FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Engels, MC
Rajarajan, K
Feistritzer, R
Sharma, A
Nielsen, UB
Schalij, MJ
De Vries, AAF
Pijnappels, DA
Wu, SM
AF Engels, M. C.
Rajarajan, K.
Feistritzer, R.
Sharma, A.
Nielsen, U. B.
Schalij, M. J.
De Vries, A. A. F.
Pijnappels, D. A.
Wu, S. M.
TI IGF promotes cardiac lineage induction by selective expansion of
cardiogenic mesoderm in vitro
SO EUROPEAN HEART JOURNAL
LA English
DT Meeting Abstract
CT Congress of the European-Society-of-Cardiology (ESC)
CY AUG 31-SEP 04, 2013
CL Amsterdam, NETHERLANDS
SP European Soc Cardiol
C1 [Engels, M. C.; Rajarajan, K.; Feistritzer, R.; Wu, S. M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Sharma, A.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Nielsen, U. B.] Silvercreek Pharmaceut, San Francisco, CA USA.
[Schalij, M. J.; De Vries, A. A. F.; Pijnappels, D. A.] Leiden Univ, Med Ctr, Dept Cardiol, Leiden, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0195-668X
EI 1522-9645
J9 EUR HEART J
JI Eur. Heart J.
PD AUG
PY 2013
VL 34
SU 1
BP 929
EP 929
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 262OH
UT WOS:000327744605466
ER
PT J
AU Magnusson, M
Wang, T
Hedblad, B
Engstrom, G
Ostling, G
Gerszten, R
Melander, O
AF Magnusson, M.
Wang, T.
Hedblad, B.
Engstrom, G.
Ostling, G.
Gerszten, R.
Melander, O.
TI High levels of arginine, citrulline and ADMA are independent predictors
of cardiovascular disease
SO EUROPEAN HEART JOURNAL
LA English
DT Meeting Abstract
CT Congress of the European-Society-of-Cardiology (ESC)
CY AUG 31-SEP 04, 2013
CL Amsterdam, NETHERLANDS
SP European Soc Cardiol
C1 [Magnusson, M.] Lund Univ, Skane Univ Hosp, Dept Heart Failure & Valvular Dis, Malmo, Sweden.
[Wang, T.; Gerszten, R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[Hedblad, B.; Engstrom, G.; Ostling, G.; Melander, O.] Lund Univ, Skane Univ Hosp, Dept Clin Sci, Malmo, Sweden.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0195-668X
EI 1522-9645
J9 EUR HEART J
JI Eur. Heart J.
PD AUG
PY 2013
VL 34
SU 1
BP 1058
EP 1059
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 262OH
UT WOS:000327744606409
ER
PT J
AU Evans, MC
Paquet, AC
Huang, W
Napolitano, L
Frantzell, A
Toma, J
Stawiski, EW
Goetz, MB
Petropoulos, CJ
Whitcomb, J
Coakley, E
Haddad, M
AF Evans, Mark C.
Paquet, Agnes C.
Huang, Wei
Napolitano, Laura
Frantzell, Arne
Toma, Jonathan
Stawiski, Eric W.
Goetz, Matthew Bidwell
Petropoulos, Christos J.
Whitcomb, Jeannette
Coakley, Eoin
Haddad, Mojgan
TI A CASE-BASED REASONING SYSTEM FOR GENOTYPIC PREDICTION OF HIV-1
CO-RECEPTOR TROPISM
SO JOURNAL OF BIOINFORMATICS AND COMPUTATIONAL BIOLOGY
LA English
DT Article
DE Tropism prediction; genotypic algorithm; HIV-1 co-receptor; V3
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HIDDEN MARKOV-MODELS; PHENOTYPE
PREDICTION; CLINICAL MANAGEMENT; USAGE; INFECTION; SEQUENCE; DISEASE;
ASSAY
AB Accurate co-receptor tropism (CRT) determination is critical for making treatment decisions in HIV management. We created a genotypic tropism prediction tool by utilizing the case-based reasoning (CBR) technique that attempts to solve new problems through applying the solution from similar past problems. V3 loop sequences from 732 clinical samples with diverse characteristics were used to build a case library. Additional sequence and molecular properties of the V3 loop were examined and used for similarity assessment. A similarity metric was defined based on each attribute's frequency in the CXCR4-using viruses. We implemented three other genotype-based tropism predictors, support vector machines (SVM), position specific scoring matrices (PSSM), and the 11/25 rule, and evaluated their performance as the ability to predict CRT compared to Monogram's enhanced sensitivity Trofile (R) assay (ESTA). Overall concordance of the CBR based tropism prediction algorithm was 81%, as compared to ESTA. Sensitivity to detect CXCR4 usage was 90% and specificity was at 73%. In comparison, sensitivity of the SVM, PSSM, and the 11/25 rule were 85%, 81%, and 36% respectively while achieving a specificity of 90% by SVM, 75% by PSSM, and 97% by the 11/25 rule. When we evaluated these predictors in an unseen dataset, higher sensitivity was achieved by the CBR algorithm (87%), compared to SVM (82%), PSSM (76%), and the 11/25 rule (33%), while maintaining similar level of specificity. Overall this study suggests that CBR can be utilized as a genotypic tropism prediction tool, and can achieve improved performance in independent datasets compared to model or rule based methods.
C1 [Evans, Mark C.; Paquet, Agnes C.; Stawiski, Eric W.; Haddad, Mojgan] Monogram Biosci Inc, Bioinformat Biostat, San Francisco, CA 94080 USA.
[Huang, Wei; Frantzell, Arne; Toma, Jonathan; Petropoulos, Christos J.] Monogram Biosci Inc, Res & Dev, San Francisco, CA 94080 USA.
[Napolitano, Laura; Coakley, Eoin] Monogram Biosci Inc, Clin Res, San Francisco, CA 94080 USA.
[Whitcomb, Jeannette] Monogram Biosci Inc, Operat, San Francisco, CA 94080 USA.
[Goetz, Matthew Bidwell] Univ Calif Los Angeles, David Geffen Sch Med, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
RP Haddad, M (reprint author), Monogram Biosci Inc, Bioinformat Biostat, San Francisco, CA 94080 USA.
EM mhaddad@monogrambio.com
OI Goetz, Matthew/0000-0003-4542-992X
FU National Institutes of Health [U01 AI-42170, U01 AI-46362, U01 AI-68641]
FX The authors would like to acknowledge the Monogram Biosciences clinical
reference and R&D laboratories for performance of all phenotype and
genotype assays. The CPCRA and INSIGHT networks are funded by the
National Institutes of Health (U01 AI-42170, U01 AI-46362, U01
AI-68641).
NR 32
TC 1
Z9 1
U1 0
U2 3
PU IMPERIAL COLLEGE PRESS
PI LONDON
PA 57 SHELTON ST, COVENT GARDEN, LONDON WC2H 9HE, ENGLAND
SN 0219-7200
EI 1757-6334
J9 J BIOINF COMPUT BIOL
JI J. Bioinform. Comput. Biol.
PD AUG
PY 2013
VL 11
IS 4
AR 1350006
DI 10.1142/S0219720013500066
PG 17
WC Biochemical Research Methods; Computer Science, Interdisciplinary
Applications; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Computer Science; Mathematical &
Computational Biology
GA 268IO
UT WOS:000328163800004
PM 23859270
ER
PT J
AU Morgan, AM
Lo, J
Fisher, DE
AF Morgan, Ann M.
Lo, Jennifer
Fisher, David E.
TI How does pheomelanin synthesis contribute to melanomagenesis? Two
distinct mechanisms could explain the carcinogenicity of pheomelanin
synthesis
SO BIOESSAYS
LA English
DT Article
DE melanoma; pheomelanin; pigmentation; reactive oxygen species
ID OXYGEN PHOTOCONSUMPTION; TRANSIENT ABSORPTION; CELLS; MELANOGENESIS;
PIGMENTATION; SPECTROSCOPY; GENERATION; EUMELANIN; EMISSION; REMOVAL
AB Recently, we reported that melanoma risk in redheads is linked not only to pale skin, but also to the synthesis of the pigment - called pheomelanin - that gives red hair its color. We demonstrated that pheomelanin synthesis is associated with increased oxidative stress in the skin, yet we have not uncovered the chemical pathway between the molecule pheomelanin and the DNA damage that drives melanoma formation. Here, we hypothesize two possible pathways. On one hand, pheomelanin might generate reactive oxygen species (ROS) that directly or indirectly cause oxidative DNA damage. On the other hand, pheomelanin synthesis might consume cellular antioxidant stores and make the cell nucleus more vulnerable to other endogenous ROS. Uncovering the mechanistic pathway between pheomelanin and oxidative DNA damage will be an important step in developing strategies to lower melanoma risk in redheads.
C1 [Morgan, Ann M.; Lo, Jennifer; Fisher, David E.] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA.
RP Morgan, AM (reprint author), Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA USA.
EM amorgan@college.harvard.edu
FU NIAMS NIH HHS [R01 AR043369]; NIGMS NIH HHS [T32 GM007753]
NR 25
TC 14
Z9 14
U1 0
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0265-9247
EI 1521-1878
J9 BIOESSAYS
JI Bioessays
PD AUG
PY 2013
VL 35
IS 8
BP 672
EP 676
DI 10.1002/bies.201300020
PG 5
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics
GA 262YR
UT WOS:000327774300004
PM 23650156
ER
PT J
AU Ahmed, FA
Kamnaksh, A
Kovesdi, E
Long, JB
Agoston, DV
AF Ahmed, Farid A.
Kamnaksh, Alaa
Kovesdi, Erzsebet
Long, Joseph B.
Agoston, Denes V.
TI Long-term consequences of single and multiple mild blast exposure on
select physiological parameters and blood-based biomarkers
SO ELECTROPHORESIS
LA English
DT Article
DE Animal models; Brain trauma; Experimental; Physiology; Proteomics
ID TRAUMATIC BRAIN-INJURY; CONCUSSION; RATS
AB Mild traumatic brain injury (mTBI), especially when it is repeated (rmTBI), can lead to progressive degenerative diseases and lasting neuropsychiatric abnormalities. To better understand the long-term pathobiological changes in mTBI and rmTBI, we exposed rats to single or repeated (5 total; administered on consecutive days) mild blast overpressure, monitored changes in physiological parameters, and determined the plasma levels of select biomarkers at 42 days post injury by proteomics. We unexpectedly found comparable changes in arterial oxygen saturation levels and heart rates of single-injured (SI) and multiple-injured (MI) rats throughout the observation period. Our analyses indicated lasting oxidative stress, vascular abnormalities, and neuronal and glial cell loss in both injured groups. However, MI rats exhibited a relatively more pronounced increase in the plasma levels of most of the tested markers-particularly those associated with inflammation-albeit the differences between the two injured groups were not statistically significant. Our findings indicate that the frequency of blast exposures is an important determinant of the resulting cumulative damage in rmTBI.
C1 [Ahmed, Farid A.; Kamnaksh, Alaa; Agoston, Denes V.] Uniformed Serv Univ Hlth Sci, Dept Anat Physiol & Genet, Bethesda, MD 20814 USA.
[Ahmed, Farid A.; Kamnaksh, Alaa; Agoston, Denes V.] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
[Kovesdi, Erzsebet] US Dept Vet Affairs, Vet Affairs Cent Off, Washington, DC USA.
[Long, Joseph B.] Walter Reed Army Inst Res, Blast Induced Neurotrauma Branch, Ctr Mil Psychiat & Neurosci, Silver Spring, MD USA.
RP Agoston, DV (reprint author), Uniformed Serv Univ Hlth Sci, Sch Med, Dept Anat Physiol & Genet, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM vagoston@usuhs.edu
FU Center for Neuroscience and Regenerative Medicine [G1703F]
FX We thank the Neurotrauma Team at the Walter Reed Army Institute of
Research for their technical help during the exposures. This work was
supported by the Center for Neuroscience and Regenerative Medicine grant
number G1703F. The views, opinions, and/or findings contained herein are
those of the authors and should not be construed as an official
position, policy, or decision of the Department of the Army or the
Department of Defense. The authors have no financial disclosures. Animal
handling and treatments were conducted in compliance with the Animal
Welfare Act and other Federal statutes and regulations related to
animals and experiments involving animals, and adhered to principles
stated in the Guide to the Care and Use of Laboratory Animals, National
Research Council. The facilities are fully accredited by the Association
for Assessment and Accreditation of Laboratory Animal Care
International.
NR 18
TC 13
Z9 14
U1 0
U2 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0173-0835
EI 1522-2683
J9 ELECTROPHORESIS
JI Electrophoresis
PD AUG
PY 2013
VL 34
IS 15
BP 2229
EP 2233
DI 10.1002/elps.201300077
PG 5
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 261KJ
UT WOS:000327663600012
PM 23712899
ER
PT J
AU Buttenheim, AM
Cherng, ST
Asch, DA
AF Buttenheim, Alison M.
Cherng, Sarah T.
Asch, David A.
TI Provider dismissal policies and clustering of vaccine-hesitant families
An agent-based modeling approach
SO HUMAN VACCINES & IMMUNOTHERAPEUTICS
LA English
DT Article
DE vaccination; immunization; immunization schedule; decision-making;
parents
ID DISEASE OUTBREAKS; REFUSES VACCINES; DYNAMICS; BEHAVIOR; IMMUNIZATION;
EPIDEMIOLOGY; EXPERIENCE; NETWORKS; CHILDREN; HEALTH
AB Many pediatric practices have adopted vaccine policies that require parents who refuse to vaccinate according to the ACIP schedule to find another health care provider. Such policies may inadvertently cluster unvaccinated patients into practices that tolerate non-vaccination or alternative schedules, turning them into risky pockets of low herd immunity. The objective of this study was to assess the effect of provider zero-tolerance vaccination policies on the clustering of intentionally unvaccinated children. We developed an agent-based model of parental vaccine hesitancy, provider non-vaccination tolerance, and selection of patients into pediatric practices. We ran 84 experiments across a range of parental hesitancy and provider tolerance scenarios. When the model is initialized, all providers accommodate refusals and intentionally unvaccinated children are evenly distributed across providers. As provider tolerance decreases, hesitant children become more clustered in a smaller number of practices and eventually are not able to find a practice that will accept them. Each of these effects becomes more pronounced as the level of hesitancy in the population rises. Heterogeneity in practice tolerance to vaccine-hesitant parents has the unintended result of concentrating susceptible individuals within a small number of tolerant practices, while providing little if any compensatory protection to adherent individuals. These externalities suggest an agenda for stricter policy regulation of individual practice decisions.
C1 [Buttenheim, Alison M.] Univ Penn, Sch Nursing, Dept Family & Community Hlth, Philadelphia, PA 19104 USA.
[Buttenheim, Alison M.; Asch, David A.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Cherng, Sarah T.] Univ Michigan, Ctr Studies Complex Syst, Ann Arbor, MI 48109 USA.
[Asch, David A.] Philadelphia VA Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
RP Buttenheim, AM (reprint author), Univ Penn, Sch Nursing, Dept Family & Community Hlth, Philadelphia, PA 19104 USA.
EM abutt@nursing.upenn.edu
OI Asch, David/0000-0002-7970-286X
FU Robert Wood Johnson Foundation Health and Society Scholars Program at
the University of Pennsylvania; National Cancer Institute
[1KM1CA156715-01]
FX This research was supported by the Robert Wood Johnson Foundation Health
and Society Scholars Program at the University of Pennsylvania and by
the National Cancer Institute (1KM1CA156715-01).
NR 33
TC 7
Z9 7
U1 2
U2 11
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2164-5515
EI 2164-554X
J9 HUM VACC IMMUNOTHER
JI Human Vaccines Immunother.
PD AUG 1
PY 2013
VL 9
IS 8
BP 1819
EP 1824
DI 10.4161/hv.25635
PG 6
WC Biotechnology & Applied Microbiology; Immunology
SC Biotechnology & Applied Microbiology; Immunology
GA 259SY
UT WOS:000327547800035
PM 23831786
ER
PT J
AU Zhou, JY
Krovvidi, RK
Gao, YQ
Gao, H
Petritis, BO
De, AK
Miller-Graziano, CL
Bankey, PE
Petyuk, VA
Nicora, CD
Clauss, TR
Moore, RJ
Shi, TJ
Brown, JN
Kaushal, A
Xiao, WZ
Davis, RW
Maier, RV
Tompkins, RG
Qian, WJ
Camp, DG
Smith, RD
AF Zhou, Jian-Ying
Krovvidi, Ravi K.
Gao, Yuqian
Gao, Hong
Petritis, Brianne O.
De, Asit K.
Miller-Graziano, Carol L.
Bankey, Paul E.
Petyuk, Vladislav A.
Nicora, Carrie D.
Clauss, Therese R.
Moore, Ronald J.
Shi, Tujin
Brown, Joseph N.
Kaushal, Amit
Xiao, Wenzhong
Davis, Ronald W.
Maier, Ronald V.
Tompkins, Ronald G.
Qian, Wei-Jun
Camp, David G., II
Smith, Richard D.
CA Inflammation Host Response Injury
TI Trauma-associated human neutrophil alterations revealed by comparative
proteomics profiling
SO PROTEOMICS CLINICAL APPLICATIONS
LA English
DT Article
DE Genomics; Human neutrophil; LC-MS; MS; Trauma
ID NF-KAPPA-B; TANDEM MASS-SPECTROMETRY; INFLAMMATORY RESPONSE; SHOTGUN
PROTEOMICS; CELL-PROLIFERATION; PROTEIN-SYNTHESIS; GENE-EXPRESSION;
CANCER-CELLS; APOPTOSIS; ACTIVATION
AB PurposePolymorphonuclear neutrophils (PMNs) play an important role in mediating the innate immune response after severe traumatic injury; however, the cellular proteome response to traumatic condition is still largely unknown.
Experimental designWe applied 2D-LC-MS/MS-based shotgun proteomics to perform comparative proteome profiling of human PMNs from severe trauma patients and healthy controls.
ResultsA total of 197 out of approximate to 2500 proteins (being identified with at least two peptides) were observed with significant abundance changes following the injury. The proteomics data were further compared with transcriptomics data for the same genes obtained from an independent patient cohort. The comparison showed that the protein abundance changes for the majority of proteins were consistent with the mRNA abundance changes in terms of directions of changes. Moreover, increased protein secretion was suggested as one of the mechanisms contributing to the observed discrepancy between protein and mRNA abundance changes. Functional analyses of the altered proteins showed that many of these proteins were involved in immune response, protein biosynthesis, protein transport, NRF2-mediated oxidative stress response, the ubiquitin-proteasome system, and apoptosis pathways.
Conclusions and clinical relevanceOur data suggest increased neutrophil activation and inhibited neutrophil apoptosis in response to trauma. The study not only reveals an overall picture of functional neutrophil response to trauma at the proteome level, but also provides a rich proteomics data resource of trauma-associated changes in the neutrophil that will be valuable for further studies of the functions of individual proteins in PMNs.
C1 [Zhou, Jian-Ying; Krovvidi, Ravi K.; Gao, Yuqian; Petritis, Brianne O.; Petyuk, Vladislav A.; Nicora, Carrie D.; Clauss, Therese R.; Moore, Ronald J.; Shi, Tujin; Brown, Joseph N.; Qian, Wei-Jun; Camp, David G., II; Smith, Richard D.] Pacific NW Natl Lab, Div Biol Sci, Richland, WA 99352 USA.
[Zhou, Jian-Ying; Krovvidi, Ravi K.; Gao, Yuqian; Petritis, Brianne O.; Petyuk, Vladislav A.; Nicora, Carrie D.; Clauss, Therese R.; Moore, Ronald J.; Shi, Tujin; Brown, Joseph N.; Qian, Wei-Jun; Camp, David G., II; Smith, Richard D.] Pacific NW Natl Lab, Environm Mol Sci Lab, Richland, WA 99352 USA.
[De, Asit K.; Miller-Graziano, Carol L.; Bankey, Paul E.] Univ Rochester, Sch Med, Dept Surg, Rochester, NY USA.
[Gao, Hong; Kaushal, Amit; Xiao, Wenzhong; Davis, Ronald W.] Stanford Univ, Sch Med, Stanford Genome Technol Ctr, Palo Alto, CA 94304 USA.
[Xiao, Wenzhong; Maier, Ronald V.] Univ Washington, Harborview Med Ctr, Dept Surg, Seattle, WA 98104 USA.
[Tompkins, Ronald G.] Harvard Univ, Sch Med, Dept Surg, Shriners Burn Ctr, Boston, MA 02115 USA.
[Tompkins, Ronald G.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
RP Smith, RD (reprint author), Pacific NW Natl Lab, Environm Mol Sci Lab, POB 999,MSIN K8-98, Richland, WA 99352 USA.
EM rds@pnnl.gov
RI Smith, Richard/J-3664-2012; Shi, Tujin/O-1789-2014;
OI Smith, Richard/0000-0002-2381-2349; Baker, Henry/0000-0002-8273-5320;
Petyuk, Vladislav/0000-0003-4076-151X
FU NIH [U54 GM-62119-02, T32 GM-008256, P41 GM103493, DP2OD006668]; EMSL
(Environmental Molecular Science Laboratory); US Department of Energy
(DOE) Office of Biological and Environmental Research on the Pacific
Northwest National Laboratory (PNNL) campus in Richland, Washington; DOE
[DE-AC05-76RLO-1830]
FX Portions of this research were supported by NIH grants U54 GM-62119-02
(to R.G.T.) and T32 GM-008256 (to R.G.T.), P41 GM103493 (to R.D.S.),
DP2OD006668 (to W.J.Q.), and EMSL (Environmental Molecular Science
Laboratory). EMSL is a national scientific user facility sponsored by
the US Department of Energy (DOE) Office of Biological and Environmental
Research on the Pacific Northwest National Laboratory (PNNL) campus in
Richland, Washington. PNNL is operated by Battelle for the DOE under
contract DE-AC05-76RLO-1830.
NR 81
TC 4
Z9 4
U1 0
U2 3
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA BOSCHSTRASSE 12, D-69469 WEINHEIM, GERMANY
SN 1862-8346
EI 1862-8354
J9 PROTEOM CLIN APPL
JI Proteom. Clin. Appl.
PD AUG
PY 2013
VL 7
IS 7-8
SI SI
BP 571
EP 583
DI 10.1002/prca.201200109
PG 13
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 263FQ
UT WOS:000327792800011
PM 23589343
ER
PT J
AU Kashyap, SR
Bhatt, DL
Wolski, K
Watanabe, RM
Abdul-Ghani, M
Abood, B
Pothier, CE
Brethauer, S
Nissen, S
Gupta, M
Kirwan, JP
Schauer, PR
AF Kashyap, Sangeeta R.
Bhatt, Deepak L.
Wolski, Kathy
Watanabe, Richard M.
Abdul-Ghani, Muhammad
Abood, Beth
Pothier, Claire E.
Brethauer, Stacy
Nissen, Steven
Gupta, Manjula
Kirwan, John P.
Schauer, Philip R.
TI Metabolic Effects of Bariatric Surgery in Patients With Moderate Obesity
and Type 2 Diabetes Analysis of a randomized control trial comparing
surgery with intensive medical treatment
SO DIABETES CARE
LA English
DT Article
ID GASTRIC BYPASS-SURGERY; BETA-CELL FUNCTION; LIFE-STYLE INTERVENTION;
GLUCAGON-LIKE PEPTIDE-1; GLUCOSE-TOLERANCE; INSULIN-SECRETION; GLYCEMIC
CONTROL; INCRETIN LEVELS; WEIGHT-LOSS; THERAPY
AB OBJECTIVETo evaluate the effects of two bariatric procedures versus intensive medical therapy (IMT) on -cell function and body composition.RESEARCH DESIGN AND METHODSThis was a prospective, randomized, controlled trial of 60 subjects with uncontrolled type 2 diabetes (HbA(1c) 9.7 1%) and moderate obesity (BMI 36 2 kg/m(2)) randomized to IMT alone, IMT plus Roux-en-Y gastric bypass, or IMT plus sleeve gastrectomy. Assessment of -cell function (mixed-meal tolerance testing) and body composition was performed at baseline and 12 and 24 months.RESULTSGlycemic control improved in all three groups at 24 months (N = 54), with a mean HbA(1c) of 6.7 +/- 1.2% for gastric bypass, 7.1 +/- 0.8% for sleeve gastrectomy, and 8.4 +/- 2.3% for IMT (P < 0.05 for each surgical group versus IMT). Reduction in body fat was similar for both surgery groups, with greater absolute reduction in truncal fat in gastric bypass versus sleeve gastrectomy (-16 vs. -10%; P = 0.04). Insulin sensitivity increased significantly from baseline in gastric bypass (2.7-fold; P = 0.004) and did not change in sleeve gastrectomy or IMT. -Cell function (oral disposition index) increased 5.8-fold in gastric bypass from baseline, was markedly greater than IMT (P = 0.001), and was not different between sleeve gastrectomy versus IMT (P = 0.30). At 24 months, -cell function inversely correlated with truncal fat and prandial free fatty acid levels.CONCLUSIONSBariatric surgery provides durable glycemic control compared with intensive medical therapy at 2 years. Despite similar weight loss as sleeve gastrectomy, gastric bypass uniquely restores pancreatic -cell function and reduces truncal fat, thus reversing the core defects in diabetes.
C1 [Kashyap, Sangeeta R.; Abood, Beth; Gupta, Manjula] Cleveland Clin, Endocrinol & Metab Inst, Cleveland, OH 44106 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.
[Wolski, Kathy; Pothier, Claire E.; Nissen, Steven] Cleveland Clin, Miller Family Heart & Vasc Inst, Cleveland, OH 44106 USA.
[Watanabe, Richard M.] Univ So Calif, Dept Physiol & Biophys, Los Angeles, CA 90089 USA.
[Abdul-Ghani, Muhammad] Univ Texas Hlth Sci Ctr San Antonio, Diabet Div, San Antonio, TX 78229 USA.
[Brethauer, Stacy; Schauer, Philip R.] Cleveland Clin, Bariatr & Metab Inst, Cleveland, OH 44106 USA.
[Kirwan, John P.] Cleveland Clin, Lerner Res Inst, Cleveland, OH 44106 USA.
RP Kashyap, SR (reprint author), Cleveland Clin, Endocrinol & Metab Inst, Cleveland, OH 44106 USA.
EM kashyas@ccf.org
FU Ethicon Endo-Surgery EES IIS [19900]; American Diabetes Association
[1-11-26 CT]; National Institutes of Health [R01-DK089547]; Ethicon
Endo-Surgery; Amarin; AstraZeneca; Bristol-Myers Squibb; Eisai; Ethicon;
Medtronic; Sanofi; Medicines Company; FlowCo; Nestle Inc.; ScottCare;
Bard-Davol; Stryker Endoscopy; Gore; Baxter; Covidien; Allergan
FX Primary funding for the STAMPEDE trial is from Ethicon Endo-Surgery EES
IIS 19900 (to P.R.S.). The American Diabetes Association clinical
translational award (1-11-26 CT) to S.R.K. provided ancillary funding
for STAMPEDE. A grant from the National Institutes of Health
(R01-DK089547) to S.R.K., P.R.S., and J.P.K. was provided.; S.R.K.
obtained research grants from Ethicon Endo-Surgery, National Institutes
of Health, and American Diabetes Association. D.L.B. is a member of the
Advisory Board for Medscape Cardiology, is on the Board of Directors for
Boston VA Research Institute and Society of Chest Pain Centers, is the
Chair of American Heart Association Get With The Guidelines Science
Subcommittee, received honoraria from American College of Cardiology
(Editor, Clinical Trials, Cardiosource), Duke Clinical Research
Institute (clinical trial steering committees), Slack Publications
(Chief Medical Editor, Cardiology Today Intervention), and WebMD (CME
steering committees), is the Senior Associate Editor of Journal of
Invasive Cardiology, received research grants from Amarin, AstraZeneca,
Bristol-Myers Squibb, Eisai, Ethicon, Medtronic, Sanofi, The Medicines
Company, and FlowCo, and performed unfunded research for PLx Pharma and
Takeda. D.L.B. receives honoraria from Ethicon Endo-Surgery as
scientific advisory board member, consultant, and speaker, and has
received honoraria from Covidien for speaking. J.P.K. receives grant
funding from National Institutes of Health, Nestle Inc., and ScottCare.
P.R.S. obtained research grants from Ethicon Endo-surgery, National
Institutes of Health, and Bard-Davol; received educational grants from
Stryker Endoscopy, Gore, Baxter, Covidien, and Allergan; and received
honoraria from Ethicon Endo-surgery as a scientific advisory board
member, consultant, and speaker. P.R.S. has been a consultant/advisory
board member for RemedyMD, StrykerEndoscopy, Bard-Davol, Gore,
Barosense, Surgiquest, and Carefusion. S.N. has consulted with Orexigen
and Vivus. S.R.K., P.R.S., and the Cleveland Clinic Coordinating Center
for Clinical Research had full and independent access to all of the data
in the study. The sponsor participated in discussions regarding study
design and protocol development and provided logistical support during
the trial. The database, statistical analysis, and monitoring were all
performed by the Cleveland Clinic Coordinating Center for Clinical
Research. The manuscript was prepared by the corresponding author and
modified after consultation with co-authors. The sponsor was permitted
to review the manuscript and suggest changes, but the final decision on
content and submission was exclusively retained by the academic authors.
J. Michael Henderson, MD (Chair), James B. Young, MD, and Venu Menon,
MD, Cleveland Clinic, Cleveland, Ohio, are members of the Data and
Safety Monitoring Board. No other potential conflicts of interest
relevant to this article were reported.
NR 31
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD AUG
PY 2013
VL 36
IS 8
BP 2175
EP 2182
DI 10.2337/dc12-1596
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 255PP
UT WOS:000327252600027
PM 23439632
ER
PT J
AU Strickland, LR
Guo, FJ
Lok, K
Garvey, WT
AF Strickland, Leah R.
Guo, Fangjian
Lok, Kerry
Garvey, W. Timothy
TI Type 2 Diabetes With Partial Lipodystrophy of the Limbs A new
lipodystrophy phenotype
SO DIABETES CARE
LA English
DT Article
ID FAMILIAL PARTIAL LIPODYSTROPHY; LEPTIN-REPLACEMENT THERAPY;
FATTY-ACID-METABOLISM; INSULIN-RESISTANCE; INHERITED LIPODYSTROPHIES;
ADIPOSE-TISSUE; GLUCOSE-UPTAKE; BODY-FAT; MACROPHAGES; MICE
AB OBJECTIVELipodystrophies are categorized by the extent of fat loss (generalized vs. partial) and by inheritance (congenital vs. acquired). We examined whether a group of patients with partial lipodystrophy of the limbs (PLL), type 2 diabetes mellitus (T2DM), and an absence of a family history of lipodystrophy constitute a new clinical subtype.RESEARCH DESIGN AND METHODSTen women with T2DM and PLL were identified in academic diabetes clinics and were matched by age, sex, BMI, ethnicity, and diabetes status with 10 women with control T2DM without lipodystrophy. All patients were characterized by clinical evaluation and hyperinsulinemic clamp.RESULTSPatients with T2DM and PLL exhibited symmetrical loss of subcutaneous fat in forearms, or forearms plus calves, and acanthosis nigricans. Maximally stimulated glucose disposal rates were markedly reduced by 56% in the T2DM with PLL group compared with the control T2DM patients, whether normalized by body weight or surface area. Most PLL patients exhibited little or no insulin-mediated glucose uptake after subtraction of non-insulin-mediated glucose uptake. The T2DM with PLL group also had greater elevations in hepatic transaminases and triglycerides and earlier onset of diabetes compared with control T2DM.CONCLUSIONST2DM with PLL represents a previously unrecognized phenotype of lipodystrophy and of T2DM. These T2DM patients exhibit symmetrical lipodystrophy of the distal limbs, acanthosis nigricans, marked insulin resistance with little insulin-mediated glucose uptake, hypertriglyceridemia, and hepatic transaminase elevations, which are greater in severity than observed in patients with common T2DM.
C1 [Strickland, Leah R.; Guo, Fangjian; Lok, Kerry; Garvey, W. Timothy] Univ Alabama Birmingham, Dept Nutr Sci, Birmingham, AL 35294 USA.
[Strickland, Leah R.] Univ Alabama Birmingham, Sch Med, Birmingham, AL 35294 USA.
[Garvey, W. Timothy] Birmingham Vet Affairs Med Ctr, Birmingham, AL USA.
RP Garvey, WT (reprint author), Univ Alabama Birmingham, Dept Nutr Sci, Birmingham, AL 35294 USA.
EM garveyt@uab.edu
RI Guo, Fangjian/B-7705-2015
OI Guo, Fangjian/0000-0003-3729-2724
FU National Institutes of Health [DK-083562, DK-038764]; Department of
Veterans Affairs; National Institute of Diabetes and Digestive and
Kidney Diseases [P60-DK-079626]; Amylin Pharmaceuticals, Inc.; Merck
Co.; UAB Obesity Training Program [T32 DK-062710]
FX This work was supported by grants from the National Institutes of Health
(DK-083562, DK-038764) to W.T.G, and the Merit Review program of the
Department of Veterans Affairs to W.T.G. L.R.S. was supported by a
Summer Research Fellowship for Medical Students provided by National
Institute of Diabetes and Digestive and Kidney Diseases to the
University of Alabama (UAB) Diabetes Research and Training Center
(P60-DK-079626) and administered by the UAB Obesity Training Program
(T32 DK-062710).; W.T.G. has received speaker honoraria from Merck &
Co.; has served on advisory boards for Vivus, Daiichi-Sankyo,
LipoScience, Janssen, and Alkermes; and has received research support
from Amylin Pharmaceuticals, Inc. and Merck & Co. No other potential
conflicts of interest relevant to this article were reported.
NR 28
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD AUG
PY 2013
VL 36
IS 8
BP 2247
EP 2253
DI 10.2337/dc12-1529
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 255PP
UT WOS:000327252600037
PM 23423695
ER
PT J
AU Nathan, DM
Buse, JB
Kahn, SE
Krause-Steinrauf, H
Larkin, ME
Staten, M
Wexler, D
Lachin, JM
AF Nathan, David M.
Buse, John B.
Kahn, Steven E.
Krause-Steinrauf, Heidi
Larkin, Mary E.
Staten, Myrlene
Wexler, Deborah
Lachin, John M.
CA GRADE Study Res Grp
TI Rationale and Design of the Glycemia Reduction Approaches in Diabetes: A
Comparative Effectiveness Study (GRADE)
SO DIABETES CARE
LA English
DT Article
ID IMPAIRED GLUCOSE-TOLERANCE; CARDIOVASCULAR-DISEASE; GLYBURIDE
MONOTHERAPY; LIFE-STYLE; FOLLOW-UP; MELLITUS; METFORMIN; HYPERGLYCEMIA;
ASSOCIATION; PREVENTION
AB OBJECTIVEThe epidemic of type 2 diabetes (T2DM) threatens to become the major public health problem of this century. However, a comprehensive comparison of the long-term effects of medications to treat T2DM has not been conducted. GRADE, a pragmatic, unmasked clinical trial, aims to compare commonly used diabetes medications, when combined with metformin, on glycemia-lowering effectiveness and patient-centered outcomes.RESEARCH DESIGN AND METHODSGRADE was designed with support from a U34 planning grant from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The consensus protocol was approved by NIDDK and the GRADE Research Group. Eligibility criteria for the 5,000 metformin-treated subjects include <5 years' diabetes duration, 30 years of age at time of diagnosis, and baseline hemoglobin A(1c) (A1C) of 6.8-8.5% (51-69 mmol/mol). Medications representing four classes (sulfonylureas, dipeptidyl peptidase 4 inhibitors, glucagon-like peptide 1 receptor agonists, and insulin) will be randomly assigned and added to metformin (minimum-maximum 1,000-2,000 mg/day). The primary metabolic outcome is the time to primary failure defined as an A1C 7% (53 mmol/mol), subsequently confirmed, over an anticipated mean observation period of 4.8 years (range 4-7 years). Other long-term metabolic outcomes include the need for the addition of basal insulin after a confirmed A1C >7.5% (58 mmol/mol) and, ultimately, the need to implement an intensive basal/bolus insulin regimen. The four drugs will also be compared with respect to selected microvascular complications, cardiovascular disease risk factors, adverse effects, tolerability, quality of life, and cost-effectiveness.CONCLUSIONSGRADE will compare the long-term effectiveness of major glycemia-lowering medications and provide guidance to clinicians about the most appropriate medications to treat T2DM. GRADE begins recruitment at 37 centers in the U.S. in 2013.
C1 [Nathan, David M.; Larkin, Mary E.; Wexler, Deborah] Massachusetts Gen Hosp, Diabet Res Ctr, Boston, MA 02114 USA.
[Nathan, David M.; Larkin, Mary E.; Wexler, Deborah] Harvard Univ, Sch Med, Boston, MA USA.
[Buse, John B.] Univ N Carolina, Dept Med, Div Endocrinol, Chapel Hill, NC USA.
[Kahn, Steven E.] VA Puget Sound Hlth Care Syst, Dept Med, Div Metab Endocrinol & Nutr, Seattle, WA USA.
[Kahn, Steven E.] Univ Washington, Seattle, WA 98195 USA.
[Krause-Steinrauf, Heidi; Lachin, John M.] George Washington Univ, Ctr Biostat, Rockville, MD 20852 USA.
[Staten, Myrlene] Natl Inst Diabet & Digest & Kidney Dis, Bethesda, MD USA.
RP Krause-Steinrauf, H (reprint author), George Washington Univ, Ctr Biostat, Rockville, MD 20852 USA.
EM heidi@bsc.gwu.edu
OI Lachin, John/0000-0001-9838-2841; Kahn, Steven/0000-0001-7307-9002
FU NIDDK, NIH [5U34-DK-088043-02]; American Diabetes Association; Abbott;
Amylin; Andromeda; AstraZeneca; Bayhill Therapeutics; BD Research
Laboratories; Boehringer Ingelheim; Bristol-Myers Squibb; Catabasis;
Cebix; Diartis, Elcelyx; Eli Lilly; Exsulin; Genentech; GI Dynamics;
GlaxoSmithKline; Halozyme; Hoffman-La Roche; Johnson Johnson;
LipoScience; Medtronic; Merck; Metabolic Solutions Development Company;
Metabolon; Novan; Novella; Novartis; Novo Nordisk; Orexigen; Osiris;
Pfizer; Rhythm; Sanofi; Spherix; Takeda; Tolerex; TransPharma; Veritas;
Verva; [1U01-DK-098246-01]
FX The planning of GRADE was supported by a U34 planning grant from the
NIDDK, NIH (5U34-DK-088043-02). The American Diabetes Association
provided funds for the initial planning meeting for developing the U34
proposal. GRADE is supported by a U01 grant (1U01-DK-098246-01).
Educational materials have been provided by the National Diabetes
Education Program. Material support in the form of donated medications
and supplies has been provided by BD, Bristol-Myers Squibb, Merck, Novo
Nordisk, Roche Diagnostics, and Sanofi.; J.B.B.'s employer (the
University of North Carolina) has received payments for his work as a
consultant or investigator from Abbott, Amylin, Andromeda, AstraZeneca,
Bayhill Therapeutics, BD Research Laboratories, Boehringer Ingelheim,
Bristol-Myers Squibb, Catabasis, Cebix, Diartis, Elcelyx, Eli Lilly,
Exsulin, Genentech, GI Dynamics, GlaxoSmithKline, Halozyme, Hoffman-La
Roche, Johnson & Johnson, LipoScience, Medtronic, Merck, Metabolic
Solutions Development Company, Metabolon, Novan, Novella, Novartis, Novo
Nordisk, Orexigen, Osiris, Pfizer, Rhythm, Sanofi, Spherix, Takeda,
Tolerex, TransPharma, Veritas, and Verva. S.E.K. has received honoraria
for consulting from Boehringer Ingelheim, Bristol-Myers Squibb, Eli
Lilly, GlaxoSmithKline, Intarcia Therapeutics, Janssen, Merck, Novo
Nordisk, and Receptos and honoraria for speaking from Boehringer
Ingelheim and Merck. J.M.L. has received honoraria for consulting from
Merck, Boehringer Ingelheim, Eli Lilly, Novartis, and Janssen. No other
potential conflicts of interest relevant to this article were reported.
NR 40
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD AUG
PY 2013
VL 36
IS 8
BP 2254
EP 2261
DI 10.2337/dc13-0356
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 255PP
UT WOS:000327252600038
PM 23690531
ER
PT J
AU Lopes-Virella, MF
Baker, NL
Hunt, KJ
Cleary, PA
Klein, R
Virella, G
AF Lopes-Virella, Maria F.
Baker, Nathaniel L.
Hunt, Kelly J.
Cleary, Patricia A.
Klein, Richard
Virella, Gabriel
CA DCCT EDIC Res Grp
TI Baseline Markers of Inflammation Are Associated With Progression to
Macroalbuminuria in Type 1 Diabetic Subjects
SO DIABETES CARE
LA English
DT Article
ID EURODIAB PROSPECTIVE COMPLICATIONS; TNF RECEPTORS 1; RISK-FACTORS;
MICROVASCULAR COMPLICATIONS; MACROVASCULAR COMPLICATIONS; ENDOTHELIAL
DYSFUNCTION; VASCULAR-DISEASE; DCCT/EDIC COHORT; FOLLOW-UP; NEPHROPATHY
AB OBJECTIVEThe current study aimed to determine in the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications cohort whether or not abnormal levels of markers of inflammation and endothelial dysfunction measured in samples collected at DCCT baseline were able to predict the development of macroalbuminuria.RESEARCH DESIGN AND METHODSLevels of inflammation and endothelial cell dysfunction biomarkers were measured in 1,237 of 1,441 patients enrolled in the DCCT study who were both free of albuminuria and cardiovascular disease at baseline. To test the association of log-transformed biomarkers with albuminuria, generalized logistic regression models were used to quantify the association of increased levels of biomarkers and development of abnormal albuminuria. Normal, micro-, and macroalbuminuria were the outcomes of interest.RESULTSIn the logistic regression models adjusted by DCCT treatment assignment, baseline albumin excretion rate, and use of ACE/angiotensin receptor blocker drugs, one unit increase in the standardized levels of soluble E-selectin (sE-selectin) was associated with an 87% increase in the odds to develop macroalbuminuria and one unit increase in the levels of interleukin-6 (IL-6), plasminogen activator inhibitor 1 (PAI-1; total and active), and soluble tumor necrosis factor receptors (TNFR)-1 and -2 lead to a 30-50% increase in the odds to develop macroalbuminuria. Following adjustment for DCCT baseline retinopathy status, age, sex, HbA(1c), and duration of diabetes, significant associations remained for sE-selectin and TNFR-1 and -2 but not for IL-6 or PAI-1.CONCLUSIONSOur study indicates that high levels of inflammatory markers, mainly E-selectin and sTNRF-1 and -2, are important predictors of macroalbuminuria in patients with type 1 diabetes.
C1 [Lopes-Virella, Maria F.] Med Univ S Carolina, Dept Med & Lab Serv, Charleston, SC 29425 USA.
[Lopes-Virella, Maria F.; Klein, Richard] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
[Baker, Nathaniel L.; Hunt, Kelly J.] Med Univ S Carolina, Dept Publ Hlth Serv, Charleston, SC 29425 USA.
[Cleary, Patricia A.] George Washington Univ, Ctr Biostat, Washington, DC USA.
[Virella, Gabriel] Med Univ S Carolina, Dept Microbiol & Immunol, Charleston, SC 29425 USA.
RP Lopes-Virella, MF (reprint author), Med Univ S Carolina, Dept Med & Lab Serv, Charleston, SC 29425 USA.
EM virellam@musc.edu
FU National Institutes of Health/National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK); Research Service of the Ralph H.
Johnson Department of the Veterans Affairs Medical Center; Division of
Diabetes, Endocrinology and Metabolic Diseases (NIDDK) of the National
Institutes of Health; National Center for Research Resources through the
General Clinical Research Centers program; Genentech, Inc.;
[R01-DK-081352]
FX This work was supported by the Grant R01-DK-081352 funded by the
National Institutes of Health/National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK) and by the Research Service of the
Ralph H. Johnson Department of the Veterans Affairs Medical Center.; The
DCCT/EDIC was sponsored through research contracts from the Division of
Diabetes, Endocrinology and Metabolic Diseases (NIDDK) of the National
Institutes of Health. Additional support was provided by the National
Center for Research Resources through the General Clinical Research
Centers program and by Genentech, Inc., through a Cooperative Research
and Development Agreement with the NIDDK. No other potential conflicts
of interest relevant to this article were reported.
NR 27
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD AUG
PY 2013
VL 36
IS 8
BP 2317
EP 2323
DI 10.2337/dc12-2521
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 255PP
UT WOS:000327252600047
PM 23514730
ER
PT J
AU Chirinos, JA
Segers, P
Gillebert, TC
Buyzere, ML
Van Daele, CM
Khan, ZA
Khawar, U
Bacquer, D
Rietzschel, ER
AF Chirinos, Julio A.
Segers, Patrick
Gillebert, Thierry C.
De Buyzere, Marc L.
Van Daele, Caroline M.
Khan, Zubair A.
Khawar, Umair
De Bacquer, Dirk
Rietzschel, Ernst R.
CA Asklepios Investigators
TI Central Pulse Pressure and Its Hemodynamic Determinants in Middle-Aged
Adults With Impaired Fasting Glucose and Diabetes
SO DIABETES CARE
LA English
DT Article
ID AORTIC ROOT DILATATION; CARDIOVASCULAR RISK-FACTORS; BODY-SURFACE AREA;
ARTERIAL STIFFNESS; NONINVASIVE EVALUATION; ESSENTIAL-HYPERTENSION; WAVE
REFLECTIONS; PLASMA-GLUCOSE; ORGAN DAMAGE; OLDER-ADULTS
AB OBJECTIVEPulse pressure (PP), a strong predictor of cardiovascular events in type 2 diabetes, is a composite measure affected by several hemodynamic factors. Little is known about the hemodynamic determinants of central PP in type 2 diabetes or whether abnormalities in central pulsatile hemodynamics are already present in individuals with impaired fasting glucose (IFG). In a population-based study, we aimed to compare central PP and its hemodynamic determinants among adults with normal fasting glucose (n = 1654), IFG (n = 240), and type 2 diabetes (n = 33).RESEARCH DESIGN AND METHODSWe measured carotid pressure, left ventricular outflow, aortic root diameter, carotid artery flow, and distension in order to measure various structural and hemodynamic arterial parameters.RESULTSIFG was associated with a greater mean arterial pressure (MAP) but was not associated with intrinsic aortic stiffening or abnormal aortic pulsatile indices after adjustment for MAP. After adjustment for age, sex, and MAP, type 2 diabetes was associated with a higher aortic root characteristic impedance (Zc), aortic root elastance-thickness product (Eh), and aortic root pulse wave velocity (but not aortic root diameter), a greater carotid-femoral pulse wave velocity, and lower total arterial compliance and wave reflection magnitude. Carotid size, Zc, distensibility, or Eh did not significantly differ between the groups.CONCLUSIONSType 2 diabetes, but not IFG, is associated with greater large artery stiffness, without abnormalities in aortic root diameter or carotid stiffness. Subjects with type 2 diabetes demonstrate a decreased reflection magnitude, which may indicate an increased penetration of pulsatile energy to distal vascular beds.
C1 [Chirinos, Julio A.; Khan, Zubair A.; Khawar, Umair] Univ Penn, Sch Med, Hosp Univ Penn, Philadelphia, PA 19104 USA.
[Chirinos, Julio A.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[Segers, Patrick] Univ Ghent, Inst Biomed Technol, B-9000 Ghent, Belgium.
[Gillebert, Thierry C.; De Buyzere, Marc L.; Van Daele, Caroline M.; Rietzschel, Ernst R.] Ghent Univ Hosp, Dept Cardiovasc Dis, Ghent, Belgium.
[De Bacquer, Dirk; Rietzschel, Ernst R.] Univ Ghent, Dept Publ Hlth, B-9000 Ghent, Belgium.
RP Chirinos, JA (reprint author), Univ Penn, Sch Med, Hosp Univ Penn, Philadelphia, PA 19104 USA.
EM julio.chirinos@uphs.upenn.edu
OI Khan, Zubair/0000-0002-0451-9155; Gillebert, Thierry/0000-0002-3832-919X
FU Fonds voor Wetenschappelijk Onderzoek Vlaanderen Grant [G.0.838.10];
American Heart Association [0885031N]; National Institutes of Health;
Atcor Medical; Cardiodynamics; APC Cardiovascular Ltd.
FX This study was supported by Fonds voor Wetenschappelijk Onderzoek
Vlaanderen Grant G.0.838.10 and the American Heart Association Research
Award 0885031N. J.A.C. received significant (>$10,000) grants from the
National Institutes of Health and the American Heart Association for
research studies related to arterial hemodynamics and has received minor
support (equipment loans) from Atcor Medical, Cardiodynamics, and APC
Cardiovascular Ltd. No other potential conflicts of interest relevant to
this article were reported.
NR 41
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD AUG
PY 2013
VL 36
IS 8
BP 2359
EP 2365
DI 10.2337/dc12-1463
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 255PP
UT WOS:000327252600053
PM 23610081
ER
PT J
AU Hill, JO
Galloway, JM
Goley, A
Marrero, DG
Minners, R
Montgomery, B
Peterson, GE
Ratner, RE
Sanchez, E
Aroda, VR
AF Hill, James O.
Galloway, James M.
Goley, April
Marrero, David G.
Minners, Regan
Montgomery, Brenda
Peterson, Gregory E.
Ratner, Robert E.
Sanchez, Eduardo
Aroda, Vanita R.
TI Scientific Statement: Socioecological Determinants of Prediabetes and
Type 2 Diabetes
SO DIABETES CARE
LA English
DT Article
ID POSTCHALLENGE PLASMA-GLUCOSE; SUGAR-SWEETENED BEVERAGES; SCHOOL-BASED
INTERVENTION; TELEVISION VIEWING TIME; LIFE-STYLE INTERVENTION;
ALL-CAUSE MORTALITY; PHYSICAL-ACTIVITY; BUILT ENVIRONMENT; SEDENTARY
TIME; SITTING TIME
C1 [Hill, James O.] Univ Colorado, Sch Med, Denver, CO USA.
[Galloway, James M.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Goley, April] Univ N Carolina, Sch Med, Div Endocrinol, Chapel Hill, NC USA.
[Marrero, David G.] Indiana Univ, Indianapolis, IN 46204 USA.
[Minners, Regan; Ratner, Robert E.] Amer Diabet Assoc, Sci & Med Div, Alexandria, VA USA.
[Montgomery, Brenda] Univ Washington, Seattle, WA 98195 USA.
[Montgomery, Brenda] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Peterson, Gregory E.] Des Moines Univ, Des Moines, IA USA.
[Sanchez, Eduardo] Amer Heart Assoc, Natl Ctr, Dallas, TX USA.
[Aroda, Vanita R.] Georgetown Univ, Sch Med, MedStar Hlth Res Inst, Washington, DC USA.
RP Ratner, RE (reprint author), Amer Diabet Assoc, Sci & Med Div, Alexandria, VA USA.
EM rratner@diabetes.org
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PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD AUG
PY 2013
VL 36
IS 8
BP 2430
EP 2439
DI 10.2337/dc13-1161
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 255PP
UT WOS:000327252600063
PM 23788649
ER
PT J
AU Beverly, EA
Weinger, K
AF Beverly, Elizabeth A.
Weinger, Katie
TI Response to Comment on: Beverly et al. Do Older Adults Aged 60-75 Years
Benefit From Diabetes Behavioral Interventions? Diabetes Care
2013;36:1501-1506
SO DIABETES CARE
LA English
DT Letter
ID EDUCATION
C1 [Beverly, Elizabeth A.] Joslin Diabet Ctr, Boston, MA 02215 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Weinger, K (reprint author), Joslin Diabet Ctr, Boston, MA 02215 USA.
EM katie.weinger@joslin.harvard.edu
NR 5
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
EI 1935-5548
J9 DIABETES CARE
JI Diabetes Care
PD AUG
PY 2013
VL 36
IS 8
BP E126
EP E126
DI 10.2337/dc13-0723
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 255PP
UT WOS:000327252600011
PM 23881979
ER
PT J
AU Dougherty, DD
AF Dougherty, Darin D.
TI This issue: Deep Brain Stimulation
SO PSYCHIATRIC ANNALS
LA English
DT Editorial Material
C1 [Dougherty, Darin D.] Massachusetts Gen Hosp, Dept Psychiat, Neurotherapeut Div, Boston, MA 02114 USA.
[Dougherty, Darin D.] Massachusetts Gen Hosp, Psychiat Neuroimaging Grp, Mood Disorders Sect, Boston, MA 02114 USA.
[Dougherty, Darin D.] Massachusetts Gen Hosp, Psychiat Neuroimaging Grp, Boston, MA 02114 USA.
[Dougherty, Darin D.] Massachusetts Gen Hosp, Obsess Compuls Disorder Inst, Boston, MA 02114 USA.
[Dougherty, Darin D.] Massachusetts Gen Hosp, Trichotillomania Clinic, Boston, MA 02114 USA.
[Dougherty, Darin D.] Harvard Univ, Sch Med, MIT, Hlth Sci & Technol Clin Investigator Training Pro, Cambridge, MA 02138 USA.
RP Dougherty, DD (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Neurotherapeut Div, Boston, MA 02114 USA.
NR 2
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PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0048-5713
EI 1938-2456
J9 PSYCHIAT ANN
JI Psychiatr. Ann.
PD AUG
PY 2013
VL 43
IS 8
BP 348
EP 349
DI 10.3928/00485713-20130806-02
PG 2
WC Psychiatry
SC Psychiatry
GA 256MF
UT WOS:000327314100002
ER
PT J
AU Corse, AK
Chou, T
Arulpragasam, AR
Kaur, N
Deckersbach, T
Cusin, C
AF Corse, Andrew K.
Chou, Tina
Arulpragasam, Amanda R.
Kaur, Navneet
Deckersbach, Thilo
Cusin, Cristina
TI Deep Brain Stimulation for Obsessive-Compulsive Disorder
SO PSYCHIATRIC ANNALS
LA English
DT Article
ID SUBTHALAMIC NUCLEUS STIMULATION; ELECTRICAL-STIMULATION; CAPSULAR
STIMULATION; PARKINSONS-DISEASE; ACCUMBENS; OUTCOMES; TRIAL
C1 [Corse, Andrew K.; Chou, Tina; Arulpragasam, Amanda R.; Kaur, Navneet; Deckersbach, Thilo; Cusin, Cristina] Massachusetts Gen Hosp, Dept Psychiat, Div Neurotherapeut, Boston, MA 02114 USA.
[Chou, Tina] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Deckersbach, Thilo; Cusin, Cristina] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Cusin, Cristina] Harvard Univ, Massachusetts Gen Hosp, Depress Clin & Res Program, Sch Med,Dept Psychiat, Cambridge, MA 02138 USA.
RP Cusin, C (reprint author), Massachusetts Gen Hosp, Depress Clin & Res Program, 1 Bowdoin Sq,Suite 634, Boston, MA 02114 USA.
EM ccusin@partners.org
NR 29
TC 0
Z9 0
U1 0
U2 0
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0048-5713
EI 1938-2456
J9 PSYCHIAT ANN
JI Psychiatr. Ann.
PD AUG
PY 2013
VL 43
IS 8
BP 351
EP 357
DI 10.3928/00485713-20130806-03
PG 7
WC Psychiatry
SC Psychiatry
GA 256MF
UT WOS:000327314100003
ER
PT J
AU Kaur, N
Chou, T
Corse, AK
Arulpragasam, AR
Deckersbach, T
Evans, KC
AF Kaur, Navneet
Chou, Tina
Corse, Andrew K.
Arulpragasam, Amanda R.
Deckersbach, Thilo
Evans, Karleyton C.
TI Deep Brain Stimulation for Treatment-Resistant Depression
SO PSYCHIATRIC ANNALS
LA English
DT Article
ID OBSESSIVE-COMPULSIVE DISORDER; REFRACTORY MAJOR DEPRESSION;
NUCLEUS-ACCUMBENS; DEFINITION; DIAGNOSIS; CIRCUITS; HABENULA
C1 [Kaur, Navneet; Chou, Tina; Corse, Andrew K.; Arulpragasam, Amanda R.; Deckersbach, Thilo; Evans, Karleyton C.] Massachusetts Gen Hosp, Dept Psychiat, Div Neurotherapeut, Charlestown, MA 02129 USA.
[Chou, Tina] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Deckersbach, Thilo; Evans, Karleyton C.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Evans, KC (reprint author), Massachusetts Gen Hosp, Dept Psychiat, CNY2625,149 13th St, Charlestown, MA 02129 USA.
EM kcevans@partners.org
NR 35
TC 0
Z9 0
U1 0
U2 4
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0048-5713
EI 1938-2456
J9 PSYCHIAT ANN
JI Psychiatr. Ann.
PD AUG
PY 2013
VL 43
IS 8
BP 358
EP 365
DI 10.3928/00485713-20130806-04
PG 8
WC Psychiatry
SC Psychiatry
GA 256MF
UT WOS:000327314100004
ER
PT J
AU Arulpragasam, AR
Chou, T
Kaur, N
Corse, AK
Deckersbach, T
Camprodon, JA
AF Arulpragasam, Amanda R.
Chou, Tina
Kaur, Navneet
Corse, Andrew K.
Deckersbach, Thilo
Camprodon, Joan A.
TI Future Directions of Deep Brain Stimulation: Current Disorders, New
Technologies
SO PSYCHIATRIC ANNALS
LA English
DT Article
ID NUCLEUS-ACCUMBENS; TOURETTES-SYNDROME; ALZHEIMERS-DISEASE; COCAINE;
RATS; CIRCUITS; SEEKING; OBESITY; MODELS; TICS
C1 [Arulpragasam, Amanda R.; Chou, Tina; Kaur, Navneet; Corse, Andrew K.; Deckersbach, Thilo] Massachusetts Gen Hosp, Dept Psychiat, Div Neurotherapeut, Charlestown, MA 02129 USA.
[Chou, Tina] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
[Deckersbach, Thilo] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Camprodon, Joan A.] Harvard Univ, Massachusetts Gen Hosp, Dept Psychiat, Div Neurotherapeut,Sch Med, Cambridge, MA 02138 USA.
[Camprodon, Joan A.] Harvard Univ, Massachusetts Gen Hosp, Dept Psychiat, Lab Neuropsychiat & Neuromodulat,Sch Med, Cambridge, MA 02138 USA.
RP Camprodon, JA (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Lab Neuropsychiat & Neuromodulat, CNY2654,149 13th St, Charlestown, MA 02129 USA.
EM camprodon.joan@mgh.harvard.edu
NR 33
TC 0
Z9 0
U1 1
U2 8
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0048-5713
EI 1938-2456
J9 PSYCHIAT ANN
JI Psychiatr. Ann.
PD AUG
PY 2013
VL 43
IS 8
BP 366
EP 373
DI 10.3928/00485713-20130806-05
PG 8
WC Psychiatry
SC Psychiatry
GA 256MF
UT WOS:000327314100005
ER
PT J
AU Oliva, EM
Bowe, T
Harris, AHS
Trafton, JA
AF Oliva, Elizabeth M.
Bowe, Thomas
Harris, Alex H. S.
Trafton, Jodie A.
TI Datapoints False Starts in Psychotherapy for Substance Use Disorders and
PTSD in the VHA
SO PSYCHIATRIC SERVICES
LA English
DT Editorial Material
C1 [Oliva, Elizabeth M.; Bowe, Thomas; Harris, Alex H. S.; Trafton, Jodie A.] US Dept Vet Affairs, Program Evaluat & Resource Ctr, Palo Alto Hlth Care Syst, Menlo Pk, CA 94025 USA.
RP Oliva, EM (reprint author), US Dept Vet Affairs, Program Evaluat & Resource Ctr, Palo Alto Hlth Care Syst, 795 Willow Rd,152 MPD, Menlo Pk, CA 94025 USA.
EM elizabeth.oliva@va.gov
NR 1
TC 2
Z9 2
U1 0
U2 1
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 1075-2730
EI 1557-9700
J9 PSYCHIAT SERV
JI Psychiatr. Serv.
PD AUG
PY 2013
VL 64
IS 8
BP 722
EP 722
PG 1
WC Health Policy & Services; Public, Environmental & Occupational Health;
Psychiatry
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Psychiatry
GA 255YN
UT WOS:000327276100006
PM 23903602
ER
PT J
AU Gorrindo, T
Goldfarb, E
Chevalier, L
Hoeppner, BB
Birnbaum, RJ
Meller, B
Alpert, JE
Herman, J
Weiss, AP
AF Gorrindo, Tristan
Goldfarb, Elizabeth
Chevalier, Lydia
Hoeppner, Bettina B.
Birnbaum, Robert J.
Meller, Benjamin
Alpert, Jonathan E.
Herman, John
Weiss, Anthony P.
TI Interprofessional Differences in Disposition Decisions: Results From a
Standardized Web-Based Patient Assessment
SO PSYCHIATRIC SERVICES
LA English
DT Article
ID PSYCHIATRIC EMERGENCY SERVICE; INTERRATER AGREEMENT; HOSPITALIZATION;
DETERMINANTS
AB Objective: This study examined differences in disposition decisions among mental health professionals using a standardized Web-based simulation. Methods: Using a Web-based simulation that described, across users, the same complex psychiatric patient, credentialed clinicians in a psychiatry department conducted a violence risk assessment and selected a level of follow-up care. Results: Of 410 clinicians who completed the simulation, 60% of psychiatrists were more likely than other types of clinicians to select higher levels of care (inpatient or emergency services) for the standardized virtual patient (odds ratio=2.67, 95% confidence interval=1.67-4.25), even after adjustment for other factors. Virtual actions taken, such as contracting with the patient for safety and discussing hospitalization, elucidated these training differences. Conclusions: Training backgrounds were important determinants of clinicians' actions and the dispositions they recommended for a psychiatric patient at high risk of self-harm and harm to others in the educational setting and may suggest the need for further training to standardize and optimize care.
C1 [Gorrindo, Tristan; Goldfarb, Elizabeth; Chevalier, Lydia; Birnbaum, Robert J.; Meller, Benjamin; Alpert, Jonathan E.; Herman, John; Weiss, Anthony P.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Hoeppner, Bettina B.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
RP Gorrindo, T (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 1 Bowdoin Sq,Suite 700, Boston, MA 02114 USA.
EM tristan.gorrindo@mgh.harvard.edu
OI Alpert, Jonathan/0000-0002-4332-908X
FU NIDA NIH HHS [K01 DA027097]
NR 13
TC 3
Z9 3
U1 1
U2 3
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 1075-2730
EI 1557-9700
J9 PSYCHIAT SERV
JI Psychiatr. Serv.
PD AUG
PY 2013
VL 64
IS 8
BP 808
EP 811
DI 10.1176/appi.ps.201200461
PG 4
WC Health Policy & Services; Public, Environmental & Occupational Health;
Psychiatry
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Psychiatry
GA 255YN
UT WOS:000327276100021
PM 23903607
ER
PT J
AU Kowalczyk, KJ
Choueiri, TK
Hevelone, ND
Trinh, QD
Lipsitz, SR
Nguyen, PL
Lynch, JH
Hu, JC
AF Kowalczyk, Keith J.
Choueiri, Toni K.
Hevelone, Nathanael D.
Quoc-Dien Trinh
Lipsitz, Stuart R.
Nguyen, Paul L.
Lynch, John H.
Hu, Jim C.
TI Comparative effectiveness, costs and trends in treatment of small renal
masses from 2005 to 2007
SO BJU INTERNATIONAL
LA English
DT Article
DE ablation; complications; kidney cancer; nephron-sparing surgery; renal
insufficiency; small renal masses; SEER
ID CHRONIC KIDNEY-DISEASE; LAPAROSCOPIC PARTIAL NEPHRECTOMY; INITIAL
CASE-REPORT; RADICAL NEPHRECTOMY; CELL CARCINOMA; CANCER; MORBIDITY;
MORTALITY; OUTCOMES
AB Objective To perform a comprehensive analysis of the outcomes and costs for treatments for small renal masses (SRM) using a population-based approach. Partial nephrectomy may be associated with improved survival, although level-one evidence has questioned this survival advantage.
Patients and Methods Using Surveillance, Epidemiology and End Results-Medicare data, we identified 1682 subjects who were diagnosed with SRM from 2005 to 2007. Treatment included open radical nephrectomy (ORN; n = 404), minimally-invasive radical nephrectomy (MIRN; n = 535), open partial nephrectomy (OPN; n = 330), minimally-invasive partial nephrectomy (MIPN; n = 160), ablation (n = 211) and surveillance (n = 42). Postoperative complications, renal insufficiency diagnosis, overall mortality, cancer-specific mortality and postoperative costs were compared. Covariates were balanced before outcomes analysis using propensity score methods.
Results Although the use of nephron-sparing surgery (NSS) increased over the study period, radical nephrectomy remained the predominant approach for SRM in 2007. Minimally-invasive approaches had shorter lengths of stay (P < 0.001), whereas open approaches had more overall complications, respiratory complications and intensive care unit admissions (all P < 0.003). MIRN and ORN were associated with more peri-operative medical complications, acute renal failure, haemodialysis use and long-term chronic renal insufficiency diagnosis vs NSS (all P < 0.001). Ablation, MIRN and ORN were associated with the highest overall mortality rates (P < 0.001), whereas MIRN and ORN were associated with the highest cancer-specific mortality rates (P < 0.001). Treatment costs were lowest for surveillance ($2911) followed by ablation ($10730), MIRN ($15373), MIPN ($15695), OPN ($16986) and ORN ($17803).
Conclusions Although not the predominant treatment approach for SRM over the study period, the use of NSS increased and was associated with improved survival, fewer complications and less renal insufficiency. Minimally-invasive approaches confer lower costs.
C1 [Kowalczyk, Keith J.; Lynch, John H.] Georgetown Univ Hosp, Dept Urol, Washington, DC 20007 USA.
[Choueiri, Toni K.] Harvard Univ, Sch Med, Lank Ctr Genitourinary Oncol, Boston, MA USA.
[Nguyen, Paul L.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol,Lank Ctr Genitourinary Oncol, Boston, MA 02115 USA.
[Hevelone, Nathanael D.; Lipsitz, Stuart R.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Surg & Publ Hlth, Boston, MA 02115 USA.
[Quoc-Dien Trinh] Henry Ford Hlth Syst, Vattikuti Urol Inst, Detroit, MI USA.
[Hu, Jim C.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Urol, Los Angeles, CA 90095 USA.
[Quoc-Dien Trinh] Univ Montreal, Ctr Hlth, Canc Prognost & Hlth Outcomes Unit, Montreal, PQ, Canada.
RP Kowalczyk, KJ (reprint author), Georgetown Univ Hosp, Dept Urol, 3800 Reservoir Rd NW, Washington, DC 20007 USA.
EM keith.kowalczyk@gunet.georgetown.edu
OI Hevelone, Nathanael/0000-0003-4740-2085
FU Department of Defense Physician Training Award [W81XWH-08-1-0283]
FX Jim C. Hu receives salary support from Department of Defense Physician
Training Award W81XWH-08-1-0283.
NR 32
TC 11
Z9 11
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1464-4096
EI 1464-410X
J9 BJU INT
JI BJU Int.
PD AUG
PY 2013
VL 112
IS 4
BP E273
EP E280
DI 10.1111/j.1464-410X.2012.11776.x
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 255CZ
UT WOS:000327218200015
PM 23452093
ER
PT J
AU Brown, EN
Purdon, PL
AF Brown, Emery N.
Purdon, Patrick L.
TI The aging brain and anesthesia
SO CURRENT OPINION IN ANESTHESIOLOGY
LA English
DT Review
DE anesthesia; delirium; electroencephalogram; functional imaging; normal
aging; postoperative cognitive dysfunction
ID POSTOPERATIVE DELIRIUM; COGNITIVE DECLINE; ALZHEIMERS-DISEASE;
GENERAL-ANESTHESIA; BURST SUPPRESSION; OXIDATIVE STRESS; NORMAL ADULTS;
PROPOFOL; ISOFLURANE; HYPOTHESIS
AB Purpose of reviewTo review the neurophysiology and neuroanatomy of normal aging and the recent recommendations for the clinical management of general anesthesia and sedation in the elderly.Recent findingsAs the population ages, the number of elderly patients having surgery is likewise increasing and with it, the prevalence of postoperative cognitive disorders. Postoperative cognitive disorders including delirium and postoperative cognitive dysfunction are common postanesthesia complications in elderly patients. Several risk factors for postoperative disorders have been identified, and anesthesiologists commonly adapt their practice habits when taking care of elderly patients to try to mitigate the effects of the anesthetics on postoperative cognitive function. These practices are reasonable and prudent; yet, they are not well supported by an understanding of the aging brain and specifics of how the anesthetic effects on the brain change with age. Through functional imaging and electrophysiological studies, much is being learned about the neurophysiology and the neuroanatomy of normal aging.SummaryOur analysis suggests that understanding the neurophysiology and neuroanatomy should be part of the standard working knowledge of anesthesiologists and that this knowledge can guide their use of the electroencephalogram to track more accurately the brain states of elderly patients receiving anesthesia care.
C1 [Brown, Emery N.; Purdon, Patrick L.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Brown, Emery N.] MIT, Inst Med Engn & Sci, Cambridge, MA 02139 USA.
[Brown, Emery N.] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
RP Brown, EN (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, GRB 444,55 Fruit St, Boston, MA 02114 USA.
EM enb@neurostat.mit.edu
FU National Institutes of Health (NIH) [DP1-OD003646, R01 GM104948-01,
R01-MH071847, DP2-OD006454, K25-NS057580]; Massachusetts General
Hospital Department of Anesthesia, Critical Care, and Pain Medicine;
[R01-EB006385]
FX This research was supported by a National Institutes of Health (NIH)
Director's Pioneer Award DP1-OD003646, an NIH Director's Transformative
Research Award R01 GM104948-01 and NIH Grant R01-MH071847 (to E.N.B.),
by NIH New Innovator Award DP2-OD006454 and K-Award K25-NS057580 (to P.
L. P.) and by R01-EB006385 (to E.N.B., P. L. P. and K. F. K. W.). This
work was also supported by the Massachusetts General Hospital Department
of Anesthesia, Critical Care, and Pain Medicine.
NR 47
TC 11
Z9 13
U1 0
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0952-7907
EI 1473-6500
J9 CURR OPIN ANESTHESIO
JI Curr. Opin. Anesthesiol.
PD AUG
PY 2013
VL 26
IS 4
BP 414
EP 419
DI 10.1097/ACO.0b013e328362d183
PG 6
WC Anesthesiology
SC Anesthesiology
GA 253LS
UT WOS:000327088700004
PM 23820102
ER
PT J
AU Coaker, H
Bradner, JE
AF Coaker, Hannah
Bradner, James E.
TI Interview with James Bradner
SO FUTURE MEDICINAL CHEMISTRY
LA English
DT Editorial Material
AB James E Bradner is an Assistant Professor in Medicine at Harvard Medical School (MA, USA) as well as a Staff Physician in the Division of Hematologic Malignancies at Dana-Farber Cancer Institute (MA, USA). The present research focus of the Bradner laboratory concerns the discovery and optimization of prototype drugs targeting cancer gene regulation. The clinical objective of the Bradner group is to deliver novel therapeutics for human clinical investigation in hematologic diseases. Bradner's awards and honors include the Damon Runyon-Rachleff Innovation Award, the Smith Family Award for Excellence in Biomedical Research, the Dunkin' Donuts Rising Star Award and the HMS Distinguished Excellence in Teaching Award. He is a member of the American Society of Clinical Investigation, the American Society of Hematology, the American Chemical Society and the American Association of Cancer Research. His recent research has been published in Nature, Cell, Nature Chemical Biology and the Journal of the American Chemical Society. He has authored more than 20 US Patent applications, licensed to five pharmaceutical companies, and is a scientific founder of Acetylon Pharmaceuticals, SHAPE Pharmaceuticals, Tensha Therapeutics and Syros Pharmaceuticals. Bradner received his AB from Harvard University, his MD from the University of Chicago (IL, USA) and a MMS from Harvard Medical School. He completed his postgraduate training in Internal Medicine at Brigham & Women's Hospital (MA, USA), followed by a fellowship in Medical Oncology and Hematology at Dana-Farber Cancer Institute. Following additional post-doctoral training in Chemistry at Harvard University and the Broad Institute (MA, USA) with Professor Stuart Schreiber, Bradner joined the research faculty of Dana-Farber in 2008. Interview conducted by Hannah Coaker, Assistant Commissioning Editor.
C1 [Bradner, James E.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
EM james_bradner@dfci.harvard.edu
NR 0
TC 2
Z9 2
U1 2
U2 6
PU FUTURE SCI LTD
PI LONDON
PA UNITED HOUSE, 2 ALBERT PL, LONDON, N3 1QB, ENGLAND
SN 1756-8919
EI 1756-8927
J9 FUTURE MED CHEM
JI Future Med. Chem.
PD AUG
PY 2013
VL 5
IS 12
BP 1373
EP 1376
DI 10.4155/fmc.13.124
PG 4
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 254TC
UT WOS:000327188900007
ER
PT J
AU Yoon, TJ
Shao, HL
Weissleder, R
Lee, H
AF Yoon, Tae-Jong
Shao, Huilin
Weissleder, Ralph
Lee, Hakho
TI Oxidation Kinetics and Magnetic Properties of Elemental Iron
Nanoparticles
SO PARTICLE & PARTICLE SYSTEMS CHARACTERIZATION
LA English
DT Article
DE iron nanoparticles; magnetism; nanoparticles; oxidation
ID CORE-SHELL NANOPARTICLES; MONODISPERSE FE NANOPARTICLES; OXIDE FILM
GROWTH; PARTICLES; NANOCRYSTALS; THERAPY
C1 [Yoon, Tae-Jong] CHA Univ, Dept Appl Biosci, Seoul 135081, South Korea.
[Shao, Huilin; Weissleder, Ralph; Lee, Hakho] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Weissleder, Ralph] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
RP Yoon, TJ (reprint author), CHA Univ, Dept Appl Biosci, Seoul 135081, South Korea.
EM hlee@mgh.harvard.edu
FU B.S.-Ph.D. National Science Scholarship; Agency for Science, Technology
and Research, Singapore; NIH [R01HL113156, R01EB004626,
HHSN268201000044C, U54-CA151844]
FX H.S. acknowledges financial support from the B.S.-Ph.D. National Science
Scholarship awarded by the Agency for Science, Technology and Research,
Singapore. This work was supported in part by NIH Grants (R01HL113156,
R01EB004626, HHSN268201000044C, and U54-CA151844).
NR 33
TC 3
Z9 3
U1 2
U2 21
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA BOSCHSTRASSE 12, D-69469 WEINHEIM, GERMANY
SN 0934-0866
EI 1521-4117
J9 PART PART SYST CHAR
JI Part. Part. Syst. Charact.
PD AUG
PY 2013
VL 30
IS 8
BP 667
EP 671
DI 10.1002/ppsc.201300013
PG 5
WC Chemistry, Physical; Nanoscience & Nanotechnology; Materials Science,
Multidisciplinary
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA 255OT
UT WOS:000327250400006
PM 24077230
ER
PT J
AU Wanderer, JP
Charnin, J
Driscoll, WD
Bailin, MT
Baker, K
AF Wanderer, Jonathan P.
Charnin, Jonathan
Driscoll, William D.
Bailin, Michael T.
Baker, Keith
TI Decision Support Using Anesthesia Information Management System Records
and Accreditation Council for Graduate Medical Education Case Logs for
Resident Operating Room Assignments
SO ANESTHESIA AND ANALGESIA
LA English
DT Article
AB Our goal in this study was to develop decision support systems for resident operating room (OR) assignments using anesthesia information management system (AIMS) records and Accreditation Council for Graduate Medical Education (ACGME) case logs and evaluate the implementations. We developed 2 Web-based systems: an ACGME case-log visualization tool, and Residents Helping in Navigating OR Scheduling (Rhinos), an interactive system that solicits OR assignment requests from residents and creates resident profiles. Resident profiles are snapshots of the cases and procedures each resident has done and were derived from AIMS records and ACGME case logs. A Rhinos pilot was performed for 6 weeks on 2 clinical services. One hundred sixty-five requests were entered and used in OR assignment decisions by a single attending anesthesiologist. Each request consisted of a rank ordered list of up to 3 ORs. Residents had access to detailed information about these cases including surgeon and patient name, age, procedure type, and admission status. Success rates at matching resident requests were determined by comparing requests with AIMS records. Of the 165 requests, 87 first-choice matches (52.7%), 27 second-choice matches (16.4%), and 8 third-choice matches (4.8%) were made. Forty-three requests were unmatched (26.1%). Thirty-nine first-choice requests overlapped (23.6%). Full implementation followed on 8 clinical services for 8 weeks. Seven hundred fifty-four requests were reviewed by 15 attending anesthesiologists, with 339 first-choice matches (45.0%), 122 second-choice matches (16.2%), 55 third-choice matches (7.3%), and 238 unmatched (31.5%). There were 279 overlapping first-choice requests (37.0%). The overall combined match success rate was 69.4%. Separately, we developed an ACGME case-log visualization tool that allows individual resident experiences to be compared against case minimums as well as resident peer groups. We conclude that it is feasible to use ACGME case-log data in decision support systems for informing resident OR assignments. Additional analysis will be necessary to assess the educational impact of these systems.
C1 [Wanderer, Jonathan P.] Vanderbilt Univ, Dept Anesthesiol, Nashville, TN 37235 USA.
[Charnin, Jonathan; Driscoll, William D.; Baker, Keith] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Driscoll, William D.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bailin, Michael T.] Baystate Med Ctr, Dept Anesthesiol, Springfield, MA USA.
RP Wanderer, JP (reprint author), Vanderbilt Clin, Dept Anesthesiol, 1301 Med Ctr Dr,Suite 4648, Nashville, TN 37212 USA.
EM jonathan.p.wanderer@vanderbilt.edu
NR 6
TC 7
Z9 7
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-2999
EI 1526-7598
J9 ANESTH ANALG
JI Anesth. Analg.
PD AUG
PY 2013
VL 117
IS 2
BP 494
EP 499
DI 10.1213/ANE.0b013e318294fb64
PG 6
WC Anesthesiology
SC Anesthesiology
GA 246BO
UT WOS:000326511500029
PM 23749442
ER
PT J
AU Guyer, AC
Long, AA
AF Guyer, Autumn Chandler
Long, Aidan Angelo
TI Long-acting anticholinergics in the treatment of asthma
SO CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Review
DE anticholinergics; asthma; ipratropium bromide; severe asthma; tiotropium
bromide
ID OBSTRUCTIVE PULMONARY-DISEASE; UNCONTROLLED ASTHMA; TIOTROPIUM BROMIDE;
LUNG-FUNCTION; THERAPY; SALMETEROL; FLUTICASONE; PHENOTYPE; COPD;
EXACERBATIONS
AB Purpose of reviewThe use of anticholinergic medications is well established as maintenance therapy for chronic obstructive pulmonary disease (COPD). There is a growing interest in the use of anticholinergic medications in the treatment of moderate to severe asthma. The purpose of this review is to summarize the scientific evidence for the use of anticholinergic therapy in the management of asthma.Recent findingsEarly case reports and small studies evaluated the use of the anticholinergic agent, tiotropium bromide, as maintenance therapy in asthma. Included in this review are several recent clinical trials which provide additional evidence for the use of tiotropium as add-on therapy for asthma. The use of tiotropium was demonstrated to be superior to doubling the dose of an inhaled corticosteroid (ICS) and more effective than placebo based on change in morning peak expiratory flow (PEF). Two large multinational trials provide evidence for the use of tiotropium in a subset of asthmatic patients who have not achieved control using combination therapy with an ICS and a long-acting (2) agonist (LABA).SummaryThe use of the long-acting anticholinergic agent, tiotropium, as maintenance of therapy in asthma, has been shown to be effective in some patients with moderate to severe asthma who are uncontrolled on combination therapy with ICS and LABA. Further studies are needed to better define which phenotypic subset of patients would benefit from the use of tiotropium.
C1 [Guyer, Autumn Chandler; Long, Aidan Angelo] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Long, AA (reprint author), Massachusetts Gen Hosp, 55 Fruit St,Cox 201, Boston, MA 02114 USA.
EM Aalong@partners.org
NR 37
TC 8
Z9 8
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1528-4050
EI 1473-6322
J9 CURR OPIN ALLERGY CL
JI Curr. Opin. Allergy Clin. Immunol.
PD AUG
PY 2013
VL 13
IS 4
BP 392
EP 398
DI 10.1097/ACI.0b013e328362a775
PG 7
WC Allergy; Immunology
SC Allergy; Immunology
GA 247GL
UT WOS:000326604700012
PM 23756872
ER
PT J
AU Rudders, SA
Banerji, A
AF Rudders, Susan A.
Banerji, Aleena
TI An update on self-injectable epinephrine
SO CURRENT OPINION IN ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Review
DE anaphylaxis; auto-injector; epinephrine; food allergy; stinging insect
allergy
ID AUTOINJECTOR DELIVERY-SYSTEMS; EMERGENCY-DEPARTMENT; AUTO-INJECTORS;
UNINTENTIONAL INJECTION; ALLERGIC REACTIONS; FOOD ALLERGIES; PEANUT
ALLERGY; NEEDLE LENGTH; ANAPHYLAXIS; CHILDREN
AB Purpose of reviewEpinephrine is an important life-saving treatment in patients with anaphylaxis. However, despite the guidelines recommending the use of epinephrine in the management of all patients with anaphylaxis, many patients are either not prescribed epinephrine auto-injectors (EAIs) or remain hesitant to use them.Recent findingsIn this review, we examine our current knowledge base regarding EAIs, including issues related to dosing, medication availability and new modes of administration. Our findings suggest that all patients at risk for anaphylaxis should always carry two epinephrine doses. Once an EAI is prescribed, the patient should receive appropriate education on when and how to use it and it should be administered without delay. Current EAI devices have been redesigned to address limitations and decrease unintentional injury.SummaryEpinephrine remains the cornerstone of anaphylaxis treatment and EAIs are critical because of their ability to rapidly deliver this potentially life-saving medication outside of a medical setting. Continued efforts are needed to establish evidence-based parameters for delivery of this medication and to optimize education of healthcare providers and patients on the use of EAIs.
C1 [Rudders, Susan A.] Rhode Isl Hosp, Dept Pediat, Div Allergy & Immunol, Providence, RI 02906 USA.
[Banerji, Aleena] Massachusetts Gen Hosp, Dept Med, Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA.
RP Rudders, SA (reprint author), Rhode Isl Hosp, Hasbro Childrens Hosp, 593 Eddy St, Providence, RI 02906 USA.
EM srudders@lifespan.org
NR 55
TC 5
Z9 5
U1 2
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1528-4050
EI 1473-6322
J9 CURR OPIN ALLERGY CL
JI Curr. Opin. Allergy Clin. Immunol.
PD AUG
PY 2013
VL 13
IS 4
BP 432
EP 437
DI 10.1097/ACI.0b013e328362b8aa
PG 6
WC Allergy; Immunology
SC Allergy; Immunology
GA 247GL
UT WOS:000326604700017
PM 23743514
ER
PT J
AU Gomez, CA
Singh, N
AF Gomez, Carlos A.
Singh, Nina
TI Donor-derived filamentous fungal infections in solid organ transplant
recipients
SO CURRENT OPINION IN INFECTIOUS DISEASES
LA English
DT Review
DE aspergillosis; donor-derived infection; mold infections; mucormycosis;
solid-organ transplantation; transplant infections
ID COMMERCIAL RENAL-TRANSPLANTATION; KIDNEY-TRANSPLANTATION; INVASIVE
ASPERGILLOSIS; MUCORMYCOSIS; ALLOGRAFT; RUPTURE; TOURISM; GRAFT;
TRANSMISSION; MULTICENTER
AB Purpose of reviewFilamentous fungal infections due to rare opportunistic moulds can be transmitted with an allograft. However, epidemiologic and clinical characteristics of donor-derived filamentous fungal infections (DDFFIs) in transplant recipients are poorly understood. Hence, the aim of this article is to describe donor-related risk factors, clinical presentation, graft and recipient outcomes associated with DDFFIs.Recent findingsTo date, 23 cases of donor-derived opportunistic filamentous fungal infections have been reported; a majority (91%) occurred in kidney transplant recipients. Aspergillus spp. was the most common organism (71%). Risk factors for DDFFIs include immunosuppressive state of the donor (transplant recipients serving as organ donors), near-drowning events, and transplant-tourism practices. DDFFIs manifested as vascular complications related to graft vasculature (65%), allograft dysfunction (43%) and unexplained febrile illness (39%) in the recipient. Rates of graft loss and overall mortality were 83 and 17%, respectively.SummaryDonor-transmitted filamentous mycoses have a unique spectrum of illness and clinical settings under which transmission occurs. Prompt recognition, early surgical intervention and specific antifungal therapy are necessary for achieving optimal graft and recipient outcomes.
C1 [Gomez, Carlos A.] Univ Pittsburgh, Dept Med, Med Ctr, Pittsburgh, PA USA.
[Singh, Nina] Univ Pittsburgh, VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
RP Singh, N (reprint author), Vet Adm Med Ctr, Infect Dis Sect, Univ Dr C, Pittsburgh, PA 15240 USA.
EM nis5@pitt.edu
NR 49
TC 8
Z9 9
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0951-7375
EI 1473-6527
J9 CURR OPIN INFECT DIS
JI Curr. Opin. Infect. Dis.
PD AUG
PY 2013
VL 26
IS 4
BP 309
EP 316
DI 10.1097/QCO.0b013e3283630e4d
PG 8
WC Infectious Diseases
SC Infectious Diseases
GA 248VL
UT WOS:000326733200003
PM 23806894
ER
PT J
AU Kawai, T
Sachs, DH
AF Kawai, Tatsuo
Sachs, David H.
TI Tolerance induction: hematopoietic chimerism
SO CURRENT OPINION IN ORGAN TRANSPLANTATION
LA English
DT Review
DE chimerism; chronic immunosuppression; donor bone marrow transplantation;
kidney transplantation; mixed chimerism; tolerance
ID RENAL-ALLOGRAFT REJECTION; KIDNEY-TRANSPLANT RECIPIENTS;
BONE-MARROW-TRANSPLANTATION; DONOR-SPECIFIC TOLERANCE; MEMORY T-CELLS;
MIXED CHIMERISM; NONHUMAN-PRIMATES; STEM-CELL; CYNOMOLGUS MONKEYS;
IMMUNOSUPPRESSIVE DRUGS
AB Purpose of reviewAlthough numerous experimental models to induce allograft tolerance have been reported, it has been difficult to translate these basic studies to clinical transplantation. However, successful induction of tolerance in HLA-mismatched kidney transplantation has recently been reported. In this review, recent progress in tolerance induction in preclinical (nonhuman primates) and clinical transplantation is summarized.Recent findingsAmong many clinical trials to induce renal allograft tolerance, success has so far been achieved only by combining donor bone marrow with organ transplantation. Induction of renal allograft tolerance by transient or durable mixed chimerism has been reported in HLA-matched or mismatched kidney transplant recipients. More recently, renal allograft tolerance by induction of full donor chimerism has also been reported using a more intensified preparative conditioning regimen.SummaryDurable allograft tolerance has been achieved by induction of hematopoietic chimerism in clinical kidney transplantation, with outstanding long-term results in successful cases. However, these approaches have been associated with higher early complications than are seen following transplantation with conventional immunosuppression. Improvements in the consistency and safety of tolerance induction and extension of successful protocols to other organs will be the next steps in bringing tolerance to a wider range of clinical applications.
C1 [Kawai, Tatsuo] Massachusetts Gen Hosp, Transplant Ctr, Boston, MA 02114 USA.
[Sachs, David H.] Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Dept Surg, Boston, MA 02114 USA.
RP Kawai, T (reprint author), Massachusetts Gen Hosp, MGH White 521,55 Fruit St, Boston, MA 02114 USA.
EM tkawai@partners.org
FU NIH [AI102405-01]; Immune Tolerance Network [N01-AI-15416]
FX Supported in part by NIH AI102405-01 and the Immune Tolerance Network
(N01-AI-15416).
NR 84
TC 16
Z9 17
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1087-2418
EI 1531-7013
J9 CURR OPIN ORGAN TRAN
JI Curr. Opin. Organ Transpl.
PD AUG
PY 2013
VL 18
IS 4
BP 402
EP 407
DI 10.1097/MOT.0b013e328363621d
PG 6
WC Transplantation
SC Transplantation
GA 249AC
UT WOS:000326747400003
PM 23838644
ER
PT J
AU Turka, LA
Li, XC
Susal, C
AF Turka, Laurence A.
Li, Xian Chang
Suesal, Caner
TI Untitled
SO CURRENT OPINION IN ORGAN TRANSPLANTATION
LA English
DT Editorial Material
C1 [Turka, Laurence A.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Turka, Laurence A.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Turka, Laurence A.] Univ Penn, Philadelphia, PA 19104 USA.
[Turka, Laurence A.; Li, Xian Chang] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Turka, Laurence A.] Amer Soc Transplantat, Mt Laurel, NJ USA.
[Turka, Laurence A.] NIAID, Board Sci Counselors, Bethesda, MD USA.
[Li, Xian Chang] Methodist Hosp, Houston, TX 77030 USA.
[Li, Xian Chang] Methodist Hosp, Transplant Immunol Ctr, Res Inst, Houston, TX 77030 USA.
RP Turka, LA (reprint author), Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1087-2418
EI 1531-7013
J9 CURR OPIN ORGAN TRAN
JI Curr. Opin. Organ Transpl.
PD AUG
PY 2013
VL 18
IS 4
DI 10.1097/MOT.0b013e3283646caa
PG 2
WC Transplantation
SC Transplantation
GA 249AC
UT WOS:000326747400016
ER
PT J
AU Faris, C
Lindsay, R
AF Faris, Callum
Lindsay, Robin
TI Current thoughts and developments in facial nerve reanimation
SO CURRENT OPINION IN OTOLARYNGOLOGY & HEAD AND NECK SURGERY
LA English
DT Review
DE facial nerve injury; facial paralysis; facial reanimation; free gracilis
muscle transfer
ID LENGTHENING TEMPORALIS MYOPLASTY; GRACILIS MUSCLE TRANSPLANTATION;
QUALITY-OF-LIFE; MOTOR-NERVE; PARALYZED FACE; THERAPEUTIC STRATEGIES;
COMPREHENSIVE APPROACH; TENDON TRANSPOSITION; ADULT PATIENTS; MASSETER
AB Purpose of reviewTo present the most current literature regarding the management of acute and chronic facial paralysis. This review will focus primarily on smile reanimation in the setting of acute and chronic facial paralysis. The management of the flaccid and the hypertonic face will be discussed.
Recent findingsRecent developments include advances in neural repair with fibrin glue and the use of cadaveric nerve grafts as interposition grafts. Advances in nerve substitutes have been shown to limit donor-site morbidity and provide similar outcomes to autografts. Techniques for muscle transfer continue to evolve to improve smile outcomes.
