE-11-0778
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 865YX
UT WOS:000298347900017
PM 22004906
ER
PT J
AU Richardson, PG
Laubach, JP
Schlossman, RL
Ghobrial, IM
Mitsiades, CS
Rosenblatt, J
Mahindra, A
Raje, N
Munshi, N
Anderson, KC
AF Richardson, Paul G.
Laubach, Jacob P.
Schlossman, Robert L.
Ghobrial, Irene M.
Mitsiades, Constantine S.
Rosenblatt, Jacalyn
Mahindra, Anuj
Raje, Noopur
Munshi, Nikhil
Anderson, Kenneth C.
TI The Medical Research Council Myeloma IX trial: the impact on treatment
paradigms*
SO EUROPEAN JOURNAL OF HAEMATOLOGY
LA English
DT Review
DE bisphosphonate; clodronate; multiple myeloma; pamidronate; zoledronic
acid
ID BISPHOSPHONATE ZOLEDRONIC ACID; MULTIPLE-MYELOMA; STAGING SYSTEM;
CELL-LINES; BONE-DISEASE; IN-VIVO; DEXAMETHASONE; SURVIVAL;
STRATIFICATION; THALIDOMIDE
AB Osteolytic bone disease is a hallmark of symptomatic multiple myeloma. Bisphosphonates have been the mainstay of treatment to preserve skeletal integrity and prevent skeletal-related events in patients with myeloma-related bone disease. Recently, the MRC Myeloma IX trial demonstrated for the first time improved survival and delayed disease progression with the use of an intravenous amino-bisphosphonate, zoledronic acid, vs. an oral agent, clodronate, with intensive and non-intensive anti-myeloma treatment regimens in patients with newly diagnosed multiple myeloma. These results validate a large body of preclinical, translational and other clinical data suggesting anti-myeloma effects of amino-bisphosphonates. In addition, this trial also provided the first head-to-head evidence for superiority of one bisphosphonate over another (zoledronic acid vs. clodronate) for reducing skeletal morbidity in patients with multiple myeloma, as well as a prospective comparison of toxicities. Despite the use of non-bortezomib containing anti-myeloma treatment regimens in the MRC Myeloma IX trial, these results are encouraging and provide an impetus to continue to evaluate current treatment guidelines for myeloma-associated bone disease.
C1 [Richardson, Paul G.; Laubach, Jacob P.; Schlossman, Robert L.; Ghobrial, Irene M.; Mitsiades, Constantine S.; Munshi, Nikhil; Anderson, Kenneth C.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Rosenblatt, Jacalyn] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Mahindra, Anuj; Raje, Noopur] Harvard Univ, Sch Med, Div Hematol Oncol, Boston, MA USA.
RP Richardson, PG (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St,Dana 1B02, Boston, MA 02115 USA.
EM paul_richardson@dfci.harvard.edu
FU Rick Corman Multiple Myeloma Research Fund; Novartis Pharmaceuticals;
AstraZeneca; Acetylon; Celgene
FX Funding for administrative assistance and for medical writing support
was provided in part by the Rick Corman Multiple Myeloma Research Fund
and Novartis Pharmaceuticals.; PGR - Advisory Board: Celgene,
Millennium, Novartis, Johnson & Johnson, BMS. IMG - Advisory Board:
Celgene, Millennium, Novartis, Onyx. NR - Advisory Board: Celgene,
Novartis, Amgen, Research Funding: AstraZeneca, Acetylon, Celgene. KCA -
Advisory Board: Novartis, Millennium, Celgene, Onyx, BMS, Merck. Founder
of Acetylon. JR - Research Funding: Celgene, Millennium. AM - Advisory
Board: Millennium. JPL, RLS - have no competing interests.
NR 42
TC 4
Z9 4
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0902-4441
J9 EUR J HAEMATOL
JI Eur. J. Haematol.
PD JAN
PY 2012
VL 88
IS 1
BP 1
EP 7
DI 10.1111/j.1600-0609.2011.01721.x
PG 7
WC Hematology
SC Hematology
GA 862KM
UT WOS:000298089600001
PM 21991938
ER
PT J
AU van der Pol, A
Domian, I
van der Meer, P
AF van der Pol, Atze
Domian, Ibrahim
van der Meer, Peter
TI Cardiac regeneration in left ventricular dysfunction: are we asking the
right questions?
SO EUROPEAN JOURNAL OF HEART FAILURE
LA English
DT Editorial Material
ID ACUTE MYOCARDIAL-INFARCTION; PROGENITOR CELLS; PARACRINE MECHANISMS;
HEART-FAILURE; STEM-CELLS; REPAIR; TRANSPLANTATION; CARDIOMYOCYTES;
INSIGHTS; MUSCLE
C1 [van der Pol, Atze; van der Meer, Peter] Univ Groningen, Univ Med Ctr Groningen, Dept Cardiol, NL-9713 GZ Groningen, Netherlands.
[Domian, Ibrahim] Massachusetts Gen Hosp, Div Cardiol, Cardiovasc Res Ctr, Boston, MA 02114 USA.
RP van der Meer, P (reprint author), Univ Groningen, Univ Med Ctr Groningen, Dept Cardiol, Hanzepl 1, NL-9713 GZ Groningen, Netherlands.
EM p.van.der.meer@umcg.nl
FU NHLBI NIH HHS [K08 HL091209]
NR 20
TC 2
Z9 2
U1 1
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1388-9842
J9 EUR J HEART FAIL
JI Eur. J. Heart Fail.
PD JAN
PY 2012
VL 14
IS 1
BP 1
EP 4
DI 10.1093/eurjhf/hfr160
PG 4
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 866LN
UT WOS:000298382400001
PM 22147203
ER
PT J
AU Fagerness, JA
Yu, Y
Maller, JB
Neale, BM
Reynolds, RC
Daly, MJ
Seddon, JM
AF Fagerness, Jesen A.
Yu, Yi
Maller, Julian B.
Neale, Benjamin M.
Reynolds, Robyn C.
Daly, Mark J.
Seddon, Johanna M.
TI Reply to Cipriani et al
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Letter
C1 [Fagerness, Jesen A.; Maller, Julian B.; Neale, Benjamin M.; Daly, Mark J.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Fagerness, Jesen A.; Maller, Julian B.; Neale, Benjamin M.; Daly, Mark J.] Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA USA.
[Yu, Yi; Reynolds, Robyn C.; Seddon, Johanna M.] Tufts Med Ctr, New England Eye Ctr, Ophthalm Epidemiol & Genet Serv, Boston, MA USA.
[Maller, Julian B.] Univ Oxford, Dept Stat, Oxford OX1 3TG, England.
[Seddon, Johanna M.] Tufts Univ, Sch Med, Dept Ophthalmol, Boston, MA 02111 USA.
RP Fagerness, JA (reprint author), Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
EM jseddon@tuftsmedicalcenter.org
NR 3
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD JAN
PY 2012
VL 20
IS 1
BP 3
EP 3
DI 10.1038/ejhg.2011.177
PG 1
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 863MF
UT WOS:000298167700005
ER
PT J
AU Abusief, ME
Missmer, SA
Ginsburg, ES
Weeks, JC
Partridge, AH
AF Abusief, Mary E.
Missmer, Stacey A.
Ginsburg, Elizabeth S.
Weeks, Jane C.
Partridge, Ann H.
TI Relationship between reproductive history, anthropometrics, lifestyle
factors, and the likelihood of persistent chemotherapy-related
amenorrhea in women with premenopausal breast cancer
SO FERTILITY AND STERILITY
LA English
DT Article
DE Chemotherapy-related amenorrhea; breast cancer; gravidity; parity;
lifestyle factors; premature menopause
ID INDUCED OVARIAN FAILURE; NATURAL MENOPAUSE; ADJUVANT CHEMOTHERAPY;
CIGARETTE-SMOKING; AGE; RISK; FERTILITY; MENARCHE; THERAPY;
CYCLOPHOSPHAMIDE
AB Objective: To determine the association between patient characteristics at diagnosis of premenopausal breast cancer, including gravidity, parity, age at menarche, age at first birth, alcohol use, smoking history, weight, height, and body mass index (BMI), with the development of persistent chemotherapy-related amenorrhea (CRA) in follow-up.
Design: Retrospective cohort study.
Setting: Dana Farber Cancer Institute and Brigham and Women's Hospital.
Patient(s): Premenopausal women with breast cancer.
Intervention(s): We identified all premenopausal women who received standard adjuvant chemotherapy during 1997-2005 for whom menstrual data were available. Multivariable logistic regression models evaluating persistent amenorrhea at >= 6 month after completion of chemotherapy were conducted.
Main Outcome Measure(s): Persistent chemotherapy-related amenorrhea (CRA) at >= 6 months from completion of chemotherapy.
Result(s): A total of 431 women met eligibility criteria and had >= 6-months' follow-up. Women with older (>13 years) vs. younger (12-13 years) age at menarche were more than twice as likely to remain amenorrheic. Current smokers had 2.4 greater odds of CRA vs. never smokers, although this association was not statistically significant (95% confidence interval, 0.86-6.75).
Conclusion(s): Few identifiable factors contribute to the variability in CRA among premenopausal women after adjuvant chemotherapy for breast cancer. Further research to improve the prediction of CRA, premature menopause, and infertility in young breast cancer survivors is warranted. (Fertil Steril (R) 2012;97:154-9. (C) 2012 by American Society for Reproductive Medicine.)
C1 [Abusief, Mary E.; Missmer, Stacey A.; Ginsburg, Elizabeth S.] Brigham & Womens Hosp, Dept Obstet Gynecol & Reprod Biol, Boston, MA 02115 USA.
[Missmer, Stacey A.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Weeks, Jane C.; Partridge, Ann H.] Harvard Univ, Sch Med, Boston, MA USA.
[Missmer, Stacey A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Weeks, Jane C.; Partridge, Ann H.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Abusief, ME (reprint author), Brigham & Womens Hosp, Dept Obstet Gynecol & Reprod Biol, 75 Francis St, Boston, MA 02115 USA.
EM maskelya@msn.com
FU NCI NIH HHS [K05 CA166208]; NCRR NIH HHS [M01 RR002635]
NR 52
TC 8
Z9 8
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD JAN
PY 2012
VL 97
IS 1
BP 154
EP 159
DI 10.1016/j.fertnstert.2011.10.005
PG 6
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 866GD
UT WOS:000298367600029
PM 22192139
ER
PT J
AU Styskal, J
Van Remmen, H
Richardson, A
Salmon, AB
AF Styskal, JennaLynn
Van Remmen, Holly
Richardson, Arlan
Salmon, Adam B.
TI Oxidative stress and diabetes: What can we learn about insulin
resistance from antioxidant mutant mouse models?
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Review
DE Oxidative stress; Diabetes; Obesity; Adipose; Insulin resistance
ID EXTRACELLULAR-SUPEROXIDE-DISMUTASE; CELLULAR GLUTATHIONE-PEROXIDASE;
METHIONINE SULFOXIDE REDUCTASE; MEMBRANE LIPID-PEROXIDATION; OXIDANT
TISSUE-INJURY; RAT SKELETAL-MUSCLE; GENE-TARGETED MICE; ALPHA-LIPOIC
ACID; RED-BLOOD-CELLS; NF-KAPPA-B
AB The development of metabolic dysfunctions like diabetes and insulin resistance in mammals is regulated by a myriad of factors. Oxidative stress seems to play a central role in this process as recent evidence shows a general increase in oxidative damage and a decrease in oxidative defense associated with several metabolic diseases. These changes in oxidative stress can be directly correlated with increased fat accumulation, obesity, and consumption of high-calorie/high-fat diets. Modulation of oxidant protection through either genetic mutation or treatment with antioxidants can significantly alter oxidative stress resistance and accumulation of oxidative damage in laboratory rodents. Antioxidant mutant mice have previously been utilized to examine the role of oxidative stress in other disease models, but have been relatively unexplored as models to study the regulation of glucose metabolism. In this review, we will discuss the evidence for oxidative stress as a primary mechanism linking obesity and metabolic disorders and whether alteration of antioxidant status in laboratory rodents can significantly alter the development of insulin resistance or diabetes. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Styskal, JennaLynn; Van Remmen, Holly; Richardson, Arlan; Salmon, Adam B.] Univ Texas Hlth Sci Ctr San Antonio, Sam & Ann Barshop Inst Longev & Aging Studies, San Antonio, TX 78245 USA.
[Styskal, JennaLynn; Van Remmen, Holly; Richardson, Arlan] Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA.
[Van Remmen, Holly; Richardson, Arlan; Salmon, Adam B.] S Texas Vet Hlth Care Syst, Geriatr Res Educ & Clin Ctr, San Antonio, TX 78229 USA.
[Salmon, Adam B.] Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA.
RP Salmon, AB (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Sam & Ann Barshop Inst Longev & Aging Studies, 15355 Lambda Dr,MSC 7755, San Antonio, TX 78245 USA.
EM salmona@uthscsa.edu
FU NIH [T32 AG021890-05, R01AG015908, R01AG023843, P01AG19316, P01AG020591,
R37AG026557]; Department of Veterans Affairs; San Antonio Nathan Shock
Center of Excellence in the Basic Biology of Aging
FX This work was supported by NIH Training Grant T32 AG021890-05, NIH
Grants R01AG015908, R01AG023843, P01AG19316, P01AG020591, and
R37AG026557, the Department of Veterans Affairs (Merit Grants and a
Research Enhancement Award Program), and the Mitocondrial Function and
Oxidative Damage Core Facility of the San Antonio Nathan Shock Center of
Excellence in the Basic Biology of Aging.
NR 184
TC 90
Z9 91
U1 1
U2 25
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD JAN 1
PY 2012
VL 52
IS 1
BP 46
EP 58
DI 10.1016/j.freeradbiomed.2011.10.441
PG 13
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 874RJ
UT WOS:000298975500005
PM 22056908
ER
PT J
AU Rungruang, B
Miller, A
Richard, SD
Hamilton, CA
Rodriguez, N
Bookman, MA
Maxwell, GL
Krivak, TC
Horowitz, NS
AF Rungruang, Bunja
Miller, Austin
Richard, Scott D.
Hamilton, Chad A.
Rodriguez, Noah
Bookman, Michael A.
Maxwell, G. Larry
Krivak, Thomas C.
Horowitz, Neil S.
TI Should stage IIIC ovarian cancer be further stratified by
intraperitoneal vs. retroperitoneal only disease?: A Gynecologic
Oncology Group study
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE Ovarian cancer; Lymphadenopathy; FIGO staging
ID PRIMARY CYTOREDUCTIVE SURGERY; NODE INVOLVEMENT; CARCINOMA; SURVIVAL;
LYMPHADENECTOMY; METASTASIS; IMPACT; TRIAL
AB Objective. To examine whether clinical outcomes varied with intraperitoneal (IP) and/or retroperitoneal (RP) involvement in stage IIIC epithelial ovarian cancer (EOC) patients with microscopic residual disease after cytoreduction.
Methods. Retrospective review was performed for EOC patients enrolled in Gynecologic Oncology Group (GOG)-182 who underwent primary cytoreduction to microscopic residual disease. Patients were divided into 3 groups: stage IIIC by lymphadenopathy with <2 cm IF spread (RP): >2 cm IP spread and negative nodes (IP/RP-): and >2 cm IP dissemination and positive lymphadenopathy (IP/RP+). Product-limit and multivariate proportional hazards modeling were used.
Results. Analyses included 417 stage IIIC women who underwent primary cytoreduction with lymphadenectomy to microscopic residual. There were 203, 123, and 91 in the RP, IP/RP-, and IP/RP+ groups, respectively. IP/RP+ and IP/RP- were associated with worse progression-free survival (PFS) (Hazard Ratio (HR) 1.68, 95% confidence interval (CI) 1.23-2.30: HR 1.38, 95% CI 1.04-1.84) vs. RP only. IP/RP+ was associated with worse overall survival (OS) (HR 1.79, 95% CI 1.24-2.57) while IP/RP- trended towards worse OS (HR 1.21, 95% CI 0.85-1.73) vs. RP only. Median PFS for IP/RP+ and IP/RP- groups was 21 and 29 months, respectively, vs. 48 months in the RP group (p = 0.0007) and median OS of 63 and 79 months vs. "not reached," respectively (p = 0.0038).
Conclusions. Among EOC patients surgically cytoreduced to microscopic residual disease, those upstaged to IIIC by retroperitoneal involvement demonstrated significant improvement in PFS and OS compared to patients with intraperitoneal tumor, suggesting that these women may represent a unique subset of FIGO stage IIIC patients. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Rungruang, Bunja; Richard, Scott D.; Krivak, Thomas C.] UPMC, Magee Womens Hosp, Dept Obstet & Gynecol, Div Gynecol Oncol, Pittsburgh, PA USA.
[Miller, Austin] Roswell Pk Canc Inst, Stat & Data Ctr, Gynecol Oncol Grp, Buffalo, NY 14263 USA.
[Hamilton, Chad A.; Maxwell, G. Larry] Walter Reed Army Med Ctr, Dept Obstet & Gynecol, Div Gynecol Oncol, Washington, DC 20307 USA.
[Rodriguez, Noah; Horowitz, Neil S.] Brigham & Womens Hosp, Div Gynecol Oncol, Boston, MA 02115 USA.
[Bookman, Michael A.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
RP Horowitz, NS (reprint author), Massachusetts Gen Hosp, 75 Francis St, Boston, MA 02115 USA.
EM nhorowitz@partners.org
FU National Cancer Institute [CA 27469, CA 37517]
FX This study was supported by National Cancer Institute grants to the
Gynecologic Oncology Group (COG) Administrative Office (CA 27469) and
the Gynecologic Oncology Group Statistical Office (CA 37517). The
following Gynecologic Oncology Group member institutions participated in
the primary treatment studies: University of Alabama at Birmingham,
Oregon Health Sciences University, Duke University Medical Center,
Abington Memorial Hospital, University of Rochester Medical Center,
Walter Reed Army Medical Center, Wayne State University, University of
Minnesota Medical School, University of Southern California at Los
Angeles, University of Mississippi Medical Center, Colorado Gynecologic
Oncology Group P.C., University of California at Los Angeles, University
of Washington. University of Pennsylvania Cancer Center, University of
Miami School of Medicine, Milton S. Hershey Medical Center, Georgetown
University Hospital, University of Cincinnati, University of North
Carolina School of Medicine. University of Iowa Hospitals and Clinics.
University of Texas Southwestern Medical Center at Dallas, Indiana
University School of Medicine, Wake Forest University School of
Medicine, Albany Medical College, University of California Medical
Center at Irvine, Tufts-New England Medical Center,
Rush-Presbyterian-St. Luke's Medical Center, University of Kentucky,
Eastern Virginia Medical School, The Cleveland Clinic Foundation, Johns
Hopkins Oncology Center, State University of New York at Stony Brook,
Eastern Pennsylvania GYN/ONC Center, P.C., Southwestern Oncology Group,
Washington University School of Medicine, Memorial Sloan-Kettering
Cancer Center, Columbus Cancer Council, University of Massachusetts
Medical School, Fox Chase Cancer Center, Medical University of South
Carolina, Women's Cancer Center, University of Oklahoma. University of
Virginia Health Sciences Center, University of Chicago, University of
Arizona Health Science Center, Tacoma General Hospital, Eastern
Collaborative Oncology Group, Thomas Jefferson University Hospital, Case
Western Reserve University, and Tampa Bay Cancer Consortium.
NR 25
TC 4
Z9 6
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0090-8258
J9 GYNECOL ONCOL
JI Gynecol. Oncol.
PD JAN
PY 2012
VL 124
IS 1
BP 53
EP 58
DI 10.1016/j.ygyno.2011.09.024
PG 6
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 864BV
UT WOS:000298212900012
PM 22032836
ER
PT J
AU van Hanegem, N
Barroilhet, LM
Nucci, MR
Bernstein, M
Feldman, S
AF van Hanegem, Nehalennia
Barroilhet, Lisa M.
Nucci, Marisa R.
Bernstein, Marilyn
Feldman, Sarah
TI Fertility-sparing treatment in younger women with adenocarcinoma in situ
of the cervix
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE Adenocarcinoma in situ; Cervix; Loop excision; Cold knife conization
ID SQUAMOUS-CELL CARCINOMA; ELECTROSURGICAL EXCISION PROCEDURE; COLD-KNIFE
CONIZATION; UTERINE CERVIX; INTRAEPITHELIAL NEOPLASIA; CONSERVATIVE
TREATMENT; UNITED-STATES; CONE BIOPSY; MANAGEMENT; MARGINS
AB Objective. For women who have completed childbearing, the treatment of choice for adenocarcinoma in situ (ACIS) of the cervix is hysterectomy. In women who desire future fertility, however, conservative therapy is an acceptable alternative. In this study we compare the outcomes for young women who underwent loop conization or were treated with cold knife conization.
Methods. We performed a retrospective analysis in 112 patients with ACIS, age 30 or younger, treated with cold knife conization or loop conization between 1998 and 2010. Decision to perform office loop conization was based on the size of the cervix and the colposcopic lesion. Main outcomes were negative margins after the procedure and recurrence of ACIS.
Results. Fifty-eight patients (52%) were treated with cold knife conization and 54 (48%) underwent loop conization. The odds ratio for cold knife conization to achieve negative cone margins compared with loop conization was 1.4 (95% CI 0.6-3.5). We observed no difference in residual or recurrent ACIS between patients treated with loop conization versus cold knife conization.
Conclusions. In select young patients who desire future fertility, loop conization and cold knife conization have equivalent rates of negative margins and negative follow-up. For optimal results, patients must have a lesion which can be removed in one pass of a loop, confirmed by expert colposcopy. Loop excision should be considered the treatment of choice in this specific group of patients. (C) 2011 Published by Elsevier Inc.
C1 [van Hanegem, Nehalennia; Barroilhet, Lisa M.; Bernstein, Marilyn; Feldman, Sarah] Harvard Univ, Brigham & Womens Hosp, Dept Obstet & Gynecol, Div Gynecol Oncol,Dana Farber Canc Inst,Med Sch, Boston, MA 02115 USA.
[van Hanegem, Nehalennia] Univ Amsterdam, Acad Med Ctr, Dept Obstet & Gynecol, NL-1105 AZ Amsterdam, Netherlands.
[Nucci, Marisa R.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Womens & Perinatal Pathol,Dept Pathol, Boston, MA 02115 USA.
RP Feldman, S (reprint author), Harvard Univ, Brigham & Womens Hosp, Dept Obstet & Gynecol, Div Gynecol Oncol,Dana Farber Canc Inst,Med Sch, 75 Francis St, Boston, MA 02115 USA.
EM sfeldman@partners.org
NR 33
TC 20
Z9 20
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0090-8258
J9 GYNECOL ONCOL
JI Gynecol. Oncol.
PD JAN
PY 2012
VL 124
IS 1
BP 72
EP 77
DI 10.1016/j.ygyno.2011.09.006
PG 6
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 864BV
UT WOS:000298212900016
PM 22030403
ER
PT J
AU Parshall, MB
Carle, AC
Ice, U
Taylor, R
Powers, J
AF Parshall, Mark B.
Carle, Adam C.
Ice, Unchalee
Taylor, Robert
Powers, Joyce
TI Validation of a three-factor measurement model of dyspnea in
hospitalized adults with heart failure
SO HEART & LUNG
LA English
DT Article
DE Chronic obstructive pulmonary disease; Confirmatory factor analysis;
Dyspnea; Respiratory sensation
ID OBSTRUCTIVE PULMONARY-DISEASE; CO2-INDUCED AIR HUNGER; RESPIRATORY
SENSATIONS; CARDIORESPIRATORY DISEASES; VENTILATED QUADRIPLEGICS;
RESPONSE CHARACTERISTICS; QUALITATIVE ASPECTS; CLINICAL-TRIALS; FIT
INDEXES; BREATHLESSNESS
AB OBJECTIVE: The purpose of this study was to validate a 3-factor measurement model of dyspnea sensory quality (WORK-EFFORT, TIGHTNESS, SMOTHERING-AIR HUNGER) originally derived in patients with exacerbated chronic obstructive pulmonary disease.
METHODS: In this validation study, adult patients with heart failure were enrolled after hospital admission (median hospital day 1) and asked to rate the intensity of dyspnea sensory quality descriptors on the day of enrollment (study day 1; N = 119) and in a recall version for the day of admission (study day 0; n = 97).
RESULTS: Confirmatory factor analysis demonstrated good model fit for both days. Cronbach's alpha for each factor was greater than .87 for both study days.
CONCLUSION: This is the first study to validate a previously specified measurement model of dyspnea sensory quality in an independent sample. Results indicate that measurement of dyspnea sensory quality in exacerbated cardiopulmonary disease does not necessarily require disease-specific questionnaires.
Cite this article: Parshall, M. B., Carle, A. C., Ice, U., Taylor, R., & Powers, J. (2012, JANUARY/FEBRUARY). Validation of a three-factor measurement model of dyspnea in hospitalized adults with heart failure. Heart & Lung, 41(1), 44-56. doi:10.1016/j.hrtlng.2011.05.003.
C1 [Parshall, Mark B.; Ice, Unchalee] Univ New Mexico, Coll Nursing, Hlth Sci Ctr, Albuquerque, NM 87131 USA.
[Carle, Adam C.] Univ Cincinnati, Coll Med, James M Anderson Ctr Hlth Syst Excellence, Cincinnati, OH USA.
[Taylor, Robert] Univ New Mexico, Sch Med, Dept Internal Med, Div Cardiol,Hlth Sci Ctr, Albuquerque, NM 87131 USA.
[Powers, Joyce] US Dept Vet Affairs, Raymond G Murphy VA Med Ctr, Albuquerque, NM USA.
RP Parshall, MB (reprint author), Univ New Mexico, Coll Nursing, Hlth Sci Ctr, MSC 09 5350,1 Univ New Mexico, Albuquerque, NM 87131 USA.
EM mparshall@salud.unm.edu
FU National Institute of Nursing Research [1 R15 NR008883]
FX Funded by a grant from the National Institute of Nursing Research (1 R15
NR008883). The opinions expressed in this article are solely those, of
the authors.
NR 78
TC 6
Z9 6
U1 1
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0147-9563
J9 HEART LUNG
JI Heart Lung
PD JAN-FEB
PY 2012
VL 41
IS 1
BP 44
EP 56
DI 10.1016/j.hrtlng.2011.05.003
PG 13
WC Cardiac & Cardiovascular Systems; Nursing; Respiratory System
SC Cardiovascular System & Cardiology; Nursing; Respiratory System
GA 875KE
UT WOS:000299028000008
PM 21794918
ER
PT J
AU Maleki, N
Becerra, L
Upadhyay, J
Burstein, R
Borsook, D
AF Maleki, Nasim
Becerra, Lino
Upadhyay, Jaymin
Burstein, Rami
Borsook, David
TI Direct optic nerve pulvinar connections defined by diffusion MR
tractography in humans: Implications for photophobia
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE tractography; nonimage forming pathway; visual pathway; thalamus;
central sensitization; migraine; pain
ID MACAQUE MONKEY; MOTOR CORTEX; NUCLEUS; PROJECTIONS; THALAMUS; BRAIN;
MIGRAINE; PATHWAY; SYSTEM; AREAS
AB The pathway that underlies exacerbation of migraine headache by light has not been elucidated in the human brain but has recently been reported in a rodent model. We employ diffusion weighted imaging and probabilistic tractography to map connectivity of direct pathways from the optic nerve to the pulvinar implicated with whole-body allodynia during migraine. Nine healthy subjects were recruited to the study and underwent scanning on a 3T magnet. We were able to define well-known image-forming (optic nerve -> lateral geniculate -> visual cortex) as well as a less known nonimage forming visual pathway from the optic chiasm to the pulvinar, and from the pulvinar to several associative cortical brain regions. Such pathway may allow photic signals to converge on a thalamic region we described recently to be selectively activated during migraine headache. Consistent with physiological and anatomical studies in rats, the data provide an anatomical substrate for exacerbation of migraine headache by light in the human. Hum Brain Mapp, 2012. (C) 2011 Wiley Periodicals, Inc.
C1 [Maleki, Nasim; Becerra, Lino; Upadhyay, Jaymin; Borsook, David] Harvard Univ, Sch Med, McLean Hosp, PAIN Grp,Brain Imaging Ctr, Belmont, MA 02478 USA.
[Becerra, Lino] Massachusetts Gen Hosp, Martinos Ctr, Charlestown, MA USA.
[Burstein, Rami] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Anesthesia & Crit Care, Belmont, MA 02478 USA.
RP Borsook, D (reprint author), Harvard Univ, Sch Med, McLean Hosp, PAIN Grp,Brain Imaging Ctr, 115 Mill St, Belmont, MA 02478 USA.
EM dborsook@partners.org
FU NINDS [R01 NS056195, K24 NS064050]
FX NINDS; Contract grant numbers: R01 NS056195, K24 NS064050.
NR 60
TC 30
Z9 31
U1 1
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1065-9471
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD JAN
PY 2012
VL 33
IS 1
BP 75
EP 88
DI 10.1002/hbm.21194
PG 14
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 869IH
UT WOS:000298591100007
PM 21337474
ER
PT J
AU Anderson, J
Wagner, J
Bessesen, M
Williams, LC
AF Anderson, Judith
Wagner, Julia
Bessesen, Mary
Williams, Linda C.
TI Usability testing in the hospital
SO HUMAN FACTORS AND ERGONOMICS IN MANUFACTURING & SERVICE INDUSTRIES
LA English
DT Article
DE Patient safety; Usability; Hospital; Healthcare; Human factors
engineering
ID CONSULTATION; IMPROVE
AB It is not unusual for hospitals to purchase equipment, devices, and materials based on preferences expressed by staff, based on economics and the best offer, or based on the promise of improvement by a new version. However, routinely subjecting potential purchases to basic usability testing provides valuable information upon which to base the decisions. Responsible manufacturers are interested in knowing of needed improvements to their products. Usability testing will also guide training for implementation. Usability testing is included in an introductory human factors engineering (HFE) session as part of a patient safety training course for physicians. Clinicians equipped with this skill are able to build evidence to support purchase decisions, make demands for improved design, and encourage a more thorough HFE evaluation by experts. (c) 2011 Wiley Periodicals, Inc.
C1 [Anderson, Judith] VA Natl Ctr Patient Safety, Denver, CO USA.
[Wagner, Julia; Bessesen, Mary] Denver VAMC, Denver, CO USA.
[Williams, Linda C.] VA Natl Ctr Patient Safety, Ann Arbor, MI USA.
RP Williams, LC (reprint author), 24 Frank Lloyd Wright Dr,M2100, Ann Arbor, MI 48106 USA.
EM linbywilliams@gmail.com
OI Bessesen, Mary/0000-0001-9305-1293
NR 16
TC 1
Z9 1
U1 2
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1090-8471
J9 HUM FACTOR ERGON MAN
JI Hum. Factors Ergonom. Manuf. Serv. Ind.
PD JAN-FEB
PY 2012
VL 22
IS 1
SI SI
BP 52
EP 63
DI 10.1002/hfm.20277
PG 12
WC Engineering, Manufacturing; Ergonomics
SC Engineering
GA 869JG
UT WOS:000298593600006
ER
PT J
AU Lesselroth, BJ
Dorr, DA
Adams, K
Church, V
Adams, S
Mazur, D
Russ, Y
Felder, R
Douglas, DM
AF Lesselroth, Blake J.
Dorr, David A.
Adams, Kathleen
Church, Victoria
Adams, Shawn
Mazur, Dennis
Russ, Yelizaveta
Felder, Robert
Douglas, David M.
TI Medication review software to improve the accuracy of outpatient
medication histories: protocol for a randomized controlled trial
SO HUMAN FACTORS AND ERGONOMICS IN MANUFACTURING & SERVICE INDUSTRIES
LA English
DT Review
DE Medication reconciliation; Medication errors; Technology assessment;
Biomedical; Adverse drug events; Medical records systems; Computerized;
Consumer health information
ID ADVERSE DRUG EVENTS; HOSPITAL DISCHARGE; CLINICAL IMPORTANCE;
RECONCILIATION; DISCREPANCIES; ERRORS; CARE; IMPLEMENTATION; ADMISSION;
DESIGN
AB Medication-prescribing errors generated at interfaces-in-care are the most common cause of preventable health care errors and contribute substantially to adverse patient outcomes. For this reason, standardized medication reconciliation (MR) processes need to be inserted at these interfaces. However, MR is an inherently complex task, and little data exist to inform system-based operationalization. The Portland Informatics Center addressed this challenge by creating an electronic patient-directed multimedia survey to automate the medication history collection. This article describes a research protocol designed to compare the software's medication discrepancy detection rate with traditional history collection strategies. For this randomized, controlled, single-blind trial, participants are randomly allocated into one of two groups: the control group reviews a paper list printed from the electronic record, whereas the intervention group uses a computer-assisted reconciliation survey that includes display of visual data (i.e., medication pictures). (c) 2011 Wiley Periodicals, Inc.
C1 [Lesselroth, Blake J.; Adams, Kathleen; Church, Victoria; Adams, Shawn; Mazur, Dennis; Russ, Yelizaveta; Felder, Robert; Douglas, David M.] Portland Oregon Vet Affairs Med Ctr, Portland, OR USA.
[Lesselroth, Blake J.; Dorr, David A.; Mazur, Dennis] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
RP Lesselroth, BJ (reprint author), Portland VA Med Ctr, P3 MED,3710 SW US Vet Hosp Dr, Portland, OR 97239 USA.
EM blake.lesselroth@va.gov
FU VA National Center for Patient Safety
FX The authors thank the VA National Center for Patient Safety for support
of this project. The authors also thank Ms. Kelly Finley for assistance
preparing this manuscript for publication.
NR 56
TC 4
Z9 4
U1 1
U2 12
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1090-8471
J9 HUM FACTOR ERGON MAN
JI Hum. Factors Ergonom. Manuf. Serv. Ind.
PD JAN-FEB
PY 2012
VL 22
IS 1
SI SI
BP 72
EP 86
DI 10.1002/hfm.20287
PG 15
WC Engineering, Manufacturing; Ergonomics
SC Engineering
GA 869JG
UT WOS:000298593600008
ER
PT J
AU Gerhard-Herman, M
Smoot, LB
Wake, N
Kieran, MW
Kleinman, ME
Miller, DT
Schwartzman, A
Giobbie-Hurder, A
Neuberg, D
Gordon, LB
AF Gerhard-Herman, Marie
Smoot, Leslie B.
Wake, Nicole
Kieran, Mark W.
Kleinman, Monica E.
Miller, David T.
Schwartzman, Armin
Giobbie-Hurder, Anita
Neuberg, Donna
Gordon, Leslie B.
TI Mechanisms of Premature Vascular Aging in Children With
Hutchinson-Gilford Progeria Syndrome
SO HYPERTENSION
LA English
DT Article
DE Hutchinson-Gilford progeria syndrome; atherosclerosis; arteriosclerosis;
arterial stiffness; lamin; aging
ID ARTERIAL STIFFNESS; INDEPENDENT PREDICTOR; AORTIC STIFFNESS;
CARDIOVASCULAR-DISEASE; HYPERTENSIVE PATIENTS; SENESCENCE; PHENOTYPE;
MORTALITY; VELOCITY; DEFECTS
AB Hutchinson-Gilford progeria syndrome is a rare, segmental premature aging syndrome of accelerated atherosclerosis and early death from myocardial infarction or stroke. This study sought to establish comprehensive characterization of the fatal vasculopathy in Hutchinson-Gilford progeria syndrome and its relevance to normal aging. We performed cardiovascular assessments at a single clinical site on the largest prospectively studied cohort to date. Carotid-femoral pulse wave velocity was dramatically elevated (mean: 13.00 +/- 3.83 m/s). Carotid duplex ultrasound echobrightness, assessed in predefined tissue sites as a measure of arterial wall density, was significantly greater than age-and sex-matched controls in the intima-media (P < 0.02), near adventitia (P < 0.003), and deep adventitia (P < 0.01), as was internal carotid artery mean flow velocity (P < 0.0001). Ankle-brachial indices were abnormal in 78% of patients. Effective disease treatments may be heralded by normalizing trends of these noninvasive cardiovascular measures. The data demonstrate that, along with peripheral vascular occlusive disease, accelerated vascular stiffening is an early and pervasive mechanism of vascular disease in Hutchinson-Gilford progeria syndrome. There is considerable overlap with cardiovascular changes of normal aging, which reinforces the view that defining mechanisms of cardiovascular disease in Hutchinson-Gilford progeria syndrome provides a unique opportunity to isolate a subset of factors influencing cardiovascular disease in the general aging population. (Hypertension. 2012;59:92-97.). Online Data Supplement
C1 [Gordon, Leslie B.] Brown Univ, Dept Pediat, Hasbro Childrens Hosp, Warren Alpert Med Sch, Providence, RI 02903 USA.
[Gerhard-Herman, Marie; Wake, Nicole] Brigham & Womens Hosp, Div Cardiol, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Smoot, Leslie B.] Childrens Hosp, Dept Cardiol, Boston, MA 02115 USA.
[Kleinman, Monica E.; Gordon, Leslie B.] Childrens Hosp, Dept Anesthesia, Boston, MA 02115 USA.
[Miller, David T.] Childrens Hosp, Dept Genet, Boston, MA 02115 USA.
[Kieran, Mark W.] Childrens Hosp, Dept Pediat Oncol, Boston, MA 02115 USA.
[Kieran, Mark W.] Dana Farber Canc Inst, Div Pediat Oncol, Boston, MA 02115 USA.
[Schwartzman, Armin; Giobbie-Hurder, Anita; Neuberg, Donna] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Schwartzman, Armin; Neuberg, Donna] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
RP Gordon, LB (reprint author), Brown Univ, Dept Pediat, Hasbro Childrens Hosp, Warren Alpert Med Sch, 593 Eddy St, Providence, RI 02903 USA.
EM Leslie.Gordon@brown.edu
OI Kieran, Mark/0000-0003-2184-7692; Schwartzman, Armin/0000-0001-5335-1611
FU Progeria Research Foundation, Peabody, MA [PRFCLIN2007-01]; National
Institutes of Health [MO1-RR02172, UL1 RR025758-01]
FX The study was funded by the Progeria Research Foundation
(PRFCLIN2007-01), Peabody, MA and by National Institutes of Health
grants to the Children's Hospital Boston General Clinical Research
Center (MO1-RR02172) and to the Harvard Catalyst Clinical and
Translational Study Unit (UL1 RR025758-01).
NR 36
TC 33
Z9 36
U1 2
U2 16
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD JAN
PY 2012
VL 59
IS 1
BP 92
EP U229
DI 10.1161/HYPERTENSIONAHA.111.180919
PG 11
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 866SS
UT WOS:000298403800019
PM 22083160
ER
PT J
AU Young, B
Hacker, MR
Rana, S
AF Young, Brett
Hacker, Michele R.
Rana, Sarosh
TI Physicians' Knowledge of Future Vascular Disease in Women with
Preeclampsia
SO HYPERTENSION IN PREGNANCY
LA English
DT Article
DE Preeclampsia; Cardiovascular disease; Ischemic heart disease; Stroke;
Primary prevention
ID LONG-TERM MORTALITY; RETROSPECTIVE COHORT; RISK; PREGNANCY; HEALTH
AB Objective. Preeclampsia, a hypertensive disorder of pregnancy, affects 5-8% of women. Large studies demonstrate a strong association between preeclampsia and future cardiovascular disease (CVD). Despite CVD being the leading cause of mortality for women, there has been little education for internal medicine physicians or obstetrician-gynecologists (ob-gyns) about this association; published guidelines do not include preeclampsia as a risk factor for future CVD. Therefore, women with a history of preeclampsia may not receive adequate risk-reduction counseling for CVD. It is unclear whether primary care physicians are aware of the association; thus, we sought to determine whether primary care providers at our institution were aware of preeclampsia's association with future CVD and whether they were providing appropriate counseling. Methods. An anonymous online survey was sent to all internists and (ob-gyns) at our hospital. Results. Although most internists (95%) and (ob-gyns) (70%) provide routine cardiovascular risk-reduction counseling, a substantial proportion of them were unaware of any health risk associated with a history of preeclampsia. Many internists were unsure or did not know whether preeclampsia is associated with ischemic heart disease (56%), stroke (48%), and decreased life expectancy (79%). The corresponding proportions for (ob-gyns) were 23, 38, and 77%, respectively. Only 9% of internists and 38% of obstetrician-gynecologists were providing cardiovascular risk-reduction counseling to women with a history of preeclampsia. Conclusion. There is limited knowledge of the association between preeclampsia and future CVD; this deficiency may limit the application of this risk factor to clinical care.
C1 [Rana, Sarosh] Beth Israel Deaconess Med Ctr, Dept Obstet & Gynecol, Div Maternal Fetal Med, Boston, MA 02215 USA.
[Young, Brett] Massachusetts Gen Hosp, Dept Obstet & Gynecol, Div Maternal Fetal Med, Boston, MA 02114 USA.
[Hacker, Michele R.] Beth Israel Deaconess Med Ctr, Dept Obstet & Gynecol, Div Reprod Endocrinol, Boston, MA 02215 USA.
RP Rana, S (reprint author), Beth Israel Deaconess Med Ctr, Dept Obstet & Gynecol, Div Maternal Fetal Med, Res N 363,99 Brookline Ave, Boston, MA 02215 USA.
EM srana1@bidmc.harvard.edu
OI Hacker, Michele/0000-0003-0217-9991
FU NICHD NIH HHS [K12 HD001255, K12 HD001255-10]
NR 17
TC 24
Z9 26
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1064-1955
J9 HYPERTENS PREGNANCY
JI Hypertens. Pregnancy
PY 2012
VL 31
IS 1
BP 50
EP 58
DI 10.3109/10641955.2010.544955
PG 9
WC Obstetrics & Gynecology; Physiology; Peripheral Vascular Disease
SC Obstetrics & Gynecology; Physiology; Cardiovascular System & Cardiology
GA 865FG
UT WOS:000298295800006
PM 21332326
ER
PT J
AU Wang, LJ
Trebicka, E
Fu, Y
Ellenbogen, S
Hong, CC
Babitt, JL
Lin, HY
Cherayil, BJ
AF Wang, Lijian
Trebicka, Estela
Fu, Ying
Ellenbogen, Shiri
Hong, Charles C.
Babitt, Jodie L.
Lin, Herbert Y.
Cherayil, Bobby J.
TI The bone morphogenetic protein-hepcidin axis as a therapeutic target in
inflammatory bowel disease
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE inflammation; iron; bone morphogenetic protein; hepcidin
ID HEREDITARY HEMOCHROMATOSIS; IRON-METABOLISM; IL-10-DEFICIENT MICE; MOUSE
MODEL; EXPRESSION; COLITIS; HFE; BMP6; GENE; DEFICIENCY
AB Background: A debilitating anemia associated with low serum iron often accompanies inflammatory bowel disease (IBD). Increased production of the iron regulatory hormone hepcidin is implicated in its pathogenesis and may also contribute to the inflammatory process itself. Hepcidin expression is dependent on bone morphogenetic proteins (BMPs) like BMP6, but the mechanisms that increase hepcidin levels during intestinal inflammation are not clear. Here we test the hypothesis that inhibiting hepcidin expression may have beneficial effects in IBD, and also shed light on the mechanism of colitis-induced hepcidin upregulation.
C1 [Wang, Lijian; Trebicka, Estela; Fu, Ying; Ellenbogen, Shiri; Cherayil, Bobby J.] Massachusetts Gen Hosp, Mucosal Immunol Lab, Charlestown, MA USA.
[Hong, Charles C.] Vanderbilt Univ, Med Ctr, Vet Affairs TVHS, Nashville, TN USA.
[Hong, Charles C.] Vanderbilt Univ, Med Ctr, Div Cardiovasc Med, Nashville, TN USA.
[Babitt, Jodie L.; Lin, Herbert Y.] Massachusetts Gen Hosp, Div Nephrol, Program Membrane Biol, Boston, MA 02114 USA.
[Babitt, Jodie L.; Lin, Herbert Y.] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Cherayil, Bobby J.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
RP Cherayil, BJ (reprint author), MGH E, Pediat Gastroenterol Unit, Bldg 114,16th St, Boston, MA 02129 USA.
EM cherayil@helix.mgh.harvard.edu
RI Fu, Ying/G-2899-2015
FU Broad Medical Research Program [IBD-0253]; National Institutes of Health
[R56 AI089700]; Wyeth Nutrition
FX Supported by grants from the Broad Medical Research Program (IBD-0253)
and the National Institutes of Health (R56 AI089700) to B.J.C., and by
an unrestricted educational grant from Wyeth Nutrition to L.W.
NR 41
TC 29
Z9 33
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1078-0998
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD JAN
PY 2012
VL 18
IS 1
BP 112
EP 119
DI 10.1002/ibd.21675
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 865TL
UT WOS:000298333100018
PM 21351217
ER
PT J
AU Viswanathan, AN
Moughan, J
Small, W
Levenback, C
Iyer, R
Hymes, S
Dicker, AP
Miller, B
Erickson, B
Gaffney, DK
AF Viswanathan, Akila N.
Moughan, Jennifer
Small, William, Jr.
Levenback, Charles
Iyer, Revathy
Hymes, Sharon
Dicker, Adam P.
Miller, Brigitte
Erickson, Beth
Gaffney, David K.
TI The Quality of Cervical Cancer Brachytherapy Implantation and the Impact
on Local Recurrence and Disease-Free Survival in Radiation Therapy
Oncology Group Prospective Trials 0116 and 0128
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
LA English
DT Article
DE Brachytherapy quality; Cervical cancer
ID EXTENDED-FIELD IRRADIATION; SQUAMOUS-CELL CARCINOMA; ILIAC LYMPH-NODES;
UTERINE CERVIX; CISPLATIN CHEMOTHERAPY; RADIOTHERAPY PRACTICE; PATTERNS;
CARE; RTOG-0116; CELECOXIB
AB Purpose: The objective of the study was to determine the impact of brachytherapy implant quality on outcome among cervical cancer patients treated on Radiation Therapy Oncology Group prospective trials 0116 and 0128.
Methods: All enrolled patients received concurrent chemoradiation followed by brachytherapy. Individual brachytherapy parameters, including the symmetry of ovoids in relation to the tandem, displacement of ovoids in relation to the cervical os, tandem bisecting the ovoids, tandem in the midpelvis, and appropriateness of packing, were scored for each implant. Multivariate Cox proportional hazards models were constructed for each parameter for local recurrence (LR), regional recurrence, distant recurrence, disease-free survival (DFS), and overall survival.
Results: Records for 103 patients were analyzed. The median follow-up time was 24.5 months. Patients with unacceptable symmetry of ovoids to the tandem had a significantly higher risk of LR than patients in the acceptable group (hazard ratio [HR], 2.67; 95% confidence interval [CI], 1.11-6.45; P = 0.03). Patients with displacement of ovoids in relation to the cervical os had a significantly increased risk of LR (HR, 2.50; 95% CI, 1.05-5.93; P = 0.04) and a lower DFS rate (HR, 2.28; 95% CI, 1.18-4.41; P = 0.01). Inappropriate placement of packing resulted in a lower DFS rate (HR, 2.06; 95% CI, 1.08-3.92; P = 0.03).
Conclusions: Assessment of the quality of a brachytherapy implant is imperative, as proper placement has an impact on patient DFS. If feasible, inappropriate placements should be corrected before treatment initiation. Brachytherapy applicators for cervical cancer should preferably be placed and assessed by experienced practitioners.
C1 [Viswanathan, Akila N.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst,Dept Radiat Oncol, Boston, MA 02115 USA.
[Moughan, Jennifer] Amer Coll Radiol, Ctr Stat, Radiat Therapy Oncol Grp, Philadelphia, PA 90034 USA.
[Small, William, Jr.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
[Levenback, Charles; Iyer, Revathy; Hymes, Sharon] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Dicker, Adam P.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Miller, Brigitte] Batte Canc Ctr, Concord, NC USA.
[Erickson, Beth] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Gaffney, David K.] Univ Utah, Huntsman Canc Ctr, Salt Lake City, UT USA.
RP Viswanathan, AN (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst,Dept Radiat Oncol, 75 Francis St,L2, Boston, MA 02115 USA.
EM aviswanathan@lroc.harvard.edu
OI Dicker, Adam/0000-0003-0733-3337
FU NCI NIH HHS [U10 CA21661, U10 CA021661, U10 CA037422, U10 CA37422, K07
CA117979, K07 CA117979-05]
NR 27
TC 24
Z9 24
U1 0
U2 1
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 JAN
PY 2012
VL 22
IS 1
BP 123
EP 131
DI 10.1097/IGC.0b013e31823ae3c9
PG 9
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 869WI
UT WOS:000298628800022
PM 22193645
ER
PT J
AU Young, RH
AF Young, Robert H.
TI History of Gynecological Pathology XXIV. Dr Cuthbert Lockyer
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY
LA English
DT Biographical-Item
DE Cuthbert Lockyer; Historical essay; Histopathology
C1 Harvard Univ, James Homer Wright Pathol Labs, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
RP Young, RH (reprint author), Harvard Univ, James Homer Wright Pathol Labs, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
EM rhyoung@partners.org
NR 1
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 JAN
PY 2012
VL 31
IS 1
BP 38
EP 47
DI 10.1097/PGP.0b013e31823bb0d9
PG 10
WC Obstetrics & Gynecology; Pathology
SC Obstetrics & Gynecology; Pathology
GA 863EW
UT WOS:000298146600006
PM 22123722
ER
PT J
AU Zietman, AL
AF Zietman, Anthony L.
TI RECEIVING THE TORCH
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
RP Zietman, AL (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Cox 302,100 Blossom St, Boston, MA 02114 USA.
EM azietman@partners.org
NR 0
TC 9
Z9 9
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 JAN
PY 2012
VL 82
IS 1
BP 1
EP 2
DI 10.1016/j.ijrobp.2011.10.008
PG 2
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 868LZ
UT WOS:000298526100001
ER
PT J
AU Chen, WC
Kim, J
Kim, E
Silverman, P
Overmoyer, B
Cooper, BW
Anthony, S
Shenk, R
Leeming, R
Hanks, SH
Lyons, JA
AF Chen, William C.
Kim, Janice
Kim, Edward
Silverman, Paula
Overmoyer, Beth
Cooper, Brenda W.
Anthony, Sue
Shenk, Robert
Leeming, Rosemary
Hanks, Shelli H.
Lyons, Janice A.
TI A PHASE II STUDY OF RADIOTHERAPY AND CONCURRENT PACLITAXEL CHEMOTHERAPY
IN BREAST-CONSERVING TREATMENT FOR NODE-POSITIVE BREAST CANCER
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Breast; Radiation; Chemoradiation
ID CELL LUNG-CANCER; RADIATION-THERAPY; CONSERVATIVE SURGERY; ADJUVANT
CHEMOTHERAPY; LOCAL-CONTROL; STAGE-II; RISK; CHEMORADIOTHERAPY;
DOXORUBICIN; CYCLOPHOSPHAMIDE
AB Purpose: Administering adjuvant chemotherapy before breast radiotherapy decreases the risk of systemic recurrence, but delays in radiotherapy could yield higher local failure. We assessed the feasibility and efficacy of placing radiotherapy earlier in the breast-conserving treatment course for lymph node positive breast cancer. Methods and
Materials: Between June 2000 and December 2004, 44 women with node-positive Stage II and III breast cancer were entered into this trial. Breast-conserving surgery and 4 cycles of doxorubicin (60 mg/m(2))/cyclophosphamide (600 mg/m2) were followed by 4 cycles of paclitaxel (175 mg/m2) delivered every 3 weeks. Radiotherapy was concurrent with the first 2 cycles of paclitaxel. The breast received 39.6 Gy in 22 fractions with a tumor bed boost of 14 Gy in 7 fractions. Regional lymphatics were included when indicated. Functional lung volume was assessed by use of the diffusing capacity for carbon monoxide as a proxy. Breast cosmesis was evaluated with the Harvard criteria.
Results: The 5-year actuarial rate of disease-free survival is 88%, and overall survival is 93%. There have been no local failures. Median follow-up is 75 months. No cases of radiation pneumonitis developed. There was no significant change in the diffusing capacity for carbon monoxide either immediately after radiotherapy (p = 0.51) or with extended follow-up (p = 0.63). Volume of irradiated breast tissue correlated with acute cosmesis, and acute Grade 3 skin toxicity developed in 2 patients. Late cosmesis was not adversely affected.
Conclusions: Concurrent paclitaxel chemotherapy and radiotherapy after breast-conserving surgery shortened total treatment time, provided excellent local control, and was well tolerated. (C) 2012 Elsevier Inc.
C1 [Chen, William C.; Anthony, Sue; Lyons, Janice A.] Univ Hosp Case Med Ctr, Dept Radiat Oncol, Cleveland, OH 44106 USA.
[Silverman, Paula; Cooper, Brenda W.] Univ Hosp Case Med Ctr, Dept Med, Cleveland, OH 44106 USA.
[Shenk, Robert; Leeming, Rosemary] Univ Hosp Case Med Ctr, Dept Surg, Cleveland, OH 44106 USA.
[Kim, Janice] Univ Washington, Med Ctr, Dept Radiat Oncol, Seattle, WA 98195 USA.
[Kim, Edward] Ohio State Univ, Med Ctr, Dept Radiat Oncol, Columbus, OH 43210 USA.
[Overmoyer, Beth] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Hanks, Shelli H.] Arizona Inst Urol, Tucson, AZ USA.
RP Lyons, JA (reprint author), Univ Hosp Case Med Ctr, Dept Radiat Oncol, 11100 Euclid Ave, Cleveland, OH 44106 USA.
EM janice.lyons@uhhospitals.org
NR 42
TC 4
Z9 5
U1 0
U2 5
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 JAN
PY 2012
VL 82
IS 1
BP 14
EP 20
DI 10.1016/j.ijrobp.2010.08.051
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 868LZ
UT WOS:000298526100005
PM 21035961
ER
PT J
AU Kelly, PJ
Lin, YIB
Yu, AY
Alexander, BM
Hacker, F
Marcus, KJ
Weiss, SE
AF Kelly, Paul J.
Lin, Yijie Brittany
Yu, Alvin Y.
Alexander, Brian M.
Hacker, Fred
Marcus, Karen J.
Weiss, Stephanie E.
TI STEREOTACTIC IRRADIATION OF THE POSTOPERATIVE RESECTION CAVITY FOR BRAIN
METASTASIS: A FRAMELESS LINEAR ACCELERATOR-BASED CASE SERIES AND REVIEW
OF THE TECHNIQUE
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Stereotactic radiosurgery; Hypofractionated stereotactic radiotherapy;
Brain metastasis; Resection cavity; Whole brain radiotherapy
ID CEREBRAL METASTASES; RADIOSURGERY BOOST; SINGLE METASTASES;
RANDOMIZED-TRIAL; RADIOTHERAPY; RADIATION; PROGRESSION; DISEASE
AB Purpose: Whole-brain radiation therapy (WBRT) is the standard of care after resection of a brain metastasis. However, concern regarding possible neurocognitive effects and the lack of survival benefit with this approach has led to the use of stereotactic radiosurgery (SRS) to the resection cavity in place of WBRT. We report our initial experience using an image-guided linear accelerator-based frameless stereotactic system and review the technical issues in applying this technique.
Methods and Materials: We retrospectively reviewed the setup accuracy, treatment outcome, and patterns of failure of the first 18 consecutive cases treated at Brigham and Women's Hospital. The target volume was the resection cavity without a margin excluding the surgical track.
Results: The median number of brain metastases per patient was 1 (range; 1-3). The median planning target volume was 3.49 mL. The median prescribed dose was 18 Gy (range, 15-18 Gy) with normalization ranging from 68% to 85%. In all cases, 99% of the planning target volume was covered by the prescribed dose. The median conformity index was 1.6 (range, 1.41-1.92). The SRS was delivered with submillimeter accuracy. At a median follow-up of 12.7 months, local control was achieved in 16/18 cavities treated. True local recurrence occurred in 2 patients. No marginal failures occurred. Distant recurrence occurred in 6/17 patients. Median time to any failure was 7.4 months. No Grade 3 or higher toxicity was recorded. A long interval between initial cancer diagnosis and the development of brain metastasis was the only factor that trended toward a significant association with the absence of recurrence (local or distant) (log-rank p = 0.097).
Conclusions: Frameless stereotactic irradiation of the resection cavity after surgery for a brain metastasis is a safe and accurate technique that offers durable local control and defers the use of WBRT in select patients. This technique should be tested in larger prospective studies. (C) 2012 Elsevier Inc.
C1 [Kelly, Paul J.; Alexander, Brian M.; Hacker, Fred; Marcus, Karen J.; Weiss, Stephanie E.] Dana Farber Brigham & Womens Canc Ctr, Dept Radiat Oncol, Boston, MA USA.
[Lin, Yijie Brittany; Yu, Alvin Y.] Harvard Univ, Sch Med, Boston, MA USA.
RP Kelly, PJ (reprint author), Brigham & Womens Hosp, Dept Radiat Oncol, 75 Francis St,ASB1,L2, Boston, MA 02115 USA.
EM pkelly@lroc.harvard.edu
OI Hacker, Fred/0000-0001-7535-7598
FU European Association of Neurooncology
FX This abstract was presented as an oral presentation at the 9th Congress
of the European Association of Neurooncology, Maastricht, Netherlands,
September 16-19, 2010. A travel grant was awarded by the European
Association of Neurooncology.
NR 22
TC 35
Z9 36
U1 1
U2 8
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 JAN
PY 2012
VL 82
IS 1
BP 95
EP 101
DI 10.1016/j.ijrobp.2010.10.043
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 868LZ
UT WOS:000298526100016
PM 21168282
ER
PT J
AU Kachnic, LA
Tsai, HK
Coen, JJ
Blaszkowsky, LS
Hartshorn, K
Kwak, EL
Willins, JD
Ryan, DP
Hong, TS
AF Kachnic, Lisa A.
Tsai, Henry K.
Coen, John J.
Blaszkowsky, Lawrence S.
Hartshorn, Kevan
Kwak, Eunice L.
Willins, John D.
Ryan, David P.
Hong, Theodore S.
TI DOSE-PAINTED INTENSITY-MODULATED RADIATION THERAPY FOR ANAL CANCER: A
MULTI-INSTITUTIONAL REPORT OF ACUTE TOXICITY AND RESPONSE TO THERAPY
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Anal cancer; Chemoradiation; IMRT; Acute toxicity
ID HIV-POSITIVE PATIENTS; SQUAMOUS-CELL CARCINOMA; RANDOMIZED-TRIAL;
CONCURRENT CHEMOTHERAPY; TREATMENT TOLERANCE; CANAL CARCINOMA; PHASE-II;
RADIOTHERAPY; IMRT; MITOMYCIN
AB Purpose: Chemoradiation for anal cancer yields effective tumor control, but is associated with significant acute toxicity. We report our multi-institutional experience using dose-painted IMRT (DP-IMRT).
Patients and Methods: Between August 2005 and May 2009,43 patients were treated with DP-IMRT and concurrent chemotherapy for biopsy-proven, squamous cell carcinoma of the anal canal at two academic medical centers. DP-IMRT was prescribed as follows: T2N0: 42 Gy, 1.5 Gy/fraction (fx) to elective nodal planning target volume (PTV) and 50.4 Gy, 1.8 Gy/fx to anal tumor PTV; T3-4N0-3: 45 Gy, 1.5 Gy/fx to elective nodal PTV, and 54 Gy, 1.8 Gy/fx to the anal tumor and metastatic nodal PTV >3 cm with 50.4 Gy, 1.68 Gy/fx to nodal PTVs <= 3 cm in size. Acute and late toxicity was reported by the treating physician. Actuarial analysis was performed using the Kaplan-Meier method.
Results: Median age was 58 years; 67% female; 16% Stage I, 37% II; 42% III; 5% IV. Fourteen patients were immunocompromised: 21% HIV-positive and 12% on chronic immunosuppression. Median follow-up was 24 months (range, 0.6-43.5 months). Sixty percent completed chemoradiation without treatment interruption; median duration of treatment interruption was 2 days (range, 2-24 days). Acute Grade 3+ toxicity included: hematologic 51%, dermatologic 10%, gastrointestinal 7%, and genitourinary 7%. Two-year local control, overall survival, colostomy-free survival, and metastasis-free survival were 95%, 94%, 90%, and 92%, respectively.
Conclusions: Dose-painted IMRT appears effective and well-tolerated as part of a chemoradiation therapy regimen for the treatment of anal canal cancer. (C) 2012 Elsevier Inc.
C1 [Kachnic, Lisa A.; Willins, John D.] Boston Med Ctr, Dept Radiat Oncol, LL, Boston, MA 02118 USA.
[Hartshorn, Kevan] Boston Med Ctr, Dept Med, Boston, MA 02118 USA.
[Tsai, Henry K.] Harvard Univ, Sch Med, Harvard Radiat Oncol Program, Boston, MA USA.
[Kachnic, Lisa A.; Coen, John J.; Willins, John D.; Hong, Theodore S.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Blaszkowsky, Lawrence S.; Kwak, Eunice L.; Ryan, David P.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Kachnic, LA (reprint author), Boston Med Ctr, Dept Radiat Oncol, LL, 830 Harrison Ave, Boston, MA 02118 USA.
EM lisa.kachnic@bmc.org
OI Hartshorn, Kevan/0000-0002-7196-7433
NR 25
TC 61
Z9 63
U1 0
U2 9
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 JAN
PY 2012
VL 82
IS 1
BP 153
EP 158
DI 10.1016/j.ijrobp.2010.09.030
PG 6
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 868LZ
UT WOS:000298526100024
PM 21095071
ER
PT J
AU Viswanathan, AN
Creutzberg, CL
Craighead, P
McCormack, M
Toita, T
Narayan, K
Reed, N
Long, H
Kim, HJ
Marth, C
Lindegaard, JC
Cerrotta, A
Small, W
Trimble, E
AF Viswanathan, Akila N.
Creutzberg, Carien L.
Craighead, Peter
McCormack, Mary
Toita, Takafumi
Narayan, Kailash
Reed, Nicholas
Long, Harry
Kim, Hak-Jae
Marth, Christian
Lindegaard, Jacob C.
Cerrotta, Annmarie
Small, William, Jr.
Trimble, Edward
TI INTERNATIONAL BRACHYTHERAPY PRACTICE PATTERNS: A SURVEY OF THE
GYNECOLOGIC CANCER INTERGROUP (GCIG)
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Brachytherapy; Cervical cancer; Radiation dose
ID HIGH-DOSE-RATE; CERVICAL-CANCER; INTRACAVITARY BRACHYTHERAPY;
FRACTIONATION SCHEDULE; RADIOTHERAPY; RECOMMENDATIONS; CARCINOMA; TRIAL
AB Purpose: To determine current practice patterns with regard to gynecologic high-dose-rate (HDR) brachytherapy among international members of the Gynecologic Cancer Intergroup (GCIG) in Japan/Korea (Asia), Australia/New Zealand (ANZ), Europe (E), and North America (NAm).
Methods and Materials: A 32-item survey was developed requesting information on brachytherapy practice patterns and standard management for Stage IB-IVA cervical cancer. The chair of each GCIG member cooperative group selected radiation oncology members to receive the survey.
Results: A total of 72 responses were analyzed; 61 respondents (85%) used HDR. The three most common HDR brachytherapy fractionation regimens for Stage IB-IIA patients were 6 Gy for five fractions (18%), 6 Gy for four fractions (15%), and 7 Gy for three fractions (11%); for Stage IIB-IVA patients they were 6 Gy for five fractions (19%), 7 Gy for four fractions (8%), and 7 Gy for three fractions (8%). Overall, the mean combined external-beam and brachytherapy equivalent dose (EQD2) was 81.1 (standard deviation [SD] 10.16). The mean EQD2 recommended for Stage IB-IIA patients was 78.9 Gy (SD 10.7) and for Stage IIB-IVA was 83.3 Gy (SD 11.2) (p = 0.02). By region, the mean combined EQD2 was as follows: Asia, 71.2 Gy (SD 12.65); ANZ, 81.18 (SD 4:96); E, 83.24 (SD 10.75); and NAm, 81.66 (SD, 6.05;p = 0.02 for Asia vs. other regions). The ratio of brachytherapy to total prescribed dose was significantly higher for Japan (p = 0.0002).
Conclusion: Although fractionation patterns may vary, the overall mean doses administered for cervical cancer are similar in Australia/New Zealand, Europe, and North America, with practitioners in Japan administering a significantly lower external-beam dose but higher brachytherapy dose to the cervix. Given common goals, standardization should be possible in future clinical trials. (C) 2012 Elsevier Inc.
C1 [Viswanathan, Akila N.] Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02115 USA.
[Viswanathan, Akila N.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Creutzberg, Carien L.] Leiden Univ, Med Ctr, Dept Clin Oncol, Leiden, Netherlands.
[Craighead, Peter] Tom Baker Canc Clin, Calgary, AB, Canada.
[McCormack, Mary] Univ Coll London Hosp, Dept Oncol, London, England.
[Toita, Takafumi] Univ Ryukyus, Grad Sch Med Sci, Dept Radiol, Okinawa, Japan.
[Narayan, Kailash] Univ Melbourne, Peter MacCallum Canc Ctr, Div Radiat Oncol, Melbourne, Vic, Australia.
[Narayan, Kailash] Univ Melbourne, Dept Obstet & Gynecol, Melbourne, Vic, Australia.
[Reed, Nicholas] Western Infirm & Associated Hosp, Beatson Oncol Ctr, Glasgow G11 6NT, Lanark, Scotland.
[Long, Harry] Mayo Clin, Coll Med, Dept Oncol, Div Med Oncol, Rochester, MN USA.
[Kim, Hak-Jae] Seoul Natl Univ Hosp, Dept Oncol, Seoul 110744, South Korea.
[Marth, Christian] Med Univ Innsbruck, Innsbruck, Austria.
[Lindegaard, Jacob C.] Aarhus Univ Hosp, DK-8000 Aarhus, Denmark.
[Cerrotta, Annmarie] Fdn IRCCS Ist Nazl Tumori, Dept Radiat Therapy, Milan, Italy.
[Small, William, Jr.] Robert H Lurie Comprehens Canc NW Univ, Chicago, IL USA.
[Trimble, Edward] NCI, Bethesda, MD 20892 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
RI Cerrotta, Annamaria/D-8063-2017;
OI Cerrotta, Annamaria/0000-0001-7926-3716; Viswanathan,
Akila/0000-0002-2003-0392
FU NCI NIH HHS [K07 CA117979]
NR 20
TC 59
Z9 60
U1 2
U2 9
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 JAN
PY 2012
VL 82
IS 1
BP 250
EP 255
DI 10.1016/j.ijrobp.2010.10.030
PG 6
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 868LZ
UT WOS:000298526100037
PM 21183288
ER
PT J
AU Schoenfeld, JD
Sher, DJ
Norris, CM
Haddad, RI
Posner, MR
Balboni, TA
Tishler, RB
AF Schoenfeld, Jonathan D.
Sher, David J.
Norris, Charles M., Jr.
Haddad, Robert I.
Posner, Marshall R.
Balboni, Tracy A.
Tishler, Roy B.
TI SALIVARY GLAND TUMORS TREATED WITH ADJUVANT INTENSITY-MODULATED
RADIOTHERAPY WITH OR WITHOUT CONCURRENT CHEMOTHERAPY
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Chemoradiotherapy; Salivary gland cancers; Intensity-modulated
radiotherapy; Adenoid cystic carcinoma; Mucoepidermoid carcinoma
ID ADENOID CYSTIC CARCINOMA; COOPERATIVE-ONCOLOGY-GROUP; SQUAMOUS-CELL
CARCINOMA; RADIATION-THERAPY; NECK-CANCER; PHASE-II; HEAD; SURGERY;
CHEMORADIOTHERAPY; MALIGNANCIES
AB Purpose: To analyze the recent single-institution experience of patients with salivary gland tumors who had undergone adjuvant intensity-modulated radiotherapy (IMRT), with or without concurrent chemotherapy.
Patients and Methods: We performed a retrospective analysis of 35 salivary gland carcinoma patients treated primarily at the Dana-Farber Cancer Institute between 2005 and 2010 with surgery and adjuvant IMRT. The primary endpoints were local control, progression-free survival, and overall survival. The secondary endpoints were acute and chronic toxicity. The median follow-up was 2.3 years (interquartile range, 1.2-2.8) among the surviving patients.
Results: The histologic types included adenoid cystic carcinoma in 15 (43%), mucoepidermoid carcinoma in 6 (17%), adenocarcinoma in 3 (9%), acinic cell carcinoma in 3 (9%), and other in 8 (23%). The primary sites were the parotid gland in 17 (49%), submandibular glands in 6 (17%), tongue in 4 (11%), palate in 4 (11%), and other in 4(11%). The median radiation dose was 66 Gy, and 22 patients (63%) received CRT. The most common chemotherapy regimen was carboplatin and paclitaxel (n = 14, 64%). A trend was seen for patients undergoing CRT to have more adverse prognostic factors, including Stage T3-T4 disease (CRT, n = 12, 55% vs. n = 4, 31%, p = .29), nodal positivity (CRT, n = 8, 36% vs. n = 1, 8%, p = .10), and positive margins (n = 13, 59% vs. n = 5, 38%, p = .30). One patient who had undergone CRT developed an in-field recurrence, resulting in an overall actuarial 3-year local control rate of 92%. Five patients (14%) developed distant metastases (1 who had undergone IMRT only and 4 who had undergone CRT). Acute Grade 3 mucositis, esophagitis, and dermatitis occurred in 8%, 8%, and 8% (1 each) of IMRT patients and in 18%, 5%, and 14% (4, 1, and 3 patients) of the CRT group, respectively. No acute Grade 4 toxicity occurred. The most common late toxicity was Grade 1 xerostomia (n = 8, 23%).
Conclusions: Treatment of salivary gland malignancies with postoperative IMRT was well tolerated with a high rate of local control. Chemoradiotherapy resulted in excellent local control in a subgroup of patients with adverse prognostic factors and might be warranted in select patients. (C) 2012 Elsevier Inc.
C1 [Schoenfeld, Jonathan D.] Harvard Radiat Oncol Program, Dept Radiat Oncol, Boston, MA 02114 USA.
[Sher, David J.; Balboni, Tracy A.; Tishler, Roy B.] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
[Norris, Charles M., Jr.] Brigham & Womens Hosp, Div Otolaryngol, Dept Surg, Boston, MA 02115 USA.
[Haddad, Robert I.; Posner, Marshall R.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Haddad, Robert I.; Posner, Marshall R.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
RP Schoenfeld, JD (reprint author), Harvard Radiat Oncol Program, Dept Radiat Oncol, 75 Francis St, Boston, MA 02114 USA.
EM jdschoenfeld@partners.org
NR 25
TC 32
Z9 33
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 JAN
PY 2012
VL 82
IS 1
BP 308
EP 314
DI 10.1016/j.ijrobp.2010.09.042
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 868LZ
UT WOS:000298526100045
PM 21075557
ER
PT J
AU Haglund, KE
Raut, CP
Nascimento, AF
Wang, Q
George, S
Baldini, EH
AF Haglund, Karl E.
Raut, Chandrajit P.
Nascimento, Alessandra F.
Wang, Qian
George, Suzanne
Baldini, Elizabeth H.
TI RECURRENCE PATTERNS AND SURVIVAL FOR PATIENTS WITH INTERMEDIATE- AND
HIGH-GRADE MYXOFIBROSARCOMA
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Myxofibrosarcoma; surgery; radiation therapy; amputalion; extremity
sarcoma
ID SOFT-TISSUE SARCOMAS; LIMB-SPARING SURGERY; PROGNOSTIC-FACTORS; SURGICAL
MARGINS; RADIATION-THERAPY; RANDOMIZED-TRIAL; LOCAL RECURRENCE;
CLINICOPATHOLOGICAL ANALYSIS; POSTOPERATIVE RADIOTHERAPY; ADJUVANT
CHEMOTHERAPY
AB Purpose: Myxofibrosarcoma (MFS) is a rare sarcoma with a predilection for multiple local recurrences (LR), for which optimal treatment has not been defined. We reviewed our experience to determine the impact of surgery and radiation therapy (RT) on pattern of recurrence, limb salvage, and overall survival (OS).
Methods and Materials: Between 1995 and 2005, 36 patients with localized intermediate-or high-grade MFS were treated at our institution. Data on clinicopathologic features, treatments, and patient outcomes were reviewed and analyzed.
Results: Median age was 72.5 years (range, 42-96 years). Median tumor size was 7.5 cm, and 34 tumors (94%) were high grade. All patients underwent surgery at our institution, including re-resections in 20 patients (56%) after initial surgery elsewhere. Margins were microscopically positive in 9 patients (25%). RT was given to 28 patients (78%) pre - and/or postoperatively. After a median follow-up of 3.5 years (range, 0.4-12.4 years), 11 patients (31%) developed LR. There were no significant predictors for L:R on univariate analysis, including margin status or use of RT. Limb salvage was ultimately achieved in only 5 of 11 LRs (45%) because of multiple subsequent LRs. Distant recurrence (DR) occurred in 6 patients (17%). Median and 4-year OS were 96 months and 65%, respectively. Seven patients (19%) died of tumor-related causes, 6 of whom had DRs. On univariate analysis, tumor size was associated with OS.
Conclusions: Despite aggressive surgery and RT, intermediate-and high-grade MFS are associated with a high rate of LR that adversely affects limb preservation. More aggressive local treatment strategies are necessary. (C) 2012 Elsevier Inc.
C1 [Baldini, Elizabeth H.] Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02115 USA.
[Raut, Chandrajit P.] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Nascimento, Alessandra F.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[George, Suzanne] Brigham & Womens Hosp, Dept Med Oncol, Boston, MA 02115 USA.
[Haglund, Karl E.] Brigham & Womens Hosp, Harvard Radiat Oncol Program, Boston, MA 02115 USA.
[Raut, Chandrajit P.; Wang, Qian; George, Suzanne; Baldini, Elizabeth H.] Dana Farber Canc Inst, Ctr Sarcoma & Bone Oncol, Boston, MA 02115 USA.
RP Baldini, EH (reprint author), Brigham & Womens Hosp, Dept Radiat Oncol, 75 Francis St,ASB1-L2, Boston, MA 02115 USA.
EM ebaldini@LROC.Harvard.edu
NR 34
TC 19
Z9 19
U1 1
U2 5
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 JAN
PY 2012
VL 82
IS 1
BP 361
EP 367
DI 10.1016/j.ijrobp.2010.08.042
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 868LZ
UT WOS:000298526100053
PM 20951504
ER
PT J
AU Bradley, J
Bae, K
Choi, N
Forster, K
Siegel, BA
Brunetti, J
Purdy, J
Faria, S
Vu, T
Thorstad, W
Choy, H
AF Bradley, Jeffrey
Bae, Kyounghwa
Choi, Noah
Forster, Ken
Siegel, Barry A.
Brunetti, Jacqueline
Purdy, James
Faria, Sergio
Vu, Toni
Thorstad, Wade
Choy, Hak
TI A PHASE II COMPARATIVE STUDY OF GROSS TUMOR VOLUME DEFINITION WITH OR
WITHOUT PET/CT FUSION IN DOSIMETRIC PLANNING FOR NON-SMALL-CELL LUNG
CANCER (NSCLC): PRIMARY ANALYSIS OF RADIATION THERAPY ONCOLOGY GROUP
(RTOG) 0515
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Lung cancer; FDG-PET; Mediastinal nodal staging; mediastinum
AB Background: Radiation Therapy Oncology Group (RTOG) 0515 is a Phase II prospective trial designed to quantify the impact of positron emission tomography (PET)/computed tomography (CT) compared with CT alone on radiation treatment plans (RTPs) and to determine the rate of elective nodal failure for PET/CT-derived volumes.
Methods: Each enrolled patient underwent definitive radiation therapy for non small-cell lung cancer (>= 60 Gy) and had two RTP datasets generated: gross tumor volume (GTV) derived with CTalone and with PET/CT. Patients received treatment using the PET/CT-derived plan. The primary end point, the impact of PET/CT fusion on treatment plans was measured by differences of the following variables for each patient: GTV, number of involved nodes, nodal station, mean lung dose (MLD), volume of lung exceeding 20 Gy (V20), and mean esophageal dose (MED). Regional failure rate was a secondary end point. The nonparametric Wilcoxon matched-pairs signed-ranks test was used with Bonferroni adjustment for an overall significance level of 0.05.
Results: RTOG 0515 accrued 52 patients, 47 of whom are evaluable. The follow-up time for all patients is 12.9 months (2.7-22.2). Tumor staging was as follows: 11 = 6%; IIIA = 40%; and IIIB = 54%. The GTV was statistically significantly smaller for PET/CT-derived volumes (98.7 vs. 86.2 mL; p < 0.0001). MLDs for PET/CT plans were slightly lower (19 vs. 17.8 Gy; p = 0.06). There was no significant difference in the number of involved nodes (2.1 vs. 2.4), V20 (32% vs. 30.8%), or MED (28.7 vs. 27.1 Gy). Nodal contours were altered by PET/CT for 51% of patients. One patient (2%) has developed an elective nodal failure.
Conclusions: PET/CT-derived tumor volumes were smaller than those derived by CT alone. PET/CT changed nodal GTV contours in 51% of patients. The elective nodal failure rate for GTVs derived by PET/CT is quite low, supporting the RTOG standard of limiting the target volume to the primary tumor and involved nodes. (C) 2012 Elsevier Inc.
C1 [Bradley, Jeffrey] Washington Univ, Sch Med, Dept Radiat Oncol, Alvin J Siteman Comprehens Canc Ctr, Washington, DC USA.
[Bae, Kyounghwa] RTOG, Dept Stat, Philadelphia, PA USA.
[Choi, Noah] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Forster, Ken] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Brunetti, Jacqueline] Holy Name Med Ctr, Teaneck, NJ USA.
