FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Fang, QQ
AF Fang, Qianqian
TI Mesh-based Monte Carlo method using fast ray-tracing in Plucker
coordinates
SO BIOMEDICAL OPTICS EXPRESS
LA English
DT Article
AB We describe a fast mesh-based Monte Carlo (MC) photon migration algorithm for static and time-resolved imaging in 3D complex media. Compared with previous works using voxel-based media discretization, a mesh-based approach can be more accurate in modeling targets with curved boundaries or locally refined structures. We implement an efficient ray-tracing technique using Plucker Coordinates. The Barycentric coordinates computed from Plucker-formed ray-tracing enables us to use linear Lagrange basis functions to model both media properties and fluence distribution, leading to further improvement in accuracy. The Plucker-coordinate ray-polygon intersection test can be extended to hexahedral or high-order elements. Excellent agreement is found when comparing mesh-based MC with the analytical diffusion model and 3D voxel-based MC code in both homogeneous and heterogeneous cases. Realistic time-resolved imaging results are observed for a complex human brain anatomy using mesh-based MC. We also include multi-threading support in the software and will port it to a graphics processing unit platform in the near future. (C) 2010 Optical Society of America
C1 Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
RP Fang, QQ (reprint author), Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, 149 13th St, Charlestown, MA 02129 USA.
EM fangq@nmr.mgh.harvard.edu
FU Harvard Catalyst Pilot Grant
FX QF would like to thank the funding support from Harvard Catalyst Pilot
Grant. He also would like to thank David Boas for the helpful
discussions on the analytical diffusion solutions of a sphere.
NR 39
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U1 0
U2 8
PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 2156-7085
J9 BIOMED OPT EXPRESS
JI Biomed. Opt. Express
PD AUG 2
PY 2010
VL 1
IS 1
BP 165
EP 175
PG 11
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
Medical Imaging
GA V21LC
UT WOS:000208208100016
PM 21170299
ER
PT J
AU Fang, QQ
Moore, RH
Kopans, DB
Boas, DA
AF Fang, Qianqian
Moore, Richard H.
Kopans, Daniel B.
Boas, David A.
TI Compositional-prior-guided image reconstruction algorithm for
multi-modality imaging
SO BIOMEDICAL OPTICS EXPRESS
LA English
DT Article
AB The development of effective multi-modality imaging methods typically requires an efficient information fusion model, particularly when combining structural images with a complementary imaging modality that provides functional information. We propose a composition-based image segmentation method for X-ray digital breast tomosynthesis (DBT) and a structural-prior-guided image reconstruction for a combined DBT and diffuse optical tomography (DOT) breast imaging system. Using the 3D DBT images from 31 clinically measured healthy breasts, we create an empirical relationship between the X-ray intensities for adipose and fibroglandular tissue. We use this relationship to then segment another 58 healthy breast DBT images from 29 subjects into compositional maps of different tissue types. For each breast, we build a weighted-graph in the compositional space and construct a regularization matrix to incorporate the structural priors into a finite-element-based DOT image reconstruction. Use of the compositional priors enables us to fuse tissue anatomy into optical images with less restriction than when using a binary segmentation. This allows us to recover the image contrast captured by DOT but not by DBT. We show that it is possible to fine-tune the strength of the structural priors by changing a single regularization parameter. By estimating the optical properties for adipose and fibroglandular tissue using the proposed algorithm, we found the results are comparable or superior to those estimated with expert-segmentations, but does not involve the time-consuming manual selection of regions-of-interest. (C) 2010 Optical Society of America
C1 [Fang, Qianqian; Boas, David A.] Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Moore, Richard H.; Kopans, Daniel B.] Massachusetts Gen Hosp, Avon Fdn Comprehens Breast Evaluat Ctr, Boston, MA 02114 USA.
RP Fang, QQ (reprint author), Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, 149 13th St, Charlestown, MA 02129 USA.
EM fangq@nmr.mgh.harvard.edu
FU NIH [R01-CA97305, U54-CA105480]; Harvard Catalyst Pilot Grant
FX The authors would like to thank Jayne Cormier and Donna Burgess for the
assistance in the clinical experiments for this study. The authors also
acknowledge the NIH funding support under grants R01-CA97305 and
U54-CA105480. QF is partly supported by Harvard Catalyst Pilot Grant.
NR 37
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U2 6
PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 2156-7085
J9 BIOMED OPT EXPRESS
JI Biomed. Opt. Express
PD AUG 2
PY 2010
VL 1
IS 1
BP 223
EP 235
PG 13
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
Medical Imaging
GA V21LC
UT WOS:000208208100021
PM 21258460
ER
PT J
AU Mesquita, RC
Franceschini, MA
Boas, DA
AF Mesquita, Rickson C.
Franceschini, Maria A.
Boas, David A.
TI Resting state functional connectivity of the whole head with
near-infrared spectroscopy
SO BIOMEDICAL OPTICS EXPRESS
LA English
DT Article
AB Resting state connectivity aims to identify spontaneous cerebral hemodynamic fluctuations that reflect neuronal activity at rest. In this study, we investigated the spatial-temporal correlation of hemoglobin concentration signals over the whole head during the resting state. By choosing a source-detector pair as a seed, we calculated the correlation value between its time course and the time course of all other source-detector combinations, and projected them onto a topographic map. In all subjects, we found robust spatial interactions in agreement with previous fMRI and NIRS findings. Strong correlations between the two opposite hemispheres were seen for both sensorimotor and visual cortices. Correlations in the prefrontal cortex were more heterogeneous and dependent on the hemodynamic contrast. HbT provided robust, well defined maps, suggesting that this contrast may be used to better localize functional connectivity. The effects of global systemic physiology were also investigated, particularly low frequency blood pressure oscillations which give rise to broad regions of high correlation and mislead interpretation of the results. These results confirm the feasibility of using functional connectivity with optical methods during the resting state, and validate its use to investigate cortical interactions across the whole head. (C) 2010 Optical Society of America
C1 [Mesquita, Rickson C.; Franceschini, Maria A.; Boas, David A.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Mesquita, Rickson C.] Univ Penn, Dept Phys & Astron, Philadelphia, PA 19104 USA.
RP Mesquita, RC (reprint author), Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
EM rickson@nmr.mgh.harvard.edu
RI Mesquita, Rickson/N-9119-2013
OI Mesquita, Rickson/0000-0003-1945-6713
FU CNPq [140273/2005-0]; CAPES [2860/06-6]; National Institutes of Health
[R01-EB006385, R01-EB001954, P41-RR14075]
FX RCM acknowledges funding from CNPq and CAPES agencies through
140273/2005-0 and 2860/06-6, respectively. We would like to thank
Christiana Andre, and Shalini Nadgir for the help collecting these data.
This work was supported by the National Institutes of Health through
R01-EB006385, R01-EB001954, and P41-RR14075.
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PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 2156-7085
J9 BIOMED OPT EXPRESS
JI Biomed. Opt. Express
PD AUG 2
PY 2010
VL 1
IS 1
BP 324
EP 336
PG 13
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
Medical Imaging
GA V21LC
UT WOS:000208208100031
PM 21258470
ER
PT J
AU Cui, XQ
Ren, JA
Tearney, GJ
Yang, CH
AF Cui, Xiquan
Ren, Jian
Tearney, Guillermo J.
Yang, Changhuei
TI Wavefront image sensor chip
SO OPTICS EXPRESS
LA English
DT Article
ID PHASE MICROSCOPY; CONTRAST; VISUALIZATION
AB We report the implementation of an image sensor chip, termed wavefront image sensor chip (WIS), that can measure both intensity/amplitude and phase front variations of a light wave separately and quantitatively. By monitoring the tightly confined transmitted light spots through a circular aperture grid in a high Fresnel number regime, we can measure both intensity and phase front variations with a high sampling density (11 mu m) and high sensitivity (the sensitivity of normalized phase gradient measurement is 0.1 mrad under the typical working condition). By using WIS in a standard microscope, we can collect both bright-field (transmitted light intensity) and normalized phase gradient images. Our experiments further demonstrate that the normalized phase gradient images of polystyrene microspheres, unstained and stained starfish embryos, and strongly birefringent potato starch granules are improved versions of their corresponding differential interference contrast (DIC) microscope images in that they are artifact-free and quantitative. Besides phase microscopy, WIS can benefit machine recognition, object ranging, and texture assessment for a variety of applications. (C) 2010 Optical Society of America
C1 [Cui, Xiquan; Ren, Jian; Tearney, Guillermo J.; Yang, Changhuei] CALTECH, Dept Elect Engn, Pasadena, CA 91125 USA.
[Tearney, Guillermo J.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Tearney, Guillermo J.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Cui, XQ (reprint author), CALTECH, Dept Elect Engn, Pasadena, CA 91125 USA.
EM xiquan@caltech.edu
FU NNIN network; Wallace Coulter Foundation; NSF [BES-0547657]; NIH
[R21EB008867]
FX We are grateful for the constructive discussions with and the generous
help from Professor Paul Sternberg, Professor Scott Fraser, Professor
Colin J.R. Sheppard, Shan Shan Kou, Dr. Thomas Vangsness, Dr. Jigang Wu,
Emily Mcdowell, Andrea Choe, Sean Pang, Guoan Zheng, Tony Wu, and Anne
Sullivan. A portion of this work was done in the UCSB nanofabrication
facility, part of the NSF funded NNIN network. The assistance from
Caltech Kavli Nanoscience Institute, Watson cleanroom, and Aptina
Imaging is much appreciated. This project is funded by the Wallace
Coulter Foundation, NSF career award BES-0547657 and NIH R21EB008867.
NR 24
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U1 0
U2 1
PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 1094-4087
J9 OPT EXPRESS
JI Opt. Express
PD AUG 2
PY 2010
VL 18
IS 16
BP 16685
EP 16701
DI 10.1364/OE.18.016685
PG 17
WC Optics
SC Optics
GA 640IB
UT WOS:000281042400045
PM 20721059
ER
PT J
AU Biederman, J
Wozniak, J
Faraone, S
Mick, E
AF Biederman, J.
Wozniak, J.
Faraone, S.
Mick, E.
TI A controlled family study of children with DSM-IV bipolar-I disorder
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 23rd Congress Meeting of European-College-of-Neuropsychopharmacology
CY AUG 28-SEP 01, 2010
CL Amsterdam, NETHERLANDS
SP European Coll Neuropsychopharmacol
C1 [Biederman, J.; Wozniak, J.; Mick, E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Faraone, S.] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY USA.
[Faraone, S.] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD AUG
PY 2010
VL 20
SU 3
BP S611
EP S611
PG 1
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 673UB
UT WOS:000283687800821
ER
PT J
AU Johansen, KL
Smith, MW
Unruh, ML
Siroka, AM
O'Connor, TZ
Palevsky, PM
AF Johansen, Kirsten L.
Smith, Mark W.
Unruh, Mark L.
Siroka, Andrew M.
O'Connor, Theresa Z.
Palevsky, Paul M.
CA VA NIH Acute Renal Failure Trial N
TI Predictors of Health Utility among 60-Day Survivors of Acute Kidney
Injury in the Veterans Affairs/National Institutes of Health Acute Renal
Failure Trial Network Study
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; LONG-TERM OUTCOMES; COGNITIVE IMPAIRMENT; REPLACEMENT
THERAPY; INTENSIVE-CARE; DISEASE; DIALYSIS; BURDEN; INDEX; MORTALITY
AB Background and objectives: Health-related quality of life (HRQOL) after acute kidney injury (AKI) is an area of great importance to patients. It was hypothesized that HRQOL after AKI would relate to intensity of dialysis during AKI and dialysis dependence at follow-up.
Design, setting, participants, & measurements: The Veterans Affairs/National Institutes of Health Acute Renal Failure Trial Network Study was a multicenter, prospective, randomized trial of intensive versus less intensive renal replacement therapy in critically ill patients with AKI. Of 1124 participants, 415 survived at least 60 days and completed the Health Utilities Index (HUI), which measures 8 health attributes and calculates an overall HRQOL score, also called a utility score. How strongly pre-intensive care unit (ICU) health, severity of illness, hospital course, intensity of dialysis, and outcome were associated with 60-day HUI scores was assessed, after adjustment for demographics.
Results: The overall HUI score was 0.40 +/- 0.37, indicating severely compromised health utility and was associated with only admission from home and hospital and ICU length of stay (LOS). Ambulation was better among those with a shorter hospital and ICU LOS. Better cognition was associated with dialysis independence and with fewer comorbid chronic illnesses. Emotion was associated with only hospital LOS. Pain was associated with ICU LOS.
Conclusions: Health utility was low in this cohort of patients after AKI, and intensity of dialysis did not affect subsequent health utility. The effects of a lengthy hospitalization generally outweighed the effects of delayed recovery of kidney function on HRQOL after AKI. Clin J Am Soc Nephrol 5: 1366-1372, 2010. doi: 10.2215/CJN.02570310
C1 [Johansen, Kirsten L.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Johansen, Kirsten L.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Smith, Mark W.; Siroka, Andrew M.] VA Palo Alto Healthcare Syst, Palo Alto, CA USA.
[Smith, Mark W.] Stanford Sch Med, Ctr Primary Care & Outcomes Res, Stanford, CA USA.
[Unruh, Mark L.; Palevsky, Paul M.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[O'Connor, Theresa Z.] VA Connecticut Healthcare Syst, W Haven Cooperat Studies Program Coordinating Ctr, West Haven, CT USA.
[Palevsky, Paul M.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
RP Johansen, KL (reprint author), San Francisco VA Med Ctr 111J, Nephrol Sect, 4150 Clement St, San Francisco, CA 94121 USA.
EM kirsten.johansen@ucsf.edu
RI Smith, Mark/G-1522-2012;
OI Smith, Mark/0000-0002-4582-9088; Palevsky, Paul/0000-0002-7334-5400
FU U.S. Department of Veterans Affairs Office of Research and Development;
U.S. National Institutes of Diabetes and Digestive and Kidney Diseases
[Y1-DK-3508-01]
FX This study was supported by the Cooperative Studies Program of the U.S.
Department of Veterans Affairs Office of Research and Development and by
the U.S. National Institutes of Diabetes and Digestive and Kidney
Diseases (interagency agreement Y1-DK-3508-01). This work was presented
as a Free Communication at the 42nd Annual Meeting and Scientific
Exposition of the American Society of Nephrology; October 27 through
November 1, 2009; San Diego, CA.
NR 35
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U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
EI 1555-905X
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD AUG
PY 2010
VL 5
IS 8
BP 1366
EP 1372
DI 10.2215/CJN.02570310
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 635WZ
UT WOS:000280689600004
PM 20507953
ER
PT J
AU Rhee, EP
Laliberte, KA
Niles, JL
AF Rhee, Eugene P.
Laliberte, Karen A.
Niles, John L.
TI Rituximab as Maintenance Therapy for Anti-Neutrophil Cytoplasmic
Antibody-Associated Vasculitis
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID ANCA-ASSOCIATED VASCULITIS; WEGENERS-GRANULOMATOSIS;
RHEUMATOID-ARTHRITIS; AUTOIMMUNE-DISEASES; MONOCLONAL-ANTIBODY; NEGATIVE
PATIENTS; METHOTREXATE; EXPERIENCE; REMISSION; DEPLETION
AB Background and objectives: Ongoing randomized trials seek to validate the efficacy of rituximab as an induction agent for anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). However, no studies directly address the role of rituximab as maintenance therapy.
Design, setting, participants, & measurements: This retrospective study reports the authors' experience with continuous rituximab administration in 39 patients in complete or partial remission at the time of rituximab initiation. All 39 patients had at least 1 year of follow-up, and 20 had 2 years of follow-up.
Results: Disease activity, as measured by a modified Birmingham Vasculitis Activity Score, decreased from a median of 1 at baseline to 0 at 12 (P < 0.001) and 24 months (P = 0.02). Three patients experienced nonorgan-threatening flares during 708 patient-months of follow-up. Each flare occurred after at least 20 months of follow-up. The percentage of patients on cytotoxic immunosuppression decreased from 87% at baseline to 41% at 12 months (P < 0.001) and 30% at 24 months (P = 0.002). The percentage of patients on prednisone decreased from 92% at baseline to 59% at 12 months (P < 0.001) and 55% at 24 months (P = 0.02). Two patients developed late-onset neutropenia; both responded to treatment with recombinant granulocyte colony-stimulating factor.
Conclusions: The successful use of continuous anti-B cell therapy in patients with AAV in complete or partial remission is reported. This extends the potential role of rituximab beyond induction to include maintenance therapy. However, more data are required regarding the delayed adverse effects of rituximab. Clin J Am Soc Nephrol 5: 1394-1400, 2010. doi: 10.2215/CJN.08821209
C1 [Rhee, Eugene P.; Laliberte, Karen A.; Niles, John L.] Massachusetts Gen Hosp, Renal Unit, Boston, MA 02114 USA.
RP Niles, JL (reprint author), Massachusetts Gen Hosp, Renal Unit, 151 Merrimac St,3rd Floor, Boston, MA 02114 USA.
EM jniles@partners.org
NR 34
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U1 0
U2 2
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
EI 1555-905X
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD AUG
PY 2010
VL 5
IS 8
BP 1394
EP 1400
DI 10.2215/CJN.08821209
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 635WZ
UT WOS:000280689600008
PM 20498238
ER
PT J
AU Adler, SG
Schwartz, S
Williams, ME
Arauz-Pacheco, C
Bolton, WK
Lee, T
Li, DX
Neff, TB
Urquilla, PR
Sewell, KL
AF Adler, Sharon G.
Schwartz, Sherwyn
Williams, Mark E.
Arauz-Pacheco, Carlos
Bolton, Warren K.
Lee, Tyson
Li, Dongxia
Neff, Thomas B.
Urquilla, Pedro R.
Sewell, K. Lea
TI Phase 1 Study of Anti-CTGF Monoclonal Antibody in Patients with Diabetes
and Microalbuminuria
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID TISSUE GROWTH-FACTOR; GLOMERULAR MESSENGER-RNAS; FACTOR GENE-EXPRESSION;
SMOOTH-MUSCLE-CELLS; MESANGIAL CELLS; ANGIOTENSIN-II; RENAL-DISEASE;
FACTOR-BETA; FACTOR EXCRETION; NEPHROPATHY
AB Background and objectives: This report summarizes the first phase 1 trial treating patients with microalbuminuric diabetic kidney disease (DKD) using FG-3019, a human monoclonal antibody to connective tissue growth factor (CTGF). CTGF is critically involved in processes of progressive fibrosis, including DKD. This phase 1, open-label, dose-escalation trial evaluated safety, pharmacokinetics, and possible therapeutic effects of FG-3019 on albuminuria, proteinuria, and tubular proteins.
Design, setting, participants, and measurements: Microalbuminuric subjects (n = 24) with type 2 (79%) or type 1 (21%) diabetes received 3 or 10 mg/kg FG-3019 dosed intravenously every 14 days for four doses. Albuminuria and safety follow-up were to days 62 and 365, respectively.
Results: No infusion was interrupted for symptoms, although 5 of 24 subjects had mild infusion-day adverse events thought to be possibly drug-related. No subject developed anti-FG-3019 antibodies. FG-3019 clearance was lower at 10 mg/kg than at 3 mg/kg, suggesting a saturable elimination pathway. Although this study was not designed for efficacy testing, it was notable that urinary albumin/creatinine ratio (ACR) decreased significantly from mean pretreatment ACR of 48 mg/g to mean post-treatment (day 56) ACR of 20 mg/g (P = 0.027) without evidence for a dose-response relationship.
Conclusions: Treatment of microalbuminuric DKD subjects using FG-3019 was well tolerated and associated with a decrease in albuminuria. The data demonstrate a saturable pathway for drug elimination, minimal infusion adverse events, and no significant drug-attributable adverse effects over the year of follow-up. Changes in albuminuria were promising but require validation in a prospective, randomized, blinded study. Clin J Am Soc Nephrol 5: 1420-1428, 2010. doi: 10.2215/CJN.09321209
C1 [Adler, Sharon G.] Los Angeles BioMed Res Inst, Div Nephrol & Hypertens, Torrance, CA 90502 USA.
[Schwartz, Sherwyn] Diabet & Glandular Dis Clin, San Antonio, TX USA.
[Williams, Mark E.] Joslin Clin, Renal Unit, Boston, MA USA.
[Arauz-Pacheco, Carlos] Radiant Res, Dallas, TX USA.
[Bolton, Warren K.] Univ Virginia, Sch Med, Div Nephrol, Charlottesville, VA 22908 USA.
[Lee, Tyson; Li, Dongxia; Neff, Thomas B.; Urquilla, Pedro R.; Sewell, K. Lea] FibroGen Inc, San Francisco, CA USA.
RP Adler, SG (reprint author), Los Angeles BioMed Res Inst, Div Nephrol & Hypertens, 1124 W Carson St,Bldg C1 Annex, Torrance, CA 90502 USA.
EM sadler@labiomed.org
FU FibroGen, Inc.
FX The authors' institutional or corporate grant offices received financial
support from FibroGen, Inc. for clinical trial execution, and M.W. was a
consultant for a FibroGen development meeting during the trial. T.L.,
D.L., and T.N. are employees of FibroGen, Inc. and therefore have direct
financial relationships. P.U. and L.S. are former employees of FibroGen,
Inc. This was an industry-sponsored study funded by FibroGen, Inc.
Employees at FibroGen performed the analyses. Upon data sharing, the
manuscript was written through a process of close collaboration of all
of the cited authors.
NR 49
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U2 2
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
EI 1555-905X
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD AUG
PY 2010
VL 5
IS 8
BP 1420
EP 1428
DI 10.2215/CJN.09321209
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 635WZ
UT WOS:000280689600011
PM 20522536
ER
PT J
AU Lopez, L
Wilper, AP
Cervantes, MC
Betancourt, JR
Green, AR
AF Lopez, Lenny
Wilper, Andrew P.
Cervantes, Marina C.
Betancourt, Joseph R.
Green, Alexander R.
TI Racial and Sex Differences in Emergency Department Triage Assessment and
Test Ordering for Chest Pain, 1997-2006
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Article; Proceedings Paper
CT 32nd Annual National Meeting of the
Society-for-General-Internal-Medicine
CY MAY 13-16, 2009
CL Miami, FL
SP Soc Gen Internal Med (SGIM)
DE chest pain; triage; coronary disease; tests; diagnosis; ethnic groups
ID ACUTE MYOCARDIAL-INFARCTION; ACUTE CORONARY SYNDROMES; UNSTABLE
ANGINA-PECTORIS; CARDIAC-CATHETERIZATION; CARDIOVASCULAR PROCEDURES;
INSURANCE STATUS; UNITED-STATES; RACE; DISPARITIES; MANAGEMENT
AB P>Objectives:
This study assessed whether sociodemographic differences exist in triage assignment and whether these differences affect initial diagnostic testing in the emergency department (ED) for patients presenting with chest pain.
Methods:
A nationally representative ED data sample for all adults (>= 18 years) was obtained from the National Hospital Ambulatory Health Care Survey of EDs for 1997-2006. Weighted logistic regression was used to examine the associations between race and presenting symptom, triage assignment, and test ordering, adjusting for patient and hospital characteristics.
Results:
Over 10 years, an estimated 78 million visits to the ED presented with a complaint of chest pain. Of those presenting with chest pain, African Americans (odds ratio [OR] = 0.70; 99% confidence interval [CI] = 0.53 to 0.92), Hispanics (OR = 0.74; 99% CI = 0.51to 0.99), Medicaid patients (OR = 0.72; 99% CI = 0.54 to 0.94), and uninsured patients (OR = 0.65; 99% CI = 0.51 to 0.84) were less likely to be triaged emergently. African Americans (OR = 0.86; 99% CI = 0.70 to 0.99), Medicaid patients (OR = 0.70; 99% CI = 0.55 to 0.88), and uninsured patients (OR = 0.70; 99% CI = 0.55 to 0.89) were less likely to have an electrocardiogram (ECG) ordered. African Americans (OR = 0.69; 99% CI = 0.49 to 0.97), Medicaid patients (OR = 0.67; 99% CI = 0.47 to 0.95), and uninsured patients (OR = 0.66; 99% CI = 0.44 to 0.96) were less likely to have cardiac enzymes ordered. Similarly, African Americans and Hispanics were less likely to have a cardiac monitor and pulse oximetry ordered, and Medicaid and uninsured patients were less likely to have a cardiac monitor ordered.
Conclusions:
Persistent racial, sex, and insurance differences in triage categorization and basic cardiac testing exist. Eliminating triage disparities may affect "downstream" clinical care and help eliminate observed disparities in cardiac outcomes.
C1 [Lopez, Lenny; Cervantes, Marina C.; Betancourt, Joseph R.; Green, Alexander R.] Massachusetts Gen Hosp, Mongan Inst Hlth Policy, Boston, MA 02114 USA.
[Lopez, Lenny] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Lopez, Lenny; Cervantes, Marina C.; Betancourt, Joseph R.; Green, Alexander R.] Massachusetts Gen Hosp, Dispar Solut Ctr, Boston, MA 02114 USA.
[Lopez, Lenny; Betancourt, Joseph R.; Green, Alexander R.] Harvard Univ, Sch Med, Boston, MA USA.
[Lopez, Lenny] Brigham & Womens Hosp, Brigham & Womens Acad Hospitalist Program, Boston, MA 02115 USA.
[Wilper, Andrew P.] Boise VA Med Ctr, Boise, ID USA.
[Wilper, Andrew P.] Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA.
RP Lopez, L (reprint author), Massachusetts Gen Hosp, Mongan Inst Hlth Policy, Boston, MA 02114 USA.
EM llopez1@partners.org
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PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1069-6563
EI 1553-2712
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD AUG
PY 2010
VL 17
IS 8
BP 801
EP 808
DI 10.1111/j.1553-2712.2010.00823.x
PG 8
WC Emergency Medicine
SC Emergency Medicine
GA 632SX
UT WOS:000280449500003
PM 20670316
ER
PT J
AU Blue, AV
Mitcham, M
Smith, T
Raymond, J
Greenberg, R
AF Blue, Amy V.
Mitcham, Maralynne
Smith, Thomas
Raymond, John
Greenberg, Raymond
TI Changing the Future of Health Professions: Embedding Interprofessional
Education Within an Academic Health Center
SO ACADEMIC MEDICINE
LA English
DT Article
ID STUDENTS
AB Institutions are increasingly considering interprofessional education (IPE) as a means to improve health care and reduce medical errors in the United States. Effective implementation of IPE within health professions education requires a strategic institutional approach to ensure longevity and sustainability. In 2007, the Medical University of South Carolina (MUSC) established Creating Collaborative Care (C(3)), an IPE initiative that takes a multifaceted approach to weaving interprofessional collaborative experiences throughout MUSC's culture to prepare students to participate in interprofessional, collaborative health care and research settings.
In this article, the authors describe C(3)'s guiding conceptual foundation and student learning goals. They present its implementation framework to illustrate how C(3) is embedded within the institutional culture. It is housed in the provost's office, and an overarching implementation committee functions as a central coordinating group. Faculty members develop and implement C(3) activities across professions by contributing to four collaborating domains-curricular, extracurricular, faculty development, and health care simulation-each of which captures an IPE component. The authors provide examples of IPE activities developed by each domain to illustrate the breadth of IPE at MUSC. The authors believe that MUSC's efforts, including the conceptual foundation and implementation framework, can be generalized to other institutions intent on developing IPE within their organizational cultures.
C1 [Blue, Amy V.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Mitcham, Maralynne] Med Univ S Carolina, Coll Hlth Profess, Div Occupat Therapy, Charleston, SC 29425 USA.
[Smith, Thomas] Med Univ S Carolina, Ctr Acad Excellence, Charleston, SC 29425 USA.
[Smith, Thomas] Med Univ S Carolina, Writing Ctr, Charleston, SC 29425 USA.
[Raymond, John] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
RP Blue, AV (reprint author), 45 Courtenay Dr,Suite SS448,MSC 175, Charleston, SC 29425 USA.
EM blueav@musc.edu
NR 25
TC 28
Z9 28
U1 2
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD AUG
PY 2010
VL 85
IS 8
BP 1290
EP 1295
DI 10.1097/ACM.0b013e3181e53e07
PG 6
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA 632UD
UT WOS:000280453500010
PM 20671454
ER
PT J
AU Nappi, JJ
AF Naeppi, Janne J.
TI CADe Prompts and Observer Performance: A Game of Confidence
SO ACADEMIC RADIOLOGY
LA English
DT Editorial Material
ID COMPUTER-AIDED DETECTION; CT COLONOGRAPHY; TOMOGRAPHIC COLONOGRAPHY;
SCREENING MAMMOGRAPHY; MASS DETECTION; READER; SYSTEM; SUPINE;
CONSPICUOUSNESS; INFORMATION
C1 [Naeppi, Janne J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Naeppi, Janne J.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Nappi, JJ (reprint author), Massachusetts Gen Hosp, 25 New Chardon St,Suite 400C, Boston, MA 02114 USA.
EM jnappi@partners.org
NR 39
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1076-6332
J9 ACAD RADIOL
JI Acad. Radiol.
PD AUG
PY 2010
VL 17
IS 8
BP 945
EP 947
DI 10.1016/j.acra.2010.05.012
PG 3
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 627IO
UT WOS:000280032900001
PM 20599154
ER
PT J
AU Tuller, DM
Bangsberg, DR
Senkungu, J
Ware, NC
Emenyonu, N
Weiser, SD
AF Tuller, David M.
Bangsberg, David R.
Senkungu, Jude
Ware, Norma C.
Emenyonu, Nneka
Weiser, Sheri D.
TI Transportation Costs Impede Sustained Adherence and Access to HAART in a
Clinic Population in Southwestern Uganda: A Qualitative Study
SO AIDS AND BEHAVIOR
LA English
DT Article
DE HIV/AIDS; Transportation; ARVs; Adherence; Access; Uganda
ID HIV ANTIRETROVIRAL THERAPY; RESOURCE-POOR SETTINGS; SUB-SAHARAN AFRICA;
ART ADHERENCE; BARRIERS; AIDS; FACILITATORS; PROGRAM; CHENNAI; INDIA
AB The cost of transportation for monthly clinic visits has been identified as a potential barrier to antiretroviral (ARV) adherence in sub-Saharan Africa and elsewhere, although there is limited data on this issue. We conducted open-ended interviews with 41 individuals living with HIV/AIDS and attending a clinic in Mbarara, Uganda, to understand structural barriers to ARV adherence and clinical care. Almost all respondents cited the need to locate funds for the monthly clinic visit as a constant source of stress and anxiety, and lack of money for transportation was a key factor in cases of missed doses and missed medical appointments. Participants struggled with competing demands between transport costs and other necessities such as food, housing and school fees. Our findings suggest that transportation costs can compromise both ARV adherence and access to care. Interventions that address this barrier will be important to ensure the success of ARV programs in sub-Saharan Africa.
C1 [Tuller, David M.] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
[Bangsberg, David R.; Emenyonu, Nneka] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Harvard Initiat Global Hlth, Boston, MA 02115 USA.
[Senkungu, Jude] Mbarara Univ Sci & Technol, Mbarara, Uganda.
[Ware, Norma C.] Harvard Univ, Sch Med, Dept Social Med, Boston, MA 02115 USA.
[Weiser, Sheri D.] Univ Calif San Francisco, San Francisco Gen Hosp, Posit Hlth Program, San Francisco, CA 94143 USA.
[Weiser, Sheri D.] Univ Calif San Francisco, Ctr AIDS Prevent Studies, San Francisco, CA 94143 USA.
RP Tuller, DM (reprint author), Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA.
EM davetuller@berkeley.edu
NR 27
TC 48
Z9 50
U1 1
U2 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1090-7165
J9 AIDS BEHAV
JI AIDS Behav.
PD AUG
PY 2010
VL 14
IS 4
BP 778
EP 784
DI 10.1007/s10461-009-9533-2
PG 7
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 629UW
UT WOS:000280226400005
ER
PT J
AU Reisner, SL
Perkovich, B
Mimiaga, MJ
AF Reisner, Sari L.
Perkovich, Brandon
Mimiaga, Matthew J.
TI A Mixed Methods Study of the Sexual Health Needs of New England Transmen
Who Have Sex with Nontransgender Men
SO AIDS PATIENT CARE AND STDS
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TO-MALE TRANSSEXUALS; TRANSGENDER PERSONS;
HIV PREVALENCE; HIDDEN POPULATIONS; RISK BEHAVIORS; SAN-FRANCISCO;
UNITED-STATES; EPIDEMIOLOGY; PREVENTION
AB The sexual health of transmen-individuals born or assigned female at birth and who identify as male-remains understudied. Given the increasing rates of HIV and sexually transmitted diseases (STDs) among gay and bisexual men in the United States, understanding the sexual practices of transmen who have sex with men (TMSM) may be particularly important to promote sexual health or develop focused HIV prevention interventions. Between May and September 2009, 16 transmen who reported sexual behavior with nontransgender men completed a qualitative interview and a brief interviewer-administered survey. Interviews were conducted until redundancy in responses was achieved. Participants (mean age, 32.5, standard deviation [SD] = 11.1; 87.5% white; 75.0% "queer") perceived themselves at moderately high risk for HIV and STDs, although 43.8% reported unprotected sex with an unknown HIV serostatus nontransgender male partner in the past 12 months. The majority (62.5%) had used the Internet to meet sexual partners and "hook-up" with an anonymous nontransgender male sex partner in the past year. A lifetime STD history was reported by 37.5%; 25.0% had not been tested for HIV in the prior 2 years; 31.1% had not received gynecological care (including STD screening) in the prior 12 months. Integrating sexual health information "by and for" transgender men into other healthcare services, involving peer support, addressing mood and psychological wellbeing such as depression and anxiety, Internet-delivered information for transmen and their sexual partners, and training for health care providers were seen as important aspects of HIV and STD prevention intervention design and delivery for this population. "Embodied scripting" is proposed as a theoretical framework to understand sexual health among transgender populations and examining transgender sexual health from a life course perspective is suggested.
C1 [Reisner, Sari L.; Perkovich, Brandon; Mimiaga, Matthew J.] Fenway Hlth, Fenway Inst, Boston, MA 02215 USA.
[Reisner, Sari L.; Mimiaga, Matthew J.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Perkovich, Brandon] Harvard Univ, Cambridge, MA USA.
[Mimiaga, Matthew J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
RP Reisner, SL (reprint author), Fenway Hlth, Fenway Inst, 1340 Boylston St,8th Floor, Boston, MA 02215 USA.
EM sreisner@fenwayhealth.org
FU National Institute of Child Health and Human Development (NICHD)
[R21HD051178]; National Institute on Drug Abuse (NIDA) [R03DA023393];
Center for Population Research in LGBT Health at The Fenway Institute
FX The project described was supported by The Center for Population
Research in LGBT Health at The Fenway Institute and by the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(NICHD) under Award Number R21HD051178 (PI: J. Bradford). Some of the
investigator time on this project was also support by grant number
R03DA023393 from the National Institute on Drug Abuse (NIDA; PI: M.
Mimiaga). The content is solely the responsibility of the authors and
does not necessarily represent the official views of the NICHD, NIDA, or
the National Institutes of Health.
NR 60
TC 26
Z9 26
U1 3
U2 11
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 AUG
PY 2010
VL 24
IS 8
BP 501
EP 513
DI 10.1089/apc.2010.0059
PG 13
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 639EW
UT WOS:000280955000006
PM 20666586
ER
PT J
AU Gubner, NR
Wilhelm, CJ
Phillips, TJ
Mitchell, SH
AF Gubner, Noah R.
Wilhelm, Clare J.
Phillips, Tamara J.
Mitchell, Suzanne H.
TI Strain Differences in Behavioral Inhibition in a Go/No-go Task
Demonstrated Using 15 Inbred Mouse Strains
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Impulsivity; Inhibition; Mice; Inbred Strains; Heritability; Go; No-go;
Locomotion; Ethanol
ID GENETIC-DETERMINANTS; ETHANOL WITHDRAWAL; IMPULSIVE BEHAVIOR; MICE;
CONSUMPTION; SENSITIZATION; RESPONSES; SEVERITY; DRINKING; RATS
AB Background:
High levels of impulsivity have been associated with a number of substance abuse disorders including alcohol abuse. Research has not yet revealed whether these high levels predate the development of alcohol abuse.
Methods:
The current study examined impulsivity in 15 inbred strains of mice (A/HeJ, AKR/J, BALB/cJ, C3H/HeJ, C57BL/6J, C57L/J, C58/J, CBA/J, DBA/1J, DBA/2J, NZB/B1NJ, PL/J, SJL/J, SWR/J, and 129P3/J) using a Go/No-go task, which was designed to measure a subject's ability to inhibit a behavior. Numerous aspects of response to ethanol and other drugs of abuse have been examined in these strains.
Results:
There were significant strain differences in the number of responses made during the No-go signal (false alarms) and the extent to which strains responded differentially during the Go and No-go signals (d'). The rate of responding prior to the cue did not differ among strains, although there was a statistically significant correlation between false alarms and precue responding that was not related to basal activity level. Interstrain correlations suggested that false alarms and rate of responding were associated with strain differences in ethanol-related traits from the published literature.
Conclusions:
The results of this study do support a link between innate level of impulsivity and response to ethanol and are consistent with a genetic basis for some measures of behavioral inhibition.
C1 [Gubner, Noah R.; Wilhelm, Clare J.; Phillips, Tamara J.; Mitchell, Suzanne H.] Oregon Hlth & Sci Univ, Dept Behav Neurosci, Portland, OR 97239 USA.
[Phillips, Tamara J.; Mitchell, Suzanne H.] Portland Alcohol Res Ctr, Portland, OR USA.
[Phillips, Tamara J.] Portland VA Med Ctr, Portland, OR USA.
RP Mitchell, SH (reprint author), Oregon Hlth & Sci Univ, Dept Behav Neurosci L470, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM mitchesu@ohsu.edu
OI Mitchell, Suzanne/0000-0002-0225-7200
FU The Portland Alcohol Research Center (PARC); Department of Veterans
Affairs; [P60AA010760]
FX We wish to thank John Crabbe, Pam Metten, and Andy Cameron for help
analyzing the genetic correlation data. The authors also thank William
Guethlein, Vanessa Wilson, Kirigin Elstad, and Carly Levine for
technical assistance. This research was supported by The Portland
Alcohol Research Center (PARC), P60AA010760 and the Department of
Veterans Affairs.
NR 33
TC 26
Z9 26
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD AUG
PY 2010
VL 34
IS 8
BP 1353
EP 1362
DI 10.1111/j.1530-0277.2010.01219.x
PG 10
WC Substance Abuse
SC Substance Abuse
GA 629KA
UT WOS:000280195200006
PM 20491731
ER
PT J
AU Cury, RC
Magalhaes, TA
Borges, AC
Shiozaki, AA
Lemos, PA
Soares, J
Meneghetti, JC
Cury, RC
Rochitte, CE
AF Cury, Roberto C.
Magalhaes, Tiago A.
Borges, Anna C.
Shiozaki, Afonso A.
Lemos, Pedro A.
Soares Junior, Jose
Meneghetti, Jose Claudio
Cury, Ricardo C.
Rochitte, Carlos E.
TI Dipyridamole Stress and Rest Myocardial Perfusion by 64-Detector Row
Computed Tomography in Patients With Suspected Coronary Artery Disease
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID DIAGNOSTIC-ACCURACY; ADENOSINE STRESS; CT ANGIOGRAPHY; 64-ROW; HEART
AB Recently, stress myocardial computed tomographic perfusion (CTP) was shown to detect myocardial ischemia. Our main objective was to evaluate the feasibility of dipyridamole stress CTP and compare it to single-photon emission computed tomography (SPECT) to detect significant coronary stenosis using invasive conventional coronary angiography (CCA; stenosis >70%) as the reference method. Thirty-six patients (62 +/- 8 years old, 20 men) with previous positive results with SPECT (<2 months) as the primary inclusion criterion and suspected coronary artery disease underwent a customized multidetector-row CT protocol with myocardial perfusion evaluation at rest and during stress and coronary CT angiography (CTA). Multidetector-row computed tomography was performed in a 64-slice scanner with dipyridamole stress perfusion acquisition before a second perfusion/CT angiographic acquisition at rest. Independent blinded observers performed analysis of images from CTP, CTA, and CCA. All 36 patients completed the CT protocol with no adverse events (mean radiation dose 14.7 +/- 3.0 mSv) and with interpretable scans. CTP results were positive in 27 of 36 patients (75%). From the 9 (25%) disagreements, 6 patients had normal coronary arteries and 2 had no significant stenosis (8 false-positive results with SPECT, 22%). The remaining patient had an occluded artery with collateral flow confirmed by conventional coronary angiogram. Good agreement was demonstrated between CTP and SPECT on a per-patient analysis (kappa 0.53). In 26 patients using CCA as reference, sensitivity, specificity, and positive and negative predictive values were 88.0%, 79.3%, 66.7%, and 93.3% for CTP and 68.8, 76.1%, 66.7%, and 77.8%, for SPECT, respectively (p = NS). In conclusion, dipyridamole CT myocardial perfusion at rest and during stress is feasible and results are similar to single-photon emission CT scintigraphy. The anatomical-perfusion information provided by this combined CT protocol may allow identification of false-positive results by SPECT. (C) 2010 Elsevier Inc. All rights reserved. (Am J Cardiol 2010;106:310-315)
C1 [Cury, Roberto C.; Magalhaes, Tiago A.; Shiozaki, Afonso A.; Rochitte, Carlos E.] Univ Sao Paulo Med, Heart Inst InCor, Cardiovasc MR & CT Sect, Sao Paulo, Brazil.
[Borges, Anna C.; Soares Junior, Jose; Meneghetti, Jose Claudio] Univ Sao Paulo Med, Heart Inst InCor, Nucl Imaging Sect, Sao Paulo, Brazil.
[Lemos, Pedro A.] Univ Sao Paulo Med, Heart Inst InCor, Invas Cardiol Sect, Sao Paulo, Brazil.
[Cury, Ricardo C.] Baptist Cardiac & Vasc Inst, Cardiovasc MR & CT Program, Miami, FL USA.
[Cury, Ricardo C.] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
[Cury, Ricardo C.] Harvard Univ, Sch Med, Boston, MA USA.
RP Rochitte, CE (reprint author), Univ Sao Paulo Med, Heart Inst InCor, Cardiovasc MR & CT Sect, Sao Paulo, Brazil.
EM rochitte@incor.usp.br
RI Lemos, Pedro/G-5758-2013
OI Lemos, Pedro/0000-0002-6782-750X
FU Fundacao de Amparo a Pesquisa do Estado de Sao Paulo, Sao Paulo/Brazil
[2007/56214-8]; Zerbini Foundation, Sao Paulo/Brazil
FX This work was supported by Grant-in-Aid 2007/56214-8 from the Fundacao
de Amparo a Pesquisa do Estado de Sao Paulo, Sao Paulo/Brazil, and the
Zerbini Foundation, Sao Paulo/Brazil.
NR 17
TC 73
Z9 80
U1 0
U2 3
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9149
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD AUG 1
PY 2010
VL 106
IS 3
BP 310
EP 315
DI 10.1016/j.amjcard.2010.03.025
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 635ZS
UT WOS:000280697700003
PM 20643238
ER
PT J
AU Sun, B
Williams, JS
Svetkey, LP
Kolatkar, NS
Conlin, PR
AF Sun, Bei
Williams, Jonathan S.
Svetkey, Laura P.
Kolatkar, Nikheel S.
Conlin, Paul R.
TI beta(2)-Adrenergic receptor genotype affects the
renin-angiotensin-aldosterone system response to the Dietary Approaches
to Stop Hypertension (DASH) dietary pattern
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID BLOOD-PRESSURE RESPONSE; CLINICAL-TRIAL; POLYMORPHISM; LINKAGE; HUMANS;
SODIUM; SUSCEPTIBILITY; ISOPROTERENOL; VASODILATION; ASSOCIATION
AB Background: beta(2)-Adrenergic receptor (beta(2)-AR) is a susceptibility locus for hypertension, and polymorphisms at this site relate to salt sensitivity and low plasma renin activity (PRA). The Dietary Approaches to Stop Hypertension (DASH) dietary pattern lowers blood pressure and appears to interact with the renin-angiotensin-aldosterone system (RAAS).
Objective: We hypothesized that the DASH diet associates with increased RAAS activity, and genotype status at beta(2)-AR G46A modifies this response.
Design: We genotyped participants in the DASH-Sodium study (n = 372) at beta(2)-AR G46A to determine the association with blood pressure, RAAS components, and consumption of the DASH diet. We used 2-way mixed linear regression and an additive model for all primary analyses.
Results: Mean (+/-SEM) PRA was significantly higher in participants in the DASH group than in participants in the control group (0.68 +/- 0.03 compared with 0.54 +/- 0.03 ng . mL(-1) . h(-1), P = 0.002). Serum aldosterone, urinary aldosterone, and urinary potassium concentrations were also significantly higher in the DASH group (P, 0.01 for all). We observed significant gene-diet interactions for changes in systolic blood pressure (SBP) and concentrations of aldosterone and urinary potassium (P for interaction = 0.048, 0.017, and 0.001 for SBP and aldosterone and urinary potassium concentrations, respectively). There was an association between the A allele of beta(2)-AR G46A and greater blood pressure reduction and blunted aldosterone and PRA responses to the DASH diet.
Conclusions: Our results indicate that the DASH diet lowers blood pressure and increases PRA and aldosterone concentrations. There is an association between the G46A polymorphism of beta(2)-AR and blood pressure and RAAS responses to the DASH diet, which suggests that beta(2)-AR may be a genetic modifier of DASH-diet responsiveness. This trial was registered at clinicaltrials.gov as NCT00000608. Am J Clin Nutr 2010; 92:444-9.
C1 [Sun, Bei; Williams, Jonathan S.; Conlin, Paul R.] Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA.
[Sun, Bei; Williams, Jonathan S.; Conlin, Paul R.] Harvard Univ, Sch Med, Boston, MA USA.
[Svetkey, Laura P.] Duke Univ, Med Ctr, Duke Hypertens Ctr, Durham, NC USA.
[Kolatkar, Nikheel S.] GlaxoSmithKline Res & Dev Ltd, Cardiovasc Metab Med Dev Ctr, King Of Prussia, PA USA.
[Kolatkar, Nikheel S.] Univ Penn, Sch Med, Philadelphia Vet Affairs Med Ctr, Philadelphia, PA 19104 USA.
[Conlin, Paul R.] VA Boston Healthcare Syst, Boston, MA USA.
RP Williams, JS (reprint author), Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, 221 Longwood Ave, Boston, MA 02115 USA.
EM jwilliams5@partners.org
OI Williams, Jonathan/0000-0001-7152-765X
FU National Institutes of Health [R01 HL57114, R01 HL77234, K24 DK63214,
K23 HL084236]
FX Supported by grants R01 HL57114, R01 HL77234, K24 DK63214, and K23
HL084236 from the National Institutes of Health.
NR 29
TC 12
Z9 12
U1 0
U2 2
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD AUG
PY 2010
VL 92
IS 2
BP 444
EP 449
DI 10.3945/ajcn.2009.28924
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 628UZ
UT WOS:000280149700025
PM 20519561
ER
PT J
AU Zeliadt, SB
Ramsey, SD
Van Den Eeden, SK
Hamilton, AS
Oakley-Girvan, I
Penson, DF
Fairweather, ME
Arora, NK
Potosky, AL
AF Zeliadt, Steven B.
Ramsey, Scott D.
Van Den Eeden, Stephen K.
Hamilton, Ann S.
Oakley-Girvan, Ingrid
Penson, David F.
Fairweather, Megan E.
Arora, Neeraj K.
Potosky, Arnold L.
TI Patient Recruitment Methods to Evaluate Treatment Decision Making for
Localized Prostate Cancer
SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS
LA English
DT Article
DE prostate cancer; decision making; recruitment; registry
ID BREAST-CANCER; STRATEGIES; MANAGEMENT; TRIAL; MEN; SURVEILLANCE;
CARCINOMA
AB Objective: To examine methods for identifying and recruiting prostate cancer patients prior to initiating treatment to gain insight into the treatment decision process and avoid recall bias.
Study Design and Setting: One recruitment strategy involved providers and nursing staff approaching patients in community and academic urology clinics. The second recruitment strategy used electronic pathology reports to identify newly diagnosed cases in real time in an integrated health system. Our recruitment goal was to have patients complete the survey about the decision-making process prior to initiating therapy.
Results: The two recruitment methods yielded different response rates. Of the 226 eligible participants approached in urology clinics, 187 (83%) returned a completed baseline survey. Of the 1177 surveys mailed to potentially eligible participants at KPNC, 617 (52%) returned a completed baseline survey. The number of surveys completed prior to treatment was 125 (67%) for the clinic recruitment approach and 437 (71%) for the electronic medical record approach. Younger participants and patients with less aggressive clinical characteristics were more likely to complete the survey before initiating treatment. Other patient demographic and clinical factors were not associated with the timing of survey return.
Conclusions: Recruiting newly diagnosed patients prior to initiating treatment is feasible with both approach methods. The use of electronic medical records to identify subjects was more cost efficient, although it results in a lower response rate.
C1 [Zeliadt, Steven B.; Ramsey, Scott D.; Fairweather, Megan E.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Zeliadt, Steven B.] VA Puget Sound Hlth Care Syst, Hlth Serv Res, Seattle, WA USA.
[Zeliadt, Steven B.] VA Puget Sound Hlth Care Syst, Dev Ctr Excellence, Seattle, WA USA.
[Van Den Eeden, Stephen K.] Kaiser Permanente, Div Res, Oakland, CA USA.
[Hamilton, Ann S.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Oakley-Girvan, Ingrid] No Calif Canc Ctr, Fremont, CA USA.
[Penson, David F.] Vanderbilt Univ, Med Ctr, Vanderbilt Inst Med & Publ Hlth, Nashville, TN USA.
[Arora, Neeraj K.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Potosky, Arnold L.] Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
RP Ramsey, SD (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1100 Fairview Ave N,Box 19024,M3-B232, Seattle, WA 98109 USA.
EM sramsey@fhcrc.org
FU National Cancer Institute [N01-PC-35142, N01-PC-35139, N01-PC-35136]
FX Supported by the National Cancer Institute contracts: N01-PC-35142,
N01-PC-35139, and N01-PC-35136.
NR 33
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-3732
EI 1537-453X
J9 AM J CLIN ONCOL-CANC
JI Am. J. Clin. Oncol.-Cancer Clin. Trials
PD AUG
PY 2010
VL 33
IS 4
BP 381
EP 386
DI 10.1097/COC.0b013e3181b215d5
PG 6
WC Oncology
SC Oncology
GA 635OX
UT WOS:000280666200011
PM 20010079
ER
PT J
AU Martin, MA
Hallmark, KC
Sharkey, FE
AF Martin, Matthew A.
Hallmark, Kelly C.
Sharkey, Francis E.
TI Periodic Review of Pathology Training Program Teaching Files A Quality
Improvement Study
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE Pathology resident education; Quality improvement; Teaching file
ID SURGICAL PATHOLOGY; ASSURANCE
AB Pathology training programs typically retain teaching files of classic and unusual diagnostic cases. Since diagnostic criteria and terminology are mutable, we reviewed a surgical pathology teaching archive to determine if the materials continued to be acceptable for educational purposes. Each case (from 2001-2003) consisted of 1 to 3 slides and a 3 x 5 card with clinical information and the diagnosis. Cases were reviewed at a daily faculty consensus conference and categorized as follows: no diagnostic change; diagnosis added; or changed diagnosis. Slides were entirely missing from 79 (35.0%) of the 226 cases reviewed. Of the remaining 147 cases, 28 (19.0%) required additional clinical information and/or slides. The final disposition of the 147 cases was as follows: diagnosis unchanged, 126 (85.7%); diagnosis added, 15 (10.2%); and diagnosis changed, 6 (4.1%). Teaching files should be subject to prospective and retrospective controls to preserve the quality of the educational experience.
C1 [Martin, Matthew A.; Sharkey, Francis E.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, San Antonio, TX 78229 USA.
[Hallmark, Kelly C.] Audie L Murphy Mem Vet Adm Med Ctr, Dept Pathol & Lab Med, San Antonio, TX USA.
RP Sharkey, FE (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
NR 6
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 AUG
PY 2010
VL 134
IS 2
BP 332
EP 334
DI 10.1309/AJCPKXBOAK5PMI8G
PG 3
WC Pathology
SC Pathology
GA 627UE
UT WOS:000280067600022
PM 20660339
ER
PT J
AU Schiavetti, R
Garcia-Godoy, F
Toledano, M
Mazzitelli, C
Barlattani, A
Ferrari, M
Osorio, R
AF Schiavetti, Remo
Garcia-Godoy, Franklin
Toledano, Manuel
Mazzitelli, Claudia
Barlattani, Alberto
Ferrari, Marco
Osorio, Raquel
TI Comparison of fracture resistance of bonded glass fiber posts at
different lengths
SO AMERICAN JOURNAL OF DENTISTRY
LA English
DT Article
ID ENDODONTICALLY TREATED TEETH; FINITE-ELEMENT-ANALYSIS; 3-POINT BENDING
TEST; ROOT-CANAL POSTS; PULPLESS TEETH; STRESS-DISTRIBUTION; SEM
EVALUATION; RESIN; RESTORATION; RETENTION
AB Purpose To evaluate in vitro the fracture resistance of quartz fiber posts for three different dowel lengths Methods 30 single-rooted human premolars with similar root length and diameter were endodontically treated and randomly divided into three experimental groups (n=10) according to the post space depth created (1) 5 mm, (2) 7 mm, (3) 9 mm Quartz fiber posts (Endo Light post) were cemented using a dual cured resin cement with its adhesive system (Prime&Bond NT + Fluorocore 2) After 24 hours, specimens were embedded in acrylic resin and loaded under continuous compressive force at the extruding coronal part of the post (45-degree angle) to the long tooth axis (cross-head speed 0 75 mm/minute) Forces at fracture (Newtons) were recorded One-way ANOVA and Tukey tests were used for the statistical analysis (P< 0 05) Results Mean strength values (SD) were (1) 40 52 (3 14), (2) 41 68 (5 31), (3) 44 88 (6 77), respectively No statistically significant differences were found among the groups (Am J Dent 2010,23 227-230)
C1 [Schiavetti, Remo; Mazzitelli, Claudia; Ferrari, Marco] Univ Siena, Dept Fixed Prosthodont & Restorat Dent, I-53100 Siena, Italy.
[Garcia-Godoy, Franklin] Univ Tennessee, Hlth Sci Ctr, Res Coll Dent, Memphis, TN USA.
[Garcia-Godoy, Franklin] Univ Memphis, Dept Biomed Engn, Memphis, TN 38152 USA.
[Garcia-Godoy, Franklin] Forsyth Inst, Boston, MA USA.
[Osorio, Raquel] Univ Granada, Dept Dent Mat, Sch Dent, E-18071 Granada, Spain.
[Barlattani, Alberto] Univ Roma Tor Vergata, Dept Fixed Prosthodont, Rome, Italy.
[Ferrari, Marco] Tufts Univ, Sch Dent Med, Boston, MA 02111 USA.
RP Ferrari, M (reprint author), Univ Siena, Sch Dent Med, Dept Fixed Prosthodont & Dent Mat, Policlin Le Scotte, Viale Bracci, I-53100 Siena, Italy.
NR 44
TC 10
Z9 10
U1 1
U2 2
PU MOSHER & LINDER, INC
PI WESTON
PA 318 INDIAN TRACE SUITE 500, WESTON, FL 33326 USA
SN 0894-8275
J9 AM J DENT
JI Am. J. Dent.
PD AUG
PY 2010
VL 23
IS 4
BP 227
EP 230
PG 4
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 677GH
UT WOS:000283976600010
PM 21250575
ER
PT J
AU Piris, A
Scopsi, L
Clemente, C
Serbelloni, FC
Mihm, MC
Hoang, MP
AF Piris, Adriano
Scopsi, Lucio
Clemente, Claudio
Serbelloni, Federica Cetti
Mihm, Martin C., Jr.
Hoang, Mai P.
TI Epidermal Growth Factor Receptor Gene Status by Fluorescence In Situ
Hybridization in Malignant, Atypical, and Benign Hidradenomas
SO AMERICAN JOURNAL OF DERMATOPATHOLOGY
LA English
DT Article
DE epidermal growth factor receptor; fluorescence in situ hybridization;
hidradenocarcinoma; polysomy; trisomy
ID CELL LUNG-CANCER; COPY NUMBER; METASTATIC HIDRADENOCARCINOMA; PROTEIN
OVEREXPRESSION; BREAST-CANCER; EGFR GENE; AMPLIFICATION; GEFITINIB;
CARCINOMA; EXPRESSION
AB Background: Epidermal growth factor receptor (EGFR) protein overexpression and gene amplification are important prognostic factors in various tumors and EGFR inhibitors are now available as promising chemotherapeutic agents. There is little information in the literature regarding the EGFR protein and gene status in hidradenocarcinomas which has an aggressive biologic course characterized by repeated local recurrences and systemic metastasis. We have previously reported EGFR protein overexpression in malignant, atypical, and benign hidradenomas and would like to further evaluate their gene status by fluorescence in situ hybridization.
Methods: Fluorescence in situ hybridization by 2-color probe Vysis LSI EGFR SpectrumOrange/CEP 7 SpectrumGreen Probe (Abbott Molecular) and EGFR immunostain (H11, Dakocytomation) were performed in 15 malignant, 15 atypical, and 7 benign hidradenomas.
Results: High polysomy and low trisomy was noted in 1 and 4 hidradenocarcinoma, respectively; however, EGFR overexpression was seen only in 1 low trisomy case. Disomy is noted in the remaining 29 cases (9 hidradenocarcinomas, 15 atypical hidradenomas, and 5 benign hidradenomas). EGFR overexpression was seen in 3/12 (25%) malignant hidradenomas, 7/15 (47%) atypical hidradenomas, and 3/5 (60%) benign hidradenomas; none of these cases demonstrated EGFR gene amplification.
Conclusions: Polysomy/trisomy is more frequently seen in hidradenocarcinoma than atypical and benign hidradenomas. The role of EGFR inhibitor therapy in hidradenocarcinoma cases with protein overexpression remains unclear. Lack of correlation between the protein expression and polysomy/gene amplification suggests that molecular mechanisms other than gene amplification play a role in EGFR overexpression in malignant, atypical, and benign hidradenomas.
C1 [Piris, Adriano; Mihm, Martin C., Jr.; Hoang, Mai P.] Massachusetts Gen Hosp, Dermatopathol Unit, Dept Pathol, Boston, MA 02114 USA.
[Piris, Adriano; Mihm, Martin C., Jr.; Hoang, Mai P.] Harvard Univ, Sch Med, Boston, MA USA.
[Clemente, Claudio; Serbelloni, Federica Cetti] Casa de Cura San PioX, Anat Patol, Milan, Italy.
RP Hoang, MP (reprint author), Massachusetts Gen Hosp, Dermatopathol Unit, Dept Pathol, 55 Fruit St,Warren 820, Boston, MA 02114 USA.
EM mhoang@partners.org
NR 32
TC 5
Z9 5
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0193-1091
J9 AM J DERMATOPATH
JI Am. J. Dermatopathol.
PD AUG
PY 2010
VL 32
IS 6
BP 586
EP 592
DI 10.1097/DAD.0b013e3181cd64f2
PG 7
WC Dermatology
SC Dermatology
GA 629JN
UT WOS:000280192800009
PM 20534988
ER
PT J
AU Driver, JA
Yung, R
Gaziano, JM
Kurth, T
AF Driver, Jane A.
Yung, Rachel
Gaziano, J. Michael
Kurth, Tobias
TI Chronic Disease in Men With Newly Diagnosed Cancer: A Nested
Case-Control Study
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE aging; case-control studies; geriatrics; neoplasms; risk
ID PARKINSONS-DISEASE; CARDIOVASCULAR-DISEASE; PHYSICIANS HEALTH;
ALZHEIMER-DISEASE; BETA-CAROTENE; COMORBIDITY; MORTALITY; SURVIVAL;
COHORT; AGE
AB The authors performed a matched case-control study (1982-2007) nested in a prospective cohort of 22,071 US men to determine the prevalence of chronic diseases of aging in those with newly diagnosed cancer. They matched one control by age to each of 5,622 men who developed cancer over the 25 years of follow-up, as of the date of cancer diagnosis. A modified Charlson score was calculated that reflected comorbidities prior to the matching date, and the authors used conditional logistic regression to determine the odds ratios of various diseases. No substantial differences were found between the scores of cases and controls overall, by cancer subtype, or by age at diagnosis. Overall, men who developed cancer were less likely to have had hypercholesterolemia (odds ratio (OR) = 0.79, 95% confidence interval (CI): 0.72, 0.87) or coronary artery disease (OR = 0.85, 95% CI: 0.77, 0.96). Compared with controls, men with cancers for which there is routine screening had fewer diseases, whereas those with smoking-related cancers had more. Prostate cancer was inversely associated with both coronary artery disease (OR = 0.72, 95% CI: 0.62, 0.84) and diabetes (OR = 0.72, 95% CI: 0.58, 0.89). Overall, men who developed cancer had no more comorbidity or frequent history of chronic disease than their age-matched controls.
C1 [Driver, Jane A.; Gaziano, J. Michael; Kurth, Tobias] Harvard Univ, Div Aging, Brigham & Womens Hosp, Sch Med,Dept Med, Boston, MA 02120 USA.
[Gaziano, J. Michael; Kurth, Tobias] Harvard Univ, Div Prevent Med, Brigham & Womens Hosp, Sch Med,Dept Med, Boston, MA 02120 USA.
[Yung, Rachel] Harvard Univ, Sch Med, Dana Farber Canc Res Inst, Dept Oncol, Boston, MA 02120 USA.
[Kurth, Tobias] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02120 USA.
[Driver, Jane A.] Ctr Geriatr Res Educ & Clin, Boston, MA USA.
[Gaziano, J. Michael] Harvard Univ, VA Boston Healthcare Syst, Massachusetts Vet Epidemiol Res Informat Ctr, Sch Med, Boston, MA 02120 USA.
[Kurth, Tobias] INSERM, Neuroepidemiol U708, Paris, France.
[Kurth, Tobias] Univ Paris 06, Fac Med, Paris, France.
RP Driver, JA (reprint author), Harvard Univ, Div Aging, Brigham & Womens Hosp, Sch Med,Dept Med, 1620 Tremont St, Boston, MA 02120 USA.
EM jdriver@partners.org
RI Kurth, Tobias/A-9243-2012
OI Kurth, Tobias/0000-0001-7169-2620
FU Hartford Foundation's Center of Excellence in Geriatric Medicine at
Harvard Medical School; Eleanor and Miles Shore/Harvard Medical School;
National Cancer Institute [CA-34944, CA-40360, CA-097193]; National
Heart, Lung, and Blood Institute, Bethesda, Maryland [HL-26490,
HL-34595]; Hartford Foundation; Parkinson's Disease Foundation (New
York, New York); Harvard Medical School; Veterans Administration
(Washington, DC); Department of Veterans Affairs (Washington, DC);
National Institutes of Health (Bethesda, Maryland); VeroScience LLC
(Tiverton, Rhode Island); Amgen Inc. (Washington, DC); National
Institutes of Health; McNeil Consumer & Specialty Pharmaceuticals (Fort
Washington, Pennsylvania); Merck Co., Inc.; Wyeth Consumer Healthcare
(Mountain View, California)
FX This work was supported by a grant from the Hartford Foundation's Center
of Excellence in Geriatric Medicine at Harvard Medical School and the
Eleanor and Miles Shore/Harvard Medical School Scholars in Medicine
Program. The Physicians' Health Study is supported by grants from the
National Cancer Institute (CA-34944, CA-40360, and CA-097193) and grants
to the National Heart, Lung, and Blood Institute (HL-26490 and
HL-34595), Bethesda, Maryland.; Dr. Driver has received research grants
from the Hartford Foundation, the Parkinson's Disease Foundation (New
York, New York), and Harvard Medical School and is the recipient of a
Career Development Award from the Veterans Administration (Washington,
DC). Dr. Gaziano has received investigator-initiated research grants
from the Department of Veterans Affairs (Washington, DC), National
Institutes of Health (Bethesda, Maryland), VeroScience LLC (Tiverton,
Rhode Island), and Amgen Inc. (Washington, DC); has served as a
consultant for and has received honoraria from Bayer AG (Leverkusen,
Germany); and has served as an expert witness for Merck & Co., Inc.
(Whitehouse Station, New Jersey). Dr. Kurth has received
investigator-initiated research funds from the National Institutes of
Health, McNeil Consumer & Specialty Pharmaceuticals (Fort Washington,
Pennsylvania), Merck & Co., Inc., and Wyeth Consumer Healthcare
(Mountain View, California; he is a consultant to i3 Drug Safety
(Minneapolis, Minnesota) and World Health Information Science
Consultants, LLC (Newton, Massachusetts); and he has received honoraria
from Genzyme Corporation (Cambridge, Massachusetts), Merck & Co., Inc.,
and Pfizer Inc. (New York, New York) for educational lectures.
NR 26
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Z9 13
U1 1
U2 7
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD AUG 1
PY 2010
VL 172
IS 3
BP 299
EP 308
DI 10.1093/aje/kwq127
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 633UB
UT WOS:000280531100008
PM 20603278
ER
PT J
AU Kanwal, F
Barkun, A
Gralnek, IM
Asch, SM
Kuipers, EJ
Bardou, M
Sung, J
Enns, R
Agreus, L
Armstrong, D
Spiegel, BMR
AF Kanwal, Fasiha
Barkun, Alan
Gralnek, Ian M.
Asch, Steven M.
Kuipers, Ernst J.
Bardou, Marc
Sung, Joseph
Enns, Robert
Agreus, Lars
Armstrong, David
Spiegel, Brennan M. R.
TI Measuring Quality of Care in Patients With Nonvariceal Upper
Gastrointestinal Hemorrhage: Development of an Explicit Quality
Indicator Set
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID PROTON PUMP INHIBITORS; DOUBLE-BLIND TRIAL; CONSENSUS RECOMMENDATIONS;
HOSPITALIZED-PATIENTS; RHEUMATOID-ARTHRITIS; PEPTIC-ULCER; ENDOSCOPY;
MEDICATIONS; MANAGEMENT; INFUSION
AB OBJECTIVES: With an increasing emphasis on quality in health care and recognition of inconsistencies in the management of patients with nonvariceal upper gastrointestinal hemorrhage (NVUGIH), it is critical to establish a set of explicit quality indicators (QIs) in NVUGIH.
METHODS: We conducted a nine-member, multidisciplinary expert panel and followed modified Delphi methods to systematically identify a set of QIs for NVUGIH. The panel performed independent ratings of each candidate QI using a nine-point RAND appropriateness scale, then met in person and re-voted using an iterative process of discussion. The final set comprised QIs with a median RAND Appropriateness Score >= 7 and no disagreement among experts.
RESULTS: Among 116 candidate QIs, the panel rated 26 as valid measures of quality care. The selected QIs cover pre-endoscopy, endoscopy, and post-endoscopy care, including diagnosis, early resuscitation, risk stratification, endoscopic care, Helicobacter pylori management, and proton pump inhibitor therapy.
CONCLUSIONS: We have developed an explicit set of evidence-based QIs in NVUGIH, providing physicians and institutions with a tool to identify processes amenable to quality improvement. This tool is intended to be applicable in all institutions providing care for NVUGIH patients.
C1 [Asch, Steven M.; Spiegel, Brennan M. R.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Kanwal, Fasiha] St Louis Vet Adm VA, St Louis, MO USA.
[Kanwal, Fasiha] St Louis Univ, St Louis, MO 63103 USA.
[Barkun, Alan] McGill Univ, Montreal Gen Hosp, GI Div, Montreal, PQ H3G 1A4, Canada.
[Gralnek, Ian M.] Technion Israel Inst Technol, Haifa, Israel.
[Gralnek, Ian M.] Rambam Med Ctr, Haifa, Israel.
[Asch, Steven M.; Spiegel, Brennan M. R.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Kuipers, Ernst J.] Erasmus MC, Rotterdam, Netherlands.
[Bardou, Marc] Univ Burgundy, Fac Med, Dijon, France.
[Sung, Joseph] Chinese Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China.
[Enns, Robert] Univ British Columbia, St Pauls Hosp, Vancouver, BC V5Z 1M9, Canada.
[Agreus, Lars] Karolinska Inst, Stockholm, Sweden.
[Armstrong, David] McMaster Univ, Hamilton, ON, Canada.
RP Spiegel, BMR (reprint author), VA Greater Los Angeles Healthcare Syst, 11301 Wilshire Blvd,Bldg 115,Room 215, Los Angeles, CA 90073 USA.
EM bspiegel@mednet.ucla.edu
RI Hossain, Sarah /C-7332-2009
OI Hossain, Sarah /0000-0003-1355-0979
FU Canadian Association of Gastroenterology; European Association for
Gastroenterology and Endoscopy; Asian Pacific Society of Digestive
Endoscopy; Canadian Institutes of Health Research (Institute of
Diabetes, Metabolism and Nutrition); AstraZeneca Molndal; Abbott Canada;
Olympus Canada
FX Canadian Association of Gastroenterology; European Association for
Gastroenterology and Endoscopy; Asian Pacific Society of Digestive
Endoscopy; Canadian Institutes of Health Research (Institute of
Diabetes, Metabolism and Nutrition). Sponsors: AstraZeneca Molndal,
Abbott Canada, Olympus Canada through individual unrestricted grants to
the Canadian Association of Gastroenterology. The supporting agencies
and the sponsors had no role in the conduct of the study.
NR 44
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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 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD AUG
PY 2010
VL 105
IS 8
BP 1710
EP 1718
DI 10.1038/ajg.2010.180
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 635LJ
UT WOS:000280656800001
PM 20686458
ER
PT J
AU Ananthakrishnan, AN
McGinley, EL
Saeian, K
AF Ananthakrishnan, Ashwin N.
McGinley, Emily L.
Saeian, Kia
TI Length of Office Visits for Gastrointestinal Disease: Impact of
Physician Specialty
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID IRRITABLE-BOWEL-SYNDROME; PRIMARY-CARE PHYSICIANS; PATIENT SATISFACTION;
TIME SPENT; DURATION; MANAGEMENT; ADHERENCE; IMPROVE
AB OBJECTIVES: Physician-visit length is an important determinant of patient satisfaction and outcomes. Our objective was to compare visit length for gastrointestinal disorders between gastroenterologists and primary-care providers (PCPs).
METHODS: From the National Ambulatory Medical Care Survey, visits to office-based physician practices between 1993 and 2004 were identified and multivariate regression was used to identify predictors of visit duration.
RESULTS: There were 3135, 3391, and 3964 office visits associated with gastrointestinal disease, corresponding to 71, 140, and 180 million visits nationwide in 1993-1996, 1997-2000, and 2001-2004 respectively. Visit duration to all physicians increased from 17.3 minutes in 1993-1996 to 20.2 minutes in 2001-2004. Among gastroenterologists, visit length remained constant, from 21.0 minutes in 1993-1996 to 22.3 minutes in 2001-2004. On multivariate regression, age >50 years (1.8 minutes), new-patient encounters (7.4 minutes), and visits in 1997-2000 (2.7 minutes) and 2001-2004 (3.4 minutes) were associated with longer visit length. Encounters with gastroenterologists (3.3 minutes) were associated with longer visit duration than those with PCPs. The greatest adjusted difference in visit length between the two was seen for visits associated with constipation (5.7 minutes favoring gastroenterologists) and irritable bowel syndrome (2.4 minutes).
CONCLUSIONS: There has been an overall increase in length of physician visits associated with gastrointestinal disease. Both patient and provider factors predict visit length.
C1 [Ananthakrishnan, Ashwin N.; Saeian, Kia] Med Coll Wisconsin, Div Gastroenterol & Hepatol, Milwaukee, WI 53226 USA.
[McGinley, Emily L.] Med Coll Wisconsin, Div Epidemiol, Milwaukee, WI 53226 USA.
RP Ananthakrishnan, AN (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, 165 Cambridge St, Boston, MA 02114 USA.
EM aananthakrishnan@partners.org
NR 23
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Z9 3
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD AUG
PY 2010
VL 105
IS 8
BP 1719
EP 1725
DI 10.1038/ajg.2010.172
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 635LJ
UT WOS:000280656800002
PM 20686459
ER
PT J
AU Dienstag, JL
AF Dienstag, Jules L.
TI Peginterferon Therapy for HBeAg-Negative Chronic Hepatitis B: Less Than
Meets the Eye
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Editorial Material
ID BIOCHEMICAL RESPONSE; VIRUS-INFECTION; ALPHA-2A 40KD; FOLLOW-UP;
LAMIVUDINE; COMBINATION; RIBAVIRIN
AB Pegylated interferon (PEG IFN) has been recommended as a first-line therapy for hepatitis B e antigen (HBeAg)-negative chronic hepatitis B; however, data supporting this recommendation are derived from a single randomized controlled trial. In this issue of the Journal, Rijckborst et al. report the results of a second randomized controlled PEG IFN trial in 138 HBeAg-negative patients. The trial was undertaken to test the efficacy of adding ribavirin to PEG IFN; however, the results were unequivocal in concluding that adding ribavirin was not effective. Moreover, the efficacy of PEG IFN for these HBeAg-negative subjects was disappointing; only 7.5% of the study cohort had undetectable hepatitis B virus DNA (<400 copies/ml) 24 weeks after a 48-week course of therapy, and none lost hepatitis B surface antigen. This study challenges the value and limits the appeal of PEG IFN therapy for HBeAg-negative chronic hepatitis B.
C1 [Dienstag, Jules L.] Massachusetts Gen Hosp, Dept Med, Gastrointestinal Unit, Med Serv, Boston, MA 02114 USA.
[Dienstag, Jules L.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Dienstag, JL (reprint author), Massachusetts Gen Hosp, Dept Med, Gastrointestinal Unit, Med Serv, Jackson 7,55 Fruit St, Boston, MA 02114 USA.
EM jdienstag@partners.org
NR 17
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 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD AUG
PY 2010
VL 105
IS 8
BP 1770
EP 1772
DI 10.1038/ajg.2010.187
PG 3
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 635LJ
UT WOS:000280656800009
PM 20686463
ER
PT J
AU Stoffel, EM
Mercado, RC
Kohlmann, W
Ford, B
Grover, S
Conrad, P
Blanco, A
Shannon, KM
Powell, M
Chung, DC
Terdiman, J
Gruber, SB
Syngal, S
AF Stoffel, Elena M.
Mercado, Rowena C.
Kohlmann, Wendy
Ford, Beth
Grover, Shilpa
Conrad, Peggy
Blanco, Amie
Shannon, Kristen M.
Powell, Mark
Chung, Daniel C.
Terdiman, Jonathan
Gruber, Stephen B.
Syngal, Sapna
TI Prevalence and Predictors of Appropriate Colorectal Cancer Surveillance
in Lynch Syndrome
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID MISMATCH-REPAIR GENES; COLON-CANCER; LONG-TERM; MICROSATELLITE
INSTABILITY; BETHESDA GUIDELINES; SCREENING PRACTICES; MUTATION
CARRIERS; HIGH-RISK; HNPCC; FAMILIES
AB OBJECTIVES: Lynch syndrome (LS) is a hereditary cancer syndrome that conveys a high risk of colorectal cancer (CRC). Guidelines recommend colonoscopy every 1 to 2 years. There is limited information about screening compliance in this high-risk group.
METHODS: Data about cancer screening behaviors were obtained from subjects recruited through four US cancer genetics clinics. The main outcome was prevalence of appropriate CRC surveillance for LS.
RESULTS: A total of 181 individuals had a family history that met the Amsterdam criteria for LS (n = 154) and/or had an identified mutation in a mismatch repair (MMR) gene (n = 105). Of these 181 individuals, 131 (73%) had appropriate LS surveillance with colonoscopies at least every 2 years for their age >= 25 years. Of those with inadequate surveillance, 26/49 (53%) had colonoscopies at 3- to 5-year intervals. There were no significant differences in health-care setting, perceived risk of CRC, or compliance with screening for other cancers. Rates of appropriate surveillance were higher among individuals who had been referred for genetic evaluation for LS compared with those who had not (109/136 (80%) vs. 23/45 (51%), respectively, P = 0.0004). In multivariate analysis, personal history of CRC (odds ratio (OR) 2.81), having a first-degree relative with CRC at age <50 years (OR 2.61), and having undergone a genetic evaluation (OR 4.62) were associated with appropriate CRC surveillance for LS.
CONCLUSIONS: The time between colonoscopic exams in patients with LS is often longer than recommended by current guidelines and may place them at risk for interval cancers. Recognizing clinical features of LS and providing genetic counseling, evaluation, and intensive surveillance may improve cancer prevention for those at the highest risk for CRC.
C1 [Stoffel, Elena M.; Grover, Shilpa; Syngal, Sapna] Brigham & Womens Hosp, Div Gastroenterol, Boston, MA 02115 USA.
[Stoffel, Elena M.; Mercado, Rowena C.; Ford, Beth; Syngal, Sapna] Dana Farber Canc Inst, Div Populat Sci, Boston, MA 02115 USA.
[Stoffel, Elena M.; Chung, Daniel C.; Syngal, Sapna] Harvard Univ, Sch Med, Boston, MA USA.
[Kohlmann, Wendy; Gruber, Stephen B.] Univ Michigan, Med Ctr, Div Mol Med & Genet, Ann Arbor, MI USA.
[Conrad, Peggy; Blanco, Amie; Terdiman, Jonathan] Univ Calif San Francisco, Ctr Canc, San Francisco, CA 94143 USA.
[Shannon, Kristen M.; Chung, Daniel C.] Massachusetts Gen Hosp, Ctr Canc Risk Anal, Boston, MA 02114 USA.
[Powell, Mark] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Chung, Daniel C.] Massachusetts Gen Hosp, Gastroenterol Unit, Boston, MA 02114 USA.
RP Stoffel, EM (reprint author), Brigham & Womens Hosp, Div Gastroenterol, 75 Francis St, Boston, MA 02115 USA.
EM estoffel@partners.org
OI Blanco, Amie/0000-0003-3690-0038
FU American College of Gastroenterology; GlaxoSmithKline; National
Institutes of Health/National Cancer Institute [K07 NCI CA 120448-01-A2,
K24 NCI CA 113433]
FX This study was supported in part by the American College of
Gastroenterology Junior Faculty Award (2004, Stoffel) and
GlaxoSmithKline GIDH Clinical Research Award (2004, Stoffel). Stoffel is
supported by the National Institutes of Health/National Cancer Institute
career development award K07 NCI CA 120448-01-A2 (Stoffel) and K24 NCI
CA 113433 (Syngal).
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U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD AUG
PY 2010
VL 105
IS 8
BP 1851
EP 1860
DI 10.1038/ajg.2010.120
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 635LJ
UT WOS:000280656800021
PM 20354509
ER
PT J
AU Rabin, DU
Kuter, DJ
Liebman, HA
Bussel, JB
AF Rabin, Daniel U.
Kuter, David J.
Liebman, Howard A.
Bussel, James B.
TI What do healthcare providers ask their patients with immune
thrombocytopenia?
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Letter
ID QUALITY-OF-LIFE; PURPURA; ROMIPLOSTIM; DISEASE; ADULTS
AB Clinical signs suggestive of immune thrombocytopenia (ITP) include bruising, petechiae, nose bleeds, genitourinary (GU) bleeding, gum bleeding, gastrointestinal (GI) bleeding, and gynecologic bleeding [1]. Clinical experience and adverse events in clinical trials reveal other lip-associated symptoms such as arthritis, abdominal pain, sleep disturbances, headache, and fatigue. Asking patients about such symptoms supplements the platelet count in assessing disease status and impact, and thus helps in the design of a patient-specific management plan. A short practice patterns survey was administered to healthcare providers attending ITP Continuing Medical Education (CME) activities to assess the questions they ask patients in monitoring visits. A high percentage of respondents routinely ask about signs of bleeding and associated symptoms but not as frequently about health-related quality of life (HRQOL). Only 39% of respondents ask about difficulty with sleep. A short standardized questionnaire may be a useful tool to help healthcare providers gather information about their patients with ITP.
C1 [Rabin, Daniel U.] France Fdn, Old Lyme, CT 06371 USA.
[Kuter, David J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol,MGH Canc Ctr, Boston, MA USA.
[Liebman, Howard A.] Univ So Calif, Keck Sch Med, Jane Anne Nohl Div Hematol, Los Angeles, CA 90033 USA.
[Liebman, Howard A.] Univ So Calif, Keck Sch Med, Ctr Study Blood Dis, Los Angeles, CA 90033 USA.
[Bussel, James B.] Cornell Univ, Weill Med Coll, Dept Pediat Hematol Oncol, New York, NY 10021 USA.
RP Rabin, DU (reprint author), France Fdn, 230 Shore Rd, Old Lyme, CT 06371 USA.
EM drabin@francefoundation.com
NR 10
TC 0
Z9 0
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD AUG
PY 2010
VL 85
IS 8
BP 629
EP 631
DI 10.1002/ajh.21764
PG 3
WC Hematology
SC Hematology
GA 634EQ
UT WOS:000280562800022
PM 20658595
ER
PT J
AU Jagannath, AD
Rastogi, U
Spooner, AE
Lin, AE
Agnihotri, AK
AF Jagannath, Anand D.
Rastogi, Ujjwal
Spooner, Amy E.
Lin, Angela E.
Agnihotri, Arvind K.
TI Aortic Dissection and Moyamoya Disease in Turner Syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE aortic dilation; aortic dissection; Turner syndrome; vascular disease;
vasculopathy
ID DILATATION; REVASCULARIZATION; VASCULOPATHY; DYSFUNCTION; PREVALENCE;
ANEURYSMS; CHILDREN; WOMEN
AB Aortic dilation and dissection are well-recognized cardiac abnormalities in women with Turner syndrome (TS), although the underlying pathophysiology is not fully understood. We report on a 46-year-old Hispanic woman who was previously diagnosed with moyamoya disease on magnetic resonance imaging after a presentation with stroke-like symptoms. Her features were consistent with TS and chromosome analysis revealed mosaicism in which 17% of the cells showed a pseudoisodicentric Y chromosome: 45,X (25)146,X psu idic (Y)(11.2) (5). A preceding screening transthoracic echocardiogram had shown a bicuspid aortic valve (BAV) with an aortic diameter of 3.2 cm; at the time of moyamoya diagnosis, the aorta was 3.5 cm with mild aortic stenosis and mild aortic regurgitation. Four years later, the patient had had an acute aortic dissection, Stanford type A, which was repaired successfully. This case report is the third individual with TS associated with moyamoya disease and the first associated with dissection. The small number of cases does not allow detailed analysis other than noting patient age (two older than 40 years), karyotype (two others associated with isochrome Xq), and associated cardiac risk factors (one with BAV). Although this may be a chance occurrence, we hypothesize that moyamoya disease could be a manifestation of the vasculopathy in TS. (C) 2010 Wiley-Liss, Inc.
C1 [Agnihotri, Arvind K.] Massachusetts Gen Hosp, Dept Surg, Div Cardiac Surg, Boston, MA 02114 USA.
[Spooner, Amy E.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Lin, Angela E.] MassGen Hosp Children, Genet Unit, Boston, MA USA.
RP Agnihotri, AK (reprint author), Massachusetts Gen Hosp, Dept Surg, Div Cardiac Surg, Cox Bldg,Room 642,55 Fruit St, Boston, MA 02114 USA.
EM aagnihotri@partners.org
NR 26
TC 4
Z9 4
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD AUG
PY 2010
VL 152A
IS 8
BP 2085
EP 2089
DI 10.1002/ajmg.a.33539
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 638VO
UT WOS:000280925800032
PM 20635402
ER
PT J
AU Shargorodsky, J
Curhan, GC
Farwell, WR
AF Shargorodsky, Josef
Curhan, Gary C.
Farwell, Wildon R.
TI Prevalence and Characteristics of Tinnitus among US Adults
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Article
DE Anxiety; Depression; Epidemiology; Hearing loss; Tinnitus
ID HEARING-LOSS; DEPRESSION; EPIDEMIOLOGY; SUFFERERS; PATIENT; ANXIETY;
TRAUMA
AB BACKGROUND: Tinnitus is common; however, few risk factors for tinnitus are known.
METHODS: We examined cross-sectional relations between several potential risk factors and self-reported tinnitus in 14,178 participants in the 1999-2004 National Health and Nutrition Examination Surveys, a nationally representative database. We calculated the prevalence of any and frequent (at least daily) tinnitus in the overall US population and among subgroups. Logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI) after adjusting for multiple potential confounders.
RESULTS: Approximately 50 million US adults reported having any tinnitus, and 16 million US adults reported having frequent tinnitus in the past year. The prevalence of frequent tinnitus increased with increasing age, peaking at 14.3% between 60 and 69 years of age. Non-Hispanic whites had higher odds of frequent tinnitus compared with other racial/ethnic groups. Hypertension and former smoking were associated with an increase in odds of frequent tinnitus. Loud leisure-time, firearm, and occupational noise exposure also were associated with increased odds of frequent tinnitus. Among participants who had an audiogram, frequent tinnitus was associated with low-mid frequency (OR 2.37; 95% CI, 1.76-3.21) and high frequency (OR 3.00; 95% CI, 1.78-5.04) hearing impairment. Among participants who were tested for mental health conditions, frequent tinnitus was associated with generalized anxiety disorder (OR 6.07; 95% CI, 2.33-15.78) but not major depressive disorder (OR 1.58; 95% CI, 0.54-4.62).
CONCLUSIONS: The prevalence of frequent tinnitus is highest among older adults, non-Hispanic whites, former smokers, and adults with hypertension, hearing impairment, loud noise exposure, or generalized anxiety disorder. Prospective studies of risk factors for tinnitus are needed. Published by Elsevier Inc. The American Journal of Medicine (2010) 123, 711-718
C1 [Farwell, Wildon R.] Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MA 02115 USA.
[Shargorodsky, Josef; Curhan, Gary C.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Farwell, Wildon R.] Harvard Univ, Sch Med, Boston, MA USA.
[Farwell, Wildon R.] VA Boston Healthcare Syst, Massachusetts Vet Epidemiol Res & Informat Ctr, Boston, MA 02130 USA.
[Shargorodsky, Josef] Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA.
RP Farwell, WR (reprint author), VA Boston Healthcare Syst, Boston Div 151 MAV, 150 S Huntington Ave, Boston, MA 02130 USA.
EM wildon.farwell@va.gov
FU Massachusetts Eye and Ear Infirmary Foundation
FX This work was supported by the Massachusetts Eye and Ear Infirmary
Foundation and with resources and the use of facilities at the
Massachusetts Veterans Epidemiology Research and Information Center, VA
Boston Healthcare System.
NR 29
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Z9 218
U1 7
U2 42
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 AUG
PY 2010
VL 123
IS 8
BP 711
EP 718
DI 10.1016/j.amjmed.2010.02.015
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 631UG
UT WOS:000280374200012
PM 20670725
ER
PT J
AU Williams, LH
Rutter, CM
Katon, WJ
Reiber, GE
Ciechanowski, P
Heckbert, SR
Lin, EHB
Ludman, EJ
Oliver, MM
Young, BA
Von Korff, M
AF Williams, Lisa H.
Rutter, Carolyn M.
Katon, Wayne J.
Reiber, Gayle E.
Ciechanowski, Paul
Heckbert, Susan R.
Lin, Elizabeth H. B.
Ludman, Evette J.
Oliver, Malia M.
Young, Bessie A.
Von Korff, Michael
TI Depression and Incident Diabetic Foot Ulcers: A Prospective Cohort Study
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Article
DE Complications; Depression; Diabetes; Foot ulcers
ID PERIPHERAL ARTERIAL-DISEASE; RANDOMIZED CONTROLLED-TRIAL; SELF-CARE;
AFRICAN-AMERICANS; LEG SYMPTOMS; RISK; MORTALITY; ASSOCIATION;
COMPLICATIONS; PREVENTION
AB OBJECTIVE: To test whether depression is associated with an increased risk of incident diabetic foot ulcers.
METHODS: The Pathways Epidemiologic Study is a population-based prospective cohort study of 4839 patients with diabetes in 2000-2007. The present analysis included 3474 adults with type 2 diabetes and no prior diabetic foot ulcers or amputations. Mean follow-up was 4.1 years. Major and minor depression assessed by the Patient Health Questionnaire-9 were the exposures of interest. The outcome of interest was incident diabetic foot ulcers. We computed the hazard ratio and 95% confidence interval (CI) for incident diabetic foot ulcers, comparing patients with major and minor depression with those without depression and adjusting for sociodemographic characteristics, medical comorbidity, glycosylated hemoglobin, diabetes duration, insulin use, number of diabetes complications, body mass index, smoking status, and foot self-care. Sensitivity analyses also adjusted for peripheral neuropathy and peripheral arterial disease as defined by diagnosis codes.
RESULTS: Compared with patients without depression, patients with major depression by Patient Health Questionnaire-9 had a 2-fold increase in the risk of incident diabetic foot ulcers (adjusted hazard ratio 2.00; 95% CI, 1.24-3.25). There was no statistically significant association between minor depression by Patient Health Questionnaire-9 and incident diabetic foot ulcers (adjusted hazard ratio 1.37; 95% CI, 0.77-2.44).
CONCLUSION: Major depression by Patient Health Questionnaire-9 is associated with a 2-fold higher risk of incident diabetic foot ulcers. Future studies of this association should include better measures of peripheral neuropathy and peripheral arterial disease, which are possible confounders or mediators. (C) 2010 Elsevier Inc. All rights reserved. The American Journal of Medicine (2010) 123, 748-754
C1 [Williams, Lisa H.] Univ Washington, Div Dermatol, Dept Med, Seattle, WA 98195 USA.
[Rutter, Carolyn M.; Heckbert, Susan R.; Lin, Elizabeth H. B.; Ludman, Evette J.; Oliver, Malia M.; Von Korff, Michael] Grp Hlth Ctr Hlth Studies, Seattle, WA USA.
[Katon, Wayne J.; Ciechanowski, Paul] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Reiber, Gayle E.] Univ Washington, Hlth Serv Res & Dev Ctr Excellence, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Heckbert, Susan R.] Univ Washington, Dept Epidemiol, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Reiber, Gayle E.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
[Young, Bessie A.] Univ Washington, Epidemiol Res & Informat Ctr, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Young, Bessie A.] Univ Washington, Dept Med, Div Nephrol, Seattle, WA 98195 USA.
RP Williams, LH (reprint author), 125 16th Ave E,Mail Stop CSB 5, Seattle, WA 98112 USA.
EM lisahw@u.washington.edu
FU National Institutes of Health [MH-073686]; National Institutes of
Health/American Skin Association [F32 AR-056380]; Dermatology Foundation
FX This research was supported by National Institutes of Health grant
MH-073686. Dr Williams was supported by National Institutes of
Health/American Skin Association grant F32 AR-056380 and a Dermatology
Foundation Dermatologist Investigator Research Fellowship.
NR 31
TC 30
Z9 34
U1 4
U2 12
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 AUG
PY 2010
VL 123
IS 8
BP 748
EP U151
DI 10.1016/j.amjmed.2010.01.023
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 631UG
UT WOS:000280374200017
PM 20670730
ER
PT J
AU Gingo, M
Risbano, MG
Russ, PD
Chan, ED
AF Gingo, Matthew
Risbano, Michael G.
Russ, Paul D.
Chan, Edward D.
TI Not Your Otitis Media 101
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Letter
ID INTRACRANIAL COMPLICATIONS
C1 [Chan, Edward D.] Natl Jewish Hlth, Denver, CO 80206 USA.
[Gingo, Matthew; Risbano, Michael G.; Chan, Edward D.] Univ Colorado, Dept Med, Denver, CO USA.
[Gingo, Matthew; Risbano, Michael G.; Chan, Edward D.] Univ Colorado, Div Pulm Sci & Crit Care, Denver, CO USA.
[Russ, Paul D.] Univ Colorado, Dept Radiol, Denver, CO USA.
[Russ, Paul D.; Chan, Edward D.] Denver Vet Affairs Med Ctr, Hlth Sci Ctr, Denver, CO USA.
RP Chan, ED (reprint author), Natl Jewish Hlth, K720,Goodman Bldg,1400 Jackson St, Denver, CO 80206 USA.
EM chane@njhealth.org
RI Gingo, Matthew/K-7203-2013;
OI Risbano, Michael/0000-0003-3334-7046
NR 5
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 0002-9343
J9 AM J MED
JI Am. J. Med.
PD AUG
PY 2010
VL 123
IS 8
BP E9
EP E11
DI 10.1016/j.amjmed.2009.12.038
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 631UG
UT WOS:000280374200024
PM 20670714
ER
PT J
AU Hollander, DA
Giaconi, JA
Holland, GN
Yu, F
Caprioli, J
Aldave, AJ
Coleman, AL
Casey, R
Law, SK
Mondino, BJ
AF Hollander, David A.
Giaconi, Joann A.
Holland, Gary N.
Yu, Fei
Caprioli, Joseph
Aldave, Anthony J.
Coleman, Anne L.
Casey, Richard
Law, Simon K.
Mondino, Bartly J.
TI Graft Failure After Penetrating Keratoplasty in Eyes With Ahmed Valves
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID GLAUCOMA DRAINAGE DEVICE; ENDOTHELIAL-CELL DENSITY; RISK-FACTORS;
MOLTENO IMPLANT; TUBE SHUNT; FOLLOW-UP; SURVIVAL; OUTCOMES; THERAPY
AB PURPOSE: To determine incidence and risk factors for graft failure following penetrating keratoplasty (PK) in eyes with Ahmed valves (AV).
DESIGN: Retrospective, observational cohort study.
METHODS: Patients who underwent PK after AV implantation (both performed at our institution through 2004) were studied. Intervals to graft failure (defined as either dysfunction [stromal thickening with retention of clarity] or decompensation [central microcystic edema or loss of clarity]) were analyzed using Kaplan-Meier technique. Risk factors for graft failure were analyzed using Cox proportional hazard models.
RESULTS: Included were 77 eyes (77 patients; first procedure 1993). Following PK, 40 eyes (52%) required increased numbers of glaucoma medications; 10 eyes (13%) required additional glaucoma drainage device(s). Graft failure at 1, 2, and 3 years was 42.4% (95% confidence interval: 32.0%-54.6%), 57.1% (45.6%-69.1%), and 59.1% (47.5%-71.2%), respectively. Prior PK (HR 2.38, P = .006) and stromal vessels (HR 2.90, P = .0005) were associated with increased risk of graft failure. Use of glaucoma medications (HR 0.27, P = .009) and evidence of lower intraocular pressures (IOP) during follow-up (excluding hypotony; HR 0.92, P = .010) were associated with reduced risk of graft failure. Endothelial rejection episodes were observed in 13 eyes (17%); however, rejection was not a risk factor for graft failure (P = .98).
CONCLUSIONS: Long-term survival of corneal grafts is poor in eyes with AV. The majority of graft failures are associated with progressive loss of endothelial function, without observed immunologic rejection. Despite the presence of an AV, escalation in glaucoma therapy often follows PK; graft failure may be related to poor IOP control. (Am J Ophthalmol 2010;150:169-178. Published by Elsevier Inc.)
C1 [Hollander, David A.; Giaconi, Joann A.; Holland, Gary N.; Yu, Fei; Caprioli, Joseph; Aldave, Anthony J.; Coleman, Anne L.; Casey, Richard; Law, Simon K.; Mondino, Bartly J.] Univ Calif Los Angeles, Jules Stein Eye Inst, Los Angeles, CA 90095 USA.
[Hollander, David A.; Giaconi, Joann A.; Holland, Gary N.; Yu, Fei; Caprioli, Joseph; Aldave, Anthony J.; Coleman, Anne L.; Casey, Richard; Law, Simon K.; Mondino, Bartly J.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Ophthalmol, Los Angeles, CA 90095 USA.
[Hollander, David A.; Giaconi, Joann A.; Holland, Gary N.] Greater Los Angeles Vet Adm Healthcare Syst, Los Angeles, CA USA.
RP Giaconi, JA (reprint author), Univ Calif Los Angeles, Jules Stein Eye Inst, 100 Stein Plaza, Los Angeles, CA 90095 USA.
EM giaconi@jsei.ucla.edu
OI Caprioli, Joseph/0000-0002-2383-7263
FU HEED OPHTHALMIC FOUNDATION CLEVELAND, OHIO; Research to Prevent
Blindness (RPB), Inc, New York, New York; Vernon O. Underwood Family
Endowed Professorship; RPB
FX PUBLICATION OF THIS STUDY WAS SUPPORTED BY THE HEED OPHTHALMIC
FOUNDATION CLEVELAND, OHIO (DR HOLLANDER); Research to Prevent Blindness
(RPB), Inc, New York, New York (Dr Holland); and the Vernon O. Underwood
Family Endowed Professorship (Dr Holland). Dr Holland was recipient of
an RPB Physician-Scientist Award. Dr Hollander is currently an employee
of Allergan, Inc. Funding entities had no role in the conduction or
presentation of this study. Involved in study design (D.A.H., J.A.G.,
G.N.H., F.Y.); data collection (D.A.H., JAG., G.N.H., J.C., A.J.A.,
A.L.C., R.C., S.K.L., B.J.M.); data management and analysis (D.A.H.,
JAG., G.N.H., F.Y.); data interpretation (D.A.H., JAG., G.N.H., F.Y.,
J.C., A.J.A., A.L.C., B.J.M.); preparation of initial draft of
manuscript (D.A.H., JAG., G.N.H., F.Y.); and review and approval of
manuscript (D.A.H., JAG., G.N.H., F.Y., J.C., A.J.A., A.L.C., R.C.,
S.K.L., B.J.M.). D. Hollander and J. Giaconi contributed equally to the
preparation of this article. This study was approved by the
Institutional Review Board at UCLA.
NR 26
TC 24
Z9 24
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD AUG
PY 2010
VL 150
IS 2
BP 169
EP 178
DI 10.1016/j.ajo.2010.02.014
PG 10
WC Ophthalmology
SC Ophthalmology
GA 635ZT
UT WOS:000280697800006
PM 20537311
ER
PT J
AU Kohno, RI
Hata, Y
Mochizuki, Y
Arita, R
Kawahara, S
Kita, T
Miyazaki, M
Hisatomi, T
Ikeda, Y
Aiello, LP
Ishibashi, T
AF Kohno, Ri-Ichiro
Hata, Yasuaki
Mochizuki, Yasutaka
Arita, Ryoichi
Kawahara, Shuhei
Kita, Takeshi
Miyazaki, Masanori
Hisatomi, Toshio
Ikeda, Yasuhiro
Aiello, Lloyd Paul
Ishibashi, Tatsuro
TI Histopathology of Neovascular Tissue From Eyes With Proliferative
Diabetic Retinopathy After Intravitreal Bevacizumab Injection
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; RETINAL VEIN OCCLUSION; MACULAR DEGENERATION;
PRIMATE EYE; AVASTIN; GLAUCOMA; MONKEY
AB PURPOSE: To examine the histopathologic effect of a single intravitreal injection of bevacizumab on newly formed vessels in eyes with proliferative diabetic retinopathy (PDR).
DESIGN: Interventional case series and laboratory investigation.
METHODS: Two days after intravitreal injection of bevacizumab (1.25 mg/eye), pars plana vitrectomy or trabeculectomy was performed for the treatment of PDR or neovascular glaucoma (NVG) associated with PDR. Ten surgically removed preretinal proliferative tissues and 6 deep scleral flaps containing trabecular meshwork were fixed in 2% glutaraldehyde or 4% paraformaldehyde and were subjected to transmission electron microscopic analysis, immunohistochemical analysis, and terminal deoxyuridiine triphosphate (dUTP) nick-end labeling staining. Two surgically removed preretinal proliferative tissues and 2 deep scleral flaps from patients with PDR and NVG, but without preoperative intravitreal injection of bevacizumab (IVB), served as controls.
RESULTS: In control tissues, vascular endothelial cells possessed many fenestrations and were accompanied by pericytes. Apoptotic vascular endothelial cells frequently were observed in tissue after intravitreal injection of bevacizumab, whereas they were not observed in control tissues. Additionally, no apparent fenestration was observed in newly formed vessels from either proliferative tissue or trabecular meshwork after intravitreal injection of bevacizumab. In both PDR and NVG tissues after intravitreal injection of bevacizumab, overexpression of smooth muscle actin was observed in newly formed vessels, suggesting that the treatment may have increased pericytes on the vasculature as compared with control tissue.
CONCLUSIONS: Intravitreal injection of bevacizumab may induce changes in immature, newly formed vessels of PDR or NVG tissue, leading to endothelial apoptosis with vascular regression, while inducing normalization of premature vessels by increasing pericyte coverage and reducing vessel fenestration. (Am J Ophthalmol 2010;150:223-229. (C) 2010 by Elsevier Inc. All rights reserved.)
C1 [Hata, Yasuaki] Fukuoka Dent Coll, Dept Med, Sect Ophthalmol, Sawara Ku, Fukuoka 8140193, Japan.
[Kohno, Ri-Ichiro; Mochizuki, Yasutaka; Arita, Ryoichi; Kawahara, Shuhei; Kita, Takeshi; Miyazaki, Masanori; Hisatomi, Toshio; Ikeda, Yasuhiro; Ishibashi, Tatsuro] Kyushu Univ, Dept Ophthalmol, Grad Sch Med Sci, Fukuoka 812, Japan.
[Aiello, Lloyd Paul] Harvard Univ, Sch Med, Joslin Diabet Ctr, Beetham Eye Inst, Boston, MA 02115 USA.
[Aiello, Lloyd Paul] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA.
RP Hata, Y (reprint author), Fukuoka Dent Coll, Dept Med, Sect Ophthalmol, Sawara Ku, 2-15-1 Tamura, Fukuoka 8140193, Japan.
EM hatachan@med.kyushu-u.ac.jp
OI Hisatomi, Toshio/0000-0003-2552-9595
FU Ministry of Education, Science, Sports and Culture, Tokyo, Japan
[21592233]
FX PUBLICATION OF THIS STUDY IS SUPPORTED IN PART BY GRANT-IN-AID FOR
SCIENTIFIC RESEARCH 21592233 FROM THE Ministry of Education, Science,
Sports and Culture, Tokyo, Japan. The authors indicate no financial
conflict of interest. Involved in design of study (R.I., Y.H., L.P.A.,
T.I.); Conduct of study (RA., S.K., T.H.); Data collection (R.K., Y.H.,
Y.M., MM.); Provision of material (Y.H., Y.M., RA., S.K., M.M., T.H.,
Y.I.); Analysis of data (R.A., S.K., T.H.); Statistical experience
(R.A., S.K., T.K.); Obtaining funding (R.I., Y.H., Y.M., R.A., S.K.,
T.K., MM., T.H., Y.I., T.I.); Literature search (R.I., R.A., S.K.,
T.K.); Administrative support (Y.H., L.P.A.); Writing the article (R.I.,
Y.H., L.P.A.); Critical revision (Y.H., Y.M., R.A., S.K., T.K., M.M.,
T.H., Y.I., L.P.P., T.I.); and Final approval (R.I., Y.H., Y.M., R.A.,
S.K., T.K., MM., T.H., Y.I., L.P.P., T.I.). This study was carried out
with approval from the Institutional Review Board at Kyushu University
Hospital and was performed in accordance with the ethical standards of
the 1989 Declaration of Helsinki. Written informed consent was obtained
from all 15 patients.
NR 23
TC 21
Z9 25
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD AUG
PY 2010
VL 150
IS 2
BP 223
EP 229
DI 10.1016/j.ajo.2010.03.016
PG 7
WC Ophthalmology
SC Ophthalmology
GA 635ZT
UT WOS:000280697800014
PM 20542485
ER
PT J
AU Jakobiec, FA
Bhat, P
AF Jakobiec, Frederick A.
Bhat, Pooja
TI Retrocorneal Membranes: A Comparative Immunohistochemical Analysis of
Keratocytic, Endothelial, and Epithelial Origins
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID CORNEAL ENDOTHELIUM; PERFORATING INJURY; GROWTH-FACTOR; DYSTROPHY;
CELLS; PROLIFERATION; KERATOPLASTY; CYTOKERATINS; EXPRESSION; FEATURES
AB PURPOSE: To determine through the use of immunohistochemistry the origins of retrocorneal cellular and fibrillar membranes.
DESIGN: Retrospective, clinicopathologic study using surgically removed human corneal tissues.
METHODS: Clinical records of patients' ocular diseases and surgical procedures were reviewed. Immunohistochemical staining was performed on 5 enucleated control globes, 32 penetrating keratoplasty specimens, and 6 Descemet stripping endothelial keratoplasty specimens to analyze: (1) the normal corneal epithelium, stroma, and endothelium; and (2) stromal scars, endothelial abnormalities, and retrocorneal membranes. Paraffin sections were stained with hematoxylin and eosin, periodic acid-Schiff, and Masson trichrome methods, and immunohistochemical analyses were performed with commonly available monoclonal and polyclonal antibodies for various cytokeratins (CKs), CD34, alpha-smooth muscle actin (SMA), and vimentin.
RESULTS: Five subtypes among 28 retrocorneal membranes were characterized. Twelve fibrous (keratocytic) membranes of stromal origin had coarse collagen and immunostained negatively for all CKs, but strongly for vimentin and alpha-SMA, the last the only marker of diagnostic value. Nine metaplastic endothelium-derived membranes produced delicate collagenous matrices and immunoreacted with CK7, vimentin, and alpha-SMA. Two epithelial multilaminar or monolaminar membranes reacted with CK cocktail and wide-spectrum CK, mildly with CK7 (not observed in orthotopic surface epithelium), and negatively for alpha-SMA and vimentin. The final 2 categories were indeterminate or nonimmunoreactive (3 specimens) and mixed (2 specimens).
CONCLUSIONS: Immunohistochemistry can diagnose retrocorneal membranes of different provenances reliably in most cases. Clinical correlations established that these membranes develop after serious inflammatory disorders, prolonged wounding or ulcerations, and multiple surgeries (an average of 3.4 per patient). (Am J Ophthalmol 2010; 150:230-242. (C) 2010 by Elsevier Inc. All rights reserved.)
C1 [Jakobiec, Frederick A.; Bhat, Pooja] Massachusetts Eye & Ear Infirm, David G Cogan Ophthalm Pathol Lab, Boston, MA 02114 USA.
[Jakobiec, Frederick A.; Bhat, Pooja] Harvard Univ, Sch Med, Dept Ophthalmol, Massachusetts Eye & Ear Infirm, Boston, MA USA.
RP Jakobiec, FA (reprint author), Massachusetts Eye & Ear Infirm, David G Cogan Ophthalm Pathol Lab, 243 Charles St,Suite 321, Boston, MA 02114 USA.
EM Fred_Jakobiec@meei.harvard.edu
NR 40
TC 22
Z9 23
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD AUG
PY 2010
VL 150
IS 2
BP 230
EP 242
DI 10.1016/j.ajo.2010.03.011
PG 13
WC Ophthalmology
SC Ophthalmology
GA 635ZT
UT WOS:000280697800015
PM 20579631
ER
PT J
AU Kanoff, JM
Turalba, AV
Andreoli, MT
Andreoli, CM
AF Kanoff, Justin M.
Turalba, Angela V.
Andreoli, Michael T.
Andreoli, Christopher M.
TI Characteristics and Outcomes of Work-Related Open Globe Injuries
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID EYE INJURIES; RISK-FACTORS; TRAUMA; ENDOPHTHALMITIS; EPIDEMIOLOGY;
WORKPLACE
AB PURPOSE: To evaluate the characteristics and outcomes of patients treated for open globe injuries sustained at work and to compare these results to patients injured outside of work.
DESIGN: Retrospective chart review of 812 consecutive patients with open globe injuries treated at the Massachusetts Eye and Ear Infirmary between 1999 and 2008.
METHODS: A total of 146 patients with open globe injuries sustained at work were identified and their characteristics and outcomes were compared with the rest of the patients in the database.
RESULTS: Of the patients injured at work, 98% were men, and the average age of the patients was 35.8 years (17-72 years). The most common mechanism of injury was penetrating trauma (56%); 38 patients examined had intraocular foreign bodies (IOFB). Nine work-related open globe injuries resulted in enucleation. There was a higher incidence of IOFBs (P = .0001) and penetrating injuries (P = .0005) in patients injured at work. Both the preoperative (P = .0001) and final best-corrected visual acuity (P = .0001) was better in the work-related group. The final visual acuity was better than 20/200 in 74.1% of cases of work-related open globe injuries. However, there was no difference observed in the rate of enucleations (P = .4).
CONCLUSIONS: Work-related injuries can cause significant morbidity in a young population of patients. Based on average patient follow-up and final visual acuity, those injured at work do at least as well as, if not potentially better than, those with open globe injuries sustained outside of work. While the statistically higher rate of IOFB in the work population is not surprising, it does emphasize the importance of strict adherence to the use of eye protection in the workplace. (Am J Ophthalmol 2010;150:265-269. (C) 2010 by Elsevier Inc. All rights reserved.)
C1 [Kanoff, Justin M.; Turalba, Angela V.; Andreoli, Christopher M.] Harvard Univ, Sch Med, Boston, MA USA.
[Kanoff, Justin M.; Turalba, Angela V.] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Andreoli, Michael T.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Andreoli, Christopher M.] Harvard Vanguard Med Associates, Boston, MA USA.
RP Kanoff, JM (reprint author), Dept Ophthalmol, 243 Charles St, Boston, MA 02114 USA.
EM Justin_Kanoff@meei.harvard.edu
NR 15
TC 26
Z9 26
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD AUG
PY 2010
VL 150
IS 2
BP 265
EP 269
DI 10.1016/j.ajo.2010.02.015
PG 5
WC Ophthalmology
SC Ophthalmology
GA 635ZT
UT WOS:000280697800019
PM 20522411
ER
PT J
AU Kong, JA
Kim, GH
Wei, MJ
Sun, T
Li, G
Liu, SQ
Li, XM
Bhan, I
Zhao, Q
Thadhani, R
Li, YC
AF Kong, Juan
Kim, Gene H.
Wei, Minjie
Sun, Tao
Li, George
Liu, Shu Q.
Li, Xinmin
Bhan, Ishir
Zhao, Qun
Thadhani, Ravi
Li, Yan Chun
TI Therapeutic Effects of Vitamin D Analogs on Cardiac Hypertrophy in
Spontaneously Hypertensive Rats
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID RENIN-ANGIOTENSIN SYSTEM; DIABETIC-NEPHROPATHY; GENE-EXPRESSION;
D-RECEPTOR; 1,25-DIHYDROXYVITAMIN D-3; CARDIOVASCULAR MORTALITY; AT1
RECEPTOR; RISK; 25-HYDROXYVITAMIN-D; ALISKIREN
AB Vitamin D inhibits renin expression and blocks the compensatory induction of renin associated with the use of renin-angiotensin system inhibitors. Here we test the therapeutic effects of two commonly used vitamin D analogs and their combination with losartan on the development of left ventricular hypertrophy. One-month-old male spontaneously hypertensive rats were treated with vehicle, losartan, paricalcitol, doxercalciferol, a combination of losartan and paricalcitol, or a combination of losartan and doxercalciferol for 2 months. Blood pressure was markedly reduced by losartan, but not by paricalcitol or doxercalciferol alone. Echocardiograpy demonstrated a 65 to 80% reduction in left ventricular wall thickness with losartan, paricalcitol, or doxercalciferol monotherapy and almost complete prevention of left ventricular hypertrophy with the combination therapies. Attenuation of cardiac and cardiomyocyte hypertrophy, and suppression of atrial and brain natriuretic peptides, were most marked in the combination therapy groups. These changes were well correlated with left ventricular gene and microRNA expression profiles in the different treatment groups. Renal and cardiac renin expression was markedly increased in losartan-treated animals, but nearly normalized with combination therapy. The same vitamin D analogs suppressed plasma renin activity in patients receiving chronic hemodialysis. These data demonstrate that vitamin D analogs have potent anti-hypertrophic activity in part via suppression of renin in the kidney and heart, and combination of these analogs with losartan achieves much better therapeutic effects because of the blockade of the compensatory renin increase. (Am J Pathol 2010, 177:622-631; DOI: 10.2353/ajpath.2010.091292)
C1 [Kong, Juan; Wei, Minjie; Zhao, Qun; Li, Yan Chun] China Med Univ, Shengjing Hosp, Lab Metab Dis Res & Drug Dev, Shenyang, Peoples R China.
[Kong, Juan; Kim, Gene H.; Sun, Tao; Li, George; Li, Yan Chun] Univ Chicago, Dept Med, Div Biol Sci, Chicago, IL 60637 USA.
[Liu, Shu Q.] Northwestern Univ, Dept Biomed Engn, Evanston, IL 60208 USA.
[Li, Xinmin] Univ Calif Los Angeles, Dept Pathol, Los Angeles, CA 90024 USA.
[Bhan, Ishir; Thadhani, Ravi] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Nephrol, Boston, MA USA.
RP Li, YC (reprint author), China Med Univ, Shengjing Hosp, Lab Metab Dis Res & Drug Dev, 900 E 57th St,KCBD,Mailbox 9, Shenyang, Peoples R China.
EM thadhani.ravi@mgh.harvard.edu; cyan@medicine.bsd.uchicago.edu
RI Liu, Shu/B-7626-2009; Sun, Tao/F-8233-2012
FU Genzyme Corp.; Abbott Laboratories; National Natural Science Foundation
of China [30971401]; National Institutes of Health-National Heart, Lung,
and Blood Institute [HL085793, HL093954]
FX Supported by research grants from Genzyme Corp., Abbott Laboratories,
National Natural Science Foundation of China (grant 30971401), and
National Institutes of Health-National Heart, Lung, and Blood Institute
(grants HL085793 and HL093954).
NR 48
TC 51
Z9 60
U1 0
U2 7
PU AMER SOC INVESTIGATIVE PATHOLOGY, INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3993 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD AUG
PY 2010
VL 177
IS 2
BP 622
EP 631
DI 10.2353/ajpath.2010.091292
PG 10
WC Pathology
SC Pathology
GA 638KU
UT WOS:000280894600014
PM 20616348
ER
PT J
AU Annamalai, L
Bhaskar, V
Pauley, DR
Knight, H
Williams, K
Lentz, M
Ratai, E
Westmoreland, SV
Gonzalez, RG
O'Neil, SP
AF Annamalai, Lakshmanan
Bhaskar, Veena
Pauley, Douglas R.
Knight, Heather
Williams, Kenneth
Lentz, Margaret
Ratai, Eva
Westmoreland, Susan V.
Gonzalez, R. Gilberto
O'Neil, Shawn P.
TI Impact of Short-Term Combined Antiretroviral Therapy on Brain Virus
Burden in Simian Immunodeficiency Virus-Infected and CD8(+)
Lymphocyte-Depleted Rhesus Macaques
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID CENTRAL-NERVOUS-SYSTEM; NECROSIS-FACTOR-ALPHA; HIV-ASSOCIATED DEMENTIA;
POLYMERASE-CHAIN-REACTION; CEREBROSPINAL-FLUID; CELLULAR-LOCALIZATION;
COMBINATION THERAPY; NEURONAL INJURY; VIRAL LOAD; TNF-ALPHA
AB Antiretroviral drugs suppress virus burden in the cerebrospinal fluid of HIV-infected individuals; however, the direct effect of antiretrovirals on virus replication in brain parenchyma is poorly understood. We investigated the effect of short-term combined antiretroviral therapy (CART) on brain virus burden in rhesus monkeys using the CD8-depletion model of accelerated simian immunodeficiency virus (SW) encephalitis. Four monkeys received CART (consisting of the nonpenetrating agents PMPA and RCV) for four weeks, beginning 28 days after SW inoculation. Lower virus burdens were measured by real-time RT-PCR in four of four regions of brain from monkeys that received CART as compared with four SIV-infected, untreated controls; however, the difference was only significant for the frontal cortex (P < 0.05). In contrast, significantly lower virus burdens were measured in plasma and four of five lymphoid compartments from animals that received CART. Surprisingly, despite normalization of neuronal function in treated animals, the numbers of activated macrophages/microglia and the magnitude of TNF-alpha mRNA expression in brain were similar between treated animals and controls. These results suggest that short-term therapy with antiretrovirals that fail to penetrate the blood-cerebrospinal fluid barrier can reduce brain virus burden provided systemic virus burden is suppressed; however, longer treatment may be required to completely resolve encephalitic lesions and microglial activation, which may reflect the longer half-life of the principal target cells of HIV/SIV in the brain (macrophages) versus lymphoid tissues (T lymphocytes). (Am J Patbol 2010, 177:777-791; DOI: 10.2353/ajpatb.2010.091248; DOI: 10.2353/ajpatb.2010.091248)
C1 [Annamalai, Lakshmanan; Pauley, Douglas R.; Knight, Heather; Westmoreland, Susan V.; O'Neil, Shawn P.] Harvard Univ, Div Comparat Pathol, New England Primate Res Ctr, Sch Med, Southborough, MA 01772 USA.
[Bhaskar, Veena; Lentz, Margaret; Ratai, Eva; Gonzalez, R. Gilberto] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA USA.
[Williams, Kenneth] Boston Coll, Dept Biol, Chestnut Hill, MA 02167 USA.
RP Westmoreland, SV (reprint author), Harvard Univ, Div Comparat Pathol, New England Primate Res Ctr, Sch Med, 1 Pine Hill Dr, Southborough, MA 01772 USA.
EM susan_westmoreland@hms.harvard.edu
RI ANNAMALAI, LAKSHMANAN/F-4220-2011
FU National Institutes of Health; National Institute of Neurological
Disorders and Stroke; National Center for Research Resources [RR000150,
NS048831, NS050041, NS40237]
FX Supported in part by grants from the National Institutes of Health,
National Institute of Neurological Disorders and Stroke, and National
Center for Research Resources, including RR000150 (S.P.O.), NS048831 (to
S.P.O.), NS050041 (R.G.G.), and NS40237 (K.W.).
NR 96
TC 12
Z9 12
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
EI 1525-2191
J9 AM J PATHOL
JI Am. J. Pathol.
PD AUG
PY 2010
VL 177
IS 2
BP 777
EP 791
DI 10.2353/ajpath.2010.091248
PG 15
WC Pathology
SC Pathology
GA 638KU
UT WOS:000280894600028
PM 20595631
ER
PT J
AU Morgenroth, DC
Orendurff, MS
Shakir, A
Segal, A
Shofer, J
Czerniecki, JM
AF Morgenroth, David C.
Orendurff, Michael S.
Shakir, Ali
Segal, Ava
Shofer, Jane
Czerniecki, Joseph M.
TI The Relationship Between Lumbar Spine Kinematics during Gait and
Low-Back Pain in Transfemoral Amputees
SO AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITATION
LA English
DT Article
DE Amputation; Biomechanics; Low-Back Pain; Rehabilitation
ID TRANS-FEMORAL AMPUTEES; LEVEL WALKING; RESIDUAL LIMB; MOTION;
OSTEOARTHRITIS; DEGENERATION; AMPUTATIONS; RELIABILITY; DISABILITY; DISC
AB Objective: Low-back pain is an important cause of secondary disability in transfemoral amputees. The primary aim of our study is to assess the differences in lumbar spine kinematics during gait between transfemoral amputees with and without low-back pain.
Design: Lumbar spine kinematics in three planes were measured when the subjects walked in a motion analysis laboratory. Nine transfemoral amputees with low-back pain, eight transfemoral amputees without low-back pain, and six healthy, nonamputee subjects participated.
Results: The Amputee Pain and Amputee No Pain groups were essentially the same in terms of all demographic and potentially confounding variable measures. Transfemoral amputees with low-back pain showed greater transverse plane rotational excursion in their lumbar spine during walking when compared with transfemoral amputees without low-back pain (P = 0.029; effect size = 1.03). There were no significant differences in sagittal or coronal plane lumbar spine excursions during walking between these two groups.
Conclusions: Although our study design does not allow for proving causation, increased transverse plane rotation has been associated with intervertebral disc degeneration, suggesting that increased transverse plane rotation secondary to walking with a prosthetic limb may be a causative factor in the etiology of low-back pain in transfemoral amputees. Identifying differences in lumbar motion can lead to potential preventative and therapeutic intervention strategies.
C1 [Morgenroth, David C.; Orendurff, Michael S.; Shakir, Ali; Shofer, Jane; Czerniecki, Joseph M.] VA Puget Sound Hlth Care Syst, Ctr Excellence Limb Loss Prevent & Prosthet Engn, Seattle, WA USA.
[Morgenroth, David C.; Czerniecki, Joseph M.] Univ Washington, Dept Rehabil Med, Seattle, WA 98195 USA.
[Segal, Ava] Western Reserve Spine & Pain Inst, Kent, OH USA.
RP Morgenroth, DC (reprint author), VAPSHCS, Rehabil Care Serv RCS 117, 1660 S Columbian Way, Seattle, WA 98108 USA.
OI Morgenroth, David/0000-0002-0226-7775
NR 39
TC 21
Z9 22
U1 5
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0894-9115
J9 AM J PHYS MED REHAB
JI Am. J. Phys. Med. Rehabil.
PD AUG
PY 2010
VL 89
IS 8
BP 635
EP 643
DI 10.1097/PHM.0b013e3181e71d90
PG 9
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 628JK
UT WOS:000280115400004
PM 20647781
ER
PT J
AU Cifu, DX
Cohen, SI
Lew, HL
Jaffee, M
Sigford, B
AF Cifu, David X.
Cohen, Sara I.
Lew, Henry L.
Jaffee, Michael
Sigford, Barbara
TI The History and Evolution of Traumatic Brain Injury Rehabilitation in
Military Service Members and Veterans
SO AMERICAN JOURNAL OF PHYSICAL MEDICINE & REHABILITATION
LA English
DT Review
DE Rehabilitation; War; Veterans; Brain Injury
ID COGNITIVE REHABILITATION; HEAD-INJURY; FOLLOW-UP; BLAST; POLYTRAUMA;
WAR; SOLDIERS; IMPAIRMENTS; INVOLVEMENT; EPILEPSY
AB The field of traumatic brain injury has evolved since the time of the Civil War in response to the needs of patients with injuries and disabilities resulting from war. The Department of Veterans Affairs and the Defense and Veterans Brain Injury Center have been in the forefront of the development of the interdisciplinary approach to the rehabilitation of soldiers with traumatic brain injury, particularly those injured from the recent conflicts in Iraq and Afghanistan. The objectives of this literature review are to examine how the casualties resulting from major wars in the past led to the establishment of the current model of evaluation and treatment of traumatic brain injury and to review how the field has expanded in response to the growing cohort of military service members and veterans with TBI.
C1 [Cifu, David X.] Virginia Commonwealth Univ, PM&R Serv, Hunter Holmes McGuire VA Healthcare Syst, Richmond, VA 23284 USA.
[Lew, Henry L.] Virginia Commonwealth Univ, Dept Phys Med & Rehabil, Richmond, VA 23284 USA.
[Cohen, Sara I.] VA Boston Healthcare Syst, Boston, MA USA.
[Cohen, Sara I.] Harvard Univ, Sch Med, Boston, MA USA.
[Jaffee, Michael] Def & Vet Brain Injury Ctr, Washington, DC USA.
RP Lew, HL (reprint author), Virginia Commonwealth Univ, Def & Vet Brain Injury Ctr, 730 E Broad St, Richmond, VA 23284 USA.
NR 45
TC 10
Z9 10
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0894-9115
J9 AM J PHYS MED REHAB
JI Am. J. Phys. Med. Rehabil.
PD AUG
PY 2010
VL 89
IS 8
BP 688
EP 694
DI 10.1097/PHM.0b013e3181e722ad
PG 7
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 628JK
UT WOS:000280115400011
PM 20647782
ER
PT J
AU Yu, T
Wu, X
Gupta, KB
Kucik, DF
AF Yu, Tao
Wu, Xing
Gupta, Kiran B.
Kucik, Dennis F.
TI Affinity, lateral mobility, and clustering contribute independently to
beta(2)-integrin-mediated adhesion
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Article
DE single particle tracking; intracellular cell adhesion molecule-1;
E-selectin; flow chamber; rolling
ID INSIDE-OUT ACTIVATION; CELL-ADHESION; EXTENDED CONFORMATIONS; LEUKOCYTE
TRAFFICKING; MECHANICAL-PROPERTIES; INTEGRIN ACTIVATION; AVIDITY
MODULATION; ACTIN CYTOSKELETON; STRUCTURAL BASIS; LIGAND-BINDING
AB Yu T, Wu X, Gupta KB, Kucik DF. Affinity, lateral mobility, and clustering contribute independently to beta(2)-integrin-mediated adhesion. Am J Physiol Cell Physiol 299: C399-C410, 2010. First published May 5, 2010; doi: 10.1152/ajpcell.00039.2009.-Affinity changes and avidity modulation both contribute to activation of beta(2)-integrin-mediated adhesion, an essential, early step in inflammation. Avidity modulation, defined as an increase in adhesiveness independent of integrin conformational changes, might be due to integrin clustering, motion, or both. Increased integrin diffusion upon leukocyte activation has been demonstrated, but whether it is proadhesive in itself, or just constitutes a mechanism for integrin clustering, remains unclear. To understand the proadhesive effects of integrin affinity changes, clustering, and motion, an experimental system was devised to separate them. Clustering and integrin motion together were induced by cytochalasin D (CD) without inducing high-affinity; integrin motion could then be frozen by fixation; and high affinity was induced independently by Mn2+. Adhesion was equivalent for fixed and unfixed cells except following pretreatment with CD or Mn2+, which increased adhesion for both. However, fixed cells were less adhesive than unfixed cells after CD, even though integrin clustering was similar. A simple explanation is that CD induces both clustering and integrin motion, fixation then stops motion on fixed cells, but integrins continue to diffuse on unfixed cells, increasing the kinetics of integrin/ICAM-1 interactions to enhance adhesion. Affinity changes are then independent of, and additive to, avidity effects.
C1 [Yu, Tao; Wu, Xing; Gupta, Kiran B.; Kucik, Dennis F.] Univ Alabama, Dept Pathol, Birmingham, AL 35294 USA.
[Kucik, Dennis F.] Univ Alabama, Dept Biomed Engn, Birmingham, AL 35294 USA.
[Kucik, Dennis F.] Birmingham Vet Affairs Med Ctr, Birmingham, AL USA.
RP Kucik, DF (reprint author), Univ Alabama, Dept Pathol, Kaul Bldg,Rm 640A,619 S 19th St, Birmingham, AL 35294 USA.
EM kucik@uab.edu
RI Yu, Tao/B-5352-2012
FU Department of Veterans Affairs
FX This work was supported by a Department of Veterans Affairs Merit Award.
NR 46
TC 11
Z9 11
U1 0
U2 6
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 AUG
PY 2010
VL 299
IS 2
BP C399
EP C410
DI 10.1152/ajpcell.00039.2009
PG 12
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA 632CK
UT WOS:000280397600024
PM 20445173
ER
PT J
AU Lauritzen, HPMM
Schertzer, JD
AF Lauritzen, Hans P. M. M.
Schertzer, Jonathan D.
TI Measuring GLUT4 translocation in mature muscle fibers
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Review
DE glucose transporter 4; green fluorescent protein; exofacial-tag;
diabetes; glucose transport; metabolism; insulin resistance; confocal
microscopy; intravital microscopy
ID RAT SKELETAL-MUSCLE; CELL-SURFACE GLUT4; INCREASES GLUCOSE-TRANSPORT;
TRANSVERSE TUBULAR SYSTEM; GREEN-FLUORESCENT PROTEIN; LIVING MICE;
T-TUBULES; GENE-TRANSFER; INSULIN STIMULATION; VESICLE DYNAMICS
AB Lauritzen HP, Schertzer JD. Measuring GLUT4 translocation in mature muscle fibers. Am J Physiol Endocrinol Metab 299: E169-E179, 2010. First published May 25, 2010; doi:10.1152/ajpendo.00066.2010.-Skeletal muscle is the major tissue for postprandial glucose disposal. Facilitated glucose uptake into muscle fibers is mediated by increases in surface membrane levels of the glucose transporter GLUT4 via insulin-and/or muscle contraction-mediated GLUT4 translocation. However, the regulatory mechanisms controlling GLUT4 translocation in skeletal muscle have been difficult to characterize at the cell biology level due to muscle tissue complexity. Muscle cell culture models have improved our understanding of GLUT4 translocation and glucose transport regulation, but in vitro muscle models lack many of the characteristics of mature muscle fibers. Thus, the molecular and cellular details of GLUT4 translocation in mature skeletal muscle are deficient. The objective of this review is to highlight how advances in recent experimental approaches translate into an enhanced understanding of the regulation of GLUT4 translocation and glucose transport in mature skeletal muscle.
C1 [Lauritzen, Hans P. M. M.] Joslin Diabet Ctr, Div Res, Boston, MA 02215 USA.
[Lauritzen, Hans P. M. M.] Harvard Univ, Sch Med, Boston, MA USA.
[Schertzer, Jonathan D.] Hosp Sick Children, Cell Biol Program, Toronto, ON M5G 1X8, Canada.
RP Lauritzen, HPMM (reprint author), Joslin Diabet Ctr, Div Res, Room 525,1 Joslin Pl, Boston, MA 02215 USA.
EM Hans.Lauritzen@joslin.harvard.edu
FU Weimann Foundation; Faculty of Health Sciences, University of
Copenhagen; Beckett Foundation; Danish National Research Foundation;
Canadian Institutes of Health Research; Canadian Diabetes Association
FX This work was supported by the Weimann Foundation; the Faculty of Health
Sciences, University of Copenhagen; the Beckett Foundation; and the
Danish National Research Foundation. J. D. Schertzer is supported by the
Canadian Institutes of Health Research and the Canadian Diabetes
Association.
NR 65
TC 17
Z9 18
U1 1
U2 7
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 AUG
PY 2010
VL 299
IS 2
BP E169
EP E179
DI 10.1152/ajpendo.00066.2010
PG 11
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 622IG
UT WOS:000279654600004
PM 20501875
ER
PT J
AU Chen, KT
Malo, MS
Moss, AK
Zeller, S
Johnson, P
Ebrahimi, F
Mostafa, G
Alam, SN
Ramasamy, S
Warren, HS
Hohmann, EL
Hodin, RA
AF Chen, Kathryn T.
Malo, Madhu S.
Moss, Angela K.
Zeller, Skye
Johnson, Paul
Ebrahimi, Farzad
Mostafa, Golam
Alam, Sayeda N.
Ramasamy, Sundaram
Warren, H. Shaw
Hohmann, Elizabeth L.
Hodin, Richard A.
TI Identification of specific targets for the gut mucosal defense factor
intestinal alkaline phosphatase
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Article
DE lipopolysaccharide; Toll-like receptors
ID INFLAMMATORY-BOWEL-DISEASE; ANTIBIOTIC-INDUCED RELEASE;
PARENTERAL-NUTRITION; ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; ENTERAL
NUTRITION; GENE-EXPRESSION; KNOCKOUT MICE; BACTERIAL-DNA;
LIPOPOLYSACCHARIDE
AB Chen KT, Malo MS, Moss AK, Zeller S, Johnson P, Ebrahimi F, Mostafa G, Alam SN, Ramasamy S, Warren HS, Hohmann EL, Hodin RA. Identification of specific targets for the gut mucosal defense factor intestinal alkaline phosphatase. Am J Physiol Gastro-intest Liver Physiol 299: G467-G475, 2010. First published May 20, 2010; doi: 10.1152/ajpgi.00364.2009.-Intestinal alkaline phosphatase (IAP) is a small intestinal brush border enzyme that has been shown to function as a gut mucosal defense factor, but its precise mechanism of action remains unclear. We investigated the effects of IAP on specific bacteria and bacterial components to determine its molecular targets. Purulent fluid from a cecal ligation and puncture model, specific live and heat-killed bacteria (Escherichia coli, Salmonella typhimurium, and Listeria monocytogenes), and a variety of proinflammatory ligands (LPS, CpG DNA, Pam-3-Cys, flagellin, and TNF) were incubated with or without calf IAP (cIAP). Phosphate release was determined by using a malachite green assay. The various fluids were applied to target cells (THP-1, parent HT-29, and IAP-expressing HT-29 cells) and IL-8 secretion measured by ELISA. cIAP inhibited IL-8 induction by purulent fluid in THP-1 cells by >35% (P < 0.005). HT29-IAP cells had a reduced IL-8 response specifically to gram-negative bacteria; >90% reduction compared with parent cells (P < 0.005). cIAP had no effect on live bacteria but attenuated IL-8 induction by heat-killed bacteria by >40% (P < 0.005). cIAP exposure to LPS and CpG DNA caused phosphate release and reduced IL-8 in cell culture by >50% (P < 0.005). Flagellin exposure to cIAP also resulted in reduced IL-8 secretion by >40% (P < 0.005). In contrast, cIAP had no effect on TNF or Pam-3-Cys. The mechanism of IAP action appears to be through dephosphorylation of specific bacterial components, including LPS, CpG DNA, and flagellin, and not on live bacteria themselves. IAP likely targets these bacterially derived molecules in its role as a gut mucosal defense factor.
C1 [Chen, Kathryn T.; Malo, Madhu S.; Moss, Angela K.; Ebrahimi, Farzad; Mostafa, Golam; Alam, Sayeda N.; Ramasamy, Sundaram; Hodin, Richard A.] Harvard Univ, Dept Surg, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
[Zeller, Skye; Johnson, Paul; Warren, H. Shaw; Hohmann, Elizabeth L.] Harvard Univ, Div Infect Dis, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
[Chen, Kathryn T.] Univ Minnesota, Dept Surg, Minneapolis, MN 55455 USA.
RP Hodin, RA (reprint author), Harvard Univ, Dept Surg, Massachusetts Gen Hosp, Sch Med, 15 Parkman St,Wang 460, Boston, MA 02114 USA.
EM rhodin@partners.org
OI Kuhnen, Angela/0000-0003-4944-9143
FU National Institute of Diabetes and Digestive and Kidney Diseases
[R01DK050623, R01DK047186, T325T3DK007754]
FX This study was supported by National Institute of Diabetes and Digestive
and Kidney Diseases Grants R01DK050623, R01DK047186, and T325T3DK007754.
NR 51
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U1 0
U2 7
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1857
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD AUG
PY 2010
VL 299
IS 2
BP G467
EP G475
DI 10.1152/ajpgi.00364.2009
PG 9
WC Gastroenterology & Hepatology; Physiology
SC Gastroenterology & Hepatology; Physiology
GA 633EU
UT WOS:000280483200020
PM 20489044
ER
PT J
AU Vaporidi, K
Francis, RC
Bloch, KD
Zapol, WM
AF Vaporidi, Katerina
Francis, Roland C.
Bloch, Kenneth D.
Zapol, Warren M.
TI Nitric oxide synthase 3 contributes to ventilator-induced lung injury
SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
LA English
DT Article
DE superoxide; pulmonary edema; inflammation
ID TIDAL VOLUME; ENDOTHELIAL-CELLS; MECHANICAL-STRESS; REDOX REGULATION;
DEFICIENT MICE; MOUSE MODEL; KAPPA-B; TETRAHYDROBIOPTERIN; INHIBITION;
KINASE
AB Vaporidi K, Francis RC, Bloch KD, Zapol WM. Nitric oxide synthase 3 contributes to ventilator-induced lung injury. Am J Physiol Lung Cell Mol Physiol 299: L150-L159, 2010. First published May 7, 2010; doi: 10.1152/ajplung.00341.2009.-Nitric oxide synthase ( NOS) depletion or inhibition reduces ventilator-induced lung injury (VILI), but the responsible mechanisms remain incompletely defined. The aim of this study was to elucidate the role of endothelial NOS, NOS3, in the pathogenesis of VILI in an in vivo mouse model. Wild-type and NOS3-deficient mice were ventilated with high-tidal volume (HVT; 40 ml/kg) for 4 h, with and without adding NO to the inhaled gas. Additional wild-type mice were pretreated with tetrahydrobiopterin and ascorbic acid, agents that can prevent NOS-generated superoxide production. Arterial blood gas tensions, histology, and lung mechanics were evaluated after 4 h of HVT ventilation. The concentration of protein, IgM, cytokines, malondialdehyde, and 8-isoprostane were measured in bronchoalveolar lavage fluid (BALF). Myeloperoxidase activity, total and oxidized glutathione levels, and NOS-derived superoxide production were measured in lung tissue homogenates. HVT ventilation induced VILI in wild-type mice, as reflected by decreased lung compliance, increased concentrations of protein and cytokines in BALF, and oxidative stress. All indices of VILI were ameliorated in NOS3-deficient mice. Augmenting pulmonary NO levels by breathing NO during mechanical ventilation did not increase lung injury in NOS3-deficient mice. HVT ventilation increased NOS-inhibitable superoxide production in lung extracts from wild-type mice but not in those from NOS3-deficient mice. Administration of tetrahydrobiopterin and ascorbic acid ameliorated VILI in wild-type mice. Our results indicate that NOS3 contributes to ventilator-induced lung injury via increased production of superoxide.
C1 [Zapol, Warren M.] Harvard Univ, Dept Anesthesia & Crit Care, Anesthesia Ctr Crit Care Res, Massachusetts Gen Hosp,Sch Med, Boston, MA 02114 USA.
RP Zapol, WM (reprint author), Harvard Univ, Dept Anesthesia & Crit Care, Anesthesia Ctr Crit Care Res, Massachusetts Gen Hosp,Sch Med, 55 Fruit St, Boston, MA 02114 USA.
EM wzapol@partners.org
FU National Heart, Lung, and Blood Institute [HL-42397]; Massachusetts
General Hospital (MGH); IKARIA
FX This work was supported, in part, by National Heart, Lung, and Blood
Institute Grant HL-42397 ( to W. M. Zapol) and by a sponsored research
agreement between the Massachusetts General Hospital (MGH) and IKARIA.
NR 42
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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 AUG
PY 2010
VL 299
IS 2
BP L150
EP L159
DI 10.1152/ajplung.00341.2009
PG 10
WC Physiology; Respiratory System
SC Physiology; Respiratory System
GA 644OQ
UT WOS:000281389000002
PM 20453164
ER
PT J
AU O'Tierney, PF
Anderson, DF
Faber, JJ
Louey, S
Thornburg, KL
Giraud, GD
AF O'Tierney, P. F.
Anderson, D. F.
Faber, J. J.
Louey, S.
Thornburg, K. L.
Giraud, G. D.
TI Reduced systolic pressure load decreases cell-cycle activity in the
fetal sheep heart
SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE
PHYSIOLOGY
LA English
DT Article
DE blood pressure; enalaprilat; hyperplasia; cardiomyocyte
ID CARDIAC MYOCYTES; VENOUS HYPERTENSION; ANGIOTENSIN-II; NEWBORN LAMBS;
OVINE FETUS; RAT HEARTS; CARDIOMYOCYTES; HYPERTROPHY; MATURATION; PLASMA
AB O'Tierney PF, Anderson DF, Faber JJ, Louey S, Thornburg KL, Giraud GD. Reduced systolic pressure load decreases cell-cycle activity in the fetal sheep heart. Am J Physiol Regul Integr Comp Physiol 299: R573-R578, 2010. First published May 19, 2010; doi: 10.1152/ajpregu.00754.2009.-The fetal heart is highly sensitive to changes in mechanical load. We have previously demonstrated that increased cardiac load can stimulate cell cycle activity and maturation of immature cardiomyocytes, but the effects of reduced load are not known. Sixteen fetal sheep were given either continuous intravenous infusion of lactated Ringer solution (LR) or enalaprilat, an angiotensin-converting enzyme inhibitor beginning at 127 days gestational age. After 8 days, fetal arterial pressure in the enalaprilat-infused fetuses (23.8 +/- 2.8 mmHg) was lower than that of control fetuses (47.5 +/- 4.7 mmHg) (P < 0.0001). Although the body weights of the two groups of fetuses were similar, the heart weight-to-body weight ratios of the enalaprilat-infused fetuses were less than those of the LR-infused fetuses (5.6 +/- 0.5 g/kg vs. 7.0 +/- 0.6 g/kg, P < 0.0001). Dimensions of ventricular myocytes were not different between control and enalaprilat-infused fetuses. However, there was a significant decrease in cell cycle activity in both the right ventricle (P < 0.005) and the left ventricle (P < 0.002) of the enalaprilat-infused fetuses. Thus, we conclude a sustained reduction in systolic pressure load decreases hyperplastic growth in the fetal heart.
C1 [O'Tierney, P. F.; Anderson, D. F.; Faber, J. J.; Louey, S.; Thornburg, K. L.; Giraud, G. D.] Oregon Hlth & Sci Univ, Heart Res Ctr, Portland, OR 97239 USA.
[Thornburg, K. L.; Giraud, G. D.] Oregon Hlth & Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97239 USA.
[Anderson, D. F.; Faber, J. J.; Louey, S.; Thornburg, K. L.; Giraud, G. D.] Oregon Hlth & Sci Univ, Dept Med Cardiovasc Med, Portland, OR 97239 USA.
[Giraud, G. D.] Portland VA Med Ctr, Portland, OR USA.
RP Giraud, GD (reprint author), Oregon Hlth & Sci Univ, Heart Res Ctr CH15H, Div Cardiovasc Med, Portland, OR 97239 USA.
EM giraudg@ohsu.edu
FU American Heart Association [0720139Z]; National Institutes of Health
[P01HD34430]
FX Perrie O'Tierney is a recipient of an American Heart Association
Postdoctoral Fellowship (0720139Z). This research was funded by a
National Institutes of Health Program Project Grant (P01HD34430), the
Department of Veterans Affairs, and the M. Lowell Edwards Endowment.
NR 24
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U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6119
J9 AM J PHYSIOL-REG I
JI Am. J. Physiol.-Regul. Integr. Comp. Physiol.
PD AUG
PY 2010
VL 299
IS 2
BP R573
EP R578
DI 10.1152/ajpregu.00754.2009
PG 6
WC Physiology
SC Physiology
GA 634GW
UT WOS:000280569800019
PM 20484695
ER
PT J
AU Mount, DB
AF Mount, David B.
TI Regulated endocytosis of NCC
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
ID NA+-CL-COTRANSPORTER; SODIUM-CHLORIDE COTRANSPORTER; BLOOD-PRESSURE;
MOLECULAR PHYSIOLOGY; SIGNALING PATHWAY; DIETARY SALT; WNK KINASES;
RAT-KIDNEY; PHOSPHORYLATION; HYPERTENSION
C1 [Mount, David B.] VABHS, Div Renal, Boston, MA 02130 USA.
[Mount, David B.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA USA.
RP Mount, DB (reprint author), VABHS, Div Renal, 150 S Huntington Ave, Boston, MA 02130 USA.
EM dmount@rics.bwh.harvard.edu
FU NIDDK NIH HHS [DK070756]
NR 35
TC 2
Z9 2
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD AUG
PY 2010
VL 299
IS 2
BP F297
EP F299
DI 10.1152/ajprenal.00280.2010
PG 3
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 634FV
UT WOS:000280566600002
PM 20504880
ER
PT J
AU Baggett, TP
Rigotti, NA
AF Baggett, Travis P.
Rigotti, Nancy A.
TI Cigarette Smoking and Advice to Quit in a National Sample of Homeless
Adults
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID ADVERSE CHILDHOOD EXPERIENCES; NUTRITION EXAMINATION SURVEY; HEALTH
INTERVIEW SURVEY; UNITED-STATES; RISK-FACTORS; FOOD INSUFFICIENCY;
SUBSTANCE-ABUSE; CESSATION; WOMEN; OCCUPATION
AB Background: Cigarette smoking is common among homeless people, but its characteristics in this vulnerable population have not been studied at a national level. Whether homeless smokers receive advice to quit from healthcare providers is also unknown.
Purpose: To determine the prevalence and predictors of current cigarette smoking, smoking cessation, and receipt of clinician advice to quit in a national sample of homeless adults.
Methods: This study analyzed data from 966 adult respondents to the 2003 Health Care for the Homeless User Survey, representing more than 436,000 people nationally. Using multivariable logistic regression, the independent predictors of smoking, quitting, and receiving advice to quit were identified. Analyses were conducted in 2008-2009.
Results: The prevalence of current smoking was 73%. The lifetime quit rate among ever smokers was 9%. Among past-year smokers, 54% reported receiving clinician advice to quit. Factors independently associated with current smoking included out-of-home placement in childhood (AOR=2.79, 95% CI=1.03, 7.52); victimization while homeless (AOR=2.36, 95% CI=1.15, 4.83); past-year employment (AOR=2.52, 95% CI=1.13, 5.58); and prior illicit drug use (AOR=7.21, 95% CI=3.11, 16.7) or problem alcohol use (AOR=7.42, 95% CI=2.51, 21.9). Respondents with multiple homeless episodes had higher odds of receiving quit advice (AOR=2.51, 95% CI=1.30, 4.83) but lower odds of quitting (AOR=0.47, 95% CI=0.29, 0.78).
Conclusions: Compared to the general population, homeless people are far more likely to smoke and much less likely to quit, even though more than half of smokers received quit advice in the past year. Interventions for homeless smokers should address the unique comorbidities and vulnerabilities of this population. (Am J Prey Med 2010;39(2):164-172) (C) 2010 American Journal of Preventive Medicine
C1 [Baggett, Travis P.; Rigotti, Nancy A.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Rigotti, Nancy A.] Massachusetts Gen Hosp, Tobacco Res & Treatment Ctr, Boston, MA 02114 USA.
[Baggett, Travis P.; Rigotti, Nancy A.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Baggett, TP (reprint author), 5 Staniford St,9th Floor, Boston, MA 02114 USA.
EM tbaggett@partners.org
FU NHLBI NIH HHS [K24 HL4440]
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U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD AUG
PY 2010
VL 39
IS 2
BP 164
EP 172
DI 10.1016/j.amepre.2010.03.024
PG 9
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 632MP
UT WOS:000280429100008
PM 20621264
ER
PT J
AU Baldessarini, RJ
Tondo, L
Ghiani, C
Lepri, B
AF Baldessarini, Ross J.
Tondo, Leonardo
Ghiani, Carmen
Lepri, Beatrice
TI Illness Risk Following Rapid Versus Gradual Discontinuation of
Antidepressants
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID LONG-TERM TREATMENT; LITHIUM TREATMENT; BIPOLAR DISORDER; MAJOR
DEPRESSION; DRUG-TREATMENT; WITHDRAWAL; ABRUPT; MAINTENANCE; PREVENTION;
MANAGEMENT
AB Objective: Rapid discontinuation of some psychotropic medications is followed by discontinuation symptoms as well as an increased risk of early illness recurrence. Recurrence occurs earlier after rapid than after gradual discontinuation with lithium and antipsychotics. The authors compared illness recurrence after rapid versus gradual discontinuation of antidepressants.
Method: The authors compared 398 patients with a DSM-IV diagnosis of recurrent major depressive disorder (N=224), panic disorder (N=75), bipolar II disorder (N=62), or bipolar I disorder (N=37). Two-thirds were women, the mean age was 42 years, and patients were treated with antidepressants for a mean of 8.5 months. Antidepressants were discontinued clinically, either rapidly (over 1-7 days; N=188) or gradually (over 14 days or more; N=210), with a mean follow-up duration of 2.8 years; patients who were ill at discontinuation were excluded from the analysis. The authors compared latency to first new illness episodes using survival analysis and Cox multivariate modeling.
Results: The latency to first illness with rapid discontinuation was 0.4 times that with gradual discontinuation, and the latency after rapid discontinuation was one-fourth the estimated average previous interepisode interval in the same patients. The effect was similar across antidepressant classes and across years; the pace of discontinuation had less effect with drugs of prolonged half-life. The effect also varied by diagnosis (bipolar I >= panic > bipolar II >= major depressive disorder) but not by episodes per year, duration of index illness, use of concomitant treatment, or antidepressant dose or duration.
Conclusions: The recurrence risk for depression or panic was much shorter after rapid than after gradual discontinuation of antidepressants. These findings have implications for both clinical management and the design and interpretation of clinical trials.
C1 Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Psychopharmacol Program, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Int Consortium Mood Disorders Res, McLean Div, Boston, MA 02114 USA.
Univ Cagliari, Dept Psychol, Sardinia, Italy.
Lucio Bini Mood Disorders Ctr, Cagliari, Italy.
RP Baldessarini, RJ (reprint author), McLean Hosp, Mailman Res Ctr 312, 115 Mill St, Belmont, MA 02478 USA.
EM rjb@mclean.org
FU AstraZeneca; Auritec; Biotrofix; Eli Lilly; IFI; Janssen; JDS-Noven;
Luitpold; Merck; NeuroHealing; Novartis; Pfizer; SK Bio-Pharmaceuticals;
Solvay Corporation; Solvay; NIH [MH-073579]; Lucio Bini Private Donors
Mood Disorders Research Fund; Bruce J. Anderson Foundation; McLean
Private Donors Psychopharmacology Research Fund
FX Dr. Baldessarini has been a consultant to or received research support
from AstraZeneca, Auritec, Biotrofix, Eli Lilly, IFI, Janssen,
JDS-Noven, Luitpold, Merck, NeuroHealing, Novartis, Pfizer, SK
Bio-Pharmaceuticals, and Solvay Corporation and has taught or prepared
CME materials for New England Educational Institute and Pri-Med. Dr.
Tondo has been a consultant to or received research support from IFI,
Janssen, Eli Lilly, Merck, and Solvay. Drs. Ghiani and Lepri report no
financial relationships with commercial interests.; Supported in part by
NIH grant MH-073579 to Drs. Tondo and Baldessarini; the Lucio Bini
Private Donors Mood Disorders Research Fund to Dr. Tondo and a grant
from the Bruce J. Anderson Foundation and the McLean Private Donors
Psychopharmacology Research Fund to Dr. Baldessarini.
NR 36
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U1 1
U2 11
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 AUG
PY 2010
VL 167
IS 8
BP 934
EP 941
DI 10.1176/appi.ajp.2010.09060880
PG 8
WC Psychiatry
SC Psychiatry
GA 634OS
UT WOS:000280593400010
PM 20478876
ER
PT J
AU Papakostas, GI
Mischoulon, D
Shyu, I
Alpert, JE
Fava, M
AF Papakostas, George I.
Mischoulon, David
Shyu, Irene
Alpert, Jonathan E.
Fava, Maurizio
TI S-Adenosyl Methionine (SAMe) Augmentation of Serotonin Reuptake
Inhibitors for Antidepressant Nonresponders With Major Depressive
Disorder: A Double-Blind, Randomized Clinical Trial
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID STAR-ASTERISK-D; OUTCOMES
AB Objective: Despite the progressive increase in the number of antidepressants, many patients with major depressive disorder continue to be symptomatic. Clearly, there is an urgent need to develop better tolerated and more effective treatments for this disorder. The use of S-adenosyl methionine (SAMe), a naturally occurring molecule that serves as a methyl donor in human cellular metabolism, as adjunctive treatment for antidepressant nonresponders with major depressive disorder represents one such effort toward novel pharmacotherapy development.
Method: Participants were 73 serotonin reuptake inhibitor (SRI) nonresponders with major depressive disorder enrolled in a 6-week, double-blind, randomized trial of adjunctive oral SAMe (target dose: 800 mg/twice daily). Patients continued to receive their SRI treatment at a stable dose throughout the 6-week trial. The primary outcome measure for the study was the response rates according to the 17-item Hamilton Depression Rating Scale (HAM D).
Results: The HAM D response and remission rates were higher for patients treated with adjunctive SAMe (36.1% and 25.8%, respectively) than adjunctive placebo (17.6% versus 11.7%, respectively). The number needed to treat for response and remission was approximately one in six and one in seven, respectively. There was no statistically significant difference in the proportion of SAMe- versus placebo-treated patients who discontinued the trial for any reason (20.6% versus 29.5%, respectively), due to adverse events (5.1% versus 8.8%, respectively), or due to inefficacy (5.1% versus 11.7%, respectively).
Conclusions: These preliminary results suggest that SAMe can be an effective, well-tolerated, and safe adjunctive treatment strategy for SRI nonresponders with major depressive disorder and warrant replication.
C1 [Papakostas, George I.; Mischoulon, David; Shyu, Irene; Alpert, Jonathan E.; Fava, Maurizio] Harvard Univ, Massachusetts Gen Hosp, Depress Clin & Res Program, Sch Med,Ctr Treatment Resistant Depress, Boston, MA 02114 USA.
RP Papakostas, GI (reprint author), Harvard Univ, Massachusetts Gen Hosp, Depress Clin & Res Program, Sch Med,Ctr Treatment Resistant Depress, 15 Parkman St,WACC 812, Boston, MA 02114 USA.
EM gpapakostas@partners.org
RI Papakostas, George/I-6905-2013;
OI Papakostas, George/0000-0002-2465-5103; Alpert,
Jonathan/0000-0002-4332-908X
FU Bristol-Myers Squibb; Forest Pharmaceuticals; National Institute of
Mental Health [5-K23 MH-069629]; Pamlab; Pfizer; Ridge Diagnostics;
Abbott Laboratories; Alkermes; Aspect Medical Systems; AstraZeneca;
Cephalon; Cyberonics; Eli Lilly; GlaxoSmithKline; J and J
Pharmaceuticals; Lichtwer Pharma GmbH; Lorex Pharmaceuticals; Novartis;
Organon; Pharmavite; Roche; Sanofi/Synthelabo; Solvay Pharmaceuticals;
Wyeth-Ayerst Laboratories; Bio Research; Brain-Cells; Clinical Trial
Solutions; Ganeden Biotech; NARSAD; National Center for Complementary
and Alternative Medicine; National Institute on Drug and Alcohol Abuse;
Organon Inc.; Sanofi-Aventis; Shire; Synthelabo; Advanced Meeting
Partners; American Psychiatric Association; Belvoir;
Boehringer-Ingelheim; Imedex; PharmaStar; Massachusetts General Hospital
Psychiatry Academy/Primedia; Massachusetts General Hospital Psychiatry
Academy/Reed-Elsevier; UBC Pharma
FX Dr. Papakostas has served as a consultant for AstraZeneca, Bristol-Myers
Squibb, Eli Lilly, GlaxoSmithKline, Evotec AG, Inflabloc
Pharmaceuticals, Jazz Pharmaceuticals, Otsuka Pharmaceuticals, Pamlab,
Pfizer, Pierre Fabre Laboratories, Shire Pharmaceuticals, and Wyeth; has
received honoraria from AstraZeneca, Bristol-Myers Squibb, Eli Lilly,
Evotec AG, GlaxoSmithKline, Inflabloc Pharmaceuticals, Jazz
Pharmaceuticals, Lundbeck, Otsuka Pharmaceuticals, Pamlab, Pfizer,
Pierre Fabre Laboratories, Shire Pharmaceuticals, Titan Pharmaceuticals,
and Wyeth; he has received research support from Bristol-Myers Squibb,
Forest Pharmaceuticals, the National Institute of Mental Health, Pamlab,
Pfizer, and Ridge Diagnostics (formerly known as Precision Human
Biolaboratories); and he has served on the speaker's bureau for
Bristol-Myers Squibb and Pfizer. Dr. Mischoulon has received research
support for other clinical trials in the form of donated medications
from Amarin (Laxdale), Bristol-Myers Squibb, Cederroth, Lichtwer Pharma
GmbH, Nordic Naturals, and Swiss Medica; he has received consulting and
writing honoraria from Pamlab; he has received speaking honoraria from
Bristol-Myers Squibb, Nordic Naturals, Pfizer, Pamlab, and Virbac as
well as from Reed Medical Education (a company working as a logistics
collaborator for the Massachusetts General Hospital Psychiatry Academy);
and he has received royalty income from Back Bay Scientific for PMS
Escape (patent application pending). Dr. Alpert has received research
support from Abbott Laboratories, Alkermes, Aspect Medical Systems,
AstraZeneca, Cephalon, Bristol-Myers Squibb, Cyberonics, Eli Lilly,
Forest Pharmaceuticals, GlaxoSmithKline, J and J Pharmaceuticals,
Lichtwer Pharma GmbH, Lorex Pharmaceuticals, Novartis, Organon, Pamlab,
Pfizer, Pharmavite, Roche, Sanofi/Synthelabo, Solvay Pharmaceuticals,
and Wyeth-Ayerst Laboratories; he has participated on the advisory
boards of or as a consultant to Eli Lilly, Pamlab, and Pharmavite; and
he has received speaker's honoraria from Eli Lilly, Janssen, Organon,
and Reed Medical Education. Dr. Fava has received research support from
Abbott Laboratories, Alkermes, Aspect Medical Systems, AstraZeneca, Bio
Research, Brain-Cells, Bristol-Myers Squibb, Cephalon, Clinical Trial
Solutions, Eli Lilly, Forest Pharmaceuticals, Ganeden Biotech,
GlaxoSmithKline, J and J Pharmaceuticals, Lichtwer Pharma GmbH, Lorex
Pharmaceuticals, NARSAD, the National Center for Complementary and
Alternative Medicine, the National Institute on Drug and Alcohol Abuse,
the National Institute of Mental Health, Novartis, Organon Inc.; ,
Pamlab, Pfizer, Pharmavite, Roche, Sanofi-Aventis, Shire, Solvay
Pharmaceuticals, Synthelabo, and Wyeth-Ayerst Laboratories; he has
served on the advisory boards of or as a consultant to Abbott
Laboratories, Amarin, Aspect Medical Systems, AstraZeneca, Auspex
Pharmaceuticals, Bayer AG, Best Practice Project Management, BioMarin
Pharmaceuticals, Biovail Pharmaceuticals, Brain-Cells, Bristol-Myers
Squibb, Cephalon, Clinical Trials Solutions, CNS Response, Compellis,
Cypress Pharmaceuticals, Dov Pharmaceuticals, Eli Lilly, EPIX
Pharmaceuticals, Euthymics Bioscience, Fabre-Kramer Pharmaceuticals,
Forest Pharmaceuticals, GlaxoSmithKline, Grunenthal GmbH Janssen
Pharmaceutica, Jazz Pharmaceuticals, J and J Pharmaceuticals, Knoll
Pharmaceuticals, Labopharm, Lorex Pharmaceuticals, Lundbeck, MedAvante,
Merck, Methylation Sciences, Neuronetics, Novartis, Nutrition 21,
Organon, Pamlab, Pfizer, PharmaStar, Pharmavite, Precision Human
Biolaboratory, PsychoGenics, Roche, Sanoi-Aventis, Sepracor,
Schering-Plough, Solvay Pharmaceuticals, Somaxon, Somerset
Pharmaceuticals, Synthelabo, Takeda, Tetragenex, Trans-Form
Pharmaceuticals, Transcept Pharmaceuticals, Vanda Pharmaceuticals, and
Wyeth-Ayerst Laboratories; he has received speaker and publishing fees
from Advanced Meeting Partners, the American Psychiatric Association,
AstraZeneca, Belvoir, Boehringer-Ingelheim, Bristol-Myers Squibb,
Cephalon, Eli Lilly, Forest Pharmaceuticals, GlaxoSmithKline, Imedex,
Novartis, Organon, Pfizer, PharmaStar, Massachusetts General Hospital
Psychiatry Academy/Primedia, Massachusetts General Hospital Psychiatry
Academy/Reed-Elsevier, UBC Pharma, and Wyeth-Ayerst Laboratories; he is
a shareholder with Compellis; he has patent applications for sequential
parallel comparison of design and for a combination of azapirones and
bupropion in major depressive disorder; and he receives copyright
royalties for the following Massachusetts General Hospital assessment
tools: the Cognitive and Physical Functioning Questionnaire, the Sexual
Functioning Inventory, the Antidepressant Treatment Response
Questionnaire, the Discontinuation-Emergent Sign and Symptom scale, and
SAFER. Ms. Shyu reports no financial relationships with commercial
interests.; Funded by a National Institute of Mental Health grant (5-K23
MH-069629).
NR 16
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U1 4
U2 12
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 AUG
PY 2010
VL 167
IS 8
BP 942
EP 948
DI 10.1176/appi.ajp.2009.09081198
PG 7
WC Psychiatry
SC Psychiatry
GA 634OS
UT WOS:000280593400011
PM 20595412
ER
PT J
AU Kimerling, R
Street, AE
Pavao, J
Smith, MW
Cronkite, RC
Holmes, TH
Frayne, SM
AF Kimerling, Rachel
Street, Amy E.
Pavao, Joanne
Smith, Mark W.
Cronkite, Ruth C.
Holmes, Tyson H.
Frayne, Susan M.
TI Military-Related Sexual Trauma Among Veterans Health Administration
Patients Returning From Afghanistan and Iraq
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID MENTAL-HEALTH; ASSAULT HISTORY; FEMALE VETERANS; WOMEN; CARE; WAR;
OUTPATIENTS; HARASSMENT; PREVALENCE; DISCLOSURE
AB We examined military-related sexual trauma among deployed Operation Enduring Freedom and Operation Iraqi Freedom veterans. Of 125729 veterans who received Veterans Health Administration primary care or mental health services, 15.1% of the women and 0.7% of the men reported military sexual trauma when screened. Military sexual trauma was associated with increased odds of a mental disorder diagnosis, including post-traumatic stress disorder, other anxiety disorders, depression, and substance use disorders. Sexual trauma is an important postdeployment mental health issue in this population. (Am J Public Health. 2010;100:1409-1412. doi:10.2105/ AJPH.2009.171793)
C1 [Kimerling, Rachel; Pavao, Joanne] VA Palo Alto Hlth Care Syst, Natl Ctr PTSD, Menlo Pk, CA 94025 USA.
[Kimerling, Rachel; Cronkite, Ruth C.; Frayne, Susan M.] VA Palo Alto Hlth Care Syst, Ctr Hlth Care Evaluat, Menlo Pk, CA 94025 USA.
[Street, Amy E.] VA Boston Hlth Care Syst, Natl Ctr Posttraumat Stress Disorder, Boston, MA USA.
[Street, Amy E.] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA.
[Smith, Mark W.] VA Palo Alto Hlth Care Syst, Hlth Econ Resource Ctr, Menlo Pk, CA 94025 USA.
[Smith, Mark W.; Cronkite, Ruth C.] Stanford Univ, Ctr Primary Care & Outcomes Res, Sch Med, Stanford, CA 94305 USA.
[Holmes, Tyson H.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
[Frayne, Susan M.] Stanford Univ, Sch Med, Div Gen Internal Med, Stanford, CA 94305 USA.
RP Kimerling, R (reprint author), VA Palo Alto Hlth Care Syst, Natl Ctr PTSD, 795 Willow Rd,334 PTSD, Menlo Pk, CA 94025 USA.
EM rachel.kinzerling@va.gov
RI Smith, Mark/G-1522-2012;
OI Smith, Mark/0000-0002-4582-9088; Kimerling, Rachel/0000-0003-0996-4212
FU Health Services Research and Development Service, US Department of
Veterans Affairs [IAE 05-291, SDR 07-331]
FX Funding was provided by the Health Services Research and Development
Service, US Department of Veterans Affairs (IAE 05-291 and SDR 07-331).
NR 29
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U1 0
U2 13
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 AUG
PY 2010
VL 100
IS 8
BP 1409
EP 1412
DI 10.2105/AJPH.2009.171793
PG 4
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 656RR
UT WOS:000282354800015
PM 20558808
ER
PT J
AU Lillie-Blanton, M
Stone, VE
Jones, AS
Levi, J
Golub, ET
Cohen, MH
Hessol, NA
Wilson, TE
AF Lillie-Blanton, Marsha
Stone, Valerie E.
Jones, Alison Snow
Levi, Jeffrey
Golub, Elizabeth T.
Cohen, Mardge H.
Hessol, Nancy A.
Wilson, Tracey E.
TI Association of Race, Substance Abuse, and Health Insurance Coverage With
Use of Highly Active Antiretroviral Therapy Among HIV-Infected Women,
2005
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID INTERAGENCY HIV; UNITED-STATES; DRUG-USE; COHORT; CARE
AB Objectives. We examined racial/ethnic disparities in highly active antiretroviral therapy (HAART) use and whether differences are moderated by substance use or insurance status, using data from the Women's Interagency HIV Study (WIHS).
Methods. Logistic regression examined HAART use in a longitudinal cohort of women for whom HAART was clinically indicated in 2005 (N=1354).
Results. Approximately 3 of every 10 eligible women reported not taking HAART. African American and Hispanic women were less likely than were White women to use HAART. After we adjusted for potential confounders, the higher likelihood of not using HAART persisted for African American but not for Hispanic women. Uninsured and privately insured women, regardless of race/ethnicity, were less likely than were Medicaid enrollees to use HAART. Although alcohol use was related to HAART nonuse, illicit drug use was not.
Conclusions. These findings suggest that expanding and improving insurance coverage should increase access to antiretroviral therapy across racial/ethnic groups, but it is not likely to eliminate the disparity in use of HAART between African American and White women with HIV/AIDS. (Am J Public Health. 2010; 100:1493-1499. doi:10.2105/AJPH.2008.158949)
C1 [Lillie-Blanton, Marsha; Levi, Jeffrey] George Washington Univ, Sch Publ Hlth & Hlth Serv, Dept Hlth Policy, Washington, DC 20006 USA.
[Stone, Valerie E.] Massachusetts Gen Hosp, Primary Care Residency Program, Boston, MA 02114 USA.
[Stone, Valerie E.] Massachusetts Gen Hosp, Womens HIV AIDS Program, Boston, MA 02114 USA.
[Jones, Alison Snow] Wake Forest Univ, Bowman Gray Sch Med, Dept Social Sci & Hlth Policy, Winston Salem, NC USA.
[Golub, Elizabeth T.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Cohen, Mardge H.] Cook Cty Stroger Hosp, Chicago, IL USA.
[Hessol, Nancy A.] Univ Calif San Francisco, Dept Clin Pharm & Med, San Francisco, CA 94143 USA.
[Wilson, Tracey E.] Suny Downstate Med Ctr, Dept Community Hlth Sci, Brooklyn, NY 11203 USA.
RP Lillie-Blanton, M (reprint author), George Washington Univ, Sch Publ Hlth & Hlth Serv, Dept Hlth Policy, 2021 K St NW,Suite 800, Washington, DC 20006 USA.
EM lblanton@gwu.edu
FU 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 Institute on Drug Abuse; National Cancer Institute; National
Institute on Deafness and Other Communication Disorders; National Center
for Research Resources (UCSF-CTSI) [UL1 RR024131]
FX The Women's Interagency HIV Study (Wit-IS) is funded by the National
Institute of Allergy and Infectious Diseases (UO1-AI-35004,
UO1-AI-31834, UO1-AI-34994, UO1-AI-34989, UO1-AI-34993, and
UO1-AI-42590) and the National Institute of Child Health and Human
Development (UO1-HD-32632). The WIHS is cofunded by the National
Institute on Drug Abuse, the National Cancer Institute, and the National
Institute on Deafness and Other Communication Disorders. Funding is also
provided by the National Center for Research Resources (UCSF-CTSI grant
UL1 RR024131). The National Institute on Drug Abuse provided primary
funding for our study.
NR 18
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U1 2
U2 7
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 AUG
PY 2010
VL 100
IS 8
BP 1493
EP 1499
DI 10.2105/AJPH.2008.158949
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 656RR
UT WOS:000282354800029
PM 19910347
ER
PT J
AU Nishino, M
Jagannathan, JP
Ramaiya, NH
van den Abbeele, AD
AF Nishino, Mizuki
Jagannathan, Jyothi P.
Ramaiya, Nikhil H.
van den Abbeele, Annick D.
TI Revised RECIST Guideline Version 1.1: What Oncologists Want to Know and
What Radiologists Need to Know
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE CT; oncologic imaging; response assessment; Response Evaluation Criteria
in Solid Tumors; RECIST; RECIST 1.1; tumor measurement
ID GASTROINTESTINAL STROMAL TUMOR; IMATINIB MESYLATE;
HEPATOCELLULAR-CARCINOMA; RESPONSE EVALUATION; SOLID TUMORS;
LUNG-CANCER; CRITERIA; CAVITATION; EVALUATE; THERAPY
AB OBJECTIVE. The objectives of this article are to review the new Response Evaluation Criteria in Solid Tumors (RECIST) guideline, version 1.1, highlighting the major changes in the new version compared with the original RECIST guideline (version 1.0), and to present case examples with representative imaging.
CONCLUSION. Familiarity with the revised RECIST is essential in day-to-day oncologic imaging practice to provide up-to-date service to oncologists and their patients. Some of the changes in the revised RECIST affect how radiologists select, measure, and report target lesions.
C1 [Nishino, Mizuki; Jagannathan, Jyothi P.; Ramaiya, Nikhil H.; van den Abbeele, Annick D.] Dana Farber Canc Inst, Dept Imaging, Boston, MA 02115 USA.
RP Nishino, M (reprint author), Dana Farber Canc Inst, Dept Imaging, 44 Binney St, Boston, MA 02115 USA.
EM Mizuki_Nishino@dfci.harvard.edu
FU Agfa Healthcare/RSNA
FX M. Nishino is supported by a 2009-2011 Agfa Healthcare/RSNA research
scholar grant.
NR 15
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U1 2
U2 6
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 AUG
PY 2010
VL 195
IS 2
BP 281
EP 289
DI 10.2214/AJR.09.4110
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 629KT
UT WOS:000280197800003
PM 20651182
ER
PT J
AU de Prost, N
Tucci, MR
Melo, MFV
AF de Prost, Nicolas
Tucci, Mauro R.
Melo, Marcos F. Vidal
TI Assessment of Lung Inflammation With (18)F-FDG PET During Acute Lung
Injury
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Review
DE acute lung injury; acute respiratory distress syndrome; adults;
(18)F-FDG; PET
ID RESPIRATORY-DISTRESS-SYNDROME; POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL
GLUCOSE-UTILIZATION; DUAL-TIME-POINT; STANDARDIZED UPTAKE VALUES; HUMAN
ENDOTHELIAL-CELLS; FDG-PET; METABOLIC-ACTIVITY; ATHEROSCLEROTIC PLAQUES;
MECHANICAL VENTILATION
AB OBJECTIVE. The purpose of this review is to describe the current experimental and clinical data regarding the fundamentals and applications of (18)F-FDG PET during acute lung injury (ALI) and acute respiratory distress syndrome ( ARDS).
CONCLUSION. Lung inflammation is a key feature of ALI. During ALI, FDG PET can be used to monitor lung neutrophils, which are essential cells in the pathophysiologic mechanisms of ALI. Pulmonary FDG kinetics are altered during experimental and human ALI and are associated with regional lung dysfunction, histologic abnormalities, and prognosis. FDG PET may be a valuable noninvasive method for gaining comprehensive understanding of the mechanisms of ALI/ARDS and for evaluating therapeutic interventions.
C1 [de Prost, Nicolas; Tucci, Mauro R.; Melo, Marcos F. Vidal] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
RP Melo, MFV (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, 55 Fruit St, Boston, MA 02114 USA.
EM mvidalmelo@partners.org
OI de Prost, Nicolas/0000-0002-4833-4320
FU NIH [HL 5R01HL086827]; LEEM Recherche; Societe de Pneumologie de Langue
Francaise; CAPES (Brazilian Ministry of Education)
FX Supported by NIH grant HL 5R01HL086827. N. de Prost received a
scholarship from LEEM Recherche and the Societe de Pneumologie de Langue
Francaise. M. R. Tucci received a scholarship from CAPES (Brazilian
Ministry of Education).
NR 89
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U1 2
U2 4
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 AUG
PY 2010
VL 195
IS 2
BP 292
EP 300
DI 10.2214/AJR.10.4499
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 629KT
UT WOS:000280197800004
PM 20651183
ER
PT J
AU Ho, W
Broughton, DE
Donelan, K
Gazelle, GS
Hur, C
AF Ho, Wendy
Broughton, Darcy E.
Donelan, Karen
Gazelle, G. Scott
Hur, Chin
TI Analysis of Barriers to and Patients' Preferences for CT Colonography
for Colorectal Cancer Screening in a Nonadherent Urban Population
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE colorectal cancer screening; CT colonography; patient preferences
ID COMPUTED TOMOGRAPHIC COLONOGRAPHY; COLLEGE-OF-RADIOLOGY;
SOCIETY-TASK-FORCE; CONVENTIONAL COLONOSCOPY; VIRTUAL COLONOSCOPY;
ADENOMATOUS POLYPS; JOINT GUIDELINE; SURVEILLANCE; ACCEPTANCE
AB OBJECTIVE. The aim of this study was to evaluate patients' barriers against colorectal cancer screening tests and to assess patients' preferences and cost influences for CT colonography (CTC) in a nonadherent urban subpopulation.
SUBJECTS AND METHODS. Patients who had been offered colorectal cancer screening but were nonadherent were asked to participate in this questionnaire study. Patients' demographic information was obtained, and patients' reasons for not being screened were explored. Subjects were given an information sheet that described a CTC procedure and then were asked about their willingness to undergo CTC and about other relevant factors, such as fees.
RESULTS. One hundred seventy-five patients were invited to participate; 53 declined and 54 did not respond, which left 68 subjects to be included in the analysis. After being informed about CTC screening, most (83%) subjects stated that they would be willing to undergo a CTC study. However, 70% stated that they would not be willing to pay out-of-pocket fees if insurance did not cover the study, and even among the 30% who were willing to pay the fees, the average amount they were willing to pay ( mean, $244; median, $150) was well below currently charged rates.
CONCLUSION. Our study suggests that most nonadherent patients would be willing to undergo CTC as long as out-of-pocket fees are reasonable.
C1 [Ho, Wendy; Broughton, Darcy E.; Hur, Chin] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Ho, Wendy] Univ Calif Los Angeles, Ctr Digest Dis, Los Angeles, CA USA.
[Donelan, Karen; Gazelle, G. Scott; Hur, Chin] Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA.
[Donelan, Karen] Massachusetts Gen Hosp, Inst Hlth Policy, Boston, MA 02114 USA.
[Donelan, Karen; Gazelle, G. Scott; Hur, Chin] Harvard Univ, Sch Med, Boston, MA USA.
[Gazelle, G. Scott] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Gazelle, G. Scott] Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA.
RP Hur, C (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
EM chur@mgh-ita.org
OI Hur, Chin/0000-0002-2819-7576
FU American Gastroenterological Association's; National Cancer Institute
[K07CA107060]
FX This work was supported in part by the American Gastroenterological
Association's Research Scholar Award (grant to C. Hur) and the National
Cancer Institute (grant K07CA107060 to C. Hur).
NR 14
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U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD AUG
PY 2010
VL 195
IS 2
BP 393
EP 397
DI 10.2214/AJR.09.3500
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 629KT
UT WOS:000280197800016
PM 20651195
ER
PT J
AU Blake, MA
Prakash, P
Cronin, CG
AF Blake, Michael A.
Prakash, Priyanka
Cronin, Carmel G.
TI PET/CT for Adrenal Assessment
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Review
DE adrenal glands; adrenal incidentalomas; adrenal masses; PET/CT
ID POSITRON-EMISSION-TOMOGRAPHY; F-18-FDG PET/CT; MASSES; TUMORS; CT;
LESIONS; GLAND
C1 [Blake, Michael A.; Prakash, Priyanka; Cronin, Carmel G.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Blake, Michael A.; Prakash, Priyanka; Cronin, Carmel G.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Blake, MA (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St, Boston, MA 02114 USA.
EM mblake2@partners.org
NR 17
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Z9 5
U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD AUG
PY 2010
VL 195
IS 2
BP W91
EP W95
DI 10.2214/AJR.09.3845
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 629KT
UT WOS:000280197800039
PM 20651179
ER
PT J
AU Roh, JH
Srivastava, A
Lauwers, GY
An, J
Jang, KT
Park, CK
Sohn, TS
Kim, S
Kim, KM
AF Roh, Ji Hyeon
Srivastava, Amitabh
Lauwers, Gregory Y.
An, Jungsuk
Jang, Kee-Taek
Park, Cheol Keun
Sohn, Tae Sung
Kim, Sung
Kim, Kyoung-Mee
TI Micropapillary Carcinoma of Stomach A Clinicopathologic and
Immunohistochemical Study of 11 Cases
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE gastric; micropapillary; adenocarcinoma; immunohistochemistry
ID SALIVARY DUCT CARCINOMA; PROGNOSTIC-SIGNIFICANCE; GASTRIC-CANCER; SEROUS
CARCINOMA; POOR-PROGNOSIS; CELL CARCINOMA; PAROTID-GLAND;
ADENOCARCINOMA; EXPRESSION; MUC6
AB Micropapillary carcinoma (MPC) of the stomach is a rare, newly recognized entity, and only 2 patients with this histology have been reported. We investigated clinicopathologic features, expression of mucin (MUC2, MUC5AC, MUC6, CD10) and cytokeratin profiles (CK7 and CK20), epidermal growth factor receptors (EGFR and HER2), prognostic markers (p53 and Ki-67), and outcomes in 11 MPCs of the stomach. The proportion of MPC component ranged from 5% to 70%. Micropapillary features were often found at the deep advancing edge of the tumor. Endolymphatic tumor emboli were found in 10 cases (91%) and lymph node metastases were found in 4 cases (36%). In MPCs, positive expression was observed for Ki-67 (82%), CK7 (73%), EGFR (64%), p53 (64%), MUC5AC (45%), MUC6 (36%), and CK20 (27%). However, MUC2, CD10, and HER2 expression was negative in all cases. In 9 conventional adenocarcinomas and 11 papillary adenocarcinomas with multiple endolymphatic tumor emboli, used as control, positive expression was observed for Ki-67 (100%), CK7 (90%), EGFR (80%), CK20 (70%), p53 (70%), MUC5AC (70%), MUC6 (60%), MUC2 (40%), CD10 (25%), and HER2 (15%). Expression of MUC2, CK20, and the Ki-67 labeling index was significantly higher in control adenocarcinomas as compared with MPCs (P < 0.05). However, there was no significant difference in other clinicopathologic features and overall patient survival. Subclassification of MPCs into 2 subgroups according to the proportion of micropapillary component (cut-off value was 20%) failed to find any significant clinicopathologic differences (P > 0.05). Although MPCs in other organs show a poor prognosis, this does not seem to be true for gastric MPCs. Further larger studies are necessary to confirm our initial findings.
C1 [Roh, Ji Hyeon; An, Jungsuk; Jang, Kee-Taek; Park, Cheol Keun; Kim, Kyoung-Mee] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol, Seoul 135710, South Korea.
[Sohn, Tae Sung; Kim, Sung] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Surg, Seoul 135710, South Korea.
[Srivastava, Amitabh] Dartmouth Hitchcock Med Ctr Lebanon, Dartmouth Med Sch, Dept Pathol, Lebanon, NH USA.
[Lauwers, Gregory Y.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Kim, KM (reprint author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol, 50 Ilwon Dong, Seoul 135710, South Korea.
EM kkmkys@skku.edu
RI Kim, Sung/G-4114-2014
NR 36
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U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD AUG
PY 2010
VL 34
IS 8
BP 1139
EP 1146
DI 10.1097/PAS.0b013e3181e7043b
PG 8
WC Pathology; Surgery
SC Pathology; Surgery
GA 631TV
UT WOS:000280372900007
PM 20661012
ER
PT J
AU Sholl, LM
Barletta, JA
Yeap, BY
Chirieac, LR
Hornick, JL
AF Sholl, Lynette M.
Barletta, Justine A.
Yeap, Beow Y.
Chirieac, Lucian R.
Hornick, Jason L.
TI Sox2 Protein Expression is an Independent Poor Prognostic Indicator in
Stage I Lung Adenocarcinoma
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE Sox2; prognosis; lung; adenocarcinoma; immunohistochemistry; biomarkers
ID NONSMALL CELL; STEM-CELLS; CANCER; SURVIVAL; CARCINOMAS; SIGNATURE;
GENOME
AB Many patients with stage I nonsmall cell lung carcinoma will develop recurrence after surgical excision. Sox2 is a marker of embryonic stem cell pluripotency that is associated with aggressive tumor behavior and is expressed in a subset of lung adenocarcinomas. We hypothesized that Sox2 expression may provide prognostic information in early stage lung adenocarcinomas. We evaluated formalin-fixed, paraffinembedded tissue from 104 stage I lung adenocarcinomas resected between 1997 and 2000. Sox2 expression was analyzed by immunohistochemistry and compared with clinicopathologic features, time-to-progression, and overall survival (OS). Sox2 expression was detected in 50% of the cases and was more frequent in tumors from older and male patients but not significantly associated with smoking status, tumor stage, grade, or histologic subtype. Compared with Sox2-negative tumors, Sox2 expression predicted a shorter time-to-progression (49% vs. 82% at 5 y; P = 0.0006) and shorter OS (54% vs. 79% at 5 y; P = 0.004). By multivariate analysis, Sox2 expression predicted a greater risk of progression among men [hazard ratio (HR) 5.6; 95% confidence interval (CI) 2.3-13.8] and women (HR 2.1; 95% CI 0.8-5.7). Sox2 expression was associated with significantly shorter OS among men (HR 2.5; 95% CI 1.2-5.1), but not in women. Sox2 seems to be an independent predictor of poor outcome in stage I lung adenocarcinomas and may help stratify patients at increased risk for recurrence.
C1 [Sholl, Lynette M.; Barletta, Justine A.; Chirieac, Lucian R.; Hornick, Jason L.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Yeap, Beow Y.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA USA.
RP Hornick, JL (reprint author), Brigham & Womens Hosp, Dept Pathol, 75 Francis St, Boston, MA 02115 USA.
EM jhornick@partners.org
FU Dana-Farber/Harvard Cancer Center Specialized Programs of Research
Excellence (SPORE) [2P50 CA090578-06]
FX Supported in part by Dana-Farber/Harvard Cancer Center Specialized
Programs of Research Excellence (SPORE) in Lung Cancer 2P50 CA090578-06
(LRC). The authors have no financial disclosures.
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U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD AUG
PY 2010
VL 34
IS 8
BP 1193
EP 1198
DI 10.1097/PAS.0b013e3181e5e024
PG 6
WC Pathology; Surgery
SC Pathology; Surgery
GA 631TV
UT WOS:000280372900015
PM 20631605
ER
PT J
AU Afrin, LB
AF Afrin, Lawrence B.
TI Fatal Copper Deficiency From Excessive Use of Zinc-Based Denture
Adhesive
SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES
LA English
DT Article
DE Zinc toxicity; Copper deficiency; Sensorimotor neuropathy;
Myelodysplasia; Denture adhesive
ID NEUROLOGIC DISEASE; HYPOCUPREMIA; NEUROPATHY
AB Introduction: Human stores of zinc and copper exist in dynamic equilibrium; an increase in one causes a fall in the other, and clinical consequences of toxicity or deficiency of one or the other may result. Some of the most widely used denture adhesives are zinc based, creating a potential for zinc toxicity and corresponding copper deficiency. A case of denture adhesive-based zinc toxicity with corresponding copper deficiency leading to fatal ascending sensorimotor polyneuropathy was identified. The objectives of this study were to illustrate the evolution, and disparate response to treatment, of neurologic and hematologic abnormalities resulting from copper deficiency, and to discuss opportunities to mitigate denture adhesive-related zinc toxicity. Methods: Detailed clinical and laboratory data for the subject patient were compiled. The patient received copper supplementation. Copper and zinc levels were obtained posttreatment at varying intervals. Results: Hematologic and neurologic abnormalities progressed, as excessive use of zinc-based denture adhesive persisted. Hematologic and neurologic consultants were initially considered purely hematologic or neurologic diagnoses. Eventual consideration of unifying hypotheses led to definitive diagnosis 10 months after presentation. Hematologic abnormalities responded to copper supplementation, but neurologic abnormalities did not. The patient died of aspiration likely due to severe sensorimotor polyneuropathy. Conclusions: Early recognition of copper deficiency and improved warnings regarding excessive use of zinc-based denture adhesives may be the routes to improved outcomes.
C1 [Afrin, Lawrence B.] Med Univ S Carolina, Div Hematol Oncol, Charleston, SC 29425 USA.
[Afrin, Lawrence B.] Ralph H Johnson Vet Affairs Med Ctr, Hematol Oncol Sect, Med Serv, Charleston, SC USA.
RP Afrin, LB (reprint author), Med Univ S Carolina, Div Hematol Oncol, CSB903,MSC635,96 Jonathan Lucas St, Charleston, SC 29425 USA.
EM afrinl@musc.edu
NR 26
TC 13
Z9 13
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0002-9629
J9 AM J MED SCI
JI Am. J. Med. Sci.
PD AUG
PY 2010
VL 340
IS 2
BP 164
EP 168
DI 10.1097/MAJ.0b013e3181e3648c
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 635TC
UT WOS:000280678200016
PM 20555248
ER
PT J
AU Leach, JR
Rayz, VL
Soares, B
Wintermark, M
Mofrad, MRK
Saloner, D
AF Leach, Joseph R.
Rayz, Vitaliy L.
Soares, Bruno
Wintermark, Max
Mofrad, Mohammad R. K.
Saloner, David
TI Carotid Atheroma Rupture Observed In Vivo and FSI-Predicted Stress
Distribution Based on Pre-rupture Imaging
SO ANNALS OF BIOMEDICAL ENGINEERING
LA English
DT Article
DE Patient-specific; Vulnerable plaque; Atherosclerosis; Image-based
ID MULTIDETECTOR COMPUTED-TOMOGRAPHY; ATHEROSCLEROTIC PLAQUE RUPTURE;
FLUID-STRUCTURE INTERACTIONS; AMERICAN-HEART-ASSOCIATION;
HISTOPATHOLOGICAL CORRELATION; ASYMPTOMATIC INDIVIDUALS; CIRCUMFERENTIAL
STRESS; STRUCTURAL-ANALYSIS; SHEAR-STRESS; FIBROUS CAP
AB Atherosclerosis at the carotid bifurcation is a major risk factor for stroke. As mechanical forces may impact lesion stability, finite element studies have been conducted on models of diseased vessels to elucidate the effects of lesion characteristics on the stresses within plaque materials. It is hoped that patient-specific biomechanical analyses may serve clinically to assess the rupture potential for any particular lesion, allowing better stratification of patients into the most appropriate treatments. Due to a sparsity of in vivo plaque rupture data, the relationship between various mechanical descriptors such as stresses or strains and rupture vulnerability is incompletely known, and the patient-specific utility of biomechanical analyses is unclear. In this article, we present a comparison between carotid atheroma rupture observed in vivo and the plaque stress distribution from fluid-structure interaction analysis based on pre-rupture medical imaging. The effects of image resolution are explored and the calculated stress fields are shown to vary by as much as 50% with sub-pixel geometric uncertainty. Within these bounds, we find a region of pronounced elevation in stress within the fibrous plaque layer of the lesion with a location and extent corresponding to that of the observed site of plaque rupture.
C1 [Leach, Joseph R.] San Francisco VA Med Ctr, Dept Radiol, San Francisco, CA 94121 USA.
[Leach, Joseph R.; Mofrad, Mohammad R. K.; Saloner, David] UC Berkeley UC San Francisco Joint Grad Grp Bioen, Berkeley, CA USA.
[Leach, Joseph R.; Rayz, Vitaliy L.; Soares, Bruno; Wintermark, Max; Saloner, David] Univ Calif San Francisco, Med Ctr, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA.
RP Leach, JR (reprint author), San Francisco VA Med Ctr, Dept Radiol, Box 114D,4150 Clement St, San Francisco, CA 94121 USA.
EM joseph.leach@ucsf.edu
OI Wintermark, Max/0000-0002-6726-3951; Soares, Bruno/0000-0003-4185-6940
FU American Heart Association [0715072Y]; NIH [1K25NS059891]; VA; NINDS
[NS059944]
FX The authors would like to thank Tarik Tihan for review of the
image-based plaque geometry. Funding support was provided by the
following grants: American Heart Association Pre-doctoral Fellowship
0715072Y (JL), NIH Grant 1K25NS059891 (VR), VA MERIT Review Award (DS),
and NS059944 from the NINDS.
NR 54
TC 21
Z9 24
U1 3
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0090-6964
J9 ANN BIOMED ENG
JI Ann. Biomed. Eng.
PD AUG
PY 2010
VL 38
IS 8
BP 2748
EP 2765
DI 10.1007/s10439-010-0004-8
PG 18
WC Engineering, Biomedical
SC Engineering
GA 622RD
UT WOS:000279682000023
PM 20232151
ER
PT J
AU Farabaugh, A
Sonawalla, S
Johnson, DP
Witte, J
Papakostas, GI
Goodness, T
Clain, A
Baer, L
Mischoulon, D
Fava, M
Harley, R
AF Farabaugh, Amy
Sonawalla, Shamsah
Johnson, Daniel P.
Witte, Janet
Papakostas, George I.
Goodness, Tracie
Clain, Alisabet
Baer, Lee
Mischoulon, David
Fava, Maurizio
Harley, Rebecca
TI Early improvements in anxiety, depression, and anger/hostility symptoms
and response to antidepressant treatment
SO ANNALS OF CLINICAL PSYCHIATRY
LA English
DT Article
DE major depressive disorder; anxiety; hostility; depression; Symptom
Questionnaire
ID DISORDER; FLUOXETINE; PREDICTORS
AB BACKGROUND: The purpose of this study was to examine whether treatment response to fluoxetine by depressed outpatients was predicted by early improvement on any of 3 subscales (Anxiety, Depression, and Anger/Hostility) of the Symptom Questionnaire (SQ).
METHODS: We evaluated 169 depressed outpatients (52.6% female) between ages 18 and 65 (mean age, 40.3 +/- 10.6 years) meeting DSM-III-R criteria for major depressive disorder (MDD). All patients completed the SQ at baseline (week 0) and at weeks 2, 4, and 8 of treatment with fluoxetine 20 mg/d. We defined treatment response as a >= 50% reduction in score on the 17-item Hamilton Rating Scale for Depression, and early improvement on 3 SQ subscales (Anxiety, Depression, and Anger/Hostility) as a >= 30% reduction in score by week 2.
RESULTS: The percentage of patients with significant early improvement in anger was significantly greater than the percentage of those with early improvements in anxiety or depression. When early improvement on the Anxiety, Depression, and Anger/Hostility subscales of the SQ were assessed independently by logistic regression, all 3 subscales were predictors of response to treatment.
CONCLUSIONS: Early improvement in anger, anxiety, and depressive symptoms may predict response to antidepressant treatment among outpatients with MDD.
C1 [Farabaugh, Amy; Johnson, Daniel P.; Witte, Janet; Papakostas, George I.; Goodness, Tracie; Clain, Alisabet; Baer, Lee; Mischoulon, David; Fava, Maurizio] Massachusetts Gen Hosp, Depress Clin & Res Program, Dept Psychiat, Boston, MA 02114 USA.
[Sonawalla, Shamsah] Jaslok Hosp & Res Ctr, Mumbai, Maharashtra, India.
[Sonawalla, Shamsah] Duke Univ, Dept Psychiat & Behav Sci, Med Ctr, Durham, NC USA.
RP Farabaugh, A (reprint author), Massachusetts Gen Hosp, Depress Clin & Res Program, Dept Psychiat, 50 Staniford St,Suite 401, Boston, MA 02114 USA.
EM afarabaugh@partners.org
RI Papakostas, George/I-6905-2013
OI Papakostas, George/0000-0002-2465-5103
FU National Institute of Mental Health [5R10MH056057-05]; Forest
Pharmaceuticals; Bristol-Myers Squibb; Pamlab L.L.C.; Pfizer Inc; Ridge
Diagnostic
FX This research was supported in part by a grant to M. Fava from the
National Institute of Mental Health (5R10MH056057-05).; Dr. Farabaugh
has received research support from Forest Pharmaceuticals.; Dr.
Papakostas has served as a consultant for AstraZeneca, Bristol-Myers
Squibb, Eli Lilly and Company, Evotec AG, GlaxoSmithKline, Inflabloc
Pharmaceuticals, Jazz Pharmaceuticals, Otsuka Pharmaceuticals, Pamlab
L.L.C., Pfizer Inc, Pierre Fabre Laboratories, Shire Pharmaceuticals,
and Wyeth Pharmaceuticals. He has received honoraria from AstraZeneca,
Bristol-Myers Squibb, Eli Lilly and Company, Evotec AG, GlaxoSmithKline,
lnflabloc Pharmaceuticals, Jazz Pharmaceuticals, Lundbeck, Pamlab
L.L.C., Pfizer Inc, Pierre Fabre Laboratories, Shire Pharmaceuticals,
Titan Pharmaceuticals, and Wyeth Pharmaceuticals. He has received
research support from Bristol-Myers Squibb, Forest Pharmaceuticals, the
National Institute of Mental Health, Pamlab L.L.C., Pfizer Inc, and
Ridge Diagnostic (formerly known as Precision Human Biolaboratories). He
has served on the speakers bureau of Bristol-Myers Squibb and Pfizer
Inc. Dr. Fava has received research support from Abbott Laboratories,
Alkermes, Aspect Medical Systems, AstraZeneca, Bristol-Myers Squibb,
Cephalon, Clinical Trial Solutions L.L.C., Eli Lilly and Company, Forest
Pharmaceuticals, Ganeden, GlaxoSmithKline, J & J Pharmaceuticals,
Lichtwer Pharma GmbH, Lorex Pharmaceuticals, NARSAD, NCCAM, NIDA, NIMH,
Novartis, Organon Inc., Pamlab L.L.C., Pfizer Inc, Pharmavite, Roche,
Sanofi/Synthelabo, Shire Pharmaceuticals, Solvay Pharmaceuticals, and
Wyeth Pharmaceuticals. He has served as a consultant/advisor for Abbott
Laboratories, Affectis Pharmaceuticals, Amarinn, Aspect Medical Systems,
AstraZeneca, Auspex Pharmaceuticals, Bayer AG, Best Practice Project
Management, Inc., BioMarin Pharmaceuticals, Biovail Pharmaceuticals,
Inc., BrainCells, Inc., Bristol-Myers Squibb, Cephalon, Clinical Trials
Solutions L.L.C, CNS Response, Cornpenis, Cypress Pharmaceuticals, Dov
Pharmaceuticals, Eisai, Eli Lilly and Company, EPIX Pharmaceuticals,
Euthymics Bioscience, Inc., Fabre-Kramer Pharmaceuticals, Inc., Forest
Pharmaceuticals, GlaxoSmithKline, Grunenthal GmBH, Janssen L.P., Jazz
Pharmaceuticals, J & J Pharmaceuticals, Knoll Pharmaceutical Company,
Labopharm, Lorex Pharmaceuticals, Lundbeck, MedAvante, Inc., Merck,
Methylation Sciences, Neuronetics, Novartis, Nutrition 21, Organon,
Pamlab, L.L.C., Pfizer Inc, PharmaStar, Pharmavite, Precision Human
Biolaboratory, PsychoGenics, Psylin Neurosciences, Inc., Ridge
Diagnostics, Inc., Roche, Sanofi/Synthelabo, Sepracor Inc.,
Schering-Plough, Solvay Pharmaceuticals, Somaxon, Somerset
Pharmaceuticals, Takeda, Tetragenex, TransForm Pharmaceuticals, Inc.,
Transcept Pharmaceuticals, Vanda Pharmaceuticals, Inc., and Wyeth
Pharmaceuticals. He has served on the speakers bureau of AstraZeneca,
Boehringer Ingelheim, BristolMyers Squibb, Cephalon, Eli Lilly and
Company, Forest Pharmaceuticals, GlaxoSmithKline, Novartis, Organon,
Pfizer Inc, PharmaStar, and Wyeth Pharmaceuticals. He has equity
holdings with Compellis. Dr. Mischoulon has received research support
from Ganeden, Laxdale (Amarin), and Nordic Naturals. He has served as a
consultant/advisor for Bristol-Myers Squibb. He is a speaker for and has
received writing support from Pamlab, L.L.C. He receives royalty/patent
income from PMS Escape (patent co-holder). Dr. Sonawalla, Mr. Johnson,
Ms. Goodness, Ms. Clain, Dr. Baer, and Dr. Harley report no financial
relationships with any company whose products are mentioned in this
article or with manufacturers of competing products.