SummaryThe goal of facial reanimation surgery is to restore meaningful facial movement. The goal should be to have quality-driven clinical practice guidelines to better facilitate patient care. This process must be initiated by facial reanimation surgeons deciding to use consistent outcome measures to report their results. Currently, it is impossible to make a direct comparison between different surgical techniques because of inconsistent methods of evaluation. Despite the lack of consistent quantitative evaluation, there have been many exciting advances in the field.
C1 [Faris, Callum] Univ Nottingham Hosp, Queens Med Ctr, Dept Otolaryngol Head & Neck Surg, Nottingham NG7 2UH, England.
[Lindsay, Robin] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otolaryngol Head & Neck Surg, Boston, MA USA.
RP Lindsay, R (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol Head & Neck Surg, 243 Charles St, Boston, MA 02114 USA.
EM robin_lindsay@meei.harvard.edu
NR 47
TC 4
Z9 4
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1068-9508
EI 1531-6998
J9 CURR OPIN OTOLARYNGO
JI Curr. Opin. Otolaryngol. Head Neck Surg.
PD AUG
PY 2013
VL 21
IS 4
BP 346
EP 352
DI 10.1097/MOO.0b013e328362a56e
PG 7
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 248XV
UT WOS:000326740200008
PM 23756337
ER
PT J
AU Bhama, P
Bhrany, AD
AF Bhama, Prabhat
Bhrany, Amit D.
TI Ocular protection in facial paralysis
SO CURRENT OPINION IN OTOLARYNGOLOGY & HEAD AND NECK SURGERY
LA English
DT Review
DE ectropion; facial paralysis; lagophthalmos; ocular protection
ID GOLD WEIGHT; BOTULINUM TOXIN; CORNEAL PROTECTION; LAGOPHTHALMOS;
MANAGEMENT; SURGERY; GRAFT; ECTROPION; PTOSIS; EYE
AB Purpose of reviewFacial nerve paralysis has a profound impact on patients' quality of life, of which one of the most important sequelae is a risk of corneal surface disease. Herein, we discuss methods to protect the eye following insult to the facial nerve.
Recent findingsProtection of the ocular surface in patients with facial nerve injury is of paramount importance to prevent corneal injury and potential blindness. Many interventions on the eye are temporary and therefore easily reversible. A systematic approach to managing the eye is required in these patients.
SummaryThis article provides a review of current methods used for ocular protection in patients with facial nerve paralysis.
C1 [Bhama, Prabhat] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Div Facial Plast & Reconstruct Surg,Dept Otol & L, Boston, MA USA.
[Bhrany, Amit D.] Univ Washington, Sch Med, Dept Otolaryngol Head & Neck Surg, Seattle, WA 98195 USA.
RP Bhrany, AD (reprint author), Univ Washington, Sch Med, Dept Otolaryngol Head & Neck Surg, Box 356515, Seattle, WA 98195 USA.
EM abhrany@uw.edu
NR 25
TC 3
Z9 3
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1068-9508
EI 1531-6998
J9 CURR OPIN OTOLARYNGO
JI Curr. Opin. Otolaryngol. Head Neck Surg.
PD AUG
PY 2013
VL 21
IS 4
BP 353
EP 357
DI 10.1097/MOO.0b013e32836239cf
PG 5
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 248XV
UT WOS:000326740200009
PM 23689596
ER
PT J
AU Winter, HS
Di Lorenzo, C
Benninga, MA
Gilger, MA
Kearns, GL
Hyman, PE
Vandeplassche, L
Ausma, J
Hoppenbrouwers, M
AF Winter, Harland S.
Di Lorenzo, Carlo
Benninga, Marc A.
Gilger, Mark A.
Kearns, Gregory L.
Hyman, Paul E.
Vandeplassche, Lieve
Ausma, Jannie
Hoppenbrouwers, Mieke
TI Oral Prucalopride in Children With Functional Constipation
SO JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION
LA English
DT Article
DE efficacy; functional constipation; pharmacokinetics; prucalopride;
tolerability
ID PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; CHILDHOOD CONSTIPATION;
INTRACTABLE CONSTIPATION; HEALTHY-VOLUNTEERS; COLONIC MOTILITY;
CISAPRIDE; TRANSIT; AGONIST
AB Background and Objectives:Prucalopride is a selective, high-affinity 5-HT4 receptor agonist with gastrointestinal prokinetic activities. The aim of this study was to evaluate the pharmacokinetics, efficacy, safety, and tolerability of prucalopride oral solution in children, ages 4 years or older to 12 years or younger, with functional constipation.Methods:A single oral dose of 0.03 mg/kg prucalopride was administered to 38 children to characterize prucalopride pharmacokinetics (NCT01674166). Thereafter, 37 children entered an open-label extension period in which 0.01 to 0.03 mg/kg of prucalopride was administered once per day for 8 weeks to investigate efficacy, safety, and tolerability (NCT01670669).Results:Mean (standard deviation [SD]) C-max, t(max), and AUC (area under the plasma concentration-time curve from time 0 to infinity) were 3.8 (0.6) ng/mL, 1.8 (0.9) hour, and 65.3 (10.6) ng h(-1) mL(-1), respectively, with limited (16%) variability in C-max and AUC. Mean (SD) t(1/2) was 19.0 (3.1) hours. On average, mean (SD) renal clearance (0.25 [0.08] L h(-1) kg(-1)) accounted for 54% of the apparent total plasma clearance (0.46 [0.07] L h(-1) kg(-1)). The apparent volume of distribution was 12.6 (2.6) L/kg. Prucalopride treatment resulted in a mean bowel movement frequency of 6.8/week, normal stool consistency, and reduced frequency of fecal incontinence. During the 8-week extension, 70% of study participants had at least 1 adverse event (all but 1 of mild/moderate intensity, 19% considered related to prucalopride). No children discontinued prucalopride because of adverse events.Conclusions:The pharmacokinetic profile of a single dose of prucalopride oral solution (0.03 mg kg(-1) day(-1)) generally resembled the profile in adults (2-mg tablet) but reflected lower systemic exposure in children. Prucalopride treatment for 8 weeks demonstrated an apparent favorable efficacy and tolerability profile in children with functional constipation.
C1 [Winter, Harland S.] MassGen Hosp Children, Boston, MA 02114 USA.
[Di Lorenzo, Carlo] Nationwide Childrens Hosp, Columbus, OH USA.
[Benninga, Marc A.] Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, NL-1105 AZ Amsterdam, Netherlands.
[Gilger, Mark A.] Texas Childrens Hosp, Houston, TX 77030 USA.
[Kearns, Gregory L.] Childrens Mercy Hosp, Kansas City, MO 64108 USA.
[Hyman, Paul E.] Childrens Hosp, New Orleans, LA USA.
[Vandeplassche, Lieve; Ausma, Jannie; Hoppenbrouwers, Mieke] Shire Movetis NV, Turnhout, Belgium.
RP Winter, HS (reprint author), MassGen Hosp Children, Pediat GI Unit, CRPZ 5-560,175 Cambridge St, Boston, MA 02114 USA.
EM hwinter@partners.org
FU UCB, Nutricia; Pediatric IBD Foundation; Autism Research Institute;
Warner-Chilcott.; Redhill Biopharma; QOL Medical; Otsuka Pharmaceutical
Inc; National Institutes of Health [NO1 A1 25465]; Bristol-Myers Squibb;
National Institutes of Health; Janssen Research Foundation, Beerse,
Belgium; Shire-Movetis NV, Turnhout, Belgium
FX H.S.W. has current research grants from Janssen, UCB, Nutricia, The
Pediatric IBD Foundation, Autism Research Institute, and
Warner-Chilcott. He has current consulting agreements with Prometheus
Laboratories, Salix, Janssen Pharmaceuticals, and Shire-Movetis NV. C.
D. has consulting agreements with Janssen Pharmaceuticals, Abbott
Laboratories, Ironwood Pharmaceuticals, and QOL Medical. M. A. B. has
consulting agreements with Shire-Movetis NV and Danone. M. A. G. has
current research grants from Redhill Biopharma, QOL Medical, Otsuka
Pharmaceutical Inc, and the National Institutes of Health (NO1 A1
25465). G. L. K. has active consulting agreements with Upsher-Smith
Laboratories, Inc, Solginex, Inc, and Bristol-Myers Squibb. He has
current research grants from Bristol-Myers Squibb and the National
Institutes of Health. L. V., J.A., and M. H. are employees of
Shire-Movetis NV and own stock in Shire. P. E. H. reports no conflicts
of interest.; The clinical research was funded by the Janssen Research
Foundation, Beerse, Belgium, and Shire-Movetis NV, Turnhout, Belgium.
Although Janssen Research Foundation and Shire-Movetis NV were involved
in the design, collection, analysis, interpretation, and fact checking
of the information, the content of this manuscript, the ultimate
interpretation, and the decision to submit it for publication was made
by the authors independently.
NR 29
TC 13
Z9 13
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-2116
EI 1536-4801
J9 J PEDIATR GASTR NUTR
JI J. Pediatr. Gastroenterol. Nutr.
PD AUG
PY 2013
VL 57
IS 2
BP 197
EP 203
DI 10.1097/MPG.0b013e318292f9ea
PG 7
WC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics
SC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics
GA 249AM
UT WOS:000326748700017
PM 23535761
ER
PT J
AU Golwala, HB
Thadani, U
Liang, L
Stavrakis, S
Butler, J
Yancy, CW
Bhatt, DL
Hernandez, AF
Fonarow, GC
AF Golwala, Harsh B.
Thadani, Udho
Liang, Li
Stavrakis, Stavros
Butler, Javed
Yancy, Clyde W.
Bhatt, Deepak L.
Hernandez, Adrian F.
Fonarow, Gregg C.
TI Use of Hydralazine-Isosorbide Dinitrate Combination in African American
and Other Race/Ethnic Group Patients With Heart Failure and Reduced Left
Ventricular Ejection Fraction
SO JOURNAL OF THE AMERICAN HEART ASSOCIATION
LA English
DT Article
DE guideline adherence; heart failure; quality; race/ethnicity; registry
ID RANDOMIZED-TRIAL; MORTALITY; SURVIVAL; MORBIDITY; ENALAPRIL; GENDER;
ASSOCIATION; CARVEDILOL; GUIDELINES; HF
AB Background-Hydralazine-isosorbide dinitrate (H-ISDN) therapy is recommended for African American patients with moderate to severe heart failure with reduced ejection fraction (<40%) (HFrEF), but use, temporal trends, and clinical characteristics associated with H-ISDN therapy in clinical practice are unknown.
Methods and Results-An observational analysis of 54 622 patients admitted with HFrEF and discharged home from 207 hospitals participating in the Get With The Guidelines-Heart Failure registry from April 2008 to March 2012 was conducted to assess prescription, trends, and predictors of use of H-ISDN among eligible patients. Among 11 185 African American patients eligible for H-ISDN therapy, only 2500 (22.4%) received H-ISDN therapy at discharge. In the overall eligible population, 5115 of 43 498 (12.6%) received H-ISDN at discharge. Treatment rates increased over the study period from 16% to 24% among African Americans and from 10% to 13% among the entire HFrEF population. In a multivariable model, factors associated with H-ISDN use among the entire cohort included younger age; male sex; African American/Hispanic ethnicity; and history of diabetes, hypertension, anemia, renal insufficiency, higher systolic blood pressure, and lower heart rate. In African American patients, these factors were similar; in addition, being uninsured was associated with lower use.
Conclusions-Overall, few potentially eligible patients with HFrEF are treated with H-ISDN, and among African-Americans fewer than one-fourth of eligible patients received guideline-recommended H-ISDN therapy. Improved ways to facilitate use of H-ISDN therapy in African American patients with HFrEF are needed.
C1 [Golwala, Harsh B.; Thadani, Udho; Stavrakis, Stavros] Univ Oklahoma, Hlth Sci Ctr, VA Med Ctr, Oklahoma City, OK USA.
[Liang, Li; Hernandez, Adrian F.] Duke Clin Res Inst, Durham, NC USA.
[Butler, Javed] Emory Univ, Div Cardiol, Atlanta, GA 30322 USA.
[Yancy, Clyde W.] Northwestern Univ, Div Cardiol, Chicago, IL 60611 USA.
[Bhatt, Deepak L.] Harvard Univ, Sch Med, Brigham & Womens Hosp, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Fonarow, Gregg C.] Ronald Reagan UCLA Med Ctr, Los Angeles, CA USA.
RP Fonarow, GC (reprint author), Ahmanson UCLA Cardiomyopathy Ctr, Ronald Reagan UCLA Med Ctr, 10833 LeConte Ave,Room 47-123 CHS, Los Angeles, CA 90095 USA.
EM gfonarow@mednet.ucla.edu
FU Medtronic; GlaxoSmithKline; Ortho-McNeil; American Heart Association
Pharmaceutical Roundtable
FX The Get With The Guidelines-Heart Failure (GWTG-HF) program is provided
by the American Heart Association. GWTG-HF has been funded in the past
through support from Medtronic, GlaxoSmithKline, Ortho-McNeil, and the
American Heart Association Pharmaceutical Roundtable.
NR 24
TC 10
Z9 10
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2047-9980
J9 J AM HEART ASSOC
JI J. Am. Heart Assoc.
PD AUG
PY 2013
VL 2
IS 4
AR e000214
DI 10.1161/JAHA.113.000214
PG 11
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 243TP
UT WOS:000326340900013
PM 23966379
ER
PT J
AU Larsen, M
Bartnes, K
Tsai, TT
Eagle, KA
Evangelista, A
Nienaber, CA
Suzuki, T
Fattori, R
Froehlich, JB
Hutchison, S
Sundt, TM
Januzzi, JL
Isselbacher, EM
Montgomery, DG
Myrmel, T
AF Larsen, Magnus
Bartnes, Kristian
Tsai, Thomas T.
Eagle, Kim A.
Evangelista, Arturo
Nienaber, Christoph A.
Suzuki, Toru
Fattori, Rossella
Froehlich, James B.
Hutchison, Stuart
Sundt, Thoralf M.
Januzzi, James L.
Isselbacher, Eric M.
Montgomery, Daniel G.
Myrmel, Truls
TI Extent of Preoperative False Lumen Thrombosis Does Not Influence
Long-Term Survival in Patients With Acute Type A Aortic Dissection
SO JOURNAL OF THE AMERICAN HEART ASSOCIATION
LA English
DT Article
DE aortic dissection; prognosis; surgery; thrombosis
ID INTERNATIONAL-REGISTRY; RISK-FACTORS; OPERATIVE STRATEGY; ARCH
REPLACEMENT; REPAIR; INSIGHTS; OUTCOMES; PATENCY; FATE; IRAD
AB Background-Partial thrombosis of the false lumen has been related to aortic growth, reoperations, and death in the chronic phase of type B and repaired type A aortic dissections. The impact of preoperative false lumen thrombosis has not been studied previously. We used data from a contemporary, multinational database on aortic dissections to evaluate whether different degrees of preoperative false lumen thrombosis influenced long-term prognosis.
Methods and Results-We examined the records of 522 patients with surgically treated acute type A aortic dissections who survived to discharge between 1996 and 2011. At the preoperative imaging, 414 (79.3%) patients had patent false lumens, 84 (16.1%) had partial thrombosis of the false lumen, and 24 (4.6%) had complete thrombosis of the false lumen. The annual median (interquartile range) aortic growth rates were 0.5 (-0.3 to 2.0) mm in the aortic arch, 2.0 (0.2 to 4.0) mm in the descending thoracic aorta, and similar regardless of the degree of false lumen thrombosis. The overall 5-year survival rate was 84.7%, and it was not influenced by false lumen thrombosis (P=0.86 by the log-rank test). Independent predictors of long-term mortality were age >70 years (hazard ratio [HR], 2.34; 95% confidence interval [CI], 1.20 to 4.56, P=0.012) and postoperative cerebrovascular accident, coma, and/or renal failure (HR, 2.62; 95% CI, 1.40 to 4.92, P=0.003).
Conclusions-Patients with acute type A aortic dissection who survive to discharge have a favorable prognosis. Preoperative false lumen thrombosis does not influence long-term mortality, reintervention rates, or aortic growth.
C1 [Larsen, Magnus; Bartnes, Kristian; Myrmel, Truls] Univ Hosp North Norway, Dept Cardiothorac & Vasc Surg, N-9038 Tromso, Norway.
[Larsen, Magnus; Bartnes, Kristian; Myrmel, Truls] Univ Tromso, Fac Med, Tromso, Norway.
[Tsai, Thomas T.] Univ Colorado Hosp, Aurora, CO USA.
[Eagle, Kim A.; Froehlich, James B.; Montgomery, Daniel G.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Evangelista, Arturo] Univ Vall DHebron, Gen Hosp, Barcelona, Spain.
[Nienaber, Christoph A.] Univ Hosp Eppendorf Rostock, Rostock, Germany.
[Suzuki, Toru] Univ Tokyo, Tokyo, Japan.
[Fattori, Rossella] Univ Hosp S Orsola, Bologna, Italy.
[Hutchison, Stuart] Univ Calgary, Med Ctr, Calgary, AB, Canada.
[Sundt, Thoralf M.; Januzzi, James L.; Isselbacher, Eric M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Larsen, M (reprint author), Univ Hosp North Norway, Dept Cardiothorac & Vasc Surg, N-9038 Tromso, Norway.
EM magnus.larsen@unn.no
FU W.L. Gore & Associates, Inc; Varbedian Fund for Aortic Research; Hewlett
Foundation; Mardigian Foundation; University of Michigan Group Practise;
Terumo; Norwegian Health Association, Norwegian Council on
Cardiovascular Diseases, Oslo, Norway
FX The International Registry of Acute Aortic Dissections receives funding
from the following sources: W.L. Gore & Associates, Inc, the Varbedian
Fund for Aortic Research, Hewlett Foundation, the Mardigian Foundation,
the University of Michigan Group Practise and Terumo. Dr Larsen is
supported by a research grant from the Norwegian Health Association,
Norwegian Council on Cardiovascular Diseases, Oslo, Norway.
NR 33
TC 7
Z9 7
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2047-9980
J9 J AM HEART ASSOC
JI J. Am. Heart Assoc.
PD AUG
PY 2013
VL 2
IS 4
AR e000112
DI 10.1161/JAHA.113.000112
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 243TP
UT WOS:000326340900020
PM 23817468
ER
PT J
AU Rodriguez, F
Hong, C
Chang, YC
Oertel, LB
Singer, DE
Green, AR
Lopez, LL
AF Rodriguez, Fatima
Hong, Clemens
Chang, Yuchiao
Oertel, Lynn B.
Singer, Daniel E.
Green, Alexander R.
Lopez, Lenny L.
TI Limited English Proficient Patients and Time Spent in Therapeutic Range
in a Warfarin Anticoagulation Clinic
SO JOURNAL OF THE AMERICAN HEART ASSOCIATION
LA English
DT Article
DE adverse drug events; limited English proficiency; outcomes research;
quality of care; warfarin
ID NONVALVULAR ATRIAL-FIBRILLATION; QUALITY-OF-CARE; HEALTH-CARE; LANGUAGE
BARRIERS; UNITED-STATES; INTERPRETER SERVICES; ORAL ANTICOAGULANT;
STROKE PREVENTION; ADVERSE EVENTS; US HISPANICS
AB Background-While anticoagulation clinics have been shown to deliver tailored, high-quality care to patients receiving warfarin therapy, communication barriers with limited English proficient (LEP) patients may lead to disparities in anticoagulation outcomes.
Methods and Results-We analyzed data on 3770 patients receiving care from the Massachusetts General Hospital Anticoagulation Management Service (AMS) from 2009 to 2010. This included data on international normalized ratio (INR) tests and patient characteristics, including language and whether AMS used a surrogate for primary communication. We calculated percent time in therapeutic range (TTR for INR between 2.0 and 3.0) and time in danger range (TDR for INR <1.8 or >3.5) using the standard Rosendaal interpolation method. There were 241 LEP patients; LEP patients, compared with non-LEP patients, had a higher number of comorbidities (3.2 versus 2.9 comorbidities, P=0.004), were more frequently uninsured (17.0% versus 4.3%, P<0.001), and less educated (47.7% versus 6.0% <= high school education, P<0.001). LEP patients compared with non-LEP patients spent less TTR (71.6% versus 74.0%, P=0.007) and more TDR (12.9% versus 11.3%, P=0.018). In adjusted analyses, LEP patients had lower TTR as compared with non-LEP patients (OR 1.5, 95% CI [ 1.1, 2.2]). LEP patients who used a communication surrogate spent less TTR and more TDR.
Conclusion-Even within a large anticoagulation clinic with a high average TTR, a small but significant decrease in TTR was observed for LEP patients compared with English speakers. Future studies are warranted to explore how the use of professional interpreters impact TTR for LEP patients.
C1 [Lopez, Lenny L.] Brigham & Womens Hosp, Div Gen Internal Med, Boston, MA 02115 USA.
[Rodriguez, Fatima; Lopez, Lenny L.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Rodriguez, Fatima; Hong, Clemens; Chang, Yuchiao; Singer, Daniel E.; Green, Alexander R.; Lopez, Lenny L.] Harvard Univ, Sch Med, Boston, MA USA.
[Hong, Clemens; Chang, Yuchiao; Singer, Daniel E.; Lopez, Lenny L.] Massachusetts Gen Hosp, Gen Med Div, Boston, MA 02114 USA.
[Oertel, Lynn B.] Massachusetts Gen Hosp, Anticoagulat Management Serv, Boston, MA 02114 USA.
[Green, Alexander R.; Lopez, Lenny L.] Massachusetts Gen Hosp, Disparities Solut Ctr, Boston, MA 02114 USA.
[Lopez, Lenny L.] Massachusetts Gen Hosp, Mongan Inst Hlth Policy, Boston, MA 02114 USA.
RP Rodriguez, F (reprint author), Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
EM farodriguez@partners.org
FU Daiichi Sankyo; Johnson and Johnson
FX Daniel E. Singer has received research grants from Daiichi Sankyo and
Johnson and Johnson and served as a consultant to Bayer Healthcare,
Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi Sankyo, Johnson and
Johnson, and Pfizer, all manufacturers of novel anticoagulants. The
other authors have no conflicts to declare.
NR 43
TC 5
Z9 5
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2047-9980
J9 J AM HEART ASSOC
JI J. Am. Heart Assoc.
PD AUG
PY 2013
VL 2
IS 4
AR e000170
DI 10.1161/JAHA.113.000170
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 243TP
UT WOS:000326340900032
PM 23832325
ER
PT J
AU Shah, RV
Abbasi, SA
Neilan, TG
Hulten, E
Coelho, O
Hoppin, A
Levitsky, L
de Ferranti, S
Rhodes, ET
Traum, A
Goodman, E
Feng, H
Heydari, B
Harris, WS
Hoefner, DM
McConnell, JP
Seethamraju, R
Rickers, C
Kwong, RY
Jerosch-Herold, M
AF Shah, Ravi V.
Abbasi, Siddique A.
Neilan, Tomas G.
Hulten, Edward
Coelho-Filho, Otavio
Hoppin, Alison
Levitsky, Lynne
de Ferranti, Sarah
Rhodes, Erinn T.
Traum, Avram
Goodman, Elizabeth
Feng, Henry
Heydari, Bobak
Harris, William S.
Hoefner, Daniel M.
McConnell, Joseph P.
Seethamraju, Ravi
Rickers, Carsten
Kwong, Raymond Y.
Jerosch-Herold, Michael
TI Myocardial Tissue Remodeling in Adolescent Obesity
SO JOURNAL OF THE AMERICAN HEART ASSOCIATION
LA English
DT Article
DE CT or MRI; obesity; type 2 diabetes
ID CARDIOVASCULAR MAGNETIC-RESONANCE; LEFT-VENTRICULAR MASS;
TRANSCYTOLEMMAL WATER-EXCHANGE; EXTRACELLULAR-MATRIX EXPANSION;
INSULIN-RESISTANCE; HEART-DISEASE; DIABETIC CARDIOMYOPATHY; VOLUME
FRACTION; CHILDREN; ASSOCIATION
AB Background-Childhood obesity is a significant risk factor for cardiovascular disease in adulthood. Although ventricular remodeling has been reported in obese youth, early tissue-level markers within the myocardium that precede organ-level alterations have not been described.
Methods and Results-We studied 21 obese adolescents (mean age, 17.7 +/- 2.6 years; mean body mass index [BMI], 41.9 +/- 9.5 kg/m(2), including 11 patients with type 2 diabetes [T2D]) and 12 healthy volunteers (age, 15.1 +/- 4.5 years; BMI, 20.1 +/- 3.5 kg/m(2)) using biomarkers of cardiometabolic risk and cardiac magnetic resonance imaging (CMR) to phenotype cardiac structure, function, and interstitial matrix remodeling by standard techniques. Although left ventricular ejection fraction and left atrial volumes were similar in healthy volunteers and obese patients (and within normal body size-adjusted limits), interstitial matrix expansion by CMR extracellular volume fraction (ECV) was significantly different between healthy volunteers (median, 0.264; interquartile range [IQR], 0.253 to 0.271), obese adolescents without T2D (median, 0.328; IQR, 0.278 to 0.345), and obese adolescents with T2D (median, 0.376; IQR, 0.336 to 0.407; P=0.0001). ECV was associated with BMI for the entire population (r=0.58, P<0.001) and with high-sensitivity C-reactive protein (r=0.47, P<0.05), serum triglycerides (r=0.51, P<0.05), and hemoglobin A1c (r=0.76, P<0.0001) in the obese stratum.
Conclusions-Obese adolescents (particularly those with T2D) have subclinical alterations in myocardial tissue architecture associated with inflammation and insulin resistance. These alterations precede significant left ventricular hypertrophy or decreased cardiac function.
C1 [Shah, Ravi V.; Abbasi, Siddique A.; Neilan, Tomas G.; Hulten, Edward; Feng, Henry; Heydari, Bobak; Kwong, Raymond Y.; Jerosch-Herold, Michael] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med,Cardiovasc Div,Noninvas Cardiovasc Imagi, Boston, MA 02115 USA.
[Shah, Ravi V.; Abbasi, Siddique A.; Neilan, Tomas G.; Hulten, Edward; Feng, Henry; Heydari, Bobak; Kwong, Raymond Y.; Jerosch-Herold, Michael] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Shah, Ravi V.; Neilan, Tomas G.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02115 USA.
[Coelho-Filho, Otavio] State Univ Campinas UNICAMP, Div Cardiol, Campinas, SP, Brazil.
[Hoppin, Alison] MassGen Hosp Children, Div Gastroenterol, Boston, MA USA.
[Levitsky, Lynne] MassGen Hosp Children, Div Endocrinol, Boston, MA USA.
[Traum, Avram] MassGen Hosp Children, Div Nephrol, Boston, MA USA.
[Goodman, Elizabeth] MassGen Hosp Children, Ctr Child & Adolescent Hlth Res & Policy, Boston, MA USA.
[de Ferranti, Sarah] Boston Childrens Hosp, Boston, MA USA.
[Rhodes, Erinn T.] Boston Childrens Hosp, Div Endocrinol, Boston, MA USA.
[Harris, William S.; Hoefner, Daniel M.; McConnell, Joseph P.] Hlth Diagnost Lab, Richmond, VA USA.
[Seethamraju, Ravi] Siemens Healthcare, Erlangen, Germany.
RP Jerosch-Herold, M (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Radiol, 75 Francis St, Boston, MA 02115 USA.
EM mjerosch-herold@partners.org
FU Harvard Catalyst; Harvard Clinical and Translational Science Center
(National Center for Research Resources); Harvard Clinical and
Translational Science Center (National Center for Advancing
Translational Sciences, National Institutes of Health)
[8UL1TR000170-05]; Harvard University; American Heart Association
[11POST000002, 12FTF12060588]; Heart Failure NIH Clinical Research
Network [U01-HL084877]; NIH [R01-HL091157]
FX This work was conducted with support from Harvard Catalyst, the Harvard
Clinical and Translational Science Center (National Center for Research
Resources and the National Center for Advancing Translational Sciences,
National Institutes of Health Award 8UL1TR000170-05, and financial
contributions from Harvard University and its affiliated academic health
care centers). The content is solely the responsibility of the authors
and does not necessarily represent the official views of Harvard
Catalyst, Harvard University and its affiliated academic health care
centers, or the National Institutes of Health. Dr Shah is supported by
an American Heart Association Post-Doctoral Fellowship Award
(11POST000002) and a training grant from the Heart Failure NIH Clinical
Research Network (U01-HL084877). Dr Neilan is supported by a grant from
the American Heart Association Fellow-to-Faculty Award (12FTF12060588).
Dr Jerosch-Herold is supported by NIH grant R01-HL091157. Studies were,
in part, donated by Siemens Healthcare.
NR 48
TC 18
Z9 18
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2047-9980
J9 J AM HEART ASSOC
JI J. Am. Heart Assoc.
PD AUG
PY 2013
VL 2
IS 4
AR e000279
DI 10.1161/JAHA.113.000279
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 243TP
UT WOS:000326340900038
PM 23963758
ER
PT J
AU Burstein, H
AF Burstein, Harold
TI Expert opinion vs guideline based care: The St. Gallen Case study
SO BREAST
LA English
DT Editorial Material
C1 Harvard Univ, Brigham & Womens Hosp, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Burstein, H (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0960-9776
EI 1532-3080
J9 BREAST
JI Breast
PD AUG 1
PY 2013
VL 22
SU 2
BP S1
EP S2
DI 10.1016/j.breast.2013.07.036
PG 2
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 243JG
UT WOS:000326312100001
PM 23906475
ER
PT J
AU Burstein, HJ
AF Burstein, Harold J.
TI Patients with triple negative breast cancer: Is there an optimal
adjuvant treatment?
SO BREAST
LA English
DT Editorial Material
ID RANDOMIZED-TRIALS; DOCETAXEL; CYCLOPHOSPHAMIDE; PACLITAXEL; SURVIVAL;
SUBTYPES; WOMEN; HER2
C1 [Burstein, Harold J.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Burstein, HJ (reprint author), Dana Farber Canc Inst, 450 Brookline Ave,44 Binney St, Boston, MA 02115 USA.
EM hburstein@partners.org
NR 13
TC 4
Z9 5
U1 0
U2 0
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0960-9776
EI 1532-3080
J9 BREAST
JI Breast
PD AUG 1
PY 2013
VL 22
SU 2
BP S147
EP S148
DI 10.1016/j.breast.2013.07.027
PG 2
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 243JG
UT WOS:000326312100029
PM 24074776
ER
PT J
AU Freedman, RA
Partridge, AH
AF Freedman, Rachel A.
Partridge, Ann H.
TI Management of breast cancer in very young women
SO BREAST
LA English
DT Article
DE Breast cancer; Young women; Age; Premenopausal
ID CONSERVING THERAPY; RANDOMIZED-TRIALS; CONSERVATION THERAPY; ADJUVANT
TAMOXIFEN; LARGE COHORT; SURVIVAL; AGE; RECURRENCE; DIAGNOSIS; STAGE
AB Breast cancer is the leading cause of cancer-related deaths in women age 40 and younger in developed countries, and although generally improving, survival rates for young women with breast cancer remain lower than for older women. Young women are more likely to develop more aggressive subtypes of breast cancer and previous research has suggested that young age is an independent risk factor for disease recurrence and death, and there may be unique biologic features of breast cancer that occurs in young women. Certainly, there are host differences biologically as well as psychosocially that affect the management of breast cancer and survivorship concerns for young women compared to older women. Multi-agent chemotherapy and biologic therapy targeting the tumor similar to the treatment in older women is standard, with careful attention to unique survivorship concerns including genetics, infertility, and psychosocial issues. Select young women will do well with hormone therapy only, although at present, the optimal hormonal therapy for very young women remains unclear. Recent data demonstrating that 10 years of tamoxifen improves outcomes compared to 5 may be particularly beneficial for young women with hormone receptor-positive tumors given the risk benefit profile. Future and ongoing studies focused on breast cancer in young women, addressing both biology as well as psychosocial issues, including supportive care interventions should improve outcomes for young women with breast cancer. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Freedman, Rachel A.; Partridge, Ann H.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Partridge, AH (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM rafreedman@partners.org; ahpartridge@partners.org
NR 44
TC 12
Z9 13
U1 1
U2 6
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0960-9776
EI 1532-3080
J9 BREAST
JI Breast
PD AUG 1
PY 2013
VL 22
SU 2
BP S176
EP S179
DI 10.1016/j.breast.2013.07.034
PG 4
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 243JG
UT WOS:000326312100036
PM 24074783
ER
PT J
AU Mouw, KW
Harris, JR
AF Mouw, Kent W.
Harris, Jay R.
TI Hypofractionation in the era of modulated radiotherapy (RT)
SO BREAST
LA English
DT Article
DE Breast-conserving therapy; Hypofractionation
ID EARLY BREAST-CANCER; 20-YEAR FOLLOW-UP; RANDOMIZED-TRIAL;
RADIATION-THERAPY; CONSERVING SURGERY; UK STANDARDIZATION; LOCAL
RECURRENCE; MASTECTOMY; BOOST; COMPLICATIONS
AB The use of radiation therapy (RI) as a component of breast-conserving therapy (BCT) has been shown to reduce the risk of local-regional recurrence and improve overall survival. As has been the common practice in the United States and Continental Europe, the majority of studies that demonstrated these benefits utilized daily radiation doses ranging from 1.8 to 2.0 Gray (Gy) per day given for approximately 5 weeks. However, due to geographic limitations, patient preferences, and financial considerations, there have been continued attempts to evaluate the efficacy and safety of abbreviated or hypofractionated courses of whole-breast radiation. Two key factors in these attempts have been: 1) advances in radiobiology allowing for a more precise estimation of equivalent dosing, and 2) advances in the delivery of RT ('modulation') that have resulted in substantially improved dose homogeneity in the target volume. Hypofractionated schedules have been compared to conventional radiation courses in several randomized controlled trials, as well as many prospective and retrospective experiences. These studies, now with about 10 years of follow-up, have demonstrated equivalent rates of local-regional recurrence, disease-free survival, and overall survival. The rates of toxicity have generally not been increased with hypofractionated regimens; however, certain toxicities may take decades to manifest. The generalizability of these results is unclear, as the majority of patients in the trials were elderly with early-stage hormone-receptor positive disease. Nevertheless, there is now sufficient evidence to recommend hypofractionated whole breast RI for a substantial percentage of patients. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Mouw, Kent W.] Harvard Radiat Oncol Program, Boston, MA USA.
[Harris, Jay R.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Harris, Jay R.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Harris, JR (reprint author), Dana Farber Canc Inst, Dana Bldg Room 1622,450 Brookline Ave, Boston, MA 02115 USA.
EM jharris@lroc.harvard.edu
NR 34
TC 2
Z9 4
U1 0
U2 2
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0960-9776
EI 1532-3080
J9 BREAST
JI Breast
PD AUG 1
PY 2013
VL 22
SU 2
BP S129
EP S136
DI 10.1016/j.breast.2013.07.024
PG 8
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 243JG
UT WOS:000326312100026
PM 24074773
ER
PT J
AU Strasser-Weippl, K
Badovinac-Crnjevic, T
Fan, L
Goss, PE
AF Strasser-Weippl, Kathrin
Badovinac-Crnjevic, Tanja
Fan, Lei
Goss, Paul E.
TI Extended adjuvant endocrine therapy in hormone-receptor positive breast
cancer
SO BREAST
LA English
DT Article
DE Extended treatment; Breast cancer; Endocrine; Adjuvant
ID TO-TREAT ANALYSIS; RANDOMIZED-TRIAL; POSTMENOPAUSAL WOMEN; TAMOXIFEN
THERAPY; UPDATED FINDINGS; NCICCTG MA.17; LETROZOLE; EXEMESTANE;
METAANALYSIS; OUTCOMES
AB A high ongoing recurrence rate in patients with endocrine responsive breast cancer provides the rationale for offering endocrine treatment for more than five years. The MA.17 study, comparing the aromatase inhibitor (AI) letrozole for five years after an initial five years of tamoxifen to no further treatment, provided the proof-of-principle for extended endocrine treatment. These results have meanwhile been confirmed by several other studies and an EBCTCG meta-analysis. More recently, data from the ATLAS trial, comparing 10 to five years of tamoxifen, have been published, similarly showing a benefit for longer endocrine treatment with tamoxifen. In postmenopausal women -including those who had been premenopausal at initial diagnosis - a cross-trial comparison of ATLAS and the AI studies indicates superiority of switching to letrozole versus ongoing tamoxifen, similar to superiority of the AIs over tamoxifen in the metastatic and early breast cancer settings. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Strasser-Weippl, Kathrin] Wilhelminen Hosp, Ctr Oncol Hematol & Palliat Care, A-1160 Vienna, Austria.
[Badovinac-Crnjevic, Tanja; Fan, Lei; Goss, Paul E.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Badovinac-Crnjevic, Tanja; Fan, Lei; Goss, Paul E.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Goss, PE (reprint author), Massachusetts Gen Hosp, Ctr Canc, 55 Fruit St,Lawrence House LRH-302, Boston, MA 02114 USA.
EM Kathrin.strasserweippl@gmail.com; pgoss@partners.org
FU GSK; Novartis; Pfizer
FX Paul Goss has received speaker's fees from GSK, Novartis and Pfizer.
NR 31
TC 12
Z9 12
U1 0
U2 1
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0960-9776
EI 1532-3080
J9 BREAST
JI Breast
PD AUG 1
PY 2013
VL 22
SU 2
BP S171
EP S175
DI 10.1016/j.breast.2013.07.033
PG 5
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 243JG
UT WOS:000326312100035
PM 24074782
ER
PT J
AU Stewart, AJ
Hepel, JT
O'Farrell, DA
Devlin, PM
Price, LL
Dale, RG
Wazer, DE
AF Stewart, Alexandra J.
Hepel, Jaroslaw T.
O'Farrell, Desmond A.
Devlin, Phillip M.
Price, Lori Lyn
Dale, Roger G.
Wazer, David E.
TI Equivalent uniform dose for accelerated partial breast irradiation using
the MammoSite applicator
SO RADIOTHERAPY AND ONCOLOGY
LA English
DT Article
DE Equivalent uniform dose; MammoSite catheter; Radiobiology; Toxicity
analysis
ID HOSPITAL EXPERIENCE; BRACHYTHERAPY; TOXICITY; OPTIMIZATION; CANCER
AB Introduction: This study aims to quantify the radiobiology of the MammoSite applicator and examine whether there is a relationship between equivalent uniform dose (EUD) and radiotherapy-associated toxicity.
Methods and materials: A previously-published version of the linear quadratic (LQ) model, designed to address the impact of dose-gradients in brachytherapy applications, was used to determine the biological effective dose (BED), equivalent dose in 2 Gray per fraction (EQD(2)) and EUD for the most common fractionation scheme for the MammoSite catheter (34 Gy in 10 fractions prescribed to 1 cm from the balloon surface), using a range of balloon sizes in a series of patients treated with single or multiple dwell positions. Toxicity from the MammoSite catheter was assessed and statistical associations with the calculated EUDs were investigated.
Results: The acute- and late-toxicity EUDs respectively range from 34.8-39.4 Gy and 33.4-37.6 Gy, with EUD decreasing as balloon diameter increases and/or the number of dwell positions increases. There was a positive association between EUD and hyperpigmentation and telangiectasia.
Conclusions: For APBI using the Mammosite applicator, EUD is higher than the marginal prescription dose and, for the dose-fractionation patterns considered here, was associated with acute and late skin toxicity. EUD is a potentially useful parameter to characterize non-uniform dose distributions related to brachytherapy treatments. Further evaluation in future studies is warranted. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Stewart, Alexandra J.] Royal Surrey Cty Hosp, St Lukes Canc Ctr, Guildford GU2 7XX, Surrey, England.
[Hepel, Jaroslaw T.; Wazer, David E.] Tufts Univ, Tufts Med Ctr, Dept Radiat Oncol, Boston, MA 02111 USA.
[Hepel, Jaroslaw T.; Wazer, David E.] Brown Univ, Rhode Isl Hosp, Dept Radiat Oncol, Providence, RI 02903 USA.
[O'Farrell, Desmond A.; Devlin, Phillip M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Brigham & Womens Hosp, Boston, MA 02115 USA.
[Price, Lori Lyn] Tufts Med Ctr, Inst Clin Res & Hlth Policy Studies, Biostat Res Ctr, Boston, MA USA.
[Dale, Roger G.] Univ London Imperial Coll Sci Technol & Med, Fac Med, Dept Surg & Canc, London, England.
RP Stewart, AJ (reprint author), Royal Surrey Cty Hosp, St Lukes Canc Ctr, Egerton Rd, Guildford GU2 7XX, Surrey, England.
EM Alexandra.stewart@nhs.net
NR 20
TC 6
Z9 6
U1 0
U2 0
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0167-8140
J9 RADIOTHER ONCOL
JI Radiother. Oncol.
PD AUG
PY 2013
VL 108
IS 2
BP 232
EP 235
DI 10.1016/j.radonc.2013.06.030
PG 4
WC Oncology; Radiology, Nuclear Medicine & Medical Imaging
SC Oncology; Radiology, Nuclear Medicine & Medical Imaging
GA 241AR
UT WOS:000326139300009
PM 23891101
ER
PT J
AU Rogus-Pulia, N
Robbins, J
AF Rogus-Pulia, Nicole
Robbins, JoAnne
TI Approaches to the Rehabilitation of Dysphagia in Acute Poststroke
Patients
SO SEMINARS IN SPEECH AND LANGUAGE
LA English
DT Article
DE Dysphagia; stroke; acute; rehabilitation; evidence
ID NEUROMUSCULAR ELECTRICAL-STIMULATION; ACUTE STROKE PATIENTS; RANDOMIZED
CONTROLLED-TRIAL; ACUTE ISCHEMIC-STROKE; OROPHARYNGEAL DYSPHAGIA;
SWALLOWING DISORDERS; PHARYNGEAL DYSPHAGIA; ASPIRATION PNEUMONIA;
NEUROGENIC DYSPHAGIA; EMERGENCY-DEPARTMENT
AB Dysphagia occurs frequently following stroke and may result in serious health consequences including pneumonia, malnutrition, dehydration, and mortality. Prevention of these negative health outcomes requires early identification and treatment of dysphagia. The speech-language pathologist, as part of a multidisciplinary team, holds the primary responsibility for selection of an effective dysphagia rehabilitation program for these patients. Because much research has focused on patients with chronic dysphagia, this review will focus on treatment of patients within the acute phase of recovery poststroke. Although some acute patients may experience transient dysphagia that resolves spontaneously, many will go on to develop chronic dysphagia that may be prevented with provision of early and intensive treatment. An overview of dysphagia following stroke will be provided with information regarding incidence, complications, evaluation, and causes of dysphagia. A thorough discussion of evidence supporting varying approaches to dysphagia rehabilitation will follow with inclusion of several current, novel, and experimental techniques. The importance of the multidisciplinary team and regular reevaluation will be emphasized as well.
C1 [Rogus-Pulia, Nicole; Robbins, JoAnne] William S Middleton Mem Vet Adm Med Ctr, GRECC, Madison, WI 53705 USA.
[Rogus-Pulia, Nicole; Robbins, JoAnne] Univ Wisconsin, Dept Med, Sch Med & Publ Hlth, Div Gastroenterol & Hepatol, Madison, WI USA.
RP Rogus-Pulia, N (reprint author), William S Middleton Mem Vet Adm Med Ctr, 2500 Overlook Terrace,Madison GRECC 11G,Room D521, Madison, WI 53705 USA.
EM nicolepulia@gmail.com
NR 126
TC 5
Z9 6
U1 1
U2 20
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0734-0478
EI 1098-9056
J9 SEMIN SPEECH LANG
JI Semin. Speech Lang.
PD AUG
PY 2013
VL 34
IS 3
BP 154
EP 169
DI 10.1055/s-0033-1358368
PG 16
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 242IF
UT WOS:000326231800004
PM 24166190
ER
PT J
AU Kobayashi, K
Hosseini, A
Sakamoto, M
Qi, W
Rubash, HE
Li, GA
AF Kobayashi, Koichi
Hosseini, Ali
Sakamoto, Makoto
Qi, Wei
Rubash, Harry E.
Li, Guoan
TI In Vivo Kinematics of the Extensor Mechanism of the Knee During Deep
Flexion
SO JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME
LA English
DT Article
DE patellofemoral contact; weight-bearing activity; patellar tendon force;
quadriceps force; knee biomechanics
ID PATELLOFEMORAL CONTACT PRESSURES; ANTERIOR CRUCIATE LIGAMENT;
3-DIMENSIONAL TRACKING; TIBIOFEMORAL JOINT; PATELLAR TRACKING;
ARTHROPLASTY; STRESS; BIOMECHANICS; FORCES; TENDON
AB While various factors have been assumed to affect knee joint biomechanics, few data have been reported on the function of the extensor mechanism in deep flexion of the knee. This study analyzed the patellofemoral joint contact kinematics and the ratio of the quadriceps and patellar tendon forces in living subjects when they performed a single leg lunge up to 150 deg of flexion. The data revealed that in the proximal-distal direction, the patellofemoral articular contact points were in the central one-third of the patellar cartilage. Beyond 90 deg of flexion, the contact points moved towards the medial-lateral edges of the patellar surface. At low flexion angles, the patellar tendon and quadriceps force ratio was approximately 1.0 but reduced to about 0.7 after 60 deg of knee flexion, implying that the patella tendon carries lower loads than the quadriceps. These data may be valuable for improvement of contemporary surgical treatments of diseased knees that are aimed to achieve deep knee flexion.
C1 [Kobayashi, Koichi; Hosseini, Ali; Qi, Wei; Rubash, Harry E.; Li, Guoan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Orthoped Surg,Bioengn Lab, Boston, MA 02114 USA.
[Kobayashi, Koichi; Sakamoto, Makoto] Niigata Univ, Sch Med, Dept Hlth Sci, Niigata, Japan.
RP Li, GA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Orthoped Surg,Bioengn Lab, Boston, MA 02114 USA.
EM gli1@partners.org
FU National Institutes of Health [R01AR055612]; Japan Society for the
Promotion of Science [C22560074]
FX This work was supported by a National Institutes of Health Grant
R01AR055612 and a Grant-in-Aid for Scientific Research C22560074 by the
Japan Society for the Promotion of Science.
NR 37
TC 3
Z9 3
U1 0
U2 9
PU ASME
PI NEW YORK
PA TWO PARK AVE, NEW YORK, NY 10016-5990 USA
SN 0148-0731
EI 1528-8951
J9 J BIOMECH ENG-T ASME
JI J. Biomech. Eng.-Trans. ASME
PD AUG
PY 2013
VL 135
IS 8
AR 081002
DI 10.1115/1.4024284
PG 7
WC Biophysics; Engineering, Biomedical
SC Biophysics; Engineering
GA 240HE
UT WOS:000326085100003
PM 23719832
ER
PT J
AU Mort, EA
Demehin, AA
Marple, KB
McCullough, KY
Meyer, GS
AF Mort, Elizabeth A.
Demehin, Akinluwa A.
Marple, Keith B.
McCullough, Kathryn Y.
Meyer, Gregg S.
TI Setting Quality and Safety Priorities in a Target-Rich Environment: An
Academic Medical Center's Challenge
SO ACADEMIC MEDICINE
LA English
DT Article
ID CARE
AB Hospitals are continually challenged to provide safer and higher-quality patient care despite resource constraints. With an ever-increasing range of quality and safety targets at the national, state, and local levels, prioritization is crucial in effective institutional quality goal setting and resource allocation.
Organizational goal-setting theory is a performance improvement methodology with strong results across many industries. The authors describe a structured goal-setting process they have established at Massachusetts General Hospital for setting annual institutional quality and safety goals. Begun in 2008, this process has been conducted on an annual basis. Quality and safety data are gathered from many sources, both internal and external to the hospital. These data are collated and classified, and multiple approaches are used to identify the most pressing quality issues facing the institution. The conclusions are subject to stringent internal review, and then the top quality goals of the institution are chosen. Specific tactical initiatives and executive owners are assigned to each goal, and metrics are selected to track performance. A reporting tool based on these tactics and metrics is used to deliver progress updates to senior hospital leadership.
The hospital has experienced excellent results and strong organizational buy-in using this effective, low-cost, and replicable goal-setting process. It has led to improvements in structural, process, and outcomes aspects of quality.
C1 [Mort, Elizabeth A.; Marple, Keith B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Mort, Elizabeth A.] Massachusetts Gen Phys Org, Boston, MA USA.
[Mort, Elizabeth A.] Partners Healthcare, Boston, MA USA.
[Demehin, Akinluwa A.] Amer Hosp Assoc, Washington, DC USA.
[McCullough, Kathryn Y.] Massachusetts Gen Hosp Phys Org, Vasc Ultrasound Core Lab, Boston, MA USA.
[Meyer, Gregg S.] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
RP Mort, EA (reprint author), Massachusetts Gen Hosp, Bulfinch 270,55 Fruit St, Boston, MA 02114 USA.
EM emort@partners.org
NR 20
TC 1
Z9 1
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
EI 1938-808X
J9 ACAD MED
JI Acad. Med.
PD AUG
PY 2013
VL 88
IS 8
BP 1099
EP 1104
DI 10.1097/ACM.0b013e31829a3ee8
PG 6
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA 235FO
UT WOS:000325702400023
PM 23807111
ER
PT J
AU Wanderer, JP
Leffert, LR
Mhyre, JM
Kuklina, EV
Callaghan, WM
Bateman, BT
AF Wanderer, Jonathan P.
Leffert, Lisa R.
Mhyre, Jill M.
Kuklina, Elena V.
Callaghan, William M.
Bateman, Brian T.
TI Epidemiology of Obstetric-Related ICU Admissions in Maryland: 1999-2008
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE critical care; intensive care; maternal health; maternal health
services; maternal mortality
ID INTENSIVE-CARE-UNIT; RISK-FACTORS; PREGNANCY; OUTCOMES; STATES;
MORBIDITY; MORTALITY; DELIVERY; TRENDS; HOSPITALIZATIONS
AB Objective: To define the prevalence, indications, and temporal trends in obstetric-related ICU admissions.
Design: Descriptive analysis of utilization patterns.
Setting: All hospitals within the state of Maryland.
Patients: All antepartum, delivery, and postpartum patients who were hospitalized between 1999 and 2008.
Interventions: None.
Measurements and Main Results: We identified 2,927 ICU admissions from 765,598 admissions for antepartum, delivery, or postpartum conditions using appropriate International Classification of Diseases, 9th Revision, Clinical Modification codes. The overall rate of ICU utilization was 419.1 per 100,000 deliveries, with rates of 162.5, 202.6, and 54.0 per 100,000 deliveries for the antepartum, delivery, and postpartum periods, respectively. The leading diagnoses associated with ICU admission were pregnancy-related hypertensive disease (present in 29.9% of admissions), hemorrhage (18.8%), cardiomyopathy or other cardiac disease (18.3%), genitourinary infection (11.5%), complications from ectopic pregnancies and abortions (10.3%), nongenitourinary infection (10.1%), sepsis (7.1%), cerebrovascular disease (5.8%), and pulmonary embolism (3.7%). We assessed for changes in the most common diagnoses in the ICU population over time and found rising rates of sepsis (10.1 per 100,000 deliveries to 16.6 per 100,000 deliveries, p = 0.003) and trauma (9.2 per 100,000 deliveries to 13.6 per 100,000 deliveries, p = 0.026) with decreasing rates of anesthetic complications (11.3 per 100,000 to 4.7 per 100,000, p = 0.006). The overall frequency of obstetric-related ICU admission and the rates for other indications remained relatively stable.
Conclusions: Between 1999 and 2008, 419.1 per 100,000 deliveries in Maryland were complicated by ICU admission. Hospitals providing obstetric services should plan for appropriate critical care management and/or transfer of women with severe morbidities during pregnancy.
C1 [Wanderer, Jonathan P.] Vanderbilt Univ, Dept Anesthesia, Nashville, TN 37235 USA.
[Leffert, Lisa R.; Bateman, Brian T.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Mhyre, Jill M.] Univ Michigan Hlth Syst, Dept Anesthesiol, Ann Arbor, MI USA.
[Kuklina, Elena V.] Ctr Dis Control & Prevent, Div Heart Dis & Stroke Prevent, Natl Ctr Chron Dis Prevent & Hlth Promot, Washington, DC USA.
[Callaghan, William M.] Ctr Dis Control & Prevent, Div Reprod Hlth, Natl Ctr Chron Dis Prevent & Hlth Promot, Washington, DC USA.
RP Wanderer, JP (reprint author), Vanderbilt Univ, Dept Anesthesia, 221 Kirkland Hall, Nashville, TN 37235 USA.
EM jonathan.p.wanderer@vanderbilt.edu
FU Massachusetts General Hospital; National Institute of Health [GM007592];
NY PGA 66th Assembly; NIH
FX Supported, in part, by Massachusetts General Hospital departmental and
National Institute of Health funds (BTB, grant GM007592).; Dr. Mhyre has
received royalties from Chestnut Principles and Practices of Anesthesia,
5th Ed; payment for development of educational presentations from NY PGA
66th Assembly; travel/accommodations from ACOG Maternal Mortality Expert
Panel, Joint Commission Panel on High Risk Pregnancy. Dr. Bateman
received funding from the NIH. The remaining authors have disclosed that
they do not have any potential conflicts of interest.
NR 32
TC 26
Z9 30
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
EI 1530-0293
J9 CRIT CARE MED
JI Crit. Care Med.
PD AUG
PY 2013
VL 41
IS 8
BP 1844
EP 1852
DI 10.1097/CCM.0b013e31828a3e24
PG 9
WC Critical Care Medicine
SC General & Internal Medicine
GA 235FH
UT WOS:000325701500017
PM 23648568
ER
PT J
AU Elmer, J
Hou, P
Wilcox, SR
Chang, YC
Schreiber, H
Okechukwu, I
Pontes-Neto, O
Bajwa, E
Hess, DR
Avery, L
Duran-Mendicuti, MA
Camargo, CA
Greenberg, SM
Rosand, J
Pallin, DJ
Goldstein, JN
AF Elmer, Jonathan
Hou, Peter
Wilcox, Susan R.
Chang, Yuchiao
Schreiber, Hannah
Okechukwu, Ikenna
Pontes-Neto, Octavio
Bajwa, Ednan
Hess, Dean R.
Avery, Laura
Duran-Mendicuti, Maria Alejandra
Camargo, Carlos A., Jr.
Greenberg, Steven M.
Rosand, Jonathan
Pallin, Daniel J.
Goldstein, Joshua N.
TI Acute Respiratory Distress Syndrome After Spontaneous Intracerebral
Hemorrhage
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE acute lung injury; hemorrhagic stroke; mechanical ventilation; tidal
volume; ventilator-induced lung injury
ID ACUTE LUNG INJURY; NEUROGENIC PULMONARY-EDEMA; INTENSIVE-CARE-UNIT;
GLASGOW COMA SCALE; SUBARACHNOID HEMORRHAGE; MECHANICAL VENTILATION;
HEMATOMA EXPANSION; SEVERE SEPSIS; TIDAL VOLUME; BRAIN-INJURY
AB Objectives: Acute respiratory distress syndrome develops commonly in critically ill patients in response to an injurious stimulus. The prevalence and risk factors for development of acute respiratory distress syndrome after spontaneous intracerebral hemorrhage have not been reported. We sought to determine the prevalence of acute respiratory distress syndrome after intracerebral hemorrhage, characterize risk factors for its development, and assess its impact on patient outcomes.
Design: Retrospective cohort study at two academic centers.
Patients: We included consecutive patients presenting from June 1, 2000, to November 1, 2010, with intracerebral hemorrhage requiring mechanical ventilation. We excluded patients with age less than 18 years, intracerebral hemorrhage secondary to trauma, tumor, ischemic stroke, or structural lesion; if they required intubation only during surgery; if they were admitted for comfort measures; or for a history of immunodeficiency.
Interventions: None.
Measurements and Main Results: Data were collected both prospectively as part of an ongoing cohort study and by retrospective chart review. Of 1,665 patients identified by database query, 697 met inclusion criteria. The prevalence of acute respiratory distress syndrome was 27%. In unadjusted analysis, high tidal volume ventilation was associated with an increased risk of acute respiratory distress syndrome (hazard ratio, 1.79 [95% CI, 1.13-2.83]), as were male sex, RBC and plasma transfusion, higher fluid balance, obesity, hypoxemia, acidosis, tobacco use, emergent hematoma evacuation, and vasopressor dependence. In multivariable modeling, high tidal volume ventilation was the strongest risk factor for acute respiratory distress syndrome development (hazard ratio, 1.74 [95% CI, 1.08-2.81]) and for inhospital mortality (hazard ratio, 2.52 [95% CI, 1.46-4.34]).
Conclusions: Development of acute respiratory distress syndrome is common after intubation for intracerebral hemorrhage. Modifiable risk factors, including high tidal volume ventilation, are associated with its development and in-patient mortality.
C1 [Elmer, Jonathan] Univ Pittsburgh, Med Ctr, Dept Crit Care Med, Pittsburgh, PA 15260 USA.
[Hou, Peter; Schreiber, Hannah; Pallin, Daniel J.] Brigham & Womens Hosp, Dept Emergency Med, Boston, MA 02115 USA.
[Hou, Peter] Brigham & Womens Hosp, Dept Surg, Div Burn Trauma & Surg Crit Care, Boston, MA 02115 USA.
[Hou, Peter; Wilcox, Susan R.; Chang, Yuchiao; Bajwa, Ednan; Hess, Dean R.; Avery, Laura; Duran-Mendicuti, Maria Alejandra; Camargo, Carlos A., Jr.; Greenberg, Steven M.; Rosand, Jonathan; Pallin, Daniel J.; Goldstein, Joshua N.] Harvard Univ, Sch Med, Boston, MA USA.
[Wilcox, Susan R.; Okechukwu, Ikenna; Camargo, Carlos A., Jr.; Goldstein, Joshua N.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Wilcox, Susan R.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Chang, Yuchiao] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Pontes-Neto, Octavio; Greenberg, Steven M.; Rosand, Jonathan] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Bajwa, Ednan] Massachusetts Gen Hosp, Pulm & Crit Care Unit, Boston, MA 02114 USA.
[Hess, Dean R.] Massachusetts Gen Hosp, Dept Resp Care, Boston, MA 02114 USA.
[Avery, Laura] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Duran-Mendicuti, Maria Alejandra] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Rosand, Jonathan; Goldstein, Joshua N.] Massachusetts Gen Hosp, Div Neurocrit Care & Emergency Neurol, Boston, MA 02114 USA.
RP Elmer, J (reprint author), Univ Pittsburgh, Med Ctr, Dept Crit Care Med, Pittsburgh, PA 15260 USA.
EM elmerjp@upmc.edu
RI Pontes-Neto, Octavio/G-4294-2012; Pallin, Daniel/H-6382-2013; Goldstein,
Joshua/H-8953-2016;
OI Pontes-Neto, Octavio/0000-0003-0317-843X; Pallin,
Daniel/0000-0002-8517-9702; Wilcox, Susan/0000-0001-7477-7531
FU Emergency Medicine Foundation/Emergency Medicine Resident's Association;
Wuerz Award from the Department of Emergency Medicine at Brigham and
Women's Hospital; National Institutes of Health [R01NS073344,
R01NS059727, 5K23NS059774]; U of Texas-Grand Rounds [5R01AG026484-08,
5R01NS070834-03]; National Institutes of Health; Mass Medical Society;
NINDS
FX Supported, in part, by a grant from the Emergency Medicine
Foundation/Emergency Medicine Resident's Association, the Wuerz Award
from the Department of Emergency Medicine at Brigham and Women's
Hospital, and by the National Institutes of Health (R01NS073344,
R01NS059727, and 5K23NS059774).; Dr. Hess has consulted for Philips
Respironics, ResMed, Breathe Technology, and Pari. Dr. Greenberg has
consulted for Hoffman La-Roche, received grants 5R01AG026484-08 and
5R01NS070834-03, and received payment for lectures from U of Texas-Grand
Rounds. Dr. Rosand has received grant support from the National
Institutes of Health. Dr. Goldstein has received grant support from the
Mass Medical Society, the National Institutes of Health and NINDS. He
has consulted for CSL Behring. The remaining authors have disclosed that
they do not have any potential conflicts of interest.
NR 54
TC 19
Z9 20
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
EI 1530-0293
J9 CRIT CARE MED
JI Crit. Care Med.
PD AUG
PY 2013
VL 41
IS 8
BP 1992
EP 2001
DI 10.1097/CCM.0b013e31828a3f4d
PG 10
WC Critical Care Medicine
SC General & Internal Medicine
GA 235FH
UT WOS:000325701500034
PM 23760151
ER
PT J
AU Lien, S
Verreault, DJ
Alston, TA
AF Lien, Susan
Verreault, David J.
Alston, Theodore A.
TI Sustained airway pressure after transient occlusion of a valve venting a
self-inflating manual resuscitator
SO JOURNAL OF CLINICAL ANESTHESIA
LA English
DT Letter
C1 [Lien, Susan] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Lien, S (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
EM talston@partners.org
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 0952-8180
EI 1873-4529
J9 J CLIN ANESTH
JI J. Clin. Anesth.
PD AUG
PY 2013
VL 25
IS 5
BP 424
EP 425
DI 10.1016/j.jclinane.2013.02.008
PG 2
WC Anesthesiology
SC Anesthesiology
GA 235PJ
UT WOS:000325732900015
PM 23965202
ER
PT J
AU Kao, SY
Kempfle, JS
Jensen, JB
Perez-Fernandez, D
Lysaght, AC
Edge, AS
Stankovic, KM
AF Kao, Shyan-Yuan
Kempfle, Judith S.
Jensen, Jane B.
Perez-Fernandez, Deborah
Lysaght, Andrew C.
Edge, Albert S.
Stankovic, Konstantina M.
TI Loss of osteoprotegerin expression in the inner ear causes degeneration
of the cochlear nerve and sensorineural hearing loss
SO NEUROBIOLOGY OF DISEASE
LA English
DT Article
DE Osteoprotegerin; Spiral ganglion cells; Cochlear neurons; Sensorineural
hearing loss; Auditory stem cell
ID SPIRAL GANGLION NEURONS; PAGETS-DISEASE; OTIC CAPSULE; CELL-DEATH;
STEM-CELLS; TEMPORAL BONE; MICE; OSTEOPOROSIS; OTOSCLEROSIS; ERK
AB Osteoprotegerin (OPG) is a key regulator of bone remodeling. Mutations and variations in the OPG gene cause many human diseases that are characterized by not only skeletal abnormalities but also poorly understood hearing loss: Paget's disease, osteoporosis, and celiac disease. To gain insight into the mechanisms of hearing loss in OPG deficiency, we studied OPG knockout (Opg(-/-)) mice. We show that they develop sensorineural hearing loss, in addition to conductive hearing loss due to abnormal middle-ear bones. OPG deficiency caused demyelination and degeneration of the cochlear nerve in vivo. It also activated ERK, sensitized spiral ganglion cells (SGC) to apoptosis, and inhibited proliferation and survival of cochlear stem cells in vitro, which could be rescued by treatment with exogenous OPG, an ERK inhibitor, or bisphosphonate. Our results demonstrate a novel role for OPG in the regulation of SGC survival, and suggest a mechanism for sensorineural hearing loss in OPG deficiency. (c) 2013 Elsevier Inc. All rights reserved.
C1 Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Eaton Peabody Labs, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02114 USA.
RP Stankovic, KM (reprint author), Massachusetts Eye & Ear Infirm, 243 Charles St, Boston, MA 02114 USA.
EM Konstantina_stankovic@meei.harvard.edu
FU National Institute on Deafness and Other Communication Disorders
[NIH-NIDCD K08 DC010419]; Massachusetts Life Sciences Center; Boston
Foundation; Bertarelli Foundation
FX This work was supported by grants from the National Institute on
Deafness and Other Communication Disorders (NIH-NIDCD K08 DC010419), the
Massachusetts Life Sciences Center, the Boston Foundation and the
Bertarelli Foundation to K.M.S. We thank Drs. Charles Liberman and
Gabriel Corfas for helpful comments.
NR 47
TC 10
Z9 10
U1 0
U2 10
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
EI 1095-953X
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD AUG
PY 2013
VL 56
BP 25
EP 33
DI 10.1016/j.nbd.2013.04.008
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 210RX
UT WOS:000323853300004
PM 23607938
ER
PT J
AU Yu, ZY
Liu, N
Li, YD
Xu, JF
Wang, XY
AF Yu, Zhanyang
Liu, Ning
Li, Yadan
Xu, Jianfeng
Wang, Xiaoying
TI Neuroglobin overexpression inhibits oxygen-glucose deprivation-induced
mitochondrial permeability transition pore opening in primary cultured
mouse cortical neurons
SO NEUROBIOLOGY OF DISEASE
LA English
DT Article
DE Neuroglobin; Oxygen/glucose deprivation; Mitochondria permeability
transition pore (mPTP); NAD(+) release; Mitochondria swelling;
Cytochrome c
ID DEPENDENT ANION CHANNEL; FOCAL CEREBRAL-ISCHEMIA; CELL-DEATH;
CYCLOSPORINE-A; CYCLOPHILIN-D; CYTOCHROME-C; ENDOGENOUS NEUROPROTECTANT;
HIPPOCAMPAL-NEURONS; REPERFUSION INJURY; IN-VITRO
AB Neuroglobin (Ngb) is an endogenous neuroprotective molecule against hypoxic/ischemic brain injury, but the underlying mechanisms remain largely undefined. Our recent study revealed that Ngb can bind to voltage-dependent anion channel (VDAC), a regulator of mitochondria permeability transition (MPT). In this study we examined the role of Ngb in MPT pore (mPTP) opening following oxygen-glucose deprivation (OGD) in primary cultured mouse cortical neurons. Co-immunoprecipitation (Co-IP) and immunocytochemistry showed that the binding between Ngb and VDAC was increased after OGD compared to normoxia, indicating the OGD-enhanced Ngb-VDAC interaction. Ngb overexpression protected primary mouse cortical neurons from OGD-induced neuronal death, to an extent comparable to mPTP opening inhibitor, cyclosporine A (CsA) pretreatment. We further measured the role of Ngb in OGD-induced mPTP opening using Ngb overexpression and knockdown approaches in primary cultured neurons, and recombinant Ngb exposure to isolated mitochondria. Same as CsA pretreatment, Ngb overexpression significantly reduced OGD-induced mPTP opening markers including mitochondria swelling, mitochondrial NAD(+) release, and cytochrome c (Cyt c) release in primary cultured neurons. Recombinant Ngb incubation significantly reduced OGD-induced NAD(+) release and Cyt c release from isolated mitochondria. In contrast, Ngb knockdown significantly increased OGD-induced neuron death, and increased OGD-induced mitochondrial NAD(+) release and Cyt c release as well, and these outcomes could be rescued by CsA pretreatment In summary, our results demonstrated that Ngb overexpression can inhibit OGD-induced mPTP opening in primary cultured mouse cortical neurons, which may be one of the molecular mechanisms of Ngb's neuroprotection. (c) 2013 Elsevier Inc. All rights reserved.
C1 Massachusetts Gen Hosp, Neuroprotect Res Lab, Dept Neurol, Charlestown, MA 02129 USA.
Massachusetts Gen Hosp, Neuroprotect Res Lab, Dept Radiol, Charlestown, MA 02129 USA.
Harvard Univ, Sch Med, Program Neurosci, Charlestown, MA 02129 USA.
RP Yu, ZY (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neuroprotect Res Lab,Dept Neurol, 149 13th St,Room 2401, Charlestown, MA 02129 USA.
EM zyu@partners.org; wangxi@helix.mgh.harvard.edu
FU NIH [R01-NS049476]; American Heart Association [12POST9720007]
FX This work was supported in part by NIH grant R01-NS049476 (to X.W.) and
postdoctoral fellowship (12POST9720007) from the American Heart
Association (to Z.Y.). We thank Ms. Jessica Poppe for language editorial
assistance. We appreciate Dr. Eng H. Lo for his very helpful discussion.
The authors declare no conflict of interest.
NR 53
TC 27
Z9 27
U1 1
U2 11
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
EI 1095-953X
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD AUG
PY 2013
VL 56
BP 95
EP 103
DI 10.1016/j.nbd.2013.04.015
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 210RX
UT WOS:000323853300011
PM 23639789
ER
PT J
AU Potter, WB
Basu, T
O'Riordan, KJ
Kirchner, A
Rutecki, P
Burger, C
Roopra, A
AF Potter, Wyatt B.
Basu, Trina
O'Riordan, Kenneth J.
Kirchner, Allison
Rutecki, Paul
Burger, Corinna
Roopra, Avtar
TI Reduced Juvenile Long-Term Depression in Tuberous Sclerosis Complex Is
Mitigated in Adults by Compensatory Recruitment of mGluR5 and Erk
Signaling
SO PLOS BIOLOGY
LA English
DT Article
ID METABOTROPIC GLUTAMATE RECEPTORS; TEMPORAL-LOBE EPILEPSY;
FRAGILE-X-SYNDROME; TUMOR-SUPPRESSOR COMPLEX; INITIATION-FACTOR 4E;
MAMMALIAN TARGET; MOUSE MODEL; PROTEIN-SYNTHESIS; 3-KINASE/AKT PATHWAY;
SYNAPTIC PLASTICITY
AB Tuberous sclerosis complex (TSC) is a multisystem genetic disease that manifests with mental retardation, tumor formation, autism, and epilepsy. Heightened signaling through the mammalian target of rapamycin (mTOR) pathway is involved in TSC pathology, however it remains unclear how other signaling pathways are perturbed and contribute to disease symptoms. Reduced long-term depression (LTD) was recently reported in TSC mutant mice. We find that although reduced LTD is a feature of the juvenile mutant hippocampus, heightened expression of metabotropic glutamate receptor 5 and constitutively activated Erk signaling in the adult hippocampus drives wild-type levels of LTD. Increased mGluR5 and Erk results in a novel mTOR-independent LTD in CA1 hippocampus of adult mice, and contributes to the development of epileptiform bursting activity in the TSC2(+/-) CA3 region of the hippocampus. Inhibition of mGluR5 or Erk signaling restores appropriate mTOR-dependence to LTD, and significantly reduces epileptiform bursting in TSC2(+/-) hippocampal slices. We also report that adult TSC2(+/-) mice exhibit a subtle perseverative behavioral phenotype that is eliminated by mGluR5 antagonism. These findings highlight the potential of modulating the mGluR5-Erk pathway in a developmental stage-specific manner to treat TSC.
C1 [Potter, Wyatt B.; Basu, Trina; Kirchner, Allison; Roopra, Avtar] Univ Wisconsin, Med Sci Ctr, Dept Neurosci, Madison, WI USA.
[Potter, Wyatt B.; Basu, Trina] Univ Wisconsin, Neurosci Training Program, Madison, WI 53706 USA.
[O'Riordan, Kenneth J.; Rutecki, Paul; Burger, Corinna] Univ Wisconsin, William S Middleton Mem Vet Adm Hosp, Dept Neurol, Madison, WI USA.
[O'Riordan, Kenneth J.; Rutecki, Paul; Burger, Corinna] Univ Wisconsin, Madison, WI USA.
RP Potter, WB (reprint author), Univ Wisconsin, Med Sci Ctr, Dept Neurosci, Madison, WI USA.
EM asroopra@wisc.edu
OI Burger, Corinna/0000-0002-9432-0114; O'Riordan, Kenneth
J/0000-0003-0081-6010
FU Neuroscience Training Program [NIH/NIGMS T32GM007507]; Epilepsy
Foundation individual pre-doctoral fellowship; CURE Multidisciplinary
Award; NIH/NINDS [RO1NS065067]
FX Neuroscience Training Program grant NIH/NIGMS T32GM007507. WBP was
supported by an Epilepsy Foundation individual pre-doctoral fellowship.
CURE Multidisciplinary Award to AR, CB, and PR. NIH/NINDS RO1NS065067 to
AR. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 52
TC 9
Z9 10
U1 1
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1545-7885
J9 PLOS BIOL
JI PLoS. Biol.
PD AUG
PY 2013
VL 11
IS 8
AR e1001627
DI 10.1371/journal.pbio.1001627
PG 12
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics
GA 209PR
UT WOS:000323771900008
PM 23966835
ER
PT J
AU Scirica, BM
Kadakia, MB
de Lemos, JA
Roe, MT
Morrow, DA
Li, S
Wiviott, SD
Kontos, MC
AF Scirica, Benjamin M.
Kadakia, Mitul B.
de Lemos, James A.
Roe, Matthew T.
Morrow, David A.
Li, Shuang
Wiviott, Stephen D.
Kontos, Michael C.
CA Natl Cardiovasc Data Registry
TI Association between Natriuretic Peptides and Mortality among Patients
Admitted with Myocardial Infarction: A Report from the ACTION Registry
(R)-GWTG (TM)
SO CLINICAL CHEMISTRY
LA English
DT Article
ID ACUTE CORONARY SYNDROMES; INTERVENTION OUTCOMES NETWORK; PROGNOSTIC
VALUE; ARTERY-DISEASE; RISK SCORE; TROPONIN-T; BIOMARKERS; PERFORMANCE;
REGISTRY; ASSAYS
AB BACKGROUND: Patients with increased blood concentrations of natriuretic peptides (NPs) have poor cardiovascular outcomes after myocardial infarction (MI). The objectives of this analysis were to evaluate the utilization and the prognostic value of NP in a large, real-world MI cohort.
METHODS: Data from 41 683 patients with non-ST-segment elevation MI (NSTEMI) and 27 860 patients with ST-segment elevation MI (STEMI) at 309 US hospitals were collected as part of the ACTION Registry (R)-GWTG (TM) (Acute Coronary Treatment and Intervention Outcomes Network Registry-Get with the Guidelines) (AR-G) between July 2008 and September 2009.
RESULTS: B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) was measured in 19 528 (47%) of NSTEMI and 9220 (33%) of STEMI patients. Patients in whom NPs were measured were older and had more comorbidities, including prior heart failure or MI. There was a stepwise increase in the risk of in-hospital mortality with increasing BNP quartiles for both NSTEMI (1.3% vs 3.2% vs 5.8% vs 11.1%) and STEMI (1.9% vs 3.9% vs 8.2% vs 17.9%). The addition of BNP to the AR-G clinical model improved the C statistic from 0.796 to 0.807 (P < 0.001) for NSTEMI and from 0.848 to 0.855 (P < 0.003) for STEMI. The relationship between NPs and mortality was similar in patients without a history of heart failure or cardiogenic shock on presentation and in patients with preserved left ventricular function.
CONCLUSIONS: NPs are measured in almost 50% of patients in the US admitted with MI and appear to be used in patients with more comorbidities. Higher NP concentrations were strongly and independently associated with in-hospital mortality in the almost 30 000 patients in whom NPs were assessed, including patients without heart failure. (c) 2013 American Association for Clinical Chemistry
C1 [Scirica, Benjamin M.; Morrow, David A.; Wiviott, Stephen D.] Brigham & Womens Hosp, TIMI Study Grp, Cardiovasc Div, Boston, MA 02115 USA.
[Scirica, Benjamin M.; Morrow, David A.; Wiviott, Stephen D.] Harvard Univ, Sch Med, Boston, MA USA.
[Kadakia, Mitul B.] Hosp Univ Penn, Cardiovasc Div, Philadelphia, PA 19104 USA.
[de Lemos, James A.] Univ Texas SW Med Ctr Dallas, Div Cardiol, Dallas, TX 75390 USA.
[Roe, Matthew T.; Li, Shuang] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC USA.
[Roe, Matthew T.; Li, Shuang] Duke Univ, Med Ctr, Div Cardiol, Durham, NC 27710 USA.
[Kontos, Michael C.] Virginia Commonwealth Univ, Pauley Heart Ctr, Div Cardiol, Richmond, VA USA.
RP Scirica, BM (reprint author), Brigham & Womens Hosp, TIMI Study Grp, Cardiovasc Div, 75 Francis St, Boston, MA 02115 USA.
EM bscirica@partners.org
FU Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership; Genentech;
Schering-Plough Corporation; Abbott; AstraZeneca; Amgen; Bayer
Healthcare; Bristol-Myers Squibb; Daichii Sankyo; Eli Lilly; Gilead;
GlaxoSmithKline; Merck (SPRI); Novartis; Pfizer; Roche Diagnostics;
sanofi-aventis; Johnson Johnson; Alere, Inc.; Abbott Diagnostics;
American College of Cardiology; Eisai
FX The NCDR (R) ACTION Registry (R)-GWTG (TM) is administered by the
American College of Cardiology Foundation (ACCF) and sponsored by
Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership, Genentech, and
Schering-Plough Corporation, who provide material support for the
operation of the data collection and infrastructure. B.M. Scirica and
D.A. Morrow, The TIMI Study Group, Brigham and Women's Hospital and
Harvard Medical School, has received research grants from Abbott,
AstraZeneca, Amgen, Bayer Healthcare, Bristol-Myers Squibb, Daichii
Sankyo, Eli Lilly, Gilead, GlaxoSmithKline, Merck (SPRI), Novartis,
Pfizer, Roche Diagnostics, sanofi-aventis, and Johnson & Johnson. J.A.
de Lemos, Alere, Inc., Roche Diagnostics, and Abbott Diagnostics; M.T.
Roe, American College of Cardiology; S.D. Wiviott, Eli Lilly, Daiichi
Sankyo, AstraZeneca, Bristol Myers Squibb, and Eisai; M.C. Kontos,
Research Astellas.
NR 25
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Z9 8
U1 0
U2 0
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
EI 1530-8561
J9 CLIN CHEM
JI Clin. Chem.
PD AUG
PY 2013
VL 59
IS 8
BP 1205
EP 1214
DI 10.1373/clinchem.2012.198556
PG 10
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 231EW
UT WOS:000325398100012
PM 23630179
ER
PT J
AU Amri, R
Bordeianou, LG
Sylla, P
Berger, DL
AF Amri, Ramzi
Bordeianou, Liliana G.
Sylla, Patricia
Berger, David L.
TI Impact of Screening Colonoscopy on Outcomes in Colon Cancer Surgery
SO JAMA SURGERY
LA English
DT Article
ID COLORECTAL-CANCER; ADENOMAS
AB IMPORTANCE Screening colonoscopy seemingly decreases colorectal cancer rates in the United States. In addition to removing benign lesions and preventing progression to malignancy, screening colonoscopy theoretically identifies asymptomatic patients with early-stage disease, potentially leading to higher survival rates.
OBJECTIVES To assess the effect of screening colonoscopy on outcomes of colon cancer surgery by reviewing differences in staging, disease-free interval, risk of recurrence, and survival and to identify whether diagnosis through screening improves long-term outcomes independent of staging.
DESIGN Retrospective review of prospectively maintained, institutional review board-approved database.
SETTING Tertiary care center with high patient volume.
PATIENTS All patients who underwent colon cancer surgery at Massachusetts General Hospital from January 1, 2004, through December 31, 2011.
INTERVENTION Colon cancer surgery.
MAIN OUTCOMES AND MEASURES Postoperative staging, death, and recurrence, measured as incidence and time to event.
RESULTS A total of 1071 patients were included, with 217 diagnosed through screening. Patients not diagnosed through screening were at risk for a more invasive tumor (>= T3: relative risk [RR] = 1.96; P < .001), nodal disease (RR = 1.92; P < .001), and metastatic disease on presentation (RR = 3.37; P < .001). In follow-up, these patients had higher death rates (RR = 3.02; P < .001) and recurrence rates (RR = 2.19; P = .004) as well as shorter survival (P < .001) and disease-free intervals (P < .001). Cox and logistic regression controlling for staging and baseline characteristics revealed that death rate (P = .02) and survival duration (P = .01) were better stage for stage with diagnosis through screening. Death and metastasis rates also remained significantly lower in tumors without nodal or metastatic spread (all P < .001).
CONCLUSIONS AND RELEVANCE Patients with colon cancer identified on screening colonoscopy not only have lower-stage disease on presentation but also have better outcomes independent of their staging. Compliance to screening colonoscopy guidelines can play an important role in prolonging longevity, improving quality of life, and reducing health care costs through early detection of colon cancer.
C1 [Berger, David L.] Massachusetts Gen Hosp, Div Gen & Gastrointestinal Surg, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Berger, DL (reprint author), Massachusetts Gen Hosp, Div Gen & Gastrointestinal Surg, 15 Parkman St, Boston, MA 02114 USA.
EM berger.david@mgh.harvard.edu
OI Amri, Ramzi/0000-0001-7416-6650
FU Harvard Catalyst/The Harvard Clinical and Translational Science Center
from the National Center for Research Resources and National Center for
Advancing Translational Sciences, National Institutes of Health
[8UL1TR000170- 05]; Dutch Cancer Society; Dutch Digestive Society;
Amsterdam University Funds; Fulbright Foundation
FX This work was conducted with support from Harvard Catalyst/The Harvard
Clinical and Translational Science Center (grant 8UL1TR000170- 05 from
the National Center for Research Resources and National Center for
Advancing Translational Sciences, National Institutes of Health and
financial contributions from Harvard University and its affiliated
academic health care centers). This work was also supported by the Dutch
Cancer Society, the Dutch Digestive Society, the Amsterdam University
Funds, and the Fulbright Foundation.
NR 10
TC 21
Z9 21
U1 2
U2 7
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6254
J9 JAMA SURG
JI JAMA Surg.
PD AUG
PY 2013
VL 148
IS 8
BP 747
EP 754
DI 10.1001/jamasurg.2013.8
PG 8
WC Surgery
SC Surgery
GA 206XB
UT WOS:000323558100013
PM 23784448
ER
PT J
AU Chiyomaru, T
Yamamura, S
Fukuhara, S
Yoshino, H
Kinoshita, T
Majid, S
Saini, S
Chang, I
Tanaka, Y
Enokida, H
Seki, N
Nakagawa, M
Dahiya, R
AF Chiyomaru, Takeshi
Yamamura, Soichiro
Fukuhara, Shinichiro
Yoshino, Hirofumi
Kinoshita, Takashi
Majid, Shahana
Saini, Sharanjot
Chang, Inik
Tanaka, Yuichiro
Enokida, Hideki
Seki, Naohiko
Nakagawa, Masayuki
Dahiya, Rajvir
TI Genistein Inhibits Prostate Cancer Cell Growth by Targeting miR-34a and
Oncogenic HOTAIR
SO PLOS ONE
LA English
DT Article
ID LONG NONCODING RNA; HEPATOCELLULAR-CARCINOMA; SIGNALING PATHWAYS;
EXPRESSION; BETA; MICRORNA-27A; PROGRESSION; SOX17; RISK
AB Objective: Genistein is a soy isoflavone that has antitumor activity both in vitro and in vivo. It has been shown that genistein inhibits many type of cancers including prostate cancer (PCa) by regulating several cell signaling pathways and microRNAs (miRNAs). Recent studies suggest that the long non-coding RNAs (lncRNAs) are also involved in many cellular processes. At present there are no reports about the relationship between gensitein, miRNAs and lncRNAs. In this study, we focused on miRNAs, lncRNA that are regulated by genistein and investigated their functional role in PCa.
Method: Microarray (SurePrint G3 Human GE 8x60K) was used for expression profiling of genistein treated and control PCa cells (PC3 and DU145). Functional assay (cell proliferation, migration, invasion, apoptosis and cell cycle assays) were performed with the PCa cell lines, PC3 and DU145. Both in vitro and in vivo (nude mouse) models were used for growth assays. Luciferase reporter assays were used for binding of miR-34a to HOTAIR.
Results: LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells.
Conclusions: Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.
C1 [Chiyomaru, Takeshi; Yamamura, Soichiro; Fukuhara, Shinichiro; Majid, Shahana; Saini, Sharanjot; Chang, Inik; Tanaka, Yuichiro; Dahiya, Rajvir] San Francisco VA Med Ctr, Dept Urol, San Francisco, CA USA.
[Chiyomaru, Takeshi; Yamamura, Soichiro; Fukuhara, Shinichiro; Majid, Shahana; Saini, Sharanjot; Chang, Inik; Tanaka, Yuichiro; Dahiya, Rajvir] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Yoshino, Hirofumi; Enokida, Hideki] Kagoshima Univ, Dept Urol, Grad Sch Med & Dent Sci, Kagoshima 890, Japan.
[Kinoshita, Takashi; Seki, Naohiko; Nakagawa, Masayuki] Chiba Univ, Dept Funct Genom, Grad Sch Med, Chiba, Japan.
RP Dahiya, R (reprint author), San Francisco VA Med Ctr, Dept Urol, San Francisco, CA USA.
EM rdahiya@urology.ucsf.edu
FU National Center for Research Resources of the National Institutes of
Health [R01CA160079, R01CA138642, T32DK007790]; VA Merit Review and VA
Program Project
FX This research was supported by the National Center for Research
Resources of the National Institutes of Health through Grant Number
R01CA160079, R01CA138642, T32DK007790 and VA Merit Review and VA Program
Project. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 44
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Z9 71
U1 1
U2 24
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 1
PY 2013
VL 8
IS 8
AR e70372
DI 10.1371/journal.pone.0070372
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 219PB
UT WOS:000324518400062
PM 23936419
ER
PT J
AU Hunter, RM
Davie, C
Rudd, A
Thompson, A
Walker, H
Thomson, N
Mountford, J
Schwamm, L
Deanfield, J
Thompson, K
Dewan, B
Mistry, M
Quoraishi, S
Morris, S
AF Hunter, Rachael Maree
Davie, Charles
Rudd, Anthony
Thompson, Alan
Walker, Hilary
Thomson, Neil
Mountford, James
Schwamm, Lee
Deanfield, John
Thompson, Kerry
Dewan, Bikash
Mistry, Minesh
Quoraishi, Sadik
Morris, Stephen
TI Impact on Clinical and Cost Outcomes of a Centralized Approach to Acute
Stroke Care in London: A Comparative Effectiveness Before and After
Model
SO PLOS ONE
LA English
DT Article
AB Background: In July 2010 a new multiple hub-and-spoke model for acute stroke care was implemented across the whole of London, UK, with continuous specialist care during the first 72 hours provided at 8 hyper-acute stroke units (HASUs) compared to the previous model of 30 local hospitals receiving acute stroke patients. We investigated differences in clinical outcomes and costs between the new and old models.
Methods: We compared outcomes and costs 'before' (July 2007-July 2008) vs. 'after' (July 2010-June 2011) the introduction of the new model, adjusted for patient characteristics and national time trends in mortality and length of stay. We constructed 90-day and 10-year decision analytic models using data from population based stroke registers, audits and published sources. Mortality and length of stay were modelled using survival analysis.
Findings: In a pooled sample of 307 patients 'before' and 3156 patients 'after', survival improved in the 'after' period (age adjusted hazard ratio 0.54; 95% CI 0.41-0.72). The predicted survival rates at 90 days in the deterministic model adjusted for national trends were 87.2% 'before' % (95% CI 86.7%-87.7%) and 88.7% 'after' (95% CI 88.6%-88.8%); a relative reduction in deaths of 12% (95% CI 8%-16%). Based on a cohort of 6,438 stroke patients, the model produces a total cost saving of 5.2 pound million per year at 90 days (95% CI 4.9- pound 5.5 pound million; 811 pound per patient).
Conclusion: A centralized model for acute stroke care across an entire metropolitan city appears to have reduced mortality for a reduced cost per patient, predominately as a result of reduced hospital length of stay.
C1 [Hunter, Rachael Maree] UCL, Res Dept Primary Care & Populat Hlth, London, England.
[Davie, Charles; Thompson, Kerry; Dewan, Bikash] Royal Free London NHS Fdn Trust, Dept Clin Neurosci, London, England.
[Rudd, Anthony] Kings Coll London, Div Hlth & Social Care Res, London, England.
[Rudd, Anthony] Guys & St Thomas NHS Fdn Trust, Natl Inst Hlth Res, Comprehens Biomed Res Ctr, London, England.
[Thompson, Alan] UCL, Inst Neurol, London, England.
[Walker, Hilary] North Cent London CardioVasc & Stroke Network, London, England.
[Thomson, Neil] London Ambulance Serv NHS Trust, London, England.
[Mountford, James] UCLPartners, London, England.
[Schwamm, Lee] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Deanfield, John] UCL, Ctr Cardiovasc Prevent & Outcomes, London, England.
[Mistry, Minesh; Quoraishi, Sadik] UCL, UCL Med Sch, London, England.
[Morris, Stephen] UCL, Dept Appl Hlth Res, London, England.
RP Hunter, RM (reprint author), UCL, Res Dept Primary Care & Populat Hlth, London, England.
EM r.hunter@ucl.ac.uk
RI Thompson, Alan/C-2654-2008;
OI Thompson, Alan/0000-0002-4333-8496; Schwamm, Lee/0000-0003-0592-9145
FU NHS London; National Institute for Health Research (NIHR)
[RP-PG-0407-10184]; Department of Health's NIHR Biomedical Research
Centres funding scheme
FX The study was funded by NHS London. This study uses data obtained via
independent research commissioned by the National Institute for Health
Research (NIHR) under its Programme Grants for Applied Research funding
scheme (RP-PG-0407-10184). The views expressed are not necessarily those
of the NHS, the NIHR or the Department of Health. This work was
undertaken at UCLH/UCL who received a proportion of funding from the
Department of Health's NIHR Biomedical Research Centres funding scheme.
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 21
TC 21
Z9 21
U1 1
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 1
PY 2013
VL 8
IS 8
AR e70420
DI 10.1371/journal.pone.0070420
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 219PB
UT WOS:000324518400066
PM 23936427
ER
PT J
AU Neufeld, T
Ludwig, B
Barkai, U
Weir, GC
Colton, CK
Evron, Y
Balyura, M
Yavriyants, K
Zimermann, B
Azarov, D
Maimon, S
Shabtay, N
Rozenshtein, T
Lorber, D
Steffen, A
Willenz, U
Bloch, K
Vardi, P
Taube, R
de Vos, P
Lewis, EC
Bornstein, SR
Rotem, A
AF Neufeld, Tova
Ludwig, Barbara
Barkai, Uriel
Weir, Gordon C.
Colton, Clark K.
Evron, Yoav
Balyura, Maria
Yavriyants, Karina
Zimermann, Baruch
Azarov, Dmitri
Maimon, Shiri
Shabtay, Noa
Rozenshtein, Tania
Lorber, Dana
Steffen, Anja
Willenz, Udi
Bloch, Konstantine
Vardi, Pnina
Taube, Ran
de Vos, Paul
Lewis, Eli C.
Bornstein, Stefan R.