[Purdy, James] Univ Calif Davis, Davis, CA 95616 USA.
[Faria, Sergio] McGill Univ, Montreal, PQ, Canada.
[Vu, Toni] Univ Montreal, Notre Dame Hosp, Ctr Hosp Univ Montreal, Montreal, PQ H3C 3J7, Canada.
[Choy, Hak] Univ Texas SW, Dallas, TX USA.
RP Bradley, J (reprint author), Washington Univ, Sch Med, Dept Radiat Oncol, Alvin J Siteman Comprehens Canc Ctr, 4921 Parkview Pl, Washington, DC USA.
EM jbradley@wustl.edu
FU RTOG [U10 CA21661]; CCOP [U10 CA37422]; National Cancer Institute (NCI)
[U24 CA81647]
FX This project was supported by RTOG grant U10 CA21661, CCOP grant U10
CA37422, and ATC grant U24 CA81647 from the National Cancer Institute
(NCI).
NR 6
TC 28
Z9 30
U1 1
U2 10
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 JAN
PY 2012
VL 82
IS 1
BP 435
EP 441
DI 10.1016/j.ijrobp.2010.09.033
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 868LZ
UT WOS:000298526100062
PM 21075551
ER
PT J
AU Gandhi, NR
Andrews, JR
Brust, JCM
Montreuil, R
Weissman, D
Heo, M
Moll, AP
Friedland, GH
Shah, NS
AF Gandhi, N. R.
Andrews, J. R.
Brust, J. C. M.
Montreuil, R.
Weissman, D.
Heo, M.
Moll, A. P.
Friedland, G. H.
Shah, N. S.
TI Risk factors for mortality among MDR- and XDR-TB patients in a high HIV
prevalence setting
SO INTERNATIONAL JOURNAL OF TUBERCULOSIS AND LUNG DISEASE
LA English
DT Article
DE MDR-TB; XDR-TB; risk factors; mortality; TB-HIV co-infection
ID MULTIDRUG-RESISTANT TUBERCULOSIS; SOUTH-AFRICA; ANTIRETROVIRAL THERAPY;
TREATMENT OUTCOMES
AB SETTING : Recent studies suggest that the prevalence of drug-resistant tuberculosis (TB) in sub-Saharan Africa may be rising. This is of concern, as human immunodeficiency virus (HIV) co-infection in multidrug-resistant (MDR) and extensively drug-resistant (XDR) TB has been associated with exceedingly high mortality rates.
OBJECTIVE: To identify risk factors associated with mortality in MDR- and XDR-TB patients co-infected with HIV in South Africa.
DESIGN: Case-control study of patients who died of all causes within 2 years of diagnosis with MDR- or XDR-TB.
RESULTS: Among 123 MDR-TB patients, 78 (63%) died following diagnosis. CD4 count <= 50 (HR 4.64, P = 0.01) and 51-200 cells/mm(3) (HR 4.17, P = 0.008) were the strongest independent risk factors for mortality. Among 139 XDR-TB patients, 111 (80%) died. CD4 count <= 50 cells/mm(3) (HR 4.46, P = 0.01) and resistance to all six drugs tested (HR 2.54, P = 0.04) were the principal risk factors. Use of antiretroviral therapy (ART) was protective (HR 0.34, P = 0.009).
CONCLUSIONS: Mortality due to MDR- and XDR-TB was associated with greater degree of immunosuppression and drug resistance. Efforts to reduce mortality must focus on preventing the amplification of resistance by strengthening TB treatment programs, as well as reducing the pool of immunosuppressed HIV-infected patients through aggressive HIV testing and ART initiation.
C1 [Gandhi, N. R.] Montefiore Med Ctr, Div Gen Internal Med, Dept Med, Bronx, NY 10467 USA.
[Gandhi, N. R.; Heo, M.; Shah, N. S.] Montefiore Med Ctr, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Andrews, J. R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, Boston, MA USA.
[Moll, A. P.] Philanjalo & Church Scotland Hosp, Tugela Ferry, Kwazulu Natal, South Africa.
[Friedland, G. H.] Yale Univ, Sch Med, New Haven, CT USA.
RP Gandhi, NR (reprint author), Montefiore Med Ctr, Div Gen Internal Med, Dept Med, 111 E 210 St, Bronx, NY 10467 USA.
EM neelgandhi@alumni.williams.edu
OI Andrews, Jason/0000-0002-5967-251X
FU Doris Duke Charitable Foundation [NRG 2007070, NSS 2007071, 2007018];
Gilead Foundation; Irene Diamond Fund [R05130]
FX The authors are grateful to the dedicated, courageous, and inspiring
staff of the Church of Scotland Hospital, the Umzinyathi District
Department of Health, and the KwaZulu-Natal Province TB Control Program.
They thank the National Health and Laboratory Services of the Inkosi
Albert Luthuli Central Hospital for performing all TB culture and DST
for patients from Tugela Ferry. This work would not have been possible
without the medical students, residents, research assistants, and data
capturers who contributed to data collection and data cleaning. The
authors also thank X Li for his helpful comments during the analysis of
these data. NRG and NSS are both recipients of the Doris Duke Charitable
Foundation Clinical Scientist Development Award (NRG 2007070, NSS
2007071). GF is also supported by the Doris Duke Charitable Foundation
(2007018), the Gilead Foundation, and The Irene Diamond Fund (R05130).
Statistical support was provided by the Center for AIDS Research (CFAR)
of Albert Einstein College of Medicine/Montefiore Medical Center. The
funders had no role in study design, data collection and analysis,
decision to publish or preparation of the manuscript.
NR 26
TC 29
Z9 29
U1 0
U2 8
PU INT UNION AGAINST TUBERCULOSIS LUNG DISEASE (I U A T L D)
PI PARIS
PA 68 BOULEVARD SAINT-MICHEL,, 75006 PARIS, FRANCE
SN 1027-3719
J9 INT J TUBERC LUNG D
JI Int. J. Tuberc. Lung Dis.
PD JAN
PY 2012
VL 16
IS 1
BP 90
EP 97
DI 10.5588/ijtld.11.0153
PG 8
WC Infectious Diseases; Respiratory System
SC Infectious Diseases; Respiratory System
GA 871GU
UT WOS:000298726700017
PM 22236852
ER
PT J
AU Jiang, T
Kambadakone, A
Kulkarni, NM
Zhu, AX
Sahani, DV
AF Jiang, Tao
Kambadakone, Avinash
Kulkarni, Naveen M.
Zhu, Andrew X.
Sahani, Dushyant V.
TI Monitoring Response to Antiangiogenic Treatment and Predicting Outcomes
in Advanced Hepatocellular Carcinoma Using Image Biomarkers, CT
Perfusion, Tumor Density, and Tumor Size (RECIST)
SO INVESTIGATIVE RADIOLOGY
LA English
DT Article
DE hepatocellular carcinoma; antiangiogenic treatment; image biomarker; CT
perfusion; RECIST
ID GUIDELINE VERSION 1.1; COMPUTED-TOMOGRAPHY; SOLID TUMORS; EVALUATION
CRITERIA; INITIAL-EXPERIENCE; COLORECTAL-CANCER; FUNCTIONAL-CT; RAT
MODEL; LIVER; ANGIOGENESIS
AB Purpose: Our aim was to investigate the hypothesis that the CT perfusion (CTP) is a more sensitive image biomarker when compared with tumor burden (Response Evaluation Criteria in Solid Tumors [RECIST]) and tumor density (HU) for monitoring treatment changes and for predicting long-term outcome in advanced hepatocellular carcinoma (HCC) treated with a combination of antiangiogenic treatment and chemotherapy.
Material and Methods: In this phase II clinical trial, 33 patients with advanced HCC were enrolled and 23 were included in the current study. A diagnostic dual-phase contrast-enhanced CT and perfusion CT was performed at baseline and days 10 to 12 after initiation of antiangiogenic treatment (Bevacizumab). The patients subsequently received bevacizumab in combination with gemcitabine and oxaliplatin (GEMOX-B) and contrast-enhanced CT was performed at the end of treatment (after completing 3 cycles of GEMOX-B chemotherapy) and after every 8 week until there was evidence of disease progression or intolerable toxicity. The CTP protocol included a targeted dynamic cine acquisition for 25 to 30 seconds after 50 to 70 mL of iodinated contrast media injection at 5 to 7 mL/s. The CTP parameters were compared with tumor size (according to Response Evaluation Criteria in Solid Tumors, RECIST 1.1) and density measurements (HU) before and after treatment and correlated with patient's outcome in groups with and without tumor thrombus. A one-sided P value was calculated and the Bonferroni correction was used to address the issue of multiple comparisons.
Results: On days 10 to 12 after initiation of bevacizumab, significant decrease in CTP parameters was noted (P < 0.005). There was a mild reduction in mean tumor density (P = 0.016) without any significant change in mean tumor size. Tumors with higher baseline mean transit time values on CTP correlated with favorable clinical outcome (partial response and stable disease) and had better 6 months progression-free survival (P = 0.002 and P = 0.005, respectively). The baseline transfer constant (Ktrans) of responders (1425.19 +/- 609.47 mL/1000mL/min) was significantly higher than that of nonresponders (935.96 +/- 189.47 mL/1000 mL/min). The tumor thrombus in the portal vein demonstrated baseline perfusion values and post-treatment change values similar to the HCC.
Conclusion: In advanced HCC, CTP is a more sensitive image biomarker for monitoring early antiangiogenic treatment effects as well as in predicting outcome at the end of treatment and progression-free survival as compared with RECIST and tumor density.
C1 [Jiang, Tao; Kambadakone, Avinash; Kulkarni, Naveen M.; Sahani, Dushyant V.] Harvard Univ, Sch Med, Div Abdominal Imaging & Intervent, Boston, MA 02114 USA.
[Zhu, Andrew X.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Jiang, Tao] Second Mil Med Univ, ChangZheng Hosp, Dept Radiol, Shanghai, Peoples R China.
RP Sahani, DV (reprint author), Harvard Univ, Sch Med, Div Abdominal Imaging & Intervent, 55 Fruit St,White 270, Boston, MA 02114 USA.
EM dsahani@partners.org
NR 37
TC 76
Z9 79
U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0020-9996
EI 1536-0210
J9 INVEST RADIOL
JI Invest. Radiol.
PD JAN
PY 2012
VL 47
IS 1
BP 11
EP 17
DI 10.1097/RLI.0b013e3182199bb5
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 866RR
UT WOS:000298400100004
PM 21512396
ER
PT J
AU Lichterfeld, M
Gandhi, RT
Simmons, RP
Flynn, T
Sbrolla, A
Yu, XG
Basgoz, N
Mui, S
Williams, K
Streeck, H
Burgett-Yandow, N
Roy, G
Janssens, M
Pedneault, L
Vandepapeliere, P
Koutsoukos, M
Demoitie, MA
Bourguignon, P
McNally, L
Voss, G
Altfeld, M
AF Lichterfeld, Mathias
Gandhi, Rajesh T.
Simmons, Rachel P.
Flynn, Theresa
Sbrolla, Amy
Yu, Xu G.
Basgoz, Nesli
Mui, Stanley
Williams, Katie
Streeck, Hendrik
Burgett-Yandow, Nicole
Roy, Gilbert
Janssens, Michel
Pedneault, Louise
Vandepapeliere, Pierre
Koutsoukos, Marguerite
Demoitie, Marie-Ange
Bourguignon, Patricia
McNally, Lisa
Voss, Gerald
Altfeld, Marcus
TI Induction of Strong HIV-1-Specific CD4(+) T-Cell Responses Using an
HIV-1 gp120/NefTat Vaccine Adjuvanted With AS02(A) in
Antiretroviral-Treated HIV-1-Infected Individuals
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE HIV-1; HIV-1-specific CD4(+) cells; therapeutic vaccination; vaccination
ID VIRUS TYPE-1 HIV-1; TREATMENT INTERRUPTION; INFECTED PATIENTS; VIRAL
REPLICATION; IMMUNE CONTROL; FOLLOW-UP; THERAPY; IMMUNODEFICIENCY; AIDS;
MEMORY
AB Background: Induction of HIV-1-specific CD4(+) T-cell responses by therapeutic vaccination represents an attractive intervention to potentially increase immune control of HIV-1.
Methods: We performed a double-blinded, randomized, placebo-controlled clinical trial to determine the safety and immunogenicity of GlaxoSmithKline Biologicals' HIV-1 gp120/NefTat subunit protein vaccine formulated with the AS02(A) Adjuvant System in subjects with well-controlled chronic HIV-1 infection on highly active antiretroviral therapy. Ten individuals received the vaccine; whereas adjuvant alone or placebo was given to 5 subjects each. Immunogenicity was monitored by intracellular cytokine flow cytometry and carboxyfluorescein succinimidyl ester-based proliferation assays.
Results: The vaccine was well tolerated with no related serious adverse events. Vaccine recipients had significantly stronger gp120-specific CD4(+) T-cell responses which persisted until week 48 and greater gp120-specific CD4(+) T-cell proliferation activity as compared with controls. In the vaccine group, the number of participants who demonstrated positive responses for both gp120-specific CD4(+) T-cell interleukin-2 production and gp120-specific CD8(+) T-cell proliferation were significantly higher at week 6.
Conclusions: The gp120/NefTat/AS02(A) vaccine induced strong gp120-specific CD4(+) T-cell responses and a higher number of vaccinees developed both HIV-1-specific CD4(+) T-cell responses and CD8(+) T-cell proliferation. The induction of these responses may be important in enhancing immune-mediated viral control.
C1 [Lichterfeld, Mathias; Gandhi, Rajesh T.; Simmons, Rachel P.; Flynn, Theresa; Sbrolla, Amy; Yu, Xu G.; Basgoz, Nesli; Mui, Stanley; Williams, Katie; Streeck, Hendrik; Burgett-Yandow, Nicole; Roy, Gilbert; Altfeld, Marcus] Massachusetts Gen Hosp, Ragon Inst, MIT, Boston, MA USA.
[Lichterfeld, Mathias; Gandhi, Rajesh T.; Simmons, Rachel P.; Flynn, Theresa; Sbrolla, Amy; Yu, Xu G.; Basgoz, Nesli; Mui, Stanley; Williams, Katie; Streeck, Hendrik; Burgett-Yandow, Nicole; Roy, Gilbert; Altfeld, Marcus] Massachusetts Gen Hosp, Infect Dis Unit, Boston, MA USA.
[Janssens, Michel; Koutsoukos, Marguerite; Demoitie, Marie-Ange; Bourguignon, Patricia; McNally, Lisa; Voss, Gerald] GlaxoSmithKline Biol, Rixensart, Belgium.
[Pedneault, Louise] Populat Council, New York, NY 10021 USA.
[Vandepapeliere, Pierre] Neovacs SA, Paris, France.
RP Altfeld, M (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ragon Inst,MIT, 149 13th St, Charlestown, MA 02129 USA.
EM maltfeld@partners.org
OI Simmons, Rachel/0000-0003-2498-7965
FU National Institutes of Health [RO1 AI50429]; Doris Duke Charitable
Foundation; GlaxoSmithKline Biologicals
FX Supported by the National Institutes of Health (M.A., RO1 AI50429), the
Doris Duke Charitable Foundation (M.A., M.L., R.S.), and GlaxoSmithKline
Biologicals.
NR 49
TC 10
Z9 10
U1 0
U2 4
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 JAN 1
PY 2012
VL 59
IS 1
BP 1
EP 9
DI 10.1097/QAI.0b013e3182373b77
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 865DW
UT WOS:000298292000005
PM 21963936
ER
PT J
AU Bassett, IV
Chetty, S
Wang, BX
Mazibuko, M
Giddy, J
Lu, ZG
Walensky, RP
Freedberg, KA
Losina, E
AF Bassett, Ingrid V.
Chetty, Senica
Wang, Bingxia
Mazibuko, Matilda
Giddy, Janet
Lu, Zhigang
Walensky, Rochelle P.
Freedberg, Kenneth A.
Losina, Elena
TI Loss to Follow-Up and Mortality Among HIV-Infected People Co-Infected
With TB at ART Initiation in Durban, South Africa
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE HIV; long-term outcomes; mortality; South Africa; tuberculosis
ID ANTIRETROVIRAL THERAPY; SCALE-UP; TUBERCULOSIS; OUTCOMES; PROGRAM; CARE
AB Objective: To quantify the impact of tuberculosis (TB) co-infection on death and loss to follow-up (LTFU) 12 months after entry into an ART program.
Design: Prospective intervention study.
Methods: From May 2007 to 2008, patients undergoing pre-ART training in Durban, South Africa, were screened for pulmonary TB using mycobacterial culture. Subjects missing appointments for >3 months were phoned. Patients who could not be reached were considered LTFU. Deaths were ascertained by report from family members. We used the Kaplan-Meier method to estimate time to LTFU or death for 3 groups at enrollment as follows: (1) newly diagnosed with TB by sputum culture; (2) on TB treatment (ie, previously diagnosed); and (3) TB free. We evaluated the role of TB on mortality and LTFU using Cox proportional hazards models.
Results: Nine hundred fifty-one HIV-infected subjects were enrolled; 59% were female, and median baseline CD4 count was 90 cells per microliter (IQR: 41-148 cells/mL). One hundred forty-four (15%) were newly diagnosed with TB by sputum culture; an additional 199 (21%) were already on TB treatment. By 12 months, 26% newly diagnosed with TB at enrollment died or were LTFU, compared with 19% already on TB treatment, and 14% who were TB free (P = 0.001). Controlling for age, sex, smoking, CD4, and opportunistic infection history, subjects newly diagnosed with pulmonary TB were 76% more likely to die or be LTFU (hazard ratio: 1.76, 95% confidence interval: 1.20 to 2.60) than those without TB.
Conclusions: HIV/TB co-infected individuals are more likely to die or be LTFU within 12 months of ART clinic entry in South Africa. These patients require intensive follow-up during ART initiation.
C1 [Bassett, Ingrid V.; Walensky, Rochelle P.; Freedberg, Kenneth A.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Bassett, Ingrid V.; Wang, Bingxia; Lu, Zhigang; Walensky, Rochelle P.; Freedberg, Kenneth A.; Losina, Elena] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Chetty, Senica; Mazibuko, Matilda; Giddy, Janet] McCord Hosp, Durban, South Africa.
[Wang, Bingxia; Walensky, Rochelle P.; Freedberg, Kenneth A.; Losina, Elena] Harvard Univ, Harvard Ctr AIDS Res CFAR, Boston, MA 02115 USA.
[Walensky, Rochelle P.] Boston Univ, Sch Publ Hlth, Div Infect Dis, Boston, MA USA.
[Freedberg, Kenneth A.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Losina, Elena] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Losina, Elena] Brigham & Womens Hosp, Dept Orthoped, Boston, MA 02115 USA.
RP Bassett, IV (reprint author), 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM ibassett@partners.org
OI Walensky, Rochelle P./0000-0002-8795-379X
FU National Institute of Allergy and Infectious Disease [K23 AI 068458];
PEPFAR supplement [R01 AI058736]; Harvard University Center for AIDS
Research [P30 AI060354]; National Institute of Mental Health [R01
MH090326, R01 MH073445]; National Institute of Arthritis and
Musculoskeletal and Skin Diseases [K24AR057827]; Doris Duke Charitable
Foundation; Operations Research on AIDS Care and Treatment in Africa;
[K24 AI062476]
FX Supported in part by the National Institute of Allergy and Infectious
Disease: K23 AI 068458 (I.V.B.); a PEPFAR supplement to R01 AI058736
(K.A.F.); K24 AI062476 (K.A.F.); the Harvard University Center for AIDS
Research P30 AI060354; the National Institute of Mental Health: R01
MH090326 (I.V.B.); R01 MH073445 (R.P.W.); the National Institute of
Arthritis and Musculoskeletal and Skin Diseases: K24AR057827 (E.L.); the
Doris Duke Charitable Foundation, Clinical Scientist Development Award
(R.P.W.) and Operations Research on AIDS Care and Treatment in Africa
(K.A.F.).
NR 21
TC 22
Z9 22
U1 0
U2 2
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 JAN 1
PY 2012
VL 59
IS 1
BP 25
EP 30
DI 10.1097/QAI.0b013e31823d3aba
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 865DW
UT WOS:000298292000008
PM 22027877
ER
PT J
AU Izadi, N
Goetz, MB
Graber, CJ
AF Izadi, Neema
Goetz, Matthew Bidwell
Graber, Christopher J.
TI Inverse Correlation of Initial CD8 Lymphocyte Count and CD4 Lymphocyte
Response to Combination Antiretroviral Therapy in Treatment-Naive
HIV-Infected Patients
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Letter
ID T-CELL-ACTIVATION; HIV-1-INFECTED PATIENTS; COLLABORATIVE ANALYSIS;
IMMUNE ACTIVATION; PREDICT; COHORT; SUPPRESSION; RECOVERY; MARKER; DEATH
C1 [Izadi, Neema; Goetz, Matthew Bidwell; Graber, Christopher J.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Goetz, Matthew Bidwell; Graber, Christopher J.] VA Greater Los Angeles Healthcare Syst, Dept Med, Infect Dis Sect, Los Angeles, CA USA.
RP Izadi, N (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
OI Goetz, Matthew/0000-0003-4542-992X
NR 19
TC 1
Z9 1
U1 0
U2 0
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 JAN 1
PY 2012
VL 59
IS 1
BP E1
EP E3
DI 10.1097/QAI.0b013e31823d3277
PG 3
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 865DW
UT WOS:000298292000001
PM 22156822
ER
PT J
AU Hattangadi, JA
Taback, N
Neville, BA
Harris, JR
Punglia, RS
AF Hattangadi, Jona A.
Taback, Nathan
Neville, Bridget A.
Harris, Jay R.
Punglia, Rinaa S.
TI Accelerated Partial Breast Irradiation Using Brachytherapy for Breast
Cancer: Patterns in Utilization and Guideline Concordance
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID RADIATION-THERAPY SYSTEM; MAMMOSITE REGISTRY TRIAL; 20-YEAR FOLLOW-UP;
CONSERVING THERAPY; AMERICAN SOCIETY; RANDOMIZED-TRIALS; STAGE-I;
CONSENSUS STATEMENT; REGIONAL-VARIATIONS; ONCOLOGY ASTRO
AB Accelerated partial breast irradiation using brachytherapy (APBIb) is an alternative to whole-breast irradiation (WBI) after breast-conserving surgery. We evaluated patterns of APBIb use with respect to 2009 American Society for Radiation Oncology consensus guidelines (ASTRO-G) in a population-based cohort.
From Surveillance, Epidemiology, and End Results data, we identified 138 815 American women with breast cancer diagnosed between January 1, 2000, and December 31, 2007, who underwent WBI or APBIb after breast-conserving surgery and classified them as suitable, cautionary, or unsuitable for APBIb according to ASTRO-G criteria. Logistic regression was applied to study APBIb use overall and within each guideline category. All P values are from two-sided tests.
Overall, 2.6% of patients received APBIb, and 65.8% of them were classified as cautionary or unsuitable. APBIb was used by 5% of suitable, 3.4% of cautionary, and 1.6% of unsuitable patients by ASTRO-G criteria (P < .001). APBIb use increased from 0.4% in 2000 to 6.6% in 2007 and varied widely (0%-7%) between localities. Variables associated with APBIb use among suitable patients included other vs white race (odds ratio [OR] = 0.51, P < .001), region (OR = 2.60-8.62, P < .001), and more recent year (OR = 20.3, P < .001). Among cautionary patients, variables associated with APBIb use included black vs white race (OR = 0.76, P = .027), other vs white race (OR = 0.57, P < .001), Hispanic ethnicity (OR = 0.75, P = .036), region (OR = 3.10-10.2, P < .001), nonmetropolitan or rural location (OR = 0.53, P = .012), and more recent year (OR = 17.6, P < .001). Among unsuitable patients, black vs white race (OR = 0.77, P = .008), other vs white race (OR = 0.46, P < .001), region (OR = 3.33-21.6, P < .001), and more recent year (OR = 12.7, P < .001) were associated with APBIb use.
APBIb after breast-conserving surgery has been rapidly adopted in the United States. Use varied by race, ethnicity, and widely by region, especially among patients who may not be suitable for this radiation technique.
C1 [Hattangadi, Jona A.] Harvard Radiat Oncol Program, Boston, MA USA.
[Taback, Nathan; Neville, Bridget A.] Dana Farber Canc Inst, Ctr Outcomes & Policy Res, Boston, MA 02115 USA.
[Hattangadi, Jona A.; Harris, Jay R.; Punglia, Rinaa S.] Harvard Univ, Brigham & Womens Hosp, Dept Radiat Oncol, Dana Farber Canc Inst,Sch Med, Boston, MA 02115 USA.
RP Hattangadi, JA (reprint author), Harvard Univ, Brigham & Womens Hosp, Dept Radiat Oncol, Dana Farber Canc Inst,Sch Med, 75 Francis St,L-2 Level, Boston, MA 02115 USA.
EM jhattangadi@partners.org
FU Joint Center for Radiation Therapy Foundation, Boston, MA
FX This study was supported by a grant from the Joint Center for Radiation
Therapy Foundation (JAH), Boston, MA.
NR 57
TC 37
Z9 37
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD JAN
PY 2012
VL 104
IS 1
BP 29
EP 41
DI 10.1093/jnci/djr495
PG 13
WC Oncology
SC Oncology
GA 873OH
UT WOS:000298892200008
PM 22180643
ER
PT J
AU Baldessarini, RJ
Salvatore, P
Khalsa, HMK
Imaz-Etxeberria, H
Gonzalez-Pinto, A
Tohen, M
AF Baldessarini, R. J.
Salvatore, P.
Khalsa, H. -M. K.
Imaz-Etxeberria, H.
Gonzalez-Pinto, A.
Tohen, M.
TI Episode cycles with increasing recurrences in first-episode bipolar-I
disorder patients
SO JOURNAL OF AFFECTIVE DISORDERS
LA English
DT Article
DE Bipolar disorder; Cycle-length; First-episodes; Progression;
Recurrences; Wellness-intervals
ID PROSPECTIVE FOLLOW-UP; MANIC-DEPRESSIVE PSYCHOSIS; MAJOR
AFFECTIVE-DISORDER; MOOD DISORDERS; CASE REGISTER; PROGNOSIS; INSANITY;
RECOVERY; ILLNESS; PERIODICITY
AB Background: Preliminary review of a century of studies of the course of manic-depressive syndromes produced 40 reports, of which approximately one-third report evidence of shortening wellness intervals or cycle-lengths with more recurrences, and two-thirds did not.
Methods: We evaluated inter-episode intervals (cycle-length) in 128 clinically-treated, DSM-IV bipolar-I disorder patients followed prospectively and systematically over 5.7 years, with 6.5 episodes/person.
Results: As expected, cycle-length varied inversely with total cycle-count/person: however, multivariate linear regression found only longer initial hospitalization and fewer total cycles to be associated with cycle-length, whereas cycle-number (1, 2, 3, etc.), sex, intake-age, and first-episode polarity were not. Regression of within-subject cycle-length versus cycle-number yielded individual slope-functions with pseudo-random distribution (28% fell within +/- 1 month/cycle of the null [zero-slope]). Mean duration of early and late euthymic intervals (cycles 2 vs. 5) in patients with matched recurrence-counts was nearly identical.
Conclusions: The course of bipolar-I disorder from onset was largely random or chaotic over nearly 6 years from onset. Only a minority of patients showed either cycle-acceleration or slowing, without changes in wellness intervals. The findings may be influenced by treatment-effects, but seem to indicate that most current bipolar-I disorder patients are unlikely to show progressive shortening of recurrence-cycles. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Baldessarini, R. J.; Salvatore, P.; Khalsa, H. -M. K.] Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp,McLean Div,Int Consortium, Boston, MA 02115 USA.
[Salvatore, P.] Univ Parma, Dept Neurosci, Sect Psychiat, I-43100 Parma, Italy.
[Imaz-Etxeberria, H.; Gonzalez-Pinto, A.] Vittoria Med Ctr, Dept Psychiat, Vittoria, Spain.
[Tohen, M.] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
RP Baldessarini, RJ (reprint author), McLean Hosp, Mailman Res Ctr 312, 115 Mill St, Belmont, MA 02478 USA.
EM rbaldessarini@mclean.harvard.edu
FU Bruce J. Anderson Foundation; McLean Private Donors Bipolar Disorder
Research Fund; NARSAD; Atlas Foundation
FX Supported in part by a grant from the Bruce J. Anderson Foundation and
the McLean Private Donors Bipolar Disorder Research Fund (to RJB), by a
grant from NARSAD (to PS), and by the Atlas Foundation (to MT). These
funding sources had no influence on the design, analysis, or reporting
of this study.
NR 52
TC 20
Z9 20
U1 0
U2 1
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 JAN
PY 2012
VL 136
IS 1-2
BP 149
EP 154
DI 10.1016/j.jad.2011.08.037
PG 6
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 867JW
UT WOS:000298451700019
PM 21943930
ER
PT J
AU Watson, KE
Dovi, WF
Conhaim, RL
AF Watson, Kal E.
Dovi, William F.
Conhaim, Robert L.
TI Evidence for active control of perfusion within lung microvessels
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE pulmonary circulation; microcirculation; vasoconstriction; circulatory
control; vasoreactivity
ID ESTIMATED FUNCTIONAL DIAMETER; ALVEOLAR SEPTAL MICROVESSELS; ISOLATED
RAT LUNGS; PULMONARY-HYPERTENSION; VASCULAR-RESISTANCE; THROMBOXANE;
CONTRACTILE; CIRCULATION; HYPOXIA; MUSCLE
AB Watson KE, Dovi WF, Conhaim RL. Evidence for active control of perfusion within lung microvessels. J Appl Physiol 112: 48-53, 2012. First published October 13, 2011; doi:10.1152/japplphysiol.00820.2011.-Vasoconstrictors cause contraction of pulmonary microvascular endothelial cells in culture. We wondered if this meant that contraction of these cells in situ caused active control of microvascular perfusion. If true, it would mean that pulmonary microvessels were not simply passive tubes and that control of pulmonary microvascular perfusion was not mainly due to the contraction and dilation of arterioles. To test this idea, we vasoconstricted isolated perfused rat lungs with angiotensin II, bradykinin, serotonin, or U46619 (a thromboxane analog) at concentrations that produced equal flows. We also perfused matched-flow controls. We then infused a bolus of 3 mu m diameter particles into each lung and measured the rate of appearance of the particles in the venous effluent. We also measured microscopic trapping patterns of particles retained within each lung. Thirty seconds after particle infusion, venous particle concentrations were significantly lower (P <= 0.05) for lungs perfused with angiotensin II or bradykinin than for those perfused with U46619, but not significantly different from serotonin perfused lungs or matched flow controls. Microscopic clustering of particles retained within the lungs was significantly greater (P <= 0.05) for lungs perfused with angiotensin II, bradykinin, or serotonin, than for lungs perfused with U46619 or for matched flow controls. Our results suggest that these agents did not produce vasoconstriction by a common mechanism and support the idea that pulmonary microvessels possess a level of active control and are not simply passive exchange vessels.
C1 [Dovi, William F.; Conhaim, Robert L.] Univ Wisconsin, Sch Med & Publ Hlth, William S Middleton Mem Vet Hosp, Madison, WI USA.
[Watson, Kal E.; Conhaim, Robert L.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Surg, Madison, WI USA.
RP Conhaim, RL (reprint author), H5-301 BX3236,600 Highland Ave, Madison, WI 53792 USA.
EM conhaim@surgery.wisc.edu
FU Veterans Health Administration, Office of Research and Development,
Department of Veterans Affairs, Biomedical Laboratory Research and
Development Service
FX This work was supported by the Veterans Health Administration, Office of
Research and Development, Department of Veterans Affairs, Biomedical
Laboratory Research and Development Service.
NR 23
TC 3
Z9 3
U1 1
U2 1
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 JAN
PY 2012
VL 112
IS 1
BP 48
EP 53
DI 10.1152/japplphysiol.00820.2011
PG 6
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 866SR
UT WOS:000298403700007
PM 21998262
ER
PT J
AU Wongviriyawong, C
Harris, RS
Zheng, H
Kone, M
Winkler, T
Venegas, JG
AF Wongviriyawong, C.
Harris, R. S.
Zheng, H.
Kone, M.
Winkler, T.
Venegas, J. G.
TI Functional effect of longitudinal heterogeneity in constricted airways
before and after lung expansion
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE airway resistance; asthma; airway hyperresponsiveness
ID ASTHMA; VENTILATION; HYPERRESPONSIVENESS; MODEL; BRONCHOCONSTRICTION;
SEGMENTATION; METHACHOLINE; VARIABILITY; RESISTANCE; MECHANICS
AB Wongviriyawong C, Harris RS, Zheng H, Kone M, Winkler T, Venegas JG. Functional effect of longitudinal heterogeneity in constricted airways before and after lung expansion. J Appl Physiol 112: 237-245, 2012. First published September 22, 2011; doi: 10.1152/japplphysiol.01400.2010.-Heterogeneity in narrowing among individual airways is an important contributor to airway hyperresponsiveness. This paper investigates the contribution of longitudinal heterogeneity (the variability along the airway in cross-sectional area and shape) to airway resistance (R(aw)). We analyzed chest high-resolution computed tomography scans of 8 asthmatic (AS) and 9 nonasthmatic (NA) subjects before and after methacholine (MCh) challenge, and after lung expansion to total lung capacity. In each subject, R(aw) was calculated for 35 defined central airways with >2 mm diameter. Ignoring the area variability and noncircular shape results in an underestimation of R(aw) (%U(total)) that was substantial in some airways (similar to 50%) but generally small (median <6%). The average contribution of the underestimation of Raw caused by longitudinal heterogeneity in the area (%U(area)) to % Utotal was 36%, while the rest was due to the noncircularity of the shape (%U(shape)). After MCh challenge, %U(area) increased in AS and NA (P < 0.05). A lung volume increase to TLC reduced % U(total) and % U(area) in both AS and NA (P < 0.0001, except for %U(total) in AS with P < 0.01). Only in NA, %U(shape) had a significant reduction after increasing lung volume to TLC (P < 0.005). %U(area) was highly correlated, but not identical to the mean-normalized longitudinal heterogeneity in the cross-sectional area [CV(2)(A)] and %U(shape) to the average eccentricity of the elliptical shape. This study demonstrates that R(aw) calculated assuming a cylindrical shape and derived from an average area along its length may, in some airways, substantially underestimate R(aw). The observed changes in underestimations of R(aw) with the increase in lung volume to total lung capacity may be consistent with, and contribute in part to, the differences in effects of deep inhalations in airway function between AS and NA subjects.
C1 [Wongviriyawong, C.; Winkler, T.; Venegas, J. G.] Harvard Univ, Sch Med, Dept Anesthesia Crit Care & Pain Med, Massachusetts Gen Hosp, Boston, MA USA.
[Wongviriyawong, C.] MIT, Dept Mech Engn, Cambridge, MA 02139 USA.
[Harris, R. S.] Harvard Univ, Sch Med, Dept Med, Pulm & Crit Care Unit, Boston, MA USA.
[Zheng, H.; Kone, M.] Harvard Univ, Sch Med, Ctr Biostat, Massachusetts Gen Hosp, Boston, MA USA.
RP Venegas, JG (reprint author), 55 Fruit St,Thier 429, Boston, MA 02114 USA.
EM jvenegas@habanero.mgh.harvard.edu
RI Winkler, Tilo/B-5337-2009
OI Winkler, Tilo/0000-0002-7276-5550
FU National Heart, Lung, and Blood Institute [HL68011]
FX This research was funded by National Heart, Lung, and Blood Institute
Grant HL68011.
NR 31
TC 3
Z9 3
U1 0
U2 2
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 JAN
PY 2012
VL 112
IS 1
BP 237
EP 245
DI 10.1152/japplphysiol.01400.2010
PG 9
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 866SR
UT WOS:000298403700028
PM 21940845
ER
PT J
AU Micheli, BR
Wannomae, KK
Lozynsky, AJ
Christensen, SD
Muratoglu, OK
AF Micheli, Brad R.
Wannomae, Keith K.
Lozynsky, Andrew J.
Christensen, Steven D.
Muratoglu, Orhun K.
TI Knee Simulator Wear of Vitamin E Stabilized Irradiated Ultrahigh
Molecular Weight Polyethylene
SO JOURNAL OF ARTHROPLASTY
LA English
DT Article
DE polyethylene; wear; fatigue; oxidation; vitamin E; knee arthroplasty
ID CROSS-LINKED POLYETHYLENE; MECHANICAL-PROPERTIES; ORTHOPEDIC UHMWPE;
ALPHA-TOCOPHEROL; FREE-RADICALS; OXIDATION; RADIATION; IMPLANTS;
RESISTANCE; LINKING
AB Wear and damage of ultrahigh molecular weight polyethylene (UHMWPE) tibial inserts used in total knee arthroplasty are accelerated by oxidation. Radiation crosslinking reduces wear but produces residual free radicals adversely affecting stability. One alternative to stabilize radiation-crosslinked UHMWPE is to infuse the material with vitamin E (vit E). We investigated the properties of 100-kGy e-beam-irradiated UHMWPE that was subsequently doped with vitamin E in comparison with conventional UHMWPE. Both polymers were sterilized with gamma irradiation in vacuum packaging. Vitamin E-doped UHMWPE showed lower wear before and after aging (2.4 +/- 0.5 and 2.5 +/- 0.8 mg/million cycle, respectively, vs 26.9 +/- 3.5 and 40.8 +/- 3.0 mg/million cycle for conventional UHMWPE). Conventional UHMWPE showed oxidation after accelerated aging, and its mechanical properties were adversely affected, whereas vit E-doped UHMWPE showed no oxidation or changes in its mechanical properties. Vitamin E stabilization of radiation-crosslinked UHMWPE resulted in low wear and high oxidation resistance; it is an alternative load-bearing material for total knee applications.
C1 [Micheli, Brad R.; Wannomae, Keith K.; Lozynsky, Andrew J.; Christensen, Steven D.; Muratoglu, Orhun K.] Massachusetts Gen Hosp, Harris Orthopaed Lab, Boston, MA 02114 USA.
[Muratoglu, Orhun K.] Harvard Univ, Sch Med, Boston, MA USA.
RP Muratoglu, OK (reprint author), Massachusetts Gen Hosp, Harris Orthopaed Lab, 55 Fruit St,GRJ-1206, Boston, MA 02114 USA.
FU Biomet, Inc.
FX This study was funded by a research grant from Biomet, Inc.
NR 22
TC 11
Z9 12
U1 0
U2 11
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 0883-5403
J9 J ARTHROPLASTY
JI J. Arthroplast.
PD JAN
PY 2012
VL 27
IS 1
BP 95
EP 104
DI 10.1016/j.arth.2011.03.006
PG 10
WC Orthopedics
SC Orthopedics
GA 873HP
UT WOS:000298872000016
PM 21550762
ER
PT J
AU Kwon, YM
AF Kwon, Young-Min
TI Untitled Reply
SO JOURNAL OF ARTHROPLASTY
LA English
DT Letter
C1 Harvard Univ, Sch Med, Dept Orthoped Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Kwon, YM (reprint author), Harvard Univ, Sch Med, Dept Orthoped Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 0883-5403
J9 J ARTHROPLASTY
JI J. Arthroplast.
PD JAN
PY 2012
VL 27
IS 1
BP 160
EP 161
DI 10.1016/j.arth.2011.09.003
PG 2
WC Orthopedics
SC Orthopedics
GA 873HP
UT WOS:000298872000028
ER
PT J
AU Hovik, H
Yu, WH
Olsen, I
Chen, T
AF Hovik, Hedda
Yu, Wen-Han
Olsen, Ingar
Chen, Tsute
TI Comprehensive Transcriptome Analysis of the Periodontopathogenic
Bacterium Porphyromonas gingivalis W83
SO JOURNAL OF BACTERIOLOGY
LA English
DT Article
ID GENOMIC TILING MICROARRAYS; SMALL NONCODING RNAS; GENE-EXPRESSION;
ESCHERICHIA-COLI; DIFFERENTIAL EXPRESSION; INSERTION-SEQUENCE; OXIDATIVE
STRESS; EPITHELIAL-CELLS; REGULATORY RNAS; OUTER-MEMBRANE
AB High-density tiling microarray and RNA sequencing technologies were used to analyze the transcriptome of the periodontopathogenic bacterium Porphyromonas gingivalis. The compiled P. gingivalis transcriptome profiles were based on total RNA samples isolated from three different laboratory culturing conditions, and the strand-specific transcription profiles generated covered the entire genome, including both protein coding and noncoding regions. The transcription profiles revealed various operon structures, 5'- and 3'-end untranslated regions (UTRs), differential expression patterns, and many novel, not-yet-annotated transcripts within intergenic and antisense regions. Further transcriptome analysis identified the majority of the genes as being expressed within operons and most 5' and 3' ends to be protruding UTRs, of which several 3' UTRs were extended to overlap genes carried on the opposite/antisense strand. Extensive antisense RNAs were detected opposite most insertion sequence (IS) elements. Pairwise comparative analyses were also performed among transcriptome profiles of the three culture conditions, and differentially expressed genes and metabolic pathways were identified. With the growing realization that noncoding RNAs play important biological functions, the discovery of novel RNAs and the comprehensive transcriptome profiles compiled in this study may provide a foundation to further understand the gene regulation and virulence mechanisms in P. gingivalis. The transcriptome profiles can be viewed at and downloaded from the Microbial Transcriptome Database website, http://bioinformatics.forsyth.org/mtd.
C1 [Yu, Wen-Han; Chen, Tsute] Forsyth Inst, Dept Mol Genet, Cambridge, MA USA.
[Hovik, Hedda; Olsen, Ingar] Univ Oslo, Fac Dent, Dept Oral Biol, Oslo, Norway.
RP Chen, T (reprint author), Forsyth Inst, Dept Mol Genet, Cambridge, MA USA.
EM tchen@forsyth.org
FU National Institute for Dental and Craniofacial Research [R21 DE018803];
Faculty of Dentistry, University of Oslo, Oslo, Norway
FX This project was funded by grant R21 DE018803 from the National
Institute for Dental and Craniofacial Research. H. Hovik was supported
by a Ph.D. stipend and mobility grant from the Faculty of Dentistry,
University of Oslo, Oslo, Norway.
NR 92
TC 16
Z9 16
U1 0
U2 10
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 JAN
PY 2012
VL 194
IS 1
BP 100
EP 114
DI 10.1128/JB.06385-11
PG 15
WC Microbiology
SC Microbiology
GA 866AA
UT WOS:000298350800012
PM 22037400
ER
PT J
AU Trivedi, RB
Piette, J
Fihn, SD
Edelman, D
AF Trivedi, Ranak B.
Piette, John
Fihn, Stephan D.
Edelman, David
TI Examining the Interrelatedness of Patient and Spousal Stress in Heart
Failure Conceptual Model and Pilot Data
SO JOURNAL OF CARDIOVASCULAR NURSING
LA English
DT Article
DE caregivers; heart failure; patient compliance; social support; spouse
ID SELF-CARE; PSYCHOSOCIAL INTERVENTIONS; PROGNOSTIC IMPORTANCE; HOSPITAL
READMISSION; MARITAL QUALITY; CHRONIC ILLNESS; SOCIAL SUPPORT;
RISK-FACTOR; DEPRESSION; FAMILY
AB Background and Research Objective: Recent research has highlighted the positive influence that spouses can have on patient outcomes. It is not clear whether patients and spouses influence each other's well-being reciprocally or whether spousal well-being affects the success of patients' disease management. Our goals were 2-fold: (a) to propose a conceptual framework to examine the reciprocity between patient and spouses' well-being, especially as it relates to disease management, and (b) to begin to assess the validity of this model using pilot data. Subjects and Methods: Twenty-three veterans with heart failure (HF) and their spouses were recruited into a pilot cross-sectional observational study. Participants completed psychosocial surveys to assess depressive symptoms, caregiver burden, relationship satisfaction, and disease management. Descriptive analyses and bivariate correlations between these measures were calculated. Results: Using standard cutoffs, analyses suggested clinically significant depressive symptoms in patients (Center for Epidemiological Studies-Depression score >16; mean, 21.8 [SD, 13]) and a high level of caregiver burden among spouses (Zarit Burden Interview score >15; mean, 22.4 [SD, 15.4]). Both patients and spouses reported high relationship satisfaction levels (Dyadic Adjustment Scale score >100; mean, 112.6 [SD, 26.5] and 115.9 [SD, 14.4], respectively). On average, patients reported poor disease management (Self-care of Heart Failure Index subscale <70 across all subscales: confidence = 53.3 [SD, 28.2]; maintenance = 59.7 [SD, 17.3]; management = 54.0 [SD, 19.4]). Patient depressive symptoms were positively correlated with spouse depressive symptoms (r = 0.53) and caregiver burden (r = 0.64; all P's < .05). Spouses' depressive symptoms were additionally correlated with lower levels of perceived social support among patients (r = -0.47), poor patient relationship satisfaction (r = -0.51), and worse patient confidence in HF management (r = -0.48). Greater caregiver burden was associated with more patient disease complaints (r = 0.49), poorer patients' relationship satisfaction (r = -0.72), and poorer patients' perceived social support (r = -0.73). Conclusions: These results provide preliminary support to the proposed conceptual model. Further research is necessary to determine which spousal factors appear to be most relevant to disease management. Disease management interventions may benefit from engaging spouses in a way that enhances their role without adding to their burden.
C1 [Trivedi, Ranak B.] VA Puget Sound Hlth Care Syst, NW HSR&D Ctr Excellence, Seattle, WA USA.
[Fihn, Stephan D.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
[Piette, John] Ann Arbor HSR&D Ctr Excellence, Ann Arbor, MI USA.
[Fihn, Stephan D.] Vet Affairs Puget Sound, NW HSR&D Ctr Excellence, Seattle, WA USA.
[Edelman, David] Duke Univ, Med Ctr, Durham, NC USA.
RP Trivedi, RB (reprint author), 1100 Olive Way,Suite 1400, Seattle, WA 98101 USA.
EM ranak.trivedi@va.gov
OI Edelman, David/0000-0001-7112-6151
FU VA Puget Sound Health Care System; Durham VA Medical Center
FX This work was supported in part by the resources provided by the VA
Puget Sound Health Care System and the
NR 46
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Z9 9
U1 5
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0889-4655
J9 J CARDIOVASC NURS
JI J. Cardiovasc. Nurs.
PD JAN-FEB
PY 2012
VL 27
IS 1
BP 24
EP 32
DI 10.1097/JCN.0b013e3182129ce7
PG 9
WC Cardiac & Cardiovascular Systems; Nursing
SC Cardiovascular System & Cardiology; Nursing
GA 866JO
UT WOS:000298376900004
PM 21743348
ER
PT J
AU Liu, R
Kalva, SP
AF Liu, Raymond
Kalva, Sanjeeva P.
TI Multidetector CT for GI Bleeding First-line Diagnostic Study?
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Editorial Material
ID ENTEROGRAPHY; ANGIOGRAPHY; HEMORRHAGE
C1 [Liu, Raymond; Kalva, Sanjeeva P.] Massachusetts Gen Hosp, Dept Imaging, Div Vasc Imaging & Intervent, Boston, MA 02114 USA.
RP Kalva, SP (reprint author), Massachusetts Gen Hosp, Dept Imaging, Div Vasc Imaging & Intervent, Boston, MA 02114 USA.
EM skalva@partners.org
NR 11
TC 4
Z9 4
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0192-0790
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD JAN
PY 2012
VL 46
IS 1
BP 6
EP 7
DI 10.1097/MCG.0b013e31823a4b2f
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 863FA
UT WOS:000298147000006
PM 22157219
ER
PT J
AU Davila, JA
Duan, ZG
McGlynn, KA
El-Serag, HB
AF Davila, Jessica A.
Duan, Zhigang
McGlynn, Katherine A.
El-Serag, Hashem B.
TI Utilization and Outcomes of Palliative Therapy for Hepatocellular
Carcinoma A Population-based Study in the United States
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE hepatocellular carcinoma; palliative treatment; chemotherapy
ID RANDOMIZED CONTROLLED TRIAL; CHEMOEMBOLIZATION; DOXORUBICIN
AB Goals: To evaluate the utilization and determinants of receiving palliative treatment for hepatocellular carcinoma (HCC), and its effect on survival.
Background: Palliative treatment for HCC, including transarterial chemoembolization (TACE) and systemic chemotherapy, is available for patients who do not receive potentially curative therapy. The utilization and outcomes of these therapies in clinical practice are unknown.
Study: We conducted a population-based cohort study using the Surveillance, Epidemiology, and End-Results Registry data linked to Medicare claims of HCC patients aged above 65 years diagnosed during 2000 to 2005 who did not receive liver transplant, resection, or ablation. The proportions of patients who received TACE or systemic chemotherapy were calculated by tumor stage, liver disease status, and non-HCC comorbidity. Determinants of receiving palliative therapy were examined in logistic regression models and propensity scores were calculated. Cox proportional hazards models were used to evaluate mortality risk.
Results: We identified 3163 HCC patients (median age, 75 y; 67% men) who did not receive potentially curative treatment. Approximately 12.5% of patients received TACE and 11.0% received chemotherapy. In patients with early or intermediate stage HCC, no liver decompensation, and little or no comorbidity, only 22.8% received TACE and 13.8% received chemotherapy. Median survival was significantly higher among patients who received TACE (14.0 mo) compared with who received chemotherapy (5.0 mo) or no therapy (2.0 mo). A significant reduction in overall mortality was observed for TACE (54%) and chemotherapy (33%).
Conclusions: Utilization of palliative treatment for HCC is low, which could not be explained by clinical features. However, misclassification could have occurred due to the data source. Receipt of TACE or systemic chemotherapy was associated with a reduction in mortality.
C1 [Davila, Jessica A.; Duan, Zhigang] Houston Vet Affairs Med Ctr, Sect Hlth Serv Res, Houston, TX USA.
[El-Serag, Hashem B.] Houston Vet Affairs Med Ctr, Gastroenterol Sect, Houston, TX USA.
Baylor Coll Med, Houston, TX 77030 USA.
RP Davila, JA (reprint author), Michael E DeBakey VA Med Ctr, 2002 Holcombe Blvd,152, Houston, TX 77030 USA.
EM jdavila@bcm.tmc.edu
FU Onyx Pharmaceuticals; Houston VA HSR&D Center of Excellence [HFP90-020]
FX Supported in part by Onyx Pharmaceuticals and the Houston VA HSR&D
Center of Excellence (HFP90-020).
NR 19
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Z9 30
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0192-0790
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD JAN
PY 2012
VL 46
IS 1
BP 71
EP 77
DI 10.1097/MCG.0b013e318224d669
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 863FA
UT WOS:000298147000016
PM 22157221
ER
PT J
AU Cushman, WC
Davis, BR
Pressel, SL
Cutler, JA
Einhorn, PT
Ford, CE
Oparil, S
Probstfield, JL
Whelton, PK
Wright, JT
Alderman, MH
Basile, JN
Black, HR
Grimm, RH
Hamilton, BP
Haywood, LJ
Ong, ST
Piller, LB
Simpson, LM
Stanford, C
Weiss, RJ
AF Cushman, William C.
Davis, Barry R.
Pressel, Sara L.
Cutler, Jeffrey A.
Einhorn, Paula T.
Ford, Charles E.
Oparil, Suzanne
Probstfield, Jeffrey L.
Whelton, Paul K.
Wright, Jackson T., Jr.
Alderman, Michael H.
Basile, Jan N.
Black, Henry R.
Grimm, Richard H., Jr.
Hamilton, Bruce P.
Haywood, L. Julian
Ong, Stephen T.
Piller, Linda B.
Simpson, Lara M.
Stanford, Carol
Weiss, Robert J.
CA ALLHAT Collaborative Res Grp
TI Mortality and Morbidity During and After the Antihypertensive and
Lipid-Lowering Treatment to Prevent Heart Attack Trial
SO JOURNAL OF CLINICAL HYPERTENSION
LA English
DT Article
ID CONVERTING-ENZYME-INHIBITOR; BLOOD-PRESSURE; CARDIOVASCULAR EVENTS;
FOLLOW-UP; ALLHAT; OUTCOMES; THERAPY; RISK; PARTICIPANTS; HYPERTENSION
AB A randomized, double-blind, active-controlled, multicenter trial assigned 32,804 participants aged 55 years and older with hypertension and =1 other coronary heart disease risk factors to receive chlorthalidone (n=15,002), amlodipine (n=8898), or lisinopril (n=8904) for 4 to 8 years, when double-blinded therapy was discontinued. Passive surveillance continued for a total follow-up of 8 to 13 years using national administrative databases to ascertain deaths and hospitalizations. During the post-trial period, fatal outcomes and nonfatal outcomes were available for 98% and 65% of participants, respectively, due to lack of access to administrative databases for the remainder. This paper assesses whether mortality and morbidity differences persisted or new differences developed during the extended follow-up. Primary outcome was cardiovascular mortality and secondary outcomes were mortality, stroke, coronary heart disease, heart failure, cardiovascular disease, and end-stage renal disease. For the post-trial period, data are not available on medications or blood pressure levels. No significant differences (P<.05) appeared in cardiovascular mortality for amlodipine (hazard ratio [HR], 1.00; 95% confidence interval [CI], 0.931.06) or lisinopril (HR, 0.97; CI, 0.901.03), each compared with chlorthalidone. The only significant differences in secondary outcomes were for heart failure, which was higher with amlodipine (HR, 1.12; CI, 1.021.22), and stroke mortality, which was higher with lisinopril (HR, 1.20; CI, 1.011.41), each compared with chlorthalidone. Similar to the previously reported in-trial result, there was a significant treatment-by-race interaction for cardiovascular disease for lisinopril vs chlorthalidone. Black participants had higher risk than non-black participants taking lisinopril compared with chlorthalidone. After accounting for multiple comparisons, none of these results were significant. These findings suggest that neither calcium channel blockers nor angiotensin-converting enzyme inhibitors are superior to diuretics for the long-term prevention of major cardiovascular complications of hypertension. J Clin Hypertens (Greenwich). 2012; 14: 20-31. (C) 2011 Wiley Periodicals, Inc.
C1 [Pressel, Sara L.] Univ Texas Hlth Sci Ctr Houston, Univ Texas Houston, ALLHAT Clin Trials Ctr, Sch Publ Hlth, Houston, TX 77030 USA.
[Cushman, William C.] Memphis Vet Affairs Med Ctr, Memphis, TN USA.
[Cutler, Jeffrey A.; Einhorn, Paula T.] Natl Heart Lung & Blood Inst, Bethesda, MD USA.
[Oparil, Suzanne] Univ Alabama Birmingham, Sch Med, Birmingham, AL USA.
[Probstfield, Jeffrey L.] Univ Washington, Med Ctr, Seattle, WA 98195 USA.
[Whelton, Paul K.] Loyola Univ, Med Ctr, Maywood, IL 60153 USA.
[Wright, Jackson T., Jr.] Case Western Reserve Univ, Med Ctr, Cleveland, OH 44106 USA.
[Alderman, Michael H.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Basile, Jan N.] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
[Black, Henry R.] NYU, Langone Med Ctr, New York, NY USA.
[Grimm, Richard H., Jr.] Berman Ctr Outcomes & Clin Res, Minneapolis, MN USA.
[Hamilton, Bruce P.] Baltimore Vet Adm, Med Ctr, Baltimore, MD USA.
[Haywood, L. Julian] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Ong, Stephen T.] Healthcare Greater Washington, Oxon Hill, MD USA.
[Stanford, Carol] Univ Missouri, Kansas City Sch Med, Kansas City, MO 64110 USA.
[Weiss, Robert J.] Androscoggin Cardiol Associates, Auburn, AL USA.
RP Pressel, SL (reprint author), Univ Texas Hlth Sci Ctr Houston, Univ Texas Houston, ALLHAT Clin Trials Ctr, Sch Publ Hlth, RAS W908,,1200 Herman Pressler Dr, Houston, TX 77030 USA.
EM sara.l.pressel@uth.tmc.edu
FU National Heart, Lung, and Blood Institute (NHLBI) [NO1-HC-35130];
Pfizer; AstraZeneca; Bristol-Myers Squibb; Pfizer Inc.; Merck;
GlaxoSmithKline; Forest; Novartis; Takeda
FX This study was supported by contract NO1-HC-35130 with the National
Heart, Lung, and Blood Institute (NHLBI). ALLHAT investigators received
contributions of study medications supplied by Pfizer (amlodipine
besylate and doxazosin mesylate), AstraZeneca (atenolol and lisinopril),
and Bristol-Myers Squibb (pravastatin), and financial support provided
by Pfizer Inc. The authors report no conflicts of interest with regard
to this paper. Michael H. Alderman has consulted for AstraZeneca, Merck,
and Sankyo; has received honoraria from Bristol-Myers Squibb and Merck;
has had grants/contracts with Sankyo; and has held a financial interest
in Merck. Jan N. Basile has consulted for Abbott Laboratories,
Boehringer Ingelheim, Daiichi Sankyo, Forest Laboratories, Forest
Pharmaceuticals, Merck, Novartis, Reddy Pharmaceuticals, Sankyo, and
SmithKline Beecham/Glaxo Wellcome; and has received honoraria from
Abbott Laboratories, AstraZeneca, Boehringer Ingelheim, Daiichi Sankyo,
Forest Laboratories, Merck, Novartis, and Pfizer; Henry R. Black has
consulted for Abbott Laboratories, AstraZeneca, Aventis, Bayer
Corporation, Biovail, Boehringer Ingelheim, Bristol-Meyers Squibb, CVRx,
Daiichi Sankyo, Forest Pharmaceuticals, Gilead, GlaxoSmithKline,
Horizons Pharmaceuticals, Inter-cure, Merck, Novartis, Pfizer, Sankyo,
Sanofi Aventis, Sanofi-Synthelabo, Servier, and Takeda; has received
honoraria from Biovail, Boehringer Ingelheim, Bristol-Myers Squibb, CV
Therapeutics, Forest Laboratories, Merck, Novartis, Pfizer,
Sanofi-Synthelabo, and Servier; and has had grants/contracts with
Pfizer. William C. Cushman has consulted for Abbott Laboratories,
Bristol-Myers Squibb, Calpis, Daiichi Sankyo, Forest Pharmaceuticals,
Gilead Colorado, Johnson and Johnson, King, Myogen, Novartis, Pfizer,
Pharmacopeia, Reddy Pharmaceuticals, Roche, Sankyo, Sanofi Aventis,
Sanofi-Synthelabo, Sciele, Takeda, and Theravance; has received
honoraria from Abbott Laboratories, AstraZeneca, Boehringer Ingelheim,
Bristol-Myers Squibb, Forest Pharmaceuticals, King, and Novartis and has
had grants/contracts with Abbott Laboratories, Biovail, King, and
Novartis. Barry R. Davis has consulted for BioMarin, Forest
Pharmaceuticals, GlaxoSmithKline, Merck, Proctor and Gamble, and Takeda;
and has held a financial interest in Amgen. Charles E. Ford has
consulted for BioMarin. Richard H. Grimm, Jr has consulted for Calpis,
Merck, Merck/SP, Novartis, Pfizer, and Takeda; has received honoraria
from AstraZeneca, Merck, Novartis, and Takeda; and has had
grants/contracts with Merck, Novartis, and Pfizer. Bruce P. Hamilton has
had grants/contracts with GlaxoSmithKline. L. Julian Haywood has held a
financial interest in Pfizer. Stephen T. Ong has received honoraria from
Novartis; and has had grants/contracts with Abbott Laboratories, Arena,
Daiichi Sankyo, Ferring, Forest Pharmaceutical, Gilead Colorado,
GlaxoSmithKline, Mylan Bertek, Novartis, Pharmacopeia, Roche, Sankyo,
and Sanofi Aventis. Suzanne Oparil has consulted for Boehringer
Ingelheim, Daiichi Sankyo, Eli Lilly, Encysive Pharm, Forest
Pharmaceuticals, GlaxoSmithKline, Merck, NicOx, Novartis, Pfizer, Salt
Institute, Sankyo, Sanofi Aventis, Schering Plough, and SmithKline
Beecham/Glaxo Wellcome; has received honoraria from Boehringer
Ingelheim, Bristol-Myers Squibb, and Encysive Pharm; has had
grants/contracts with Daiichi Sankyo, Eisai Medical Research, Encysive
Pharm, Gilead, Novartis, Pfizer, Sankyo, and Takeda; and has held a
financial interest in Encysive Pharm. Jeffrey L.; Prob-stfield has
consulted for Boehringer Ingelheim, King, and King
Pharmceuticals/Monarch; has received honoraria from Boehringer
Ingelheim; and has had grants/contracts with Boehringer Ingelheim, King,
King Pharmaceuticals/Monarch, KOS, and Sanofi Aventis. Carol Stanford
has held a financial interest in Pfizer. Robert J. Weiss has had
grants/contracts with Forest, Novartis, and Takeda. Jackson T. Wright,
Jr has consulted for Abbott Laboratories, AstraZeneca, Bayer
Corporation, Biovail, CV Therapeutics, CVRx, Daiichi Sankyo, Forest
Pharmaceuticals, GlaxoSmithKline, Merck, NitroMed, Novartis, Pfizer,
Reliant Pharm, Sankyo, Sanofi Aventis, Sanofi-Synthelabo, and SmithKline
Beecham/Glaxo Wellcome; and has had grants/contracts with
GlaxoSmithKline and Novartis. Jeffrey A. Cutler, Paula T. Einhorn, Linda
B. Piller, Sara L. Pressel, Lara M. Simpson, and Paul K. Whelton have no
financial conflicts of interest to report. The NHLBI sponsored the study
and was involved in all aspects other than direct operations of the
study centers. This included collection, analysis, and interpretation of
the data plus the decision to submit the manuscript for publication.
Pfizer Inc, AstraZeneca, and Bristol-Myers Squibb had no role in the
design and conduct of the study, the collection, analysis, and
interpretation of the data or the preparation or approval of the
manuscript. Editorial assistance was provided by Ellen Breckenridge, an
employee of the ALLHAT Collaborative Research Group. The position was
paid for by grant funds provided by the NHLBI for the ALLHAT project.
NR 27
TC 20
Z9 23
U1 2
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1524-6175
EI 1751-7176
J9 J CLIN HYPERTENS
JI J. Clin. Hypertens.
PD JAN
PY 2012
VL 14
IS 1
BP 20
EP 31
DI 10.1111/j.1751-7176.2011.00568.x
PG 12
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 871IV
UT WOS:000298732400006
PM 22235820
ER
PT J
AU Panigrahy, D
Edin, ML
Lee, CR
Huang, S
Bielenberg, DR
Butterfield, CE
Barnes, CM
Mammoto, A
Mammoto, T
Luria, A
Benny, O
Chaponis, DM
Dudley, AC
Greene, ER
Vergilio, JA
Pietramaggiori, G
Scherer-Pietramaggiori, SS
Short, SM
Seth, M
Lih, FB
Tomer, KB
Yang, J
Schwendener, RA
Hammock, BD
Falck, JR
Manthati, VL
Ingber, DE
Kaipainen, A
D'Amore, PA
Kieran, MW
Zeldin, DC
AF Panigrahy, Dipak
Edin, Matthew L.
Lee, Craig R.
Huang, Sui
Bielenberg, Diane R.
Butterfield, Catherine E.
Barnes, Carmen M.
Mammoto, Akiko
Mammoto, Tadanori
Luria, Ayala
Benny, Ofra
Chaponis, Deviney M.
Dudley, Andrew C.
Greene, Emily R.
Vergilio, Jo-Anne
Pietramaggiori, Giorgio
Scherer-Pietramaggiori, Sandra S.
Short, Sarah M.
Seth, Meetu
Lih, Fred B.
Tomer, Kenneth B.
Yang, Jun
Schwendener, Reto A.
Hammock, Bruce D.
Falck, John R.
Manthati, Vijaya L.
Ingber, Donald E.
Kaipainen, Arja
D'Amore, Patricia A.
Kieran, Mark W.
Zeldin, Darryl C.
TI Epoxyeicosanoids stimulate multiorgan metastasis and tumor dormancy
escape in mice
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID SOLUBLE EPOXIDE HYDROLASE; ISCHEMIA-REPERFUSION INJURY; IN-VIVO;
ENDOTHELIAL EXPRESSION; THERAPEUTIC TARGET; CORONARY-ARTERIES;
ANGIOGENIC SWITCH; BLOOD-PRESSURE; CANCER-CELLS; NUDE-MICE
AB Epoxyeicosatrienoic acids (EETs) are small molecules produced by cytochrome P450 epoxygenases. They are lipid mediators that act as autocrine or paracrine factors to regulate inflammation and vascular tone. As a result, drugs that raise EET levels are in clinical trials for the treatment of hypertension and many other diseases. However, despite their pleiotropic effects on cells, little is known about the role of these epoxyeicosanoids in cancer. Here, using genetic and pharmacological manipulation of endogenous EET levels, we demonstrate that EETs are critical for primary tumor growth and metastasis in a variety of mouse models of cancer. Remarkably, we found that EETs stimulated extensive multiorgan metastasis and escape from tumor dormancy in several tumor models. This systemic metastasis was not caused by excessive primary tumor growth but depended on endothelium-derived EETs at the site of metastasis. Administration of synthetic EETs recapitulated these results, while EET antagonists suppressed tumor growth and metastasis, demonstrating in vivo that pharmacological modulation of EETs can affect cancer growth. Furthermore, inhibitors of soluble epoxide hydrolase (sEH), the enzyme that metabolizes EETs, elevated endogenous EET levels and promoted primary tumor growth and metastasis. Thus, our data indicate a central role for EETs in tumorigenesis, offering a mechanistic link between lipid signaling and cancer and emphasizing the critical importance of considering possible effects of EET-modulating drugs on cancer.
C1 [Panigrahy, Dipak; Bielenberg, Diane R.; Butterfield, Catherine E.; Barnes, Carmen M.; Mammoto, Akiko; Mammoto, Tadanori; Benny, Ofra; Chaponis, Deviney M.; Dudley, Andrew C.; Greene, Emily R.; Short, Sarah M.; Seth, Meetu; Ingber, Donald E.; Kieran, Mark W.] Childrens Hosp Boston, Vasc Biol Program, Boston, MA USA.
[Panigrahy, Dipak; Chaponis, Deviney M.; Greene, Emily R.; Kieran, Mark W.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Div Pediat Oncol, Boston, MA 02115 USA.
[Edin, Matthew L.; Lee, Craig R.; Lih, Fred B.; Tomer, Kenneth B.; Zeldin, Darryl C.] NIEHS, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
[Lee, Craig R.] Univ N Carolina, Eshelman Sch Pharm, Div Pharmacotherapy & Expt Therapeut, Chapel Hill, NC USA.
[Huang, Sui] Univ Calgary, Inst Biocomplex & Informat, Calgary, AB, Canada.
[Huang, Sui] Inst Syst Biol, Seattle, WA USA.
[Luria, Ayala; Yang, Jun; Hammock, Bruce D.] UCD, Dept Entomol, Davis, CA USA.
[Luria, Ayala; Yang, Jun; Hammock, Bruce D.] UCD, Ctr Canc, Davis, CA USA.
[Vergilio, Jo-Anne] Harvard Univ, Sch Med, Dept Pathol, Childrens Hosp Boston, Boston, MA 02115 USA.
[Pietramaggiori, Giorgio; Scherer-Pietramaggiori, Sandra S.] Univ Lausanne, Div Plast Surg, Lausanne, Switzerland.
[Schwendener, Reto A.] Univ Zurich, Inst Mol Canc Res, Zurich, Switzerland.
[Falck, John R.; Manthati, Vijaya L.] Univ Texas SW Med Ctr Dallas, Dept Biochem, Dallas, TX 75390 USA.
[Ingber, Donald E.] Harvard Univ, Wyss Inst Biol Inspired Engn, Boston, MA 02115 USA.
[Kaipainen, Arja] Univ Calgary, Dept Biochem & Mol Biol, Calgary, AB, Canada.
[D'Amore, Patricia A.] Harvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02115 USA.
RP Panigrahy, D (reprint author), 300 Longwood Ave, Boston, MA 02115 USA.
EM dipak.panigrahy@childrens.harvard.edu; sui.huang@systemsbiology.org;
mark_kieran@dfci.harvard.edu; zeldin@niehs.nih.gov
RI Yang, Jun/B-2262-2010; Tomer, Kenneth/E-8018-2013;
OI Yang, Jun/0000-0002-4630-3838; Kieran, Mark/0000-0003-2184-7692; Falck,
John/0000-0002-9219-7845; Edin, Matthew/0000-0002-7042-500X; Lee,
Craig/0000-0003-3595-5301
FU National Cancer Institute [R01CA148633-01A1]; Stop and Shop Pediatric
Brain Tumor Fund; C.J. Buckley Pediatric Brain Tumor Fund; Division of
Intramural Research of the NIH, National Institute of Environmental
Health Sciences [Z01 ES025034, Z01 ES050167]; NIH [R01 GM088199,
CA045548]; Robert A. Welch Foundation; NIEHS [NIH P42 ES004699, NIH R01
ES002710, NIH R01 ES013933]
FX We thank and gratefully acknowledge Kristin Johnson for photography and
preparation of the figures; J. Alyce Bradbury, Joan P. Graves, Laura M.
DeGraff, Ricky Sanchez, Lyndsay Leach, and Tony Walshe for excellent
technical assistance; and Sung Hee Hwang for sEH inhibitors and
eicosanoid profiling assays. We thank Isaiah J. Fidler for PC3M-LN4
cells. This work was supported by National Cancer Institute grant
R01CA148633-01A1 (to D. Panigrahy); the Stop and Shop Pediatric Brain
Tumor Fund and the C.J. Buckley Pediatric Brain Tumor Fund (to M.W.
Kieran); Division of Intramural Research of the NIH, National Institute
of Environmental Health Sciences grants Z01 ES025034 and Z01 ES050167
(to D.C. Zeldin and K.B. Tomer); NIH grant R01 GM088199 (to C.R. Lee);
the Robert A. Welch Foundation (to J.R Falck); NIEHS Superfund Basic
Research Program grants NIH P42 ES004699, NIH R01 ES002710, and NIH R01
ES013933 (to B.D. Hammock); and NIH grant CA045548 (to D.E. Ingber).
B.D. Hammock is a George and Judy Marcus Senior Fellow of the American
Asthma Foundation.
NR 62
TC 88
Z9 90
U1 2
U2 21
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD JAN
PY 2012
VL 122
IS 1
BP 178
EP 191
DI 10.1172/JCI58128
PG 14
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 871WW
UT WOS:000298769400023
PM 22182838
ER
PT J
AU Yoshioka, J
Chutkow, WA
Lee, S
Kim, JB
Yan, J
Tian, R
Lindsey, ML
Feener, EP
Seidman, CE
Seidman, JG
Lee, RT
AF Yoshioka, Jun
Chutkow, William A.
Lee, Samuel
Kim, Jae Bum
Yan, Jie
Tian, Rong
Lindsey, Merry L.
Feener, Edward P.
Seidman, Christine E.
Seidman, Jonathan G.
Lee, Richard T.
TI Deletion of thioredoxin-interacting protein in mice impairs
mitochondrial function but protects the myocardium from
ischemia-reperfusion injury
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID CARBOHYDRATE RESPONSE ELEMENT; OXIDATIVE STRESS; PERMEABILITY
TRANSITION; CARDIAC MITOCHONDRIA; PRESSURE-OVERLOAD; NITRIC-OXIDE;
HELA-CELLS; EXPRESSION; GLUCOSE; DYSFUNCTION
AB Classic therapeutics for ischemic heart disease are less effective in individuals with the metabolic syndrome. As the prevalence of the metabolic syndrome is increasing, better understanding of cardiac metabolism is needed to identify potential new targets for therapeutic intervention. Thioredoxin-interacting protein (Txnip) is a regulator of metabolism and an inhibitor of the antioxidant thioredoxins, but little is known about its roles in the myocardium. We examined hearts from Txnip-KO mice by polony multiplex analysis of gene expression and an independent proteomic approach; both methods indicated suppression of genes and proteins participating in mitochondrial metabolism. Consistently, Txnip-KO mitochondria were functionally and structurally altered, showing reduced oxygen consumption and ultrastructural derangements. Given the central role that mitochondria play during hypoxia, we hypothesized that Txnip deletion would enhance ischemia-reperfusion damage. Surprisingly, Txnip-KO hearts had greater recovery of cardiac function after an ischemia-reperfusion insult. Similarly, cardiomyocyte-specific Txnip deletion reduced infarct size after reversible coronary ligation. Coordinated with reduced mitochondrial function, deletion of Txnip enhanced anaerobic glycolysis. Whereas mitochondrial ATP synthesis was minimally decreased by Txnip deletion, cellular ATP content and lactate formation were higher in Txnip-KO hearts after ischemia-reperfusion injury. Pharmacologic inhibition of glycolytic metabolism completely abolished the protection afforded the heart by Txnip deficiency under hypoxic conditions. Thus, although Txnip deletion suppresses mitochondrial function, protection from myocardial ischemia is enhanced as a result of a coordinated shift to enhanced anaerobic metabolism, which provides an energy source outside of mitochondria.
C1 [Yoshioka, Jun; Chutkow, William A.; Lee, Samuel; Kim, Jae Bum; Yan, Jie; Tian, Rong; Seidman, Christine E.; Lee, Richard T.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
[Lindsey, Merry L.] Univ Texas Hlth Sci Ctr UTHSCSA, Dept Med, Div Cardiol, San Antonio, TX USA.
[Feener, Edward P.] Joslin Diabet Ctr, Div Res, Boston, MA 02215 USA.
[Seidman, Christine E.; Seidman, Jonathan G.] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
[Lee, Richard T.] Harvard Stem Cell Inst, Cambridge, MA USA.
RP Lee, RT (reprint author), 65 Landsdowne St,Room 279, Cambridge, MA 02139 USA.
EM rlee@partners.org
RI Lindsey, Merry/B-2650-2012;
OI Tian, Rong/0000-0002-3676-3830
FU American Heart Association [0835484N]; Deutsche Forschungsgemeinschaft
[LE 2728/1-1]; NIH [HL088977, NHLBI268201000036C-0-0-1, HL048743,
HL103582]
FX We thank Hayden Huang (Columbia University) and Kenichi Imahashi
(National Institute of Environmental Health Sciences) for their
technical advice. We also thank Joseph Gannon and Qiuxia Dai for their
technical assistance. This work was supported by American Heart
Association Scientist Development Grant 0835484N (to J. Yoshioka);
Deutsche Forschungsgemeinschaft LE 2728/1-1 (to S. Lee); and NIH grants
HL088977 (to W.A. Chutkow), NHLBI268201000036C-0-0-1 for the UTHSCSA
Cardiovascular Proteomics Center (to M.L. Lindsey), and HL048743 and
HL103582 (to R.T. Lee).
NR 56
TC 55
Z9 56
U1 2
U2 13
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD JAN
PY 2012
VL 122
IS 1
BP 267
EP 279
DI 10.1172/JCI44927
PG 13
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 871WW
UT WOS:000298769400030
PM 22201682
ER
PT J
AU Kearney, DJ
McDermott, K
Malte, C
Martinez, M
Simpson, TL
AF Kearney, David J.
McDermott, Kelly
Malte, Carol
Martinez, Michelle
Simpson, Tracy L.
TI Association of participation in a mindfulness program with measures of
PTSD, depression and quality of life in a veteran sample
SO JOURNAL OF CLINICAL PSYCHOLOGY
LA English
DT Article
DE mindfulness; posttraumatic stress disorder; acceptance; depression;
meditation
ID POSTTRAUMATIC-STRESS-DISORDER; PROSTATE-CANCER OUTPATIENTS; NATIONAL
COMORBIDITY SURVEY; BEHAVIORAL ACTIVATION; REDUCTION PROGRAM; COGNITIVE
THERAPY; SEXUAL TRAUMA; SCALE BADS; SYMPTOMS; MEDITATION
AB Objectives: To assess outcomes of veterans who participated in mindfulness-based stress reduction (MBSR). Design: Posttraumatic stress disorder (PTSD) symptoms, depression, functional status, behavioral activation, experiential avoidance, and mindfulness were assessed at baseline, and 2 and 6 months after enrollment. Results: At 6 months, there were significant improvements in PTSD symptoms (standardized effect size, d = -0.64, p< 0.001); depression (d = -0.70, p<0.001); behavioral activation (d = 0.62, p<0.001); mental component summary score of the Short Form-8 (d = 0.72, p<0.001); acceptance (d = 0.67, p<0.001); and mindfulness (d = 0.78, p<0.001), and 47.7% of veterans had clinically significant improvements in PTSD symptoms. Conclusions: MBSR shows promise as an intervention for PTSD and warrants further study in randomized controlled trials. (c) 2011 Wiley Periodicals, Inc. J Clin Psychol 68:116, 2012.
C1 [Kearney, David J.; McDermott, Kelly; Malte, Carol; Martinez, Michelle; Simpson, Tracy L.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
RP Kearney, DJ (reprint author), Seattle VAMC 111GI,1660 S Columbian Way, Seattle, WA 98108 USA.
EM david.kearney@va.gov
RI Schueter, nicos/A-3625-2014
NR 59
TC 72
Z9 72
U1 8
U2 55
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9762
J9 J CLIN PSYCHOL
JI J. Clin. Psychol.