NR 12
TC 10
Z9 10
U1 0
U2 2
PU DOWDEN HEALTH MEDIA
PI MONTVALE
PA 110 SUMMIT AVE, MONTVALE, NJ 07645-1712 USA
SN 1040-1237
J9 ANN CLIN PSYCHIATRY
JI Ann. Clin. Psychiatry
PD AUG
PY 2010
VL 22
IS 3
BP 166
EP 171
PG 6
WC Psychiatry
SC Psychiatry
GA 640DM
UT WOS:000281028300005
PM 20680189
ER
PT J
AU Nyer, M
Kasckow, J
Fellows, I
Lawrence, EC
Golshan, S
Solorzano, E
Zisook, S
AF Nyer, Maren
Kasckow, John
Fellows, Ian
Lawrence, Edith C.
Golshan, Shah
Solorzano, Ellen
Zisook, Sidney
TI The relationship of marital status and clinical characteristics in
middle-aged and older patients with schizophrenia and depressive
symptoms
SO ANNALS OF CLINICAL PSYCHIATRY
LA English
DT Article
DE marriage; quality of life; suicide; subsyndromal depression; marital
status; divorce
ID QUALITY-OF-LIFE; INTIMATE-RELATIONSHIPS; GENDER-DIFFERENCES;
UNITED-STATES; RATING-SCALE; SUICIDE; MARRIAGE; BEHAVIOR; MEN; DISORDERS
AB BACKGROUND: This study examines the relationship of marital status to depression, positive and negative symptoms, quality of life, and suicidal ideation among 211 patients with schizophrenia-spectrum disorders and subsyndromal depressive symptoms. We hypothesized that single participants would have more severe symptomatology than married and cohabitating participants.
METHODS: Outpatients, age 40 or older, were diagnosed with schizophrenia or schizoaffective disorders using the MINI Structured Clinical Interview for DSM-IV Axis 1 Disorders. Participants exhibited a score of >= 8 on the Hamilton Rating Scale for Depression but did not meet criteria for a major depressive episode.
RESULTS: Participants who were married or cohabitating had a later age of onset of first psychotic episode or hospitalization than those who were single (age, 29.35 vs 24.21). Married participants rated their quality of life higher than those who were single (mean Quality of Life Scale scores, 72.28 vs 53.87) and had less suicidal ideation than those who were divorced, widowed, or separated (7.4% vs 29.2%).
CONCLUSIONS: In middle-aged and older individuals with schizophrenia or schizoaffective disorder and depressive symptoms, marriage appeared. to enhance quality of life and protect against suicidal ideation. Efforts that focus on providing additional support for those who are experiencing divorce or separation could prove to be lifesaving for these individuals.
C1 [Nyer, Maren; Lawrence, Edith C.] Univ Virginia, Dept Human Serv, Curry Sch Educ, Charlottesville, VA 22903 USA.
[Kasckow, John] Univ Pittsburgh, Western Psychiat Inst & Clin, Dept Psychiat, VA Pittsburgh Healthcare Syst, Pittsburgh, PA 15213 USA.
[Fellows, Ian; Golshan, Shah; Solorzano, Ellen; Zisook, Sidney] Univ Calif San Diego, Dept Psychiat, Div Geriatr Psychiat 116A 1, San Diego, CA 92103 USA.
[Zisook, Sidney] VA San Diego Healthcare Syst, San Diego, CA USA.
RP Nyer, M (reprint author), Univ Virginia, Dept Human Serv, Curry Sch Educ, 405 Emmet St, Charlottesville, VA 22903 USA.
EM mbn4k@virginia.edu
FU [MH 063931]; [MH6398]
FX Supported by MH 063931(SZ) MH6398 (JWK), the VISN 4 and VISN 22 MIRECC,
and the University of California, San Diego Center for Community-based
Research in Older People with Psychoses. In addition J.W.K. was
supported by a VISN 4 CPPF grant. We also wish to thank the Cincinnati
VA Medical Center and the University of Cincinnati College of Medicine
for all of their support.
NR 49
TC 10
Z9 13
U1 1
U2 5
PU DOWDEN HEALTH MEDIA
PI MONTVALE
PA 110 SUMMIT AVE, MONTVALE, NJ 07645-1712 USA
SN 1040-1237
J9 ANN CLIN PSYCHIATRY
JI Ann. Clin. Psychiatry
PD AUG
PY 2010
VL 22
IS 3
BP 172
EP 179
PG 8
WC Psychiatry
SC Psychiatry
GA 640DM
UT WOS:000281028300006
PM 20680190
ER
PT J
AU Ginde, AA
Sullivan, AF
Camargo, CA
AF Ginde, Adit A.
Sullivan, Ashley F.
Camargo, Carlos A., Jr.
TI Attrition From Emergency Medicine Clinical Practice in the United States
SO ANNALS OF EMERGENCY MEDICINE
LA English
DT Article
ID OCCUPATIONAL STRESS; PHYSICIANS; SATISFACTION; BURNOUT
AB Study objective: We estimate the annual attrition from emergency medicine clinical practice.
Methods: We performed a cross-sectional analysis of the American Medical Association's 2008 Physician Masterfile, which includes data on all physicians who have ever obtained a medical license in at least 1 US state. We restricted the analysis to physicians who completed emergency medicine residency training or who obtained emergency medicine board certification. We defined attrition as not being active in emergency medicine clinical practice. Attrition was reported as cumulative and annualized rates, with stratification by years since training graduation. Death rates were estimated from life tables for the US population.
Results: Of the 30,864 emergency medicine trained or emergency medicine board-certified physicians, 26,826 (87%) remain active in emergency medicine clinical practice. Overall, type of attrition was 45% to non emergency medicine clinical practice, 22% retired, 14% administration, and 10% research/teaching. Immediate attrition (<2 years since training graduation) was 6.5% The cumulative attrition rates from 2 to 15 years postgraduation were stable (5% to 9%) and thereafter were progressively higher, with 18% having left emergency medicine clinical practice at 20 years postgraduation and 25% at 30 years postgraduation. Annualized attrition rates were highest for the first 5 years postgraduation and after 40 years postgraduation; between 5 and 40 years, the rates remained low (<1%). The overall annual attrition rate from emergency medicine clinical practice, including estimated death rate, was approximately 1.7%.
Conclusion: Despite the high stress and demands of emergency medicine, overall attrition remains low and compares favorably with that of other medical specialties. These data have positive implications for the emergency physician workforce and are important for accurate estimation of and planning for emergency physician workforce needs. [Ann Emerg Med. 2010;56:166-171.]
C1 [Ginde, Adit A.] Univ Colorado Denver, Sch Med, Dept Emergency Med, Aurora, CO 80045 USA.
[Sullivan, Ashley F.; Camargo, Carlos A., Jr.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA USA.
RP Ginde, AA (reprint author), Univ Colorado Denver, Sch Med, Dept Emergency Med, 12401 E 17th Ave,B-215, Aurora, CO 80045 USA.
EM adit.ginde@ucdenver.edu
RI Siry, Bonnie/D-7189-2017
NR 27
TC 8
Z9 8
U1 1
U2 2
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 AUG
PY 2010
VL 56
IS 2
BP 166
EP 171
DI 10.1016/j.annemergmed.2009.11.002
PG 6
WC Emergency Medicine
SC Emergency Medicine
GA 635ZM
UT WOS:000280697000014
PM 20036032
ER
PT J
AU Wen, LS
AF Wen, Leana S.
TI All Quiet on Cambridge Street
SO ANNALS OF EMERGENCY MEDICINE
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Wen, LS (reprint author), Massachusetts Gen Hosp, Brigham & Womens Hosp, 75 Francis St,Nevilee House 236-A, Boston, MA 02115 USA.
EM LWen@partners.org
OI Wen, Leana/0000-0003-0259-0537
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 0196-0644
J9 ANN EMERG MED
JI Ann. Emerg. Med.
PD AUG
PY 2010
VL 56
IS 2
BP 187
EP 187
DI 10.1016/j.annemergmed.2009.12.026
PG 1
WC Emergency Medicine
SC Emergency Medicine
GA 635ZM
UT WOS:000280697000019
PM 20643269
ER
PT J
AU Debette, S
Beiser, A
Hoffmann, U
DeCarli, C
O'Donnell, CJ
Massaro, JM
Au, R
Himali, JJ
Wolf, PA
Fox, CS
Seshadri, S
AF Debette, Stephanie
Beiser, Alexa
Hoffmann, Udo
DeCarli, Charles
O'Donnell, Christopher J.
Massaro, Joseph M.
Au, Rhoda
Himali, Jayandra J.
Wolf, Philip A.
Fox, Caroline S.
Seshadri, Sudha
TI Visceral Fat Is Associated with Lower Brain Volume in Healthy
Middle-Aged Adults
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID BODY-MASS INDEX; ADIPOSE-TISSUE VOLUMES; WHITE-MATTER LESIONS; STROKE
RISK PROFILE; FOLLOW-UP; ALZHEIMERS-DISEASE; CENTRAL OBESITY; COGNITIVE
FUNCTION; GENE-EXPRESSION; DEMENTIA
AB Objective: Mid life obesity has been associated with an increased risk of dementia. The underlying mechanisms are poorly understood. Our aim was to examine the cross-sectional association of body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), and computed tomography (CT)-based measurements of subcutaneous (SAT) and visceral (VAT) adipose tissue with various magnetic resonance imaging (MRI) markers of brain aging in middle-aged community adults.
Methods: Participants from the Framingham Offspring cohort were eligible if in addition to having measurements of BMI, WC, WHR, SAT, and VAT, they had undergone a volumetric brain MRI scan with measurements of total brain volume (TCBV), temporal horn volume (THV), white matter hyperintensity volume (WMHV), and MRI-defined brain infarcts (BI). All analyses were adjusted for age, sex, and time interval between abdominal CT and brain MRI.
Results: In a sample of 733 community participants (mean age, 60 years; 53% women), we observed an inverse association of BMI (estimate by standard deviation unit +/- standard error = -0.27 +/- 0.12; p = 0.02), WC (-0.30 +/- 0.12; p = 0.01), WHR (-0.37 +/- 0.12; p = 0.02), SAT (-0.23 +/- 0.11; p = 0.04), and VAT (-0.36 +/- 0.12; p = 0.002) with TCBV, independent of vascular risk factors. The association between VAT and TCBV was the strongest and most robust, and was also independent of BMI (-0.35 +/- 0.15; p = 0.02) and insulin resistance (-0.32 +/- 0.13; p = 0.01). When adjusting for C-reactive protein levels, the associations were attenuated (-0.17 +/- 0.13; p = 0.17 for VAT). No consistently significant association was observed between the anthropometric or CT-based abdominal fat measurements and THV, WMHV, or BI.
Interpretation: In middle-aged community participants, we observed a significant inverse association of anthropometric and CT-based measurements of abdominal, especially visceral, fat with total brain volume. ANN NEUROL 2010;68:136-144
C1 [Debette, Stephanie; Beiser, Alexa; Au, Rhoda; Himali, Jayandra J.; Wolf, Philip A.; Seshadri, Sudha] Boston Univ, Sch Med, Dept Neurol, Framingham Heart Study, Boston, MA 02118 USA.
[Debette, Stephanie; Beiser, Alexa; O'Donnell, Christopher J.; Massaro, Joseph M.; Au, Rhoda; Himali, Jayandra J.; Wolf, Philip A.; Fox, Caroline S.; Seshadri, Sudha] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Beiser, Alexa; Massaro, Joseph M.; Himali, Jayandra J.] Boston Univ, Sch Med, Dept Biostat, Boston, MA 02118 USA.
[Hoffmann, Udo; Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol Metab & Diabet, Boston, MA 02115 USA.
[Hoffmann, Udo; O'Donnell, Christopher J.; Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[DeCarli, Charles] Univ Calif Davis, Dept Neurol, Sacramento, CA 95817 USA.
[O'Donnell, Christopher J.] Massachusetts Gen Hosp, Dept Cardiol, Boston, MA 02114 USA.
RP Seshadri, S (reprint author), Boston Univ, Sch Med, Dept Neurol, Framingham Heart Study, B602,72 E Concord St, Boston, MA 02118 USA.
EM suseshad@bu.edu
RI DeCarli, Charles/B-5541-2009;
OI /0000-0003-1391-9481
FU Framingham Heart Study's National Heart, Lung, and Blood Institute
[N01-HC-25195]; National Institute of Neurological Disorders and Stroke
[R01 NS17950]; National Institute on Aging [R01 AG16495, AG08122,
AG033193, AG031287, AG033040, P30AG013846]; Bettencourt-Schueller
Foundation
FX This work was supported by the Framingham Heart Study's National Heart,
Lung, and Blood Institute contract (N01-HC-25195) and by grants from the
National Institute of Neurological Disorders and Stroke (R01 NS17950 to
PAW.) and from the National Institute on Aging (R01 AG16495 to P.A.W.,
AG08122 to P.A.W., AG033193 to S.S., AG031287 to S.S., AG033040 to
P.A.W., P30AG013846 to S.S.).; Dr Debette received an award from the
Bettencourt-Schueller Foundation.
NR 58
TC 80
Z9 81
U1 1
U2 11
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD AUG
PY 2010
VL 68
IS 2
BP 136
EP 144
DI 10.1002/ana.22062
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 636HD
UT WOS:000280721500007
PM 20695006
ER
PT J
AU Gandy, S
Simon, AJ
Steele, JW
Lublin, AL
Lah, JJ
Walker, LC
Levey, AI
Krafft, GA
Levy, E
Checler, F
Glabe, C
Bilker, WB
Abel, T
Schmeidler, J
Ehrlich, ME
AF Gandy, Sam
Simon, Adam J.
Steele, John W.
Lublin, Alex L.
Lah, James J.
Walker, Lary C.
Levey, Allan I.
Krafft, Grant A.
Levy, Efrat
Checler, Frederic
Glabe, Charles
Bilker, Warren B.
Abel, Ted
Schmeidler, James
Ehrlich, Michelle E.
TI Days to Criterion as an Indicator of Toxicity Associated with Human
Alzheimer Amyloid-beta Oligomers
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID HEREDITARY CEREBRAL-HEMORRHAGE; IMPAIR SYNAPTIC PLASTICITY; MOUSE MODEL;
A-BETA; NATURAL OLIGOMERS; TRANSGENIC MICE; DISEASE; MEMORY; DEFICITS;
PEPTIDE
AB Objective: Recent evidence suggests that high molecular weight soluble oligomeric A beta (oA beta) assemblies (also known as A beta-derived diffusible ligands, or ADDLs) may represent a primary neurotoxic basis for cognitive failure in Alzheimer disease (AD). To date, most in vivo studies of oA beta/ADDLs have involved injection of assemblies purified from the cerebrospinal fluid of human subjects with AD or from the conditioned media of A beta-secreting cells into experimental animals. We sought to study the bioactivities of endogenously formed oA beta/ADDLs generated in situ from the physiological processing of human amyloid precursor protein (APP) and presenitin1 (PS1) transgenes.
Methods: We produced and histologically characterized single transgenic mice overexpressing APPE(693Q) or APP(E693Q) X PS1 Delta E9 bigenic mice. APP(E693Q) mice were studied in the Morris water maze (MWM) task at 6 and 12 months of age. Following the second MWM evaluation, mice were sacrificed, and brains were assayed for A beta total, A beta 40, A beta 42, and oA beta/ADDLs by enzyme-linked immunosorbent assay (ELISA) and were also histologically examined. Based on results from the oA beta/ADDL ELISA, we assigned individual APP(E693Q) mice to either an undetectable oA beta/ADDLs group or a readily detectable oA beta/ADDLs group. A days to criterion (DTC) analysis was used to determine delays in acquisition of the MWM task.
Results: Both single transgenic and bigenic mice developed intraneuronal accumulation of APP/A beta, although only APP(E693Q) X PS1 Delta 9 bigenic mice developed amyloid plaques. The APP(E693Q) mice did not develop amyloid plaques at any age studied, up to 30 months. APP(E693Q) mice were tested for spatial learning and memory, and only 12-month-old APP(E693Q) mice with readily detectable oA beta/ADDLs displayed a significant delay in acquisition of the MWM task when compared to nontransgenic littermates.
Interpretation: These data suggest that cerebral oA beta/ADDL assemblies generated in brain in situ from human APP transgenes may be associated with cognitive impairment. We propose that a DTC analysis may be a sensitive method for assessing the cognitive impact in mice of endogenously generated oligomeric human A beta assemblies. ANN NEUROL 2010;68:220-330
C1 [Gandy, Sam; Steele, John W.; Lublin, Alex L.; Ehrlich, Michelle E.] Mt Sinai Sch Med, Dept Neurol, New York, NY 10029 USA.
[Gandy, Sam; Steele, John W.; Lublin, Alex L.; Schmeidler, James] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
[Gandy, Sam; Steele, John W.; Lublin, Alex L.; Ehrlich, Michelle E.] Mt Sinai Sch Med, Alzheimers Dis Res Ctr, New York, NY 10029 USA.
[Gandy, Sam] James J Peters VA Med Ctr, Bronx, NY USA.
[Simon, Adam J.] AJ Simon Enterprises LLC, Yardley, PA USA.
[Lah, James J.; Walker, Lary C.; Levey, Allan I.] Emory Univ, Dept Neurol, Ctr Neurodegenerat Dis, Atlanta, GA 30322 USA.
[Walker, Lary C.] Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Krafft, Grant A.] Acumen Pharmaceut Inc, Livermore, CA USA.
[Levy, Efrat] NYU, Sch Med, Dept Psychiat, New York, NY USA.
[Levy, Efrat] NYU, Sch Med, Dept Pharmacol, New York, NY USA.
[Levy, Efrat] Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA.
[Checler, Frederic] Fdn Rech Med, Inst Mol & Cellular Pharmacol, Valbonne, France.
[Glabe, Charles] Univ Calif Irvine, Sch Med, Dept Neurol, Irvine, CA 92717 USA.
[Bilker, Warren B.] Univ Penn, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Abel, Ted] Univ Penn, Dept Biol, Philadelphia, PA 19104 USA.
[Ehrlich, Michelle E.] Mt Sinai Sch Med, Dept Pediat, New York, NY 10029 USA.
RP Gandy, S (reprint author), Mt Sinai Sch Med, Dept Neurol, 1 Gustave L Levy Pl,Box 1137, New York, NY 10029 USA.
EM samuel.gandy@mssm.edu
RI Walker, L/J-6541-2015; Checler, Frederic/C-1241-2009
OI Walker, L/0000-0001-9166-3261; Checler, Frederic/0000-0003-2098-1750
FU Cure Alzheimer's Fund; VA MERIT [1I01BX000348-01]; National Institute on
Aging [P01AG10491, P50AG017623, P50AG025688, P50AG05138, P01AG02219];
National Center for Research Resources [RR-00165]; National Institute of
General Medical Sciences [T32GM062754]; Fondation pour la Recherche
Medicale; Conseil General des Alpes Maritimes
FX S.G., A.L.L., J.W.S. and M.E.E. were supported by the Cure Alzheimer's
Fund, VA MERIT review grant 1I01BX000348-01, and National Institute on
Aging grant P01AG10491. T.A. was supported by National Institute on
Aging grant P50AG017623. J.J.L. and A.I.L. were supported by National
Institute on Aging grant P50AG025688. L.C.W. was supported by National
Center for Research Resources grant RR-00165. J.S. was supported by
National Institute on Aging grants P50AG05138 and P01AG02219. J.W.S. is
a trainee in the Integrated Pharmacological Sciences Training Program
supported by grant T32GM062754 from the National Institute of General
Medical Sciences. F.C. was supported by the Fondation pour la Recherche
Medicale and by the Conseil General des Alpes Maritimes.
NR 36
TC 54
Z9 54
U1 0
U2 7
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD AUG
PY 2010
VL 68
IS 2
BP 220
EP 230
DI 10.1002/ana.22052
PG 11
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 636HD
UT WOS:000280721500016
PM 20641005
ER
PT J
AU Colwell, AS
Gadd, M
Smith, BL
Austen, WG
AF Colwell, Amy S.
Gadd, Michele
Smith, Barbara L.
Austen, William G., Jr.
TI An Inferolateral Approach to Nipple-Sparing Mastectomy Optimizing
Mastectomy and Reconstruction
SO ANNALS OF PLASTIC SURGERY
LA English
DT Article
DE breast cancer reconstruction; implants; nipple-sparing; AlloDerm
AB An increasing number of women presenting with early stage breast cancer or a strong family history are choosing mastectomy as a therapeutic or prophylactic treatment option. In these selected patients, conservation of the nipple areolar complex is considered to improve cosmesis and body image. Incision placement is an important consideration in breast appearance after surgery. Functionally, the incision must allow adequate access for mastectomy and implant positioning. In addition, preservation of blood supply is critical to maintain a viable nipple. This article describes an inferolateral curvilinear incision on the breast mound, which can be designed de novo or as an extension of a preexisting lateral scar. The incision allows adequate access and hides the scar on anterior view, thus optimizing both the mastectomy and reconstruction. In patients with a preexisting lateral scar, this may be the incision of choice.
C1 [Colwell, Amy S.; Austen, William G., Jr.] Mass Gen Hosp, Div Plast Surg, Boston, MA 02114 USA.
[Gadd, Michele; Smith, Barbara L.] Mass Gen Hosp, Div Surg Oncol, Boston, MA 02114 USA.
RP Colwell, AS (reprint author), Mass Gen Hosp, Div Plast Surg, 15 Parkman St,WACC 435, Boston, MA 02114 USA.
EM acolwell@partners.org
NR 5
TC 13
Z9 14
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-7043
J9 ANN PLAS SURG
JI Ann. Plast. Surg.
PD AUG
PY 2010
VL 65
IS 2
BP 140
EP 143
DI 10.1097/SAP.0b013e3181c1fe77
PG 4
WC Surgery
SC Surgery
GA 630AT
UT WOS:000280244200007
PM 20606592
ER
PT J
AU Hsu, WM
Carraro, A
Kulig, KM
Miller, ML
Kaazempur-Mofrad, M
Weinberg, E
Entabi, F
Albadawi, H
Watkins, MT
Borenstein, JT
Vacanti, JP
Neville, C
AF Hsu, Wen-Ming
Carraro, Amedeo
Kulig, Katherine M.
Miller, Mark L.
Kaazempur-Mofrad, Mohammad
Weinberg, Eli
Entabi, Fateh
Albadawi, Hassan
Watkins, Michael T.
Borenstein, Jeffrey T.
Vacanti, Joseph P.
Neville, Craig
TI Liver-Assist Device With a Microfluidics-Based Vascular Bed in an Animal
Model
SO ANNALS OF SURGERY
LA English
DT Article
ID BIOARTIFICIAL LIVER; IN-VITRO; HEPATOCYTES; CHANNELS; FAILURE; ALBUMIN;
FUTURE
AB Objective: This study evaluates a novel liver-assist device platform with a microfluidics-modeled vascular network in a femoral arteriovenous shunt in rats.
Summary of Background Data: Liver-assist devices in clinical trials that use pumps to force separated plasma through packed beds of parenchymal cells exhibited significant necrosis with a negative impact on function.
Methods: Microelectromechanical systems technology was used to design and fabricate a liver-assist device with a vascular network that supports a hepatic parenchymal compartment through a nanoporous membrane. Sixteen devices with rat primary hepatocytes and 12 with human HepG2/C3A cells were tested in athymic rats in a femoral arteriovenous shunt model. Several parenchymal tube configurations were evaluated for pressure profile and cell survival. The blood flow pattern and perfusion status of the devices was examined by laser Doppler scanning. Cell viability and serum protein secretion functions were assessed.
Results: Femoral arteriovenous shunt was successfully established in all animals. Blood flow was homogeneous through the vascular bed and replicated native flow patterns. Survival of seeded liver cells was highly dependent on parenchymal chamber pressures. The tube configuration that generated the lowest pressure supported excellent cell survival and function.
Conclusions: This device is the first to incorporate a microfluidics network in the systemic circulatory system. The microvascular network supported viability and function of liver cells in a short-term ex vivo model. Parenchymal chamber pressure generated in an arteriovenous shunt model is a critical parameter that affects viability and must be considered in future designs. The microfluidics-based vascular network is a promising platform for generating a large-scale medical device capable of augmenting liver function in a clinical setting.
C1 [Hsu, Wen-Ming; Kulig, Katherine M.; Vacanti, Joseph P.; Neville, Craig] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
[Entabi, Fateh; Albadawi, Hassan; Watkins, Michael T.] Massachusetts Gen Hosp, Dept Surg, Div Vasc & Endovascu Surg, Boston, MA 02114 USA.
[Hsu, Wen-Ming] Natl Taiwan Univ, Coll Med, Natl Taiwan Univ Hosp, Dept Surg, Taipei 10764, Taiwan.
[Carraro, Amedeo] Ist Oncol Veneto, Dept Surg Oncol, Padua, Italy.
[Miller, Mark L.; Watkins, Michael T.; Vacanti, Joseph P.; Neville, Craig] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Kaazempur-Mofrad, Mohammad; Weinberg, Eli] Univ Calif Berkeley, Dept Bioengn, Berkeley, CA 94720 USA.
[Borenstein, Jeffrey T.] Charles Stark Draper Lab Inc, Ctr Biomed Engn, Cambridge, MA 02139 USA.
RP Neville, C (reprint author), Massachusetts Gen Hosp, Ctr Regenerat Med, 185 Cambridge St,CPZN-4809, Boston, MA 02114 USA.
EM neville@helix.mgh.harvard.edu
OI HSU, WEN-MING/0000-0002-5145-9538
FU Center for Integration of Medicine and Innovative Technology (US Army)
[DAMD17-02-2-0006]
FX Supported by the Center for Integration of Medicine and Innovative
Technology (US Army DAMD17-02-2-0006).
NR 23
TC 17
Z9 18
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-4932
EI 1528-1140
J9 ANN SURG
JI Ann. Surg.
PD AUG
PY 2010
VL 252
IS 2
BP 351
EP 357
DI 10.1097/SLA.0b013e3181e982ba
PG 7
WC Surgery
SC Surgery
GA 634OQ
UT WOS:000280593000022
PM 20647924
ER
PT J
AU Tanabe, KK
Jara, S
Michaelson, J
AF Tanabe, Kenneth K.
Jara, Sebastian
Michaelson, James
TI Creating and Providing Predictions of Melanoma Outcome
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Editorial Material
ID LYMPH-NODES CONTRIBUTES; CANCER DEATH; PRIMARY SITE; RISK
C1 [Tanabe, Kenneth K.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Tanabe, KK (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
EM ktanabe@partners.org
NR 8
TC 0
Z9 0
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 AUG
PY 2010
VL 17
IS 8
BP 1981
EP 1982
DI 10.1245/s10434-010-1054-8
PG 2
WC Oncology; Surgery
SC Oncology; Surgery
GA 622HY
UT WOS:000279653600003
PM 20373038
ER
PT J
AU Tomkiewicz, D
Casadei, G
Larkins-Ford, J
Moy, TI
Garner, J
Bremner, JB
Ausubel, FM
Lewis, K
Kelso, MJ
AF Tomkiewicz, Danuta
Casadei, Gabriele
Larkins-Ford, Jonah
Moy, Terence I.
Garner, James
Bremner, John B.
Ausubel, Frederick M.
Lewis, Kim
Kelso, Michael J.
TI Berberine-INF55 (5-Nitro-2-Phenylindole) Hybrid Antimicrobials: Effects
of Varying the Relative Orientation of the Berberine and INF55
Components
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID MULTIDRUG EFFLUX TRANSPORTER; STAPHYLOCOCCUS-AUREUS; ANTIBACTERIAL
AGENTS; PUMP INHIBITOR; FLUOROQUINOLONE RESISTANCE; NORA; MECHANISMS;
ELEGANS; PROTEIN; CLONING
AB Hybrid antimicrobials containing an antibacterial linked to a multidrug resistance (MDR) pump inhibitor make up a promising new class of agents for countering efflux-mediated bacterial drug resistance. This study explores the effects of varying the relative orientation of the antibacterial and efflux pump inhibitor components in three isomeric hybrids (SS14, SS14-M, and SS14-P) which link the antibacterial alkaloid and known substrate for the NorA MDR pump berberine to different positions on INF55 (5-nitro-2-phenylindole), an inhibitor of NorA. The MICs for all three hybrids against wild-type, NorA-knockout, and NorA-overexpressing Staphylococcus aureus cells were found to be similar (9.4 to 40.2 mu M), indicating that these compounds are not effectively effluxed by NorA. The three hybrids were also found to have similar curing effects in a Caenorhabditis elegans live infection model. Each hybrid was shown to accumulate in S. aureus cells to a greater extent than either berberine or berberine in the presence of INF55, and the uptake kinetics of SS14 were found to differ from those of SS14-M and SS14-P. The effects on the uptake and efflux of the NorA substrate ethidium bromide into S. aureus cells in the presence or absence of the hybrids were used to confirm MDR inhibition by the hybrids. MDR-inhibitory activity was confirmed for SS14-M and SS14-P but not for SS14. Molecular dynamics simulations revealed that SS14 prefers to adopt a conformation that is not prevalent in either SS14-M or SS14-P, which may explain why some properties of SS14 diverge from those of its two isomers. In summary, subtle repositioning of the pump-blocking INF55 moiety in berberine-INF55 hybrids was found to have a minimal effect on their antibacterial activities but to significantly alter their effects on MDR pumps.
C1 [Garner, James; Bremner, John B.; Kelso, Michael J.] Univ Wollongong, Sch Chem, Wollongong, NSW 2522, Australia.
[Tomkiewicz, Danuta; Casadei, Gabriele; Lewis, Kim] Northeastern Univ, Dept Biol, Boston, MA 02115 USA.
[Tomkiewicz, Danuta; Casadei, Gabriele; Lewis, Kim] Northeastern Univ, Antimicrobial Discovery Ctr, Boston, MA 02115 USA.
[Larkins-Ford, Jonah; Moy, Terence I.; Ausubel, Frederick M.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA.
[Larkins-Ford, Jonah; Moy, Terence I.; Ausubel, Frederick M.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
RP Kelso, MJ (reprint author), Univ Wollongong, Sch Chem, Northfields Ave, Wollongong, NSW 2522, Australia.
EM mkelso@uow.edu.au
OI Kelso, Michael/0000-0001-7809-6637
FU University of Wollongong, NSW, Australia; Harvard Medical School;
Northeastern University, Boston, MA; NHMRC [252922]; American Cancer
Society [PF-02-130-01-MBC]; NIH [R21 AI059483, R01 AI072508, R01
AI076372]; Broad Institute of Harvard and MIT
FX We thank the University of Wollongong, NSW, Australia; Harvard Medical
School; and Northeastern University, Boston, MA, for supporting this
work. The award of an NHMRC C. J. Martin fellowship (fellowship 252922
to Michael J. Kelso) and an American Cancer Society postdoctoral
fellowship (fellowship PF-02-130-01-MBC to Terence I. Moy) are
gratefully acknowledged. The work was supported by grants R21 AI059483,
R01 AI072508, and R01 AI076372 from the NIH and a grant from the Broad
Institute of Harvard and MIT, awarded to Frederick M. Ausubel.
NR 36
TC 16
Z9 17
U1 0
U2 7
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD AUG
PY 2010
VL 54
IS 8
BP 3219
EP 3224
DI 10.1128/AAC.01715-09
PG 6
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 626JW
UT WOS:000279963300019
PM 20498327
ER
PT J
AU Chaiswing, L
Oberley, TD
AF Chaiswing, Luksana
Oberley, Terry D.
TI Extracellular/Microenvironmental Redox State
SO ANTIOXIDANTS & REDOX SIGNALING
LA English
DT Review
ID EXTRACELLULAR-SUPEROXIDE-DISMUTASE; GAMMA-GLUTAMYL-TRANSPEPTIDASE;
X(C)(-) CYSTINE/GLUTAMATE ANTIPORTER; PLASMA GLUTATHIONE-PEROXIDASE;
PROTEIN DISULFIDE-ISOMERASE; NITRIC-OXIDE SYNTHASE; RENAL-CELL
CARCINOMA; HYDROGEN-PEROXIDE; PROSTATE-CANCER; GROWTH-FACTOR
AB Extracellular redox (reduction-oxidation) state is a factor that serves as an important regulator of cell-microenvironmental interactions and is determined by several known variables; including redox-modulating proteins that are located on the plasma membrane or outside of cells, extracellular thiol/disulfide couples, and reactive oxygen species (ROS)/reactive nitrogen species (RNS) that are capable of traveling across plasma membranes into the extracellular space. The extracellular redox state works in concert with the intracellular redox state to control both the influx and efflux of ROS/RNS that may serve to modulate redox signaling or to perturb normal cellular processes or both. Under physiologic conditions, the extracellular space is known to have a relatively more-oxidized redox state than the interior of the cell. During pathologic conditions, such as cancer, the extracellular redox state may be altered, causing specific proteins such as proteases, soluble factors, or the extracellular matrix to have altered functions or activities. Recent studies have strongly supported an important relation between the extracellular redox state and cancer cell aggressiveness. The purpose of this review is to identify redox buffer networks in extracellular spaces and to emphasize the possible roles of the extracellular redox state in cancer, knowledge that may contribute to potential therapeutic interventions. Antioxid. Redox Signal. 13, 449-465.
C1 [Oberley, Terry D.] William S Middleton Mem Vet Adm Med Ctr, Pathol & Lab Med Serv, Madison, WI 53705 USA.
[Chaiswing, Luksana; Oberley, Terry D.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Pathol & Lab Med, Madison, WI 53706 USA.
RP Oberley, TD (reprint author), William S Middleton Mem Vet Adm Med Ctr, Pathol & Lab Med Serv, Room A-35,2500 Overlook Terrace, Madison, WI 53705 USA.
EM toberley@wisc.edu
FU Office of Research and Development, Biomedical Laboratory Research and
Development Service; Department of Veterans Affairs (TDO)
FX This material is based on work supported by the Office of Research and
Development, Biomedical Laboratory Research and Development Service, and
Department of Veterans Affairs (TDO).
NR 123
TC 51
Z9 51
U1 0
U2 4
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1523-0864
EI 1557-7716
J9 ANTIOXID REDOX SIGN
JI Antioxid. Redox Signal.
PD AUG
PY 2010
VL 13
IS 4
BP 449
EP 465
DI 10.1089/ars.2009.3020
PG 17
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 619KI
UT WOS:000279428700006
PM 20017602
ER
PT J
AU Salloum, S
Kluge, SF
Kim, AY
Roggendorf, M
Timm, J
AF Salloum, Shadi
Kluge, Silvia F.
Kim, Arthur Y.
Roggendorf, Michael
Timm, Joerg
TI The resistance mutation R155K in the NS3/4A protease of hepatitis C
virus also leads the virus to escape from HLA-A*68-restricted CD8 T
cells
SO ANTIVIRAL RESEARCH
LA English
DT Article
DE CD8 T cell; Immune escape; Drug resistance; STAT-C; Protease inhibitor;
BILN 2061
ID TREATMENT-NAIVE; CONFERRING RESISTANCE; DRUG-RESISTANCE; RNA
REPLICATION; INHIBITOR; HCV; SENSITIVITY; TELAPREVIR; POLYMERASE;
INFECTION
AB The NS3/4A serine protease of the hepatitis C virus (HCV) is one of the most attractive targets for specific antiviral agents. However, mutations conferring resistance may decrease the efficacy of these drugs. Although the level of resistance associated with specific mutations differs between different compounds, substitutions R155K and A156T reduce susceptibility to all protease inhibitors published so far. Interestingly, variants harboring the resistant mutation R155K were also detected as the predominant quasispecies in some treatment-naive patients. Of note, key positions for resistance overlap with the HLA-A*68-restricted epitope HAVGIFRAAV(1175-1184). The aim of our study was to analyze the impact of protease inhibitor resistance mutations on the replication level and the antiviral CD8 T cell response against this HCV epitope. Our findings suggest that the R155K variant is associated with a relatively high replication level and with a substantial loss of cross-recognition by specific CD8 T cells targeting the epitope HAVGIFRAAV(1175-1184), providing a possible explanation for its existence in the absence of drug selection pressure. (C) 2010 Elsevier B.V. All rights reserved.
C1 [Salloum, Shadi; Kluge, Silvia F.; Roggendorf, Michael; Timm, Joerg] Univ Duisburg Essen, Inst Virol, D-45147 Essen, Germany.
[Kim, Arthur Y.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Infect Dis, Boston, MA USA.
RP Timm, J (reprint author), Univ Duisburg Essen, Inst Virol, Virchowstr 179, D-45147 Essen, Germany.
EM joerg.timm@uni-due.de
NR 21
TC 9
Z9 9
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
J9 ANTIVIR RES
JI Antiviral Res.
PD AUG
PY 2010
VL 87
IS 2
SI SI
BP 272
EP 275
DI 10.1016/j.antiviral.2010.05.006
PG 4
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA 639KC
UT WOS:000280972700020
PM 20488208
ER
PT J
AU Alora-Palli, MB
Brouda, I
Green, B
Kimball, AB
AF Alora-Palli, Maria B.
Brouda, Irina
Green, Barbara
Kimball, Alexandra B.
TI A Cost-effectiveness Comparison of Liquor Carbonis Distillate Solution
and Calcipotriol Cream in the Treatment of Moderate Chronic Plaque
Psoriasis
SO ARCHIVES OF DERMATOLOGY
LA English
DT Letter
ID COAL-TAR; EFFICACY
C1 [Alora-Palli, Maria B.] Massachusetts Gen Hosp, Clin Unit Res Trials Skin, Boston, MA 02114 USA.
[Brouda, Irina; Green, Barbara] NeoStrata Co Inc, Princeton, NJ USA.
RP Kimball, AB (reprint author), Massachusetts Gen Hosp, Clin Unit Res Trials Skin, 50 Staniford St,Ste 240, Boston, MA 02114 USA.
EM harvardskinstudies@partners.org
NR 9
TC 3
Z9 3
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-987X
J9 ARCH DERMATOL
JI Arch. Dermatol.
PD AUG
PY 2010
VL 146
IS 8
BP 919
EP 922
DI 10.1001/archdermatol.2010.167
PG 4
WC Dermatology
SC Dermatology
GA 642VS
UT WOS:000281249700023
PM 20713833
ER
PT J
AU Herskovits, AZ
Growdon, JH
AF Herskovits, A. Zara
Growdon, John H.
TI Sharpen That Needle
SO ARCHIVES OF NEUROLOGY
LA English
DT Editorial Material
ID ALZHEIMERS-DISEASE; COGNITIVE DECLINE; BIOMARKERS
C1 [Growdon, John H.] Massachusetts Gen Hosp, Dept Neurol, Wang Ambulatory Care Ctr 729, Boston, MA 02114 USA.
[Herskovits, A. Zara] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Growdon, JH (reprint author), Massachusetts Gen Hosp, Dept Neurol, Wang Ambulatory Care Ctr 729, Boston, MA 02114 USA.
EM jgrowdon@partners.org
NR 12
TC 12
Z9 13
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD AUG
PY 2010
VL 67
IS 8
BP 918
EP 920
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 637HU
UT WOS:000280809000001
PM 20697041
ER
PT J
AU Goldstein, JN
Marrero, M
Masrur, S
Pervez, M
Barrocas, AM
Abdullah, A
Oleinik, A
Rosand, J
Smith, EE
Dzik, WH
Schwamm, LH
AF Goldstein, Joshua N.
Marrero, Marisela
Masrur, Shihab
Pervez, Muhammad
Barrocas, Alex M.
Abdullah, Abdul
Oleinik, Alexandra
Rosand, Jonathan
Smith, Eric E.
Dzik, Walter H.
Schwamm, Lee H.
TI Management of Thrombolysis-Associated Symptomatic Intracerebral
Hemorrhage
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID TISSUE-PLASMINOGEN-ACTIVATOR; ACUTE ISCHEMIC-STROKE; QUALITY-OF-CARE;
INTRACRANIAL HEMORRHAGE; GUIDELINES-STROKE; THERAPY; TRANSFORMATION;
INTRAARTERIAL; WARFARIN; OUTCOMES
AB Background: Symptomatic intracerebral hemorrhage (sICH) is the most devastating complication of thrombolytic therapy for acute stroke. It is not clear whether patients with sICH continue to bleed after diagnosis, nor has the most appropriate treatment been determined.
Methods: We performed a retrospective analysis of our prospectively collected Get With the Guidelines Stroke database between April 1, 2003, and December 31, 2007. Radiologic images and all procoagulant agents used were reviewed. Multivariable logistic regression was performed to identify factors associated with in-hospital mortality.
Results: Of 2362 patients with acute ischemic stroke during the study period, sICH occurred in 19 of the 311 patients (6.1%) who received intravenous tissue plasminogen activator and 2 of the 72 (2.8%) who received intra-arterial thrombolysis. In-hospital mortality was significantly higher in patients with sICH than in those without (15 of 20 [75.0]% vs 56 of 332 [16.9%], P < .001). Eleven of 20 patients (55.0%) received therapy for co-agulopathy: 7 received fresh frozen plasma; 5, cryoprecipitate; 4, phytonadione (vitamin K(1)); 3, platelets; and 1, aminocaproic acid. Independent predictors of in-hospital mortality included sICH (odds ratio, 32.6; 95% confidence interval, 8.8-120.2), increasing National Institutes of Health Stroke Scale score (1.2; 1.1-1.2), older age (1.3; 1.0-1.7), and intra-arterial thrombolysis (2.9; 1.4-6.0). Treatment for coagulopathy was not associated with outcome. Continued bleeding (>33% increase in intracerebral hemorrhage volume) occurred in 4 of 10 patients with follow-up scans available (40.0%).
Conclusions: In many patients with sICH after thrombolysis, coagulopathy goes untreated. Our finding of continued bleeding after diagnosis in 40.0% of patients suggests a powerful opportunity for intervention. A multicenter registry to analyze management of thrombolysis-associated intracerebral hemorrhage and outcomes is warranted.
C1 [Goldstein, Joshua N.; Marrero, Marisela] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Masrur, Shihab; Pervez, Muhammad; Abdullah, Abdul; Oleinik, Alexandra; Rosand, Jonathan; Schwamm, Lee H.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Dzik, Walter H.] Massachusetts Gen Hosp, Dept Hematol, Boston, MA 02114 USA.
[Barrocas, Alex M.] Mt Sinai Med Ctr, Dept Radiol, Miami Beach, FL 33140 USA.
[Smith, Eric E.] Univ Calgary, Calgary Stroke Program, Calgary, AB, Canada.
RP Goldstein, JN (reprint author), Massachusetts Gen Hosp, Dept Emergency Med, 0 Emerson Pl,Ste 3B, Boston, MA 02114 USA.
EM jgoldstein@partners.org
RI Goldstein, Joshua/H-8953-2016;
OI Schwamm, Lee/0000-0003-0592-9145; Smith, Eric/0000-0003-3956-1668
FU NINDS [NS059774]
FX This study was funded in part by K23 career development award NS059774
from the NINDS (Dr Goldstein).
NR 31
TC 35
Z9 38
U1 0
U2 5
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD AUG
PY 2010
VL 67
IS 8
BP 965
EP 969
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA 637HU
UT WOS:000280809000008
PM 20697046
ER
PT J
AU Buracchio, T
Dodge, HH
Howieson, D
Wasserman, D
Kaye, J
AF Buracchio, Teresa
Dodge, Hiroko H.
Howieson, Diane
Wasserman, Dara
Kaye, Jeffrey
TI The Trajectory of Gait Speed Preceding Mild Cognitive Impairment
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID OLDER PERSONS; PARKINSONIAN SIGNS; ALZHEIMER-DISEASE; COMMUNITY
POPULATION; DECLINE; PEOPLE; RISK; DYSFUNCTION; DEMENTIA; PROGRESSION
AB Objectives: To compare the trajectory of motor decline, as measured by gait speed and finger-tapping speed, between elderly people who developed mild cognitive impairment (MCI) and those who remained cognitively intact. We also sought to determine the approximate time at which the decline in motor function accelerated in persons who developed MCI.
Design: Longitudinal cohort study.
Participants: Participants were 204 healthy seniors (57.8% women) from the Oregon Brain Aging Study evaluated for up to 20 years using annual neurologic, neuropsychological, and motor examinations.
Main Outcome Measures: The pattern of motor decline with aging was compared using a mixed-effects model with an interaction term for age and a clinical diagnosis of MCI. The time before diagnosis of MCI, when the change in gait or finger-tapping speed accelerates, was assessed using a mixed-effects model with a change point for men and women, separately and combined, who developed MCI.
Results: The rates of change, with aging, in gait speed (P < .001) and finger-tapping speed in the dominant hand (P=.003) and nondominant hand (P < .001) were significantly different between participants who developed MCI (converters) and those who did not (nonconverters). Using a change point analysis for MCI converters, the decrease in gait speed accelerated by 0.023 m/s/y (P < .001), occurring 12.1 years before the onset of MCI. An acceleration in gait speed decline occurred earlier in men than women. For tapping speed, the change point occurred after the onset of MCI for both dominant and nondominant hands when men and women were combined.
Conclusions: Motor decline as indexed by gait speed accelerates up to 12 years before MCI. Longitudinal changes in motor function may be useful in the early detection of dementia during preclinical stages, when the utility of disease-modifying therapies would be greatest.
C1 [Buracchio, Teresa; Kaye, Jeffrey] Portland VA Med Ctr, Portland, OR USA.
[Kaye, Jeffrey] Oregon Ctr Aging & Technol, Portland, OR USA.
[Buracchio, Teresa; Dodge, Hiroko H.; Howieson, Diane; Wasserman, Dara; Kaye, Jeffrey] Oregon Hlth & Sci Univ, Dept Neurol, Layton Aging & Alzheimers Dis Ctr, Portland, OR 97239 USA.
RP Buracchio, T (reprint author), Oregon Hlth & Sci Univ, Dept Neurol, Layton Aging & Alzheimers Dis Ctr, 3181 SW Sam Jackson Pk Rd,Mail Code CR-131, Portland, OR 97239 USA.
EM buracchi@ohsu.edu
OI Kaye, Jeffrey/0000-0002-9971-3478
FU Department of Veterans Affairs [P30AG008017, R01AG024059]; National
Institute on Aging [K01AG023014]; National Center for Research Resources
FX This study was supported by the Department of Veterans Affairs; grants
P30AG008017, R01AG024059, and K01AG023014 from the National Institute on
Aging; and the National Center for Research Resources.
NR 40
TC 107
Z9 108
U1 2
U2 16
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD AUG
PY 2010
VL 67
IS 8
BP 980
EP 986
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 637HU
UT WOS:000280809000011
PM 20697049
ER
PT J
AU Hayden, KM
Breitner, JCS
Welsh-Bohmer, KA
AF Hayden, Kathleen M.
Breitner, John C. S.
Welsh-Bohmer, Kathleen A.
TI Apolipoprotein E epsilon 4 Status and Cognitive Decline With and Without
Dementia Reply
SO ARCHIVES OF NEUROLOGY
LA English
DT Letter
ID DISEASE; APOE
C1 [Hayden, Kathleen M.] Duke Univ, Dept Psychiat & Behav Sci, Joseph & Kathleen Bryan Alzheimers Dis Res Ctr, Durham, NC 27705 USA.
[Hayden, Kathleen M.; Welsh-Bohmer, Kathleen A.] Duke Univ, Div Neurol, Joseph & Kathleen Bryan Alzheimers Dis Res Ctr, Dept Med,Med Ctr, Durham, NC 27705 USA.
[Breitner, John C. S.] Univ Washington, Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Breitner, John C. S.] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
RP Hayden, KM (reprint author), Duke Univ, Dept Psychiat & Behav Sci, Joseph & Kathleen Bryan Alzheimers Dis Res Ctr, 2200 W Main St,Ste A-200, Durham, NC 27705 USA.
EM khayden@duke.edu
RI Hayden, Kathleen/B-6442-2012
OI Hayden, Kathleen/0000-0002-7745-3513
NR 4
TC 0
Z9 0
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD AUG
PY 2010
VL 67
IS 8
BP 1036
EP 1037
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 637HU
UT WOS:000280809000028
ER
PT J
AU Ku, TK
Rutar, T
Han, Y
Porco, TC
Naseri, A
AF Ku, Tina K.
Rutar, Tina
Han, Ying
Porco, Travis C.
Naseri, Ayman
TI Resident-Performed Phacoemulsification Surgery in Tamsulosin-Treated
Patients
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Article
ID FLOPPY-IRIS-SYNDROME; BENIGN PROSTATIC HYPERTROPHY; CATARACT-SURGERY;
CLINICAL FINDINGS; VITREOUS LOSS; IFIS; COMPLICATIONS; ASSOCIATION;
PROPHYLAXIS; EPINEPHRINE
AB Objectives: To compare intraoperative complication rates and visual outcomes for patients treated and not treated with tamsulosin hydrochloride who underwent resident-performed phacoemulsification, and to determine whether the recognition of intraoperative floppy iris syndrome in 2005 affected the subsequent complication rates for tamsulosin-treated patients.
Methods: This comparative retrospective cohort study included 101 tamsulosin-treated eyes and 404 non tamsulosin-treated eyes from January 1, 1998, to August 31, 2008. Main outcome measures were major and minor complication rates and postoperative best-corrected visual acuity. Complication rates were compared between August 11, 1999, to December 31, 2005, and January 1, 2006, to September 3, 2008, for both tamsulosin-treated and non tamsulosin-treated eyes.
Results: The major complication rates were 3.0% for tamsulosin-treated eyes and 8.9% for non-tamsulosin-treated eyes (P=.08), while the minor complication rates were 24.8% and 12.1%, respectively (P=.002). Both groups had an equal likelihood of attaining better than 20/40 postoperative visual acuities (82.2% vs 82.9%, rdspectively; P=.85). Frequency of major complications between tamsulosin-treated and non tamsulosin-treated eyes was 6.0% vs 15.8%, respectively (P=.09), from August 11, 1999, to December 31, 2005, compared with 0.0% vs 2.0%, respectively (P>.99), from January 1, 2006, to September 3, 2008.
Conclusions: Differences in the major complication rates for tamsulosin-treated and non tamsulosin-treated eyes were not significant, whereas tamsulosin exposure was associated with a significant increase in minor complications. Both groups had similar, good postoperative visual outcomes. After 2005, a reduction in major complications was seen in both groups, attributed to programmatic changes in surgical education. Recognition of intraoperative floppy iris syndrome did not impart a significant additional protective effect in preventing major complications.
C1 [Naseri, Ayman] San Francisco VA Med Ctr, Dept Ophthalmol, San Francisco, CA 94121 USA.
[Ku, Tina K.; Rutar, Tina; Han, Ying; Porco, Travis C.; Naseri, Ayman] Univ Calif San Francisco, Dept Ophthalmol, San Francisco, CA 94143 USA.
[Porco, Travis C.] Univ Calif San Francisco, Dept Epidemiol & Biostat, Div Prevent Med & Publ Hlth, San Francisco, CA 94143 USA.
[Porco, Travis C.; Naseri, Ayman] Francis I Proctor Fdn Res Ophthalmol, San Francisco, CA USA.
RP Naseri, A (reprint author), San Francisco VA Med Ctr, Dept Ophthalmol, 4150 Clement St, San Francisco, CA 94121 USA.
EM ayman.naseri@va.gov
FU Research to Prevent Blindness; University of California [NIH P30]; That
Man May See
FX This work was supported in part by unrestricted grants from Research to
Prevent Blindness, the University of California Institutional Core Grant
For Vision Research (NIH P30), and That Man May See, a non-profit
organization.
NR 37
TC 3
Z9 3
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD AUG
PY 2010
VL 128
IS 8
BP 967
EP 972
PG 6
WC Ophthalmology
SC Ophthalmology
GA 638QJ
UT WOS:000280909700002
PM 20696995
ER
PT J
AU Lane, AM
Egan, KM
Kim, IK
Gragoudas, ES
AF Lane, Anne Marie
Egan, Kathleen M.
Kim, Ivana K.
Gragoudas, Evangelos S.
TI Mortality After Diagnosis of Small Melanocytic Lesions of the Choroid
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Article
ID NATIONAL DEATH INDEX; MALIGNANT MELANOMAS; UVEAL MELANOMA; CILIARY BODY;
HOST FACTORS; NEVI; RISK; GROWTH; HISTOGENESIS; ENUCLEATION
AB Objective: To evaluate the risk of dying of metastatic choroidal melanoma in patients with small, indeterminate, pigmented lesions of the uveal tract.
Methods: A cohort of 1063 consecutive patients were evaluated in the Ocular Oncology Clinic of the Massachusetts Eye and Ear Infirmary between January 1976 and June 1996 with definite choroidal nevus (n = 256), indeterminate lesions (n = 334), or small melanoma (n = 373). Deaths occurring up to December 1998 were identified through active follow-up or by a search of the National Death Index. Cumulative death rates were compared among diagnostic groups using the Kaplan-Meier method.
Results: Mean lesion diameter was 4.6 mm in the nevi, 7.0 mm in the indeterminate lesions, and 8.1 mm in the small melanomas. Patients ranged in age from 3 to 95 years (median, 64 years). A total of 15 deaths due to ocular melanoma were ascertained (median follow-up of survivors, 8.2 years), 13 in the melanoma group and 2 in the indeterminate lesion group; actuarial tumor-specific death rates at 10 years after evaluation were 5% (95% confidence interval, 3%-8%) and 1% (95% confidence interval 0%-3%), respectively. No deaths due to ocular melanoma occurred in the nevus group.
Conclusions: These data document the very low malignant potential of most indeterminate melanocytic lesions of the choroid and support the current practice of monitoring these tumors, with treatment provided when growth and other signs of malignant transformation are observed.
C1 [Lane, Anne Marie] Massachusetts Eye & Ear Infirm, Retina Serv, Boston, MA 02114 USA.
[Egan, Kathleen M.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
RP Lane, AM (reprint author), Massachusetts Eye & Ear Infirm, Retina Serv, 243 Charles St, Boston, MA 02114 USA.
EM alane@meei.harvard.edu
FU Research to Prevent Blindness
FX This study was supported by Research to Prevent Blindness (Dr Kim).
NR 31
TC 5
Z9 5
U1 0
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD AUG
PY 2010
VL 128
IS 8
BP 996
EP 1000
PG 5
WC Ophthalmology
SC Ophthalmology
GA 638QJ
UT WOS:000280909700006
PM 20696999
ER
PT J
AU Brigger, MT
Cunningham, MJ
Hartnick, CJ
AF Brigger, Matthew T.
Cunningham, Michael J.
Hartnick, Christopher J.
TI Dexamethasone Administration and Postoperative Bleeding Risk in Children
Undergoing Tonsillectomy
SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY
LA English
DT Article
ID PEDIATRIC TONSILLECTOMY; ADENOTONSILLECTOMY; HEMORRHAGE; MANAGEMENT;
PAIN; METAANALYSIS; MORBIDITY; SAFETY; NAUSEA
AB Objective: To assess whether administration of dexamethasone during tonsillectomy is associated with a dose-dependent increased rate of postoperative tonsillectomy hemorrhage.
Design: Retrospective review of 2788 children and adolescents who underwent tonsillectomy with or without adenoidectomy for sleep-disordered breathing or infectious tonsillitis and received perioperative dexamethasone between January 1, 2002, and March 3, 2009.
Patients underwent 1 of 3 methods of tonsillectomy, including extracapsular electrosurgical tonsillectomy, extracapsular radiofrequency ablation tonsillectomy, or intracapsular microdebrider tonsillotomy.
Setting: Massachusetts Eye and Ear Infirmary.
Patients: Two thousand seven hundred eighty-eight children and adolescents aged 2 to 18 years (hereinafter referred to as children) who underwent tonsillectomy with or without adenoidectomy.
Interventions: Each child received 1 of 2 distinct intravenous doses of perioperative dexamethasone (0.5 mg/kg or 1.0 mg/kg) based on the protocol of the surgeon who performed the tonsillectomy; other aspects of care, including anesthetic technique, perioperative an-algesia, and postoperative care, were equivalent between children.
Main Outcome Measures: Occurrence of postoperative hemorrhage based on 3 severity stratification levels.
Results: Ninety-four of the 2788 children experienced 104 episodes of postoperative hemorrhage. After adjusting for age, sex, primary diagnosis, and surgical technique, the odds ratio of experiencing a postoperative hemorrhage of any severity in children who received the 1.0-mg/kg compared with the 0.5-mg/kg dose was 0.66 (95% confidence interval [CI], 0.42-1.05). Children requiring readmission with or without the need for operative intervention demonstrated an adjusted odds ratio of 0.83 (95% Cl, 0.51-1.36). An adjusted odds ratio of 0.71 (95% Cl, 0.39-1.28) was seen in children requiring operative intervention.
Conclusion: In this observational review of children undergoing tonsillectomy or adenotonsillectomy, perioperative dexamethasone administration is not associated with a dose-dependent elevation of postoperative hemorrhage rates after adjusting for age, sex, primary diagnosis, and surgical technique.
C1 [Brigger, Matthew T.] Naval Med Ctr San Diego, Dept Otolaryngol Head & Neck Surg, San Diego, CA 92134 USA.
[Cunningham, Michael J.; Hartnick, Christopher J.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Massachusetts Eye & Ear Infirm, Boston, MA 02115 USA.
RP Brigger, MT (reprint author), Naval Med Ctr San Diego, Dept Otolaryngol Head & Neck Surg, 34800 Bob Wilson Dr, San Diego, CA 92134 USA.
EM matt.brigger@alumni.vanderbilt.edu
NR 31
TC 15
Z9 15
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0886-4470
J9 ARCH OTOLARYNGOL
JI Arch. Otolaryngol. Head Neck Surg.
PD AUG
PY 2010
VL 136
IS 8
BP 766
EP 772
PG 7
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 640FD
UT WOS:000281033300002
PM 20713751
ER
PT J
AU Kakarala, K
Brigger, MT
Faquin, WC
Hartnick, CJ
Cunningham, MJ
AF Kakarala, Kiran
Brigger, Matthew T.
Faquin, William C.
Hartnick, Christopher J.
Cunningham, Michael J.
TI Cystic Pilomatrixoma A Diagnostic Challenge
SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY
LA English
DT Article
ID CALCIFYING EPITHELIOMA; BETA-CATENIN; HEAD; NECK; CHILDREN; MUTATION
AB Pilomatrixoma is a benign neoplasm of ectodermal hair follicle germinal matrix cell origin. At least 50% of pilomatrixomas are reported to arise in the head and neck, and 40% occur before the age of 10 years.(1-3) Pilomatrixoma is the third most common reason for excision of a cervicofacial mass in children, after lymphadenopathy and epidermoid cysts.
C1 [Kakarala, Kiran; Hartnick, Christopher J.; Cunningham, Michael J.] Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA.
[Kakarala, Kiran; Hartnick, Christopher J.; Cunningham, Michael J.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA USA.
[Faquin, William C.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Brigger, Matthew T.] Naval Med Ctr, Dept Otolaryngol Head & Neck Surg, San Diego, CA USA.
RP Kakarala, K (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, 243 Charles St, Boston, MA 02114 USA.
EM kiran_kakarala@meei.harvard.edu
OI Kakarala, Kiran/0000-0002-1003-8024
NR 15
TC 3
Z9 4
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0886-4470
J9 ARCH OTOLARYNGOL
JI Arch. Otolaryngol. Head Neck Surg.
PD AUG
PY 2010
VL 136
IS 8
BP 830
EP 833
PG 4
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 640FD
UT WOS:000281033300015
PM 20713764
ER
PT J
AU Silver, AL
Masia, R
Hasserjian, RP
Deschler, DG
AF Silver, Amanda L.
Masia, Ricard
Hasserjian, Robert P.
Deschler, Daniel G.
TI Pathology Quiz Case 1 Diffuse large B-cell lymphoma (DLBCL)
SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY
LA English
DT Editorial Material
ID CRANIAL NERVE PALSIES; NON-HODGKIN-LYMPHOMA; CENTRAL SKULL BASE; MR
C1 [Silver, Amanda L.; Deschler, Daniel G.] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Masia, Ricard; Hasserjian, Robert P.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Silver, AL (reprint author), Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
NR 10
TC 0
Z9 0
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0886-4470
J9 ARCH OTOLARYNGOL
JI Arch. Otolaryngol. Head Neck Surg.
PD AUG
PY 2010
VL 136
IS 8
BP 840
EP +
PG 3
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 640FD
UT WOS:000281033300019
PM 20713768
ER
PT J
AU Joehl, RJ
AF Joehl, Raymond J.
TI Mom Is Not Permitted to Be Ill
SO ARCHIVES OF SURGERY
LA English
DT Editorial Material
C1 [Joehl, Raymond J.] US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Surg Serv, Hines, IL 60141 USA.
[Joehl, Raymond J.] Loyola Univ, Med Ctr, Maywood, IL 60153 USA.
RP Joehl, RJ (reprint author), Hines VA Hosp, 5000 S 5th Ave, Hines, IL 60141 USA.
EM raymond.joehl@va.gov
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0004-0010
J9 ARCH SURG-CHICAGO
JI Arch. Surg.
PD AUG
PY 2010
VL 145
IS 8
BP 780
EP 780
PG 1
WC Surgery
SC Surgery
GA 640FB
UT WOS:000281033000016
PM 20737736
ER
PT J
AU Napadow, V
LaCount, L
Park, K
As-Sanie, S
Clauw, DJ
Harris, RE
AF Napadow, Vitaly
LaCount, Lauren
Park, Kyungmo
As-Sanie, Sawsan
Clauw, Daniel J.
Harris, Richard E.
TI Intrinsic Brain Connectivity in Fibromyalgia Is Associated With Chronic
Pain Intensity
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID RESTING-STATE CONNECTIVITY; FUNCTIONAL CONNECTIVITY; SPONTANEOUS
FLUCTUATIONS; RESPONSE FUNCTION; DEFAULT NETWORK; WORKING-MEMORY; BOLD
SIGNAL; CORTEX; DYNAMICS; TASK
AB Objective. Fibromyalgia (FM) is considered to be the prototypical central chronic pain syndrome and is associated with widespread pain that fluctuates spontaneously. Multiple studies have demonstrated altered brain activity in these patients. The objective of this study was to investigate the degree of connectivity between multiple brain networks in patients with FM, as well as how activity in these networks correlates with the level of spontaneous pain.
Methods. Resting-state functional magnetic resonance imaging (FMRI) data from 18 patients with FM and 18 age-matched healthy control subjects were analyzed using dual-regression independent components analysis, which is a data-driven approach for the identification of independent brain networks. Intrinsic, or resting-state, connectivity was evaluated in multiple brain networks: the default mode network (DMN), the executive attention network (EAN), and the medial visual network (MVN), with the MVN serving as a negative control. Spontaneous pain levels were also analyzed for covariance with intrinsic connectivity.
Results. Patients with FM had greater connectivity within the DMN and right EAN (corrected P [P(corr)] < 0.05 versus controls), and greater connectivity between the DMN and the insular cortex, which is a brain region known to process evoked pain. Furthermore, greater intensity of spontaneous pain at the time of the FMRI scan correlated with greater intrinsic connectivity between the insula and both the DMN and right EAN (P(corr) < 0.05).
Conclusion. These findings indicate that resting brain activity within multiple networks is associated with spontaneous clinical pain in patients with FM. These findings may also have broader implications for how subjective experiences such as pain arise from a complex interplay among multiple brain networks.
C1 [Napadow, Vitaly] Massachusetts Gen Hosp, Dept Radiol, Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Napadow, Vitaly] Logan Coll Chiropract, Chesterfield, MO USA.
[Park, Kyungmo] Kyung Hee Univ, Yongin, South Korea.
[As-Sanie, Sawsan; Clauw, Daniel J.; Harris, Richard E.] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Napadow, V (reprint author), Massachusetts Gen Hosp, Dept Radiol, Martinos Ctr Biomed Imaging, 149 13th St 2301, Charlestown, MA 02129 USA.
EM vitaly@nmr.mgh.harvard.edu
RI Harris, Richard/F-1307-2011
FU NIH (National Center for Complementary and Alternative Medicine)
[K01-A002166, R01-AT-004714, F05-AT-003770, P01-AT-002048,
K01-AT-01111]; National Center for Research Resources [P41-RR-14075];
GCRC [M01-RR-01066]; Mental Illness and Neuroscience Discovery
Institute; Pfizer Inc.; Institute of Information Technology Advancement,
Korea [IITA-2008 [C1090-0801-0002]]; US Department of Defense
[DAMD-W81XWH-07-2-0050]; Dana Foundation
FX Supported by the NIH (National Center for Complementary and Alternative
Medicine grants K01-A002166 and R01-AT-004714 [to Dr. Napadow],
F05-AT-003770 [to Dr. Park], and P01-AT-002048, K01-AT-01111 [to Dr.
Harris], and National Center for Research Resources grants P41-RR-14075
and GCRC M01-RR-01066), the Mental Illness and Neuroscience Discovery
Institute, and Pfizer Inc. Dr. Park's work also was supported by the
Institute of Information Technology Advancement, Korea (IITA-2008
[C1090-0801-0002]). Dr. Harris' work also was supported by the US
Department of Defense (Army grant DAMD-W81XWH-07-2-0050); he is
recipient of a Dana Foundation Award in Brain and Immuno-Imaging.
NR 50
TC 203
Z9 208
U1 1
U2 31
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD AUG
PY 2010
VL 62
IS 8
BP 2545
EP 2555
DI 10.1002/art.27497
PG 11
WC Rheumatology
SC Rheumatology
GA 661WA
UT WOS:000282762100042
PM 20506181
ER
PT J
AU Liao, KP
Cai, TX
Gainer, V
Goryachev, S
Zeng-Treitler, Q
Raychaudhuri, S
Szolovits, P
Churchill, S
Murphy, S
Kohane, I
Karlson, EW
Plenge, RM
AF Liao, Katherine P.
Cai, Tianxi
Gainer, Vivian
Goryachev, Sergey
Zeng-Treitler, Qing
Raychaudhuri, Soumya
Szolovits, Peter
Churchill, Susanne
Murphy, Shawn
Kohane, Isaac
Karlson, Elizabeth W.
Plenge, Robert M.
TI Electronic Medical Records for Discovery Research in Rheumatoid
Arthritis
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID HEALTH RECORDS; AUTOMATED IDENTIFICATION; NECROSIS-FACTOR;
UNITED-STATES; ANTI-CCP; SENSITIVITY; DIAGNOSIS; RISK; ASSOCIATION;
SPECIFICITY
C1 [Plenge, Robert M.] Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA.
[Cai, Tianxi] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Gainer, Vivian; Goryachev, Sergey; Churchill, Susanne] Partners Healthcare Syst, Boston, MA USA.
[Zeng-Treitler, Qing] Univ Utah, Salt Lake City, UT USA.
[Raychaudhuri, Soumya; Plenge, Robert M.] Broad Inst, Cambridge, MA USA.
[Szolovits, Peter] MIT, Cambridge, MA 02139 USA.
[Murphy, Shawn] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Plenge, RM (reprint author), Brigham & Womens Hosp, Div Rheumatol Allergy & Immunol, 77 Ave Louis Pasteur,Suite 168, Boston, MA 02115 USA.
EM rplenge@partners.org
RI Kohane, Isaac Kohane/K-3716-2012;
OI Kohane, Isaac Kohane/0000-0003-2192-5160; Szolovits,
Peter/0000-0001-8411-6403
FU National Library of Medicine [U54LM008748]; NIH [T32-AR055885,
R01-LM007222, R01-DK075837, R01-LM009966, R21-NR0101710-01,
R21-NS067463, K08-AR-055688-01A1, UL1-RR02578-01, R01-HL091495-01A1,
R01-AR049880, P60-AR047782, K24-AR0524-01, R01-AR057108, R01-AR056768,
U54-LM00878]; i2b2 [NIH U54-LM008748]
FX Supported by award U54LM008748 from the National Library of Medicine.
Dr. Liao's work was supported by the NIH (grant T32-AR055885). Drs. Cai,
Goryachev, Szolovits, Churchill, and Kohane's work was supported by the
i2b2 grant (NIH U54-LM008748). Dr. Zeng-Treitler's work was supported by
the NIH (grants R01-LM007222, R01-DK075837, R01-LM009966,
R21-NR0101710-01, and R21-NS067463) and the i2b2 grant (NIH
U54-LM008748). Dr. Raychaudhuri's work was supported by the NIH (grant
K08-AR-055688-01A1). Dr. Murphy's work was supported by the NIH (grants
UL1-RR02578-01 and R01-HL091495-01A1) and the i2b2 grant (NIH
U54-LM008748). Dr. Karlson's work was supported by the NIH (grants
R01-AR049880, P60-AR047782, and K24-AR0524-01) and the i2b2 grant (NIH
U54-LM008748). Dr. Plenge's work was supported by the NIH (grants
R01-AR057108, R01-AR056768, and U54-LM00878) and a Career Award for
Medical Scientists from the Burroughs Wellcome Fund.
NR 34
TC 86
Z9 86
U1 0
U2 8
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 2151-464X
J9 ARTHRIT CARE RES
JI Arthritis Care Res.
PD AUG
PY 2010
VL 62
IS 8
BP 1120
EP 1127
DI 10.1002/acr.20184
PG 8
WC Rheumatology
SC Rheumatology
GA 639NA
UT WOS:000280980300009
PM 20235204
ER
PT J
AU Fitzgerald, ML
Mujawar, Z
Tamehiro, N
AF Fitzgerald, Michael L.
Mujawar, Zahedi
Tamehiro, Norimasa
TI ABC transporters, atherosclerosis and inflammation
SO ATHEROSCLEROSIS
LA English
DT Review
DE ABCA1; ABCG1; ABCG5; ABCG8; Tangier disease; Sitosterolemia;
Atherosclerosis; Inflammation
ID HIGH-DENSITY-LIPOPROTEIN; APOLIPOPROTEIN-A-I; CORONARY-HEART-DISEASE;
REVERSE CHOLESTEROL TRANSPORT; INCREASED SITOSTEROL ABSORPTION; BINDING
CASSETTE TRANSPORTER-1; RANDOMIZED CONTROLLED-TRIAL; RECEPTOR-DEFICIENT
MICE; ABCG1(-/-) BONE-MARROW; TRANSFER PROTEIN GENE
AB Atherosclerosis, driven by inflamed lipid-laden lesions, can occlude the coronary arteries and lead to myocardial infarction. This chronic disease is a major and expensive health burden. However, the body is able to mobilize and excrete cholesterol and other lipids, thus preventing atherosclerosis by a process termed reverse cholesterol transport (RCT). Insight into the mechanism of RCT has been gained by the study of two rare syndromes caused by the mutation of ABC transporter loci. In Tangier disease, loss of ABCA1 prevents cells from exporting cholesterol and phospholipid, thus resulting in the build-up of cholesterol in the peripheral tissues and a loss of circulating HDL. Consistent with HDL being an athero-protective particle, Tangier patients are more prone to develop atherosclerosis. Likewise, sitosterolemia is another inherited syndrome associated with premature atherosclerosis. Here mutations in either the ABCG5 or G8 loci, prevents hepatocytes and enterocytes from excreting cholesterol and plant sterols, including sitosterol, into the bile and intestinal lumen. Thus, ABCG5 and G8, which from a heterodimer, constitute a transporter that excretes cholesterol and dietary sterols back into the gut, while ABCA1 functions to export excess cell cholesterol and phospholipid during the biogenesis of HDL. Interestingly, a third protein, ABCG1, that has been shown to have anti-atherosclerotic activity in mice, may also act to transfer cholesterol to mature HDL particles. Here we review the relationship between the lipid transport activities of these proteins and their anti-atherosclerotic effect, particularly how they may reduce inflammatory signaling pathways. Of particular interest are recent reports that indicate both ABCA1 and ABCG1 modulate cell surface cholesterol levels and inhibit its partitioning into lipid rafts. Given lipid rafts may provide platforms for innate immune receptors to respond to inflammatory signals, it follows that loss of ABCA1 and ABCG1 by increasing raft content will increase signaling through these receptors, as has been experimentally demonstrated. Moreover, additional reports indicate ABCA1, and possibly SR-BI, another HDL receptor, may directly act as anti-inflammatory receptors independent of their lipid transport activities. Finally, we give an update on the progress and pitfalls of therapeutic approaches that seek to stimulate the flux of lipids through the RCT pathway. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
C1 [Fitzgerald, Michael L.; Mujawar, Zahedi; Tamehiro, Norimasa] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Lipid Metab Unit, Boston, MA 02114 USA.
[Fitzgerald, Michael L.; Mujawar, Zahedi; Tamehiro, Norimasa] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
RP Fitzgerald, ML (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Lipid Metab Unit, 185 Cambridge St, Boston, MA 02114 USA.
EM mfitzgerald@ccib.mgh.harvard.edu
FU NIH-NHLBI; American Heart Association [HL074136, 09GRNT2260352]; Uehara
Memorial Foundation; Nagai Foundation of Tokyo; Japan Heart Foundation
FX This work was supported by NIH-NHLBI and American Heart Association
grants to ML Fitzgerald (HL074136, 09GRNT2260352) and by fellowship
training grants from the Uehara Memorial Foundation, the Nagai
Foundation of Tokyo and the Japan Heart Foundation (N Tamehiro), the
American Heart Association (Z Mujawar).
NR 168
TC 86
Z9 98
U1 1
U2 19
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 AUG
PY 2010
VL 211
IS 2
BP 361
EP 370
DI 10.1016/j.atherosclerosis.2010.01.011
PG 10
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 634VC
UT WOS:000280612700002
PM 20138281
ER
PT J
AU Blankstein, R
Ferencik, M
AF Blankstein, Ron
Ferencik, Maros
TI The vulnerable plaque: Can it be detected with Cardiac CT?
SO ATHEROSCLEROSIS
LA English
DT Editorial Material
DE Vulnerable plaque; Cardiac CT; Acute coronary syndrome
ID ACUTE CORONARY SYNDROME; MULTISLICE COMPUTED-TOMOGRAPHY; ACUTE
MYOCARDIAL-INFARCTION; INTRAVASCULAR ULTRASOUND ANALYSIS; RADIOFREQUENCY
DATA-ANALYSIS; STABLE ANGINA-PECTORIS; VIRTUAL HISTOLOGY;
ARTERY-DISEASE; PROGNOSTIC VALUE; ATHEROSCLEROTIC PLAQUES
C1 [Blankstein, Ron] Harvard Univ, Brigham & Womens Hosp, Sch Med, Noninvas Cardiovasc Imaging Program,Dept Med,Card, Boston, MA 02115 USA.
[Ferencik, Maros] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Cardiol Div, Boston, MA 02115 USA.
RP Blankstein, R (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Noninvas Cardiovasc Imaging Program,Dept Med,Card, 75 Francis St, Boston, MA 02115 USA.
EM rblankstein@partners.org
NR 39
TC 8
Z9 8
U1 0
U2 1
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 AUG
PY 2010
VL 211
IS 2
BP 386
EP 389
DI 10.1016/j.atherosclerosis.2010.06.014
PG 4
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 634VC
UT WOS:000280612700006
PM 20619414
ER
PT J
AU Damrauer, SM
Fisher, MD
Wada, H
Siracuse, JJ
da Silva, CG
Moon, K
Csizmadia, E
Maccariello, ER
Patel, VI
Studer, P
Essayagh, S
Aird, WC
Daniel, S
Ferran, C
AF Damrauer, Scott M.
Fisher, Mark D.
Wada, Hiromi
Siracuse, Jeffrey J.
da Silva, Cleide G.
Moon, Karam
Csizmadia, Eva
Maccariello, Elizabeth R.
Patel, Virendra I.
Studer, Peter
Essayagh, Sanah
Aird, William C.
Daniel, Soizic
Ferran, Christiane
TI A20 inhibits post-angioplasty restenosis by blocking macrophage
trafficking and decreasing adventitial neovascularization
SO ATHEROSCLEROSIS
LA English
DT Article
DE Neointimal hyperplasia; Vascular endothelial growth factor;
Neovascularization; Macrophage
ID ENDOTHELIAL GROWTH-FACTOR; MONOCYTE CHEMOATTRACTANT PROTEIN-1;
FACTOR-KAPPA-B; MUSCLE-CELL PROLIFERATION; INTIMAL HYPERPLASIA;
NEOINTIMAL HYPERPLASIA; IN-VITRO; ATHEROSCLEROTIC LESIONS; ADHESION
MOLECULE-1; HEMATOPOIETIC STEM
AB Objective: Neointimal hyperplasia is an inflammatory and proliferative process that occurs as a result of injury to the vessel wall. We have shown that the homeostatic protein A20 prevents neointimal hyperplasia by affecting endothelial cell (EC) and smooth muscle cell (SMC) responses to injury. In this work, we questioned whether A20 impacts other pathogenic effectors of neointimal hyperplasia including homing of monocyte/macrophages and EC/SMC precursors to the site of vascular injury, vascular endothelial growth factor (VEGF) secretion, and adventitial neovascularization.
Methods and results: Carotid balloon angioplasty was performed on rat recipients of a bone marrow transplant from green fluorescent rats. Adenoviral delivery of A20 prevented neointimal hyperplasia and decreased macrophage infiltration. This was associated with decreased ICAM-1 and MCP-1 expression in vitro. Additionally, A20 reduced neovascularization in the adventitia of balloon injured carotid arteries, which correlated with fewer VEGF positive cells.
Conclusions: A20 downregulates adhesion markers, chemokine production, and adventitial angiogenesis, all of which are required for macrophage trafficking to sites of vascular injury. This, in turn, diminishes the inflammatory milieu to prevent neointimal hyperplasia. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
C1 [Ferran, Christiane] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Ctr Vasc Biol Res,Div Vasc Surg, Boston, MA 02215 USA.
[Wada, Hiromi; Aird, William C.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Mol Med, Boston, MA 02215 USA.
[Ferran, Christiane] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Transplant Inst, Boston, MA 02215 USA.
[Ferran, Christiane] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Nephrol,Dept Med, Boston, MA 02215 USA.
[Damrauer, Scott M.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
RP Ferran, C (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Ctr Vasc Biol Res,Div Vasc Surg, RN 370F G,99 Brookline Ave, Boston, MA 02215 USA.
EM cferran@caregroup.harvard.edu
OI Moon, Karam/0000-0002-7984-5801
FU NIH [RO1 HL080130, RO1 DK063275, RO1 HL57791, T32 HL07734]; Juvenile
Diabetes Research Foundation [1-2007-567]
FX This research was supported by NIH grant RO1 HL080130 and in part by NIH
grants RO1 DK063275, RO1 HL57791, Juvenile Diabetes Research Foundation
grant 1-2007-567 to CF. SMD, MDF, JJS, and VIP were supported by NIH T32
HL07734.
NR 32
TC 12
Z9 13
U1 0
U2 13
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 AUG
PY 2010
VL 211
IS 2
BP 404
EP 408
DI 10.1016/j.atherosclerosis.2010.03.029
PG 5
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 634VC
UT WOS:000280612700011
PM 20430393
ER
PT J
AU Otto, MW
McHugh, RK
Simon, NM
Farach, FJ
Worthington, JJ
Pollack, MH
AF Otto, Michael W.
McHugh, R. Kathryn
Simon, Naomi M.
Farach, Frank J.
Worthington, John J.
Pollack, Mark H.
TI Efficacy of CBT for benzodiazepine discontinuation in patients with
panic disorder: Further evaluation
SO BEHAVIOUR RESEARCH AND THERAPY
LA English
DT Article
DE Benzodiazepines; Panic disorder; Cognitive behavior therapy; Drug
withdrawal
ID COGNITIVE-BEHAVIORAL THERAPY; ALPRAZOLAM DISCONTINUATION;
PHARMACOLOGICAL TREATMENT; ANXIETY DISORDER; FOLLOW-UP; WITHDRAWAL;
METAANALYSIS; TRIAL; AGORAPHOBIA; DEPRESSION
AB Despite its acute efficacy for the treatment of panic disorder, benzodiazepines (BZs) are associated with a withdrawal syndrome that closely mimics anxiety sensations, leading to difficulty with treatment discontinuation and often disorder relapse. An exposure-based cognitive-behavioral treatment for BZ discontinuation, Panic Control Treatment for BZ Discontinuation (CBT) targets the fear of these sensations and has demonstrated efficacy in preventing disorder relapse and facilitating successful BZ discontinuation among patients with panic disorder. In this randomized controlled trial, CBT was compared to taper alone and a taper plus a relaxation condition to control for the effect of therapist contact and support among 47 patients with panic disorder seeking taper from BZs. Based on the primary outcome of successful discontinuation of BZ use, results indicate that adjunctive CBT provided additive benefits above both taper alone and taper plus relaxation, with consistently medium and large effect sizes over time that reached significance at the six month follow-up evaluation. The efficacy of CBT relative to either of the other taper conditions reflected very large and significant effect sizes at that time. These findings suggest that CBT provides specific efficacy for the successful discontinuation from BZs, even when controlling for therapist contact and relaxation training. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Otto, Michael W.] Boston Univ, Ctr Anxiety & Related Disorders, Dept Psychol, Boston, MA 02215 USA.
[Simon, Naomi M.; Farach, Frank J.; Worthington, John J.; Pollack, Mark H.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
RP Otto, MW (reprint author), Boston Univ, Ctr Anxiety & Related Disorders, Dept Psychol, 648 Beacon St,6th Floor,5th Floor, Boston, MA 02215 USA.
EM mwotto@bu.edu
OI McHugh, R. Kathryn/0000-0002-3011-8697; Farach,
Frank/0000-0002-2145-0145
FU NIDA NIH HHS [R10 DA009692]
NR 51
TC 23
Z9 23
U1 1
U2 11
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0005-7967
J9 BEHAV RES THER
JI Behav. Res. Ther.
PD AUG
PY 2010
VL 48
IS 8
BP 720
EP 727
DI 10.1016/j.brat.2010.04.002
PG 8
WC Psychology, Clinical
SC Psychology
GA 641CP
UT WOS:000281102400005
PM 20546699
ER
PT J
AU Forcione, DG
Brugge, WR
AF Forcione, David G.
Brugge, William R.
TI New kid on the block? Autoimmune pancreatitis
SO BEST PRACTICE & RESEARCH IN CLINICAL GASTROENTEROLOGY
LA English
DT Article
ID LYMPHOPLASMACYTIC SCLEROSING PANCREATITIS; IMMUNOGLOBULIN G4-ASSOCIATED
CHOLANGITIS; IDIOPATHIC CHRONIC-PANCREATITIS; IGG4-RELATED
SYSTEMIC-DISEASE; HELICOBACTER-PYLORI INFECTION; PRIMARY
SJOGRENS-SYNDROME; OF-THE-LITERATURE; DIAGNOSTIC-CRITERIA;
STEROID-THERAPY; CARBONIC-ANHYDRASE
C1 [Forcione, David G.; Brugge, William R.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
RP Brugge, WR (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
EM wbrugge@partners.org
NR 125
TC 6
Z9 7
U1 1
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1521-6918
EI 1532-1916
J9 BEST PRACT RES CL GA
JI Best Pract. Res. Clin. Gastroenterol.
PD AUG
PY 2010
VL 24
IS 4
BP 361
EP 378
DI 10.1016/j.bpg.2010.04.002
PG 18
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 670AN
UT WOS:000283392300002
PM 20833341
ER
PT J
AU Lansdorp-Vogelaar, I
Knudsen, AB
Brenner, H
AF Lansdorp-Vogelaar, Iris
Knudsen, Amy B.
Brenner, Hermann
TI Cost-effectiveness of colorectal cancer screening - An overview
SO BEST PRACTICE & RESEARCH IN CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE Colorectal neoplasms; Mass screening; Cost-benefit analysis; Occult
blood; Colonoscopy; Sigmoidoscopy; Colonography, Computed tomographic;
Stool DNA; Capsule endoscopy
ID FECAL-OCCULT-BLOOD; SERVICES TASK-FORCE; COLON-CANCER; FLEXIBLE
SIGMOIDOSCOPY; PERSONALIZED MEDICINE; IMMUNOCHEMICAL TEST; CAPSULE
ENDOSCOPY; CT COLONOGRAPHY; DETECTION RATES; UNITED-STATES
AB There are several modalities available for a colorectal cancer (CRC) screening program. When determining which CRC screening program to implement, the costs of such programs should be considered in comparison to the health benefits they are expected to provide. Cost-effectiveness analysis provides a tool to do this. In this paper we review the evidence on the cost-effectiveness of CRC screening. Published studies universally indicate that when compared with no CRC screening, all screening modalities provide additional years of life at a cost that is deemed acceptable by most industrialized nations. Many recent studies even find CRC screening to be cost-saving. However, when the alternative CRC screening strategies are compared against each other in an incremental cost-effectiveness analysis, no single optimal strategy emerges across the studies. There is consensus that the new technologies of stool DNA testing, computed tomographic colonography and capsule endoscopy are not yet cost-effective compared with the established CRC screening tests. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Lansdorp-Vogelaar, Iris] Erasmus MC, Univ Med Ctr, Dept Publ Hlth, NL-3000 CA Rotterdam, Netherlands.
[Knudsen, Amy B.] Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA.
[Brenner, Hermann] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, D-69115 Heidelberg, Germany.
RP Lansdorp-Vogelaar, I (reprint author), Erasmus MC, Univ Med Ctr, Dept Publ Hlth, POB 2040, NL-3000 CA Rotterdam, Netherlands.
EM i.vogelaar@erasmusmc.nl; aknudsen@mgh-ita.org;
h.brenner@Dkfz-Heidelberg.de
RI Brenner, Hermann/B-4627-2017
OI Brenner, Hermann/0000-0002-6129-1572
FU National Cancer Institute [U01-CA-097426, U01-CA-115953, U01-CA-088204]
FX Drs. Lansdorp-Vogelaar and Knudsen are supported in part by Cancer
Intervention and Surveillance Modeling Network grants from the National
Cancer Institute: (U01-CA-097426 (Lansdorp-Vogelaar), U01-CA-115953
(Lansdorp-Vogelaar), and U01-CA-088204 (Knudsen)).
NR 91
TC 21
Z9 22
U1 1
U2 8
PU BAILLIERE TINDALL
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1521-6918
J9 BEST PRACT RES CL GA
JI Best Pract. Res. Clin. Gastroenterol.
PD AUG
PY 2010
VL 24
IS 4
BP 439
EP 449
DI 10.1016/j.bpg.2010.04.004
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 670AN
UT WOS:000283392300009
PM 20833348
ER
PT J
AU Wheeler, JM
Guthrie, CR
Kraemer, BC
AF Wheeler, Jeanna M.
Guthrie, Chris R.
Kraemer, Brian C.
TI The role of MSUT-2 in tau neurotoxicity: a target for neuroprotection in
tauopathy?
SO BIOCHEMICAL SOCIETY TRANSACTIONS
LA English
DT Article
DE aggresome; Alzheimer's disease; neurodegeneration; neurofibrillary
tangle; protein aggregation; tau
ID CAENORHABDITIS-ELEGANS; PROTEIN AGGREGATION; AGGRESOME FORMATION;
MISFOLDED PROTEINS; MISSENSE MUTATIONS; FTDP-17 MUTATIONS; POLYADENOSINE
RNA; DEMENTIA FTDP-17; INCLUSION-BODIES; MOUSE MODEL
AB We previously developed a transgenic Caenorhabditis elegons model of human tauopathy disorders by expressing human tau in nematode worm neurons to explore genetic pathways contributing to tau-induced neurodegeneration. This animal model recapitulates several hallmarks of human tauopathies, including altered behaviour, accumulation of detergent-insoluble phosphorylated tau protein and neurodegeneration. To identify genes required for tau neurotoxicity, we carried out a forward genetic screen for mutations that suppress tau neurotoxicity. We ultimately cloned the sut-2 (suppressor of tau pathology-2) gene, mutations in which alleviate tau neurotoxicity in C. elegons. SUT-2 encodes a novel subtype of CCCH zinc-finger protein conserved across animal phyla. SUT-2 shares significant identity with the mammalian SUT-2 (MSUT-2). We identified components of the aggresome as binding partners of MSUT-2. Thus we hypothesize that MSUT-2 plays a role in the formation and/or clearance of protein aggregates. We are currently exploring the role of MSUT-2 in tauopathy using mammalian systems. The identification of sut-2 as a gene required for tau neurotoxicity in C. elegons suggests new neuroprotective strategies targeting MSUT-2 that may be effective in modulating tau neurotoxicity in human tauopathy disorders.
C1 [Kraemer, Brian C.] Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Seattle Div, Seattle, WA 98108 USA.
Univ Washington, Dept Med, Div Gerontol, Seattle, WA 98195 USA.
Univ Washington, Dept Med, Div Geriatr Med, Seattle, WA 98195 USA.
RP Kraemer, BC (reprint author), Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Seattle Div, 1660 S Colombian Way, Seattle, WA 98108 USA.
EM kraemerb@u.washington.edu
FU Department of Veterans Affairs; National Institute of Neurological
Disorders and Stroke [R01NS064131]
FX This work was Supported by a Department of Veterans Affairs Merit Review
Grant and by the National Institute of Neurological Disorders and Stroke
[grant number R01NS064131 (to B.C.K.)].
NR 39
TC 6
Z9 7
U1 1
U2 2
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0300-5127
J9 BIOCHEM SOC T
JI Biochem. Soc. Trans.
PD AUG
PY 2010
VL 38
BP 973
EP 976
DI 10.1042/BST0380973
PN 4
PG 4
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 636QL
UT WOS:000280753600021
PM 20658987
ER
PT J
AU Merkulova, M
Bakulina, A
Thaker, YR
Gruber, G
Marshansky, V
AF Merkulova, Maria
Bakulina, Anastasia
Thaker, Youg Raj
Grueber, Gerhard
Marshansky, Vladimir
TI Specific motifs of the V-ATPase a2-subunit isoform interact with
catalytic and regulatory domains of ARNO
SO BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
LA English
DT Article
DE V-type ATPase; Arf-GEF ARNO; Sec7-domain; PB-domain; BIAcore; NMR;
Peptide structure; Phosphorylation
ID VACUOLAR H+-ATPASE; NUCLEOTIDE EXCHANGE FACTORS; RENAL TUBULAR-ACIDOSIS;
A-SUBUNIT; PROTON PUMP; ARF; YEAST; PHYSIOLOGY; ALDOLASE; FAMILY
AB We have previously shown that the V-ATPase a2-subunit isoform interacts specifically, and in an intra-endosomal acidification-dependent manner, with the Arf-GEF ARNO. In the present study, we examined the molecular mechanism of this interaction using synthetic peptides and purified recombinant proteins in protein-association assays. In these experiments, we revealed the involvement of multiple sites on the N-terminus of the V-ATPase a2-subunit (a2N) in the association with ARNO. While six a2N-derived peptides interact with wild-type ARNO, only two of them (named a2N-01 and a2N-03) bind to its catalytic Sec7-domain. However, of these, only the a2N-01 peptide (MGSLFRSESMCLAQLFL) showed specificity towards the Sec7-domain compared to other domains of the ARNO protein. Surface plasmon resonance kinetic analysis revealed a very strong binding affinity between this a2N-01 peptide and the Sec7-domain of ARNO, with dissociation constant K(D) = 3.44 x 10(-7) M. similar to the K(D) = 3.13 x 10(-7) M binding affinity between wild-type a2N and the full-length ARNO protein. In further pull-down experiments, we also revealed the involvement of multiple sites on ARNO itself in the association with a2N. However, while its catalytic Sec7-domain has the strongest interaction, the PH-, and PB-domains show much weaker binding to a2N. Interestingly, an interaction of the a2N to a peptide corresponding to ARNO's PB-domain was abolished by phosphorylation of ARNO residue Ser(392). The 3D-structures of the non-phosphorylated and phosphorylated peptides were resolved by NMR spectroscopy, and we have identified rearrangements resulting from Ser(392) phosphorylation. Homology modeling suggests that these alterations may modulate the access of the a2N to its interaction pocket on ARNO that is formed by the Sec7 and PB-domains. Overall, our data indicate that the interaction between the a2-subunit of V-ATPase and ARNO is a complex process involving various binding sites on both proteins. Importantly, the binding affinity between the a2-subunit and ARNO is in the same range as those previously reported for the intramolecular association of subunits within V-ATPase complex itself, indicating an important cell biological role for the interaction between the V-ATPase and small GTPase regulatory proteins. (C) 2010 Elsevier B.V. All rights reserved.
C1 [Marshansky, Vladimir] Massachusetts Gen Hosp, CPZN, Ctr Syst Biol, Program Membrane Biol, Boston, MA 02114 USA.
[Merkulova, Maria; Marshansky, Vladimir] Massachusetts Gen Hosp, Div Nephrol, Dept Med, Boston, MA 02114 USA.
[Merkulova, Maria; Marshansky, Vladimir] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Bakulina, Anastasia] State Res Ctr Virol & Biotechnol VECTOR, Koltsov 630559, Novosibirsk Reg, Russia.
[Thaker, Youg Raj; Grueber, Gerhard] Nanyang Technol Univ, Div Struct & Computat Biol, Sch Biol Sci, Singapore 637551, Singapore.
[Grueber, Gerhard] Bioinformat Inst ASTAR, Singapore 138671, Singapore.
RP Marshansky, V (reprint author), Massachusetts Gen Hosp, CPZN, Ctr Syst Biol, Program Membrane Biol, 185 Cambridge St,Suite 8212, Boston, MA 02114 USA.
EM Vladimir_Marshansky@hms.harvard.edu
RI Bakulina, Anastasia/A-6215-2014; Thaker, Youg/K-6083-2016;
OI thaker, youg/0000-0002-6496-1017
FU National Institutes of Health (NIH) [DK038452]; Boston Area Diabetes
Endocrinology Research Center (BADERC) [DK057521-08]; School of
Biological Sciences, Nanyang Technological University (NTU) [SUG/31/05]
FX We would like to thank Dr. Dennis Brown and Dr. Masamitsu Futai for the
critical reading and constructive suggestions during the preparation of
this manuscript. We also would like to thank Dr. Ashok Khatri, (Director
of Partners/MGH Peptide/Protein Core Facility) for the assistance with
peptide synthesis. We are grateful to Dr. James Casanova for his
generous gift of the cDNA construct of human ARNO. We are also grateful
to S. Gayen, School of Biological Sciences, NTU, for the assistance in
generating the NMR related figures. This study was supported by a
National Institutes of Health (NIH) grant DK038452 and by Boston Area
Diabetes Endocrinology Research Center (BADERC) grant DK057521-08 (to
VM) as well as by the School of Biological Sciences, Nanyang
Technological University (NTU) grant SUG/31/05 (to GG). Y.R. Thaker is
grateful to the authority of NTU for awarding a research scholarship.
NR 50
TC 20
Z9 20
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0005-2728
J9 BBA-BIOENERGETICS
JI Biochim. Biophys. Acta-Bioenerg.
PD AUG
PY 2010
VL 1797
IS 8
BP 1398
EP 1409
DI 10.1016/j.bbabio.2010.02.009
PG 12
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 625IM
UT WOS:000279888700006
PM 20153292
ER
PT J
AU Bhattacharyya, R
Kovacs, DM
AF Bhattacharyya, Raja
Kovacs, Dora M.
TI ACAT inhibition and amyloid beta reduction
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
LA English
DT Review
DE Alzheimer's disease; A beta; ACAT; Cholesterol; Cholesteryl ester; Lipid
droplet
ID A-CHOLESTEROL ACYLTRANSFERASE; LOW-DENSITY-LIPOPROTEIN; CORONARY-ARTERY
ATHEROSCLEROSIS; DOMINANT-NEGATIVE MUTANT; TRANSGENIC MOUSE MODEL;
MAMMALIAN ACYL-COA; ALZHEIMERS-DISEASE; LIPID DROPLETS; PRECURSOR
PROTEIN; APOLIPOPROTEIN-E
AB Alzheimer's disease (AD) is a devastating neurodegenerative disorder. Accumulation and deposition of the beta-amyloid (A beta) peptide generated from its larger amyloid precursor protein (APP) is one of the pathophysiological hallmarks of AD. Intracellular cholesterol was shown to regulate A beta production. Recent genetic and biochemical studies indicate that not only the amount, but also the distribution of intracellular cholesterol is critical to regulate A beta generation. Acyl-coenzyme A: cholesterol acyl-transferase (ACAT) is a family of enzymes that regulates the cellular distribution of cholesterol by converting membrane cholesterol into hydrophobic cholesteryl esters for cholesterol storage and transport. Using pharmacological inhibitors and transgenic animal models, we and others have identified ACAT1 as a potential therapeutic target to lower A beta generation and accumulation. Here we discuss data focusing on ACAT inhibition as an effective strategy for the prevention and treatment of AD. (C) 2010 Elsevier B.V. All rights reserved.
C1 [Bhattacharyya, Raja; Kovacs, Dora M.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neurobiol Dis Lab,Genet & Aging Res Unit,MIND, Charlestown, MA 02129 USA.
RP Kovacs, DM (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neurobiol Dis Lab,Genet & Aging Res Unit,MIND, Charlestown, MA 02129 USA.
EM dora_kovacs@hms.harvard.edu
FU Cure Alzheimer's Fund; U.S. National Institutes of Health [R01 NS45860]
FX This study was supported by grants from the Cure Alzheimer's Fund
(D.M.K.) and the U.S. National Institutes of Health (R01 NS45860;
D.M.K.).
NR 112
TC 29
Z9 29
U1 0
U2 5
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 AUG
PY 2010
VL 1801
IS 8
SI SI
BP 960
EP 965
DI 10.1016/j.bbalip.2010.04.003
PG 6
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 620CG
UT WOS:000279476000028
PM 20398792
ER
PT J
AU Dominy, JE
Lee, Y
Gerhart-Hines, Z
Puigserver, P
AF Dominy, John E., Jr.
Lee, Yoonjin
Gerhart-Hines, Zachary
Puigserver, Pere
TI Nutrient-dependent regulation of PGC-1 alpha's acetylation state and
metabolic function through the enzymatic activities of Sirt1/GCN5
SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS
LA English
DT Review
DE PGC-1 alpha; GCN5; Sirt1; Acetylation
ID TRANSCRIPTIONAL COACTIVATOR PGC-1-ALPHA; HEPATIC GLUCOSE-PRODUCTION;
PPAR-GAMMA COACTIVATOR-1; NAD(+) SALVAGE PATHWAY; FATTY-ACID OXIDATION;
RECEPTOR-GAMMA; DEACETYLASE SIRT1; MODULATES GLUCONEOGENESIS;
MITOCHONDRIAL-FUNCTION; INSULIN SENSITIVITY
AB Mammals possess an intricate regulatory system for controlling flux through fuel utilization pathways in response to the dietary availability of particular macronutrients. Under fasting conditions, for instance, mammals initiate a whole body metabolic response that limits glucose utilization and favors fatty acid oxidation. Understanding the underlying mechanisms by which this process occurs will facilitate the development of new treatments for metabolic disorders such as type II diabetes and obesity. One of the recently identified components of the signal transduction pathway involved in metabolic reprogramming is PGC-1 alpha. This transcriptional coactivator is able to coordinate the expression of a wide array of genes involved in glucose and fatty acid metabolism. The nutrient-mediated control of PGC-1 alpha activity is tightly correlated with its acetylation state. In this review, we evaluate how the nutrient regulation of PGC-1 alpha activity squares with the regulation of its acetylation state by the deacetylase Sirt1 and the acetyltransferase GCN5. We also propose an outline of additional experimental directives that will help to shed additional light on this very powerful transcriptional coactivator. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Puigserver, Pere] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
RP Puigserver, P (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM pere_puigserver@dfci.harvard.edu
FU NIDDK NIH HHS [R01 DK069966, R01 DK069966-01A1, R01 DK069966-02, R01
DK069966-03, R01 DK069966-04, R01 DK069966-05]
NR 70
TC 74
Z9 77
U1 1
U2 9
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 AUG
PY 2010
VL 1804
IS 8
SI SI
BP 1676
EP 1683
DI 10.1016/j.bbapap.2009.11.023
PG 8
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 621JA
UT WOS:000279571200014
PM 20005308
ER
PT J
AU Wang, J
Fivecoat, H
Ho, L
Pan, Y
Ling, E
Pasinetti, GM
AF Wang, Jun
Fivecoat, Hayley
Ho, Lap
Pan, Yong
Ling, Emi
Pasinetti, Giulio Maria
TI The role of Sirt1: At the crossroad between promotion of longevity and
protection against Alzheimer's disease neuropathology
SO BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS
LA English
DT Review
DE Sirtuins; Caloric restriction; Neurodegeneration; Alzheimer's disease;
Dementia
ID CALORIC RESTRICTION; LIFE-SPAN; SACCHAROMYCES-CEREVISIAE; AMYLOID
NEUROPATHOLOGY; MOUSE MODEL; MECHANISM; PROTEIN; DEACETYLATION;
NICOTINAMIDE; YEAST
AB Sirt1, a mammalian member of the sirtuin gene family, holds great potential for promoting longevity, preventing against disease and increasing cell survival. For example, studies suggest that the beneficial impact of caloric restriction in promoting longevity and cellular function may be mediated, in part, by Sirt1 through mechanisms involving PGC-1 alpha, which plays important role in the regulation of cellular metabolism and inflammatory and antioxidant responses. Sirt1 may also interfere with mechanisms implicated in pathological disorders. We will present recent evidence indicating that Sirt1 may protect against Alzheimer's disease by interfering with the generation of beta-amyloid peptides. We will discuss Sirt1 as a potential novel target, in addition to the development of Sirt1 activators for the prevention and treatment of Alzheimer's disease. Published by Elsevier B.V.
C1 [Wang, Jun; Fivecoat, Hayley; Ho, Lap; Pan, Yong; Ling, Emi; Pasinetti, Giulio Maria] Mt Sinai Sch Med, Dept Neurol,Brain Inst, Ctr Excellence Novel Approaches Neurodiagnost & N, Ctr Excellence Res Complementary & Alternat Med A, New York, NY 10029 USA.
[Pasinetti, Giulio Maria] James J Peters Vet Affairs Med Ctr, GRECC, Biomed Res & Training Program, Bronx, NY 10468 USA.
RP Pasinetti, GM (reprint author), Mt Sinai Sch Med, Dept Neurol,Brain Inst, Ctr Excellence Novel Approaches Neurodiagnost & N, Ctr Excellence Res Complementary & Alternat Med A, 1 Gustave L Levy Pl,Box 1230, New York, NY 10029 USA.
EM giulio.pasinetti@mssm.edu
FU Atkins Foundation
FX The studies reported in this review article were generously supported by
the Atkins Foundation.
NR 38
TC 38
Z9 42
U1 0
U2 8
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 AUG
PY 2010
VL 1804
IS 8
SI SI
BP 1690
EP 1694
DI 10.1016/j.bbapap.2009.11.015
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 621JA
UT WOS:000279571200016
PM 19945548
ER
PT J
AU Hook, V
Hook, G
Kindy, M
AF Hook, Vivian
Hook, Gregory
Kindy, Mark
TI Pharmacogenetic features of cathepsin B inhibitors that improve memory
deficit and reduce beta-amyloid related to Alzheimer's disease
SO BIOLOGICAL CHEMISTRY
LA English
DT Article; Proceedings Paper
CT 6th General Meeting of the International-Proteolysis-Society
CY OCT 26-30, 2009
CL Gold Coast, AUSTRALIA
SP Int Proteolysis Soc
DE Alzheimer's disease; beta-amyloid; cathepsin B; cleavage site;
inhibitor; memory; pharmacogenetics; protease; transgenic AD mice
ID REGULATED SECRETORY VESICLES; PRECURSOR PROTEIN; TRANSGENIC MICE;
WILD-TYPE; IN-VIVO; SELECTIVE INHIBITOR; CHROMAFFIN CELLS; THERAPEUTICS;
PEPTIDES; BACE1
AB Beta-amyloid (A beta) in the brain is a major factor involved in Alzheimer's disease (AD) that results in severe memory deficit. Our recent studies demonstrate pharmacogenetic differences in the effects of inhibitors of cathepsin B to improve memory and reduce A beta in different mouse models of AD. The inhibitors improve memory and reduce brain A beta in mice expressing the wild-type (WT) beta-secretase site of human APP, expressed in most AD patients. However, these inhibitors have no effect in mice expressing the rare Swedish (Swe) mutant amyloid precursor protein (APP). Knockout of the cathepsin B decreased brain A beta in mice expressing WT APP, validating cathepsin B as the target. The specificity of cathepsin B to cleave the WT beta-secretase site, but not the Swe mutant site, of APP for A beta production explains the distinct inhibitor responses in the different AD mouse models. In contrast to cathepsin B, the BACE1 beta-secretase prefers to cleave the Swe mutant site. Discussion of BACE1 data in the field indicate that they do not preclude cathepsin B as also being a beta-secretase. Cathepsin B and BACE1 could participate jointly as beta-secretases. Significantly, the majority of AD patients express WT APP and, therefore, inhibitors of cathepsin B represent candidate drugs for AD.
C1 [Hook, Vivian] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, La Jolla, CA 92093 USA.
[Hook, Vivian] Univ Calif San Diego, Dept Neurosci, Sch Med, La Jolla, CA 92093 USA.
[Hook, Vivian] Univ Calif San Diego, Dept Pharmacol, Sch Med, La Jolla, CA 92093 USA.
[Hook, Vivian] Univ Calif San Diego, Dept Med, Sch Med, La Jolla, CA 92093 USA.
[Hook, Gregory] Amer Life Sci Pharmaceut Inc, San Diego, CA 92109 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.
RP Hook, V (reprint author), Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, La Jolla, CA 92093 USA.
EM vhook@ucsd.edu
FU NIA NIH HHS [R21 AG027446, R44 AG032784, R44 AG030865, 1R44AG032784];
NIDA NIH HHS [R01 DA004271]
NR 47
TC 16
Z9 18
U1 2
U2 7
PU WALTER DE GRUYTER & CO
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1431-6730
J9 BIOL CHEM
JI Biol. Chem.
PD AUG
PY 2010
VL 391
IS 8
BP 861
EP 872
DI 10.1515/BC.2010.110
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 642HL
UT WOS:000281198700004
PM 20536395
ER
PT J
AU Alyea, EP
DeAngelo, DJ
Moldrem, J
Pagel, JM
Przepiorka, D
Sadelin, M
Young, JW
Giralt, S
Bishop, M
Riddell, S
AF Alyea, Edwin P.
DeAngelo, Daniel J.
Moldrem, Jeffrey
Pagel, John M.
Przepiorka, Donna
Sadelin, Michel
Young, James W.
Giralt, Sergio
Bishop, Michael
Riddell, Stan
TI NCI First International Workshop on the Biology, Prevention and
Treatment of Relapse after Allogeneic Hematopoietic Cell
Transplantation: Report from the Committee on Prevention of Relapse
Following Allogeneic Cell Transplantation for Hematologic Malignancies
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Allogeneic hematopoietic cell transplantation; Relapse prevention; Acute
graft-versus-host disease; Immunotherapy; Resistant leukemia
ID CHRONIC MYELOID-LEUKEMIA; BONE-MARROW-TRANSPLANTATION;
VERSUS-HOST-DISEASE; CHRONIC LYMPHOCYTIC-LEUKEMIA; CHRONIC MYELOGENOUS
LEUKEMIA; HUMAN T-CELLS; ANTIGEN-PRESENTING CELLS; ACUTE
LYMPHOBLASTIC-LEUKEMIA; TOTAL-BODY IRRADIATION; REDUCED-INTENSITY
TRANSPLANTATION
AB Prevention of relapse after allogeneic hematopoietic stem cell transplantation is the most likely approach to improve survival of patients treated for hematologic malignancies. Herein we review the limits of currently available transplant therapies and the innovative strategies being developed to overcome resistance to therapy or to fill therapeutic modalities not currently available. These novel strategies include nonimmunologic therapies, such as targeted preparative regimens and posttransplant drug therapy, as well as immunologic interventions, including graft engineering, donor lymphocyte infusions, T cell engineering, vaccination, and dendritic cell-based approaches. Several aspects of the biology of the malignant cells as well as the host have been identified that obviate success of even these newer strategies. To maximize the potential for success, we recommend pursuing research to develop additional targeted therapies to be used in the preparative regimen or as maintenance posttransplant, better characterize the T cell and dendritic cells subsets involved in graft-versus-host disease and the graft-versus-leukemia/tumor effect, identify strategies for timing immunologic or nonimmunologic therapies to eliminate the noncycling cancer stem cell, identify more targets for immunotherapies, develop new vaccines that will not be limited by HLA, and develop methods to identify populations at very high risk for relapse to accelerate clinical development and avoid toxicity in patients not at risk for relapse. Biol Blood Marrow Transplant 16: 1037-1069 (2010) (C) 2010 American Society for Blood and Marrow Transplantation
C1 [Alyea, Edwin P.; DeAngelo, Daniel J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Moldrem, Jeffrey; Giralt, Sergio] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Pagel, John M.; Riddell, Stan] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Pagel, John M.; Riddell, Stan] Univ Washington, Seattle, WA 98195 USA.
[Przepiorka, Donna] US FDA, Rockville, MD 20857 USA.
[Sadelin, Michel; Young, James W.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Bishop, Michael] NCI, Bethesda, MD 20892 USA.
RP Alyea, EP (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM edwin_alyea@dfci.harvard.edu
FU NCI NIH HHS [P01 CA018029, P01 CA018029-36]
NR 280
TC 23
Z9 25
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
EI 1523-6536
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD AUG
PY 2010
VL 16
IS 8
BP 1037
EP 1069
DI 10.1016/j.bbmt.2010.05.005
PG 33
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 628RH
UT WOS:000280137800002
PM 20580849
ER
PT J
AU Schriber, J
Agovi, MA
Ho, V
Ballen, KK
Bacigalupo, A
Lazarus, HM
Bredeson, CN
Gupta, V
Maziarz, RT
Hale, GA
Litzow, MR
Logan, B
Bornhauser, M
Giller, RH
Isola, L
Marks, DI
Rizzo, JD
Pasquini, MC
AF Schriber, Jeffrey
Agovi, Manza-A
Ho, Vincent
Ballen, Karen K.
Bacigalupo, Andrea
Lazarus, Hillard M.
Bredeson, Christopher N.
Gupta, Vikas
Maziarz, Richard T.
Hale, Gregory A.
Litzow, Mark R.
Logan, Brent
Bornhauser, Martin
Giller, Roger H.
Isola, Luis
Marks, David I.
Rizzo, J. Douglas
Pasquini, Marcelo C.
TI Second Unrelated Donor Hematopoietic Cell Transplantation for Primary
Graft Failure
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Graft failure; Second transplant; Nonengraftment
ID BONE-MARROW-TRANSPLANTATION; COLONY-STIMULATING FACTOR; APLASTIC-ANEMIA;
BLOOD; FLUDARABINE; REJECTION; RISK
AB Failure to engraft donor cells is a devastating complication after allogeneic hematopoietic cell transplantation (HCT). We describe the results of 122 patients reported to the National Marrow Donor Program between 1990 and 2005, who received a second unrelated donor HCT after failing to achieve an absolute neutrophil count of >= 500/mu L without recurrent disease. Patients were transplanted for leukemia (n = 83), myelodysplastic disorders (n = 16), severe aplastic anemia (n = 20), and other diseases (n = 3). The median age was 29 years. Twenty-four patients received second grafts from a different unrelated donor. Among 98 patients who received a second graft from the same donor, 28 received products that were previously collected and cryopreserved for the first transplantation. One-year overall survival (OS) after second transplant was 11%, with 10 patients alive at last follow-up. We observed no differences between patients who received grafts from the same or different donors, or in those who received fresh or cryopreserved product. The outcomes after a second allogeneic HCT for primary graft failure are dismal. Identifying risk factors for primary graft failure can decrease the incidence of this complication. Further studies are needed to test whether early recognition and hastened procurement of alternative grafts can improve transplant outcomes for primary graft failure. Biol Blood Marrow Transplant 16: 1099-1106 (2010) (C) 2010 American Society for Blood and Marrow Transplantation
C1 [Agovi, Manza-A; Logan, Brent; Rizzo, J. Douglas; Pasquini, Marcelo C.] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI 53226 USA.
[Schriber, Jeffrey] Banner Blood Marrow Transplant Program, Phoenix, AZ USA.
[Schriber, Jeffrey] City Hope Banner, Phoenix, AZ USA.
[Ho, Vincent] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ballen, Karen K.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bacigalupo, Andrea] Osped San Martino Genova, Genoa, Italy.
[Lazarus, Hillard M.] Univ Hosp Case Med Ctr, Cleveland, OH USA.
[Bredeson, Christopher N.] Med Coll Wisconsin, Froedtert Mem Lutheran Hosp, Milwaukee, WI 53226 USA.
[Gupta, Vikas] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Hale, Gregory A.] Univ S Florida, All Childrens Hosp, St Petersburg, FL 33701 USA.
[Litzow, Mark R.] Mayo Clin, Rochester, MN USA.
[Bornhauser, Martin] Univ Klinikum Carl Gustav Carus, Dresden, Germany.
[Giller, Roger H.] Univ Colorado, Childrens Hosp, Aurora, CO USA.
[Isola, Luis] Mt Sinai Hosp, New York, NY 10029 USA.
[Marks, David I.] Bristol Childrens Hosp, Bristol, Avon, England.
RP Pasquini, MC (reprint author), Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, 9200 W Wisconsin Ave,Suite CC5500, Milwaukee, WI 53226 USA.
EM mpasquin@mcw.edu
RI Bornhauser, Martin/F-8101-2010
FU National Cancer Institute (NCI) [U24-CA76518]; National Heart, Lung, and
Blood Institute (NHLBI) [5U01HL069294]; National Institute of Allergy
and Infectious Diseases (NIAID); Health Resources and Services
Administration (HRSA/DHHS) [HHSH234200637015C]; Office of Naval Research
[N00014-06-1-0704, N00014-08-1-0058]; AABB; Aetna; American Society for
Blood and Marrow Transplantation; Amgen, Inc.; Astellas Pharma US, Inc.;
Baxter International, Inc.; Bayer HealthCare Pharmaceuticals; Be the
Match Foundation; Biogen IDEC; BioMarin Pharmaceutical, Inc.; Biovitrum
AB; BloodCenter of Wisconsin; Blue Cross and Blue Shield Association;
Bone Marrow Foundation; Canadian Blood and Marrow Transplant Group;
CaridianBCT; Celgene Corporation; CellGenix, GmbH; Centers for Disease
Control and Prevention; Children's Leukemia Research Association;
ClinImmune Labs; CTI Clinical Trial and Consulting Services; Cubist
Pharmaceuticals; Cylex Inc.; CytoTherm; DOR BioPharma, Inc.; Dynal
Biotech, an Invitrogen Company; Eisai, Inc.; Enzon Pharmaceuticals,
Inc.; European Group for Blood and Marrow Transplantation; Gamida Cell,
Ltd.; GE Healthcare; Genentech, Inc.; Genzyme Corporation;
Histogenetics, Inc.; HKS Medical Information Systems; Hospira, Inc.;
Infectious Diseases Society of America; Kiadis Pharma; Kirin Brewery
Co., Ltd.; The Leukemia & Lymphoma Society; Merck Company; The Medical
College of Wisconsin; MGI Pharma, Inc.; Michigan Community Blood
Centers; Millennium Pharmaceuticals, Inc.; Miller Pharmacal Group;
Milliman USA, Inc.; Miltenyi Biotec, Inc.; National Marrow Donor
Program; Nature Publishing Group; New York Blood Center; Novartis
Oncology; Oncology Nursing Society; Osiris Therapeutics, Inc.; Otsuka
America Pharmaceutical, Inc.; Pall Life Sciences; Pfizer Inc; Saladax
Biomedical, Inc.; Schering Corporation; Society for Healthcare
Epidemiology of America; Soligenix, Inc.; StemCyte, Inc.; StemSoft
Software, Inc.; Sysmex America, Inc.; THERAKOS, Inc.; Thermogenesis
Corporation; Vidacare Corporation; Vion Pharmaceuticals, Inc.; ViraCor
Laboratories; ViroPharma, Inc.; Wellpoint, Inc.
FX The CIBMTR is supported by Public Health Service Grant/Cooperative
Agreement U24-CA76518 from the National Cancer Institute (NCI), the
National Heart, Lung, and Blood Institute (NHLBI) and the National
Institute of Allergy and Infectious Diseases (NIAID); a
Grant/Cooperative Agreement 5U01HL069294 from NHLBI and NCI; a contract
HHSH234200637015C with Health Resources and Services Administration
(HRSA/DHHS); 2 Grants, N00014-06-1-0704 and N00014-08-1-0058, from the
Office of Naval Research; and grants from AABB; Aetna; American Society
for Blood and Marrow Transplantation; Amgen, Inc.; anonymous donation to
the Medical College of Wisconsin; Astellas Pharma US, Inc.; Baxter
International, Inc.; Bayer HealthCare Pharmaceuticals; Be the Match
Foundation; Biogen IDEC; BioMarin Pharmaceutical, Inc.; Biovitrum AB;
BloodCenter of Wisconsin; Blue Cross and Blue Shield Association; Bone
Marrow Foundation; Canadian Blood and Marrow Transplant Group;
CaridianBCT; Celgene Corporation; CellGenix, GmbH; Centers for Disease
Control and Prevention; Children's Leukemia Research Association;
ClinImmune Labs; CTI Clinical Trial and Consulting Services; Cubist
Pharmaceuticals; Cylex Inc.; CytoTherm; DOR BioPharma, Inc.; Dynal
Biotech, an Invitrogen Company; Eisai, Inc.; Enzon Pharmaceuticals,
Inc.; European Group for Blood and Marrow Transplantation; Gamida Cell,
Ltd.; GE Healthcare; Genentech, Inc.; Genzyme Corporation;
Histogenetics, Inc.; HKS Medical Information Systems; Hospira, Inc.;
Infectious Diseases Society of America; Kiadis Pharma; Kirin Brewery
Co., Ltd.; The Leukemia & Lymphoma Society; Merck & Company; The Medical
College of Wisconsin; MGI Pharma, Inc.; Michigan Community Blood
Centers; Millennium Pharmaceuticals, Inc.; Miller Pharmacal Group;
Milliman USA, Inc.; Miltenyi Biotec, Inc.; National Marrow Donor
Program; Nature Publishing Group; New York Blood Center; Novartis
Oncology; Oncology Nursing Society; Osiris Therapeutics, Inc.; Otsuka
America Pharmaceutical, Inc.; Pall Life Sciences; Pfizer Inc; Saladax
Biomedical, Inc.; Schering Corporation; Society for Healthcare
Epidemiology of America; Soligenix, Inc.; StemCyte, Inc.; StemSoft
Software, Inc.; Sysmex America, Inc.; THERAKOS, Inc.; Thermogenesis
Corporation; Vidacare Corporation; Vion Pharmaceuticals, Inc.; ViraCor
Laboratories; ViroPharma, Inc.; and Wellpoint, Inc.
NR 19
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U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD AUG
PY 2010
VL 16
IS 8
BP 1099
EP 1106
DI 10.1016/j.bbmt.2010.02.013
PG 8
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 628RH
UT WOS:000280137800007
PM 20172038
ER
PT J
AU Cutler, C
Kim, HT
Ayanian, S
Bradwin, G
Revta, C
Aldridge, J
Ho, V
Alyea, E
Koreth, J
Armand, P
Soiffer, R
Ritz, J
Richardson, PG
Antin, JH
AF Cutler, Corey
Kim, Haesook T.
Ayanian, Shake
Bradwin, Gary
Revta, Carolyn
Aldridge, Julie
Ho, Vincent
Alyea, Edwin
Koreth, John
Armand, Philippe
Soiffer, Robert
Ritz, Jerome
Richardson, Paul G.
Antin, Joseph H.
TI Prediction of Veno-Occlusive Disease Using Biomarkers of Endothelial
Injury
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Veno-occlusive disease; Endothelium; Sirolimus
ID STEM-CELL TRANSPLANTATION; BONE-MARROW-TRANSPLANTATION;
VON-WILLEBRAND-FACTOR; THROMBOTIC MICROANGIOPATHY; GROWTH-FACTOR;
SIROLIMUS; LIVER; DEFIBROTIDE; PARAMETERS; MARKERS
AB Predicting the development of veno-occlusive disease (VOD) of the liver remains challenging. We hypothesized that biomarkers of endothelial injury in myeloablative allogeneic transplantation recipients could predict VOD occurrence. We evaluated 4 biomarkers-von Willebrand Factor (vWF), thrombomodulin, E-selectin, and soluble intercellular adhesion molecule-1 (sICAM-1)-weekly in the peritransplantation period in an attempt to predict VOD. In the patients who received sirolimus, vWF, thrombomodulin, and sICAM-1 levels were significantly elevated in patients with VOD compared with those without VOD on day - 1 (P <= .035), day +7 (P <= .0001), and day +14 (P <= .004). E-selectin was predictive on day +7 (P = .007). Levels of vWF >= 1400 IU/mL and thrombomodulin >= 100 ng/mL on day +7 were both 100% sensitive and 100% specific in predicting VOD. These biomarkers were informative when adjusted for other risk factors for VOD in regression analysis. Among patients not receiving sirolimus, biomarkers of endothelial injury were not informative. We conclude that vWF, thrombomodulin, and sICAM-1 elevations before and early after transplantation may be useful in predicting VOD in patients receiving sirolimus. Biol Blood Marrow Transplant 16: 1180-1185 (2010) (C) 2010 American Society for Blood and Marrow Transplantation
C1 [Cutler, Corey; Revta, Carolyn; Ho, Vincent; Alyea, Edwin; Koreth, John; Armand, Philippe; Soiffer, Robert; Ritz, Jerome; Richardson, Paul G.; Antin, Joseph H.] Dana Farber Canc Inst, Dept Med Oncol, Div Hematol Oncol, Boston, MA 02115 USA.
[Kim, Haesook T.; Aldridge, Julie] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Ayanian, Shake; Bradwin, Gary] Childrens Hosp Boston, Boston, MA 02115 USA.
RP Cutler, C (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Div Hematol Oncol, 44 Binney St,D1B13, Boston, MA 02115 USA.
EM corey_cutler@dfci.harvard.edu
OI Ritz, Jerome/0000-0001-5526-4669
FU Ted and Eileen Pasquarello Research Fund; National Institutes of Health
[AI29530, CA142106, HL070149]; Stem Cell Cyclists of the Pan-Mass
Challenge
FX This work was supported by the Ted and Eileen Pasquarello Research Fund
and National Institutes of Health Grants AI29530, CA142106, and
HL070149. Corey Cutler is supported by the Stem Cell Cyclists of the
Pan-Mass Challenge.
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD AUG
PY 2010
VL 16
IS 8
BP 1180
EP 1185
DI 10.1016/j.bbmt.2010.02.016
PG 6
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 628RH
UT WOS:000280137800017
PM 20184961
ER
PT J
AU Moskowitz, JS
Blaisse, MR
Samuel, RE
Hsu, HP
Harris, MB
Martin, SD
Lee, JC
Spector, M
Hammond, PT
AF Moskowitz, Joshua S.
Blaisse, Michael R.
Samuel, Raymond E.
Hsu, Hu-Ping
Harris, Mitchel B.
Martin, Scott D.
Lee, Jean C.
Spector, Myron
Hammond, Paula T.
TI The effectiveness of the controlled release of gentamicin from
polyelectrolyte multilayers in the treatment of Staphylococcus aureus
infection in a rabbit bone model
SO BIOMATERIALS
LA English
DT Article
DE Antibacterial; Animal model; Bone; Controlled drug release;
Layer-by-layer; Coating
ID LAYER THIN-FILMS; IN-VIVO; EXPONENTIAL-GROWTH; POLY(ACRYLIC ACID);
DRUG-RELEASE; PLASMID DNA; PMMA BEADS; OSTEOMYELITIS; IMPLANTS; COATINGS
AB While the infection rate of orthopedic implants is low, the required treatment, which can involve six weeks of antibiotic therapy and two additional surgical operations, is life threatening and expensive, and thus motivates the development of a one-stage re-implantation procedure. Polyelectrolyte multilayers incorporating gentamicin were fabricated using the layer-by-layer deposition process for use as a device coating to address an existing bone infection in a direct implant exchange operation. The films eluted about 70% of their payload in vitro during the first three days and subsequently continued to release drug for more than four additional weeks, reaching a total average release of over 550 mu g/cm(2). The coatings were demonstrated to be bactericidal against Staphylococcus aureus, and degradation products were generally nontoxic towards MC3T3-E1 murine preosteoblasts. Film-coated titanium implants were compared to uncoated implants in an in vivo S. aureus bone infection model. After a direct exchange procedure, the antimicrobial-coated devices yielded bone homogenates with a significantly lower degree of infection than uncoated devices at both day four (p < 0.004) and day seven (p < 0.03). This study has demonstrated that a self-assembled ultrathin film coating is capable of effectively treating an experimental bone infection in vivo and lays the foundation for development of a multi-therapeutic film for optimized, synergistic treatment of pain, infection, and osteomyelitis. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Moskowitz, Joshua S.; Blaisse, Michael R.; Samuel, Raymond E.; Hammond, Paula T.] MIT, Dept Chem Engn, Cambridge, MA 02139 USA.
[Hsu, Hu-Ping; Spector, Myron] VA Boston Healthcare Syst, Tissue Engn Labs, Boston, MA 02130 USA.
[Hsu, Hu-Ping; Harris, Mitchel B.; Martin, Scott D.; Spector, Myron] Brigham & Womens Hosp, Dept Orthoped Surg, Boston, MA 02115 USA.
[Hsu, Hu-Ping; Harris, Mitchel B.; Martin, Scott D.; Lee, Jean C.; Spector, Myron] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Lee, Jean C.] Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA.
RP Hammond, PT (reprint author), 77 Massachusetts Ave,Room 66-352, Cambridge, MA 02139 USA.
EM hammond@mit.edu
FU National Institutes of Health, National Institute of Aging
[5R01AG029601-03]
FX This work was financially supported by the National Institutes of
Health, National Institute of Aging (5R01AG029601-03). We thank Catrina
Wong, Alison Hayward, DVM, and Alison Darby, DVM (animal support staff.
Division of Comparative Medicine, MIT) for care, handling, and
anesthesia of animals, Ellen Buckley and Nikki Lew (microbiologists,
Division of Comparative Medicine, MIT) for blood analyses, cultures, and
biofilm studies, Wayne Schwark, DVM, PhD (Professor of Pharmacology,
Department of Molecular Medicine, Cornell University), for gentamicin
assays, and Helen Chuang, PhD (Research Scientist, ChromoLogic,
Pasadena, CA), for consultation on in vitro film studies. The authors
greatly appreciate the use of equipment available at the Institute for
Soldier Nanotechnologies (ISN), as well as the Robert Langer Laboratory
for scintillation counting, the Center for Materials Science and
Engineering for profilometry, and the Division of Comparative Medicine's
animal facilities for all in vivo work.
NR 52
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PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0142-9612
J9 BIOMATERIALS
JI Biomaterials
PD AUG
PY 2010
VL 31
IS 23
BP 6019
EP 6030
DI 10.1016/j.biomaterials.2010.04.011
PG 12
WC Engineering, Biomedical; Materials Science, Biomaterials
SC Engineering; Materials Science
GA 623DZ
UT WOS:000279719600013
PM 20488534
ER
PT J
AU Felts, AS
Lindsley, SR
Lamb, JP
Rodriguez, AL
Menon, UN
Jadhav, S
Jones, CK
Conn, PJ
Lindsley, CW
Emmitte, KA
AF Felts, Andrew S.
Lindsley, Stacey R.
Lamb, Jeffrey P.
Rodriguez, Alice L.
Menon, Usha N.
Jadhav, Satyawan
Jones, Carrie K.
Conn, P. Jeffrey
Lindsley, Craig W.
Emmitte, Kyle A.
TI 3-Cyano-5-fluoro-N-arylbenzamides as negative allosteric modulators of
mGlu(5): Identification of easily prepared tool compounds with CNS
exposure in rats
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE mGlu5; GPCR; Allosteric modulator; CNS; GERD; Fragile X syndrome;
Addiction; PD-LID
ID MGLUR5 ANTAGONIST MPEP; METABOTROPIC GLUTAMATE-RECEPTOR-5 ANTAGONIST;
RECEPTOR SUBTYPE-5 ANTAGONISTS; CUE-INDUCED REINSTATEMENT; GLUTAMATE
RECEPTORS; GASTROESOPHAGEAL-REFLUX; SQUIRREL-MONKEYS; SEEKING BEHAVIOR;
COCAINE SEEKING; POTENT
AB Development of SAR in a 3-cyano-5-fluoro-N-arylbenzamide series of non-competitive antagonists of mGlu(5) using a functional cell-based assay is described in this Letter. Further characterization of selected potent compounds in in vitro assays designed to measure their metabolic stability and protein binding is also presented. Subsequent evaluation of two new compounds in pharmacokinetic studies using intraperitoneal dosing in rats demonstrated good exposure in both plasma and brain samples. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Felts, Andrew S.; Lindsley, Stacey R.; Lamb, Jeffrey P.; Rodriguez, Alice L.; Menon, Usha N.; Jadhav, Satyawan; Jones, Carrie K.; Conn, P. Jeffrey; Lindsley, Craig W.; Emmitte, Kyle A.] Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA.
[Felts, Andrew S.; Lindsley, Stacey R.; Lamb, Jeffrey P.; Rodriguez, Alice L.; Menon, Usha N.; Jadhav, Satyawan; Jones, Carrie K.; Conn, P. Jeffrey; Lindsley, Craig W.; Emmitte, Kyle A.] Vanderbilt Univ, Med Ctr, Vanderbilt Program Drug Discovery, Nashville, TN 37232 USA.
[Jones, Carrie K.; Lindsley, Craig W.] Vanderbilt Univ, Dept Chem, Nashville, TN 37232 USA.
[Jones, Carrie K.] Tennesse Valley Healthcare Syst, US Dept Vet Affairs, Nashville, TN 37212 USA.
RP Emmitte, KA (reprint author), Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA.
EM kyle.a.emmitte@Vanderbilt.edu
RI Conn, Peter/D-7848-2012
FU NIDA [RO1 DA023947-01]; Seaside Therapeutics [VUMC33842]
FX We thank NIDA (RO1 DA023947-01) and Seaside Therapeutics (VUMC33842) for
their support of our programs in the development of non-competitive
antagonist of mGlu5. Matt Mulder, Chris Denicola, and Sichen
Chang are also thanked for the purification of compounds using the
mass-directed HPLC system.
NR 48
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U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD AUG 1
PY 2010
VL 20
IS 15
BP 4390
EP 4394
DI 10.1016/j.bmcl.2010.06.064
PG 5
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA 625BK
UT WOS:000279866300020
PM 20598884
ER
PT J
AU Reilly-Harrington, NA
DeBonis, D
Leon, AC
Sylvia, L
Perlis, R
Lewis, D
Sachs, GS
AF Reilly-Harrington, Noreen A.
DeBonis, Daniel
Leon, Andrew C.
Sylvia, Louisa
Perlis, Roy
Lewis, Daniel
Sachs, Gary S.
TI The interactive computer interview for mania
SO BIPOLAR DISORDERS
LA English
DT Article
DE bipolar disorder; computerized interviews; rater reliability
ID SAMPLE-SIZE REQUIREMENTS; CLINICAL-TRIALS; MEASUREMENT ERROR;
DEPRESSION; EFFICACY; AGREEMENT; VALIDITY; DESIGN
AB Objectives:
The Interactive Computer Interview for Mania (ICI-M) is a computer-administered interview that presents probes to assess symptom severity and utilizes a scoring algorithm to select follow-up questions and rate subject responses in accordance with rating scale anchor points. The current study examines the acceptability, feasibility, and reliability of the ICI-M as a potential method for evaluating the performance of human raters.
Methods:
Participants with a diagnosis of bipolar I or II disorder completed both a live interview of the Young Mania Rating Scale with a human rater (LR) and the ICI-M. A panel of three expert raters reviewed each videotaped LR and assigned a consensus rating (CR). Participants completed a modified version of the Client Satisfaction Questionnaire to assess each method.
Results:
Intraclass correlation coefficients were 0.91 between the ICI-M and CR and 0.97 between the LR and CR (n = 100), providing empirical support for the inter-rater reliability of each approach. Coefficient alphas indicated comparable internal consistency reliability: ICI-M = 0.82, LR = 0.83, and CR = 0.84. The ICI-M was significantly more sensitive in detecting symptomatology than the LR (p < 0.001) and the CR (p < 0.001), and resulted in significantly higher ratings than CR on mood, speech, psychotic content, and disruptive-aggressive behavior. While participants endorsed significantly higher overall satisfaction with LR, no significant differences emerged between ICI-M and LR regarding willingness to participate again or ability to understand the questions.
Conclusions:
The ICI-M is a well-accepted and reliable method for assessing manic symptoms. The ICI-M is a tool with adequate sensitivity to elicit symptoms and rate severity and is recommended as a tool to monitor and improve rater performance, not as a replacement of a human rater.
C1 [Reilly-Harrington, Noreen A.] Massachusetts Gen Hosp, Bipolar Clin, Boston, MA 02114 USA.
[Reilly-Harrington, Noreen A.; DeBonis, Daniel; Sylvia, Louisa; Perlis, Roy; Lewis, Daniel; Sachs, Gary S.] Concordant Rater Syst, Boston, MA USA.
[Reilly-Harrington, Noreen A.; Sylvia, Louisa; Perlis, Roy; Sachs, Gary S.] Harvard Univ, Sch Med, Boston, MA USA.
[Leon, Andrew C.] Cornell Univ, Weill Med Coll, New York, NY 10021 USA.
RP Reilly-Harrington, NA (reprint author), Massachusetts Gen Hosp, Bipolar Clin, 50 Staniford St,Suite 580, Boston, MA 02114 USA.
EM nhreilly@partners.org
FU NIMH [1 R43 MH65796-01A1]; AstraZeneca; Eli Lilly Co.; Pfizer;
GlaxoSmithKline; Bristol-Myers Squibb
FX This study was funded by NIMH Grant 1 R43 MH65796-01A1 to NAR-H,
Principal Investigator.; NAR-H is a shareholder and consultant for
Concordant Rater Systems and receives royalties from Oxford University
Press and the American Psychological Association. DD is president and
shareholder of Concordant Rater Systems. ACL serves on the Data and
Safety Monitoring Boards for AstraZeneca, Dainippon Sumitomo Pharma
America, and Pfizer; has served as a consultant/advisor to the FDA,
NIMH, Cyberonics, MedAvante, Schering Plough, and Takeda; and has equity
in MedAvante. LS is a consultant for Concordant Rater Systems. RP has
received speaker's fees/honoraria from AstraZeneca, Eli Lilly & Co.,
Pfizer, GlaxoSmithKline, and Bristol-Myers Squibb; has served on the
consulting/advisory boards for AstraZeneca, Eli Lilly & Co., Pfizer,
Bristol-Myers Squibb, and Proteus LLC; and has received royalties from
Concordant Rater Systems. DL is a shareholder in Concordant Rater
Systems. GSS serves on the speakers bureaus of Abbott, AstraZeneca,
Bristol-Myers Squibb, Eli Lilly & Co., GlaxoSmithKline, Janssen, Memory
Pharmaceuticals, Novartis, Pfizer, Sanofi-aventis, and Wyeth; serves as
an advisory board member or consultant for Abbott, AstraZeneca,
Bristol-Myers Squibb, Cephalon, CNS Response, Concordant Rater Systems,
Elan Pharmaceuticals, Eli Lilly & Co., GlaxoSmithKline, Janssen, Memory
Pharmaceuticals, Merck, Novartis, Organon, Otsuka, Pfizer, Repligen,
Sanofi-aventis, Schering Plough, Sepracor, Shire, Sigma-Tau, Solvay
Pharmaceuticals, and Wyeth; and his spouse holds shares in Concordant
Rater Systems.
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PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD AUG
PY 2010
VL 12
IS 5
BP 521
EP 527
DI 10.1111/j.1399-5618.2010.00844.x
PG 7
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 639PX
UT WOS:000280987800007
PM 20712753
ER
PT J
AU Altshuler, LL
Abulseoud, OA
Foland-Ross, L
Bartzokis, G
Chang, S
Mintz, J
Hellemann, G
Vinters, HV
AF Altshuler, Lori L.
Abulseoud, Osama A.
Foland-Ross, Lara
Bartzokis, George
Chang, Sean
Mintz, Jim
Hellemann, Gerhard
Vinters, Harry V.
TI Amygdala astrocyte reduction in subjects with major depressive disorder
but not bipolar disorder
SO BIPOLAR DISORDERS
LA English
DT Article
DE amygdala; astrocyte; bipolar disorder; depression; glial cell; neuron
ID MAGNETIC-RESONANCE SPECTROSCOPY; DORSOLATERAL PREFRONTAL CORTEX;
ANTERIOR CINGULATE CORTEX; FIBRILLARY ACIDIC PROTEIN; TEMPORAL-LOBE
STRUCTURES; GAMMA-AMINOBUTYRIC-ACID; GLIAL-CELL DENSITY; MOOD DISORDERS;
NEUROPATHOLOGY CONSORTIUM; GLUTAMINE-SYNTHETASE
AB Objectives:
Several magnetic resonance imaging studies have found changes in amygdala volumes in adults with mood disorders. The cellular basis for these changes has not been explored in detail. Specifically, it is not known whether differences in the density and/or volume of neurons or glial cells contribute to tissue volume changes seen on magnetic resonance images.
Methods:
Postmortem amygdala samples were obtained from the Stanley Foundation Neuropathology Consortium from subjects diagnosed with bipolar disorder (n = 10), major depressive disorder (n = 11), and schizophrenia (n = 9), and from normal controls (n = 14). Samples were first stained with glial fibrillary acidic protein (GFAP) and counter-stained with hematoxylin to ascertain neuron and glia (astrocyte) densities.
Results:
No significant differences in neuronal densities were found between groups. However, a reduction in the density of GFAP immunoreactive astrocytes was observed in the amygdala of subjects with major depressive disorder compared to the bipolar disorder, schizophrenia, and normal control postmortem samples.
Conclusions:
A decrease in density of GFAP immunoreactive astrocytes in the amygdala of depressed subjects is consistent with prior histologic reports and might contribute to amygdala volume reductions reported in several in vivo neuroimaging studies.
C1 [Altshuler, Lori L.; Bartzokis, George; Hellemann, Gerhard] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Altshuler, Lori L.; Bartzokis, George; Mintz, Jim] VA Greater Angeles Healthcare Syst, W Los Angeles Healthcare Ctr, Los Angeles, CA USA.
[Abulseoud, Osama A.] Univ So Calif, Dept Psychiat & Behav Sci, Los Angeles, CA USA.
[Foland-Ross, Lara; Bartzokis, George] Univ Calif Los Angeles, David Geffen Sch Med, Lab Neuroimaging, Dept Neurol,Div Brain Mapping, Los Angeles, CA 90095 USA.
[Chang, Sean] Albert Einstein Jacobi Med Ctr, Dept Radiol, Bronx, NY USA.
[Vinters, Harry V.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
[Vinters, Harry V.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
RP Altshuler, LL (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, 300 UCLA Med Plaza,Suite 1544,Box 6, Los Angeles, CA 90095 USA.
EM laltshuler@mednet.ucla.edu
RI Bartzokis, George/K-2409-2013
FU Stanley Medical Research Institute (Bethesda, MD, USA); Daljit S. and
Elaine Sarkaria Chair in Diagnostic Medicine; Janssen
FX Postmortem brain tissue was donated by the Stanley Medical Research
Institute's brain collection. Financial support for this research was
provided by the Stanley Medical Research Institute (Bethesda, MD, USA).
HHV is supported in part by the Daljit S. and Elaine Sarkaria Chair in
Diagnostic Medicine. We are grateful to Arnold Scheibel for consultation
regarding identification of amygdala nuclei, and to Teri English for
editorial assistance.; LLA is on the scientific advisory board for
Forest Laboratories (for matters related to s-citalopram). GB has
received grant support from Janssen and is on the speakers bureaus for
and receives honoraria from Pfizer and Novartis, none for matters
related to bipolar disorder. HVV has stock holdings in the following
pharmaceutical companies: Pfizer, GlaxoSmithKline Beecham, and Teva. All
authors report that they do not have any conflict of interest relevant
to this manuscript.
NR 72
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PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD AUG
PY 2010
VL 12
IS 5
BP 541
EP 549
DI 10.1111/j.1399-5618.2010.00838.x
PG 9
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 639PX
UT WOS:000280987800010
PM 20712756
ER
PT J
AU Cipriano, LE
Barth, WH
Zaric, GS
AF Cipriano, L. E.
Barth, W. H., Jr.
Zaric, G. S.
TI The cost-effectiveness of targeted or universal screening for vasa
praevia at 18-20 weeks of gestation in Ontario
SO BJOG-AN INTERNATIONAL JOURNAL OF OBSTETRICS AND GYNAECOLOGY
LA English
DT Article
DE Cost effectiveness analysis; prenatal diagnosis; screening;
ultrasonography; ultrasound; vasa praevia
ID UMBILICAL-CORD; COLOR DOPPLER; VELAMENTOUS INSERTION;
PRENATAL-DIAGNOSIS; ULTRASOUND; TECHNOLOGY; SONOGRAPHY; GUIDELINES
AB Objectives To estimate the cost-effectiveness of targeted and universal screening for vasa praevia at 18-20 weeks of gestation in singleton and twin pregnancies.
Design Cost-utility analysis based on a decision-analytic model comparing relevant strategies and life-long outcomes for mother and infant(s).
Setting Ontario, Canada.
Population A cohort of pregnant women in 1 year.
Methods We constructed a decision-analytic model to estimate the lifetime incremental costs and benefits of screening for vasa praevia. Inputs were estimated from the literature. Costs were collected from the London Health Sciences Centre, the Ontario Health Insurance Program, and other sources. We used one-way, scenario and probabilistic sensitivity analysis to determine the robustness of the results.
Main outcome measures Incremental costs, life expectancy, quality-adjusted life-years (QALY) and incremental cost-effectiveness ratio (ICER).
Results Universal transvaginal ultrasound screening of twin pregnancies has an ICER of $5488 per QALY-gained. Screening all singleton pregnancies with the risk factors low-lying placentas, in vitro fertilisation (IVF) conception, accessory placental lobes, or velamentous cord insertion has an ICER of $15,764 per QALY-gained even though identifying some of these risk factors requires routine use of colour Doppler during transabdominal examinations. Screening women with a marginal cord insertion costs an additional $27,603 per QALY-gained. Universal transvaginal screening for vasa praevia in singleton pregnancies costs $579,164 per QALY compared with targeted screening.
Conclusions Compared with current practice, screening all twin pregnancies for vasa praevia with transvaginal ultrasound is cost-effective. Among the alternatives considered, the use of colour Doppler at all transabdominal ultrasound examinations of singleton pregnancies and targeted use of transvaginal ultrasound for IVF pregnancies or when the placenta has been found to be associated with one or more risk factors is cost-effective. Universal screening of singleton pregnancies is not cost-effective compared with targeted screening.
C1 [Zaric, G. S.] Univ Western Ontario, Richard Ivey Sch Business, London, ON N6A 3K7, Canada.
[Cipriano, L. E.] Stanford Univ, Dept Management Sci & Engn, Stanford, CA 94305 USA.
[Barth, W. H., Jr.] Massachusetts Gen Hosp, Div Maternal Fetal Med, Boston, MA 02114 USA.
[Barth, W. H., Jr.] Harvard Univ, Sch Med, Boston, MA USA.
RP Zaric, GS (reprint author), Univ Western Ontario, Richard Ivey Sch Business, 1151 Richmond St N, London, ON N6A 3K7, Canada.
EM gzaric@ivey.uwo.ca
RI Zaric, Gregory/B-7665-2013; Cipriano, Lauren/C-3521-2017
OI Cipriano, Lauren/0000-0001-5568-4516
FU Natural Science and Engineering Research Council of Canada (NSERC)
FX This work was funded by the Natural Science and Engineering Research
Council of Canada (NSERC).
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PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1470-0328
J9 BJOG-INT J OBSTET GY
JI BJOG
PD AUG
PY 2010
VL 117
IS 9
BP 1108
EP 1118
DI 10.1111/j.1471-0528.2010.02621.x
PG 11
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 620WN
UT WOS:000279532500011
PM 20560948
ER
PT J
AU Araldi, E
Schipani, E
AF Araldi, Elisa
Schipani, Ernestina
TI Hypoxia, HIFs and bone development
SO BONE
LA English
DT Article
DE Chondrocyte; Osteoblast; Hypoxia; HIF-1alpha; HIF-2alpha
ID ARTICULAR CHONDROCYTE PHENOTYPE; INDUCIBLE FACTOR 1-ALPHA; CELL-CYCLE
ARREST; GROWTH-PLATE; TRANSCRIPTIONAL ACTIVITY; GENE-EXPRESSION;
DISTRACTION OSTEOGENESIS; MICRORNA TARGETS; LYSYL OXIDASE; STEM-CELLS
AB Oxygen is not only an obviously important substrate, but it is also a regulatory signal that controls expression of a specific genetic program. Crucial mediator of the adaptive response of cells to hypoxia is the family of Hypoxia-inducible Transcription Factors (HIFs). The fetal growth plate, which is an avascular structure of mesenchymal origin, has a unique out-in gradient of oxygenation. HIF-1 alpha is necessary for chondrogenesis in vivo by controlling a complex homeostatic response that allows chondrocytes to survive and differentiate in a hypoxic environment. Moreover. HIFs are also essential in osteogenesis and joint development. This brief Perspective summarizes the critical role of HIFs in endochondral bone development. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Schipani, Ernestina] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Schipani, E (reprint author), Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
EM schipani@helix.mgh.harvard.edu
FU NIH [RO1 AR048191 -06]
FX This paper was supported by NIH RO1 AR048191 -06 to E.S.
NR 111
TC 50
Z9 53
U1 2
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 AUG
PY 2010
VL 47
IS 2
BP 190
EP 196
DI 10.1016/j.bone.2010.04.606
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 632SW
UT WOS:000280449300003
PM 20444436
ER
PT J
AU Sahyoun, CP
Belliveau, JW
Mody, M
AF Sahyoun, Cherif P.
Belliveau, John W.
Mody, Maria
TI White matter integrity and pictorial reasoning in high-functioning
children with autism
SO BRAIN AND COGNITION
LA English
DT Article
DE High-functioning autism; Pictorial reasoning; Language; White matter
ID SUPERIOR TEMPORAL GYRUS; SPECTRUM DISORDERS; WORKING-MEMORY; SENTENCE
COMPREHENSION; CORPUS-CALLOSUM; FRONTAL-CORTEX; DIFFUSION; LANGUAGE;
BRAIN; CONNECTIVITY
AB The current study investigated the neurobiological role of white matter in visuospatial versus linguistic processing abilities in autism using diffusion tensor imaging. We examined differences in white matter integrity between high-functioning children with autism (HFA) and typically developing controls (CTRL), in relation to the groups' response times (RT) on a pictorial reasoning task under three conditions: visuospatial, V. semantic. S, and V + S. a hybrid condition allowing language use to facilitate visuospatial transformations.
Diffusion-weighted images were collected from HFA and CTRL participants, matched on age and IQ and significance maps were computed for group differences in fractional anisotropy (FA) and in RT-FA association for each condition.
Typically developing children showed increased FA within frontal white matter and the superior longitudinal fasciculus (SLF). HFA showed increased FA within peripheral white matter, including the ventral temporal lobe. Additionally, RT-FA relationships in the semantic condition (5) implicated white matter near the STG and in the SLF within the temporal and frontal lobes to a greater extent in CTRL Performance in visuospatial reasoning (V, V + S), in comparison, was related to peripheral parietal and superior precentral white matter in HFA, but to the SLF, callosal, and frontal white matter in CTRL
Our results appear to support a preferential use of linguistically-mediated pathways in reasoning by typically developing children, whereas autistic cognition may rely more on visuospatial processing networks. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Sahyoun, Cherif P.; Mody, Maria] Massachusetts Gen Hosp, MGH MIT HMS Athinoula A Martinos Ctr Biomed Imagi, Charlestown, MA 02129 USA.
MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Sahyoun, CP (reprint author), Massachusetts Gen Hosp, MGH MIT HMS Athinoula A Martinos Ctr Biomed Imagi, 149 13th St, Charlestown, MA 02129 USA.
EM cherif@mit.edu; maria@nmr.mgh.harvard.edu
FU National Institutes of Health [NS037462, HD40712]; National Center for
Research Resources [P41RR14075]
FX This research was supported by funding from the National Institutes of
Health (NS037462; HD40712) and in part by the National Center for
Research Resources (P41RR14075). We would like to thank all the children
and parents for their willingness to participate in the study. We thank
Seppo Ahlfors, Douglas Greve, Saad Jbabdi, Shira Schwartz, and Isabelle
Soulieres for various aspects of analysis and interpretation.
NR 78
TC 28
Z9 28
U1 0
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0278-2626
J9 BRAIN COGNITION
JI Brain Cogn.
PD AUG
PY 2010
VL 73
IS 3
BP 180
EP 188
DI 10.1016/j.bandc.2010.05.002
PG 9
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 627DV
UT WOS:000280020300005
PM 20542370
ER
PT J
AU Lin, NU
AF Lin, Nancy U.
TI Concordance of HER2 in primary tumor and leptomeningeal metastases: now
what?
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Editorial Material
ID NERVOUS-SYSTEM METASTASES; BREAST-CANCER; MENINGEAL CARCINOMATOSIS;
INTRATHECAL TRASTUZUMAB; BRAIN METASTASES; MET; RESISTANCE; EXPRESSION;
SURVIVAL; SITES
C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Lin, NU (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM nlin@partners.org
NR 27
TC 5
Z9 5
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 AUG
PY 2010
VL 123
IS 1
BP 129
EP 131
DI 10.1007/s10549-009-0720-7
PG 3
WC Oncology
SC Oncology
GA 627SP
UT WOS:000280063200014
PM 20054640
ER
PT J
AU Gunnarsdottir, KA
Jensen, MB
Zahrieh, D
Gelber, RD
Knoop, A
Bonetti, M
Mouridsen, H
Ejlertsen, B
AF Gunnarsdottir, Katrin A.
Jensen, Maj-Britt
Zahrieh, David
Gelber, Richard D.
Knoop, Ann
Bonetti, Marco
Mouridsen, Henning
Ejlertsen, Bent
TI CEF is superior to CMF for tumours with TOP2A aberrations: a
Subpopulation Treatment Effect Pattern Plot (STEPP) analysis on Danish
Breast Cancer Cooperative Group Study 89D
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Breast cancer; TOP2A; Treatment; Anthracycline; STEPP
ID TOPOISOMERASE-II-ALPHA; TREATMENT-COVARIATE INTERACTIONS; ADJUVANT
CHEMOTHERAPY; PREMENOPAUSAL WOMEN; PREDICTIVE MARKERS; RANDOMIZED-TRIAL;
CYCLOPHOSPHAMIDE; METHOTREXATE; FLUOROURACIL; DOXORUBICIN
AB The aim of this study was to examine TOP2A gene copy number changes as a means to identify groups of breast cancer patients with superior benefit from treatment with anthracyclines. Tumour tissue was retrospectively collected and successfully analysed for TOP2A in 773 of 980 Danish patients randomly assigned to receive intravenous CMF (cyclophosphamide, methotrexate and fluorouracil) or CEF (cyclophosphamide, epirubicin and fluorouracil) in DBCG trial 89D. Subgroup analyses on this material published by Knoop et al. (J Clin Oncol 23:7483-7490, 2005) and updated by Nielsen et al. (Acta Oncol 47:725-734, 2008) demonstrated that superiority of CEF over CMF is limited to patients with TOP2A aberrations, defined as patients whose tumours have TOP2A ratio below 0.8 or above 2.0. The Subpopulation Treatment Effect Pattern Plot (STEPP) technique was applied to these data to explore the pattern of treatment effect relative to TOP2A and to compare that pattern to the ranges previously used to define 'aberrations'. The pattern of treatment effect illustrated by the STEPP analysis confirmed that the superiority of CEF over CMF is indeed limited to patients whose tumours have high or low TOP2A ratios. The hypothesis of no treatment effect-covariate interaction was rejected (P = 0.02). Furthermore, results indicated that the interval of TOP2A ratios hitherto denoted as 'normal' could be narrower than previously assumed. A more optimal separation of TOP2A subgroups could be obtained by altering cut-points currently used to define TOP2A amplified and TOP2A deleted tumours by narrowing the TOP2A normal interval, and consequently enlarging the population with TOP2A aberrated tumours.
C1 [Gunnarsdottir, Katrin A.; Jensen, Maj-Britt; Knoop, Ann; Mouridsen, Henning; Ejlertsen, Bent] Rigshosp, Danish Breast Canc Cooperat Grp DBCG, DBCG Secretariat, DK-2100 Copenhagen, Denmark.
[Zahrieh, David; Gelber, Richard D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bonetti, Marco] Bocconi Univ, Milan, Italy.
RP Jensen, MB (reprint author), Rigshosp, Danish Breast Canc Cooperat Grp DBCG, DBCG Secretariat, Bldg 2501,9 Blegdamsvej, DK-2100 Copenhagen, Denmark.
EM mj@dbcg.dk
RI Knoop, Ann/L-7436-2016;
OI Knoop, Ann/0000-0003-2898-1093; Bonetti, Marco/0000-0003-2304-4180
FU United States National Cancer Institute [CA-75362]
FX This study was supported in part by Grant No. CA-75362 from the United
States National Cancer Institute.
NR 24
TC 10
Z9 10
U1 0
U2 2
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 AUG
PY 2010
VL 123
IS 1
BP 163
EP 169
DI 10.1007/s10549-010-0931-y
PG 7
WC Oncology
SC Oncology
GA 627SP
UT WOS:000280063200019
PM 20464479
ER
PT J
AU Paridaens, RJ
Gelber, S
Cole, BF
Gelber, RD
Thurlimann, B
Price, KN
Holmberg, SB
Crivellari, D
Coates, AS
Goldhirsch, A
AF Paridaens, Robert J.
Gelber, Shari
Cole, Bernard F.
Gelber, Richard D.
Thuerlimann, Beat
Price, Karen N.
Holmberg, Stig B.
Crivellari, Diana
Coates, Alan S.
Goldhirsch, Aron
TI Adjuvant (c) Online estimation of chemotherapy effectiveness when added
to ovarian function suppression plus tamoxifen for premenopausal women
with estrogen-receptor-positive breast cancer
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Adjuvant (c); Online; Estrogen receptor; Premenopausal; Chemotherapy;
Endocrine therapy; International Breast Cancer Study Group
ID RANDOMIZED-TRIALS; THERAPY; CYCLOPHOSPHAMIDE; FLUOROURACIL;
METHOTREXATE; GOSERELIN; SURVIVAL; BLOCKADE; PROGRAM
AB Adjuvant!(A (c)) Online (Adjuvant!) is a user-friendly, web-based tool that provides estimates of adjuvant therapy outcomes for individual patients. While reliable evidence underpins estimates for most patient cohorts, there is a paucity of data on the effect of adding chemotherapy to complete estrogen blockade for premenopausal women with estrogen-receptor positive breast cancer. International Breast Cancer Study Group (IBCSG) Trial 11-93 enrolled 174 premenopausal women with estrogen-receptor positive, node-positive breast cancer. Among these patients, 55% had one positive axillary lymph node and 97% had three or fewer positive nodes. Patients were randomized to receive ovarian function suppression plus 5 years of tamoxifen with or without anthracycline-based chemotherapy. Estimated hazard rates and corresponding 10-year relapse-free survival percentages obtained from Trial 11-93 data were compared with those predicted using Adjuvant!. The 10-year relapse-free survival percentages predicted from Adjuvant! were 64.4% (95% CI, 61.9-67.2%) for endocrine therapy alone and 74.9% (95% CI, 73.1-76.8%) for chemoendocrine therapy. By contrast, these estimates in Trial 11-93 were 76.4% (95% CI, 65.8-84.0%) for endocrine therapy alone and 74.9% (95% CI, 64.5-82.7%) for chemoendocrine therapy. The Adjuvant! estimate for the endocrine-alone control group is lower than that observed in Trial 11-93 (P = 0.03), while the estimates for the two chemoendocrine therapy groups are similar. Adjuvant! appears to underestimate the effectiveness of adjuvant endocrine therapy alone for premenopausal women with endocrine responsive breast cancer, thus overestimating the added benefit, if any, from chemotherapy for this patient population.
C1 [Paridaens, Robert J.] Catholic Univ Louvain, Univ Hosp Gasthuisberg, Dept Med Oncol, B-3000 Louvain, Belgium.
[Gelber, Shari; Cole, Bernard F.; Gelber, Richard D.; Price, Karen N.] IBCSG Stat Ctr, Dana Farber Canc Inst, Boston, MA USA.
[Gelber, Shari; Gelber, Richard D.; Price, Karen N.] Frontier Sci & Technol Res Fdn Inc, Boston, MA USA.
[Cole, Bernard F.] Univ Vermont, Dept Math & Stat, Coll Engn & Math Sci, Burlington, VT 05405 USA.
[Gelber, Richard D.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Thuerlimann, Beat] Kantonsspital, Breast Ctr, St Gallen, Switzerland.
[Thuerlimann, Beat] Swiss Grp Clin Canc Res SAKK, Bern, Switzerland.
[Holmberg, Stig B.] Sahlgrens Univ Hosp, Dept Surg, Gothenburg, Sweden.
[Crivellari, Diana] Ctr Riferimento Oncol, Aviano, Italy.
[Coates, Alan S.] Univ Sydney, Sydney, NSW 2006, Australia.
[Goldhirsch, Aron] European Inst Oncol, Milan, Italy.
[Goldhirsch, Aron] Oncol Inst So Switzerland, Bellinzona, Switzerland.
RP Paridaens, RJ (reprint author), Catholic Univ Louvain, Univ Hosp Gasthuisberg, Dept Med Oncol, Herestr 49, B-3000 Louvain, Belgium.
EM robert.paridaens@uz.kuleuven.ac.be; shari@jimmy.harvard.edu;
ccole@cems.uvm.edu; gelber@jimmy.harvard.edu; beat.thuerlimann@kssg.ch;
price@jimmy.harvard.edu; stig.holmberge@vgregion.se; dcrivellari@cro.it;
alan.coates@ibcsg.org; aron.goldhirsch@ibcsg.org
FU International Breast Cancer Study Group (IBCSG); Swedish Cancer Society;
Cancer Council Australia; Australian New Zealand Breast Cancer Trials
Group (NHMRC) [940892]; Frontier Science and Technology Research
Foundation; Swiss Group for Clinical Cancer Research (SAKK); Cancer
Research Switzerland/Oncosuisse; Foundation for Clinical Research of
Eastern Switzerland (OSKK); United States National Cancer Institute
[CA-75362]
FX The International Breast Cancer Study Group (IBCSG) funded this
research. The IBCSG is funded by the Swedish Cancer Society; The Cancer
Council Australia; Australian New Zealand Breast Cancer Trials Group
(NHMRC grant number 940892); The Frontier Science and Technology
Research Foundation, the Swiss Group for Clinical Cancer Research
(SAKK); Cancer Research Switzerland/Oncosuisse, the Foundation for
Clinical Research of Eastern Switzerland (OSKK); and the United States
National Cancer Institute (CA-75362). We thank Love Nickerson for
collecting information on patient population from Adjuvant(C) Online.
NR 18
TC 12
Z9 12
U1 0
U2 1
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 AUG
PY 2010
VL 123
IS 1
BP 303
EP 310
DI 10.1007/s10549-010-0794-2
PG 8
WC Oncology
SC Oncology
GA 627SP
UT WOS:000280063200036
PM 20195744
ER
PT J
AU Richardson, PG
Badros, AZ
Jagannath, S
Tarantolo, S
Wolf, JL
Albitar, M
Berman, D
Messina, M
Anderson, KC
AF Richardson, Paul G.
Badros, Ashraf Z.
Jagannath, Sundar
Tarantolo, Stefano
Wolf, Jeffrey L.
Albitar, Maher
Berman, David
Messina, Marianne
Anderson, Kenneth C.
TI Tanespimycin with bortezomib: activity in relapsed/refractory patients
with multiple myeloma
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE tanespimycin; bortezomib; HSP90; HSP70; peripheral neuropathy
ID HEAT-SHOCK PROTEINS; PHASE-I TRIAL; ADVANCED CANCER; REFRACTORY MYELOMA;
ADULT PATIENTS; HSP90; DEXAMETHASONE; COMBINATION; THERAPY;
17-(ALLYLAMINO)-17-DEMETHOXYGELDANAMYCIN
AB P>Tanespimycin (17-allylamino-17-demethoxygeldanamycin, 17-AAG) disrupts heat shock protein 90 (HSP90), a key molecular chaperone for signal transduction proteins critical to myeloma growth, survival and drug resistance. In previous studies, tanespimycin monotherapy was well tolerated and active in heavily pretreated patients with relapsed/refractory multiple myeloma (MM). Preclinical data have shown antitumour synergy between tanespimycin and bortezomib, with more pronounced intracellular accumulation of ubiquitinated proteins than either drug alone, an effect attributed to the synergistic suppression of chymotryptic activity in the 20S proteasome. HSP70 induction has been observed in all Phase 1 tanespimycin studies in which it has been measured, with several separate reports of HSP70 overexpression protecting against peripheral nerve injury. In this Phase 2, open-label multicentre study, we compared 1 center dot 3 mg/m2 bortezomib + three doses of tanespimycin: 50, 175 and 340 mg/m2 in heavily pretreated patients with relapsed and refractory MM and measured HSP70 expression and proteasome activity levels in plasma of treated patients. The study was closed prematurely for resource-based reasons, precluding dose comparison. Nonetheless, antitumour activity was observed, with promising response rates and promising severity of peripheral neuropathy.
C1 [Richardson, Paul G.; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Badros, Ashraf Z.] Univ Maryland, Med Ctr, Baltimore, MD 21201 USA.
[Jagannath, Sundar] St Vincents Comprehens Canc Ctr, New York, NY USA.
[Wolf, Jeffrey L.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Albitar, Maher] Quest Diagnost Nichols Inst, San Juan Capistrano, CA USA.
[Berman, David] Bristol Myers Squibb Co, Princeton, NJ USA.
[Messina, Marianne] Bristol Myers Squibb Co, Wallingford, CT 06492 USA.
RP Richardson, PG (reprint author), Dana Farber Canc Inst, 44 Binney St,Dana 1B02, Boston, MA 02115 USA.
EM paul_richardson@dfci.harvard.edu
FU Bristol-Myers Squibb; Millennium Pharmaceuticals; Celgene Corporation;
Novartis
FX The authors wish to thank all of the patients and their families, and
the research nurses, physicians, coordinators, and other staff at the
study sites. We would also like to thank Katie Redman for administrative
assistance; and Anne Lambert for editorial assistance. This study was
sponsored by Bristol-Myers Squibb (and previously Kosan Biosciences).;
Conflicts of Interest; Dr. Richardson serves on advisory boards for
Millennium Pharmaceuticals and Celgene Corporation and receives research
funding from Millennium Pharmaceuticals. Drs. Badros, Jagannath,
Tarantolo, Wolf and Albitar have no other relevant conflicts of interest
to disclose. Dr. Berman and Ms. Messina are employees of Bristol-Myers
Squibb and have no other relevant conflicts of interest to disclose. Dr.
Anderson is a consultant and has received honoraria and research funding
from Celgene Corporation, Novartis, Millennium Pharmaceuticals, and
Bristol-Myers Squibb.
NR 43
TC 42
Z9 42
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD AUG
PY 2010
VL 150
IS 4
BP 428
EP 437
DI 10.1111/j.1365-2141.2010.08264.x
PG 10
WC Hematology
SC Hematology
GA 635AZ
UT WOS:000280629300004
PM 20618338
ER
PT J
AU Richardson, PG
Chanan-Khan, AA
Alsina, M
Albitar, M
Berman, D
Messina, M
Mitsiades, CS
Anderson, KC
AF Richardson, Paul G.
Chanan-Khan, Asher A.
Alsina, Melissa
Albitar, Maher
Berman, David
Messina, Marianne
Mitsiades, Constantine S.
Anderson, Kenneth C.
TI Tanespimycin monotherapy in relapsed multiple myeloma: results of a
phase 1 dose-escalation study
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE Multiple myeloma; tanespimycin; HSP90; HSP70; 17-AAG
ID ADVANCED CANCER; I TRIAL; REFRACTORY MYELOMA; ADULT PATIENTS;
BORTEZOMIB; 17-(ALLYLAMINO)-17-DEMETHOXYGELDANAMYCIN;
17-ALLYLAMINO-17-DEMETHOXYGELDANAMYCIN; 17-DEMETHOXYGELDANAMYCIN;
17-ALLYLAMINO; DEXAMETHASONE
AB P>Tanespimycin, a heat shock protein 90 (HSP90) inhibitor, induces apoptosis in drug-sensitive and -resistant MM cell lines and in tumour cells from patients with relapsed MM. In this phase 1 dose-escalation study, the safety, plasma pharmacokinetics, and biological/antitumour activity of tanespimycin were evaluated in heavily pretreated patients with relapsed/refractory MM. Tanespimycin (150-525 mg/m2) was given on days 1, 4, 8, and 11 of each 3-week cycle for up to 8 cycles. Non-haematological AEs included diarrhoea (59%), back pain (35%), fatigue (38%), and nausea (35%); haematological AEs included anaemia (24%) and thrombocytopenia (21%). One patient (3%) achieved minimal response (MR), with a progression-free survival (PFS) of 3 months, a 41% decrease from baseline in urine M protein, and a 33% decrease from baseline in serum M protein. Fifteen patients (52%) achieved SD with a median PFS of 2 center dot 1 months; 5/15 had reductions in serum M protein ranging from 7% to 38% and in urine M protein ranging from 6% to 91%. Mean HSP70 levels increased from day 1 h 0 to day 1 h 4 with further increases on day 11 h 0 and day 11 h 4, consistent with a therapeutic treatment effect. Tanespimycin monotherapy was well tolerated and demonstrated activity across all doses tested.
C1 [Richardson, Paul G.; Mitsiades, Constantine S.; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Chanan-Khan, Asher A.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Alsina, Melissa] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Albitar, Maher] Quest Diagnost Nichols Inst, San Juan Capistrano, CA USA.
[Berman, David] Bristol Myers Squibb Co, Princeton, NJ USA.
[Messina, Marianne] Bristol Myers Squibb Co, Res & Dev, Wallingford, CT 06492 USA.
RP Richardson, PG (reprint author), Dana Farber Canc Inst, 44 Binney St,Dana 1B02, Boston, MA 02115 USA.
EM paul_richardson@dfci.harvard.edu
FU Bristol-Myers Squibb; Millennium Pharmaceuticals
FX The authors gratefully acknowledge Alison L. Hannah, MD, consultant, for
her contributions to the study and study design. The authors would
especially like to thank the patients and their families, as well as the
research nurses, physicians, coordinators, and other staff at the study
sites including: Dana-Farber Cancer Institute; Roswell Park Cancer
Institute; H. Lee Moffitt Cancer Center and Research Institute; and
Quest Diagnostics Nichols Institute. We would also like to thank Katie
Redman for administrative assistance, and Lauren Cerruto and AOI
Communications, L. P., for editorial assistance in the preparation of
this manuscript. This study was sponsored by Bristol-Myers Squibb (and
previously Kosan Biosciences).; Dr. Richardson serves on advisory
committees for Millennium Pharmaceuticals and Celgene Corporation and
also receives research funding from Millennium Pharmaceuticals. Dr.
Chanan-Khan is on a speakers bureau and receives honoraria from Celgene
Corporation, ImmunoGen, Inc., and Millennium Pharmaceuticals. Dr. Alsina
has received commercial research grants from Millennium Pharmaceuticals
and Centocor Ortho Biotech Inc., and is a consultant for Millennium
Pharmaceuticals and Celgene Corporation. Dr. Albitar has no other
relevant conflicts of interest to disclose. Dr. Berman and Ms. Messina
are employees of Bristol-Myers Squibb and have no relevant conflicts of
interest to disclose. Dr. Mitsiades is a consultant for Millennium
Pharmaceuticals, Novartis, Bristol-Myers Squibb, Merck & Co., Pharmion
and Centocor. He receives research funding from OSI Pharmaceuticals,
Amgen Pharmaceuticals, AVEO Pharma, EMD Serono, Sunesis Pharmaceuticals,
and Gloucester Pharmaceuticals. He has received honoraria from
Millennium Pharmaceuticals, Novartis, Bristol-Myers Squibb, Merck & Co.,
and Pharmion. He receives royalties from patents from PharmaMar. Dr.
Anderson is a consultant and has received honoraria and research funding
from Celgene Corporation, Novartis, Millennium Pharmaceuticals, and
Bristol- Myers Squibb.
NR 22
TC 40
Z9 42
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD AUG
PY 2010
VL 150
IS 4
BP 438
EP 445
DI 10.1111/j.1365-2141.2010.08265.x
PG 8
WC Hematology
SC Hematology
GA 635AZ
UT WOS:000280629300005
PM 20618337
ER
PT J
AU Lopez-Posadas, R
Ballester, I
Mascaraque, C
Suarez, MD
Zarzuelo, A
Martinez-Augustin, O
de Medina, FS
AF Lopez-Posadas, R.
Ballester, I.
Mascaraque, C.
Suarez, M. D.
Zarzuelo, A.
Martinez-Augustin, O.
Sanchez de Medina, F.
TI Flavonoids exert distinct modulatory actions on cyclooxygenase 2 and
NF-kappa B in an intestinal epithelial cell line (IEC18)
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE flavonoids; cyclooxygenase 2; NF-kappa B; intestinal epithelial cells
ID INFLAMMATORY-BOWEL-DISEASE; TOLL-LIKE-RECEPTORS; EXPERIMENTAL COLITIS;
GENE-EXPRESSION; ACID; MACROPHAGES; QUERCETIN; COLON; RAT;
PHOSPHORYLATION
AB Background and purpose:
Cyclooxygenase 2 (COX-2) is involved in inflammatory bowel disease, but the effect of flavonoids at the intestinal epithelial level is unknown. We aimed to characterize the effect and structure-activity relationship of nine selected flavonoids on COX-2 expression in intestinal epithelial cell (IEC)18 cells. We also investigated the signal transduction pathway(s) responsible for the effects observed.
Experimental approach:
Intestinal epithelial cell 18, a non-tumour cell line with intestinal epithelial phenotype, was used. COX-2 was measured by Western blot and the involvement of the NF-kappa B pathway assessed by Western blot, pharmacological inhibition, luciferase reporter assays and nuclear translocation experiments.
Key results:
The effect of flavonoids on COX-2 expression depended on the experimental conditions tested [non-stimulated and lipopolysaccharide (LPS)-stimulated]. Flavonoids caused an increase in COX-2 expression and NF-kappa B-dependent gene transcription under basal conditions. Conversely, under LPS stimulation flavonoids increased, decreased or did not affect COX-2 levels depending on the specific type. Variable effects were observed on extracellular signal regulated kinase/p38/c-Jun N-terminal kinase phosphorylation and p50/65 nuclear translocation.
Conclusion and implications:
The effect of flavonoids on COX-2 expression depended on the balance of the interference with I kappa B-alpha phosphorylation and other signalling targets, and therefore depends on the experimental conditions and on the type of flavonoids. This is expected to result in different effects in inflammatory conditions. In general, flavonoids may limit epithelial COX-2 expression in inflammatory conditions while favouring it when inflammation is not present.
C1 [Lopez-Posadas, R.; Mascaraque, C.; Zarzuelo, A.; Sanchez de Medina, F.] Univ Granada, Sch Pharm, Dept Pharmacol, CIBERehd, E-18071 Granada, Spain.
[Suarez, M. D.; Martinez-Augustin, O.] Univ Granada, Sch Pharm, Dept Biochem & Mol Biol 2, CIBERehd, E-18071 Granada, Spain.
[Ballester, I.] Massachusetts Gen Hosp, Gastrointestinal Unit GRJ716, Boston, MA 02114 USA.
RP de Medina, FS (reprint author), Univ Granada, Sch Pharm, Dept Pharmacol, CIBERehd, Campus Cartuja S-N, E-18071 Granada, Spain.
EM fsanchez@ugr.es
RI Zarzuelo, Antonio/L-2840-2014; Lorente, M Dolores/N-1313-2014; Suarez
Ortega, Maria Dolores/H-1240-2015; Martinez Augustin, Olga/K-6720-2014
OI Suarez Ortega, Maria Dolores/0000-0003-3197-2518; Martinez Augustin,
Olga/0000-0001-8291-3468
FU Instituto de Salud Carlos III [PI051625, PI051651]; Ministry of Science
and Innovation [SAF2008-01432, AGL2008-04332]; CIBERehd; Ministerio de
Educacion y Ciencia, Spain; European Regional Development Fund
[BFU2007-30688-E/BFI]
FX This work was supported by grants from the Instituto de Salud Carlos III
(PI051625 and PI051651) and the Ministry of Science and Innovation
(SAF2008-01432 and AGL2008-04332). The CIBERehd is funded by the
Instituto de Salud Carlos III. IB and RLP are funded by the Ministry of
Science and Innovation. CM is funded by CIBERehd. The group is member of
the Network for Cooperative Research on Membrane Transport Proteins
(REIT), co-funded by the Ministerio de Educacion y Ciencia, Spain and
the European Regional Development Fund (Grant BFU2007-30688-E/BFI).
NR 39
TC 12
Z9 13
U1 2
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1188
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD AUG
PY 2010
VL 160
IS 7
BP 1714
EP 1726
DI 10.1111/j.1476-5381.2010.00827.x
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 621WM
UT WOS:000279616400015
PM 20649574
ER
PT J
AU Lorenz, KA
Malin, JL
AF Lorenz, Karl A.
Malin, Jennifer L.
TI How Might VA-Medicare Differences Inform the Delivery of End-of-Life
Cancer Care?
SO CANCER
LA English
DT Editorial Material
ID UNITED-STATES; ASSOCIATIONS; ACCESS; HEALTH; COSTS
C1 [Lorenz, Karl A.] Vet Adm Greater Los Angeles Healthcare Syst, Div Gen Internal Med, Los Angeles, CA USA.
[Lorenz, Karl A.] Vet Adm Greater Los Angeles Healthcare Syst, Div Palliat Care, Los Angeles, CA USA.
[Lorenz, Karl A.; Malin, Jennifer L.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Malin, Jennifer L.] Vet Adm Greater Los Angeles Healthcare Syst, Div Hematol Oncol, Los Angeles, CA USA.
RP Lorenz, KA (reprint author), Vet Adm Greater Los Angeles, VA Palliat Care Qual Improvement Resource Ctr, Vet Integrated Palliat Program, 11301 Wilshire Blvd,Code 111-G, Los Angeles, CA 90073 USA.
EM karl.lorenz@va.gov
NR 16
TC 2
Z9 2
U1 0
U2 0
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 AUG 1
PY 2010
VL 116
IS 15
BP 3533
EP 3536
DI 10.1002/cncr.25101
PG 4
WC Oncology
SC Oncology
GA 629TS
UT WOS:000280223200004
PM 20564077
ER
PT J
AU Wadlow, RC
Ryan, DP
AF Wadlow, Raymond C.
Ryan, David P.
TI The Role of Targeted Agents in Preoperative Chemoradiation for Rectal
Cancer
SO CANCER
LA English
DT Review
DE rectal cancer; chemoradiation; targeted therapy; biomarkers;
angiogenesis
ID METASTATIC COLORECTAL-CANCER; GROWTH-FACTOR-RECEPTOR; PHASE-II TRIAL;
TYROSINE KINASE INHIBITOR; TOTAL MESORECTAL EXCISION; VENOUS INFUSION
5-FLUOROURACIL; PATHOLOGICAL COMPLETE RESPONSE; FLUOROURACIL PLUS
LEUCOVORIN; EXTERNAL-BEAM RADIOTHERAPY; K-RAS MUTATION
AB In the United States, randomized trials have established preoperative chemoradiation as the standard of care for patients with locally advanced rectal cancer. Pathologic complete response (pCR) rates occur in 10% to 16% of patients and have been shown to be correlated with both disease-free and overall survival. Therefore, recent efforts incorporating newer cytotoxic and molecularly targeted agents into chemoradiotherapy regimens have reported the pCR rate to be a surrogate marker of clinical outcomes. Substitution of oral fluoropyrimidines, including capecitabine, for infusional 5-fluorouracil reportedly generated pCR rates of up to 32% in phase 2 studies, but definitive evaluation awaits results from the National Surgical Adjuvant Breast and Bowel Project (NSABP) R-04 trial. Similarly, regimens incorporating irinotecan generated pCR rates as high as 38%, but to the authors' knowledge have not been evaluated in randomized trials. In contrast, 2 large randomized trials reported that the addition of weekly oxaliplatin to fluoropyrimidine-based chemoradiation led to an increase in grade 3/4 toxicity but no difference in pCR rates. Early phase trials evaluating the anti-epidermal growth factor receptor (EGFF) antibody cetuximab in combination with chemoradiation reported modest pCR rates of 5% to 12%, and efforts have focused on identifying biomarkers of response including EGFR copy number, k-ras mutational status, and both serum and tumor-specific expression of EGFR ligands. Finally, incorporation of the anti-vascular endothelial growth factor antibody bevacizumab into chemoradiation appears to be safe and feasible, with initial studies reporting a beneficial effect on vascular normalization and correlations between circulating biomarkers of angiogenesis and pathologic response. Future efforts should include prospective studies of these agents in biomarker-defined subpopulations, as well as studies of novel agents that target angiogenesis, tumor-stromal interaction, and the cell signaling pathways implicated in colorectal cancer. Cancer 2010;116;3537-48. (C) 2070 American Cancer Society.
C1 [Wadlow, Raymond C.; Ryan, David P.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol Oncol, Boston, MA 02114 USA.
RP Ryan, DP (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Hematol Oncol, 55 Fruit St,Yawkey 7, Boston, MA 02114 USA.
EM dpryan@partners.org
NR 102
TC 15
Z9 17
U1 0
U2 4
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 AUG 1
PY 2010
VL 116
IS 15
BP 3537
EP 3548
DI 10.1002/cncr.25155
PG 12
WC Oncology
SC Oncology
GA 629TS
UT WOS:000280223200005
PM 20564106
ER
PT J
AU Keating, NL
Landrum, MB
Lamont, EB
Earle, CC
Bozeman, SR
McNeil, BJ
AF Keating, Nancy L.
Landrum, Mary Beth
Lamont, Elizabeth B.
Earle, Craig C.
Bozeman, Samuel R.
McNeil, Barbara J.
TI End-of-Life Care for Older Cancer Patients in the Veterans Health
Administration Versus the Private Sector
SO CANCER
LA English
DT Article
DE end-of-life care; lung cancer; colorectal cancer; metastatic cancer
ID MEDICARE BENEFICIARIES; MYOCARDIAL-INFARCTION; PROPENSITY SCORE;
QUALITY; INDICATORS; HOSPICE; SYSTEM; PLACE; DEATH; AGGRESSIVENESS
AB BACKGROUND: Treatment of older cancer patients at the end of life has become increasingly aggressive, despite the absence of evidence for better outcomes. We compared aggressiveness of end-of-life care of older metastatic cancer patients treated in the Veterans Health Administration (VHA) and those under fee-for-service Medicare arrangements. METHODS: Using propensity score methods, we matched 2913 male veterans who were diagnosed with stage IV lung or colorectal cancer in 2001-2002 and died before 2006 with 2913 similar men enrolled in fee-for-service Medicare living in Surveillance, Epidemiology, and End Result (SEER) areas. We assessed chemotherapy within 14 days of death, intensive care unit (ICU) admissions within 30 days of death, and >1 emergency room visit within 30 days of death. RESULTS: Among matched cohorts, men treated in the VHA were less likely than men in the private sector to receive chemotherapy within 14 days of death (4.6% vs 7.5%, P < .001), be admitted to an ICU within 30 days of death (12.5% vs 19.7%, P < .001), or have >1 emergency room visit within 30 days of death (13.1 vs 14.7, P = .09). CONCLUSIONS: Older men with metastatic lung or colorectal cancer treated in the VHA healthcare system received less aggressive end-of-life care than similar men in fee-for-service Medicare. This may result from the absence of financial incentives for more intensive care in the VHA or because this integrated delivery system is better structured to limit potentially overly aggressive care. Additional studies are needed to assess whether men undergoing less aggressive end-of-life care also experience better outcomes. Cancer 2010;116;3732-9. (C) 2010 American Cancer Society.
C1 [Keating, Nancy L.; Landrum, Mary Beth; Lamont, Elizabeth B.; McNeil, Barbara J.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Keating, Nancy L.] Brigham & Womens Hosp, Div Gen Internal Med, Boston, MA 02115 USA.
[Lamont, Elizabeth B.] Massachusetts Gen Hosp, Div Adult Oncol, Boston, MA 02114 USA.
[Earle, Craig C.] Sunnybrook Hlth Sci Ctr, Inst Clin Evaluat Sci, Toronto, ON M4N 3M5, Canada.
[Bozeman, Samuel R.] ABT Associates Inc, Cambridge, MA 02138 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 Department of Veterans Affairs through the Office of Policy and Planning
FX This work was funded by the Department of Veterans Affairs through the
Office of Policy and Planning as part of a larger evaluation of oncology
care.
NR 37
TC 37
Z9 38
U1 0
U2 0
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 AUG 1
PY 2010
VL 116
IS 15
BP 3732
EP 3739
DI 10.1002/cncr.25077
PG 8
WC Oncology
SC Oncology
GA 629TS
UT WOS:000280223200027
PM 20564065
ER
PT J
AU Michaud, DS
Vrieling, A
Jiao, L
Mendelsohn, JB
Steplowski, E
Lynch, SM
Wactawski-Wende, J
Arslan, AA
Bueno-de-Mesquita, HB
Fuchs, CS
Gross, M
Helzlsouer, K
Jacobs, EJ
LaCroix, A
Petersen, G
Zheng, W
Allen, N
Ammundadottir, L
Bergmann, MM
Boffetta, P
Buring, JE
Canzian, F
Chanock, SJ
Clavel-Chapelon, F
Clipp, S
Freiberg, MS
Gaziano, JM
Giovannucci, EL
Hankinson, S
Hartge, P
Hoover, RN
Hubbell, FA
Hunter, DJ
Hutchinson, A
Jacobs, K
Kooperberg, C
Kraft, P
Manjer, J
Navarro, C
Peeters, PHM
Shu, XO
Stevens, V
Thomas, G
Tjonneland, A
Tobias, GS
Trichopoulos, D
Tumino, R
Vineis, P
Virtamo, J
Wallace, R
Wolpin, BM
Yu, K
Zeleniuch-Jacquotte, A
Stolzenberg-Solomon, RZ
AF Michaud, Dominique S.
Vrieling, Alina
Jiao, Li
Mendelsohn, Julie B.
Steplowski, Emily
Lynch, Shannon M.
Wactawski-Wende, Jean
Arslan, Alan A.
Bueno-de-Mesquita, H. Bas
Fuchs, Charles S.
Gross, Myron
Helzlsouer, Kathy
Jacobs, Eric J.
LaCroix, Andrea
Petersen, Gloria
Zheng, Wei
Allen, Naomi
Ammundadottir, Laufey
Bergmann, Manuela M.
Boffetta, Paolo
Buring, Julie E.
Canzian, Federico
Chanock, Stephen J.
Clavel-Chapelon, Francoise
Clipp, Sandra
Freiberg, Matthew S.
Gaziano, J. Michael
Giovannucci, Edward L.
Hankinson, Susan
Hartge, Patricia
Hoover, Robert N.
Hubbell, F. Allan
Hunter, David J.
Hutchinson, Amy
Jacobs, Kevin
Kooperberg, Charles
Kraft, Peter
Manjer, Jonas
Navarro, Carmen
Peeters, Petra H. M.
Shu, Xiao-Ou
Stevens, Victoria
Thomas, Gilles
Tjonneland, Anne
Tobias, Geoffrey S.
Trichopoulos, Dimitrios
Tumino, Rosario
Vineis, Paolo
Virtamo, Jarmo
Wallace, Robert
Wolpin, Brian M.
Yu, Kai
Zeleniuch-Jacquotte, Anne
Stolzenberg-Solomon, Rachael Z.
TI Alcohol intake and pancreatic cancer: a pooled analysis from the
pancreatic cancer cohort consortium (PanScan)
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Alcohol; Pancreatic cancer; Pooled analysis
ID BASE-LINE CHARACTERISTICS; GENOME-WIDE ASSOCIATION; LIFE-STYLE FACTORS;
WOMENS HEALTH; UNITED-STATES; COFFEE CONSUMPTION; RISK; TOBACCO; DESIGN;
SUSCEPTIBILITY
AB The literature has consistently reported no association between low to moderate alcohol consumption and pancreatic cancer; however, a few studies have shown that high levels of intake may increase risk. Most single studies have limited power to detect associations even in the highest alcohol intake categories or to examine associations by alcohol type. We analyzed these associations using 1,530 pancreatic cancer cases and 1,530 controls from the Pancreatic Cancer Cohort Consortium (PanScan) nested case-control study. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression, adjusting for potential confounders. We observed no significant overall association between total alcohol (ethanol) intake and pancreatic cancer risk (OR = 1.38, 95% CI = 0.86-2.23, for 60 or more g/day vs. > 0 to < 5 g/day). A statistically significant increase in risk was observed among men consuming 45 or more grams of alcohol from liquor per day (OR = 2.23, 95% CI = 1.02-4.87, compared to 0 g/day of alcohol from liquor, P-trend = 0.12), but not among women (OR = 1.35, 95% CI = 0.63-2.87, for 30 or more g/day of alcohol from liquor, compared to none). No associations were noted for wine or beer intake. Overall, no significant increase in risk was observed, but a small effect among heavy drinkers cannot be ruled out.
C1 [Michaud, Dominique S.; Peeters, Petra H. M.; Vineis, Paolo] Univ London Imperial Coll Sci Technol & Med, Div Epidemiol Publ Hlth & Primary Care, London, England.
[Michaud, Dominique S.; Giovannucci, Edward L.; Hankinson, Susan] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Vrieling, Alina; Bueno-de-Mesquita, H. Bas] Natl Inst Publ Hlth & Environm RIVM, Bilthoven, Netherlands.
[Jiao, Li; Mendelsohn, Julie B.; Ammundadottir, Laufey; Chanock, Stephen J.; Hartge, Patricia; Hoover, Robert N.; Hutchinson, Amy; Jacobs, Kevin; Thomas, Gilles; Tobias, Geoffrey S.; Yu, Kai; Stolzenberg-Solomon, Rachael Z.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Steplowski, Emily] Informat Management Serv Inc, Silver Spring, MD USA.
[Lynch, Shannon M.] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Wactawski-Wende, Jean] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
[Arslan, Alan A.] NYU, Dept Obstet & Gynecol, Sch Med, New York, NY 10016 USA.
[Arslan, Alan A.; Zeleniuch-Jacquotte, Anne] NYU, Dept Environm Med, Sch Med, New York, NY 10016 USA.
[Arslan, Alan A.; Zeleniuch-Jacquotte, Anne] NYU Canc Inst, New York, NY USA.
[Fuchs, Charles S.; Wolpin, Brian M.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Fuchs, Charles S.; Giovannucci, Edward L.; Hankinson, Susan; Hunter, David J.; Wolpin, Brian M.] Harvard Univ, Sch Med, Channing Lab, Dept Med,Brigham & Womens Hosp, Boston, MA 02115 USA.
[Gross, Myron] Univ Minnesota, Sch Med, Dept Lab Med Pathol, Minneapolis, MN 55455 USA.
[Helzlsouer, Kathy] Mercy Med Ctr, Prevent & Res Ctr, Baltimore, MD USA.
[Jacobs, Eric J.; Stevens, Victoria] Amer Canc Soc, Dept Epidemiol, Atlanta, GA 30329 USA.
[LaCroix, Andrea; Kooperberg, Charles] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Petersen, Gloria] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Zheng, Wei; Shu, Xiao-Ou] Vanderbilt Univ, Dept Med, Nashville, TN USA.
[Zheng, Wei; Shu, Xiao-Ou] Vanderbilt Univ, Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Allen, Naomi] Univ Oxford, Canc Epidemiol Unit, Oxford, England.
[Ammundadottir, Laufey; Chanock, Stephen J.] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, US Dept HHS,NIH, Bethesda, MD 20892 USA.
[Bergmann, Manuela M.] German Inst Human Nutr, Dept Epidemiol, Potsdam, Germany.
[Boffetta, Paolo] Int Agcy Res Canc, F-69372 Lyon, France.
[Boffetta, Paolo] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
[Buring, Julie E.; Gaziano, J. Michael] Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA.
[Buring, Julie E.; Gaziano, J. Michael] Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MA 02115 USA.
[Buring, Julie E.] Harvard Univ, Sch Med, Dept Ambulatory Care & Prevent, Boston, MA USA.
[Canzian, Federico] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Clavel-Chapelon, Francoise] Inst Gustave Roussy, Villejuif, France.
[Clavel-Chapelon, Francoise] INSERM, Villejuif, France.
[Clipp, Sandra] George W Comstock Ctr Publ Hlth Res & Prevent, Johns Hopkins Bloomberg Sch Publ Hlth, Hagerstown, MD USA.
[Freiberg, Matthew S.] Univ Pittsburgh, Ctr Res Hlth Care, Pittsburgh, PA USA.
[Gaziano, J. Michael] Vet Affairs Boston Healthcare Syst, Massachusetts Vet Epidemiol Res & Informat Ctr, Boston, MA USA.
[Giovannucci, Edward L.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Hubbell, F. Allan] Univ Calif Irvine, Sch Med, Irvine, CA 92717 USA.
[Tumino, Rosario] Univ Athens, Sch Med, Dept Hyg & Epidemiol, Athens, Greece.
[Tumino, Rosario] Civile MP Arezzo Hosp, Canc Registry, Ragusa, Italy.
[Tumino, Rosario] Civile MP Arezzo Hosp, Dept Histopathol, Ragusa, Italy.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Wallace, Robert] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA USA.
[Wallace, Robert] Univ Iowa, Dept Internal Med, Coll Publ Hlth, Iowa City, IA 52242 USA.
[Wallace, Robert] Univ Iowa, Coll Med, Dept Epidemiol, Iowa City, IA 52242 USA.
[Wallace, Robert] Univ Iowa, Coll Med, Dept Internal Med, Iowa City, IA 52242 USA.
RP Michaud, DS (reprint author), Univ London Imperial Coll Sci Technol & Med, Div Epidemiol Publ Hlth & Primary Care, London, England.
EM d.michaud@imperial.ac.uk
RI Clavel-Chapelon, Francoise/G-6733-2014; Michaud, Dominique/I-5231-2014;
Vrieling, Alina/A-2725-2016; Tobias, Geoffrey/M-4135-2016;
OI Tobias, Geoffrey/0000-0002-2878-8253; Zeleniuch-Jacquotte,
Anne/0000-0001-9350-1303
FU NCI NIH HHS [P01 CA087969, P01 CA087969-12, R01 CA082729, R01 CA124908,
R37 CA070867]
NR 41
TC 42
Z9 44
U1 0
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD AUG
PY 2010
VL 21
IS 8
BP 1213
EP 1225
DI 10.1007/s10552-010-9548-z
PG 13
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 627TI
UT WOS:000280065400007
PM 20373013
ER
PT J
AU Barnett, CM
Nielson, CM
Shannon, J
Chan, JM
Shikany, JM
Bauer, DC
Hoffman, AR
Barrett-Connor, E
Orwoll, E
Beer, TM
AF Barnett, Christine M.
Nielson, Carrie M.
Shannon, Jackie
Chan, June M.
Shikany, James M.
Bauer, Douglas C.
Hoffman, Andrew R.
Barrett-Connor, Elizabeth
Orwoll, Eric
Beer, Tomasz M.
TI Serum 25-OH vitamin D levels and risk of developing prostate cancer in
older men
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Vitamin D; Prostate cancer
ID UNITED-STATES; 1,25-DIHYDROXYVITAMIN D-3; SUBSEQUENT DEVELOPMENT;
ULTRAVIOLET-RADIATION; D METABOLITES; COLON-CANCER; D DEFICIENCY;
IN-VIVO; 25-HYDROXYVITAMIN-D; MORTALITY
AB Multiple studies have shown clear evidence of vitamin D's anti-tumor effects on prostate cancer cells in laboratory experiments, but the evidence has not been consistent in humans. We sought to examine the association between vitamin D and prostate cancer risk in a cohort of older men.
We conducted a prospective case-cohort study nested within the multicenter Osteoporotic Fractures in Men (MrOS) study. Baseline serum 25-OH vitamin D was measured in a randomly selected sub-cohort of 1,433 men a parts per thousand yen65 years old without a history of prostate cancer and from all participants with an incident diagnosis of prostate cancer (n = 297). Cox proportional hazards models were used to evaluate the associations between quartiles of total 25-OH vitamin D and incident prostate cancer, as well as Gleason score.
In comparison with the lowest quartile of 25-OH vitamin D, the hazard ratio for the highest quartile of 25-OH vitamin D was 1.22 (CI 0.50-1.72, p = 0.25), no trend across quartiles (p = 0.94) or association with Gleason score was observed. Adjustment for covariates did not alter the results.
In this prospective cohort of older men, we found no association between serum 25-OH vitamin D levels and subsequent risk of prostate cancer.
C1 [Barnett, Christine M.; Beer, Tomasz M.] Oregon Hlth & Sci Univ, Div Hematol & Med Oncol, Portland, OR 97239 USA.
[Barnett, Christine M.; Beer, Tomasz M.] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97239 USA.
[Nielson, Carrie M.; Shannon, Jackie] Oregon Hlth & Sci Univ, Dept Publ Hlth & Prevent Med, Portland, OR 97239 USA.
[Shannon, Jackie] Oregon Hlth & Sci Univ, Portland VA Med Ctr, Portland, OR 97239 USA.
[Shannon, Jackie] Oregon Hlth & Sci Univ, CROET, Portland, OR 97239 USA.
[Chan, June M.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Chan, June M.] Univ Calif San Francisco, Dept Urol, San Francisco, CA 94143 USA.
[Shikany, James M.] Univ Alabama, Div Prevent Med, Birmingham, AL USA.
[Hoffman, Andrew R.] Stanford Univ, Dept Med, Stanford, CA 94305 USA.
[Barrett-Connor, Elizabeth] Univ Calif San Diego, Dept Family & Prevent Med, Div Epidemiol, San Diego, CA 92103 USA.