Rotem, Avi
TI The Efficacy of an Immunoisolating Membrane System for Islet
Xenotransplantation in Minipigs
SO PLOS ONE
LA English
DT Article
ID PIG ISLETS; EDMONTON PROTOCOL; PANCREATIC-ISLETS; BLOOD-FLOW;
TRANSPLANTATION; PRIMATES; IMMUNOSUPPRESSION; SURVIVAL; MONKEYS; GROWTH
AB Developing a device that protects xenogeneic islets to allow treatment and potentially cure of diabetes in large mammals has been a major challenge in the past decade. Using xenogeneic islets for transplantation is required in light of donor shortage and the large number of diabetic patients that qualify for islet transplantation. Until now, however, host immunoreactivity against the xenogeneic graft has been a major drawback for the use of porcine islets. Our study demonstrates the applicability of a novel immunoprotective membrane that allows successful xenotransplantation of rat islets in diabetic minipigs without immunosuppressive therapy. Rat pancreatic islets were encapsulated in highly purified alginate and integrated into a plastic macrochamber covered by a poly-membrane for subcutaneous transplantation. Diabetic Sinclair pigs were transplanted and followed for up to 90 days. We demonstrated a persistent graft function and restoration of normoglycemia without the need for immunosuppressive therapy. This concept could potentially offer an attractive strategy for a more widespread islet replacement therapy that would restore endogenous insulin secretion in diabetic patients without the need for immunosuppressive drugs and may even open up an avenue for safe utilization of xenogeneic islet donors.
C1 [Neufeld, Tova; Evron, Yoav; Zimermann, Baruch; Azarov, Dmitri; Maimon, Shiri; Lorber, Dana; Rotem, Avi] Beta O2 Technol, Dept Technol, Rosh Haayin, Israel.
[Ludwig, Barbara; Barkai, Uriel; Balyura, Maria; Steffen, Anja; Bornstein, Stefan R.] Univ Hosp Carl Gustav Carus, Dept Med 3, Dresden, Germany.
[Barkai, Uriel; Balyura, Maria; Yavriyants, Karina; Shabtay, Noa; Rozenshtein, Tania] Beta O2 Technol, Islet Dept, Rosh Haayin, Israel.
[Weir, Gordon C.] Joslin Diabet Ctr, Sect Islet Trasnplantat & Cell Biol, Boston, MA 02215 USA.
[Colton, Clark K.] MIT, Dept Chem Engn, Cambridge, MA 02139 USA.
[Willenz, Udi] Lahav Res Inst, Vet Dept, Lahav, Israel.
[Bloch, Konstantine; Vardi, Pnina] Tel Aviv Univ, Fac Med, Diabet & Obes Res Lab, IL-49100 Petah Tiqwa, Israel.
[Taube, Ran] Ben Gurion Univ Negev, Dept Microbiol Immunol & Genet, IL-84105 Beer Sheva, Israel.
[de Vos, Paul] Univ Groningen, Univ Med Ctr Groningen, Dept Pathol & Lab Med, NL-9713 AV Groningen, Netherlands.
[Lewis, Eli C.] Ben Gurion Univ Negev, Dept Clin Biochem & Pharmacol, IL-84105 Beer Sheva, Israel.
RP Weir, GC (reprint author), Joslin Diabet Ctr, Sect Islet Trasnplantat & Cell Biol, Boston, MA 02215 USA.
EM gordon.weir@joslin.harvard.edu
RI de Vos, Paul/A-3170-2013
FU Beta-O2; Deutsche Forschungsgemeinschaft [SFB TRR 127, BR 1179, KFO
252]; Dresden Centre of Excellence; Centre for Regenerative Therapies
Dresden; Paul Langerhans Institute Dresden - The German Center for
Diabetes Research
FX This work was funded by Beta-O2 (http://www.beta-o2.com/), the Deutsche
Forschungsgemeinschaft grants (http://www.dfg.de/en/) SFB TRR 127
"Biology of xenogeneic cell, tissue and organ transplantation" (to BL,
SRB), BR 1179 (to BL), and KFO 252 (to BL, SRB), Dresden Centre of
Excellence (http://ccoe-dresden.de/), Centre for Regenerative Therapies
Dresden (http://www.crt-dresden.de/), Paul Langerhans Institute Dresden
- The German Center for Diabetes Research (http://www.dzd-ev.de/en). The
funders (except for Beta-O2) had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript. Beta-O2 had a role in study design, data collection, and
analysis.
NR 28
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U1 3
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 1
PY 2013
VL 8
IS 8
AR e70150
DI 10.1371/journal.pone.0070150
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 219PB
UT WOS:000324518400039
PM 23936385
ER
PT J
AU Strangman, GE
Li, Z
Zhang, Q
AF Strangman, Gary E.
Li, Zhi
Zhang, Quan
TI Depth Sensitivity and Source-Detector Separations for Near Infrared
Spectroscopy Based on the Colin27 Brain Template
SO PLOS ONE
LA English
DT Article
ID ADULT HEAD MODEL; LIGHT-PROPAGATION; PHOTON MIGRATION; SUPERFICIAL
TISSUE; FREQUENCY-DOMAIN; THICKNESS; SCATTERING; TRANSPORT; SCALP;
INTERFERENCE
AB Understanding the spatial and depth sensitivity of non-invasive near-infrared spectroscopy (NIRS) measurements to brain tissue-i.e., near-infrared neuromonitoring (NIN) - is essential for designing experiments as well as interpreting research findings. However, a thorough characterization of such sensitivity in realistic head models has remained unavailable. In this study, we conducted 3,555 Monte Carlo (MC) simulations to densely cover the scalp of a well-characterized, adult male template brain (Colin27). We sought to evaluate: (i) the spatial sensitivity profile of NIRS to brain tissue as a function of source-detector separation, (ii) the NIRS sensitivity to brain tissue as a function of depth in this realistic and complex head model, and (iii) the effect of NIRS instrument sensitivity on detecting brain activation. We found that increasing the source-detector (SD) separation from 20 to 65 mm provides monotonic increases in sensitivity to brain tissue. For every 10 mm increase in SD separation (up to similar to 45 mm), sensitivity to gray matter increased an additional 4%. Our analyses also demonstrate that sensitivity in depth (S) decreases exponentially, with a "rule-of-thumb" formula S = 0.75*0.85(depth). Thus, while the depth sensitivity of NIRS is not strictly limited, NIN signals in adult humans are strongly biased towards the outermost 10-15 mm of intracranial space. These general results, along with the detailed quantitation of sensitivity estimates around the head, can provide detailed guidance for interpreting the likely sources of NIRS signals, as well as help NIRS investigators design and plan better NIRS experiments, head probes and instruments.
C1 [Strangman, Gary E.; Li, Zhi; Zhang, Quan] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neural Syst Grp, Charlestown, MA USA.
RP Strangman, GE (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neural Syst Grp, Charlestown, MA USA.
EM strang@nmr.mgh.harvard.edu
FU National Space Biomedical Research Institute through NASA [NCC 9-58]
FX This work was supported by the National Space Biomedical Research
Institute through NASA NCC 9-58. The funder had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 63
TC 25
Z9 25
U1 1
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD AUG 1
PY 2013
VL 8
IS 8
AR e66319
DI 10.1371/journal.pone.0066319
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 219PB
UT WOS:000324518400003
PM 23936292
ER
PT J
AU Bressani, AEL
Mariath, AAS
Haas, AN
Garcia-Godoy, F
de Araujo, FB
AF Lemes Bressani, Ana Eliza
Souza Mariath, Adriela Azevedo
Haas, Alex Nogueira
Garcia-Godoy, Franklin
de Araujo, Fernando Borba
TI Incomplete caries removal and indirect pulp capping in primary molars: A
randomized controlled trial
SO AMERICAN JOURNAL OF DENTISTRY
LA English
DT Article
ID DEEP CARIOUS LESIONS; MICROBIOLOGICAL VALIDATION; PRIMARY TEETH;
MICROORGANISMS; DENTIN
AB Purpose: To compare the effect of incomplete caries removal (ICR) and indirect pulp capping (IPC) with calcium hydroxide (CH) or an inert material (wax) on color, consistency and contamination of the remaining dentin of primary molars. Methods: This double-blind, parallel-design, randomized controlled trial included 30 children presenting one primary molar with deep caries lesion. Children were randomly assigned after ICR to receive IPC with CH or wax. All-teeth were then restored with resin composite. Baseline dentin color and consistency were evaluated after ICR, and dentin samples were collected for contamination analyses using scanning electron microscopy. After 3 months, restorations were removed and the three parameters were re-evaluated. In both groups, dentin became significantly darker after 3 months. Results: No cases of yellow dentin were observed after 3 months with CH compared to 33.3% of the wax cases (P< 0.05). A statistically significant difference over time was observed only for CH regarding consistency. CH stimulated a dentin hardening process in a statistically higher number of cases than wax (86.7% vs. 33.3%; P= 0.008). Contamination changed significantly over time in CH and wax without significant difference between groups. It was concluded that CH and wax arrested the carious process of the remaining carious dentin after indirect pulp capping, but CH showed superior dentin color and consistency after 3 months.
C1 [Lemes Bressani, Ana Eliza; Souza Mariath, Adriela Azevedo; de Araujo, Fernando Borba] Univ Fed Rio Grande do Sul, Fac Dent, Dept Pediat Dent, Porto Alegre, RS, Brazil.
[Haas, Alex Nogueira] Univ Fed Rio Grande do Sul, Fac Dent, Dept Periodontol, Porto Alegre, RS, Brazil.
[Garcia-Godoy, Franklin] Univ Tennessee, Ctr Hlth Sci, Coll Dent, Biosci Res Ctr, Memphis, TN 38163 USA.
[Garcia-Godoy, Franklin] Forsyth Inst, Cambridge, MA USA.
RP de Araujo, FB (reprint author), Rua Ramiro Barcelos 2492, BR-90035003 Porto Alegre, RS, Brazil.
EM fernando.araujo@ufrgs.br
OI Araujo, Fernando/0000-0001-6471-5564; Haas, Alex/0000-0003-0531-6234
NR 27
TC 2
Z9 2
U1 2
U2 11
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 2013
VL 26
IS 4
BP 196
EP 200
PG 5
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 221KZ
UT WOS:000324659100005
PM 24693629
ER
PT J
AU Welzel, TM
Graubard, BI
Quraishi, S
Zeuzem, S
Davila, JA
El-Serag, HB
McGlynn, KA
AF Welzel, Tania M.
Graubard, Barry I.
Quraishi, Sabah
Zeuzem, Stefan
Davila, Jessica A.
El-Serag, Hashem B.
McGlynn, Katherine A.
TI Population-Attributable Fractions of Risk Factors for Hepatocellular
Carcinoma in the United States
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID PRIMARY LIVER-CANCER; C VIRUS-INFECTION; NONALCOHOLIC STEATOHEPATITIS;
DIABETES-MELLITUS; HEPATITIS-B; ALCOHOL; DISEASE; COHORT; EPIDEMIOLOGY;
ASSOCIATION
AB OBJECTIVES: Risk factors for hepatocellular carcinoma (HCC) include hepatitis B and C viruses (HBV, HCV), excessive alcohol consumption, rare genetic disorders and diabetes/obesity. The population attributable fractions (PAF) of these factors, however, have not been investigated in population-based studies in the United States.
METHODS: Persons >= 68 years diagnosed with HCC (n = 6,991) between 1994 and 2007 were identified in the SEER-Medicare database. A 5 % random sample (n = 255,702) of persons residing in SEER locations were selected for comparison. For each risk factor, odds ratios (ORs), 95 % confidence intervals (95 % CI) and PAFs were calculated.
RESULTS: As anticipated, the risk of HCC was increased in relationship to each factor: HCV (OR 39.89, 95 % CI: 36.29-43.84), HBV (OR 11.17, 95 % CI: 9.18-13.59), alcohol-related disorders (OR 4.06, 95 % CI: 3.82-4.32), rare metabolic disorders (OR 3.45, 95 % CI: 2.97-4.02), and diabetes and/or obesity (OR 2.47, 95 % CI: 2.34-2.61). The PAF of all factors combined was 64.5 % (males 65.6 %; females 62.2 %). The PAF was highest among Asians (70.1 %) and lowest among black persons (52.4 %). Among individual factors, diabetes/obesity had the greatest PAF (36.6 %), followed by alcohol-related disorders (23.5%), HCV (22.4%), HBV (6.3%) and rare genetic disorders (3.2%). While diabetes/obesity had the greatest PAF among both males (36.4%) and females (36.7%), alcohol-related disorders had the second greatest PAF among males (27.8%) and HCV the second greatest among females (28.1%). Diabetes/obesity had the greatest PAF among whites (38.9%) and Hispanics (38.1%), while HCV had the greatest PAF among Asians (35.4%) and blacks (34.9%). The second greatest PAF was alcohol-related disorders in whites (25.6%), Hispanics (30.1%) and blacks (and 18.5%) and HBV in Asians (28.5%).
CONCLUSIONS: The dominant risk factors for HCC in the United States among persons = 68 years differ by sex and race/ethnicity. Overall, eliminating diabetes/obesity could reduce the incidence of HCC more than the elimination of any other factor.
C1 [Welzel, Tania M.; Zeuzem, Stefan] Johann Wolfgang Goethe Univ Hosp, Frankfurt, Germany.
[Graubard, Barry I.; Quraishi, Sabah; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Rockville, MD 20852 USA.
[Davila, Jessica A.; El-Serag, Hashem B.] Houston Vet Affairs Med Ctr, Houston, TX USA.
[Davila, Jessica A.; El-Serag, Hashem B.] Baylor Coll Med, Houston, TX 77030 USA.
RP McGlynn, KA (reprint author), NCI, DCEG, NIH, EPS 5022,6120 Execut Blvd, Rockville, MD 20852 USA.
EM mcglynnk@mail.nih.gov
FU Intramural Research Program of the National Cancer Institute, National
Institutes of Health
FX This work was funded by the Intramural Research Program of the National
Cancer Institute, National Institutes of Health.
NR 32
TC 74
Z9 74
U1 0
U2 9
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 2013
VL 108
IS 8
BP 1314
EP 1321
DI 10.1038/ajg.2013.160
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 222BM
UT WOS:000324704800013
PM 23752878
ER
PT J
AU Dominitz, JA
Robertson, DJ
AF Dominitz, Jason A.
Robertson, Douglas J.
TI Interval Cancers: Learning from the Past as We Build for the Future
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Editorial Material
ID SERVICES TASK-FORCE; COLORECTAL-CANCER; SCREENING COLONOSCOPY;
ASYMPTOMATIC ADULTS; COST-EFFECTIVENESS; MISS RATE; RISK; PREDICTORS;
RATIONALE; MORTALITY
AB While colonoscopy is the gold standard for the evaluation of the colon, research on post-colonoscopy colorectal cancers has increased our awareness of its limitations. In this issue of the Journal, Erichsen et al. provide evidence to suggest that post-colonoscopy colorectal cancers are most likely due to missed cancers at the time of the index colonoscopy, rather than due to aggressive tumor biology. Ultimately, studies demonstrating the shortcomings of colonoscopy are a call to action for the gastroenterology community to develop strategies and new technologies to improve the effectiveness of colonoscopy.
C1 [Dominitz, Jason A.] Univ Washington, Sch Med, VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Robertson, Douglas J.] Geisel Sch Med Dartmouth, White River Junct VA Med Ctr, White River Junction, VA USA.
RP Dominitz, JA (reprint author), VA Puget Sound Hlth Care Syst, 1660 S Columbian Way 111 Gastro, Seattle, WA 98108 USA.
EM jason.dominitz@va.gov
OI Dominitz, Jason/0000-0002-8070-7086
NR 32
TC 2
Z9 2
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 2013
VL 108
IS 8
BP 1341
EP 1343
DI 10.1038/ajg.2013.177
PG 3
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 222BM
UT WOS:000324704800016
PM 23912407
ER
PT J
AU Tacheva-Grigorova, SK
Santos, AJM
Boucrot, E
Kirchhausen, T
AF Tacheva-Grigorova, Silvia K.
Santos, Antonio J. M.
Boucrot, Emmanuel
Kirchhausen, Tom
TI Clathrin-Mediated Endocytosis Persists during Unperturbed Mitosis
SO CELL REPORTS
LA English
DT Article
ID SURFACE FUNCTIONS; TRANSFERRIN RECEPTOR; COATED PITS; CELLS; INHIBITOR;
INTERNALIZATION; PINOCYTOSIS; INTERPHASE; MICROSCOPY; CYCLE
AB How does mitosis influence the critical process of endocytosis? Some experiments lead to the conclusion that endocytosis arrests completely during mitosis, whereas others indicate that endocytosis persists. We have resolved this apparent discrepancy by showing how conditions of the experiment influence its outcome. The dynamics of clathrincoated pit formation and the uptake of transferrin are maintained in naturally dividing cells but are nearly absent in mitotic cells arrested chemically by treatment with nocodazole, S-Trityl-L-cysteine, or RO-3306. Moreover, sequentially incubating cells at 4 degrees C and then shifting them to 37 degrees C or to serum starvation artificially increases the amount of transferrin receptor at the surface of naturally dividing cells, leading to the incorrect conclusion that endocytosis has ceased during mitosis. Thus, our data show that endocytosis is unaffected during all stages of natural cell division.
C1 [Tacheva-Grigorova, Silvia K.; Kirchhausen, Tom] Boston Childrens Hosp, Program Cellular & Mol Med, Boston, MA 02115 USA.
[Santos, Antonio J. M.] Univ London Imperial Coll Sci Technol & Med, MRC Ctr Mol Bacteriol & Infect, Sect Microbiol, London SW7 2AZ, England.
[Santos, Antonio J. M.] Univ Porto, Grad Program Areas Basic & Appl Biol GABBA, P-4099002 Oporto, Portugal.
[Boucrot, Emmanuel] UCL, Div Biosci, Inst Struct & Mol Biol, London WC1E 6BT, England.
[Kirchhausen, Tom] Harvard Univ, Dept Cell Biol, Sch Med, Boston, MA 02115 USA.
[Kirchhausen, Tom] Harvard Univ, Dept Pediat, Sch Med, Boston, MA 02115 USA.
RP Boucrot, E (reprint author), UCL, Div Biosci, Inst Struct & Mol Biol, Mortimer St, London WC1E 6BT, England.
EM e.boucrot@ucl.ac.uk; kirchhausen@crystal.harvard.edu
OI Santos, Antonio/0000-0001-6514-7423
FU NIH [GM-075252, U54 AI057159]; Fundacao para a Ciencia e Tecnologia;
Biological Sciences Research Council (BBSRC)
FX We thank E. Marino for maintaining the imaging resources in the
Kirchhausen laboratory and R. Massol for making IMAB available. This
work was supported in part by NIH grants GM-075252 (to T. K.) and U54
AI057159 (New England Regional Center of Excellence in Biodefense and
Emerging Infectious Disease, Core Imaging Facility), the Fundacao para a
Ciencia e Tecnologia (to A.J.M.S.), and a Biological Sciences Research
Council (BBSRC) David Phillips Research Fellowship (to E.B.).
NR 22
TC 15
Z9 15
U1 1
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD AUG
PY 2013
VL 4
IS 4
BP 659
EP 668
DI 10.1016/j.celrep.2013.07.017
PG 10
WC Cell Biology
SC Cell Biology
GA 216LU
UT WOS:000324285700006
PM 23954786
ER
PT J
AU Grenon, NN
AF Grenon, Nina N.
TI Managing Toxicities Associated With Antiangiogenic Biologic Agents in
Combination With Chemotherapy for Metastatic Colorectal Cancer
SO CLINICAL JOURNAL OF ONCOLOGY NURSING
LA English
DT Article
ID EVIDENCE-BASED INTERVENTIONS; PHASE-II TRIAL; CLINICAL-PRACTICE
GUIDELINE; COOPERATIVE-ONCOLOGY-GROUP; PUTTING EVIDENCE;
AMERICAN-SOCIETY; INFUSIONAL FLUOROURACIL; 1ST-LINE TREATMENT;
RANDOMIZED-TRIAL; VEGF-TRAP
AB Toxicities commonly associated with antiangiogenic agents include hypertension, proteinuria, wound-healing complications, bleeding or hemorrhage, thromboembolic events, hypersensitivity reactions, and gastrointestinal perforation; however, toxicities most often attributed to chemotherapy include nausea, vomiting, diarrhea, constipation, fatigue, neuropathy, mucositis, hand-foot syndrome, hypersensitivity reactions, and myelosuppression. Patients with metastatic colorectal cancer (mCRC) who receive an antiangiogenic agent in combination with chemotherapy may experience toxicities related to both chemotherapy and the antiangiogenic agent. If possible, evidence-based interventions should be used for the management of toxicities. Patient education about expected toxicities and optimal toxicity management can promote the optimal use of therapy to improve survival and quality of life. Oncology nurses are well positioned to educate patients and their families on anticipated treatment and management of side effects. This article summarizes the incidence of toxicities associated with the antiangiogenic biologic agents aflibercept and bevacizumab, in combination with chemotherapy for patients with mCRC, and provides strategies for managing these toxicities based on clinical practice guidelines.
C1 Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Grenon, NN (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA.
EM nina_grenon@dfci.harvard.edu
NR 56
TC 4
Z9 4
U1 1
U2 6
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 1092-1095
EI 1538-067X
J9 CLIN J ONCOL NURS
JI Clin. J. Oncol. Nurs.
PD AUG
PY 2013
VL 17
IS 4
BP 425
EP 433
DI 10.1188/13.CJON.425-433
PG 9
WC Oncology; Nursing
SC Oncology; Nursing
GA 220EE
UT WOS:000324564000013
PM 23899982
ER
PT J
AU Friedlander, AH
Aghazadehsanai, N
Chang, TI
Harada, N
Garrett, NR
AF Friedlander, A. H.
Aghazadehsanai, N.
Chang, T. I.
Harada, N.
Garrett, N. R.
TI Prevalence of calcified carotid artery atheromas on panoramic images of
individuals with primary hyperparathyroidism
SO DENTOMAXILLOFACIAL RADIOLOGY
LA English
DT Article
DE primary hyperparathyroidism; atherosclerosis; carotid artery; panoramic
images
ID PARATHYROID-HORMONE; CARDIOVASCULAR RISK; RADIOGRAPHY; MORTALITY;
POPULATION; DISEASE
AB Objectives: Primary hyperparathyroidism (PHPT), affecting 1% of the population, is associated with increased cardiovascular morbidity and mortality. The presence of calcified carotid artery plaque (CCAP) on panoramic images is a validated risk indicator of future adverse cardiovascular events. We hypothesized that military veterans aged 50 years or older diagnosed with PHPT by increased parathyroid hormone and calcium levels would frequently have CCAP on their images.
Methods: We determined the prevalence rates of CCAP on the images of patients diagnosed with PHPT and evaluated their atherogenic risk profiles, including hypertension, dyslipidaemia, diabetes and obesity. Comparisons of atherogenic risk factors were made between subjects with and without observed CCAP on their panoramic images.
Results: Of the 60 patients (86.7% males and 13.3% females, mean age 73.2 +/- 11.3 years) with PHPT, 40% had atheromas. There were no significant differences between CCAP+ and CCAP- groups in gender or race (p > 0.05). The atherogenic profile (age, body mass index, hypertension, diabetes, hyperlipidaemia) in the CCAP+ and CCAP- groups was not significantly different (p > 0.05).
Conclusions: Calcified carotid artery atheromas are often seen on the panoramic images of patients with PHPT. Thus, dentists must be uniquely vigilant for these lesions when evaluating these studies.
C1 [Friedlander, A. H.; Aghazadehsanai, N.; Chang, T. I.] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Friedlander, A. H.] Ronald Reagan UCLA Med Ctr, Hosp Dent Serv, Los Angeles, CA USA.
[Friedlander, A. H.; Chang, T. I.] Univ Calif Los Angeles, Sch Dent, Los Angeles, CA 90024 USA.
[Aghazadehsanai, N.; Chang, T. I.] Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Harada, N.] Vet Affairs Greater Los Angeles Healthcare Syst, Grad Med Educ, Member Geriatr Res Educ & Clin Ctr, Los Angeles, CA 90073 USA.
[Harada, N.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Garrett, N. R.] Univ Calif Los Angeles, Sch Dent, Los Angeles, CA 90024 USA.
RP Friedlander, AH (reprint author), Vet Affairs Greater Los Angeles Healthcare Syst, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM arthur.friedlander@va.gov
NR 26
TC 1
Z9 2
U1 0
U2 2
PU BRITISH INST RADIOLOGY
PI LONDON
PA 36 PORTLAND PLACE, LONDON W1N 4AT, ENGLAND
SN 0250-832X
J9 DENTOMAXILLOFAC RAD
JI Dentomaxillofac. Radiol.
PD AUG
PY 2013
VL 42
IS 8
AR 20130118
DI 10.1259/dmfr.20130118
PG 4
WC Dentistry, Oral Surgery & Medicine; Radiology, Nuclear Medicine &
Medical Imaging
SC Dentistry, Oral Surgery & Medicine; Radiology, Nuclear Medicine &
Medical Imaging
GA 223FA
UT WOS:000324788900003
PM 23775925
ER
PT J
AU Salamone, JD
Collins-Praino, LE
Pardo, M
Podurgiel, SJ
Baqi, Y
Muller, CE
Schwarzschild, MA
Correa, M
AF Salamone, John D.
Collins-Praino, Lyndsey E.
Pardo, Marta
Podurgiel, Samantha J.
Baqi, Younis
Mueller, Christa E.
Schwarzschild, Michael A.
Correa, Merce
TI Conditional neural knockout of the adenosine A(2A) receptor and
pharmacological A(2A) antagonism reduce pilocarpine-induced tremulous
jaw movements: Studies with a mouse model of parkinsonian tremor
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE Motor; Parkinson's disease; Parkinsonism; Striatum; Muscarinic receptor;
Acetylcholine
ID C-FOS EXPRESSION; ORAL TREMOR; RATS; DISEASE; MICE; ISTRADEFYLLINE;
TROPICAMIDE; SYMPTOMS; AGONISTS; MOTOR
AB Tremulous jaw movements are rapid vertical deflections of the lower jaw that resemble chewing but are not directed at any particular stimulus. In rats, tremulous jaw movements can be induced by a number of conditions that parallel those seen in human parkinsonism, including dopamine depletion, dopamine antagonism, and cholinomimetic drugs. Moreover, tremulous jaw movements in rats can be attenuated using antiparkinsonian agents such as L-DOPA, dopamine agonists, muscarinic antagonists, and adenosine A(2A) antagonists. In the present studies, a mouse model of tremulous jaw movements was established to investigate the effects of adenosine A(2A) antagonism, and a conditional neuronal knockout of adenosine A(2A) receptors, on cholinomimetic-induced tremulous jaw movements. The muscarinic agonist pilocarpine significantly induced tremulous jaw movements in a dose-dependent manner (0.25-1.0 mg/kg IP). These movements occurred largely in the 3-7.5 Hz local frequency range. Administration of the adenosine A(2A) antagonist MSX-3 (2.5-10.0 mg/kg IP) significantly attenuated pilocarpine-induced tremulous jaw movements. Furthermore, adenosine A(2A) receptor knockout mice showed a significant reduction in pilocarpine-induced tremulous jaw movements compared to littermate controls. These results demonstrate the feasibility of using the tremulous jaw movement model in mice, and indicate that adenosine A(2A) receptor antagonism and deletion are capable of reducing cholinomimetic-induced tremulous jaw movements in mice. Future studies should investigate the effects of additional genetic manipulations using the mouse tremulous jaw movement model. (C) 2013 Elsevier B.V. and ECNP. All rights reserved.
C1 [Salamone, John D.; Collins-Praino, Lyndsey E.; Pardo, Marta; Podurgiel, Samantha J.; Correa, Merce] Univ Connecticut, Dept Psychol, Behav Neurosci Div, Storrs, CT 06269 USA.
[Pardo, Marta; Correa, Merce] Univ Jaume 1, Dept Psychobiol, Castellon de La Plana, Spain.
[Baqi, Younis; Mueller, Christa E.] Univ Bonn, Inst Pharmazeut, Pharma Zentrum Bonn, Bonn, Germany.
[Schwarzschild, Michael A.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
RP Salamone, JD (reprint author), Univ Connecticut, Dept Psychol, Behav Neurosci Div, Storrs, CT 06269 USA.
EM john.salamone@uconn.edu
RI Salamone, John/H-8165-2015; CORREA, MERCE/G-6125-2011; Baqi,
Younis/I-8240-2016; Muller, Christa/C-7748-2014
OI Salamone, John/0000-0001-6435-9635; CORREA, MERCE/0000-0002-9868-3131;
Baqi, Younis/0000-0002-9659-8419; Muller, Christa/0000-0002-0013-6624
FU University of Connecticut Research Foundation; NIH [K24NS60991]; DoD
[W81XWH-11-1-0150]; Fundacio Bancaixa-UJI [P1.1B2010-43]; Caja Navarra;
Fundacio Bancaixa-UJI
FX This work was supported by grants to John Salamone from the University
of Connecticut Research Foundation, which paid for all animals, supplies
and equipment, except for the A2A knockout mice and
littermate controls, which were provided by a grant from Michael
Schwarzschild from NIH (K24NS60991) and DoD (W81XWH-11-1-0150), Merce
Correa was supported by a grant from Fundacio Bancaixa-UJI
(P1.1B2010-43) and Caja Navarra, and Marta Pardo received a travel grant
from Fundacio Bancaixa-UJI.
NR 33
TC 8
Z9 8
U1 0
U2 7
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 2013
VL 23
IS 8
BP 972
EP 977
DI 10.1016/j.euroneuro.2012.08.004
PG 6
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 220QT
UT WOS:000324602700027
PM 22947264
ER
PT J
AU Lagali, N
Eden, U
Utheim, TP
Chen, XJ
Riise, R
Dellby, A
Fagerholm, P
AF Lagali, Neil
Eden, Ulla
Utheim, Tor Paaske
Chen, Xiangjun
Riise, Ruth
Dellby, Anette
Fagerholm, Per
TI In Vivo Morphology of the Limbal Palisades of Vogt Correlates With
Progressive Stem Cell Deficiency in Aniridia-Related Keratopathy
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
DE limbal palisades of Vogt; corneal stem cells; corneal epithelium;
subbasal nerves; aniridia; in vivo confocal microscopy; stem cell
deficiency
ID CONFOCAL MICROSCOPIC EVALUATION; CORNEAL INNERVATION; EXPRESSION;
EPITHELIUM; PHENOTYPE; DENSITY
AB PURPOSE. To investigate morphologic alterations in the limbal palisades of Vogt in a progressive form of limbal stem cell deficiency.
METHODS. Twenty Norwegian subjects (40 eyes) with congenital aniridia and 9 healthy family members (18 eyes) without aniridia were examined. Clinical grade of aniridia-related keratopathy (ARK) was assessed by slit-lamp biomicroscopy, and tear production and quality, corneal thickness, and sensitivity were additionally measured. The superior and inferior limbal palisades of Vogt and central cornea were examined by laser scanning in vivo confocal microscopy (IVCM).
RESULTS. In an aniridia patient with grade 0 ARK, a transparent cornea and normal limbal palisade morphology were found. In grade 1 ARK, 5 of 12 eyes had degraded palisade structures. In the remaining grade 1 eyes and in all 20 eyes with stage 2, 3, and 4 ARK, palisade structures were absent by IVCM. Increasing ARK grade significantly correlated with reduced visual acuity and corneal sensitivity, increased corneal thickness, degree of degradation of superior and inferior palisade structures, reduced peripheral nerves, increased inflammatory cell invasion, and reduced density of basal epithelial cells and central subbasal nerves. Moreover, limbal basal epithelial cell density and central corneal subbasal nerve density were both significantly reduced in aniridia compared to healthy corneas (P = 0.002 and 0.003, respectively).
CONCLUSIONS. Progression of limbal stem cell deficiency in aniridia correlates with degradation of palisade structures, gradual transformation of epithelial phenotype, onset of inflammation, and a corneal nerve deficit. IVCM can be useful in monitoring early-to late-stage degenerative changes in stem cell-deficient patients.
C1 [Lagali, Neil; Eden, Ulla; Dellby, Anette; Fagerholm, Per] Linkoping Univ, Fac Hlth Sci, Dept Clin & Expt Med, SE-58183 Linkoping, Sweden.
[Utheim, Tor Paaske] Oslo Univ Hosp, Dept Med Biochem, Oslo, Norway.
[Utheim, Tor Paaske] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Schepens Eye Res Inst, Boston, MA USA.
[Chen, Xiangjun] Synslaser Kirurgi AS, Oslo, Norway.
[Riise, Ruth] Innland Hosp, Dept Ophthalmol, Elverum, Norway.
RP Lagali, N (reprint author), Linkoping Univ, Fac Hlth Sci, Inst Clin & Expt Med, Dept Ophthalmol, SE-58183 Linkoping, Sweden.
EM neil.lagali@liu.se
OI Chen, Xiangjun/0000-0003-0331-9028; Lagali, Neil/0000-0003-1079-4361
FU Crown Princess Margareta's Foundation for the Visually Impaired; Carmen
and Bertil Regners Foundation for Research in Eye Disease; County
Council of Ostergotland; Konung Gustav V and Drottning Viktorias
Frimurarestiftelse; The Swedish Research Council; Aniridia Norway
FX Supported by Crown Princess Margareta's Foundation for the Visually
Impaired, Carmen and Bertil Regners Foundation for Research in Eye
Disease, the County Council of Ostergotland, Konung Gustav V and
Drottning Viktorias Frimurarestiftelse, The Swedish Research Council,
and Aniridia Norway. The authors alone are responsible for the content
and writing of the paper.
NR 25
TC 22
Z9 23
U1 0
U2 3
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 2013
VL 54
IS 8
BP 5333
EP 5342
DI 10.1167/iovs.13-11780
PG 10
WC Ophthalmology
SC Ophthalmology
GA 228EA
UT WOS:000325167200024
PM 23860752
ER
PT J
AU Keller, KE
Vranka, JA
Haddadin, RI
Kang, MH
Oh, DJ
Rhee, DJ
Yang, YF
Sun, YY
Kelley, MJ
Acott, TS
AF Keller, Kate E.
Vranka, Janice A.
Haddadin, Ramez I.
Kang, Min-Hyung
Oh, Dong-Jin
Rhee, Douglas J.
Yang, Yong-feng
Sun, Ying Ying
Kelley, Mary J.
Acott, Ted S.
TI The Effects of Tenascin C Knockdown on Trabecular Meshwork Outflow
Resistance
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
DE tenascin C; trabecular meshwork; outflow resistance; extracellular
matrix
ID EXTRACELLULAR-MATRIX TURNOVER; LOWER INTRAOCULAR-PRESSURES; OPEN-ANGLE
GLAUCOMA; HEPARIN-II DOMAIN; JUXTACANALICULAR TISSUE; MATRICELLULAR
PROTEINS; ANTERIOR SEGMENTS; AQUEOUS OUTFLOW; ORGAN-CULTURE;
CELL-FUNCTION
AB PURPOSE. Tenascin C (TNC) is a matricellular glycoprotein whose expression in adult tissue is indicative of tissue remodeling. The purpose of the current study was to determine the localization of TNC in trabecular meshwork (TM) tissue and to analyze the effects of TNC on intraocular pressure (IOP).
METHODS. Human TM frontal sections were immunostained with anti-TNC and imaged by confocal microscopy. TNC mRNA and protein levels were quantitated in anterior segments perfused at physiological and elevated pressure. Short, hairpin RNA (shRNA) silencing lentivirus targeting full-length TNC (shTNC) was applied to anterior segment perfusion organ cultures. The IOPs and central corneal thickness (CCT) of wild-type, TNC-/-, and tenascin X (TNX-/-) knockout mice were measured.
RESULTS. TNC was distributed in the juxtacanalicular (JCT) region of adult human TM, predominantly in the basement membrane underlying the inner wall of Schlemm's canal. Application of shTNC lentivirus to human and porcine anterior segments in perfusion culture did not significantly affect outflow rate. Although TNC was upregulated in response to pressure, there was no difference in outflow rate when shTNC-silenced anterior segments were subjected to elevated pressure. Furthermore, IOPs and CCTs were not significantly different between TNC-/- or TNX-/- and wild-type mice.
CONCLUSIONS. TNC does not appear to contribute directly to outflow resistance. However, TNC immunolocalization in the JCT of adult human eyes suggests that certain areas of the TM are being continuously remodeled with or without an IOP increase.
C1 [Keller, Kate E.; Vranka, Janice A.; Yang, Yong-feng; Sun, Ying Ying; Kelley, Mary J.; Acott, Ted S.] Oregon Hlth & Sci Univ, Casey Eye Inst, Portland, OR 97201 USA.
[Haddadin, Ramez I.; Kang, Min-Hyung; Oh, Dong-Jin; Rhee, Douglas J.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Boston, MA USA.
RP Keller, KE (reprint author), Casey Eye Inst, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM gregorka@ohsu.edu
FU NIH [EY019643, EY003279, EY008247, EY010572, EY019654]; Fight for Sight
Summer Research Program; Northwest Health Foundation; Research to
Prevent Blindness, New York, New York
FX Supported by NIH Grants EY019643 (KEK), EY003279, EY008247, EY010572
(TSA), EY019654 (DJR); the Fight for Sight Summer Research Program
(RIH); the Northwest Health Foundation (MJK); and an unrestricted grant
to the Casey Eye Institute from Research to Prevent Blindness, New York,
New York.
NR 58
TC 8
Z9 8
U1 0
U2 2
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 2013
VL 54
IS 8
BP 5613
EP 5623
DI 10.1167/iovs.13-11620
PG 11
WC Ophthalmology
SC Ophthalmology
GA 228EA
UT WOS:000325167200060
PM 23882691
ER
PT J
AU Waldo, SW
Armstrong, EJ
Kulkarni, A
Hoffmayer, KS
Hsue, P
Ganz, P
McCabe, JM
AF Waldo, Stephen W.
Armstrong, Ehrin J.
Kulkarni, Ameya
Hoffmayer, Kurt S.
Hsue, Priscilla
Ganz, Peter
McCabe, James M.
TI Clinical Characteristics and Reperfusion Times Among Patients With an
Isolated Posterior Myocardial Infarction
SO JOURNAL OF INVASIVE CARDIOLOGY
LA English
DT Article
DE acute coronary syndromes; posterior myocardial infarction; reperfusion
time
ID ST-SEGMENT ELEVATION; PERCUTANEOUS CORONARY INTERVENTION;
ACTIVATE-SF-REGISTRY; TO-BALLOON TIME; PROGNOSTIC-SIGNIFICANCE;
DEPRESSION; MANAGEMENT; LEADS; THROMBOLYSIS; PREVALENCE
AB Background. An isolated posterior myocardial infarction (PMI) is associated with significant morbidity and mortality. Because physicians often fail to recognize this diagnosis, there may be delays in the timely revascularization of these patients. The present study sought to identify the clinical characteristics and reperfusion times among patients presenting with isolated PMI. Methods. We identified subjects with isolated PMI within a registry of all catheterization laboratory activations for ST-elevation myocardial infarction (STEMI) from 2008 to 2012. Association between PMI and revascularization within 90 minutes was evaluated by logistic regression. Results. Among 318 patients who underwent revascularization for STEMI, a total of 20 (6%) had electrocardiographic evidence of an isolated PMI. Compared to non-PMI STEMI, subjects with PMI were more often female (45% vs 22%; P=.02) and less likely to have chest pain (40% vs 75%; P<.01). The median door-to-activation (25.5 min vs 12 min; P<.01), activation-to-laboratory (36.5 min vs 29 min; P<.01) and door-to-balloon times (107 min vs 72 min; P<.01) were longer among subjects with PMI, with fewer patients achieving reperfusion within 90 minutes (30% vs 71%; P<.01). After multivariable adjustment, individuals with PMI had 82% lower odds (adjusted odds ratio, 0.18; 95% confidence interval, 0.06-0.50) of achieving coronary reperfusion within 90 minutes. Door-to-activation time accounted for 96% of variation in the total revascularization time (R-2=0.96; P<.0001). Conclusions. Door-to-activation time was prolonged for those with PMI, resulting in longer door-to-balloon times and fewer patients revascularized within the recommended time. An isolated PMI should be considered among individuals presenting with symptoms consistent with myocardial infarction.
C1 [Waldo, Stephen W.; Hoffmayer, Kurt S.; Hsue, Priscilla; Ganz, Peter] Univ Calif San Francisco, Dept Med, Div Cardiol, San Francisco, CA 94134 USA.
[Armstrong, Ehrin J.] Univ Calif San Francisco, Dept Med, Div Cardiovasc Med, San Francisco, CA 94134 USA.
[Kulkarni, Ameya] Massachusetts Gen Hosp, Dept Med, Div Cardiovasc Med, Boston, MA 02114 USA.
[McCabe, James M.] Brigham & Womens Hosp, Dept Med, Div Cardiovasc Med, Boston, MA 02115 USA.
RP Waldo, SW (reprint author), Univ Calif San Francisco, Dept Med, Div Cardiol, 505 Parnassus Ave,Box 0124, San Francisco, CA 94134 USA.
EM stephen.waldo@ucsf.edu
NR 24
TC 4
Z9 4
U1 2
U2 3
PU H M P COMMUNICATIONS
PI MALVERN
PA 83 GENERAL WARREN BLVD, STE 100, MALVERN, PA 19355 USA
SN 1042-3931
J9 J INVASIVE CARDIOL
JI J. Invasive Cardiol.
PD AUG
PY 2013
VL 25
IS 8
BP 371
EP 375
PG 5
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 224HC
UT WOS:000324872700008
PM 23913600
ER
PT J
AU Arokiaraj, M
Guerrero, L
Levine, R
Palacios, I
AF Arokiaraj, Mark
Guerrero, Luis
Levine, Robert
Palacios, Igor
TI A Theoretical Cardiac Resynchronization Therapy Method to Augment
Ventricular Contraction Using Polymer-Based Actuators and Mitral
Regurgitation Reduction With Devices Over Left Ventricular Endocardial
Pacing Wire - An In-Vitro Study
SO JOURNAL OF INVASIVE CARDIOLOGY
LA English
DT Article
DE heart failure; ejection fraction; mitral regurgitation; cardiac
resynchronization therapy; polymer actuators; new device
ID HEART-FAILURE
AB Background. To investigate a potential cardiac resynchronization method using high force density actuators and mitral regurgitation (MR) reduction devices. Methods. An 8-cm long, 0.4-mm thick, and 2-mm wide polymeric actuator strip was attached to the right ventricular (RV) pacemaker lead 4.0 cm from the edge of the leads, and 035 wire and step-up voltages (2-9 V) were given. Deformation of the pacemaker lead with polymer was studied under cine-fluoroscopy in the air and immersing it in 0.9% saline. Cantilever function was assessed by the addition of gold rings. The left ventricular (LV) lead was reinforced with dual polymer and a side branching 035 wire Y-attachment and studied. A novel nitinol-based Gore-Tex device and polymer-based technology was developed and positioned abutting the mitral valves, and was evaluated in sheep heart preparations by cine-fluoroscopy. Results. The mean deformation at 9 V for the LV leads, RV leads, and 035 wires was 3.5 +/- 0.2 mm, 1.1 +/- 0.1 mm, and 1.4 +/- 0.1 mm, respectively, and the stopping weight was 3.8 +/- 0.2 g, 3.2 +/- 0.1 g, and 3.6 +/- 0.3 g, respectively. With dual surfacing of polymer and driven by separate actuation circuits simultaneously, the stopping weight parameters increased to 4.8 +/- 0.2 g, 4.0 +/- 0.2 g, and 4.6 +/- 0.1 g, respectively (>25% each; P<.01 for all). The nitinol-based Gore-Tex device and the polymer device appeared to have reduced MR significantly from grade IV to grade I (>60% by visual quantification). Conclusion. There is potential for a novel theoretical cardiac resynchronization therapy method using polymer-based actuators and devices to control MR.
C1 [Arokiaraj, Mark] Pondicherry Inst Med Sci, Pondicherry 605014, India.
[Guerrero, Luis; Levine, Robert; Palacios, Igor] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP Arokiaraj, M (reprint author), Pondicherry Inst Med Sci, Pondicherry 605014, India.
EM christomark@gmail.com
FU NHLBI NIH HHS [R01 HL072265]
NR 7
TC 0
Z9 0
U1 0
U2 0
PU H M P COMMUNICATIONS
PI MALVERN
PA 83 GENERAL WARREN BLVD, STE 100, MALVERN, PA 19355 USA
SN 1042-3931
J9 J INVASIVE CARDIOL
JI J. Invasive Cardiol.
PD AUG
PY 2013
VL 25
IS 8
BP 415
EP 420
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 224HC
UT WOS:000324872700017
PM 23913609
ER
PT J
AU Lam, DY
O'Hare, AM
Vig, EK
AF Lam, Daniel Y.
O'Hare, Ann M.
Vig, Elizabeth K.
TI Decisions About Dialysis Initiation in the Elderly
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; STAGE RENAL-DISEASE; STARTING DIALYSIS;
UNITED-STATES; END; PREVALENCE; LIFE; HEMODIALYSIS; MANAGEMENT; SURVIVAL
C1 [Lam, Daniel Y.; O'Hare, Ann M.; Vig, Elizabeth K.] Univ Washington, Seattle, WA 98195 USA.
[O'Hare, Ann M.; Vig, Elizabeth K.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
RP Lam, DY (reprint author), Univ Washington, Med Ctr, Div Nephrol, 1959 NE Pacific St,Box 356521, Seattle, WA 98195 USA.
EM dlam34@u.washington.edu
NR 20
TC 1
Z9 1
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0885-3924
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD AUG
PY 2013
VL 46
IS 2
BP 298
EP 302
DI 10.1016/j.jpainsymman.2013.05.014
PG 5
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA 213AU
UT WOS:000324026100019
PM 23938186
ER
PT J
AU Muller, AM
Sadoghi, P
Lucas, R
Audige, L
Delaney, R
Klein, M
Valderrabano, V
Vavken, P
AF Mueller, Andreas M.
Sadoghi, Patrick
Lucas, Robert
Audige, Laurent
Delaney, Ruth
Klein, Maria
Valderrabano, Victor
Vavken, Patrick
TI Effectiveness of bracing in the treatment of nonosseous restriction of
elbow mobility: a systematic review and meta-analysis of 13 studies
SO JOURNAL OF SHOULDER AND ELBOW SURGERY
LA English
DT Article
DE Elbow; stiffness; brace; conservative
ID STATIC PROGRESSIVE STRETCH; DISTAL RADIUS FRACTURE; FLEXION
CONTRACTURES; SPLINTING APPROACH; WRIST STIFFNESS; SECONDARY; MOTION;
TRAUMA; BURNS; KNEE
AB Background: Restriction of elbow mobility is a very frequent complaint after trauma or surgery. The objective of this study was to assess and compare the effectiveness of dynamic, static, or staticprogressive bracing in patients with elbow stiffness of traumatic or postoperative origin and without evidence of ossification. For the purpose of this study, effectiveness was measured as the increase in total range of motion, as well as extension and flexion.
Materials and methods: We performed a systematic search of the keywords "elbow AND (stiffness OR stiff) AND (brace OR splint OR conservative)" in the online databases PubMed, EMBASE, CINAHL (Cumulative Index to Nursing and Allied Health Literature), and the Cochrane Library. We included all clinical studies using dynamic or static bracing in patients with elbow stiffness. Eligible outcomes were changes in total range of motion, flexion, and extension; sustainability of results; and complications.
Results: We included 13 eligible studies, providing data on 14 treated groups in 247 patients. The mean age of these patients was 34.5 +/- 10.4 years, and female patients comprised 46% +/- 12%. The mean duration from the incident to the start of brace treatment was 6.9 +/- 5.1 months. The mean improvement in range of motion during the course of treatment was 38.4 degrees +/- 8.9 degrees (95% confidence interval, 39.5 degrees-41.8 degrees).
Conclusions: The current evidence strongly supports the use of static-progressive stretching 3 times 30 minutes per day in each direction as a first line of treatment in patients with post-traumatic and postsurgical elbow stiffness. If this treatment fails or if reasons for stiffness other than soft-tissue incompliance are identified, further surgical interventions should be considered.
Level of evidence: Level IV, Systematic Review. (C) 2013 Journal of Shoulder and Elbow Surgery Board of Trustees.
C1 [Mueller, Andreas M.; Klein, Maria; Valderrabano, Victor; Vavken, Patrick] Univ Basel, Univ Basel Hosp, Dept Orthopaed, Basel, Switzerland.
[Mueller, Andreas M.] Beth Israel Deaconess Med Ctr, Ctr Adv Orthoped Studies, Boston, MA 02215 USA.
[Sadoghi, Patrick] Med Univ Graz, Dept Orthoped Surg, Graz, Austria.
[Lucas, Robert] Univ Calif San Francisco, Dept Orthoped Surg, San Francisco, CA 94143 USA.
[Audige, Laurent] Schulthess Clin, Dept Upper Extrem Surg, Zurich, Switzerland.
[Delaney, Ruth] Massachusetts Gen Hosp, Harvard Combined Residency Program, Boston, MA 02114 USA.
[Vavken, Patrick] Harvard Univ, Childrens Hosp, Sch Med, Dept Orthoped Surg, Boston, MA 02115 USA.
[Vavken, Patrick] Harvard Univ, Sch Publ Hlth, Ctr Populat & Dev Studies, Boston, MA 02115 USA.
RP Sadoghi, P (reprint author), Auenbruggerpl 5, A-8036 Graz, Austria.
EM patricksadoghi@gmx.at
OI Sadoghi, Patrick/0000-0003-1767-555X
NR 27
TC 4
Z9 4
U1 0
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1058-2746
J9 J SHOULDER ELB SURG
JI J. Shoulder Elbow Surg.
PD AUG
PY 2013
VL 22
IS 8
BP 1146
EP 1152
DI 10.1016/j.jse.2013.04.003
PG 7
WC Orthopedics; Sport Sciences; Surgery
SC Orthopedics; Sport Sciences; Surgery
GA 221EO
UT WOS:000324640700026
PM 23796383
ER
PT J
AU Ring, D
AF Ring, David
TI Regarding "Patients that request reconstruction are different"
SO JOURNAL OF SHOULDER AND ELBOW SURGERY
LA English
DT Letter
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Ring, D (reprint author), Massachusetts Gen Hosp, Yawkey 2100,55 Fruit St, Boston, MA 02114 USA.
EM dring@partners.org
NR 1
TC 0
Z9 0
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1058-2746
J9 J SHOULDER ELB SURG
JI J. Shoulder Elbow Surg.
PD AUG
PY 2013
VL 22
IS 8
BP E22
EP E22
DI 10.1016/j.jse.2013.01.013
PG 1
WC Orthopedics; Sport Sciences; Surgery
SC Orthopedics; Sport Sciences; Surgery
GA 221EO
UT WOS:000324640700008
PM 23422515
ER
PT J
AU Strand, JJ
Kamdar, MM
Carey, EC
AF Strand, Jacob J.
Kamdar, Mihir M.
Carey, Elise C.
TI Top 10 Things Palliative Care Clinicians Wished Everyone Knew About
Palliative Care
SO MAYO CLINIC PROCEEDINGS
LA English
DT Editorial Material
ID OF-LIFE CARE; RANDOMIZED CONTROLLED-TRIAL; CONGESTIVE-HEART-FAILURE;
SERIOUSLY ILL PATIENTS; CELL LUNG-CANCER; END; PAIN; ASSOCIATIONS;
PREVALENCE; SYMPTOMS
AB With a focus on improving quality of life for patients, palliative care is a rapidly growing medical subspecialty focusing on the care of patients with serious illness. Basic symptom management, discussions of prognostic understanding, and eliciting treatment goals are essential pieces in the practice of nearly all physicians. Nonetheless, many complex patients with a serious, life-threatening illness benefit from consultation with palliative care specialists, who are trained and experienced in complex symptom management and challenging communication interactions, including medical decision making and aligning goals of care. This article discusses the changing role of modern palliative care, addresses common misconceptions, and presents an argument for early integration of palliative care in the treatment of patients dealing with serious illness. (C) 2013 Mayo Foundation for Medical Education and Research
C1 [Strand, Jacob J.; Carey, Elise C.] Mayo Clin, Palliat Care Sect, Dept Internal Med, Rochester, MN 55905 USA.
[Kamdar, Mihir M.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Dept Internal Med, Palliat Care Serv, Boston, MA 02114 USA.
RP Strand, JJ (reprint author), Mayo Clin, Palliat Care Sect, Dept Internal Med, 200 1st St SW,Gonda 17, Rochester, MN 55905 USA.
EM strand.jacob@mayo.edu
NR 52
TC 12
Z9 14
U1 2
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0025-6196
J9 MAYO CLIN PROC
JI Mayo Clin. Proc.
PD AUG
PY 2013
VL 88
IS 8
BP 859
EP 865
DI 10.1016/j.mayocp.2013.05.020
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 217CE
UT WOS:000324333400016
PM 23910412
ER
PT J
AU Shampo, MA
Kyle, RA
Steensma, DP
AF Shampo, Marc A.
Kyle, Robert A.
Steensma, David P.
TI Tadeus Reichstein-Work on Hormones of the Adrenal Glands
SO MAYO CLINIC PROCEEDINGS
LA English
DT Editorial Material
C1 [Shampo, Marc A.; Kyle, Robert A.] Mayo Clin, Rochester, MN 55905 USA.
[Steensma, David P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Shampo, MA (reprint author), Mayo Clin, Rochester, MN 55905 USA.
OI Steensma, David/0000-0001-5130-9284
NR 0
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 0025-6196
J9 MAYO CLIN PROC
JI Mayo Clin. Proc.
PD AUG
PY 2013
VL 88
IS 8
BP E85
EP E85
DI 10.1016/j.mayocp.2012.01.031
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 217CE
UT WOS:000324333400002
PM 23910422
ER
PT J
AU Yoo, JW
Nakagawa, S
Kim, S
AF Yoo, Ji Won
Nakagawa, Shunichi
Kim, Sulgi
TI Relationships among advance directives, principal diagnoses, and
discharge outcomes in critically ill older adults
SO PALLIATIVE & SUPPORTIVE CARE
LA English
DT Article
DE Critical care; Health services for the aged; Advance directives;
Diagnosis-related groups
ID LENGTH-OF-STAY; SEVERE SEPSIS; CARE-UNIT; RESOURCE USE; SURVIVORS;
ADMISSION; MEDICARE; MEDICINE; HOSPICE; STATES
AB Objective: The purpose of this study was to determine the relationships among advance directive status, principal diagnoses, and the discharge outcomes in community-dwelling, critically ill older adults.
Method: Using administrative and clinical data (n = 1673), multinomial logit regressions were used to examine the relationships among advance directive status, principal diagnoses, and discharge outcomes (in-hospital deaths, hospice discharges, and transition to institutions).
Results: In the overall sample, the adjusted probability of in-hospital deaths with advance directives (12%) was lower than that without advance directives (17%; odds ratio [OR] 0.56; p = 0.007) and the adjusted probability of hospice discharges with advance directives (11%) was higher than that without advance directives (7%; OR = 1.96; p = 0.03). Subgroup analysis showed that the magnitude of the abovementioned changes was aggregated when their principal diagnoses were a group of diseases with more difficult prognostication (circulatory and respiratory diseases) and more potential for reversibility (infectious diseases). By contrast, the magnitude of the abovementioned findings was diminished with other principal diagnoses. On the other hand, the presence of advance directives did not make a contribution to transition from communities to institutions.
Significance of results: Significantly fewer in-hospital deaths in addition to higher hospice discharges were observed with any advance directives in community-dwelling, critically ill older adults. The magnitude of these findings was aggregated when their principal diagnoses were a group of diseases with more difficult prognostication (circulatory and respiratory diseases) and more potential for reversibility (infectious diseases). By contrast, the magnitude of these findings was diminished with other principal diagnoses.
C1 [Yoo, Ji Won] Univ Michigan, Sch Med, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Nakagawa, Shunichi] Mt Sinai Sch Med, Dept Geriatr & Palliat Med, New York, NY USA.
[Nakagawa, Shunichi] James J Peters Vet Affairs Med Ctr, Educ & Clin Ctr, Bronx, NY USA.
[Kim, Sulgi] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Yoo, Ji Won] Korea Univ, Dept Internal Med, Seoul, South Korea.
RP Yoo, JW (reprint author), Univ Michigan, Sch Med, 300 North Ingalls Bldg,Room 932, Ann Arbor, MI 48109 USA.
EM yoojiw@trinity-health.org
NR 37
TC 1
Z9 1
U1 3
U2 8
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1478-9515
J9 PALLIAT SUPPORT CARE
JI Palliat. Support Care
PD AUG
PY 2013
VL 11
IS 4
BP 315
EP 322
DI 10.1017/S1478951512000259
PG 8
WC Health Policy & Services
SC Health Care Sciences & Services
GA 219XL
UT WOS:000324544900005
PM 22892195
ER
PT J
AU Stiens, SA
Fawber, HL
Yuhas, SA
AF Stiens, Steven A.
Fawber, Heidi L.
Yuhas, Steven A.
TI The Person with a Spinal Cord Injury An Evolving Prototype for Life Care
Planning
SO PHYSICAL MEDICINE AND REHABILITATION CLINICS OF NORTH AMERICA
LA English
DT Article
DE Spinal cord injury; Life care plan; Problem list; Patient-centered care;
Cost of care; Outcome; Prevention
ID QUALITY-OF-LIFE; NEUROGENIC BOWEL; MEDICINE; ADJUSTMENT; EMPLOYMENT;
PEOPLE
AB The sequela of spinal cord injury (SCI) can provide a prototype for life care planning because the segmental design of the vertebrate body allows assessments to be quantitative, repeatable, and predictive of the injured person's impairments, self-care capabilities, and required assistance. Life care planning for patients with SCI uses a standard method that is comparable between planner, yet individualizes assessment and seeks resources that meet unique patient-centered needs in their communities of choice. Clinical care and rehabilitation needs organized with an SCI problem list promotes collaboration by the interdisciplinary team, caregivers, and family in efficient achievement of patient-centered goals and completion of daily care plans.
C1 [Stiens, Steven A.] Univ Washington, Dept Rehabil Med, Seattle, WA 98195 USA.
[Stiens, Steven A.] Univ Washington, Seattle, WA 98195 USA.
[Stiens, Steven A.] Univ Hosp, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Fawber, Heidi L.; Yuhas, Steven A.] Int Assoc Rehabil Profess, Int Acad Life Care Planners Sect, Glenview, IL 60025 USA.
[Yuhas, Steven A.] Direct Grp Inc, Mt Pleasant, SC 29464 USA.
RP Stiens, SA (reprint author), Univ Hosp, VA Puget Sound Hlth Care Syst, POB 356490,Hlth Sci Bldg,1959 North East Pacific, Seattle, WA 98195 USA.
EM Steven.Stiens@va.gov
FU Lou and Virginia Muhlhofer, Cincinnati, OH, USA
FX Lou and Virginia Muhlhofer, Cincinnati, OH, USA.
NR 51
TC 1
Z9 1
U1 1
U2 8
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1047-9651
J9 PHYS MED REH CLIN N
JI Phys. Med. Rehabil. Clin. N. Am.
PD AUG
PY 2013
VL 24
IS 3
BP 419
EP +
DI 10.1016/j.pmr.2013.03.006
PG 27
WC Rehabilitation
SC Rehabilitation
GA 214QG
UT WOS:000324149800004
PM 23910484
ER
PT J
AU Harshman, LC
Taplin, ME
AF Harshman, Lauren C.
Taplin, Mary-Ellen
TI Abiraterone Acetate: Targeting Persistent Androgen Dependence in
Castration-Resistant Prostate Cancer
SO ADVANCES IN THERAPY
LA English
DT Review
DE Abiraterone; Androgen dependence; Castration-resistant prostate cancer;
CYP17 inhibitor; Oncology; Prostate cancer; Survival
ID MITOXANTRONE PLUS PREDNISONE; I CLINICAL-TRIAL; LEUKEMIA GROUP-B;
PHASE-II; INCREASED SURVIVAL; HORMONAL-THERAPY; RANDOMIZED-TRIAL;
END-POINTS; C-MET; RECEPTOR
AB Abiraterone acetate is the first second-line hormonal agent proven to improve survival in metastatic castration-resistant prostate cancer. It selectively inhibits cytochrome P450 17 (CYP17) alpha-hydroxylase and cytochrome(17,20) (C-17,C-20)-lyase, which are enzymes critical for androgen synthesis. Abiraterone acetate was initially approved in the United States in 2011 after demonstrating a 4-month survival benefit in docetaxel-refractory metastatic prostate cancer. The FDA recently expanded its indication for use in the pre-chemotherapy setting after it elicited significant delays in disease progression and a strong trend for increased overall survival in phase III studies. Ongoing investigations of abiraterone are evaluating its efficacy in earlier disease states, exploring its synergy in combination with other therapeutic agents, and assessing the necessity for administration of concurrent steroids and gonadal suppression. The identification and development of predictive biomarkers will optimize the incorporation of abiraterone into the management of advanced prostate cancer.
C1 [Harshman, Lauren C.; Taplin, Mary-Ellen] Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Harshman, LC (reprint author), Dana Farber Canc Inst, 450 Brookline Ave,DANA 1230, Boston, MA 02215 USA.
EM laurenc_harshman@dfci.harvard.edu
FU Fairweather and Uribe Prostate Cancer Research Funds
FX This work was supported in part by the Fairweather and Uribe Prostate
Cancer Research Funds. Drs. Harshman and Taplin contributed equally to
the original design, writing, and revision of this review article. No
editorial or medical writing assistance was utilized. Prior to peer
review, Janssen was offered the opportunity to review this paper for
scientific accuracy. Dr. Harshman is the guarantor for this article, and
takes responsibility for the integrity of the work as a whole.
NR 72
TC 7
Z9 8
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0741-238X
J9 ADV THER
JI Adv. Ther.
PD AUG
PY 2013
VL 30
IS 8
BP 727
EP 747
DI 10.1007/s12325-013-0050-3
PG 21
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 216ZH
UT WOS:000324325400002
PM 23979793
ER
PT J
AU Pannucci, NL
Li, D
Sahay, S
Thomas, EK
Chen, R
Tala, I
Hu, T
Ciccarelli, BT
Megjugorac, NJ
Adams, HC
Rodriguez, PL
Fitzpatrick, ER
Lagunoff, D
Williams, DA
Whitehead, IP
AF Pannucci, N. L.
Li, D.
Sahay, S.
Thomas, E. K.
Chen, R.
Tala, I.
Hu, T.
Ciccarelli, B. T.
Megjugorac, N. J.
Adams, H. C., III
Rodriguez, P. L.
Fitzpatrick, E. R.
Lagunoff, D.
Williams, D. A.
Whitehead, I. P.
TI Loss of the xeroderma pigmentosum group B protein binding site impairs
p210 BCR/ABL1 leukemogenic activity
SO BLOOD CANCER JOURNAL
LA English
DT Article
DE chronic myelogenous leukemia; p210 BCR/ABL1; XPB; NER; DNA repair
ID CHRONIC MYELOGENOUS LEUKEMIA; NUCLEOTIDE EXCISION-REPAIR; BASIC
TRANSCRIPTION FACTOR; C-MYC EXPRESSION; BCR-ABL; DNA-DAMAGE;
MYELOPROLIFERATIVE DISEASE; INDUCED APOPTOSIS; BTF2 TFIIH; RESISTANCE
AB Previous studies have demonstrated that p210 BCR/ABL1 interacts directly with the xeroderma pigmentosum group B (XPB) protein, and that XPB is phosphorylated on tyrosine in cells that express p210 BCR/ABL1. In the current study, we have constructed a p210 BCR/ABL1 mutant that can no longer bind to XPB. The mutant has normal kinase activity and interacts with GRB2, but can no longer phosphorylate XPB. Loss of XPB binding is associated with reduced expression of c-MYC and reduced transforming potential in ex-vivo clonogenicity assays, but does not affect nucleotide excision repair in lymphoid or myeloid cells. When examined in a bone marrow transplantation (BMT) model for chronic myelogenous leukemia, mice that express the mutant exhibit attenuated myeloproliferation and lymphoproliferation when compared with mice that express unmodified p210 BCR/ABL1. Thus, the mutant-transplanted mice show predominantly neutrophilic expansion and altered progenitor expansion, and have significantly extended lifespans. This was confirmed in a BMT model for B-cell acute lymphoblastic leukemia, wherein the majority of the mutant-transplanted mice remain disease free. These results suggest that the interaction between p210 BCR/ABL1 and XPB can contribute to disease progression by influencing the lineage commitment of lymphoid and myeloid progenitors.
C1 [Pannucci, N. L.; Li, D.; Sahay, S.; Chen, R.; Tala, I.; Hu, T.; Ciccarelli, B. T.; Megjugorac, N. J.; Adams, H. C., III; Rodriguez, P. L.; Fitzpatrick, E. R.; Lagunoff, D.; Whitehead, I. P.] Univ Med & Dent New Jersey, New Jersey Med Sch, Univ Hosp Canc Ctr, Newark, NJ 07101 USA.
[Thomas, E. K.] Cincinnati Childrens Hosp Med Ctr, Cincinnati Childrens Res Fdn, Div Expt Hematol, Cincinnati, OH 45229 USA.
[Williams, D. A.] Harvard Univ, Sch Med, Hematol Oncol Div, Childrens Hosp Boston, Boston, MA USA.
[Williams, D. A.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Whitehead, IP (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Univ Hosp Canc Ctr, Canc Ctr Level H, 205 South Orange Ave, Newark, NJ 07101 USA.
EM whiteip@umdnj.edu
RI Hu, Tinghui/F-3213-2015
FU Public Health Service [CA097066, DK62757]; New Jersey Commission for
Cancer Research
FX This work was supported by the Public Health Service grants CA097066
(IPW) and DK62757 (DAW). NLP, PLR and ERF is a recipient of a fellowship
from the New Jersey Commission for Cancer Research. NLP are recipients
of fellowships from NJCCR.
NR 42
TC 2
Z9 2
U1 2
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2044-5385
J9 BLOOD CANCER J
JI Blood Cancer J.
PD AUG
PY 2013
VL 3
AR UNSP e135
DI 10.1038/bcj.2013.36
PG 10
WC Oncology
SC Oncology
GA 214XK
UT WOS:000324171500007
PM 23955590
ER
PT J
AU Chen, BB
Glasser, JR
Coon, TA
Mallampalli, RK
AF Chen, B. B.
Glasser, J. R.
Coon, T. A.
Mallampalli, R. K.
TI Skp-cullin-F box E3 ligase component FBXL2 ubiquitinates Aurora B to
inhibit tumorigenesis
SO CELL DEATH & DISEASE
LA English
DT Article
DE ubiquitin; tumor; proteolysis; drug; small molecule
ID CTP-PHOSPHOCHOLINE CYTIDYLYLTRANSFERASE; SPINDLE ASSEMBLY CHECKPOINT;
HISTONE H3 PHOSPHORYLATION; KINASE INHIBITOR; KINETOCHORE ORIENTATION;
CHROMOSOME CONDENSATION; MITOTIC PROGRESSION; REGULATORY ENZYME;
HUMAN-CELLS; PROTEIN
AB Aurora B kinase is an integral regulator of cytokinesis, as it stabilizes the intercellular canal within the midbody to ensure proper chromosomal segregation during cell division. Here we identified that the ubiquitin E3 ligase complex SCFFBXL2 mediates Aurora B ubiquitination and degradation within the midbody, which is sufficient to induce mitotic arrest and apoptosis. Three molecular acceptor sites (K-102, K-103 and K-207) within Aurora B protein were identified as important sites for its ubiquitination. A triple Lys mutant of Aurora B (K-102/103/207R) exhibited optimal resistance to SCFFBXL2-directed polyubiquitination, and overexpression of this variant resulted in a significant delay in anaphase onset, resulting in apoptosis. A unique small molecule F-box/LRR-repeat protein 2 (FBXL2) activator, BC-1258, stabilized and increased levels of FBXL2 protein that promoted Aurora B degradation, resulting in tetraploidy, mitotic arrest and apoptosis of tumorigenic cells, and profoundly inhibiting tumor formation in athymic nude mice. These findings uncover a new proteolytic mechanism targeting a key regulator of cell replication that may serve as a basis for chemotherapeutic intervention in neoplasia.
C1 [Chen, B. B.; Glasser, J. R.; Coon, T. A.; Mallampalli, R. K.] Univ Pittsburgh, Dept Med Pulm Allergy & Crit Care Med, UPMC Montefiore, Pittsburgh, PA 15213 USA.
[Chen, B. B.] Univ Pittsburgh, Dept Acute Lung Injury Ctr Excellence, Pittsburgh, PA 15213 USA.
[Mallampalli, R. K.] Univ Pittsburgh, Dept Cell Biol & Physiol, Pittsburgh, PA 15213 USA.
[Mallampalli, R. K.] Vet Affairs Pittsburgh Healthcare Syst, Med Specialty Serv Line, Pittsburgh, PA USA.
RP Chen, BB (reprint author), Univ Pittsburgh, Dept Med Pulm Allergy & Crit Care Med, UPMC Montefiore, 3459 5th Ave,NW 628, Pittsburgh, PA 15213 USA.
EM chenb@upmc.edu
FU US Department of Veterans Affairs, Veterans Health Administration,
Office of Research and Development; Biomedical Laboratory Research and
Development; US Department of Veterans Affairs; National Institutes of
Health [HL116472, HL096376, HL097376, HL098174]
FX We thank DW Gerlich for providing pH2B-mCherry-IRES-puro2 and
pMyrPalm-mEGFP plasmids. This material is based upon work supported, in
part, by the US Department of Veterans Affairs, Veterans Health
Administration, Office of Research and Development, and Biomedical
Laboratory Research and Development. This work was supported by a Merit
Review Award from the US Department of Veterans Affairs and National
Institutes of Health R01 grants HL116472 (to BBC), HL096376, HL097376
and HL098174 (to RKM).
NR 49
TC 14
Z9 14
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD AUG
PY 2013
VL 4
AR e759
DI 10.1038/cddis.2013.271
PG 10
WC Cell Biology
SC Cell Biology
GA 214PK
UT WOS:000324146000016
PM 23928698
ER
PT J
AU Clark, KB
Eisenstein, EM
AF Clark, Kevin B.
Eisenstein, E. M.
TI Targeting Host Store-Operated Ca2+ Release to Attenuate Viral Infections
SO CURRENT TOPICS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE diarrhea; intracellular Ca2+ signaling; IP3 pathway and receptors;
protein-protein allostery; T cells; viral replication; virus-associated
dementia; virus-induced cytotoxicity
ID INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; EPSTEIN-BARR-VIRUS;
ENDOPLASMIC-RETICULUM MEMBRANE; CEREBELLAR PURKINJE-CELLS;
POLYAMINE-SENSITIVE-SITE; LONG-TERM POTENTIATION; NA+/H+ EXCHANGER NHE3;
D-ASPARTATE RECEPTOR; LIGAND-BINDING SITE; TRISPHOSPHATE RECEPTOR
AB Viruses coopt host intracellular Ca2+ signaling pathways to optimize timing and effectiveness of infection stages against barriers to invasion, pathogenesis, replication, and release. Virus-induced changes in free cytosolic Ca2+ levels facilitate virus adsorption, uncoating, catalysis, toxin production, structural assembly and stabilization, trafficking, and fusion and budding. Ca2+-associated alterations in virus status also selectively precipitate host cytopathologies through, among other events, retardation or induction of apoptosis, elevation of metabolic stress and reactive oxygen species production, and promotion of proinflammatory cytokine and chemokine synthesis and release. Viral particles and proteins tune spatiotemporal dynamics of host free cytosolic Ca2+ concentrations by modulating Ca2+ entry from the extracellular environment, upstream first or second messengers, ion-and ATP-dependent Ca2+ pumps that sequester or extrude free cytosolic Ca2+, store-operated Ca2+ mobilization and leakage, and viral capsid/envelope and downstream host Ca2+ binding proteins and sensors. Each of these major viral mechanisms, briefly reviewed in this article, presents a suitable drug target capable of mitigating the severity and incidence of viral infections. Given its pivotal role in cellular response regulation, bioenergetics, posttranslational protein and lipid modification and transport, homeostasis, cell motility and morphogenesis, and T lymphocyte proliferation, targeting virally stimulated inositol 1,4,5-trisphoshate (IP3)-mediated store-operated Ca2+ release especially offers unique, predictable benefits for augmenting immunoprotection in vertebrate clinical populations. We appraise possibilities of modulating this system with experimental proteins that gate activation kinetics of endoplasmic-reticulum-localized Ca2+-conducting IP3 receptors via allosteric protein-protein interactions. Such compounds are expected to be valuable in treating primary disease symptoms and sequelae, including virus-associated dementia.
C1 [Eisenstein, E. M.] Vet Affairs Greater Los Angeles Hlth Care Syst, Res & Dev Serv, Los Angeles, CA 90073 USA.
RP Clark, KB (reprint author), 4229 SE Harney St, Portland, OR 97206 USA.
EM kbclarkphd@yahoo.com
NR 220
TC 3
Z9 3
U1 4
U2 8
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1568-0266
J9 CURR TOP MED CHEM
JI Curr. Top. Med. Chem.
PD AUG
PY 2013
VL 13
IS 16
BP 1916
EP 1932
PG 17
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 214WH
UT WOS:000324167500003
PM 23895094
ER
PT J
AU Klassert, TB
Hanisch, A
Brauer, J
Mansour, MK
Vyas, JM
Tam, JM
Slevogt, H
AF Klassert, T. B.
Hanisch, A.
Braeuer, J.
Mansour, M. K.
Vyas, J. M.
Tam, J. M.
Slevogt, H.
TI Modulatory role of nuclear receptors on the C. albicans-induced immune
response in human monocytes
SO INFECTION
LA English
DT Meeting Abstract
C1 [Klassert, T. B.; Hanisch, A.; Braeuer, J.; Slevogt, H.] Jena Univ Hosp, Sept Res Ctr, Jena, Germany.
[Klassert, T. B.; Hanisch, A.; Braeuer, J.; Slevogt, H.] Univ Jena, Jena, Germany.
[Hanisch, A.] Jena Univ Hosp, Ctr Sepsis Control & Care, Jena, Germany.
[Mansour, M. K.; Vyas, J. M.; Tam, J. M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Div Infect Dis, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0300-8126
J9 INFECTION
JI Infection
PD AUG
PY 2013
VL 41
SU 1
MA 132
BP S29
EP S29
PG 1
WC Infectious Diseases
SC Infectious Diseases
GA 216KG
UT WOS:000324281600057
ER
PT J
AU Assoumou, SA
Panther, LA
Feng, Y
Gelman, RS
Fugelso, DK
Mayer, KH
AF Assoumou, S. A.
Panther, L. A.
Feng, Y.
Gelman, R. S.
Fugelso, D. K.
Mayer, K. H.
TI Treatment of high-grade anal dysplasia in high-risk patients: outcome at
an urban community health centre (vol 24, pg 134, 2013)
SO INTERNATIONAL JOURNAL OF STD & AIDS
LA English
DT Correction
C1 [Assoumou, S. A.] Boston Med Ctr, Dept Med, Infect Dis Sect, Boston, MA USA.
[Panther, L. A.; Mayer, K. H.] Fenway Inst, Boston, MA USA.
[Panther, L. A.; Mayer, K. H.] Beth Israel Deaconess Med Ctr, Dept Med, Div Infect Dis, Boston, MA 02215 USA.
[Feng, Y.; Gelman, R. S.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Gelman, R. S.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Fugelso, D. K.] Beth Israel Deaconess Med Ctr, Dept Surg, Boston, MA 02215 USA.
RP Assoumou, SA (reprint author), Boston Med Ctr, Dept Med, Infect Dis Sect, Boston, MA USA.
NR 1
TC 0
Z9 0
U1 0
U2 2
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0956-4624
J9 INT J STD AIDS
JI Int. J. STD AIDS
PD AUG
PY 2013
VL 24
IS 8
BP 683
EP 683
DI 10.1177/0956462413501415
PG 1
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 214EP
UT WOS:000324114200015
ER
PT J
AU Fattori, R
Montgomery, D
Lovato, L
Kische, S
Di Eusanio, M
Ince, H
Eagle, KA
Isselbacher, EM
Nienaber, CA
AF Fattori, Rossella
Montgomery, Daniel
Lovato, Luigi
Kische, Stephan
Di Eusanio, Marco
Ince, Hueseyin
Eagle, Kim A.
Isselbacher, Eric M.
Nienaber, Christoph A.
TI Survival After Endovascular Therapy in Patients With Type B Aortic
Dissection A Report From the International Registry of Acute Aortic
Dissection (IRAD)
SO JACC-CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE aorta; stent graft; survival
ID STENT-GRAFT PLACEMENT; LONG-TERM SURVIVAL; EXPERIENCE; REPAIR; INSIGHTS;
DETERMINANTS; ANEURYSMS; LESSONS; STILL
AB Objectives This study sought to evaluate long-term survival in type B aortic dissection patients treated with thoracic endovascular aortic repair (TEVAR) therapy.
Background Historical data have supported medical therapy in type B acute aortic dissection (TBAAD) patients. Recent advances in TEVAR appear to improve in-hospital mortality.
Methods We examined 1,129 consecutive patients with TBAAD enrolled in IRAD (International Registry of Acute Aortic Dissection) between 1995 and 2012 who received medical (n = 853, 75.6%) or TEVAR (n = 276, 24.4%) therapy.
Results Clinical history was similar between groups. TEVAR patients were more likely to present with a pulse deficit (28.3% vs. 13.4%, p < 0.001) and lower extremity ischemia (16.8% vs. 3.6%, p < 0.001), and to characterize their pain as the "worst pain ever" (27.5% vs. 15.7%, p < 0.001). TEVAR patients were also most likely to present with complicated acute aortic dissection, defined as shock, periaortic hematoma, signs of malperfusion, stroke, spinal cord ischemia, mesenteric ischemia, and/or renal failure (61.7% vs. 37.2%). In-hospital mortality was similar in patients managed with endovascular repair (10.9 % vs. 8.7%, p = 0.273) compared with medically managed patients. One-year mortality was also similar in both groups (8.1% endovascular vs. 9.8% medical, p = 0.604). Among adverse events during follow-up, aortic growth/new aneurysm was most common, occurring in 73.3% of patients with medical therapy and in 62.7% of patients after TEVAR, based on 5-year Kaplan-Meier estimates. Kaplan-Meier survival estimates showed that patients undergoing TEVAR had a lower death rate (15.5% vs. 29.0%, p = 0.018) at 5 years.
Conclusions Results from IRAD show that TEVAR is associated with lower mortality over a 5-year period than medical therapy for TBAAD. Further randomized trials with long-term follow-up are needed. (C) 2013 by the American College of Cardiology Foundation
C1 [Fattori, Rossella] San Salvatore Hosp, Intervent Cardiol Unit, I-61121 Pesaro, Italy.
[Montgomery, Daniel; Eagle, Kim A.] Univ Michigan, Ctr Cardiovasc, Ann Arbor, MI 48109 USA.
[Lovato, Luigi; Di Eusanio, Marco] Univ Hosp S Orsola, Cardiothoracovasc Dept, Bologna, Italy.
[Kische, Stephan; Ince, Hueseyin; Nienaber, Christoph A.] Univ Rostock, Ctr Heart, D-18055 Rostock, Germany.
[Isselbacher, Eric M.] Massachusetts Gen Hosp, Thorac Aort Ctr, Boston, MA 02114 USA.
RP Fattori, R (reprint author), San Salvatore Hosp, Int Cardiol Unit, Piazzale Cinelli 4, I-61121 Pesaro, Italy.
EM rossella.fattori@unibo.it
FU W.L. Gore & Associates, Inc.; Varbedian Aortic Research Fund; Hewlett
Foundation; Mardigian Foundation; UM Faculty Group Practice; Terumo;
Gore
FX IRAD was funded by W.L. Gore & Associates, Inc., Varbedian Aortic
Research Fund, Hewlett Foundation, Mardigian Foundation, UM Faculty
Group Practice, and Terumo. Dr. Eagle has received research funding from
Gore; and is a consultant for the National Heart, Lung, and Blood
Institute, National Institutes of Health. All other authors have
reported that they have no relationships relevant to the contents of
this paper to disclose.
NR 29
TC 67
Z9 71
U1 1
U2 6
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 2013
VL 6
IS 8
BP 876
EP 882
DI 10.1016/j.jcin.2013.05.003
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 216TW
UT WOS:000324308400014
PM 23968705
ER
PT J
AU Hoge, EA
Bui, E
Marques, L
Metcalf, CA
Morris, LK
Robinaugh, DJ
Worthington, JJ
Pollack, MH
Simon, NM
AF Hoge, Elizabeth A.
Bui, Eric
Marques, Luana
Metcalf, Christina A.
Morris, Laura K.
Robinaugh, Donald J.
Worthington, John J.
Pollack, Mark H.
Simon, Naomi M.
TI Randomized Controlled Trial of Mindfulness Meditation for Generalized
Anxiety Disorder: Effects on Anxiety and Stress Reactivity
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID COGNITIVE-BEHAVIORAL THERAPY; OLDER-ADULTS; PSYCHOMETRIC PROPERTIES;
CLINICAL-TRIALS; ATTENUATION; RELAXATION; INSTRUMENT; PREDICTORS;
SYMPTOMS; VALIDITY
AB Objective: Mindfulness meditation has met increasing interest as a therapeutic strategy for anxiety disorders, but prior studies have been limited by methodological concerns, including a lack of an active comparison group. This is the first randomized, controlled trial comparing the manualized Mindfulness-Based Stress Reduction (MBSR) program with an active control for generalized anxiety disorder (GAD), a disorder characterized by chronic worry and physiologic hyperarousal symptoms.
Method: Ninety-three individuals with DSM-IV-diagnosed GAD were randomly assigned to an 8-week group intervention with MBSR or to an attention control, Stress Management Education (SME), between 2009 and 2011. Anxiety symptoms were measured with the Hamilton Anxiety Rating Scale (HAMA; primary outcome measure), the Clinical Global Impressions-Severity of Illness and -Improvement scales (CGI-S and CGI-I), and the Beck Anxiety Inventory (BAI). Stress reactivity was assessed by comparing anxiety and distress during pretreatment and posttreatment administration of the Trier Social Stress Test (TSST).
Results: A modified intent-to-treat analysis including participants who completed at least 1 session of MBSR (n=48) or SME (n=41) showed that both interventions led to significant (P < .0001) reductions in HAMA scores at endpoint, but did not significantly differ. MBSR, however, was associated with a significantly greater reduction in anxiety as measured by the CGI-S, the CGI-I, and the BAI (all P values < .05). MBSR was also associated with greater reductions than SME in anxiety and distress ratings in response to the TSST stress challenge (P < .05) and a greater increase in positive self-statements (P=.004).
Conclusions: These results suggest that MBSR may have a beneficial effect on anxiety symptoms in GAD and may also improve stress reactivity and coping as measured in a laboratory stress challenge.
Trial Registration: ClinicalTrials.gov identifier: NCT01033851 (C) Copyright 2013 Physicians Postgraduate Press, Inc.
C1 [Hoge, Elizabeth A.; Bui, Eric; Marques, Luana; Metcalf, Christina A.; Morris, Laura K.; Robinaugh, Donald J.; Worthington, John J.; Simon, Naomi M.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Pollack, Mark H.] Rush Univ, Dept Psychiat, Med Ctr, Chicago, IL 60612 USA.
RP Hoge, EA (reprint author), Massachusetts Gen Hosp, Ctr Anxiety & Traumat Stress Disorders, 1 Bowdoin Sq,6th Floor, Boston, MA 02114 USA.
EM ehoge@partners.org
RI Hoge, Elizabeth/H-5879-2012; Bui, Eric/J-8347-2015
OI Hoge, Elizabeth/0000-0002-5513-2292; Bui, Eric/0000-0002-1413-6473
FU National Center on Complementary and Alternative Medicine, National
Institutes of Health [K23AT4432]; Highland Street Foundation
FX This study was primarily supported by grant K23AT4432 from the National
Center on Complementary and Alternative Medicine, National Institutes of
Health (Dr Hoge, principal investigator). The Highland Street Foundation
provided additional support, including to Drs Bui, Marques, Pollack, and
Simon and Ms Metcalf.
NR 45
TC 38
Z9 38
U1 9
U2 130
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 752870, MEMPHIS, TN 38175-2870 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD AUG
PY 2013
VL 74
IS 8
BP 786
EP 792
DI 10.4088/JCP.12m08083
PG 7
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 212NI
UT WOS:000323989700001
PM 23541163
ER
PT J
AU Rosenberg, PB
Lanctot, KL
Drye, LT
Herrmann, N
Scherer, RW
Bachman, DL
Mintzer, JE
AF Rosenberg, Paul B.
Lanctot, Krista L.
Drye, Lea T.
Herrmann, Nathan
Scherer, Roberta W.
Bachman, David L.
Mintzer, Jacobo E.
CA ADMET Investigators
TI Safety and Efficacy of Methylphenidate for Apathy in Alzheimer's
Disease: A Randomized, Placebo-Controlled Trial
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID DEXTROAMPHETAMINE CHALLENGE; NEUROPSYCHIATRIC SYMPTOMS; DEMENTIA;
DEPRESSION; RELIABILITY; SERTRALINE; DOPAMINE; VALIDITY; DESIGN; CARE
AB Objective: In a recent crossover trial, methylphenidate treatment decreased apathy in Alzheimer's disease. We further assessed this finding in the Apathy in Dementia Methylphenidate Trial (ADMET).
Method: Six-week, randomized, double-blind, placebo-controlled multicenter trial enrolling Alzheimer's disease participants (NINCDS-ADRDA criteria) with apathy assigned to methylphenidate 20 mg daily or placebo, conducted from June 2010 to December 2011. Primary outcomes were change in Apathy Evaluation Scale (AES) score and modified Alzheimer's Disease Cooperative Study-Clinical Global Impression of Change (ADCS-CGI-C). Secondary outcomes included change in Neuropsychiatric Inventory (NPI) apathy score, Mini-Mental State Examination (MMSE) score, and safety.
Results: 60 participants were randomly assigned (29 methylphenidate, 31 placebo). At baseline, mean (SD) age = 76 (8) years, MMSE score = 20 (5), AES score = 51 (12), NPI total score = 16 (8), and 62% of the participants (n=37) were female. After 6 weeks' treatment, mean (SD) change in AES score was -1.9 (1.5) for methylphenidate and 0.6 (1.4) for placebo (P = .23). Odds ratio for improvement in ADCS-CGI-C was 3.7 (95% CI, 1.3 to 10.8) (P = .02), with 21% of methylphenidate versus 3% of placebo rated as moderately or markedly improved. NPI apathy score improvement was 1.8 points (95% CI, 0.3 to 3.4) greater on methylphenidate than on placebo (P = .02). MMSE trended toward improvement on methylphenidate (P = .06). There were trends toward greater anxiety and weight loss >2% in the methylphenidate-treated group.
Conclusions: Methylphenidate treatment of apathy in Alzheimer's disease was associated with significant improvement in 2 of 3 efficacy outcomes and a trend toward improved global cognition with minimal adverse events, supporting the safety and efficacy of methylphenidate treatment for apathy in Alzheimer's disease.
Trial Registration: ClinicalTrials.gov identifier: NCT01117181 (C) Copyright 2013 Physicians Postgraduate Press, Inc.
C1 [Rosenberg, Paul B.] Johns Hopkins Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD USA.
[Drye, Lea T.; Scherer, Roberta W.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Lanctot, Krista L.; Herrmann, Nathan] Univ Toronto, Sunnybrook Res Inst, Dept Psychiat, Toronto, ON M5S 1A1, Canada.
[Lanctot, Krista L.; Herrmann, Nathan] Univ Toronto, Sunnybrook Res Inst, Brain Sci Res Program, Toronto, ON M5S 1A1, Canada.
[Lanctot, Krista L.; Herrmann, Nathan] Univ Toronto, Dept Psychiat, Toronto, ON M5S 1A1, Canada.
[Lanctot, Krista L.; Herrmann, Nathan] Univ Toronto, Dept Pharmacol Toxicol, Toronto, ON M5S 1A1, Canada.
[Bachman, David L.; Mintzer, Jacobo E.] Med Univ S Carolina, Dept Neurosci, Alzheimers Res Program, Charleston, SC 29425 USA.
[Bachman, David L.; Mintzer, Jacobo E.] Med Univ S Carolina, Dept Neurosci, Alzheimers Clin Program, Charleston, SC 29425 USA.
[Bachman, David L.; Mintzer, Jacobo E.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
RP Mintzer, JE (reprint author), Alzheimers Res Program, 5900 Core Rd,Ste 203, Charleston, SC 29406 USA.
EM mintzerj@musc.edu
OI Drye, Lea/0000-0002-2964-1878
FU National Institute on Aging [R01 AG033032-01, 1 K08 AG029157-01A1]
FX National Institute on Aging (R01 AG033032-01 and 1 K08 AG029157-01A1).
NR 27
TC 31
Z9 35
U1 1
U2 6
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 752870, MEMPHIS, TN 38175-2870 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD AUG
PY 2013
VL 74
IS 8
BP 810
EP 816
DI 10.4088/JCP.12m08099
PG 7
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 212NI
UT WOS:000323989700004
PM 24021498
ER
PT J
AU Teo, AR
Du, YB
Escobar, JI
AF Teo, Alan R.
Du, Ye B.
Escobar, Javier I.
TI How can we better manage difficult patient encounters?
SO JOURNAL OF FAMILY PRACTICE
LA English
DT Editorial Material
ID CARE; OUTCOMES; HEALTH
C1 [Teo, Alan R.] Portland VA Med Ctr, Portland, OR USA.
[Teo, Alan R.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Du, Ye B.] Columbia Univ, Dept Psychiat, New York, NY USA.
[Escobar, Javier I.] Rutgers Robert Wood Johnson Med Sch, Dept Psychiat & Family Med, New Brunswick, NJ USA.
RP Teo, AR (reprint author), 3710 SW US Vet Hosp Rd,R&D66, Portland, OR 97239 USA.
EM alan.teo@va.gov
NR 19
TC 5
Z9 5
U1 0
U2 3
PU DOWDEN HEALTH MEDIA
PI MONTVALE
PA 110 SUMMIT AVE, MONTVALE, NJ 07645-1712 USA
SN 0094-3509
J9 J FAM PRACTICE
JI J. Fam. Pract.
PD AUG
PY 2013
VL 62
IS 8
BP 414
EP 421
PG 6
WC Primary Health Care; Medicine, General & Internal
SC General & Internal Medicine
GA 218WW
UT WOS:000324464300005
PM 24143334
ER
PT J
AU Silverberg, ND
Lange, RT
Millis, SR
Rose, A
Hopp, G
Leach, S
Iverson, GL
AF Silverberg, Noah D.
Lange, Rael T.
Millis, Scott R.
Rose, Alice
Hopp, Grace
Leach, Suzanne
Iverson, Grant L.