PD JAN
PY 2012
VL 68
IS 1
BP 101
EP 116
DI 10.1002/jclp.20853
PG 16
WC Psychology, Clinical
SC Psychology
GA 865HE
UT WOS:000298301000009
PM 22125187
ER
PT J
AU Mayotte-Blum, J
Slavin-Mulford, J
Lehmann, M
Pesale, F
Becker-Matero, N
Hilsenroth, M
AF Mayotte-Blum, Jason
Slavin-Mulford, Jenelle
Lehmann, Meaghan
Pesale, Frank
Becker-Matero, Nikaya
Hilsenroth, Mark
TI Therapeutic Immediacy Across Long-Term Psychodynamic Psychotherapy: An
Evidence-Based Case Study
SO JOURNAL OF COUNSELING PSYCHOLOGY
LA English
DT Article
DE therapeutic immediacy; psychodynamic psychotherapy; case study;
self-disclosure; transference
ID CONSENSUAL QUALITATIVE RESEARCH; TRANSFERENCE INTERPRETATIONS;
INTERPERSONAL PROBLEMS; PERSONALITY-DISORDERS; DYNAMIC PSYCHOTHERAPY;
THERAPIST IMMEDIACY; SOCIAL-ADJUSTMENT; SELF-REPORT; ALLIANCE; PATIENT
AB C. E. Hill (2004) recently developed the concept of therapist immediacy to capture discussion by the therapist about the therapeutic relationship that occurs in the here-and-now of a therapy session. This concept has been expanded to include discussion about the therapeutic relationship by both the client and therapist, captured by the term therapeutic immediacy (K. Kuutmann & M. Hilsenroth, 2011). Although prior research has examined the use of therapeutic immediacy across short-term treatment, the present study is the first to examine the use of immediacy across a long-term (4 years) psychotherapy. Also, this is the first study to assess the interrater reliability of therapeutic immediacy, which was found to achieve good to excellent levels across raters. The most frequently used categories of client and therapist immediacy are presented. Finally, the authors provide an in-depth qualitative examination of 5 therapeutic immediacy segments across the treatment judged by the raters to have high levels of depth/intensity (4.5 or higher out of 5) to examine the role of therapeutic immediacy in exploring meaningful treatment issues. Clinical utility, potential limitations, and future research on therapeutic immediacy are discussed.
C1 [Mayotte-Blum, Jason; Lehmann, Meaghan; Pesale, Frank; Becker-Matero, Nikaya; Hilsenroth, Mark] Adelphi Univ, Derner Inst Adv Psychol Studies, Garden City, NY 11530 USA.
[Slavin-Mulford, Jenelle] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Slavin-Mulford, Jenelle] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Mayotte-Blum, J (reprint author), Adelphi Univ, Derner Inst Adv Psychol Studies, Hy Weinberg Bldg,158 Cambridge Ave, Garden City, NY 11530 USA.
EM jasonblum@nyc.rr.com
NR 39
TC 12
Z9 12
U1 1
U2 15
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-0167
J9 J COUNS PSYCHOL
JI J. Couns. Psychol.
PD JAN
PY 2012
VL 59
IS 1
BP 27
EP 40
DI 10.1037/a0026087
PG 14
WC Psychology, Educational; Psychology, Applied
SC Psychology
GA 875SB
UT WOS:000299053900004
PM 22059428
ER
PT J
AU Li, Y
Rimbara, E
Thirumurthi, S
Trespalacios, A
Reddy, R
Sabounchi, S
Attumi, TA
Graham, DY
AF Li, Yuan
Rimbara, Emiko
Thirumurthi, Selvi
Trespalacios, Alba
Reddy, Rita
Sabounchi, Saman
Attumi, Taraq Assed
Graham, David Yates
TI Detection of clarithromycin resistance in Helicobacter pylori following
noncryogenic storage of rapid urease tests for 30 days
SO JOURNAL OF DIGESTIVE DISEASES
LA English
DT Article
DE clarithromycin resistance; Helicobacter pylori; noncryogenic storage;
polymerase chain reaction; rapid urease test; susceptibility test
ID POLYMERASE-CHAIN-REACTION; 23S RIBOSOMAL-RNA; ANTIBIOTIC-RESISTANCE;
BIOPSY SPECIMENS; GASTRIC TISSUE; INFECTION; SUSCEPTIBILITY;
POLYMORPHISM; PREVALENCE; MUTATIONS
AB OBJECTIVE: Traditional Helicobacter pylori (H. pylori) eradication therapy has been undermined by increasing antimicrobial, especially clarithromycin, resistance. Susceptibility testing in some areas is difficult to achieve or unavailable. We aimed to determine whether gastric biopsy specimens stored at room temperature for rapid urease test (RUT) were suitable for clarithromycin susceptibility testing of H. pylori.
METHODS: After 30 days of storage at room temperature, DNA was extracted from gastric biopsies present in RUTs (Hpfast). H. pylori status and clarithromycin susceptibility were evaluated using H. pylori- specific polymerase chain reaction (PCR) for ureA, vacA, and allele- specific primer- PCR of the 23S rRNA genes. The PCR results were compared with histology, RUT, and culture results. H. pylori positive was defined as RUT and either culture or histology positive; H. pylori negative as RUT, culture and histology negative.
RESULTS: Samples from 31 patients were evaluated; 11 were H. pylori positive including 9 by culture; seven of which had allele- specific primer- PCR results from the RUT specimen for the detection of mutations of the 23S rRNA gene. When both tests were available, culture and PCR results were concordant in 7 cases. In 15 of the 20 histology, RUT and culture negative patients, three PCR were negative. In one patient, all of the three tests were positive; and in three only the 23S rRNA was positive and in one only ureA was positive.
CONCLUSION: Gastric biopsy specimens stored in the gel of RUT for 30 days can be used for molecular testing to confirm the diagnosis of H. pylori infection and test for clarithromycin susceptibility.
C1 [Li, Yuan; Rimbara, Emiko; Thirumurthi, Selvi; Trespalacios, Alba; Reddy, Rita; Sabounchi, Saman; Attumi, Taraq Assed; Graham, David Yates] Baylor Coll Med, Ben Taub Gen Hosp, Dept Med, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
RP Graham, DY (reprint author), Baylor Coll Med, Dept Med, Michael E DeBakey Vet Affairs, Affairs Med Ctr, 2002 Holcombe Blvd, Houston, TX 77030 USA.
EM dgraham@bcm.edu
RI Rimbara, Emiko/F-4113-2017
OI Rimbara, Emiko/0000-0001-8847-1840
FU Office of Research and Development Medical Research Service, Department
of Veterans Affairs, Public Health Service [DK56338]; Texas Medical
Center Digestive Diseases Center [DK067366, CA116845]
FX Dr GRAHAM is supported in part by the Office of Research and Development
Medical Research Service, Department of Veterans Affairs, Public Health
Service grant DK56338 which funds the Texas Medical Center Digestive
Diseases Center, DK067366 and CA116845. The contents are solely the
responsibility of the authors and do not necessarily represent the
official views of the Veterans Affairs or National Institutes of Health.
Dr GRAHAM is an unpaid consultant for Novartis in relation to vaccine
development for the treatment or prevention of H. pylori infection. Dr
GRAHAM is also a paid consultant for Otsuka Pharmaceuticals regarding
diagnostic testing and has received royalties on the Baylor College of
Medicine patent covering materials related to the 13C-urea
breath test. The other authors have nothing to declare.
NR 21
TC 8
Z9 9
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1751-2972
J9 J DIGEST DIS
JI J. Dig. Dis.
PD JAN
PY 2012
VL 13
IS 1
BP 54
EP 59
DI 10.1111/j.1751-2980.2011.00549.x
PG 6
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 867UK
UT WOS:000298480100009
PM 22188917
ER
PT J
AU Smith, KW
Proctor, SP
Ozonoff, AL
McClean, MD
AF Smith, Kristen W.
Proctor, Susan P.
Ozonoff, A. L.
McClean, Michael D.
TI Urinary biomarkers of occupational jet fuel exposure among air force
personnel
SO JOURNAL OF EXPOSURE SCIENCE AND ENVIRONMENTAL EPIDEMIOLOGY
LA English
DT Article
DE jet fuel; JP8; urinary biomarkers; 1-naphthol; 2-naphthol; naphthalene
ID DERMAL EXPOSURE; WORKERS; JP-8; NAPHTHALENE; PENETRATION; 1-NAPHTHOL;
COMPONENTS; ABSORPTION; INHALATION; NAPHTHOLS
AB There is a potential for widespread occupational exposure to jet fuel among military and civilian personnel. Urinary metabolites of naphthalene have been suggested for use as short-term biomarkers of exposure to jet fuel (jet propulsion fuel 8 (JP8)). In this study, urinary biomarkers of JP8 were evaluated among US Air Force personnel. Personnel (n = 24) were divided a priori into high, moderate, and low exposure groups. Pre- and post-shift urine samples were collected from each worker over three workdays and analyzed for metabolites of naphthalene (1- and 2-naphthol). Questionnaires and breathingzone naphthalene samples were collected from each worker during the same workdays. Linear mixed-effects models were used to evaluate the exposure data. Post-shift levels of 1- and 2-naphthol varied significantly by a priori exposure group (levels in high group>moderate group>low group), and breathing-zone naphthalene was a significant predictor of post-shift levels of 1-and 2-naphthol, indicating that for every unit increase in breathing-zone naphthalene, there was an increase in naphthol levels. These results indicate that post-shift levels of urinary 1-and 2-naphthol reflect JP8 exposure during the work-shift and may be useful surrogates of JP8 exposure. Among the high exposed workers, significant job-related predictors of post-shift levels of 1-and 2-naphthol included entering the fuel tank, repairing leaks, direct skin contact with JP8, and not wearing gloves during the work-shift. The job-related predictors of 1-and 2-naphthol emphasize the importance of reducing inhalation and dermal exposure through the use of personal protective equipment while working in an environment with JP8. Journal of Exposure Science and Environmental Epidemiology (2012) 22, 35-45; doi: 10.1038/jes.2011.38; published online 2 November 2011
C1 [Smith, Kristen W.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Smith, Kristen W.; Proctor, Susan P.; McClean, Michael D.] Boston Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA USA.
[Smith, Kristen W.; Proctor, Susan P.] USA, Mil Performance Div, Environm Med Res Inst, Natick, MA 01760 USA.
[Proctor, Susan P.] VA Boston Healthcare Syst, Boston, MA USA.
[Ozonoff, A. L.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
RP Smith, KW (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, 665 Huntington Ave,Bldg 1,Room 1402, Boston, MA 02115 USA.
EM ksmith@hsph.harvard.edu
RI McClean, Michael/J-2934-2015;
OI McClean, Michael/0000-0002-3902-8823; Ozonoff, Al/0000-0003-4233-5899
FU US Air Force personnel; US Army Medical Research and Materiel Command
[W81XWH-06-10105]; Henry M. Jackson Foundation of the Advancement of
Military Medicine
FX We sincerely thank the US Air Force personnel for their cooperation and
generous participation in this research project. This work was supported
by the US Army Medical Research and Materiel Command award
(W81XWH-06-10105) to the Henry M. Jackson Foundation of the Advancement
of Military Medicine (PI: SP Proctor). The opinions or assertions
contained herein are the private views of the author(s) and are not to
be construed as official or as reflecting the views of the Army or the
Department of Defense.
NR 28
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Z9 5
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1559-0631
J9 J EXPO SCI ENV EPID
JI J. Expo. Sci. Environ. Epidemiol.
PD JAN-FEB
PY 2012
VL 22
IS 1
BP 35
EP 45
DI 10.1038/jes.2011.38
PG 11
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 864NZ
UT WOS:000298248200004
PM 22044926
ER
PT J
AU Drazner, MH
Brown, RN
Kaiser, PA
Cabuay, B
Lewis, NP
Semigran, MJ
Torre-Amione, G
Naftel, DC
Kirklin, JK
AF Drazner, Mark H.
Brown, Robert N.
Kaiser, Patricia A.
Cabuay, Barry
Lewis, Neil. P.
Semigran, Marc J.
Torre-Amione, Guillermo
Naftel, David C.
Kirklin, James K.
TI Relationship of right- and left-sided filling pressures in patients with
advanced heart failure: A 14-year multi-institutional analysis
SO JOURNAL OF HEART AND LUNG TRANSPLANTATION
LA English
DT Article
DE hemodynamics; physical examination; heart failure; outcomes; survival;
cardiac transplantation
AB BACKGROUND: Jugular venous pressure (JVP) is assessed to estimate volume status in patients with heart failure because right atrial pressure (RAP) reflects pulmonary capillary wedge pressure (PCWP). In a large cohort of heart failure patients spanning 14 years, we sought to further characterize the relationship between RAP and PCWP, including identifying temporal trends, to optimize estimates of PCWP by JVP. We also sought to determine whether the RAP to PCWP relationship impacts post-transplant mortality.
METHODS: Hemodynamic data were obtained from 4,079 patients before cardiac transplantation. Elevated RAP was defined as >= 10 mm Hg and elevated PCWP >= 22 mm Hg. Hemodynamics were "concordant" when both RAP and PCWP were elevated or when both were not elevated. The frequency of concordant hemodynamics was assessed over 3 eras (1993 to 1997, 1998 to 2002, 2003 to 2007). Baseline characteristics were compared among quartiles of the ratio (RAP+1)/PCWP. The association of (RAP+1)/PCWP with 2-year mortality after cardiac transplantation was assessed using multivariate models.
RESULTS: The frequency of concordant hemodynamics over time was stable (74%, 72%, 73%; p = 0.4). Increasing (RAP+ 1)/PCWP was associated with the following variables: female gender; cardiomyopathy etiology besides ischemic or non-ischemic; prior sternotomies; and lower creatinine clearance (p < 0.01 for all). Elevated (RAP+1)/PCWP was associated with post-transplant mortality (relative risk 1.2, 95% confidence interval 1.02 to 1.37, p = 0.02).
CCONCLUSIONS: RAP and PCWP remain concordant in most heart failure patients, supporting the ongoing use of JVP to estimate PCWP. Easily identifiable patient characteristics were associated with an increased RAP/PCWP ratio, and their presence should alert clinicians that PCWP may be overestimated by JVP assessment. A higher RAP/PCWP ratio was an adverse risk factor for post cardiac transplant survival. J Heart Lung Transplant 2012;31:67-72 (C) 2012 International Society for Heart and Lung Transplantation. All rights reserved.
C1 [Drazner, Mark H.; Kaiser, Patricia A.] Univ Texas SW Med Ctr Dallas, Div Cardiol, Dept Internal Med, Dallas, TX 75390 USA.
[Brown, Robert N.; Naftel, David C.; Kirklin, James K.] Univ Alabama, Dept Surg, Birmingham, AL 35294 USA.
[Cabuay, Barry] Univ Iowa, Dept Cardiovasc Med, Iowa City, IA USA.
[Lewis, Neil. P.] Virginia Commonwealth Univ, Dept Cardiol, Richmond, VA USA.
[Lewis, Neil. P.] McGuire VA Med Ctr, Richmond, VA USA.
[Semigran, Marc J.] Massachusetts Gen Hosp, Dept Med, Div Cardiol, Boston, MA 02114 USA.
[Torre-Amione, Guillermo] Methodist Hosp, Methodist DeBakey Heart Ctr, Houston, TX 77030 USA.
RP Drazner, MH (reprint author), Univ Texas SW Med Ctr Dallas, Div Cardiol, Dept Internal Med, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM mark.drazner@utsouthwestern.edu
FU James M. Wooten Chair in Cardiology
FX The authors have no conflicts of interest to disclose. M.H.D. was
supported by the James M. Wooten Chair in Cardiology.
NR 6
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Z9 17
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1053-2498
J9 J HEART LUNG TRANSPL
JI J. Heart Lung Transplant.
PD JAN
PY 2012
VL 31
IS 1
BP 67
EP 72
DI 10.1016/j.healun.2011.09.003
PG 6
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery;
Transplantation
SC Cardiovascular System & Cardiology; Respiratory System; Surgery;
Transplantation
GA 867GF
UT WOS:000298442200009
PM 22071240
ER
PT J
AU Jilg, N
Chung, RT
AF Jilg, Nikolaus
Chung, Raymond T.
TI Adding to the toolbox: Receptor tyrosine kinases as potential targets in
the treatment of hepatitis C
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE HCV; HCV entry; Entry factors; EGFR; Host factors; Receptor tyrosine
kinases
ID FUNCTIONAL GENOMIC SCREEN; VIRUS-REPLICATION; INFECTION
AB Hepatitis C virus (HCV) is a major cause of liver disease, but therapeutic options are limited and there are no prevention strategies. Viral entry is the first step of infection and requires the cooperative interaction of several host cell factors. Using a functional RNAi kinase screen, we identified epidermal growth factor receptor and ephrin receptor A2 as host cofactors for HCV entry. Blocking receptor kinase activity by approved inhibitors broadly impaired infection by all major HCV genotypes and viral escape variants in cell culture and in a human liver chimeric mouse model in vivo. The identified receptor tyrosine kinases (RTKs) mediate HCV entry by regulating co-receptor associations and viral glycoprotein-dependent membrane fusion. These results identify RTKs as previously unknown HCV entry cofactors and show that tyrosine kinase inhibitors have substantial antiviral activity. Inhibition of RTK function may constitute a new approach for prevention and treatment of HCV infection. (C) 2011 European Association for the study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Jilg, Nikolaus; Chung, Raymond T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
RP Chung, RT (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, 55 Fruit St, Boston, MA 02114 USA.
EM rtchung@partners.org
NR 12
TC 2
Z9 2
U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD JAN
PY 2012
VL 56
IS 1
BP 282
EP 284
PG 3
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 867WC
UT WOS:000298484500044
PM 21784050
ER
PT J
AU Burks, DJ
Robbins, R
AF Burks, Derek J.
Robbins, Rockey
TI Psychologists' Authenticity: Implications for Work in Professional and
Therapeutic Settings
SO JOURNAL OF HUMANISTIC PSYCHOLOGY
LA English
DT Article
DE authenticity; genuineness; humanistic psychotherapy; therapeutic
relationship
ID QUALITATIVE RESEARCH; CONCEPTUALIZATION
AB Psychologists engage in a multitude of social roles of varying degrees of emotionality, subjectivity, and objectivity because of the nature of their profession as well as their unique backgrounds that have drawn them to that profession. This study sought to understand how psychologists recognize and experience the concept of authenticity in the context of their professional lives. A purposeful sample of 17 clinical psychologists from metropolitan areas in the Southwest and the Pacific Northwest were interviewed. Using a phenomenological, qualitative research design, 262 significant statements were extracted and grouped together, resulting in 11 emergent themes specifically relating to a therapeutic, health care context. Rigor and thoroughness were achieved via multiple validation procedures. Psychologists defined authenticity as the matching of one's inner thoughts, beliefs, and feelings with one's outer presentation and behaviors. They believed that authenticity involves sensory and emotional qualities rather than purely cognitive or verbal qualities. Concepts of self-disclosure and mindful awareness were discussed as related to authenticity. It is of note that both humanistic and nonhumanistically inclined psychologists equally valued authenticity in the professional and therapeutic setting. Participants also discussed how authenticity and inauthenticity are experienced and modified in the therapeutic relationship, as well as the negative effects of inauthenticity in professional contexts.
C1 [Robbins, Rockey] Univ Oklahoma, Coll Educ, Norman, OK 73019 USA.
RP Burks, DJ (reprint author), Portland VA Med Ctr, P3MIRECC,POB 1034, Portland, OR 97207 USA.
EM derek.burks@va.gov
NR 41
TC 2
Z9 4
U1 1
U2 10
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-1678
J9 J HUMANIST PSYCHOL
JI J. Humanist. Psychol.
PD JAN
PY 2012
VL 52
IS 1
BP 75
EP 104
DI 10.1177/0022167810381472
PG 30
WC Psychology, Multidisciplinary
SC Psychology
GA 868YR
UT WOS:000298563000005
ER
PT J
AU Ling, MT
Tu, WW
Han, Y
Mao, HW
Chong, WP
Guan, J
Liu, M
Lam, KT
Law, HKW
Peiris, JSM
Takahashi, K
Lau, YL
AF Ling, Man To
Tu, Wenwei
Han, Yan
Mao, Huawei
Chong, Wai Po
Guan, Jing
Liu, Ming
Lam, Kwok Tai
Law, Helen K. W.
Peiris, J. S. Malik
Takahashi, K.
Lau, Yu Lung
TI Mannose-Binding Lectin Contributes to Deleterious Inflammatory Response
in Pandemic H1N1 and Avian H9N2 Infection
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID INFLUENZA-A-VIRUS; PATTERN-RECOGNITION MOLECULE; CYTOKINE RESPONSES;
PROTEIN FUNCTIONS; GENE-EXPRESSION; HOST-DEFENSE; MICE; INTERLEUKIN-1;
PATHOGENESIS; MACROPHAGES
AB Background. Mannose-binding lectin (MBL) is a pattern-recognition molecule, which functions as a first line of host defense. Pandemic H1N1 (pdmH1N1) influenza A virus caused massive infection in 2009 and currently circulates worldwide. Avian influenza A H9N2 (H9N2/G1) virus has infected humans and has the potential to be the next pandemic virus. Antiviral function and immunomodulatory role of MBL in pdmH1N1 and H9N2/G1 virus infection have not been investigated.
Methods. In this study, MBL wild-type (WT) and MBL knockout (KO) murine models were used to examine the role of MBL in pdmH1N1 and H9N2/G1 virus infection.
Results. Our study demonstrated that in vitro, MBL binds to pdmH1N1 and H9N2/G1 viruses, likely via the carbohydrate recognition domain of MBL. Wild-type mice developed more severe disease, as evidenced by a greater weight loss than MBL KO mice during influenza virus infection. Furthermore, MBL WT mice had enhanced production of proinflammatory cytokines and chemokines compared with MBL KO mice, suggesting that MBL could upregulate inflammatory responses that may potentially worsen pdmH1N1 and H9N2/G1 virus infections.
Conclusions. Our study provided the first in vivo evidence that MBL may be a risk factor during pdmH1N1 and H9N2/G1 infection by upregulating proinflammatory response.
C1 [Ling, Man To; Tu, Wenwei; Han, Yan; Mao, Huawei; Chong, Wai Po; Guan, Jing; Lam, Kwok Tai; Law, Helen K. W.; Lau, Yu Lung] Univ Hong Kong, Dept Paediat & Adolescent Med, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China.
[Peiris, J. S. Malik] Univ Hong Kong, Dept Microbiol, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China.
[Liu, Ming] Guangzhou Med Coll, Guangzhou Inst Resp Dis, Guangzhou, Guangdong, Peoples R China.
[Takahashi, K.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pediat, Boston, MA USA.
RP Lau, YL (reprint author), Univ Hong Kong, Dept Paediat & Adolescent Med, Queen Mary Hosp, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China.
EM lauylung@hkucc.hku.hk
RI Mao, Huawei/C-9255-2012; Lau, Yu Lung/C-4322-2009
FU National Institutes of Health [U01AI074503]; University Grants Committee
of the Hong Kong Special Administrative Region, China [AoE/M-12/06];
Hong Kong SAR government [Lab-11]; Chung Ko Lee and Cheung Yuen Kan
Education and Research Fund in Paediatric Immunology
FX This work was supported in part by the National Institutes of Health
(U01AI074503); the Area of Excellence program on influenza supported by
the University Grants Committee of the Hong Kong Special Administrative
Region, China (AoE/M-12/06); the Research Fund for the Control of
Infectious Diseases, Hong Kong SAR government (Lab-11); and the Chung Ko
Lee and Cheung Yuen Kan Education and Research Fund in Paediatric
Immunology.
NR 50
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Z9 23
U1 1
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD JAN 1
PY 2012
VL 205
IS 1
BP 44
EP 53
DI 10.1093/infdis/jir691
PG 10
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 866MW
UT WOS:000298386200009
PM 22080095
ER
PT J
AU Grobman, LE
Wu, DY
Dong, DZ
Wu, PC
AF Grobman, L. E.
Wu, D. Y.
Dong, D. Z.
Wu, P. C.
TI THE ROLE OF COXSACKIE-ADENOVIRUS RECEPTOR AS A SENESCENCE BIOMARKER
DURING RECTAL CANCER TREATMENT
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Grobman, L. E.; Wu, D. Y.; Wu, P. C.] Univ Washington, Seattle, WA 98195 USA.
[Wu, D. Y.; Dong, D. Z.; Wu, P. C.] VA Puget Sound, Seattle, WA 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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 148
EP 148
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634401081
ER
PT J
AU MIller, M
Knaub, L
Reusch, JE
AF MIller, M.
Knaub, L.
Reusch, J. E.
TI ATTENUATION OF ACUTE EXERCISE-INDUCED MITOCHONDRIAL BIOGENESIS AND
OXIDANT DEFENSE IN A MODEL OF INSULIN RESISTANT DIABETES
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [MIller, M.; Knaub, L.; Reusch, J. E.] Univ Colorado, Sch Med, Aurora, CO USA.
[Reusch, J. E.] 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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 176
EP 176
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634401178
ER
PT J
AU Hartvigson, PE
Erikson, MA
Banks, WA
AF Hartvigson, P. E.
Erikson, M. A.
Banks, W. A.
TI SYSTEMIC INFLAMMATION INHIBITS LOW-DENSITY LIPOPROTEIN RECEPTOR-RELATED
PROTEIN-1 MEDIATED CLEARANCE OF AMYLOID-beta FROM BLOOD: IMPLICATIONS
FOR ALZHEIMER'S DISEASE
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Hartvigson, P. E.; Erikson, M. A.; Banks, W. A.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Hartvigson, P. E.; Banks, W. A.] Univ Washington, Sch Med, Seattle, WA USA.
[Erikson, M. A.] St Louis Univ, St Louis, MO 63103 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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 240
EP 240
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634401409
ER
PT J
AU Obioha, O
Bassett, J
Saigal, C
Bennett, C
AF Obioha, O.
Bassett, J.
Saigal, C.
Bennett, C.
TI DISSEMINATION OF TOBACCO CONTROL GUIDELINES TO A SPECIALTY CARE SETTING:
A UROLOGIC PERSPECTIVE
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Obioha, O.; Bassett, J.; Saigal, C.; Bennett, C.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Bassett, J.; Saigal, C.; Bennett, C.] W Los Angeles VA Hosp, 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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 244
EP 245
PG 2
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634401424
ER
PT J
AU Bains, S
Egede, LE
AF Bains, S.
Egede, L. E.
TI ASSOCIATIONS BETWEEN HEALTH LITERACY AND PREVENTATIVE CARE BEHAVIOR:
ANALYSIS OF A NATIONAL SAMPLE
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Bains, S.; Egede, L. E.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Egede, L. E.] Ralph H Johnson VAMC, Charleston, SC 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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 353
EP 353
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634402152
ER
PT J
AU Vasquez, K
Wagner, BT
AF Vasquez, K.
Wagner, B. T.
TI NEPHROGENIC SYSTEMIC FIBROSIS: THE CONTRIBUTION OF BONE MARROW-DERIVED
FIBROCYTES TO SKIN LESIONS AND ASSOCIATION WITH L-CATHEPSIN
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Vasquez, K.; Wagner, B. T.] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
[Vasquez, K.; Wagner, B. T.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 425
EP 425
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634402416
ER
PT J
AU Billue, K
Safford, M
Salanitro, A
Houston, T
Curry, W
Kim, Y
Allison, J
Estrada, C
AF Billue, K.
Safford, M.
Salanitro, A.
Houston, T.
Curry, W.
Kim, Y.
Allison, J.
Estrada, C.
TI DIABETES MEDICATION INTENSIFICATION IN RURAL PRIMARY CARE PRACTICES: A
CLUSTER-RANDOMIZED EFFECTIVENESS TRIAL
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Billue, K.; Safford, M.; Salanitro, A.; Curry, W.; Kim, Y.; Estrada, C.] Univ Alabama, Birmingham, AL USA.
[Estrada, C.] Birmingham VAMC, Birmingham, AL USA.
[Houston, T.; Allison, J.] Univ Massachusetts, Sch Med, Worcester, MA USA.
RI Houston, Thomas/F-2469-2013
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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 460
EP 461
PG 2
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634402541
ER
PT J
AU Bains, S
Egede, LE
AF Bains, S.
Egede, L. E.
TI DEMOGRAPHIC, GEOGRAPHIC AND LANGUAGE PREDICTORS OF HEALTH LITERACY:
ANALYSIS OF THE 2003 NATIONAL ASSESSMENT OF ADULT LITERACY SURVEY
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Bains, S.; Egede, L. E.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Egede, L. E.] Ralph H Johnson VAMC, Charleston, SC 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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 463
EP 463
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634402551
ER
PT J
AU Newsom, J
Taylor, B
AF Newsom, J.
Taylor, B.
TI CAN MEDICAL TEAM MEMBERS PREDICT 30-DAY READMISSION RISK ON ADMISSION?
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Newsom, J.; Taylor, B.] Univ Alabama, Birmingham, AL USA.
[Newsom, J.; Taylor, B.] Birmingham VA Med Ctr, Birmingham, AL 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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 463
EP 464
PG 2
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634402552
ER
PT J
AU Newsom, J
Kraemer, R
Estrada, C
Morris, J
Willett, L
AF Newsom, J.
Kraemer, R.
Estrada, C.
Morris, J.
Willett, L.
TI EXTERNAL VALIDATION OF A CLINICAL VIGNETTE SCORING TOOL
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Newsom, J.; Kraemer, R.; Estrada, C.; Morris, J.; Willett, L.] Univ Alabama, Birmingham, AL USA.
[Newsom, J.; Estrada, C.] Birmingham VA Med Ctr, Birmingham, AL 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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 464
EP 464
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634402553
ER
PT J
AU Kertesz, S
Steward, J
Johnson, N
Pollio, D
Holt, C
Austin, E
Gordon, A
Stringfellow, E
Granstaff, U
AF Kertesz, S.
Steward, J.
Johnson, N.
Pollio, D.
Holt, C.
Austin, E.
Gordon, A.
Stringfellow, E.
Granstaff, U.
TI COMPARISON OF CUSTOMIZED VERSUS MAINSTREAM PRIMARY CARE FOR HOMELESS
INDIVIDUALS: THE PRIMARY CARE QUALITY-HOMELESS SURVEY
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Western Regional Meeting
CY JAN 25-28, 2012
CL Carmel, CA
C1 [Kertesz, S.; Johnson, N.; Austin, E.; Granstaff, U.] Birmingham VAMC, Birmingham, AL USA.
[Kertesz, S.; Steward, J.] Univ Alabama, Birmingham, AL USA.
[Pollio, D.] Univ Alabama, Tuscaloosa, AL USA.
[Holt, C.] Univ Maryland, Baltimore, MD 21201 USA.
[Gordon, A.] Pittsburgh VAMC, Pittsburgh, PA USA.
[Stringfellow, E.] Boston HCH, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD JAN
PY 2012
VL 60
IS 1
BP 465
EP 465
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 869XV
UT WOS:000298634402556
ER
PT J
AU Potter, RM
Harikumar, KG
Wu, SV
Miller, LJ
AF Potter, Ross M.
Harikumar, Kaleeckal G.
Wu, S. Vincent
Miller, Laurence J.
TI Differential sensitivity of types 1 and 2 cholecystokinin receptors to
membrane cholesterol
SO JOURNAL OF LIPID RESEARCH
LA English
DT Article
DE receptor binding; biological activity; chimeric receptors; G
protein-coupled receptors; perfringolysin
ID PROTEIN-COUPLED RECEPTOR; PERFRINGOLYSIN-O; BETA(2)-ADRENERGIC RECEPTOR;
CANNABINOID RECEPTORS; INTRACELLULAR LOOP; HUMAN GALLBLADDERS;
PLASMA-MEMBRANE; LIGAND-BINDING; CCK RECEPTOR; II-RECEPTOR
AB Recent studies indicate that membrane cholesterol can associate with G protein-coupled receptors (GPCRs) and affect their function. Previously, we reported that manipulation of membrane cholesterol affects ligand binding and signal transduction of the type 1 cholecystokinin receptor (CCK1R), a Class A GPCR. We now demonstrate that the closely related type 2 cholecystokinin receptor (CCK2R) does not share this cholesterol sensitivity. The sequences of both receptors reveal almost identical cholesterol interaction motifs in analogous locations in transmembrane segments two, three, four, and five. The disparity in cholesterol sensitivity between these receptors, despite their close structural relationship, provides a unique opportunity to define the possible structural basis of cholesterol sensitivity of CCK1R. To evaluate the relative contributions of different regions of CCK1R to cholesterol sensitivity, we performed ligand binding studies and biological activity assays of wildtype and CCK2R/CCK1R chimeric receptor-bearing Chinese hamster ovary cells after manipulation of membrane cholesterol. We also extended these studies to site-directed mutations within the cholesterol interaction motifs. The results contribute to a better understanding of the structural requirements for cholesterol sensitivity in CCK1R and provides insight into the function of other cholesterol-sensitive Class A GPCRs.-Potter, R.M., K.G. Harikumar, S.V. Wu, and L.J. Miller. Differential sensitivity of types 1 and 2 cholecystokinin receptors to membrane cholesterol. J. Lipid Res. 2012. 53: 137-148.
C1 [Potter, Ross M.; Harikumar, Kaleeckal G.; Miller, Laurence J.] Mayo Clin, Dept Mol Pharmacol & Expt Therapeut, Scottsdale, AZ 85259 USA.
[Wu, S. Vincent] Vet Adm Greater Los Angeles Healthcare Syst, Dept Med, Los Angeles, CA 90073 USA.
RP Miller, LJ (reprint author), Mayo Clin, Dept Mol Pharmacol & Expt Therapeut, Scottsdale, AZ 85259 USA.
EM miller@mayo.edu
FU National Institutes of Health [DK-32878]; Mayo Clinic
FX This work was supported by Grant DK-32878 from the National Institutes
of Health and by the Mayo Clinic-Kinney Career Development Award. Its
contents are solely the responsibility of the authors and do not
necessarily represent the official views of the National Institutes of
Health or other granting agencies.
NR 62
TC 17
Z9 17
U1 0
U2 8
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0022-2275
J9 J LIPID RES
JI J. Lipid Res.
PD JAN
PY 2012
VL 53
IS 1
BP 137
EP 148
DI 10.1194/jlr.M020065
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 866TI
UT WOS:000298405900014
PM 22021636
ER
PT J
AU Richman, AR
Coronado, GD
Arnold, LD
Fernandez, ME
Glenn, BA
Allen, JD
Wilson, KM
Brewer, NT
AF Richman, Alice R.
Coronado, Gloria D.
Arnold, Lauren D.
Fernandez, Maria E.
Glenn, Beth A.
Allen, Jennifer D.
Wilson, Katherine M.
Brewer, Noel T.
TI Cognitive Testing of Human Papillomavirus Vaccine Survey Items for
Parents of Adolescent Girls
SO JOURNAL OF LOWER GENITAL TRACT DISEASE
LA English
DT Article
DE cognitive interviewing; survey design; cervical cancer; human
papillomavirus; HPV vaccine
ID EPIDEMIOLOGIC RESEARCH; HEALTH-SERVICES; ACCEPTABILITY; INSTRUMENT
AB Objective. Many studies have been conducted to understand what factors are associated with human papillomavirus (HPV) vaccine acceptability and completion of the 3-dose vaccination series, but few have examined whether people understand the survey items used to assess these relationships. Through a multisite collaborative effort, we developed and cognitively tested survey items that represent constructs known to affect vaccine acceptability and completion.
Materials and Methods. Investigators from 7 research centers in the United States used cognitive interviewing techniques and in-person and telephone interviews to test 21 items. Four rounds of testing, revising, and retesting were conducted among racially and ethnically diverse parents (n = 62) of girls between the ages of 9 and 17 years.
Results. The final survey contained 20 items on attitudes and beliefs relevant to HPV vaccine. Some parents misinterpreted statements about hypothetical vaccine harms as statements of fact. Others were unwilling to answer items about perceived disease likelihood and perceived vaccine effectiveness, because they said the items seemed to have a "right" answer that they did not know. On the basis of these and other findings from cognitive testing, we revised the wording of 14 questions to improve clarity and comprehension. We also revised instructions, response options, and item order.
Conclusions. Cognitive testing of HPV vaccine survey items revealed important differences between intended and ascribed item meaning by participants. Use of the tested survey questions presented here may increase measurement validity and researchers' ability to compare findings across studies and populations. Additional testing using quantitative methods can help to further validate these items.
C1 [Richman, Alice R.] Univ N Carolina, Dept Hlth Behav & Hlth Educ, Gillings Sch Global Publ Hlth, Chapel Hill, NC 27516 USA.
[Coronado, Gloria D.] Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
[Arnold, Lauren D.] Washington Univ, Sch Med, Dept Surg, Siteman Canc Ctr, St Louis, MO 63110 USA.
[Fernandez, Maria E.] Univ Texas Houston, Hlth Sci Ctr, Houston, TX USA.
[Glenn, Beth A.] Univ Calif Los Angeles, Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA 90024 USA.
[Glenn, Beth A.] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA.
[Allen, Jennifer D.] Harvard Univ, Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA USA.
[Wilson, Katherine M.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Brewer, Noel T.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
RP Richman, AR (reprint author), Univ N Carolina, Dept Hlth Behav & Hlth Educ, Gillings Sch Global Publ Hlth, 325 Rosenau Hall,CB 7440, Chapel Hill, NC 27516 USA.
EM richmana@ecu.edu; ntb1@unc.edu
RI Allen, Jennifer/M-2113-2015
FU Centers for Disease Control and Prevention; National Cancer Institute
for the Cancer Prevention and Control Research Network at the University
of California at Los Angeles School of Public Health [1-U48-DP000056];
Harvard School of Public Health/Boston School of Public Health
[1-U48-DP000064]; University of North Carolina at Chapel Hill, Gillings
School of Global Public Health [5-U48-DP000059]; University of Texas
School of Public Health [1-U48-DP000057]; University of Washington
School of Public Health and Community Medicine/Fred Hutchinson Cancer
Research Center [1-U48-DP000050]; Washington University School of
Medicine, Department of Surgery, Siteman Cancer Center [5-U48-DP000060];
American Cancer Society [MSRG-06-259-01-CPPB]
FX Research for this publication was supported by the Centers for Disease
Control and Prevention and the National Cancer Institute cooperative
agreements for the Cancer Prevention and Control Research Network at the
University of California at Los Angeles School of Public Health
(1-U48-DP000056); Harvard School of Public Health/Boston School of
Public Health (1-U48-DP000064); University of North Carolina at Chapel
Hill, Gillings School of Global Public Health (5-U48-DP000059);
University of Texas School of Public Health (1-U48-DP000057); University
of Washington School of Public Health and Community Medicine/Fred
Hutchinson Cancer Research Center (1-U48-DP000050); and Washington
University School of Medicine, Department of Surgery, Siteman Cancer
Center (5-U48-DP000060). In addition, the research at the University of
North Carolina was supported by grants from the American Cancer Society
(MSRG-06-259-01-CPPB). The findings and conclusions in this report are
those of the authors and do not necessarily represent the official
position of the Centers for Disease Control and Prevention.
NR 22
TC 3
Z9 3
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1089-2591
J9 J LOW GENIT TRACT DI
JI J. Low. Genit. Tract. Dis.
PD JAN
PY 2012
VL 16
IS 1
BP 16
EP 23
DI 10.1097/LGT.0b013e3182293a49
PG 8
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 870KP
UT WOS:000298668500005
PM 21964205
ER
PT J
AU Eatesam, M
Noworolski, SM
Tien, PC
Nystrom, M
Dodge, JL
Merriman, RB
Qayyum, A
AF Eatesam, Mamak
Noworolski, Susan M.
Tien, Phyllis C.
Nystrom, Michelle
Dodge, Jennifer L.
Merriman, Raphael B.
Qayyum, Aliya
TI Liver diffusivity in healthy volunteers and patients with chronic liver
disease: Comparison of breathhold and free-breathing techniques
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE diffusion-weighted imaging (DWI); breathhold (BH); free-breathing (FB);
nonalcoholic fatty liver disease (NAFLD); hepatitis C (HCV)
ID WOMENS INTERAGENCY HIV; WEIGHTED MRI; FIBROSIS; COEFFICIENT; EXPERIENCE;
DIAGNOSIS; CIRRHOSIS; REPRODUCIBILITY; PARAMETERS; HEPATITIS
AB Purpose: To compare liver ADC obtained with breathhold and free-breathing diffusion weighted imaging (DWI) in healthy volunteers and patients with liver disease.
Materials and Methods: Twenty-eight subjects, 12 healthy volunteers and 16 patients (9 NAFLD, 7 chronic active HCV), underwent breathhold (BH) and free-breathing (FB) DWI MRI at 1.5 Tesla. Pearson's correlation coefficient was used to determine correlation while paired t-tests assessed differences between BH and FB ADC. Estimated bias was calculated using the Bland-Altman method.
Results: Liver ADC (x10(-3) mm(2)/s) was lower on BH for all groups (mean difference 0.36 +/- 0.20; P < 0.01). ADC was higher in healthy volunteers (BH 1.80 +/- 0.18; FB 2.24 +/- 0.20) compared with NAFLD patients (BH 1.43 +/- 0.27; FB 1.78 +/- 0.28) (P < 0.001) and HCV patients (BH 1.63 +/- 0.191; FB 1.88 +/- 0.12). Overall correlation between BH and FB ADC was (r = 0.75), greatest in NAFLD (r = 0.90) compared with the correlation in HCV (r = 0.24) and healthy subjects (r = 0.34). Bland-Altman plots did not show agreement in mean absolute difference and estimated bias between subjects.
Conclusion: Correlation between BH and FB liver ADC is moderate indicating that BH and FB should not be used interchangeably. Additionally, the lower ADC values in BH versus FB should be accounted for when comparing different liver DWI studies.
C1 [Eatesam, Mamak; Noworolski, Susan M.; Nystrom, Michelle; Qayyum, Aliya] Univ Calif San Francisco, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA.
[Noworolski, Susan M.] Univ Calif San Francisco & Berkeley, Grad Grp Bioengn, Berkeley, CA USA.
[Tien, Phyllis C.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Tien, Phyllis C.] San Francisco VA Med Ctr, Med Serv, San Francisco, CA USA.
[Dodge, Jennifer L.] Univ Calif San Francisco, Dept Internal Med, Fresno Med Educ Program, San Francisco, CA 94143 USA.
[Merriman, Raphael B.] Calif Pacific Med Ctr, Dept Med, San Francisco, CA USA.
RP Qayyum, A (reprint author), Univ Calif San Francisco, Dept Radiol & Biomed Imaging, Box 0628,M-372,505 Parnassus Ave, San Francisco, CA 94143 USA.
EM aliya.qayyum@radiology.ucsf.edu
FU NIH [K23 AI-66943, UO1 AI-34989, MO1-RR-00083, R01 DK061738-SI, R01
DK074718-01]; National Institute of Allergy and Infectious Diseases
[UO1-AI-35004, UO1-AI-31834, UO1-AI-34994, UO1-AI-34989, UO1-AI-34993,
UO1-AI-42590]; National Institute of Child Health and Human Development
[UO1-HD-32632]; National Cancer Institute; National Institute on Drug
Abuse; National Institute on Deafness and Other Communication Disorders;
National Center for Research Resources (UCSF-CTSI) [UL1 RR024131]; UCSF
FX Contract grant sponsor: NIH; Contract grant number: K23 AI-66943, UO1
AI-34989, MO1-RR-00083, R01 DK061738-SI, R01 DK074718-01; Contract grant
sponsor: National Institute of Allergy and Infectious Diseases; Contract
grant number: UO1-AI-35004, UO1-AI-31834, UO1-AI-34994, UO1-AI-34989,
UO1-AI-34993, UO1-AI-42590; Contract grant sponsor: National Institute
of Child Health and Human Development; Contract grant number:
UO1-HD-32632; Contract grant sponsor: National Cancer Institute;
Contract grant sponsor: National Institute on Drug Abuse; Contract grant
sponsor: National Institute on Deafness and Other Communication
Disorders; Contract grant sponsor: National Center for Research
Resources (UCSF-CTSI); Contract grant number: UL1 RR024131; Contract
grant sponsor: UCSF Hellman Family Award.
NR 30
TC 3
Z9 4
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1053-1807
J9 J MAGN RESON IMAGING
JI J. Magn. Reson. Imaging
PD JAN
PY 2012
VL 35
IS 1
BP 103
EP 109
DI 10.1002/jmri.22748
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 862LT
UT WOS:000298093200011
PM 22034200
ER
PT J
AU Biederman, J
Fried, R
Petty, CR
Henin, A
Wozniak, J
Corkum, L
Claudat, K
Faraone, SV
AF Biederman, Joseph
Fried, Ronna
Petty, Carter R.
Henin, Aude
Wozniak, Janet
Corkum, Lyndsey
Claudat, Kim
Faraone, Stephen V.
TI Examining the Association Between Stimulant Treatment and Cognitive
Outcomes Across the Life Cycle of Adults With
Attention-Deficit/Hyperactivity Disorder A Controlled Cross-Sectional
Study
SO JOURNAL OF NERVOUS AND MENTAL DISEASE
LA English
DT Article
DE ADHD; adults; stimulants; adult ADHD and cognition; ADHD over lifespan
ID DEFICIT-HYPERACTIVITY DISORDER; EXECUTIVE FUNCTION; NEUROPSYCHOLOGICAL
FUNCTION; BIPOLAR DISORDER; CHILDREN; PERFORMANCE; ADHD; ADOLESCENTS;
MEDICATION; VIGILANCE
AB Few studies have evaluated the effects of stimulants on cognition in adults with attention-deficit/hyperactivity disorder (ADHD). We evaluated the impact of stimulant treatment on neurocognition in a cross-sectional sample of adults with ADHD. Comparisons were made between adults with ADHD who received (n = 105) and who had never received pharmacotherapy (n = 116) and 146 controls. The subjects were assessed cross-sectionally using a structured diagnostic interview and a neurocognitive battery. We modeled cognitive measures as a function of age and group status using linear regression. Treated ADHD subjects had statistically significantly better scores on measures of IQ than did untreated ones. The treated group also had better (not statistically significant) scores on neuropsychological measures. The direction of the effects of stimulant on neurocognition suggests that either good cognitive functioning may be a determinant of seeking treatment or that stimulant treatment may improve cognition in adults with ADHD. However, this does not indicate a clear causal relationship.
C1 [Biederman, Joseph] Massachusetts Gen Hosp, Pediat Psychopharmacol Program, Clin & Res Programs Pediat Psychiat & Adult ADHD, Boston, MA 02114 USA.
[Biederman, Joseph; Fried, Ronna; Henin, Aude; Wozniak, Janet] Harvard Univ, Sch Med, Dept Psychiat, Cambridge, MA 02138 USA.
[Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY USA.
[Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY USA.
RP Biederman, J (reprint author), Massachusetts Gen Hosp, Pediat Psychopharmacol Program, Clin & Res Programs Pediat Psychiat & Adult ADHD, 55 Fruit St,YAW 6A-6900, Boston, MA 02114 USA.
EM jbiederman@partners.org
OI Faraone, Stephen/0000-0002-9217-3982
FU Neal-Kimmerly MGH; MGH Pediatric Psychopharmacology Philanthropy Fund;
National Institutes of Health [R01MH57934]; Elminda; Janssen; McNeil;
Next Wave Pharmaceuticals; Shire; Fundacion Areces (Spain); Medice
Pharmaceuticals (Germany); Spanish Child Psychiatry Association; Abbott;
Alza; AstraZeneca; Bristol Myers Squibb; Celltech; Cephalon; Eli Lilly
and Co.; Esai; Forest; Glaxo; Gliatech; Merck; NARSAD; NIDA; New River;
NICHD; NIMH; Novartis; Noven; Neurosearch; Organon; Otsuka; Pfizer;
Pharmacia; Prechter Foundation; Stanley Foundation; UCB Pharma, Inc.;
Wyeth; Johnson and Johnson; Independent Medical Education; Lilly; McNeil
Pediatrics; Forest Laboratories Inc.; Sanofi Aventis; Bristol-Myers
Squibb; National Institutes of Health (NIH)
FX This study was supported, in part, by the Neal-Kimmerly MGH Fund for the
Study of Cognition, the MGH Pediatric Psychopharmacology Philanthropy
Fund and by grants to S. Faraone from the National Institutes of Health
(R01MH57934).; Dr. Joseph Biederman is currently receiving research
support from the following sources: Elminda, Janssen, McNeil, Next Wave
Pharmaceuticals, and Shire. In 2011, Dr. Joseph Biederman gave a single
unpaid talk for Juste Pharmaceutical Spain and received honoraria from
the MGH Psychiatry Academy for a tuition-funded CME course. He also
received an honorarium from Cambridge University Press for a chapter
publication. Dr. Biederman received royalties from a copyrighted rating
scale used for ADHD diagnoses. These royalties are paid to the
Department of Psychiatry at MGH. During the past year, Dr. Biederman,
through the MGH Department of Psychiatry, has received royalty payments
from Eli Lilly, Shire, and AstraZeneca. In 2010, Dr. Joseph Biederman
received a speaker's fee from a single talk given at Fundacion Dr.
Manuel Camelo A. C. in Monterrey, Mexico. Dr. Biederman provided single
consultations for Shionogi Pharma Inc. and Cipher Pharmaceuticals Inc.;
the honoraria for these consultations were paid to the Department of
Psychiatry at the MGH. Dr. Biederman received honoraria from the MGH
Psychiatry Academy for a tuition-funded CME course. In 2009, Dr. Joseph
Biederman received a speaker's fee from the following sources: Fundacion
Areces (Spain), Medice Pharmaceuticals (Germany), and the Spanish Child
Psychiatry Association. In previous years, Dr. Joseph Biederman received
research support, consultation fees, or speaker's fees for/from the
following additional sources: Abbott, Alza, AstraZeneca, Bristol Myers
Squibb, Celltech, Cephalon, Eli Lilly and Co., Esai, Forest, Glaxo,
Gliatech, Janssen, McNeil, Merck, NARSAD, NIDA, New River, NICHD, NIMH,
Novartis, Noven, Neurosearch, Organon, Otsuka, Pfizer, Pharmacia, The
Prechter Foundation, Shire, The Stanley Foundation, UCB Pharma, Inc.,
and Wyeth.; Dr. Janet Wozniak, MD, is the author of "Is Your Child
Bipolar,'' published in May 2008 by Bantam Books. She is a speaker for
Primedia/MGH Psychiatry Academy. She received research support from the
following: McNeil, Shire, Janssen, Johnson and Johnson. Her spouse, John
Winkelman, MD, PhD, is a member of the speaker's bureau for the
following: Sanofi-Aventis, Sepracor. He is a consultant/advisory board
member for Covance, GlaxoSmithKline, Impax Laboratories, Luitpold
Pharmaceuticals, Neurogen, Pfizer, UCB, Zeo Inc. He received research
support from GlaxoSmithKline and Sepracor.; In the past 12 months, Dr.
Henin has been a consultant for Concordant Rater Systems and Pfizer. She
receives royalties from Oxford University Press. She has also received
honoraria from the MGH Psychiatry Academy. The education programs
conducted by the MGH Psychiatry Academy were, in part, supported though
Independent Medical Education grants from pharmaceutical companies,
including AstraZeneca, Lilly, McNeil Pediatrics, Shire, Forest
Laboratories Inc., Sanofi Aventis, Janssen, Bristol-Myers Squibb, and
Pfizer.; In the past year, Dr. Faraone received consulting fees and was
on advisory boards for Shire Development and received research support
from Shire and the National Institutes of Health (NIH). In previous
years, he received consulting fees or was on advisory boards or
participated in continuing medical education programs sponsored by
Shire, McNeil, Janssen, Novartis, Pfizer, and Eli Lilly. In previous
years, he received research support from Eli Lilly, Shire, Pfizer and
the NIH. Dr. Faraone receives royalties from a book published by
Guilford Press named Straight Talk About Your Child's Mental Health.
NR 37
TC 1
Z9 1
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3018
J9 J NERV MENT DIS
JI J. Nerv. Ment. Dis.
PD JAN
PY 2012
VL 200
IS 1
BP 69
EP 75
DI 10.1097/NMD.0b013e31823e55ef
PG 7
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 869YP
UT WOS:000298636600009
PM 22210365
ER
PT J
AU Rei, ALDP
Bui, E
Bousquet, B
Simon, NM
Rieu, J
Schmitt, L
Billard, J
Rodgers, R
Birmes, P
AF Rei, Agnes Ladois-Do Pilar
Bui, Eric
Bousquet, Benjamin
Simon, Naomi M.
Rieu, Julie
Schmitt, Laurent
Billard, Julien
Rodgers, Rachel
Birmes, Philippe
TI Peritraumatic Reactions and Posttraumatic Stress Disorder Symptoms After
Psychiatric Admission
SO JOURNAL OF NERVOUS AND MENTAL DISEASE
LA English
DT Article
DE Posttraumatic stress disorder; admission; hospitalization; peritraumatic
distress; peritraumatic dissociation
ID PTSD CHECKLIST; SECLUSION; RESTRAINT; TRAUMA
AB The present study aimed to explore exposure to stressful events during a psychiatric admission and the predictive power of peritraumatic distress and dissociation in the development of posttraumatic stress disorder (PTSD) symptoms after exposure to such events. Psychiatric inpatients (N = 239) were asked to report exposure to stressful events during their admission within 48 hours of being admitted. Individuals reporting at least one stressful event during admission (n = 70, 29%) were assessed for peritraumatic dissociation and distress in relation to this event and, 5 weeks later, were reassessed for PTSD symptoms. Eight participants (12.3%) scored above the cutoff for probable PTSD. Multiple regression analyses revealed that peritraumatic distress was a significant predictor of 5-week PTSD symptoms. Our findings suggest that individuals experiencing increased peritraumatic distress in relation to a stressful event experienced during a psychiatric admission might be at risk of PTSD symptoms and might benefit from increased attention.
C1 [Rei, Agnes Ladois-Do Pilar; Bui, Eric; Schmitt, Laurent; Rodgers, Rachel; Birmes, Philippe] Univ Toulouse, UPS, Lab Stress Traumat LST EA 4560, F-31059 Toulouse 9, France.
[Bui, Eric; Simon, Naomi M.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Bousquet, Benjamin; Rieu, Julie; Billard, Julien] Hop Casselardit Psychiat, Toulouse, France.
[Rodgers, Rachel] Univ Toulouse 2, Ctr Etud & Rech Psychopathol, Toulouse, France.
RP Bui, E (reprint author), Univ Toulouse, UPS, Lab Stress Traumat LST EA 4560, CHU Toulouse,Hop Casselardit, 170 Av Casselardit,TSA 40031, F-31059 Toulouse 9, France.
EM bui.e@chu-toulouse.fr
RI Bui, Eric/J-8347-2015
OI Bui, Eric/0000-0002-1413-6473
NR 15
TC 2
Z9 2
U1 2
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3018
J9 J NERV MENT DIS
JI J. Nerv. Ment. Dis.
PD JAN
PY 2012
VL 200
IS 1
BP 88
EP 90
DI 10.1097/NMD.0b013e31823fafb9
PG 3
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 869YP
UT WOS:000298636600012
ER
PT J
AU Buhlmann, U
Marques, LM
Wilhelm, S
AF Buhlmann, Ulrike
Marques, Luana M.
Wilhelm, Sabine
TI Traumatic Experiences in Individuals With Body Dysmorphic Disorder
SO JOURNAL OF NERVOUS AND MENTAL DISEASE
LA English
DT Article
DE Body dysmorphic disorder; traumatic experience; sexual abuse; physical
abuse; emotional abuse; body image
ID OBSESSIVE-COMPULSIVE SCALE; IMAGE DISTORTION; SEXUAL ABUSE; RELIABILITY
AB Individuals with body dysmorphic disorder (BDD) are excessively concerned about perceived defects in their appearance (e.g., blemishes on their skin). BDD is a severe mental disorder often associated with increased suicidality as well as significant social and occupational interference (e.g., J Clin Psychiatry 2005; 66: 717Y725). Recently, investigators have begun to explore variables that might function as risk factors in the development of BDD, such as traumatic experiences (e. g., Child Abuse Negl 2006; 30: 1105-1115). As such, one of the goals of the current study was to examine the role of early-life sexual, physical, or emotional abuse in BDD. Specifically, the Traumatic Stress Institute Life Event Questionnaire (Treat Abuse Today 1992; 2: 9-11) was used to examine whether individuals with BDD (n = 18) self-reported having experienced more traumatic events than mentally healthy controls (n = 19). The BDD group reported more retrospective experiences of sexual and physical abuse in childhood or adolescence than did healthy controls. Surprisingly, there was no significant group difference in reports of emotional abuse in early life. This study provides preliminary evidence of the importance of examining abuse as a potential risk factor in the development of BDD.
C1 [Wilhelm, Sabine] Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp,Body Dysmorph Disorder Cli, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Wilhelm, S (reprint author), Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp,Body Dysmorph Disorder Cli, 185 Cambridge St, Boston, MA 02114 USA.
EM wilhelm@psych.mgh.harvard.edu
FU German Research Society (DFG) [BU 1814/7-1, BU 1814/7-2]; NIMH;
Obsessive-Compulsive Foundation; Tourette Syndrome Association
FX Dr. Buhlmann has received research support from the German Research
Society (DFG; Grant #s BU 1814/7-1 and BU 1814/7-2).; Dr. Wilhelm has
received research support from NIMH, the Obsessive-Compulsive
Foundation, and the Tourette Syndrome Association. Forest Laboratories
provided her with medication and placebo for an NIMH-funded study. She
is a presenter for the Massachusetts General Hospital Psychiatry Academy
in educational programs supported through independent medical education
grants from pharmaceutical companies; and has received royalties from
Elsevier Publications, Guilford Publications, and New Harbinger
Publications from Oxford University Press. She has also received
speaking honorarium from various academic institutions.
NR 25
TC 4
Z9 4
U1 0
U2 20
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3018
J9 J NERV MENT DIS
JI J. Nerv. Ment. Dis.
PD JAN
PY 2012
VL 200
IS 1
BP 95
EP 98
DI 10.1097/NMD.0b013e31823f6775
PG 4
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 869YP
UT WOS:000298636600014
PM 22210370
ER
PT J
AU Meyers, PM
Blackham, KA
Abruzzo, TA
Gandhi, CD
Higashida, RT
Hirsch, JA
Moran, CJ
Narayanan, S
Prestigiacomo, CJ
Tarr, R
AF Meyers, P. M.
Blackham, K. A.
Abruzzo, T. A.
Gandhi, C. D.
Higashida, R. T.
Hirsch, J. A.
Moran, C. J.
Narayanan, S.
Prestigiacomo, C. J.
Tarr, R.
CA Soc NeuroInterventional Surg
TI Society of NeuroInterventional Surgery Standards of Practice: general
considerations
SO JOURNAL OF NEUROINTERVENTIONAL SURGERY
LA English
DT Article
ID CLINICAL-PRACTICE GUIDELINES; REPORTING STANDARDS; AMERICAN-COLLEGE;
ANGIOPLASTY; STROKE
AB This is the first in a set of documents intended to standardize techniques, procedures, and practices in the field of endovascular surgical neuroradiology. Standards are meant to define core practices for peer review, comparison, and improvement. Standards and guidelines also form the basic dialogue, reporting, and recommendations for ongoing practices and future development.
C1 [Meyers, P. M.] Columbia Univ, Dept Radiol & Neurol Surg, Coll Phys & Surg, New York, NY 10032 USA.
[Blackham, K. A.] Univ Hosp, Case Med Ctr, Cleveland, OH USA.
[Abruzzo, T. A.; Tarr, R.] Univ Cincinnati, Med Ctr, Cincinnati, OH 45267 USA.
[Gandhi, C. D.] UMDNJ New Jersey Med Sch, Newark, NJ USA.
[Higashida, R. T.] Univ Calif San Francisco, Med Ctr, San Francisco, CA USA.
[Hirsch, J. A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Moran, C. J.] Edward Mallinckrodt Inst Radiol, St Louis, MO 63110 USA.
[Narayanan, S.] Wayne State Univ, Dept Neurosurg & Neurol, Detroit Med Ctr, Detroit, MI USA.
[Prestigiacomo, C. J.] Univ Med & Dent New Jersey, Newark, NJ 07103 USA.
RP Meyers, PM (reprint author), Columbia Univ, Dept Radiol & Neurol Surg, Coll Phys & Surg, 710 W 168th St,Rm 428, New York, NY 10032 USA.
EM pmm2002@columbia.edu
NR 12
TC 8
Z9 8
U1 0
U2 1
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1759-8478
J9 J NEUROINTERV SURG
JI J. NeuroInterventional Surg.
PD JAN
PY 2012
VL 4
IS 1
BP 11
EP 15
DI 10.1136/neurintsurg-2011-010180
PG 5
WC Neuroimaging; Surgery
SC Neurosciences & Neurology; Surgery
GA 866XF
UT WOS:000298418800005
PM 22166819
ER
PT J
AU Oh, DC
Hirsch, JA
Yoo, AJ
AF Oh, Daniel C.
Hirsch, Joshua A.
Yoo, Albert J.
TI Novel use of Onyx for treatment of intracranial vertebral artery
dissection
SO JOURNAL OF NEUROINTERVENTIONAL SURGERY
LA English
DT Article
ID ENDOVASCULAR MANAGEMENT; SUBARACHNOID HEMORRHAGE; ANEURYSMS
AB This report describes a patient who presented with subarachnoid hemorrhage and extensive right posterior inferior cerebellar artery territory infarct secondary to a dissecting aneurysm of the right intracranial vertebral artery. Urgent endovascular treatment was undertaken with plans for trapping of the diseased segment with coils. However, significant intralesional stenosis limited distal microcatheter access. Therefore, using proximal flow arrest and adjunctive coiling, the liquid embolic agent Onyx was injected within the pseudoaneurysm and was able to traverse the stenosis, resulting in proximal and distal parent vessel closure. There were no embolic complications. During the 3 month hospital stay, there was no rebleeding. The patient was discharged to skilled nursing facility and was lost to follow-up.
C1 [Oh, Daniel C.; Hirsch, Joshua A.; Yoo, Albert J.] Massachusetts Gen Hosp, Dept Intervent Neuroradiol Endovasc Neurosurg, Boston, MA 02114 USA.
RP Yoo, AJ (reprint author), Massachusetts Gen Hosp, Dept Intervent Neuroradiol Endovasc Neurosurg, Gray 241,55 Fruit St, Boston, MA 02114 USA.
EM ajyoo@partners.org
NR 7
TC 3
Z9 4
U1 0
U2 0
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1759-8478
J9 J NEUROINTERV SURG
JI J. NeuroInterventional Surg.
PD JAN
PY 2012
VL 4
IS 1
BP 31
EP 33
DI 10.1136/jnis.2011.004952
PG 3
WC Neuroimaging; Surgery
SC Neurosciences & Neurology; Surgery
GA 866XF
UT WOS:000298418800010
PM 21990480
ER
PT J
AU Bruguera, C
Tremble, T
Hirsch, JA
AF Bruguera, Carolyn
Tremble, Thomas
Hirsch, Joshua A.
TI Coming soon to a state near you?
SO JOURNAL OF NEUROINTERVENTIONAL SURGERY
LA English
DT Editorial Material
C1 [Bruguera, Carolyn] Micrus Corp, San Jose, CA USA.
[Tremble, Thomas] Adv Med Technol Assoc AdvaMed, State Govt Relat & Reg Affairs, Washington, DC USA.
[Hirsch, Joshua A.] Massachusetts Gen Hosp, Neuroendovasc Program, Boston, MA 02114 USA.
RP Bruguera, C (reprint author), 2810 Belmont Canyon Rd, Belmont, CA 94002 USA.
EM carolyn.bruguera@gmail.com
NR 12
TC 1
Z9 1
U1 2
U2 2
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1759-8478
J9 J NEUROINTERV SURG
JI J. NeuroInterventional Surg.
PD JAN
PY 2012
VL 4
IS 1
BP 75
EP 78
DI 10.1136/neurintsurg-2011-010120
PG 4
WC Neuroimaging; Surgery
SC Neurosciences & Neurology; Surgery
GA 866XF
UT WOS:000298418800019
PM 22006867
ER
PT J
AU Walcott, BP
Nahed, BV
Kahle, KT
Duhaime, AC
Sharma, N
Eskandar, EN
AF Walcott, Brian P.
Nahed, Brian V.
Kahle, Kristopher T.
Duhaime, Ann-Christine
Sharma, Nutan
Eskandar, Emad N.
TI Deep brain stimulation for medically refractory life-threatening status
dystonicus in children Report of 3 cases
SO JOURNAL OF NEUROSURGERY-PEDIATRICS
LA English
DT Article
DE deep brain stimulation; globus pallidus; movement disorder;
rhabdomyolysis; status dystonicus; functional neurosurgery
ID HALLERVORDEN-SPATZ-DISEASE; GENERALIZED DYSTONIA; PALLIDOTOMY;
MANAGEMENT; EXPERIENCE
AB Generalized dystonic syndromes may escalate into persistent episodes of generalized dystonia known as status dystonicus that can be life-threatening due to dystonia-induced rhabdomyolysis and/or respiratory compromise. Treatment of these conditions usually entails parenteral infusion of antispasmodic agents and sedatives and occasionally necessitates a medically induced coma for symptom control. The authors report a series of 3 children who presented with medically intractable, life-threatening status dystonicus and were successfully treated with bilateral pallidal deep brain stimulation. Bilateral globus pallidus internus stimulation appears to be effective in the urgent treatment of medically refractory and life-threatening movement disorders. (http://thejns.org/doi/abs/10.3171/2011.10.PEDS11360)
C1 [Walcott, Brian P.; Nahed, Brian V.; Kahle, Kristopher T.; Duhaime, Ann-Christine; Eskandar, Emad N.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Sharma, Nutan] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Sharma, Nutan] Harvard Univ, Sch Med, Boston, MA USA.
RP Walcott, BP (reprint author), Massachusetts Gen Hosp, Dept Neurosurg, 55 Fruit St,White Bldg Room 502, Boston, MA 02114 USA.
EM walcott.brian@mgh.harvard.edu
FU NINDS NIH HHS [P50 NS037409]
NR 24
TC 12
Z9 12
U1 0
U2 1
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 1933-0707
J9 J NEUROSURG-PEDIATR
JI J. Neurosurg.-Pediatr.
PD JAN
PY 2012
VL 9
IS 1
BP 99
EP 102
DI 10.3171/2011.10.PEDS11360
PG 4
WC Clinical Neurology; Pediatrics; Surgery
SC Neurosciences & Neurology; Pediatrics; Surgery
GA 869WW
UT WOS:000298630700018
PM 22208329
ER
PT J
AU Erickson, JI
AF Erickson, Jeanette Ives
TI 200 Years of Nursing-A Chief Nurse's Reflections on Practice, Theory,
Policy, Education, and Research
SO JOURNAL OF NURSING ADMINISTRATION
LA English
DT Editorial Material
ID CLINICAL EXCELLENCE
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Erickson, JI (reprint author), Massachusetts Gen Hosp, Bulfinch 230B,55 Fruit St, Boston, MA 02114 USA.
EM jiveserickson@partners.org
NR 17
TC 1
Z9 1
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0002-0443
J9 J NURS ADMIN
JI J. Nurs. Adm.
PD JAN
PY 2012
VL 42
IS 1
BP 9
EP 11
DI 10.1097/NNA.0b013e31823c1710
PG 3
WC Nursing
SC Nursing
GA 863HL
UT WOS:000298153300004
PM 22157375
ER
PT J
AU Adams, JM
AF Adams, Jeffrey M.
TI Exploring Influential Nurse Executive Leadership An Interview With Marla
Weston
SO JOURNAL OF NURSING ADMINISTRATION
LA English
DT Editorial Material
C1 [Adams, Jeffrey M.] Massachusetts Gen Hosp, Yvonne L Munn Ctr Nursing Res, Boston, MA 02114 USA.
[Adams, Jeffrey M.] Massachusetts Gen Hosp, Ctr Innovat Care Delivery, Boston, MA 02114 USA.
RP Adams, JM (reprint author), Massachusetts Gen Hosp, Yvonne L Munn Ctr Nursing Res, 275 Cambridge St,POB 4, Boston, MA 02114 USA.
EM jadams9@partners.org
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 0002-0443
J9 J NURS ADMIN
JI J. Nurs. Adm.
PD JAN
PY 2012
VL 42
IS 1
BP 12
EP 14
DI 10.1097/NNA.0b013e31823c17e0
PG 3
WC Nursing
SC Nursing
GA 863HL
UT WOS:000298153300005
PM 22157376
ER
PT J
AU Yip, S
Butterfield, YS
Morozova, O
Chittaranjan, S
Blough, MD
An, JH
Birol, I
Chesnelong, C
Chiu, R
Chuah, E
Corbett, R
Docking, R
Firme, M
Hirst, M
Jackman, S
Karsan, A
Li, HY
Louis, DN
Maslova, A
Moore, R
Moradian, A
Mungall, KL
Perizzolo, M
Qian, J
Roldan, G
Smith, EE
Tamura-Wells, J
Thiessen, N
Varhol, R
Weiss, S
Wu, W
Young, S
Zhao, YJ
Mungall, AJ
Jones, SJM
Morin, GB
Chan, JA
Cairncross, JG
Marra, MA
AF Yip, Stephen
Butterfield, Yaron S.
Morozova, Olena
Chittaranjan, Suganthi
Blough, Michael D.
An, Jianghong
Birol, Inanc
Chesnelong, Charles
Chiu, Readman
Chuah, Eric
Corbett, Richard
Docking, Rod
Firme, Marlo
Hirst, Martin
Jackman, Shaun
Karsan, Aly
Li, Haiyan
Louis, David N.
Maslova, Alexandra
Moore, Richard
Moradian, Annie
Mungall, Karen L.
Perizzolo, Marco
Qian, Jenny
Roldan, Gloria
Smith, Eric E.
Tamura-Wells, Jessica
Thiessen, Nina
Varhol, Richard
Weiss, Samuel
Wu, Wei
Young, Sean
Zhao, Yongjun
Mungall, Andrew J.
Jones, Steven J. M.
Morin, Gregg B.
Chan, Jennifer A.
Cairncross, J. Gregory
Marra, Marco A.
TI Concurrent CIC mutations, IDH mutations, and 1p/19q loss distinguish
oligodendrogliomas from other cancers
SO JOURNAL OF PATHOLOGY
LA English
DT Article
DE glioma; oligodendroglioma; next-generation sequencing; Capicua; IDH1
ID ANAPLASTIC OLIGODENDROGLIOMAS; SIGNALING PATHWAY; MSH6 MUTATIONS;
BRAIN-TUMORS; CELL; GLIOMAS; CAPICUA; SURVIVAL; ALIGNMENT; ATAXIN-1
AB Oligodendroglioma is characterized by unique clinical, pathological, and genetic features. Recurrent losses of chromosomes 1p and 19q are strongly associated with this brain cancer but knowledge of the identity and function of the genes affected by these alterations is limited. We performed exome sequencing on a discovery set of 16 oligodendrogliomas with 1p/19q co-deletion to identify new molecular features at base-pair resolution. As anticipated, there was a high rate of IDH mutations: all cases had mutations in either IDH1 (14/16) or IDH2 (2/16). In addition, we discovered somatic mutations and insertions/deletions in the CIC gene on chromosome 19q13.2 in 13/16 tumours. These discovery set mutations were validated by deep sequencing of 13 additional tumours, which revealed seven others with CIC mutations, thus bringing the overall mutation rate in oligodendrogliomas in this study to 20/29 (69%). In contrast, deep sequencing of astrocytomas and oligoastrocytomas without 1p/19q loss revealed that CIC alterations were otherwise rare (1/60; 2%). Of the 21 non-synonymous somatic mutations in 20 CIC-mutant oligodendrogliomas, nine were in exon 5 within an annotated DNA-interacting domain and three were in exon 20 within an annotated protein-interacting domain. The remaining nine were found in other exons and frequently included truncations. CIC mutations were highly associated with oligodendroglioma histology, 1p/19q co-deletion, and IDH1/2 mutation (p < 0.001). Although we observed no differences in the clinical outcomes of CIC mutant versus wild-type tumours, in a background of 1p/19q co-deletion, hemizygous CIC mutations are likely important. We hypothesize that the mutant CIC on the single retained 19q allele is linked to the pathogenesis of oligodendrogliomas with IDH mutation. Our detailed study of genetic aberrations in oligodendroglioma suggests a functional interaction between CIC mutation, IDH1/2 mutation, and 1p/19q co-deletion. Copyright (C) 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
C1 [Yip, Stephen; Karsan, Aly; Young, Sean] BC Canc Agcy, Dept Pathol & Lab Med, Vancouver, BC, Canada.
[Butterfield, Yaron S.; Morozova, Olena; Chittaranjan, Suganthi; An, Jianghong; Birol, Inanc; Chiu, Readman; Chuah, Eric; Corbett, Richard; Docking, Rod; Firme, Marlo; Hirst, Martin; Jackman, Shaun; Karsan, Aly; Li, Haiyan; Maslova, Alexandra; Moore, Richard; Moradian, Annie; Mungall, Karen L.; Qian, Jenny; Tamura-Wells, Jessica; Thiessen, Nina; Varhol, Richard; Zhao, Yongjun; Mungall, Andrew J.; Jones, Steven J. M.; Morin, Gregg B.; Marra, Marco A.] BC Canc Agcy, Michael Smith Genome Sci Ctr, Vancouver, BC, Canada.
[Blough, Michael D.; Chesnelong, Charles; Chan, Jennifer A.] Univ Calgary, So Alberta Canc Res Inst, Calgary, AB, Canada.
[Louis, David N.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Louis, David N.] Harvard Univ, Sch Med, Boston, MA USA.
[Perizzolo, Marco; Chan, Jennifer A.] Univ Calgary, Dept Pathol & Lab Med, Calgary, AB, Canada.
[Roldan, Gloria] Univ Calgary, Dept Med, Calgary, AB, Canada.
[Smith, Eric E.] Univ Calgary, Dept Clin Neurosci, Hotchkiss Brain Inst, Calgary, AB, Canada.
[Weiss, Samuel] Univ Calgary, Dept Cell Biol & Anat, Hotchkiss Brain Inst, Calgary, AB, Canada.
[Wu, Wei] Univ Calgary, Dept Biol Sci, Inst Biocomplex & Bioinformat, Calgary, AB T2N 1N4, Canada.
[Marra, Marco A.] Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada.
RP Cairncross, JG (reprint author), Foothills Prov Gen Hosp, Dept Clin Neurosci, 1403-29th St NW, Calgary, AB T2N 2T9, Canada.
EM jgcairnx@ucalgary.ca; mmarra@bcgsc.ca
RI Morin, Gregg/E-9123-2012; Blough, Michael/O-1186-2013; Tang,
Macy/B-9798-2014; Karsan, Aly/K-2067-2015; Hirst, Martin/B-7684-2016;
Smith, Eric/C-5443-2012; Jones, Steven/C-3621-2009; Birol,
Inanc/G-5440-2011; Marra, Marco/B-5987-2008;
OI Morin, Gregg/0000-0001-8949-4374; Smith, Eric/0000-0003-3956-1668;
Birol, Inanc/0000-0003-0950-7839; Docking, Rod/0000-0003-3248-4081
FU BC Cancer Foundation; Western Economic Diversification; Genome Canada;
Genome British Columbia
FX We would like to acknowledge Dr John Kelly for cell lines, Dr Peter
Forsyth and the Calgary Brain Tumour Bank for tissues, Colleen Anderson
and Susan Hui for technical assistance, Alberta Innovates Health
Solutions (JAC, EES), the Brain Tumour Foundation of Canada (JGC), the
Alberta Cancer Foundation (JGC), and the Clark Smith Family. We also
acknowledge Dr Robert Jenkins for performing mFISH on the brain
tumour-initiating cell lines BT054 and BT088 and sharing the data. MAM
acknowledges the support of the BC Cancer Foundation, Western Economic
Diversification, Genome Canada, and Genome British Columbia. MAM is also
grateful to Dr Brian Thiessen, BCCA, for early conversations that helped
shape the project. SY acknowledges the generous support of BrainCare BC
and the BCCA Hershey and Yvette Porte Neuro-Oncology Endowment Fund. We
would also like to acknowledge Maria Mendez-Lago, Diane Trinh, Kane Tse,
and Thomas Zeng at the BCGSC for invaluable scientific advice and
technical support.
NR 52
TC 120
Z9 125
U1 0
U2 27
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3417
J9 J PATHOL
JI J. Pathol.
PD JAN
PY 2012
VL 226
IS 1
BP 7
EP 16
DI 10.1002/path.2995
PG 10
WC Oncology; Pathology
SC Oncology; Pathology
GA 864RJ
UT WOS:000298257300002
PM 22072542
ER
PT J
AU Tran, P
Skolnick, P
Czobor, P
Huang, NY
Bradshaw, M
McKinney, A
Fava, M
AF Tran, Pierre
Skolnick, Phil
Czobor, Pal
Huang, N. Y.
Bradshaw, Mark
McKinney, Anthony
Fava, Maurizio
TI Efficacy and tolerability of the novel triple reuptake inhibitor
amitifadine in the treatment of patients with major depressive disorder:
A randomized, double-blind, placebo-controlled trial
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE Amitifadine; Anhedonia; Major depressive disorder; Sexual function;
Triple reuptake inhibitor; Weight
ID BROAD-SPECTRUM ANTIDEPRESSANTS; SEXUAL DYSFUNCTION; TRICYCLIC
ANTIDEPRESSANTS; PHARMACOLOGICAL-TREATMENT; PSYCHIATRIC-DISORDERS;
CLINICAL-TRIALS; NEXT-GENERATION; SEROTONIN; METAANALYSIS; DOPAMINE
AB Amitifadine (EB-1010, formerly DOV 21,947) is a serotonin-preferring triple reuptake inhibitor with a relative potency to inhibit serotonin, norepinephrine, and dopamine uptake of similar to 1:2:8, respectively. This 6-week, multicenter, randomized, double-blind, parallel, placebo-controlled study evaluated the efficacy and tolerability of amitifadine in 63 patients with major depressive disorder. Eligible patients (17-item Hamilton Depression Rating Scale [HAMD-17] >= 22 at baseline) were randomized to amitifadine 25 mg twice daily (BID) for 2 weeks, then 50 mg BID for 4 weeks or placebo. Mean baseline scores in the modified intent-to-treat population (n = 56) were 31.4 for the Montgomery-Asberg Depression Rating Scale (MADRS), 29.6 for the HAMD-17, and 25.4 for the Derogatis Interview for Sexual Functioning - Self Report (DISF-SR). At the end of the 6-week double-blind treatment, estimated least squares mean change from baseline (mixed-model repeated measures [MMRM]) in MADRS total score was statistically significantly superior for amitifadine compared to placebo (18.2 vs. 22.0; p = 0.028), with an overall statistical effect size of -0.601 (Cohen's d). Amitifadine also was statistically significantly superior to placebo (p = 0.03) for the Clinical Global Impression of Change Improvement. An anhedonia factor score grouping of MADRS Items 1 (apparent sadness), 2 (reported sadness), 6 (concentration difficulties), 7 (lassitude), and 8 (inability to feel) demonstrated a statistically significant difference in favor of amitifadine compared to placebo (p = 0.049). No differences were observed between treatments in DISF-SR scores. Amitifadine was well-tolerated. Two patients on each treatment discontinued the study early due to adverse events: however, no serious adverse events were reported. This initial clinical trial in patients with severe major depression demonstrated significant antidepressant activity with amitifadine, including attenuating symptoms of anhedonia, and a tolerability profile that was comparable to placebo. The efficacy and tolerability of amitifadine for major depressive disorder are being investigated in additional clinical trials. (C )2011 Elsevier Ltd. All rights reserved.