[Orwoll, Eric] Oregon Hlth & Sci Univ, Div Endocrinol, Bone & Mineral Unit, Portland, OR 97239 USA.
RP Beer, TM (reprint author), Oregon Hlth & Sci Univ, Div Hematol & Med Oncol, CH-14R,3303 SW Bond Ave, Portland, OR 97239 USA.
EM beert@ohsu.edu
OI Orwoll, Eric/0000-0002-8520-7355
FU NIA NIH HHS [U01 AG042140]
NR 47
TC 25
Z9 26
U1 0
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD AUG
PY 2010
VL 21
IS 8
BP 1297
EP 1303
DI 10.1007/s10552-010-9557-y
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 627TI
UT WOS:000280065400015
PM 20383574
ER
PT J
AU Mekary, RA
Wu, KN
Giovannucci, E
Sampson, L
Fuchs, C
Spiegelman, D
Willett, WC
Smith-Warner, SA
AF Mekary, Rania A.
Wu, Kana
Giovannucci, Edward
Sampson, Laura
Fuchs, Charles
Spiegelman, Donna
Willett, Walter C.
Smith-Warner, Stephanie A.
TI Total antioxidant capacity intake and colorectal cancer risk in the
Health Professionals Follow-up Study
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Total antioxidant capacity (TAC); FRAP; Colorectal cancer; Nutrition
ID FOOD-FREQUENCY QUESTIONNAIRE; PLANT FOODS; REPRODUCIBILITY; PREVENTION;
VALIDITY; DISEASE
AB To examine the association between total antioxidant capacity (TAC) intake and colorectal cancer incidence.
TAC intake was assessed in 1986 and every 4 years thereafter in the Health Professionals Follow-up Study, a prospective cohort study of 47,339 men. Between 1986 and 2004, 952 colorectal cancer cases were diagnosed. Cox proportional hazards regression models were used to estimate relative risks (RR) and 95% confidence intervals (CI).
Comparing the highest versus lowest quintile, TAC intake from foods only (dietary TAC) was not associated with colorectal (multivariate-RR: 0.98; 95% CI: 0.78, 1.23) or colon (multivariate-RR: 1.20; 95% CI: 0.90, 1.61) cancer risk, but was inversely associated with rectal cancer risk (multivariate-RR: 0.58; 95% CI: 0.35, 0.96). For the same comparison, TAC intake from foods and supplements (total TAC) was not associated with colorectal (multivariate-RR: 0.91; 95% CI: 0.73, 1.14), colon (multivariate-RR: 1.01; 95% CI: 0.77, 1.33), or rectal (multivariate-RR: 0.85; 95% CI: 0.52, 1.38) cancer risk.
Dietary and total TAC intakes were not associated with colorectal and colon cancer risk. Dietary, but not total, TAC intake was inversely associated with rectal cancer risk, suggesting antioxidants per se may not be associated with rectal cancer risk.
C1 [Mekary, Rania A.; Wu, Kana; Giovannucci, Edward; Sampson, Laura; Willett, Walter C.; Smith-Warner, Stephanie A.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Mekary, Rania A.; Giovannucci, Edward; Spiegelman, Donna; Willett, Walter C.; Smith-Warner, Stephanie A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Giovannucci, Edward; Fuchs, Charles; Willett, Walter C.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Lab, Boston, MA USA.
[Fuchs, Charles] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Spiegelman, Donna] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
RP Mekary, RA (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 665 Huntington Ave,Bldg 2,Rm 355A, Boston, MA 02115 USA.
EM Rmekary@hsph.harvard.edu
FU National Institutes for Health [CA098566, CA55075]
FX This work was supported by CA098566 and CA55075 from the National
Institutes for Health.
NR 22
TC 19
Z9 19
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD AUG
PY 2010
VL 21
IS 8
BP 1315
EP 1321
DI 10.1007/s10552-010-9559-9
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 627TI
UT WOS:000280065400017
PM 20390446
ER
PT J
AU Chiorean, EG
Malireddy, S
Younger, AE
Jones, DR
Waddell, MJ
Sloop, MI
Yu, MG
Hall, SD
Schneider, B
Sweeney, CJ
AF Chiorean, E. Gabriela
Malireddy, Srikar
Younger, Anne E.
Jones, David R.
Waddell, Mary-Jane
Sloop, Melissa I.
Yu, Menggang
Hall, Stephen D.
Schneider, Bryan
Sweeney, Christopher J.
TI A phase I dose escalation and pharmacokinetic study of vatalanib
(PTK787/ZK 222584) in combination with paclitaxel in patients with
advanced solid tumors
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Paclitaxel; Phase I; PTK/ZK; VEGFR
ID ENDOTHELIAL GROWTH-FACTOR; ADVANCED COLORECTAL-CANCER; RECEPTOR TYROSINE
KINASES; METASTATIC BREAST-CANCER; HUMAN LIVER-MICROSOMES; CELL
LUNG-CANCER; OVARIAN-CANCER; INHIBITOR; CARBOPLATIN; METABOLISM
AB To define the maximum-tolerated dose (MTD) for weekly paclitaxel administered in combination with daily vatalanib (PTK787/ZK 222584, PTK/ZK) and assess for a drug-drug interaction.
Patients were treated with escalating doses of weekly paclitaxel (75-85 mg/m(2)), and daily PTK/ZK (250-1,000 mg). During the first cycle only, paclitaxel was given on days 1 and 15, and PTK/ZK on days 3-28. Pharmacokinetic studies were conducted on cycle 1 days 1 and 15 for paclitaxel, and on cycle 1 day 15 for PTK/ZK. Therapy was given until disease progression.
Twenty-seven patients were accrued to four dose levels. Two of five patients treated with paclitaxel 85 mg/m(2) and PTK/ZK 1,000 mg had Grade 3 transaminase elevation as dose-limiting toxicity. Paired PK analyses demonstrated a significant increase in paclitaxel clearance on day 15 (p = 0.006). Activity included one partial response and 11 patients with stable disease a parts per thousand yen4 months, including patients previously treated with paclitaxel.
The MTD for weekly paclitaxel plus daily PTK/ZK is 75 mg/m(2) and 750 mg. PK analysis revealed a significant drug-drug interaction, with an increase in paclitaxel clearance. This combination was well tolerated with evidence of anti-cancer activity and provides guidance for phase 2 planning.
C1 [Sweeney, Christopher J.] Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol, Dept Med, Boston, MA 02115 USA.
[Yu, Menggang] Indiana Univ, Dept Biostat, Indianapolis, IN 46204 USA.
[Chiorean, E. Gabriela; Malireddy, Srikar; Younger, Anne E.; Jones, David R.; Waddell, Mary-Jane; Sloop, Melissa I.; Hall, Stephen D.; Schneider, Bryan; Sweeney, Christopher J.] Indiana Univ, Dept Med, Simon Canc Ctr, Indianapolis, IN USA.
RP Sweeney, CJ (reprint author), Dana Farber Canc Inst, Lank Ctr Genitourinary Oncol, Dept Med, 44 Binney St,Rm 1230, Boston, MA 02115 USA.
EM Christopher_Sweeney@dfci.harvard.edu
FU Novartis Pharmaceuticals; Indiana University School of Medicine
[M01RR00750]
FX Supported by Novartis Pharmaceuticals; General Clinical Research Center
at Indiana University School of Medicine M01RR00750.
NR 27
TC 4
Z9 4
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 AUG
PY 2010
VL 66
IS 3
BP 441
EP 448
DI 10.1007/s00280-009-1179-2
PG 8
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 611PJ
UT WOS:000278831600004
PM 20091169
ER
PT J
AU Grundmark, B
Garmo, H
Loda, M
Busch, C
Holmberg, L
Zethelius, B
AF Grundmark, Birgitta
Garmo, Hans
Loda, Massimo
Busch, Christer
Holmberg, Lars
Zethelius, Bjorn
TI The Metabolic Syndrome and the Risk of Prostate Cancer under Competing
Risks of Death from Other Causes
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID BODY-MASS INDEX; MYOCARDIAL-INFARCTION; MEN; COHORT; SIZE; PREVENTION;
COMPONENTS; PREDICTOR; SURVIVAL; REGISTER
AB Background: Associations between metabolic syndrome (MetS) components and prostate cancer development have not been studied comprehensively; results have been divergent. Using the National Cholesterol Education Program Adult Treatment panel III (NCEP) and International Diabetes Federation (IDF) definitions of the MetS, we investigated such associations taking competing risks of death into consideration.
Methods: In the prospective Uppsala Longitudinal Study of Adult Men of 2,322 Caucasian men with 34 years of follow-up baseline, MetS measurements at age 50 years were used. Cumulative incidence of prostate cancer and death with/without the MetS were calculated. Competing risk of dying was taken into account by calculating the conditional probability of prostate cancer with/without the MetS.
Results: Two hundred and thirty-seven prostate cancers were identified. Prostate cancer probability by age 80 years with baseline MetS compared with without MetS was nonsignificantly higher [5.2 percent units (confidence interval (CI), -0.8% to 11.3%; NCEP); 2.7 percent units (CI, -2.7% to 8.0%; IDF)]; cumulative incidence proportions of death was significantly higher [19.3 percent units (CI, 13.4-25.3%; NCEP); 15.3 percent units (CI, 9.5-21.1%; IDF)]; and conditional probability of prostate cancer considering death from other causes was significantly higher [7.3 percent-units (CI, 0.2-14.5%); odds ratio of 1.64 (CI, 1.03-2.23; NCEP)] and nonsignificantly higher [5.0 percent-units (CI, -1.6% to 11.6%); odds ratio of 1.43 (CI, 0.89-1.90; IDF].
Conclusions: The MetS by the NCEP definition is associated with prostate cancer, taking the competing risk of early death from other causes into account.
Impact: The results further highlight the public health effect of the increasing prevalence of MetS and the importance of considering competing risks when studying risk factors for cancer. Cancer Epidemiol Biomarkers Prev; 19(8); 2088-96. (C) 2010 AACR.
C1 [Grundmark, Birgitta; Garmo, Hans; Holmberg, Lars] Uppsala Univ, Dept Surg Sci, Uppsala, Sweden.
[Busch, Christer] Uppsala Univ, Dept Genet & Pathol, Uppsala, Sweden.
[Zethelius, Bjorn] Uppsala Univ, Dept Publ Hlth & Caring Sci Geriatr, Uppsala, Sweden.
[Grundmark, Birgitta; Garmo, Hans; Holmberg, Lars] Univ Uppsala Hosp, Reg Oncol Ctr Uppsala Orebro Reg, SE-75185 Uppsala, Sweden.
[Grundmark, Birgitta; Zethelius, Bjorn] Med Prod Agcy, Uppsala, Sweden.
[Garmo, Hans; Holmberg, Lars] Kings Coll London, Sch Med, Div Canc Studies, London WC2R 2LS, England.
[Loda, Massimo] Harvard Univ, Sch Med, Dept Pathol, Dana Farber Canc Inst,Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Grundmark, B (reprint author), Univ Uppsala Hosp, Reg Oncol Ctr, SE-75185 Uppsala, Sweden.
EM birgitta.grundmark@surgsci.uu.se
OI Garmo, Hans/0000-0001-7181-7083
FU Ernfors Family; Thuring; Thureus; Ake Wiberg Foundations; Swedish
Diabetes Association; Swedish Medical Products Agency; Swedish Cancer
Society; Cancer Research UK; Prostate Cancer Foundation; National Cancer
Institute [RO1CA131945, P50 CA90381]; Dana-Farber Cancer Institute;
Linda and Arthur Gelb Center for Translational Research
FX Grants from the Ernfors Family(B. Zethelius), the Thuring (B.
Zethelius), the Thureus (B. Zethelius) and the Ake Wiberg (B. Zethelius)
Foundations, the Swedish Diabetes Association Research Fund (B.
Zethelius), the Swedish Medical Products Agency (B. Grundmark and B.
Zethelius), The Swedish Cancer Society (B. Grundmark and L. Holmberg),
Cancer Research UK (H. Garmo and L. Holmberg), the Prostate Cancer
Foundation (M. Loda), the National Cancer Institute grant RO1CA131945,
P50 CA90381 (M. Loda), the Dana-Farber Cancer Institute-Novartis Drug
Development Program (M. Loda), and the Linda and Arthur Gelb Center for
Translational Research, a gift from Nuclea Biomarkers (M. Loda).
NR 40
TC 33
Z9 33
U1 0
U2 0
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD AUG
PY 2010
VL 19
IS 8
BP 2088
EP 2096
DI 10.1158/1055-9965.EPI-10-0112
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 635RY
UT WOS:000280675000023
PM 20647401
ER
PT J
AU Ghosh, SK
Kim, P
Zhang, XA
Yun, SH
Moore, A
Lippard, SJ
Medarova, Z
AF Ghosh, Subrata K.
Kim, Pilhan
Zhang, Xiao-an
Yun, Seok-Hyun
Moore, Anna
Lippard, Stephen J.
Medarova, Zdravka
TI A Novel Imaging Approach for Early Detection of Prostate Cancer Based on
Endogenous Zinc Sensing
SO CANCER RESEARCH
LA English
DT Article
ID UPTAKE TRANSPORTER; TRANSGENIC MOUSE; TUMORS; RECEPTOR; ANTIGEN; CELLS;
MODEL
AB The early detection of prostate cancer is a life-saving event in patients harboring potentially aggressive disease. With the development of malignancy, there is a dramatic reduction in the zinc content of prostate tissue associated with the inability of cancer cells to accumulate the ion. In the current study, we used endogenous zinc as an imaging biomarker for prostate cancer detection and progression monitoring. We employed a novel fluorescent sensor for mobile zinc (ZPP1) to detect and monitor the development of prostate cancer in a transgenic mouse model of prostate adenocarcinoma, using in vivo optical imaging correlated with biological fluid-based methods. We showed that the progression of prostate cancer could be monitored in vivo judging by the decreasing zinc content in the prostates of tumor-bearing mice in an age-dependent manner. In a novel quantitative assay, we determined the concentration of mobile zinc in both prostate cell lysates and mouse prostate extracts through simple titration of the ZPP1 sensor. Our findings fulfill the promise of zinc-based prostate cancer diagnostics with the prospect for immediate clinical translation. Cancer Res; 70(15); 6119-27. (C) 2010 AACR.
C1 [Ghosh, Subrata K.; Moore, Anna; Medarova, Zdravka] Harvard Univ, Mol Imaging Lab, MGH MIT HMS Athinoula A Martinos Ctr Biomed Imagi, Sch Med,Dept Radiol,Massachusetts Gen Hosp, Charlestown, MA 02129 USA.
[Kim, Pilhan; Yun, Seok-Hyun] Harvard Univ, Wellman Ctr Photomed, Dept Dermatol, Sch Med,Massachusetts Gen Hosp, Charlestown, MA 02129 USA.
[Zhang, Xiao-an; Lippard, Stephen J.] MIT, Dept Chem, Cambridge, MA 02139 USA.
RP Medarova, Z (reprint author), Harvard Univ, Mol Imaging Lab, MGH MIT HMS Athinoula A Martinos Ctr Biomed Imagi, Sch Med,Dept Radiol,Massachusetts Gen Hosp, Bldg 75,13th St, Charlestown, MA 02129 USA.
EM amoore@helix.mgh.harvard.edu; lippard@mit.edu; zmedarova@partners.org
RI Kim, Pilhan/C-1836-2011; Zhang, Xiao-an/E-4458-2016
OI Kim, Pilhan/0000-0001-8388-1840; Zhang, Xiao-an/0000-0001-9417-4228
FU National Institute of General Medical Sciences [GM065519]; National
Cancer Institute [R00CA129070]; National Institute of Diabetes and
Digestive and Kidney Diseases [RC1DK086242]; Tosteson Postdoctoral
Fellowship
FX Work at the Massachusetts Institute of Technology was supported under
grant GM065519 from the National Institute of General Medical Sciences.
Work at the Martinos Center for Biomedical Imaging was supported in part
under grant R00CA129070 from the National Cancer Institute. Work at the
Wellman Center for Photomedicine was supported in part under grant
RC1DK086242 from the National Institute of Diabetes and Digestive and
Kidney Diseases and a Tosteson Postdoctoral Fellowship.
NR 23
TC 47
Z9 47
U1 4
U2 22
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 AUG 1
PY 2010
VL 70
IS 15
BP 6119
EP 6127
DI 10.1158/0008-5472.CAN-10-1008
PG 9
WC Oncology
SC Oncology
GA 634CQ
UT WOS:000280557500002
PM 20610630
ER
PT J
AU Monte, NM
Webster, KA
Neuberg, D
Dressler, GR
Mutter, GL
AF Monte, Nicolas M.
Webster, Kaitlyn A.
Neuberg, Donna
Dressler, Gregory R.
Mutter, George L.
TI Joint Loss of PAX2 and PTEN Expression in Endometrial Precancers and
Cancer
SO CANCER RESEARCH
LA English
DT Article
ID INTRAEPITHELIAL-NEOPLASIA; TUMOR-SUPPRESSOR; WILMS-TUMOR; CARCINOMA;
PROGRESSION; MARKER; BREAST; HYPERPLASIA; MUTATIONS; TAMOXIFEN
AB Latent endometrial carcinoma precancers are normal-appearing endometrial glands with sporadic loss of tumor suppressor gene function such as PTEN. Progression to carcinoma is inefficient and requires additional genetic damage that creates a histologic precursor lesion called endometrial intraepithelial neoplasia (EIN). In this study, we examined loss of PAX2 expression, a gene required for embryonic uterine development, during endometrial carcinogenesis. Normal proliferative, EIN, and malignant (endometrial adenocarcinoma) endometrial tissues were immunostained for PTEN and PAX2. Proliferative samples with loss of protein in at least one gland were scored as latent precancers. EIN and cancer lesions were scored by the majority pattern. Overall prevalence and topography of joint PAX2-PTEN expression loss was examined. The prevalence of PAX2 protein loss in the sequence of normal to precancer to cancer was 36%, 71%, and 77%, respectively, and for PTEN, it was 49%, 44%, and 68%, respectively. The normal endometrial prevalence of PAX2- or PTEN-deficient latent precancers was unaffected by biopsy indication, but increased significantly with age. Coincident loss of PAX2 and PTEN expression in an individual normal endometrium was seen in 21% of patients, but usually involved different glands. Coincident loss was more common in precancers (31%) and carcinoma (55%), in which case, both markers were protein null in an overlapping clonal distribution. PAX2 and PTEN protein loss occurs independently and accumulates with increasing age in latent precancers of normal premenopausal endometrium. Loss of function of both genes in an overlapping distribution characterizes the clinical emergence of a premalignant lesion which is carried forward to carcinoma. Cancer Res; 70(15); 6225-32. (C) 2010 AACR.
C1 [Mutter, George L.] Brigham & Womens Hosp, Div Womens & Perinatal Pathol, Dept Pathol, Boston, MA 02115 USA.
[Neuberg, Donna] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Dressler, Gregory R.] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Mutter, GL (reprint author), Brigham & Womens Hosp, Div Womens & Perinatal Pathol, Dept Pathol, 75 Francis St, Boston, MA 02115 USA.
EM gmutter@rics.bwh.harvard.edu
FU NIH [RO1-CA100833]
FX NIH grant RO1-CA100833 (G. Mutter).
NR 30
TC 36
Z9 40
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD AUG 1
PY 2010
VL 70
IS 15
BP 6225
EP 6232
DI 10.1158/0008-5472.CAN-10-0149
PG 8
WC Oncology
SC Oncology
GA 634CQ
UT WOS:000280557500012
PM 20631067
ER
PT J
AU Tyner, JW
Fletcher, LB
Wang, EQ
Yang, WF
Rutenberg-Schoenberg, ML
Beadling, C
Mori, M
Heinrich, MC
Deininger, MW
Druker, BJ
Loriaux, MM
AF Tyner, Jeffrey W.
Fletcher, Luke B.
Wang, Ellen Q.
Yang, Wayne F.
Rutenberg-Schoenberg, Michael L.
Beadling, Carol
Mori, Motomi
Heinrich, Michael C.
Deininger, Michael W.
Druker, Brian J.
Loriaux, Marc M.
TI MET Receptor Sequence Variants R970C and T992I Lack Transforming
Capacity
SO CANCER RESEARCH
LA English
DT Article
ID CELL LUNG-CANCER; ACTIVATING MUTATIONS; FUNCTIONAL-ANALYSIS;
MYELOID-LEUKEMIA; FOLLOW-UP; C-MET; PROTOONCOGENE; EXPRESSION;
GEFITINIB; CARCINOMA
AB High-throughput sequencing promises to accelerate the discovery of sequence variants, but distinguishing oncogenic mutations from irrelevant "passenger" mutations remains a major challenge. Here we present an analysis of two sequence variants of the MET receptor (hepatocyte growth factor receptor) R970C and T992I (also designated R988C and T1010I). Previous reports indicated that these sequence variants are transforming and contribute to oncogenesis. We screened patients with chronic lymphocytic leukemia (CLL), acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML), colorectal cancer, endometrial cancer, thyroid cancer, or melanoma, as well as individuals without cancer, and found these variants at low frequencies in most cohorts, including normal individuals. No evidence of increased phosphorylation or transformative capacity by either sequence variant was found. Because small-molecule inhibitors for MET are currently in development, it will be important to distinguish between oncogenic sequence variants and rare single-nucleotide polymorphisms to avoid the use of unnecessary, and potentially toxic, cancer therapy agents. Cancer Res; 70(15); 6233-7. (C) 2010 AACR.
C1 [Tyner, Jeffrey W.; Fletcher, Luke B.; Wang, Ellen Q.; Yang, Wayne F.; Rutenberg-Schoenberg, Michael L.; Beadling, Carol; Mori, Motomi; Heinrich, Michael C.; Deininger, Michael W.; Druker, Brian J.; Loriaux, Marc M.] Oregon Hlth & Sci Univ, Knight Canc Inst, Portland, OR 97239 USA.
[Tyner, Jeffrey W.; Fletcher, Luke B.; Wang, Ellen Q.; Yang, Wayne F.; Rutenberg-Schoenberg, Michael L.; Deininger, Michael W.; Druker, Brian J.; Loriaux, Marc M.] Oregon Hlth & Sci Univ, Div Hematol & Med Oncol, Portland, OR 97239 USA.
[Beadling, Carol; Heinrich, Michael C.] Portland VA Med Ctr, Portland, OR USA.
[Mori, Motomi] Oregon Hlth & Sci Univ, Div Biostat, Dept Publ Hlth & Prevent Med, Portland, OR 97239 USA.
[Druker, Brian J.] Howard Hughes Med Inst, Portland, OR USA.
[Loriaux, Marc M.] Oregon Hlth & Sci Univ, Dept Pathol, Portland, OR 97239 USA.
RP Tyner, JW (reprint author), Oregon Hlth & Sci Univ, Knight Canc Inst, 3181 SW Sam Jackson Pk Rd,Mailcode L592, Portland, OR 97239 USA.
EM tynerj@ohsu.edu
OI Tyner, Jeffrey/0000-0002-2133-0960
FU Leukemia and Lymphoma Society; TJ Martell Foundation; Doris Duke
Charitable Foundation; William Lawrence and Blanche Hughes Fund;
National Center for Research Resources (NRCC); VA Merit Review Grant;
OHSU cancer center [5 p30 CA069533]; Knight Cancer Institute
[5P50CA069533]; Oregon Clinical & Translational Research Institute [UL1
RR024140]
FX The Leukemia and Lymphoma Society, the TJ Martell Foundation, and the
Doris Duke Charitable Foundation. J.W. Tyner is supported by grants from
the William Lawrence and Blanche Hughes Fund, and the Oregon Clinical
and Translational Research Institute (OCTRI) grant number UL1 RR024140
from the National Center for Research Resources (NRCC), a component of
the NIH, and NIH Roadmap for Medical Research. M. C. Heinrich is
supported in part by a VA Merit Review Grant. B.J. Druker is an
investigator of the Howard Hughes Medical Institute and principal
investigator of the OHSU cancer center support grant 5 p30 CA069533. M.
M. Loriaux is supported by the Leukemia and Lymphoma Society and the TJ
Martell Foundation. Biostatistics support (M. Mori) is in part provided
by the Biostatistics Shared Resource of the Knight Cancer Institute
(5P50CA069533) and the Biostatistics & Design Program of the Oregon
Clinical & Translational Research Institute (UL1 RR024140).
NR 22
TC 37
Z9 37
U1 1
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD AUG 1
PY 2010
VL 70
IS 15
BP 6233
EP 6237
DI 10.1158/0008-5472.CAN-10-0429
PG 5
WC Oncology
SC Oncology
GA 634CQ
UT WOS:000280557500013
PM 20670955
ER
PT J
AU Sasajima, J
Mizukami, Y
Sugiyama, Y
Nakamura, K
Kawamoto, T
Koizumi, K
Fujii, R
Motomura, W
Sato, K
Suzuki, Y
Tanno, S
Fujiya, M
Sasaki, K
Shimizu, N
Karasaki, H
Kono, T
Kawabe, J
Ii, M
Yoshiara, H
Kamiyama, N
Ashida, T
Bardeesy, N
Chung, DC
Kohgo, Y
AF Sasajima, Junpei
Mizukami, Yusuke
Sugiyama, Yoshiaki
Nakamura, Kazumasa
Kawamoto, Toru
Koizumi, Kazuya
Fujii, Rie
Motomura, Wataru
Sato, Kazuya
Suzuki, Yasuaki
Tanno, Satoshi
Fujiya, Mikihiro
Sasaki, Katsunori
Shimizu, Norihiko
Karasaki, Hidenori
Kono, Toru
Kawabe, Jun-ichi
Ii, Masaaki
Yoshiara, Hiroki
Kamiyama, Naohisa
Ashida, Toshifumi
Bardeesy, Nabeel
Chung, Daniel C.
Kohgo, Yutaka
TI Transplanting Normal Vascular Proangiogenic Cells to Tumor-Bearing Mice
Triggers Vascular Remodeling and Reduces Hypoxia in Tumors
SO CANCER RESEARCH
LA English
DT Article
ID ENDOTHELIAL PROGENITOR CELLS; PANCREATIC-CANCER CELLS; STEM-CELLS; ADULT
NEOVASCULARIZATION; HEDGEHOG PROMOTES; ANGIOGENESIS; GROWTH;
GEMCITABINE; METASTASIS; EXPRESSION
AB Blood vessels deliver oxygen and nutrients to tissues, and vascular networks are spatially organized to meet the metabolic needs for maintaining homeostasis. In contrast, the vasculature of tumors is immature and leaky, resulting in insufficient delivery of nutrients and oxygen. Vasculogenic processes occur normally in adult tissues to repair "injured" blood vessels, leading us to hypothesize that bone marrow mononuclear cells (BMMNC) may be able to restore appropriate vessel function in the tumor vasculature. Culturing BMMNCs in endothelial growth medium resulted in the early outgrowth of spindle-shaped attached cells expressing CD11b/Flt1/Tie2/c-Kit/CXCR4 with proangiogenic activity. Intravenous administration of these cultured vascular proangiogenic cells (VPC) into nude mice bearing pancreatic cancer xenografts and Pdx1-Cre; LSL-Kras(G12D);p53(lox/+) genetically engineered mice that develop pancreatic ductal adenocarcinoma significantly reduced areas of hypoxia without enhancing tumor growth. The resulting vasculature structurally mimicked normal vessels with intensive pericyte coverage. Increases in vascularized areas within VPC-injected xenografts were visualized with an ultrasound diagnostic system during injection of a microbubble-based contrast agent (Sonazoid), indicating a functional "normalization" of the tumor vasculature. In addition, gene expression profiles in the VPC-transplanted xenografts revealed a marked reduction in major factors involved in drug resistance and "stemness" of cancer cells. Together, our findings identify a novel alternate approach to regulate abnormal tumor vessels, offering the potential to improve the delivery and efficacy of anticancer drugs to hypoxic tumors. Cancer Res; 70(15); 6283-92. (C) 2010 AACR.
C1 [Sasajima, Junpei; Mizukami, Yusuke; Sugiyama, Yoshiaki; Nakamura, Kazumasa; Kawamoto, Toru; Koizumi, Kazuya; Fujii, Rie; Motomura, Wataru; Sato, Kazuya; Suzuki, Yasuaki; Tanno, Satoshi; Fujiya, Mikihiro; Sasaki, Katsunori; Kohgo, Yutaka] Asahikawa Med Coll, Div Gastroenterol & Hematol Oncol, Dept Med, Asahikawa, Hokkaido 0788510, Japan.
[Shimizu, Norihiko] Asahikawa Med Coll, Dept Anim Facil, Asahikawa, Hokkaido 0788510, Japan.
[Karasaki, Hidenori; Kono, Toru] Asahikawa Med Coll, Div Gastroenterol & Gen Surg, Dept Surg, Asahikawa, Hokkaido 0788510, Japan.
[Kawabe, Jun-ichi] Asahikawa Med Coll, Dept Cardiovasc Regenerat & Innovat, Asahikawa, Hokkaido 0788510, Japan.
[Ii, Masaaki] Osaka Med Coll, Dept Pharmacol, Osaka, Japan.
[Yoshiara, Hiroki; Kamiyama, Naohisa] Toshiba Med Syst Corp, Otawara, Tochigi, Japan.
[Ashida, Toshifumi] Sapporo Higashi Tokusyukai Hosp, Ctr IBD, Sapporo, Hokkaido, Japan.
[Bardeesy, Nabeel; Chung, Daniel C.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bardeesy, Nabeel; Chung, Daniel C.] Harvard Univ, Sch Med, Boston, MA USA.
RP Mizukami, Y (reprint author), Asahikawa Med Coll, Div Gastroenterol & Hematol Oncol, Dept Med, 2-1 Midorigaoka Higashi, Asahikawa, Hokkaido 0788510, Japan.
EM mizu@asahikawa-med.ac.jp
FU New Energy and Industrial Technology Development Organization of Japan
[07A05010a]
FX New Energy and Industrial Technology Development Organization of Japan
grant 07A05010a (Y. Mizukami).
NR 51
TC 16
Z9 16
U1 0
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 AUG 1
PY 2010
VL 70
IS 15
BP 6283
EP 6292
DI 10.1158/0008-5472.CAN-10-0412
PG 10
WC Oncology
SC Oncology
GA 634CQ
UT WOS:000280557500019
PM 20631070
ER
PT J
AU d'Othee, BJ
Walker, TG
Kalva, SP
Ganguli, S
Davison, B
AF d'Othee, Bertrand Janne
Walker, T. Gregory
Kalva, Sanjeeva P.
Ganguli, Suvranu
Davison, Brian
TI Endovenous Laser Ablation of the Small Saphenous Vein Sparing the
Saphenopopliteal Junction
SO CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
DE Varicose vein; Endovenous ablation; Saphenous veins; Laser; Endovenous
thermal ablation; Small saphenous vein
ID RADIOFREQUENCY OBLITERATION; ARTERIOVENOUS-FISTULA; VENOUS
INSUFFICIENCY; VARICOSE-VEINS; REFLUX; EXPERIENCE
AB To assess outcomes after endovenous laser ablation (EVLA) of the small saphenous vein (SSV). Retrospective review was performed of all consecutive EVLA procedures performed over a 39-month period at three neighboring vein practices for symptomatic, duplex ultrasound-proven incompetence of the SSV. EVLA was performed under ultrasound guidance with an 810- or 980-nm diode laser in continuous mode using the pullback method while sparing the deep, most cephalad segment of the SSV near the saphenopopliteal junction. Follow-up after EVLA included patient symptoms, physical examination, and duplex ultrasound. Pretreatment variables were similar across all three practices. EVLA was performed to treat 67 incompetent SSVs in 63 patients (86% women; mean age and 95% confidence interval, 50 +/- A 3 years; range, 20-82 years). Average energy delivered was 92 J/cm. Immediate technical success and occlusion of the treated vein at 1-2 weeks was 100%. Imaging follow-up length was 243 +/- A 65 days (range, 3-893 days). Clinical follow-up (243 +/- A 66 days) showed symptomatic improvement in 66 (99%) of 67 patients; one patient had recanalization with recurrent reflux by ultrasound (2%). Complications included one case of paresthesias lasting beyond 1 month of follow-up (2%) and three cases of superficial phlebitis (4%), but no deep vein thrombosis, skin burns, or other complications. Although ablation involved only the superficial portion of the SSV and spared its deep segment in the popliteal fossa, SSV occlusion typically extended up to the saphenopopliteal junction or to a gastrocnemial collateral, without popliteal vein involvement. EVLA of the SSV is safe and effective when the saphenopopliteal junction and popliteal fossa are avoided. This approach may help reduce the risk of paresthesias or other complications while maintaining low recanalization rates.
C1 [d'Othee, Bertrand Janne] Univ Maryland, Sch Med, Dept Diagnost Radiol & Nucl Med, Div Vasc & Intervent Radiol, Baltimore, MD 21201 USA.
[d'Othee, Bertrand Janne; Walker, T. Gregory; Kalva, Sanjeeva P.; Ganguli, Suvranu; Davison, Brian] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Vasc Imaging & Intervent,Dept Imaging, Boston, MA 02114 USA.
[d'Othee, Bertrand Janne; Ganguli, Suvranu] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Radiol, Boston, MA 02215 USA.
[Davison, Brian] Lincoln Med Ctr, TVV, Framingham, MA 01702 USA.
RP d'Othee, BJ (reprint author), Univ Maryland, Sch Med, Dept Diagnost Radiol & Nucl Med, Div Vasc & Intervent Radiol, 22 S Greene St, Baltimore, MD 21201 USA.
EM bjannedothee@umm.edu
NR 16
TC 4
Z9 4
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0174-1551
EI 1432-086X
J9 CARDIOVASC INTER RAD
JI Cardiovasc. Interv. Radiol.
PD AUG
PY 2010
VL 33
IS 4
BP 766
EP 771
DI 10.1007/s00270-010-9806-1
PG 6
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 629UQ
UT WOS:000280225800017
ER
PT J
AU Robbins, CS
Swirski, FK
AF Robbins, Clinton S.
Swirski, Filip K.
TI The multiple roles of monocyte subsets in steady state and inflammation
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Review
DE Monocyte subsets; Inflammation; Hematopoietic system; Macrophage;
Dendritic cell
ID HUMAN PERIPHERAL-BLOOD; CD8(+) T-CELLS; COUNTERFLOW CENTRIFUGATION
ELUTRIATION; ATHEROSCLEROTIC LESION FORMATION; DENDRITIC CELLS; LYMPHOID
ORGANS; BONE-MARROW; IN-VIVO; BACTERIAL-INFECTION; MYD88-DEPENDENT
ACTIVATION
AB Monocytes participate importantly in immunity. Produced in the bone marrow and released into the blood, they circulate in blood or reside in a spleen reservoir before entering tissue and giving rise to macrophages or dendritic cells. Monocytes are more than transitional cells that adapt to a particular tissue environment indiscriminately. Accumulating evidence now indicates that monocytes are heterogeneous in several species and are themselves predetermined for particular function in the steady state and inflammation. Future therapeutics may harness this heterogeneity to target harmful functions while sparing those that are beneficial. Here, we review recent advances on the ontogeny and function of monocytes and their subsets in humans and mice.
C1 [Robbins, Clinton S.; Swirski, Filip K.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
RP Swirski, FK (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Syst Biol, Simches Res Bldg,185 Cambridge St, Boston, MA 02114 USA.
EM fswirski@mgh.harvard.edu
FU NIH [1R01HL095612]; AHA
FX This work was funded by NIH grant 1R01HL095612 (to FKS) and an AHA
postdoctoral fellowship (to CSR).
NR 109
TC 64
Z9 68
U1 0
U2 11
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1420-682X
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD AUG
PY 2010
VL 67
IS 16
BP 2685
EP 2693
DI 10.1007/s00018-010-0375-x
PG 9
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 634FF
UT WOS:000280564600002
PM 20437077
ER
PT J
AU Mishra, BB
Moura-Alves, P
Sonawane, A
Hacohen, N
Griffiths, G
Moita, LF
Anes, E
AF Mishra, Bibhuti B.
Moura-Alves, Pedro
Sonawane, Avinash
Hacohen, Nir
Griffiths, Gareth
Moita, Luis F.
Anes, Elsa
TI Mycobacterium tuberculosis protein ESAT-6 is a potent activator of the
NLRP3/ASC inflammasome
SO CELLULAR MICROBIOLOGY
LA English
DT Article
ID INTERLEUKIN-1-BETA CONVERTING-ENZYME; CASPASE-1 ACTIVATION; MURINE
MACROPHAGES; NALP3 INFLAMMASOME; MURAMYL DIPEPTIDE; INDUCED APOPTOSIS;
INFECTION; SECRETION; RECOGNITION; RECEPTORS
AB P>Interleukin-1 beta (IL-1 beta) represents one of the most important mediators of inflammation and host responses to infection. Mycobacterium tuberculosis (Mtb), the causative agent of human tuberculosis, induces IL-1 beta secretion at the site of infection, but the underlying mechanism(s) are poorly understood. In this work we show that Mtb infection of macrophages stimulates caspase-1 activity and promotes the secretion of IL-1 beta. This stimulation requires live intracellular bacteria expressing a functional ESX-1 secretion system. ESAT-6, an ESX-1 substrate implicated in membrane damage, is both necessary and sufficient for caspase-1 activation and IL-1 beta secretion. ESAT-6 promotes the access of other immunostimulatory agents such as AG85 into the macrophage cytosol, indicating that this protein may contribute to caspase-1 activation largely by perturbing host cell membranes. Using a high-throughput shRNA-based screen we found that numerous NOD-like receptors (NLRs) and CARD domain-containing proteins (CARDs) were important for IL-1 beta secretion upon Mtb infection. Most importantly, NLRP3, ASC and caspase-1 form an infection-inducible inflammasome complex that is essential for IL-1 beta secretion. In summary, we show that recognition of Mtb infection by the NLRP3 inflammasome requires the activity of the bacterial virulence factor ESAT-6, and the subsequent IL-1 beta response is regulated by a number of NLR/CARD proteins.
C1 [Moura-Alves, Pedro; Moita, Luis F.] Univ Lisbon, Fac Med, Inst Mol Med, Cell Biol Immune Syst Unit, P-1649028 Lisbon, Portugal.
[Mishra, Bibhuti B.; Anes, Elsa] Univ Lisbon, Fac Farm, Ctr Patogenese Mol, Unidade Retrovirus & Infeccoes Associadas, P-1649028 Lisbon, Portugal.
[Mishra, Bibhuti B.; Anes, Elsa] Univ Lisbon, Fac Farm, Inst Mol Med, P-1649028 Lisbon, Portugal.
[Moura-Alves, Pedro] Univ Porto, Abel Salazar Inst Biomed Sci, Grad Program Basic & Appl Biol, P-4099003 Oporto, Portugal.
[Sonawane, Avinash; Griffiths, Gareth] Univ Oslo, Dept Mol Biosci, N-0316 Oslo, Norway.
[Hacohen, Nir] Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Div Rheumatol Allergy & Immunol, Charlestown, MA 02129 USA.
[Hacohen, Nir] Broad Inst Harvard, Cambridge, MA 02142 USA.
[Hacohen, Nir] MIT, Cambridge, MA 02142 USA.
RP Moita, LF (reprint author), Univ Lisbon, Fac Med, Inst Mol Med, Cell Biol Immune Syst Unit, P-1649028 Lisbon, Portugal.
EM lmoita@fm.ul.pt; eanes@ff.ul.pt
RI Moita, Luis/L-1296-2013; iMed.ULisboa, iMed.ULisboa/C-6292-2014; Anes,
Elsa/K-3124-2013; iMed.ULisboa, HPI /B-4239-2014
OI Moita, Luis/0000-0003-0707-315X; Anes, Elsa/0000-0001-5934-0198;
iMed.ULisboa, HPI /0000-0001-5934-0198
FU National Foundation for Science-FCT [PPCDT/BIA-BCM/55327/2004,
PIC/IC/82859/2007, SFRH/BD/28173/2006, SFRH/BD/15238/2004]; Human
Frontier Science Program; FLAD; FCT [PTDC/SAU-MII/69280/2006,
PTDC/SAU-MII/78333/2006]
FX We thank Dr Christopher Sassetti for his critical review of the
manuscript and helpful suggestions. We are thankful to Drs Fernando
Maltez, Amelia Pimpao and Lurdes Fernandes for providing us the blood
samples from TB patients. We thank Dr Takahashi Miyashita for providing
the p11-GFP and p45-GFP plasmids. We are also grateful for the reagents
provided by the Colorado State University, USA and by the Centralised
Facility for AIDS Reagents (NISB). We thank Professor David R Sherman of
the Seattle Biomedical Research Institute, USA for providing us the Mtb
mutant strains. This work was supported by grants from the National
Foundation for Science-FCT project PPCDT/BIA-BCM/55327/2004,
PIC/IC/82859/2007 to E.A., SFRH/BD/28173/2006 fellowship to B.B.M. and
SFRH/BD/15238/2004 fellowship to P.M.-A. L.F.M. is a Young Investigator
from the Human Frontier Science Program and receives support from FLAD
and FCT (PTDC/SAU-MII/69280/2006 and PTDC/SAU-MII/78333/2006).
NR 64
TC 130
Z9 133
U1 2
U2 20
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1462-5814
J9 CELL MICROBIOL
JI Cell Microbiol.
PD AUG
PY 2010
VL 12
IS 8
BP 1046
EP 1063
DI 10.1111/j.1462-5822.2010.01450.x
PG 18
WC Cell Biology; Microbiology
SC Cell Biology; Microbiology
GA 623ER
UT WOS:000279721400004
PM 20148899
ER
PT J
AU Stevens, WD
Buckner, RL
Schacter, DL
AF Stevens, W. Dale
Buckner, Randy L.
Schacter, Daniel L.
TI Correlated Low-Frequency BOLD Fluctuations in the Resting Human Brain
Are Modulated by Recent Experience in Category-Preferential Visual
Regions
SO CEREBRAL CORTEX
LA English
DT Article
DE fMRI; functional connectivity; intrinsic activity; network;
resting-state
ID STATE FUNCTIONAL CONNECTIVITY; DEFAULT-MODE NETWORK; FUSIFORM FACE AREA;
EVENT-RELATED FMRI; STRUCTURAL CONNECTIVITY; ALZHEIMERS-DISEASE;
COMPONENT ANALYSIS; NEURAL ACTIVITY; CORTEX; MEMORY
AB The resting brain is associated with significant intrinsic activity fluctuations, such as the correlated low-frequency (IF) blood oxygen level-dependent (BOLD) fluctuations measured by functional magnetic resonance imaging. Despite a recent expansion of studies investigating resting-state LF-BOLD correlations, their nature and function are poorly understood. A major constraint on IF-BOLD correlations appears to be stable properties of anatomic connectivity. There is also evidence that coupling can be modulated by recent or ongoing task performance, suggesting that certain components of correlated dynamics are malleable on short timescales. Here, we compared activity during extended periods of rest following performance of 2 distinct cognitive tasks using different categories of visual stimuli faces and complex scenes. Prolonged exposure to these distinct categories of visual information caused frontal networks to couple differentially with posterior category-preferential visual regions during subsequent periods of rest. In addition, we report preliminary evidence suggesting that conditions exist in which the degree of modulation of LF-BOLD correlations predicts subsequent memory. The finding that resting-state IF-BOLD correlations are modulated by recent experience in functionally specific brain regions engaged during prior task performance clarifies their role as a dynamic phenomenon which may be involved in mnemonic processes.
C1 [Stevens, W. Dale; Buckner, Randy L.; Schacter, Daniel L.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Stevens, W. Dale; Buckner, Randy L.; Schacter, Daniel L.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Buckner, Randy L.] Harvard Univ, Howard Hughes Med Inst, Cambridge, MA 02138 USA.
RP Stevens, WD (reprint author), Harvard Univ, Dept Psychol, 33 Kirkland St, Cambridge, MA 02138 USA.
EM dstevens@wjh.harvard.edu
OI Schacter, Daniel/0000-0002-2460-6061
FU National Institutes of Health [MH060941, AG021910]; Howard Hughes
Medical Institute
FX National Institutes of Health (MH060941 to D.L.S.); Howard Hughes
Medical Institute and a National Institutes of Health (AG021910 to
R.L.B.).
NR 68
TC 90
Z9 91
U1 1
U2 9
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
J9 CEREB CORTEX
JI Cereb. Cortex
PD AUG
PY 2010
VL 20
IS 8
BP 1997
EP 2006
DI 10.1093/cercor/bhp270
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 634QD
UT WOS:000280597100022
PM 20026486
ER
PT J
AU O'Donnell, CR
Bankier, AA
Stiebellehner, L
Reilly, JJ
Brown, R
Loring, SH
AF O'Donnell, Carl R.
Bankier, Alexander A.
Stiebellehner, Leopold
Reilly, John J.
Brown, Robert
Loring, Stephen H.
TI Comparison Among Different Methods on Measurement of Total Lung Capacity
in COPD Response
SO CHEST
LA English
DT Letter
ID VOLUMES
C1 [O'Donnell, Carl R.] Beth Israel Deaconess Med Ctr, Div Pulm & Crit Care Med, Dept Pulm & Crit Care Med, Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Bankier, Alexander A.] Beth Israel Deaconess Med Ctr, Dept Radiol, Boston, MA USA.
[Loring, Stephen H.] Beth Israel Deaconess Med Ctr, Dept Anesthesia & Crit Care, Boston, MA USA.
[Stiebellehner, Leopold] Med Univ Vienna, Dept Pulmonol, Vienna, Austria.
[Reilly, John J.] Univ Pittsburgh, Div Pulm & Crit Care Med, Pittsburgh, PA USA.
[Brown, Robert] Massachusetts Gen Hosp, Pulm & Crit Care Med Unit, Boston, MA 02114 USA.
RP O'Donnell, CR (reprint author), Beth Israel Deaconess Med Ctr, Div Pulm & Crit Care Med, Dept Pulm & Crit Care Med, Beth Israel Deaconess Med Ctr, E Dana 717,330 Brookline Ave, Boston, MA 02215 USA.
RI Reilly, John/H-8755-2012
NR 6
TC 0
Z9 0
U1 0
U2 0
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD AUG
PY 2010
VL 138
IS 2
BP 459
EP 460
DI 10.1378/chest.10-1093
PG 2
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 636NI
UT WOS:000280743600038
ER
PT J
AU Hawkins, AO
Danielson, CK
de Arellano, MA
Hanson, RF
Ruggiero, KJ
Smith, DW
Saunders, BE
Kilpatrick, DG
AF Hawkins, Alesia Oscea
Danielson, Carla Kmett
de Arellano, Michael A.
Hanson, Rochelle F.
Ruggiero, Kenneth J.
Smith, Daniel W.
Saunders, Benjamin E.
Kilpatrick, Dean G.
TI Ethnic/Racial Differences in the Prevalence of Injurious Spanking and
Other Child Physical Abuse in a National Survey of Adolescents
SO CHILD MALTREATMENT
LA English
DT Article
DE adolescent victims; ethnic minority populations; physical abuse
ID VIOLENCE; VICTIMIZATION; MALTREATMENT; PUNISHMENT; YOUTH
AB Limited research has examined whether similar patterns in injurious spanking and other forms of child physical abuse (CPA) exist across specific ethnic/racial groups. The authors examined and compared differences in the lifetime prevalence of injurious spanking and CPA in two national samples of adolescents across ethnic/racial groups and over time. Participants were 4,023 youth (12-17 years) and 3,614 youth (12-17 years) who participated in the 1995 National Survey of Adolescents (NSA) and 2005 National Survey of Adolescents-Replication (NSA-R), respectively. Adolescents, who were identified through random digit dial procedures, completed a telephone interview assessment. Results indicated significant ethnic/racial variation across groups in reports of injurious spanking in the NSA and the NSA-R samples; however, significant differences were not observed within groups between the two samples over time. Ethnic/racial differences also were found between groups in reports of CPA in the NSA-R sample. Limitations and future directions of this research are discussed.
C1 [Hawkins, Alesia Oscea] Univ Illinois, Coll Med Rockford, Dept Family & Community Med, Rockford, IL 61107 USA.
[de Arellano, Michael A.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Natl Crime Victims Res & Treatment Ctr, COPE, Charleston, SC 29425 USA.
[Ruggiero, Kenneth J.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
RP Hawkins, AO (reprint author), Univ Illinois, Coll Med Rockford, Dept Family & Community Med, 1601 Parkview Ave, Rockford, IL 61107 USA.
EM alesiah@uic.edu
FU NICHD NIH HHS [R01 HD046830]; NIDA NIH HHS [K23DA018686]
NR 21
TC 18
Z9 18
U1 1
U2 11
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1077-5595
J9 CHILD MALTREATMENT
JI Child Maltreatment
PD AUG
PY 2010
VL 15
IS 3
BP 242
EP 249
DI 10.1177/1077559510367938
PG 8
WC Family Studies; Social Work
SC Family Studies; Social Work
GA 628PJ
UT WOS:000280132400005
PM 20498129
ER
PT J
AU Thanassoulis, G
Massaro, JM
O'Donnell, CJ
Hoffmann, U
Levy, D
Ellinor, PT
Wang, TJ
Schnabel, RB
Vasan, RS
Fox, CS
Benjamin, EJ
AF Thanassoulis, George
Massaro, Joseph M.
O'Donnell, Christopher J.
Hoffmann, Udo
Levy, Daniel
Ellinor, Patrick T.
Wang, Thomas J.
Schnabel, Renate B.
Vasan, Ramachandran S.
Fox, Caroline S.
Benjamin, Emelia J.
TI Pericardial Fat Is Associated With Prevalent Atrial Fibrillation The
Framingham Heart Study
SO CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY
LA English
DT Article
DE atrial fibrillation; pericardial adipose tissue; obesity; epidemiology;
risk factor
ID EPICARDIAL ADIPOSE-TISSUE; P-WAVE DISPERSION; CORONARY-ARTERY-DISEASE;
VISCERAL ABDOMINAL FAT; LIPOMATOUS HYPERTROPHY; OBESE SUBJECTS;
INTERATRIAL SEPTUM; WEIGHT-LOSS; CLINICAL-SIGNIFICANCE; MORPHOLOGIC
FEATURES
AB Background-Obesity represents an important risk factor for atrial fibrillation (AF). We tested the hypothesis that pericardial fat, a unique fat deposit in close anatomic proximity to cardiac structures and autonomic fibers, is associated with prevalent AF.
Methods and Results-Participants from the Framingham Heart Study underwent multidetector computed tomography from 2002 to 2005. We estimated the association between quantitative pericardial, intrathoracic and visceral adipose tissue volumes (per standard deviation of volume) with prevalent AF adjusting for established AF risk factors (age, sex, systolic blood pressure, blood pressure treatment, PR interval, and clinically significant valvular disease). Of the 3217 eligible participants (mean age, 50.6 +/- 10.1 years; 48% women), 54 had a confirmed diagnosis of AF. Pericardial fat but not intrathoracic or visceral abdominal fat was associated with prevalent AF in multivariable-adjusted models (odds ratio per standard deviation of pericardial fat volume, 1.28; 95% confidence intervals, 1.03 to 1.58). Further adjustments for body mass index, heart failure, myocardial infarction, and intrathoracic fat volume did not materially change the association between pericardial fat and AF.
Conclusions-Pericardial fat was associated with prevalent AF even after adjustment for AF risk factors, including body mass index. If this association is replicated, further investigations into the mechanisms linking pericardial fat to AF are merited. (Circ Arrhythm Electrophysiol. 2010;3:345-350.)
C1 [Thanassoulis, George; O'Donnell, Christopher J.; Levy, Daniel; Schnabel, Renate B.; Vasan, Ramachandran S.; Fox, Caroline S.; Benjamin, Emelia J.] Boston Univ, Framingham, MA 01702 USA.
NHLBI, NIH, Framingham, MA 01702 USA.
[Thanassoulis, George; Benjamin, Emelia J.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Massaro, Joseph M.; Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[O'Donnell, Christopher J.; Hoffmann, Udo; Ellinor, Patrick T.; Wang, Thomas J.; Fox, Caroline S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Hoffmann, Udo] MGH PET MR CT Program, Boston, MA USA.
[O'Donnell, Christopher J.; Levy, Daniel; Fox, Caroline S.] NIH, Div Intramural Res, Bethesda, MD 20892 USA.
RP Benjamin, EJ (reprint author), Boston Univ, 73 Mt Wayte Ave,2, Framingham, MA 01702 USA.
EM emelia@bu.edu
RI Schnabel, Renate/F-6527-2014;
OI Massaro, Joseph/0000-0002-2682-4812; Ramachandran,
Vasan/0000-0001-7357-5970; Benjamin, Emelia/0000-0003-4076-2336
FU Framingham Heart Study, Boston University; National Institutes of
Health/National Heart, Lung, and Blood Institute [N01-HC 25195];
Canadian Institute of Health Research; Fonds de Recherche en Sante
Quebec; [1R01HL092577]; [RO1 HL076784]; [1RC1HL101056]; [R01
AG028321]; [R01-DK-080739]
FX This study was supported by the Framingham Heart Study, Boston
University and the National Institutes of Health/National Heart, Lung,
and Blood Institute, grant N01-HC 25195. Dr Thanassoulis is supported by
a Research Fellowship from the Canadian Institute of Health Research and
the Fonds de Recherche en Sante Quebec. Dr Benjamin was supported in
part by grants 1R01HL092577, RO1 HL076784, 1RC1HL101056, and R01
AG028321. Dr Vasan was supported in part by grant R01-DK-080739.
NR 46
TC 112
Z9 114
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-3149
J9 CIRC-ARRHYTHMIA ELEC
JI Circ.-Arrhythmia Electrophysiol.
PD AUG
PY 2010
VL 3
IS 4
BP 345
EP 350
DI 10.1161/CIRCEP.109.912055
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 639WI
UT WOS:000281006700008
PM 20558845
ER
PT J
AU Mills, RW
Milan, DJ
AF Mills, Robert W.
Milan, David J.
TI Trpm4-Linked Isolated Cardiac Conduction Defects Bad Trafficking Causes
Electrical Gridlock
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Editorial Material
DE Editorials; conduction; genetics
ID PR INTERVAL; HEART; SUMOYLATION; ARRHYTHMIA; DISEASES; TRPM4
C1 [Milan, David J.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Mills, Robert W.; Milan, David J.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA USA.
RP Milan, DJ (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
EM DMilan@Partners.org
NR 18
TC 4
Z9 4
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1942-325X
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD AUG
PY 2010
VL 3
IS 4
BP 311
EP 313
DI 10.1161/CIRCGENETICS.110.957670
PG 3
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 639WH
UT WOS:000281006600002
PM 20716750
ER
PT J
AU Keebler, ME
Deo, RC
Surti, A
Konieczkowski, D
Guiducci, C
Burtt, N
Buxbaum, SG
Sarpong, DF
Steffes, MW
Wilson, JG
Taylor, HA
Kathiresan, S
AF Keebler, Mary E.
Deo, Rahul C.
Surti, Aarti
Konieczkowski, David
Guiducci, Candace
Burtt, Noel
Buxbaum, Sarah G.
Sarpong, Daniel F.
Steffes, Michael W.
Wilson, James G.
Taylor, Herman A.
Kathiresan, Sekar
TI Fine-Mapping in African Americans of 8 Recently Discovered Genetic Loci
for Plasma Lipids The Jackson Heart Study
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE lipids; genetics; epidemiology; risk factors
ID GENOME-WIDE ASSOCIATION; CHOLESTEROL; ADMIXTURE; VARIANTS; DISEASE; RISK
AB Background-Genome-wide association studies in cohorts of European descent have identified novel genomic regions as associated with lipids, but their relevance in African Americans remains unclear.
Methods and Results-We genotyped 8 index single nucleotide polymorphisms (SNPs) and 488 tagging SNPs across 8 novel lipid loci in the Jackson Heart Study, a community-based cohort of 4605 African Americans. For each trait, we calculated residuals adjusted for age, sex, and global ancestry and performed multivariable linear regression to detect genotype-phenotype association with adjustment for local ancestry. To explore admixture effects, we conducted stratified analyses in individuals with a high probability of 2 African ancestral alleles or at least 1 European allele at each locus. We confirmed 2 index SNPs as associated with lipid traits in African Americans, with suggestive association for 3 more. However, the effect sizes for 4 of the 5 associated SNPs were larger in the European local ancestry subgroup compared with the African local ancestry subgroup, suggesting that the replication is driven by European ancestry segments. Through fine-mapping, we discovered 3 new SNPs with significant associations, 2 with consistent effect on triglyceride levels across ancestral groups: rs636523 near DOCK7/ANGPTL3 and rs780093 in GCKR. African linkage disequilibrium patterns did not assist in narrowing association signals.
Conclusions-We confirm that 5 genetic regions associated with lipid traits in European-derived populations are relevant in African Americans. To further evaluate these loci, fine-mapping in larger African American cohorts and/or resequencing will be required. (Circ Cardiovasc Genet. 2010; 3: 358-364.)
C1 [Kathiresan, Sekar] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02115 USA.
[Keebler, Mary E.; Surti, Aarti; Konieczkowski, David; Guiducci, Candace; Burtt, Noel; Kathiresan, Sekar] Broad Inst, Cambridge, MA USA.
[Buxbaum, Sarah G.; Sarpong, Daniel F.; Taylor, Herman A.] Jackson State Univ, Jackson, MS USA.
[Steffes, Michael W.] Univ Minnesota, Minneapolis, MN USA.
[Wilson, James G.] GV Sonny Montgomery VA Med Ctr, Jackson, MS USA.
[Wilson, James G.; Taylor, Herman A.] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Taylor, Herman A.] Tougaloo Coll, Tougaloo, MS USA.
RP Kathiresan, S (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, 185 Cambridge St,CZPN 5-252, Boston, MA 02115 USA.
EM skathiresan@partners.org
RI Buxbaum, Sarah/E-1970-2013
OI Buxbaum, Sarah/0000-0002-4886-3564
FU NHLBI NIH HHS [N01 HC095171, K08 HL098361, K08 HL098361-01A1, K08
HL098361-02, K23 HL083102, K23 HL083102-01A1, N01 HC095170, N01
HC095172, N01-HC-95170, N01-HC-95171, N01-HC-95172, N01HC95170,
N01HC95171, N01HC95172, R01 HL084107, R01 HL084107-01, R01-HL-084107];
NIGMS NIH HHS [T32 GM007753]
NR 14
TC 19
Z9 21
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1942-325X
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD AUG
PY 2010
VL 3
IS 4
BP 358
EP U149
DI 10.1161/CIRCGENETICS.109.914267
PG 8
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 639WH
UT WOS:000281006600008
PM 20570916
ER
PT J
AU Stein, PD
Matta, F
Yaekoub, AY
Kazerooni, EA
Cahill, JE
Goodman, LR
Sostman, HD
Hales, CA
Denier, JE
Weg, JG
Ghumman, D
Chan, KM
Woodard, PK
Kwun, Y
AF Stein, Paul D.
Matta, Fadi
Yaekoub, Abdo Y.
Kazerooni, Ella A.
Cahill, Jennifer Ellis
Goodman, Lawrence R.
Sostman, H. Dirk
Hales, Charles A.
Denier, James E.
Weg, John G.
Ghumman, Dilraj
Chan, Kevin M.
Woodard, Pamela K.
Kwun, Yoojin
TI CT Venous Phase Venography With 64-Detector CT Angiography in the
Diagnosis of Acute Pulmonary Embolism
SO CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS
LA English
DT Article
DE pulmonary embolism; deep venous thrombosis; CT angiography; CT
venography; 64-detector CT
ID COMPUTED-TOMOGRAPHY VENOGRAPHY; THROMBOEMBOLIC DISEASE;
RADIATION-EXPOSURE; PIOPED-II; MULTIDETECTOR CT; HELICAL CT; D-DIMER;
THROMBOSIS; SONOGRAPHY; MANAGEMENT
AB The value of computed tomographic (CT) venography in combination with CT pulmonary angiography has been questioned because of the potential dangers of radiation. Accordingly, we retrospectively evaluated the diagnostic yield of 64-detector CT angiography with CT venography. Among patients who routinely underwent CT venography with CT angiography, the CT angiogram showed acute pulmonary embolism (PE) in 206 of 1903 patients (10.8%). A positive CT venogram in a patient with a negative CT angiogram was shown in 25 of 1903 patients (1.3%). Either the CT angiogram or the CT venogram showed venous thromboembolism in 231 of 1903 patients (12.1%). The proportion of patients with venous thromboembolism diagnosed only by a CT venogram was 25 of 231 (10.8%). In conclusion, the proportion of patients with venous thromboembolism diagnosed only by a CT venogram is sufficiently high to merit consideration of its use especially in those at high risk for DVT.
C1 [Stein, Paul D.; Matta, Fadi; Yaekoub, Abdo Y.; Denier, James E.; Ghumman, Dilraj] St Joseph Mercy Oakland Hosp, Dept Res, Pontiac, MI USA.
[Stein, Paul D.] Wayne State Univ, Dept Med, Detroit, MI 48202 USA.
[Kazerooni, Ella A.; Weg, John G.; Chan, Kevin M.; Kwun, Yoojin] Univ Michigan, Dept Radiol, Ann Arbor, MI 48109 USA.
[Cahill, Jennifer Ellis; Hales, Charles A.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Cahill, Jennifer Ellis; Hales, Charles A.] Harvard Univ, Sch Med, Boston, MA USA.
[Goodman, Lawrence R.] Med Coll Wisconsin, Dept Radiol, Milwaukee, WI 53226 USA.
[Sostman, H. Dirk] Weill Cornell Med Coll, Houston, TX USA.
[Sostman, H. Dirk] Methodist Hosp, Houston, TX 77030 USA.
[Woodard, Pamela K.] Washington Univ, Dept Radiol, St Louis, MO USA.
RP Stein, PD (reprint author), St Joseph Mercy Oakland, 44405 Woodward Ave, Pontiac, MI 48341 USA.
EM steinp@trinity-health.org
NR 36
TC 6
Z9 6
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1076-0296
J9 CLIN APPL THROMB-HEM
JI Clin. Appl. Thromb.-Hemost.
PD AUG
PY 2010
VL 16
IS 4
BP 422
EP 429
DI 10.1177/1076029609335502
PG 8
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 628PA
UT WOS:000280131300007
PM 19520677
ER
PT J
AU Charles, RC
Sheikh, A
Krastins, B
Harris, JB
Bhuiyan, MS
LaRocque, RC
Logvinenko, T
Sarracino, DA
Kudva, IT
Eisenstein, J
Podolsky, MJ
Kalsy, A
Brooks, WA
Ludwig, A
John, M
Calderwood, SB
Qadri, F
Ryan, ET
AF Charles, Richelle C.
Sheikh, Alaullah
Krastins, Bryan
Harris, Jason B.
Bhuiyan, M. Saruar
LaRocque, Regina C.
Logvinenko, Tanya
Sarracino, David A.
Kudva, Indira T.
Eisenstein, Jana
Podolsky, Michael J.
Kalsy, Anuj
Brooks, W. Abdullah
Ludwig, Albrecht
John, Manohar
Calderwood, Stephen B.
Qadri, Firdausi
Ryan, Edward T.
TI Characterization of Anti-Salmonella enterica Serotype Typhi Antibody
Responses in Bacteremic Bangladeshi Patients by an Immunoaffinity
Proteomics-Based Technology
SO CLINICAL AND VACCINE IMMUNOLOGY
LA English
DT Article
ID T-CELL RESPONSES; OUTER-MEMBRANE PROTEINS; C-TERMINAL DOMAIN; SYSTEM
PHOP-PHOQ; SEROVAR TYPHI; ESCHERICHIA-COLI; IMMUNE-RESPONSES; HUMAN
INFECTION; VIBRIO-CHOLERAE; PARATYPHI-A
AB Salmonella enterica serotype Typhi is the cause of typhoid fever and a human-restricted pathogen. Currently available typhoid vaccines provide 50 to 90% protection for 2 to 5 years, and available practical diagnostic assays to identify individuals with typhoid fever lack sensitivity and/or specificity. Identifying immunogenic S. Typhi antigens expressed during human infection could lead to improved diagnostic assays and vaccines. Here we describe a platform immunoaffinity proteomics-based technology (IPT) that involves the use of columns charged with IgG, IgM, or IgA antibody fractions recovered from humans bacteremic with S. Typhi to capture S. Typhi proteins that were subsequently identified by mass spectrometry. This screening tool identifies immunogenic proteins recognized by antibodies from infected hosts. Using this technology and the plasma of patients with S. Typhi bacteremia in Bangladesh, we identified 57 proteins of S. Typhi, including proteins known to be immunogenic (PagC, HlyE, OmpA, and GroEL) and a number of proteins present in the human-restricted serotypes S. Typhi and S. Paratyphi A but rarely found in broader-host-range Salmonella spp. (HlyE, CdtB, PltA, and STY1364). We categorized identified proteins into a number of major groupings, including those involved in energy metabolism, protein synthesis, iron homeostasis, and biosynthetic and metabolic functions and those predicted to localize to the outer membrane. We assessed systemic and mucosal anti-HlyE responses in S. Typhi-infected patients and detected anti-HlyE responses at the time of clinical presentation in patients but not in controls. These findings could assist in the development of improved diagnostic assays.
C1 [Charles, Richelle C.; Harris, Jason B.; LaRocque, Regina C.; Eisenstein, Jana; Podolsky, Michael J.; Kalsy, Anuj; Calderwood, Stephen B.; Ryan, Edward T.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Charles, Richelle C.; Harris, Jason B.; LaRocque, Regina C.; Calderwood, Stephen B.; Ryan, Edward T.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Sheikh, Alaullah; Bhuiyan, M. Saruar; Brooks, W. Abdullah; Qadri, Firdausi] Int Ctr Diarrhoeal Dis Res, Dhaka 1000, Bangladesh.
[Krastins, Bryan; Sarracino, David A.] Thermo Fisher Sci, Cambridge, MA USA.
[Logvinenko, Tanya] Tufts Univ, Biostat Res Ctr, Med Ctr, ICRHPS, Boston, MA 02111 USA.
[Kudva, Indira T.] ARS, Food Safety & Enter Pathogens Res Unit, Natl Ctr Anim Hlth, USDA, Ames, IA USA.
[Ludwig, Albrecht] Klinikum Johann Wolfgang Goethe Univ, Inst Med Mikrobiol & Krankenhaushyg, Frankfurt, Germany.
[John, Manohar] Pathovacs Inc, Ames, IA USA.
[Calderwood, Stephen B.] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA.
[Ryan, Edward T.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Charles, RC (reprint author), Massachusetts Gen Hosp, Div Infect Dis, Jackson 504,55 Fruit St, Boston, MA 02114 USA.
EM rccharles@partners.org
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases [AI072599, AI077883, AI058935, NS059429]; Johns
Hopkins Bloomberg School of Public Health; Fogarty International Center
[TW05572, TW05572-09S1, TW007409, TW07144]; NIAID [AI089721]; Howard
Hughes Medical Institute; Deutsche Forschungsgemeinschaft [LU 842/1-1]
FX This work was supported by the ICDDR, B, grants from the National
Institutes of Health, including the National Institute of Allergy and
Infectious Diseases (AI072599 [E. T. R.], AI077883 [E. T. R.], AI058935
[R. C. C. and S. B. C.], NS059429 [J.B.H.]), the PneumoADIP Project of
the Johns Hopkins Bloomberg School of Public Health (W. A. B.), an
ICDDRB-US Centers for Disease Control and Prevention Cooperative
Agreement (W. A. B.), a Training Grant in Vaccine Development from the
Fogarty International Center, including an ARRA supplement (TW05572 [A.
S., M. S. B., and F. Q.] and TW05572-09S1 [R. C. C.]), Career
Development Awards (K01) from the Fogarty International Center (TW007409
[J.B.H.], TW07144 [R. C. L.]) and (K08) from the NIAID (AI089721 [R. C.
C.]), a Physician Scientist Early Career Award from the Howard Hughes
Medical Institute (R. C. L.), and a grant from the Deutsche
Forschungsgemeinschaft (LU 842/1-1 [A. L.]).
NR 57
TC 16
Z9 17
U1 0
U2 5
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1556-6811
J9 CLIN VACCINE IMMUNOL
JI Clin. Vaccine Immunol.
PD AUG
PY 2010
VL 17
IS 8
BP 1188
EP 1195
DI 10.1128/CVI.00104-10
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 633XG
UT WOS:000280539900004
PM 20573880
ER
PT J
AU Arndt, CAS
Koshkina, NV
Inwards, CY
Hawkins, DS
Krailo, MD
Villaluna, D
Anderson, PM
Goorin, AM
Blakely, ML
Bernstein, M
Bell, SA
Ray, K
Grendahl, DC
Marina, N
Kleinerman, ES
AF Arndt, Carola A. S.
Koshkina, Nadya V.
Inwards, Carrie Y.
Hawkins, Douglas S.
Krailo, Mark D.
Villaluna, Doojduen
Anderson, Peter M.
Goorin, Allen M.
Blakely, Martin L.
Bernstein, Mark
Bell, Sharon A.
Ray, Kaylee
Grendahl, Darryl C.
Marina, Neyssa
Kleinerman, Eugenie S.
TI Inhaled Granulocyte-Macrophage Colony Stimulating Factor for First
Pulmonary Recurrence of Osteosarcoma: Effects on Disease-Free Survival
and Immunomodulation. A Report From the Children's Oncology Group
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID EARLY LYMPHOCYTE RECOVERY; GM-CSF; AEROSOL GEMCITABINE; ANTITUMOR
IMMUNITY; PROGNOSTIC-FACTORS; LUNG METASTASES; FAS EXPRESSION; CELLS;
CHEMOTHERAPY; THERAPY
AB Purpose: Osteosarcoma most commonly recurs in the lung. Based on preliminary data on the antitumor effects of granulocyte-macrophage colony stimulating factor (GM-CSF) in animal models, and promising phase I trials, we embarked on a feasibility study of inhaled GM-CSF in patients with first isolated pulmonary recurrence of osteosarcoma.
Experimental Design: Forty-three eligible patients received inhaled GM-CSF at doses from 250 to 1,750 mu g twice daily on alternate weeks. Following two cycles, patients underwent thoracotomy to resect tumor and analyze pulmonary nodules for expression of Fas/Fas ligand (Fas/FasL), and the presence of dendritic cells by immunostaining for CD1a, clusterin, and S100. Following surgery, patients received 12 additional cycles of therapy on alternating weeks or until progression. Event-free survival and survival, and feasibility of therapy delivery were evaluated.
Results: Dose escalation to 1,750 mu g twice daily was feasible with no dose-limiting toxicity. Mean scores for Fas/FasL in nodules from patients with bilateral recurrence who underwent unilateral thoracotomy pretreatment (using a scoring system of 0-3) were 1.3 and 0.88, respectively, compared with 0.78 and 0.62 in nodules resected following two cycles of therapy. Only 11 of 30 nodules postinhalation were positive for CD1a, 4 of 30 for S100, and 6 of 30 for clusterin. Event-free and overall survival at 3 years were 7.8% and 35.4%, respectively.
Conclusions: Inhalation of GM-CSF at doses from 250 to 1,750 mu g twice daily on alternate weeks was feasible with low toxicity. However, no detectable immunostimulatory effect in pulmonary metastases or improved outcome postrelapse was seen. Clin Cancer Res; 16(15); 4024-30. (C) 2010 AACR.
C1 [Arndt, Carola A. S.; Inwards, Carrie Y.; Bell, Sharon A.; Grendahl, Darryl C.] Mayo Clin, Rochester, MN 55905 USA.
[Koshkina, Nadya V.; Anderson, Peter M.; Kleinerman, Eugenie S.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Hawkins, Douglas S.] Seattle Childrens Hosp, Seattle, WA USA.
[Krailo, Mark D.] Univ So Calif, Los Angeles, CA USA.
[Villaluna, Doojduen] Childrens Oncol Grp, Arcadia, CA USA.
[Goorin, Allen M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Blakely, Martin L.] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Bernstein, Mark] IWK Hlth Ctr, Halifax, NS, Canada.
[Ray, Kaylee] Doernbecher Hosp Children, Portland, OR USA.
[Marina, Neyssa] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
RP Arndt, CAS (reprint author), Mayo Clin, 200 1st St SW, Rochester, MN 55905 USA.
EM carndt@mayo.edu
FU [U10 CA98543]; [U10 CA98413]
FX Grant U10 CA98543 and U10 CA98413.
NR 30
TC 26
Z9 29
U1 1
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 AUG 1
PY 2010
VL 16
IS 15
BP 4024
EP 4030
DI 10.1158/1078-0432.CCR-10-0662
PG 7
WC Oncology
SC Oncology
GA 633TT
UT WOS:000280530300023
PM 20576718
ER
PT J
AU Refaat, MM
Hashash, JG
Shalaby, AA
AF Refaat, Marwan M.
Hashash, Jana G.
Shalaby, Alaa A.
TI Late Perforation by Cardiac Implantable Electronic Device Leads:
Clinical Presentation, Diagnostic Clues, and Management
SO CLINICAL CARDIOLOGY
LA English
DT Review
ID RIGHT-VENTRICULAR PERFORATION; PERMANENT PACEMAKER LEAD;
OF-THE-LITERATURE; CARDIOVERTER-DEFIBRILLATOR; ICD LEAD; SUBCUTANEOUS
TISSUES; DELAYED PERFORATION; LUNG PERFORATION; EXTRACTION; HEART
AB Late intracardiac lead perforation is defined as migration and perforation of an implanted lead after 1 month of cardiac electronic device implantation. It is an under-recognized complication with significant morbidity and mortality, particularly if not recognized early. Two patients with late perforation caused by passive-fixation leads are reported and the clinical features of their presentation and management are reviewed. We conducted a thorough review of the available English language literature pertaining to this complication to draw relevant conclusions regarding presentation, diagnosis, and management. Early recognition of this complication is important as the indications for and numbers of patients who receive cardiac implantable electronic devices continue to expand.
C1 [Refaat, Marwan M.; Shalaby, Alaa A.] VA Pittsburgh Healthcare Syst, Div Cardiol, Pittsburgh, PA 15240 USA.
[Hashash, Jana G.] Univ Pittsburgh, Dept Internal Med, Med Ctr, Pittsburgh, PA USA.
RP Shalaby, AA (reprint author), VA Pittsburgh Healthcare Syst, Univ Dr Div, 111C-U, Pittsburgh, PA 15240 USA.
EM alaa.shalaby@va.gov
NR 41
TC 20
Z9 21
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0160-9289
J9 CLIN CARDIOL
JI Clin. Cardiol.
PD AUG
PY 2010
VL 33
IS 8
BP 466
EP 475
DI 10.1002/clc.20803
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645RM
UT WOS:000281482200002
PM 20734443
ER
PT J
AU Zerilli, F
Bonanno, C
Shehi, E
Amicarelli, G
Adlerstein, D
Makrigiorgos, GM
AF Zerilli, Francesco
Bonanno, Cinzia
Shehi, Erlet
Amicarelli, Giulia
Adlerstein, Daniel
Makrigiorgos, G. Mike
TI Methylation-Specific Loop-Mediated Isothermal Amplification for
Detecting Hypermethylated DNA in Simplex and Multiplex Formats
SO CLINICAL CHEMISTRY
LA English
DT Article
ID CELL LUNG-CANCER; GENE; EPIGENETICS; BIOMARKERS; VIRUS; TUMOR; ASSAY;
PCR
AB BACKGROUND: Aberrant DNA methylation of gene promoters and the associated silencing of tumor suppressor genes are recognized as mechanisms contributing to tumor development. Therefore, detection of promoter hypermethylation is becoming important for diagnosis, prognosis, and aiding the design of cancer therapies. We describe a novel isothermal method for the detection of DNA hypermethylation.
METHODS: Methylation-specific loop-mediated isothermal amplification (MS-LAMP) is a novel adaptation of LAMP. MS-LAMP was used for the highly specific detection of hypermethylated CpGs in the promoters of the CDKN2A [cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)], GATA5 (GATA binding protein 5), and DAPK1 (death-associated protein kinase 1) genes. The reactions occurred under isothermal conditions with 3 primer sets specific for methylated promoters. Both turbidimetry and fluorescence were used for detection. The MS-LAMP assay was validated with bisulfite-treated plasmid and genomic DNA controls of known methylation status and was applied to detect hypermethylation in 18 clinical tumor samples. A multiplex MS-LAMP for CDKN2A, GATA5, and DAPK1 was also validated with the aid of synthetic positive and negative controls.
RESULTS: The MS-LAMP assay showed high specificity with plasmid and genomic DNA targets in reactions carried out in <1 h. The assay had a detection limit of approximately 30 copies of methylated target sequence and a selectivity of 0.5% methylated DNA in a mixture with unmethylated DNA. Compared with methylation-specific PCR, the MS-LAMP assay detected lower rates of methylation in lung adenocarcinoma samples. Simultaneous multiplex detection of hypermethylation in the 3 targets (CDKN2A, GATA5, and DAPK1) was readily achieved with the MS-LAMP assay in both the turbidimetric and fluorescence detection formats.
CONCLUSIONS: MS-LAMP provides a highly specific isothermal method for methylation detection and is well suited for multiplex approaches. (C) 2010 American Association for Clinical Chemistry
C1 [Zerilli, Francesco] Univ Milano Bicocca, Dipartimento Biotecnol & Biosci, Milan, Italy.
[Bonanno, Cinzia; Shehi, Erlet; Amicarelli, Giulia; Adlerstein, Daniel] DiaSorin SpA, Saluggia, VC, Italy.
[Makrigiorgos, G. Mike] Dana Farber Brigham & Womens Canc Ctr, Div Med Phys & Biophys, Dept Radiat Oncol, Boston, MA USA.
[Makrigiorgos, G. Mike] Dana Farber Brigham & Womens Canc Ctr, Div Genome Stabil & DNA Repair, Boston, MA USA.
RP Adlerstein, D (reprint author), Biotrin Ltd, 93 Rise, Mt Merrion, Co Dublin, Ireland.
EM daniel.adlerstein@biotrin.ie
NR 33
TC 14
Z9 15
U1 4
U2 17
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 AUG
PY 2010
VL 56
IS 8
BP 1287
EP 1296
DI 10.1373/clinchem.2010.143545
PG 10
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 633KP
UT WOS:000280501400017
PM 20551384
ER
PT J
AU Melmed, GY
Spiegel, BM
Bressler, B
Cheifetz, AS
Devlin, SM
Harrell, LE
Irving, PM
Jones, J
Kaplan, GG
Kozuch, PL
Velayos, FS
Baidoo, L
Sparrow, MP
Siegel, CA
AF Melmed, Gil Y.
Spiegel, Brennan M.
Bressler, Brian
Cheifetz, Adam S.
Devlin, Shane M.
Harrell, Laura E.
Irving, Peter M.
Jones, Jennifer
Kaplan, Gilaad G.
Kozuch, Patricia L.
Velayos, Fernando S.
Baidoo, Leonard
Sparrow, Miles P.
Siegel, Corey A.
TI The Appropriateness of Concomitant Immunomodulators With Anti-Tumor
Necrosis Factor Agents for Crohn's Disease: One Size Does Not Fit All
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Crohn's Disease; Inflammatory Bowel Disease; Infliximab; Adalimumab;
Certolizumab; Anti-Tumor Necrosis alpha Therapy
ID INFLAMMATORY-BOWEL-DISEASE; T-CELL LYMPHOMA; MAINTENANCE INFLIXIMAB;
CERTOLIZUMAB PEGOL; RANDOMIZED-TRIAL; THERAPY; ADALIMUMAB; EFFICACY
AB BACKGROUND & AIMS: There is no consensus on the appropriateness of concomitant immunomodulators with antitumor necrosis factor (TNF) therapy for Crohn's disease Some patients benefit from concomitant immunomodulators, but concerns related to infections and lymphoma risk have dampened enthusiasm for this approach We applied the RAND/University of California Los Angeles Appropriateness Method toward establishing appropriateness of concomitant immunomodulators and anti-TNF therapies for Crohn's disease METHODS: A literature review was conducted regarding efficacy and safety of concomitant immunomodulators in the setting of anti-TNF therapy for Crohn's disease and presented to the Building Research in Inflammatory Bowel Disease Globally group, a globally diverse panel of 13 gastroenterologists clinically experienced in inflammatory bowel disease A total of 134 scenarios were constructed using several clinical variables Panelists used a modified Delphi method to rate the appropriateness of concomitant immunomodulators, and met to discuss and re-rate appropriateness Disagreement was assessed using a validated index RESULTS: Concomitant immunomodulators were generally rated appropriate for 63 scenarios, uncertain for 60 scenarios, and inappropriate for 11 scenarios In general, concomitant immunomodulators were appropriate for those with extensive disease, shorter duration of disease, perianal involvement, prior surgery, females, and older patients (>26 y) Concomitant immunomodulators were generally rated inappropriate for young males, and in some scenarios involving uncomplicated disease Smoking and the particular anti-TNF medication did not Influence ratings Disagreement was observed in 6 of 134 scenarios CONCLUSIONS: The appropriateness of concomitant immunomodulators with anti-TNF therapy for Crohn's disease was determined through a modified Delphi panel approach based on expert interpretation of the available literature. Clinicians should consider multiple factors when considering concomitant immunomodulators with anti-TNF treatment.
C1 [Melmed, Gil Y.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Spiegel, Brennan M.] Univ Calif Los Angeles, Los Angeles Vet Adm Ctr Outcomes Res & Educ, VA Greater Los Angeles Healthcare Syst, Ctr Ulcer Res & Educ,Digest Dis Res Ctr, Los Angeles, CA USA.
[Melmed, Gil Y.; Spiegel, Brennan M.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Bressler, Brian] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
[Cheifetz, Adam S.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
[Devlin, Shane M.; Kaplan, Gilaad G.] Univ Calgary, Calgary, AB T2N 1N4, Canada.
[Harrell, Laura E.] Univ Chicago, Chicago, IL 60637 USA.
[Irving, Peter M.] Guys Hosp, London SE1 9RT, England.
[Irving, Peter M.] St Thomas Hosp, London, England.
[Jones, Jennifer] Univ Saskatchewan, Saskatoon, SK, Canada.
[Kozuch, Patricia L.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Velayos, Fernando S.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Baidoo, Leonard] Univ Pittsburgh, Pittsburgh, PA USA.
[Sparrow, Miles P.] Alfred Hosp, Dept Gastroenterol, Melbourne, Vic, Australia.
[Siegel, Corey A.] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
RP Melmed, GY (reprint author), Cedars Sinai Med Ctr, 8635 W 3rd St,960-W, Los Angeles, CA 90048 USA.
OI kozuch, patricia/0000-0002-7465-9671; Kaplan, Gilaad/0000-0003-2719-0556
FU Centocor; Setpoint; Amgen; Celgene; Elan; PG; AstraZeneca; Bristol Meyer
Squibb; Salix; Takeda; Rose Pharmaceuticals; Prometheus; Schering-Plough
Canada; UCB Pharma; Shire; Abbott; Ferring Pharmaceuticals; Abbott
Pharmaceuticals; Proctor and Gamble Pharmaceuticals; Crohn's and Colitis
Foundation of America; National Institute of Diabetes and Digestive and
Kidney Diseases [K23DK078678]; National Institutes of Health/NCRR/OD
[KL2 RR024130]
FX These authors disclose the following: Gil Melmed was a consultant and/or
received research support from Centocor, Setpoint, Amgen, and Celgene,
was on the speakers bureaus of Abbott. P&G. and Shire, and was on the
advisory board of UCB: Corey Siegel was on the advisory boards of
Abbott. UCB, and P&G, was a consultant and received research support
from Elan and P&G. and performed CME activities for Abbott and UCB;
Brennan Spiegel received research funding from AstraZeneca, Amgen,
Bristol Meyer Squibb, Salix, Takeda, Rose Pharmaceuticals, and
Prometheus, and was on the advisory Boards of Takeda. Prometheus, and
Ironwood, Brian Bressler was on the advisory boards of Abbott.
Schering-Plough Canada, UCB, Shire. P&G. and Ferring, and was on the
speaker's bureaus of Abbott, Schering-Plough Canada, and Shire. Adam
Cheifetz was on the speaker's bureau of Centocor, UCB, and Abbott, and
the advisory boards of Abbott and UCB. Jennifer Jones was a consultant,
on the speaker's bureaus, and received educational funding from
Schering-Plough Canada, UCB Pharma, Shire, P&G, and Abbott. Miles
Sparrow received research support from Ferring Pharmaceuticals and
Abbott Pharmaceuticals, and was on the advisory board of Schering-Plough
Pharmaceuticals; Fernando Velayos was on the speaker's bureau of
Centocor, Peter Irving was on the advisory board and speaker's bureau of
Abbott; Shane Devlin was on the speaker's bureaus for Schering-Plough
and Abbott, and on the advisory boards for Abbott, Centocor, and UCB;
Gilaad Kaplan was on the advisory boards of Schering-Plough. Abbott,
UCB, and Shire. and Laura Harrell was a consultant for Abbott The
remaining authors disclose no conflicts.; Unrestricted funding for the
in-person Dallas RAND Appropriateness Panel meeting generously was
provided by Proctor and Gamble Pharmaceuticals Unrestricted funding for
the Building Research in Inflammatory Bowel Disease Globally group is
provided by Abbott, Shire, and Proctor and Gamble Pharmaceuticals,; Dr
Kaplan is a Canadian Institutes of Health Research New Investigator and
an Alberta Heritage Foundation for Medical Research Population Health
Investigator; Dr Harrell is supported by a Crohn's and Colitis
Foundation of America Career Development Award: Dr Siegel is supported
by a Crohn's and Colitis Foundation of America Career Development Award
and by grant number K23DK078678 from the National Institute of Diabetes
and Digestive and Kidney Diseases. Dr Velayos is supported by a Crohn's
and Colitis Foundation of America Career Development Award and the
National Institutes of Health/NCRR/OD UCSF-CTSI award (KL2 RR024130)
NR 20
TC 24
Z9 24
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD AUG
PY 2010
VL 8
IS 8
BP 655
EP 659
DI 10.1016/j.cgh.2010.04.023
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 638YX
UT WOS:000280938200007
PM 20451665
ER
PT J
AU Kanwal, F
Kramer, J
Asch, SM
El-Serag, H
Spiegel, BMR
Edmundowicz, S
Sanyal, AJ
Dominitz, JA
McQuaid, KR
Martin, P
Keeffe, EB
Friedman, LS
Ho, SB
Durazo, F
Bacon, BR
AF Kanwal, Fasiha
Kramer, Jennifer
Asch, Steven M.
El-Serag, Hashem
Spiegel, Brennan M. R.
Edmundowicz, Steven
Sanyal, Arun J.
Dominitz, Jason A.
McQuaid, Kenneth R.
Martin, Paul
Keeffe, Emmet B.
Friedman, Lawrence S.
Ho, Samuel B.
Durazo, Francisco
Bacon, Bruce R.
TI An Explicit Quality Indicator Set for Measurement of Quality of Care in
Patients With Cirrhosis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Quality of Care; Cirrhosis; Delphi Panel; Performance Measures
ID PORTAL-HYPERTENSION; LIVER-TRANSPLANTATION; RHEUMATOID-ARTHRITIS;
VARICEAL HEMORRHAGE; ADULT PATIENTS; MANAGEMENT; GUIDELINES; DIAGNOSIS;
WORKSHOP; ASCITES
AB BACKGROUND & AIMS: Cirrhosis is a prevalent and expensive condition With an increasing emphasis on quality in health care and recognition of inconsistencies in the management of patients with cirrhosis, we established a set of explicit quality indicators (QIs) for their treatment METHODS: We organized an 11-member, multidisciplinary expert panel and followed modified Delphi methods to systematically identify a set of QIs for cirrhosis We provided the panel with a report that summarized the results of a comprehensive literature review of data linking candidate QIs to outcomes The panel performed independent ratings of each candidate QI by using a standard 9-point RAND appropriateness scale (RAS) (ranging from 1 = not appropriate to 9 = most appropriate) The panel members then met, reviewed the ratings, and voted again by using an iterative process of discussion The final set of QIs was selected, QIs had a median RAS >7, and panel members agreed on those selected RESULTS: Among 169 candidate QIs, the panel rated 41 QIs as valid measures of quality care The selected QIs cover 6 domains of care including ascites (13 QIs), variceal bleeding (18 QIs), hepatic encephalopathy (4 QIs), hepatocellular cancer (1 QI), liver transplantation (2 QIs), and general cirrhosis care (3 QIs) Content coverage included prevention, diagnosis, treatment, timeliness, and follow-up CONCLUSIONS: We developed an explicit set of evidence-based QIs for treatment of cirrhosis. These provide physicians and institutions with a tool to identify processes amenable to quality improvement. This tool is intended to be applicable in any setting where care for patients with cirrhosis is provided.
C1 [Kanwal, Fasiha] St Louis Vet Adm VA, St Louis, MO USA.
[Kanwal, Fasiha; Bacon, Bruce R.] St Louis Univ, Sch Med, Dept Gastroenterol & Hepatol, St Louis, MO 63141 USA.
[Kramer, Jennifer; El-Serag, Hashem] Michael E DeBakey VA Med Ctr, Houston, TX USA.
[Kramer, Jennifer; El-Serag, Hashem] Baylor Coll Med, Dept Med, Div Gastroenterol, Houston, TX 77030 USA.
[Asch, Steven M.; Spiegel, Brennan M. R.] Greater Los Angeles VA Healthcare Syst, Dept Med & Hlth Serv Res, Los Angeles, CA USA.
[Asch, Steven M.; Spiegel, Brennan M. R.; Durazo, Francisco] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
[Edmundowicz, Steven] Washington Univ, Sch Med, St Louis, MO USA.
[Sanyal, Arun J.] Virginia Commonwealth Univ, Med Ctr, Dept Internal Med, Div Gastroenterol Hepatol & Nutr, Richmond, VA USA.
[Dominitz, Jason A.] Univ Washington, Sch Med, VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[McQuaid, Kenneth R.] Univ Calif San Francisco, Vet Affairs Med Ctr, San Francisco, CA 94143 USA.
[McQuaid, Kenneth R.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
[Martin, Paul] Univ Miami, Sch Med, Div Gastroenterol & Hepatol, Miami, FL USA.
[Keeffe, Emmet B.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Friedman, Lawrence S.] Newton Wellesley Hosp, Dept Med, Newton, MA USA.
[Ho, Samuel B.] VA San Diego Healthcare Syst, Dept Med, San Diego, CA USA.
[Ho, Samuel B.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Durazo, Francisco] Univ Calif Los Angeles, David Geffen Sch Med, UCLA Dumont Liver Transplant Ctr, Los Angeles, CA 90095 USA.
RP Kanwal, F (reprint author), St Louis VA Med Ctr, 915 N Grand,111 JC GI, St Louis, MO 63141 USA.
EM fkanwal@yahoo.com
OI Edmundowicz, Steven/0000-0002-6541-3485; Dominitz,
Jason/0000-0002-8070-7086
FU American Society for Gastrointestinal Endoscopy; American College of
Gastroenterology
FX This material is based on work supported by the 2008 American Society
for Gastrointestinal Endoscopy Quality of Care Award and by the 2009
American College of Gastroenterology Clinical Research Award.
NR 31
TC 45
Z9 45
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD AUG
PY 2010
VL 8
IS 8
BP 709
EP 717
DI 10.1016/j.cgh.2010.03.028
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 638YX
UT WOS:000280938200016
PM 20385251
ER
PT J
AU Simchowitz, B
Shiman, L
Spencer, J
Brouillard, D
Gross, A
Connor, M
Weingart, SN
AF Simchowitz, Brett
Shiman, Lawrence
Spencer, Justin
Brouillard, Daniela
Gross, Anne
Connor, Maureen
Weingart, Saul N.
TI Perceptions and Experiences of Patients Receiving Oral Chemotherapy
SO CLINICAL JOURNAL OF ONCOLOGY NURSING
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; INTRAVENOUS FLUOROURACIL; PALLIATIVE
CHEMOTHERAPY; SAFETY PROFILE; PHASE-III; THERAPY; LEUCOVORIN;
CAPECITABINE
AB Although many patients prefer orally administered cancer therapy (including oral chemotherapy) because of its convenience, the shift from hospital to home-based administration creates concerns. This article explores the perceptions and experiences of oral chemotherapy users and their caregivers to assess vulnerabilities and improvement opportunities at each stage of the medication process: choosing oral chemotherapy, prescribing, dispensing, administering, and monitoring. The authors recruited 15 current and former oral chemotherapy users, as well as caregivers who administered the medications to children, to participate in one of two focus group sessions at a comprehensive cancer center. Participants largely were satisfied with oral cancer therapy but raised concerns regarding their lack of preparedness for side effects and their unfamiliarity with the possible techniques to mitigate drug toxicity. Participants also described difficulties obtaining medications through retail pharmacies. Parents of pediatric patients with cancer indicated concerns regarding their children's emotional health and correct medication administration. Participants believed that the initial prescribing encounter should have included more education, and they also wanted more frequent follow-up by healthcare practitioners. As oral cancer therapy is used more widely, oncology healthcare providers will need to create robust mechanisms to support their safe use.
C1 [Brouillard, Daniela; Gross, Anne; Weingart, Saul N.] Dana Farber Canc Inst, Adult Ambulatory Serv, Boston, MA 02115 USA.
[Simchowitz, Brett] Univ Calif San Francisco, Sch Med, San Francisco, CA USA.
[Connor, Maureen] Qual & Patient Safety Consultant, Arlington, MA USA.
RP Weingart, SN (reprint author), Dana Farber Canc Inst, Adult Ambulatory Serv, Boston, MA 02115 USA.
FU U.S. Agency for Healthcare Research and Quality [1 P20HS017123]
FX The authors take full responsibility for the content of the article. The
study was supported by a grant from the U.S. Agency for Healthcare
Research and Quality (grant # 1 P20HS017123). The authors did not
receive honoraria for this work. The content of this article has been
reviewed by independent peer reviewers to ensure that it is balanced,
objective, and free from commercial bias. No financial relationships
relevant to the content of this article have been disclosed by the
authors, planners, independent peer reviewers, or editorial staff.
NR 19
TC 16
Z9 16
U1 1
U2 11
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 1092-1095
J9 CLIN J ONCOL NURS
JI Clin. J. Oncol. Nurs.
PD AUG
PY 2010
VL 14
IS 4
BP 447
EP 453
DI 10.1188/10.CJON.447-453
PG 7
WC Oncology; Nursing
SC Oncology; Nursing
GA 636NK
UT WOS:000280743800011
PM 20682500
ER
PT J
AU Walsh, MC
AF Walsh, Michele C.
TI Impact of Treatment-Related Cardiac Toxicity on Lymphoma Survivors: An
Institutional Approach for Risk Reduction and Management
SO CLINICAL JOURNAL OF ONCOLOGY NURSING
LA English
DT Article
ID LONG-TERM SURVIVORS; QUALITY-OF-LIFE; HODGKINS-DISEASE; CARE PLANS;
CARDIOMYOPATHY; THERAPY; CHEST
AB Despite improvements in treatment and overall survival rates, survivors of lymphoma may have long-term and late effects. Given the immense risk for cardiac disease after treatment for Hodgkin lymphoma and non-Hodgkin lymphoma, healthcare providers should focus on prevention of secondary adverse effects. The Dana-Farber Cancer Institute has been working to develop guidelines to address the cardiotoxicities that impact the lymphoma survivor population.
C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Walsh, MC (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM michele_walsh@dfci.harvard.edu
NR 24
TC 0
Z9 0
U1 1
U2 1
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 1092-1095
J9 CLIN J ONCOL NURS
JI Clin. J. Oncol. Nurs.
PD AUG
PY 2010
VL 14
IS 4
BP 505
EP 507
DI 10.1188/10.CJON.505-507
PG 3
WC Oncology; Nursing
SC Oncology; Nursing
GA 636NK
UT WOS:000280743800018
PM 20682507
ER
PT J
AU Schroen, AT
Petroni, GR
Wang, H
Gray, R
Wang, XFF
Cronin, W
Sargent, DJ
Benedetti, J
Wickerham, DL
Djulbegovic, B
Slingluff, CL
AF Schroen, Anneke T.
Petroni, Gina R.
Wang, Hongkun
Gray, Robert
Wang, Xiaofei F.
Cronin, Walter
Sargent, Daniel J.
Benedetti, Jacqueline
Wickerham, Donald L.
Djulbegovic, Benjamin
Slingluff, Craig L., Jr.
TI Preliminary evaluation of factors associated with premature trial
closure and feasibility of accrual benchmarks in phase III oncology
trials
SO CLINICAL TRIALS
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIALS; CANCER CLINICAL-TRIALS; PARTICIPATION;
BARRIERS; ENROLLMENT; ATTITUDES
AB Background A major challenge for randomized phase III oncology trials is the frequent low rates of patient enrollment, resulting in high rates of premature closure due to insufficient accrual.
Purpose We conducted a pilot study to determine the extent of trial closure due to poor accrual, feasibility of identifying trial factors associated with sufficient accrual, impact of redesign strategies on trial accrual, and accrual benchmarks designating high failure risk in the clinical trials cooperative group (CTCG) setting.
Methods A subset of phase III trials opened by five CTCGs between August 1991 and March 2004 was evaluated. Design elements, experimental agents, redesign strategies, and pretrial accrual assessment supporting accrual predictions were abstracted from CTCG documents. Percent actual/predicted accrual rate averaged per month was calculated. Trials were categorized as having sufficient or insufficient accrual based on reason for trial termination. Analyses included univariate and bivariate summaries to identify potential trial factors associated with accrual sufficiency.
Results Among 40 trials from one CTCG, 21 (52.5%) trials closed due to insufficient accrual. In 82 trials from five CTCGs, therapeutic trials accrued sufficiently more often than nontherapeutic trials (59% vs 27%, p = 0.05). Trials including pretrial accrual assessment more often achieved sufficient accrual than those without (67% vs 47%, p = 0.08). Fewer exclusion criteria, shorter consent forms, other CTCG participation, and trial design simplicity were not associated with achieving sufficient accrual. Trials accruing at a rate much lower than predicted (< 35% actual/predicted accrual rate) were consistently closed due to insufficient accrual.
Limitations This trial subset under-represents certain experimental modalities. Data sources do not allow accounting for all factors potentially related to accrual success.
Conclusion Trial closure due to insufficient accrual is common. Certain trial design factors appear associated with attaining sufficient accrual. Defining accrual benchmarks for early trial termination or redesign is feasible, but better accrual prediction methods are critically needed. Future studies should focus on identifying trial factors that allow more accurate accrual predictions and strategies that can salvage open trials experiencing slow accrual. Clinical Trials 2010; 7: 312-321. http://ctj.sagepub.com.
C1 [Schroen, Anneke T.; Slingluff, Craig L., Jr.] Univ Virginia, Dept Surg, Charlottesville, VA 22903 USA.
[Petroni, Gina R.; Wang, Hongkun] Univ Virginia, Dept Publ Hlth Sci, Charlottesville, VA USA.
[Gray, Robert] Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA.
[Wang, Xiaofei F.] Duke Univ, Dept Biostat & Bioinformat, Durham, NC USA.
[Cronin, Walter; Wickerham, Donald L.] NSABP Operat Ctr, Pittsburgh, PA USA.
[Sargent, Daniel J.] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Benedetti, Jacqueline] SW Oncol Grp Stat Ctr, Seattle, WA USA.
[Djulbegovic, Benjamin] Univ S Florida, Dept Med, Tampa, FL USA.
RP Schroen, AT (reprint author), Univ Virginia, Dept Surg, Charlottesville, VA 22903 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 Commonwealth Foundation for Cancer Research
FX This research was supported by the Commonwealth Foundation for Cancer
Research support to the University of Virginia Cancer Center.
NR 23
TC 34
Z9 34
U1 0
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
J9 CLIN TRIALS
JI Clin. Trials
PD AUG
PY 2010
VL 7
IS 4
BP 312
EP 321
DI 10.1177/1740774510374973
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 636MV
UT WOS:000280741400002
PM 20595245
ER
PT J
AU Yeh, HC
Clark, JM
Emmons, KE
Moore, RH
Bennett, GG
Warner, ET
Sarwer, DB
Jerome, GJ
Miller, ER
Volger, S
Louis, TA
Wells, B
Wadden, TA
Colditz, GA
Appel, LJ
AF Yeh, Hsin-Chieh
Clark, Jeanne M.
Emmons, Karen E.
Moore, Renee H.
Bennett, Gary G.
Warner, Erica T.
Sarwer, David B.
Jerome, Gerald J.
Miller, Edgar R., III
Volger, Sheri
Louis, Thomas A.
Wells, Barbara
Wadden, Thomas A.
Colditz, Graham A.
Appel, Lawrence J.
TI Independent but coordinated trials: insights from the Practice-based
Opportunities for Weight Reduction Trials Collaborative Research Group
SO CLINICAL TRIALS
LA English
DT Article
ID UNITED-STATES; RANDOMIZED-TRIAL; OBESITY; INTERVENTIONS; OVERWEIGHT;
ADULTS
AB Background The National Heart, Lung, and Blood Institute (NHLBI) funded three institutions to conduct effectiveness trials of weight loss interventions in primary care settings. Unlike traditional multi-center clinical trials, each study was established as an independent trial with a distinct protocol. Still, efforts were made to coordinate and standardize several aspects of the trials. The three trials formed a collaborative group, the 'Practice-based Opportunities for Weight Reduction (POWER) Trials Collaborative Research Group.'
Purpose We describe the common and distinct features of the three trials, the key characteristics of the collaborative group, and the lessons learned from this novel organizational approach.
Methods The Collaborative Research Group consists of three individual studies: 'Be Fit, Be Well' (Washington University in St. Louis/Harvard University), 'POWER Hopkins' (Johns Hopkins), and 'POWER-UP' (University of Pennsylvania). There are a total of 15 participating clinics with similar to 1100 participants. The common primary outcome is change in weight at 24 months of follow-up, but each protocol has trial-specific elements including different interventions and different secondary outcomes. A Resource Coordinating Unit at Johns Hopkins provides administrative support.
Results The Collaborative Research Group established common components to facilitate potential cross-site comparisons. The main advantage of this approach is to develop and evaluate several interventions, when there is insufficient evidence to test one or two approaches, as would be done in a traditional multi-center trial.
Limitations The challenges of the organizational design include the complex decision-making process, the extent of potential data pooling, time intensive efforts to standardize reports, and the additional responsibilities of the DSMB to monitor three distinct protocols.
C1 [Yeh, Hsin-Chieh] Johns Hopkins Univ, Welch Ctr Prevent Epidemiol & Clin Res, Dept Med, Baltimore, MD 21218 USA.
[Yeh, Hsin-Chieh; Clark, Jeanne M.; Miller, Edgar R., III; Appel, Lawrence J.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Emmons, Karen E.; Bennett, Gary G.] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Emmons, Karen E.; Bennett, Gary G.] Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA 02115 USA.
[Moore, Renee H.] Univ Penn, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Moore, Renee H.; Sarwer, David B.; Volger, Sheri; Wadden, Thomas A.] Univ Penn, Dept Psychiat, Ctr Weight & Eating Disorders, Philadelphia, PA 19104 USA.
[Bennett, Gary G.] Duke Univ, Dept Psychol & Neurosci, Durham, NC USA.
[Bennett, Gary G.] Duke Univ, Duke Global Hlth Inst, Durham, NC USA.
[Warner, Erica T.; Colditz, Graham A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Jerome, Gerald J.] Towson Univ, Dept Kinesiol, Towson, MD USA.
[Louis, Thomas A.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD USA.
[Wells, Barbara] NHLBI, Div Cardiovasc Sci, NIH, Bethesda, MD 20892 USA.
[Colditz, Graham A.] Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA.
[Colditz, Graham A.] Washington Univ, Alvin J Siteman Canc Ctr, St Louis, MO 63110 USA.
[Appel, Lawrence J.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Baltimore, MD USA.
RP Yeh, HC (reprint author), Johns Hopkins Univ, Welch Ctr Prevent Epidemiol & Clin Res, Dept Med, Baltimore, MD 21218 USA.
EM hyeh1@jhmi.edu
RI Colditz, Graham/A-3963-2009;
OI volger, sheri/0000-0002-1689-1173; Colditz, Graham/0000-0002-7307-0291;
Jerome, Gerald/0000-0003-0612-2626
FU NHLBI [U01HL087071, U01HL087085, U01HL087072, NCT00661817, NCT00783315,
NCT00826774]
FX The POWER Trials Collaborative Research Group is supported by NHLBI
grants: U01HL087071 (Washington University), U01HL087085 (Johns Hopkins
University), and U01HL087072 (University of Pennsylvania). The
ClinicalTrials.gov identifiers are NCT00661817 (Washington University),
NCT00783315 (Johns Hopkins University), and NCT00826774 (University of
Pennsylvania).
NR 15
TC 25
Z9 25
U1 0
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
J9 CLIN TRIALS
JI Clin. Trials
PD AUG
PY 2010
VL 7
IS 4
BP 322
EP 332
DI 10.1177/1740774510374213
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 636MV
UT WOS:000280741400003
PM 20573639
ER
PT J
AU Chang, KM
AF Chang, Kyong-Mi
TI Hepatitis B Immunology for Clinicians
SO CLINICS IN LIVER DISEASE
LA English
DT Article
DE Hepatitis B; Innate immunity; Adaptive immunity; Regulatory T cells;
Costimulation; Pathogenesis; Programmed death 1
ID REGULATORY T-CELLS; PLASMACYTOID DENDRITIC CELLS; NATURAL-KILLER-CELLS;
ADAPTIVE IMMUNE-RESPONSES; ACUTE VIRAL-HEPATITIS; CHRONIC HBV INFECTION;
VIRUS-INFECTION; LIVER-DAMAGE; LYMPHOCYTE RESPONSE; ANTIVIRAL THERAPY
AB Hepatitis B virus (HBV) is a hepatotrophic DNA virus that causes acute and chronic hepatitis. Despite an effective vaccine, more than 350 million people are chronically infected with HBV worldwide and are at risk for progressive liver disease. There are marked geographic variations in HBV prevalence (ranging from 0.1% to 2% in low prevalence areas and 10% to 20% in high prevalence areas) related to the timing and mode of HBV exposure. In many developed countries, HBV exposure typically occurs in adults via sexual transmission with a low chronicity rate (5%). In regions with high HBV prevalence (eg, Asia, sub-Saharan Africa), HBV exposure tends to occur in the perinatal period (eg, vertical transmission from mother to infant) with a high rate of persistence in the absence of timely vaccination. The course of viral infection is defined by the interplay between the virus and host immune defense. This article introduces the innate and adaptive immune defense mechanisms in general and as related to HBV. In particular, the current concepts regarding the innate and adaptive immune components contributing to the clinical, virologic and therapeutic outcome in acute and chronic hepatitis B are examined.
C1 [Chang, Kyong-Mi] Philadelphia VA Med Ctr, Div Gastroenterol, Philadelphia, PA 19104 USA.
[Chang, Kyong-Mi] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
RP Chang, KM (reprint author), Philadelphia VA Med Ctr, Div Gastroenterol, A412-A424 Med Res Bldg, Philadelphia, PA 19104 USA.
EM kmchang@mail.med.upenn.edu
FU NIH [UO1 DK082866, RO1 AI047519]
FX This work was supported in part by NIH UO1 DK082866 and NIH RO1 AI047519
NR 82
TC 7
Z9 7
U1 0
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1089-3261
J9 CLIN LIVER DIS
JI Clin. Liver Dis.
PD AUG
PY 2010
VL 14
IS 3
BP 409
EP +
DI 10.1016/j.cld.2010.05.012
PG 18
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 639OP
UT WOS:000280984400004
PM 20638022
ER
PT J
AU Nierenberg, AA
AF Nierenberg, Andrew A.
TI My Mother's Levetiracetam
SO CNS SPECTRUMS
LA English
DT Editorial Material
C1 [Nierenberg, Andrew A.] Harvard Univ, Psychiat, Sch Med, Cambridge, MA 02138 USA.
[Nierenberg, Andrew A.] Massachusetts Gen Hosp, Bipolar Clin, Boston, MA 02114 USA.
[Nierenberg, Andrew A.] Massachusetts Gen Hosp, Res Program, Boston, MA 02114 USA.
[Nierenberg, Andrew A.] Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 02114 USA.
RP Nierenberg, AA (reprint author), Harvard Univ, Psychiat, Sch Med, Cambridge, MA 02138 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1092-8529
EI 2165-6509
J9 CNS SPECTRUMS
JI CNS Spectr.
PD AUG
PY 2010
VL 15
IS 8
BP 487
EP 488
DI 10.1017/S1092852900000419
PG 2
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA V44BS
UT WOS:000209725100001
PM 20703195
ER
PT J
AU Dording, CM
Mischoulon, D
Goodness, TM
Baer, L
Clain, A
Stewart, JW
Matthews, JD
McGrath, PJ
Nierenberg, AA
Fava, M
Papakostas, GI
AF Dording, Christina M.
Mischoulon, David
Goodness, Tracie M.
Baer, Lee
Clain, Alisabet
Stewart, Jonathan W.
Matthews, John D.
McGrath, Patrick J.
Nierenberg, Andrew A.
Fava, Maurizio
Papakostas, George I.
TI Psychoticism and Paranoid Ideation in Patients With Nonpsychotic Major
Depressive Disorder: Prevalence, Response to Treatment, and Impact on
Short- and Long-Term Treatment Outcome
SO CNS SPECTRUMS
LA English
DT Article
AB Objective/Introduction: We sought to characterize the impact of the 90-item Symptom Checklist (SCL-90) subscales for paranoid ideation (PI) and psychoticism (P) in patients with major depressive disorder (MDD), on acute antidepressant response and on relapse prevention.
Methods: Subjects with Structured Clinical Interview for DSM Disorders-diagnosed non psychotic MDD were recruited into a clinical trial of open-label fluoxetine 10-60 mg/day for 12 weeks, followed by double-blind randomization of responders (n=262) to fluoxetine continuation or placebo for 12 months. PI and P were assessed with the patient-rated SCL-90. The association of these symptoms with response to treatment was assessed by logistic regression.
Results: We found significant decreases in PI and P during acute treatment phase for fluoxetine responders and nonresponders, although only 10.3% and 7.5% of patients experienced a >50% reduction in PI and P scores, respectively. Neither PI nor P scores significantly predicted time to relapse. P scores predicted a lower response rate to treatment with fluoxetine.
Discussion:The results of the present study suggest that there is a significant relationship between the presence of psychoticism in patients with nonpsychotic MDD, and the likelihood of overall depressive symptom improvement following a trial of monotherapy with fluoxetine.
Conclusion: An increased burden of psychoticism in depressed subjects may confer poorer response to fluoxetine, but not increased risk of relapse among fluoxetine responders.
C1 [Dording, Christina M.] Harvard Univ, Sch Med, Sexual Behav Studies, Boston, MA USA.
[Dording, Christina M.; Mischoulon, David; Nierenberg, Andrew A.; Fava, Maurizio; Papakostas, George I.] Harvard Univ, Sch Med, Psychiat, Boston, MA USA.
[Mischoulon, David] Massachusetts Gen Hosp, Res, Boston, MA 02114 USA.
[Mischoulon, David] Massachusetts Gen Hosp, Psychiat, Boston, MA 02114 USA.
[Goodness, Tracie M.; Clain, Alisabet; Nierenberg, Andrew A.; Fava, Maurizio] Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 02114 USA.
[Baer, Lee] Harvard Univ, Sch Med, Psychol, Boston, MA USA.
[Baer, Lee] Massachusetts Gen Hosp, Dept Psychiat, Psychol, Boston, MA 02114 USA.
[Stewart, Jonathan W.; McGrath, Patrick J.] Columbia Univ Coll Phys & Surg, Psychiat Clin, 630 W 168th St, New York, NY 10032 USA.
[Stewart, Jonathan W.] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Matthews, John D.] Massachusetts Gen Hosp, Inpatient Res & Training, Boston, MA USA.
[Matthews, John D.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[McGrath, Patrick J.] New York State Psychiat Inst & Hosp, Depress Evaluat Serv, New York, NY 10032 USA.
[Nierenberg, Andrew A.] NIMH, Bipolar Trials Network, Bethesda, MD USA.
[Nierenberg, Andrew A.] Massachusetts Gen Hosp, Bipolar Clin, Boston, MA USA.
[Nierenberg, Andrew A.] Massachusetts Gen Hosp, Res Program, Boston, MA USA.
[Fava, Maurizio] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Fava, Maurizio] Massachusetts Gen Hosp, Clin Trials Network & Inst, Boston, MA 02114 USA.
[Papakostas, George I.] Massachusetts Gen Hosp, Treatment Resistant Depress Studies, Boston, MA 02114 USA.
RP Dording, CM (reprint author), Massachusetts Gen Hosp, 50 Staniford St,401, Boston, MA 02114 USA.
EM cdording@partners.org
NR 34
TC 0
Z9 0
U1 0
U2 3
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1092-8529
EI 2165-6509
J9 CNS SPECTRUMS
JI CNS Spectr.
PD AUG
PY 2010
VL 15
IS 8
BP 515
EP 521
DI 10.1017/S1092852900000468
PG 7
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA V44BS
UT WOS:000209725100006
PM 20703198
ER
PT J
AU Greenberg, JL
Wilhelm, S
AF Greenberg, Jennifer L.
Wilhelm, Sabine
TI SPECIAL SERIES: COGNITIVE-BEHAVIORAL TREATMENT OF BODY IMAGE DISORDERS
Introduction
SO COGNITIVE AND BEHAVIORAL PRACTICE
LA English
DT Editorial Material
ID DYSMORPHIC DISORDER; EATING-DISORDERS; VISUAL-ATTENTION; PREVALENCE;
WOMEN; DISTURBANCE; POPULATION; SAMPLE; PARTS; BIAS
C1 [Wilhelm, Sabine] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Greenberg, Jennifer L.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Wilhelm, S (reprint author), Massachusetts Gen Hosp, 185 Cambridge St, Boston, MA 02114 USA.
EM wilhelm@psych.mgh.harvard.edu
NR 29
TC 1
Z9 1
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1077-7229
J9 COGN BEHAV PRACT
JI Cogn. Behav. Pract.
PD AUG
PY 2010
VL 17
IS 3
BP 237
EP 240
PG 4
WC Psychology, Clinical
SC Psychology
GA 615PU
UT WOS:000279148000001
ER
PT J
AU Wilhelm, S
Buhlmann, U
Hayward, LC
Greenberg, JL
Dimaite, R
AF Wilhelm, Sabine
Buhlmann, Ulrike
Hayward, Laura C.
Greenberg, Jennifer L.
Dimaite, Ruta
TI A Cognitive-Behavioral Treatment Approach for Body Dysmorphic Disorder
SO COGNITIVE AND BEHAVIORAL PRACTICE
LA English
DT Article
ID OBSESSIVE-COMPULSIVE DISORDER; OPEN-LABEL; CLINICAL-FEATURES; IMAGINED
UGLINESS; 200 INDIVIDUALS; PREVALENCE; TRIAL; COMORBIDITY; DERMATOLOGY;
FLUVOXAMINE
AB Although body dysmorphic disorder (BDD) has been described in the literature for mow than a century, there has been only a limited focus on the development of cognitive behavioral treatments for BDD. Our case report provides a data dad description of a course of cognitive behavioral treatment (CBT) for an individual with BDD. The patient was treated for 10 weekly 50-minute individual sessions. The treatment focused on psychoeducation cognitive restructuring, exposure and response prevention, and perceptual retraining exercises. The patient's BDD symptoms significantly improved over the course of the treatment. This case study illustrates several clinical strategies and provides further support. for CBT as a promising treatment for individuals suffering from BDD.
C1 [Wilhelm, Sabine; Greenberg, Jennifer L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Wilhelm, Sabine; Dimaite, Ruta] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Buhlmann, Ulrike] Humboldt Univ, Berlin, Germany.
RP Wilhelm, S (reprint author), Massachusetts Gen Hosp, 185 Cambridge St, Boston, MA 02114 USA.
EM wilhelm@psych.mgh.harvard.edu
NR 44
TC 16
Z9 16
U1 2
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1077-7229
J9 COGN BEHAV PRACT
JI Cogn. Behav. Pract.
PD AUG
PY 2010
VL 17
IS 3
BP 241
EP 247
PG 7
WC Psychology, Clinical
SC Psychology
GA 615PU
UT WOS:000279148000002
ER
PT J
AU Greenberg, JL
Markowitz, S
Petronko, MR
Taylor, CE
Wilhelm, S
Wilson, GT
AF Greenberg, Jennifer L.
Markowitz, Sarah
Petronko, Michael R.
Taylor, Caitlin E.
Wilhelm, Sabine
Wilson, G. Terence
TI Cognitive-Behavioral Therapy for Adolescent Body Dysmorphic Disorder
SO COGNITIVE AND BEHAVIORAL PRACTICE
LA English
DT Article
ID OBSESSIVE-COMPULSIVE SCALE; RANDOMIZED CLINICAL-TRIAL; RESPONSE
PREVENTION; ANXIETY DISORDERS; RELIABILITY; SERTRALINE; CHILDREN;
VALIDITY; SCHIZOPHRENIA; MAINTENANCE
AB The onset of appearance-related concerns associated with body dysmorphic disorder (BDD) typically occurs in adolescence, and these concerns are often severe enough to interfere with normal development and psychosocial functioning. Cognitive behavioral therapy (CBT) is an effective treatment for adults with BDD. However, no treatment studies focusing on adolescents with BDD have been conducted. The need for an. effective treatment in this population led to the development of a brief CBT protocol with family involvement. The treatment focuses on. enhancing an adolescent's quality of life through the reduction of maladaptive thoughts and behaviors, and incorporates skills training and parent training. Similar treatment packages have already been shown to be efficacious for children and adolescents with similar disorders, such as obsessive-compulsive disorder and social phobia. The following case illustrates the application of this brief CBT protocol for BDD in an adolescent, and highlights clinical considerations needed when adapting CBT for a pediatric population. Treatment was associated with clinically significant improvement in symptoms of BDD, self-esteem, depression, and quality of life. This report extends extant literature by suggesting that CBT may be a helpful treatment for adolescents with BDD.
C1 [Greenberg, Jennifer L.; Markowitz, Sarah; Taylor, Caitlin E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Greenberg, Jennifer L.; Markowitz, Sarah; Wilhelm, Sabine] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Petronko, Michael R.; Wilson, G. Terence] Rutgers State Univ, Piscataway, NJ 08855 USA.
RP Greenberg, JL (reprint author), Massachusetts Gen Hosp, 185 Cambridge St, Boston, MA 02114 USA.
EM jlgreenberg@partners.org
NR 50
TC 15
Z9 15
U1 2
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1077-7229
J9 COGN BEHAV PRACT
JI Cogn. Behav. Pract.
PD AUG
PY 2010
VL 17
IS 3
BP 248
EP 258
PG 11
WC Psychology, Clinical
SC Psychology
GA 615PU
UT WOS:000279148000003
ER
PT J
AU Delinsky, SS
Wilson, GT
AF Delinsky, Sherrie S.
Wilson, G. Terence
TI Cognitive Behavior Therapy With Body Image Exposure for Bulimia Nervosa:
A Case Example
SO COGNITIVE AND BEHAVIORAL PRACTICE
LA English
DT Article
ID QUESTIONNAIRE EDE-Q; EATING-DISORDERS; MIRROR EXPOSURE; SHAPE
QUESTIONNAIRE; ANOREXIA-NERVOSA; DISSATISFACTION; PSYCHOTHERAPY;
ADOLESCENTS; DISTURBANCE; INTERVIEW
AB Cognitive behavior therapy (CBT) is an effective treatment for bulimia nervosa (BN). However, among patients with BN, symptom improvement is more pronounced for behavioral eating symptoms (i.e., bingeing and purging) than for body image disturbance, and the persistence of body image disturbance is associated with relapse. The need for more effective body image interventions led to the development of mirror exposure, which focuses on encouraging patients to view themselves in a holistic, nonjudgmental, mindful fashion. Behavioral manifestations of body image disturbance-body checking and avoidance-are also targeted in order to reduce and eliminate such behaviors and their associated preoccupation and distress. A preliminary trial of Body Image Exposure has shown. promise, but it has not yet been tested in the context of CBT for BN. The case of "Sara" illustrates the application of this targeted treatment for body image disturbance. Central clinical issues around the perceptual, cognitive, and behavioral components of body image are delineated as they arose in treatment, as are issues of motivation and compliance. Treatment was associated with improvement in eating symptoms, body image, and mood.
C1 [Delinsky, Sherrie S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Delinsky, Sherrie S.] McLean Hosp, Belmont, MA USA.
[Wilson, G. Terence] Rutgers State Univ, Piscataway, NJ 08855 USA.
RP Delinsky, SS (reprint author), 332 Washington St,Suite 265, Wellesley, MA 02481 USA.
EM sdelinsky@gmail.com
RI gray, stephen/G-6729-2011
NR 41
TC 10
Z9 11
U1 5
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1077-7229
J9 COGN BEHAV PRACT
JI Cogn. Behav. Pract.
PD AUG
PY 2010
VL 17
IS 3
BP 270
EP 277
PG 8
WC Psychology, Clinical
SC Psychology
GA 615PU
UT WOS:000279148000005
ER
PT J
AU Flessner, CA
Penzel, F
Keuthen, NJ
AF Flessner, Christopher A.
Penzel, Fred
Keuthen, Nancy J.
CA Trichotillomania Learning Ctr Sci
TI Current Treatment Practices for Children and Adults With
Trichotillomania: Consensus Among Experts
SO COGNITIVE AND BEHAVIORAL PRACTICE
LA English
DT Article
ID COGNITIVE-BEHAVIORAL THERAPY; DOUBLE-BLIND; DESCRIPTIVE PSYCHOPATHOLOGY;
FUNCTIONAL IMPAIRMENT; HABIT REVERSAL; LONG-TERM; FLUOXETINE; TRIAL;
CLOMIPRAMINE; COMORBIDITY
C1 [Flessner, Christopher A.] Brown Univ, Warren Alpert Sch Med, Bradley Hasbro Child Res Ctr, Providence, RI 02912 USA.
[Penzel, Fred] Western Suffolk Psychol Serv, Huntington, NY USA.
[Keuthen, Nancy J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cambridge, MA 02138 USA.
RP Flessner, CA (reprint author), Rhode Isl Hosp, Dept Child & Adolescent Psychiat, Bradley Hasbro Childrens Res Ctr, 1 Hoppin St,Suite 204, Providence, RI 02903 USA.
EM cflessner@lifespan.org
RI Citations, TLC SAB/C-4006-2011; Flessner, Christopher/K-1483-2015
NR 32
TC 15
Z9 15
U1 1
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1077-7229
J9 COGN BEHAV PRACT
JI Cogn. Behav. Pract.
PD AUG
PY 2010
VL 17
IS 3
BP 290
EP 300
PG 11
WC Psychology, Clinical
SC Psychology
GA 615PU
UT WOS:000279148000008
ER
PT J
AU Daughters, SB
Magidson, JF
Schuster, RM
Safren, SA
AF Daughters, Stacey B.
Magidson, Jessica F.
Schuster, Randi M.
Safren, Steven A.
TI ACT HEALTHY: A Combined Cognitive-Behavioral Depression and Medication
Adherence Treatment for HIV-Infected Substance Users
SO COGNITIVE AND BEHAVIORAL PRACTICE
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; TREATMENT RETENTION; COCAINE DEPENDENCE;
CANCER-PATIENTS; RISK BEHAVIORS; DRUG-ABUSE; VIRAL LOAD; THERAPY; CARE;
COMORBIDITY
AB The two most common comorbid conditions with HIV are substance use disorders and depression, and individuals with comorbid HIV, depression, and substance dependence face a more chronic and treatment-resistant course. As an example of how to adapt evidence-based approaches to a complex comorbid population, the current case study examined the integration of a combined depression and HIV medication adherence treatment. The resulting intervention, ACT HEALTHY, combines a brief behavioral activation approach specifically developed to treat depression in individuals receiving residential substance abuse treatment (LETS ACT; Daughters et al., 2008) with a brief cognitive-behavioral approach to improving HIV medication adherence (Life-Steps; Safren el al., 1999; Safren et al., 2009). The current case series demonstrates the use of ACT HEALTHY among 3 depressed HIV-positive, low-income African Americans entering residential substance abuse treatment.
C1 [Daughters, Stacey B.] Univ Maryland, Dept Publ & Community Hlth, College Pk, MD 20742 USA.
[Safren, Steven A.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Safren, Steven A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Daughters, SB (reprint author), Univ Maryland, Dept Publ & Community Hlth, College Pk, MD 20742 USA.
EM daughter@umd.edu
FU NIDA NIH HHS [R01 DA022974-01A2, R01 DA022974]
NR 58
TC 27
Z9 27
U1 2
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1077-7229
J9 COGN BEHAV PRACT
JI Cogn. Behav. Pract.
PD AUG
PY 2010
VL 17
IS 3
BP 309
EP 321
PG 13
WC Psychology, Clinical
SC Psychology
GA 615PU
UT WOS:000279148000010
PM 21709737
ER
PT J
AU Perrimon, N
Ni, JQ
Perkins, L
AF Perrimon, Norbert
Ni, Jian-Quan
Perkins, Lizabeth
TI In vivo RNAi: Today and Tomorrow
SO COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
LA English
DT Article
ID DOUBLE-STRANDED-RNA; TRANSMEMBRANE PROTEIN SID-1; FUNCTIONAL GENOMIC
ANALYSIS; HIGH-THROUGHPUT RNAI; DROSOPHILA-MELANOGASTER;
CAENORHABDITIS-ELEGANS; C-ELEGANS; GENETIC INTERFERENCE;
BACTERIAL-INFECTION; TRANSGENIC RNAI
AB RNA interference (RNAi) provides a powerful reverse genetics approach to analyze gene functions both in tissue culture and in vivo. Because of its widespread applicability and effectiveness it has become an essential part of the tool box kits of model organisms such as Caenorhabditis elegans, Drosophila, and the mouse. In addition, the use of RNAi in animals in which genetic tools are either poorly developed or nonexistent enables a myriad of fundamental questions to be asked. Here, we review the methods and applications of in vivo RNAi to characterize gene functions in model organisms and discuss their impact to the study of developmental as well as evolutionary questions. Further, we discuss the applications of RNAi technologies to crop improvement, pest control and RNAi therapeutics, thus providing an appreciation of the potential for phenomenal applications of RNAi to agriculture and medicine.
C1 [Perrimon, Norbert; Ni, Jian-Quan] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Perrimon, Norbert; Ni, Jian-Quan] Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02175 USA.
[Perkins, Lizabeth] Harvard Univ, Sch Med, Pediat Surg Res Labs, Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Perrimon, N (reprint author), Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
EM perrimon@receptor.med.harvard.edu
FU HHMI; [GM084947]
FX We thank Rui Zhou and Stephanie Mohr for comments on the manuscript and
Luping Liu, Donghui Yang-Zhou and Martha Reed assistance on the figures.
This work is supported by GM084947 to N.P. and the HHMI.
NR 90
TC 80
Z9 85
U1 3
U2 41
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1943-0264
J9 CSH PERSPECT BIOL
JI Cold Spring Harbor Perspect. Biol.
PD AUG
PY 2010
VL 2
IS 8
AR a003640
DI 10.1101/cshperspect.a003640
PG 11
WC Cell Biology
SC Cell Biology
GA 634MY
UT WOS:000280588200001
PM 20534712
ER
PT J
AU Storer, NY
Zon, LI
AF Storer, Narie Y.
Zon, Leonard I.
TI Zebrafish Models of p53 Functions
SO COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
LA English
DT Article
ID DEVELOPMENTAL ABNORMALITIES; NEUROFIBROMATOSIS TYPE-1; INSERTIONAL
MUTAGENESIS; EMBRYONIC LETHALITY; MDM2-DEFICIENT MICE; GERMLINE
MUTATIONS; SPONTANEOUS TUMORS; BRAF MUTATIONS; HIGH-FREQUENCY;
DANIO-RERIO
AB Zebrafish models have significantly contributed to our understanding of vertebrate development and, more recently, human disease. The growing number of genetic tools available in zebrafish research has resulted in the identification of many genes involved in developmental and disease processes. In particular, studies in the zebrafish have clarified roles of the p53 tumor suppressor in the formation of specific tumor types, as well as roles of p53 family members during embryonic development. The zebrafish has also been instrumental in identifying novel mechanisms of p53 regulation and highlighting the importance of these mechanisms in vivo. This article will summarize how zebrafish models have been used to reveal numerous, important aspects of p53 function.
C1 [Zon, Leonard I.] Harvard Univ, Stem Cell Program, Sch Med, Boston, MA 02115 USA.
Harvard Univ, Div Hematol Oncol, Sch Med, Childrens Hosp Boston, Boston, MA 02115 USA.
Harvard Univ, Dana Farber Canc Inst, Howard Hughes Med Inst, Sch Med,Harvard Stem Cell Inst, Boston, MA 02115 USA.
RP Zon, LI (reprint author), Harvard Univ, Stem Cell Program, Sch Med, Boston, MA 02115 USA.
EM zon@enders.tch.harvard.edu
RI Xie, Huangming/B-2260-2012
FU National Institutes of Health (NIH) [GM07226, 5R01 CA103846-07]
FX We thank Craig Ceol and Gessingga Storer for critical reading of this
manuscript. N.Y.S. was supported in part by National Institutes of
Health (NIH) Cell and Developmental Biology Training Grant GM07226.
Cancer research by L.I.Z. is funded by NIH Grant 5R01 CA103846-07.
NR 71
TC 23
Z9 23
U1 0
U2 7
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI WOODBURY
PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
SN 1943-0264
J9 CSH PERSPECT BIOL
JI Cold Spring Harbor Perspect. Biol.
PD AUG
PY 2010
VL 2
IS 8
AR a001123
DI 10.1101/cshperspect.a001123
PG 12
WC Cell Biology
SC Cell Biology
GA 634MY
UT WOS:000280588200005
PM 20679337
ER
PT J
AU Jakobiec, FA
Sandhu, H
Bhat, P
Colby, K
AF Jakobiec, Frederick A.
Sandhu, Harpal
Bhat, Pooja
Colby, Kathryn
TI Bilateral Conjunctival Melanocytic Nevi of Simultaneous Onset Simulating
Conjunctivitis in a Child
SO CORNEA
LA English
DT Article
DE conjunctival nevus; junctional nevus; melanocytic nevus; bilateral nevi;
immunohistochemistry
ID LESIONS
AB A healthy 10-year-old girl developed synchronous, bilateral, temporal redness of the eyes regarded as sectoral conjunctivitis for 5 years that was unresponsive to topical steroids and antihistamines. Finely vascularized, minimally elevated, amelanotic or faintly focally pigmented, epibulbar conjunctival lesions were present bilaterally. The lesions were completely excised. Histopathologic and immunohistochemical evaluations confirmed that they were both predominantly junctional nevi with conspicuous chronic inflammation. Juvenile conjunctival nevi frequently have atypical histopathologic traits that in an adult could be suggestive of melanoma. The differential diagnosis of much less likely disorders includes leukemia, lymphoid tumor (salmon patch), and conjunctival sarcoidosis, among other conditions. The patient has had no recurrence 3 years after surgery.
C1 [Jakobiec, Frederick A.; Bhat, Pooja] Massachusetts Eye & Ear Infirm, David G Cogan Ophthalm Pathol Lab, Boston, MA 02114 USA.
[Jakobiec, Frederick A.; Sandhu, Harpal; Bhat, Pooja; Colby, Kathryn] Harvard Univ, Sch Med, Boston, MA USA.
[Colby, Kathryn] Massachusetts Eye & Ear Infirm, Cornea Serv, Dept Ophthalmol, Boston, MA 02114 USA.
RP Jakobiec, FA (reprint author), Massachusetts Eye & Ear Infirm, David G Cogan Ophthalm Pathol Lab, Suite 321,3rd Floor,243 Charles St, Boston, MA 02114 USA.
EM fred_jakobiec@meei.harvard.edu
NR 13
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-3740
J9 CORNEA
JI Cornea
PD AUG
PY 2010
VL 29
IS 8
BP 937
EP 940
DI 10.1097/ICO.0b013e3181c84480
PG 4
WC Ophthalmology
SC Ophthalmology
GA 630ED
UT WOS:000280254500020
PM 20508514
ER
PT J
AU Jakobiec, FA
Nguyen, J
Bhat, P
Fay, A
AF Jakobiec, Frederick A.
Nguyen, John
Bhat, Pooja
Fay, Aaron
TI Recurrent Blue Nevus of the Corneoscleral Limbus
SO CORNEA
LA English
DT Article
DE blue nevus; cornea; limbus; recurrent; immunohistochemistry; cryotherapy
ID CONJUNCTIVAL MELANOCYTIC LESIONS; MALIGNANT-MELANOMA; CRYOTHERAPY;
FEATURES
AB Purpose: To describe an unusual corneoscleral blue nevus.
Methods: Review of clinical and histopathological characteristics and previous relevant literature supplemented with immunohistochemical studies.
Results: A 13-year-old Pakistani girl presented with a 5 X 2-mm, superotemporal, nonmovable, recurrent, black, limbal nodule. The lesion had been incompletely removed two and a half years earlier. Nonfascicular, variably pigmented, banal, spindle melanocytes with bland nuclei were discovered histopathologically in the conjunctival substantia propria and superficial sclera in the original and recurrent specimens. HMB-45+ and MART-1+ immunostainings established that all the variably pigmented spindle cells were melanocytes. Dispersed plump melanophages displayed clumped melanin granules and were shown to have small nuclei after decolorization. The Ki-67 proliferation index was very low (0.05%), supporting a benign diagnosis. No residual pigmentation after excision and cryotherapy was observed in follow-up examinations during a year and a half.
Conclusions: Careful histopathological and immunohistochemical evaluation of recurrent, incompletely excised, blue nevi can determine if they remain benign. Adjunctive cryotherapy was performed to prevent further recurrence, based on results from published data.
C1 [Jakobiec, Frederick A.] Massachusetts Eye & Ear Infirm, David G Cogan Ophthalm Pathol Lab, Boston, MA 02114 USA.
Massachusetts Eye & Ear Infirm, Dept Ophthalmol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
Massachusetts Eye & Ear Infirm, Oculoplast Serv, Boston, MA 02114 USA.
RP Jakobiec, FA (reprint author), Massachusetts Eye & Ear Infirm, David G Cogan Ophthalm Pathol Lab, 243 Charles St,Room 321, Boston, MA 02114 USA.
EM fred_jakobiec@meei.harvard.edu
NR 28
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-3740
J9 CORNEA
JI Cornea
PD AUG
PY 2010
VL 29
IS 8
BP 947
EP 951
DI 10.1097/ICO.0b013e3181ca6d1b
PG 5
WC Ophthalmology
SC Ophthalmology
GA 630ED
UT WOS:000280254500023
PM 20508501
ER
PT J
AU Patterson, JE
Malani, PN
Maragakis, LL
AF Patterson, Jan E.
Malani, Preeti N.
Maragakis, Lisa L.
TI Infection control in the intensive care unit: Progress and challenges in
systems and accountability
SO CRITICAL CARE MEDICINE
LA English
DT Article
ID SAFETY NETWORK
AB Attention to the improvement of safety in healthcare lately has focused on healthcare-associated infections, including many that occur in the intensive care unit, such as catheter-related bloodstream infections and ventilator-associated pneumonias. Great strides have been made in decreasing the rates of intensive care unit hospital-acquired infections in the past decade. This is attributable to a number of factors, including standardization of care, technological advances, provider payment reform, and consumer activism. Teamwork and communication remain the most important facets in patient safety. The papers in this supplement examine the roles of human factors and process engineering, survey a spectrum of infection control and safety challenges encountered by critical care practitioners, and assess the future challenges for continued improvement in our systems of care. (Crit Care Med 2010; 38[Suppl.]:S265-S268)
C1 [Patterson, Jan E.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Patterson, Jan E.] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
[Malani, Preeti N.] Univ Michigan Hlth Syst, Vet Affairs Ann Arbor Healthcare Syst, Ann Arbor, MI USA.
[Malani, Preeti N.] Geriatr Res Educ & Clin Ctr, Ann Arbor, MI USA.
[Maragakis, Lisa L.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
RP Patterson, JE (reprint author), Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
EM pattersonj@uthscsa.edu
FU Basilea; Merck; Pfizer; Schering-Plough
FX Dr. Patterson disclosed that her spouse received grant support from
Basilea, Merck, Pfizer, and Schering-Plough and is a consultant for
Merck, Pfizer, and Basilea. The remaining authors did not disclose any
potential conflicts of interest.
NR 28
TC 5
Z9 7
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD AUG
PY 2010
VL 38
IS 8
SU S
BP S265
EP S268
DI 10.1097/CCM.0b013e3181e69d48
PG 4
WC Critical Care Medicine
SC General & Internal Medicine
GA 628IP
UT WOS:000280112100001
PM 20647783
ER
PT J
AU Flynn, RL
Zou, L
AF Flynn, Rachel Litman
Zou, Lee
TI Oligonucleotide/oligosaccharide-binding fold proteins: a growing family
of genome guardians
SO CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY
LA English
DT Review
DE OB fold; DNA damage; checkpoint; telomere; DNA repair
ID SINGLE-STRANDED-DNA; HOLLIDAY JUNCTION DISSOLVASOME;
TOPOISOMERASE-III-ALPHA; OB-FOLD; DAMAGE RESPONSE; HUMAN POT1; A RPA;
TELOMERASE PROCESSIVITY; ESSENTIAL COMPONENT; PROTECTS TELOMERES
AB The maintenance of genomic stability relies on the coordinated action of a number of cellular processes, including activation of the DNA-damage checkpoint, DNA replication, DNA repair, and telomere homeostasis. Many proteins involved in these cellular processes use different types of functional modules to regulate and execute their functions. Recent studies have revealed that many DNA-damage checkpoint and DNA repair proteins in human cells possess the oligonucleotide/oligosaccharide-binding (OB) fold domains, which are known to bind single-stranded DNA in both prokaryotes and eukaryotes. Furthermore, during the DNA damage response, the OB folds of the human checkpoint and DNA repair proteins play critical roles in DNA binding, protein complex assembly, and regulating protein-protein interactions. These findings suggest that the OB fold is an evolutionarily conserved functional module that is widely used by genome guardians. In this review, we will highlight the functions of several well-characterized or newly discovered eukaryotic OB-fold proteins in the DNA damage response.
C1 [Zou, Lee] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Flynn, Rachel Litman; Zou, Lee] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA USA.
RP Zou, L (reprint author), Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
EM zou.lee@mgh.harvard.edu
FU NIH [GM076388]; ACS [0902501]
FX L.Z. is supported by a NIH grant (GM076388) and is an Ellison New
Scholar on Aging. R. L. F. is supported by an ACS fellowship 0902501.
NR 93
TC 60
Z9 60
U1 5
U2 12
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 1040-9238
J9 CRIT REV BIOCHEM MOL
JI Crit. Rev. Biochem. Mol. Biol.
PD AUG
PY 2010
VL 45
IS 4
BP 266
EP 275
DI 10.3109/10409238.2010.488216
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 636TJ
UT WOS:000280763700002
PM 20515430
ER
PT J
AU Menze, MA
Chakraborty, N
Clavenna, M
Banerjee, M
Liu, XH
Toner, M
Hand, SC
AF Menze, Michael A.
Chakraborty, Nilay
Clavenna, Matthew
Banerjee, Mitali
Liu, Xiang-Hong
Toner, Mehmet
Hand, Steven C.
TI Metabolic preconditioning of cells with AICAR-riboside: Improved
cryopreservation and cell-type specific impacts on energetics and
proliferation
SO CRYOBIOLOGY
LA English
DT Article
DE AICAR; Adenylate levels; ATP; Metabolism; Cell stasis; Biostabilization
ID ACTIVATED PROTEIN-KINASE; KILLIFISH AUSTROFUNDULUS-LIMNAEUS; SANDWICH
CONFIGURATION; COLLAGEN SANDWICH; RAT HEPATOCYTES; ENERGY-CHARGE;
INHIBITION; DEPRESSION; TOLERANCE; DIAPAUSE
AB In species whose evolutionary history has provided natural tolerance to dehydration and freezing, metabolic depression is often a pre-requisite for survival. We tested the hypothesis that preconditioning of mammalian cells with 5-aminoimidazole-4-carboxamide-1-b-o-ribofuranoside (AICAR) to achieve metabolic depression will promote greater survivorship during cryopreservation. AICAR is used extensively to stimulate AMP-activated protein kinase (AMPK), which can result in downregulation of biosynthetic processes. We showed that the metabolic interconversion of AICAR was cell-type dependent. Accumulation of 5-aminoimidazole-4-carboxamide-1b-D-ribofuranosyl-5'-monophosphate (ZMP), as well as other metabolites that possess multiple phosphates (i.e., ZDP, ZTP), varied approximately 3.5-fold across the cell lines tested. AICAR treatment also significantly influenced the concentrations of cellular adenylates (ATP, ADP, and AMP). Depression of cell metabolism and proliferation with AICAR treatment differed among cell lines. Proliferation for a given cell line was negatively correlated with the fold-increase achieved in the 'effective adenylate ratio' ([AMP] + [ZMP])/[ATP]) after AICAR treatment. Metabolic preconditioning with AICAR promoted a significant increase in viability post-freezing in J774.A1 macrophages, HepG2/C3A cells and primary hepatocytes but not in NIH/3T3 fibroblasts or OMK cells. The effect of AICAR on viability after freezing was positively correlated (r(2) = 0.94) with the fold-increase in the 'effective adenylate ratio'. Thus for each cell line, the greater the depression of metabolism and proliferation due to preconditioning with AICAR, the greater was the survivorship post-freezing. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Menze, Michael A.; Clavenna, Matthew; Hand, Steven C.] Louisiana State Univ, Dept Biol Sci, Div Cellular Dev & Integrat Biol, Baton Rouge, LA 70803 USA.
[Chakraborty, Nilay; Banerjee, Mitali; Liu, Xiang-Hong; Toner, Mehmet] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Engn Med & Surg Serv, Boston, MA 02114 USA.
[Chakraborty, Nilay; Banerjee, Mitali; Liu, Xiang-Hong; Toner, Mehmet] Shriners Hosp Children, Boston, MA 02114 USA.
RP Menze, MA (reprint author), Louisiana State Univ, Dept Biol Sci, Div Cellular Dev & Integrat Biol, 202 Life Sci Bldg, Baton Rouge, LA 70803 USA.
EM menze@lsu.edu
RI Chakraborty, Nilay/C-3118-2009;
OI Menze, Michael/0000-0003-1072-5462
FU National Institutes of Health [2-RO1-DK046270-14A1]
FX This study was supported by National Institutes of Health Grant
2-RO1-DK046270-14A1.
NR 45
TC 14
Z9 14
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0011-2240
J9 CRYOBIOLOGY
JI Cryobiology
PD AUG
PY 2010
VL 61
IS 1
BP 79
EP 88
DI 10.1016/j.cryobiol.2010.05.004
PG 10
WC Biology; Physiology
SC Life Sciences & Biomedicine - Other Topics; Physiology
GA 640SY
UT WOS:000281073900013
PM 20510224
ER
PT J
AU BuAbbud, JC
Al-latayfeh, MM
Sun, JK
AF BuAbbud, John C.
Al-latayfeh, Motasem M.
Sun, Jennifer K.
TI Optical Coherence Tomography Imaging for Diabetic Retinopathy and
Macular Edema
SO CURRENT DIABETES REPORTS
LA English
DT Article
DE Diabetic retinopathy; Diabetic macular edema; Optical coherence
tomography; OCT; Spectral domain; Time domain
ID RETINAL THICKNESS; FUNDUS PHOTOGRAPHY; VISUAL-ACUITY; TIME-DOMAIN; EYES;
BIOMICROSCOPY; PATTERNS; SPEED; OCT
AB Optical coherence tomography (OCT) is a noninvasive imaging modality that uses low-coherent interferometry to visualize an optical cross-section of biological tissues. Over the past two decades, the ability to perform OCT imaging of the neural retina has afforded clinicians and researchers a highly reproducible method of diagnosing and following diabetic macular edema (DME) that compares favorably to other methods of DME assessment such as clinical examination and fundus photography. Although central subfield mean thickness has been the OCT parameter most commonly used to evaluate DME in clinical research trials, OCT also allows evaluation of morphologic changes that occur in DME, including compact retinal thickening, intraretinal cystic changes, subretinal fluid, and vitreomacular traction. OCT parameters have been shown to be only moderately correlated with visual acuity. However, improvements in technology leading to higher resolution, faster acquisition speed, image registration, and three-dimensional imaging that are available with newer spectral domain OCT models may allow future identification of valid OCT-derived surrogate markers for visual function in patients with diabetes.
C1 [BuAbbud, John C.; Al-latayfeh, Motasem M.; Sun, Jennifer K.] Joslin Diabet Ctr, Beetham Eye Inst, Boston, MA 02215 USA.
[BuAbbud, John C.; Al-latayfeh, Motasem M.] Joslin Diabet Ctr, Eye Res Sect, Boston, MA 02215 USA.
[Sun, Jennifer K.] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02215 USA.
RP Sun, JK (reprint author), Joslin Diabet Ctr, Beetham Eye Inst, 1 Joslin Pl, Boston, MA 02215 USA.
EM Jennifer.sun@joslin.harvard.edu
NR 32
TC 11
Z9 13
U1 0
U2 4
PU CURRENT MEDICINE GROUP
PI PHILADELPHIA
PA 400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA
SN 1534-4827
J9 CURR DIABETES REP
JI Curr. Diabetes Rep.
PD AUG
PY 2010
VL 10
IS 4
BP 264
EP 269
DI 10.1007/s11892-010-0129-z
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 615IT
UT WOS:000279128900002
PM 20556548
ER
PT J
AU Feener, EP
AF Feener, Edward P.
TI Plasma Kallikrein and Diabetic Macular Edema
SO CURRENT DIABETES REPORTS
LA English
DT Article
DE Diabetic macular edema; Diabetic retinopathy; Plasma kallikrein;
Kallikrein kinin system; Bradykinin; Diabetes; Inflammation; Vascular
permeability; Vitreous fluid; Retina; Proteomics; Complement 1
inhibitor; Angioedema
ID RETINAL VASCULAR-PERMEABILITY; HUMAN OCULAR-TISSUES; KININ B-1
RECEPTORS; FACTOR-XII; RETINOPATHY; BRADYKININ; ACTIVATION; RATS;
PREKALLIKREIN; SYSTEM
AB Recent proteomic studies have identified components of the kallikrein kinin system, including plasma kallikrein, factor XII, and kininogen, in vitreous obtained from individuals with advanced diabetic retinopathy. In rodent models, activation of plasma kallikrein in vitreous increases retinal vascular permeability; whereas inhibition of the kallikrein kinin system reduces retinal leakage induced by diabetes and hypertension. These findings suggest that intraocular activation of the plasma kallikrein pathway may contribute to excessive retinal vascular permeability that can lead to diabetic macular edema. The kallikrein kinin system contains two separate and independently regulated serine proteases that generate bradykinin peptides: plasma kallikrein and tissue kallikrein. Tissue kallikrein is expressed in the retina and ciliary body, where it has been implicated in exerting autocrine or paracrine effects via bradykinin receptors that are colocalized in these tissues. Emerging evidence suggests that plasma kallikrein inhibitors may provide a new therapeutic opportunity to reduce retinal vascular permeability.
C1 Harvard Univ, Sch Med, Joslin Diabet Ctr, Dept Med,Res Div, Boston, MA 02215 USA.
RP Feener, EP (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Dept Med,Res Div, 1 Joslin Pl, Boston, MA 02215 USA.
EM Edward.Feener@joslin.harvard.edu
FU US National Institutes of Health [EY019029, DK 36836]; Juvenile Diabetes
Research Foundation
FX This work was supported in part by the US National Institutes of Health
(grants EY019029, DK 36836) and the Juvenile Diabetes Research
Foundation.
NR 47
TC 16
Z9 16
U1 0
U2 4
PU CURRENT MEDICINE GROUP
PI PHILADELPHIA
PA 400 MARKET STREET, STE 700, PHILADELPHIA, PA 19106 USA
SN 1534-4827
J9 CURR DIABETES REP
JI Curr. Diabetes Rep.
PD AUG
PY 2010
VL 10
IS 4
BP 270
EP 275
DI 10.1007/s11892-010-0127-1
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 615IT
UT WOS:000279128900003
PM 20535647
ER
PT J
AU Rothenberg, SM
Settleman, J
AF Rothenberg, S. Michael
Settleman, Jeff
TI Discovering Tumor Suppressor Genes Through Genome-Wide Copy Number
Analysis
SO CURRENT GENOMICS
LA English
DT Article
DE Array CGH; copy number analysis; cancer; tumor suppressor genes
ID ARRAY-CGH DATA; RECESSIVE JUVENILE PARKINSONISM; NUCLEOTIDE POLYMORPHISM
ARRAYS; ACUTE LYMPHOBLASTIC-LEUKEMIA; METASTATIC BREAST-CANCER;
HOMOZYGOUS DELETIONS; WILMS-TUMOR; LUNG-CANCER; OLIGONUCLEOTIDE ARRAYS;
PANCREATIC-CARCINOMA
AB Classical tumor suppressor gene discovery has largely involved linkage analysis and loss-of-heterozygosity (LOH) screens, followed by detailed mapping of relatively large chromosomal regions. Subsequent efforts made use of genome-wide PCR-based methods to detect rare homozygous deletions. More recently, high-resolution genomic arrays have been applied to cancer gene discovery. However, accurate characterization of regions of genomic loss is particularly challenging due to sample heterogeneity, the small size of deleted regions and the high frequency of germline copy number polymorphisms. Here, we review the application of genome-wide copy number analysis to the specific problem of identifying tumor suppressor genes.
C1 [Settleman, Jeff] Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02129 USA.
[Settleman, Jeff] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
RP Settleman, J (reprint author), Massachusetts Gen Hosp, Ctr Canc, 149 13th St, Charlestown, MA 02129 USA.
EM settleman@helix.mgh.harvard.edu
FU MGH Tosteson Postdoctoral Fellowship
FX The authors wish to thank Miguel N. Rivera for critical reading of the
manuscript. S. M. Rothenberg is supported by the MGH Tosteson
Postdoctoral Fellowship.
NR 85
TC 9
Z9 9
U1 0
U2 2
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-2029
J9 CURR GENOMICS
JI Curr. Genomics
PD AUG
PY 2010
VL 11
IS 5
BP 297
EP 310
PG 14
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 632XV
UT WOS:000280463800001
PM 21286308
ER
PT J
AU Jung, HJ
Yang, MZ
Kwon, KH
Yenari, MA
Choi, YJ
Lee, WT
Park, KA
Lee, JE
AF Jung, Hyun Joo
Yang, Mei Zi
Kwon, Ki Hyo
Yenari, Midori A.
Choi, Yoon Jung
Lee, Won Taek
Park, Kyung Ah
Lee, Jong Eun
TI Endogenous Agmatine Inhibits Cerebral Vascular Matrix Metalloproteinases
Expression by Regulating Activating Transcription Factor 3 and
Endothelial Nitric Oxide Synthesis
SO CURRENT NEUROVASCULAR RESEARCH
LA English
DT Article
DE Arginine decarboxylase; agmatine; activating transcription factor 3;
endothelial cell; matrix metalloproteinases; endothelial nitric oxide
synthase
ID BLOOD-BRAIN-BARRIER; ALPHA-INDUCED APOPTOSIS; RETINAL GANGLION-CELLS;
RAT-BRAIN; TISSUE INHIBITORS; ATF3 EXPRESSION; MULTIPLE ROLES; C-JUN;
ISCHEMIA; MATRIX-METALLOPROTEINASE-9
AB Earlier investigations from our laboratory demonstrated that the expression of matrix metalloproteinases (MMPs) was down-regulated by exogenously administered agmatine against ischemia-like injuries in the murine brain capillary endothelial (bEnd.3) cells. In our present study, we intended to investigate the mechanism involved in the inhibition of MMPs in bEnd.3 cells infected with retroviral containing human arginine decarboxylase (hADC) gene which can synthesize agmatine endogenously (ADC Delta bEnd.3 cells). The ADC Delta bEnd.3 cells were subjected to oxygen glucose deprivation (OGD, 6 hrs) with reperfusion (18 hrs). High performance liquid chromatography (HPLC) analysis revealed the high levels of agmatine in the ADC Delta bEnd.3 cells compared to other experimental groups. The results demonstrated significant decrease in cell death and increase in the nitric oxide (NO) production in the ADC Delta bEnd.3 cells. The increased expression of MMP-2 and MMP-9, and decreased expression of endothelial nitric oxide synthase (eNOS) by ischemic injury was attenuated in ADC Delta bEnd.3 cells. Moreover, the expression of activating transcription factor 3 (ATF3) was increased significantly in ADC Delta bEnd.3 cells. In addition, the suppression of the MMP-2 and MMP-9 expression in ADC Delta bEnd.3 cells was prevented with ATF3 small interfering RNA (siRNA) treatment. These results suggest that the endogenous agmatine in ADC Delta bEnd.3 cells inhibits the MMPs expression mediated via the regulation of eNOS, NO and ATF3.
C1 [Jung, Hyun Joo; Kwon, Ki Hyo; Choi, Yoon Jung; Lee, Won Taek; Park, Kyung Ah; Lee, Jong Eun] Yonsei Univ, Coll Med, Dept Anat, Seoul 120752, South Korea.
[Jung, Hyun Joo; Yang, Mei Zi; Lee, Jong Eun] Yonsei Univ, Coll Med, BK Project Med Sci 21, Seoul 120752, South Korea.
[Yang, Mei Zi] Binzhou Med Univ, Yantai 264003, Peoples R China.
[Yenari, Midori A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Yenari, Midori A.] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Lee, JE (reprint author), Yonsei Univ, Coll Med, Dept Anat, 134 Shinchon Dong, Seoul 120752, South Korea.
EM jelee@yumc.yonsei.ac.kr
OI Lee, Jong Eun/0000-0001-6203-7413
FU Korea government (MEST) [2009-0052626]
FX This work was supported by the Korea Science and Engineering Foundation
(KOSEF) grant funded by the Korea government (MEST) (No. 2009-0052626).
NR 60
TC 13
Z9 13
U1 0
U2 3
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1567-2026
J9 CURR NEUROVASC RES
JI Curr. Neurovasc. Res.
PD AUG
PY 2010
VL 7
IS 3
BP 201
EP 212
PG 12
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 633MG
UT WOS:000280506500004
PM 20560878
ER
PT J
AU Beerman, I
Maloney, WJ
Weissmann, IL
Rossi, DJ
AF Beerman, Isabel
Maloney, William J.
Weissmann, Irving L.
Rossi, Derrick J.
TI Stem cells and the aging hematopoietic system
SO CURRENT OPINION IN IMMUNOLOGY
LA English
DT Review
ID AGE-RELATED-CHANGES; MYELODYSPLASTIC SYNDROMES; DISEASE PROGRESSION;
BONE-MARROW; DNA-REPAIR; DIFFERENTIATION; GENE; TRANSPLANTATION;
METHYLATION; MECHANISM
AB Advancing age is accompanied by a number of clinically significant conditions arising in the hematopoietic system that include: diminution and decreased competence of the adaptive immune system, elevated incidence of certain autoimmune diseases, increased hematological malignancies, and elevated incidence of age-associated anemia. As with most tissues, the aged hematopoietic system also exhibits a reduced capacity to regenerate and return to normal homeostasis after injury or stress. Evidence suggests age-dependent functional alterations within the hematopoietic stem cell compartment significantly contribute to many of these pathophysiologies. Recent developments have shed light on how aging of the hematopoietic stem cell compartment contributes to hematopoietic decline through diverse mechanisms.
C1 [Beerman, Isabel; Rossi, Derrick J.] Harvard Univ, Dept Pathol,Childrens Hosp Boston, Harvard Stem Cell Inst, Immune Dis Inst,Program Cellular & Mol Med, Boston, MA 02115 USA.
[Maloney, William J.] Stanford Univ, Orthopaed Res Labs, Dept Orthopaed Surg, Sch Med, Stanford, CA 94305 USA.
[Weissmann, Irving L.] Stanford Univ, Stanford Inst Stem Cell Biol & Regenerat Med, Ctr Canc, Stanford, CA 94305 USA.
[Weissmann, Irving L.] Stanford Univ, Dept Pathol, Sch Med, Stanford, CA 94305 USA.
RP Beerman, I (reprint author), Harvard Univ, Dept Pathol,Childrens Hosp Boston, Harvard Stem Cell Inst, Immune Dis Inst,Program Cellular & Mol Med, 200 Longwood Ave,Warren Alpert Bldg,Room 253, Boston, MA 02115 USA.
EM beerman@idi.harvard.edu
NR 50
TC 68
Z9 71
U1 0
U2 11
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0952-7915
EI 1879-0372
J9 CURR OPIN IMMUNOL
JI Curr. Opin. Immunol.
PD AUG
PY 2010
VL 22
IS 4
BP 500
EP 506
DI 10.1016/j.coi.2010.06.007
PG 7
WC Immunology
SC Immunology
GA 645MH
UT WOS:000281462800013
PM 20650622
ER
PT J
AU Chung, RJ
Burke, PJ
Goodman, E
AF Chung, Richard J.
Burke, Pamela J.
Goodman, Elizabeth
TI Firm foundations: strength-based approaches to adolescent chronic
disease
SO CURRENT OPINION IN PEDIATRICS
LA English
DT Review
DE adolescents; chronic disease; motivational interviewing; strength-based
approach
ID RANDOMIZED CONTROLLED-TRIAL; HEALTH-CARE SETTINGS; YOUTH DEVELOPMENT;
MOTIVATIONAL-INTERVENTION; PHYSICAL-ACTIVITY; RISK; PREVENTION;
OUTCOMES; PROGRAM; OBESITY
AB Purpose of review
Chronic disease management is an increasingly important aspect of caring for adolescents. Strength-based approaches hold tremendous promise in the face of current challenges. Recent clinical innovations and research findings that provide evidence of the efficacy of strength-based approaches and represent a fundamental evolution in the clinical approach to adolescent care are reviewed. Recent findings
Resilience and positive youth development are important conceptual frameworks in adolescent health, which have recently been brought into the clinic setting in the form of the strength-based approach to care. In parallel, studies of motivational interviewing, a strength-based technique with known efficacy in behavioral change, have begun to demonstrate clinical efficacy in various adolescent chronic disease applications. The coupling of a strength-based approach with motivational interviewing holds promise for not only modifying end behaviors but also helping teens to develop strengths and assets to promote general well-being and healthy development. This distinction in goals might be described as the difference between being transiently problem-free and durably problem-resistant.
Summary
Strength-based approaches, including motivational interviewing, hold tremendous potential for equipping providers to address the rapidly increasing burden of chronic disease in adolescents.
C1 [Chung, Richard J.; Burke, Pamela J.] Harvard Univ, Div Adolescent Young Adult Med, Childrens Hosp Boston, Sch Med,Dept Med, Boston, MA 02115 USA.
[Goodman, Elizabeth] MassGen Hosp Children, Ctr Child & Adolescent Hlth Policy, Boston, MA USA.
RP Chung, RJ (reprint author), Harvard Univ, Div Adolescent Young Adult Med, Childrens Hosp Boston, Sch Med,Dept Med, 300 Longwood Ave, Boston, MA 02115 USA.
EM richard.chung@childrens.harvard.edu
OI Goodman, Elizabeth/0000-0002-9640-9884
FU Maternal and Child Health Bureau, Health Resources and Services
Administration [T71MC00009]
FX Supported in part by the Leadership Education in Adolescent Health
Training grant no. T71MC00009 from the Maternal and Child Health Bureau,
Health Resources and Services Administration.
NR 52
TC 8
Z9 8
U1 1
U2 18
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8703
J9 CURR OPIN PEDIATR
JI CURR. OPIN. PEDIATR.
PD AUG
PY 2010
VL 22
IS 4
BP 389
EP 397
DI 10.1097/MOP.0b013e32833a468e
PG 9
WC Pediatrics
SC Pediatrics
GA 625QW
UT WOS:000279911100002
PM 20489640
ER
PT J
AU Borus, JS
Laffel, L
AF Borus, Joshua S.
Laffel, Lori
TI Adherence challenges in the management of type 1 diabetes in
adolescents: prevention and intervention
SO CURRENT OPINION IN PEDIATRICS
LA English
DT Review
DE adherence; adolescent; motivational interviewing; type 1 diabetes
ID RANDOMIZED CONTROLLED-TRIAL; POOR GLYCEMIC CONTROL; SELF-CARE; SOCIAL
SUPPORT; BLOOD-GLUCOSE; MEDICATION ADHERENCE; DEPRESSIVE SYMPTOMS;
INTENSIVE TREATMENT; METABOLIC-CONTROL; NATURAL-HISTORY
AB Purpose of review
Despite the availability of effective therapies, adolescents with type 1 diabetes demonstrate poorer adherence to treatment regimens compared with other pediatric age groups. Nonadherence is tightly linked to suboptimal glycemic control, increasing morbidity, and risk for premature mortality. This article will review barriers to adherence and discuss interventions that have shown promise in improving outcomes for this population.
Recent findings
Adolescents face numerous obstacles to adherence, including developmental behaviors, flux in family dynamics, and perceived social pressures, which compound the relative insulin resistance brought on by pubertal physiology. Some successful interventions have relied on encouraging nonjudgmental family support in the daily tasks of blood glucose monitoring and insulin administration. Other interventions overcome these barriers through the use of motivational interviewing and problem-solving techniques, flexibility in dietary recommendations, and extending provider outreach and support with technology.
Summary
Effective interventions build on teens' internal and external supports (family, technology, and internal motivation) in order to simplify their management of diabetes and provide opportunities for the teens to share the burdens of care. Although such strategies help to minimize the demands placed upon teens with diabetes, suboptimal glycemic control will likely persist for the majority of adolescents until technological breakthroughs allow for automated insulin delivery in closed loop systems.
C1 [Borus, Joshua S.] Harvard Univ, Sch Med, Div Adolescent Young Adult Med, Childrens Hosp Boston,Dept Med, Boston, MA 02115 USA.
[Laffel, Lori] Harvard Univ, Sch Med, Pediat Adolescent & Young Adult Sect, Genet & Epidemiol Sect,Joslin Diabet Ctr, Boston, MA 02115 USA.
RP Borus, JS (reprint author), Harvard Univ, Sch Med, Div Adolescent Young Adult Med, Childrens Hosp Boston,Dept Med, 300 Longwood Ave, Boston, MA 02115 USA.
EM joshua.borus@childrens.harvard.edu
RI Hanghoj, Signe/E-2440-2012
FU Maternal and Child Health Bureau, Health Resources and Services
Administration [T71MC00009]; National Institute of Diabetes, Digestive
and Kidney Diseases [K12 DK6369605, P30DK036836]; Charles H. Hood
Foundation; Maria Griffin Drury Pediatric Fund; Katherine Adler Astrove
Youth Education Fund
FX Supported in part by the Leadership Education in Adolescent Health
training grant no. T71MC00009 from the Maternal and Child Health Bureau,
Health Resources and Services Administration. Other supports, K12
DK6369605 and P30DK036836, were from the National Institute of Diabetes,
Digestive and Kidney Diseases; the Charles H. Hood Foundation; the Maria
Griffin Drury Pediatric Fund; and the Katherine Adler Astrove Youth
Education Fund.
NR 52
TC 53
Z9 54
U1 7
U2 30
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8703
EI 1531-698X
J9 CURR OPIN PEDIATR
JI CURR. OPIN. PEDIATR.
PD AUG
PY 2010
VL 22
IS 4
BP 405
EP 411
DI 10.1097/MOP.0b013e32833a46a7
PG 7
WC Pediatrics
SC Pediatrics
GA 625QW
UT WOS:000279911100004
PM 20489639
ER
PT J
AU Cypess, AM
Kahn, CR
AF Cypess, Aaron M.
Kahn, C. Ronald
TI The role and importance of brown adipose tissue in energy homeostasis
SO CURRENT OPINION IN PEDIATRICS
LA English
DT Review
DE brown adipose tissue; energy balance; PET-computed tomography;
uncoupling protein 1
ID MITOCHONDRIAL UNCOUPLING PROTEIN; INDUCED THERMOGENESIS; ADULT HUMANS;
BETA(3)-ADRENOCEPTOR AGONIST; NONSHIVERING THERMOGENESIS; F-18-FDG
PET/CT; WHITE FAT; COLD; OBESITY; ADIPOCYTES
AB Purpose of review
Children and adults have two major types of adipocytes, which represent the predominant cells in white adipose tissue, which is involved in energy storage, and brown adipose tissue (BAT), which is responsible for thermogenesis and energy expenditure. This review discusses BAT physiology and evaluates the recent discoveries regarding its development, identification, and function.
Recent findings
Last year, multiple independent research teams using combined PET and computed tomography imaging, immunohistochemistry, and gene and protein expression have proven conclusively that adult humans have functional BAT. In parallel, basic studies defined BAT origins, its transcriptional regulation, and the role of hormones in BAT growth and activation. These methods have begun to be applied to children to understand pediatric BAT anatomy and physiology.
Summary
Adult humans have functional BAT, which plays a role in energy balance. BAT is more prevalent in children, suggesting an even greater physiological role than that seen in adults. Future studies will identify safe ways to quantify BAT mass and activity and which interventions might be used to increase BAT mass, thermogenesis, or both to treat obesity.
C1 [Cypess, Aaron M.; Kahn, C. Ronald] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02215 USA.
RP Kahn, CR (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, 1 Joslin Pl, Boston, MA 02215 USA.
EM c.ronald.kahn@joslin.harvard.edu
FU Eli Lilly Foundation; National Institutes of Health (NIH) [DK082659,
DK046200, DK081604, DK087317, RR025757]; National Institute of Diabetes
and Digestive and Kidney Diseases (NIDDK) [P30 DK036836]
FX This work was supported in part by the Eli Lilly Foundation and National
Institutes of Health (NIH) grant numbers DK082659 (to C.R.K.), DK046200,
DK081604, DK087317, RR025757 (to A.M.C.), and P30 DK036836 from the
National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK). The content is solely the responsibility of the authors and
does not necessarily represent the official views of the National NIDDK
or the NIH.
NR 65
TC 25
Z9 28
U1 1
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-8703
J9 CURR OPIN PEDIATR
JI CURR. OPIN. PEDIATR.
PD AUG
PY 2010
VL 22
IS 4
BP 478
EP 484
DI 10.1097/MOP.0b013e32833a8d6e
PG 7
WC Pediatrics
SC Pediatrics
GA 625QW
UT WOS:000279911100015
PM 20489634
ER
PT J
AU Tseng, KAS
Beane, WS
Lemire, JM
Masi, A
Levin, M
AF Tseng, Kelly Ai-Sun
Beane, Wendy S.
Lemire, Joan M.
Masi, Alessio
Levin, Michael
TI Na-v-mediated sodium transport is required for vertebrate appendage
regeneration
SO DEVELOPMENTAL BIOLOGY
LA English
DT Meeting Abstract
CT 69th Annual Meeting of the
Society-for-Developmental-Biology/Japanese-Society-of-Developmental-Biol
ogists
CY AUG 05-09, 2010
CL Albuquerque, NM
SP Soc Dev Biol, Japanese Soc Dev Biologists
C1 [Tseng, Kelly Ai-Sun; Beane, Wendy S.; Lemire, Joan M.; Levin, Michael] Tufts Univ, Ctr Reg & Dev Biol, Medford, MA 02155 USA.
[Masi, Alessio; Levin, Michael] Forsyth Inst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0012-1606
J9 DEV BIOL
JI Dev. Biol.
PD AUG 1
PY 2010
VL 344
IS 1
MA 369
BP 519
EP 519
DI 10.1016/j.ydbio.2010.05.376
PG 1
WC Developmental Biology
SC Developmental Biology
GA 632LO
UT WOS:000280426400393
ER
PT J
AU Horton, ES
Silberman, C
Davis, KL
Berria, R
AF Horton, Edward S.
Silberman, Cheryl
Davis, Keith L.
Berria, Rachele
TI Weight Loss, Glycemic Control, and Changes in Cardiovascular Biomarkers
in Patients With Type 2 Diabetes Receiving Incretin Therapies or Insulin
in a Large Cohort Database
SO DIABETES CARE
LA English
DT Article
ID DIPEPTIDYL PEPTIDASE-4 INHIBITOR; DISEASE RISK-FACTORS; EXENATIDE
TREATMENT; HEPATIC BIOMARKERS; INTERIM ANALYSIS; OBESITY; METFORMIN;
INDIVIDUALS; SITAGLIPTIN; PREVENTION
AB OBJECTIVE Weight loss in patients with type 2 diabetes can improve glycemic control, lower blood pressure, and improve dyslipidemia. Glucagon-like peptide (GLP-1) receptor agonists are associated with weight loss and have potentially beneficial effects on cardiovascular risk biomarkers; however, there is limited information to indicate whether these effects remain outside of clinical trials.
RESEARCH DESIGN AND METHODS Medical records from the General Electric Centricity research database were analyzed retrospectively to evaluate the relationship between weight loss and glycemic control and changes in blood pressure and lipids in patients with type 2 diabetes initiating therapy with exenatide, sitagliptin, or insulin. Baseline and follow-up (90-365 days after the index date) for weight, A1C, fasting blood glucose (FBG), blood pressure, triglycerides, and LDL, HDL, and total cholesterol were assessed.
RESULTS A total of 6,280, 5,861, and 32,398 patients receiving exenatide, sitagliptin, or insulin, respectively, were included in the analysis. Exenatide-treated patients lost a mean SD of 3.0 +/- 7.33 kg, sitagliptin-treated patients lost 1.1 +/- 5.39 kg, and insulin-treated patients gained 0.6 +/- 9.49 kg. There was a significant association between weight loss and a reduction in A1C and FBG with exenatide only and a reduction in blood pressure for all therapies. Weight loss was associated with some improvements in lipids, primarily in the GLP-1 receptor agonist group, with little association in the insulin group.
CONCLUSIONS Weight reduction with GLP-1 receptor agonists was associated with a shift toward a more favorable cardiovascular risk profile. Outcome trials are needed to determine whether improvement in biomarkers translates into a reduction in cardiovascular events in patients with type 2 diabetes.
C1 [Horton, Edward S.] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Silberman, Cheryl; Berria, Rachele] Roche Labs, Nutley, NJ USA.
[Davis, Keith L.] RTI Hlth Solut, Res Triangle Pk, NC USA.
RP Horton, ES (reprint author), Joslin Diabet Ctr, Boston, MA 02215 USA.
EM edward.horton@joslin.harvard.edu
FU Roche; Amylin; Eli Lilly
FX This research was supported by Roche. Editorial assistance was provided
by Susan Sutch, PharmD, of Evidence Scientific Solutions, which was
funded by Roche.; E.S.H. has research grants from Amylin and Eli Lilly
and serves on advisory boards or is a consultant for Abbott,
AstraZeneca, Bristol Myers-Squibb, Daiichi-Sankyo, Medtronic, Merck,
Metabasis, Novartis, Roche, Sanofi-Aventis, Takeda, and Tethys. C.S. is
an employee and R.B. was an employee of Roche Laboratories at the time
of the research and writing of the manuscript, which is developing a
GLP-1 receptor agonist. K.L.D. is an employee of RTI, which was paid by
Roche to conduct this research. No other potential conflicts of interest
to this study were reported.
NR 21
TC 75
Z9 84
U1 0
U2 5
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 AUG
PY 2010
VL 33
IS 8
BP 1759
EP 1765
DI 10.2337/dc09-2062
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 645AF
UT WOS:000281422600014
PM 20460445
ER
PT J
AU Borg, R
Kuenen, JC
Carstensen, B
Zheng, H
Nathan, DM
Heine, RJ
Nerup, J
Borch-Johnsen, K
Witte, DR
AF Borg, R.
Kuenen, J. C.
Carstensen, B.
Zheng, H.
Nathan, D. M.
Heine, R. J.
Nerup, J.
Borch-Johnsen, K.
Witte, D. R.
CA ADAG Study Grp
TI Real-life glycaemic profiles in non-diabetic individuals with low
fasting glucose and normal HbA(1c): the A1C-Derived Average Glucose
(ADAG) study
SO DIABETOLOGIA
LA English
DT Article
DE Continuous glucose monitoring; Glucose monitoring; Glycaemia in healthy
individuals; Non-diabetic glucose exposure; Normoglycaemia
ID TOLERANCE
AB Real-life glycaemic profiles of healthy individuals are poorly studied. Our aim was to analyse to what extent individuals without diabetes exceed OGTT thresholds for impaired glucose tolerance (IGT) and diabetes.
In the A1C-Derived Average Glucose (ADAG) study, 80 participants without diabetes completed an intensive glucose monitoring period of 12 weeks. From these data, we calculated the average 24 h glucose exposure as time spent above different plasma glucose thresholds. We also derived indices of postprandial glucose levels, glucose variability and HbA(1c).
We found that 93% of participants reached glucose concentrations above the IGT threshold of 7.8 mmol/l and spent a median of 26 min/day above this level during continuous glucose monitoring. Eight individuals (10%) spent more than 2 h in the IGT range. They had higher HbA(1c), fasting plasma glucose (FPG), age and BMI than those who did not. Seven participants (9%) reached glucose concentrations above 11.1 mmol/l during monitoring.
Even though the non-diabetic individuals monitored in the ADAG study were selected on the basis of a very low level of baseline FPG, 10% of these spent a considerable amount of time at glucose levels considered to be 'prediabetic' or indicating IGT. This highlights the fact that exposure to moderately elevated glucose levels remains under-appreciated when individuals are classified on the basis of isolated glucose measurements.
C1 [Borg, R.; Carstensen, B.; Nerup, J.; Borch-Johnsen, K.; Witte, D. R.] Steno Diabet Ctr, DK-2820 Gentofte, Denmark.
[Kuenen, J. C.; Heine, R. J.] Vrije Univ Amsterdam Med Ctr, Amsterdam, Netherlands.
[Heine, R. J.] Eli Lilly & Co, Indianapolis, IN 46285 USA.
[Zheng, H.; Nathan, D. M.] Massachusetts Gen Hosp, Ctr Diabet, Boston, MA 02114 USA.
[Zheng, H.; Nathan, D. M.] Massachusetts Gen Hosp, Dept Biostat, Boston, MA 02114 USA.
[Zheng, H.; Nathan, D. M.] Harvard Univ, Sch Med, Boston, MA USA.
RP Borg, R (reprint author), Steno Diabet Ctr, Niels Steensens Vej 2-4, DK-2820 Gentofte, Denmark.
EM RBrg@steno.dk
RI Witte, Daniel/C-1722-2008
OI Witte, Daniel/0000-0002-0769-2922
FU American Diabetes Association; European Association; Abbott Diabetes
Care; Bayer Healthcare; GlaxoSmithKline; sanofi-aventis Netherlands;
Merck; Lifescan; Medtronic Minimed; Sehested Hansen Foundation; Clinical
Development Foundation at Steno Diabetes Center; Danish Diabetes
Association
FX The ADAG study was supported by research grants from the American
Diabetes Association and the European Association for the Study of
Diabetes. Financial support was also provided by Abbott Diabetes Care,
Bayer Healthcare, GlaxoSmithKline, sanofi-aventis Netherlands, Merck,
Lifescan and Medtronic Minimed. Supplies and equipment were provided by
Medtronic Minimed, Lifescan and HemoCue.; The Steno substudy was
supported by research grants from the Sehested Hansen Foundation, the
Clinical Development Foundation at Steno Diabetes Center and the Danish
Diabetes Association.
NR 6
TC 15
Z9 20
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD AUG
PY 2010
VL 53
IS 8
BP 1608
EP 1611
DI 10.1007/s00125-010-1741-9
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 616FG
UT WOS:000279193800011
PM 20396998
ER
PT J
AU Gianani, R
Campbell-Thompson, M
Sarkar, SA
Wasserfall, C
Pugliese, A
Solis, JM
Kent, SC
Hering, BJ
West, E
Steck, A
Bonner-Weir, S
Atkinson, MA
Coppieters, K
von Herrath, M
Eisenbarth, GS
AF Gianani, R.
Campbell-Thompson, M.
Sarkar, S. A.
Wasserfall, C.
Pugliese, A.
Solis, J. M.
Kent, S. C.
Hering, B. J.
West, E.
Steck, A.
Bonner-Weir, S.
Atkinson, M. A.
Coppieters, K.
von Herrath, M.
Eisenbarth, G. S.
TI Dimorphic histopathology of long-standing childhood-onset diabetes (vol
53, pg 690, 2010)
SO DIABETOLOGIA
LA English
DT Correction
C1 [Gianani, R.; Sarkar, S. A.; Solis, J. M.; West, E.; Steck, A.; Eisenbarth, G. S.] Univ Colorado Denver, Barbara Davis Ctr Childhood Diabet, Aurora, CO 80055 USA.
[Campbell-Thompson, M.; Wasserfall, C.; Atkinson, M. A.] Univ Florida, Dept Pathol, Gainesville, FL 32611 USA.
[Pugliese, A.] Diabet Res Inst, Miami, FL USA.
[Kent, S. C.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Neurol Dis, Boston, MA 02115 USA.
[Hering, B. J.] Univ Minnesota, Schulze Diabet Inst, Minneapolis, MN USA.
[Bonner-Weir, S.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Coppieters, K.; von Herrath, M.] La Jolla Inst Allergol & Immunol, La Jolla, CA USA.
RP Gianani, R (reprint author), Univ Colorado Denver, Barbara Davis Ctr Childhood Diabet, 1775 Aurora Court, Aurora, CO 80055 USA.
EM roberto.gianani@ucdenver.edu
RI wasserfall, clive/J-9078-2012
OI wasserfall, clive/0000-0002-3522-8932
NR 1
TC 1
Z9 1
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD AUG
PY 2010
VL 53
IS 8
BP 1811
EP 1812
DI 10.1007/s00125-010-1769-x
PG 2
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 616FG
UT WOS:000279193800035
ER
PT J
AU Markland, AD
Greer, WJ
Vogt, A
Redden, DT
Goode, PS
Burgio, KL
Richter, HE
AF Markland, Alayne D.
Greer, W. Jerod
Vogt, Alicia
Redden, David T.
Goode, Patricia S.
Burgio, Kathryn L.
Richter, Holly E.
TI Factors Impacting Quality of Life in Women With Fecal Incontinence
SO DISEASES OF THE COLON & RECTUM
LA English
DT Article
DE Bowel symptoms; Fecal incontinence; Quality of life; Urinary
incontinence; Women
ID URINARY-INCONTINENCE; ANAL INCONTINENCE; SEVERITY INDEX; RISK-FACTORS;
PREVALENCE; COMMUNITY; ADULTS; OLDER; SYMPTOMS; RELIABILITY
AB PURPOSE: The aim of this study was to characterize differences in health-related quality of life among women presenting for treatment of fecal incontinence.
METHODS: Among 155 women presenting for treatment of fecal incontinence in a specialty clinic, validated questionnaires measured impact on quality of life (Modified Manchester Health Questionnaire) and severity (the Fecal Incontinence Severity Index). Bowel symptoms, including frequency, urgency, and stool consistency, were ascertained. Comorbid diseases were self-reported. Linear regression models were constructed from significant univariate variables to examine differences observed in quality of life scores.
RESULTS: The average age was 58.7 +/- 11.5 years, with no differences found in quality of life scores according to race, body mass index, or number of vaginal deliveries (P > .05). Younger age, increased urinary incontinence symptoms, prior cholecystectomy, prior hysterectomy, and severity of bowel symptoms correlated with a negative impact on quality of life in univariate analysis (P < .05). Average severity scores were 30.5 +/- 13.7, with moderate correlation seen with increasing severity and quality of life scores (R(2) = 0.60). After controlling for severity, women had increased quality of life scores with more bowel urgency (15 points; 95% CI, 8.1-21.2), harder stool consistency (10 points; 95% CI, 3.8-16.3), and prior hysterectomy (9 points; 95% CI, 2.7-15.4).
CONCLUSION: Bowel symptoms and having undergone a hysterectomy had the greatest negative impact on quality of life in women seeking treatment for fecal incontinence. Targeting individualized treatments to improve bowel symptoms may improve quality of life for women with fecal incontinence.
C1 [Markland, Alayne D.; Redden, David T.; Goode, Patricia S.; Burgio, Kathryn L.] Birmingham Atlanta Geriatr Res Educ & Clin Ctr, Dept Vet Affairs Med Ctr, Birmingham, AL USA.
[Markland, Alayne D.; Goode, Patricia S.; Burgio, Kathryn L.] Univ Alabama, Dept Med, Div Gerontol Geriatr & Palliat Care, Birmingham, AL 35294 USA.
[Greer, W. Jerod; Vogt, Alicia; Richter, Holly E.] Univ Alabama, Dept Obstet & Gynecol, Div Womens Pelv Med & Reconstruct Surg, Birmingham, AL 35294 USA.
[Redden, David T.] Univ Alabama, Birmingham Sch Publ Hlth, Birmingham, AL USA.
RP Markland, AD (reprint author), Birmingham VA Med Ctr, GRECC 11G, 700 19th St S, Birmingham, AL 35233 USA.
EM amarkland@aging.uab.edu
OI Markland, Alayne/0000-0002-6567-6744
FU National Institutes of Health [K24DK068389-03]; Veterans Health
Administration [CDA-2]; Hartford/Southeast Center of Excellence in
Geriatric Medicine
FX This work was supported by National Institutes of Health grant
K24DK068389-03 to Dr Richter; Veterans Health Administration Career
Development Award (CDA-2) to Dr Markland; and a Hartford/Southeast
Center of Excellence in Geriatric Medicine Grant to Dr Markland.
NR 27
TC 11
Z9 11
U1 0
U2 1
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 AUG
PY 2010
VL 53
IS 8
BP 1148
EP 1154
DI 10.1007/DCR.0b013e3181d5da6c
PG 7
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA 625DF
UT WOS:000279872600009
PM 20628278
ER
PT J
AU Hayeck, TJ
Kong, CY
Spechler, SJ
Gazelle, GS
Hur, C
AF Hayeck, T. J.
Kong, C. Y.
Spechler, S. J.
Gazelle, G. S.
Hur, C.
TI The prevalence of Barrett's esophagus in the US: estimates from a
simulation model confirmed by SEER data
SO DISEASES OF THE ESOPHAGUS
LA English
DT Article
DE adenocarcinoma; Barrett's esophagus; computer models; computer
simulation; esophageal cancer; SEER program
ID GASTROESOPHAGEAL-REFLUX DISEASE; CLINICAL SPECTRUM; GASTRIC CARDIA;
ADENOCARCINOMA; POPULATION; RISK; SYMPTOMS; CANCER; SURVEILLANCE; TRENDS
AB P>Barrett's esophagus (BE) is the precursor and the biggest risk factor for esophageal adenocarcinoma (EAC), the solid cancer with the fastest rising incidence in the US and western world. Current strategies to decrease morbidity and mortality from EAC have focused on identifying and surveying patients with BE using upper endoscopy. An accurate estimate of the number of patients with BE in the population is important to inform public health policy and to prioritize resources for potential screening and management programs. However, the true prevalence of BE is difficult to ascertain because the condition frequently is symptomatically silent, and the numerous clinical studies that have analyzed BE prevalence have produced a wide range of estimates. The aim of this study was to use a computer simulation disease model of EAC to determine the estimates for BE prevalence that best align with US Surveillance Epidemiology and End Results (SEER) cancer registry data. A previously developed mathematical model of EAC was modified to perform this analysis. The model consists of six health states: normal, gastroesophageal reflux disease (GERD), BE, undetected cancer, detected cancer, and death. Published literature regarding the transition rates between these states were used to provide boundaries. During the one million computer simulations that were performed, these transition rates were systematically varied, producing differing prevalences for the numerous health states. Two filters were sequentially applied to select out superior simulations that were most consistent with clinical data. First, among these million simulations, the 1000 that best reproduced SEER cancer incidence data were selected. Next, of those 1000 best simulations, the 100 with an overall calculated BE to Detected Cancer rates closest to published estimates were selected. Finally, the prevalence of BE in the final set of best 100 simulations was analyzed. We present histogram data depicting BE prevalences for all one million simulations, the 1000 simulations that best approximate SEER data, and the final set of 100 simulations. Using the best 100 simulations, we estimate the prevalence of BE to be 5.6% (5.49-5.70%). Using our model, an estimated prevalence for BE in the general population of 5.6% (5.49-5.70%) accurately predicts incidence rates for EAC reported to the US SEER cancer registry. Future clinical studies are needed to confirm our estimate.
C1 [Hayeck, T. J.; Kong, C. Y.; Gazelle, G. S.; Hur, C.] Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA.
[Hayeck, T. J.; Hur, C.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Kong, C. Y.; Gazelle, G. S.; Hur, C.] Harvard Univ, Sch Med, Boston, MA USA.
[Spechler, S. J.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
RP Hur, C (reprint author), Massachusetts Gen Hosp, Inst Technol Assessment, 101 Merrimac St,10th Floor, Boston, MA 02114 USA.
EM chur@mgh-ita.org
OI Hur, Chin/0000-0002-2819-7576
FU NIH/NCI [CA107060]
FX NIH/NCI Grant CA107060 (C.H.). No potential financial conflicts to
report.
NR 34
TC 46
Z9 48
U1 2
U2 6
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1120-8694
J9 DIS ESOPHAGUS
JI Dis. Esophagus
PD AUG
PY 2010
VL 23
IS 6
BP 451
EP 457
DI 10.1111/j.1442-2050.2010.01054.x
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 641NQ
UT WOS:000281135000003
PM 20353441
ER
PT J
AU Green, TC
Kershaw, T
Lin, HQ
Heimer, R
Goulet, JL
Kraemer, KL
Gordon, AJ
Maisto, SA
Day, NL
Bryant, K
Fiellin, DA
Justice, AC
AF Green, Traci C.
Kershaw, Trace
Lin, Haiqun
Heimer, Robert
Goulet, Joseph L.
Kraemer, Kevin L.
Gordon, Adam J.
Maisto, Steve A.
Day, Nancy L.
Bryant, Kendall
Fiellin, David A.
Justice, Amy C.
TI Patterns of drug use and abuse among aging adults with and without HIV:
A latent class analysis of a US Veteran cohort
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE Aging; Veterans; HIV; Substance-related disorders; Latent class
analysis; Illicit drugs; Cohort studies
ID ACTIVE ANTIRETROVIRAL THERAPY; SUBSTANCE USE DISORDERS; VIRUS-INFECTED
VETERANS; HEALTH-CARE UTILIZATION; NEW-YORK-CITY; DEVELOPMENTAL
TRAJECTORIES; YOUNG ADULTHOOD; UNITED-STATES; MARIJUANA USE;
OLDER-ADULTS
AB This study characterized the extent and patterns of self-reported drug use among aging adults with and without HIV, assessed differences in patterns by HIV status, and examined pattern correlates. Data derived from 6351 HIV-infected and uninfected adults enrolled in an eight-site matched cohort, the Veterans Aging Cohort Study (VACS). Using clinical variables from electronic medical records and socio-demographics, drug use consequences, and frequency of drug use from baseline surveys, we performed latent class analyses (LCA) stratified by HIV status and adjusted for clinical and socio-demographic covariates. Participants were, on average, age 50 (range 22-86), primarily male (95%) and African-American (64%). Five distinct patterns emerged: non-users, past primarily marijuana users, past multidrug users, current high consequence multidrug users, and current low consequence primarily marijuana users. HIV status strongly influenced class membership. Non-users were most prevalent among HIV uninfected (36.4%) and current high consequence multidrug users (25.5%) were most prevalent among HIV-infected. While problems of obesity marked those not currently using drugs, current users experienced higher prevalences of medical or mental health disorders. Multimorbidity was highest among past and current multidrug users. HIV-infected participants were more likely than HIV-uninfected participants to be current low consequence primarily marijuana users. In this sample, active drug use and abuse were common. HIV-infected and uninfected Veterans differed on extent and patterns of drug use and on important characteristics within identified classes. Findings have the potential to inform screening and intervention efforts in aging drug users with and without HIV. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
C1 [Green, Traci C.; Kershaw, Trace] Yale Univ, Sch Publ Hlth, Div Chron Dis Epidemiol, New Haven, CT USA.
[Green, Traci C.; Kershaw, Trace; Heimer, Robert; Goulet, Joseph L.; Fiellin, David A.; Justice, Amy C.] Yale Ctr Interdisciplinary Res AIDS, New Haven, CT USA.
[Lin, Haiqun] Yale Univ, Sch Publ Hlth, Div Biostat, New Haven, CT USA.
[Heimer, Robert] Yale Univ, Sch Publ Hlth, Div Epidemiol Microbial Dis, New Haven, CT USA.
[Goulet, Joseph L.; Justice, Amy C.] Vet Affairs Connecticut Healthcare Syst, West Haven, CT USA.
[Goulet, Joseph L.; Fiellin, David A.; Justice, Amy C.] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA.
[Kraemer, Kevin L.; Gordon, Adam J.] Univ Pittsburgh, Sch Med, Div Gen Internal Med, Ctr Res Hlth Care, Pittsburgh, PA USA.
[Gordon, Adam J.] VA Pittsburgh Healthcare Syst, Mental Illness Res Educ & Clin Ctr Comorbid VISN, Pittsburgh, PA USA.
[Gordon, Adam J.] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Maisto, Steve A.] Syracuse Univ, Dept Psychol, Ctr Hlth & Behav, Syracuse, NY USA.
[Day, Nancy L.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA.
[Bryant, Kendall] NIAAA, Bethesda, MD USA.
[Fiellin, David A.] Yale Univ, Sch Med, Investigat Med Program, New Haven, CT USA.
RP Green, TC (reprint author), 111 Plain St Bldg,Rm 111, Providence, RI 02903 USA.
EM traci.c.green@brown.edu
RI Day, Nancy/H-3171-2016;
OI Goulet, Joseph/0000-0002-0842-804X; Fiellin, David/0000-0002-4006-010X
FU National Institutes of Health, National Institute on Drug Abuse
[1F31DA023862-01A1]; National Institute on Alcohol Abuse and Alcoholism
[U10 AA 13566]; VHA Public Health Strategic Health Core Group
FX Research for this manuscript was supported by the National Institutes of
Health, National Institute on Drug Abuse grant 1F31DA023862-01A1 to TCG.
The Veterans Aging Cohort Study funded by: National Institute on Alcohol
Abuse and Alcoholism (U10 AA 13566) and VHA Public Health Strategic
Health Core Group. The funding sources had no further involvement in the
study design, data collection, analysis, writing, preparation or
decision to submit this manuscript for publication.
NR 94
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U1 2
U2 11
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0376-8716
J9 DRUG ALCOHOL DEPEN
JI Drug Alcohol Depend.
PD AUG 1
PY 2010
VL 110
IS 3
BP 208
EP 220
DI 10.1016/j.drugalcdep.2010.02.020
PG 13
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 634ZU
UT WOS:000280626200005
PM 20395074
ER
PT J
AU George, E
Becerra, L
Upadhyay, J
Schmidt, U
Borsook, D
AF George, Edward
Becerra, Lino
Upadhyay, Jaymin
Schmidt, Ulrich
Borsook, David
TI Evaluation of novel drugs using fMRI in early-phase clinical trials:
safety monitoring
SO DRUG DISCOVERY TODAY
LA English
DT Review
ID FUNCTIONAL MRI; NEURAL BASIS; EXPERIENCE; BENEFIT; FUTURE
AB A advances in functional magnetic resonance imaging (fMRI) permit the possibility of helping with dose ranging, as well as potential drug efficacy and side-effect profiles. However there are no current guidelines or standards for fMRI that meet established standards of care. Guidelines must be adopted to be used when patients are exposed to novel drugs, in particular, when immediate access to the patient is limited. When used in initial, MRI mandates certain safety standards because subjects are positioned in the magnet thereby limiting direct observation, communication or immediate access in an emergency; in testing new drugs using fMRI, we suggest that safety guidelines merit discussion and definition. This could lead to the adoption of standards. Some of these issues are unique to the application of the technology in early-phase trials.
C1 [George, Edward; Becerra, Lino; Upadhyay, Jaymin] Harvard Univ, Sch Med, McLean Hosp, Brain Imaging Ctr, Belmont, MA 02478 USA.
[George, Edward; Schmidt, Ulrich] Harvard Univ, Sch Med, McLean Hosp, Dept Anesthesia,Brain Imaging Ctr, Belmont, MA 02478 USA.
[Becerra, Lino; Borsook, David] Harvard Univ, Sch Med, Mclean & Massachusetts Gen Hosp, Dept Psychiat,Brain Imaging Ctr,McLean Hosp, Belmont, MA 02478 USA.
[Becerra, Lino; Borsook, David] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol,Brain Imaging Ctr,McLean Hosp, Belmont, MA 02478 USA.
RP George, E (reprint author), Harvard Univ, Sch Med, McLean Hosp, Brain Imaging Ctr, 115 Mill St, Belmont, MA 02478 USA.
EM edgeorge@partners.org
FU L Herlands fund for pain research; K24 NINDS [NS064050]
FX Supported by the L Herlands fund for pain research (D.B. and L.B.) and
K24 NINDS NS064050 (D.B.).
NR 23
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6446
J9 DRUG DISCOV TODAY
JI Drug Discov. Today
PD AUG
PY 2010
VL 15
IS 15-16
BP 684
EP 689
DI 10.1016/j.drudis.2010.05.008
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 641OU
UT WOS:000281138600013
PM 20553959
ER
PT J
AU Milsom, MD
Williams, DA
AF Milsom, Michael D.
Williams, David A.
TI Gaining the hard yard: pre-clinical evaluation of lentiviral-mediated
gene therapy for the treatment of beta-thalassemia
SO EMBO MOLECULAR MEDICINE
LA English
DT Editorial Material
DE gene therapy; haematopoiesis; insertional mutagenesis; lentivirus;
beta-thalassemia
ID SCID-X1
AB Gene therapy is one potential novel therapeutic avenue for the treatment of inherited monogenic disorders. Diseases of the blood are frequent targets for gene therapy because it is relatively easy to harvest haematopoietic stem cells (HSCs) from the bone marrow, genetically modify the cells ex vivo, and then re-administer the corrected cells back into the patient via intra-venous injection. In this Closeup, Milsom and Williams discuss the work of Roselli et al, who describe the pre-clinical evaluation of the treatment for beta-thalassemia in erythroid cells via the genetic correction of patient HSCs using a lentiviral vector.
C1 [Milsom, Michael D.; Williams, David A.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Milsom, Michael D.; Williams, David A.] Childrens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Milsom, Michael D.; Williams, David A.] Harvard Univ, Sch Med, Boston, MA USA.
[Williams, David A.] Harvard Stem Cell Inst, Boston, MA USA.
[Williams, David A.] Dana Farber Canc Inst, Brookline, MA USA.
RP Williams, DA (reprint author), Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
EM dawilliams@childrens.harvard.edu
NR 6
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1757-4676
J9 EMBO MOL MED
JI EMBO Mol. Med.