TI Post-Concussion Symptom Reporting after Multiple Mild Traumatic Brain
Injuries
SO JOURNAL OF NEUROTRAUMA
LA English
DT Article
DE concussion; cumulative effects; head trauma; mild traumatic brain
injury; post-concussion syndrome
ID SPORT-RELATED CONCUSSION; POSTCONCUSSION-LIKE SYMPTOMS; COLLEGIATE
FOOTBALL PLAYERS; HEAD-INJURY; NEUROCOGNITIVE PERFORMANCE; TEMPORAL
WINDOW; PROFESSIONAL FOOTBALL; RECURRENT CONCUSSION; HISTORY;
VULNERABILITY
AB The relationship between previous mild traumatic brain injury/ injuries (MTBI) and recovery from a subsequent MTBI may be complex. The present study investigated three factors hypothesized to influence this relation: (1) the number of prior MTBIs, (2) the interval between MTBIs, and (3) the certainty level of previous MTBIs. The study design was retrospective cross-sectional. Participants (N = 105) were evaluated at a concussion clinic on average 1 month after sustaining an MTBI, defined by World Health Organization diagnostic criteria. Approximately half the sample had at least one previous MTBI. Subgroups with 0, 1, or 2 + previous MTBIs did not differ in levels of current post-concussion symptom reporting on the British Columbia Post-Concussion Symptom Inventory. Time since the most recent previous MTBI was significantly associated with current post-concussion symptom reporting. This relation was best characterized as logarithmic; i.e., the impact of previous MTBI(s) lessens exponentially as time elapses to a subsequent MTBI. Defining previous MTBIs with a higher certainty level (i.e., probable versus possible) was not consistently associated with greater post-concussion symptom reporting. In conclusion, participants with multiple MTBIs did not report more post-concussion symptoms than those with no history of MTBI. Previous MTBI(s), however, were associated with increased symptom reporting from a subsequent MTBI to the extent they occurred closer in time. Having one or two previous remote MTBIs was not associated with worse outcome from subsequent MTBI in this sample.
C1 [Silverberg, Noah D.] Univ British Columbia, Div Phys Med & Rehabil, Dept Med, GF Strong Rehab Ctr, Vancouver, BC V5Z 2G9, Canada.
[Lange, Rael T.] Walter Reed Natl Mil Med Ctr, Def & Vet Brain Injury Ctr, North Bethesda, MD USA.
[Lange, Rael T.] Univ British Columbia, Dept Psychiat, Vancouver, BC V5Z 2G9, Canada.
[Millis, Scott R.] Wayne State Univ, Sch Med, Dept Phys Med & Rehabil, Detroit, MI USA.
[Rose, Alice] GF Strong Rehab Ctr, Vancouver, BC, Canada.
[Hopp, Grace] Independent Practice, Port Coquitlam, BC, Canada.
[Leach, Suzanne] Simon Fraser Univ, Ctr Students Disabil, Burnaby, BC V5A 1S6, Canada.
[Iverson, Grant L.] Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Red Sox Fdn, Boston, MA USA.
[Iverson, Grant L.] Massachusetts Gen Hosp, Home Base Program, Boston, MA 02114 USA.
RP Silverberg, ND (reprint author), Univ British Columbia, Div Phys Med & Rehabil, Dept Med, GF Strong Rehab Ctr, 4255 Laurel St, Vancouver, BC V5Z 2G9, Canada.
EM noah.silverberg@vch.ca
NR 57
TC 10
Z9 10
U1 2
U2 26
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0897-7151
J9 J NEUROTRAUM
JI J. Neurotrauma
PD AUG
PY 2013
VL 30
IS 16
BP 1398
EP 1404
DI 10.1089/neu.2012.2827
PG 7
WC Critical Care Medicine; Clinical Neurology; Neurosciences
SC General & Internal Medicine; Neurosciences & Neurology
GA 199JB
UT WOS:000322989500003
PM 23458451
ER
PT J
AU Edwards, SD
Lipson, JA
Ikeda, DM
Lee, JM
AF Edwards, Sonya D.
Lipson, Jafi A.
Ikeda, Debra M.
Lee, Janie M.
TI Updates and Revisions to the BI-RADS Magnetic Resonance Imaging Lexicon
SO MAGNETIC RESONANCE IMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE Breast; MRI; BI-RADS; Lexicon
ID BREAST IMPLANT RUPTURE; BACKGROUND PARENCHYMAL ENHANCEMENT;
CONTRAST-MEDIUM ENHANCEMENT; COMPUTER-AIDED EVALUATION; POSITIVE
PREDICTIVE-VALUE; DIFFERENTIAL-DIAGNOSIS; FOLLOW-UP; NONMASSLIKE
ENHANCEMENT; ENHANCING LESIONS; SIGNAL INTENSITY
AB This article summarizes the updates and revisions to the second edition of the BI-RADS MRI lexicon. A new feature in the lexicon is background parenchymal enhancement and its descriptors. Another major focus is on revised terminology for masses and non-mass enhancement. A section on breast implants and associated lexicon terms has also been added. Because diagnostic breast imaging increasingly includes multimodality evaluation, the new edition of the lexicon also contains revised recommendations for combined reporting with mammography and ultrasound if these modalities are included as comparison, and clarification on the use of final assessment categories in MR imaging.
C1 [Edwards, Sonya D.; Lipson, Jafi A.; Ikeda, Debra M.] Stanford Univ, Med Ctr, Dept Radiol, Stanford Comprehens Canc Ctr, Stanford, CA 94305 USA.
[Lee, Janie M.] Massachusetts Gen Hosp, Dept Radiol, Inst Technol Assessment, Boston, MA 02114 USA.
RP Lee, JM (reprint author), Massachusetts Gen Hosp, Dept Radiol, Inst Technol Assessment, 101 Merrimac St,10th Floor, Boston, MA 02114 USA.
EM janie@mgh-ita.org
NR 58
TC 13
Z9 16
U1 2
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 1064-9689
J9 MAGN RESON IMAGING C
JI Magn. Reson. Imaging Clin. N. Am.
PD AUG
PY 2013
VL 21
IS 3
BP 483
EP +
DI 10.1016/j.mric.2013.02.005
PG 12
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 214QN
UT WOS:000324150500004
PM 23928239
ER
PT J
AU Scahill, L
Woods, DW
Himle, MB
Peterson, AL
Wilhelm, S
Piacentini, JC
McNaught, K
Walkup, JT
Mink, JW
AF Scahill, Lawrence
Woods, Douglas W.
Himle, Michael B.
Peterson, Alan L.
Wilhelm, Sabine
Piacentini, John C.
McNaught, Kevin
Walkup, John T.
Mink, Jonathan W.
TI Current controversies on the role of behavior therapy in Tourette
syndrome
SO MOVEMENT DISORDERS
LA English
DT Article
DE Tourette syndrome; tics; habit reversal therapy; evidence-based
treatment
ID RANDOMIZED CONTROLLED-TRIAL; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND;
HABIT-REVERSAL; TIC DISORDERS; CHILDREN; GUIDELINES; EFFICACY; BRAIN
AB Comprehensive behavioral intervention for tics (CBIT) is a safe and effective treatment for managing the tics of Tourette syndrome (TS). In contrast to most current medications used for the treatment of tics, the efficacy of CBIT has been demonstrated in 2 relatively large, multisite trials. It also shows durability of benefit over time. Similar to psychopharmacological intervention, skilled practitioners are required to implement the intervention. Despite concerns about the effort required to participate in CBIT, patients with TS and parents of children with TS appear willing to meet the requirements of the CBIT program. Efforts are under way to increase the number of trained CBIT providers in the United States. Based on available evidence, recent published guidelines suggest that CBIT can be considered a first-line treatment for persons with tic disorders. (c) 2013 Movement Disorder Society
C1 [Scahill, Lawrence] Emory Univ, Sch Med, Marcus Ctr, Atlanta, GA 30329 USA.
[Woods, Douglas W.] Univ Wisconsin Milwaukee, Milwauke, WI USA.
[Himle, Michael B.] Univ Utah, Salt Lake City, UT USA.
[Peterson, Alan L.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Wilhelm, Sabine] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Piacentini, John C.] Univ Calif Los Angeles, Los Angeles, CA USA.
[McNaught, Kevin] Tourette Syndrome Assoc, Bayside, NY USA.
[Walkup, John T.] Weill Cornell Med Coll, New York, NY USA.
[Mink, Jonathan W.] Univ Rochester, Sch Med, Rochester, NY USA.
RP Scahill, L (reprint author), Emory Univ, Sch Med, Marcus Ctr, 1920 Briarcliff Rd, Atlanta, GA 30329 USA.
EM lawrence.scahill@emory.edu
OI Scahill, Lawrence/0000-0001-5073-1707
FU National Institute of Mental Health (NIMH) [R01MH069874, 5R01MH069877,
RO1MH069875, R01MH070802]
FX This work was supported by grants from the National Institute of Mental
Health (NIMH) to Lawrence Scahill (R01MH069874), Sabine Wilhelm
(5R01MH069877), Alan L. Peterson (RO1MH069875), and John C. Piacentini
(R01MH070802).
NR 37
TC 22
Z9 23
U1 2
U2 19
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0885-3185
J9 MOVEMENT DISORD
JI Mov. Disord.
PD AUG
PY 2013
VL 28
IS 9
BP 1179
EP 1183
DI 10.1002/mds.25488
PG 5
WC Clinical Neurology
SC Neurosciences & Neurology
GA 210KA
UT WOS:000323830100005
PM 23681719
ER
PT J
AU Jafari, S
Etminan, M
Aminzadeh, F
Samii, A
AF Jafari, Siavash
Etminan, Mahyar
Aminzadeh, Farhad
Samii, Ali
TI Head injury and risk of Parkinson disease: A systematic review and
meta-analysis
SO MOVEMENT DISORDERS
LA English
DT Review
DE Parkinson's disease; head injury; head trauma; traumatic brain injury;
inflammation; meta-analysis; systematic review
ID TRAUMATIC BRAIN-INJURY; ENVIRONMENTAL-FACTORS; YOUNG-ONSET; POPULATION;
EPIDEMIOLOGY; HISTORY; LIFE
AB Head trauma has been implicated in the etiopathogenesis of Parkinson's disease (PD). We performed a meta-analysis to investigate the association between head trauma and the risk of developing PD. We included observational studies if they (1) clearly defined PD, (2) defined head trauma leading to concussion, and (3) presented odds ratios (ORs) and 95% confidence intervals (CIs) or provided data to compute these statistics. Random effect model was used to estimate the pooled, adjusted OR. Heterogeneity between studies was evaluated with the Q test and the I-2 statistic. We conducted a sensitivity analysis to assess the influence of each study and repeated the analysis by excluding the studies with the largest weights. We used funnel plot to assess the presence of publication bias. After reviewing more than 636 article titles, 34 articles were selected for full review. In total, 22 studies (19 case-control studies, 2 nested case-control studies, and 1 cohort study) were included in the meta-analysis. The pooled OR for the association of PD and head trauma was 1.57 (95% CI, 1.35-1.83). The results of our meta-analysis indicate that a history of head trauma that results in concussion is associated with a higher risk of developing PD. (c) 2013 Movement Disorder Society
C1 [Jafari, Siavash] Univ British Columbia, Fac Med, Sch Populat & Publ Hlth, Vancouver, BC, Canada.
[Etminan, Mahyar] Univ British Columbia, Fac Med, Prov Hlth Serv, Therapeut Evaluat Unit, Vancouver, BC, Canada.
[Aminzadeh, Farhad] St Georges Univ, Sch Med, Newcastle Upon Tyne, Tyne & Wear, England.
[Samii, Ali] Univ Washington, Dept Neurol, Seattle, WA 98195 USA.
[Samii, Ali] Vet Affairs Puget Sound Hlth Care Syst, Seattle Parkinson Dis Res Educ & Clin Ctr, Seattle, WA 98108 USA.
RP Samii, A (reprint author), Univ Washington, Vet Affairs Puget Hlth Care Syst, Seattle Parkinson Dis Res Educ & Clin Ctr, 1660 S Columbian Way, Seattle, WA 98108 USA.
EM asamii@u.washington.edu
NR 52
TC 31
Z9 32
U1 0
U2 20
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0885-3185
J9 MOVEMENT DISORD
JI Mov. Disord.
PD AUG
PY 2013
VL 28
IS 9
BP 1222
EP 1229
DI 10.1002/mds.25458
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 210KA
UT WOS:000323830100015
PM 23609436
ER
PT J
AU Sung, VW
Nicholas, AP
AF Sung, Victor W.
Nicholas, Anthony P.
TI Nonmotor Symptoms in Parkinson's Disease Expanding the View of
Parkinson's Disease Beyond a Pure Motor, Pure Dopaminergic Problem
SO NEUROLOGIC CLINICS
LA English
DT Article
DE Parkinson's disease; Nonmotor symptoms; Motor symptoms; Dopaminergic
ID QUALITY STANDARDS SUBCOMMITTEE; SLEEP BEHAVIOR DISORDER; L-DOPA;
AMERICAN-ACADEMY; PRACTICE PARAMETER; RATING-SCALES; REM-SLEEP;
QUESTIONNAIRE; DEPRESSION; RECOMMENDATIONS
AB Nonmotor symptoms (NMS) of Parkinson's disease (PD) are critical to identify and treat because of their impact on quality of life. Despite growing evidence of the importance of NMS on patients' quality of life, gaps remain in their recognition and treatment. The result is a need for increased information and understanding of specific NMS and the clinical approaches for their assessment and management in the context of PD as a whole. This article discusses the NMS of PD, their relationship to the pathologic basis of PD, and how NMS can be best managed.
C1 [Sung, Victor W.; Nicholas, Anthony P.] Univ Alabama Birmingham, Dept Neurol, Birmingham, AL 35294 USA.
[Sung, Victor W.; Nicholas, Anthony P.] Birmingham VA Med Ctr, Birmingham, AL 35294 USA.
RP Sung, VW (reprint author), Univ Alabama Birmingham, Dept Neurol, SC 360C,1720 7th Ave South, Birmingham, AL 35294 USA.
EM vsung@uab.edu
OI Sung, Victor/0000-0003-1024-3404
NR 78
TC 14
Z9 15
U1 1
U2 12
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0733-8619
J9 NEUROL CLIN
JI Neurol. Clin.
PD AUG
PY 2013
VL 31
IS 3
SU S
BP S1
EP +
DI 10.1016/j.ncl.2013.04.013
PG 17
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 218PV
UT WOS:000324445500002
PM 23931951
ER
PT J
AU Partridge, AH
AF Partridge, Ann H.
TI Cancer Survivorship and the Young Breast Cancer Patient: Addressing the
Important Issues
SO ONCOLOGIST
LA English
DT Editorial Material
ID PREMATURE OVARIAN FAILURE; ADJUVANT CHEMOTHERAPY; MENOPAUSAL SYMPTOMS;
WOMEN; FERTILITY
C1 [Partridge, Ann H.] Dana Farber Canc Inst, Program Young Women Breast Canc, Boston, MA 02115 USA.
RP Partridge, AH (reprint author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02115 USA.
EM ahpartridge@partners.org
NR 12
TC 4
Z9 4
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 2013
VL 18
IS 8
BP E19
EP E20
DI 10.1634/theoncologist.2013-0300
PG 2
WC Oncology
SC Oncology
GA 214AC
UT WOS:000324101200001
PM 23986342
ER
PT J
AU Bonilla-Velez, J
Mroz, EA
Hammon, RJ
Rocco, JW
AF Bonilla-Velez, Juliana
Mroz, Edmund A.
Hammon, Rebecca J.
Rocco, James W.
TI Impact of Human Papillomavirus on Oropharyngeal Cancer Biology and
Response to Therapy Implications for Treatment
SO OTOLARYNGOLOGIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE HPV-positive oropharyngeal cancer; Clinical implications; Treatment
implications
ID SQUAMOUS-CELL CARCINOMA; PHASE-III TRIAL; NECK-CANCER; UNITED-STATES;
CONCURRENT CHEMORADIATION; FUTURE-DIRECTIONS; CERVICAL-CANCER; HEAD;
SURVIVAL; HPV
AB Oropharyngeal squamous cell carcinoma (OPSCC) originating from human papillomavirus infection has emerged as a new entity in head and neck cancer, defining a subset of patients with distinct carcinogenesis, risk factor profiles, and clinical presentation that show markedly improved survival than patients with classic OPSCC. De-escalation of therapy and identification of relevant biomarkers to aid in patient selection are actively being investigated. This review addresses the implications of these findings in clinical care.
C1 [Bonilla-Velez, Juliana; Hammon, Rebecca J.; Rocco, James W.] Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Boston, MA 02114 USA.
[Mroz, Edmund A.; Rocco, James W.] Massachusetts Gen Hosp, Ctr Canc Res, Boston, MA 02114 USA.
[Mroz, Edmund A.; Rocco, James W.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
RP Rocco, JW (reprint author), Massachusetts Gen Hosp, Jackson 904G,55 Fruit St, Boston, MA 02114 USA.
EM jrocco@partners.org
FU Flight Attendant Medical Research Institute; NIH NIDCR [R01 DE022087];
NCI [R21 CA119591]; NIDCD [T32 DC000020]; AAO-HNSF Resident Research
Award; Principles and Practice of Clinical Research and Latin American
Initiative program, Harvard Medical School
FX Funding Sources and Support: Flight Attendant Medical Research
Institute; NIH NIDCR R01 DE022087; NCI R21 CA119591; NIDCD T32 DC000020;
2012 AAO-HNSF Resident Research Award; Principles and Practice of
Clinical Research and Latin American Initiative program, Harvard Medical
School.
NR 69
TC 15
Z9 15
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 0030-6665
J9 OTOLARYNG CLIN N AM
JI Otolaryngol. Clin. N. Am.
PD AUG
PY 2013
VL 46
IS 4
BP 521
EP +
DI 10.1016/j.otc.2013.04.009
PG 24
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 214QI
UT WOS:000324150000003
PM 23910468
ER
PT J
AU Hasegawa, K
Tsugawa, Y
Camargo, CA
Hiraide, A
Brown, DFM
AF Hasegawa, Kohei
Tsugawa, Yusuke
Camargo, Carlos A., Jr.
Hiraide, Atsushi
Brown, David F. M.
TI Regional variability in survival outcomes of out-of-hospital cardiac
arrest: The All-Japan Utstein Registry
SO RESUSCITATION
LA English
DT Article
DE Out-of-hospital cardiac arrest; Epidemiology; Regional variation;
Outcomes; Emergency medical service; Health services research
ID AMERICAN-HEART-ASSOCIATION; AUSTRALIAN-RESUSCITATION-COUNCIL; ELEVATION
MYOCARDIAL-INFARCTION; CARDIOPULMONARY-RESUSCITATION; COMATOSE
SURVIVORS; STROKE-FOUNDATION; TASK-FORCE; CARE; MORTALITY; STATEMENT
AB Objective: There is a paucity of studies on the degree of regional variability in out-of-hospital cardiac arrest (OHCA) outcomes, particularly in neurological outcome. This study aimed to determine whether there is a significant regional variation in survival outcomes of OHCA across Japan.
Methods: We analyzed a prospective, nation-wide, population-based database (All-Japan Utstein Registry) involving all Japanese individuals who had non-traumatic OHCA resuscitated by emergency responders from January 2005 through December 2010. The primary study endpoint was favourable neurological survival at 1 month, defined as Cerebral Performance Category 1 or 2. We compared unadjusted and multivariable-adjusted rates of the outcome among seven geographic regions.
Results: In the total catchment population of 128 million, there were 539,641 non-traumatic OHCA patients. Unadjusted neurologically favourable survival varied across regions from 1.9% to 3.1% (rate difference, 1.2%; 95% CI, 1.0-1.3%); the Northeast region had a significantly lower rate compared to the Midwest region (unadjusted rate ratio, 0.62; 95% CI, 0.60-0.64). This disparity became larger after adjusting for patient-and prehospital-level confounders (adjusted rate ratio, 0.52; 95% CI, 0.51-0.54). Among 35,153 OHCA patients with return of spontaneous circulation, unadjusted neurologically favourable survival varied from 26.4% to 34.7% (rate difference, 8.3%; 95% CI, 6.6-10.1%); the East region had a significantly lower rate compared to the Midwest region (adjusted rate ratio, 0.72; 95% CI, 0.68-0.76).
Conclusion: In this prospective, nation-wide, population-based study in Japan, we found a two-fold regional difference in neurologically favourable survival after OHCA, suggesting regional disparities in prehospital care and in-hospital post-resuscitation care. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Hasegawa, Kohei; Camargo, Carlos A., Jr.; Brown, David F. M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA USA.
[Tsugawa, Yusuke] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Gen Med & Primary Care, Boston, MA 02215 USA.
[Tsugawa, Yusuke] St Lukes Life Sci Inst, Ctr Clin Epidemiol, Tokyo, Japan.
[Hiraide, Atsushi] Kinki Univ, Fac Med, Dept Acute Med, Osaka, Japan.
RP Hasegawa, K (reprint author), Massachusetts Gen Hosp, Dept Emergency Med, 326 Cambridge St,Suite 410, Boston, MA 02114 USA.
EM khasegawa1@partners.org
FU Fire and Disaster Management Agency
FX This study was supported in part by the grant for emergency management
scientific research from the Fire and Disaster Management Agency (to Dr
Hiraide, on behalf of the study group concerning strategy for applying
the results of Utstein report for improvement of emergency service). The
Fire and Disaster Management Agency gathered and managed the data but
had no role in the design and conduct of the study; analysis and
interpretation of the data; and preparation, review, or approval of the
manuscript.
NR 37
TC 34
Z9 37
U1 1
U2 4
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0300-9572
J9 RESUSCITATION
JI Resuscitation
PD AUG
PY 2013
VL 84
IS 8
BP 1099
EP 1107
DI 10.1016/j.resuscitation.2013.03.007
PG 9
WC Critical Care Medicine; Emergency Medicine
SC General & Internal Medicine; Emergency Medicine
GA 214BA
UT WOS:000324103800030
PM 23499636
ER
PT J
AU Najita, JS
Catalano, PJ
AF Najita, Julie S.
Catalano, Paul J.
TI On Determining the BMD from Multiple Outcomes in Developmental Toxicity
Studies when One Outcome is Intentionally Missing
SO RISK ANALYSIS
LA English
DT Article
DE Benchmark dose; dose-response modeling; fetal toxicity; subset selection
ID QUANTITATIVE RISK-ASSESSMENT; LATENT VARIABLE MODELS; DOSE-RESPONSE
MODEL; FETAL WEIGHT; TERATOLOGICAL EXPERIMENTS; REGRESSION-MODEL;
CLUSTERED BINARY; LITTER SIZE; DISCRETE; TOXICOLOGY
AB Public health concerns over the occurrence of developmental abnormalities that can occur as a result of prenatal exposure to drugs, chemicals, and other environmental factors has led to a number of developmental toxicity studies and the use of the benchmark dose (BMD) for risk assessment. To characterize risk from multiple sources, more recent analytic methods involve a joint modeling approach, accounting for multiple dichotomous and continuous outcomes. For some continuous outcomes, evaluating all subjects may not be feasible, and only a subset may be evaluated due to limited resources. The subset can be selected according to a prespecified probability model and the unobserved data can be viewed as intentionally missing in the sense that subset selection results in missingness that is experimentally planned. We describe a subset selection model that allows for sampling pups with malformations and healthy pups at different rates, and includes the well-known simple random sample (SRS) as a special case. We were interested in understanding how sampling rates that are selected beforehand influence the precision of the BMD. Using simulations we show how improvements over the SRS can be obtained by oversampling malformations, and how some sampling rates can yield precision that is substantially worse than the SRS. We also illustrate the potential for cost saving with oversampling. Simulations are based on a joint mixed effects model, and to account for subset selection, use of case weights to obtain valid dose-response estimates.
C1 [Najita, Julie S.; Catalano, Paul J.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02215 USA.
[Najita, Julie S.; Catalano, Paul J.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
RP Najita, JS (reprint author), Dana Farber Canc Inst, Dept Biostat & Computat Biol, MS CLS11007,450 Brookline Ave, Boston, MA 02215 USA.
EM jnajita@jimmy.harvard.edu
FU National Institute of Environmental Health Sciences of the U.S. National
Institutes of Health [ES07142]
FX The authors thank the reviewers for helpful comments that improved the
article. This work was supported in part by grant ES07142 from the
National Institute of Environmental Health Sciences of the U.S. National
Institutes of Health.
NR 31
TC 1
Z9 1
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0272-4332
J9 RISK ANAL
JI Risk Anal.
PD AUG
PY 2013
VL 33
IS 8
BP 1500
EP 1509
DI 10.1111/j.1539-6924.2012.01939.x
PG 10
WC Public, Environmental & Occupational Health; Mathematics,
Interdisciplinary Applications; Social Sciences, Mathematical Methods
SC Public, Environmental & Occupational Health; Mathematics; Mathematical
Methods In Social Sciences
GA 202IA
UT WOS:000323206100013
PM 23231656
ER
PT J
AU Michaelson, MD
Stadler, WM
AF Michaelson, M. Dror
Stadler, Walter M.
TI Predictive Markers in Advanced Renal Cell Carcinoma
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID TARGETED THERAPY; CANCER; HYPERTENSION; SORAFENIB; SUNITINIB; BIOMARKER;
SURVIVAL; TRIAL; PAZOPANIB; BEVACIZUMAB
AB Predictive markers of response to therapy are increasingly important in advanced renal cell carcinoma (RCC) due to the proliferation of treatment options in recent years. Different types of potential predictive markers may include clinical, toxicity-based, serum, tissue, and radiologic biomarkers. Clinical factors are commonly used in overall prognostic models of RCC but have limited utility in predicting response to therapy. Correlation between development of particular toxicities and response to therapy has been noted, such as the correlation between hypertension and response to angiogenesis-targeted therapy. Serum and tissue biomarkers will be covered in detail elsewhere, but factors such as serum lactate dehydrogenase (LDH) and circulating cytokines show promise in this regard. Finally, baseline or early treatment radiology studies may have predictive ability for longer term efficacy, with most studies to date focusing on functional imaging modalities such as positron emission tomography (PET) scans, dynamic contrast-enhanced (DCE) magnetic resonance imaging (MRI), and DCE ultrasound (US). The ultimate goal of developing predictive biomarkers is to enable rational and personalized treatment strategies for patients with advanced RCC. (C) 2013 Elsevier Inc. All nights reserved.
C1 [Michaelson, M. Dror] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Stadler, Walter M.] Univ Chicago Med, Dept Med, Chicago, IL USA.
[Stadler, Walter M.] Univ Chicago Med, Dept Surg, Chicago, IL USA.
RP Michaelson, MD (reprint author), Massachusetts Gen Hosp, Ctr Canc, 55 Fruit St,Yawkey 7E, Boston, MA 02114 USA.
EM dmichaelson1@partners.org
NR 32
TC 10
Z9 10
U1 1
U2 11
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0093-7754
EI 1532-8708
J9 SEMIN ONCOL
JI Semin. Oncol.
PD AUG
PY 2013
VL 40
IS 4
BP 459
EP 464
DI 10.1053/j.seminonco1.2013.05.001
PG 6
WC Oncology
SC Oncology
GA 214QF
UT WOS:000324149700007
PM 23972709
ER
PT J
AU McDermott, DF
Atkins, MB
AF McDermott, David F.
Atkins, Michael B.
TI Immune Therapy for Kidney Cancer: A Second Dawn?
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID RENAL-CELL CARCINOMA; DOSE RECOMBINANT INTERLEUKIN-2; RANDOMIZED
CONTROLLED-TRIAL; CARBONIC-ANHYDRASE-IX; PHASE-III TRIAL;
INTERFERON-ALPHA; SUBCUTANEOUS INTERLEUKIN-2; T-CELLS; IMMUNOTHERAPY;
SUNITINIB
AB Agents targeting the immune system have been a historical standard of care in metastatic renal cell carcinoma (RCC), but have largely been supplanted by newer targeted therapy. Recent insights into the regulation of an anti-tumor immune response has led to the development of agents that can activate immune responses primarily within the tumor, enabling the possibility of achieving durable tumor response in the absence of significant systemic toxicity. In addition, a better understanding of tumor immunology has raised the potential of developing predictive biomarkers of response to immunotherapy. Novel approaches including inhibition of immune checkpoints has entered clinical testing in RCC. (C) 2013 Elsevier Inc. All rights reserved.
C1 [McDermott, David F.] Beth Israel Deaconess Med Ctr, Biol Therapy Program, Boston, MA 02215 USA.
[McDermott, David F.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[McDermott, David F.] Dana Farber Harvard Canc Ctr, Kidney Canc Program, Boston, MA USA.
[Atkins, Michael B.] Georgetown Univ, Med Ctr, Georgetown Lombardi Comprehens Canc Ctr, Dept Oncol & Med, Washington, DC 20007 USA.
RP McDermott, DF (reprint author), Beth Israel Deaconess Med Ctr, 375 Longwood Ave,MS-428, Boston, MA 02215 USA.
EM dmcdermo@bidmc.harvard.edu
FU DF/HCC Renal Cancer SPORE [P50 CA101942-01]
FX Supported in part by the DF/HCC Renal Cancer SPORE: P50 CA101942-01.
NR 51
TC 6
Z9 7
U1 0
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0093-7754
EI 1532-8708
J9 SEMIN ONCOL
JI Semin. Oncol.
PD AUG
PY 2013
VL 40
IS 4
BP 492
EP 498
DI 10.1053/j.seminonco1.2013.05.008
PG 7
WC Oncology
SC Oncology
GA 214QF
UT WOS:000324149700011
PM 23972713
ER
PT J
AU Pongas, G
Dasgupta, SK
Thiagarajan, P
AF Pongas, Georgios
Dasgupta, Swapan Kumar
Thiagarajan, Perumal
TI Antiplatelet factor 4/heparin antibodies in patients with gram negative
bacteremia
SO THROMBOSIS RESEARCH
LA English
DT Article
ID HEPARIN-INDUCED THROMBOCYTOPENIA; DEEP-VEIN THROMBOSIS;
CHLAMYDIA-PNEUMONIAE; PLATELET ACTIVATION; IGG-SEROPOSITIVITY;
SPONTANEOUS HIT; PLATELET-FACTOR-4; BINDING; COMPLICATIONS; PURIFICATION
AB Heparin-induced thrombocytopenia (HIT) is an antibody-mediated syndrome of thrombocytopenia and prothrombotic state that follows exposure to heparin. However, spontaneous HIT has been described in the setting of infection, without evidence of previous heparin administration. Since PF4 binds to lipid A portion of lipopolysaccharide, we tested for the presence of antiPF4/heparin antibodies in patients with gram-negative bacteremia. Patients with bacteremia had higher titers of antiPF4/heparin antibodies compared to normal controls 26.3 +/- SD 34 units, N = 32 versus 6.3 +/- SD 2.38 units, N = 10, P = 0.001. FITC-labeled PF4 interacted with lipopolysaccharide in a concentration-dependent manner as determined by quenching of the emission spectrum following excitation at lambda 488. In addition, immunoaffinity purified antiPF4/Heparin antibodies from 3 patients with HIT cross-reacted with PF4/heparin complex. These results show that PF4/LPS complex is immunogenic and can elicit cross-reacting antibodies against PF4/Heparin, providing an explanation for the presence of these antibodies in individuals, who were never been exposed to heparin before. These antibodies may also be at least partly responsible for the thrombocytopenia associated with infection. Published by Elsevier Ltd.
C1 [Pongas, Georgios; Thiagarajan, Perumal] Baylor Coll Med, Dept Med, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
[Dasgupta, Swapan Kumar] Baylor Coll Med, Dept Pathol, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
RP Thiagarajan, P (reprint author), Michael E DeBakey VA Med Ctr, Mail Stop 113,2002 Holcombe Blvd, Houston, TX 77030 USA.
EM perumalt@bcm.edu
OI Thiagarajan, Perumal/0000-0003-2186-7036
FU Department of Veterans Affairs; National Blood Foundation
FX GP and PT designed and perform the experiments and wrote the paper. SKG
isolated the PF4 and performed fluorescence measurements. This study was
supported in part by grants from the Department of Veterans Affairs (to
PT) and by a grant from the National Blood Foundation (to SKD).
NR 26
TC 6
Z9 6
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0049-3848
J9 THROMB RES
JI Thromb. Res.
PD AUG
PY 2013
VL 132
IS 2
BP 217
EP 220
DI 10.1016/j.thromres.2013.06.013
PG 4
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 213LV
UT WOS:000324059600028
PM 23830968
ER
PT J
AU Aston-Mourney, K
Subramanian, SL
Zraika, S
Samarasekera, T
Meier, DT
Goldstein, LC
Hull, RL
AF Aston-Mourney, Kathryn
Subramanian, Shoba L.
Zraika, Sakeneh
Samarasekera, Thanya
Meier, Daniel T.
Goldstein, Lynn C.
Hull, Rebecca L.
TI One year of sitagliptin treatment protects against islet
amyloid-associated beta-cell loss and does not induce pancreatitis or
pancreatic neoplasia in mice
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE DPP-4 inhibitor; IAPP; beta-cell mass; amyloid; exocrine pancreas
pathology
ID ENDOPLASMIC-RETICULUM STRESS; TRANSGENIC MOUSE; DIPEPTIDYL PEPTIDASE-4;
GLYCEMIC CONTROL; DIABETES-MELLITUS; INCRETIN THERAPY; DPP-4 INHIBITOR;
RODENT MODEL; POLYPEPTIDE; METFORMIN
AB The dipeptidyl peptidase-4 (DPP-4) inhibitor sitagliptin is an attractive therapy for diabetes, as it increases insulin release and may preserve beta-cell mass. However, sitagliptin also increases beta-cell release of human islet amyloid polypeptide (hIAPP), the peptide component of islet amyloid, which is cosecreted with insulin. Thus, sitagliptin treatment may promote islet amyloid formation and its associated beta-cell toxicity. Conversely, metformin treatment decreases islet amyloid formation by decreasing beta-cell secretory demand and could therefore offset sitagliptin's potential proamyloidogenic effects. Sitagliptin treatment has also been reported to be detrimental to the exocrine pancreas. We investigated whether long-term sitagliptin treatment, alone or with metformin, increased islet amyloid deposition and beta-cell toxicity and induced pancreatic ductal proliferation, pancreatitis, and/or pancreatic metaplasia/neoplasia. hIAPP transgenic and nontransgenic littermates were followed for 1 yr on no treatment, sitagliptin, metformin, or the combination. Islet amyloid deposition, beta-cell mass, insulin release, and measures of exocrine pancreas pathology were determined. Relative to untreated mice, sitagliptin treatment did not increase amyloid deposition, despite increasing hIAPP release, and prevented amyloid-induced beta-cell loss. Metformin treatment alone or with sitagliptin decreased islet amyloid deposition to a similar extent vs untreated mice. Ductal proliferation was not altered among treatment groups, and no evidence of pancreatitis, ductal metaplasia, or neoplasia were observed. Therefore, long-term sitagliptin treatment stimulates beta-cell secretion without increasing amyloid formation and protects against amyloid-induced beta-cell loss. This suggests a novel effect of sitagliptin to protect the beta-cell in type 2 diabetes that appears to occur without adverse effects on the exocrine pancreas.
C1 [Aston-Mourney, Kathryn; Subramanian, Shoba L.; Zraika, Sakeneh; Samarasekera, Thanya; Meier, Daniel T.; Hull, Rebecca L.] Vet Affairs Puget Sound Hlth Care Syst, Div Metab Endocrinol & Nutr, Dept Med, Seattle, WA USA.
[Aston-Mourney, Kathryn; Subramanian, Shoba L.; Zraika, Sakeneh; Samarasekera, Thanya; Meier, Daniel T.; Hull, Rebecca L.] Univ Washington, Seattle, WA 98195 USA.
[Aston-Mourney, Kathryn] Deakin Univ, Sch Med, Metab Res Unit, Geelong, Vic 3217, Australia.
[Goldstein, Lynn C.] PhenoPath Labs, Seattle, WA USA.
RP Hull, RL (reprint author), VA Puget Sound Hlth Care Syst 151, 1660 S Columbian Way, Seattle, WA 98108 USA.
EM rhull@uw.edu
FU National Institute of Diabetes and Digestive and Kidney Diseases
[K99-DK-080945, T32-DK-007247, P30-DK-017047]; University of Washington
McAbee Fellowship; American Diabetes Association Mentor Award;
Department of Veterans Affairs
FX This work was supported by the Department of Veterans Affairs and
National Institute of Diabetes and Digestive and Kidney Diseases grants,
K99-DK-080945 (S. Zraika), T32-DK-007247, and P30-DK-017047 (Cellular
and Molecular Imaging Core of the University of Washington Diabetes
Research Center). K. Aston-Mourney was supported by the University of
Washington McAbee Fellowship and an American Diabetes Association Mentor
Award (to Dr. S. E. Kahn).
NR 47
TC 19
Z9 20
U1 0
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 2013
VL 305
IS 4
BP E475
EP E484
DI 10.1152/ajpendo.00025.2013
PG 10
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 205GT
UT WOS:000323432000002
PM 23736544
ER
PT J
AU Ferrari, G
Nalassamy, N
Downs, H
Dana, R
Oaklander, AL
AF Ferrari, Giulio
Nalassamy, Nambi
Downs, Heather
Dana, Reza
Oaklander, Anne Louise
TI Corneal innervation as a window to peripheral neuropathies
SO EXPERIMENTAL EYE RESEARCH
LA English
DT Article
DE corneal nerves; peripheral neuropathy
ID CONFOCAL MICROSCOPY; PACLITAXEL
AB The cornea receives the densest sensory innervation of the body, which is exclusively from small-fiber nociceptive (pain-sensing) neurons. These are similar to those in the skin of the legs, the standard location for neurodiagnostic skin biopsies used to diagnose small-fiber peripheral polyneuropathies. Many cancer chemotherapy agents cause dose-related, therapy-limiting, sensory-predominant polyneuropathy. Because corneal innervation can be detected non-invasively, it is a potential surrogate biomarker for skin biopsy measurements. Therefore, we compared hindpaw-skin and cornea innervation in mice treated with neurotoxic chemotherapy. Paclitaxel (0, 5, 10, or 20 mg/kg) was administered to C57/Bl6 mice and peri-mortem cornea and skin biopsies were immunolabeled to reveal and permit quantitation of innervation. Both tissues demonstrated dose-dependent, highly correlated (r = 0.66) nerve fiber damage. These findings suggest that the quantification of corneal nerves may provide a useful surrogate marker for skin peripheral innervation. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Ferrari, Giulio; Nalassamy, Nambi; Dana, Reza] Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Schepens Eye Res Inst, Boston, MA 02114 USA.
[Ferrari, Giulio] Ist Sci San Raffaele, I-20132 Milan, Italy.
[Downs, Heather; Oaklander, Anne Louise] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02114 USA.
[Downs, Heather; Oaklander, Anne Louise] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol Neuropathol, Boston, MA 02114 USA.
[Oaklander, Anne Louise] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
RP Ferrari, G (reprint author), Hosp San Raffaele, Eye Repair Lab, Cornea & Ocular Surface Unit, Via Olgettina 60, I-20122 Milan, Italy.
EM giulio.ferrari@schepens.harvard.edu
RI ferrari, giulio/J-9260-2016
OI ferrari, giulio/0000-0001-6474-9908
FU Public Health Service [NINDS K24-NS059892, NEI RO1-EY20889]
FX Supported in part by the Public Health Service (NINDS K24-NS059892 and
NEI RO1-EY20889). Presented in abstract form at the annual meetings of
the Association for Research in Vision and Ophthalmology and the
American Neurologic Association.
NR 9
TC 9
Z9 10
U1 0
U2 3
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0014-4835
J9 EXP EYE RES
JI Exp. Eye Res.
PD AUG
PY 2013
VL 113
BP 148
EP 150
DI 10.1016/j.exer.2013.05.016
PG 3
WC Ophthalmology
SC Ophthalmology
GA 198OH
UT WOS:000322931700019
PM 23769950
ER
PT J
AU Burstein, HJ
AF Burstein, Harold J.
TI Breast Cancer Treatment in the Era of Individualized Care Preface
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Editorial Material
C1 Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Burstein, HJ (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM hburstein@partners.org
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 0889-8588
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD AUG
PY 2013
VL 27
IS 4
BP XIII
EP XV
DI 10.1016/j.hoc.2013.05.013
PG 3
WC Oncology; Hematology
SC Oncology; Hematology
GA 209ZB
UT WOS:000323798000001
PM 23915750
ER
PT J
AU Stan, D
Loprinzi, CL
Ruddy, KJ
AF Stan, Daniela
Loprinzi, Charles L.
Ruddy, Kathryn J.
TI Breast Cancer Survivorship Issues
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Vasomotor symptoms; Sexual dysfunction; Infertility; Osteoporosis;
Musculoskeletal pain; Cognitive changes; Neuropathy; Treatment-related
cancers
ID RANDOMIZED CONTROLLED-TRIAL; BONE-MINERAL DENSITY; QUALITY-OF-LIFE;
ADJUVANT ENDOCRINE THERAPY; INDUCED PERIPHERAL NEUROPATHY; ACUTE
MYELOID-LEUKEMIA; HOT FLASHES; POSTMENOPAUSAL WOMEN; DOUBLE-BLIND;
PHASE-III
AB Survivors of breast cancer are confronted with a plethora of cancer treatment-related long-term symptoms, the most common being fatigue, hot flashes, sexual dysfunction, arthralgias, neuropathy, and cognitive dysfunction. Survivors of breast cancer also face cancer treatment-related disease states, such as osteoporosis, cardiac dysfunction, obesity, infertility, and secondary cancers. Evidence-based recommendations for screening, prevention, and early intervention should be implemented to improve quality of life and decrease comorbidities in this population.
C1 [Stan, Daniela] Mayo Clin, Div Gen Internal Med, Rochester, MN 55905 USA.
[Loprinzi, Charles L.] Mayo Clin, Rochester, MN 55905 USA.
[Ruddy, Kathryn J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Stan, D (reprint author), Mayo Clin, Div Gen Internal Med, 200 1st St Southwest, Rochester, MN 55905 USA.
EM stan.daniela@mayo.edu
FU United States National Institutes of Health [CA 124477]
FX Dr D. Stan: Internal Mayo Clinic funds; Dr C.L. Loprinzi: This work was
supported by United States National Institutes of Health Grant-CA
124477; Dr K.J. Ruddy: Internal Dana Farber Cancer Institute funds.
NR 146
TC 22
Z9 22
U1 0
U2 15
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8588
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD AUG
PY 2013
VL 27
IS 4
BP 805
EP +
DI 10.1016/j.hoc.2013.05.005
PG 24
WC Oncology; Hematology
SC Oncology; Hematology
GA 209ZB
UT WOS:000323798000011
PM 23915746
ER
PT J
AU Hassett, MJ
Elkin, EB
AF Hassett, Michael J.
Elkin, Elena B.
TI What Does Breast Cancer Treatment Cost and What Is It Worth?
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Breast cancer; Cost; Value; Cost-effectiveness; Chemotherapy;
Hospitalization
ID IXABEPILONE PLUS CAPECITABINE; ADJUVANT CHEMOTHERAPY; UNITED-STATES;
AROMATASE INHIBITORS; POSTMENOPAUSAL WOMEN; FEBRILE NEUTROPENIA;
CONSERVING SURGERY; COLORECTAL-CANCER; ECONOMIC BURDEN; THERAPY
AB The costs of breast cancer care are substantial and growing, and they extend across the spectrum of care. Medical therapies and hospitalizations account for a significant proportion of these costs. Cost-effectiveness analysis (CEA) is the preferred method for assessing the health benefits of medical interventions relative to their costs. Although many CEAs have been conducted for a wide range of breast cancer treatments, these analyses are not used routinely to guide coverage or utilization decisions in the United States. Currently, patients and providers may not consider costs when making most treatment decisions; this is likely to change as payment reform spreads.
C1 [Hassett, Michael J.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Hassett, Michael J.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Elkin, Elena B.] Mem Sloan Kettering Canc Ctr, Dept Biostat & Epidemiol, New York, NY 10065 USA.
RP Hassett, MJ (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM michael_hassett@dfci.harvard.edu
FU Cure; NCI; AHRQ
FX Funding Sources: Dr M.J. Hassett: Susan G. Komen for the Cure, NCI,
AHRQ. Dr E.B. Elkin: NO.
NR 86
TC 3
Z9 3
U1 1
U2 14
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8588
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD AUG
PY 2013
VL 27
IS 4
BP 829
EP +
DI 10.1016/j.hoc.2013.05.011
PG 14
WC Oncology; Hematology
SC Oncology; Hematology
GA 209ZB
UT WOS:000323798000012
PM 23915747
ER
PT J
AU Pineles, SL
Suvak, MK
Liverant, GI
Gregor, K
Wisco, BE
Pitman, RK
Orr, SP
AF Pineles, Suzanne L.
Suvak, Michael K.
Liverant, Gabrielle I.
Gregor, Kristin
Wisco, Blair E.
Pitman, Roger K.
Orr, Scott P.
TI Psychophysiologic Reactivity, Subjective Distress, and Their
Associations With PTSD Diagnosis
SO JOURNAL OF ABNORMAL PSYCHOLOGY
LA English
DT Article
DE PTSD; trauma cues; psychophysiology; self-reported distress; imagery
ID POSTTRAUMATIC-STRESS-DISORDER; ANXIETY DISORDERS; COMBAT VETERANS;
SEXUAL-ABUSE; IMAGERY; PSYCHOPATHOLOGY; WAR
AB Intense subjective distress and physiologic reactivity upon exposure to reminders of the traumatic event are each diagnostic features of posttraumatic stress disorder (PTSD). However, subjective reports and psychophysiological data often suggest different conclusions. For the present study, we combined data from five previous studies to assess the contributions of these two types of measures in predicting PTSD diagnosis. One hundred fifty trauma-exposed participants who were classified into PTSD or non-PTSD groups based on structured diagnostic interviews completed the same script-driven imagery procedure, which quantified measures of psychophysiologic reactivity and self-reported emotional responses. We derived four discriminant functions (DiscFxs) that each maximally separated the PTSD from the non-PTSD group using (1) psychophysiologic measures recorded during personal mental imagery of the traumatic event; (2) self-report ratings in response to the trauma imagery; (3) psychophysiologic measures recorded during personal mental imagery of another highly stressful experience unrelated to the index traumatic event; and (4) self-report ratings in response to this other stressor. When PTSD status was simultaneously regressed on all four DiscFxs, trauma-related psychophysiological reactivity was a significant predictor, but physiological reactivity resulting from the highly stressful, but not traumatic script, was not. Self-reported distress to the traumatic experience and the other stressful event were both predictive of PTSD diagnosis. Trauma-related psychophysiologic reactivity was the best predictor of PTSD diagnosis, but self-reported distress contributed additional variance. These results are discussed in relation to the Research Domain Criteria framework.
C1 [Pineles, Suzanne L.; Gregor, Kristin; Wisco, Blair E.] VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA USA.
[Pineles, Suzanne L.; Liverant, Gabrielle I.; Gregor, Kristin; Wisco, Blair E.] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02215 USA.
[Suvak, Michael K.] Suffolk Univ, Dept Psychol, Boston, MA USA.
[Liverant, Gabrielle I.] VA Boston Healthcare Syst, Boston, MA USA.
[Pitman, Roger K.; Orr, Scott P.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Pitman, Roger K.; Orr, Scott P.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Pineles, SL (reprint author), VA Boston Healthcare Syst 116B 3, 150 South Huntington Ave, Boston, MA 02130 USA.
EM Suzanne.Pineles@va.gov
NR 37
TC 9
Z9 9
U1 4
U2 15
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0021-843X
J9 J ABNORM PSYCHOL
JI J. Abnorm. Psychol.
PD AUG
PY 2013
VL 122
IS 3
BP 635
EP 644
DI 10.1037/a0033942
PG 10
WC Psychology, Clinical; Psychology, Multidisciplinary
SC Psychology
GA 210CO
UT WOS:000323807100003
PM 24016006
ER
PT J
AU Hilbert, A
Hartmann, AS
Czaja, J
Schoebi, D
AF Hilbert, Anja
Hartmann, Andrea S.
Czaja, Julia
Schoebi, Dominik
TI Natural Course of Preadolescent Loss of Control Eating
SO JOURNAL OF ABNORMAL PSYCHOLOGY
LA English
DT Article
DE binge eating disorder; loss of control eating; depression; childhood;
adolescence
ID PRIMARY-SCHOOL CHILDREN; RISK-FACTORS; ADOLESCENT GIRLS; DISORDER
EXAMINATION; CLINICAL-SIGNIFICANCE; BODY DISSATISFACTION; COMMUNITY
SAMPLE; NEGATIVE AFFECT; ADULT OBESITY; WEIGHT-GAIN
AB Cross-sectional evidence shows that loss of control (LOC) eating is a common and psychopathologically relevant experience in preadolescence. This study sought to investigate the natural course of preadolescent LOC eating in relation to psychopathology and body weight trajectory. A community sample of 55 children ages 8-13 years with LOC eating, defined as at least one episode of LOC eating within the past 3 months (LOC+), and 59 matched children without LOC history (LOC), were assessed with the Eating Disorder Examination adapted for Children and self-report questionnaires every 6 months over a 2-year follow-up. Of the LOC+ children, 54.5% of children remitted from LOC eating, 3.6% showed persistent LOC eating, and 41.8% showed recurring LOC eating over the follow-up period. Of the LOC children, 19% revealed an onset of LOC episodes, mostly with a low level of stability. Multilevel modeling showed that LOC eating predicted a partial binge eating disorder diagnosis and greater global eating disorder psychopathology, but not depressive symptoms or growth in body fatness. Between-person higher shape concern and weight-related teasing, as well as within-person decreases in shape concern and increases in depression, predicted a greater likelihood of subsequent LOC eating. The results indicate a moderate stability of LOC eating in preadolescent children, with prognostic significance for clinically relevant eating problems and eating disorder psychopathology.
C1 [Hilbert, Anja] Univ Leipzig, Med Ctr, Integrated Res & Treatment Ctr AdiposityDis, Dept Med Psychol & Med Sociol, D-04103 Leipzig, Germany.
[Hartmann, Andrea S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Hartmann, Andrea S.] Harvard Univ, Sch Med, Dept Psychiat, Cambridge, MA 02138 USA.
[Czaja, Julia] Univ Marburg, Dept Psychol, D-35032 Marburg, Germany.
[Schoebi, Dominik] Univ Fribourg, Dept Psychol, CH-1700 Fribourg, Switzerland.
RP Hilbert, A (reprint author), Univ Leipzig, Med Ctr, Integrated Res & Treatment Ctr AdiposityDis, Dept Med Psychol & Med Sociol, Philipp Rosenthal Str 27, D-04103 Leipzig, Germany.
EM anja.hilbert@medizin.uni-leipzig.de
OI Schoebi, Dominik/0000-0003-3991-2712
NR 61
TC 23
Z9 23
U1 3
U2 15
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0021-843X
J9 J ABNORM PSYCHOL
JI J. Abnorm. Psychol.
PD AUG
PY 2013
VL 122
IS 3
BP 684
EP 693
DI 10.1037/a0033330
PG 10
WC Psychology, Clinical; Psychology, Multidisciplinary
SC Psychology
GA 210CO
UT WOS:000323807100008
PM 24016009
ER
PT J
AU Jarosiewicz, B
Masse, NY
Bacher, D
Cash, SS
Eskandar, E
Friehs, G
Donoghue, JP
Hochberg, LR
AF Jarosiewicz, Beata
Masse, Nicolas Y.
Bacher, Daniel
Cash, Sydney S.
Eskandar, Emad
Friehs, Gerhard
Donoghue, John P.
Hochberg, Leigh R.
TI Advantages of closed-loop calibration in intracortical brain-computer
interfaces for people with tetraplegia
SO JOURNAL OF NEURAL ENGINEERING
LA English
DT Article
ID PRIMATE MOTOR CORTEX; CORTICAL CONTROL; NEUROPROSTHETIC DEVICES; MACHINE
INTERFACES; CELL DISCHARGE; NEURAL-CONTROL; ARM MOVEMENTS; NEURONS;
ALGORITHM; DIRECTION
AB Objective. Brain-computer interfaces (BCIs) aim to provide a means for people with severe motor disabilities to control their environment directly with neural activity. In intracortical BCIs for people with tetraplegia, the decoder that maps neural activity to desired movements has typically been calibrated using 'open-loop' (OL) imagination of control while a cursor automatically moves to targets on a computer screen. However, because neural activity can vary across contexts, a decoder calibrated using OL data may not be optimal for 'closed-loop' (CL) neural control. Here, we tested whether CL calibration creates a better decoder than OL calibration even when all other factors that might influence performance are held constant, including the amount of data used for calibration and the amount of elapsed time between calibration and testing. Approach. Two people with tetraplegia enrolled in the BrainGate2 pilot clinical trial performed a center-out-back task using an intracortical BCI, switching between decoders that had been calibrated on OL versus CL data. Main results. Even when all other variables were held constant, CL calibration improved neural control as well as the accuracy and strength of the tuning model. Updating the CL decoder using additional and more recent data resulted in further improvements. Significance. Differences in neural activity between OL and CL contexts contribute to the superiority of CL decoders, even prior to their additional 'adaptive' advantage. In the near future, CL decoder calibration may enable robust neural control without needing to pause ongoing, practical use of BCIs, an important step toward clinical utility.
C1 [Jarosiewicz, Beata; Masse, Nicolas Y.; Donoghue, John P.] Brown Univ, Dept Neurosci, Providence, RI 02912 USA.
[Jarosiewicz, Beata; Masse, Nicolas Y.; Bacher, Daniel; Donoghue, John P.; Hochberg, Leigh R.] Brown Univ, Brown Inst Brain Sci, Providence, RI 02912 USA.
[Jarosiewicz, Beata; Donoghue, John P.; Hochberg, Leigh R.] Dept Vet Affairs Med Ctr, Rehabil R&D Serv, Ctr Neurorestorat & Neurotechnol, Providence, RI USA.
[Bacher, Daniel; Donoghue, John P.; Hochberg, Leigh R.] Brown Univ, Sch Engn, Providence, RI 02912 USA.
[Cash, Sydney S.; Eskandar, Emad; Hochberg, Leigh R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Friehs, Gerhard] Rhode Isl Hosp, Dept Neurosurg, Providence, RI USA.
RP Jarosiewicz, B (reprint author), Brown Univ, Dept Neurosci, 2 Stimson Ave,Box 1994, Providence, RI 02912 USA.
EM beata@brown.edu
OI Hochberg, Leigh/0000-0003-0261-2273
FU Craig H Neilsen Foundation fellowship; Rehabilitation R&D Service,
Department of Veterans Affairs [B6453R, B6310N, B6459L, A6779I]; NIH:
NIDCD [R01DC009899]; NINDS/NICHD [RC1HD063931]; NICHD-NCMRR [N01HD53403,
N01HD10018]; NINDS-Javits [NS25074]; Doris Duke Charitable Foundation;
MGH-Deane Institute for Integrated Research on Atrial Fibrillation and
Stroke; Katie Samson Foundation
FX The authors would like to thank participants S3 and T1 and their
families, The Boston Home and their staff, and John Simeral, Sergey
Stavisky, Katie Centrella, Erin Gallivan, and Etsub Berhanu for their
contributions to this study. Thanks also to Michael Black for comments
on an earlier draft of the manuscript, to Naveen Rao, Steven Chase, and
Wasim Malik for useful discussions, and to Laurie Barefoot, Beth
Travers, and David Rosler for research support. Funding was provided by
the Craig H Neilsen Foundation fellowship (BJ); Rehabilitation R&D
Service, Department of Veterans Affairs (Merit Review Awards: B6453R and
A6779I, Career Development Transition Award: B6310N, Senior Research
Career Scientist Award: B6459L); NIH: NIDCD (R01DC009899), NINDS/NICHD
(RC1HD063931), NICHD-NCMRR (N01HD53403, N01HD10018), NINDS-Javits
(NS25074); the Doris Duke Charitable Foundation; the MGH-Deane Institute
for Integrated Research on Atrial Fibrillation and Stroke; and the Katie
Samson Foundation. The contents do not represent the views of the
Department of Veterans Affairs or the United States Government.
NR 59
TC 25
Z9 25
U1 0
U2 11
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 1741-2560
J9 J NEURAL ENG
JI J. Neural Eng.
PD AUG
PY 2013
VL 10
IS 4
AR 046012
DI 10.1088/1741-2560/10/4/046012
PG 10
WC Engineering, Biomedical; Neurosciences
SC Engineering; Neurosciences & Neurology
GA 188UW
UT WOS:000322221600019
PM 23838067
ER
PT J
AU Liberman, MY
Ching, SN
Chemali, J
Brown, EN
AF Liberman, Max Y.
Ching, ShiNung
Chemali, Jessica
Brown, Emery N.
TI A closed-loop anesthetic delivery system for real-time control of burst
suppression
SO JOURNAL OF NEURAL ENGINEERING
LA English
DT Article
ID QUANTITATIVE EEG ANALYSIS; STATE-SPACE MODEL; BISPECTRAL INDEX;
PERFORMANCE ASSESSMENT; PROPOFOL ANESTHESIA; FEEDBACK-CONTROL;
REMIFENTANIL; SURGERY; HUMANS; FEASIBILITY
AB Objective. There is growing interest in using closed-loop anesthetic delivery (CLAD) systems to automate control of brain states (sedation, unconsciousness and antinociception) in patients receiving anesthesia care. The accuracy and reliability of these systems can be improved by using as control signals electroencephalogram (EEG) markers for which the neurophysiological links to the anesthetic-induced brain states are well established. Burst suppression, in which bursts of electrical activity alternate with periods of quiescence or suppression, is a well-known, readily discernible EEG marker of profound brain inactivation and unconsciousness. This pattern is commonly maintained when anesthetics are administered to produce a medically-induced coma for cerebral protection in patients suffering from brain injuries or to arrest brain activity in patients having uncontrollable seizures. Although the coma may be required for several hours or days, drug infusion rates are managed inefficiently by manual adjustment. Our objective is to design a CLAD system for burst suppression control to automate management of medically-induced coma. Approach. We establish a CLAD system to control burst suppression consisting of: a two-dimensional linear system model relating the anesthetic brain level to the EEG dynamics; a new control signal, the burst suppression probability (BSP) defining the instantaneous probability of suppression; the BSP filter, a state-space algorithm to estimate the BSP from EEG recordings; a proportional-integral controller; and a system identification procedure to estimate the model and controller parameters. Main results. We demonstrate reliable performance of our system in simulation studies of burst suppression control using both propofol and etomidate in rodent experiments based on Vijn and Sneyd, and in human experiments based on the Schnider pharmacokinetic model for propofol. Using propofol, we further demonstrate that our control system reliably tracks changing target levels of burst suppression in simulated human subjects across different epidemiological profiles. Significance. Our results give new insights into CLAD system design and suggest a control-theory framework to automate second-to-second control of burst suppression for management of medically-induced coma.
C1 [Liberman, Max Y.; Ching, ShiNung; Chemali, Jessica; Brown, Emery N.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Ching, ShiNung; Brown, Emery N.] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
[Brown, Emery N.] MIT, Inst Med Engn & Sci, Cambridge, MA 02139 USA.
RP Liberman, MY (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
EM enb@neurostat.mit.edu
FU NIH [DP1-OD003646, R01GM10498]; Burroughs-Wellcome Fund [1010625]
FX This work was supported by: NIH Awards DP1-OD003646 and R01GM10498
(ENB), and the Burroughs-Wellcome Fund Award 1010625 (SC).
NR 51
TC 11
Z9 12
U1 0
U2 6
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 1741-2560
EI 1741-2552
J9 J NEURAL ENG
JI J. Neural Eng.
PD AUG
PY 2013
VL 10
IS 4
AR 046004
DI 10.1088/1741-2560/10/4/046004
PG 13
WC Engineering, Biomedical; Neurosciences
SC Engineering; Neurosciences & Neurology
GA 188UW
UT WOS:000322221600011
PM 23744607
ER
PT J
AU Thompson, JW
Forrester, MT
Moseley, MA
Foster, MW
AF Thompson, J. Will
Forrester, Michael T.
Moseley, M. Arthur
Foster, Matthew W.
TI Solid-phase capture for the detection and relative quantification of
S-nitrosoproteins by mass spectrometry
SO METHODS
LA English
DT Review
DE Nitric oxide; S-nitrosylation; S-nitrosothiol; Redox; Proteomics; Mass
spectrometry; Nitrosative; Palmitoylation
ID NITROSO-L-CYSTEINE; RESIN-ASSISTED CAPTURE; BIOTIN-SWITCH ASSAY;
CYSTIC-FIBROSIS; ACCURATE MASS; NITRIC-OXIDE; NITROSYLATION;
IDENTIFICATION; PROTEINS; PROTEOME
AB The proteomic analysis of S-nitrosylated protein (SNO-proteins) has long depended on the biotin switch technique (BST), which requires blocking of free thiols, ascorbate-based denitrosylation of SNO-Cys, biotinylation of nascent thiol and avidin-based affinity isolation. A more recent development is resin assisted-capture of SNO-proteins (SNO-RAC), which substitutes thiopropyl Sepharose (TPS) for biotin-avidin, thus reducing the number of steps required for enrichment of S-nitrosylated proteins. In addition, SNO-RAC facilitates on-resin proteolytic digestion following SNO-protein capture, greatly simplifying the purification of peptides containing sites of S-nitrosylation ("SNO-sites"). This resin-based approach has also now been applied to detection of alternative Cys-based modifications, including S-palmitoylation (Acyl-RAC) and S-oxidation (Ox-RAC). Here, we review the important steps to minimize false-positive identification of SNO-proteins, give detailed methods for processing of protein-bound TPS for mass spectrometry (MS) based analysis, and discuss the various quantitative MS methods that are compatible with SNO-RAC. We also discuss strategies to overcome the current limitations surrounding MS-based SNO-site localization in peptides containing more than one potential target Cys residue. This article therefore serves as a starting point and guide for the MS-focused exploration of SNO-proteomes by SNO-RAC. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Thompson, J. Will; Moseley, M. Arthur] Duke Univ, Med Ctr, Inst Genome Sci & Policy, Durham, NC 27710 USA.
[Forrester, Michael T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA 02114 USA.
[Foster, Matthew W.] Duke Univ, Med Ctr, Div Pulm Allergy & Crit Care Med, Durham, NC 27710 USA.
RP Foster, MW (reprint author), Duke Univ, Med Ctr, Box 2629 Res Dr, Durham, NC 27710 USA.
EM mwfoster@duke.edu
FU National Institutes of Health [HL106121]
FX This work was supported in part by a grant from the National Institutes
of Health (HL106121).
NR 55
TC 7
Z9 7
U1 4
U2 23
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1046-2023
J9 METHODS
JI Methods
PD AUG 1
PY 2013
VL 62
IS 2
BP 130
EP 137
DI 10.1016/j.ymeth.2012.10.001
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 210WN
UT WOS:000323865700003
PM 23064468
ER
PT J
AU Caruso, PA
Johnson, J
Thibert, R
Rapalino, O
Rincon, S
Ratai, EM
AF Caruso, Paul A.
Johnson, Jason
Thibert, Ron
Rapalino, Otto
Rincon, Sandra
Ratai, Eva-Maria
TI The Use of Magnetic Resonance Spectroscopy in the Evaluation of Epilepsy
SO NEUROIMAGING CLINICS OF NORTH AMERICA
LA English
DT Article
DE H-1 MR spectroscopy; Epilepsy; Inborn error of metabolism; Focal
cortical dysplasia
ID AUTOMATED SPECTRAL-ANALYSIS; TEMPORAL-LOBE EPILEPSY; CREATINE
TRANSPORTER DEFICIENCY; PROSPECTIVE MOTION CORRECTION; RESPIRATORY-CHAIN
DEFECTS; PROTON NMR-SPECTROSCOPY; HUMAN-BRAIN INVIVO; MR SPECTROSCOPY;
CHEMICAL-SHIFT; MITOCHONDRIAL DISORDERS
AB Magnetic resonance spectroscopy (MRS) is indicated in the imaging protocol of the patient with epilepsy to screen for metabolic derangements such as inborn errors of metabolism and to characterize masses that may be equivocal on conventional magnetic resonance imaging for dysplasia versus neoplasia. Single-voxel MRS with echo time of 35 milliseconds may be used for this purpose as a quick screening tool in the epilepsy imaging protocol. MRS is useful in the evaluation of both focal and generalized epilepsy.
C1 [Caruso, Paul A.; Johnson, Jason; Rapalino, Otto; Rincon, Sandra; Ratai, Eva-Maria] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Neuroradiol,Dept Radiol, Boston, MA 02114 USA.
[Thibert, Ron] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Epilepsy Serv,Dept Neurol, Boston, MA 02114 USA.
[Ratai, Eva-Maria] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02129 USA.
RP Caruso, PA (reprint author), Massachusetts Gen Hosp, Dept Radiol, Div Neuroradiol, 55 Fruit St, Boston, MA 02114 USA.
EM pcaruso@partners.org
NR 101
TC 7
Z9 7
U1 1
U2 8
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1052-5149
J9 NEUROIMAG CLIN N AM
JI Neuroimaging Clin. N. Am.
PD AUG
PY 2013
VL 23
IS 3
BP 407
EP +
DI 10.1016/j.nic.2012.12.012
PG 19
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 209ZX
UT WOS:000323800200006
PM 23928197
ER
PT J
AU Calkins, AS
Iglehart, JD
Lazaro, JB
AF Calkins, Anne S.
Iglehart, J. Dirk
Lazaro, Jean-Bernard
TI DNA damage-induced inhibition of rRNA synthesis by DNA-PK and PARP-1
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID DEPENDENT PROTEIN-KINASE; POLYMERASE-I TRANSCRIPTION; POLY(ADP-RIBOSE)
POLYMERASE; NUCLEOLAR PROTEIN; HISTONE CHAPERONE; ADP-RIBOSYLATION;
BINDING-PROTEIN; KU ANTIGEN; CELL-CYCLE; PHOSPHORYLATION
AB RNA synthesis and DNA replication cease after DNA damage. We studied RNA synthesis using an in situ run-on assay and found ribosomal RNA (rRNA) synthesis was inhibited 24 h after UV light, gamma radiation or DNA cross-linking by cisplatin in human cells. Cisplatin led to accumulation of cells in S phase. Inhibition of the DNA repair proteins DNA-dependent protein kinase (DNA-PK) or poly(ADP-ribose) polymerase 1 (PARP-1) prevented the DNA damage-induced block of rRNA synthesis. However, DNA-PK and PARP-1 inhibition did not prevent the cisplatin-induced arrest of cell cycle in S phase, nor did it induce de novo BrdU incorporation. Loss of DNA-PK function prevented activation of PARP-1 and its recruitment to chromatin in damaged cells, suggesting regulation of PARP-1 by DNA-PK within a pathway of DNA repair. From these results, we propose a sequential activation of DNA-PK and PARP-1 in cells arrested in S phase by DNA damage causes the interruption of rRNA synthesis after DNA damage.
C1 [Calkins, Anne S.; Iglehart, J. Dirk; Lazaro, Jean-Bernard] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
[Iglehart, J. Dirk] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
RP Lazaro, JB (reprint author), Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
EM jiglehart@partners.org; jlazaro@partners.org
FU Pallotta Investigator Fund; Susan F. Smith Center for Women's Cancers;
Marjorie Powell Allen Memorial Fund
FX Pallotta Investigator Fund (to J.B.L.); the Susan F. Smith Center for
Women's Cancers; the Marjorie Powell Allen Memorial Fund and Barbara and
Paul Ferry. Funding for open access charge: The Pallotta Investigator
Fund.
NR 51
TC 15
Z9 17
U1 1
U2 19
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD AUG
PY 2013
VL 41
IS 15
BP 7378
EP 7386
DI 10.1093/nar/gkt502
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 212GL
UT WOS:000323970700024
PM 23775790
ER
PT J
AU Chen, EY
Dobrinski, KP
Brown, KH
Clagg, R
Edelman, E
Ignatius, MS
Chen, JYH
Brockmann, J
Nielsen, GP
Ramaswamy, S
Keller, C
Lee, C
Langenau, DM
AF Chen, Eleanor Y.
Dobrinski, Kimberly P.
Brown, Kim H.
Clagg, Ryan
Edelman, Elena
Ignatius, Myron S.
Chen, Jin Yun Helen
Brockmann, Jillian
Nielsen, G. Petur
Ramaswamy, Sridhar
Keller, Charles
Lee, Charles
Langenau, David M.
TI Cross-Species Array Comparative Genomic Hybridization Identifies Novel
Oncogenic Events in Zebrafish and Human Embryonal Rhabdomyosarcoma
SO PLOS GENETICS
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; ACUTE LYMPHOBLASTIC-LEUKEMIA; TRANSGENIC
ZEBRAFISH; RAS GENES; PHASE-II; CYCLIN D; CANCER; TUMORS; CELLS;
EXPRESSION
AB Human cancer genomes are highly complex, making it challenging to identify specific drivers of cancer growth, progression, and tumor maintenance. To bypass this obstacle, we have applied array comparative genomic hybridization (array CGH) to zebrafish embryonal rhabdomyosaroma (ERMS) and utilized cross-species comparison to rapidly identify genomic copy number aberrations and novel candidate oncogenes in human disease. Zebrafish ERMS contain small, focal regions of low-copy amplification. These same regions were commonly amplified in human disease. For example, 16 of 19 chromosomal gains identified in zebrafish ERMS also exhibited focal, low-copy gains in human disease. Genes found in amplified genomic regions were assessed for functional roles in promoting continued tumor growth in human and zebrafish ERMS - identifying critical genes associated with tumor maintenance. Knockdown studies identified important roles for Cyclin D2 (CCND2), Homeobox Protein C6 (HOXC6) and PlexinA1 (PLXNA1) in human ERMS cell proliferation. PLXNA1 knockdown also enhanced differentiation, reduced migration, and altered anchorage-independent growth. By contrast, chemical inhibition of vascular endothelial growth factor (VEGF) signaling reduced angiogenesis and tumor size in ERMS-bearing zebrafish. Importantly, VEGFA expression correlated with poor clinical outcome in patients with ERMS, implicating inhibitors of the VEGF pathway as a promising therapy for improving patient survival. Our results demonstrate the utility of array CGH and cross-species comparisons to identify candidate oncogenes essential for the pathogenesis of human cancer.
C1 [Chen, Eleanor Y.; Clagg, Ryan; Ignatius, Myron S.; Brockmann, Jillian; Langenau, David M.] Massachusetts Gen Hosp, Div Mol Pathol, Charlestown, MA 02129 USA.
[Chen, Eleanor Y.; Clagg, Ryan; Ignatius, Myron S.; Langenau, David M.] Harvard Stem Cell Inst, Boston, MA USA.
[Chen, Eleanor Y.; Clagg, Ryan; Edelman, Elena; Ignatius, Myron S.; Ramaswamy, Sridhar; Langenau, David M.] Massachusetts Gen Hosp, Dept Med, Ctr Canc, Boston, MA 02114 USA.
[Chen, Eleanor Y.; Dobrinski, Kimberly P.; Brown, Kim H.; Ignatius, Myron S.; Chen, Jin Yun Helen; Ramaswamy, Sridhar; Lee, Charles; Langenau, David M.] Harvard Univ, Sch Med, Boston, MA USA.
[Dobrinski, Kimberly P.; Brown, Kim H.; Chen, Jin Yun Helen; Lee, Charles] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Dobrinski, Kimberly P.] Univ S Florida, Coll Med, Dept Pathol & Cell Biol, Tampa, FL USA.
[Brown, Kim H.] Portland State Univ, Dept Biol, Portland, OR 97207 USA.
[Nielsen, G. Petur] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Keller, Charles] Oregon Hlth & Sci Univ, Dept Pediat, Pediat Canc Biol Program, Portland, OR 97201 USA.
RP Chen, EY (reprint author), Massachusetts Gen Hosp, Div Mol Pathol, Charlestown, MA 02129 USA.
EM dlangenau@partners.org
FU NIH [K01 AR055619, RO1 CA154923, R21 CA156056, K08 AR063165-01]; Alex's
Lemonade Stand Foundation (ALSF); American Cancer Society; Harvard Stem
Cell Institute; St. Baldrick's Foundation Scholar Award; NIH-National
Institute of Environmental Health Sciences [K99/R00 ES018892]; "A'' ALSF
ward; NIH-National Cancer Institute [5R01CA111560]; NIH-National Human
Genome Research Institute [5P41HG004421]
FX DML was supported by NIH grants K01 AR055619, RO1 CA154923, and R21
CA156056, the Alex's Lemonade Stand Foundation (ALSF), the American
Cancer Society, and the Harvard Stem Cell Institute. EYC was supported
by NIH K08 AR063165-01 and St. Baldrick's Foundation Scholar Award. KHB
was supported by Grant K99/R00 ES018892 (NIH-National Institute of
Environmental Health Sciences). MSI was supported by an "A'' ALSF ward.
CL is supported by Grants 5R01CA111560 (NIH-National Cancer Institute)
and 5P41HG004421 (NIH-National Human Genome Research Institute). The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript
NR 49
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U1 0
U2 4
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 2013
VL 9
IS 8
AR e1003727
DI 10.1371/journal.pgen.1003727
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 210KB
UT WOS:000323830300069
PM 24009521
ER
PT J
AU He, X
Sanders, SJ
Liu, L
De Rubeis, S
Lim, ET
Sutcliffe, JS
Schellenberg, GD
Gibbs, RA
Daly, MJ
Buxbaum, JD
State, MW
Devlin, B
Roeder, K
AF He, Xin
Sanders, Stephan J.
Liu, Li
De Rubeis, Silvia
Lim, Elaine T.
Sutcliffe, James S.
Schellenberg, Gerard D.
Gibbs, Richard A.
Daly, Mark J.
Buxbaum, Joseph D.
State, Matthew W.
Devlin, Bernie
Roeder, Kathryn
TI Integrated Model of De Novo and Inherited Genetic Variants Yields
Greater Power to Identify Risk Genes
SO PLOS GENETICS
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; COPY-NUMBER VARIATION; FUNCTIONAL IMPACT;
RARE VARIANTS; MUTATIONS; ASSOCIATION; DISEASE; DISCOVERY; COL25A1;
EXOMES
AB De novo mutations affect risk for many diseases and disorders, especially those with early-onset. An example is autism spectrum disorders (ASD). Four recent whole-exome sequencing (WES) studies of ASD families revealed a handful of novel risk genes, based on independent de novo loss-of-function (LoF) mutations falling in the same gene, and found that de novo LoF mutations occurred at a twofold higher rate than expected by chance. However successful these studies were, they used only a small fraction of the data, excluding other types of de novo mutations and inherited rare variants. Moreover, such analyses cannot readily incorporate data from case-control studies. An important research challenge in gene discovery, therefore, is to develop statistical methods that accommodate a broader class of rare variation. We develop methods that can incorporate WES data regarding de novo mutations, inherited variants present, and variants identified within cases and controls. TADA, for Transmission And De novo Association, integrates these data by a gene-based likelihood model involving parameters for allele frequencies and gene-specific penetrances. Inference is based on a Hierarchical Bayes strategy that borrows information across all genes to infer parameters that would be difficult to estimate for individual genes. In addition to theoretical development we validated TADA using realistic simulations mimicking rare, large-effect mutations affecting risk for ASD and show it has dramatically better power than other common methods of analysis. Thus TADA's integration of various kinds of WES data can be a highly effective means of identifying novel risk genes. Indeed, application of TADA to WES data from subjects with ASD and their families, as well as from a study of ASD subjects and controls, revealed several novel and promising ASD candidate genes with strong statistical support.
C1 [He, Xin; Roeder, Kathryn] Carnegie Mellon Univ, Lane Ctr Computat Biol, Pittsburgh, PA 15213 USA.
[Sanders, Stephan J.; State, Matthew W.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Sanders, Stephan J.; State, Matthew W.] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA.
[Liu, Li; Roeder, Kathryn] Carnegie Mellon Univ, Dept Stat, Pittsburgh, PA 15213 USA.
[De Rubeis, Silvia; Buxbaum, Joseph D.] Icahn Mt Sinai Sch Med, Seaver Autism Ctr Res & Treatment, New York, NY USA.
[De Rubeis, Silvia; Buxbaum, Joseph D.] Icahn Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Lim, Elaine T.; Daly, Mark J.] Massachusetts Gen Hosp, Dept Med, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
[Lim, Elaine T.; Daly, Mark J.] Harvard Univ, Sch Med, Boston, MA USA.
[Lim, Elaine T.; Daly, Mark J.] Broad Inst Harvard & MIT, Program Med & Populat Genet, Cambridge, MA USA.
[Sutcliffe, James S.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Vanderbilt Brain Inst, Nashville, TN 37232 USA.
[Sutcliffe, James S.] Vanderbilt Univ, Dept Psychiat, Vanderbilt Brain Inst, Nashville, TN 37235 USA.
[Schellenberg, Gerard D.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Gibbs, Richard A.] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
[Buxbaum, Joseph D.] Icahn Mt Sinai Sch Med, Dept Genet & Genom Sci, New York, NY USA.
[Buxbaum, Joseph D.] Icahn Mt Sinai Sch Med, Friedman Brain Inst, New York, NY USA.
[Devlin, Bernie] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA.
RP He, X (reprint author), Carnegie Mellon Univ, Lane Ctr Computat Biol, Pittsburgh, PA 15213 USA.
EM roeder@stat.cmu.edu
RI Liu, Li/G-1897-2015; De Rubeis, Silvia/E-9852-2013;
OI De Rubeis, Silvia/0000-0001-9383-6883; Sutcliffe,
James/0000-0001-5200-6007; Buxbaum, Joseph/0000-0001-8898-8313; Sanders,
Stephan/0000-0001-9112-5148
FU NIH [R01MH089208, R01 MH089025, R01 MH089004, R01MH089175, R01 MH089482,
RO1 MH057881, R01 MH061009, 1U01MH100233-01, 1U01MH100209]
FX This work was directly supported by NIH grants R01MH089208 (MJD), R01
MH089025 (JDB), R01 MH089004 (GDS), R01MH089175 (RAG), R01 MH089482
(JSS), RO1 MH057881 (BD), R01 MH061009 (JSS), 1U01MH100233-01 (JDB), and
1U01MH100209 (BD). This work was also supported by a grant from the
Simons Foundation. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 40
TC 50
Z9 50
U1 0
U2 12
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 2013
VL 9
IS 8
AR e1003671
DI 10.1371/journal.pgen.1003671
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 210KB
UT WOS:000323830300023
PM 23966865
ER
PT J
AU Ibrahim, MK
Barnes, JL
Anstead, GM
Jimenez, F
Travi, BL
Peniche, AG
Osorio, EY
Ahuja, SS
Melby, PC
AF Ibrahim, Marwa K.
Barnes, Jeffrey L.
Anstead, Gregory M.
Jimenez, Fabio
Travi, Bruno L.
Peniche, Alex G.
Osorio, E. Yaneth
Ahuja, Seema S.
Melby, Peter C.
TI The Malnutrition-Related Increase in Early Visceralization of Leishmania
donovani Is Associated with a Reduced Number of Lymph Node Phagocytes
and Altered Conduit System Flow
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID PROTEIN-ENERGY MALNUTRITION; BONE-MARROW-CELLS; IMMUNE-RESPONSE;
MALNOURISHED RATS; DENDRITIC CELLS; SOUTHERN SUDAN; RISK-FACTOR;
KALA-AZAR; INFECTION; NUTRITION
AB In a murine model of moderate childhood malnutrition we found that polynutrient deficiency led to a 4-5-fold increase in early visceralization of L. donovani (3 days post-infection) following cutaneous infection and a 16-fold decrease in lymph node barrier function (p<0.04 for all). To begin to understand the mechanistic basis for this malnutrition-related parasite dissemination we analyzed the cellularity, architecture, and function of the skin-draining lymph node. There was no difference in the localization of multiple cell populations in the lymph node of polynutrient deficient (PND) mice, but there was reduced cellularity with fewer CD11c(+) dendritic cells (DCs), fibroblastic reticular cells (FRCs), MOMA-2(+) macrophages, and CD169(+) subcapsular sinus macrophage (p<0.05 for all) compared to the well-nourished (WN) mice. The parasites were equally co-localized with DCs associated with the lymph node conduit network in the WN and PND mice, and were found in the high endothelial venule into which the conduits drain. When a fluorescent low molecular weight (10 kD) dextran was delivered in the skin, there was greater efflux of the marker from the lymph node conduit system to the spleens of PND mice (p<0.04), indicating that flow through the conduit system was altered. There was no evidence of disruption of the conduit or subcapsular sinus architecture, indicating that the movement of parasites into the subcortical conduit region was due to an active process and not from passive movement through a leaking barrier. These results indicate that the impaired capacity of the lymph node to act as a barrier to dissemination of L. donovani infection is associated with a reduced number of lymph node phagocytes, which most likely leads to reduced capture of parasites as they transit through the sinuses and conduit system.
C1 [Ibrahim, Marwa K.; Melby, Peter C.] Univ Texas Hlth Sci Ctr San Antonio, Dept Microbiol & Immunol, San Antonio, TX 78229 USA.
[Ibrahim, Marwa K.; Barnes, Jeffrey L.; Anstead, Gregory M.; Jimenez, Fabio; Ahuja, Seema S.] South Texas Vet Hlth Care Syst, San Antonio, TX USA.
[Barnes, Jeffrey L.; Anstead, Gregory M.; Jimenez, Fabio; Ahuja, Seema S.] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, San Antonio, TX 78229 USA.
[Travi, Bruno L.; Peniche, Alex G.; Osorio, E. Yaneth; Melby, Peter C.] Univ Texas Med Branch, Dept Internal Med, Galveston, TX 77555 USA.
[Travi, Bruno L.; Melby, Peter C.] Univ Texas Med Branch, Ctr Trop Dis, Galveston, TX 77555 USA.
[Travi, Bruno L.; Melby, Peter C.] Univ Texas Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA.
[Travi, Bruno L.; Melby, Peter C.] Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA.
RP Ibrahim, MK (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Microbiol & Immunol, San Antonio, TX 78229 USA.
EM pcmelby@utmb.edu
OI Ibrahim, Marwa/0000-0002-2603-8280
NR 67
TC 4
Z9 4
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD AUG
PY 2013
VL 7
IS 8
AR e2329
DI 10.1371/journal.pntd.0002329
PG 16
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 211WE
UT WOS:000323941500008
PM 23967356
ER
PT J
AU Salloum, S
Wang, HL
Ferguson, C
Parton, RG
Tai, AW
AF Salloum, Shadi
Wang, Hongliang
Ferguson, Charles
Parton, Robert G.
Tai, Andrew W.
TI Rab18 Binds to Hepatitis C Virus NS5A and Promotes Interaction between
Sites of Viral Replication and Lipid Droplets
SO PLOS PATHOGENS
LA English
DT Article
ID NONSTRUCTURAL PROTEIN 5A; 4-KINASE III ALPHA; CELL-CULTURE SILAC; RNA
REPLICATION; CORE PROTEIN; IN-VITRO; EFFICIENT REPLICATION; DIRECT
VISUALIZATION; INFECTIOUS VIRUS; AMINO-ACIDS
AB Hepatitis C virus (HCV) is a single-stranded RNA virus that replicates on endoplasmic reticulum-derived membranes. HCV particle assembly is dependent on the association of core protein with cellular lipid droplets (LDs). However, it remains uncertain whether HCV assembly occurs at the LD membrane itself or at closely associated ER membranes. Furthermore, it is not known how the HCV replication complex and progeny genomes physically associate with the presumed sites of virion assembly at or near LDs. Using an unbiased proteomic strategy, we have found that Rab18 interacts with the HCV nonstructural protein NS5A. Rab18 associates with LDs and is believed to promote physical interaction between LDs and ER membranes. Active (GTP-bound) forms of Rab18 bind more strongly to NS5A than a constitutively GDP-bound mutant. NS5A colocalizes with Rab18-positive LDs in HCV-infected cells, and Rab18 appears to promote the physical association of NS5A and other replicase components with LDs. Modulation of Rab18 affects genome replication and possibly also the production of infectious virions. Our results support a model in which specific interactions between viral and cellular proteins may promote the physical interaction between membranous HCV replication foci and lipid droplets.
C1 [Salloum, Shadi; Wang, Hongliang; Tai, Andrew W.] Univ Michigan, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Ferguson, Charles; Parton, Robert G.] Univ Queensland, Inst Mol Biosci, Brisbane, Qld, Australia.
[Ferguson, Charles; Parton, Robert G.] Univ Queensland, Ctr Microscopy & Microanal, Brisbane, Qld, Australia.
[Tai, Andrew W.] Ann Arbor Vet Adm Hlth Syst, Dept Internal Med, Div Gastroenterol, Ann Arbor, MI USA.
RP Salloum, S (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
EM andrewwt@med.umich.edu
OI Parton, Robert/0000-0002-7494-5248; Tai, Andrew/0000-0002-6877-450X
FU National Institutes of Health [AI083785, DK097374]; Michigan
Gastrointestinal Peptide Research Center [NIDDK 5P30DK034933]; Greenview
Foundation Hepatitis C Research Fund; National Health and Medical
Research Council of Australia [569542, 511005]
FX This work was supported by grants AI083785 and DK097374 from the
National Institutes of Health, the Michigan Gastrointestinal Peptide
Research Center (NIDDK 5P30DK034933), and the Greenview Foundation
Hepatitis C Research Fund (to AWT), as well as by a fellowship (no.
569542) and grant (no. 511005) from the National Health and Medical
Research Council of Australia (to RGP). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 70
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U1 1
U2 16
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD AUG
PY 2013
VL 9
IS 8
AR e1003513
DI 10.1371/journal.ppat.1003513
PG 16
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 211EQ
UT WOS:000323888200017
PM 23935497
ER
PT J
AU Kubicki, M
Shenton, ME
Maciejewski, PK
Pelavin, PE
Hawley, KJ
Ballinger, T
Swisher, T
Jabbar, GA
Thermenos, HW
Keshavan, MS
Seidman, LJ
DeLisi, LE
AF Kubicki, M.
Shenton, M. E.
Maciejewski, P. K.
Pelavin, P. E.
Hawley, K. J.
Ballinger, T.
Swisher, T.
Jabbar, G. A.
Thermenos, H. W.
Keshavan, M. S.
Seidman, L. J.
DeLisi, L. E.
TI Decreased axial diffusivity within language connections: A possible
biomarker of schizophrenia risk
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Increased familial risk; Schizophrenia; Diffusion tensor imaging; White
matter maturation
ID HIGH GENETIC RISK; WHITE-MATTER MICROSTRUCTURE; ULTRA-HIGH-RISK; RADIAL
DIFFUSIVITY; HUMAN BRAIN; 1ST-EPISODE SCHIZOPHRENIA; MULTIPLE-SCLEROSIS;
TRACTOGRAPHY; PSYCHOSIS; MRI
AB Siblings of patients diagnosed with schizophrenia are at elevated risk for developing this disorder. The nature of such risk associated with brain abnormalities, and whether such abnormalities are similar to those observed in schizophrenia, remain unclear. Deficits in language processing are frequently reported in increased risk populations. Interestingly, white matter pathology involving fronto-temporal language pathways, including arcuate fasciculus (AF), uncinate fasciculus (UF), and inferior occipitofrontal fasciculus (IOFF), are frequently reported in schizophrenia. In this study, high spatial and directional resolution diffusion MRI data was obtained on a 3 T magnet from 33 subjects with increased familial risk for developing schizophrenia, and 28 control subjects. Diffusion tractography was performed to measure white matter integrity within AF, UF, and IOFF. To understand these abnormalities, Fractional Anisotropy (FA, a measure of tract integrity) and Trace (a measure of overall diffusion), were combined with more specific measures of axial diffusivity (AX, a putative measure of axonal integrity) and radial diffusivity (RD, a putative measure of myelin integrity). Results revealed a significant decrease in Trace within IOFF, and a significant decrease in AX in all tracts. FA and RD anomalies, frequently reported in schizophrenia, were not observed. Moreover, AX group effect was modulated by age, with increased risk subjects demonstrating a deviation from normal maturation trajectory. Findings suggest that familial risk for schizophrenia may be associated with abnormalities in axonal rather than myelin integrity, and possibly associated with disruptions in normal brain maturation. AX should be considered a possible biomarker of risk for developing schizophrenia. (C) 2013 Elsevier B. V. All rights reserved.
C1 [Kubicki, M.; Shenton, M. E.; Pelavin, P. E.; Hawley, K. J.; Ballinger, T.; Swisher, T.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Psychiat Neuroimaging Lab, Boston, MA 02115 USA.
[Shenton, M. E.; DeLisi, L. E.] VA Boston Healthcare Syst, Brockton, MA USA.
[Maciejewski, P. K.; Jabbar, G. A.; Thermenos, H. W.; Keshavan, M. S.; Seidman, L. J.; DeLisi, L. E.] Harvard Univ, Sch Med, Boston, MA USA.
[Seidman, L. J.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Thermenos, H. W.; Keshavan, M. S.; Seidman, L. J.] Beth Israel Deaconess Med Ctr, Dept Psychiat, Boston, MA 02215 USA.
[Thermenos, H. W.; Keshavan, M. S.; Seidman, L. J.] Massachusetts Mental Hlth Ctr, Div Publ Psychiat, Boston, MA 02115 USA.
RP Kubicki, M (reprint author), Psychiat Neuroimaging Lab, 1249 Boylston St, Boston, MA 02215 USA.
EM kubicki@bwh.harvard.edu
FU National Alliance for Medical Image Computing (NA-MIC); National
Institutes of Health Roadmap for Medical Research [U54 EB005149]; VA
Merit; National Institute of Health [R01 MH 074794];
[NIMH-R21MH083205]; [MH 64023]
FX This study was supported, in part, by the National Alliance for Medical
Image Computing (NA-MIC), supported through the National Institutes of
Health Roadmap for Medical Research, Grant U54 EB005149 (MK, CFW, PG);
VA Merit (MS); National Institute of Health (R01 MH 074794 to CFW and
MK); NIMH-R21MH083205 (LED); and MH 64023 (MSK, LS).
NR 60
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Z9 14
U1 2
U2 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD AUG
PY 2013
VL 148
IS 1-3
BP 67
EP 73
DI 10.1016/j.schres.2013.06.014
PG 7
WC Psychiatry
SC Psychiatry
GA 211UL
UT WOS:000323936600011
PM 23800617
ER
PT J
AU Woods, SW
Addington, J
Bearden, CE
Cadenhead, KS
Cannon, TD
Cornblatt, BA
Mathalon, DH
Perkins, DO
Seidman, LJ
Tsuang, MT
Walker, EF
McGlashan, TH
AF Woods, Scott W.
Addington, Jean
Bearden, Carrie E.
Cadenhead, Kristin S.
Cannon, Tyrone D.
Cornblatt, Barbara A.
Mathalon, Daniel H.
Perkins, Diana O.
Seidman, Larry J.
Tsuang, Ming T.
Walker, Elaine F.
McGlashan, Thomas H.
TI Psychotropic medication use in youth at high risk for psychosis:
Comparison of baseline data from two research cohorts 1998-2005 and
2008-2011
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Psychosis; High risk; Risk syndrome; Psychotropic medication;
Antipsychotic medication
ID RANDOMIZED CONTROLLED-TRIAL; ANTIPSYCHOTIC MEDICATIONS; PRODROMAL
SYMPTOMS; 2ND-GENERATION ANTIPSYCHOTICS; PREDICTIVE-VALIDITY;
META-ANALYSIS; INTERRATER RELIABILITY; EPISODE PSYCHOSIS; YOUNG-PEOPLE;
1ST EPISODE
AB Background: Antipsychotic medication use rates have generally been rising among youth with psychiatric disorders, but little is known about use rates of antipsychotics or other psychotropic medications in patients at high risk for psychosis.