C1 [Tran, Pierre; McKinney, Anthony] Euthym Biosci Inc, Cambridge, MA 02141 USA.
[Skolnick, Phil; Czobor, Pal; Huang, N. Y.] DOV Pharmaceut, Somerset, NJ USA.
[Bradshaw, Mark] Global Consulting Partners, Princeton, NJ USA.
[Fava, Maurizio] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Tran, P (reprint author), Euthym Biosci Inc, 43 Thorndike St,Suite S1-3, Cambridge, MA 02141 USA.
EM ptran@euthymics.com
FU Euthymics Bioscience, Cambridge, MA
FX The authors acknowledge the editorial assistance of Richard S. Perry,
PharmD in the preparation of this manuscript, which was supported by
Euthymics Bioscience, Cambridge, MA.
NR 65
TC 42
Z9 44
U1 4
U2 15
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD JAN
PY 2012
VL 46
IS 1
BP 64
EP 71
DI 10.1016/j.jpsychires.2011.09.003
PG 8
WC Psychiatry
SC Psychiatry
GA 868MR
UT WOS:000298527900009
PM 21925682
ER
PT J
AU Lydecker, JA
Pisetsky, EM
Mitchell, KS
Thornton, LM
Kendler, KS
Reichborn-Kjennerud, T
Lichtenstein, P
Bulik, CM
Mazzeo, SE
AF Lydecker, Janet A.
Pisetsky, Emily M.
Mitchell, Karen S.
Thornton, Laura M.
Kendler, Kenneth S.
Reichborn-Kjennerud, Ted
Lichtenstein, Paul
Bulik, Cynthia M.
Mazzeo, Suzanne E.
TI Association between co-twin sex and eating disorders in opposite sex
twin pairs: Evaluations in North American, Norwegian, and Swedish
samples
SO JOURNAL OF PSYCHOSOMATIC RESEARCH
LA English
DT Article
DE Eating disorders; Estrogen; Opposite sex twin pairs; Prenatal hormone
exposure; Testosterone; Twin study
ID SAME-SEX; OVARIAN HORMONES; BULIMIA-NERVOSA; FEMALE RATS; BEHAVIOR;
TESTOSTERONE; EXPOSURE; ANOREXIA; REGISTRY; WOMEN
AB Objective: These three studies examined the hypothesis that prenatal exposure to sex hormones influences twins' risk for eating disorders based on co-twin sex, such that individuals with a female co-twin would be more likely than individuals with a male co-twin to meet diagnostic criteria for an eating disorder.
Methods: Male and female twins from the United States (N=2607), Norway (N=2796) and Sweden (N=16,458) with known co-twin sex and zygosity were assessed for eating disorders.
Results: In the U.S. and Swedish samples, sex was significantly associated with eating disorder diagnoses, and although co-twin sex was not associated with eating disorders overall, it was associated with broadly defined bulimia nervosa in the Swedish sample. The effects for bulimia were not sustained when monozygotic twins were excluded, suggesting that the effects of prenatal sex hormones play a minor role in influencing eating disorders. Sex and co-twin sex were not associated with eating disorders in the Norwegian sample.
Conclusion: The prenatal sex hormone hypothesis, which proposes that prenatal hormone exposure is associated with later eating disorder symptomatology, was not supported in these three population-based twin samples. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Lydecker, Janet A.; Mitchell, Karen S.; Mazzeo, Suzanne E.] Virginia Commonwealth Univ, Dept Psychol, Richmond, VA 23284 USA.
[Pisetsky, Emily M.] Univ N Carolina, Dept Psychol, Chapel Hill, NC USA.
[Mitchell, Karen S.; Kendler, Kenneth S.; Mazzeo, Suzanne E.] Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Richmond, VA USA.
[Mitchell, Karen S.] VA Boston Healthcare Syst, Womens Hlth Sci Div, Natl Ctr PTSD, Boston, MA USA.
[Mitchell, Karen S.] Boston Univ, Dept Psychiat, Boston, MA 02215 USA.
[Thornton, Laura M.; Bulik, Cynthia M.] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA.
[Kendler, Kenneth S.] Virginia Commonwealth Univ, Dept Psychiat, Richmond, VA USA.
[Reichborn-Kjennerud, Ted] Norwegian Inst Publ Hlth, Div Mental Hlth, Oslo, Norway.
[Reichborn-Kjennerud, Ted] Univ Oslo, Inst Psychiat, N-0316 Oslo, Norway.
[Reichborn-Kjennerud, Ted] Columbia Univ, Dept Epidemiol, New York, NY USA.
[Lichtenstein, Paul] Karolinska Inst, Dept Med Epidemiol & Biostat, S-10401 Stockholm, Sweden.
[Bulik, Cynthia M.] Univ N Carolina, Dept Nutr, Chapel Hill, NC USA.
[Mazzeo, Suzanne E.] Virginia Commonwealth Univ, Dept Pediat, Richmond, VA USA.
RP Mazzeo, SE (reprint author), 806 W Franklin St,POB 842018, Richmond, VA 23220 USA.
EM semazzeo@vcu.edu
RI Lydecker, Janet/B-3349-2016;
OI Lydecker, Janet/0000-0001-6425-514X; lichtenstein,
paul/0000-0003-3037-5287
FU NIMH NIH HHS [K01 MH068520-05]
NR 36
TC 12
Z9 12
U1 0
U2 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3999
EI 1879-1360
J9 J PSYCHOSOM RES
JI J. Psychosomat. Res.
PD JAN
PY 2012
VL 72
IS 1
BP 73
EP 77
DI 10.1016/j.jpsychores.2011.05.014
PG 5
WC Psychiatry
SC Psychiatry
GA 874DU
UT WOS:000298936400014
PM 22200526
ER
PT J
AU Sorrentino, R
AF Sorrentino, Renee
TI Degarelix: An Antagonist to GnRHu-Theoretical and Treatment
Considerations in Paraphilia
SO JOURNAL OF SEXUAL MEDICINE
LA English
DT Letter
ID HORMONE-II; BEHAVIOR
C1 Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Sorrentino, R (reprint author), Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp, Boston, MA 02115 USA.
NR 10
TC 2
Z9 2
U1 2
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1743-6095
J9 J SEX MED
JI J. Sex. Med.
PD JAN
PY 2012
VL 9
IS 1
BP 327
EP 329
DI 10.1111/j.1743-6109.2011.02540.x
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA 872HE
UT WOS:000298799100042
PM 22082230
ER
PT J
AU Saoiabi, S
El Asri, S
Laghzizil, A
Masse, S
Ackerman, JL
AF Saoiabi, Sanaa
El Asri, Sanae
Laghzizil, Abdelaziz
Masse, Sylvie
Ackerman, Jerome L.
TI Synthesis and characterization of nanoapatites organofunctionalized with
aminotriphosphonate agents
SO JOURNAL OF SOLID STATE CHEMISTRY
LA English
DT Article
DE Apatite; Functionalized surface; Mesoporous materials; Surface
properties
ID CALCIUM HYDROXYAPATITE; SURFACE MODIFICATION; AQUEOUS-SOLUTION;
PHOSPHATE; BONE; REMOVAL; SPECTROSCOPY; KINETICS; COATINGS; APATITES
AB Organofunctionalized apatite nanoparticles were prepared using a one step process involving dissolution/precipitation of natural phosphate rock and covalent grafting of nitrilotris(methylene)triphosphonate (NTP). The synthesized materials were characterized by Brunauer-Emmett-Teller (BET) surface measurement, thermogravimetry, inductively coupled plasma emission spectroscopy (ICP-ES), elemental analysis, multinuclear solid state cross-polarization/magic angle spinning (CP/MAS) and single-pulse NMR spectroscopy, transmission electron microscopy (TEM) and energy dispersive X-ray analysis (EDXA). After grafting BET measurements yielded particle specific surface areas ranging from 88 to 193 m(2) g(-1) depending on the grafted phosphonate. The results show that the surfaces of the nanoapatite particles can be covered with functional groups bound through a variable number of R-P-O-Ca bonds to render them organoapatites. Published by Elsevier Inc.
C1 [Saoiabi, Sanaa; El Asri, Sanae; Laghzizil, Abdelaziz] Univ Mohamed V Agdal, Fac Sci, Lab Chim Phys Gen, Rabat, Morocco.
[Saoiabi, Sanaa; Masse, Sylvie] Univ Paris 06, UMR 7574, F-75005 Paris, France.
[Saoiabi, Sanaa; Ackerman, Jerome L.] Massachusetts Gen Hosp, Dept Radiol, Biomat Lab, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Saoiabi, Sanaa; Ackerman, Jerome L.] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
RP Laghzizil, A (reprint author), Univ Mohamed V Agdal, Fac Sci, Lab Chim Phys Gen, BP 1014, Rabat, Morocco.
EM laghzizi@fsr.ac.ma; jerry@nmr.mgh.harvard.edu
RI Ackerman, Jerome/E-2646-2015
OI Ackerman, Jerome/0000-0001-5176-7496
FU Office Cherifien des Phosphates (OCP); Center d'Etudes et de Recherches
des Phosphates Mineraux (CERPHOS); National Institutes of Health
[P41RR14075]; Fulbright Foundation
FX The authors would like to thank the Office Cherifien des Phosphates
(OCP) and the Center d'Etudes et de Recherches des Phosphates Mineraux
(CERPHOS) for their support, UATRS-CNRST-Rabat for chemical analyses,
the Martinos Center for Biomedical Imaging at Massachusetts General
Hospital and National Institutes of Health grant P41RR14075. S. Saoiabi
wishes to acknowledge the Moroccan-American Commission for Educational
and Cultural Exchange (MACECE) and the Fulbright Foundation for
fellowship support.
NR 38
TC 6
Z9 6
U1 0
U2 10
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4596
J9 J SOLID STATE CHEM
JI J. Solid State Chem.
PD JAN
PY 2012
VL 185
BP 95
EP 100
DI 10.1016/j.jssc.2011.10.031
PG 6
WC Chemistry, Inorganic & Nuclear; Chemistry, Physical
SC Chemistry
GA 874EA
UT WOS:000298937000015
PM 22287800
ER
PT J
AU Baer, JS
Carpenter, KM
Beadnell, B
Stoner, SA
Ingalsbe, MH
Hartzler, B
Rosengren, DB
Drager, Z
AF Baer, John S.
Carpenter, Kelly M.
Beadnell, Blair
Stoner, Susan A.
Ingalsbe, Michelle Hansten
Hartzler, Bryan
Rosengren, David B.
Drager, Zach
TI Computer Assessment of Simulated Patient Interviews (CASPI):
Psychometric Properties of a Web-Based System for the Assessment of
Motivational Interviewing Skills
SO JOURNAL OF STUDIES ON ALCOHOL AND DRUGS
LA English
DT Article
ID VIDEO ASSESSMENT; CLINICIAN; COMPETENCE; VALIDITY; RELIABILITY;
VALIDATION; ADDICTION; BEHAVIOR; SCALE; VASE
AB Objective: Benefits of empirically supported interventions hinge on clinician skill, particularly for motivational interviewing (MI). Existing MI skill assessments are limited with respect to validity (e.g., self-report) and practicality (e.g., coding session tapes). To address these limitations, we developed and evaluated two versions of a web-based assessment of MI skills, the Computer Assessment of Simulated Patient Interviews (CASPI). Method: Ninety-six counselors from the community and 24 members of the Motivational Interviewing Network of Trainers (MINT) completed the CASPI (N = 120), in which they verbally responded via microphones to video clips comprising three 9-item vignettes. Three coders used an emergent coding scheme, which was compared with alternative MI skills measures. Results: CASPI demonstrated excellent internal consistency when averaging across two or three vignettes (alpha's = .86.89). Intraclass correlations were above 40 for most items. Confirmatory factor analyses supported a correlated three-factor model: MI-consistent, resistance-engendering, and global change talk orientation rating. Means and factor loadings were invariant across forms (i.e., the two alternative versions of CASPI), and factor loadings were invariant across subgroup (i.e., community counselor or MINT member). Test retest reliability was good for MI-consistent and resistance-engendering scores (r = .74 and .80, respectively) but low for change talk orientation (r = .29) unless coder was taken into account (r = .69). CASPI showed excellent construct and criterion-related validity. Conclusions: CASPI represents a promising method of assessing MI skills. Future studies are needed to establish its performance in real-world contexts. (J. Stud. Alcohol Drugs, 73, 154-164, 2012)
C1 [Baer, John S.] Univ Washington, Dept Psychol, Seattle, WA 98195 USA.
[Baer, John S.; Ingalsbe, Michelle Hansten; Hartzler, Bryan; Rosengren, David B.] Univ Washington, Inst Alcohol & Drug Abuse, Seattle, WA 98195 USA.
[Carpenter, Kelly M.; Stoner, Susan A.; Drager, Zach] Talaria Inc, Seattle, WA USA.
[Beadnell, Blair] Univ Washington, Sch Social Work, Seattle, WA 98195 USA.
[Beadnell, Blair; Rosengren, David B.] Prevent Res Inst, Lexington, KY USA.
RP Baer, JS (reprint author), VA Puget Sound HCS, S-116-ATC,1660 S Columbian Way, Seattle, WA 98108 USA.
EM jsbaer@uw.edu
FU National Institute on Drug Abuse [R42 DA020284]
FX This research was supported by a Small Business Technology Transfer
grant from the National Institute on Drug Abuse (R42 DA020284).
NR 24
TC 4
Z9 4
U1 0
U2 2
PU ALCOHOL RES DOCUMENTATION INC CENT ALCOHOL STUD RUTGERS UNIV
PI PISCATAWAY
PA C/O DEIRDRE ENGLISH, 607 ALLISON RD, PISCATAWAY, NJ 08854-8001 USA
SN 1937-1888
J9 J STUD ALCOHOL DRUGS
JI J. Stud. Alcohol Drugs
PD JAN
PY 2012
VL 73
IS 1
BP 154
EP 164
PG 11
WC Substance Abuse; Psychology
SC Substance Abuse; Psychology
GA 873QP
UT WOS:000298898400020
PM 22152673
ER
PT J
AU Klein, AA
Slaymaker, VJ
Dugosh, KL
Mckay, JR
AF Klein, Audrey A.
Slaymaker, Valerie J.
Dugosh, Karen L.
Mckay, James R.
TI Computerized continuing care support for alcohol and drug dependence: A
preliminary analysis of usage and outcomes
SO JOURNAL OF SUBSTANCE ABUSE TREATMENT
LA English
DT Article
DE Alcohol dependence; Drug dependence; Continuing care; Computer based;
Residential treatment
ID RANDOMIZED CONTROLLED-TRIAL; COGNITIVE-BEHAVIORAL THERAPY; ASSISTED
INTERVENTION; PROBLEM DRINKERS; CLINICAL-TRIAL; DIABETES CARE;
FOLLOW-UP; RELIABILITY; PROGRAM; INSTRUMENT
AB The central aim of this administrative data analysis was to examine usage of a Web-based disease management program designed to provide continuing recovery support to patients discharged from residential drug and alcohol treatment. Tailored clinical content was delivered in a multimedia format over the course of 18 months posttreatment. The program also included access to a recovery coach across the 18 months. Consistent with other disease management programs, program usage decreased over time. A small subsample of patients accessed a large number of program modules in the year following treatment; these patients had significantly higher abstinence rates and consumed less alcohol than patients accessing few or no modules. Regression analyses revealed a significant relationship between the number of modules accessed and substance use outcomes in the year following treatment when controlling for motivation, self-efficacy, and pretreatment substance use. Limiting the analyses to only the more compliant patients did not reduce the magnitude of these effects. These preliminary results suggest that computerized support programs may be beneficial to patients recently treated for drug and alcohol issues. Methods to increase program engagement need additional study. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Klein, Audrey A.; Slaymaker, Valerie J.] Hazelden Fdn, Butler Ctr Res, Ctr City, MN 55012 USA.
[Dugosh, Karen L.] Treatment Res Inst, Philadelphia, PA USA.
[Mckay, James R.] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA.
[Mckay, James R.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
RP Klein, AA (reprint author), Hazelden Fdn, Butler Ctr Res, POB 11,BC-4, Ctr City, MN 55012 USA.
EM aklein@hazelden.org
NR 27
TC 14
Z9 15
U1 0
U2 9
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0740-5472
J9 J SUBST ABUSE TREAT
JI J. Subst. Abus. Treat.
PD JAN
PY 2012
VL 42
IS 1
BP 25
EP 34
DI 10.1016/j.jsat.2011.07.002
PG 10
WC Psychology, Clinical; Substance Abuse
SC Psychology; Substance Abuse
GA 860OF
UT WOS:000297956900004
PM 21862275
ER
PT J
AU Brewster, LP
Palmatier, J
Manley, CJ
Hall, DE
Brems, JJ
AF Brewster, Luke P.
Palmatier, Jason
Manley, C. J.
Hall, Daniel E.
Brems, J. J.
TI Limitations on Surrogate Decision-Making for Emergent Liver
Transplantation
SO JOURNAL OF SURGICAL RESEARCH
LA English
DT Article
DE surrogate consent; ethics; fulminant hepatic failure; liver
transplantation
ID RISK-RELATED STANDARDS; INFORMED-CONSENT; OF-LIFE; COMPETENCE; ACCURACY;
PERSPECTIVE; DEBATE; ETHICS; CARE
AB Background. Surrogate consent is an accepted form of promoting patient autonomy when patients cannot consent, but it can lead to surrogate duress and may be unreliable. Since consent for liver transplantation in patients with fulminant hepatic failure (FHF) is typically performed by surrogates and these patients typically regain decisional capacity, we chose this population to query patients' opinion on the surrogate consent process.
Materials and Methods. We developed a questionnaire that queried transplanted patients' experience and opinion on surrogate consent, suitability of surrogates, and return of decisional capacity. This survey was then sent to consecutive survivors of liver transplantation for FHF at our institution.
Results. Eleven of 14 patients eligible to participate completed the questionnaire. The mean follow-up for all survivors was 41 mo, with a range of survival since transplant of 5 mo to 10 y. Although 10/11 respondents agreed with their surrogates to consent to liver transplantation, all 11 patients thought that surrogates should not be able to decline liver transplantation for this condition. In distinction, 3/11 patients believed patients could decline liver transplantation.
Conclusions. This is the first study to demonstrate that liver transplant patients do not think surrogate decision-makers should be permitted to contravene physician recommendations regarding transplant. In clinical settings when patients cannot speak for themselves, it may be appropriate for surrogates and clinicians to act together according to the patients' best interest rather than attempt to determine what the patient would want. This approach might reduce surrogate distress, better represent patient preferences, and improve the decision-making process for affected patients. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Brewster, Luke P.] Emory Univ Hosp, Dept Surg, Atlanta, GA 30322 USA.
[Palmatier, Jason; Manley, C. J.] Loyola Univ, Stritch Sch Med, Maywood, IL 60153 USA.
[Hall, Daniel E.] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Hall, Daniel E.] Univ Pittsburgh, Dept Surg, Med Ctr, Pittsburgh, PA USA.
[Brems, J. J.] Sherman Hosp, Dept Surg, Elgin, IL USA.
RP Brewster, LP (reprint author), Emory Univ Hosp, Dept Surg, 676 N Parkwood Rd, Decatur, GA 30030 USA.
EM lukebrewst@aol.com
RI Hall, Daniel/H-4843-2013;
OI Hall, Daniel/0000-0001-6382-0522
NR 31
TC 1
Z9 1
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4804
J9 J SURG RES
JI J. Surg. Res.
PD JAN
PY 2012
VL 172
IS 1
BP 48
EP 52
DI 10.1016/j.jss.2011.04.042
PG 5
WC Surgery
SC Surgery
GA 864DK
UT WOS:000298217000007
PM 21696773
ER
PT J
AU Mukherjee, R
Snipes, JM
Saunders, SM
Zavadzkas, JA
Spinale, FG
AF Mukherjee, Rupak
Snipes, Jonathan M.
Saunders, Stuart M.
Zavadzkas, Juozas A.
Spinale, Francis G.
TI Discordant Activation of Gene Promoters for Matrix Metalloproteinases
and Tissue Inhibitors of the Metalloproteinases Following Myocardial
Infarction
SO JOURNAL OF SURGICAL RESEARCH
LA English
DT Article
DE matrix metalloproteinase; tissue inhibitor of metalloproteinase;
myocardial infarction; remodeling
ID LEFT-VENTRICULAR ENLARGEMENT; EXTRACELLULAR-MATRIX; HEART-FAILURE;
TRANSCRIPTIONAL REGULATION; TARGETED DELETION; TRANSGENIC MICE; CARDIAC
RUPTURE; EXPRESSION; RAT; INDUCTION
AB Background. Left ventricular (LV) remodeling following myocardial infarction (MI) is associated with increased levels of specific matrix metalloproteinases (MMPs) and relative reduction of endogenous tissue inhibitors of the MMPs (TIMPs). However, transcriptional mechanisms for the disparate post-MI MMP/TIMP expression remain unknown. Using murine constructs designed to report gene promoter activation, this study tested the hypothesis that distinctly different temporal profiles of MMP-2, MMP-9, and TIMP-1 transcription occurs post-MI.
Methods/Results. Transcriptional activity (beta-galactosidase (beta-gal) reporter constructs) of MMP-2 (n = 49), MMP-9 (n = 62), or TIMP-1 (n = 40) was assayed at 1 h (acute), and 1-28 d after MI (coronary ligation) in transgenic reporter mice. At 7 d post-MI, the area of promoter activation normalized to LV area was increased from acute values for MMP-2 (63.4 +/- 5.8 versus 1.1% +/- 1.0%, P < 0.05) and MMP-9 (53.1 +/- 6.1 versus 1.3% +/- 0.9%, P < 0.05). While TIMP-1 promoter activation at 7 d post-MI increased from acute values (3.6 +/- 1.3 versus 0.3% +/- 0.5%, P < 0.05), this increase was smaller than that for MMP-2 or MMP-9 (both P < 0.05). MMP-2 promoter activation peaked in the MI region at 7 d post-MI and MMP-9 promoter activation was highest in the border region at 7 and 14 d post-MI. TIMP-1 promoter activation peaked within the MI region at 7 d post-MI and within the remote region at 14 d post-MI.
Conclusions. These findings provided direct in vivo evidence that discordant changes in temporal and spatial patterns of MMP/TIMP transcription occurs with MI. Restoration of TIMP-1 promoter activation may represent a molecular therapeutic target to attenuate/prevent adverse post-MI LV remodeling. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Mukherjee, Rupak; Snipes, Jonathan M.; Saunders, Stuart M.; Zavadzkas, Juozas A.; Spinale, Francis G.] Med Univ S Carolina, Div Cardiothorac Surg, Charleston, SC 29425 USA.
[Spinale, Francis G.] Ralph H Johnson Vet Adm Med Ctr, Charleston, SC USA.
RP Mukherjee, R (reprint author), Med Univ S Carolina, Div Cardiothorac Surg, Strom Thurmond Res Bldg,770 MUSC Complex,Suite 62, Charleston, SC 29425 USA.
EM mukherr@musc.edu
FU National Institutes of Health [HL-66029, HL-45024, HL-97012,
PO1-HL48788]
FX This study was supported by National Institutes of Health grants
HL-66029 (RM), HL-45024, HL-97012, and PO1-HL48788 (FGS).
NR 36
TC 2
Z9 4
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-4804
J9 J SURG RES
JI J. Surg. Res.
PD JAN
PY 2012
VL 172
IS 1
BP 59
EP 67
DI 10.1016/j.jss.2010.06.015
PG 9
WC Surgery
SC Surgery
GA 864DK
UT WOS:000298217000009
PM 20863528
ER
PT J
AU Wilens, TE
Bukstein, O
Brams, M
Cutler, AJ
Childress, A
Rugino, T
Lyne, A
Grannis, K
Youcha, S
AF Wilens, Timothy E.
Bukstein, Oscar
Brams, Matthew
Cutler, Andrew J.
Childress, Ann
Rugino, Thomas
Lyne, Andrew
Grannis, Kara
Youcha, Sharon
TI A Controlled Trial of Extended-Release Guanfacine and Psychostimulants
for Attention-Deficit/Hyperactivity Disorder
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE Attention-deficit/hyperactivity disorder; alpha(2)-adrenoceptor agonist
ID DEFICIT HYPERACTIVITY DISORDER; COMORBIDITY SURVEY REPLICATION;
PLACEBO-CONTROLLED EVALUATION; RANDOMIZED CONTROLLED-TRIAL;
DOUBLE-BLIND; LISDEXAMFETAMINE DIMESYLATE; LIFETIME PREVALENCE;
CHILDREN; ADOLESCENTS; ADHD
AB Objective: To examine efficacy, tolerability, and safety of guanfacine extended release (GXR; <= 4 mg/d) adjunctive to a long-acting psychostimulant for the treatment of attention-deficit/hyperactivity disorder (ADHD) in children and adolescents 6 to 17 years of age with suboptimal, but partial, response to psychostimulant alone. Method: In this multicenter, 9-week, double-blind, placebo-controlled, dose-optimization study, subjects (N = 461) continued their stable dose of psychostimulant given in the morning and were randomized to receive GXR in the morning (GXR AM), GXR in the evening (GXR PM), or placebo. Efficacy measures included ADHD Rating Scale IV (ADHD-RS-IV) and Clinical Global Impressions of Severity of Illness (CGI-S) and Improvement (CGI-I) scales. Safety measures included adverse events (AEs), vital signs, electrocardiograms, and laboratory evaluations. Results: At endpoint, GXR treatment groups showed significantly greater improvement from baseline ADHD-RS-IV total scores compared with placebo plus psychostimulant (GXR AM, p = .002; GXR PM, p < .001). Significant benefits of GXR treatment versus placebo plus psychostimulant were observed on the CGI-S (GXR AM, p = .013; GXR PM, p < .001) and CGI-I (GXR AM, p = .024; GXR PM, p = .003). At endpoint, small mean decreases in pulse, systolic, and diastolic blood pressure were observed in GXR treatment groups versus placebo plus psychostimulant. No new safety signals emerged following administration of GXR with psychostimulants versus psychostimulants alone. Most AEs were mild to moderate in severity. Conclusions: Morning or evening GXR administered adjunctively to a psychostimulant showed significantly greater improvement over placebo plus psychostimulant in ADHD symptoms and generated no new safety signals. J. Am. Acad. Child Adolesc. Psychiatry, 2012; 51(1):74-85. Clinical trial registration information Efficacy and Safety of SPD503 in Combination With Psychostimulants; http://www.clinicaltriaLs.gov; NCT00734578.
C1 [Wilens, Timothy E.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Wilens, Timothy E.] Harvard Univ, Sch Med, Boston, MA USA.
[Bukstein, Oscar] Univ Texas Houston, Houston, TX USA.
[Brams, Matthew] Bayou City Res, Houston, TX USA.
[Cutler, Andrew J.] Florida Clin Res Ctr LLC, Bradenton, FL USA.
[Childress, Ann] Ctr Psychiat & Behav Med, Las Vegas, NV USA.
[Rugino, Thomas] Childrens Specialized Hosp, Toms River, NJ USA.
[Lyne, Andrew] Shire Pharmaceut Dev Ltd, Basingstoke, Hants, England.
[Grannis, Kara; Youcha, Sharon] Shire Dev Inc, Wayne, PA USA.
RP Wilens, TE (reprint author), Massachusetts Gen Hosp, Dept Psychiat, YAW 6900,55 Fruit St, Boston, MA 02114 USA.
EM twilens@partners.org
FU Shire Development Inc., Wayne, PA; Shire Development Inc.; Abbott; Eli
Lilly and Co.; McNeil; Merck; National Institutes of Health (NIH);
National Institute on Drug Abuse (NIDA); Shire; AstraZeneca; Addremax;
Bristol-Myers Squibb; Cephalon; GlaxoSmithKline; Janssen; Johnson and
Johnson; Novartis; Ortho McNeil; Otsuka; Pfizer; Sepracor; Shionogi;
Sunovion; AstraZeneca Pharmaceuticals; Jazz Pharmaceuticals; McNeil
Pharmaceuticals; Memory Pharmaceuticals; Sanofi; Solvay; Supernus;
Targacept; NextWave; Janssen Scientific Affairs; Rhodes; Somerset;
Forest Research Institute; Lexicor
FX This study was supported by Shire Development Inc., Wayne, PA.; Clinical
research was funded by the sponsor, Shire Development Inc. The primary
manuscript was written by Dr. Wilens after discussion about the
manuscript's content with the independent authors. Under the direction
of the authors, Jennifer Steeber, PhD, an employee of SCI Scientific
Communications and Information SCI), provided additional writing
assistance for this publication. Editorial assistance in formatting,
proofreading, copy editing, and fact checking was also provided by SCI.
Jonathan Rubin, M.D., M.B.A., Ryan Dammerman, M.D., Ph.D., Carla White,
B.Sc., C.Stat., Edward Johnson, Michael Kahn, and Gina D'Angelo,
Pharm.D., M.B.A., from Shire Development Inc., also reviewed and edited
the manuscript for scientific accuracy. Shire Development Inc. provided
funding to OCHSC for support in writing and editing this manuscript.
Although the sponsor was involved in the design, collection, analysis,
interpretation, and fact checking of information, the content of this
manuscript, the ultimate interpretation, and the decision to submit it
for publication in Journal of the American Academy of Child and
Adolescent Psychiatry were mode by the authors independently.; Dr.
Wilens receives or has received grant support from Abbott, Eli Lilly and
Co., McNeil, Merck, the National Institutes of Health (NIH), National
Institute on Drug Abuse (NIDA), and Shire. He has served as a speaker
for Eli Lilly and Co., McNeil, Novartis, and Shire. He has served as a
consultant for Abbott, AstraZeneca, Eli Lilly and Co., Euthymics,
McNeil, Merck, NextWave, NIH, NIDA, Novortis, and Shire. Dr. Wilens
receives royalties from Guilford Press. Dr. Bukstein receives or has
received research support from McNeil and Shire. He has acted as a
consultant, and/or served on a speakers' bureau for Cephalon, McNeil,
Novartis, and Shire. He receives royalties from Routledge Press. Dr.
Brams has served on the speakers' bureau and as a consultant for
AstraZeneca, Eli Lilly and Co., Cephalon, McNeil, Novartis, Pfizer,
Shire, Shionogi, Sunovion. He has received research support from
AstraZeneca, Addremax, Bristol-Myers Squibb, Cephalon, GlaxoSmithKline,
Janssen, Johnson and Johnson, Merck, Novartis, Ortho McNeil, Otsuka,
Pfizer, Sepracor, Shionogi, Shire, and Sunovion. Dr. Cutler has received
research grants from Abbott, Addrenex, AstraZeneca Pharmaceuticals,
Bristol-Myers Squibb, Cephalon, Eli Lilly and Co., GlaxoSmithKline,
Janssen, Jazz Pharmaceuticals, Johnson and Johnson, McNeil
Pharmaceuticals, Memory Pharmaceuticals, Merck, Novartis, Ortho-McNeil,
Otsuka, Pfizer, Sanofi, Sepracor, Shionogi, Shire, Solvay, Supernus, and
Targacept. He has served as a consultant for Abbott, Addrenex,
AstraZeneca, Bristol-Myers Squibb, Cephalon, Eli Lilly and Co.,
GlaxoSmithKline, Janssen, Johnson and Johnson, Neuroscience Education
Institute, Novartis, Ortho-McNeil, Otsuka, Pfizer, Sepracor, Shionogi,
Shire, Supernus, and Targacept. He has served on the speakers' bureau
for Abbott, AstraZeneca, Bristol-Myers Squibb, Eli Lilly and Co.,
GlaxoSmithKline, Janssen, Neuroscience Education Institute, Novartis,
Ortho-McNeil, Pfizer, Sepracor, Shionogi, and Shire. He has received
continuing medical education credits from an advisory board for
Neuroscience Education Institute. Dr. Childress has served as a
consultant for NextWave, Novartis, and Shire. She has served on the
speakers' bureau for Bristol-Myers Squibb, GlaxoSmithKline, Shire, and
Novartis. She receives research support from Abbott, Bristol-Myers
Squibb, Eli Lilly and Co., Johnson and Johnson, NextWave, Novartis,
Ortho-McNeill, Otsuka, Janssen Scientific Affairs, Rhodes, Sepracor,
Shire, and Somerset. Dr. Rugino has served as a consultant for Lexicor,
Bristol-Myers Squibb, and Shire. He has served on the speakers' bureau
for Shire. Children's Specialized Hospital received research support
from Bristol-Myers Squibb, Eli Lilly and Co., Forest Research Institute,
Lexicor, Novartis, and Shire. Ms. Grannis holds stock and/or stock
options in Shire. Mr. Lyne holds stock and/or stock options in Shire.
Dr. Youcha holds stock and/or stock options in Shire.
NR 41
TC 39
Z9 39
U1 3
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD JAN
PY 2012
VL 51
IS 1
BP 74
EP 85
DI 10.1016/j.jaac.2011.10.012
PG 12
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 868NP
UT WOS:000298530300009
PM 22176941
ER
PT J
AU Kardos, M
Kimball, AB
AF Kardos, Marisa
Kimball, Alexa Boer
TI Time for a change? Updated guidelines using interferon gamma release
assays for detection of latent tuberculosis infection in the office
setting
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Editorial Material
DE anti-tumor necrosis factor; interferon gamma release assay; latent
tuberculosis; psoriasis; screening
ID ANTITUMOR NECROSIS FACTOR; FACTOR ANTAGONISTS; SKIN-TEST; PSORIASIS;
THERAPY; PERFORMANCE; AGENTS; RISK
AB Treatment with tumor necrosis factor-alfa inhibitors and other systemic medications increases the risk of reactivating a latent tuberculosis (TB) infection. Therefore, screening for latent TB infection is important in dermatology patients eligible for treatment with these medications. Although the tuberculin skin test (TST) has its limitations, it has been the standard choice for diagnosis of latent TB infection. Since the development of interferon gamma release assays (IGRAs), the role of the TST has been re-evaluated and IGRAs have increasingly been incorporated into national guidelines. Although there are situations when either test may be performed, in individuals who have received a BCG vaccination and in those who are unlikely to return for a TST reading, IGRAs may be particularly helpful in distinguishing patients at risk for TB. This article discusses the advantages and disadvantages of both the TST and the IGRA and presents a summary of the Centers for Disease Control and Prevention 2010 guidelines for using IGRAs. (J Am Acacl Dermatol 2012;66:148-52.)
C1 [Kardos, Marisa; Kimball, Alexa Boer] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
RP Kimball, AB (reprint author), 50 Staniford St,Suite 240, Boston, MA 02114 USA.
EM harvardskinstudies@partners.org
NR 22
TC 8
Z9 8
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD JAN
PY 2012
VL 66
IS 1
BP 148
EP 152
DI 10.1016/j.jaad.2011.09.007
PG 5
WC Dermatology
SC Dermatology
GA 871BH
UT WOS:000298712100021
PM 22177633
ER
PT J
AU Lang, RM
Badano, LP
Tsang, W
Adams, DH
Agricola, E
Buck, T
Faletra, FF
Franke, A
Hung, J
de Isla, LP
Kamp, O
Kasprzak, JD
Lancellotti, P
Marwick, TH
McCulloch, ML
Monaghan, MJ
Nihoyannopoulos, P
Pandian, NG
Pellikka, PA
Pepi, M
Roberson, DA
Shernan, SK
Shirali, GS
Sugeng, L
Ten Cate, FJ
Vannan, MA
Zamorano, JL
Zoghbi, WA
AF Lang, Roberto M.
Badano, Luigi P.
Tsang, Wendy
Adams, David H.
Agricola, Eustachio
Buck, Thomas
Faletra, Francesco F.
Franke, Andreas
Hung, Judy
Perez de Isla, Leopoldo
Kamp, Otto
Kasprzak, Jaroslaw D.
Lancellotti, Patrizio
Marwick, Thomas H.
McCulloch, Marti L.
Monaghan, Mark J.
Nihoyannopoulos, Petros
Pandian, Natesa G.
Pellikka, Patricia A.
Pepi, Mauro
Roberson, David A.
Shernan, Stanton K.
Shirali, Girish S.
Sugeng, Lissa
Ten Cate, Folkert J.
Vannan, Mani A.
Luis Zamorano, Jose
Zoghbi, William A.
TI EAE/ASE Recommendations for Image Acquisition and Display Using
Three-Dimensional Echocardiography
SO JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY
LA English
DT Article
DE Echocardiography; Two-dimensional; Three-dimensional; Transthoracic;
Transesophageal
ID DOBUTAMINE-STRESS-ECHOCARDIOGRAPHY; LEFT-VENTRICULAR VOLUMES; CARDIAC
MAGNETIC-RESONANCE; VENA CONTRACTA AREA; CORONARY-ARTERY-DISEASE; LEFT
ATRIAL APPENDAGE; AORTIC-VALVE AREA; 3D TRANSESOPHAGEAL
ECHOCARDIOGRAPHY; FUNCTIONAL TRICUSPID REGURGITATION; COLOR
DOPPLER-ECHOCARDIOGRAPHY
C1 [Lang, Roberto M.; Tsang, Wendy] Univ Chicago, Chicago, IL 60637 USA.
[Badano, Luigi P.] Univ Padua, Padua, Italy.
[Adams, David H.] Mt Sinai Med Ctr, New York, NY 10029 USA.
[Agricola, Eustachio] Hosp San Raffaele, I-20132 Milan, Italy.
[Buck, Thomas] Univ Duisburg Essen, Essen, Germany.
[Faletra, Francesco F.] Fdn Cardioctr Ticino, Lugano, Switzerland.
[Franke, Andreas] Klinikum Reg Hannover Siloah, Hannover, Germany.
[Hung, Judy] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Perez de Isla, Leopoldo; Luis Zamorano, Jose] Univ Clin San Carlos, Madrid, Spain.
[Kamp, Otto] Vrije Univ Amsterdam Med Ctr, Amsterdam, Netherlands.
[Kasprzak, Jaroslaw D.] Med Univ Lodz, Lodz, Poland.
[Lancellotti, Patrizio] Univ Liege, Liege, Belgium.
[Marwick, Thomas H.] Cleveland Clin, Cleveland, OH 44106 USA.
[McCulloch, Marti L.; Zoghbi, William A.] Methodist Hosp, Methodist DeBakey Heart & Vasc Ctr, Houston, TX 77030 USA.
[Monaghan, Mark J.] Kings Coll Hosp London, London, England.
[Nihoyannopoulos, Petros] Univ London Imperial Coll Sci Technol & Med, London, England.
[Pandian, Natesa G.] Tufts Univ, Med Ctr, Boston, MA 02111 USA.
[Pellikka, Patricia A.] Mayo Clin, Rochester, MN USA.
[Pepi, Mauro] IRCCS, Ctr Cardiol Monzino, Milan, Italy.
[Roberson, David A.] Heart Inst Children, Oak Lawn, IL USA.
[Shernan, Stanton K.] Harvard Univ, Sch Med, Boston, MA USA.
[Shirali, Girish S.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Sugeng, Lissa] Yale Univ, New Haven, CT USA.
[Ten Cate, Folkert J.] Erasmus MC, Rotterdam, Netherlands.
[Vannan, Mani A.] ASE Writing Grp, Morrisville, NC USA.
RP Lang, RM (reprint author), Amer Soc Echocardiog, 2100 Gateway Ctr Blvd,Suite 310, Morrisville, NC 27560 USA.
RI Marwick, Thomas/C-7261-2013; Kasprzak, Jaroslaw/S-4496-2016;
OI Marwick, Thomas/0000-0001-9065-0899; Badano, Luigi/0000-0002-0379-3283
NR 153
TC 192
Z9 202
U1 2
U2 21
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0894-7317
J9 J AM SOC ECHOCARDIOG
JI J. Am. Soc. Echocardiogr.
PD JAN
PY 2012
VL 25
IS 1
BP 3
EP 46
DI 10.1016/j.echo.2011.11.010
PG 44
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 864YN
UT WOS:000298276500003
PM 22183020
ER
PT J
AU Stavitsky, K
Neargarder, S
Bogdanova, Y
McNamara, P
Cronin-Golomb, A
AF Stavitsky, Karina
Neargarder, Sandy
Bogdanova, Yelena
McNamara, Patrick
Cronin-Golomb, Alice
TI The Impact of Sleep Quality on Cognitive Functioning in Parkinson's
Disease
SO JOURNAL OF THE INTERNATIONAL NEUROPSYCHOLOGICAL SOCIETY
LA English
DT Article
DE Parkinson's disease; Sleep; Cognition; Executive function; Actigraphy;
Memory
ID REM-SLEEP; BEHAVIOR DISORDER; CHRONIC INSOMNIA; MEMORY CONSOLIDATION;
SUBJECTIVE MEASURES; DAYTIME SLEEPINESS; PREFRONTAL CORTEX;
WORKING-MEMORY; OLDER-ADULTS; PERFORMANCE
AB In healthy individuals and those with insomnia, poor sleep quality is associated with decrements in performance on tests of cognition, especially executive function. Sleep disturbances and cognitive deficits are both prevalent in Parkinson's disease (PD). Sleep problems occur in over 75% of patients, with sleep fragmentation and decreased sleep efficiency being the most common sleep complaints, but their relation to cognition is unknown. We examined the association between sleep quality and cognition in PD. In 35 non-demented individuals with PD and 18 normal control adults (NC), sleep was measured using 24-hr wrist actigraphy over 7 days. Cognitive domains tested included attention and executive function, memory and psychomotor function. In both groups, poor sleep was associated with worse performance on tests of attention/executive function but not memory or psychomotor function. In the PD group, attention/executive function was predicted by sleep efficiency, whereas memory and psychomotor function were not predicted by sleep quality. Psychomotor and memory function were predicted by motor symptom severity. This study is the first to demonstrate that sleep quality in PD is significantly correlated with cognition and that it differentially impacts attention and executive function, thereby furthering our understanding of the link between sleep and cognition. (JINS, 2012, 18, 108-117)
C1 [Stavitsky, Karina; Neargarder, Sandy; Bogdanova, Yelena; Cronin-Golomb, Alice] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
[Neargarder, Sandy] Bridgewater State Univ, Dept Psychol, Bridgewater, MA USA.
[Bogdanova, Yelena] VA Boston Healthcare Syst, Boston, MA USA.
[Bogdanova, Yelena] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[McNamara, Patrick] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[McNamara, Patrick] VA Boston Healthcare Syst, Dept Neurol, Boston, MA USA.
RP Cronin-Golomb, A (reprint author), Boston Univ, Dept Psychol, 648 Beacon St,2nd Floor, Boston, MA 02215 USA.
EM alicecg@bu.edu
FU National Institute of Neurological Disorders and Stroke [1F31NS061555,
R01 NS050446]; Clara Mayo Foundation from the Department of Psychology,
Boston University
FX This study was supported by a Ruth L. Kirschstein National Research
Service Award from the National Institute of Neurological Disorders and
Stroke (1F31NS061555) and a Clara Mayo Foundation fellowship from the
Department of Psychology, Boston University (K. S.), and by NINDS grant
R01 NS050446 (A. C. G.). We report no conflicts of interest. Marie
Saint-Hilaire, MD, FRCPC, Cathi Thomas, RN, MS, and Denyse Turpin, RN,
MPH of the Department of Neurology, Boston Medical Center, provided
valuable support of our participant recruitment efforts. Chase Ansok,
Erica Appleman, Sophie Blease, Eric Griffith, Patricia Johnson, Barrett
Phillips, and Jessica Saurman assisted with testing participants and
scoring data. We acknowledge with gratitude the efforts of these
colleagues and especially the efforts of all of the individuals who
participated in this study.
NR 75
TC 12
Z9 14
U1 3
U2 13
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1355-6177
J9 J INT NEUROPSYCH SOC
JI J. Int. Neuropsychol. Soc.
PD JAN
PY 2012
VL 18
IS 1
BP 108
EP 117
DI 10.1017/S1355617711001482
PG 10
WC Clinical Neurology; Neurosciences; Psychiatry; Psychology
SC Neurosciences & Neurology; Psychiatry; Psychology
GA 874LL
UT WOS:000298958800011
PM 22152279
ER
PT J
AU Kanai, R
Rabkin, SD
Yip, S
Sgubin, D
Zaupa, CM
Hirose, Y
Louis, DN
Wakimoto, H
Martuza, RL
AF Kanai, Ryuichi
Rabkin, Samuel D.
Yip, Stephen
Sgubin, Donatella
Zaupa, Cecile M.
Hirose, Yuichi
Louis, David N.
Wakimoto, Hiroaki
Martuza, Robert L.
TI Oncolytic Virus-Mediated Manipulation of DNA Damage Responses: Synergy
With Chemotherapy in Killing Glioblastoma Stem Cells
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID HERPES-SIMPLEX-VIRUS; DOUBLE-STRAND BREAKS; ATAXIA-TELANGIECTASIA;
MALIGNANT GLIOMA; GENE-EXPRESSION; REPAIR PROTEINS; BRAIN-TUMOR;
TEMOZOLOMIDE; CANCER; REPLICATION
AB Although both the alkylating agent temozolomide (TMZ) and oncolytic viruses hold promise for treating glioblastoma, which remains uniformly lethal, the effectiveness of combining the two treatments and the mechanism of their interaction on cancer stem cells are unknown.
We investigated the efficacy of combining TMZ and the oncolytic herpes simplex virus (oHSV) G47 delta in killing glioblastoma stem cells (GSCs), using Chou-Talalay combination index analysis, immunocytochemistry and fluorescence microscopy, and neutral comet assay. The role of treatment-induced DNA double-strand breaks, activation of DNA damage responses, and virus replication in the cytotoxic interaction between G47 delta and TMZ was examined with a panel of pharmacological inhibitors and short-hairpin RNA (shRNA)-mediated knockdown of DNA repair pathways. Comparisons of cell survival and virus replication were performed using a two-sided t test (unpaired). The survival of athymic mice (n = 6-8 mice per group) bearing GSC-derived glioblastoma tumors treated with the combination of G47 delta and TMZ was analyzed by the Kaplan-Meier method and evaluated with a two-sided log-rank test.
The combination of G47 delta and TMZ acted synergistically in killing GSCs but not neurons, with associated robust induction of DNA damage. Pharmacological and shRNA-mediated knockdown studies suggested that activated ataxia telangiectasia mutated (ATM) is a crucial mediator of synergy. Activated ATM relocalized to HSV DNA replication compartments where it likely enhanced oHSV replication and could not participate in repairing TMZ-induced DNA damage. Sensitivity to TMZ and synergy with G47 delta decreased with O(6)-methylguanine-DNA-methyltransferase (MGMT) expression and MSH6 knockdown. Combined G47 delta and TMZ treatment extended survival of mice bearing GSC-derived intracranial tumors, achieving long-term remission in four of eight mice (median survival = 228 days; G47 delta alone vs G47 delta + TMZ, hazard ratio of survival = 7.1, 95% confidence interval = 1.9 to 26.1, P = .003) at TMZ doses attainable in patients.
The combination of G47 delta and TMZ acts synergistically in killing GSCs through oHSV-mediated manipulation of DNA damage responses. This strategy is highly efficacious in representative preclinical models and warrants clinical translation.
C1 [Kanai, Ryuichi; Rabkin, Samuel D.; Sgubin, Donatella; Zaupa, Cecile M.; Wakimoto, Hiroaki] Massachusetts Gen Hosp, Dept Neurosurg, Brain Tumor Res Ctr, Boston, MA 02114 USA.
[Kanai, Ryuichi; Rabkin, Samuel D.; Yip, Stephen; Sgubin, Donatella; Zaupa, Cecile M.; Louis, David N.; Wakimoto, Hiroaki; Martuza, Robert L.] Harvard Univ, Sch Med, Boston, MA USA.
[Yip, Stephen; Louis, David N.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Yip, Stephen] BC Canc Agcy, Dept Pathol & Lab Med, Vancouver, BC, Canada.
[Hirose, Yuichi] Fujita Hlth Univ, Dept Neurosurg, Toyoake, Aichi, Japan.
RP Martuza, RL (reprint author), Massachusetts Gen Hosp, Dept Neurosurg, Brain Tumor Res Ctr, White Bldg,Rm 502,55 Fruit St, Boston, MA 02114 USA.
EM rmartuza@partners.org
RI rabkin, samuel/C-2443-2012
OI rabkin, samuel/0000-0003-2344-2795
FU National Institutes of Health [NS-032677, CA57683]; Department of
Defense [W81XWH-07-1-0359]; Royal College of Physicians and Surgeons of
Canada; BrainCare BC
FX This work was supported by the National Institutes of Health (NS-032677
to R. L. M. and CA57683 to D.N.L.), and the Department of Defense
(W81XWH-07-1-0359 to S. D. R.). S.Y. was supported by a Clinician
Investigator Fellowship from the Royal College of Physicians and
Surgeons of Canada and BrainCare BC.
NR 58
TC 35
Z9 36
U1 0
U2 17
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD JAN
PY 2012
VL 104
IS 1
BP 42
EP 55
DI 10.1093/jnci/djr509
PG 14
WC Oncology
SC Oncology
GA 873OH
UT WOS:000298892200009
PM 22173583
ER
PT J
AU Burstein, HJ
AF Burstein, Harold J.
TI JNCCN Reaches 10
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Editorial Material
C1 [Burstein, Harold J.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Burstein, Harold J.] Dana Farber Canc Inst, Boston, MA USA.
[Burstein, Harold J.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Burstein, HJ (reprint author), Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD JAN
PY 2012
VL 10
IS 1
BP 3
EP 3
PG 1
WC Oncology
SC Oncology
GA 875CL
UT WOS:000299007500002
PM 22223863
ER
PT J
AU Ettinger, DS
Akerley, W
Borghaei, H
Chang, A
Cheney, RT
Chirieac, LR
D'Amico, TA
Demmy, TL
Ganti, AKP
Govindan, R
Grannis, FW
Horn, L
Jahan, TM
Jahanzeb, M
Kessinger, A
Komaki, R
Kong, FM
Kris, MG
Krug, LM
Lennes, IT
Loo, BW
Martins, R
O'Malley, J
Osarogiagbon, RU
Otterson, GA
Patel, JD
Pinder-Schenck, M
Pisters, KM
Reckamp, K
Riely, GJ
Rohren, E
Swanson, SJ
Wood, DE
Yang, SC
AF Ettinger, David S.
Akerley, Wallace
Borghaei, Hossein
Chang, Andrew
Cheney, Richard T.
Chirieac, Lucian R.
D'Amico, Thomas A.
Demmy, Todd L.
Ganti, Apar Kishor P.
Govindan, Ramaswamy
Grannis, Frederic W., Jr.
Horn, Leora
Jahan, Thierry M.
Jahanzeb, Mohammad
Kessinger, Anne
Komaki, Ritsuko
Kong, Feng-Ming (Spring)
Kris, Mark G.
Krug, Lee M.
Lennes, Inga T.
Loo, Billy W., Jr.
Martins, Renato
O'Malley, Janis
Osarogiagbon, Raymond U.
Otterson, Gregory A.
Patel, Jyoti D.
Pinder-Schenck, Mary
Pisters, Katherine M.
Reckamp, Karen
Riely, Gregory J.
Rohren, Eric
Swanson, Scott J.
Wood, Douglas E.
Yang, Stephen C.
CA NCCN Clinical Practice Guidelines
TI Malignant Pleural Mesothelioma
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Review
DE NCCN Clinical Practice Guidelines; NCCN Guidelines; malignant pleural
mesothelioma; asbestos; chemotherapy; surgery; radiation therapy;
pleural effusion
ID INTENSITY-MODULATED RADIOTHERAPY; POSITRON-EMISSION-TOMOGRAPHY;
PEMETREXED PLUS CISPLATIN; MULTICENTER PHASE-II; MEGAKARYOCYTE
POTENTIATING FACTOR; DOSE HEMITHORACIC RADIATION; RANDOMIZED
CONTROLLED-TRIAL; EXPANDED ACCESS PROGRAM; EXTRAPLEURAL PNEUMONECTOMY;
TRIMODALITY THERAPY
C1 [Ettinger, David S.; Yang, Stephen C.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
[Akerley, Wallace] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[Borghaei, Hossein] Fox Chase Canc Ctr, Philadelphia, PA USA.
[Chang, Andrew; Kong, Feng-Ming (Spring)] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Cheney, Richard T.; Demmy, Todd L.] Roswell Pk Canc Inst, Buffalo, NY USA.
[Chirieac, Lucian R.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Govindan, Ramaswamy] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO USA.
[Govindan, Ramaswamy] Washington Univ, Sch Med, St Louis, MO 63130 USA.
[Grannis, Frederic W., Jr.; Reckamp, Karen] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Horn, Leora] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Jahanzeb, Mohammad; Osarogiagbon, Raymond U.] Univ Tennessee, St Jude Childrens Hosp, Inst Canc, Knoxville, TN 37996 USA.
[Kessinger, Anne] Nebraska Med Ctr, UNMC Eppley Canc Ctr, Omaha, NE USA.
[Komaki, Ritsuko; Pisters, Katherine M.; Rohren, Eric] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
[Kris, Mark G.; Krug, Lee M.; Riely, Gregory J.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[Lennes, Inga T.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Loo, Billy W., Jr.] Stanford Canc Inst, Stanford, CA USA.
[Martins, Renato; Wood, Douglas E.] Fred Hutchinson Canc Res Ctr, Seattle, WA USA.
[O'Malley, Janis] Univ Alabama, Ctr Comprehens Canc, Birmingham, AL USA.
[Otterson, Gregory A.] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Patel, Jyoti D.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Pinder-Schenck, Mary] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Swanson, Scott J.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
RP Ettinger, DS (reprint author), Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
RI Ganti, Apar Kishor/D-5498-2015;
OI Ganti, Apar Kishor/0000-0003-3724-2671; Chang,
Andrew/0000-0001-9506-0425; Reckamp, Karen/0000-0002-9213-0325
NR 116
TC 19
Z9 19
U1 2
U2 6
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD JAN
PY 2012
VL 10
IS 1
BP 26
EP 41
PG 16
WC Oncology
SC Oncology
GA 875CL
UT WOS:000299007500006
PM 22223867
ER
PT J
AU O'Brien, S
Abboud, CN
Akhtari, M
Altman, J
Berman, E
DeAngelo, DJ
Devine, S
Fathi, AT
Gotlib, J
Jagasia, M
Moore, JO
Pinilla-Ibarz, J
Radich, JP
Reddy, VVB
Shah, NP
Shami, PJ
Smith, BD
Snyder, DS
Wetzler, M
Yunus, F
AF O'Brien, Susan
Abboud, Camille N.
Akhtari, Mojtaba
Altman, Jessica
Berman, Ellin
DeAngelo, Daniel J.
Devine, Steven
Fathi, Amir T.
Gotlib, Jason
Jagasia, Madan
Moore, Joseph O.
Pinilla-Ibarz, Javier
Radich, Jerald P.
Reddy, Vishnu V. B.
Shah, Neil P.
Shami, Paul J.
Smith, B. Douglas
Snyder, David S.
Wetzler, Meir
Yunus, Furhan
CA NCCN Clinical Practice
TI Chronic Myelogenous Leukemia
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Review
DE NCCN Clinical Practice Guidelines; NCCN Guidelines; chronic myelogenous
leukemia; BCR-ABL; tyrosine kinase inhibitor; stem cell transplant;
imatinib; dasatinib; nilotinib
ID CHRONIC MYELOID-LEUKEMIA; STEM-CELL TRANSPLANTATION; TYROSINE KINASE
INHIBITORS; IMATINIB MESYLATE THERAPY; BONE-MARROW-TRANSPLANTATION;
POLYMERASE-CHAIN-REACTION; COMPLETE CYTOGENETIC RESPONSE; IN-SITU
HYBRIDIZATION; EARLY CHRONIC-PHASE; HIGH-DOSE IMATINIB
C1 [O'Brien, Susan] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Abboud, Camille N.] Washington Univ, Sch Med, St Louis, MO 63130 USA.
[Abboud, Camille N.] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO USA.
[Akhtari, Mojtaba] Nebraska Med Ctr, UNMC Eppley Canc Ctr, Omaha, NE USA.
[Altman, Jessica] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Berman, Ellin] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[Devine, Steven] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Fathi, Amir T.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Gotlib, Jason] Stanford Comprehens Canc Ctr, Stanford, CA USA.
[Jagasia, Madan] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Pinilla-Ibarz, Javier] Univ S Florida, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33620 USA.
[Radich, Jerald P.] Fred Hutchinson Canc Res Ctr, Seattle, WA USA.
[Reddy, Vishnu V. B.] Univ Alabama Birmingham, Ctr Comprehens Canc, Birmingham, AL USA.
[Shah, Neil P.] UCSF Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
[Shami, Paul J.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[Smith, B. Douglas] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
[Snyder, David S.] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Wetzler, Meir] Roswell Pk Canc Inst, Buffalo, NY USA.
[Yunus, Furhan] Univ Tennessee, Inst Canc, St Jude Childrens Res Hosp, Knoxville, TN 37996 USA.
RP O'Brien, S (reprint author), Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
OI Reddy, Vishnu/0000-0001-5474-3289
FU NCI NIH HHS [P30 CA016672]
NR 263
TC 9
Z9 11
U1 1
U2 5
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD JAN
PY 2012
VL 10
IS 1
BP 64
EP 110
PG 47
WC Oncology
SC Oncology
GA 875CL
UT WOS:000299007500009
PM 22223870
ER
PT J
AU Wright, CD
AF Wright, Cameron D.
TI Historical perspectives of The American Association for Thoracic
Surgery: Edward D. Churchill (1895-1972)
SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
LA English
DT Biographical-Item
C1 Massachusetts Gen Hosp, Dept Thorac Surg, Boston, MA 02114 USA.
RP Wright, CD (reprint author), Massachusetts Gen Hosp, Dept Thorac Surg, Blake 1570,55 Fruit St, Boston, MA 02114 USA.
EM wright.cameron@mgh.harvard.edu
NR 1
TC 0
Z9 0
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5223
J9 J THORAC CARDIOV SUR
JI J. Thorac. Cardiovasc. Surg.
PD JAN
PY 2012
VL 143
IS 1
BP 1
EP 3
DI 10.1016/j.jtcvs.2011.06.032
PG 3
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 863GW
UT WOS:000298151800005
PM 21820679
ER
PT J
AU Yarbrough, WM
Mukherjee, R
Stroud, RE
Rivers, WT
Oelsen, JM
Dixon, JA
Eckhouse, SR
Ikonomidis, JS
Zile, MR
Spinale, FG
AF Yarbrough, William M.
Mukherjee, Rupak
Stroud, Robert E.
Rivers, William T.
Oelsen, J. Marshall
Dixon, Jennifer A.
Eckhouse, Shaina R.
Ikonomidis, John S.
Zile, Michael R.
Spinale, Francis G.
TI Progressive induction of left ventricular pressure overload in a large
animal model elicits myocardial remodeling and a unique matrix signature
SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
LA English
DT Article; Proceedings Paper
CT 91st Annual Meeting of the American-Association-for-Thoracic-Surgery
CY MAY 07-11, 2011
CL Philadelphia, PA
SP Amer Assoc Thorac Surg
ID AORTIC-VALVE-REPLACEMENT; HEART-FAILURE; TISSUE INHIBITOR;
GENE-EXPRESSION; DIASTOLIC DYSFUNCTION; CARDIAC FIBROBLASTS; DEPENDENT
CHANGES; FIBROSIS; HYPERTROPHY; DISEASE
AB Objective: Patients with severe left ventricular pressure overload secondary to aortic stenosis can present with signs and symptoms of heart failure despite normal left ventricular ejection fraction. This process occurs, at least in part, as a result of left ventricular pressure overload-induced extracellular matrix remodeling that promulgates increased left ventricular stiffness and impaired diastolic function. However, the determinants that drive extracellular matrix remodeling in this form of left ventricular pressure overload remain to be fully defined.
Methods: Left ventricular pressure overload was induced in mature pigs (n = 15) by progressive ascending aortic cuff inflation (once per week for 4 weeks), whereby left ventricular mass, left ventricular ejection fraction, and regional myocardial stiffness (rK(m)) were compared with referent controls (n = 12). Determinants of extracellular matrix remodeling were assessed by measuring levels of mRNA expression for fibrillar collagens, matrix metalloproteinases, and tissue inhibitors of matrix metalloproteinase 1 and 4.
Results: With left ventricular pressure overload, left ventricular mass and rK(m) increased by 2- and 3-fold, respectively, compared with control, with no change in left ventricular ejection fraction. Left ventricular myocardial collagen increased approximately 2-fold, which was accompanied by reduced solubility (ie, increased cross-linking) with left ventricular pressure overload, but mRNA expression for fibrillar collagen and matrix metalloproteinases remained relatively unchanged. In contrast, a robust increase in mRNA expression for tissue inhibitors of matrix metalloproteinase-1 and 4 occurred with left ventricular pressure overload.
Conclusions: In a progressive model of left ventricular pressure overload, which recapitulates the phenotype of aortic stenosis, increased extracellular matrix accumulation and subsequently increased myocardial stiffness were not due to increased fibrillar collagen expression but rather to determinants of post-translational control that included increased collagen stability (thereby resistant to matrix metalloproteinase degradation) and increased endogenous matrix metalloproteinase inhibition. Targeting these extracellular matrix post-translational events with left ventricular pressure overload may hold both diagnostic and therapeutic relevance. (J Thorac Cardiovasc Surg 2012;143:215-23)
C1 [Spinale, Francis G.] Univ S Carolina, Sch Med, CBA, Cardiovasc Translat Res Ctr, Columbia, SC 29208 USA.
[Yarbrough, William M.] Sisters Char Providence Hosp, Columbia, SC USA.
[Zile, Michael R.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Mukherjee, Rupak; Stroud, Robert E.; Rivers, William T.; Oelsen, J. Marshall; Dixon, Jennifer A.; Eckhouse, Shaina R.; Ikonomidis, John S.; Spinale, Francis G.] Div Cardiothorac Surg & Adult Cardiol, Charleston, SC USA.
[Zile, Michael R.; Spinale, Francis G.] Ralph H Johnson Vet Adm Med Ctr, Charleston, SC USA.
RP Spinale, FG (reprint author), Univ S Carolina, Sch Med, CBA, Cardiovasc Translat Res Ctr, 6439 Garners Ferry Rd, Columbia, SC 29208 USA.
EM cvctrc@uscmed.sc.edu
FU NHLBI NIH HHS [R01 HL095608, T32 HL007260, HL059165, R01 HL059165-08,
R01 HL095608-03, R01 HL057952, HL057952, HL095608, R01 HL111090, R01
HL059165, R01 HL057952-12, HL 57952]
NR 32
TC 20
Z9 21
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5223
J9 J THORAC CARDIOV SUR
JI J. Thorac. Cardiovasc. Surg.
PD JAN
PY 2012
VL 143
IS 1
BP 215
EP 223
DI 10.1016/j.jtcvs.2011.09.032
PG 9
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 863GW
UT WOS:000298151800031
PM 22056365
ER
PT J
AU Ranasinghe, S
Flanders, M
Cutler, S
Soghoian, DZ
Ghebremichael, M
Davis, I
Lindqvist, M
Pereyra, F
Walker, BD
Heckerman, D
Streeck, H
AF Ranasinghe, Srinika
Flanders, Michael
Cutler, Sam
Soghoian, Damien Z.
Ghebremichael, Musie
Davis, Isaiah
Lindqvist, Madelene
Pereyra, Florencia
Walker, Bruce D.
Heckerman, David
Streeck, Hendrik
TI HIV-Specific CD4 T Cell Responses to Different Viral Proteins Have
Discordant Associations with Viral Load and Clinical Outcome
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID COMPREHENSIVE ANALYSIS; INFECTION; EPITOPES; GAG; INDIVIDUALS; HELP
AB A successful prophylactic vaccine is characterized by long-lived immunity, which is critically dependent on CD4 T cell-mediated helper signals. Indeed, most licensed vaccines induce antigen-specific CD4 T cell responses, in addition to high-affinity antibodies. However, despite the important role of CD4 T cells in vaccine design and natural infection, few studies have characterized HIV-specific CD4 T cells due to their preferential susceptibility to HIV infection. To establish at the population level the impact of HIV-specific CD4 T cells on viral control and define the specificity of HIV-specific CD4 T cell peptide targeting, we conducted a comprehensive analysis of these responses to the entire HIV proteome in 93 subjects at different stages of HIV infection. We show that HIV-specific CD4 T cell responses were detectable in 92% of individuals and that the breadth of these responses showed a significant inverse correlation with the viral load (P = 0.009, R = -0.31). In particular, CD4 T cell responses targeting Gag were robustly associated with lower levels of viremia (P = 0.0002, R = -0.45). Importantly, differences in the immunodominance profile of HIV-specific CD4 T cell responses distinguished HIV controllers from progressors. Furthermore, Gag/Env ratios were a potent marker of viral control, with a high frequency and magnitude of Gag responses and low proportion of Env responses associated with effective immune control. At the epitope level, targeting of three distinct Gag peptides was linked to spontaneous HIV control (P = 0.60 to 0.85). Inclusion of these immunogenic proteins and peptides in future HIV vaccines may act as a critical cornerstone for enhancing protective T cell responses.
C1 [Ranasinghe, Srinika; Flanders, Michael; Cutler, Sam; Soghoian, Damien Z.; Ghebremichael, Musie; Davis, Isaiah; Lindqvist, Madelene; Pereyra, Florencia; Walker, Bruce D.; Streeck, Hendrik] Massachusetts Gen Hosp, Ragon Inst MGH MIT & Harvard, Boston, MA 02114 USA.
[Ranasinghe, Srinika; Flanders, Michael; Cutler, Sam; Soghoian, Damien Z.; Ghebremichael, Musie; Davis, Isaiah; Lindqvist, Madelene; Pereyra, Florencia; Walker, Bruce D.; Streeck, Hendrik] Harvard Univ, Sch Med, Boston, MA USA.
[Walker, Bruce D.] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Heckerman, David] Microsoft Res, Redmond, WA USA.
RP Streeck, H (reprint author), Massachusetts Gen Hosp, Ragon Inst MGH MIT & Harvard, Boston, MA 02114 USA.
EM hstreeck@partners.org
FU National Institutes of Health [1R01AI091450-01, 1R01AI094602-01]; Bill
and Melinda Gates Foundation
FX This study was funded by the National Institutes of Health
(1R01AI091450-01 and 1R01AI094602-01) and the Bill and Melinda Gates
Foundation.
NR 28
TC 47
Z9 47
U1 0
U2 4
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD JAN
PY 2012
VL 86
IS 1
BP 277
EP 283
DI 10.1128/JVI.05577-11
PG 7
WC Virology
SC Virology
GA 865YV
UT WOS:000298347700026
PM 22031937
ER
PT J
AU Dehghan, S
Liu, EB
Seto, J
Torres, SF
Hudson, NR
Kajon, AE
Metzgar, D
Dyer, DW
Chodosh, J
Jones, MS
Seto, D
AF Dehghan, Shoaleh
Liu, Elizabeth B.
Seto, Jason
Torres, Sarah F.
Hudson, Nolan R.
Kajon, Adriana E.
Metzgar, David
Dyer, David W.
Chodosh, James
Jones, Morris S.
Seto, Donald
TI Five Genome Sequences of Subspecies B1 Human Adenoviruses Associated
with Acute Respiratory Disease
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID COMPUTATIONAL ANALYSIS; RECOMBINATION; INFECTION; GENE
AB Five genomes of human subspecies B1 adenoviruses isolated from cases of acute respiratory disease have been sequenced and archived for reference. These include representatives of two prevalent genomic variants of HAdV-7, i.e., HAdV-7h and HAdV7d2. The other three are HAdV-3/16, HAdV-16 strain E26, and HAdV-3+7 strain Takeuchi. All are recombinant genomes. Genomics and bioinformatics provide detailed views into the genetic makeup of these pathogens and insight into their molecular evolution. Retrospective characterization of particularly problematic older pathogens such as HAdV-7h (1987) and intriguing isolates such as HAdV-3+7 strain Takeuchi (1958) may provide clues to their phenotypes and serology and may suggest protocols for prevention and treatment.
C1 [Dehghan, Shoaleh; Liu, Elizabeth B.; Seto, Jason; Seto, Donald] George Mason Univ, Sch Syst Biol, Manassas, VA 20110 USA.
[Torres, Sarah F.; Hudson, Nolan R.] David Grant USAF Med Ctr, Clin Invest Facil, Travis AFB, CA 94535 USA.
[Kajon, Adriana E.] Lovelace Resp Res Inst, Albuquerque, NM 87108 USA.
[Metzgar, David] USN, Dept Resp Dis Res, Hlth Res Ctr, San Diego, CA 92106 USA.
[Dyer, David W.] Univ Oklahoma, Hlth Sci Ctr, Dept Microbiol & Immunol, Oklahoma City, OK 73104 USA.
[Chodosh, James] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Howe Lab, Boston, MA 02114 USA.
[Jones, Morris S.] Calif Dept Publ Hlth, Viral & Rickettsial Dis Lab, Richmond, CA 94804 USA.
RP Seto, D (reprint author), George Mason Univ, Sch Syst Biol, Manassas, VA 20110 USA.
EM dseto@gmu.edu
RI Valle, Ruben/A-7512-2013
FU U.S. Public Health Service NIH [EY013124, P30EY014104]; Research to
Prevent Blindness, Inc.
FX This work was supported in part by U.S. Public Health Service NIH grants
EY013124 (D. S., M.S.J., D. W. D., and J.C.) and P30EY014104 (J.C.).
J.C. is also funded by an unrestricted grant to the Department of
Ophthalmology, Harvard Medical School, from Research to Prevent
Blindness, Inc.
NR 13
TC 8
Z9 10
U1 0
U2 0
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD JAN
PY 2012
VL 86
IS 1
BP 635
EP 636
DI 10.1128/JVI.06593-11
PG 2
WC Virology
SC Virology
GA 865YV
UT WOS:000298347700066
PM 22158846
ER
PT J
AU He, JC
Chuang, PY
Ma'ayan, A
Iyengar, R
AF He, John Cijiang
Chuang, Peter Y.
Ma'ayan, Avi
Iyengar, Ravi
TI Systems biology of kidney diseases
SO KIDNEY INTERNATIONAL
LA English
DT Review
DE cell signaling; gene transcription; kidney disease; microarray analysis;
protein interaction
ID HUMAN DIABETIC-NEPHROPATHY; FOCAL SEGMENTAL GLOMERULOSCLEROSIS;
GENOME-WIDE ASSOCIATION; BLOOD-PRESSURE REGULATION; VEGF-A EXPRESSION;
GENE-EXPRESSION; PROTEOMIC ANALYSIS; AFRICAN-AMERICANS; HUMAN URINE;
3-DIMENSIONAL RECONSTRUCTION
AB Kidney diseases manifest in progressive loss of renal function, which ultimately leads to complete kidney failure. The mechanisms underlying the origins and progression of kidney diseases are not fully understood. Multiple factors involved in the pathogenesis of kidney diseases have made the traditional candidate gene approach of limited value toward full understanding of the molecular mechanisms of these diseases. A systems biology approach that integrates computational modeling with large-scale data gathering of the molecular changes could be useful in identifying the multiple interacting genes and their products that drive kidney diseases. Advances in biotechnology now make it possible to gather large data sets to characterize the role of the genome, epigenome, transcriptome, proteome, and metabolome in kidney diseases. When combined with computational analyses, these experimental approaches will provide a comprehensive understanding of the underlying biological processes. Multiscale analysis that connects the molecular interactions and cell biology of different kidney cells to renal physiology and pathology can be utilized to identify modules of biological and clinical importance that are perturbed in disease processes. This integration of experimental approaches and computational modeling is expected to generate new knowledge that can help to identify marker sets to guide the diagnosis, monitor disease progression, and identify new therapeutic targets. Kidney International (2012) 81, 22-39; doi:10.1038/ki.2011.314; published online 31 August 2011
C1 [He, John Cijiang] Mt Sinai Sch Med, Dept Med, Div Nephrol, New York, NY 10029 USA.
[He, John Cijiang; Ma'ayan, Avi; Iyengar, Ravi] Mt Sinai Sch Med, Dept Pharmacol & Syst Therapeut, New York, NY 10029 USA.
[He, John Cijiang] James J Peters VAMC, Dept Med, New York, NY USA.
[Ma'ayan, Avi; Iyengar, Ravi] Mt Sinai Sch Med, Syst Biol Ctr New York, New York, NY 10029 USA.
RP He, JC (reprint author), Mt Sinai Sch Med, Dept Med, Div Nephrol, 1 Gustave L Levy Pl, New York, NY 10029 USA.
EM cijiang.he@mssm.edu
FU NIH [1R01DK078897, 1R01DK088541, 1RC4DK090860, RC2LM010994-01,
5R01DK087650, 5K08DK082760]; Systems Biology Center [5P50GM071558]
FX JCH is supported by NIH 1R01DK078897 and VA Merit Award; JCH and AM are
supported by NIH 1R01DK088541 and 1RC4DK090860; AM is supported by NIH
RC2LM010994-01. RI and AM are supported by the Systems Biology Center
grant 5P50GM071558; RI and JCH are supported by NIH 5R01DK087650. PYC is
supported by NIH 5K08DK082760.
NR 127
TC 39
Z9 39
U1 0
U2 21
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
J9 KIDNEY INT
JI Kidney Int.
PD JAN
PY 2012
VL 81
IS 1
BP 22
EP 39
DI 10.1038/ki.2011.314
PG 18
WC Urology & Nephrology
SC Urology & Nephrology
GA 869XP
UT WOS:000298633600006
PM 21881558
ER
PT J
AU Berman, DM
Bosenberg, MW
Orwant, RL
Thurberg, BL
Draetta, GF
Fletcher, CDM
Loda, M
AF Berman, David M.
Bosenberg, Marcus W.
Orwant, Robin L.
Thurberg, Beth L.
Draetta, Gulio F.
Fletcher, Christopher D. M.
Loda, Massimo
TI Investigative pathology: leading the post-genomic revolution
SO LABORATORY INVESTIGATION
LA English
DT Article
DE career development; collaborative research; genomics; industry;
pathobiology; pharmaceuticals
ID BREAST-CANCER; MUTATIONS; CARCINOMAS; RECURRENCE; PATTERNS; REVEALS;
PATIENT; IMPACT; TUMORS; ASSAY
AB The completion of the Human Genome Project and the development of genome-based technologies over the past decade have set the stage for a new era of personalized medicine. By all rights, molecularly trained investigative pathologists should be leading this revolution. Singularly well suited for this work, molecular pathologists have the rare ability to wed genomic tools with unique diagnostic skills and tissue-based pathology techniques for integrated diagnosis of human disease. However, the number of pathologists with expertise in genome-based research has remained relatively low due to outdated training methods and a reluctance among some traditional pathologists to embrace new technologies. Moreover, because budding pathologists may not appreciate the vast selection of jobs available to them, they often end up choosing jobs that focus almost entirely on routine diagnosis rather than new frontiers in molecular pathology. This review calls for changes aimed at rectifying these troubling trends to ensure that pathology continues to guide patient care in a post-genomic era. Laboratory Investigation (2012) 92, 4-8; doi: 10.1038/labinvest.2011.147; published online 10 October 2011
C1 [Berman, David M.] Johns Hopkins Univ, Sch Med, Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21231 USA.
[Berman, David M.] Johns Hopkins Med Inst, Dept Oncol, Baltimore, MD 21205 USA.
[Berman, David M.] Johns Hopkins Med Inst, Dept Urol, Baltimore, MD 21205 USA.
[Bosenberg, Marcus W.] Yale Univ, Sch Med, Dept Dermatol, New Haven, CT 06510 USA.
[Draetta, Gulio F.] Dana Farber Canc Inst, Belfer Inst Appl Canc Sci, Boston, MA 02115 USA.
[Thurberg, Beth L.] Genzyme Corp, Dept Pathol, Framingham, MA 01701 USA.
[Fletcher, Christopher D. M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Loda, Massimo] Harvard Univ, Brigham & Womens Hosp, Sch Med,Dept Pathol, Ctr Mol Oncol Pathol,Dana Farber Canc Inst, Boston, MA 02115 USA.
[Loda, Massimo] Harvard Univ, Brigham & Womens Hosp, Sch Med,Dept Med Oncol, Ctr Mol Oncol Pathol,Dana Farber Canc Inst, Boston, MA 02115 USA.
[Loda, Massimo] Broad Inst Harvard & MIT, Cambridge, MA USA.
[Loda, Massimo] Kings Coll London, Div Canc Studies, London WC2R 2LS, England.