PD AUG
PY 2010
VL 2
IS 8
BP 291
EP 293
DI 10.1002/emmm.201000086
PG 3
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 646ER
UT WOS:000281520500002
PM 20677209
ER
PT J
AU Wang, N
Guo, LK
Rueda, BR
Tilly, JL
AF Wang, Ning
Guo, Lankai
Rueda, Bo R.
Tilly, Jonathan L.
TI Cables1 protects p63 from proteasomal degradation to ensure deletion of
cells after genotoxic stress
SO EMBO REPORTS
LA English
DT Article
DE p63; Cables1; proteasome; oocyte; apoptosis
ID MOUSE OOCYTES; C-ABL; PHOSPHORYLATION; EXPRESSION; CANCER; DEATH; MICE;
WEE1; P73
AB The p63 gene product regulates epithelial morphogenesis and female germline integrity. In this study, we show that cyclin-dependent kinase 5 and Abl enzyme substrate 1 (Cables1) interacts with the trans-activating (TA) p63 alpha isoform to protect it from proteasomal degradation. Using the female germline of Cables1-null mice as an in vivo model, we demonstrate further that oocytes lacking Cables1 exhibit lower basal levels of TAp63 alpha and reduced accumulation of phosphorylated TAp63 alpha in response to genotoxic stress. This in turn enhances the survival of these cells after ionizing radiation exposure. Thus, Cables1 modulates p63 protein stability and function during genotoxic stress.
C1 [Wang, Ning; Guo, Lankai; Rueda, Bo R.; Tilly, Jonathan L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Obstet & Gynecol,Vincent Ctr Reprod Biol, Boston, MA 02114 USA.
RP Tilly, JL (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Obstet & Gynecol,Vincent Ctr Reprod Biol, THR 901B,55 Fruit St, Boston, MA 02114 USA.
EM jtilly@partners.org
FU Massachusetts General Hospital; National Institute on Aging
[R37-AG012279]; National Institutes of Health [R01-CA098333]; Henry and
Vivian Rosenberg Philanthropic Fund; Sea Breeze Foundation; Vincent
Memorial Research Funds
FX We thank F. McKeon for TAp63 antibody and T. Ohta for helpful
discussions regarding the ubiquitination assay. N.W. is a recipient of a
Massachusetts General Hospital Fund for Medical Discovery award. This
study was supported by National Institute on Aging MERIT Award
R37-AG012279, National Institutes of Health R01-CA098333, the Henry and
Vivian Rosenberg Philanthropic Fund, the Sea Breeze Foundation and
Vincent Memorial Research Funds.
NR 26
TC 10
Z9 10
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1469-221X
J9 EMBO REP
JI EMBO Rep.
PD AUG
PY 2010
VL 11
IS 8
BP 633
EP 639
DI 10.1038/embor.2010.82
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 630YS
UT WOS:000280313400017
PM 20559324
ER
PT J
AU Ouyang, H
Quinn, J
AF Ouyang, Helen
Quinn, James
TI Diagnosis and Evaluation of Syncope in the Emergency Department
SO EMERGENCY MEDICINE CLINICS OF NORTH AMERICA
LA English
DT Article
DE Syncope; Diagnosis; Evaluation; Prognosis
ID CAROTID-SINUS SYNDROME; LONG QT SYNDROME; HYPERTROPHIC CARDIOMYOPATHY;
CLINICAL CHARACTERISTICS; ORTHOSTATIC HYPOTENSION; UNEXPLAINED SYNCOPE;
BLOOD-PRESSURE; POPULATION; RULE; MANAGEMENT
AB With a careful history, physical examination, and directed investigation, physicians can determine the likely cause of syncope in more than 50% and perhaps up to 80% of patients. Understanding the cause of syncope allows clinicians to determine the disposition of high- and low-risk patients. Patients with a potential malignant cause, such as a cardiac or neurologic condition, should be treated and admitted. Those with benign causes can be safely discharged. This article reviews the diagnosis and ED work-up of syncope, the different classifications of syncope, and prognosis The use of specific decision rules in risk stratification and syncope in the pediatric population are discussed in another article
C1 [Ouyang, Helen] Brigham & Womens Hosp, Dept Emergency Med, Boston, MA 02115 USA.
[Ouyang, Helen] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Quinn, James] Stanford Univ, Div Emergency Med, Palo Alto, CA 94304 USA.
RP Ouyang, H (reprint author), Brigham & Womens Hosp, Dept Emergency Med, 75 Francis St,Neville House, Boston, MA 02115 USA.
NR 67
TC 3
Z9 4
U1 1
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0733-8627
EI 1558-0539
J9 EMERG MED CLIN N AM
JI Emerg. Med. Clin. N. Am.
PD AUG
PY 2010
VL 28
IS 3
BP 471
EP +
DI 10.1016/j.emc.2010.03.007
PG 16
WC Emergency Medicine
SC Emergency Medicine
GA 649AN
UT WOS:000281737700005
PM 20709239
ER
PT J
AU Fugate, JMB
Gouzoules, H
Barrett, LF
AF Fugate, Jennifer M. B.
Gouzoules, Harold
Barrett, Lisa Feldman
TI Reading Chimpanzee Faces: Evidence for the Role of Verbal Labels in
Categorical Perception of Emotion
SO EMOTION
LA English
DT Article
DE facial expressions; emotion; categorical perception; verbal labeling;
expertise
ID NEWLY LEARNED FACES; FACIAL EXPRESSIONS; 12-MONTH-OLD INFANTS;
CATEGORIZATION; DISCRIMINATION; RECOGNITION; INVITATIONS; LANGUAGE;
MUSCLES; WORDS
AB Categorical perception (CP) occurs when continuously varying stimuli are perceived as belonging to discrete categories. Thereby, perceivers are more accurate at discriminating between stimuli of different categories than between stimuli within the same category (Hamad, 1987; Goldstone, 1994). The current experiments investigated whether the structural information in the face is sufficient for CP to occur. Alternatively, a perceiver's conceptual knowledge, by virtue of expertise or verbal labeling, might contribute. In two experiments, people who differed in their conceptual knowledge (in the form of expertise, Experiment 1; or verbal label learning, Experiment 2) categorized chimpanzee facial expressions. Expertise alone did not facilitate CP. Only when perceivers first explicitly learned facial expression categories with a label were they more likely to show CP. Overall, the results suggest that the structural information in the face alone is often insufficient for CP; CP is facilitated by verbal labeling.
C1 [Fugate, Jennifer M. B.; Barrett, Lisa Feldman] Boston Coll, Dept Psychol, Chestnut Hill, MA 02467 USA.
[Gouzoules, Harold] Emory Univ, Dept Psychol, Atlanta, GA 30322 USA.
[Barrett, Lisa Feldman] Massachusetts Gen Hosp, Dept Psychiat, Charlestown, MA USA.
[Barrett, Lisa Feldman] Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA USA.
RP Fugate, JMB (reprint author), Boston Coll, Dept Psychol, 140 Commonwealth Ave, Chestnut Hill, MA 02467 USA.
EM fugatej@bc.edu
FU NIH HHS [DP1 OD003312-01, DP1OD003312, DP1 OD003312]; NIMH NIH HHS [F32
MH083455]
NR 40
TC 13
Z9 14
U1 0
U2 6
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1528-3542
J9 EMOTION
JI Emotion
PD AUG
PY 2010
VL 10
IS 4
BP 544
EP 554
DI 10.1037/a0019017
PG 11
WC Psychology, Experimental
SC Psychology
GA 637PE
UT WOS:000280829700009
PM 20677871
ER
PT J
AU Guo, J
Liu, ML
Yang, DH
Bouxsein, ML
Thomas, CC
Schipani, E
Bringhurst, FR
Kronenberg, HM
AF Guo, Jun
Liu, Minlin
Yang, Dehong
Bouxsein, Mary L.
Thomas, Clare C.
Schipani, Ernestina
Bringhurst, F. Richard
Kronenberg, Henry M.
TI Phospholipase C Signaling via the Parathyroid Hormone (PTH)/PTH-Related
Peptide Receptor Is Essential for Normal Bone Responses to PTH
SO ENDOCRINOLOGY
LA English
DT Article
ID GROWTH-PLATE CHONDROCYTES; RAT OSTEOBLASTIC CELLS; PROTEIN-KINASE;
IN-VIVO; PTH/PTHRP RECEPTOR; ADENYLYL-CYCLASE; LLC-PK1 CELLS;
DIFFERENTIATION; PROLIFERATION; INTERMITTENT
AB We have previously shown that differentiation of hypertrophic chondrocytes is delayed in mice expressing a mutated PTH/PTHrP receptor (PTHR) (called DSEL here) that stimulates adenylyl cyclase normally but fails to activate phospholipase C (PLC). To better understand the role of PLC signaling via the PTHR in skeletal and mineral homeostasis, we examined these mice fed a normal or calcium-deficient diet. On a standard diet, DSEL mice displayed a modest decrease in bone mass. Remarkably, when fed a low-calcium diet or infused with PTH, DSEL mice exhibited strikingly curtailed peritrabecular stromal cell responses and attenuated new bone formation when compared with Wt mice. Attenuated in vitro colony formation was also observed in bone marrow cells derived from DSEL mice fed a low-calcium diet. Furthermore, PTH stimulated proliferation and increased mRNAs encoding cyclin D1 in primary osteoblasts derived from Wt but not from DSEL mice. Our data indicate that PLC signaling through the PTHR is required for skeletal homeostasis. (Endocrinology 151: 3502-3513, 2010)
C1 [Guo, Jun; Liu, Minlin; Yang, Dehong; Thomas, Clare C.; Schipani, Ernestina; Bringhurst, F. Richard; Kronenberg, Henry M.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Bouxsein, Mary L.] Beth Israel Deaconess Med Ctr, Orthoped Biomech Lab, Boston, MA 02215 USA.
RP Kronenberg, HM (reprint author), Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
EM hkronenberg@partners.org
FU National Institutes of Health [DK11794]
FX This work was supported by National Institutes of Health Grant DK11794
(to H.M.K.).
NR 45
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U1 2
U2 8
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD AUG
PY 2010
VL 151
IS 8
BP 3502
EP 3513
DI 10.1210/en.2009-1494
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 629CH
UT WOS:000280171100005
PM 20501677
ER
PT J
AU D'Andrea, AD
AF D'Andrea, A. D.
TI The Fanconi Anemia Pathway in DNA Interstrand Crosslink Repair
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Meeting Abstract
CT 41st Annual Meeting of Environmental-Mutagen-Society
CT 41st Annual Meeting of Complex Systems in Biology and Risk Assessment
CY OCT 23-27, 2010
CY OCT 23-27, 2010
CL Ft Worth, TX
CL Ft Worth, TX
SP Environ Mutagen Soc
SP Environ Mutagen Soc
C1 [D'Andrea, A. D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[D'Andrea, A. D.] Harvard Univ, Sch Med, Boston, MA USA.
[D'Andrea, A. D.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0893-6692
EI 1098-2280
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PD AUG
PY 2010
VL 51
IS 7
BP 687
EP 687
PG 1
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 639XE
UT WOS:000281009600014
ER
PT J
AU Price, BD
AF Price, B. D.
TI Histone Methylation The Link between Chromatin Structure and DNA Repair
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Meeting Abstract
CT 41st Annual Meeting of Environmental-Mutagen-Society
CT 41st Annual Meeting of Complex Systems in Biology and Risk Assessment
CY OCT 23-27, 2010
CY OCT 23-27, 2010
CL Ft Worth, TX
CL Ft Worth, TX
SP Environ Mutagen Soc
SP Environ Mutagen Soc
C1 [Price, B. D.] Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0893-6692
EI 1098-2280
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PD AUG
PY 2010
VL 51
IS 7
BP 699
EP 699
PG 1
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 639XE
UT WOS:000281009600062
ER
PT J
AU Leeman, BA
AF Leeman, Beth A.
TI Remote memory deficits in epilepsy and the role of failed consolidation
SO EPILEPSY & BEHAVIOR
LA English
DT Letter
C1 [Leeman, Beth A.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Leeman, Beth A.] Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA.
[Leeman, Beth A.] Harvard Univ, Sch Med, Boston, MA USA.
RP Leeman, BA (reprint author), Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
EM baleeman@partners.org
OI Macklin, Eric/0000-0003-1618-3502
NR 5
TC 0
Z9 0
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 1525-5050
J9 EPILEPSY BEHAV
JI Epilepsy Behav.
PD AUG
PY 2010
VL 18
IS 4
BP 498
EP 499
DI 10.1016/j.yebeh.2010.03.003
PG 2
WC Behavioral Sciences; Clinical Neurology; Psychiatry
SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry
GA 643ON
UT WOS:000281306600027
PM 20708577
ER
PT J
AU Roberts, JD
Davies, RW
Lubitz, SA
Thibodeau, IL
Nery, PB
Birnie, DH
Benjamin, EJ
Lemery, R
Ellinor, PT
Gollob, MH
AF Roberts, Jason D.
Davies, Robert W.
Lubitz, Steven A.
Thibodeau, Isabelle L.
Nery, Pablo B.
Birnie, David H.
Benjamin, Emelia J.
Lemery, Robert
Ellinor, Patrick T.
Gollob, Michael H.
TI Evaluation of non-synonymous NPPA single nucleotide polymorphisms in
atrial fibrillation
SO EUROPACE
LA English
DT Article
DE Atrial fibrillation; Atrial natriuretic peptide; Single nucleotide
polymorphism; Genetics
ID OF-FUNCTION MUTATION; BLOOD-PRESSURE PROGRESSION; NATRIURETIC-PEPTIDE;
FAMILIAL AGGREGATION; INCIDENT HYPERTENSION; GENE POLYMORPHISMS;
ISCHEMIC-STROKE; HEART-DISEASE; RISK-FACTOR; VARIANTS
AB Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, is an important cause of morbidity and mortality. A genetic mutation in the NPPA gene, which encodes the atrial natriuretic peptide, has been identified as the putative causative factor in a family with an autosomal dominant pattern of inheritance for AF. Two common single nucleotide polymorphisms (SNPs) in NPPA, rs5063 and rs5065, result in amino acid changes of the primary peptide and have been previously implicated in conditions associated with AF, including stroke and hypertension. Recently, the rs5063 SNP has been reported to confer an increased risk of AF development in a Chinese population. We sought to examine the associations of both rs5063 and rs5065 with AF in two separate North American cohorts of European ancestry.
Patients with early-onset AF, along with healthy controls, were recruited at the University of Ottawa Heart Institute (UOHI) and the Massachusetts General Hospital (MGH). Study participants were genotyped for rs5063 and rs5065 using a combination of restriction fragment length polymorphism analysis and DNA microarrays. The study genotyped a total of 620 AF cases and 2446 healthy controls. The UOHI arm of the study identified an odds ratio (OR) of 0.72 [95% confidence interval (CI): 0.42-1.24] for rs5063, whereas an OR of 1.33 (95% CI: 0.80-2.21) was observed in the MGH arm. The combined OR approximated unity (OR 0.99; 95% CI: 0.54-1.80). Analysis of rs5065 revealed an OR of 1.12 (95% CI: 0.84-1.48) in UOHI, 1.08 (95% CI 0.80-1.45) in MGH, and 1.10 (95% CI 0.90-1.35) when combined.
Common non-synonymous genetic variants within NPPA in these two large North American cohorts of European ancestry are not associated with the development of AF.
C1 [Roberts, Jason D.; Thibodeau, Isabelle L.; Gollob, Michael H.] Univ Ottawa, Inst Heart, Arrhythmia Res Lab, Ottawa, ON K1Y 4W7, Canada.
[Davies, Robert W.] Univ Ottawa, Inst Heart, Cardiovasc Res Methods Ctr, Ottawa, ON K1Y 4W7, Canada.
[Lubitz, Steven A.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Lubitz, Steven A.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
[Nery, Pablo B.; Birnie, David H.; Lemery, Robert; Gollob, Michael H.] Univ Ottawa, Inst Heart, Arrhythmia Serv, Ottawa, ON K1Y 4W7, Canada.
[Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
[Benjamin, Emelia J.] NHLBI, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Cardiol & Prevent Med Sect, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02118 USA.
RP Gollob, MH (reprint author), Univ Ottawa, Inst Heart, Arrhythmia Res Lab, 40 Ruskin St, Ottawa, ON K1Y 4W7, Canada.
EM mgollob@ottawaheart.ca
RI Nery, Pablo/D-1754-2011;
OI Benjamin, Emelia/0000-0003-4076-2336
FU Heart and Stroke Foundation of Ontario; Canadian Institutes of Health
Research; NIH [HL092577, RC1-HL01056, DA027021, T32HL00757]
FX This work was supported by grants from the Heart and Stroke Foundation
of Ontario and Canadian Institutes of Health Research to M.H.G. and
grants from the NIH: HL092577 to P.T.E. and E.J.B.; RC1-HL01056 to
E.J.B.; and DA027021 to P.T.E.; S.A.L. was supported by a training grant
from the NIH (T32HL00757).
NR 42
TC 13
Z9 13
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1099-5129
J9 EUROPACE
JI Europace
PD AUG
PY 2010
VL 12
IS 8
BP 1078
EP 1083
DI 10.1093/europace/euq161
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 633VV
UT WOS:000280535800009
PM 20543198
ER
PT J
AU Hildebrandt, P
Collinson, PO
Doughty, RN
Fuat, A
Gaze, DC
Gustafsson, F
Januzzi, J
Rosenberg, J
Senior, R
Richards, M
AF Hildebrandt, Per
Collinson, Paul O.
Doughty, Robert N.
Fuat, Ahmet
Gaze, David C.
Gustafsson, Finn
Januzzi, James
Rosenberg, Jens
Senior, Roxy
Richards, Mark
TI Age-dependent values of N-terminal pro-B-type natriuretic peptide are
superior to a single cut-point for ruling out suspected systolic
dysfunction in primary care(dagger)
SO EUROPEAN HEART JOURNAL
LA English
DT Article
DE Natriuretic peptides; Chronic heart failure; Diagnosis; Decision limits
ID HEART-FAILURE; PRIMARY-CARE; DIAGNOSTIC-ACCURACY; METAANALYSIS;
POPULATION; PROGNOSIS; STATEMENT; COMMUNITY; SURVIVAL; MARKER
AB The study evaluated the use of age-related decision limits for N-terminal pro-B-type natriuretic peptide (NT-proBNP), for ruling out suspected systolic dysfunction in symptomatic patients in primary care, compared with the present standards.
Data were obtained from 5508 patients from 10 studies in the UK, New Zealand, Europe, and USA. All have had NT-proBNP analysis and echocardiography. The median age was 62 years (range 18-100 years) with a prevalence of reduced left ventricular systolic function (left ventricular ejection fraction < 40%) of 18%. In a receiver operating characteristic curve analysis, overall area under the curve (AUC) was 0.89. When looking at different age groups, AUC was highest (0.95) for < 50 years, intermediate (0.90) for 50-75 years, and lowest (0.82) for > 75 years. Using optimized decision limits, sensitivity, specificity, and negative predictive values (NPVs) were: < 50 years (50 ng/L): 99.2, 57.2, and 99.7%; 50-75 years (75 ng/L): 95.9, 51.0, and 96.8%; and > 75 years (250 ng/L): 87.9, 53.7, and 92.4%, respectively. Using only a single decision value (125 ng/L for all ages) gave sensitivities of 89.1, 91.9, and 94.3%; specificities of 84.0, 69.1, and 29.3% and NPVs of 97.7, 97.6, and 93.4%. A decision value of 400 ng/L for all ages gave much lower sensitivities.
In a large population of patients in primary care, the use of age-stratified NT-proBNP decision limits considerably improves performance over current standards, with an excellent NPV for exclusion of reduced left ventricular systolic function.
C1 [Hildebrandt, Per] Glostrup Univ Hosp, Dept Cardiol & Med, Glostrup, Denmark.
[Collinson, Paul O.; Gaze, David C.] St George Hosp, Dept Chem Pathol, London, England.
[Collinson, Paul O.] St George Hosp, Dept Cardiol, London, England.
[Doughty, Robert N.] Univ Auckland, Dept Med, Fac Med & Hlth Sci, Auckland, New Zealand.
[Fuat, Ahmet] Univ Durham, Dept Cardiol, Darlington Mem Hosp, Ctr Integrated Hlth Care Res, Durham, England.
[Gustafsson, Finn] State Univ Hosp, Dept Cardiol, Copenhagen, Denmark.
[Januzzi, James] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Rosenberg, Jens] Frederiksberg Univ Hosp, Dept Cardiol & Endocrinol, Frederiksberg, Denmark.
[Senior, Roxy] Northwick Pk Hosp & Clin Res Ctr, Dept Cardiol, Middlesex, England.
[Richards, Mark] Christchurch Sch Med & Hlth Sci, Christchurch Cardioendocrine Res Grp, Christchurch, New Zealand.
RP Hildebrandt, P (reprint author), Glostrup Univ Hosp, Dept Cardiol & Med, Glostrup, Denmark.
EM p.hildebrandt@dadlnet.dk
OI Gustafsson, Finn/0000-0003-2144-341X
FU Roche Diagnostics
FX P.H., P.O.C., R.N.D., J.J., and M.R. received research support from
Roche Diagnostics.
NR 33
TC 41
Z9 42
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0195-668X
J9 EUR HEART J
JI Eur. Heart J.
PD AUG
PY 2010
VL 31
IS 15
BP 1881
EP 1889
DI 10.1093/eurheartj/ehq163
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 636CA
UT WOS:000280704300014
PM 20519241
ER
PT J
AU Hjortnaes, J
Butcher, J
Figueiredo, JL
Riccio, M
Kohler, RH
Kozloff, KM
Weissleder, R
Aikawa, E
AF Hjortnaes, Jesper
Butcher, Jonathan
Figueiredo, Jose-Luiz
Riccio, Mark
Kohler, Rainer H.
Kozloff, Kenneth M.
Weissleder, Ralph
Aikawa, Elena
TI Arterial and aortic valve calcification inversely correlates with
osteoporotic bone remodelling: a role for inflammation
SO EUROPEAN HEART JOURNAL
LA English
DT Article
DE Aortic valve calcification; Atherosclerosis; Inflammation; Bone mineral
density; Molecular imaging
ID VASCULAR CALCIFICATION; POSTMENOPAUSAL WOMEN; MINERAL DENSITY; DEFICIENT
MICE; DISEASE; CELLS; OSTEOPROTEGERIN; PLAQUE; MECHANISMS; MATRIX
AB Aims Westernized countries face a growing burden of cardiovascular calcification and osteoporosis. Despite its vast clinical significance, the precise nature of this reciprocal relationship remains obscure. We hypothesize that cardiovascular calcification progresses with inflammation and inversely correlates with bone tissue mineral density (TMD).
Methods and results Arterial, valvular, and bone metabolism were visualized using near-infrared fluorescence (NIRF) molecular imaging agents, targeting macrophages and osteogenesis. We detected significant arterial and aortic valve calcification in apoE(-/-) mice with or without chronic renal disease (CRD, 30 weeks old; n = 28), correlating with the severity of atherosclerosis. We demonstrated decreases in osteogenic activity in the femurs of apoE(-/-) mice when compared with WT mice, which was further reduced with CRD. Three-dimensional micro-computed tomography imaging of the cortical and cancellous regions of femurs quantified structural remodelling and reductions in TMD in apoE(-/-) and CRD apoE(-/-) mice. We established significant correlations between arterial and valvular calcification and loss of TMD (R(2) = 0.67 and 0.71, respectively). Finally, we performed macrophage-targeted molecular imaging to explore a link between inflammation and osteoporosis in vivo. Although macrophage burden, visualized as uptake of NIRF-conjugated iron nanoparticles, was directly related to the degree of arterial and valvular inflammation and calcification, the same method inversely correlated inflammation with TMD (R(2) = 0.73; 0.83; 0.75, respectively).
Conclusion This study provides direct in vivo evidence that in arteries and aortic valves, macrophage burden and calcification associate with each other, whereas inflammation inversely correlates with bone mineralization. Thus, understanding inflammatory signalling mechanisms may offer insight into selective abrogation of divergent calcific phenomena.
C1 [Hjortnaes, Jesper; Figueiredo, Jose-Luiz; Kohler, Rainer H.; Weissleder, Ralph; Aikawa, Elena] Massachusetts Gen Hosp, Ctr Mol Imaging Res, Boston, MA 02114 USA.
[Butcher, Jonathan] Cornell Univ, Dept Biomed Engn, Ithaca, NY USA.
[Butcher, Jonathan; Riccio, Mark] Cornell Univ, Preclin Imaging Facil, Ithaca, NY USA.
[Figueiredo, Jose-Luiz; Aikawa, Elena] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Kozloff, Kenneth M.] Univ Michigan, Dept Orthopaed Surg, Ann Arbor, MI 48109 USA.
RP Aikawa, E (reprint author), Massachusetts Gen Hosp, Ctr Mol Imaging Res, Boston, MA 02114 USA.
EM eaikawa@partners.org
RI Butcher, Jonathan/D-2280-2012
OI Butcher, Jonathan/0000-0002-9309-6296
FU Wijck-Casper-Stam Foundation; American Heart Association [0835460N,
0830384N]; NYSTAR CAT Award; Donald W. Reynolds Foundation; Leducq
Foundation [07CVD04]; Translational Program of Excellence in
Nanotechnology [5-UO1-HL080731]
FX This study was supported in part by Wijck-Casper-Stam Foundation (J.H.),
American Heart Association Scientist Development Grants (0835460N, E.A.;
0830384N, J.B.), NYSTAR CAT Award (J.B., M.R.), Donald W. Reynolds
Foundation (R.W., E.A.), Leducq Foundation (07CVD04; E.A., J.B.) and
Translational Program of Excellence in Nanotechnology (5-UO1-HL080731;
R.W.). Funding to pay the Open Access publication charges for this
article was provided by research grants to Dr Aikawa.
NR 39
TC 80
Z9 88
U1 1
U2 17
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0195-668X
J9 EUR HEART J
JI Eur. Heart J.
PD AUG
PY 2010
VL 31
IS 16
BP 1975
EP 1984
DI 10.1093/eurheartj/ehq237
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 643IP
UT WOS:000281289100012
PM 20601388
ER
PT J
AU Scirica, BM
Morrow, DA
Bode, C
Ruzyllo, W
Ruda, M
Ophuis, AJMO
Lopez-Sendon, J
Swedberg, K
Ogorek, M
Rifai, N
Lukashevich, V
Maboudian, M
Cannon, CP
McCabe, CH
Braunwald, E
AF Scirica, Benjamin M.
Morrow, David A.
Bode, Christoph
Ruzyllo, Witold
Ruda, Mikhail
Ophuis, Anthonius J. M. Oude
Lopez-Sendon, Jose
Swedberg, Karl
Ogorek, Michal
Rifai, Nader
Lukashevich, Valentina
Maboudian, Mojdeh
Cannon, Christopher P.
McCabe, Carolyn H.
Braunwald, Eugene
TI Patients with acute coronary syndromes and elevated levels of
natriuretic peptides: the results of the AVANT GARDE-TIMI 43 Trial
SO EUROPEAN HEART JOURNAL
LA English
DT Article
DE Natriuretic peptides; Acute coronary syndrome;
Renin-angiotensin-aldosteron system
ID ACUTE MYOCARDIAL-INFARCTION; LEFT-VENTRICULAR DYSFUNCTION; RENIN
INHIBITOR ALISKIREN; HEART-FAILURE; PROGNOSTIC VALUE; ARTERY-DISEASE;
DOUBLE-BLIND; ANTIHYPERTENSIVE EFFICACY; ORAL CAPTOPRIL; MORTALITY
AB Aims Elevated natriuretic peptides (NPs) are associated with an increased cardiovascular risk following acute coronary syndromes (ACSs). However, the therapeutic implications are still undefined. We hypothesized that early inhibition of renin angiotensin aldosterone system (RAAS) in patients with preserved left ventricular function but elevated NPs but following ACS would reduce haemodynamic stress as reflected by a greater reduction NP compared with placebo.
Methods and results AVANT GARDE-TIMI 43 trial, a multinational, double-blind trial, randomized 1101 patients stabilized after ACS without clinical evidence of heart failure or left ventricular function <= 40% but with an increased level of NP 3-10 days after admission to aliskiren, valsartan, their combination, and placebo. The primary endpoint was the change in NT-proBNP from baseline to Week 8. NT-proBNP declined significantly in each treatment arm, including placebo, by Week 8, though there were no differences in the reduction between treatment strategies (42% in placebo, 44% in aliskiren, 39% in valsartan, and 36% in combination arm). Although several subgroups had higher baseline levels of NP and greater reductions over the study period, there were no differences among treatment groups in any subgroup. There were no differences in clinical outcomes but there were more adverse events, including serious events and adverse events leading to early study drug discontinuation, in patients treated with active therapy.
Conclusion In this study of a high-risk population with elevated levels of NPs but relatively preserved systolic function and no evidence of heart failure following ACS, there was no evidence for a benefit of early initiation of inhibition of RAAS with valsartan, aliskiren, or their combination compared with placebo with respect to a reduction in NP over 8 weeks of therapy. Moreover, adverse events were reported more frequently in patients assigned to active therapy.
C1 [Scirica, Benjamin M.; Morrow, David A.; Cannon, Christopher P.; McCabe, Carolyn H.; Braunwald, Eugene] Brigham & Womens Hosp, Div Cardiovasc, TIMI Study Grp, Boston, MA 02115 USA.
[Scirica, Benjamin M.; Morrow, David A.; Cannon, Christopher P.; McCabe, Carolyn H.; Braunwald, Eugene] Harvard Univ, Sch Med, Boston, MA USA.
[Bode, Christoph] Med Univ Klin, Freiburg, Germany.
[Ruzyllo, Witold] Inst Cardiol, Warsaw, Poland.
[Ruda, Mikhail] Cardiol Res Ctr, Moscow 121552, Russia.
[Ophuis, Anthonius J. M. Oude] Canisiud Wilhelmina Ziekenhuis, Nijmegen, Netherlands.
[Lopez-Sendon, Jose] Hosp Univ La Paz, Madrid, Spain.
[Swedberg, Karl] Univ Gothenburg, Sahlgrenska Acad, Gothenburg, Sweden.
[Ogorek, Michal] Samodzielny Szpital Wojewodzki, Piotrkow Trybunalski, Poland.
[Rifai, Nader] Childrens Hosp, Boston, MA 02115 USA.
[Lukashevich, Valentina; Maboudian, Mojdeh] Novartis Pharmaceut, E Hanover, NJ USA.
RP Scirica, BM (reprint author), Brigham & Womens Hosp, Div Cardiovasc, TIMI Study Grp, 75 Francis St, Boston, MA 02115 USA.
EM bscirica@partners.org
FU CV Therapeutics; Novartis; AstraZeneca; Daiichi-Sankyo; Bristol
Meyer-Squibb; Roche Diagnostics; Michael Lerner Foundation; Otsuka;
Servier
FX B.M.S. reports research support from CV Therapeutics, Novartis,
AstraZeneca, Daiichi-Sankyo, Bristol Meyer-Squibb, and Roche
Diagnostics, honoraria for educational presentations from CV
Therapeutics, Novartis, Merck, Schering-Plough, sanofi-aventis, Lilly,
Daiichi-Sankyo, has served as a consultant for AstraZeneca, Novartis,
and Cogentus and received an unrestricted research grant from the
Michael Lerner Foundation. D.M.M. has received honoraria for educational
presentations from CV Therapeutics and Eli Lilly has served as a
consultant for Beckman-Coulter, Critical Diagnostics, Genentech, Ikaria,
Menarini, OrthoClinical Diagnostics, Roche Diagnostics, Sanofi Aventis,
Schering Plough, and Siemens, and was compensated as a member of a
Clinical Events Committee for a clinical trial by AstraZeneca. J.L.-S.
has received research grants from Novartis. K.S. reports having research
support and honoraria from Astrazeneca, Novartis, Otsuka, Servier. V.L.
and M.M. are employees of Novartis. C.P.C. reports research funding from
Accumetrics, AstraZeneca, Bristol-Myers Squibb/Sanofi Partnership, Glaxo
Smith Kline, Intekrin Therapeutics, Merck, Merck/Schering Plough
Partnership, Novartis, and Takeda and acted as a Clinical Advisor and
having equity in Automedics Medical Systems. E.B. has received honoraria
from Bristol Myers Squibb, Merck, and Pfizer and has served as a
consultant to Bristol-Myers Squibb, and Pfizer. Others report no
conflicts.
NR 30
TC 30
Z9 32
U1 1
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0195-668X
J9 EUR HEART J
JI Eur. Heart J.
PD AUG
PY 2010
VL 31
IS 16
BP 1993
EP 2005
DI 10.1093/eurheartj/ehq190
PG 13
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 643IP
UT WOS:000281289100014
PM 20558431
ER
PT J
AU Brick, DJ
Gerweck, AV
Meenaghan, E
Lawson, EA
Misra, M
Fazeli, P
Johnson, W
Klibanski, A
Miller, KK
AF Brick, D. J.
Gerweck, A. V.
Meenaghan, E.
Lawson, E. A.
Misra, M.
Fazeli, P.
Johnson, W.
Klibanski, A.
Miller, K. K.
TI Determinants of IGF1 and GH across the weight spectrum: from anorexia
nervosa to obesity
SO EUROPEAN JOURNAL OF ENDOCRINOLOGY
LA English
DT Article
ID GROWTH-HORMONE-SECRETION; FACTOR-I; CARDIOVASCULAR RISK; REPLACEMENT
THERAPY; NORMAL WOMEN; TESTOSTERONE; DEFICIENCY; AXIS; AGE; OVERWEIGHT
AB Context: Chronic starvation is characterized by GH resistance, and obesity is characterized by decreased GH secretion. In both extremes, IGF1 levels may be low and androgen levels may be abnormal.
Objective: To investigate the determinants of IGF1 and GH across the weight spectrum in women.
Design: Cross-sectional study.
Setting: Clinical research center.
Study participants: In total, 32 women had participated in the study: 11 women with anorexia nervosa (AN), 11 normal-weight women, and 10 obese women of comparable mean age.
Intervention: None.
Main outcome measures: Pooled hourly overnight serum samples assayed for IGF1, GH, estradiol (E-2), testosterone, SHBG, insulin, free fatty acids, and trunk fat.
Results: Free testosterone was higher in obese women and lower in women with AN than in normal-weight women, and was the only independent (and positive) predictor of IGF1 levels, accounting for 14% of the variability (P=0.032) in the group as a whole. This relationship was stronger when obese women were excluded, with free testosterone accounting for 36% of the variability (P=0.003). Trunk fat accounted for 49% of the variability (P<0.0001) of GH, with an additional 7% of the variability attributable to E-2 (P=0.042) in the group as a whole, but was not a significant determinant of GH secretion when obese women were excluded.
Conclusions: Free testosterone is a significant determinant of IGF1 levels in women across the body weight spectrum. In contrast, GH secretion is differentially regulated at the extremes of the weight spectrum.
C1 [Miller, K. K.] Massachusetts Gen Hosp, Neuroendocrine Unit, Dept Med, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Miller, KK (reprint author), Massachusetts Gen Hosp, Neuroendocrine Unit, Dept Med, Bulfinch 457B, Boston, MA 02114 USA.
EM kkmiller@partners.org
RI Perez , Claudio Alejandro/F-8310-2010
OI Perez , Claudio Alejandro/0000-0001-9688-184X
FU NIH [R01 HL077674, R01 DK52525, MO1 RR01066, UL1 RR025758]
FX This work was supported in part by the following NIH grants: R01
HL077674, R01 DK52525, MO1 RR01066, and UL1 RR025758.
NR 31
TC 14
Z9 14
U1 1
U2 1
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 0804-4643
EI 1479-683X
J9 EUR J ENDOCRINOL
JI Eur. J. Endocrinol.
PD AUG
PY 2010
VL 163
IS 2
BP 185
EP 191
DI 10.1530/EJE-10-0365
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 633FJ
UT WOS:000280484800002
PM 20501597
ER
PT J
AU Dhingra, R
Gona, P
Benjamin, EJ
Wang, TJ
Aragam, J
D'Agostino, RB
Kannel, WB
Vasan, RS
AF Dhingra, Ravi
Gona, Philimon
Benjamin, Emelia J.
Wang, Thomas J.
Aragam, Jayashri
D'Agostino, Ralph B., Sr.
Kannel, William B.
Vasan, Ramachandran S.
TI Relations of serum phosphorus levels to echocardiographic left
ventricular mass and incidence of heart failure in the community
SO EUROPEAN JOURNAL OF HEART FAILURE
LA English
DT Article
DE Phosphorus; Congestive heart failure; Ventricle; Epidemiology; Risk
factors
ID PARATHYROID-HORMONE SECRETION; BLOOD-PRESSURE; CARDIOVASCULAR-DISEASE;
PHOSPHATE LEVEL; RISK; ASSOCIATION; FRAMINGHAM; 1,25-DIHYDROXYVITAMIN-D;
HYPERPHOSPHATEMIA; SUPPLEMENTATION
AB Aims To evaluate the association of serum phosphorus with cardiac structure/function and incident heart failure.
Methods and results We related serum phosphorus to echocardiographic left ventricular (LV) measurements cross-sectionally, and to incident heart failure prospectively in 3300 participants (mean age 44 years, 51% women) free of heart failure, myocardial infarction, and chronic kidney disease (estimated glomerular filtration rate [eGFR]<60 mL/min/1.73 m(2)). Cross-sectionally, serum phosphorus was related positively to LV mass, internal dimensions, and systolic dysfunction. On follow-up (mean 17.4 years), 157 individuals developed heart failure. In models adjusting for established risk factors as time-varying covariates, each mg/dL increment in serum phosphorus was associated with a 1.74-fold risk of heart failure [95% confidence intervals (CI) 1.17-2.59]. Individuals in the highest serum phosphorus quartile experienced a two-fold (95% CI 1.28-3.40) risk of heart failure compared with participants in the lowest quartile. These relations were maintained upon additional adjustment for LV mass/dimensions and systolic dysfunction. In analyses restricted to individuals with eGFR >90 mUmin/1.73 m(2), no proteinuria and serum phosphorus <4.5 mg/dL, the association of serum phosphorus with heart failure remained robust.
Conclusion In our community-based sample, higher serum phosphorus was associated with greater LV mass cross-sectionally, and with an increased risk of heart failure prospectively.
C1 [Dhingra, Ravi; Gona, Philimon; Benjamin, Emelia J.; Wang, Thomas J.; D'Agostino, Ralph B., Sr.; Kannel, William B.; Vasan, Ramachandran S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Dhingra, Ravi] Dartmouth Hitchcock Med Ctr, Div Cardiol, Lebanon, NH 03766 USA.
[Dhingra, Ravi] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Gona, Philimon; D'Agostino, Ralph B., Sr.] Boston Univ, Dept Math, Boston, MA 02215 USA.
[Wang, Thomas J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[Aragam, Jayashri] Vet Affairs Hosp, W Roxbury, MA USA.
[Benjamin, Emelia J.; Kannel, William B.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Cardiol Sect EJB RSV, Boston, MA 02118 USA.
[Benjamin, Emelia J.; Kannel, William B.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Dept Prevent Med & Epidemiol, Boston, MA 02118 USA.
RP Vasan, RS (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA USA.
EM vasan@bu.edu
OI Ramachandran, Vasan/0000-0001-7357-5970; Benjamin,
Emelia/0000-0003-4076-2336
FU NIH/NHLBI [N01-HC-25195, HL080124, 2K24HL4334]
FX This work was supported by the NIH/NHLBI Contract No. N01-HC-25195;
HL080124, and 2K24HL4334 (Dr R.S.V.).
NR 34
TC 44
Z9 46
U1 0
U2 10
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 AUG
PY 2010
VL 12
IS 8
BP 812
EP 818
DI 10.1093/eurjhf/hfq106
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 642HR
UT WOS:000281200100008
PM 20675668
ER
PT J
AU Shah, RV
Chen-Tournoux, AA
Picard, MH
van Kimmenade, RRJ
Januzzi, JL
AF Shah, Ravi V.
Chen-Tournoux, Annabel A.
Picard, Michael H.
van Kimmenade, Roland R. J.
Januzzi, James L.
TI Galectin-3, cardiac structure and function, and long-term mortality in
patients with acutely decompensated heart failure
SO EUROPEAN JOURNAL OF HEART FAILURE
LA English
DT Article
DE Heart failure; Echocardiography; Prognosis
ID EMERGENCY-DEPARTMENT PRIDE; DYSPNEA; PRO; MACROPHAGES; DYSFUNCTION;
BIOMARKERS; PROGNOSIS; FIBROSIS; DISEASE
AB Aims To determine the relationship between galectin-3 concentrations and cardiac structure in patients with acute dyspnoea, and to evaluate the impact of galectin-3 independent of echocardiographic measurements on long-term mortality.
Methods and results One hundred and fifteen patients presenting to the emergency department with acute dyspnoea who had galectin-3 levels and detailed echocardiographic studies on admission were studied. Galectin-3 levels were associated with older age (r = 0.26, P = 0.006), lower creatinine clearance (r = -0.42, P < 0.001), and higher levels of N-terminal-proBNP (r = 0.39, P < 0.001). Higher galectin-3 levels were associated with tissue Doppler E/E(a) ratio (r = 0.35, P = 0.01), a lower right ventricular (RV) fractional area change (r = -0.19, P = 0.05), higher RV systolic pressure (r = 0.37, P < 0.001), and more severe mitral (r = 0.30, P = 0.001) or tricuspid regurgitation (r = 0.26, P = 0.005). In patients diagnosed with heart failure (HF), the association between galectin-3 and valvular regurgitation and RV systolic pressure persisted. In a multivariate Cox regression model, galectin-3 remained a significant predictor of 4-year mortality independent of echocardiographic markers of risk. Dyspnoeic patients with HF and galectin-3 levels above the median value had a 63% mortality; patients less than the median value had a 37% mortality (P = 0.003).
Conclusion Among dyspnoeic patients with and without ADHF, galectin-3 concentrations are associated with echocardiographic markers of ventricular function. In patients with ADHF, a single admission galectin-3 level predicts mortality to 4 years, independent of echocardiographic markers of disease severity.
C1 [Shah, Ravi V.; Chen-Tournoux, Annabel A.; Picard, Michael H.; Januzzi, James L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Cardiol Div, Boston, MA 02114 USA.
[van Kimmenade, Roland R. J.] Univ Hosp Maastricht, Dept Cardiol, Maastricht, Netherlands.
RP Januzzi, JL (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Cardiol Div, 32 Fruit St,Yawkey 5984, Boston, MA 02114 USA.
EM jjanuzzi@partners.org
RI Kimmenade, R.R.J./L-4432-2015;
OI Picard, Michael/0000-0002-9264-3243
FU National Heart, Lung, and Blood Institute Heart Failure Research Network
(Boston, MA, USA); Balson Scholar Fund (Boston, MA, USA);
Interuniversity Cardiology Institute of the Netherlands
FX This work was supported by the National Heart, Lung, and Blood Institute
Heart Failure Research Network (R.V.S.; Boston, MA, USA), the Balson
Scholar Fund (J.L.J.; Boston, MA, USA), and the Interuniversity
Cardiology Institute of the Netherlands (R.R.J.K.).
NR 18
TC 140
Z9 146
U1 0
U2 8
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 AUG
PY 2010
VL 12
IS 8
BP 826
EP 832
DI 10.1093/eurjhf/hfq091
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 642HR
UT WOS:000281200100010
PM 20525986
ER
PT J
AU Bergen, SE
Maher, BS
Fanous, AH
Kendler, KS
AF Bergen, Sarah E.
Maher, Brion S.
Fanous, Ayman H.
Kendler, Kenneth S.
TI Detection of susceptibility genes as modifiers due to subgroup
differences in complex disease
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE modifier; simulation; subtyping; complex disease
ID GENOME-WIDE ASSOCIATION; SPINOCEREBELLAR ATAXIA TYPE-2;
CLINICAL-FEATURES; CYSTIC-FIBROSIS; DYSBINDIN GENE; SCHIZOPHRENIA;
GENOTYPE; SYMPTOMS; AGE; HETEROGENEITY
AB Complex diseases invariably involve multiple genes and often exhibit variable symptom profiles. The extent to which disease symptoms, course, and severity differ between affected individuals may result from underlying genetic heterogeneity. Genes with modifier effects may or may not also influence disease susceptibility. In this study, we have simulated data in which a subset of cases differ by some effect size (ES) on a quantitative trait and are also enriched for a risk allele. Power to detect this 'pseudo-modifier' gene in case-only and case-control designs was explored blind to case substructure. Simulations involved 1000 iterations and calculations for 80% power at P<0.01 while varying the risk allele frequency (RAF), sample size (SS), ES, odds ratio (OR), and proportions of the case subgroups. With realistic values for the RAF (0.20), SS (3000) and ES (1), an OR of 1.7 is necessary to detect a pseudo-modifier gene. Unequal numbers of subjects in the case groups result in little decrement in power until the group enriched for the risk allele is <30% or >70% of the total case population. In practice, greater numbers of subjects and selection of a quantitative trait with a large range will provide researchers with greater power to detect a pseudo-modifier gene. However, even under ideal conditions, studies involving alleles with low frequencies or low ORs are usually underpowered for detection of a modifier or susceptibility gene. This may explain some of the inconsistent association results for many candidate gene studies of complex diseases.
European Journal of Human Genetics (2010) 18, 960-964; doi:10.1038/ejhg.2010.39; published online 31 March 2010
C1 [Bergen, Sarah E.; Maher, Brion S.; Kendler, Kenneth S.] Virginia Commonwealth Univ, Dept Human & Mol Genet, Richmond, VA USA.
[Bergen, Sarah E.; Maher, Brion S.; Fanous, Ayman H.; Kendler, Kenneth S.] Virginia Commonwealth Univ, Virginia Inst Psychiat & Behav Genet, Richmond, VA USA.
[Maher, Brion S.; Fanous, Ayman H.; Kendler, Kenneth S.] Virginia Commonwealth Univ, Dept Psychiat, Richmond, VA USA.
[Fanous, Ayman H.] Washington VA Med Ctr, Washington, DC USA.
[Fanous, Ayman H.] Georgetown Univ, Med Ctr, Dept Psychiat, Washington, DC 20007 USA.
RP Bergen, SE (reprint author), Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Ctr Human Genet Res, 185 Cambridge St,6th Floor, Boston, MA 02114 USA.
EM sbergen@gmail.com
RI Maher, Brion/F-9185-2010; Bergen, Sarah/I-8313-2012;
OI Bergen, Sarah/0000-0002-5888-0034
FU NIH [MH41953, DE016632, MH20030]
FX This work was funded by NIH grants MH41953 to KSK, DE016632 to BSM,
training grant MH20030 supporting SEB, and a VA Merit Review Program
grant to AHF.
NR 28
TC 4
Z9 4
U1 1
U2 1
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 AUG
PY 2010
VL 18
IS 8
BP 960
EP 964
DI 10.1038/ejhg.2010.39
PG 5
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 628TO
UT WOS:000280145100016
PM 20354561
ER
PT J
AU Tedeschini, E
Fava, M
Goodness, TM
Papakostas, GI
AF Tedeschini, Enrico
Fava, Maurizio
Goodness, Tracie M.
Papakostas, George I.
TI Relationship between probability of receiving placebo and probability of
prematurely discontinuing treatment in double-blind, randomized clinical
trials for MDD: A meta-analysis
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Antidepressant; Placebo; Discontinuation; Major; Depressive; Disorder;
Adults
ID MAJOR DEPRESSION; DIAGNOSTIC CRITERIA; RATING-SCALE; RUN-IN; DISORDERS;
EFFICACY
AB An increased likelihood of receiving placebo in randomized clinical trials has been found to predict greater chances of trial success. However, patients who are less likely to receive active therapy (and more likely to receive placebo) may be at increased risk of attrition which, in turn, can limit the statistical power of a study. Therefore, in the present work, we sought to investigate the relationship between the probability of receiving placebo and the likelihood of prematurely discontinuing treatment. Medline/Pubmed publication databases were searched for RCT in MDD. A meta-regression established that the likelihood of receiving placebo did not predict either antidepressant discontinuation rates, placebo-discontinuation rates or the risk ratio of discontinuing antidepressants versus placebo. An increased likelihood of receiving placebo did not inflate discontinuation rates which did not influence the degree of antidepressant-placebo "separation". (C) 2010 Elsevier B.V. and ECNP. All rights reserved.
C1 [Tedeschini, Enrico; Fava, Maurizio; Goodness, Tracie M.; Papakostas, George I.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Depress Clin & Res Program, Boston, MA 02114 USA.
[Tedeschini, Enrico] Univ Modena & Reggio Emilia, Dept Psychiat, Modena, Italy.
RP Tedeschini, E (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Depress Clin & Res Program, 50 Staniford St, Boston, MA 02114 USA.
EM etedeschini@partners.org
RI Papakostas, George/I-6905-2013
OI Papakostas, George/0000-0002-2465-5103
FU Bristol-Myers Squibb Company; Forest Pharmaceuticals; National Institute
of Mental; Abbott Laboratories; Alkermes; Aspect Medical Systems;
Astra-Zeneca; Bio Research; Brain Cells, Inc.; Cephalon; Clinical Trial
Solutions; Eli Lilly Et Company; Forest Pharmaceuticals Inc.; Ganeden;
GlaxoSmithKline; J & J Pharmaceuticals; Lichtwer Pharma GmbH; Lorex
Pharmaceuticals; NARSAD; NCCAM; NIDA; NIMH; Novartis; Organon Inc.
FX Dr. Papakostas has served as a consultant for Astra-Zeneca PLC,
Bristol-Myers Squibb Company, Eli Lilly Co., GlaxoSmithKline, Evotec AG,
Inflabloc Pharmaceuticals, Jazz Pharmaceuticals, Otsuka Pharmaceuticals,
PAMLAB LLC, Pfizer Inc., Pierre Fabre Laboratories, Shire
Pharmaceuticals, and Wyeth, Inc.; has received honoraria from
Astra-Zeneca PLC, Bristol-Myers Squibb Company, Eli Lilly Co., Evotec
AG, GlaxoSmithKline, Inflabloc Pharmaceuticals, Jazz Pharmaceuticals,
Lundbeck, Otsuka Pharmaceuticals, PAMLAB LLC, Pfizer, Pierre Fabre
Laboratories, Shire Pharmaceuticals, Titan Pharmaceuticals, and Wyeth
Inc.; has received research support from Bristol-Myers Squibb Company,
Forest Pharmaceuticals, the National Institute of Mental; and has served
on the speaker's bureau for Bristol-Myers Squibb Co and Pfizer, Inc.;
Dr. Fava has served as an advisor/consultant for Abbott Laboratories,
Amarin, Aspect Medical Systems, Astra-Zeneca, Auspex Pharmaceuticals,
Bayer AG, Best Practice Project Management, Inc, Biovail
Pharmaceuticals, Inc., Brain Cells, Inc, BristolMyers Squibb Company,
Cephalon, Clinical Trials Solutions, CNS Response, Compel lis, Cypress
Pharmaceuticals, Dov Pharmaceuticals, Eli Lilly a Company, EPIX
Pharmaceuticals, Fabre-Kramer, Pharmaceuticals, Inc., Forest
Pharmaceuticals Inc., GlaxoSmithKline, Grunenthal GmBH Janssen
Pharmaceutica, Jazz Pharmaceuticals, J & J Pharmaceuticals, Knoll
Pharmaceutical Company, Labopharm, Lorex Pharmaceuticals, Lundbeck,
MedAvante Inc. Merck, Methylation Sciences, Neuronetics, Novartis,
Nutrition 21, Organon Inc., PamLab, LLC, Pfizer Inc, PharmaStar,
Pharmavite, Precision Human Biolaboratory, Roche, Sanofi-Aventis,
Sepracor, Schering-Plough, Solvay Pharmaceuticals, Inc., Somaxon,
Somerset Pharmaceuticals, Synthelabo, Takeda, Tetragenex, Transcept
Pharmaceuticals, Vanda Pharmaceuticals In Wyeth-Ayerst Laboratories; has
received research support from Abbott Laboratories, Alkermes, Aspect
Medical Systems, Astra-Zeneca, Bio Research, Brain Cells, Inc.,
Bristol-Myers Squibb Company, Cephalon, Clinical Trial Solutions, Eli
Lilly Et Company, Forest Pharmaceuticals Inc., Ganeden, GlaxoSmithKline,
J & J Pharmaceuticals, Lichtwer Pharma GmbH, Lorex Pharmaceuticals,
NARSAD, NCCAM, NIDA, NIMH, Novartis, Organon Inc., PamLab, LLC, Pfizer
Inc, Pharmavite, Roche, Sanofi-Aventis, Shire, Solvay Pharmaceuticals,
Inc., Synthelabo, Wyeth-Ayerst Laboratories; has served as a speaker for
Advanced Meeting Partners, American Psychiatric Association,
Astra-Zeneca, Belvoir, Boehringer-Ingelheim, Bristol-Myers Squibb
Company, Cephalon, Eli Lilly Et Company, Forest Pharmaceuticals Inc.,
GlaxoSmithKline, Imedex, Novartis, Organon Inc., Pfizer Inc, PharmaStar,
MGH Psychiatry Academy/Primedia, MGH Psychiatry Academy/Reed-Elsevier,
UBC, Wyeth-Ayerst Laboratories; has equity Holdings in Compel lis; and
has patent applications for SPCD and for a combination of azapirones and
bupropion in MDD, copyright royalties for the MGH CPFQ_, SFI, ATRQ,
DESS, and SAFER.
NR 24
TC 10
Z9 10
U1 1
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD AUG
PY 2010
VL 20
IS 8
BP 562
EP 567
DI 10.1016/j.euroneuro.2010.02.004
PG 6
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 630FL
UT WOS:000280258400005
PM 20219330
ER
PT J
AU Biederman, J
Wozniak, J
AF Biederman, J.
Wozniak, J.
TI The long term course of pediatric bipolar disorder: a five year
longitudinal follow up study
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 23rd Congress Meeting of European-College-of-Neuropsychopharmacology
CY AUG 28-SEP 01, 2010
CL Amsterdam, NETHERLANDS
SP European Coll Neuropsychopharmacol
C1 [Biederman, J.; Wozniak, J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD AUG
PY 2010
VL 20
SU 3
BP S611
EP S612
PG 2
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 673UB
UT WOS:000283687800822
ER
PT J
AU Biederman, J
Petty, C
Monuteaux, M
Faraone, S
AF Biederman, J.
Petty, C.
Monuteaux, M.
Faraone, S.
TI Psychiatric outcomes of girls with ADHD grown up: a controlled 11-year
follow-up study
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 23rd Congress Meeting of European-College-of-Neuropsychopharmacology
CY AUG 28-SEP 01, 2010
CL Amsterdam, NETHERLANDS
SP European Coll Neuropsychopharmacol
C1 [Biederman, J.; Petty, C.; Monuteaux, M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Faraone, S.] SUNY Upstate Med Univ, Dept Psychiat & Behav Sci, Syracuse, NY USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD AUG
PY 2010
VL 20
SU 3
BP S612
EP S613
PG 2
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 673UB
UT WOS:000283687800823
ER
PT J
AU Biederman, J
Fried, R
Petty, C
Faraone, S
AF Biederman, J.
Fried, R.
Petty, C.
Faraone, S.
TI Examination of the effects of stimulant treatment across the adult
lifecycle of adults with ADHD: a controlled study
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 23rd Congress Meeting of European-College-of-Neuropsychopharmacology
CY AUG 28-SEP 01, 2010
CL Amsterdam, NETHERLANDS
SP European Coll Neuropsychopharmacol
C1 [Biederman, J.; Fried, R.; Petty, C.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Faraone, S.] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY USA.
[Faraone, S.] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD AUG
PY 2010
VL 20
SU 3
BP S329
EP S329
PG 1
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 673UB
UT WOS:000283687800336
ER
PT J
AU Biederman, J
Mick, E
AF Biederman, J.
Mick, E.
TI A randomized, three phase 34 week double-blind long-term efficacy study
of extended-release methylphenidate in adults with ADHD
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 23rd Congress Meeting of European-College-of-Neuropsychopharmacology
CY AUG 28-SEP 01, 2010
CL Amsterdam, NETHERLANDS
SP European Coll Neuropsychopharmacol
C1 [Biederman, J.; Mick, E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD AUG
PY 2010
VL 20
SU 3
BP S329
EP S330
PG 2
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 673UB
UT WOS:000283687800337
ER
PT J
AU Herbert, MR
AF Herbert, M. R.
TI Environment and vulnerable physiology in autism
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 23rd Congress Meeting of European-College-of-Neuropsychopharmacology
CY AUG 28-SEP 01, 2010
CL Amsterdam, NETHERLANDS
SP European Coll Neuropsychopharmacol
ID SPECTRUM
C1 [Herbert, M. R.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, TRANSCEND, Charlestown, MA USA.
NR 3
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD AUG
PY 2010
VL 20
SU 3
BP S177
EP S177
PG 1
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 673UB
UT WOS:000283687800046
ER
PT J
AU Marder, S
Buchanan, RW
AF Marder, S.
Buchanan, R. W.
TI NIMH/FDA guidelines for clinical trials for cognition in schizophrenia:
how much have we advanced?
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 23rd Congress Meeting of European-College-of-Neuropsychopharmacology
CY AUG 28-SEP 01, 2010
CL Amsterdam, NETHERLANDS
SP European Coll Neuropsychopharmacol
C1 [Marder, S.] W Los Angeles VA Hlth Care Ctr, Los Angeles, CA USA.
[Buchanan, R. W.] Maryland Psychiat Res Ctr, Baltimore, MD 21228 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD AUG
PY 2010
VL 20
SU 3
BP S194
EP S194
PG 1
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 673UB
UT WOS:000283687800091
ER
PT J
AU Tedeschini, E
Levkovitz, Y
Papakostas, G
AF Tedeschini, E.
Levkovitz, Y.
Papakostas, G.
TI Antidepressants for late-life depression: a meta analysis of
placebo-controlled randomized trials
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 23rd Congress Meeting of European-College-of-Neuropsychopharmacology
CY AUG 28-SEP 01, 2010
CL Amsterdam, NETHERLANDS
SP European Coll Neuropsychopharmacol
C1 [Tedeschini, E.] Univ Modena & Reggio Emilia, Modena, Italy.
[Levkovitz, Y.] Emot Cognit Res Ctr, Shalvata Mental Hlth Ctr, Tel Aviv, Israel.
[Papakostas, G.] Massachusetts Gen Hosp, Psychiat DCRP, Boston, MA 02114 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD AUG
PY 2010
VL 20
SU 3
BP S382
EP S383
PG 2
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 673UB
UT WOS:000283687800428
ER
PT J
AU Killeen, RP
Arnous, S
Martos, R
Abbara, S
Quinn, M
Dodd, JD
AF Killeen, Ronan P.
Arnous, Samer
Martos, Ramon
Abbara, Suhny
Quinn, Martin
Dodd, Jonathan D.
TI Chronic mitral regurgitation detected on cardiac MDCT: differentiation
between functional and valvular aetiologies
SO EUROPEAN RADIOLOGY
LA English
DT Article
DE Cardiomyopathy; Dilated/complications; Mitral valve/anatomy; Mitral
valve insufficiency/aetiology; Computed tomography; Coronary artery
disease
ID AMERICAN-HEART-ASSOCIATION; 3-DIMENSIONAL ECHOCARDIOGRAPHY; OUTCOME
IMPLICATIONS; WALL-MOTION; DISEASE; PREVALENCE; VALVE; CT;
RECONSTRUCTION; MANAGEMENT
AB To determine whether cardiac computed tomography (MDCT) can differentiate between functional and valvular aetiologies of chronic mitral regurgitation (MR) compared with echocardiography (TTE).
Twenty-seven patients with functional or valvular MR diagnosed by TTE and 19 controls prospectively underwent cardiac MDCT. The morphological appearance of the mitral valve (MV) leaflets, MV geometry, MV leaflet angle, left ventricular (LV) sphericity and global/regional wall motion were analysed. The coronary arteries were evaluated for obstructive atherosclerosis.
All control and MR cases were correctly identified by MDCT. Significant differences were detected between valvular and control groups for anterior leaflet length (30 +/- 7 mm vs. 22 +/- 4 mm, P < 0.02) and thickness (3.0 +/- 1 mm vs. 2.2 +/- 1 mm, P < 0.01). High-grade coronary stenosis was detected in all patients with functional MR compared with no controls (P < 0.001). Significant differences in those with/without MV prolapse were detected in MV tent area (-1.0 +/- 0.6 mm vs. 1.3 +/- 0.9 mm, P < 0.0001) and MV tent height (-0.7 +/- 0.3 mm vs. 0.8 +/- 0.8 mm, P < 0.0001). Posterior leaflet angle was significantly greater for functional MR (37.9 +/- 19.1A degrees vs. 22.9 A +/- 14A degrees, P < 0.018) and less for valvular MR (0.6 A +/- 35.5A degrees vs. 22.9 A +/- 14A degrees, P < 0.017). Sensitivity, specificity, and positive and negative predictive values of MDCT were 100%, 95%, 96% and 100%.
Cardiac MDCT allows the differentiation between functional and valvular causes of MR.
C1 [Killeen, Ronan P.; Dodd, Jonathan D.] St Vincents Univ Hosp, Dept Radiol, Dublin 4, Ireland.
[Arnous, Samer; Martos, Ramon; Quinn, Martin] St Vincents Univ Hosp, Dept Cardiol, Dublin 4, Ireland.
[Abbara, Suhny] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Dodd, JD (reprint author), St Vincents Univ Hosp, Dept Radiol, Elm Pk 4, Dublin 4, Ireland.
EM j.dodd@st-vincents.ie
NR 30
TC 7
Z9 7
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0938-7994
J9 EUR RADIOL
JI Eur. Radiol.
PD AUG
PY 2010
VL 20
IS 8
BP 1886
EP 1895
DI 10.1007/s00330-010-1760-4
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 622IU
UT WOS:000279656400011
PM 20309557
ER
PT J
AU Abujudeh, HH
Boland, GW
Kaewlai, R
Rabiner, P
Halpern, EF
Gazelle, GS
Thrall, JH
AF Abujudeh, Hani H.
Boland, Giles W.
Kaewlai, Rathachai
Rabiner, Pavel
Halpern, Elkarn F.
Gazelle, G. Scott
Thrall, James H.
TI Abdominal and pelvic computed tomography (CT) interpretation:
discrepancy rates among experienced radiologists
SO EUROPEAN RADIOLOGY
LA English
DT Article
DE Peer-review system; Radiological error; Discrepancy rate; Computed
tomography; Abdomen; Pelvis
ID DIAGNOSTIC-PROCEDURES; ERROR; ACCURACY
AB To assess the discrepancy rate for the interpretation of abdominal and pelvic computed tomography (CT) examinations among experienced radiologists.
Ninety abdominal and pelvic CT examinations reported by three experienced radiologists who specialize in abdominal imaging were randomly selected from the radiological database. The same radiologists, blinded to previous interpretation, were asked to re-interpret 60 examinations: 30 of their previous interpretations and 30 interpreted by others. All reports were assessed for the degree of discrepancy between initial and repeat interpretations according to a three-level scoring system: no discrepancy, minor, or major discrepancy. Inter- and intrareader discrepancy rates and causes were evaluated.
CT examinations included in the investigation were performed on 90 patients (43 men, mean age 59 years, SD 14, range 19-88) for the following indications: follow-up/evaluation of malignancy (69/90, 77%), pancreatitis (5/90, 6%), urinary tract stone (4/90, 4%) or other (12/90, 13%). Interobserver and intraobserver major discrepancy rates were 26 and 32%, respectively. Major discrepancies were due to missed findings, different opinions regarding interval change of clinically significant findings, and the presence of recommendation.
Major discrepancy of between 26 and 32% was observed in the interpretation of abdominal and pelvic CT examinations.
C1 [Abujudeh, Hani H.; Boland, Giles W.; Kaewlai, Rathachai; Rabiner, Pavel; Halpern, Elkarn F.; Gazelle, G. Scott; Thrall, James H.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Abujudeh, Hani H.; Boland, Giles W.; Kaewlai, Rathachai; Rabiner, Pavel; Halpern, Elkarn F.; Gazelle, G. Scott; Thrall, James H.] Harvard Univ, Sch Med, Boston, MA USA.
[Halpern, Elkarn F.; Gazelle, G. Scott] Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA.
RP Abujudeh, HH (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,FND-220, Boston, MA 02114 USA.
EM habujudeh@partners.org
OI Kaewlai, Rathachai/0000-0002-0650-9380
NR 17
TC 21
Z9 21
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0938-7994
J9 EUR RADIOL
JI Eur. Radiol.
PD AUG
PY 2010
VL 20
IS 8
BP 1952
EP 1957
DI 10.1007/s00330-010-1763-1
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 622IU
UT WOS:000279656400018
PM 20336300
ER
PT J
AU Geisler, BP
AF Geisler, Benjamin P.
TI Treating anemia in heart failure patients: a review of
erythropoiesis-stimulating agents
SO EXPERT OPINION ON BIOLOGICAL THERAPY
LA English
DT Review
DE carbamylated erythropoietin; continuous erythropoietin receptor
activator; erythropoietin; heart failure; recombinant
ID CHRONIC KIDNEY-DISEASE; QUALITY-OF-LIFE; EPOETIN-ALPHA; RENAL-FUNCTION;
HEMOGLOBIN CONCENTRATION; HEMODIALYSIS-PATIENTS; RESOURCE UTILIZATION;
SECONDARY ANALYSIS; DIALYSIS PATIENTS; CONTROLLED-TRIAL
AB Importance of the field: Prevalence of chronic heart failure (CHF) is increasing, and despite improvements in the past decade the prognosis in terms of mortality and health-related quality of life remains poor. Anemia is often found concomitantly in CHF patients.
Areas covered in this review: Erythropoiesis-stimulating agents (ESAs) are a new treatment option for these anemic CHF patients, promising to decrease mortality and hospitalizations, and increase health-related quality of life.
What the reader will gain: CHF epidemiology is briefly dicussed. Currently available clinical efficacy and safety data are critically appraised. Health care utilization by CHF patients, particularly hospitalizations, are reviewed in order predict cost-effectiveness of ESAs.
Take home messages: The efficacy for the most pertinent endpoints has not been proven by a pivotal trial or a meta-analysis free of bias, and there might be increased cardiovascular events and cancer incidence rates above a currently unknown target value or with multiple doses. However, subgroups should be identified in which ESAs might prove to be more efficacious and as safe as usual care and either cost-saving or cost-effective. Nevertheless, depending on the subgroup, the budget effect for payors might be dramatic due to the large number of CHF patients.
C1 [Geisler, Benjamin P.] Massachusetts Gen Hosp, Inst Technol Assessment, Somerville, MA 02143 USA.
[Geisler, Benjamin P.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA USA.
RP Geisler, BP (reprint author), Massachusetts Gen Hosp, Inst Technol Assessment, 18 Pleasant Ave, Somerville, MA 02143 USA.
EM ben.geisler@gmail.com
RI Geisler, Benjamin/A-9244-2010
OI Geisler, Benjamin/0000-0003-1704-6067
FU Amgen, Inc.
FX The author was a subcontractor for a research project that received
unrestricted support from Amgen, Inc., a manufacturer of ESAs. The
author also received direct support from Amgen, Inc., a manufacturer of
ESAs to present the outcomes of that project at a conference.
NR 82
TC 2
Z9 2
U1 0
U2 3
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1471-2598
J9 EXPERT OPIN BIOL TH
JI Expert Opin. Biol. Ther.
PD AUG
PY 2010
VL 10
IS 8
BP 1209
EP 1216
DI 10.1517/14712598.2010.500282
PG 8
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA 629JB
UT WOS:000280191000004
PM 20557272
ER
PT J
AU Ho, L
Pasinetti, GM
AF Ho, Lap
Pasinetti, Giulio Maria
TI Polyphenolic compounds for treating neurodegenerative disorders
involving protein misfolding
SO EXPERT REVIEW OF PROTEOMICS
LA English
DT Review
DE Alzheimer's disease; beta-amyloid; grape seed polyphenolic extract;
Huntington's disease; neurodegenerative disorders; Parkinson's disease;
polyphenols; tau; tauopathy
ID ALZHEIMER TRANSGENIC MICE; PAIRED HELICAL FILAMENTS; ALPHA-SYNUCLEIN;
IN-VITRO; GRAPE SEED; HUNTINGTONS-DISEASE; PARKINSONS-DISEASE; TAU
PATHOLOGY; AGGREGATION; TAUOPATHIES
AB A diverse group of neurodegenerative diseases are characterized by progressive, age-dependent intracellular formation of misfolded protein aggregates. These include Alzheimer's disease, Huntington's disease, Parkinson's disease and a number of tau-mediated disorders. There is no effective treatment for any of these disorders; currently approved interventions are designed to treat disease symptoms and generally lead to modest modulation of clinical symptoms. None are known to mitigate underlying neuropathologic mechanisms and, thus, it is not unexpected that existing treatments appear ineffective in modulating disease progression. We note that these neurodegenerative disorders all share a common mechanistic theme in that depositions of misfolded protein in the brain is a key molecular feature underlying disease onset and/or progression. While previous studies have identified a number of drugs and nutraceuticals capable of interfering with the formation and/or stability of misfolded protein aggregates, none have been demonstrated to be effective in vivo for treating any of the neurodegenerative disorders. We hereby review accumulating evidence that a select nutraceutical grape-seed polyphenolic extract (GSPE) is effective in vitro and in vivo in mitigating certain misfolded protein-mediated neuropathologic and clinical phenotypes. We will also review evidence implicating bioavailability of GSPE components in the brain and the tolerability as well as safety of GSPE in animal models and in humans. Collectively, available information supports continued development of the GSPE for treating a variety of neurodegenerative disorders involving misfolded protein-mediated neuropathologic mechanisms.
C1 [Ho, Lap; Pasinetti, Giulio Maria] Mt Sinai Sch Med, Ctr Excellence Novel Approaches Neurodiagnost & N, Ctr Excellence Res Complementary & Alternat Med A, Dept Neurol,Brain Inst, New York, NY 10029 USA.
[Pasinetti, Giulio Maria] James J Peters Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Bronx, NY 10468 USA.
RP Pasinetti, GM (reprint author), Mt Sinai Sch Med, Ctr Excellence Novel Approaches Neurodiagnost & N, Ctr Excellence Res Complementary & Alternat Med A, Dept Neurol,Brain Inst, 1 Gustave L Levy Pl,Box 1137, New York, NY 10029 USA.
EM giulio.pasinetti@mssm.edu
NR 45
TC 13
Z9 13
U1 3
U2 14
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1478-9450
J9 EXPERT REV PROTEOMIC
JI Expert Rev. Proteomics
PD AUG
PY 2010
VL 7
IS 4
BP 579
EP 589
DI 10.1586/EPR.10.69
PG 11
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 637BH
UT WOS:000280788800015
PM 20653511
ER
PT J
AU Theodoropoulou, S
Kolovou, PE
Morizane, Y
Kayama, M
Nicolaou, F
Miller, JW
Gragoudas, E
Ksander, BR
Vavvas, DG
AF Theodoropoulou, Sofia
Kolovou, Paraskevi E.
Morizane, Yuki
Kayama, Maki
Nicolaou, Fotini
Miller, Joan W.
Gragoudas, Evangelos
Ksander, Bruce R.
Vavvas, Demetrios G.
TI Retinoblastoma cells are inhibited by aminoimidazole carboxamide
ribonucleotide (AICAR) partially through activation of AMP-dependent
kinase
SO FASEB JOURNAL
LA English
DT Article
DE cancer; energy; metabolism; eye; intraocular tumors
ID RIBOSIDE INDUCES APOPTOSIS; PROTEIN-KINASE; BILATERAL RETINOBLASTOMA;
ENERGY STATUS; KEY SENSOR; CANCER; GROWTH;
5-AMINOIMIDAZOLE-4-CARBOXAMIDE-1-BETA-D-RIBOFURANOSIDE; CHEMOREDUCTION;
CHEMOTHERAPY
AB 5-Aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), an analog of AMP, is widely used as an activator of AMP-kinase (AMPK), a protein that regulates the responses of the cell to energy change. We studied the effects of AICAR on the growth of retinoblastoma cell lines (Y79, WERI, and RB143). AICAR inhibited Rb cell growth, induced apoptosis and S-phase cell cycle arrest, and led to activation of AMPK. These effects were abolished by treatment with dypiridamole, an inhibitor that blocks entrance of AICAR into cells. Treatment with the adenosine kinase inhibitor 5-iodotubericidin to inhibit the conversion of AICAR to ZMP (the direct activator of AMPK) reversed most of the growth-inhibiting effects of AICAR, indicating that some of the antiproliferative effects of AICAR are mediated through AMPK activation. In addition, AICAR treatment was associated with inhibition of the mammalian target of rapamycin pathway, decreased phosphorylation of ribosomal protein-S6 and 4E-BP1, down-regulation of cyclins A and E, and decreased expression of p21. Our results indicate that AICAR-induced activation of AMPK inhibits retinoblastoma cell growth. This is one of the first descriptions of a nonchemotherapeutic drug with low toxicity that may be effective in treating Rb patients.-Theodoropoulou, S., Kolovou, P. E., Morizane, Y., Kayama, M., Nicolaou, F., Miller, J. W., Gragoudas, E., Ksander, B. R., Vavvas, D. G. Retinoblastoma cells are inhibited by aminoimidazole carboxamide ribonucleotide (AICAR) partially through activation of AMP-dependent kinase. FASEB J. 24, 2620-2630 (2010). www.fasebj.org
C1 [Theodoropoulou, Sofia; Morizane, Yuki; Kayama, Maki; Miller, Joan W.; Gragoudas, Evangelos; Vavvas, Demetrios G.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Angiogenesis Lab,Retina Serv,Dept Ophthalmol, Boston, MA 02114 USA.
[Kolovou, Paraskevi E.; Ksander, Bruce R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA.
[Nicolaou, Fotini] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Pediat Surg Labs, Boston, MA 02114 USA.
RP Vavvas, DG (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Angiogenesis Lab,Retina Serv,Dept Ophthalmol, Boston, MA 02114 USA.
EM demetrios_vavvas@meei.harvard.edu
OI Vavvas, Demetrios/0000-0002-8622-6478
FU Onassis Foundation; Massachusetts Lions Eye Research Fund; Research to
Prevent Blindness; U.S. National Institutes of Health [NIH EY009294]
FX D.G.V. was supported by an Onassis Foundation Scholars grant, the
Massachusetts Lions Eye Research Fund, and Research to Prevent
Blindness. B.R.K. was supported by U.S. National Institutes of Health
grant NIH EY009294.
NR 44
TC 21
Z9 22
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD AUG
PY 2010
VL 24
IS 8
BP 2620
EP 2630
DI 10.1096/fj.09-152546
PG 11
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 690LD
UT WOS:000285005400004
PM 20371623
ER
PT J
AU Anelli, V
Gault, CR
Snider, AJ
Obeid, LM
AF Anelli, Viviana
Gault, Christopher R.
Snider, Ashley J.
Obeid, Lina M.
TI Role of sphingosine kinase-1 in paracrine/transcellular angiogenesis and
lymphangiogenesis in vitro
SO FASEB JOURNAL
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; SIGNALING PATHWAYS; MOLECULAR-CLONING;
FUNCTIONAL-CHARACTERIZATION; EXTRACELLULAR RELEASE; MASS-SPECTROMETRY;
POOR SURVIVAL; G-PROTEIN; VEGF-C; 1-PHOSPHATE
AB Sphingosine-1-phosphate (S1P) is an important bioactive sphingolipid involved in angiogenesis and lymphangiogenesis, 2 important processes that influence the growth, survival, and spread of tumors. S1P acts as an extracellular mediator through binding to 5 highly specific S1P receptors, S1P(1-5). Sphingosine kinase-1 (SK1), one of 2 known sphingosine kinase enzymes responsible for S1P production, appears to be overexpressed in many tumors. Although a role for S1P in angiogenesis and lymphangiogenesis has been established, it is unclear whether S1P secreted from cancer cells has a paracrine function in a tumor environment. Here we investigated whether modulation of cellular SK1 could initiate a paracrine angiogenic and lymphangiogenic switch. We found that SK1 overexpression in HEK cells or its down-regulation in glioma or breast cancer cells modulated extracellular S1P levels accordingly, which in turn increased or decreased both migration and tube formation in cocultured vascular or lymphatic endothelial cells. In contrast, down-regulation of sphingosine kinase 2 in both glioma and breast cancer cells had no appreciable effect on cellular or secreted S1P levels. In addition, vascular endothelial growth factors VEGF and VEGF-C down-regulation in cancer cells appeared insufficient to block the angiogenic and lymphangiogenic switch triggered by these cells. Moreover, S1P initiated endothelial cell sprouting in 3-dimensional collagen matrices, which is representative of a multistep angiogenic process. Our data collectively demonstrate for the first time that SK1 plays an essential role in regulating in vitro paracrine angiogenesis and lymphangiogenesis.-Anelli, V., Gault, C. R., Snider, A.J., Obeid, L. M. Role of sphingosine kinase-1 in paracrine/transcellular angiogenesis and lymphangiogenesis in vitro. FASEB J. 24, 2727-2738 (2010). www.fasebj.org
C1 [Obeid, Lina M.] Med Univ S Carolina, Div Gen Internal Med Geriatr, Dept Med, Charleston, SC 29425 USA.
[Anelli, Viviana; Obeid, Lina M.] Med Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA.
[Anelli, Viviana] Univ Milan, Dept Med Chem Biochem & Biotechnol, Milan, Italy.
[Obeid, Lina M.] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
RP Obeid, LM (reprint author), Med Univ S Carolina, Div Gen Internal Med Geriatr, Dept Med, MSC 779, Charleston, SC 29425 USA.
EM obeidl@musc.edu
OI obeid, lina/0000-0002-0734-0847
FU National Institutes of Health [NIH/NIGMS GM062887, NIH/NCI CA097132,
NIH/P20 RR17677]; Hollings Cancer Center [P30-CA-56036]
FX The authors thank Kathy Wiita-Fisk for administrative assistance. The
authors also thank the Lipidomics Core at the Medical University of
South Carolina. Grant support came from National Institutes of Health
grants NIH/NIGMS GM062887 (L.M.O.), NIH/NCI CA097132 (L.M.O.), NIH/P20
RR17677 for the Centers of Biomedical Research Excellence (COBRE)
Lipidomics Core, and Hollings Cancer Center core grant P30-CA-56036 for
the Microscopy Core.
NR 39
TC 39
Z9 39
U1 0
U2 1
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 AUG
PY 2010
VL 24
IS 8
BP 2727
EP 2738
DI 10.1096/fj.09-150540
PG 12
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 690LD
UT WOS:000285005400014
PM 20335228
ER
PT J
AU Reindollar, RH
Regan, MM
Neumann, PJ
Levine, BS
Thornton, KL
Alper, MM
Goldman, MB
AF Reindollar, Richard H.
Regan, Meredith M.
Neumann, Peter J.
Levine, Bat-Sheva
Thornton, Kim L.
Alper, Michael M.
Goldman, Marlene B.
TI A randomized clinical trial to evaluate optimal treatment for
unexplained infertility: the fast track and standard treatment (FASTT)
trial
SO FERTILITY AND STERILITY
LA English
DT Article
DE Unexplained infertility; FASTT Trial; intrauterine insemination; in
vitro fertilization
ID IN-VITRO FERTILIZATION; HUMAN CHORIONIC-GONADOTROPIN; MULTIPLE PREGNANCY
RATE; INTRAUTERINE INSEMINATION; CLOMIPHENE CITRATE; COST; REPRODUCTION;
FECUNDITY; EFFICACY; CYCLES
AB Objective: To determine the value of gonadotropin/ intrauterine insemination (FSH/IUI) therapy for infertile women aged 21-39 years.
Design: Randomized controlled trial.
Setting: Academic medical center associated with a private infertility center.
Patient(s): Couples with unexplained infertility.
Intervention(s): Couples were randomized to receive either conventional treatment (n = 247) with three cycles of clomiphene citrate (CC)/IUI, three cycles of FSH/IUI, and up to six cycles of IVF or an accelerated treatment (n 256) that omitted the three cycles of FSH/IUI.
Main Outcome Measure(s): The time it took to establish a pregnancy that led to a live birth and cost-effectiveness, defined as the ratio of the sum of all health insurance charges between randomization and delivery divided by the number of couples delivering at least one live-born baby.
Result(s): An increased rate of pregnancy was observed in the accelerated arm (hazard ratio [HR], 1.25; 95% confidence interval [CI], 1.00-1.56) compared with the conventional arm. Median time to pregnancy was 8 and 11 months in the accelerated and conventional arms, respectively. Per cycle pregnancy rates for CC/IUI, FSH/IUI, and IVF were 7.6%, 9.8%, and 30.7%, respectively. Average charges per delivery were $9,800 lower (95% CI, $25,100 lower to $3,900 higher) in the accelerated arm compared to conventional treatment. The observed incremental difference was a savings of $2,624 per couple for accelerated treatment and 0.06 more deliveries.
Conclusion(s): A randomized clinical trial demonstrated that FSH/IUI treatment was of no added value. (Fertil Steril (R) 2010; 94: 888-99. (c) 2010 by American Society for Reproductive Medicine.)
C1 [Reindollar, Richard H.; Goldman, Marlene B.] Dartmouth Hitchcock Med Ctr, Dept Obstet & Gynecol, Dartmouth Med Sch, Lebanon, NH 03756 USA.
[Regan, Meredith M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Neumann, Peter J.; Levine, Bat-Sheva] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Neumann, Peter J.; Levine, Bat-Sheva] Tufts Med Ctr, Ctr Evaluat Value & Risk Hlth, Boston, MA USA.
[Thornton, Kim L.; Alper, Michael M.] Beth Israel Deaconess Med Ctr, Div Reprod Endocrinol & Infertil, Dept Obstet Gynecol & Reprod Biol, Boston, MA 02215 USA.
[Goldman, Marlene B.] Dartmouth Hitchcock Med Ctr, Dept Community & Family Med, Dartmouth Med Sch, Lebanon, NH 03756 USA.
RP Reindollar, RH (reprint author), Dartmouth Hitchcock Med Ctr, Dept Obstet & Gynecol, Dartmouth Med Sch, 1 Med Ctr Dr, Lebanon, NH 03756 USA.
EM Richard.H.Reindollar@Hitchcock.org
FU Ferring; Organon; Serono; Serono and General Electric,; Novo Nordisk;
Duramed; National Institute of Child Health and Human Development;
National Institutes of Health, Bethesda, Maryland [R01 HD38561]
FX R.H.R. reports receiving fellowship training funds and lecture fees from
Ferring, Organon, and Serono before 2005. M.M.R. has nothing to
disclose. P.J.N. reports receiving grant support from Elan
Pharmaceuticals and Johnson & Johnson, receiving consultant fees from
Serono and General Electric, and serving on advisory boards for Merck,
Schering Plough, and Abbott; B-S.L. reports receiving an educational
grant from Novo Nordisk. K.L.T. reports receiving fellowship training
support from Ferring, research grant support from Duramed, Organon, and
Serono, consulting fees from Organon, and lecture fees from Organon and
Serono. M.M.A. reports receiving unrestricted research grants from
Serono and Organon, consulting fees from Serono, and lecture fees from
Ferring, Organon, and Serono. M.B.G. has nothing to disclose.; Supported
by a grant from the National Institute of Child Health and Human
Development, National Institutes of Health, Bethesda, Maryland (R01
HD38561). The National Institute of Child Health and Human Development
had no role in the design or conduct of the study; collection,
management, analysis, and interpretation of the data; or preparation,
review, or approval of the manuscript. The content of this article is
solely the responsibility of the authors and does not necessarily
represent the official views of the National Institutes of Health.
NR 26
TC 74
Z9 74
U1 2
U2 10
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 AUG
PY 2010
VL 94
IS 3
BP 888
EP 899
DI 10.1016/j.fertnstert.2009.04.022
PG 12
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 632FX
UT WOS:000280407900012
PM 19531445
ER
PT J
AU Tanrikut, C
Feldman, AS
Altemus, M
Paduch, DA
Schlegel, PN
AF Tanrikut, Cigdem
Feldman, Adam S.
Altemus, Margaret
Paduch, Darius A.
Schlegel, Peter N.
TI Adverse effect of paroxetine on sperm
SO FERTILITY AND STERILITY
LA English
DT Article
DE Male infertility; semen analysis; antidepressants; sperm; DNA
fragmentation; erectile dysfunction; ejaculation; body mass index
ID CHROMATIN-STRUCTURE ASSAY; IN-VITRO FERTILIZATION; BODY-MASS INDEX;
DOUBLE-BLIND; DNA-DAMAGE; ANTIDEPRESSANTS; EJACULATION; PREGNANCY; MEN;
FRAGMENTATION
AB Objective: To assess the effects of a selective serotonin reuptake inhibitor on semen parameters.
Design: Prospective study.
Setting: Academic medical center.
Patient(s): Thirty-five healthy male volunteers, 18-65 years old.
Intervention(s): Paroxetine administration for 5 weeks.
Main Outcome Measure(s): Serum hormone levels, semen analyses, percent sperm DNA fragmentation, and questionnaire assessment of sexual function assessed before, during, and 1 month after drug administration.
Result(s): Mean sperm DNA fragmentation was significantly higher for men while on paroxetine (30.3%) versus baseline (13.8%). Before paroxetine, 9.7% of patients had a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) score >= 30% compared with 50% at week 4 of treatment. The odds ratio (OR) of having abnormal DNA fragmentation while taking paroxetine was 9.33 (95% confidence interval, 2.3-37.9). Multivariate logistic regression correcting for age and body mass index confirmed this correlation (OR, 11.12). Up to 35% of men noted significant changes in erectile function and up to 47% of men reported ejaculatory difficulties on medication. Recovery to near-normal sexual function was noted after stopping treatment. Standard semen parameters were not significantly altered during paroxetine treatment.
Conclusion(s): In men with normal semen parameters, paroxetine induced abnormal sperm DNA fragmentation in a significant proportion of subjects, without a measurable effect on semen parameters. The fertility potential of a substantial number of men on paroxetine may be adversely affected by these changes in sperm DNA integrity. (Fertil Steril (R) 2010; 94: 1021-6. (C) 2010 by American Society for Reproductive Medicine.)
C1 [Tanrikut, Cigdem; Paduch, Darius A.; Schlegel, Peter N.] Cornell Univ, Weill Med Coll, Dept Urol, James Buchanan Brady Fdn,Cornell Reprod Med Inst, New York, NY 10021 USA.
[Tanrikut, Cigdem; Feldman, Adam S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Urol, Boston, MA USA.
[Altemus, Margaret] Cornell Univ, Weill Med Coll, Dept Psychiat, New York, NY 10021 USA.
RP Schlegel, PN (reprint author), Cornell Univ, Weill Med Coll, Dept Urol, James Buchanan Brady Fdn,Cornell Reprod Med Inst, 525 E 68th St,Starr 900, New York, NY 10021 USA.
EM pnschleg@med.cornell.edu
FU New York Community Trust; Brady Urology Foundation
FX Supported by the Frederick J. and Theresa Dow Wallace Fund of the New
York Community Trust and the Brady Urology Foundation.
NR 28
TC 50
Z9 52
U1 0
U2 11
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 AUG
PY 2010
VL 94
IS 3
BP 1021
EP 1026
DI 10.1016/j.fertnstert.2009.04.039
PG 6
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 632FX
UT WOS:000280407900029
PM 19515367
ER
PT J
AU Souter, I
Baltagi, LM
Toth, TL
Petrozza, JC
AF Souter, Irene
Baltagi, Lina M.
Toth, Thomas L.
Petrozza, John C.
TI Prevalence of hyperprolactinemia and abnormal magnetic resonance imaging
findings in a population with infertility
SO FERTILITY AND STERILITY
LA English
DT Editorial Material
DE Hyperprolactinemia; infertility; pituitary MRI; microadenoma
ID SERUM PROLACTIN; PITUITARY; MICROADENOMAS; HYPOGONADISM; GALACTORRHEA;
TOMOGRAPHY; AMENORRHEA; PREGNANCY; DIAGNOSIS; WOMEN
AB Hyperprolactinemia is rare among asymptomatic patients with infertility. Its prevalence and the mean PRL levels did not differ with [1] the infertility diagnosis, [2] the presence or absence of menstrual irregularities, or [3] the severity of menstrual dysregulation. Abnormal magnetic resonance imaging findings, though, are not uncommon among women with hyperprolactinemia despite the lack of symptoms and the mild PRL elevations. (Fertil Steril (R) 2010;94:1159-62. (C)2010 by American Society for Reproductive Medicine.)
C1 [Souter, Irene] Harvard Univ, Div Reprod Endocrinol & Infertil, Massachusetts Gen Hosp, Dept Obstet & Gynecol,Sch Med,Fertil Ctr, Boston, MA 02114 USA.
RP Souter, I (reprint author), Harvard Univ, Div Reprod Endocrinol & Infertil, Massachusetts Gen Hosp, Dept Obstet & Gynecol,Sch Med,Fertil Ctr, 55 Fruit St Yawkey 10A, Boston, MA 02114 USA.
EM isouter@partners.org
NR 23
TC 13
Z9 16
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD AUG
PY 2010
VL 94
IS 3
BP 1159
EP 1162
DI 10.1016/j.fertnstert.2009.12.017
PG 4
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 632FX
UT WOS:000280407900066
PM 20116788
ER
PT J
AU Rosenzweig, TM
Hartman, S
MacKenzie, E
AF Rosenzweig, Tamara M.
Hartman, Sarah
MacKenzie, Elizabeth
TI Disease-modifying therapy in adult relapsing-remitting multiple
sclerosis
SO FORMULARY
LA English
DT Article
ID TECHNOLOGY-ASSESSMENT SUBCOMMITTEE; PLACEBO-CONTROLLED TRIAL;
ACADEMY-OF-NEUROLOGY; WEEKLY INTERFERON BETA-1A; DOUBLE-BLIND;
GLATIRAMER ACETATE; IMMUNOMODULATORY TREATMENTS; DIAGNOSTIC-CRITERIA;
COST-EFFECTIVENESS; OPEN-LABEL
AB Multiple sclerosis (MS) is a significant cause of disability among young adults, more commonly women, and usually strikes patients in the prime of their lives. Despite recent therapeutic advancements, MS remains an incurable, chronic illness. Clinical evidence supports the role of disease-modifying therapy (DMT) early in the disease course to reduce the number of acute attacks, delay disease progression, maintain quality of life, and prevent disability. However, an estimated 43% of patients are not receiving DMT. Current guidelines provide direction for making the diagnosis, identifying MS subtypes and choosing initial therapy for the relapsing-remitting forms of the disease. This review presents a summary of available DMT agents indicated for the treatment of patients with relapsing-remitting MS (RRMS), briefly touches upon the management of acute attacks, and highlights new therapies being investigated for RRMS, which show promise as adjuncts to or alternatives to currently accepted strategies. (Formulary. 2010;45:252-262.)
C1 [Rosenzweig, Tamara M.; Hartman, Sarah] Univ Massachusetts, Sch Med, Clin Pharm Serv, Amherst, MA 01003 USA.
[MacKenzie, Elizabeth] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
RP Rosenzweig, TM (reprint author), Univ Massachusetts, Sch Med, Clin Pharm Serv, Amherst, MA 01003 USA.
NR 60
TC 0
Z9 0
U1 0
U2 7
PU ADVANSTAR COMMUNICATIONS INC
PI WOODLAND HILLS
PA 6200 CANOGA AVE, 2ND FLR, WOODLAND HILLS, CA 91367 USA
SN 1082-801X
J9 FORMULARY
JI Formulary
PD AUG
PY 2010
VL 45
IS 8
BP 252
EP 262
PG 11
GA 645TN
UT WOS:000281489200002
ER
PT J
AU Tracy, EE
Wiler, JL
Holschen, JC
Patel, SS
Ligda, KO
AF Tracy, Erin E.
Wiler, Jennifer L.
Holschen, Jolie C.
Patel, Soha Sumanchandra
Ligda, Kristin Ondecko
TI Topics to Ponder: Part-Time Practice and Pay Parity
SO GENDER MEDICINE
LA English
DT Article
DE women physicians; part-time practice; pay disparity
ID WORK-LIFE BALANCE; UNITED-STATES; PHYSICIANS; MEDICINE; WOMEN;
RADIOLOGISTS; GENERATION; FACULTY
AB Background: The medical profession has undergone a significant demographic change, with a dramatic increase in the number of women applying to medical school and practicing medicine.
Objectives: In recognition of the changing demographics in the medical profession, the American Medical Association's Women Physicians Congress (AMA-WPC) conducted a members' survey to identify the issues affecting women physicians and to ascertain certain practice characteristics.
Methods: In 2008, an e-mail survey link was sent to a randomly selected nationwide sample of 4992 WPC members, and a second, identical survey was sent to 596 female AMA members, utilizing the Epocrates database (Epocrates, Inc., San Mateo, California). Two e-mail reminders were sent for the first survey, which had a 15% response rate. A quota of 148 physicians was received within 4 days and was utilized to interpret results from the second survey.
Results: Achieving work life balance was a significant concern for 91% of the respondents (n = 884). Half of the respondents believed that pay is gender neutral, and 28% indicated that they were "somewhat or very concerned about sexual harassment." When queried regarding practice patterns, 29% of respondents indicated that they had worked part-time at some point during their careers.
Conclusions: In this survey, women physicians indicated that gender pay disparity and sexual harassment remain important issues in the medical profession. Less than a third of respondents had ever worked part-time, which should be a consideration for physician workforce studies. Barriers to part-time practice may exist. (Gend Med. 2010;7:350-356) (C) 2010 Excerpta Medica Inc.
C1 [Tracy, Erin E.] Massachusetts Gen Hosp, Boston, MA 02180 USA.
[Wiler, Jennifer L.] Washington Univ, St Louis, MO USA.
[Wiler, Jennifer L.] Univ Colorado, Denver, CO 80202 USA.
[Holschen, Jolie C.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Patel, Soha Sumanchandra] Univ S Florida, Coll Med, Tampa, FL USA.
[Ligda, Kristin Ondecko] Univ Pittsburgh, Dept Anesthesiol, Pittsburgh, PA USA.
RP Tracy, EE (reprint author), Massachusetts Gen Hosp, Founders 406,55 Fruit St, Boston, MA 02180 USA.
EM EETracy@partners.org
RI Wiler, Jennifer/G-7676-2016
NR 26
TC 5
Z9 5
U1 0
U2 0
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 1550-8579
J9 GENDER MED
JI Gend. Med.
PD AUG
PY 2010
VL 7
IS 4
BP 350
EP 356
DI 10.1016/j.genm.2010.07.003
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 648VP
UT WOS:000281722800008
PM 20869635
ER
PT J
AU Bogdan, R
Perlis, RH
Fagerness, J
Pizzagalli, DA
AF Bogdan, R.
Perlis, R. H.
Fagerness, J.
Pizzagalli, D. A.
TI The impact of mineralocorticoid receptor ISO/VAL genotype (rs5522) and
stress on reward learning
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Anhedonia; cortisol; depression; endophenotype; gene; glucocorticoid;
HPA; mineralocorticoid; reward; stress
ID PERCEIVED STRESS; MAJOR DEPRESSION; HEDONIC CAPACITY; HUMANS; INCREASES;
CORTISOL; RESPONSIVENESS; NEUROENDOCRINE; CANRENOATE; DISORDERS
AB Research suggests that stress disrupts reinforcement learning and induces anhedonia. The mineralocorticoid receptor (MR) determines the sensitivity of the stress response, and the missense iso/val polymorphism (IIe180Val, rs5522) of the MR gene (NR3C2) has been associated with enhanced physiological stress responses, elevated depressive symptoms and reduced cortisol-induced MR gene expression. The goal of these studies was to evaluate whether rs5522 genotype and stress independently and interactively influence reward learning. In study 1, participants (n = 174) completed a probabilistic reward task under baseline (i.e. no-stress) conditions. In study 2, participants (n = 53) completed the task during a stress (threat-of-shock) and no-stress condition. Reward learning, i.e. the ability to modulate behavior as a function of reinforcement history, was the main variable of interest. In study 1, in which participants were evaluated under no-stress conditions, reward learning was enhanced in val carriers. In study 2, participants developed a weaker response bias toward a more frequently rewarded stimulus under the stress relative to no-stress condition. Critically, stress-induced reward learning deficits were largest in val carriers. Although preliminary and in need of replication due to small sample size, findings indicate that psychiatrically healthy individuals carrying the MR val allele, gene, which has been recently linked to depression, showed a reduced ability to modulate behavior as a function of reward when facing an acute, uncontrollable stressor. Future studies are warranted to evaluate whether rs5522 genotype interacts with naturalistic stressors to increase the risk of depression and whether stress-induced anhedonia might moderate such risk.
C1 [Bogdan, R.; Pizzagalli, D. A.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Perlis, R. H.; Fagerness, J.] Massachusetts Gen Hosp, Ctr Human Genet Res, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA.
[Perlis, R. H.] Massachusetts Gen Hosp, Bipolar Clin & Res Program, Boston, MA 02114 USA.
[Perlis, R. H.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Pizzagalli, DA (reprint author), Harvard Univ, Dept Psychol, William James Hall 1220,33 Kirkland St, Cambridge, MA 02138 USA.
EM dap@wjh.harvard.edu
OI Bogdan, Ryan/0000-0002-1430-1045
FU NIH [R01 (MH68376), R21 (MH078979)]; Sackler Scholarship; NIMH NRSA
[R90; DA023427-01]
FX This work was supported by NIH R01 (MH68376) and R21 (MH078979) grants
to D.A.P. and a Sackler Scholarship and NIMH NRSA predoctoral training
grant (R90; DA023427-01) to R.B. The authors would like to thank Jeffrey
Birk, Sara Dainese, Brian Galloway, Elena Goetz, Allison Jahn, Yuliya
Nikolova, Miles Nugent, James O'Shea, Kyle Ratner, Sara Rubinstein,
Ritchie Siburian, Sunny Dutra and Yan Emily Yuan for study assistance.
Dr D.A.P. has received consulting fees from ANT North America Inc.
(Advanced Neuro Technology) and AstraZeneca, and honoraria from
AstraZeneca. Dr R.H.P. has received speakers or consulting
fees/honoraria from AstraZeneca, BMS, Eli Lilly & Co., GSK, Pfizer,
Concordant Rater Systems and Proteus Biomedical. Dr R.H.P. is a major
stockholder in Concordant Rater Systems, LLC. R.B. and J.F. report no
competing interests.
NR 54
TC 26
Z9 27
U1 0
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD AUG
PY 2010
VL 9
IS 6
BP 658
EP 667
DI 10.1111/j.1601-183X.2010.00600.x
PG 10
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 640FA
UT WOS:000281032700012
PM 20528958
ER
PT J
AU Klusmann, JH
Godinho, FJ
Heitmann, K
Maroz, A
Koch, ML
Reinhardt, D
Orkin, SH
Li, Z
AF Klusmann, Jan-Henning
Godinho, Frank J.
Heitmann, Kirsten
Maroz, Aliaksandra
Koch, Mia Lee
Reinhardt, Dirk
Orkin, Stuart H.
Li, Zhe
TI Developmental stage-specific interplay of GATA1 and IGF signaling in
fetal megakaryopoiesis and leukemogenesis
SO GENES & DEVELOPMENT
LA English
DT Article
DE DS-AMKL; Down syndrome; GATA1; IGF signaling; IGF1R; megakaryoblastic
leukemia
ID HEMATOPOIETIC STEM-CELLS; FACTOR-II GENE; DOWN-SYNDROME; GROWTH-FACTOR;
MEGAKARYOBLASTIC LEUKEMIA; CYCLE PROGRESSION; MEGAKARYOCYTIC LEUKEMIA;
TARGET GENES; INSULIN; TRANSCRIPTION
AB Oncogene-mediated transformation of hematopoietic cells has been studied extensively, but little is known about the molecular basis for restriction of oncogenes to certain target cells and differential cellular context-specific requirements for oncogenic transformation between infant and adult leukemias. Understanding cell type-specific interplay of signaling pathways and oncogenes is essential for developing targeted cancer therapies. Here, we address the vexing issue of how developmental restriction is achieved in Down syndrome acute megakaryoblastic leukemia (DS-AMKL), characterized by the triad of fetal origin, mutated GATA1 (GATA1s), and trisomy 21. We demonstrate overactivity of insulin-like growth factor (IGF) signaling in authentic human DS-AMKL and in a DS-AMKL mouse model generated through retroviral insertional mutagenesis. Fetal but not adult megakaryocytic progenitors are dependent on this pathway. GATA1 restricts IGF-mediated activation of the E2F transcription network to coordinate proliferation and differentiation. Failure of a direct GATA1-E2F interaction in mutated GATA1s converges with overactive IGF signaling to promote cellular transformation of DS fetal progenitors, revealing a complex, fetal stage-specific regulatory network. Our study underscores context-dependent requirements during oncogenesis, and explains resistance to transformation of ostensibly similar adult progenitors.
C1 [Klusmann, Jan-Henning; Godinho, Frank J.; Orkin, Stuart H.; Li, Zhe] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Klusmann, Jan-Henning; Heitmann, Kirsten; Maroz, Aliaksandra; Koch, Mia Lee; Reinhardt, Dirk] Hannover Med Sch, Dept Pediat Hematol Oncol, D-3000 Hannover, Germany.
[Godinho, Frank J.; Orkin, Stuart H.] Howard Hughes Med Inst, Boston, MA 02115 USA.
[Koch, Mia Lee; Li, Zhe] Brigham & Womens Hosp, Div Genet, Boston, MA 02115 USA.
[Orkin, Stuart H.; Li, Zhe] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Orkin, Stuart H.; Li, Zhe] Harvard Stem Cell Inst, Boston, MA 02115 USA.
[Orkin, Stuart H.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
RP Orkin, SH (reprint author), Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
EM Stuart_Orkin@dfci.harvard.edu
RI Reinhardt, Dirk/D-3939-2011; Klusmann, Jan-Henning/M-9655-2015
OI Reinhardt, Dirk/0000-0003-4313-9056; Klusmann,
Jan-Henning/0000-0002-1070-0727
FU NCI; German National Academic Foundation [KL-2374/1-1]; NIH
FX We thank Dr. H. Hock, J. Schindler, J. Schoning, T.V. Raghavan, K.
Bohmer, M. Wackerhahn, T. Pushpanathan, Dr. J. Skokowa, K. Gupta, Dr. B.
Thakur, and Dr. Y. Fujiwara for suggestions and/or technical assistance;
M. Hamblen for general laboratory support; G. Losyev and Dr. M.
Ballmaier for cell sorting; Dr. M. Zimmermann for statistical
assistance; Drs. A. Schambach and C. Baum for providing plasmids and
assistance with lentiviral transduction; Dr. N. von Neuhoff for
providing support and assistance with protein analyses; Drs. K. Bernt
and S. Armstrong for Mll-Af9 leukemic cells; and Dr. A. Cantor for the
BioGata1/BioGata1s constructs and for sharing
unpublished data. Z.L. was a Fellow of the Leukemia and Lymphoma
Society, and was supported by a K99 Pathway-to-Independence award from
NCI. This work was supported by a grant to J.H.K. and D.R. from the
German National Academic Foundation (KL-2374/1-1), and a grant to S.H.O.
from the NIH. S.H.O. is an Investigator of the Howard Hughes Medical
Institute.
NR 51
TC 57
Z9 58
U1 0
U2 3
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI WOODBURY
PA 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2924 USA
SN 0890-9369
J9 GENE DEV
JI Genes Dev.
PD AUG 1
PY 2010
VL 24
IS 15
BP 1659
EP 1672
DI 10.1101/gad.1903410
PG 14
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 634QE
UT WOS:000280597200012
PM 20679399
ER
PT J
AU Apger, J
Reubens, M
Henderson, L
Gouge, CA
Ilic, N
Zhou, HH
Christensen, TW
AF Apger, Jennifer
Reubens, Michael
Henderson, Laura
Gouge, Catherine A.
Ilic, Nina
Zhou, Helen H.
Christensen, Tim W.
TI Multiple Functions for Drosophila Mcm10 Suggested Through Analysis of
Two Mcm10 Mutant Alleles
SO GENETICS
LA English
DT Article
ID DNA POLYMERASE-ALPHA; ORIGIN RECOGNITION COMPLEX;
SACCHAROMYCES-CEREVISIAE; HETEROCHROMATIN PROTEIN-1; REPLICATION
FACTORS; CHROMOSOME STRUCTURE; CATALYTIC SUBUNIT; BUDDING YEAST;
CHROMATIN; INITIATION
AB DNA replication and the correct packaging of DNA into different states of chromatin are both essential processes in all eukaryotic cells. High-fidelity replication of DNA is essential for the transmission of genetic material to cells. Likewise the maintenance of the epigenetic chromatin states is essential to the faithful reproduction of the transcriptional state of the cell. It is becoming more apparent that these two processes are linked through interactions between DNA replication proteins and chromatin-associated proteins. In addition, more proteins are being discovered that have dual roles in both DNA replication and the maintenance of epigenetic states. We present an analysis of two Drosophila mutants in the conserved DNA replication protein Mcm10. A hypomorphic mutant demonstrates that Mcm10 has a role in heterochromatic silencing and chromosome condensation, while the analysis of a novel C-terminal truncation allele of Mcm10 suggests that an interaction with Mcm2 is not required for chromosome condensation and heterochromatic silencing but is important for DNA replication.
C1 [Apger, Jennifer; Reubens, Michael; Henderson, Laura; Gouge, Catherine A.; Christensen, Tim W.] E Carolina Univ, Dept Biol, Greenville, NC 27858 USA.
[Ilic, Nina] Harvard Univ, Sch Med, Dept Canc Biol, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Zhou, Helen H.] ZS Associates, Boston, MA 02108 USA.
RP Christensen, TW (reprint author), E Carolina Univ, Dept Biol, Howell Sci Complex,S309, Greenville, NC 27858 USA.
EM christensent@ecu.edu
FU Hughes Undergraduate Research and Cornell Presidential Research Scholars
programs; National Science Foundation [NSF 0453773]; East Carolina
University; National Institutes of Health [1R15GM093328-01]
FX We thank and are grateful to Bik Tye for providing support for the
initial work and Ross MacIntyre for advice and reagents, especially his
contribution of expertise and flies lines for the PEV analysis. We thank
Patrick Ferree, Bonnie Bolkan, Daniel Barbash, Janice Werner, Michael
Goldberg, Byron Wilson, and members of the Cornell Superfly group for
input and advice. We also thank Alexey A. Soshnev from Carver College of
Medicine for useful advice concerning ovary dissection and nurse cell
visualization. In addition, at East Carolina University Tom Fink of the
Imaging Core supported our imaging efforts. Support for undergraduate
research on this project was provided by the Hughes Undergraduate
Research and Cornell Presidential Research Scholars programs. Support
for the initial work was provided by the National Science Foundation
(NSF 0453773). Finally we thank East Carolina University for start-up
funds and the National Institutes of Health (grant 1R15GM093328-01
awarded to T.W.C.).
NR 49
TC 16
Z9 16
U1 0
U2 2
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 0016-6731
J9 GENETICS
JI Genetics
PD AUG
PY 2010
VL 185
IS 4
BP 1151
EP U44
DI 10.1534/genetics.110.117234
PG 17
WC Genetics & Heredity
SC Genetics & Heredity
GA 651EM
UT WOS:000281907700003
PM 20498296
ER
PT J
AU Tseveleki, V
Rubio, R
Vamvakas, SS
White, J
Taoufik, E
Petit, E
Quackenbush, J
Probert, L
AF Tseveleki, Vivian
Rubio, Renee
Vamvakas, Sotiris-Spyros
White, Joseph
Taoufik, Era
Petit, Edwige
Quackenbush, John
Probert, Lesley
TI Comparative gene expression analysis in mouse models for multiple
sclerosis, Alzheimer's disease and stroke for identifying commonly
regulated and disease-specific gene changes
SO GENOMICS
LA English
DT Article
DE cDNA microarrays; Brain inflammation; Cerebral stroke; Alzheimer's
disease; Systems biology; Gene expression profiling
ID AUTOIMMUNE ENCEPHALOMYELITIS; MICROARRAY ANALYSIS; NEURITE OUTGROWTH;
ISCHEMIC-STROKE; NEURONAL DEATH; ANIMAL-MODEL; BRAIN; CELLS; BETA;
DEMYELINATION
AB The brain responds to injury and infection by activating innate defense and tissue repair mechanisms. Working upon the hypothesis that the brain defense response involves common genes and pathways across diverse pathologies, we analysed global gene expression in brain from mouse models representing three major central nervous system disorders, cerebral stroke, multiple sclerosis and Alzheimer's disease compared to normal brain using DNA microarray expression profiling. A comparison of dysregulated genes across disease models revealed common genes and pathways including key components of estrogen and TGF-beta signaling pathways that have been associated with neuroprotection as well as a neurodegeneration mediator, TRPM7. Further, for each disease model, we discovered collections of differentially expressed genes that provide novel insight into the individual pathology and its associated mechanisms. Our data provide a resource for exploring the complex molecular mechanisms that underlie brain neurodegeneration and a new approach for identifying generic and disease-specific targets for therapy. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Tseveleki, Vivian; Vamvakas, Sotiris-Spyros; Taoufik, Era; Probert, Lesley] Hellenic Pasteur Inst, Mol Genet Lab, Athens 11521, Greece.
[Rubio, Renee; White, Joseph; Quackenbush, John] Dana Farber Canc Inst, Lab Computat Biol & Funct Genom, Boston, MA 02115 USA.
[Rubio, Renee; White, Joseph; Quackenbush, John] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Petit, Edwige] Univ Caen, Ctr Cyceron, CNRS, UMR 6185, F-14032 Caen, France.
RP Probert, L (reprint author), Hellenic Pasteur Inst, Mol Genet Lab, Athens 11521, Greece.
EM vtseveleki@pasteur.gr; rrubio@jimmy.harvard.edu;
vamvakas@bio.demokritos.gr; jwhite@jimmy.harvard.edu;
etaoufik@pasteur.gr; epetit@cyceron.fr; johnq@jimmy.harvard.edu;
lesley@pasteur.gr
RI PETIT, Edwige/C-1896-2008
FU Greek Secretariat of Research and Technology, EPAN Greece-USA; European
Union; NeuroproMiSe [LSHM-CT-2005-018637]
FX This work was supported by a bidirectional collaboration research
program from the Greek Secretariat of Research and Technology, EPAN
Greece-USA and by the 6th Framework Program of the European Union,
NeuroproMiSe, LSHM-CT-2005-018637. We wish to thank Matthias Staufenbiel
(Novartis Pharma Ltd., Basel, Switzerland) for providing the APP23 mice.
We wish to extend our special thanks to Adriana Ahumada, Razvan Sultana,
Tove Anderson, Brian Frank and other members of the Quackenbush
laboratory and Nikos Simos, Anda Voulgari-Kokota and Christos Georgiadis
from the Probert laboratory for help and discussions.
NR 50
TC 30
Z9 31
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0888-7543
J9 GENOMICS
JI Genomics
PD AUG
PY 2010
VL 96
IS 2
BP 82
EP 91
DI 10.1016/j.ygeno.2010.04.004
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 632RA
UT WOS:000280443800003
PM 20435134
ER
PT J
AU Chapman, E
Venkat, P
Ko, E
Orezzoli, JP
Del Carmen, M
Garner, EIO
AF Chapman, Eloise
Venkat, Pavithra
Ko, Emily
Orezzoli, Jorge P.
Del Carmen, Marcela
Garner, Elizabeth I. O.
TI Use of multimedia as an educational tool to improve human papillomavirus
vaccine acceptability-A pilot study
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE Human papillomavirus (HPV); Vaccine; Education; Acceptability; Survey;
Disparity
ID HPV VACCINATION; PUBLIC-HEALTH; UNITED-STATES; ADOLESCENTS; PARENTS;
ACCEPTANCE; INFECTION; ATTITUDES; POLITICS; CANCER
AB Objective. To determine, through a pilot study, whether use of a video-based educational tool can influence overall human papillomavirus (HPV) vaccine acceptability, views on vaccine mandates, school vaccination, and acceptable age for vaccination.
Methods. Written surveys addressing HPV knowledge and vaccine acceptability were administered to study participants from January to March 2007. An initial 32-question survey was completed, followed by an 8-minute educational video, and a post-video assessment.
Results. Out of 256 subjects, 73.0% watched the video and completed all surveys. Eighty percent of the subjects had heard of HPV, while 65.0% knew, prior to viewing the video, that the vaccine was available. Individual vaccine acceptability increased from 66.7% to 78.0% after the video (p = .0014). Prior to the video, 54.8% of subjects supported mandatory HPV vaccination, with 51.1% supporting school vaccination, and 66.7% accepting vaccination if it were free. After the video, these percentages increased to 72.6% (p<.0001), 65.1% (p<.0001) and 86.6% (p<.0001) respectively. Initially, 56.5% of subjects would vaccinate their child at 15 years of age or younger. After the video, 94.1% approved of vaccination from age 9 (p<.0001). Secondary analysis revealed Hispanics, African Americans, and lower income families were more likely to accept HPV vaccination after the video. A perception that vaccination promotes sex, and whether or not participants talk to their children about sex, did not affect acceptability.
Conclusion. Using an educational video significantly increased overall HPV vaccine acceptability and acceptance in younger age groups. This may be an effective means of increasing awareness and acceptability of HPV vaccination. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Chapman, Eloise; Venkat, Pavithra; Ko, Emily; Garner, Elizabeth I. O.] Brigham & Womens Hosp, Dept Obstet & Gynecol, Boston, MA 02115 USA.
[Orezzoli, Jorge P.; Del Carmen, Marcela] Massachusetts Gen Hosp, Dept Obstet & Gynecol, Boston, MA 02114 USA.
[Chapman, Eloise; Ko, Emily; Orezzoli, Jorge P.; Del Carmen, Marcela; Garner, Elizabeth I. O.] Harvard Univ, Sch Med, Boston, MA USA.
RP Chapman, E (reprint author), Northwestern Univ, Sch Med, Dept Obstet & Gynecol, Div Gynecol Oncol, 250 E Super St,5-2168, Chicago, IL 60611 USA.
EM eloise.chapman@gmail.com
FU Harvard Medical School Center for Excellence in Minority Health and
Health Disparities; Yale School of Medicine
FX This study was supported by a fellowship from the Harvard Medical School
Center for Excellence in Minority Health and Health Disparities and the
Yale School of Medicine Student Research Program.
NR 24
TC 8
Z9 9
U1 1
U2 10
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 AUG 1
PY 2010
VL 118
IS 2
BP 103
EP 107
DI 10.1016/j.ygyno.2010.04.010
PG 5
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 627LB
UT WOS:000280039900002
PM 20457469
ER
PT J
AU Ruchelsman, DE
Mudgal, CS
Jupiter, JB
AF Ruchelsman, David E.
Mudgal, Chaitanya S.
Jupiter, Jesse B.
TI The Role of Locking Technology in the Hand
SO HAND CLINICS
LA English
DT Article
DE Locking plates; Metacarpal and phalanx fractures; Hand trauma
ID PROXIMAL HUMERUS FRACTURES; DISTAL RADIAL FRACTURES; INVASIVE
STABILIZATION SYSTEM; PLATE FIXATION; PHALANGEAL FRACTURES; METACARPAL
FRACTURES; MINICONDYLAR PLATE; INTERNAL-FIXATION; FEMORAL FRACTURES;
FEMUR FRACTURES
AB Locked fixed-angle plating in the hand and wrist helps to optimize outcomes following surgical fixation of select acute fractures and complex reconstructions. Select indications include unstable distal ulna head/neck fractures, periarticular metacarpal and phalangeal fractures, comminuted/multifragmentary diaphyseal fractures with bone loss (ie, combined injuries of the hand), osteopenic/pathologic fractures, non-unions and corrective osteotomy fixation, and small joint arthrodesis. Locked plating techniques in the hand should not be seen as a panacea for wrist and digital acute trauma and delayed reconstructions. An understanding of the biomechanics of fixed-angle plating and proper technical application of locking constructs will optimize outcomes and minimize complications. As clinical experience with locking technology in hand trauma broadens, new indications and applications will emerge. Currently, several systems are available. The specific implants share common features in their protocols for insertion, but unique differences in their design (ie, individual locking mechanisms, uniaxial vs polyaxial locking capability, metallurgy, and plate profiles) must be appreciated and considered preoperatively.
C1 [Ruchelsman, David E.; Mudgal, Chaitanya S.; Jupiter, Jesse B.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Hand & Upper Extrem Serv,Yawkey Ctr, Boston, MA 02114 USA.
[Ruchelsman, David E.; Mudgal, Chaitanya S.; Jupiter, Jesse B.] Harvard Univ, Sch Med, Dept Orthopaed Surg, Boston, MA 02114 USA.
RP Jupiter, JB (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Hand & Upper Extrem Serv,Yawkey Ctr, 55 Fruit St,Suite 2100, Boston, MA 02114 USA.
EM jjupiter1@partners.org
NR 63
TC 10
Z9 11
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0749-0712
J9 HAND CLIN
JI Hand Clin.
PD AUG
PY 2010
VL 26
IS 3
BP 307
EP +
DI 10.1016/j.hcl.2010.04.001
PG 14
WC Orthopedics
SC Orthopedics
GA 644CX
UT WOS:000281349800002
PM 20670796
ER
PT J
AU Monica, JT
Mudgal, CS
AF Monica, James T.
Mudgal, Chaitanya S.
TI Radial Head Arthroplasty
SO HAND CLINICS
LA English
DT Article
DE Radial head; Fracture; Arthroplasty
ID VALGUS STABILITY; FRACTURES; ELBOW; REPLACEMENT; PROSTHESIS; EXCISION
AB Radial head arthroplasty remains an encouraging treatment option for comminuted radial head fractures in an unstable elbow or forearm. This article discusses the surgical considerations related to radial head arthroplasty, including anatomy, indications, and surgical technique. Radial head arthroplasty outcomes literature and a review of current implant options are also discussed.
C1 [Monica, James T.; Mudgal, Chaitanya S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Yawkey Ctr, Hand & Upper Extrem Surg Serv,Dept Orthopaed Surg, Boston, MA 02114 USA.
RP Mudgal, CS (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med,Yawkey Ctr, Hand & Upper Extrem Surg Serv,Dept Orthopaed Surg, 55 Fruit St,Suite 2100, Boston, MA 02114 USA.
EM cmudgal@partners.org
NR 31
TC 2
Z9 2
U1 0
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0749-0712
J9 HAND CLIN
JI Hand Clin.
PD AUG
PY 2010
VL 26
IS 3
BP 403
EP +
DI 10.1016/j.hcl.2010.04.008
PG 9
WC Orthopedics
SC Orthopedics
GA 644CX
UT WOS:000281349800011
PM 20670805
ER
PT J
AU Guitton, TG
Ring, D
AF Guitton, Thierry G.
Ring, David
TI Three-Dimensional Computed Tomographic Imaging and Modeling in the Upper
Extremity
SO HAND CLINICS
LA English
DT Article
DE Computed tomography; Imaging; Modeling; Upper extremity
ID CORRECTIVE OSTEOTOMY; FRACTURES; RADIUS; RELIABILITY
AB Technologic advances in imaging of the upper extremity have taken an immense leap in the last decade. So has the amount of research that has been published on this subject. Three-dimensional (3D) reconstructions, in particular, have improved identification of fracture characteristics, such as fragments, fracture edges, and articular surfaces. Three-dimensional physical models can even increase the advantages of the 3D reconstructions. Together, 3D reconstructions and physical modeling may outweigh the disadvantages of increased cost, resource usage, and additional time, as research has shown that it can benefit both the surgeon and the patient significantly.
C1 [Guitton, Thierry G.; Ring, David] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Orthopaed Hand & Upper Extrem Serv,Yawkey Ctr, Boston, MA 02114 USA.
RP Ring, D (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Orthopaed Hand & Upper Extrem Serv,Yawkey Ctr, Suite 2100,55 Fruit St, Boston, MA 02114 USA.
EM dring@partners.org
OI Guitton, Thierry/0000-0002-2599-1985
NR 12
TC 8
Z9 8
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 0749-0712
J9 HAND CLIN
JI Hand Clin.
PD AUG
PY 2010
VL 26
IS 3
BP 447
EP +
DI 10.1016/j.hcl.2010.04.007
PG 8
WC Orthopedics
SC Orthopedics
GA 644CX
UT WOS:000281349800015
PM 20670809
ER
PT J
AU Francis, NA
Guinan, JJ
AF Francis, Nikolas A.
Guinan, John J., Jr.
TI Acoustic stimulation of human medial olivocochlear efferents reduces
stimulus-frequency and click-evoked otoacoustic emission delays:
Implications for cochlear filter bandwidths
SO HEARING RESEARCH
LA English
DT Article
ID SUPERIOR OLIVARY COMPLEX; AUDITORY-NERVE RESPONSES; TUNING CURVES;
CONTRALATERAL SUPPRESSION; WAVELET ANALYSIS; REFLEX; DEPENDENCE; PHASE;
MODEL; SOUND
AB Filter theory indicates that changes in cochlear filter bandwidths are accompanied by changes in cochlear response latencies. Previous reports indicate that otoacoustic emission (OAE) delays are reduced by exciting medial olivocochlear (MOC) efferents with contralateral broad-band noise (CBBN). These delay reductions are consistent with MOC-induced widening of cochlear filters. We quantified the MOC-induced changes in human cochlear filter-related delays using stimulus-frequency and click-evoked OAEs (SFOAE and CEOAEs), recorded with and without MOC activity elicited by 60 dB SPL CBBN. MOC-induced delay changes were measured from the slopes of SFOAE phase functions and from cross-correlation of 500 Hz-wide CEOAE frequency-band waveform magnitudes. The delay changes measured from CEOAEs and SFOAEs were statistically indistinguishable. Both showed greater delay reductions at lower frequencies (a 5% decrease in the 0.5-2 kHz frequency region). These data indicate that cochlear filters are widened 5% by the MOC activity from moderate-level CBBN. Psychophysically, the large changes in cochlear response latencies, implied by the 0.5 ms change in OAE delay at low frequencies, would have a profound effect on binaural localization if they were not balanced in the central nervous system, or by the MOC system producing similar changes in both ears. (C) 2010 Elsevier B.V. All rights reserved.
C1 [Francis, Nikolas A.; Guinan, John J., Jr.] Harvard MIT Div Hlth Sci & Technol, Speech & Hearing Biosci & Technol, Cambridge, MA 02139 USA.
[Francis, Nikolas A.; Guinan, John J., Jr.] Massachusetts Eye & Ear Infirm, Eaton Peabody Labs Auditory Physiol, Dept Otolaryngol, Boston, MA 02114 USA.
[Guinan, John J., Jr.] Harvard Univ, Dept Otol & Laryngol, Sch Med, Boston, MA 02115 USA.
RP Francis, NA (reprint author), Massachusetts Eye & Ear Infirm, Eaton Peabody Lab, 243 Charles St, Boston, MA 02114 USA.
EM nfu@mit.edu
FU NIH NIDCD [RO1 DC005977, P30 DC005209, T32 DC00038]
FX We thank Radha Kalluri, Jeffery Lichtenhan and Christopher Shera for
comments on the manuscript. Supported by NIH NIDCD RO1 DC005977, P30
DC005209 and T32 DC00038.
NR 62
TC 31
Z9 31
U1 2
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-5955
J9 HEARING RES
JI Hear. Res.
PD AUG 1
PY 2010
VL 267
IS 1-2
BP 36
EP 45
DI 10.1016/j.heares.2010.04.009
PG 10
WC Audiology & Speech-Language Pathology; Neurosciences;
Otorhinolaryngology
SC Audiology & Speech-Language Pathology; Neurosciences & Neurology;
Otorhinolaryngology
GA 631MO
UT WOS:000280351700005
PM 20430088
ER
PT J
AU Hou, JB
Qi, H
Zhang, MM
Ma, LJ
Liu, HM
Han, ZG
Meng, LB
Yang, SA
Zhang, SS
Yu, B
Jang, IK
AF Hou, Jingbo
Qi, Hai
Zhang, Maomao
Ma, Lijia
Liu, Huimin
Han, Zhigang
Meng, Lingbo
Yang, Shuang
Zhang, Shaosong
Yu, Bo
Jang, Ik-Kyung
TI Development of lipid-rich plaque inside bare metal stent: possible
mechanism of late stent thrombosis? An optical coherence tomography
study
SO HEART
LA English
DT Article
ID CORONARY-ARTERY-DISEASE; SIROLIMUS-ELUTING STENT; FOLLOW-UP; BALLOON
ANGIOPLASTY; IMPLANTATION; PLACEMENT
AB Aims To study in-stent tissue characteristics by optical coherence tomography (OCT) at long-term follow-up in patients with previous bare metal stent implantation.
Methods and results Among 1636 patients who underwent bare metal stent (BMS) implantation between 1999 and 2006, 39 patients with 60 BMS who developed recurrent ischaemia underwent repeat catheterisation and OCT imaging between June 2008 and August 2009. The average time interval between initial BMS implantation and OCT imaging was 6.5 +/- 1.3 years. A lesion that had features of lipid-rich plaque was found in 20 stents (33.3%) in 16 patients (41%). Fibrous intima was observed in the remaining 40 stents. In the group with lipid-rich plaque, average fibrous cap thickness was 56.7 +/- 5.8 mu m and lipid arc was 173 +/- 58. Six patients had evidence of recent plaque disruption and another six patients had mural thrombus. Hypertension and smoking were more common in these patients than in those with fibrous intima.
Conclusions Lipid-rich plaque with a thin fibrous cap was seen in patients with previous BMS implantation and recurrent ischaemia at late follow-up. This may be one possible mechanism for late stent thrombosis.
C1 [Hou, Jingbo; Qi, Hai; Zhang, Maomao; Ma, Lijia; Liu, Huimin; Han, Zhigang; Meng, Lingbo; Yang, Shuang; Yu, Bo] Harbin Med Coll, Affiliated Hosp 2, Dept Cardiol, Key Labs Educ,Minist Myocardial Ischaemia Mech &, Harbin, Heilongjiang, Peoples R China.
[Zhang, Shaosong] LightLab Imaging Inc, Westford, MA USA.
[Jang, Ik-Kyung] Harvard Univ, Massachusetts Gen Hosp, Sch Med, CLIPI,Cardiol Div, Boston, MA USA.
RP Yu, B (reprint author), Harbin Med Coll, Affiliated Hosp 2, Dept Cardiol, Key Labs Educ,Minist Myocardial Ischaemia Mech &, Harbin, Heilongjiang, Peoples R China.
EM yubodr@163.com
FU LightLab Imaging
FX SZ is an employee of LightLab Imaging; IKJ received research grant from
LightLab Imaging.
NR 20
TC 34
Z9 35
U1 1
U2 3
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1355-6037
J9 HEART
JI Heart
PD AUG
PY 2010
VL 96
IS 15
BP 1187
EP 1190
DI 10.1136/hrt.2010.194381
PG 4
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 626HJ
UT WOS:000279956700005
PM 20639235
ER
PT J
AU Milan, DJ
Lubitz, SA
Kaab, S
Ellinor, PT
AF Milan, David J.
Lubitz, Steven A.
Kaeaeb, Stefan
Ellinor, Patrick T.
TI Genome-wide association studies in cardiac electrophysiology: Recent
discoveries and implications for clinical practice
SO HEART RHYTHM
LA English
DT Article
DE Genome wide association study; atrial fibrillation; gene; mutation
ID QT INTERVAL DURATION; ATRIAL-FIBRILLATION; COMMON VARIANTS; PR INTERVAL;
POTASSIUM CHANNEL; GENETIC-VARIATION; CHROMOSOME 4Q25; RISK;
POPULATIONS; MUTATIONS
AB Genome-wide association studies have been increasingly used to study the genetics of complex human diseases. Within the field of cardiac electrophysiology, this technique has been applied to conditions such as atrial fibrillation, and several electrocardiographic parameters including the QT interval. While these studies have identified multiple genomic regions associated with each trait, questions remain, including the best way to explore the pathophysiology of each association and the potential for clinical utility. This review will summarize recent genome-wide association study results within cardiac electrophysiology and discuss their broader implications in basic science and clinical medicine.
C1 [Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Milan, David J.; Lubitz, Steven A.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA USA.
[Lubitz, Steven A.] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
[Kaeaeb, Stefan] Univ Munich, Univ Hosp Grosshadern, Dept Med 1, Munich, Germany.
RP Ellinor, PT (reprint author), Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Cardiovasc Res Ctr, Boston, MA 02114 USA.
EM pellinor@partners.org
RI Kaab, Stefan/H-3915-2012
FU National Institutes of Health [K08HL076361, R21DA026982, HL092577,
DA027021, T32HL007575]; Fondation Leducq [07-CVD 03]; German National
Genome Research Network (NGFN) [01GS0838]; German AF-Net [01 GI 0204/N];
Exzellenzinitiative at Ludwig-Maximilians University, Munich
FX Supported by grants from the National Institutes of Health (K08HL076361,
R21DA026982, HL092577, DA027021, T32HL007575), Fondation Leducq (07-CVD
03), German National Genome Research Network (NGFN, 01GS0838), German
AF-Net (01 GI 0204/N), and Exzellenzinitiative at Ludwig-Maximilians
University, Munich. Address reprint requests and correspondence: Patrick
T. Ellinor, Cardiac Arrhythmia Service, Cardiovascular Research Center,
Massachusetts General Hospital, Boston, Massachusetts 02114. E-mail
address: pellinor@partners.org. (Received March 17, 2010; accepted April
21, 2010.)
NR 40
TC 14
Z9 14
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1547-5271
J9 HEART RHYTHM
JI Heart Rhythm
PD AUG
PY 2010
VL 7
IS 8
BP 1141
EP 1148
DI 10.1016/j.hrthm.2010.04.021
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 629ZE
UT WOS:000280239300022
PM 20423731
ER
PT J
AU Rimbara, E
Shulman, RJ
Abraham, BP
Sabounchi, S
Attumi, TA
Opekun, AR
Graham, DY
AF Rimbara, E.
Shulman, R. J.
Abraham, B. P.
Sabounchi, S.
Attumi, T. A.
Opekun, A. R.
Graham, D. Y.
CA Baylor IBD Study Grp
TI Detection of non-pylori Helicobacter species from IBD, IBS and healthy
subjects: preliminary results
SO HELICOBACTER
LA English
DT Meeting Abstract
CT 23rd International Workshop on Helicobacter and Related Bacteria in
Chronic Digestive Inflammation and Gastric Cancer
CY SEP 16-18, 2010
CL Rotterdam, NETHERLANDS
C1 [Rimbara, E.; Sabounchi, S.; Attumi, T. A.; Graham, D. Y.] VA Med Ctr, Houston, TX USA.
[Shulman, R. J.; Abraham, B. P.; Opekun, A. R.] Baylor Coll Med, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1083-4389
J9 HELICOBACTER
JI Helicobacter
PD AUG
PY 2010
VL 15
IS 4
BP 325
EP 325
PG 1
WC Gastroenterology & Hepatology; Microbiology
SC Gastroenterology & Hepatology; Microbiology
GA 626SC
UT WOS:000279986200042
ER
PT J
AU El-Serag, HB
Talwalkar, J
Kim, WR
AF El-Serag, Hashem B.
Talwalkar, Jayant
Kim, W. Ray
TI Efficacy, Effectiveness, and Comparative Effectiveness in Liver Disease
SO HEPATOLOGY
LA English
DT Editorial Material
ID HEPATITIS-C; UNITED-STATES; HEALTH-CARE; PREDICTORS; DISPARITIES;
POPULATION; VETERANS; MEDICINE
C1 [Talwalkar, Jayant; Kim, W. Ray] Mayo Clin, Div Gastroenterol & Hepatol, Coll Med, Rochester, MN 55906 USA.
[Talwalkar, Jayant; Kim, W. Ray] Mayo Clin, Div Healthcare Policy & Res, Coll Med, Rochester, MN 55906 USA.
[El-Serag, Hashem B.] Michael E DeBakey Dept Vet Affairs Med Ctr, Gastroenterol Sect, Houston, TX USA.
[El-Serag, Hashem B.] Michael E DeBakey Dept Vet Affairs Med Ctr, Sect Hlth Serv Res, Houston, TX USA.
[El-Serag, Hashem B.] Baylor Coll Med, Houston, TX 77030 USA.
RP Kim, WR (reprint author), Mayo Clin, Div Gastroenterol & Hepatol, Coll Med, PL 6,200 1st St SW, Rochester, MN 55906 USA.
EM kim.ray@mayo.edu
NR 16
TC 24
Z9 25
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD AUG
PY 2010
VL 52
IS 2
BP 403
EP 407
DI 10.1002/hep.23819
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 633OZ
UT WOS:000280513900001
PM 20683939
ER
PT J
AU Afzali, A
Weiss, NS
Boyko, EJ
Ioannou, GN
AF Afzali, Anita
Weiss, Noel S.
Boyko, Edward J.
Ioannou, George N.
TI Association Between Serum Uric Acid Level and Chronic Liver Disease in
the United States
SO HEPATOLOGY
LA English
DT Article
ID ALANINE AMINOTRANSFERASE ACTIVITY; CIRRHOSIS-RELATED DEATH;
CARDIOVASCULAR RISK; HYPERURICEMIA; POPULATION; PREVALENCE;
HOSPITALIZATION; CONSUMPTION; PREDICTORS; OBESITY
AB Elevated serum uric acid (UA) levels strongly reflect and may even cause oxidative stress, insulin resistance, and metabolic syndrome, which are risk factors for the progression of liver disease. We sought to determine whether serum UA levels are associated with the development of cirrhosis or the presence of elevated serum liver enzymes. We used cohort data from the first National Health and Nutrition Examination Survey (NHANES I) to determine whether the baseline serum UA level was associated with the incidence of hospitalization or death due to cirrhosis among 5518 participants during a mean follow-up of 12.9 years (range = 4-21 years) after the exclusion of the first 4 years of follow-up. We also used cross-sectional data from NHANES 1988-1994 (n = 10,993) and NHANES 19992006 (n = 6186) to determine whether the serum UA level was associated with elevated serum alanine aminotransferase (ALT) or gamma-glutamyl transferase (GGT), two markers of hepatic necroinflammation. Compared to persons in the lower third of the distribution of serum UA (<4.8 mg/dL), those in the top third (>6 mg/dL) had a higher risk of cirrhosis-related hospitalization or death [adjusted hazard ratio (AHR) = 2.8, 95% confidence interval (CI) =1.3-5.7], whereas the risk was not substantially increased in persons within the middle third (serum UA level = 2.6-4.8 mg/dL, AHR = 1.3, 95% CI = 0.6-2.7). A higher serum UA level was associated with greater mean serum ALT and GGT levels and a greater probability of elevated serum ALT and GGT. Conclusion: The serum UA level is associated with the development of cirrhosis and the presence of elevated serum liver enzymes after adjustments for important causes and risk factors of chronic liver disease. (HEPATOLOGY 2010;52:578-589)
C1 [Afzali, Anita; Ioannou, George N.] Vet Affairs Puget Sound Hlth Care Syst, Dept Med, Div Gastroenterol, Seattle, WA 98108 USA.
[Afzali, Anita; Ioannou, George N.] Vet Affairs Puget Sound Hlth Care Syst, Res Enhancement Award Program, Seattle, WA 98108 USA.
[Boyko, Edward J.] Vet Affairs Puget Sound Hlth Care Syst, Seattle Epidemiol Res & Informat Ctr, Seattle, WA 98108 USA.
[Weiss, Noel S.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Afzali, Anita; Ioannou, George N.] Univ Washington, Dept Med, Div Gastroenterol, Seattle, WA USA.
[Boyko, Edward J.] Univ Washington, Dept Med, Div Internal Med, Seattle, WA USA.
RP Ioannou, GN (reprint author), Vet Affairs Puget Sound Hlth Care Syst, Dept Med, Div Gastroenterol, S-111 Gastro,1660 S Columbian Way, Seattle, WA 98108 USA.
EM georgei@medicine.washington.edu
FU NIDDK NIH HHS [P30 DK-17047]
NR 27
TC 35
Z9 38
U1 0
U2 3
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD AUG
PY 2010
VL 52
IS 2
BP 578
EP 589
DI 10.1002/hep.23717
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 633OZ
UT WOS:000280513900020
PM 20683957
ER
PT J
AU Mader, C
Stolzmann, P
Leschka, S
Alkadhi, H
Scheffel, H
AF Mader, C.
Stolzmann, P.
Leschka, S.
Alkadhi, H.
Scheffel, Hans
TI Hemoptysis - a sign of primary cardiac malignancy
SO HERZ
LA English
DT Editorial Material
C1 [Stolzmann, P.; Alkadhi, H.; Scheffel, Hans] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
[Stolzmann, P.; Alkadhi, H.; Scheffel, Hans] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Mader, C.; Stolzmann, P.; Alkadhi, H.; Scheffel, Hans] Univ Zurich Hosp, Inst Diagnost & Intervent Radiol, Zurich, Switzerland.
[Leschka, S.] Canton Hosp St Gallen, Inst Radiol, St Gallen, Switzerland.
RP Scheffel, H (reprint author), Massachusetts Gen Hosp, Cardiac MR PET CT Program, 100 Charles River Plaza, Boston, MA 02114 USA.
EM hscheffel@partners.org
NR 2
TC 0
Z9 0
U1 0
U2 0
PU URBAN & VOGEL
PI MUNICH
PA NEUMARKTER STRASSE 43, D-81673 MUNICH, GERMANY
SN 0340-9937
J9 HERZ
JI Herz
PD AUG
PY 2010
VL 35
IS 5
BP 355
EP 356
DI 10.1007/s00059-010-3357-8
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 641GL
UT WOS:000281112700007
PM 20607199
ER
PT J
AU Tomas, E
Stanojevic, V
Habener, JF
AF Tomas, E.
Stanojevic, V.
Habener, J. F.
TI GLP-1 (9-36) Amide Metabolite Suppression of Glucose Production in
Isolated Mouse Hepatocytes
SO HORMONE AND METABOLIC RESEARCH
LA English
DT Article
DE hepatic insulin resistance; hyperglycemia; diabetes
ID GLUCAGON-LIKE PEPTIDE-1; INSULIN-RESISTANCE; TISSUE DISTRIBUTION;
RECEPTOR; EXPRESSION; EXENDIN-4; MICE; SENSITIVITY; SECRETION; HUMANS
AB The glucoincretin hormone glucagon-like peptide-1 (GLP-1) augments glucose-stimulated insulin secretion and is in use as an effective treatment for diabetes. However, after its secretion from the intestine, the insulinotropic GLP-1 (7-36) amide hormone is rapidly inactivated by enzymatic cleavage by the diaminopeptidyl peptidase-4 giving rise to GLP-1 (9-36) amide. Inasmuch as most of the circulating GLP-1 is in the form of the metabolite GLP-1 (9-36) amide it has been suggested that it has insulin-like actions on peripheral insulin-sensitive tissues. In earlier studies, infusions of GLP-1 (9-36) amide in obese insulin-resistant subjects showed a marked suppression of hepatic glucose production. However, it remained uncertain whether the effects on glucose production were due to direct effects on hepatocytes, involved central or portal vein-mediated actions, or were mediated by insulin secretion. Here we show that GLP-1 (9-36) amide directly suppresses glucose production in isolated mouse hepatocytes ex vivo independent of the GLP-1 receptor. These findings support direct insulinomimetic actions of the GLP-1 metabolite on gluconeogenesis in hepatocytes that are independent of insulin action and the GLP-1 receptor, and suggest that GLP-1 (9-36) amide-based peptides might present a novel therapy for the treatment of excessive hepatic glucose production in individuals with insulin-resistant diabetes.
C1 [Tomas, E.; Stanojevic, V.; Habener, J. F.] Massachusetts Gen Hosp, Mol Endocrinol Lab, Boston, MA 02114 USA.
RP Habener, JF (reprint author), Massachusetts Gen Hosp, Mol Endocrinol Lab, Thier 306,55 Fruit St, Boston, MA 02114 USA.
EM jhabener@partners.org
FU Merck Company
FX We thank Karen McManus for important help with the studies. This work
was supported in part by an Investigator-initiated Studies Program Pilot
Grant from Merck & Company.
NR 30
TC 25
Z9 30
U1 0
U2 1
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0018-5043
J9 HORM METAB RES
JI Horm. Metab. Res.
PD AUG
PY 2010
VL 42
IS 9
BP 657
EP 662
DI 10.1055/s-0030-1253421
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 631TG
UT WOS:000280370400007
PM 20645222
ER
PT J
AU Pawlyk, BS
Bulgakov, OV
Liu, XQ
Xu, XY
Adamian, M
Sun, X
Khani, SC
Berson, EL
Sandberg, MA
Li, TS
AF Pawlyk, Basil S.
Bulgakov, Oleg V.
Liu, Xiaoqing
Xu, Xiaoyun
Adamian, Michael
Sun, Xun
Khani, Shahrokh C.
Berson, Eliot L.
Sandberg, Michael A.
Li, Tiansen
TI Replacement Gene Therapy with a Human RPGRIP1 Sequence Slows
Photoreceptor Degeneration in a Murine Model of Leber Congenital
Amaurosis
SO HUMAN GENE THERAPY
LA English
DT Article
ID RECOMBINANT ADENOASSOCIATED VIRUS; REGULATOR (RPGR)-INTERACTING PROTEIN;
RETINITIS-PIGMENTOSA; ROD PHOTORECEPTOR; RESTORES VISION; MUTATIONS;
IDENTIFICATION; MORPHOGENESIS; LOCALIZATION; TRANSDUCTION
AB RPGR-interacting protein-1 (RPGRIP1) is localized in the photoreceptor-connecting cilium, where it anchors the RPGR (retinitis pigmentosa GTPase regulator) protein, and its function is essential for photoreceptor maintenance. Genetic defect in RPGRIP1 is a known cause of Leber congenital amaurosis (LCA), a severe, early-onset form of retinal degeneration. We evaluated the efficacy of replacement gene therapy in a murine model of LCA carrying a targeted disruption of RPGRIP1. The replacement construct, packaged in an adeno-associated virus serotype 8 (AAV8) vector, used a rhodopsin kinase gene promoter to drive RPGRIP1 expression. Both promoter and transgene were of human origin. After subretinal delivery of the replacement gene in the mutant mice, human RPGRIP1 was expressed specifically in photoreceptors, localized correctly in the connecting cilia, and restored the normal localization of RPGR. Electroretinogram and histological examinations showed better preservation of rod and cone photoreceptor function and improved photoreceptor survival in the treated eyes. This study demonstrates the efficacy of human gene replacement therapy and validates a gene therapy design for future clinical trials in patients afflicted with this condition. Our results also have therapeutic implications for other forms of retinal degenerations attributable to a ciliary defect.
C1 [Pawlyk, Basil S.; Bulgakov, Oleg V.; Liu, Xiaoqing; Xu, Xiaoyun; Adamian, Michael; Sun, Xun; Berson, Eliot L.; Sandberg, Michael A.; Li, Tiansen] Harvard Univ, Sch Med, Berman Gund Lab Study Retinal Degenerat, Boston, MA 02114 USA.
[Pawlyk, Basil S.; Bulgakov, Oleg V.; Liu, Xiaoqing; Xu, Xiaoyun; Adamian, Michael; Sun, Xun; Berson, Eliot L.; Sandberg, Michael A.; Li, Tiansen] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Khani, Shahrokh C.] Harvard Univ, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA.
RP Li, TS (reprint author), NEI, Neurobiol Neurodegenerat & Repair Lab, Bethesda, MD 20892 USA.
EM Tiansen.Li@nih.gov
FU National Eye Institute [EY10581]; NEI [P30EY14104]; Foundation Fighting
Blindness; Foundation for Retina Research; Massachusetts Lions Eye
Research Fund
FX The authors thank Dr. Jeng-Shin Lee at the Research Vector Core of
Harvard Medical School for AAV vector packaging, the National Disease
Research Interchange for providing human retinal tissue, and Norman
Michaud for select tissue processing for light microscopy. This work was
supported by National Eye Institute grant EY10581, an NEI core grant for
Vision Research (P30EY14104), the Foundation Fighting Blindness, the
Foundation for Retina Research, and the Massachusetts Lions Eye Research
Fund.
NR 43
TC 41
Z9 42
U1 0
U2 1
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD AUG
PY 2010
VL 21
IS 8
BP 993
EP 1004
DI 10.1089/hum.2009.218
PG 12
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 636RK
UT WOS:000280757200009
PM 20384479
ER
PT J
AU Schumacher, FR
Cheng, I
Freedman, ML
Mucci, L
Allen, NE
Pollak, MN
Hayes, RB
Stram, DO
Canzian, F
Henderson, BE
Hunter, DJ
Virtamo, J
Manjer, J
Gaziano, JM
Kolonel, LN
Tjonneland, A
Albanes, D
Calle, EE
Giovannucci, E
Crawford, ED
Haiman, CA
Kraft, P
Willett, WC
Thun, MJ
Marchand, LL
Kaaks, R
Feigelson, HS
Bueno-De-Mesquita, HB
Palli, D
Riboli, E
Lund, E
Amiano, P
Andriole, G
Dunning, AM
Trichopoulos, D
Stampfer, MJ
Key, TJ
Ma, J
AF Schumacher, Fredrick R.
Cheng, Iona
Freedman, Matthew L.
Mucci, Lorelei
Allen, Naomi E.
Pollak, Michael N.
Hayes, Richard B.
Stram, Daniel O.
Canzian, Frederico
Henderson, Brian E.
Hunter, David J.
Virtamo, Jarmo
Manjer, Jonas
Gaziano, J. Michael
Kolonel, Laurence N.
Tjonneland, Anne
Albanes, Demetrius
Calle, Eugenia E.
Giovannucci, Edward
Crawford, E. David
Haiman, Christopher A.
Kraft, Peter
Willett, Walter C.
Thun, Michael J.
Marchand, Loic Le
Kaaks, Rudolf
Feigelson, Heather Spencer
Bueno-de-Mesquita, H. Bas
Palli, Domenico
Riboli, Elio
Lund, Eliv
Amiano, Pilar
Andriole, Gerald
Dunning, Alison M.
Trichopoulos, Dimitrios
Stampfer, Meir J.
Key, Timothy J.
Ma, Jing
TI A comprehensive analysis of common IGF1, IGFBP1 and IGFBP3 genetic
variation with prospective IGF-I and IGFBP-3 blood levels and prostate
cancer risk among
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GROWTH-FACTOR-I; GENOME-WIDE ASSOCIATION; FACTOR-BINDING PROTEIN-3;
BREAST-CANCER; MULTIETHNIC COHORT; CIRCULATING LEVELS; FACTOR (IGF)-I;
SERUM-LEVELS; MENDELIAN RANDOMIZATION; MISSING HERITABILITY
AB The insulin-like growth factor (IGF) pathway has been implicated in prostate development and carcinogenesis. We conducted a comprehensive analysis, utilizing a resequencing and tagging single-nucleotide polymorphism (SNP) approach, between common genetic variation in the IGF1, IGF binding protein (BP) 1, and IGFBP3 genes with IGF-I and IGFBP-3 blood levels, and prostate cancer (PCa) risk, among Caucasians in the NCI Breast and Prostate Cancer Cohort Consortium. We genotyped 14 IGF1 SNPs and 16 IGFBP1/IGFBP3 SNPs to capture common [minor allele frequency (MAF) >= 5%] variation among Caucasians. For each SNP, we assessed the geometric mean difference in IGF blood levels (N = 5684) across genotypes and the association with PCa risk (6012 PCa cases/6641 controls). We present two-sided statistical tests and correct for multiple comparisons. A non-synonymous IGFBP3 SNP in exon 1, rs2854746 (Gly32Ala), was associated with IGFBP-3 blood levels (P-adj = 8.8 x 10(-43)) after adjusting for the previously established IGFBP3 promoter polymorphism A-202C (rs2854744); IGFBP-3 blood levels were 6.3% higher for each minor allele. For IGF1 SNP rs4764695, the risk estimates among heterozygotes was 1.01 (99% CI: 0.90-1.14) and 1.20 (99% CI: 1.06-1.37) for variant homozygotes with overall PCa risk. The corrected allelic P-value was 8.7 x 10(-3). IGF-I levels were significantly associated with PCa risk (P-trend = 0.02) with a 21% increase of PCa risk when compared with the highest quartile to the lowest quartile. We have identified SNPs significantly associated with IGFBP-3 blood levels, but none of these alter PCa risk; however, a novel IGF1 SNP, not associated with IGF-I blood levels, shows preliminary evidence for association with PCa risk among Caucasians.
C1 [Mucci, Lorelei; Hunter, David J.; Giovannucci, Edward; Stampfer, Meir J.; Ma, Jing] Harvard Univ, Sch Med, Channing Lab, Boston, MA 02115 USA.
[Schumacher, Fredrick R.; Stram, Daniel O.; Henderson, Brian E.; Haiman, Christopher A.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Cheng, Iona; Kolonel, Laurence N.; Marchand, Loic Le] Univ Hawaii, Canc Res Ctr, Program Epidemiol, Honolulu, HI 96813 USA.
[Freedman, Matthew L.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Mucci, Lorelei; Giovannucci, Edward; Willett, Walter C.; Stampfer, Meir J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Hunter, David J.; Kraft, Peter] Harvard Univ, Sch Publ Hlth, Program Mol & Genet Epidemiol, Boston, MA 02115 USA.
[Gaziano, J. Michael] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
[Gaziano, J. Michael] VA Boston Healthcare Syst, MAVERIC, Boston, MA 02115 USA.
[Allen, Naomi E.; Key, Timothy J.] Univ Oxford, Canc Epidemiol Unit, Oxford OX3 7BN, England.
[Pollak, Michael N.] McGill Univ, Jewish Gen Hosp, Lady Davis Res Inst, Dept Med & Oncol,Canc Prevent Res Unit, Montreal, PQ H3T 1E2, Canada.
[Hayes, Richard B.] NYU, Sch Med, New York, NY 10016 USA.
[Kaaks, Rudolf] German Canc Res Ctr, Div Canc Epidemiol, D-69120 Heidelberg, Germany.
[Virtamo, Jarmo] Natl Publ Hlth Inst, Dept Hlth Promot & Chron Dis Prevent, FIN-00300 Helsinki, Finland.
[Manjer, Jonas] Malmo Univ Hosp, Dept Surg, S-20502 Malmo, Sweden.
[Tjonneland, Anne] Danish Canc Soc, Inst Canc Epidemiol, DK-2100 Copenhagen, Denmark.
[Albanes, Demetrius] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20892 USA.
[Calle, Eugenia E.; Thun, Michael J.; Feigelson, Heather Spencer] Amer Canc Soc, Dept Epidemiol & Surveillance Res, Atlanta, GA 30303 USA.
[Crawford, E. David] Univ Colorado, Denver Hlth Sci Ctr, Denver, CO 80045 USA.
[Feigelson, Heather Spencer] Kaiser Permanente, Denver, CO 80237 USA.
[Bueno-de-Mesquita, H. Bas; Amiano, Pilar] Natl Inst Publ Hlth & Environm, RIVM, NL-3720 BA Bilthoven, Netherlands.
[Palli, Domenico] ISPO Canc Res & Prevent Inst, Mol & Nutrit Epidemiol Unit, I-50139 Florence, Italy.
[Riboli, Elio] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Publ Hlth, London SW7 2AZ, England.
[Lund, Eliv] Univ Tromso, Inst Community Med, N-9019 Tromso, Norway.
[Andriole, Gerald] Washington Univ, Sch Med, Div Urol Surg, St Louis, MO 63110 USA.
[Dunning, Alison M.] Univ Cambridge, Dept Oncol, Cambridge CB2 1TN, England.
[Trichopoulos, Dimitrios] Univ Athens, Sch Med, Dept Hyg & Epidemiol, Athens 11527, Greece.
RP Ma, J (reprint author), Brigham & Womens Hosp, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.
EM jing.ma@channing.harvard.edu
RI Pollak, Michael/G-9094-2011; Albanes, Demetrius/B-9749-2015;
OI Pollak, Michael/0000-0003-3047-0604; Dunning, Alison
Margaret/0000-0001-6651-7166; PALLI, Domenico/0000-0002-5558-2437
FU National Cancer Institute (NCI) [U01 CA098216, U01 CA098233, U01
CA098758, U01 CA098710, CA-34944, CA-40360, CA-097193]; National
Research Service Award Training Program in Cancer Epidemiology [T32
CA009001-32]; NHLBI [HL-26490, HL-34595]; Department of Health and Human
Services, National Cancer Institute [N01-CN-45165, N01-RC-45035,
N01-RC-37004]; [CA54281]; [CA63464]
FX This work was funded by National Cancer Institute (NCI) grants U01
CA098216 (EPIC), U01 CA098233 (Harvard), U01 CA098758 (MEC) and U01
CA098710 (ACS). F. R. S. was supported by the National Research Service
Award Training Program in Cancer Epidemiology (T32 CA009001-32). The
Physicians' Health Study was supported by the NCI (CA-34944, CA-40360
and CA-097193) and the NHLBI (HL-26490 and HL-34595). The Multiethnic
Cohort was supported by CA54281 and CA63464. The ATBC Study was
supported by US Public Health Service contracts N01-CN-45165,
N01-RC-45035 and N01-RC-37004 from the Department of Health and Human
Services, National Cancer Institute.
NR 97
TC 32
Z9 32
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD AUG 1
PY 2010
VL 19
IS 15
BP 3089
EP 3101
DI 10.1093/hmg/ddq210
PG 13
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 633HA
UT WOS:000280491200015
PM 20484221
ER
PT J
AU Boisvert, H
Duncan, MJ
AF Boisvert, Heike
Duncan, Margaret J.
TI Translocation of Porphyromonas gingivalis Gingipain Adhesin Peptide A44
to Host Mitochondria Prevents Apoptosis
SO INFECTION AND IMMUNITY
LA English
DT Article
ID STAUROSPORINE-INDUCED APOPTOSIS; TRACHOMATIS-INFECTED CELLS; HUMAN
EPITHELIAL-CELLS; CYTOCHROME-C; BACTERIAL PATHOGENS; BCL-2; ACTIVATION;
PROTEIN; INHIBITION; RELEASE
AB Porphyromonas gingivalis, a Gram-negative oral anaerobe, is associated with periodontal diseases that, in some form, affect up to 80% of the U. S. population. The organism is highly proteolytic, and noncatalytic adhesin domains of the major proteases, gingipains, are involved in bacterium-host interactions. Recently, we showed that gingipain adhesin peptide A44 hijacks the host's clathrin-dependent endocytosis system, allowing the peptide and whole bacteria to be internalized by epithelial cells. In the present study, we found by cell fractionation assays and confocal microscopy that peptide A44 translocated to host mitochondria. Cell viability assays and quantitative real-time PCR showed that the peptide interacted with the cell death machinery by triggering upregulation of antiapoptotic factors bcl-2 and bcl-XL and prevented staurosporine-induced apoptosis for up to 12 h. We confirmed these findings with Western blot analyses of caspase-9 activation in time course experiments with staurosporine. Finally, we verified a similar antiapoptotic effect for P. gingivalis, showing for the first time that the organism manipulated mitochondrial functions during the first hours of infection, thus resisting host cell clearance by apoptosis of infected cells. This mechanism may enable the bacteria to persist in the protected cellular environment until the next step in pathogenesis, progression or resolution of infection.
C1 [Boisvert, Heike; Duncan, Margaret J.] Forsyth Inst, Dept Mol Genet, Boston, MA 02115 USA.
RP Boisvert, H (reprint author), Forsyth Inst, Dept Mol Genet, Boston, MA 02115 USA.
EM hboisvert@forsyth.org
FU U.S. National Institutes of Health [R01-DE015931, T32-DE007327-08]
FX This work was supported by U.S. National Institutes of Health grants
R01-DE015931 and T32-DE007327-08.
NR 48
TC 9
Z9 9
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD AUG
PY 2010
VL 78
IS 8
BP 3616
EP 3624
DI 10.1128/IAI.00187-10
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 626TQ
UT WOS:000279990400030
PM 20547744
ER
PT J
AU Lipsky, BA
Kollef, MH
Miller, LG
Sun, XW
Johannes, RS
Tabak, YP
AF Lipsky, Benjamin A.
Kollef, Marin H.
Miller, Loren G.
Sun, Xiaowu
Johannes, Richard S.
Tabak, Ying P.
TI Predicting Bacteremia among Patients Hospitalized for Skin and
Skin-Structure Infections: Derivation and Validation of a Risk Score
SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY
LA English
DT Article
ID SOFT-TISSUE INFECTIONS; RESISTANT STAPHYLOCOCCUS-AUREUS; BLOOD-STREAM
INFECTION; INADEQUATE ANTIMICROBIAL TREATMENT; INAPPROPRIATE
ANTIBIOTIC-THERAPY; INTENSIVE-CARE-UNIT; LARGE US DATABASE; ADULT
PATIENTS; NEEDLE ASPIRATION; CELLULITIS
AB OBJECTIVE. Bacteremia is relatively common in patients with skin and skin-structure infection (SSSI) severe enough to require hospitalization. We used selected demographic and clinical characteristics easily assessable at initial evaluation to develop a model for the early identification of patients with SSSI who are at higher risk for bacteremia.
PARTICIPANTS. A large database of adults hospitalized with SSSI at 97 hospitals in the United States during the period from 2003 through 2007 and from whom blood samples were obtained for culture at admission.
METHODS. We compared selected candidate predictor variables for patients shown to have bacteremia and patients with no demonstrated bacteremia. Using stepwise logistic regression to identify independent risk factors for bacteremia, we derived a model by using 75% of a randomly split cohort, converted the model coefficients into a risk score system, and then we validated it by using the remaining 25% of the cohort.
RESULTS. Bacteremia was documented in 1,021 (11.7%) of the 8,747 eligible patients. Independent predictors of bacteremia (P < .001) were infected device or prosthesis, respiratory rate less than 10 or more than 29 breaths per minute, pulse rate less than 49 or more than 125 beats per minute, temperature less than 35.6 degrees C or at least 38.0 degrees C, white blood cell band percentage of 7% or more, white blood cell count greater than 11 x 10(9)/L, healthcare-associated infection, male sex, and older age. The bacteremia rates ranged from 3.7% (lowest decile) to 30.6% (highest decile) (P < .001). The model C statistic was 0.71; the Hosmer-Lemeshow test P value was .36, indicating excellent model calibration.
CONCLUSIONS. Using data available at hospital admission, we developed a risk score that differentiated SSSI patients at low risk for bacteremia from patients at high risk. This score may help clinicians identify patients who require more intensive monitoring or antimicrobial regimens appropriate for treating bacteremia. Infect Control Hosp Epidemiol 2010; 31(8): 828-837
C1 [Lipsky, Benjamin A.] VA Puget Sound Hlth Care Syst, Primary Care Clin S 111 PCC, Gen Med Serv, Seattle, WA 98108 USA.
[Lipsky, Benjamin A.] Univ Washington, Dept Med, Seattle, WA USA.
[Kollef, Marin H.] Washington Univ, Sch Med, St Louis, MO USA.
[Miller, Loren G.] UCLA Sch Med, Los Angeles, CA USA.
[Miller, Loren G.] Harbor UCLA Med Ctr, Los Angeles, CA USA.
[Sun, Xiaowu; Johannes, Richard S.; Tabak, Ying P.] CareFusion, MedMined Serv, Clin Res, Marlborough, MA USA.
[Johannes, Richard S.] Harvard Univ, Sch Med, Boston, MA USA.
RP Lipsky, BA (reprint author), VA Puget Sound Hlth Care Syst, Primary Care Clin S 111 PCC, Gen Med Serv, 1660 S Columbian Way, Seattle, WA 98108 USA.
EM balipsky@uw.edu
OI Lipsky, Benjamin A./0000-0001-9886-5114
FU CareFusion Corporation; Cubis; Pfizer
FX We thank CareFusion Clinical Research team members Karen Derby, Vikas
Gupta, and Linda Hyde for their contributions in database management,
analysis, and technical and administrative support. Editorial support
was provided by Hamilton House, Virginia Beach, Virginia, and funded by
CareFusion Corporation.; B. A. L. reports that he has served as a
consultant to Cubist, Pfizer, Merck, Wyeth-Ayerst, and Ortho-McNeil. M.
H. K. reports that he has been a member of the the speakers' bureau or
served as a consultant for Astrazeneca, Pfizer, Merck, Elan, Bard, and
Kimberly-Clark and has served as a consultant for Astellas, Cubist, and
Bayer. L. G. M. reports that he has received research grants from Cubist
and Pfizer and served as a consultant to Theravance. X. S., R.S.J., and
Y.P.T. report that they are employees of CareFusion Corporation.
NR 36
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Z9 10
U1 0
U2 1
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 AUG
PY 2010
VL 31
IS 8
BP 828
EP 837
DI 10.1086/654007
PG 10
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 621SC
UT WOS:000279601800009
PM 20586653
ER
PT J
AU Cullen, G
Sands, BE
Yajnik, V
AF Cullen, Garret
Sands, Bruce E.
Yajnik, Vijay
TI Babesiosis in a Patient on Infliximab for Crohn's Disease
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Letter
ID MALARIA
C1 [Cullen, Garret; Sands, Bruce E.; Yajnik, Vijay] Massachusetts Gen Hosp, Crohns & Colitis Ctr, Boston, MA 02114 USA.
RP Cullen, G (reprint author), Massachusetts Gen Hosp, Crohns & Colitis Ctr, Boston, MA 02114 USA.
NR 8
TC 1
Z9 1
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1078-0998
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD AUG
PY 2010
VL 16
IS 8
BP 1269
EP 1270
DI 10.1002/ibd.21158
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 640TZ
UT WOS:000281077400002
PM 19885904
ER
PT J
AU Herfarth, HH
Osterman, MI
Isaacs, KL
Lewis, JD
Sands, BE
AF Herfarth, Hans H.
Osterman, Mark I.
Isaacs, Kim L.
Lewis, James D.
Sands, Bruce E.
TI Efficacy of Methotrexate in Ulcerative Colitis: Failure or Promise
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Review
DE methotrexate; ulcerative colitis; inflammatory bowel disease
ID INFLAMMATORY-BOWEL-DISEASE; LOW-DOSE METHOTREXATE; ISRAELI MULTICENTER
TRIAL; PEDIATRIC CROHNS-DISEASE; OF-THE-LITERATURE;
RHEUMATOID-ARTHRITIS; ORAL METHOTREXATE; DOUBLE-BLIND; PARENTERAL
METHOTREXATE; MAINTAINING REMISSION
AB Background: Low-dose methotrexate is a widely used and efficacious therapy in chronic inflammatory disorders such as psoriasis and rheumatoid arthritis. Prospective randomized controlled trials have demonstrated the efficacy of parenteral methotrexate in Crohn's disease (CD). We performed a systematic review of the efficacy of methotrexate in ulcerative colitis (UC) and discuss the results in the context of the known pharmacokinetics and adverse events of methotrexate therapy in inflammatory bowel diseases and other inflammatory conditions.
Materials and Methods: We performed a systematic review of the literature in Medline, Embase, and Web of Science. All publications describing patients with UC treated with methotrexate were included.
Results: We identified 12 studies or retrospective case series and 5 meeting abstracts that met the inclusion criteria. Only I study reported a prospective randomized placebo-controlled trial using methotrexate at a dose of 12.5 mg orally with no significant clinical benefit. However, the majority of uncontrolled retrospective analyses suggest a clinical response to methotrexate therapy in a range of 30%-80% when the drug is applied by parenteral route in doses between 20-25 mg.
Conclusions: The only randomized controlled trial of methotrexate in UC employed oral dosing and doses lower than those shown to be effective in CD and did not demonstrate efficacy, whereas uncontrolled, retrospective studies using doses and routes of administration similar to those employed in CD suggest benefit. Well-designed, prospective, placebo-controlled trials of methotrexate in UC are needed.
C1 [Herfarth, Hans H.] Univ N Carolina, Div Gastroenterol & Hepatol, Dept Med, Chapel Hill, NC 27599 USA.
[Osterman, Mark I.; Lewis, James D.] Univ Penn, Div Gastroenterol, Philadelphia, PA 19104 USA.
[Osterman, Mark I.; Lewis, James D.] Univ Penn, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Sands, Bruce E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, MGH Crohns & Colitis Ctr, Boston, MA USA.
[Sands, Bruce E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit, Boston, MA USA.
RP Herfarth, HH (reprint author), Univ N Carolina, Div Gastroenterol & Hepatol, Dept Med, Bioinformat Bldg,CB 7080, Chapel Hill, NC 27599 USA.
EM hherf@med.unc.edu
FU National Institutes of Health [1U34DK084511-01]; Crohn's and Colitis
Foundation of America (CCFA)
FX Drs. Herfarth, Isaacs, Lewis, Osterman, and Sands are supported by a
National Institutes of Health grant 1U34DK084511-01 and the Crohn's and
Colitis Foundation of America (CCFA).
NR 60
TC 16
Z9 18
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1078-0998
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD AUG
PY 2010
VL 16
IS 8
BP 1421
EP 1430
DI 10.1002/ibd.21246
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 640TZ
UT WOS:000281077400023
PM 20186931
ER
PT J
AU Leatherman, S
Ferris, TG
Berwick, D
Omaswa, F
Crisp, N
AF Leatherman, Sheila
Ferris, Timothy G.
Berwick, Donald
Omaswa, Francis
Crisp, Nigel
TI The role of quality improvement in strengthening health systems in
developing countries
SO INTERNATIONAL JOURNAL FOR QUALITY IN HEALTH CARE
LA English
DT Article
DE quality improvement; healthcare systems; healthcare systems; developing
countries
ID RESOURCE-POOR SETTINGS; IMMUNIZATION COVERAGE; CARES EXPERIENCES;
OBSTETRIC CARE; SOUTH-AFRICA; MANAGEMENT; SERVICES; RWANDA; PERFORMANCE;
ADHERENCE
AB Quality of care was recognized as a key element for improved health outcomes and efficiency in the World Health Organization's (WHO) widely adopted framework for health system strengthening in resource-poor countries. Although modern approaches to improving quality are increasingly used globally, their adoption remains sporadic in developing countries. Healthcare leaders and improvement experts representing 15 countries met in October 2008 to catalyze the adoption of quality improvement (QI) methods to improve healthcare quality in resource-poor settings. This paper describes the evidence used to frame deliberations, the proceedings and a proposal for incorporating QI methods into plans for strengthening health systems. The conference participants presented case reports and reviewed a growing body of evidence from peer-reviewed journals demonstrating that QI methods can make significant contributions in resource poor settings. Deliberations focused on the barriers to adoption of QI methods and potential strategies for addressing those barriers. Attendees concluded that QI has the potential to optimize the use of limited resources available from governments and global initiatives targeted at achieving shared aims. Demonstrable improvements in quality may encourage greater investment in health systems in developing countries by increasing donor, population and governmental confidence that resources are being used well.
C1 [Ferris, Timothy G.] Mass Gen Hosp, Boston, MA USA.
[Leatherman, Sheila] Univ N Carolina, Sch Publ Hlth, London Sch Econ, Minneapolis, MN USA.
[Berwick, Donald; Crisp, Nigel] Inst Healthcare Improvement, Cambridge, MA USA.
[Omaswa, Francis] African Ctr Global Hlth & Social Transformat, Kampala, Uganda.
RP Ferris, TG (reprint author), Massachusetts Gen Phy Org, 55 Fruit St,Bulfinch 205E, Boston, MA 02114 USA.
EM tferris@partners.org
FU Institute for Healthcare Improvement and The Rockefeller Foundation
FX The authors would also like to acknowledge the Institute for Healthcare
Improvement and The Rockefeller Foundation for their joint support in
hosting the October 2008 meeting in Bellagio.
NR 42
TC 53
Z9 54
U1 1
U2 15
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1353-4505
J9 INT J QUAL HEALTH C
JI Int. J. Qual. Health Care
PD AUG
PY 2010
VL 22
IS 4
BP 237
EP 243
DI 10.1093/intqhc/mzq028
PG 7
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 630MT
UT WOS:000280278200001
PM 20543209
ER
PT J
AU Schartel, J
Mori, DL
AF Schartel, Janell
Mori, DeAnna L.
TI THE RELATIONSHIP OF ANXIETY TO MULTIPLE ASPECTS OF TREATMENT ADHERENCE
IN PATIENTS WITH ESRD
SO INTERNATIONAL JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Meeting Abstract
C1 [Schartel, Janell] VA Boston Healthcare Syst, Boston, MA USA.
[Mori, DeAnna L.] Boston Univ, Sch Med, Boston, MA 02118 USA.
EM janell.schartel@va.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1070-5503
J9 INT J BEHAV MED
JI Int. J. Behav. Med.
PD AUG
PY 2010
VL 17
SU 1
BP 2
EP 3
PG 2
WC Psychology, Clinical
SC Psychology
GA 628BG
UT WOS:000280088500002
ER
PT J
AU Campbell, MK
Rosenstien, D
Jones, A
Andersen, B
Syrjala, K
Baker, S
Miller, K
Jacobs, L
McCabe, M
Ganz, P
Gellin, M
Tessaro, I
Manning, M
AF Campbell, Marci K.
Rosenstien, Donald
Jones, Alison
Andersen, Barbara
Syrjala, Karen
Baker, Scott
Miller, Kenneth
Jacobs, Linda
McCabe, Mary
Ganz, Patricia
Gellin, Mindy
Tessaro, Irene
Manning, Michelle
TI CREATING A SURVIVORSHIP PROGRAM-WHAT DOES IT TAKE TO BE SUCCESSFUL?
SO INTERNATIONAL JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Meeting Abstract
C1 [Campbell, Marci K.; Rosenstien, Donald; Gellin, Mindy; Tessaro, Irene; Manning, Michelle] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hll, NC 27599 USA.
[Jacobs, Linda] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Miller, Kenneth] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Syrjala, Karen; Baker, Scott] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[McCabe, Mary] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Andersen, Barbara] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Andersen, Barbara] Solove Res Inst, Columbus, OH USA.
[Ganz, Patricia] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA.
[Jones, Alison] Univ Colorado, Ctr Canc, Denver, CO 80262 USA.
EM mindy_gellin@med.unc.edu
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1070-5503
J9 INT J BEHAV MED
JI Int. J. Behav. Med.
PD AUG
PY 2010
VL 17
SU 1
BP 325
EP 326
PG 2
WC Psychology, Clinical
SC Psychology
GA 628BG
UT WOS:000280088500734
ER
PT J
AU Fischer, SEJ
AF Fischer, Sylvia E. J.
TI Small RNA-mediated gene silencing pathways in C. elegans
SO INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
LA English
DT Article
DE RNAi; miRNA; siRNA; Silencing; C. elegans
ID DOUBLE-STRANDED-RNA; TRANSMEMBRANE PROTEIN SID-1;
CAENORHABDITIS-ELEGANS; MESSENGER-RNA; REGULATORY RNA;
POSTTRANSCRIPTIONAL REGULATION; MICROPROCESSOR COMPLEX; MICRORNA
PRECURSORS; SLICER ACTIVITY; GW182 PROTEINS
AB Small RNA pathways, including the RNA interference (RNAi) pathway and the microRNA (miRNA) pathway, regulate gene expression, defend against transposable elements and viruses, and, in some organisms, guide genome rearrangements. The nematode Caenorhabditis elegans (C. elegans) has been at the forefront of small RNA research; not only were the first miRNAs and their function as regulators of gene expression discovered in C elegans, but also double-stranded RNA-induced gene silencing by RNAi was discovered in this model organism. Since then, genetic and RNAi-mediated screens, candidate gene approaches, and biochemical studies have uncovered numerous factors in the small RNA pathways and painted a rich palette of interacting pathways. Here we review the different small RNAs that have been discovered in C. elegans and discuss our understanding of their biogenesis pathways and mechanisms of action. (C) 2010 Elsevier Ltd. All rights reserved.
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Mol Biol,Dept Genet, Boston, MA 02114 USA.
RP Fischer, SEJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Mol Biol,Dept Genet, 185 Cambridge St, Boston, MA 02114 USA.
EM fischer@molbio.mgh.harvard.edu
NR 113
TC 31
Z9 32
U1 1
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1357-2725
J9 INT J BIOCHEM CELL B
JI Int. J. Biochem. Cell Biol.
PD AUG
PY 2010
VL 42
IS 8
BP 1306
EP 1315
DI 10.1016/j.biocel.2010.03.006
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 631XN
UT WOS:000280384100012
PM 20227516
ER
PT J
AU Kuan, CT
Srivastava, N
McLendon, RE
Marasco, WA
Zalutsky, MR
Bigner, DD
AF Kuan, Chien-Tsun
Srivastava, Nidhi
McLendon, Roger E.
Marasco, Wayne A.
Zalutsky, Michael R.
Bigner, Darell D.
TI Recombinant single-chain variable fragment antibodies against
extracellular epitopes of human multidrug resistance protein MRP3 for
targeting malignant gliomas
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE GBM; MRP3; scFv antibody; phage display
ID SOLID TUMORS; STEM-CELLS; RAT-LIVER; EXPRESSION; HETEROGENEITY;
TRANSPORTERS; IMMUNIZATION; XENOGRAFTS; MARKERS
AB Multidrug resistance protein 3 (MRP3), a multidrug resistance protein identified by serial analysis of gene expression as a glioblastoma multiforme (GBM)-associated molecule, is highly expressed in GBM, but not in normal brain cells. Thus, MRP3 is a candidate for GBM immunotargeting, but to date, no monoclonal antibody has been isolated that can target an extracellular MRP3 epitope. By phage display, we have isolated 3 recombinant, fully human, single-chain Fv (scFv) antibodies, M25, M58 and M89, which specifically react with the extracellular N-terminus of human MRP3. In ELISA, these scFvs reacted only with the peptide used for screening and not with other MRP3-derived peptides. Flow cytometric analysis revealed that these scFv fragments bind specifically to viable human GBM cells displaying different MRP3 expression levels, but not to MRP3-null cells. Furthermore, these scFv antibodies failed to react with tumor cells overexpressing other MRP proteins, including MRP1, MRP2, MRP4 and MRP5. M25 and M58 also bound to viable neurospheres. lodogen-labeled scFvs demonstrated a yield of 56-76%. The immunoreactive fractions of the radiolabeled M25, M58 and M89 scFvs were 32, 52 and 69%, respectively. M25 exhibited 20% internalization into D2159MG neurospheres, M58, 33% into D54MG cells and M89, 26% into D247MG. Immunohistochemical evaluation of human gliomas to determine the localization of MRP3 antigen using scFvs M25 and M58 showed a dense cytoplasmic and membranous staining pattern. These Fv-based recombinant antibodies, which possess superior tumor penetration capabilities and selectively target tumor cells that express MRP3, may potentially be used in immunotherapy and diagnosis for brain tumors and other cancers.
C1 [Kuan, Chien-Tsun; Srivastava, Nidhi; McLendon, Roger E.; Bigner, Darell D.] Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA.
[Kuan, Chien-Tsun; Srivastava, Nidhi; McLendon, Roger E.; Bigner, Darell D.] Duke Univ, Med Ctr, Preston Robert Tisch Brain Tumor Ctr, Durham, NC 27710 USA.
[Marasco, Wayne A.] Harvard Univ, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Zalutsky, Michael R.] Duke Univ, Med Ctr, Dept Radiol, Durham, NC 27710 USA.
RP Kuan, CT (reprint author), Duke Univ, Med Ctr, Dept Pathol, Box 3156, Durham, NC 27710 USA.
EM kuan@duke.edu; bigne001@mc.duke.edu
FU NIH, National Center for Research Resources [MO1 RR30]; NINDS [5P50
NS20023]; NCI SPORE [5P50 CA 108786, CA 74886]; NIH [R37 CA 011898];
Finding Cures for Glioma Grants
FX Grant sponsor: NIH (General Clinical Research Centers Program, National
Center for Research Resources); Grant number: MO1 RR30; Grant sponsor:
NINDS; Grant number: 5P50 NS20023; Grant sponsor: NCI SPORE; Grant
numbers: 5P50 CA 108786, CA 74886; Grant sponsor: NIH Merit Award; Grant
number: R37 CA 011898; Grant sponsor: Finding Cures for Glioma Grants
NR 47
TC 12
Z9 15
U1 0
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD AUG 1
PY 2010
VL 127
IS 3
BP 598
EP 611
DI 10.1002/ijc.25062
PG 14
WC Oncology
SC Oncology
GA 615JP
UT WOS:000279131300011
PM 19937796
ER
PT J
AU Campos, SM
Berlin, ST
Parker, LM
Chen, WY
Bunnell, CA
Atkinson, T
Lee, J
Matulonis, U
Hirsch, MS
Harris, L
Krasner, CN
AF Campos, Susana M.
Berlin, Suzanne T.
Parker, Leroy M.
Chen, Wendy Y.
Bunnell, Craig A.
Atkinson, Tina
Lee, Julie
Matulonis, Ursula
Hirsch, Michelle S.
Harris, Lyndsay
Krasner, Carolyn N.
TI Phase I trial of liposomal doxorubicin and ZD1839 in patients with
refractory gynecological malignancies or metastatic breast cancer
SO INTERNATIONAL JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
DE ZD1839; Liposomal doxorubicin; Breast cancer; Gynecological cancer;
Toxicity
ID EPIDERMAL-GROWTH-FACTOR; CELL LUNG-CANCER; TYROSINE KINASE INHIBITOR;
ADVANCED OVARIAN-CANCER; PLATINUM-RESISTANT OVARIAN; FACTOR RECEPTOR;
III TRIAL; MONOCLONAL-ANTIBODY; MULTICENTER TRIAL; ORAL ETOPOSIDE
AB Pegylated liposomal doxorubicin has activity in both breast and ovarian cancer. Preclinical data noted that ZD1839 acts synergistically with chemotherapy. Given the lack of cross-resistance between these two agents, a phase I trial was initiated examining the safety and efficacy of the combination of liposomal doxorubicin and ZD1839 in patients with recurrent gynecologic or metastatic breast cancer.
Dose-limiting toxicity (DLT) was defined within the first two cycles of treatment. Escalating doses of liposomal doxorubicin were administered every 4 weeks with ZD1839. Pharmacokinetic analysis and correlative studies were performed.
Thirty-five patients were enrolled in this study: six in each cohort. One DLT (febrile neutropenia) was observed in cohort 2. Dose level 3 was determined to be the maximum tolerated dose (MTD), and an additional ten patients were accrued. Serious adverse events (SAEs) included one patient with mental status changes believed secondary to disease progression and two central nervous system (CNS) bleeds believed to be unrelated to the combination of study agents. Toxicities were generally mild except for skin and gastrointestinal toxicity. No cardiac toxicity was observed. The best response to therapy included four partial responses and 20 patients with stable disease.
Liposomal doxorubicin with ZD1839 is an active regimen but is associated with increased skin toxicity in patients with advanced breast and gynecologic cancer.
C1 [Campos, Susana M.; Berlin, Suzanne T.; Atkinson, Tina; Lee, Julie; Matulonis, Ursula] Dana Farber Canc Inst, Dept Gynecol Oncol, Boston, MA 02115 USA.
[Parker, Leroy M.; Chen, Wendy Y.; Bunnell, Craig A.] Dana Farber Canc Inst, Dept Breast Oncol, Boston, MA 02115 USA.
[Krasner, Carolyn N.] Massachusetts Gen Hosp, Dept Gynecol Oncol, Boston, MA 02114 USA.
[Hirsch, Michelle S.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Harris, Lyndsay] Yale Univ, Dept Med Oncol, New Haven, CT USA.
RP Campos, SM (reprint author), Dana Farber Canc Inst, Dept Gynecol Oncol, 44 Binney St, Boston, MA 02115 USA.
EM scampos@partners.org
FU Ortho-Biotech; AstraZeneca; Genentech
FX Susana M. Campos serves as a medical consultant to Genentech, Inc, and
GSK, Inc. and has received research funding from Ortho-Biotech,
AstraZeneca and Genentech. Ursula Matulonis has received research
funding from AstraZeneca.
NR 59
TC 2
Z9 2
U1 0
U2 1
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
JAPAN
SN 1341-9625
EI 1437-7772
J9 INT J CLIN ONCOL
JI Int. J. Clin. Oncol.
PD AUG
PY 2010
VL 15
IS 4
BP 390
EP 398
DI 10.1007/s10147-010-0073-6
PG 9
WC Oncology
SC Oncology
GA 637HZ
UT WOS:000280809500009
PM 20405155
ER
PT J
AU Sala, E
DeSouza, N
Lee, SI
Atri, M
Hricak, H
AF Sala, Evis
DeSouza, Nandita
Lee, Susanna I.
Atri, Mostafa
Hricak, Hedvig
CA Gynaecological Canc InterGrp
TI Ovarian Cancer The Role of Functional Imaging as an End Point in
Clinical Trials
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
LA English
DT Article
DE Ovarian cancer; Functional imaging; Biomarker; Clinical trial
ID APPARENT DIFFUSION-COEFFICIENT; POSITRON-EMISSION-TOMOGRAPHY; DIAGNOSTIC
ONCOLOGY GROUP; CONTRAST-ENHANCED MRI; COMPUTED-TOMOGRAPHY; PET-CT;
PERITONEAL CARCINOMATOSIS; NEOADJUVANT CHEMOTHERAPY; 2ND-LOOK
LAPAROTOMY; PREDICTING RESPONSE
AB The Gynaecological Cancer InterGroup conducts collaborative trials in gynecologic cancer and also aims to develop standards that can be used to strengthen all aspects of study methodology. There is an urgent need to develop more refined imaging end points that can be used as early treatment response biomarkers in ovarian cancer. Therefore, the Gynaecological Cancer InterGroup commissioned an expert position paper on the role of functional imaging as an end point in clinical trials in ovarian cancer. In this position paper, we state the limitation of current anatomical imaging methods used in clinical trials, highlight the potential of functional imaging, and provide key recommendations on the use of functional imaging as an end point in ovarian cancer clinical trials.
C1 [Sala, Evis] Addenbrookes Hosp, Dept Radiol, Cambridge CB2 0QQ, England.
[DeSouza, Nandita] Inst Canc Res, Surrey, England.
[DeSouza, Nandita] Royal Marsden Hosp, Surrey, England.
[Lee, Susanna I.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Atri, Mostafa] Univ Toronto, Abdominal Div, Toronto, ON M5S 1A1, Canada.
[Hricak, Hedvig] Mem Sloan Kettering Canc Ctr, Dept Radiol, New York, NY 10021 USA.
RP Sala, E (reprint author), Addenbrookes Hosp, Dept Radiol, Box 218,Hills Rd, Cambridge CB2 0QQ, England.
EM es220@radiol.cam.ac.uk
RI 李, 海明/I-2405-2012
NR 79
TC 1
Z9 1
U1 0
U2 5
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 AUG
PY 2010
VL 20
IS 6
BP 971
EP 978
DI 10.1111/IGC.0b013e3181e0a353
PG 8
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 634HR
UT WOS:000280572000010
PM 20683404
ER
PT J
AU Righi, V
Apidianakis, Y
Mintzopoulos, D
Astrakas, L
Rahme, LG
Tzika, AA
AF Righi, Valeria
Apidianakis, Yiorgos
Mintzopoulos, Dionyssios
Astrakas, Loukas
Rahme, Laurence G.
Tzika, A. Aria
TI In vivo high-resolution magic angle spinning magnetic resonance
spectroscopy of Drosophila melanogaster at 14.1 T shows trauma in aging
and in innate immune-deficiency is linked to reduced insulin signaling
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Article
DE magnetic resonance spectroscopy; high resolution magic angle spinning;
total through bond correlation spectroscopy; Drosophila melanogaster;
biomarkers; immunity; insulin signaling; obesity; aging
ID INTRAMYOCELLULAR LIPID-CONTENT; RESISTANCE FOLLOWING INJURY; PROTON
NMR-SPECTROSCOPY; SKELETAL-MUSCLE; FATTY-ACIDS; INDUCED APOPTOSIS;
RELAXATION-TIMES; BURN-TRAUMA; METABOLISM; H-1
AB In vivo magnetic resonance spectroscopy (MRS), a non-destructive biochemical tool for investigating live organisms, has yet to be used in the fruit fly Drosophila melanogaster, a useful model organism for investigating genetics and physiology. We developed and implemented a high-resolution magic-angle-spinning (HRMAS) MRS method to investigate live Drosophila at 14.1 T. We demonstrated, for the first time, the feasibility of using HRMAS MRS for molecular characterization of Drosophila with a conventional MR spectrometer equipped with an HRMAS probe. We showed that the metabolic HRMAS MRS profiles of injured, aged wild-type (wt) flies and of immune deficient (imd) flies were more similar to chico flies mutated at the chico gene in the insulin signaling pathway, which is analogous to insulin receptor substrate 1-4 (IRS1-4) in mammals and less to those of adipokinetic hormone receptor (akhr) mutant flies, which have an obese phenotype. We thus provide evidence for the hypothesis that trauma in aging and in innate immune-deficiency is linked to insulin signaling. This link may explain the mitochondrial dysfunction that accompanies insulin resistance and muscle wasting that occurs in trauma, aging and immune system deficiencies, leading to higher susceptibility to infection. Our approach advances the development of novel in vivo non-destructive research approaches in Drosophila, suggests biomarkers for investigation of biomedical paradigms, and thus may contribute to novel therapeutic development.
C1 [Righi, Valeria; Apidianakis, Yiorgos; Mintzopoulos, Dionyssios; Astrakas, Loukas; Tzika, A. Aria] Harvard Univ, Sch Med, Massachusetts Gen Hosp, NMR Surg Lab,Dept Surg, Boston, MA 02114 USA.
[Righi, Valeria; Apidianakis, Yiorgos; Mintzopoulos, Dionyssios; Astrakas, Loukas; Tzika, A. Aria] Harvard Univ, Sch Med, Shriners Burn Inst, Boston, MA 02114 USA.
[Righi, Valeria; Mintzopoulos, Dionyssios; Astrakas, Loukas; Tzika, A. Aria] Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Apidianakis, Yiorgos; Rahme, Laurence G.] Massachusetts Gen Hosp, Dept Surg, Mol Surg Lab, Boston, MA 02114 USA.
RP Tzika, AA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, NMR Surg Lab,Dept Surg, 51 Blossom St,Room 261, Boston, MA 02114 USA.
EM atzika@hms.harvard.edu
RI Astrakas, Loukas/F-5918-2011;
OI Apidianakis, Yiorgos/0000-0002-7465-3560; Righi,
Valeria/0000-0003-2394-8462
FU National Institute Institutes of Health (NIH) [P50GM021700, AI063433];
Shriner's Hospital for Children [8893]
FX This work was supported in part by a National Institute Institutes of
Health (NIH) Center Grant (no. P50GM021700) to Ronald G. Tompkins (A.
Aria Tzika, Director of the NMR core), NIH grant no. AI063433 to
Laurence G. Rahme and a Shriner's Hospital for Children research grant
(no. 8893) to A. Aria Tzika. We thank Ovidiu Andronesi Ph.D. for
assistance with the TOBSY pulse sequence. We also thank Ann Power Smith
Ph.D. of Write Science Right for editorial assistance.
NR 82
TC 10
Z9 10
U1 2
U2 14
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD AUG
PY 2010
VL 26
IS 2
BP 175
EP 184
DI 10.3892/ijmm_00000450
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 628JO
UT WOS:000280115900002
PM 20596596
ER
PT J
AU Ademi, Z
Walls, HL
Peeters, A
Liew, D
Hollingsworth, B
Stevenson, C
Steg, PG
Bhatt, DL
Reid, CM
AF Ademi, Z.
Walls, H. L.
Peeters, A.
Liew, D.
Hollingsworth, B.
Stevenson, C.
Steg, Ph-G
Bhatt, D. L.
Reid, C. M.
CA REACH Registry Investigators
TI Economic implications of obesity among people with atherothrombotic
disease
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Article
DE atherothrombosis; direct health-care costs; pharmaceuticals
ID HEALTH-CARE COSTS; BODY-MASS INDEX; CARDIOVASCULAR RISK-FACTORS;
SERVICES USE; INDIVIDUALS; PREVALENCE; AUSTRALIA
AB Objective: The purpose of this study was to ascertain the impact of obesity on the cost of disease management in people with or at high risk of atherothrombotic disease from a governmental perspective using a bottom-up approach to cost estimation. In addition, the aim was also to explore the causes of any differences found.
Method: The health-care costs of obesity were estimated from 2819 participants recruited into the nationwide Australian REACH Registry with established atherothrombotic disease or at least three risk factors for atherothrombosis. Enrollment was in 2004, through primary care general practices. Information was collected on the use of cardiovascular drugs, hospitalizations and ambulatory care services. 'Bottom-up' costing was undertaken by assigning unit costs to each health-care item, based on Australian Government-reimbursed figures 2006-2007. Linear-mixed models were used to estimate associations between direct medical costs and body mass index (BMI) categories.
Results: Annual pharmaceutical costs per person increased with increasing BMI category, even after adjusting for gender, age, living place, formal education, smoking status, hypertension and diabetes. Adjusted annual pharmaceutical costs of overweight and obese participants were higher ($7 (P = 0.004) and $144 (<0.001), respectively) than those of the normal weight participants. This was due to participants in higher BMI categories receiving more pharmaceuticals than normal weight participants. There was no significant change across the BMI categories in annual ambulatory care costs and annual hospital costs.
Conclusion: In these participants with or at high risk of atherothrombotic disease, annual pharmaceutical costs were greater in participants of higher BMI category, but there was not such a gradient in the annual hospital or ambulatory care costs. The greater cardiovascular pharmaceutical costs for participants of higher BMI categories remained even after adjusting for a range of demographic factors and comorbidities. Our results suggest that these costs are explained by the higher number of drugs used among people with atherothrombotic disease. Further investigation is needed to understand the reasons for this level of drug use. International Journal of Obesity (2010) 34, 1284-1292; doi: 10.1038/ijo.2010.42; published online 2 March 2010
C1 [Ademi, Z.; Walls, H. L.; Peeters, A.; Stevenson, C.; Reid, C. M.] Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic 3004, Australia.
[Liew, D.] Univ Melbourne, Dept Med, St Vincents Hosp, Melbourne, Vic 3010, Australia.
[Hollingsworth, B.] Monash Univ, Ctr Hlth Econ, Melbourne, Vic 3004, Australia.
[Steg, Ph-G] Univ Paris 07, INSERM, U698, AP HP, Paris, France.
[Bhatt, D. L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Bhatt, D. L.] VA Boston Healthcare Syst, Boston, MA USA.
RP Ademi, Z (reprint author), Monash Univ, Dept Epidemiol & Prevent Med, Sch Publ Hlth & Prevent Med, Alfred Hosp, Commercial Rd, Melbourne, Vic 3004, Australia.
EM Zanfina.Ademi@med.monash.edu.au
RI Peeters, Anna/B-3663-2013;
OI Hollingsworth, Bruce/0000-0002-4314-6523; Liew,
Danny/0000-0002-0131-623X
FU sanofi-aventis; Bristol-Myers Squibb; Waksman Foundation (Tokyo, Japan);
Monash University; Australian Research Council [LP077532]; National
Health and Medical Research Council [465130]
FX Zanfina Ademi, Helen Walls, Anna Peteers, Danny Liew, Bruce
Hollingsworth, Christopher Stevenson and Christopher Reid declare no
conflict of interest. Ph Gabriel Steg has the following disclosures:
research grant from sanofi-aventis. Speakers bureau:
Boehringer-Ingelheim, Bristol-Myers Squibb, GlaxoSmithKline, Medtronic,
Nycomed, sanofi-aventis, Servier. Consulting/advisory board: Astellas,
AstraZeneca, Bayer, Boehringer-Ingelheim, Bristol-Myers Squibb, Endotis,
GlaxoSmithKline, Medtronic, MSD, Nycomed, sanofi-aventis, Servier, The
Medicines Company. Deepak L Bhatt has received research grants from
sanofi-aventis and Bristol-Myers Squibb who have funded the REACH
Registry. He has also received institutional research support from
AstraZeneca, Eisai, Ethicon, Heartscape and The Medicines Company.; The
global REACH Registry is sponsored by sanofi-aventis, Bristol-Myers
Squibb, and the Waksman Foundation (Tokyo, Japan), and is endorsed by
the World Heart Federation. The REACH Registry enforces a
no-ghostwriting policy. A complete list of global REACH investigators is
available at www.reachregistry.org. This work was supported by Monash
University. In addition, this work was supported in part by the
Australian Research Council Linkage Project LP077532, National Health
and Medical Research Council grant (No. 465130).
NR 25
TC 3
Z9 3
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0307-0565
J9 INT J OBESITY
JI Int. J. Obes.
PD AUG
PY 2010
VL 34
IS 8
BP 1284
EP 1292
DI 10.1038/ijo.2010.42
PG 9
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 636KK
UT WOS:000280732400007
PM 20195286
ER
PT J
AU Wynn, JK
Horan, WP
Kring, AM
Simons, RF
Green, MF
AF Wynn, Jonathan K.
Horan, William P.
Kring, Ann M.
Simons, Robert F.
Green, Michael F.
TI Impaired anticipatory event-related potentials in schizophrenia
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Article
DE Schizophrenia; Event-related potentials (ERP); Anticipation
ID STIMULUS-PRECEDING NEGATIVITY; STRIATAL REWARD PREDICTION; SLOW BRAIN
POTENTIALS; PHYSICAL ANHEDONIA; FEEDBACK STIMULI; HEART-RATE; TASK;
INFORMATION; DYSFUNCTION; PLEASURE
AB Deficits in anticipation are implicated across a variety of cognitive and emotional processes in schizophrenia. Although diminished anticipatory event-related potentials (ERPs) have been detected during tasks requiring motor response preparation in schizophrenia, no prior ERP study has examined non-motor-related anticipatory processes or used motivationally engaging stimuli. Thirty-four schizophrenia outpatients and 36 healthy controls completed a cued, reaction-time contingent picture viewing task to assess two types of anticipatory ERPs, one involving motor response preparation (Contingent Negative Variation [CNV]) and one not involving motor preparation (Stimulus Preceding Negativity [SPN]). The ERP paradigm included emotional and non-emotional pictures, and participants also completed trait anhedonia questionnaires. Patients and controls demonstrated similar patterns of reaction time and self-reported emotional responses to the pictures. However, patients demonstrated generally lower CNV and SPN across pleasant, neutral, and unpleasant picture conditions. Patients also reported lower anticipatory pleasure than controls on a trait questionnaire. Schizophrenia patients demonstrate diminished motor- and non-motor-related anticipatory processing, which may have wide-ranging adverse functional consequences. Published by Elsevier B.V.
C1 [Wynn, Jonathan K.; Horan, William P.; Green, Michael F.] Univ Calif Los Angeles, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Kring, Ann M.] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Simons, Robert F.] Univ Delaware, Newark, DE 19716 USA.