Method: Baseline psychotropic medication use rates were compared in two research cohorts of patients at high risk for psychosis that enrolled between 1998-2005 (n = 391) and 2008-2011 (n = 346). Treatment durations and antipsychotic doses were described for cohort 2.
Results: Median age was 17 years in cohort 1 and 18 years in cohort 2. The rate of prescription of any psychotropic at baseline was roughly 40% for each cohort. Antipsychotic prescription rates were 24% among sites that permitted baseline antipsychotic use in cohort 1 and 18% in the cohort 2; the decline did not quite reach statistical significance (p = 0.064). In cohort 2 the mean +/- SD baseline chlorpromazine-equivalent dose was 121 +/- 108 mg/d, and lifetime duration of antipsychotic treatment was 3.8 +/- 5.9 months.
Discussion: Although the rate of antipsychotic prescription among high-risk youth may have fallen slightly, the nearly one-in-five rate in the second cohort still constitutes a significant exposure. Mitigating factors were that doses and durations of treatment were low. As for other nonpsychotic conditions, it is incumbent on our field to develop alternative treatments for high-risk patients and to generate additional evidence for or against the efficacy of antipsychotics to help define their appropriate role if alternative treatments fail. (C) 2013 Elsevier B. V. All rights reserved.
C1 [Woods, Scott W.; McGlashan, Thomas H.] Yale Univ, Dept Psychiat, New Haven, CT 06519 USA.
[Addington, Jean] Univ Calgary, Dept Psychiat, Calgary, AB T2N 1N4, Canada.
[Bearden, Carrie E.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
[Bearden, Carrie E.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA.
[Cadenhead, Kristin S.; Tsuang, Ming T.] Univ Calif San Diego, Dept Psychiat, San Diego, CA USA.
[Cannon, Tyrone D.] Yale Univ, Dept Psychol, New Haven, CT 06519 USA.
[Cornblatt, Barbara A.] Zucker Hillside Hosp, Dept Psychiat, Long Isl City, NY USA.
[Mathalon, Daniel H.] UCSF, Dept Psychiat, San Francisco, CA USA.
[Perkins, Diana O.] UCSF, Univ N Carolina, Dept Psychiat, San Francisco, CA USA.
[Seidman, Larry J.] Harvard Univ, Beth Israel Deaconess Med Ctr, Massachusetts Gen Hosp, Dept Psychiat,Med Sch, Boston, MA 02215 USA.
[Walker, Elaine F.] Emory Univ, Dept Psychol, Atlanta, GA 30322 USA.
[Walker, Elaine F.] Emory Univ, Dept Psychiat, Atlanta, GA 30322 USA.
RP Woods, SW (reprint author), Yale Univ, Sch Med, Connecticut Mental Hlth Ctr, 34 Pk St, New Haven, CT 06519 USA.
EM scott.woods@yale.edu
OI Mathalon, Daniel/0000-0001-6090-4974
FU National Institute of Mental Health [U01 MH066160, U01 MH082022, U01
MH066134, U01 MH081984, U01 MH060720, R01 MH60720, U01 MH081944, K24
MH76191, U01 MH065079, MH081902, U01 MH061523, U01 MH081857, U01
MH066069, U01 MH082004, U01 MH065562, U01 MH081928, P50 MH080272];
National Institute of Mental Health (Commonwealth of Massachusetts)
[SCDMH82101008006, U01 MH062066, U01 MH081988]
FX This study was supported by the National Institute of Mental Health
(grants U01 MH066160 and U01 MH082022 to Dr Woods; grants U01 MH066134
and U01 MH081984 to Dr Addington; grants U01 MH060720, R01 MH60720, U01
MH081944 and K24 MH76191 to Dr Cadenhead; grants U01 MH065079 and
MH081902 to Dr Cannon; grants U01 MH061523 and U01 MH081857 to Dr
Cornblatt; grants U01 MH066069 and U01 MH082004 to Dr Perkins; grants
U01 MH065562, U01 MH081928, P50 MH080272 and Commonwealth of
Massachusetts SCDMH82101008006 to Dr Seidman; and grants U01 MH062066 to
EFW and U01 MH081988 to Dr Walker). The NIMH had no further role in
study design; in the collection, analysis and interpretation of data; in
the writing of the report; or in the decision to submit the paper for
publication.
NR 55
TC 14
Z9 14
U1 4
U2 15
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD AUG
PY 2013
VL 148
IS 1-3
BP 99
EP 104
DI 10.1016/j.schres.2013.05.019
PG 6
WC Psychiatry
SC Psychiatry
GA 211UL
UT WOS:000323936600016
PM 23787224
ER
PT J
AU Amato, RJ
Felts, AS
Rodriguez, AL
Venable, DF
Morrison, RD
Byers, FW
Daniels, JS
Niswender, CM
Conn, PJ
Lindsley, CW
Jones, CK
Emmitte, KA
AF Amato, Russell J.
Felts, Andrew S.
Rodriguez, Alice L.
Venable, Daryl F.
Morrison, Ryan D.
Byers, Frank W.
Daniels, J. Scott
Niswender, Colleen M.
Conn, P. Jeffrey
Lindsley, Craig W.
Jones, Carrie K.
Emmitte, Kyle A.
TI Substituted 1-Phenyl-3-(pyridin-2-yl)urea Negative Allosteric Modulators
of mGlu(5): Discovery of a New Tool Compound VU0463841 with Activity in
Rat Models of Cocaine Addiction
SO ACS CHEMICAL NEUROSCIENCE
LA English
DT Article
DE mGlu(5); negative allosteric modulator; noncompetitive antagonist; CNS;
cocaine; addiction
ID METABOTROPIC GLUTAMATE RECEPTORS; MGLUR5 ANTAGONIST MPEP;
2-METHYL-6-(PHENYLETHYNYL)-PYRIDINE MPEP; SQUIRREL-MONKEYS; DRUG
DISCOVERY; CNS EXPOSURE; PHARMACOLOGY; SEEKING; REWARD; POTENT
AB Cocaine is a powerful and highly addictive stimulant that disrupts the normal reward circuitry in the central nervous system (CNS), producing euphoric effects. Cocaine use can lead to acute and life threatening emergencies, and abuse is associated with increased risk for contracting infectious diseases. Though certain types of behavioral therapy have proven effective for treatment of cocaine addiction, relapse remains high, and there are currently no approved medications for the treatment of cocaine abuse. Evidence has continued to accumulate that indicates a critical role for the metabotropic glutamate receptor subtype 5 (mGlu(5)) in the modulation of neural circuitry associated with the addictive properties of cocaine. While the small molecule mGlu(5) negative allosteric modulator (NAM) field is relatively advanced, investigation into the potential of small molecule mGlu(5) NAMs for the treatment of cocaine addiction remains an area of high interest. Herein we describe the discovery and characterization of a potent and selective compound 29 (VU0463841) with good CNS exposure in rats. The utility of 29 (VU0463841) was demonstrated by its ability to attenuate drug seeking behaviors in relevant rat models of cocaine addiction.
C1 [Amato, Russell J.; Felts, Andrew S.; Rodriguez, Alice L.; Venable, Daryl F.; Morrison, Ryan D.; Byers, Frank W.; Daniels, J. Scott; Niswender, Colleen M.; Conn, P. Jeffrey; Lindsley, Craig W.; Jones, Carrie K.; Emmitte, Kyle A.] Vanderbilt Univ Sch Med, Dept Pharmacol, Nashville, TN 37232 USA.
[Lindsley, Craig W.; Emmitte, Kyle A.] Vanderbilt Univ Sch Med, Dept Chem, Nashville, TN 37232 USA.
[Amato, Russell J.; Felts, Andrew S.; Rodriguez, Alice L.; Venable, Daryl F.; Morrison, Ryan D.; Byers, Frank W.; Daniels, J. Scott; Niswender, Colleen M.; Conn, P. Jeffrey; Lindsley, Craig W.; Jones, Carrie K.; Emmitte, Kyle A.] Vanderbilt Univ Sch Med, Vanderbilt Ctr Neurosci Drug Discovery, Nashville, TN 37232 USA.
[Jones, Carrie K.] US Dept Vet Affairs, Tennessee Valley Healthcare Syst, Nashville, TN 37212 USA.
RP Jones, CK (reprint author), Vanderbilt Univ Sch Med, Vanderbilt Ctr Neurosci Drug Discovery, 1205 Light Hall, Nashville, TN 37232 USA.
EM carrie.jones@vanderbilt.edu; kyle.a.emmitte@vanderbilt.edu
FU NIH; NIMH; NIDA [R01 DA023947]; Alzheimer's Association; Bristol-Myers
Squibb; AstraZeneca; Tennessee Valley Healthcare System (U.S. Dept. of
Veteran's Affairs); NINDS; Seaside Therapeutics [VUMC33842]
FX C.W.L. receives funding from NIH, NIMH, NIDA, the Alzheimer's
Association, Bristol-Myers Squibb, and AstraZeneca. C.K.J. receives
funding from NIMH and Tennessee Valley Healthcare System (U.S. Dept. of
Veteran's Affairs), Bristol-Myers Squibb, and AstraZeneca. C.M.N.
receives funding from NINDS, Bristol-Myers Squibb, and AstraZeneca.
P.J.C. receives funding from NIH, NIMH, NINDS, Bristol-Myers Squibb, and
AstraZeneca. K.A.E. receives funding from NIMH. The authors thank NIDA
(R01 DA023947) and Seaside Therapeutics (VUMC33842) for their support of
our programs in the development of mGlu5 NAMs.
NR 58
TC 8
Z9 8
U1 0
U2 5
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1948-7193
J9 ACS CHEM NEUROSCI
JI ACS Chem. Neurosci.
PD AUG
PY 2013
VL 4
IS 8
BP 1217
EP 1228
DI 10.1021/cn400070k
PG 12
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Neurosciences
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Neurosciences
& Neurology
GA 206PZ
UT WOS:000323535900010
PM 23682684
ER
PT J
AU Rifkin, DE
Katz, R
Chonchol, M
Shlipak, MG
Sarnak, MJ
Fried, LF
Newman, AB
Siscovick, DS
Peralta, CA
AF Rifkin, Dena E.
Katz, Ronit
Chonchol, Michel
Shlipak, Michael G.
Sarnak, Mark J.
Fried, Linda F.
Newman, Anne B.
Siscovick, David S.
Peralta, Carmen A.
TI Blood Pressure Components and Decline in Kidney Function in
Community-Living Older Adults: The Cardiovascular Health Study
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Article
DE blood pressure; cystatin C; diastolic blood pressure; elderly;
hypertension; kidney function; systolic blood pressure
ID ISOLATED SYSTOLIC HYPERTENSION; STAGE RENAL-DISEASE; CYSTATIN-C;
UNITED-STATES; RISK; MORTALITY; ASSOCIATION; PREVALENCE; CREATININE
AB BACKGROUND
Although hypertension contributes to kidney dysfunction in the general population, the contributions of elevated systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP) to kidney function decline in community-dwelling older adults are unknown.
METHODS
We used linear and logistic regression to examine the separate and combined associations of SBP, DBP, and PP at baseline with kidney function decline among 4,365 older adults in the Cardiovascular Health Study. We used cystatin C to estimate glomerular filtration rate on 3 occasions over 7 years of follow-up. We defined rapid decline >= 3 ml/min/year.
RESULTS
Average age was 72.2 and mean (standard deviation) SBP, DBP, and PP were 135 (21), 71 (11), and 65 (18) mm Hg, respectively. SBP and PP, rather than DBP, were most significantly associated with kidney function decline. In adjusted linear models, each 10-mm Hg increment in SBP and PP was associated with 0.13 ml/min/year (-0.19, -0.08, P < 0.001) and 0.15-ml/min/year faster decline (-0.21, -0.09, P < 0.001), respectively. Each 10-mm Hg increment in DBP was associated with a nonsignificant 0.10-ml/min/year faster decline (95% confidence interval, -0.20, 0.01). In adjusted logistic models, SBP had the strongest associations with rapid decline, with 14% increased hazard of rapid decline (95% confidence interval, 10% to 17%, P < 0.01) per 10 mm Hg. In models combining BP components, only SBP consistently had independent associations with rapid decline.
CONCLUSIONS
Our findings suggest that elevated BP, particularly SBP, contributes to declining kidney function in older adults.
C1 [Rifkin, Dena E.] Univ Calif San Diego, Div Nephrol, San Diego, CA 92103 USA.
[Rifkin, Dena E.] Univ Calif San Diego, Div Family & Prevent Med, San Diego, CA 92103 USA.
[Rifkin, Dena E.] Vet Affairs Med Ctr, San Diego, CA 92161 USA.
[Katz, Ronit] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Chonchol, Michel] Univ Colorado, Div Renal Dis & Hypertens, Denver, CO 80202 USA.
[Shlipak, Michael G.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Sarnak, Mark J.] Tufts Med Ctr, Div Nephrol, Boston, MA USA.
[Fried, Linda F.] Vet Affairs Pittsburgh Healthcare Syst, Renal Sect, Pittsburgh, PA USA.
[Newman, Anne B.] Univ Pittsburgh, Dept Epidemiol, Sch Med, Div Geriatr Med, Pittsburgh, PA 15261 USA.
[Siscovick, David S.] Univ Washington, Dept Med, Seattle, WA USA.
[Siscovick, David S.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Peralta, Carmen A.] Univ Calif San Francisco, Div Nephrol, San Francisco, CA 94143 USA.
RP Rifkin, DE (reprint author), Univ Calif San Diego, Div Nephrol, San Diego, CA 92103 USA.
EM drifkin@ucsd.edu
RI Newman, Anne B./C-6408-2013
OI Newman, Anne B./0000-0002-0106-1150
FU NHLBI [HHSN268201200036C, N01-HC-85239, N01-HC-85079, N01-HC-85086,
N01-HC-35129, N01 HC-15103, N01 HC-55222, N01-HC-75150, N01-HC-45133,
HL080295]; NIA [AG-023629, AG-15928, AG-20098, AG-027058]
FX This work was supported by NHLBI contracts HHSN268201200036C,
N01-HC-85239, N01-HC-85079 through N01-HC-85086; N01-HC-35129, N01
HC-15103, N01 HC-55222, N01-HC-75150, N01-HC-45133 and NHLBI grant
HL080295, with additional contribution from NINDS. Additional support
was provided through AG-023629, AG-15928, AG-20098, and AG-027058 from
the NIA. See also http://www.chs-nhlbi.org/pi.htm.
NR 23
TC 9
Z9 11
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0895-7061
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD AUG
PY 2013
VL 26
IS 8
BP 1037
EP 1044
DI 10.1093/ajh/hpt067
PG 8
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 182CO
UT WOS:000321718300014
PM 23709568
ER
PT J
AU Miloslavsky, EM
Specks, U
Merkel, PA
Seo, P
Spiera, R
Langford, CA
Hoffman, GS
Kallenberg, CGM
St Clair, EW
Tchao, NK
Viviano, L
Ding, L
Sejismundo, LP
Mieras, K
Ikle, D
Jepson, B
Mueller, M
Brunetta, P
Allen, NB
Fervenza, FC
Geetha, D
Keogh, K
Kissin, EY
Monach, PA
Peikert, T
Stegeman, C
Ytterberg, SR
Stone, JH
AF Miloslavsky, E. M.
Specks, U.
Merkel, P. A.
Seo, P.
Spiera, R.
Langford, C. A.
Hoffman, G. S.
Kallenberg, C. G. M.
St Clair, E. W.
Tchao, N. K.
Viviano, L.
Ding, L.
Sejismundo, L. P.
Mieras, K.
Ikle, D.
Jepson, B.
Mueller, M.
Brunetta, P.
Allen, N. B.
Fervenza, F. C.
Geetha, D.
Keogh, K.
Kissin, E. Y.
Monach, P. A.
Peikert, T.
Stegeman, C.
Ytterberg, S. R.
Stone, J. H.
CA Rituximab ANCA-Associated
TI Clinical Outcomes of Remission Induction Therapy for Severe
Antineutrophil Cytoplasmic Antibody-Associated Vasculitis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID ANCA-ASSOCIATED VASCULITIS; DAILY ORAL CYCLOPHOSPHAMIDE;
RANDOMIZED-TRIAL; FOLLOW-UP; RITUXIMAB; MAINTENANCE; AUTOANTIBODIES;
GRANULOMATOSIS; AZATHIOPRINE; METHOTREXATE
AB Objective. To evaluate the reasons that complete remission is not achieved or maintained with original treatment in some patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) treated with rituximab (RTX) or with cyclophosphamide/azathioprine (CYC/AZA).
Methods. The Rituximab in AAV trial was a randomized, double-blind, placebo-controlled trial comparing the rate of remission induction among patients treated with RTX (n = 99) and patients treated with CYC followed by AZA (n = 98). Glucocorticoids were tapered over a period of 5 months. The primary outcome measure was lack of disease activity without glucocorticoid treatment at 6 months. To determine the most important reason for failure to achieve the primary outcome, 7 hierarchical categories of reasons were defined retrospectively (uncontrolled disease, adverse event leading to therapy discontinuation, severe flare, limited flare, Birmingham Vasculitis Activity Score for Wegener's Granulomatosis >0, prednisone treatment at any dosage, and other).
Results. Although remission (lack of disease activity) was achieved in 170 of the 197 patients (86%) in the first 6 months, the primary outcome measure was not achieved in 42%. There were 3 deaths. Twenty-four percent of the patients failed to achieve the primary end point due to active disease: 10 (5%) experienced uncontrolled disease in the first month and 37 (19%) experienced flares after initial improvement. In the majority of such patients, treatment with blinded crossover or according to best medical judgment led to disease control. Ninety-one percent of patients who had uncontrolled disease or experienced a severe flare had proteinase 3 (PR3)-ANCA. When patients with uncontrolled disease were excluded from analysis, those who were PR3-ANCA positive were found to experience fewer flares when treated with RTX compared to CYC/AZA (8 of 59 [14%] versus 20 of 62 [32%]; P = 0.02). Neither ANCA titers nor B cell counts predicted disease flare.
Conclusion. Current treatment regimens are largely successful in controlling AAV, but in approximately one-fourth of patients, active disease persists or recurs in the first 6 months despite treatment. PR3- ANCA positivity is a risk factor for recurrence or persistence of severe disease. ANCA titers and B cell detectability are poor predictors of both disease relapse and disease quiescence in the first 6 months.
C1 [Miloslavsky, E. M.; Stone, J. H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Specks, U.; Mieras, K.; Fervenza, F. C.; Keogh, K.; Peikert, T.; Ytterberg, S. R.] Mayo Clin, Rochester, MN USA.
[Merkel, P. A.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Seo, P.; Sejismundo, L. P.; Geetha, D.] Johns Hopkins Univ, Baltimore, MD USA.
[Spiera, R.] Hosp Special Surg, New York, NY 10021 USA.
[Langford, C. A.; Hoffman, G. S.] Cleveland Clin, Cleveland, OH 44106 USA.
[Kallenberg, C. G. M.; Stegeman, C.] Univ Groningen, Univ Med Ctr Groningen, Groningen, Netherlands.
[Kallenberg, C. G. M.; Stegeman, C.] Univ Groningen, Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
[St Clair, E. W.; Allen, N. B.] Duke Univ, Med Ctr, Durham, NC USA.
[Tchao, N. K.] Immune Tolerance Network, San Francisco, CA USA.
[Viviano, L.; Ding, L.] NIAID, NIH, Bethesda, MD 20892 USA.
[Ikle, D.; Jepson, B.] Rho, Chapel Hill, NC USA.
[Mueller, M.] US FDA, Silver Spring, MD USA.
[Brunetta, P.] Genentech Inc, San Francisco, CA 94080 USA.
[Kissin, E. Y.; Monach, P. A.] Boston Univ, Sch Med, Boston, MA 02118 USA.
RP Stone, JH (reprint author), Massachusetts Gen Hosp, Rheumatol Unit, Yawkey 2C,55 Fruit St, Boston, MA 02114 USA.
EM jhstone@partners.org
FU Immune Tolerance Network (NIH), an international clinical research
consortium headquartered at the University of California San Francisco
[N01-AI-15416, ITN021AI]; NIH (National Institute of Allergy and
Infectious Diseases) [N01-AI-15416, ITN021AI]; Juvenile Diabetes
Research Foundation; Genentech; Biogen Idec; NIH (Mayo Clinic: National
Center for Research Resources Clinical and Translational Science)
[RR-024150-01]; NIH (Johns Hopkins University: National Center for
Research Resources Clinical and Translational Science) [RR-025005,
K23-AR-052820, K24-AR-049185, RR-025771, M01-RR-00533, K24-AR-02224];
Arthritis Foundation
FX The Rituximab in ANCA-Associated Vasculitis (RAVE) trial was performed
with the support of the Immune Tolerance Network (NIH contract
N01-AI-15416, protocol number ITN021AI), an international clinical
research consortium headquartered at the University of California San
Francisco and supported by the NIH (National Institute of Allergy and
Infectious Diseases contract N01-AI-15416, protocol number ITN021AI) and
the Juvenile Diabetes Research Foundation. Genentech and Biogen Idec
provided the study medications and partial funding for the RAVE trial.
At the Mayo Clinic, Johns Hopkins University, and Boston University
School of Medicine, the RAVE trial was supported by the NIH (Mayo
Clinic: National Center for Research Resources Clinical and
Translational Science award RR-024150-01; Johns Hopkins University:
National Center for Research Resources Clinical and Translational
Science grant RR-025005 and career development awards K23-AR-052820 to
Dr. Seo and K24-AR-049185 to Dr. Stone; Boston University: National
Center for Research Resources Clinical and Translational Science award
RR-025771, grant M01-RR-00533, and career development award K24-AR-02224
to Dr. Merkel). Dr. Miloslavsky's work was supported by Genentech
(Clinical Immunology Fellowship). Dr. Monach's work was supported by the
Arthritis Foundation (Arthritis Investigator Award).
NR 21
TC 37
Z9 39
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD AUG
PY 2013
VL 65
IS 9
BP 2441
EP 2449
DI 10.1002/art.38044
PG 9
WC Rheumatology
SC Rheumatology
GA 205YR
UT WOS:000323481400027
PM 23754238
ER
PT J
AU Xie, G
Roshandel, D
Sherva, R
Monach, PA
Lu, EY
Kung, T
Carrington, K
Zhang, SS
Pulit, SL
Ripke, S
Carette, S
Dellaripa, PF
Edberg, JC
Hoffman, GS
Khalidi, N
Langford, CA
Mahr, AD
St Clair, EW
Seo, P
Specks, U
Spiera, RF
Stone, JH
Ytterberg, SR
Raychaudhuri, S
de Bakker, PIW
Farrer, LA
Amos, CI
Merkel, PA
Siminovitch, KA
AF Xie, Gang
Roshandel, Delnaz
Sherva, Richard
Monach, Paul A.
Lu, Emily Yue
Kung, Tabitha
Carrington, Keisha
Zhang, Steven S.
Pulit, Sara L.
Ripke, Stephan
Carette, Simon
Dellaripa, Paul F.
Edberg, Jeffrey C.
Hoffman, Gary S.
Khalidi, Nader
Langford, Carol A.
Mahr, Alfred D.
St Clair, E. William
Seo, Philip
Specks, Ulrich
Spiera, Robert F.
Stone, John H.
Ytterberg, Steven R.
Raychaudhuri, Soumya
de Bakker, Paul I. W.
Farrer, Lindsay A.
Amos, Christopher I.
Merkel, Peter A.
Siminovitch, Katherine A.
TI Association of Granulomatosis With Polyangiitis (Wegener's) With
HLA-DPB1*04 and SEMA6A Gene Variants: Evidence Grom Genome-Wide Analysis
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID COPY NUMBER VARIATION; RHEUMATOID-ARTHRITIS; SYSTEMIC VASCULITIS;
CHROMOSOME 6P21.3; INTERFERON-GAMMA; POLYMORPHISMS; RISK;
SUSCEPTIBILITY; SEMAPHORINS; DISEASE
AB Objective. To identify genetic determinants of granulomatosis with polyangiitis (Wegener's) (GPA).
Methods. We carried out a genome-wide association study (GWAS) of 492 GPA cases and 1,506 healthy controls (white subjects of European descent), followed by replication analysis of the most strongly associated signals in an independent cohort of 528 GPA cases and 1,228 controls.
Results. Genome-wide significant associations were identified in 32 single-nucleotide polymorphic (SNP) markers across the HLA region, the majority of which were located in the HLA-DPB1 and HLA-DPA1 genes encoding the class II major histocompatibility complex (MHC) DP chain 1 and DP chain 1 proteins, respectively. Peak association signals in these 2 genes, emanating from SNPs rs9277554 (for DP chain 1) and rs9277341 (DP chain 1) were strongly replicated in an independent cohort (in the combined analysis of the initial cohort and the replication cohort, P = 1.92 x 10(-50) and 2.18 x 10(-39), respectively). Imputation of classic HLA alleles and conditional analyses revealed that the SNP association signal was fully accounted for by the classic HLA-DPB1*04 allele. An independent single SNP, rs26595, near SEMA6A (the gene for semaphorin 6A) on chromosome 5, was also associated with GPA, reaching genome-wide significance in a combined analysis of the GWAS and replication cohorts (P = 2.09 x 10(-8)).
Conclusion. We identified the SEMA6A and HLA-DP loci as significant contributors to risk for GPA, with the HLA-DPB1*04 allele almost completely accounting for the MHC association. These two associations confirm the critical role of immunogenetic factors in the development of GPA.
C1 [Xie, Gang; Roshandel, Delnaz; Kung, Tabitha; Carrington, Keisha; Zhang, Steven S.; Carette, Simon] Mt Sinai Hosp, Toronto, ON M5G 1X5, Canada.
[Xie, Gang; Roshandel, Delnaz; Kung, Tabitha; Carrington, Keisha; Zhang, Steven S.; Carette, Simon; Siminovitch, Katherine A.] Univ Toronto, Toronto, ON, Canada.
[Sherva, Richard; Monach, Paul A.; Farrer, Lindsay A.; Merkel, Peter A.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Lu, Emily Yue; Amos, Christopher I.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Pulit, Sara L.; Dellaripa, Paul F.; de Bakker, Paul I. W.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Pulit, Sara L.; de Bakker, Paul I. W.] Broad Inst, Boston, MA USA.
[Pulit, Sara L.; de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Utrecht, Netherlands.
[Ripke, Stephan; Stone, John H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Edberg, Jeffrey C.] Univ Alabama Birmingham, Birmingham, AL USA.
[Hoffman, Gary S.; Langford, Carol A.] Cleveland Clin, Cleveland, OH 44106 USA.
[Khalidi, Nader] McMaster Univ, Hamilton, ON, Canada.
[Mahr, Alfred D.] Hop St Louis, Paris, France.
[Mahr, Alfred D.] Univ Paris 07, Paris, France.
[St Clair, E. William] Duke Univ, Med Ctr, Durham, NC USA.
[Seo, Philip] Johns Hopkins Univ, Baltimore, MD USA.
[Specks, Ulrich; Ytterberg, Steven R.] Mayo Clin, Rochester, MN USA.
[Spiera, Robert F.] Hosp Special Surg, New York, NY 10021 USA.
[Raychaudhuri, Soumya] Brigham & Womens Hosp, Broad Inst, Boston, MA 02115 USA.
[Raychaudhuri, Soumya] Partners Ctr Personalized Genet Med, Boston, MA USA.
[Raychaudhuri, Soumya] Univ Manchester, Manchester, Lancs, England.
[Amos, Christopher I.] Geisel Sch Med Dartmouth, Hanover, NH USA.
[Merkel, Peter A.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Siminovitch, Katherine A.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto Gen Res Inst, Toronto, ON M5G 1X5, Canada.
RP Siminovitch, KA (reprint author), Mt Sinai Hosp, 600 Univ Ave,Room 778D, Toronto, ON M5G 1X5, Canada.
EM ksimin@mshri.on.ca
RI de Bakker, Paul/B-8730-2009; Siminovitch, Katherine/K-1475-2013;
OI de Bakker, Paul/0000-0001-7735-7858; Farrer, Lindsay/0000-0001-5533-4225
FU Erna Baird Memorial Grant; Vasculitis Foundation Canada; Ontario
Research Fund [RE-01-061]; Vasculitis Foundation; Vasculitis Clinical
Research Consortium (NIH) [U54-RR-019497, U54-AR-47785, R01-AR-047799,
R01-AG025259]; Arthritis Foundation; Societe Nationale Francaise de
Medecine Interne; Netherlands Organization for Scientific Research;
Mid-Career Development Award in Clinical Investigation (NIH-National
Institute of Arthritis and Musculoskeletal and Skin Diseases)
[K24-AR-02224]; Sanofi-Aventis; Roche; Genentech
FX Supported by an Erna Baird Memorial Grant, the Vasculitis Foundation
Canada, the Ontario Research Fund (RE-01-061), the Vasculitis
Foundation, and the Vasculitis Clinical Research Consortium (NIH grants
U54-RR-019497, U54-AR-47785, R01-AR-047799, and R01-AG025259). Dr.
Monach's work was supported by the Arthritis Foundation. Dr. Mahr's work
was supported in part by a grant from the Societe Nationale Francaise de
Medecine Interne. Dr. de Bakker is recipient of a Vidi Award from The
Netherlands Organization for Scientific Research. Dr. Merkel's work was
supported by a Mid-Career Development Award in Clinical Investigation
(NIH-National Institute of Arthritis and Musculoskeletal and Skin
Diseases grant K24-AR-02224). Dr. Siminovitch is a Tier 1 Canada
Research Chair and the Sherman Family Chair in Genomic Medicine.; Dr.
Hoffman has received consulting fees, speaking fees, and/or honoraria
from Sanofi-Aventis, Roche, and Genentech (less than $10,000 each).
NR 51
TC 31
Z9 32
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD AUG
PY 2013
VL 65
IS 9
BP 2457
EP 2468
DI 10.1002/art.38036
PG 12
WC Rheumatology
SC Rheumatology
GA 205YR
UT WOS:000323481400029
PM 23740775
ER
PT J
AU Hicks, CW
Weinstein, M
Wakamatsu, M
Pulliam, S
Savitt, L
Bordeianou, L
AF Hicks, C. W.
Weinstein, M.
Wakamatsu, M.
Pulliam, S.
Savitt, L.
Bordeianou, L.
TI Are rectoceles the cause or the result of obstructed defaecation
syndrome? A prospective anorectal physiology study
SO COLORECTAL DISEASE
LA English
DT Article
DE Rectocele; obstructed defaecation syndrome; anorectal physiology
ID TRANSANAL RECTAL RESECTION; LONG-TERM OUTCOMES; FECAL INCONTINENCE;
PROLAPSE; INTUSSUSCEPTION; DEFECOGRAPHY; VOLUNTEERS; REPAIR; TRIAL
AB Aim To determine the relationship between obstructed defaecation syndrome (ODS) and rectoceles.
Method From December 2007 to November 2011, all female patients with ODS were prospectively evaluated with full interview, clinical examination and anorectal physiology testing. The characteristics of patients with and without rectoceles were compared, and logistic regression was utilized to identify factors predictive of patients having a rectocele beyond the introitus.
Results Of 239 patients with ODS, 90 (mean age: 52.3 +/- 1.7 years) had a rectocele. Patients with rectoceles (R+) had a similar prevalence of incomplete emptying compared with patients with no rectocele (R-) (P >= 0.21), but only R+ patients reported splinting with defaecation (36.7% vs 0%; P < 0.0001). Anorectal manometry measurements, including mean resting pressure, maximum resting pressure and maximum squeeze pressure, were similar between groups (P >= 0.12). There were also no significant differences in rectal compliance (maximum tolerated volume) or rectal sensitivity (volume of first sensation) (P >= 0.65). R+ patients had greater difficulty expelling a 60 cm 3 balloon (70.1% R+ patients vs 57.5% R- patients; P = 0.05), but the prevalence of pelvic floor dyssynergia, as quantified by nonrelaxation on electromyography (EMG) testing, was similar to that of R- patients (P = 0.49). Logistic regression suggested that only difficulty with balloon expulsion was associated with higher odds of having a rectocele (OR = 3.00; P = 0.002), whereas mean resting pressure, EMG nonrelaxation and symptoms of incomplete emptying were not (P >= 0.12).
Conclusion Rectoceles are not associated with an increased severity of ODS-type symptoms, anorectal abnormalities or pelvic floor dyssynergia in patients with ODS. This suggests that rectoceles may be the result, rather than the cause, of ODS.
C1 [Hicks, C. W.; Savitt, L.; Bordeianou, L.] Massachusetts Gen Hosp, Dept Surg, Pelv Floor Disorders Serv, Boston, MA 02114 USA.
[Hicks, C. W.] Johns Hopkins Univ Hosp, Dept Surg, Baltimore, MD 21287 USA.
[Weinstein, M.; Wakamatsu, M.; Pulliam, S.] Massachusetts Gen Hosp, Pelv Floor Disorders Serv, Dept Gynecol, Boston, MA 02114 USA.
RP Bordeianou, L (reprint author), Massachusetts Gen Hosp, Dept Surg, 15 Parkman St,ACC 460, Boston, MA 02114 USA.
EM lbordeianou@partners.org
NR 31
TC 12
Z9 15
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1462-8910
J9 COLORECTAL DIS
JI Colorectal Dis.
PD AUG
PY 2013
VL 15
IS 8
BP 993
EP 999
DI 10.1111/codi.12213
PG 7
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA 208KW
UT WOS:000323678700023
PM 23527537
ER
PT J
AU Ho, JE
Larson, MG
Vasan, RS
Ghorbani, A
Cheng, S
Rhee, EP
Florez, JC
Clish, CB
Gerszten, RE
Wang, TJ
AF Ho, Jennifer E.
Larson, Martin G.
Vasan, Ramachandran S.
Ghorbani, Anahita
Cheng, Susan
Rhee, Eugene P.
Florez, Jose C.
Clish, Clary B.
Gerszten, Robert E.
Wang, Thomas J.
TI Metabolite Profiles During Oral Glucose Challenge
SO DIABETES
LA English
DT Article
ID BILE-ACID SYNTHESIS; INSULIN SENSITIVITY; TOLERANCE TEST; PLASMA;
APPROPRIATE; RESISTANCE; INDUCTION; DIAGNOSIS; GLYCEMIA; DISEASE
AB To identify distinct biological pathways of glucose metabolism, we conducted a systematic evaluation of biochemical changes after an oral glucose tolerance test (OGTT) in a community-based population. Metabolic profiling was performed on 377 nondiabetic Framingham Offspring cohort participants (mean age 57 years, 42% women, BMI 30 kg/m(2)) before and after OGTT. Changes in metabolite levels were evaluated with paired Student t tests, cluster-based analyses, and multivariable linear regression to examine differences associated with insulin resistance. Of 110 metabolites tested, 91 significantly changed with OGTT (P <= 0.0005 for all). Amino acids, B-hydroxybutyrate, and tricarboxylic acid cycle intermediates decreased after OGTT, and glycolysis products increased, consistent with physiological insulin actions. Other pathways affected by OGTT included decreases in serotonin derivatives, urea cycle metabolites, and B vitamins. We also observed an increase in conjugated, and a decrease in unconjugated, bile acids. Changes in p-hydroxybutyrate, isoleucine, lactate, and pyridoxate were blunted in those with insulin resistance. Our findings demonstrate changes in 91 metabolites representing distinct biological pathways that are perturbed in response to an OGTT. We also identify metabolite responses that distinguish individuals with and without insulin resistance. These findings suggest that unique metabolic phenotypes can be unmasked by OGTT in the prediabetic state. Diabetes 62:2689-2698, 2013
C1 [Ho, Jennifer E.; Larson, Martin G.; Vasan, Ramachandran S.; Cheng, Susan; Wang, Thomas J.] Framingham Heart Study Natl Heart Lung & Blood In, Framingham, MA USA.
[Ho, Jennifer E.; Larson, Martin G.; Vasan, Ramachandran S.; Cheng, Susan; Wang, Thomas J.] Boston Univ, Sch Med, Framingham, MA USA.
[Ho, Jennifer E.] Boston Univ, Med Ctr, Dept Med, Cardiovasc Med Sect, Boston, MA USA.
[Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Vasan, Ramachandran S.] Boston Univ, Dept Med, Div Cardiol & Prevent Med, Boston, MA 02215 USA.
[Ghorbani, Anahita; Gerszten, Robert E.; Wang, Thomas J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiol Div,Dept Med, Boston, MA USA.
[Cheng, Susan] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiol, Boston, MA 02115 USA.
[Rhee, Eugene P.; Gerszten, Robert E.; Wang, Thomas J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiovasc Res Ctr, Boston, MA USA.
[Rhee, Eugene P.] Harvard Univ, Massachusetts Gen Hosp, Dept Med, Div Renal, Boston, MA 02115 USA.
[Rhee, Eugene P.; Clish, Clary B.; Gerszten, Robert E.] Broad Inst Massachusetts Inst Technol & Harvard U, Cambridge, MA USA.
[Florez, Jose C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Florez, Jose C.] Massachusetts Gen Hosp, Diabet Unit, Diabet Res Ctr, Boston, MA 02114 USA.
[Florez, Jose C.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Florez, Jose C.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Wang, TJ (reprint author), Framingham Heart Study Natl Heart Lung & Blood In, Framingham, MA USA.
EM tjwang@partners.org
OI Larson, Martin/0000-0002-9631-1254; Ho, Jennifer/0000-0002-7987-4768;
Ramachandran, Vasan/0000-0001-7357-5970
FU National Institutes of Health [NO1-HC-25195, R01-DK-HL-081572]; American
Heart Association; Leducq Foundation; Ellison Foundation
FX This work was supported by the National Institutes of Health
(NO1-HC-25195 and R01-DK-HL-081572), the American Heart Association, the
Leducq Foundation, and the Ellison Foundation.
NR 38
TC 49
Z9 49
U1 1
U2 21
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD AUG
PY 2013
VL 62
IS 8
BP 2689
EP 2698
DI 10.2337/db12-0754
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 191RU
UT WOS:000322431100014
PM 23382451
ER
PT J
AU Lessard, SJ
Rivas, DA
Alves-Wagner, AB
Hirshman, MF
Gallagher, IJ
Constantin-Teodosiu, D
Atkins, R
Greenhaff, PL
Qi, NR
Gustafsson, T
Fielding, RA
Timmons, JA
Britton, SL
Koch, LG
Goodyear, LJ
AF Lessard, Sarah J.
Rivas, Donato A.
Alves-Wagner, Ana B.
Hirshman, Michael F.
Gallagher, Iain J.
Constantin-Teodosiu, Dumitru
Atkins, Ryan
Greenhaff, Paul L.
Qi, Nathan R.
Gustafsson, Thomas
Fielding, Roger A.
Timmons, James A.
Britton, Steven L.
Koch, Lauren G.
Goodyear, Laurie J.
TI Resistance to Aerobic Exercise Training Causes Metabolic Dysfunction and
Reveals Novel Exercise-Regulated Signaling Networks
SO DIABETES
LA English
DT Article
ID ALL-CAUSE MORTALITY; PROTEIN-KINASE-II; SKELETAL-MUSCLE;
INSULIN-RESISTANCE; CARDIORESPIRATORY FITNESS; CARDIOVASCULAR-DISEASE;
ARTIFICIAL SELECTION; GENE-EXPRESSION; CAPACITY; RISK
AB Low aerobic exercise capacity is a risk factor for diabetes and a strong predictor of mortality, yet some individuals are "exercise-resistant" and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease risk, we used selective breeding for 15 generations to develop rat models of low and high aerobic response to training. Before exercise training, rats selected as low and high responders had similar exercise capacities. However, after 8 weeks of treadmill training, low responders failed to improve their exercise capacity, whereas high responders improved by 54%. Remarkably, low responders to aerobic training exhibited pronounced metabolic dysfunction characterized by insulin resistance and increased adiposity, demonstrating that the exercise-resistant phenotype segregates with disease risk. Low responders had impaired exercise-induced angiogenesis in muscle; however, mitochondrial capacity was intact and increased normally with exercise training, demonstrating that mitochondria are not limiting for aerobic adaptation or responsible for metabolic dysfunction in low responders. Low responders had increased stress/inflammatory signaling and altered transforming growth factor-8 signaling, characterized by hyperphosphorylation of a novel exercise-regulated phosphorylation site on SMAD2. Using this powerful biological model system, we have discovered key pathways for low exercise training response that may represent novel targets for the treatment of metabolic disease. Diabetes 62:2717-2727, 2013
C1 [Lessard, Sarah J.; Alves-Wagner, Ana B.; Hirshman, Michael F.; Goodyear, Laurie J.] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Rivas, Donato A.; Fielding, Roger A.] Tufts Univ, Human Nutr Res Ctr Aging, Jean Mayer US Dept Agr, Boston, MA 02111 USA.
[Gallagher, Iain J.] Univ Stirling, Stirling FK9 4LA, Scotland.
[Constantin-Teodosiu, Dumitru; Atkins, Ryan; Greenhaff, Paul L.] Univ Nottingham, Nottingham NG7 2RD, England.
[Qi, Nathan R.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Gustafsson, Thomas; Timmons, James A.] Karolinska Inst, Huddinge, Sweden.
[Timmons, James A.] Univ Loughborough, Loughborough, Leics, England.
[Britton, Steven L.; Koch, Lauren G.] Univ Michigan, Dept Anesthesiol, Ann Arbor, MI 48109 USA.
RP Goodyear, LJ (reprint author), Joslin Diabet Ctr, Boston, MA 02215 USA.
EM laurie.goodyear@joslin.harvard.edu
RI Alves Wagner, Ana Barbara/E-4556-2013; Timmons, James/J-4698-2014;
OI Alves Wagner, Ana Barbara/0000-0002-3070-9454; Timmons,
James/0000-0002-2255-1220; Gustafsson, Thomas/0000-0002-1559-4206;
Rivas, Donato/0000-0002-4500-6233
FU National Institutes of Health [RO1AR042238, DK068626, RO1 DK077200];
Diabetes Research Center [5P30 DK 36836, DK089503]; Department of
Anesthesiology, University of Michigan Medical School, Michigan Diabetes
Research and Training Center [NIH5P60 DK20572-P/FS]; National Center for
Research Resources [R24 RR017718]; Office of Research Infrastructure
Programs/OD grant from the National Institutes of Health [ROD012098A];
FP7 EU grant; Wallenberg Foundation, Sweden; United States Department of
Agriculture [58-1950-0-014]; Boston Claude D. Pepper Older Americans
Independence Center [1P30AG031679]; American Physiological Society
(Physiological Genomics); Canadian Diabetes Association
FX This work was supported by National Institutes of Health grants
RO1AR042238 and DK068626 (L.J.G.) and by Diabetes Research Center 5P30
DK 36836 (Joslin Diabetes Center) and DK089503 (University of Michigan).
The HRT and LRT rat models are supported by the Department of
Anesthesiology, University of Michigan Medical School, Michigan Diabetes
Research and Training Center (NIH5P60 DK20572-P/FS; L.G.K.), National
Center for Research Resources (R24 RR017718; L.G.K. and S.L.B.), and
current support by Office of Research Infrastructure Programs/OD grant
(ROD012098A) from the National Institutes of Health (L.G.K. and S.L.B.).
This work also was supported by FP7 EU grant (J.A.T., T.G., and P.L.G.;
METAPREDICT) and a grant from the Wallenberg Foundation, Sweden (T.G.).;
S.L.B. was supported by National Institutes of Health grant RO1
DK077200. R.A.F. is supported by the United States Department of
Agriculture under agreement 58-1950-0-014. D.A.R. is supported by the
Boston Claude D. Pepper Older Americans Independence Center
(1P30AG031679). S.J.L. is supported by postdoctoral fellowships from the
American Physiological Society (Physiological Genomics) and the Canadian
Diabetes Association.
NR 58
TC 18
Z9 18
U1 1
U2 24
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD AUG
PY 2013
VL 62
IS 8
BP 2717
EP 2727
DI 10.2337/db13-0062
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 191RU
UT WOS:000322431100017
PM 23610057
ER
PT J
AU Richardson, P
Lokhorst, H
Palumbo, A
Nahi, H
Laubach, J
Gimsing, P
Lisby, S
Cakana, A
Brun, NC
Plesner, T
AF Richardson, P.
Lokhorst, H.
Palumbo, A.
Nahi, H.
Laubach, J.
Gimsing, P.
Lisby, S.
Cakana, A.
Brun, N. Constantin
Plesner, T.
TI DARATUMUMAB Anti-CD38 Monoclonal Antibody, Treatment of Multiple Myeloma
SO DRUGS OF THE FUTURE
LA English
DT Article
DE Transmembrane glycoprotein; Immunotherapy; Multiple myeloma; Daratumumab
ID IMMUNOMODULATORY DRUGS IMIDS; HUMAN CD38; PROTEASOME INHIBITORS;
TREATMENT STRATEGIES; THERAPY; IMMUNOTHERAPY; SURVIVAL; LENALIDOMIDE;
COMBINATION; BORTEZOMIB
AB CD38 is a type II transmembrane glycoprotein that is highly expressed in hematological malignancies, including multiple myeloma (MM). Therefore, CD38 is a promising target for antibody immunotherapy. Daratumumab is a human monoclonal antibody with broad-spectrum killing activity. In vitro, daratumumab induces anti-MM effects via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis. Synergistic activity was demonstrated in vitro in combination with standard MM therapies, including bortezomib and lenalidomide. Protective bone marrow stromal cells did not influence daratumumab-induced CDC and ADCC, suggesting that daratumumab may have activity in the bone marrow microenvironment in vivo. Indeed, significant daratumumab-mediated tumor growth inhibition was shown in MM mouse xenograft models. A phase I/II clinical study is ongoing in patients with relapsed/refractory MM. This review discusses the preclinical pharmacology, pharmacokinetics and preliminary clinical efficacy of daratumumab and its potential in MM therapy.
C1 [Richardson, P.; Laubach, J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Lokhorst, H.] Univ Med Ctr, Utrecht, Netherlands.
[Palumbo, A.] Univ Turin, Turin, Italy.
[Nahi, H.] Karolinska Inst, Stockholm, Sweden.
[Gimsing, P.] Copenhagen Univ Hosp, Copenhagen, Denmark.
[Lisby, S.; Brun, N. Constantin] Genmab AS, Copenhagen, Denmark.
[Cakana, A.] Janssen Res & Dev, High Wycombe, Bucks, England.
[Plesner, T.] Vejle Hosp, Vejle, Denmark.
RP Richardson, P (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA.
EM paul_richardson@dfci.harvard.edu
OI nahi, hareth/0000-0003-4711-5094
FU Genmab
FX The authors gratefully acknowledge the writing support of Steve Hill, of
FireKite, which was funded by Genmab, in the preparation of this
manuscript. The authors also gratefully acknowledge the administrative
assistance of Michelle Maglio and Vibeke Leth.
NR 69
TC 0
Z9 0
U1 0
U2 9
PU PROUS SCIENCE, SAU-THOMSON REUTERS
PI BARCELONA
PA 398 PROVENCA, 08025 BARCELONA, SPAIN
SN 0377-8282
J9 DRUG FUTURE
JI Drug Future
PD AUG
PY 2013
VL 38
IS 8
BP 545
EP 554
DI 10.1358/dof.2013.38.8.2025424
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 208KT
UT WOS:000323678300002
ER
PT J
AU Perkins, PS
Slane, JD
Klump, KL
AF Perkins, Patrick Scott
Slane, Jennifer D.
Klump, Kelly L.
TI Personality clusters and family relationships in women with disordered
eating symptoms
SO EATING BEHAVIORS
LA English
DT Article
DE Personality clusters; Family relationships; Disordered eating
ID PARENTAL-BONDING INSTRUMENT; BEHAVIORAL RISK-FACTORS; ANOREXIA-NERVOSA;
BULIMIA-NERVOSA; STRUCTURAL-ANALYSIS; ADOLESCENT GIRLS;
SOCIAL-ADJUSTMENT; SELF-REPORT; DSM-IV; SUBTYPES
AB Personality clusters in women with eating disorders predict important clinical variables (e.g., social functioning) better than eating disorder diagnoses. However, it is unknown whether these findings generalize to samples with subclinical pathology. Further, little is known about associations between personality clusters and family relationships. This study sought to address these limitations by replicating personality clusters in a college sample of women with disordered eating symptoms Based on reported symptoms, women were divided into a restricting, binging and purging, or control (i.e., symptom free) group. Participants completed measures of personality, social functioning, and family relationships. Cluster analyses suggested three personality groups (i.e., Adaptive, Rigid, Dysregulated) which corresponded to those identified previously in clinical samples. Personality clusters, and not disordered eating groups, significantly predicted social functioning, and these clusters were differentially associated with family conflict type. Meaningful personality clusters are present in subclinical populations and have clinical utility in predicting social functioning and family relationships. Published by Elsevier Ltd.
C1 [Perkins, Patrick Scott] Weill Cornell Med Coll, Dept Psychiat, New York, NY USA.
[Slane, Jennifer D.] VA Pittsburgh Healthcare Syst, VISN Mental Illness Res Educ & Clin Ctr 4, Pittsburgh, PA USA.
[Slane, Jennifer D.] Univ Pittsburgh, Dept Psychiat, Med Ctr, Pittsburgh, PA USA.
[Klump, Kelly L.] Michigan State Univ, Dept Psychol, E Lansing, MI 48824 USA.
RP Slane, JD (reprint author), 7180 Highland Dr,Suite 201N,Bldg 4,2nd Floor, Pittsburgh, PA 15206 USA.
EM jennifer.slane@va.gov
NR 71
TC 4
Z9 5
U1 1
U2 20
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1471-0153
EI 1873-7358
J9 EAT BEHAV
JI Eat. Behav.
PD AUG
PY 2013
VL 14
IS 3
BP 299
EP 308
DI 10.1016/j.eatbeh.2013.05.007
PG 10
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 207GK
UT WOS:000323586700012
PM 23910771
ER
PT J
AU Popa, SM
Moriyama, RM
Caligioni, CS
Yang, JJ
Cho, CM
Concepcion, TL
Oakley, AE
Lee, IH
Sanz, E
Amieux, PS
Caraty, A
Palmiter, RD
Navarro, VM
Chan, YM
Seminara, SB
Clifton, DK
Steiner, RA
AF Popa, Simina M.
Moriyama, Ryutaro M.
Caligioni, Claudia S.
Yang, Jasmine J.
Cho, Caroline M.
Concepcion, Tessa L.
Oakley, Amy E.
Lee, In Hae
Sanz, Elisenda
Amieux, Paul S.
Caraty, Alain
Palmiter, Richard D.
Navarro, Victor M.
Chan, Yee-Ming
Seminara, Stephanie B.
Clifton, Donald K.
Steiner, Robert A.
TI Redundancy in Kiss1 Expression Safeguards Reproduction in the Mouse
SO ENDOCRINOLOGY
LA English
DT Article
ID LUTEINIZING-HORMONE SURGE; ARCUATE NUCLEUS; NEUROKININ B; HYPOTHALAMIC
NOREPINEPHRINE; GONADOTROPIN-SECRETION; MESSENGER-RNA; BRAIN GRAFTS;
BODY-WEIGHT; FEMALE RATS; NEURONS
AB Kisspeptin (Kiss1) signaling to GnRH neurons is widely acknowledged to be a prerequisite for puberty and reproduction. Animals lacking functional genes for either kisspeptin or its receptor exhibit low gonadotropin secretion and infertility. Paradoxically, a recent study reported that genetic ablation of nearly all Kiss1-expressing neurons (Kiss1 neurons) does not impair reproduction, arguing that neither Kiss1 neurons nor their products are essential for sexual maturation. We posited that only minute quantities of kisspeptin are sufficient to support reproduction. If this were the case, animals having dramatically reduced Kiss1 expression might retain fertility, testifying to the redundancy of Kiss1 neurons and their products. To test this hypothesis and to determine whether males and females differ in the required amount of kisspeptin needed for reproduction, we used a mouse (Kiss1-CreGFP) that has a severe reduction in Kiss1 expression. Mice that are heterozygous and homozygous for this allele (Kiss1(Cre/+) and Kiss1(Cre/Cre)) have similar to 50% and 95% reductions in Kiss1 transcript, respectively. We found that although male Kiss1(Cre/Cre) mice sire normal-sized litters, female Kiss1(Cre/Cre) mice exhibit significantly impaired fertility and ovulation. These observations suggest that males require only 5% of normal Kiss1 expression to be reproductively competent, whereas females require higher levels for reproductive success.
C1 [Popa, Simina M.] Univ Washington, Mol & Cellular Biol Program, Seattle, WA 98195 USA.
[Popa, Simina M.; Moriyama, Ryutaro M.; Cho, Caroline M.; Concepcion, Tessa L.; Lee, In Hae; Clifton, Donald K.; Steiner, Robert A.] Univ Washington, Dept Obstet & Gynecol, Seattle, WA 98195 USA.
[Oakley, Amy E.; Steiner, Robert A.] Univ Washington, Dept Physiol & Biophys, Seattle, WA 98195 USA.
[Sanz, Elisenda; Amieux, Paul S.] Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA.
[Palmiter, Richard D.] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
[Palmiter, Richard D.] Univ Washington, Howard Hughes Med Inst, Seattle, WA 98195 USA.
[Moriyama, Ryutaro M.] Kinki Univ, Dept Life Sci, Higashiosaka, Osaka 5778502, Japan.
[Caligioni, Claudia S.; Yang, Jasmine J.; Chan, Yee-Ming; Seminara, Stephanie B.] Massachusetts Gen Hosp, Dept Med, Harvard Reprod Sci Ctr, Boston, MA 02114 USA.
[Caligioni, Claudia S.; Yang, Jasmine J.; Chan, Yee-Ming; Seminara, Stephanie B.] Massachusetts Gen Hosp, Dept Med, Reprod Endocrine Unit, Boston, MA 02114 USA.
[Chan, Yee-Ming] Boston Childrens Hosp, Dept Med, Div Endocrinol, Boston, MA 02115 USA.
[Navarro, Victor M.] Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Caraty, Alain] Univ Tours, Haras Nationaux, CNRS, INRA,UMR 6175, F-37380 Nouzilly, France.
RP Steiner, RA (reprint author), Univ Washington, Dept Physiol & Biophys, Box 357290, Seattle, WA 98195 USA.
EM steiner@uw.edu
RI Sanz, Elisenda/I-2765-2015
OI Sanz, Elisenda/0000-0002-7932-8556
FU National Institutes of Health (NIH) [2 R01 HD049651, U54 HD028138]; JSPS
KAKENHI [23780282]; Developmental Biology Training Grant at the
University of Washington [NIH T32HD007183]; Eunice Kennedy Shriver
National Institute of Child Health and Human Development/NIH
(Specialized Cooperative Centers Program in Reproduction and Infertility
Research) [U54-HD28934]
FX This research was supported by National Institutes of Health (NIH) Grant
2 R01 HD049651 (to R.A.S.), U54 HD028138 (to S.B.S.), and JSPS KAKENHI
23780282 (to R.M.M.). We acknowledge support from the Developmental
Biology Training Grant at the University of Washington (NIH
T32HD007183). We are grateful to the University of Virginia Center for
Research in Reproduction Ligand Assay and Analysis Core (supported by
the Eunice Kennedy Shriver National Institute of Child Health and Human
Development/NIH (Specialized Cooperative Centers Program in Reproduction
and Infertility Research) Grant U54-HD28934)
NR 39
TC 25
Z9 25
U1 0
U2 13
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 2013
VL 154
IS 8
BP 2784
EP 2794
DI 10.1210/en.2013-1222
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 186SC
UT WOS:000322063900024
PM 23736293
ER
PT J
AU Ananthakrishnan, AN
AF Ananthakrishnan, Ashwin N.
TI Personalizing therapy for inflammatory bowel diseases
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE biologics; Crohn's disease; genetics; serology; ulcerative colitis
ID POPULATION-BASED COHORT; POSTOPERATIVE CROHNS-DISEASE; POUCH-ANAL
ANASTOMOSIS; ANTINEUTROPHIL CYTOPLASMIC ANTIBODY; ULCERATIVE-COLITIS
PATIENTS; NATURAL-HISTORY; SEROLOGICAL MARKERS; INFLIXIMAB THERAPY;
CLINICAL-COURSE; HOSPITALIZATION RATES
AB Inflammatory bowel diseases (IBDs; e.g., Crohn's disease [CD] and ulcerative colitis [UC]) are chronic immunologically mediated diseases characterized by frequent relapses, often requiring hospitalization and surgery. There is substantial heterogeneity in the progressive natural history of disease with cumulative accrual of bowel damage and impairment of functioning. Recent advances in therapeutics have significantly improved our ability to achieve disease remission; yet therapies remain expensive and are associated with significant side effects precluding widespread use in all patients with IBD. Consequently, algorithms for the management of patients with IBD require a personalized approach incorporating an individual's projected likely natural history, the probability of response to a specific therapeutic agent and an informed approach to management of loss of response to current therapies.
C1 [Ananthakrishnan, Ashwin N.] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Ananthakrishnan, Ashwin N.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Ananthakrishnan, AN (reprint author), Massachusetts Gen Hosp, Div Gastroenterol, 165 Cambridge St,9th Floor, Boston, MA 02114 USA.
EM aananthakrishnan@partners.org
FU US National Institutes of Health [K23 DK097142]
FX AN Ananthakrishnan is supported by funding from the US National
Institutes of Health (K23 DK097142). The author has served on the
scientific advisory boards for Prometheus, Inc. and Janssen, Inc. The
authors have no other relevant affiliations or financial involvement
with any organization or entity with a financial interest in or
financial conflict with the subject matter or materials discussed in the
manuscript apart from those disclosed.
NR 113
TC 5
Z9 5
U1 0
U2 8
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD AUG
PY 2013
VL 7
IS 6
BP 549
EP 558
DI 10.1586/17474124.2013.824693
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 208CE
UT WOS:000323652800010
PM 23985004
ER
PT J
AU Ring, D
AF Ring, David
TI Symptoms and Disability After Major Peripheral Nerve Injury
SO HAND CLINICS
LA English
DT Article
DE Peripheral nerve injury; Coping strategy; Cognitive behavioral therapy;
symptoms; Disability
ID QUALITY-OF-LIFE; COLD INTOLERANCE; PATIENT SATISFACTION; HAND INJURIES;
PAIN; SENSITIVITY; DEPRESSION; PREDICTORS; TRANSFERS
AB Laceration and irrecoverable stretch, crush, or avulsion of a major peripheral nerve in the upper extremity causes substantial impairment in an adult patient. Hand care professionals who treat these patients encounter a wide range of coping strategies leading to varied courses of recovery and strikingly different final outcomes. There is evidence that the cognitive, emotional, and behavioral aspects of recovery (not to mention the circumstantial aspects such as worker compensation and litigation) are as important as the physical aspects. Awareness of the factors that facilitate or hinder these aspects of recovery might improve the quality and effectiveness of our care.
C1 Massachusetts Gen Hosp, MGH Hand Serv, Boston, MA 02114 USA.
RP Ring, D (reprint author), Massachusetts Gen Hosp, MGH Hand Serv, Yawkey 2100,55 Fruit St, Boston, MA 02114 USA.
EM dring@partners.org
NR 15
TC 1
Z9 3
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 2013
VL 29
IS 3
BP 421
EP +
DI 10.1016/j.hcl.2013.04.008
PG 6
WC Orthopedics
SC Orthopedics
GA 207TR
UT WOS:000323627800011
PM 23895722
ER
PT J
AU Fisher, DE
Geller, AC
AF Fisher, David E.
Geller, Alan C.
TI Disproportionate Burden of Melanoma Mortality in Young US Men The
Possible Role of Biology and Behavior
SO JAMA DERMATOLOGY
LA English
DT Editorial Material
ID UNITED-STATES
C1 [Fisher, David E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol, Boston, MA 02114 USA.
[Geller, Alan C.] Harvard Univ, Massachusetts Gen Hosp, Sch Publ Hlth, Dept Social & Behav Sci, Boston, MA 02114 USA.
RP Fisher, DE (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol, Bartlett Hall,55 Fruit St, Boston, MA 02114 USA.
EM dfisher3@partners.org
NR 5
TC 7
Z9 7
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6068
J9 JAMA DERMATOL
JI JAMA Dermatol.
PD AUG
PY 2013
VL 149
IS 8
BP 903
EP 904
DI 10.1001/jamadermatol.2013.4437
PG 2
WC Dermatology
SC Dermatology
GA 208ZH
UT WOS:000323721400003
PM 23804228
ER
PT J
AU Strazzula, L
Nigwekar, SU
Steele, D
Tsiaras, W
Sise, M
Bis, S
Smith, GP
Kroshinsky, D
AF Strazzula, Lauren
Nigwekar, Sagar U.
Steele, David
Tsiaras, William
Sise, Meghan
Bis, Sabina
Smith, Gideon P.
Kroshinsky, Daniela
TI Intralesional Sodium Thiosulfate for the Treatment of Calciphylaxis
SO JAMA DERMATOLOGY
LA English
DT Article
ID CALCIFIC UREMIC ARTERIOLOPATHY; THERAPY; PATIENT
AB IMPORTANCE Calciphylaxis is a potentially fatal disorder of abnormal calcium deposition. Patients commonly present with painful retiform to stellate purpuric lesions that often undergo ulceration and necrosis, increasing the risk of infection and life-threatening sepsis. Treatment is multifaceted, and improved outcomes have been demonstrated with intravenous sodium thiosulfate; however, the use of this medication can be limited by its adverse effects. The use of topical sodium thiosulfate has been successfully reported for superficial calcium deposits in the skin from other processes. Therefore, we hypothesized that intralesional (IL) sodium thiosulfate may be an effective treatment for the deeper lesions of cutaneous calciphylaxis. We provide a retrospective case review of 4 patients with calciphylaxis who were treated with IL sodium thiosulfate.
OBSERVATIONS Four patients with biopsy-proven cutaneous calciphylaxis were treated with IL sodium thiosulfate (250 mg/mL) in areas of clinically active disease. The patients tolerated the medication well, with only transient localized discomfort during injection. All 4 patients had complete healing of their ulcers and remission of disease.
CONCLUSIONS AND RELEVANCE Intralesional sodium thiosulfate may be an effective and well-tolerated treatment for localized calciphylaxis. This novel approach requires further research and investigation.
C1 [Strazzula, Lauren; Tsiaras, William; Bis, Sabina; Smith, Gideon P.; Kroshinsky, Daniela] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Nigwekar, Sagar U.; Steele, David] Massachusetts Gen Hosp, Dept Nephrol, Boston, MA 02114 USA.
[Sise, Meghan] Massachusetts Gen Hosp, Dept Internal Med, Boston, MA 02114 USA.
RP Kroshinsky, D (reprint author), Massachusetts Gen Hosp, Dept Dermatol, 50 Staniford St, Boston, MA 02114 USA.
EM dkroshinsky@partners.org
OI Tsiaras, William/0000-0002-4080-4762
NR 14
TC 19
Z9 20
U1 1
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6068
J9 JAMA DERMATOL
JI JAMA Dermatol.
PD AUG
PY 2013
VL 149
IS 8
BP 946
EP 949
DI 10.1001/jamadermatol.2013.4565
PG 4
WC Dermatology
SC Dermatology
GA 208ZH
UT WOS:000323721400012
PM 23760631
ER
PT J
AU Blacker, D
AF Blacker, Deborah
TI Food for Thought
SO JAMA NEUROLOGY
LA English
DT Editorial Material
ID CARDIOVASCULAR-DISEASE; ALZHEIMERS-DISEASE; DEMENTIA
C1 [Blacker, Deborah] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gerontol Res Unit,Dept Psychiat, Boston, MA USA.
[Blacker, Deborah] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
RP Blacker, D (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Gerontol Res Unit, 149 13th St, Charlestown, MA 02129 USA.
EM blacker@psych.mgh.harvard.edu
FU NIA NIH HHS [P50 AG005134-28, U01 AG032984-03, 1P01AG036694]; NINDS NIH
HHS [R01 NS062028-04]
NR 10
TC 0
Z9 0
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6149
J9 JAMA NEUROL
JI JAMA Neurol.
PD AUG
PY 2013
VL 70
IS 8
BP 967
EP 968
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 206ZO
UT WOS:000323565900002
PM 23779081
ER
PT J
AU Hanson, AJ
Bayer-Carter, JL
Green, PS
Montine, TJ
Wilkinson, CW
Baker, LD
Watson, S
Bonner, LM
Callaghan, M
Leverenz, JB
Tsai, E
Postupna, N
Zhang, J
Lampe, J
Craft, S
AF Hanson, Angela J.
Bayer-Carter, Jennifer L.
Green, Pattie S.
Montine, Thomas J.
Wilkinson, Charles W.
Baker, Laura D.
Watson, Stennis
Bonner, Laura M.
Callaghan, Maureen
Leverenz, James B.
Tsai, Elaine
Postupna, Nadia
Zhang, Jing
Lampe, Johanna
Craft, Suzanne
TI Effect of Apolipoprotein E Genotype and Diet on Apolipoprotein E
Lipidation and Amyloid Peptides Randomized Clinical Trial
SO JAMA NEUROLOGY
LA English
DT Article
ID A-BETA OLIGOMERS; SPORADIC ALZHEIMERS-DISEASE; MILD COGNITIVE
IMPAIRMENT; HIGH-DENSITY-LIPOPROTEIN; TRANSGENIC MOUSE MODEL;
CEREBROSPINAL-FLUID; INSULIN-RESISTANCE; BRAIN INSULIN;
DIABETES-MELLITUS; PRECURSOR PROTEIN
AB IMPORTANCE Sporadic Alzheimer disease (AD) is caused in part by decreased clearance of the beta-amyloid (A beta) peptide breakdown products. Lipid-depleted (LD) apolipoproteins are less effective at binding and clearing A beta, and LD A beta peptides are more toxic to neurons. However, not much is known about the lipid states of these proteins in human cerebrospinal fluid.
OBJECTIVE To characterize the lipidation states of A beta peptides and apolipoprotein E in the cerebrospinal fluid in adults with respect to cognitive diagnosis and APOE epsilon 4 allele carrier status and after a dietary intervention.
DESIGN Randomized clinical trial.
SETTING Veterans Affairs Medical Center clinical research unit.
PARTICIPANTS Twenty older adults with normal cognition (mean [SD] age, 69 [7] years) and 27 with amnestic mild cognitive impairment (67 [6] years).
INTERVENTIONS Randomization to a diet high in saturated fat content and with a high glycemic index (High diet; 45% of energy from fat [>25% saturated fat], 35%-40% from carbohydrates with a mean glycemic index >70, and 15%-20% from protein) or a diet low in saturated fat content and with a low glycemic index (Low diet; 25% of energy from fat [<7% saturated fat], 55%-60% from carbohydrates with a mean glycemic index <55, and 15%-20% from protein).
MAIN OUTCOMES AND MEASURES Lipid-depleted A beta 42 and A beta 40 and apolipoprotein E in cerebrospinal fluid.
RESULTS Baseline levels of LD A beta were greater for adults with mild cognitive impairment compared with adults with normal cognition (LD A beta 42, P =.05; LD A beta 40, P = .01). These findings were magnified in adults with mild cognitive impairment and the epsilon 4 allele, who had higher LD apolipoprotein E levels irrespective of cognitive diagnosis (P < .001). The Low diet tended to decrease LD A beta levels, whereas the High diet increased these fractions (LD A beta 42, P = .01; LD A beta 40, P = .15). Changes in LD A beta levels with the Low diet negatively correlated with changes in cerebrospinal fluid levels of insulin (LD A beta 42 and insulin, r = -0.68 [P = .01]; LD A beta 40 and insulin, r = -0.78 [P = .002]).
CONCLUSIONS AND RELEVANCE The lipidation states of apolipoproteins and A beta peptides in the brain differ depending on APOE genotype and cognitive diagnosis. Concentrations can be modulated by diet. These findings may provide insight into the mechanisms through which apolipoprotein E4 and unhealthy diets impart risk for developing AD.
C1 [Hanson, Angela J.; Bayer-Carter, Jennifer L.; Green, Pattie S.; Wilkinson, Charles W.; Baker, Laura D.; Watson, Stennis; Bonner, Laura M.; Callaghan, Maureen; Craft, Suzanne] Univ Washington, Sch Med, Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA USA.
[Montine, Thomas J.] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA.
[Leverenz, James B.] Univ Washington, Sch Med, Vet Affairs Puget Sound Hlth Care Syst, Educ & Clin Ctr,Dept Neurol, Seattle, WA USA.
[Hanson, Angela J.; Green, Pattie S.; Tsai, Elaine] Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA.
[Bayer-Carter, Jennifer L.; Wilkinson, Charles W.; Baker, Laura D.; Watson, Stennis; Bonner, Laura M.; Postupna, Nadia; Zhang, Jing; Craft, Suzanne] Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Leverenz, James B.; Lampe, Johanna] Univ Washington, Sch Med, Dept Neurol, Seattle, WA USA.
Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
RP Craft, S (reprint author), Wake Forest Univ, Sch Med, Dept Internal Med, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM suzcraft@wakehealth.edu
FU Hartford Center of Excellence scholarship; National Institute on Aging
[R37-AG-10880, P50 AG-05136]; Nancy and Buster Alvord Endowment;
Department of Veterans Affairs; [T32 AG-000258-13]
FX This study was supported by grant T32 AG-000258-13 and a Hartford Center
of Excellence scholarship (Dr Hanson); by grants R37-AG-10880 (Dr Craft)
and P50 AG-05136 (Dr Montine) from the National Institute on Aging; by
the Nancy and Buster Alvord Endowment; and by the Department of Veterans
Affairs.
NR 67
TC 22
Z9 23
U1 0
U2 14
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6149
EI 2168-6157
J9 JAMA NEUROL
JI JAMA Neurol.
PD AUG
PY 2013
VL 70
IS 8
BP 972
EP 980
DI 10.1001/jamaneurol.2013.396
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 206ZO
UT WOS:000323565900004
PM 23779114
ER
PT J
AU Falcone, GJ
Biffi, A
Brouwers, HB
Anderson, CD
Battey, TWK
Ayres, AM
Vashkevich, A
Schwab, K
Rost, NS
Goldstein, JN
Viswanathan, A
Greenberg, SM
Rosand, J
AF Falcone, Guido J.
Biffi, Alessandro
Brouwers, H. Bart
Anderson, Christopher D.
Battey, Thomas W. K.
Ayres, Alison M.
Vashkevich, Anastasia
Schwab, Kristin
Rost, Natalia S.
Goldstein, Joshua N.
Viswanathan, Anand
Greenberg, Steven M.
Rosand, Jonathan
TI Predictors of Hematoma Volume in Deep and Lobar Supratentorial
Intracerebral Hemorrhage
SO JAMA NEUROLOGY
LA English
DT Article
ID BLOOD-PRESSURE REDUCTION; ACTIVATED FACTOR-VII; EXPANSION; MORTALITY;
INTERACT; WARFARIN; GROWTH; TRIAL
AB IMPORTANCE Hematoma volume is the strongest predictor of outcome in intracerebral hemorrhage (ICH). Despite known differences in the underlying biology between deep and lobar ICHs, limited data are available on location specificity of factors reported to affect hematoma volume.
OBJECTIVE To evaluate whether determinants of ICH volume differ by topography, we sought to estimate location-specific effects for potential predictors of this radiological outcome.
DESIGN Prospective cohort study.
SETTING Academic medical center.
PARTICIPANTS A total of 744 supratentorial primary ICH patients (388 deep and 356 lobar) aged older than 18 years admitted between January 1, 2000, and December 31, 2010.
MAIN OUTCOMES AND MEASURES Intracerebral hemorrhage volume measured from the computed tomography scan obtained on presentation to the emergency department. Linear regression analysis, stratified by ICH location, was implemented to identify determinants of log-transformed ICH volume.
RESULTS Median ICH volume was larger in lobar hemorrhages (39 mL; interquartile range, 16-75 mL) than in deep hemorrhages (13 mL; interquartile range, 5-40 mL; P < .001). In multivariable linear regression, independent predictors of deep ICH volume were intensity of anticoagulation (beta = 0.32; standard error [SE] = 0.08; P < .001; test for trend across 4 categories of the international normalized ratio), history of coronary artery disease (beta = 0.33; SE = 0.17; P =.05), male sex (beta = 0.28; SE = 0.14; P =.05), and age (beta = -0.02; SE = 0.01; P = .001). Independent predictors of lobar ICH volume were intensity of anticoagulation (beta = 0.14; SE = 0.06; P = .02) and antiplatelet treatment (beta = 0.27; SE = 0.13; P = .03).
CONCLUSIONS AND RELEVANCE Predictors of hematoma volume only partially overlap between deep and lobar ICHs. These findings suggest that the mechanisms that determine the extent of bleeding differ for deep and lobar ICHs. Further studies are needed to characterize the specific biological pathways that underlie the observed associations.
C1 [Falcone, Guido J.; Biffi, Alessandro; Brouwers, H. Bart; Anderson, Christopher D.; Battey, Thomas W. K.; Rost, Natalia S.; Rosand, Jonathan] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Falcone, Guido J.; Biffi, Alessandro; Brouwers, H. Bart; Anderson, Christopher D.; Battey, Thomas W. K.; Ayres, Alison M.; Vashkevich, Anastasia; Schwab, Kristin; Rost, Natalia S.; Viswanathan, Anand; Greenberg, Steven M.; Rosand, Jonathan] Massachusetts Gen Hosp, Hemorrhag Stroke Res Grp, Boston, MA 02114 USA.
[Falcone, Guido J.; Biffi, Alessandro; Brouwers, H. Bart; Anderson, Christopher D.; Battey, Thomas W. K.; Rost, Natalia S.; Rosand, Jonathan] Massachusetts Gen Hosp, Dept Neurol, Div Neurocrit Care & Emergency Neurol, Boston, MA 02114 USA.
[Goldstein, Joshua N.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Falcone, Guido J.; Biffi, Alessandro; Brouwers, H. Bart; Anderson, Christopher D.; Battey, Thomas W. K.; Rost, Natalia S.; Rosand, Jonathan] Massachusetts Gen Hosp, Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Falcone, Guido J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
RP Rosand, J (reprint author), Massachusetts Gen Hosp, Ctr Human Genet Res, 185 Cambridge St,CPZN 6818, Boston, MA 02114 USA.
EM jrosand@partners.org
RI Goldstein, Joshua/H-8953-2016; Falcone, Guido/L-2287-2016;
OI Falcone, Guido/0000-0002-6407-0302; Ayres, Alison/0000-0002-5492-1695;
Anderson, Christopher/0000-0002-0053-2002
FU National Institutes of Health/National Institute of Neurological
Disorders and Stroke [R01NS073344, R01NS059727, 5K23NS059774]; American
Heart Association [0755984T]
FX This study was supported by grants R01NS073344, R01NS059727, and
5K23NS059774 from the National Institutes of Health/National Institute
of Neurological Disorders and Stroke and grant 0755984T from the
American Heart Association.
NR 21
TC 20
Z9 21
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6149
J9 JAMA NEUROL
JI JAMA Neurol.
PD AUG
PY 2013
VL 70
IS 8
BP 988
EP 994
DI 10.1001/jamaneurol.2013.98
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 206ZO
UT WOS:000323565900006
PM 23733000
ER
PT J
AU Diercks, GR
Ojha, S
Infusino, S
Maurer, R
Hartnick, CJ
AF Diercks, Gillian R.
Ojha, Shilpa
Infusino, Scott
Maurer, Rie
Hartnick, Christopher J.
TI Consistency of Voice Frequency and Perturbation Measures in Children
Using Cepstral Analyses A Movement Toward Increased Recording Stability
SO JAMA OTOLARYNGOLOGY-HEAD & NECK SURGERY
LA English
DT Article
ID CONTINUOUS SPEECH; DYSPHONIA SEVERITY; ACOUSTIC INDEX; DISORDERS;
DATABASE
AB IMPORTANCE Few studies have evaluated the pediatric voice objectively using acoustic measurements. Furthermore, consistency of these measurements across time, particularly for continuous speech, has not been evaluated.
OBJECTIVES (1) To evaluate normal pediatric voice frequency and perturbation using both time-based and frequency-based acoustic measurements, and (2) to determine if continuous speech samples facilitate increased recording stability.
DESIGN Prospective, longitudinal study.
SETTING Pediatric otolaryngology practice within a tertiary hospital.
PARTICIPANTS Forty-three children, ages 4 to 17 years.
INTERVENTION OR EXPOSURE Sustained vowel utterances and continuous speech samples, which included 4 Consensus Auditory-Perceptual Evaluation of Voice (CAPE-V) sentences and the first sentence of the "rainbow passage" ("A rainbow is a division of white light into many beautiful colors that takes the shape of a long round arch, with its path high above and its 2 ends apparently beyond the horizon") were obtained at 2 time points
MAIN OUTCOME AND MEASURE Intraclass correlation coefficients (ICCs) were calculated to assess reliability between speech samples.
RESULTS Fundamental frequency of sustained vowel utterances had excellent reliability (ICC >= 0.94). Time-based analyses of perturbation in sustained vowel utterances demonstrated poor reliability (ICC < 0.40), while frequency-based analyses of perturbation for these utterances demonstrated good to excellent reliability (ICC > 0.40). Fundamental frequency of continuous speech sample had excellent reliability (ICC > 0.94). Frequency-based analyses of continuous speech samples demonstrated excellent reliability (ICC > 0.75) for all but 1 variable, which demonstrated good reliability (cepstral-spectral index of dysphonia of the all voiced sample; ICC = 0.72).
CONCLUSIONS AND RELEVANCE Sustained vowel utterance and continuous speech samples provide consistent measures of fundamental frequency. Frequency-based analysis of sustained vowel recordings improves the reliability of perturbation measures. Continuous speech recordings can be obtained in children and demonstrate good to excellent reliability across recordings. This suggests that frequency-based analysis of continuous speech may be more representative of a child's voice and therefore may be of use in the study both of the developmental changes of the pediatric voice as well as the study of vocal changes pretreatment and posttreatment in children with voice disorders.
C1 [Diercks, Gillian R.; Ojha, Shilpa; Infusino, Scott; Hartnick, Christopher J.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otolaryngol Head & Neck Surg, Boston, MA 02114 USA.
[Maurer, Rie] Brigham & Womens Hosp, Ctr Clin Investigat, Boston, MA 02115 USA.
[Maurer, Rie] Harvard Clin & Translat Sci Ctr, Harvard Catalyst, Boston, MA USA.
RP Diercks, GR (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otolaryngol Head & Neck Surg, 243 Charles St, Boston, MA 02114 USA.
EM Gillian_Diercks@meei.harvard.edu
NR 21
TC 3
Z9 3
U1 1
U2 5
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6181
J9 JAMA OTOLARYNGOL
JI JAMA Otolaryngol-Head Neck Surg.
PD AUG
PY 2013
VL 139
IS 8
BP 811
EP 816
DI 10.1001/jamaoto.2013.3926
PG 6
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 206TM
UT WOS:000323545800009
PM 23949356
ER
PT J
AU Chambers, KJ
Sedaghat, AR
Roberts, DS
Caradonna, DS
AF Chambers, Kyle J.
Sedaghat, Ahmad R.
Roberts, Daniel S.
Caradonna, David S.
TI Nasal Obstruction and Anosmia Respiratory epithelial adenomatoid
hamartoma (REAH)
SO JAMA OTOLARYNGOLOGY-HEAD & NECK SURGERY
LA English
DT Editorial Material
ID OLFACTORY CLEFTS
C1 [Chambers, Kyle J.; Sedaghat, Ahmad R.; Roberts, Daniel S.] Massachusetts Eye & Ear Infirm, Dept Otolaryngol Head & Neck Surg, Boston, MA 02114 USA.
[Chambers, Kyle J.; Sedaghat, Ahmad R.; Roberts, Daniel S.; Caradonna, David S.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
[Caradonna, David S.] Beth Israel Deaconess Med Ctr, Div Otolaryngol Head & Neck Surg, Boston, MA 02215 USA.
RP Chambers, KJ (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, 243 Charles St, Boston, MA 02114 USA.
EM kyle_chambers@meei.harvard.edu
NR 8
TC 0
Z9 0
U1 1
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6181
J9 JAMA OTOLARYNGOL
JI JAMA Otolaryngol-Head Neck Surg.
PD AUG
PY 2013
VL 139
IS 8
BP 851
EP 852
DI 10.1001/jamaoto.2013.3823
PG 2
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 206TM
UT WOS:000323545800017
PM 23949364
ER
PT J
AU Taveras, EM
Gillman, MW
Kleinman, KP
Rich-Edwards, JW
Rifas-Shiman, SL
AF Taveras, Elsie M.
Gillman, Matthew W.
Kleinman, Ken P.
Rich-Edwards, Janet W.
Rifas-Shiman, Sheryl L.
TI Reducing Racial/Ethnic Disparities in Childhood Obesity The Role of
Early Life Risk Factors
SO JAMA PEDIATRICS
LA English
DT Article
ID BODY-MASS INDEX; INCOME PRESCHOOL-CHILDREN; US CHILDREN; BLOOD-PRESSURE;
WEIGHT-GAIN; SOCIOECONOMIC-STATUS; UNITED-STATES; OVERWEIGHT;
ADOLESCENTS; PREVALENCE
AB IMPORTANCE Many early life risk factors for childhood obesity are more prevalent among blacks and Hispanics than among whites and may explain the higher prevalence of obesity among racial/ethnic minority children.
OBJECTIVE To examine the extent to which racial/ethnic disparities in adiposity and overweight are explained by differences in risk factors during pregnancy (gestational diabetes and depression), infancy (rapid infant weight gain, feeding other than exclusive breastfeeding, and early introduction of solid foods), and early childhood (sleeping <12 h/d, presence of a television set in the room where the child sleeps, and any intake of sugar-sweetened beverages or fast food).
DESIGN Prospective prebirth cohort study.
SETTING Multisite group practice in Massachusetts.
PARTICIPANTS Participants included 1116 mother-child pairs (63% white, 17% black, and 4% Hispanic)
EXPOSURE Mother's report of child's race/ethnicity.
MAIN OUTCOMES AND MEASURES Age- and sex-specific body mass index (BMI) z score, total fat mass index from dual-energy x-ray absorptiometry, and overweight or obesity, defined as a BMI in the 85th percentile or higher at age 7 years.
RESULTS Black (0.48 U [95% CI, 0.31 to 0.64]) and Hispanic (0.43 [0.12 to 0.74]) children had higher BMI z scores, as well as higher total fat mass index and overweight/obesity prevalence, than white children. After adjustment for socioeconomic confounders and parental BMI, differences in BMI z score were attenuated for black and Hispanic children (0.22 U [0.05 to 0.40] and 0.22 U [-0.08 to 0.52], respectively). Adjustment for pregnancy risk factors did not substantially change these estimates. However, after further adjustment for infancy and childhood risk factors, we observed only minimal differences in BMI z scores between whites, blacks (0.07 U [-0.11 to 0.26]), and Hispanics (0.04 U [-0.27 to 0.35]). We observed similar attenuation of racial/ethnic differences in adiposity and prevalence of overweight or obesity.
CONCLUSIONS AND RELEVANCE Racial/ethnic disparities in childhood adiposity and obesity are determined by factors operating in infancy and early childhood. Efforts to reduce obesity disparities should focus on preventing early life risk factors.
C1 [Taveras, Elsie M.; Gillman, Matthew W.; Kleinman, Ken P.; Rifas-Shiman, Sheryl L.] Harvard Univ, Sch Med, Dept Populat Med, Obes Prevent Program, Boston, MA USA.
[Taveras, Elsie M.; Gillman, Matthew W.; Kleinman, Ken P.; Rifas-Shiman, Sheryl L.] Harvard Pilgrim Hlth Care Inst, Boston, MA USA.
[Taveras, Elsie M.] Boston Childrens Hosp, Div Gen Pediat, Boston, MA USA.
[Rich-Edwards, Janet W.] Brigham & Womens Hosp, Connors Ctr Womens Hlth & Gender Biol, Boston, MA 02115 USA.
RP Taveras, EM (reprint author), MassGen Hosp Children, Div Gen Pediat, 100 Cambridge St,15th Floor, Boston, MA 02114 USA.
EM etaveras@partners.org
FU National Institute on Minority Health and Health Disparities [MD 003963]
FX This study was supported by grant MD 003963 from the National Institute
on Minority Health and Health Disparities.
NR 53
TC 48
Z9 50
U1 7
U2 59
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6203
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD AUG
PY 2013
VL 167
IS 8
BP 731
EP 738
DI 10.1001/jamapediatrics.2013.85
PG 8
WC Pediatrics
SC Pediatrics
GA 206VE
UT WOS:000323551200010
PM 23733179
ER
PT J
AU Goel, S
Gupta, N
Walcott, BP
Snuderl, M
Kesler, CT
Kirkpatrick, ND
Heishi, T
Huang, YH
Martin, JD
Ager, E
Samuel, R
Wang, SH
Yazbek, J
Vakoc, BJ
Peterson, RT
Padera, TP
Duda, DG
Fukumura, D
Jain, RK
AF Goel, Shom
Gupta, Nisha
Walcott, Brian P.
Snuderl, Matija
Kesler, Cristina T.
Kirkpatrick, Nathaniel D.
Heishi, Takahiro
Huang, Yuhui
Martin, John D.
Ager, Eleanor
Samuel, Rekha
Wang, Shuhan
Yazbek, John
Vakoc, Benjamin J.
Peterson, Randall T.
Padera, Timothy P.
Duda, Dan G.
Fukumura, Dai
Jain, Rakesh K.
TI Effects of Vascular-Endothelial Protein Tyrosine Phosphatase Inhibition
on Breast Cancer Vasculature and Metastatic Progression
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID BLOOD-VESSEL DEVELOPMENT; TUMOR-GROWTH; OVEREXPRESSING ANGIOPOIETIN-1;
ANTIANGIOGENIC THERAPY; ANGIOGENESIS; NORMALIZATION; VEGF; SURVIVAL;
OXYGENATION; PERFUSION
AB The solid tumor microvasculature is characterized by structural and functional abnormality and mediates several deleterious aspects of tumor behavior. Here we determine the role of vascular endothelial protein tyrosine phosphatase (VE-PTP), which deactivates endothelial cell (EC) Tie-2 receptor tyrosine kinase, thereby impairing maturation of tumor vessels.
AKB-9778 is a first-in-class VE-PTP inhibitor. We examined its effects on ECs in vitro and on embryonic angiogenesis in vivo using zebrafish assays. We studied the impact of AKB-9778 therapy on the tumor vasculature, tumor growth, and metastatic progression using orthotopic models of murine mammary carcinoma as well as spontaneous and experimental metastasis models. Finally, we used endothelial nitric oxide synthase (eNOS)deficient mice to establish the role of eNOS in mediating the effects of VE-PTP inhibition. All statistical tests were two-sided.
AKB-9778 induced ligand-independent Tie-2 activation in ECs and impaired embryonic zebrafish angiogenesis. AKB-9778 delayed the early phase of mammary tumor growth by maintaining vascular maturity (P < .01, t test); slowed growth of micrometastases (P < .01, (2) test) by preventing extravasation of tumor cells (P < 0.01, Fisher exact test), resulting in a trend toward prolonged survival (27.0 vs 36.5 days; hazard ratio of death 0.33, 95% confidence interval 0.11 to 1.03; P .05, MantelCox test); and stabilized established primary tumor blood vessels, enhancing tumor perfusion (P .03 for 4T1 tumor model and 0.05 for E0771 tumor model, by two-sided t tests) and, hence, radiation response (P < .01, analysis of variance; n 7 mice per group). The effects of AKB-9778 on tumor vessels were mediated in part by endothelial nitric oxide synthase activation.
Our results demonstrate that pharmacological VE-PTP inhibition can normalize the structure and function of tumor vessels through Tie-2 activation, which delays tumor growth, slows metastatic progression, and enhances response to concomitant cytotoxic treatments.
C1 [Goel, Shom; Gupta, Nisha; Snuderl, Matija; Kesler, Cristina T.; Kirkpatrick, Nathaniel D.; Heishi, Takahiro; Huang, Yuhui; Martin, John D.; Ager, Eleanor; Samuel, Rekha; Padera, Timothy P.; Duda, Dan G.; Fukumura, Dai; Jain, Rakesh K.] Massachusetts Gen Hosp, Edwin L Steele Lab Tumor Biol, Dept Radiat Oncol, Boston, MA 02114 USA.
[Vakoc, Benjamin J.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Walcott, Brian P.; Peterson, Randall T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Walcott, Brian P.; Peterson, Randall T.] Harvard Univ, Sch Med, Charlestown, MA USA.
[Wang, Shuhan] MIT, Dept Biol, Cambridge, MA 02139 USA.
[Yazbek, John] MIT, Dept Chem Engn, Cambridge, MA 02139 USA.
RP Fukumura, D (reprint author), Massachusetts Gen Hosp, Edwin L Steele Lab Tumor Biol, Cox 7,100 Blossom St, Boston, MA 02114 USA.
EM dai@steele.mgh.harvard.edu; jain@steele.mgh.harvard.edu
RI Martin, John/L-6892-2016;
OI Martin, John/0000-0002-9828-8203; Ager, Eleanor/0000-0002-7849-9206;
Huang, Yuhui/0000-0003-1985-3575; Padera, Timothy/0000-0002-3453-9384;
Snuderl, Matija/0000-0003-0752-0917
FU NCI NIH HHS [R01 CA163528, 2K12CA090354-11, P01-CA080124, R00 CA137167,
R00-CA137167, R01-CA096915, R01-CA126642, R01-CA159258, R01-CA163528,
T32-CA073479]; NCRR NIH HHS [S10-RR027070]; NIBIB NIH HHS [P41 EB015903,
P41EB015903]; NIH HHS [DP2 OD008780, DP2OD008780]
NR 41
TC 27
Z9 28
U1 2
U2 18
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD AUG
PY 2013
VL 105
IS 16
BP 1188
EP 1201
DI 10.1093/jnci/djt164
PG 14
WC Oncology
SC Oncology
GA 207YR
UT WOS:000323641300008
PM 23899555
ER
PT J
AU Hasham, A
Zhang, WJ
Lotay, V
Haggerty, S
Stefan, M
Concepcion, E
Dieterich, DT
Tomer, Y
AF Hasham, Alia
Zhang, Weijia
Lotay, Vaneet
Haggerty, Shannon
Stefan, Mihaela
Concepcion, Erlinda
Dieterich, Douglas T.