RP Berman, DM (reprint author), Johns Hopkins Univ, Sch Med, Johns Hopkins Med Inst, Dept Pathol, 1550 Orleans St,CRB2 Room 545, Baltimore, MD 21231 USA.
EM dberman@jhmi.edu
FU National Institutes of Health [RO1DK072000, R01CA131945]; Prostate
Cancer Foundation
FX We thank the journal's reviewers for insightful and significant
contributions to the manuscript. We also gratefully acknowledge the
USCAP Education Committee, including Dr J Goldblum and Dr D Huntsman,
for hosting a course on investigative pathology careers, which formed
the basis of this review. Finally, we thank our financial supporters:
the National Institutes of Health (RO1DK072000 and R01CA131945) and the
Prostate Cancer Foundation.
NR 23
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Z9 14
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD JAN
PY 2012
VL 92
IS 1
BP 4
EP 8
DI 10.1038/labinvest.2011.147
PG 5
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 871MZ
UT WOS:000298743600001
PM 21986811
ER
PT J
AU Barchue, SM
AF Barchue, Sylvia M.
TI Should Children Visit Patients in an Intensive Care Unit (ICU)?
SO MCN-THE AMERICAN JOURNAL OF MATERNAL-CHILD NURSING
LA English
DT Editorial Material
C1 James J Peters VA Med Ctr, Patient Care Ctr, Med Surg Units, ICU,ED & Pulm Care, Bronx, NY USA.
RP Barchue, SM (reprint author), James J Peters VA Med Ctr, Patient Care Ctr, Med Surg Units, ICU,ED & Pulm Care, Bronx, NY USA.
NR 3
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0361-929X
J9 MCN-AM J MATERN-CHIL
JI MCN-Am. J. Matern.-Child Nurs.
PD JAN-FEB
PY 2012
VL 37
IS 1
BP 8
EP 8
PG 1
WC Nursing
SC Nursing
GA 864OR
UT WOS:000298250000002
ER
PT J
AU Morgan, A
AF Morgan, Aneita
TI Coordinated by Kathleen Leask Capitulo, DNSc, RN, FAAN
SO MCN-THE AMERICAN JOURNAL OF MATERNAL-CHILD NURSING
LA English
DT Editorial Material
C1 James J Peters VA Med Ctr, Clin Care Team, Intens Care Unit, Bronx, NY USA.
RP Morgan, A (reprint author), James J Peters VA Med Ctr, Clin Care Team, Intens Care Unit, Bronx, NY USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0361-929X
J9 MCN-AM J MATERN-CHIL
JI MCN-Am. J. Matern.-Child Nurs.
PD JAN-FEB
PY 2012
VL 37
IS 1
BP 9
EP 9
PG 1
WC Nursing
SC Nursing
GA 864OR
UT WOS:000298250000003
ER
PT J
AU Epstein, AJ
Ketcham, JD
Rathore, SS
Groeneveld, PW
AF Epstein, Andrew J.
Ketcham, Jonathan D.
Rathore, Saif S.
Groeneveld, Peter W.
TI Variations in the Use of an Innovative Technology by Payer The Case of
Drug-Eluting Stents
SO MEDICAL CARE
LA English
DT Article
DE variations in care; technology; access
ID ACUTE CORONARY SYNDROMES; HEALTH-CARE COSTS; INSURANCE TYPE; OUTCOMES;
CLOPIDOGREL; PREDICTORS; REGISTRY; THERAPY; ARTERY
AB Background: Despite receiving identical reimbursement for treating heart disease patients with bare metal stents (BMS) or drug-eluting coronary stents (DES), cardiologists' use of the new technology (DES) may have varied by patient payer type as DES diffused. Payer-related factors that differ between hospitals and/or differential treatment inside hospitals might explain any overall differences by payer type.
Objectives: To assess the association between payer and DES use and to examine between-hospital and within-hospital variation in DES use over time.
Methods: We conducted a retrospective analysis of 4.1 million hospitalizations involving DES or BMS from 2003 to 2008 Nationwide Inpatient Sample. We estimated hybrid-fixed effects logit models and calculated the adjusted within-quarter, cross-payer differences in DES use.
Results: Coronary stent patients with Medicaid or without insurance were significantly less likely to receive DES than were patients with private insurance throughout the study period. The differences fluctuated over time as the popularity of DES relative to BMS increased and decreased. The within-hospital gaps paralleled the overall differences, and were largest in Q3 2003 (Medicaid: 11.9, uninsured: 10.9% points) and Q4 2008 (Medicaid: 12.8, uninsured: 20.7% points), and smallest in Q4 2004 (Medicaid: 1.4, uninsured: 1.1% points). The between-hospital adjusted differences in DES use by payer were small and rarely significant.
Conclusions: We found substantial differences in DES use by payer within hospitals, suggesting physicians selected the new technology for patients in a manner associated with patients' payer type.
C1 [Epstein, Andrew J.; Groeneveld, Peter W.] Univ Penn, Sch Med, Dept Med, Div Gen Internal Med, Philadelphia, PA 19104 USA.
[Epstein, Andrew J.] Philadelphia Vet Affairs Med Ctr, Dept Vet Affairs, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
[Epstein, Andrew J.; Groeneveld, Peter W.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Ketcham, Jonathan D.] Arizona State Univ, WP Carey Sch Business, Dept Mkt, Tempe, AZ USA.
[Rathore, Saif S.] Yale Univ, Sch Med, MD PhD Program, New Haven, CT USA.
RP Epstein, AJ (reprint author), Univ Penn, Sch Med, Dept Med, Div Gen Internal Med, 423 Guardian Dr,11th Floor, Philadelphia, PA 19104 USA.
EM eandrew@mail.med.upenn.edu
FU National Heart, Lung, and Blood Institute [1R01HL086919]; Agency for
Healthcare Research and Quality [1R01HS018403]
FX This research was supported by the National Heart, Lung, and Blood
Institute (1R01HL086919) and by the Agency for Healthcare Research and
Quality (1R01HS018403). The content of this study does not reflect the
views of the VA or the United States government.
NR 38
TC 8
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U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD JAN
PY 2012
VL 50
IS 1
BP 1
EP 9
DI 10.1097/MLR.0b013e31822d5de9
PG 9
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 863IY
UT WOS:000298157200001
PM 22167062
ER
PT J
AU Epstein, AJ
Polsky, D
Yang, FF
Yang, L
Groeneveld, PW
AF Epstein, Andrew J.
Polsky, Daniel
Yang, Feifei
Yang, Lin
Groeneveld, Peter W.
TI Geographic Variation in Implantable Cardioverter-Defibrillator Use and
Heart Failure Survival
SO MEDICAL CARE
LA English
DT Article
DE cardiovascular disease; congestive heart failure; health care
technology; mortality; utilization
ID CARDIAC RESYNCHRONIZATION THERAPY; PROPHYLACTIC IMPLANTATION; PRIMARY
PREVENTION; PROPENSITY SCORE; COMORBIDITY; DYSFUNCTION; COMMUNITY
AB Background: Implantable cardioverter-defibrillators and cardiac resynchronization therapy-defibrillators (ICD/CRT-Ds) are evidence-based preventative treatments for many patients with heart failure (HF), yet large numbers of eligible patients remain untreated. It is uncertain if localities with more frequent ICD/CRT-D use have had better rates of HF survival.
Objectives: To determine if US Hospital Referral Regions (HRRs) with larger increases in the rate of ICD/CRT-D utilization during 2002 to 2007 also had commensurate increases in HF survival.
Research Design: Retrospective cohort.
Participants: Medicare beneficiaries age 66 to 80 nonelectively hospitalized for HF from 2002 to 2007.
Measures: Each HRR's annual ICD/CRT-D rate was estimated from the cohort's Medicare procedure claims. Survival duration was determined from Medicare mortality records. HRR-year-level panel regression models were estimated to assess whether an HRR's ICD/CRT-D rate predicted HF survival, adjusting for baseline differences in survival across HRRs and secular trends.
Results: A total of 883,002 HF patients were propensity-score matched within HRR across 2002 to 2007. Across HRRs, growth in ICD/CRT-D use among such patients varied from 1 to 12 percentage points. Regression models indicated that a 1 percentage point increase in an HRR's ICD/CRT-D utilization among hospitalized HF patients was associated with an increase in 1-year survival of 0.12% [95% confidence interval (CI), 0.03%-0.21%, P = 0.009] and with a 0.26% increase in HF survival at 2 years (95% CI, 0.14%-0.37%, P < 0.001).
Conclusions: Localities with greater increases in ICD/CRT-D utilization from 2002 to 2007 also had greater improvements in HF survival. Areas with persistently low ICD/CRT-D use may be good targets for programs designed to increase the evidence-based use of defibrillators.
C1 [Epstein, Andrew J.; Groeneveld, Peter W.] Philadelphia Vet Affairs Med Ctr, Ctr Hlth Equ Res & Promot, Dept Vet Affairs, Philadelphia, PA USA.
[Epstein, Andrew J.; Polsky, Daniel; Yang, Feifei; Yang, Lin; Groeneveld, Peter W.] Univ Penn, Sch Med, Dept Med, Div Gen Internal Med, Philadelphia, PA 19104 USA.
[Epstein, Andrew J.; Polsky, Daniel; Groeneveld, Peter W.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
RP Groeneveld, PW (reprint author), 1229 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM petergro@mail.med.upenn.edu
FU National Heart, Lung, and Blood Institute [1R01HL086919]; Agency for
Healthcare Research and Quality [1R01HS018403]; Department of Veterans
Affairs' Health Services Research and Development Service, Washington,
DC; Pennsylvania Department of Health
FX Supported by the National Heart, Lung, and Blood Institute
(1R01HL086919) and by the Agency for Healthcare Research and Quality
(1R01HS018403). Dr Groeneveld was additionally supported by a Career
Development Transition Award from the Department of Veterans Affairs'
Health Services Research and Development Service, Washington, DC. This
project was also funded, in part, under a grant from the Pennsylvania
Department of Health, which specifically disclaims responsibility for
any analyses, interpretations, or conclusions.
NR 27
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U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD JAN
PY 2012
VL 50
IS 1
BP 10
EP 17
DI 10.1097/MLR.0b013e3182293510
PG 8
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 863IY
UT WOS:000298157200002
PM 22167063
ER
PT J
AU Keyhani, S
Arling, G
Williams, LS
Ross, JS
Ordin, DL
Myers, J
Tyndall, G
Vogel, B
Bravata, DM
AF Keyhani, Salomeh
Arling, Greg
Williams, Linda S.
Ross, Joseph S.
Ordin, Diana L.
Myers, Jennifer
Tyndall, Gary
Vogel, Bruce
Bravata, Dawn M.
TI The Use and Misuse of Thrombolytic Therapy Within the Veterans Health
Administration
SO MEDICAL CARE
LA English
DT Article
DE stroke; thrombolytic therapy; health services research
ID ACUTE ISCHEMIC-STROKE; TISSUE-PLASMINOGEN ACTIVATOR; QUALITY-OF-CARE;
ASSOCIATION; IMPROVEMENT; GUIDELINES; CENTERS; SYSTEM; ATTACK
AB Background: Within the Veterans Health Administration (VHA), approximately 6000 veterans are hospitalized with acute ischemic stroke annually. We examined the use and misuse of thrombolytic therapy with tissue plasminogen activator (tPA) in a national sample of veterans who were admitted to a VHA Medical Center (VAMC) with acute ischemic stroke.
Methods: Medical record reviews were conducted on 5000 acute stroke patients who were admitted to a VAMC in 2007. Patients were defined as eligible to receive tPA if they arrived at the hospital within 3 hours of stroke symptom onset and had no contra-indications to tPA. We compared eligible patients who received tPA to those who did not and examined the distribution of eligible patients across the 129 VAMCs included in this study.
Results: Among the 3931 ischemic stroke patients, 174 (4.4%) were eligible for tPA. Among the 135 patients who arrived within 2 hours of symptom onset which allowed adequate time for testing and evaluation, 19 (14.1%) received tPA. An additional 11 patients received tPA but did not meet eligibility criteria. Eligible patients receiving tPA were similar to eligible patients not receiving tPA in terms of clinical conditions and time to brain imaging. Among the 30 patients that received tPA, 5 (16.6%) received the wrong dose. Among the 85 VAMCs that received Z1 eligible patient, on average 2.3 patients were eligible for tPA annually.
Conclusions: Relatively few eligible veterans receive thrombolysis across the VHA system. Strategies to improve thrombolysis delivery will have to account for the low annual volume of eligible stroke patients cared for at individual VAMCs.
C1 [Keyhani, Salomeh] Univ Calif San Francisco, Dept Vet Affairs VHA, Hlth Serv Res & Dev Serv HSR&D, REAP, San Francisco, CA 94143 USA.
[Keyhani, Salomeh] Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA.
[Keyhani, Salomeh; Williams, Linda S.; Ordin, Diana L.; Myers, Jennifer; Vogel, Bruce; Bravata, Dawn M.] VHA HSR&D Stroke Qual Enhancement Res Initiat QUE, Indianapolis, IN USA.
[Arling, Greg] Indiana Univ Sch Med, Indiana Univ Ctr Aging Res, Indianapolis, IN USA.
[Arling, Greg; Williams, Linda S.; Bravata, Dawn M.] Regenstrief Inst Hlth Care, Indianapolis, IN USA.
[Williams, Linda S.; Myers, Jennifer; Bravata, Dawn M.] Richard L Roudebush VA Med Ctr, VHA HSR&D Ctr Excellence Implementing Evidence Ba, Indianapolis, IN USA.
[Williams, Linda S.] Indiana Univ Sch Med, Dept Neurol, Indianapolis, IN USA.
[Ross, Joseph S.] Yale Univ, Sch Med, Washington, DC USA.
[Ordin, Diana L.] VHA Off Qual & Performance OQP, Washington, DC USA.
[Tyndall, Gary] Syracuse VA Med Ctr, Emergency Dept, Syracuse, NY USA.
[Vogel, Bruce] N Florida S Georgia Vet Hlth Syst, VHA Rehabil Outcomes Res Ctr RORC, Gainesville, FL USA.
[Bravata, Dawn M.] Indiana Univ Sch Med, Dept Internal Med, Indianapolis, IN USA.
RP Keyhani, S (reprint author), San Francisco VA Med Ctr, 4150 Clement,111A1, San Francisco, CA 94121 USA.
EM salomeh.keyhani@va.gov
OI Tyndall, Gary/0000-0001-9984-4809
FU Department of Veterans Affairs; Veterans Health Administration (VHA);
Office of Quality and Performance and Health Services Research and
Development Service Quality Enhancement Research Initiative [RRP
09-184]; VA HSRD
FX The project reported here was supported by the Department of Veterans
Affairs, Veterans Health Administration (VHA), Office of Quality and
Performance and Health Services Research and Development Service Quality
Enhancement Research Initiative (RRP 09-184). Dr. Keyhani is also
supported by a VA HSR&D Career Development Award.
NR 25
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U1 2
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD JAN
PY 2012
VL 50
IS 1
BP 66
EP 73
DI 10.1097/MLR.0b013e3182294092
PG 8
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 863IY
UT WOS:000298157200009
PM 22182924
ER
PT J
AU Rosen, AK
Itani, KMF
Cevasco, M
Kaafarani, HMA
Hanchate, A
Shin, M
Shwartz, M
Loveland, S
Chen, Q
Borzecki, A
AF Rosen, Amy K.
Itani, Kamal M. F.
Cevasco, Marisa
Kaafarani, Haytham M. A.
Hanchate, Amresh
Shin, Marlena
Shwartz, Michael
Loveland, Susan
Chen, Qi
Borzecki, Ann
TI Validating the Patient Safety Indicators in the Veterans Health
Administration Do They Accurately Identify True Safety Events?
SO MEDICAL CARE
LA English
DT Article
DE patient safety; ICD-9-CM coding; criterion validation; adverse events;
administrative data
ID POSITIVE PREDICTIVE-VALUE; POSTOPERATIVE HEMORRHAGE; ADVERSE EVENTS;
CARE RESEARCH; VALIDITY; HOSPITALS; HEMATOMA; TRAUMA; AGENCY; RATES
AB Background: The Agency for Healthcare Research and Quality (AHRQ) Patient Safety Indicators (PSIs) use administrative data to detect potentially preventable in-hospital adverse events. However, few studies have determined how accurately the PSIs identify true safety events.
Objectives: We examined the criterion validity, specifically the positive predictive value (PPV), of 12 selected PSIs using clinical data abstracted from the Veterans Health Administration (VA) electronic medical record as the gold standard.
Methods: We identified PSI-flagged cases from 28 representative hospitals by applying the AHRQ PSI software (v.3.1a) to VA fiscal year 2003 to 2007 administrative data. Trained nurse-abstractors used standardized abstraction tools to review a random sample of flagged medical records (112 records per PSI) for the presence of true adverse events. Interrater reliability was assessed. We evaluated PPVs and associated 95% confidence intervals of each PSI and examined false positive (FP) cases to determine why they were incorrectly flagged and gain insight into how each PSI might be improved.
Results: PPVs ranged from 28% (95% CI, 15%-43%) for Postoperative Hip Fracture to 87% (95% CI, 79%-92%) for Postoperative Wound Dehiscence. Common reasons for FPs included conditions that were present on admission (POA), coding errors, and lack of coding specificity. PSIs with the lowest PPVs had the highest proportion of FPs owing to POA.
Conclusions: Overall, PPVs were moderate for most of the PSIs. Implementing POA codes and using more specific ICD-9-CM codes would improve their validity. Our results suggest that additional coding improvements are needed before the PSIs evaluated herein are used for hospital reporting or pay for performance.
C1 [Rosen, Amy K.; Hanchate, Amresh; Shin, Marlena; Shwartz, Michael; Loveland, Susan; Chen, Qi] VA Boston Healthcare Syst, COLMR, Boston, MA 02130 USA.
[Rosen, Amy K.; Chen, Qi; Borzecki, Ann] Boston Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA USA.
[Rosen, Amy K.; Itani, Kamal M. F.; Hanchate, Amresh; Borzecki, Ann] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Itani, Kamal M. F.; Cevasco, Marisa] VA Boston Healthcare Syst, Dept Surg, Boston, MA 02130 USA.
[Itani, Kamal M. F.] Harvard Univ, Sch Med, Boston, MA USA.
[Cevasco, Marisa] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Kaafarani, Haytham M. A.] Tufts Med Ctr, Dept Surg, Boston, MA USA.
[Kaafarani, Haytham M. A.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Shwartz, Michael] Boston Univ, Sch Management, Dept Operat & Technol Management, Boston, MA 02215 USA.
[Borzecki, Ann] Bedford VAMC, Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA USA.
RP Rosen, AK (reprint author), VA Boston Healthcare Syst, COLMR, 150 S Huntington Ave,152 M, Boston, MA 02130 USA.
EM akrosen@bu.edu
OI Hanchate, Amresh/0000-0002-7038-4463
FU VA [HSRD SDR-07-002]
FX Supported by VA grant HSR&D SDR-07-002.
NR 50
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U1 2
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD JAN
PY 2012
VL 50
IS 1
BP 74
EP 85
DI 10.1097/MLR.0b013e3182293edf
PG 12
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 863IY
UT WOS:000298157200010
PM 21993057
ER
PT J
AU Lin, WC
Chien, HL
Willis, G
O'Connell, E
Rennie, KS
Bottella, HM
Ferris, TG
AF Lin, Wen-Chieh
Chien, Hung-Lun
Willis, Georgianna
O'Connell, Elizabeth
Rennie, Kate Staunton
Bottella, Heather M.
Ferris, Timothy G.
TI The Effect of a Telephone-based Health Coaching Disease Management
Program on Medicaid Members With Chronic Conditions
SO MEDICAL CARE
LA English
DT Article
DE disease management; chronic condition; Medicaid;
difference-in-differences
ID CARE UTILIZATION; HEART-FAILURE; BENEFICIARIES; DISORDERS; QUALITY;
IMPACT; EXPENDITURES; DEPRESSION; ASTHMA; COSTS
AB Background: Despite the growing popularity of disease management programs for chronic conditions, evidence regarding the effect of these programs has been mixed. In addition, few peer-reviewed studies have examined the effect of these programs on publicly insured populations.
Objectives: To examine the effect of a telephone-based health coaching disease management program on healthcare utilization and expenditures in Medicaid members with chronic conditions.
Research Design: Using a difference-in-differences analysis, we examined changes in hospitalizations, emergency department (ED) visits, ambulatory care visits, and Medicaid expenditures among program members for 1 year before and 2 years after their enrollment compared with a matched comparison group.
Subjects: Medicaid members aged 18 to 64 with a diagnosis of qualifying chronic conditions and 2 acute health service events of hospitalizations and/or ED visits within a 12-month period.
Results: Changes in acute hospitalizations, ambulatory care visits, and Medicaid expenditures before and after program enrollment were similar between the 2 study groups. However, during the second year after enrollment, program members had a significantly smaller decrease in ED visits than the comparisons (8% in program members and 23% in comparisons, P value = 0.03).
Conclusions: Compared with a matched comparison group, the telephone-based health coaching disease management program did not demonstrate significant effects on healthcare utilization and expenditures in Medicaid members with chronic conditions.
C1 [Lin, Wen-Chieh; Chien, Hung-Lun; Willis, Georgianna; O'Connell, Elizabeth] Univ Massachusetts, Sch Med, Ctr Hlth Policy & Res, Shrewsbury, MA 01545 USA.
[Lin, Wen-Chieh] Univ Massachusetts, Sch Med, Dept Family Med & Community Hlth, Worcester, MA USA.
[Rennie, Kate Staunton] Massachusetts Execut Off Hlth & Human Serv, MassHlth Off Acute & Ambulatory Care, Boston, MA USA.
[Bottella, Heather M.] Humana, Louisville, KY USA.
[Ferris, Timothy G.] Mass Gen Hosp, Mongan Inst Hlth Policy, Boston, MA USA.
RP Lin, WC (reprint author), Univ Massachusetts, Sch Med, Ctr Hlth Policy & Res, 333 South St, Shrewsbury, MA 01545 USA.
EM wen.lin@umassmed.edu
NR 26
TC 15
Z9 16
U1 5
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
EI 1537-1948
J9 MED CARE
JI Med. Care
PD JAN
PY 2012
VL 50
IS 1
BP 91
EP 98
DI 10.1097/MLR.0b013e31822dcedf
PG 8
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 863IY
UT WOS:000298157200012
PM 21993059
ER
PT J
AU Teal, CR
Gill, AC
Green, AR
Crandall, S
AF Teal, Cayla R.
Gill, Anne C.
Green, Alexander R.
Crandall, Sonia
TI Helping medical learners recognise and manage unconscious bias toward
certain patient groups
SO MEDICAL EDUCATION
LA English
DT Article
ID IMPLICIT ASSOCIATION TEST; DIAGNOSTIC ERROR; CULTURAL COMPETENCE;
PROVIDERS CONTRIBUTE; COGNITIVE-PSYCHOLOGY; AVERSIVE RACISM; CARE;
HEALTH; DISPARITIES; STUDENTS
AB CONTEXT For the last 30 years, developments in cognitive sciences have demonstrated that human behaviour, beliefs and attitudes are shaped by automatic and unconscious cognitive processes. Only recently has much attention been paid to how unconscious biases based on certain patient characteristics may: (i) result in behaviour that is preferential toward or against specific patients; (ii) influence treatment decisions, and (iii) adversely influence the patient-doctor relationship. Partly in response to accreditation requirements, medical educators are now exploring how they might help students and residents to develop awareness of their own potential biases and strategies to mitigate them.
METHODS In this paper, we briefly review key cognition concepts and describe the limited published literature about educational strategies for addressing unconscious bias.
DISCUSSION We propose a developmental model to illustrate how individuals might move from absolute denial of unconscious bias to the integration of strategies to mitigate its influence on their interactions with patients and offer recommendations to educators and education researchers.
C1 [Teal, Cayla R.; Gill, Anne C.] Baylor Coll Med, Off Undergrad Med Educ, Houston, TX 77030 USA.
[Teal, Cayla R.] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Gill, Anne C.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
[Gill, Anne C.] Baylor Coll Med, Dept Med Eth, Houston, TX 77030 USA.
[Green, Alexander R.] Massachusetts Gen Hosp, Dispar Solut Ctr, Boston, MA 02114 USA.
[Green, Alexander R.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Crandall, Sonia] Wake Forest Sch Med, Dept Family & Community Med, Winston Salem, NC USA.
[Crandall, Sonia] Wake Forest Sch Med, Dept Phys Assistant Studies, Winston Salem, NC USA.
RP Teal, CR (reprint author), Baylor Coll Med, Off Undergrad Med Educ, 1 Baylor Plaza,MS BCM300, Houston, TX 77030 USA.
EM cteal@bcm.edu
NR 59
TC 30
Z9 30
U1 3
U2 29
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0308-0110
J9 MED EDUC
JI Med. Educ.
PD JAN
PY 2012
VL 46
IS 1
BP 80
EP 88
DI 10.1111/j.1365-2923.2011.04101.x
PG 9
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA 862KV
UT WOS:000298090500014
PM 22150199
ER
PT J
AU Ngwa, W
Makrigiorgos, GM
Berbeco, RI
AF Ngwa, Wilfred
Makrigiorgos, G. Mike
Berbeco, Ross I.
TI Gold nanoparticle-aided brachytherapy with vascular dose painting:
Estimation of dose enhancement to the tumor endothelial cell nucleus
SO MEDICAL PHYSICS
LA English
DT Article
DE brachytherapy; gold nanoparticles; vascular disrupting agents; dose
enhancement
ID RADIATION RESPONSE; DISRUPTING AGENTS; SOLID TUMORS; IN-VIVO; THERAPY;
SIZE; SURFACE; CANCER; ENERGY; RADIOTHERAPY
AB Purpose: Theoretical microdosimetry at the subcellular level is employed in this study to estimate the dose enhancement to tumor endothelial cell nuclei, caused by radiation-induced photo/Auger electrons originating from gold nanoparticles (AuNPs) targeting the tumor endothelium, during brachytherapy.
Methods: A tumor vascular endothelial cell (EC) is modeled as a slab of 2 mu m (thickness) x 10 mu m (length) x 10 mu m (width). The EC contains a nucleus of 5 mu m diameter and thickness of 0.5-1 mu m, corresponding to nucleus size 5%-10% of cellular volume, respectively. Analytic calculations based on the electron energy loss formula of Cole were carried out to estimate the dose enhancement to the nucleus caused by photo/Auger electrons from AuNPs attached to the exterior surface of the EC. The nucleus dose enhancement factor (nDEF), representing the ratio of the dose to the nucleus with and without the presence of gold nanoparticles was calculated for different AuNP local concentrations. The investigated concentration range considers the potential for significantly higher local concentration near the EC due to preferential accumulation of AuNP in the tumor vasculature. Four brachytherapy sources: I-125, Pd-103, Yb-169, and 50 kVp x-rays were investigated.
Results: For nucleus size of 10% of the cellular volume and AuNP concentrations ranging from 7 to 140 mg/g, brachytherapy sources Pd-103, I-125, 50 kVp, and Yb-169 yielded nDEF values of 5.6-73, 4.8-58.3, 4.7-56.6, and 3.2-25.8, respectively. Meanwhile, for nucleus size 5% of the cellular volume in the same concentration range, Pd-103, I-125, 50 kVp, and Yb-169 yielded nDEF values of 6.9-79.2, 5.1-63.2, 5.0-61.5, and 3.3-28.3, respectively.
Conclusions: The results predict that a substantial dose boost to the nucleus of endothelial cells can be achieved by applying tumor vasculature-targeted AuNPs in combination with brachytherapy. Such vascular dose boosts could induce tumor vascular shutdown, prompting extensive tumor cell death. (C) 2012 American Association of Physicists in Medicine. [DOI: 10.1118/1.3671905]
C1 [Ngwa, Wilfred] Brigham & Womens Hosp, Dana Farber Canc Inst, Div Med Phys & Biophys, Dept Radiat Oncol, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Ngwa, W (reprint author), Brigham & Womens Hosp, Dana Farber Canc Inst, Div Med Phys & Biophys, Dept Radiat Oncol, 75 Francis St, Boston, MA 02115 USA.
EM wngwa@lroc.harvard.edu
NR 55
TC 24
Z9 25
U1 3
U2 14
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD JAN
PY 2012
VL 39
IS 1
BP 392
EP 398
DI 10.1118/1.3671905
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 872LX
UT WOS:000298812200041
PM 22225308
ER
PT J
AU Khosroshahi, A
Carruthers, MN
Deshpande, V
Unizony, S
Bloch, DB
Stone, JH
AF Khosroshahi, Arezou
Carruthers, Mollie N.
Deshpande, Vikram
Unizony, Sebastian
Bloch, Donald B.
Stone, John H.
TI Rituximab for the Treatment of IgG4-Related Disease Lessons From 10
Consecutive Patients
SO MEDICINE
LA English
DT Article
ID AUTOIMMUNE PANCREATITIS; SYSTEMIC-DISEASE; SCLEROSING DISEASE;
CLINICOPATHOLOGICAL-ENTITY; RHEUMATOID-ARTHRITIS; THERAPY; FEATURES;
AZATHIOPRINE; SAFETY
AB Patients with IgG4-related disease (IgG4-RD) typically have elevated serum concentrations of IgG4 and share histopathologic features that are similar across affected organ(s). IgG4-RD patients frequently require prolonged treatment with glucocorticoids and are often unable to taper these medications. Traditional disease-modifying antirheumatic drugs (DMARDs) are generally ineffective. We assessed the clinical and serologic responses to B lymphocyte depletion therapy in 10 consecutive patients with steroid-and DMARD-refractory IgG4-RD.
Ten patients with IgG4-RD were treated with rituximab (RTX) (2 infusions of 1000 mg, 15 days apart). Clinical improvement was assessed by monitoring the patient's ability to taper prednisone to discontinuation and to stop DMARDs; by serial measurements of total IgG and IgG subclasses; and by follow-up radiologic assessments guided by the patient's particular pattern of organ involvement. We also developed and retrospectively applied the IgG4-RD Disease Activity Index and Flare Tool.
Organ involvement included the pancreas, biliary tree, aorta, salivary glands (submandibular and parotid), lacrimal glands, lymph nodes, thyroid gland, and retroperitoneum. Nine of 10 patients demonstrated striking clinical improvement within 1 month of starting RTX. One patient with advanced thyroid fibrosis associated with Riedel thyroiditis and a history of disease in multiple other organ systems did not have improvement in the thyroid gland, but the disease did not progress to involve new organs. All 10 patients were able to discontinue prednisone and DMARDs following RTX therapy. Significant decreases in IgG concentrations were observed for the IgG4 subclass only. Four patients were re-treated with RTX after 6 months because of either symptom recurrence and increasing IgG4 concentration at the time of peripheral B cell reconstitution (n = 2) or because of physician discretion (n = 2). Repeated courses of RTX maintained their effectiveness and resulted in further decreases in IgG4 concentrations. In patients who had an increased IgG4 concentration at the time of presentation, the level of serum IgG4 appeared to be a reliable measure of disease activity.
IgG4-RD is an idiopathic, multiorgan inflammatory disease in which diverse organ manifestations are linked by characteristic histopathologic and immunohistochemical features. Treatment with RTX led to prompt clinical and serologic improvement in refractory IgG4-RD in all patients with active inflammation. Serial treatments with RTX may lead to progressive declines in serum IgG4 concentrations and better disease control. Serum IgG4 concentrations may remain low, and clinical disease activity may remain quiescent even after B cell reconstitution in a significant proportion of patients.
C1 [Khosroshahi, Arezou; Carruthers, Mollie N.; Unizony, Sebastian; Bloch, Donald B.; Stone, John H.] Massachusetts Gen Hosp, Rheumatol Unit, Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA.
[Deshpande, Vikram] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Stone, JH (reprint author), Massachusetts Gen Hosp, Rheumatol Unit, Div Rheumatol Allergy & Immunol, 55 Fruit St, Boston, MA 02114 USA.
EM jhstone@partners.org
FU Genentech
FX Dr. Deshpande has served as a consultant for Chugai Pharmaceutical. Dr.
Stone has served as a consultant and his institution has a grant pending
with Genentech. The other authors declare no funding or conflicts of
interest.
NR 35
TC 178
Z9 195
U1 1
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7974
J9 MEDICINE
JI Medicine (Baltimore)
PD JAN
PY 2012
VL 91
IS 1
BP 57
EP 66
DI 10.1097/MD.0b013e3182431ef6
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 873CD
UT WOS:000298857600007
PM 22210556
ER
PT J
AU Tracy, EE
Speakman, E
AF Tracy, Erin E.
Speakman, Elizabeth
TI Intimate partner violence: not just a concern of the reproductive ages
SO MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY
LA English
DT Editorial Material
ID WOMEN; FAMILY; ABUSE
C1 [Tracy, Erin E.; Speakman, Elizabeth] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Tracy, EE (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 18
TC 3
Z9 3
U1 2
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1072-3714
J9 MENOPAUSE
JI Menopause-J. N. Am. Menopause Soc.
PD JAN
PY 2012
VL 19
IS 1
BP 3
EP 5
DI 10.1097/gme.0b013e318239c985
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 870IJ
UT WOS:000298662300002
PM 22198633
ER
PT J
AU Sugita, M
Sugita, H
Kim, M
Mao, J
Yasuda, Y
Habiro, M
Shinozaki, S
Yasuhara, S
Shimizu, N
Martyn, JAJ
Kaneki, M
AF Sugita, Michiko
Sugita, Hiroki
Kim, Minhye
Mao, Ji
Yasuda, Yoshikazu
Habiro, Mayu
Shinozaki, Shohei
Yasuhara, Shingo
Shimizu, Nobuyuki
Martyn, J. A. Jeevendra
Kaneki, Masao
TI Inducible nitric oxide synthase deficiency ameliorates skeletal muscle
insulin resistance but does not alter unexpected lower blood glucose
levels after burn injury in C57BL/6 mice
SO METABOLISM-CLINICAL AND EXPERIMENTAL
LA English
DT Article
ID CRITICAL ILLNESS POLYNEUROPATHY; RECEPTOR SUBSTRATE-1; TARGETED
DISRUPTION; ADIPOSE-TISSUE; PROTEIN-KINASE; LIVER; INFLAMMATION;
OBESITY; HYPERGLYCEMIA; CARBOHYDRATE
AB Burn injury is associated with inflammatory responses and metabolic alterations including insulin resistance. Impaired insulin receptor substrate-1 (IRS-1)-mediated insulin signal transduction is a major component of insulin resistance in skeletal muscle following bum injury. To further investigate molecular mechanisms that underlie bum injury-induced insulin resistance, we study a role of inducible nitric oxide synthase (iNOS), a major mediator of inflammation, on burn-induced muscle insulin resistance in iNOS-deficient mice. Full-thickness third-degree bum injury comprising 12% of total body surface area was produced in wild-type and iNOS-deficient C57BL/6 mice. Insulin-stimulated activation (phosphorylation) of IR, IRS-1, and Akt was assessed by immunoblotting and immunoprecipitation. Insulin-stimulated glucose uptake by skeletal muscle was evaluated ex vivo. Burn injury caused induction of iNOS in skeletal muscle of wild-type mice. The increase of iNOS expression paralleled the increase of insulin resistance, as evidenced by decreased tyrosine phosphorylation of IR and IRS-1, IRS-1 expression, insulin-stimulated activation of phosphatidylinositol 3-kinase and Akt/PKB, and insulin-stimulated glucose uptake in mouse skeletal muscle. The absence of iNOS in genetically engineered mice significantly lessened burn injury-induced insulin resistance in skeletal muscle. In wild-type mice, insulin tolerance test revealed whole-body insulin resistance in burned mice compared with sham-burned controls. This effect was reversed by iNOS deficiency. Unexpectedly, however, blood glucose levels were depressed in both wild-type and iNOS-deficient mice after burn injury. Gene disruption of iNOS ameliorated the effect of burn on IRS-1-mediated insulin signaling in skeletal muscle of mice. These findings indicate that iNOS plays a significant role in burn injury-induced skeletal muscle insulin resistance. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Sugita, Michiko; Sugita, Hiroki; Kim, Minhye; Mao, Ji; Yasuda, Yoshikazu; Habiro, Mayu; Shinozaki, Shohei; Yasuhara, Shingo; Shimizu, Nobuyuki; Martyn, J. A. Jeevendra; Kaneki, Masao] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Sugita, Michiko; Sugita, Hiroki; Mao, Ji; Yasuda, Yoshikazu; Shinozaki, Shohei; Yasuhara, Shingo; Shimizu, Nobuyuki; Martyn, J. A. Jeevendra; Kaneki, Masao] Shriners Hosp Children, Boston, MA 02114 USA.
RP Kaneki, M (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Charlestown, MA 02129 USA.
EM mkaneki@helix.mgh.harvard.edu
FU National Institutes of Health [R01-DK-058127, R01-GM-31569,
R01-GM-055082, R01-GM-61411, GM-21700]; Shriners Hospitals for Children
[8540, 71000, 8530, 8510, 8830]
FX This work was supported by grants from the National Institutes of Health
(R01-DK-058127 to M Kaneki; R01-GM-31569, R01-GM-055082, R01-GM-61411,
and GM-21700 [Project IV] to JAJ Martyn) and by the Shriners Hospitals
for Children grants 8540 and 71000 (to M Kaneki), 8530 and 8510 (to JAJ
Martyn), and 8830 (to S Yasuhara).
NR 41
TC 12
Z9 12
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 0026-0495
J9 METABOLISM
JI Metab.-Clin. Exp.
PD JAN
PY 2012
VL 61
IS 1
BP 127
EP 136
DI 10.1016/j.metabol.2011.06.001
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 864DH
UT WOS:000298216700019
PM 21816442
ER
PT J
AU Afrin, LB
AF Afrin, Lawrence B.
TI Mast Cell Activation Syndrome Masquerading as Agranulocytosis
SO MILITARY MEDICINE
LA English
DT Article
ID SYSTEMIC MASTOCYTOSIS; DISEASE; KIT
AB Acquired agranulocytosis is a Tare, life-threatening disorder. The few known causes/associations usually are readily identifiable (e.g., drug reaction. Felty syndrome, megaloblastosis, large granular lymphocytic leukemia, etc.). We report a novel association with mast cell disease. A 61-year-old morbidly obese man developed rheumatoid arthritis unresponsive to several medications. Agranulocytosis developed shortly alter sulfasalazine was started but did not improve when the drug was soon stopped. Other symptoms across many systems developed including hives and presyncope. Marrow aspiration and biopsy showed only neutropenia. Serum tryptase was mildly elevated; urinary prostaglandin D, was markedly elevated. Other causes were not found. Mast cell activation syndrome (MCAS) was diagnosed. Oral antihistamines, montelukast, and cromolyn were unhelpful; aspirin was initially felt contraindicated. Imatinib immediately increased neutrophils from 0% to 25% but did not help symptoms; subsequent addition of aspirin increased neutrophils further and abated symptoms. Different presentations of different MCAS patients reflect elaboration of different mediators likely consequent to different Kit mutations. Mast cells (MCs) help regulate adipocytes, and adipocytes can inhibit granulopoiesis; thus, a Kit-mutated MC clone may have directly and/or indirectly driven agranulocytosis. MCAS should be considered in otherwise idiopathic agranulocytosis presenting with comorbidities best explained by MC mediator release.
C1 [Afrin, Lawrence B.] Ralph H Johnson Vet Affairs Med Ctr, Hematol Oncol Sect, Med Serv, Charleston, SC 29401 USA.
[Afrin, Lawrence B.] Med Univ S Carolina, Div Hematol Oncol, Charleston, SC 29425 USA.
RP Afrin, LB (reprint author), Ralph H Johnson Vet Affairs Med Ctr, Hematol Oncol Sect, Med Serv, 103 Bee St, Charleston, SC 29401 USA.
NR 16
TC 6
Z9 6
U1 0
U2 1
PU ASSOC MILITARY SURG US
PI BETHESDA
PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 USA
SN 0026-4075
J9 MIL MED
JI Milit. Med.
PD JAN
PY 2012
VL 177
IS 1
BP 113
EP 117
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 874RP
UT WOS:000298976100025
PM 22338992
ER
PT J
AU Wan, M
Easton, RM
Gleason, CE
Monks, BR
Ueki, K
Kahn, CR
Birnbaum, MJ
AF Wan, Min
Easton, Rachael M.
Gleason, Catherine E.
Monks, Bobby R.
Ueki, Kohjiro
Kahn, C. Ronald
Birnbaum, Morris J.
TI Loss of Akt1 in Mice Increases Energy Expenditure and Protects against
Diet-Induced Obesity
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID BROWN ADIPOSE-TISSUE; SKELETAL-MUSCLE; GLUCOSE-HOMEOSTASIS;
INSULIN-RESISTANCE; UNCOUPLING PROTEIN-3; KINASE-B; METABOLIC SYNDROME;
HEPATIC STEATOSIS; EXERCISE; LACKING
AB Akt is encoded by a gene family for which each isoform serves distinct but overlapping functions. Based on the phenotypes of the germ line gene disruptions, Akt1 has been associated with control of growth, whereas Akt2 has been linked to metabolic regulation. Here we show that Akt1 serves an unexpected role in the regulation of energy metabolism, as mice deficient for Akt1 exhibit protection from diet-induced obesity and its associated insulin resistance. Although skeletal muscle contributes most of the resting and exercising energy expenditure, muscle-specific deletion of Akt1 does not recapitulate the phenotype, indicating that the role of Akt1 in skeletal muscle is cell nonautonomous. These data indicate a previously unknown function of Akt1 in energy metabolism and provide a novel target for treatment of obesity.
C1 [Wan, Min; Easton, Rachael M.; Gleason, Catherine E.; Monks, Bobby R.; Birnbaum, Morris J.] Univ Penn, Inst Diabet Obes & Metab, Philadelphia, PA 19104 USA.
[Ueki, Kohjiro] Univ Tokyo, Grad Sch Med, Tokyo, Japan.
[Kahn, C. Ronald] Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, Boston, MA 02115 USA.
RP Birnbaum, MJ (reprint author), Univ Penn, Inst Diabet Obes & Metab, Philadelphia, PA 19104 USA.
EM birnbaum@mail.med.upenn.edu
OI Birnbaum, Morris/0000-0001-9972-8680
FU NIH [RO1 DK56886, PO1 DK49210]; Diabetes and Endocrinology Research
Center, University of Pennsylvania [NIH DK-19525]
FX This work was supported by NIH grants RO1 DK56886 and PO1 DK49210 to
M.J.B. The Mouse Phenotyping, Physiology and Metabolism Core and the
Radioimmunoassay and Biomarker Core were supported by the Diabetes and
Endocrinology Research Center, University of Pennsylvania (NIH
DK-19525).
NR 42
TC 17
Z9 17
U1 0
U2 5
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 JAN
PY 2012
VL 32
IS 1
BP 96
EP 106
DI 10.1128/MCB.05806-11
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 866FN
UT WOS:000298366000009
PM 22037765
ER
PT J
AU Huang, SC
Ou, AC
Park, J
Yu, F
Yu, B
Lee, A
Yang, G
Zhou, A
Benz, EJ
AF Huang, Shu-Ching
Ou, Alexander C.
Park, Jennie
Yu, Faye
Yu, Brian
Lee, Angela
Yang, Guang
Zhou, Anyu
Benz, Edward J., Jr.
TI RBFOX2 Promotes Protein 4.1R Exon 16 Selection via U1 snRNP Recruitment
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID PRE-MESSENGER-RNA; 5' SPLICE SITE; ERYTHROID-DIFFERENTIATION; MEMBRANE
STABILITY; COMPLEX-FORMATION; SR PROTEINS; FOX-1; INTRON; BINDING; GENE
AB The erythroid differentiation-specific splicing switch of protein 4.1R exon 16, which encodes a spectrin/actin-binding peptide critical for erythrocyte membrane stability, is modulated by the differentiation-induced splicing factor RBFOX2. We have now characterized the mechanism by which RBFOX2 regulates exon 16 splicing through the downstream intronic element UGCAUG. Exon 16 possesses a weak 5' splice site (GAG/GTTTGT), which when strengthened to a consensus sequence (GAG/GTAAGT) leads to near-total exon 16 inclusion. Impaired RBFOX2 binding reduces exon 16 inclusion in the context of the native weak 5' splice site, but not the engineered strong 5' splice site, implying that RBFOX2 achieves its effect by promoting utilization of the weak 5' splice site. We further demonstrate that RBFOX2 increases U1 snRNP recruitment to the weak 5' splice site through direct interaction between its C-terminal domain (CTD) and the zinc finger region of U1C and that the CTD is required for the effect of RBFOX2 on exon 16 splicing. Our data suggest a novel mechanism for exon 165' splice site activation in which the binding of RBFOX2 to downstream intronic splicing enhancers stabilizes the pre-mRNA-U1 snRNP complex through interactions with U1 C.
C1 [Huang, Shu-Ching; Ou, Alexander C.; Park, Jennie; Yu, Faye; Yu, Brian; Lee, Angela; Yang, Guang; Zhou, Anyu; Benz, Edward J., Jr.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Huang, Shu-Ching; Yang, Guang; Zhou, Anyu; Benz, Edward J., Jr.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Benz, Edward J., Jr.] Harvard Univ, Sch Med, Dana Farber Harvard Canc Inst, Boston, MA 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 NIH [HL24385]; Claudia Barr Award
FX This work was supported by NIH grant HL24385 (to E.J.B.) and the Claudia
Barr Award (to S.C.H.).
NR 52
TC 10
Z9 10
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 JAN
PY 2012
VL 32
IS 2
BP 513
EP 526
DI 10.1128/MCB.06423-11
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 875HD
UT WOS:000299020100023
PM 22083953
ER
PT J
AU Avila-Elchiver, M
Nagrath, D
Yarmush, ML
AF Avila-Elchiver, Marco
Nagrath, Deepak
Yarmush, Martin L.
TI Optimality and thermodynamics determine the evolution of transcriptional
regulatory networks
SO MOLECULAR BIOSYSTEMS
LA English
DT Article
ID ESCHERICHIA-COLI; IN-SILICO; CULTURED-HEPATOCYTES; SIGNAL-TRANSDUCTION;
ADAPTIVE EVOLUTION; COMPLEX NETWORKS; MOTIFS; OPTIMIZATION; EQUILIBRIUM;
FRAMEWORK
AB Transcriptional motifs are small regulatory interaction patterns that regulate biological functions in highly-interacting cellular networks. Recently, attempts have been made to explain the significance of transcriptional motifs through dynamic function. However, fundamental questions remain unanswered. Why are certain transcriptional motifs with similar dynamic function abundant while others occur rarely? What are the criteria for topological generalization of these motifs into complex networks? Here, we present a novel paradigm that combines non-equilibrium thermodynamics with multiobjective-optimality for network analysis. We found that energetic cost, defined herein as specific dissipation energy, is minimal at the optimal environmental conditions and it correlates inversely with the abundance of the network motifs obtained experimentally for E. coli and S. cerevisiae. This yields evidence that dissipative energetics is the underlying criteria used during evolution for motif selection and that biological systems during transcription tend towards evolutionary selection of subgraphs which produces minimum specific heat dissipation under optimal conditions, thereby explaining the abundance/rare occurrence of some motifs. We show that although certain motifs had similar dynamical functionality, they had significantly different energetic cost, thus explaining the abundance/rare occurrence of these motifs. The presented insights may establish global thermodynamic analysis as a backbone in designing and understanding complex networks systems, such as metabolic and protein interaction networks.
C1 [Avila-Elchiver, Marco; Yarmush, Martin L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Avila-Elchiver, Marco; Yarmush, Martin L.] Harvard Univ, Sch Med, Shriners Hosp Children, Boston, MA 02114 USA.
[Nagrath, Deepak] Rice Univ, Chem & Biomol Engn Dept, Houston, TX 77005 USA.
RP Yarmush, ML (reprint author), Massachusetts Gen Hosp, 51 Blossom St, Boston, MA 02114 USA.
EM ireis@sbi.org; dn7@rice.edu
OI Nagrath, Deepak/0000-0002-8999-2282
FU NIBIB NIH HHS [P41 EB002503]
NR 52
TC 2
Z9 2
U1 0
U2 8
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 1742-206X
EI 1742-2051
J9 MOL BIOSYST
JI Mol. Biosyst.
PY 2012
VL 8
IS 2
BP 511
EP 530
DI 10.1039/c1mb05177f
PG 20
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 874YP
UT WOS:000298994900011
PM 22076617
ER
PT J
AU Wray, NR
Pergadia, ML
Blackwood, DHR
Penninx, BWJH
Gordon, SD
Nyholt, DR
Ripke, S
MacIntyre, DJ
McGhee, KA
Maclean, AW
Smit, JH
Hottenga, JJ
Willemsen, G
Middeldorp, CM
de Geus, EJC
Lewis, CM
McGuffin, P
Hickie, IB
van den Oord, EJCG
Liu, JZ
Macgregor, S
McEvoy, BP
Byrne, EM
Medland, SE
Statham, DJ
Henders, AK
Heath, AC
Montgomery, GW
Martin, NG
Boomsma, DI
Madden, PAF
Sullivan, PF
AF Wray, N. R.
Pergadia, M. L.
Blackwood, D. H. R.
Penninx, B. W. J. H.
Gordon, S. D.
Nyholt, D. R.
Ripke, S.
MacIntyre, D. J.
McGhee, K. A.
Maclean, A. W.
Smit, J. H.
Hottenga, J. J.
Willemsen, G.
Middeldorp, C. M.
de Geus, E. J. C.
Lewis, C. M.
McGuffin, P.
Hickie, I. B.
van den Oord, E. J. C. G.
Liu, J. Z.
Macgregor, S.
McEvoy, B. P.
Byrne, E. M.
Medland, S. E.
Statham, D. J.
Henders, A. K.
Heath, A. C.
Montgomery, G. W.
Martin, N. G.
Boomsma, D. I.
Madden, P. A. F.
Sullivan, P. F.
TI Genome-wide association study of major depressive disorder: new results,
meta-analysis, and lessons learned
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE major depressive disorder; depression; genome-wide association study;
CACNA1C; ADCY3; GAL
ID NATIONAL COMORBIDITY SURVEY; SEROTONIN TRANSPORTER GENE; MOOD DISORDERS;
PSYCHIATRIC-DISORDERS; BIPOLAR DISORDER; TWIN SAMPLE; GALANIN;
POPULATION; HERITABILITY; STABILITY
AB Major depressive disorder (MDD) is a common complex disorder with a partly genetic etiology. We conducted a genome-wide association study of the MDD2000+ sample (2431 cases, 3673 screened controls and >1M imputed single-nucleotide polymorphisms (SNPs)). No SNPs achieved genome-wide significance either in the MDD2000+ study, or in meta-analysis with two other studies totaling 5763 cases and 6901 controls. These results imply that common variants of intermediate or large effect do not have main effects in the genetic architecture of MDD. Suggestive but notable results were (a) gene-based tests suggesting roles for adenylate cyclase 3 (ADCY3, 2p23.3) and galanin (GAL, 11q13.3); published functional evidence relates both of these to MDD and serotonergic signaling; (b) support for the bipolar disorder risk variant SNP rs1006737 in CACNA1C (P = 0.020, odds ratio = 1.10); and (c) lack of support for rs2251219, a SNP identified in a meta-analysis of affective disorder studies (P = 0.51). We estimate that sample sizes 1.8- to 2.4-fold greater are needed for association studies of MDD compared with those for schizophrenia to detect variants that explain the same proportion of total variance in liability. Larger study cohorts characterized for genetic and environmental risk factors accumulated prospectively are likely to be needed to dissect more fully the etiology of MDD. Molecular Psychiatry (2012) 17, 36-48; doi:10.1038/mp.2010.109; published online 2 November 2010
C1 [Pergadia, M. L.; Heath, A. C.; Madden, P. A. F.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
[Blackwood, D. H. R.; MacIntyre, D. J.; McGhee, K. A.; Maclean, A. W.] Univ Edinburgh, Royal Edinburgh Hosp, Div Psychiat, Edinburgh, Midlothian, Scotland.
[Penninx, B. W. J. H.; Smit, J. H.; Hottenga, J. J.; Willemsen, G.; Middeldorp, C. M.; de Geus, E. J. C.; Boomsma, D. I.] Vrije Univ Amsterdam, Dept Biol Psychol, Amsterdam, Netherlands.
[Penninx, B. W. J. H.; Smit, J. H.; Hottenga, J. J.; Willemsen, G.; Middeldorp, C. M.; de Geus, E. J. C.; Boomsma, D. I.] Vrije Univ Amsterdam, Med Ctr, Amsterdam, Netherlands.
[Ripke, S.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Ripke, S.] Broad Inst Harvard & MIT, Cambridge, MA USA.
[Lewis, C. M.; McGuffin, P.] Kings Coll London, MRC SGDP Ctr, Inst Psychiat, Dept Med & Mol Genet, London WC2R 2LS, England.
[Hickie, I. B.] Univ Sydney, Brain & Mind Res Inst, Clin Res Unit, Sydney, NSW 2006, Australia.
[van den Oord, E. J. C. G.] Virginia Commonwealth Univ, Ctr Biomarker Res & Personalized Med, Richmond, VA USA.
[Sullivan, P. F.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Wray, N. R.; Gordon, S. D.; Nyholt, D. R.; Liu, J. Z.; Macgregor, S.; McEvoy, B. P.; Byrne, E. M.; Medland, S. E.; Statham, D. J.; Henders, A. K.; Montgomery, G. W.; Martin, N. G.] Queensland Inst Med Res, Psychiat Genet Lab, Brisbane, Qld 4029, Australia.
[Wray, N. R.; Gordon, S. D.; Nyholt, D. R.; Liu, J. Z.; Macgregor, S.; McEvoy, B. P.; Byrne, E. M.; Medland, S. E.; Statham, D. J.; Henders, A. K.; Montgomery, G. W.; Martin, N. G.] Queensland Inst Med Res, Genet Epidemiol Lab, Brisbane, Qld 4029, Australia.
[Wray, N. R.; Gordon, S. D.; Nyholt, D. R.; Liu, J. Z.; Macgregor, S.; McEvoy, B. P.; Byrne, E. M.; Medland, S. E.; Statham, D. J.; Henders, A. K.; Montgomery, G. W.; Martin, N. G.] Queensland Inst Med Res, Mol Epidemiol Lab, Brisbane, Qld 4029, Australia.
[Wray, N. R.; Gordon, S. D.; Nyholt, D. R.; Liu, J. Z.; Macgregor, S.; McEvoy, B. P.; Byrne, E. M.; Medland, S. E.; Statham, D. J.; Henders, A. K.; Montgomery, G. W.; Martin, N. G.] Queensland Inst Med Res, Queensland Stat Genet Lab, Brisbane, Qld 4029, Australia.
RP Wray, NR (reprint author), Queensland Inst Med Res, Psychiat Genet Lab, Herston Rd, Brisbane, Qld 4029, Australia.
EM naomi.wray@qimr.edu.au; pfsulliv@med.unc.edu
RI Lewis, Cathryn/A-5225-2010; Medland, Sarah/C-7630-2013; Macgregor,
Stuart/C-6442-2009; Nyholt, Dale/C-8384-2013; McGuffin,
Peter/A-1565-2012; Wray, Naomi/C-8639-2015; de Geus, Eco/M-9318-2015;
Montgomery, Grant/B-7148-2008;
OI Middeldorp, Christel/0000-0002-6218-0428; Martin,
Nicholas/0000-0003-4069-8020; Lewis, Cathryn/0000-0002-8249-8476;
Medland, Sarah/0000-0003-1382-380X; Macgregor,
Stuart/0000-0001-6731-8142; McGuffin, Peter/0000-0002-9888-2907; Wray,
Naomi/0000-0001-7421-3357; de Geus, Eco/0000-0001-6022-2666; Montgomery,
Grant/0000-0002-4140-8139; MacIntyre, Donald J/0000-0001-6963-1335
FU Australian National Health and Medical Research Council [241944, 339462,
389927, 389875, 389891, 389892, 389938, 442915, 442981, 496675, 496739,
552485, 552498, 613608]; FP-5 GenomEUtwin Project [QLG2-CT-2002-01254];
US National Institutes of Health [AA07535, AA10248, AA13320, AA13321,
AA13326, AA14041, MH66206, DA12854, DA019951]; Netherlands Scientific
Organization (NWO) [480-05-003]; National Health and Medical Research
Council; Australian Research Council; Netherlands Scientific
Organization [904-61-090, 904-61-193, 480-04-004, 400-05-717];
Neuroscience Campus Amsterdam and the EMGO+ institute; European Union
[EU/WLRT-2001-01254]; ZonMW (Geestkracht program) [10-000-1002];
National Institute of Mental Health Schizophrenia (NIMH) [RO1 MH059160,
MH080403]; NESDA; NTR; Wellcome Trust, London; Chief Scientist Office of
the Scottish Government; [NWO-SPI 56-464-1419]
FX We thank the twins and their families registered at the Australian Twin
Registry for their participation in the many studies that have
contributed to this research. We thank Dixie Statham (sample
collection); Leanne Wallace, Anthony Caracella and staff of the
Molecular Epidemiology Laboratory (DNA processing); David Smyth, Harry
Beeby, and Daniel Park (IT support). Funding was provided by the
Australian National Health and Medical Research Council (241944, 339462,
389927, 389875, 389891, 389892, 389938, 442915, 442981, 496675, 496739,
552485, 552498, 613608), the FP-5 GenomEUtwin Project
(QLG2-CT-2002-01254), and the US National Institutes of Health (NIH
grants AA07535, AA10248, AA13320, AA13321, AA13326, AA14041, MH66206,
DA12854, DA019951). A portion of the genotyping on which this study was
based (Illumina 370K scans on 4300 individuals) was carried out at the
Center for Inherited Disease Research, Baltimore through an access award
to our late colleague Dr Richard Todd (Psychiatry, Washington University
School of Medicine, St Louis). Statistical analyses were partly
conducted at the Genetic Cluster Computer
(http://www.geneticcluster.org), which is financially supported by the
Netherlands Scientific Organization (NWO 480-05-003). SEM, SM and GWM
are supported by the National Health and Medical Research Council
Fellowship Scheme. NRW and DRN are supported by the Australian Research
Council Future Fellowship Scheme.; Funding support was provided by the
Netherlands Scientific Organization (904-61-090, 904-61-193, 480-04-004,
400-05-717, Centre for Medical Systems Biology (NWO Genomics), the
Neuroscience Campus Amsterdam and the EMGO+ institute; the European
Union (EU/WLRT-2001-01254), ZonMW (Geestkracht program, 10-000-1002),
NIMH (RO1 MH059160) and matching funds from participating institutes in
NESDA and NTR. The NTR controls were genotyped in the Genomics platform
(certified service provider (CSPro(R)) for Illumina) at the LIFE and
BRAIN Center Bonn (funded by NWO-SPI 56-464-1419).; We would like to
record our appreciation for much practical support from our late
colleague Walter J Muir, Professor of Developmental Psychiatry at the
University of Edinburgh and especially for his many stimulating ideas
for genetic studies in depression. We thank Margaret Van Beck for sample
collection and Lee Murphy, Wellcome Trust Clinical Research Facility,
Western General Hospital, Crewe Road South, Edinburgh, for sample
management. The collection of the Edinburgh cohort was supported by
grants from The Wellcome Trust, London and the Chief Scientist Office of
the Scottish Government.; Additional funding was provided by National
Institute of Mental Health Schizophrenia (NIMH) grant MH080403 to
EJGCvdO and PFS. Control subjects from the NIMH Genetics Initiative,
data and biomaterials are being collected by the 'Molecular Genetics of
Schizophrenia II' collaboration. The investigators and coinvestigators
are: ENH/Northwestern University, Evanston, IL, MH059571, Pablo V
Gejman, MD (Collaboration Coordinator; PI), Alan R Sanders, MD; Emory
University School of Medicine, Atlanta, GA, MH59587, Farooq Amin, MD
(PI); Louisiana State University Health Sciences Center; New Orleans,
Louisiana, MH067257, Nancy Buccola APRN, BC, MSN (PI); University of
California-Irvine, Irvine, CA, MH60870, William Byerley, MD (PI);
Washington University, St Louis, MO, U01, MH060879, C Robert Cloninger,
MD (PI); University of Iowa, Iowa, IA, MH59566, Raymond Crowe, MD (PI),
Donald Black, MD; University of Colorado, Denver, CO, MH059565, Robert
Freedman, MD (PI); University of Pennsylvania, Philadelphia, PA,
MH061675, Douglas Levinson, MD (PI); University of Queensland,
Queensland, Australia, MH059588, Bryan Mowry, MD (PI); Mt. Sinai School
of Medicine, New York, NY, MH59586, Jeremy Silverman, PhD (PI).
NR 59
TC 156
Z9 160
U1 7
U2 40
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD JAN
PY 2012
VL 17
IS 1
BP 36
EP 48
DI 10.1038/mp.2010.109
PG 13
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 875EU
UT WOS:000299014000009
PM 21042317
ER
PT J
AU Zhang, W
Fulci, G
Buhrman, JS
Stemmer-Rachamimov, AO
Chen, JW
Wojtkiewicz, GR
Weissleder, R
Rabkin, SD
Martuza, RL
AF Zhang, Wei
Fulci, Giulia
Buhrman, Jason S.
Stemmer-Rachamimov, Anat O.
Chen, John W.
Wojtkiewicz, Gregory R.
Weissleder, Ralph
Rabkin, Samuel D.
Martuza, Robert L.
TI Bevacizumab With Angiostatin-armed oHSV Increases Antiangiogenesis and
Decreases Bevacizumab-induced Invasion in U87 Glioma
SO MOLECULAR THERAPY
LA English
DT Article
ID HERPES-SIMPLEX-VIRUS; VESICULAR STOMATITIS-VIRUS; INNATE
IMMUNE-RESPONSES; ANTITUMOR EFFICACY; ONCOLYTIC VIRUSES; VIRAL
REPLICATION; COMBINATION THERAPY; MALIGNANT GLIOMAS; CANCER-CELLS;
FUSION GENE
AB Bevacizumab (BEV) is an antiangiogenic drug approved for glioblastoma (GBM) treatment. However, it does not increase survival and is associated with glioma invasion. Angiostatin is an antiangiogenic polypeptide that also inhibits migration of cancer cells, but is difficult to deliver. Oncolytic viruses (OV) can potentially spread throughout the tumor, reach isolated infiltrating cells, kill them and deliver anticancer agents to uninfected cells. We have tested a combination treatment of BEV plus an OV expressing angiostatin (G47 Delta-mAngio) in mice-bearing human GBM. Using a vascular intracranial human glioma model (U87) in athymic mice, we performed histopathological,analysis of tumors treated with G47 Delta-mAngio or BEV alone or in combination, followed tumor response by magnetic resonance imaging (MRI), and assessed animal survival. Our results indicate that injection of G47 Delta-mAngio during BEV treatment allows increased virus distribution, tumor lysis, and angiostatin-mediated inhibition of vascular endothelial growth factor (VEGF) expression and of BEV-induced invasion markers (matrix metalloproteinases-2 (MMP2), MMP9, and collagen). This leads to increased survival and antiangiogenesis and decreased invasive phenotypes. We show for the first time the possibility of improving the antiangiogenic effect of BEV while decreasing the tumor invasive-like phenotype induced by this drug, and demonstrate the therapeutic advantage of combining systemic and local antiangiogenic treatments with viral oncolytic therapy.
C1 [Zhang, Wei; Fulci, Giulia; Buhrman, Jason S.; Rabkin, Samuel D.; Martuza, Robert L.] Massachusetts Gen Hosp, Brain Tumor Res Ctr, Dept Neurosurg, Boston, MA 02114 USA.
[Zhang, Wei] Fourth Mil Med Univ, Xijing Hosp, Dept Neurosurg, Xian 710032, Peoples R China.
[Stemmer-Rachamimov, Anat O.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Chen, John W.; Wojtkiewicz, Gregory R.; Weissleder, Ralph] Massachusetts Gen Hosp, Ctr Syst Biol & Mol Imaging Res, Boston, MA 02114 USA.
RP Martuza, RL (reprint author), Massachusetts Gen Hosp, Brain Tumor Res Ctr, Dept Neurosurg, 55 Fruit St, Boston, MA 02114 USA.
EM rmartuza@partners.org
RI rabkin, samuel/C-2443-2012
OI rabkin, samuel/0000-0003-2344-2795
FU China Scholarship Council (CSC); National Institute for Neurological
Disorders [R01-NS032677, P30-NS045776, U24CA092782, R01-NS070835,
R01-NS072167]; National Heart, Lung and Blood Institute at the National
Institutes of Health, USA [K08-HL081170]
FX We thank Prof Xiang Zhang (Department of Neurosurgery, Xijing Hospital,
P.R. China) and Prof Takashi Tamiya (Department of Neurological Surgery,
Kagawa University Faculty of Medicine, Japan) for their great spiritual
inspiration and editorial assistance. We thank Christopher J. Owen for
his help in computer assistance. We thank the support from Postgraduate
Scholarship Program of China Scholarship Council (CSC). This work was
supported in part by grants from the National Institute for Neurological
Disorders (R01-NS032677 to R.L.M., P30-NS045776 to S.D.R. for the
real-time PCR core, U24CA092782 to R.W. for imaging core, R01-NS070835
and R01-NS072167 to J.W.C.) and the National Heart, Lung and Blood
Institute (K08-HL081170 to J.W.C.) at the National Institutes of Health,
USA. The authors declared no conflict of interest.
NR 49
TC 23
Z9 24
U1 1
U2 16
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1525-0016
J9 MOL THER
JI Mol. Ther.
PD JAN
PY 2012
VL 20
IS 1
BP 37
EP 45
DI 10.1038/mt.2011.187
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 875HV
UT WOS:000299021900009
PM 21915104
ER
PT J
AU Parekkadan, B
Fletcher, AL
Li, M
Tjota, MY
Bellemare-Pelletier, A
Milwid, JM
Lee, JW
Yarmush, ML
Turley, SJ
AF Parekkadan, Biju
Fletcher, Anne L.
Li, Matthew
Tjota, Melissa Y.
Bellemare-Pelletier, Angelique
Milwid, Jack M.
Lee, Je-Wook
Yarmush, Martin L.
Turley, Shannon J.
TI Aire Controls Mesenchymal Stem Cell-mediated Suppression in Chronic
Colitis
SO MOLECULAR THERAPY
LA English
DT Article
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; COLLAGEN-INDUCED ARTHRITIS;
PROLIFERATION IN-VITRO; NATURAL-KILLER-CELLS; VERSUS-HOST-DISEASE;
BONE-MARROW; STROMAL CELLS; T-CELLS; MYOCARDIAL-INFARCTION; DENDRITIC
CELLS
AB Mesenchymal stem cells (MSCs) are emerging as a promising immunotherapeutic, based largely on their overt suppression of T lymphocytes under inflammatory and autoimmune conditions. While paracrine crosstalk between MSCs and T cells has been well-studied, an intrinsic transcriptional switch that programs MSCs for immunomodulation has remained undefined. Here we show that bone marrow-derived MSCs require the transcriptional regulator Aire to suppress T cell-mediated pathogenesis in a mouse model of chronic colitis. Surprisingly, Aire did not control MSC suppression of T cell proliferation in vitro. Instead, Aire reduced T cell mitochondrial reductase by negatively regulating a proinflammatory cytokine, early T cell activation factor (Eta)-1. Neutralization of Eta-1 enabled Aire(-/-) MSCs to ameliorate colitis, reducing the number of infiltrating effector T cells in the colon, and normalizing T cell reductase levels. We propose that Aire represents an early molecular switch imposing a suppressive MSC phenotype via regulation of Eta-1. Monitoring Aire expression in MSCs may thus be a critical parameter for clinical use.
C1 [Parekkadan, Biju; Li, Matthew; Milwid, Jack M.; Yarmush, Martin L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Engn Med & Surg Serv,Dept Surg, Boston, MA USA.
[Parekkadan, Biju; Li, Matthew; Milwid, Jack M.; Yarmush, Martin L.] Shriners Hosp Children, Boston, MA USA.
[Fletcher, Anne L.; Tjota, Melissa Y.; Bellemare-Pelletier, Angelique; Lee, Je-Wook; Turley, Shannon J.] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
[Fletcher, Anne L.; Tjota, Melissa Y.; Bellemare-Pelletier, Angelique; Lee, Je-Wook; Turley, Shannon J.] Harvard Univ, Sch Med, Dept Microbiol & Immunol, Boston, MA USA.
RP Turley, SJ (reprint author), 44 Binney St, Boston, MA 02115 USA.
EM biju_parekkadan@hms.harvard.edu; shannon_turley@dfci.harvard.edu
OI Tjota, Melissa/0000-0002-5869-3175
FU National Institutes of Health [DK074500, AI045757, DK059766-06,
DK087770]; NHMRC Australia [546259]; Broad Foundation [BMRP498382];
Shriners Hospitals for Children
FX We thank the Dana Farber Microarray and Biostatistics Core Facility for
hybridizing cDNA chips and performing computational analysis. We thank
Myriam Armant for kindly providing amniotic fluid-derived MSCs. We thank
Veronika Lukacs-Kornek for thoughtful opinions on the manuscript. This
work was supported by the National Institutes of Health (DK074500,
AI045757, DK059766-06, and DK087770), NHMRC Australia: (546259), the
Broad Medical Research Program of The Broad Foundation (BMRP498382) and
Shriners Hospitals for Children.
NR 50
TC 8
Z9 9
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1525-0016
J9 MOL THER
JI Mol. Ther.
PD JAN
PY 2012
VL 20
IS 1
BP 178
EP 186
DI 10.1038/mt.2011.192
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 875HV
UT WOS:000299021900024
PM 21952165
ER
PT J
AU Sips, M
Sciaranghella, G
Diefenbach, T
Dugast, AS
Berger, CT
Liu, Q
Kwon, D
Ghebremichael, M
Estes, JD
Carrington, M
Martin, JN
Deeks, SG
Hunt, PW
Alter, G
AF Sips, M.
Sciaranghella, G.
Diefenbach, T.
Dugast, A-S
Berger, C. T.
Liu, Q.
Kwon, D.
Ghebremichael, M.
Estes, J. D.
Carrington, M.
Martin, J. N.
Deeks, S. G.
Hunt, P. W.
Alter, G.
TI Altered distribution of mucosal NK cells during HIV infection
SO MUCOSAL IMMUNOLOGY
LA English
DT Article
ID NATURAL-KILLER-CELLS; INTRA-EPITHELIAL LYMPHOCYTES; CD4(+) T-CELLS;
GASTROINTESTINAL-TRACT; INTRAEPITHELIAL LYMPHOCYTES;
FUNCTIONAL-CHARACTERISTICS; LYMPHADENOPATHY SYNDROME; INTESTINAL
EPITHELIUM; COLLAGEN DEPOSITION; CYTOLYTIC FUNCTION
AB The human gut mucosa is a major site of human immunodeficiency virus (HIV) infection and infection-associated pathogenesis. Increasing evidence shows that natural killer (NK) cells have an important role in control of HIV infection, but the mechanism(s) by which they mediate antiviral activity in the gut is unclear. Here, we show that two distinct subsets of NK cells exist in the gut, one localized to intraepithelial spaces (intraepithelial lymphocytes, IELs) and the other to the lamina propria (LP). The frequency of both subsets of NK cells was reduced in chronic infection, whereas IEL NK cells remained stable in spontaneous controllers with protective killer immunoglobulin-like receptor/human leukocyte antigen genotypes. Both IEL and LP NK cells were significantly expanded in immunological non-responsive patients, who incompletely recovered CD4 + T cells on highly active antiretroviral therapy (HAART). These data suggest that both IEL and LP NK cells may expand in the gut in an effort to compensate for compromised CD4 + T-cell recovery, but that only IEL NK cells may be involved in providing durable control of HIV in the gut.
C1 [Sips, M.; Sciaranghella, G.; Diefenbach, T.; Dugast, A-S; Berger, C. T.; Liu, Q.; Kwon, D.; Ghebremichael, M.; Carrington, M.; Alter, G.] Harvard Univ & Massachusetts Inst Technol, Ragon Inst Massachusetts Gen Hosp, Boston, MA USA.
[Estes, J. D.] Frederick Inc, NCI, AIDS & Canc Virus Program, Frederick, MD USA.
[Carrington, M.] SAIC Frederick Inc, NCI Frederick, Canc & Inflammat Program, Expt Immunol Lab, Frederick, MD USA.
[Martin, J. N.; Deeks, S. G.; Hunt, P. W.] Univ Calif San Francisco, Dept Med, Posit Hlth Program, San Francisco, CA USA.
RP Alter, G (reprint author), Harvard Univ & Massachusetts Inst Technol, Ragon Inst Massachusetts Gen Hosp, Boston, MA USA.
EM galter@partners.org
RI Dugast, AnneSophie/L-9541-2015
FU NCI NIH HHS [HHSN261200800001E]; NIAID NIH HHS [K08 AI084546, P30
AI027763, R01 AI080289]
NR 51
TC 24
Z9 24
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1933-0219
J9 MUCOSAL IMMUNOL
JI Mucosal Immunol.
PD JAN
PY 2012
VL 5
IS 1
BP 30
EP 40
DI 10.1038/mi.2011.40
PG 11
WC Immunology
SC Immunology
GA 866UP
UT WOS:000298411100005
PM 21993602
ER
PT J
AU Andres, PL
Skerry, LM
Munsat, TL
Thornell, BJ
Szymonifka, J
Schoenfeld, DA
Cudkowicz, ME
AF Andres, Patricia L.
Skerry, Linda M.
Munsat, Theodore L.
Thornell, Brenda J.
Szymonifka, Jackie
Schoenfeld, David A.
Cudkowicz, Merit E.
TI Validation of a new strength measurement device for amyotrophic lateral
sclerosis clinical trials
SO MUSCLE & NERVE
LA English
DT Article
DE ALS; neuromuscular; outcomes measures; reliability; strength testing
ID VOLUNTARY ISOMETRIC CONTRACTION; NATURAL-HISTORY; ALSFRS-R; SURVIVAL
AB Introduction: Strength measures with reduced variability and higher sensitivity could improve efficiency in clinical trials of amyotrophic lateral sclerosis (ALS). The Accurate Test of Limb Isometric Strength (ATLIS) was developed to precisely and conveniently measure force in 12 muscle groups. In this study we evaluate the reliability and validity of the ATLIS testing protocol. Methods: Twenty healthy adults and 10 patients with ALS were tested twice by the same or by different evaluators to determine test-retest and interrater reliability. Twenty healthy adults were examined using ATLIS and a wellvalidated strength testing protocol (TQNE) to assess criterionbased validity. Results: Mean absolute variation between tests was 8.6%, and intraclass correlation coefficients for each muscle group were high (range 0.82-0.99). The Pearson correlation coefficient of mean ATLIS and TQNE scores was 0.90. A subject survey demonstrated high user acceptance of ATLIS. Conclusions: ATLIS is convenient for patients and evaluators, produces precise strength measurements, and is easily moved between examining rooms.
C1 [Andres, Patricia L.; Skerry, Linda M.; Thornell, Brenda J.; Cudkowicz, Merit E.] Massachusetts Gen Hosp, Neurol Clin Trials Unit, Charlestown, MA 02129 USA.
[Munsat, Theodore L.] Tufts Med Ctr, Dept Neurol, Boston, MA USA.
[Szymonifka, Jackie; Schoenfeld, David A.] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
RP Andres, PL (reprint author), Massachusetts Gen Hosp, Neurol Clin Trials Unit, 149 13th St,Room 2274, Charlestown, MA 02129 USA.
EM pandres1@partners.org
FU ALS Association; Muscular Dystrophy Association; ALS Therapy Alliance
FX The authors gratefully acknowledge the support of the ALS Association,
the Muscular Dystrophy Association, and the ALS Therapy Alliance.
NR 36
TC 10
Z9 10
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0148-639X
J9 MUSCLE NERVE
JI Muscle Nerve
PD JAN
PY 2012
VL 45
IS 1
BP 81
EP 85
DI 10.1002/mus.22253
PG 5
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 867TI
UT WOS:000298477000016
PM 22190312
ER
PT J
AU Creton, S
Aardema, MJ
Carmichael, PL
Harvey, JS
Martin, FL
Newbold, RF
O'Donovan, MR
Pant, K
Poth, A
Sakai, A
Sasaki, K
Scott, AD
Schechtman, LM
Shen, RR
Tanaka, N
Yasaei, H
AF Creton, Stuart
Aardema, Marilyn J.
Carmichael, Paul L.
Harvey, James S.
Martin, Francis L.
Newbold, Robert F.
O'Donovan, Michael R.
Pant, Kamala
Poth, Albrecht
Sakai, Ayako
Sasaki, Kiyoshi
Scott, Andrew D.
Schechtman, Leonard M.
Shen, Rhine R.
Tanaka, Noriho
Yasaei, Hemad
TI Cell transformation assays for prediction of carcinogenic potential:
state of the science and future research needs
SO MUTAGENESIS
LA English
DT Article
ID DISCRIMINATE RODENT CARCINOGENS; VITRO GENOTOXICITY TESTS; HAMSTER
EMBRYO CELLS; MORPHOLOGICAL TRANSFORMATION; EXPERIMENTAL-MODELS;
RELATIVE PREDICTIVITY; ALTERNATIVE MODELS; RESEARCH-PROGRAM; HUMAN
CANCER; TUMOR-CELLS
AB Cell transformation assays (CTAs) have long been proposed as in vitro methods for the identification of potential chemical carcinogens. Despite showing good correlation with rodent bioassay data, concerns over the subjective nature of using morphological criteria for identifying transformed cells and a lack of understanding of the mechanistic basis of the assays has limited their acceptance for regulatory purposes. However, recent drivers to find alternative carcinogenicity assessment methodologies, such as the Seventh Amendment to the EU Cosmetics Directive, have fuelled renewed interest in CTAs. Research is currently ongoing to improve the objectivity of the assays, reveal the underlying molecular changes leading to transformation and explore the use of novel cell types. The UK NC3Rs held an international workshop in November 2010 to review the current state of the art in this field and provide directions for future research. This paper outlines the key points highlighted at this meeting.