RP Wynn, JK (reprint author), Univ Calif Los Angeles, VA Greater Los Angeles Healthcare Syst, MIRECC 210A,Bldg 210,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM jkwynn@ucla.edu
RI Wynn, Jonathan/H-3749-2014
OI Wynn, Jonathan/0000-0002-1763-8540
FU NIMH NIH HHS [R01 MH043292, R01 MH043292-19, R01 MH065707, R01
MH065707-05, R03 MH077141, R03 MH077141-01]
NR 59
TC 24
Z9 28
U1 3
U2 15
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD AUG
PY 2010
VL 77
IS 2
BP 141
EP 149
DI 10.1016/j.ijpsycho.2010.05.009
PG 9
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 633WZ
UT WOS:000280539000008
PM 20573584
ER
PT J
AU D'Amico, AV
Braccioforte, MH
Moran, BJ
Chen, MH
AF D'Amico, Anthony V.
Braccioforte, Michelle H.
Moran, Brian J.
Chen, Ming-Hui
TI CAUSES OF DEATH IN MEN WITH PREVALENT DIABETES AND NEWLY DIAGNOSED HIGH-
VERSUS FAVORABLE-RISK PROSTATE CANCER
SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS
LA English
DT Article
DE Diabetes; prostate cancer; cause of death
ID ANDROGEN DEPRIVATION THERAPY; RANDOMIZED CONTROLLED-TRIAL; RADICAL
PROSTATECTOMY; RADIATION-THERAPY; COMPETING RISK; RADIOTHERAPY;
MORTALITY; SURVIVAL; ADJUVANT; BRACHYTHERAPY
AB Purpose: To determine whether prevalent diabetes mellitus (pDM) affects the presentation, extent of radiotherapy, or prostate cancer (PCa)-specific mortality (PCSM) and whether PCa aggressiveness affects the risk of non-PCSM, DM-related mortality, and all-cause mortality in men with pDM.
Methods: Between October 1997 and July 2907, 5,279 men treated at the Chicago Prostate Cancer Center with radiotherapy for PCa were included in the study. Logistic and competing risk regression analyses were performed to assess whether pDM was associated with high-grade PCa, less aggressive radiotherapy, and an increased risk of PCSM. Competing risks and Cox regression analyses were performed to assess whether PCa aggressiveness described by risk group in men with pDM was associated with the risk of non-PCSM, DM-related mortality, and all-cause mortality. Analyses were adjusted for predictors of high-grade PCa and factors that could affect treatment extent and mortality.
Results: Men with pDM were more likely (adjusted hazard ratio [AHR], 1.9; 95% confidence interval [CI], 1.3-2.7; p = .002) to present with high-grade PCa but were not treated less aggressively (p = .33) and did not have an increased risk of PCSM (p = .58) compared to men without pDM. Among the men with pDM, high-risk PCa was associated with a greater risk of non-PCSM (AHR, 2.2; 95% CI, 1.1-4.5; p = .035), DM-related mortality (AHR, 5.2; 95% CI, 2.0-14.0; p = .001), and all-cause mortality (AHR, 2.4; 95% Cl, 1.2-4.7; p = .01) compared to favorable-risk PCa.
Conclusion: Aggressive management of pDM is warranted in men with high-risk PCa. (C) 2010 Elsevier Inc.
C1 [D'Amico, Anthony V.] Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02215 USA.
[D'Amico, Anthony V.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Braccioforte, Michelle H.; Moran, Brian J.] Prostate Canc Fdn Chicago, Dept Radiat Oncol, Westmont, IL USA.
[Chen, Ming-Hui] Univ Connecticut, Dept Stat, Storrs, CT 06269 USA.
RP D'Amico, AV (reprint author), Brigham & Womens Hosp, Dept Radiat Oncol, 75 Francis St,L-2 Level, Boston, MA 02215 USA.
EM adamico@partners.org
NR 33
TC 21
Z9 21
U1 0
U2 1
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 AUG 1
PY 2010
VL 77
IS 5
BP 1329
EP 1337
DI 10.1016/j.ijrobp.2009.06.051
PG 9
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 632WJ
UT WOS:000280459700007
PM 19879061
ER
PT J
AU Hachinski, V
Donnan, GA
Gorelick, PB
Hacke, W
Cramer, SC
Kaste, M
Fisher, M
Brainin, M
Buchan, AM
Lo, EH
Skolnick, BE
Furie, KL
Hankey, GJ
Kivipelto, M
Morris, J
Rothwell, PM
Sacco, RL
Smith, SC
Wang, YL
Bryer, A
Ford, GA
Iadecola, C
Martins, SCO
Saver, J
Skvortsova, V
Bayley, M
Bednar, MM
Duncan, P
Enney, L
Finklestein, S
Jones, TA
Kalra, L
Kleim, J
Nitkin, R
Teasell, R
Weiller, C
Desai, B
Goldberg, MP
Heiss, WD
Saarelma, O
Schwamm, LH
Shinohara, Y
Trivedi, B
Wahlgren, N
Wong, LK
Hakim, A
Norrving, B
Prudhomme, S
Bornstein, NM
Davis, SM
Goldstein, LB
Leys, D
Tuomilehto, J
AF Hachinski, Vladimir
Donnan, Geoffrey A.
Gorelick, Philip B.
Hacke, Werner
Cramer, Steven C.
Kaste, Markku
Fisher, Marc
Brainin, Michael
Buchan, Alastair M.
Lo, Eng H.
Skolnick, Brett E.
Furie, Karen L.
Hankey, Graeme J.
Kivipelto, Miia
Morris, John
Rothwell, Peter M.
Sacco, Ralph L.
Smith, Sidney C., Jr.
Wang, Yulun
Bryer, Alan
Ford, Gary A.
Iadecola, Costantino
Martins, Sheila C. O.
Saver, Jeff
Skvortsova, Veronika
Bayley, Mark
Bednar, Martin M.
Duncan, Pamela
Enney, Lori
Finklestein, Seth
Jones, Theresa A.
Kalra, Lalit
Kleim, Jeff
Nitkin, Ralph
Teasell, Robert
Weiller, Cornelius
Desai, Bhupat
Goldberg, Mark P.
Heiss, Wolf-Dieter
Saarelma, Osmo
Schwamm, Lee H.
Shinohara, Yukito
Trivedi, Bhargava
Wahlgren, Nils
Wong, Lawrence K.
Hakim, Antoine
Norrving, Bo
Prudhomme, Stephen
Bornstein, Natan M.
Davis, Stephen M.
Goldstein, Larry B.
Leys, Didier
Tuomilehto, Jaakko
TI Stroke: working toward a prioritized world agenda
SO INTERNATIONAL JOURNAL OF STROKE
LA English
DT Editorial Material
DE prevention; rehabilitation; stroke; translational; treatment
ID VASCULAR COGNITIVE IMPAIRMENT; TISSUE-PLASMINOGEN ACTIVATOR; TRANSIENT
ISCHEMIC ATTACK; HEALTHY LIFE-STYLE; PRIMARY PREVENTION; POLICY
STATEMENT; CARE; RECOMMENDATIONS; PROGRESS; BRAIN
AB Background and Purpose
The aim of the Synergium was to devise and prioritize new ways of accelerating progress in reducing the risks, effects, and consequences of stroke.
Methods
Preliminary work was performed by seven working groups of stroke leaders followed by a synergium (a forum for working synergistically together) with approximately 100 additional participants. The resulting draft document had further input from contributors outside the synergium.
Results
Recommendations of the Synergium are:
Basic Science, Drug Development and Technology: There is a need to develop: (1) New systems of working together to break down the prevalent 'silo' mentality; (2) New models of vertically integrated basic, clinical, and epidemiological disciplines; and (3) Efficient methods of identifying other relevant areas of science.
Stroke Prevention: (1) Establish a global chronic disease prevention initiative with stroke as a major focus. (2) Recognize not only abrupt clinical stroke, but subtle subclinical stroke, the commonest type of cerebrovascular disease, leading to impairments of executive function. (3) Develop, implement and evaluate a population approach for stroke prevention. (4) Develop public health communication strategies using traditional and novel (eg, social media/marketing) techniques.
Acute Stroke Management: Continue the establishment of stroke centers, stroke units, regional systems of emergency stroke care and telestroke networks.
Brain Recovery and Rehabilitation: (1) Translate best neuroscience, including animal and human studies, into poststroke recovery research and clinical care. (2) Standardize poststroke rehabilitation based on best evidence. (3) Develop consensus on, then implementation of, standardized clinical and surrogate assessments. (4) Carry out rigorous clinical research to advance stroke recovery.
Into the 21st Century: Web, Technology and Communications: (1) Work toward global unrestricted access to stroke-related information. (2) Build centralized electronic archives and registries.
Foster Cooperation Among Stakeholders (large stroke organizations, nongovernmental organizations, governments, patient organizations and industry) to enhance stroke care.
Educate and energize professionals, patients, the public and policy makers by using a 'Brain Health' concept that enables promotion of preventive measures.
Conclusions
To accelerate progress in stroke, we must reach beyond the current status scientifically, conceptually, and pragmatically. Advances can be made not only by doing, but ceasing to do. Significant savings in time, money, and effort could result from discontinuing practices driven by unsubstantiated opinion, unproven approaches, and financial gain. Systematic integration of knowledge into programs coupled with careful evaluation can speed the pace of progress.
C1 [Hachinski, Vladimir] Univ Western Ontario, London Hlth Sci Ctr, Dept Clin Neurol Sci, London, ON N6A 5A5, Canada.
[Donnan, Geoffrey A.] Florey Neurosci Inst, Carlton S Victoria, Australia.
[Gorelick, Philip B.] Univ Illinois, Chicago, IL USA.
[Hacke, Werner] Univ Heidelberg, Heidelberg, Germany.
[Cramer, Steven C.] Univ Calif Irvine, Orange, CA 92668 USA.
[Kaste, Markku] Univ Helsinki, Cent Hosp, Helsinki, Finland.
[Fisher, Marc] Univ Massachusetts, Sch Med, Worcester, MA USA.
[Brainin, Michael] Univ Krems, Univ Donau, Krems, Austria.
[Buchan, Alastair M.] Univ Oxford, Oxford, England.
[Lo, Eng H.; Furie, Karen L.; Schwamm, Lee H.] Massachusetts Gen Hosp, Charlestown, MA USA.
[Skolnick, Brett E.] Novo Nordisk AS, Princeton, NJ USA.
[Hankey, Graeme J.] Royal Perth Hosp, Perth, WA, Australia.
[Kivipelto, Miia] Karolinska Inst, Stockholm, Sweden.
[Morris, John; Goldberg, Mark P.] Washington Univ, Sch Med, St Louis, MO USA.
[Rothwell, Peter M.] John Radcliffe Hosp, Oxford OX3 9DU, England.
[Sacco, Ralph L.] Univ Miami, AHA, Miami, FL USA.
[Smith, Sidney C., Jr.] Univ N Carolina, Ctr Cardiovasc Sci & Med, Chapel Hill, NC USA.
World Heart Federat, Geneva, Switzerland.
[Wang, Yulun] InTouch Hlth, Goleta, CA USA.
[Bryer, Alan] Univ Cape Town, ZA-7925 Cape Town, South Africa.
[Bryer, Alan] Groote Schuur Hosp, ZA-7925 Cape Town, South Africa.
[Ford, Gary A.] Univ Newcastle, Newcastle Upon Tyne, Tyne & Wear, England.
[Iadecola, Costantino] Weill Cornell Med Coll, New York, NY USA.
[Martins, Sheila C. O.] Hosp Clin, Porto Alegre, RS, Brazil.
[Saver, Jeff] Univ Calif Los Angeles, Stroke Ctr, Los Angeles, CA USA.
[Skvortsova, Veronika] Russian State Res Stroke Inst, Moscow, Russia.
[Bayley, Mark] Toronto Rehabil Inst, Toronto, ON, Canada.
[Bednar, Martin M.] Pfizer Inc, Neurosci Res Unit, Groton, CT 06340 USA.
[Duncan, Pamela] Duke Univ, Durham, NC USA.
[Enney, Lori] GlaxoSmithKline Inc, Durham, NC USA.
[Finklestein, Seth] Biotrofix Inc, Waltham, MA USA.
[Jones, Theresa A.] Univ Texas Austin, Austin, TX 78712 USA.
[Kalra, Lalit] Kings Coll London, London WC2R 2LS, England.
[Kleim, Jeff] Univ Florida, Gainesville, FL USA.
[Nitkin, Ralph] NICHHD, Natl Ctr Med Rehabil, NIH, Rockville, MD USA.
[Teasell, Robert] St Josephs Healthcare London, London, ON, Canada.
[Weiller, Cornelius] Univ Freiburg, Freiburg, Germany.
[Desai, Bhupat] Pomona Valley Hosp Med Ctr, Pomona, CA USA.
[Heiss, Wolf-Dieter] Max Planck Inst Neurol Res, Cologne, Germany.
[Saarelma, Osmo] Terveystalo Med Ctr, Helsinki, Finland.
[Shinohara, Yukito] Tachikawa Hosp, Tokyo, Japan.
[Trivedi, Bhargava] So Illinois Healthcare, Carbondale, IL USA.
[Wahlgren, Nils] Karolinska Inst, Stockholm, Sweden.
[Wong, Lawrence K.] Chinese Univ Hong Kong, Sha Tin, Hong Kong, Peoples R China.
Ottawa Hosp Res Inst, Ottawa, ON, Canada.
[Hakim, Antoine] Univ Ottawa, Canadian Stroke Network, Ottawa, ON, Canada.
[Norrving, Bo] Univ Lund Hosp, S-22185 Lund, Sweden.
[Prudhomme, Stephen] Amer Heart Assoc, Dallas, TX USA.
[Bornstein, Natan M.] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, IL-69978 Tel Aviv, Israel.
Univ Melbourne, Melbourne, Vic, Australia.
[Davis, Stephen M.] Royal Melbourne Hosp, Melbourne, Vic, Australia.
[Goldstein, Larry B.] Duke Univ, Durham, NC USA.
[Goldstein, Larry B.] Durham VA Med Ctr, Durham, NC USA.
[Leys, Didier] Univ Lille Nord France, Lille, France.
[Tuomilehto, Jaakko] Univ Helsinki, Helsinki, Finland.
RP Hachinski, V (reprint author), Univ Western Ontario, Univ Hosp, 339 Windermere Rd, London, ON N6A 5A5, Canada.
EM Vladimir.Hachinski@lhsc.on.ca
RI Jones, Theresa/F-1182-2010; Skolnick, Brett/B-5140-2009; Ford,
Gary/A-6353-2012; Buchan, Alastair/B-9095-2009; Hankey, Graeme
/H-4968-2014;
OI Kaste, Markku/0000-0001-6557-6412; Jones, Theresa/0000-0003-0906-6439;
Buchan, Alastair/0000-0002-2918-5200; Hankey, Graeme
/0000-0002-6044-7328; Donnan, Geoffrey/0000-0001-6324-3403; Saver,
Jeffrey/0000-0001-9141-2251; Norrving, Bo/0000-0002-8024-5096; Schwamm,
Lee/0000-0003-0592-9145; Kivipelto, Miia/0000-0003-0992-3875
FU Medical Research Council [G0500495]; NINDS NIH HHS [P01 NS055104, RC2
NS069335]
NR 87
TC 17
Z9 18
U1 0
U2 16
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1747-4930
J9 INT J STROKE
JI Int. J. Stroke
PD AUG
PY 2010
VL 5
IS 4
BP 238
EP 256
DI 10.1111/j.1747-4949.2010.00442.x
PG 19
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 619RC
UT WOS:000279446600002
PM 20636706
ER
PT J
AU Jura, Y
Townsend, M
Grodstein, F
AF Jura, Y.
Townsend, M.
Grodstein, F.
TI CAFFEINE INTAKE AND RISK OF STRESS, URGENCY, AND MIXED URINARY
INCONTINENCE
SO INTERNATIONAL UROGYNECOLOGY JOURNAL
LA English
DT Meeting Abstract
C1 [Jura, Y.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Townsend, M.] Harvard Univ, Sch Publ Hlth, Cambridge, MA 02138 USA.
[Grodstein, F.] Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0937-3462
J9 INT UROGYNECOL J
JI Int. Urogynecol. J.
PD AUG
PY 2010
VL 21
SU 1
MA 165
BP S234
EP S235
PG 2
WC Obstetrics & Gynecology; Urology & Nephrology
SC Obstetrics & Gynecology; Urology & Nephrology
GA 640OV
UT WOS:000281061800166
ER
PT J
AU Weinstein, M
Pulliam, S
Wakamatsu, M
AF Weinstein, M.
Pulliam, S.
Wakamatsu, M.
TI MINIMALLY-INVASIVE SACRAL COLPOPEXY: COMPARISON OF OPERATIVE
CHARACTERISTICS OF LAPAROSCOPIC AND ROBOTIC APPROACHES.
SO INTERNATIONAL UROGYNECOLOGY JOURNAL
LA English
DT Meeting Abstract
C1 [Weinstein, M.; Pulliam, S.; Wakamatsu, M.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cambridge, MA 02138 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0937-3462
J9 INT UROGYNECOL J
JI Int. Urogynecol. J.
PD AUG
PY 2010
VL 21
SU 1
MA 256
BP S367
EP S368
PG 2
WC Obstetrics & Gynecology; Urology & Nephrology
SC Obstetrics & Gynecology; Urology & Nephrology
GA 640OV
UT WOS:000281061800257
ER
PT J
AU Wang, DY
Ray, A
Rodgers, K
Ergorul, C
Hyman, BT
Huang, W
Grosskreutz, CL
AF Wang, Dan Yi
Ray, Arjun
Rodgers, Kathryn
Ergorul, Ceren
Hyman, Bradley T.
Huang, Wei
Grosskreutz, Cynthia L.
TI Global Gene Expression Changes in Rat Retinal Ganglion Cells in
Experimental Glaucoma
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID LASER CAPTURE MICRODISSECTION; OPTIC-NERVE TRANSECTION; MICROARRAY
ANALYSIS; INTRAOCULAR-PRESSURE; MODEL; ACTIVATION; SURVIVAL;
PHOSPHORYLATION; MECHANISMS; NEURONS
AB PURPOSE. Intraocular pressure (IOP) is an important risk factor in glaucoma. Gene expression changes were studied in glaucomatous rat retinal ganglion cells (RGCs) to elucidate altered transcriptional pathways.
METHODS. RGCs were back-labeled with Fluorogold. Unilateral IOP elevation was produced by injection of hypertonic saline into the episcleral veins. Laser capture microdissection (LCM) was used to capture an equal number of RGCs from normal and glaucomatous retinal sections. RNA was extracted and amplified, labeled, and hybridized to rat genome microarrays, and data analysis was performed. After selected microarray data were confirmed by RT-qPCR and immunohistochemistry, biological pathway analyses were performed.
RESULTS. Significant changes were found in the expression of 905 genes, with 330 genes increasing and 575 genes decreasing in glaucomatous RGCs. Multiple cellular pathways were involved. Ingenuity pathway analysis demonstrated significant changes in cardiac beta-adrenergic signaling, interferon signaling, glutamate receptor signaling, cAMP-mediated signaling, chemokine signaling, 14-3-3-mediated signaling, and G-protein-coupled receptor signaling. Gene set enrichment analysis showed that the genes involved in apoptotic pathways were enriched in glaucomatous RGCs. The prosurvival gene Stat3 was upregulated in response to elevated IOP, and immunohistochemistry confirmed that Stat3 and phosphorylated-Stat3 levels were increased in RGCs in experimental glaucoma. In addition, the expression of several prosurvival genes normally expressed in RGCs was decreased.
CONCLUSIONS. There are extensive changes in gene expression in glaucomatous RGCs involving multiple molecular pathways, including prosurvival and prodeath genes. The alteration in the balance between prosurvival and prodeath may contribute to RGC death in glaucoma. (Invest Ophthalmol Vis Sci. 2010;51:4084-4095) DOI:10.1167/iovs.09-4864
C1 [Wang, Dan Yi; Ray, Arjun; Rodgers, Kathryn; Ergorul, Ceren; Huang, Wei; Grosskreutz, Cynthia L.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA 02114 USA.
[Hyman, Bradley T.] Harvard Univ, MassGen Inst Neurodegenerat Dis, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
RP Grosskreutz, CL (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, 243 Charles St, Boston, MA 02114 USA.
EM cynthia_grosskreutz@meei.harvard.edu
FU National Eye Institute [R01-EY13399, EY014104]; Cannistraro Fund;
Margolis fund
FX Supported by the Massachusetts Lions Eye Research Fund, National Eye
Institute Grant R01-EY13399, the Cannistraro Fund, the Margolis fund,
and National Eye Institute Core Facility Grant EY014104.
NR 35
TC 27
Z9 28
U1 0
U2 1
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD AUG
PY 2010
VL 51
IS 8
BP 4084
EP 4095
DI 10.1167/iovs.09-4864
PG 12
WC Ophthalmology
SC Ophthalmology
GA 629JT
UT WOS:000280194100037
PM 20335623
ER
PT J
AU Fan, BJ
Liu, K
Wang, DY
Tham, CCY
Tam, POS
Lam, DSC
Pang, CP
AF Fan, Bao Jian
Liu, Ke
Wang, Dan Yi
Tham, Clement C. Y.
Tam, Pancy O. S.
Lam, Dennis S. C.
Pang, Chi Pui
TI Association of Polymorphisms of Tumor Necrosis Factor and Tumor Protein
p53 with Primary Open-Angle Glaucoma
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID NORMAL-TENSION GLAUCOMA; NITRIC-OXIDE SYNTHASE; S-TRANSFERASE M1;
METHYLENETETRAHYDROFOLATE REDUCTASE GENE; ALPHA PROMOTER POLYMORPHISMS;
CODON 72 POLYMORPHISM; TNF-ALPHA; PSEUDOEXFOLIATION GLAUCOMA; OPA1
POLYMORPHISMS; RISK-FACTOR
AB PURPOSE. To evaluate the variants of 10 genes for association with primary open-angle glaucoma (POAG) in a Chinese population.
METHODS. A total of 405 unrelated patients with POAG (255 high-tension glaucoma [HTG], 100 normal-tension glaucoma [NTG], and 50 juvenile-onset open-angle glaucoma [JOAG]) and 201 control subjects were recruited. Seventeen variants in 10 genes with reported association with POAG were geno-typed for analysis of allele and haplotype frequencies between cases and control subjects. These genes included CDH1 (cadherin 1, type 1, E-cadherin), CDKN1A (cyclin-dependent kinase inhibitor 1A), CYP1B1 (cytochrome P450, family 1, subfamily B, polypeptide 1), GSTM1 (glutathione S-transferase mu 1), GSTT1 (glutathione S-transferase theta 1), MTHFR (5,10-methylenetetrahydrofolate reductase), NOS3 (nitric oxide synthase 3), OPA1 (optic atrophy 1), TNF (tumor necrosis factor), and TP53 (tumor protein p53).
RESULTS. One SNP (-308G>A; rs1800629) in TNF demonstrated a significant association with HTG (P = 0.012). The allele G frequency was higher in HTG patients than in control subjects (94.6% vs. 90.3%; OR = 1.89). One haplotype consisting of rs1799724 and rs1800629 was significantly associated with HTG (P = 0.015, corrected P = 0.045). One SNP (R72P; rs1042522) in TP53 was significantly associated with NTG (P = 0.018). The allele G frequency was higher in NTG patients than in control subjects (56.1% vs. 45.8%; OR = 1.52). The significance of these associations survived the Bonferroni correction (corrected P < 0.024). Other gene variants were not significantly associated with HTG (P > 0.063) or NTG (P > 0.13). None of the studied variants was significantly associated with JOAG (P > 0.17).
CONCLUSIONS. The findings suggest that variants in TNF and TP53 are risk factors for POAG, whereas variants in other studied genes are not major risk factors for POAG, at least in the Chinese population. (Invest Ophthalmol Vis Sci. 2010;51:4110-4116) DOI:10.1167/iovs.09-4974
C1 [Fan, Bao Jian; Liu, Ke; Wang, Dan Yi; Tham, Clement C. Y.; Tam, Pancy O. S.; Lam, Dennis S. C.; Pang, Chi Pui] Chinese Univ Hong Kong, Dept Ophthalmol & Visual Sci, Kowloon, Hong Kong, Peoples R China.
[Fan, Bao Jian; Wang, Dan Yi] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA USA.
RP Pang, CP (reprint author), Chinese Univ Hong Kong, Hong Kong Eye Hosp, Dept Ophthalmol & Visual Sci, 147K Argyle St, Kowloon, Hong Kong, Peoples R China.
EM cppang@cuhk.edu.hk
RI Pang, Chi/I-5388-2014;
OI Fan, Baojian/0000-0002-6851-2737
FU University Grants Committee, Hong Kong; Research Grant Council, Hong
Kong [2140597]
FX Supported in part by a block grant from the University Grants Committee,
Hong Kong, and by General Research Fund Grant 2140597 from the Research
Grant Council, Hong Kong.
NR 78
TC 44
Z9 45
U1 1
U2 6
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD AUG
PY 2010
VL 51
IS 8
BP 4110
EP 4116
DI 10.1167/iovs.09-4974
PG 7
WC Ophthalmology
SC Ophthalmology
GA 629JT
UT WOS:000280194100040
PM 20357201
ER
PT J
AU Christen, T
Sheikine, Y
Rocha, VZ
Hurwitz, S
Goldfine, AB
Di Carli, M
Libby, P
AF Christen, Thomas
Sheikine, Yuri
Rocha, Viviane Z.
Hurwitz, Shelley
Goldfine, Allison B.
Di Carli, Marcelo
Libby, Peter
TI Increased Glucose Uptake in Visceral Versus Subcutaneous Adipose Tissue
Revealed by PET Imaging
SO JACC-CARDIOVASCULAR IMAGING
LA English
DT Article
DE adipose tissue; adipocytes; stromal vascular cells; fluorodeoxyglucose;
positron emission tomography; glucose uptake; inflammation
ID CARDIOVASCULAR-DISEASE; INSULIN STIMULATION; ABDOMINAL OBESITY; FAT
DEPOT; TOMOGRAPHY; ADIPOCYTES; CELLS; BASAL; RISK
AB OBJECTIVES The current study tested the hypothesis that glucose utilization differs between visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT), and investigated potential mechanisms for such a finding.
BACKGROUND VAT burden correlates better with cardiovascular risk than does SAT burden. Beyond volumetric measurement, glucose uptake in adipose tissue (AT) might reflect metabolic activity and provide pathophysiologic insight and aid risk stratification.
METHODS We retrospectively studied tissue-specific glucose uptake in vivo in clinically obtained whole-body fluorodeoxyglucose positron emission tomography (FDG-PET) scans in humans. We also assessed glucose uptake in vitro, using stromal vascular cells isolated from SAT and VAT of diet-induced obese C57BL/6 mice. Quantitative polymerase chain reaction (PCR) evaluated the expression of multiple genes involved in cellular glucose metabolism, including glucose transporters (GLUT-1, -3, and -4) and hexokinases (HK-1 and -2) in SAT and VAT of obese C57BL/6 mice.
RESULTS We analyzed whole-body FDG-PET scans from 31 obese and 26 lean patients. VAT exhibited higher FDG uptake compared with SAT (p < 0.0001) independent of age, sex, body mass index, comorbidities, and medications. To investigate mechanisms underlying this observation, we studied glucose uptake in the stromal vascular cell fraction of AT, which is rich in inflammatory cells. Stromal vascular cells from VAT of diet-induced obese C57BL/6 mice exhibited higher glucose uptake than those from SAT (p = 0.01). Evaluation of expression of glucose transporters (GLUT-1, -3, and -4) and hexokinases (HK-1 and -2), revealed increased expression of HK-1 in VAT-derived compared with SAT-derived stromal vascular cells, and also in visceral versus subcutaneous unfractionated AT.
CONCLUSIONS In humans in vivo, VAT has increased glucose uptake compared with SAT, as determined noninvasively with FDG PET imaging. Differential stromal metabolic activity may be 1 mechanism underlying differences in metabolic activity of visceral and subcutaneous AT. (J Am Coll Cardiol Img 2010;3:843-51) (C) 2010 by the American College of Cardiology Foundation
C1 [Christen, Thomas; Rocha, Viviane Z.; Di Carli, Marcelo; Libby, Peter] Brigham & Womens Hosp, Div Cardiovasc Med, Boston, MA 02115 USA.
[Sheikine, Yuri; Di Carli, Marcelo] Brigham & Womens Hosp, Dept Radiol, Div Nucl Med & Mol Imaging, Boston, MA 02115 USA.
[Sheikine, Yuri; Di Carli, Marcelo] Brigham & Womens Hosp, Noninvas Cardiovasc Imaging Program, Dept Med Cardiol, Boston, MA 02115 USA.
[Sheikine, Yuri; Di Carli, Marcelo] Brigham & Womens Hosp, Dept Radiol, Noninvas Cardiovasc Imaging Program, Boston, MA 02115 USA.
[Goldfine, Allison B.] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
RP Libby, P (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc,Dept Med, 77 Ave Louis Pasteur, Boston, MA 02115 USA.
EM plibby@rics.bwh.harvard.edu
FU Donald W. Reynolds Foundation [U01HL080731]
FX From the *Division of Cardiovascular Medicine, Brigham and Women's
Hospital, Boston, Massachusetts, dagger Division of Nuclear Medicine and
Molecular Imaging, Department of Radiology, Brigham and Women's
Hospital, Boston, Massachusetts, double dagger Noninvasive
Cardiovascular Imaging Program, Departments of Medicine (Cardiology) and
Radiology, Brigham and Women's Hospital, Boston, Massachusetts,
Department of Medicine, Brigham and Women's Hospital, Boston,
Massachusetts; and the parallel to Joslin Diabetes Center, Harvard
Medical School, Boston, Massachusetts. This work was funded in part by
the Donald W. Reynolds Foundation, Translational Program of Excellence
in Nanotechnology grant U01HL080731. Drs. Christen, Sheikine, and Rocha
contributed equally to this study. An alternative spelling of Dr.
Sheikine's name is Yury Sheykin.
NR 20
TC 35
Z9 36
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-878X
J9 JACC-CARDIOVASC IMAG
JI JACC-Cardiovasc. Imag.
PD AUG
PY 2010
VL 3
IS 8
BP 843
EP 851
DI 10.1016/j.jcmg.2010.06.004
PG 9
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 647OE
UT WOS:000281627000008
PM 20705265
ER
PT J
AU Donnelly, P
Maurovich-Horvat, P
Vorpahl, M
Nakano, M
Kaple, RK
Warger, W
Tanaka, A
Tearney, G
Virmani, R
Hoffmann, U
AF Donnelly, Patrick
Maurovich-Horvat, Pal
Vorpahl, Marc
Nakano, Masataka
Kaple, Ryan K.
Warger, William
Tanaka, Atsushi
Tearney, Guillermo
Virmani, Renu
Hoffmann, Udo
TI Multimodality Imaging Atlas of Coronary Atherosclerosis
SO JACC-CARDIOVASCULAR IMAGING
LA English
DT Editorial Material
ID AMERICAN-HEART-ASSOCIATION; VASCULAR-LESIONS; ARTERIOSCLEROSIS;
CLASSIFICATION; DEFINITION; COMMITTEE; COUNCIL; PLAQUE
C1 [Donnelly, Patrick; Maurovich-Horvat, Pal; Hoffmann, Udo] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA.
[Kaple, Ryan K.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Warger, William; Tanaka, Atsushi; Tearney, Guillermo] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Maurovich-Horvat, Pal] Semmelweis Univ, Ctr Heart, Budapest, Hungary.
[Vorpahl, Marc; Nakano, Masataka; Virmani, Renu] CV Path Inst Inc, Gaithersburg, MD USA.
[Tearney, Guillermo] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Tearney, Guillermo] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Hoffmann, U (reprint author), Massachusetts Gen Hosp, Cardiac MR PET CT Program, 165 Cambridge St,Suite 400, Boston, MA 02114 USA.
EM uhoffmann@partners.org
NR 8
TC 6
Z9 6
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-878X
J9 JACC-CARDIOVASC IMAG
JI JACC-Cardiovasc. Imag.
PD AUG
PY 2010
VL 3
IS 8
BP 876
EP 880
DI 10.1016/j.jcmg.2010.06006
PG 5
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 647OE
UT WOS:000281627000013
PM 20705270
ER
PT J
AU Pride, YB
Tung, P
Mohanavelu, S
Zorkun, C
Wiviott, SD
Antman, EM
Giugliano, R
Braunwald, E
Gibson, CM
AF Pride, Yuri B.
Tung, Patricia
Mohanavelu, Satishkumar
Zorkun, Cafer
Wiviott, Stephen D.
Antman, Elliott M.
Giugliano, Robert
Braunwald, Eugene
Gibson, C. Michael
CA TIMI Study Grp
TI Angiographic and Clinical Outcomes Among Patients With Acute Coronary
Syndromes Presenting With Isolated Anterior ST-Segment Depression A
TRITON TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by
Optimizing Platelet Inhibition With Prasugrel Thrombolysis In Myocardial
Infarction 38) Substudy
SO JACC-CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE acute coronary syndrome; ST-segment elevation myocardial infarction;
electrocardiography
ID ELEVATION; MORTALITY; EMERGENCY; MULTICENTER; REPERFUSION; CLOPIDOGREL;
IMPACT; ARTERY
AB Objectives This study sought to determine angiographic and clinical outcomes among patients with acute coronary syndrome (ACS) presenting with isolated anterior ST-segment depression on 12-lead electrocardiogram (ECG).
Background In patients with ACS, anterior ST-segment depression on 12-lead ECG may represent plaque rupture with: 1) acute thrombotic occlusion with elevation of cardiac biomarkers (+Tn); 2) a patent artery with +Tn; or 3) a patent artery with -Tn.
Methods The TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis In Myocardial Infarction 38) enrolled 13,608 ACS patients. Those with isolated anterior (leads V(1) to V(4)) ST-segment depression were analyzed. Angiograms and ECGs were interpreted by local investigators.
Results There were 1,198 (8.8%) patients with isolated anterior ST-segment depression. Of those, 314 (26.2%) had an occluded culprit artery (TIMI flow grade 0/1) and +Tn, 641 (53.5%) had a patent culprit artery (TIMI flow grade 2/3) and +Tn, and 243 (20.3%) had TIMI flow grade 2/3 and -Tn. Among patients with an occluded artery, the culprit artery was most often the left circumflex artery (48.4%). The 30-day incidence of the composite of death and MI was significantly higher among patients with an occluded artery (8.6%) than among those with a patent culprit artery and either +Tn (6.3%) or -Tn (2.9%) (3-way p = 0.006). Among patients with an occluded artery, the median time from ECG to percutaneous coronary intervention was 29.4 h (interquartile range 26.1 to 44.1 h).
Conclusions Among ACS patients presenting with isolated anterior ST-segment depression, over one-quarter had an occluded culprit artery and elevated cardiac biomarkers. These patients had significantly worse clinical outcomes, and few underwent urgent angiography. (J Am Coll Cardiol Intv 2010;3:806-11) (c) 2010 by the American College of Cardiology Foundation
C1 [Gibson, C. Michael] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Cardiovasc, Boston, MA 02115 USA.
[Mohanavelu, Satishkumar; Wiviott, Stephen D.; Antman, Elliott M.; Giugliano, Robert; Braunwald, Eugene] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, TIMI Study Grp, Boston, MA 02115 USA.
[Pride, Yuri B.; Tung, Patricia; Zorkun, Cafer] Beth Israel Deaconess Med Ctr, Dept Med, Div Cardiovasc, Boston, MA USA.
RP Gibson, CM (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Cardiovasc, 350 Longwood Ave,1st Floor, Boston, MA 02115 USA.
EM mgibson@perfuse.org
FU Daiichi-Sankyo Company, Ltd.; Eli Lilly and Company; Schering-Plough;
Sanofi-Aventis; AstraZeneca; ARENA; Novartis; Merck; Bristol-Myers
Squibb
FX The TRITON TEVII 38 study was supported by a grant from Daiichi-Sankyo
Company, Ltd. and Eli Lilly and Company. Dr. Braunwald has received
grant support from Eli Lilly and Company and Daiichi-Sankyo, recieves
lecture fees from Eli Lilly and Company, and is a member of the Advisory
Board of Daiichi-Sankyo. Dr. Wiviott has received research grants from
Eli Lilly and Company, Daiichi-Sankyo, Schering-Plough, consulting fees
from Sanofi-Aventis, AstraZeneca, and ARENA, and has received lecture
fees from Eli Lilly and Company, Daiichi-Sankyo, AstraZeneca, and
Novartis. Dr. Giugliano has received lecture fees from Sanofi-Aventis,
Merck, and Bristol-Myers Squibb, is a consultant for Merck, HeartScape,
Sanofi-Aventis, Daiichi-Sankyo, and Angel Med, and has participated in
clinical trials/research support for Daiichi-Sanlcyo and Merck. All
other authors report that they have no relationships to disclose.
NR 22
TC 24
Z9 24
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-8798
J9 JACC-CARDIOVASC INTE
JI JACC-Cardiovasc. Interv.
PD AUG
PY 2010
VL 3
IS 8
BP 806
EP 811
DI 10.1016/j.jcin.2010.05.012
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645LI
UT WOS:000281458700004
PM 20723851
ER
PT J
AU Hatano, H
Lampiris, H
Fransen, S
Gupta, S
Huang, W
Hoh, R
Martin, JN
Lalezari, J
Bangsberg, D
Petropoulos, C
Deeks, SG
AF Hatano, Hiroyu
Lampiris, Harry
Fransen, Signe
Gupta, Soumi
Huang, Wei
Hoh, Rebecca
Martin, Jeffrey N.
Lalezari, Jacob
Bangsberg, David
Petropoulos, Christos
Deeks, Steven G.
TI Evolution of Integrase Resistance During Failure of Integrase
Inhibitor-Based Antiretroviral Therapy
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE integrase inhibitors; drug resistance; virologic failure
ID TREATMENT-EXPERIENCED PATIENTS; HIV-1 INFECTION; CONTROLLED-TRIAL;
RALTEGRAVIR; EFFICACY; SAFETY; REPLICATION; SUBGROUP
AB Background: Although integrase inhibitors are highly effective in the management of drug-resistant HIV, some patients fail to achieve durable viral suppression. The long-term consequences of integrase inhibitor failure have not been well defined.
Methods: We identified 29 individuals who exhibited evidence of incomplete viral suppression on a regimen containing an integrase inhibitor (23 raltegravir, 6 elvitegravir). Before initiating the integrase inhibitor-based regimen, the median CD4(+) T-cell count and plasma HIV RNA levels were 62 cells/mm(3) and 4.65 log(10) copies/mL, respectively.
Results: At the first failure time-point, the most common integrase resistance pattern for subjects taking raltegravir was wild-type, followed in order of frequency by Q148H/K/R+G140S, N155H, and Y143R/H/C. The most common resistance pattern for subjects taking elvitegravir was E92Q. Long-term failure was associated with continued viral evolution, emergence of high-level phenotypic resistance, and a decrease in replicative capacity.
Conclusions: Although wild-type failure during early integrase inhibitor failure is common, most patients eventually develop high-level phenotypic drug resistance. This resistance evolution is gradual and associated with declines in replicative capacity.
C1 [Hatano, Hiroyu; Lampiris, Harry; Hoh, Rebecca; Martin, Jeffrey N.; Deeks, Steven G.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Lampiris, Harry] San Francisco VA Med Ctr, San Francisco, CA 94143 USA.
[Fransen, Signe; Gupta, Soumi; Huang, Wei; Petropoulos, Christos] Monogram Biosci, San Francisco, CA USA.
[Lalezari, Jacob] Quest Clin Res, San Francisco, CA USA.
[Bangsberg, David] Harvard Univ, Sch Med, Boston, MA USA.
RP Hatano, H (reprint author), San Francisco Gen Hosp, Bldg 80,Ward 84,995 Potrero Ave, San Francisco, CA 94110 USA.
EM hhatano@php.ucsf.edu
FU NIAID [K23AI075985, K24 AI069994]; UCSF/Gladstone Center for AIDS
Research [P30 AI27763, P30 MH59037]; Center for AIDS Prevention Studies
[P30 MH62246]; UCSF Clinical and Translational Science Institute [UL1
RR024131-01]; NIH NIAID [SBIR- R43 AI057074-01]; Merck; Monogram
Biosciences; Gilead
FX This work was supported by grants from the NIAID (K23AI075985, K24
AI069994), the UCSF/Gladstone Center for AIDS Research (P30 AI27763, P30
MH59037), the Center for AIDS Prevention Studies (P30 MH62246), and the
UCSF Clinical and Translational Science Institute (UL1 RR024131-01). The
development of the PhenoSense (R) Integrase assay was partially
supported by NIH NIAID SBIR- R43 AI057074-01.; Potential conflicts of
interest. SG, SF, WH, and CP are employees of Monogram Biosciences. HH
has received research support from Merck and Monogram Biosciences. SD
has received research support from Merck, Gilead, and Monogram
Biosciences.
NR 13
TC 38
Z9 39
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 AUG 1
PY 2010
VL 54
IS 4
BP 389
EP 393
DI 10.1097/QAI.0b013e3181c42ea4
PG 5
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 627BR
UT WOS:000280013600008
PM 20300008
ER
PT J
AU Willig, JH
Nevin, CR
Raper, JL
Saag, MS
Mugavero, MJ
Willig, AL
Burkhardt, JH
Schumacher, JE
Johnson, VA
AF Willig, James H.
Nevin, Christa R.
Raper, James L.
Saag, Michael S.
Mugavero, Michael J.
Willig, Amanda L.
Burkhardt, Jeffrey H.
Schumacher, Joseph E.
Johnson, Victoria A.
TI Cost Ramifications of Increased Reporting of Detectable Plasma HIV-1 RNA
Levels by the Roche COBAS AmpliPrep/COBAS TaqMan HIV-1 Version 1.0 Viral
Load Test
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Letter
ID VIRUS TYPE-1 RNA; ANTIRETROVIRAL THERAPY; AMPLICOR; ASSAY; FAILURE;
MONITOR
C1 [Willig, James H.; Nevin, Christa R.; Raper, James L.; Saag, Michael S.; Mugavero, Michael J.; Johnson, Victoria A.] Birmingham Vet Affairs Med Ctr, Div Infect Dis, Dept Internal Med, Birmingham, AL USA.
[Willig, Amanda L.] Birmingham Vet Affairs Med Ctr, Dept Nutr Sci, Birmingham, AL USA.
[Burkhardt, Jeffrey H.] Birmingham Vet Affairs Med Ctr, Dept Hlth Serv Adm, Birmingham, AL USA.
[Schumacher, Joseph E.] Birmingham Vet Affairs Med Ctr, Dept Med, Div Prevent Med, Birmingham, AL USA.
RP Willig, JH (reprint author), Birmingham Vet Affairs Med Ctr, Div Infect Dis, Dept Internal Med, Birmingham, AL USA.
OI Willig, Amanda/0000-0001-8802-4311
FU NCI NIH HHS [CA 47888, R25 CA047888]; NIAID NIH HHS [P30 AI027767, R24
AI067039-04, R24 AI067039, 1 R24 AI067039-1, P30-AI27767, P30
AI027767-21A1]
NR 12
TC 9
Z9 9
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 AUG 1
PY 2010
VL 54
IS 4
BP 442
EP 444
DI 10.1097/QAI.0b013e3181d01d1d
PG 3
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 627BR
UT WOS:000280013600016
PM 20611035
ER
PT J
AU Tyer-Viola, LA
Duffy, ME
AF Tyer-Viola, Lynda A.
Duffy, Mary E.
TI The Pregnant Women with HIV Attitude Scale: development and initial
psychometric evaluation
SO JOURNAL OF ADVANCED NURSING
LA English
DT Article
DE HIV; AIDS; instrument development; midwives; obstetric nurses; Pregnant
Women with HIV Attitude Scale; psychometric evaluation
ID POSITIVE WOMEN; NURSES ATTITUDES; CARE PROVIDERS; MATERNITY CARE;
HIV/AIDS; STIGMA; AIDS; KNOWLEDGE; PERCEPTIONS; INFECTION
AB P>Title.
The Pregnant Women with HIV Attitude Scale: development and initial psychometric evaluation.
Aim.
This paper is a report of the development and initial psychometric evaluation of the Pregnant Women with HIV Attitude Scale.
Background.
Previous research has identified that attitudes toward persons with HIV/AIDS have been judgmental and could affect clinical care and outcomes. Stigma towards persons with HIV has persisted as a barrier to nursing care globally. Women are more vulnerable during pregnancy. An instrument to specifically measure obstetric care provider's attitudes toward this population is needed to target identified gaps in providing respectful care.
Methods.
Existing literature and instruments were analysed and two existing measures, the Attitudes about People with HIV Scale and the Attitudes toward Women with HIV Scale, were combined to create an initial item pool to address attitudes toward HIV-positive pregnant women. The data were collected in 2003 with obstetric nurses attending a national conference in the United States of America (N = 210). Content validity was used for item pool development and principal component analysis and analysis of variance were used to determine construct validity. Reliability was analysed using Cronbach's Alpha.
Results.
The new measure demonstrated high internal consistency (alpha estimates = 0 center dot 89). Principal component analysis yielded a two-component structure that accounted for 45% of the total variance: Mothering-Choice (alpha estimates = 0 center dot 89) and Sympathy-Rights (alpha estimates = 0 center dot 72).
Conclusion.
These data provided initial evidence of the psychometric properties of the Pregnant Women with HIV Attitude Scale. Further analysis is required of the validity of the constructs of this scale and its reliability with various obstetric care providers.
C1 [Tyer-Viola, Lynda A.] Massachusetts Gen Hosp Inst Hlth Profess, Boston, MA USA.
[Duffy, Mary E.] Massachusetts Gen Hosp, Yvonne L Munn Ctr Nursing Res, Boston, MA 02114 USA.
RP Tyer-Viola, LA (reprint author), Massachusetts Gen Hosp Inst Hlth Profess, Boston, MA USA.
EM ltyerviola@partners.org
FU Alpha Chi Chapter of Sigma Theta Tau; Yvonne L. Munn Center for Nursing
Research, Massachusetts General Hospital
FX Funding for this study was from The Alpha Chi Chapter of Sigma Theta Tau
and The Yvonne L. Munn Center for Nursing Research, Massachusetts
General Hospital.
NR 71
TC 1
Z9 1
U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0309-2402
J9 J ADV NURS
JI J. Adv. Nurs.
PD AUG
PY 2010
VL 66
IS 8
BP 1852
EP 1863
DI 10.1111/j.1365-2648.2009.05234.x
PG 12
WC Nursing
SC Nursing
GA 619RG
UT WOS:000279447100020
PM 20557397
ER
PT J
AU Vassallo, MF
Camargo, CA
AF Vassallo, Milo F.
Camargo, Carlos A., Jr.
TI Potential mechanisms for the hypothesized link between sunshine, vitamin
D, and food allergy in children
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Food allergy; vitamin D; vitamin D deficiency; mucosal immunity;
epithelial barrier; microbial ecology; infections; sensitization; atopy
ID REGULATORY T-CELLS; BODY-MASS INDEX; D DEFICIENCY; ATOPIC-DERMATITIS;
1,25-DIHYDROXYVITAMIN D-3; UNITED-STATES; ORAL TOLERANCE; IMMUNE-SYSTEM;
US CHILDREN; D-RECEPTOR
AB Epidemiologic data suggest that the incidence of food allergy (FA) is increasing among children, yet a satisfactory model of its pathogenesis remains elusive. FA is the consequence of maladaptive immune responses to common and otherwise innocuous food antigens. Concurrent with the increase in FA is an epidemic of vitamin D deficiency (VDD) caused by several factors, especially decreased sunlight/UVB exposure. There is growing appreciation of the importance of the pleiotropic hormone vitamin D in the development of tolerance, immune system defenses, and epithelial barrier integrity. We propose a "multiplehit'' model in which VDD in a developmentally critical period increases susceptibility to colonization with abnormal intestinal microbial flora and gastrointestinal infections, contributing to abnormal intestinal barrier permeability and excess and inappropriate exposure of the immune system to dietary allergens. A compounding effect (and additional "hit'') of VDD is the promotion of a pro-sensitization immune imbalance that might compromise immunologic tolerance and contribute to FA. We propose that early correction of VDD might promote mucosal immunity, healthy microbial ecology, and allergen tolerance and thereby blunt the FA epidemic in children. (J Allergy Clin Immunol 2010;126:217-22.)
C1 [Vassallo, Milo F.; Camargo, Carlos A., Jr.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol,Dept Med, Boston, MA 02114 USA.
[Camargo, Carlos A., Jr.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Camargo, Carlos A., Jr.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
RP Camargo, CA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol,Dept Med, 326 Cambridge St,Suite 410, Boston, MA 02114 USA.
EM ccamargo@partners.org
FU National Institutes of Health (Bethesda, Md) [T32 AI-060548];
Massachusetts General Hospital Center for D-receptor Activation Research
(Boston, Mass); Food Allergy and Anaphylaxis Network (Fairfax, Va)
FX M. F. V. was supported by T32 AI-060548 from the National Institutes of
Health (Bethesda, Md). C. A. C. was supported, in part, by the
Massachusetts General Hospital Center for D-receptor Activation Research
(Boston, Mass) and the Food Allergy and Anaphylaxis Network (Fairfax,
Va).
NR 67
TC 75
Z9 77
U1 3
U2 14
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD AUG
PY 2010
VL 126
IS 2
BP 217
EP 222
DI 10.1016/j.jaci.2010.06.011
PG 6
WC Allergy; Immunology
SC Allergy; Immunology
GA 642IL
UT WOS:000281203800004
PM 20624647
ER
PT J
AU Lange, NE
Rifas-Shiman, SL
Camargo, CA
Gold, DR
Gillman, MW
Litonjua, AA
AF Lange, Nancy E.
Rifas-Shiman, Sheryl L.
Camargo, Carlos A., Jr.
Gold, Diane R.
Gillman, Matthew W.
Litonjua, Augusto A.
TI Maternal dietary pattern during pregnancy is not associated with
recurrent wheeze in children
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Asthma; dietary pattern; Mediterranean diet; healthy diet; principal
components; childhood wheeze; pregnancy
ID MAJOR CHRONIC DISEASE; OBSTRUCTIVE PULMONARY-DISEASE;
GUIDELINES-FOR-AMERICANS; MEDITERRANEAN DIET; VITAMIN-D; 5-YEAR-OLD
CHILDREN; ANTIOXIDANT INTAKE; CHILDHOOD ASTHMA; FOOD-CONSUMPTION; RISK
AB Background: The rise in asthma prevalence over the last few decades may be a result of changes in prenatal or early-life environment, including maternal diet during pregnancy. Previous studies have found associations between individual foods or nutrients consumed during pregnancy and asthma or wheeze in children, but these may be confounded by overall dietary pattern.
Objective: To determine whether overall maternal dietary pattern during pregnancy is associated with recurrent wheeze in children.
Methods: A total of 1376 mother-infant pairs from Project Viva, a longitudinal prebirth cohort, who had responses for food frequency questionnaires in the first and second trimester and outcome data at 3 years of age were included. Multivariable logistic regression was used to look at associations between dietary pattern and the primary outcome of recurrent wheeze at 3 years. Overall dietary pattern was examined by using Mediterranean diet score, Alternate Healthy Eating Index modified for pregnancy (AHEI-P), and principal components analysis to look at Western and Prudent diets.
Results: None of these dietary patterns was associated with the primary outcome of recurrent wheeze in children in either the crude or the multivariable model (multivariable model, odds ratio per 1-point increase in Mediterranean diet, 0.98 [95% CI, 0.89-1.08]; AHEI-P, 1.07 [0.87-1.30]; Prudent, 1.02 [0.83-1.26]; Western, 0.98 [0.81-1.19]).
Conclusion: Overall dietary pattern during pregnancy is not associated with recurrent wheeze in this cohort. Maternal intake of individual nutrients may be more important determinants of offspring wheeze-associated illness than is dietary pattern. (J Allergy Clin Immunol 2010;126:250-5.)
C1 [Lange, Nancy E.; Camargo, Carlos A., Jr.; Gold, Diane R.; Litonjua, Augusto A.] Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA.
[Lange, Nancy E.; Gold, Diane R.; Litonjua, Augusto A.] Brigham & Womens Hosp, Div Pulm & Crit Care Med, Boston, MA 02115 USA.
[Lange, Nancy E.; Gold, Diane R.; Litonjua, Augusto A.] Harvard Univ, Sch Med, Dept Populat Med, Boston, MA USA.
[Rifas-Shiman, Sheryl L.; Gillman, Matthew W.] Harvard Pilgrim Hlth Care Inst, Boston, MA USA.
[Camargo, Carlos A., Jr.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Gillman, Matthew W.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
RP Lange, NE (reprint author), Brigham & Womens Hosp, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.
EM nlange@partners.org
OI Litonjua, Augusto/0000-0003-0422-5875
FU NIH [HL61907, HL64925, HD34568, AI35786, HL68041, HL007427];
AstraZeneca; Dey; GlaxoSmithKline; Merck
FX Supported by NIH HL61907, HL64925, HD34568, AI35786, HL68041, and
HL007427.; C. A. Camargo Jr is a consultant and speaker for AstraZeneca;
is on the advisory board for Dey; is a consultant, is a speaker, and is
on the advisory board for GlaxoSmithKline; is a speaker of Merck; is a
consultant and is on the advisory board for Novartis; and has received
research support from the National Institutes of Health, AstraZeneca,
Dey, GlaxoSmithKline, and Merck. D. R. Gold has received research
support from the National Institutes of Health. The rest of the authors
have declared that they have no conflict of interest.
NR 54
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U1 2
U2 10
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD AUG
PY 2010
VL 126
IS 2
BP 250
EP U13
DI 10.1016/j.jaci.2010.05.009
PG 10
WC Allergy; Immunology
SC Allergy; Immunology
GA 642IL
UT WOS:000281203800008
PM 20584543
ER
PT J
AU Rudders, SA
Banerji, A
Vassallo, MF
Clark, S
Camargo, CA
AF Rudders, Susan A.
Banerji, Aleena
Vassallo, Milo F.
Clark, Sunday
Camargo, Carlos A., Jr.
TI Trends in pediatric emergency department visits for food-induced
anaphylaxis
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Letter
ID ALLERGY; PREVALENCE
C1 [Rudders, Susan A.] Childrens Hosp, Div Allergy & Immunol, Boston, MA 02115 USA.
[Rudders, Susan A.; Vassallo, Milo F.; Camargo, Carlos A., Jr.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Banerji, Aleena; Vassallo, Milo F.; Camargo, Carlos A., Jr.] Massachusetts Gen Hosp, Dept Med, Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA.
[Clark, Sunday] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
RP Rudders, SA (reprint author), Childrens Hosp, Div Allergy & Immunol, 300 Longwood Ave, Boston, MA 02115 USA.
EM ccamargo@partners.org
FU NIAID NIH HHS [T32-AI-007512]
NR 9
TC 48
Z9 50
U1 0
U2 7
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD AUG
PY 2010
VL 126
IS 2
BP 385
EP 388
DI 10.1016/j.jaci.2010.05.018
PG 5
WC Allergy; Immunology
SC Allergy; Immunology
GA 642IL
UT WOS:000281203800026
PM 20621344
ER
PT J
AU Kunisawa, T
Nagashima, M
Suzuki, A
Takahata, O
Iwasaki, H
AF Kunisawa, Takayuki
Nagashima, Michio
Suzuki, Akihiro
Takahata, Osamu
Iwasaki, Hiroshi
TI The range of values of "variable alpha" when predicting plasma
concentrations and/or effect site concentrations of remifentanil is huge
SO JOURNAL OF ANESTHESIA
LA English
DT Letter
C1 [Kunisawa, Takayuki; Suzuki, Akihiro; Takahata, Osamu; Iwasaki, Hiroshi] Asahikawa Med Coll, Dept Anesthesiol & Crit Care Med, Asahikawa, Hokkaido 0788510, Japan.
[Kunisawa, Takayuki] Asahikawa Med Coll Hosp, Surg Operat Dept, Asahikawa, Hokkaido, Japan.
[Nagashima, Michio] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
[Nagashima, Michio] Harvard Univ, Sch Med, Boston, MA USA.
RP Kunisawa, T (reprint author), Asahikawa Med Coll, Dept Anesthesiol & Crit Care Med, 2-1-1-1 Midorigaoka Higashi, Asahikawa, Hokkaido 0788510, Japan.
EM taka.kunisawa@nifty.ne.jp
OI Nagashima, Michio/0000-0001-7416-5367
NR 3
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER TOKYO
PI TOKYO
PA 1-11-11 KUDAN-KITA, CHIYODA-KU, TOKYO, 102-0073, JAPAN
SN 0913-8668
J9 J ANESTH
JI J. Anesth.
PD AUG
PY 2010
VL 24
IS 4
BP 656
EP 657
DI 10.1007/s00540-010-0961-y
PG 2
WC Anesthesiology
SC Anesthesiology
GA 635IG
UT WOS:000280648200031
PM 20505958
ER
PT J
AU Crompton, JA
North, DS
Yoon, M
Steenbergen, JN
Lamp, KC
Forrest, GN
AF Crompton, Jason A.
North, Donald S.
Yoon, MinJung
Steenbergen, Judith N.
Lamp, Kenneth C.
Forrest, Graeme N.
TI Outcomes with daptomycin in the treatment of Staphylococcus aureus
infections with a range of vancomycin MICs
SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY
LA English
DT Article
DE lipopeptides; S; aureus; CORE
ID MINIMUM INHIBITORY CONCENTRATION; BACTERICIDAL ACTIVITY; PROSPECTIVE
MULTICENTER; CLINICAL-OUTCOMES; RISK-FACTORS; BACTEREMIA;
SUSCEPTIBILITY; ENDOCARDITIS; RESISTANCE; EFFICACY
AB Recent recommendations by the Infectious Diseases Society of America for the treatment of Staphylococcus aureus suggest the use of alternative agents when vancomycin MIC values are >= 2 mg/L. This study examines the outcome of patients treated with daptomycin for S. aureus infections with documented vancomycin MICs.
All patients with skin, bacteraemia and endocarditis infections due to S. aureus with vancomycin MIC values in CORE 2005-08, a retrospective, multicentre, observational registry, were studied. The outcome (cure, improved, failure or non-evaluable) was the investigator assessment at the end of daptomycin therapy. Success was defined as cure or improved.
Five hundred and forty-seven clinically evaluable patients were identified with discrete vancomycin MIC values [MIC < 2 mg/L: 451 (82%); MIC >= 2 mg/L: 96 (18%)]. The vancomycin MIC groups were well matched for patient characteristics, types of infections, first-line daptomycin use (19%) and prior vancomycin use (58%). Clinical success was reported in 94% of patients. No differences were detected in the daptomycin success rate by the vancomycin MIC group overall or by the infection type. A multivariate logistic regression also failed to identify vancomycin MIC as a predictor of daptomycin failure. Adverse event (AE) rates were not different when analysed by MIC group; both groups had similar to 17% of patients with one AE.
In this diverse population, daptomycin was associated with similar outcomes for patients, regardless of whether the vancomycin MIC was categorized as < 2 or >= 2 mg/L. Further studies are warranted.
C1 [Crompton, Jason A.; North, Donald S.; Yoon, MinJung; Steenbergen, Judith N.; Lamp, Kenneth C.] Cubist Pharmaceut, Lexington, MA 02421 USA.
[Forrest, Graeme N.] Portland VA Med Ctr, Portland, OR 97239 USA.
RP Lamp, KC (reprint author), Cubist Pharmaceut, 65 Hayden Ave, Lexington, MA 02421 USA.
EM kenneth.lamp@cubist.com
FU Cubist Pharmaceuticals, Inc.
FX This work was supported by Cubist Pharmaceuticals, Inc. The decision to
submit this analysis for publication was made by Cubist Pharmaceuticals
and the authors. No financial support or honorarium was given to the
non-Cubist Pharmaceuticals author for the development of this
manuscript. The Cubist Pharmaceuticals authors were not awarded any
additional support outside of their salary for their participation in
this study.
NR 33
TC 16
Z9 18
U1 1
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-7453
J9 J ANTIMICROB CHEMOTH
JI J. Antimicrob. Chemother.
PD AUG
PY 2010
VL 65
IS 8
BP 1784
EP 1791
DI 10.1093/jac/dkq200
PG 8
WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy
GA 627DD
UT WOS:000280018400037
PM 20554570
ER
PT J
AU Neal-Barnett, A
Flessner, C
Franklin, ME
Woods, DW
Keuthen, NJ
Stein, DJ
AF Neal-Barnett, Angela
Flessner, Christopher
Franklin, Martin E.
Woods, Douglas W.
Keuthen, Nancy J.
Stein, Dan J.
TI Ethnic differences in trichotillomania: Phenomenology, interference,
impairment, and treatment efficacy
SO JOURNAL OF ANXIETY DISORDERS
LA English
DT Article
DE Minorities; Trichotillomania; Internet study
ID AFRICAN-AMERICAN WOMEN; MGH HAIRPULLING SCALE; ANXIETY STRESS SCALES;
PSYCHOMETRIC PROPERTIES; ISSUES; COMMUNITY; DISORDER; THERAPY; SAMPLES;
IMPACT
AB In this Internet study, we explore differences among minority and Caucasian participants in the phenomenology of, interference and impairment related to, and perceived efficacy of treatments for trichotillomania (TTM) symptoms. A demographic difference was found for number of children only. Results indicate that the minority sample was less likely to report pulling from their eyebrows and eyelashes than the Caucasian sample. Minorities were less likely to report increased tension before a pulling episode. Minorities reported high levels of TTM interference with home management but Caucasians reported higher TTM interference with their academic life. Caucasians with TTM reported higher daily stress than their minority counterparts. Although minorities were less likely to utilize treatment, no significant differences were found for treatment improvement. This Internet study sheds important light on differences in TIN symptoms among minorities and Caucasians. The lack of economic and education differences between groups is a strength of this research. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Neal-Barnett, Angela] Kent State Univ, Dept Psychol, Kent, OH 44242 USA.
[Flessner, Christopher] Brown Univ, Providence, RI 02912 USA.
[Franklin, Martin E.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Woods, Douglas W.] Univ Wisconsin Milwaukee, Milwaukee, WI USA.
[Keuthen, Nancy J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cambridge, MA 02138 USA.
[Stein, Dan J.] Univ Cape Town, ZA-7700 Rondebosch, South Africa.
RP Neal-Barnett, A (reprint author), Kent State Univ, Dept Psychol, Kent, OH 44242 USA.
EM aneal@kent.edu
RI Citations, TLC SAB/C-4006-2011; Flessner, Christopher/K-1483-2015;
Stein, Dan/A-1752-2008
OI Stein, Dan/0000-0001-7218-7810
NR 36
TC 5
Z9 5
U1 2
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0887-6185
J9 J ANXIETY DISORD
JI J. Anxiety Disord.
PD AUG
PY 2010
VL 24
IS 6
BP 553
EP 558
DI 10.1016/j.janxdis.2010.03.014
PG 6
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 607CU
UT WOS:000278476900002
PM 20413254
ER
PT J
AU Chen, NC
Gill, TJ
Martin, SD
AF Chen, Neal C.
Gill, Thomas J.
Martin, Scott D.
TI Quantitative Anatomy of Medial Femoral Perforators of the Distal Thigh
SO JOURNAL OF ARTHROPLASTY
LA English
DT Article
DE knee anatomy; vastus medialis; total knee arthroplasty; mini-incision;
perforator
ID TOTAL KNEE ARTHROPLASTY; SUBVASTUS APPROACH; MIDVASTUS APPROACH; MUSCLE
AB The purpose of the study was to quantitatively examine the anatomical organization of medial femoral perforators. Mini-incision approaches to total knee arthroplasty are being used more often; however, no studies have examined the quantitative anatomy of perforating vessels into the distal intermuscular septum. Fourteen embalmed cadaveric knees were dissected to identify where vascular perforators pierced the medial intermuscular septum. Quantitative measurements were made from the perforators to the medial epicondyle of the femur. The mean measurements from the medial epicondyle to each of the vascular perforators were 7.1, 10.5, and 13.5 cm. The closest perforator to the medial epicondyle was found at a distance of 5.5 cm. During mini-incision approaches to the knee, vascular perforators are at potential risk of injury when dissection proceeds 5 cm proximal to the medial epicondyle.
C1 [Chen, Neal C.] Univ Michigan, Dept Orthopaed Surg, Ann Arbor, MI 48106 USA.
[Gill, Thomas J.] Massachusetts Gen Hosp, Dept Orthopaed, Boston, MA 02114 USA.
[Martin, Scott D.] Brigham & Womens Hosp, Dept Orthoped, Boston, MA 02115 USA.
RP Chen, NC (reprint author), Univ Michigan, Dept Orthopaed Surg, 24 Frank Lloyd Wright Dr, Ann Arbor, MI 48106 USA.
NR 13
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 AUG
PY 2010
VL 25
IS 5
BP 803
EP 806
DI 10.1016/j.arth.2009.05.031
PG 4
WC Orthopedics
SC Orthopedics
GA 639ZE
UT WOS:000281015200021
PM 19628367
ER
PT J
AU Menconi, F
Huber, A
Osman, R
Concepcion, E
Jacobson, EM
Stefan, M
David, CS
Tomer, Y
AF Menconi, Francesca
Huber, Amanda
Osman, Roman
Concepcion, Erlinda
Jacobson, Eric M.
Stefan, Mihaela
David, Chela S.
Tomer, Yaron
TI Tg.2098 is a major human thyroglobulin T-cell epitope
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Thyroglobulin; HLA; Gene; Thyroiditis
ID AUTOIMMUNE THYROID-DISEASE; MHC CLASS-II; UNIQUE TETRANUCLEOTIDE
SEQUENCES; MOLECULAR-DYNAMICS SIMULATIONS; GENETIC SUSCEPTIBILITY;
HASHIMOTO THYROIDITIS; DNA OLIGONUCLEOTIDES; RHEUMATOID-ARTHRITIS;
GRAVES-DISEASE; RAS-RAF
AB An HLA-DR variant containing Arginine at position 74 of the DR beta 1 chain confers a strong genetic susceptibility to autoimmune thyroid diseases (AITD), Graves' disease (GD) and Hashimoto's thyroiditis (HT), while Glutamine at position DR beta 1-74 is protective. We hypothesized that the DR beta 1-Arg74 variant is able to present pathogenic thyroglobulin (Tg) peptides to T-cells more efficiently, thereby triggering thyroid autoimmunity. Indeed, we have previously identified 4 human Tg (hTg) peptides that bind specifically to DR beta 1-Arg74 with much weaker binding to the protective variant DR beta 1-Gln74. The aim of our study was to examine in vivo whether an hTg peptide that binds strongly and specifically to DR beta 1-Arg74 is capable of stimulating T-cells during the induction of thyroiditis in a "humanized" mouse expressing human DR3, and in patients positive for Tg antibodies. Sequencing of exon 2 of the DR transgene in the DR3 mice, null for endogenous MHC II molecules, confirmed that they expressed the disease-associated DR beta 1-Arg74 variant, thus making them an ideal in vivo model to test the presentation of hTg peptides by DR beta 1-Arg74 HLA-DR. Induction of EAT in the DR3 mice lead to T-cell stimulation and proliferation to Tg.2098, a strong and specific DR beta 1-Arg74 binder, while a non-binding control peptide. Tg.2766 did not induce this response. Moreover, Tg.2098 stimulated T-cells from 4 individuals who were positive for thyroglobulin antibodies, demonstrating that Tg.2098 is an immunogenic peptide capable of being presented in vivo and activating T-cells in EAT and AITD. Energetic analysis of the complex formed by Tg.2098 and DR beta-Arg74 has shown that the origin of the affinity was determined by residues 1, 7 and 9 in the peptide, while the selectivity of the peptide for the MHC was determined by the Asp in position 4. The disease-protective substitution R74Q leads to reduction in affinity due to changes in local interaction with D4 as well as non-local interaction with other residues. The electrostatic potential on the surface of the DR beta-Arg74 Tg.2098 complex has a unique signature which may be recognized by T-cell receptors leading to autoimmune thyroiditis. Taken together these findings suggest that Tg.2098, a strong and specific binder to the disease-associated HLA-DR beta-Arg74, is a major human T-cell epitope and participant in the pathoetiology of AITD. Published by Elsevier Ltd.
C1 [Menconi, Francesca; Huber, Amanda; Concepcion, Erlinda; Stefan, Mihaela; Tomer, Yaron] Mt Sinai Med Ctr, Dept Med, Div Endocrinol, New York, NY 10029 USA.
[Osman, Roman] Mt Sinai Sch Med, Dept Struct & Chem Biol, New York, NY USA.
[Jacobson, Eric M.] Univ Cincinnati, Dept Canc & Cell Biol, Cincinnati, OH USA.
[David, Chela S.] Mayo Clin, Coll Med, Dept Immunol, Rochester, MN USA.
[Tomer, Yaron] James J Peters VA Med Ctr, Bronx, NY USA.
RP Tomer, Y (reprint author), Mt Sinai Med Ctr, Dept Med, Div Endocrinol, Box 1118,1 Gustave L Levy Pl, New York, NY 10029 USA.
EM Yaron.Tomer@mssm.edu
FU NIDDK [DK61659, DK067555, DK073681]; American Thyroid Association
FX This work was supported in part by grants DK61659, DK067555, & DK073681
from NIDDK (to YT), and by a grant from the American Thyroid Association
(to EMJ).
NR 37
TC 10
Z9 11
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
J9 J AUTOIMMUN
JI J. Autoimmun.
PD AUG
PY 2010
VL 35
IS 1
BP 45
EP 51
DI 10.1016/j.jaut.2010.01.004
PG 7
WC Immunology
SC Immunology
GA 616HV
UT WOS:000279200700006
PM 20303712
ER
PT J
AU Elo, LL
Mykkanen, J
Nikula, T
Jarvenpaa, H
Simell, S
Aittokallio, T
Hyoty, H
Ilonen, J
Veijola, R
Simell, T
Knip, M
Simell, O
Lahesmaa, R
AF Elo, Laura L.
Mykkanen, Juha
Nikula, Tuomas
Jarvenpaa, Henna
Simell, Satu
Aittokallio, Tero
Hyoty, Heikki
Ilonen, Jorma
Veijola, Riitta
Simell, Tuula
Knip, Mikael
Simell, Olli
Lahesmaa, Riitta
TI Early suppression of immune response pathways characterizes children
with prediabetes in genome-wide gene expression profiling
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Type 1 diabetes; Prediabetes; Autoantibodies; Longitudinal data;
Differential gene expression; Molecular networks; Pathway analysis
ID LYMPHOID TYROSINE PHOSPHATASE; COMPLEX CLASS-I; DEPENDENT
DIABETES-MELLITUS; T-CELL ANERGY; PERIPHERAL-BLOOD; HUMAN THYMUS;
B-CELLS; TYPE-1; ANTIGEN; VARIANT
AB Type 1 diabetes (T1D) is caused by autoimmune destruction of insulin-producing pancreatic p cells in the islets of Langerhans. Although defects in various T cell subsets have been linked to the disease pathogenesis, mechanisms initiating or enhancing the autoimmunity in prediabetes remain poorly understood. To unravel genes and molecular pathways affected by the diabetes-associated autoimmunity, we investigated transcriptomic profiles of prospective whole-blood samples from children who have developed T1D-associated autoantibodies and eventually clinical T1D. Gene-level investigation of the data showed systematic differential expression of 520 probesets. A network-based analysis revealed then a highly significant down-regulated network of genes involved in antigen presentation as well as T-cell receptor and insulin signaling. Finally, detection of dynamic changes in the affected pathways at the early or late phases of autoimmunity showed down-regulation of several novel T1D-associated pathways as well as known key components of immune response. The longitudinal genome-wide data generated in the present study allows the detection of dynamic changes relevant to the disease that may be completely missed in conventional cross-sectional studies or in genome-wide association studies. Taken together, our analysis showed systemic high-level repression of immune response pathways associated with T1D autoimmunity. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Elo, Laura L.; Mykkanen, Juha; Nikula, Tuomas; Jarvenpaa, Henna; Aittokallio, Tero; Lahesmaa, Riitta] Univ Turku, Turku Ctr Biotechnol, FI-20521 Turku, Finland.
[Elo, Laura L.; Mykkanen, Juha; Nikula, Tuomas; Jarvenpaa, Henna; Aittokallio, Tero; Lahesmaa, Riitta] Abo Akad Univ, FI-20521 Turku, Finland.
[Elo, Laura L.; Aittokallio, Tero] Univ Turku, Dept Math, FI-20014 Turku, Finland.
[Simell, Satu; Simell, Tuula; Simell, Olli] Univ Turku, Dept Pediat, FI-20014 Turku, Finland.
[Ilonen, Jorma] Univ Turku, Immunogenet Lab, FI-20014 Turku, Finland.
[Hyoty, Heikki] Univ Tampere, Dept Virol, FI-33014 Tampere, Finland.
[Hyoty, Heikki] Tampere Univ Hosp, Ctr Lab Med, FI-33520 Tampere, Finland.
[Ilonen, Jorma] Univ Kuopio, Dept Clin Microbiol, FI-70211 Kuopio, Finland.
[Veijola, Riitta] Univ Oulu, Dept Pediat, FI-90014 Oulu, Finland.
[Knip, Mikael] Univ Helsinki, Hosp Children & Adolescents, FI-00014 Helsinki, Finland.
[Knip, Mikael] Univ Helsinki, Folkhalsan Res Ctr, FI-00014 Helsinki, Finland.
[Knip, Mikael] Tampere Univ Hosp, Dept Pediat, FI-33521 Tampere, Finland.
[Lahesmaa, Riitta] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
RP Lahesmaa, R (reprint author), Univ Turku, Turku Ctr Biotechnol, FI-20521 Turku, Finland.
EM laura.elo@utu.fi; juha.mykkanen@utu.fi; toumas.nikula@perkinelmer.fi;
henna.jarvenpaa@btk.fi; satu.simell@tyks.fi; tero.aittokallio@utu.fi;
heikki.hyoty@uta.fi; jorma.ilonen@utu.fi; riitta.veijola@oulu.fi;
tuula.simell@utu.fi; mikael.knip@helsinki.fi; olli.simell@utu.fi;
riitta.lahesmaa@btk.fi
RI Aittokallio, Tero/B-6583-2009; Mykkanen, Juha/Q-1663-2015;
OI Aittokallio, Tero/0000-0002-0886-9769; Mykkanen,
Juha/0000-0001-9898-2660; Elo, Laura/0000-0001-5648-4532
FU Juvenile Diabetes Research Foundation (JDRF); Academy of Finland; Turku
University; Finnish Funding Agency for Technology and Innovation
(Tekes); Sigrid Juselius Foundation; DIPP
FX We thank all the staff of the DIPP team for their expert help and
contribution. DIPP families are thanked for their support. We are
grateful for Katja Waenerberg and the Finnish DNA Microarray Centre at
Turku Centre for Biotechnology for excellent technical assistance. This
study was financially supported by the Juvenile Diabetes Research
Foundation (JDRF), the Academy of Finland, the Turku University Hospital
Research Fund, the Finnish Funding Agency for Technology and Innovation
(Tekes), and the Sigrid Juselius Foundation.
NR 56
TC 20
Z9 20
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
J9 J AUTOIMMUN
JI J. Autoimmun.
PD AUG
PY 2010
VL 35
IS 1
BP 70
EP 76
DI 10.1016/j.jaut.2010.03.001
PG 7
WC Immunology
SC Immunology
GA 616HV
UT WOS:000279200700009
PM 20356713
ER
PT J
AU Hoover, SE
Xu, WH
Xiao, WZ
Burkholder, WF
AF Hoover, Sharon E.
Xu, Weihong
Xiao, Wenzhong
Burkholder, William F.
TI Changes in DnaA-Dependent Gene Expression Contribute to the
Transcriptional and Developmental Response of Bacillus subtilis to
Manganese Limitation in Luria-Bertani Medium
SO JOURNAL OF BACTERIOLOGY
LA English
DT Article
ID REPLICATION INITIATION; PEROXIDE STRESS; DEINOCOCCUS-RADIODURANS;
HYDROGEN-PEROXIDE; SPORE FORMATION; PROTEIN DNAA; METAL-IONS;
CELL-CYCLE; SPORULATION; BACTERIA
AB The SOS response to DNA damage in bacteria is a well-known component of the complex transcriptional responses to genotoxic environmental stresses such as exposure to reactive oxygen species, alkylating agents, and many of the antibiotics targeting DNA replication. However, bacteria such as Bacillus subtilis also respond to conditions that perturb DNA replication via a transcriptional response mediated by the replication initiation protein DnaA. In addition to regulating the initiation of DNA replication, DnaA directly regulates the transcription of specific genes. Conditions that perturb DNA replication can trigger the accumulation of active DnaA, activating or repressing the transcription of genes in the DnaA regulon. We report here that simply growing B. subtilis in LB medium altered DnaA-dependent gene expression in a manner consistent with the accumulation of active DnaA and that this was part of a general transcriptional response to manganese limitation. The SOS response to DNA damage was not induced under these conditions. One of the genes positively regulated by DnaA in Bacillus subtilis encodes a protein that inhibits the initiation of sporulation, Sda. Sda expression was induced as cells entered stationary phase in LB medium but not in LB medium supplemented with manganese, and the induction of Sda inhibited sporulation-specific gene expression and the onset of spore morphogenesis. In the absence of Sda, manganese-limited cells initiated spore development but failed to form mature spores. These data highlight that DnaA-dependent gene expression may influence the response of bacteria to a range of environmental conditions, including conditions that are not obviously associated with genotoxic stress.
C1 [Hoover, Sharon E.; Burkholder, William F.] Stanford Univ, Dept Biol, Stanford, CA 94305 USA.
[Xu, Weihong; Xiao, Wenzhong] Stanford Univ, Stanford Genome Technol Ctr, Palo Alto, CA 94304 USA.
[Xiao, Wenzhong] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Burkholder, WF (reprint author), Stanford Univ, Dept Biol, 371 Serra Mall, Stanford, CA 94305 USA.
EM burkholder@stanford.edu
OI xiao, wenzhong/0000-0003-4944-6380
FU NIH [5T32GM007276]; National Science Foundation [ID 0744872]
FX S. E. H. was supported by an NIH predoctoral training grant
(5T32GM007276). This work was supported by National Science Foundation
award ID 0744872.
NR 61
TC 16
Z9 16
U1 1
U2 7
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 AUG
PY 2010
VL 192
IS 15
BP 3915
EP 3924
DI 10.1128/JB.00210-10
PG 10
WC Microbiology
SC Microbiology
GA 623XZ
UT WOS:000279782000008
PM 20511500
ER
PT J
AU Bensing, BA
Sullam, PM
AF Bensing, Barbara A.
Sullam, Paul M.
TI Transport of Preproteins by the Accessory Sec System Requires a Specific
Domain Adjacent to the Signal Peptide
SO JOURNAL OF BACTERIOLOGY
LA English
DT Article
ID STREPTOCOCCUS-GORDONII DL1; BINDING PROTEIN-GSPB; SECONDARY STRUCTURE
PREDICTION; SURFACE GLYCOPROTEINS GSPB; SERINE-RICH ADHESIN;
SIALIC-ACID; ESCHERICHIA-COLI; STAPHYLOCOCCUS-AUREUS; TRANSLOCATION
CHANNEL; SEQUENCE RECOGNITION
AB The accessory Sec (SecA2/Y2) systems of streptococci and staphylococci are dedicated to the transport of large serine-rich repeat (SRR) glycoproteins to the bacterial cell surface. The means by which the glycosylated preproteins are selectively recognized by the accessory Sec system have not been fully characterized. In Streptococcus gordonii, the SRR glycoprotein GspB has a 90-residue amino-terminal signal sequence that is essential for transport by SecA2/Y2 but is not sufficient to mediate the transport of heterologous proteins by this specialized transporter. We now report that a preprotein must remain at least partially unfolded prior to transport by the accessory Sec system. In addition, a region of approximately 20 residues from the amino-terminal end of mature GspB (the accessory Sec transport or AST domain) is essential for SecA2/Y2-dependent transport. The replacement of several AST domain residues with glycine strongly interferes with export, which suggests that a helical conformation may be important. Analysis of GspB variants with alterations in the AST domain, in combination with the results with a SecY2 variant, indicates that the AST domain is essential both for targeting to the SecA2/Y2 translocase and for initiating translocation through the SecY2 channel. The combined results suggest a unique mechanism that ensures the transport of a single substrate by the SecA2/Y2 system.
C1 San Francisco VA Med Ctr, San Francisco, CA USA.
Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Sullam, PM (reprint author), Vet Affairs Med Ctr, Div Infect Dis, 111W,4150 Clement St, San Francisco, CA 94121 USA.
EM paul.sullam@ucsf.edu
FU Department of Veterans Affairs; National Institutes of Health
[RO1AI41513, RO1AI057433]
FX This work was supported by the Department of Veterans Affairs and the VA
Merit Review program and by grants RO1AI41513 and RO1AI057433 from the
National Institutes of Health.
NR 54
TC 16
Z9 16
U1 0
U2 4
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 AUG
PY 2010
VL 192
IS 16
BP 4223
EP 4232
DI 10.1128/JB.00373-10
PG 10
WC Microbiology
SC Microbiology
GA 632FL
UT WOS:000280406300016
PM 20562303
ER
PT J
AU Sevick, MA
Stone, RA
Zickmund, S
Wang, YY
Korytkowski, M
Burke, LE
AF Sevick, Mary Ann
Stone, Roslyn A.
Zickmund, Susan
Wang, Yuanyuan
Korytkowski, Mary
Burke, Lora E.
TI Factors associated with probability of personal digital assistant-based
dietary self-monitoring in those with type 2 diabetes
SO JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Handheld computer; Randomized clinical trial; Behavioral research;
Compliance
ID WEIGHT-LOSS PROGRAM; BEHAVIOR-CHANGE; PAPER DIARIES; HEALTH;
INTERVENTION; DIVIDE; TECHNOLOGY; COMPUTERS; ADHERENCE; INTERNET
AB Knowledge of factors associated with the use of technology could inform the design of technology-based behavioral interventions. This study examined modifiable and nonmodifiable factors associated with technology-based self-monitoring. 123 participants with type 2 diabetes self-monitored diet using a personal digital assistant in a 6-month behavioral intervention. Multinomial logistic regression was used to examine probability of nonadherent and suboptimally adherent behavior relative to adherent behavior. Sociodemographic characteristics were not associated with probability of self-monitoring. Probability of adherence generally was greater in the weeks preceding no group session, and lower in the weeks following no group session or following skipped sessions. Non-modifiable factors suggested by the literature to be associated with poorer access to technology (lower income, older age, minority race, and lower education) were not associated with probability of self-monitoring in this population.
C1 [Sevick, Mary Ann; Zickmund, Susan; Korytkowski, Mary] Univ Pittsburgh, Sch Med, Pittsburgh, PA 15260 USA.
[Sevick, Mary Ann; Stone, Roslyn A.; Zickmund, Susan] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Sevick, Mary Ann] VA Pittsburgh Healthcare Syst, Ctr Geriatr Res Educ & Clin, Pittsburgh, PA USA.
[Sevick, Mary Ann; Stone, Roslyn A.; Wang, Yuanyuan; Burke, Lora E.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
[Burke, Lora E.] Univ Pittsburgh, Sch Nursing, Pittsburgh, PA 15261 USA.
RP Sevick, MA (reprint author), Univ Pittsburgh, Sch Med, Pittsburgh, PA 15260 USA.
EM sevick@pitt.edu
FU NCRR NIH HHS [M01-RR000056, UL1-RR024153]; NIDDK NIH HHS [DK-046204];
NINR NIH HHS [NR-R01008792]
NR 54
TC 10
Z9 11
U1 1
U2 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0160-7715
J9 J BEHAV MED
JI J. Behav. Med.
PD AUG
PY 2010
VL 33
IS 4
BP 315
EP 325
DI 10.1007/s10865-010-9257-9
PG 11
WC Psychology, Clinical
SC Psychology
GA 628OE
UT WOS:000280129000007
PM 20232131
ER
PT J
AU Aguilar, D
Chan, WY
Bozkurt, B
Ramasubbu, K
Deswal, A
AF Aguilar, David
Chan, Wenyaw
Bozkurt, Biykem
Ramasubbu, Kumudha
Deswal, Anita
TI Metformin Use and Mortality in Ambulatory Patients With Diabetes and
Heart Failure
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 14th Annual Scientific Meeting of the Heart-Failure-Society-of-America
CY SEP 12-15, 2010
CL San Diego, CA
SP Heart Failure Soc Amer
C1 [Aguilar, David; Bozkurt, Biykem; Ramasubbu, Kumudha; Deswal, Anita] Baylor Coll Med, Houston, TX 77030 USA.
[Aguilar, David; Bozkurt, Biykem; Ramasubbu, Kumudha; Deswal, Anita] Michael E Debakey Med Ctr, Houston, TX USA.
[Chan, Wenyaw] Univ Texas Hlth Sci Ctr, Sch Publ Hlth, Houston, TX USA.
NR 0
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 1071-9164
J9 J CARD FAIL
JI J. Card. Fail.
PD AUG
PY 2010
VL 16
IS 8
SU 1
MA 272
BP S83
EP S84
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645YJ
UT WOS:000281501800272
ER
PT J
AU Aleong, R
Sauer, WH
Pellegnni, CN
Yang, YF
Keung, E
Heidenreich, P
Rumsfeld, JS
Massie, BM
Varosy, PD
AF Aleong, Ryan
Sauer, William H.
Pellegnni, Cara N.
Yang, Yanfei
Keung, Edmund
Heidenreich, Paul
Rumsfeld, John S.
Massie, Barry M.
Varosy, Paul D.
TI Clinical Subtype of Atrial Fibrillation at the Time of Implantation and
Subsequent Mortality among Veterans With Implantable Defibrillators
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 14th Annual Scientific Meeting of the Heart-Failure-Society-of-America
CY SEP 12-15, 2010
CL San Diego, CA
SP Heart Failure Soc Amer
C1 [Aleong, Ryan; Sauer, William H.; Rumsfeld, John S.; Varosy, Paul D.] Univ Colorado Denver, Aurora, CO USA.
[Pellegnni, Cara N.; Yang, Yanfei; Keung, Edmund; Massie, Barry M.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Pellegnni, Cara N.; Yang, Yanfei; Keung, Edmund; Massie, Barry M.] UCSF, San Francisco, CA USA.
[Heidenreich, Paul] Palo Alto VAMC, Palo Alto, CA USA.
[Heidenreich, Paul] Stanford Univ, Palo Alto, CA 94304 USA.
[Rumsfeld, John S.; Varosy, Paul D.] VA Eastern Colorado Hlth Care Syst, Denver, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 1071-9164
J9 J CARD FAIL
JI J. Card. Fail.
PD AUG
PY 2010
VL 16
IS 8
SU 1
MA 185
BP S58
EP S58
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645YJ
UT WOS:000281501800186
ER
PT J
AU Deswal, A
Richardson, P
Bozkurt, B
Mann, DL
AF Deswal, Anita
Richardson, Peter
Bozkurt, Biykem
Mann, Douglas L.
TI Randomized Trial of Aldosterone AntagonisM in Diastolic Heart Failure
(RAAM-DHF)
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 14th Annual Scientific Meeting of the Heart-Failure-Society-of-America
CY SEP 12-15, 2010
CL San Diego, CA
SP Heart Failure Soc Amer
C1 [Deswal, Anita; Richardson, Peter; Bozkurt, Biykem] VA Med Ctr, Houston, TX USA.
[Deswal, Anita; Richardson, Peter; Bozkurt, Biykem] Baylor Coll Med, Houston, TX 77030 USA.
[Mann, Douglas L.] Washington Univ, Sch Med, St Louis, MO USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 1071-9164
J9 J CARD FAIL
JI J. Card. Fail.
PD AUG
PY 2010
VL 16
IS 8
SU 1
MA 017
BP S7
EP S7
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645YJ
UT WOS:000281501800018
ER
PT J
AU Lewis, GD
Murphy, RM
Shah, R
Pappagianopoulos, PP
Malhotra, R
Bloch, KD
Systrom, DM
Semigran, MJ
AF Lewis, Gregory D.
Murphy, Ryan M.
Shah, Ravi
Pappagianopoulos, Paul P.
Malhotra, Rajeev
Bloch, Kenneth D.
Systrom, David M.
Semigran, Marc J.
TI Right Ventricular and Pulmonary Vascular Response Patterns To Exercise
Predict Exercise Capacity and Outcomes in Heart Failure
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 14th Annual Scientific Meeting of the Heart-Failure-Society-of-America
CY SEP 12-15, 2010
CL San Diego, CA
SP Heart Failure Soc Amer
C1 [Lewis, Gregory D.; Murphy, Ryan M.; Shah, Ravi; Pappagianopoulos, Paul P.; Malhotra, Rajeev; Bloch, Kenneth D.; Systrom, David M.; Semigran, Marc J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
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 AUG
PY 2010
VL 16
IS 8
SU 1
MA 007
BP S3
EP S3
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645YJ
UT WOS:000281501800008
ER
PT J
AU Mather, P
Alexis, J
Sheppard, R
Thohan, V
Markham, D
Dec, GW
Liu, P
McNamara, D
AF Mather, Paul
Alexis, Jeffrey
Sheppard, Richard
Thohan, Vinay
Markham, David
Dec, G. William
Liu, Peter
McNamara, Dennis
TI Impact of Blood Pressure on Myocardial Recovery and Outcomes in Recent
Onset Cardiomyopathy: Results of IMAC2
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 14th Annual Scientific Meeting of the Heart-Failure-Society-of-America
CY SEP 12-15, 2010
CL San Diego, CA
SP Heart Failure Soc Amer
C1 [Mather, Paul] Thomas Jefferson Univ, Jefferson Med Coll, Philadelphia, PA 19107 USA.
[Alexis, Jeffrey] Univ Rochester, Rochester, NY USA.
[Sheppard, Richard] McGill SMBD Jewish Gen, Montreal, PQ, Canada.
[Thohan, Vinay] Wake Forest Univ, Baptist Med Ctr, Winston Salem, NC 27109 USA.
[Markham, David] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Dec, G. William] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Liu, Peter] Univ Toronto, Toronto, ON, Canada.
Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
NR 0
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 1071-9164
J9 J CARD FAIL
JI J. Card. Fail.
PD AUG
PY 2010
VL 16
IS 8
SU 1
MA 314
BP S95
EP S95
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645YJ
UT WOS:000281501800313
ER
PT J
AU Moslehi, J
Minamishima, YA
Padera, R
Liao, R
Kaelin, WG
AF Moslehi, Javid
Minamishima, Yoji Andy
Padera, Robert
Liao, Ronglih
Kaelin, William G.
TI Loss of PHD Prolyl Hydroxylase Activity in Cardiomyocytes Phenocopies
Ischemic Cardiomyopathy
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 14th Annual Scientific Meeting of the Heart-Failure-Society-of-America
CY SEP 12-15, 2010
CL San Diego, CA
SP Heart Failure Soc Amer
C1 [Moslehi, Javid; Padera, Robert] Brigham & Womens Hosp, Dept Med, Div Cardiovasc Med, Boston, MA 02115 USA.
[Moslehi, Javid; Minamishima, Yoji Andy; Liao, Ronglih; Kaelin, William G.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kaelin, William G.] Howard Hughes Med Inst, Chevy Chase, MD USA.
RI Minamishima, Yoji/E-5380-2010
OI Minamishima, Yoji/0000-0001-7995-9318
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 1071-9164
J9 J CARD FAIL
JI J. Card. Fail.
PD AUG
PY 2010
VL 16
IS 8
SU 1
MA 004
BP S2
EP S2
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645YJ
UT WOS:000281501800005
ER
PT J
AU Subramanian, D
Subramanian, V
Deswal, A
Mann, DL
AF Subramanian, Devika
Subramanian, Venkataraman
Deswal, Anita
Mann, Douglas L.
TI Improved Predictive Models of Mortality in Chronic Heart Failure Using
Time-Series Measurements of Inflammatory Biomarkers
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 14th Annual Scientific Meeting of the Heart-Failure-Society-of-America
CY SEP 12-15, 2010
CL San Diego, CA
SP Heart Failure Soc Amer
C1 Rice Univ, Houston, TX USA.
Univ Nottingham Hosp, Nottingham NG7 2UH, England.
VA Med Ctr, Houston, TX USA.
Baylor Coll Med, Houston, TX 77030 USA.
Washington Univ, Sch Med, St Louis, MO USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 1071-9164
J9 J CARD FAIL
JI J. Card. Fail.
PD AUG
PY 2010
VL 16
IS 8
SU 1
MA 307
BP S93
EP S93
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645YJ
UT WOS:000281501800306
ER
PT J
AU Thomas, MK
Weaver, C
LaCroix, B
Prokunina-Olsson, M
Hall, JL
AF Thomas, Melissa K.
Weaver, Cyprian
LaCroix, Bonnie
Prokunina-Olsson, Mila
Hall, Jennifer L.
TI Defining the Role of the Transcription Factor TCF7L2 in Type 2 Diabetes
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 14th Annual Scientific Meeting of the Heart-Failure-Society-of-America
CY SEP 12-15, 2010
CL San Diego, CA
SP Heart Failure Soc Amer
C1 Mass Gen Hosp, Boston, MA USA.
Univ Minnesota, Lillehei Heart Inst, Minneapolis, MN USA.
NCI, Bethesda, MD 20892 USA.
NR 0
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 1071-9164
J9 J CARD FAIL
JI J. Card. Fail.
PD AUG
PY 2010
VL 16
IS 8
SU 1
MA 113
BP S37
EP S37
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 645YJ
UT WOS:000281501800114
ER
PT J
AU Ehrenfeld, JM
Mulvoy, W
Sandberg, WS
AF Ehrenfeld, Jesse M.
Mulvoy, William
Sandberg, Warren S.
TI Performance Comparison of Right- and Left-Sided Double-Lumen Tubes Among
Infrequent Users
SO JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA
LA English
DT Article
DE lung isolation; equipment safety; anesthesia; intubation; intratracheal;
respiration; artificial; thoracic surgical procedures
ID THORACIC-SURGERY; ENDOTRACHEAL-TUBES
AB Objective: To compare performance of right- versus left-sided double-lumen tubes (DLTs) among infrequent users by evaluating the incidence and severity of hypoxemia, hypercapnia, and high airway pressures.
Design: A retrospective, cohort study.
Setting: A university hospital.
Participants: Ninety-eight patients undergoing left-sided DLT placement (53.9 +/- 21.2 years old) and 98 patients undergoing right-sided DLT placement (62.3 +/- 20.6 years old). Cases performed by thoracic anesthesia specialists were excluded.
Interventions: The authors retrospectively reviewed electronic anesthetic records from a 2-year period to determine the incidence and severity of hypoxia (SpO(2) < 90%), hypercapnia (end-tidal carbon dioxide > 45 mmHg) and high airway pressures (peak inspiratory pressure >35 cmH(2)O) during one-lung ventilation via right and left DLTs.
Measurements and Main Results: Right-sided (n = 98) DLTs were almost exclusively used on the side contralateral to surgery by infrequent users, whereas left-sided (n = 98) DLTs were used for ipsilateral surgery one third of the time. Hypoxia lasted longer in left versus right DLTs, but the frequency of hypoxia was the same for each tube type among infrequent users. Hypercapnia and high airway pressures occurred more frequently with left-sided DLTs.
Conclusions: Left-sided DLTs are perceived to be safer because they may be less prone to malpositioning during lung isolation. However, the supposition that left-sided DLTs are safer than right-sided DLTs when intraoperative hypoxia, hypercapnia, and high airway pressures are used as criteria, even when these tubes are used by infrequent users, is not supported by the data. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Ehrenfeld, Jesse M.; Mulvoy, William; Sandberg, Warren S.] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
RP Ehrenfeld, JM (reprint author), Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, 55 Fruit St,Jackson 460, Boston, MA 02114 USA.
EM jehrenfeld@partners.org
OI Ehrenfeld, Jesse/0000-0003-3427-0140; Sandberg,
Warren/0000-0002-9246-777X
NR 9
TC 2
Z9 2
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 1053-0770
J9 J CARDIOTHOR VASC AN
JI J. Cardiothorac. Vasc. Anesth.
PD AUG
PY 2010
VL 24
IS 4
BP 598
EP 601
DI 10.1053/j.jvca.2009.09.007
PG 4
WC Anesthesiology; Cardiac & Cardiovascular Systems; Respiratory System;
Peripheral Vascular Disease
SC Anesthesiology; Cardiovascular System & Cardiology; Respiratory System
GA 636IS
UT WOS:000280726000010
PM 19942453
ER
PT J
AU Xavier, A
Erlich, J
Lerner, AB
AF Xavier, Andrea
Erlich, Jason
Lerner, Adam B.
TI Coronary Artery Bypass Graft Surgery and Moderate Aortic Stenosis: When
To Leave Well Enough Alone
SO JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA
LA English
DT Article
DE aortic stenosis; coronary artery bypass graft surgery; aortic valve
replacement; transesophageal; echocardiography; combined aortic valve
replacement/coronary artery bypass graft surgery
C1 [Xavier, Andrea; Erlich, Jason; Lerner, Adam B.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA USA.
RP Lerner, AB (reprint author), BIDMC, Dept Anesthesia, 1 Deaconess Rd,CC 470, Boston, MA 02215 USA.
EM alerner@bidmc.harvard.edu
NR 0
TC 0
Z9 0
U1 0
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1053-0770
J9 J CARDIOTHOR VASC AN
JI J. Cardiothorac. Vasc. Anesth.
PD AUG
PY 2010
VL 24
IS 4
BP 712
EP 713
DI 10.1053/j.jvca.2010.05.001
PG 2
WC Anesthesiology; Cardiac & Cardiovascular Systems; Respiratory System;
Peripheral Vascular Disease
SC Anesthesiology; Cardiovascular System & Cardiology; Respiratory System
GA 636IS
UT WOS:000280726000027
PM 20673750
ER
PT J
AU Prystowsky, EN
Camm, J
Lip, GYH
Allessie, M
Bergmann, JF
Breithardt, G
Brugada, J
Crijns, H
Ellinor, PT
Mark, D
Naccarelli, G
Packer, D
Tamargo, J
AF Prystowsky, Eric N.
Camm, John
Lip, Gregory Y. H.
Allessie, Maurits
Bergmann, Jean-Francois
Breithardt, Guenter
Brugada, Josep
Crijns, Harry
Ellinor, Patrick T.
Mark, Daniel
Naccarelli, Gerald
Packer, Douglas
Tamargo, Juan
TI The Impact of New and Emerging Clinical Data on Treatment Strategies for
Atrial Fibrillation
SO JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY
LA English
DT Article
DE atrial fibrillation; stroke; thromboembolism; heart failure; catheter
ablation
ID RADIOFREQUENCY CATHETER ABLATION; RISK STRATIFICATION SCHEMES;
CONGESTIVE-HEART-FAILURE; STROKE PREVENTION; ANTITHROMBOTIC THERAPY;
ANTICOAGULANT-THERAPY; CARDIOVASCULAR EVENTS; COST-EFFECTIVENESS;
CONTROLLED-TRIAL; UNITED-STATES
AB AF Treatment Strategies. Introduction: The Atrial Fibrillation (AF) Exchange Group, an international multidisciplinary group concerned with the management of AF, was convened to review recent advances in the field and the potential impact on treatment strategies.
Methods: Issues discussed included epidemiology and the impact of the rising incidence of AF on health care systems, developments in pharmacological and surgical interventions in the management of arrhythmias and thromboprophylaxis, the potential to affect treatment strategies, and barriers to implementing them.
Results: The incidence of AF and the associated burden on health care systems are increasing with aging populations, prevalence of comorbidities and more effective treatment of cardiovascular diseases. Advances in available medical treatments, in particular dronedarone and dabigatran, with other products in development, offer the possibility of changes in treatment paradigms and a greater emphasis on reducing hospitalizations and improvement in long-term outcomes instead of a symptom/safety-driven approach in which the priority is symptom suppression without provoking drug toxicity. Developments in catheter ablation techniques may mean that, in experienced centers, ablation may be offered as first-line treatment in selected patient populations. Barriers to optimal treatment include underdiagnosis, lack of recognition as a serious condition and as a risk factor for stroke, limited access to care, inadequate implementation of guidelines, and poor adherence to treatment.
Conclusions: The focus of the management of AF may be changing as a consequence of new treatments based on the outcome improvements they offer. However, the benefits will not be fully realized if guidelines and guidance are not observed in routine clinical practice. (J Cardiovasc Electrophysiol, Vol. 21, pp. 946-958, August 2010)
C1 [Prystowsky, Eric N.] Care Grp, Indianapolis, IN 46260 USA.
[Camm, John] St Georges Univ London, London, England.
[Lip, Gregory Y. H.] Univ Birmingham, Ctr Cardiovasc Sci, City Hosp, Birmingham, W Midlands, England.
[Allessie, Maurits] Univ Maastricht, Dept Physiol, Maastricht, Netherlands.
[Bergmann, Jean-Francois] Hop Lariboisiere, Serv Med Interne A, F-75475 Paris, France.
[Bergmann, Jean-Francois; Breithardt, Guenter] Hosp Univ Munster, Dept Cardiol & Angiol, Munster, Germany.
[Brugada, Josep] Univ Barcelona, Hosp Clin, Cardiovasc Inst, Arrhythmia Sect, Barcelona, Spain.
[Crijns, Harry] Univ Hosp Maastricht, Dept Cardiol, Cardiovasc Res Inst Maastricht CARIM, Maastricht, Netherlands.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Mark, Daniel] Duke Univ, Med Ctr, Dept Med Cardiovasc Med, Durham, NC USA.
[Naccarelli, Gerald] Penn State Heart & Vasc Inst, Div Cardiol, Hershey, PA USA.
[Packer, Douglas] Mayo Clin, Rochester, MN USA.
[Tamargo, Juan] Univ Complutense Madrid, Fac Med, Dept Pharmacol, E-28040 Madrid, Spain.
RP Prystowsky, EN (reprint author), Care Grp, 8333 Naab Rd,Suite 400, Indianapolis, IN 46260 USA.
EM eprystow@TheCareGroup.com
RI Tamargo, Juan/J-7772-2016;
OI Tamargo, Juan/0000-0002-7979-7758; Mark, Daniel/0000-0001-6340-8087;
BRUGADA, JOSEP/0000-0002-5662-8302
FU Sanofi-aventis; Daiichi; Pfizer; BMS; Cardiome; Merck; Astellas; Astra
Zeneca; Biotronic; Alexion Pharmaceuticals; Eli Lilly; Proctor Gamble;
Medtronic; Medicure; Innocoll; St. Jude Medical; Glaxo Smith Kline;
Boehringer-Ingelheim; Boston Scientific; Bristol Myers Squibb; Portola;
Otsuka; Gilead; Novartis; Xention; Biocritique; Biosense Webster;
Cryocath; Siemens USA
FX E. Prystowsky reports participation in a new antiarrhythmic drug study
supported by Sanofi-aventis and consultancy for the same; he consults
for Boehringer-Ingelheim; he has received honoraria relevant to this
topic. J. Camm reports participation in multicenter trials supported by
Daiichi, Pfizer, BMS, Cardiome, and Merck; he received compensation for
participation on a speaker's bureau from Sanofi-aventis, Cardiome,
Merck, and Astellas; he serves as a consultant or on the advisory boards
of Merck, Sanofi-aventis, Boehringer-Ingelheim, Daiichi, and Medtronic.
G. Lip reports participation in research studies supported by Astellas,
Astra Zeneca, Biotronic, Cardiome; he serves as a consultant or on the
advisory boards of Bayer, Astellas, Astra Zeneca, Sanofi-aventis,
Biotronic, Cardiome, Boehringer-Ingelheim. M. Allessie reports
compensation on a speakers bureau, but did not name the sponsor. J.-F.
Bergmann reports honoraria from Sanofi-aventis and Glaxo H. Crijns
reports participation on a research grant supported by Sanofi-aventis,
as well as participation on a speakers bureau and serving as a
consultant or on the advisory board of that company. P. Ellinor reports
participation on multiple research grants, including CHS, FHS,
Rotterdam, MONICA/KORA, and PREVENT-IT studies; he serves as a
consultant or on the advisory boards of Sanofi-aventis and
Ortho-MacNeil. D. Mark reports participation on research grants
supported by Alexion Pharmaceuticals, Eli Lilly, Proctor & Gamble,
Pfizer, Medtronic, Medicure, Innocoll, and St. Jude Medical; he serves
as a consultant or on the advisory board of Sanofi-aventis. G.
Naccarelli reports participation on research grants supported by Glaxo
Smith Kline, Boehringer-Ingelheim, Boston Scientific, and
Sanofi-aventis; he has received consultant fees or honoraria from
Sanofi-aventis, St. Jude Medical, Bristol Myers Squibb, Merck, Portola,
Otsuka, Boehringer-Ingelheim, Pfizer, Astra Zeneca, Medtronic, Gilead,
Cardiome, Novartis, Xention, Astellas, Glaxo Smith Kline, and
Biocritique. D. Packer reports participation on research grants
supported by St. Jude Medical, Biosense Webster, Boston Scientific,
Medtronic, Cryocath, and Siemens USA; he serves as a consultant or on
the advisory boards of Medtronic, St. Jude Medical, Siemans,
Sanofi-aventis, Biosense Webster, and Cryocath; he reports a patent on
mapping technology. J. Tamargo reports speakers bureau fees and
honoraria, as well as serving as a consultant or on advisory board, but
does not name the sponsors/companies.
NR 80
TC 17
Z9 18
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1045-3873
J9 J CARDIOVASC ELECTR
JI J. Cardiovasc. Electrophysiol.
PD AUG
PY 2010
VL 21
IS 8
BP 946
EP 958
DI 10.1111/j.1540-8167.2010.01770.x
PG 13
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 635MX
UT WOS:000280660900023
PM 20384658
ER
PT J
AU Benson, EK
Lee, SW
Aaronson, SA
AF Benson, Erica K.
Lee, Sam W.
Aaronson, Stuart A.
TI Role of progerin-induced telomere dysfunction in HGPS premature cellular
senescence
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE Cellular senescence; DNA damage; Nuclear lamins; Telomerase; Telomere
dysfunction; Tumor suppressors
ID HUTCHINSON-GILFORD-PROGERIA; LAMIN-A; NUCLEAR ARCHITECTURE; HUMAN
FIBROBLASTS; INSTABILITY SYNDROMES; GENOMIC INSTABILITY; STEM-CELLS;
HUMAN SKIN; DNA; MUTANT
AB Hutchinson-Gilford Progeria Syndrome (HGPS) is a premature-aging syndrome caused by a dominant mutation in the gene encoding lamin A, which leads to an aberrantly spliced and processed protein termed progerin. Previous studies have shown that progerin induces early senescence associated with increased DNA-damage signaling and that telomerase extends HGPS cellular lifespan. We demonstrate that telomerase extends HGPS cellular lifespan by decreasing progerin-induced DNA-damage signaling and activation of p53 and Rb pathways that otherwise mediate the onset of premature senescence. We show further that progerin-induced DNA-damage signaling is localized to telomeres and is associated with telomere aggregates and chromosomal aberrations. Telomerase amelioration of DNA-damage signaling is relatively rapid, requires both its catalytic and DNA-binding functions, and correlates in time with the acquisition by HGPS cells of the ability to proliferate. All of these findings establish that HGPS premature cellular senescence results from progerin-induced telomere dysfunction.
C1 [Benson, Erica K.; Aaronson, Stuart A.] Mt Sinai Sch Med, Dept Oncol Sci, New York, NY 10012 USA.
[Lee, Sam W.] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA.
[Lee, Sam W.] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
RP Aaronson, SA (reprint author), Mt Sinai Sch Med, Dept Oncol Sci, Box 1130,1 Gustave L Levy Pl, New York, NY 10012 USA.
EM stuart.aaronson@mssm.edu
FU NCI [PO1CA80058, T32 CA078207]; New York State Stem Cell [C024313];
NIGMS [T32 GM008553]; NIH-NCI [5R24 CA095823-04]; NSF [DBI-9724504]; NIH
[1 S10 RR0 9145-01]
FX This work was supported by grant number PO1CA80058 from the NCI and the
New York State Stem Cell contract #C024313. E. B. was supported by the
NCI Training Program in Cancer Biology (T32 CA078207) and the NIGMS
Training Program in Cellular and Molecular Biology (T32 GM008553).
Confocal laser scanning microscopy was performed at the MSSM-Microscopy
Shared Resource Facility, supported with funding from NIH-NCI shared
resources grant (5R24 CA095823-04), NSF Major Research Instrumentation
grant (DBI-9724504) and NIH shared instrumentation grant (1 S10 RR0
9145-01). We thank Elizabeth Blackburn (UCSF) for providing us with TERT
mutant constructs, N125A+T126A and D868A, in the pBABE-puro backbone. We
thank Titia de Lange (Rockefeller University) for the TRF1 (#370)
antibody and for a TRF2Delta B Delta M construct obtained via
Addgene. We also thank Bo Zhao and Cesar Munoz-Fontela for helpful
discussions. Deposited in PMC for release after 12 months.
NR 65
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U1 0
U2 15
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD AUG 1
PY 2010
VL 123
IS 15
BP 2605
EP 2612
DI 10.1242/jcs.067306
PG 8
WC Cell Biology
SC Cell Biology
GA 629CN
UT WOS:000280172000009
PM 20605919
ER
PT J
AU Young, AP
Wagers, AJ
AF Young, Arthur P.
Wagers, Amy J.
TI Pax3 induces differentiation of juvenile skeletal muscle stem cells
without transcriptional upregulation of canonical myogenic regulatory
factors
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE Pax3; Pax7; Muscle stem cells; Satellite cells; C2C12; Myogenic
differentiation; Myogenic regulatory factors
ID SATELLITE CELLS; PROGENITOR CELLS; PRECURSOR CELLS; SELF-RENEWAL; GENE
MYF-5; MYOD; EXPRESSION; MICE; LIMB; SPECIFICATION
AB Pax3 is an essential myogenic regulator of fetal and embryonic development, but its role in postnatal myogenesis remains a topic of debate. We show that constitutive expression of Pax3 in postnatal, juvenile mouse skeletal muscle stem cells, a subset of the heterogeneous satellite cell pool highly enriched for myogenic activity, potently induces differentiation. This differentiation-promoting activity stands in contrast to the differentiation-inhibiting effects of Pax3 in the commonly used mouse myoblast cell line C2C12. Pax3 mRNA levels in distinct muscles correlate with the rate of myogenic differentiation of their muscle stem cells. Although Pax3 controls embryonic myogenesis through regulation of the canonical myogenic regulatory factors (MRFs) Myf-5, MyoD, myogenin and Mrf4, we find that in postnatal muscle stem cells, ectopic Pax3 expression fails to induce expression of any of these factors. Unexpectedly, overexpression of neither Myf-5 nor myogenin is sufficient to induce differentiation of juvenile stem cells; and knockdown of Myf-5, rather than inhibiting differentiation, promotes it. Taken together, our results suggest that there are distinct myogenic regulatory pathways that control the embryonic development, juvenile myogenesis and adult regeneration of skeletal myofibers.
C1 [Young, Arthur P.; Wagers, Amy J.] Joslin Diabet Ctr, Sect Dev & Stem Cell Biol, Boston, MA 02115 USA.
[Young, Arthur P.; Wagers, Amy J.] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
[Young, Arthur P.; Wagers, Amy J.] Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
RP Wagers, AJ (reprint author), Joslin Diabet Ctr, Sect Dev & Stem Cell Biol, 1 Joslin Pl, Boston, MA 02115 USA.
EM amy.wagers@joslin.harvard.edu
FU Burroughs Wellcome Fund; Beckman Foundation; NIH/NIDDK [T32 DK07260-30]
FX We thank Joyce LaVecchio and Girijesh Buruzula at the JDC/HSCI Flow Core
for cell sorting and flow cytometry analysis, Jennifer Shadrach for
laboratory management, Andrew Lassar for provision of cDNAs, and Andrew
Brack and Andrew Lassar for critically reviewing the manuscript. This
work was supported in part by a Burroughs Wellcome Fund career award
(A.J.W.), Beckman Foundation Young Investigators Award, and NIH/NIDDK
training grant T32 DK07260-30 (A.P.Y.). Deposited in PMC for release
after 12 months.
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PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD AUG 1
PY 2010
VL 123
IS 15
BP 2632
EP 2639
DI 10.1242/jcs.061606
PG 8
WC Cell Biology
SC Cell Biology
GA 629CN
UT WOS:000280172000012
PM 20605921
ER
PT J
AU Mancuso, E
Faro, A
Joshi, G
Geller, DA
AF Mancuso, Elizabeth
Faro, Alyssa
Joshi, Gagan
Geller, Daniel A.
TI Treatment of Pediatric Obsessive-Compulsive Disorder: A Review
SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY
LA English
DT Review
ID SEROTONIN REUPTAKE INHIBITORS; COGNITIVE-BEHAVIORAL THERAPY;
PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; NEUROPSYCHIATRIC DISORDERS;
STREPTOCOCCAL INFECTIONS; CLOMIPRAMINE TREATMENT; PSYCHIATRIC-DISORDERS;
TOURETTES-SYNDROME; MULTICENTER TRIAL
AB Recently, research in pediatric obsessive-compulsive disorder (OCD) has expanded to include large family genetic studies, elaboration of phenotypic dimensions, description of co-morbid disorders and their moderating effects on treatment response and outcome, research on immune-based neuropsychiatric causes, randomized controlled trials of selective serotonin re-uptake inhibitors (SSRIs), randomized controlled trials of cognitive behavioral therapy (CBT), comparative treatment trials; new approaches in behavior therapy, and increased awareness of newer approaches to treatment. The purpose of this article is to review assessment and treatment strategies to include current advances in research.
C1 [Mancuso, Elizabeth; Faro, Alyssa; Joshi, Gagan; Geller, Daniel A.] Massachusetts Gen Hosp, Dept Psychiat, Clin & Res Program Pediat Psychopharmacol, Boston, MA 02114 USA.
[Geller, Daniel A.] Harvard Univ, Sch Med, Boston, MA USA.
RP Geller, DA (reprint author), Massachusetts Gen Hosp, Pediat OCD Program, 185 Alewife Brook Pkwy,Suite 2000, Cambridge, MA 02138 USA.
EM dageller@partners.org
FU Boehringer Ingelheim; Otsuka; Eli Lilly; Pediatric Obsessive-compulsive
and Related Disorders fund; Eli Lilly and Co.; Forest Laboratories;
Glaxo-SmithKline; Pfizer; Ethel DuPont Warren Fellowship; American
Academy of Child and Adolescent Psychiatry [2005]; National Institute of
Mental Health; McNeil Pediatrics; SynerMed Communications; Bristol Myers
Squibb; Glaxo Smith Kline; Shire; Johnson Johnson; Merck; Cephlon;
McNeil; Eli-Lily; Abbott; Novartis; Organon; Takeda; New River
Pharmaceuticals
FX Dr. Daniel Geller receives/d in last 36 months (to April 2010) research
support from Boehringer Ingelheim, Otsuka, Eli Lilly, Pediatric
Obsessive-compulsive and Related Disorders fund (philanthropic); speaker
honoraria from Eli Lilly; is on the Medical Advisory Boards/Consulting
for Eli Lilly; private foundations, McIngvale Family Foundation,
National Institutes of Health, National Institute of Neurological
Disorders and Stroke, National Institute of Mental Health. He has
receives/d lifetime research support from Eli Lilly and Co., Forest
Laboratories, GlaxoSmithKline, Pfizer, Boehringer Ingelheim, Otsuka;
speaker honoraria from Alza, Bristol-Myers-Squibb, Eli Lilly, Forest
Laboratories, Glaxo-SmithKline, Novartis, Pfizer, Shire, Wyeth; is on
the Medical Advisory Boards/Consulting for Eli Lilly, Solvay, Lundbeck,
and Glaxo-SmithKline; private foundations, Obsessive-compulsive
Foundation, Tourette Syndrome Association, Wallace Foundation, McIngvale
Family Foundation Rogers Memorial Hospital; educational consultant/guest
lecture for American Psychiatric Publishing: honorarium for textbook
Network for Continuing Medical; education, Neuroscience e journal club
lecturer; National Institutes of Health, National Institute of Mental
Health, National Institute of Neurological Disorders and Stroke. Gagan
Joshi has received the Ethel DuPont Warren Fellowship Award 2005-2006,
Pilot Research Award from the American Academy of Child and Adolescent
Psychiatry 2005, National Institute of Mental Health (reviewer and
member of the NIMH Editorial Board), McNeil Pediatrics (CME sponsored by
SynerMed Communications), Bristol Myers Squibb (Site PI for
Multi-centered Trial), Glaxo Smith Kline (Site PI for Multi-centered
Trial), Shire (member of national advisory board), Subinvestigator for
clinical trials sponsored by Shire, Johnson & Johnson, Pfizer, Merck,
Cephlon, McNeil, Eli-Lily, Abbott, Novartis, Bristol Myers Squibb,
Organon, Otsuka, Takeda, & New River Pharmaceuticals. Elizabeth Mancuso
and Alyssa Faro have no conflicts of interest or financial ties to
disclose.
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U1 9
U2 25
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1044-5463
J9 J CHILD ADOL PSYCHOP
JI J. Child Adolesc. Psychopharmacol.
PD AUG
PY 2010
VL 20
IS 4
SI SI
BP 299
EP 308
DI 10.1089/cap.2010.0040
PG 10
WC Pediatrics; Pharmacology & Pharmacy; Psychiatry
SC Pediatrics; Pharmacology & Pharmacy; Psychiatry
GA 645FG
UT WOS:000281435700008
PM 20807068
ER
PT J
AU Preis, SR
Massaro, JM
Hoffmann, U
D'Agostino, RB
Levy, D
Robins, SJ
Meigs, JB
Vasan, RS
O'Donnell, CJ
Fox, CS
AF Preis, Sarah Rosner
Massaro, Joseph M.
Hoffmann, Udo
D'Agostino, Ralph B., Sr.
Levy, Daniel
Robins, Sander J.
Meigs, James B.
Vasan, Ramachandran S.
O'Donnell, Christopher J.
Fox, Caroline S.
TI Neck Circumference as a Novel Measure of Cardiometabolic Risk: The
Framingham Heart Study
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID VISCERAL ADIPOSE-TISSUE; FATTY-ACID-METABOLISM; INSULIN-RESISTANCE;
SLEEP-APNEA; ASSOCIATION; OBESITY; HYPERTENSION; CHOLESTEROL;
POPULATION; COMMUNITY
AB Background: Neck circumference, a proxy for upper-body sc fat, may be a unique fat depot that confers additional cardiovascular risk above and beyond central body fat.
Methods and Results: Participants with neck circumference measures who underwent multidetector computed tomography to assess visceral adipose tissue (VAT) were included [n = 3307, 48% women; mean age = 51 yr; mean body mass index (BMI) = 27.8 kg/m(2); mean neck circumference = 40.5 cm (men) and 34.2 cm (women)]. Sex-specific linear regression models were used to assess the association between SD increase in neck circumference and cardiovascular disease (CVD) risk factors (systolic and diastolic blood pressure; total, low-density lipoprotein, and high-density lipoprotein cholesterol and triglycerides; and fasting plasma glucose, insulin, proinsulin, and homeostasis model assessment of insulin resistance). Neck circumference was correlated with VAT [r = 0.63 (men); r = 0.74 (women); P < 0.001] and BMI [r = 0.79 (men); r = 0.80 (women); P < 0.001]. After further adjustment for VAT, neck circumference was positively associated with systolic blood pressure, diastolic blood pressure in men only, triglycerides, fasting plasma glucose in women only, insulin, proinsulin, and homeostasis model assessment of insulin resistance and was inversely associated with high-density lipoprotein (all P values < 0.01). Similar results were observed in models that adjusted for both VAT and BMI. In a secondary analysis of incident CVD as an outcome, there was no statistically significant association observed for neck circumference in multivariable-adjusted models.
Conclusions: Neck circumference is associated with CVD risk factors even after adjustment for VAT and BMI. These findings suggest that upper-body sc fat may be a unique, pathogenic fat depot. (J Clin Endocrinol Metab 95: 3701-3710, 2010)
C1 [Preis, Sarah Rosner; D'Agostino, Ralph B., Sr.; Levy, Daniel; Robins, Sander J.; Vasan, Ramachandran S.; O'Donnell, Christopher J.; Fox, Caroline S.] NHLBI, Framingham, MA 01702 USA.
[Preis, Sarah Rosner; D'Agostino, Ralph B., Sr.; Levy, Daniel; Robins, Sander J.; Vasan, Ramachandran S.; O'Donnell, Christopher J.; Fox, Caroline S.] Boston Univ, Framingham Heart Study, Framingham, MA 01702 USA.
[Preis, Sarah Rosner; Levy, Daniel; O'Donnell, Christopher J.; Fox, Caroline S.] NHLBI, Ctr Populat Studies, NIH, Bethesda, MD 20824 USA.
[Massaro, Joseph M.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02114 USA.
[Robins, Sander J.; Vasan, Ramachandran S.] Massachusetts Gen Hosp, Sect Prevent Med, Boston, MA 02114 USA.
[Robins, Sander J.; Vasan, Ramachandran S.] Massachusetts Gen Hosp, Serv Cardiol, Boston, MA 02114 USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Meigs, James B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
[O'Donnell, Christopher J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[D'Agostino, Ralph B., Sr.] Boston Univ, Dept Math, Boston, MA 02215 USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol & Metab, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Fox, CS (reprint author), 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM foxca@nhlbi.nih.gov
OI Preis, Sarah/0000-0002-9360-4166; Massaro, Joseph/0000-0002-2682-4812;
Ramachandran, Vasan/0000-0001-7357-5970
FU National Heart, Lung, and Blood Institute [N01-HC-25195]; American
Diabetes Association
FX This work was supported by the National Heart, Lung, and Blood
Institute's Framingham Heart Study (N01-HC-25195) and by an American
Diabetes Association Career Development Award (to J.B.M.).
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U2 6
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD AUG
PY 2010
VL 95
IS 8
BP 3701
EP 3710
DI 10.1210/jc.2009-1779
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 635JW
UT WOS:000280652400021
PM 20484490
ER
PT J
AU Beckman, JA
Goldfine, AB
Goldin, A
Prsic, A
Kim, S
Creager, MA
AF Beckman, Joshua A.
Goldfine, Allison B.
Goldin, Alison
Prsic, Adnan
Kim, Sora
Creager, Mark A.
TI Inhibition of Protein Kinase C beta Does Not Improve Endothelial
Function in Type 2 Diabetes
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID PERIPHERAL NEUROPATHY; CLINICAL-TRIAL; RUBOXISTAURIN; MELLITUS; RATS;
VASODILATION; ACTIVATION; DILATION; LY333531; OXYGEN
AB Context: Antagonism of protein kinase C beta (PKC beta) restores endothelial function in experimental models of diabetes and prevents vascular dysfunction in response to hyperglycemia in healthy humans.
Objective: We tested the hypothesis that PKC beta antagonism would improve vascular function in subjects with type 2 diabetes compared with healthy control subjects.
Design: The effect of PKC beta was evaluated in a randomized, placebo-controlled, double-blinded crossover trial.
Setting: The study was performed in the outpatient setting of a university medical center.
Participants: Thirteen subjects with type 2 diabetes without evidence of cardiovascular disease and 15 healthy control subjects were recruited via newspaper advertisement.
Intervention: Subjects underwent a randomized, double-blind, crossover, placebo-controlled trial of the selective PKC beta antagonist ruboxistaurin mesylate. Subjects received each treatment for 14 d.
Main Outcome Measure: Endothelium-dependent and endothelium-independent vasodilation of forearm resistance vessels was measured with mercury-in-silastic, strain-gauge plethysmography during intraarterial administration of methacholine chloride and verapamil, respectively. Markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress were measured after each treatment.
Results: Endothelium-dependent vasodilation of forearm resistance vessels was attenuated in diabetic subjects when compared with healthy subjects (P = 0.001). Endothelium-independent vasodilation did not differ between groups (P value not significant). Ruboxistaurin did not significantly change endothelium-dependent or endothelium-independent vasodilation or blood-based markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress in either diabetic or healthy subjects.
Conclusion: Endothelial dysfunction of forearm resistance vessels was not improved by 2 wk of selective PKC beta inhibition in patients with diabetes. These results suggest that PKC beta does not contribute significantly to vascular dysfunction in otherwise healthy patients with type 2 diabetes. (J Clin Endocrinol Metab 95: 3783-3787, 2010)
C1 [Beckman, Joshua A.; Goldin, Alison; Prsic, Adnan; Kim, Sora; Creager, Mark A.] Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA.
[Goldfine, Allison B.] Joslin Diabet Ctr, Div Cellular & Mol Physiol, Boston, MA 02215 USA.
RP Beckman, JA (reprint author), Brigham & Womens Hosp, Div Cardiovasc, 75 Francis St, Boston, MA 02115 USA.
EM jbeckman@partners.org
OI Beckman, Joshua/0000-0001-8332-8439
FU NIH [P01 HL48743, K23 HL-04169]; American Diabetes Association [ADA
1-06-CD-01]; Eli Lilly
FX This work has been supported by grants from the NIH (P01 HL48743 and K23
HL-04169), the American Diabetes Association (ADA 1-06-CD-01), and Eli
Lilly. M. A. C. is the Simon C. Fireman Scholar in Cardiovascular
Medicine at Brigham and Women's Hospital.
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U1 0
U2 1
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD AUG
PY 2010
VL 95
IS 8
BP 3783
EP 3787
DI 10.1210/jc.2010-0286
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 635JW
UT WOS:000280652400033
PM 20444914
ER
PT J
AU Roth, MY
Page, ST
Lin, K
Anawalt, BD
Matsumoto, AM
Snyder, CN
Marck, BT
Bremner, WJ
Amory, JK
AF Roth, M. Y.
Page, S. T.
Lin, K.
Anawalt, B. D.
Matsumoto, A. M.
Snyder, C. N.
Marck, B. T.
Bremner, W. J.
Amory, J. K.
TI Dose-Dependent Increase in Intratesticular Testosterone by Very Low-Dose
Human Chorionic Gonadotropin in Normal Men with Experimental
Gonadotropin Deficiency
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID HORMONE ANTAGONIST; MASS-SPECTROMETRY; HEALTHY-YOUNG; INFERTILE MEN;
HUMAN TESTIS; SPERMATOGENESIS; MAINTENANCE; DIHYDROTESTOSTERONE;
SUPPRESSION; FLUID
AB Context and Objective: In men with infertility secondary to gonadotropin deficiency, treatment with relatively high dosages of human chorionic gonadotropin (hCG) stimulates intratesticular testosterone (IT-T) biosynthesis and spermatogenesis. Previously we found that lower dosages of hCG stimulated IT-T to normal. However, the minimal dose of hCG needed to stimulate IT-T and the dose-response relationship between very low doses of hCG and IT-T and serum testosterone in normal men is unknown.
Design, Setting, Patients, and Intervention: We induced experimental gonadotropin deficiency in 37 normal men with the GnRH antagonist acyline and randomized them to receive one of four low doses of hCG: 0, 15, 60, or 125 IU sc every other day or 7.5 g daily testosterone gel for 10 d. Testicular fluid was obtained by percutaneous aspiration for steroid measurements at baseline and after 10 d of treatment and correlated with contemporaneous serum hormone measurements.
Results: Median (25th, 75th percentile) baseline IT-T was 2508 nmol/liter (1753, 3502 nmol/liter). IT-T concentrations increased in a dose-dependent manner with very low-dosage hCG administration from 77 nmol/liter (40, 122 nmol/liter) to 923 nmol/liter (894, 1017 nmol/liter) in the 0- and 125-IU groups, respectively (P < 0.001). Moreover, serum hCG was significantly correlated with both IT-T and serum testosterone (P < 0.01).
Conclusion: Doses of hCG far lower than those used clinically increase IT-T concentrations in a dose-dependent manner in normal men with experimental gonadotropin deficiency. Assessment of IT-T provides a valuable tool to investigate the hormonal regulation of spermatogenesis in man. (J Clin Endocrinol Metab 95: 3806-3813, 2010)
C1 [Roth, M. Y.; Page, S. T.; Anawalt, B. D.; Matsumoto, A. M.; Snyder, C. N.; Bremner, W. J.; Amory, J. K.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
[Lin, K.] Univ Washington, Dept Obstet & Gynecol, Seattle, WA 98195 USA.
[Roth, M. Y.; Page, S. T.; Anawalt, B. D.; Matsumoto, A. M.; Snyder, C. N.; Bremner, W. J.; Amory, J. K.] Univ Washington, Ctr Res Reprod & Contracept, Seattle, WA 98195 USA.
[Matsumoto, A. M.; Marck, B. T.] Vet Affairs Puget Sound Hlth Care Syst, Ctr Geriatr Res Educ & Clin, Seattle, WA 98108 USA.
RP Roth, MY (reprint author), Univ Washington, Dept Med, 1959 NE Pacific St,Box 357138, Seattle, WA 98195 USA.
EM mylang@u.washington.edu
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [U54-HD-12629, U54-HD-42454]; Diabetes, Obesity, and
Metabolism Grant [T32 DK007247]; Department of Veterans Affairs;
National Institute of Aging, a division of the National Institutes of
Health [K23 AG027238]
FX This work was supported by the Eunice Kennedy Shriver National Institute
of Child Health and Human Development through cooperative agreements
U54-HD-12629 and U54-HD-42454 as part of the specialized Cooperative
Centers Program in Reproductive Research and the Cooperative
Contraceptive Research Centers Program. M.Y.R. is supported by the
Diabetes, Obesity, and Metabolism Grant T32 DK007247. A. M. M. is
supported by the Department of Veterans Affairs. S. T. P. is supported
by Grant K23 AG027238 from the National Institute of Aging, a division
of the National Institutes of Health.
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U2 3
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD AUG
PY 2010
VL 95
IS 8
BP 3806
EP 3813
DI 10.1210/jc.2010-0360
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 635JW
UT WOS:000280652400036
PM 20484472
ER
PT J
AU Lima, MMO
Pareja, JC
Alegre, SM
Geloneze, SR
Kahn, SE
Astiarraga, BD
Chaim, EA
Geloneze, B
AF Lima, Marcelo M. O.
Pareja, Jose C.
Alegre, Sarah M.
Geloneze, Sylka R.
Kahn, Steven E.
Astiarraga, Brenno D.
Chaim, Elinton A.
Geloneze, Bruno
TI Acute Effect of Roux-En-Y Gastric Bypass on Whole-Body Insulin
Sensitivity: A Study with the Euglycemic-Hyperinsulinemic Clamp
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID TYPE-2 DIABETIC SUBJECTS; BETA-CELL FUNCTION; BARIATRIC SURGERY;
WEIGHT-LOSS; OBESE-PATIENTS; METABOLIC SYNDROME; MORBID-OBESITY;
RESISTANCE; RESTORATION; ADIPONECTIN
AB Context: Insulin resistance ameliorates after bariatric surgery, yet there is still a need for data on the acute effect of Roux-en-Y gastric bypass (RYGBP) on insulin sensitivity.
Objective: The objective of the study was to describe the acute effect of RYGBP on insulin sensitivity, measured by both the euglycemic-hyperinsulinemic clamp and homeostasis model assessment insulin resistance index (HOMA-IR).
Design and Setting: Evaluations were conducted before and 1 month after RYGBP at State University of Campinas (Sao Paulo, Brazil).
Patients: Patients included 19 premenopausal women with metabolic syndrome aged 35.3 (6.7) yr, body mass index 45.50 (3.74) kg/m(2) [mean (SD)]. Six had mild type 2 diabetes, seven impaired glucose tolerance, and six normal glucose tolerance.
Interventions and Main Outcome Measures: The volunteers underwent RYGBP either alone or combined with omentectomy. Euglycemic-hyperinsulinemic clamp, HOMA-IR, nonesterified fatty acids, leptin, ultrasensitive C-reactive protein, adiponectin, and IL-6 were assessed at baseline and 4.5 (0.9) wk postoperatively.
Results: Fasting glucose decreased [99.2 (13.1) to 83.6 (8.1) mg/dl, P < 0.01] along with a reduction in fasting insulin [30.4 (17.0) to 11.4 (6.3) mU/liter, P < 0.01]. M value did not improve postoperatively [25.82 (6.30) to 22.02 (6.05) mu mol/kg(FFM) . min] despite of a decrease in body weight [114.8 (14.5) to 102.3 (14.5) kg, P < 0.001]. This finding was discordant to the observation of an improvement in HOMA-IR [3.85 (2.10) to 1.42 (0.76), P < 0.01]. Nonesterified fatty acids increased. Leptin and C-reactive protein decreased. IL-6 and adiponectin remained unchanged.
Conclusions: A month after RYGBP, fasting glucose metabolism improves independent of a change in peripheral insulin sensitivity. (J Clin Endocrinol Metab 95: 3871-3875, 2010)
C1 [Lima, Marcelo M. O.; Pareja, Jose C.; Geloneze, Sylka R.; Astiarraga, Brenno D.; Geloneze, Bruno] State Univ Campinas UNICAMP, Lab Invest Metab & Diabet Gastroctr, BR-13081970 Campinas, SP, Brazil.
[Pareja, Jose C.; Chaim, Elinton A.] State Univ Campinas UNICAMP, Dept Surg, BR-13081970 Campinas, SP, Brazil.
[Alegre, Sarah M.; Astiarraga, Brenno D.] State Univ Campinas UNICAMP, Dept Internal Med, BR-13081970 Campinas, SP, Brazil.
[Kahn, Steven E.] Vet Affairs Puget Sound Hlth Care Syst, Div Metab Endocrinol & Nutr, Dept Med, Seattle, WA 98108 USA.
Univ Washington, Seattle, WA 98108 USA.
RP Lima, MMO (reprint author), State Univ Campinas UNICAMP, Lab Invest Metab & Diabet Gastroctr, 420 Cidade Univ, BR-13081970 Campinas, SP, Brazil.
EM endo.marcelolima@hotmail.com
RI 5, INCT/H-4505-2013; Diabetes, Inct/I-2186-2013;
OI Kahn, Steven/0000-0001-7307-9002
FU Fundacao de Apoio a Pesquisa do Estado de Sao Paulo, Sao Paulo, Brazil
[05/58627-2]; U.S. Department of Veterans Affairs
FX This work was supported by Fundacao de Apoio a Pesquisa do Estado de Sao
Paulo, Sao Paulo, Brazil (Protocol 05/58627-2) and in part by the U.S.
Department of Veterans Affairs. This study is registered at
www.clinicaltrials.gov (NCT00545805).
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U2 8
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD AUG
PY 2010
VL 95
IS 8
BP 3871
EP 3875
DI 10.1210/jc.2010-0085
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 635JW
UT WOS:000280652400044
PM 20484482
ER
PT J
AU Chillambhi, S
Turan, S
Hwang, DY
Chen, HC
Juppner, H
Bastepe, M
AF Chillambhi, Smitha
Turan, Serap
Hwang, Daw-Yang
Chen, Hung-Chun
Jueppner, Harald
Bastepe, Murat
TI Deletion of the Noncoding GNAS Antisense Transcript Causes
Pseudohypoparathyroidism Type Ib and Biparental Defects of GNAS
Methylation in cis
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID XL-ALPHA-S; IMPRINTING CONTROL ELEMENT; G-PROTEIN; AUTOSOMAL-DOMINANT;
CONTROL REGION; EPIGENETIC DEFECTS; LOCUS; IDENTIFICATION; CLUSTER; GENE
AB Context: GNAS encodes the alpha-subunit of the stimulatory G protein as well as additional imprinted transcripts including the maternally expressed NESP55 and the paternally expressed XL alpha s, antisense, and A/B transcripts. Most patients with pseudohypoparathyroidism type Ib (PHP-Ib) exhibit imprinting defects affecting the maternal GNAS allele, which are thought to reduce/abolish Gs alpha expression in renal proximal tubules and thereby cause resistance to PTH.
Objective: Our objective was to define the genetic defect in a previously unreported family with autosomal dominant PHP-Ib.
Design and Setting: Analyses of serum and urine chemistries and of genomic DNA and lymphoblastoid-derived RNA were conducted at a tertiary hospital and research laboratory.
Patients: Affected individuals presented with muscle weakness and/or paresthesia and showed hypocalcemia, hyperphosphatemia, and elevated serum PTH. Obligate carriers were healthy and revealed no obvious abnormality in mineral ion homeostasis.
Results: A novel 4.2-kb microdeletion was discovered in the affected individuals and the obligate carriers, ablating two noncoding GNAS antisense exons while preserving the NESP55 exon. On maternal transmission, the deletion causes loss of all maternal GNAS imprints, partial gain of NESP55 methylation, and PTH resistance. Paternal transmission of the mutation leads to epigenetic alterations in cis, including a partial loss of NESP55 methylation and a partial gain of A/B methylation.
Conclusions: The identified deletion points to a unique cis-acting element located telomeric of the NESP55 exon that is critical for imprinting both GNAS alleles. These findings provide novel insights into the molecular mechanisms underlying PHP and GNAS imprinting. (J Clin Endocrinol Metab 95: 3993-4002, 2010)
C1 [Chillambhi, Smitha; Turan, Serap; Jueppner, Harald; Bastepe, Murat] Massachusetts Gen Hosp, Endocrine Unit, Dept Med, Boston, MA 02114 USA.
[Chillambhi, Smitha; Jueppner, Harald] Massachusetts Gen Hosp, Pediat Nephrol Unit, Dept Pediat, Boston, MA 02114 USA.
[Chillambhi, Smitha; Jueppner, Harald] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Turan, Serap] Marmara Univ, Sch Med, Dept Pediat Endocrinol, TR-34722 Istanbul, Turkey.
[Hwang, Daw-Yang; Chen, Hung-Chun] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Nephrol, Kaohsiung 80708, Taiwan.
RP Juppner, H (reprint author), Massachusetts Gen Hosp, Endocrine Unit, Dept Med, 50 Blossom St Thier 10, Boston, MA 02114 USA.
EM jueppner@helix.mgh.harvard.edu; bastepe@helix.mgh.harvard.edu
FU National Institutes of Health/National Institute of Diabetes and
Digestive and Kidney Diseases [R01 DK073911, R37 DK46718]; Scientific
and Technical Research Council of Turkey (TUBITAK); Scientific Human
Resources Development (BAYG)
FX This work was supported by research grants from National Institutes of
Health/National Institute of Diabetes and Digestive and Kidney Diseases
(R01 DK073911 to M. B. and R37 DK46718 to H.J.). S. T. was the recipient
of a fellowship from the Scientific and Technical Research Council of
Turkey (TUBITAK), Scientific Human Resources Development (BAYG) within
the framework of the Postdoctoral Research Fellowship program.
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U2 4
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD AUG
PY 2010
VL 95
IS 8
BP 3993
EP 4002
DI 10.1210/jc.2009-2205
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 635JW
UT WOS:000280652400059
PM 20444925
ER
PT J
AU Sox, HC
Helfand, M
Grimshaw, J
Dickersin, K
Tovey, D
Knottnerus, JA
Tugwell, P
AF Sox, Harold C.
Helfand, Mark
Grimshaw, Jeremy
Dickersin, Kay
Tovey, David
Knottnerus, J. Andre
Tugwell, Peter
CA PLoS Med Editors
TI Comparative Effectiveness Research: Challenges for Medical Journals
SO JOURNAL OF CLINICAL EPIDEMIOLOGY
LA English
DT Article
C1 [Helfand, Mark] Oregon Hlth & Sci Univ, Portland VA Med Ctr, Portland, OR 97201 USA.
[Sox, Harold C.] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dartmouth Inst, Hanover, NH 03756 USA.
[Grimshaw, Jeremy] Ottawa Hosp Res Inst, Clin Epidemiol Program, Ottawa, ON, Canada.
[Dickersin, Kay] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Tovey, David] Cochrane Lib, London, England.
[Knottnerus, J. Andre] Univ Maastricht, Dept Gen Practice, Maastricht, Netherlands.
[Tugwell, Peter] Univ Ottawa, Dept Med, Ottawa, ON, Canada.
[Tugwell, Peter] Univ Ottawa, Dept Epidemiol & Community Med, Ottawa, ON, Canada.
RP Helfand, M (reprint author), Oregon Hlth & Sci Univ, Portland VA Med Ctr, Portland, OR 97201 USA.
EM helfand@ohsu.edu
RI Grimshaw, Jeremy/D-8726-2013; Knottnerus, Andre/F-4866-2013; Knottnerus,
Johannes/A-3829-2009;
OI Grimshaw, Jeremy/0000-0001-8015-8243; Barbour,
Virginia/0000-0002-2358-2440; Tugwell, Peter/0000-0001-5062-0556; Clark,
Jocalyn/0000-0002-8014-3989
FU Public Library of Science
FX Funding: The PLoS Medicine Editors are each paid a salary by the Public
Library of Science, and they contributed to this editorial during their
salaried time. The other authors received no specific funding for this
article.
NR 7
TC 5
Z9 5
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0895-4356
J9 J CLIN EPIDEMIOL
JI J. Clin. Epidemiol.
PD AUG
PY 2010
VL 63
IS 8
BP 862
EP 864
DI 10.1016/j.jclinepi.2010.03.001
PG 3
WC Health Care Sciences & Services; Public, Environmental & Occupational
Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 619OQ
UT WOS:000279439900010
PM 20434882
ER
PT J
AU Bloch, MJ
Basile, JN
AF Bloch, Michael J.
Basile, Jan N.
TI EXISTING KIDNEY DISEASE CLASSIFICATION GUIDELINE NEEDS TO INCORPORATE
DEGREE OF PROTEINURIA WITH ESTIMATED GLOMERULAR FILTRATION RATE TO MORE
ACCURATELY PREDICT CARDIOVASCULAR AND RENAL RISK
SO JOURNAL OF CLINICAL HYPERTENSION
LA English
DT Editorial Material
C1 [Bloch, Michael J.] St Marys Reg Med Ctr, Risk Reduct Ctr, Reno, NV 89503 USA.
[Bloch, Michael J.] Univ Nevada, Sch Med, Dept Med, Reno, NV 89557 USA.
[Basile, Jan N.] Med Univ S Carolina, Seinsheimer Cardiovasc Hlth Program, Div Gen Internal Med Geriatr, Charleston, SC 29425 USA.
[Basile, Jan N.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
RP Bloch, MJ (reprint author), St Marys Reg Med Ctr, Risk Reduct Ctr, 645 N Arlington St,Suite 460, Reno, NV 89503 USA.
EM mbloch@aol.com
NR 0
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U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1524-6175
J9 J CLIN HYPERTENS
JI J. Clin. Hypertens.
PD AUG
PY 2010
VL 12
IS 8
BP 627
EP 630
DI 10.1111/j.1751-7176.2010.00325.x
PG 4
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 635GX
UT WOS:000280644700011
PM 20695941
ER
PT J
AU Path, ME
AF Path, Mary-Elizabeth
TI Rehashing endocannabinoid antagonists: can we selectively target the
periphery to safely treat obesity and type 2 diabetes?
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Editorial Material
ID CANNABINOID RECEPTOR; SYSTEM; METABOLISM; INSULIN
AB A growing body of evidence supports an important role for the endocannabinoid system as a regulator of appetite, body weight, and systemic metabolism, which is overactive in obesity and type 2 diabetes. While initial attempts to target this system using the cannabinoid receptor inverse agonist rimonabant were successful in producing modest weight loss and improving obesity-related metabolic complications in humans, adverse central nervous system side effects precluded introduction of this drug into clinical practice. However, new data, presented by Tam and colleagues in this issue of the JCI, demonstrate that selective blockade of peripheral cannabinoid receptors may be a novel successful therapeutic approach.
C1 [Path, Mary-Elizabeth] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Path, Mary-Elizabeth] Harvard Univ, Sch Med, Boston, MA USA.
RP Path, ME (reprint author), Joslin Diabet Ctr, Boston, MA 02215 USA.
EM mary.elizabeth.patti@joslin.harvard.edu
NR 20
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U1 0
U2 0
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 AUG
PY 2010
VL 120
IS 8
BP 2646
EP 2648
DI 10.1172/JCI44099
PG 3
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 633HI
UT WOS:000280492100001
ER
PT J
AU Sun, SH
Sprenger, CCT
Vessella, RL
Haugk, K
Soriano, K
Mostaghel, EA
Page, ST
Coleman, IM
Nguyen, HM
Sun, HY
Nelson, PS
Plymate, SR
AF Sun, Shihua
Sprenger, Cynthia C. T.
Vessella, Robert L.
Haugk, Kathleen
Soriano, Kathryn
Mostaghel, Elahe A.
Page, Stephanie T.
Coleman, Ilsa M.
Nguyen, Holly M.
Sun, Huiying
Nelson, Peter S.
Plymate, Stephen R.
TI Castration resistance in human prostate cancer is conferred by a
frequently occurring androgen receptor splice variant
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID GROWTH-FACTOR-I; TUMOR-CELL LINES; MEDICAL CASTRATION; EPITHELIAL-CELLS;
GENE-EXPRESSION; T-ANTIGEN; IGF-IR; PROGRESSION; ACTIVATION; MUTATIONS
AB Progression of prostate cancer following castration is associated with increased androgen receptor (AR) expression and signaling despite AR blockade. Recent studies suggest that these activities are due to the generation of constitutively active AR splice variants, but the mechanisms by which these splice variants could mediate such effects are not fully understood. Here we have identified what we believe to be a novel human AR splice variant in which exons 5, 6, and 7 are deleted (AR(v567es)) and demonstrated that this variant can contribute to cancer progression in human prostate cancer xenograft models in mice following castration. We determined that, in human prostate cancer cell lines, AR(v567es) functioned as a constitutively active receptor, increased expression of full-length AR (AR(fl)), and enhanced the transcriptional activity of AR. In human xenografts, human prostate cancer cells transfected with AR(v567es) cDNA formed tumors that were resistant to castration. Furthermore, the ratio of AR(v567es) to AR(fl) expression within the xenografts positively correlated with resistance to castration. Importantly, we also detected AR(v567es) frequently in human prostate cancer metastases. In summary, these data indicate that constitutively active AR splice variants can contribute to the development of castration-resistant prostate cancers and may serve as biomarkers for patients who are likely to suffer from early recurrence and are candidates for therapies directly targeting the AR rather than ligand.
C1 [Plymate, Stephen R.] Univ Washington, Sch Med, Harborview Med Ctr, Dept Med, Seattle, WA 98104 USA.
[Vessella, Robert L.; Nguyen, Holly M.; Nelson, Peter S.; Plymate, Stephen R.] Univ Washington, Sch Med, Dept Urol, Seattle, WA 98104 USA.
[Vessella, Robert L.; Haugk, Kathleen; Plymate, Stephen R.] Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Seattle, WA USA.
[Mostaghel, Elahe A.; Coleman, Ilsa M.; Nelson, Peter S.] Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98104 USA.
[Sun, Huiying] Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
[Sun, Huiying] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
RP Plymate, SR (reprint author), Univ Washington, Sch Med, Harborview Med Ctr, Dept Med, Box 359625,325 9th Ave, Seattle, WA 98104 USA.
EM splymate@u.washington.edu
FU NIH-NCI [PO1 CA 85859]; Pacific Northwest Prostate Cancer SPORE [P50 CA
097186]; Veterans Affairs Research Program
FX We would like to thank Jennifer Wu and Marco Marcelli for critical
review of the manuscript and Martin Escandon for assistance with
manuscript preparation. Grants from the NIH-NCI (PO1 CA 85859 to S.R.
Plymate, R. Vessella, and P.S. Nelson), the Pacific Northwest Prostate
Cancer SPORE (P50 CA 097186 to S.R. Plymate, R. Vessella, and P.S.
Nelson), and the Veterans Affairs Research Program (to S.R. Plymate)
supported this work.
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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 AUG
PY 2010
VL 120
IS 8
BP 2715
EP 2730
DI 10.1172/JCI41824
PG 16
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 633HI
UT WOS:000280492100010
PM 20644256
ER
PT J
AU Cao, HL
Yu, SB
Yao, Z
Galson, DL
Jiang, Y
Zhang, XY
Fan, J
Lu, BF
Guan, YF
Luo, M
Lai, YM
Zhu, YB
Kurihara, N
Patrene, K
Roodman, GD
Xiao, GZ
AF Cao, Huiling
Yu, Shibing
Yao, Zhi
Galson, Deborah L.
Jiang, Yu
Zhang, Xiaoyan
Fan, Jie
Lu, Binfeng
Guan, Youfei
Luo, Min
Lai, Yumei
Zhu, Yibei
Kurihara, Noriyoshi
Patrene, Kenneth
Roodman, G. David
Xiao, Guozhi
TI Activating transcription factor 4 regulates osteoclast differentiation
in mice
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID BONE-MINERAL-DENSITY; OSTEOCALCIN GENE-EXPRESSION; MARROW STROMAL CELLS;
LACKING C-FOS; PARATHYROID-HORMONE; KEY REGULATOR; T-CELLS; OSTEOBLAST
DIFFERENTIATION; RECEPTOR ACTIVATOR; NUCLEAR-FACTOR
AB Activating transcription factor 4 (ATF4) is a critical transcription factor for osteoblast (OBL) function and bone formation; however, a direct role in osteoclasts (OCLs) has not been established. Here, we targeted expression of ATF4 to the OCL lineage using the Trap promoter or through deletion of Aft4 in mice. OCL differentiation was drastically decreased in Atf4(-/-) bone marrow monocyte (BMM) cultures and bones. Coculture of Atf4(-/-) BMMs with WT OBLs or a high concentration of RANKL failed to restore the OCL differentiation defect. Conversely, Trap-Atf4-tg mice displayed severe osteopenia with dramatically increased osteoclastogenesis and bone resorption. We further showed that ATF4 was an upstream activator of the critical transcription factor Nfatc1 and was critical for RANKL activation of multiple MAPK pathways in OCL progenitors. Furthermore, ATF4 was crucial for M-CSF induction of RANK expression on BMMs, and lack of ATF4 caused a shift in OCL precursors to macrophages. Finally, ATF4 was largely modulated by M-CSF signaling and the PI3K/AKT pathways in BMMs. These results demonstrate that ATF4 plays a direct role in regulating OCL differentiation and suggest that it may be a therapeutic target for treating bone diseases associated with increased OCL activity.
C1 [Cao, Huiling; Yu, Shibing; Galson, Deborah L.; Zhang, Xiaoyan; Luo, Min; Kurihara, Noriyoshi; Patrene, Kenneth; Roodman, G. David; Xiao, Guozhi] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Cao, Huiling; Yao, Zhi] Tianjin Med Univ, Educ Minist China, Key Lab, Dept Immunol, Tianjin, Peoples R China.
[Jiang, Yu; Lai, Yumei] Univ Pittsburgh, Dept Pharmacol & Chem Biol, Pittsburgh, PA USA.
[Zhang, Xiaoyan; Guan, Youfei] Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing, Peoples R China.
[Fan, Jie] Univ Pittsburgh, Dept Surg, Pittsburgh, PA USA.
[Lu, Binfeng; Zhu, Yibei] Univ Pittsburgh, Dept Immunol, Pittsburgh, PA USA.
[Xiao, Guozhi] Nankai Univ, Coll Life Sci, Tianjin 300071, Peoples R China.
RP Xiao, GZ (reprint author), VA Pittsburgh Healthcare Syst, Rm 2E-107,151-U, Pittsburgh, PA 15240 USA.
EM xiaog@upmc.edu
RI YU, SHIBING/B-7648-2012; Galson, Deborah/E-9370-2010
OI Galson, Deborah/0000-0002-2045-8807
FU NIH [DK072230, AR057310]; Department of Defense [W81XWH-07-1-0160];
Chinese Ministry of Science and Technology [2009CB918902]
FX We thank Renny T. Franceschi (University of Michigan, Ann Arbor,
Michigan, USA) for critical reading of this manuscript. Thanks to Harry
Blair (University of Pittsburgh, Pittsburgh, Pennsylvania, USA) for
expert advice on bone histomorphometry. This work was in part supported
by NIH grant DK072230, Department of Defense grant W81XWH-07-1-0160, and
Chinese Ministry of Science and Technology grant 2009CB918902 (to G.
Xiao) as well as by NIH grant AR057310 (to D.L. Galson).
NR 67
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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 AUG
PY 2010
VL 120
IS 8
BP 2755
EP 2766
DI 10.1172/JCI42106
PG 12
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 633HI
UT WOS:000280492100013
PM 20628199
ER
PT J
AU Liew, CW
Bochenski, J
Kawamori, D
Hu, J
Leech, CA
Wanic, K
Malecki, M
Warram, JH
Qi, L
Krolewski, AS
Kulkarni, RN
AF Liew, Chong Wee
Bochenski, Jacek
Kawamori, Dan
Hu, Jiang
Leech, Colin A.
Wanic, Krzysztof
Malecki, Maciej
Warram, James H.
Qi, Ling
Krolewski, Andrzej S.
Kulkarni, Rohit N.
TI The pseudokinase tribbles homolog 3 interacts with ATF4 to negatively
regulate insulin exocytosis in human and mouse beta cells
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID FUNCTIONAL Q84R POLYMORPHISM; PANCREATIC-ISLETS; TRB3; GLUCOSE; GENE;
ACTIVATION; RESISTANCE; EXPRESSION; SECRETION; TRIB3
AB Insufficient insulin secretion and reduced pancreatic beta cell mass are hallmarks of type 2 diabetes (T2DM). Here, we confirm that a previously identified polymorphism (rs2295490/Q84R) in exon 2 of the pseudokinase-encoding gene tribbles 3 (TRB3) is associated with an increased risk for T2DM in 2 populations of people of mixed European descent. Carriers of the 84R allele had substantially reduced plasma levels of C-peptide, the product of proinsulin processing to insulin, suggesting a role for TRB3 in beta cell function. Overexpression of TRB3 84R in mouse beta cells, human islet cells, and the murine beta cell line MIN6 revealed reduced insulin exocytosis, associated with a marked reduction in docked insulin granules visualized by electron microscopy. Conversely, knockdown of TRB3 in MIN6 cells restored insulin secretion and expression of exocytosis genes. Further analysis in MIN6 cells demonstrated that TRB3 interacted with the transcription factor ATF4 and that this complex acted as a competitive inhibitor of cAMP response element-binding (CREB) transcription factor in the regulation of key exocytosis genes. In addition, the 84R TRB3 variant exhibited greater protein stability than wild-type TRB3 and increased binding affinity to Akt. Mice overexpressing TRB3 84R in beta cells displayed decreased beta cell mass, associated with reduced proliferation and enhanced apoptosis rates. These data link a missense polymorphism in human TRB3 to impaired insulin exocytosis and thus increased risk for T2DM.
C1 [Liew, Chong Wee; Kawamori, Dan; Hu, Jiang; Kulkarni, Rohit N.] Harvard Univ, Sch Med, Sect Islet Cell & Regenerat Med, Boston, MA USA.
[Bochenski, Jacek; Wanic, Krzysztof; Warram, James H.; Krolewski, Andrzej S.] Harvard Univ, Sch Med, Sect Genet & Epidemiol, Joslin Diabet Ctr,Res Div, Boston, MA USA.
[Bochenski, Jacek; Wanic, Krzysztof; Warram, James H.; Krolewski, Andrzej S.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Leech, Colin A.] SUNY Upstate Med Univ, Dept Med, Syracuse, NY USA.
[Wanic, Krzysztof; Malecki, Maciej] Jagiellonian Univ, Sch Med, Dept Metab Disorders, Krakow, Poland.
[Qi, Ling] Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA.
[Qi, Ling] Salk Inst Biol Studies, Labs Peptide Biol, La Jolla, CA 92037 USA.
RP Kulkarni, RN (reprint author), Joslin Diabet Ctr, Room 602,1 Joslin Pl, Boston, MA 02215 USA.
EM Rohit.Kulkarni@joslin.harvard.edu
FU NIH [RO1 DK 67536, RO1 DK47475, RO1 TW01351, P30 DK36836,
1RL9EB008539-01]; Graetz Bridge Funds; Manpei Suzuki Diabetes
Foundation, Japan; JDRF
FX The authors thank M. Montminy and C.R. Kahn for providing reagents and
discussions; J. Pessin, G.W. Sharp, and S. Bonner-Weir for advice; L.
Huse and E. Morgan for excellent assistance in the preparation of this
manuscript; H. Li for assistance with hormone assays; and C. Cahill for
assistance with electron microscopy. This work was supported by NIH
grant RO1 DK 67536 and the Graetz Bridge Funds (to R.N. Kulkarni), NIH
grant RO1 DK47475 (to A.S. Krolewski), NIH grant RO1 TW01351 (to A.S.
Krolewski), and the Joslin DERC Specialized Assay and Advanced
Microscopy Cores (NIH P30 DK36836). C.W. Liew was supported by a Mary K.
Iacocca Postdoctoral Fellowship and an NIH Interdisciplinary training
grant (1RL9EB008539-01) (SysCODE). D. Kawamori is the recipient of a
research fellowship (Manpei Suzuki Diabetes Foundation, Japan) and a
JDRF postdoctoral fellowship.
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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 AUG
PY 2010
VL 120
IS 8
BP 2876
EP 2888
DI 10.1172/JCI36849
PG 13
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 633HI
UT WOS:000280492100023
PM 20592469
ER
PT J
AU DiVall, SA
Williams, TR
Carver, SE
Koch, L
Bruning, JC
Kahn, CR
Wondisford, F
Radovick, S
Wolfe, A
AF DiVall, Sara A.
Williams, Tameeka R.
Carver, Sarah E.
Koch, Linda
Bruening, Jens C.
Kahn, C. Ronald
Wondisford, Fredric
Radovick, Sally
Wolfe, Andrew
TI Divergent roles of growth factors in the GnRH regulation of puberty in
mice
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID FEMALE REPRODUCTIVE FUNCTION; NEURONAL CELL-LINE; HIGH-FAT DIET;
FACTOR-I; GENE-EXPRESSION; BODY-WEIGHT; INSULIN-RECEPTOR; HORMONE
NEURONS; SEXUAL-MATURATION; DENDRITIC SPINES
AB Pubertal onset, initiated by pulsatile gonadotropin-releasing hormone (GnRH), only occurs in a favorable, anabolic hormonal milieu. Anabolic factors that may signal nutritional status to the hypothalamus include the growth factors insulin and IGF-1. It is unclear which hypothalamic neuronal subpopulation these factors affect to ultimately regulate GnRH neuron function in puberty and reproduction. We examined the direct role of the GnRH neuron in growth factor regulation of reproduction using the Cre/lox system. Mice with the IR or IGF-1R deleted specifically in GnRH neurons were generated. Male and female mice with the IR deleted in GnRH neurons displayed normal pubertal timing and fertility, but male and female mice with the IGF-1R deleted in GnRH neurons experienced delayed pubertal development with normal fertility. With IGF-1 administration, puberty was advanced in control females, but not in females with the IGF-1R deleted in GnRH neurons, in control males, or in knockout males. These mice exhibited developmental differences in GnRH neuronal morphology but normal number and distribution of neurons. These studies define the role of IGF-1R signaling in the coordination of somatic development with reproductive maturation and provide insight into the mechanisms regulating pubertal timing in anabolic states.
C1 [DiVall, Sara A.] Johns Hopkins Univ, Div Pediat Endocrinol, Dept Pediat, Baltimore, MD 21212 USA.
[Koch, Linda; Bruening, Jens C.] Univ Cologne, Inst Genet, Dept Mouse Genet & Metab, D-5000 Cologne, Germany.
[Bruening, Jens C.] Univ Hosp Cologne, Dept Internal Med, Cologne, Germany.
[Bruening, Jens C.] Max Planck Inst Biol Aging, Cologne, Germany.
[Kahn, C. Ronald] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
RP DiVall, SA (reprint author), Johns Hopkins Univ, Div Pediat Endocrinol, Dept Pediat, 600 N Wolfe St,CMSC 406, Baltimore, MD 21212 USA.
EM sdivall1@jhmi.edu
OI Koch, Linda/0000-0002-2943-1993
FU Lawson Wilkins Pediatric Endocrine Society (LWPES); NIH [K08HD056139,
R01HD044608]; Deutsche Forschungsgemeinschaft (DFG) [Br1492-7]; Eunice
Kennedy Shriver NICHD/NIH [U54HD41859]
FX The authors thank Brigitte Mann of the Northwestern University Ligand
Assay Core Facility for performing the LH radioimmunoassays. We also
thank Andrea Gore for helpful advice regarding GnRH and IGF-1R
immunofluorescence staining. This work was supported by the Lawson
Wilkins Pediatric Endocrine Society (LWPES) Clinical Scholars Award and
NIH K08HD056139 to S.A. DiVall, Deutsche Forschungsgemeinschaft (DFG)
Br1492-7 to J.C. Bruning, NIH R01HD044608 to A. Wolfe, and the Eunice
Kennedy Shriver NICHD/NIH through cooperative agreement U54HD41859 as
part of the Specialized Cooperative Centers Program in Reproduction and
Infertility Research.
NR 48
TC 60
Z9 63
U1 1
U2 6
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 AUG
PY 2010
VL 120
IS 8
BP 2900
EP 2909
DI 10.1172/JCI41069
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 633HI
UT WOS:000280492100025
PM 20628204
ER
PT J
AU Baruch, L
Agarwal, S
Gupta, B
Haynos, A
Johnson, S
Kelly-Johnson, K
Eng, C
AF Baruch, Lawrence
Agarwal, Sanjay
Gupta, Bhanu
Haynos, Ann
Johnson, Swapna
Kelly-Johnson, Katelyn
Eng, Calvin
TI Is directly measured low-density lipoprotein clinically equivalent to
calculated low-density lipoprotein?
SO JOURNAL OF CLINICAL LIPIDOLOGY
LA English
DT Article
DE Health policy; Hypercholesterolemia; LDL-C cholesterol; Lipids
ID CORONARY-HEART-DISEASE; TREATMENT PANEL-III; CARDIOVASCULAR-DISEASE;
POSITION STATEMENT; APOLIPOPROTEIN-B; HIGH-RISK; CHOLESTEROL; EVENTS;
RATIOS
AB BACKGROUND: Low-density lipoprotein cholesterol (LDL-C) can either be calculated or measured directly. Clinical guidelines recommend the use of calculated LDL-C (C-LDL-C) to guide therapy because the evidence base for cholesterol management is derived almost exclusively from trials that use C-LDL-C, with direct measurement of LDL-C (D-LDL-C) being reserved for those patients who are nonfasting or with significant hypertriglyceridemia.
OBJECTIVE: Our aim was to determine the clinical equivalence of directly measured-LDL-C, using a Siemens Advia Chemistry System, and fasting C-LDL-C.
METHODS: Eighty-one subjects recruited for two cholesterol treatment studies had at least one C-LDL-C and D-LDL-C performed simultaneously; 64 had a repeat lipid assessment after 4 to 6 weeks of therapy, resulting in 145 pairs of C-LDL-C and D-LDL-C.
RESULTS: There was significant correlation between D-LDL-C and C-LDL-C (r(2) = 0.86). Correlation was significantly better in those with lower total cholesterol, triglycerides, and high-density lipoprotein. In 60% of subjects, the difference between D-LDL-C and C-LDL-C was more than 5 mg/dL and greater than 6%. Clinical concordance between D-LDL-C and C-LDL-C was present in 40% of patients, whereas clinical discordance was noted in 25%. One-third had greater than a 15 ing/dL difference between D-LDL-C and C-LDL-C, whereas 25% had a greater than 20 mg/dL difference. In 47% of subjects, the difference between D-LDL-C and C-LDL-C at baseline and follow-up changed by a minimum of 10% or 10 mg/dL.
CONCLUSIONS: Our findings suggest that D-LDL-C is not clinically equivalent to C-LDL-C. This puts into question the current recommendation of using D-LDL-C in situations in which C-LDL-C would be inaccurate. Published by Elsevier Inc on behalf of the National Lipid Association.
C1 [Baruch, Lawrence; Johnson, Swapna; Kelly-Johnson, Katelyn; Eng, Calvin] James J Peters VA Med Ctr, Med Serv, Bronx, NY 10468 USA.
[Baruch, Lawrence; Eng, Calvin] Mt Sinai Sch Med, New York, NY USA.
[Agarwal, Sanjay] Valley Hosp, Ridgewood, NJ USA.
[Gupta, Bhanu] Mayo Clin, Rochester, MN USA.
[Haynos, Ann] Univ Nevada, Reno, NV 89557 USA.
RP Baruch, L (reprint author), James J Peters VA Med Ctr, Med Serv, 130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM lawrence.baruch@va.gov
NR 14
TC 7
Z9 7
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1933-2874
J9 J CLIN LIPIDOL
JI J. Clin. Lipidol.
PD AUG
PY 2010
VL 4
IS 4
BP 259
EP 264
DI 10.1016/j.jacl.2010.05.003
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 647LB
UT WOS:000281618900004
PM 21122658
ER
PT J
AU Nahed, BV
Walcott, BP
Ortman, AJ
Kahle, KT
Aghi, M
Peterfreund, RA
Coumans, JV
AF Nahed, Brian V.
Walcott, Brian P.
Ortman, Amy J.
Kahle, Kristopher T.
Aghi, Manish
Peterfreund, Robert A.
Coumans, Jean-Valery
TI Interval, acute onset airway obstruction associated with a fracture of
the C4 vertebra in a patient with ankylosing spondylitis
SO JOURNAL OF CLINICAL NEUROSCIENCE
LA English
DT Editorial Material
DE Airway obstruction; Ankylosing spondylitis; Cervical collar; Cervical
fracture; Spinal instability
ID CERVICAL-SPINE; MOTION; STABILIZATION; COMPLICATIONS; LARYNGOSCOPY;
INTUBATION; INJURIES; SURGERY
AB We report a 92-year-old female with ankylosing spondylitis who suffered a non-displaced cervical fracture of the C4 vertebral body as the result of a mechanical fall. A rigid cervical collar was used to maintain stability. The patient later went on to develop upper airway obstruction as a result of fracture displacement. She was emergently intubated for airway protection. To our knowledge, this is the first report of interval, acute onset upper airway obstruction caused by cervical instability following trauma and fracture in a patient with ankylosing spondylitis. This example highlights one of the potential complications of rigid cervical collar immobilization in patients with spinal instability. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Nahed, Brian V.; Walcott, Brian P.; Kahle, Kristopher T.; Coumans, Jean-Valery] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Ortman, Amy J.; Peterfreund, Robert A.] Harvard Univ, Sch Med, Dept Anesthesia Crit Care & Pain Med, Boston, MA USA.
[Aghi, Manish] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA 94143 USA.
RP Coumans, JV (reprint author), Massachusetts Gen Hosp, Dept Neurosurg, 15 Parkman St, Boston, MA 02114 USA.
EM jcoumans@partners.org
NR 15
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0967-5868
J9 J CLIN NEUROSCI
JI J. Clin. Neurosci.
PD AUG
PY 2010
VL 17
IS 8
BP 1085
EP 1088
DI 10.1016/j.jocn.2009.12.010
PG 4
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 623GK
UT WOS:000279726700037
PM 20580996
ER
PT J
AU Liu, F
Williams, RM
Liu, HE
Chien, NH
AF Liu, Fen
Williams, Rhonda M.
Liu, Hsueh-Erh
Chien, Nai-Hui
TI The lived experience of persons with lower extremity amputation
SO JOURNAL OF CLINICAL NURSING
LA English
DT Article
DE lived experience; lower extremity amputation; nurses; nursing;
qualitative research
ID LOWER-LIMB AMPUTATION; DIABETIC-PATIENTS; REHABILITATION; ADJUSTMENT;
MANAGEMENT; TRAUMA; DEFINITION; AMPUTEES; CARE
AB Aim.
The aim of this study was to describe and understand the lived experience of people with lower extremity amputation.
Background.
The loss of a body part can cause physical, psychological and social disturbances. The majority of previous studies in this area focus on the impact of amputation or the effectiveness of rehabilitation programmes. This is the first study in Taiwan exploring the holistic experiences of persons with amputation.
Design.
A phenomenological research design was used.
Methods.
Semi-structured interviews were performed with 22 people with lower extremity amputation. Interviews were tape-recorded and transcribed verbatim. Data were analysed using Colaizzi's phenomenological analysis method.
Results.
The lived experience of persons with lower extremity amputation could be categorised into the following four themes: 'lost in the dark woods', 'emotional collapse', 'difficulty in passing through the shadow' and 'igniting a gleam of hope'.
Conclusions.
Participants described suffering in physical, psychological and sociocultural realms and the ways they strived to cope with these challenges. The findings of this study provide an enhanced understanding of the experiences of people with lower extremity amputation and underscore the importance of truly listening and responding to their concerns. The need to appreciate cultural context and to develop the peer-based support programme was highlighted.
Relevance to clinical practice.
Health professionals need to acknowledge the real needs of people with lower extremity amputation and provide them a clear explanation regarding the short-term and long-term health issues associated with amputation during the pre- and post-amputation phase. Health professionals also need to expand the scope of services beyond a physical and prosthetic focus. Supportive psychological and social interventions such as formal support groups and peer support programmes may provide a powerful and inexpensive addition to routine care. Currently, such programmes are unavailable in Taiwan.
C1 [Liu, Hsueh-Erh] Chang Gung Univ, Sch Nursing, Tao Yuan, Taiwan.
[Liu, Fen] Chang Gung Univ, Coll Med, Grad Inst Clin Med Sci, Tao Yuan, Taiwan.
[Liu, Fen; Chien, Nai-Hui] Chang Gung Inst Technol, Dept Nursing, Tao Yuan, Taiwan.
[Williams, Rhonda M.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Williams, Rhonda M.] Univ Washington, Seattle, WA 98195 USA.
RP Liu, HE (reprint author), Room 33,7F,2nd Med Bldg,259 Wen Haw 1st Rd, Tao Yuan, Taiwan.
EM sarah@mail.cgu.edu.tw
FU Chang Gung Institute of Technology
FX We thank all persons who participated in this study and the prosthetic
rehabilitation centres that provided us with access to these
participants. Funding for this study was received gratefully from Chang
Gung Institute of Technology.
NR 45
TC 11
Z9 12
U1 2
U2 20
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0962-1067
J9 J CLIN NURS
JI J. Clin. Nurs.
PD AUG
PY 2010
VL 19
IS 15-16
BP 2152
EP 2161
DI 10.1111/j.1365-2702.2010.03256.x
PG 10
WC Nursing
SC Nursing
GA 626AI
UT WOS:000279937600010
PM 20659195
ER
PT J
AU Kindler, HL
Niedzwiecki, D
Hollis, D
Sutherland, S
Schrag, D
Hurwitz, H
Innocenti, F
Mulcahy, MF
O'Reilly, E
Wozniak, TF
Picus, J
Bhargava, P
Mayer, RJ
Schilsky, RL
Goldberg, RM
AF Kindler, Hedy Lee
Niedzwiecki, Donna
Hollis, Donna
Sutherland, Susan
Schrag, Deborah
Hurwitz, Herbert
Innocenti, Federico
Mulcahy, Mary Frances
O'Reilly, Eileen
Wozniak, Timothy F.
Picus, Joel
Bhargava, Pankaj
Mayer, Robert J.
Schilsky, Richard L.
Goldberg, Richard M.
TI Gemcitabine Plus Bevacizumab Compared With Gemcitabine Plus Placebo in
Patients With Advanced Pancreatic Cancer: Phase III Trial of the Cancer
and Leukemia Group B (CALGB 80303)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; COOPERATIVE-ONCOLOGY-GROUP; METASTATIC
BREAST-CANCER; CLINICAL-TRIALS; NUDE-MICE; ANGIOGENESIS; COMBINATION;
ANTIBODY; TUMOR; MICROENVIRONMENT
AB Purpose
The combination of gemcitabine plus bevacizumab produced a 21% response rate and a median survival of 8.8 months in a multicenter phase II trial in patients with metastatic pancreatic cancer. These encouraging data led Cancer and Leukemia Group B (CALGB) to conduct a double-blind, placebo-controlled, randomized phase III trial of gemcitabine/bevacizumab versus gemcitabine/placebo in advanced pancreatic cancer patients.
Patients and Methods
Eligible patients had no prior therapy for advanced disease, Eastern Cooperative Oncology Group (ECOG) performance status 0 to 2, no tumor invasion of adjacent organs, and no increased bleeding risk. The primary end point was overall survival. Patients were stratified by performance status, extent of disease, and prior radiotherapy. Patients received gemcitabine at 1,000 mg/m(2) over 30 minutes on days 1, 8, and 15 every 28 days and bevacizumab at 10 mg/kg or placebo on days 1 and 15 every 28 days.
Results
Between June 2004 and April 2006, 602 patients were enrolled onto the study and 535 were treated. Median overall survival was 5.8 months for gemcitabine/bevacizumab and 5.9 months for gemcitabine/placebo (P = .95). Median progression-free survival was 3.8 and 2.9 months, respectively (P = .07). Overall response rates were 13% and 10%, respectively. Patients with a performance status of 0, 1, and 2 survived a median of 7.9, 4.8, and 2.4 months, respectively. The only statistically significant differences in grades 3 and 4 toxicity occurred for hypertension (10% v 3%; P < .001) and proteinuria (5% v 1%; P = .002); venous thrombosis grade >= 3 was equivalent in both arms (14% and 15%, respectively).
Conclusion
The addition of bevacizumab to gemcitabine does not improve survival in advanced pancreatic cancer patients.
C1 [Kindler, Hedy Lee] Univ Chicago, Canc Res Ctr, Hematol Oncol Sect, Chicago, IL 60637 USA.
NW Univ Feinberg, Sch Med, Chicago, IL USA.
Duke Univ, Med Ctr, Canc & Leukemia Grp, Stat Ctr B, Durham, NC 27706 USA.
Univ N Carolina, Chapel Hill, NC USA.
Dana Farber Canc Inst, Boston, MA 02115 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Delaware Christiana Care Community Clin Oncol Pro, Wilmington, DE USA.
Helen F Graham Canc Ctr, Wilmington, DE USA.
Washington Univ, Sch Med, St Louis, MO USA.
RP Kindler, HL (reprint author), Univ Chicago, Canc Res Ctr, Hematol Oncol Sect, 5841 S Maryland Ave,MC 2115, Chicago, IL 60637 USA.
EM hkindler@medicine.bsd.uchicago.edu
RI Goldberg , Richard/M-1311-2013
FU National Cancer Institute to Cancer [CA31946]; Leukemia Group B [80303];
CALGB Statistical Center [CA33601]; Hedy Lee Kindler; Eli Lilly;
Genentech; Herbert Hurwitz; Roche; Richard M. Goldberg; [CA41287]; [CA
32291]; [CA47577]; [CA21115]; [CA17145]; [CA77651]; [CA45418];
[CA77440]; [CA47559]
FX Supported, in part, by Grants No. CA31946 from the National Cancer
Institute to Cancer and Leukemia Group B 80303 (CALGB 80303) trial (R.
L. S.), No. CA33601 to the CALGB Statistical Center (S. G.), and No.
CA41287, CA 32291, CA47577, CA21115, CA17145, CA77651, CA45418, CA77440,
and CA47559.; Stock Ownership: None Honoraria: Herbert Hurwitz, Roche
Research Funding: Hedy Lee Kindler, Eli Lilly, Genentech; Herbert
Hurwitz, Genentech, Roche; Richard M. Goldberg, Genentech Expert
Testimony: None Other Remuneration: Pankaj Bhargava, AVEO
Pharmaceuticals
NR 37
TC 388
Z9 398
U1 3
U2 19
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD AUG 1
PY 2010
VL 28
IS 22
BP 3617
EP 3622
DI 10.1200/JCO.2010.28.1386
PG 6
WC Oncology
SC Oncology
GA 633GA
UT WOS:000280486700013
PM 20606091
ER
PT J
AU Lin, N
Moy, B
Come, S
Winer, E
AF Lin, Nancy
Moy, Beverly
Come, Steven
Winer, Eric
TI Dose-Dense Doxorubicin and Cyclophosphamide Followed by Weekly
Paclitaxel With Trastuzumab and Lapatinib in
HER2/neu-Overexpressed/Amplified Breast Cancer Is Not Feasible Because
of Excessive Diarrhea (vol 28, pg 2982, 2010)
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Correction
C1 [Lin, Nancy; Moy, Beverly; Come, Steven; Winer, Eric] Dana Farber Canc Inst, Harvard Canc Ctr, Boston, MA 02115 USA.
RP Lin, N (reprint author), Dana Farber Canc Inst, Harvard Canc Ctr, Boston, MA 02115 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD AUG 1
PY 2010
VL 28
IS 22
BP 3670
EP 3670
DI 10.1200/JCO.2010.31.3510
PG 1
WC Oncology
SC Oncology
GA 633GA
UT WOS:000280486700021
ER
PT J
AU Chang, T
Fava, M
AF Chang, Trina
Fava, Maurizio
TI The Future of Psychopharmacology of Depression
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID SEROTONIN REUPTAKE INHIBITORS; NICOTINIC ACETYLCHOLINE-RECEPTORS;
POSITRON-EMISSION-TOMOGRAPHY; BUPROPION SUSTAINED-RELEASE; SUBSTANCE-P
RECEPTORS; MAJOR DEPRESSION; SEXUAL DYSFUNCTION; DOUBLE-BLIND;
ANTIDEPRESSANT TREATMENT; VENLAFAXINE-XR
AB There are clear limitations to the currently approved pharmacotherapies of depression, including the fact that they are all essentially monoamine-based, have modest efficacy and a relatively slow onset of efficacy, and suffer from significant tolerability issues, particularly in the long term, including sexual dysfunction, weight gain, and cognitive impairments. This article reviews some of the most promising novel mechanisms that are not represented in compounds currently approved for depression in either the United States or Europe and that May represent the future of the psychopharmacologic treatment of depression, potentially addressing some of the efficacy and tolerability issues of antidepressants on the market. These potential antidepressant treatments include the multimodal serotonergic agents, the triple uptake inhibitors, the neurokinin-based novel therapies, the glutamatergic treatments, the nicotinic receptor-based treatments, the neurogenesis-based treatments, and antiglucocorticoid therapies. Some of these mechanisms appear to be more advanced in terms of drug development than others, but they all contribute to the global effort to develop more effective and better tolerated treatments for major depressive disorder. J Clin Psychiatry 2010;71(8):971-975 (C) Copyright 2010 Physicians Postgraduate Press, Inc.
C1 [Chang, Trina; Fava, Maurizio] Massachusetts Gen Hosp, Depress Clin & Res Program, Boston, MA 02114 USA.
RP Fava, M (reprint author), Massachusetts Gen Hosp, Depress Clin & Res Program, 55 Fruit St,Bulfinch 351, Boston, MA 02114 USA.
EM MFava@Partners.org
FU GlaxoSmithKline; Harvard Medical School; Abbott; Alkermes; Aspect
Medical Systems; AstraZeneca; BioResearch; BrainCells; Bristol-Myers
Squibb; Cephalon; Clinical Trials Solutions; Covidien; Eli Lilly;
EnVivo; Forest; Ganeden Biotech; Johnson Johnson; Lichtwer; Lorex;
Novartis; Organon; PamLab; Pfizer; Roche; RTC Logic; Sanofi-Aventis;
Shire; Solvay; Synthelabo; Wyeth-Ayerst; T-32 Research [MH-19126]
FX Dr Chang has received grant/research support from GlaxoSmithKline and
Harvard Medical School. Dr Fava has received research support from
Abbott, Alkermes, Aspect Medical Systems, AstraZeneca, BioResearch,
BrainCells, Bristol-Myers Squibb, Cephalon, Clinical Trials Solutions,
Covidien, Eli Lilly, EnVivo, Forest, Ganeden Biotech, GlaxoSmithKline,
Johnson & Johnson, Lichtwer, Lorex, Novartis, Organon, PamLab, Pfizer,
Roche, RTC Logic, Sanofi-Aventis, Shire, Solvay, Synthelabo, and
Wyeth-Ayerst; has been an advisor/consultant for Abbott, Affectis,
Amarin, Aspect Medical Systems, AstraZeneca, Auspex, Bayer, Best
Practice Project Management, BioMarin, Biovail, BrainCells,
Bristol-Myers Squibb, CeNeRx, Cephalon, Clinical Trials Solutions', CNS
Response, Compellis, Cypress, Dov, Eisai, Eli Lilly, EPIX, Euthymics
Bioscience; Fabre-Kramer, Forest, GenOmind, GlaxoSmithKline, Gruenthal,
Janssen, Jazz, Johnson & Johnson, Knoll, Labopharm, Lorex, Lundbeck,
MedAvante, Merck, Methylation Sciences, Neuronetics, Novartis, Nutrition
21, Organon, PamLab, Pfizer, PharmaStar, Pharmavite, Precision Human
Biolaboratory, Prexa, PsychoGenics, Psylin Neurosciences, Rexahn, Ridge
Diagnostics, Roche, RCT Logic, Sanofi-Aventis, Sepracor,
Schering-Plough, Solvay, Somaxon, Somerset, Synthelabo, Takeda,
Tetragenex, TransForm, Transcept, Vanda, and Wyeth-Ayerst; has had
speaking/publishing affiliations with Adamed, Advanced Meeting Partners,
American Psychiatric Association, American Society of Clinical
Psychopharmacology, AstraZeneca, Belvoir Media Group, Boehringer
Ingelheim, Bristol-Myers Squibb, Cephalon, Eli Lilly, Forest,
GlaxoSmithKline, Imedex, MGH Psychiatry Academy/Primedia, MGH Psychiatry
Academy/Reed Elsevier, Novartis, Organon, Pfizer, PharmaStar, United
BioSource, and Wyeth-Ayerst; has equity holdings in Compellis; holds a
patent for SPCD and has a patent application for a combination of
azapirones and bupropion in MDD; and has received copyright royalties
for the MGH CPFQ, SFI, ATRQ, DESS, and SAFER.; Dr Chang is supported in
part by a T-32 Research Training Grant MH-19126 through the American
Psychiatric Association's Program for Minority Research Training in
Psychiatry.
NR 60
TC 21
Z9 22
U1 1
U2 6
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 AUG
PY 2010
VL 71
IS 8
BP 971
EP 975
DI 10.4088/JCP.10m06223blu
PG 5
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 643KY
UT WOS:000281296500001
PM 20797377
ER
PT J
AU Cizza, G
Nguyen, VT
Eskandari, F
Duan, ZG
Wright, EC
Reynolds, JC
Ahima, RS
Blackman, MR
AF Cizza, Giovanni
Nguyen, Vi T.
Eskandari, Farideh
Duan, Zhigang
Wright, Elizabeth C.
Reynolds, James C.
Ahima, Rexford S.
Blackman, Marc R.
CA POWER Study Grp
TI Low 24-Hour Adiponectin and High Nocturnal Leptin Concentrations in a
Case-Control Study of Community-Dwelling Premenopausal Women With Major
Depressive Disorder: The Premenopausal, Osteopenia/Osteoporosis, Women,
Alendronate, Depression (POWER) Study
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID PLASMA ADIPONECTIN; WEIGHT-LOSS; MARKERS; RISK; ASSOCIATION;
PULSATILITY; PREVALENCE; ADIPOKINES; BIOMARKERS; DYNAMICS
AB Objective: Major depressive disorder (MDD) is associated with immune system dysfunction and disruption of multiple circadian systems. Adiponectin is an adipo-cytokine with anti-inflammatory and antiatherogenic effects: Circulating concentrations are inversely related to adiposity and risks of metabolic syndrome and diabetes mellitus. Our goals were (1) to establish whether premenopausal women with MDD exhibit decreased plasma adiponectin concentrations and/or disruption of circadian adiponectin rhythmicity; (2) to assess whether there is a relationship between adiponectin and MDD; and (3) to explore the temporal relationships among adiponectin, leptin, corticotropin, and cortisol secretion.
Method: We conducted a case-control study of community-dwelling premenopausal women with DSM-IV MDD (n=23) and age- and body mass index (BMI)-matched control subjects (n=23). Main outcome measures were circulating concentrations of adiponectin, leptin, corticotropin, and cortisol measured hourly for 24 hours. Subjects were recruited from July 1, 2001, to February 28, 2003.
Results: Women with MDD had approximately 30% lower mean 24-hour concentration of adiponectin than did control subjects. Adiponectin concentration was inversely related to depression severity and total duration of disease, suggesting a causal link. In contrast, mean nocturnal leptin concentration was higher in the MDD versus control groups. Mean leptin concentration was inversely related to cortisol and adiponectin concentrations, both in subjects with depression and in control subjects. In cross-correlation analyses, the relationship between corticotropin and cortisol concentrations was stronger in women with MDD than in control subjects, a finding consistent with hypothalamic-pituitary-adrenal (HPA) axis activation in MDD.
Conclusions: In premenopausal women with MDD, reduced daily adiponectin production may increase the risk of diabetes mellitus, and elevated leptin may contribute to osteoporosis. J Clin Psychiatry 2010;71(8):1079-1087 (C) Copyright 2010 Physicians Postgraduate Press, Inc.
C1 [Cizza, Giovanni] NIDDK, Clin Endocrine Sect, Clin Endocrinol Branch, NIH,CRC, Bethesda, MD 20892 USA.
[Nguyen, Vi T.] Massachusetts Gen Hosp, Pediat Endocrine Unit, Boston, MA 02114 USA.
[Eskandari, Farideh] NIMH, Sect Neuroendocrine Immunol & Behav, Integrat Neural Immune Program, Intramural Res Program,NIH, Bethesda, MD 20892 USA.
[Duan, Zhigang; Wright, Elizabeth C.] NIDDK, Off Director, Bethesda, MD 20892 USA.
[Reynolds, James C.] NIH, Dept Radiol, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Ahima, Rexford S.] Univ Penn, Sch Med, Dept Med, Div Endocrinol Diabet & Metab, Philadelphia, PA 19104 USA.
[Blackman, Marc R.] NIH, Endocrine Sect, NCCAM, Bethesda, MD 20892 USA.
[Blackman, Marc R.] Vet Affairs Med Ctr, Res Serv, Washington, DC 20422 USA.
RP Cizza, G (reprint author), NIDDK, Clin Endocrine Sect, Clin Endocrinol Branch, NIH,CRC, Bldg 10,Rm 6-3940, Bethesda, MD 20892 USA.
EM cizzag@intra.niddk.nih.gov
FU NIMH; NIDDK; NCCAM, NIH, Bethesda, Maryland
FX The study was fully supported by the Intramural Research Programs of the
NIMH; NIDDK; and NCCAM, NIH, Bethesda, Maryland.
NR 45
TC 36
Z9 40
U1 0
U2 5
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 AUG
PY 2010
VL 71
IS 8
BP 1079
EP 1087
DI 10.4088/JCP.09m05314blu
PG 9
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 643KY
UT WOS:000281296500016
PM 20492842
ER
PT J
AU Fang, YR
Yuan, CM
Xu, YF
Chen, J
Wu, ZG
Cao, L
Yi, ZH
Hong, W
Wang, Y
Jiang, KD
Gao, KM
Cui, XJ
Nierenberg, AA
AF Fang, Yiru
Yuan, Chengmei
Xu, Yifeng
Chen, Jun
Wu, Zhiguo
Cao, Lan
Yi, Zhenghui
Hong, Wu
Wang, Yong
Jiang, Kaida
Gao, Keming
Cui, Xingjia
Nierenberg, Andrew A.
CA OPERATION Study Team
TI Comparisons of the Efficacy and Tolerability of Extended-Release
Venlafaxine, Mirtazapine, and Paroxetine in Treatment-Resistant
Depression A Double-Blind, Randomized Pilot Study in a Chinese
Population
SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Article
DE treatment-resistant depression; switch strategies; extended-release
venlafaxine; mirtazapine; paroxetine
ID STAR-ASTERISK-D; SEROTONIN REUPTAKE INHIBITORS; SWITCHING
ANTIDEPRESSANTS; REMISSION RATES; DISORDER; TRIAL; ALTERNATIVES;
OUTPATIENTS; DEFINITION; FLUOXETINE
AB To compare the efficacy and tolerability of antidepressants switch with extended-release venlafaxine (venlafaxine-XR), mirtazapine, and paroxetine in Chinese patients with major depressive disorder who had 2 consecutive unsuccessful antidepressant trials. One hundred fifty adult patients with treatment-resistant depression according to their medical records and/or response to current treatments were randomly assigned to receive fixed-dosage treatment of venlafaxine-XR 225 mg/d (n = 50), mirtazapine 45 mg/d (n = 55), or paroxetine 20 mg/d (n = 45) for 8 weeks. The primary outcome was the remission rates that were defined as a score 7 or lower on the 17-item Hamilton Rating Scale for Depression (HRSD-17). Secondary outcomes included the remission rate defined by the Self-Rating Depression Scale of 50 or lower and the response rate defined by a 50% reduction or greater on the HRSD-17 total score, and the improvement of patients' general health functions. The completion rates were 82% for venlafaxine-XR, 81.8% for mirtazapine, and 82.2% for paroxetine. Only one patient in paroxetine arm discontinued the study owing to an adverse event. The remission rates based on the HRSD-17 were 42.0% for venlafaxine-XR, 36.4% for mirtazapine, and 46.7% for paroxetine. There were no statistical significances between treatment arms in remission rates. Similarly, there were also no significant differences between groups in secondary outcome measure. Venlafaxine-XR, mirtazapine, and paroxetine were equally effective in the treatment of Chinese patients with major depressive disorder who failed at least 2 previous antidepressant treatments. Selecting any of these 3 antidepressants as a third-step antidepressant is a reasonable choice for this group of patients.
C1 [Fang, Yiru] Shanghai Jiao Tong Univ, Sch Med, Dept Psychiat, Div Mood Disorder,Shanghai Mental Hlth Ctr, Shanghai 200030, Peoples R China.
[Gao, Keming] Case Western Reserve Univ, Sch Med, Dept Psychiat,Mood & Anxiety Clin, Mood Disorders Program,Univ Hosp Case Med Ctr, Cleveland, OH 44106 USA.
[Cui, Xingjia] Univ Rochester, Med Ctr, Dept Psychiat, Rochester, NY 14642 USA.
[Cui, Xingjia] Canandaigua VA Med Ctr, Rochester, NY USA.
[Nierenberg, Andrew A.] Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Fang, YR (reprint author), Shanghai Jiao Tong Univ, Sch Med, Dept Psychiat, Div Mood Disorder,Shanghai Mental Hlth Ctr, 600 S Wan Ping Rd, Shanghai 200030, Peoples R China.
EM yirufang@yahoo.com.cn
FU Ministry of Science and Technology of China [2004BA720A21-02,
2006AA02Z430]; Science and Technology Commission of Shanghai
Municipality [064119533]; AstraZeneca; National Alliance for Research on
Schizophrenia and Depression; Pfizer; Bristol-Myers Squibb; Cederroth;
Cyberonics; Eli Lilly; Forest Pharmaceuticals; GlaxoSmithKline; Janssen
Pharmaceutica; Lichtwer Pharma; National Institute of Mental Health;
Organon; Stanley Foundation; Wyeth-Ayerst Laboratories
FX This work was supported by the "10th Five-year Plan"of National Key
Technologies R&D Program grants 2004BA720A21-02 (Ministry of Science and
Technology of China) and the "Climbing Mountain Action Plan" Program
grants 064119533 (Science and Technology Commission of Shanghai
Municipality) and partly supported by National High-tech R&D Program
(863 Program) grants 2006AA02Z430 (Ministry of Science and Technology of
China).; Dr Gao received grant support from AstraZeneca and National
Alliance for Research on Schizophrenia and Depression and was on an
advisory board of Schering-Plough and a speaker's bureau of Pfizer.; Dr
Nierenberg has provided scientific consultation for Bristol-Myers
Squibb, Janssen Pharmaceutica, Eli Lilly, Genaissance, GlaxoSmithKline,
Innapharma, Neuronetics, Pfizer, Sepracor, and Shire and has received
research support from Bristol-Myers Squibb, Cederroth, Cyberonics, Eli
Lilly, Forest Pharmaceuticals, GlaxoSmithKline, Janssen Pharmaceutica,
Lichtwer Pharma, National Alliance for Research on Schizophrenia and
Depression, National Institute of Mental Health, Organon, Pfizer,
Stanley Foundation, and Wyeth-Ayerst Laboratories. Dr Nierenberg has
also received honoraria from Cyberonics, Eli Lilly, GlaxoSmithKline, and
Wyeth-Ayerst Laboratories.
NR 41
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U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0271-0749
J9 J CLIN PSYCHOPHARM
JI J. Clin. Psychopharmacol.
PD AUG
PY 2010
VL 30
IS 4
BP 357
EP 364
DI 10.1097/JCP.0b013e3181e7784f
PG 8
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA 625MY
UT WOS:000279900700002
PM 20571433
ER
PT J
AU Myrick, H
Li, XB
Randall, PK
Henderson, S
Voronin, K
Anton, RF
AF Myrick, Hugh
Li, Xingbao
Randall, Patrick K.
Henderson, Scott
Voronin, Konstantin
Anton, Raymond F.
TI The Effect of Aripiprazole on Cue-Induced Brain Activation and Drinking
Parameters in Alcoholics
SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Article
DE neuroimaging; alcoholism; craving; aripiprazole
ID RAT NUCLEUS-ACCUMBENS; CLINICAL LABORATORY PARADIGM; EXTRACELLULAR
DOPAMINE; VENTRAL STRIATUM; ANTIPSYCHOTIC-DRUG; DOUBLE-BLIND; RECEPTOR
AVAILABILITY; RELAPSE PREVENTION; DEPENDENT SUBJECTS; PARTIAL AGONIST
AB Because the effects of alcohol and its environmental cues on brain dopamine have been implicated in the maintenance of heavy drinking, drugs that modify dopamine might be useful in reducing drinking or promoting abstinence. The goal of the current study was to use an established brain imaging paradigm to explore the effect of aripiprazole (final dose 15 mg over a 14-day period), a dopamine stabilizer medication, on alcohol cue-induced brain activation and drinking in alcoholics. Non-treatment-seeking alcoholics were randomly assigned aripiprazole (n = 14) or identical placebo (n = 16) and reported their alcohol use while taking study medication for 14 days before an alcohol cue-induced brain functional magnetic resonance imaging study. In a Philips 3.0-T magnetic resonance imaging scanner, subjects were given a sip of alcohol before viewing a randomized presentation alcoholic-and nonalcoholic-beverage photographs while subjects rated their urge to drink. During photograph presentation, changes in regional brain activity were measured, and differences between viewing alcoholic beverage and nonalcoholic beverages were compared within and between groups. Brain activity analysis revealed increased activation for placebo-treated subjects in the right ventral striatum (P < 0.005; threshold 15 voxels), while there was a blunting of activation in this area in the aripiprazole-treated subjects. Aripiprazole-treated subjects, compared with placebo-treated subjects, also had significantly less heavy drinking during the 14-day medication period. The study provides both novel and valuable information regarding the effect of aripiprazole on cue-induced brain activation and voluntary drinking during treatment.
C1 [Myrick, Hugh; Henderson, Scott] Med Univ S Carolina, Ralph H Johnson Dept Vet Affairs Med Ctr, Res & Dev Serv, Charleston, SC 29425 USA.
[Myrick, Hugh; Li, Xingbao; Randall, Patrick K.; Henderson, Scott; Voronin, Konstantin; Anton, Raymond F.] Med Univ S Carolina, Alcohol Res Ctr, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA.