Tomer, Yaron
TI Genetic analysis of interferon induced thyroiditis (IIT): Evidence for a
key role for MHC and apoptosis related genes and pathways
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Interferon; Thyroiditis; Autoimmunity; Thyroid
ID CHRONIC HEPATITIS-C; GRAVES-DISEASE; AUTOIMMUNITY; ALPHA; ASSOCIATION;
POPULATION; CELLS; TAP1; PML; POLYMORPHISMS
AB Autoimmune thyroid diseases (AITD) have become increasingly recognized as a complication of interferon-alpha (IFN alpha) therapy in patients with chronic Hepatitis C virus (HCV) infection. Interferon-induced thyroiditis (IIT) can manifest as clinical thyroiditis in approximately 15% of HCV patients receiving IFN alpha and subclinical thyroiditis in up to 40% of patients, possibly resulting in either dose reduction or discontinuation of IFN alpha treatment. However, the exact mechanisms that lead to the development of IIT are unknown and may include IFN alpha-mediated immune-recruitment as well as direct toxic effects on thyroid follicular cells. We hypothesized that IIT develops in genetically predisposed individuals whose threshold for developing thyroiditis is lowered by IFN alpha. Therefore, our aim was to identify the susceptibility genes for IIT. We used a genomic convergence approach combining genetic association data with transcriptome analysis of genes upregulated by IFN alpha. Integrating results of genetic association, transcriptome data, pathway, and haplotype analyses enabled the identification of 3 putative loci, SP100/110/140 (2q37.1), HLA (6p21.3), and TAP1 (6p21.3) that may be involved in the pathogenesis of IIT. Immune-regulation and apoptosis emerged as the predominant mechanisms underlying the etiology of IIT. (C) Published by Elsevier Ltd.
C1 [Hasham, Alia; Stefan, Mihaela; Concepcion, Erlinda; Tomer, Yaron] Mt Sinai Sch Med, Dept Med, Div Endocrinol, New York, NY USA.
[Hasham, Alia; Stefan, Mihaela; Tomer, Yaron] James J Peters VA Med Ctr, Bronx, NY USA.
[Zhang, Weijia; Lotay, Vaneet] Mt Sinai Sch Med, Dept Med Bioinformat Core, New York, NY USA.
[Haggerty, Shannon] Univ Cincinnati, Coll Med, Div Endocrinol, Cincinnati, OH USA.
[Dieterich, Douglas T.] Mt Sinai Sch Med, Dept Med, Div Liver Dis, New York, NY USA.
RP Tomer, Y (reprint author), Mt Sinai Med Ctr, Div Endocrinol, Box 1055,1 Gustave L Levy Pl, New York, NY 10029 USA.
EM Yaron.Tomer@mssm.edu
FU VA Merit award from Department of Veterans Affairs [1I01BX002031]; NIDDK
[DK61659, DK073681]
FX This work was supported in part by a VA Merit award 1I01BX002031 from
the Department of Veterans Affairs, and by grants DK61659, and DK073681
from NIDDK (to YT). We thank Dr. David A. Greenberg (Battelle Center for
Mathematical Medicine and Department of Neurology, Nationwide Children's
Hospital, Columbus, Ohio) for his suggestions and expert review of this
manuscript.
NR 39
TC 7
Z9 10
U1 3
U2 6
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 2013
VL 44
BP 61
EP 70
DI 10.1016/j.jaut.2013.04.002
PG 10
WC Immunology
SC Immunology
GA 208PJ
UT WOS:000323691300008
PM 23683877
ER
PT J
AU Benz, EJ
Nathan, DG
AF Benz, Edward J., Jr.
Nathan, David G.
TI A tribute to Emil Frei III Obituary
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Biographical-Item
C1 [Benz, Edward J., Jr.; Nathan, David G.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Benz, EJ (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM edward_benz@dfci.harvard.edu; David_Nathan@dfci.harvard.edu
NR 1
TC 0
Z9 0
U1 0
U2 2
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 2013
VL 123
IS 8
BP 3188
EP 3189
PG 2
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 196CH
UT WOS:000322750500002
ER
PT J
AU Richardson, A
AF Richardson, Arlan
TI Rapamycin, anti-aging, and avoiding the fate of Tithonus
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Editorial Material
ID EXTENDS LIFE-SPAN; GENETICALLY HETEROGENEOUS MICE; MAMMALIAN TARGET;
MTOR; INHIBITION
AB The discovery that rapamycin increased the lifespan of mice was recognized by Science as one of the top 10 scientific breakthroughs of 2009. In addition to increasing lifespan, Neff and colleagues show that while rapamycin improves several functions/pathologies that change with age, it has little effect on the majority of the physiological and structural parameters they evaluated. What do these data tell us about the ability of rapamycin to delay aging and improve quality of life, i.e., prevent the fate of Tithonus?
C1 [Richardson, Arlan] Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst Longev & Aging Studies, San Antonio, TX 78229 USA.
[Richardson, Arlan] South Texas Vet Hlth Care Syst, Geriatr Res Educ & Clin Ctr, San Antonio, TX USA.
RP Richardson, A (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM richardsona@uthscsa.edu
FU NIA NIH HHS [RC2 AG036613]
NR 23
TC 12
Z9 12
U1 0
U2 3
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 2013
VL 123
IS 8
BP 3204
EP 3206
DI 10.1172/JCI70800
PG 3
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 196CH
UT WOS:000322750500005
PM 24063054
ER
PT J
AU Woo, AJ
Wieland, K
Huang, H
Akie, TE
Piers, T
Kim, J
Cantor, AB
AF Woo, Andrew J.
Wieland, Karen
Huang, Hui
Akie, Thomas E.
Piers, Taylor
Kim, Jonghwan
Cantor, Alan B.
TI Developmental differences in IFN signaling affect GATA1s-induced
megakaryocyte hyperproliferation
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID ACUTE MEGAKARYOBLASTIC LEUKEMIA; TRANSIENT MYELOPROLIFERATIVE DISORDER;
RECOMBINANT INTERFERON-ALPHA; DOWN-SYNDROME; GATA1 MUTATIONS;
GENE-EXPRESSION; ACQUIRED MUTATIONS; MYELOID-LEUKEMIA; NATURAL-HISTORY;
MEGAKARYOPOIESIS
AB About 10% of Down syndrome (DS) infants are born with a transient myeloproliferative disorder (DS-TMD) that spontaneously resolves within the first few months of life. About 20%-30% of these infants subsequently develop acute megakaryoblastic leukemia (DS-AMKL). Somatic mutations leading to the exclusive production of a short GATA1 isoform (GATA1s) occur in all cases of DS-TMD and DS-AMKL. Mice engineered to exclusively produce GATA1s have marked megakaryocytic progenitor (MkP) hyperproliferation during early fetal liver (FL) hematopoiesis, but not during postnatal BM hematopoiesis, mirroring the spontaneous resolution of DS-TMD. The mechanisms that underlie these developmental stage-specific effects are incompletely understood. Here, we report a striking upregulation of type I IFN-responsive gene expression in prospectively isolated mouse BM- versus FL-derived MkPs. Exogenous IFN-alpha markedly reduced the hyperproliferation FL-derived MkPs of GATA1s mice in vitro. Conversely, deletion of the alpha/beta IFN receptor 1 (Ifnar1) gene or injection of neutralizing IFN-alpha/beta antibodies increased the proliferation of BM-derived MkPs of GATA1s mice beyond the initial postnatal period. We also found that these differences existed in human FL versus BM mega-karyocytes and that primary DS-TMD cells expressed type I IFN-responsive genes. We propose that increased type I IFN signaling contributes to the developmental stage-specific effects of GATA1s and possibly the spontaneous resolution of DS-TMD.
C1 [Woo, Andrew J.; Wieland, Karen; Huang, Hui; Akie, Thomas E.; Piers, Taylor; Cantor, Alan B.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Div Pediat Hematol Oncol,Boston Childrens Hosp, Boston, MA 02115 USA.
[Kim, Jonghwan] Univ Texas Austin, Inst Cellular & Mol Biol, Austin, TX 78712 USA.
[Cantor, Alan B.] Harvard Stem Cell Inst, Cambridge, MA USA.
RP Cantor, AB (reprint author), Childrens Hosp Boston, 300 Longwood Ave,Karp 7, Boston, MA 02115 USA.
EM alan.cantor@childrens.harvard.edu
FU German Academic Research Service; NIH [R01 HL075705]; American Society
for Hematology
FX We thank Stuart Orkin for providing GATA1s mice, Genhong Cheng for
providing Ifnar1-/- mice, Jonathan Keller for providing the
Ifi205 (p205) antibody, Mark Fleming and Theonia Boyd for assisting with
procurement of human BM and FL pathology specimens, and Andrei Kristov
and Grigoriy Losyev for advice and assistance with cell sorting. We
thank Zhe Li and Martha Sola-Visner for advice and critical review of
the manuscript. This work was supported by grants from the German
Academic Research Service (to K. Wieland), the NIH (R01 HL075705; to
A.B. Cantor), and the American Society for Hematology (to A.B. Cantor).
NR 44
TC 5
Z9 5
U1 0
U2 1
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 2013
VL 123
IS 8
BP 3292
EP 3304
DI 10.1172/JCI40609
PG 13
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 196CH
UT WOS:000322750500013
ER
PT J
AU Navaratna, D
Fan, X
Leung, W
Lok, J
Guo, SZ
Xing, CH
Wang, XY
Lo, EH
AF Navaratna, Deepti
Fan, Xiang
Leung, Wendy
Lok, Josephine
Guo, Shuzhen
Xing, Changhong
Wang, Xiaoying
Lo, Eng H.
TI Cerebrovascular degradation of TRKB by MMP9 in the diabetic brain
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID KUNGSHOLMEN PROJECT; ISCHEMIC-STROKE; APOE GENE; DEMENTIA; RISK;
MELLITUS; NEURONS; CELLS
AB Diabetes elevates the risk for neurological diseases, but little is known about the underlying mechanisms. Brain-derived neurotrophic factor (BDNF) is secreted by microvascular endothelial cells (ECs) in the brain, functioning as a neuroprotectant through the activation of the neurotrophic tyrosine kinase receptor TRKB. In a rat model of streptozotocin-induced hyperglycemia, we found that endothelial activation of MMP9 altered TRKB-dependent trophic pathways by degrading TRKB in neurons. Treatment of brain microvascular ECs with advanced glycation endproducts (AGE), a metabolite commonly elevated in diabetic patients, increased MMP9 activation, similar to in vivo findings. Recombinant human MMP9 degraded the TRKB ectodomain in primary neuronal cultures, suggesting that TRKB could be a substrate for MMP9 proteolysis. Consequently, AGE-conditioned endothelial media with elevated MMP9 activity degraded the TRKB ectodomain and simultaneously disrupted the ability of endothelium to protect neurons against hypoxic injury. Our findings demonstrate that neuronal TRKB trophic function is ablated by MMP9-mediated degradation in the diabetic brain, disrupting cerebrovascular trophic coupling and leaving the brain vulnerable to injury.
C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neuroprotect Res Lab,Dept Radiol, Charlestown, MA USA.
Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neuroprotect Res Lab,Dept Neurol, Charlestown, MA USA.
Harvard Univ, Sch Med, Massachusetts Gen Hosp, Neuroprotect Res Lab,Dept Pediat, Charlestown, MA USA.
RP Lo, EH (reprint author), Neuroprotect Res Lab, MGH East 149-2401,13th St, Charlestown, MA 02129 USA.
EM deeptinavaratna@gmail.com; Lo@helix.mgh.harvard.edu
FU NIH [R01-NS76694, RC2-NS69335, P01-NS55104]; American Heart Founders
Postdoctoral Fellowship; Rappaport Foundation
FX This work was supported in part by NIH grants (R01-NS76694, RC2-NS69335,
P01-NS55104), an American Heart Founders Postdoctoral Fellowship, and
the Rappaport Foundation.
NR 14
TC 6
Z9 8
U1 0
U2 4
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 2013
VL 123
IS 8
BP 3373
EP 3377
DI 10.1172/JCI65767
PG 5
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 196CH
UT WOS:000322750500020
PM 23867621
ER
PT J
AU Arora, P
Wu, C
Khan, AM
Bloch, DB
Davis-Dusenbery, BN
Ghorbani, A
Spagnolli, E
Martinez, A
Ryan, A
Tainsh, LT
Kim, S
Rong, J
Huan, TX
Freedman, JE
Levy, D
Miller, KK
Hata, A
del Monte, F
Vandenwijngaert, S
Swinnen, M
Janssens, S
Holmes, TM
Buys, ES
Bloch, KD
Newton-Cheh, C
Wang, TJ
AF Arora, Pankaj
Wu, Connie
Khan, Abigail May
Bloch, Donald B.
Davis-Dusenbery, Brandi N.
Ghorbani, Anahita
Spagnolli, Ester
Martinez, Andrew
Ryan, Allicia
Tainsh, Laurel T.
Kim, Samuel
Rong, Jian
Huan, Tianxiao
Freedman, Jane E.
Levy, Daniel
Miller, Karen K.
Hata, Akiko
del Monte, Federica
Vandenwijngaert, Sara
Swinnen, Melissa
Janssens, Stefan
Holmes, Tara M.
Buys, Emmanuel S.
Bloch, Kenneth D.
Newton-Cheh, Christopher
Wang, Thomas J.
TI Atrial natriuretic peptide is negatively regulated by microRNA-425
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID BLOOD-PRESSURE; SODIUM-INTAKE; TARGETS; ASSOCIATION
AB Numerous common genetic variants have been linked to blood pressure, but no underlying mechanism has been elucidated. Population studies have revealed that the variant rs5068 (A/G) in the 3' untranslated region of NPPA, the gene encoding atrial natriuretic peptide (ANP), is associated with blood pressure. We selected individuals on the basis of rs5068 genotype (AG vs. AA) and fed them a low- or high-salt diet for 1 week, after which they were challenged with an intravenous saline infusion. On both diets, before and after saline administration, ANP levels were up to 50% higher in AG individuals than in AA individuals, a difference comparable. to the changes induced by high-salt diet or saline infusion. In contrast, B-type natriuretic peptide levels did not differ by rs5068 genotype. We identified a microRNA, miR-425, that is expressed in human atria and ventricles and is predicted to bind the sequence spanning rs5068 for the A, but not the G, allele. miR-425 silenced NPPA mRNA in an allele-specific manner, with the G allele conferring resistance to miR-425. This study identifies miR-425 as a regulator of ANP production, raising the possibility that miR-425 antagonists could be used to treat disorders of salt overload, including hypertension and heart failure.
C1 [Arora, Pankaj; Ghorbani, Anahita; Martinez, Andrew; Ryan, Allicia; Bloch, Kenneth D.; Newton-Cheh, Christopher; Wang, Thomas J.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Arora, Pankaj; Ghorbani, Anahita; Bloch, Kenneth D.; Newton-Cheh, Christopher; Wang, Thomas J.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Arora, Pankaj; Martinez, Andrew; Ryan, Allicia; Kim, Samuel; Newton-Cheh, Christopher] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Arora, Pankaj; Newton-Cheh, Christopher] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Wu, Connie; Spagnolli, Ester; Tainsh, Laurel T.; Buys, Emmanuel S.; Bloch, Kenneth D.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Khan, Abigail May] Univ Penn, Sch Med, Div Cardiovasc Med, Philadelphia, PA 19104 USA.
[Bloch, Donald B.] Massachusetts Gen Hosp, Div Rheumatol Allergy & Clin Immunol, Boston, MA 02114 USA.
[Bloch, Donald B.] Massachusetts Gen Hosp, Ctr Immunol & Inflammatory Dis, Boston, MA 02114 USA.
[Davis-Dusenbery, Brandi N.] Harvard Univ, Cambridge, MA 02138 USA.
[Rong, Jian; Huan, Tianxiao; Levy, Daniel] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Rong, Jian; Huan, Tianxiao; Levy, Daniel] Boston Univ, Sch Med, Framingham, MA USA.
[Rong, Jian; Huan, Tianxiao; Levy, Daniel] NHLBI, Ctr Populat Studies, NIH, Bethesda, MD 20892 USA.
[Rong, Jian; Huan, Tianxiao; Levy, Daniel] NHLBI, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Freedman, Jane E.] Univ Massachusetts, Sch Med, Dept Med, Worcester, MA USA.
[Miller, Karen K.] Massachusetts Gen Hosp, Neuroendocrine Unit, Div Endocrinol, Boston, MA 02114 USA.
[Hata, Akiko] UCSF, Cardiovasc Res Inst, San Francisco, CA USA.
[del Monte, Federica] Beth Israel Deaconess Med Ctr, Cardiovasc Inst, Boston, MA 02215 USA.
[Vandenwijngaert, Sara; Swinnen, Melissa; Janssens, Stefan] Univ Louvain, Univ Hosp Gasthuisberg, Dept Cardiovasc Sci, Louvain, Belgium.
[Holmes, Tara M.] Massachusetts Gen Hosp, Clin Res Ctr, Boston, MA 02114 USA.
[Wang, Thomas J.] Vanderbilt Univ, Div Cardiovasc Med, Nashville, TN 37232 USA.
RP Bloch, KD (reprint author), Anesthesia Ctr Crit Care Res, Dept Anesthesia & Crit Care, Jackson 4,55 Fruit St, Boston, MA 02114 USA.
EM kdbloch@partners.org; cnewtoncheh@chgr.mgh.harvard.edu;
thomas.j.wang@vanderbilt.edu
RI Huan, Tianxiao/D-6020-2014; Davis-Dusenbery, Brandi/N-2798-2013;
OI Davis-Dusenbery, Brandi/0000-0001-7811-8613; Arora,
Pankaj/0000-0003-2420-3550
FU NIH [R01-HL098283]; National Center for Research Resources [1
UL1-RR025758-01]; Fondation LeDucq; Research Council of the University
of Leuven [PF/10/014]
FX The authors thank the Massachusetts General Hospital Clinical Research
Center staff and the Center for Human Genetic Research extraction and
genotyping core. We also acknowledge support from NIH R01-HL098283 and 1
UL1-RR025758-01 from the National Center for Research Resources. The
research was also supported by a grant from the Fondation LeDucq and
from the Research Council of the University of Leuven (PF/10/014).
NR 13
TC 40
Z9 42
U1 0
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 2013
VL 123
IS 8
BP 3378
EP 3382
DI 10.1172/JCI67383
PG 5
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 196CH
UT WOS:000322750500021
PM 23867623
ER
PT J
AU van der Lans, AAJJ
Hoeks, J
Brans, B
Vijgen, GHEJ
Visser, MGW
Vosselman, MJ
Hansen, J
Jorgensen, JA
Wu, J
Mottaghy, FM
Schrauwen, P
Lichtenbelt, WDV
AF van der Lans, Anouk A. J. J.
Hoeks, Joris
Brans, Boudewijn
Vijgen, Guy H. E. J.
Visser, Marielle G. W.
Vosselman, Maarten J.
Hansen, Jan
Joergensen, Johanna A.
Wu, Jun
Mottaghy, Felix M.
Schrauwen, Patrick
Lichtenbelt, Wouter D. van Marken
TI Cold acclimation recruits human brown fat and increases nonshivering
thermogenesis
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID INDUCED ADAPTIVE THERMOGENESIS; ADIPOSE-TISSUE ACTIVITY;
SKELETAL-MUSCLE; PHYSIOLOGICAL SIGNIFICANCE; MITOCHONDRIAL DYSFUNCTION;
ENERGY-EXPENDITURE; ADULT HUMANS; TEMPERATURE; ADIPOCYTES; RESPONSES
AB In recent years, it has been shown that humans have active brown adipose tissue (BAT) depots, raising the question of whether activation and recruitment of BAT can be a target to counterbalance the current obesity pandemic. Here, we show that a 10-day cold acclimation protocol in humans increases BAT activity in parallel with an increase in nonshivering thermogenesis (NST). No sex differences in BAT presence and activity were found either before or after cold acclimation. Respiration measurements in permeabilized fibers and isolated mitochondria revealed no significant contribution of skeletal muscle mitochondrial uncoupling to the increased NST. Based on cell-specific markers and on uncoupling protein-1 (characteristic of both BAT and beige/brite cells), this study did not show "browning" of abdominal subcutaneous white adipose tissue upon cold acclimation. The observed physiological acclimation is in line with the subjective changes in temperature sensation; upon cold acclimation, the subjects judged the environment warmer, felt more comfortable in the cold, and reported less shivering. The combined results suggest that a variable indoor environment with frequent cold exposures might be an acceptable and economic manner to increase energy expenditure and may contribute to counteracting the current obesity epidemic.
C1 [van der Lans, Anouk A. J. J.; Hoeks, Joris; Vijgen, Guy H. E. J.; Vosselman, Maarten J.; Hansen, Jan; Joergensen, Johanna A.; Schrauwen, Patrick; Lichtenbelt, Wouter D. van Marken] MUMC, Dept Human Biol, NUTRIM, Sch Nutr Toxicol & Metab, Maastricht, Netherlands.
[Brans, Boudewijn; Visser, Marielle G. W.; Mottaghy, Felix M.] MUMC, Dept Nucl Med, Maastricht, Netherlands.
[Vijgen, Guy H. E. J.] MUMC, Dept Surg, Maastricht, Netherlands.
[Wu, Jun] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Wu, Jun] Harvard Univ, Sch Med, Boston, MA USA.
[Mottaghy, Felix M.] Univ Hosp RWTH Aachen, Dept Nucl Med, Aachen, Germany.
RP Lichtenbelt, WDV (reprint author), Maastricht Univ, Dept Human Biol, NUTRIM, Sch Nutr Toxicol & Metab, POB 616, NL-6200 MD Maastricht, Netherlands.
EM markenlichtenbelt@maastrichtuniversity.nl
OI schrauwen, patrick/0000-0002-0973-847X
FU Netherlands Organization for Scientific Research [TOP 91209037]; EU
[HEALTH-F2-2011-278373]
FX This work is financed by the Netherlands Organization for Scientific
Research (TOP 91209037 to W.D. van Marken Lichtenbelt) and by the EU FP7
project DIABAT (HEALTH-F2-2011-278373 to W.D. van Marken Lichtenbelt).
We thank Sabina Paglialunga and Kyra Jansen (Maastricht University
Medical Centre+) for assistance during the experiments and Ivo Pooters,
Matthias Bauwens, Nancy Hendrix, Paul Menheere, and Jos Stegen
(Maastricht University Medical Centre+) for their assistance with the
biochemical analyses. Furthermore technical support of Boris Kingma,
Roel Wierts, Loek Wouters, and Paul Schoffelen (Maastricht University
Medical Centre+) is highly appreciated Finally, we thank our Literature
Club for all the fruitful discussions.
NR 49
TC 200
Z9 200
U1 18
U2 71
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 2013
VL 123
IS 8
BP 3395
EP 3403
DI 10.1172/JCI68993
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 196CH
UT WOS:000322750500023
PM 23867626
ER
PT J
AU Ramsey, MR
Wilson, C
Ory, B
Rothenberg, SM
Faquin, W
Mills, AA
Ellisen, LW
AF Ramsey, Matthew R.
Wilson, Catherine
Ory, Benjamin
Rothenberg, S. Michael
Faquin, William
Mills, Alea A.
Ellisen, Leif W.
TI FGFR2 signaling underlies p63 oncogenic function in squamous cell
carcinoma
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID TYROSINE KINASE INHIBITOR; PHASE-II TRIAL; GROWTH-FACTOR; NECK-CANCER;
TUMOR PROGRESSION; METASTATIC HEAD; SKIN TUMORS; MOUSE MODEL;
EXPRESSION; MICE
AB Oncogenic transcription factors drive many human cancers, yet identifying and therapeutically targeting the resulting deregulated pathways has proven difficult. Squamous cell carcinoma (SCC) is a common and lethal human cancer, and relatively little progress has been made in improving outcomes for SCC due to a poor understanding of its underlying molecular pathogenesis. While SCCs typically lack somatic oncogene-activating mutations, they exhibit frequent overexpression of the p53-related transcription factor p63. We developed an in vivo murine tumor model to investigate the function and key transcriptional programs of p63 in SCC. Here, we show that established SCCs are exquisitely dependent on p63, as acute genetic ablation of p63 in advanced, invasive SCC induced rapid and dramatic apoptosis and tumor regression. In vivo genome-wide gene expression analysis identified a tumor-survival program involving p63-regulated FGFR2 signaling that was activated by ligand emanating from abundant tumor-associated stroma. Correspondingly, we demonstrate the therapeutic efficacy of extinguishing this signaling axis in endogenous SCCs using the clinical FGFR2 inhibitor AZD4547. Collectively, these results reveal an unanticipated role for p63-driven paracrine FGFR2 signaling as an addicting pathway in human cancer and suggest a new approach for the treatment of SCC.
C1 [Ramsey, Matthew R.; Wilson, Catherine; Ory, Benjamin; Ellisen, Leif W.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Ramsey, Matthew R.; Wilson, Catherine; Ory, Benjamin; Rothenberg, S. Michael; Faquin, William; Ellisen, Leif W.] Harvard Univ, Sch Med, Boston, MA USA.
[Rothenberg, S. Michael; Faquin, William] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Mills, Alea A.] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA.
RP Ellisen, LW (reprint author), Massachusetts Gen Hosp, Ctr Canc, GRJ 904,55 Fruit St, Boston, MA 02114 USA.
EM ellisen@helix.mgh.harvard.edu
RI ory, benjamin/K-8231-2015;
OI Ramsey, Matthew/0000-0003-2402-8502
FU NIDCR [R01 DE015945]; NCI [K99 CA 157730]; American Cancer Society/Mass
Biotech Council Cancer Research Challenge-AstraZeneca Pharmaceuticals LP
Fellowship [PF-09-100-01 MGO]
FX We wish to thank Nabeel Bardeesy, James Rocco, William Michaud, Mike
Dennis, and Zach Nash for advice, reagents, and technical support; and
Nabeel Bardeesy, Andrea McClatchey, and members of the Ellisen
laboratory for comments on the manuscript. The Dana-Farber/Harvard
Cancer Center Specialized Histopathology Core Facility assisted in
processing and staining of murine tumors, and the Harvard Stem Cell
Institute/Center for Regenerative Medicine (HSCI/CRM) Flow Cytometry
Core Facility assisted with tumor sample sorting. AZD4547 used in this
study was provided by AstraZeneca Pharmaceuticals LP. This work was
supported by NIDCR R01 DE015945 (to L.W. Ellisen), by NCI K99 CA 157730
(to M.R. Ramsey), and by the American Cancer Society/Mass Biotech
Council Cancer Research Challenge-AstraZeneca Pharmaceuticals LP
Fellowship PF-09-100-01 MGO (to M.R. Ramsey).
NR 81
TC 35
Z9 35
U1 3
U2 16
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD AUG
PY 2013
VL 123
IS 8
BP 3525
EP 3538
DI 10.1172/JCI68899
PG 14
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 196CH
UT WOS:000322750500034
PM 23867503
ER
PT J
AU Gabrielian, S
Yuan, A
Rubenstein, L
Andersen, RM
Gelberg, L
AF Gabrielian, Sonya
Yuan, Anita
Rubenstein, Lisa
Andersen, Ronald M.
Gelberg, Lillian
TI Serving homeless Veterans in the VA Desert Pacific Healthcare Network: A
needs assessment to inform quality improvement endeavors
SO JOURNAL OF HEALTH CARE FOR THE POOR AND UNDERSERVED
LA English
DT Article
DE Homeless people; Veterans; quality improvement; needs assessment
ID SERIOUS MENTAL-ILLNESS; MEDICAL-CARE; ADULTS
AB This report describes a needs assessment of VA programs for homeless Veterans in Southern California and Nevada, the geographic region with the most homeless Veterans in the nation. The assessment was formulated through key informant interviews. Current service provisions are discussed, along with salient unmet needs for this vulnerable population.
C1 [Gabrielian, Sonya; Gelberg, Lillian] Vet Adm Greater Los Angeles, Mental Illness Res Educ & Clin Ctr, Los Angeles, CA USA.
[Yuan, Anita] VA GLA, Dept Primary Care, Los Angeles, CA USA.
[Rubenstein, Lisa] VA GLA, Hlth Serv Res & Dev Ctr Excellence Study Healthca, Los Angeles, CA USA.
[Rubenstein, Lisa] RAND Corp, Santa Monica, CA 90406 USA.
[Andersen, Ronald M.; Gelberg, Lillian] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90024 USA.
[Gelberg, Lillian] Univ Calif Los Angeles, Dept Family Med, Los Angeles, CA 90024 USA.
RP Gabrielian, S (reprint author), VA Greater Los Angeles WLA, 11301 Wilshire Blvd,Bldg 210A, Los Angeles, CA 90073 USA.
EM sonya.gabrielian@va.gov
FU Intramural VA [VA999999]; NIDA NIH HHS [R01 DA022445, DA 022445]; NIMHD
NIH HHS [P20MD000148/P20MD000182, P20 MD000148, P20 MD000182]
NR 18
TC 0
Z9 0
U1 0
U2 8
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
21218-4363 USA
SN 1049-2089
J9 J HEALTH CARE POOR U
JI J. Health Care Poor Underserved
PD AUG
PY 2013
VL 24
IS 3
BP 1344
EP 1352
PG 9
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 206OR
UT WOS:000323532500033
PM 23974403
ER
PT J
AU Prabhakar, AM
Harvey, HB
Wicky, S
Hirsch, JA
Thrall, JH
Oklu, R
AF Prabhakar, Anand M.
Harvey, H. Benjamin
Wicky, Stephan
Hirsch, Joshua A.
Thrall, James H.
Oklu, Rahmi
TI What's Brewing: How Interventional Radiologists Can Learn From the
Reinvention of Starbucks
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Editorial Material
C1 [Prabhakar, Anand M.; Harvey, H. Benjamin; Wicky, Stephan; Hirsch, Joshua A.; Thrall, James H.; Oklu, Rahmi] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA.
RP Prabhakar, AM (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, 55 Fruit St,White 270, Boston, MA 02114 USA.
EM amp@alumni.upenn.edu
NR 19
TC 2
Z9 2
U1 0
U2 9
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 2013
VL 10
IS 8
BP 559
EP 561
DI 10.1016/j.jacr.2012.12.021
PG 3
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 204UP
UT WOS:000323397000004
PM 23453724
ER
PT J
AU Iii, E
Breslau, J
Barr, RM
Liebscher, LA
Bohl, M
Hoffman, T
Boland, GWL
Sherry, C
Kim, W
Shah, SS
Tilking, M
AF Silva, Ezequiel, III
Breslau, Jonathan
Barr, Robert M.
Liebscher, Lawrence A.
Bohl, Michael
Hoffman, Thomas
Boland, Giles W. L.
Sherry, Cynthia
Kim, Woojin
Shah, Samir S.
Tilking, Mike
TI ACR White Paper on Teleradiology Practice: A Report From the Task Force
on Teleradiology Practice
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Article
DE Quality of care; technology; teleradiology; teleradiologist;
teleradiology company; regulatory issues; end-user standards; patient
primacy; business standards of practice; disintermediation
ID RADIOLOGY; MALPRACTICE; ERGONOMICS; PACS
AB Teleradiology services are now embedded into the workflow of many radiology practices in the United States, driven largely by an expanding corporate model of services. This has brought opportunities and challenges to both providers and recipients of teleradiology services and has heightened the need to create best-practice guidelines for teleradiology to ensure patient primacy. To this end, the ACR Task Force on Teleradiology Practice has created this white paper to update the prior ACR communication on teleradiology and discuss the current and possible future state of teleradiology in the United States. This white paper proposes comprehensive best-practice guidelines for the practice of teleradiology, with recommendations offered regarding future actions.
C1 [Silva, Ezequiel, III] South Texas Radiol Grp, San Antonio, TX 78229 USA.
[Silva, Ezequiel, III] Univ Texas Hlth Sci Ctr San Antonio, Dept Radiol, San Antonio, TX 78229 USA.
[Breslau, Jonathan] Radiol Associates Sacramento Med Grp Inc, Sacramento, CA USA.
[Barr, Robert M.] Mecklenburg Radiol Associates, Charlotte, NC USA.
[Liebscher, Lawrence A.] Cedar Valley Med Specialists, Waterloo, IA USA.
[Bohl, Michael] Radliol Grp, Davenport, IA USA.
[Hoffman, Thomas; Tilking, Mike] Amer Coll Radiol, Reston, VA USA.
[Boland, Giles W. L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Sherry, Cynthia] Texas Hlth Presbyterian Hosp, Dallas, TX USA.
[Kim, Woojin] Univ Penn, Dept Radiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Shah, Samir S.] Virtual Radiol, Eden Prairie, MN USA.
RP Iii, E (reprint author), South Texas Radiol Grp, 8401 Datapoint,Suite 600, San Antonio, TX 78229 USA.
EM zeitesilva3@gmail.com
OI Barr, Robert/0000-0002-9214-9448
NR 40
TC 0
Z9 0
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 2013
VL 10
IS 8
BP 575
EP 585
DI 10.1016/j.jacr.2013.03.018
PG 11
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 204UP
UT WOS:000323397000009
ER
PT J
AU Bhargava, P
Robinson, TJ
Lyer, RS
Seyal, AR
Munsell, A
Moshiri, M
Dighe, MK
Richardson, ML
Weinberger, E
AF Bhargava, Puneet
Robinson, Tracy J.
Lyer, Ramesh S.
Seyal, Adeel R.
Munsell, Andrew
Moshiri, Mariam
Dighe, Manjiri K.
Richardson, Michael L.
Weinberger, Edward
TI Sharing a Collection of Radiology Educational Websites as Bookmarks
Among Radiologists
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Editorial Material
ID RESOURCES; INTERNET; FUTURE
C1 [Bhargava, Puneet; Robinson, Tracy J.; Lyer, Ramesh S.; Munsell, Andrew; Moshiri, Mariam; Dighe, Manjiri K.; Richardson, Michael L.; Weinberger, Edward] Univ Washington, Sch Med, Dept Radiol, Seattle, WA USA.
[Bhargava, Puneet] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Lyer, Ramesh S.; Munsell, Andrew; Weinberger, Edward] Seattle Childrens Hosp, Seattle, WA USA.
[Seyal, Adeel R.] Harrison Med Ctr, Bremerton, WA USA.
RP Bhargava, P (reprint author), VA Puget Sound Hlth Care Syst, Dept Radiol, 1660 S Columbian Way,Mailbox 358280,S-114-Radiol, Seattle, WA 98108 USA.
EM bhargp@uw.edu
OI Bhargava, Puneet/0000-0002-3849-9666
NR 8
TC 1
Z9 1
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1546-1440
J9 J AM COLL RADIOL
JI J. Am. Coll. Radiol.
PD AUG
PY 2013
VL 10
IS 8
BP 627
EP 632
DI 10.1016/j.jacr.2012.12.015
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 204UP
UT WOS:000323397000017
PM 23453725
ER
PT J
AU Mitin, T
Hunt, D
Shipley, WU
Kaufman, DS
Uzzo, R
Wu, CL
Buyyounouski, MK
Sandler, H
Zietman, AL
AF Mitin, Timur
Hunt, Daniel
Shipley, William U.
Kaufman, Donald S.
Uzzo, Robert
Wu, Chin-Lee
Buyyounouski, Mark K.
Sandler, Howard
Zietman, Anthony L.
TI Transurethral surgery and twice-daily radiation plus
paclitaxel-cisplatin or fluorouracil-cisplatin with selective bladder
preservation and adjuvant chemotherapy for patients with muscle invasive
bladder cancer (RTOG 0233): a randomised multicentre phase 2 trial
SO LANCET ONCOLOGY
LA English
DT Article
ID TRANSITIONAL-CELL CARCINOMA; RADICAL CYSTECTOMY; ORGAN PRESERVATION;
RESECTION; THERAPY; RADIOTHERAPY; SERIES
AB Background We assessed effectiveness, safety, and tolerability of paclitaxel or fluorouracil when added to radiation plus cisplatin followed by adjuvant chemotherapy in a programme of selected bladder preservation for patients with muscle invasive bladder cancer.
Methods In our randomised phase 2 trial, we enrolled patients with T2-4a transitional cell carcinoma of the bladder at 24 medical centres in the USA. We randomly allocated patients to receive paclitaxel plus cisplatin (paclitaxel group) or fluorouracil plus cisplatin (fluorouracil group) with twice-daily radiation in random block sizes per site on the basis of clinical T-stage (T2 vs T3-4). Patients and physicians were aware of treatment assignment. All patients had transurethral resection of bladder tumour and twice-daily radiotherapy to 40.3 Gy, along with allocated chemotherapy, followed by cystoscopic and biopsy assessment of response. Patients who had a tumour response with downstaging to T0, Tcis, or Ta received consolidation chemoradiotherapy to 64.3 Gy, with the same chemotherapy regimen as in the induction phase. Patients received adjuvant cisplatin-gemcitabine-paclitaxel after the end of chemo radiotherapy. If, after induction, persistent disease was graded as T1 or worse, we recommended patients undergo cystectomy and adjuvant chemotherapy. We assessed the primary endpoints of rates of treatment completion and toxic effects in all randomly allocated patients. This study is registered with ClinicalTrials.gov, number NCT00055601.
Findings Between Dec 13, 2002, and Jan 11, 2008, we enrolled 97 patients, of whom 93 were eligible for analysis. Median follow-up was 5.0 years (IQR 5.0-6.2). Of 46 patients in the paclitaxel group, 45 (98%) completed induction (16 [35%] with grade 3-4 toxicity), 39 (85%) completed induction and consolidation (11 [24%] with grade 3-4 toxicity due to consolidation), and 31 (67%) completed the entire protocol with adjuvant chemotherapy. 34 (85%) of 40 assessable patients in the paclitaxel group had grade 3-4 toxicity during adjuvant chemotherapy. Of 47 patients in the fluorouracil group, 45 (96%) completed induction (nine [19%] with grade 3-4 toxicity), 39 (83%) completed induction and consolidation (12 [26%] had grade 3-4 toxicity due to consolidation), and 25 (53%) completed the entire protocol with adjuvant chemotherapy. 31 (76%) of 41 assessable patients in the fluorouracil group had grade 3-4 toxicity during adjuvant chemotherapy. Five (11%) patients treated with the paclitaxel regimen and three (6%) patients treated with the fluorouracil regimen developed late grade 3-4 radiotherapy toxicities. 11 (24%) patients treated with the paclitaxel regimen and 16 (34%) patients treated with the fluorouracil regimen developed late grade 3-4 toxicities unrelated to radiotherapy. One patient (in the fluorouracil group) died during follow-up. Six (13%) patients in the paclitaxel group and in three (6%) patients in the fluorouracil group discontinued due to treatment-related toxicity.
Interpretation In the absence of phase 3 data, our findings could inform selection of a bladder-sparing trimodality chemotherapy regimen for patients with muscle invasive bladder cancer.
C1 [Mitin, Timur; Shipley, William U.; Kaufman, Donald S.; Wu, Chin-Lee; Zietman, Anthony L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Hunt, Daniel] Ctr Stat, Radiat Therapy Oncol Grp, Philadelphia, PA USA.
[Uzzo, Robert; Buyyounouski, Mark K.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Sandler, Howard] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
RP Mitin, T (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, 55 Fruit St, Boston, MA 02114 USA.
EM tmitin@partners.org
FU RTOG [U10 CA21661]; Community Clinical Oncology Program grant from the
US National Cancer Institute (NCI) [U10 CA37422]
FX This trial was undertaken by the RTOG, and was supported by RTOG grant
U10 CA21661 and Community Clinical Oncology Program grant U10 CA37422
from the US National Cancer Institute (NCI).
NR 32
TC 34
Z9 34
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD AUG
PY 2013
VL 14
IS 9
BP 863
EP 872
DI 10.1016/S1470-2045(13)70255-9
PG 10
WC Oncology
SC Oncology
GA 205DZ
UT WOS:000323423400043
PM 23823157
ER
PT J
AU Barton, SE
Najita, JS
Ginsburg, ES
Leisenring, WM
Stovall, M
Weathers, RE
Sklar, CA
Robison, LL
Diller, L
AF Barton, Sara E.
Najita, Julie S.
Ginsburg, Elizabeth S.
Leisenring, Wendy M.
Stovall, Marilyn
Weathers, Rita E.
Sklar, Charles A.
Robison, Leslie L.
Diller, Lisa
TI Infertility, infertility treatment, and achievement of pregnancy in
female survivors of childhood cancer: a report from the Childhood Cancer
Survivor Study cohort
SO LANCET ONCOLOGY
LA English
DT Article
ID LONG-TERM SURVIVORS; ANTI-MULLERIAN HORMONE; DOSE RECONSTRUCTION;
HODGKINS LYMPHOMA; OVARIAN FAILURE; BREAST-CANCER; CHEMOTHERAPY;
FERTILITY; WOMEN; RADIOTHERAPY
AB Background Previous studies have shown decreased pregnancy rates and early menopause in female cancer survivors; however, infertility rates and reproductive interventions have not been studied. We investigated infertility and time to pregnancy in female childhood cancer survivors, and analysed treatment characteristics associated with infertility and subsequent pregnancy.
Methods The Childhood Cancer Survivor Study (CCSS) is a cohort study including 5 year cancer survivors from 26 Canadian and US institutions who were younger than 21 years at the time of diagnosis between Jan 1, 1970, and Dec 31, 1986, and a sibling control group. We included women aged 18-39 years who had ever been sexually active. We gathered demographic, medical, and reproductive data via a baseline questionnaire, and quantified exposure to alkylating agents and radiation therapy. Self-reported infertility, medical treatment for infertility, time to first pregnancy in survivors and siblings, and the risk of infertility in survivors by demographic, disease, and treatment variables were analysed.
Findings 3531 survivors and 1366 female sibling controls who enrolled between Nov 3, 1992, and April 4, 2004, were included. Compared with their siblings, survivors had an increased risk (relative risk [RR] 1.48 [95% CI 1.23-1.78]; p<0.0001) of clinical infertility (ie, >1 year of attempts at conception without success), which was most pronounced at early reproductive ages (RR 2.92 [95% CI 1.18-7.20], p=0.020, in participants <= 24 years; 1.61 [1.05-2.48], p=0.029, in those aged 25-29 years; and 1.37 [1.11-1.69], p=0.0035, in those aged 30-40 years). Despite being equally likely to seek treatment for infertility, survivors were less likely than were their siblings to be prescribed drugs for treatment of infertility (0.57 [95% CI 0.46-0.70], p<0.0001). Increasing doses of uterine radiation and alkylating agent chemotherapy were strongly associated with infertility. Although survivors had an increased time to pregnancy compared with their siblings (p=0.032), 292 (64%) of 455 participants with self-reported clinical infertility achieved a pregnancy.
Interpretation A more comprehensive understanding of infertility after cancer is crucial for counselling and decision making about future conception attempts and fertility preservation.
C1 [Barton, Sara E.; Ginsburg, Elizabeth S.] Brigham & Womens Hosp, Dept Obstet & Gynecol, Boston, MA 02115 USA.
[Barton, Sara E.; Ginsburg, Elizabeth S.] Harvard Univ, Sch Med, Boston, MA USA.
[Najita, Julie S.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Leisenring, Wendy M.] Fred Hutchinson Canc Res Ctr, Clin Stat Program, Seattle, WA 98104 USA.
[Leisenring, Wendy M.] Fred Hutchinson Canc Res Ctr, Canc Prevent Program, Seattle, WA 98104 USA.
[Stovall, Marilyn; Weathers, Rita E.] Univ Texas MD Anderson Canc Ctr, Dept Radiat Phys, Houston, TX 77030 USA.
[Sklar, Charles A.] Mem Sloan Kettering Canc Ctr, Dept Pediat, New York, NY 10021 USA.
[Robison, Leslie L.] St Jude Childrens Res Hosp, Dept Epidemiol & Canc Control, Memphis, TN USA.
[Diller, Lisa] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Diller, Lisa] Dana Farber Boston Childrens Hosp Canc Ctr, Boston, MA USA.
RP Barton, SE (reprint author), Brigham & Womens Hosp, Ctr Infertil & Reprod Surg, 75 Francis St, Boston, MA 02115 USA.
EM sarabarton5@gmail.com
FU US National Cancer Institute [U24 CA55727]; American Lebanese Syrian
Associated Charities; Swim Across America
FX This study was funded by grant U24 CA55727 (awarded to LLR, the
principal investigator) from the US National Cancer Institute, support
to St Jude Children's Research Hospital from the American Lebanese
Syrian Associated Charities, and support to LD from Swim Across America.
NR 29
TC 62
Z9 63
U1 4
U2 19
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 2013
VL 14
IS 9
BP 873
EP 881
DI 10.1016/S1470-2045(13)70251-1
PG 9
WC Oncology
SC Oncology
GA 205DZ
UT WOS:000323423400044
PM 23856401
ER
PT J
AU Quinn, DI
Tangen, CM
Hussain, M
Lara, PN
Goldkorn, A
Moinpour, CM
Garzotto, MG
Mack, PC
Carducci, MA
Monk, JP
Twardowski, PW
Van Veldhuizen, PJ
Agarwal, N
Higano, CS
Vogelzang, NJ
Thompson, IM
AF Quinn, David I.
Tangen, Catherine M.
Hussain, Maha
Lara, Primo N., Jr.
Goldkorn, Amir
Moinpour, Carol M.
Garzotto, Mark G.
Mack, Philip C.
Carducci, Michael A.
Monk, J. Paul
Twardowski, Przemyslaw W.
Van Veldhuizen, Peter J.
Agarwal, Neeraj
Higano, Celestia S.
Vogelzang, Nicholas J.
Thompson, Ian M., Jr.
TI Docetaxel and atrasentan versus docetaxel and placebo for men with
advanced castration-resistant prostate cancer (SWOG S0421): a randomised
phase 3 trial
SO LANCET ONCOLOGY
LA English
DT Article
ID BONE METASTASES; DOUBLE-BLIND; III TRIAL; COMPARING DOCETAXEL;
ENDOTHELIN RECEPTOR; INCREASED SURVIVAL; PLUS PREDNISONE; PAIN;
CHEMOTHERAPY; MITOXANTRONE
AB Background The endothelin pathway has a role in bone metastases, which are characteristic of advanced prostate cancer. Atrasentan, an endothelin receptor antagonist, has shown activity in prostate cancer. We therefore assessed its effect on survival in patients with castration-resistant prostate cancer with bone metastases.
Methods In a double-blind phase 3 trial, men with metastatic castration-resistant prostate cancer, stratified for progression type (prostate-specific antigen or radiological), baseline pain, extraskeletal metastases, and bisphosphonate use, were randomly assigned in a 1:1 ratio to docetaxel (75 mg/m(2) every 21 days, intravenously) with atrasentan (10 mg/day, orally) or placebo for up to 12 cycles and treated until disease progression or unacceptable toxicity. Patients who did not progress on treatment were permitted to continue atrasentan or placebo for up to 52 weeks. Coprimary endpoints were progression-free survival (PFS) and overall survival. Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00134056.
Findings 498 patients were randomly assigned to the atrasentan group and 496 to the placebo group. The trial was halted early for futility in April, 2011, after a planned interim analysis. Median PFS was 9.2 months (95% CI 8.5-9.9) in the atrasentan group and 9.1 months (8.4-10.2) in the placebo group (hazard ratio 1.02, 0.89-1.16; p=0.81). Median overall survival was 17.8 months (16.4-19.8) in the atrasentan group versus 17.6 months (16.4-20.1) in the placebo group (1.04, 0.90-1.19; p=0.64). 278 (57%) of 492 patients in the atrasentan group had grade 3 and greater toxicity compared with 294 (60%) of 486 in the placebo group (p=0.22). Three deaths in the atrasentan group and seven in the placebo group were judged to be possibly or probably due to protocol treatment.
Interpretation Atrasentan, when added to docetaxel, does not improve overall survival or PFS in men with castration-resistant prostate cancer and bone metastases; therefore, single-agent docetaxel should remain as one of the standard treatments.
C1 [Quinn, David I.; Goldkorn, Amir] Univ So Calif, Norris Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Tangen, Catherine M.; Moinpour, Carol M.] SWOG Stat Ctr, Seattle, WA USA.
[Hussain, Maha] Univ Michigan, Ann Arbor, MI 48109 USA.
[Lara, Primo N., Jr.; Mack, Philip C.] Univ Calif Davis, Sacramento, CA 95817 USA.
[Garzotto, Mark G.] Portland VA Med Ctr, Portland, OR USA.
[Carducci, Michael A.] Johns Hopkins Kimmel Canc Ctr, Baltimore, MD USA.
[Monk, J. Paul] Ohio State Univ, Columbus, OH 43210 USA.
[Twardowski, Przemyslaw W.] City Hope Natl Med Ctr, Med Ctr, Duarte, CA USA.
[Van Veldhuizen, Peter J.] Univ Kansas, Kansas City, KS USA.
[Agarwal, Neeraj] Univ Utah, Salt Lake City, UT USA.
[Higano, Celestia S.] Seattle Canc Care Alliance, Puget Sound Oncol Consortium, Seattle, WA USA.
[Higano, Celestia S.] Univ Washington, Seattle, WA 98195 USA.
[Vogelzang, Nicholas J.] US Oncol Res, Ctr Comprehens Canc, Las Vegas, NV USA.
[Thompson, Ian M., Jr.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
RP Quinn, DI (reprint author), Univ So Calif, Norris Comprehens Canc Ctr, 1441 Eastlake Ave,Suite 3440, Los Angeles, CA 90033 USA.
EM diquinn@med.usc.edu
RI Quinn, David/F-4343-2015
OI Quinn, David/0000-0002-1411-0417
FU Public Health Service; National Cancer Institute, Department of Health
and Human Services [CA32102, CA38926, CA46368, CA46441, CA58882,
CA58861, CA12644, CA22433, CA46282, CA27057, CA58416, CA45807, CA45808,
CA45450, CA42777, CA35281, CA20319, CA35090, CA76429, CA14028, CA67575,
CA45377, CA68183, CA63848, CA74647, CA16385, CA35192, CA63844, CA11083,
CA63845, CA76447]; Sanofi-Aventis; Abbott Laboratories
FX The investigation was supported, partly, by the following Public Health
Service Cooperative Agreement grant numbers awarded by the National
Cancer Institute, Department of Health and Human Services: CA32102,
CA38926, CA46368, CA46441, CA58882, CA58861, CA12644, CA22433, CA46282,
CA27057, CA58416, CA45807, CA45808, CA45450, CA42777, CA35281, CA20319,
CA35090, CA76429, CA14028, CA67575, CA45377, CA68183, CA63848, CA74647,
CA16385, CA35192, CA63844, CA11083, CA63845, CA76447, CA35128, CA13612,
CA35431, CA76448, CA35178, CA35176, CA35119, CA35421, CA128567, CA04919,
CA68183, CA45560, CA37981, CA58723, CA21115, CA16116, and CA31949; and,
partly, by Sanofi-Aventis and Abbott Laboratories. The authors report on
behalf of a large team and would like to acknowledge the contribution of
clinicians, research teams, patients, and their families through ECOG,
CALGB, and the Clinical Trials Support Unit in completing SWOG S0421.
NR 33
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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 2013
VL 14
IS 9
BP 893
EP 900
DI 10.1016/S1470-2045(13)70294-8
PG 8
WC Oncology
SC Oncology
GA 205DZ
UT WOS:000323423400046
PM 23871417
ER
PT J
AU Chawla, S
Henshaw, R
Seeger, L
Choy, E
Blay, JY
Ferrari, S
Kroep, J
Grimer, R
Reichardt, P
Rutkowski, P
Schuetze, S
Skubitz, K
Staddon, A
Thomas, D
Qian, Y
Jacobs, I
AF Chawla, Sant
Henshaw, Robert
Seeger, Leanne
Choy, Edwin
Blay, Jean-Yves
Ferrari, Stefano
Kroep, Judith
Grimer, Robert
Reichardt, Peter
Rutkowski, Piotr
Schuetze, Scott
Skubitz, Keith
Staddon, Arthur
Thomas, David
Qian, Yi
Jacobs, Ira
TI Safety and efficacy of denosumab for adults and skeletally mature
adolescents with giant cell tumour of bone: interim analysis of an
open-label, parallel-group, phase 2 study
SO LANCET ONCOLOGY
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; OSTEOCLAST PRECURSORS; RECEPTOR ACTIVATOR;
ZOLEDRONIC ACID; GENE-EXPRESSION; KAPPA-B; CRITERIA; CANCER; LIGAND
AB Background Giant cell tumour of bone (GCTB) is a very rare, aggressive, and progressive osteolytic tumour for which no standard medicinal treatment or chemotherapy exists. We report interim safety and efficacy results from a phase 2 study of denosumab in patients with GCTB.
Methods We did an international, open-label, parallel-group, phase 2 trial of patients with histologically confirmed GCTB and radiographically measurable active disease. Eligible patients were adults or skeletally mature adolescents with radiographic evidence of at least one mature long bone who were at least 12 years old and weighed at least 45 kg. We divided patients into three cohorts-those with surgically unsalvageable GCTB (cohort 1), those with salvageable GCTB whose surgery was associated with severe morbidity (cohort 2), and those who transferred from a previous study of denosumab for GCTB (cohort 3). Patients in cohorts 1 and 2 received 120 mg of subcutaneous denosumab every 4 weeks with loading doses on days 8 and 15 of the first cycle; those in cohort 3 continued the regimen from the previous study. Investigator-determined disease status and clinical benefit were assessed every 4 weeks. Our primary endpoint was the safety profile of denosumab in terms of adverse events and laboratory abnormalities. Prespecified secondary endpoints were time to disease progression in cohort 1 and the proportion of patients without any surgery at 6 months in cohort 2. Safety analyses included all patients who received at least one dose of denosumab. Efficacy analyses included all eligible patients who received at least one dose of denosumab. This study is registered with ClinicalTrials.gov, identifier NCT00680992.
Findings 282 patients, including ten adolescents, were included between Sept 9, 2008, and March 25, 2011. Of the 281 patients analysable for safety, three (1%) had osteonecrosis of the jaw and 15 (5%) hypocalcaemia. The most common grade 3-4 adverse events were hypophosphataemia, which occurred in nine (3%) patients, and anaemia, back pain, and pain in extremities, each of which occurred in three patients (1%). Serious adverse events were reported in 25 (9%) patients. No treatment-related deaths were reported. On the basis of investigators' assessment of disease status, 163 of 169 (96%) analysable patients in cohort 1 had no disease progression after median follow-up of 13 months (IQR 5.8-21.0). In cohort 2, 74 of 100 (74%) analysable patients had no surgery and 16 of 26 (62%) patients who had surgery underwent a less morbid procedure than planned. Median follow-up in cohort 2 was 9.2 months (IQR 4.2-12.9).
Interpretation Adverse events were consistent with the known safety profile of denosumab. Denosumab was associated with tumour responses and reduced the need for morbid surgery in patients with GCTB. Denosumab represents a new treatment option for patients with GCTB.
C1 [Chawla, Sant] Sarcoma Oncol Ctr, Santa Monica, CA 90403 USA.
[Henshaw, Robert] Georgetown Univ, Washington Canc Inst, Medstar Washington Hosp Ctr, Washington, DC USA.
[Seeger, Leanne] UCLA Hlth Syst, Musculoskeletal Imaging, Los Angeles, CA USA.
[Choy, Edwin] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Blay, Jean-Yves] Univ Lyon 1, F-69365 Lyon, France.
[Blay, Jean-Yves] Ctr Leon Berard, F-69373 Lyon, France.
[Ferrari, Stefano] Ist Ortoped Rizzoli, Bologna, Italy.
[Kroep, Judith] Leiden Univ, Med Ctr, Leiden, Netherlands.
[Grimer, Robert] Royal Orthopaed Hosp, Birmingham B31 2AP, W Midlands, England.
[Reichardt, Peter] HELIOS Klinikum Berlin Buch, Berlin, Germany.
[Rutkowski, Piotr] Maria Sklodowska Curie Mem Canc Ctr, Warsaw, Poland.
[Rutkowski, Piotr] Inst Oncol, Warsaw, Poland.
[Schuetze, Scott] Univ Michigan, Ann Arbor, MI 48109 USA.
[Skubitz, Keith] Univ Minnesota, Minneapolis, MN USA.
[Staddon, Arthur] Penn Oncol Hematol Associates, Philadelphia, PA USA.
[Thomas, David] Peter MacCallum Canc Ctr, East Melbourne, Vic, Australia.
[Qian, Yi; Jacobs, Ira] Amgen Inc, Thousand Oaks, CA USA.
RP Chawla, S (reprint author), Sarcoma Oncol Ctr, 2811 Wilshire Blvd,Suite 414, Santa Monica, CA 90403 USA.
EM santchawla@sarcomaoncology.com
RI Blay, Jean-Yves/N-3966-2016;
OI Blay, Jean-Yves/0000-0001-7190-120X; Choy, Edwin/0000-0001-9896-8084;
Rutkowski, Piotr/0000-0002-8920-5429
FU Amgen
FX This study was funded by Amgen. We thank Ada Braun for writing
contributions, data interpretation, and critical review, and Lori Gorton
for providing medical writing, editing, and formatting assistance.
NR 25
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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 2013
VL 14
IS 9
BP 901
EP 908
DI 10.1016/S1470-2045(13)70277-8
PG 8
WC Oncology
SC Oncology
GA 205DZ
UT WOS:000323423400047
PM 23867211
ER
PT J
AU Chavarri-Guerra, Y
Sullivan, R
Goss, PE
AF Chavarri-Guerra, Yanin
Sullivan, Richard
Goss, Paul E.
TI Cancer control in Chile Reply
SO LANCET ONCOLOGY
LA English
DT Letter
C1 [Chavarri-Guerra, Yanin] Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Dept Hematol Oncol, Salvador Zubiran, Mexico.
[Sullivan, Richard] Kings Coll London, Kings Hlth Partners, Integrated Canc Ctr, Guys Hosp, London WC2R 2LS, England.
[Goss, Paul E.] Massachusetts Gen Hosp, Ctr Canc, Canc Ctr Excellence, Avon Breast, Boston, MA 02114 USA.
RP Chavarri-Guerra, Y (reprint author), Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Dept Hematol Oncol, Salvador Zubiran, Mexico.
EM pgoss@partners.org
NR 4
TC 0
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U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
J9 LANCET ONCOL
JI Lancet Oncol.
PD AUG
PY 2013
VL 14
IS 9
BP E338
EP E338
PG 1
WC Oncology
SC Oncology
GA 205DZ
UT WOS:000323423400003
PM 23896269
ER
PT J
AU Lapierre, LR
De Magalhaes, CD
McQuary, PR
Chu, CC
Visvikis, O
Chang, JT
Gelino, S
Ong, B
Davis, AE
Irazoqui, JE
Dillin, A
Hansen, M
AF Lapierre, Louis R.
De Magalhaes Filho, C. Daniel
McQuary, Philip R.
Chu, Chu-Chiao
Visvikis, Orane
Chang, Jessica T.
Gelino, Sara
Ong, Binnan
Davis, Andrew E.
Irazoqui, Javier E.
Dillin, Andrew
Hansen, Malene
TI The TFEB orthologue HLH-30 regulates autophagy and modulates longevity
in Caenorhabditis elegans
SO NATURE COMMUNICATIONS
LA English
DT Article
ID LIFE-SPAN EXTENSION; MESSENGER-RNA TRANSLATION; C-ELEGANS; DIETARY
RESTRICTION; TRANSCRIPTION FACTORS; LYSOSOMAL BIOGENESIS;
LIPID-METABOLISM; GENES; GENETICS; CONSUMPTION
AB Autophagy is a cellular recycling process that has an important anti-aging role, but the underlying molecular mechanism is not well understood. The mammalian transcription factor EB (TFEB) was recently shown to regulate multiple genes in the autophagy process. Here we show that the predicted TFEB orthologue HLH-30 regulates autophagy in Caenorhabditis elegans and, in addition, has a key role in lifespan determination. We demonstrate that hlh-30 is essential for the extended lifespan of Caenorhabditis elegans in six mechanistically distinct longevity models, and overexpression of HLH-30 extends lifespan. Nuclear localization of HLH-30 is increased in all six Caenorhabditis elegans models and, notably, nuclear TFEB levels are augmented in the livers of mice subjected to dietary restriction, a known longevity-extending regimen. Collectively, our results demonstrate a conserved role for HLH-30 and TFEB in autophagy, and possibly longevity, and identify HLH-30 as a uniquely important transcription factor for lifespan modulation in Caenorhabditis elegans.
C1 [Lapierre, Louis R.; McQuary, Philip R.; Chu, Chu-Chiao; Chang, Jessica T.; Gelino, Sara; Ong, Binnan; Davis, Andrew E.; Hansen, Malene] Sanford Burnham Med Res Inst, Aging & Stem Cell Res Ctr, Program Dev & Aging, La Jolla, CA USA.
[De Magalhaes Filho, C. Daniel; Dillin, Andrew] Salk Inst Biol Studies, Howard Hughes Med Inst, Glenn Ctr Aging Res, La Jolla, CA 92037 USA.
[McQuary, Philip R.; Gelino, Sara] Sanford Burnham Med Res Inst, Grad Sch Biomed Sci, La Jolla, CA USA.
[Visvikis, Orane; Irazoqui, Javier E.] Harvard Univ, Sch Med, Dept Pediat, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Hansen, M (reprint author), Sanford Burnham Med Res Inst, Aging & Stem Cell Res Ctr, Program Dev & Aging, 10901 N Torrey Pines Rd, La Jolla, CA USA.
EM mhansen@sanfordburnham.org
RI di Ronza, Alberto/H-7674-2016; VISVIKIS, ORANE/N-1818-2016;
OI di Ronza, Alberto/0000-0002-9813-5143; VISVIKIS,
ORANE/0000-0001-7719-5836; Lapierre, Louis/0000-0002-8154-141X;
Irazoqui, Javier/0000-0001-6553-1329
FU NIH/UCSD [P50 AG005131-29]; Glenn Foundation for Aging Research
fellowship; Fund for Medical Discovery postdoctoral fellowship from the
Massachusetts General Hospital; NIH/NIA [F31 AG039222, R01 AG027463, R01
AG038664, R01 AG039756]; NIH/NIGMS [R01 GM101056]
FX We thank all Hansen lab members for helpful discussions, and Drs H.
Aguilaniu, A. Ghazi, C. Kumsta, A. O'Rourke, E. Troemel and D. Wilkinson
for comments on the manuscript. We thank the Mitani lab for the
hlh-30(tm1978) strain. L.R.L. was funded by the NIH/UCSD (P50
AG005131-29), C.D.D.M.F. by a Glenn Foundation for Aging Research
fellowship, O.V. by a Fund for Medical Discovery postdoctoral fellowship
from the Massachusetts General Hospital, P.R.M. by NIH/NIA (F31
AG039222), J.E.I. by NIH/NIGMS (R01 GM101056), A.D. by NIH/NIA (R01
AG027463) and M.H. by NIH/NIA (R01 AG038664 and R01 AG039756).
NR 40
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U1 1
U2 14
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD AUG
PY 2013
VL 4
AR 2267
DI 10.1038/ncomms3267
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 209JG
UT WOS:000323751200007
PM 23925298
ER
PT J
AU Hoppe, BS
Hodgson, DC
Advani, R
Dabaja, BS
Flowers, CR
Ha, CS
Metzger, ML
Plastaras, JP
Roberts, KB
Shapiro, R
Terezakis, SA
Winkfield, KM
Younes, A
Constine, LS
AF Hoppe, Bradford S.
Hodgson, David C.
Advani, Ranjana
Dabaja, Bouthaina S.
Flowers, Christopher R.
Ha, Chul S.
Metzger, Monika L.
Plastaras, John P.
Roberts, Kenneth B.
Shapiro, Ronald
Terezakis, Stephanie A.
Winkfield, Karen M.
Younes, Anas
Constine, Louis S.
TI ACR APPROPRIATENESS CRITERIA (R) Localized Nodal Indolent Lymphoma
SO ONCOLOGY-NEW YORK
LA English
DT Review
ID NON-HODGKINS-LYMPHOMA; INTERNATIONAL PROGNOSTIC INDEX; TERM-FOLLOW-UP;
INVOLVED-FIELD RADIOTHERAPY; FOLLICULAR LYMPHOMA; LOW-GRADE; STAGE-I;
NATIONAL LYMPHOCARE; RADIATION-THERAPY; UNITED-STATES
AB The present guidelines review epidemiology, pathology, presentation, workup, staging, prognostic factors, and treatment options for patients with localized nodal indolent lymphoma, with an emphasis on radiation guidelines, including radiation dose, field design, and radiation techniques. Following a discussion of the current literature and available data for treatment and outcomes of patients with indolent lymphoma, several different example cases are reviewed to help. physicians make appropriate treatment decisions. The American College of Radiology Appropriateness Criteria are evidence-based guidelines for specific clinical conditions that are reviewed every 2 years by a multidisciplinary expert panel. The guideline development and review include an extensive analysis of current medical literature from peer-reviewed journals and the application of a well-established consensus methodology (modified Delphi) by which the panel rates the appropriateness of imaging and treatment procedures. In those instances where evidence is lacking or not definitive, expert opinion may be used to recommend imaging or treatment.
C1 [Hoppe, Bradford S.] Univ Florida, Proton Therapy Inst, Jacksonville, FL 32209 USA.
[Hodgson, David C.] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Advani, Ranjana] Stanford Canc Ctr, Stanford, CA USA.
[Dabaja, Bouthaina S.; Younes, Anas] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Flowers, Christopher R.] Emory Univ, Atlanta, GA 30322 USA.
[Ha, Chul S.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Metzger, Monika L.] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
[Plastaras, John P.] Univ Penn Hlth Syst, Philadelphia, PA USA.
[Roberts, Kenneth B.] Yale Univ, Sch Med, New Haven, CT USA.
[Shapiro, Ronald] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[Terezakis, Stephanie A.] Johns Hopkins Univ Hosp, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21287 USA.
[Winkfield, Karen M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Constine, Louis S.] Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
RP Hoppe, BS (reprint author), Univ Florida, Proton Therapy Inst, Jacksonville, FL 32209 USA.
RI Flowers, Christopher/F-1953-2010;
OI Flowers, Christopher/0000-0002-9524-3990; Terezakis,
Stephanie/0000-0003-4933-6712; Hoppe, Bradford/0000-0002-2312-5418
FU Novartis; Johnson Johnson; Seattle Genetics; Merck; Genentech; Infinity;
Gilead
FX Christopher R. Flowers, MD, MS reports: "I provide consultation for the
Prescription Solutions Pharmacy & Therapeutics Division. My consultation
involves advice on FDA regulated drugs only. None of my consultation
overlaps with existing or planned ACR guidelines." Anas Younes, MD,
reports: "Honoraria from Novartis, Seattle Genetics, Millennium,
Celgene, Curis, Sanofi, Pharmacyclics, and Incyte; research support from
Novartis, Johnson & Johnson, Seattle Genetics, Merck, Genentech,
Infinity, and Gilead."
NR 46
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U1 0
U2 1
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 2013
VL 27
IS 8
BP 786
EP 794
PG 9
WC Oncology
SC Oncology
GA 208NM
UT WOS:000323686400009
PM 24133827
ER
PT J
AU Richardson, PG
Laubach, J
Paba-Prada, C
Anderson, KC
AF Richardson, Paul G.
Laubach, Jacob
Paba-Prada, Claudia
Anderson, Kenneth C.
TI IgD and IgE Variants of Myeloma: Valuable Insights and Therapeutic
Opportunities THE PANDEY/KYLE ARTICLE REVIEWED
SO ONCOLOGY-NEW YORK
LA English
DT Editorial Material
ID MULTIPLE-MYELOMA; EXTRAMEDULLARY DISEASE; PRESENTING FEATURES;
TRANSPLANTATION; AMYLOIDOSIS; SURVIVAL
C1 [Richardson, Paul G.; Laubach, Jacob; Paba-Prada, Claudia; Anderson, Kenneth C.] Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Div Hematol Malignancies, Boston, MA 02115 USA.
RP Richardson, PG (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Jerome Lipper Multiple Myeloma Ctr, Div Hematol Malignancies, Boston, MA 02115 USA.
NR 22
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U1 0
U2 1
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 2013
VL 27
IS 8
BP 803
EP +
PG 3
WC Oncology
SC Oncology
GA 208NM
UT WOS:000323686400012
PM 24133830
ER
PT J
AU Schulz, CF
Davis, TT
Fung, DA
AF Schulz, Carolyn F.
Davis, Timothy T.
Fung, Daniel A.
TI Epidural Lipomatosis as a Cause for High Impedance Values During a
Spinal Cord Stimulator Trial
SO PM&R
LA English
DT Article
ID MECHANISMS
C1 [Schulz, Carolyn F.] Univ Calif Los Angeles, Greater Los Angeles Vet Affairs Hlth Care Syst, Los Angeles, CA USA.
[Davis, Timothy T.; Fung, Daniel A.] Ctr Spine & Joint Restorat, Santa Monica, CA 90043 USA.
RP Fung, DA (reprint author), Ctr Spine & Joint Restorat, 2811 Wilshire Blvd,Suite 850, Santa Monica, CA 90043 USA.
EM DFUNGMD@gmail.com
FU Medtronic
FX Disclosures outside this publication: board membership (no money), ABNM;
consultancy, Medtronic; payment for lectures including service on
speakers bureaus, Medtronic; payment for development of educational
presentations, Medtronic; travel/accommodations/meeting expenses,
Medtronic
NR 9
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1934-1482
J9 PM&R
JI PM&R
PD AUG
PY 2013
VL 5
IS 8
BP 729
EP 731
DI 10.1016/j.pmrj.2013.04.021
PG 3
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 207JK
UT WOS:000323594500019
PM 23643840
ER
PT J
AU DeLelys, ME
Ochoa, G
Cserti-Gazdewich, CM
Vietz, C
Preffer, FI
Dzik, W
AF DeLelys, Michelle E.
Ochoa, Gorka
Cserti-Gazdewich, Christine M.
Vietz, Christine
Preffer, Frederic I.
Dzik, Walter
TI Relationship between ABO genotype and A antigen expression on platelets
SO TRANSFUSION
LA English
DT Article
ID BLOOD-GROUP-A; TRANSFUSION; INCREMENTS; INDIVIDUALS; DELETION; ALLELES;
DISEASE
AB BACKGROUND: Although platelets (PLTs) are known to express ABH antigens, the extent of expression is different on PLTs compared with red blood cells and the relationship between PLT ABH expression and genotype has not been thoroughly investigated.
STUDY DESIGN AND METHODS: We measured blood group H and A antigens on PLTs from 100 normal volunteers using fluorescent-conjugated reagents and flow cytometry. Individuals were also genotyped at the ABO locus using a commercially available genotyping system.
RESULTS: Expression of A and H antigen varied widely on PLTs from different individuals. Among group A and AB persons, H antigen expression was significantly greater than A antigen (p<0.0001). The ratio of H-to-A antigen expression varied more than 100-fold in a predictable fashion according to genotype with values lowest in A(1)/A(1)18 years) ED visits resulting in discharge in 2007. Candidate predictors included index hospital structural characteristics such as ownership, teaching affiliation, trauma status, and index ED size, along with index visit patient characteristics of demographic information, day of service, against medical advice or eloped disposition, insurance, and ED primary discharge diagnosis. We fit a nnultivariable, hierarchic logistic regression to account for clustering of ED visits by hospitals.
Results: The study cohort contained a total of 5,035,833 visits to 288 facilities in 2007. Bounce-back admission within 7 days occurred in 130,526 (2.6%) visits and was associated with Medicaid (odds ratio [OR] 1.42; 95% confidence interval [CI] 1.40 to 1.45) or Medicare insurance (OR 1.53; 95% CI 1.50 to 1.55) and a disposition of leaving against medical advice or before the evaluation was complete (OR 1.90; 95% CI 1.89 to 2.0). The 3 most common age-adjusted index ED discharge diagnoses associated with a bounce-back admission were chronic renal disease, not end stage (OR 3.3; 95% CI 2.8 to 3.8), end-stage renal disease (OR 2.9; 95% CI 2.4 to 3.6), and congestive heart failure (OR 2.5; 95% CI 2.3 to 2.6). Hospital characteristics associated with a higher bounce-back admission rate were for-profit status (OR 1.2; 95% CI 1.1 to 1.3) and teaching affiliation (OR 1.2; 95% CI 1.0 to 1.3).
Conclusion: We found 2.6% of discharged patients from California EDs to have a bounce-back admission within 7 days. We identified vulnerable populations, such as the very old and the use of Medicaid insurance, and chronic or end-stage renal disease as being especially at risk. Our findings suggest that quality improvement efforts focus on high-risk individuals and that the disposition plan of patients consider vulnerable populations.
C1 [Gabayan, Gelareh Z.; Zingmond, David; Liang, Li-Jung] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Gabayan, Gelareh Z.] Greater Los Angeles Vet Affairs Healthcare Syst, Div Emergency Med, Los Angeles, CA USA.
[Gabayan, Gelareh Z.] Ronald Reagan UCLA, Ctr Emergency Med, Los Angeles, CA USA.
[Asch, Steven M.] Vet Affairs Palo Alto Healthcare Syst, Div Gen Med Disciplines, Palo Alto, CA USA.
[Asch, Steven M.] Stanford Sch Med, Palo Alto, CA USA.
[Hsia, Renee Y.] Univ Calif San Francisco, Dept Emergency Med, San Francisco, CA 94143 USA.
[Han, Weijuan; McCreath, Heather; Weiss, Robert E.] UCLA Fielding Sch Publ Hlth, Dept Biostat, Los Angeles, CA USA.
[Sun, Benjamin C.] Oregon Hlth & Sci Univ, Dept Emergency Med, Portland, OR 97201 USA.
RP Gabayan, GZ (reprint author), Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
EM gelareh@gabayan.com
FU Emergency Medicine Foundation; Agency for Healthcare Research and
Quality [R03 HS18098]; UCLA Older American Independence Center
NIH/National Institute on Aging (NIA) grant; NIH/NCRR/OD UCSF-CTSI grant
[KL2RR024130]; Robert Wood Johnson Foundation Physician Faculty
Scholars; NIH/NCRR/NCATS UCLA CTSI [KL2TR000122]
FX By Annals policy, all authors are required to disclose any and all
commercial, financial, and other relationships in any way related to the
subject of this article as per ICMJE conflict of interest guidelines
(see www.icmje.org). The authors have stated that no such relationships
exist. This research was supported by the Emergency Medicine Foundation
(Dr. Sun), the Agency for Healthcare Research and Quality (Dr. Sun, R03
HS18098), the UCLA Older American Independence Center NIH/National
Institute on Aging (NIA) grant (Dr. McCreath, Mrs. Han), the NIH/NCRR/OD
UCSF-CTSI grant (Dr. Hsia, KL2RR024130), and the Robert Wood Johnson
Foundation Physician Faculty Scholars (Dr. Hsia). Dr. Gabayan receives
support from the NIH/NCRR/NCATS UCLA CTSI (grant KL2TR000122). The
content is solely the responsibility of the authors and does not
necessarily represent the official views of the National Institutes of
Health or the NIA. The funding organizations did not have a role in the
design and conduct of the study; management, analysis, and
interpretation of the data; and preparation, review, or approval of the
article.
NR 42
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U1 0
U2 14
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 2013
VL 62
IS 2
BP 136
EP 144
DI 10.1016/j.annemergmed.2013.01.017
PG 9
WC Emergency Medicine
SC Emergency Medicine
GA 199SC
UT WOS:000323014800008
PM 23465554
ER
PT J
AU Doran, KM
Raven, MC
Rosenheck, RA
AF Doran, Kelly M.
Raven, Maria C.
Rosenheck, Robert A.
TI What Drives Frequent Emergency Department Use in an Integrated Health
System? National Data From the Veterans Health Administration
SO ANNALS OF EMERGENCY MEDICINE
LA English
DT Article
ID UTILIZATION PATTERNS; MENTAL-DISORDERS; RANDOMIZED-TRIAL;
CASE-MANAGEMENT; MEDICAL-CARE; RISK-FACTORS; SERVICES; OUTCOMES;
DEFINITIONS; POPULATION
AB Study objective: There is widespread concern about patients with frequent emergency department (ED) use. We identify sociodemographic and clinical factors most strongly associated with frequent ED use within the Veterans Health Administration (VHA) nationally.
Methods: We conducted a cross-sectional analysis of national VHA databases (N=5,531,379) in 2010. The primary outcome measure was the number of VHA ED visits categorized into 6 frequency levels.
Results: In 2010, 4,600,667 (83.2%) VHA patients had no ED visit, whereas 493,391 (8.9%) had 1 visit, 356,258 (6.4%) had 2 to 4 visits, 70,741 (1.3%) had 5 to 10 visits, 9,705 (0.2%) had 11 to 25 visits, and 617 (0.01%) had greater than 25 visits. Increasing ED use frequency was associated with homelessness, medical diagnoses, substance abuse and psychiatric diagnoses, receipt of psychotropic and opioid prescriptions, and more frequent use of outpatient medical and mental health services. In multivariable analyses, factors most strongly associated with all levels of ED use were schizophrenia (odds ratio [OR] range 1.44 [95% confidence interval {Cl} 1.41 to 1.47] to 6.86 [95% Cl 5.55 to 8.48] across categories of increasing ED use), homelessness (OR range 1.41 [95% CI 1.38 to 1.43] to 6.60 [95% Cl 5.36 to 8.12]), opioid prescriptions filled (OR range 2.09 [95% Cl 2.07 to 2.10] to 5.08 [95% Cl 4.16 to 6.19]), and heart failure (OR range 1.64 [95% Cl 1.63 to 1.66] to 3.53 [95% Cl 2.64 to 4.72]).
Conclusion: Frequent ED use occurs even in a coordinated health care system that provides ready access to outpatient care. Frequent ED users are characterized by traits that represent high levels of psychosocial and medical needs. The correlates we identified for frequent ED use were consistent across multiple distinct levels of ED use.
C1 [Doran, Kelly M.] Yale Univ, Sch Med, Robert Wood Johnson Fdn Clin Scholars Program, New Haven, CT 06520 USA.
[Doran, Kelly M.] US Dept Vet Affairs, New Haven, CT USA.
[Doran, Kelly M.] Yale Univ, Sch Med, Dept Emergency Med, New Haven, CT USA.
[Rosenheck, Robert A.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Raven, Maria C.] Univ Calif San Francisco, Dept Emergency Med, San Francisco, CA 94143 USA.
[Rosenheck, Robert A.] VA New England Mental Illness Res Educ & Clin Ctr, West Haven, CT USA.
RP Doran, KM (reprint author), Yale Univ, Sch Med, Robert Wood Johnson Fdn Clin Scholars Program, New Haven, CT 06520 USA.
EM kelly.doran@yale.edu
FU VA New England Mental Illness Research and Education Center
FX By Annals policy, all authors are required to disclose any and all
commercial, financial, and other relationships in any way related to the
subject of this article as per ICMJE conflict of interest guidelines
(see www.icmje.org). The authors have stated that no such relationships
exist. Support was provided by the VA New England Mental Illness
Research and Education Center. The funder had no role in the design and
conduct of the study; collection, management, analysis, and
interpretation of the data; and the preparation, review, or approval of
the article.
NR 44
TC 35
Z9 35
U1 2
U2 15
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 2013
VL 62
IS 2
BP 151
EP 159
DI 10.1016/j.annemergmed.2013.02.016
PG 9
WC Emergency Medicine
SC Emergency Medicine
GA 199SC
UT WOS:000323014800011
PM 23582617
ER
PT J
AU Dutta, S
Long, WJ
Brown, DFM
Reisner, AT
AF Dutta, Sayon
Long, William J.
Brown, David F. M.
Reisner, Andrew T.
TI Automated Detection Using Natural Language Processing of Radiologists
Recommendations for Additional Imaging of Incidental Findings
SO ANNALS OF EMERGENCY MEDICINE
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the American-College-of-Emergency-Physicians
CY OCT 15-16, 2011
CL San Francisco, CA
SP Amer Coll Emergency Phys
ID PREVALENCE; RECORDS; CANCER; SCANS
AB Study objective: As use of radiology studies increases, there is a concurrent increase in incidental findings (eg, lung nodules) for which the radiologist issues recommendations for additional imaging for follow-up. Busy emergency physicians may be challenged to carefully communicate recommendations for additional imaging not relevant to the patient's primary evaluation. The emergence of electronic health records and natural language processing algorithms may help address this quality gap. We seek to describe recommendations for additional imaging from our institution and develop and validate an automated natural language processing algorithm to reliably identify recommendations for additional imaging.
Methods: We developed a natural language processing algorithm to detect recommendations for additional imaging, using 3 iterative cycles of training and validation. The third cycle used 3,235 radiology reports (1,600 for algorithm training and 1,635 for validation) of discharged emergency department (ED) patients from which we determined the incidence of discharge-relevant recommendations for additional imaging and the frequency of appropriate discharge documentation. The test characteristics of the 3 natural language processing algorithm iterations were compared, using blinded chart review as the criterion standard.
Results: Discharge-relevant recommendations for additional imaging were found in 4.5% (95% confidence interval [Cl] 3.5% to 5.5%) of ED radiology reports, but 51% (95% Cl 43% to 59%) of discharge instructions failed to note those findings. The final natural language processing algorithm had 89% (95% Cl 82% to 94%) sensitivity and 98% (95% Cl 97% to 98%) specificity for detecting recommendations for additional imaging. For discharge-relevant recommendations for additional imaging, sensitivity improved to 97% (95% Cl 89% to 100%).
Conclusion: Recommendations for additional imaging are common, and failure to document relevant recommendations for additional imaging in ED discharge instructions occurs frequently. The natural language processing algorithm's performance improved with each iteration and offers a promising error-prevention tool.
C1 [Dutta, Sayon; Brown, David F. M.; Reisner, Andrew T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA 02115 USA.
[Long, William J.] MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.
RP Dutta, S (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA 02115 USA.
EM sdutta1@partners.org
NR 29
TC 9
Z9 9
U1 0
U2 6
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 2013
VL 62
IS 2
BP 162
EP 169
DI 10.1016/j.annemergmed.2013.02.001
PG 8
WC Emergency Medicine
SC Emergency Medicine
GA 199SC
UT WOS:000323014800013
PM 23548405
ER
PT J
AU Bekris, LM
Lutz, F
Montine, TJ
Yu, CE
Tsuang, D
Peskind, ER
Leverenz, JB
AF Bekris, Lynn M.
Lutz, Franziska
Montine, Thomas J.
Yu, Chang En
Tsuang, Debby
Peskind, Elaine R.
Leverenz, James B.
TI MicroRNA in Alzheimer's disease: an exploratory study in brain,
cerebrospinal fluid and plasma
SO BIOMARKERS
LA English
DT Article
DE Amyloid; biomarker; braak stage; miR-15a; miR-370; miR-328; miR-138;
miR-132; plaque
ID ENDOGENOUS CONTROL GENES; NEUROPATHOLOGIC ASSESSMENT; PROSTATE-CANCER;
NEURONAL LOSS; EXPRESSION; IDENTIFICATION; DEMENTIA; MIRNA; BIOMARKERS;
DIAGNOSIS
AB MicroRNA (miRNA) may be potential biomarkers of Alzheimer's disease (AD). The objective of this investigation was to demonstrate that miRNAs in human brain or biofluids are differentially expressed according to disease status, tissue type, neuritic plaque score or Braak stage. Post-mortem brain (PMB) miRNA were profiled using arrays and validated using quantitative RT-PCR (qRT-PCR). Five gRT-PCR-validated miRNAs were measured in an independent sample of PMB, cerebrospinal fluid and plasma from the same subjects. Plasma miR-15a was found to be associated with plaque score in the independent sample. In conclusion, miRNA present in human biofluids may offer utility as biomarkers of AD.
C1 [Bekris, Lynn M.; Lutz, Franziska; Yu, Chang En; Tsuang, Debby; Leverenz, James B.] VA Puget Sound Hlth Care Syst, Dept Geriatr GRECC, Res Ctr, Seattle, WA USA.
[Bekris, Lynn M.; Lutz, Franziska; Yu, Chang En; Tsuang, Debby; Leverenz, James B.] VA Puget Sound Hlth Care Syst, Dept Geriatr GRECC, Educ Ctr, Seattle, WA USA.
[Bekris, Lynn M.; Lutz, Franziska; Yu, Chang En; Tsuang, Debby; Leverenz, James B.] VA Puget Sound Hlth Care Syst, Dept Geriatr GRECC, Ctr Clin, Seattle, WA USA.
[Bekris, Lynn M.; Lutz, Franziska; Yu, Chang En] Univ Washington, Dept Med, Seattle, WA 98108 USA.
[Montine, Thomas J.] Univ Washington, Dept Pathol, Seattle, WA 98108 USA.
[Tsuang, Debby; Peskind, Elaine R.; Leverenz, James B.] VA Puget Sound Hlth Care Syst, Dept Mental Illness MIRECC, Res Ctr, Seattle, WA USA.
[Tsuang, Debby; Peskind, Elaine R.; Leverenz, James B.] VA Puget Sound Hlth Care Syst, Dept Mental Illness MIRECC, Educ Ctr, Seattle, WA USA.
[Tsuang, Debby; Peskind, Elaine R.; Leverenz, James B.] VA Puget Sound Hlth Care Syst, Dept Mental Illness MIRECC, Ctr Clin, Seattle, WA USA.
[Tsuang, Debby; Peskind, Elaine R.; Leverenz, James B.] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98108 USA.
[Leverenz, James B.] VA Puget Sound Hlth Care Syst, Dept Parkinsons Dis PADRECC, Res Ctr, Seattle, WA USA.
[Leverenz, James B.] VA Puget Sound Hlth Care Syst, Dept Parkinsons Dis PADRECC, Educ Ctr, Seattle, WA USA.
[Leverenz, James B.] VA Puget Sound Hlth Care Syst, Dept Parkinsons Dis PADRECC, Ctr Clin, Seattle, WA USA.
[Leverenz, James B.] Univ Washington, Dept Neurol, Seattle, WA 98108 USA.
RP Bekris, LM (reprint author), Univ Washington, Dept Med, Div Gerontol & Geriatr Med, Box 358280 VAPSHCS GRECC S182,1660 South Columbia, Seattle, WA 98108 USA.
EM lbekris@uw.edu
RI Tsuang, Debby/L-7234-2016
OI Tsuang, Debby/0000-0002-4716-1894
FU U.S. Department of Veterans Affairs, Office of Research and Development
Clinical Research and Development Program; Biomedical Laboratory
Research Program; NIH [P50AG005136-27, P50NS062684-01A1, P50 NS062684,
K99AG034214-02/R00AG034214-03]
FX This work is supported, in part, by the U.S. Department of Veterans
Affairs, Office of Research and Development Clinical Research and
Development Program, the Biomedical Laboratory Research Program and NIH
Grants: P50AG005136-27, P50NS062684-01A1, P50 NS062684 and
K99AG034214-02/R00AG034214-03.
NR 79
TC 31
Z9 34
U1 0
U2 36
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1354-750X
J9 BIOMARKERS
JI Biomarkers
PD AUG
PY 2013
VL 18
IS 5
BP 455
EP 466
DI 10.3109/1354750X.2013.814073
PG 12
WC Biotechnology & Applied Microbiology; Toxicology
SC Biotechnology & Applied Microbiology; Toxicology
GA 200RF
UT WOS:000323085900012
PM 23822153
ER
PT J
AU Tracy, MS
Rosenberg, SM
Dominici, L
Partridge, AH
AF Tracy, Michaela S.
Rosenberg, Shoshana M.
Dominici, Laura
Partridge, Ann H.
TI Contralateral prophylactic mastectomy in women with breast cancer:
trends, predictors, and areas for future research
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Review
DE Contralateral prophylactic mastectomy; Breast cancer; Surgery
ID QUALITY-OF-LIFE; YOUNG-WOMEN; TUMOR CHARACTERISTICS; GERMLINE MUTATIONS;
FAMILY-HISTORY; DECISION AID; SURVIVAL; RISK; EFFICACY; RECONSTRUCTION
AB Recent studies have revealed increasing rates of contralateral prophylactic mastectomy (CPM) among women with unilateral early stage breast cancer. This trend has raised concerns, given the lack of evidence for a survival benefit from CPM and the relatively low risk of contralateral breast cancer for most women in this setting. In this article, we review available data regarding the value of CPM, predictors, and outcomes related to CPM, and areas for future research and potential intervention.
C1 [Tracy, Michaela S.; Rosenberg, Shoshana M.; Dominici, Laura; Partridge, Ann H.] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Partridge, AH (reprint author), Brigham & Womens Hosp, Dana Farber Canc Inst, 450 Brookline Ave Boston, Boston, MA 02215 USA.
EM ahpartridge@partners.org
FU National Cancer Institute [NIH 5 R25 CA057711]
FX Dr. Rosenberg receives funding from the National Cancer Institute (NIH 5
R25 CA057711).
NR 46
TC 20
Z9 20
U1 2
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
EI 1573-7217
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD AUG
PY 2013
VL 140
IS 3
BP 447
EP 452
DI 10.1007/s10549-013-2643-6
PG 6
WC Oncology
SC Oncology
GA 202UP
UT WOS:000323245400002
PM 23893127
ER
PT J
AU Specht, MC
Miller, CL
Russell, TA
Horick, N
Skolny, MN
O'Toole, JA
Jammallo, LS
Niemierko, A
Sadek, BT
Shenouda, MN
Finkelstein, DM
Smith, BL
Taghian, AG
AF Specht, Michelle C.
Miller, Cynthia L.
Russell, Tara A.
Horick, Nora
Skolny, Melissa N.
O'Toole, Jean A.
Jammallo, Lauren S.
Niemierko, Andrzej
Sadek, Betro T.
Shenouda, Mina N.
Finkelstein, Dianne M.
Smith, Barbara L.
Taghian, Alphonse G.
TI Defining a threshold for intervention in breast cancer-related
lymphedema: what level of arm volume increase predicts progression?
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Lymphedema; Quality of life; Compression therapy; Threshold for
intervention; Early intervention
ID SENTINEL NODE BIOPSY; RISK-FACTORS; FOLLOW-UP; AXILLARY DISSECTION;
CONSERVING THERAPY; EARLY-DIAGNOSIS; LIMB VOLUME; GROUP TRIAL;
SURVIVORS; SURGERY
AB The purpose of this study is to evaluate arm volume measurements and clinico-pathologic characteristics of breast cancer patients to define a threshold for intervention in breast cancer-related lymphedema. We prospectively performed arm volume measurements on breast cancer patients using a Perometer. Arm measurements were performed pre- and post-operatively, and change in arm volume was quantified using a relative volume change (RVC) equation. Patient and treatment risk factors were evaluated. Cox proportional hazards models with time-dependent covariates for RVC were used to evaluate whether RVC elevations of a parts per thousand yen3 to < 5 % or a parts per thousand yen5 to < 10 % occurring a parts per thousand currency sign3 months or > 3 months after surgery were associated with progression to a parts per thousand yen10 % RVC. 1,173 patients met eligibility criteria with a median of 27 months post-operative follow-up. The cumulative incidence of a parts per thousand yen10 % RVC at 24 months was 5.26 % (95 % CI 4.01-6.88 %). By multivariable analysis, a measurement of a parts per thousand yen5 to < 10 % RVC occurring > 3 months after surgery was significantly associated with an increased risk of progression to a parts per thousand yen10 % RVC (HR 2.97, p < 0.0001), but a measurement of a parts per thousand yen3 to < 5 % RVC during the same time period was not statistically significantly associated (HR 1.55, p = 0.10). Other significant risk factors included a measurement a parts per thousand currency sign3 months after surgery with RVC of a parts per thousand yen3 to < 5 % (p = 0.007), a parts per thousand yen5 to < 10 % (p < 0.0001), or a parts per thousand yen10 % (p = 0.023), axillary lymph node dissection (ALND) (p < 0.0001), and higher BMI at diagnosis (p = 0.0028). Type of breast surgery, age, number of positive or number of lymph nodes removed, nodal radiation, chemotherapy, and hormonal therapy were not significant (p > 0.05). Breast cancer patients who experience a relative arm volume increase of a parts per thousand yen3 to < 5 % occurring > 3 months after surgery do not have a statistically significant increase in risk of progression to a parts per thousand yen10 %, a common lymphedema criterion. Our data support utilization of a a parts per thousand yen5 to < 10 % threshold for close monitoring or intervention, warranting further assessment. Additional risk factors for progression to a parts per thousand yen10 % include ALND, higher BMI, and post-operative arm volume elevation.