C1 [Creton, Stuart] Natl Ctr Replacement Refinement & Reduct Anim Res, London NW1 2BE, England.
[Aardema, Marilyn J.] Marilyn Aardema Consulting LLC, Fairfield, OH 45014 USA.
[Carmichael, Paul L.; Scott, Andrew D.] Unilever Safety & Environm Assurance Ctr, Sharnbrook MK44 1LQ, Beds, England.
[Harvey, James S.] GlaxoSmithKline Plc, Genet Toxicol, Ware SG12 0DP, Herts, England.
[Martin, Francis L.] Univ Lancaster, Ctr Biophoton, Lancaster Environm Ctr, Lancaster LA1 4YQ, England.
[Newbold, Robert F.; Yasaei, Hemad] Brunel Univ, Brunel Inst Canc Genet & Pharmacogen, Uxbridge UB8 3PH, Middx, England.
[O'Donovan, Michael R.] AstraZeneca R&D, Macclesfield SK10 4TG, Cheshire, England.
[Pant, Kamala] Bioreliance Corp, Rockville, MD 20850 USA.
[Poth, Albrecht] Harlan Cytotest Cell Res GmbH, D-64380 Rossdorf, Germany.
[Sakai, Ayako; Sasaki, Kiyoshi; Tanaka, Noriho] Food & Drug Safety Ctr, Hatano Res Inst, Div Alternat Res, Kanagawa 2578523, Japan.
[Schechtman, Leonard M.] Innovat Toxicol Consulting LLC, Lake Worth, FL 33467 USA.
[Shen, Rhine R.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Creton, S (reprint author), Natl Ctr Replacement Refinement & Reduct Anim Res, Gibbs Bldg,215 Euston Rd, London NW1 2BE, England.
EM stuart.creton@nc3rs.org.uk
RI Yasaei, Hemad/A-6351-2014;
OI L Martin, Francis/0000-0001-8562-4944
FU UK NC3Rs; UK Environmental Mutagen Society
FX The CTA workshop was funded by the UK NC3Rs with additional sponsorship
for the meeting provided by the UK Environmental Mutagen Society.; The
authors are grateful to the UK Environmental Mutagen Society for
financial sponsorship of the workshop.
NR 61
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U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0267-8357
EI 1464-3804
J9 MUTAGENESIS
JI Mutagenesis
PD JAN
PY 2012
VL 27
IS 1
BP 93
EP 101
DI 10.1093/mutage/ger053
PG 9
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 866MP
UT WOS:000298385400010
PM 21852270
ER
PT J
AU Ghosh, K
Kanapathipillai, M
Korin, N
McCarthy, JR
Ingber, DE
AF Ghosh, Kaustabh
Kanapathipillai, Mathumai
Korin, Netanel
McCarthy, Jason R.
Ingber, Donald E.
TI Polymeric Nanomaterials for Islet Targeting and Immunotherapeutic
Delivery
SO NANO LETTERS
LA English
DT Article
DE Diabetes; pancreatic islet; nanoparticle; drug delivery; vascular
endothelium; inflammation; tissue targeting
ID DIABETES PREVENTION TRIAL-TYPE-1; RECENT-ONSET; DRUG-DELIVERY; TYPE-1;
THERAPY; CELLS; IMMUNOSUPPRESSION; NANOTECHNOLOGY; NANOPARTICLES;
INFLAMMATION
AB Here we report a proof-of-concept for development of pancreatic islet-targeting nanoparticles for immunomodulatory therapy of autoimmune type 1 diabetes. Modified with a unique islet-homing peptide, these polymeric nanomaterials exhibit 3-fold greater binding to islet endothelial cells and a 200-fold greater anti-inflammatory effect through targeted islet endothelial cell delivery of an immunosuppressant drug. Our findings also underscore the need to carefully tailor drug loading and nanoparticle dosage to achieve maximal vascular targeting and immunosuppression.
C1 [Ghosh, Kaustabh; Ingber, Donald E.] Childrens Hosp, Dept Pathol, Vasc Biol Program, Boston, MA 02115 USA.
[Ghosh, Kaustabh; Ingber, Donald E.] Childrens Hosp, Dept Surg, Vasc Biol Program, Boston, MA 02115 USA.
[Ghosh, Kaustabh; McCarthy, Jason R.; Ingber, Donald E.] Harvard Univ, Sch Med, Boston, MA USA.
[Ghosh, Kaustabh; Kanapathipillai, Mathumai; Korin, Netanel; Ingber, Donald E.] Harvard Univ, Wyss Inst Biol Inspired Engn, Boston, MA 02115 USA.
[McCarthy, Jason R.] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Ingber, Donald E.] Harvard Univ, Sch Engn & Appl Sci, Cambridge, MA 02138 USA.
RP Ingber, DE (reprint author), Childrens Hosp, Dept Pathol, Vasc Biol Program, Boston, MA 02115 USA.
EM don.ingber@wyss.harvard.edu
FU NIH [1RL9EB008539-01, RL1 DE019023-01]; Wyss Institute for Biologically
Inspired Engineering at Harvard University
FX This work was supported by NIH U54 sysCODE Postdoctoral Training grant
(1RL9EB008539-01 to KG.), NIH U54 sysCODE grant (RL1 DE019023-01 to
D.E.I), and the Wyss Institute for Biologically Inspired Engineering at
Harvard University.
NR 27
TC 14
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U1 2
U2 23
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1530-6984
J9 NANO LETT
JI Nano Lett.
PD JAN
PY 2012
VL 12
IS 1
BP 203
EP 208
DI 10.1021/nl203334c
PG 6
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied;
Physics, Condensed Matter
SC Chemistry; Science & Technology - Other Topics; Materials Science;
Physics
GA 874GJ
UT WOS:000298943100036
PM 22196766
ER
PT J
AU Trowbridge, JJ
Orkin, SH
AF Trowbridge, Jennifer J.
Orkin, Stuart H.
TI Dnmt3a silences hematopoietic stem cell self-renewal
SO NATURE GENETICS
LA English
DT Editorial Material
ID NOVO DNA METHYLTRANSFERASE; METHYLATION; MUTATIONS
C1 [Trowbridge, Jennifer J.] Childrens Hosp Boston, Dept Pediat Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
Childrens Hosp Boston, Div Hematol Oncol, Boston, MA USA.
RP Trowbridge, JJ (reprint author), Childrens Hosp Boston, Dept Pediat Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
EM trowbridge@bloodgroup.tch.harvard.edu; stuart_orkin@dfci.harvard.edu
NR 12
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U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD JAN
PY 2012
VL 44
IS 1
BP 13
EP 14
DI 10.1038/ng.1043
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 870JA
UT WOS:000298664000006
PM 22200773
ER
PT J
AU Zhang, JW
Jackson, AF
Naito, T
Dose, M
Seavitt, J
Liu, FF
Heller, EJ
Kashiwagi, M
Yoshida, T
Gounari, F
Petrie, HT
Georgopoulos, K
AF Zhang, Jiangwen
Jackson, Audrey F.
Naito, Taku
Dose, Marei
Seavitt, John
Liu, Feifei
Heller, Elizabeth J.
Kashiwagi, Mariko
Yoshida, Toshimi
Gounari, Fotini
Petrie, Howard T.
Georgopoulos, Katia
TI Harnessing of the nucleosome-remodeling-deacetylase complex controls
lymphocyte development and prevents leukemogenesis
SO NATURE IMMUNOLOGY
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; DNA-BINDING PROTEINS; GENE-EXPRESSION;
POLYCOMB GROUP; CELL-FATE; CHROMATIN; IKAROS; TRANSCRIPTION; NETWORK;
COHESIN
AB Cell fate depends on the interplay between chromatin regulators and transcription factors. Here we show that activity of the Mi-2 beta nucleosome-remodeling and histone-deacetylase (NuRD) complex was controlled by the Ikaros family of lymphoid lineage-determining proteins. Ikaros, an integral component of the NuRD complex in lymphocytes, tethered this complex to active genes encoding molecules involved in lymphoid differentiation. Loss of Ikaros DNA-binding activity caused a local increase in chromatin remodeling and histone deacetylation and suppression of lymphoid cell-specific gene expression. Without Ikaros, the NuRD complex also redistributed to transcriptionally poised genes that were not targets of Ikaros (encoding molecules involved in proliferation and metabolism), which induced their reactivation. Thus, release of NuRD from Ikaros regulation blocks lymphocyte maturation and mediates progression to a leukemic state by engaging functionally opposing epigenetic and genetic networks.
C1 [Jackson, Audrey F.; Naito, Taku; Seavitt, John; Liu, Feifei; Heller, Elizabeth J.; Kashiwagi, Mariko; Yoshida, Toshimi; Georgopoulos, Katia] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cuteneous Biol Res Ctr, Charlestown, MA USA.
[Zhang, Jiangwen] Harvard Univ, Fac Arts & Sci Res Comp, Cambridge, MA 02138 USA.
[Petrie, Howard T.] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Petrie, Howard T.] Scripps Res Inst, Dept Canc Biol, Jupiter, FL USA.
RP Georgopoulos, K (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cuteneous Biol Res Ctr, Charlestown, MA USA.
EM katia.georgopoulos@cbrc2.mgh.harvard.edu
RI Zhang, Jiangwen/A-7654-2013;
OI Dose, Marei/0000-0001-5394-9779
FU US National Institutes of Health [2T32AI007529, 5R01AI042254,
R01CA158006]
FX We thank P. Gomez for analysis of the expression of Mi-2 beta protein in
thymocytes; the Kingston laboratory (Massachusetts General Hospital) for
the hSWI-SNF complex and help with setting up the mononucleosome and 5S
array assays; I. Joshi for help with cell sorting; B. Czyzewski for
mouse husbandry; and B. Morgan for discussions of the project and
critical review of the manuscript. Protein microsequencing was done at
the Microchemistry and Proteomics Facility of Harvard University,
Cambridge, and at the Taplin Mass Spectrometry Facility of Harvard
Medical School, Boston, and high-throughput DNA sequencing and RNA
profiling were done at the Bauer Center for Genomic Research of Harvard
University, Cambridge. Supported by the US National Institutes of Health
(2T32AI007529 to A.F.J.; and 5R01AI042254 and R01CA158006 to K.G.).
NR 47
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U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD JAN
PY 2012
VL 13
IS 1
BP 86
EP U132
DI 10.1038/ni.2150
PG 10
WC Immunology
SC Immunology
GA 866VB
UT WOS:000298412800015
PM 22080921
ER
PT J
AU Tschop, MH
Speakman, JR
Arch, JRS
Auwerx, J
Bruning, JC
Chan, L
Eckel, RH
Farese, RV
Galgani, JE
Hambly, C
Herman, MA
Horvath, TL
Kahn, BB
Kozma, SC
Maratos-Flier, E
Muller, TD
Munzberg, H
Pfluger, PT
Plum, L
Reitman, ML
Rahmouni, K
Shulman, GI
Thomas, G
Kahn, CR
Ravussin, E
AF Tschoep, Matthias H.
Speakman, John R.
Arch, Jonathan R. S.
Auwerx, Johan
Bruening, Jens C.
Chan, Lawrence
Eckel, Robert H.
Farese, Robert V., Jr.
Galgani, Jose E.
Hambly, Catherine
Herman, Mark A.
Horvath, Tamas L.
Kahn, Barbara B.
Kozma, Sara C.
Maratos-Flier, Eleftheria
Mueller, Timo D.
Muenzberg, Heike
Pfluger, Paul T.
Plum, Leona
Reitman, Marc L.
Rahmouni, Kamal
Shulman, Gerald I.
Thomas, George
Kahn, C. Ronald
Ravussin, Eric
TI A guide to analysis of mouse energy metabolism
SO NATURE METHODS
LA English
DT Article
ID CHRONIC SOCIAL STRESS; DIET-INDUCED OBESITY; FAT-FREE MASS;
BODY-COMPOSITION; LABORATORY MICE; FOOD-INTAKE; EXPENDITURE; TISSUE;
AGE; BEHAVIOR
AB We present a consolidated view of the complexity and challenges of designing studies for measurement of energy metabolism in mouse models, including a practical guide to the assessment of energy expenditure, energy intake and body composition and statistical analysis thereof. We hope this guide will facilitate comparisons across studies and minimize spurious interpretations of data. We recommend that division of energy expenditure data by either body weight or lean body weight and that presentation of group effects as histograms should be replaced by plotting individual data and analyzing both group and body-composition effects using analysis of covariance (ANCOVA). The epidemic of obesity has generated a large
C1 [Muenzberg, Heike; Ravussin, Eric] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Tschoep, Matthias H.; Mueller, Timo D.; Pfluger, Paul T.] Tech Univ Munich, Dept Med, Helmholz Ctr Munich, Inst Diabet & Obes, Munich, Germany.
[Speakman, John R.; Hambly, Catherine] Univ Aberdeen, Inst Biol & Environm Sci, Aberdeen, Scotland.
[Speakman, John R.] Chinese Acad Sci, Inst Genet & Dev Biol, Beijing, Peoples R China.
[Arch, Jonathan R. S.] Univ Buckingham, Clore Lab, Buckingham, England.
[Auwerx, Johan] Ecole Polytech Fed Lausanne, Lausanne, Switzerland.
[Bruening, Jens C.] Max Planck Inst Neurol Res, D-50931 Cologne, Germany.
[Chan, Lawrence] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Chan, Lawrence] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA.
[Eckel, Robert H.] Univ Colorado Denver Sch Med, Div Endocrinol Diabet & Metab, Dept Med, Aurora, CO USA.
[Farese, Robert V., Jr.] Univ Calif San Francisco, Gladstone Inst Cardiovasc Dis, San Francisco, CA 94143 USA.
[Galgani, Jose E.] Univ Chile, Fac Med, Dept Nutr, Santiago 7, Chile.
[Herman, Mark A.; Kahn, Barbara B.; Maratos-Flier, Eleftheria] Beth Israel Deaconess Med Ctr, Dept Med, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA.
[Horvath, Tamas L.] Yale Univ, Sch Med, Comparat Med Sect, Program Integrat Cell Signaling & Neurobiol Met, New Haven, CT 06510 USA.
[Kozma, Sara C.; Thomas, George] Univ Cincinnati, Coll Med, Dept Canc & Cell Biol, Metab Dis Inst, Cincinnati, OH USA.
[Plum, Leona] Columbia Univ, Naomi Berrie Diabet Ctr, New York, NY USA.
[Plum, Leona] Columbia Univ, Dept Med, New York, NY USA.
[Reitman, Marc L.] NIDDKD, Diabet Endocrinol & Obes Branch, US Natl Inst Hlth, Bethesda, MD 20892 USA.
[Rahmouni, Kamal] Univ Iowa Carver Coll Med, Ctr Funct Genom Hypertens, Dept Internal Med, Iowa City, IA USA.
[Shulman, Gerald I.] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA.
[Kahn, C. Ronald] Harvard Univ, Sch Med, Joslin Diabet Ctr, Div Res, Boston, MA 02115 USA.
RP Ravussin, E (reprint author), Pennington Biomed Res Ctr, Baton Rouge, LA USA.
EM c.ronald.kahn@joslin.harvard.edu; e.ravussin@pbrc.edu
RI Herman, Mark/H-3232-2012; Reitman, Marc/B-4448-2013; John,
Speakman/A-9494-2008; Tschoep, Matthias/I-5443-2014; Thomas,
George/K-9235-2014;
OI Reitman, Marc/0000-0002-0426-9475; John, Speakman/0000-0002-2457-1823;
Thomas, George/0000-0003-3518-8149; Tschoep,
Matthias/0000-0002-4744-371X
FU Biotechnology and Biological Sciences Research Council [BB/G009953/1];
NHLBI NIH HHS [R01 HL051586]; NIDDK NIH HHS [R01 DK056084, R01 DK040936,
R01 DK082659, R37 DK031036, R37 DK043051, U24 DK059635]
NR 56
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U1 3
U2 49
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
J9 NAT METHODS
JI Nat. Methods
PD JAN
PY 2012
VL 9
IS 1
BP 57
EP 63
DI 10.1038/NMETH.1806
PG 7
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 870KB
UT WOS:000298667000028
PM 22205519
ER
PT J
AU Barabasi, AL
AF Barabasi, Albert-Laszlo
TI The network takeover
SO NATURE PHYSICS
LA English
DT Editorial Material
ID COMPLEX NETWORKS
AB Reductionism, as a paradigm, is expired, and complexity, as a field, is tired. Data-based mathematical models of complex systems are offering a fresh perspective, rapidly developing into a new discipline: network science.
C1 [Barabasi, Albert-Laszlo] Northeastern Univ, Ctr Complex Network Res, Boston, MA 02115 USA.
[Barabasi, Albert-Laszlo] Northeastern Univ, Dept Phys Comp Sci & Biol, Boston, MA 02115 USA.
[Barabasi, Albert-Laszlo] Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA.
[Barabasi, Albert-Laszlo] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA.
RP Barabasi, AL (reprint author), Northeastern Univ, Ctr Complex Network Res, Boston, MA 02115 USA.
EM alb@neu.edu
NR 11
TC 91
Z9 93
U1 8
U2 61
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1745-2473
J9 NAT PHYS
JI Nat. Phys.
PD JAN
PY 2012
VL 8
IS 1
BP 14
EP 16
PG 3
WC Physics, Multidisciplinary
SC Physics
GA 866YV
UT WOS:000298423000009
ER
PT J
AU Olson, EM
Lin, NU
Krop, IE
Winer, EP
AF Olson, Erin M.
Lin, Nancy U.
Krop, Ian E.
Winer, Eric P.
TI Use of discard pleural fluid in molecular research
SO NATURE REVIEWS CLINICAL ONCOLOGY
LA English
DT Letter
ID LUNG-CANCER; GEFITINIB
C1 [Lin, Nancy U.; Krop, Ian E.; Winer, Eric P.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02215 USA.
[Olson, Erin M.] Ohio State Univ, Coll Med, Richard J Solove Res Inst, Columbus, OH 43210 USA.
[Olson, Erin M.] Ohio State Univ, Coll Med, Arthur G James Canc Hosp, Columbus, OH 43210 USA.
RP Winer, EP (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM ewiner@partners.org
NR 8
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4774
J9 NAT REV CLIN ONCOL
JI Nat. Rev. Clin. Oncol.
PD JAN
PY 2012
VL 9
IS 1
DI 10.1038/nrclinonc.2011.114-c2
PG 1
WC Oncology
SC Oncology
GA 866TQ
UT WOS:000298407300013
ER
PT J
AU Jensen, DM
AF Jensen, Dennis M.
TI ULCER Prediction and prevention of peptic ulcer rebleeding
SO NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Editorial Material
ID UPPER-GASTROINTESTINAL HEMORRHAGE
C1 VA Greater Los Angeles Healthcare Syst, CURE DDRC, Los Angeles, CA 90073 USA.
RP Jensen, DM (reprint author), VA Greater Los Angeles Healthcare Syst, CURE DDRC, Room 318,Bldg 115,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM djensen@mednet.ucla.edu
NR 9
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5045
J9 NAT REV GASTRO HEPAT
JI Nat. Rev. Gastroenterol. Hepatol.
PD JAN
PY 2012
VL 9
IS 1
BP 7
EP 8
DI 10.1038/nrgastro.2011.243
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 866FY
UT WOS:000298367100001
PM 22143269
ER
PT J
AU Mercier, FE
Ragu, C
Scadden, DT
AF Mercier, Francois E.
Ragu, Christine
Scadden, David T.
TI The bone marrow at the crossroads of blood and immunity
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Review
ID HEMATOPOIETIC STEM-CELLS; HYPOXIA-INDUCIBLE FACTOR;
SYMPATHETIC-NERVOUS-SYSTEM; RENEWAL IN-VIVO; ENDOTHELIAL-CELLS;
PROGENITOR CELLS; SELF-RENEWAL; B-CELLS; STROMAL CELLS; MESENCHYMAL STEM
AB Progenitor cells that are the basis for all blood cell production share the bone marrow with more mature elements of the adaptive immune system. Specialized niches within the bone marrow guide and, at times, constrain the development of haematopoietic stem and progenitor cells (HSPCs) and lineage-restricted immune progenitor cells. Specific niche components are organized into distinct domains to create a diversified landscape in which specialized cell differentiation or population expansion programmes proceed. Local cues that reflect the tissue and organismal state affect cellular interactions to alter the production of a range of cell types. Here, we review the organization of regulatory elements in the bone marrow and discuss how these elements provide a dynamic means for the host to modulate stem cell and adaptive immune cell responses to physiological challenges.
C1 [Mercier, Francois E.; Ragu, Christine; Scadden, David T.] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
[Mercier, Francois E.; Ragu, Christine; Scadden, David T.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Mercier, Francois E.; Ragu, Christine; Scadden, David T.] Harvard Univ, Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
[Mercier, Francois E.; Ragu, Christine; Scadden, David T.] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
RP Scadden, DT (reprint author), Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
EM dscadden@mgh.harvard.edu
OI Ragu, Christine/0000-0002-1150-1105
FU Canadian Institutes of Health Research; Massachusetts General Hospital;
Ellison Medical Foundation; National Heart, Lung and Blood Institute
[U01HL10042, R01HL44851]
FX The authors would like to thank D. B. Sykes, L. Silberstein and I.
Droujinine for their comments on the manuscript. Thanks also go to J.-P.
Levesque and S. Mendez-Ferrer for generously contributing to FIG. 3. F.
E. M. is a recipient of a Clinician Scientist Training Award from the
Canadian Institutes of Health Research. C. R. was funded by
Massachusetts General Hospital institutional funds. This work was
supported by the Ellison Medical Foundation and the National Heart, Lung
and Blood Institute (grants U01HL10042 and R01HL44851).
NR 125
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U1 1
U2 37
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1733
EI 1474-1741
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD JAN
PY 2012
VL 12
IS 1
BP 49
EP 60
DI 10.1038/nri3132
PG 12
WC Immunology
SC Immunology
GA 866GM
UT WOS:000298368500013
PM 22193770
ER
PT J
AU Dranoff, G
AF Dranoff, Glenn
TI Experimental mouse tumour models: what can be learnt about human cancer
immunology?
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Article
ID REGULATORY T-CELLS; METHYLCHOLANTHRENE-INDUCED SARCOMAS; RESISTANT
PROSTATE-CANCER; COMBINATION IMMUNOTHERAPY; ESTABLISHED TUMORS; ADOPTIVE
IMMUNOTHERAPY; IMMUNE-RESPONSE; CTLA-4 BLOCKADE; ANIMAL-MODELS;
SIPULEUCEL-T
AB The recent demonstration that cancer immunotherapy extends patient survival has reinvigorated interest in elucidating the role of immunity in tumour pathogenesis. Experimental mouse tumour models have provided key mechanistic insights into host antitumour immune responses, and these have guided the development of novel treatment strategies. To accelerate the translation of these findings into clinical benefits, investigators need to gain a better understanding of the strengths and limitations of mouse model systems as tools for deciphering human antitumour immune responses.
C1 [Dranoff, Glenn] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Dranoff, Glenn] Dana Farber Canc Inst, Canc Vaccine Ctr, Boston, MA 02215 USA.
[Dranoff, Glenn] Brigham & Womens Hosp, Dept Med, Boston, MA 02215 USA.
[Dranoff, Glenn] Harvard Univ, Sch Med, Boston, MA 02215 USA.
RP Dranoff, G (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
EM glenn_dranoff@dfci.harvard.edu
FU US National Cancer Institute; Leukemia and Lymphoma Society; Melanoma
Research Alliance; Alliance for Cancer Gene Therapy; Research Foundation
for the Treatment of Ovarian Cancer
FX Glenn Dranoff is supported by grants from the US National Cancer
Institute, the Leukemia and Lymphoma Society, the Melanoma Research
Alliance, the Alliance for Cancer Gene Therapy and the Research
Foundation for the Treatment of Ovarian Cancer.
NR 61
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U1 3
U2 20
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1733
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD JAN
PY 2012
VL 12
IS 1
BP 61
EP 66
DI 10.1038/nri3129
PG 6
WC Immunology
SC Immunology
GA 866GM
UT WOS:000298368500014
ER
PT J
AU Barkhof, F
Simon, JH
Fazekas, F
Rovaris, M
Kappos, L
de Stefano, N
Polman, CH
Petkau, J
Radue, EW
Sormani, MP
Li, DK
O'Connor, P
Montalban, X
Miller, DH
Filippi, M
AF Barkhof, Frederik
Simon, Jack H.
Fazekas, Franz
Rovaris, Marco
Kappos, Ludwig
de Stefano, Nicola
Polman, Chris H.
Petkau, John
Radue, Ernst W.
Sormani, Maria P.
Li, David K.
O'Connor, Paul
Montalban, Xavier
Miller, David H.
Filippi, Massimo
TI MRI monitoring of immunomodulation in relapse-onset multiple sclerosis
trials
SO NATURE REVIEWS NEUROLOGY
LA English
DT Review
ID PLACEBO-CONTROLLED TRIAL; GADOLINIUM-ENHANCED MRI; SURROGATE END-POINTS;
CONTROLLED PHASE IIB; DOUBLE-BLIND; CLINICAL-TRIALS; SPINAL-CORD; ORAL
FINGOLIMOD; INTRAMUSCULAR INTERFERON; CONTROLLED MULTICENTER
AB Over the past 15 years, MRI lesion activity has become the accepted surrogate primary outcome measure in proof-of-concept placebo-controlled clinical trials of new immunomodulating therapies in relapse-onset multiple sclerosis (MS). In parallel, the number of patients that are available for the placebo arm of trials has declined, and more-aggressive drugs are being developed. A critical review is warranted to ensure efficient MRI-and patient-resource utilization. Recently, an international panel reviewed the methodology for efficient use of MRI-monitored trials in relapse-onset MS. In this article, we provide up-to-date recommendations for scan acquisition, image analysis, outcome-measure definition and standards of reporting. Factors to consider for optimizing trial design, such as outcome measure selection and the unique requirements of phase II and phase III trials, including active-comparator studies, are outlined. Finally, we address safety considerations in the use of MRI in MS trials, and the safety-related responsibilities of the various parties involved in conducting such trials.
C1 [Barkhof, Frederik; Polman, Chris H.] Vrije Univ Amsterdam Med Ctr, Amsterdam, Netherlands.
[Simon, Jack H.] Portland VA Med Ctr, Portland, OR USA.
[Fazekas, Franz] Med Univ Graz, Graz, Austria.
[Rovaris, Marco] Sci Inst Fdn Don Gnocchi, Milan, Italy.
[Kappos, Ludwig; Radue, Ernst W.] Univ Basel Hosp, Basel, Switzerland.
[de Stefano, Nicola] Univ Siena, I-53100 Siena, Italy.
[Petkau, John; Li, David K.] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
[Sormani, Maria P.] Univ Genoa, I-16126 Genoa, Italy.
[O'Connor, Paul] St Michaels Hosp, Toronto, ON M5B 1W8, Canada.
[Montalban, Xavier] Hosp Valle De Hebron, Barcelona, Spain.
[Miller, David H.] UCL, London WC1E 6BT, England.
[Filippi, Massimo] Inst Sci, Milan, Italy.
[Filippi, Massimo] Univ Hosp San Raffaele, Milan, Italy.
RP Barkhof, F (reprint author), Vrije Univ Amsterdam Med Ctr, Amsterdam, Netherlands.
EM f.barkhof@vumc.nl
FU MAGNIMS; US National Multiple Sclerosis Society; Multiple Sclerosis
Society of Canada; Bayer-Schering Pharma
FX This work is based on a workshop of the Magnetic Resonance Imaging
Network in Multiple Sclerosis (MAGNIMS) working group, co-sponsored by
MAGNIMS, the US National Multiple Sclerosis Society and the Multiple
Sclerosis Society of Canada, and supported by an unrestricted
educational grant by Bayer-Schering Pharma. We thank A. Thompson and J.
Palace for their helpful input.
NR 80
TC 22
Z9 22
U1 1
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4758
EI 1759-4766
J9 NAT REV NEUROL
JI Nat. Rev. Neurol.
PD JAN
PY 2012
VL 8
IS 1
BP 13
EP 21
DI 10.1038/nrneurol.2011.190
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 866VT
UT WOS:000298415000006
PM 22143362
ER
PT J
AU Spires-Jones, T
Knafo, S
AF Spires-Jones, Tara
Knafo, Shira
TI Spines, Plasticity, and Cognition in Alzheimer's Model Mice
SO NEURAL PLASTICITY
LA English
DT Review
ID AMYLOID PRECURSOR PROTEIN; TRANSGENIC MOUSE MODEL; LONG-TERM
POTENTIATION; CONTEXTUAL FEAR EXTINCTION; TANGLE-BEARING NEURONS; A-BETA
OLIGOMERS; SYNAPTIC PLASTICITY; IN-VIVO; DENDRITIC SPINES; MEMORY
DEFICITS
AB The pathological hallmarks of Alzheimer's disease (AD)-widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (A beta) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles-have been known for many decades, but the links between AD pathology and dementia and effective therapeutic strategies remain elusive. Transgenic mice have been developed based on rare familial forms of AD and frontotemporal dementia, allowing investigators to test in detail the structural, functional, and behavioral consequences of AD-associated pathology. Here, we review work on transgenic AD models that investigate the degeneration of dendritic spine structure, synaptic function, and cognition. Together, these data support a model of AD pathogenesis in which soluble A beta initiates synaptic dysfunction and loss, as well as pathological changes in tau, which contribute to both synaptic and neuronal loss. These changes in synapse structure and function as well as frank synapse and neuronal loss contribute to the neural system dysfunction which causes cognitive deficits. Understanding the underpinnings of dementia in AD will be essential to develop and evaluate therapeutic approaches for this widespread and devastating disease.
C1 [Spires-Jones, Tara] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Charlestown, MA 02129 USA.
[Knafo, Shira] Univ Autonoma Madrid, E-28049 Madrid, Spain.
[Knafo, Shira] CSIC, Ctr Biol Mol Severo Ochoa, E-28049 Madrid, Spain.
RP Spires-Jones, T (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, 114 16th St, Charlestown, MA 02129 USA.
EM tspires@partners.org; sknafo@cbm.uam.es
OI Knafo, Shira/0000-0002-4478-7584; Spires-Jones, Tara/0000-0003-2530-0598
NR 145
TC 35
Z9 35
U1 2
U2 12
PU HINDAWI PUBLISHING CORPORATION
PI NEW YORK
PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA
SN 0792-8483
J9 NEURAL PLAST
JI Neural. Plast.
PY 2012
AR 319836
DI 10.1155/2012/319836
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 871NP
UT WOS:000298745200001
ER
PT J
AU Kremen, WS
Panizzon, MS
Neale, MC
Fennema-Notestine, C
Prom-Wormley, E
Eyler, LT
Stevens, A
Franz, CE
Lyons, MJ
Grant, MD
Jak, AJ
Jernigan, TL
Xian, H
Fischl, B
Thermenos, HW
Seidman, LJ
Tsuang, MT
Dale, AM
AF Kremen, William S.
Panizzon, Matthew S.
Neale, Michael C.
Fennema-Notestine, Christine
Prom-Wormley, Elizabeth
Eyler, Lisa T.
Stevens, Allison
Franz, Carol E.
Lyons, Michael J.
Grant, Michael D.
Jak, Amy J.
Jernigan, Terry L.
Xian, Hong
Fischl, Bruce
Thermenos, Heidi W.
Seidman, Larry J.
Tsuang, Ming T.
Dale, Anders M.
TI Heritability of brain ventricle volume: Converging evidence from
inconsistent results
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Aging; Alzheimer's Disease; Endophenotype; Genetics; Lateral ventricles;
Mild cognitive impairment; Structural MRI; Twins
ID DISEASE PROGRESSION; ALZHEIMERS-DISEASE; GENETIC INFLUENCES; TWIN;
POWER; SAMPLE
AB Twin studies generally show great consistency for the heritability of brain structures. Ironically, the lateral ventricles-perhaps the most reliably measured brain regions of interest-are the most inconsistent when it comes to estimating genetic influences on their volume. Heritability estimates in twin studies have ranged from zero to almost 0.80. Here we aggregate heritability estimates from extant twin studies, and we review and reinterpret some of the findings. Based on our revised estimates, we conclude that lateral ventricular volume is indeed heritable. The weighted average heritability of the revised estimates was 0.54. Although accumulated environmental insults might seem most logical as the predominant cause of age-related ventricular expansion, the data strongly suggest that genetic influences on lateral ventricular volume are increasing with age. Genetic influences accounted for 32-35% of the variance in lateral ventricular volume in childhood, but about 75% of the variance in late middle and older age. These conclusions have implications for the basic understanding of the genetic and environmental underpinnings of normative and pathological brain aging. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Kremen, William S.; Panizzon, Matthew S.; Fennema-Notestine, Christine; Eyler, Lisa T.; Franz, Carol E.; Jak, Amy J.; Jernigan, Terry L.; Tsuang, Ming T.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Kremen, William S.; Tsuang, Ming T.] Univ Calif San Diego, Ctr Behav Genom, La Jolla, CA 92093 USA.
[Kremen, William S.; Eyler, Lisa T.; Jak, Amy J.; Tsuang, Ming T.] VA Hlth Care Syst, San Diego, CA 92093 USA.
[Neale, Michael C.; Prom-Wormley, Elizabeth] Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Sch Med, Richmond, VA 23219 USA.
[Fennema-Notestine, Christine; Dale, Anders M.] Univ Calif San Diego, Dept Radiol, La Jolla, CA 92093 USA.
[Stevens, Allison; Fischl, Bruce; Thermenos, Heidi W.; Seidman, Larry J.] Massachusetts Gen Hosp, AA Martinos Ctr, Dept Radiol, Boston, MA 02129 USA.
[Lyons, Michael J.; Grant, Michael D.] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
[Xian, Hong] Washington Univ, VA Med Ctr, Sch Med, St Louis, MO 63108 USA.
[Xian, Hong] Washington Univ, Dept Internal Med, Sch Med, St Louis, MO 63108 USA.
[Thermenos, Heidi W.; Seidman, Larry J.] Harvard Univ, Sch Med, Boston, MA 02215 USA.
[Dale, Anders M.] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA.
RP Kremen, WS (reprint author), Univ Calif San Diego, Dept Psychiat, 9500 Gilman Dr,MC 0738, La Jolla, CA 92093 USA.
EM wkremen@ucsd.edu
OI Lyons, Michael/0000-0001-6516-9219; Prom-Wormley,
Elizabeth/0000-0001-9230-9723; Fennema-Notestine,
Christine/0000-0002-6527-6361
FU National Institute on Aging [AG022381, AG018384, AG018386, AG022982];
National Center for Research Resources [P41-RR14075, BIRN002]; National
Institute for Biomedical Imaging and Bioengineering [R01EB006758];
National Institute for Neurological Disorders and Stroke [R01
NS052585-01]; Mental Illness and Neuroscience Discovery (MIND)
Institute; National Alliance for Medical Image Computing (nemic);
National Institutes of Health through the NIH Roadmap for Medical
Research [U54 EB005149]; Autism and Dyslexia Project; Ellison Medical
Foundation; US Department of Veterans Affairs
FX This work was supported by National Institute on Aging (AG022381,
AG018384, AG018386, AG022982); National Center for Research Resources
(P41-RR14075; NCRR Birn Morphometric Project BIRN002); National
Institute for Biomedical Imaging and Bioengineering (R01EB006758);
National Institute for Neurological Disorders and Stroke (R01
NS052585-01); Mental Illness and Neuroscience Discovery (MIND)
Institute, part of the National Alliance for Medical Image Computing
(nemic), funded by the National Institutes of Health through the NIH
Roadmap for Medical Research Grants U54 EB005149. Additional support was
provided by the Autism and Dyslexia Project funded by the Ellison
Medical Foundation. The US Department of Veterans Affairs has provided
financial support for the development and maintenance of the Vietnam Era
Twin (VET) Registry. Numerous organizations have provided invaluable
assistance in the conduct of this study, including: 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; the Institute for Survey Research, Temple University. Most
importantly, the authors gratefully acknowledge the continued
cooperation and participation of the members of the VET Registry and
their families. Without their contribution this research would not have
been possible.
NR 32
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Z9 11
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD JAN
PY 2012
VL 33
IS 1
BP 1
EP 8
DI 10.1016/j.neurobiolaging.2010.02.007
PG 8
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 860FR
UT WOS:000297934700001
PM 20363053
ER
PT J
AU Voineskos, AN
Rajji, TK
Lobaugh, NJ
Miranda, D
Shenton, ME
Kennedy, JL
Pollock, BG
Mulsant, BH
AF Voineskos, Aristotle N.
Rajji, Tarek K.
Lobaugh, Nancy J.
Miranda, Dielle
Shenton, Martha E.
Kennedy, James L.
Pollock, Bruce G.
Mulsant, Benoit H.
TI Age-related decline in white matter tract integrity and cognitive
performance: A DTI tractography and structural equation modeling study
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Aging; Anisotropy; Cognition; Diffusion tensor imaging; White matter
ID MAGNETIC-RESONANCE DIFFUSION; TENSOR IMAGING TRACTOGRAPHY; HUMAN BRAIN;
CORPUS-CALLOSUM; FIBER TRACKING; IN-VIVO; NEUROPSYCHOLOGICAL STATUS;
UNCINATE FASCICULUS; REPEATABLE BATTERY; EXECUTIVE FUNCTION
AB Age-related decline in microstructural integrity of certain white matter tracts may explain cognitive decline associated with normal aging. Whole brain tractography and a clustering segmentation in 48 healthy individuals across the adult lifespan were used to examine: interhemispheric (corpus callosum), intrahemispheric association (cingulum, uncinate, arcuate, inferior longitudinal, inferior occipitofrontal), and projection (corticospinal) fibers. Principal components analysis reduced cognitive tests into 6 meaningful factors: (1) memory and executive function; (2) visuomotor dexterity; (3) motor speed; (4) attention and working memory; (5) set-shifting/ flexibility; and (6) visuospatial construction. Using theory-based structural equation modeling, relationships among age, white matter tract integrity, and cognitive performance were investigated. Parsimonious model fit demonstrated relationships where decline in white matter integrity may explain age-related decline in cognitive performance: inferior longitudinal fasciculus (ILF) with visuomotor dexterity; the inferior occipitofrontal fasciculus with visuospatial construction; and posterior fibers (i. e., splenium) of the corpus callosum with memory and executive function. Our findings suggest that decline in the microstructural integrity of white matter fibers can account for cognitive decline in normal aging. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Voineskos, Aristotle N.; Rajji, Tarek K.; Miranda, Dielle; Pollock, Bruce G.; Mulsant, Benoit H.] Univ Toronto, Geriatr Mental Hlth Program, Ctr Addict & Mental Hlth, Dept Psychiat, Toronto, ON M6J 1H4, Canada.
[Voineskos, Aristotle N.; Kennedy, James L.] Univ Toronto, Dept Neurosci, Ctr Addict & Mental Hlth, Dept Psychiat, Toronto, ON M6J 1H4, Canada.
[Lobaugh, Nancy J.] Univ Toronto, Sunnybrook Hlth Sci Ctr, Dept Med, Toronto, ON M6J 1H4, Canada.
[Shenton, Martha E.] Harvard Univ, Brigham & Womens Hosp, Psychiat Neuroimaging Lab, Dept Psychiat,Med Sch, Boston, MA 02115 USA.
[Shenton, Martha E.] Harvard Univ, VA Boston Healthcare Syst, Brockton Div, Sch Med, Brockton, MA 02401 USA.
[Pollock, Bruce G.] Univ Toronto, Rotman Res Inst, Baycrest Hosp, Dept Psychiat, Toronto, ON M6J 1H4, Canada.
RP Mulsant, BH (reprint author), Univ Toronto, Geriatr Mental Hlth Program, Ctr Addict & Mental Hlth, Dept Psychiat, Toronto, ON M6J 1H4, Canada.
EM benoit_mulsant@camh.net
RI Voineskos, Aristotle/J-5014-2013;
OI Kennedy, Kristen/0000-0001-5373-9026
FU Canadian Institutes of Health Research; APA/APIRE AstraZeneca; National
Institutes of Health (NIH) [MH074794, MH 50, 740, 1P50, MH08272]; NIG/HS
Nih [GM072977-01]; VA merit; VA Schizophrenia Center; Sandra A. Rotman
Research Institute; Centre for Addiction and Mental Health
FX This work was supported by the Canadian Institutes of Health Research
Clinician scientist Award (ANV); APA/APIRE AstraZeneca Young Minds in
Psychiatry Award (ANV); Canadian Institutes of Health Research
Fellowship (TKR); National Institutes of Health (NIH) [R01, grant no.
MH074794] (MES), [R01, grant number MH 50,740] (MES), NIH [1P50, grant
no. MH08272] (MES), NIG/HS Nih [U54 grant no. GM072977-01] (MES), VA
merit (MES), VA Schizophrenia Center Grant (MES), the Sandra A. Rotman
Research Institute (BGP), and the Centre for Addiction and Mental
Health.
NR 88
TC 94
Z9 96
U1 1
U2 27
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD JAN
PY 2012
VL 33
IS 1
BP 21
EP 34
DI 10.1016/j.neurobiolaging.2010.02.009
PG 14
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 860FR
UT WOS:000297934700003
PM 20363050
ER
PT J
AU Aasly, JO
Shi, M
Sossi, V
Stewart, T
Johansen, KK
Wszolek, ZK
Uitti, RJ
Hasegawa, K
Yokoyama, T
Zabetian, CP
Kim, HM
Leverenz, JB
Ginghina, C
Armaly, J
Edwards, KL
Snapinn, KW
Stoessl, AJ
Zhang, J
AF Aasly, J. O.
Shi, M.
Sossi, V.
Stewart, T.
Johansen, K. K.
Wszolek, Z. K.
Uitti, R. J.
Hasegawa, K.
Yokoyama, T.
Zabetian, C. P.
Kim, H. M.
Leverenz, J. B.
Ginghina, C.
Armaly, J.
Edwards, K. L.
Snapinn, K. W.
Stoessl, A. J.
Zhang, J.
TI Cerebrospinal fluid amyloid beta and tau in LRRK2 mutation carriers
SO NEUROLOGY
LA English
DT Article
ID PARKINSONS-DISEASE; ALPHA-SYNUCLEIN; COGNITIVE DECLINE; ALZHEIMERS; PET
AB Objective: The goal of the current investigation was to examine a cohort of symptomatic and asymptomatic LRRK2 mutation carriers, in order to address whether the reported alterations in amyloid beta (A beta) and tau species in the CSF of patients with sporadic Parkinson disease (PD) are a part of PD pathogenesis, the aging process, or a comorbid disease in patients with PD, and to explore the possibility of A beta and tau as markers of early or presymptomatic PD.
Methods: CSF A beta 42, total tau, and phosphorylated tau were measured with Luminex assays in 26 LRRK2 mutation carriers, who were either asymptomatic (n = 18) or had a phenotype resembling sporadic PD (n = 8). All patients also underwent PET scans with (18)F-6-fluoro-L-dopa (FD), (11)C-(+/-)-alpha-dihydrotetrabenazine (DTBZ), and (11)C-d-threo-methylphenidate (MP) to measure dopaminergic function in the striatum. The levels of CSF markers were then compared to each PET measurement.
Results: Reduced CSF A beta 42 and tau levels correlated with lower striatal dopaminergic function as determined by all 3 PET tracers, with a significant association between A beta 42 and FD uptake. When cases were restricted to carriers of the G2019S mutation, the most common LRRK2 variant in our cohort, significant correlations were also observed for tau.
Conclusions: The disposition of A beta and tau is likely important in both LRRK2-related and sporadic PD, even during early phases of the disease. A better understanding of their production, aggregation, and degradation, including changes in their CSF levels, may provide insights into the pathogenesis of PD and the potential utility of these proteins as biomarkers. Neurology (R) 2012;78:55-61
C1 [Shi, M.; Stewart, T.; Ginghina, C.; Armaly, J.; Zhang, J.] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA.
[Aasly, J. O.; Johansen, K. K.] Norwegian Univ Sci & Technol, Dept Neurosci, N-7034 Trondheim, Norway.
[Aasly, J. O.; Johansen, K. K.] St Olavs Univ Hosp, Dept Neurol, Trondheim, Norway.
[Zabetian, C. P.; Kim, H. M.; Leverenz, J. B.] Univ Washington, Sch Med, Dept Neurol, Seattle, WA USA.
[Leverenz, J. B.] Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Sossi, V.] Univ British Columbia, Dept Phys & Astron, Vancouver Hosp & Hlth Sci Ctr, Vancouver, BC V5Z 1M9, Canada.
[Wszolek, Z. K.; Uitti, R. J.] Mayo Clin Florida, Dept Neurol, Jacksonville, FL USA.
[Hasegawa, K.; Yokoyama, T.] Sagamihara Natl Hosp, Natl Hosp Org, Dept Neurol, Sagamihara, Kanagawa, Japan.
[Zabetian, C. P.] Vet Affairs Puget Sound Hlth Care Syst, Ctr Geriatr Res Educ & Clin, Seattle, WA USA.
[Zabetian, C. P.; Kim, H. M.; Leverenz, J. B.] Vet Affairs Puget Sound Hlth Care Syst, Parkinsons Dis Res Educ & Clin Ctr, Seattle, WA USA.
[Leverenz, J. B.] Vet Affairs Puget Sound Hlth Care Syst, Mental Illness Res Educ & Clin Ctr, Seattle, WA USA.
[Edwards, K. L.; Snapinn, K. W.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
[Stoessl, A. J.] Univ British Columbia, Pacific Parkinsons Res Ctr, Vancouver, BC V5Z 1M9, Canada.
[Stoessl, A. J.] Vancouver Coastal Hlth, Vancouver, BC, Canada.
RP Zhang, J (reprint author), Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA.
EM zhangj@uw.edu
RI Shi, Min/G-6165-2012
OI Shi, Min/0000-0002-6901-2558
FU NIH [AG025327, AG033398, P30ES007033-6364, ES004696-5897, ES012703,
ES016873, NS057567, NS060252, P50NS062684, NS065070, P50NS072187];
Department of Veterans Affairs [1I01BX000531]; Canadian Institutes of
Health Research; Michael Smith Foundation for Health Research; Pacific
Alzheimer Research Foundation; Canada Research Chairs program; Mayo
Clinic Florida Research Committee; Research Committee of CNS
Degenerative Diseases; Ministry of Health, Labour and Welfare of Japan;
Lundbeck Inc.; Allergan, Inc.; NIH/NINDS; Pacific Alzheimer Research
Foundation (Canada); CIHR; NIH; NIH (NINDS/NIA); US Department of
Veterans Affairs; Parkinson's Disease Foundation; American Parkinson
Disease Association; NIH/NIND; Michael J. Fox Foundation; Washington
Chapter American Parkinson's Disease Association/Northwest Collaborative
Care; Centers for Disease Control
FX Supported by NIH (AG025327, AG033398, P30ES007033-6364, ES004696-5897,
ES012703, ES016873, NS057567, NS060252 to J.Z., P50NS062684 to C.P.Z.,
J.B.L., and J.Z., NS065070 to C.P.Z., NS057567 and P50NS072187 to Z.K.W.
and R.J.U.), Department of Veterans Affairs (to J.B.L. and H. M. K., and
1I01BX000531 to C.P.Z.), Canadian Institutes of Health Research (to
A.J.S.), Michael Smith Foundation for Health Research (to A.J.S.),
Pacific Alzheimer Research Foundation (to A.J.S.), Canada Research
Chairs program (to A.J.S.), TRIUMF (to A.J.S.), Mayo Clinic Florida
Research Committee CR program (to Z.K.W. and R.J.U.), the gift from Carl
Edward Bolch, Jr. and Susan Bass Bolch (to Z.K.W. and R.J.U.), and
Grants-in-Aid from the Research Committee of CNS Degenerative Diseases,
the Ministry of Health, Labour and Welfare of Japan (to K.H. and T.Y.).;
Dr. Aasly serves on the editorial boards of Parkinsonism and Related
Disorders, Parkinson's Disease, and the Journal of the Norwegian Medical
Association; and his institution receives annual royalties from Lundbeck
Inc. from the licensing of the technology related to PARK8/LRRK2. Dr.
Shi reports no disclosures. Dr. Sossi has received research support from
Pacific Alzheimer Research Foundation. Dr. Stewart and Dr. Johansen
report no disclosures. Dr. Wszolek serves as Co-Editor-in-Chief of
Parkinsonism and Related Disorders, Regional Editor of the European
Journal of Neurology, and on the editorial boards of Neurologia i
Neurochirurgia Polska, Advances in Rehabilitation, the Medical Journal
of the Rzeszow University, and Clinical and Experimental Medical
Letters; holds and has contractual rights for receipt of future royalty
payments from patents re: A novel polynucleotide involved in heritable
Parkinson's disease; receives royalties from publishing Parkinsonism and
Related Disorders (Elsevier, 2007, 2008, 2009) and the European Journal
of Neurology (Wiley-Blackwell, 2007, 2008, 2009); and receives research
support from Allergan, Inc., the NIH/NINDS, Mayo Clinic Florida Research
Committee CR program, the Pacific Alzheimer Research Foundation
(Canada), the CIHR, the Mayo Clinic Florida Research Committee CR
program, and a gift from Carl Edward Bolch, Jr., and Susan Bass Bolch.
Dr. Uitti serves as an Associate Editor of Neurology (R); has received
research support from Advanced Neuromodulations Systems and from the
NIH; and his institution receives annual royalties from Lundbeck Inc.
from the licensing of the technology related to PARK8/LRRK2. Dr.
Hasegawa and Dr. Yokoyama report no disclosures. Dr. Zabetian has
received research support from NIH (NINDS/NIA), the US Department of
Veterans Affairs, the Parkinson's Disease Foundation, and the American
Parkinson Disease Association. Dr. Kim reports no disclosures. Dr.
Leverenz has served as a consultant for Bayer Schering Pharma, Novartis,
and Teva Pharmaceutical Industries Ltd.; has received speaker honoraria
from Novartis; and receives research support from the NIH/NIND, the
Michael J. Fox Foundation, the Washington Chapter American Parkinson's
Disease Association/Northwest Collaborative Care, and the US Department
of Veterans Affairs. Dr. Ginghina and J. Armaly report no disclosures.
Dr. Edwards has received research support from the NIH and the Centers
for Disease Control. K. W. Snapinn has received research support from
the NIH, the US Department of Veterans Affairs, and the Centers for
Disease Control. Dr. Stoessl serves on a scientific advisory board for
Biovail Corporation/Medgenesis; has received funding for travel and
speaker honoraria from Novartis, Teva Pharmaceutical Industries Ltd.,
Allergan, Inc., and Abbott; serves on the editorial boards of Annals of
Neurology, Lancet Neurology, and Parkinsonism & Related Disorders; and
receives research support from CIHR, the Michael Smith Foundation for
Health Research, the Michael J. Fox Foundation, and the Pacific
Alzheimer Research Foundation. Dr. Zhang serves on the editorial boards
of Neurological Disease, Neurochemical Research, the Journal of
Alzheimer's Disease, and Proteomics; and has received research support
from the NIH.
NR 20
TC 22
Z9 22
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 JAN
PY 2012
VL 78
IS 1
BP 55
EP 61
DI 10.1212/WNL.0b013e31823ed101
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 869YG
UT WOS:000298635700011
PM 22170881
ER
PT J
AU Deason, RG
Hussey, EP
Ally, BA
Budson, AE
AF Deason, Rebecca G.
Hussey, Erin P.
Ally, Brandon A.
Budson, Andrew E.
TI Changes in Response Bias With Different Study-Test Delays: Evidence From
Young Adults, Older Adults, and Patients With Alzheimer's Disease
SO NEUROPSYCHOLOGY
LA English
DT Article
DE recognition memory; Alzheimer's disease; response bias; familiarity;
recollection
ID MILD COGNITIVE IMPAIRMENT; RECOGNITION MEMORY; FALSE RECOGNITION;
EPISODIC MEMORY; PARIETAL LOBE; FRONTAL-LOBE; ASSOCIATIVE RECOGNITION;
CRITERION SHIFT; RECOLLECTION; LESIONS
AB Objective: Along with impaired discrimination, patients with Alzheimer's disease ( AD) often show an abnormally liberal response bias ( greater tendency to respond "old"). Previously we matched discrimination by varying study-test list length and found that participants' usual bias is maintained, such that patients with AD were more liberal than healthy controls. However, this pattern could be a result of the way in which discrimination was matched. In this experiment, we examined whether matching discrimination with the use of a delay would lead to a liberal response bias in healthy younger and older adults as it might lead to the use of more similar memorial processing to the patients with AD. Method: Younger adults, older adults, and patients with AD were run in 2 study-test sessions, with study and recognition test separated by either a 1-min or 1-day delay. Results: With the 1-min delay, both younger adults and healthy older adults showed a conservative response bias, while patients with AD showed a liberal response bias. When discrimination was matched between patients with AD and controls by the use of a delay, response bias was also matched, with all participants showing a more liberal response bias. Conclusions: The current study suggests that how discrimination is matched between patients with AD and controls matters greatly. Potentially, this liberal bias is a result of healthy younger and older adults relying primarily on familiarity at the longer delay, thus using more similar memorial processes to patients with AD who are dependent on familiarity at any delay.
C1 [Deason, Rebecca G.; Budson, Andrew E.] VA Boston Healthcare Syst, Ctr Translat Cognit Neurosci, Boston, MA 02130 USA.
[Deason, Rebecca G.; Budson, Andrew E.] Boston Univ, Sch Med, Alzheimers Dis Ctr, Boston, MA 02215 USA.
[Hussey, Erin P.; Ally, Brandon A.] Vanderbilt Univ, Dept Neurol, Nashville, TN USA.
[Ally, Brandon A.] Vanderbilt Univ, Dept Psychiat & Psychol, Nashville, TN USA.
RP Deason, RG (reprint author), VA Boston Healthcare Syst, Ctr Translat Cognit Neurosci, 150 S Huntington Ave,Mailstop 151-C, Boston, MA 02130 USA.
EM rdeason@bu.edu
OI Ally, Brandon/0000-0002-6034-7968
FU National Institute on Aging [R01 AG025815, K23 AG031925, P30 AG13846];
Department of Veterans Affairs, Veterans Health Administration
FX This research was supported by National Institute on Aging, grants R01
AG025815 (AEB), K23 AG031925 (BAA), P30 AG13846 (AEB); and a Department
of Veterans Affairs, Veterans Health Administration, VISN 1 Early Career
Development Award to RGD. This material is also the result of work
supported with resources and the use of facilities at the Bedford VA
Hospital in Bedford, MA and the VA Boston Healthcare System, Boston, MA.
NR 55
TC 6
Z9 6
U1 2
U2 9
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0894-4105
J9 NEUROPSYCHOLOGY
JI Neuropsychology
PD JAN
PY 2012
VL 26
IS 1
BP 119
EP 126
DI 10.1037/a0026330
PG 8
WC Psychology, Clinical; Neurosciences; Psychology
SC Psychology; Neurosciences & Neurology
GA 867XI
UT WOS:000298487700011
PM 22409339
ER
PT J
AU Almandoz, JED
Jagadeesan, BD
Moran, CJ
Cross, DT
Zipfel, GJ
Lee, JM
Romero, JM
Derdeyn, CP
AF Almandoz, Josser E. Delgado
Jagadeesan, Bharathi D.
Moran, Christopher J.
Cross, DeWitte T., III
Zipfel, Gregory J.
Lee, Jin-Moo
Romero, Javier M.
Derdeyn, Colin P.
TI Independent Validation of the Secondary Intracerebral Hemorrhage Score
With Catheter Angiography and Findings of Emergent Hematoma Evacuation
SO NEUROSURGERY
LA English
DT Article
DE Aneurysm; Arteriovenous malformation; Catheter angiography; Dural venous
sinus thrombosis; Intracerebral hemorrhage
ID CENTRAL-NERVOUS-SYSTEM; SPOT SIGN SCORE; ARTERIOVENOUS-MALFORMATIONS;
HIGHEST RISK; IDENTIFIES PATIENTS; BENIGN ANGIOPATHY; NATURAL-HISTORY;
CT ANGIOGRAPHY; FOLLOW-UP; EXPANSION
AB BACKGROUND: The secondary intracerebral hemorrhage (SICH) score, derived from a cohort of patients with intracerebral hemorrhage examined with computed tomographic (CT) angiography, predicts a patient's risk of harboring a vascular etiology.
OBJECTIVE: To validate the SICH score in an independent patient population.
METHODS: We retrospectively reviewed all adults with nontraumatic ICH who presented to our institution during a 5.4-year period and were evaluated with catheter angiography or underwent emergent hematoma evacuation, and applied the SICH score to this cohort. Receiver operating characteristic analysis was performed to determine the area under the curve (AUC) and maximum operating point (MOP). Patients with subarachnoid hemorrhage in the basal cisterns were excluded.
RESULTS: The study included 341 patients, with a mean age of 57.2 years (range, 18-88). Of these, 179 patients were male (52.5%) and 162 were female (47.5%). Two hundred ninety-two patients were evaluated with catheter angiography (85.6%), and 49 underwent emergent hematoma evacuation (14.4%). The SICH score successfully predicted an increasing risk of underlying vascular etiologies in the independent patient cohort, which was similar to the cohort examined with CT angiography. The MOP was reached at a SICH score >2, with the highest incidence of vascular etiologies in patients with SICH scores of 3 (18.8%), 4 (39%), and 5 (79.2%). There was no significant difference in the AUC between the 2 cohorts (0.82-0.87).
CONCLUSION: The SICH score successfully predicted the risk of a patient with ICH of harboring a vascular etiology in an independent patient population. This scoring system could be used to select patients with ICH for neurovascular evaluation to exclude an underlying vascular abnormality.
C1 [Almandoz, Josser E. Delgado; Jagadeesan, Bharathi D.; Moran, Christopher J.; Cross, DeWitte T., III; Derdeyn, Colin P.] Washington Univ, Mallinckrodt Inst Radiol, Div Neuroradiol, St Louis, MO 63110 USA.
[Almandoz, Josser E. Delgado; Romero, Javier M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Neuroradiol,Dept Radiol, Boston, MA USA.
[Moran, Christopher J.; Cross, DeWitte T., III; Zipfel, Gregory J.; Derdeyn, Colin P.] Washington Univ, Dept Neurol Surg, St Louis, MO 63110 USA.
[Zipfel, Gregory J.; Lee, Jin-Moo; Derdeyn, Colin P.] Washington Univ, Dept Neurol, St Louis, MO 63110 USA.
RP Almandoz, JED (reprint author), Washington Univ, Mallinckrodt Inst Radiol, Div Neuroradiol, Campus Box 8131,510 S Kingshighway Blvd, St Louis, MO 63110 USA.
EM josser.delgado@gmail.com
OI Derdeyn, Colin/0000-0002-5932-2683
FU National Institute of Neurological Disorders and Stroke [P5055977]
FX National Institute of Neurological Disorders and Stroke grant # P5055977
was used, in part, for the preparation of this manuscript. The authors
have no personal financial or institutional interest in any of the
drugs, materials, or devices described in this article.
NR 17
TC 7
Z9 7
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-396X
J9 NEUROSURGERY
JI Neurosurgery
PD JAN
PY 2012
VL 70
IS 1
BP 131
EP 140
DI 10.1227/NEU.0b013e31822fbf43
PG 10
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 863EP
UT WOS:000298145900032
ER
PT J
AU Ropper, AE
Cahill, KS
Hanna, JW
McCarthy, EF
Gokaslan, ZL
Chi, JH
AF Ropper, Alexander E.
Cahill, Kevin S.
Hanna, John W.
McCarthy, Edward F.
Gokaslan, Ziya L.
Chi, John H.
TI Primary Vertebral Tumors: A Review of Epidemiologic, Histological and
Imaging Findings, Part II: Locally Aggressive and Malignant Tumors
SO NEUROSURGERY
LA English
DT Review
DE Bone tumors; Chondrosarcoma; Chordoma; Multiple myeloma; Osteosarcoma;
Primary vertebral tumor; Spinal malignancies
ID GIANT-CELL TUMOR; EWINGS-SARCOMA; MULTIPLE-MYELOMA; MOBILE SPINE;
SOLITARY PLASMACYTOMA; SACRAL CHORDOMA; BONE-TUMORS; SKULL BASE;
OSTEOSARCOMA; EXPERIENCE
AB This second part of a comprehensive review of primary vertebral tumors focuses on locally aggressive and malignant tumors. As discussed in the earlier part of the review, both benign and malignant types of these tumors affect the adult and the pediatric population, and an understanding of their subtleties may increase their effective resection. In this review, we discuss the epidemiologic, histological, and imaging features of the most common locally aggressive primary vertebral tumors (chordoma and giant-cell tumor) and malignant tumors (chondrosarcoma, Ewing sarcoma, multiple myeloma or plasmacytoma, and osteosarcoma). The figures used for illustration are from operative patients of the senior authors (Z.L.G. and J.H.C.). Taken together, parts 1 and 2 of this article provide a thorough and illustrative review of primary vertebral tumors.
C1 [Ropper, Alexander E.; Cahill, Kevin S.; Chi, John H.] Harvard Univ, Dana Farber Canc Inst, Sch Med, Brigham & Womens Hosp,Dept Neurosurg, Boston, MA 02115 USA.
[Hanna, John W.] Harvard Univ, Dana Farber Canc Inst, Sch Med, Brigham & Womens Hosp,Dept Pathol, Boston, MA 02115 USA.
[McCarthy, Edward F.] Johns Hopkins Univ, Sch Med, Dept Pathol, Johns Hopkins Hosp, Baltimore, MD 21205 USA.
[Gokaslan, Ziya L.] Johns Hopkins Univ, Sch Med, Dept Neurosurg, Johns Hopkins Hosp, Baltimore, MD 21205 USA.
RP Chi, JH (reprint author), Harvard Univ, Dana Farber Canc Inst, Sch Med, Brigham & Womens Hosp,Dept Neurosurg, 15 Francis St, Boston, MA 02115 USA.
EM jchi@partners.org
NR 55
TC 13
Z9 13
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-396X
J9 NEUROSURGERY
JI Neurosurgery
PD JAN
PY 2012
VL 70
IS 1
BP 211
EP 219
DI 10.1227/NEU.0b013e31822d5f17
PG 9
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 863EP
UT WOS:000298145900051
PM 21768918
ER
PT J
AU Vogelbaum, MA
Jost, S
Aghi, MK
Heimberger, AB
Sampson, JH
Wen, PY
Macdonald, DR
Van den Bent, MJ
Chang, SM
AF Vogelbaum, Michael A.
Jost, Sarah
Aghi, Manish K.
Heimberger, Amy B.
Sampson, John H.
Wen, Patrick Y.
Macdonald, David R.
Van den Bent, Martin J.
Chang, Susan M.
TI Application of Novel Response/Progression Measures for Surgically
Delivered Therapies for Gliomas: Response Assessment in Neuro-Oncology
(RANO) Working Group
SO NEUROSURGERY
LA English
DT Article
DE Brain surgery; Clinical trials; End points; Macdonald criteria; Response
evaluation
ID HIGH-GRADE GLIOMAS; RECURRENT MALIGNANT GLIOMA;
MAGNETIC-RESONANCE-SPECTROSCOPY; PROGRESSION-FREE SURVIVAL; TUMOR VOLUME
DELINEATION; ADULT BRAIN-TUMORS; GLIOBLASTOMA-MULTIFORME; RADIATION
NECROSIS; CONTRAST ENHANCEMENT; PROGNOSTIC-FACTORS
AB BACKGROUND: The Response Assessment in Neuro-Oncology (RANO) Working Group is an international, multidisciplinary effort to develop new standardized response criteria for clinical trials in brain tumors. The RANO group identified knowledge gaps relating to the definitions of tumor response and progression after the use of surgical or surgically based treatments.
OBJECTIVE: To outline a proposal for new response and progression criteria for the assessment of the effects of surgery and surgically delivered therapies for patients with gliomas.
METHODS: The Surgery Working Group of RANO identified surgically related end-point evaluation problems that were not addressed in the original Macdonald criteria, performed an extensive literature review, and used a consensus-building process to develop recommendations for how to address these issues in the setting of clinical trials.
RESULTS: Recommendations were formulated for surgically related issues, including imaging changes associated with surgical resection or surgically mediated adjuvant local therapies, the determination of progression in the setting where all enhancing tumor has been removed, and how new enhancement should be interpreted in the setting where local therapies that are known to produce nonspecific enhancement have been used. Additionally, the terminology used to describe the completeness of surgical resections has been recognized to be inconsistently applied to enhancing vs nonenhancing tumors, and a new set of descriptors is proposed.
CONCLUSION: The RANO process is intended to produce end-point criteria for clinical trials that take into account the effects of prior and ongoing therapies. The RANO criteria will continue to evolve as new therapies and technologies are introduced into clinical trial and/or practice.
C1 [Vogelbaum, Michael A.] Cleveland Clin, Dept Neurosurg, Neurol Inst, Brain Tumor & Neurooncol Ctr, Cleveland, OH 44195 USA.
[Jost, Sarah] Swedish Neurosci Inst, Dept Neurosurg, Ivy Ctr Adv Brain Tumor Treatment, Seattle, WA USA.
[Aghi, Manish K.] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA USA.
[Heimberger, Amy B.] Univ Texas MD Anderson Canc Ctr, Dept Neurosurg, Houston, TX 77030 USA.
[Sampson, John H.] Duke Univ, Med Ctr, Preston Robert Tisch Brain Tumor Ctr, Durham, NC USA.
[Wen, Patrick Y.] Brigham & Womens Hosp, Dana Farber Brigham & Womens Canc Ctr, Ctr Neurooncol, Boston, MA 02115 USA.
[Wen, Patrick Y.] Brigham & Womens Hosp, Div Neurol, Boston, MA 02115 USA.
[Macdonald, David R.] Univ Western Ontario, Dept Oncol, London Reg Canc Program, London, ON, Canada.
[Van den Bent, Martin J.] Erasmus Univ Hosp Rotterdam, Daniel den Hoed Canc Ctr, Neurooncol Unit, Rotterdam, Netherlands.
[Chang, Susan M.] Univ Calif San Francisco, Dept Neurol Surg, Div Neurooncol, San Francisco, CA USA.
RP Vogelbaum, MA (reprint author), Cleveland Clin, Dept Neurosurg, Neurol Inst, Brain Tumor & Neurooncol Ctr, 9500 Euclid Ave ND40, Cleveland, OH 44195 USA.
EM vogelbm@ccf.org
NR 78
TC 83
Z9 83
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-396X
J9 NEUROSURGERY
JI Neurosurgery
PD JAN
PY 2012
VL 70
IS 1
BP 234
EP 243
DI 10.1227/NEU.0b013e318223f5a7
PG 10
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 863EP
UT WOS:000298145900055
PM 21593697
ER
PT J
AU Ferreira, M
Nahed, BV
Babu, MA
Walcott, BP
Ellenbogen, RG
Sekhar, LN
AF Ferreira, Manuel
Nahed, Brian V.
Babu, Maya A.
Walcott, Brian P.
Ellenbogen, Richard G.
Sekhar, Laligam N.
TI Trapped Fourth Ventricle Phenomenon Following Aneurysm Rupture of the
Posterior Circulation: Case Reports
SO NEUROSURGERY
LA English
DT Article
DE Aneurysm; Cerebrospinal fluid; Clipping; Fourth ventricle; Microsurgery;
Shunt
ID ISOLATED 4TH VENTRICLE; ENDOSCOPIC TREATMENT; STENT PLACEMENT;
HYDROCEPHALUS; SHUNT; HEMORRHAGE; STENOSIS; CHILDREN
AB BACKGROUND AND IMPORTANCE: Cerebral ventricular noncommunication has been described in the setting of infection and acutely in the setting of intracranial hemorrhage. We describe the first adult case series of individuals who developed delayed isolated fourth ventricles after rupture of intracranial posterior circulation aneurysms and define treatment modality.
CLINICAL PRESENTATION: A retrospective review was performed of all patients with aneurysms treated at a single institution from 2005 to 2009. Both microsurgical obliteration and endovascular cases were queried. Of 1044 aneurysms treated in this period, 3 patients were identified who required fourth ventricular shunting, for the treatment of the isolated ventricle. All 3 patients underwent microsurgical clip obliteration of their aneurysms and had subsequent frontal approach ventriculoperitoneal cerebrospinal fluid diversion. These patients had no evidence of infection of the cerebrospinal fluid as measured by serial cultures. Subsequently, all 3 patients presented in a delayed fashion with symptoms attributable to a dilated fourth ventricle and syringomyelia or syringobulbia. Either exploration or percutaneous tapping confirmed the function of the supratentorial shunt. These patients then underwent fourth ventriculoperitoneal cerebrospinal fluid diversion by the use of a low-pressure shunt system. The symptoms attributable to the isolated fourth ventricle resolved rapidly in all 3 patients after shunting. This clinical improvement correlated with the fourth ventricular size.
CONCLUSION: Isolated fourth ventricle, in an adult, is a rare phenomenon associated with intracranial posterior circulation aneurysm rupture treated with microsurgical clip obliteration. Fourth ventriculoperitoneal cerebrospinal fluid diversion is effective at resolving the symptoms attributed to the trapped ventricle and associated syrinx.
C1 [Ferreira, Manuel] Univ Washington, Harborview Med Ctr, Dept Neurosurg, UW Med,Med Sch, Seattle, WA 98104 USA.
[Nahed, Brian V.; Walcott, Brian P.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Nahed, Brian V.; Walcott, Brian P.] Harvard Univ, Sch Med, Boston, MA USA.
[Babu, Maya A.] Mayo Clin, Coll Med, Dept Neurosurg, Rochester, MN USA.
RP Ferreira, M (reprint author), Univ Washington, Harborview Med Ctr, Dept Neurosurg, UW Med,Med Sch, Box 359924,325 9Th Ave, Seattle, WA 98104 USA.
EM manuelf3@u.washington.edu
NR 28
TC 2
Z9 2
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-396X
J9 NEUROSURGERY
JI Neurosurgery
PD JAN
PY 2012
VL 70
IS 1
BP E253
EP E258
DI 10.1227/NEU.0b013e31822abf95
PG 6
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 863EP
UT WOS:000298145900059
PM 21795864
ER
PT J
AU Barr, JC
Ogilvy, CS
AF Barr, John C.
Ogilvy, Christopher S.
TI Selection of Treatment Modalities or Observation of Arteriovenous
Malformations
SO NEUROSURGERY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Arteriovenous malformations; Surgical excision; Endovascular
embolization; Radiosurgery
ID GAMMA-KNIFE RADIOSURGERY; SEIZURE CONTROL; INTRACRANIAL HEMORRHAGE;
MULTIMODALITY TREATMENT; ARTERIAL ANEURYSMS; GRADING SYSTEM; BRAIN;
SURGERY; EMBOLIZATION; RISK
AB This article provides management guidelines for arteriovenous malformations (AVMs). Management options include observation, surgical excision, endovascular embolization, and radiosurgery. Each of these can be used individually or combined for multimodal therapy based on the characteristics of the lesion. The article stratifies each lesion based on the AVM and patient characteristics to either observation or a single or multimodal treatment arm. The treatment of an AVM must be carefully weighed in each patient because of the risk of neurologic injury in functional areas of the brain and weighed against the natural history of hemorrhage.
C1 [Barr, John C.; Ogilvy, Christopher S.] Massachusetts Gen Hosp, Neurosurg Serv, Boston, MA 02114 USA.
RP Ogilvy, CS (reprint author), Massachusetts Gen Hosp, Neurosurg Serv, WAC-745,55 Fruit St, Boston, MA 02114 USA.
EM cogilvy@partners.org
NR 61
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 1042-3680
J9 NEUROSURG CLIN N AM
JI Neurosurg. Clin. N. Am.
PD JAN
PY 2012
VL 23
IS 1
BP 63
EP +
DI 10.1016/j.nec.2011.09.010
PG 14
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 865LI
UT WOS:000298312000008
PM 22107859
ER
PT J
AU Nagel, JM
Brinkoetter, M
Magkos, F
Liu, X
Chamberland, JP
Shah, S
Zhou, JR
Blackburn, G
Mantzoros, CS
AF Nagel, Jutta M.
Brinkoetter, Mary
Magkos, Faidon
Liu, Xiaowen
Chamberland, John P.
Shah, Sunali
Zhou, Jinrong
Blackburn, George
Mantzoros, Christos S.
TI Dietary walnuts inhibit colorectal cancer growth in mice by suppressing
angiogenesis
SO NUTRITION
LA English
DT Article
DE Nuts; Linseed; Colon cancer; Xenograft; VEGF
ID ALPHA-LINOLENIC ACID; CARDIOVASCULAR RISK-FACTORS; COLON-TUMOR
DEVELOPMENT; DOUBLE-BLIND; IN-VIVO; FLAXSEED; METASTASIS; CELLS; WOMEN;
XENOGRAFTS
AB Objective: Animal studies have demonstrated that dietary supplementation with flaxseed oil inhibits colorectal cancer growth. Recent data indicate that walnuts have strong antiproliferative properties against colon cancer cells in vitro but no previous study has assessed the effects of walnuts in vivo or performed a joint evaluation of flaxseed oil and walnuts. The aim of the present study was to examine the effect of dietary walnuts on colorectal cancer in vivo and to comparatively evaluate their efficacy in relation to flaxseed oil.
Methods: HT-29 human colon cancer cells were injected in 6-wk-old female nude mice. After a 1-wk acclimation period, mice (n = 48) were randomized to diets containing similar to 19% of total energy from walnuts, flaxseed oil, or corn oil (control) and were subsequently studied for 25 d.
Results: Tumor growth rate was significantly slower in walnut-fed and flaxseed-fed mice compared with corn oil-fed animals (P < 0.05) by 27% and 43%, respectively. Accordingly, final tumor weight was reduced by 33% and 44%, respectively (P < 0.05 versus control); the differences between walnut and flaxseed diets did not reach significance. We found no differences among groups in metabolic and hormonal profile, serum antioxidant capacity, or inflammation (P > 0.05). However, walnuts and flaxseed oil significantly reduced serum expression levels of angiogenesis factors, including vascular endothelial growth factor (by 30% and 80%, respectively), and approximately doubled total necrotic areas despite smaller tumor sizes (P < 0.05 versus control). Dietary walnuts significantly decreased angiogenesis (CD34 staining; P = 0.017 versus control), whereas this effect did not reach significance in the flaxseed oil group (P = 0.454 versus control).
Conclusion: We conclude that walnuts in the diet inhibit colorectal cancer growth by suppressing angiogenesis. Further studies are needed to confirm our findings in humans and explore underlying mechanisms. Published by Elsevier Inc.
C1 [Nagel, Jutta M.; Brinkoetter, Mary; Magkos, Faidon; Liu, Xiaowen; Chamberland, John P.; Shah, Sunali; Mantzoros, Christos S.] Harvard Univ, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Sch Med, Boston, MA 02215 USA.
[Zhou, Jinrong; Blackburn, George] Harvard Univ, Beth Israel Deaconess Med Ctr, Dept Surg, Sch Med, Boston, MA 02215 USA.
[Mantzoros, Christos S.] Boston VA Healthcare Syst, Boston, MA USA.
RP Mantzoros, CS (reprint author), Harvard Univ, Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Sch Med, Boston, MA 02215 USA.
EM cmantzor@bidmc.harvard.edu
OI Chamberland, John/0000-0002-7862-1371
FU National Institutes of Health [DK081913]; American Institute for Cancer
Research; California Walnut Commission
FX This work was supported by the National Institutes of Health (DK081913)
and the American Institute for Cancer Research and the California Walnut
Commission; sponsors had no input on interpretation or reporting of the
findings.
NR 43
TC 15
Z9 16
U1 1
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0899-9007
EI 1873-1244
J9 NUTRITION
JI Nutrition
PD JAN
PY 2012
VL 28
IS 1
BP 67
EP 75
DI 10.1016/j.nut.2011.03.004
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 873RF
UT WOS:000298900000012
PM 21795022
ER
PT J
AU Flanagan, J
Winters, LN
Habin, K
Cashavelly, B
AF Flanagan, Jane
Winters, Loren N.
Habin, Karleen
Cashavelly, Barbara
TI Women's Experiences With Antiestrogen Therapy to Treat Breast Cancer
SO ONCOLOGY NURSING FORUM
LA English
DT Article
ID QUALITY-OF-LIFE; POSTMENOPAUSAL WOMEN; AFRICAN-AMERICAN; TAMOXIFEN
THERAPY; CONTROLLED-TRIAL; ADJUVANT BREAST; SURVIVORS; INTERVENTIONS;
LETROZOLE; SYMPTOMS
AB Purpose/Objectives: To understand the experiences of women undergoing antiestrogen therapy (AET) to treat breast cancer.
Research Approach: Content analysis of tape-recorded focus group interviews.
Setting: Breast oncology center of a large medical center in the northeastern United States.
Participants: Purposive sample of 21 women undergoing AFT to treat breast cancer.
Methodologic Approach: A nonexperimental qualitative, descriptive design using open-ended interviews and content analysis to isolate themes.
Main Research Variables: Women's experiences with AET.
Findings: Five themes were isolated and were focused on the overall experience of having breast cancer: symptoms related to AET, shared decision making, being strong for others, discovering new priorities, and recognizing vulnerability.
Conclusions: Oral therapies are an increasingly popular treatment option for various types of cancer, particularly in women with estrogen-sensitive breast cancer. Although this type of treatment has been efficacious in terms of disease-free and overall survival, women undergoing AET face many challenges related to treatment. Healthcare providers need to understand women's perceptions of AFT and its effects as a first step in the process of developing interventions to improve care.
Interpretation: More research is needed to distinguish whether the presence of preexisting chronic illness, differences in type of AET, age, and ethnicity impact the overall experience of women on AET. Individual interviews may be necessary to fully explore the experience. Oncology nurses should implement surveillance care to explore the effects of AET on women with breast cancer.