[Myrick, Hugh; Li, Xingbao] Med Univ S Carolina, Ctr Adv Imaging Res, Charleston, SC 29425 USA.
RP Myrick, H (reprint author), Med Univ S Carolina, Ralph H Johnson Dept Vet Affairs Med Ctr, Res & Dev Serv, IOP 4N,67 President St,MSC 861, Charleston, SC 29425 USA.
EM myrickh@musc.edu
FU Charleston Alcohol Research Center [NIAAA P50 AA10761]; NIAAA [K23
AA00314]; VA Research and Development Service, Ralph H. Johnson
Department of Veterans Affairs Medical Center; Bristol-Myers Squibb
FX This work was funded by the Charleston Alcohol Research Center (NIAAA
P50 AA10761). Dr Myrick is also funded through NIAAA K23 AA00314 and the
VA Research and Development Service, Ralph H. Johnson Department of
Veterans Affairs Medical Center.; Drs Anton and Myrick have received
grant support from Bristol-Myers Squibb. Dr Myrick is a member of the
Bristol-Myers Squibb speakers' bureau, and Dr Anton has been a
consultant for Bristol-Myers Squibb. Drs Voronin, Li, and Randall and Mr
Henderson reported no biomedical financial interests or potential
conflicts of interest.
NR 72
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U1 5
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0271-0749
J9 J CLIN PSYCHOPHARM
JI J. Clin. Psychopharmacol.
PD AUG
PY 2010
VL 30
IS 4
BP 365
EP 372
DI 10.1097/JCP.0b013e3181e75cff
PG 8
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA 625MY
UT WOS:000279900700004
PM 20571434
ER
PT J
AU Schutt, RK
Schapira, L
Maniates, J
Santiccioli, J
Henlon, S
Bigby, J
AF Schutt, Russell K.
Schapira, Lidia
Maniates, Jennifer
Santiccioli, Jessica
Henlon, Silas
Bigby, JudyAnn
TI Community Health Workers' Support for Cancer Clinical Trials:
Description and Explanation
SO JOURNAL OF COMMUNITY HEALTH
LA English
DT Article
DE Community health workers; Cancer clinical trials; Medical research;
Community attitudes; Health care disparities
ID AGE-BASED DISPARITIES; MEDICAL-RESEARCH; AFRICAN-AMERICANS;
PARTICIPATION; CARE; RECRUITMENT; ATTITUDES; WOMEN
AB Ethnic differences in participation in cancer clinical trials slow advances in medical knowledge that can reduce health care disparities. Community health workers (CHWs) are an increasingly important bridge between the health care system and underserved communities and could play an important role in increasing rates of clinical trial participation. We investigated community health workers' orientations to medical research and cancer clinical trials with a mixed methods design: two focus groups, 11 intensive interviews, and a structured survey of 76 CHW training workshop participants. CHWs demonstrated high levels of commitment to improving the health of community members but considerable distrust of researchers' motives, low levels of knowledge about cancer clinical trials, and frequent perceptions of bias in the health care system. Support for research is associated with more research experience, self-assessed knowledge, and Hispanic ethnicity, but with less seniority as a CHW. Neither actual knowledge of cancer clinical trials nor perceptions of bias in the health care system were related to degree of support for medical research. Community health workers perceive bias in the health care system but recognize the importance of medical research and are interested in learning more about cancer clinical trials. Research experience increases support for medical research; education increases perceptions of health care system bias.
C1 [Schutt, Russell K.] Univ Massachusetts, Dept Sociol, Boston, MA 02125 USA.
[Schapira, Lidia] Massachusetts Gen Hosp, Ctr Canc, Gillette Ctr Breast Canc, Boston, MA 02114 USA.
[Maniates, Jennifer] Execut Off Hlth & Human Serv, Off Behav Hlth MassHlth, Boston, MA 02111 USA.
[Santiccioli, Jessica] Business Knowledge Serv, Holliston, MA 01746 USA.
[Bigby, JudyAnn] Commonwealth Massachusetts, Execut Off Hlth & Human Serv, Boston, MA 02108 USA.
RP Schutt, RK (reprint author), Univ Massachusetts, Dept Sociol, 100 Morrissey Blvd, Boston, MA 02125 USA.
EM russell.schutt@umb.edu
NR 36
TC 3
Z9 3
U1 1
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0094-5145
J9 J COMMUN HEALTH
JI J. Community Health
PD AUG
PY 2010
VL 35
IS 4
BP 417
EP 422
DI 10.1007/s10900-010-9267-0
PG 6
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 642TB
UT WOS:000281239700010
PM 20352478
ER
PT J
AU Harrington, EF
Crowther, JH
Shipherd, JC
AF Harrington, Ellen F.
Crowther, Janis H.
Shipherd, Jillian C.
TI Trauma, Binge Eating, and the "Strong Black Woman"
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
DE trauma; binge eating; Strong Black Woman; sociocultural factors
ID POSTTRAUMATIC-STRESS-DISORDER; SEXUAL EXPERIENCES SURVEY;
NATURAL-ENVIRONMENT; DIAGNOSTIC SCALE; BULIMIA-NERVOSA; AMERICAN WOMEN;
RISK-FACTORS; SELF; ABUSE; VALIDATION
AB Objective: The primary goal of this study was to test a culturally specific model of binge eating in African American female trauma survivors, investigating potential mechanisms through which trauma exposure and distress were related to binge eating symptomatology. Method: Participants were 179 African American female trauma survivors who completed questionnaires about traumatic experiences; emotional inhibition/regulation difficulties; self-silencing (prioritizing others' needs and adopting external self-evaluation standards); eating for psychological reasons; binge eating; and internalization of "Strong Black Woman" (SBW) ideology, an important cultural symbol emphasizing strength and self-sufficiency. Results: Structural path analysis supported the proposed model in which SBW ideology, emotional inhibition/regulation difficulties, and eating for psychological reasons mediated the relationship between trauma exposure/distress and binge eating. The proposed model provided better fit to the data than several competing models. Conclusions: These findings suggest that among African American trauma survivors, trauma exposure and distress predict greater internalization of SBW ideology, which is associated with emotional inhibition/regulation difficulties, eating for psychological reasons, and ultimately binge eating. Implications of these findings for assessment, treatment, and prevention efforts are discussed.
C1 [Harrington, Ellen F.; Shipherd, Jillian C.] VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA USA.
[Harrington, Ellen F.; Crowther, Janis H.] Kent State Univ, Dept Psychol, Kent, OH 44242 USA.
[Shipherd, Jillian C.] Boston Univ, Sch Med, Boston, MA 02215 USA.
RP Harrington, EF (reprint author), St Thomas Hosp, Summa Hlth Syst, Ctr Treatment & Study Traumat Stress, 4th Floor Ambulatory Bldg, Akron, OH 44310 USA.
EM harringtone@summa-health.org
NR 59
TC 29
Z9 29
U1 1
U2 8
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD AUG
PY 2010
VL 78
IS 4
BP 469
EP 479
DI 10.1037/a0019174
PG 11
WC Psychology, Clinical
SC Psychology
GA 637MV
UT WOS:000280823100003
PM 20658804
ER
PT J
AU Lester, K
Resick, PA
Young-Xu, Y
Artz, C
AF Lester, Kristin
Resick, Patricia A.
Young-Xu, Yinong
Artz, Caroline
TI Impact of Race on Early Treatment Termination and Outcomes in
Posttraumatic Stress Disorder Treatment
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
DE African Americans; posttraumatic stress disorder; cognitive processing
therapy; prolonged exposure; dropout
ID COGNITIVE-PROCESSING THERAPY; ADMINISTERED PTSD SCALE; BEHAVIORAL
THERAPY; AFRICAN-AMERICAN; RAPE VICTIMS; SELF-REPORT; PSYCHOTHERAPY;
AGORAPHOBIA; PREVALENCE; SERVICES
AB Objective: The present study investigated the influence of race on posttraumatic stress disorder (PTSD) treatment among 94 African American and 214 Caucasian female victims of interpersonal violence participating in 2 studies of cognitive behavioral treatment for PTSD that were conducted sequentially and continuously. Method: In each study, participants were randomized into 1 of 3 conditions. The first study compared cognitive processing therapy with prolonged exposure and a delayed treatment condition. In the second study, cognitive processing therapy was compared with its constituent components: cognitive therapy only and written accounts. Participants were assessed with the Clinician Administered PTSD Scale and the Structured Clinical Interview for DSM-IV, as well as through self-report measures of PTSD. Results: Analyses revealed that African Americans were significantly less likely to complete treatment compared with Caucasians (45% vs. 73%, respectively, p < .001) and that the differences held even after controlling for education and income. Despite racial differences in treatment completion status, analyses with the intent-to-treat sample indicated no racial differences in outcomes on PTSD measures. Conclusions: The lack of difference in treatment outcomes despite racial differences in dropout may be explained by greater symptom improvement of African Americans who dropped out compared with Caucasians who dropped out. Implications of these findings and practical approaches to addressing sociocultural barriers to care are explored.
C1 [Lester, Kristin; Resick, Patricia A.; Artz, Caroline] Vet Affairs Boston Healthcare Syst, Natl Ctr PTSD, Womens Hlth Sci Div, Boston, MA USA.
[Resick, Patricia A.] Boston Univ, Dept Psychiat, Boston, MA 02215 USA.
[Resick, Patricia A.] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
[Young-Xu, Yinong] Vet Affairs Med Ctr, Natl Ctr PTSD, Execut Div, White River Jct, VT USA.
RP Lester, K (reprint author), Dept Vet Affairs Tuscaloosa, 116-PSY,3701 Loop Rd, Tuscaloosa, AL 35404 USA.
EM kristin.lester@va.gov
NR 39
TC 31
Z9 31
U1 3
U2 7
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD AUG
PY 2010
VL 78
IS 4
BP 480
EP 489
DI 10.1037/a0019551
PG 10
WC Psychology, Clinical
SC Psychology
GA 637MV
UT WOS:000280823100004
PM 20658805
ER
PT J
AU Hirshfeld-Becker, DR
Masek, B
Henin, A
Blakely, LR
Pollock-Wurman, RA
McQuade, J
DePetrillo, L
Briesch, J
Endick, TH
Rosenbaum, JF
Biederman, J
AF Hirshfeld-Becker, Dina R.
Masek, Bruce
Henin, Aude
Blakely, Lauren Raezer
Pollock-Wurman, Rachel A.
McQuade, Julia
DePetrillo, Lillian
Briesch, Jacquelyn
Endick, Thomas H.
Rosenbaum, Jerrold F.
Biederman, Joseph
TI Cognitive Behavioral Therapy for 4-to 7-Year-Old Children With Anxiety
Disorders: A Randomized Clinical Trial
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
DE childhood anxiety disorders; cognitive behavioral therapy; preschoolers;
behavioral inhibition; randomized clinical trial
ID PRESCHOOL-CHILDREN; FOLLOW-UP; PSYCHIATRIC-DISORDERS; PSYCHOSOCIAL
IMPAIRMENT; EARLY INTERVENTION; CHILDHOOD ANXIETY; REFERRED CHILDREN;
ANXIOUS CHILDREN; SOCIAL ANXIETY; PANIC DISORDER
AB Objective: To examine the efficacy of a developmentally appropriate parent child cognitive behavioral therapy (CBI) protocol for anxiety disorders in children ages 4-7 years. Method: Design: Randomized wait-list controlled trial. Conduct: Sixty-four children (53% female, mean age 5.4 years, 80% European American) with anxiety disorders were randomized to a parent child CBT intervention (n = 34) or a 6-month wait-list condition (n = 30). Children were assessed by interviewers blind to treatment assignment, using structured diagnostic interviews with parents, laboratory assessments of behavioral inhibition, and parent questionnaires. Analysis: Chi-square analyses of outcome rates and linear and ordinal regression of repeated measures, examining time by intervention interactions. Results: The response rate (much or very much improved on the Clinical Global Impression Scale for Anxiety) among 57 completers was 69% versus 32% (CBT vs. controls), p < .01; intent-to-treat: 59% vs. 30%, p = .016. Treated children showed a significantly greater decrease in anxiety disorders (effect size [ES] = .55) and increase in parent-rated coping (ES = .69) than controls, as well as significantly better CGI improvement on social phobia/avoidant disorder (ES = .95), separation anxiety disorder (ES = .82), and specific phobia (ES = .78), but not on generalized anxiety disorder. Results on the Child Behavior Checklist Internalizing scale were not significant and were limited by low return rates. Treatment response was unrelated to age or parental anxiety but was negatively predicted by behavioral inhibition. Gains were maintained at 1-year follow-up. Conclusions: Results suggest that developmentally modified parent child CBT may show promise in 4- to 7-year-old children.
C1 [Hirshfeld-Becker, Dina R.; Masek, Bruce; Henin, Aude; Blakely, Lauren Raezer; Pollock-Wurman, Rachel A.; McQuade, Julia; DePetrillo, Lillian; Briesch, Jacquelyn; Rosenbaum, Jerrold F.; Biederman, Joseph] Massachusetts Gen Hosp, Dept Psychiat, Cambridge, MA 02138 USA.
[Hirshfeld-Becker, Dina R.; Masek, Bruce; Henin, Aude; Pollock-Wurman, Rachel A.; Rosenbaum, Jerrold F.; Biederman, Joseph] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Endick, Thomas H.] Virginia Polytech Inst & State Univ, Dept Psychol, Blacksburg, VA 24061 USA.
RP Hirshfeld-Becker, DR (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 185 Alewife Brook Pkway,Suite 2000, Cambridge, MA 02138 USA.
EM dhirshfeld@partners.org
OI McQuade, Julia/0000-0001-9278-3345
FU NIMH NIH HHS [K08 MH001538]
NR 63
TC 79
Z9 80
U1 2
U2 33
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD AUG
PY 2010
VL 78
IS 4
BP 498
EP 510
DI 10.1037/a0019055
PG 13
WC Psychology, Clinical
SC Psychology
GA 637MV
UT WOS:000280823100006
PM 20658807
ER
PT J
AU Holmbeck, GN
DeLucia, C
Essner, B
Kelly, L
Zebracki, K
Friedman, D
Jandasek, B
AF Holmbeck, Grayson N.
DeLucia, Christian
Essner, Bonnie
Kelly, Lauren
Zebracki, Kathy
Friedman, Deborah
Jandasek, Barbara
TI Trajectories of Psychosocial Adjustment in Adolescents With Spina
Bifida: A 6-Year, Four-Wave Longitudinal Follow-Up
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
DE spina bifida; psychosocial adjustment; growth analyses; adolescence
ID EXECUTIVE FUNCTIONS; FAMILIES; CHILDREN; PERSPECTIVE; MULTIMETHOD;
PSYCHOLOGY; TRANSITION; ATTENTION; CONFLICT; ILLNESS
AB Objective: As a follow-up to an earlier cross-sectional study (Holmbeck et al., 2003), the current multimethod, multi-informant investigation examined individual growth in psychosocial adjustment across the adolescent transition in 2 samples: young adolescents with spina bifida (SB) and typically developing adolescents (N = 68 in both groups at Time 1). Method: Growth curve modeling procedures were used to describe the developmental course of psychosocial adjustment across 4 waves of data collection from ages 8 to 15. Child gender was included in the models as a moderator of associations between illness status and adjustment trajectories. Results and Conclusions: Findings revealed that preadolescent differences between groups were maintained for several adjustment variables, indicating that adolescents with SB have enduring academic and attention problems and difficulties with social development (e.g., fewer friends and less influence during family interactions). For other outcomes, trajectories of adjustment levels for adolescents with SB converged on levels observed in comparison adolescents, indicating some areas of resilience. Girls with SB were at risk for increasing levels of social difficulties and negative perceptions of their physical appearance. Clinical implications are discussed.
C1 [Holmbeck, Grayson N.; Essner, Bonnie; Kelly, Lauren] Loyola Univ, Dept Psychol, Chicago, IL 60626 USA.
[DeLucia, Christian] Nova SE Univ, Ctr Psychol Studies, Ft Lauderdale, FL 33314 USA.
[Zebracki, Kathy] Shriners Hosp Children, Dept Psychol, Chicago, IL USA.
[Friedman, Deborah] Massachusetts Gen Hosp, Dept Child & Adolescent Psychiat, Boston, MA 02114 USA.
[Jandasek, Barbara] Bradley Hasbro Childrens Res Ctr, Dept Child & Adolescent Psychiat, Providence, RI USA.
RP Holmbeck, GN (reprint author), Loyola Univ, Dept Psychol, 6525 N Sheridan Rd, Chicago, IL 60626 USA.
EM gholmbe@luc.edu
FU NICHD NIH HHS [R01 HD048629]
NR 48
TC 24
Z9 24
U1 1
U2 7
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD AUG
PY 2010
VL 78
IS 4
BP 511
EP 525
DI 10.1037/a0019599
PG 15
WC Psychology, Clinical
SC Psychology
GA 637MV
UT WOS:000280823100007
PM 20658808
ER
PT J
AU Mueser, KT
Pratt, SI
Bartels, SJ
Swain, K
Forester, B
Cather, C
Feldman, J
AF Mueser, Kim T.
Pratt, Sarah I.
Bartels, Stephen J.
Swain, Karin
Forester, Brent
Cather, Corinne
Feldman, James
TI Randomized Trial of Social Rehabilitation and Integrated Health Care for
Older People With Severe Mental Illness
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
DE severe mental illness; social skills training; psychiatric
rehabilitation; aging; health management
ID LIVING SKILLS; PSYCHOSOCIAL INTERVENTION; SCHIZOPHRENIA-PATIENTS;
CONSENSUS STATEMENT; PSYCHOTIC DISORDERS; NEGATIVE SYMPTOMS;
SELF-EFFICACY; COMMUNITY; BEHAVIOR; GENDER
AB Objective: The Helping Older People Experience Success (HOPES) program was developed to improve psychosocial functioning and reduce long-term medical burden in older people with severe mental illness (SMI) living in the community. HOPES includes 1 year of intensive skills training and health management, followed by a 1-year maintenance phase. Method: To evaluate effects of HOPES on social skills and psychosocial functioning, we conducted a randomized controlled trial with 183 older adults with SMI (58% schizophrenia spectrum) age 50 and older at 3 sites who were assigned to HOPES or treatment as usual with blinded follow-up assessments at baseline and 1- and 2-year follow-up. Results: Retention in the HOPES program was high (80%). Intent-to-treat analyses showed significant improvements for older adults assigned to HOPES compared to treatment as usual in performance measures of social skill, psychosocial and community functioning, negative symptoms, and self-efficacy, with effect sizes in the moderate (.37-.63) range. Exploratory analyses indicated that men improved more than women in the HOPES program, whereas benefit from the program was not related to psychiatric diagnosis, age, or baseline levels of cognitive functioning, psychosocial functioning, or social skill. Conclusions: The results support the feasibility of engaging older adults with SMI in the HOPES program, an intensive psychiatric rehabilitation intervention that incorporates skills training and medical case management, and improves psychosocial functioning in this population. Further research is needed to better understand gender differences in benefit from the HOPES program.
C1 [Mueser, Kim T.; Pratt, Sarah I.; Swain, Karin] Dartmouth Psychiat Res Ctr, Concord, NH 03301 USA.
[Mueser, Kim T.; Pratt, Sarah I.; Swain, Karin] Dartmouth Med Sch, Dept Psychiat, Concord, NH USA.
[Mueser, Kim T.; Pratt, Sarah I.; Bartels, Stephen J.; Swain, Karin] Dartmouth Med Sch, Dept Community & Family Med, Concord, NH USA.
[Bartels, Stephen J.] Dartmouth Inst Hlth Care Policy & Clin Practice, Ctr Aging Res, Hanover, NH USA.
[Forester, Brent; Cather, Corinne; Feldman, James] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Forester, Brent] McLean Hosp, Boston, MA USA.
[Cather, Corinne] Massachusetts Gen Hosp, Schizophrenia Program, Boston, MA 02114 USA.
[Feldman, James] Massachusetts Mental Hlth Ctr, Boston, MA 02115 USA.
RP Mueser, KT (reprint author), Dartmouth Psychiat Res Ctr, Main Bldg,105 Pleasant St, Concord, NH 03301 USA.
EM kim.t.mueser@dartmouth.edu
FU NIMH NIH HHS [R01 MH062324, K23 MH080021, K23 MH080021-01A1, K23
MH080021-02, K23 MH080021-03, R01 MH062324-01A1, R01 MH62324]
NR 62
TC 32
Z9 32
U1 1
U2 7
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD AUG
PY 2010
VL 78
IS 4
BP 561
EP 573
DI 10.1037/a0019629
PG 13
WC Psychology, Clinical
SC Psychology
GA 637MV
UT WOS:000280823100011
PM 20658812
ER
PT J
AU Cao, H
Wang, J
Li, X
Florez, S
Huang, Z
Venugopalan, SR
Elangovan, S
Skobe, Z
Margolis, HC
Martin, JF
Amendt, BA
AF Cao, H.
Wang, J.
Li, X.
Florez, S.
Huang, Z.
Venugopalan, S. R.
Elangovan, S.
Skobe, Z.
Margolis, H. C.
Martin, J. F.
Amendt, B. A.
TI MicroRNAs Play a Critical Role in Tooth Development
SO JOURNAL OF DENTAL RESEARCH
LA English
DT Article
DE Dicer1; dental stem cells; craniofacial and tooth microRNAs; epithelial
differentiation
ID STEM-CELLS; AMELOGENESIS IMPERFECTA; DENTAL EPITHELIUM; MOUSE
DEVELOPMENT; DIFFERENTIATION; AMELOBLASTIN; PITX2; DICER
AB MicroRNAs are known to regulate gene function in many tissues and organs, but their expression and function, if any, in tooth development are elusive. We sought to identify them by microRNA screening analyses and reveal their overall roles by inactivating Dicer1 in the dental epithelium and mesenchyme. Discrete sets of microRNAs are expressed in molars compared with incisors as well as epithelium compared with mesenchyme. Conditional knockout (cKO) of Dicer1 (mature microRNAs) in the dental epithelium of the Pitx2-Cre mouse results in multiple and branched enamel-free incisors and cuspless molars, and change in incisor patterning and in incisor and molar size and shape. Analyses of differentiating dental epithelial markers reveal a defect in ameloblast differentiation. Conversely, the cervical loop (stem cell niche) is expanded in Dicer1 cKO. These results demonstrate that tooth development is tightly controlled by microRNAs and that specific microRNAs regulate tooth epithelial stem cell differentiation.
C1 [Cao, H.; Wang, J.; Li, X.; Florez, S.; Huang, Z.; Venugopalan, S. R.; Martin, J. F.; Amendt, B. A.] Texas A&M Hlth Sci Ctr, Inst Biosci & Technol, Houston, TX 77030 USA.
[Elangovan, S.; Skobe, Z.; Margolis, H. C.] Forsyth Inst, Dept Biomineralizat, Boston, MA USA.
RP Amendt, BA (reprint author), Texas A&M Hlth Sci Ctr, Inst Biosci & Technol, 2121 W Holcombe Blvd, Houston, TX 77030 USA.
EM bamendt@ibt.tamhsc.edu
FU National Institute of Dental and Craniofacial Research [DE 13941]
FX We thank Drs. Tord A. Hjalt (University of Lund, Sweden) and Robert
Schwartz (TAMHSC-IBT) for reagents and technical advice, and members of
the Amendt laboratory for helpful discussions. Support for this research
was provided from grant DE 13941 from the National Institute of Dental
and Craniofacial Research to Brad A. Amendt.
NR 25
TC 49
Z9 49
U1 1
U2 9
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-0345
J9 J DENT RES
JI J. Dent. Res.
PD AUG
PY 2010
VL 89
IS 8
BP 779
EP 784
DI 10.1177/0022034510369304
PG 6
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 629JY
UT WOS:000280194800004
PM 20505045
ER
PT J
AU Chun, YHP
Yamakoshi, Y
Yamakoshi, F
Fukae, M
Hu, JCC
Bartlett, JD
Simmer, JP
AF Chun, Y. -H. P.
Yamakoshi, Y.
Yamakoshi, F.
Fukae, M.
Hu, J. C. -C.
Bartlett, J. D.
Simmer, J. P.
TI Cleavage Site Specificity of MMP-20 for Secretory-stage Ameloblastin
SO JOURNAL OF DENTAL RESEARCH
LA English
DT Article
DE proteases; enamel; tooth; fluorescent peptides
ID AMELOGENESIS IMPERFECTA PHENOTYPE; SHEATH PROTEINS; CALCIUM-BINDING;
ENAMEL PROTEINS; IMMATURE ENAMEL; MICE DISPLAY; RAT INCISOR; PORCINE;
EXPRESSION; CLONING
AB Ameloblastin is processed by protease(s) during enamel formation. We tested the hypothesis that MMP-20 (enamelysin) catalyzes the cleavages that generate secretory-stage ameloblastin cleavage products. We isolated a 23-kDa ameloblastin cleavage product from developing enamel and determined its N-terminus sequence. Ameloblastin was stably expressed and secreted from HEK293-H cells, purified, and digested with MMP-20 or Klk4 (kallikrein 4). The digests were analyzed by SDS-PAGE and Western blotting, and cleavage products were characterized by N-terminal sequencing. Six fluorescent peptides were digested with MMP-20 and Klk4 and analyzed by RP-HPLC and by mass spectrometry. MMP-20 cleaved each peptide exactly at the sites corresponding to ameloblastin cleavages catalyzed in vivo. Klk4 cleaved ameloblastin and the fluorescent peptides at sites not observed in vivo, and cleaved at only a single correct site: before Leu(171). We conclude that MMP-20 is the enzyme that processes ameloblastin during the secretory stage of amelogenesis, and we present a hypothesis about the sequence of ameloblastin cleavages.
C1 [Chun, Y. -H. P.] Univ Texas Hlth Sci Ctr San Antonio, Dept Periodont, San Antonio, TX 78229 USA.
[Fukae, M.] Tsurumi Univ, Sch Dent Med, Dept Biochem, Tsurumi Ku, Yokohama, Kanagawa 230, Japan.
[Bartlett, J. D.] Forsyth Inst, Dept Cytokine Biol, Boston, MA 02115 USA.
[Chun, Y. -H. P.; Yamakoshi, Y.; Yamakoshi, F.; Hu, J. C. -C.; Simmer, J. P.] Univ Michigan, Sch Dent, Dept Biol & Mat Sci, Ann Arbor, MI 48109 USA.
RP Simmer, JP (reprint author), Univ Michigan, Dent Res Lab, 1210 Eisenhower Pl, Ann Arbor, MI 48108 USA.
EM jsimmer@umich.edu
FU NIDCR/NIH [DE015846, DE0 16276]
FX We thank Mr. Tom Forton, Manager of the Michigan State University Meat
Laboratory, for assistance in obtaining fresh developing molars from
pigs slaughtered at that facility; Dr. Myron Crawford, Director of the
W. M. Keck Foundation Bio technology Resource Laboratory at Yale
University, and Nancy Williams for protein sequencing; and David Allen
of NextGen Sciences, Inc., for mass spectrometry. This research was
supported by USPHS Research Grants DE015846 and DE0 16276 (NIDCR/NIH).
All authors declare that there are no conflicting interests.
NR 35
TC 31
Z9 31
U1 0
U2 5
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-0345
J9 J DENT RES
JI J. Dent. Res.
PD AUG
PY 2010
VL 89
IS 8
BP 785
EP 790
DI 10.1177/0022034510366903
PG 6
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 629JY
UT WOS:000280194800005
PM 20400724
ER
PT J
AU Hoy, WE
Ingelfinger, JR
Hallan, S
Hughson, MD
Mott, SA
Bertram, JF
AF Hoy, W. E.
Ingelfinger, J. R.
Hallan, S.
Hughson, M. D.
Mott, S. A.
Bertram, J. F.
TI The early development of the kidney and implications for future health
SO JOURNAL OF DEVELOPMENTAL ORIGINS OF HEALTH AND DISEASE
LA English
DT Review
DE kidney development
ID LOW-BIRTH-WEIGHT; MATERNAL PROTEIN RESTRICTION; AUSTRALIAN ABORIGINAL
COMMUNITY; INTRAUTERINE GROWTH-RETARDATION; INDIVIDUAL GLOMERULAR
VOLUMES; SHORT PRENATAL EXPOSURE; ISCHEMIC-HEART-DISEASE;
CHRONIC-RENAL-FAILURE; MICE LACKING GDNF; BLOOD-PRESSURE
C1 [Hoy, W. E.; Mott, S. A.] Univ Queensland, Ctr Chron Dis, Herston, Qld 4029, Australia.
[Ingelfinger, J. R.] Harvard Univ, Harvard Med Sch, Boston, MA 02115 USA.
[Ingelfinger, J. R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Hallan, S.] Norwegian Univ Sci & Technol, Dept Canc Res & Mol Med, Trondheim, Norway.
[Hughson, M. D.] Univ Mississippi, Med Ctr, Dept Pathol, Jackson, MS 39216 USA.
[Bertram, J. F.] Monash Univ, Dept Anat & Dev Biol, Melbourne, Vic 3004, Australia.
RP Hoy, WE (reprint author), Univ Queensland, Ctr Chron Dis, Royal Brisbane& Womens Hosp, Hlth Sci Bldg Level 8, Herston, Qld 4029, Australia.
EM w.hoy@uq.edu.au
RI Hoy, Wendy/A-7325-2010; mott, susan/F-6262-2010; Bertram,
John/I-2588-2014
OI Hoy, Wendy/0000-0002-8405-1539; mott, susan/0000-0003-0117-4718;
Bertram, John/0000-0001-5863-6464
NR 177
TC 42
Z9 53
U1 1
U2 3
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
SN 2040-1744
J9 J DEV ORIG HLTH DIS
JI J. Dev. Orig. Health Dis.
PD AUG
PY 2010
VL 1
IS 4
BP 216
EP 233
DI 10.1017/S204017441000022X
PG 18
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 755DO
UT WOS:000289907100002
PM 25141870
ER
PT J
AU Manini, AF
McAfee, AT
Noble, VE
Bohan, JS
AF Manini, Alex F.
McAfee, Andrew T.
Noble, Vicki E.
Bohan, J. Stephen
TI PROGNOSTIC VALUE OF THE DUKE TREADMILL SCORE FOR EMERGENCY DEPARTMENT
PATIENTS WITH CHEST PAIN
SO JOURNAL OF EMERGENCY MEDICINE
LA English
DT Article
DE treadmill test; myocardial infarction; chest pain
ID CORONARY-ARTERY DISEASE; ASSOCIATION TASK-FORCE; PRACTICE GUIDELINES
COMMITTEE; AMERICAN-HEART-ASSOCIATION; ACUTE CARDIAC ISCHEMIA; CHRONIC
STABLE ANGINA; LOW-RISK PATIENTS; MYOCARDIAL-INFARCTION; UNSTABLE
ANGINA; EXERCISE SCORE
AB Background: The potential clinical utility of the Duke Treadmill Score (DTS) in the Emergency Department (ED) to risk-stratify patients with chest pain but negative cardiac biomarkers and non-diagnostic electrocardiograms is unclear. Objective: We evaluated whether DTS was associated with 30-day adverse cardiac outcomes for low-risk ED patients with chest pain. Methods: For this prospective, observational cohort study, the primary outcome was any of the following at 30 days: cardiac death, myocardial infarction, or coronary revascularization. DTS risk categories (low, intermediate, high) were compared with 30-day cardiac outcomes. Results: We enrolled 191 patients, of whom 20 (10%) were lost to follow-up, leaving 171 patients (mean age 53.3 +/- 12.4 years, 54% female, 3.5% adverse event rate) for evaluation. Sensitivity and specificity of DTS for 30-day events were 83.3% and 71.5%, respectively, with a 99.2% negative predictive value (confidence interval 95.4-99.9) for 30-day event-free survival. Conclusions: In this cohort of low-risk ED patients with chest pain, DTS demonstrated excellent negative predictive value for 30-day event-free survival and facilitated safe disposition of a large subset of patients. (C) 2010 Elsevier Inc.
C1 [Manini, Alex F.] Harvard Affiliated Emergency Med Residency, Boston, MA USA.
[McAfee, Andrew T.; Bohan, J. Stephen] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Emergency Med, Boston, MA USA.
[McAfee, Andrew T.] i3 Drug Safety, Auburndale, MA USA.
[Noble, Vicki E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA USA.
RP Manini, AF (reprint author), Mt Sinai Sch Med, 1 Gustave L Levy Pl,Box 1620, New York, NY 10029 USA.
FU Harvard Affiliated Emergency Medicine Residency; Dade Behring
Corporation
FX The study was supported by the Richard C. Wuerz Scholarship for
emergency medicine research from the Harvard Affiliated Emergency
Medicine Residency, and an unrestricted grant provided by the Dade
Behring Corporation.
NR 35
TC 9
Z9 10
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0736-4679
J9 J EMERG MED
JI J. Emerg. Med.
PD AUG
PY 2010
VL 39
IS 2
BP 135
EP 142
DI 10.1016/j.jemermed.2007.12.034
PG 8
WC Emergency Medicine
SC Emergency Medicine
GA 643IY
UT WOS:000281290000001
PM 19062225
ER
PT J
AU Yiadom, MYAB
AF Yiadom, Maame Yaa Maya A. B.
TI CLOPIDOGREL USE IN ST-ELEVATION MYOCARDIAL INFARCTION (STEMI)
SO JOURNAL OF EMERGENCY MEDICINE
LA English
DT Letter
ID ANTIPLATELET THERAPY
C1 [Yiadom, Maame Yaa Maya A. B.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Yiadom, Maame Yaa Maya A. B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Brigham & Womens Hosp, 75 Francis St, Boston, MA 02115 USA.
NR 5
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 0736-4679
J9 J EMERG MED
JI J. Emerg. Med.
PD AUG
PY 2010
VL 39
IS 2
BP 217
EP 218
DI 10.1016/j.jemermed.2008.08.025
PG 2
WC Emergency Medicine
SC Emergency Medicine
GA 643IY
UT WOS:000281290000017
PM 19168312
ER
PT J
AU Pallin, DJ
Sullivan, AF
Auerbach, BS
Camargo, CA
AF Pallin, Daniel J.
Sullivan, Ashley F.
Auerbach, Bruce S.
Camargo, Carlos A., Jr.
TI ADOPTION OF INFORMATION TECHNOLOGY IN MASSACHUSETTS EMERGENCY
DEPARTMENTS
SO JOURNAL OF EMERGENCY MEDICINE
LA English
DT Article
DE information technology; patient safety; medical error; medical
informatics; computerized patient order entry; decision support
AB Background: Information technology improves outcomes (e.g., by reducing error), and universal implementation of electronic medical records throughout the United States is a national goal. Prior studies have shown low rates of implementation. Objectives: To assess the current state of acquisition and implementation of information technology tools in Massachusetts emergency departments (EDs). Methods: This was part of a larger survey that sought to describe various attributes of all non-federal Massachusetts EDs. We asked about implementation of technologies listed below, and report proportions (95% confidence intervals) and medians (interquartile ranges). We compare responding to non-responding EDs to guard against response bias. Results: We identified and surveyed 74 non-federal EDs; 61 (82%) responded. Of these, the following number (%) reported full implementation of the following technologies: medication ordering, 9 (15%); medication error checking, 7 (11%); current visit information (e.g., chief complaint), 25 (41 %); computerized management recommendations based on clinical decision rules, 6 (10%); electronic laboratory results, 55 (90%); computerized clinical reminders, 10 (17%); tracking information, 31 (51%); hospital discharge summaries, 50 (82%); current outpatient medications, 15 (25%); ED visit notes, 30 (49%); radiographic images from a prior visit, 39 (64%); old electrocardiograms, 33 (54%); and computer system to collect real-time clinical data, 23 (38%). Conclusion: Massachusetts EDs have been slow to adopt evidence-based information technologies. A collaborative approach to determining the best available technologies and their implementation would decrease duplication of effort, frustration, and financial waste (due to non-implementation of acquired systems), and would facilitate inter-operability of ED computer systems. (C) 2010 Elsevier Inc.
C1 [Pallin, Daniel J.] Brigham & Womens Hosp, Dept Emergency Med, Boston, MA 02115 USA.
[Pallin, Daniel J.] Childrens Hosp, Div Emergency Med, Boston, MA 02115 USA.
[Sullivan, Ashley F.; Camargo, Carlos A., Jr.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Auerbach, Bruce S.] Sturdy Mem Hosp, Dept Emergency Med, Attleboro, MA USA.
RP Pallin, DJ (reprint author), Brigham & Womens Hosp, Dept Emergency Med, 75 Francis St, Boston, MA 02115 USA.
RI Pallin, Daniel/H-6382-2013
OI Pallin, Daniel/0000-0002-8517-9702
NR 9
TC 5
Z9 5
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0736-4679
J9 J EMERG MED
JI J. Emerg. Med.
PD AUG
PY 2010
VL 39
IS 2
BP 240
EP 243
DI 10.1016/j.jemermed.2008.09.030
PG 4
WC Emergency Medicine
SC Emergency Medicine
GA 643IY
UT WOS:000281290000022
PM 19232877
ER
PT J
AU El Muayed, M
Billings, LK
Raja, MR
Zhang, XM
Park, PJ
Newman, MV
Kaufman, DB
O'Halloran, TV
Lowe, WL
AF El Muayed, Malek
Billings, Liana K.
Raja, Meera R.
Zhang, Xiaomin
Park, Paul J.
Newman, Marsha V.
Kaufman, Dixon B.
O'Halloran, Thomas V.
Lowe, William L., Jr.
TI Acute cytokine-mediated downregulation of the zinc transporter ZnT8
alters pancreatic beta-cell function
SO JOURNAL OF ENDOCRINOLOGY
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; ACRODERMATITIS-ENTEROPATHICA GENE; INDUCIBLE
INSULIN-SECRETION; ACTIVATED PROTEIN-KINASES; NITRIC-OXIDE;
GLUCOSE-HOMEOSTASIS; NEURONAL DEATH; FASTING GLUCOSE; RAT THYMOCYTES;
RISK LOCI
AB Genetic studies suggest that Zn transporters such as ZnT8 play a role in insulin secretion by pancreatic beta-cells; however, little is known about the dynamic roles of Zn trafficking pathways on beta-cell physiology. To test the acute effects of the inflammatory cytokines interleukin 1 beta (IL1 beta) and tumor necrosis factor alpha (TNF alpha) on Zn homeostasis, the mRNA expression profile of Zn transporters of the ZnT and ZIP families was examined. Exposure of MIN6 cells or primary murine islets to IL1 beta or TNF alpha altered the mRNA expression profile of Zn transporters; most notable was decreased ZnT8 mRNA levels. siRNA-mediated gene knockdown was used to examine the effects of decreased ZnT8 expression in primary dispersed murine islet cells from C57/BL6 mice and MIN6 cells. ZnT8 knockdown in these murine islets led to reduced glucose stimulated insulin secretion without altering the total cellular insulin content or cell viability at normal or supraphysiological Zn concentrations. The labile Zn content determined by flow cytometry after loading with the Zn-specific sensor FluoZin-3 AM was decreased in MIN6 cells following ZnT8 knockdown or IL1 beta treatment. These results suggest that an acute decrease in ZnT8 levels impairs beta-cell function and Zn homeostasis, and may contribute to inflammatory cytokine-induced alterations in beta-cell function. Journal of Endocrinology (2010) 206, 159-169
C1 [El Muayed, Malek; Newman, Marsha V.; Lowe, William L., Jr.] Northwestern Univ, Feinberg Sch Med, Div Endocrinol Metab & Mol Med, Chicago, IL 60611 USA.
[Billings, Liana K.] Harvard Univ, Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Raja, Meera R.; O'Halloran, Thomas V.] Northwestern Univ, Chem Life Proc Inst, Evanston, IL 60208 USA.
[Raja, Meera R.; O'Halloran, Thomas V.] Northwestern Univ, Dept Chem, Evanston, IL 60208 USA.
[Zhang, Xiaomin; Kaufman, Dixon B.] Northwestern Univ, Feinberg Sch Med, Div Transplant Surg, Chicago, IL 60611 USA.
RP El Muayed, M (reprint author), Northwestern Univ, Feinberg Sch Med, Div Endocrinol Metab & Mol Med, 303 E Chicago Ave,Tarry 15-755, Chicago, IL 60611 USA.
EM m-muayed@northwestern.edu
FU Northwestern Memorial Foundation; NIH [R37GM038784, U42RR023245, T32
DK007169-27]; CCSG [P30 CA060553]; NASA Ames Research Center
[NNA04CC36G]
FX This study was funded by a Northwestern Memorial Foundation MD-Scientist
Fellowship in Genetic Medicine award for ME. The study was also funded
by two NIH grants: R37GM038784 (TVO) and U42RR023245 (TVO) and T32
DK007169-27 NRSA Institutional Training Grant (LKB). Imaging was
performed at the Northwestern University Cell Imaging Facility
generously supported by CCSG P30 CA060553 awarded to the Robert H Lurie
Comprehensive Cancer Center. ICP-MS Metal analysis was performed at the
Northwestern University Quantitative Bioelemental Imaging Center
generously supported by NASA Ames Research Center NNA04CC36G.
NR 75
TC 31
Z9 31
U1 0
U2 2
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 0022-0795
J9 J ENDOCRINOL
JI J. Endocrinol.
PD AUG
PY 2010
VL 206
IS 2
BP 159
EP 169
DI 10.1677/JOE-09-0420
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 626BM
UT WOS:000279940900002
PM 20508080
ER
PT J
AU Ayotte, BJ
Kressin, NR
AF Ayotte, Brian J.
Kressin, Nancy R.
TI Race Differences in Cardiac Catheterization: The Role of Social
Contextual Variables
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE race; differences; cardiac; catheterization
ID RACIAL-DIFFERENCES; DECISION-MAKING; PREFERENCES; DISPARITIES; HEALTH;
CARE; EXPERIENCES; BELIEFS; DISEASE; SURGERY
AB Race differences in the receipt of invasive cardiac procedures are well-documented but the etiology remains poorly understood.
We examined how social contextual variables were related to race differences in the likelihood of receiving cardiac catheterization in a sample of veterans who were recommended to undergo the procedure by a physician.
Prospective observational cohort study.
A subsample from a study examining race disparities in cardiac catheterization of 48 Black/African American and 189 White veterans who were recommended by a physician to undergo cardiac catheterization.
We assessed social contextual variables (e.g., knowing somebody who had the procedure, being encouraged by family or friends), clinical variables (e.g., hypertension, maximal medical therapy), and if participants received cardiac catheterization at any point during the study.
Blacks/African Americans were less likely to undergo cardiac catheterization compared to Whites even after controlling for age, education, and clinical variables (OR = 0.31; 95% CI, 0.13, 0.75). After controlling for demographic and clinical variables, three social contextual variables were significantly related to increased likelihood of receiving catheterization: knowing someone who had undergone the procedure (OR = 3.14; 95% CI, 1.70, 8.74), social support (OR = 2.05; 95% CI, 1.17, 2.78), and being encouraged by family to have procedure (OR = 1.45; 95% CI, 1.08, 1.90). After adding the social contextual variables, race was no longer significantly related to the likelihood of receiving catheterization, thus suggesting that social context plays an important role in the relationship between race and cardiac catheterization.
Our results suggest that social contextual factors are related to the likelihood of receiving recommended care. In addition, accounting for these relationships attenuated the observed race disparities between Whites and Blacks/African Americans who were recommended to undergo cardiac catheterization by their physicians.
C1 [Ayotte, Brian J.] VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA 02130 USA.
[Kressin, Nancy R.] Bedford VA Med Ctr, Ctr Hlth Qual Outcomes & Econ Res, Boston, MA USA.
[Kressin, Nancy R.] Boston Univ, Sch Med, Gen Internal Med Sect, Hlth Care Dispar Res Program, Boston, MA 02118 USA.
RP Ayotte, BJ (reprint author), VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, 150 S Huntington Ave 152M, Boston, MA 02130 USA.
EM brian.ayotte@va.gov
OI Kressin, Nancy/0000-0003-2767-4286
FU VA Health Services Research and Development Service (HSRD) [ECV97-022]
FX This research was supported by funding from the VA Health Services
Research and Development Service (HSR & D; ECV97-022, N. Kressin, P.
I.). Dr. Kressin is a Research Career Scientist, VA HSR&D (RCS
02-066-1); Dr. Ayotte is a VA HSR&D Post-doctoral fellow. 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 22
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PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD AUG
PY 2010
VL 25
IS 8
BP 814
EP 818
DI 10.1007/s11606-010-1324-y
PG 5
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 620MZ
UT WOS:000279505300017
PM 20383600
ER
PT J
AU Manze, M
Rose, AJ
Orner, MB
Berlowitz, DR
Kressin, NR
AF Manze, Meredith
Rose, Adam J.
Orner, Michelle B.
Berlowitz, Dan R.
Kressin, Nancy R.
TI Understanding Racial Disparities in Treatment Intensification for
Hypertension Management
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE disparities; treatment intensification; hypertension
ID BLOOD-PRESSURE CONTROL; UNITED-STATES; COGNITIVE REPRESENTATION;
MEDICATION ADHERENCE; THERAPEUTIC INERTIA; PREVALENCE; AWARENESS;
BELIEFS; CARE; QUESTIONNAIRE
AB Disparities in blood pressure (BP) control may be a function of disparities in treatment intensification (TI).
To examine racial differences in TI, understand modifiable factors that may mediate this relationship, and explore the relative effects of TI and race on blood pressure.
Prospective cohort study.
Participants were 819 black and white patients with hypertension from an urban, safety-net hospital
We sequentially explored the effects of patient race, sociodemographic and clinical characteristics, beliefs about BP/medications, perceptions of provider/discrimination, sodium intake, medication adherence, and provider counseling on TI, performing a series of random effects analyses. To assess the effects of race and TI on BP, we performed linear regressions, using systolic BP (SBP) as the outcome.
Unadjusted analyses and those including sociodemographic and clinical characteristics revealed that black patients had less TI than whites (-0.31 vs.-0.24, p < 0.001), but adjustment for patient beliefs and experiences eliminated the effects of race (beta =-0.02, p = 0.5). Increased patient concerns about BP medications were related to lower TI, as was more provider counseling (beta =-0.06, p = 0.02 and beta = -0.01, p = 0.001, respectively). In the unadjusted analysis, black race was a significant predictor of SBP (134 mm/Hg for blacks vs. 131 mm/Hg for whites, p = 0.009), but when both race and TI were included in the model, TI was a significant predictor of SBP (final SBP 2.0 mm/Hg lower for each additional therapy increase per 10 visits, p < 0.001), while race was not (Blacks 1.6 mm/Hg higher than whites, p = 0.17).
Improved patient-provider communication targeted towards addressing patient concerns about medications may have the potential to reduce racial disparities in TI and ultimately, BP control.
C1 [Manze, Meredith; Rose, Adam J.; Kressin, Nancy R.] Boston Univ, Sch Med, Gen Internal Med Sect, Boston, MA 02118 USA.
[Manze, Meredith; Berlowitz, Dan R.] Boston Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02118 USA.
[Rose, Adam J.; Orner, Michelle B.; Berlowitz, Dan R.; Kressin, Nancy R.] Bedford VA Med Ctr, Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA USA.
[Manze, Meredith; Kressin, Nancy R.] VA Boston Healthcare Syst, Boston, MA USA.
RP Manze, M (reprint author), VA Boston Healthcare Syst, Boston, MA USA.
EM meredith.manze@bmc.org
OI Kressin, Nancy/0000-0003-2767-4286
FU NIH/National Heart, Lung and Blood Institute [R01 HL072814]; Department
of Veterans Affairs Health Services Research and Development Service
FX This work was supported by the NIH/National Heart, Lung and Blood
Institute grant R01 HL072814 (N. Kressin, PI). Dr. Kressin is supported
in part by a Research Career Scientist Award from the Department of
Veterans Affairs Health Services Research and Development Service. Dr.
Rose is funded by a career development award from the Department of
Veterans Affairs Health Services Research and Development Service.
NR 28
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U2 13
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD AUG
PY 2010
VL 25
IS 8
BP 819
EP 825
DI 10.1007/s11606-010-1342-9
PG 7
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 620MZ
UT WOS:000279505300018
PM 20386998
ER
PT J
AU Pabon-Nau, LP
Cohen, A
Meigs, JB
Grant, RW
AF Pabon-Nau, Lina P.
Cohen, Amy
Meigs, James B.
Grant, Richard W.
TI Hypertension and Diabetes Prevalence Among US Hispanics by Country of
Origin: The National Health Interview Survey 2000-2005
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article; Proceedings Paper
CT 31st Annual Meeting of the Society-of-General-Internal-Medicine
CY APR 09-12, 2008
CL Pittsburgh, PA
SP Soc Gen Internal Med
DE diabetes; health status; hypertension; immigrant health; vulnerable
populations
ID NUTRITION-EXAMINATION-SURVEY; SELF-REPORTED HYPERTENSION; SAN-ANTONIO
HEART; CARDIOVASCULAR-DISEASE; MEXICAN-AMERICANS; UNITED-STATES;
PUERTO-RICANS; METABOLIC SYNDROME; CUBAN AMERICANS; RISK-FACTORS
AB Despite their diverse cultural origins, Hispanics in the US are generally studied as a single ethnic group.
1) Assess demographic and disease-related differences among U.S. Hispanics by country of origin, and 2) Examine the mediating roles of socioeconomic status and acculturation on disease prevalence in these subgroups.
Using data from the 2000-2005 National Health Interview Survey (NHIS), we compared characteristics of Mexican-Americans with Hispanics originally from: Mexico, Puerto Rico, Central/South America, Cuba, and Dominican Republic (n = 31,240). We stratified the analysis by foreign versus US-born Hispanic subgroups and modeled hypertension and diabetes prevalence, adjusting for demographic and acculturation differences.
The six Hispanic subgroups were significantly diverse in all measured variables. Prevalence of hypertension (32%) and diabetes (15%) was highest in foreign-born Puerto Ricans. After adjusting for age, BMI, smoking, socioeconomic status and acculturation in foreign-born Hispanics, Puerto Ricans (OR = 1.76 [95% CI: 1.23, 2.50], p = 0.002) and Dominicans (OR = 1.93 [1.24, 3.00], p = 0.004), had higher prevalence of hypertension relative to Mexican-Americans. Adjusted diabetes prevalence among foreign-born Hispanics was half or less in Cubans (OR = 0.42 [0.25, 0.68] p < 0.001), Dominicans (OR = 0.48 [0.26, 0.91], p = 0.02) and Central/South Americans (OR = 0.51 [0.33, 0.78], p = 0.002) relative to Mexican-Americans. Among US-born Hispanic subgroups, Cubans had lower hypertension (OR = 0.53, [0.33, 0.83], p = 0.006) and Mexicans (OR = 0.76 [0.60, 0.98], p = 0.03) had lower diabetes prevalence compared to Mexican-Americans in adjusted models.
The prevalence of hypertension and diabetes varies significantly among Hispanics by country of origin. Health disparities research should include representation from all Hispanic subgroups.
C1 [Pabon-Nau, Lina P.; Meigs, James B.; Grant, Richard W.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Cohen, Amy] Harvard Univ, Sch Publ Hlth, Dept Informat Technol, Boston, MA 02115 USA.
[Pabon-Nau, Lina P.] Massachusetts Gen Hosp, Dispar Solut Ctr, Boston, MA 02114 USA.
RP Pabon-Nau, LP (reprint author), Massachusetts Gen Hosp, Div Gen Med, 50 Staniford St,9th Floor, Boston, MA 02114 USA.
EM lpabon1@partners.org
OI Grant, Richard/0000-0002-6164-8025
FU NIDDK NIH HHS [K23 DK067452, K24 DK080140]; PHS HHS [NIDDK K24 DK080140,
T32HP11001]
NR 43
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U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD AUG
PY 2010
VL 25
IS 8
BP 847
EP 852
DI 10.1007/s11606-010-1335-8
PG 6
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 620MZ
UT WOS:000279505300022
PM 20490949
ER
PT J
AU Dublin, S
Glazer, NL
Smith, NL
Psaty, BM
Lumley, T
Wiggins, KL
Page, RL
Heckbert, SR
AF Dublin, Sascha
Glazer, Nicole L.
Smith, Nicholas L.
Psaty, Bruce M.
Lumley, Thomas
Wiggins, Kerri L.
Page, Richard L.
Heckbert, Susan R.
TI Diabetes Mellitus, Glycemic Control, and Risk of Atrial Fibrillation
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE arrhythmia; atrial fibrillation; diabetes mellitus; glycemic control;
diabetes complications
ID C-REACTIVE PROTEIN; OBSTRUCTIVE SLEEP-APNEA; INSULIN SENSITIVITY;
GLUCOSE-METABOLISM; INDEPENDENT RISK; PREVALENCE; POPULATION; OBESITY;
HEART; OLDER
AB Diabetes may be an independent risk factor for atrial fibrillation. However, results from prior studies are in conflict, and no study has examined diabetes duration or glycemic control.
To examine the association of diabetes with risk of atrial fibrillation and to describe risk according to diabetes duration and glycemic control.
A population-based case-control study.
Within a large, integrated healthcare delivery system, we identified 1,410 people with newly-recognized atrial fibrillation from ICD-9 codes and validated cases by review of medical records. 2,203 controls without atrial fibrillation were selected from enrollment lists, stratified on age, sex, hypertension, and calendar year.
Information on atrial fibrillation, diabetes and other characteristics came from medical records. Diabetes was defined based on physician diagnoses recorded in the medical record, and pharmacologically treated diabetes was defined as receiving antihyperglycemic medications. Information about hemoglobin A1c levels came from computerized laboratory data.
Among people with atrial fibrillation, 252/1410 (17.9%) had pharmacologically treated diabetes compared to 311/2203 (14.1%) of controls. The adjusted OR for atrial fibrillation was 1.40 (95% CI 1.15-1.71) for people with treated diabetes compared to those without diabetes. Among those with treated diabetes, the risk of developing atrial fibrillation was 3% higher for each additional year of diabetes duration (95% CI 1-6%). Compared to people without diabetes, the adjusted OR for people with treated diabetes with average hemoglobin A1c a parts per thousand currency sign7 was 1.06 (95% CI 0.74-1.51); for A1c > 7 but a parts per thousand currency sign8, 1.48 (1.09-2.01); for A1c > 8 but a parts per thousand currency sign9, 1.46 (1.02-2.08); and for A1c > 9, 1.96 (1.22-3.14).
Diabetes was associated with higher risk of developing atrial fibrillation, and risk was higher with longer duration of treated diabetes and worse glycemic control. Future research should identify and test approaches to reduce the risk of atrial fibrillation in people with diabetes.
C1 [Dublin, Sascha; Psaty, Bruce M.; Heckbert, Susan R.] Grp Hlth Res Inst, Seattle, WA 98101 USA.
[Dublin, Sascha; Smith, Nicholas L.; Psaty, Bruce M.; Heckbert, Susan R.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Glazer, Nicole L.; Psaty, Bruce M.; Wiggins, Kerri L.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
[Psaty, Bruce M.] Univ Washington, Dept Hlth Serv, Seattle, WA 98195 USA.
[Lumley, Thomas] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Page, Richard L.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Med, Madison, WI USA.
[Smith, Nicholas L.] VA Puget Sound Hlth Care Syst, Seattle Epidemiol Res & Informat Ctr, Seattle, WA USA.
RP Dublin, S (reprint author), Grp Hlth Res Inst, 1730 Minor Ave,Suite 1600, Seattle, WA 98101 USA.
EM dublin.s@ghc.org
FU National Heart, Lung and Blood Institute [HL 68986, HL 43201, HL 73410,
HL 68639]; Veterans' Affairs Health Services Research Development;
National Institute on Aging [K23AG028954]; Group Health Research
Institute; American Federation for Aging Research; Hartford Foundation;
Atlantic Philanthropies; Starr Foundation
FX This research was funded by grants HL 68986, HL 43201, HL 73410, and HL
68639 from the National Heart, Lung and Blood Institute. Dr. Dublin was
funded through a Veterans' Affairs Health Services Research &
Development fellowship, a Paul Beeson Career Development Award from the
National Institute on Aging (K23AG028954), and Group Health Research
Institute internal funds. The Beeson Award is also supported in part by
the American Federation for Aging Research, the Hartford Foundation, the
Atlantic Philanthropies and the Starr Foundation.
NR 40
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PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD AUG
PY 2010
VL 25
IS 8
BP 853
EP 858
DI 10.1007/s11606-010-1340-y
PG 6
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 620MZ
UT WOS:000279505300023
PM 20405332
ER
PT J
AU Keenan, CR
Dhaliwal, G
Henderson, MC
Bowen, JL
AF Keenan, Craig R.
Dhaliwal, Gurpreet
Henderson, Mark C.
Bowen, Judith L.
TI A 43-Year-Old Woman with Abdominal Pain and Fever
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Editorial Material
DE pattern recognition; analytic reasoning; problem representation;
clinical diagnostic reasoning
C1 [Keenan, Craig R.; Henderson, Mark C.] UC Davis Med Ctr, Dept Internal Med, Sacramento, CA 95817 USA.
[Dhaliwal, Gurpreet] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Dhaliwal, Gurpreet] San Francisco VA Med Ctr, San Francisco, CA USA.
[Bowen, Judith L.] Oregon Hlth & Sci Univ, Dept Med Informat & Clin Epidemiol, Portland, OR 97201 USA.
RP Keenan, CR (reprint author), UC Davis Med Ctr, Dept Internal Med, 4150 V St,Suite 2400, Sacramento, CA 95817 USA.
EM craig.keenan@ucdmc.ucdavis.edu
NR 7
TC 5
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U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD AUG
PY 2010
VL 25
IS 8
BP 874
EP 877
DI 10.1007/s11606-010-1372-3
PG 4
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 620MZ
UT WOS:000279505300027
PM 20440575
ER
PT J
AU Bray-Hall, S
Schmidt, K
Aagaard, E
AF Bray-Hall, Susan
Schmidt, Katrina
Aagaard, Eva
TI Toward Safe Hospital Discharge: A Transitions in Care Curriculum for
Medical Students
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE care transitions; curriculum development/evaluation; home visit;
undergraduate medical education; hospital discharge
ID RANDOMIZED CONTROLLED-TRIAL; FOLLOW-UP; INTERVENTION; QUALITY; EVENTS;
NEEDS
AB Medical errors often occur when patients move between care settings. Physicians generally receive little formal education on improving patient care transitions.
To develop a sustainable and effective Transition in Care Curriculum (TICC). Specific goals were to increase student confidence in and knowledge of skills necessary during care transitions at the time of hospital discharge, and to quantify the frequency of student-identified medication discrepancies during a post-discharge home visit.
TICC was delivered to 136 3rd-year medical students during their required inpatient medicine clerkship at six urban Denver hospitals. TICC consists of small and large group interactive sessions and self-directed learning exercises to provide foundational knowledge of care transitions. Experiential learning occurs through direct patient care at the time of discharge and during a follow-up home, hospice, or skilled nursing visit. Students completed a pre-post confidence measure, short answer and multiple choice questions, a post-clerkship satisfaction survey, and a standardized medication discrepancy tool.
Overall combined confidence in transitional care skills improved following the TICC from an average score of 2.7 (SD 0.9) to 4.0 (SD 0.8) (p < 0.01) on a 5-point confidence scale. They scored an average of 77% on the written discharge plan portion of the final exam. Students rated the usefulness of TICC at a mean of 3.1 (SD 0.7), above the combined mean of 2.7 for project work in all required clerkships. Students identified medication discrepancies during 43% of post-discharge visits (58 of 136). The most common reasons for discrepancies were patient lack of understanding of instructions and intentional non-adherence to medication plan.
TICC represents a feasible and effective program to teach evidence-based transitional care.
C1 [Bray-Hall, Susan] Denver VA Med Ctr, Denver, CO 80220 USA.
[Bray-Hall, Susan] Univ Colorado, Dept Med, Div Geriatr, Aurora, CO USA.
[Schmidt, Katrina] St Joseph Hosp, Dept Surg, Denver, CO USA.
RP Bray-Hall, S (reprint author), Denver VA Med Ctr, 1055 Clermont St 111-D, Denver, CO 80220 USA.
EM Susan.Bray-Hall@va.gov
FU John A. Hartford Foundation, Center of Excellence, Division of
Geriatrics, University of Colorado; John A. Hartford Center of
Excellence, University of Colorado Denver
FX Dr. Bray-Hall has received funding from the John A. Hartford Foundation,
Center of Excellence, Division of Geriatrics, University of Colorado.;
No sponsors or funders were involved in curricula design, data
collection, management, analysis and interpretation, or the preparation,
review and approval of the manuscript. This protocol was approved by the
Colorado and VA IRB as exempt.; This study was supported by a grant from
the John A. Hartford Center of Excellence, University of Colorado
Denver. The authors wish to thank Dr. Adam Abraham who helped secure the
grant and Drs. Daniel Matlock, Ethan Cumbler, and Jeannette Guerrasio
for facilitating the small group sessions.
NR 21
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U1 2
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD AUG
PY 2010
VL 25
IS 8
BP 878
EP 881
DI 10.1007/s11606-010-1364-3
PG 4
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 620MZ
UT WOS:000279505300028
PM 20443072
ER
PT J
AU Boulton, CL
Salzler, M
Mudgal, CS
AF Boulton, Christina L.
Salzler, Matthew
Mudgal, Chaitanya S.
TI Intramedullary Cannulated Headless Screw Fixation of a Comminuted
Subcapital Metacarpal Fracture: Case Report
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Article
DE Fixation; fracture; intramedullary; metacarpal; subcapital
ID PHALANGEAL FRACTURES; PLATE FIXATION; DISTAL RADIUS; HAND
AB This case report describes an alternative technique for the fixation of displaced comminuted subcapital fractures of the metacarpal with limited distal bone stock. Using a cannulated headless screw as an intramedullary device placed through the articular surface, we were able to secure proximal and distal bone purchase without excessive soft tissue stripping or disruption of the fracture hematoma. This technique allows early rehabilitation, and our patient went on to uneventful healing with excellent functional results. (J Hand Surg 2010; 35A:1260-1263. (C) 2010 Published by Elsevier Inc. on behalf of the American Society for Surgery of the Hand.)
C1 [Mudgal, Chaitanya S.] Harvard Univ, Orthopaed Hand Serv, Massachusetts Gen Hosp,Yawkey Ctr,Med Sch, Harvard Combined Orthopaed Residency Program, Boston, MA 02114 USA.
Harvard Univ, Orthopaed Hand Serv, Massachusetts Gen Hosp,Med Sch, Dept Orthopaed Surg, Boston, MA 02114 USA.
RP Mudgal, CS (reprint author), Harvard Univ, Orthopaed Hand Serv, Massachusetts Gen Hosp,Yawkey Ctr,Med Sch, Harvard Combined Orthopaed Residency Program, Suite 2100,55 Fruit St, Boston, MA 02114 USA.
EM cmudgal@partners.org
NR 13
TC 5
Z9 5
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 0363-5023
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD AUG
PY 2010
VL 35A
IS 8
BP 1260
EP 1263
DI 10.1016/j.jhsa.2010.04.032
PG 4
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 637MS
UT WOS:000280822800005
PM 20619555
ER
PT J
AU Ring, D
Barth, R
Barsky, A
AF Ring, David
Barth, Robert
Barsky, Arthur
TI Evidence-Based Medicine: Disproportionate Pain and Disability
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Editorial Material
C1 [Ring, David] Harvard Univ, Dept Orthopaed Surg, Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv,Med Sch, Boston, MA 02114 USA.
Brigham & Womens Hosp, Dept Psychiat, Boston, MA 02115 USA.
Parkridge Hosp, Chattanooga, TN USA.
RP Ring, D (reprint author), Harvard Univ, Dept Orthopaed Surg, Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv,Med Sch, Yawkey 2100,55 Fruit St, Boston, MA 02114 USA.
EM dring@partners.org
NR 15
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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 0363-5023
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD AUG
PY 2010
VL 35A
IS 8
BP 1345
EP 1347
DI 10.1016/j.jhsa.2010.06.007
PG 3
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 637MS
UT WOS:000280822800021
PM 20684932
ER
PT J
AU Delahanty, LM
AF Delahanty, L. M.
TI An expanded role for dietitians in maximising retention in nutrition and
lifestyle intervention trials: implications for clinical practice
SO JOURNAL OF HUMAN NUTRITION AND DIETETICS
LA English
DT Review
DE diabetes; lifestyle intervention; obesity; retention
ID DIABETES PREVENTION PROGRAM; CARDIOVASCULAR-DISEASE; COMPLICATIONS
TRIAL; REDUCTION; WEIGHT; DESIGN
AB The demand for clinical trials targeting lifestyle intervention has increased as a result of the escalation in obesity, diabetes mellitus and cardiovascular disease. Little is published about the strategies that dietitians have used to successfully screen potential study volunteers, implement interventions and maximise adherence and retention in large multicentre National Institutes of Health funded nutrition and lifestyle intervention clinical trials. This paper discusses an expanded role for the contributions of dietitians as members of an interdisciplinary team based on research experiences in the Diabetes Control and Complications Trial, Diabetes Prevention Program and Look AHEAD (Action for Health in Diabetes). Many of the strategies and insights discussed are also relevant to effective clinical practice. Dietitians need to broaden their scope of practice so that they are integrated proactively into the screening and intervention phases of large clinical trials to maximise retention and adherence to assigned nutrition, lifestyle and behavioural interventions. The skills of dietitians are a unique fit for this work and it is important that investigators and project managers consider including them in both the screening and intervention phases of such clinical trials to maximise retention results.
C1 Massachusetts Gen Hosp, Ctr Diabet, Boston, MA 02114 USA.
RP Delahanty, LM (reprint author), Massachusetts Gen Hosp, Ctr Diabet, Suite 340,50 Staniford St, Boston, MA 02114 USA.
EM ldelahanty@partners.org
NR 23
TC 12
Z9 12
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0952-3871
EI 1365-277X
J9 J HUM NUTR DIET
JI J. Hum. Nutr. Diet.
PD AUG
PY 2010
VL 23
IS 4
BP 336
EP 343
DI 10.1111/j.1365-277X.2009.01037.x
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 626AL
UT WOS:000279937900002
PM 20163510
ER
PT J
AU Delahanty, LM
AF Delahanty, L. M.
TI Research charting a course for evidence-based clinical dietetic practice
in diabetes
SO JOURNAL OF HUMAN NUTRITION AND DIETETICS
LA English
DT Review
DE diabetes; lifestyle intervention; obesity; retention
ID LIFE-STYLE INTERVENTION; IMPAIRED GLUCOSE-TOLERANCE; PREVENTION-PROGRAM;
COMPLICATIONS TRIAL; INTENSIVE THERAPY; CARDIOVASCULAR-DISEASE;
WEIGHT-LOSS; MELLITUS; METFORMIN; DESIGN
AB Nutrition and lifestyle interventions have been a critical component in three of the four largest clinical trials that focused on diabetes in the past two decades. Evidence of the effectiveness of nutrition and lifestyle interventions with resepect to achieving diabetes-related outcomes for diabetes prevention and a reduction in diabetes complications for people with diabetes is clearly mounting. The Diabetes Control and Complications Trial (1983-1993), the Diabetes Prevention Program (1996-2001) and the Look AHEAD (Action for Health in Diabetes) Trial (2001-2012) have been providing key evidence for the dietitian's role in delivering effective nutrition and lifestyle interventions for people with prediabetes, type 1 and type 2 diabetes. The dietitians in these multicentre efficacy trials contributed to this evidence base by expanding their roles beyond implementing the protocol defined goal-based nutrition and lifestyle interventions to conducting ancillary research and using problem-solving strategies that tailor counselling approaches toward participants' barriers to goal achievement. As lifestyle coaches and case managers, dietitians had the opportunity to work with the same group of study participants over extended periods of time and use their clinical and research expertise to uncover important insights and strategies that helped achieve clinical goals related to glycaemia control, weight loss and activity. The present review will 'chart the course' of how the evidence base for nutrition and lifestyle interventions emanated from these trials and discuss the implications for clinical dietetic practice. Dietitians can use insights gleaned from these experiences with the research process to expand their roles and guide cutting edge evidence-based clinical dietetic practice in diabetes.
C1 Massachusetts Gen Hosp, Ctr Diabet, Boston, MA 02114 USA.
RP Delahanty, LM (reprint author), Massachusetts Gen Hosp, Ctr Diabet, 50 Staniford St Suite 340, Boston, MA 02114 USA.
EM ldelahanty@partners.org
NR 41
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U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0952-3871
EI 1365-277X
J9 J HUM NUTR DIET
JI J. Hum. Nutr. Diet.
PD AUG
PY 2010
VL 23
IS 4
BP 360
EP 370
DI 10.1111/j.1365-277X.2010.01065.x
PG 11
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 626AL
UT WOS:000279937900005
PM 20456590
ER
PT J
AU Breen, N
Rao, SR
Meissner, HI
AF Breen, Nancy
Rao, Sowmya R.
Meissner, Helen I.
TI Immigration, Health Care Access, and Recent Cancer Tests Among
Mexican-Americans in California
SO JOURNAL OF IMMIGRANT AND MINORITY HEALTH
LA English
DT Article
DE Mexican-American; Mammography; Pap; FOBT; Colorectal endoscopy; Access
to care; Immigration; Language; Cancer testing; CHIS
ID UNITED-STATES; SCREENING PRACTICES; HISPANIC WOMEN; INTERVIEW SURVEY;
BEHAVIORAL-MODEL; ASIAN-AMERICAN; BREAST; ACCULTURATION; INSURANCE;
LANGUAGE
AB Immigrants' lower rates of cancer testing may be due to lack of fluency in English and other skills and knowledge about navigating US health care markets, lack of access to health services, or both. We analyzed 9,079 Mexican-American respondents to the 2001 California Health Interview Survey (CHIS) grouped as born in the US, living in the US 10 or more years, or living in the US less than 10 years. The CHIS provides the largest Mexican-American sample in a US survey. Access to care meant having health insurance coverage and a usual source of care. English proficiency meant the respondent took the interview in English. Multivariate logistic regression was used to predict outcomes. Respondents reporting more time in the US were more likely to report access to medical care and to report getting a cancer screening exam. Regardless of time in the US, respondents reporting access had similar test rates. Regression results indicate that time in the US and primary language were not significant relative to use of cancer screening tests, but access to care was. Cancer screening tests that are covered by Every Woman Counts, California's breast and cervical cancer early detection program, had smaller gaps among groups than colorectal cancer screening which is not covered by a program. California is the only state with a survey able to monitor changes in small population groups. Understanding barriers specific to subgroups is key to developing appropriate policy and interventions to increase use of cancer screening exams.
C1 [Breen, Nancy] NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Rockville, MD 20892 USA.
[Rao, Sowmya R.] Massachusetts Gen Hosp, Inst Hlth Policy, Ctr Biostat, Boston, MA 02114 USA.
[Meissner, Helen I.] NCI, Behav Res Program, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Breen, N (reprint author), NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci, Execut Plaza N,Room 4005,6130 Execut Blvd,MSC 734, Rockville, MD 20892 USA.
EM Breenn@mail.nih.gov
NR 47
TC 14
Z9 14
U1 2
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1557-1912
J9 J IMMIGR MINOR HEALT
JI J. Immigr. Minor. Health
PD AUG
PY 2010
VL 12
IS 4
BP 433
EP 444
DI 10.1007/s10903-008-9198-3
PG 12
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 645ZY
UT WOS:000281505900002
PM 19052868
ER
PT J
AU Rabquer, BJ
Amin, MA
Teegala, N
Shaheen, MK
Tsou, PS
Ruth, JH
Lesch, CA
Imhof, BA
Koch, AE
AF Rabquer, Bradley J.
Amin, Mohammad A.
Teegala, Nanditha
Shaheen, Matthew K.
Tsou, Pei-Suen
Ruth, Jeffrey H.
Lesch, Charles A.
Imhof, Beat A.
Koch, Alisa E.
TI Junctional Adhesion Molecule-C Is a Soluble Mediator of Angiogenesis
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID RHEUMATOID-ARTHRITIS; CELL-ADHESION; IMMUNOGLOBULIN SUPERFAMILY;
ENDOTHELIAL-CELLS; E-SELECTIN; LEUKOCYTE ADHESION; GROWTH-FACTOR;
IN-VIVO; JAM-C; PROTEIN
AB Junctional adhesion molecule-C (JAM-C) is an adhesion molecule expressed by endothelial cells (ECs) that plays a role in tight junction formation, leukocyte adhesion, and transendothelial migration. In the current study, we investigated whether JAM-C is found in soluble form and whether soluble JAM-C (sJAM-C) mediates angiogenesis. We found that JAM-C is present in soluble form in normal serum and elevated in rheumatoid arthritis (RA) serum. The concentration of sJAM-C is also elevated locally in RA synovial fluid compared with RA serum or osteoarthritis synovial fluid. sJAM-C was also present in the culture supernatant of human microvascular ECs (HMVECs) and immortalized human dermal microvascular ECs, and its concentration was increased following cytokine stimulation. In addition, sJAM-C cleavage from the cell surface was mediated in part by a disintegrin and metalloproteinases 10 and 17. In functional assays, sJAM-C was both chemotactic and chemokinetic for HMVECs and induced HMVEC tube formation on Matrigel in vitro. Neutralizing anti-JAM-C Abs inhibited RA synovial fluid-induced HMVEC chemotaxis and sJAM-C-induced HMVEC tube formation on Matrigel. sJAM-C also induced angiogenesis in vivo in the Matrigel plug and sponge granuloma models. Moreover, sJAM-C-mediated HMVEC chemotaxis was dependent on Src, p38, and PI3K. Our results show that JAM-C exists in soluble form and suggest that modulation of sJAM-C may provide a novel route for controlling pathological angiogenesis. The Journal of Immunology, 2010, 185: 1777-1785.
C1 [Rabquer, Bradley J.] Univ Michigan, Sch Med, Div Rheumatol, Dept Med, Ann Arbor, MI 48109 USA.
[Koch, Alisa E.] US Dept Vet Affairs, Vet Affairs Med Serv, Ann Arbor, MI 48109 USA.
[Imhof, Beat A.] Univ Geneva, Dept Pathol, CH-1211 Geneva, Switzerland.
RP Rabquer, BJ (reprint author), Univ Michigan, Sch Med, Div Rheumatol, Dept Med, 4388 BSRB,109 Zina Pitcher Dr, Ann Arbor, MI 48109 USA.
EM brabquer@umich.edu
RI Koch, Alisa/B-6894-2011
FU National Institutes of Health [HL094017, AR052482, AR48267]; Office of
Research and Development, Medical Research Service, Department of
Veterans Affairs; Frederick G.L. Huetwell and William D. Robinson
FX This work was supported by National Institutes of Health Grants HL094017
(to B.J.R.), AR052482 (to M.A.A.), and AR48267 (to A.E.K.), the Office
of Research and Development, Medical Research Service, Department of
Veterans Affairs, and the Frederick G.L. Huetwell and William D.
Robinson, M.D., Professorship in Rheumatology.
NR 44
TC 27
Z9 31
U1 0
U2 2
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD AUG 1
PY 2010
VL 185
IS 3
BP 1777
EP 1785
DI 10.4049/jimmunol.1000556
PG 9
WC Immunology
SC Immunology
GA 629EI
UT WOS:000280177400055
PM 20592283
ER
PT J
AU Carbo, C
Duerschmied, D
Goerge, T
Hattori, H
Sakai, J
Cifuni, SM
White, GC
Chrzanowska-Wodnicka, M
Luo, HR
Wagner, DD
AF Carbo, Carla
Duerschmied, Daniel
Goerge, Tobias
Hattori, Hidenori
Sakai, Jiro
Cifuni, Stephen M.
White, Gilbert C., II
Chrzanowska-Wodnicka, Magdalena
Luo, Hongbo R.
Wagner, Denisa D.
TI Integrin-independent role of CalDAG-GEFI in neutrophil chemotaxis
SO JOURNAL OF LEUKOCYTE BIOLOGY
LA English
DT Article
DE Rap1; adhesion; F-actin; polarization
ID BLOOD POLYMORPHONUCLEAR LEUKOCYTES; RANDOM LOCOMOTION; CLOSE QUARTERS;
CELL-ADHESION; CAIDAG-GEFI; NULL MICE; ACTIVATION; RAP1B; INFLAMMATION;
POLARIZATION
AB Chemotaxis and integrin activation are essential processes for neutrophil transmigration in response to injury. CalDAG-GEFI plays a key role in the activation of beta 1, beta 2, and beta 3 integrins in platelets and neutrophils by exchanging a GDP for a GTP on Rap1. Here, we explored the role of CalDAG-GEFI and Rap1b in integrin-independent neutrophil chemotaxis. In a transwell assay, CalDAG-GEFI(-/-) neutrophils had a 46% reduction in transmigration compared with WT in response to a low concentration of LTB(4). Visualization of migrating neutrophils in the presence of 10 mM EDTA revealed that CalDAG-GEFI(-/-) neutrophils had abnormal chemotactic behavior compared with WT neutrophils, including reduced speed and directionality. Interestingly, Rap1b(-/-) neutrophils had a similar phenotype in this assay, suggesting that CalDAG-GEFI may be acting through Rap1b. We investigated whether the deficit in integrin-independent chemotaxis in CalDAG-GEFI(-/-) neutrophils could be explained by defective cytoskeleton rearrangement. Indeed, we found that CalDAG-GEFI(-/-) neutrophils had reduced formation of F-actin pseudopodia after LTB(4) stimulation, suggesting that they have a defect in polarization. Overall, our studies show that CalDAG-GEFI helps regulate neutrophil chemotaxis, independent of its established role in integrin activation, through a mechanism that involves actin cytoskeleton and cellular polarization. J. Leukoc. Biol. 88: 313-319; 2010.
C1 [Carbo, Carla; Duerschmied, Daniel; Cifuni, Stephen M.; Wagner, Denisa D.] Harvard Univ, Sch Med, Childrens Hosp, Immune Dis Inst, Boston, MA 02115 USA.
[Carbo, Carla; Duerschmied, Daniel; Cifuni, Stephen M.; Wagner, Denisa D.] Harvard Univ, Sch Med, Childrens Hosp, Program Cellular & Mol Med, Boston, MA 02115 USA.
[Hattori, Hidenori; Sakai, Jiro; Luo, Hongbo R.] Harvard Univ, Sch Med, Childrens Hosp, Dept Lab Med, Boston, MA 02115 USA.
[Carbo, Carla; Duerschmied, Daniel; Hattori, Hidenori; Sakai, Jiro; Luo, Hongbo R.; Wagner, Denisa D.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Goerge, Tobias] Univ Hosp Muenster, Dept Dermatol, Munster, Germany.
[Hattori, Hidenori; Sakai, Jiro; Luo, Hongbo R.] Dana Farber Harvard Canc Ctr, Boston, MA USA.
[White, Gilbert C., II; Chrzanowska-Wodnicka, Magdalena] Blood Ctr Wisconsin, Blood Res Inst, Milwaukee, WI USA.
RP Wagner, DD (reprint author), Harvard Univ, Sch Med, Childrens Hosp, Immune Dis Inst, 3 Blackfan Circle, Boston, MA 02115 USA.
EM wagner@idi.harvard.edu
OI Sakai, Jiro/0000-0002-2526-2766; Chrzanowska-Wodnicka,
Magdalena/0000-0003-4182-2126
FU National Heart, Lung and Blood Institute of the National Institutes of
Health [P01 HL056949, P01 HL066105]; DFG [GO1360/4-1]; IMF Munster; NIH
[HL085100, AI076471, HL092020, GM076084]; American Cancer Society
FX This work was supported by the National Heart, Lung and Blood Institute
of the National Institutes of Health grants P01 HL056949 and P01
HL066105 (both to D. D. W.); grant DFG GO1360/4-1 and IMF Munster (T.
G.); NIH grants HL085100, AI076471, HL092020, and GM076084; and a
research scholar grant from the American Cancer Society (H. R. L.). We
thank Kulandayan Subramanian and Ian del Conde for helpful discussions
and Lesley Cowan for assistance in preparing the manuscript. We thank
Ann Graybiel, David Housman, and Jill Crittenden for providing the
CalDAG-GEFI-deficient mice.
NR 35
TC 14
Z9 15
U1 0
U2 2
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 AUG
PY 2010
VL 88
IS 2
BP 313
EP 319
DI 10.1189/jlb.0110049
PG 7
WC Cell Biology; Hematology; Immunology
SC Cell Biology; Hematology; Immunology
GA 692YQ
UT WOS:000285192200011
PM 20413728
ER
PT J
AU Sun, PZ
AF Sun, Phillip Zhe
TI Simplified and scalable numerical solution for describing multi-pool
chemical exchange saturation transfer (CEST) MRI contrast
SO JOURNAL OF MAGNETIC RESONANCE
LA English
DT Article
DE Amide proton transfer (APT); Chemical exchange saturation transfer
(CEST); Numerical solution
ID MAGNETIZATION-TRANSFER; PROTON-EXCHANGE; QUANTITATIVE DESCRIPTION;
PARACEST AGENTS; CROSS-RELAXATION; WATER PROTONS; HUMAN BRAIN; IN-VIVO;
RESONANCE; RATES
AB Chemical exchange saturation transfer (CEST) imaging is sensitive to dilute labile proton and microenvironment properties such as pH and temperature, and provides vital information complementary to the conventional MRI methods. Whereas the Bloch equations coupled by exchange terms (i.e., Bloch-McConnell equations) have been utilized to quantify 2-pool CEST contrast, it is tedious to extend the Bloch-McConnell equations to describe CEST contrast beyond four saturation transfer sites. Hence, it is necessary to develop a scalable yet reasonably accurate numerical solution to describe the complex multi-pool CEST contrast. It is postulated here that the multi-pool CEST contrast can be quantified by modifying the classic 2-pool model. Although the direct exchange among labile proton groups is often negligible, labile protons may be coupled indirectly through their interaction with bulk water protons, which has to be quantified. The coupling term was solved empirically, and the proposed simplified solution was shown in good agreement with the conventional simulation. Moreover, the proposed solution is scalable, and can be easily extended to describe multi-pool CEST contrast. In sum, our study established a simplified and scalable, yet reasonably accurate numerical solution, suitable for quantitatively describing multi-pool CEST contrast. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Sun, Phillip Zhe] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol,Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Sun, Phillip Zhe] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
RP Sun, PZ (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol,Ctr Biomed Imaging, Rm 2301,149 13th St, Charlestown, MA 02129 USA.
EM pzhesun@nmr.mgh.harvard.edu
FU AHA/SDG [0835384N]; NIH/NIBIB [1K01EB009771-01]; [NIH/R21NS061119-02]
FX This study was supported in part by Grants from AHA/SDG 0835384N,
NIH/NIBIB 1K01EB009771-01 and NIH/R21NS061119-02.
NR 37
TC 29
Z9 29
U1 3
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1090-7807
J9 J MAGN RESON
JI J. Magn. Reson.
PD AUG
PY 2010
VL 205
IS 2
BP 235
EP 241
DI 10.1016/j.jmr.2010.05.004
PG 7
WC Biochemical Research Methods; Physics, Atomic, Molecular & Chemical;
Spectroscopy
SC Biochemistry & Molecular Biology; Physics; Spectroscopy
GA 627SZ
UT WOS:000280064500007
PM 20570196
ER
PT J
AU Emmer, BJ
van Osch, MJ
Wu, O
Steup-Beekman, GM
Steens, SC
Huizinga, TW
van Buchem, MA
van der Grond, J
AF Emmer, Bart J.
van Osch, Matthias J.
Wu, Ona
Steup-Beekman, Gerda M.
Steens, Stefan C.
Huizinga, Tom W.
van Buchem, Mark A.
van der Grond, Jeroen
TI Perfusion MRI in Neuro-Psychiatric Systemic Lupus Erthemathosus
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE perfusion MR; systemic lupus erythematosus; neuropsychiatric;
immunological disorder; ischemia
ID CEREBRAL-BLOOD-FLOW; EMISSION COMPUTED-TOMOGRAPHY; HIGH-RESOLUTION
MEASUREMENT; TRACER BOLUS PASSAGES; ERYTHEMATOSUS; INVOLVEMENT; BRAIN;
MANIFESTATIONS; AUTOANTIBODIES; IMMUNITY
AB Purpose: To use perfusion weighted MR to quantify any perfusion abnormalities and to determine their contribution to neuropsychiatric (NP) involvement in systemic lupus erythematosus (SLE).
Materials and methods: We applied dynamic susceptibility contrast (DSC) perfusion MRI in 15 active NPSLE, 26 inactive NPSLE patients. and 11 control subjects. Cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) maps were reconstructed and regions of interest were compared between groups. In addition, the effect of SLE criteria, NPSLE syndromes. immunological coagulation disorder, and medication on CBF. CBV, and MTT was investigated.
Results: No significant differences were found between the groups in CBF, CBV, and MTT. No significant influence of SLE criteria or NPSLE syndromes on CBF, CBV, or MTT was found. No significant influence of anti-cardiolipin antibodies, lupus anti-coagulant, the presence of anti-phospholipid syndrome (APS), or medication on CBF, CBV. or MTT was found.
Conclusion: Our findings suggest CBF. CBV, and MTT in the white and the gray matter in SLE patients is not significantly different from healthy controls or between patients with and without specific symptoms or with and without immunological disorder involving coagulation.
C1 [Emmer, Bart J.] Leiden Univ, Med Ctr, Dept Radiol, NL-2300 RC Leiden, Zuid Holland, Netherlands.
[Wu, Ona] Massachusetts Gen Hosp, Athinoula A Martinos Ctr, Charlestown, MA USA.
RP Emmer, BJ (reprint author), Leiden Univ, Med Ctr, Dept Radiol, C2-S, NL-2300 RC Leiden, Zuid Holland, Netherlands.
EM b.j.emmer@lumc.nl
RI Emmer, Bart/B-3957-2012; Steens, Stefan/L-4670-2015
OI Steens, Stefan/0000-0001-8580-4726
FU Dutch Arthritis Foundation
FX Contract grant sponsor: Dutch Arthritis Foundation.
NR 22
TC 7
Z9 7
U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1053-1807
J9 J MAGN RESON IMAGING
JI J. Magn. Reson. Imaging
PD AUG
PY 2010
VL 32
IS 2
BP 283
EP 288
DI 10.1002/jmri.22251
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 632SF
UT WOS:000280447300004
PM 20677252
ER
PT J
AU Bredella, MA
Ghomi, RH
Thomas, BJ
Miller, KK
Torriani, M
AF Bredella, Miriam A.
Ghomi, Reza Hosseini
Thomas, Bijoy J.
Miller, Karen K.
Torriani, Martin
TI Comparison of 3.0 T Proton Magnetic Resonance Spectroscopy Short and
Long Echo-Time Measures of Intramyocellular Lipids in Obese and
Normal-Weight Women
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE IMCL; 1H-MR spectroscopy; echo-time; obesity
ID SKELETAL-MUSCLE; INSULIN SENSITIVITY; TRIGLYCERIDE CONTENT; BODY-FAT;
QUANTIFICATION; RESISTANCE; HUMANS; LCMODEL; SPECTRA
AB Purpose: To compare correlations of intramyocellular lipids (IMCL) measured by short and long echo-time proton magnetic resonance spectroscopy (1H-MRS) with indices of body composition and insulin resistance in obese and normal-weight women.
Materials and Methods: We quantified IMCL of tibialis anterior (TA) and soleus (SOL) muscles in 52 premenopausal women (37 obese and 15 normal weight) using single-voxel 1H-MRS PRESS at 3.0 T with short (30 msec) and long (144 msec) echo times. Statistical analyses were performed to determine correlations of IMCL with body composition as determined by computed tomography (CT) and insulin resistance indices and to compare correlation coefficients from short and long echo-time data. Signal-to-noise ratio (SNR), linewidth, and coefficients of variation (CV) of short and long echo-time spectra were calculated.
Results: Short and long echo-time IMCL from TA and SQL significantly correlated with body mass index (BMI) and abdominal fat depots (r = 0.32 to 0.70, P = <0.05), liver density (r = -0.39 to -0.50, P < 0.05), and glucose area under the curve as a measure of insulin resistance (r = 0.47 to 0.49, P < 0.05). There was no significant difference between correlation coefficients of short and long echo-time spectra (P > 0.5). Short echo-time IMCL in both muscles showed significantly higher SNR (P < 0.0001) and lower CVs when compared to long echo-time acquisitions. Linewidth measures were not significantly different between groups.
Conclusion: IMCL quantification using short and long echo-time 1H-MRS at 3.0 T is useful to detect differences in muscle lipid content in obese and normal-weight subjects. In addition, IMCL correlates with body composition and markers of insulin resistance in this population with no significant difference in correlations between short and long echo-times. Short echo-time IMCL quantification of TA and SOL muscles at 3.0 T was superior to long echo-time due to better SNR and better reproducibility.
C1 [Bredella, Miriam A.; Ghomi, Reza Hosseini; Thomas, Bijoy J.; Torriani, Martin] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Miller, Karen K.] Massachusetts Gen Hosp, Dept Med, Neuroendocrine Unit, Boston, MA 02114 USA.
RP Bredella, MA (reprint author), Massachusetts Gen Hosp, Dept Radiol, Yawkey 6E,55 Fruit St, Boston, MA 02114 USA.
EM mbredella@partners.org
OI Hosseini Ghomi, Reza/0000-0003-4369-8237
FU National Institutes of Health [RO1 HL-077674, UL1 RR025758, K23
RR-23090]
FX Contract grant sponsor: National Institutes of Health: Contract grant
numbers: RO1 HL-077674, UL1 RR025758, K23 RR-23090.
NR 23
TC 19
Z9 20
U1 1
U2 6
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1053-1807
J9 J MAGN RESON IMAGING
JI J. Magn. Reson. Imaging
PD AUG
PY 2010
VL 32
IS 2
BP 388
EP 393
DI 10.1002/jmri.22226
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 632SF
UT WOS:000280447300019
PM 20677267
ER
PT J
AU Marini, RP
Muthupalani, S
Shen, ZL
Buckley, EM
Alvarado, C
Taylor, NS
Dewhirst, FE
Whary, MT
Patterson, MM
Fox, JG
AF Marini, Robert P.
Muthupalani, Sureshkumar
Shen, Zeli
Buckley, Ellen M.
Alvarado, Cynthia
Taylor, Nancy S.
Dewhirst, Floyd E.
Whary, Mark T.
Patterson, Mary M.
Fox, James G.
TI Persistent infection of rhesus monkeys with 'Helicobacter macacae' and
its isolation from an animal with intestinal adenocarcinoma
SO JOURNAL OF MEDICAL MICROBIOLOGY
LA English
DT Article
ID INFLAMMATORY-BOWEL-DISEASE; CHRONIC IDIOPATHIC COLITIS; COLON-CANCER;
RAG2-DEFICIENT MICE; HEPATICUS; CARCINOGENESIS; LIVER; GASTROENTERITIS;
CINAEDI; MULATTA
AB A novel helicobacter, 'Helicobacter macacae', was previously isolated from a colony of rhesus and cynomolgus monkeys in which diarrhoea from chronic idiopathic colitis was enzootic. A survey performed in a second colony of rhesus monkeys without a history of chronic diarrhoea determined that 57% were faecal-culture positive for Helicobacter species. Ten years after the survey, one of the animals from which 'H. macacae' had been isolated, a 23-year-old, intact male rhesus monkey (Macaca mulatta), presented with partial inappetence and progressive weight loss. Subsequent evaluation of the monkey revealed anaemia, hypoproteinaemia, hypoalbuminaemia and a palpable abdominal mass. Contrast radiography suggested partial intestinal obstruction. The animal was euthanized and a diagnosis was made of intestinal adenocarcinoma of the ileocaecocolic junction with metastasis to regional lymph nodes and liver. Microaerobic culture of caecal tissue yielded a helicobacter organism identified as 'H. macacae' by 16S rRNA gene sequencing - the same species of bacteria isolated 10 years previously. The liver, small intestine and colon were also positive by PCR for Helicobacter species. Intestinal adenocarcinoma is the most common malignancy of aged macaques. Faeces or caecal tissue from five out of five monkeys that remained from the original cohort and that were colonized with 'H. macacae' in the initial survey were positive for the organism. The apparent persistence of 'H. macacae' in these animals, the isolation of the bacterium from animals with colitis and the recognition of the importance of inflammation in carcinogenesis raise the possibility of an aetiological role in the genesis of intestinal adenocarcinoma in aged rhesus monkeys.
C1 [Marini, Robert P.; Shen, Zeli; Buckley, Ellen M.; Alvarado, Cynthia; Taylor, Nancy S.; Whary, Mark T.; Patterson, Mary M.; Fox, James G.] MIT, Div Comparat Med, Cambridge, MA 02139 USA.
[Dewhirst, Floyd E.] Forsyth Inst, Dept Mol Genet, Boston, MA 02115 USA.
RP Fox, JG (reprint author), MIT, Div Comparat Med, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM jgfox@mit.edu
FU [RO1 CA 67529]; [T32 RR07036]; [P30 - ES02109]
FX This work was supported by grants RO1 CA 67529, T32 RR07036 and P30 -
ES02109.
NR 33
TC 13
Z9 13
U1 0
U2 1
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-2615
J9 J MED MICROBIOL
JI J. Med. Microbiol.
PD AUG
PY 2010
VL 59
IS 8
BP 961
EP 969
DI 10.1099/jmm.0.019117-0
PG 9
WC Microbiology
SC Microbiology
GA 638WL
UT WOS:000280928700014
PM 20413623
ER
PT J
AU Siddappa, NB
Wassermann, K
Wang, W
Watkins, J
Kramer, VG
Lakhashe, S
Santosuosso, M
Poznansky, MC
Novembre, FJ
Else, JG
Montefiori, DC
Ruprecht, RM
AF Siddappa, Nagadenahalli B.
Wassermann, Klemens
Wang, Wendy
Watkins, Jennifer
Kramer, Victor G.
Lakhashe, Samir
Santosuosso, Michael
Poznansky, Mark C.
Novembre, Francis J.
Else, James G.
Montefiori, David C.
Ruprecht, Ruth M.
TI NATURAL EVOLUTION OF CLADE C SHIV NEUTRALIZATION SENSITIVITY FROM TIER 1
TO TIER 2 IS LINKED TO DIFFERENCES IN V1 AND V2 LOOP SEQUENCES IN ENV
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Siddappa, Nagadenahalli B.; Wassermann, Klemens; Wang, Wendy; Watkins, Jennifer; Kramer, Victor G.; Lakhashe, Samir; Ruprecht, Ruth M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Santosuosso, Michael; Poznansky, Mark C.] Massachusetts Gen Hosp E, Partners AIDS Res Ctr & Infect Dis Med, Charlestown, MA 02129 USA.
[Novembre, Francis J.] Emory Univ, Div Microbiol & Immunol, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Else, James G.] Emory Univ, Div Anim Resources, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Montefiori, David C.] Duke Univ, Dept Surg, Med Ctr, Durham, NC 27710 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0047-2565
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD AUG
PY 2010
VL 39
IS 4
MA 5
BP 268
EP 268
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 619RV
UT WOS:000279448900014
ER
PT J
AU Finstad, SL
Zhang, GL
Linde, C
Muik, A
Hermann, F
Evans, V
de la Rosa, M
Zahn, R
Gaufin, T
Reimann, K
Apetrei, C
Miller, C
McCune, J
Picker, L
Veazey, R
Brusic, V
Letvin, N
Schmitz, J
AF Finstad, Samantha L.
Zhang, Guanglan
Linde, Caitlyn
Muik, Alexander
Hermann, Fabian
Evans, Valerie
de la Rosa, Maurus
Zahn, Roland
Gaufin, Thaidra
Reimann, Keith
Apetrei, Cristian
Miller, Christopher
McCune, Joseph
Picker, Louis
Veazey, Ronald
Brusic, Vladimir
Letvin, Norman
Schmitz, Joern
TI INFLUENCE OF FC Gamma-RECEPTOR POLYMORPHISMS ON EFFICACY OF
ANTIBODY-MEDIATED LYMPHOCYTE DEPLETION IN RHESUS MACAQUES
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Finstad, Samantha L.; Linde, Caitlyn; Muik, Alexander; Hermann, Fabian; Evans, Valerie; de la Rosa, Maurus; Zahn, Roland; Reimann, Keith; Letvin, Norman; Schmitz, Joern] Beth Israel Deaconess Med Ctr, Div Viral Pathogenesis, Boston, MA 02215 USA.
[Zhang, Guanglan; Brusic, Vladimir] Dana Farber Canc Inst, Canc Vaccine Ctr, Boston, MA 02115 USA.
[Gaufin, Thaidra; Apetrei, Cristian; Veazey, Ronald] Tulane Univ, Hlth Sci Ctr, Tulane Natl Primate Res Ctr, Covington, LA USA.
[Miller, Christopher] Calif Natl Primate Res Ctr, Davis, CA USA.
[McCune, Joseph] Univ Calif San Francisco, Div Expt Med, San Francisco, CA 94143 USA.
[Picker, Louis] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Portland, OR 97201 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 0047-2565
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD AUG
PY 2010
VL 39
IS 4
MA 40
BP 279
EP 280
PG 2
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 619RV
UT WOS:000279448900049
ER
PT J
AU de la Rosa, M
Finstad, S
Zahn, R
Chugh, P
Evans, V
Rett, M
Linde, C
Carville, A
Letvin, N
Schmitz, J
AF de la Rosa, Maurus
Finstad, Samantha
Zahn, Roland
Chugh, Prithi
Evans, Valerie
Rett, Melissa
Linde, Caitlyn
Carville, Angela
Letvin, Norman
Schmitz, Joern
TI B CELL SUBSET CHANGES FOLLOWING SIV INFECTION
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [de la Rosa, Maurus; Finstad, Samantha; Zahn, Roland; Chugh, Prithi; Evans, Valerie; Rett, Melissa; Linde, Caitlyn; Letvin, Norman; Schmitz, Joern] Harvard Univ, Sch Med, Div Viral Pathogenesis, BIDMC, Boston, MA 02115 USA.
[Carville, Angela] Harvard Univ, New England Reg Primate Res Ctr, Sch Med, Southborough, MA 01772 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 0047-2565
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD AUG
PY 2010
VL 39
IS 4
MA 67
BP 290
EP 290
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 619RV
UT WOS:000279448900079
ER
PT J
AU Annamalai, L
Bailey, C
Bhaskar, V
Boisvert, K
Gonzalez, RG
Westmoreland, SV
AF Annamalai, Lakshmanan
Bailey, Charles
Bhaskar, Veena
Boisvert, Karen
Gonzalez, Ramon Gilberto
Westmoreland, Susan V.
TI HIGHER LEVELS OF EXPRESSION OF CXCR3 LIGANDS AND ACTIVATION OF MICROGLIA
IN SIMIAN IMMUNODEFICIENCY VIRUS ENCEPHALITIS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Annamalai, Lakshmanan; Bailey, Charles; Boisvert, Karen; Westmoreland, Susan V.] Harvard Univ, Sch Med, Dept Comparat Med & Pathol, NEPRC, Southborough, MA 01772 USA.
[Bhaskar, Veena; Gonzalez, Ramon Gilberto] Massachusetts Gen Hosp, Neuroradiol Div, Charlestown, MA USA.
[Bhaskar, Veena; Gonzalez, Ramon Gilberto] Massachusetts Gen Hosp, Martinos Ctr Biomed Imaging, Charlestown, MA 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 0047-2565
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD AUG
PY 2010
VL 39
IS 4
MA 70
BP 291
EP 291
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 619RV
UT WOS:000279448900082
ER
PT J
AU Ratai, EM
Joo, CG
Bombardier, JP
He, JL
Hakimelahi, R
Campbell, J
Burdo, T
Autissier, P
Annamalai, L
Westmoreland, SV
Williams, K
Gonzalez, RG
Martinos, AA
AF Ratai, Eva-Maria
Joo, Chan-Gyu
Bombardier, Jeffrey P.
He, Julian
Hakimelahi, Reza
Campbell, Jennifer
Burdo, Tricia
Autissier, Patrick
Annamalai, Lakshmanan
Westmoreland, Susan V.
Williams, Kenneth
Gonzalez, Ramon Gilberto
Martinos, A. A.
TI 1H MR SPECTROSCOPY REVEALS NEUROPROTECTION BY MINOCYCLINE IN AN
ACCELERATED RHESUS MACAQUE MODEL OF NEUROAIDS
SO JOURNAL OF MEDICAL PRIMATOLOGY
LA English
DT Meeting Abstract
C1 [Ratai, Eva-Maria; Joo, Chan-Gyu; Bombardier, Jeffrey P.; He, Julian; Hakimelahi, Reza; Gonzalez, Ramon Gilberto; Martinos, A. A.] Massachusetts Gen Hosp, Dept Radiol, Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Campbell, Jennifer; Burdo, Tricia; Autissier, Patrick; Williams, Kenneth] Boston Coll, Dept Biol, Boston, MA 02467 USA.
[Annamalai, Lakshmanan; Westmoreland, Susan V.] New England Reg Primate Res Ctr, Dept Pathol, Southborough, MA 01772 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0047-2565
J9 J MED PRIMATOL
JI J. Med. Primatol.
PD AUG
PY 2010
VL 39
IS 4
MA 73
BP 292
EP 292
PG 1
WC Veterinary Sciences; Zoology
SC Veterinary Sciences; Zoology
GA 619RV
UT WOS:000279448900085
ER
PT J
AU Janle, EM
Lila, MA
Grannan, M
Wood, L
Higgins, A
Yousef, GG
Rogers, RB
Kim, H
Jackson, GS
Ho, L
Weaver, CM
AF Janle, Elsa M.
Lila, Mary Ann
Grannan, Michael
Wood, Lauren
Higgins, Aine
Yousef, Gad G.
Rogers, Randy B.
Kim, Helen
Jackson, George S.
Ho, Lap
Weaver, Connie M.
TI Pharmacokinetics and Tissue Distribution of C-14-Labeled Grape
Polyphenols in the Periphery and the Central Nervous System Following
Oral Administration
SO JOURNAL OF MEDICINAL FOOD
LA English
DT Article
DE blood-brain barrier; brain kinetics; grape; grape cell culture;
interstitial fluid kinetics; neurodegenerative diseases;
pharmacokinetics; polyphenols; tissue distribution
ID ACCELERATOR MASS-SPECTROMETRY; CELL SUSPENSION-CULTURES;
ALZHEIMERS-DISEASE; RED WINE; SEED EXTRACT; COGNITIVE DETERIORATION;
IN-VIVO; BIOAVAILABILITY; RATS; ULTRAFILTRATION
AB Grape polyphenols confer potential health benefits, including prevention of neurodegenerative diseases. To determine the absorption and tissue distribution of the complex grape polyphenol mixture, C-14-labeled polyphenols were biosynthesized by grape cell suspension cultures, during co-incubation with radioisotopically labeled sucrose, and fractionated into polyphenolic subfractions. The pharmacokinetics and distribution of grape polyphenols into blood, brain, and peripheral interstitial fluid were determined by tracking the C-14 label. The blood peak C-14 concentration of the fractions ranged from 15 minutes to 4 hours. Absorption and tissue distribution varied greatly between fractions. Concentrations in interstitial fluid were lower than in blood. The amount of residual label in the brain at 24 hours ranged from 0.1% to 1.7% of the dose, depending on the fraction. (14)Clabel found in the brain tissue and brain microdialysate indicated that grape polyphenols or their metabolites are able to cross the blood-brain barrier. Using C-14-labeled plant polyphenols it is possible to track the compounds or their metabolic products into any tissue and determine distribution patterns in spite of low concentrations. A central question regarding the potential role of dietary polyphenolics in neurodegenerative research is whether they are bioavailable in the brain. Our observations indicate that some grape-derived polyphenolics do reach the brain, which suggests their potential value for applications in neurodegenerative disorders.
C1 [Janle, Elsa M.; Grannan, Michael; Wood, Lauren; Higgins, Aine; Weaver, Connie M.] Purdue Univ, Dept Foods & Nutr, W Lafayette, IN 47907 USA.
[Lila, Mary Ann; Rogers, Randy B.] Univ Illinois, Dept Nat Resources & Environm Sci, Urbana, IL 61801 USA.
[Jackson, George S.] Purdue Univ, Dept Phys, W Lafayette, IN 47907 USA.
[Kim, Helen] Univ Alabama, Dept Pharmacol & Toxicol, Birmingham, AL USA.
[Ho, Lap] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Ho, Lap] James J Peters Vet Affairs Med Ctr, Geriatr Res & Clin Ctr, Bronx, NY USA.
RP Janle, EM (reprint author), Purdue Univ, Dept Foods & Nutr, 700 W State St, W Lafayette, IN 47907 USA.
EM janle@purdue.edu
FU Purdue University-University of Alabama at Birmingham Botanical Center
for Age Related Diseases; NCCAM [P50 AT 00477]
FX The authors thank Pamela Lachcik, Jane Einstein, and Tom Kubley for
technical assistance. This project was supported by Purdue
University-University of Alabama at Birmingham Botanical Center for Age
Related Diseases funded by the Office of Dietary Supplements and NCCAM
grant P50 AT 00477.
NR 35
TC 24
Z9 25
U1 0
U2 8
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-620X
J9 J MED FOOD
JI J. Med. Food
PD AUG
PY 2010
VL 13
IS 4
BP 926
EP 933
DI 10.1089/jmf.2009.0157
PG 8
WC Chemistry, Medicinal; Food Science & Technology; Nutrition & Dietetics
SC Pharmacology & Pharmacy; Food Science & Technology; Nutrition &
Dietetics
GA 633FL
UT WOS:000280485000023
PM 20673061
ER
PT J
AU Kang, DK
Suter, MJ
Boudoux, C
Yachimski, PS
Puricelli, WP
Nishioka, NS
Mino-Kenudson, M
Lauwers, GY
Bouma, BE
Tearney, GJ
AF Kang, D. K.
Suter, M. J.
Boudoux, C.
Yachimski, P. S.
Puricelli, W. P.
Nishioka, N. S.
Mino-Kenudson, M.
Lauwers, G. Y.
Bouma, B. E.
Tearney, G. J.
TI Co-registered spectrally encoded confocal microscopy and optical
frequency domain imaging system
SO JOURNAL OF MICROSCOPY
LA English
DT Article
DE Confocal microscopy; co-registered imaging; multi-modality imaging;
optical coherence tomography
ID COHERENCE TOMOGRAPHY; ESOPHAGUS
AB P>Spectrally encoded confocal microscopy and optical frequency domain imaging are two non-contact optical imaging technologies that provide images of tissue cellular and architectural morphology, which are both used for histopathological diagnosis. Although spectrally encoded confocal microscopy has better transverse resolution than optical frequency domain imaging, optical frequency domain imaging can penetrate deeper into tissues, which potentially enables the visualization of different morphologic features. We have developed a co-registered spectrally encoded confocal microscopy and optical frequency domain imaging system and have obtained preliminary images from human oesophageal biopsy samples to compare the capabilities of these imaging techniques for diagnosing oesophageal pathology.
C1 [Kang, D. K.; Suter, M. J.; Boudoux, C.; Nishioka, N. S.; Bouma, B. E.; Tearney, G. J.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Kang, D. K.; Suter, M. J.; Boudoux, C.; Yachimski, P. S.; Puricelli, W. P.; Nishioka, N. S.; Mino-Kenudson, M.; Lauwers, G. Y.; Bouma, B. E.; Tearney, G. J.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Yachimski, P. S.; Puricelli, W. P.; Nishioka, N. S.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Lauwers, G. Y.; Bouma, B. E.; Tearney, G. J.] Massachusetts Gen Hosp, Pathol Serv, Boston, MA 02114 USA.
RP Tearney, GJ (reprint author), Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
EM gtearney@partners.org
RI Boudoux, Caroline/A-6399-2012; Kang, Dongkyun/C-1085-2013
OI Kang, Dongkyun/0000-0001-5063-5387
FU National Cancer Institute [R21CA122161]
FX This research is supported by National Cancer Institute (grant number
R21CA122161). Caroline Boudoux is currently with Ecole Polytechnique
Montreal, Canada, and Patrick S. Yachimski is with Vanderbilt University
Medical Center, Nashville, Tennessee, U.S.A.
NR 12
TC 8
Z9 8
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-2720
J9 J MICROSC-OXFORD
JI J. Microsc..
PD AUG
PY 2010
VL 239
IS 2
BP 87
EP 91
DI 10.1111/j.1365-2818.2010.03367.x
PG 5
WC Microscopy
SC Microscopy
GA 626AP
UT WOS:000279938300001
PM 20629914
ER
PT J
AU Asnaani, A
Richey, JA
Dimaite, R
Hinton, DE
Hofmann, SG
AF Asnaani, Anu
Richey, J. Anthony
Dimaite, Ruta
Hinton, Devon E.
Hofmann, Stefan G.
TI A Cross-Ethnic Comparison of Lifetime Prevalence Rates of Anxiety
Disorders
SO JOURNAL OF NERVOUS AND MENTAL DISEASE
LA English
DT Article
DE Anxiety disorders; cultural differences; epidemiology; national
comorbidity survey-replication (NCS-R); collaborative psychiatric
epidemiology surveys (CPES)
ID NATIONAL-COMORBIDITY-SURVEY; MENTAL-HEALTH SURVEYS; UNITED-STATES;
ASIAN-AMERICAN; PSYCHIATRIC-DISORDERS; SURVEY REPLICATION; PANIC
DISORDER; LATINO; VALIDITY; EPIDEMIOLOGY
AB To examine race-ethnic differences in the lifetime prevalence rates of common anxiety disorders, we examined data from the Collaborative Psychiatric Epidemiology Studies. The samples included 6870 White Americans, 4598 African Americans, 3615 Hispanic Americans, and 1628 Asian Americans. White Americans were more likely to be diagnosed with social anxiety disorder, generalized anxiety disorder, and panic disorder than African Americans, Hispanic Americans, and Asian Americans. African Americans more frequently met criteria for post-traumatic stress disorder (PTSD) than White Americans, Hispanic Americans, and Asian Americans. Asian Americans were also less likely to meet the diagnoses for generalized anxiety disorder and PTSD than Hispanic Americans, and were less likely to receive social anxiety disorder, generalized anxiety disorder, panic disorder, and PTSD diagnoses than White Americans. The results suggest that race and ethnicity need to be considered when assigning an anxiety disorder diagnosis. Possible reasons for the observed differences in prevalence rates between racial groups are discussed.
C1 [Asnaani, Anu; Richey, J. Anthony; Dimaite, Ruta; Hofmann, Stefan G.] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
[Dimaite, Ruta; Hinton, Devon E.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
RP Hofmann, SG (reprint author), Boston Univ, Dept Psychol, 648 Beacon St,6th Floor, Boston, MA 02215 USA.
EM shofmann@bu.edu
RI Hofmann, Stefan/B-8769-2014
OI Hofmann, Stefan/0000-0002-3548-9681
FU NIMH [1R01MH078308, R01MH079032]
FX Supported by NIMH grant 1R01MH078308 and R01MH079032 (to S.G.H. and
D.E.H., respectively).
NR 30
TC 73
Z9 73
U1 6
U2 17
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 AUG
PY 2010
VL 198
IS 8
BP 551
EP 555
DI 10.1097/NMD.0b013e3181ea169f
PG 5
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 640QQ
UT WOS:000281067000004
PM 20699719
ER
PT J
AU Hearst, SM
Lopez, ME
Shao, QM
Liu, Y
Vig, PJS
AF Hearst, Scoty M.
Lopez, Mariper E.
Shao, Qingmei
Liu, Yong
Vig, Parminder J. S.
TI Dopamine D-2 receptor signaling modulates mutant ataxin-1 S776
phosphorylation and aggregation
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE ataxin-1; cerebellum; dopamine 2 receptor; phosphorylation; S100B
protein; spinocerebellar ataxia
ID SCA1 TRANSGENIC MICE; SPINOCEREBELLAR ATAXIA; PROTEIN-KINASE;
TRINUCLEOTIDE REPEAT; LOCOMOTOR IMPAIRMENT; NEURITE OUTGROWTH;
ADENYLATE-CYCLASE; S100 PROTEINS; TYPE-1 GENE; CELL-LINE
AB P>Spinocerebellar ataxia 1 (SCA1) is a dominantly inherited neurodegenerative disease associated with progressive ataxia resulting from the loss of cerebellar Purkinje cells (PCs) and neurons in the brainstem. In PCs of SCA1 transgenic mice, the disease causing ataxin-1 protein mediates the formation of S100B containing cytoplasmic vacuoles and further self-aggregates to form intranuclear inclusions. The exact function of the ataxin-1 protein is not fully understood. However, the aggregation and neurotoxicity of the mutant ataxin-1 protein is dependent on the phosphorylation at serine 776 (S776). Although protein kinase A (PKA) has been implicated as the S776 kinase, the mechanism of PKA/ataxin-1 regulation in SCA1 is still not clear. We propose that a dopamine D-2 receptor (D2R)/S100B pathway may be involved in modulating PKA activity in PCs. Using a D2R/S100B HEK stable cell line transiently transfected with GFP-ataxin-1[82Q], we demonstrate that stimulation of the D2R/S100B pathway caused a reduction in mutant ataxin-1 S776 phosphorylation and ataxin-1 aggregation. Activation of PKA by forskolin resulted in an enhanced S776 phosphorylation and increased ataxin-1 nuclear aggregation, which was suppressed by treatment with D2R agonist bromocriptine and PKA inhibitor H89. Furthermore, treating SCA1 transgenic PC slice cultures with forskolin induced neurodegenerative morphological abnormalities in PC dendrites consistent with those observed in vivo. Taken together our data support a mechanism where PKA dependent mutant ataxin-1 phosphorylation and aggregation can be regulated by D2R/S100B signaling.
C1 [Hearst, Scoty M.; Lopez, Mariper E.; Shao, Qingmei; Vig, Parminder J. S.] Univ Mississippi, Med Ctr, Dept Neurol, Jackson, MS 39216 USA.
[Hearst, Scoty M.; Vig, Parminder J. S.] Univ Mississippi, Med Ctr, Dept Biochem, Jackson, MS 39216 USA.
[Liu, Yong] Oregon Hlth & Sci Univ, Dept Behav Neurosci, Portland, OR 97201 USA.
[Liu, Yong] Portland VA Med Ctr, Portland, OR USA.
RP Vig, PJS (reprint author), Univ Mississippi, Med Ctr, Dept Neurol, 2500 N State St, Jackson, MS 39216 USA.
EM pvig@neurology.umsmed.edu
FU National Institutes of Health; National Ataxia Foundation
FX This work was partly supported by grants from the National Institutes of
Health and National Ataxia Foundation. We would like to thank Dr. Kim
Neve, Department of Behavioral Neuroscience, Oregon Health & Science
University and Portland Veterans Affairs Medical Center for providing
the D2R/S100B HEK cell lines and for his advice in preparing this
manuscript. In addition, we would like to thank Dr. Michael Hebert,
Department of Biochemistry, the University of Mississippi Medical
Center, for his help with cell culture and ataxin-1 plasmid propagation.
NR 63
TC 14
Z9 14
U1 0
U2 3
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 AUG
PY 2010
VL 114
IS 3
BP 706
EP 716
DI 10.1111/j.1471-4159.2010.06791.x
PG 11
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 620ZI
UT WOS:000279541900008
PM 20477910
ER
PT J
AU Gallagher, A
Grant, EP
Madan, N
Jarrett, DY
Lyczkowski, DA
Thiele, EA
AF Gallagher, Anne
Grant, Ellen P.
Madan, Neel
Jarrett, Delma Y.
Lyczkowski, David A.
Thiele, Elizabeth A.
TI MRI findings reveal three different types of tubers in patients with
tuberous sclerosis complex
SO JOURNAL OF NEUROLOGY
LA English
DT Article
DE Tuber classification; MRI signal intensity; Brain lesion; Epilepsy; TSC
mutation
ID INFANTILE SPASMS; CORTICAL TUBERS; EPILEPTOGENIC TUBERS; BRAIN; TSC2;
ABNORMALITIES; MUTATIONS; DIAGNOSIS; SEVERITY; EPILEPSY
AB Cortical tubers are very common in tuberous sclerosis complex (TSC) and widely vary in size, appearance and location. The relationship between tuber features and clinical phenotype is unclear. The aim of the study is to propose a classification of tuber types along a spectrum of severity, using magnetic resonance imaging (MRI) characteristics in 35 patients with TSC and history of epilepsy, and to investigate the relationship between tuber types and genetics, as well as clinical manifestations. Three types of tubers were identified based on the MRI signal intensity of their subcortical white matter component. (1) Tubers Type A are isointense on volumetric T1 images and subtly hyperintense on T2 weighted and fluid-attenuated inversion recovery (FLAIR); (2) Type B are hypointense on volumetric T1 images and homogeneously hyperintense on T2 weighted and FLAIR; (3) Type C are hypointense on volumetric T1 images, hyperintense on T2 weighted, and heterogeneous on FLAIR characterized by a hypointense central region surrounded by a hyperintense rim. Based on the dominant tuber type present, three distinct patient groups were also identified: Patients with Type A tuber dominance have a milder phenotype. Patients with Type C tuber dominance have more MRI abnormalities such as subependymal giant cell tumors, and were more likely to have an autism spectrum disorder, a history of infantile spasms, and a higher frequency of epileptic seizures, compared to patients who have a dominance in Type B tubers, and especially to those with a Type A dominance.
C1 [Thiele, Elizabeth A.] Carol & James Herscot Ctr Tuberous Sclerosis, Boston, MA 02114 USA.
[Gallagher, Anne; Lyczkowski, David A.; Thiele, Elizabeth A.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Gallagher, Anne; Grant, Ellen P.; Madan, Neel; Jarrett, Delma Y.; Lyczkowski, David A.; Thiele, Elizabeth A.] Harvard Univ, Sch Med, Boston, MA USA.
[Grant, Ellen P.] Childrens Hosp Boston, Fetal Neonatal Neuroimaging & Dev Sci Ctr, Boston, MA USA.
[Madan, Neel] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Jarrett, Delma Y.] Childrens Hosp Boston, Dept Radiol, Boston, MA USA.
RP Thiele, EA (reprint author), Carol & James Herscot Ctr Tuberous Sclerosis, Complex,175 Cambridge St,Suite 340, Boston, MA 02114 USA.
EM ethiele@partners.org
FU Canadian Institutes of Health Research (CIHR)
FX We are grateful to Miguel Chagnon, Adam Numis and Larry MacDonald for
providing advice and information regarding statistical analysis. This
work was supported by a scholarship by the Canadian Institutes of Health
Research (CIHR), awarded to Anne Gallagher, Ph.D. as well as by the
Carol and James Herscot Center for Tuberous Sclerosis Complex.
NR 44
TC 21
Z9 24
U1 0
U2 5
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0340-5354
J9 J NEUROL
JI J. Neurol.
PD AUG
PY 2010
VL 257
IS 8
BP 1373
EP 1381
DI 10.1007/s00415-010-5535-2
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 632AW
UT WOS:000280393400023
PM 20352250
ER
PT J
AU Huttunen, HJ
Havas, D
Peach, C
Barren, C
Duller, S
Xia, WM
Frosch, MP
Hutter-Paier, B
Windisch, M
Kovacs, DM
AF Huttunen, Henri J.
Havas, Daniel
Peach, Camilla
Barren, Cory
Duller, Stephan
Xia, Weiming
Frosch, Matthew P.
Hutter-Paier, Birgit
Windisch, Manfred
Kovacs, Dora M.
TI The Acyl-Coenzyme A:Cholesterol Acyltransferase Inhibitor CI-1011
Reverses Diffuse Brain Amyloid Pathology in Aged Amyloid Precursor
Protein Transgenic Mice
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE Alzheimer disease; Cholesterol transport; Glia; Lipids;
Neurodegeneration; Transgenic
ID GAMMA-SECRETASE INHIBITOR; SPORADIC ALZHEIMERS-DISEASE; BETA-PEPTIDE
GENERATION; MOUSE MODEL; DOWN-SYNDROME; PLAQUE DEPOSITION; IN-VIVO;
CHOLESTEROL; APP; INFLAMMATION
AB Cerebral accumulation of amyloid-beta (A beta) is characteristic of Alzheimer disease and of amyloid precursor protein (APP) transgenic mice. Here, we assessed the efficacy of CI-1011, an inhibitor of acylcoenzyme A: cholesterol acyltransferase, which is suitable for clinical use, in reducing amyloid pathology in both young (6.5 months old) and aged (16 months old) human APP transgenic mice. Treatment of young animals with CI-1011 decreased amyloid plaque load in the cortex and hippocampus and reduced the levels of insoluble A beta(40) and A beta(42) and C-terminal fragments of APP in brain extracts. In aged mice, CI-1011 specifically reduced diffuse amyloid plaques with a minor effect on thioflavin S-positive dense-core plaques. Reduced diffusible amyloid was accompanied by suppression of astrogliosis and enhanced microglial activation. Collectively, these data suggest that CI-1011 treatment reduces amyloid burden in human APP mice by limiting generation and increasing clearance of diffusible A beta.
C1 [Huttunen, Henri J.; Peach, Camilla; Barren, Cory; Kovacs, Dora M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neurobiol Dis Lab,Genet & Aging Res Unit, Charlestown, MA 02129 USA.
[Huttunen, Henri J.; Peach, Camilla; Barren, Cory; Frosch, Matthew P.; Kovacs, Dora M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, MassGen Inst Neurodegenerat Dis, Charlestown, MA 02129 USA.
[Huttunen, Henri J.; Peach, Camilla; Barren, Cory; Frosch, Matthew P.; Kovacs, Dora M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Charlestown, MA 02129 USA.
[Huttunen, Henri J.] Univ Helsinki, Ctr Neurosci, Helsinki, Finland.
[Havas, Daniel; Duller, Stephan; Hutter-Paier, Birgit; Windisch, Manfred] JSW Res Forschungslab GmbH, Inst Expt Pharmacol, Grambach Graz, Austria.
[Xia, Weiming] Brigham & Womens Hosp, Ctr Neurol Dis, Boston, MA 02115 USA.
[Xia, Weiming] Harvard Univ, Sch Med, Boston, MA USA.
RP Kovacs, DM (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neurobiol Dis Lab,Genet & Aging Res Unit, 114 16th St, Charlestown, MA 02129 USA.
EM Dora_Kovacs@hms.harvard.edu
RI xia, weiming/E-5465-2016;
OI xia, weiming/0000-0002-7463-3295; Huttunen, Henri/0000-0002-9867-4438
FU Cure Alzheimer's Fund; National Institutes of Health [R01 NS45860]
FX This study was supported by grants from the Cure Alzheimer's Fund and
the National Institutes of Health (R01 NS45860). The authors declare no
conflict of interest.
NR 61
TC 22
Z9 23
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD AUG
PY 2010
VL 69
IS 8
BP 777
EP 788
DI 10.1097/NEN.0b013e3181e77ed9
PG 12
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 633DD
UT WOS:000280478800002
PM 20613640
ER
PT J
AU Benn, CL
Luthi-Carter, R
Kuhn, A
Sadri-Vakili, G
Blankson, KL
Dalai, SC
Goldstein, DR
Spires, TL
Pritchard, J
Olson, JM
van Dellen, A
Hannan, AJ
Cha, JHJ
AF Benn, Caroline L.
Luthi-Carter, Ruth
Kuhn, Alexandre
Sadri-Vakili, Ghazaleh
Blankson, Kwabena L.
Dalai, Sudeb C.
Goldstein, Darlene R.
Spires, Tara L.
Pritchard, Joel
Olson, James M.
van Dellen, Anton
Hannan, Anthony J.
Cha, Jang-Ho J.
TI Environmental Enrichment Reduces Neuronal Intranuclear Inclusion Load
But Has No Effect on Messenger RNA Expression in a Mouse Model of
Huntington Disease
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE Huntington disease; In situ hybridization; Microarray gene expression
profiling; Neuronal intranuclear inclusions; Neurotransmitter receptors;
Real-time RT-PCR; Receptor binding; Transcriptional dysregulation
ID AGE-OF-ONSET; GENE-EXPRESSION; TRANSGENIC MICE; POLYGLUTAMINE
AGGREGATION; RECEPTOR EXPRESSION; MUTANT HUNTINGTIN; WILD-TYPE; BRAIN;
EXPERIENCE; DEFICITS
AB Huntington disease (HD) is a fatal neurodegenerative disease with no effective treatment. In the R6/1 mouse model of HD, environmental enrichment delays the neurologic phenotype onset and prevents cerebral volume loss by unknown molecular mechanisms. We examined the effects of environmental enrichment on well-characterized neuropathological parameters in a mouse model of HD. We found a trend toward preservation of downregulated neurotransmitter receptors in striatum of environmentally enriched mice and assessed possible enrichment-related modifications in gene expression using microarrays. We observed similar gene expression changes in R6/1 and R6/2 transgenic mice but found no specific changes in enrichment-related microarray expression profiles in either transgenic or wild-type mice. Furthermore, specific corrections in transprotein-induced transcriptional dysregulation in R6/1 mice were not detected by microarray profiling. However, gene-specific analyses suggested that long-term environmental enrichment may beneficially modulate gene expression dysregulation. Finally, environmental enrichment significantly decreased neuronal intranuclear inclusion load, despite unaffected transgene expression levels. Thus, the therapeutic effects of environmental enrichment likely contribute to decreasing aggregated polyglutamine protein levels without exerting strong effects on gene expression.
C1 [Cha, Jang-Ho J.] Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Charlestown, MA 02129 USA.
[Luthi-Carter, Ruth; Kuhn, Alexandre; Goldstein, Darlene R.] Ecole Polytech Fed Lausanne, Lausanne, Switzerland.
[Pritchard, Joel; Olson, James M.] Fred Hutchinson Canc Res Ctr, Human Biol Div, Seattle, WA 98104 USA.
[van Dellen, Anton; Hannan, Anthony J.] Univ Oxford, Univ Lab Physiol, Oxford, England.
[Hannan, Anthony J.] Univ Melbourne, Howard Florey Inst, Florey Neurosci Inst, Melbourne, Vic 3010, Australia.
[Hannan, Anthony J.] Univ Melbourne, Dept Anat & Cell Biol, Melbourne, Vic 3010, Australia.
RP Cha, JHJ (reprint author), Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, 114 16th St, Charlestown, MA 02129 USA.
EM cha@helix.mgh.harvard.edu
OI Spires-Jones, Tara/0000-0003-2530-0598
FU Huntington's Disease Society of America Coalition for the Cure;
Hereditary Disease Foundation's Cure Huntington's Disease Initiative;
Glendorn Foundation; National Institutes of Health [NS38106, NS45242,
AG00277, AG13617]; Ecole Polytechnique Federale de Lausanne; UK Medical
Research Council; National Science Foundation
FX This work was supported by grants from the Huntington's Disease Society
of America Coalition for the Cure, the Hereditary Disease Foundation's
Cure Huntington's Disease Initiative, the Glendorn Foundation, the
National Institutes of Health (NS38106, NS45242, AG00277, and AG13617),
the Ecole Polytechnique Federale de Lausanne, the UK Medical Research
Council, and the National Science Foundation.
NR 57
TC 17
Z9 17
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD AUG
PY 2010
VL 69
IS 8
BP 817
EP 827
DI 10.1097/NEN.0b013e3181ea167f
PG 11
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 633DD
UT WOS:000280478800005
PM 20613636
ER
PT J
AU Nelson, PT
Frosch, MP
AF Nelson, Peter T.
Frosch, Matthew P.
TI Correspondence Regarding: Thinking Outside the Box: Alzheimer-Type
Neuropathology That Does Not Map Directly Onto Current Consensus
Recommendations. J Neuropathol Exp Neurol 2010;69:449-54 Reply
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Letter
C1 [Nelson, Peter T.] Univ Kentucky, Lexington, KY 40506 USA.
[Frosch, Matthew P.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Nelson, PT (reprint author), Univ Kentucky, Lexington, KY 40506 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 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD AUG
PY 2010
VL 69
IS 8
BP 864
EP 865
DI 10.1097/01.jnen.0000384006.06660.a2
PG 2
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 633DD
UT WOS:000280478800010
ER
PT J
AU Robinson, JD
AF Robinson, Jennifer D.
TI Raising Awareness of Heparin-Induced Thrombocytopenia in Subarachnoid
Hemorrhage
SO JOURNAL OF NEUROSCIENCE NURSING
LA English
DT Article
C1 Massachusetts Gen Hosp, Neurosci ICU, Boston, MA 02114 USA.
RP Robinson, JD (reprint author), Massachusetts Gen Hosp, Neurosci ICU, Boston, MA 02114 USA.
EM Jenrobinson80@gmail.com
NR 9
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0888-0395
J9 J NEUROSCI NURS
JI J. Neurosci. Nurs.
PD AUG
PY 2010
VL 42
IS 4
BP 208
EP 211
PG 4
WC Clinical Neurology; Nursing
SC Neurosciences & Neurology; Nursing
GA 632PG
UT WOS:000280436100006
PM 20804115
ER
PT J
AU Palazzolo, I
Nedelsky, NB
Askew, CE
Harmison, GG
Kasantsev, AG
Taylor, JP
Fischbeck, KH
Pennuto, M
AF Palazzolo, Isabella
Nedelsky, Natalia B.
Askew, Caitlin E.
Harmison, George G.
Kasantsev, Aleksey G.
Taylor, J. Paul
Fischbeck, Kenneth H.
Pennuto, Maria
TI B2 Attenuates Polyglutamine-Expanded Androgen Receptor Toxicity in Cell
and Fly Models of Spinal and Bulbar Muscular Atrophy
SO JOURNAL OF NEUROSCIENCE RESEARCH
LA English
DT Article
DE polyglutamine disease; SBMA; androgen receptor; B2; inclusions
ID TRANSGENIC MOUSE MODEL; INTRANUCLEAR INCLUSIONS; TRANSCRIPTIONAL
REGULATION; KENNEDY-DISEASE; PROTEIN-KINASE; NEURODEGENERATION;
HUNTINGTIN; NUCLEAR; BINDING; ACETYLATION
AB Expanded polyglutamine tracts cause neurodegeneration through a toxic gain-of-function mechanism. Generation of inclusions is a common feature of polyglutamine diseases and other protein misfolding disorders. Inclusion formation is likely to be a defensive response of the cell to the presence of unfolded protein. Recently, the compound B2 has been shown to increase inclusion formation and decrease toxicity of polyglutamine-expanded huntingtin in cultured cells. We explored the effect of B2 on spinal and bulbar muscular atrophy (SBMA). SBMA is caused by expansion of polyglutamine in the androgen receptor (AR) and is characterized by the loss of motor neurons in the brain-stem and spinal cord. We found that B2 increases the deposition of mutant AR into nuclear inclusions, without altering the ligand-induced aggregation, expression, or subcellular distribution of the mutant protein. The effect of B2 on inclusions was associated with a decrease in AR transactivation function. We show that B2 reduces mutant AR toxicity in cell and fly models of SBMA, further supporting the idea that accumulation of polyglutamine-expanded protein into inclusions is protective. Our findings suggest B2 as a novel approach to therapy for SBMA. (C) 2010 Wiley-Liss, inc.
C1 [Pennuto, Maria] Italian Inst Technol, Dept Neurosci, I-16163 Genoa, Italy.
[Palazzolo, Isabella; Askew, Caitlin E.; Harmison, George G.; Fischbeck, Kenneth H.] NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
[Palazzolo, Isabella] Univ Milan, Inst Endocrinol, Milan, Italy.
[Nedelsky, Natalia B.; Taylor, J. Paul] St Jude Childrens Hosp, Dept Dev Neurobiol, Memphis, TN 38105 USA.
[Nedelsky, Natalia B.] Univ Penn, Neurosci Grad Grp, Philadelphia, PA 19104 USA.
[Kasantsev, Aleksey G.] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Pennuto, M (reprint author), Italian Inst Technol, Dept Neurosci & Brain Technol, Via Morego 30, I-16163 Genoa, Italy.
EM maria.pennuto@iit.it
OI Pennuto, Maria/0000-0001-8634-0767
FU NINDS-NIH; Kennedy's Disease Association; Muscular Dystrophy
Association; NIH [NS053825]
FX Contract grant sponsor: NINDS-NIH; Contract grant sponsor: Kennedy's
Disease Association (to M.P.); Contract grant sponsor: Muscular
Dystrophy Association (to M.P., J.P.T.); Contract grant sponsor: NIH;
Contract grant number: NS053825 (to J.P.T.).
NR 48
TC 17
Z9 17
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0360-4012
J9 J NEUROSCI RES
JI J. Neurosci. Res.
PD AUG 1
PY 2010
VL 88
IS 10
BP 2207
EP 2216
DI 10.1002/jnr.22389
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 622ZM
UT WOS:000279706200013
PM 20336775
ER
PT J
AU Shin, HK
Lee, HR
Lee, DH
Hong, KW
Lee, JH
Park, SY
Lee, SJ
Lee, JS
Lee, WS
Rhim, BY
Kim, CD
AF Shin, Hwa Kyoung
Lee, Hye Rin
Lee, Dong Hyung
Hong, Ki Whan
Lee, Jeong Hyun
Park, So Youn
Lee, Seung Jin
Lee, Jun Sik
Lee, Won Suk
Rhim, Byung Yong
Kim, Chi Dae
TI Cilostazol Enhances Neovascularization in the Mouse Hippocampus After
Transient Forebrain Ischemia
SO JOURNAL OF NEUROSCIENCE RESEARCH
LA English
DT Article
DE CD31; cilostazol; endothelial progenitor cells; transient forebrain
ischemia; vasculogenesis
ID ENDOTHELIAL PROGENITOR CELLS; DELAYED NEURONAL DEATH; BONE-MARROW;
NEUROTROPHIC FACTOR; DENTATE GYRUS; GROWTH-FACTOR; STEM-CELLS; IN-VITRO;
NEUROGENESIS; ANGIOGENESIS
AB Cilostazol is known to be a specific type III phosphodiesterase inhibitor, which promotes increased intracellular cAMP levels. We assessed the effect of cilostazol on production of angioneurins and chemokines and recruitment of new endothelial cells for vasculogenesis in a mouse model of transient forebrain ischemia. Pyramidal cell loss was prominently evident 3-28 days postischemia, which was markedly ameliorated by cilostazol treatment. Expression of angioneurins, including endothelial nitric oxide synthase, vascular endothelial growth factor, and brain-derived neurotrophic factor, was up-regulated by cilostazol treatment in the postischemic hippocampus. Cilostazol also increased Sca-1/vascular endothelial growth factor receptor-2 positive cells in the bone marrow and circulating peripheral blood and the number of stromal cell-derived factor-1 alpha-positive cells in the molecular layer of the hippocampus, which colocalized with CD31. CXCR4 chemokine receptors were up-regulated by cilostazol in mouse bone marrow-derived endothelial progenitor cells, suggesting that cilostazol may be important in targeting or homing in of bone marrow-derived stem cells to areas of injured tissues. CD31-positive cells were colocalized with almost all bromodeoxyuridine-positive cells in the molecular layer, indicating stimulation of endothelial cell proliferation by cilostazol. These data suggest that cilostazol markedly enhances neovascularization in the hippocampus CA1 area in a mouse model of transient forebrain ischemia, providing a beneficial interface in which both bone marrow-derived endothelial progenitor cells and angioneurins influence neurogenesis in injured tissue. (C) 2010 Wiley-Liss, Inc.
C1 [Lee, Won Suk; Rhim, Byung Yong; Kim, Chi Dae] Pusan Natl Univ, Sch Med, Dept Pharmacol, Pusan 609735, South Korea.
[Lee, Dong Hyung] Pusan Natl Univ, Sch Med, Dept Obstet & Gynecol, Pusan 609735, South Korea.
[Shin, Hwa Kyoung] Pusan Natl Univ, Sch Korean Med, Div Meridian & Struct Med, Pusan 609735, South Korea.
[Lee, Hye Rin; Hong, Ki Whan; Park, So Youn; Lee, Seung Jin; Lee, Won Suk; Kim, Chi Dae] Pusan Natl Univ, MRC Ischem Tissue Regenerat, Pusan 609735, South Korea.
[Lee, Jeong Hyun] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Stroke & Neurovasc Regulat Lab,Dept Radiol, Charlestown, MA USA.
[Lee, Jun Sik] Albert Einstein Coll Med, Sch Med, Dept Microbiol & Immunol, Bronx, NY 10467 USA.
RP Kim, CD (reprint author), Pusan Natl Univ, Sch Med, Dept Pharmacol, Yangsan Si 626870, Gyeongsangnam D, South Korea.
EM chidkim@pusan.ac.kr
RI Lee, Jeong Hyun/G-1676-2013
OI Lee, Jeong Hyun/0000-0003-0504-0119
FU Ministry of Education, Science and Technology [KRF-2008-313-E00477,
R13-2005-009]; Pusan National University
FX Contract grant sponsor: National Research Foundation of Korea funded by
the Ministry of Education, Science and Technology; Contract grant
number: Basic Science Research Program KRF-2008-313-E00477; Contract
grant number: MRC program R13-2005-009; Contract grant sponsor: Pusan
National University Research Grant, 2009.
NR 32
TC 12
Z9 12
U1 0
U2 6
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0360-4012
J9 J NEUROSCI RES
JI J. Neurosci. Res.
PD AUG 1
PY 2010
VL 88
IS 10
BP 2228
EP 2238
DI 10.1002/jnr.22376
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 622ZM
UT WOS:000279706200015
PM 20175201
ER
PT J
AU Li, LN
Quang, TS
Brady, LW
AF Li, Linna
Quang, Tony S.
Brady, Luther W.
TI Monoclonal antibodies Response
SO JOURNAL OF NEUROSURGERY
LA English
DT Editorial Material
ID MALIGNANT GLIOMA; RADIOTHERAPY; GLIOBLASTOMA; PROGRESSION
C1 [Li, Linna] Drexel Univ, Coll Med, Fox Chase Canc Ctr, Philadelphia, PA 19104 USA.
[Brady, Luther W.] Drexel Univ, Coll Med, Dept Radiat Oncol, Philadelphia, PA 19104 USA.
[Quang, Tony S.] Univ Washington, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
RP Li, LN (reprint author), Drexel Univ, Coll Med, Fox Chase Canc Ctr, Philadelphia, PA 19104 USA.
NR 7
TC 0
Z9 0
U1 1
U2 2
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
J9 J NEUROSURG
JI J. Neurosurg.
PD AUG
PY 2010
VL 113
IS 2
BP 190
EP 191
PG 2
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 632FH
UT WOS:000280405900011
ER
PT J
AU Li, LN
Quang, TS
Gracely, EJ
Kim, JH
Emrich, JG
Yaeger, TE
Jenrette, JM
Cohen, SC
Black, P
Brady, LW
AF Li, Linna
Quang, Tony S.
Gracely, Ed J.
Kim, Ji H.
Emrich, Jacqueline G.
Yaeger, Theodore E.
Jenrette, Joseph M.
Cohen, Steven C.
Black, Perry
Brady, Luther W.
TI A Phase II study of anti-epidermal growth factor receptor
radioimmunotherapy in the treatment of glioblastoma multiforme Clinical
article
SO JOURNAL OF NEUROSURGERY
LA English
DT Article
DE radioimmunotherapy; glioblastoma multiforme; temozolomide;
(125)iodine-labeled monoclonal antibody 425; anti-epidermal growth
factor receptor
ID NEWLY-DIAGNOSED GLIOBLASTOMA; ONCOLOGY-GROUP TRIAL; HIGH-GRADE GLIOMA;
RADIATION-THERAPY; SUPRATENTORIAL GLIOBLASTOMA; MALIGNANT GLIOMAS;
STEREOTACTIC RADIOSURGERY; MONOCLONAL ANTIBODY-425; ADJUVANT
CHEMOTHERAPY; INTERFERON-BETA
AB Object. This single-institution Phase II study tests the efficacy of adjuvant radioimmunotherapy with I-125-labeled anti epidermal growth factor receptor 425 murine monoclonal antibody (I-125-mAb 425) in patients with newly diagnosed glioblastoma multiforme (GBM).
Methods. A total of 192 patients with GBM were treated with I-125-mAb 425 over a course of 3 weekly intravenous injections of 1.8 GBq following surgery and radiation therapy. The primary end point was overall survival, and the secondary end point was toxicity. Additional subgroup analyses were performed comparing treatment with I-125-mAb 425 (RIT, 132 patients), I-125-mAb 425 and temozolomide (TMZ+RIT, 60 patients), and a historical control group (CTL, 81 patients).
Results. The median age was 53 years (range 19-78 years), and the median Karnofsky Performance Scale score was 80 (range 60-100). The percentage of patients who underwent debulking surgery was 77.6% and that of those receiving temozolomide was 31.3%. The overall median survival was 15.7 months (95% CI 13.6-17.8 months). The 1- and 2-year survivals were 62.5 and 25.5%, respectively. For subgroups RIT and TMZ+RIT, the median survivals were 14.5 and 20.2 months, respectively. No Grade 3 or 4 toxicity was seen with the administration of I-125-mAb 425. The CTL patients lacked Karnofsky Performance Scale scores, had poorer survival, were older, and were less likely to receive radiation therapy. On multivariate analysis, the hazard ratios for RIT versus CTL, TMZ+RIT versus CTL, and TMZ+RIT versus RIT were 0.49 (p < 0.001), 0.30 (p < 0.001), and 0.62 (p = 0.008), respectively.
Conclusions. In this large Phase II study of 192 patients with GBM treated with anti epidermal growth factor receptor I-125-mAb 425 radioimmunotherapy, survival was 15.7 months, and treatment was safe and well tolerated. (DOI: 10.3171/2010.2.JNS091211)
C1 [Li, Linna] Fox Chase Canc Ctr, Dept Radiat Oncol, Philadelphia, PA 19111 USA.
[Gracely, Ed J.] Drexel Univ, Coll Med, Dept Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Emrich, Jacqueline G.; Brady, Luther W.] Drexel Univ, Coll Med, Dept Radiat Oncol, Philadelphia, PA 19104 USA.
[Black, Perry] Drexel Univ, Coll Med, Dept Surg Neurosurg, Philadelphia, PA 19104 USA.
[Cohen, Steven C.] Bryn Mawr Hosp, Dept Hematol & Oncol, Philadelphia, PA USA.
[Quang, Tony S.] Univ Washington, VA Puget Sound Hlth Care Syst, Dept Radiat Oncol, Seattle, WA 98195 USA.
[Kim, Ji H.] City Hope Natl Med Ctr, Dept Radiat Oncol, Duarte, CA USA.
[Yaeger, Theodore E.] Wake Forest Univ, Sch Med, Dept Radiat Oncol, Winston Salem, NC 27109 USA.
[Jenrette, Joseph M.] Med Univ S Carolina, Dept Radiat Oncol, Charleston, SC 29425 USA.
RP Li, LN (reprint author), Fox Chase Canc Ctr, Dept Radiat Oncol, 333 Cottman Ave, Philadelphia, PA 19111 USA.
EM linna.li@fccc.edu
NR 54
TC 37
Z9 37
U1 0
U2 2
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
EI 1933-0693
J9 J NEUROSURG
JI J. Neurosurg.
PD AUG
PY 2010
VL 113
IS 2
BP 192
EP 198
DI 10.3171/2010.2.JNS091211
PG 7
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 632FH
UT WOS:000280405900012
PM 20345222
ER
PT J
AU Beckham, JD
Tuttle, KD
Tyler, KL
AF Beckham, J. David
Tuttle, Kathryn D.
Tyler, Kenneth L.
TI Caspase-3 activation is required for reovirus-induced encephalitis in
vivo
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Article
DE apoptosis; caspase; encephalitis; neuron; reovirus
ID CENTRAL-NERVOUS-SYSTEM; JAPANESE ENCEPHALITIS; CELL-DEATH; PERSISTENT
INFECTIONS; INDUCED APOPTOSIS; VIRUS INFECTION; PATHOGENESIS;
REPLICATION; INHIBITOR; MUTATIONS
AB Reovirus infection of neonatal mice provides a classic experimental system for understanding the molecular pathogenesis of central nervous system (CNS) viral infection. CNS tissue injury, caused by many human neurotropic viruses, including herpes viruses and West Nile virus, is associated with caspase-dependent apoptotic neuronal cell death. We have previously shown that reovirus-induced CNS tissue injury results from apoptosis and is associated with activation of both death-receptor and mitochondrial apoptotic pathways culminating in the activation of the downstream effector caspase, caspase-3. In order to directly investigate the role of caspase-3 in virus-induced neuronal death and CNS tissue injury during encephalitis, we have compared the pathogenesis of reovirus CNS infection in mice lacking the caspase-3 gene (caspase-3 (-/-)) to syngeneic wild-type mice. Prior studies of antiapoptotic treatments for reovirus-infected mice have indicated that protection from reovirus-induced neuronal injury can occur without altering the viral titer in the brains of infected mice. We now show that reovirus infection of caspase-3 (-/-) mice was associated with dramatic reduction in severity of CNS tissue injury, decreased viral antigen and titer in the brain, and enhanced survival of infected mice. Following intracerebral inoculation, the authors also show that virus spread from the brain to the eyes in reovirus-infected caspase-3 (-/-) mice, indicating that viral spread was intact in these mice. Examination of brains of long-term survivors of reovirus infection among caspase-3 (-/-) mice showed that these mice eventually clear their CNS viral infection, and do not manifest residual or delayed CNS tissue injury. Journal of NeuroVirology (2010) 16, 306-317.
C1 [Beckham, J. David] Univ Colorado Denver, Dept Med, Div Infect Dis, Aurora, CO 80045 USA.
[Tyler, Kenneth L.] Denver Vet Affairs Med Ctr, Denver, CO USA.
RP Beckham, JD (reprint author), Univ Colorado Denver, Dept Med, Div Infect Dis, Bldg Res 2,12700 E 19th Ave,B168, Aurora, CO 80045 USA.
EM david.beckham@ucdenver.edu
OI Tyler, Kenneth/0000-0003-3294-5888
FU VA; NIH [5K08AI076518, 5R01NS050138, 1R01NS051403]; ASCI
FX This work was supported in part by VA Merit funding, NIH 5K08AI076518,
NIH 5R01NS050138, NIH 1R01NS051403, and ASCI Young Investigator Award.
NR 37
TC 14
Z9 14
U1 0
U2 2
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 1355-0284
J9 J NEUROVIROL
JI J. Neurovirol.
PD AUG
PY 2010
VL 16
IS 4
BP 306
EP 317
DI 10.3109/13550284.2010.499890
PG 12
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA 647JA
UT WOS:000281613400006
PM 20626234
ER
PT J
AU Le, AD
Lee, JS
Dodson, TB
Kademani, D
Feinberg, SE
Shetty, V
Wohlford, ME
Zuniga, JR
Cunningham, LL
AF Le, Anh D.
Lee, Janice S.
Dodson, Thomas B.
Kademani, Deepak
Feinberg, Stephen E.
Shetty, Vivek
Wohlford, Mark E.
Zuniga, John R.
Cunningham, Larry L., Jr.
TI Proceedings of the American Association of Oral and Maxillofacial
Surgeons 2009 Research Summit
SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
ID AAOMS RESEARCH SUMMIT; BRANCHING MORPHOGENESIS; SURFACE MODIFICATIONS;
TISSUE; STIMULATION; ACTIVATION; PAIN; FMRI; REPRESENTATION; METHYLATION
C1 [Cunningham, Larry L., Jr.] Univ Kentucky, Coll Dent, Coll Dent, Lexington, KY 40536 USA.
[Le, Anh D.] Univ So Calif, Los Angeles, CA USA.
[Lee, Janice S.] Univ Calif San Francisco, Dept Oral & Maxillofacial Surg, San Francisco, CA 94143 USA.
[Dodson, Thomas B.] Harvard Univ, Sch Dent Med, Boston, MA 02115 USA.
[Dodson, Thomas B.] Massachusetts Gen Hosp, Ctr Appl Clin Invest CACI, Dept Oral & Maxillofacial Surg, Boston, MA 02114 USA.
[Kademani, Deepak] Univ Minnesota, Sch Dent, Dept Oral & Maxillofacial Surg, Minneapolis, MN 55455 USA.
[Feinberg, Stephen E.] Univ Michigan Hosp, Dept Oral & Maxillofacial Surg, Ann Arbor, MI 48109 USA.
[Shetty, Vivek] Univ Calif Los Angeles, Ctr Hlth Sci, Facial Injury Research Ctr, Los Angeles, CA 90024 USA.
[Zuniga, John R.] Univ Texas SW Med Ctr Dallas, Dept Oral & Maxillofacial Surg, Dallas, TX 75390 USA.
RP Cunningham, LL (reprint author), Univ Kentucky, Coll Dent, Coll Dent, 800 Rose St,D-508, Lexington, KY 40536 USA.
EM llcunn2@email.uky.edu
OI zuniga, john/0000-0002-8602-2811
NR 45
TC 0
Z9 0
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 0278-2391
J9 J ORAL MAXIL SURG
JI J. Oral Maxillofac. Surg.
PD AUG
PY 2010
VL 68
IS 8
BP 1711
EP 1722
DI 10.1016/j.joms.2010.02.062
PG 12
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 635TT
UT WOS:000280680200002
PM 20542614
ER
PT J
AU Katsnelson, A
Tartakovsky, JV
Miloro, M
AF Katsnelson, Alexander
Tartakovsky, Julia V.
Miloro, Michael
TI Review of the Literature for Mandibular Metastasis Illustrated by a Case
of Lung Metastasis to the Temporomandibular Joint in an HIV-Positive
Patient
SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
ID CONDYLAR METASTASIS; BREAST ADENOCARCINOMA; HEPATOCELLULAR-CARCINOMA;
BRONCHOGENIC-CARCINOMA; TUMORS; MOUTH; JAWS; NEOPLASMS; CANCER
C1 [Miloro, Michael] Univ Illinois, Dept Oral & Maxillofacial Surg, Coll Dent, Chicago, IL USA.
[Tartakovsky, Julia V.] Harvard Univ, Cambridge, MA 02138 USA.
RP Katsnelson, A (reprint author), Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, 55 Fruit St,Warren 1201, Boston, MA 02114 USA.
EM akatsnelson@partners.org
NR 67
TC 2
Z9 2
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 0278-2391
J9 J ORAL MAXIL SURG
JI J. Oral Maxillofac. Surg.
PD AUG
PY 2010
VL 68
IS 8
BP 1960
EP 1964
DI 10.1016/j.joms.2009.07.075
PG 5
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 635TT
UT WOS:000280680200035
PM 20381938
ER
PT J
AU Kwon, JY
Chacko, AT
Kadzielski, JJ
Appleton, PT
Rodriguez, EK
AF Kwon, John Y.
Chacko, Aron T.
Kadzielski, John J.
Appleton, Paul T.
Rodriguez, Edward K.
TI A Novel Methodology for the Study of Injury Mechanism: Ankle Fracture
Analysis Using Injury Videos Posted on YouTube.com
SO JOURNAL OF ORTHOPAEDIC TRAUMA
LA English
DT Article
DE ankle fracture; video; Lauge Hansen; injury mechanism; youtube
ID LAUGE-HANSEN CLASSIFICATION; MALLEOLAR FRACTURES; OBSERVER VARIATION
AB Purpose: An inherent deficiency in the understanding of the biomechanics of fractures is the reliance on cadaveric or other nonphysiological injury models resulting from the prohibitive ethical and practical considerations of conducting injury studies in live participants. We describe a novel methodology for studying injury mechanisms using in vivo injury videos obtained from Youtube.com demonstrating injuries as they occur in real time and correlating them with the resulting injury radiographs.
Methods: Over 1000 video clips of potential ankle fractures were assessed for clear visualization of the mechanism of injury, including the foot position and deforming force. Candidate videos were selected if the mechanism of injury was classifiable by those described by Lauge-Hansen and there appeared to be a significant mechanism to likely cause fracture. X-rays were then requested from the individuals posting the video clips. Videos and x-rays were reviewed and classified using the Lauge-Hansen system in a blinded manner. The deforming mechanism in the video clips was classified as supination external rotation, supination adduction (SAD), pronation external rotation (PER), or pronation abduction. X-ray fracture patterns were similarly classified.
Results: Two hundred forty videos were selected and individuals posting the videos were contacted. Of 96 initial positive responses, we collected 15 videos with their corresponding radiographs. Eight had SAD-deforming trauma and seven had PER-deforming trauma as appreciated in the videos. There were 12 true ankle fractures. All five fractures judged by video to be SAD injuries resulted in a corresponding SAD pattern radiographic ankle fractures. Of the seven fractures judged by video to be PER injuries, only two resulted in PER pattern radiographic ankle fractures. Five PER injuries resulted in supination external rotation ankle fracture patterns.
Conclusion: Our series shows that when in vivo injury videos are matched to their corresponding x-rays, the Lauge-Hansen system is only 58% overall accurate in predicting fracture patterns from deforming injury mechanism as pertaining to SAD and PER injury mechanisms. All SAD injuries correlated but only 29% of PER injuries resulted in a PER fracture pattern. This study illustrates the ethical and practical difficulties of using public access Internet YouTube videos for the study of injury dynamics. The current case series illustrates the method's potential and may lead to future research analyzing the validity of the Lauge-Hansen classification system as applied to in vivo injuries.
C1 [Chacko, Aron T.; Appleton, Paul T.; Rodriguez, Edward K.] Harvard Univ, Dept Orthopaed Surg, Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Kwon, John Y.; Kadzielski, John J.] Massachusetts Gen Hosp, Harvard Combined Orthopaed Residency Program, Boston, MA 02114 USA.
RP Rodriguez, EK (reprint author), Harvard Univ, Dept Orthopaed Surg, Beth Israel Deaconess Med Ctr, 330 Brookline Ave,Stoneman 10, Boston, MA 02215 USA.
EM ekrodrig@bidmc.harvard.edu
FU AO [S-09-39R]
FX Part of the study was supported by AO research grant S-09-39R.
NR 17
TC 16
Z9 17
U1 1
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0890-5339
J9 J ORTHOP TRAUMA
JI J. Orthop. Trauma
PD AUG
PY 2010
VL 24
IS 8
BP 477
EP 482
DI 10.1097/BOT.0b013e3181c99264
PG 6
WC Orthopedics; Sport Sciences
SC Orthopedics; Sport Sciences
GA 630CK
UT WOS:000280249100012
PM 20657256
ER
PT J
AU Cook, DB
Stegner, AJ
Ellingson, LD
AF Cook, Dane B.
Stegner, Aaron J.
Ellingson, Laura D.
TI Exercise Alters Pain Sensitivity in Gulf War Veterans With Chronic
Musculoskeletal Pain
SO JOURNAL OF PAIN
LA English
DT Article
DE Gulf War; pain; exercise; veterans; fibromyalgia; hyperalgesia
ID FIBROMYALGIA SYNDROME; TEMPORAL SUMMATION; MAJOR DEPRESSION; CLINICAL
PAIN; MUSCLE; PERCEPTION; ILLNESSES; QUESTIONNAIRE; CONSEQUENCES;
STIMULATION
AB Since returning from the Persian Gulf, nearly 100,000 veterans of the first Gulf War (GVs) have reported numerous symptoms with no apparent medical explanation. A primary complaint of these individuals is chronic musculoskeletal pain (CMP). CMP symptoms in GVs are similar to those reported by patients with fibromyalgia (FM), but have not received equivalent scientific attention. Exercise research in CMP patients suggests that acute exercise may exacerbate pain while chronic exercise can reduce pain and improve other symptoms. However, the influence of exercise on GVs with CMP is largely unexplored. This study examined the impact of an acute bout of exercise on pain sensitivity in GVs with CMP. Thirty-two GVs (CMP, n = 15; Control, n = 17) were recruited to complete a series of psychophysical assessments to determine pain sensitivity to heat and pressure stimuli before and after exercise. In response to heat-pain stimuli, GVs with CMP reported higher pain intensity and affect ratings than healthy GVs and exhibited a significant increase in ratings following exercise. GVs with CMP rated exercise as more painful and effortful and were generally more sensitive to heat-pain stimuli than healthy GVs. These results are similar to what has been reported for acute exercise in patients with FM.
Perspective: Gulf War veterans with CMP perceive exercise as more painful and effortful than healthy GVs and experience increased pain sensitivity following exercise. These results suggest that similar abnormalities in central nervous system processing of nociceptive information documented in FM may also be occurring in GVs with CMP (C) 2010 by the American Pain Society
C1 [Cook, Dane B.] Univ Wisconsin, Dept Kinesiol, Unit 2, Madison, WI 53706 USA.
[Cook, Dane B.] William S Middleton Mem Vet Adm Med Ctr, Res Serv, Madison, WI USA.
RP Cook, DB (reprint author), Univ Wisconsin, Dept Kinesiol, Unit 2, 2000 Observ Dr, Madison, WI 53706 USA.
EM dcook@education.wisc.edu
FU Office of Research and Development, VA Central Office, Department of
Veterans Affairs [561-00215]
FX Supported by the Office of Research and Development, VA Central Office,
Department of Veterans Affairs (Grant #561-00215).
NR 49
TC 22
Z9 22
U1 1
U2 5
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 1526-5900
J9 J PAIN
JI J. Pain
PD AUG
PY 2010
VL 11
IS 8
BP 764
EP 772
DI 10.1016/j.jpain.2009.11.010
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 639KP
UT WOS:000280974000008
PM 20338824
ER
PT J
AU Penrod, JD
Deb, P
Dellenbaugh, C
Burgess, JF
Zhu, CW
Christiansen, CL
Luhrs, CA
Cortez, T
Livote, E
Allen, V
Morrison, RS
AF Penrod, Joan D.
Deb, Partha
Dellenbaugh, Cornelia
Burgess, James F., Jr.
Zhu, Carolyn W.
Christiansen, Cindy L.
Luhrs, Carol A.
Cortez, Therese
Livote, Elayne
Allen, Veleka
Morrison, R. Sean
TI Hospital-Based Palliative Care Consultation: Effects on Hospital Cost
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Article
ID QUALITY-OF-LIFE; INSTRUMENTAL VARIABLES; RANDOMIZED-TRIAL;
CANCER-PATIENTS; UNITED-STATES; OUTCOMES; END; SATISFACTION; CAREGIVERS;
MODELS
AB Context: Palliative care consultation teams in hospitals are becoming increasingly more common. Palliative care improves the quality of hospital care for patients with advanced disease. Less is known about its effects on hospital costs.
Objective: To evaluate the relationship between palliative care consultation and hospital costs in patients with advanced disease.
Design, setting, and patients: An observational study of 3321 veterans hospitalized with advanced disease between October 1, 2004 and September 30, 2006. The sample includes 606 (18%) veterans who received palliative care and 2715 (82%) who received usual hospital care. October 1, 2004 and September 30, 2006.
Main outcome measures: We studied the costs and intensive care unit (ICU) use of palliative versus usual care for patients in five Veterans Affairs hospitals over a 2-year period. We used an instrumental variable approach to control for unmeasured characteristics that affect both treatment and outcome.
Results: The average daily total direct hospital costs were $464 a day lower for the 606 patients receiving palliative compared to the 2715 receiving usual care (p < 0.001). Palliative care patients were 43.7 percentage points less likely to be admitted to ICU during the hospitalization than usual care patients (p < 0.001).
Comments: Palliative care for patients hospitalized with advanced disease results in lower costs of care and less utilization of intensive care compared to similar patients receiving usual care. Selection on unobserved characteristics plays an important role in the determination of costs of care.
C1 [Penrod, Joan D.; Dellenbaugh, Cornelia; Zhu, Carolyn W.; Livote, Elayne; Allen, Veleka] James J Peters VA Med Ctr, Hlth Serv REAP GRECC, Bronx, NY 10468 USA.
[Deb, Partha] CUNY Hunter Coll, Dept Econ, New York, NY 10021 USA.
[Burgess, James F., Jr.] VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA USA.
[Christiansen, Cindy L.] Boston Univ, Dept Hlth Policy & Management, Boston, MA 02215 USA.
[Luhrs, Carol A.] VA New York Harbor Healthcare Syst, Dept Oncol, Brooklyn, NY USA.
[Cortez, Therese] VA New York Harbor Healthcare Syst, Dept Palliat Care, New York, NY USA.
[Morrison, R. Sean] Mt Sinai Sch Med, Brookdale Dept Geriatr, Hertzberg Palliat Care Inst, New York, NY USA.
RP Penrod, JD (reprint author), James J Peters VA Med Ctr, Hlth Serv REAP GRECC, 130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM joan.penrod@mssm.edu
OI Burgess, James/0000-0002-6646-7071; Christiansen,
Cindy/0000-0001-9951-480X
FU Department Of Veteran Affairs, Health Services Research and Development
Service [IAD-06-060-2]
FX Funding for this study came from the Department Of Veteran Affairs,
Health Services Research and Development Service (grant # IAD-06-060-2).
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 44
TC 72
Z9 73
U1 0
U2 9
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-6218
J9 J PALLIAT MED
JI J. Palliat. Med.
PD AUG
PY 2010
VL 13
IS 8
BP 973
EP 979
DI 10.1089/jpm.2010.0038
PG 7
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 639HY
UT WOS:000280967100010
PM 20642361
ER
PT J
AU Lu, H
Trancik, E
Bailey, FA
Ritchie, C
Rosenfeld, K
Shreve, S
Furman, C
Smith, D
Wolff, C
Casarett, D
AF Lu, Hien
Trancik, Emily
Bailey, F. Amos
Ritchie, Christine
Rosenfeld, Kenneth
Shreve, Scott
Furman, Christian
Smith, Dawn
Wolff, Catherine
Casarett, David
TI Families' Perceptions of End-of-Life Care in Veterans Affairs versus
Non-Veterans Affairs Facilities
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Article
ID PALLIATIVE CARE; QUALITY; SATISFACTION; PROJECT; ACCESS; ACOVE; OLDER
AB Background: The Veterans Affairs (VA) has made significant investments in care for veterans. However, it is not known whether these investments have produced improvements in end-of-life care in the VA compared to other settings. Therefore, the goal of this study was to compare families' perceptions of end-of-life care among patients who died in VA and non-VA facilities.
Design: Retrospective 32-item telephone surveys were conducted with family members of patients who died in VA and non-VA facilities.
Setting: Five Veterans Affairs medical centers and their affiliated nursing homes and outpatient clinics.
Participants: Patients were eligible if they received any care from a participating VA facility in the last month of life and if they died in an inpatient setting. One family member per patient completed the survey.
Results: In bivariate analysis, patients who died in VA facilities (n = 520) had higher mean satisfaction scores compared to those who died in non-VA facilities (n = 89; 59 versus 51; rank sum test p = 0.002). After adjusting for medical center, the overall score was still significantly higher for those dying in the VA (beta = 0.07; confidence interval [CI] 0.02-0.11; p = 0.004), as was the domain measuring care around the time of death (beta = 0.11; CI = 0.04-0.17; p = 0.001).
Conclusion: Families of patients who died in VA facilities rated care as being better than did families of those who died in non-VA facilities. These results provide preliminary evidence that the VA's investment in end-of-life care has contributed to improvements in care in VA facilities compared to non-VA facilities.
C1 [Lu, Hien; Wolff, Catherine; Casarett, David] Univ Penn, Sch Med, Div Geriatr, Philadelphia, PA 19104 USA.
[Trancik, Emily] Villanova Univ, Philadelphia, PA USA.
[Bailey, F. Amos; Ritchie, Christine] Birmingham VA, Birmingham, AL USA.
[Rosenfeld, Kenneth] Greater Los Angeles VA, Los Angeles, CA USA.
[Shreve, Scott] Lebanon VA, Lebanon, PA USA.
[Furman, Christian] Louisville VA, Louisville, KY USA.
[Smith, Dawn; Casarett, David] Philadelphia VA Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
RP Casarett, D (reprint author), 3615 Chestnut St, Philadelphia, PA 19104 USA.
EM Casarett@mail.med.upenn.edu
FU VA Merit Award [IIR 03-128-2]; Presidential Early Career Award for
Scientists and Engineers
FX This study was supported by a VA Merit Award (IIR 03-128-2), by a VA
Advanced Research Career Development Award (Dr. Casarett), and by a
Presidential Early Career Award for Scientists and Engineers (Dr.
Casarett).
NR 27
TC 15
Z9 15
U1 1
U2 1
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-6218
J9 J PALLIAT MED
JI J. Palliat. Med.
PD AUG
PY 2010
VL 13
IS 8
BP 991
EP 996
DI 10.1089/jpm.2010.0044
PG 6
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 639HY
UT WOS:000280967100012
PM 20649437
ER
PT J
AU Demiris, G
Oliver, DP
Washington, K
Fruehling, LT
Haggarty-Robbins, D
Doorenbos, A
Wechkin, H
Berry, D
AF Demiris, George
Oliver, Debra Parker
Washington, Karla
Fruehling, Lynne Thomas
Haggarty-Robbins, Donna
Doorenbos, Ardith
Wechkin, Hope
Berry, Donna
TI A Problem Solving Intervention for Hospice Caregivers: A Pilot Study
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Article
ID HEALTH; CANCER; CARE
AB The Problem Solving Intervention (PSI) is a structured, cognitive-behavioral intervention that provides people with problem-solving coping skills to help them face major negative life events and daily challenges. PSI has been applied to numerous settings but remains largely unexplored in the hospice setting. The aim of this pilot study was to demonstrate the feasibility of PSI targeting informal caregivers of hospice patients. We enrolled hospice caregivers who were receiving outpatient services from two hospice agencies. The intervention included three visits by a research team member. The agenda for each visit was informed by the problem-solving theoretical framework and was customized based on the most pressing problems identified by the caregivers. We enrolled 29 caregivers. Patient's pain was the most frequently identified problem. On average, caregivers reported a higher quality of life and lower level of anxiety postintervention than at baseline. An examination of the caregiver reaction assessment showed an increase of positive esteem average and a decrease of the average value of lack of family support, impact on finances, impact on schedules, and on health. After completing the intervention, caregivers reported lower levels of anxiety, improved problem solving skills, and a reduced negative impact of caregiving. Furthermore, caregivers reported high levels of satisfaction with the intervention, perceiving it as a platform to articulate their challenges and develop a plan to address them. Findings demonstrate the value of problem solving as a psycho-educational intervention in the hospice setting and call for further research in this area.
C1 [Demiris, George; Fruehling, Lynne Thomas; Haggarty-Robbins, Donna; Doorenbos, Ardith] Univ Washington, Sch Nursing, Seattle, WA 98195 USA.
[Oliver, Debra Parker] Univ Missouri, Sch Med, Columbia, MO USA.
[Washington, Karla] Univ Louisville, Raymond A Kent Sch Social Work, Louisville, KY 40292 USA.
[Berry, Donna] Dana Farber Canc Inst, Harvard Canc Ctr, Boston, MA 02115 USA.
[Wechkin, Hope] Univ Washington, Evergreen Hosp, Seattle, WA 98195 USA.
[Wechkin, Hope] Univ Washington, Sch Med, Seattle, WA 98195 USA.
RP Demiris, G (reprint author), Univ Washington, Sch Nursing, BNHS Box 357266, Seattle, WA 98195 USA.
EM gdemiris@u.washington.edu
OI Washington, Karla T./0000-0002-1100-9524; Demiris,
George/0000-0002-6318-5829
FU National Institutes of Health National Institute of Nursing [R21
NR010744-01]
FX This project was funded in part by the National Institutes of Health
National Institute of Nursing Research Grant Nr. R21 NR010744-01 (A
Technology Enhanced Nursing Intervention for Hospice Caregivers, Demiris
PI).
NR 22
TC 17
Z9 17
U1 0
U2 6
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-6218
J9 J PALLIAT MED
JI J. Palliat. Med.
PD AUG
PY 2010
VL 13
IS 8
BP 1005
EP 1011
DI 10.1089/jpm.2010.0022
PG 7
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 639HY
UT WOS:000280967100014
PM 20649438
ER
PT J
AU Delgado-Borrego, A
Healey, D
Negre, B
Christofi, M
Sabharwal, S
Ludwig, DA
Chung, RT
Jonas, MM
AF Delgado-Borrego, Aymin
Healey, David
Negre, Betania
Christofi, Marielle
Sabharwal, Sabina
Ludwig, David A.
Chung, Raymond T.
Jonas, Maureen M.
TI Influence of Body Mass Index on Outcome of Pediatric Chronic Hepatitis C
Virus Infection
SO JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION
LA English
DT Article
DE fibrosis; interferon; obesity; pediatric; steatosis
ID FATTY LIVER-DISEASE; INSULIN-RESISTANCE; UNITED-STATES; CHILDHOOD
OVERWEIGHT; ANTIVIRAL THERAPY; OBESITY; STEATOSIS; CHILDREN; FIBROSIS;
IMPACT
AB Background and Aims: Evidence demonstrates that obesity is associated with progression of chronic hepatitis C virus (HCV) infection and poor response to interferon therapy among HCV-infected adults. However, this evidence has been confounded by multiple comorbidities present in adult cohorts and the use of single adult doses.
Patients and Methods: We performed a retrospective investigation to evaluate the role of body mass index (BMI) in chronic HCV progression and response to therapy in the children. One hundred twenty-three children and teenagers studied at Children's Hospital Boston for HCV infection between 1998 and 2007 were included. Patients' weight and height at the time of liver biopsy or before and after HCV therapy were obtained and BMI was calculated.
Results: The presence of steatosis was statistically associated with higher mean (+/- SE) BMI percentiles (72nd +/- 5.8 vs 58th +/- 3.5) percentile; F(1,101) = 4.2, P = 0.04. Nonresponders to treatment had a higher mean (+SE) BMI percentile (70th + 7.4) when compared with responders (50th +/- 6.5) in univariate and multivariate analyses (P = 0.04, P = 0.02, respectively). Using a multivariate model, it was calculated that 1 standard deviation (1 z-score unit) increase in baseline BMI z score is associated with a 12% decrease in the probability of sustained virologic response.
Conclusions: Overweight adversely affects the progression of chronic HCV liver disease and is associated with diminished response to antiviral therapy using weight-based dosing in a cohort with minimal comorbidities.
C1 [Delgado-Borrego, Aymin; Negre, Betania; Ludwig, David A.] Univ Miami, Dept Pediat, Batchelor Childrens Res Inst, Div Clin Res, Miami, FL 33152 USA.
[Delgado-Borrego, Aymin; Negre, Betania; Ludwig, David A.] Univ Miami, Dept Pediat, Batchelor Childrens Res Inst, Div Gastroenterol, Miami, FL 33152 USA.
[Healey, David; Christofi, Marielle; Jonas, Maureen M.] Childrens Hosp, Dept Pediat, Div Gastroenterol Hepatol & Nutr, Boston, MA 02115 USA.
[Sabharwal, Sabina; Chung, Raymond T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Dept Med, Boston, MA 02114 USA.
RP Chung, RT (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Dept Med, 55 Fruit St,GRJ 724, Boston, MA 02114 USA.
EM rtchung@partners.org
FU NIH [DK070022, DK78772]; Robert Wood Johnson Foundation
FX This work was supported by NIH DK070022 (A.D.B.), DK78772 (RTC), and the
Robert Wood Johnson Foundation (A.D.B.).
NR 36
TC 15
Z9 17
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-2116
J9 J PEDIATR GASTR NUTR
JI J. Pediatr. Gastroenterol. Nutr.
PD AUG
PY 2010
VL 51
IS 2
BP 191
EP 197
DI 10.1097/MPG.0b013e3181d32756
PG 7
WC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics
SC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics
GA 631HY
UT WOS:000280338600015
PM 20531022
ER
PT J
AU Stengel, A
Goebel, M
Wang, L
Rivier, J
Kobelt, P
Monnikes, H
Tache, Y
AF Stengel, A.
Goebel, M.
Wang, L.
Rivier, J.
Kobelt, P.
Monnikes, H.
Tache, Y.
TI SELECTIVE CENTRAL ACTIVATION OF SOMATOSTATIN RECEPTOR 2 INCREASES FOOD
INTAKE, GROOMING BEHAVIOR AND RECTAL TEMPERATURE IN RATS
SO JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
LA English
DT Article
DE somatostatin; somatostatin receptor-2; behavior; body temperature; food
intake; gastric emptying; rat; feeding; grooming
ID CENTRAL-NERVOUS-SYSTEM; GHRELIN SECRETION; BARREL ROTATION;
GROWTH-HORMONE; CHOLINERGIC STIMULATION; IN-VITRO; HYPOTHALAMUS;
SUPPRESSION; AGONISTS; SUBTYPE
AB The consequences of selective activation of brain somatostatin receptor-2 (sst(2)) were assessed using the sst(2) agonist, des-AA(1,4-6,11-13)-[DPhe(2),Aph7(Cbm),DTrp(8)]-Cbm-SST-Thr-NH(2). Food intake (FI) was monitored in ad libitum fed rats chronically implanted with an intracerebroventricular (icy.) cannula. The sst(2) agonist injected i.c.v. at 0.1 and 1 mu g/rat dose-dependently increased light phase FI from 2 to 6 hours post injection (2.3 +/- 0.5 and 7.5 +/- 1.2 respectively vs. vehicle: 0.2 +/- 0.2 g/300 g bw, P<0.001). Peptide action was reversed by i.c.v, injection of the sst2 antagonist, des-AA(1,4-6,11-13)-[pNO(2)-Phe(2),DCys(3),Tyr(7),DAph(Cbm)(8)]-SST-2NaI-NH(2) and not reproduced by intraperitoneal injection (30 mu g/rat). The sst(2) antagonist alone i.c.v, significantly decreased the cumulative 14-hours dark phase FI by 29.5%. Other behaviors, namely grooming, drinking and locomotor activity were also increased by the sst2 agonist (1 mu g/rat, i.c.v.) as monitored during the 2(nd) hour post injection while gastric emptying of solid food was unaltered. Rectal temperature rose 1 hour after the sst(2) agonist (1 mu g/rat, i.c.v.) with a maximal response maintained from 1 to 4 hours post injection. These data show that selective activation of the brain sst(2) receptor induces a feeding response in the light phase not associated with changes in gastric emptying. The food intake reduction following sst(2) receptor blockade suggests a role of this receptor in the orexigenic drive during the dark phase.
C1 [Tache, Y.] Vet Affairs Greater Los Angeles Healthcare Syst, Ctr Neurobiol Stress, Los Angeles, CA 90073 USA.
[Stengel, A.; Goebel, M.; Wang, L.; Tache, Y.] Univ Calif Los Angeles, CURE Digest Dis Res Ctr, Los Angeles, CA USA.
[Stengel, A.; Goebel, M.; Wang, L.; Tache, Y.] Univ Calif Los Angeles, Dept Med, Ctr Neurobiol Stress, Div Digest Dis, Los Angeles, CA 90024 USA.
[Rivier, J.] Salk Inst Biol Studies, Peptide Biol Labs, La Jolla, CA USA.
[Kobelt, P.] Univ Med Berlin, Div Psychosomat Med & Psychotherapy, Dept Med, Charite, Berlin, Germany.
[Monnikes, H.] Martin Luther Krankenhaus, Dept Med, Berlin, Germany.
[Monnikes, H.] Martin Luther Krankenhaus, Inst Neurogastroenterol, Berlin, Germany.
RP Tache, Y (reprint author), Vet Affairs Greater Los Angeles Healthcare Syst, Ctr Neurobiol Stress, CURE Bldg 115,Room 117,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM ytache@mednet.ucla.edu
FU German Research Foundation [STE 1765/1-1, GO 1718/1-1]; Veterans
Administration Research Career Scientist Award [R01 NIH DK-33061,
DK-41301]
FX This work was supported by German Research Foundation Grants STE
1765/1-1 (A.S.), GO 1718/1-1 (M.G.), Veterans Administration Research
Career Scientist Award, R01 NIH DK-33061 and Center Grant DK-41301
(Animal Core) (Y.T). J. R. is the Dr. Frederik Paulsen Chair in
Neurosciences Professor. We are grateful to Mrs. Honghui Liang for her
excellent technical support and we thank Ms. Eugenia Hu for reviewing
the manuscript.
NR 62
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U1 0
U2 2
PU POLISH PHYSIOLOGICAL SOC
PI GRZEGORZECKA
PA JAGIELLONIAN UNIV SCHOOL MED, INST PHYSIOLOGY, 31-531 KRAKOW, 16
GRZEGORZECKA, POLAND
SN 0867-5910
J9 J PHYSIOL PHARMACOL
JI J. Physiol. Pharmacol.
PD AUG
PY 2010
VL 61
IS 4
BP 399
EP 407
PG 9
WC Physiology
SC Physiology
GA 646IZ
UT WOS:000281534500004
PM 20814067
ER
PT J
AU O'Tierney, PF
Chattergoon, NN
Louey, S
Giraud, GD
Thornburg, KL
AF O'Tierney, P. F.
Chattergoon, N. N.
Louey, S.
Giraud, G. D.
Thornburg, K. L.
TI Atrial natriuretic peptide inhibits angiotensin II-stimulated
proliferation in fetal cardiomyocytes
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; SMOOTH-MUSCLE CELLS; A-DEFICIENT MICE;
CARDIAC-HYPERTROPHY; MESANGIAL CELLS; CLEARANCE RECEPTOR; VENOUS
HYPERTENSION; GENE-EXPRESSION; SHEEP HEART; RAT HEART
AB The role of atrial natriuretic peptide (ANP) in regulating fetal cardiac growth is poorly understood. Angiotensin II (Ang II) stimulates proliferation in fetal sheep cardiomyocytes when growth is dependent on the activity of the mitogen-activated protein kinase (MAPK) and phosphoinositol-3-kinase (PI3K) pathways. We hypothesized that ANP would suppress near-term fetal cardiomyocyte proliferation in vitro and inhibit both the MAPK and PI3K pathways. Forty-eight hour 5-bromodeoxyuridine (BrdU) uptake (used as an index of proliferation) was measured in cardiomyocytes isolated from fetal sheep (135 day gestational age) in response to 100 nm Ang II with or without ANP (0.003-100 nm) or 1 mu m 8-bromo-cGMP. The effects of these compounds on the MAPK and PI3K pathways were assessed by measuring extracellular signal-regulated kinase (ERK) and AKT phosphorylation following 10 min of treatment with Ang II, ANP or 8-bromo-cGMP. In right ventricular myocytes (RV), the lowest dose of ANP (0.003 nm) inhibited Ang II-stimulated BrdU uptake by 68%. Similarly, 8-bromo-cGMP suppressed Ang II-stimulated proliferation by 62%. The same effects were observed in left ventricular (LV) cardiomyoytes but the RV was more sensitive to the inhibitory effects of ANP than the LV (P < 0.0001). Intracellular cGMP was increased by 4-fold in the presence of 100 nm ANP. Ang II-stimulated ERK and Akt phosphorylation was inhibited by 100 nm ANP. The activity of ANP may in part be cGMP dependent, as 8-bromo-cGMP had similar effects on the cardiomyocytes.
C1 [O'Tierney, P. F.; Chattergoon, N. N.; Louey, S.; Giraud, G. D.; Thornburg, K. L.] Oregon Hlth & Sci Univ, Heart Res Ctr, Portland, OR 97239 USA.
[Thornburg, K. L.] Oregon Hlth & Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97239 USA.
[Louey, S.; Giraud, G. D.; Thornburg, K. L.] Oregon Hlth & Sci Univ, Dept Cardiovasc Med, Portland, OR 97239 USA.
[Giraud, G. D.] Portland VA Med Ctr, Portland, OR USA.
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 National Institute of Child Health and Human Development Program
[P01HD34430]; American Heart Association; Tartar Trust Foundation;
Department of Veterans Affairs
FX This work at Oregon Health and Science University was supported by the
National Institute of Child Health and Human Development Program Project
Grant (P01HD34430), an American Heart Association Fellowship
(O'Tierney), the Tartar Trust Foundation and the Department of Veterans
Affairs. The authors have no conflicts of interest to declare.
NR 56
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U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3751
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD AUG 1
PY 2010
VL 588
IS 15
BP 2879
EP 2889
DI 10.1113/jphysiol.2010.191098
PG 11
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 635EL
UT WOS:000280638300015
PM 20519318
ER
PT J
AU Chang, BH
Casey, A
Dusek, JA
Benson, H
AF Chang, Bei-Hung
Casey, Aggie
Dusek, Jeffery A.
Benson, Herbert
TI Relaxation response and spirituality: Pathways to improve psychological
outcomes in cardiac rehabilitation
SO JOURNAL OF PSYCHOSOMATIC RESEARCH
LA English
DT Article
DE Spirituality; Mind/body medicine; Relaxation response; Cardiac
rehabilitation; Psychological distress; Mediation effects
ID CORONARY-ARTERY-DISEASE; QUALITY-OF-LIFE; RANDOMIZED-TRIAL; STYLE
PROFILE; NITRIC-OXIDE; HEALTH; RELIGION; MANAGEMENT; DISTRESS; SCALE
AB Objectives: Studies have shown beneficial effects from practicing the relaxation response (RR). Various pathways for these effects have been investigated. Previous small studies suggest that spirituality might be a pathway for the health effects of the RR. In this study, we tested the hypothesis that increased spiritual well-being by eliciting the RR is one pathway resulting in improved psychological outcomes. Methods: This observational study included 845 outpatients who completed a 13-week mind/body Cardiac Rehabilitation Program. Patients self-reported RR practice time in a questionnaire before and after the 13-week program. Similarly, data on spiritual well-being, measured by the subscale of Spiritual Growth of the Health-Promoting Lifestyle Profile II, were collected. The psychological distress levels were measured by the Symptom Checklist-90-Revised. We tested the mediation effect of spiritual well-being using regression analyses. Results: Significant increases in RR practice time (75 min/week, effect size/ES=1.05) and spiritual well-being scores (ES=0.71) were observed after participants completed the program (P<.0001). Patients also improved on measures of depression, anxiety, hostility and the global severity index with medium effect sizes (0.25 to 0.48, P<.0001). Greater increases in RR practice time were associated with enhanced spiritual well-being (beta=.08, P=.01); and enhanced spiritual well-being was associated with improvements in psychological outcomes (beta=-0.14 to -0.22, P<.0001). Conclusion: Our data demonstrated a possible dose response relationship among RR practice, spiritual and psychological well-being. Furthermore, the data support the hypothesis that spiritual well-being may serve as a pathway of how RR elicitation improves psychological outcomes. These findings might contribute to improved psychological care of cardiac patients. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Chang, Bei-Hung] Boston Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA USA.
[Chang, Bei-Hung] VA Boston Hlth Care Syst, Boston, MA USA.
[Casey, Aggie; Dusek, Jeffery A.; Benson, Herbert] Massachusetts Gen Hosp, Benson Henry Inst Mind Body Med, Boston, MA 02114 USA.
[Dusek, Jeffery A.] Abbott NW Hosp, Penny George Inst Hlth & Healing, Minneapolis, MN 55407 USA.
RP Chang, BH (reprint author), 150 S Huntington Ave 152H,Bldg 9,4th Floor, Boston, MA 02130 USA.
EM bhchang@bu.edu
OI Dusek, Jeffery/0000-0001-9581-0564
FU Center for Disease Control and Prevention [H75/CCH119124-05, 5 R01
DP000339]
FX We thank Yue Zhao, M.S., for performing the data analyses. We would also
like to thank Ann Hendricks, Ph.D., for providing valuable editorial
comments. The study was partially funded by the Center for Disease
Control and Prevention: Grant Number H75/CCH119124-05 and 5 R01
DP000339.
NR 56
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U1 1
U2 11
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3999
J9 J PSYCHOSOM RES
JI J. Psychosomat. Res.
PD AUG
PY 2010
VL 69
IS 2
BP 93
EP 100
DI 10.1016/j.jpsychores.2010.01.007
PG 8
WC Psychiatry
SC Psychiatry
GA 631BX
UT WOS:000280322700002
PM 20624507
ER
PT J
AU Sakamoto, FH
Lopes, JD
Anderson, RR
AF Sakamoto, Fernanda H.
Lopes, Jose Daniel
Anderson, R. Rox
TI Photodynamic therapy for acne vulgaris: A critical review from basics to
clinical practice Part I. Acne vulgaris: When and why consider
photodynamic therapy?
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Article
DE 5-aminolevulinic acid; lasers; light; methyl 5-aminolevulinate;
photochemotherapy; porphyrins; therapeutics; ultraviolet
ID TOPICAL AMINOLEVULINIC ACID; CARBON-DIOXIDE LASER;
PROPIONIBACTERIUM-ACNES; 5-AMINOLEVULINIC ACID; ORAL ISOTRETINOIN;
SEBACEOUS GLANDS; DOSE-RESPONSE; MATRIX METALLOPROTEINASES;
CORYNEBACTERIUM-ACNES; NODULOCYSTIC ACNE
AB The first-line treatments for acne vulgaris are conventional topical and/or oral medications. However, many patients have contraindications, only partial response, significant adverse effects, or recurrence. Light-based treatments and photodynamic therapy (PDT) using topical precursors of porphyrins are off-label alternative treatments for acne vulgaris, with their own advantages and disadvantages. To date, there is no consensus on PDT methodology and parameters. An understanding of pathophysiology of acne, light tissue interactions, and PDT mechanisms of action is helpful whenever PDT is considered as an alternative treatment. In general, blue light alone improves acne because of its antiinflammatory effects. PDT using 5-aminolevulenic acid (ALA) or ALA derivatives induces transient antimicrobial and antiinflammatory effects. At high doses, red light PDT may induce inhibition or destruction of sebaceous glands, resulting in clinical improvement. (J Am Acad Dermatol 2010;63:183-93.)
C1 [Anderson, R. Rox] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Sakamoto, Fernanda H.] Univ Fed Sao Paulo, Dept Dermatol, Escola Paulista Med UNIFESP EPM, Sao Paulo, Brazil.
[Lopes, Jose Daniel] Univ Fed Sao Paulo, Dept Immunol, Escola Paulista Med, Sao Paulo, Brazil.
RP Anderson, RR (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Ctr Photomed, 55 Fruit St,BHX 630, Boston, MA 02114 USA.
EM rranderson@partners.org
NR 101
TC 54
Z9 55
U1 1
U2 22
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 AUG
PY 2010
VL 63
IS 2
BP 183
EP 193
DI 10.1016/j.jaad.2009.09.056
PG 11
WC Dermatology
SC Dermatology
GA 630DJ
UT WOS:000280252100001
PM 20633796
ER
PT J
AU Sakamoto, FH
Torezan, L
Anderson, RR
AF Sakamoto, Fernanda H.
Torezan, Luis
Anderson, R. Rox
TI Photodynamic therapy for acne vulgaris: A critical review from basics to
clinical practice Part II. Understanding parameters for acne treatment
with photodynamic therapy
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Article
DE adverse effects; 5-aminolevulinic acid; lasers; light; methyl
5-aminolevulinate; photochemotherapy; porphyrins; therapeutics
ID DELTA-AMINOLEVULINIC-ACID; TOPICAL 5-AMINOLEVULINIC ACID; ALLERGIC
CONTACT-DERMATITIS; INTENSE PULSED-LIGHT; BASAL-CELL CARCINOMAS; METHYL
AMINOLEVULINATE; IN-VIVO; FACIAL ACNE; HUMAN-SKIN; SELECTIVE
PHOTOTHERMOLYSIS
AB Photodynamic therapy requires a photosensitizer, oxygen, and activating light. For acne, pilosebaceous units are "target" structures. Porphyrins are synthesized in vivo from 5-aminolevulinic acid (ALA), particularly in pilosebaceous units. Different photosensitizers and drug delivery methods have been reported for acne treatment. There are a variety of porphyrin precursors with different pharmacokinetic properties. Among them, ALA and methyl-ester of ALA (MAT.) are available for possible off-label treatment of acne vulgaris. In addition, various light sources, light dosimetry, drug incubation time, and pre- and posttreatment care also change efficacy and side effects. None of these variables has been optimized for acne treatment, but a number of clinical trials provide helpful guidance. In this paper, we critically analyze clinical trials, case reports, and series of cases published through 2009. (J Am Acad Dermatol 2010;63:195-211.)
C1 [Sakamoto, Fernanda H.; Anderson, R. Rox] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Sakamoto, Fernanda H.] Univ Fed Sao Paulo, Dept Dermatol, Escola Paulista Med, Sao Paulo, Brazil.
[Torezan, Luis] Univ Sao Paulo, Fac Med, Sao Paulo, Brazil.
RP Anderson, RR (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Wellman Ctr Photomed, 55 Fruit St,BHX 630, Boston, MA 02114 USA.
EM rranderson@partners.org
NR 63
TC 55
Z9 55
U1 1
U2 31
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 AUG
PY 2010
VL 63
IS 2
BP 195
EP 211
DI 10.1016/j.jaad.2009.09.057
PG 17
WC Dermatology
SC Dermatology
GA 630DJ
UT WOS:000280252100002
PM 20633797
ER
PT J
AU Patti, JA
AF Patti, John A.
TI A World in Turmoil: Chaos, or a New World Order?
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Patti, JA (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,FND 202, Boston, MA 02114 USA.
EM jpatti@partners.org
NR 0
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 1546-1440
J9 J AM COLL RADIOL
JI J. Am. Coll. Radiol.
PD AUG
PY 2010
VL 7
IS 8
SI SI
BP 551
EP 551
DI 10.1016/j.jacr.2010.06.021
PG 1
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA V23SR
UT WOS:000208363000001
PM 20678719
ER
PT J
AU Zalis, M
Harris, M
AF Zalis, Michael
Harris, Mitchell
TI Advanced Search of the Electronic Medical Record: Augmenting Safety and
Efficiency in Radiology
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Article
DE Electronic medical record (EMR); decision support; search; workflow
efficiency; quality and safety improvement
AB The integration of electronic medical record (EMR) systems into clinical practice has been spurred by general consensus and recent federal incentives and is set to become a standard feature of clinical practice in the US. We discuss how the addition of advanced search capabilities to the EMR can improve the radiologist's ability to integrate contextual data into workflows associated with both for diagnostic and interventional procedures.
C1 [Zalis, Michael; Harris, Mitchell] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Zalis, M (reprint author), Massachusetts Gen Hosp, Dept Radiol, 25 New Chardon St,Suite 400A, Boston, MA 02114 USA.
EM mzalis@mgh.harvard.edu
FU Department of Radiology, Massachusetts General Hospital (Boston, Mass);
Partners Healthcare Information Systems (Boston, Mass)
FX This study was funded by the Department of Radiology, Massachusetts
General Hospital (Boston, Mass), and by a research grant (2005-2006)
from Partners Healthcare Information Systems (Boston, Mass), Michael
Zalis, MD, principal investigator.
NR 10
TC 11
Z9 11
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1546-1440
J9 J AM COLL RADIOL
JI J. Am. Coll. Radiol.
PD AUG
PY 2010
VL 7
IS 8
SI SI
BP 625
EP 633
DI 10.1016/j.jacr.2010.03.011
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA V23SR
UT WOS:000208363000014
PM 20678732
ER
PT J
AU Ingraham, AM
Cohen, ME
Ko, CY
Hall, BL
AF Ingraham, Angela M.
Cohen, Mark E.
Ko, Clifford Y.
Hall, Bruce Lee
TI A Current Profile and Assessment of North American Cholecystectomy:
Results from the American College of Surgeons National Surgical Quality
Improvement Program
SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS
LA English
DT Article; Proceedings Paper
CT 95th Annual Clinical Congress of the American-College-of-Surgeons/64th
Annual Sessions of the Owen H Wangensteen Forum on Fundamental Surgical
Problems
CY OCT 11-15, 2009
CL Chicago, IL
SP Amer Coll Surg
ID 8 COMMON OPERATIONS; BILE-DUCT INJURY; LAPAROSCOPIC CHOLECYSTECTOMY;
ACUTE CHOLECYSTITIS; RISK-FACTORS; OUTCOMES; VOLUME; COMPLICATIONS;
TRIAL; NSQIP
AB BACKGROUND: Cholecystectomy is among the most common surgical procedures performed in the United States. The current state of cholecystectomy outcomes, including variations in hospital performance, is unclear. The objective of this study is to compare the risk factors, indications, and 30-day outcomes, as well as variations in hospital performance associated with laparoscopic (LC) versus open cholecystectomy (OC) at 221 hospitals during a 4-year period.
STUDY DESIGN: Using the American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) database (2005-2008), patients were identified who underwent cholecystectomy and related procedures (cholangiogram and/or common bile duct exploration). Four outcomes were studied, ie, 30-day overall morbidity, serious morbidity, surgical site infections, and mortality. Forward stepwise logistic regressions yielded patient-level predicted probabilities, and hospital-level observed-to-expected ratios were determined.
RESULTS: Of 65,511 patients, 58,659(89.5%) underwent LC; 6,852 (10.5%) underwent OC. OC patients were considerably older with a higher comorbidity burden. LC patients were less likely to experience any morbidity (3.1% versus 17.8%; p < 0.0001), a serious morbidity (1.4% versus 11.1%; p < 0.0001), or a surgical site infection (1.3% versus 8.4%; p < 0.0001), and less likely to die (0.3% versus 2.8%; p < 0.0001). Observed-to-expected ratios for overall morbidity ranged from 0 to 3.55; for serious morbidity, 0 to 3.23; for surgical site infection, 0 to 7.02; for mortality, 0 to 13.05.
CONCLUSIONS: Although overall incidence of adverse events is low after LC, substantial morbidity and mortality are associated with OC. Additionally, controlling for patient- and operation-related factors, considerable variations exist in hospital performance when evaluating 30-day outcomes after cholecystectomy. (J Am Coll Surg 2010;211:176-186. (C) 2010 by the American College of Surgeons)
C1 [Ingraham, Angela M.; Cohen, Mark E.; Ko, Clifford Y.] Amer Coll Surg, Div Res & Optimal Patient Care, Chicago, IL 60611 USA.
[Ingraham, Angela M.] Univ Cincinnati, Coll Med, Dept Surg, Cincinnati, OH 45267 USA.
[Ko, Clifford Y.] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90024 USA.
[Ko, Clifford Y.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Hall, Bruce Lee] Washington Univ, Sch Med, Dept Surg, John Cochran Vet Affairs Med Ctr, St Louis, MO 63110 USA.
[Hall, Bruce Lee] Barnes Jewish Hosp, St Louis, MO 63110 USA.
[Hall, Bruce Lee] Washington Univ, Ctr Hlth Policy, St Louis, MO USA.
[Hall, Bruce Lee] Washington Univ, John M Olin Sch Business, St Louis, MO 63130 USA.
RP Ingraham, AM (reprint author), Amer Coll Surg, Div Res & Optimal Patient Care, 633 N St Clair St,Floor 22NE, Chicago, IL 60611 USA.
EM aingraham@facs.org
NR 26
TC 52
Z9 52
U1 0
U2 3
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 AUG
PY 2010
VL 211
IS 2
BP 176
EP 186
DI 10.1016/j.jamcollsurg.2010.04.003
PG 11
WC Surgery
SC Surgery
GA 638VY
UT WOS:000280927200003
PM 20670855
ER
PT J
AU Aspinall, SL
Zhao, XH
Handler, SM
Stone, RA
Kosmoski, JC
Libby, EA
Francis, SD
Goodman, DA
Roman, RD
Bieber, HL
Voisine, JM
Jeffery, SM
Hepfinger, CA
Hagen, DG
Martin, MM
Hanlon, JT
AF Aspinall, Sherrie L.
Zhao, Xinhua
Handler, Steven M.
Stone, Roslyn A.
Kosmoski, Janine C.