C1 [Specht, Michelle C.; Smith, Barbara L.] Massachusetts Gen Hosp, Div Surg Oncol, Boston, MA 02114 USA.
[Miller, Cynthia L.; Russell, Tara A.; Skolny, Melissa N.; Jammallo, Lauren S.; Niemierko, Andrzej; Sadek, Betro T.; Shenouda, Mina N.; Taghian, Alphonse G.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Horick, Nora; Finkelstein, Dianne M.] Massachusetts Gen Hosp, Dept Biostat, Boston, MA 02114 USA.
[O'Toole, Jean A.] Massachusetts Gen Hosp, Dept Phys & Occupat Therapy, Boston, MA 02114 USA.
RP Taghian, AG (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, 100 Blossom St, Boston, MA 02114 USA.
EM ataghian@partners.org
RI Sadek, Betro/I-7734-2013
OI Sadek, Betro/0000-0003-0119-7207
FU National Cancer Institute [R01CA139118, P50CA089393]
FX This project was supported by Award R01CA139118 (AGT), and Award
P50CA089393 (AGT) from the National Cancer Institute. The content is
solely the responsibility of the authors and does not necessarily
represent the views of the National Cancer Institute or the National
Institutes of Health. In addition, we would like to acknowledge Nadine
R. Taghian, whose dedication helped expedite completion of this project.
The authors are greatly appreciative of her efforts.
NR 65
TC 20
Z9 20
U1 0
U2 11
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 2013
VL 140
IS 3
BP 485
EP 494
DI 10.1007/s10549-013-2655-2
PG 10
WC Oncology
SC Oncology
GA 202UP
UT WOS:000323245400006
PM 23912961
ER
PT J
AU Porthan, K
Viitasalo, M
Toivonen, L
Havulinna, AS
Jula, A
Tikkanen, JT
Vaananen, H
Nieminen, MS
Huikuri, HV
Newton-Cheh, C
Salomaa, V
Oikarinen, L
AF Porthan, Kimmo
Viitasalo, Matti
Toivonen, Lauri
Havulinna, Aki S.
Jula, Antti
Tikkanen, Jani T.
Vaeaenaenen, Heikki
Nieminen, Markku S.
Huikuri, Heikki V.
Newton-Cheh, Christopher
Salomaa, Veikko
Oikarinen, Lasse
TI Predictive Value of Electrocardiographic T-Wave Morphology Parameters
and T-Wave Peak to T-Wave End Interval for Sudden Cardiac Death in the
General Population
SO CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY
LA English
DT Article
DE electrocardiography; epidemiology; prognosis; repolarization; sudden
death
ID CORONARY-HEART-DISEASE; VENTRICULAR REPOLARIZATION; CARDIOVASCULAR
MORTALITY; ALL-CAUSE; QT INTERVAL; POSTMENOPAUSAL WOMEN;
AMERICAN-INDIANS; RISK-FACTORS; HETEROGENEITY; MEN
AB Background-Previous population studies have found an association between electrocardiographic T-wave morphology parameters and cardiovascular mortality, but their relationship to sudden cardiac death (SCD) is not clear. To our knowledge, there are no follow-up studies assessing the association between electrocardiographic T-wave peak to T-wave end interval (TPE) and SCD. We assessed the predictive value of electrocardiographic T-wave morphology parameters and TPE for SCD in an adult general population sample.
Methods and Results-A total of 4 T-wave morphology parameters (principal component analysis ratio, T-wave morphology dispersion, total cosine R-to-T, T-wave residuum) as well as TPE were measured from digital standard 12-lead ECGs in 5618 adults (46% men; mean age 50.9 +/- 12.5 years) participating in the Finnish population-based Health 2000 Study. After a mean follow-up time of 7.7 +/- 1.4 years, 72 SCDs had occurred. In univariable analyses, all T-wave morphology parameters were associated with an increased SCD risk. In multivariable Cox models, T-wave morphology dispersion and total cosine R-to-T remained as predictors of SCD, with T-wave morphology dispersion showing the highest SCD risk (hazard ratio of 1.4 [95% confidence interval 1.1-1.7, P=0.001] per 1 SD increase in the log(e) T-wave morphology dispersion). In contrast, TPE was not associated with SCD in univariable or multivariable analyses.
Conclusions-Electrocardiographic T-wave morphology parameters describing the 3-dimensional shape of the T-wave stratify SCD risk in the general population, but we did not find an association between TPE and SCD.
C1 [Porthan, Kimmo; Viitasalo, Matti; Toivonen, Lauri; Nieminen, Markku S.; Oikarinen, Lasse] Univ Helsinki, Cent Hosp, Dept Med, Div Cardiol, Helsinki 00029, Finland.
[Havulinna, Aki S.; Salomaa, Veikko] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Jula, Antti] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Turku, Finland.
[Tikkanen, Jani T.; Huikuri, Heikki V.] Univ Oulu, Inst Clin Med, Dept Internal Med, SF-90100 Oulu, Finland.
[Tikkanen, Jani T.; Huikuri, Heikki V.] Univ Cent Hosp Oulu, Oulu, Finland.
[Huikuri, Heikki V.] Aalto Univ, Dept Biomed Engn & Computat Sci, Helsinki, Finland.
[Newton-Cheh, Christopher] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Newton-Cheh, Christopher] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Newton-Cheh, Christopher] Harvard Univ, Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Newton-Cheh, Christopher] MIT, Cambridge, MA 02139 USA.
RP Porthan, K (reprint author), Univ Helsinki, Cent Hosp, Dept Med, Div Cardiol, Haartmaninkatu 4,POB 340, Helsinki 00029, Finland.
EM kimmo.porthan@fimnet.fi
FU Aarne Koskelo Foundation; Finnish Foundation for Cardiovascular
Research; Finnish Medical Foundation; Orion-Farmos Research Foundation;
Finnish Cultural Foundation; Academy of Finland [129494, 139635]
FX Dr Porthan was supported by grants from the Aarne Koskelo Foundation,
the Finnish Foundation for Cardiovascular Research, the Finnish Medical
Foundation, and the Orion-Farmos Research Foundation. Drs Viitasalo,
Huikuri, and Oikarinen were supported by grants from the Finnish
Foundation for Cardiovascular Research. Dr Tikkanen was supported by
grants from the Finnish Foundation for Cardiovascular Research, the
Finnish Cultural Foundation, and the Finnish Medical Foundation. Dr
Salomaa was supported by the Academy of Finland (grant numbers 129494
and 139635) and the Finnish Foundation for Cardiovascular Research.
NR 37
TC 21
Z9 22
U1 0
U2 6
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 2013
VL 6
IS 4
BP 690
EP 696
DI 10.1161/CIRCEP.113.000356
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 203WB
UT WOS:000323323900016
PM 23881778
ER
PT J
AU Sayadi, O
Merchant, FM
Puppala, D
Mela, T
Singh, JP
Heist, EK
Owen, C
Armoundas, AA
AF Sayadi, Omid
Merchant, Faisal M.
Puppala, Dheeraj
Mela, Theofanie
Singh, Jagmeet P.
Heist, E. Kevin
Owen, Chris
Armoundas, Antonis A.
TI A Novel Method for Determining the Phase of T-Wave Alternans: Diagnostic
and Therapeutic Implications
SO CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY
LA English
DT Article
DE alternans; arrhythmia (heart rhythm disorders); defibrillators,
implantable; intracardiac electrogram; pacing
ID IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR; REPOLARIZATION ALTERNANS;
VENTRICULAR TACHYARRHYTHMIAS; RISK STRATIFICATION; CARDIAC ALTERNANS;
FIBRILLATION; HEART; ELECTROGRAMS; TACHYCARDIA; MECHANISMS
AB Background-T-wave alternans (TWA) has been implicated in the pathogenesis of ventricular arrhythmias and sudden cardiac death. However, to estimate and suppress TWA effectively, the phase of TWA must be accurately determined.
Methods and Results-We developed a method that computes the beat-by-beat integral of the T-wave morphology, over time points within the T-wave with positive alternans. Then, we estimated the signed derivative of the T-wave integral sequence, which allows the classification of each beat to a binary phase index. In animal studies, we found that this method was able to accurately identify the T-wave phase in artificially induced alternans (P<0.0001). The coherence of the phase increased consistently after acute ischemia induction in all body-surface and intracardiac leads (P<0.0001). Also, we developed a phase-resetting detection algorithm that enhances the diagnostic utility of TWA. We further established an algorithm that uses the phase of TWA to deliver appropriate polarity-pacing pulses (all interventions compared with baseline, P<0.0001 for alternans voltage; P<0.0001 for K-score), to suppress TWA. Finally, we demonstrated that using the phase of TWA we can suppress spontaneous TWA during acute ischemia; 77.6% for alternans voltage (P<0.0001) and 92.5% for K-score (P<0.0001).
Conclusions-We developed a method to quantify the temporal variability of the TWA phase. This method is expected to enhance the utility of TWA in predicting ventricular arrhythmias and sudden cardiac death and raises the possibility of using upstream therapies to abort a ventricular tachyarrhythmia before its onset.
C1 [Sayadi, Omid; Puppala, Dheeraj; Armoundas, Antonis A.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Mela, Theofanie; Singh, Jagmeet P.; Heist, E. Kevin] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Owen, Chris] Massachusetts Gen Hosp, Div Neurosurg, Boston, MA 02114 USA.
[Merchant, Faisal M.] Emory Univ, Sch Med, Div Cardiol, Atlanta, GA 30322 USA.
[Armoundas, Antonis A.] MIT, Inst Med Engn & Sci, Cambridge, MA 02139 USA.
RP Armoundas, AA (reprint author), Massachusetts Gen Hosp, Cardiovasc Res Ctr, 149 13th St, Charlestown, MA 02129 USA.
EM aarmoundas@partners.org
FU Scientist Development Grant [0635127 N]; American Heart Association
[12POST9310001]; National Institutes of Health (NIH) [1R21AG035128];
Center for Integration of Medicine and Innovative Technology (CIMIT);
Deane Institute for Integrative Research in Atrial Fibrillation and
Stroke; Cardiovascular Research Society; Harvard Catalyst; Harvard
Clinical and Translational Science Center (National Center for Research
Resources); Harvard Clinical and Translational Science Center (National
Center for Advancing Translational Sciences, NIH) [8UL1TR000170-05];
Harvard University and its affiliated academic healthcare centers)
FX The work was supported by a Scientist Development Grant (#0635127 N) and
a Founders Affiliate Post-doctoral Fellowship (#12POST9310001) from the
American Heart Association, and by National Institutes of Health (NIH)
grant 1R21AG035128. This work was also supported by a Fellowship and a
Science Award from the Center for Integration of Medicine and Innovative
Technology (CIMIT), the Deane Institute for Integrative Research in
Atrial Fibrillation and Stroke, and the Cardiovascular Research Society.
This work was performed with support from Harvard Catalyst, The Harvard
Clinical and Translational Science Center (National Center for Research
Resources and the National Center for Advancing Translational Sciences,
NIH Award 8UL1TR000170-05, and financial contributions from Harvard
University and its affiliated academic healthcare centers). The content
is solely the responsibility of the authors and does not necessarily
represent the official views of Harvard Catalyst, Harvard University and
its affiliated academic healthcare centers, or the NIH.
NR 29
TC 1
Z9 2
U1 0
U2 3
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 2013
VL 6
IS 4
BP 818
EP 826
DI 10.1161/CIRCEP.113.000114
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 203WB
UT WOS:000323323900033
PM 23884196
ER
PT J
AU Gutierrez, A
Tsai, TT
Stanislawski, MA
Vidovich, M
Bryson, CL
Bhatt, DL
Grunwald, GK
Rumsfeld, J
Rao, SV
AF Gutierrez, Antonio
Tsai, Thomas T.
Stanislawski, Maggie A.
Vidovich, Mladen
Bryson, Christopher L.
Bhatt, Deepak L.
Grunwald, Gary K.
Rumsfeld, John
Rao, Sunil V.
TI Adoption of Transradial Percutaneous Coronary Intervention and Outcomes
According to Center Radial Volume in the Veterans Affairs Healthcare
System Insights From the Veterans Affairs Clinical Assessment,
Reporting, and Tracking (CART) Program
SO CIRCULATION-CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE blood transfusion; hemorrhage; percutaneous coronary intervention;
radial artery
ID ACUTE MYOCARDIAL-INFARCTION; FEMORAL ACCESS; TASK-FORCE; ANGIOGRAPHY;
ASSOCIATION; MORTALITY; IMPACT; TRIAL; GUIDELINES; SOCIETY
AB Background-Studies examining the association between radial approach and post-percutaneous coronary intervention (PCI) bleeding and mortality have reached conflicting conclusions. There are no current data about the use and outcomes of transradial PCI (r-PCI) in the Veterans Affairs system.
Methods and Results-Consecutive veterans (n=24143 patients) undergoing PCI in the Veterans Affairs between 2007 and 2010 were examined. On the basis of propensity to undergo r-PCI, 3 cohorts matched with veterans undergoing transfemoral access were constructed among sites performing >= 1 r-PCI, >= 50 r-PCI (high volume), and <50 r-PCI (low volume). Cox proportional hazard models were used to determine the association between PCI access site, blood transfusion, and mortality. The prevalence of r-PCI increased over time (2007=2.1%; 2010=8.8%). Overall, there was no difference in procedure success between matched groups (r-PCI 97.3% versus transfemoral PCI 96.6%; P=0.182), or in the risk of postprocedure transfusion or mortality. Among matched patients treated at high r-PCI volume sites, radial access was associated with a decreased risk of post-PCI blood transfusion (hazard ratio, 0.4; 95% confidence interval, 0.3-0.7; P<0.001), and no significant difference in the risk of mortality (hazard ratio, 0.7; 95% confidence interval, 0.4-1.3; P=0.279).
Conclusions-Within the Veterans Affairs, the use of r-PCI increased over time. r-PCI may be associated with a significant decreased risk of post-PCI blood transfusion among higher volume r-PCI sites. These data demonstrate that potential benefits of r-PCI in terms of reduced post-PCI blood transfusions may be more pronounced at sites that routinely use radial access.
C1 [Gutierrez, Antonio; Bhatt, Deepak L.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Tsai, Thomas T.; Stanislawski, Maggie A.; Grunwald, Gary K.; Rumsfeld, John] Univ Colorado Denver, VA Eastern Colorado Healthcare Syst, Aurora, CO USA.
[Vidovich, Mladen] Univ Illinois, VA Med Ctr, Chicago, IL USA.
[Bryson, Christopher L.] Seattle VA Med Ctr, Seattle, WA USA.
[Bhatt, Deepak L.] VA Boston Healthcare Syst, West Roxbury, MA USA.
[Rao, Sunil V.] Duke Clin Res Inst, Durham VA Med Ctr, Durham, NC USA.
RP Gutierrez, A (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, 75 Francis St, Boston, MA 02115 USA.
EM Antonio.Gutierrez3@va.gov
NR 28
TC 15
Z9 15
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7640
J9 CIRC-CARDIOVASC INTE
JI Circ.-Cardiovasc. Interv.
PD AUG
PY 2013
VL 6
IS 4
BP 336
EP 346
DI 10.1161/CIRCINTERVENTIONS.113.000110
PG 11
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 203VX
UT WOS:000323323300007
PM 23941860
ER
PT J
AU Goodrich, DE
Kilbourne, AM
Nord, KM
Bauer, MS
AF Goodrich, David E.
Kilbourne, Amy M.
Nord, Kristina M.
Bauer, Mark S.
TI Mental Health Collaborative Care and its Role in Primary Care Settings
SO CURRENT PSYCHIATRY REPORTS
LA English
DT Article
DE Mental health; Co-occurring conditions; Primary care; PCP; Integrated
care; Collaborative care; Chronic care model; CCM; Accountable care
organization; ACO; Patient-centered medical home; Screening; Diagnosis;
Treatment; Access; Mental health services; Psychiatry; Bipolar disorder;
Mood disorder; Substance abuse disorder; Anxiety disorder; Serious
mental illness
ID RANDOMIZED-CONTROLLED-TRIAL; MAJOR DEPRESSIVE DISORDER; BIPOLAR
DISORDER; UNITED-STATES; MEDICATION ADHERENCE; PSYCHIATRIC-SERVICES;
COST-EFFECTIVENESS; BRIEF INTERVENTION; FAMILY PHYSICIANS; COMPLEX
PATIENTS
AB Collaborative care models (CCMs) provide a pragmatic strategy to deliver integrated mental health and medical care for persons with mental health conditions served in primary care settings. CCMs are team-based intervention to enact system-level redesign by improving patient care through organizational leadership support, provider decision support, and clinical information systems, as well as engaging patients in their care through self-management support and linkages to community resources. The model is also a cost-efficient strategy for primary care practices to improve outcomes for a range of mental health conditions across populations and settings. CCMs can help achieve integrated care aims underhealth care reform yet organizational and financial issues may affect adoption into routine primary care. Notably, successful implementation of CCMs in routine care will require alignment of financial incentives to support systems redesign investments, reimbursements for mental health providers, and adaptation across different practice settings and infrastructure to offer all CCM components.
C1 [Goodrich, David E.; Kilbourne, Amy M.; Nord, Kristina M.] VA Ann Arbor Ctr Clin Management Res, Ann Arbor, MI 48109 USA.
[Goodrich, David E.; Kilbourne, Amy M.; Nord, Kristina M.] Univ Michigan, Sch Med, Dept Psychiat, Ann Arbor, MI USA.
[Bauer, Mark S.] VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA USA.
[Bauer, Mark S.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
RP Kilbourne, AM (reprint author), VA Ann Arbor Ctr Clin Management Res, North Campus Res Complex,2800 Plymouth Rd,Bldg 16, Ann Arbor, MI 48109 USA.
EM amykilbo@umich.edu
OI Goodrich, David/0000-0003-3232-2189
FU Department of Veterans Affairs, Veterans Health Administration, Health
Services Research and Development [HSRD IIR 10-340]; VA Health Services
Research and Development Center for Organization, Leadership, and
Management Research (COLMR); National Institute of Mental Health [RO1 MH
79994, R34 MH 74509]; University of Michigan Comprehensive Depression
Center
FX This work was supported by the Department of Veterans Affairs, Veterans
Health Administration, Health Services Research and Development [HSRD
IIR 10-340], the VA Health Services Research and Development Center for
Organization, Leadership, and Management Research (COLMR), the National
Institute of Mental Health [RO1 MH 79994 and R34 MH 74509], and the
University of Michigan Comprehensive Depression Center (Director's
Innovation Fund). 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 98
TC 15
Z9 15
U1 2
U2 44
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3812
J9 CURR PSYCHIAT REP
JI Curr. Psychiatry Rep.
PD AUG
PY 2013
VL 15
IS 8
AR 383
DI 10.1007/s11920-013-0383-2
PG 12
WC Psychiatry
SC Psychiatry
GA 202VN
UT WOS:000323248300009
PM 23881714
ER
PT J
AU Peterfreund, RA
Philip, JH
AF Peterfreund, Robert A.
Philip, James H.
TI Critical parameters in drug delivery by intravenous infusion
SO EXPERT OPINION ON DRUG DELIVERY
LA English
DT Review
DE drug delivery by infusion; infusion pumps; intravenous infusion;
medication safety
ID BLOOD-STREAM INFECTIONS; INTENSIVE-CARE UNITS; SYRINGE PUMPS;
ADMINISTRATION SETS; DROP SIZE; FLOW-RATE; IN-VITRO; POLYVINYL-CHLORIDE;
DEAD-VOLUME; FLUID-FLOW
AB Introduction: Intravenous infusion is commonly used to deliver medications and fluids to patients. The duration of an infusion is short (hours) in the operating room where intravenous agents are infused to anesthetize patients and to manage circulation. Critically ill patients often receive infusions for days. Infusion technology has become increasingly sophisticated and complex. The technical advances broaden the clinical application of intravenous infusion methodology and provide safety features.
Areas covered: This article provides an historical overview of intravenous infusion and discusses components of infusion systems. A section describes configuration of components to meet clinical needs. The article describes physical properties of infusion systems, emphasizing how critical parameters of resistance to flow, infusion pump performance and interactions between fluid flows and the dead volume influence medication and fluid delivery. The authors emphasize the use of infusions in the intensive care and operating room environments, although the general principles apply to other clinical settings.
Expert opinion: Intravenous infusion systems contribute significantly to clinical care, but in a deceptively simple way. Several critical parameters combine to influence the performance of an infusion system, with a number of pitfalls potentially confounding utility of the technology. Safe and effective clinical application of intravenous infusion technology depends on an appreciation of this complexity which impacts the performance of infusion systems.
C1 [Peterfreund, Robert A.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Philip, James H.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Anesthesiol Perioperat & Pain Med, Boston, MA 02115 USA.
RP Peterfreund, RA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Jackson 439,55 Fruit St, Boston, MA 02114 USA.
EM RPeterfreund@Partners.org
NR 62
TC 8
Z9 8
U1 3
U2 12
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1742-5247
J9 EXPERT OPIN DRUG DEL
JI Expert Opin. Drug Deliv.
PD AUG
PY 2013
VL 10
IS 8
BP 1095
EP 1108
DI 10.1517/17425247.2013.785519
PG 14
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 198OL
UT WOS:000322932100006
PM 23565777
ER
PT J
AU Borzutzky, A
Camargo, CA
AF Borzutzky, Arturo
Camargo, Carlos A., Jr.
TI Role of vitamin D in the pathogenesis and treatment of atopic dermatitis
SO EXPERT REVIEW OF CLINICAL IMMUNOLOGY
LA English
DT Review
DE allergy; atopic dermatitis; cathelicidin; dendritic cells; epidermal
barrier; filaggrin; latitude; Staphylococcus aureus; tolerance; vitamin
D
ID PLASMACYTOID DENDRITIC CELLS; SERUM 25-HYDROXYVITAMIN D; CD4(+) T-CELLS;
RANDOMIZED CONTROLLED-TRIAL; HUMAN BETA-DEFENSINS; 1,25-DIHYDROXYVITAMIN
D-3; D SUPPLEMENTATION; TH2 CELLS; IN-VITRO; EPIDERMAL DIFFERENTIATION
AB Atopic dermatitis (AD) is a highly prevalent allergic skin disease that affects children worldwide. Epidemiological, clinical and basic immunological studies have suggested an association between vitamin D (VD) deficiency and the development of AD and other allergic diseases. Low levels of VD, a pleiotropic hormone that has widespread effects on the immune system and skin integrity, appear to be inversely correlated with AD severity, and VD deficiency at birth is associated with higher risk of developing AD. Recent randomized trials have reported inconsistent, but still promising, results on whether VD supplementation may improve AD severity. The apparent differences are likely due to small samples, different regimens and different patient populations. The mechanisms underlying this potential improvement in AD severity remain under investigation.
C1 [Borzutzky, Arturo] Pontificia Univ Catolica Chile, Allergy Immunol & Rheumatol Unit, Div Pediat, Sch Med, Santiago, Chile.
[Borzutzky, Arturo] Pontificia Univ Catolica Chile, Sch Med, Millennium Inst Immunol & Immunotherapy, Santiago, Chile.
[Camargo, Carlos A., Jr.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA USA.
[Camargo, Carlos A., Jr.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Rheumatol Allergy & Immunol,Dept Med, Boston, MA USA.
RP Borzutzky, A (reprint author), Pontificia Univ Catolica Chile, Allergy Immunol & Rheumatol Unit, Div Pediat, Sch Med, Alameda 340, Santiago, Chile.
EM arturobor@med.puc.cl
OI Borzutzky, Arturo/0000-0002-7904-262X
FU Fondecyt [1130615]; NIH [R01 AI093723, U01 AI087881]
FX A Borzutzky is supported by Fondecyt Grant 1130615. CA Camargo is
supported by NIH grants R01 AI093723 and U01 AI087881. The authors have
no other relevant affiliations or financial involvement with any
organization or entity with a financial interest in or financial
conflict with the subject matter or materials discussed in the
manuscript apart from those disclosed.
NR 102
TC 5
Z9 6
U1 1
U2 12
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1744-666X
J9 EXPERT REV CLIN IMMU
JI Expert Rev. Clin. Immunol.
PD AUG
PY 2013
VL 9
IS 8
BP 751
EP 760
DI 10.1586/1744666X.2013.816493
PG 10
WC Immunology
SC Immunology
GA 205FP
UT WOS:000323428600008
PM 23971753
ER
PT J
AU Vaduganathan, M
Gheorghiade, M
Butler, J
AF Vaduganathan, Muthiah
Gheorghiade, Mihai
Butler, Javed
TI Expanding the Scope of the "Polypill" to Heart Failure
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Editorial Material
ID REDUCED EJECTION FRACTION; READMISSION; THERAPY
C1 [Vaduganathan, Muthiah] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Gheorghiade, Mihai] Northwestern Univ, Feinberg Sch Med, Ctr Cardiovasc Innovat, Chicago, IL 60611 USA.
[Butler, Javed] Emory Univ Hosp, Div Cardiol, Atlanta, GA 30322 USA.
RP Vaduganathan, M (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Med, 55 Fruit St,GRB 740, Boston, MA 02114 USA.
EM mvaduganathan@partners.org
NR 9
TC 2
Z9 2
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 2013
VL 19
IS 8
BP 540
EP 541
DI 10.1016/j.cardfail.2013.05.017
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 201LF
UT WOS:000323142400003
PM 23910582
ER
PT J
AU Manzano-Fernandez, S
Flores-Blanco, PJ
Perez-Calvo, JI
Ruiz-Ruiz, FJ
Carrasco-Sanchez, FJ
Morales-Rull, JL
Galisteo-Almeda, L
Pascual-Figal, D
Valdes, M
Januzzi, JL
AF Manzano-Fernandez, Sergio
Flores-Blanco, Pedro J.
Perez-Calvo, Juan I.
Ruiz-Ruiz, Francisco J.
Carrasco-Sanchez, Francisco J.
Morales-Rull, Jose L.
Galisteo-Almeda, Luis
Pascual-Figal, Domingo
Valdes, Mariano
Januzzi, James L.
TI Comparison of Risk Prediction With the CKD-EPI and MDRD Equations in
Acute Decompensated Heart Failure
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Article
DE Acute heart failure; prognosis; CKD-EPI; MDRD
ID GLOMERULAR-FILTRATION-RATE; BETA-TRACE-PROTEIN; SERUM CYSTATIN-C;
CHRONIC KIDNEY-DISEASE; RENAL-FUNCTION; CARDIOVASCULAR EVENTS;
PROGNOSTIC VALUE; ELDERLY PERSONS; ESTIMATING GFR; CREATININE
AB Background: Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations estimate glomerular filtration rate (eGFR) more accurately than the Modification of Diet in Renal Disease (MDRD) equation. The aim of this study was to evaluate whether CKD-EPI equations based on. serum creatinine and/or cystatin C (CysC) predict risk for adverse outcomes more accurately than the MDRD equation in a hospitalized cohort of patients with acute decompensated heart failure (ADHF).
Methods and Results: A total of 526 subjects with ADHF were studied. Blood was collected within 48 hours from admission. eGFR was calculated with the use of MDRD and CKD-EPI equations. The occurrences of mortality and heart failure (HF) hospitalization were recorded. Over the study period (median 365 days [interquartile range 238-370]), 305 patients (58%) died or were rehospitalized for FIEF. Areas under the receiver operator characteristic curves for CKD-EPI CysC and CKD-EPI creatinine-CysC equations were significantly higher than that for the MDRD equation, especially in patients with >60 mL min(-1) 1.73 m(-2). After multivariate adjustment, all eGFR equations were independent predictors of adverse outcomes (P < .001). However, only CKD-EPI CysC and CKD-EPI creatinine-CysC equations were associated with significant improvement in reclassification analyses (net reclassification improvements 10.8% and 12.5%, respectively).
Conclusions: In patients with ADHF, CysC-based CKD-EPI equations were superior to the MDRD equation for predicting mortality and/or HF hospitalization especially in patients with >60 mL min(-1) 1.73 m(-2), and both CKD-EPI equations improved clinical risk stratification.
C1 [Manzano-Fernandez, Sergio; Flores-Blanco, Pedro J.; Pascual-Figal, Domingo; Valdes, Mariano] Univ Murcia, Univ Hosp Virgen de la Arrixaca, Div Cardiol, Sch Med, Murcia 30120, Spain.
[Perez-Calvo, Juan I.; Ruiz-Ruiz, Francisco J.] Univ Zaragoza, Fac Med, Hosp Clin Univ Lozano Blesa, Med Interna Serv, Zaragoza, Spain.
[Perez-Calvo, Juan I.] Inst Invest Sanitaria Aragon, Zaragoza, Spain.
[Carrasco-Sanchez, Francisco J.] Hosp Juan Ramon Jimenez, Med Interna Serv, Huelva, Spain.
[Morales-Rull, Jose L.] Hosp Arnau Vilanova, Med Interna Serv, Lerida, Spain.
[Galisteo-Almeda, Luis] Hosp Juan Ramon Jimenez, Serv Bioquim Clin & Lab, Huelva, Spain.
[Januzzi, James L.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP Manzano-Fernandez, S (reprint author), Univ Murcia, Univ Hosp Virgen de la Arrixaca, Div Cardiol, Sch Med, Carretera Madrid Cartagena S-N, Murcia 30120, Spain.
EM sergiosmf13@hotmail.com
RI Pascual Figal, Domingo /B-3794-2008;
OI Pascual Figal, Domingo /0000-0002-4993-9540; Perez-Calvo, Juan
Ignacio/0000-0003-2361-9941
NR 29
TC 14
Z9 15
U1 3
U2 9
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 2013
VL 19
IS 8
BP 583
EP 591
DI 10.1016/j.cardfail.2013.05.011
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 201LF
UT WOS:000323142400010
PM 23910589
ER
PT J
AU Fourman, LT
Meyer, BR
AF Fourman, Lindsay T.
Meyer, B. Robert
TI Autoimmune Hepatitis in Association With Ramelteon
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE ramelteon; melatonin; hepatitis; autoimmunity
ID ALCOHOLIC LIVER-DISEASE; MELATONIN RECEPTORS; HEPATOTOXICITY;
CITALOPRAM; CELLS
AB Ramelteon is a nonscheduled insomnia medication that lacks the abuse potential and residual effects common for other sedative-hypnotics. Distinct in its mechanism, the drug is a melatonin agonist with a high affinity for the membrane receptors MT1 and MT2. Although it therapeutically targets the suprachiasmatic nucleus of the hypothalamus, many organ systems have melatonin receptors and thus may be influenced by ramelteon. A growing body of research on melatonin indicates that it modulates the immune system. Indeed, immune cells have been shown to synthesize and to respond to this compound through receptors including MT1 and MT2. Melatonin's effects are generally immunostimulatory, and there is evidence to suggest that the chemical may potentiate autoimmunty. Here, we describe a case of autoimmune hepatitis that developed in a 50-year-old man after starting ramelteon for insomnia. The temporal association between ramelteon initiation and disease development, as well as the immunomodulatory properties of melatonergic compounds, suggest a role for ramelteon in the etiology of his illness.
C1 [Fourman, Lindsay T.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Meyer, B. Robert] New York Presbyterian Hosp, Weill Cornell Med Ctr, Dept Med, New York, NY USA.
RP Fourman, LT (reprint author), Massachusetts Gen Hosp, Dept Med, 55 Fruit St, Boston, MA 02114 USA.
EM lindsayfourman@gmail.com
NR 24
TC 3
Z9 3
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0192-0790
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD AUG
PY 2013
VL 47
IS 7
BP 651
EP 654
DI 10.1097/MCG.0b013e31829174f0
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 202OS
UT WOS:000323228000014
PM 23632362
ER
PT J
AU Lerman, MA
Burnham, JM
Chang, PY
Daniel, E
Foster, CS
Hennessy, S
Jabs, DA
Joffe, MM
Kacmaz, RO
Levy-Clarke, GA
Mills, MD
Nussenblatt, RB
Rosenbaum, JT
Suhler, EB
Thorne, JE
Kempen, JH
AF Lerman, Melissa A.
Burnham, Jon M.
Chang, Peter Y.
Daniel, Ebenezer
Foster, C. Stephen
Hennessy, Sean
Jabs, Douglas A.
Joffe, Marshall M.
Kacmaz, R. Oktay
Levy-Clarke, Grace A.
Mills, Monte D.
Nussenblatt, Robert B.
Rosenbaum, James T.
Suhler, Eric B.
Thorne, Jennifer E.
Kempen, John H.
TI Response of Pediatric Uveitis to Tumor Necrosis Factor-alpha Inhibitors
SO JOURNAL OF RHEUMATOLOGY
LA English
DT Article
DE UVEITIS; TUMOR NECROSIS FACTOR ANTAGONIST; JUVENILE IDIOPATHIC ARTHRITIS
ID JUVENILE IDIOPATHIC ARTHRITIS; CHRONIC NONINFECTIOUS UVEITIS; REFRACTORY
CHILDHOOD UVEITIS; OCULAR INFLAMMATORY DISEASES; TERM-FOLLOW-UP;
RHEUMATOID-ARTHRITIS; INFLIXIMAB THERAPY; RISK-FACTORS; CASE SERIES;
CHILDREN
AB Objective. To evaluate the outcome of tumor necrosis factor-alpha inhibition (anti-TNF) for pediatric uveitis.
Methods. We retrospectively assessed children (age <= 18 yrs) with noninfectious uveitis receiving anti-TNF at 5 uveitis centers and 1 pediatric rheumatology center. Incident treatment success was defined as minimal or no uveitis activity at >= 2 consecutive ophthalmological examinations L 28 days apart while taking no oral and <= 2 eyedrops/day of corticosteroids. Eligible children had active uveitis and/or were taking higher corticosteroid doses.
Results. Among 56 eligible children followed over 33.73 person-years, 52% had juvenile idiopathic arthritis (JIA) and 75% had anterior uveitis (AU). The Kaplan-Meier estimated proportion achieving treatment success within 12 months was 75% (95% CI 62%-87%). Complete absence of inflammatory signs with discontinuation of all corticosteroids was observed in an estimated 64% by 12 months (95% CI 51%-76%). Diagnoses of JIA or AU were associated with greater likelihood of success, as was the oligoarticular subtype among JIA cases. In a multivariable model, compared to those with JIA-associated AU, those with neither or with JIA or AU alone had a 75%-80% lower rate of achieving quiescence under anti-TNF, independent of the number of immunomodulators previously or concomitantly prescribed. Uveitis reactivated within 12 months of achieving quiescence in 14% of those continuing anti-TNF (95% CI 6%-31%). The incidence of discontinuation for adverse effects was 8%/year (95% CI 1%-43%).
Conclusion. Treatment with anti-TNF was successful and sustained in a majority of children with noninfectious uveitis, and treatment-limiting toxicity was infrequent. JIA-associated AU may be especially responsive to anti-TNF.
C1 Childrens Hosp Philadelphia, Div Rheumatol, Philadelphia, PA 19104 USA.
Univ Penn, Scheie Eye Inst, Dept Ophthalmol, Ctr Clin Epidemiol & Biostat,Dept Epidemiol & Bio, Philadelphia, PA 19104 USA.
Univ Penn, Perelman Sch Med SOM, Philadelphia, PA 19104 USA.
Ocular Immunol & Uveitis Fdn, Massachusetts Eye Res & Surg Inst, Cambridge, MA USA.
[Chang, Peter Y.] New York Eye & Ear Infirm, New York, NY 10003 USA.
[Foster, C. Stephen] Harvard Univ, Sch Med, Boston, MA USA.
Mt Sinai Sch Med, Dept Med, New York, NY USA.
Mt Sinai Sch Med, Dept Ophthalmol, New York, NY USA.
Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
Johns Hopkins Univ, Sch Med, Dept Ophthalmol, Baltimore, MD 21218 USA.
[Kacmaz, R. Oktay] Allergan Pharmaceut Inc, Irvine, CA 92715 USA.
[Nussenblatt, Robert B.] NEI, Immunol Lab, Bethesda, MD 20892 USA.
[Levy-Clarke, Grace A.] Johnson & Johnson Vis Care, Jacksonville, FL USA.
Childrens Hosp Philadelphia, Div Ophthalmol, Philadelphia, PA 19104 USA.
Oregon Hlth & Sci Univ, Dept Ophthalmol, Portland, OR USA.
Oregon Hlth & Sci Univ, Div Rheumatol, Dept Internal Med, Portland, OR USA.
Portland VA Med Ctr, Dept Ophthalmol, Portland, OR USA.
RP Lerman, MA (reprint author), Childrens Hosp Philadelphia, Div Rheumatol, Abramson Res Ctr, Suite 1102,3615 Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM lermanm@email.chop.edu
FU Rheumatology Research Foundation Scientist Development Award;
Autoimmunity Centers of Excellence, National Institute of Allergy and
Infectious Diseases; National Eye Institute (NEI), US National
Institutes of Health (NIH) [R01 EY014943]; National Institute on Aging
[AG025152, AG035751]; NEI [U10 EY08052]; NIH [U10 EY08052]; Johns
Hopkins University Bloomberg School of Public Health [U10 EY08057];
University of Wisconsin [U10 EY08067]; US Department of Veterans
Affairs; Abbott; LuxBio Genentech; Bristol Myers Squibb; Novartis;
EyeGate; RPB Sybil B. Harrington Special Scholars Award; Research to
Prevent Blindness; Paul and Evanina Mackall Foundation
FX Supported by a Rheumatology Research Foundation Scientist Development
Award (Dr. Lerman); Autoimmunity Centers of Excellence, National
Institute of Allergy and Infectious Diseases (Dr. Burnham); R01 EY014943
National Eye Institute (NEI), US National Institutes of Health (NIH;
Drs. Daniel, Rosenbaum, Suhler, Thorne, and Kempen); grants AG025152 and
AG035751 from the National Institute on Aging (Dr. Hennessy);
cooperative agreements from the NEI and the NIH to the Mount Sinai
School of Medicine (U10 EY08052), the Johns Hopkins University Bloomberg
School of Public Health, (U10 EY08057), and the University of Wisconsin
(U10 EY08067; Dr. Jabs); intramural funding from the NEI (Dr.
Levy-Clarke, and previously, Dr. Nussenblatt); The US Department of
Veterans Affairs (Dr. Suhler); research grants from Abbott, LuxBio
Genentech, Bristol Myers Squibb, Novartis, EyeGate, and the RPB Sybil B.
Harrington Special Scholars Award (Dr. Thorne); and Research to Prevent
Blindness, and the Paul and Evanina Mackall Foundation (Dr. Kempen).
NR 50
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U1 0
U2 1
PU J RHEUMATOL PUBL CO
PI TORONTO
PA 365 BLOOR ST E, STE 901, TORONTO, ONTARIO M4W 3L4, CANADA
SN 0315-162X
J9 J RHEUMATOL
JI J. Rheumatol.
PD AUG
PY 2013
VL 40
IS 8
BP 1394
EP 1403
DI 10.3899/jrheum.121180
PG 10
WC Rheumatology
SC Rheumatology
GA 202CY
UT WOS:000323192300025
PM 23818712
ER
PT J
AU Busl, KM
Nogueira, RG
Yoo, AJ
Hirsch, JA
Schwamm, LH
Rost, NS
AF Busl, Katharina M.
Nogueira, Raul G.
Yoo, Albert J.
Hirsch, Joshua A.
Schwamm, Lee H.
Rost, Natalia S.
TI Prestroke Dementia is Associated With Poor Outcomes After Reperfusion
Therapy Among Elderly Stroke Patients
SO JOURNAL OF STROKE & CEREBROVASCULAR DISEASES
LA English
DT Article
DE Acute stroke; dementia; outcome; reperfusion therapy; tissue plasminogen
activator
ID ACUTE ISCHEMIC-STROKE; TISSUE-PLASMINOGEN ACTIVATOR; 80 YEARS OLD;
RT-PA; INTRACEREBRAL HEMORRHAGE; THROMBOLYTIC THERAPY; INTRAVENOUS
THROMBOLYSIS; CONTROLLED-TRIAL; DOUBLE-BLIND; EXPERIENCE
AB Background: In elderly acute stroke patients, reperfusion therapy is often withheld. We sought to determine whether prestroke dementia contributed to poor outcomes after reperfusion therapy in these patients. Methods: All consecutive patients >= 80 years of age who received intravenous (IV) or intra-arterial reperfusion therapy (IAT) were identified in our Get With the Guidelines Stroke (GWTG-S) database. Vascular risk factors, presence of dementia, and outcomes were abstracted from the medical record. Dementia was recorded when listed in the medical history or when under medical treatment. Primary outcome was in-hospital mortality. Secondary outcome was discharge destination, "favorable" (home or rehabilitation facility) versus "unfavorable" (skilled nursing facility, hospice, or death). Multivariate logistic regression models were used to assess outcomes. Results: Of 153 patients, 72% received IV tissue plasminogen activator (tPA), 35% IAT, and 7% both. The mean age was 85.8 +/- 4.6 years; 13.6% had prestroke dementia. The in-hospital mortality rate was 35%. The likelihood of death increased with National Institutes of Health Stroke Scale (NIHSS; odds ratio [OR] 1.14; 95% confidence interval [CI] 1.07-1.21), IAT (OR 3.43; 95% CI 1.70-6.92), and dementia (OR 3.61; 95% CI 1.39-9.37), and decreased with IV tPA (OR 0.34; 95% CI 0.17-0.71). Increasing NIHSS (OR 0.90; 95% CI 0.85-0.95), symptomatic intracranial hemorrhage (OR 0.08; 95% CI 0.01-0.67), IAT (OR 0.43; 95% CI 0.22-0.84), and dementia (OR 0.37; 95% CI 0.14-0.97) decreased the likelihood of favorable discharge. In multivariate analysis, only NIHSS (OR 1.13; 95% CI 1.06-1.22) and dementia (OR 5.64; 95% CI 1.88-16.89) independently predicted death and unfavorable discharge destination. Conclusions: Among the elderly, prestroke dementia is a powerful independent predictor of in-hospital mortality after acute reperfusion therapy for stroke. Future investigations of thrombolysis outcomes in the elderly are warranted.
C1 [Busl, Katharina M.; Nogueira, Raul G.; Schwamm, Lee H.; Rost, Natalia S.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol,Stroke Serv, Boston, MA USA.
[Yoo, Albert J.; Hirsch, Joshua A.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol,Neurointervent Div, Boston, MA USA.
[Nogueira, Raul G.] Emory Univ, Sch Med, Dept Neurol, Atlanta, GA 30322 USA.
RP Rost, NS (reprint author), Massachusetts Gen Hosp, 175 Cambridge St,Ste 300, Boston, MA 02114 USA.
EM nrost@partners.org
OI Schwamm, Lee/0000-0003-0592-9145
FU National Institute of Neurological Disorders and Stroke (NINDS)
[K23NS064052]; Penumbra, Inc.
FX Dr Rost is supported by the National Institute of Neurological Disorders
and Stroke (NINDS) (K23NS064052). Dr Nogueira is a member of the
Physician Advisory Board for Concentric Medical, ev3 Neurovascular,
Coaxia, Rapid Medical, and Neurointervention, and the site PI for the
TREVO-2 Trial. He does not receive any consulting fees. Dr Yoo receives
research funding from Penumbra, Inc. Dr Schwamm serves as chair of the
AHA GWTG National Steering Committee (unpaid), a member of the
international steering committee of the DIAS-4 trial (Lundbeck), and a
stroke systems consultant to the Massachusetts Department of Public
Health. The other authors have nothing to disclose.
NR 28
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U1 1
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1052-3057
J9 J STROKE CEREBROVASC
JI J. Stroke Cerebrovasc. Dis.
PD AUG
PY 2013
VL 22
IS 6
BP 718
EP 724
DI 10.1016/j.jstrokecerebrovasdis.2011.11.005
PG 7
WC Neurosciences; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 206DM
UT WOS:000323497700004
PM 22182760
ER
PT J
AU Yoo, AJ
Sheth, KN
Kimberly, WT
Chaudhry, ZA
Elm, JJ
Jacobson, S
Davis, SM
Donnan, GA
Albers, GW
Stern, BJ
Gonzalez, RG
AF Yoo, Albert J.
Sheth, Kevin N.
Kimberly, W. Taylor
Chaudhry, Zeshan A.
Elm, Jordan J.
Jacobson, Sven
Davis, Stephen M.
Donnan, Geoffrey A.
Albers, Gregory W.
Stern, Barney J.
Gonzalez, R. Gilberto
TI Validating Imaging Biomarkers of Cerebral Edema in Patients With Severe
Ischemic Stroke
SO JOURNAL OF STROKE & CEREBROVASCULAR DISEASES
LA English
DT Article
DE Acute ischemic stroke; biomarker subject codes 44 and 45; cerebral
edema; magnetic resonance imaging; malignant stroke
ID BRAIN EDEMA; ARTERY INFARCTION
AB Background: There is no validated neuroimaging marker for quantifying brain edema. We sought to test whether magnetic resonance imaging (MRI)-based metrics would reliably change during the early subacute period in a manner consistent with edema and whether they would correlate with relevant clinical endpoints. Methods: Serial MRI studies from patients in the Echoplanar Imaging Thrombolytic Evaluation Trial with initial diffusion-weighted imaging (DWI) lesion volume >82 cm(3) were analyzed. Two independent readers outlined the hemisphere and lateral ventricle on the involved side and calculated respective volumes at baseline and days 3 to 5. We assessed interrater agreement, volume change between scans, and the association of volume change with early neurologic deterioration (National Institutes of Health Stroke Scale score worsening of >= 4 points), a 90-day modified Rankin scale (mRS) score of 0 to 4, and mortality. Results: Of 12 patients who met study criteria, average baseline and follow-up DWI lesion size was 138 cm(3) and 234 cm(3), respectively. The mean time to follow-up MRI was 62 hours. Concordance correlation coefficients between readers were >0.90 for both hemisphere and ventricle volume assessment. Mean percent hemisphere volume increase was 16.2 +/- 8.3% (P < .0001), and the mean percent ventricle volume decrease was 45.6 +/- 16.9% (P < .001). Percent hemisphere growth predicted early neurologic deterioration (area under the curve [AUC] 0.92; P = .0005) and 90-day mRS 0 to 4 (AUC 0.80; P = .02). Conclusions: In this exploratory analysis of severe ischemic stroke patients, statistically significant changes in hemisphere and ventricular volumes within the first week are consistent with expected changes of cerebral edema. MRI-based analysis of hemisphere growth appears to be a suitable biomarker for edema formation.
C1 [Yoo, Albert J.; Chaudhry, Zeshan A.; Gonzalez, R. Gilberto] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Kimberly, W. Taylor] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Sheth, Kevin N.; Stern, Barney J.] Univ Maryland, Sch Med, Dept Neurol, Baltimore, MD 21201 USA.
[Elm, Jordan J.] Med Univ S Carolina, Div Biostat & Epidemiol, Charleston, SC 29425 USA.
[Jacobson, Sven] Remedy Pharmaceut, New York, NY USA.
[Davis, Stephen M.] Royal Melbourne Hosp, Dept Med & Neurol, Parkville, Vic 3050, Australia.
[Donnan, Geoffrey A.] Univ Melbourne, Florey Neurosci Inst, Parkville, Vic 3052, Australia.
[Albers, Gregory W.] Stanford Univ, Med Ctr, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA.
[Albers, Gregory W.] Stanford Stroke Ctr, Stanford, CA USA.
RP Sheth, KN (reprint author), 110 S Paca St,3rd Fl, Baltimore, MD 21201 USA.
EM ksheth@som.umaryland.edu
RI Davis, Stephen/L-5260-2013;
OI Davis, Stephen/0000-0003-0962-2300; Donnan, Geoffrey/0000-0001-6324-3403
FU Penumbra, Inc; American Academy of Neurology Clinical Research Award;
American Heart Association Clinical Research Award; Remedy
Pharmaceuticals, Inc.; Clinical Investigator Training Program: Beth
Israel Deaconess Medical Center; Harvard Medical School; Pfizer, Inc;
Merck Co [NIH 1K23NS076597]; Sanofi-Aventis; Boehringer Ingelheim;
National Institutes of Health and Lundbeck; National Institutes of
Health
FX Dr. Yoo has received support from Penumbra, Inc for core imaging
laboratory activities. Dr. Sheth is supported by research funding from
the American Academy of Neurology Clinical Research Award, American
Heart Association Clinical Research Award, and Remedy Pharmaceuticals,
Inc. Dr. Kimberly is supported by an American Academy of Neurology
Clinical Research Award, Clinical Investigator Training Program: Beth
Israel Deaconess Medical Center, Harvard Medical School, in
collaboration with Pfizer, Inc and Merck & Co (NIH 1K23NS076597). Mr.
Jacobson is the CEO of Remedy Pharmaceticals. Dr. Davis serves on the
advisory boards of PAION, Servier, and Novo Nordisk, and has received
honoraria from Novo Nordisk, Sanofi-Aventis, Pfizer, and Boehringer
Ingelheim. Dr. Donnan serves on the advisory boards of Boehringer
Ingelheim, PAION, Servier, and Sanofi-Aventis; has received honoraria or
consulting payments from and has had costs of participating in
scientific meetings reimbursed by Boehringer Ingelheim, Sanofi-Aventis,
and Servier; and has received grant funding from Sanofi-Aventis and
grants and consultancy payments from Boehringer Ingelheim. Dr. Albers
has received grant funding from the National Institutes of Health and
Lundbeck; is a consultant for Lundbeck; and holds equity in iSchema
View. Dr. Stern is supported by the National Institutes of Health. Drs.
Chaudhry, Elm, and Gonzalez have no conflicts of interest to declare.
NR 14
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U1 1
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1052-3057
J9 J STROKE CEREBROVASC
JI J. Stroke Cerebrovasc. Dis.
PD AUG
PY 2013
VL 22
IS 6
BP 742
EP 749
DI 10.1016/j.jstrokecerebrovasdis.2012.01.002
PG 8
WC Neurosciences; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 206DM
UT WOS:000323497700008
PM 22325573
ER
PT J
AU Fang, PA
Margolis, HC
Conway, JF
Simmer, JP
Beniash, E
AF Fang, Ping-An
Margolis, Henry C.
Conway, James F.
Simmer, James P.
Beniash, Elia
TI CryoTEM study of effects of phosphorylation on the hierarchical assembly
of porcine amelogenin and its regulation of mineralization in vitro
SO JOURNAL OF STRUCTURAL BIOLOGY
LA English
DT Article
DE Biomineralization; Cryo Transmission Electron Microscopy; Single
particle reconstruction; Self-assembly; Enamel; Amelogenin
ID CALCIUM-PHOSPHATE FORMATION; ENAMEL MATRIX; TOOTH ENAMEL; IMPERFECTA
PHENOTYPE; MOUSE AMELOGENINS; MICE DISPLAY; PROTEIN; BIOMINERALIZATION;
TEMPERATURE; IDENTIFICATION
AB Amelogenin, the major extracellular enamel matrix protein, plays a critical role in regulating the growth and organization of enamel. Assembly and mineralization of full-length native (P173) and recombinant (rP172) porcine amelogenins were studied by cryogenic Transmission Electron Microscopy (cryoTEM). The cryoTEM revealed that both native and recombinant porcine amelogenins undergo step-wise self-assembly. Although the overall structural organization of P173 and rP172 oligomers was similar and resembled oligomers of murine recombinant amelogenin rM179, there were subtle differences suggesting that a single phosphorylated serine present in P173 might affect amelogenin self-assembly. Our mineralization studies demonstrated that both P173 and rP172 oligomers stabilize initial mineral clusters. Importantly, however, rP172 regulated the organization of initial mineral clusters into linear chains and guided the formation of parallel arrays of elongated mineral particles, which are the hallmark of enamel structural organization. These results are similar to those obtained previously using full-length recombinant murine amelogenin (Fang et al., 2011a). In contrast to that seen with rP172, phosphorylated P173 strongly inhibits mineralization for extended periods of time. We propose that these differences might be due to the differences in the structural organization and charge distribution between P173 and rP172. Overall our studies indicate that self-assembly of amelogenin and the mechanisms of its control over mineralization might be universal across different mammalian species. Our data also provide new insight into the effect of phosphorylation on amelogenin self-assembly and its regulation of mineralization. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Fang, Ping-An; Beniash, Elia] Univ Pittsburgh, Dept Oral Biol, Ctr Craniofacial Regenerat, McGowan Inst Regenerat Med, Pittsburgh, PA 15261 USA.
[Margolis, Henry C.] Forsyth Inst, Ctr Biomineralizat, Dept Appl Oral Sci, Cambridge, MA 02142 USA.
[Conway, James F.] Univ Pittsburgh, Dept Biol Struct, Pittsburgh, PA 15261 USA.
[Simmer, James P.] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Beniash, E (reprint author), Univ Pittsburgh, Dept Oral Biol, Ctr Craniofacial Regenerat, McGowan Inst Regenerat Med, Pittsburgh, PA 15261 USA.
EM ebeniash@pitt.edu
FU NIH [R56DE016376, R01DE023091, R56DE016703]
FX These studies were supported by NIH grants R56DE016376 (to H.C.M.),
R01DE023091 (to H.C.M.), and R56DE016703 (to E.B.).
NR 47
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U1 2
U2 29
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1047-8477
EI 1095-8657
J9 J STRUCT BIOL
JI J. Struct. Biol.
PD AUG
PY 2013
VL 183
IS 2
BP 250
EP 257
DI 10.1016/j.jsb.2013.05.011
PG 8
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 204XU
UT WOS:000323405400016
PM 23707542
ER
PT J
AU Cohen, ME
Ko, CY
Bilimoria, KY
Zhou, L
Huffman, K
Wang, X
Liu, YM
Kraemer, K
Meng, XJ
Merkow, R
Chow, W
Matel, B
Richards, K
Hart, AJ
Dimick, JB
Hall, BL
AF Cohen, Mark E.
Ko, Clifford Y.
Bilimoria, Karl Y.
Zhou, Lynn
Huffman, Kristopher
Wang, Xue
Liu, Yaoming
Kraemer, Kari
Meng, Xiangju
Merkow, Ryan
Chow, Warren
Matel, Brian
Richards, Karen
Hart, Amy J.
Dimick, Justin B.
Hall, Bruce L.
TI Optimizing ACS NSQIP Modeling for Evaluation of Surgical Quality and
Risk: Patient Risk Adjustment, Procedure Mix Adjustment, Shrinkage
Adjustment, and Surgical Focus
SO JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS
LA English
DT Article
ID SUPPORT VECTOR MACHINE; IMPROVEMENT PROGRAM; HOSPITAL OUTCOMES;
PREDICTION MODELS; MORTALITY-RATE; REPORT CARDS; ROC CURVE; SURGERY;
PERFORMANCE; REGRESSION
AB The American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) collects detailed clinical data from participating hospitals using standardized data definitions, analyzes these data, and provides participating hospitals with reports that permit risk-adjusted comparisons with a surgical quality standard. Since its inception, the ACS NSQIP has worked to refine surgical outcomes measurements and enhance statistical methods to improve the reliability and validity of this hospital profiling. From an original focus on controlling for between-hospital differences in patient risk factors with logistic regression, ACS NSQIP has added a variable to better adjust for the complexity and risk profile of surgical procedures (procedure mix adjustment) and stabilized estimates derived from small samples by using a hierarchical model with shrinkage adjustment. New models have been developed focusing on specific surgical procedures (eg, "Procedure Targeted" models), which provide opportunities to incorporate indication and other procedure-specific variables and outcomes to improve risk adjustment. In addition, comparative benchmark reports given to participating hospitals have been expanded considerably to allow more detailed evaluations of performance. Finally, procedures have been developed to estimate surgical risk for individual patients. This article describes the development of, and justification for, these new statistical methods and reporting strategies in ACS NSQIP. (C) 2013 by the American College of Surgeons
C1 [Cohen, Mark E.; Ko, Clifford Y.; Bilimoria, Karl Y.; Zhou, Lynn; Huffman, Kristopher; Wang, Xue; Liu, Yaoming; Kraemer, Kari; Meng, Xiangju; Merkow, Ryan; Chow, Warren; Matel, Brian; Richards, Karen; Hart, Amy J.; Hall, Bruce L.] Amer Coll Surg, Div Res & Optimal Patient Care, Chicago, IL 60611 USA.
[Bilimoria, Karl Y.] Northwestern Univ, Surg Outcomes & Qual Improvement Ctr, Dept Surg, Feinberg Sch Med, Chicago, IL 60611 USA.
[Ko, Clifford Y.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Surg, Los Angeles, CA 90095 USA.
[Ko, Clifford Y.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Dimick, Justin B.] Univ Michigan, Dept Surg, Michigan Surg Collaborat Outcomes Res & Evaluat, Ann Arbor, MI 48109 USA.
[Hall, Bruce L.] Washington Univ, Dept Surg, St Louis, MO USA.
[Hall, Bruce L.] Washington Univ, BJC Healthcare, St Louis, MO USA.
[Hall, Bruce L.] Washington Univ, Ctr Hlth Policy, St Louis, MO USA.
[Hall, Bruce L.] Washington Univ, John M Olin Sch Business, St Louis, MO 63130 USA.
[Hall, Bruce L.] John Cochran Vet Affairs Med Ctr, St Louis, MO USA.
RP Cohen, ME (reprint author), Amer Coll Surg, 633 N St Clair St,22nd Floor, Chicago, IL 60611 USA.
EM markcohen@facs.org
NR 47
TC 141
Z9 142
U1 4
U2 19
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 2013
VL 217
IS 2
BP 336
EP +
DI 10.1016/j.jamcollsurg.2013.02.027
PG 12
WC Surgery
SC Surgery
GA 201TX
UT WOS:000323167000022
PM 23628227
ER
PT J
AU Hanlon, JT
Schmader, KE
Semla, TP
AF Hanlon, Joseph T.
Schmader, Kenneth E.
Semla, Todd P.
TI Update of Studies on Drug-Related Problems in Older Adults
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE aged; drug utilization; adverse drug event
ID HOSPITALIZATIONS
C1 [Hanlon, Joseph T.] Univ Pittsburgh, Dept Med, Div Geriatr, Pittsburgh, PA 15213 USA.
[Hanlon, Joseph T.] Univ Pittsburgh, Sch Med, Dept Biomed Informat, Pittsburgh, PA 15213 USA.
[Hanlon, Joseph T.] Univ Pittsburgh, Sch Pharm, Dept Pharm & Therapeut, Pittsburgh, PA 15213 USA.
[Hanlon, Joseph T.] Univ Pittsburgh, Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15213 USA.
[Hanlon, Joseph T.] Univ Pittsburgh, Geriatr Pharmaceut Outcomes & Geroinformat Res &, Pittsburgh, PA 15213 USA.
[Hanlon, Joseph T.] Univ Pittsburgh, Clin & Translat Sci Inst, Pittsburgh, PA 15213 USA.
[Hanlon, Joseph T.] Vet Affairs Pittsburgh Healthcare Syst, Geriatr Res Educ & Clin Ctr, Pittsburgh, PA USA.
[Hanlon, Joseph T.] Vet Affairs Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Schmader, Kenneth E.] Duke Univ, Med Ctr, Dept Med, Div Geriatr, Durham, NC 27710 USA.
[Schmader, Kenneth E.] Durham Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Durham, NC USA.
[Semla, Todd P.] Pharm Benefits Management, Dept Vet Affairs, Hines, IL USA.
[Semla, Todd P.] Northwestern Univ, Dept Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Semla, Todd P.] Northwestern Univ, Feinberg Sch Med, Dept Psychiat & Behav Sci, Chicago, IL 60611 USA.
RP Hanlon, JT (reprint author), Univ Pittsburgh, Dept Geriatr Med, Kaufman Med Bldg,Suite 514,3471 5th Ave, Pittsburgh, PA 15213 USA.
EM jth14@pitt.edu
FU Agency for Healthcare Research and Quality [R01 HS018721, K12 HS019461];
National Institute of Aging [P30AG024827, T32 AG021885, K07AG033174,
R01A G027017, R01 AG037451]
FX The editor in chief has reviewed the conflict of interest checklist
provided by the authors and has determined that the authors have no
financial or any other kind of personal conflicts with this paper. Dr.
Semla serves on the Omnicare Pharmacy and Therapeutics Committee
(long-term care). He is an author and editor for LexiComp, Inc; his
spouse is an employee of Abbott Labs. Dr. Hanlon is supported by Agency
for Healthcare Research and Quality Grants R01 HS018721, and K12
HS019461 and National Institute of Aging Grants P30AG024827, T32
AG021885, K07AG033174, R01A G027017, and R01 AG037451.
NR 13
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Z9 10
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD AUG
PY 2013
VL 61
IS 8
BP 1365
EP 1368
DI 10.1111/jgs.12354
PG 4
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 198ZY
UT WOS:000322964500016
PM 23731022
ER
PT J
AU Hicks, JW
Parkes, J
Sadovski, O
Tong, JC
Houle, S
Vasdev, N
Wilson, AA
AF Hicks, Justin W.
Parkes, Jun
Sadovski, Oleg
Tong, Junchao
Houle, Sylvain
Vasdev, Neil
Wilson, Alan A.
TI Synthesis and preclinical evaluation of [C-11-carbonyl]PF-04457845 for
neuroimaging of fatty acid amide hydrolase
SO NUCLEAR MEDICINE AND BIOLOGY
LA English
DT Article
DE FAAH; Positron emission tomography; Rodent models; Carbon-11;
Radiotracer
AB Introduction: Fatty acid amide hydrolase (FAAH) has a significant role in regulating endocannabinoid signaling in the central nervous system. As such, FAAH inhibitors are being actively sought for pain, addiction, and other indications. This has led to the recent pursuit of positron emission tomography (PET) radiotracers targeting FAAH. We report herein the preparation and preclinical evaluation of [C-11-carbonyl]PF-04457845, an isotopologue of the potent irreversible FAAH inhibitor.
Methods: PF-04457845 was radiolabeled at the carbonyl position via automated [C-11]CO2-fixation. Ex vivo brain biodistribution of [C-11-carbonyl]PF-04457845 was carried out in conscious rats. Specificity was determined by pre-administration of PF-04457845 or URB597 prior to [C-11-carbonyl]PF-04457845. In a separate experiment, rats injected with the title radiotracer had whole brains excised, homogenized and extracted to examine irreversible binding to brain parenchyma.
Results: The title compound was prepared in 5 +/- 1% (n = 4) isolated radiochemical yield based on starting [C-11]CO2 (decay uncorrected) within 25 min from end-of-bombardment in >98% radiochemical purity and a specific activity of 73.5 +/- 8.2 GBq/mu mol at end-of-synthesis. Uptake of [C-11-carbonyl]PF-04457845 into the rat brain was high (range of 1.2-4.4 SUV), heterogeneous, and in accordance with reported FAAH distribution. Saturable binding was demonstrated by a dose-dependent reduction in brain radioactivity uptake following pre-treatment with PF-04457845. Pre-treatment with the prototypical FAAH inhibitor, URB597, reduced the brain radiotracer uptake in all regions by 71-81%, demonstrating specificity for FAAH. The binding of [C-11-carbonyl]PF-04457845 to FAAH at 40 min post injection was irreversible as 98% of the radioactivity in the brain could not be extracted.
Conclusions: [C-11-carbonyl]PF-04457845 was rapidly synthesized via an automated radiosynthesis. Ex vivo biodistribution studies in conscious rodents demonstrate that [C-11 PF-04457845 is a promising candidate radiotracer for imaging FAAH in the brain with PET. These results coupled with the known pharmacology and toxicology of PF-04457845 should facilitate clinical translation of this radiotracer. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Hicks, Justin W.; Parkes, Jun; Sadovski, Oleg; Tong, Junchao; Houle, Sylvain; Wilson, Alan A.] Ctr Addict & Mental Hlth, Res Imaging Ctr, Toronto, ON M5T 1R8, Canada.
[Hicks, Justin W.; Wilson, Alan A.] Univ Toronto, Inst Med Sci, Toronto, ON M5S 1A8, Canada.
[Houle, Sylvain; Wilson, Alan A.] Univ Toronto, Dept Psychiat, Toronto, ON M5T 1R8, Canada.
[Vasdev, Neil] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02114 USA.
[Vasdev, Neil] Massachusetts Gen Hosp, Div Nucl Med & Mol Imaging, Boston, MA 02114 USA.
RP Wilson, AA (reprint author), CAMH, Res Imaging Ctr, Toronto, ON M5T 1R8, Canada.
EM alan.wilson@camhpet.ca
RI Wilson, Alan/A-1788-2011
FU NIH [1R21MH094424-01]; Ontario Ministry of Research and Development
Early Researcher award; University of Toronto Institute of Medical
Science Open Fellowship award
FX This work was supported by NIH Grant # 1R21MH094424-01 to AAW, an
Ontario Ministry of Research and Development Early Researcher award to
NV, and a University of Toronto Institute of Medical Science Open
Fellowship award to JWH. We would like to thank Armando Garcia, Winston
Stableford, MM Wong, Virginia S. Wilson, Patrick McCormick, and Alvina
Ng for their assistance with the radiochemistry and animal dissection
experiments.
NR 45
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U1 3
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0969-8051
J9 NUCL MED BIOL
JI Nucl. Med. Biol.
PD AUG
PY 2013
VL 40
IS 6
BP 740
EP 746
DI 10.1016/j.nucmedbio.2013.04.008
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 200RS
UT WOS:000323087200004
PM 23731552
ER
PT J
AU Dearling, JLJ
Barnes, JW
Panigrahy, D
Zimmerman, RE
Fahey, F
Treves, ST
Morrison, MS
Kieran, MW
Packard, AB
AF Dearling, Jason L. J.
Barnes, Jessica W.
Panigrahy, Dipak
Zimmerman, Robert E.
Fahey, Frederic
Treves, S. Ted
Morrison, Matthew S.
Kieran, Mark W.
Packard, Alan B.
TI Specific uptake of Tc-99m-NC100692, an alpha(v)beta(3)-targeted imaging
probe, in subcutaneous and orthotopic tumors
SO NUCLEAR MEDICINE AND BIOLOGY
LA English
DT Article
DE Angiogenesis; NC100692; MicroSPECT; alpha(v)beta(3); Brain tumor; RGD
peptides; Cilengitide
AB Introduction: The alpha(v)beta(3) integrin, which is expressed by angiogenic epithelium and some tumor cells, is an attractive target for the development of both imaging agents and therapeutics. While optimal implementation of alpha(v)beta(3)-targeted therapeutics will require a priori identification of the presence of the target, the clinical evaluation of these compounds has typically not included parallel studies with alpha(v)beta(3)-targeted diagnostics. This is at least partly due to the relatively limited availability of PET radiopharmaceuticals in comparison to those labeled with Tc-99m. In an effort to begin to address this limitation, we evaluated the tumor uptake of Tc-99m-NC100692, a cyclic RGD peptide that binds to alpha(v beta 3) with similar to 1-nM affinity, in an alpha(v)beta(3)-positive tumor model as well as its in vivo specificity.
Methods: MicroSPECT imaging was used to assess the ability of cilengitide, a therapeutic with high affinity for alpha(v)beta(3), to block and displace Tc-99m-NC100692 in an orthotopic U87 glioma tumor. The specificity of Tc-99m-NC100692 was quantitatively evaluated in mice bearing subcutaneous U87MG tumors, by comparison of the biodistribution of Tc-99m-NC100692 with that of the non-specific structural analogue Tc-99m-AH-111744 and by blocking uptake of Tc-99m-NC100692 with excess unlabeled NC100692.
Results: MicroSPECT imaging studies demonstrated that uptake of Tc-99m-NC100692 in the intracranial tumor model was both blocked and displaced by the alpha(v)beta(3)-targeted therapeutic cilengitide. Biodistribution studies provided quantitative confirmation of these imaging results. Tumor uptake of Tc-99m-NC100692 at 1 h post-injection was 2.8 +/- 0.7% ID/g compared to 0.38 +/- 0.1% ID/g for Tc-99m-AH-111744 (p < 0.001). Blocking Tc-99m-NC100692 uptake by pre-injecting the mice with excess unlabeled NC100692 reduced tumor uptake by approximately five-fold, to 0.68 +/- 0.3% ID/g (p = 0.01).
Conclusion: These results confirm that Tc-99m-NC100692 does, in fact, target the alpha(v)beta(3) integrin and may, therefore, be useful in identifying patients prior to anti-alpha(v)beta(3) therapy as well as monitoring the response of these patients to therapy. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Dearling, Jason L. J.; Fahey, Frederic; Treves, S. Ted; Packard, Alan B.] Boston Childrens Hosp, Dept Radiol, Div Nucl Med & Mol Imaging, Boston, MA 02115 USA.
[Dearling, Jason L. J.; Barnes, Jessica W.; Panigrahy, Dipak; Zimmerman, Robert E.; Fahey, Frederic; Treves, S. Ted; Kieran, Mark W.; Packard, Alan B.] Harvard Univ, Sch Med, Boston, MA USA.
[Barnes, Jessica W.; Panigrahy, Dipak; Kieran, Mark W.] Boston Childrens Hosp, Vasc Biol Program, Boston, MA 02115 USA.
[Barnes, Jessica W.; Panigrahy, Dipak; Kieran, Mark W.] Dana Farber Canc Inst, Div Pediat Oncol, Boston, MA USA.
[Barnes, Jessica W.; Panigrahy, Dipak; Kieran, Mark W.] Dana Farber Childrens Hosp Canc Ctr, Boston, MA USA.
[Barnes, Jessica W.; Panigrahy, Dipak; Kieran, Mark W.] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Zimmerman, Robert E.] Grove Ctr, GE Healthcare, Amersham HP7 9LL, England.
RP Dearling, JLJ (reprint author), Boston Childrens Hosp, Dept Radiol, Div Nucl Med & Mol Imaging, Boston, MA 02115 USA.
EM jason.dearling@childrens.harvard.edu
FU Childhood Brain Tumor Foundation; Kyle Johnson Brain Tumor Fund; CJ
Buckley Brain Tumor Research Fund; Stop&Shop Pediatric Brain Tumor
Research Fund; Ralph and Andrea Faber Fund for Radiological Research;
NIH [S10-RR17224]
FX We thank Patricia Dunning, Erin Snay, Deviney Chaponis, Amanda Baker and
Emily Greene for technical assistance. The assistance of Sharon Peled,
PhD, in the acquisition of the MRI studies is gratefully acknowledged.
Alice Carmel, BS, assisted with the mouse microSPECT studies. Kristin
Johnson assisted with image preparation. NC100692 (maraciclatide) was
provided by GE Healthcare (Amersham, UK). EMD121974 (cilengitide) was
provided by Merck KGaA (Darmstadt, Germany). This work was supported by
the Childhood Brain Tumor Foundation, the Kyle Johnson Brain Tumor Fund,
the CJ Buckley Brain Tumor Research Fund, the Stop&Shop Pediatric Brain
Tumor Research Fund and the Ralph and Andrea Faber Fund for Radiological
Research. The microSPECT camera was purchased with NIH Grant
S10-RR17224.
NR 21
TC 8
Z9 8
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0969-8051
J9 NUCL MED BIOL
JI Nucl. Med. Biol.
PD AUG
PY 2013
VL 40
IS 6
BP 788
EP 794
DI 10.1016/j.nucmedbio.2013.04.006
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 200RS
UT WOS:000323087200009
PM 23701702
ER
PT J
AU Hatoum, IJ
Kaplan, LM
AF Hatoum, Ida J.
Kaplan, Lee M.
TI Advantages of Percent Weight Loss as a Method of Reporting Weight Loss
After Roux-en-Y Gastric Bypass
SO OBESITY
LA English
DT Article
ID BODY-MASS INDEX; BARIATRIC SURGERY; MORBID-OBESITY; BLOOD-PRESSURE;
RISK-FACTORS; PREDICTOR; OVERWEIGHT; RATS
AB Objective: Although Roux-en-Y gastric bypass (RYGB) is an effective treatment for severe obesity, weight loss (WL) after this operation is highly variable. Accurate predictors of outcome would thus be useful in identifying those patients who would most benefit from this invasive therapy. WL has been characterized using several different metrics, including the number of BMI units lost (Delta BMI), percent baseline WL (%WL), and percent excess body WL (%EBWL). To identify clinically relevant predictors most sensitively, it is necessary to avoid confounding by other factors, including preoperative BMI (pBMI), the strongest known predictor of RYGB-induced WL.
Design and Methods: To determine the WL measure least associated with pBMI, outcomes of 846 patients undergoing RYGB were analyzed.
Results: Patients in this cohort had an average pBMI of 50.0 kg/m(2) at baseline. At weight nadir, they lost an average 19.4 kg/m(2), 38.7% WL, and 81.2% EBWL. pBMI was strongly and positively associated with DBMI at both 1 year (r = 0.56, P = 4.7 x 10(-51)) and nadir (r = 0.58, P = 2.8 x 10(-77)) and strongly but negatively associated with %EBWL at 1 year (r = -0.52, P = 3.8 x 10(-44)) and nadir (r = -0.45, P = 7.2 x 10(-43)). In contrast, pBMI was not significantly associated with %WL at 1 year (r = 0.04, P = 0.33) and only weakly associated at nadir (r = 0.13, P = 0.0002).
Conclusions: Of the metrics examined, %WL is the parameter describing WL after RYGB least influenced by pBMI. It thus improves comparison of WL outcomes across studies of patients undergoing surgery and facilitates the most sensitive identification of novel predictors of surgery-induced WL. We therefore is recommend that %WL be adopted more broadly in reporting weight loss after RYGB.
C1 [Hatoum, Ida J.; Kaplan, Lee M.] Massachusetts Gen Hosp, Obes Metab & Nutr Inst, Boston, MA 02114 USA.
[Hatoum, Ida J.; Kaplan, Lee M.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Hatoum, Ida J.; Kaplan, Lee M.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Kaplan, LM (reprint author), Massachusetts Gen Hosp, Obes Metab & Nutr Inst, Boston, MA 02114 USA.
EM LMKaplan@partners.org
FU NIH [DK093257, DK088661, DK090956]
FX This work was supported by NIH grants DK093257 (IJH), DK088661 (LMK),
and DK090956 (LMK). Additional Supporting Information may be found in
the online version of this article.
NR 41
TC 18
Z9 18
U1 2
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD AUG
PY 2013
VL 21
IS 8
BP 1519
EP 1525
DI 10.1002/oby.20186
PG 7
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 206LE
UT WOS:000323521500004
PM 23670991
ER
PT J
AU Murabito, JM
Massaro, JM
Clifford, B
Hoffmann, U
Fox, CS
AF Murabito, Joanne M.
Massaro, Joseph M.
Clifford, Brian
Hoffmann, Udo
Fox, Caroline S.
TI Depressive Symptoms Are Associated with Visceral Adiposity in a
Community-Based Sample of Middle-Aged Women and Men
SO OBESITY
LA English
DT Article
ID CORONARY HEART-DISEASE; MAJOR DEPRESSION; ABDOMINAL OBESITY; TISSUE
VOLUMES; OLDER PERSONS; FAT; MARKERS; HEALTH; OVERWEIGHT; DISORDERS
AB Objective: To examine the relation between measures of adiposity and depressive symptoms in a large well characterized community-based sample, we examined the relations of visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) to depressive symptoms in 1,581 women (mean age 52.2 years) and 1,718 men (mean age 49.8 years) in the Framingham Heart Study.
Design and Methods: Depressive symptoms were measured using the Center for Epidemiologic Studies Depression (CES-D) scale. Regression models were created to examine the association between each fat depot (exposure) and depressive symptoms (outcome). Sex-specific models were adjusted for age, body mass index, smoking, alcohol consumption, diabetes, hypertension, total and HDL cholesterol, lipid lowering treatment, CVD, menopause, C-reactive protein, and physical activity.
Results: Mean CES-D scores were 6.8 and 5.6 in women and men. High levels of depressive symptoms were present in 22.5% of women and 12.3% of men. In women, one standard deviation increase in VAT was associated with a 1.3 point higher CES-D score after adjusting for age and BMI (P < 0.01) and remained significant in the fully adjusted model (P = 0.03). The odds ratio of depressive symptoms per 1 standard deviation increase in VAT in women was 1.33 (P = 0.015); results were attenuated in fully adjusted models (OR 1.29, P = 0.055). In men, the association between VAT and CES-D score and depressive symptoms was not significant. SAT was not associated with CES-D score or depressive symptoms.
Conclusions: This study supports an association between VAT and depressive symptoms in women. Further work is needed to uncover the complex biologic mechanisms mediating the association.
C1 [Murabito, Joanne M.; Clifford, Brian] Boston Univ, Sch Med, Dept Med, Gen Internal Med Sect, Boston, MA 02118 USA.
[Murabito, Joanne M.; Fox, Caroline S.] Natl Heart Lung & Blood Inst Framingham Heart Stu, Framingham, MA USA.
[Massaro, Joseph M.] Boston Univ, Dept Math, Boston, MA 02215 USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Cardiac MR PET CT, Boston, MA 02114 USA.
[Hoffmann, Udo; Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol, Boston, MA 02115 USA.
RP Murabito, JM (reprint author), Boston Univ, Sch Med, Dept Med, Gen Internal Med Sect, Boston, MA 02118 USA.
EM murabito@bu.edu
OI Murabito, Joanne/0000-0002-0192-7516; Massaro,
Joseph/0000-0002-2682-4812
FU National Heart Blood and Lung Institute [N01-HC-25195]
FX The Framingham Heart Study is funded by National Heart Blood and Lung
Institute (contract N01-HC-25195).
NR 33
TC 9
Z9 9
U1 2
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1930-7381
J9 OBESITY
JI Obesity
PD AUG
PY 2013
VL 21
IS 8
BP 1713
EP 1719
DI 10.1002/oby.20130
PG 7
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 206LE
UT WOS:000323521500031
PM 23666906
ER
PT J
AU Plagge, JM
Lu, MW
Lovejoy, TI
Karl, AI
Dobscha, SK
AF Plagge, Jane M.
Lu, Mary W.
Lovejoy, Travis I.
Karl, Andrea I.
Dobscha, Steven K.
TI Treatment of Comorbid Pain and PTSD in Returning Veterans: A
Collaborative Approach Utilizing Behavioral Activation
SO PAIN MEDICINE
LA English
DT Article
DE Pain; Posttraumatic Stress Disorder; Veterans; Behavioral Activation;
Collaborative Care
ID POSTTRAUMATIC-STRESS-DISORDER; MENTAL-HEALTH TREATMENT; MUSCULOSKELETAL
PAIN; PRIMARY-CARE; PSYCHOMETRIC PROPERTIES; DEPRESSION; AFGHANISTAN;
SCALE; IRAQ; INTERVENTION
AB Objective. We explore preliminary clinical effectiveness and feasibility of an intervention utilizing collaborative care components and behavioral activation (BA) to treat comorbid chronic pain and posttraumatic stress disorder (PTSD).
Design. Descriptive, including pre- and posttreatment assessment results.
Setting. Portland Veterans Affairs Medical Center. Participants. Fifty-eight Iraq and Afghanistan veterans with chronic pain and PTSD symptoms.
Interventions. Veterans participated in a biopsychosocial evaluation and up to eight BA sessions using a collaborative approach involving primary care, mental health, and other clinicians. A physiatrist assisted the psychologist in providing recommendations to primary care providers.
Outcome Measures. Participants were administered pre-and posttreatment measures of PTSD, pain severity, pain interference, mental health, quality of life, satisfaction, and global ratings of change with the purpose of assessing progress and improving quality.
Results. Of the 58 participants, 30 completed treatment. Common recommendations included physical therapy and exercise programs, pain medication or pain medication adjustments, and additional diagnostic workups, such as imaging. Participants who completed the program showed significant improvements on measures of PTSD, pain severity, and pain interference. Improvements were also evident on measures of mental health and quality of life. Overall, participants were satisfied with the program, and on average reported feeling "somewhat better."
Conclusions. These findings suggest that a collaborative approach that includes BA is feasible and a potentially effective treatment for comorbid chronic pain and PTSD.
C1 [Plagge, Jane M.; Lu, Mary W.; Lovejoy, Travis I.; Dobscha, Steven K.] Portland VA Med Ctr, Mental Hlth & Clin Neurosci Div, Portland, OR 97239 USA.
[Karl, Andrea I.] Portland VA Med Ctr, Dept Rehabil Med, Portland, OR 97239 USA.
[Dobscha, Steven K.] Portland VA Med Ctr, Portland Ctr Study Chron Comorbid Mental & Phys D, Portland, OR 97239 USA.
[Plagge, Jane M.; Lu, Mary W.; Dobscha, Steven K.] Oregon Hlth & Sci Univ, Dept Psychiat, Portland, OR 97201 USA.
RP Dobscha, SK (reprint author), Portland VA Med Ctr, Mental Hlth & Neurosci Div, 3710 SW US Vet Hosp Rd,POB 1034,P3MHADM, Portland, OR 97239 USA.
EM steven.dobscha@va.gov
FU Pacific Northwest Mental Illness Research and Education and Clinical
Center (MIRECC); VA Mental Health Services
FX No author reports having any financial or other potential conflict of
interest with this study. 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 or the United States government. This
work was supported by the Pacific Northwest Mental Illness Research and
Education and Clinical Center (MIRECC) and VA Mental Health Services.
The authors acknowledge Alex Linke, BS, for assistance with utilization
data extraction, and Amy Wagner, PhD, for assistance in implementing
behavioral activation and for reviewing the manuscript.
NR 44
TC 5
Z9 5
U1 5
U2 21
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1526-2375
J9 PAIN MED
JI Pain Med.
PD AUG
PY 2013
VL 14
IS 8
BP 1164
EP 1172
DI 10.1111/pme.12155
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 202FP
UT WOS:000323199400008
PM 23746043
ER
PT J
AU Singh, JA
Lewallen, DG
AF Singh, Jasvinder A.
Lewallen, David G.
TI Medical Comorbidity is Associated with Persistent Index Hip Pain after
Total Hip Arthroplasty
SO PAIN MEDICINE
LA English
DT Article
DE Pain; Function; Functional Limitation; Total Hip Replacement; Primary;
Arthroplasty; Joint Replacement; Outcomes; Patient-Reported Outcomes
ID QUALITY-OF-LIFE; CHRONIC KIDNEY-DISEASE; KNEE ARTHROPLASTY;
RHEUMATOID-ARTHRITIS; FUNCTIONAL STATUS; REVISION HIP; OUTCOMES;
REPLACEMENT; HEALTH; RISK
AB Objective. To characterize whether medical comorbidity predicts persistent moderate-severe pain after total hip arthroplasty (THA).
Methods. We analyzed the prospectively collected data from the Mayo Clinic Total Joint Registry for patients who underwent primary or revision THA between 1993 and 2005. Using multivariable-adjusted logistic regression analyses, we examined whether certain medical comorbidities were associated with persistent moderate-severe hip pain 2 or 5 years after primary or revision THA. Odds ratios (ORs), along with 95% confidence intervals (CIs) and P value, are presented.
Results. The primary THA cohort consisted of 5,707 THAs and 3,289 THAs at 2 and 5 years, and revision THA, 2,687 and 1,627 THAs, respectively. In multivariable-adjusted logistic regression models, in the primary THA cohort, renal disease was associated with lower odds of moderate-severe hip pain (OR 0.6; 95% CI 0.3, 1.0) at 2 years. None of the comorbidities were significantly associated at 5 years. In the revision THA cohort, heart disease was significantly associated with higher risk (OR 1.7; 95% CI 1.1, 2.6) at 2 years and connective tissue disease with lower risk (OR 0.5; 95% CI 0.3, 0.9) of moderate-severe hip pain at 5-year follow-up.
Conclusion. This study identified new correlates of moderate-severe hip pain after primary or revision THA, a much-feared outcome of hip arthroplasty. Patients with these comorbidities should be informed regarding the risk of moderate-severe index hip pain, so that they can have a fully informed consent and realistic expectations.
C1 [Singh, Jasvinder A.] Birmingham VA Med Ctr, Med Serv, Birmingham, AL USA.
[Singh, Jasvinder A.] Birmingham VA Med Ctr, Ctr Surg Med Acute Care Res & Transit SMART, Birmingham, AL USA.
[Singh, Jasvinder A.] Univ Alabama Birmingham, Sch Med, Dept Med, Birmingham, AL USA.
[Singh, Jasvinder A.] Univ Alabama Birmingham, Sch Publ Hlth, Div Epidemiol, Birmingham, AL 35294 USA.
[Singh, Jasvinder A.; Lewallen, David G.] Mayo Clin, Coll Med, Dept Orthoped Surg, Rochester, MN USA.
RP Singh, JA (reprint author), Univ Alabama Birmingham, Fac Off Tower 805B,510 20th St S, Birmingham, AL 35294 USA.
EM jasvinder.md@gmail.com
OI singh, jasvinder/0000-0003-3485-0006
FU Mayo Clinic Orthopedic Surgery research funds; National Institutes of
Health (NIH) Clinical Translational Science Award [1 KL2 RR024151-01];
Agency for Health Quality and Research Center for Education and Research
on Therapeutics (CERTs), National Institute of Aging and National Cancer
Institute
FX This material is the result of work supported with research grants from
the Mayo Clinic Orthopedic Surgery research funds, National Institutes
of Health (NIH) Clinical Translational Science Award 1 KL2 RR024151-01
(Mayo Clinic Center for Clinical and Translational Research) and the
resources and use of facilities at the Birmingham VA Medical Center,
Alabama, USA. J.A.S. is also supported by grants from the Agency for
Health Quality and Research Center for Education and Research on
Therapeutics (CERTs), National Institute of Aging and National Cancer
Institute.
NR 35
TC 8
Z9 8
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1526-2375
J9 PAIN MED
JI Pain Med.
PD AUG
PY 2013
VL 14
IS 8
BP 1222
EP 1229
DI 10.1111/pme.12153
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 202FP
UT WOS:000323199400014
PM 23742141
ER
PT J
AU Huang, LW
Choi, SY
Chacon-Heszele, M
Ryu, YK
McKenna, S
Zuo, XF
Kuruvilla, R
Lipschutz, J
AF Huang, Liwei
Choi, Soo Young
Chacon-Heszele, Maria
Ryu, Yun Kyoung
McKenna, Sarah
Zuo, Xiaofeng
Kuruvilla, Rejji
Lipschutz, Josh
TI The Role of Wnt5a in Pronephric and Metanephric Kidney Development
SO PEDIATRIC NEPHROLOGY
LA English
DT Meeting Abstract
C1 [Huang, Liwei; Choi, Soo Young; Chacon-Heszele, Maria; McKenna, Sarah; Zuo, Xiaofeng; Lipschutz, Josh] Univ Penn, Philadelphia, PA 19104 USA.
[Ryu, Yun Kyoung; Kuruvilla, Rejji] Johns Hopkins Univ, Baltimore, MD USA.
[Lipschutz, Josh] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0931-041X
J9 PEDIATR NEPHROL
JI Pediatr. Nephrol.
PD AUG
PY 2013
VL 28
IS 8
BP 1348
EP 1348
PG 1
WC Pediatrics; Urology & Nephrology
SC Pediatrics; Urology & Nephrology
GA 177PJ
UT WOS:000321387201012
ER
PT J
AU Siever, L
AF Siever, Larry
TI Paranoid case vignette
SO PERSONALITY AND MENTAL HEALTH
LA English
DT Editorial Material
C1 [Siever, Larry] Icahn Sch Med Mt Sinai, New York, NY USA.
[Siever, Larry] James J Peters VA Med Ctr, Psychiat Program, Bronx, NY USA.
RP Siever, L (reprint author), James J Peters VA Med Ctr, Psychiat Program, Bronx, NY USA.
EM larry.siever@mssm.edu
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1932-8621
J9 PERSONAL MENT HEALTH
JI Personal. Ment. Health
PD AUG
PY 2013
VL 7
IS 3
BP 262
EP 263
DI 10.1002/pmh.1243
PG 2
WC Psychiatry; Psychology, Social
SC Psychiatry; Psychology
GA 201OS
UT WOS:000323151900010
PM 24343970
ER
PT J
AU Kosten, TA
Shen, XY
O'Malley, PW
Kinsey, BM
Lykissa, ED
Orson, FM
Kosten, TR
AF Kosten, Therese A.
Shen, Xiaoyun Y.
O'Malley, Patrick W.
Kinsey, Berma M.
Lykissa, Ernest D.
Orson, Frank M.
Kosten, Thomas R.
TI A morphine conjugate vaccine attenuates the behavioral effects of
morphine in rats
SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Antinociception; Conditioned place preference; Heroin metabolites;
Immunotherapy; Opioid dependence
ID SERUM-ALBUMIN; HEROIN; METHADONE; PHARMACOTHERAPY; METABOLITES;
ANTIBODIES; DEPENDENCE; ADDICTION; EFFICACY; COCAINE
AB Vaccines for opioid dependence may provide a treatment that would reduce or slow the distribution of the drug to brain, thus reducing the drug's reinforcing effects. We tested whether a conjugate vaccine against morphine (keyhole limpet hemocyanin-6-succinylmorphine; KLH-6-SM) administered to rats would produce antibodies and show specificity for morphine or other heroin metabolites. The functional effects of the vaccine were tested with antinociceptive and conditioned place preference (CPP) tests. Rats were either vaccinated with KLH-6-SM and received two boosts 3 and 16 weeks later or served as controls and received KLH alone. Anti-morphine antibodies were produced in vaccinated rats; levels increased and were sustained at moderate levels through 24 weeks. Antibody binding was inhibited by free morphine and other heroin metabolites as demonstrated by competitive inhibition ELISA. Vaccinated rats showed reduced morphine CPP, tested during weeks 4 to 6, and decreased antinociceptive responses to morphine, tested at week 7. Brain morphine levels, assessed using gas-chromatography coupled to mass spectrometry (GC-MS) on samples obtained at 26 weeks, were significantly lower in vaccinated rats. This suggests that morphine entry into the brain was reduced or slowed. These results provide support for KLH-6-SM as a candidate vaccine for opioid dependence. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Shen, Xiaoyun Y.; O'Malley, Patrick W.; Kosten, Thomas R.] Baylor Coll Med, Menninger Dept Psychiat & Behav Sci, Houston, TX 77030 USA.
[Kosten, Therese A.; Shen, Xiaoyun Y.; Kinsey, Berma M.; Orson, Frank M.] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Orson, Frank M.; Kosten, Thomas R.] Michael E Debakey Vet Med Affairs Ctr, Houston, TX USA.