C1 [Flanagan, Jane] Boston Coll, Connell Sch Nursing, Chestnut Hill, MA 02167 USA.
[Winters, Loren N.; Habin, Karleen] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
RP Flanagan, J (reprint author), Boston Coll, Connell Sch Nursing, Chestnut Hill, MA 02167 USA.
EM flanagjg@bc.edu
FU Boston College; Yvonne L. Munn Research Grant
FX Jane Flanagan, PhD, ANP-BC, is an assistant professor of nursing in the
Connell School of Nursing at Boston College in Massachusetts; and Loren
N. Winters, MSN, ANP-BC, RCN, OCN (R), is a nurse practitioner and
Karleen Habin, RN, is a research nurse, both in the Cancer Center, and
Barbara Cashavelly, RN, MSN, AOCN (R), is the nurse director, all at
Massachusetts General Hospital in Boston. This study was funded, in
part, by a Boston College Research Expense Grant and an Yvonne L. Munn
Research Grant. Flanagan can be reached at flanagjg@bc.edu, with copy to
editor at ONFEditor@ons.org. (Submitted January 2011. Accepted for
publication March 11, 2011.)
NR 36
TC 3
Z9 3
U1 0
U2 7
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 0190-535X
EI 1538-0688
J9 ONCOL NURS FORUM
JI Oncol. Nurs. Forum
PD JAN
PY 2012
VL 39
IS 1
BP 70
EP 77
DI 10.1188/12.ONF.70-77
PG 8
WC Oncology; Nursing
SC Oncology; Nursing
GA 873RW
UT WOS:000298901700009
PM 22201657
ER
PT J
AU Kang, JH
Loomis, S
Wiggs, JL
Stein, JD
Pasquale, LR
AF Kang, Jae Hee
Loomis, Stephanie
Wiggs, Janey L.
Stein, Joshua D.
Pasquale, Louis R.
TI Demographic and Geographic Features of Exfoliation Glaucoma in 2 United
States-Based Prospective Cohorts
SO OPHTHALMOLOGY
LA English
DT Article
ID OPEN-ANGLE GLAUCOMA; RETINAL VEIN OCCLUSION; PSEUDOEXFOLIATION SYNDROME;
NORTHERN SWEDEN; REYKJAVIK EYE; FOLLOW-UP; PREVALENCE; POPULATION;
VARIANTS; EPIDEMIOLOGY
AB Purpose: To examine prospectively the association between demographic and geographic factors in relation to exfoliation glaucoma (EG) or exfoliation glaucoma suspect (EGS).
Design: Prospective cohort study.
Participants: Seventy-eight thousand nine hundred fifty-five women in the Nurses' Health Study and 41 191 men in the Health Professionals Follow-up Study.
Methods: Female and male health professionals were followed prospectively from 1980 through 2008 and from 1986 through 2008, respectively. Eligible participants were 40 years of age or older, did not have EG or EGS at baseline, and reported undergoing eye examinations during follow-up. Information regarding demographic features, lifetime geographic residence, and potential confounders was collected. During follow-up, 348 EG or EGS cases were confirmed with medical record review. The relative risk of EG or EGS in each cohort was estimated separately and the results were pooled with meta-analysis.
Main Outcome Measures: Multivariate rate ratios (MVRRs) of EG or EGS and their 95% confidence intervals (CIs).
Results: Exfoliation glaucoma or EGS was strongly age related with subjects 75 years of age or older at 46.22-fold (95% CI, 22.77-93.80) increased risk compared with those between 40 and 55 years of age. Although men were 68% less likely to develop EG or EGS than women (MVRR, 0.32; 95% CI, 0.23-0.46), no predisposition to EG or EGS by ancestry, particularly Scandinavian ancestry, emerged. Compared with a lifetime of living in the northern tier of the continental United States, lifetime residence in the middle geographic tier (MVRR, 0.53; 95% CI, 0.40-0.71) and in the southern geographic tier (MVRR, 0.25; 95% CI, 0.09-0.71) was associated with markedly reduced risks of EG or EGS.
Conclusions: In this mainly white cohort from the United States, increasing age and female gender were significant risk factors for EG or EGS; however, Scandinavian heritage was not. Living in the middle or southern regions of the United States relative to living in the northern region was associated with a reduced risk of EG or EGS.
Financial Disclosure(s): The author(s) have no proprietary or commercial interest in any materials discussed in this article. Ophthalmology 2012; 119: 27-35 (C) 2012 by the American Academy of Ophthalmology.
C1 [Loomis, Stephanie; Wiggs, Janey L.; Pasquale, Louis R.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA 02114 USA.
[Kang, Jae Hee; Pasquale, Louis R.] Harvard Univ, Dept Med, Sch Med, Channing Lab, Boston, MA 02114 USA.
[Kang, Jae Hee; Pasquale, Louis R.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Stein, Joshua D.] Univ Michigan, Dept Ophthalmol & Visual Sci, Ann Arbor, MI 48109 USA.
RP Pasquale, LR (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, 243 Charles St, Boston, MA 02114 USA.
EM Louis_Pasquale@meei.harvard.edu
FU Research to Prevent Blindness, Inc., New York, New York; National
Institutes of Health, Bethesda, Maryland [CA87969, CA55075, EY09611,
HL35464, EY019511, EY015473]; Arthur Ashley Williams Foundation,
Holliston, Massachusetts; Harvard Glaucoma Center of Excellence, Boston,
Massachusetts
FX A Physician Scientist Award from Research to Prevent Blindness, Inc.,
New York, New York, supports Dr. Pasquale. The National Institutes of
Health, Bethesda, Maryland (grant nos.: CA87969, CA55075, EY09611,
HL35464, EY019511, EY015473 [LRP]); the Arthur Ashley Williams
Foundation, Holliston, Massachusetts; and the Harvard Glaucoma Center of
Excellence (JLW and LRP), Boston, Massachusetts.
NR 50
TC 27
Z9 28
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0161-6420
J9 OPHTHALMOLOGY
JI Ophthalmology
PD JAN
PY 2012
VL 119
IS 1
BP 27
EP 35
DI 10.1016/j.ophtha.2011.06.018
PG 9
WC Ophthalmology
SC Ophthalmology
GA 869ZS
UT WOS:000298639500006
PM 21982415
ER
PT J
AU Jea, SY
Francis, BA
Vakili, G
Filippopoulos, T
Rhee, DJ
AF Jea, Seung Youn
Francis, Brian A.
Vakili, Ghazal
Filippopoulos, Theodoros
Rhee, Douglas J.
TI Ab Interno Trabeculectomy Versus Trabeculectomy for Open-Angle Glaucoma
SO OPHTHALMOLOGY
LA English
DT Article
ID FLUOROURACIL FILTERING SURGERY; FOLLOW-UP; MITOMYCIN-C; COMPLICATIONS;
5-FLUOROURACIL; TRIAL; TUBE
AB Purpose: To compare the effect of ab interno trabeculectomy with trabeculectomy.
Design: Retrospective, cohort study.
Participants: A total of 115 patients who underwent ab interno trabeculectomy (study group) compared with 102 patients who underwent trabeculectomy with intraoperative mitomycin as an initial surgical procedure (trabeculectomy group). Inclusion criteria were open-angle glaucoma, age >= 40 years, and uncontrolled on maximally tolerated medical therapy. Exclusion criterion was concurrent surgery.
Methods: Clinical variables were collected from patient medical records.
Main Outcome Measures: Intraocular pressure (IOP) and Cox proportional hazard ratio (HR) and Kaplan-Meier survival analyses with failure defined as IOP >21 mmHg or less than 20% reduction below baseline on 2 consecutive follow-up visits after 1 month; IOP <= 5 mmHg on 2 consecutive follow-up visits after 1 month; additional glaucoma surgery; or loss of light perception vision. Secondary outcome measures include number of glaucoma medications and occurrence of complications.
Results: Mean follow-up was 27.3 and 25.5 months for the study and trabeculectomy groups, respectively. Intraocular pressure decreased from 28.1 +/- 8.6 mmHg at baseline to 15.9 +/- 4.5 mmHg (43.5% reduction) at month 24 in the study group, and from 26.3 +/- 10.9 mmHg at baseline to 10.2 +/- 4.1 mmHg (61.3% reduction) at month 24 in the trabeculectomy group. The success rates at 2 years were 22.4% and 76.1% in the study and trabeculectomy groups, respectively (P < 0.001). Younger age (P = 0.037; adjusted HR, 0.98 per year; 95% confidence interval [CI], 0.97-0.99) and lower baseline IOP (P = 0.016; adjusted HR, 0.96 per 1 mmHg; 95% CI, 0.92-0.99) were significant risk factors for failure in the multivariate analysis of the study group. With the exception of hyphema, the occurrence of postoperative complications was more frequent in the trabeculectomy group (P < 0.001). More additional glaucoma procedures were performed after ab interno trabeculectomy (43.5%) than after trabeculectomy (10.8%, P < 0.001).
Conclusions: Ab interno trabeculectomy has a lower success rate than trabeculectomy.
Financial Disclosure(s): Proprietary or commercial disclosure may be found after the references. Ophthalmology 2012; 119: 36-42 (C) 2012 by the American Academy of Ophthalmology.
C1 [Jea, Seung Youn; Filippopoulos, Theodoros; Rhee, Douglas J.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA 02114 USA.
[Francis, Brian A.; Vakili, Ghazal] Univ So Calif, Keck Sch Med, Doheny Eye Inst, Los Angeles, CA 90033 USA.
RP Rhee, DJ (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, 243 Charles St, Boston, MA 02114 USA.
EM dougrhee@aol.com
NR 20
TC 30
Z9 30
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0161-6420
J9 OPHTHALMOLOGY
JI Ophthalmology
PD JAN
PY 2012
VL 119
IS 1
BP 36
EP 42
DI 10.1016/j.ophtha.2011.06.046
PG 7
WC Ophthalmology
SC Ophthalmology
GA 869ZS
UT WOS:000298639500007
PM 21982416
ER
PT J
AU Yoon, N
Kwon, JW
Seo, SW
Ahn, G
Choi, YL
AF Yoon, Nara
Kwon, Jong Won
Seo, Sung Wook
Ahn, Geunghwan
Choi, Yoon-La
TI Sclerosing epithelioid fibrosarcoma: Cytogenetic analysis of FUS
rearrangement
SO PATHOLOGY INTERNATIONAL
LA English
DT Article
DE beta-catenin; FUS; sclerosing epithelioid fibrosarcoma
ID GRADE FIBROMYXOID SARCOMA; DESMOID TUMORS; BETA-CATENIN; GENE
AB Sclerosing epithelioid fibrosarcoma (SEF) is a rare but distinct variant of fibrosarcoma. A 43-year-old man presented with a lesion in his back that had been present for three years but had recently increased in size. Magnetic resonance imaging (MRI) revealed a 6-cm sized ovoid mass showing low intensities on T1 and T2 weighted images. Histologically, the tumor was of moderate cellularity, and the cells were relatively uniform in size and shape. The cells were epithelioid, round, oval and polygonal with clear and slightly eosinophilic cytoplasm, forming nests, cords, or sheet-like patterns with a dense collagenous and hyalinized matrix. The tumor was positive for vimentin, but negative for smooth muscle actin, desmin, HMB45, and CD34. Although the tumor showed nuclear overexpression of beta-catenin protein, the CTNNB1 exon3 mutation was not detected. Fluorescent in situ hybridization for FUS using dual color break-apart probes showed rearrangement of the FUS. In accordance with previous studies, our case showed positive findings of FUS rearrangement, reinforcing the notion of a close relationship between low grade fibromyxoid sarcoma and SEF.
C1 [Choi, Yoon-La] Sungkyunkwan Univ, Dept Pathol, Samsung Med Ctr, Sch Med,Coll Med, Seoul 135710, South Korea.
[Kwon, Jong Won] Sungkyunkwan Univ, Dept Radiol, Samsung Med Ctr, Coll Med, Seoul 135710, South Korea.
[Seo, Sung Wook] Sungkyunkwan Univ, Dept Orthoped Surg, Samsung Med Ctr, Coll Med, Seoul 135710, South Korea.
[Ahn, Geunghwan] Univ Calif San Francisco, San Francisco Vet Affairs Med Ctr, Dept Pathol, San Francisco, CA 94143 USA.
RP Choi, YL (reprint author), Sungkyunkwan Univ, Dept Pathol, Samsung Med Ctr, Sch Med,Coll Med, 50 Ilwondong, Seoul 135710, South Korea.
EM ylachoi@skku.edu
NR 15
TC 6
Z9 6
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1320-5463
J9 PATHOL INT
JI Pathol. Int.
PD JAN
PY 2012
VL 62
IS 1
BP 65
EP 68
DI 10.1111/j.1440-1827.2011.02752.x
PG 4
WC Pathology
SC Pathology
GA 867US
UT WOS:000298480900010
PM 22192807
ER
PT J
AU Rosen, LJ
Ben Noach, M
Winickoff, JP
Hovell, MF
AF Rosen, Laura J.
Ben Noach, Michal
Winickoff, Jonathan P.
Hovell, Mel F.
TI Parental Smoking Cessation to Protect Young Children: A Systematic
Review and Meta-analysis
SO PEDIATRICS
LA English
DT Review
DE parenting; second hand smoke; smoking cessation; systematic reviews;
tobacco use/smoking
ID ENVIRONMENTAL TOBACCO-SMOKE; RANDOMIZED CONTROLLED-TRIAL; RELAPSE
PREVENTION INTERVENTION; LOW-INCOME CHILDREN; PASSIVE SMOKING;
ASTHMATIC-CHILDREN; MATERNAL SMOKING; RESPIRATORY ILLNESS; ETS EXPOSURE;
LATINO CHILDREN
AB BACKGROUND: Young children can be protected from much of the harm from tobacco smoke exposure if their parents quit smoking. Some researchers encourage parents to quit for their children's benefit, but the evidence for effectiveness of such approaches is mixed.
OBJECTIVE: To perform a systematic review and meta-analysis to quantify the effects of interventions that encourage parental cessation.
METHODS: We searched PubMed, the Cochrane Library, Web of Science, and PsycINFO. Controlled trials published before April 2011 that targeted smoking parents of infants or young children, encouraged parents to quit smoking for their children's benefit, and measured parental quit rates were included. Study quality was assessed. Relative risks and risk differences were calculated by using the DerSimonian and Laird random-effects model.
RESULTS: Eighteen trials were included. Interventions took place in hospitals, pediatric clinical settings, well-baby clinics, and family homes. Quit rates averaged 23.1% in the intervention group and 18.4% in the control group. The interventions successfully increased the parental quit rate. Subgroups with significant intervention benefits were children aged 4 to 17 years, interventions whose primary goal was cessation, interventions that offered medications, and interventions with high follow-up rates (>80%).
CONCLUSIONS: Interventions to achieve cessation among parents, for the sake of the children, provide a worthwhile addition to the arsenal of cessation approaches, and can help protect vulnerable children from harm due to tobacco smoke exposure. However, most parents do not quit, and additional strategies to protect children are needed. Pediatrics 2012; 129: 141-152
C1 [Rosen, Laura J.; Ben Noach, Michal] Tel Aviv Univ, Sch Publ Hlth, Sackler Fac Med, Dept Hlth Promot, IL-69978 Ramat Aviv, Israel.
[Winickoff, Jonathan P.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pediat, Boston, MA USA.
[Hovell, Mel F.] San Diego State Univ, Sch Publ Hlth, Ctr Behav Epidemiol & Community Hlth, San Diego, CA 92182 USA.
RP Rosen, LJ (reprint author), Tel Aviv Univ, Sch Publ Hlth, Fac Med, Dept Hlth Promot, POB 39040, IL-69978 Ramat Aviv, Israel.
EM rosenl@post.tau.ac.il
FU Flight Attendants' Medical Research Institute (FAMRI) [072086_YCSA]
FX This work was funded by the Flight Attendants' Medical Research
Institute (FAMRI) FAMRI Award 072086_YCSA.
NR 89
TC 82
Z9 84
U1 5
U2 28
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD JAN
PY 2012
VL 129
IS 1
BP 141
EP 152
DI 10.1542/peds.2010-3209
PG 12
WC Pediatrics
SC Pediatrics
GA 870BT
UT WOS:000298644800052
PM 22201152
ER
PT J
AU Bienvenu, OJ
Samuels, JF
Wuyek, LA
Liang, KY
Wang, Y
Grados, MA
Cullen, BA
Riddle, MA
Greenberg, BD
Rasmussen, SA
Fyer, AJ
Pinto, A
Rauch, SL
Pauls, DL
McCracken, JT
Piacentini, J
Murphy, DL
Knowles, JA
Nestadt, G
AF Bienvenu, O. J.
Samuels, J. F.
Wuyek, L. A.
Liang, K-Y.
Wang, Y.
Grados, M. A.
Cullen, B. A.
Riddle, M. A.
Greenberg, B. D.
Rasmussen, S. A.
Fyer, A. J.
Pinto, A.
Rauch, S. L.
Pauls, D. L.
McCracken, J. T.
Piacentini, J.
Murphy, D. L.
Knowles, J. A.
Nestadt, G.
TI Is obsessive-compulsive disorder an anxiety disorder, and what, if any,
are spectrum conditions? A family study perspective
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Anxiety disorders; genetic epidemiology; obsessive-compulsive disorder;
obsessive-compulsive personality disorder; obsessive-compulsive spectrum
ID HOPKINS OCD FAMILY; DSM-V; PERSONALITY-DISORDERS; MAJOR DEPRESSION;
PANIC DISORDER; COMORBIDITY; RELATIVES; HYPOCHONDRIASIS; PROBANDS; LA
AB Background. Experts have proposed removing obsessive-compulsive disorder (OCD) from the anxiety disorders section and grouping it with putatively related conditions in DSM-5. The current study uses co-morbidity and familiality data to inform these issues.
Method. Case family data from the OCD Collaborative Genetics Study (382 OCD-affected probands and 974 of their first-degree relatives) were compared with control family data from the Johns Hopkins OCD Family Study (73 non-OCD-affected probands and 233 of their first-degree relatives).
Results. Anxiety disorders (especially agoraphobia and generalized anxiety disorder), cluster C personality disorders (especially obsessive-compulsive and avoidant), tic disorders, somatoform disorders (hypochondriasis and body dysmorphic disorder), grooming disorders (especially trichotillomania and pathological skin picking) and mood disorders (especially unipolar depressive disorders) were more common in case than control probands; however, the prevalences of eating disorders (anorexia and bulimia nervosa), other impulse-control disorders (pathological gambling, pyromania, kleptomania) and substance dependence (alcohol or drug) did not differ between the groups. The same general pattern was evident in relatives of case versus control probands. Results in relatives did not differ markedly when adjusted for demographic variables and proband diagnosis of the same disorder, though the strength of associations was lower when adjusted for OCD in relatives. Nevertheless, several anxiety, depressive and putative OCD-related conditions remained significantly more common in case than control relatives when adjusting for all of these variables simultaneously.
Conclusions. On the basis of co-morbidity and familiality, OCD appears related both to anxiety disorders and to some conditions currently classified in other sections of DSM-IV.
C1 [Bienvenu, O. J.; Samuels, J. F.; Wuyek, L. A.; Wang, Y.; Grados, M. A.; Cullen, B. A.; Riddle, M. A.; Nestadt, G.] Johns Hopkins Univ, Dept Psychiat & Behav Sci, Sch Med, Baltimore, MD 21287 USA.
[Liang, K-Y.] Johns Hopkins Univ, Dept Biostat, Bloomberg Sch Publ Hlth, Baltimore, MD 21287 USA.
[Greenberg, B. D.; Rasmussen, S. A.] Brown Med Sch, Dept Psychiat & Human Behav, Providence, RI USA.
[Fyer, A. J.; Pinto, A.] Columbia Univ, Coll Phys & Surg, New York, NY USA.
[Fyer, A. J.; Pinto, A.] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Rauch, S. L.; Pauls, D. L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Rauch, S. L.; Pauls, D. L.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[McCracken, J. T.; Piacentini, J.] Univ Calif Los Angeles, Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
[Murphy, D. L.] NIMH, Clin Sci Lab, Bethesda, MD 20892 USA.
[Knowles, J. A.] Univ So Calif, Keck Sch Med, Dept Psychiat & Behav Sci, Los Angeles, CA 90033 USA.
RP Bienvenu, OJ (reprint author), Johns Hopkins Univ, Dept Psychiat & Behav Sci, Sch Med, Meyer 115,600 N Wolfe St, Baltimore, MD 21287 USA.
EM jbienven@jhmi.edu
RI Pinto, Anthony/D-2718-2017;
OI Pinto, Anthony/0000-0002-6078-7242; Samuels, Jack/0000-0002-6715-7905
FU American Psychiatric Association; National Institutes of Health
[MH50125, RR00052, NS42609, MH64543, MH80221, MH66284]
FX This study was commissioned and funded by the American Psychiatric
Association to support the work of the DSM-5 Anxiety,
Obsessive-Compulsive Spectrum, Post-Traumatic, and Dissociative
Disorders Work Group. National Institutes of Health grants MH50125,
RR00052, NS42609, MH64543, MH80221 and MH66284 also supported this work.
NR 43
TC 62
Z9 63
U1 6
U2 37
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
J9 PSYCHOL MED
JI Psychol. Med.
PD JAN
PY 2012
VL 42
IS 1
BP 1
EP 13
DI 10.1017/S0033291711000742
PG 13
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 874MG
UT WOS:000298961600001
PM 21733222
ER
PT J
AU Perlis, RH
Iosifescu, DV
Castro, VM
Murphy, SN
Gainer, VS
Minnier, J
Cai, T
Goryachev, S
Zeng, Q
Gallagher, PJ
Fava, M
Weilburg, JB
Churchill, SE
Kohane, IS
Smoller, JW
AF Perlis, R. H.
Iosifescu, D. V.
Castro, V. M.
Murphy, S. N.
Gainer, V. S.
Minnier, J.
Cai, T.
Goryachev, S.
Zeng, Q.
Gallagher, P. J.
Fava, M.
Weilburg, J. B.
Churchill, S. E.
Kohane, I. S.
Smoller, J. W.
TI Using electronic medical records to enable large-scale studies in
psychiatry: treatment resistant depression as a model
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Antidepressant; classification; machine learning; natural language
processing; remission; treatment resistant depression
ID REPORT QIDS-SR; AUTOMATED IDENTIFICATION; PSYCHOMETRIC EVALUATION; QUICK
INVENTORY; DISORDER; REMISSION; SYMPTOMATOLOGY; AUGMENTATION;
TECHNOLOGY; VALIDATION
AB Background. Electronic medical records (EMR) provide a unique opportunity for efficient, large-scale clinical investigation in psychiatry. However, such studies will require development of tools to define treatment outcome.
Method. Natural language processing (NLP) was applied to classify notes from 127 504 patients with a billing diagnosis of major depressive disorder, drawn from out-patient psychiatry practices affiliated with multiple, large New England hospitals. Classifications were compared with results using billing data (ICD-9 codes) alone and to a clinical gold standard based on chart review by a panel of senior clinicians. These cross-sectional classifications were then used to define longitudinal treatment outcomes, which were compared with a clinician-rated gold standard.
Results. Models incorporating NLP were superior to those relying on billing data alone for classifying current mood state (area under receiver operating characteristic curve of 0.85-0.88 v. 0.54-0.55). When these cross-sectional visits were integrated to define longitudinal outcomes and incorporate treatment data, 15% of the cohort remitted with a single antidepressant treatment, while 13% were identified as failing to remit despite at least two antidepressant trials. Non-remitting patients were more likely to be non-Caucasian (p < 0.001).
Conclusions. The application of bioinformatics tools such as NLP should enable accurate and efficient determination of longitudinal outcomes, enabling existing EMR data to be applied to clinical research, including biomarker investigations. Continued development will be required to better address moderators of outcome such as adherence and co-morbidity.
C1 [Perlis, R. H.; Iosifescu, D. V.; Fava, M.; Weilburg, J. B.] Massachusetts Gen Hosp, Dept Psychiat, Depress Clin & Res Program, Boston, MA 02114 USA.
[Perlis, R. H.; Gallagher, P. J.; Smoller, J. W.] Massachusetts Gen Hosp, Dept Psychiat, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA.
[Iosifescu, D. V.] Mt Sinai Hosp, Dept Psychiat, Mood & Anxiety Disorders Program, New York, NY 10029 USA.
[Castro, V. M.; Gainer, V. S.; Goryachev, S.] Partners HealthCare Syst, Partners Res Comp, Boston, MA USA.
[Murphy, S. N.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Minnier, J.; Cai, T.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Zeng, Q.] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Churchill, S. E.] Partners HealthCare Syst, Informat Syst, Boston, MA USA.
[Kohane, I. S.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
RP Perlis, RH (reprint author), Simches Res Bldg,185 Cambridge St,6th Floor, Boston, MA 02114 USA.
EM rperlis@partners.org
RI Kohane, Isaac Kohane/K-3716-2012;
OI Kohane, Isaac Kohane/0000-0003-2192-5160; Minnier,
Jessica/0000-0002-3527-2757
FU National Library of Medicine [U54LM008748]; National Institute of Mental
Health [R01MH086026, R01MH085542]; Proteus Biomedical; Concordant Rater
Systems; Genomind; RID Ventures; Aspect Medical Systems; Forest
Laboratories; Janssen Pharmaceuticals; NARSAD; NIH; Abbott Laboratories;
Alkermes, Inc.; AstraZeneca; Bio-Research; BrainCells Inc.;
Bristol-Myers Squibb; Cephalon, Inc.; Clinical Trials Solutions, LLC;
Covidien; Eli Lilly and Company; EnVivo Pharmaceuticals, Inc.; Forest
Pharmaceuticals, Inc.; Ganeden Biotech, Inc.; GlaxoSmithKline; Johnson &
Johnson Pharmaceutical Research Development; Lichtwer Pharma GmbH; Lorex
Pharmaceuticals; Novartis AG; Organon Pharmaceuticals; PamLab, LLC;
Pfizer Inc.; Pharmavite(R) LLC; Roche; RTC Logic, LLC; Sanofi-Aventis US
LLC; Shire; Solvay Pharmaceuticals, Inc.; Synthelabo; Wyeth-Ayerst
Laboratories
FX The project described was supported by Award # U54LM008748 from the
National Library of Medicine (to ISK) and R01MH086026 and R01MH085542
from the National Institute of Mental Health (to R. H. P. and J.W.S.,
respectively). The content is solely the responsibility of the authors
and does not necessarily represent the official view of the National
Library of Medicine or the National Institutes of Health.; Roy Perlis
has received consulting fees from Proteus Biomedical, Concordant Rater
Systems, Genomind, and RID Ventures.; Dan Iosifescu has received grant
support from Aspect Medical Systems, Forest Laboratories, Janssen
Pharmaceuticals, NARSAD, and NIH. He has received speaker honoraria from
Eli & Co., Pfizer, Inc., Forest Laboratories, and Reed Medical
Education.; Research Support: Abbott Laboratories; Alkermes, Inc.;
Aspect Medical Systems; AstraZeneca; Bio-Research; BrainCells Inc.;
Bristol-Myers Squibb; Cephalon, Inc.; Clinical Trials Solutions, LLC;
Covidien; Eli Lilly and Company; EnVivo Pharmaceuticals, Inc.; Forest
Pharmaceuticals, Inc.; Ganeden Biotech, Inc.; GlaxoSmithKline; Johnson &
Johnson Pharmaceutical Research & Development; Lichtwer Pharma GmbH;
Lorex Pharmaceuticals; Novartis AG; Organon Pharmaceuticals; PamLab,
LLC.; Pfizer Inc.; Pharmavite (R) LLC; Roche; RTC Logic, LLC;
Sanofi-Aventis US LLC; Shire; Solvay Pharmaceuticals, Inc.; Synthelabo;
Wyeth-Ayerst Laboratories.
NR 34
TC 46
Z9 47
U1 1
U2 15
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
J9 PSYCHOL MED
JI Psychol. Med.
PD JAN
PY 2012
VL 42
IS 1
BP 41
EP 50
DI 10.1017/S0033291711000997
PG 10
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 874MG
UT WOS:000298961600004
PM 21682950
ER
PT J
AU Jahshan, C
Cadenhead, KS
Rissling, AJ
Kirihara, K
Braff, DL
Light, GA
AF Jahshan, C.
Cadenhead, K. S.
Rissling, A. J.
Kirihara, K.
Braff, D. L.
Light, G. A.
TI Automatic sensory information processing abnormalities across the
illness course of schizophrenia
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE MMN; prodromal; P300; RON; schizophrenia
ID MISMATCH NEGATIVITY GENERATION; EVENT-RELATED POTENTIALS; NEUROCOGNITIVE
DEFICITS; 1ST-EPISODE SCHIZOPHRENIA; 1ST EPISODE; PRODROMAL
SCHIZOPHRENIA; INVOLUNTARY ATTENTION; AUDITORY DISTRACTION;
SELECTIVE-ATTENTION; SPECTRUM DISORDERS
AB Background. Deficits in automatic sensory discrimination, as indexed by a reduction in the mismatch negativity (MMN) and P3a event-related potential amplitudes, are well documented in chronic schizophrenia. However, MMN and P3a have not been sufficiently studied early in the course of psychotic illness. The present study aimed to investigate MMN, P3a and reorienting negativity (RON) across the course of schizophrenia.
Method. MMN, P3a, and RON were assessed in 118 subjects across four groups: (1) individuals at risk for psychosis (n=26); (2) recent-onset patients (n=31); (3) chronic patients (n=33); and (4) normal controls (n=28) using a duration-deviant auditory oddball paradigm.
Results. Frontocentral deficits in MMN and P3a were present in all patient groups. The at-risk group's MMN and P3a amplitudes were intermediate to those of the control and recent-onset groups. The recent-onset and chronic patients, but not the at-risk subjects, showed significant RON amplitude reductions, relative to the control group. Associations between MMN, P3a, RON and psychosocial functioning were present in the chronic patients. In the at-risk subjects, P3a and RON deficits were significantly associated with higher levels of negative symptoms.
Conclusions. Abnormalities in the automatic processes of sensory discrimination, orienting and reorienting of attention are evident in the early phases of schizophrenia and raise the possibility of progressive worsening across stages of the illness. The finding that MMN and P3a, but not RON, were reduced before psychosis onset supports the continued examination of these components as potential early biomarkers of schizophrenia.
C1 [Cadenhead, K. S.; Rissling, A. J.; Kirihara, K.; Braff, D. L.; Light, G. A.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Jahshan, C.] Vet Affairs Greater Los Angeles Healthcare Syst, Mental Illness Res Educ & Clin Ctr, Los Angeles, CA USA.
RP Light, GA (reprint author), Univ Calif San Diego, Dept Psychiat, 9500 Gilman Dr, La Jolla, CA 92093 USA.
EM glight@ucsd.edu
FU Department of Veteran Affairs (VISN 22 Mental Illness Research,
Education, and Clinical Center); National Institute of Mental Health
[MH079777, MH042228, MH065571]
FX This work was supported by grants from the Department of Veteran Affairs
(VISN 22 Mental Illness Research, Education, and Clinical Center) and
National Institute of Mental Health (MH079777; MH042228, and MH065571).
The authors wish to thank Jason Nunag, Steven Reding, Kathleen Shafer,
Marlena Pela, Joyce Sprock, and Richard Sharp for their assistance.
NR 86
TC 52
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U1 0
U2 4
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
EI 1469-8978
J9 PSYCHOL MED
JI Psychol. Med.
PD JAN
PY 2012
VL 42
IS 1
BP 85
EP 97
DI 10.1017/S0033291711001061
PG 13
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 874MG
UT WOS:000298961600008
PM 21740622
ER
PT J
AU Dutra, SJ
Stoeckel, LE
Carlini, SV
Pizzagalli, DA
Evins, AE
AF Dutra, Sunny J.
Stoeckel, Luke E.
Carlini, Sara V.
Pizzagalli, Diego A.
Evins, A. Eden
TI Varenicline as a smoking cessation aid in schizophrenia: effects on
smoking behavior and reward sensitivity
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Nicotine; Schizophrenia; Varenicline; Reward; Anhedonia; Affective
flattening; Smoking cessation
ID NICOTINE DEPENDENCE; NEGATIVE SYMPTOMS; DOPAMINE-D-2 RECEPTOR;
CIGARETTE-SMOKING; TRANSDERMAL NICOTINE; VENTRAL STRIATUM; HUMANS;
HYPOTHESIS; NONSMOKERS; SYSTEMS
AB Smoking rates are up to five times higher in people with schizophrenia than in the general population, placing these individuals at high risk for smoking-related health problems. Varenicline, an alpha 4 beta 2 nicotinic acetylcholine receptor partial agonist, is a promising aid for smoking cessation in this population. To maximize treatment efficacy while minimizing risks, it is critical to identify reliable predictors of positive response to varenicline in smokers with schizophrenia.
Negative symptoms of schizophrenia are related to dysfunctions in the brain reward system, are associated with nicotine dependence, and may be improved by nicotine or nicotinic receptor agonists, suggesting that smoking cessation may be especially difficult for patients with substantial negative symptoms. The purpose of the study was to evaluate negative symptoms as predictors of response to varenicline.
Patients with schizophrenia (N = 53) completed a 12-week smoking cessation trial combining varenicline with cognitive behavioral therapy. Negative symptoms were assessed via the Scale for the Assessment of Negative Symptoms (Andreasen 1983). Outcomes included smoking abstinence as assessed by self-report and expired carbon monoxide. Change in performance on a probabilistic reward task was used as an index of change in reward sensitivity during treatment.
At week 12, 32 participants met criteria for 14-day point-prevalence abstinence. Patients with lower baseline symptoms of affective flattening (more typical affect) were more likely to achieve smoking abstinence and demonstrated larger increases in reward sensitivity during treatment.
These data suggest that affective flattening symptoms in smokers with schizophrenia may predict response to varenicline.
C1 [Dutra, Sunny J.] Yale Univ, Dept Psychol, New Haven, CT 06520 USA.
[Stoeckel, Luke E.; Carlini, Sara V.; Evins, A. Eden] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Pizzagalli, Diego A.] McLean Hosp, Dept Psychiat, Belmont, MA 02478 USA.
RP Evins, AE (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 60 Staniford St, Boston, MA 02114 USA.
EM a_eden_evins@hms.harvard.edu
FU NIDA [R01 DA021245]; Harvard Medical School; NIMH [R01MH68376,
R21MH078979]; GSK; Janssen; Pfizer; Boehringer-Ingelheim; ANT Inc.;
AstraZeneca
FX The study was funded by NIDA R01 DA021245 (Evins). This grant supported
Dr. Evins' effort on the project. During the study, Dr. Stoeckel was
partially supported by the Harvard Medical School Zinberg Fellowship in
Clinical Addiction Research and a NIDA Loan Repayment Program Grant, and
Dr. Pizzagalli was partially supported by NIMH grants R01MH68376 and
R21MH078979.; The authors declare no competing financial interests. Dr.
Evins has received research support from GSK, Janssen and Pfizer, and
honoraria or consulting fees from Boehringer-Ingelheim and Pfizer. Dr.
Pizzagalli has received research support and consulting fees from ANT
Inc. and honoraria and consulting fee from AstraZeneca.
NR 69
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U1 1
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD JAN
PY 2012
VL 219
IS 1
BP 25
EP 34
DI 10.1007/s00213-011-2373-6
PG 10
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 870BX
UT WOS:000298645200003
PM 21695488
ER
PT J
AU Brink, JA
Goske, MJ
Patti, JA
AF Brink, James A.
Goske, Marilyn J.
Patti, John A.
TI Informed Decision Making Trumps Informed Consent for Medical Imaging
with Ionizing Radiation
SO RADIOLOGY
LA English
DT Editorial Material
ID CANCER-RISKS; EXPOSURE; PATIENT; RATHER; CT
C1 [Brink, James A.] Yale Univ, Dept Diagnost Radiol, Sch Med, New Haven, CT 06520 USA.
[Goske, Marilyn J.] Cincinnati Childrens Hosp, Med Ctr, Dept Radiol, Cincinnati, OH USA.
[Patti, John A.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Brink, JA (reprint author), Yale Univ, Dept Diagnost Radiol, Sch Med, 789 Howard Ave,Room TE2-230, New Haven, CT 06520 USA.
EM james.brink@yale.edu
NR 23
TC 32
Z9 32
U1 0
U2 2
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD JAN
PY 2012
VL 262
IS 1
BP 11
EP 14
DI 10.1148/radiol.11111421
PG 4
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 869PY
UT WOS:000298611500004
PM 22190652
ER
PT J
AU Su, HS
Nahrendorf, M
Panizzi, P
Breckwoldt, MO
Rodriguez, E
Iwamoto, Y
Aikawa, E
Weissleder, R
Chen, JW
AF Su, Henry S.
Nahrendorf, Matthias
Panizzi, Peter
Breckwoldt, Michael O.
Rodriguez, Elisenda
Iwamoto, Yoshiko
Aikawa, Elena
Weissleder, Ralph
Chen, John W.
TI Vasculitis: Molecular Imaging by Targeting the Inflammatory Enzyme
Myeloperoxidase
SO RADIOLOGY
LA English
DT Article
ID ANCA-ASSOCIATED VASCULITIDES; LARGE VESSEL VASCULITIS; GIANT-CELL
ARTERITIS; KAWASAKI-DISEASE; CARDIOVASCULAR-DISEASE; EULAR
RECOMMENDATIONS; SYSTEMIC VASCULITIS; ANIMAL-MODEL; 3T MRI; MICE
AB Purpose:
To determine if a molecular imaging approach targeting the highly oxidative enzyme myeloperoxidase (MPO) can help noninvasively identify and confirm sites of vascular wall inflammation in a murine model of vasculitis.
Materials and Methods:
Animal experiments were approved by the institutional animal care committee. Twenty-six mice were studied, including eight MPO-deficient and six sham-operated mice as controls. Vasculitis was induced with intraperitoneal injection of Candida albicans water-soluble fraction (CAWS). Aortic root magnetic resonance imaging was performed after intravenous injection of the activatable MPO sensor (bis-5-hydroxytryptamide-diethylenetriaminepentatacetate gadolinium) (n = 23), referred to as MPO-Gd, or gadopentetate dimeglumine (n = 10). Seven mice were randomly assigned to receive either MPO-Gd or gadopentetate dimeglumine first. Aortic root specimens were collected for biochemical and histopathologic analyses to validate imaging findings. Statistical significance was calculated for contrast-to-noise ratios (CNRs) by using the paired t test.
Results:
In the aortic root, the mean MPO-Gd CNRs after agent injection (CNR = 28.1) were more than 2.5-fold higher than those of sham-operated mice imaged with MPO-Gd and vasculitis mice imaged with gadopentetate dimeglumine (CNR = 10.6) (P > .05). MPO-Gd MR imaging helped identify areas of vasculitis that were not seen at unenhanced and contrast material-enhanced imaging with gadopentetate dimeglumine. Histopathologic and biochemical analyses for MPO and myeloid cells confirmed imaging findings. In MPO-deficient mice, injection of CAWS did not result in a vasculitis phenotype, implying a key role of the imaging target in disease cause.
Conclusion:
Molecular imaging targeting MPO can be a useful biomarker to noninvasively detect and confirm inflammation in vasculitis by using a murine model of Kawasaki disease. (C) RSNA, 2011
C1 [Su, Henry S.; Nahrendorf, Matthias; Panizzi, Peter; Breckwoldt, Michael O.; Rodriguez, Elisenda; Iwamoto, Yoshiko; Aikawa, Elena; Weissleder, Ralph; Chen, John W.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res,Ctr Syst Biol, Boston, MA 02114 USA.
[Su, Henry S.; Chen, John W.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Neuroradiol,Dept Radiol, Boston, MA 02114 USA.
RP Chen, JW (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res,Ctr Syst Biol, Boston, MA 02114 USA.
EM jwchen@mgh.harvard.edu
OI Panizzi, Peter/0000-0003-0141-8807
FU European Commission; National Institutes of Health [K08 HL081170, R01
NS070835, R01 NS072167, R01 HL078641]; Pfizer; Elsevier for a book
FX From the Center for Molecular Imaging Research, Center for Systems
Biology, Massachusetts General Hospital, Harvard Medical School, Boston,
Mass (H.S.S., M.N., P.R.P., M.O.B., E.R., Y.I., E.A., R.W., J.W.C.); and
Division of Neuroradiology, Department of Radiology, Massachusetts
General Hospital, Harvard Medical School, 55 Fruit St, Gray 2, Boston,
MA 02114 (H.S.S., J.W.C.). From the 2008 RSNA Annual Meeting. Received
January 5, 2011; revision requested March 23; revision received June 21;
accepted July 21; final version accepted August 15. E.R. supported by a
Marie Curie Fellowship from the European Commission. Address
correspondence to J.W.C. (e-mail: jwchen@mgh.harvard.edu).; This
research was supported by the National Institutes of Health (grants K08
HL081170, R01 NS070835, R01 NS072167, and R01 HL078641).; Disclosures of
Potential Conflicts of Interest: H.S.S. No potential conflicts of
interest to disclose. M.N. No potential conflicts of interest to
disclose. P.R.P. No potential conflicts of interest to disclose. M.O.B.
No potential conflicts of interest to disclose. E.R. No potential
conflicts of interest to disclose. Y.I. No potential conflicts of
interest to disclose. E.A. No potential conflicts of interest to
disclose. R.W. Financial activities related to the present article: none
to disclose. Financial activities not related to the present article:
author receives money for board membership to T2 BioSystems (author is
founder) and has stock in T2 BioSystems; author is consultant for
Lumicell; author is employee of Massachusetts General Hospital;
institution has many grants pending; author has many patents. Other
relationships: none to disclose. J.W.C. Financial activities related to
the present article: none to disclose. Financial activities not related
to the present article: author is employee of Massachusetts General
Hospital; institution has grants pending from Pfizer; author receives
royalties from Elsevier for a book. Other relationships: none to
disclose.
NR 41
TC 9
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U1 0
U2 9
PU RADIOLOGICAL SOC NORTH AMERICA
PI OAK BROOK
PA 820 JORIE BLVD, OAK BROOK, IL 60523 USA
SN 0033-8419
J9 RADIOLOGY
JI Radiology
PD JAN
PY 2012
VL 262
IS 1
BP 181
EP 190
DI 10.1148/radiol.11110040
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 869PY
UT WOS:000298611500022
PM 22084204
ER
PT J
AU Nanji, KC
Cooper, JB
AF Nanji, Karen C.
Cooper, Jeffrey B.
TI It Is Time to Use Checklists for Anesthesia Emergencies Simulation Is
the Vehicle for Testing and Learning
SO REGIONAL ANESTHESIA AND PAIN MEDICINE
LA English
DT Editorial Material
ID PERFORMANCE
C1 [Nanji, Karen C.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Nanji, Karen C.; Cooper, Jeffrey B.] Harvard Univ, Sch Med, Boston, MA USA.
RP Nanji, KC (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, 55 Fruit St, Boston, MA 02114 USA.
EM knanji@partners.org
NR 12
TC 9
Z9 9
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1098-7339
J9 REGION ANESTH PAIN M
JI Region. Anesth. Pain Med.
PD JAN-FEB
PY 2012
VL 37
IS 1
BP 1
EP 2
DI 10.1097/AAP.0b013e31823e75b2
PG 2
WC Anesthesiology
SC Anesthesiology
GA 866FS
UT WOS:000298366500001
PM 22189573
ER
PT J
AU Lambrechts, G
Van Leeuwen, K
Boonen, H
Maes, B
Noens, I
AF Lambrechts, Greet
Van Leeuwen, Karla
Boonen, Hannah
Maes, Bea
Noens, Ilse
TI Parenting behaviour among parents of children with autism spectrum
disorder (vol 5, pg 1143, 2011)
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Correction
C1 [Lambrechts, Greet; Van Leeuwen, Karla; Boonen, Hannah; Maes, Bea; Noens, Ilse] Katholieke Univ Leuven, Parenting & Special Educ Res Grp, B-3000 Louvain, Belgium.
[Lambrechts, Greet; Boonen, Hannah; Noens, Ilse] Katholieke Univ Leuven, Leuven Autism Res Consortium LAuRes, B-3000 Louvain, Belgium.
[Noens, Ilse] Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA.
RP Lambrechts, G (reprint author), Katholieke Univ Leuven, Parenting & Special Educ Res Grp, Vesaliusstr 2,POB 3765, B-3000 Louvain, Belgium.
EM Greet.Lambrechts@ped.kuleuven.be; Karla.Vanleeuwen@ped.kuleuven.be;
Hannah.Boonen@ped.kuleuven.be; Bea.Maes@ped.kuleuven.be;
Ilse.Noens@ped.kuleuven.be
NR 1
TC 0
Z9 0
U1 1
U2 14
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD JAN-MAR
PY 2012
VL 6
IS 1
BP 311
EP 312
DI 10.1016/j.rasd.2011.06.001
PG 2
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 858TU
UT WOS:000297826400036
ER
PT J
AU Barch, DM
Moore, H
Nee, DE
Manoach, DS
Luck, SJ
AF Barch, Deanna M.
Moore, Holly
Nee, Derek E.
Manoach, Dara S.
Luck, Steven J.
TI CNTRICS Imaging Biomarkers Selection: Working Memory
SO SCHIZOPHRENIA BULLETIN
LA English
DT Article
DE schizophrenia; treatment; working memory; prefrontal cortex; capacity
ID PREDICTS INDIVIDUAL-DIFFERENCES; DORSOLATERAL PREFRONTAL CORTEX;
INTERFERENCE-CONTROL PROCESSES; POSTERIOR PARIETAL CORTEX;
SHORT-TERM-MEMORY; PROACTIVE-INTERFERENCE; COGNITIVE NEUROSCIENCE;
SCHIZOPHRENIC SUBJECTS; NEURAL MECHANISMS; CAPACITY LIMIT
AB The sixth meeting of the Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia (CNTRICS) consortium was focused on selecting promising imaging biomarker measures for each of the cognitive constructs selected in the first CNTRICS meeting. In the domain of working memory (WM), the 2 constructs of interest were "goal maintenance" and "interference control." CNTRICS received 7 task nominations for goal maintenance and 3 task nominations for interference control. For goal maintenance, the breakout group for WM recommended the AX Continuous Performance Test/Dot Pattern Expectancy (DPX) and the Switching Stroop task for translation and further development for use in clinical trial contexts in schizophrenia research. Notably, these same 2 paradigms were recommended for "rule generation and selection" in executive control, a highly related construct. For interference control, the breakout group recommended the Suppress Task and the Sternberg Item Recognition Paradigm for translation for use in clinical trials. This manuscript describes the ways in which each of these tasks met the criteria used by the breakout group to recommend tasks for further development. In addition, the group revisited the construct of WM capacity. Since the initial CNTRICS meeting, a growing body of work has emerged on the neurobiological substrates of WM capacity, making measure of this construct ready for translation. The group suggested a promising imaging biomarker measure for capacity, a version of the change detection task that measures delay activity over posterior parietal and occipital cortex.
C1 [Barch, Deanna M.] Washington Univ, Dept Psychol, St Louis, MO 63130 USA.
[Barch, Deanna M.] Washington Univ, Dept Psychiat, St Louis, MO 63130 USA.
[Barch, Deanna M.] Washington Univ, Dept Radiol, St Louis, MO 63130 USA.
[Moore, Holly] Columbia Univ, Dept Psychiat, New York, NY USA.
[Moore, Holly] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Nee, Derek E.] Indiana Univ, Dept Psychol & Brain Sci, Bloomington, IN USA.
[Nee, Derek E.] Univ Michigan, Dept Psychol, Ann Arbor, MI USA.
[Manoach, Dara S.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Manoach, Dara S.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Luck, Steven J.] Univ Calif Davis, Dept Psychol, Ctr Mind & Brain, Davis, CA 95616 USA.
RP Barch, DM (reprint author), Washington Univ, Dept Psychol, St Louis, MO 63130 USA.
EM dbarch@artsci.wustl.edu
RI Barch, Deanna/G-8638-2013;
OI Nee, Derek/0000-0001-7858-6871
FU National Institutes of Mental Health [5R 13MH078710]; National Institute
of Health (NIH); McDonnell Center for Higher Brain Function; National
Alliance for Research on Schizophrenia and Depression (NARSAD); New York
State Office of Mental Health; Sidney R. Baer Jr Foundation; national
science foundation (NSF)
FX National Institutes of Mental Health (5R 13MH078710).; We would also
like to thank Deb Tussing and Carol Cox, whose efforts have been
invaluable in the CNTRICS process. In addition, we would like to thank
the other members of the Working Memory breakout group, including.
Financial Disclosures: D.M.B. receives funding from the National
Institute of Health (NIH), the McDonnell Center for Higher Brain
Function, and National Alliance for Research on Schizophrenia and
Depression (NARSAD). H.M. receives funding from the NIH, the New York
State Office of Mental Health, and the Sidney R. Baer Jr Foundation.
D.E.N. receives funding from national science foundation (NSF) and NIH.
D.S.M. receives funding from National Institutes of Mental Health and
NARSAD. S.J.L. receives funding from NSF and NIH.
NR 50
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U2 12
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0586-7614
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PD JAN
PY 2012
VL 38
IS 1
BP 43
EP 52
DI 10.1093/schbul/sbr160
PG 10
WC Psychiatry
SC Psychiatry
GA 875DZ
UT WOS:000299011900008
PM 22080498
ER
PT J
AU Butler, PD
Chen, Y
Ford, JM
Geyer, MA
Silverstein, SM
Green, MF
AF Butler, Pamela D.
Chen, Yue
Ford, Judith M.
Geyer, Mark A.
Silverstein, Steven M.
Green, Michael F.
TI Perceptual Measurement in Schizophrenia: Promising Electrophysiology and
Neuroimaging Paradigms From CNTRICS
SO SCHIZOPHRENIA BULLETIN
LA English
DT Article
DE perception; CNTRICS; sensory processes; gain control; integration
ID PREPULSE INHIBITION; COROLLARY DISCHARGE; MISMATCH NEGATIVITY; AUDITORY
HALLUCINATIONS; EVOKED-POTENTIALS; MOTION PERCEPTION; ACOUSTIC STARTLE;
GATING DEFICITS; VISUAL-CORTEX; HUMANS
AB The sixth meeting of the Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia (CNTRICS) focused on selecting promising imaging paradigms for each of the cognitive constructs selected in the first CNTRICS meeting. In the domain of perception, the 2 constructs of interest were "gain control" and "visual integration." CNTRICS received 6 task nominations for imaging paradigms for gain control and 3 task nominations for integration. The breakout group for perception evaluated the degree to which each of these tasks met prespecified criteria. For gain control, the breakout group believed that one task (mismatch negativity) was already mature and was being incorporated into multisite clinical trials. The breakout group recommended that I visual task (steady-state visual evoked potentials to magnocellular- vs parvocellular-biased stimuli) and 2 auditory measures (an event-related potential (ERP) measure of corollary discharge and a functional magnetic resonance imaging (fMRI) version of prepulse inhibition of startle) be adapted for use in clinical trials in schizophrenia research. For visual integration, the breakout group recommended that fMRI and ERP versions of a contour integration test and an fMRI version of a coherent motion test be adapted for use in clinical trials. This manuscript describes the ways in which each of these tasks met the criteria used in the breakout group to evaluate and recommend tasks for further development.
C1 [Butler, Pamela D.] Schizophrenia Res Ctr, Nathan Kline Inst Psychiat Res, Orangeburg, NY USA.
[Butler, Pamela D.] NYU, Sch Med, Dept Psychiat, New York, NY USA.
[Chen, Yue] Harvard Univ, McLean Hosp, Sch Med, Dept Psychiat, Belmont, MA USA.
[Ford, Judith M.] Univ Calif San Francisco, VA Med Ctr, Dept Psychiat, San Francisco, CA 94143 USA.
[Geyer, Mark A.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Silverstein, Steven M.] Univ Behav HealthCare, Univ Med & Dent New Jersey, Div Schizophrenia Res, Piscataway, NJ USA.
[Silverstein, Steven M.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Psychiat, Piscataway, NJ 08854 USA.
[Green, Michael F.] Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Los Angeles, CA USA.
[Green, Michael F.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
RP Butler, PD (reprint author), 140 Old Orangeburg Rd, Orangeburg, NY 10962 USA.
EM butler@nki.rfmh.org
FU National Institutes of Health [MH84848, MH61824, MH58262, MH067967,
MH052885, MH084828, MH043292]; Veteran's Administration VISN 22 Mental
Illness Research, Education, and Clinical Center; VA Merit
FX National Institutes of Health (MH84848 to P.D.B., MH61824 to Y.C.,
MH58262 and MH067967 to J.M.F., MH052885 to M.A.G., MH084828 to S.M.S.,
MH043292 to M.F.G.); Veteran's Administration VISN 22 Mental Illness
Research, Education, and Clinical Center to M.F.G. and M.A.G.; VA Merit
to J.M.F.
NR 50
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U1 2
U2 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0586-7614
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PD JAN
PY 2012
VL 38
IS 1
BP 81
EP 91
DI 10.1093/schbul/sbr106
PG 11
WC Psychiatry
SC Psychiatry
GA 875DZ
UT WOS:000299011900012
PM 21890745
ER
PT J
AU Zietman, A
Ibbott, G
AF Zietman, Anthony
Ibbott, Geoffrey
TI A Clinical Approach to Technology Assessment: How Do We and How Should
We Choose the Right Treatment?
SO SEMINARS IN RADIATION ONCOLOGY
LA English
DT Article
ID PROSTATE-CANCER; DECISIONS; PATIENT
AB The evidence required to support the use of new technology in medicine differs from that required for new drugs. On one extreme, very little may be required for small devices, but on the other strong evidence is required to support the use of truly novel, potentially dangerous, and high-cost machines. The randomized controlled trial is built into the evaluation of drugs and suits them well. It is not so well suited to the evaluation of major devices in which installation costs and return on investment are important. We discuss where the randomized controlled trial may still play a role and what alternatives may exist when this is not possible. We also discuss the role that independent bodies may have in determining whether or not a new device is not only safe but also adds to the medical landscape in a way that justifies its cost. Semin Radiat Oncol 22:11-17 (C) 2012 Elsevier Inc. All rights reserved.
C1 [Zietman, Anthony] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Ibbott, Geoffrey] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Zietman, A (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Fruit St, Boston, MA 02114 USA.
EM azietman@partners.org
NR 16
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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 1053-4296
J9 SEMIN RADIAT ONCOL
JI Semin. Radiat. Oncol.
PD JAN
PY 2012
VL 22
IS 1
BP 11
EP 17
DI 10.1016/j.semradonc.2011.09.008
PG 7
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 867GI
UT WOS:000298442500003
PM 22177874
ER
PT J
AU Boriani, S
Bandiera, S
Casadei, R
Boriani, L
Donthineni, R
Gasbarrini, A
Pignotti, E
Biagini, R
Schwab, JH
AF Boriani, Stefano
Bandiera, Stefano
Casadei, Roberto
Boriani, Luca
Donthineni, Rakesh
Gasbarrini, Alessandro
Pignotti, Elettra
Biagini, Roberto
Schwab, Joseph H.
TI Giant Cell Tumor of the Mobile Spine A Review of 49 Cases
SO SPINE
LA English
DT Review
DE giant cell tumor of bone; mobile spine; local recurrence
ID BONE-TUMORS; RADIATION-THERAPY; SOFT-TISSUE; CRYOSURGERY; SARCOMA;
RADIOTHERAPY; MANAGEMENT; RESECTION
AB Study Design. This is a retrospective review of 49 cases of giant cell tumor (GCT) of the mobile spine treated surgically.
Objective. Our goal was to determine which factors influenced local recurrence.
Summary of Background Data. GCT is a benign, locally aggressive tumor that rarely occurs in the spine. The management of local recurrence can be challenging.
Methods. We performed a retrospective analysis of GCTs of the mobile spine managed between 1970 and 2005. Median follow-up was 145 months with a minimum of 2 years or until death. We used the Kaplan-Meier method to test whether Enneking stage, surgery type, and surgical margin had statistically significant impact on local recurrence. The log rank test was used for comparison, and a P value of less than 0.05 was deemed significant.
Results. Of the 49 patients, 11 (22%) local recurrences occurred. The latest recurrence occurred at 60 months. Age less than 25 years was associated with a worse relapse-free survival (P = 0.03). En bloc resection was associated with better local control with Enneking stage III tumors (P = 0.01); however, intralesional resection provided adequate control of Enneking stage II tumors. There were 6 (12%) cases of metastasis, and 2 patients died from the progression of their disease. One patient died from the complications of the surgery.
Conclusion. En bloc resection should be considered for Enneking stage III GCTs of the mobile spine. The choice of en bloc resection must be balanced with the inherent risks of the procedure. Intralesional resection of Enneking stage II tumors provides adequate local control. Patients should be followed for at least 5 years because local relapse can occur late.
C1 [Schwab, Joseph H.] Massachusetts Gen Hosp, Sect Orthoped Oncol, Dept Orthoped Surg, Boston, MA 02114 USA.
[Boriani, Stefano; Bandiera, Stefano; Gasbarrini, Alessandro] Rizzoli Inst, Dept Spine Oncol, Bologna, Italy.
[Casadei, Roberto; Boriani, Luca] Rizzoli Inst, Dept Surg Oncol, Bologna, Italy.
[Donthineni, Rakesh] Alta Bates Med Ctr, Berkeley, CA USA.
[Pignotti, Elettra] Rizzoli Inst, Stat Anal TF, Bologna, Italy.
[Biagini, Roberto] IFO, Dept Orthoped Oncol, Rome, Italy.
RP Schwab, JH (reprint author), Massachusetts Gen Hosp, Sect Orthoped Oncol, Dept Orthoped Surg, 55 Fruit St, Boston, MA 02114 USA.
EM jhschwab@partners.org
OI Biagini, Roberto/0000-0002-6819-2841
NR 40
TC 26
Z9 29
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0362-2436
J9 SPINE
JI SPINE
PD JAN 1
PY 2012
VL 37
IS 1
BP E37
EP E45
DI 10.1097/BRS.0b013e3182233ccd
PG 9
WC Clinical Neurology; Orthopedics
SC Neurosciences & Neurology; Orthopedics
GA 866UN
UT WOS:000298410500007
PM 22179322
ER
PT J
AU Reeves, MJ
Fonarow, GC
Smith, EE
Pan, WQ
Olson, D
Hernandez, AF
Peterson, ED
Schwamm, LH
AF Reeves, Mathew J.
Fonarow, Gregg C.
Smith, Eric E.
Pan, Wenqin
Olson, DaiWai
Hernandez, Adrian F.
Peterson, Eric D.
Schwamm, Lee H.
TI Representativeness of the Get With The Guidelines-Stroke Registry
Comparison of Patient and Hospital Characteristics Among Medicare
Beneficiaries Hospitalized With Ischemic Stroke
SO STROKE
LA English
DT Article
DE ischemic stroke; Medicare; registries; representativeness
ID EXPERIENCE; OUTCOMES; ATTACK; CARE
AB Background and Purpose-Get With The Guidelines (GWTG)-Stroke is a large quality improvement-based registry of acute stroke; however, its generalizability is unclear. We used fee-for-service Medicare claims to ascertain the representativeness of ischemic stroke admissions in GWTG-Stroke.
Methods-All 228 815 ischemic stroke admissions aged >= 65 years enrolled in GWTG-Stroke between April 2003 and December 2007 were linked to 926 756 unique fee-for-service Medicare patients with ischemic stroke (primary International Classification of Diseases, 9th Revision discharge code 434 or 436) from the same period. Patient characteristics and in-hospital outcomes were compared between the linked GWTG-Stroke Medicare cohort and the remaining unlinked Medicare cohort. Characteristics of GWTG-Stroke hospitals were compared with non-GWTG-Stroke hospitals.
Results-A total of 144 344 of the 228,815 GWTG-Stroke admissions (63.1%) were successfully linked to the 926 756 Medicare ischemic stroke beneficiaries, leaving 782 412 unlinked Medicare patients. Differences in patient characteristics, including age, race, gender, and comorbidities, between the linked and unlinked Medicare cohorts were minimal. Length of stay and rate of discharge home were almost identical between the linked and unlinked groups; however, in-hospital mortality was slightly lower in the linked Medicare cohort (6.3%) compared with the unlinked cohort (7.0%). There were large differences in hospital characteristics between GWTG-Stroke and non-GWTG-Stroke hospitals; GWTG-Stroke hospitals tended to be larger, urban, teaching centers.
Conclusions-Despite substantial differences between GWTG-Stroke and non-GWTG-Stroke hospitals, Medicare beneficiaries with acute ischemic stroke entered in the GWTG-Stroke program were similar to other Medicare beneficiaries. These data suggest that the Medicare-aged GWTG-Stroke ischemic stroke admissions are generally representative of the national fee-for-service Medicare ischemic stroke population. (Stroke. 2012;43:44-49.)
C1 [Reeves, Mathew J.] Michigan State Univ, Dept Epidemiol, E Lansing, MI 48824 USA.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Div Cardiol, Los Angeles, CA USA.
[Smith, Eric E.] Univ Calgary, Dept Clin Neurosci, Calgary, AB, Canada.
[Pan, Wenqin; Olson, DaiWai; Hernandez, Adrian F.; Peterson, Eric D.] Duke Clin Res Inst, Durham, NC USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
RP Reeves, MJ (reprint author), Michigan State Univ, Dept Epidemiol, B601 W Fee Hall, E Lansing, MI 48824 USA.
EM reevesm@msu.edu
RI Smith, Eric/C-5443-2012; Hernandez, Adrian F./A-7818-2016
OI Smith, Eric/0000-0003-3956-1668; Schwamm, Lee/0000-0003-0592-9145;
Hernandez, Adrian F./0000-0003-3387-9616
FU Michigan Stroke Registry; National Institutes of Health (NIH); Agency
for Healthcare Research and Quality; Canadian Stroke Network; Heart and
Stroke Foundation of Canada; Canadian Institute for Health Research;
Bristol-Myers Squibb; Sanofi-Aventis; Merck; Ortho McNeil
Pharmaceuticals
FX M.J.R. receives salary support from the Michigan Stroke Registry and
serves on several American Heart Association Get With The Guidelines
(AHA GWTG) Committees. G. C. F. serves as a member of the AHA GWTG
Steering Committee; receives research support from the National
Institutes of Health (NIH; significant) and the Agency for Healthcare
Research and Quality (significant); and serves as a consultant to
Novartis (significant). E. E. S. serves as a member of the GWTG
Subcommittee and receives research support from the NIH and the Canadian
Stroke Network and salary support from the Heart and Stroke Foundation
of Canada and the Canadian Institute for Health Research. W. P. is a
member of the Duke Clinical Research Institute (DCRI), which serves as
the AHA GWTG data coordinating center. D. O. is a member of the DCRI,
which serves as the AHA GWTG data coordinating center. A. F. H. is a
member of the DCRI, which serves as the AHA GWTG data coordinating
center. A. F. H. is a recipient of an AHA Pharmaceutical Roundtable
grant. E. D. P. has received research grants from Bristol-Myers Squibb,
Sanofi-Aventis, Merck, and Ortho McNeil Pharmaceuticals. E. D. P. serves
as Principal Investigator of the Data Analytic Center for AHA GWTG. L.
H. S. serves as chair of the AHA GWTG Steering Committee and serves as a
consultant to the Massachusetts Department of Public Health.
NR 13
TC 42
Z9 42
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD JAN
PY 2012
VL 43
IS 1
BP 44
EP 49
DI 10.1161/STROKEAHA.111.626978
PG 6
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 866LY
UT WOS:000298383600027
PM 21980197
ER
PT J
AU Parker, C
Schwamm, LH
Fonarow, GC
Smith, EE
Reeves, MJ
AF Parker, Carol
Schwamm, Lee H.
Fonarow, Gregg C.
Smith, Eric E.
Reeves, Mathew J.
TI Stroke Quality Metrics Systematic Reviews of the Relationships to
Patient-Centered Outcomes and Impact of Public Reporting
SO STROKE
LA English
DT Article
DE acute stroke; outcomes; public reporting; quality metrics
ID ACUTE MYOCARDIAL-INFARCTION; TRANSIENT ISCHEMIC ATTACK; OF-CARE;
PERFORMANCE-MEASURES; GUIDELINES-STROKE; HOSPITAL OUTCOMES;
MORTALITY-RATES; ASSOCIATION; REHABILITATION; IMPROVEMENTS
AB Background and Purpose-Stroke quality metrics play an increasingly important role in quality improvement and policies related to provider reimbursement, accreditation, and public reporting. We conducted 2 systematic reviews examining the relationships between compliance with stroke quality metrics and patient-centered outcomes, and public reporting of stroke metrics and quality improvement, quality of care, or outcomes.
Methods-MEDLINE and EMBASE databases were searched to identify studies that evaluated the relationship between stroke quality metric compliance and patient-centered outcomes in acute hospital settings and public reporting of stroke quality metrics and quality improvement activities, quality of care, or patient outcomes. We specifically excluded studies that evaluated the effect of stroke units or hospital certification.
Results-Fourteen studies met eligibility criteria for the review of stroke quality metric compliance and patient-centered outcomes; 9 found mostly positive associations, whereas 5 found no or very limited associations. Only 2 eligible studies were found that directly addressed the public reporting of stroke quality metrics.
Conclusions-Some studies have found positive associations between stroke metric compliance and improved patient-centered outcomes. However, high-quality studies are lacking and several methodological difficulties make the interpretation of the reported associations challenging. Information on the impact of public reporting of stroke quality metric data is extremely limited. Legitimate questions remain as to whether public reporting of stroke metrics is accurate, effective, or has the potential for unintended consequences. The generation of high-quality data examining quality metrics and stroke outcomes as well as the impact of public reporting should be given priority. (Stroke. 2012;43:155-162.)
C1 [Parker, Carol; Reeves, Mathew J.] Michigan State Univ, Dept Epidemiol, E Lansing, MI 48824 USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Div Cardiol, Los Angeles, CA USA.
[Smith, Eric E.] Dept Clin Neurosci, Calgary, AB, Canada.
RP Reeves, MJ (reprint author), Michigan State Univ, Dept Epidemiol, B601 W Fee Hall, E Lansing, MI 48824 USA.
EM reevesm@msu.edu
OI Schwamm, Lee/0000-0003-0592-9145; Smith, Eric/0000-0003-3956-1668
FU National Institutes of Health; Agency of Healthcare Research and
Quality; Canadian Institutes for Health Research; Canadian Stroke
Network; Heart and Stroke Foundation of Canada; Michigan Paul Coverdell
Stroke Registry
FX L. H. S. serves as chair of the American Heart Association (AHA) Get
With The Guidelines (GWTG) Steering Committee, is a consultant to the
Massachusetts Department of Public Health, and provided expert medical
opinions in malpractice lawsuits regarding stroke treatment and
prevention. G. C. F. is a member of the AHA GWTG Steering Committee, is
a consultant to Novartis, and receives research support from the
National Institutes of Health and the Agency of Healthcare Research and
Quality. E. E. S. serves as chair of the AHA GWTG-Stroke Science
Subcommittee and reports research funding from the National Institutes
of Health, Canadian Institutes for Health Research, Canadian Stroke
Network, and Heart and Stroke Foundation of Canada. M.J.R. serves as a
member of the AHA GWTG Quality Improvement and Stroke Science
Subcommittees and receives salary support from the Michigan Paul
Coverdell Stroke Registry.
NR 50
TC 21
Z9 21
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD JAN
PY 2012
VL 43
IS 1
BP 155
EP 162
DI 10.1161/STROKEAHA.111.635011
PG 8
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 866LY
UT WOS:000298383600046
PM 21980213
ER
PT J
AU Yung, LM
Wei, Y
Qin, T
Wang, YM
Smith, CD
Waeber, C
AF Yung, Lai Ming
Wei, Ying
Qin, Tao
Wang, Yumei
Smith, Charles D.
Waeber, Christian
TI Sphingosine Kinase 2 Mediates Cerebral Preconditioning and Protects the
Mouse Brain Against Ischemic Injury
SO STROKE
LA English
DT Article
DE cell death; cerebral ischemia; hypoxia; isoflurane; neurons;
preconditioning; sphingosine kinase 2
ID HIPPOCAMPAL SLICE CULTURES; NITRIC-OXIDE SYNTHASE; FOCAL ISCHEMIA;
UP-REGULATION; RAT-BRAIN; ISOFLURANE; HYPOXIA; TOLERANCE; FTY720; STROKE
AB Background and Purpose-Cerebral preconditioning provides insights into endogenous mechanisms that protect the brain from ischemic injury. Hypoxia and the anesthetic isoflurane are powerful preconditioning agents. Recent data show that sphingosine 1-phosphate receptor stimulation improves outcome in rodent models of stroke. Endogenous sphingosine 1-phosphate levels are controlled by the expression and activity of sphingosine kinases (SPK). We hypothesize that SPK upregulation mediates preconditioning induced by isoflurane and hypoxia and reduces ischemic injury.
Methods-Male wild-type C57BL/J, SPK1(-/-) and SPK2(-/-) mice were exposed to isoflurane or hypoxia preconditioning before transient middle cerebral artery occlusion. Infarct volume and neurological outcome were measured 24 hours later. SPK inhibitors (SKI-II and ABC294640) were used to test the involvement of SPK2. Expressions of SPK1, SPK2, and hypoxia-inducible factor 1 alpha were determined. Primary cultures of mouse cortical neurons were exposed to isoflurane before glutamate-or hydrogen peroxide-induced cell death.
Results-Isoflurane preconditioning and hypoxia preconditioning significantly reduced infarct volume and improved neurological outcome in wild-type and SPK1 (/) mice but not in SPK2 (/) mice. Pretreatment with SKI-II or ABC294640 abolished the isoflurane preconditioning-induced tolerance. Western blot showed a rapid and sustained increase in SPK2 level, whereas SPK1 level was similar between preconditioned mice and controls. Hypoxia-inducible factor 1 alpha was upregulated in wild-type isoflurane-preconditioned mice but not in SPK2(-/-). Isoflurane preconditioning protected primary neurons against cell death, which was abolished in ABC294640-treated cells.
Conclusions-Applying genetic and pharmacological approaches, we demonstrate that neuronal SPK2 isoform plays an important role in cerebral preconditioning. (Stroke. 2012;43:199-204.)
C1 [Yung, Lai Ming; Wei, Ying; Qin, Tao; Wang, Yumei; Waeber, Christian] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Stroke & Neurovasc Regulat Lab,Dept Radiol, Charlestown, MA USA.
[Smith, Charles D.] Apogee Biotechnol Corp, Hummelstown, PA USA.
RP Waeber, C (reprint author), MGH, Bldg 149,Room 6403, Charlestown, MA 02129 USA.
EM waeber@helix.mgh.harvard.edu
RI Waeber, Christian/A-8333-2009
OI Waeber, Christian/0000-0001-6078-0027
FU National Institutes of Health [NS049263, NS055104]; Interdepartmental
Neuroscience Center [P30NS045776]
FX This work was supported by National Institutes of Health grants
(NS049263 and NS055104) to C.W. and grant P30NS045776 (Interdepartmental
Neuroscience Center).
NR 48
TC 26
Z9 26
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD JAN
PY 2012
VL 43
IS 1
BP 199
EP U377
DI 10.1161/STROKEAHA.111.626911
PG 17
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 866LY
UT WOS:000298383600052
PM 21980199
ER
PT J
AU Schlunk, F
Van Cott, EM
Hayakawa, K
Pfeilschifter, W
Lo, EH
Foerch, C
AF Schlunk, Frieder
Van Cott, Elizabeth M.
Hayakawa, Kazuhide
Pfeilschifter, Waltraud
Lo, Eng H.
Foerch, Christian
TI Recombinant Activated Coagulation Factor VII and Prothrombin Complex
Concentrates Are Equally Effective in Reducing Hematoma Volume in
Experimental Warfarin-Associated Intracerebral Hemorrhage
SO STROKE
LA English
DT Article
DE animal models; anticoagulation; ICH; intracerebral hemorrhage; warfarin
ID ANTICOAGULATION; REVERSAL; MODEL
AB Background and Purpose-Based on an experimental model of warfarin-associated intracerebral hemorrhage, we investigated whether the rapid reversal of anticoagulation using prothrombin complex concentrates (PCC) or recombinant activated coagulation factor VII (rFVIIa) reduces hematoma volume.
Methods-Mice were orally pretreated with warfarin (2 mg/kg). Intracerebral hemorrhage was induced by collagenase injection into the right striatum. Forty-five minutes later, PCC (100 IE/kg), rFVIIa (1 mg/kg), or an equal volume of saline was administered intravenously. Hematoma volume after 24 hours was quantified using a photometric hemoglobin assay.
Results-International normalized ratio was 4.3 +/- 0.4 in saline-treated mice, 0.9 +/- 0.1 in rFVIIa mice, and 1.4 +/- 0.2 in PCC mice. Intracerebral hemorrhage volume was 29.0 +/- 19.7 mu L in the saline group (n=7), 8.6 +/- 4.3 mu L in the rFVIIa group (n=6), and 6.1 +/- 1.8 mu L in the PCC group (n=7; analysis of variance between-group differences P=0.004; post hoc rFVIIa versus saline P=0.021; PCC versus saline P=0.007). No significant difference was found between PCC- and rFVIIa-treated animals.
Conclusions-Our results suggest that PCC and rFVIIa are equally effective in restoring coagulation and preventing excessive hematoma growth in acute warfarin-associated intracerebral hemorrhage. (Stroke. 2012;43:246-249.)
C1 [Schlunk, Frieder; Pfeilschifter, Waltraud; Foerch, Christian] Goethe Univ Frankfurt, Dept Neurol, D-60528 Frankfurt, Germany.
[Schlunk, Frieder; Hayakawa, Kazuhide; Lo, Eng H.; Foerch, Christian] Massachusetts Gen Hosp, Neuroprotect Res Lab, Charlestown, MA USA.
[Van Cott, Elizabeth M.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Foerch, C (reprint author), Goethe Univ Frankfurt, Dept Neurol, Schleusenweg 2-16, D-60528 Frankfurt, Germany.
EM foerch@em.uni-frankfurt.de
RI Pfeilschifter, Waltraud/K-6134-2012
OI Pfeilschifter, Waltraud/0000-0001-6935-8842
FU NINDS NIH HHS [R37 NS037074, P01 NS055104, R01 NS076694, RC2 NS069335]
NR 13
TC 17
Z9 19
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD JAN
PY 2012
VL 43
IS 1
BP 246
EP 249
DI 10.1161/STROKEAHA.111.629360
PG 4
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 866LY
UT WOS:000298383600061
PM 21998055
ER
PT J
AU Wallace, ZS
Khosroshahi, A
Jakobiec, FA
Deshpande, V
Hatton, MP
Ritter, J
Ferry, JA
Stone, JH
AF Wallace, Zachary S.
Khosroshahi, Arezou
Jakobiec, Frederick A.
Deshpande, Vikram
Hatton, Mark P.
Ritter, Jill
Ferry, Judith A.
Stone, John H.
TI IgG4-Related Systemic Disease as a Cause of "Idiopathic" Orbital
Inflammation, Including Orbital Myositis, and Trigeminal Nerve
Involvement
SO SURVEY OF OPHTHALMOLOGY
LA English
DT Review
DE dacryoadenitis; Idiopathic Inflammation; IgG4-related systemic disease;
myositis; orbital pseudotumor; rituximab
ID PATHOLOGICAL FEATURES; SCLEROSING DISEASE; RITUXIMAB THERAPY; DIAGNOSIS;
TUMOR
AB IgG4-related systemic disease (IgG4-RD) is an inflammatory condition of unknown etiology that has been identified as the cause of tumefactive lesions in a number of tissues and organs. The role of the IgG4 remains to be clarified fully, but the histopathologic diagnosis hinges upon the finding of IgG4-bearing plasma cells in addition to characteristic morphologic features, with or without elevated scum IgG4. We present a 56-year-old man with orbital pseudotumor in whom, after 30 years of intractable disease, biopsy showed IgG4-RD involving the lacrimal gland, extraocular muscles, intraconal fat, and trigeminal nerve. Six months after initiating treatment with rituximab, his disease remained dormant, with improvement in his proptosis and normalization of serum IgG4 levels. We review the differential of idiopathic orbital inflammatory disease, including IgG4-RD, and emphasize the need for biopsy for accurate diagnosis and to guide appropriate treatment. (Surv Ophthalmol 57:26-33, 2012. (C) 2012 Elsevier Inc. All rights reserved.)
C1 [Wallace, Zachary S.; Khosroshahi, Arezou; Stone, John H.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Jakobiec, Frederick A.; Deshpande, Vikram; Ferry, Judith A.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Hatton, Mark P.] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA.
[Khosroshahi, Arezou; Stone, John H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Khosroshahi, Arezou; Stone, John H.] Massachusetts Eye & Ear Infirm, Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA.
[Jakobiec, Frederick A.] Massachusetts Eye & Ear Infirm, Cogan Eye Pathol Lab, Boston, MA 02114 USA.
RP Stone, JH (reprint author), Massachusetts Gen Hosp, Rheumatol Unit, Yawkey 2,55 Fruit St, Boston, MA 02114 USA.
EM jhstone@partners.org
NR 25
TC 68
Z9 75
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-6257
J9 SURV OPHTHALMOL
JI Surv. Ophthalmol.
PD JAN-FEB
PY 2012
VL 57
IS 1
BP 26
EP 33
DI 10.1016/j.survophthal.2011.07.004
PG 8
WC Ophthalmology
SC Ophthalmology
GA 862WG
UT WOS:000298124200002
PM 22018678
ER
PT J
AU Rossi, A
Baumgart, F
van Hoek, AN
Verkman, AS
AF Rossi, Andrea
Baumgart, Florian
van Hoek, Alfred N.
Verkman, A. S.