Libby, Elizabeth A.
Francis, Susan Dove
Goodman, David A.
Roman, Rebecca D.
Bieber, Heather L.
Voisine, Jennifer M.
Jeffery, Sean M.
Hepfinger, Charley A.
Hagen, Diane G.
Martin, Micki M.
Hanlon, Joseph T.
TI The Quality of Warfarin Prescribing and Monitoring in Veterans Affairs
Nursing Homes
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE warfarin; healthcare quality assurance; nursing homes
ID ATRIAL-FIBRILLATION; ANTICOAGULATION CONTROL; MANAGEMENT; FREQUENCY;
INTENSITY; THERAPY; EVENTS; DRUG; METAANALYSIS; RISK
AB OBJECTIVES
To describe the quality of warfarin prescribing and monitoring in Veterans Affairs (VA) nursing homes and to assess the factors associated with maintaining a therapeutic international normalized ratio (INR).
DESIGN
Retrospective cohort.
SETTING
Five VA nursing homes.
PARTICIPANTS
All veterans who received warfarin between January 1 and June 30, 2008, at the nursing homes.
MEASUREMENTS
Using medical records, the percentage of person-time spent in the target INR range, the proportion of patients with INRs in the therapeutic range on 50% or more of their person-days, and the frequency of INR monitoring were estimated. Multivariable logistic regression was used to identify factors associated with maintaining a therapeutic INR 50% or more of the time.
RESULTS
Over 6 months, 160 patients received 10,380 person-days of warfarin. INRs were in the therapeutic range for 55% of the person-days, and 99% of the INR tests were repeated within 4 weeks of the previous result. On an individual level, 49% of patients had INRs in the target range for 50% or more of their person-days. Achieving this outcome was more likely in patients with prevalent warfarin use than with new use (adjusted odds ratio (AOR)=2.86, 95% confidence interval (CI)=1.06-7.72). Conversely, patients with a history of a stroke (AOR=0.38, 95% CI =0.18-0.80) were less likely to have therapeutic INRs for 50% or more of their days.
CONCLUSION
Warfarin appears to be prescribed and monitored effectively in VA nursing home patients. Future studies should focus on increasing time in therapeutic range in patients with poor INR control.
C1 [Aspinall, Sherrie L.; Zhao, Xinhua; Handler, Steven M.; Stone, Roslyn A.; Hanlon, Joseph T.] VA Pittsburgh Healthcare Syst, Ctr Hlth Equity Res & Promot, Pittsburgh, PA 15206 USA.
[Aspinall, Sherrie L.; Zhao, Xinhua] Vet Affairs Ctr Medicat Safety, Hines, IL USA.
[Handler, Steven M.; Hanlon, Joseph T.] VA Pittsburgh Healthcare Syst, Geriatr Res Educ & Clin Ctr, Pittsburgh, PA 15206 USA.
[Goodman, David A.; Roman, Rebecca D.] VA Pittsburgh Healthcare Syst, Dept Pharm, Pittsburgh, PA 15206 USA.
[Aspinall, Sherrie L.; Hanlon, Joseph T.] Univ Pittsburgh, Sch Pharm, Pittsburgh, PA USA.
[Handler, Steven M.; Hanlon, Joseph T.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Stone, Roslyn A.] Univ Pittsburgh, Grad Sch Publ Hlth, Pittsburgh, PA USA.
[Kosmoski, Janine C.; Francis, Susan Dove] Durham Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Durham, NC USA.
[Libby, Elizabeth A.; Hepfinger, Charley A.; Hagen, Diane G.; Martin, Micki M.] Phoenix Vet Affairs Hlth Care Syst, Dept Pharm, Phoenix, AZ USA.
[Bieber, Heather L.] Lake City Vet Affairs Med Ctr, Dept Pharm, Lake City, FL USA.
[Voisine, Jennifer M.; Jeffery, Sean M.] Vet Affairs Connecticut Healthcare Syst, Dept Pharm, West Haven, CT USA.
RP Aspinall, SL (reprint author), VA Pittsburgh Healthcare Syst, Ctr Hlth Equity Res & Promot, 7180 Highland Dr 151C-H, Pittsburgh, PA 15206 USA.
EM sherrie.aspinall@va.gov
OI Handler, Steven/0000-0002-3940-3224
FU VA Center for Medication Safety/VA Pharmacy Benefits Management
Services, Hines, IL; VA Pittsburgh Healthcare System, Pittsburgh, PA; VA
Connecticut Healthcare System, West Haven, CT; Durham VA Medical Center,
Durham, NC; Lake City VA Medical Center, Lake City, FL; Phoenix VA
Health Care System, Phoenix, AZ; National Institute of Aging
[R01AG027017, P30AG024827, T32 AG021885, K07AG033174, R01AG034056];
National Institute of Mental Health [R34 MH082682]; National Institute
of Nursing Research [R01 NR010135]; Agency for Healthcare Research and
Quality [R01 HS017695]; VA Health Services [IIR-06-062]
FX These findings are the result of work supported by the VA Center for
Medication Safety/VA Pharmacy Benefits Management Services, Hines, IL;
VA Pittsburgh Healthcare System (especially the Geriatric Research,
Education and Clinical Center and the VA Center for Health Equity
Research and Promotion), Pittsburgh, PA; VA Connecticut Healthcare
System, West Haven, CT; Durham VA Medical Center (especially the
Geriatric Research, Education and Clinical Center), Durham, NC; Lake
City VA Medical Center, Lake City, FL; and Phoenix VA Health Care
System, Phoenix, AZ.; Dr. Handler was supported by National Institutes
of Health Roadmap Multidisciplinary Clinical Research Career Development
Award Grant K12 RR023267.; Dr. Hanlon was supported by National
Institute of Aging Grants R01AG027017, P30AG024827, T32 AG021885,
K07AG033174, and R01AG034056; National Institute of Mental Health Grant
R34 MH082682; National Institute of Nursing Research Grant R01 NR010135;
Agency for Healthcare Research and Quality Grant R01 HS017695; and VA
Health Services Research Grant IIR-06-062.
NR 26
TC 8
Z9 9
U1 0
U2 6
PU WILEY-BLACKWELL PUBLISHING, INC
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 AUG
PY 2010
VL 58
IS 8
BP 1475
EP 1480
DI 10.1111/j.1532-5415.2010.02967.x
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 635GN
UT WOS:000280643700008
PM 20662956
ER
PT J
AU Rudolph, JL
Zanin, NM
Jones, RN
Marcantonio, ER
Fong, TG
Yang, FM
Yap, LA
Inouye, SK
AF Rudolph, James L.
Zanin, Nicole M.
Jones, Richard N.
Marcantonio, Edward R.
Fong, Tamara G.
Yang, Frances M.
Yap, Liang
Inouye, Sharon K.
TI Hospitalization in Community-Dwelling Persons with Alzheimer's Disease:
Frequency and Causes
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE hospitalization; geriatrics; dementia; Alzheimer's disease; delirium
ID OLDER PERSONS; DEMENTIA; DELIRIUM; COSTS; ASSOCIATION; POPULATION;
PREVALENCE; VALIDATION; ADMISSIONS; DIAGNOSIS
AB OBJECTIVES
To examine the rates of and risk factors for acute hospitalization in a prospective cohort of older community-dwelling patients with Alzheimer's disease (AD).
DESIGN
Longitudinal patient registry.
SETTING
AD research center.
PARTICIPANTS
Eight hundred twenty-seven older persons with AD.
MEASUREMENTS
Acute hospitalization after AD research center visit was determined from a Medicare database. Risk factor variables included demographics, dementia-related, comorbidity and diagnoses and were measured in interviews and according to Medicare data.
RESULTS
Of the 827 eligible patients seen at the ADRC during 1991 to 2006 (median follow-up 3.0 years), 542 (66%) were hospitalized at least once, and 389 (47%) were hospitalized two or more times, with a median of 3 days spent in the hospital per person-year. Leading reasons for admission were syncope or falls (26%), ischemic heart disease (17%), gastrointestinal disease (9%), pneumonia (6%), and delirium (5%). Five significant independent risk factors for hospitalization were higher comorbidity (hazard ratio (HR)=1.87, 95% confidence interval (CI)=1.57-2.23), previous acute hospitalization (HR=1.65, 95% CI=1.37-1.99), older age (HR=1.51, 95% CI=1.26-1.81), male sex (HR=1.27, 95% CI=1.04-1.54), and shorter duration of dementia symptoms (HR=1.26, 95% CI=1.02-1.56). Cumulative risk of hospitalization increased with number of risk factors present at baseline: 38% with zero factors, 57% with one factor, 70% with two or three factors, and 85% with four or five factors (P(trend)<.001).
CONCLUSION
In a community-dwelling population with generally mild AD, hospitalization is frequent, occurring in two-thirds of participants over a median follow-up time of 3 years. With these results, clinicians may be able to identify dementia patients at high risk for hospitalization.
C1 [Rudolph, James L.; Zanin, Nicole M.; Jones, Richard N.; Marcantonio, Edward R.; Fong, Tamara G.; Yang, Frances M.; Yap, Liang; Inouye, Sharon K.] Hebrew SeniorLife, Inst Aging Res, Aging Brain Ctr, Boston, MA USA.
[Rudolph, James L.; Inouye, Sharon K.] Geriatr Res Educ & Clin Ctr, Vet Affairs Boston Healthcare Syst, Boston, MA USA.
[Zanin, Nicole M.] Wright State Univ, Boonshoft Sch Med, Dayton, OH 45435 USA.
[Jones, Richard N.; Marcantonio, Edward R.; Yang, Frances M.; Inouye, Sharon K.] Beth Israel Deaconess Med Ctr, Div Gerontol, Boston, MA 02215 USA.
[Marcantonio, Edward R.] Beth Israel Deaconess Med Ctr, Div Gen Med & Primary Care, Boston, MA 02215 USA.
[Fong, Tamara G.] Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA.
[Yap, Liang] Massachusetts Gen Hosp, Massachusetts Alzheimers Dis Res Ctr, Boston, MA 02114 USA.
[Rudolph, James L.; Jones, Richard N.; Marcantonio, Edward R.; Fong, Tamara G.; Yang, Frances M.; Inouye, Sharon K.] Harvard Univ, Sch Med, Boston, MA USA.
RP Rudolph, JL (reprint author), VABHS GRECC, 150 S Huntington Ave, Boston, MA 02130 USA.
EM jrudolph@partners.org
RI Jones, Richard/J-3488-2013
OI Jones, Richard/0000-0002-1049-218X
FU Veterans Affairs Research Career Development Award; American Federation
for Aging Research Medical Student Training in Aging [T35AG026781];
National Institute on Aging (NIA) [K24AG000949, R03AG029861];
Alzheimer's Association [IIRG-08-88737]; Aging Brain Center, Institute
for Aging Research, Hebrew SeniorLife; National Institutes of Health
[NIA P50AG005134]
FX Dr. Inouye holds the Milton and Shirley F. Levy Family Chair in
Alzheimer's disease. Dr. Rudolph is funded by a Veterans Affairs
Research Career Development Award.; This study is supported in part by
the American Federation for Aging Research Medical Student Training in
Aging Research program T35AG026781 (NMZ, JLR) and Grants K24AG000949
(SKI) and R03AG029861 (JLR) from the National Institute on Aging (NIA),
IIRG-08-88737 (SKI) from the Alzheimer's Association, and the Aging
Brain Center, Institute for Aging Research, Hebrew SeniorLife. The MADRC
database is funded by National Institutes of Health, NIA P50AG005134.
NR 38
TC 50
Z9 51
U1 1
U2 9
PU WILEY-BLACKWELL PUBLISHING, INC
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 AUG
PY 2010
VL 58
IS 8
BP 1542
EP 1548
DI 10.1111/j.1532-5415.2010.02924.x
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 635GN
UT WOS:000280643700018
PM 20553338
ER
PT J
AU Kang, HG
Mahoney, DF
Hoenig, H
Hirth, VA
Bonato, P
Hajjar, I
Lipsitz, LA
AF Kang, Hyun Gu
Mahoney, Diane F.
Hoenig, Helen
Hirth, Victor A.
Bonato, Paolo
Hajjar, Ihab
Lipsitz, Lewis A.
CA Ctr Integration Med & Innovative T
TI In Situ Monitoring of Health in Older Adults: Technologies and Issues
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE monitoring; telehealth; ethics; gerontechnology
ID HEART-RATE-VARIABILITY; BIPOLAR DISORDER; HOME; MOBILITY; INTERVENTION;
REHABILITATION; POPULATION; COMMUNITY; SLEEP; FALLS
AB With the upcoming reform of the healthcare system and the greater emphasis on care in the home and other living environments, geriatric providers will need alternate ways of monitoring disease, activity, response to therapy, and patient safety. Current understanding of the dynamic nature of chronic illnesses, their effects on health over time, and the ability to manage them in the community are limited to measuring a set of variables at discrete points in time, which does not account for the dynamic interactions between physiological systems and the environments of daily life. Recent developments of sensors, data recorders, and communication networks allow the unprecedented measurements of physiological and sociological data for use in geriatrics care. This article identifies and discusses the important issues regarding the use of monitoring technologies in elderly patients. The goals are fourfold. First, some emerging technology that may improve the lives of older adults and improve care are highlighted. Second, the possible applications of technology in geriatrics settings are discussed, with a focus on acute falls, dementia, and cardiac conditions. Third, real and perceived concerns in using monitoring technology are identified and addressed, including technology adoption by elderly people; stigma; and the reduction in social contact; ethical concerns of privacy, autonomy, and consent; concerns of clinicians, including information overload, licensure, and liability; current reimbursement schemes for using technology; and the reliability and infrastructure needed for monitoring technology. Fourth, future approaches to make monitoring technology useful and available in geriatrics are recommended.
C1 [Kang, Hyun Gu] Calif State Polytech Univ Pomona, Pomona, CA 91768 USA.
[Mahoney, Diane F.] Massachusetts Gen Hosp, Inst Hlth Profess, Sch Nursing, Charlestown, MA USA.
[Mahoney, Diane F.; Bonato, Paolo; Hajjar, Ihab; Lipsitz, Lewis A.] Harvard Univ, Sch Med, Boston, MA USA.
[Hoenig, Helen] Durham Vet Affairs Hosp, Durham, NC USA.
[Hoenig, Helen] Duke Univ, Ctr Study Aging & Human Dev, Durham, NC USA.
[Hirth, Victor A.] Univ S Carolina, Sch Med, Dept Internal Med, Columbia, SC 29208 USA.
[Hirth, Victor A.] Palmetto Hlth, Internal Med, Columbia, SC USA.
[Bonato, Paolo] Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, Charlestown, MA USA.
[Hajjar, Ihab; Lipsitz, Lewis A.] Hebrew SeniorLife, Inst Aging Res, Boston, MA USA.
[Hajjar, Ihab; Lipsitz, Lewis A.] Beth Israel Deaconess Med Ctr, Gerontol Div, Boston, MA 02215 USA.
RP Kang, HG (reprint author), Calif State Polytech Univ Pomona, 3801 W Temple Ave, Pomona, CA 91768 USA.
EM hgkang@csupomona.edu
OI Mahoney, Diane/0000-0002-6415-475X
FU Center for Integration of Medicine and Innovative Technologies [08-380];
Veterans Affairs Rehabilitation Research and Development [B4492R];
Beeson Collaborative Research Award
FX Funding was received from Center for Integration of Medicine and
Innovative Technologies Award 08-380, Veterans Affairs Rehabilitation
Research and Development Grant B4492R, and a Beeson Collaborative
Research Award.
NR 58
TC 42
Z9 42
U1 5
U2 37
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 AUG
PY 2010
VL 58
IS 8
BP 1579
EP 1586
DI 10.1111/j.1532-5415.2010.02959.x
PG 8
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 635GN
UT WOS:000280643700023
PM 20646105
ER
PT J
AU Sedor, JR
Watnick, S
Patel, UD
Cheung, A
Harmon, W
Himmelfarb, J
Hostetter, TH
Inrig, JK
Mehrotra, R
Robinson, E
Smedberg, PC
Shaffer, RN
AF Sedor, John R.
Watnick, Suzanne
Patel, Uptal D.
Cheung, Alfred
Harmon, William
Himmelfarb, Jonathan
Hostetter, Thomas H.
Inrig, Jula K.
Mehrotra, Rajnish
Robinson, Emily
Smedberg, Paul C.
Shaffer, Rachel N.
CA Amer Soc Nephrology ESRD Task Forc
TI ASN End-Stage Renal Disease Task Force: Perspective on Prospective
Payments for Renal Dialysis Facilities
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
C1 [Sedor, John R.] Dept Med, Cleveland, OH USA.
[Sedor, John R.] Case Western Reserve Univ, Ctr Study Kidney Dis & Biol, Cleveland, OH 44106 USA.
[Sedor, John R.; Watnick, Suzanne] Case Western Reserve Univ, Sch Med, Cleveland, OH 44106 USA.
Portland VA Med Ctr, Portland, OR USA.
[Patel, Uptal D.] Duke Univ, Duke Clin Res Inst, Durham, NC USA.
[Patel, Uptal D.] Duke Univ, Dept Med, Durham, NC USA.
[Patel, Uptal D.] Duke Univ, Dept Pediat, Durham, NC USA.
[Cheung, Alfred] Univ Utah, Sch Med, Div Nephrol & Hypertens, Salt Lake City, UT USA.
[Harmon, William] Childrens Hosp Boston, Dept Pediat, Boston, MA USA.
[Himmelfarb, Jonathan] Univ Washington, Sch Med, Dept Med, Kidney Res Inst,Div Nephrol, Seattle, WA 98195 USA.
Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA.
[Inrig, Jula K.] Univ Texas SW Med Ctr Dallas, Div Nephrol, Dept Med, Dallas, TX 75390 USA.
[Mehrotra, Rajnish] Harbor UCLA Med Ctr, Dept Med, Los Angeles, CA USA.
[Mehrotra, Rajnish] Harbor UCLA, Los Angeles Biomed Res Inst, Torrace, CA USA.
[Mehrotra, Rajnish] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
[Robinson, Emily] Brigham & Womens Hosp, Div Renal Med, Boston, MA 02115 USA.
RP Hostetter, TH (reprint author), Albert Einstein Coll Med, Div Nephrol, Room 615,Ullmann Bldg,1300 Morris Pk Ave, Bronx, NY 10461 USA.
FU National Institutes of Health (NIH) [K23DK075929, K23 HL092297];
NIH/National Institute of Allergy and Infectious Diseases
FX U.D.P. is supported by the National Institutes of Health (NIH) grant
K23DK075929, W H receives grants from NIH/National Institute of Allergy
and Infectious Diseases, and J K I is supported by NIH grant K23
HL092297.
NR 6
TC 9
Z9 9
U1 1
U2 1
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD AUG
PY 2010
VL 21
IS 8
BP 1235
EP 1237
DI 10.1681/ASN.2010060656
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA 636OE
UT WOS:000280746200002
PM 20675502
ER
PT J
AU Fried, LF
AF Fried, Linda F.
TI Higher Incidence of ESRD than Mortality in the AASK Study
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Editorial Material
ID CHRONIC KIDNEY-DISEASE; STAGE RENAL-DISEASE; UNITED-STATES;
RACIAL-DIFFERENCES; FOLLOW-UP; DEATH; POPULATION; OUTCOMES; RISK; CKD
C1 [Fried, Linda F.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA 15240 USA.
[Fried, Linda F.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Fried, Linda F.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
RP Fried, LF (reprint author), VA Pittsburgh Healthcare Syst, Univ Dr, Pittsburgh, PA 15240 USA.
NR 18
TC 2
Z9 2
U1 0
U2 1
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD AUG
PY 2010
VL 21
IS 8
BP 1244
EP 1246
DI 10.1681/ASN.2010060623
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA 636OE
UT WOS:000280746200007
PM 20651162
ER
PT J
AU Burstein, HJ
AF Burstein, Harold J.
TI Avastin, ODAC, and the FDA: Are We Drafting the Right Players?
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), 275 Commerce Dr,Suite 300, Ft Washington, PA 19034 USA.
EM JNCCN@nccn.org
NR 0
TC 3
Z9 3
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 AUG
PY 2010
VL 8
IS 8
BP 833
EP 834
PG 2
WC Oncology
SC Oncology
GA 647PK
UT WOS:000281630600001
PM 20870630
ER
PT J
AU Miller, SJ
Alam, M
Andersen, J
Berg, D
Bichakjian, CK
Bowen, G
Cheney, RT
Glass, LF
Grekin, RC
Kessinger, A
Lee, NY
Liegeois, N
Lydiatt, DD
Michalski, J
Morrison, WH
Nehal, KS
Nelson, KC
Nghiem, P
Olencki, T
Perlis, CS
Rosenberg, EW
Shaha, AR
Urist, MM
Wang, LC
Zic, JA
AF Miller, Stanley J.
Alam, Murad
Andersen, James
Berg, Daniel
Bichakjian, Christopher K.
Bowen, Glen
Cheney, Richard T.
Glass, L. Frank
Grekin, Roy C.
Kessinger, Anne
Lee, Nancy Y.
Liegeois, Nanette
Lydiatt, Daniel D.
Michalski, Jeff
Morrison, William H.
Nehal, Kishwer S.
Nelson, Kelly C.
Nghiem, Paul
Olencki, Thomas
Perlis, Clifford S.
Rosenberg, E. William
Shaha, Ashok R.
Urist, Marshall M.
Wang, Linda C.
Zic, John A.
TI Basal Cell and Squamous Cell Skin Cancers
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
DE NCCN Clinical Practice Guidelines; NCCN Guidelines; non-melanoma skin
cancers; skin carcinoma; sunlight and cancer; precancerous lesions;
basosquamous carcinoma; Bowen's disease
ID TOPICAL METHYL AMINOLEVULINATE; ORGAN TRANSPLANT RECIPIENTS; CUTANEOUS
BASOSQUAMOUS CARCINOMA; MOHS MICROGRAPHIC SURGERY; LOCALLY ADVANCED
HEAD; PHOTODYNAMIC THERAPY; RADIATION-THERAPY; RECURRENCE RATES; ACTINIC
KERATOSIS; ADJUVANT RADIOTHERAPY
C1 [Miller, Stanley J.; Liegeois, Nanette] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Sidney, BC, Canada.
[Alam, Murad] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Andersen, James] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Berg, Daniel] Univ Washington, Seattle Canc Care Alliance, Seattle, WA 98195 USA.
[Bichakjian, Christopher K.] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Bowen, Glen] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[Cheney, Richard T.] Roswell Pk Canc Inst, Buffalo, NY USA.
[Lee, Nancy Y.; Nehal, Kishwer S.; Shaha, Ashok R.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[Michalski, Jeff] Washington Univ, Sch Med, St Louis, MO 63130 USA.
[Michalski, Jeff] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO USA.
[Morrison, William H.] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
[Nghiem, Paul] Fred Hutchinson Canc Res Ctr, Seattle Canc Care Alliance, Seattle, WA USA.
[Olencki, Thomas] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Perlis, Clifford S.] Fox Chase Canc Ctr, Philadelphia, PA USA.
[Rosenberg, E. William] Univ Tennessee, Inst Canc, St Jude Childrens Res Hosp, Knoxville, TN 37996 USA.
[Urist, Marshall M.] Univ Alabama, Birmingham Comprehens Canc Ctr, Tuscaloosa, AL 35487 USA.
[Wang, Linda C.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Zic, John A.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
RP Miller, SJ (reprint author), Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Sidney, BC, Canada.
RI Nghiem, Paul/A-9210-2011
OI Nghiem, Paul/0000-0003-2784-963X
NR 141
TC 39
Z9 40
U1 0
U2 9
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 AUG
PY 2010
VL 8
IS 8
BP 836
EP 864
PG 29
WC Oncology
SC Oncology
GA 647PK
UT WOS:000281630600002
PM 20870631
ER
PT J
AU Weinstock, MA
Fisher, DE
AF Weinstock, Martin A.
Fisher, David E.
TI Indoor Ultraviolet Tanning: What the Data Do and Do Not Show Regarding
Risk of Melanoma and Keratinocyte Malignancies
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
DE Indoor tanning; ultraviolet; melanoma; skin cancer; DNA damage;
addiction
ID VITAMIN-D STATUS; CONTROLLED-TRIAL; SUN EXPOSURE; BASAL-CELL; SKIN;
SUPPLEMENTATION; POPULATION; PREVENTION; TANNERS
AB Recreational indoor tanning with ultraviolet (UV) radiation has become popular in recent decades, particularly among teenagers and young adults. The consequences for public health have become an important area of concern. The link between this form of UV exposure and both melanoma and non-melanoma skin cancers has been clarified through multiple lines of evidence from epidemiology and laboratory science reflected in recent reports by multiple prestigious bodies. Some have suggested that this form of indoor tanning has a role in vitamin D generation, but a review of existing evidence suggests that indoor tanning is neither a reliable nor advisable source. In addition, laboratory data suggest that tanning promotes a common molecular intermediate in skin carcinogenesis, DNA damage, which thus precludes the concept of a "safe tan." Finally, emerging evidence links UV signaling in skin to dependency/addiction, thus having implications for the organic (rather than cosmetic) impact of the process. This article presents the epidemiologic and mechanistic data relevant to the safety considerations for indoor tanning. (JNCCN 2010;8:867-873)
C1 [Weinstock, Martin A.] Brown Med Sch, Dept Dermatol, Providence, RI USA.
[Fisher, David E.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
RP Fisher, DE (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Dermatol, 55 Fruit St, Boston, MA 02114 USA.
EM dfisher3@partners.org
FU NIAMS NIH HHS [R01 AR043369]
NR 28
TC 9
Z9 9
U1 0
U2 4
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 AUG
PY 2010
VL 8
IS 8
BP 867
EP 873
PG 7
WC Oncology
SC Oncology
GA 647PK
UT WOS:000281630600003
PM 20870632
ER
PT J
AU Berger, AM
Abernethy, AP
Atkinson, A
Barsevick, AM
Breitbart, WS
Cella, D
Cimprich, B
Cleeland, C
Eisenberger, MA
Escalante, CP
Jacobsen, PB
Kaldor, P
Ligibel, JA
Murphy, BA
O'Connor, T
Pirl, WF
Rodler, E
Rugo, HS
Thomas, J
Wagner, LI
AF Berger, Ann M.
Abernethy, Amy Pickar
Atkinson, Ashley
Barsevick, Andrea M.
Breitbart, William S.
Cella, David
Cimprich, Bernadine
Cleeland, Charles
Eisenberger, Mario A.
Escalante, Carmen P.
Jacobsen, Paul B.
Kaldor, Phyllis
Ligibel, Jennifer A.
Murphy, Barbara A.
O'Connor, Tracey
Pirl, William F.
Rodler, Eve
Rugo, Hope S.
Thomas, Jay
Wagner, Lynne I.
TI Cancer-Related Fatigue
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
DE NCCN Clinical Practice Guidelines; NCCN Guidelines; fatigue;
chemotherapy; radiation therapy; bone marrow transplantation; carcinoma
treatment; screening; evaluation; intervention
ID QUALITY-OF-LIFE; RANDOMIZED CONTROLLED-TRIAL; STEM-CELL TRANSPLANTATION;
PATIENTS RECEIVING CHEMOTHERAPY; BONE-MARROW-TRANSPLANTATION;
L-CARNITINE SUPPLEMENTATION; HODGKINS-DISEASE SURVIVORS; RELAXATION
BREATHING EXERCISE; COGNITIVE-BEHAVIORAL THERAPY; PLACEBO-CONTROLLED
TRIAL
C1 [Atkinson, Ashley] Univ Alabama, Ctr Comprehens Canc, Birmingham, AL USA.
[Barsevick, Andrea M.] Fox Chase Canc Ctr, Philadelphia, PA USA.
[Breitbart, William S.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[Cella, David; Wagner, Lynne I.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Cimprich, Bernadine] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Cleeland, Charles; Escalante, Carmen P.] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
[Kaldor, Phyllis] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Ligibel, Jennifer A.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Murphy, Barbara A.] Vanderbilt Ingram Canc Inst, Nashville, TN USA.
[O'Connor, Tracey] Roswell Pk Canc Inst, Buffalo, NY USA.
[Pirl, William F.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Rodler, Eve] Seattle Canc Care Alliance, Fred Hutchinson Canc Res Ctr, Seattle, WA USA.
[Thomas, Jay] City Hope Comprehens Canc Ctr, Duarte, CA USA.
OI Barsevick, Andrea/0000-0003-1829-6826
NR 220
TC 64
Z9 65
U1 3
U2 14
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 AUG
PY 2010
VL 8
IS 8
BP 904
EP 931
PG 28
WC Oncology
SC Oncology
GA 647PK
UT WOS:000281630600007
PM 20870636
ER
PT J
AU Oyeku, SO
Feldman, HA
Ryan, K
Muret-Wagstaff, S
Neufeld, EJ
AF Oyeku, Suzette O.
Feldman, Henry. A.
Ryan, Kathleen
Muret-Wagstaff, Sharon
Neufeld, Ellis J.
TI Primary Care Clinicians' Knowledge and Confidence About Newborn
Screening for Sickle Cell Disease: Randomized Assessment of Educational
Strategies
SO JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
LA English
DT Article
DE sickle cell anemia; infant health
ID CONTINUING MEDICAL-EDUCATION; CHANGE PHYSICIAN BEHAVIOR; FOLLOW-UP;
CHILDREN
AB Objective: In Massachusetts, primary care clinicians receive and act upon hemoglobinopathy newborn screening results. We assessed clinicians' knowledge, confidence, and practices regarding hemoglobinopathy newborn screening, and the effect of mailed educational materials vs interactive seminar on knowledge and confidence.
Methods: A randomized educational intervention trial was performed at 15 community health sites. Practices were randomized to determine the order in which the educational interventions were administered: mailed educational materials first or interactive seminars on the management of hemoglobinopathy newborn screening results first. Clinicians' demographics, knowledge, confidence, and practices were assessed by a survey. Posttests were administered soon after the intervention.
Results: Responses came from 85 of 170 eligible providers (50%). Twenty-nine percent of respondents provided both pretests and posttests. In respondents with paired data, knowledge on a 5-point scale improved by 1.4 +/- 0.4 (mean +/- standard error of the mean, p = .003), while self-efficacy on a 16-point scale increased by 1.3 +/- 0.3, p = .002. There were no significant differences between seminar and mailed-materials groups.
Conclusions: Both educational strategies led to modest improvements in knowledge about newborn screening for hemoglobin disorders. Enhancing knowledge and confidence about newborn screening-related tasks may improve clinicians' capacity to act upon newborn screening results for hemoglobinopathies.
C1 [Oyeku, Suzette O.] Childrens Hosp Montefiore, Div Gen Pediat, Bronx, NY 10467 USA.
[Oyeku, Suzette O.] Yeshiva Univ, Albert Einstein Coll Med, Bronx, NY USA.
[Feldman, Henry. A.] Childrens Hosp, Clin Res Program, Boston, MA 02115 USA.
[Neufeld, Ellis J.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Neufeld, Ellis J.] Dana Farber Canc Inst, Boston, MA USA.
[Ryan, Kathleen] Boston Univ, Program Hlth Serv Res, Dept Hlth Policy & Management, Sch Publ Hlth, Boston, MA 02215 USA.
[Muret-Wagstaff, Sharon] Beth Israel Deaconess Med Ctr, Dept Anesthesia Crit Care & Pain Med, Boston, MA USA.
[Feldman, Henry. A.; Muret-Wagstaff, Sharon; Neufeld, Ellis J.] Harvard Univ, Sch Med, Boston, MA USA.
RP Oyeku, SO (reprint author), Childrens Hosp Montefiore, Div Gen Pediat, 3444 Kossuth Ave,1st Floor, Bronx, NY 10467 USA.
EM soyeku@montefiore.org
RI Neufeld, Ellis/F-9331-2011
FU Health Resources and Services Administration [T32PE10018]; Maternal and
Child Health Bureau, Health Resources and Services Administration
[1H4600232]; National Heart, Lung, and Blood Institute [HL004184]
FX This study is supported in part by grant T32PE10018 from the Health
Resources and Services Administration to the Harvard Pediatric Health
Services Research Fellowship Program (Jonathan Finkelstein, principal
investigator) and grant 1H4600232 from the Maternal and Child Health
Bureau, Health Resources and Services Administration and National Heart,
Lung, and Blood Institute K24 grant HL004184 (Dr Neufeld). Previous
Presentation: Results from this study were presented
NR 20
TC 8
Z9 8
U1 0
U2 2
PU NATL MED ASSOC
PI WASHINGON
PA 1012 10TH ST, N W, WASHINGON, DC 20001 USA
SN 0027-9684
J9 J NATL MED ASSOC
JI J. Natl. Med. Assoc.
PD AUG
PY 2010
VL 102
IS 8
BP 676
EP 682
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 641MC
UT WOS:000281129500001
PM 20806678
ER
PT J
AU Nelson, BA
Lee, EY
French, CA
Bauer, DE
Vargas, SO
AF Nelson, Benjamin A.
Lee, Edward Y.
French, Christopher A.
Bauer, Daniel E.
Vargas, Sara O.
TI BRD4-NUT Carcinoma of the Mediastinum in a Pediatric Patient
Multidetector Computed Tomography Imaging Findings
SO JOURNAL OF THORACIC IMAGING
LA English
DT Article
DE NUT midline carcinoma; mediastinum; multidetector computed tomography;
pediatric patient
ID NUT REARRANGEMENT; MIDLINE CARCINOMA; FUSION ONCOGENE; DIFFERENTIATION;
TRACT
AB Midline carcinoma with chromosomal rearrangement of the gene nuclear protein in testis (NUT) is termed NUT midline carcinoma (NMC), and is a rare and highly lethal neoplasm. The gene BRD4 is its most common translocation partner, forming a BRD4-NUT fusion oncogene. NMCs typically occur in the midline, most commonly in the head, neck, or mediastinum, as poorly differentiated carcinomas with variable degrees of squamous differentiation. This is a recently characterized tumor, and thus is still largely unfamiliar to radiologists. We report a 10-year-old boy with NMC involving the posterior mediastinum and invading the left pulmonary vein with an extension into the left atrium; these findings are presented with an emphasis on multidetector computed tomography imaging.
C1 [Lee, Edward Y.] Childrens Hosp, Dept Radiol, Div Pulm, Boston, MA 02115 USA.
[Lee, Edward Y.] Childrens Hosp, Dept Med, Div Pulm, Boston, MA 02115 USA.
[Vargas, Sara O.] Childrens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Bauer, Daniel E.; Vargas, Sara O.] Harvard Univ, Sch Med, Boston, MA USA.
[Nelson, Benjamin A.] Massachusetts Gen Hosp, Dept Pediat, Div Pulm, Boston, MA 02114 USA.
[French, Christopher A.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Bauer, Daniel E.] Dana Farber Canc Inst, Dept Med, Childrens Hosp Boston, Dept Pediat Hematol Oncol, Boston, MA 02115 USA.
RP Lee, EY (reprint author), Childrens Hosp, Dept Radiol, Div Pulm, 300 Longwood Ave, Boston, MA 02115 USA.
EM Edward.Lee@childrens.harvard.edu
FU GE-AUR Research Award; The Society of Thoracic Radiology Research; The
Society for Pediatric Radiology Research
FX This work was supported in part by a GE-AUR Research Award, The Society
of Thoracic Radiology Research Grant, and The Society for Pediatric
Radiology Research Fellow Grant (E. Y. L.).
NR 12
TC 9
Z9 10
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0883-5993
J9 J THORAC IMAG
JI J. Thorac. Imaging
PD AUG
PY 2010
VL 25
IS 3
BP W93
EP W96
PG 4
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 641HD
UT WOS:000281114500020
PM 20395873
ER
PT J
AU Alam, HB
Chipman, JG
Luchette, FA
Shapiro, MJ
Spain, DA
Cioffi, W
AF Alam, Hasan B.
Chipman, Jeffrey G.
Luchette, Fred A.
Shapiro, Marc J.
Spain, David A.
Cioffi, William
CA Surg Crit Care Program Directors S
TI Training and Certification in Surgical Critical Care: A Position Paper
by the Surgical Critical Care Program Directors Society
SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE
LA English
DT Article
ID UNITED-STATES; MEDICINE; RECOMMENDATIONS; MORTALITY; SERVICES; ILL
AB Delivery of Surgical Critical Care in the United States is facing multiple challenges including increasing complexity of care, escalating costs, shortage of well-trained physicians, and controversies about appropriate training and credentialing methods. In this position paper, the Surgical Critical Care Program Directors Society discusses some of these important issues and suggests a number of possible solutions.
C1 [Alam, Hasan B.; Chipman, Jeffrey G.; Luchette, Fred A.; Shapiro, Marc J.; Spain, David A.; Cioffi, William; Surg Crit Care Program Directors S] Massachusetts Gen Hosp, Div Trauma Emergency Surg & Surg Crit Care, Boston, MA 01124 USA.
RP Alam, HB (reprint author), Massachusetts Gen Hosp, Div Trauma Emergency Surg & Surg Crit Care, 165 Cambridge St,Suite 810, Boston, MA 01124 USA.
EM hbalam@partners.org
OI Luchette, Fred/0000-0002-8857-9111
NR 20
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-5282
J9 J TRAUMA
JI J. Trauma-Injury Infect. Crit. Care
PD AUG
PY 2010
VL 69
IS 2
BP 471
EP 474
DI 10.1097/TA.0b013e3181e93159
PG 4
WC Critical Care Medicine; Surgery
SC General & Internal Medicine; Surgery
GA 638JN
UT WOS:000280890800045
PM 20699761
ER
PT J
AU Fredman, SJ
Monson, CM
Schumm, JA
Adair, KC
Taft, CT
Resick, PA
AF Fredman, Steffany J.
Monson, Candice M.
Schumm, Jeremiah A.
Adair, Kathryn C.
Taft, Casey T.
Resick, Patricia A.
TI Associations Among Disaster Exposure, Intimate Relationship Adjustment,
and PTSD Symptoms: Can Disaster Exposure Enhance a Relationship?
SO JOURNAL OF TRAUMATIC STRESS
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; SOCIAL SUPPORT; DEPRESSION; VICTIMS;
FLOOD
AB This study examined associations among disaster characteristics, relationship adjustment, and posttraumatic stress disorder (PTSD) symptomatology 9 months postdisaster in 205 women exposed to extensive flooding. Bivariately, threat/harm and loss exposure dimensions were related to each other but differentially related to relationship adjustment and PTSD symptoms. Results from structural equation modeling revealed a positive and significant direct association between threat/harm and PTSD symptoms Conversely, loss was not significantly associated with PTSD symptoms, but was positively and significantly associated with relationship adjustment. Relationship adjustment was negatively and significantly related to PTSD symptoms. These data suggest that some aspects of disaster exposure can have a mobilizing and positive effect on intimate relationships. In turn, positive intimate relationships may buffer individuals against PTO symptoms.
C1 [Fredman, Steffany J.; Monson, Candice M.; Adair, Kathryn C.; Taft, Casey T.; Resick, Patricia A.] VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA USA.
[Fredman, Steffany J.; Monson, Candice M.; Taft, Casey T.; Resick, Patricia A.] Boston Univ, Sch Med, Boston, MA 02215 USA.
[Schumm, Jeremiah A.] Cincinnati VA Med Ctr, Cincinnati, OH USA.
[Schumm, Jeremiah A.] Univ Cincinnati, Coll Med, Cincinnati, OH 45221 USA.
RP Fredman, SJ (reprint author), VA Boston Healthcare Syst 116B 3, 150 S Huntington Ave, Boston, MA 02130 USA.
FU NIMH NIH HHS [1-R01-MH55542, R01 MH055542, R03 MH052513, R03
MH052513-01]
NR 29
TC 8
Z9 8
U1 1
U2 2
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-9867
J9 J TRAUMA STRESS
JI J. Trauma Stress
PD AUG
PY 2010
VL 23
IS 4
BP 446
EP 451
DI 10.1002/jts.20555
PG 6
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 645YF
UT WOS:000281501400004
PM 20623594
ER
PT J
AU Bromley, B
Shipp, TD
Mitchell, MA
Benacerraf, BR
AF Bromley, Bryann
Shipp, Thomas D.
Mitchell, Mary Ann
Benacerraf, Beryl R.
TI Tricks for Obtaining a Nuchal Translucency Measurement on the Fetus in a
Difficult Position
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Editorial Material
C1 [Bromley, Bryann; Shipp, Thomas D.; Mitchell, Mary Ann; Benacerraf, Beryl R.] Diagnost Ultrasound Associates PC, Boston, MA 02115 USA.
[Bromley, Bryann; Shipp, Thomas D.; Benacerraf, Beryl R.] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Bromley, Bryann; Shipp, Thomas D.; Benacerraf, Beryl R.] Brigham & Womens Hosp, Dept Obstet & Gynecol, Boston, MA 02115 USA.
[Bromley, Bryann; Benacerraf, Beryl R.] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Bromley, Bryann; Benacerraf, Beryl R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Obstet & Gynecol, Boston, MA USA.
RP Bromley, B (reprint author), Diagnost Ultrasound Associates PC, 333 Longwood Ave,Suite 400, Boston, MA 02115 USA.
EM bbsono@aol.com
NR 3
TC 2
Z9 2
U1 0
U2 0
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
USA
SN 0278-4297
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD AUG
PY 2010
VL 29
IS 8
BP 1261
EP 1264
PG 4
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 634WB
UT WOS:000280615500017
PM 20660464
ER
PT J
AU Garzotto, M
AF Garzotto, Mark
TI The Association Between Statin Use and the Diagnosis of Prostate Cancer
in a Population Based Cohort EDITORIAL COMMENT
SO JOURNAL OF UROLOGY
LA English
DT Editorial Material
C1 Oregon Hlth & Sci Univ, Portland VA Med Ctr, Portland, OR 97201 USA.
RP Garzotto, M (reprint author), Oregon Hlth & Sci Univ, Portland VA Med Ctr, Portland, OR 97201 USA.
NR 0
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 0022-5347
J9 J UROLOGY
JI J. Urol.
PD AUG
PY 2010
VL 184
IS 2
BP 500
EP 500
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA 623AA
UT WOS:000279707700025
PM 20620407
ER
PT J
AU Burgio, KL
Goode, PS
Richter, HE
Markland, AD
Johnson, TM
Redden, DT
AF Burgio, Kathryn L.
Goode, Patricia S.
Richter, Holly E.
Markland, Alayne D.
Johnson, Theodore M.
Redden, David T.
TI Combined Behavioral and Individualized Drug Therapy Versus
Individualized Drug Therapy Alone for Urge Urinary Incontinence in Women
SO JOURNAL OF UROLOGY
LA English
DT Article
DE urinary incontinence; behavioral therapy; drug therapy; clinical trial
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY-OF-LIFE; OLDER WOMEN; OVERACTIVE
BLADDER; EFFICACY; TOLTERODINE; BIOFEEDBACK; PROGRAM; IMPACT
AB Purpose: We tested whether individualized drug therapy enhanced with behavioral training would result in better outcomes than individualized drug therapy alone.
Materials and Methods: Participants were community dwelling women with urge predominant incontinence. Using a randomized clinical trial design women were randomized to 8 weeks (4 visits) of drug therapy alone (32) or drug therapy plus behavioral training (32). Drug therapy was individually titrated, extended release oxybutynin with proactive management of side effects. Behavioral training included pelvic floor muscle training and urge suppression techniques. The primary outcome measure was reduction in frequency of incontinence episodes on bladder diary at 8 weeks (with followup at 6 and 12 months). Secondary outcomes included patient satisfaction, global perception of improvement, Urogenital Distress Inventory and Incontinence Impact Questionnaire.
Results: In intent to treat analysis frequency of incontinence was reduced a mean of 88.5% in the drug alone group and 78.3% in the combined therapy group (p = 0.16). Outcomes were not significantly different between the groups in the analysis of completers (91.5% vs 86.2%, p = 0.34), or in either analysis at 6 or 12 months. The groups also did not differ significantly on secondary outcomes at any point. Participants in the drug alone group tended to be taking higher doses of oxybutynin at 8 weeks but the final dose did not differ significantly between the groups. Based on a conditional power calculation the trial was stopped early for futility.
Conclusions: When drug therapy is implemented with frequent individualized dose titration, daily bladder diaries and careful management of side effects, initiating concurrent behavioral training does not enhance outcomes for urge incontinence in women.
C1 [Burgio, Kathryn L.; Goode, Patricia S.; Markland, Alayne D.; Johnson, Theodore M.; Redden, David T.] Birmingham Atlanta Geriatr Res Educ & Clin Ctr, Dept Vet Affairs, Birmingham, AL USA.
[Burgio, Kathryn L.; Goode, Patricia S.; Markland, Alayne D.; Johnson, Theodore M.; Redden, David T.] Birmingham Atlanta Geriatr Res Educ & Clin Ctr, Dept Vet Affairs, Atlanta, GA USA.
[Burgio, Kathryn L.; Goode, Patricia S.; Richter, Holly E.; Markland, Alayne D.; Redden, David T.] Univ Alabama, Birmingham, AL USA.
[Johnson, Theodore M.] Emory Univ, Atlanta, GA 30322 USA.
RP Burgio, KL (reprint author), Birmingham VA Med Ctr, GRECC-11G,700 19th St S, Birmingham, AL 35233 USA.
EM kburgio@aging.uab.edu
OI Markland, Alayne/0000-0002-6567-6744
FU Department of Veterans Affairs; Veterans Health Administration;
Rehabilitation Research and Development Service; Birmingham/Atlanta
Geriatric Research Education and Clinical Center, Birmingham VA Medical
Center; Pfizer; Astellas; Xanodyne; Yamanouchi; Ortho McNeil; Boehringer
Ingelheim; Johnson Johnson
FX Supported by a grant from the Department of Veterans Affairs, Veterans
Health Administration, Rehabilitation Research and Development Service,
and the Female Veterans Project, Birmingham/Atlanta Geriatric Research
Education and Clinical Center, Birmingham VA Medical Center.; Financial
interest and/or other relationship with Pfizer and Astellas.; Financial
interest and/or other relationship with Xanodyne, Pfizer and Astellas.;
Financial interest and/or other relationship with Aventis, Yamanouchi,
Ortho McNeil, Boehringer Ingelheim, Johnson & Johnson and Pfizer.
NR 24
TC 15
Z9 16
U1 3
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5347
J9 J UROLOGY
JI J. Urol.
PD AUG
PY 2010
VL 184
IS 2
BP 598
EP 603
DI 10.1016/j.juro.2010.03.141
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 623AA
UT WOS:000279707700066
PM 20639023
ER
PT J
AU Flanders, VL
Gervais, DA
AF Flanders, Vincent L.
Gervais, Debra A.
TI Ablation of Liver Metastases: Current Status
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Review
ID PERCUTANEOUS RADIOFREQUENCY ABLATION; HEPATIC COLORECTAL METASTASES;
MICROWAVE COAGULATION THERAPY; BREAST-CANCER; HEPATOCELLULAR-CARCINOMA;
OVARIAN-CANCER; SURGICAL MARGIN; CYTOREDUCTIVE STRATEGY; NEUROENDOCRINE
TUMORS; CRYOSURGICAL ABLATION
AB Local ablative therapy for the treatment of metastatic disease to the liver has been evaluated most extensively in colorectal cancer with 5-year survival rates up to 55% after RF ablation. Recent findings suggest selected patients with other malignant processes may benefit as well, but conclusive evidence is limited. This article reviews the available literature regarding the use of radiofrequency ablation, microwave ablation, and cryoablation in the treatment of metastatic disease to the liver. The published results of each of these modalities in the treatment of metastatic disease to the liver are promising, and outcomes continue to be evaluated.
C1 [Flanders, Vincent L.; Gervais, Debra A.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Gervais, DA (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,White 270, Boston, MA 02114 USA.
EM dgervais@partners.org
FU Covidien
FX D.A.G. is a paid consultant for, and received a research grant from,
Covidien; it was not used to fund this paper. V.L.F. has not identified
a conflict of interest.
NR 103
TC 25
Z9 26
U1 0
U2 7
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 AUG
PY 2010
VL 21
IS 8
SU S
BP S214
EP S222
DI 10.1016/j.jvir.2010.01.046
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 640IT
UT WOS:000281045600006
PM 20656231
ER
PT J
AU Abularrage, CJ
Conrad, MF
Hackney, LA
Paruchuri, V
Crawford, RS
Kwolek, CJ
LaMuraglia, GM
Cambria, RP
AF Abularrage, Christopher J.
Conrad, Mark F.
Hackney, Lauren A.
Paruchuri, Vikram
Crawford, Robert S.
Kwolek, Christopher J.
LaMuraglia, Glenn M.
Cambria, Richard P.
TI Long-term outcomes of diabetic patients undergoing endovascular
infrainguinal interventions
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Article
ID CRITICAL LIMB ISCHEMIA; SUPERFICIAL FEMORAL-ARTERY; PERCUTANEOUS
INTERVENTIONS; OCCLUSIVE DISEASE; VASCULAR-SURGERY; PERONEAL ARTERY;
BYPASS; ANGIOPLASTY; REVASCULARIZATION; INSULIN
AB Objective: Diabetes mellitus (DM) has traditionally predicted poor outcomes after lower extremity revascularization for peripheral vascular disease (PVD). This study assessed the influence of DM on long-term outcomes of percutaneous transluminal angioplasty, with or without stenting (PTA/stent), in patients with PVD.
Methods: From January 2002 to December 2007, 920 patients underwent 1075 PTA/stent procedures. Patients were stratified into DM and non-DM cohorts. Study end points included primary patency (PP), assisted patency (AP), limb salvage, and survival and were evaluated using Kaplan-Meier and Cox regression analyses.
Results: There were 533 DM and 542 non-DM limbs. Median follow-up was 34 months. Overall, the 5-year actuarial PP was 42% +/- 2.4%, AP was 81% +/- 2.0%, limb salvage was 89% +/- 1.6%, and survival was 60% +/- 2.4%. On univariate analysis, DM vs non-DM was associated with inferior 5-year PP (37% +/- 3.4% vs 46% +/- 3.3%; P = .009), limb salvage (84% +/- 2.6% vs 93% +/- 1.8%, P < .0001), and survival (52% +/- 3.5% vs 68% +/- 3.1%, P = .0001). AP did not differ between DM and non-DM patients (P = .18). In the entire cohort, DM (hazard ratio [HR], 1.25; 95% confidence interval [CI], 1.01-1.54; P = .04), single-vessel peroneal runoff (HR, 1.54; 95% CI, 1.16-2.08; P = .003), and dialysis (HR, 1.59; 95% CI, 1.10-2.33; P = .02) were associated with decreased PP on multivariate analysis. The only variables on multivariate analysis to predict limb loss and death were critical limb ischemia (HR, 9.09; 95% CI, 4.17-20.00; P <. 0001; HR, 2.99; 95% CI, 2.01-4.44; P < .0001, respectively) and dialysis (HR, 2.94; 95% CI, 1.39-5.00; P = .003; HR, 4.24; 95% CI 2.80-6.45; P < .0001, respectively).
Conclusions: DM is an independent predictor of decreased long-term primary patency after PTA/stent. Although acceptable assisted patency rates can be achieved with close surveillance and reintervention, long-term limb salvage remains inferior in diabetic patients compared with non-diabetic patients due to a more severe clinical presentation and poor runoff. (J Vasc Surg 2010;52:314-22.)
C1 [Conrad, Mark F.] Massachusetts Gen Hosp, Div Vasc & Endovasc Surg, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Conrad, MF (reprint author), Massachusetts Gen Hosp, Div Vasc & Endovasc Surg, WAC440,15 Parkman St, Boston, MA 02114 USA.
EM mconrad@partners.org
OI Goldman, Lauren/0000-0002-8469-2416
NR 37
TC 27
Z9 32
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD AUG
PY 2010
VL 52
IS 2
BP 314
EP 322
DI 10.1016/j.jvs.2010.03.015
PG 9
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 632VA
UT WOS:000280455900010
PM 20591601
ER
PT J
AU Kang, JW
Albadawi, H
Casey, PJ
Abbruzzese, TA
Patel, VI
Yoo, HJ
Cambria, RP
Watkins, MT
AF Kang, Jeanwan
Albadawi, Hassan
Casey, Patrick J.
Abbruzzese, Thomas A.
Patel, Virendra I.
Yoo, Hyung-Jin
Cambria, Richard P.
Watkins, Michael T.
TI The effects of systemic hypothermia on a murine model of thoracic aortic
ischemia reperfusion
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Article
ID THORACOABDOMINAL ANEURYSM REPAIR; DELAYED PARAPLEGIA; SURGERY; GRAFT;
RISK
AB Introduction: Hypothermia is widely used to mediate ischemia-reperfusion injury associated with repair of the thoracoabdominal aorta. Experiments were designed in a murine model of thoracic aortic ischemia-reperfusion (TAR) to evaluate the effect of moderate systemic hypothermia on neurologic function, spinal cord morphology, and indices of inflammation in critical organs.
Methods: C57BL/6 mice were subjected to TAR under hypothermic (34 degrees C) or normothermic (38 degrees C) conditions, followed by 24 or 48 hours of normothermic reperfusion. Neurologic functions were assessed during reperfusion. Spinal cords were examined at 24 and 48 hours after reperfusion, and the degree of injury qualified by counting the number of viable motor neurons within the anterior horns. Keratinocyte chemokine, interleukin-6, and myeloperoxidase levels were measured from lung, liver, and kidney at 24 and 48 hours.
Results: Normothermic TAB. resulted in a dense neurologic deficit in all mice throughout the reperfusion period. Mice subjected to TAR under hypothermic conditions had transient, mild neurologic deficit during the initial periods of reperfusion. Between 24 and 48 hours, delayed paralysis developed in half of these mice, whereas the other half remained neurologically intact. Spinal cord histology showed a graded degree of injury that correlated with neurologic function. There was no correlation between markers of inflammation in various organs and neurologic outcomes following TAR.
Conclusion: Systemic moderate hypothermia was protective against immediate paralysis after TAR in all cases and was associated with delayed paralysis in 50% of mice. This study suggests that delayed-onset paralysis may be the result of a local insult, rather than a systemic inflammatory event, precipitating spinal cord injury. (J Vase Surg 2010;52:435-43.)
Clinical Relevance: Spinal cord injury is one of the most devastating complications of vascular surgery on the thoracoabdominal aorta. This study used a murine model that replicates the phenotypic and histologic characteristics of spinal cord injury in humans after thoracic aortic ischemia, followed by reperfusion. The findings indicate that subtle injury that exhibits minimal disability during the early periods after thoracic aortic ischemia-reperfusion may be a harbinger of delayed paralysis. This early injury, obvious in mice, may not be evident in an intubated critically ill patient. Delayed paralysis in mice was not associated with a delayed systemic inflammatory response but was associated with direct evidence of graded motor neuron injury. These data suggest that early intervention during the ischemic period may be necessary to avoid creating a scenario where the spinal cord will be susceptible to delayed injury.
C1 [Kang, Jeanwan; Albadawi, Hassan; Patel, Virendra I.; Yoo, Hyung-Jin; Cambria, Richard P.; Watkins, Michael T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Vasc & Endovasc Surg, Boston, MA USA.
[Casey, Patrick J.] Dalhousie Univ, Dept Surg, Sch Med, Halifax, NS B3H 4H2, Canada.
[Abbruzzese, Thomas A.] Gen & Vasc Surg Specialists Inc, Boynton Beach, FL USA.
RP Watkins, MT (reprint author), 15 Parkman St,Ste 444, Boston, MA 02114 USA.
EM mtwatkins@partners.org
RI Ji, Haofeng/G-6206-2012
FU Foundation for Accelerated Research; Massachusetts General Hospital;
Division of Vascular and Endovascular Surgery; Department of Surgery at
the Massachusetts General Hospital
FX Support was received from the Foundation for Accelerated Research (Wylie
Scholar in Vascular Surgery), the Geneen Fund at the Massachusetts
General Hospital, the Division of Vascular and Endovascular Surgery, and
the Linton Research Fellowship from the Department of Surgery at the
Massachusetts General Hospital. Dr Watkins is the Isenberg Fellow in
Academic Surgery at the Massachusetts General Hospital.
NR 20
TC 13
Z9 13
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD AUG
PY 2010
VL 52
IS 2
BP 435
EP 443
DI 10.1016/j.jvs.2010.03.021
PG 9
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 632VA
UT WOS:000280455900027
PM 20541344
ER
PT J
AU Ketteler, R
Tomov, V
Neunkirchner, A
Xie, QA
Pickl, WF
Seed, B
AF Ketteler, Robin
Tomov, Vesselin
Neunkirchner, Alina
Xie, Qiang
Pickl, Winfried F.
Seed, Brian
TI Host-encoded reporters for the detection and purification of multiple
enveloped viruses
SO JOURNAL OF VIROLOGICAL METHODS
LA English
DT Article
DE High-throughput screening; Alkaline phosphatase; Enveloped virus;
Flag-tagged virus purification
ID FUNCTIONAL GENOMIC SCREEN; PLASMA-MEMBRANE; CELLULAR COFACTORS; HIV-1
REPLICATION; PROTEINS; CELLS; INFECTION; FUSION; VPR; EXPRESSION
AB The identification of host cell factors for virus replication holds great promise for the development of new antiviral therapies Recently, high-throughput screening methods have emerged as powerful tools to identify candidate host factors for therapeutic intervention. The development of assay systems suitable for large-scale automated screening is of particular importance for novel viruses with high pathogenic potential for which limited biological information can be developed in a short period of time. This report presents a general enzymatic reporter system for the detection and characterization of multiple enveloped viruses that does not rely on engineering of the virus. Instead, reporter enzymes are incorporated into virus particles by targeting to lipid microdomains in producer cells. The approach allows a variety of human pathogenic enveloped viruses to be detected by sensitive, inexpensive and automatable enzymatic assays. Tagged viruses can be purified quickly and efficiently by a magnetic bead-based capture method The method allows general detection of enveloped viruses without prior reference to their sequence (C) 2010 Elsevier B V All rights reserved
C1 [Ketteler, Robin; Tomov, Vesselin; Xie, Qiang; Seed, Brian] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
[Ketteler, Robin; Tomov, Vesselin; Xie, Qiang; Seed, Brian] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA.
[Neunkirchner, Alina; Pickl, Winfried F.] Med Univ Vienna, Inst Immunol, Ctr Physiol Pathophysiol & Immunol, Vienna, Austria.
RP Seed, B (reprint author), Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, 185 Cambridge St, Boston, MA 02114 USA.
RI Pickl, Winfried/E-5682-2011;
OI Ketteler, Robin/0000-0002-2786-7291
FU Deutsche Forschungsgemeinschaft [Ke904/2-1]; Austrian Science Foundation
[SFB F1816]
FX R.K. was supported by the Deutsche Forschungsgemeinschaft (Ke904/2-1).
W.F.P. and A.N. were supported by the Austrian Science Foundation (SFB
F1816). We thank Slim Sassi and Zahedi Mujawar for critically reading
the manuscript.
NR 38
TC 1
Z9 1
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-0934
J9 J VIROL METHODS
JI J. Virol. Methods
PD AUG
PY 2010
VL 167
IS 2
BP 178
EP 185
DI 10.1016/j.jviromet.2010.04.002
PG 8
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Virology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Virology
GA 621HT
UT WOS:000279567400011
PM 20399809
ER
PT J
AU Miura, T
Brumme, ZL
Brockman, MA
Rosato, P
Sela, J
Brumme, CJ
Pereyra, F
Kaufmann, DE
Trocha, A
Block, BL
Daar, ES
Connick, E
Jessen, H
Kelleher, AD
Rosenberg, E
Markowitz, M
Schafer, K
Vaida, F
Iwamoto, A
Little, S
Walker, BD
AF Miura, Toshiyuki
Brumme, Zabrina L.
Brockman, Mark A.
Rosato, Pamela
Sela, Jennifer
Brumme, Chanson J.
Pereyra, Florencia
Kaufmann, Daniel E.
Trocha, Alicja
Block, Brian L.
Daar, Eric S.
Connick, Elizabeth
Jessen, Heiko
Kelleher, Anthony D.
Rosenberg, Eric
Markowitz, Martin
Schafer, Kim
Vaida, Florin
Iwamoto, Aikichi
Little, Susan
Walker, Bruce D.
TI Impaired Replication Capacity of Acute/Early Viruses in Persons Who
Become HIV Controllers
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID T-LYMPHOCYTE EPITOPES; REVERSE-TRANSCRIPTASE; ESCAPE MUTATIONS;
IN-VITRO; ANTIRETROVIRAL THERAPY; ELITE SUPPRESSORS; VIRAL LOAD;
EX-VIVO; RESISTANCE MUTATIONS; DISEASE PROGRESSION
AB Human immunodeficiency virus type 1 (HIV-1) controllers maintain viremia at <2,000 RNA copies/ml without antiretroviral therapy. Viruses from controllers with chronic infection were shown to exhibit impaired replication capacities, in part associated with escape mutations from cytotoxic-T-lymphocyte (CTL) responses. In contrast, little is known about viruses during acute/early infection in individuals who subsequently become HIV controllers. Here, we examine the viral replication capacities, HLA types, and virus sequences from 18 HIV-1 controllers identified during primary infection. gag-protease chimeric viruses constructed using the earliest postinfection samples displayed significantly lower replication capacities than isolates from persons who failed to control viremia (P = 0.0003). Protective HLA class I alleles were not enriched in these early HIV controllers, but viral sequencing revealed a significantly higher prevalence of drug resistance mutations associated with impaired viral fitness in controllers than in noncontrollers (6/15 [40.0%] versus 10/80 [12.5%], P = 0.018). Moreover, of two HLA-B57-positive (B57(+)) controllers identified, both harbored, at the earliest time point tested, signature escape mutations within Gag that likewise impair viral replication capacity. Only five controllers did not express "protective" alleles or harbor viruses with drug resistance mutations; intriguingly, two of them displayed typical B57 signature mutations (T242N), suggesting the acquisition of attenuated viruses from B57(+) donors. These data indicate that acute/early stage viruses from persons who become controllers have evidence of reduced replication capacity during the initial stages of infection which is likely associated with transmitted or acquired CTL escape mutations or transmitted drug resistance mutations. These data suggest that viral dynamics during acute infection have a major impact on HIV disease outcome.
C1 [Miura, Toshiyuki; Brumme, Zabrina L.; Brockman, Mark A.; Rosato, Pamela; Sela, Jennifer; Brumme, Chanson J.; Pereyra, Florencia; Kaufmann, Daniel E.; Trocha, Alicja; Block, Brian L.; Rosenberg, Eric; Walker, Bruce D.] Ragon Inst MGH MIT & Harvard, Boston, MA USA.
[Miura, Toshiyuki; Brumme, Zabrina L.; Brockman, Mark A.; Pereyra, Florencia; Kaufmann, Daniel E.; Block, Brian L.; Rosenberg, Eric; Walker, Bruce D.] Harvard Univ, Ctr AIDS Res, Boston, MA 02115 USA.
[Miura, Toshiyuki; Trocha, Alicja; Walker, Bruce D.] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Miura, Toshiyuki; Iwamoto, Aikichi] Univ Tokyo, Div Infect Dis, Adv Clin Res Ctr, Tokyo, Japan.
[Miura, Toshiyuki; Iwamoto, Aikichi] Univ Tokyo, Inst Med Sci, Tokyo, Japan.
[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.
[Daar, Eric S.] Univ Calif Los Angeles, Harbor Med Ctr, Los Angeles Biomed Res Inst, David Geffen Sch Med, Torrance, CA 90509 USA.
[Connick, Elizabeth] Univ Colorado Denver, Div Infect Dis, Aurora, CO USA.
[Jessen, Heiko] Jessen Praxis, Berlin, Germany.
[Kelleher, Anthony D.] Univ New S Wales, Natl Ctr HIV Epidemiol & Clin Res, Darlinghurst, NSW, Australia.
[Markowitz, Martin] Rockefeller Univ, Aaron Diamond AIDS Res Ctr, New York, NY 10021 USA.
[Schafer, Kim; Little, Susan] Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA.
[Vaida, Florin] Univ Calif San Diego, Div Biostat & Bioinformat, Dept Family & Prevent Med, San Diego, CA 92103 USA.
RP Walker, BD (reprint author), Massachusetts Gen Hosp, Ragon Inst MGH MIT & Harvard, 149 13th St,Room 5212, Charlestown, MA 02129 USA.
EM miura523@ims.u-tokyo.ac.jp; bwalker@partners.org
OI Brumme, Chanson/0000-0003-2722-5288; Brockman, Mark/0000-0001-6432-1426
FU NIAID/NIH [AI028568, AI030914, AI55356, AI041534, AI047033]; Howard
Hughes Medical Institute; Harvard University Center for AIDS Research
(HU CFAR); Mark and Lisa Schwartz Foundation; International AIDS Vaccine
Initiative (IAVI); Bill and Melinda Gates Foundation; Canadian
Institutes for Health Research (CIHR); Australian Government Department
of Health and Ageing; NHMRC
FX This work was supported by grants AI028568 and AI030914 (B.D.W.),
AI55356 (E.C.), and AI041534 and AI047033 (M.M.) from the NIAID/NIH and
by the Howard Hughes Medical Institute, the Harvard University Center
for AIDS Research (HU CFAR), the Mark and Lisa Schwartz Foundation, the
International AIDS Vaccine Initiative (IAVI), and the Bill and Melinda
Gates Foundation. Z.L.B. is supported by a New Investigator Award from
the Canadian Institutes for Health Research (CIHR). NCHECR is funded by
the Australian Government Department of Health and Ageing and is
affiliated with the Faculty of Medicine, the University of New South
Wales. A.D.K. is supported by an NHMRC Practitioner Fellowship.
NR 60
TC 79
Z9 80
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD AUG
PY 2010
VL 84
IS 15
BP 7581
EP 7591
DI 10.1128/JVI.00286-10
PG 11
WC Virology
SC Virology
GA 626TK
UT WOS:000279989800015
PM 20504921
ER
PT J
AU Lynch, CP
McTigue, KM
Bost, JE
Tinker, LF
Vitolins, M
Adams-Campbell, L
Sarto, GE
Hays-Grudo, J
Manson, JE
Kuller, LH
AF Lynch, Cheryl P.
McTigue, Kathleen M.
Bost, James E.
Tinker, Lesley F.
Vitolins, Mara
Adams-Campbell, Lucile
Sarto, Gloria E.
Hays-Grudo, Jennifer
Manson, Joann E.
Kuller, Lewis H.
TI Excess Weight and Physical Health-Related Quality of Life in
Postmenopausal Women of Diverse Racial/Ethnic Backgrounds
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID BODY-MASS INDEX; OLDER-ADULTS; SOCIAL SUPPORT; US ADULTS; OBESITY;
IMPACT; ASSOCIATION; OVERWEIGHT; MORTALITY; AGE
AB Background: Studies of weight and health-related quality of life (HRQOL) generally focus on white populations. This analysis examines the association between clinical weight categories and physical HRQOL in five racial/ethnic groups of older women and determines the extent to which emotional/psychological (social support, caregiver burden) and physical health (diabetes, osteoarthritis) factors modify this relationship.
Methods: The cross-sectional analysis, completed in 2007, used baseline data from postmenopausal women enrolled in the Women's Health Initiative (WHI) during the 5-year recruitment period (1993-1998).
Results: Of 161,393 women, 83% were non-Hispanic white, 9% were African American, 4% were Hispanic/Latina, 3% were Asian/Pacific Islander, and <1% were American Indian/Alaska Native. Obesity (body mass index [BMI] >= 30 kg/m(2)) was most common in non-Asian minority groups. Regression modeling showed higher odds of poor physical HRQOL with increasing weight category in all groups. In the total sample, these odds were at least 6 times as high in women with class 3 obesity as in women of normal weight and were only mildly attenuated after the analysis adjusted for emotional/psychological factors. Further adjustment for physical health factors made odds ratio (OR) estimates drop from 2.36 to 1.59 for class 1 obesity and from 6.96 to 3.71 for class 3 obesity. This pattern generally persisted within each racial/ethnic group.
Conclusions: Heavier weight negatively affects physical HRQOL in postmenopausal women across diverse racial/ethnic backgrounds. Weight-relevant physical health factors have a greater impact on this weight-HRQOL association than do emotional/psychological factors.
C1 [Lynch, Cheryl P.] Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA.
[Lynch, Cheryl P.] Med Univ S Carolina, Ralph H Johnson VA Med Ctr, Charleston, SC 29425 USA.
[McTigue, Kathleen M.; Bost, James E.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[McTigue, Kathleen M.; Kuller, Lewis H.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Tinker, Lesley F.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Vitolins, Mara] Wake Forest Univ, Baptist Med Ctr, Winston Salem, NC 27109 USA.
[Adams-Campbell, Lucile] Georgetown Univ, Med Ctr, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
[Sarto, Gloria E.] Univ Wisconsin, Dept Obstet & Gynecol, Madison, WI 53706 USA.
[Hays-Grudo, Jennifer] Univ Oklahoma, Dept Internal Med, Tulsa, OK USA.
[Manson, Joann E.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Prevent Med, Boston, MA 02115 USA.
RP Lynch, CP (reprint author), Med Univ S Carolina, Dept Med, 135 Rutledge Ave,MSC 593, Charleston, SC 29425 USA.
EM lynchcp@musc.edu
RI Sriwisit, Sukhumaphorn/G-1405-2011;
OI Hays-Grudo, Jennifer/0000-0002-8107-1243
FU National Heart, Lung, and Blood Institute, U.S. Department of Health and
Human Services; Division of General Internal Medicine, University of
Pittsburgh
FX The WHI program is funded by the National Heart, Lung, and Blood
Institute, U.S. Department of Health and Human Services. C. P. L.
received an internal developmental award from the Division of General
Internal Medicine, University of Pittsburgh, for statistical support to
conduct the analyses. The funding agencies had no role in the design and
conduct of this study, in the collection, analysis, and interpretation
of the data, or in the preparation, review, or approval of the article.
NR 54
TC 10
Z9 10
U1 1
U2 9
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD AUG
PY 2010
VL 19
IS 8
BP 1449
EP 1458
DI 10.1089/jwh.2009.1652
PG 10
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 634KH
UT WOS:000280579300004
PM 20629574
ER
PT J
AU Tello, MA
Jenckes, M
Gaver, J
Anderson, JR
Moore, RD
Chander, G
AF Tello, Monique A.
Jenckes, Mollie
Gaver, Jennifer
Anderson, Jean R.
Moore, Richard D.
Chander, Geetanjali
TI Barriers to Recommended Gynecologic Care in an Urban United States HIV
Clinic
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; AFRICAN-AMERICAN WOMEN; CERVICAL-CANCER;
ANTIRETROVIRAL THERAPY; INFECTED WOMEN; HEALTH-CARE; SUBSTANCE USE;
FOLLOW-UP; ADHERENCE; PREVALENCE
AB Background: Despite an increased risk for cervical cytologic abnormalities, HIV-infected women frequently miss their gynecology appointments. We examined barriers to adherence with gynecologic care in an urban HIV clinic.
Methods: We conducted a cross-sectional survey of 200 women receiving gynecologic services in an urban HIV clinic, followed by focus groups. Primary outcomes included (1) missed gynecology appointments and (2) receipt of a Pap smear in the previous year. Independent variables included sociodemographic characteristics, child care responsibilities, substance use, depressive symptoms, social support, interpersonal violence, CD4 count, and HIV-1 RNA. We conducted multivariable logistic regression to examine associations between independent variables and outcomes. We then held two focus groups designed to gather opinions on and increase our understanding of the key findings from the survey.
Results: Of 200 women, 69% missed at least one gynecology appointment, and 22% had no Pap smear in the past year. In logistic regression, moderate (odds ratio [OR] 3.1, 95% confidence interval [CI] 1.4-6.7) and severe (OR 3.1, 95% CI 1.3-7.5) depressive symptoms and past-month substance use (OR 2.3, 95% CI 1.0-5.3) were associated with missing an appointment in the prior year. An education level of less than high school (OR 0.3, 95% CI 0.1-0.6) compared with high school diploma or greater was associated with not having a Pap smear in the previous year. When analyses were limited to women with a cervix (n = 166), moderate (OR 2.5, 95% CI 1.1-5.7) and severe (OR 2.5, 95% CI 1.0-6.3) depressive systems remained significantly associated with missing a gynecology appointment in the previous year and age > 50 (OR 0.3, 95% CI 0.1-0.9), an HIV-1 RNA > 50 (OR 0.4, 95% CI 0.2-0.9), and education level less than high school (OR 0.2, 95% CI 0.1-0.5) were associated with not having a Pap smear in the past 12 months. Qualitative analysis of the focus group data suggested that fear, inclement weather, and forgetting appointments may contribute to missed gynecology appointments.
Conclusion: Gynecologic healthcare is underused among HIV-infected women. We found that depressive symptoms, substance use, fear of the gynecologic examination, and simply forgetting about the appointment may be barriers to gynecologic care. Interventions targeting these barriers may improve use of gynecologic care among this population.
C1 [Tello, Monique A.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Jenckes, Mollie; Gaver, Jennifer; Moore, Richard D.; Chander, Geetanjali] Johns Hopkins Med Inst, Dept Med, Div Gen Internal Med, Baltimore, MD 21205 USA.
[Gaver, Jennifer; Anderson, Jean R.] Johns Hopkins Med Inst, Dept Gynecol & Obstet, Baltimore, MD 21205 USA.
RP Tello, MA (reprint author), MGH Womens Hlth Associates, Yawkey 4B,Suite 4700,55 Fruit St, Boston, MA 02114 USA.
EM mtello@partners.org
FU Society of General Internal Medicine, NIH [R01 DA11602, K24DA00432,
K23AA015313, R01AA105032]
FX This work was supported by a Lawrence S. Linn Award, Society of General
Internal Medicine, NIH R01 DA11602, K24DA00432, K23AA015313 and
R01AA105032.
NR 39
TC 15
Z9 15
U1 2
U2 4
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD AUG
PY 2010
VL 19
IS 8
BP 1511
EP 1518
DI 10.1089/jwh.2009.1670
PG 8
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 634KH
UT WOS:000280579300011
PM 20629573
ER
PT J
AU Ligibel, JA
Partridge, A
Giobbie-Hurder, A
Campbell, N
Shockro, L
Salinadri, T
Winer, EP
AF Ligibel, Jennifer A.
Partridge, Ann
Giobbie-Hurder, Anita
Campbell, Nancy
Shockro, Laura
Salinadri, Taylor
Winer, Eric P.
TI Physical and Psychological Outcomes Among Women in a Telephone-Based
Exercise Intervention During Adjuvant Therapy for Early Stage Breast
Cancer
SO JOURNAL OF WOMENS HEALTH
LA English
DT Article
ID QUALITY-OF-LIFE; BODY-IMAGE; WEIGHT-GAIN; SURVIVORS; DIAGNOSIS;
QUESTIONNAIRE; ADJUSTMENT; QLQ-C30; HEALTH
AB Background: Many women gain weight after breast cancer diagnosis. Weight gain has been associated with poor quality of life (QOL), dissatisfaction with one's body, increased risk of postoperative complications, and possibly even an increased risk of breast cancer recurrence. Studies have suggested that decreases in physical activity during treatment may contribute to weight gain in breast cancer patients.
Methods: In this single-arm pilot study, 41 sedentary women with early stage breast cancer participated in a 12-week, moderate-intensity aerobic exercise intervention during adjuvant chemotherapy and/or radiation. The target exercise goal was 150 minutes of activity/week. Participants underwent evaluation of exercise behaviors, fitness, and psychological and anthropometric measures at baseline and after the 12-week intervention.
Results: Most participants were premenopausal, and 80% were treated with intensive chemotherapy regimens that included both an anthracycline and a taxane. In the 34 patients for whom baseline and week 12 measures were available, weekly exercise increased from 13 minutes to 116 minutes at week 12 (p < 0.001). Cardiorespiratory fitness and QOL improved significantly (p < 0.003 and p - 0.001, respectively), and there was a trend toward improvements in fatigue (p - 0.08). Participants also avoided weight gain and increases in body fat over the course of the 12-week protocol.
Conclusions: Women participating in a home-based exercise intervention during adjuvant therapy significantly increased activity and avoided weight gain, which has been associated with poor QOL and cancer outcomes in early stage breast cancer.
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Ligibel, JA (reprint author), 44 Binney St, Boston, MA 02115 USA.
EM jligibel@partners.org
NR 30
TC 11
Z9 11
U1 2
U2 8
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD AUG
PY 2010
VL 19
IS 8
BP 1553
EP 1559
DI 10.1089/jwh.2009.1760
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 634KH
UT WOS:000280579300016
PM 20629579
ER
PT J
AU Chuang, PY
He, JC
AF Chuang, Peter Y.
He, John C.
TI JAK/STAT signaling in renal diseases
SO KIDNEY INTERNATIONAL
LA English
DT Editorial Material
ID DIABETIC-NEPHROPATHY; STAT3; PROLIFERATION; TRANSDUCER; ACTIVATOR;
PATHWAY; INJURY
AB The Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway is a pleiotropic cascade essential to cytokine and growth hormone receptor signaling. Signaling through the JAK/STAT pathway is important for the kidney's response to injury in disease. Pang et al. confirm that activation of STAT3 mediates renal fibrosis in the unilateral ureteral obstruction experimental model. Kidney International (2010) 78, 231-234. doi: 10.1038/ki.2010.158
C1 [Chuang, Peter Y.; He, John C.] Mt Sinai Sch Med, Div Nephrol, Dept Med, New York, NY 10029 USA.
[He, John C.] Mt Sinai Sch Med, Dept Pharmacol & Syst Therapeut, New York, NY 10029 USA.
[He, John C.] James J Peters VA Med Ctr, York, NY USA.
RP He, JC (reprint author), Mt Sinai Sch Med, Dept Med Nephrol, 1 Gustave L Levy Pl,Box 1243, New York, NY 10029 USA.
EM cijiang.he@mssm.edu
FU NIDDK NIH HHS [K08 DK082760]
NR 10
TC 21
Z9 22
U1 0
U2 5
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 AUG
PY 2010
VL 78
IS 3
BP 231
EP 234
DI 10.1038/ki.2010.158
PG 4
WC Urology & Nephrology
SC Urology & Nephrology
GA 626QV
UT WOS:000279982800001
PM 20631733
ER
PT J
AU Schreiner, R
Frindt, G
Diaz, F
Carvajal-Gonzalez, JM
Bay, AEP
Palmer, LG
Marshansky, V
Brown, D
Philp, NJ
Rodriguez-Boulan, E
AF Schreiner, Ryan
Frindt, Gustavo
Diaz, Fernando
Carvajal-Gonzalez, Jose M.
Bay, Andres E. Perez
Palmer, Lawrence G.
Marshansky, Vladimir
Brown, Dennis
Philp, Nancy J.
Rodriguez-Boulan, Enrique
TI The absence of a clathrin adapter confers unique polarity essential to
proximal tubule function
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE AP1B; IGF2R/CI-MPR; polarity; proximal tubule; PTH receptor; sorting
ID RETINAL-PIGMENT EPITHELIUM; ADHESION MOLECULE-C; DARBY CANINE KIDNEY;
MDCK CELLS; PROTEIN TRAFFICKING; SORTING SIGNALS; LDL RECEPTOR; JAM-C;
LOCALIZATION; EXPRESSION
AB It is well established that many cognate basolateral plasma membrane proteins are expressed apically in proximal tubule cells thus optimizing the reabsorption capacity of the kidney. The protein clathrin and its adapter proteins normally regulate basolateral polarity. Here we tested whether the unique proximal tubule polarity is dependent on an epithelial-specific basolateral clathrin adapter, AP1B, present in most other epithelia. Quantitative PCR of isolated mouse renal tubules showed that AP1B was absent in proximal tubules but present in medullary and cortical thick ascending limbs of Henle, and cortical collecting ducts. Western blot confirmed the absence of AP1B in three established proximal tubule cell lines. Knockdown of AP1B by shRNA in prototypical distal tubule MDCK cells resulted in redistribution of the basolateral parathyroid hormone receptor, the insulin-like growth factor II receptor/calciumin dependent mannose-6-phosphate receptor, and the junctional adhesion molecule, JAM-C, to a proximal tubule-like nonpolar localization. Yeast two-hybrid assays detected direct interactions between the cytoplasmic tails of these plasma membrane proteins and the cargo-binding region of the AP1B complex. Hence, our results show that differential expression of AP1B contributes to normal kidney function and illustrates possible roles of this adapter protein in kidney development, physiology, and pathology. Kidney International (2010) 78, 382-388; doi:10.1038/ki.2010.166; published online 9 June 2010
C1 [Schreiner, Ryan; Diaz, Fernando; Carvajal-Gonzalez, Jose M.; Bay, Andres E. Perez; Rodriguez-Boulan, Enrique] Cornell Univ, Dept Ophthalmol, Dyson Vis Res Inst, Weill Med Coll, New York, NY 10065 USA.
[Schreiner, Ryan; Frindt, Gustavo; Palmer, Lawrence G.] Cornell Univ, Weill Med Coll, Dept Physiol & Biophys, New York, NY 10065 USA.
[Marshansky, Vladimir; Brown, Dennis] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Nephrol,Program Membrane Biol,Ctr Syst Biol, Boston, MA USA.
[Philp, Nancy J.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA.
RP Rodriguez-Boulan, E (reprint author), Cornell Univ, Dept Ophthalmol, Dyson Vis Res Inst, Weill Cornell Med Coll, 1300 York Ave,LC300,Box 233, New York, NY 10065 USA.
EM boulan@med.cornell.edu
OI Schreiner, Ryan/0000-0002-7457-6606; Carvajal-Gonzalez, Jose
Maria/0000-0001-6576-830X
FU NIH [EY08538, GM34107, EY-012042, DK27847, DK42956, DK38452, EY07138];
EMBO
FX This work was supported by NIH Grants EY08538 and GM34107 to ER-B,
EY-012042 to NJP, DK27847 to LGP, DK42956 to DB, DK38452 to VM, RS was
supported by EY07138. JMC-G was supported by a fellowship from the EMBO.
NR 38
TC 28
Z9 28
U1 0
U2 10
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 AUG
PY 2010
VL 78
IS 4
BP 382
EP 388
DI 10.1038/ki.2010.166
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 633TE
UT WOS:000280528000008
PM 20531453
ER
PT J
AU Seckl, MJ
Sebire, NJ
Berkowitz, RS
AF Seckl, Michael J.
Sebire, Neil J.
Berkowitz, Ross S.
TI Gestational trophoblastic disease
SO LANCET
LA English
DT Article
ID HUMAN CHORIONIC-GONADOTROPIN; COMPLETE HYDATIDIFORM MOLE; POLYMERASE
CHAIN-REACTION; RETROSPECTIVE COHORT SURVEY; REPEAT UTERINE EVACUATION;
HIGH-DOSE CHEMOTHERAPY; FREE BETA-SUBUNIT; SUBSEQUENT PREGNANCY;
ACTINOMYCIN-D; VINCRISTINE CHEMOTHERAPY
AB Gestational trophoblastic disease encompasses a range of pregnancy-related disorders, consisting of the premalignant disorders of complete and partial hydatidiform mole, and the malignant disorders of invasive mole, choriocarcinoma, and the rare placental-site trophoblastic tumour. These malignant forms are termed gestational trophoblastic tumours or neoplasia. Improvements in management and follow-up protocols mean that overall cure rates can exceed 98% with fertility retention, whereas most women would have died from malignant disease 60 years ago This success can be explained by the development of effective treatments, the use of human chorionic gonadotropin as a biomarker, and centralisation of care. We summarise strategies for management of gestational trophoblastic disease and address some of the controversies and future research directions.
C1 [Seckl, Michael J.] Univ London Imperial Coll Sci Technol & Med, Charing Cross Hosp Campus, Charing Cross Gestat Trophoblast Dis Ctr, Dept Canc Med, London W6 8RF, England.
[Sebire, Neil J.] Univ London Imperial Coll Sci Technol & Med, Charing Cross Hosp Campus, Charing Cross Gestat Trophoblast Dis Ctr, Dept Histopathol, London W6 8RF, England.
[Berkowitz, Ross S.] Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst,Div Gynecol Oncol,Sch Med, Dept Obstet & Gynecol,New England Trophoblast Dis, Boston, MA 02115 USA.
RP Seckl, MJ (reprint author), Univ London Imperial Coll Sci Technol & Med, Charing Cross Hosp Campus, Charing Cross Gestat Trophoblast Dis Ctr, Dept Canc Med, London W6 8RF, England.
FU Department of Health; National Commissioning Group; Cancer Treatment and
Research Trust; Imperial College Experimental Cancer Medicine Centre;
Biomedical Research Centre; Donald P Goldstein MD Trophoblaslic Registry
Endowment Fund; Chonocarenoma Research Fund
FX MJS and NJS thank the Department of Health, National Commissioning
Group, and the Cancer Treatment and Research Trust for their continued
support MJS acknowledges support from the Imperial College Experimental
Cancer Medicine Centre and Biomedical Research Centre grants RSB
acknowledges the Donald P Goldstein MD Trophoblaslic Registry Endowment
Fund and the Chonocarenoma Research Fund
NR 153
TC 194
Z9 212
U1 5
U2 34
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
J9 LANCET
JI Lancet
PD AUG-SEP
PY 2010
VL 376
IS 9742
BP 717
EP 729
DI 10.1016/S0140-6736(10)60280-2
PG 13
WC Medicine, General & Internal
SC General & Internal Medicine
GA 646YW
UT WOS:000281582900031
PM 20673583
ER
PT J
AU Yang, P
Jen, J
Li, YF
Wang, LA
de Andrade, M
Chang, SC
Zhang, ZF
Christiani, DC
Wu, XF
AF Yang, Ping
Jen, Jin
Li, Yafei
Wang, Liang
de Andrade, Mariza
Chang, Shen-Chih
Zhang, Zuo-Feng
Christiani, David C.
Wu, Xifeng
TI GPC5 rs2352028 variant and risk of lung cancer in never smokers Reply
SO LANCET ONCOLOGY
LA English
DT Editorial Material
C1 [Yang, Ping; Li, Yafei; de Andrade, Mariza] Mayo Clin, Coll Med, Dept Hlth Sci Res, Rochester, MN 55905 USA.
[Jen, Jin] Mayo Clin, Coll Med, Dept Pulm & Crit Care Med, Rochester, MN 55905 USA.
[Wang, Liang] Mayo Clin, Coll Med, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
[Chang, Shen-Chih; Zhang, Zuo-Feng] Univ Calif Los Angeles, Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA 90024 USA.
[Chang, Shen-Chih; Zhang, Zuo-Feng] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA.
[Christiani, David C.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Christiani, David C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Pulm & Crit Care Unit,Dept Med, Boston, MA USA.
[Wu, Xifeng] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
RP Yang, P (reprint author), Mayo Clin, Coll Med, Dept Hlth Sci Res, Rochester, MN 55905 USA.
NR 1
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
J9 LANCET ONCOL
JI Lancet Oncol.
PD AUG
PY 2010
VL 11
IS 8
BP 716
EP 716
DI 10.1016/S1470-2045(10)70180-7
PG 1
WC Oncology
SC Oncology
GA 639XD
UT WOS:000281009500012
ER
PT J
AU Vakharia, KT
Shapiro, NL
Bhattacharyya, N
AF Vakharia, Kalpesh T.
Shapiro, Nina L.
Bhattacharyya, Neil
TI Demographic Disparities Among Children With Frequent Ear Infections in
the United States
SO LARYNGOSCOPE
LA English
DT Article
DE Otitis media; disparities; access to care; epidemiology
ID OTITIS-MEDIA; ETHNIC DISPARITIES; PRIMARY-CARE; US CHILDREN;
HEALTH-CARE; ACCESS; PREVALENCE; CANCER; BURDEN
AB Objectives/Hypothesis: To evaluate current racial/ethnic and socioeconomic disparities in the prevalence of frequent ear infections (FEI) among children in the United States.
Study Design: Cross-sectional study.
Methods: The National Health Interview Survey (years 1997 to 2006) was utilized to evaluate children who were reported by their parent/guardian to have "3 or more ear infections during the past 12 months." Demographic variables evaluated included age, sex, race/ethnicity, income level, and insurance status. Multivariate analyses determined the influence of demographic variables on the prevalence of FEI in children.
Results: Among an annualized population of 72.6 million children (average age, 8.55 +/- 0.19 years), 4.65 +/- 0.07 million children (6.6 +/- 0.1%) reported FEI. FEI was more commonly reported in white (7.0 +/- 0.1%) and Hispanic (6.2 +/- 0.2%) than in black (5.0 +/- 0.2%) and other race/ethnic groups (4.5 +/- 0.3%, P<.001). A larger portion of children in households below the poverty level reported FEI (8.0 +/- 0.3%, P<.001). Of children with no health insurance 5.4 +/- 0.3% had FEI. On multivariate analysis, black, Hispanic and other race/ethnic group had decreased odds ratio for FEI relative to white children (odds ratios: 0.63, 0.76, and 0.60, respectively, all P<.001). Income below poverty level also predicted FEI (odds ratio, 1.322, P<.001), whereas lack of insurance coverage did not (P=.181).
Conclusions: Despite increasing awareness, there are still notable racial/ethnic and socioeconomic disparities among children with FEI. Further efforts to eliminate these disparities and improve the care of children with FEI are needed.
C1 [Vakharia, Kalpesh T.] Massachusetts Eye & Ear Infirm, Dept Otol & Laryngol, Boston, MA 02114 USA.
[Bhattacharyya, Neil] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
[Shapiro, Nina L.] Univ Calif Los Angeles, Div Otolaryngol Head & Neck Surg, Los Angeles, CA USA.
[Bhattacharyya, Neil] Brigham & Womens Hosp, Div Otolaryngol Head & Neck Surg, Boston, MA 02115 USA.
RP Bhattacharyya, N (reprint author), Div Otolaryngol, 45 Francis St, Boston, MA 02115 USA.
EM neiloy@massmed.org
NR 19
TC 21
Z9 21
U1 1
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0023-852X
J9 LARYNGOSCOPE
JI Laryngoscope
PD AUG
PY 2010
VL 120
IS 8
BP 1667
EP 1670
DI 10.1002/lary.20961
PG 4
WC Medicine, Research & Experimental; Otorhinolaryngology
SC Research & Experimental Medicine; Otorhinolaryngology
GA 635YW
UT WOS:000280695000029
PM 20564719
ER
PT J
AU Hashmi, JT
Huang, YY
Sharma, SK
Kurup, DB
De Taboada, L
Carroll, JD
Hamblin, MR
AF Hashmi, Javad T.
Huang, Ying-Ying
Sharma, Sulbha K.
Kurup, Divya Balachandran
De Taboada, Luis
Carroll, James D.
Hamblin, Michael R.
TI Effect of Pulsing in Low-Level Light Therapy
SO LASERS IN SURGERY AND MEDICINE
LA English
DT Review
DE low level light therapy; photobiomodulation; frequency; pulse duration;
duty cycle; clinical trials
ID CARPAL-TUNNEL-SYNDROME; PULSED ELECTROMAGNETIC-FIELDS; ENERGY LASER
IRRADIATION; DEEP BRAIN-STIMULATION; NEAR-INFRARED LIGHT; AS 904 NM;
MAGNETIC-FIELDS; DOUBLE-BLIND; NERVE-STIMULATION; CONTROLLED-TRIAL
AB Background and Objective: Low level laser (light) therapy (LLLT) is a rapidly growing modality used in physical therapy, chiropractic, sports medicine and increasingly in mainstream medicine LLLT is used to increase wound healing and tissue regeneration, to relieve pain and inflammation, to prevent tissue death, to mitigate degeneration in many neurological indications While some agreement has emerged on the best wavelengths of light and a range of acceptable dosages to be used (irradiance and fluence), there is no agreement on whether continuous wave or pulsed light is best and on what factors govern the pulse parameters to be chosen
Study Design/Materials and Methods: Published peer-reviewed literature between 1970 and 2010 was reviewed
Results: The basic molecular and cellular mechanisms of LLLT are discussed. The type of pulsed light sources available and the parameters that govern their pulse structure are outlined. Studies that have compared continuous wave and pulsed light in both animals and patients are reviewed. Frequencies used in other pulsed ElectroMagnetic treatment modalities modalities used in physical therapy and biomedicine are compared to those used in LLLT.
Conclusion: There is some evidence that pulsed light does have effects that are different from those of continuous wave light However further work is needed to define these effects for different disease conditions and pulse structures Lasers Surg. Med 42:450-466, 2010. (C) 2010 Wiley-Liss, Inc.
C1 [Hashmi, Javad T.; Huang, Ying-Ying; Sharma, Sulbha K.; Kurup, Divya Balachandran; Hamblin, Michael R.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Huang, Ying-Ying; Hamblin, Michael R.] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Huang, Ying-Ying] Guangxi Med Univ, Aesthet & Plast Ctr, Nanning, Peoples R China.
[De Taboada, Luis] PhotoThera Inc, Carlsbad, CA USA.
[Carroll, James D.; Hamblin, Michael R.] THOR Photomed Ltd, Chesham HP5 1HQ, England.
[Hamblin, Michael R.] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Hamblin, MR (reprint author), 40 Blossom St, Boston, MA 02114 USA.
RI Huang, Ying-ying/G-3153-2011;
OI Huang, Ying-ying/0000-0003-3066-6981; Carroll,
James/0000-0002-9205-1061; Hamblin, Michael/0000-0001-6431-4605
FU NIH [R01AI050875]; Center for Integration of Medicine and Innovative
Technology [DAMD17-02-2-0006]; CDMRP Program in TBI [W81XWH-09-1-0514];
Air Force Office of Scientific Research [FA9950-04-1-0079]
FX Contract grant sponsor NIH, Contract grant number R01AI050875, Contract
grant sponsor Center for Integration of Medicine and Innovative
Technology, Contract grant number DAMD17-02-2-0006, Contract grant
sponsor CDMRP Program in TBI, Contract grant number W81XWH-09-1-0514;
Contract grant sponsor Air Force Office of Scientific Research, Contract
grant number FA9950-04-1-0079
NR 71
TC 76
Z9 76
U1 4
U2 32
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0196-8092
J9 LASER SURG MED
JI Lasers Surg. Med.
PD AUG
PY 2010
VL 42
IS 6
BP 450
EP 466
DI 10.1002/lsm.20950
PG 17
WC Dermatology; Surgery
SC Dermatology; Surgery
GA 639XC
UT WOS:000281009400002
PM 20662021
ER
PT J
AU Kim, Y
Oh, S
Yun, HS
Oh, S
Kim, SH
AF Kim, Y.
Oh, S.
Yun, H. S.
Oh, S.
Kim, S. H.
TI Cell-bound exopolysaccharide from probiotic bacteria induces autophagic
cell death of tumour cells
SO LETTERS IN APPLIED MICROBIOLOGY
LA English
DT Article
DE antitumour activity; autophagy; cb-EPS; two-dimensional polyacrylamide
gel electrophoresis (2D-PAGE)
ID ESCHERICHIA-COLI O157-H7; STRESS-INDUCED AUTOPHAGY; EXPRESSION;
BECLIN-1; GENE; INHIBITION; TUMORIGENESIS; SUPPRESSOR; PROTEINS; THERAPY
AB Aim:
Lactic acid bacteria (LAB) are beneficial micro-organisms that have been associated with several probiotic effects in both humans and animals. Here, using proteome analysis, we investigate the antitumour effects of cell-bound exopolysaccharides (cb-EPS) isolated from Lactobacillus acidophilus 606 on colon cancer cells and explore the proteins critical for their antitumour activity.
Methods and Results:
cb-EPS inhibited the proliferation of HT-29 colon cancer cells by directly affecting cell morphology and not the cell cycle. Using two-dimensional polyacrylamide gel electrophoresis coupled with matrix-assisted laser desorption-ionization time-of-flight mass spectrometry (MALDI-TOF/MS) and immunoblot analysis, we found that cb-EPS dramatically induced Beclin-1 and GRP78, and affected Bcl-2 and Bak regulation.
Conclusions:
The results of this study indicate that cb-EPS are antitumourigenic against HT-29 colon cancer cells and that this activity is because of the activation of autophagic cell death promoted directly by the induction of Beclin-1 and GRP78, as well as indirectly through the induction of Bcl-2 and Bak.
Significance and Impact of the Study:
These results may contribute to understanding the novel mechanisms by which probiotic bacteria induce tumour cell death via autophagy.
C1 [Yun, H. S.; Kim, S. H.] Korea Univ, Div Food Biosci & Technol, Seoul 136701, South Korea.
[Kim, Y.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, Boston, MA USA.
[Oh, S.] Korea Univ, Div Cellular & Dev Biol, Brain Korea Program Biomed Sci 21, Seoul 136701, South Korea.
[Oh, S.] Chonnam Natl Univ, Dept Anim Sci, Kwangju, South Korea.
RP Kim, SH (reprint author), Korea Univ, Div Food Biosci & Technol, 1,5 Ka Anam Dong, Seoul 136701, South Korea.
EM saehkim@korea.ac.kr
FU Korea government (MEST) [R01-2008-000-20593-0]; Korean Government
(MOEHRD) [KRF-F00025]
FX This study was supported by a Korea Science and Engineering Foundation
(KOSEF) grant funded by the Korea government (MEST)
(R01-2008-000-20593-0). Y. Kim was supported by a Korea Research
Foundation Grant funded by the Korean Government (MOEHRD) (KRF-F00025).
NR 26
TC 34
Z9 36
U1 0
U2 13
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0266-8254
J9 LETT APPL MICROBIOL
JI Lett. Appl. Microbiol.
PD AUG
PY 2010
VL 51
IS 2
BP 123
EP 130
DI 10.1111/j.1472-765X.2010.02859.x
PG 8
WC Biotechnology & Applied Microbiology; Microbiology
SC Biotechnology & Applied Microbiology; Microbiology
GA 623OB
UT WOS:000279750600001
PM 20536712
ER
PT J
AU Brown, JR
AF Brown, Jennifer R.
TI Immunomodulators in chronic lymphocytic leukemia: where does
lenalidomide belong?
SO LEUKEMIA & LYMPHOMA
LA English
DT Article
DE CLL; lenalidomide; tumor flare
ID CLINICAL-EFFICACY; FLARE REACTION; TUMOR FLARE; PHASE-I; CLL;
COMBINATION; RITUXIMAB; CELLS
AB The significant clinical activity of lenalidomide in relapsed CLL was first described several years ago. Since then the problems of tumor flare and tumor lysis have emerged, and upfront single agent studies have reported response rates that were perhaps a little disappointing. Interest in elucidating the place of lenalidomide in CLL therapy remains intense, however, and combination studies are in progress. As laboratory efforts start to provide more insight into the mechanisms of antitumor efficacy and tumor flare, rational strategies for combination therapy will soon follow.
C1 Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Brown, JR (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM jbrown2@partners.org
NR 18
TC 3
Z9 3
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 1042-8194
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD AUG
PY 2010
VL 51
IS 8
BP 1382
EP 1385
DI 10.3109/10428194.2010.496017
PG 4
WC Oncology; Hematology
SC Oncology; Hematology
GA 647SK
UT WOS:000281639200005
PM 20624030
ER
PT J
AU Albrecht, J
Werth, VP
AF Albrecht, J.
Werth, V. P.
TI Clinical outcome measures for cutaneous lupus erythematosus
SO LUPUS
LA English
DT Review
DE cutaneous lupus erythematosus; disease activity; patient outcome
assessment; reproducibility of results; skin; validity
ID QUALITY-OF-LIFE; DISEASE SEVERITY; ATOPIC-DERMATITIS; SURFACE-AREA;
INDEX; RELIABILITY; PSORIASIS; ACNE; INSTRUMENTS; VALIDATION
AB Cutaneous lupus erythematosus (CLE) is a clinically heterogeneous group of rare skin diseases that only rarely have been subjected to controlled clinical trials. This may have been partly due to a lack of suitable validated outcome instruments. Recently, the Food and Drug Administration (FDA) mandated that organ-specific trials for lupus erythematosus need to use a combination of different outcome measures. The patient's condition needs to be assessed in terms of quality of life, the patient's global response, and organ-specific instruments that measure activity of the disease as well as damage due to the disease. For the skin, the only formally validated and published instrument is currently the Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI). This paper discusses the background of the development of the CLASI as well as issues related to its use and interpretation in the context of clinical research of CLE. Lupus (2010) 19, 1137-1143.
C1 [Albrecht, J.] John H Stroger Jr Hosp Cook Cty, Div Dermatol, Dept Med, Chicago, IL 60612 USA.
[Werth, V. P.] Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
[Werth, V. P.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
RP Werth, VP (reprint author), Univ Penn, Dept Dermatol, 2 Maloney 3600 Spruce St, Philadelphia, PA 19119 USA.
EM werth@mail.med.upenn.edu
FU National Institutes of Health [K24-AR 02207]; Department of Veterans
Affairs, Veterans Health Administration, Office of Research and
Development, Biomedical Laboratory Research and Development
FX This material is based upon work supported by the National Institutes of
Health, including NIH K24-AR 02207 (Werth). This work was also partially
supported by a Merit Review Grant from the Department of Veterans
Affairs, Veterans Health Administration, Office of Research and
Development, Biomedical Laboratory Research and Development.
NR 43
TC 8
Z9 10
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0961-2033
J9 LUPUS
JI Lupus
PD AUG
PY 2010
VL 19
IS 9
SI SI
BP 1137
EP 1143
DI 10.1177/0961203310370049
PG 7
WC Rheumatology
SC Rheumatology
GA 635UW
UT WOS:000280683400016
PM 20693208
ER
PT J
AU Prabhakar, PD
Prabhakar, AM
Prabhakar, HB
Sahani, D
AF Prabhakar, Priya D.
Prabhakar, Anand M.
Prabhakar, Hima B.
Sahani, Duyshant
TI Magnetic Resonance Cholangiopancreatography of Benign Disorders of the
Biliary System
SO MAGNETIC RESONANCE IMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE MRCP; Benign liver disorders; Biliary; Imaging
ID PRIMARY SCLEROSING CHOLANGITIS; ENDOSCOPIC RETROGRADE
CHOLANGIOPANCREATOGRAPHY; MR-IMAGING FINDINGS; RECURRENT PYOGENIC
CHOLANGITIS; BILE-DUCT STRICTURES; CONGENITAL-ANOMALIES;
MIRIZZI-SYNDROME; PATHOLOGICAL CORRELATION; LIVER-TRANSPLANTATION;
CLINICAL-APPLICATIONS
AB Magnetic resonance cholangiopancreatography (MRCP) is an elegant MR technique for noninvasively delineating the biliary system. Technologic advances in MRCP acquisition and processing and the routine availability of three-dimensional sequences have facilitated detailed assessment of biliary anatomy and pathologic or congenital processes; therefore, invasive endoscopic retrograde cholangiopancreatography is rarely needed for establishing a diagnosis. MRCP can be combined with contrast-enhanced MR imaging to enable concurrent evaluation of organs such as the liver and pancreas in addition to functional biliary imaging. This review focuses on the current use of MRCP to evaluate nonmalignant processes affecting the biliary system.
C1 [Prabhakar, Anand M.; Sahani, Duyshant] Massachusetts Gen Hosp, Dept Radiol, Div Abdominal Imaging & Intervent, Boston, MA 02114 USA.
[Prabhakar, Hima B.] S Texas Radiol, San Antonio, TX USA.
[Prabhakar, Priya D.] Wilmington Vet Adm Hosp, Wilmington, DE USA.
RP Sahani, D (reprint author), Massachusetts Gen Hosp, Dept Radiol, Div Abdominal Imaging & Intervent, 55 Fruit St,White 270, Boston, MA 02114 USA.
EM DSAHANI@partners.org
NR 72
TC 9
Z9 10
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1064-9689
J9 MAGN RESON IMAGING C
JI Magn. Reson. Imaging Clin. N. Am.
PD AUG
PY 2010
VL 18
IS 3
BP 497
EP +
DI 10.1016/j.mric.2010.08.007
PG 19
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 701VF
UT WOS:000285851200010
PM 21094452
ER
PT J
AU Aslam, R
Yeh, BM
Yee, J
AF Aslam, Rizwan
Yeh, Benjamin M.
Yee, Judy
TI MR Imaging Evaluation of the Hepatic Vasculature
SO MAGNETIC RESONANCE IMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE Hepatic vasculature; Liver injury; MR imaging; Portal veins; Hepatic
veins
ID PORTAL-VEIN THROMBOSIS; MAGNETIC-RESONANCE ANGIOGRAPHY;
BUDD-CHIARI-SYNDROME; DONOR CANDIDATES; ECHO SEQUENCE; VENOUS SYSTEM;
BLOOD-FLOW; CONTRAST; PORTOGRAPHY; VOLUNTEERS
AB Assessment of the hepatic vasculature is essential for tumor staging, surgical planning, and understanding of liver disease. Technological advances have made contrast-enhanced magnetic resonance (MR) imaging comparable to multidetector-row computed tomography for diagnostic vascular imaging with respect to spatial resolution. Unenhanced MR angiographic sequences enable reasonable clinical assessment of vessels without contrast agents in patients with contraindications or renal insufficiency. Furthermore, MR angiography may be used to provide directional information through manipulation of the signal intensity of flowing blood. A major limitation to consistent contrast-enhanced MR angiography is the timing of MR image acquisition with arrival of the contrast bolus in the structures of interest. In this article, the authors discuss currently available techniques for imaging of the hepatic vasculature.
C1 [Aslam, Rizwan; Yeh, Benjamin M.] Univ Calif San Francisco, Sch Med, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA.
[Aslam, Rizwan; Yeh, Benjamin M.; Yee, Judy] San Francisco VA Med Ctr, Dept Radiol, San Francisco, CA 94121 USA.
RP Yeh, BM (reprint author), Univ Calif San Francisco, Sch Med, Dept Radiol & Biomed Imaging, 505 Parnassus Ave,M372,Box 0628, San Francisco, CA 94143 USA.
EM ben.yeh@radiology.ucsf.edu
NR 29
TC 2
Z9 2
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 1064-9689
J9 MAGN RESON IMAGING C
JI Magn. Reson. Imaging Clin. N. Am.
PD AUG
PY 2010
VL 18
IS 3
BP 515
EP +
DI 10.1016/j.mric.2010.08.005
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 701VF
UT WOS:000285851200011
PM 21094453
ER
PT J
AU Stolzmann, KL
Meterko, M
Shwartz, M
Young, GJ
Pekoz, EA
Benzer, JK
Osatuke, K
White, B
Mohr, DC
AF Stolzmann, Kelly L.
Meterko, Mark
Shwartz, Michael
Young, Gary J.
Pekoz, Erol A.
Benzer, Justin K.
Osatuke, Katerine
White, Bert
Mohr, David C.
TI Accounting for Variation in Technical Quality and Patient Satisfaction
The Contribution of Patient, Provider, Team, and Medical Center
SO MEDICAL CARE
LA English
DT Article
DE performance measurement; quality of care; patient satisfaction; quality
improvement
ID PAY-FOR-PERFORMANCE; HEALTH-CARE; MEANINGFUL VARIATION; HOSPITAL-CARE;
INCENTIVES; IMPROVE; RATES
AB Background: The delivery of healthcare depends on individual providers, coordination within teams, and the structure of the work setting. We analyzed the amount of variation in technical quality and patient satisfaction accounted for at the patient, provider, team, and medical center level.
Methods: Data abstracted from Veterans Health Administration patient medical records for 2007 were used to calculate measures of technical quality based on adherence to best practice guidelines in 5 domains. Outpatient satisfaction was obtained from a 2007 standardized national mail survey. Hierarchical linear models that accounted for the clustering of patients within providers, providers within teams, and teams within medical centers were used to partition the variation in technical quality and satisfaction across patients and components of the system (ie, providers, teams, and medical centers).
Results: Providers accounted for the largest percent of system-level variance for all technical quality domains, ranging from 46.5% to 71.9%. For the single-item measure of patient satisfaction, medical centers, teams, and providers accounted for about the same percent of system-level variance (31%-34%). For the doctor/patient interaction scale providers explained 59.9% of system-level variance, more than double that of teams and medical centers. For all the measures, the residual variance (composed of patient-level and random error) explained the largest proportion of the total variance.
Conclusions: Providers explained the greatest amount of system-level variation in technical quality and patient satisfaction. However, in both of these domains, differences between patients were the predominant source of nonrandom variance.
C1 [Stolzmann, Kelly L.; Meterko, Mark; Shwartz, Michael; Young, Gary J.; Benzer, Justin K.; White, Bert; Mohr, David C.] VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA 02130 USA.
[Shwartz, Michael; Pekoz, Erol A.] Boston Univ, Sch Management, Boston, MA 02215 USA.
[Young, Gary J.] Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA.
RP Stolzmann, KL (reprint author), VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Mail Stop 152M,150 S Huntington Ave, Boston, MA 02130 USA.
EM kelly.stolzmann@va.gov
OI Benzer, Justin/0000-0001-5151-2127
FU VHA HSRD [IIR 05-221]
FX This research was supported by VHA HSR&D grant number: IIR 05-221.
NR 40
TC 6
Z9 6
U1 2
U2 7
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 AUG
PY 2010
VL 48
IS 8
BP 676
EP 682
DI 10.1097/MLR.0b013e3181e35b1f
PG 7
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 628JM
UT WOS:000280115700003
PM 20613661
ER
PT J
AU Borzecki, AM
Christiansen, CL
Loveland, S
Chew, P
Rosen, AK
AF Borzecki, Ann M.
Christiansen, Cindy L.
Loveland, Susan
Chew, Priscilla
Rosen, Amy K.
TI Trends in the Inpatient Quality Indicators The Veterans Health
Administration Experience
SO MEDICAL CARE
LA English
DT Article
DE quality of care; administrative data; quality improvement
ID ACUTE MYOCARDIAL-INFARCTION; DUTY HOUR REFORM; MEDICARE BENEFICIARIES;
OF-CARE; PATIENT OUTCOMES; UNITED-STATES; MORTALITY; AFFAIRS; HOSPITALS;
PROGRAM
AB Background: The Agency for Healthcare Research and Quality Inpatient Quality Indicators (IQIs), which include in-hospital mortality and utilization rates, have received little attention in the Veterans Health Administration (VA), despite extensive private sector use for quality improvement.
Objectives: We examined the following: the feasibility of applying the IQIs to VA data; temporal trends in national VA IQI rates; temporal and regional IQI trends in geographic areas defined by Veterans Integrated Service Networks' (VISNs); and VA versus non-VA (Nationwide Inpatient Sample) temporal trends.
Methods: We derived VA- and VISN-level IQI observed rates, risk-adjusted rates, and observed to expected ratios (O/Es), using VA inpatient data (2004-2007). We examined the trends in VA- and VISN-level rates using weighted linear regression, variation in VISN-level O/Es, and compared VA to non-VA trends.
Results: VA in-hospital mortality rates from selected medical conditions (stroke, hip fracture, pneumonia) decreased significantly over time; procedure-related mortality rates were unchanged. Laparoscopic cholecystectomy rates increased significantly. A few VISNs were consistently high or low outliers for the medical-related mortality IQIs. Within any given year, utilization indicators, especially cardiac catheterization and cholecystectomy, showed the most inter-VISN variation. Compared with the non-VA, VA medical-related mortality rates for the above-mentioned conditions decreased more rapidly, whereas laparascopic cholecystectomy rates rose more steeply.
Conclusions: The IQIs are easily applied to VA administrative data. They can be useful to tracks rate trends over time, reveal variation between sites, and for trend comparisons with other healthcare systems. By identifying potential quality events related to mortality and utilization, they may complement existing VA quality improvement initiatives.
C1 [Borzecki, Ann M.; Christiansen, Cindy L.; Chew, Priscilla] Bedford VAMC, Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA USA.
[Borzecki, Ann M.; Christiansen, Cindy L.; Loveland, Susan; Rosen, Amy K.] Boston Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA USA.
[Borzecki, Ann M.] Boston Univ, Sch Med, Gen Internal Med Sect, Boston, MA 02118 USA.
[Loveland, Susan; Rosen, Amy K.] VA Boston Healthcare Syst, W Roxbury, MA USA.
[Rosen, Amy K.] Boston Univ, Sch Med, Dept Family Med, Boston, MA 02118 USA.
RP Borzecki, AM (reprint author), Bedford VA Hosp 152, 200 Springs Rd, Bedford, MA 01730 USA.
EM amb@bu.edu
OI Christiansen, Cindy/0000-0001-9951-480X
FU Veterans Health Administration
FX Supported by Veterans Health Administration.
NR 47
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U1 0
U2 4
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 AUG
PY 2010
VL 48
IS 8
BP 694
EP 702
DI 10.1097/MLR.0b013e3181e419e3
PG 9
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 628JM
UT WOS:000280115700005
PM 20613657
ER
PT J
AU Lin, GA
Redberg, RF
Anderson, HV
Shaw, RE
Milford-Beland, S
Peterson, ED
Rao, SV
Werner, RM
Dudley, RA
AF Lin, Grace A.
Redberg, Rita F.
Anderson, H. Vernon
Shaw, Richard E.
Milford-Beland, Sarah
Peterson, Eric D.
Rao, Sunil V.
Werner, Rachel M.
Dudley, R. Adams
TI Impact of Changes in Clinical Practice Guidelines on Assessment of
Quality of Care
SO MEDICAL CARE
LA English
DT Article
DE performance measurement; clinical practice guidelines; quality of care;
percutaneous coronary intervention
ID PERCUTANEOUS CORONARY INTERVENTIONS; ELEVATION MYOCARDIAL-INFARCTION;
ASSOCIATION TASK-FORCE; ANGIOGRAPHY-AND-INTERVENTIONS; DRUG-ELUTING
STENTS; REGISTRY ACC-NCDR; AMERICAN-COLLEGE; APPROPRIATENESS CRITERIA;
PERFORMANCE-MEASURES; ACC/AHA GUIDELINES
AB Background: Measures for pay-for-performance and public reporting programs may be based on clinical practice guidelines. The impact of guideline changes over time-and whether evolving clinical evidence can render measures based on prior guidelines misleading-is not known.
Objective: To assess the impact of using different percutaneous coronary intervention (PCI) guidelines when evaluating whether PCI was indicated.
Research Design: PCIs from the National Cardiovascular Data Registry's CathPCI registry performed in 2003-2004 were categorized into indication classes (Class I, IIa, IIb, III), using 2001 American College of Cardiology/American Heart Association guidelines for PCI, the guidelines available at the time of the procedures. The same procedures were recategorized using 2005 guidelines, which reflect the best evidence available to clinicians at the time of PCI. Procedures unable to be categorized were labeled as "Not Certain."
Subjects: Patients undergoing PCI for stable or unstable angina in 394 hospitals.
Measures: Number of procedures changing classification categories using 2001 versus 2005 guidelines.
Results: A total of 345,779 PCIs were evaluated. Applying 2001 guidelines, 47.9% had Class I indications; 33.3% Class IIa; 5.9% Class IIb; 3.7% Class III; and 9.2% Not Certain. Applying 2005 guidelines to the same procedures, 25.1% had Class I indications; 57.5% Class IIa; 5.5% Class IIb; 3.7% Class III; and 8.3% Not Certain; 41.1% of procedures changed the classification overall.
Conclusions: The changes in guidelines resulted in a marked shift in whether PCIs done in 2003-2004 were considered indicated. Guideline-based performance measures should be carefully evaluated before implementation to avoid incorrect assessments of quality of care.
C1 [Lin, Grace A.] Univ Calif San Francisco, Div Gen Internal Med, San Francisco, CA 94143 USA.
[Lin, Grace A.; Dudley, R. Adams] Univ Calif San Francisco, Philip R Lee Inst Hlth Policy Studies, San Francisco, CA 94143 USA.
[Redberg, Rita F.] Univ Calif San Francisco, Div Cardiol, San Francisco, CA 94143 USA.
[Anderson, H. Vernon] Univ Texas Hlth Sci Ctr, Houston, TX USA.
[Shaw, Richard E.] Calif Pacific Med Ctr, Dept Clin Res, San Francisco, CA USA.
[Milford-Beland, Sarah; Peterson, Eric D.; Rao, Sunil V.] Duke Clin Res Inst, Durham, NC USA.
[Werner, Rachel M.] Philadelphia Vet Affairs Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
[Werner, Rachel M.] Univ Penn, Div Gen Internal Med, Sch Med, Philadelphia, PA 19104 USA.
[Werner, Rachel M.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
RP Lin, GA (reprint author), Univ Calif San Francisco, Div Gen Internal Med, 400 Parnassus Ave,A-405,Box 0320, San Francisco, CA 94143 USA.
EM glin@medicine.ucsf.edu
FU Blue Shield of California Foundation; American Heart Association; Robert
Wood Johnson Foundation
FX Supported by Blue Shield of California Foundation; a portion of Dr.
Lin's work was supported by a Fellow-to-Faculty Transition Award from
the American Heart Association; and a portion of Dr. Dudley's work was
supported by an Investigator Award in Health Policy from the Robert Wood
Johnson Foundation.
NR 48
TC 6
Z9 6
U1 1
U2 4
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 AUG
PY 2010
VL 48
IS 8
BP 733
EP 738
DI 10.1097/MLR.0b013e3181e35b3a
PG 6
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 628JM
UT WOS:000280115700010
PM 20613660
ER
PT J
AU Koo, S
Klompas, M
Marty, FM
AF Koo, Sophia
Klompas, Michael
Marty, Francisco M.
TI Fonsecaea monophora cerebral phaeohyphomycosis: case report of
successful surgical excision and voriconazole treatment and review
SO MEDICAL MYCOLOGY
LA English
DT Review
DE Fonsecaea monophora; cerebral phaeohyphomycosis; beta-glucan;
voriconazole
ID CENTRAL-NERVOUS-SYSTEM; CLADOPHIALOPHORA-BANTIANA; INFECTIONS; THERAPY;
FUNGI
AB We report a case of Fonsecaea monophora cerebral phaeohyphomycosis successfully treated with surgical excision and voriconazole monotherapy in a patient receiving maintenance immunosuppression therapy for 8 years after cadaveric renal transplantation. She presented with a severe frontal headache in the absence of any constitutional or neurologic symptoms. Brain magnetic resonance imaging showed an irregular 3.1 x 3.4 cm ring-enhancing lesion in her left frontal lobe. The patient underwent craniotomy and resection of her mass, with intraoperative spillage of some of her abscess contents into her lateral ventricle. Histopathology of her resected mass showed necrotic fragments of brain parenchyma with granulomatous inflammation and numerous pigmented fungal forms. A mold, recovered from cultures inoculated with portions of her brain resection specimen, was later definitively identified as Fonsecaea monophora. Initial serum (1 -> 3) beta-D-glucan (BG) levels exceeded 500 pg/ml. The patient received voriconazole, which she tolerated well, without recurrent headaches or abscess formation noted on serial brain imaging. Her BG declined to < 31 pg/ml one year following her abscess resection. She discontinued antifungal therapy after an 18-month treatment course, and has remained free of any clinical or radiographic evidence of recurrent abscess formation three years later.
C1 [Koo, Sophia; Klompas, Michael; Marty, Francisco M.] Brigham & Womens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Koo, Sophia; Marty, Francisco M.] Dana Farber Canc Inst, Boston, MA USA.
[Koo, Sophia; Klompas, Michael; Marty, Francisco M.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Koo, S (reprint author), Brigham & Womens Hosp, Div Infect Dis, 75 Francis St,PBB-A4, Boston, MA 02115 USA.
EM skoo@partners.org
OI Koo, Sophia/0000-0002-4973-7439
NR 13
TC 14
Z9 17
U1 0
U2 2
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 1369-3786
J9 MED MYCOL
JI Med. Mycol.
PD AUG
PY 2010
VL 48
IS 5
BP 769
EP 774
DI 10.3109/13693780903471081
PG 6
WC Infectious Diseases; Mycology; Veterinary Sciences
SC Infectious Diseases; Mycology; Veterinary Sciences
GA 636AU
UT WOS:000280700800012
PM 20100141
ER
PT J
AU Winey, BA
Zygmanski, P
Cormack, RA
Lyatskaya, Y
AF Winey, B. A.
Zygmanski, P.
Cormack, R. A.
Lyatskaya, Y.
TI Balancing dose and image registration accuracy for cone beam
tomosynthesis (CBTS) for breast patient setup
SO MEDICAL PHYSICS
LA English
DT Article
DE cone beam tomosynthesis; patient setup verification; cone beam CT;
breast irradiation; kV dosimetry
ID COMPARING DIGITAL TOMOSYNTHESIS; COMPUTED-TOMOGRAPHY; RADIATION-THERAPY;
SURGICAL CLIPS; POSITION VERIFICATION; LUMPECTOMY CAVITY; IRRADIATION;
CT; RECONSTRUCTION; LOCALIZATION
AB Purpose: To balance dose reduction and image registration accuracy in breast setup imaging. In particular, the authors demonstrate the relationship between scan angle and dose delivery for cone beam tomosynthesis (CBTS) when employed for setup verification of breast cancer patients with surgical clips.
Methods: The dose measurements were performed in a female torso phantom for varying scan angles of CBTS. Setup accuracy was measured using three registration methods: Clip centroid localization accuracy and the accuracy of two semiautomatic registration algorithms. The dose to the organs outside of the ipsilateral breast and registration accuracy information were compared to determine the optimal scan angle for CBTS for breast patient setup verification. Isocenter positions at the center of the patient and at the breast-chest wall interface were considered.
Results: Image registration accuracy was within 1 mm for the CBTS scan angles theta above 20 degrees for some scenarios and as large as 80 degrees for the worst case, depending on the imaged breast and registration algorithm. Registration accuracy was highest based on clip centroid localization. For left and right breast imaging with the isocenter at the chest wall, the dose to the contralateral side of the patient was very low (<0.5 cGy) for all scan angles considered. For central isocenter location, the optimal scan angles were 30 degrees-50 degrees for the left breast imaging and 40 degrees-50 degrees for the right breast imaging, with the difference due to the geometric asymmetry of the current clinical imaging system.
Conclusions: The optimal scan angles for CBTS imaging were found to be between 10 degrees and 50 degrees, depending on the isocenter location and ipsilateral breast. Use of the isocenter at the breast-chest wall locations always resulted in greater accuracy of image registration (<1 mm) at smaller angles (10 degrees-20 degrees) and at lower doses (<0.1 cGy) to the contralateral organs. For chest wall isocenters, doses delivered to organs outside of the target breast were much smaller than the scattered and leakage doses of the treatment beams. The complete volumetric information of all clips in the region of interest, combined with the small dose to the contralateral organs and the small scan angle, could result in an advantage for small angle CBTS with off center isocenters over simple orthogonal pairs. (C) 2010 American Association of Physicists in Medicine. [DOT: 10.1118/1.3464716]
C1 [Winey, B. A.; Zygmanski, P.; Cormack, R. A.; Lyatskaya, Y.] Harvard Univ, Sch Med, Dept Radiat Oncol, Dana Farber Brigham & Womens Canc Ctr, Boston, MA 02115 USA.
RP Winey, BA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, Boston, MA 02114 USA.
EM bwiney@partners.org
OI Cormack, Robert/0000-0001-5553-9984
NR 29
TC 6
Z9 6
U1 0
U2 0
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD AUG
PY 2010
VL 37
IS 8
BP 4414
EP 4423
DI 10.1118/1.3464716
PG 10
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 641GN
UT WOS:000281112900049
PM 20879600
ER
PT J
AU Knapp, H
Anaya, HD
AF Knapp, Herschel
Anaya, Henry D.
TI Facilitating HIV Testing: Exploring Provider and Patient-Centered
Barriers
SO MILITARY MEDICINE
LA English
DT Editorial Material
ID IMMUNODEFICIENCY-VIRUS-INFECTION; NEEDLE PHOBIA; BAD-NEWS; CARE;
INDIVIDUALS; BEHAVIOR; SUICIDE; IMPACT; RISK
C1 [Knapp, Herschel; Anaya, Henry D.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
RP Knapp, H (reprint author), VA Greater Los Angeles Healthcare Syst, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
NR 27
TC 1
Z9 1
U1 0
U2 1
PU ASSOC MILITARY SURG US
PI BETHESDA
PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 USA
SN 0026-4075
EI 1930-613X
J9 MIL MED
JI Milit. Med.
PD AUG
PY 2010
VL 175
IS 8
BP 541
EP 543
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 632VB
UT WOS:000280456000002
PM 20731255
ER
PT J
AU Scheble, VJ
Braun, M
Beroukhim, R
Mermel, CH
Ruiz, C
Wilbertz, T
Stiedl, AC
Petersen, K
Reischl, M
Kuefer, R
Schilling, D
Fend, F
Kristiansen, G
Meyerson, M
Rubin, MA
Bubendorf, L
Perner, S
AF Scheble, Veit J.
Braun, Martin
Beroukhim, Rameen
Mermel, Craig H.
Ruiz, Christian
Wilbertz, Theresia
Stiedl, Ann-Cathrin
Petersen, Karen
Reischl, Markus
Kuefer, Rainer
Schilling, David
Fend, Falko
Kristiansen, Glen
Meyerson, Matthew
Rubin, Mark A.
Bubendorf, Lukas
Perner, Sven
TI ERG rearrangement is specific to prostate cancer and does not occur in
any other common tumor
SO MODERN PATHOLOGY
LA English
DT Article
DE ERG rearrangement; prostate cancer; carcinoma
ID TMPRSS2/ERG FUSION GENE; TMPRSS2-ERG FUSION; RECURRENT FUSION;
HETEROGENEITY; CARCINOMAS; EXPRESSION; EVENT
AB Identification of specific somatic gene alterations is crucial for the insight into the development, progression, and clinical behavior of individual cancer types. The recently discovered recurrent ERG rearrangement in prostate cancer might represent a prostate cancer-specific alteration that has not been systematically assessed in tumors other than prostate cancer. Aim of this study was to assess, whether the ERG rearrangement and the distinct deletion site between TMPRSS2 and ERG, both predominantly resulting in a TMPRSS2-ERG fusion, occur in tumors other than prostate cancer. We assessed 54 different tumor types (2942 samples in total) for their ERG rearrangement status by fluorescence in situ hybridization (FISH). To calibrate, we analyzed 285 prostate cancer samples for the ERG rearrangement frequency. Additionally, we interrogated a high-resolution single nucleotide polymorphism (SNP) data set across 3131 cancer specimens (26 tumor types) for copy number alterations. None of the 54 different tumor types assessed by FISH harbored an ERG rearrangement, whereas the prostate cancer samples revealed an ERG rearrangement in 49.5% of cases. Furthermore, within the 26 tumor types assessed for copy number alterations by SNP, the distinct deletion site between TMPRSS2 and ERG (21q22.2-3) was detectable exclusively in prostate cancer. Although Ewing's sarcoma and AML have known rearrangements rarely involving ERG, we hypothesize that the ERG rearrangement as well as the distinct deletion site on 21q22.2-3 between TMPRSS2 and ERG are prostate-cancer-specific genomic alterations. These observations provide further insight into the oncogenesis of prostate cancer and might be critical for the development of ERG rearrangement assessment as a clinical tool. Modern Pathology (2010) 23, 1061-1067; doi:10.1038/modpathol.2010.87; published online 14 May 2010
C1 [Scheble, Veit J.; Braun, Martin; Wilbertz, Theresia; Stiedl, Ann-Cathrin; Petersen, Karen; Fend, Falko; Perner, Sven] Univ Tubingen Hosp, Inst Pathol, Ctr Comprehens Canc, D-72076 Tubingen, Germany.
[Beroukhim, Rameen; Mermel, Craig H.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Beroukhim, Rameen] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA.
[Mermel, Craig H.; Meyerson, Matthew] Broad Inst MIT & Harvard, Canc Program, Med & Populat Genet Grp, Cambridge, MA USA.
[Ruiz, Christian; Bubendorf, Lukas] Univ Basel Hosp, Dept Pathol, CH-4031 Basel, Switzerland.
[Reischl, Markus] Res Ctr Karlsruhe, Inst Appl Informat, Karlsruhe, Germany.
[Kuefer, Rainer] Univ Hosp Ulm, Dept Urol, Ulm, Germany.
[Schilling, David] Univ Tubingen Hosp, Dept Urol, Ctr Comprehens Canc, D-72076 Tubingen, Germany.
[Kristiansen, Glen] Univ Zurich Hosp, Inst Surg Pathol, CH-8091 Zurich, Switzerland.
[Meyerson, Matthew] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Rubin, Mark A.] Weill Cornell Med Coll, Dept Pathol & Lab Med, New York, NY USA.
RP Perner, S (reprint author), Univ Tubingen Hosp, Inst Pathol, Ctr Comprehens Canc, Liebermeisterstr 8, D-72076 Tubingen, Germany.
EM sven.perner@medizin.uni-tuebingen.de
RI Bubendorfl, Lukas/H-5880-2011; Meyerson, Matthew/E-7123-2012; Reischl,
Markus/H-6970-2013;
OI Rubin, Mark/0000-0002-8321-9950
FU German Research Foundation (Deutsche Forschungsgemeinschaft, DFG)
[PE1179/2-1]; University Hospital of Tuebingen [1809-1-0]
FX This work was supported by a grant of the German Research Foundation
(Deutsche Forschungsgemeinschaft, DFG, Emmy-Noether-Program, PE1179/2-1)
and the University Hospital of Tuebingen (fortuene Program, No.
1809-1-0) to SP.
NR 27
TC 72
Z9 77
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD AUG
PY 2010
VL 23
IS 8
BP 1061
EP 1067
DI 10.1038/modpathol.2010.87
PG 7
WC Pathology
SC Pathology
GA 634EZ
UT WOS:000280563900003
PM 20473283
ER
PT J
AU Sugita, H
Kaneki, M
Furuhashi, S
Hirota, M
Takamori, H
Baba, H
AF Sugita, Hiroki
Kaneki, Masao
Furuhashi, Satoshi
Hirota, Masahiko
Takamori, Hiroshi
Baba, Hideo
TI Nitric Oxide Inhibits the Proliferation and Invasion of Pancreatic
Cancer Cells through Degradation of Insulin Receptor Substrate-1 Protein
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID NF-KAPPA-B; S-NITROSYLATION; TUMOR-CELLS; IN-VIVO; CARCINOMA-CELLS;
RELAXING FACTOR; SYNTHASE; GROWTH; ACTIVATION; KINASE
AB Nitric oxide (NO), which plays a role in the posttranslational modification of proteins, exhibits tumoricidal activity. However, the mechanism remains largely unclear. We investigated whether the regulation of insulin receptor substrate (IRS)-1 protein expression and insulin/insulin-like growth factor (IGF) signaling by NO is involved in the proliferation and invasion of pancreatic cancer cells. NO donor inhibited insulin/IGF-I-stimulated phosphorylation of insulin receptor/IGF-I receptor, IRS-1, Akt/PKB, and glycogen synthase kinase-3 beta along with decreased expression of IRS-1 protein in MIAPaCa-2 cells, whereas NO donor enhanced the phosphorylation of extracellular signal-regulated kinase-1/2. In contrast, a selective inducible nitric oxide synthase inhibitor, 1400W, upregulated the expression of IRS-1 protein and the phosphorylation of IRS-1, Akt/PKB, and glycogen synthase kinase-3 beta, along with enhanced proliferation and invasion of Panc-1 cells expressing inducible nitric oxide synthase protein. NO donor induced IRS-1 protein reduction through increased ubiquitination and degradation. For the detection of the site responsible for NO-induced ubiquitination, IRS-1 deletion mutant genes were transfected and overexpressed in MIAPaCa-2 cells. The results indicate that the COOH terminus of the IRS-1 protein is required for NO donor-induced ubiquitination and protein degradation. Cells stably transfected with COOH-terminal deletion mutants of IRS-1 exhibited reduced IGF signaling and cell proliferation compared with vector alone-transfected cells, with no influence of NO on IGF signaling and invasion, although stable transfectants with full-length IRS-1 protein exhibited remarkable NO-induced reduction in IGF signaling, cell proliferation, and invasion. These findings indicate that NO inhibits the proliferation and invasion of pancreatic cancer cells, at least in part, through upregulation of IRS-1 protein degradation and resultant downregulation of the insulin/IGF-I-Akt pathway. Mol Cancer Res; 8(8); 1152-63. (C) 2010 AACR.
C1 [Sugita, Hiroki; Furuhashi, Satoshi; Hirota, Masahiko; Takamori, Hiroshi; Baba, Hideo] Kumamoto Univ, Grad Sch Med Sci, Dept Surg Gastroenterol, Kumamoto 8608556, Japan.
[Kaneki, Masao] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Anesthesia & Crit Care,Shriners Hosp Childre, Boston, MA USA.
RP Sugita, H (reprint author), Kumamoto Univ, Grad Sch Med Sci, Dept Surg Gastroenterol, 1-1-1 Honjo, Kumamoto 8608556, Japan.
EM sugitaf@ba2.so-net.ne.jp
FU Japanese Society for the Promotion of Science [18591517, 20591633]
FX Grant-in-Aid for Scientific Research (grant nos. 18591517 and 20591633)
from the Japanese Society for the Promotion of Science.
NR 47
TC 13
Z9 13
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD AUG
PY 2010
VL 8
IS 8
BP 1152
EP 1163
DI 10.1158/1541-7786.MCR-09-0472
PG 12
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 639DS
UT WOS:000280951600009
PM 20663861
ER
PT J
AU Carroll, MC
Ma, MH
Agemang, A
AF Carroll, Michael C.
Ma, Minghe
Agemang, Amma
TI Reduced B cell anergy in mice deficient in CD21
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 23rd International National Complement Workshop
CY AUG 01-05, 2010
CL New York, NY
C1 Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
Harvard Univ, Sch Med, Program Cellular & Mol Med, Boston, MA USA.
Harvard Univ, Sch Med, Childrens Hosp, Boston, MA USA.
Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD AUG
PY 2010
VL 47
IS 13
SI SI
MA 167
BP 2225
EP 2225
DI 10.1016/j.molimm.2010.05.087
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 630JE
UT WOS:000280268400081
ER
PT J
AU Kim, YA
Carroll, MC
AF Kim, Young-A.
Carroll, Michael C.
TI Visualizing B cell transport of immune complexes via CD21
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 23rd International National Complement Workshop
CY AUG 01-05, 2010
CL New York, NY
C1 Harvard Univ, Sch Med, Immune Dis Inst, Childrens Hosp, Cambridge, MA 02138 USA.
Harvard Univ, Sch Med, Program Cellular & Mol Med, Childrens Hosp, Cambridge, MA 02138 USA.
Harvard Univ, Sch Med, Dept Pediat, Cambridge, MA 02138 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD AUG
PY 2010
VL 47
IS 13
SI SI
MA 172
BP 2227
EP 2227
DI 10.1016/j.molimm.2010.05.093
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 630JE
UT WOS:000280268400087
ER
PT J
AU Pitcher, LA
Gonzalez, SF
Lukacs-Kornek, V
Kuligowski, MP
Kim, YA
Martinez-Pomares, L
Gordon, S
Turley, SJ
Carroll, MC
AF Pitcher, Lisa A.
Gonzalez, Santiago F.
Lukacs-Kornek, Veronika
Kuligowski, Michael P.
Kim, Young-A.
Martinez-Pomares, Luisa
Gordon, Siamon
Turley, Shannon J.
Carroll, Michael C.
TI SIGN-R1-expressing dendritic cells are important for humoral immunity to
influenza virus
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 23rd International National Complement Workshop
CY AUG 01-05, 2010
CL New York, NY
C1 [Pitcher, Lisa A.; Gonzalez, Santiago F.; Kuligowski, Michael P.; Kim, Young-A.; Carroll, Michael C.] Harvard Univ, Sch Med, Immune Dis Inst, Childrens Hosp, Boston, MA USA.
[Pitcher, Lisa A.; Gonzalez, Santiago F.; Kuligowski, Michael P.; Kim, Young-A.; Carroll, Michael C.] Harvard Univ, Sch Med, Program Cellular & Mol Med, Childrens Hosp, Boston, MA USA.
[Pitcher, Lisa A.; Gonzalez, Santiago F.; Kuligowski, Michael P.; Kim, Young-A.; Carroll, Michael C.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Pitcher, Lisa A.; Gonzalez, Santiago F.; Kuligowski, Michael P.; Kim, Young-A.; Carroll, Michael C.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Lukacs-Kornek, Veronika; Turley, Shannon J.] Harvard Univ, Sch Med, Dept Canc Immunol, Boston, MA USA.
[Lukacs-Kornek, Veronika; Turley, Shannon J.] Harvard Univ, Sch Med, AIDS, Boston, MA USA.
[Lukacs-Kornek, Veronika; Turley, Shannon J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Lukacs-Kornek, Veronika; Turley, Shannon J.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Martinez-Pomares, Luisa] Univ Nottingham, Sch Mol Med Sci, Nottingham NG7 2RD, England.
[Gordon, Siamon] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD AUG
PY 2010
VL 47
IS 13
SI SI
MA 171
BP 2227
EP 2227
DI 10.1016/j.molimm.2010.05.092
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 630JE
UT WOS:000280268400086
ER
PT J
AU Gonzalez, SF
Degn, SE
Kuligowski, MP
Pitcher, LA
Cloninger, M
Carroll, MC
AF Gonzalez, Santiago F.
Degn, Soren E.
Kuligowski, Michael P.
Pitcher, Lisa A.
Cloninger, Mary
Carroll, Michael C.
TI Lymph node macrophages bind influenza virus in an MBL-dependent manner
but they are not required for humoral immunity to influenza
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 23rd International National Complement Workshop
CY AUG 01-05, 2010
CL New York, NY
C1 [Gonzalez, Santiago F.; Degn, Soren E.; Kuligowski, Michael P.; Pitcher, Lisa A.; Carroll, Michael C.] Harvard Univ, Sch Med, Immune Dis Inst, Childrens Hosp, Boston, MA USA.
[Gonzalez, Santiago F.; Degn, Soren E.; Kuligowski, Michael P.; Pitcher, Lisa A.; Carroll, Michael C.] Harvard Univ, Sch Med, Program Cellular & Mol Med, Childrens Hosp, Boston, MA USA.
[Gonzalez, Santiago F.; Degn, Soren E.; Kuligowski, Michael P.; Pitcher, Lisa A.; Carroll, Michael C.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Gonzalez, Santiago F.; Degn, Soren E.; Kuligowski, Michael P.; Pitcher, Lisa A.; Carroll, Michael C.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Degn, Soren E.] Aarhus Univ, Dept Med Microbiol & Immunol, Aarhus, Denmark.
[Cloninger, Mary] Montana State Univ, Dept Chem & Biochem, Bozeman, MT 59717 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD AUG
PY 2010
VL 47
IS 13
SI SI
MA 178
BP 2229
EP 2229
DI 10.1016/j.molimm.2010.05.099
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 630JE
UT WOS:000280268400093
ER
PT J
AU Heesters, BA
Gonzalez, SF
Carroll, MC
AF Heesters, Balthasar A.
Gonzalez, Santiago F.
Carroll, Michael C.
TI The role of the complement system in trafficking of a Streptococcus
vaccine in the lymph node
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 23rd International National Complement Workshop
CY AUG 01-05, 2010
CL New York, NY
C1 Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA USA.
Harvard Univ, Sch Med, Childrens Hosp, Program Cellular & Mol Med, Boston, MA USA.
Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
NR 1
TC 0
Z9 0
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD AUG
PY 2010
VL 47
IS 13
SI SI
MA 232
BP 2249
EP 2249
DI 10.1016/j.molimm.2010.05.157
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 630JE
UT WOS:000280268400150
ER
PT J
AU Takahashi, M
Iwaki, D
Endo, Y
Takahashi, K
Stahl, GL
Fujita, T
AF Takahashi, Minoru
Iwaki, Daisuke
Endo, Yuichi
Takahashi, Kazue
Stahl, Gregory L.
Fujita, Teizo
TI MBL/MASP-1 complexes efficiently cleave a zymogen of complement factor D
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 23rd International National Complement Workshop
CY AUG 01-05, 2010
CL New York, NY
C1 [Takahashi, Minoru; Iwaki, Daisuke; Endo, Yuichi; Fujita, Teizo] Fukushima Med Univ, Dept Immunol, Sch Med, Fukushima, Japan.
[Takahashi, Kazue] Harvard Univ, Sch Med, Dept Pediat, Dev Immunol Program,Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Stahl, Gregory L.] Harvard Univ, Sch Med, Ctr Expt Therapeut & Reperfus Injury, Brigham & Womens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD AUG
PY 2010
VL 47
IS 13
SI SI
MA 3
BP 2266
EP 2267
DI 10.1016/j.molimm.2010.05.206
PG 2
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 630JE
UT WOS:000280268400199
ER
PT J
AU Haas, M
Schuerpf, F
Alicot-Carroll, EM
Chiu, I
Kim, K
Sachs, D
Carroll, MC
AF Haas, M.
Schuerpf, F.
Alicot-Carroll, E. M.
Chiu, I.
Kim, K.
Sachs, D.
Carroll, M. C.
TI N2 peptide blocks natural IgM-mediated injury in a murine model of
myocardial infarction
SO MOLECULAR IMMUNOLOGY
LA English
DT Meeting Abstract
CT 23rd International National Complement Workshop
CY AUG 01-05, 2010
CL New York, NY
C1 [Kim, K.; Sachs, D.] Massachusetts Gen Hosp, Charlestown, MA USA.
[Kim, K.; Sachs, D.] Transplant Biol Res Ctr, Charlestown, MA USA.
[Carroll, M. C.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD AUG
PY 2010
VL 47
IS 13
SI SI
MA 46
BP 2273
EP 2273
DI 10.1016/j.molimm.2010.05.224
PG 1
WC Biochemistry & Molecular Biology; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 630JE
UT WOS:000280268400217
ER
PT J
AU Haake, DA
Matsunaga, J
AF Haake, David A.
Matsunaga, James
TI Leptospira: a spirochaete with a hybrid outer membrane
SO MOLECULAR MICROBIOLOGY
LA English
DT Review
ID SURFACE-EXPOSED LIPOPROTEIN; MODULATES FIBRONECTIN-BINDING; PATHOGENIC
LEPTOSPIRA; MOLECULAR-CLONING; EXTRACELLULAR RELEASE; SEQUENCE-ANALYSIS;
ESCHERICHIA-COLI; PROTEIN LIPL32; CALCIUM BINDS; C-TERMINUS
AB P>Leptospira is a genus of spirochaetes that includes organisms with a variety of lifestyles ranging from aquatic saprophytes to invasive pathogens. Adaptation to a wide variety of environmental conditions has required leptospires to acquire a large genome and a complex outer membrane with features that are unique among bacteria. The most abundant surface-exposed outer membrane proteins are lipoproteins that are integrated into the lipid bilayer by amino-terminal fatty acids. In contrast to many spirochaetes, the leptospiral outer membrane also includes lipopolysaccharide and many homologues of well-known beta-barrel transmembrane outer membrane proteins. Research on leptospiral transmembrane outer membrane proteins has lagged behind studies of lipoproteins because of their aberrant behaviour by Triton X-114 detergent fractionation. For this reason, transmembrane outer membrane proteins are best characterized by assessing membrane integration and surface exposure. Not surprisingly, some outer membrane proteins that mediate host-pathogen interactions are strongly regulated by conditions found in mammalian host tissues. For example, the leptospiral immunoglobulin-like (Lig) repeat proteins are dramatically induced by osmolarity and mediate interactions with host extracellular matrix proteins. Development of molecular genetic tools are making it possible to finally understand the roles of these and other outer membrane proteins in mechanisms of leptospiral pathogenesis.
C1 [Haake, David A.; Matsunaga, James] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Haake, David A.; Matsunaga, James] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
[Haake, David A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Urol, Los Angeles, CA 90095 USA.
[Haake, David A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA 90095 USA.
RP Haake, DA (reprint author), Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
EM dhaake@ucla.edu
FU NIAID NIH HHS [R01 AI034431, R01 AI034431-14]
NR 63
TC 26
Z9 26
U1 1
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD AUG
PY 2010
VL 77
IS 4
BP 805
EP 814
DI 10.1111/j.1365-2958.2010.07262.x
PG 10
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 635QY
UT WOS:000280672400002
PM 20598085
ER
PT J
AU Yin, L
Ahmad, R
Kosugi, M
Kufe, T
Vasir, B
Avigan, D
Kharbanda, S
Kufe, D
AF Yin, Li
Ahmad, Rehan
Kosugi, Michio
Kufe, Turner
Vasir, Baldev
Avigan, David
Kharbanda, Surender
Kufe, Donald
TI Survival of Human Multiple Myeloma Cells Is Dependent on MUC1 C-Terminal
Transmembrane Subunit Oncoprotein Function
SO MOLECULAR PHARMACOLOGY
LA English
DT Article
ID NF-KAPPA-B; IN-VITRO; EXPRESSION; GROWTH; DEATH; INHIBITION; ACTIVATION;
THERAPY; PATHWAY; PROTEIN
AB The MUC1 C-terminal transmembrane subunit (MUC1-C) oncoprotein is a direct activator of the canonical nuclear factor-kappa B (NF-kappa B) RelA/p65 pathway and is aberrantly expressed in human multiple myeloma cells. However, it is not known whether multiple myeloma cells are sensitive to the disruption of MUC1-C function for survival. The present studies demonstrate that peptide inhibitors of MUC1-C oligomerization block growth of human multiple myeloma cells in vitro. Inhibition of MUC1-C function also blocked the interaction between MUC1-C and NF-kappa B p65 and activation of the NF-kappa B pathway. In addition, inhibition of MUC1-C in multiple myeloma cells was associated with activation of the intrinsic apoptotic pathway and induction of late apoptosis/necrosis. Primary multiple myeloma cells, but not normal B-cells, were also sensitive to MUC1-C inhibition. Significantly, treatment of established U266 multiple myeloma xenografts growing in nude mice with a lead candidate MUC1-C inhibitor resulted in complete tumor regression and lack of recurrence. These findings indicate that multiple myeloma cells are dependent on intact MUC1-C function for constitutive activation of the canonical NF-kappa B pathway and for their growth and survival.
C1 [Yin, Li; Ahmad, Rehan; Kosugi, Michio; Vasir, Baldev; Kufe, Donald] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kufe, Turner; Avigan, David] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
RP Kufe, D (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM donald_kufe@dfci.harvard.edu
FU Multiple Myeloma Research Foundation; Leukemia Lymphoma Society;
National Institutes of Health National Cancer Institute [CA42802]
FX This study was supported by the Multiple Myeloma Research Foundation;
the Leukemia Lymphoma Society; and the National Institutes of Health
National Cancer Institute [Grant CA42802].
NR 37
TC 18
Z9 18
U1 0
U2 0
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0026-895X
J9 MOL PHARMACOL
JI Mol. Pharmacol.
PD AUG
PY 2010
VL 78
IS 2
BP 166
EP 174
DI 10.1124/mol.110.065011
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 625IF
UT WOS:000279888000002
PM 20444960
ER
PT J
AU Petryshen, TL
Sabeti, PC
Aldinger, KA
Fry, B
Fan, JB
Schaffner, SF
Waggoner, SG
Tahl, AR
Sklar, P
AF Petryshen, T. L.
Sabeti, P. C.
Aldinger, K. A.
Fry, B.
Fan, J. B.
Schaffner, S. F.
Waggoner, S. G.
Tahl, A. R.
Sklar, P.
TI Population genetic study of the brain-derived neurotrophic factor (BDNF)
gene
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE selection; diversity; gene association; single-nucleotide polymorphism;
haplotype; susceptibility locus
ID OBSESSIVE-COMPULSIVE DISORDER; FAMILY-BASED ASSOCIATION;
ACTIVITY-DEPENDENT SECRETION; HUMAN GENOME; VAL66MET POLYMORPHISM;
ANOREXIA-NERVOSA; EUROPEAN POPULATIONS; BIPOLAR DISORDER; EPISODIC
MEMORY; SCHIZOPHRENIA
AB Genetic variants in the brain-derived neurotrophic factor (BDNF) gene, predominantly the functional Val66Met polymorphism, have been associated with risk of bipolar disorder and other psychiatric disorders. However, not all studies support these findings, and overall the evidence for the association of BDNF with disease risk is weak. As differences in population genetic structure between patient samples could cause discrepant or spurious association results, we investigated this possibility by carrying out population genetic analyses of the BDNF genomic region. Substantial variation was detected in BDNF coding region single-nucleotide polymorphism (SNP) allele and haplotype frequencies between 58 global populations, with the derived Met allele of Val66Met ranging in frequency from 0 to 72% across populations. F(ST) analyses to assess diversity in the HapMap populations determined that the Val66Met F(ST) value was at the 99.8th percentile among all SNPs in the genome. As the BDNF population genetic differences may be due to local selection, we performed the long-range haplotype test for selection using 68 SNPs spanning the BDNF genomic region in 12 European-derived pedigrees. Evidence for positive selection was found for a high-frequency Val-carrying haplotype, with a relative extended haplotype homozygosity value above the 99th percentile compared with HapMap data (P = 4.6 x 10(-4)). In conclusion, we observed considerable BDNF allele and haplotype diversity among global populations and evidence for positive selection at the BDNF locus. These phenomena can have a profound impact on the detection of disease susceptibility genes and must be considered in gene association studies of BDNF. Molecular Psychiatry (2010) 15, 810-815; doi: 10.1038/mp.2009.24; published online 3 March 2009
C1 [Petryshen, T. L.; Aldinger, K. A.; Fan, J. B.; Waggoner, S. G.; Tahl, A. R.; Sklar, P.] Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Ctr Human Genet Res, Boston, MA 02114 USA.
[Petryshen, T. L.; Sklar, P.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Petryshen, T. L.; Sklar, P.] Harvard Univ, Sch Med, Boston, MA USA.
[Petryshen, T. L.; Aldinger, K. A.; Fan, J. B.; Waggoner, S. G.; Tahl, A. R.; Sklar, P.] Broad Inst MIT & Harvard, Stanley Ctr Psychiat Res, Cambridge, MA USA.
[Sabeti, P. C.] Harvard Univ, Dept Organism & Evolutionary Biol, Ctr Syst Biol, Cambridge, MA 02138 USA.
RP Petryshen, TL (reprint author), Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Ctr Human Genet Res, 185 Cambridge St, Boston, MA 02114 USA.
EM petryshen@chgr.mgh.harvard.edu
RI Schaffner, Stephen/D-1189-2011
FU NIMH [R01 MH062137]; Canadian Institutes for Health Research; Charles A
King Trust; Bank of America; Co-Trustee; National Alliance on
Schizophrenia and Depression; Burroughs Wellcome Career Award in the
Biomedical Sciences
FX We thank Dr Manuel Ferreira for analytical assistance, and Dr Roy
Perlis, Dr James Potash, Dr Melvin McInnis and Dr J Raymond De Paulo for
their valuable comments on the paper. The HGDR-CEPH Human Genome
Diversity Cell Line Panel DNA was obtained from David Reich, MD. This
study was supported by the NIMH grant R01 MH062137, postdoctoral
fellowships from the Canadian Institutes for Health Research (TLP) and
the Charles A King Trust, Bank of America, Co-Trustee (JBF), Young
Investigator awards from the National Alliance on Schizophrenia and
Depression (TLP and JBF), and a Burroughs Wellcome Career Award in the
Biomedical Sciences (PCS).
NR 37
TC 95
Z9 96
U1 1
U2 7
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 AUG
PY 2010
VL 15
IS 8
BP 810
EP 815
DI 10.1038/mp.2009.24
PG 6
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 637YO
UT WOS:000280854800008
PM 19255578
ER
PT J
AU Fava, M
Hwang, I
Rush, AJ
Sampson, N
Walters, EE
Kessler, RC
AF Fava, M.
Hwang, I.
Rush, A. J.
Sampson, N.
Walters, E. E.
Kessler, R. C.
TI The importance of irritability as a symptom of major depressive
disorder: results from the National Comorbidity Survey Replication
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE epidemiology; irritability; major depressive disorder; National
Comorbidity Survey Replication; adult
ID BIPOLAR SPECTRUM DISORDER; ANGER ATTACKS; FENFLURAMINE CHALLENGE;
UNIPOLAR DEPRESSION; 12-MONTH PREVALENCE; PROLACTIN RESPONSE; NCS-R;
INVENTORY; LIFETIME; SCALE
AB Irritability is a diagnostic symptom of major depressive disorder (MDD) in children and adolescents but not in adults in both the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) and International Classification of Diseases (ICD-10) systems. We explore the importance of irritability for subtyping adult DSM-IV MDD in the National Comorbidity Survey Replication (NCS-R), a national US adult household survey. The WHO Composite International Diagnostic Interview (CIDI) was used to assess prevalence of many DSM-IV disorders in the lifetime and in the year before interview (12-month prevalence). MDD was assessed conventionally (that is, requiring either persistent sadness or loss of interest), but with irritability included as one of the Criterion A symptoms. We also considered the possibility that irritability might be a diagnostic symptom of adult MDD (that is, detect cases who had neither sad mood nor loss of interest). Twelve-month MDD symptom severity was assessed with the Quick Inventory of Depressive Symptomatology and role impairment with the Sheehan Disability Scale. After excluding bipolar spectrum disorders, irritability during depressive episodes was reported by roughly half of respondents with lifetime DSM-IV MDD. Irritability in the absence of either sad mood or loss of interest, in comparison, was rare. Irritability in MDD was associated with early age of onset, lifetime persistence, comorbidity with anxiety and impulse-control disorders, fatigue and self-reproach during episodes, and disability. Irritability was especially common in MDD among respondents in the age range 18-44 and students. Further investigation is warranted of distinct family aggregation, risk factors and treatment response. Consideration should also be given to including irritability as a nondiagnostic symptom of adult MDD in DSM-V and ICD-11. Molecular Psychiatry (2010) 15, 856-867; doi: 10.1038/mp.2009.20; published online 10 March 2009
C1 [Hwang, I.; Sampson, N.; Walters, E. E.; Kessler, R. C.] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Fava, M.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Rush, A. J.] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA.
[Rush, A. J.] Univ Texas SW Med Ctr Dallas, Dept Clin Sci, Dallas, TX 75390 USA.
RP Kessler, RC (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, 180 Longwood Ave, Boston, MA 02115 USA.
EM kessler@hcp.med.harvard.edu
OI Rush, Augustus/0000-0003-2004-2382
FU National Institute of Mental Health (NIMH) [U01-MH60220]; National
Institute of Drug Abuse; Substance Abuse and Mental Health Services
Administration; Robert Wood Johnson Foundation [044780]; John WAlden
Trust; John D and Catherine T MacArthur Foundation; Pfizer Foundation;
US Public Health Service [R13MH066849, R01-MH069864, R01 DA016558]; Eli
Lilly and Company; GlaxoSmithKline; Ortho-McNeil Pharmaceutical Inc.;
Pan American Health Organization; Abbott Laboratories; Alkermes; Aspect
Medical Systems; AstraZeneca; Bristol-Myers Squibb Company; Cephalon;
Forest Pharmaceuticals Inc.; Johnson & Johnson Pharmaceuticals; Lichtwer
Pharma GmbH; Lorex Pharmaceuticals; Novartis; Organon Inc.; PamLab LLC;
Pfizer Inc.; Pharmavite; Roche; Sanofi-Synthelabo; Solvay
Pharmaceuticals Inc.; Wyeth-Ayerst Laboratories; Stanley Medical
Research Institute
FX The National Comorbidity Survey Replication (NCS-R) was supported by the
National Institute of Mental Health (NIMH; U01-MH60220) with
supplemental support from the National Institute of Drug Abuse, the
Substance Abuse and Mental Health Services Administration, the Robert
Wood Johnson Foundation (Grant No. 044780) and the John WAlden Trust.
Collaborating NCS-R investigators include Ronald C Kessler (Principal
Investigator, Harvard Medical School), Kathleen Merikangas (Co-principal
Investigator, NIMH), James Anthony (Michigan State University), William
Eaton (The Johns Hopkins University), Meyer Glantz (NIDA), Doreen Koretz
(Harvard University), Jane McLeod (Indiana University), Mark Olfson
(Columbia University College of Physicians and Surgeons), Harold Pincus
(University of Pittsburgh), Greg Simon (Group Health Cooperative), T
Bedirhan Ustun (World Health Organization), Michael Von Korff (Group
Health Cooperative), Philip Wang (Harvard Medical School), Kenneth Wells
(UCLA), Elaine Wethington (Cornell University) and Hans-Ulrich Wittchen
(Max Planck Institute of Psychiatry). The views and opinions expressed
in this report are those of the authors and should not be construed to
represent the views of any of the sponsoring organizations, agencies or
US Government. A complete list of NCS publications and the full text of
all NCS-R instruments can be found at
http://www.hcp.med.harvard.edu/ncs. Send correspondence to
NCS@hcp.med.harvard.edu. The NCSR is carried out in conjunction with the
World Health Organization World Mental Health (WMH) Survey Initiative.
We thank the staff of the WMH Data Collection and Data Analysis
Coordination Centers for assistance with instrumentation, fieldwork and
consultation on data analysis. These activities were supported by the
John D and Catherine T MacArthur Foundation, the Pfizer Foundation, the
US Public Health Service (R13MH066849, R01-MH069864 and R01 DA016558),
Eli Lilly and Company, GlaxoSmithKline, Ortho-McNeil Pharmaceutical Inc.
and the Pan American Health Organization. A complete list of WMH
publications and instruments can be found at
(http://www.hcp.med.harvard.edu/wmhcidi).; Dr Fava has research support
from Abbott Laboratories, Alkermes, Aspect Medical Systems, AstraZeneca,
Bristol-Myers Squibb Company, Cephalon, Eli Lilly and Company, Forest
Pharmaceuticals Inc., GlaxoSmithKline, Johnson & Johnson
Pharmaceuticals, Lichtwer Pharma GmbH, Lorex Pharmaceuticals, Novartis,
Organon Inc., PamLab LLC, Pfizer Inc., Pharmavite, Roche,
Sanofi-Synthelabo, Solvay Pharmaceuticals Inc. and Wyeth-Ayerst
Laboratories. He has served as an advisor/consultant for Aspect Medical
Systems, AstraZeneca, Bayer AG, Biovail Pharmaceuticals Inc., BrainCells
Inc., Bristol-Myers Squibb Company, Cephalon, Comellas, Cypress
Pharmaceuticals, DOV Pharmaceuticals, Eli Lilly and Company, EPIX
Pharmaceuticals, Fabre-Kramer Pharmaceuticals Inc., Forest
Pharmaceuticals Inc., GlaxoSmithKline, Grunenthal GmbH, Janssen
Pharmaceutica, Jazz Pharmaceuticals Inc., Johnson & Johnson
Pharmaceuticals, Knoll Pharmacuetical Company, Lundbeck, MedAvante Inc.,
Merck, Neuronetics, Novartis, Nutrition 21, Organon Inc., PamLab LLC,
Pfizer Inc., PharmaStar, Pharmavite, Roche, Sanofi-Synthelabo, Sepracor,
Solvay Pharmaceuticals Inc., Somaxon, Somerset Pharmaceuticals and
Wyeth-Ayerst Laboratories. He has been on speaker bureaus for
AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb Company,
Cephalon, Eli Lilly and Company, Forest Pharmaceuticals Inc.,
GlaxoSmithKline, Novartis, Organon Inc., Pfizer Inc., PharmaStar and
Wyeth-Ayerst Laboratories. He holds equity in Compellis and MedAvante.
Dr Kessler has been a consultant for GlaxoSmithKline Inc., Pfizer Inc.,
Wyeth-Ayerst, Sanofi-Aventis, Kaiser Permanente and Shire
Pharmaceuticals; has served on advisory boards for Eli Lilly and Company
and Wyeth-Ayerst; and has had research support for his epidemiological
studies from Bristol-Myers Squibb, Eli Lilly and Company,
GlaxoSmithKline, Johnson & Johnson Pharmaceuticals, Ortho-McNeil
Pharmaceuticals Inc., Pfizer Inc. and Sanofi-Aventis. Dr Rush has
provided scientific consultation to or served on Advisory Boards for
Advanced Neuromodulation Systems Inc., AstraZeneca, Best Practice
Project Management Inc., Bristol-Myers Squibb Company/Otsuka, Cyberonics
Inc., Forest Pharmaceuticals, GlaxoSmithKline, Jazz Pharmaceuticals, Eli
Lilly and Company, Magellan Health Services, Merck & Co. Inc.,
Neuronetics, Novartis, Ono Pharmaceutical, Organon Inc., Pamlab Pfizer
Inc. and Transcept Pharmaceuticals. He has received royalties from
Guilford Press and Healthcare Technology Systems and research/grant
support from the National Institute of Mental Health and the Stanley
Medical Research Institute; has been on speaker bureaus for Cyberonics
Inc., Forest Pharmaceuticals Inc. and GlaxoSmithKline; and owned stock
in Pfizer Inc.
NR 39
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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 AUG
PY 2010
VL 15
IS 8
BP 856
EP 867
DI 10.1038/mp.2009.20
PG 12
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 637YO
UT WOS:000280854800014
PM 19274052
ER
PT J
AU Cheng, EM
Crandall, CJ
Bever, CT
Giesser, B
Haselkorn, JK
Hays, RD
Shekelle, P
Vickrey, BG
AF Cheng, Eric M.
Crandall, Carolyn J.
Bever, Christopher T., Jr.
Giesser, Barbara
Haselkorn, Jodie K.
Hays, Ron D.
Shekelle, Paul
Vickrey, Barbara G.
TI Quality indicators for multiple sclerosis
SO MULTIPLE SCLEROSIS JOURNAL
LA English
DT Article
DE health services research; multiple sclerosis; outcome research; quality
indicators
ID TECHNOLOGY-ASSESSMENT SUBCOMMITTEE; VULNERABLE OLDER PATIENTS;
MEDICAL-CARE; HEALTH-CARE; OF-CARE; AMERICAN-ACADEMY; GUIDELINES;
ELDERS; ADULTS; THERAPEUTICS
AB Determining whether persons with multiple sclerosis (MS) receive appropriate, comprehensive healthcare requires tools for measuring quality. The objective of this study was to develop quality indicators for the care of persons with MS. We used a modified version of the RAND/UCLA Appropriateness Method in a two-stage process to identify relevant MS care domains and to assess the validity of indicators within high-ranking care domains. Based on a literature review, interviews with persons with MS, and discussions with MS providers, 25 MS symptom domains and 14 general health domains of MS care were identified. A multidisciplinary panel of 15 stakeholders of MS care, including 4 persons with MS, rated these 39 domains in a two-round modified Delphi process. The research team performed an expanded literature review for 26 highly ranked domains to draft 86 MS care indicators. Through another two-round modified Delphi process, a second panel of 18 stakeholders rated these indicators using a nine-point response scale. Indicators with a median rating in the highest tertile were considered valid. Among the most highly rated MS care domains were appropriateness and timeliness of the diagnostic work-up, bladder dysfunction, cognition dysfunction, depression, disease-modifying agent usage, fatigue, integration of care, and spasticity. Of the 86 preliminary indicators, 76 were rated highly enough to meet predetermined thresholds for validity. Following a widely accepted methodology, we developed a comprehensive set of quality indicators for MS care that can be used to assess quality of care and guide the design of interventions to improve care among persons with MS.
C1 [Cheng, Eric M.; Giesser, Barbara; Vickrey, Barbara G.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
[Cheng, Eric M.; Vickrey, Barbara G.] VA Greater Los Angeles Hlth Care Syst, Dept Neurol, Los Angeles, CA USA.
[Crandall, Carolyn J.; Hays, Ron D.; Shekelle, Paul] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
[Bever, Christopher T., Jr.] VA Maryland Hlth Care Syst, Multiple Sclerosis Ctr Excellence E, Res & Neurol Serv, Baltimore, MD USA.
[Bever, Christopher T., Jr.] Univ Maryland, Sch Med, Dept Neurol, Baltimore, MD 21201 USA.
[Haselkorn, Jodie K.] VA Puget Sound Hlth Care Syst, Multiple Sclerosis Ctr Excellence W, Seattle, WA USA.
[Haselkorn, Jodie K.] Univ Washington, Sch Med, Dept Rehabil Med, Seattle, WA 98195 USA.
[Haselkorn, Jodie K.] Univ Washington, Sch Med, Dept Epidemiol, Seattle, WA 98195 USA.
[Shekelle, Paul] VA Greater Los Angeles Hlth Care Syst, Dept Med, Los Angeles, CA USA.
RP Cheng, EM (reprint author), VA Greater Los Angeles, Dept Neurol, 11301 Wilshire Blvd,ML 127, Los Angeles, CA 90073 USA.
EM eric.cheng@va.gov
RI Hays, Ronald/D-5629-2013
FU National Multiple Sclerosis Society [HC0094]; NINDS [K23NS058571]; UCLA
Resource Center for Minority Aging Research/Center for Health
Improvement in Minority Elderly (RCMAR/CHIME); NIH/NIA [P30AG021684];
NCMHD [2P20MD000182]
FX This research was initiated, funded, and supported by the National
Multiple Sclerosis Society (HC0094). Dr Cheng is supported by a Career
Development Award from NINDS (K23NS058571). Dr Hays was supported in
part by the UCLA Resource Center for Minority Aging Research/Center for
Health Improvement in Minority Elderly (RCMAR/CHIME), NIH/NIA Grant
Award Number P30AG021684, and the UCLA/Drew Project EXPORT, NCMHD,
2P20MD000182. Dr Giesser has received compensation from Teva
Neuroscience and Serono for speaking engagements. Dr Bever received
consulting fees from Ingenix.
NR 39
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U1 1
U2 2
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 AUG
PY 2010
VL 16
IS 8
BP 970
EP 980
DI 10.1177/1352458510372394
PG 11
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 634TO
UT WOS:000280608600010
PM 20562162
ER
PT J
AU Chitnis, T
Guttmann, C
Zaitsev, A
Weinstock-Guttman, B
Yeh, E
Rodriguez, M
Ness, J
Gorman, M
Healy, BC
Waubant, E
Strober, JB
Pelletier, D
Krupp, L
Zivadinov, R
Chabas, D
AF Chitnis, Tanuja
Guttmann, Charles
Zaitsev, Alexander
Weinstock-Guttman, Bianca
Yeh, Eluen
Rodriguez, Moses
Ness, Jayne
Gorman, Mark
Healy, Brian C.
Waubant, Emmanuelle
Strober, Jonathan B.
Pelletier, Daniel
Krupp, Lauren
Zivadinov, Robert
Chabas, Dorothee
CA US Network Pediat MS Ctr Excellenc
TI Quantitative MRI characteristics of pediatric multiple sclerosis
SO MULTIPLE SCLEROSIS JOURNAL
LA English
DT Meeting Abstract
CT 15th Annual Meeting of the
Americas-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis
CY JUN, 2010
CL San Antonio, TX
SP Americas Comm Treatment & Res Multiple Sclerosis
C1 [Chitnis, Tanuja; Gorman, Mark] Massachusetts Gen Hosp, Partners Pediat MS Ctr, Boston, MA 02114 USA.
[Guttmann, Charles; Zaitsev, Alexander] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Weinstock-Guttman, Bianca; Yeh, Eluen; Zivadinov, Robert] SUNY Buffalo, Dept Neurol, Buffalo, NY 14260 USA.
[Rodriguez, Moses] Mayo Clin, Dept Immunol, Rochester, MN USA.
[Rodriguez, Moses] Mayo Clin, Dept Neurol, Rochester, MN USA.
[Ness, Jayne] Univ Alabama, Dept Pediat, Ctr Pediat Onset Demyelinating Dis, Birmingham, AL USA.
[Healy, Brian C.] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Waubant, Emmanuelle; Strober, Jonathan B.; Chabas, Dorothee] UCSF Pediat MS Ctr, Dept Neurol, San Francisco, CA USA.
[Pelletier, Daniel] Univ Calif San Francisco, Dept Neurol Dept, San Francisco, CA 94143 USA.
[Krupp, Lauren] SUNY Stony Brook, Dept Neurol, Stony Brook, NY 11794 USA.
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U1 0
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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 AUG
PY 2010
VL 16
IS 8
BP 996
EP 997
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 634TO
UT WOS:000280608600018
ER
PT J
AU Prajapati, SI
Martinez, CO
Abraham, J
Mccleish, AT
Michalek, JE
McManus, LM
Rubin, BP
Shireman, PK
Keller, C
AF Prajapati, Suresh I.
Martinez, Carlo O.
Abraham, Jinu
Mccleish, Amanda T.
Michalek, Joel E.
McManus, Linda M.
Rubin, Brian P.
Shireman, Paula K.
Keller, Charles
TI CRIMSON CARRIER, A LONG-ACTING CONTRAST AGENT FOR IN VIVO NEAR-INFRARED
IMAGING OF INJURED AND DISEASED MUSCLE
SO MUSCLE & NERVE
LA English
DT Article
DE crimson carrier; muscle injury; near-infrared contrast agent; optical
imaging; tumor imaging
ID REGENERATION; CANCER
AB The near-infrared wavelengths (700-900 nm) are the most suitable optical window for light penetration and deep tissue imaging in small animals. Herein we report a near-infrared fluorescent contrast agent, crimson carrier, which acts as a blood pool contrast agent to detect and quantify injury and disease in live animals. After determining the excitation-emission spectra and pharmacokinetics, crimson carrier was injected into myoinjured mice to monitor their recovery. Crimson carrier was also used to image transgenic mice with spontaneous tumors. Crimson carrier has maximal excitation and emission wavelengths of 745 nm and 820 nm, respectively. Elimination occurs predominantly via urinary excretion. We demonstrate the utility of this contrast agent for serial imaging of traumatized muscle as well as muscle tumors. The unique long-acting pharmacokinetics and urinary excretion route characteristics make crimson carrier a contrast agent of choice for the visualization of tumors and injured muscle or other tissues in live animal studies. Muscle Nerve 42:245-251, 2010
C1 [Prajapati, Suresh I.; Abraham, Jinu; Mccleish, Amanda T.; Keller, Charles] Univ Texas Hlth Sci Ctr San Antonio, Greehey Childrens Canc Res Inst, San Antonio, TX 78229 USA.
[Martinez, Carlo O.; Shireman, Paula K.] Univ Texas Hlth Sci Ctr San Antonio, Dept Surg, San Antonio, TX 78229 USA.
[Michalek, Joel E.] Univ Texas Hlth Sci Ctr San Antonio, Dept Epidemiol & Biostat, San Antonio, TX 78229 USA.
[McManus, Linda M.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pathol, San Antonio, TX 78229 USA.
[McManus, Linda M.] Univ Texas Hlth Sci Ctr San Antonio, Dept Peridont, San Antonio, TX 78229 USA.
[Rubin, Brian P.] Cleveland Clin, Dept Anat Pathol, Taussig Canc Ctr, Cleveland, OH 44106 USA.
[Rubin, Brian P.] Cleveland Clin, Lerner Res Inst, Cleveland, OH 44106 USA.
[Martinez, Carlo O.; Shireman, Paula K.] S Texas Vet Hlth Care Syst, Dept Surg, San Antonio, TX USA.
[Keller, Charles] Univ Texas Hlth Sci Ctr San Antonio, Dept Pediat, San Antonio, TX 78229 USA.
RP Keller, C (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Greehey Childrens Canc Res Inst, San Antonio, TX 78229 USA.
EM kellerc2@uthscsa.edu
OI Keller, Charles/0000-0003-2505-7487
FU Veterans Administration [HL090196, HL074236]; Numira Biosciences, Inc.
FX This study was supported in part by Grants HL090196 (to C.O.M.) and
HL074236 (to P.K.S.) from the Veterans Administration and a sponsored
research agreement with Numira Biosciences, Inc. (to C.K.).
NR 7
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U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0148-639X
J9 MUSCLE NERVE
JI Muscle Nerve
PD AUG
PY 2010
VL 42
IS 2
BP 245
EP 251
DI 10.1002/mus.21682
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 631UE
UT WOS:000280374000014
PM 20544935
ER
PT J
AU Polo, JM
Liu, S
Figueroa, ME
Kulalert, W
Eminli, S
Tan, KY
Apostolou, E
Stadtfeld, M
Li, YS
Shioda, T
Natesan, S
Wagers, AJ
Melnick, A
Evans, T
Hochedlinger, K
AF Polo, Jose M.
Liu, Susanna
Figueroa, Maria Eugenia
Kulalert, Warakorn
Eminli, Sarah
Tan, Kah Yong
Apostolou, Effie
Stadtfeld, Matthias
Li, Yushan
Shioda, Toshi
Natesan, Sridaran
Wagers, Amy J.
Melnick, Ari
Evans, Todd
Hochedlinger, Konrad
TI Cell type of origin influences the molecular and functional properties
of mouse induced pluripotent stem cells
SO NATURE BIOTECHNOLOGY
LA English
DT Article
ID HUMAN SOMATIC-CELLS; GENE-EXPRESSION; REPROGRAMMING FACTORS; EPIGENETIC
MEMORY; DNA METHYLATION; SKELETAL-MUSCLE; DEFINED FACTORS; GENERATION;
PATIENT; DISEASE
AB Induced pluripotent stem cells (iPSCs) have been derived from various somatic cell populations through ectopic expression of defined factors. It remains unclear whether iPSCs generated from different cell types are molecularly and functionally similar. Here we show that iPSCs obtained from mouse fibroblasts, hematopoietic and myogenic cells exhibit distinct transcriptional and epigenetic patterns. Moreover, we demonstrate that cellular origin influences the in vitro differentiation potentials of iPSCs into embryoid bodies and different hematopoietic cell types. Notably, continuous passaging of iPSCs largely attenuates these differences. Our results suggest that early-passage iPSCs retain a transient epigenetic memory of their somatic cells of origin, which manifests as differential gene expression and altered differentiation capacity. These observations may influence ongoing attempts to use iPSCs for disease modeling and could also be exploited in potential therapeutic applications to enhance differentiation into desired cell lineages.
C1 [Polo, Jose M.; Kulalert, Warakorn; Eminli, Sarah; Tan, Kah Yong; Apostolou, Effie; Stadtfeld, Matthias; Wagers, Amy J.; Hochedlinger, Konrad] Harvard Univ, Howard Hughes Med Inst, Cambridge, MA 02138 USA.
[Polo, Jose M.; Kulalert, Warakorn; Eminli, Sarah; Tan, Kah Yong; Apostolou, Effie; Stadtfeld, Matthias; Wagers, Amy J.; Hochedlinger, Konrad] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
[Polo, Jose M.; Kulalert, Warakorn; Eminli, Sarah; Tan, Kah Yong; Apostolou, Effie; Stadtfeld, Matthias; Wagers, Amy J.; Hochedlinger, Konrad] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Polo, Jose M.; Kulalert, Warakorn; Eminli, Sarah; Apostolou, Effie; Stadtfeld, Matthias; Shioda, Toshi; Hochedlinger, Konrad] Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA USA.
[Polo, Jose M.; Kulalert, Warakorn; Eminli, Sarah; Apostolou, Effie; Stadtfeld, Matthias; Hochedlinger, Konrad] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
[Polo, Jose M.; Kulalert, Warakorn; Eminli, Sarah; Tan, Kah Yong; Apostolou, Effie; Stadtfeld, Matthias; Wagers, Amy J.; Hochedlinger, Konrad] Harvard Stem Cell Inst, Cambridge, MA USA.
[Liu, Susanna; Evans, Todd] Weill Cornell Med Coll, Dept Surg, New York, NY USA.
[Figueroa, Maria Eugenia; Li, Yushan; Melnick, Ari] Weill Cornell Med Coll, Dept Med, Div Hematol Oncol, New York, NY USA.
[Tan, Kah Yong; Wagers, Amy J.] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Natesan, Sridaran] Sanofi Aventis Cambridge Genom Ctr, Cambridge, MA USA.
RP Hochedlinger, K (reprint author), Harvard Univ, Howard Hughes Med Inst, Cambridge, MA 02138 USA.
EM khochedlinger@helix.mgh.harvard.edu
OI Tan, Kah Yong/0000-0002-6825-2752; Polo, Jose M/0000-0002-2531-778X;
Stadtfeld, Matthias/0000-0002-5852-9906
FU MGH ECOR fellowship; Jane Coffin Childs fellowship; Schering fellowship;
Agency of Science, Technology and Research Singapore; Lymphoma Society,
SCOR [7132-08]; National Institutes of Health (NIH)
FX We thank N. Maherali and R. Walsh for helpful suggestions and critical
reading of the manuscript, B. Wittner for statistical advice, J.
LaVecchio, G. Buruzula, K. Folz-Donahue and L. Prickett for expert cell
sorting and K. Coser for technical assistance. J.M.P. was supported by
an MGH ECOR fellowship, E.A. by a Jane Coffin Childs fellowship, M.S. by
a Schering fellowship and K.Y.T. by the Agency of Science, Technology
and Research Singapore. Support to A.M. was from the Lymphoma Society,
SCOR no. 7132-08; to T.E. from National Institutes of Health (NIH) grant
HL056182 and NYSTEM; to A.J.W. in part from the Burroughs Wellcome Fund,
Harvard Stem Cell Institute, Peabody Foundation, and NIH 1 DP2
OD004345-01, and the Joslin Diabetes Center DERC (P30DK036836); to K.H.
from Howard Hughes Medical Institute, the NIH Director's Innovator Award
and the Harvard Stem Cell Institute. The content is solely the
responsibility
NR 52
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U1 8
U2 95
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1087-0156
J9 NAT BIOTECHNOL
JI Nat. Biotechnol.
PD AUG
PY 2010
VL 28
IS 8
BP 848
EP U130
DI 10.1038/nbt.1667
PG 10
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 636RM
UT WOS:000280757500025
PM 20644536
ER
PT J
AU Stewart, ML
Fire, E
Keating, AE
Walensky, LD
AF Stewart, Michelle L.
Fire, Emiko
Keating, Amy E.
Walensky, Loren D.
TI The MCL-1 BH3 helix is an exclusive MCL-1 inhibitor and apoptosis
sensitizer
SO NATURE CHEMICAL BIOLOGY
LA English
DT Article
ID STABILIZED ALPHA-HELICES; BCL-2 PROTEINS; MITOCHONDRIAL APOPTOSIS; TRAIL
SENSITIZATION; MIMETIC ABT-737; CELL-DEATH; X-RAY; RESISTANCE; DOMAINS;
CANCER
AB The development of selective inhibitors for discrete anti-apoptotic BCL-2 family proteins implicated in pathologic cell survival remains a formidable but pressing challenge. Such precisely tailored compounds would serve as molecular probes and targeted therapies to study and treat human diseases driven by specific anti-apoptotic blockades. In particular, MCL-1 has emerged as a major resistance factor in human cancer. By screening a library of stabilized alpha-helix of BCL-2 domains (SAHBs), we determined that the MCL-1 BH3 helix is itself a potent and exclusive MCL-1 inhibitor. X-ray crystallography and mutagenesis studies defined key binding and specificity determinants, including the capacity to harness the hydrocarbon staple to optimize affinity while preserving selectivity. MCL-1 SAHB directly targets MCL-1, neutralizes its inhibitory interaction with pro-apoptotic BAK and sensitizes cancer cells to caspase-dependent apoptosis. By leveraging nature's solution to ligand selectivity, we generated an MCL-1-specific agent that defines the structural and functional features of targeted MCL-1 inhibition.
C1 [Stewart, Michelle L.; Walensky, Loren D.] Harvard Univ, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Stewart, Michelle L.; Walensky, Loren D.] Harvard Univ, Childrens Hosp Boston, Sch Med, Boston, MA 02115 USA.
[Stewart, Michelle L.; Walensky, Loren D.] Dana Farber Canc Inst, Program Canc Chem Biol, Boston, MA 02115 USA.
[Fire, Emiko; Keating, Amy E.] MIT, Dept Biol, Cambridge, MA USA.
RP Walensky, LD (reprint author), Harvard Univ, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
EM Loren_Walensky@dfci.harvard.edu
FU US National Institutes of Health [5P01CA92625, 5RO1GM084181]; Burroughs
Wellcome Career Award; Ruth L. Kirschstein National Research Service
Award [1F31CA144566]; National Center for Research Resources at the US
National Institutes of Health [RR-15301]; US Department of Energy,
Office of Basic Energy Sciences [DE-AC02-06CH11357]
FX We thank E. Smith (Dana-Farber Cancer Institute) for editorial and
graphics support, R.A. Grant (Massachussets Institute of Technology) for
input on the crystallography experiments, X-ray data collection and
structural analysis, and C.H. Yun and M.J. Eck (Dana-Farber Cancer
Institute) for assistance in generating the hydrocarbon staple parameter
file used in the structural refinement. This work was supported by US
National Institutes of Health grant 5P01CA92625 and a Burroughs Wellcome
Career Award in the Biomedical Sciences to L.D.W., a Ruth L. Kirschstein
National Research Service Award 1F31CA144566 to M.L.S. and US National
Institutes of Health award 5RO1GM084181 to A.E.K. X-ray diffraction data
were acquired at the Advanced Photon Source on the Northeastern
Collaborative Access Team beamlines, which are supported by award
RR-15301 from the National Center for Research Resources at the US
National Institutes of Health. Use of the Advanced Photon Source is
supported by the US Department of Energy, Office of Basic Energy
Sciences, under Contract No. DE-AC02-06CH11357.
NR 45
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U1 3
U2 44
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1552-4450
J9 NAT CHEM BIOL
JI Nat. Chem. Biol.
PD AUG
PY 2010
VL 6
IS 8
BP 595
EP 601
DI 10.1038/NCHEMBIO.391
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 628EG
UT WOS:000280096600010
PM 20562877
ER
PT J
AU Johansen, CT
Wang, JA
Lanktree, MB
Cao, HN
McIntyre, AD
Ban, MR
Martins, RA
Kennedy, BA
Hassell, RG
Visser, ME
Schwartz, SM
Voight, BF
Elosua, R
Salomaa, V
O'Donnell, CJ
Dallinga-Thie, GM
Anand, SS
Yusuf, S
Huff, MW
Kathiresan, S
Hegele, RA
AF Johansen, Christopher T.
Wang, Jian
Lanktree, Matthew B.
Cao, Henian
McIntyre, Adam D.
Ban, Matthew R.
Martins, Rebecca A.
Kennedy, Brooke A.
Hassell, Reina G.
Visser, Maartje E.
Schwartz, Stephen M.
Voight, Benjamin F.
Elosua, Roberto
Salomaa, Veikko
O'Donnell, Christopher J.
Dallinga-Thie, Geesje M.
Anand, Sonia S.
Yusuf, Salim
Huff, Murray W.
Kathiresan, Sekar
Hegele, Robert A.
TI Excess of rare variants in genes identified by genome-wide association
study of hypertriglyceridemia
SO NATURE GENETICS
LA English
DT Article
ID HYPERLIPOPROTEINEMIA PHENOTYPES; POPULATION; DISEASE; LOCI; RISK;
TRIGLYCERIDES; CHOLESTEROL; CONTRIBUTE; MUTATIONS; ALLELES
AB Genome-wide association studies (GWAS) have identified multiple loci associated with plasma lipid concentrations(1-5). Common variants at these loci together explain <10% of variation in each lipid trait(4,5). Rare variants with large individual effects may also contribute to the heritability of lipid traits(6,7); however, the extent to which rare variants affect lipid phenotypes remains to be determined. Here we show an accumulation of rare variants, or a mutation skew, in GWAS-identified genes in individuals with hypertriglyceridemia (HTG). Through GWAS, we identified common variants in APOA5, GCKR, LPL and APOB associated with HTG. Resequencing of these genes revealed a significant burden of 154 rare missense or nonsense variants in 438 individuals with HTG, compared to 53 variants in 327 controls (P = 6.2 x 10(-8)), corresponding to a carrier frequency of 28.1% of affected individuals and 15.3% of controls (P = 2.6 x 10(-5)). Considering rare variants in these genes incrementally increased the proportion of genetic variation contributing to HTG.
C1 [Johansen, Christopher T.; Wang, Jian; Lanktree, Matthew B.; Cao, Henian; McIntyre, Adam D.; Ban, Matthew R.; Martins, Rebecca A.; Kennedy, Brooke A.; Hassell, Reina G.; Huff, Murray W.; Hegele, Robert A.] Univ Western Ontario, Dept Biochem, Robarts Res Inst, London, ON, Canada.
[Visser, Maartje E.; Dallinga-Thie, Geesje M.] Univ Amsterdam, Acad Med Ctr, Dept Expt Vasc Med, NL-1105 AZ Amsterdam, Netherlands.
[Visser, Maartje E.; Dallinga-Thie, Geesje M.] Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1105 AZ Amsterdam, Netherlands.
[Schwartz, Stephen M.] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Voight, Benjamin F.; Kathiresan, Sekar] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Voight, Benjamin F.; Kathiresan, Sekar] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Voight, Benjamin F.; Kathiresan, Sekar] Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA USA.
[Elosua, Roberto] Inst Municipal Invest Med, E-08003 Barcelona, Spain.
[Salomaa, Veikko] Natl Inst Hlth & Welf, Chron Dis Epidemiol Unit, Dept Hlth Promot & Chron Dis Prevent, Helsinki, Finland.
[O'Donnell, Christopher J.] Harvard Univ, Sch Med, Cardiovasc Res Ctr, Boston, MA USA.
[O'Donnell, Christopher J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[O'Donnell, Christopher J.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Anand, Sonia S.; Yusuf, Salim] McMaster Univ, Populat Hlth Res Inst, Hamilton Hlth Sci, Hamilton, ON, Canada.
[Huff, Murray W.; Hegele, Robert A.] Univ Western Ontario, Dept Med, Schulich Sch Med & Dent, London, ON, Canada.
RP Hegele, RA (reprint author), Univ Western Ontario, Dept Biochem, Robarts Res Inst, London, ON, Canada.
EM hegele@robarts.ca
RI Voight, Benjamin/F-1775-2011; Hegele, Robert/G-3301-2011;
OI Lanktree, Matthew/0000-0002-5750-6286; ELOSUA,
ROBERTO/0000-0001-8235-0095
FU US National Institutes of Health through the National Heart, Lung, and
Blood Institute [R01 HL087676]; National Center for Research Resources
[U54 RR020278]; Canadian Institutes of Health Research (CIHR)
[MOP-13430, MOP-79523, CTP-79853]; Heart and Stroke Foundation of
Ontario; Sigrid Juselius Foundation; Finnish Academy [129494]; Michael
G. DeGroote Heart and Stroke Foundation of Ontario Chair; Eli Lilly May
Cohen Chair in Women's Health Research at McMaster University; Jacob J.
Wolfe Distinguished Medical Research Chair; Edith Schulich Vinet Canada
Research Chair in Human Genetics (Tier I); Heart and Stroke Foundation
of Ontario [NA-6059, T-6018, PRG-4854]; Pfizer Jean Davignon
Distinguished Cardiovascular and Metabolic; Genome Canada through the
Ontario Genomics Institute
FX We thank the London Regional Genomics Centre (D. Carter, G. Barbe and K.
Kang) for their dedication to this project, and the Myocardial
Infarction Genetics Consortium (MIGen) study for the use of their
genotype data as control data in our study. The MIGen study was funded
by the US National Institutes of Health through the National Heart,
Lung, and Blood Institute's STAMPEED genomics research program (R01
HL087676) and the National Center for Research Resources (U54 RR020278).
This work was made possible by the facilities of the Shared Hierarchical
Academic Research Computing Network (SHARCNET). C.T.J. is supported by a
Canadian Institutes of Health Research (CIHR) Banting and Best Canada
Graduate Scholarship, a Heart and Stroke Foundation of Ontario Program
Grant and a CIHR Vascular Research Fellowship. V. S. was supported by
the Sigrid Juselius Foundation and by the Finnish Academy (grant
129494). S. S. A. is supported by the Michael G. DeGroote Heart and
Stroke Foundation of Ontario Chair and the Eli Lilly May Cohen Chair in
Women's Health Research at McMaster University. R. A. H. is supported by
the Jacob J. Wolfe Distinguished Medical Research Chair, the Edith
Schulich Vinet Canada Research Chair in Human Genetics (Tier I), the
Martha G. Blackburn Chair in Cardiovascular Research and operating
grants from the CIHR (MOP-13430, MOP-79523, CTP-79853), the Heart and
Stroke Foundation of Ontario (NA-6059, T-6018, PRG-4854), the Pfizer
Jean Davignon Distinguished Cardiovascular and Metabolic Research Award
and Genome Canada through the Ontario Genomics Institute.
NR 27
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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 AUG
PY 2010
VL 42
IS 8
BP 684
EP U59
DI 10.1038/ng.628
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 633RZ
UT WOS:000280524000012
PM 20657596
ER
PT J
AU Barretina, J
Taylor, BS
Banerji, S
Ramos, AH
Lagos-Quintana, M
DeCarolis, PL
Shah, K
Socci, ND
Weir, BA
Ho, A
Chiang, DY
Reva, B
Mermel, CH
Getz, G
Antipin, Y
Beroukhim, R
Major, JE
Hatton, C
Nicoletti, R
Hanna, M
Sharpe, T
Fennell, TJ
Cibulskis, K
Onofrio, RC
Saito, T
Shukla, N
Lau, C
Nelander, S
Silver, SJ
Sougnez, C
Viale, A
Winckler, W
Maki, RG
Garraway, LA
Lash, A
Greulich, H
Root, DE
Sellers, WR
Schwartz, GK
Antonescu, CR
Lander, ES
Varmus, HE
Ladanyi, M
Sander, C
Meyerson, M
Singer, S
AF Barretina, Jordi
Taylor, Barry S.
Banerji, Shantanu
Ramos, Alexis H.
Lagos-Quintana, Mariana
DeCarolis, Penelope L.
Shah, Kinjal
Socci, Nicholas D.
Weir, Barbara A.
Ho, Alan
Chiang, Derek Y.
Reva, Boris
Mermel, Craig H.
Getz, Gad
Antipin, Yevgenyi
Beroukhim, Rameen
Major, John E.
Hatton, Charles
Nicoletti, Richard
Hanna, Megan
Sharpe, Ted
Fennell, Tim J.
Cibulskis, Kristian
Onofrio, Robert C.
Saito, Tsuyoshi
Shukla, Neerav
Lau, Christopher
Nelander, Sven
Silver, Serena J.
Sougnez, Carrie
Viale, Agnes
Winckler, Wendy
Maki, Robert G.
Garraway, Levi A.
Lash, Alex
Greulich, Heidi
Root, David E.
Sellers, William R.
Schwartz, Gary K.
Antonescu, Cristina R.
Lander, Eric S.
Varmus, Harold E.
Ladanyi, Marc
Sander, Chris
Meyerson, Matthew
Singer, Samuel
TI Subtype-specific genomic alterations define new targets for soft-tissue
sarcoma therapy
SO NATURE GENETICS
LA English
DT Article
ID GASTROINTESTINAL STROMAL TUMORS; HUMAN CANCER GENES; DEDIFFERENTIATED
LIPOSARCOMA; ANTAGONIST NUTLIN-3A; PIK3CA GENE; MUTATIONS; CELLS;
PATHWAY; P53; CENSUS
AB Soft-tissue sarcomas, which result in approximately 10,700 diagnoses and 3,800 deaths per year in the United States(1), show remarkable histologic diversity, with more than 50 recognized subtypes(2). However, knowledge of their genomic alterations is limited. We describe an integrative analysis of DNA sequence, copy number and mRNA expression in 207 samples encompassing seven major subtypes. Frequently mutated genes included TP53 (17% of pleomorphic liposarcomas), NF1 (10.5% of myxofibrosarcomas and 8% of pleomorphic liposarcomas) and PIK3CA (18% of myxoid/round-cell liposarcomas, or MRCs). PIK3CA mutations in MRCs were associated with Akt activation and poor clinical outcomes. In myxofibrosarcomas and pleomorphic liposarcomas, we found both point mutations and genomic deletions affecting the tumor suppressor NF1. Finally, we found that short hairpin RNA (shRNA)-based knockdown of several genes amplified in dedifferentiated liposarcoma, including CDK4 and YEATS4, decreased cell proliferation. Our study yields a detailed map of molecular alterations across diverse sarcoma subtypes and suggests potential subtype-specific targets for therapy.
C1 [Taylor, Barry S.; Socci, Nicholas D.; Reva, Boris; Antipin, Yevgenyi; Major, John E.; Nelander, Sven; Lash, Alex; Greulich, Heidi; Sander, Chris] Mem Sloan Kettering Canc Ctr, Computat Biol Ctr, New York, NY 10021 USA.
[Barretina, Jordi; Banerji, Shantanu; Ramos, Alexis H.; Shah, Kinjal; Weir, Barbara A.; Chiang, Derek Y.; Mermel, Craig H.; Beroukhim, Rameen; Hatton, Charles; Nicoletti, Richard; Hanna, Megan; Winckler, Wendy; Garraway, Levi A.; Greulich, Heidi; Meyerson, Matthew] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Barretina, Jordi; Banerji, Shantanu; Ramos, Alexis H.; Weir, Barbara A.; Chiang, Derek Y.; Mermel, Craig H.; Beroukhim, Rameen; Hatton, Charles; Nicoletti, Richard; Hanna, Megan; Garraway, Levi A.; Greulich, Heidi; Meyerson, Matthew] Harvard Univ, Sch Med, Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Barretina, Jordi; Banerji, Shantanu; Ramos, Alexis H.; Shah, Kinjal; Weir, Barbara A.; Chiang, Derek Y.; Mermel, Craig H.; Getz, Gad; Beroukhim, Rameen; Sharpe, Ted; Fennell, Tim J.; Cibulskis, Kristian; Onofrio, Robert C.; Silver, Serena J.; Sougnez, Carrie; Winckler, Wendy; Garraway, Levi A.; Root, David E.; Lander, Eric S.; Meyerson, Matthew] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Taylor, Barry S.] Cornell Univ, Dept Physiol & Biophys, Weill Med Coll, New York, NY 10021 USA.
[Lagos-Quintana, Mariana; DeCarolis, Penelope L.; Singer, Samuel] Mem Sloan Kettering Canc Ctr, Dept Surg, Sarcoma Biol Lab, Sarcoma Dis Management Program, New York, NY 10021 USA.
[Ho, Alan; Schwartz, Gary K.] Mem Sloan Kettering Canc Ctr, Lab New Drug Dev, Dept Med, New York, NY 10021 USA.
[Saito, Tsuyoshi; Shukla, Neerav; Lau, Christopher; Ladanyi, Marc] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Saito, Tsuyoshi; Shukla, Neerav; Lau, Christopher; Ladanyi, Marc] Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10021 USA.
[Viale, Agnes] Sloan Kettering Inst, Genom Core Lab, New York, NY USA.
[Sellers, William R.] Novartis Inst Biomed Res, Cambridge, MA USA.
[Varmus, Harold E.] Mem Sloan Kettering Canc Ctr, Program Canc Biol & Genet, New York, NY 10021 USA.
[Meyerson, Matthew] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
RP Sander, C (reprint author), Mem Sloan Kettering Canc Ctr, Computat Biol Ctr, 1275 York Ave, New York, NY 10021 USA.
EM sanderc@mskcc.org; matthew_meyerson@dfci.harvard.edu; singers@mskcc.org
RI sander, chris/H-1452-2011; Meyerson, Matthew/E-7123-2012; Reva,
Boris/B-6436-2014;
OI Reva, Boris/0000-0002-8805-389X; Nelander, Sven/0000-0003-1758-1262;
Lash, Alex/0000-0003-3787-1590
FU Anbinder Fund; Soft Tissue Sarcoma [P01 CA047179]; Kristen Ann Carr
Fund; Starr Foundation Cancer Consortium
FX For advice and discussion, we thank W. M. Lin, J.S. Boehm, C. M.
Johannessen, A.J. Bass, M. Garber, S. Finn, J.A. Fletcher, W. C. Hahn,
T. Golub and all the members of the Spanish Group for Research on
Sarcomas (GEIS). We are grateful for the technical assistance and
support of B. S. Blumenstail, L. Ziaugra and S. B. Gabriel of the Broad
Genetic Analysis Platform; J. Baldwin of the Broad Sequencing Platform;
J. Franklin, S. Mahan and K. Ardlie of the Broad Biological Samples
Platform; and H. Le, P. Lizotte, B. Wong, A. Allen, A. Derr, C. Nguyen
and J. K. Grenier of the Broad RNAi Platform. We thank L. Borsu for
assistance with Sequenom assays at Memorial Sloan-Kettering Cancer
Center (MSKCC). The MSKCC Sequenom facility is supported by the Anbinder
Fund. We also thank the members of the MSKCC Genomics Core Laboratory
and N.H. Moraco for clinical data support. J. A. Fletcher (Department of
Pathology, Brigham and Women's Hospital, Boston, Massachusetts, USA) and
J. Nishio (Fukuoka University, Fukuoka, Japan) provided the LPS141 and
FU-DDLS-1 cell lines, respectively. J. B. is a Beatriu de Pinos fellow
of the Departament d'Universitats, Recerca i Societat de la Informacio
de la Generalitat de Catalunya. B. S. T. is a fellow of the Geoffrey
Beene Cancer Research Center at MSKCC. This work was supported in part
by the Soft Tissue Sarcoma Program Project (P01 CA047179, S. J. S., M.
L. and C. Sander), the Kristen Ann Carr Fund and the Starr Foundation
Cancer Consortium and by a generous donation from M. B. Zuckerman.
NR 54
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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 AUG
PY 2010
VL 42
IS 8
BP 715
EP U103
DI 10.1038/ng.619
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 633RZ
UT WOS:000280524000019
PM 20601955
ER
PT J
AU Means, TK
Luster, AD
AF Means, Terry K.
Luster, Andrew D.
TI Integrins limit the Toll
SO NATURE IMMUNOLOGY
LA English
DT Editorial Material
ID ACTIVATION
AB Regulation of the inflammatory response is necessary for limiting tissue destruction and preventing autoimmunity. A recent discovery shows that CD11b activated by Toll-like receptors via inside-out signaling mediates degradation of the Toll-like receptor adaptors MyD88 and TRIF.
C1 [Means, Terry K.; Luster, Andrew D.] Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Charlestown, MA USA.
[Means, Terry K.; Luster, Andrew D.] Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol, Charlestown, MA USA.
[Means, Terry K.; Luster, Andrew D.] Harvard Univ, Sch Med, Charlestown, MA USA.
RP Means, TK (reprint author), Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Charlestown, MA USA.
EM aluster@mgh.harvard.edu
FU NIAID NIH HHS [R01 AI084884]
NR 12
TC 8
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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 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD AUG
PY 2010
VL 11
IS 8
BP 691
EP 693
PG 3
WC Immunology
SC Immunology
GA 628UX
UT WOS:000280149400007
PM 20644576
ER
PT J
AU Kim, H
Seed, B
AF Kim, Hwijin
Seed, Brian
TI The transcription factor MafB antagonizes antiviral responses by
blocking recruitment of coactivators to the transcription factor IRF3
SO NATURE IMMUNOLOGY
LA English
DT Article
ID DOUBLE-STRANDED-RNA; HUMAN PANCREATIC-ISLETS; VIRUS-INFECTION;
BETA-CELLS; RIG-I; GENE-EXPRESSION; DENDRITIC CELLS; INNATE IMMUNITY;
NOD MICE; INTERFERON
AB Viral infection induces type I interferons (IFN-alpha and IFN-beta) that recruit unexposed cells in a self-amplifying response. We report that the transcription factor MafB thwarts auto-amplification by a metastable switch activity. MafB acted as a weak positive basal regulator of transcription at the IFNB1 promoter through activity at transcription factor AP-1-like sites. Interferon elicitors recruited the transcription factor IRF3 to the promoter, whereupon MafB acted as a transcriptional antagonist, impairing the interaction of coactivators with IRF3. Mathematical modeling supported the view that prepositioning of MafB on the promoter allows the system to respond rapidly to fluctuations in IRF3 activity. Higher expression of MafB in human pancreatic islet beta cells might increase cellular vulnerability to viral infections associated with the etiology of type 1 diabetes.
C1 [Kim, Hwijin; Seed, Brian] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
[Kim, Hwijin; Seed, Brian] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
RP Seed, B (reprint author), Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
EM bseed@ccib.mgh.harvard.edu
FU NIDDK NIH HHS [P30 DK057521-019001]
NR 50
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U2 4
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 AUG
PY 2010
VL 11
IS 8
BP 743
EP U113
DI 10.1038/ni.1897
PG 9
WC Immunology
SC Immunology
GA 628UX
UT WOS:000280149400016
PM 20581830
ER
PT J
AU Kharas, MG
Lengner, CJ
Al-Shahrour, F
Bullinger, L
Ball, B
Zaidi, S
Morgan, K
Tam, W
Paktinat, M
Okabe, R
Gozo, M
Einhorn, W
Lane, SW
Scholl, C
Frohling, S
Fleming, M
Ebert, BL
Gilliland, DG
Jaenisch, R
Daley, GQ
AF Kharas, Michael G.
Lengner, Christopher J.
Al-Shahrour, Fatima
Bullinger, Lars
Ball, Brian
Zaidi, Samir
Morgan, Kelly
Tam, Winnie
Paktinat, Mahnaz
Okabe, Rachel
Gozo, Maricel
Einhorn, William
Lane, Steven W.
Scholl, Claudia
Froehling, Stefan
Fleming, Mark
Ebert, Benjamin L.
Gilliland, D. Gary
Jaenisch, Rudolf
Daley, George Q.
TI Musashi-2 regulates normal hematopoiesis and promotes aggressive myeloid
leukemia
SO NATURE MEDICINE
LA English
DT Article
ID RNA-BINDING PROTEIN; ONCOGENIC PATHWAY SIGNATURES; STEM-CELLS;
GENE-EXPRESSION; THERAPEUTIC-EFFICACY; HUMAN CANCER; PROGENITOR;
TRANSFORMATION; DIFFERENTIATION; PROGRESSION
AB RNA-binding proteins of the Musashi (Msi) family are expressed in stem cell compartments and in aggressive tumors, but they have not yet been widely explored in the blood. Here we demonstrate that Msi2 is the predominant form expressed in hematopoietic stem cells (HSCs), and its knockdown leads to reduced engraftment and depletion of HSCs in vivo. Overexpression of human MSI2 in a mouse model increases HSC cell cycle progression and cooperates with the chronic myeloid leukemia-associated BCR-ABL1 oncoprotein to induce an aggressive leukemia. MSI2 is overexpressed in human myeloid leukemia cell lines, and its depletion leads to decreased proliferation and increased apoptosis. Expression levels in human myeloid leukemia directly correlate with decreased survival in patients with the disease, thereby defining MSI2 expression as a new prognostic marker and as a new target for therapy in acute myeloid leukemia (AML).
C1 [Kharas, Michael G.; Al-Shahrour, Fatima; Ball, Brian; Morgan, Kelly; Tam, Winnie; Paktinat, Mahnaz; Okabe, Rachel; Gozo, Maricel; Einhorn, William; Ebert, Benjamin L.; Gilliland, D. Gary; Daley, George Q.] Brigham & Womens Hosp, Dept Med, Div Hematol, Boston, MA 02115 USA.
[Daley, George Q.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Lengner, Christopher J.; Jaenisch, Rudolf] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA.
[Al-Shahrour, Fatima] Broad Inst Massachusetts Inst Technol & Harvard, Cambridge, MA USA.
[Bullinger, Lars; Scholl, Claudia; Froehling, Stefan] Univ Hosp Ulm, Dept Internal Med 3, Ulm, Germany.
[Zaidi, Samir; Jaenisch, Rudolf] MIT, Dept Biol, Cambridge, MA USA.
[Einhorn, William; Lane, Steven W.; Daley, George Q.] Childrens Hosp, Div Pediat Hematol Oncol, Boston, MA 02115 USA.
[Fleming, Mark] Childrens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Gilliland, D. Gary] Merck Res Labs, N Wales, PA USA.
[Daley, George Q.] Howard Hughes Med Inst, Boston, MA 02115 USA.
[Daley, George Q.] Childrens Hosp, Stem Cell Transplantat Program, Boston, MA 02115 USA.
[Daley, George Q.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Daley, George Q.] Harvard Stem Cell Inst, Cambridge, MA USA.
[Daley, George Q.] Childrens Hosp, Manton Ctr Orphan Dis Res, Boston, MA 02115 USA.
RP Kharas, MG (reprint author), Brigham & Womens Hosp, Dept Med, Div Hematol, Boston, MA 02115 USA.
EM mkharas@partners.org; george.daley@childrens.harvard.edu
RI Lane, Steven/C-3215-2012;
OI Lane, Steven/0000-0002-8050-6209; Lengner,
Christopher/0000-0002-0574-5189
FU US National Institutes of Health (NIH) National Institute of Diabetes
and Digestive and Kidney Diseases; NIH; Leukemia and Lymphoma Society;
Howard Hughes Medical Institute
FX We would like to thank S. Armstrong (Children's Hospital Boston) for
valuable reagents. We would like to acknowledge T. Zhang, D.
Kalaitzidis, K. Gritsman, P. Stern and S. Sykes for their critical
suggestions and J.-A. Kwon for assistance with microarray processing. We
would like to thank M. Wernig for his assistance with the project.
M.G.K. was supported by the US National Institutes of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases Career
Development Award. This work was supported by grants from the NIH
(D.G.G., R.J. and G.Q.D.), the Leukemia and Lymphoma Society (D.G.G. and
G.Q.D.) and the Howard Hughes Medical Institute (D.G.G. and G.Q.D.).
C.J.L. was supported by a Ruth L. Kirschstein Fellowship from the NIH.
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PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD AUG
PY 2010
VL 16
IS 8
BP 903
EP U101
DI 10.1038/nm.2187
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 635IQ
UT WOS:000280649200030
PM 20616797
ER
PT J
AU Ott, HC
Clippinger, B
Conrad, C
Schuetz, C
Pomerantseva, I
Ikonomou, L
Kotton, D
Vacanti, JP
AF Ott, Harald C.
Clippinger, Ben
Conrad, Claudius
Schuetz, Christian
Pomerantseva, Irina
Ikonomou, Laertis
Kotton, Darrell
Vacanti, Joseph P.
TI Regeneration and orthotopic transplantation of a bioartificial lung
SO NATURE MEDICINE
LA English
DT Article
ID TISSUE-ENGINEERED LUNG; MARROW-DERIVED CELLS; EMBRYONIC STEM-CELLS;
IN-VITRO; MECHANICAL FORCES; MATRIX; EPITHELIUM; COLLAGEN; BONE; VIVO
AB About 2,000 patients now await a donor lung in the United States. Worldwide, 50 million individuals are living with end-stage lung disease. Creation of a bioartificial lung requires engineering of viable lung architecture enabling ventilation, perfusion and gas exchange. We decellularized lungs by detergent perfusion and yielded scaffolds with acellular vasculature, airways and alveoli. To regenerate gas exchange tissue, we seeded scaffolds with epithelial and endothelial cells. To establish function, we perfused and ventilated cell-seeded constructs in a bioreactor simulating the physiologic environment of developing lung. By day 5, constructs could be perfused with blood and ventilated using physiologic pressures, and they generated gas exchange comparable to that of isolated native lungs. To show in vivo function, we transplanted regenerated lungs into orthotopic position. After transplantation, constructs were perfused by the recipient's circulation and ventilated by means of the recipient's airway and respiratory muscles, and they provided gas exchange in vivo for up to 6 h after extubation.
C1 [Ott, Harald C.; Clippinger, Ben; Conrad, Claudius; Schuetz, Christian; Pomerantseva, Irina; Vacanti, Joseph P.] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Ikonomou, Laertis; Kotton, Darrell] Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA.
[Ikonomou, Laertis; Kotton, Darrell] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02118 USA.
RP Ott, HC (reprint author), Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
EM hott@partners.org
RI Ikonomou, Laertis/D-4579-2009; Schuetz, Christian/K-5234-2013;
OI Ikonomou, Laertis/0000-0003-0993-6713; Schuetz,
Christian/0000-0002-6828-4543; Kotton, Darrell/0000-0002-9604-8476
FU Inflammatory Bowel Disease [DK43351]; Boston Area Diabetes and
Endocrinology Research Center [DK57521]; Department of Surgery,
Massachusetts General Hospital; Center for Integration of Medicine and
Innovative Technology (CIMIT)
FX We thank Harvard Apparatus Inc. for providing bioreactor components and,
in particular, J. Consiglio, R. Zink and T. Beha for technical support.
We thank J. Titus for assistance with animal surgeries and video
recording. We further thank E. Bassett and D. Hoganson for their help
with bioreactor parts and materials, A. Pardo for her technical support
with western blots and K. Kulig for assistance with confocal microscopy.
Electron microscopy was performed in the Microscopy Core of the Center
for Systems Biology/Program in Membrane Biology, which is partially
supported by Inflammatory Bowel Disease Grant DK43351 and Boston Area
Diabetes and Endocrinology Research Center Award DK57521. This study was
supported by a Faculty Development Grant provided by the Department of
Surgery, Massachusetts General Hospital and by a Young Clinician
Researcher Award granted by the Center for Integration of Medicine and
Innovative Technology (CIMIT).
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PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD AUG
PY 2010
VL 16
IS 8
BP 927
EP U131
DI 10.1038/nm.2193
PG 8
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 635IQ
UT WOS:000280649200034
PM 20628374
ER
PT J
AU Polyak, K
AF Polyak, Kornelia
TI Going small is the new big
SO NATURE METHODS
LA English
DT Editorial Material
ID EPIGENETIC CHARACTERIZATION; TRANSCRIPTOME; PROJECT; GENOME; ELEMENTS;
SAMPLES
C1 [Polyak, Kornelia] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Polyak, Kornelia] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Polyak, Kornelia] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Polyak, K (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM kornelia_polyak@dfci.harvard.edu
NR 15
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PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
J9 NAT METHODS
JI Nat. Methods
PD AUG
PY 2010
VL 7
IS 8
BP 597
EP 600
DI 10.1038/nmeth0810-597
PG 4
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 633KD
UT WOS:000280500000018
PM 20676079
ER
PT J
AU Tamplin, OJ
Zon, LI
AF Tamplin, Owen J.
Zon, Leonard I.
TI Fishing at the cellular level
SO NATURE METHODS
LA English
DT Editorial Material
ID IN-VIVO; ZEBRAFISH
C1 [Tamplin, Owen J.] Childrens Hosp Boston, Stem Cell Program, Boston, MA USA.
Childrens Hosp Boston, Div Hematol Oncol, Boston, MA USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Tamplin, OJ (reprint author), Childrens Hosp Boston, Stem Cell Program, Boston, MA USA.
EM zon@enders.tch.harvard.edu
RI Tamplin, Owen/C-1617-2014
OI Tamplin, Owen/0000-0001-9146-4860
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PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
J9 NAT METHODS
JI Nat. Methods
PD AUG
PY 2010
VL 7
IS 8
BP 600
EP 601
DI 10.1038/nmeth0810-600
PG 3
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 633KD
UT WOS:000280500000019
PM 20676080
ER
PT J
AU Adli, M
Zhu, JA
Bernstein, BE
AF Adli, Mazhar
Zhu, Jiang
Bernstein, Bradley E.
TI Genome-wide chromatin maps derived from limited numbers of hematopoietic
progenitors
SO NATURE METHODS
LA English
DT Article
ID STEM-CELLS; EPIGENETIC CHARACTERIZATION; CHIP; DIFFERENTIATION;
TRANSCRIPTION; PLURIPOTENT; PLASTICITY; SIGNATURES; GENES; FATE
AB Current methods for whole-genome mapping of protein-DNA interactions, performed by coupling chromatin immunoprecipitation with high-throughput sequencing (ChIP-seq), require large amounts of starting materials, which precludes their application to rare cell types. Here we combine a high-sensitivity ChIP assay with a new library preparation procedure to map histone modifications in as few as 10,000 cells. We used the technique to characterize mouse hematopoietic progenitors and thereby gain insight into their developmental program.
C1 [Adli, Mazhar; Zhu, Jiang; Bernstein, Bradley E.] Massachusetts Gen Hosp, Dept Pathol, Howard Hughes Med Inst, Boston, MA 02114 USA.
[Adli, Mazhar; Zhu, Jiang; Bernstein, Bradley E.] Harvard Univ, Sch Med, Boston, MA USA.
[Adli, Mazhar; Zhu, Jiang; Bernstein, Bradley E.] Harvard & Massachusetts Inst Technol, Broad Inst, Cambridge, MA USA.
[Adli, Mazhar; Zhu, Jiang; Bernstein, Bradley E.] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Adli, Mazhar; Zhu, Jiang; Bernstein, Bradley E.] Massachusetts Gen Hosp, Ctr Canc Res, Boston, MA 02114 USA.
RP Bernstein, BE (reprint author), Massachusetts Gen Hosp, Dept Pathol, Howard Hughes Med Inst, Boston, MA 02114 USA.
EM bernstein.bradley@mgh.harvard.edu
RI Zhu, Jiang/E-3049-2013
FU Starr Cancer Consortium; Charles E. Culpeper Scholarship; US National
Human Genome Research Institute; National Institutes of Health Roadmap
for Epigenomics; National Heart, Lung, and Blood Institute
FX We thank D. Flowers and I. Bernstein for expertise, reagents and
assistance in isolation of hematopoietic cells, N. Shoresh and T.
Mikkelsen for computational assistance and B. Knoechel, E. Mendenhall,
A. Goren and A. Chi for constructive discussions and critical reading of
the manuscript. This research was supported by funds from the Starr
Cancer Consortium, a Charles E. Culpeper Scholarship, the US National
Human Genome Research Institute, the National Institutes of Health
Roadmap for Epigenomics and the National Heart, Lung, and Blood
Institute.
NR 20
TC 89
Z9 93
U1 0
U2 6
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 AUG
PY 2010
VL 7
IS 8
BP 615
EP U24
DI 10.1038/NMETH.1478
PG 6
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 633KD
UT WOS:000280500000004
PM 20622861
ER
PT J
AU Ozsolak, F
Ting, DT
Wittner, BS
Brannigan, BW
Paul, S
Bardeesy, N
Ramaswamy, S
Milos, PM
Haber, DA
AF Ozsolak, Fatih
Ting, David T.
Wittner, Ben S.
Brannigan, Brian W.
Paul, Suchismita
Bardeesy, Nabeel
Ramaswamy, Sridhar
Milos, Patrice M.
Haber, Daniel A.
TI Amplification-free digital gene expression profiling from minute cell
quantities
SO NATURE METHODS
LA English
DT Article
ID SINGLE-CELL; RNA; TRANSCRIPTOME; ADENOCARCINOMA; GENOME; LEVEL; BIAS
AB Generating reliable expression profiles from minute cell quantities is critical for scientific discovery and potential clinical applications. Here we present low-quantity digital gene expression (LQ-DGE), an amplification-free approach involving capture of poly(A)(+) RNAs from cellular lysates onto poly(dT)-coated sequencing surfaces, followed by on-surface reverse transcription and sequencing. We applied LQ-DGE to profile malignant and nonmalignant mouse and human cells, demonstrating its quantitative power and potential applicability to archival specimens.
C1 [Ozsolak, Fatih; Milos, Patrice M.] Helicos BioSci Corp, Cambridge, MA USA.
[Ting, David T.; Wittner, Ben S.; Brannigan, Brian W.; Paul, Suchismita; Bardeesy, Nabeel; Ramaswamy, Sridhar; Haber, Daniel A.] Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA USA.
[Ting, David T.; Wittner, Ben S.; Bardeesy, Nabeel; Ramaswamy, Sridhar; Haber, Daniel A.] Harvard Univ, Sch Med, Boston, MA USA.
[Haber, Daniel A.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Howard Hughes Med Inst, Charlestown, MA USA.
RP Ozsolak, F (reprint author), Helicos BioSci Corp, Cambridge, MA USA.
EM fatihozsolak@gmail.com; haber@helix.mgh.harvard.edu
OI Ting, David/0000-0002-3261-2322
FU Pancreatic Cancer Action Network-American Association for Cancer
Research; Howard Hughes Medical Institute; US National Human Genome
Research Institute [1R44HG005279-01]
FX We thank K. Kerouac for technical assistance. D. T. T. is supported by
the Pancreatic Cancer Action Network-American Association for Cancer
Research Research Fellowship, and D. A. H. is supported by the Howard
Hughes Medical Institute. This work was supported by US National Human
Genome Research Institute grant 1R44HG005279-01 to F.O. and P.M.M.
NR 16
TC 31
Z9 32
U1 0
U2 11
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 AUG
PY 2010
VL 7
IS 8
BP 619
EP U28
DI 10.1038/NMETH.1480
PG 4
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 633KD
UT WOS:000280500000005
PM 20639869
ER
PT J
AU Kamoun, WS
Chae, SS
Lacorre, DA
Tyrrell, JA
Mitre, M
Gillissen, MA
Fukumura, D
Jain, RK
Munn, LL
AF Kamoun, Walid S.
Chae, Sung-Suk
Lacorre, Delphine A.
Tyrrell, James A.
Mitre, Mariela
Gillissen, Marijn A.
Fukumura, Dai
Jain, Rakesh K.
Munn, Lance L.
TI Simultaneous measurement of RBC velocity, flux, hematocrit and shear
rate in vascular networks
SO NATURE METHODS
LA English
DT Article
ID INTRAVITAL MICROSCOPY; TUMOR; MICROCIRCULATION; NORMALIZATION; GROWTH;
MODEL
AB Not all tumor vessels are equal. Tumor-associated vasculature includes immature vessels, regressing vessels, transport vessels undergoing arteriogenesis and peritumor vessels influenced by tumor growth factors. Current techniques for analyzing tumor blood flow do not discriminate between vessel subtypes and only measure average changes from a population of dissimilar vessels. We developed methodologies for simultaneously quantifying blood flow (velocity, flux, hematocrit and shear rate) in extended networks at single-capillary resolution in vivo. Our approach relies on deconvolution of signals produced by labeled red blood cells as they move relative to the scanning laser of a confocal or multiphoton microscope and provides fully resolved three-dimensional flow profiles within vessel networks. Using this methodology, we show that blood velocity profiles are asymmetric near intussusceptive tissue structures in tumors in mice. Furthermore, we show that subpopulations of vessels, classified by functional parameters, exist in and around a tumor and in normal brain tissue.
C1 [Kamoun, Walid S.; Chae, Sung-Suk; Lacorre, Delphine A.; Mitre, Mariela; Gillissen, Marijn A.; Fukumura, Dai; Jain, Rakesh K.; Munn, Lance L.] Massachusetts Gen Hosp, Dept Radiat Oncol, Edwin L Steele Lab, Boston, MA 02114 USA.
[Kamoun, Walid S.; Chae, Sung-Suk; Lacorre, Delphine A.; Mitre, Mariela; Gillissen, Marijn A.; Fukumura, Dai; Jain, Rakesh K.; Munn, Lance L.] Harvard Univ, Sch Med, Boston, MA USA.
[Tyrrell, James A.] Thomson Reuters, Corp Res & Dev, New York, NY USA.
RP Munn, LL (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Edwin L Steele Lab, Boston, MA 02114 USA.
EM munn@steele.mgh.harvard.edu
RI Tyrrell, James/A-6359-2010; Munn, Lance/L-3950-2016
OI Munn, Lance/0000-0003-0698-7232
FU US National Institutes of Health [R01HL064240, R01CA149285, P01CA80124];
Susan G. Komen Foundation
FX We thank T. Padera for editorial comments and S. Roberge for technical
assistance. This work was supported in part by US National Institutes of
Health grants R01HL064240 (L. L. M.), R01CA149285 (L. L. M.) and
P01CA80124 (R.K.J.) and by a postdoctoral fellowship from the Susan G.
Komen Foundation (W.S.K.).
NR 16
TC 87
Z9 87
U1 2
U2 22
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 AUG
PY 2010
VL 7
IS 8
BP 655
EP U78
DI 10.1038/NMETH.1475
PG 8
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 633KD
UT WOS:000280500000012
PM 20581828
ER
PT J
AU Lubitz, SA
Benjamin, EJ
Ruskin, JN
Fuster, V
Ellinor, PT
AF Lubitz, Steven A.
Benjamin, Emelia J.
Ruskin, Jeremy N.
Fuster, Valentin
Ellinor, Patrick T.
TI Challenges in the classification of atrial fibrillation
SO NATURE REVIEWS CARDIOLOGY
LA English
DT Review
ID QUALITY-OF-LIFE; RANDOMIZED CONTROLLED-TRIALS; RISK STRATIFICATION
SCHEMES; ASSOCIATION TASK-FORCE; VON-WILLEBRAND-FACTOR; 30-YEAR
FOLLOW-UP; CATHETER ABLATION; EMBOLIC COMPLICATIONS; STOCKHOLM COHORT;
AMERICAN-COLLEGE
AB The incidence and prevalence of atrial fibrillation (AF) are increasing worldwide. AF is of public health importance because it accounts for substantial morbidity, mortality, and health-care costs. AF may be transient initially, but many patients have progressive disease marked by increasing frequency and duration of episodes. Various classification schemes for AF have been proposed, although current guidelines are based on temporal rhythm-based patterns. We discuss existing schemes for the classification of AF, focusing on the advantages and limitations of the pattern-based scheme, in the context of new knowledge about AF pathophysiology, AF patterns, and clinical outcomes. Furthermore, we address gaps in knowledge that present opportunities to re-examine the current pattern-based classification of AF. A future classification scheme should ideally combine elements such as the risk of stroke, an assessment of symptoms, and the degree of impairment of the atrial substrate.
C1 [Ruskin, Jeremy N.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Lubitz, Steven A.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02129 USA.
[Benjamin, Emelia J.] Framingham Heart Dis Epidemiol Study, Framingham, MA 01702 USA.
[Fuster, Valentin] Mt Sinai Sch Med, Zena & Michael Wiener Cardiovasc Inst, New York, NY 10029 USA.
[Fuster, Valentin] Mt Sinai Sch Med, Marie Josee & Henry R Kravis Cardiovasc Hlth Ctr, New York, NY 10029 USA.
RP Ellinor, PT (reprint author), Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, 55 Fruit St,GRB 109, Boston, MA 02114 USA.
EM pellinor@partners.org
RI Fuster, Valentin/H-4319-2015;
OI Fuster, Valentin/0000-0002-9043-9986; Benjamin,
Emelia/0000-0003-4076-2336
FU NIH [T32HL007575, HL092577, AG028321, RC1-HL01056, DA027021]
FX S. A. Lubitz is supported by a training grant in the epidemiology of
cardiovascular disease from the NIH (T32HL007575). This work was
supported by NIH grants HL092577 to P. T. Ellinor and E. J. Benjamin,
AG028321 and RC1-HL01056 to E. J. Benjamin, and DA027021 to P. T.
Ellinor.
NR 105
TC 17
Z9 17
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5002
J9 NAT REV CARDIOL
JI Nat. Rev. Cardiol.
PD AUG
PY 2010
VL 7
IS 8
BP 451
EP 459
DI 10.1038/nrcardio.2010.86
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 633SB
UT WOS:000280524200010
PM 20567238
ER
PT J
AU Zhang, Y
Moqtaderi, Z
Rattner, BP
Euskirchen, G
Snyder, M
Kadonaga, JT
Liu, XS
Struhl, K
AF Zhang, Yong
Moqtaderi, Zarmik
Rattner, Barbara P.
Euskirchen, Ghia
Snyder, Michael
Kadonaga, James T.
Liu, X. Shirley
Struhl, Kevin
TI Evidence against a genomic code for nucleosome positioning Reply
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Letter
ID HISTONE-DNA INTERACTIONS; IN-VIVO; SEQUENCE; YEAST; POLY(DA).POLY(DT);
TRANSCRIPTION; POLY(DA-DT); RNA
C1 [Zhang, Yong; Liu, X. Shirley] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Zhang, Yong; Liu, X. Shirley] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Moqtaderi, Zarmik; Struhl, Kevin] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Rattner, Barbara P.; Kadonaga, James T.] Univ Calif San Diego, Mol Biol Sect, La Jolla, CA 92093 USA.
[Euskirchen, Ghia; Snyder, Michael] Yale Univ, Dept Mol Cellular & Dev Biol, New Haven, CT USA.
RP Zhang, Y (reprint author), Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
EM kevin@hms.harvard.edu
RI Zhang, Yong/B-4838-2011
OI Zhang, Yong/0000-0001-6316-2734
FU NIGMS NIH HHS [R37 GM030186, R01 GM030186]
NR 21
TC 39
Z9 39
U1 2
U2 9
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD AUG
PY 2010
VL 17
IS 8
BP 920
EP 923
DI 10.1038/nsmb0810-920
PG 5
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 635QD
UT WOS:000280670300003
PM 20683474
ER
PT J
AU Huang, M
D'Andrea, AD
AF Huang, Min
D'Andrea, Alan D.
TI A new nuclease member of the FAN club
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Editorial Material
ID FANCONI-ANEMIA PATHWAY; CROSS-LINK REPAIR; HOLLIDAY JUNCTION RESOLVASE;
DNA-REPAIR; MONOUBIQUITINATED FANCD2; PROTEIN COMPLEX; DAMAGE;
IDENTIFICATION; KIAA1018/FAN1; GENOME
C1 [Huang, Min; D'Andrea, Alan D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
RP Huang, M (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol, 44 Binney St, Boston, MA 02115 USA.
EM Alan_dandrea@dfci.harvard.edu
OI huang, min/0000-0001-6735-1612
FU NIDDK NIH HHS [R01-DK43889, R01 DK043889-18, R01 DK043889]
NR 29
TC 17
Z9 19
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9985
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD AUG
PY 2010
VL 17
IS 8
BP 926
EP 928
DI 10.1038/nsmb0810-926
PG 3
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 635QD
UT WOS:000280670300006
PM 20683477
ER
PT J
AU Joseph, AJ
Compton, SP
Holmes, LH
Annand, A
Self, SE
Fitzgibbon, WR
Ullian, ME
AF Joseph, Anthony J.
Compton, Susan P.
Holmes, Lewis H.
Annand, Andrew
Self, Sally E.
Fitzgibbon, Wayne R.
Ullian, Michael E.
TI Utility of percutaneous renal biopsy in chronic kidney disease
SO NEPHROLOGY
LA English
DT Article
DE chronic kidney disease; renal biopsy; renal bleeding; renal scarring;
serum creatinine
ID MANAGEMENT; THERAPY
AB Background: We tested the hypothesis that patterns of serum creatinine concentrations (S-cr) prior to percutaneous renal biopsy (PRB) predict the utility of PRB in safely making renal diagnoses, revealing treatable disease, and altering therapy in chronic kidney disease patients.
Methods: PRB specimens (170 patients) were assigned to 1 of 5 groups: S-cr never greater than 0.11 mM for at least 6 months prior to PRB (Group 1); S-cr greater than 0.11 mM but less than 0.18 mM during the 6 months prior to PRB (Groups 2); S-cr less than 0.18 mM during the 6 months prior to PRB but greater than 0.18 mM prior to these 6 months (Group 3); S-cr greater than 0.18 mM for less than 6 months prior to PRB (Group 4); S-cr greater than 0.18 mM for more than 6 months prior to PRB (Group 5).
Results: Histopathology chronicity score (0-9) increased with increasing group number: 2.1 (Group 1); 4.4 (Group 2); 4.5 (Group 3); 5.4 (Group 4); 7.0 (Group 5). Post-PRB bleeding was more common with increasing group number. New therapy was instituted after PRB most frequently in Group 4 (62%) and least frequently in Group 5 (24%).
Conclusion: After more prolonged elevations of S-cr, PRB may be less safe and less likely to reveal treatable disease and opportunities for therapy.
C1 [Joseph, Anthony J.; Compton, Susan P.; Holmes, Lewis H.; Annand, Andrew; Self, Sally E.; Fitzgibbon, Wayne R.; Ullian, Michael E.] Med Univ S Carolina, Ralph H Johnson VA Hosp, Charleston, SC 29425 USA.
RP Ullian, ME (reprint author), Med Univ S Carolina, Ralph H Johnson VA Hosp, 96 Jonathan Lucas St,MSC 629, Charleston, SC 29425 USA.
EM ullianme@musc.edu
NR 11
TC 4
Z9 5
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1320-5358
J9 NEPHROLOGY
JI Nephrology
PD AUG
PY 2010
VL 15
IS 5
BP 544
EP 548
DI 10.1111/j.1440-1797.2010.01293.x
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 631OI
UT WOS:000280356700006
PM 20649874
ER
PT J
AU David, S
Kumpers, P
Lukasz, A
Fliser, D
Martens-Lobenhoffer, J
Bode-Boger, SM
Kliem, V
Haller, H
Kielstein, JT
AF David, Sascha
Kuempers, Philipp
Lukasz, Alexander
Fliser, Danilo
Martens-Lobenhoffer, Jens
Bode-Boeger, Stefanie M.
Kliem, Volker
Haller, Hermann
Kielstein, Jan T.
TI Circulating angiopoietin-2 levels increase with progress of chronic
kidney disease
SO NEPHROLOGY DIALYSIS TRANSPLANTATION
LA English
DT Article
DE angiopoietin; CKD; dialysis; kidney donation; nephrectomy
ID STAGE RENAL-DISEASE; TIE-2 LIGAND ANGIOPOIETIN-2;
GLOMERULAR-FILTRATION-RATE; ASYMMETRIC DIMETHYLARGININE; ENDOTHELIAL
DYSFUNCTION; CARDIOVASCULAR RISK; INFLAMMATION; ATHEROSCLEROSIS;
TRANSPLANTATION; ANGIOGENESIS
AB Background. Angiopoietin-2 (Ang-2) is an antagonistic ligand of the endothelial-specific Tie2 receptor. Patients on dialysis have markedly elevated Ang-2 levels, and those correlate with their atherosclerotic burden. The aim of the current study was to investigate the relationship between the circulating levels of Ang-2 and renal function throughout all stages of chronic kidney disease (CKD). In addition, we aimed to detect a potential link between the nitric oxide (NO) synthase inhibitor asymmetric dimethylarginine (ADMA) and the Ang-2 levels.
Methods. Glomerular filtration rate (GFR) was assessed by the inulin clearance technique ((i)GFR) and compared to serum Ang-2 (immunoluminometric assay) and ADMA levels (liquid chromatography-electrospray tandem mass spectrometry) in 44 untreated non-smokers at the different stages of CKD 1-4. Ang-2 was also measured in 19 patients on dialysis (CKD stage 5). In addition, the Ang-2 and (c)GFR (cystatin C) measurements were taken in 15 healthy individuals before and 72 h after kidney donation.
Results. The median Ang-2 levels steadily increased across the following groups: healthy controls: 0.77 (0.32-1.08) ng/mL; CKD 1: 0.83 (0.67-1.09) ng/mL; CKD 2: 0.93 (0.74-1.15) ng/mL; CKD 3: 1.13 (0.87-1.49) ng/mL; CKD 4: 1.75 (1.23-2.61) ng/mL; and CKD 5: 4.87 (3.22-7.59) ng/mL, respectively (non-parametric ANOVA P < 0.0001). Ang-2 was associated with the degree of CKD as evidenced by an inverse correlation with the (i)GFR (r = -0.509, P < 0.0001) and positive correlations with homocysteine (r = 0.365, P = 0.015) and phosphate (r = 0.53, P < 0.0001). Additionally, Ang-2 correlated with the ADMA levels (r = 0.35, P = 0.01). We detected a close inverse correlation between the mean changes in GFR and circulating Ang-2 at 72 h after kidney donation (r = -0.54, P = 0.03).
Conclusions. Circulating Ang-2, a putative marker and potential mediator of accelerated atherosclerosis, is inversely related to GFR and increases with advanced CKD. The correlation between Ang-2 and ADMA points towards the hypothesis that the ADMA-driven NO deficiency might trigger Ang-2 release and account for the Ang-2 increase in CKD patients.
C1 [David, Sascha; Kuempers, Philipp; Lukasz, Alexander; Haller, Hermann; Kielstein, Jan T.] Hannover Med Sch, Div Nephrol & Hypertens, D-3000 Hannover, Germany.
[David, Sascha] Harvard Univ, Sch Med, Vasc Biol Res Ctr, BIDMC, Boston, MA USA.
[Kuempers, Philipp] Univ Hosp Munster, Dept Med D, Div Gen Internal Med Nephrol & Rheuinatol, Munster, Germany.
[Fliser, Danilo] Univ Saarland, Dept Nephrol, D-6650 Homburg, Germany.
[Martens-Lobenhoffer, Jens; Bode-Boeger, Stefanie M.] Otto von Guericke Univ, Inst Clin Pharmacol, Magdeburg, Germany.
[Kliem, Volker] Lower Saxony Ctr Nephrol, Dept Nephrol, Hannoversch Muenden, Germany.
RP David, S (reprint author), Hannover Med Sch, Div Nephrol & Hypertens, D-3000 Hannover, Germany.
EM david.sascha@web.de
OI Bode-Boger, Stefanie/0000-0002-5132-6591
NR 38
TC 24
Z9 25
U1 0
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0931-0509
J9 NEPHROL DIAL TRANSPL
JI Nephrol. Dial. Transplant.
PD AUG
PY 2010
VL 25
IS 8
BP 2571
EP 2576
DI 10.1093/ndt/gfq060
PG 6
WC Transplantation; Urology & Nephrology
SC Transplantation; Urology & Nephrology
GA 645RV
UT WOS:000281483300030
PM 20179005
ER
PT J
AU Frisoni, GB
Weiner, MW
AF Frisoni, Giovanni B.
Weiner, Michael W.
TI Alzheimer's Disease Neuroimaging Initiative special issue
SO NEUROBIOLOGY OF AGING
LA English
DT Editorial Material
ID BIOMARKERS
C1 [Frisoni, Giovanni B.] IRCCS Fatebenefratelli, Brescia, Italy.
[Weiner, Michael W.] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Frisoni, GB (reprint author), IRCCS Fatebenefratelli, Brescia, Italy.
RI Frisoni, Giovanni B/K-1360-2016
OI Frisoni, Giovanni B/0000-0002-6419-1753
NR 26
TC 7
Z9 7
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD AUG
PY 2010
VL 31
IS 8
SI SI
BP 1259
EP 1262
DI 10.1016/j.neurobiolaging.2010.05.006
PG 4
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 626UE
UT WOS:000279991800001
PM 20570400
ER
PT J
AU Desikan, RS
Cabral, HJ
Settecase, F
Hess, CP
Dillon, WP
Glastonbury, CM
Weiner, MW
Schmansky, NJ
Salat, DH
Fischl, B
AF Desikan, Rahul S.
Cabral, Howard J.
Settecase, Fabio
Hess, Christopher P.
Dillon, William P.
Glastonbury, Christine M.
Weiner, Michael W.
Schmansky, Nicholas J.
Salat, David H.
Fischl, Bruce
CA Alzheimer's Dis Neuroimaging Initi
TI Automated MRI measures predict progression to Alzheimer's disease
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Computational MRI; AD; Mild cognitive impairment; Clinical biomarker
ID MILD COGNITIVE IMPAIRMENT; SURFACE-BASED ANALYSIS; CORTICAL SURFACE;
FUNCTIONAL CONNECTIVITY; COORDINATE SYSTEM; CEREBRAL-CORTEX; AD;
ATROPHY; CONVERSION; DEMENTIA
AB The prediction of individuals with mild cognitive impairment (MCI) destined to develop Alzheimer's disease (AD) is of increasing clinical importance. In this study, using baseline T1-weighted MRI scans of 324 MCI individuals from two cohorts and automated software tools, we employed factor analyses and Cox proportional hazards models to identify a set of neuroanatomic measures that best predicted the time to progress from MCI to AD. For comparison, cerebrospinal fluid (CSF) assessments of cellular pathology and positron emission tomography (PET) measures of metabolic activity were additionally examined. By 3 years follow-up, 60 MCI individuals from the first cohort and 58 MCI individuals from the second cohort had progressed to a diagnosis of AD. Cox models on the first cohort demonstrated significant effects for the medial temporal factor [Hazards Ratio (HR) = 0.43(95% confidence interval (CI), 0.32-0.55), p<0.0001], the fronto-parietoccipital factor [HR = 0.59[95% CI, 0.48-0.80), p<0.001], and the lateral temporal factor [HR = 0.67 (95% CI, 0.52-0.871, p<0.011. When applied to the second cohort, these Cox models showed significant effects for the medial temporal factor [HR = 0.44 (0.32-0.61), p<0.0011 and lateral temporal factor [HR = 0.49 (0.38-0.62), p<0.001]. In a combined Cox model, consisting of individual CSF, PET, and MRI measures that best predicted disease progression, only the medial temporal factor [HR = 0.53 195% CI, 0.34-0.811, p<0.001] demonstrated a significant effect. These findings illustrate that automated MRI measures of the medial temporal cortex accurately and reliably predict time to disease progression, outperform cellular and metabolic measures as predictors of clinical decline, and can potentially serve as a predictive marker for AD. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Desikan, Rahul S.; Schmansky, Nicholas J.; Salat, David H.; Fischl, Bruce] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Dept Radiol, Charlestown, MA 02129 USA.
[Cabral, Howard J.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Settecase, Fabio; Hess, Christopher P.; Dillon, William P.; Glastonbury, Christine M.; Weiner, Michael W.] Univ Calif San Francisco, Dept Radiol, San Francisco, CA 94143 USA.
[Weiner, Michael W.] Dept Vet Affairs, San Francisco, CA USA.
[Fischl, Bruce] MIT, CSAIL, Cambridge, MA 02139 USA.
[Fischl, Bruce] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
RP Desikan, RS (reprint author), Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Dept Radiol, Bldg 149,13th St,Room 2301, Charlestown, MA 02129 USA.
EM rahul@nmr.mgh.harvard.edu
RI Scharre, Douglas/E-4030-2011;
OI Cabral, Howard/0000-0002-1185-8331; GLASTONBURY,
CHRISTINE/0000-0002-9611-1287; Hess, Christopher/0000-0002-5132-5302
FU National Center for Research Resources [P41-RR14075, R01 RR 16594-01A1,
BIRN002, U24 RR021382]; National Institute for Biomedical Imaging and
Bioengineering [R01 EB001550]; Mental Illness and Neuroscience Discovery
(MIND) Institute; National Institute on Aging [P50 AG05681, P01 AG03991,
AG021910]
FX The authors thank Reisa Sperling for her insightful comments on this
manuscript. This work was supported by grants from the National Center
for Research Resources (P41-RR14075, R01 RR 16594-01A1 and the NCRR Birn
Morphometric Project BIRN002, U24 RR021382), the National Institute for
Biomedical Imaging and Bioengineering (R01 EB001550), the Mental Illness
and Neuroscience Discovery (MIND) Institute, and the National Institute
on Aging (P50 AG05681, P01 AG03991, and AG021910). Data collection and
sharing for this project was funded by the Alzheimer's disease
Neuroimaging Initiative (Alzheimer's disease Neuroimaging initiative
(ADNI); Principal Investigator: Michael Weiner; NIH grant U01 AG024904).
ADNI is funded by the National Institute on Aging, the National
Institute of Biomedical Imaging and Bioengineering (NIBIB), and through
generous contributions from the following: Pfizer, Inc., Wyeth Research,
Bristol-Myers Squibb, Eli Lilly and Company, GlaxoSmithKline, Merck &
Co., Inc., AstraZeneca AB, Novartis Pharmaceuticals Corporation,
Alzheimer's Association, Eisai Global Clinical Development, Elan
Corporation, plc, Forest Laboratories, and the Institute for the Study
of Aging, with participation from the US Food and Drug Administration.
Industry partnerships are coordinated through the Foundation for the
National Institutes of Health. 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 of Neuro Imaging at the University of California, Los
Angeles.
NR 46
TC 39
Z9 41
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U2 6
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 AUG
PY 2010
VL 31
IS 8
SI SI
BP 1364
EP 1374
DI 10.1016/j.neurobiolaging.2010.04.023
PG 11
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA 626UE
UT WOS:000279991800010
PM 20570399
ER
PT J
AU Hasler, WL
Parkman, H
Rao, S
Chey, WD
Mccallum, R
Kuo, B
Koch, K
Sitrin, M
Semler, JR
AF Hasler, W. L.
Parkman, H.
Rao, S.
Chey, W. D.
Mccallum, R.
Kuo, B.
Koch, K.
Sitrin, M.
Semler, J. R.
TI Efficacy of colon propulsion in health and constipation measured by
wireless motility capsules: role of associated IBS and relation to colon
contractile activity
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Meeting Abstract
CT Joint International Meeting for Neurogastroenterology and Motility
CY AUG 26-29, 2010
CL Boston, MA
C1 [Hasler, W. L.; Chey, W. D.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Parkman, H.] Temple Univ, Philadelphia, PA 19122 USA.
[Rao, S.] Univ Iowa, Iowa City, IA USA.
[Mccallum, R.] Texas Tech Univ, El Paso, TX USA.
[Kuo, B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Koch, K.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Sitrin, M.; Semler, J. R.] SUNY Buffalo, SmartPill Corp, Buffalo, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
SU 1
SI SI
MA 25
BP 8
EP 8
PG 1
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA V45OJ
UT WOS:000209825600026
ER
PT J
AU Gourcerol, G
Wu, SV
Yuan, PQ
Miampamba, M
Larauche, M
Sanders, P
Amano, T
Rivier, J
Tache, Y
Million, M
AF Gourcerol, G.
Wu, S. V.
Yuan, P. Q.
Miampamba, M.
Larauche, M.
Sanders, P.
Amano, T.
Rivier, J.
Tache, Y.
Million, M.
TI CRF2 receptor activation blunts stress and CRF-induced colonic motor
function in rodents
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Meeting Abstract
CT Joint International Meeting for Neurogastroenterology and Motility
CY AUG 26-29, 2010
CL Boston, MA
C1 [Gourcerol, G.; Wu, S. V.; Yuan, P. Q.; Miampamba, M.; Larauche, M.; Sanders, P.; Amano, T.; Tache, Y.; Million, M.] Univ Calif Los Angeles, VA Greater Los Angeles Healthcare Syst, CURE Digest Dis Res Ctr, Los Angeles, CA USA.
[Gourcerol, G.; Wu, S. V.; Yuan, P. Q.; Miampamba, M.; Larauche, M.; Sanders, P.; Amano, T.; Tache, Y.; Million, M.] Univ Calif Los Angeles, Dept Med, VA Greater Los Angeles Healthcare Syst, Ctr Neurobiol Stress,Div Digest Dis, Los Angeles, CA 90024 USA.
[Rivier, J.] Salk Inst Biol Studies, Clayton Fdn Labs Peptide Biol, La Jolla, CA 92037 USA.
NR 0
TC 0
Z9 0
U1 0
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PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
SU 1
SI SI
MA 103
BP 31
EP 31
PG 1
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA V45OJ
UT WOS:000209825600103
ER
PT J
AU Ziogas, DC
Wang, Y
Mustafa, S
Tseng, YH
Mcdougal, L
Popov, Y
Schuppan, D
Kokkotou, E
AF Ziogas, D. C.
Wang, Y.
Mustafa, S.
Tseng, Y-H.
Mcdougal, L.
Popov, Y.
Schuppan, D.
Kokkotou, E.
TI Melanin concentrating hormone-immunoneutralization inhibits
colitis-associated intestinal fibrosis
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Meeting Abstract
CT Joint International Meeting for Neurogastroenterology and Motility
CY AUG 26-29, 2010
CL Boston, MA
C1 [Ziogas, D. C.; Wang, Y.; Mustafa, S.; Popov, Y.; Schuppan, D.; Kokkotou, E.] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Boston, MA USA.
[Tseng, Y-H.; Mcdougal, L.] Harvard Med Sch, Joslin Diabet Ctr, Boston, MA USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
SU 1
SI SI
MA 108
BP 32
EP 32
PG 1
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA V45OJ
UT WOS:000209825600108
ER
PT J
AU Brun, R
Staller, K
Viner, S
Kuo, B
AF Brun, R.
Staller, K.
Viner, S.
Kuo, B.
TI Endoscopically assisted water perfusion esophageal manometry with
minimal sedation technique
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Meeting Abstract
CT Joint International Meeting for Neurogastroenterology and Motility
CY AUG 26-29, 2010
CL Boston, MA
C1 [Brun, R.; Staller, K.; Viner, S.; Kuo, B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
SU 1
SI SI
MA 142
BP 42
EP 42
PG 1
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA V45OJ
UT WOS:000209825600142
ER
PT J
AU Staller, K
Brun, R
Viner, S
Kuo, B
AF Staller, K.
Brun, R.
Viner, S.
Kuo, B.
TI Endoscopically assisted water perfusion manometry with minimal sedation:
indications and implication on the clinical management
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Meeting Abstract
CT Joint International Meeting for Neurogastroenterology and Motility
CY AUG 26-29, 2010
CL Boston, MA
C1 [Staller, K.; Brun, R.; Viner, S.; Kuo, B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
SU 1
SI SI
MA 181
BP 52
EP 53
PG 2
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA V45OJ
UT WOS:000209825600181
ER
PT J
AU Michalek, W
Chang, K
Kuo, B
AF Michalek, W.
Chang, K.
Kuo, B.
CA Smartpill Trial Grp
TI Spectral analysis of GI motility comparing various gastric regions
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Meeting Abstract
CT Joint International Meeting for Neurogastroenterology and Motility
CY AUG 26-29, 2010
CL Boston, MA
C1 [Michalek, W.; Chang, K.; Kuo, B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Smartpill Trial Grp] SmartPill Corp, Buffalo, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
SU 1
SI SI
MA 222
BP 64
EP 64
PG 1
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA V45OJ
UT WOS:000209825600222
ER
PT J
AU Michalek, W
Kuo, B
AF Michalek, W.
Kuo, B.
CA Smartpill Trial Grp
TI Analysis of upper GI migrating motor complexes using invasive and
non-invasive techniques
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Meeting Abstract
CT Joint International Meeting for Neurogastroenterology and Motility
CY AUG 26-29, 2010
CL Boston, MA
C1 [Michalek, W.; Kuo, B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Smartpill Trial Grp] SmartPill Corp, Buffalo, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
SU 1
SI SI
MA 223
BP 64
EP 65
PG 2
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA V45OJ
UT WOS:000209825600223
ER
PT J
AU Michalek, W
Parkman, H
Rhode, B
Buckley, P
Powers, J
Semler, J
Kuo, B
AF Michalek, W.
Parkman, H.
Rhode, B.
Buckley, P.
Powers, J.
Semler, J.
Kuo, B.
TI Optimal pressure thresholds for UGI motility assessment: invasive vs
non-invasive techniques
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Meeting Abstract
CT Joint International Meeting for Neurogastroenterology and Motility
CY AUG 26-29, 2010
CL Boston, MA
C1 [Michalek, W.; Kuo, B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Parkman, H.] Temple Univ, Philadelphia, PA 19122 USA.
[Rhode, B.; Semler, J.] SmartPill Corp, Buffalo, NY USA.
[Buckley, P.; Powers, J.] Appl Sci Grp, Buffalo, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
SU 1
SI SI
MA 224
BP 65
EP 65
PG 1
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA V45OJ
UT WOS:000209825600224
ER
PT J
AU Kuo, B
Dassatti, A
Hasheminejad, N
Thurler, A
Rosenblum, J
Kagan, L
Benson, H
Fricchione, G
Denninger, J
Slawsby, EA
Brun, M
Norton, B
Rao, S
Korzenik, JR
AF Kuo, B.
Dassatti, A.
Hasheminejad, N.
Thurler, A.
Rosenblum, J.
Kagan, L.
Benson, H.
Fricchione, G.
Denninger, J.
Slawsby, E. A.
Brun, M.
Norton, B.
Rao, S.
Korzenik, J. R.
TI Impact of a GI Mind Body Intervention (MBI) upon mixed group of patients
with irritable bowel syndrome and inflammatory bowel disease
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Meeting Abstract
CT Joint International Meeting for Neurogastroenterology and Motility
CY AUG 26-29, 2010
CL Boston, MA
C1 [Kuo, B.; Dassatti, A.; Hasheminejad, N.; Thurler, A.; Rosenblum, J.; Kagan, L.; Benson, H.; Fricchione, G.; Denninger, J.; Slawsby, E. A.; Brun, M.; Norton, B.; Rao, S.; Korzenik, J. R.] Massachusetts Gen Hosp, Benson Henry Inst Mind Body Med, GI Unit, Boston, MA 02114 USA.
NR 0
TC 0
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U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
SU 1
SI SI
MA 277
BP 80
EP 80
PG 1
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA V45OJ
UT WOS:000209825600277
ER
PT J
AU Camilleri, M
Thorne, NK
Ringel, Y
Hasler, WL
Kuo, B
Esfandyari, T
Gupta, A
Scott, SM
McCallum, RW
Parkman, HP
Soffer, E
Wilding, GE
Semler, JR
Rao, SSC
AF Camilleri, M.
Thorne, N. K.
Ringel, Y.
Hasler, W. L.
Kuo, B.
Esfandyari, T.
Gupta, A.
Scott, S. M.
McCallum, R. W.
Parkman, H. P.
Soffer, E.
Wilding, G. E.
Semler, J. R.
Rao, S. S. C.
TI Wireless pH-motility capsule for colonic transit: prospective comparison
with radiopaque markers in chronic constipation
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Article
DE colonic transit time; correlation; negative agreement; positive
agreement; radiopaque markers; wireless motility capsule
ID WHOLE GUT TRANSIT; GASTROINTESTINAL PH; CLINICAL-EVALUATION;
HEALTHY-SUBJECTS; MOTOR-ACTIVITY; NORTH-AMERICA; SCINTIGRAPHY; TIMES;
DEFECATION; DISORDERS
AB Background
Colon transit (CT) measurements are used in the management of significant constipation. The radiopaque marker (ROM) method provides limited information.
Methods
We proposed to validate wireless motility capsule (WMC), that measures pH, pressure and temperature, to ROM measurement of CT in patients with symptomatic constipation evaluated at multiple centers. Of 208 patients recruited, 158 eligible patients underwent simultaneous measurement of colonic transit time (CTT) using ROM (Metcalf method, cut off for delay > 67 h), and WMC (cutoff for delay > 59 h). The study was designed to demonstrate substantial equivalence, defined as diagnostic agreement > 65% for patients who had normal or delayed ROM transit.
Key Results
Fifty-nine of 157 patients had delayed ROM CT. Transit results by the two methods differed: ROM median 55.0 h [IQR 31.0-85.0] and WMC (43.5 h [21.7-70.3], P < 0.001. The positive percent agreement between WMC and ROM for delayed transit was similar to 80%; positive agreement in 47 by WMC/59 by ROM or 0.796 (95% CI = 0.67-0.98); agreement vs null hypothesis (65%) P = 0.01. The negative percent agreement (normal transit) was similar to 91%: 89 by WMC/98 by ROM or 0.908 (95% CI = 0.83-0.96); agreement vs null hypothesis (65%), P = 0.00001. Overall device agreement was 87%. There were significant correlations (P < 0.001) between ROM and WMC transit (CTT [r = 0.707] and between ROM and combined small and large bowel transit [r = 0.704]). There were no significant adverse events.
Conclusions & Inferences
The 87% overall agreement (positive and negative) validates WMC relative to ROM in differentiating slow vs normal CT in a multicenter clinical study of constipation.
C1 [Camilleri, M.] Mayo Clin, Coll Med, Rochester, MN 55905 USA.
[Thorne, N. K.] Wake Forest Univ, Med Ctr, Winston Salem, NC USA.
[Ringel, Y.] Univ N Carolina, Med Ctr, Chapel Hill, NC USA.
[Hasler, W. L.] Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA.
[Kuo, B.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Esfandyari, T.] Univ Kansas, Med Ctr, Dept Med, Kansas City, KS 66103 USA.
[Gupta, A.] SUNY Buffalo, VA Med Ctr, Buffalo, NY 14260 USA.
[Scott, S. M.] Queen Mary Univ, London, England.
[McCallum, R. W.] Texas Tech Univ, El Paso, TX USA.
[Parkman, H. P.] Temple Univ, Dept Med, Philadelphia, PA 19122 USA.
[Soffer, E.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Wilding, G. E.] SUNY Buffalo, Dept Biostat, Buffalo, NY 14260 USA.
[Semler, J. R.] SmartPill Corp, Buffalo, NY USA.
[Rao, S. S. C.] Univ Iowa, Dept Med, Iowa City, IA 52242 USA.
RP Camilleri, M (reprint author), Mayo Clin, Coll Med, Charlton 8-110,200 1st St SW, Rochester, MN 55905 USA.
EM camilleri.michael@mayo.edu
FU New York State Foundation for Science, Technology and Innovation;
SmartPill Corporation, Buffalo, New York; National Institutes of Health
[RO1-DK-54681]; SmartPill Corporation
FX The study was supported by a 'New York State Foundation for Science,
Technology and Innovation Grant.' Funding grant support was received by
all study centers from the SmartPill Corporation, Buffalo, New York. Dr.
Camilleri was supported in part by grant RO1-DK-54681 from National
Institutes of Health. The authors acknowledge the excellent contribution
of gastroenterology colleagues at the different medical centers who
helped conduct this study: Ashok Attaluri, MD, University of Iowa;
Shanthini Daniel, MD, Jasper Clinic; Javier Gomez, MD, Temple
University; Otto Linet, MD, Jasper Clinic; Sahar D. Mohammed, MD, Queen
Mary University, London; Suwebatu Odunsi-Shiyanbade, MD, Mayo Clinic;
Irene Sarosiek, MD, Texas Tech University. Clinical Trials.gov
identifier: NCT00857363.; Dr. Camilleri serves as a consultant to
SmartPill Corporation, with compensation to Mayo Clinic, not to him. He
received grant support to participate in this study. Dr. Rao, Dr.
Hasler, Dr. Kuo, Dr. McCallum, Dr Parkman, Dr. Scott, Dr. Wilding serve
as speakers, consultants, or advisory board members for the SmartPill
Corporation. These authors and Dr. Soffer have received research funding
for other research studies from the SmartPill Corporation. Dr. Semler is
an employee of the SmartPill Corporation and owns stock in the SmartPill
Corporation.
NR 41
TC 52
Z9 57
U1 0
U2 17
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD AUG
PY 2010
VL 22
IS 8
BP 874
EP E233
DI 10.1111/j.1365-2982.2010.01517.x
PG 10
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA 622NK
UT WOS:000279670300007
PM 20465593
ER
PT J
AU Ou, WM
Nummenmaa, A
Ahveninen, J
Belliveau, JW
Hamalainen, MS
Golland, P
AF Ou, Wanmei
Nummenmaa, Aapo
Ahveninen, Jyrki
Belliveau, John W.
Haemaelaeinen, Matti S.
Golland, Polina
TI Multimodal functional imaging using fMRI-informed regional EEG/MEG
source estimation
SO NEUROIMAGE
LA English
DT Article
DE EEG; MEG; Inverse solver; fMRI; Expectation-maximization; Re-weighted
minimum-norm estimate
ID HUMAN BRAIN; AUDITORY-CORTEX; BAYESIAN FRAMEWORK;
MAGNETOENCEPHALOGRAPHY; MEG/EEG; INVERSE; LOCALIZATION; ACTIVATION;
ALGORITHM; PATTERN
AB We propose a novel method, fMRI-Informed Regional Estimation (FIRE), which utilizes information from fMRI in E/MEG source reconstruction FIRE takes advantage of the spatial alignment between the neural and the vascular activities. while allowing for substantial differences in their dynamics Furthermore, with a region-based approach, FIRE estimates the model parameters for each region independently Hence, it can be efficiently applied on a dense grid of source locations The optimization procedure at the core of FIRE is related to the re-weighted minimum-norm algorithms The weights in the proposed approach are computed from both the current source estimates and fMRI data, leading to robust estimates in the presence of silent sources in either fMRI or E/MEG measurements We employ a Monte Carlo evaluation procedure to compare the proposed method to several other joint E/MEG-fMRI algorithms Our results show that FIRE provides the best trade-off in estimation accuracy between the spatial and the temporal accuracy Analysis using human E/MEG-fMRI data reveals that FIRE significantly reduces the ambiguities in source localization present in the minimum-norm estimates, and that it accurately captures activation timing in adjacent functional regions (C) 2010 Elsevier Inc. All rights reserved
C1 [Ou, Wanmei; Golland, Polina] MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.
[Nummenmaa, Aapo; Ahveninen, Jyrki; Belliveau, John W.; Haemaelaeinen, Matti S.] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp,Martinos Ctr Biomed Imagin, Boston, MA 02115 USA.
[Nummenmaa, Aapo] Helsinki Univ Technol, Dept Biomed Engn & Computat Sci, FIN-02150 Espoo, Finland.
RP Ou, WM (reprint author), MIT, Comp Sci & Artificial Intelligence Lab, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
RI Hamalainen, Matti/C-8507-2013
FU NIH NIBIB NAMIC [U54-EB005149]; NIH NCRR NAC [P41-RR13218]; NIH NCRR
[P41-RR14075, 5R01-EB006385-03, R01-HD040712, R01-NS037462,
R01-NS048279]; NSF [0642971]; PHS [DA022759-03]; Academy of Finland
[127624]; Finnish Cultural Foundation; Finnish Foundation for Technology
Promotion
FX We thank Dr. Raij and Dr. Siracusa for the stimulating discussions. This
work was supported in part by NIH NIBIB NAMIC U54-EB005149, NIH NCRR NAC
P41-RR13218, NIH NCRR P41-RR14075, 5R01-EB006385-03, R01-HD040712,
R01-NS037462, R01-NS048279, and the NSF CAREER Award 0642971 Wanmer Ou
is partially supported by the PHS training grant DA022759-03. Aapo
Nummenmaa is supported by Academy of Finland (127624), Finnish Cultural
Foundation, and Finnish Foundation for Technology Promotion
NR 42
TC 21
Z9 21
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD AUG 1
PY 2010
VL 52
IS 1
BP 97
EP 108
DI 10.1016/j.neuroimage.2010.03.001
PG 12
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 609EJ
UT WOS:000278637700011
PM 20211266
ER
PT J
AU Agam, Y
Joseph, RM
Barton, JJS
Manoach, DS
AF Agam, Yigal
Joseph, Robert M.
Barton, Jason J. S.
Manoach, Dara S.
TI Reduced cognitive control of response inhibition by the anterior
cingulate cortex in autism spectrum disorders
SO NEUROIMAGE
LA English
DT Article
ID EVENT-RELATED FMRI; POSITRON-EMISSION-TOMOGRAPHY; HIGH-FUNCTIONING
AUTISM; FRONTAL EYE-FIELD; EMOTIONAL PROCESSING DISORDER; ANTISACCADE
TASK-PERFORMANCE; COVERT SPATIAL ATTENTION; SURFACE-BASED ANALYSIS;
EXECUTIVE FUNCTIONS; CORTICAL SURFACE
AB Response inhibition, or the suppression of prepotent, but contextually inappropriate behaviors, is essential to adaptive, flexible responding In autism spectrum disorders (ASD), difficulty inhibiting prepotent behaviors may contribute to restricted, repetitive behavior (RRB) Individuals with ASD consistently show deficient response inhibition while performing antisaccades, which require one to inhibit the prepotent response of looking towards a suddenly appearing stimulus (ie.. a prosaccade), and to substitute a gaze in the opposite direction Here, we used fMRI to identify the neural correlates of this deficit We focused on two regions that are critical for saccadic inhibition the frontal eye field (FEF), the key cortical region for generating volitional saccades, and the dorsal anterior cingulate cortex (dACC), which is thought to exert top-down control on the FEF We also compared ASD and control groups on the functional connectivity of the dACC and FEF during saccadic performance. In the context of an increased antisaccade error rate, ASD participants showed decreased functional connectivity of the FEF and dACC and decreased inhibition-related activation (based on the contrast of antisaccades and prosaccades) in both regions Decreased dACC activation correlated with a higher error rate in both groups, consistent with a role in top-down control. Within the ASD group, increased FEF activation and dACC/FEF functional connectivity were associated with more severe RRB These findings demonstrate functional abnormalities in a circuit critical for volitional ocular motor control in ASD that may contribute to deficient response inhibition and to RRB More generally, our findings suggest reduced cognitive control over behavior by the dACC in ASD (C) 2010 Elsevier Inc All rights reserved
C1 [Agam, Yigal; Manoach, Dara S.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02215 USA.
[Agam, Yigal; Manoach, Dara S.] Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Joseph, Robert M.] Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA.
[Barton, Jason J. S.] Univ British Columbia, Dept Neurol, Vancouver, BC V5Z 1M9, Canada.
[Barton, Jason J. S.] Univ British Columbia, Dept Ophthalmol & Visual Sci, Vancouver, BC V5Z 1M9, Canada.
RP Manoach, DS (reprint author), 149 13th St,Room 2608, Charlestown, MA 02129 USA.
RI Barton, Jason/A-6362-2012
FU National Institute for Mental Health [R01 MH67720]; Mental Illness
Neuroscience Discovery (MIND) Institute [DE-FG02-99ER62764]; National
Center for Research Resources [P41 RR14075]
FX National Institute for Mental Health (R01 MH67720 (DSM); Mental Illness
Neuroscience Discovery (MIND) Institute (DOE DE-FG02-99ER62764), The
National Center for Research Resources (P41 RR14075).
NR 111
TC 80
Z9 85
U1 6
U2 35
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD AUG 1
PY 2010
VL 52
IS 1
BP 336
EP 347
DI 10.1016/j.neuroimage.2010.04.010
PG 12
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 609EJ
UT WOS:000278637700034
PM 20394829
ER
PT J
AU Quant, EC
Wen, PY
AF Quant, Eudocia C.
Wen, Patrick Y.
TI Novel Medical Therapeutics in Glioblastomas, Including Targeted
Molecular Therapies, Current and Future Clinical Trials
SO NEUROIMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE Targeted therapy; Glioblastoma; Tyrosine kinase inhibitors; Clinical
trials
ID EPIDERMAL-GROWTH-FACTOR; PHASE-II TRIAL; BRAIN-TUMOR CONSORTIUM;
BEVACIZUMAB PLUS IRINOTECAN; RECURRENT MALIGNANT GLIOMAS; HIGH-GRADE
GLIOMAS; CANCER STEM-CELLS; POSITRON-EMISSION-TOMOGRAPHY; TYROSINE
KINASE INHIBITOR; SCATTER FACTOR EXPRESSION
AB The prognosis for glioblastoma is poor despite optimal therapy with surgery, radiation, and chemotherapy. New therapies that improve survival and quality of life are needed. Research has increased our understanding of the molecular pathways important for gliomagenesis and disease progression. Novel agents have been developed against these targets, including receptor tyrosine kinases, intracellular signaling molecules, epigenetic abnormalities, and tumor vasculature and microenvironment. This article reviews novel therapies for glioblastoma, with an emphasis on targeted agents.
C1 [Wen, Patrick Y.] Harvard Univ, Sch Med, Div Canc Neurol, Dept Neurol,Brigham & Womens Hosp, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Dana Farber Brigham & Womens Canc Ctr, Boston, MA 02115 USA.
RP Wen, PY (reprint author), Harvard Univ, Sch Med, Div Canc Neurol, Dept Neurol,Brigham & Womens Hosp, Boston, MA 02115 USA.
EM pwen@partners.org
FU Chris Elliott Fund for Glioblastoma Brain Cancer Research
FX We gratefully acknowledge the support of the Chris Elliott Fund for
Glioblastoma Brain Cancer Research.
NR 194
TC 14
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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 1052-5149
EI 1557-9867
J9 NEUROIMAG CLIN N AM
JI Neuroimaging Clin. N. Am.
PD AUG
PY 2010
VL 20
IS 3
BP 425
EP +
DI 10.1016/j.nic.2010.04.007
PG 25
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 649JB
UT WOS:000281763800014
PM 20708556
ER
PT J
AU Ford, JH
Verfaellie, M
Giovanello, KS
AF Ford, Jaclyn Hennessey
Verfaellie, Mieke
Giovanello, Kelly S.
TI Neural correlates of familiarity-based associative retrieval
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE Associative memory; Recollection; Familiarity; Hippocampus; Perirhinal
cortex; Medial temporal lobe; Unitization
ID MEDIAL TEMPORAL-LOBE; RECALL-TO-REJECT; RECOGNITION MEMORY; CONJUNCTION
ERRORS; HIPPOCAMPUS SUPPORTS; PERIRHINAL CORTEX; RELATIONAL MEMORY; ITEM
RECOGNITION; RECOLLECTION; AMNESIA
AB The current study compared the neural correlates of associative retrieval of compound (unitized) stimuli and unrelated (non-unitized) stimuli. Although associative recognition was nearly identical for compounds and unrelated pairs, accurate recognition of these different pair types was associated with activation in distinct regions within the medial temporal lobe (MTL). Recognition of previously presented compound words was associated with left perirhinal activity, whereas recognition of unrelated word pairs was associated with activity in left hippocampus. These results provide evidence that perirhinal cortex mediates familiarity-based associative memory of stimuli unitized at encoding, while the hippocampus is required for recollection-based associative memory. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Ford, Jaclyn Hennessey; Giovanello, Kelly S.] Univ N Carolina, Dept Psychol, Chapel Hill, NC 27599 USA.
[Verfaellie, Mieke] US Dept Vet Affairs, Boston, MA USA.
[Verfaellie, Mieke] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Giovanello, Kelly S.] Univ N Carolina, Biomed Res Imaging Ctr, Chapel Hill, NC 27599 USA.
RP Ford, JH (reprint author), Univ N Carolina, Dept Psychol, Davie Hall,CB 3270, Chapel Hill, NC 27599 USA.
EM Jahennessey@gmail.com
OI Verfaellie, Mieke/0000-0001-5535-4584
FU Medical Research Service of the Department of Veterans Affairs;
[AG028774]; [MH57681]
FX This work was supported by AG028774, MH57681, and the Medical Research
Service of the Department of Veterans Affairs.
NR 50
TC 25
Z9 27
U1 0
U2 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3932
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD AUG
PY 2010
VL 48
IS 10
BP 3019
EP 3025
DI 10.1016/j.neuropsychologia.2010.06.010
PG 7
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 642AU
UT WOS:000281175900023
PM 20547169
ER
PT J
AU Sherva, R
Kranzler, HR
Yu, Y
Logue, MW
Poling, J
Arias, AJ
Anton, RF
Oslin, D
Farrer, LA
Gelernter, J
AF Sherva, Richard
Kranzler, Henry R.
Yu, Yi
Logue, Mark W.
Poling, James
Arias, Albert J.
Anton, Raymond F.
Oslin, David
Farrer, Lindsay A.
Gelernter, Joel
TI Variation in Nicotinic Acetylcholine Receptor Genes is Associated with
Multiple Substance Dependence Phenotypes
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE genetic association; substance dependence; nicotinic acetylcholine
receptors
ID GENOME-WIDE ASSOCIATION; POPULATION-BASED SAMPLE; LUNG-CANCER;
SUSCEPTIBILITY LOCUS; EUROPEAN-AMERICANS; AFRICAN-AMERICANS; MALE TWINS;
SMOKING; RISK; LINKAGE
AB There is shared genetic risk for dependence on multiple substances, and the nicotinic receptor gene cluster on chromosome 15 harbors multiple polymorphisms that associate to this risk. Here, we report the results of an association study with 21 SNPs genotyped across the CHRNA5, CHRNA3, and CHRNB4 loci on chromosome 15q25.1. The sample consists of a discovery set (N = 1858) of European-American and African-American (AA) families, ascertained on the basis of a sibling pair with cocaine and/or opioid dependence, and a case-control replication sample (N = 3388) collected for association studies of alcohol, cocaine, and opioid dependence. We tested the SNPs for association with lifetime cocaine, opioid, nicotine, and alcohol dependence. We replicated several previous findings, including associations between rs16969968 and nicotine dependence (P = 0.002) and cocaine dependence (P = 0.02), with opposite risk alleles for each substance. We observed these associations in AAs, which is a novel finding. The strongest association signal in either sample was between rs684513 in CHRNA5 and cocaine dependence (OR = 1.43, P = 0.0004) in the AA replication set. We also observed two SNPs associated with alcohol dependence, that is, rs615470 in CHRNA5 (OR = 0.77, P = 0.0006) and rs578776 (OR = 0.78, P = 0.001). The associations between CD and rs684513, AD and rs615470, and AD and rs578776 remained significant after a permutation-based correction for multiple testing. These data reinforce the importance of variation in the chromosome 15 nicotinic receptor subunit gene cluster for risk of dependence on multiple substances, although the direction of the effects may vary across substances. Neuropsychopharmacology (2010) 35, 1921-1931; doi: 10.1038/npp.2010.64; published online 19 May 2010
C1 [Sherva, Richard; Yu, Yi; Logue, Mark W.; Farrer, Lindsay A.] Boston Univ, Sch Med, Dept Med, Genet Program, Boston, MA 02118 USA.
[Kranzler, Henry R.; Arias, Albert J.] Univ Connecticut, Dept Psychiat, Sch Med, Farmington, CT 06107 USA.
[Kranzler, Henry R.; Arias, Albert J.] Univ Connecticut, Sch Med, Dept Genet & Dev Biol, Farmington, CT USA.
[Poling, James; Gelernter, Joel] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Poling, James; Gelernter, Joel] VA CT Healthcare Syst, West Haven, CT USA.
[Anton, Raymond F.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA.
[Oslin, David] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA.
[Oslin, David] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
[Farrer, Lindsay A.] Boston Univ, Sch Med, Dept Neurol, Boston, MA 02118 USA.
[Farrer, Lindsay A.] Boston Univ, Sch Med, Dept Genet & Genom, Boston, MA 02118 USA.
[Farrer, Lindsay A.] Boston Univ, Sch Med, Dept Biostat, Boston, MA 02118 USA.
[Farrer, Lindsay A.] Boston Univ, Sch Med, Dept Epidemiol, Boston, MA 02118 USA.
[Farrer, Lindsay A.] Boston Univ, Sch Publ Hlth, Dept Neurol, Boston, MA USA.
[Farrer, Lindsay A.] Boston Univ, Sch Publ Hlth, Dept Genet & Genom, Boston, MA USA.
[Farrer, Lindsay A.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Farrer, Lindsay A.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Gelernter, Joel] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT USA.
[Gelernter, Joel] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA.
RP Gelernter, J (reprint author), Yale Univ, Sch Med, VA CT Healthcare Ctr 116A2, 950 Campbell Ave, West Haven, CT 06516 USA.
EM joel.gelernter@yale.edu
RI Arias, Albert/H-1334-2011;
OI Logue, Mark/0000-0001-9347-7892; Farrer, Lindsay/0000-0001-5533-4225;
Poling, James/0000-0002-0133-3136
FU NIDA [R01 DA12690, R01 DA12849, R01 DA018432, K24 DA22288]; NIAAA [R01
AA11330, K24 AA013736, P50 AA12870, K05 AA017435]; NCRR [M01 RR06192];
VA CT MIRECC Center; Bristol-Myers Squibb Company; Merck Co.;
Ortho-McNeil Pharmaceuticals; Eli Lilly; Merck; Hythiam; Johnson
Johnson; Janssen; Schering Plough; Lundbeck; Alkermes; GlaxoSmithKline;
Abbott; ACTIVE
FX We thank John Farrell and Michael Jervis for database management support
and An Marie Lacobelle for technical assistance. This work was supported
by NIDA grants R01 DA12690, R01 DA12849, R01 DA018432, and K24 DA22288,
NIAAA grants R01 AA11330, K24 AA013736, P50 AA12870, and K05 AA017435,
and NCRR grant M01 RR06192, and the VA CT MIRECC Center.; Dr Gelernter
reports that he has received compensation for professional services in
the previous 3 years from the following entities: the Yale University
School of Medicine, Veterans Affairs Healthcare System (VA) and the
National Institutes of Health (NIAAA, NIDA, and NIMH) and related to
academic lectures and editorial functions in various scientific venues
(including the ACNP). Dr Kranzler has received compensation for
professional services from the National Institutes of Health (NIAAA and
NIDA) and for academic lectures and editorial functions in various
scientific venues (including the ACNP). Dr Kranzler also reports
consulting arrangements with Alkermes, Elbion Pharmaceuticals,
Ortho-McNeil Pharmaceuticals, Sanofi-Aventis Pharmaceuticals, and Solvay
Pharmaceuticals, and research support from Bristol-Myers Squibb Company,
Merck & Co., and Ortho-McNeil Pharmaceuticals. Dr Anton reports the
following: being a consultant for Sanofi-Aventis, Eli Lilly, Merck,
Organon, Hythiam, Novartis, Johnson & Johnson, and GlaxoSmithKline;
serving on an Advisory Board for Solvay, Hythiam, Novartis, and Johnson
& Johnson, and receiving grant support from Eli Lilly, Merck, Hythiam,
and Johnson & Johnson. Dr Anton and Dr Kranzler also report having
associations with the following pharmaceutical companies: Eli Lilly,
Janssen, Schering Plough, Lundbeck, Alkermes, GlaxoSmithKline, Abbott,
and Johnson & Johnson, as these companies provide support to the Alcohol
Clinical Trials Initiative (ACTIVE) and both Dr Kranzler and Dr Anton
receive support from ACTIVE. These disclosures do not hold any influence
on the content of this paper.
NR 37
TC 53
Z9 53
U1 2
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD AUG
PY 2010
VL 35
IS 9
BP 1921
EP 1931
DI 10.1038/npp.2010.64
PG 11
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 625VQ
UT WOS:000279924400010
PM 20485328
ER
PT J
AU Mian, MK
Campos, M
Sheth, SA
Eskandar, EN
AF Mian, Matthew K.
Campos, Michael
Sheth, Sameer A.
Eskandar, Emad N.
TI Deep brain stimulation for obsessive-compulsive disorder: past, present,
and future
SO NEUROSURGICAL FOCUS
LA English
DT Article
DE deep brain stimulation; obsessive-compulsive disorder; psychiatric
neurosurgery; ventral striatum; subthalamic nucleus
ID SUBTHALAMIC NUCLEUS STIMULATION; INFERIOR THALAMIC PEDUNCLE;
ELECTRICAL-STIMULATION; PARKINSONS-DISEASE; NEUROSURGICAL TREATMENT;
MAJOR DEPRESSION; LONG-TERM; ORBITOFRONTAL CORTEX; CAPSULAR STIMULATION;
DECISION-MAKING
AB Obsessive-compulsive disorder (OCD) is a psychiatric illness that can lead to chronic functional impairment. Some patients with severe, chronic OCD have been treated with ablative neurosurgical techniques over the past 4 decades. More recently, deep brain stimulation (DBS) has been investigated as a therapy for refractory OCD, and the procedure was granted a limited humanitarian device exemption by the FDA in 2009. In this article, the authors review the development of DBS for OCD, describe the current understanding of the pathophysiological mechanisms of the disorder and how the underlying neural circuits might be modulated by DBS, and discuss the clinical studies that provide evidence for the use of this evolving therapy. The authors conclude with suggestions for how a combined basic science and translational research approach could drive the understanding of the neural mechanisms underlying OCD as well as the clinical effectiveness of DBS in the setting of recalcitrant disease. (DOI: 10.3171/2010.4.FOCUS10107)
C1 [Mian, Matthew K.; Campos, Michael; Sheth, Sameer A.; Eskandar, Emad N.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Mian, Matthew K.; Campos, Michael; Eskandar, Emad N.] Harvard Univ, Sch Med, Boston, MA USA.
RP Eskandar, EN (reprint author), Massachusetts Gen Hosp, Dept Neurosurg, 55 Fruit St,GRB 502, Boston, MA 02114 USA.
EM eeskandar@partners.org
FU National Eye Institute [1R01EY017658-01]; National Institute on Drug
Abuse [1R01NS063249]; National Institute of Mental Health [P50
MH086400-03]; National Science Foundation [IOB 0645886]; Howard Hughes
Medical Institute; National Institute for Neurological Disorders and
Stroke [R25 NS065743]
FX The following funding was received: National Eye Institute (Grant No.
1R01EY017658-01) to Dr. Eskandar as principal investigator; National
Institute on Drug Abuse (Grant No. 1R01NS063249) to Dr. Eskandar as
principal investigator; National Institute of Mental Health (Grant No.
P50 MH086400-03) to Dr. Eskandar as co-investigator; National Science
Foundation (Grant No. IOB 0645886) to Dr. Eskandar as principal
investigator; Howard Hughes Medical Institute (Physician Scientist Early
Career Award) to Dr. Eskandar as principal investigator; and National
Institute for Neurological Disorders and Stroke (Grant No. R25 NS065743)
to Dr. Sheth as fellow. None of the contents of this manuscript have
been previously submitted for publication or presentation. The authors
report no conflict of interest.
NR 84
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Z9 33
U1 4
U2 16
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 1092-0684
J9 NEUROSURG FOCUS
JI Neurosurg. Focus
PD AUG
PY 2010
VL 29
IS 2
AR E10
DI 10.3171/2010.4.FOCUS10107
PG 9
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 675CJ
UT WOS:000283802400011
PM 20672912
ER
PT J
AU Abolmaali, K
Rhoads, D
Tavakkolizadeh, A
AF Abolmaali, Kamran
Rhoads, David B.
Tavakkolizadeh, Alil
TI Potential Role Of Bilio-Pancreatic Limb On Intestinal Sweetness Sensing
Following Gastric Bypass Surgery
SO OBESITY SURGERY
LA English
DT Meeting Abstract
CT 15th World Congress of International Federation for the Surgery of
Obesity and Metabolic Disorders (IFSO)
CY SEP 03-07, 2010
CL Amer Soc Metabolic Bariatric Surg, Long Beach, CA
HO Amer Soc Metabolic Bariatric Surg
C1 [Abolmaali, Kamran; Tavakkolizadeh, Alil] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Rhoads, David B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0960-8923
J9 OBES SURG
JI Obes. Surg.
PD AUG
PY 2010
VL 20
IS 8
BP 982
EP 982
PG 1
WC Surgery
SC Surgery
GA 636OD
UT WOS:000280746100012
ER
PT J
AU Wisbach, G
Pratt, JS
AF Wisbach, Gordon
Pratt, Janey S.
TI Laparoscopic Gastric Bypass Technique Using Anterior Approach To
Ligament Of Treitz
SO OBESITY SURGERY
LA English
DT Meeting Abstract
CT 15th World Congress of International Federation for the Surgery of
Obesity and Metabolic Disorders (IFSO)
CY SEP 03-07, 2010
CL Amer Soc Metabolic Bariatric Surg, Long Beach, CA
HO Amer Soc Metabolic Bariatric Surg
C1 [Wisbach, Gordon] USN, Med Ctr, San Diego, CA 92152 USA.
[Pratt, Janey S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0960-8923
J9 OBES SURG
JI Obes. Surg.
PD AUG
PY 2010
VL 20
IS 8
BP 1026
EP 1026
PG 1
WC Surgery
SC Surgery
GA 636OD
UT WOS:000280746100142
ER
PT J
AU Colwell, AS
AF Colwell, Amy S.
TI Current Concepts in Post-bariatric Body Contouring
SO OBESITY SURGERY
LA English
DT Article
DE Massive weight loss; Body contouring; Panniculectomy
ID MASSIVE WEIGHT-LOSS; SURGERY; FLAP
AB Background The advent of bariatric surgery has led to a new subspecialty in plastic surgery for contouring the skin and fat remaining after massive weight loss. This field is increasingly recognized as a vital component to the multi-disciplinary treatment approach to care for the obese patient. The author sought to review key concepts in patient selection, technical advancements, and postoperative care in body contouring following weight loss surgery.
Methods A literature review in PubMed identified articles relevant to the care of massive weight loss patients presenting for plastic surgical contouring. These articles were combined with a retrospective review of the author's personal experience in management of these patients.
Results The best candidates for post-bariatric plastic surgery are those who have achieved weight loss stability with a BMI of 35 or less and who have adequate nutrition to heal the surgical excisions. Truncal deformity is the most common presenting complaint of massive weight loss patients, and the procedure of choice to address this region is a lower body lift. Post-operative care focuses on patient safety prioritizing in DVT prophylaxis and seroma prevention.
Conclusions Bariatric procedures routinely achieve sustained decreases in body mass index; however, the remaining skin in the massive-weight-loss patient serves as a reminder of their previous obese existence. Post-bariatric body contouring aims to correct this deformity and restore a sense of normalcy. By reshaping the body into its ideal proportions, the true success of the weight loss surgery is fully realized.
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Plast Surg, Boston, MA 02114 USA.
RP Colwell, AS (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Plast Surg, 15 Parkman St WACC 435, Boston, MA 02114 USA.
EM acolwell@partners.org
NR 5
TC 18
Z9 18
U1 1
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0960-8923
J9 OBES SURG
JI Obes. Surg.
PD AUG
PY 2010
VL 20
IS 8
BP 1178
EP 1182
DI 10.1007/s11695-010-0120-4
PG 5
WC Surgery
SC Surgery
GA 636OD
UT WOS:000280746100315
PM 20349284
ER
PT J
AU Russell, M
Mendes, N
Miller, KK
Rosen, CJ
Lee, H
Klibanski, A
Misra, M
AF Russell, Melissa
Mendes, Nara
Miller, Karen K.
Rosen, Clifford J.
Lee, Hang
Klibanski, Anne
Misra, Madhusmita
TI Visceral Fat Is a Negative Predictor of Bone Density Measures in Obese
Adolescent Girls
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
AB The accumulation of adipose tissue in 2 regional fat depots, visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT), have a differential impact on bone mineral density (BMD). In most studies, a positive association of SAT with bone density has been reported. There are conflicting data on the effect of VAT on bone. One recent study suggested that VAT was a negative and SAT a positive predictor of bone structural parameters in young adults. Various chemicals secreted from VAT and SAT appear to mediate these associations with bone but there is a limited knowledge of their role. Potential mediators include inflammatory cytokines such as IL-6, soluble intercellular adhesion molecules such as E-selectin, and adipokine hormones such as adiponectin and leptin. IL-6 and adiponectin can increase osteoclast activity and appear to have deleterious effects on BMD. In a previous report, VAT was an independent predictor of E-selectin and soluble intercellular adhesion molecule 1 (sICAM1), whereas SAT was a predictor of IL-6, and both SAT and VAT predicted adiponectin levels. Other studies have shown that VAT is an important determinant of levels of sICAM1 and E-selectin in obese and normal-weight girls.
This cross-sectional study investigated associations of VAT and SAT and potential chemical mediators with BMD in adolescent obese and normal-weight girls. The investigators tested the hypothesis that adolescent girls with a greater VAT to SAT ratio would have lower bone density measures mediated by inflammatory cytokines, adiponectin, and leptin. Fifteen obese girls 12 to 18 years old were matched to 15 normal-weight controls for race, ethnicity, and bone age (within 2 year). Magnetic resonance imaging was used to measure SAT and VAT at the lumbar level. Dual-energy x-ray absorptiometry assessed bone density at the spine, hip, and whole body. Fasting serum levels of leptin, adiponectin, E-selectin, sICAM, and IL-6 were determined.
The mean body mass index SD score was higher in obese subjects than in controls (3.7 +/- 1.5 versus 0.1 +/- 0.4 kg/m(2)). After controlling for SAT, VAT was a negative predictor of whole-body BMD and bone mineral content/height in the whole group, and of BMD, bone mineral apparent density, whole-body BMD, and bone mineral content/height in obese girls. As hypothesized, obese girls with the highest VAT to SAT ratio had the lowest bone density measures. E-selectin and adiponectin were negative predictors for BMD, and leptin was a positive predictor in a regression model including VAT/SAT, adipokines, and cytokines.
These findings indicate that VAT is a negative predictor of bone density in obese girls. Pro-inflammatory adhesion molecules such as E-selectin and adipokines such as adiponectin and leptin appear to mediate the association between VAT and bone density.
C1 [Russell, Melissa] Massachusetts Gen Hosp, Neuroendocrine Unit, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Pediat Endocrine Unit, Mass Gen Hosp Children, Boston, MA USA.
Harvard Univ, Sch Med, Boston, MA USA.
Harvard Catalyst, Biostat Core, Boston, MA USA.
Maine Med Ctr Res Inst, Scarborough, ME USA.
RP Russell, M (reprint author), Massachusetts Gen Hosp, Neuroendocrine Unit, Boston, MA 02114 USA.
RI Mendes Estella, Nara/E-4682-2013; Mendes Estella, Nara/A-1469-2015
NR 0
TC 0
Z9 0
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7828
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD AUG
PY 2010
VL 65
IS 8
BP 505
EP 507
DI 10.1097/OGX.0b013e3181f07b98
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 668JN
UT WOS:000283264700016
ER
PT J
AU Benacerraf, BR
Shipp, TD
Lyons, JG
Bromley, B
AF Benacerraf, Beryl R.
Shipp, Thomas D.
Lyons, Jennifer G.
Bromley, Bryann
TI Width of the Normal Uterine Cavity in Premenopausal Women and Effect of
Parity
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID UTERUS; VOLUME
AB OBJECTIVE: To estimate the width of the normal uterine cavity at the fundus and evaluate its relationship to parity, gravidity, prior cesarean delivery, uterine volume, and patient age.
METHODS: From September 1, 2009, to November 10, 2009, all premenopausal patients aged 50 years or younger who had a normal uterus by ultrasonography were included in the study. Standard measurements of the outer aspect of the uterus as well as two three-dimensional volumes of the uterus (one transverse and the other longitudinal) were done at the time of the scan. These volumes were manipulated retrospectively to obtain the coronal view of the uterine cavity. Using electronic calipers on the picture archiving and communication system, a network with a server that stores electronic images in an ultrasonography or imaging practice, the width of the uterine cavity was measured on each volume. The width of the uterine cavity was then correlated with patient gravidity, parity, previous cesarean delivery, calculated uterine volume, endometrial echo, and age.
RESULTS: The width of the uterine cavity enlarges significantly with increasing gravidity or parity. The width of the uterine cavity ranged from a mean of 27 mm in nulliparous women to 32 mm in those with more than one pregnancy. There was a strong correlation between the width of the uterine cavity and the overall uterine volume as well as width of the endometrial echo (P < .001). There was no appreciable relationship between prior cesarean delivery and width of the uterine cavity nor between patient age and the width of the uterine cavity in patients who were never pregnant. In the absence of other variables, the patients on oral contraceptives had smaller uterine cavities compared with those not on hormones (P = .016).
CONCLUSION: We have produced a standard for the measurement of the normal uterine cavity width and have shown that this width varies with gravidity and parity. The mean width of the uterine cavity of nulliparous women (27 mm) is narrower than the width of a standard intrauterine device (32 mm), suggesting that physicians should consider ultrasonography to measure the uterine cavity before inserting an intrauterine device.
C1 Brigham & Womens Hosp, Dept Obstet & Gynecol, Boston, MA 02115 USA.
Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Obstet & Gynecol, Boston, MA USA.
Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA USA.
RP Benacerraf, BR (reprint author), 333 Longwood Ave,Suite 400, Boston, MA 02115 USA.
EM berylbenacerraf@post.harvard.edu
NR 5
TC 10
Z9 10
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD AUG
PY 2010
VL 116
IS 2
BP 305
EP 310
DI 10.1097/AOG.0b013e3181e6cc10
PN 1
PG 6
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 629HI
UT WOS:000280186300009
PM 20664389
ER
PT J
AU Shifren, JL
Schiff, I
AF Shifren, Jan L.
Schiff, Isaac
TI Role of Hormone Therapy in the Management of Menopause Reply
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Letter
C1 [Shifren, Jan L.] Massachusetts Gen Hosp, Vincent Menopause Program, Boston, MA 02114 USA.
[Shifren, Jan L.; Schiff, Isaac] Harvard Univ, Sch Med, Dept Obstet Gynecol & Reprod Biol, Boston, MA 02115 USA.
[Schiff, Isaac] Massachusetts Gen Hosp, Vincent Mem Gynecol Serv, Boston, MA 02114 USA.
RP Shifren, JL (reprint author), Massachusetts Gen Hosp, Vincent Menopause Program, Boston, MA 02114 USA.
NR 1
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD AUG
PY 2010
VL 116
IS 2
BP 442
EP 443
DI 10.1097/AOG.0b013e3181eb00c5
PN 1
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 629HI
UT WOS:000280186300035
ER
PT J
AU Ciralsky, J
Papaliodis, GN
Foster, CS
Dohlman, CH
Chodosh, J
AF Ciralsky, Jessica
Papaliodis, George N.
Foster, C. Stephen
Dohlman, Claes H.
Chodosh, James
TI Keratoprosthesis in Autoimmune Disease
SO OCULAR IMMUNOLOGY AND INFLAMMATION
LA English
DT Article
DE autoimmune disease; keratoprosthesis; mucous membrane pemphigoid;
Stevens-Johnson syndrome
ID TOXIC EPIDERMAL NECROLYSIS; STEVENS-JOHNSON-SYNDROME; BOSTON TYPE-1
KERATOPROSTHESIS; TOTAL JOINT ARTHROPLASTY; BONE-CEMENT; CYTOKINES; HIP;
POLYMETHYLMETHACRYLATE; PERSPECTIVE; MANAGEMENT
AB Purpose: To describe the clinical features and course of 2 patients with autoimmune diseases and their experience with the Boston keratoprosthesis. To draw on general medical literature to try to better understand recurrent complications.
Methods: Retrospective review of 2 patients treated with Boston keratoprostheses. The clinical histories, examinations, and other diagnostics were reviewed. A literature review was performed.
Results: The first patient presented with end-stage ocular disease secondary to toxic epidermal necrolysis (TENS). The second patient presented with end-stage ocular disease secondary to mucous membrane pemphigoid (MMP). Both patients underwent treatment with the Boston keratoprosthesis. Both patients suffered numerous corneal melts requiring multiple repeat implantations.
Conclusions: Patients with corneal blindness secondary to autoimmune disease often fare poorly with available surgical treatments. Study of existing literature on prosthetic device complications in autoimmune diseases may help uncover common mechanisms of tissue destruction to establish perioperative immunomodulatory regimens targeted to specific underlying diseases.
C1 [Ciralsky, Jessica; Papaliodis, George N.; Dohlman, Claes H.; Chodosh, James] Harvard Univ, Sch Med, Dept Ophthalmol, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Foster, C. Stephen] Massachusetts Eye Res & Surg Inst, Cambridge, MA USA.
RP Chodosh, J (reprint author), Harvard Univ, Sch Med, Dept Ophthalmol, Massachusetts Eye & Ear Infirm, 243 Charles St, Boston, MA 02114 USA.
EM james_chodosh@meei.harvard.edu
FU Research to Prevent Blindness, NY, NY
FX Supported in part by an unrestricted grant to the Department of
Ophthalmology, Harvard Medical School, from Research to Prevent
Blindness, NY, NY.
NR 38
TC 19
Z9 19
U1 0
U2 2
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 0927-3948
J9 OCUL IMMUNOL INFLAMM
JI Ocul. Immunol. Inflamm.
PD AUG
PY 2010
VL 18
IS 4
BP 275
EP 280
DI 10.3109/09273941003682300
PG 6
WC Ophthalmology
SC Ophthalmology
GA 638ZD
UT WOS:000280939000007
PM 20662659
ER
PT J
AU Singh, A
Settleman, J
AF Singh, A.
Settleman, J.
TI EMT, cancer stem cells and drug resistance: an emerging axis of evil in
the war on cancer
SO ONCOGENE
LA English
DT Review
DE EMT; cancer; cancer stem cells; drug resistance
ID EPITHELIAL-MESENCHYMAL TRANSITION; TUMOR-INITIATING CELLS; ACUTE
MYELOID-LEUKEMIA; GENE-EXPRESSION SIGNATURE; BREAST-CANCER; TGF-BETA;
MIR-200 FAMILY; LUNG-CANCER; E-CADHERIN; PANCREATIC-CANCER
AB Tumors are cellularly and molecularly heterogeneous, with subsets of undifferentiated cancer cells exhibiting stem cell-like features (CSCs). Epithelial to mesenchymal transitions (EMT) are transdifferentiation programs that are required for tissue morphogenesis during embryonic development. The EMT process can be regulated by a diverse array of cytokines and growth factors, such as transforming growth factor (TGF)-beta, whose activities are dysregulated during malignant tumor progression. Thus, EMT induction in cancer cells results in the acquisition of invasive and metastatic properties. Recent reports indicate that the emergence of CSCs occurs in part as a result of EMT, for example, through cues from tumor stromal components. Recent evidence now indicates that EMT of tumor cells not only causes increased metastasis, but also contributes to drug resistance. In this review, we will provide potential mechanistic explanations for the association between EMT induction and the emergence of CSCs. We will also highlight recent studies implicating the function of TGF-beta-regulated noncoding RNAs in driving EMT and promoting CSC self-renewal. Finally we will discuss how EMT and CSCs may contribute to drug resistance, as well as therapeutic strategies to overcome this clinically. Oncogene (2010) 29, 4741-4751; doi: 10.1038/onc.2010.215; published online 7 June 2010
C1 [Settleman, J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Med,Canc Ctr, Charlestown, MA 02129 USA.
RP Settleman, J (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Med,Canc Ctr, 149 13th St, Charlestown, MA 02129 USA.
EM settleman@HELIX.MGH.HARVARD.EDU
RI Singh, Anurag/C-7347-2014
OI Singh, Anurag/0000-0003-4705-8683
FU NCI NIH HHS [K99 CA149169, K99 CA149169-01, K99 CA149169-02, R00
CA149169]
NR 102
TC 862
Z9 904
U1 81
U2 319
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD AUG
PY 2010
VL 29
IS 34
BP 4741
EP 4751
DI 10.1038/onc.2010.215
PG 11
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 643VB
UT WOS:000281326400001
PM 20531305
ER
PT J
AU Hassett, MJ
AF Hassett, Michael J.
TI The Full Burden of Cancer
SO ONCOLOGIST
LA English
DT Editorial Material
ID PATIENT NAVIGATION
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Hassett, MJ (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM michael_hassett@dfci.harvard.edu
NR 9
TC 4
Z9 5
U1 0
U2 0
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
J9 ONCOLOGIST
JI Oncologist
PD AUG
PY 2010
VL 15
IS 8
BP 793
EP 795
DI 10.1634/theoncologist.2010-0211
PG 3
WC Oncology
SC Oncology
GA 647FN
UT WOS:000281603300001
PM 20667965
ER
PT J
AU King, LY
Chung, RT
AF King, Lindsay Y.
Chung, Raymond T.
TI When Treating Cancer, Please Don't Forget Hepatitis B
SO ONCOLOGIST
LA English
DT Article
DE Hepatitis B; Reactivation; Chemotherapy; HBV
ID VIRUS REACTIVATION; CYTOTOXIC CHEMOTHERAPY; HBV REACTIVATION;
RISK-FACTORS; LAMIVUDINE; THERAPY; PREVENTION; MANAGEMENT; INFECTION;
CARRIERS
C1 [Chung, Raymond T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[King, Lindsay Y.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[King, Lindsay Y.; Chung, Raymond T.] Harvard Univ, Sch Med, Boston, MA USA.
RP Chung, RT (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Warren 1007C,55 Fruit St, Boston, MA 02114 USA.
EM rtchung@partners.org
NR 24
TC 3
Z9 3
U1 0
U2 1
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
J9 ONCOLOGIST
JI Oncologist
PD AUG
PY 2010
VL 15
IS 8
BP 826
EP 829
DI 10.1634/theoncologist.2009-0282
PG 4
WC Oncology
SC Oncology
GA 647FN
UT WOS:000281603300006
PM 20647389
ER
PT J
AU Willett, CG
Duda, DG
Ancukiewicz, M
Shah, M
Czito, BG
Bentley, R
Poleski, M
Fujita, H
Lauwers, GY
Carroll, M
Tyler, D
Mantyh, C
Shellito, P
Chung, DC
Clark, JW
Jain, RK
AF Willett, Christopher G.
Duda, Dan G.
Ancukiewicz, Marek
Shah, Mira
Czito, Brian G.
Bentley, Rex
Poleski, Martin
Fujita, Hiroshi
Lauwers, Gregory Y.
Carroll, Madeline
Tyler, Douglas
Mantyh, Christopher
Shellito, Paul
Chung, Daniel C.
Clark, Jeffrey W.
Jain, Rakesh K.
TI A Safety and Survival Analysis of Neoadjuvant Bevacizumab with Standard
Chemoradiation in a Phase I/II Study Compared with Standard
Chemoradiation in Locally Advanced Rectal Cancer
SO ONCOLOGIST
LA English
DT Article
DE Bevacizumab; Neoadjuvant; Rectal cancer; Chemoradiation; Toxicity
ID METASTATIC COLORECTAL-CANCER; ANTIANGIOGENIC THERAPY; TUMOR
ANGIOGENESIS; VEGF; FLUOROURACIL; LEUCOVORIN
AB Introduction. Bevacizumab is increasingly being tested with neoadjuvant regimens in patients with localized cancer, but its effects on metastasis and survival remain unknown. This study examines the long-term outcome of clinical stage II/III rectal cancer patients treated in a prospective phase II study of bevacizumab with chemoradiation and surgery. As a benchmark, we used data from an analysis of 42 patients with locally advanced rectal cancer treated with a contemporary approach of preoperative fluoropyrimidine-based radiation therapy.
Materials and Methods. Outcome analyses were performed on 32 patients treated prospectively with neoadjuvant bevacizumab, 5-fluorouracil, radiation therapy, and surgery as well as 42 patients treated with standard fluoropyrimidine-based chemoradiation.
Results. Overall survival, disease-free survival, and local control showed favorable trends in patients treated with bevacizumab with chemoradiation followed by surgery. Acute and postoperative toxicity appeared acceptable.
Conclusions. Neoadjuvant bevacizumab with standard chemoradiation and surgery shows promising long-term efficacy and safety profiles in locally advanced rectal cancer patients. The Oncologist 2010;15:845-851
C1 [Willett, Christopher G.; Shah, Mira; Czito, Brian G.; Carroll, Madeline] Duke Univ, Med Ctr, Dept Radiat Oncol, Durham, NC 27710 USA.
[Bentley, Rex] Duke Univ, Med Ctr, Dept Pathol, Durham, NC 27710 USA.
[Poleski, Martin; Tyler, Douglas; Mantyh, Christopher] Duke Univ, Med Ctr, Dept Med & Surg, Durham, NC 27710 USA.
[Duda, Dan G.; Ancukiewicz, Marek; Jain, Rakesh K.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Fujita, Hiroshi; Lauwers, Gregory Y.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Shellito, Paul] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Chung, Daniel C.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Clark, Jeffrey W.] Massachusetts Gen Hosp, Dept Hematol Oncol, Boston, MA 02114 USA.
RP Willett, CG (reprint author), Duke Univ, Med Ctr, Dept Radiat Oncol, Durham, NC 27710 USA.
EM christopher.willett@duke.edu; jain@steele.mgh.harvard.edu
FU NIH [R21-CA99237, P01-CA80124, R01-CA115767, R01-CA85140, R01-CA126642];
Federal Share/NCI; National Foundation for Cancer Research; Genentech;
Dyax; AstraZeneca
FX This study was partially supported by NIH grants R21-CA99237,
P01-CA80124, R01-CA115767, R01-CA85140, and R01-CA126642 and Federal
Share/NCI Proton Beam Program Income grants, and by the National
Foundation for Cancer Research.; Disclosures: Christopher G. Willett:
Honoraria: Roche; Dan G. Duda: None; Marek Ancukiewicz: None; Mira Shah:
None; Brian G. Czito: Research funding/contracted research: Genentech;
Rex Bentley: None; Martin Poleski: None; Hiroshi Fujita: None; Gregory
Y. Lauwers: None; Madeline Carroll: None; Douglas Tyler: None;
Christopher Mantyh: None; Paul Shellito: None; Daniel C. Chung: None;
Jeffrey W. Clark: None; Rakesh K. Jain: Consultant/advisory role:
Millennium, Dyax, AstraZeneca, Regeneron, SynDevRx (uncompensated);
Honoraria: Pfizer (honorarium for lecture); Research funding/contracted
research: Dyax, AstraZeneca; Ownership interest: SynDevRx.
NR 17
TC 29
Z9 30
U1 0
U2 0
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD AUG
PY 2010
VL 15
IS 8
BP 845
EP 851
DI 10.1634/theoncologist.2010-0030
PG 7
WC Oncology
SC Oncology
GA 647FN
UT WOS:000281603300009
PM 20667969
ER
PT J
AU Rauh-Hain, JA
del Carmen, MG
AF Rauh-Hain, J. Alejandro
del Carmen, Marcela G.
TI Treatment for Advanced and Recurrent Endometrial Carcinoma: Combined
Modalities
SO ONCOLOGIST
LA English
DT Article
DE Endometrial cancer; Radiation; Chemotherapy; Hormonal therapy
ID GYNECOLOGIC-ONCOLOGY-GROUP; MALIGNANT PERITONEAL CYTOLOGY; ISOLATED
VAGINAL RECURRENCES; PHASE-III TRIAL; MEDROXYPROGESTERONE ACETATE;
CYTOREDUCTIVE SURGERY; RADIATION-THERAPY; STAGE-IV; INTERSTITIAL
BRACHYTHERAPY; POSTOPERATIVE RADIOTHERAPY
AB Women with recurrent or advanced endometrial cancer constitute a heterogeneous group of patients. Depending on previous treatment, women with recurrent endometrial cancer may be appropriate candidates for surgery, radiation therapy, hormonal therapy, or chemotherapy. Women with advanced stage disease at presentation may also be appropriate candidates for systemic and local therapies. We review the treatment options available to treat recurrent and locally advanced endometrial cancer.
Treatment choice depends largely on the localization of disease, the patient's performance status and previous treatment history, as well the tumor's hormonal receptor status. Radiation therapy is appropriate for isolated vaginal recurrences in patients with no previous history of radiation therapy. Patients with recurrent low-grade tumors overexpressing estrogen and progesterone receptors may be treated with progestin therapy. Systemic therapy is appropriate for patients with disseminate recurrences or advanced stage disease at presentation, or for those with receptor-negative tumors. We review all these different treatment strategies available to patients with advanced or recurrent endometrial cancer. The Oncologist 2010;15:852 861
C1 [Rauh-Hain, J. Alejandro; del Carmen, Marcela G.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Gynecol Oncol Vincent Obstet & Gynecol, Boston, MA 02114 USA.
RP del Carmen, MG (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Gynecol Oncol Vincent Obstet & Gynecol, 55 Fruit St,Yawkey 9 E, Boston, MA 02114 USA.
EM mdelcarmen@partners.org
NR 78
TC 9
Z9 11
U1 0
U2 0
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
J9 ONCOLOGIST
JI Oncologist
PD AUG
PY 2010
VL 15
IS 8
BP 852
EP 861
DI 10.1634/theoncologist.2010-0091
PG 10
WC Oncology
SC Oncology
GA 647FN
UT WOS:000281603300010
PM 20660059
ER
PT J
AU Ligibel, JA
AF Ligibel, Jennifer A.
TI Considering Metabolic Effects When Making Breast Cancer Treatment
Decisions
SO ONCOLOGY-NEW YORK
LA English
DT Editorial Material
ID POSTMENOPAUSAL WOMEN; AROMATASE INHIBITORS; CARDIOVASCULAR RISK;
ADJUVANT TREATMENT; TAMOXIFEN THERAPY; RANDOMIZED-TRIAL; SAFETY
ANALYSIS; LETROZOLE; ANASTROZOLE
C1 Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Ligibel, JA (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
NR 18
TC 0
Z9 0
U1 0
U2 0
PU UBM MEDICA
PI NORWALK
PA 535 CONNECTICUT AVE, STE 300, NORWALK, CT 06854 USA
SN 0890-9091
J9 ONCOLOGY-NY
JI Oncology-NY
PD AUG
PY 2010
VL 24
IS 9
BP 844
EP 846
PG 3
WC Oncology
SC Oncology
GA 800DR
UT WOS:000293340500011
PM 20923041
ER
PT J
AU Pasquale, LR
Willett, WC
Rosner, BA
Kang, JH
AF Pasquale, Louis R.
Willett, Walter C.
Rosner, Bernard A.
Kang, Jae Hee
TI Anthropometric Measures and their Relation to Incident Primary
Open-Angle Glaucoma
SO OPHTHALMOLOGY
LA English
DT Article
ID VISUAL IMPAIRMENT PROJECT; TYPE-2 DIABETES-MELLITUS; BALTIMORE EYE
SURVEY; SINGAPORE MALAY EYE; ANGELES LATINO EYE; BODY-MASS INDEX; BEAVER
DAM EYE; INTRAOCULAR-PRESSURE; POSTMENOPAUSAL WOMEN; BARBADOS EYE
AB Purpose: To assess the relation between anthropometric measures and incident primary open-angle glaucoma (POAG).
Design: Prospective cohort study.
Participants: Included were 78 777 women in the Nurses' Health Study and 41 352 men in the Health Professionals Follow-up Study.
Methods: Females and male health professionals were followed prospectively from 1980 through 2004 and 1986 through 2004, respectively. Eligible participants were 40 years of age or older, did not have POAG at baseline, and reported undergoing eye examinations during follow-up. Information regarding anthropometric measures, potential confounders, and ophthalmic status was updated using biennial questionnaires. During follow-up, 980 POAG cases were identified.
Main Outcome Measures: Multivariate rate ratios (MVRR) of POAG and their 95% confidence intervals (CIs).
Results: There was no significant relation between cumulatively averaged body mass index (BMI) in kilograms per meter squared and POAG overall (P = 0.06, for trend). However, in relation to POAG with intraocular pressure (IOP) of 22 mmHg or less at diagnosis, each unit increase in BMI was associated with a 6% reduced risk in women (MVRR, 0.94; 95% CI, 0.91-0.98; P = 0.01), but not for men (MVRR, 1.02; 95% CI, 0.96-1.09; P = 0.57); this gender difference was significant (P = 0.03, for heterogeneity). In multivariate analyses to explore the independent effects of height and weight, weight (as height-adjusted weight residuals; P = 0.002, for trend), but not height (P = 0.10, for trend) seemed to account for most of the inverse association between BMI and POAG with IOP of 21 mmHg or less at diagnosis in women. There was no association between BMI and POAG with IOP of more than 21 mmHg at diagnosis for either gender (P>0.26, for trend). Among women, analyses found that the relations between anthropometric parameters and both POAG subtypes (POAG with IOP <= 21 mmHg vs. POAG with IOP>21 mmHg when diagnosed) were significantly different (P <= 0.0001).
Conclusions: Among women, higher BMI was associated with a lower risk of POAG with IOP of 21 mmHg or less at diagnosis. The factors contributing to this tendency may yield insight into the pathogenesis of POAG.
Financial Disclosure(s): The author(s) have no proprietary or commercial interest in any materials discussed in this article. Ophthalmology 2010; 117: 1521-1529 (C) 2010 by the American Academy of Ophthalmology.
C1 [Pasquale, Louis R.] Harvard Univ, Sch Med, Dept Ophthalmol, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Willett, Walter C.; Rosner, Bernard A.; Kang, Jae Hee] Harvard Univ, Sch Med, Dept Med, Channing Lab, Boston, MA USA.
[Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Willett, Walter C.; Rosner, Bernard A.; Kang, Jae Hee] Brigham & Womens Hosp, Boston, MA USA.
[Rosner, Bernard A.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
RP Pasquale, LR (reprint author), Harvard Univ, Sch Med, Dept Ophthalmol, Massachusetts Eye & Ear Infirm, 243 Charles St, Boston, MA 02114 USA.
EM Louis_Pasquale@meei.harvard.edu
FU National Institutes of Health, Bethesda, Maryland [CA87969, CA55075,
EY09611, HL35464, EY015473]
FX Supported by the National Institutes of Health, Bethesda, Maryland
(grant nos.: CA87969, CA55075, EY09611, HL35464, and EY015473).
NR 52
TC 41
Z9 41
U1 0
U2 0
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 AUG
PY 2010
VL 117
IS 8
BP 1521
EP 1529
DI 10.1016/j.ophtha.2009.12.017
PG 9
WC Ophthalmology
SC Ophthalmology
GA 634QU
UT WOS:000280598900011
PM 20382429
ER
PT J
AU Kim, IK
Lane, AM
Egan, KM
Munzenrider, J
Gragoudas, ES
AF Kim, Ivana K.
Lane, Anne Marie
Egan, Kathleen M.
Munzenrider, John
Gragoudas, Evangelos S.
TI Natural History of Radiation Papillopathy after Proton Beam Irradiation
of Parapapillary Melanoma
SO OPHTHALMOLOGY
LA English
DT Article
ID INDUCED OPTIC NEUROPATHY; HYPERBARIC-OXYGEN THERAPY; CHOROIDAL MELANOMA;
PLAQUE RADIOTHERAPY; VISUAL-LOSS
AB Purpose: To evaluate the natural history of radiation papillopathy after proton beam irradiation of parapapillary choroidal melanoma.
Design: Noncomparative case series.
Participants: Ninety-three eyes of 93 patients.
Methods: Retrospective chart review of patients with choroidal melanoma within 0 to 1 disc diameter (DD) of the optic nerve and at least 2 DD away from the fovea treated with proton beam irradiation.
Main Outcome Measures: Rates of papillopathy, visual loss, and visual improvement.
Results: Sixty-eight percent of patients developed papillopathy a median of 1.5 years (17.7 months) after radiation. Among patients who developed papillopathy, 5-year rates of vision retention were 42% for counting fingers or better and 23% for 20/200 or better. At 5 years after the onset of papillopathy, 31% of patients had spontaneous visual improvement of 3 or more lines compared with the time of papillopathy diagnosis.
Conclusions: Even in eyes receiving high doses of radiation to the optic nerve for treatment of intraocular tumors, approximately two thirds of patients develop radiation papillopathy. After the development of papillopathy, 42% of eyes retain useful vision and one third of eyes have significant spontaneous visual improvement over 5 years. The natural history of radiation papillopathy may be more favorable than previously assumed, and therefore treatments for this condition must be compared with an appropriate control group.
Financial Disclosure(s): Proprietary or commercial disclosure may be found after the references. Ophthalmology 2010; 117: 1617-1622 (C) 2010 by the American Academy of Ophthalmology.
C1 [Kim, Ivana K.; Lane, Anne Marie; Gragoudas, Evangelos S.] Harvard Univ, Sch Med, Retina Serv, Massachusetts Eye & Ear Infirm,Dept Ophthalmol, Boston, MA 02114 USA.
[Egan, Kathleen M.] Univ S Florida, H Lee Moffitt Canc Ctr, Div Populat Sci, Tampa, FL 33682 USA.
[Munzenrider, John] Harvard Univ, Sch Med, Dept Radiat Oncol, Massachusetts Gen Hosp, Boston, MA USA.
RP Kim, IK (reprint author), Harvard Univ, Sch Med, Retina Serv, Massachusetts Eye & Ear Infirm,Dept Ophthalmol, 243 Charles St, Boston, MA 02114 USA.
EM ivana_kim@meei.harvard.edu
FU Massachusetts Eye and Ear Infirmary Melanoma Research Fund; Research to
Prevent Blindness
FX Supported by the Massachusetts Eye and Ear Infirmary Melanoma Research
Fund and Research to Prevent Blindness (IKK).
NR 18
TC 14
Z9 14
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 AUG
PY 2010
VL 117
IS 8
BP 1617
EP 1622
DI 10.1016/j.ophtha.2009.12.015
PG 6
WC Ophthalmology
SC Ophthalmology
GA 634QU
UT WOS:000280598900023
PM 20363507
ER
PT J
AU Zouhary, KJ
AF Zouhary, Kenneth J.
TI Bone Graft Harvesting From Distant Sites: Concepts and Techniques
SO ORAL AND MAXILLOFACIAL SURGERY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Graft; Harvest; Iliac; Tibial; Cranial; Calvarial
ID ANTERIOR ILIAC CREST; FEMORAL CUTANEOUS NERVE; DONOR SITE; CANCELLOUS
BONE; PROXIMAL TIBIA; ANATOMIC CONSIDERATIONS; CRANIOFACIAL SKELETON;
UNUSUAL COMPLICATION; VOLUME MAINTENANCE; JAW RECONSTRUCTION
AB Bony augmentation of the moderately to severely resorbed alveolus in preparation for endosseous dental implant placement can be challenging for the oral and maxillofacial surgeon. Autogenous bone remains the gold standard for alveolar grafting. Multiple extraoral bone graft sources can be used to help meet this challenge, including the iliac crest, proximal tibia, and calvarium. This article reviews the anatomy, harvest techniques, and morbidity associated with each of these donor sites.
C1 [Zouhary, Kenneth J.] Birmingham VA Med Ctr, Dept Oral & Maxillofacial Surg, Birmingham, AL 35233 USA.
[Zouhary, Kenneth J.] Univ Alabama, Dept Oral & Maxillofacial Surg, Birmingham, AL 35233 USA.
RP Zouhary, KJ (reprint author), Birmingham VA Med Ctr, Dept Oral & Maxillofacial Surg, 700 19th St S, Birmingham, AL 35233 USA.
EM kzouhary@uab.edu
NR 59
TC 33
Z9 35
U1 0
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1042-3699
J9 ORAL MAXIL SURG CLIN
JI Oral Maxillofac. Surg. Clin. N. Am.
PD AUG
PY 2010
VL 22
IS 3
BP 301
EP +
DI 10.1016/j.coms.2010.04.007
PG 17
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 864TW
UT WOS:000298264000004
PM 20713264
ER
PT J
AU Alsan, MM
Lin, HW
AF Alsan, Marcella M.
Lin, Harrison W.
TI Tularemia presenting as a cervical abscess
SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY
LA English
DT Editorial Material
C1 [Lin, Harrison W.] Massachusetts Eye & Ear Infirm, Dept Otolaryngol Head & Neck Surg, Boston, MA 02114 USA.
[Alsan, Marcella M.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
RP Lin, HW (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol Head & Neck Surg, 243 Charles St, Boston, MA 02114 USA.
EM harrison_lin@meei.harvard.edu
FU NIAID NIH HHS [T32 AI007433]
NR 4
TC 2
Z9 2
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0194-5998
J9 OTOLARYNG HEAD NECK
JI Otolaryngol. Head Neck Surg.
PD AUG
PY 2010
VL 143
IS 2
BP 311
EP 312
DI 10.1016/j.otohns.2010.04.002
PG 2
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 632OF
UT WOS:000280433300030
PM 20647143
ER
PT J
AU Kulke, MH
Anthony, LB
Bushnell, DL
de Herder, WW
Goldsmith, SJ
Klimstra, DS
Marx, SJ
Pasieka, JL
Pommier, RF
Yao, JC
Jensen, RT
AF Kulke, Matthew H.
Anthony, Lowell B.
Bushnell, David L.
de Herder, Wouter W.
Goldsmith, Stanley J.
Klimstra, David S.
Marx, Stephen J.
Pasieka, Janice L.
Pommier, Rodney F.
Yao, James C.
Jensen, Robert T.
TI NANETS Treatment Guidelines Well-Differentiated Neuroendocrine Tumors of
the Stomach and Pancreas
SO PANCREAS
LA English
DT Article
DE islet cell; gastric; carcinoid; guidelines; review
ID ZOLLINGER-ELLISON-SYNDROME; MULTIPLE ENDOCRINE NEOPLASIA;
SOMATOSTATIN-RECEPTOR SCINTIGRAPHY; GASTRIC CARCINOID-TUMORS;
PROTON-PUMP INHIBITORS; ISLET-CELL-CARCINOMA; DUODX AFFECT RATE;
PHASE-II TRIAL; LONG-TERM; LIVER METASTASES
AB Well-differentiated neuroendocrine tumors (NETs) of the stomach and pancreas represent 2 major subtypes of gastrointestinal NETs. Historically, there has been little consensus on the classification and management of patients with these tumor subtypes. We provide an overview of well-differentiated NETs of the stomach and pancreas and describe consensus guidelines for the treatment of patients with these malignancies.
C1 [Kulke, Matthew H.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Anthony, Lowell B.] Louisiana State Univ, Div Hematol Oncol, Hlth Sci Ctr, New Orleans, LA USA.
[Bushnell, David L.] Univ Iowa Hosp & Clin, Dept Radiol, Iowa City, IA 52242 USA.
[de Herder, Wouter W.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Goldsmith, Stanley J.] Cornell Univ, Div Nucl Med, Dept Radiol, New York Presbyterian Hosp,Weill Med Coll, Ithaca, NY 14853 USA.
[Klimstra, David S.] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Marx, Stephen J.] NIDDKD, Metab Dis Branch, NIH, Bethesda, MD 20892 USA.
[Pasieka, Janice L.] Univ Calgary, Dept Surg, Calgary, AB, Canada.
[Pommier, Rodney F.] Oregon Hlth & Sci Univ, Div Surg Oncol, Dept Gen Surg, Portland, OR 97201 USA.
[Yao, James C.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
[Jensen, Robert T.] NIH, Digest Dis Branch, Bethesda, MD 20892 USA.
RP Kulke, MH (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM Matthew_kulke@dfci.harvard.edu
FU Intramural NIH HHS [Z01 DK053200-17, Z01 DK053215-02, Z99 DK999999, ZIA
DK053200-19]; NCI NIH HHS [K23 CA093401-01A2, K23 CA093401, K23
CA093401-02, K23 CA093401-03, K23 CA093401-04, K23 CA093401-05]
NR 192
TC 183
Z9 198
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD AUG
PY 2010
VL 39
IS 6
BP 735
EP 752
DI 10.1097/MPA.0b013e3181ebb168
PG 18
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 629JA
UT WOS:000280190900004
PM 20664472
ER
PT J
AU Strosberg, JR
Coppola, D
Klimstra, DS
Phan, AT
Kulke, MH
Wiseman, GA
Kvols, LK
AF Strosberg, Jonathan R.
Coppola, Domenico
Klimstra, David S.
Phan, Alexandria T.
Kulke, Matthew H.
Wiseman, Gregory A.
Kvols, Larry K.
TI The NANETS Consensus Guidelines for the Diagnosis and Management of
Poorly Differentiated (High-Grade) Extrapulmonary Neuroendocrine
Carcinomas
SO PANCREAS
LA English
DT Article
DE neuroendocrine carcinomas; neuroendocrine tumors; poorly differentiated;
high grade
ID CELL LUNG-CANCER; PHASE-III; GASTROINTESTINAL-TRACT; CISPLATIN; TUMORS;
ETOPOSIDE; TRIAL; COMBINATION
AB Extrapulmonary poorly differentiated neuroendocrine carcinomas can originate in the gastrointestinal tract, bladder, cervix, and prostate. These high-grade malignancies are characterized by aggressive histological features (high mitotic rate, extensive necrosis, and nuclear atypia) and a poor clinical prognosis. They are infrequently associated with secretory hormonal syndromes (such as the carcinoid syndrome) and rarely express somatostatin receptors.
Most poorly differentiated neuroendocrine carcinomas are locally advanced ormetastatic at presentation. First-line systemic chemotherapy with a platinum agent (cisplatin or carboplatin) and etoposide is recommended for most patients with metastatic-stage disease; however, response durations are often short. Sequential or concurrent chemoradiation is recommended for patients with loco-regional disease. In patients with localized tumors undergoing surgical resection, adjuvant treatment (chemotherapy with or without radiation) is warranted in most cases.
C1 [Strosberg, Jonathan R.; Kvols, Larry K.] H Lee Moffitt Canc Ctr & Res Inst, Dept Gastrointestinal Oncol, Tampa, FL 33612 USA.
[Klimstra, David S.] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Phan, Alexandria T.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
[Kulke, Matthew H.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Wiseman, Gregory A.] Mayo Clin, Dept Nucl Med, Rochester, MN USA.
[Coppola, Domenico] H Lee Moffitt Canc Ctr & Res Inst, Dept Anat Pathol, Tampa, FL 33612 USA.
RP Strosberg, JR (reprint author), H Lee Moffitt Canc Ctr & Res Inst, Dept Gastrointestinal Oncol, 12902 Magnolia Dr,FOB-2, Tampa, FL 33612 USA.
EM jonathan.strosberg@moffitt.org
FU NCI NIH HHS [K23 CA093401, K23 CA093401-01A2, K23 CA093401-02, K23
CA093401-03, K23 CA093401-04, K23 CA093401-05]
NR 17
TC 90
Z9 95
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
J9 PANCREAS
JI Pancreas
PD AUG
PY 2010
VL 39
IS 6
BP 799
EP 800
DI 10.1097/MPA.0b013e3181ebb56f
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 629JA
UT WOS:000280190900009
PM 20664477
ER
PT J
AU Yong, PL
Orange, JS
Sullivan, KE
AF Yong, Pierre L.
Orange, Jordan S.
Sullivan, Kathleen E.
TI Pediatric common variable immunodeficiency: Immunologic and phenotypic
associations with switched memory B cells
SO PEDIATRIC ALLERGY AND IMMUNOLOGY
LA English
DT Article
DE common variable immunodeficiency; memory B cells; autoimmune disease;
recurrent infections; IgG
ID ANTIBODY-DEFICIENCY SYNDROME; IGA DEFICIENCY; DISEASE; MUTATIONS;
CHILDREN; FEATURES; TACI; HYPOGAMMAGLOBULINEMIA; COMPLICATIONS;
SUBGROUPS
AB Recent studies suggest that patients with common variable immunodeficiency (CVID) and low numbers of switched memory B cells have lower IgG levels and higher rates of autoimmune disease, splenomegaly, and granulomatous disease; however, no prior literature has focused exclusively on pediatric cases. We examined the relationship between switched memory B cells and clinical and immunologic manifestations of CVID in a pediatric population. Forty-five patients were evaluated. Patients were categorized as Group I (< 5 switched memory B cells/ml, n = 24) or Group II (>= 5 switched memory B cells/mL, n = 21). CD3+ T-cell counts and CD19+ B-cell levels were lower among Group I patients. Only those in Group I had meningitis, sepsis, bronchiectasis, granulomatous lung disease, autoimmune cytopenias, or hematologic malignancies. Segregation of pediatric patients into high risk (Group I) and average risk (Group II) may assist in targeting surveillance appropriately.
C1 [Yong, Pierre L.] Univ Penn, Sch Med, Robert Wood Johnson Clin Scholars Program, Philadelphia, PA 19104 USA.
[Yong, Pierre L.] Hosp Univ Penn, Div Pulm Allergy & Crit Care, Philadelphia, PA 19104 USA.
[Yong, Pierre L.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Yong, Pierre L.] Univ Penn, Ctr Publ Hlth Initiat, Philadelphia, PA 19104 USA.
[Orange, Jordan S.; Sullivan, Kathleen E.] Childrens Hosp Philadelphia, Div Allergy & Immunol, Philadelphia, PA 19104 USA.
[Yong, Pierre L.] Philadelphia Vet Affairs Med Ctr, Dept Med, Philadelphia, PA USA.
RP Sullivan, KE (reprint author), Childrens Hosp Philadelphia, Div Allergy Immunol, 3615 Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM sullivak@mail.med.upenn.edu
OI orange, jordan/0000-0001-7117-7725; Sullivan,
Kathleen/0000-0003-4018-1646
FU Philadelphia Veterans Affairs Medical Center; University of Pennsylvania
FX Dr. Pierre Yong is supported by a training grant from the Philadelphia
Veterans Affairs Medical Center and the Robert Wood Johnson Clinical
Scholars Program at the University of Pennsylvania. We are grateful for
the assistance of Benjamin Garcia, who helped with data management for
this project and the assistance of Sarah Shaw, Joe McMann, and USIDNET.
NR 49
TC 22
Z9 22
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0905-6157
J9 PEDIAT ALLERG IMM-UK
JI Pediatr. Allergy Immunol.
PD AUG
PY 2010
VL 21
IS 5
BP 852
EP 858
DI 10.1111/j.1399-3038.2010.01004.x
PG 7
WC Allergy; Immunology; Pediatrics
SC Allergy; Immunology; Pediatrics
GA 629LN
UT WOS:000280200000008
PM 20337966
ER
PT J
AU Sultan, I
Casanova, M
Ferrari, A
Rihani, R
Rodriguez-Galindo, C
AF Sultan, Iyad
Casanova, Michela
Ferrari, Andrea
Rihani, Rawad
Rodriguez-Galindo, Carlos
TI Differential Features of Nasopharyngeal Carcinoma in Children and
Adults: A SEER Study
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE adolescents; children; nasopharyngeal carcinoma; prognosis; SEER
ID TUNISIAN PATIENTS; CANCER; ADOLESCENTS; AGE; YOUNG
AB Background. Nasopharyngeal carcinoma (NPC) is a rare malignancy in the United States, which is considered a low-risk country. Methods. We searched the surveillance, epidemiology, and end results (SEER) database for patients with NPC who were diagnosed from 1988 to 2006. We compared the clinical features and outcomes of children and adolescents (<20 years old) and adults. Results. The incidence for children and adolescents was 0.5 per million person-years versus 8.4 in adults. NPC was less rare in black children and adolescents (incidence, 1.5 per million person-years). Our search criteria retrieved 129 children and adolescents and 5,885 adults. Black children and adolescents represented 34.9% of patients below the age of 20 years. Younger patients had distinct features with advanced stages more frequently observed (31% and 46% of children and adolescents had stages III and IV, respectively) and 87% had WHO type III histology. Outcome was better in children and adolescents with 5-year NPC-specific survival of 83% +/- 3.9% compared to 62% +/- 0.8% in adults (P < 0.001). In a multivariate model, the following factors affected the outcome: age, race, stage, and histologic type. Young adults (20-45 years old) had almost double the risk of NPC-specific mortality when compared to children and adolescents (hazards ratio (HR), 1.93; P=0.0077]. Children and adolescents with NPC were at higher risk of getting second cancer than adults (observed-to-expected ratio of 4.36 in children and adolescents; vs. 1.41 in adults; both were significantly higher than general population). Conclusion. Despite the use of similar treatment approaches, NPC in children and adolescents may have different biologic features. Young patients are at higher risk of developing therapy related complications, including second cancer. Pediatr Blood Cancer. 2010;55:279-284. (C) 2010 Wiley-Liss, Inc.
C1 [Sultan, Iyad; Rihani, Rawad] King Hussein Canc Ctr, Dept Pediat Oncol, Amman 11941, Jordan.
[Casanova, Michela; Ferrari, Andrea] Ist Nazl Tumori, Pediat Oncol Unit, I-20133 Milan, Italy.
[Rodriguez-Galindo, Carlos] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Rodriguez-Galindo, Carlos] Harvard Univ, Sch Med, Childrens Hosp, Boston, MA 02115 USA.
RP Sultan, I (reprint author), King Hussein Canc Ctr, Dept Pediat Oncol, Queen Rania Al Abdullah St,POB 1269, Amman 11941, Jordan.
EM isultan@khcc.jo
RI Casanova, Michela/K-8436-2016;
OI Casanova, Michela/0000-0003-0368-7883; Ferrari,
Andrea/0000-0002-4724-0517
NR 18
TC 20
Z9 21
U1 1
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD AUG
PY 2010
VL 55
IS 2
BP 279
EP 284
DI 10.1002/pbc.22521
PG 6
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 621EY
UT WOS:000279559200015
PM 20582982
ER
PT J
AU Dicianno, BE
Fairman, AD
Juengst, SB
Braun, PG
Zabel, TA
AF Dicianno, Brad E.
Fairman, Andrea D.
Juengst, Shannon B.
Braun, Patricia G.
Zabel, T. Andrew
TI Using the Spina Bifida Life Course Model in Clinical Practice: An
Interdisciplinary Approach
SO PEDIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Spina bifida; Development; Milestones; Transition
ID ADULTS
AB The Life Course Model for patients, families, caregivers, teachers, and clinicians was developed with support by the National Spina Bifida Program, National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, for individuals with spina bifida. The Life Course Model facilitates a developmental approach to assessment and intervention along life's trajectory. This Life Course Model provides information about key developmental milestones for particular age groups, validated assessments that can be performed by clinicians or teachers to determine if milestones have been reached, useful suggestions for intervening in creative ways at each step, and evidence-based references. In this article, the authors introduce the viewpoints of several key clinicians who are involved in the care of individuals with spina bifida and how the Life Course Model can assist them, their patients, and their families in the process of assessment, intervention, collaboration with other clinicians, and follow-up. A case study is used to demonstrate the experience of comprehensive and collaborative management in transitioning a child and his family from infancy to adulthood.
C1 [Dicianno, Brad E.] VA Pittsburgh Healthcare Syst, Dept Vet Affairs, HERL, Pittsburgh, PA 15206 USA.
[Dicianno, Brad E.; Fairman, Andrea D.] UPMC, Adult Spina Bifida Clin, Dept Phys Med & Rehabil, Pittsburgh, PA 15213 USA.
[Fairman, Andrea D.] Univ Pittsburgh, Sch Hlth & Rehabil Sci, Dept Rehabil Sci & Technol, Pittsburgh, PA 15260 USA.
[Juengst, Shannon B.] Univ Pittsburgh, Sch Hlth & Rehabil Sci, Dept Occupat Therapy, Pittsburgh, PA 15260 USA.
[Braun, Patricia G.] No Illinois Univ, Sch Nursing & Hlth Studies, De Kalb, IL 60115 USA.
[Zabel, T. Andrew] Kennedy Krieger Inst, Philip A Keelty Ctr Spina Bifida & Related Condit, Dept Neuropsychol, Baltimore, MD 21231 USA.
[Zabel, T. Andrew] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA.
RP Dicianno, BE (reprint author), VA Pittsburgh Healthcare Syst, Dept Vet Affairs, HERL, 7180 Highland Dr,151R-1, Pittsburgh, PA 15206 USA.
EM dicianno@pitt.edu
OI Juengst, Shannon/0000-0003-4709-545X; Dicianno, Brad/0000-0003-0738-0192
FU National Center on Birth Defects and Developmental Disabilities, Centers
for Disease Control and Prevention, Atlanta, Georgia
FX This work was supported by the National Spina Bifida Program, National
Center on Birth Defects and Developmental Disabilities, Centers for
Disease Control and Prevention, Atlanta, Georgia.
NR 20
TC 0
Z9 0
U1 1
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0031-3955
J9 PEDIATR CLIN N AM
JI Pediatr. Clin. N. Am.
PD AUG
PY 2010
VL 57
IS 4
BP 945
EP +
DI 10.1016/j.pcl.2010.07.014
PG 15
WC Pediatrics
SC Pediatrics
GA 672YH
UT WOS:000283623300008
PM 20883884
ER
PT J
AU Fairman, AD
Thibadeau, JK
Dicianno, BE
Parmanto, B
AF Fairman, Andrea D.
Thibadeau, Judy K.
Dicianno, Brad E.
Parmanto, Bambang
TI Implementing a Specialty Electronic Medical Record to Document a
Life-Course Developmental Model and Facilitate Clinical Interventions in
Spina Bifida Clinics
SO PEDIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Electronic medical record; Spina bifida; Developmental model; Transition
ID HEALTH; CARE; TRANSITION; ADULTHOOD
AB This article describes the utility of a spina bifida-specific electronic medical record (SB EMR). Standardization and pooling of data through the SB EMR will facilitate development of increased knowledge for advancing interventions for SB treatment, rehabilitation, and support. Integration with a Web-based transition tool will enhance the efficiency and efficacy of interventions delivered by clinicians. The SB EMR may also be used by SB clinic staff to manage and monitor the developmental course SB through childhood and the adolescent years. Further, implementation of the SB EMR in conjunction with the life-course model will assist in the transition of young persons with SB to adult roles.
C1 [Fairman, Andrea D.] Univ Pittsburgh, Sch Hlth & Rehabil Sci, Dept Rehabil Sci & Technol, Pittsburgh, PA 15260 USA.
[Thibadeau, Judy K.] Ctr Dis Control & Prevent, Div Human Dev & Disabil, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30033 USA.
[Dicianno, Brad E.] VA Pittsburgh Healthcare Syst, Dept Vet Affairs, HERL, Pittsburgh, PA 15206 USA.
[Dicianno, Brad E.] UPMC, Dept Phys Med & Rehabil, Pittsburgh, PA 15213 USA.
[Parmanto, Bambang] Univ Pittsburgh, Sch Hlth & Rehabil Sci, Dept Hlth Informat Management, Pittsburgh, PA 15260 USA.
RP Fairman, AD (reprint author), Univ Pittsburgh, Sch Hlth & Rehabil Sci, Dept Rehabil Sci & Technol, Forbes Tower,Suite 5044,3600 Forbes Ave, Pittsburgh, PA 15260 USA.
EM adf29@pitt.edu
OI Dicianno, Brad/0000-0003-0738-0192
FU National Center on Birth Defects and Developmental Disabilities, Centers
for Disease Control and Prevention, Atlanta, Georgia
FX This work was supported by the National Spina Bifida Program, National
Center on Birth Defects and Developmental Disabilities, Centers for
Disease Control and Prevention, Atlanta, Georgia.
NR 24
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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 0031-3955
J9 PEDIATR CLIN N AM
JI Pediatr. Clin. N. Am.
PD AUG
PY 2010
VL 57
IS 4
BP 959
EP +
DI 10.1016/j.pcl.2010.07.015
PG 14
WC Pediatrics
SC Pediatrics
GA 672YH
UT WOS:000283623300009
PM 20883885
ER
PT J
AU Swanson, ME
Dicianno, BE
AF Swanson, Mark E.
Dicianno, Brad E.
TI Physiatrists and Developmental Pediatricians Working Together to Improve
Outcomes in Children with Spina Bifida
SO PEDIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Spina bifida; Physiatry; Developmental pediatrics; Interdisciplinary
care
ID YOUNG-ADULTS; ADOLESCENTS; MYELOMENINGOCELE; HISTORY; OBESITY; FAMILY
AB Based on the experience of 2 physicians from physiatry and developmental pediatrics, this article proposes a framework for improving care and outcomes for children with spina bifida. The combined skills of physiatrists and developmental pediatricians, along with other disciplines, can form the ideal team to manage the complex issues faced by this population. The developmental pediatrician is best suited for directing care for younger children through the elementary and middle school years, during which time behavioral and educational issues are prominent. As the child assumes more responsibility for self-management in adolescence, the physiatrist is ideally suited to provide major clinical input that improves functional outcomes. The addition of the discipline of physiatry to traditional, developmentally oriented pediatric interdisciplinary teams can add the much needed dimensions of activity and participation, and improve functional outcomes at the adult level by encouraging activities in adolescence that lead to full participation in adulthood.
C1 [Swanson, Mark E.] Ctr Dis Control & Prevent, Div Human Dev & Disabil, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30333 USA.
[Dicianno, Brad E.] VA Pittsburgh Healthcare Syst, Dept Vet Affairs, HERL, Pittsburgh, PA 15206 USA.
[Dicianno, Brad E.] UPMC, Adult Spina Bifida Clin, Dept Phys Med & Rehabil, Pittsburgh, PA 15213 USA.
RP Swanson, ME (reprint author), Ctr Dis Control & Prevent, Div Human Dev & Disabil, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30333 USA.
EM cfu9@cdc.gov
OI Dicianno, Brad/0000-0003-0738-0192
NR 22
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U1 1
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 0031-3955
J9 PEDIATR CLIN N AM
JI Pediatr. Clin. N. Am.
PD AUG
PY 2010
VL 57
IS 4
BP 973
EP +
DI 10.1016/j.pcl.2010.07.016
PG 10
WC Pediatrics
SC Pediatrics
GA 672YH
UT WOS:000283623300010
PM 20883886
ER
PT J
AU Co, JPT
Johnson, SA
Poon, EG
Fiskio, J
Rao, SR
Van Cleave, J
Perrin, JM
Ferris, TG
AF Co, John Patrick T.
Johnson, Sarah A.
Poon, Eric G.
Fiskio, Julie
Rao, Sowmya R.
Van Cleave, Jeanne
Perrin, James M.
Ferris, Timothy G.
TI Electronic Health Record Decision Support and Quality of Care for
Children With ADHD
SO PEDIATRICS
LA English
DT Article
DE attention-deficit/hyperactivity disorder; quality of care; electronic
health records; decision support system; chronic disease management;
child
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; CLINICAL-PRACTICE GUIDELINE;
DEFICIT HYPERACTIVITY DISORDER; INFORMATION-TECHNOLOGY; AMBULATORY-CARE;
NATIONAL-SURVEY; UNITED-STATES; PREVALENCE; CHILDHOOD; IMPACT
AB OBJECTIVES: The objective of this study was to assess the effect of electronic health record (EHR) decision support on physician management and documentation of care for children with attention-deficit/hyperactivity disorder (ADHD).
METHODS: This study involved 79 general pediatricians in 12 pediatric primary care practices that use the same EHR who were caring for 412 children who were aged 5 to 18 years and had a previous diagnosis of ADHD. We conducted a cluster randomized trial of EHR-based decision support that included (1) clinician reminders to assess ADHD symptoms every 3 to 6 months and (2) an ADHD note template with structured fields for symptoms, treatment effectiveness, and adverse effects. The main outcome measures were (1) proportion of children with visits during the 6-month study period in which ADHD was assessed and (2) quality of documentation of ADHD assessment. Generalized estimating equations were used to control for the clustering by providers.
RESULTS: Children at intervention sites were more likely to have had a visit during the study period in which their ADHD was assessed. The ADHD template was used at 32% of visits at which patients were scheduled specifically for ADHD assessment, and its use was associated with improved documentation of symptoms, treatment effectiveness, and treatment adverse effects.
CONCLUSIONS: EHR-based decision support improved the likelihood that children with ADHD had visits for as well as care related to managing this condition. Better understanding of how to optimize provider use of the decision support and templates could promote additional improvements in care. Pediatrics 2010;126:239-246
C1 [Co, John Patrick T.; Van Cleave, Jeanne; Perrin, James M.; Ferris, Timothy G.] Mass Gen Hosp Children, Ctr Child & Adolescent Hlth Policy, Boston, MA USA.
[Johnson, Sarah A.; Ferris, Timothy G.] Massachusetts Gen Hosp, Inst Hlth Policy, Boston, MA 02114 USA.
[Poon, Eric G.; Fiskio, Julie] Brigham & Womens Hosp, Div Gen Med, Boston, MA 02115 USA.
[Rao, Sowmya R.] MGH Biostat Ctr, Boston, MA USA.
RP Co, JPT (reprint author), MGH Ctr Child & Adolescent Hlth Policy, 50 Staniford St,Suite 901, Boston, MA 02114 USA.
EM jco@partners.org
FU Agency for Healthcare Research and Quality [R01 HS15002]
FX This study was funded by Agency for Healthcare Research and Quality
grant R01 HS15002.
NR 25
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Z9 23
U1 1
U2 6
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 AUG
PY 2010
VL 126
IS 2
BP 239
EP 246
DI 10.1542/peds.2009-0710
PG 8
WC Pediatrics
SC Pediatrics
GA 634FO
UT WOS:000280565700007
PM 20643719
ER
PT J
AU Fiks, AG
Localio, AR
Alessandrini, EA
Asch, DA
Guevara, JP
AF Fiks, Alexander G.
Localio, A. Russell
Alessandrini, Evaline A.
Asch, David A.
Guevara, James P.
TI Shared Decision-Making in Pediatrics: A National Perspective
SO PEDIATRICS
LA English
DT Article
DE ADHD; asthma; communication; decision-making; telephone care
ID ATTENTION-DEFICIT/HYPERACTIVITY-DISORDER; STIMULANT MEDICATION;
MULTIMODAL-TREATMENT; RANDOMIZED TRIAL; MENTAL-HEALTH; FOLLOW-UP;
E-MAIL; CHILDREN; CARE; COMMUNICATION
AB OBJECTIVES: To identify patterns of shared decision-making (SDM) among a nationally representative sample of US children with attention-deficit/hyperactivity disorder (ADHD) or asthma and determine if demographics, health status, or access to care are associated with SDM.
PATIENTS AND METHODS: We performed a cross-sectional study of the 2002-2006 Medical Expenditure Panel Survey, which represents 2 million children with ADHD and 4 million children with asthma. The outcome, high SDM, was defined by using latent class models based on 7 Medical Expenditure Panel Survey items addressing aspects of SDM. We entered factors potentially associated with SDM into logistic regression models with high SDM as the outcome. Marginal standardization then described the standardized proportion of children's households with high SDM for each factor.
RESULTS: For both ADHD and asthma, 65% of children's households had high SDM. Those who reported poor general health for their children were 13% less likely to have high SDM for ADHD (64 vs 77%) and 8% less likely for asthma (62 vs 70%) when adjusting for other factors. Results for behavioral impairment were similar. Respondent demographic characteristics were not associated with SDM. Those with difficulty contacting their clinician by telephone were 26% (ADHD: 55 vs 81%) and 29% (asthma: 48 vs 77%) less likely to have high SDM than those without difficulty.
CONCLUSIONS: These findings indicate that households of children who report greater impairment or difficulty contacting their clinician by telephone are less likely to fully participate in SDM. Future research should examine how strategies to foster ongoing communication between families and clinicians affect SDM. Pediatrics 2010;126:306-314
C1 [Fiks, Alexander G.] Childrens Hosp Philadelphia, Ctr Pediat Clin Effectiveness, Pediat Res Consortium, Philadelphia, PA 19104 USA.
[Fiks, Alexander G.] Childrens Hosp Philadelphia, Ctr Biomed Informat, Philadelphia, PA 19104 USA.
[Fiks, Alexander G.; Guevara, James P.] Childrens Hosp Philadelphia, Pediat Generalist Res Grp, Philadelphia, PA 19104 USA.
[Fiks, Alexander G.; Guevara, James P.] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.
[Localio, A. Russell] Univ Penn, Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Asch, David A.] Univ Penn, Sch Med, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Alessandrini, Evaline A.] Cincinnati Childrens Hosp Med Ctr, Div Hlth Policy, Cincinnati, OH USA.
[Alessandrini, Evaline A.] Cincinnati Childrens Hosp Med Ctr, Div Clin Effectiveness & Emergency Med, Cincinnati, OH USA.
[Asch, David A.] Philadelphia VA Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
RP Fiks, AG (reprint author), Childrens Hosp Philadelphia, Ctr Pediat Clin Effectiveness, Pediat Res Consortium, 3535 Market St,Room 1546, Philadelphia, PA 19104 USA.
EM fiks@email.chop.edu
OI Asch, David/0000-0002-7970-286X; Guevara, James/0000-0003-1665-4503
FU National Institutes of Health (NIH); Academic Pediatric Association;
Children's Hospital of Philadelphia; Eunice Kennedy Shriver National
Institute of Child Health and Human Development [K23HD059919]
FX Funded by the National Institutes of Health (NIH).; This research was
supported by an Academic Pediatric Association Young Investigator Award
and institutional development funds from the Children's Hospital of
Philadelphia. In addition, the project described was supported by award
K23HD059919 from the Eunice Kennedy Shriver National Institute of Child
Health and Human Development.
NR 45
TC 36
Z9 36
U1 2
U2 12
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 AUG
PY 2010
VL 126
IS 2
BP 306
EP 314
DI 10.1542/peds.2010-0526
PG 9
WC Pediatrics
SC Pediatrics
GA 634FO
UT WOS:000280565700020
PM 20624804
ER
PT J
AU Yager, P
Noviski, N
AF Yager, Phoebe
Noviski, Natan
TI Shock
SO PEDIATRICS IN REVIEW
LA English
DT Review
ID NEONATAL SEPTIC SHOCK; SEVERE SEPSIS; CHILDREN; LEVOSIMENDAN;
GUIDELINES; SUPPORT
C1 [Yager, Phoebe; Noviski, Natan] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Yager, Phoebe; Noviski, Natan] MassGen Hosp Children, Boston, MA USA.
RP Yager, P (reprint author), Harvard Univ, Sch Med, Boston, MA 02115 USA.
NR 9
TC 1
Z9 1
U1 1
U2 2
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0191-9601
J9 PEDIATR REV
JI Pediatr. Rev.
PD AUG
PY 2010
VL 31
IS 8
BP 311
EP 319
PG 9
WC Pediatrics
SC Pediatrics
GA 634FA
UT WOS:000280564100001
PM 20679096
ER
PT J
AU Look, AE
Flory, JD
Harvey, PD
Siever, LJ
AF Look, Amy E.
Flory, Janine D.
Harvey, Philip D.
Siever, Larry J.
TI Psychometric properties of a short form of the Affective Lability Scale
(ALS-18)
SO PERSONALITY AND INDIVIDUAL DIFFERENCES
LA English
DT Article
DE Affective Lability Scale; Affect dysregulation; Cluster B personality
ID BORDERLINE PERSONALITY-DISORDER; AFFECTIVE INSTABILITY; BIPOLAR-II
AB Psychometric properties of a short form of the Affective Lability Scale (ALS) that was developed in a non-clinical sample (i.e., undergraduate students) were examined in a sample of people diagnosed with Cluster B DSM-IV Axis II personality disorders (n = 236), other personality disorders (n = 180), and healthy comparison participants (n = 164). The total score of the ALS-18 score correlated strongly with the original 54-item scale (r = .97) and aspects of convergent and discriminant validity of the ALS-18 subscales (Anxiety/Depression, Depression/Elation, and Anger) were evaluated using self-report measures of affective and psychosocial functioning in the domains of affect intensity, anxiety, anger, and minimization/denial. Clinical utility of the scale was also demonstrated; participants diagnosed with Cluster B personality disorders reported higher affective lability scores, and healthy control participants reported lower scores, relative to individuals with Cluster A or Cluster C personality disorders (p's < .001). Confirmatory factor analyses were conducted and demonstrated reasonably good fit to the data but future research is needed to test the three factor substructure of the ALS-18 against alternative factor models in samples that include clinical and non-clinical participants. Published by Elsevier Ltd.
C1 [Flory, Janine D.] CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA.
[Look, Amy E.; Siever, Larry J.] James J Peters VA Med Ctr, MIRECC, Bronx, NY USA.
[Flory, Janine D.; Siever, Larry J.] James J Peters VA Med Ctr, Psychiat Serv, Bronx, NY USA.
[Harvey, Philip D.] Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA USA.
[Siever, Larry J.] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
RP Flory, JD (reprint author), CUNY Queens Coll, Dept Psychol, 65-30 Kissena Blvd, Flushing, NY 11367 USA.
EM janine.flory@qc.cuny.edu
FU NCRR NIH HHS [M01 RR000071-340193, M01 RR000071]; NIMH NIH HHS [K01
MH069979, K01 MH069979-01A1, R01 MH063875, R01 MH065554]
NR 20
TC 9
Z9 9
U1 0
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0191-8869
J9 PERS INDIV DIFFER
JI Pers. Individ. Differ.
PD AUG
PY 2010
VL 49
IS 3
BP 187
EP 191
DI 10.1016/j.paid.2010.03.030
PG 5
WC Psychology, Social
SC Psychology
GA 611NU
UT WOS:000278824100006
PM 20606710
ER
PT J
AU Salters-Pedneault, K
Ruef, AM
Orr, SP
AF Salters-Pedneault, Kristalyn
Ruef, Anna M.
Orr, Scott P.
TI Personality and psychophysiological profiles of police officer and
firefighter recruits
SO PERSONALITY AND INDIVIDUAL DIFFERENCES
LA English
DT Article
DE Extraversion; Five Factor Personality Model; Psychophysiology
ID POSTTRAUMATIC-STRESS-DISORDER; PHYSIOLOGICAL-RESPONSES; LOUD TONES;
SYMPTOMS
AB Some have suggested that people who join emergency-services professions have a unique set of personality and response characteristics that allow them to manage the intense stressors of their particular jobs. The nature of personality and response profiles of individuals from different emergency-services professions could have both clinical and policy implications. The present study examined self-reported personality traits of police and firefighter recruits, as well as their psychophysiological response patterns during a loud-tone procedure. Police recruits scored higher than firefighters on gregariousness, a facet of Extraversion, and on dutifulness and deliberation, facets of Conscientiousness. Compared to a normative sample, police and firefighters both scored higher on excitement-seeking, a facet of Extraversion. Comparisons with psychophysiological data from a non-rescuer sample suggest that the firefighter recruits exhibited higher heart rate and skin conductance (SC) levels, while police recruits showed larger eyeblink electromyogram (EMG) startle responses and required more trials to reach SC habituation criteria. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Salters-Pedneault, Kristalyn] VA Boston Healthcare Syst, Boston, MA USA.
[Orr, Scott P.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Orr, Scott P.] Harvard Univ, Sch Med, Boston, MA USA.
[Ruef, Anna M.; Orr, Scott P.] Vet Affairs Med Ctr, Res Serv, Manchester, NH USA.
RP Salters-Pedneault, K (reprint author), Eastern Connecticut State Univ, Dept Psychol, 83 Windham St, Willimantic, CT 06226 USA.
EM saltersk@easternct.edu
NR 15
TC 12
Z9 12
U1 1
U2 11
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0191-8869
J9 PERS INDIV DIFFER
JI Pers. Individ. Differ.
PD AUG
PY 2010
VL 49
IS 3
BP 210
EP 215
DI 10.1016/j.paid.2010.03.037
PG 6
WC Psychology, Social
SC Psychology
GA 611NU
UT WOS:000278824100010
ER
PT J
AU Hodgins, HS
Weibust, KS
Weinstein, N
Shiffman, S
Miller, A
Coombs, G
Adair, KC
AF Hodgins, Holley S.
Weibust, Kristin S.
Weinstein, Netta
Shiffman, Sara
Miller, Anita
Coombs, Garth
Adair, Kathryn C.
TI The Cost of Self-Protection: Threat Response and Performance as a
Function of Autonomous and Controlled Motivations
SO PERSONALITY AND SOCIAL PSYCHOLOGY BULLETIN
LA English
DT Article
DE defensive processes; motivation; performance; self-determination theory;
physiological processes
ID CAUSALITY ORIENTATIONS; MENTAL-HEALTH; CARDIOVASCULAR REACTIVITY; TERROR
MANAGEMENT; VERBAL-BEHAVIOR; SOCIAL-BEHAVIOR; MODEL; PERSONALITY;
AROUSAL; ESTEEM
AB Seventy-seven undergraduates, primed for autonomous or controlled motivation, were videotaped and physiologically monitored during a stressful interview and subsequent speech. Interview videotapes were coded for behavioral measures of threat response; speech videotapes were coded for performance. It was hypothesized that relative to controlled motivation, autonomous motivation would decrease interview threat response and enhance speech performance, and that threat response would mediate the effect of motivation on performance. Results support the prediction across measures of verbal, paralinguistic, smiling, vocal fundamental frequency, and cardiovascular response. Autonomously primed participants continued to show less cardiovascular threat throughout the later speech and gave better speeches. Finally, speech performance was mediated by interview threat response. Results demonstrate that relative to controlled motivation, autonomous motivation lowers threat response, which enhances performance.
C1 [Hodgins, Holley S.] Skidmore Coll, Dept Psychol, Saratoga Springs, NY 12866 USA.
[Weibust, Kristin S.] Univ Vermont, Burlington, VT 05405 USA.
[Weinstein, Netta] Univ Hamburg, Hamburg, Germany.
[Adair, Kathryn C.] VA Boston Healthcare Syst, Natl Ctr PTSD, Womens Hlth Sci Div, Boston, MA USA.
RP Hodgins, HS (reprint author), Skidmore Coll, Dept Psychol, 815 North Broadway, Saratoga Springs, NY 12866 USA.
EM hhodgins@skidmore.edu
RI Shiffman, Saul/K-7337-2012
NR 97
TC 23
Z9 23
U1 3
U2 18
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0146-1672
J9 PERS SOC PSYCHOL B
JI Pers. Soc. Psychol. Bull.
PD AUG
PY 2010
VL 36
IS 8
BP 1101
EP 1114
DI 10.1177/0146167210375618
PG 14
WC Psychology, Social
SC Psychology
GA 635VQ
UT WOS:000280685500009
PM 20693387
ER
PT J
AU Tada, DB
Singh, S
Nagesha, D
Jost, E
Levy, CO
Gultepe, E
Cormack, R
Makrigiorgos, GM
Sridhar, S
AF Tada, Dayane B.
Singh, Surinder
Nagesha, Dattatri
Jost, Evan
Levy, Craig O.
Gultepe, Evin
Cormack, Robert
Makrigiorgos, G. Mike
Sridhar, Srinivas
TI Chitosan Film Containing Poly(D,L-Lactic-Co-Glycolic Acid)
Nanoparticles: A Platform for Localized Dual-Drug Release
SO PHARMACEUTICAL RESEARCH
LA English
DT Article
DE chitosan; PLGA; paclitaxel; drug release; implants coating
ID IMPLANTED FIDUCIAL MARKERS; BREAST-CANCER; PACLITAXEL; STENT;
CHEMOTHERAPY; RESTENOSIS; THERAPY; MODEL
AB To characterize and evaluate chitosan film containing PLGA nanoparticles (NPs) as a platform for localized dual-drug release.
Fluorescent Paclitaxel (FPTX), a hydrophobic drug, was incorporated into PLGA NPs. FPTX-loaded PLGA NPs and Carboxyfluorescein (CF), a hydrophilic model drug, were embedded into chitosan films. Release of CF and NPs from chitosan and release of FPTX from PLGA NPs were monitored by fluorescence. The stability of the platform was observed through SEM and dynamic light scattering (DLS).
Chitosan films containing CF and FPTX-loaded PLGA NPs showed a biphasic release profile. In the first phase, 78% of CF and 34% of NPs were released within few days. In the second phase, the release was slower, showing an additional release of 22% of CF and 18% of NPs after 3 weeks. SEM images and DLS measurements showed that NP release depends on film degradation rate. FPTX-loaded PLGA NPs showed the release of 19.8% of total drug in 2 days, and no additional release was detected in the next 26 days.
The ability of chitosan film containing PLGA NPs to coat gold surface and to incorporate and release two different drugs of different hydrophilicity make it a promising platform for localized dual-drug release.
C1 [Tada, Dayane B.; Nagesha, Dattatri; Jost, Evan; Levy, Craig O.; Gultepe, Evin; Sridhar, Srinivas] Northeastern Univ, Elect Mat Res Inst, Boston, MA 02115 USA.
[Singh, Surinder] Univ Puerto Rico, Dept Engn Sci & Mat, Mayaguez, PR 00681 USA.
[Cormack, Robert; Makrigiorgos, G. Mike] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dana Farber Canc Inst,Dept Radiat Oncol, Boston, MA 02115 USA.
RP Sridhar, S (reprint author), Northeastern Univ, Elect Mat Res Inst, Boston, MA 02115 USA.
EM s.sridhar@neu.edu
RI Rinaldi2, Carlos/D-4479-2011; Sridhar, Srinivas/A-3688-2012; Tada,
Dayane/E-9032-2012;
OI Cormack, Robert/0000-0001-5553-9984; Singh, Surinder
P./0000-0001-9638-7673
FU IGERT Nanomedicine Science and Technology [NSF-0504331]; Brigham Womens
Hospital
FX The authors thank Dr. Bernard D. F. Casse, William Fowle and Electronic
Materials Research Institute of Northeastern University for SEM images.
This work was supported by the IGERT Nanomedicine Science and Technology
Program (NSF-0504331) and Brigham Womens Hospital.
NR 25
TC 12
Z9 13
U1 0
U2 21
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0724-8741
J9 PHARM RES-DORDR
JI Pharm. Res.
PD AUG
PY 2010
VL 27
IS 8
BP 1738
EP 1745
DI 10.1007/s11095-010-0176-9
PG 8
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
SC Chemistry; Pharmacology & Pharmacy
GA 620NH
UT WOS:000279506100023
PM 20521086
ER
PT J
AU Cheung, WY
Zhai, RH
Kulke, M
Heist, R
Asomaning, K
Ma, C
Wang, ZX
Su, L
Liu, G
Christiani, D
AF Cheung, Winson Y.
Zhai, Rihong
Kulke, Matthew
Heist, Rebecca
Asomaning, Kofi
Ma, Clement
Wang, Zhaoxi
Su, Li
Liu, Geoffrey
Christiani, David
TI Single Nucleotide Polymorphisms (SNPs) in the Matrix Metalloproteinase
(MMP) Gene Family, Gastroesophageal Reflux Disease (GERD), and Risk of
Esophageal Adenocarcinoma (EAC)
SO PHARMACOEPIDEMIOLOGY AND DRUG SAFETY
LA English
DT Meeting Abstract
C1 [Cheung, Winson Y.] British Columbia Canc Agcy, Vancouver, BC, Canada.
[Zhai, Rihong; Asomaning, Kofi; Wang, Zhaoxi; Su, Li; Christiani, David] Harvard Sch Publ Hlth, Boston, MA USA.
[Kulke, Matthew] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Heist, Rebecca] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Ma, Clement; Liu, Geoffrey] Princess Margaret Hosp, Toronto, ON, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-8569
EI 1099-1557
J9 PHARMACOEPIDEM DR S
JI Pharmacoepidemiol. Drug Saf.
PD AUG
PY 2010
VL 19
SU 1
MA 261
BP S112
EP S112
PG 1
WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
GA V45OP
UT WOS:000209826200254
ER
PT J
AU Lawler, EV
Fonda, JR
Thwin, SS
Gaziano, JM
Brophy, MT
Gagnon, DR
AF Lawler, Elizabeth V.
Fonda, Jennifer R.
Thwin, Soe Soe
Gaziano, J. Michael
Brophy, Mary T.
Gagnon, David R.
TI Lipid Lowering Agents and Non-Traumatic Tendon Rupture
SO PHARMACOEPIDEMIOLOGY AND DRUG SAFETY
LA English
DT Meeting Abstract
CT 26th International Conference on Pharmacoepidemiology and Therapeutic
Risk Management
CY AUG 19-22, 2010
CL Brighton, ENGLAND
C1 [Lawler, Elizabeth V.; Fonda, Jennifer R.; Thwin, Soe Soe; Gaziano, J. Michael; Brophy, Mary T.; Gagnon, David R.] Massachusetts Vet Epidemiol Res & Informat Ctr, VA Cooperat Studies Program, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-8569
EI 1099-1557
J9 PHARMACOEPIDEM DR S
JI Pharmacoepidemiol. Drug Saf.
PD AUG
PY 2010
VL 19
SU 1
MA 549
BP S232
EP S233
PG 2
WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
GA V45OP
UT WOS:000209826200526
ER
PT J
AU Linsky, A
Hermos, JA
Rudolph, JL
Lawler, EV
AF Linsky, Amy
Hermos, John A.
Rudolph, James L.
Lawler, Elizabeth V.
TI Factors Associated with Proton Pump Inhibitor Discontinuation in Nursing
Homes
SO PHARMACOEPIDEMIOLOGY AND DRUG SAFETY
LA English
DT Meeting Abstract
C1 [Linsky, Amy; Hermos, John A.] Boston Med Ctr, Gen Internal Med, Boston, MA USA.
[Hermos, John A.; Lawler, Elizabeth V.] VA Boston Healthcare Syst, MAVERIC, VA Cooperat Studies Program, Boston, MA USA.
[Rudolph, James L.] VA Boston Healthcare Syst, GRECC, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-8569
EI 1099-1557
J9 PHARMACOEPIDEM DR S
JI Pharmacoepidemiol. Drug Saf.
PD AUG
PY 2010
VL 19
SU 1
MA 257
BP S110
EP S110
PG 1
WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
GA V45OP
UT WOS:000209826200250
ER
PT J
AU Renouf, D
Coate, L
Zhai, RH
Kulke, M
Heist, RS
Bradbury, P
Xu, W
Chen, ZF
Asomaning, K
Wain, J
Su, L
Liu, G
Christiani, DC
AF Renouf, Daniel
Coate, Linda
Zhai, Rihong
Kulke, Matthew
Heist, Rebecca S.
Bradbury, Penelope
Xu, Wei
Chen, Zhengfei
Asomaning, Kofi
Wain, John
Su, Li
Liu, Geoffrey
Christiani, David C.
TI Early-Adulthood Obesity [EOb] Modifies the Cisplatin [C]-DNA Repair Gene
Polymorphism XPD ASP312ASN [X] Relationship in Esophageal Cancer (EC)
Survival: A Combined Pharmacogenetic-Molecular Epidemiologic Analysis
SO PHARMACOEPIDEMIOLOGY AND DRUG SAFETY
LA English
DT Meeting Abstract
CT 26th International Conference on Pharmacoepidemiology and Therapeutic
Risk Management
CY AUG 19-22, 2010
CL Brighton, ENGLAND
C1 [Renouf, Daniel; Coate, Linda; Bradbury, Penelope; Xu, Wei; Chen, Zhengfei; Liu, Geoffrey] Princess Margaret Hosp, Med Oncol, Toronto, ON, Canada.
[Zhai, Rihong; Heist, Rebecca S.; Asomaning, Kofi; Su, Li; Christiani, David C.] Harvard Sch Publ Hlth, Environm Hlth, Boston, MA USA.
[Kulke, Matthew] Dana Farber Canc Inst, Oncol, Boston, MA 02115 USA.
[Wain, John] Massachusetts Gen Hosp, Surg, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-8569
EI 1099-1557
J9 PHARMACOEPIDEM DR S
JI Pharmacoepidemiol. Drug Saf.
PD AUG
PY 2010
VL 19
SU 1
MA 485
BP S205
EP S206
PG 2
WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
GA V45OP
UT WOS:000209826200465
ER
PT J
AU Stedman, MR
Gagnon, DR
Lew, RA
Losina, E
Solomon, DH
Brookhart, MA
AF Stedman, Margaret R.
Gagnon, David R.
Lew, Robert A.
Losina, Elena
Solomon, Daniel H.
Brookhart, M. Alan
TI A Comparison of Statistical Approaches for Clustered
Pharmacoepidemiology Data with Survival Outcomes
SO PHARMACOEPIDEMIOLOGY AND DRUG SAFETY
LA English
DT Meeting Abstract
CT 26th International Conference on Pharmacoepidemiology and Therapeutic
Risk Management
CY AUG 19-22, 2010
CL Brighton, ENGLAND
C1 [Stedman, Margaret R.; Losina, Elena; Solomon, Daniel H.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Stedman, Margaret R.; Gagnon, David R.; Lew, Robert A.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Brookhart, M. Alan] Univ North Carolina Chapel Hill, Chapel Hill, NC USA.
[Gagnon, David R.; Lew, Robert A.] Boston VA Healthcare Syst, Boston, MA USA.
[Losina, Elena; Solomon, Daniel H.] Harvard Med Sch, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-8569
EI 1099-1557
J9 PHARMACOEPIDEM DR S
JI Pharmacoepidemiol. Drug Saf.
PD AUG
PY 2010
VL 19
SU 1
MA 538
BP S228
EP S228
PG 1
WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy
GA V45OP
UT WOS:000209826200516
ER
PT J
AU Geisler, T
Gawaz, M
Steinhubl, SR
Bhatt, DL
Storey, RF
Flather, M
AF Geisler, Tobias
Gawaz, Meinrad
Steinhubl, Steven R.
Bhatt, Deepak L.
Storey, Robert F.
Flather, Marcus
TI Current strategies in antiplatelet therapy - Does identification of risk
and adjustment of therapy contribute to more effective, personalized
medicine in cardiovascular disease?
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE Antiplatelet therapy; Platelets; Drugs; Cardiovascular disease;
Percutaneous coronary intervention
ID ACUTE CORONARY SYNDROMES; ELEVATION MYOCARDIAL-INFARCTION; RESIDUAL
PLATELET-AGGREGATION; GLYCOPROTEIN IIB/IIIA INHIBITION;
THROMBIN-RECEPTOR ANTAGONIST; RANDOMIZED CONTROLLED-TRIAL; ELUTING STENT
THROMBOSIS; PROTON PUMP INHIBITORS; 2007 FOCUSED UPDATE; OF-CARE
ANALYSIS
AB There is a wide consensus that intensified antiplatelet therapy contributes to the reduction of major atherothrombotic complications in cardiovascular (CV) disease. In the setting of PCI (percutaneous coronary intervention) and acute coronary syndromes, dual antiplatelet therapy at optimal dosing and timing has significantly lowered the risk of thrombotic complications. There is a growing body of evidence that there is variability in response to antiplatelet treatments and this represents a potentially important clinical problem. Understanding the mechanisms underlying this phenomenon is important in improving patient care, but due to the diversity of factors involved, a clear predictive model for responsiveness to antiplatelet therapy is still missing. Attempts have been made to characterize the efficacy of antiplatelet therapy using platelet function testing but based on current information, its routine use is not recommended particularly as costs and cost effectiveness have not been established and agreement between laboratory methods is lacking. Hence, it is necessary to identify risk factors for decreased efficacy of standard antiplatelet drug treatment It may be useful to adjust antiplatelet therapy based on individual risk assessment, especially as new platelet inhibitors are being introduced or are in development including prasugrel as well as the non-thienopyridines, ticagrelor, elinogrel, the ATP analog cangrelor, and thrombin receptor antagonists. This article focuses on antiplatelet therapy in patients at high risk for cardiovascular events and discusses the options for individual risk assessment and strategies to personalize therapy in the light of the large number of recent developments. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Geisler, Tobias; Flather, Marcus] Royal Brompton & Harefield NHS Fdn Trust, Clin Trials & Evaluat Unit, London SW3 6NP, England.
[Geisler, Tobias; Gawaz, Meinrad] Univ Tubingen, Med Klin 3, Univ Klinikum, Tubingen, Germany.
[Steinhubl, Steven R.] Medicines Co, CH-8058 Zurich, Switzerland.
[Steinhubl, Steven R.] Weis Ctr Res, Geisinger Clin, Danville, PA 17822 USA.
[Bhatt, Deepak L.] Brigham & Womens Hosp, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Bhatt, Deepak L.] Harvard Univ, Sch Med, Boston, MA USA.
[Storey, Robert F.] Univ Sheffield, Dept Cardiovasc Sci, Sheffield, S Yorkshire, England.
RP Geisler, T (reprint author), Royal Brompton & Harefield NHS Fdn Trust, Clin Trials & Evaluat Unit, Sydney St, London SW3 6NP, England.
EM t.geisler@rbht.nhs.uk
NR 126
TC 10
Z9 10
U1 0
U2 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD AUG
PY 2010
VL 127
IS 2
BP 95
EP 107
DI 10.1016/j.pharmthera.2010.04.017
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 631XV
UT WOS:000280384900001
PM 20570595
ER
PT J
AU Vincenti, A
Ventriglio, A
Baldessarini, RJ
Talamo, A
Fitzmaurice, G
Centorrino, F
AF Vincenti, A.
Ventriglio, A.
Baldessarini, R. J.
Talamo, A.
Fitzmaurice, G.
Centorrino, F.
TI Characteristics and Clinical Changes during Hospitalization in Bipolar
and Psychotic Disorder Patients with versus without Substance-Use
Disorders
SO PHARMACOPSYCHIATRY
LA English
DT Article
ID MENTAL-DISORDERS; DOUBLE-BLIND; ACUTE MANIA; DRUG-ABUSE; SCHIZOPHRENIA;
ALCOHOL; REASONS; RISK; PHARMACOTHERAPY; LAMOTRIGINE
AB Background: Co-morbid substance-use disorders (SUDs) are prevalent among patients with severe psychiatric disorders, but the characteristics of such patients remain incompletely defined, and their current treatments and responses, poorly documented.
Methods: We evaluated the records of 481 consecutive inpatients diagnosed with DSM-IV bipolar or schizoaffective disorders, or schizophrenia, admitted to McLean Hospital in 2004 or 2009. Demographic and clinical characteristics, and treatments, were extracted from hospital and pharmacy records for bivariate and multivariate analyses.
Results: SUD prevalence increased 1.84-times from 2004 (31.3%) to 2009 (57.6%). Patients with (n = 204) versus without co-morbid SUDs (n = 277) were similar in many respects, but in multivariate modeling, the following factors were more likely with SUD, in rank-order: co-morbid anxiety disorders > men more than women > greater prevalence in 2009 vs. 2004 > younger age > greater doses of mood-stabilizers > shorter hospitalization.
Conclusions: Hospitalized patients with severe primary psychiatric disorders, and comorbid SUD were more likely to be young and have anxiety disorders, to receive more combinations and higher doses of mood-stabilizers, and show more improvement in impulsivity and hostility, but otherwise differed little in treatment-responses. Prevalence of SUD rose substantially in the past five years, with increased but largely unproved use of mood-stabilizers.
C1 [Vincenti, A.; Ventriglio, A.; Centorrino, F.] McLean Hosp, Psychopharmacol Res Dept, Belmont, MA 02478 USA.
[Vincenti, A.; Talamo, A.] Univ Roma La Sapienza, Sch Med 2, Dept Neurosci Mental Hlth & Sonsory Funct NESMOS, Rome, Italy.
[Vincenti, A.; Talamo, A.] St Andrea Hosp, Unit Psychiat, Rome, Italy.
[Vincenti, A.; Ventriglio, A.; Baldessarini, R. J.; Talamo, A.; Centorrino, F.] Massachusetts Gen Hosp, McLean Div, Int Consortium Psychot & Bipolar Disorder Res, Belmont, MA USA.
[Ventriglio, A.] Univ Foggia, Dept Psychiat, Foggia, Italy.
[Baldessarini, R. J.; Talamo, A.; Fitzmaurice, G.; Centorrino, F.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
RP Centorrino, F (reprint author), McLean Hosp, Psychopharmacol Res Dept, N Belknap 3,115 Mill St, Belmont, MA 02478 USA.
EM fcentorrino@mclean.harvard.edu
OI Talamo, Alessandra/0000-0001-7321-9247; Ventriglio,
Antonio/0000-0002-3934-7007
FU Universities of Rome-La Sapienza; Foggia; Bruce J. Anderson Foundation;
McLean Private Donors Psychopharmacology Research Fund
FX Supported in part by research fellowships from Universities of Rome-La
Sapienza (Drs. Vincenti) and Foggia (Dr. Ventriglio), a grant from the
Bruce J. Anderson Foundation and by the McLean Private Donors
Psychopharmacology Research Fund (Dr. Baldessarini).
NR 40
TC 4
Z9 4
U1 3
U2 6
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0176-3679
EI 1439-0795
J9 PHARMACOPSYCHIATRY
JI Pharmacopsychiatry
PD AUG
PY 2010
VL 43
IS 6
BP 225
EP 232
DI 10.1055/s-0030-1254153
PG 8
WC Pharmacology & Pharmacy; Psychiatry
SC Pharmacology & Pharmacy; Psychiatry
GA 649KH
UT WOS:000281767200005
PM 20652858
ER
PT J
AU Reitmair, A
Lambrecht, NWG
Yakubov, I
Nieves, A
Old, D
Donde, Y
Dinh, D
Burk, R
Sachs, G
Bin Im, W
Wheeler, L
AF Reitmair, Armin
Lambrecht, Nils W. G.
Yakubov, Iskandar
Nieves, Amelia
Old, David
Donde, Yariv
Dinh, Danny
Burk, Robert
Sachs, George
Bin Im, Wha
Wheeler, Larry
TI Prostaglandin E-2 receptor subtype EP2-and EP4-regulated gene expression
profiling in human ciliary smooth muscle cells
SO PHYSIOLOGICAL GENOMICS
LA English
DT Article
DE gene regulation; glaucoma; intraocular pressure
ID TYPE-1 MATRIX-METALLOPROTEINASE; KERATINOCYTE GROWTH-FACTOR;
AQUEOUS-HUMOR DYNAMICS; NECROSIS-FACTOR-ALPHA; MORPHOGENETIC PROTEIN-2
BMP-2; EP4 PROSTANOID RECEPTORS; ELEMENT-BINDING PROTEIN;
EXTRACELLULAR-MATRIX; CYNOMOLGUS MONKEY; TISSUE INHIBITOR
AB Reitmair A, Lambrecht NW, Yakubov I, Nieves A, Old D, Donde Y, Dinh D, Burk R, Sachs G, Im WB, Wheeler L. Prostaglandin E-2 receptor subtype EP2-and EP4-regulated gene expression profiling in human ciliary smooth muscle cells. Physiol Genomics 42: 348-360, 2010. First published June 15, 2010; doi: 10.1152/physiolgenomics.00012.2010.-Prostanoids are an important class of intraocular pressure (IOP)-lowering antiglaucoma agents that act primarily via increased uveo-scleral aqueous humor outflow through the ciliary body. We have developed two novel PGE(2) analogs that are specific agonists for the PGE(2) receptor subtypes EP2 and EP4, respectively. To identify gene regulatory networks and key players that mediate the physiological effects observed in vivo, we performed genomewide expression studies using human ciliary smooth muscle cells. Quantitative real-time RT-PCR confirmed a largely overlapping gene expression profile subsequent to EP2 and EP4 agonist treatment, with 65 significantly regulated genes identified overall, 5 being specific for the EP2 agonist and 6 specific for the EP4 agonist. We found predicted functional cAMP-response elements in promoter regions of a large fraction of the predominantly upregulated genes, which suggests that the cAMP signaling pathway is the most important intracellular signaling pathway for these agonists in these cells. Several target genes were identified that, as part of complex regulatory networks, are implicated in tissue remodeling processes and osmoregulation (e. g., AREG, LOXL3, BMP2, AQP3) and thus may help elucidate the mechanism of action of these IOP-lowering drugs involving the uveo-scleral outflow path.
C1 [Reitmair, Armin; Nieves, Amelia; Bin Im, Wha; Wheeler, Larry] Allergan Pharmaceut Inc, Dept Biol Sci, Irvine, CA 92612 USA.
[Old, David; Donde, Yariv; Dinh, Danny; Burk, Robert] Allergan Pharmaceut Inc, Dept Med Chem, Irvine, CA 92612 USA.
[Lambrecht, Nils W. G.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
[Sachs, George] Univ Calif Los Angeles, David Geffen Sch Med, Dept Physiol, Los Angeles, CA 90095 USA.
[Yakubov, Iskandar; Sachs, George] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
[Lambrecht, Nils W. G.; Yakubov, Iskandar; Sachs, George] W Los Angeles Vet Affairs Med Ctr, Membrane Biol Lab, Los Angeles, CA 90073 USA.
RP Reitmair, A (reprint author), Allergan Pharmaceut Inc, Dept Biol Sci, RD3,2525 Dupont Dr, Irvine, CA 92612 USA.
EM reitmair_armin@allergan.com
OI Lambrecht, Nils/0000-0002-1275-1384
NR 122
TC 2
Z9 3
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1094-8341
J9 PHYSIOL GENOMICS
JI Physiol. Genomics
PD AUG
PY 2010
VL 42
IS 3
BP 348
EP 360
DI 10.1152/physiolgenomics.00012.2010
PG 13
WC Cell Biology; Genetics & Heredity; Physiology
SC Cell Biology; Genetics & Heredity; Physiology
GA 655UU
UT WOS:000282278700004
PM 20551148
ER
PT J
AU Bastow, R
Beynon, J
Estelle, M
Friesner, J
Grotewold, E
Lavagi, I
Lindsey, K
Meyers, B
Provart, N
Benfey, P
Birney, E
Braun, P
Brendel, V
Buell, R
Caccamo, M
Carrington, J
Cherry, M
Ecker, J
Eppig, J
Forster, M
Gutierrez, R
Hilson, P
Huala, E
Katari, M
Kersey, P
Kudla, J
Ma, H
Matsui, M
Matthews, K
May, S
Mayer, K
Millar, A
Millar, H
Mjolsness, E
Mockler, T
Nikolau, B
Nordborg, M
Rawlings, C
Schofield, P
Schoof, H
Schroeder, JI
Sen, TZ
Stanzione, D
Town, C
Toyoda, T
Vision, T
Walsh, S
Wang, XJ
Ware, D
Weckwerth, W
Yang, WC
AF Bastow, Ruth
Beynon, Jim
Estelle, Mark
Friesner, Joanna
Grotewold, Erich
Lavagi, Irene
Lindsey, Keith
Meyers, Blake
Provart, Nicholas
Benfey, Philip
Birney, Ewan
Braun, Pascal
Brendel, Volker
Buell, Robin
Caccamo, Mario
Carrington, Jim
Cherry, Mike
Ecker, Joseph
Eppig, Janan
Forster, Mark
Gutierrez, Rodrigo
Hilson, Pierre
Huala, Eva
Katari, Manpreet
Kersey, Paul
Kudla, Joerg
Ma, Hong
Matsui, Minami
Matthews, Kathy
May, Sean
Mayer, Klaus
Millar, Andrew
Millar, Harvey
Mjolsness, Eric
Mockler, Todd
Nikolau, Basil
Nordborg, Magnus
Rawlings, Chris
Schofield, Paul
Schoof, Heiko
Schroeder, Julian I.
Sen, Taner Z.
Stanzione, Dan
Town, Chris
Toyoda, Tetsuro
Vision, Todd
Walsh, Sean
Wang, Xiujie
Ware, Doreen
Weckwerth, Wolfram
Yang, Weicai
CA Int Arabidopsis Informatics Cons
TI An International Bioinformatics Infrastructure to Underpin the
Arabidopsis Community
SO PLANT CELL
LA English
DT Editorial Material
AB The future bioinformatics needs of the Arabidopsis community as well as those of other scientific communities that depend on Arabidopsis resources were discussed at a pair of recent meetings held by the Multinational Arabidopsis Steering Committee and the North American Arabidopsis Steering Committee. There are extensive tools and resources for information storage, curation, and retrieval of Arabidopsis data that have been developed over recent years primarily through the activities of The Arabidopsis Information Resource, the Nottingham Arabidopsis Stock Centre, and the Arabidopsis Biological Resource Center, among others. However, the rapid expansion in many data types, the international basis of the Arabidopsis community, and changing priorities of the funding agencies all suggest the need for changes in the way informatics infrastructure is developed and maintained. We propose that there is a need for a single core resource that is integrated into a larger international consortium of investigators. We envision this to consist of a distributed system of data, tools, and resources, accessed via a single information portal and funded by a variety of sources, under shared international management of an International Arabidopsis Informatics Consortium (IAIC). This article outlines the proposal for the development, management, operations, and continued funding for the IAIC.
C1 [Beynon, Jim] Univ Warwick, Coventry CV4 7AL, W Midlands, England.
[Estelle, Mark; Schroeder, Julian I.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Grotewold, Erich; Carrington, Jim; Mockler, Todd] Ohio State Univ, Columbus, OH 43210 USA.
[Lindsey, Keith] Univ Durham, Durham DH1 3HP, England.
[Meyers, Blake] Univ Delaware, Newark, DE 19716 USA.
[Provart, Nicholas] Univ Toronto, Toronto, ON M5S 1A1, Canada.
[Benfey, Philip] Duke Univ, Durham, NC 27706 USA.
[Braun, Pascal] Dana Farber Canc Inst, Boston, MA USA.
[Braun, Pascal] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Sen, Taner Z.] Iowa State Univ, USDA, ARS, Res Serv, Ames, IA 50011 USA.
[Buell, Robin] Michigan State Univ, E Lansing, MI 48824 USA.
[Cherry, Mike] Stanford Univ, Stanford, CA 94305 USA.
[Gutierrez, Rodrigo] Catholic Univ Chile, Santiago, Chile.
[Hilson, Pierre] VIB Ghent, Ghent, Belgium.
[Katari, Manpreet] NYU, New York, NY 10003 USA.
[Kudla, Joerg] Univ Munster, D-4400 Munster, Germany.
[Ma, Hong] Fudan Univ, Shanghai, Peoples R China.
[Ma, Hong] Penn State Univ, University Pk, PA 16802 USA.
[Matsui, Minami; Toyoda, Tetsuro] RIKEN, Wako, Saitama, Japan.
[Matthews, Kathy] Indiana Univ, Bloomington, IN 47405 USA.
[May, Sean] Univ Nottingham, Nottingham NG7 2RD, England.
[Millar, Andrew] Univ Edinburgh, Edinburgh EH8 9YL, Midlothian, Scotland.
[Millar, Harvey] Univ Western Australia, Nedlands, WA 6009, Australia.
[Mjolsness, Eric] Univ Calif Irvine, Irvine, CA USA.
[Schofield, Paul] Univ Cambridge, Cambridge CB2 1TN, England.
[Sen, Taner Z.] Iowa State Univ, MaizeGDB, Ames, IA 50011 USA.
[Stanzione, Dan] Univ Texas Austin, Austin, TX 78712 USA.
[Walsh, Sean] ETH, Zurich, Switzerland.
[Yang, Weicai] Chinese Acad Sci, Inst Genet & Dev Biol, Beijing 100864, Peoples R China.
[Ware, Doreen] ARS, USDA, Cold Spring Harbor Lab, Washington, DC USA.
[Weckwerth, Wolfram] Univ Vienna, A-1010 Vienna, Austria.
RP Bastow, R (reprint author), Univ Warwick, Coventry CV4 7AL, W Midlands, England.
RI Millar, Andrew/G-2423-2012; Weckwerth, Wolfram/G-5811-2010; Gutierrez,
Rodrigo/C-2611-2008; may, sean/B-6838-2012; Kudla, Jorg/C-2174-2012;
Millar, A. Harvey/A-5452-2008; Ecker, Joseph/B-9144-2008; Braun,
Pascal/B-9669-2013; Matsui, Minami/A-5235-2016; Mockler,
Todd/L-2609-2013; Meyers, Blake/B-6535-2012; Mayer, Klaus/M-7941-2015;
Carrington, James/A-4656-2012
OI Schroeder, Julian/0000-0002-3283-5972; Kersey, Paul/0000-0002-7054-800X;
Birney, Ewan/0000-0001-8314-8497; Rawlings,
Christopher/0000-0003-3702-1633; Millar, Andrew/0000-0003-1756-3654;
may, sean/0000-0001-5282-3250; Kudla, Jorg/0000-0002-8238-767X; Millar,
A. Harvey/0000-0001-9679-1473; Ecker, Joseph/0000-0001-5799-5895; Braun,
Pascal/0000-0003-2012-6746; Matsui, Minami/0000-0001-5162-2668; Mockler,
Todd/0000-0002-0462-5775; Meyers, Blake/0000-0003-3436-6097; Mayer,
Klaus/0000-0001-6484-1077; Carrington, James/0000-0003-3572-129X
NR 2
TC 15
Z9 15
U1 2
U2 18
PU AMER SOC PLANT BIOLOGISTS
PI ROCKVILLE
PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 USA
SN 1040-4651
J9 PLANT CELL
JI Plant Cell
PD AUG
PY 2010
VL 22
IS 8
BP 2530
EP 2536
DI 10.1105/tpc.110.078519
PG 7
WC Biochemistry & Molecular Biology; Plant Sciences; Cell Biology
SC Biochemistry & Molecular Biology; Plant Sciences; Cell Biology
GA 655SU
UT WOS:000282270600004
ER
PT J
AU Segre, AV
Groop, L
Mootha, VK
Daly, MJ
Altshuler, D
AF Segre, Ayellet V.
Groop, Leif
Mootha, Vamsi K.
Daly, Mark J.
Altshuler, David
CA DIAGRAM Consortium
MAGIC Investigators
TI Common Inherited Variation in Mitochondrial Genes Is Not Enriched for
Associations with Type 2 Diabetes or Related Glycemic Traits
SO PLOS GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; INSULIN-RESISTANCE; OXIDATIVE-PHOSPHORYLATION;
COMPLEX DISEASES; PATHWAY ANALYSIS; CANDIDATE GENES; LOCI; GLUCOSE;
SUSCEPTIBILITY; REPLICATION
AB Mitochondrial dysfunction has been observed in skeletal muscle of people with diabetes and insulin-resistant individuals. Furthermore, inherited mutations in mitochondrial DNA can cause a rare form of diabetes. However, it is unclear whether mitochondrial dysfunction is a primary cause of the common form of diabetes. To date, common genetic variants robustly associated with type 2 diabetes (T2D) are not known to affect mitochondrial function. One possibility is that multiple mitochondrial genes contain modest genetic effects that collectively influence T2D risk. To test this hypothesis we developed a method named Meta-Analysis Gene-set Enrichment of variaNT Associations (MAGENTA; http://www.broadinstitute.org/mpg/magenta). MAGENTA, in analogy to Gene Set Enrichment Analysis, tests whether sets of functionally related genes are enriched for associations with a polygenic disease or trait. MAGENTA was specifically designed to exploit the statistical power of large genome-wide association (GWA) study meta-analyses whose individual genotypes are not available. This is achieved by combining variant association p-values into gene scores and then correcting for confounders, such as gene size, variant number, and linkage disequilibrium properties. Using simulations, we determined the range of parameters for which MAGENTA can detect associations likely missed by single-marker analysis. We verified MAGENTA's performance on empirical data by identifying known relevant pathways in lipid and lipoprotein GWA meta-analyses. We then tested our mitochondrial hypothesis by applying MAGENTA to three gene sets: nuclear regulators of mitochondrial genes, oxidative phosphorylation genes, and,1,000 nuclear-encoded mitochondrial genes. The analysis was performed using the most recent T2D GWA meta-analysis of 47,117 people and meta-analyses of seven diabetes-related glycemic traits (up to 46,186 non-diabetic individuals). This well-powered analysis found no significant enrichment of associations to T2D or any of the glycemic traits in any of the gene sets tested. These results suggest that common variants affecting nuclear-encoded mitochondrial genes have at most a small genetic contribution to T2D susceptibility.
C1 [Segre, Ayellet V.; Mootha, Vamsi K.; Daly, Mark J.; Altshuler, David] Broad Inst Harvard & Massachusetts Inst Technol, Cambridge, MA USA.
[Segre, Ayellet V.; Mootha, Vamsi K.; Daly, Mark J.; Altshuler, David] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Segre, Ayellet V.; Altshuler, David] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Groop, Leif] Lund Univ, Malmo Univ Hosp, Dept Clin Sci, Diabet & Endocrinol Res Unit, S-21401 Malmo, Sweden.
[Mootha, Vamsi K.] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA USA.
[Mootha, Vamsi K.; Daly, Mark J.; Altshuler, David] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Altshuler, David] Massachusetts Gen Hosp, Diabet Unit, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
RP Segre, AV (reprint author), Broad Inst Harvard & Massachusetts Inst Technol, Cambridge, MA USA.
EM asegre@broadinstitute.org; altshuler@molbio.mgh.harvard.edu
RI Altshuler, David/A-4476-2009; Segre, Ayellet/E-9800-2010
OI Altshuler, David/0000-0002-7250-4107;
FU American Diabetes Association [7-08-MN-OK]; Swedish Research Council;
Wallenberg Foundation; Sigrid Juselius Foundation; American Diabetes
Association/Smith Family Foundation
FX For this project, AVS and DA acknowledge support from the American
Diabetes Association (Award No.: 7-08-MN-OK); LG was supported by the
Swedish Research Council (Linne grant), the Wallenberg Foundation, and
the Sigrid Juselius Foundation; and VKM was supported by the American
Diabetes Association/Smith Family Foundation. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 57
TC 164
Z9 165
U1 2
U2 13
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD AUG
PY 2010
VL 6
IS 8
AR e1001058
DI 10.1371/journal.pgen.1001058
PG 19
WC Genetics & Heredity
SC Genetics & Heredity
GA 644NG
UT WOS:000281383800014
ER
PT J
AU Wang, JL
Robida-Stubbs, S
Tullet, JMA
Rual, JF
Vidal, M
Blackwell, TK
AF Wang, Jinling
Robida-Stubbs, Stacey
Tullet, Jennifer M. A.
Rual, Jean-Francois
Vidal, Marc
Blackwell, T. Keith
TI RNAi Screening Implicates a SKN-1-Dependent Transcriptional Response in
Stress Resistance and Longevity Deriving from Translation Inhibition
SO PLOS GENETICS
LA English
DT Article
ID LIFE-SPAN EXTENSION; CAENORHABDITIS-ELEGANS; OXIDATIVE-STRESS;
C-ELEGANS; COP9 SIGNALOSOME; FACTOR SKN-1; DIETARY RESTRICTION;
GENE-EXPRESSION; MOLECULAR-BASIS; MECHANISMS
AB Caenorhabditis elegans SKN-1 (ortholog of mammalian Nrf1/2/3) is critical for oxidative stress resistance and promotes longevity under reduced insulin/IGF-1-like signaling (IIS), dietary restriction (DR), and normal conditions. SKN-1 inducibly activates genes involved in detoxification, protein homeostasis, and other functions in response to stress. Here we used genome-scale RNA interference (RNAi) screening to identify mechanisms that prevent inappropriate SKN-1 target gene expression under non-stressed conditions. We identified 41 genes for which knockdown leads to activation of a SKN-1 target gene (gcs-1) through skn-1-dependent or other mechanisms. These genes correspond to multiple cellular processes, including mRNA translation. Inhibition of translation is known to increase longevity and stress resistance and may be important for DR-induced lifespan extension. One model postulates that these effects derive from reduced energy needs, but various observations suggest that specific longevity pathways are involved. Here we show that translation initiation factor RNAi robustly induces SKN-1 target gene transcription and confers skn-1-dependent oxidative stress resistance. The accompanying increases in longevity are mediated largely through the activities of SKN-1 and the transcription factor DAF-16 (FOXO), which is required for longevity that derives from reduced IIS. Our results indicate that the SKN-1 detoxification gene network monitors various metabolic and regulatory processes. Interference with one of these processes, translation initiation, leads to a transcriptional response whereby SKN-1 promotes stress resistance and functions together with DAF-16 to extend lifespan. This stress response may be beneficial for coping with situations that are associated with reduced protein synthesis.
C1 [Wang, Jinling; Robida-Stubbs, Stacey; Tullet, Jennifer M. A.; Blackwell, T. Keith] Harvard Univ, Sch Med, Joslin Diabet Ctr, Harvard Stem Cell Inst, Boston, MA 02115 USA.
[Wang, Jinling; Robida-Stubbs, Stacey; Tullet, Jennifer M. A.; Blackwell, T. Keith] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Rual, Jean-Francois; Vidal, Marc] Dana Farber Canc Inst, Ctr Canc Syst Biol CCSB, Boston, MA 02115 USA.
[Rual, Jean-Francois; Vidal, Marc] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Rual, Jean-Francois; Vidal, Marc] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
RP Wang, JL (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Harvard Stem Cell Inst, Boston, MA 02115 USA.
EM keith.blackwell@joslin.harvard.edu
OI Rual, Jean-Francois/0000-0003-4465-8819; Tullet,
Jennifer/0000-0002-2037-526X
FU NIH [GM62891, HG001715, CA81658]; Joslin Diabetes Center DERC
[DK036836]; Juvenile Diabetes Research Foundation
FX This work was supported by NIH grants GM62891 (TKB), HG001715 (MV), and
CA81658 ( MV); by the Joslin Diabetes Center DERC (DK036836); and by a
fellowship from the Juvenile Diabetes Research Foundation
(www.jdrf.org)(JW). The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 63
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U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD AUG
PY 2010
VL 6
IS 8
AR e1001048
DI 10.1371/journal.pgen.1001048
PG 17
WC Genetics & Heredity
SC Genetics & Heredity
GA 644NG
UT WOS:000281383800004
ER
EF