TI Post-Golgi Supramolecular Assembly of Aquaporin-4 in Orthogonal Arrays
SO TRAFFIC
LA English
DT Article
DE AQP4; Golgi; NMO; OAP
ID INSENSITIVE WATER CHANNEL; NEUROMYELITIS-OPTICA; ENDOPLASMIC-RETICULUM;
CELL-ADHESION; KNOCKOUT MICE; M23 ISOFORMS; PROTEIN; BRAIN;
LOCALIZATION; MEMBRANES
AB The supramolecular assembly of aquaporin-4 (AQP4) in orthogonal arrays of particles (OAPs) involves N-terminus interactions of the M23-AQP4 isoform. We found AQP4 OAPs in cell plasma membranes but not in endoplasmic reticulum (ER) or Golgi, as shown by: (i) native gel electrophoresis of brain and AQP4-transfected cells, (ii) photobleaching recovery of green fluorescent protein-AQP4 chimeras in live cells and (iii) freeze-fracture electron microscopy (FFEM). We found that AQP4 OAP formation in plasma membranes, but not in the Golgi, was not related to AQP4 density, pH, membrane lipid composition, C-terminal PDZ domain interactions or a-syntrophin expression. Remarkably, however, fusion of AQP4-containing Golgi vesicles with (AQP4-free) plasma membrane vesicles produced OAPs, suggesting the involvement of plasma membrane factor(s) in AQP4 OAP formation. In investigating additional possible determinants of OAP assembly we discovered membrane curvature-dependent OAP assembly, in which OAPs were disrupted by extrusion of plasma membrane vesicles to similar to 110 nm diameter, but not to similar to 220 nm diameter. We conclude that AQP4 supramolecular assembly in OAPs is a post-Golgi phenomenon involving plasma membrane-specific factor(s). Post-Golgi and membrane curvature-dependent OAP assembly may be important for vesicle transport of AQP4 in the secretory pathway and AQP4-facilitated astrocyte migration, and suggests a novel therapeutic approach for neuromyelitis optica.
C1 [Rossi, Andrea; Baumgart, Florian; Verkman, A. S.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
[Rossi, Andrea; Baumgart, Florian; Verkman, A. S.] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA.
[van Hoek, Alfred N.] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[van Hoek, Alfred N.] Massachusetts Gen Hosp, Program Membrane Biol, Boston, MA 02114 USA.
[van Hoek, Alfred N.] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
[van Hoek, Alfred N.] Harvard Univ, Sch Med, Boston, MA USA.
RP Verkman, AS (reprint author), Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
EM Alan.Verkman@ucsf.edu
OI Baumgart, Florian/0000-0003-1352-8632
FU National Institutes of Health [EY13574, EB00415, DK35124, HL73856,
DK86125, DK72517]; Guthy-Jackson Charitable Foundation
FX This work was supported by grants EY13574, EB00415, DK35124, HL73856,
DK86125 and DK72517 from the National Institutes of Health and grants
from the Guthy-Jackson Charitable Foundation. We thank Cambier Stephanie
(UCSF) for providing human astrocyte cultures.
NR 47
TC 15
Z9 15
U1 1
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-9219
J9 TRAFFIC
JI Traffic
PD JAN
PY 2012
VL 13
IS 1
BP 43
EP 53
DI 10.1111/j.1600-0854.2011.01299.x
PG 11
WC Cell Biology
SC Cell Biology
GA 865RR
UT WOS:000298328500006
PM 21981006
ER
PT J
AU Fagenholz, PJ
Murray, AF
Noble, VE
Baggish, AL
Harris, NS
AF Fagenholz, Peter J.
Murray, Alice F.
Noble, Vicki E.
Baggish, Aaron L.
Harris, N. Stuart
TI ULTRASOUND FOR HIGH ALTITUDE RESEARCH
SO ULTRASOUND IN MEDICINE AND BIOLOGY
LA English
DT Review
DE Ultrasonography; Altitude sickness; Mountaineering; Biomedical research
ID OPTIC-NERVE SHEATH; ACUTE MOUNTAIN-SICKNESS; PULMONARY-ARTERY PRESSURE;
EXTRAVASCULAR LUNG WATER; INCREASED INTRACRANIAL-PRESSURE;
CEREBROSPINAL-FLUID PRESSURE; PATENT FORAMEN OVALE; INFERIOR VENA-CAVA;
DOPPLER-ECHOCARDIOGRAPHY; SONOGRAPHIC MEASUREMENT
AB This review describes ultrasound techniques of potential use to high altitude researchers and discusses technical issues related to using ultrasound for high altitude research. Ultrasound allows portable, noninvasive evaluation of many physiologic parameters of interest to high altitude researchers. We discuss techniques that have been extensively used and emerging techniques that can be used to assess parameters of particular interest to high altitude researchers. We do not provide a definitive description of all ultrasound scanning methods but references to instructive sources are included. Potential drawbacks of ultrasound use, such as the need for sometimes extensive training and the potential for interobserver variation, are discussed and strategies for mitigating these are suggested. This review is meant to encourage other high altitude researchers to consider using ultrasound, either as a primary investigative modality or as an adjunct for monitoring parameters of interest in studies of physiology, altitude illness, or therapeutics. (E-mail: pfagenholz@partners.org) (C) 2012 World Federation for Ultrasound in Medicine & Biology.
C1 [Fagenholz, Peter J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg,Div Trauma Emergency Surg & Surg Crit C, Boston, MA 02114 USA.
[Noble, Vicki E.; Harris, N. Stuart] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA 02114 USA.
[Baggish, Aaron L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA 02114 USA.
[Murray, Alice F.] Royal Infirm Edinburgh NHS Trust, Dept Emergency Med, Edinburgh, Midlothian, Scotland.
RP Fagenholz, PJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Surg,Div Trauma Emergency Surg & Surg Crit C, CPZ 810,55 Fruit St, Boston, MA 02114 USA.
EM pfagenholz@partners.org
NR 70
TC 7
Z9 9
U1 1
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0301-5629
J9 ULTRASOUND MED BIOL
JI Ultrasound Med. Biol.
PD JAN
PY 2012
VL 38
IS 1
BP 1
EP 12
DI 10.1016/j.ultrasmedbio.2011.10.004
PG 12
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 863AO
UT WOS:000298135400001
PM 22104522
ER
PT J
AU Gershman, B
Eisner, BH
AF Gershman, Boris
Eisner, Brian H.
TI Increased Risk of Urinary Tract Calculi Among Patients With Diabetes
Mellitus-A Population-based Cohort Study EDITORIAL COMMENT
SO UROLOGY
LA English
DT Editorial Material
ID STONE DISEASE
C1 [Gershman, Boris; Eisner, Brian H.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Urol, Boston, MA 02115 USA.
RP Gershman, B (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Urol, Boston, MA 02115 USA.
NR 9
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 0090-4295
J9 UROLOGY
JI Urology
PD JAN
PY 2012
VL 79
IS 1
BP 92
EP 93
DI 10.1016/j.urology.2011.08.068
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA 870LO
UT WOS:000298671000022
PM 22202545
ER
PT J
AU Stefanik, JJ
Roemer, FW
Zumwalt, AC
Zhu, YY
Gross, KD
Lynch, JA
Frey-Law, LA
Lewis, CE
Guermazi, A
Powers, CM
Felson, DT
AF Stefanik, Joshua J.
Roemer, Frank W.
Zumwalt, Ann C.
Zhu, Yanyan
Gross, K. Douglas
Lynch, John A.
Frey-Law, Laura A.
Lewis, Cora E.
Guermazi, Ali
Powers, Christopher M.
Felson, David T.
TI Association between measures of trochlear morphology and structural
features of patellofemoral joint osteoarthritis on MRI: The MOST study
SO JOURNAL OF ORTHOPAEDIC RESEARCH
LA English
DT Article
DE osteoarthritis; patellofemoral; trochlea
ID KNEE OSTEOARTHRITIS; PATELLAR ALIGNMENT; WEIGHT-BEARING; PAIN;
KINEMATICS; ALTA
AB The sulcus angle has been widely used in the literature as a measure of trochlear morphology. Recently, lateral trochlear inclination and trochlear angle have been reported as alternatives. The purpose of this study was to determine the association between measures of trochlear morphology and patellofemoral joint (PFJ) cartilage damage and bone marrow lesions (BMLs). Nine hundred seven knees were selected from the Multicenter Osteoarthritis Study, a cohort study of persons aged 5079 years with or at risk for knee OA. Trochlear morphology was measured using lateral trochlear inclination, trochlear angle, and sulcus angle on axial MRI images; cartilage damage and BMLs were graded on MRI. We determined the association between quartiles of each trochlear morphology variable with the presence or absence of cartilage damage and BMLs in the PFJ using logistic regression. The strongest associations were seen with lateral trochlear inclination and lateral PFJ cartilage damage and BMLs, with knees in the lowest quartile (flattened lateral trochlea) having more than two times the odds of lateral cartilage damage and BMLs compared to those in the highest quartile (p?0.0001). Lateral trochlear inclination may be the best method for assessment of trochlear morphology as it was strongly association with structural damage in the PFJ. (c) 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 30:18, 2012
C1 [Stefanik, Joshua J.; Roemer, Frank W.; Zumwalt, Ann C.; Zhu, Yanyan; Gross, K. Douglas; Guermazi, Ali; Felson, David T.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Roemer, Frank W.] Klinikum Augsburg, Dept Radiol, Augsburg, Germany.
[Gross, K. Douglas] Massachusetts Gen Hosp, Inst Hlth Profess, Boston, MA 02114 USA.
[Lynch, John A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Frey-Law, Laura A.] Univ Iowa, Iowa City, IA USA.
[Lewis, Cora E.] Univ Alabama, Birmingham, AL USA.
[Powers, Christopher M.] Univ So Calif, Los Angeles, CA USA.
RP Stefanik, JJ (reprint author), Boston Univ, Sch Med, 650 Albany St,Suite 200, Boston, MA 02118 USA.
EM stefanik@bu.edu
RI Lynch, John/F-8209-2012; Powers, Christopher/J-2662-2014;
OI Felson, David/0000-0002-2668-2447
FU NIH [U01-AG18820, U01-AG18832, U01-AG18947, U01-AG19069, AR-47785,
T32AR007598]; Arthritis Foundation
FX The Multicenter Osteoarthritis Study was supported by the NIH (grants
U01-AG18820, U01-AG18832, U01-AG18947, U01-AG19069, and AR-47785). Dr.
Stefanik's work was supported by a Doctoral Dissertation Award from the
Arthritis Foundation and NIH grant T32AR007598. The authors would also
like to thank the MOST Study participants.
NR 23
TC 19
Z9 22
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0736-0266
J9 J ORTHOP RES
JI J. Orthop. Res.
PD JAN
PY 2012
VL 30
IS 1
BP 1
EP 8
DI 10.1002/jor.21486
PG 8
WC Orthopedics
SC Orthopedics
GA 859ZD
UT WOS:000297913600001
PM 21710542
ER
PT J
AU Kotton, CN
AF Kotton, Camille Nelson
TI Comment on the paper by Kpodzo et al. Response
SO MEDICAL MYCOLOGY
LA English
DT Letter
C1 Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
RP Kotton, CN (reprint author), Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
EM ckotton@partners.org
NR 1
TC 0
Z9 0
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1369-3786
J9 MED MYCOL
JI Med. Mycol.
PD JAN
PY 2012
VL 50
IS 1
BP 111
EP 112
DI 10.3109/13693786.2011.635388
PG 2
WC Infectious Diseases; Mycology; Veterinary Sciences
SC Infectious Diseases; Mycology; Veterinary Sciences
GA 862OU
UT WOS:000298103400017
ER
PT J
AU Huang, JN
Schmeidler, J
Beeri, MS
Rosendorff, C
Bhatia, S
West, RK
Bespalova, IN
Mavris, R
Silverman, JM
AF Huang, Jennifer
Schmeidler, James
Beeri, Michal S.
Rosendorff, Clive
Bhatia, Simmi
West, Rebecca K.
Bespalova, Irina N.
Mavris, Rizalina
Silverman, Jeremy M.
TI Haemoglobin A(1c) and cognitive function in very old, cognitively intact
men
SO AGE AND AGEING
LA English
DT Article
ID DIABETES-MELLITUS; ALZHEIMER-DISEASE; ANTAGONISTIC PLEIOTROPY; ELDERLY
SUBJECTS; RISK-FACTORS; DECLINE; DEMENTIA; MEMORY; AGE; IMPAIRMENT
C1 [Schmeidler, James; Beeri, Michal S.; West, Rebecca K.; Bespalova, Irina N.; Silverman, Jeremy M.] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
[Beeri, Michal S.; Silverman, Jeremy M.] James J Peters Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Bronx, NY USA.
RP Silverman, JM (reprint author), Mt Sinai Sch Med, Dept Psychiat, Box 1230,1 Gustave L Levy Pl, New York, NY 10029 USA.
EM jeremy.silverman@mssm.edu
FU National Institute of Aging [P01-AG02219, K01 AG023515, P50-AG05138];
United States Department of Veterans Affairs; Berkman Charitable Trust
FX This work was supported by National Institute of Aging (grant numbers:
P01-AG02219, K01 AG023515, P50-AG05138); United States Department of
Veterans Affairs; Berkman Charitable Trust
NR 30
TC 5
Z9 5
U1 1
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 JAN
PY 2012
VL 41
IS 1
BP 125
EP 128
DI 10.1093/ageing/afr124
PG 4
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 859EL
UT WOS:000297858700025
PM 21930529
ER
PT J
AU DaRocha-Souto, B
Coma, M
Perez-Nievas, BG
Scotton, TC
Siao, M
Sanchez-Ferrer, P
Hashimoto, T
Fan, Z
Hudry, E
Barroeta, I
Sereno, L
Rodriguez, M
Sanchez, MB
Hyman, BT
Gomez-Isla, T
AF DaRocha-Souto, B.
Coma, M.
Perez-Nievas, B. G.
Scotton, T. C.
Siao, M.
Sanchez-Ferrer, P.
Hashimoto, T.
Fan, Z.
Hudry, E.
Barroeta, I.
Sereno, L.
Rodriguez, M.
Sanchez, M. B.
Hyman, B. T.
Gomez-Isla, T.
TI Activation of glycogen synthase kinase-3 beta mediates beta-amyloid
induced neuritic damage in Alzheimer's disease
SO NEUROBIOLOGY OF DISEASE
LA English
DT Article
ID TRANSGENIC MOUSE MODEL; PRECURSOR PROTEIN; SYNAPTIC PLASTICITY; NEURONAL
LOSS; IN-VIVO; NEUROFIBRILLARY DEGENERATION; MICE; GSK-3-BETA;
PHOSPHORYLATION; DEPOSITION
AB beta-Amyloid (A beta) plaques in Alzheimer (AD) brains are surrounded by severe dendritic and axonal changes, including local spine loss, axonal swellings and distorted neurite trajectories. Whether and how plaques induce these neuropil abnormalities remains unknown. We tested the hypothesis that oligomeric assemblies of A beta, seen in the periphery of plaques, mediate the neurodegenerative phenotype of AD by triggering activation of the enzyme GSK-3 beta, which in turn appears to inhibit a transcriptional program mediated by CREB. We detect increased activity of GSK-3 beta after exposure to oligomeric A beta in neurons in culture, in the brain of double transgenic APP/tau mice and in AD brains. Activation of GSK-3 beta, even in the absence of A beta, is sufficient to produce a phenocopy of A beta-induced dendritic spine loss in neurons in culture, while pharmacological inhibition of GSK-3 beta prevents spine loss and increases expression of CREB-target genes like BDNF. Of note, in transgenic mice GSK-3 beta inhibition ameliorated plaque-related neuritic changes and increased CREB-mediated gene expression. Moreover, GSK-3 beta inhibition robustly decreased the oligomeric A beta load in the mouse brain. All these findings support the idea that GSK3 beta is aberrantly activated by the presence of A beta, and contributes, at least in part, to the neuronal anatomical derangement associated with A beta plaques in AD brains and to A beta pathology itself. (C) 2011 Elsevier Inc. All rights reserved.
C1 [DaRocha-Souto, B.; Coma, M.; Perez-Nievas, B. G.; Scotton, T. C.; Siao, M.; Sanchez-Ferrer, P.; Hashimoto, T.; Fan, Z.; Hudry, E.; Hyman, B. T.; Gomez-Isla, T.] Harvard Univ, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Barroeta, I.; Sereno, L.; Rodriguez, M.; Sanchez, M. B.; Gomez-Isla, T.] Univ Autonoma Barcelona, Dept Neurol, Hosp Santa Creu & St Pau, E-08193 Barcelona, Spain.
RP Gomez-Isla, T (reprint author), Harvard Univ, Dept Neurol, Massachusetts Gen Hosp, WACC Suite 715,15th Parkman St, Boston, MA 02115 USA.
EM tgomezisla@partners.org
RI Hashimoto, Tadafumi/A-7723-2013
FU FIS [PI041887]; CIBERNED
FX This project was funded in part by FIS PI041887 and CIBERNED.
NR 61
TC 57
Z9 60
U1 3
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD JAN
PY 2012
VL 45
IS 1
BP 425
EP 437
DI 10.1016/j.nbd.2011.09.002
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 859NQ
UT WOS:000297883500048
PM 21945540
ER
PT S
AU Hatcliff, J
King, A
Lee, I
MacDonald, A
Fernando, A
Robkin, M
Vasserman, E
Weininger, S
Goldman, JM
AF Hatcliff, John
King, Andrew
Lee, Insup
MacDonald, Alasdair
Fernando, Anura
Robkin, Michael
Vasserman, Eugene
Weininger, Sandy
Goldman, Julian M.
GP IEEE Comp Soc
TI Rationale and Architecture Principles for Medical Application Platforms
SO 2012 IEEE/ACM THIRD INTERNATIONAL CONFERENCE ON CYBER-PHYSICAL SYSTEMS
(ICCPS 2012)
SE ACM-IEEE International Conference on Cyber-Physical Systems
LA English
DT Proceedings Paper
CT 3rd IEEE/ACM International Conference on Cyber-Physical Systems (ICCPS)
CY APR 17-19, 2012
CL Beijing, PEOPLES R CHINA
SP ACM, IEEE Comp Soc, IEEE
DE computing platform; medical device; interoperability; safety-critical
systems; certification
AB The concept of "system of systems" architecture is increasingly prevalent in many critical domains. Such systems allow information to be pulled from a variety of sources, analyzed to discover correlations and trends, stored to enable realtime and post-hoc assessment, mined to better inform decision-making, and leveraged to automate control of system units. In contrast, medical devices typically have been developed as monolithic stand-alone units. However, a vision is emerging of a notion of a medical application platform (MAP) that would provide device and health information systems (HIS) interoperability, safety critical network middleware, and an execution environment for clinical applications ("apps") that offer numerous advantages for safety and effectiveness in health care delivery.
In this paper, we present the clinical safety/effectiveness and economic motivations for MAPs, and describe key characteristics of MAPs that are guiding the search for appropriate technology, regulatory, and ecosystem solutions. We give an overview of the Integrated Clinical Environment (ICE) - one particular achitecture for MAPs, and the Medical Device Coordination Framework - a prototype implementation of the ICE architecture.
C1 [Hatcliff, John; Vasserman, Eugene] Kansas State Univ, Manhattan, KS 66506 USA.
[King, Andrew; Lee, Insup] Univ Penn, Philadelphia, PA 19104 USA.
[MacDonald, Alasdair] eHlth Technol, West Henrietta, NY USA.
[Fernando, Anura] Underwriters Labs, Northbrook, IL USA.
[Robkin, Michael] Anakena Solut, Woodland Hills, CA USA.
[Weininger, Sandy] US FDA, Rockville, MD 20857 USA.
[Goldman, Julian M.] Massachusetts Gen Hosp, CIMIT MD PnP Program, Boston, MA 02114 USA.
RP Hatcliff, J (reprint author), Kansas State Univ, Manhattan, KS 66506 USA.
FU National Science Foundation [0734204, 0932289, 1065887]; NIH/NIBIB
Quantum program
FX This work is supported in part by the National Science Foundation under
Grants #0734204, 0932289, 1065887, and by the NIH/NIBIB Quantum program.
NR 11
TC 5
Z9 5
U1 0
U2 0
PU IEEE COMPUTER SOC
PI LOS ALAMITOS
PA 10662 LOS VAQUEROS CIRCLE, PO BOX 3014, LOS ALAMITOS, CA 90720-1264 USA
SN 2375-8317
BN 978-0-7695-4695-7
J9 ACM IEEE INT CONF CY
PY 2012
BP 3
EP 12
DI 10.1109/ICCPS.2012.9
PG 10
WC Computer Science, Information Systems; Computer Science, Software
Engineering; Engineering, Electrical & Electronic
SC Computer Science; Engineering
GA BG9NL
UT WOS:000393451600001
ER
PT J
AU Puissant, A
Fenouille, N
Auberger, P
AF Puissant, Alexandre
Fenouille, Nina
Auberger, Patrick
TI When autophagy meets cancer through p62/SQSTM1
SO AMERICAN JOURNAL OF CANCER RESEARCH
LA English
DT Review
DE Paget's disease; mTOR; NF kappa B; NRF2; MAPK; Atg; ROS; ubiquitin;
protein aggregates; oxidative stress
AB Although p62/SQSTM1 was initially identified as an essential mediator of NF kappa B signaling, several recent studies have also highlighted its important role at the crossroad between the mTOR or MAPK signaling pathways and selective autophagy. The p62 structure containing important interaction domains attests to the ability of this protein to regulate and modulate the activation of these signaling pathways during tumor formation and propagation. The second very important function of this protein is to act as a molecular adaptor between the autophagic machinery and its substrates. Consequently, p62 is degraded following an increase in autophagic flux for which this protein currently serves as an indicator. However, the measurement of p62 expression strictly as a marker of autophagic flux is still controversial and can be misinterpreted mainly because this protein is subject to complex regulation at both the transcriptional and post-translational levels. Finally, because p62 is an autophagic substrate, it acts as a molecular link between cancer and autophagy by conferring a high level of selectivity through the degradation of important signaling molecules.
C1 [Puissant, Alexandre] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02215 USA.
[Fenouille, Nina] MIT, Cambridge, MA 02139 USA.
[Auberger, Patrick] Fac Med Nice, INSERM, U1065, Team Cell Death Differentiat Inflammat & Canc, F-06034 Nice, France.
[Auberger, Patrick] Equipe Labellisee Ligue Natl Canc 2011 2013, Nice, France.
[Auberger, Patrick] Univ Nice Sophia Antipolis, F-06189 Nice, France.
RP Auberger, P (reprint author), Ctr Mediterraneen Med Mol, INSERM U1065, INSERM DR1, Batiment ARCHIMED, F-06204 Nice 3, France.
EM auberger@unice.fr
RI PUISSANT, ALEXANDRE/O-9575-2016; AUBERGER, Patrick/G-1491-2013
OI PUISSANT, ALEXANDRE/0000-0002-3997-9282; AUBERGER,
Patrick/0000-0002-2481-8275
FU INSERM; Ligue Nationale Contre le Cancer (LNCC); INCA [PL2010-0149];
Association pour la Rechercher contre le Cancer; Fondation de France
(FDF); Contrat Hospitalier de Recherche Translationnel (CHRT) from the
CHU of Nice, France; Association pour la Recherche sur le Cancer (ARC);
Ludwig Fund for Cancer Research; equipe labellisee
FX This work was supported by INSERM, the Ligue Nationale Contre le Cancer
(LNCC), equipe labellisee 2008-2010, INCA (PL2010-0149), the Association
pour la Rechercher contre le Cancer and the Fondation de France (FDF).
P.A. is the recipient of a Contrat Hospitalier de Recherche
Translationnel (CHRT 2010-2013) from the CHU of Nice, France. A.P. is
the recipient of a fellowship from the Association pour la Recherche sur
le Cancer (ARC). N.F. is the recipient of a fellowship from The Ludwig
Fund for Cancer Research.
NR 82
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Z9 85
U1 0
U2 4
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 2156-6976
J9 AM J CANCER RES
JI Am. J. Cancer Res.
PY 2012
VL 2
IS 4
BP 397
EP 413
PG 17
WC Oncology
SC Oncology
GA V30ZV
UT WOS:000208854800004
PM 22860231
ER
PT B
AU Castro, CM
Lee, H
Weissleder, R
AF Castro, Cesar M.
Lee, Hakho
Weissleder, Ralph
BE Herold, KE
Rasooly, A
TI Cancer Cell Detection and Molecular Profiling Using Diagnostic Magnetic
Resonance
SO BIOSENSORS AND MOLECULAR TECHNOLOGIES FOR CANCER DIAGNOSTICS
SE Series in Sensors
LA English
DT Article; Book Chapter
ID LUNG-CANCER; SYSTEM
C1 [Castro, Cesar M.; Lee, Hakho; Weissleder, Ralph] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Castro, Cesar M.; Weissleder, Ralph] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Castro, Cesar M.; Lee, Hakho; Weissleder, Ralph] Harvard Univ, Sch Med, Boston, MA USA.
RP Castro, CM (reprint author), Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
NR 16
TC 0
Z9 0
U1 0
U2 0
PU CRC PRESS-TAYLOR & FRANCIS GROUP
PI BOCA RATON
PA 6000 BROKEN SOUND PARKWAY NW, STE 300, BOCA RATON, FL 33487-2742 USA
BN 978-1-4398-4166-2; 978-1-4398-4165-5
J9 SER SENSORS
PY 2012
BP 731
EP 746
D2 10.1201/b12138
PG 16
WC Biophysics; Biotechnology & Applied Microbiology; Oncology
SC Biophysics; Biotechnology & Applied Microbiology; Oncology
GA BD6CZ
UT WOS:000362079300043
ER
PT J
AU Lyman, JR
Chappell, JD
Morales, TI
Kelley, SS
Lee, GM
AF Lyman, Jeffrey R.
Chappell, Jonathan D.
Morales, Teresa I.
Kelley, Scott S.
Lee, Greta M.
TI Response of Chondrocytes to Local Mechanical Cartilage Injury in an Ex
Vivo Model
SO CARTILAGE
LA English
DT Article
DE cartilage; pseudopod; motility; collagen; repair
AB Background: Our goal was to set up an ex vivo culture system to assess whether cartilage wounding (partial-thickness defects) can induce morphological changes in neighboring chondrocytes and whether these cells can translocate to the surface of the defect. Methods: Two-millimeter partial-depth defects were created in human osteochondral explants followed by culture for up to 4 weeks. Frozen sections of defects and defect-free regions were labeled using immunofluorescence for a plasma membrane protein, CD44, and actin with TRITC-phalloidin. Viable nuclei were detected with Hoechst 33342. Differential interference contrast (DIC), confocal, and transmission electron microscopy (TEM) were used to examine process extension. Results: Significant changes in cell morphology occurred in response to wounding in the superficial and deep cartilage zones. These included cell flattening, polarization of the actin cytoskeleton, extension of pseudopods projecting towards the edge of the defect, and interactions of these filopodia with collagen fibers. Cell density decreased progressively in the 300-mu m zone adjacent to the defect to an average of approximately 25% to 35% after 3 weeks. Concomitant increases in cell density in the defect margin were observed. By contrast, minimal changes were seen in the middle cartilage zone. Conclusions: These novel observations strongly suggest active cartilage cell responses and movements in response to wounding. It is proposed that cartilage cells use contact guidance on fibrillated collagen to move into and populate defect areas in the superficial and deep zones.
C1 [Lyman, Jeffrey R.] Lyman Knee Clin, Scottsdale, AZ USA.
[Chappell, Jonathan D.] Wake Orthopaed, Raleigh, NC USA.
[Morales, Teresa I.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Kelley, Scott S.] Duke Univ, Dept Orthopaed, Durham, NC USA.
[Lee, Greta M.] Univ North Carolina Chapel Hill, Dept Orthoped, Chapel Hill, NC USA.
[Lee, Greta M.] Univ North Carolina Chapel Hill, Thurston Arthrit Res Ctr, Chapel Hill, NC USA.
RP Morales, TI (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Jackson Bldg,R1120,55 Fruit St, Boston, MA 02114 USA.
EM tmorales@fas.harvard.edu
FU NIAMS [AR43883]
FX The authors thank Marianne Tioran and Vicki Madden for technical
assistance and Dr. C. William Davis and the UNC Cystic Fibrosis Center
for the use of the Leica confocal microscope. Dr. Teresa Morales
(Harvard Medical School) contributed by helping to write the article.
This work was funded by NIAMS (AR43883).
NR 30
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Z9 6
U1 1
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1947-6035
EI 1947-6043
J9 CARTILAGE
JI Cartilage
PD JAN
PY 2012
VL 3
IS 1
BP 58
EP 69
DI 10.1177/1947603511421155
PG 12
WC Orthopedics
SC Orthopedics
GA V36NE
UT WOS:000209217700006
PM 26069619
ER
PT J
AU Johnson, LL
DeLano, MC
Spector, M
Jeng, L
Pittsley, A
Gottschalk, A
AF Johnson, Lanny L.
DeLano, Mark C.
Spector, Myron
Jeng, Lily
Pittsley, Andrew
Gottschalk, Alexander
TI The Biological Response following Autogenous Bone Grafting for
Large-Volume Defects of the Knee: Index Surgery through 12 to 21 Years'
Follow-up
SO CARTILAGE
LA English
DT Article
DE articular cartilage < tissue; biopsy < research methods; histology:
staining < research methods; magnetic resonance imaging < diagnostics;
knee < joint involved
AB Objective: This report focuses on the biological events occurring at various intervals following autogenous bone grafting of large-volume defects of the knee joint's femoral condyle secondary to osteochondritis dissecans (OCD) or osteonecrosis (ON). It was hypothesized that the autogenous bone graft would integrate and the portion exposed to the articular surface would form fibrocartilage, which would endure for years. Methods: Between September 29, 1987 and August 8, 1994, there were 51 patients treated with autogenous bone grafting for large-volume osteochondral defects. Twenty-five of the 51 patients were available for long-term follow-up up to 21 years. Patient follow-up was accomplished by clinical opportunity and intentional research. Videotapes were available on all index surgeries for review and comparison. All had preoperative and postoperative plain film radiographs. Long-term follow-up included MRI up to 21 years. Second-look arthroscopy and biopsy were obtained on 14 patients between 8 weeks and 20 years. Results: Radiological assessment showed the autogenous bone grafts integrated with the host bone. The grafts retained the physical geometry of the original placement. MRI showed soft tissue covering the grafts in all cases at long-term follow-up. Interval biopsy showed the surface covered with fibrous tissue at 8 weeks and subsequently converted to fibrocartilage with hyaline cartilage at 20 years. Conclusion: Autogenous bone grafting provides a matrix for large osteochondral defects that integrates with the host bone and results in a surface repair of fibrocartilage and hyaline cartilage that can endure for up to 20 years.
C1 [DeLano, Mark C.; Gottschalk, Alexander] Michigan State Univ, Coll Human Med, Dept Radiol, E Lansing, MI 48824 USA.
[Spector, Myron; Jeng, Lily] Harvard Univ, Brigham & Womens Hosp, Sch Med, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Jeng, Lily] MIT, Dept Biol Engn, Cambridge, MA 02139 USA.
RP Johnson, LL (reprint author), 4658 Chippewa Dr, Okemos, MI 48864 USA.
EM LLJMD@aol.com
OI DeLano, Mark/0000-0003-1550-6445
FU VA Research Career Scientist Award
FX The authors received no financial support for the research and/or
authorship of this article. M. Spector was supported by a VA Research
Career Scientist Award. The authors gratefully acknowledge receipt of
the anti-lubricin antibody from T.M. Schmid, Rush University Medical
Center, Chicago, IL.
NR 35
TC 2
Z9 2
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1947-6035
EI 1947-6043
J9 CARTILAGE
JI Cartilage
PD JAN
PY 2012
VL 3
IS 1
BP 86
EP 99
DI 10.1177/1947603511413568
PG 14
WC Orthopedics
SC Orthopedics
GA V36NE
UT WOS:000209217700009
PM 26069622
ER
PT S
AU Murakami, Y
Gunji, H
Kimura, F
Yamaguchi, M
Yamashita, Y
Saito, A
Abe, T
Sakamoto, M
Bautista, PA
Yagi, Y
AF Murakami, Yuri
Gunji, Hikaru
Kimura, Fumikazu
Yamaguchi, Masahiro
Yamashita, Yoshiko
Saito, Akira
Abe, Tokiya
Sakamoto, Michiie
Bautista, Pinky A.
Yagi, Yukako
GP IS&T
TI Color Correction in Whole Slide Digital Pathology
SO COLOR SCIENCE AND ENGINEERING SYSTEMS, TECHNOLOGIES, AND APPLICATIONS:
TWENTIETH COLOR AND IMAGING CONFERENCE
SE Color and Imaging Conference Final Program and Proceedings
LA English
DT Proceedings Paper
CT 20th Color and Imaging Conference on Color Science and Engineering
Systems, Technologies, and Applications
CY NOV 12-16, 2012
CL Los Angeles, CA
SP Soc Imag Sci & Technol, Soc Informat Display, Adobe, Canon, Kodak, hp, LENMARK, xerox, KYOCERA
AB Whole slide imaging (WSI) is a technique with both the scanning and viewing of digital images of the entire area of a glass pathology slide. The implementation of WSI has started to accelerate, and the usages of WSI are expected for variety of applications such as image analysis, education, conference, and remote diagnosis. However; for implementation of WSI to clinical applications, color variation in digital pathology images is one of the most important issues. The reasons for color variation of whole slide images are mainly in the two processes: staining tissue samples and scanning glass slides. This paper presents the methods and the results of the color correction of whole slide images, with consideration of these two reasons. For color variation caused by scanning devices, the characterization of the whole slide scanner was performed based on a traditional empirical model using a known color chart, where the color chart is a miniature transparent one arranged on a glass slide. In addition, it was also tested that color correction using Hematoxylin and Eosin stained mouse embryo slide instead of the color chart slide. For the color variation caused by staining conditions, the color distribution of images was corrected so as to fit to that of a reference image. Such correction is relatively easy for pathology image, because the color distribution of a stained pathology slide presents a characteristic color distribution decided by its staining method. The effectiveness of the color correction methods were confirmed for whole slide images of tissue samples stained by some typical staining methods.
C1 [Murakami, Yuri; Gunji, Hikaru; Kimura, Fumikazu; Yamaguchi, Masahiro] Tokyo Inst Technol, Global Sci Informat & Comp Ctr, Tokyo 152, Japan.
[Yamashita, Yoshiko; Saito, Akira] NEC Corp Ltd, Med Solut Div, Tokyo, Japan.
[Abe, Tokiya; Sakamoto, Michiie] Keio Univ, Sch Med, Dept Pathol, Tokyo 160, Japan.
[Bautista, Pinky A.; Yagi, Yukako] Harvard Univ, Massachusetts Gen Hosp, Dept Pathol, Boston, MA USA.
RP Murakami, Y (reprint author), Tokyo Inst Technol, Global Sci Informat & Comp Ctr, Tokyo 152, Japan.
OI Yamaguchi, Masahiro/0000-0003-1001-4505
NR 5
TC 1
Z9 1
U1 0
U2 1
PU SOC IMAGING SCIENCE & TECHNOLOGY
PI SPRINGFIELD
PA 7003 KILWORTH LANE, SPRINGFIELD, VA 22151 USA
SN 2166-9635
BN 978-0-89208-303-9
J9 COLOR IMAG CONF
PY 2012
BP 253
EP 258
PG 6
WC Imaging Science & Photographic Technology
SC Imaging Science & Photographic Technology
GA BC4YD
UT WOS:000353000800045
ER
PT S
AU Jalian, HR
Nelson, A
AF Jalian, H. Ray
Nelson, Andrew
BE Kim, J
Lask, G
Nelson, A
TI Laser rejuvenation
SO COMPREHENSIVE AESTHETIC REJUVENATION: A REGIONAL APPROACH
SE Series in Cosmetic and Laser Therapy
LA English
DT Article; Book Chapter
ID PULSED-DYE-LASER; ND-YAG LASER; GUINEA-PIG SKIN; FRACTIONAL
PHOTOTHERMOLYSIS; PHOTODYNAMIC THERAPY; CARBON-DIOXIDE; THERMAL-INJURY;
COMBINATION; EXPERIENCE; LIGHT
C1 [Jalian, H. Ray] Massachusetts Gen Hosp, Dept Dermatol, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Nelson, Andrew] Tufts Univ, Sch Med, Dept Dermatol, Boston, MA 02111 USA.
RP Jalian, HR (reprint author), Massachusetts Gen Hosp, Dept Dermatol, Wellman Ctr Photomed, Boston, MA 02114 USA.
NR 55
TC 0
Z9 0
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL ST, LONDON, EC2A 4LQ, ENGLAND
SN 2158-026X
BN 978-1-84184-758-0; 978-0-415-45894-8
J9 SER COSMET LASER TH
PY 2012
VL 8
BP 30
EP 42
PG 13
WC Dermatology
SC Dermatology
GA BD6NF
UT WOS:000362405700006
ER
PT S
AU Wasserman, DI
Avram, M
Nelson, A
AF Wasserman, Daniel I.
Avram, Mathew
Nelson, Andrew
BE Kim, J
Lask, G
Nelson, A
TI Approach to cellulite and fat
SO COMPREHENSIVE AESTHETIC REJUVENATION: A REGIONAL APPROACH
SE Series in Cosmetic and Laser Therapy
LA English
DT Article; Book Chapter
ID FOCUSED ULTRASOUND; RADIOFREQUENCY; DEVICE; ENDERMOLOGIE; EFFICACY;
TISSUE; LASER; SKIN; NM
C1 [Wasserman, Daniel I.] Riverchase Dermatol & Cosmet Surg, Naples, FL 34102 USA.
[Avram, Mathew] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Ctr Photomed,Dept Dermatol, Boston, MA USA.
[Nelson, Andrew] Tufts Univ, Sch Med, Dept Dermatol, Boston, MA 02111 USA.
RP Wasserman, DI (reprint author), Riverchase Dermatol & Cosmet Surg, Naples, FL 34102 USA.
NR 33
TC 0
Z9 0
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL ST, LONDON, EC2A 4LQ, ENGLAND
SN 2158-026X
BN 978-1-84184-758-0; 978-0-415-45894-8
J9 SER COSMET LASER TH
PY 2012
VL 8
BP 136
EP 144
PG 9
WC Dermatology
SC Dermatology
GA BD6NF
UT WOS:000362405700019
ER
PT S
AU Yanai, R
Thanos, A
Connor, KM
AF Yanai, Ryoji
Thanos, Aristomenis
Connor, Kip M.
BE Lambris, JD
Hajishengallis, G
TI Complement Involvement in Neovascular Ocular Diseases
SO CURRENT TOPICS IN INNATE IMMUNITY II
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Proceedings Paper
CT 7th International Aegean Conference on Innate Immunity
CY JUL 04-09, 2010
CL GREECE
DE Complement; Oxygen-induced retinopathy; Retinopathy of prematurity;
Choroidal neovascularization; Age-related macular degeneration; Diabetic
retinopathy
ID PROLIFERATIVE DIABETIC-RETINOPATHY; ENDOTHELIAL GROWTH-FACTOR; MEMBRANE
ATTACK COMPLEX; TUMOR-NECROSIS-FACTOR; C-REACTIVE PROTEIN; INDUCED
CHOROIDAL NEOVASCULARIZATION; PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA;
LECTIN ACTIVATION PATHWAY; DECAY-ACCELERATING FACTOR; AGE-RELATED
MACULOPATHY
AB Pathological neovascularization (NV) is a hallmark of late stage neovascular age-related macular degeneration (AMD), diabetic retinopathy (DR), and retinopathy of prematurity (ROP). There is accumulating evidence that alterations in inflammatory and immune system pathways that arise from genetic differences, injury, and disease can predispose individuals to retinal neovascular eye diseases. Yet the mechanism of disease progression with respect to the complement system in these maladies is not fully understood. Recent studies have implicated the complement system as an emerging player in the etiology of several retinal diseases. We will summarize herein several of the complement system pathways known to be involved in ocular neovascular pathologies. Current treatment for many neovascular eye diseases focuses on suppression of NV with laser ablation, photodynamic therapy, or anti-VEGF angiogenic inhibitors. However, these treatments do not address the underlying cause of many of these diseases. A clear understanding of the cellular and molecular mechanisms could bring a major shift in our approach to disease treatment and prevention.
C1 [Yanai, Ryoji; Thanos, Aristomenis; Connor, Kip M.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Angiogenesis Lab, Boston, MA 02114 USA.
RP Connor, KM (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Angiogenesis Lab, Boston, MA 02114 USA.
EM ryoji_yanai@meei.harvard.edu; aristomenis_thanos@meei.harvard.edu;
kip_connor@meei.harvard.edu
OI Connor, Kip/0000-0002-2048-9080
FU March of Dimes Foundation [5-FY09-535]; National Institutes of Health
[P30EY014104]; Research to Prevent Blindness
FX This work was generously supported by the March of Dimes Foundation
(Grant No. 5-FY09-535), National Institutes of Health Core Grant
(P30EY014104) and Research to Prevent Blindness Unrestricted Grant.
NR 163
TC 13
Z9 15
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING STREET, NEW YORK, NY 10013, UNITED STATES
SN 0065-2598
BN 978-1-4614-0106-3; 978-1-4614-0105-6
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2012
VL 946
BP 161
EP 183
DI 10.1007/978-1-4614-0106-3_10
PG 23
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA BA4HQ
UT WOS:000335736900011
PM 21948368
ER
PT J
AU Pfeifer, HH
AF Pfeifer, Heidi H.
BE Neal, E
TI The Low Glycaemic Index Treatment
SO DIETARY TREATMENT OF EPILEPSY: PRACTICAL IMPLEMENTATION OF KETOGENIC
THERAPY
LA English
DT Article; Book Chapter
ID KETOGENIC DIET; EPILEPSY; EXPERIENCE; EFFICACY; CHILDREN
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Pfeifer, HH (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 14
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI CHICHESTER
PA THE ATRIUM, SOUTHERN GATE, CHICHESTER, WEST SUSSEX PO19 8SQ, ENGLAND
BN 978-0-470-67041-5
PY 2012
BP 100
EP 108
D2 10.1002/9781118702772
PG 9
WC Clinical Neurology; Nutrition & Dietetics
SC Neurosciences & Neurology; Nutrition & Dietetics
GA BA8OB
UT WOS:000338331800010
ER
PT J
AU Kratz, F
Senter, P
Steinhagen, H
AF Kratz, Felix
Senter, Peter
Steinhagen, Henning
BE Kratz, F
Senter, P
Steinhagen, H
TI Drug Delivery in Oncology From Basic Research to Cancer Therapy Volume 1
Preface
SO DRUG DELIVERY IN ONCOLOGY: FROM BASIC RESEARCH TO CANCER THERAPY, VOLS
1-3
LA English
DT Editorial Material; Book Chapter
C1 [Kratz, Felix] Univ Florence, Bioinorgan Inst, I-50121 Florence, Italy.
[Kratz, Felix] Tumor Biol Ctr, Freiburg, Germany.
[Senter, Peter] Max Planck Inst, Gottingen, Germany.
[Senter, Peter] Dana Farber Canc Inst, Boston, MA USA.
[Senter, Peter] Bristol Myers Squibb, New York, NY USA.
[Senter, Peter] Seattle Genet, Seattle, WA USA.
[Steinhagen, Henning] Grunenthal GmbH, Global Drug Discovery, D-52078 Aachen, Germany.
RP Kratz, F (reprint author), Univ Florence, Bioinorgan Inst, I-50121 Florence, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PAPPELALLEE 3, W-69469 WEINHEIM, GERMANY
BN 978-3-527-32823-9
PY 2012
BP XVII
EP XVIII
PG 2
WC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
GA BA8DL
UT WOS:000338009100002
ER
PT J
AU Sutphin, PD
Flores, EJ
Harisinghani, M
AF Sutphin, Patrick D.
Flores, Efren J.
Harisinghani, Mukesh
BE Kratz, F
Senter, P
Steinhagen, H
TI Magnetic Nanoparticles in Magnetic Resonance Imaging and Drug Delivery
SO DRUG DELIVERY IN ONCOLOGY: FROM BASIC RESEARCH TO CANCER THERAPY, VOLS
1-3
LA English
DT Article; Book Chapter
ID SUPERPARAMAGNETIC IRON-OXIDE; TARGETED GENE DELIVERY; LYMPH-NODE
METASTASES; IN-VIVO; TRANSFERRIN RECEPTOR; MR LYMPHANGIOGRAPHY;
COMPUTED-TOMOGRAPHY; CONTRAST AGENT; TUMOR-CELLS; CANCER
C1 [Flores, Efren J.; Harisinghani, Mukesh] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Harisinghani, Mukesh] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Sutphin, PD (reprint author), Massachusetts Gen Hosp, Diagnost Radiol Residency Program, Boston, MA 02114 USA.
NR 52
TC 1
Z9 1
U1 0
U2 1
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PAPPELALLEE 3, W-69469 WEINHEIM, GERMANY
BN 978-3-527-32823-9
PY 2012
BP 225
EP 245
PG 21
WC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
GA BA8DL
UT WOS:000338009100011
ER
PT J
AU Alley, SC
Jeger, S
Lyon, RP
Sussman, D
Senter, PD
AF Alley, Stephen C.
Jeger, Simone
Lyon, Robert P.
Sussman, Django
Senter, Peter D.
BE Kratz, F
Senter, P
Steinhagen, H
TI Empowered Antibodies for Cancer Therapy
SO DRUG DELIVERY IN ONCOLOGY: FROM BASIC RESEARCH TO CANCER THERAPY, VOLS
1-3
LA English
DT Article; Book Chapter
ID ACUTE MYELOID-LEUKEMIA; DEPENDENT CELLULAR CYTOTOXICITY; FC-GAMMA-RIII;
GEMTUZUMAB OZOGAMICIN MYLOTARG; SENSITIVE DIPEPTIDE PRODRUGS; POTENT
ANTITUMOR-ACTIVITY; METASTATIC BREAST-CANCER; AURISTATIN-E CONJUGATE;
MONOCLONAL-ANTIBODY; TARGETED CHEMOTHERAPY
C1 [Alley, Stephen C.] Penn State Univ, University Pk, PA 16802 USA.
[Alley, Stephen C.; Jeger, Simone; Senter, Peter D.] Seattle Genet, Seattle, WA USA.
[Lyon, Robert P.] Seattle Genet, Dept Chem, Seattle, WA USA.
[Sussman, Django] Fred Hutchinson Canc Res Ctr, Seattle, WA USA.
[Senter, Peter D.] Max Planck Inst, Gottingen, Germany.
[Senter, Peter D.] Dana Farber Canc Inst, Boston, MA USA.
[Senter, Peter D.] Bristol Myers Squibb, New York, NY USA.
RP Alley, SC (reprint author), Penn State Univ, University Pk, PA 16802 USA.
NR 151
TC 0
Z9 0
U1 0
U2 0
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PAPPELALLEE 3, W-69469 WEINHEIM, GERMANY
BN 978-3-527-32823-9
PY 2012
BP 291
EP 323
PG 33
WC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
GA BA8DL
UT WOS:000338009100013
ER
PT J
AU Henderson, IC
AF Henderson, I. Craig
BE Kratz, F
Senter, P
Steinhagen, H
TI Development of PEGylated Liposomes
SO DRUG DELIVERY IN ONCOLOGY: FROM BASIC RESEARCH TO CANCER THERAPY, VOLS
1-3
LA English
DT Article; Book Chapter
ID METASTATIC BREAST-CANCER; PHASE-II TRIAL; REFRACTORY MULTIPLE-MYELOMA;
RESISTANT OVARIAN-CANCER; RECURRENT EPITHELIAL OVARIAN; DOXORUBICIN PLUS
DOCETAXEL; SOFT-TISSUE SARCOMA; HAND-FOOT SYNDROME; KAPOSIS-SARCOMA;
RANDOMIZED-TRIAL
C1 [Henderson, I. Craig] Board SEQUUS Pharmaceut, Menlo Pk, CA USA.
[Henderson, I. Craig] Dana Farber Canc Inst, Breast Evaluat Ctr, Boston, MA USA.
[Henderson, I. Craig] UCSF, San Francisco, CA USA.
[Henderson, I. Craig] UCSF, Ctr Canc, San Francisco, CA USA.
[Henderson, I. Craig] Keryx Biopharmaceut, Access Oncol, New York, NY USA.
[Henderson, I. Craig] Keryx Biopharmaceut, New York, NY USA.
RP Henderson, IC (reprint author), UCSF, San Francisco, CA USA.
NR 125
TC 0
Z9 0
U1 0
U2 0
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PAPPELALLEE 3, W-69469 WEINHEIM, GERMANY
BN 978-3-527-32823-9
PY 2012
BP 907
EP 949
PG 43
WC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
GA BA8DL
UT WOS:000338009100031
ER
PT J
AU Torchilin, VP
AF Torchilin, Vladimir P.
BE Kratz, F
Senter, P
Steinhagen, H
TI Immunoliposomes
SO DRUG DELIVERY IN ONCOLOGY: FROM BASIC RESEARCH TO CANCER THERAPY, VOLS
1-3
LA English
DT Article; Book Chapter
ID PEGYLATED-LIPOSOMAL DOXORUBICIN; STERICALLY STABILIZED LIPOSOMES; B-CELL
LYMPHOMA; SINGLE-CHAIN FV; LONG-CIRCULATING LIPOSOMES; LARGE UNILAMELLAR
LIPOSOMES; TRANS-RETINOIC ACID; COLON-CANCER CELLS; MEDIATED
INTRACELLULAR DELIVERY; COMBINED IMMUNODEFICIENT MICE
C1 [Torchilin, Vladimir P.] Northeastern Univ, Boston, MA 02115 USA.
[Torchilin, Vladimir P.] Northeastern Univ, Ctr Pharmaceut Biotechnol & Nanomed, Boston, MA 02115 USA.
[Torchilin, Vladimir P.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Torchilin, Vladimir P.] Harvard Univ, Sch Med, Chem Program, Ctr Imaging & Pharmaceut Res, Cambridge, MA 02138 USA.
[Torchilin, Vladimir P.] Amer Inst Med & Biol Engn, Washington, DC USA.
[Torchilin, Vladimir P.] AAPS, Minneapolis, MN 55455 USA.
RP Torchilin, VP (reprint author), Northeastern Univ, Boston, MA 02115 USA.
NR 279
TC 0
Z9 0
U1 0
U2 1
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PAPPELALLEE 3, W-69469 WEINHEIM, GERMANY
BN 978-3-527-32823-9
PY 2012
BP 951
EP 987
PG 37
WC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
GA BA8DL
UT WOS:000338009100032
ER
PT J
AU Schally, AV
Halmos, G
AF Schally, Andrew V.
Halmos, Gabor
BE Kratz, F
Senter, P
Steinhagen, H
TI Targeting to Peptide Receptors
SO DRUG DELIVERY IN ONCOLOGY: FROM BASIC RESEARCH TO CANCER THERAPY, VOLS
1-3
LA English
DT Article; Book Chapter
ID HORMONE-RELEASING-HORMONE; CYTOTOXIC SOMATOSTATIN ANALOG; HUMAN BREAST
CANCERS; MULTIDRUG-RESISTANCE PROTEINS; EPIDERMAL-GROWTH-FACTOR;
BOMBESIN-LIKE PEPTIDES; RENAL-CELL CARCINOMAS; HUMAN PROSTATE-CANCER;
HUMAN OVARIAN CANCERS; HUMAN ENDOMETRIAL CANCERS
C1 [Schally, Andrew V.] Univ Miami, Miller Sch Med, Coral Gables, FL 33124 USA.
[Schally, Andrew V.] Univ Miami, Miller Sch Med, Div Hematol Oncol, Dept Med, Coral Gables, FL 33124 USA.
[Schally, Andrew V.] Vet Affairs Med Ctr, Polypeptide Canc Inst, Miami, FL 33125 USA.
[Schally, Andrew V.] US Dept Vet Affairs, Ford City, PA USA.
[Halmos, Gabor] Univ Debrecen, Med & Hlth Sci Ctr, Dept Biopharm, Debrecen, Hungary.
RP Schally, AV (reprint author), Univ Miami, Miller Sch Med, Coral Gables, FL 33124 USA.
NR 140
TC 4
Z9 4
U1 0
U2 1
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PAPPELALLEE 3, W-69469 WEINHEIM, GERMANY
BN 978-3-527-32823-9
PY 2012
BP 1219
EP 1261
PG 43
WC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
GA BA8DL
UT WOS:000338009100041
ER
PT J
AU Mroz, P
Sharma, SK
Zhiyentayev, T
Huang, YY
Hamblin, MR
AF Mroz, Pawel
Sharma, Sulbha K.
Zhiyentayev, Timur
Huang, Ying-Ying
Hamblin, Michael R.
BE Kratz, F
Senter, P
Steinhagen, H
TI Photodynamic Therapy: Photosensitizer Targeting and Delivery
SO DRUG DELIVERY IN ONCOLOGY: FROM BASIC RESEARCH TO CANCER THERAPY, VOLS
1-3
LA English
DT Article; Book Chapter
ID GROWTH-FACTOR RECEPTOR; INTERNALIZING MONOCLONAL-ANTIBODIES;
CHLORIN-TYPE PHOTOSENSITIZER; BREAST-CANCER CELLS; PEG-PE MICELLES;
IN-VITRO; PHOTOCHEMICAL INTERNALIZATION; SINGLET OXYGEN; ZINC
PHTHALOCYANINE; PYROPHEOPHORBIDE-A
C1 [Mroz, Pawel] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Wellman Ctr Photomed, Cambridge, MA 02138 USA.
[Mroz, Pawel] Harvard Univ, Sch Med, Lab Dr Michael R Hamblin, Cambridge, MA 02138 USA.
[Mroz, Pawel; Hamblin, Michael R.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Mroz, Pawel] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Mroz, Pawel] Wellman Ctr, Boston, MA 02114 USA.
[Sharma, Sulbha K.; Hamblin, Michael R.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Zhiyentayev, Timur] Moscow MV Lomonosov State Univ, Moscow 117234, Russia.
[Zhiyentayev, Timur] Massachusetts Gen Hosp, Grp Dr Michael R Hamblin, Boston, MA 02114 USA.
[Zhiyentayev, Timur] CALTECH, Pasadena, CA 91125 USA.
[Huang, Ying-Ying] Massachusetts Gen Hosp, Res Grp Dr Michael R Hamblin, Wellman Ctr Photomed, Boston, MA 02114 USA.
NR 183
TC 1
Z9 1
U1 1
U2 3
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA PAPPELALLEE 3, W-69469 WEINHEIM, GERMANY
BN 978-3-527-32823-9
PY 2012
BP 1569
EP 1603
PG 35
WC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Oncology; Pharmacology & Pharmacy
GA BA8DL
UT WOS:000338009100051
ER
PT J
AU Linville, D
Brown, T
O'Neil, M
AF Linville, Deanna
Brown, Tiffany
O'Neil, Maya
TI Medical Providers' Self Perceived Knowledge and Skills for Working With
Eating Disorders: A National Survey
SO EATING DISORDERS
LA English
DT Article
AB Research indicates that individuals suffering from an eating disorder (ED) consult their general practitioners more frequently than those without an eating disorder (Mond, Myers, Crosby, Hay, & Mitchell, 2010). However, little is known about medical providers' existing knowledge of and training in ED detection, intervention, and treatment. This study aimed to examine national medical providers' self-perceived knowledge, skills, and needs around eating disorder screening and intervention strategies. Utilizing survey design, a randomized sample of national medical providers responded to a 23-question survey. Sixty-eight percent of respondents indicated that they did not think to screen for an eating disorder because it was not the presenting concern and nearly 59% of providers did not feel like they had the skills necessary to intervene with eating disorders. Training implications and future research directions are discussed.
C1 [Linville, Deanna] Univ Oregon, Coll Educ, Dept Counseling Psychol & Human Serv, Eugene, OR 97403 USA.
[Brown, Tiffany] Pacific Lutheran Univ, Dept Marriage & Family Therapy, Div Social Sci, Tacoma, WA 98447 USA.
[O'Neil, Maya] Portland VA Med Ctr, Hlth Serv Res & Dev, Portland, OR USA.
[O'Neil, Maya] Portland VA Med Ctr, Dept Psychiat, Portland, OR USA.
[O'Neil, Maya] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
RP Linville, D (reprint author), 5251 Univ Oregon, Coll Educ, Dept Counseling Psychol & Human Serv, Eugene, OR 97403 USA.
EM Linville@uoregon.edu
NR 26
TC 6
Z9 7
U1 0
U2 1
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1064-0266
EI 1532-530X
J9 EAT DISORD
JI Eat. Disord
PY 2012
VL 20
IS 1
BP 1
EP 13
DI 10.1080/10640266.2012.635557
PG 13
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA V32PE
UT WOS:000208962300001
PM 22188056
ER
PT S
AU Bergwitz, C
Juppner, H
AF Bergwitz, Clemens
Jueppner, Harald
BE KuroO, M
TI FGF23 AND SYNDROMES OF ABNORMAL RENAL PHOSPHATE HANDLING
SO ENDOCRINE FGFS AND KLOTHOS
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Book Chapter
ID FIBROBLAST GROWTH FACTOR-23; FAMILIAL TUMORAL CALCINOSIS; HEREDITARY
HYPOPHOSPHATEMIC RICKETS; X-LINKED HYPOPHOSPHATEMIA;
HYPEROSTOSIS-HYPERPHOSPHATEMIA SYNDROME; NEVUS-SEBACEOUS-SYNDROME;
MCCUNE-ALBRIGHT-SYNDROME; STIMULATORY G-PROTEIN; RESECTION-RELATED
HYPOPHOSPHATEMIA; INFANTILE ARTERIAL CALCIFICATION
AB Fibroblast growth factor 23 (FGF23) is part of a previously unrecognized hormonal bone-parathyroid-kidney axis, which is modulated by 1,25(OH)(2)-vitamin D (1,25(OH)(2)D), dietary and circulating phosphate and possibly PTHI. FGF23 was discovered as the humoral factor in tumors that causes hypophosphatemia and osteomalacia and through the identification of a mutant form of FGF23 that leads to autosomal dominant hypophosphatemic rickets (ADHR), a rare genetic disorder. FGF23 appears to be mainly secreted by osteocytes where its expression is up-regulated by 1,25(OH)(2)D and probably by increased senim phosphate levels. Its synthesis and secretion is reduced through yet unknown mechanisms that involve the phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX), dentin matrix protein 1 (DWI) and ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1). Consequently, loss-of-function mutations in these genes underlie hypophosphatemic disorders that are either X-linked or autosomal recessive. impaired O-glycosylation of FGF23 due to the lack of UDP-N-acetyl-alpha-D-galactosamine:polypeptide N-acetylgalactosaminyl-transferase 3 (GALNT3) or due to certain homozygous FGF23 mutations results in reduced secretion of intact FGF23 and leads to familial hyperphosphatemic tumoral calcinosis. FOE 23 acts through FGF-receptors and the coreceptor Klotho to reduce 1,25(OH)(2),D synthesis in the kidney and probably the synthesis of parathyroid hormone (PTH) by the parathyroid glands. It furthermore synergizes with PTH to increase renal phosphate excretion by reducing expression of the sodium-phosphate cotransporters NaPi-Ha and NaPi-Hc in the proximal tubules. Loss-of-function mutations in these two transporters lead to autosomal recessive Fanconi syndrome or to hereditary hypophosphatemic rickets with hypercalciuria, respectively.
C1 [Bergwitz, Clemens; Jueppner, Harald] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Jueppner, Harald] Massachusetts Gen Hosp, Pediat Nephrol Unit, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Juppner, H (reprint author), Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
EM hjueppner@partners.org
FU NIDDK NIH HHS [K08 DK078361, R03 DK089127]
NR 172
TC 27
Z9 28
U1 0
U2 4
PU SPRINGER-VERLAG BERLIN
PI BERLIN
PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY
SN 0065-2598
BN 978-1-4614-0886-4; 978-1-4614-0887-1
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2012
VL 728
BP 41
EP 64
D2 10.1007/978-1-4614-0887-1
PG 24
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA BA3CR
UT WOS:000334109100004
PM 22396161
ER
PT B
AU Dupuy, JM
Ostacher, MJ
Huffman, J
Perlis, RH
Nierenberg, AA
AF Dupuy, Jamie M.
Ostacher, Michael J.
Huffman, Jeffrey
Perlis, Roy H.
Nierenberg, Andrew A.
BE Stein, DJ
Lerer, B
Stahl, SM
TI Evidence-based pharmacotherapy of major depressive disorder
SO ESSENTIAL EVIDENCE-BASED PSYCHOPHARMACOLOGY, 2ND EDITION
LA English
DT Article; Book Chapter
ID SEROTONIN REUPTAKE INHIBITORS; STAR-ASTERISK-D;
PLACEBO-CONTROLLED-TRIAL; ANTIDEPRESSANT PRESCRIPTION RATES; RESISTANT
UNIPOLAR DEPRESSION; DOUBLE-BLIND; 2ND-GENERATION ANTIDEPRESSANTS;
MODAFINIL AUGMENTATION; ADJUNCTIVE TREATMENT; RESIDUAL SYMPTOMS
C1 [Dupuy, Jamie M.; Huffman, Jeffrey; Perlis, Roy H.; Nierenberg, Andrew A.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Dupuy, Jamie M.; Huffman, Jeffrey; Perlis, Roy H.; Nierenberg, Andrew A.] Harvard Univ, Sch Med, Boston, MA USA.
[Ostacher, Michael J.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
RP Dupuy, JM (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
OI Ostacher, Michael/0000-0003-0353-7535
NR 93
TC 0
Z9 0
U1 0
U2 0
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND
BN 978-1-107-40010-8; 978-1-107-00795-6
PY 2012
BP 53
EP 72
D2 10.1017/CBO9780511910395
PG 20
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA BJM92
UT WOS:000329193200005
ER
PT B
AU Ripoll, LH
Triebwasser, J
Siever, LJ
AF Ripoll, Luis H.
Triebwasser, Joseph
Siever, Larry J.
BE Stein, DJ
Lerer, B
Stahl, SM
TI Evidence-based pharmacotherapy of personality disorders
SO ESSENTIAL EVIDENCE-BASED PSYCHOPHARMACOLOGY, 2ND EDITION
LA English
DT Article; Book Chapter
ID SOCIAL ANXIETY DISORDER; PLACEBO-CONTROLLED-TRIAL;
SELF-INJURIOUS-BEHAVIOR; POSITRON-EMISSION-TOMOGRAPHY; 18-MONTH
FOLLOW-UP; POSTTRAUMATIC-STRESS-DISORDER; IMPULSIVE AGGRESSIVE-BEHAVIOR;
RANDOMIZED CONTROLLED-TRIAL; VENLAFAXINE EXTENDED-RELEASE; FEMALE
BORDERLINE-PATIENTS
C1 [Ripoll, Luis H.; Triebwasser, Joseph; Siever, Larry J.] James J Peters VA Med Ctr, Mental Illness Res Educ & Clin Ctr, Bronx, NY USA.
RP Ripoll, LH (reprint author), James J Peters VA Med Ctr, Mental Illness Res Educ & Clin Ctr, Bronx, NY USA.
NR 185
TC 0
Z9 0
U1 0
U2 0
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA THE PITT BUILDING, TRUMPINGTON ST, CAMBRIDGE CB2 1RP, CAMBS, ENGLAND
BN 978-1-107-40010-8; 978-1-107-00795-6
PY 2012
BP 278
EP 315
D2 10.1017/CBO9780511910395
PG 38
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA BJM92
UT WOS:000329193200015
ER
PT J
AU Abercrombie, HC
Wirth, MM
Jahn, AL
Hoks, RM
AF Abercrombie, Heather C.
Wirth, Michelle M.
Jahn, Allison L.
Hoks, Roxanne M.
TI Affective style and early life experiences moderate cortisol's effects
on emotional learning
SO EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
LA English
DT Meeting Abstract
DE emotional memory; learning; cortisol; early life separation; trait
negative affect
C1 [Abercrombie, Heather C.; Hoks, Roxanne M.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI USA.
[Wirth, Michelle M.] Univ Notre Dame, South Bend, IN USA.
[Jahn, Allison L.] VA Boston Healthcare Syst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 5
PU CO-ACTION PUBLISHING
PI JARFALLA
PA RIPVAGEN 7, JARFALLA, SE-175 64, SWEDEN
SN 2000-8066
J9 EUR J PSYCHOTRAUMATO
JI Eur. J. Psychotraumatol.
PY 2012
VL 3
SU 1
DI 10.3402/ejpt.v3i0.19451
PG 2
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA V31FC
UT WOS:000208868500030
ER
PT J
AU Chao, LL
Weiner, MW
Neylan, TC
AF Chao, Linda L.
Weiner, Michael W.
Neylan, Thomas C.
TI Regional cerebral volumes in veterans with current versus remitted
posttraumatic stress disorder: a study at 4 Tesla
SO EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
LA English
DT Meeting Abstract
DE veterans; PTSD; brain volume
C1 [Chao, Linda L.; Weiner, Michael W.; Neylan, Thomas C.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Chao, Linda L.; Weiner, Michael W.] Univ Calif San Francisco, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA.
[Chao, Linda L.; Weiner, Michael W.] San Francisco VA Med Ctr, Ctr Imaging Neurodegenerat Dis, San Francisco, CA USA.
[Chao, Linda L.; Neylan, Thomas C.] San Francisco VA Med Ctr, Mental Hlth Serv, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CO-ACTION PUBLISHING
PI JARFALLA
PA RIPVAGEN 7, JARFALLA, SE-175 64, SWEDEN
SN 2000-8066
J9 EUR J PSYCHOTRAUMATO
JI Eur. J. Psychotraumatol.
PY 2012
VL 3
SU 1
DI 10.3402/ejpt.v3i0.19425
PG 2
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA V31FC
UT WOS:000208868500186
ER
PT J
AU de Fouchier, C
Blanchet, A
Hopkins, W
Bui, E
Ait-Aoudia, M
Jehel, L
AF de Fouchier, Capucine
Blanchet, Alain
Hopkins, William
Bui, Eric
Ait-Aoudia, Malik
Jehel, Louis
TI Validation of a French adaptation of the Harvard Trauma Questionnaire
among torture survivors from sub-Saharan African countries
SO EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
LA English
DT Article
DE Refugees; ethnic/cultural minorities; torture; cross-cultural
assessment; questionnaire
AB Background: To date no validated instrument in the French language exists to screen for posttraumatic stress disorder (PTSD) in survivors of torture and organized violence.
Objective: The aim of this study is to adapt and validate the Harvard Trauma Questionnaire (HTQ) to this population.
Method: The adapted version was administered to 52 French-speaking torture survivors, originally from sub-Saharan African countries, receiving psychological treatment in specialized treatment centers. A structured clinical interview for DSM was also conducted in order to assess if they met criteria for PTSD.
Results: Cronbach's alpha coefficient for the HTQ Part 4 was adequate (0.95). Criterion validity was evaluated using receiver operating characteristic curve analysis that generated good classification accuracy for PTSD (0.83). At the original cut-off score of 2.5, the HTQ demonstrated high sensitivity and specificity (0.87 and 0.73, respectively).
Conclusion: Results support the reliability and validity of the French version of the HTQ.
C1 [de Fouchier, Capucine; Ait-Aoudia, Malik] Inst Victimol, Ctr Psychotrauma, Paris, France.
[de Fouchier, Capucine; Blanchet, Alain; Ait-Aoudia, Malik] Univ Paris 08, Lab Psychopathol & Neuropsychol EA 2027, St Denis, France.
[Hopkins, William] Freedom Torture, London, England.
[Bui, Eric] CHU Toulouse, Lab Stress Traumat EA 4560, Toulouse, France.
[Bui, Eric] Univ Toulouse, Toulouse, France.
[Bui, Eric] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bui, Eric] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Jehel, Louis] Univ Antilles Guyane, Ctr Hosp Univ Martin, F-97261 Fort De France, France.
[Jehel, Louis] INSERM U669, Lab Eth Med & Med Legale EA 4569, Paris, France.
RP Jehel, L (reprint author), Ctr Hosp Univ, Serv Psychiat & Psychol Med Psychotraumatol & Add, BP 632, F-97261 Fort De France, France.
EM louis.jehel@chu-fortdefrance.fr
RI Bui, Eric/J-8347-2015;
OI Bui, Eric/0000-0002-1413-6473; Blanchet, Alain/0000-0003-1068-3717
NR 37
TC 4
Z9 4
U1 2
U2 8
PU CO-ACTION PUBLISHING
PI JARFALLA
PA RIPVAGEN 7, JARFALLA, SE-175 64, SWEDEN
SN 2000-8066
J9 EUR J PSYCHOTRAUMATO
JI Eur. J. Psychotraumatol.
PY 2012
VL 3
AR 19225
DI 10.3402/ejpt.v3i0.19225
PG 9
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA V31FB
UT WOS:000208868400031
ER
PT J
AU Hazlett, EA
Fernandez, N
Sasso, S
New, AS
Goodman, M
AF Hazlett, Erin A.
Fernandez, Nicholas
Sasso, Scott
New, Antonia S.
Goodman, Marianne
TI A non-verbal, quantitative measure of emotion dysregulation in veterans:
is affective startle a potential biomarker for suicide?
SO EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
LA English
DT Meeting Abstract
DE emotion; emotion dysregulation; fear/defensive brain circuitry;
affective startle eyeblink modulation; suicide ideation; suicidal
behavior
C1 [Hazlett, Erin A.; Fernandez, Nicholas; Sasso, Scott; New, Antonia S.; Goodman, Marianne] James J Peters VA Med Ctr, Mental Illness Res Educ & Clin Ctr MIRECC VISN, New York, NY USA.
[Hazlett, Erin A.; New, Antonia S.; Goodman, Marianne] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU CO-ACTION PUBLISHING
PI JARFALLA
PA RIPVAGEN 7, JARFALLA, SE-175 64, SWEDEN
SN 2000-8066
J9 EUR J PSYCHOTRAUMATO
JI Eur. J. Psychotraumatol.
PY 2012
VL 3
SU 1
DI 10.3402/ejpt.v3i0.19368
PG 2
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA V31FC
UT WOS:000208868500183
ER
PT J
AU Inslicht, SS
Metzler, TJ
Milad, M
Pineles, S
Orr, S
Marmar, C
Neylan, TC
AF Inslicht, Sabra S.
Metzler, Thomas J.
Milad, Mohammed
Pineles, Suzanne
Orr, Scott
Marmar, Charles
Neylan, Thomas C.
TI Sex differences in fear conditioning in posttraumatic stress disorder
SO EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
LA English
DT Meeting Abstract
DE sex differences; learning; conditioning; fear; posttraumatic stress
disorder; galvanic skin response
C1 [Inslicht, Sabra S.; Metzler, Thomas J.; Neylan, Thomas C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Inslicht, Sabra S.; Metzler, Thomas J.; Neylan, Thomas C.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Milad, Mohammed; Orr, Scott] Massachusetts Gen Hosp, Charlestown, MA USA.
[Milad, Mohammed; Orr, Scott] Harvard Univ, Sch Med, Charlestown, MA USA.
[Pineles, Suzanne] Vet Affairs Boston Healthcare Syst, Boston, MA USA.
[Marmar, Charles] NYU, Langone Med Ctr, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CO-ACTION PUBLISHING
PI JARFALLA
PA RIPVAGEN 7, JARFALLA, SE-175 64, SWEDEN
SN 2000-8066
J9 EUR J PSYCHOTRAUMATO
JI Eur. J. Psychotraumatol.
PY 2012
VL 3
SU 1
DI 10.3402/ejpt.v3i0.19367
PG 1
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA V31FC
UT WOS:000208868500182
ER
PT J
AU Luxenberg, A
O'Donovan, A
Inslicht, SS
Metzler, TJ
Hlavin, J
Weiner, MW
Neylan, TC
AF Luxenberg, Adam
O'Donovan, Aoife
Inslicht, Sabra S.
Metzler, Thomas J.
Hlavin, Jennifer
Weiner, Michael W.
Neylan, Thomas C.
TI Exaggerated autonomic responding to acoustic stimuli in Gulf War
Veterans with current versus remitted post-traumatic stress disorder
SO EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
LA English
DT Meeting Abstract
DE veterans; Gulf War; PTSD; autonomic response
C1 Univ Calif San Francisco, San Francisco, CA 94143 USA.
San Francisco VA Med Ctr, San Francisco, CA USA.
Northern Calif Inst Res & Educ, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU CO-ACTION PUBLISHING
PI JARFALLA
PA RIPVAGEN 7, JARFALLA, SE-175 64, SWEDEN
SN 2000-8066
J9 EUR J PSYCHOTRAUMATO
JI Eur. J. Psychotraumatol.
PY 2012
VL 3
SU 1
DI 10.3402/ejpt.v3i0.19369
PG 2
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA V31FC
UT WOS:000208868500184
ER
PT J
AU Miller, NA
Najavits, LM
AF Miller, Niki A.
Najavits, Lisa M.
TI Creating trauma-informed correctional care: a balance of goals and
environment
SO EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
LA English
DT Article
DE trauma; incarceration; criminal justice; PTSD; substance abuse;
treatment
AB Background: Rates of posttraumatic stress disorder and exposure to violence among incarcerated males and females in the US are exponentially higher than rates among the general population; yet, abrupt detoxification from substances, the pervasive authoritative presence and sensory and environmental trauma triggers can pose a threat to individual and institutional stability during incarceration.
Objective: The authors explore the unique challenges and promises of trauma-informed correctional care and suggest strategies for administrative support, staff development, programming, and relevant clinical approaches.
Method: A review of literature includes a comparison of gendered responses, implications for men's facilities, and the compatibility of trauma recovery goals and forensic programming goals.
Results: Trauma-informed care demonstrates promise in increasing offender responsivity to evidence-based cognitive behavioral programming that reduces criminal risk factors and in supporting integrated programming for offenders with substance abuse and co-occurring disorders.
Conclusions: Incorporating trauma recovery principles into correctional environments requires an understanding of criminal justice priorities, workforce development, and specific approaches to screening, assessment, and programming that unify the goals of clinical and security
C1 [Miller, Niki A.] New Hampshire Dept Correct, Concord, NH 03302 USA.
[Najavits, Lisa M.] Boston Univ, Sch Med, VA Boston Healthcare Syst, Boston, MA 02118 USA.
RP Miller, NA (reprint author), New Hampshire Dept Correct, Concord, NH 03302 USA.
EM nmiller@ahpnet.com
NR 67
TC 9
Z9 9
U1 1
U2 4
PU CO-ACTION PUBLISHING
PI JARFALLA
PA RIPVAGEN 7, JARFALLA, SE-175 64, SWEDEN
SN 2000-8066
J9 EUR J PSYCHOTRAUMATO
JI Eur. J. Psychotraumatol.
PY 2012
VL 3
AR 17246
DI 10.3402/ejpt.v3i0.17246
PG 8
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA V31FB
UT WOS:000208868400011
ER
PT J
AU O'Donovan, A
Cohen, BE
Bertenthal, D
Margaretten, M
Seal, K
Neylan, TC
AF O'Donovan, Aoife
Cohen, Beth E.
Bertenthal, Dan
Margaretten, Mary
Seal, Karen
Neylan, Thomas C.
TI Association of posttraumatic stress disorder with increased prevalence
of autoimmune disorders in Iraq and Afghanistan veterans
SO EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
LA English
DT Meeting Abstract
DE autoimmune disorders; inflammation; post-traumatic stress disorder;
psychiatric disorders; traumatic stress; veterans
C1 [O'Donovan, Aoife; Margaretten, Mary; Seal, Karen] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Cohen, Beth E.; Bertenthal, Dan] San Francisco VA Med Ctr, San Francisco, CA USA.
[Neylan, Thomas C.] Northern Calif Inst Res & Educ, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CO-ACTION PUBLISHING
PI JARFALLA
PA RIPVAGEN 7, JARFALLA, SE-175 64, SWEDEN
SN 2000-8066
J9 EUR J PSYCHOTRAUMATO
JI Eur. J. Psychotraumatol.
PY 2012
VL 3
SU 1
DI 10.3402/ejpt.v3i0.19511
PG 1
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA V31FC
UT WOS:000208868500053
ER
PT J
AU Peskind, ER
Cross, DJ
Yarnykh, V
Pagulayan, K
Hoff, D
Hart, K
Martin, N
Richards, T
Raskind, MA
Minoshima, S
Petrie, EC
AF Peskind, Elaine R.
Cross, Donna J.
Yarnykh, Vasily
Pagulayan, Kathleen
Hoff, David
Hart, Kim
Martin, Nathalie
Richards, Todd
Raskind, Murray A.
Minoshima, Satoshi
Petrie, Eric C.
TI Neuroimaging biomarkers in veterans with blast-mild traumatic brain
injury with or without comorbid PTSD
SO EUROPEAN JOURNAL OF PSYCHOTRAUMATOLOGY
LA English
DT Meeting Abstract
DE mild traumatic brain injury; neuroimaging; biomarkers; PTSD; magnetic
resonance imaging; FDG-PET
C1 VA Puget Sound Hlth Care Syst, Seattle, WA USA.
Univ Washington, Seattle, WA 98195 USA.
RI Yarnykh, Vasily/G-8757-2016; Yarnykh, Vasiliy/N-7635-2014
OI Yarnykh, Vasily/0000-0002-1583-8979;
NR 0
TC 0
Z9 0
U1 0
U2 4
PU CO-ACTION PUBLISHING
PI JARFALLA
PA RIPVAGEN 7, JARFALLA, SE-175 64, SWEDEN
SN 2000-8066
J9 EUR J PSYCHOTRAUMATO
JI Eur. J. Psychotraumatol.
PY 2012
VL 3
SU 1
DI 10.3402/ejpt.v3i0.19376
PG 1
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA V31FC
UT WOS:000208868500185
ER
EF