[Lykissa, Ernest D.] ExperTox, Houston, TX USA.
RP Kosten, TA (reprint author), Menninger Dept Psychiat & Behav Sci, 2002 Holcombe Blvd, Houston, TX 77030 USA.
EM tkosten@bcm.edu
FU National Institute on Drug Abuse [DA026859]; VA Merit Review Program
FX Financial support was provided by a grant from the National Institute on
Drug Abuse, DA026859, and by a grant from the VA Merit Review Program.
The authors gratefully acknowledge the excellent technical assistance
provided by A. Lopez and Y. Wu and thank Dr. Reetakshi Arora for her
valuable input.
NR 34
TC 10
Z9 10
U1 1
U2 9
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0278-5846
J9 PROG NEURO-PSYCHOPH
JI Prog. Neuro-Psychopharmacol. Biol. Psychiatry
PD AUG 1
PY 2013
VL 45
BP 223
EP 229
DI 10.1016/j.pnpbp.2013.05.012
PG 7
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 202RW
UT WOS:000323238300030
PM 23739535
ER
PT J
AU Bianchi, MT
Thomas, RJ
AF Bianchi, Matt T.
Thomas, Robert J.
TI Technical advances in the characterization of the complexity of sleep
and sleep disorders
SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Actigraphy; Autonomic; Cardiopulmonary coupling; Complex system;
Hypnogram; Polysomnography; Sleep
ID TRANSCRANIAL MAGNETIC STIMULATION; ELECTROCARDIOGRAM-BASED TECHNIQUE;
PERIPHERAL ARTERIAL TONOMETRY; WORLD NETWORK ORGANIZATION; ALTERNATING
PATTERN CAP; SLOW-WAVE ACTIVITY; FUNCTIONAL CONNECTIVITY; AMBULATORY
DEVICE; NEURONAL-ACTIVITY; WAKE TRANSITIONS
AB The current clinical standard for quantifying sleep physiology is the laboratory polysomnogram, from which basic sleep-wake stages are determined. However, the complexity of sleep physiology has inspired alternative metrics that are providing additional insights into the rich dynamics of sleep. Electro-encephalography, magneto-encephalography, and functional magnetic resonance imaging represent advanced imaging modalities for understanding brain dynamics. These methods are complemented by autonomic measurements that provide additional important insights. We review here the spectrum of approaches that have been leveraged towards improved understanding of the complexity of sleep. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Bianchi, Matt T.] Massachusetts Gen Hosp, Sleep Div, Dept Neurol, Boston, MA 02114 USA.
[Thomas, Robert J.] Beth Israel Deaconess Med Ctr, Dept Med, Div Pulm Crit Care & Sleep Med, Boston, MA 02215 USA.
RP Thomas, RJ (reprint author), Beth Israel Deaconess Med Ctr, Dept Med, Div Pulm Crit Care & Sleep Med, KB-023,330 Brookline Ave, Boston, MA 02215 USA.
EM mtbianchi@partners.org; rthomas1@bidmc.harvard.edu
FU NHLBI NIH HHS [RC1 HL099749]
NR 81
TC 6
Z9 6
U1 0
U2 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0278-5846
EI 1878-4216
J9 PROG NEURO-PSYCHOPH
JI Prog. Neuro-Psychopharmacol. Biol. Psychiatry
PD AUG 1
PY 2013
VL 45
BP 277
EP 286
DI 10.1016/j.pnpbp.2012.09.017
PG 10
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 202RW
UT WOS:000323238300038
PM 23174482
ER
PT J
AU Carmody, TP
Duncan, CL
Huggins, J
Solkowitz, SN
Lee, SK
Reyes, N
Mozgai, S
Simon, JA
AF Carmody, Timothy P.
Duncan, Carol L.
Huggins, Joy
Solkowitz, Sharon N.
Lee, Sharon K.
Reyes, Norma
Mozgai, Sharon
Simon, Joel A.
TI Telephone-Delivered Cognitive-Behavioral Therapy for Pain Management
Among Older Military Veterans: A Randomized Trial
SO PSYCHOLOGICAL SERVICES
LA English
DT Article
DE pain; chronic pain; cognitive-behavioral therapy; pain management;
telemen health
ID LOW-BACK-PAIN; LUMBAR INSTRUMENTED FUSION; PRIMARY-CARE; PSYCHOLOGICAL
INTERVENTIONS; ADMINISTERED PSYCHOTHERAPY; PSYCHOMETRIC PROPERTIES;
DEPRESSION TREATMENT; COST-EFFECTIVENESS; CLINICAL-TRIAL; HEALTH-CARE
AB This study investigated the effectiveness of telephone-delivered cognitive-behavioral therapy (T-CBT) in the management of chronic pain with older military veterans enrolled in VA primary-care clinics. We conducted a randomized clinical trial comparing T-CBT with telephone-delivered pain education (T-EDU). A total of 98 military veterans with chronic pain were enrolled in the study and randomized into one of two treatment conditions. Study participants were recruited from primary-care clinics at an urban VA medical center and affiliated VA community-based outpatient clinics (CBOCs). Pain management outcomes were measured at midtreatment (10 weeks), posttreatment (20 weeks), 3-month follow-up (32 weeks), and 6-month follow-up (46 weeks). No significant differences were found between the two treatment groups on any of the outcome measures. Both treatment groups reported small but significant increases in level of physical and mental health, and reductions in pain and depressive symptoms. Improvements in all primary outcome measures were mediated by reductions in catastrophizing. Telephone-delivered CBT and EDU warrant further study as easily accessible interventions for rural-living older individuals with chronic pain.
C1 [Carmody, Timothy P.; Duncan, Carol L.; Huggins, Joy; Solkowitz, Sharon N.; Lee, Sharon K.; Reyes, Norma; Mozgai, Sharon; Simon, Joel A.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Carmody, Timothy P.; Duncan, Carol L.; Huggins, Joy; Solkowitz, Sharon N.; Lee, Sharon K.; Reyes, Norma; Mozgai, Sharon] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Simon, Joel A.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Simon, Joel A.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
RP Carmody, TP (reprint author), VA Med Ctr, 116B,4150 Clement St, San Francisco, CA 94121 USA.
EM timothy.carmody@va.gov
NR 57
TC 8
Z9 8
U1 3
U2 7
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1541-1559
J9 PSYCHOL SERV
JI Psychol. Serv.
PD AUG
PY 2013
VL 10
IS 3
SI SI
BP 265
EP 275
DI 10.1037/a0030944
PG 11
WC Psychology, Clinical
SC Psychology
GA 198HX
UT WOS:000322914400001
PM 23244028
ER
PT J
AU Santa Ana, EJ
Stallings, DL
Rounsaville, BJ
Martino, S
AF Santa Ana, Elizabeth J.
Stallings, Deidre L.
Rounsaville, Bruce J.
Martino, Steve
TI Development of an In-Home Telehealth Program for Outpatient Veterans
With Substance Use Disorders
SO PSYCHOLOGICAL SERVICES
LA English
DT Article
DE telepsychiatry; home telehealth; care coordination home telehealth;
substance abuse treatment; treatment barriers
ID COGNITIVE-BEHAVIORAL THERAPY; RANDOMIZED CONTROLLED-TRIAL; CONTROLLED
CLINICAL-TRIAL; ALCOHOL DEPENDENCE; CARE; TELEPSYCHIATRY; INTERVENTION;
TECHNOLOGY; MANAGEMENT; ADDICTION
AB A variety of obstacles (e.g., lack of transportation, less availability of treatment in rural districts) contribute to underutilization of treatment among patients with substance use disorders, warranting the need to develop innovative strategies for enhancing access to treatment for these patients. The telehealth in-home-messaging-device is a small message-delivering and monitoring device connected via landline phone to a secure server that provides assessment and disease self-management education to patients in their homes. We describe the development of a Substance Use Disorder telehealth management program (SUD program) for use on this device and a feasibility pilot of the program with six outpatient veterans with substance use disorders referred by their primary medical care providers. These patients indicated that the SUD program was acceptable, easy to use, and helpful toward addressing their substance use problems. Home telehealth technology may be an innovative and feasible approach for providing substance abuse evidence-based treatment either as an adjunct to specialty treatment for substance use disorders or as a stand-alone intervention within primary care for a larger number of patients who may otherwise not access traditional treatment services.
C1 [Santa Ana, Elizabeth J.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Div Neurosci, Charleston, SC 29401 USA.
[Santa Ana, Elizabeth J.] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
[Stallings, Deidre L.] VHA Off Telehlth Serv, Sunshine Training Ctr 08A, Lake City, FL USA.
Yale Univ, Sch Med, Dept Psychiat, West Haven, CT 06516 USA.
VA CT Healthcare Syst, West Haven, CT USA.
RP Santa Ana, EJ (reprint author), Med Univ S Carolina, Dept Psychiat & Behav Sci, Clin Neurosci Div, 109 Bee St, Charleston, SC 29401 USA.
EM santaana@musc.edu
NR 36
TC 2
Z9 2
U1 1
U2 10
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1541-1559
J9 PSYCHOL SERV
JI Psychol. Serv.
PD AUG
PY 2013
VL 10
IS 3
SI SI
BP 304
EP 314
DI 10.1037/a0026511
PG 11
WC Psychology, Clinical
SC Psychology
GA 198HX
UT WOS:000322914400007
PM 23937090
ER
PT J
AU Baker, RR
AF Baker, Rodney R.
TI The History of the Division of Psychologists in Public Service
(1946-2006)
SO PSYCHOLOGICAL SERVICES
LA English
DT Article
DE public service psychology; history of Division 18; history of APA;
history of psychology
AB The 60-year history of the American Psychological Association (APA) Division of Psychologists in Public Service (Division 18) is described. Included are relevant events in the history of the APA that led to the establishment of the division and later events within the APA that influenced the development and activities of the division.
C1 [Baker, Rodney R.] Dept Vet Affairs, San Antonio, TX USA.
RP Baker, RR (reprint author), 10710 Old Blue Lane, San Antonio, TX 78230 USA.
EM rodbaker@att.net
NR 7
TC 0
Z9 0
U1 1
U2 2
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1541-1559
J9 PSYCHOL SERV
JI Psychol. Serv.
PD AUG
PY 2013
VL 10
IS 3
SI SI
BP 353
EP 358
DI 10.1037/a0031598
PG 6
WC Psychology, Clinical
SC Psychology
GA 198HX
UT WOS:000322914400013
PM 23398088
ER
PT J
AU Pape, TLB
Guernon, A
Lundgren, S
Patil, V
Herrold, AA
Smith, B
Blahnik, M
Picon, LM
Harton, B
Peterson, M
Mallinson, T
Hoffmann, M
AF Pape, Theresa Louise-Bender
Guernon, Ann
Lundgren, Sandra
Patil, Vijaya
Herrold, Amy A.
Smith, Bridget
Blahnik, Melanie
Picon, Linda M.
Harton, Brett
Peterson, Michelle
Mallinson, Trudy
Hoffmann, Michael
TI Predicting Levels of Independence With Expressing Needs and Ideas 1 Year
After Severe Brain Injury
SO REHABILITATION PSYCHOLOGY
LA English
DT Article
DE prognoses; communication; coma; vegetative state; minimally conscious
state
ID SEVERE HEAD-INJURY; VEGETATIVE STATE; MEDICAL REHABILITATION;
CONSCIOUSNESS SCALE; FAMILY CAREGIVERS; SUPPORT NEEDS; DISORDERS;
RECOVERY; COMA; PROGNOSIS
AB Purpose/Objective: Severe brain injury (BI) is a catastrophic event often evolving into a complex chronic and severely disabling condition making activity participation possible only with sustained caregiving. One aspect of building sustainable caregiving is early provision of information about expected outcomes germane to patients and their caregivers. An analysis was conducted to determine whether 2 levels of independence with expressing needs and ideas 1-year after severe BI could be predicted using variables available early after injury. Method: The authors examined a subsample (n = 79) of participants of an outcome study who received repeated neurobehavioral evaluations with the Disorders of Consciousness Scale (DOCS) and who were assessed 1 year after injury with the Functional Independence Measures (FM). Explanatory variables included DOCS measures, patient characteristics, coexisting conditions, and interventions. The outcome is measured with the FIM Expression item. Optimal data analysis was used to construct multivariate classification tree models. Results: The 2nd (p = .004) DOCS visual measure and seizure (p = .004) entered the final model providing 79% accuracy in classifying more or less independence with expressing needs and ideas at 1 year. The model will correctly identify 78% of future severe BI survivors who will have more independence and 82% of persons who will have less independence. Conclusions: For persons incurring severe BI, it is possible to predict, early after injury,
C1 [Pape, Theresa Louise-Bender; Herrold, Amy A.; Smith, Bridget; Harton, Brett] US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Res Serv, Hines, IL 60141 USA.
[Pape, Theresa Louise-Bender; Herrold, Amy A.; Harton, Brett] US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Ctr Management Complex Chron Care Ctr Excellence, Hines, IL 60141 USA.
[Pape, Theresa Louise-Bender] Northwestern Univ, Feinberg Sch Med, Dept Phys Med & Rehabil, Evanston, IL 60208 USA.
[Guernon, Ann] Marianjoy Rehabil Hosp, Res Dept, Wheaton, IL USA.
[Lundgren, Sandra] Minneapolis VA Hlth Care Syst, Psychol Serv, Minneapolis, MN USA.
[Patil, Vijaya; Hoffmann, Michael] US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Neurol Serv, Hines, IL 60141 USA.
[Patil, Vijaya; Smith, Bridget] Loyola Univ Chicago, Stritch Sch Med, Dept Neurol, Chicago, IL USA.
[Picon, Linda M.] James A Haley Vet Hosp, Audiol & Speech Pathol Serv, Tampa, FL 33612 USA.
[Picon, Linda M.] Univ S Florida, Dept Commun Sci & Disorders, Tampa, FL 33620 USA.
[Mallinson, Trudy] Univ So Calif, Div Occupat Sci & Occupat Therapy, Los Angeles, CA 90089 USA.
RP Pape, TLB (reprint author), US Dept Vet Affairs, Vet Affairs Edward Hines Jr Hosp, Res Serv, POB 5000,M-C 151H, Hines, IL 60141 USA.
EM theresa.pape@va.gov
OI Pape, Theresa/0000-0001-7738-5963; Mallinson, Trudy/0000-0002-4888-5579
NR 51
TC 3
Z9 3
U1 0
U2 2
PU EDUCATIONAL PUBLISHING FOUNDATION-AMERICAN PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA
SN 0090-5550
J9 REHABIL PSYCHOL
JI Rehabil. Psychol.
PD AUG
PY 2013
VL 58
IS 3
BP 253
EP 262
DI 10.1037/a0032610
PG 10
WC Psychology, Clinical; Rehabilitation
SC Psychology; Rehabilitation
GA 204ZB
UT WOS:000323408700004
PM 23978083
ER
PT J
AU Schoenfeld, SR
Kasturi, S
Costenbader, KH
AF Schoenfeld, Sara R.
Kasturi, Shanthini
Costenbader, Karen H.
TI The epidemiology of atherosclerotic cardiovascular disease among
patients with SLE: A systematic review
SO SEMINARS IN ARTHRITIS AND RHEUMATISM
LA English
DT Review
DE Systemic lupus erythematosus; Atherosclerosis; Cardiovascular; Coronary
artery disease; Myocardial infarction; Epidemiology; Risk factors;
Cohort study; Risk
ID CORONARY-ARTERY-DISEASE; MULTIETHNIC US COHORT; LUPUS-ERYTHEMATOSUS
DATA; CONFER INCREASED RISK; MYOCARDIAL-INFARCTION; VASCULAR EVENTS;
RHEUMATOID-ARTHRITIS; HEART-DISEASE; WOMEN; LUMINA
AB Objective: To perform a systematic review of the literature regarding the epidemiology of the association between systemic lupus erythematosus (SLE) and atherosclerotic cardiovascular disease (CVD), including the increased risk for CVD, as well as the risk factors responsible for development of CVD in patients with SLE.
Methods: We followed the PRISMA guidelines to systematically search the PubMed database from inception to June 2012. Studies were selected using predefined eligibility criteria, and 2 authors independently extracted data. The risk of bias was measured for each study using a domain-based assessment.
Results: We report on 28 studies that met criteria for inclusion in our analysis. We found strong epidemiologic evidence that SLE patients have an increased relative risk of CVD compared to controls. There is limited information regarding relative CVD mortality risks among SLE patients. Traditional CVD risk factors, including age, male sex, hyperlipidemia, smoking, hypertension, and CRP, are associated with CVD risk among SLE patients. Several SLE-specific factors, including disease activity and duration, and possibly specific manifestations and therapies, further increase risk. Several risk factors, such as disease activity and glucocorticoid use, are closely associated, making it difficult to disentangle their effects.
Conclusions: CVD risk among SLE patients compared to the general population is at least doubled. While older SLE patients appear to have the highest absolute risks of CVD, young women have alarmingly high relative risks, given the rarity of CVD in the comparison general population. Both traditional and SLE-specific risk factors are important, although there are discrepancies within the literature. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Schoenfeld, Sara R.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Kasturi, Shanthini] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Costenbader, Karen H.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Rheumatol Allergy & Immunol,Dept Med, Boston, MA 02115 USA.
RP Costenbader, KH (reprint author), Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, 75 Francis St, Boston, MA 02115 USA.
EM KCostenbader@partners.org
NR 47
TC 51
Z9 51
U1 0
U2 8
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0049-0172
J9 SEMIN ARTHRITIS RHEU
JI Semin. Arthritis Rheum.
PD AUG
PY 2013
VL 43
IS 1
BP 77
EP 95
DI 10.1016/j.semarthrit.2012.12.002
PG 19
WC Rheumatology
SC Rheumatology
GA 202SB
UT WOS:000323238800010
PM 23422269
ER
PT J
AU Martinez-Quintanilla, J
Bhere, D
Heidari, P
He, D
Mahmood, U
Shah, K
AF Martinez-Quintanilla, Jordi
Bhere, Deepak
Heidari, Pedram
He, Derek
Mahmood, Umar
Shah, Khalid
TI Therapeutic Efficacy and Fate of Bimodal Engineered Stem Cells in
Malignant Brain Tumors
SO STEM CELLS
LA English
DT Article
DE Stem cells; Herpes simplex virus thymidine kinase; Glioblastoma
multiforme; In vivo imaging; Tumor necrosis factor apoptosis-inducing
ligand
ID POSITRON-EMISSION-TOMOGRAPHY; CANCER GENE-THERAPY; GROWTH IN-VIVO;
SUICIDE GENE; GLIOMA MODEL; HEPATOCELLULAR-CARCINOMA;
MONOCLONAL-ANTIBODY; EXPRESSION; TRAIL; MAPATUMUMAB
AB Therapeutically engineered stem cells (SC) are emerging as an effective tumor-targeted approach for different cancer types. However, the assessment of the long-term fate of therapeutic SC post-tumor treatment is critical if such promising therapies are to be translated into clinical practice. In this study, we have developed an efficient SC-based therapeutic strategy that simultaneously allows killing of tumor cells and assessment and eradication of SC after treatment of highly malignant glioblastoma multiforme (GBM). Mesenchymal stem cells (MSC) engineered to co-express the prodrug converting enzyme, herpes simplex virus thymidine kinase (HSV-TK) and a potent and secretable variant of tumor necrosis factor apoptosis-inducing ligand (S-TRAIL) induced caspase-mediated GBM cell death and showed selective MSC sensitization to the prodrug ganciclovir (GCV). A significant decrease in tumor growth and a subsequent increase in survival were observed when mice bearing highly aggressive GBM were treated with MSC coexpressing S-TRAIL and HSV-TK. Furthermore, the systemic administration of GCV post-tumor treatment selectively eliminated therapeutic MSC expressing HSV-TK in vitro and in vivo, which was monitored in real time by positron emission-computed tomography imaging using 18F-FHBG, a substrate for HSV-TK. These findings demonstrate the development and validation of a novel therapeutic strategy that has implications in translating SC-based therapies in cancer patients. STEM Cells2013;31:1706-1714
C1 [Martinez-Quintanilla, Jordi; Bhere, Deepak; He, Derek; Shah, Khalid] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Mol Neurotherapy & Imaging Lab, Boston, MA USA.
[Martinez-Quintanilla, Jordi; Bhere, Deepak; Heidari, Pedram; He, Derek; Mahmood, Umar; Shah, Khalid] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Heidari, Pedram; Mahmood, Umar] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Nucl Med & Mol Imaging, Boston, MA USA.
[Shah, Khalid] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Shah, Khalid] Harvard Univ, Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
RP Shah, K (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02115 USA.
EM kshah@mgh.harvard.edu
FU American Cancer Society; James McDonald Foundation; [RO1 CA138922];
[RO1 NS071197]; [R01 CA173077]
FX We thank Alicia Leece for the synthesis of 18F-FHBG used in this study.
This work was supported by RO1 CA138922 (K. S.), RO1 NS071197 (K. S.),
R01 CA173077 (K. S.), American Cancer Society (K. S.), and James
McDonald Foundation (K.S.).
NR 47
TC 26
Z9 27
U1 0
U2 20
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PD AUG
PY 2013
VL 31
IS 8
BP 1706
EP 1714
DI 10.1002/stem.1355
PG 9
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 205CM
UT WOS:000323418700023
PM 23389839
ER
PT J
AU Graham, DB
Xavier, RJ
AF Graham, Daniel B.
Xavier, Ramnik J.
TI From genetics of inflammatory bowel disease towards mechanistic insights
SO TRENDS IN IMMUNOLOGY
LA English
DT Review
DE inflammatory bowel disease (IBD); Crohn's disease; ulcerative colitis;
genome-wide association study (GWAS); genomics; mucosal immunity; host
defense
ID GENOME-WIDE ASSOCIATION; NATURAL-KILLER-CELLS; CROHNS-DISEASE;
SUSCEPTIBILITY LOCI; INTESTINAL INFLAMMATION; INFLAMED MUCOSA; NONCODING
RNAS; CUTTING EDGE; T-CELLS; B-CELLS
AB Advancements in human genetics now poise the field to illuminate the pathophysiology of complex genetic disease. In particular, genome-wide association studies (GWAS) have generated insights into the mechanisms driving inflammatory bowel disease (IBD) and implicated genes shared by multiple autoimmune and autoinflammatory diseases. Thus, emerging evidence suggests a central role for the mucosal immune system in mediating immune homeostasis and highlights the complexity of genetic and environmental interactions that collectively modulate the risk of disease. Nevertheless, the challenge remains to determine how genetic variation can precipitate and sustain the inappropriate inflammatory response to commensals that is observed in IBD. Here, we highlight recent advancements in immunogenetics and provide a forward-looking view of the innovations that will deliver mechanistic insights from human genetics.
C1 [Graham, Daniel B.; Xavier, Ramnik J.] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Graham, Daniel B.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Xavier, Ramnik J.] Massachusetts Gen Hosp, Gastrointestinal Unit, Ctr Study Inflammatory Bowel Dis, Boston, MA 02114 USA.
[Xavier, Ramnik J.] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
RP Graham, DB (reprint author), Broad Inst MIT & Harvard, Cambridge, MA USA.
EM dgraham@broadinstitute.org
FU Center for the Study of Inflammatory Bowel Diseases (Massachusetts
General Hospital); Helmsley Trust; NIH [R01 DK092405]
FX The authors are funded by the Center for the Study of Inflammatory Bowel
Diseases (Massachusetts General Hospital), the Helmsley Trust, and NIH
R01 DK092405.
NR 92
TC 37
Z9 39
U1 2
U2 25
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4906
J9 TRENDS IMMUNOL
JI Trends Immunol.
PD AUG
PY 2013
VL 34
IS 8
BP 371
EP 378
DI 10.1016/j.it.2013.04.001
PG 8
WC Immunology
SC Immunology
GA 207JJ
UT WOS:000323594400002
PM 23639549
ER
PT J
AU Byrne, T
Montgomery, AE
Dichter, ME
AF Byrne, Thomas
Montgomery, Ann Elizabeth
Dichter, Melissa E.
TI Homelessness Among Female Veterans: A Systematic Review of the
Literature
SO WOMEN & HEALTH
LA English
DT Review
DE homelessness; women; veterans; systematic review
ID HEALTH-CARE UTILIZATION; WOMEN VETERANS; GENDER-DIFFERENCES;
MENTAL-HEALTH; CLINICAL-OUTCOMES; SUBSTANCE-ABUSERS; PREDICTORS;
PROGRAM; ILLNESS; DETERMINANTS
AB The authors conducted a systematic, critical review of the literature to assess and summarize existing research on homelessness among female veterans. They searched seven electronic databases (ERIC, Proquest Dissertations and Theses, PsycINFO, PubMed, Social Services Abstracts, Social Science Citation Index, and Sociological Abstracts), websites of several government and research organizations, and reference lists of prior studies. They abstracted data on study design, funding source, and topic from studies meeting inclusion criteria and classified each study into one of the following categories: epidemiology, health and other services utilization, and interventions. The authors included both experimental and observational studies of interventions in the review and performed a narrative synthesis for each of the 26 studies identified. No studies were experimental, 20 were observational, and the remainder were either qualitative or descriptive. Of the 26 identified studies, 14 were epidemiologic, 7 focused on the health and additional service utilization, and 5 were intervention studies. Findings provided important baseline epidemiologic information about homelessness among female veterans and indicated that female veterans were at an increased risk of homelessness relative to their male veteran and female non-veteran counterparts. Additional research is needed to develop and implement effective, evidence-based programs to prevent and end homelessness among women veterans.
C1 [Byrne, Thomas; Montgomery, Ann Elizabeth] Natl Ctr Homelessness Vet, Philadelphia, PA 19104 USA.
[Byrne, Thomas] Univ Penn, Philadelphia, PA 19104 USA.
[Dichter, Melissa E.] Philadelphia VA Med Ctr, CHERP, Philadelphia, PA USA.
RP Byrne, T (reprint author), Natl Ctr Homelessness Vet, 4100 Chester Ave,Suite 201, Philadelphia, PA 19104 USA.
EM byrnet@sp2.upenn.edu
NR 56
TC 5
Z9 5
U1 3
U2 22
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 0363-0242
J9 WOMEN HEALTH
JI Women Health
PD AUG 1
PY 2013
VL 53
IS 6
BP 572
EP 596
DI 10.1080/03630242.2013.817504
PG 25
WC Public, Environmental & Occupational Health; Women's Studies
SC Public, Environmental & Occupational Health; Women's Studies
GA 199WF
UT WOS:000323025500003
PM 23937730
ER
PT J
AU Pompili, M
Serafini, G
Innamorati, M
Venturini, P
Fusar-Poli, P
Sher, L
Amore, M
Girardi, P
AF Pompili, Maurizio
Serafini, Gianluca
Innamorati, Marco
Venturini, Paola
Fusar-Poli, Paolo
Sher, Leo
Amore, Mario
Girardi, Paolo
TI Agomelatine, a novel intriguing antidepressant option enhancing
neuroplasticity: A critical review
SO WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY
LA English
DT Review
DE Agomelatine; antidepressant drugs; efficacy; tolerability;
neuroplasticity
ID MAJOR DEPRESSIVE DISORDER; 5HT(2C) RECEPTORS ANTAGONIST;
PLACEBO-CONTROLLED-TRIAL; DOUBLE-BLIND; MELATONIN RECEPTORS;
NEUROTROPHIC FACTOR; MESSENGER-RNA; HIPPOCAMPAL NEUROGENESIS; NEURONAL
PLASTICITY; CELLULAR RESILIENCE
AB Objectives. The treatment of major affective disorders, commonly associated with high disability and elevated social costs may be still considered unsatisfactory. Among all antidepressant drugs, predominantly acting through monoaminergic mechanisms, agomelatine is of particular interest due to another alternative mechanism of action. Targeting melatonergic receptors, agomelatine play a crucial role in synchronizing circadian rhythms, known to be altered in depressed subjects. Methods. A critical review of the literature focusing on efficacy, safety and tolerability of agomelatine in major affective disorders was performed. Additionally, we focused on the potential of agomelatine in enhancing neuroplasticity mechanisms and promote neurogenesis. A total of 136 articles from peer-reviewed journals were identified, of which 50 were assessed for eligibility and 21 were included. Results. Agomelatine, a melatonergic analogue drug acting as MT1/MT2 agonist and 5-HT2C antagonist, has been reported to be effective as antidepressant drug. Studies confirmed not only clinical efficacy but also safety and tolerability of agomelatine. Also, it enhances neuroplasticity mechanisms and adult neurogenesis in brain areas such as hippocampus and prefrontal cortex. Conclusions. Agomelatine actually represents an intriguing option in the treatment of affective disorders.
C1 [Pompili, Maurizio; Serafini, Gianluca; Innamorati, Marco; Venturini, Paola; Girardi, Paolo] Univ Roma La Sapienza, Dept Neurosci Mental Hlth & Sensory Organs, St Andrea Hosp, I-00189 Rome, Italy.
[Fusar-Poli, Paolo] Inst Psychiat, Dept Psychosis Studies, London, England.
[Sher, Leo] Mt Sinai Sch Med, James J Peters Vet Adm Med Ctr, Dept Psychiat, Bronx, NY USA.
[Amore, Mario] Univ Genoa, Sect Psychiat, Dept Neurosci Rehabil Ophthalmol Genet Maternal &, Genoa, Italy.
RP Pompili, M (reprint author), Univ Roma La Sapienza, Dept Neurosci Mental Hlth & Sensory Organs, St Andrea Hosp, Suicide Prevent Ctr, Via Grottarossa 1035-1039, I-00189 Rome, Italy.
EM maurizio.pompili@uniroma1.it; gianluca.serafini@uniroma1.it
OI Innamorati, Marco/0000-0003-1389-2290; Pompili,
Maurizio/0000-0003-1886-4977
NR 101
TC 26
Z9 27
U1 2
U2 8
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1562-2975
J9 WORLD J BIOL PSYCHIA
JI World J. Biol. Psychiatry
PD AUG
PY 2013
VL 14
IS 6
BP 412
EP 431
DI 10.3109/15622975.2013.765593
PG 20
WC Psychiatry
SC Psychiatry
GA 206CM
UT WOS:000323494100002
PM 23530731
ER
PT J
AU Sainani, NI
Arellano, RS
Shyn, PB
Gervais, DA
Mueller, PR
Silverman, SG
AF Sainani, Nisha I.
Arellano, Ronald S.
Shyn, Paul B.
Gervais, Debra A.
Mueller, Peter R.
Silverman, Stuart G.
TI The challenging image-guided abdominal mass biopsy: established and
emerging techniques 'if you can see it, you can biopsy it'
SO ABDOMINAL IMAGING
LA English
DT Review
DE Image-guided; Biopsy; Abdominal; Percutaneous; Challenging
ID NEEDLE ASPIRATION BIOPSY; TECHNICALLY EASY APPROACH; CT FLUOROSCOPY;
PERCUTANEOUS BIOPSY; ADRENAL BIOPSY; DIAGNOSTIC-ACCURACY;
INITIAL-EXPERIENCE; UPPER ABDOMEN; LIVER; LESIONS
AB Image-guided percutaneous biopsy of abdominal masses is among the most commonly performed procedures in interventional radiology. While most abdominal masses are readily amenable to percutaneous biopsy, some may be technically challenging for a number of reasons. Low lesion conspicuity, small size, overlying or intervening structures, motion, such as that due to respiration, are some of the factors that can influence the ability and ultimately the success of an abdominal biopsy. Various techniques or technologies, such as choice of imaging modality, use of intravenous contrast and anatomic landmarks, patient positioning, organ displacement or trans-organ approach, angling CT gantry, triangulation method, real-time guidance with CT fluoroscopy or ultrasound, sedation or breath-hold, pre-procedural image fusion, electromagnetic tracking, and others, when used singularly or in combination, can overcome these challenges to facilitate needle placement in abdominal masses that otherwise would be considered not amenable to percutaneous biopsy. Familiarity and awareness of these techniques allows the interventional radiologist to expand the use of percutaneous biopsy in clinical practice, and help choose the most appropriate technique for a particular patient.
C1 [Sainani, Nisha I.; Shyn, Paul B.; Silverman, Stuart G.] Brigham & Womens Hosp, Div Abdominal Imaging & Intervent, Boston, MA 02115 USA.
[Arellano, Ronald S.; Gervais, Debra A.; Mueller, Peter R.] Massachusetts Gen Hosp, Div Abdominal Imaging & Intervent, Boston, MA 02114 USA.
RP Sainani, NI (reprint author), Brigham & Womens Hosp, Div Abdominal Imaging & Intervent, 75 Francis St, Boston, MA 02115 USA.
EM nsainani@partners.org
NR 47
TC 16
Z9 16
U1 0
U2 12
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0942-8925
J9 ABDOM IMAGING
JI Abdom. Imaging
PD AUG
PY 2013
VL 38
IS 4
BP 672
EP 696
DI 10.1007/s00261-013-9980-0
PG 25
WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
GA 200FE
UT WOS:000323052400004
PM 23381506
ER
PT J
AU Quencer, KB
Nimkin, K
Mino-Kenudson, M
Gee, MS
AF Quencer, Keith B.
Nimkin, Katherine
Mino-Kenudson, Mari
Gee, Michael S.
TI Detecting active inflammation and fibrosis in pediatric Crohn's disease:
prospective evaluation of MR-E and CT-E
SO ABDOMINAL IMAGING
LA English
DT Article
DE Crohn's disease; Fibrosis; MR enterography (MR-E); CT enterography
(CT-E)
ID BOWEL-DISEASE; INTESTINAL FIBROSIS; ENTEROGRAPHY; RADIATION; EXPOSURE;
PATIENT; RISKS
AB Symptoms of Crohn's disease (CD) can be due to active inflammation or fibrosis. Differentiating these based on clinical presentation, endoscopy, laboratory parameters, and clinical scoring methods can be inaccurate and/or invasive. As therapy decisions are often directed based on whether active disease or fibrosis is present, a reliable and non-invasive test to distinguish these two etiologies would be a powerful clinical tool. CT enterography (CT-E) and MR enterography (MR-E) are two non-invasive imaging modalities tailored to evaluate the small bowel. The purpose of our study was to compare the ability of MR-E and CT-E to assess for active inflammation and mural fibrosis in patients with known CD as compared to a histologic reference standard. After obtaining MR-E and CT-E on the same day, a total of 61 histologic samples were obtained from twelve subjects aged 12-20 years via full-thickness bowel resection or endoscopy. These were evaluated by the pathologist for active inflammation and fibrosis. We found that while CT-E and MR-E were similar in their accuracies of depicting active inflammation, MR-E was significantly more sensitive in detecting fibrosis. Because of this and the lack of ionizing radiation from MR-E, we believe that MR-E rather than CT-E should serve as the primary imaging modality for the assessment of CD pediatric patients with non-acute clinical exacerbations.
C1 [Quencer, Keith B.; Nimkin, Katherine; Mino-Kenudson, Mari; Gee, Michael S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
RP Quencer, KB (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, 55 Fruit St, Boston, MA 02114 USA.
EM kquencer@partners.org
FU Harvard Medical School [UL1 RR025758-02]; National Institutes of Health
FX Supported by a Clinical and Translational Science Award UL1 RR025758-02
(to M.S.G.) from Harvard Medical School and the National Institutes of
Health.
NR 26
TC 26
Z9 27
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0942-8925
J9 ABDOM IMAGING
JI Abdom. Imaging
PD AUG
PY 2013
VL 38
IS 4
BP 705
EP 713
DI 10.1007/s00261-013-9981-z
PG 9
WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
GA 200FE
UT WOS:000323052400006
PM 23361877
ER
PT J
AU Oliva, IB
Davarpanah, AH
Rybicki, FJ
Desjardins, B
Flamm, SD
Francois, CJ
Gerhard-Herman, MD
Kalva, SP
Mansour, MA
Mohler, ER
Schenker, MP
Weiss, C
Dill, KE
AF Oliva, Isabel B.
Davarpanah, Amir H.
Rybicki, Frank J.
Desjardins, Benoit
Flamm, Scott D.
Francois, Christopher J.
Gerhard-Herman, Marie D.
Kalva, Sanjeeva P.
Mansour, M. Ashraf
Mohler, Emile R., III
Schenker, Matthew P.
Weiss, Clifford
Dill, Karin E.
TI ACR appropriateness criteria((R)) imaging of mesenteric ischemia
SO ABDOMINAL IMAGING
LA English
DT Article
DE Appropriateness criteria; Mesenteric ischemia; Acute abdomen; Abdominal
pain; Bowel ischemia
ID ACUTE BOWEL ISCHEMIA; INTESTINAL ISCHEMIA; ENDOVASCULAR TREATMENT; CT
ANGIOGRAPHY; DUPLEX ULTRASOUND; MR-ANGIOGRAPHY; PLAIN FILM; DIAGNOSIS;
OCCLUSION; CONTRAST
AB Mesenteric ischemia is a rare disease associated with high morbidity and mortality. Acute mesenteric ischemia is most commonly secondary to embolism followed by arterial thrombosis, nonocclusive ischemia, and less commonly venous thrombosis. Chronic mesenteric ischemia is almost always caused by atherosclerotic disease, with rare causes including fibromuscular dysplasia and vasculitis. The American College of Radiology Appropriateness Criteria are evidence-based guidelines for specific clinical conditions that are reviewed every 2 years by a multidisciplinary expert panel. The guideline development and review include an extensive analysis of current medical literature from peer reviewed journals and the application of a well-established consensus methodology (modified Delphi) to rate the appropriateness of imaging and treatment procedures by the panel. In those instances where evidence is lacking or not definitive, expert opinion may be used to recommend imaging or treatment. Patients with mesenteric ischemia usually present with nonspecific abdominal symptoms and laboratory findings. This document evaluates and rates the appropriateness of imaging to evaluate patients with clinically suspected mesenteric ischemia. While catheter-based angiography has been considered the reference standard and enables diagnosis and treatment, advances in computed tomography have made it a first-line test in many patients because it is a fast, widely available, and noninvasive study. Abdominal radiographs and ultrasound have a limited role in diagnosing mesenteric ischemia but are commonly the first ordered tests in patients with abdominal pain and may diagnose more common pathologies.
C1 [Oliva, Isabel B.; Davarpanah, Amir H.] Yale Univ, Sch Med, New Haven, CT 06520 USA.
[Rybicki, Frank J.; Gerhard-Herman, Marie D.; Schenker, Matthew P.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Desjardins, Benoit; Mohler, Emile R., III] Univ Penn, Philadelphia, PA 19104 USA.
[Flamm, Scott D.] Cleveland Clin, Cleveland, OH 44106 USA.
[Francois, Christopher J.] Univ Wisconsin, Madison, WI USA.
[Mohler, Emile R., III] Amer Coll Cardiol, Washington, DC USA.
[Kalva, Sanjeeva P.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Mansour, M. Ashraf] Vasc Associates, Grand Rapids, MI USA.
[Mansour, M. Ashraf] Soc Vasc Surg, Chicago, IL USA.
[Weiss, Clifford] Johns Hopkins Bayview Med Ctr, Baltimore, MD USA.
[Dill, Karin E.] Univ Chicago, Chicago, IL 60637 USA.
RP Oliva, IB (reprint author), Yale Univ, Sch Med, New Haven, CT 06520 USA.
EM isabel.oliva@yale.edu
NR 33
TC 23
Z9 24
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0942-8925
J9 ABDOM IMAGING
JI Abdom. Imaging
PD AUG
PY 2013
VL 38
IS 4
BP 714
EP 719
DI 10.1007/s00261-012-9975-2
PG 6
WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
GA 200FE
UT WOS:000323052400007
PM 23296712
ER
PT J
AU Saboo, SS
Zukotynski, K
Shinagare, AB
Krajewski, KM
Ramaiya, N
AF Saboo, Sachin S.
Zukotynski, Katherine
Shinagare, Atul B.
Krajewski, Katherine M.
Ramaiya, Nikhil
TI Anal carcinoma: FDG PET/CT in staging, response evaluation, and
follow-up
SO ABDOMINAL IMAGING
LA English
DT Article
DE Anal carcinoma; F-18-FDG PET/CT; Diagnosis; Staging; Treatment
monitoring
ID POSITRON-EMISSION-TOMOGRAPHY; CANCER; GUIDELINES; MANAGEMENT; IMPACT
AB The role of FDG PET/CT in anal cancer is becoming increasingly important. At the time of initial staging, FDG PET/CT can detect the primary site of disease more frequently than CT, is sensitive for nodal and metastatic spread and alters staging in a significant number of patients. Indeed, the NCCN guidelines for anal cancer published in April 2012 recommend FDG PET/CT for therapy planning. Metabolic activity of primary anal cancer at presentation is a potential biomarker for predicting prognosis, treatment response and survival. More intensely FDG-avid primary malignancy is associated with a higher incidence of disease spread. Metabolic response following chemoradiotherapy is associated with improved survival. The aim of this paper is to provide an up-to-date pictorial review of FDG PET/CT in anal cancer at the time of staging and to illustrate its utility for determining response to therapy and detecting recurrent disease.
C1 [Saboo, Sachin S.] Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Radiol, Boston, MA 02215 USA.
Harvard Univ, Sch Med, Boston, MA 02215 USA.
RP Saboo, SS (reprint author), Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Radiol, 450 Brookline Ave, Boston, MA 02215 USA.
EM ssaboo@partners.org
NR 21
TC 10
Z9 10
U1 1
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0942-8925
J9 ABDOM IMAGING
JI Abdom. Imaging
PD AUG
PY 2013
VL 38
IS 4
BP 728
EP 735
DI 10.1007/s00261-012-9958-3
PG 8
WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical
Imaging
GA 200FE
UT WOS:000323052400009
PM 23011550
ER
PT J
AU Gabayan, GZ
Sun, BC
Asch, SM
Timmermans, S
Sarkisian, C
Yiu, S
Lancaster, EM
Poon, KT
Kellermann, AL
Ryan, G
Miniel, NJ
Flansbaum, D
Hoffman, JR
Derose, SF
AF Gabayan, Gelareh Z.
Sun, Benjamin C.
Asch, Steven M.
Timmermans, Stefan
Sarkisian, Catherine
Yiu, Sau
Lancaster, Elizabeth M.
Poon, K. Trudy
Kellermann, Arthur L.
Ryan, Gery
Miniel, Nicholas J.
Flansbaum, Drew
Hoffman, Jerome R.
Derose, Stephen F.
TI Qualitative Factors in Patients Who Die Shortly After Emergency
Department Discharge
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Article
ID DEATH AFTER-DISCHARGE; MEDICAL LITERATURE; USERS GUIDES; HEALTH-CARE;
HOME; XXIII; FALLS; TIME
AB Objectives Early death after emergency department (ED) discharge may signal opportunities to improve care. Prior studies are limited by incomplete mortality ascertainment and lack of clinically important information in administrative data. The goal in this hypothesis-generating study was to identify patient and process of care themes that may provide possible explanations for early postdischarge mortality.
Methods This was a qualitative analysis of medical records of adult patients who visited the ED of any of six hospitals in an integrated health system (Kaiser Permanente Southern California [KPSC]) and died within 7days of discharge in 2007 and 2008. Nonmembers, visits to non-health plan hospitals, patients receiving or referred to hospice care, and patients with do not attempt resuscitation or do not intubate orders (DNAR/DNI) were excluded. Under the guidance of two qualitative research scientists, a team of three emergency physicians used grounded theory techniques to identify patient clinical presentations and processes of care that serve as potential explanations for poor outcome after discharge.
Results The source population consisted of a total of 290,092 members with 446,120 discharges from six KPSC EDs in 2007 and 2008. A total of 203 deaths occurred within 7days of ED discharge (0.05%). Sixty-one randomly chosen cases were reviewed. Patient-level themes that emerged included an unexplained persistent acute change in mental status, recent fall, abnormal vital signs, ill-appearing presentation, malfunctioning indwelling device, and presenting symptoms remaining at discharge. Process-of-care factors included a discrepancy in history of present illness, incomplete physical examination, and change of discharge plan by a third party, such as a consulting or admitting physician.
Conclusions In this hypothesis-generating study, qualitative research techniques were used to identify clinical and process-of-care factors in patients who died withindays after discharge from an ED. These potential predictors will be formally tested in a future quantitative study. (C) 2013 by the Society for Academic Emergency Medicine
C1 [Gabayan, Gelareh Z.; Sarkisian, Catherine] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Timmermans, Stefan] Univ Calif Los Angeles, Dept Sociol, Los Angeles, CA 90024 USA.
[Gabayan, Gelareh Z.; Sarkisian, Catherine] Greater Los Angeles Vet Affairs Healthcare Syst, Dept Med, Los Angeles, CA USA.
[Gabayan, Gelareh Z.; Lancaster, Elizabeth M.; Flansbaum, Drew; Hoffman, Jerome R.] Ronald Reagan UCLA, Ctr Emergency Med, Los Angeles, CA USA.
[Sun, Benjamin C.] Oregon Hlth & Sci Univ, Dept Emergency Med, Portland, OR 97201 USA.
[Asch, Steven M.] Stanford Sch Med, Dept Med, Vet Affairs Palo Alto Hlth Care Syst, Palo Alto, CA USA.
[Yiu, Sau; Lancaster, Elizabeth M.; Poon, K. Trudy; Derose, Stephen F.] Kaiser Permanente So Calif, Dept Res & Evaluat, Pasadena, CA 91101 USA.
[Kellermann, Arthur L.; Ryan, Gery] RAND Hlth, Santa Monica, CA USA.
[Miniel, Nicholas J.; Flansbaum, Drew] Olive View UCLA Emergency Med Ctr, Sylmar, CA USA.
RP Gabayan, GZ (reprint author), Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
EM Gelareh@gabayan.com
FU Kaiser Permanente Southern California; Emergency Medicine Foundation
Career Development Award [59668]; UCLA Oppenheimer Foundation; UCLA
Older Americans Independence Center (NIH/NIA K) [P30-AG028748]; National
Center for Advancing Translational Sciences [KL2TR000122]
FX This research was supported by Kaiser Permanente Southern California.
During the initial phase of the project, Dr. Gabayan received support
from the Emergency Medicine Foundation Career Development Award (59668
G. Gabayan) and the UCLA Oppenheimer Foundation, and Dr. Sun received
support from the UCLA Older Americans Independence Center (NIH/NIA K
grant P30-AG028748). Continued support was obtained for Dr. Gabayan from
the National Center for Advancing Translational Sciences, grant
KL2TR000122. The content is solely the responsibility of the authors and
does not necessarily represent the official views of the NIH or the NIA.
NR 25
TC 6
Z9 6
U1 2
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1069-6563
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD AUG
PY 2013
VL 20
IS 8
BP 778
EP 785
DI 10.1111/acem.12181
PG 8
WC Emergency Medicine
SC Emergency Medicine
GA 201IQ
UT WOS:000323134300005
PM 24033620
ER
PT J
AU Caterino, JM
Sullivan, AF
Betz, ME
Espinola, JA
Miller, I
Camargo, CA
Boudreaux, ED
AF Caterino, Jeffrey M.
Sullivan, Ashley F.
Betz, Marian E.
Espinola, Janice A.
Miller, Ivan
Camargo, Carlos A., Jr.
Boudreaux, Edwin D.
CA Emergency Dept Safety Assessment
TI Evaluating Current Patterns of Assessment for Self-harm in Emergency
Departments: A Multicenter Study
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Article
ID ATTEMPTED-SUICIDE; RISK RATIOS; VISITS; TRENDS; INJURY; ADULTS
AB Objectives The objective was to describe self-harm assessment practices in U.S. emergency departments (EDs) and to identify predictors of being assessed.
Methods This was a prospective observational cohort study of adults presenting to eight U.S. EDs. A convenience sample of adults presenting to the EDs during covered research shifts was entered into a study log. Self-harm assessment was defined as ED documentation of suicide attempt; suicidal ideation; or nonsuicidal self-injury thoughts, behaviors, or both. Institution characteristics were compared relative to percentage assessed. To identify predictive patient characteristics, multivariable generalized linear models were created controlling for weekend presentation, time of presentation, age, sex, and race and ethnicity.
Results Among 94,354 charts, self-harm assessment ranged from 3.5% to 31%, except for one outlying site at 95%. Overall, 26% were assessed (11% excluding the outlying site). Current self-harm was present in 2.7% of charts. Sites with specific self-harm assessment policies had higher assessment rates. In the complete model, adjusted risk ratios (aRR) for assessment included age 65years (0.56, 95% confidence interval [CI]=0.35 to 0.92) and male sex (1.17, 95% CI=1.10 to 1.26). There was an interaction between these variables in the smaller model (excluding outlying site), with males<65years of age being more likely to be assessed (aRR= 1.14, 95% CI=1.02 to 1.37).
Conclusions Emergency department assessment of self-harm was highly variable among institutions. Presence of specific assessment policies was associated with higher assessment rates. Assessment varied based upon patient characteristics. The identification of self-harm in 2.7% of ED patients indicates that a substantial proportion of current risk of self-harm may go unidentified, particularly in certain patient groups. (C) 2013 by the Society for Academic Emergency Medicine
C1 [Caterino, Jeffrey M.] Ohio State Univ, Dept Emergency Med, Columbus, OH 43210 USA.
[Caterino, Jeffrey M.] Ohio State Univ, Dept Internal Med, Columbus, OH 43210 USA.
[Sullivan, Ashley F.; Espinola, Janice A.; Camargo, Carlos A., Jr.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Betz, Marian E.] Univ Colorado, Dept Emergency Med, Sch Med, Aurora, CO USA.
[Miller, Ivan] Brown Univ, Dept Psychiat & Human Behav, Providence, RI 02912 USA.
[Boudreaux, Edwin D.] Univ Massachusetts, Sch Med, Dept Emergency Med, Worcester, MA USA.
[Boudreaux, Edwin D.] Univ Massachusetts, Sch Med, Dept Psychiat, Worcester, MA 01655 USA.
[Boudreaux, Edwin D.] Univ Massachusetts, Sch Med, Dept Quantitat Hlth Sci, Worcester, MA 01655 USA.
RP Caterino, JM (reprint author), Ohio State Univ, Dept Emergency Med, Columbus, OH 43210 USA.
EM jeffrey.caterino@osumc.edu
OI Betz, Marian/0000-0003-1643-6565; Boudreaux, Edwin/0000-0002-3223-6371
FU National Institute of Mental Health [U01MH088278]; National Institute on
Aging [1K23AG038351]
FX This project was supported by Award U01MH088278 from the National
Institute of Mental Health. Dr. Caterino's time was supported by Award
1K23AG038351 from the National Institute on Aging. The content is solely
the responsibility of the authors and does not necessarily represent the
official views of the National Institute of Mental Health, National
Institute on Aging, or the National Institutes of Health. The authors
declare no conflicts of interest or disclosures.
NR 28
TC 9
Z9 9
U1 1
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1069-6563
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD AUG
PY 2013
VL 20
IS 8
BP 807
EP 815
DI 10.1111/acem.12188
PG 9
WC Emergency Medicine
SC Emergency Medicine
GA 201IQ
UT WOS:000323134300009
PM 24033624
ER
PT J
AU Brunner, AM
Sadrzadeh, H
Feng, Y
Drapkin, BJ
Ballen, KK
Attar, EC
Amrein, PC
McAfee, SL
Chen, YB
Neuberg, DS
Fathi, AT
AF Brunner, Andrew M.
Sadrzadeh, Hossein
Feng, Yang
Drapkin, Benjamin J.
Ballen, Karen K.
Attar, Eyal C.
Amrein, Philip C.
McAfee, Steven L.
Chen, Yi-Bin
Neuberg, Donna S.
Fathi, Amir T.
TI Association between baseline body mass index and overall survival among
patients over age 60 with acute myeloid leukemia
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID HEMATOPOIETIC-CELL TRANSPLANTATION; ACUTE MYELOGENOUS LEUKEMIA; ADULT
PATIENTS; SURFACE AREA; LEPTIN RECEPTOR; UNITED-STATES; EARLY DEATH;
OBESITY; RISK; OVERWEIGHT
AB Acute myeloid leukemia (AML) is more common and more lethal among patients over the age of 60. Increased body mass index (BMI) has been associated with a higher incidence of various malignancies, including AML. We sought to determine whether patient BMI at the time of AML diagnosis is related to overall survival (OS) among elderly patients. We identified 97 patients with AML diagnosed after the age of 60 and treated with cytarabine-based induction chemotherapy. The median age was 68 years (range 60-87); 52% of patients were male, and our study population was predominantly white (89% of patients). The median OS for all patients was 316 days (95% CI 246-459). The hazard ratio for mortality was increased among patients with a BMI < 25 compared to BMI 30 (HR 2.14, P = 0.009, 95% CI 1.21-3.77), as well as with older age (HR 1.76, P = 0.015, 95% CI 1.12-2.79) and with secondary versus de novo disease (HR 1.95, P = 0.006, 95% CI 1.21-3.14). After multivariable analysis, we did not find a significant association between OS and other potential confounders such as coronary artery disease or diabetes among these patients. We conclude that increased BMI was independently associated with improved OS among older AML patients at our institution. Am. J. Hematol. 88:642-646, 2013. (c) 2013 Wiley Periodicals, Inc.
C1 [Brunner, Andrew M.; Sadrzadeh, Hossein; Drapkin, Benjamin J.; Ballen, Karen K.; Attar, Eyal C.; Amrein, Philip C.; McAfee, Steven L.; Chen, Yi-Bin; Fathi, Amir T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Hematol & Oncol, Boston, MA USA.
[Feng, Yang; Neuberg, Donna S.] Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA.
RP Fathi, AT (reprint author), Massachusetts Gen Hosp, 0 Emerson Pl,Suite 118, Boston, MA 02114 USA.
EM afathi@partners.org
FU NCI NIH HHS [P30 CA006516]
NR 44
TC 9
Z9 9
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD AUG
PY 2013
VL 88
IS 8
BP 642
EP 646
DI 10.1002/ajh.23462
PG 5
WC Hematology
SC Hematology
GA 187ZO
UT WOS:000322160900003
PM 23619915
ER
PT J
AU Ghosh, P
Sahoo, R
Vaidya, A
Cantel, S
Kavishwar, A
Goldfine, A
Herring, N
Bry, L
Chorev, M
Halperin, JA
AF Ghosh, Pamela
Sahoo, Rupam
Vaidya, Anand
Cantel, Sonia
Kavishwar, Amol
Goldfine, Allison
Herring, Neil
Bry, Lynn
Chorev, Michael
Halperin, Jose A.
TI A specific and sensitive assay for blood levels of glycated CD59: A
novel biomarker for diabetes
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID TERMINAL COMPLEMENT COMPLEXES; REGULATORY PROTEIN CD59; VASCULAR
COMPLICATIONS; ACTIVE-SITE; ACTIVATION; INHIBITOR; ANTIBODY; SYSTEM;
LYSIS
AB Increasing evidence links the complement system with complications of human diabetes. The complement regulatory protein CD59, an inhibitor of formation of membrane attack complex (MAC), is inhibited by hyperglycemia-induced glycation fostering increased deposition of MAC, a major effector of complement-mediated tissue damage. CD59, an ubiquitous GPI-anchored membrane protein, is shed from cell membranes by phospholipases generating a soluble form present in blood and urine. We established an enzyme-linked immunosorbent assay (ELISA) to measure serum/plasma glycated human CD59 (hCD59) (GCD59) and evaluated its potential as a diabetes biomarker. We used a synthetic peptide strategy to generate (a) a mouse monoclonal antibody to capture hCD59, (b) a rabbit monoclonal antibody to detect GCD59, and (c) a GCD59 surrogate for assay standardization. ELISA conditions were optimized for precision, reproducibility, and clinical sensitivity. The clinical utility of the assay was initially evaluated in 24 subjects with or without diabetes and further validated in a study that included 100 subjects with and 90 subjects without a diagnosis of diabetes. GCD59 (a) was significantly higher in individuals with than in individual without diabetes, (b) was independently associated with HbA1c, and (c) identified individuals with diabetes with high specificity and sensitivity. We report the development and standardization of a novel, sensitive, and specific ELISA for measuring GCD59 in blood. The assay distinguished individuals with diabetes from those without, and showed strong correlation between GCD59 and HbA1c. Because GCD59 likely contributes to the pathogenesis of diabetes complications, measurement of blood levels of GCD59 may be useful in the diagnosis and management of diabetes. Am. J. Hematol. 88:670-676, 2013. (c) 2013 Wiley Periodicals, Inc.
C1 [Ghosh, Pamela; Sahoo, Rupam; Cantel, Sonia; Kavishwar, Amol; Chorev, Michael; Halperin, Jose A.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Hematol,Dept Med, Boston, MA 02115 USA.
[Vaidya, Anand; Goldfine, Allison] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA.
[Goldfine, Allison] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Herring, Neil; Bry, Lynn] Partners Healthcare Syst, Crimson Biospecimen Core, Boston, MA USA.
RP Halperin, JA (reprint author), Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
EM jhalperin@partners.org
RI SAHOO, RUPAM/B-3935-2016;
OI Kavishwar, Amol/0000-0001-8214-6625
FU National Institutes of Health [DK62294, DK089206]; National Heart, Lung,
and Blood Institute of the National Institutes of Health [K23HL111771]
FX Contract grant sponsor: Jose A. Halperin; Contract grant number:
National Institutes of Health Grants DK62294 and DK089206.; Contract
grant sponsor: Anand Vaidya; Contract grant number: National Heart,
Lung, and Blood Institute of the National Institutes of Health Grant
K23HL111771. The content is solely the responsibility of the authors and
does not necessarily represent the official views of National Institutes
of Health.
NR 37
TC 7
Z9 7
U1 3
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD AUG
PY 2013
VL 88
IS 8
BP 670
EP 676
DI 10.1002/ajh.23478
PG 7
WC Hematology
SC Hematology
GA 187ZO
UT WOS:000322160900009
PM 23670858
ER
PT J
AU Peralta, CA
Vittinghoff, E
Bansal, N
Jacobs, D
Muntner, P
Kestenbaum, B
Lewis, C
Siscovick, D
Kramer, H
Shlipak, M
Bibbins-Domingo, K
AF Peralta, Carmen A.
Vittinghoff, Eric
Bansal, Nisha
Jacobs, David, Jr.
Muntner, Paul
Kestenbaum, Bryan
Lewis, Cora
Siscovick, David
Kramer, Holly
Shlipak, Michael
Bibbins-Domingo, Kirsten
TI Trajectories of Kidney Function Decline in Young Black and White Adults
With Preserved GFR: Results From the Coronary Artery Risk Development in
Young Adults (CARDIA) Study
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Trajectories; race; decline; kidney
ID STAGE RENAL-DISEASE; SERUM CYSTATIN-C; SERIAL MEASUREMENTS;
RACIAL-DIFFERENCES; UNITED-STATES; CREATININE; PROGRESSION; MORTALITY
AB Background: Strong racial discrepancies in end-stage renal disease exist. Whether there are race differences in kidney function loss in younger healthy persons is not well established.
Study Design: Longitudinal.
Setting & Participants: 3,348 black and white adults with at least 2 measurements of cystatin C-based estimated glomerular filtration rate (eGFR(cys)) at scheduled Coronary Artery Risk Development in Young Adults (CARDIA) examinations (years 10, 15, and 20).
Predictor: Race.
Outcomes & Measurements: We used linear mixed models to examine race differences in annualized rates of eGFR(cys) decline, adjusting for age, sex, lifetime exposure to systolic blood pressure >120 mm Hg, diabetes, and albumin-creatinine ratio. We used Poisson regression to compare racial differences in rapid decline (eGFR(cys) decline >3% per year) by study period (10-15 years after baseline examination [defining period 1] and >15-20 years after baseline examination [defining period 2]).
Results: Mean age was 35 +/- 3.6 (SD) years, and mean eGFR(cys) was 110 +/- 20 mL/min/1.73 m(2) for blacks and 104 +/- 17 mL/min/1.73 m(2) for whites at baseline. For both blacks and whites, eGFR(cys) decline was minimal at younger ages (<35 years) and eGFR(cys) loss accelerated at older ages. However, acceleration of eGFR(cys) decline occurred at earlier ages for blacks than whites. Blacks had somewhat faster annualized rates of decline compared with whites, but differences were attenuated after adjustment in period 1 (0.13 mL/min/1.73 m(2) per year faster; P = 0.2). In contrast, during period 2, blacks had significantly faster annualized rates of decline, even after adjustment (0.32 mL/min/1.73 m(2) per year faster; P = 0.003). The prevalence of rapid decline was significantly higher for blacks versus whites, with prevalence rate ratios of 1.31 (95% CI, 1.04-1.63) for period 1 and 1.24 (95% CI, 1.09-1.41) for period 2. Differences were attenuated after full adjustment: adjusted prevalence rate ratios were 1.20 (95% CI, 0.95-1.49) for period 1 and 1.10 (95% CI, 0.96-1.26) for period 2.
Limitations: No measured GFR.
Conclusions: eGFR(cys) decline differs by race at early ages, with faster annualized rates of decline for blacks. Future studies are required to explain the observed differences. (c) 2013 by the National Kidney Foundation, Inc.
C1 [Peralta, Carmen A.; Vittinghoff, Eric; Bansal, Nisha; Shlipak, Michael; Bibbins-Domingo, Kirsten] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Peralta, Carmen A.; Shlipak, Michael] San Francisco VA Med Ctr, San Francisco, CA USA.
[Jacobs, David, Jr.] Univ Minnesota, Minneapolis, MN USA.
[Muntner, Paul] Univ Alabama Birmingham, Birmingham, AL USA.
[Kestenbaum, Bryan; Siscovick, David] Univ Washington, Washington, DC USA.
[Kramer, Holly] Loyola Univ, Chicago, IL 60611 USA.
RP Peralta, CA (reprint author), 4150 Clement St,111A1, San Francisco, CA 94121 USA.
EM carmenalicia.peralta@ucsf.edu
OI Kramer, Holly/0000-0002-6374-837X
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[1K23DK082793-01, R01DK078124]; Robert Wood Johnson Harold Amos Program;
National Heart, Lung and Blood Institute (NHLBI) [N01HC48050]; National
Institute on Minority Health and Health Disparities (NIMHD),
Comprehensive Centers of Excellence [1P60MD006902]; NIDDK [P30-DK092924]
FX Dr Peralta is funded by grant 1K23DK082793-01 from the National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and the
Robert Wood Johnson Harold Amos Program. Dr Bibbins-Domingo was in part
supported by grant R01DK078124 from the National Institute of Diabetes
and Digestive and Kidney Diseases (NIDDK), grant N01HC48050 from the
National Heart, Lung and Blood Institute (NHLBI), from grant
1P60MD006902 from the National Institute on Minority Health and Health
Disparities (NIMHD), Comprehensive Centers of Excellence and from grant
P30-DK092924 from the NIDDK.
NR 17
TC 16
Z9 16
U1 0
U2 7
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD AUG
PY 2013
VL 62
IS 2
BP 261
EP 266
DI 10.1053/j.ajkd.2013.01.012
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 196OK
UT WOS:000322784700012
PM 23473985
ER
PT J
AU Kumbhani, DJ
Steg, PG
Cannon, CP
Eagle, KA
Smith, SC
Hoffman, E
Goto, S
Ohman, EM
Bhatt, DL
AF Kumbhani, Dharam J.
Steg, Ph. Gabriel
Cannon, Christopher P.
Eagle, Kim A.
Smith, Sidney C., Jr.
Hoffman, Elaine
Goto, Shinya
Ohman, E. Magnus
Bhatt, Deepak L.
CA REduc Atherothrombosis Continued H
TI Adherence to Secondary Prevention Medications and Four-year Outcomes in
Outpatients with Atherosclerosis
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Article
DE Atherosclerosis; Cardiovascular disease; Compliance/adherence; Registry;
Secondary prevention
ID ACUTE MYOCARDIAL-INFARCTION; CARDIOVASCULAR EVENT RATES;
CORONARY-ARTERY-DISEASE; GUIDELINES; ATHEROTHROMBOSIS; CARE; MORTALITY;
QUALITY; STROKE; HEART
AB BACKGROUND: Although nonadherence with evidence-based secondary prevention medications is common in patients with established atherothrombotic disease, long-term outcomes studies are scant. We assessed the prevalence and long-term outcomes of nonadherence to secondary prevention (antiplatelet agents, statins, and antihypertensive agents) medications in stable outpatients with established atherothrombosis (coronary, cerebrovascular, or peripheral artery disease) enrolled in the international REduction of Atherothrombosis for Continued Health registry.
METHODS: Adherence with these medications in eligible patients at baseline and 1-year follow-up was assessed. The primary outcome was a composite of cardiovascular death, myocardial infarction, or stroke at 4 years.
RESULTS: A total of 37,154 patients with established atherothrombotic disease were included. Adherence rates with all evidence-based medications at baseline and 1 year were 46.7% and 48.2%, respectively. Nonadherence with any medication at baseline (hazard ratio, 1.18; 95% confidence interval, 1.11-1.25) and at 1 year (hazard ratio, 1.19; 95% confidence interval, 1.11-1.28) were both significantly associated with an increased risk of the primary end point. The risk of all-cause mortality was similarly elevated. Corresponding numbers needed to treat were 31 and 25 patients for the composite end point and total mortality, respectively. This also was true for each disease-specific subgroup. Patients who were fully adherent at both time points had the lowest incidence of adverse outcomes, whereas patients who were nonadherent at both time points had the worst outcomes (P < .01).
CONCLUSIONS: Our analysis of a large international registry demonstrates that nonadherence with evidence-based secondary prevention therapies in patients with established atherothrombosis is associated with a significant increase in long-term adverse events, including mortality. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Kumbhani, Dharam J.] Univ Texas SW Med Ctr Dallas, Div Cardiol, Dallas, TX 75390 USA.
[Steg, Ph. Gabriel] INSERM, U698, Paris, France.
[Steg, Ph. Gabriel] Univ Paris Diderot, Paris, France.
[Steg, Ph. Gabriel] AP HP, Paris, France.
[Cannon, Christopher P.; Bhatt, Deepak L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Cannon, Christopher P.; Bhatt, Deepak L.] Harvard Univ, Sch Med, Boston, MA USA.
[Cannon, Christopher P.; Hoffman, Elaine; Bhatt, Deepak L.] TIMI Study Grp, Boston, MA USA.
[Eagle, Kim A.] Univ Michigan, Ctr Cardiovasc, Ann Arbor, MI 48109 USA.
[Smith, Sidney C., Jr.] Univ N Carolina, Ctr Cardiovasc Sci & Med, Chapel Hill, NC USA.
[Goto, Shinya] Tokai Univ, Sch Med, Isehara, Kanagawa 25911, Japan.
[Ohman, E. Magnus] Duke Univ, Div Cardiol, Durham, NC USA.
[Bhatt, Deepak L.] VA Boston Healthcare Syst, Boston, MA USA.
RP Bhatt, DL (reprint author), VA Boston Healthcare Syst, 1400 VFW Pkwy, Boston, MA 02132 USA.
EM dlbhattmd@post.harvard.edu
FU Sanofi-Aventis; Bristol-Myers Squibb; Waksman Foundation (Tokyo, Japan)
FX The REduction of Atherothrombosis for Continued Health (REACH) Registry
is sponsored by Sanofi-Aventis, Bristol-Myers Squibb, and the Waksman
Foundation (Tokyo, Japan). The REACH Registry is endorsed by the World
Heart Federation. The sponsors did not review this manuscript. The
statistical analyses by the TIMI Study Group were funded with a grant
from Sanofi-Aventis.
NR 34
TC 34
Z9 35
U1 0
U2 9
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 2013
VL 126
IS 8
BP 693
EP +
DI 10.1016/j.amjmed.2013.01.033
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 197CS
UT WOS:000322827200023
PM 23800583
ER
PT J
AU Booher, AM
Isselbacher, EM
Nienaber, CA
Trimarchi, S
Evangelista, A
Montgomery, DG
Froehlich, JB
Ehrlich, MP
Oh, JK
Januzzi, JL
O'Gara, P
Sundt, TM
Harris, KM
Bossone, E
Pyeritz, RE
Eagle, KA
AF Booher, Anna M.
Isselbacher, Eric M.
Nienaber, Christoph A.
Trimarchi, Santi
Evangelista, Arturo
Montgomery, Daniel G.
Froehlich, James B.
Ehrlich, Marek P.
Oh, Jae K.
Januzzi, James L.
O'Gara, Patrick
Sundt, Thoralf M.
Harris, Kevin M.
Bossone, Eduardo
Pyeritz, Reed E.
Eagle, Kim A.
CA IRAD Investigators
TI The IRAD Classification System for Characterizing Survival after Aortic
Dissection
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Article
DE Aorta; Dissecting aneurysm; Survival analyses; Thoracic surgery
ID LONG-TERM SURVIVAL; INTERNATIONAL REGISTRY; INSIGHTS; SURGERY; ANEURYSM;
OUTCOMES
AB BACKGROUND: The classification of aortic dissection into acute (<14 days from symptom onset) versus chronic (>= 14 days) is based on survival estimates of patients treated decades before modern diagnostic and treatment modalities were available. A new classification of aortic dissection in the current era may provide clinicians with a more precise method of characterizing the interaction of time, dissection location, and treatment type with survival.
METHODS: We developed separate Kaplan-Meier survival curves for Type A and Type B aortic dissection using data from the International Registry of Aortic Dissection (IRAD). Daily survival was stratified based on type of therapy provided: medical therapy alone (medical), nonsurgical intervention plus medical therapy (endovascular), and open surgery plus medical therapy (surgical). The log-rank statistic was used to compare the survival curves of each management type within Type A and Type B aortic dissection.
RESULTS: There were 1815 patients included, 67.3% male with mean age 62.0 +/- 14.2 years. When survival curves were constructed, 4 distinct time periods were noted: hyperacute (symptom onset to 24 hours), acute (2-7 days), subacute (8-30 days), and chronic (>30 days). Overall survival was progressively lower through the 4 time periods.
CONCLUSIONS: This IRAD classification system can provide clinicians with a more robust method of characterizing survival after aortic dissection over time than previous methods. This system will be useful for treating patients, counseling patients and families, and studying new diagnostic and treatment methods. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Booher, Anna M.; Montgomery, Daniel G.; Froehlich, James B.; Eagle, Kim A.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Isselbacher, Eric M.; Januzzi, James L.; Sundt, Thoralf M.] Massachusetts Gen Hosp, Thorac Aort Ctr, Boston, MA 02114 USA.
[Nienaber, Christoph A.] Univ Hosp Eppendorf Rostock, Dept Internal Med, Rostock, Germany.
[Trimarchi, Santi] IRCCS Policlin San Donato, Thorac Aort Res Ctr, San Donato Milanese, Italy.
[Evangelista, Arturo] Hosp Gen Univ Vall dHebron, Dept Cardiol, Barcelona, Spain.
[Ehrlich, Marek P.] Univ Vienna, Dept Cardiothorac Surg, A-1010 Vienna, Austria.
[Oh, Jae K.] Mayo Clin, Dept Internal Med, Rochester, MN USA.
[O'Gara, Patrick] Brigham & Womens Hosp, Div Cardiol, Boston, MA 02115 USA.
[Harris, Kevin M.] Minneapolis Heart Inst, Dept Cardiol, Minneapolis, MN USA.
[Bossone, Eduardo] Dept Cardiol, Salerno, Italy.
[Pyeritz, Reed E.] Univ Penn, Sch Med, Dept Med, Philadelphia, PA 19104 USA.
RP Booher, AM (reprint author), Univ Michigan, Cardiovasc Ctr, Cardiovasc Ctr 2344, SPC 5853,1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM amanion@med.umich.edu
RI Trimarchi, Santi/J-7361-2016
OI Trimarchi, Santi/0000-0001-5996-3264
FU University of Michigan Health System; Varbedian Fund for Aortic
Research; Hewlett Foundation; Mardigian Foundation; Gore Inc.
FX IRAD is supported by grants from the University of Michigan Health
System, the Varbedian Fund for Aortic Research, the Hewlett Foundation,
the Mardigian Foundation, and Gore Inc.
NR 14
TC 14
Z9 16
U1 0
U2 6
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 2013
VL 126
IS 8
AR 730.e19
DI 10.1016/j.amjmed.2013.01.020
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA 197CS
UT WOS:000322827200029
PM 23885677
ER
PT J
AU Sobrin, L
Seddon, JM
AF Sobrin, Lucia
Seddon, Johanna M.
TI Regular Aspirin Use and Risk of Age-Related Macular Degeneration
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Editorial Material
ID LOW-DOSE ASPIRIN; EYE; METAANALYSIS; ASSOCIATION; MACULOPATHY;
PREVENTION; DISEASE; TRIAL
C1 [Sobrin, Lucia] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA USA.
[Seddon, Johanna M.] Tufts Univ, Ophthalm Epidemiol & Genet Serv, New England Eye Ctr, Tufts Med Ctr,Sch Med, Boston, MA 02111 USA.
[Seddon, Johanna M.] Tufts Univ, Sch Med, Dept Ophthalmol, Boston, MA 02111 USA.
RP Seddon, JM (reprint author), Tufts Med Ctr, Ophthalm Epidemiol & Genet Serv, Dept Ophthalmol, 800 Washington St 450, Boston, MA 02111 USA.
EM jseddon@tuftsmalicalcenter.org
NR 15
TC 1
Z9 1
U1 0
U2 4
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 2013
VL 156
IS 2
BP 213
EP 217
DI 10.1016/j.ajo.2013.04.023
PG 5
WC Ophthalmology
SC Ophthalmology
GA 196BK
UT WOS:000322748200002
PM 23870358
ER
PT J
AU Roberts, DJ
AF Roberts, Drucilla J.
TI New Hope for Prevention of Preterm Delivery
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Editorial Material
ID CHRONIC CHORIOAMNIONITIS; CHRONIC INTERVILLOSITIS; INFLAMMATORY
RESPONSE; UNKNOWN ETIOLOGY; CHRONIC VILLITIS; PREGNANT RATS; SEPTIC
SHOCK; FETAL; BIRTH; EPIDEMIOLOGY
C1 Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Roberts, DJ (reprint author), Massachusetts Gen Hosp, Dept Pathol, 55 Blossom St, Boston, MA 02114 USA.
EM robertsd@helix.mgh.harvard.edu
NR 40
TC 1
Z9 1
U1 0
U2 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD AUG
PY 2013
VL 183
IS 2
BP 330
EP 332
DI 10.1016/j.ajpath.2013.06.001
PG 3
WC Pathology
SC Pathology
GA 194DR
UT WOS:000322611700001
PM 23810739
ER
PT J
AU Paintlia, AS
Paintlia, MK
Mohan, S
Singh, AK
Singh, I
AF Paintlia, Ajaib S.
Paintlia, Manjeet K.
Mohan, Sarumathi
Singh, Avtar K.
Singh, Inderjit
TI AMP-Activated Protein Kinase Signaling Protects Oligodendrocytes that
Restore Central Nervous System Functions in an Experimental Autoimmune
Encephalomyelitis Model
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID NECROSIS-FACTOR-ALPHA; MULTIPLE-SCLEROSIS; DEMYELINATING DISEASES;
COMBINATION THERAPY; AXON DEGENERATION; OXIDATIVE STRESS;
INTERFERON-GAMMA; PROGENITOR CELLS; NAD(P)H OXIDASE; ENERGY-BALANCE
AB AMP-activated protein kinase (AMPK) signaling is reported to protect neurons under pathologic conditions; however, its effect on oligodendrocytes (OLs) remains to be elucidated. We investigated whether AMPK signaling protects OLs to restore central nervous system (CNS) functions in an experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis. Increased inflammation and demyelination in the CNS and peripheral immune responses were consistent with the observed clinical impairments in EAE animals, which were attenuated by treatment with metformin compared with vehicle. In addition, expressions of neurotrophic factors and of signatory genes of OL lineages were increased in the CNS of metformin-treated EAE animals. Likewise, metformin attenuated inflammatory response and enhanced expressions of neurotrophic factors, thereby protecting OLs via AMPK activation in mixed glial cultures stimulated with lipopolysaccharide/interferon gamma in vitro, as evidenced by analysis of the expression of signatory genes of 01(+)/MBP+ OLs and their cellular populations. Metformin also attenuated oxidative stress and malondialdehyde-containing protein levels, with corresponding induction of anti-oxidative defenses in OLs exposed to cytokines via AMPK activation. These effects of metformin were evident in the CNS of EAE animals. These data provide evidence that AMPK signaling is crucial to protect OLs and, thus, CNS functions in EAE animals. We conclude that AMPK activators, including metformin, have the potential to limit neurologic deficits in multiple sclerosis and related neurodegenerative disorders.
C1 [Paintlia, Ajaib S.; Paintlia, Manjeet K.; Mohan, Sarumathi; Singh, Inderjit] Med Univ S Carolina, Dept Pediat, Darby Childrens Res Inst, Charleston, SC 29425 USA.
[Singh, Avtar K.] Ralph H Johnson VA Med Ctr, Dept Pathol & Lab Med, Charleston, SC USA.
RP Singh, I (reprint author), Med Univ S Carolina, Dept Pediat, 173 Ashley Ave, Charleston, SC 29425 USA.
EM singhi@musc.edu
FU NIH [VA-1BX001072, VA-BX001999, NS-22576, NS-37766, C06-RR018823]
FX Supported by NIH grants VA-1BX001072, VA-BX001999, NS-22576, NS-37766,
and C06-RR018823.
NR 65
TC 13
Z9 15
U1 1
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD AUG
PY 2013
VL 183
IS 2
BP 526
EP 541
DI 10.1016/j.ajpath.2013.04.030
PG 16
WC Pathology
SC Pathology
GA 194DR
UT WOS:000322611700021
PM 23759513
ER
PT J
AU Raff, H
Brown, D
AF Raff, Hershel
Brown, Dennis
TI Civil, sensible, and constructive peer review in APS journals
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Editorial Material
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY
C1 [Raff, Hershel] Med Coll Wisconsin, Dept Med, Milwaukee, WI 53226 USA.
[Raff, Hershel] Med Coll Wisconsin, Dept Surg, Milwaukee, WI 53226 USA.
[Raff, Hershel] Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA.
[Raff, Hershel] Aurora Res Fdn, Aurora St Lukes Med Ctr, Endocrine Res Lab, Milwaukee, WI USA.
[Brown, Dennis] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Brown, Dennis] Massachusetts Gen Hosp, Div Nephrol, Program Membrane Biol, Boston, MA 02114 USA.
[Brown, Dennis] Harvard Univ, Sch Med, Boston, MA USA.
RP Raff, H (reprint author), Aurora St Lukes Med Ctr, 2801 W KK River Pky,Suite 245, Milwaukee, WI 53215 USA.
EM hraff@mcw.edu
NR 14
TC 0
Z9 0
U1 1
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 2013
VL 305
IS 3
BP C239
EP C240
DI 10.1152/ajpcell.00135.2013
PG 2
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA 195LC
UT WOS:000322702800001
PM 23677798
ER
PT J
AU Raff, H
Brown, D
AF Raff, Hershel
Brown, Dennis
TI Civil, sensible, and constructive peer review in APS journals
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Editorial Material
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY
C1 [Raff, Hershel] Med Coll Wisconsin, Dept Med, Milwaukee, WI 53226 USA.
[Raff, Hershel] Med Coll Wisconsin, Dept Surg, Milwaukee, WI 53226 USA.
[Raff, Hershel] Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA.
[Raff, Hershel] Aurora St Lukes Med Ctr, Aurora Res Fdn, Endocrine Res Lab, Milwaukee, WI USA.
[Brown, Dennis] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Brown, Dennis] Massachusetts Gen Hosp, Program Membrane Biol, Div Nephrol, Boston, MA 02114 USA.
[Brown, Dennis] Harvard Univ, Sch Med, Boston, MA USA.
RP Raff, H (reprint author), Aurora St Lukes Med Ctr, 2801 W KK River Pky,Suite 245, Milwaukee, WI 53215 USA.
EM hraff@mcw.edu
NR 15
TC 0
Z9 0
U1 0
U2 3
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 2013
VL 305
IS 3
BP G205
EP G206
DI 10.1152/ajpgi.00154.2013
PG 2
WC Gastroenterology & Hepatology; Physiology
SC Gastroenterology & Hepatology; Physiology
GA 195KP
UT WOS:000322701400001
PM 23703653
ER
PT J
AU Yamamoto, S
Nakase, H
Matsuura, M
Honzawa, Y
Matsumura, K
Uza, N
Yamaguchi, Y
Mizoguchi, E
Chiba, T
AF Yamamoto, Shuji
Nakase, Hiroshi
Matsuura, Minoru
Honzawa, Yusuke
Matsumura, Kayoko
Uza, Norimitsu
Yamaguchi, Yu
Mizoguchi, Emiko
Chiba, Tsutomu
TI Heparan sulfate on intestinal epithelial cells plays a critical role in
intestinal crypt homeostasis via Wnt/beta-catenin signaling
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Article
DE heparan sulfate; intestinal regeneration; Wnt signaling
ID MOUSE SMALL INTESTINE; DOCKING-PROTEIN FRS2-ALPHA; STEM-CELLS;
EXTRACELLULAR-MATRIX; MOLECULAR-MECHANISM; CRYSTAL-STRUCTURE;
TUMOR-SUPPRESSOR; BARRIER FUNCTION; DIFFERENTIATION; DROSOPHILA
AB Heparan sulfate (HS), a constituent of HS proteoglycans (HSPGs), is a linear polysaccharide present on the cell surface. HSPGs modulate functions of several growth factors and signaling molecules. We examined whether small intestinal epithelial HS plays some roles in crypt homeostasis using intestinal epithelium cell (IEC)-specific HS-deficient C57Bl/6 mice. Survival rate after total body irradiation was significantly reduced in HS-deficient mice due to profound intestinal injury. HS-deficient IECs exhibited Wnt/beta-catenin pathway disruption, decreased levels of beta-catenin nuclear localization, and reduced expression of Wnt target genes, including Lgr5 during crypt regeneration. Moreover, epithelial HS increased Wnt binding affinity of IECs, promoted phosphorylation of Wnt coreceptor LRP6, and enhanced Wnt/beta-catenin signaling following ex vivo stimulation with Wnt3a, whereas activation of canonical Wnt signaling following direct inhibition of glycogen synthase kinase-3 beta by lithium chloride was similar between HS-deficient and wild-type mice. Thus HS influences the binding affinity of IECs to Wnt, thereby promoting activation of canonical Wnt signaling and facilitating regeneration of small intestinal crypts after epithelial injury.
C1 [Yamamoto, Shuji; Nakase, Hiroshi; Matsuura, Minoru; Honzawa, Yusuke; Matsumura, Kayoko; Uza, Norimitsu; Chiba, Tsutomu] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Kyoto 6068507, Japan.
[Yamamoto, Shuji] Japan Soc Promot Sci, Tokyo, Japan.
[Yamaguchi, Yu] Sanford Burnham Med Res Inst, Sanford Childrens Hlth Res Ctr, La Jolla, CA USA.
[Mizoguchi, Emiko] Massachusetts Gen Hosp, Dept Med, Gastrointestinal Unit, Boston, MA 02114 USA.
[Mizoguchi, Emiko] Harvard Univ, Sch Med, Boston, MA USA.
RP Nakase, H (reprint author), Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, 54 Shogoin Kawahara Cho, Kyoto 6068507, Japan.
EM hiropy_n@kuhp.kyoto-u.ac.jp
FU Ministry of Culture and Science of Japan [18590677]; Kato Memorial Trust
for Nambyo Research; Japan Foundation for Applied Enzymology; Shimizu
Foundation for the Promotion of Immunology Research; National Institutes
of Health in the U.S. [ROI DK 80070]; Ministry of Education, Culture,
Sports, Science, and Technology of Japan [16017240, 16017249, 17013051,
17659212, 18012029]; JSPS [15209024, 18209027]; Ministry of Health,
Labor, and Welfare, Japan [nano005]
FX This work was supported by a Grant-in-Aid for the Japan Society for the
Promotion of Science Fellows (to S. Yamamoto); a Grant-in-Aid for
Scientific Research (C) from the Ministry of Culture and Science of
Japan (grant 18590677), the Kato Memorial Trust for Nambyo Research, the
Japan Foundation for Applied Enzymology, the Shimizu Foundation for the
Promotion of Immunology Research (to H. Nakase); a research grant (ROI
DK 80070) from the National Institutes of Health in the U.S. (to E.
Mizoguchi); Grants-in-Aid for Scientific Research (16017240, 16017249,
17013051, 17659212, and 18012029) from the Ministry of Education,
Culture, Sports, Science, and Technology of Japan, Grants-in-Aid for
Scientific Research (15209024 and 18209027) from JSPS, and a
Grant-in-Aid for Research on Measures for Intractable Disease, and
Research on Advanced Medical Technology (nano005) from the Ministry of
Health, Labor, and Welfare, Japan (to T. Chiba).
NR 59
TC 6
Z9 6
U1 1
U2 6
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 2013
VL 305
IS 3
BP G241
EP G249
DI 10.1152/ajpgi.00480.2012
PG 9
WC Gastroenterology & Hepatology; Physiology
SC Gastroenterology & Hepatology; Physiology
GA 195KP
UT WOS:000322701400005
PM 23744737
ER
PT J
AU Raff, H
Brown, D
AF Raff, Hershel
Brown, Dennis
TI Civil, sensible, and constructive peer review in APS journals
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Editorial Material
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY
C1 [Raff, Hershel] Med Coll Wisconsin, Dept Med, Milwaukee, WI 53226 USA.
[Raff, Hershel] Med Coll Wisconsin, Dept Surg, Milwaukee, WI 53226 USA.
[Raff, Hershel] Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA.
[Raff, Hershel] Aurora Res Fdn, Aurora St Lukes Med Ctr, Endocrine Res Lab, Milwaukee, WI USA.
[Brown, Dennis] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Brown, Dennis] Massachusetts Gen Hosp, Div Nephrol, Program Membrane Biol, Boston, MA 02114 USA.
[Brown, Dennis] Harvard Univ, Sch Med, Boston, MA USA.
RP Raff, H (reprint author), Aurora St Lukes Med Ctr, 2801 W KK River Pky,Suite 245, Milwaukee, WI 53215 USA.
EM hraff@mcw.edu
NR 15
TC 0
Z9 0
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD AUG
PY 2013
VL 305
IS 3
BP H265
EP H266
DI 10.1152/ajpheart.00390.2013
PG 2
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 195KI
UT WOS:000322700600001
PM 23686714
ER
PT J
AU Raff, H
Brown, D
AF Raff, Hershel
Brown, Dennis
TI Civil, sensible, and constructive peer review in APS journals
SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE
PHYSIOLOGY
LA English
DT Editorial Material
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY
C1 [Raff, Hershel] Aurora Res Fdn, Med Coll Wisconsin, Dept Med, Milwaukee, WI USA.
[Raff, Hershel] Aurora Res Fdn, Med Coll Wisconsin, Dept Surg, Milwaukee, WI USA.
[Raff, Hershel] Aurora Res Fdn, Med Coll Wisconsin, Dept Physiol, Milwaukee, WI USA.
[Raff, Hershel] Aurora Res Fdn, Aurora St Lukes Med Ctr, Endocrine Res Lab, Milwaukee, WI USA.
[Brown, Dennis] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Brown, Dennis] Massachusetts Gen Hosp, Div Nephrol, Program Membrane Biol, Boston, MA 02114 USA.
[Brown, Dennis] Harvard Univ, Sch Med, Boston, MA USA.
RP Raff, H (reprint author), Aurora St Lukes Med Ctr, 2801 W KK River Pky,Suite 245, Milwaukee, WI 53215 USA.
EM hraff@mcw.edu
NR 14
TC 0
Z9 0
U1 0
U2 2
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 2013
VL 305
IS 3
BP R171
EP R172
DI 10.1152/ajpregu.00237.2013
PG 2
WC Physiology
SC Physiology
GA 195JO
UT WOS:000322698400001
PM 23678023
ER
PT J
AU Raff, H
Brown, D
AF Raff, Hershel
Brown, Dennis
TI Civil, sensible, and constructive peer review in APS journals
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Editorial Material
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY
C1 [Raff, Hershel] Med Coll Wisconsin, Dept Med Surg & Physiol, Milwaukee, WI 53226 USA.
[Raff, Hershel] Aurora Res Fdn, Aurora St Lukes Med Ctr, Endocrine Res Lab, Milwaukee, WI USA.
[Brown, Dennis] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Brown, Dennis] Massachusetts Gen Hosp, Program Membrane Biol, Div Nephrol, Boston, MA 02114 USA.
[Brown, Dennis] Harvard Univ, Sch Med, Boston, MA USA.
RP Raff, H (reprint author), Aurora St Lukes Med Ctr, 2801 W KK River Pky,Suite 245, Milwaukee, WI 53215 USA.
EM hraff@mcw.edu
NR 15
TC 0
Z9 0
U1 1
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 2013
VL 305
IS 3
BP F227
EP F228
DI 10.1152/ajprenal.00269.2013
PG 2
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 195JU
UT WOS:000322699000001
PM 23678044
ER
PT J
AU Criscitiello, C
Azim, HA
Agbor-tarh, D
de Azambuja, E
Piccart, M
Baselga, J
Eidtmann, H
Di Cosimo, S
Bradbury, I
Rubio, IT
AF Criscitiello, C.
Azim, H. A., Jr.
Agbor-tarh, D.
de Azambuja, E.
Piccart, M.
Baselga, J.
Eidtmann, H.
Di Cosimo, S.
Bradbury, I.
Rubio, I. T.
TI Factors associated with surgical management following neoadjuvant
therapy in patients with primary HER2-positive breast cancer: results
from the NeoALTTO phase III trial
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE breast cancer; neoadjuvant; HER2; surgery; breast conservation;
trastuzumab
ID ADJUVANT BREAST; PREOPERATIVE CHEMOTHERAPY; CONSERVING SURGERY; SYSTEMIC
TREATMENT; RANDOMIZED-TRIAL; OPEN-LABEL; TRASTUZUMAB; COUNTRIES;
CONSENSUS; METAANALYSIS
AB The NeoALTTO trial showed that dual HER2 blockade nearly doubles the rate of pathologic complete response (pCR) in patients with primary HER2-positive breast cancer. However, this did not translate into a higher rate of breast-conserving surgery (BCS).
In NeoALTTO, patients with HER2-positive breast cancer were randomly assigned to either trastuzumab, lapatinib or their combination with paclitaxel before surgery with pCR as the primary end point. We investigated the association between the surgery type and clinicopathological factors and response to treatment, adjusting for the treatment arm.
Four hundred and twenty-nine patients were subjected to breast surgery. Two hundred and forty-two (56%) and 187 (44%) patients underwent mastectomy and BCS, respectively. In a logistic regression model, negative estrogen receptor (ER), multicentricity and the presence of a palpable mass before surgery were significantly associated with a low chance of BCS. Conversely, patients with small tumors and those eligible for BCS at diagnosis were managed more with BCS, independent of the treatment arm. Radiological response was not associated with the surgical decision.
Tumor characteristics before neoadjuvant therapy play a main role in deciding the type of surgery calling for a clear consensus on the role of BCS in patients responding to neoadjuvant therapy.
C1 [Criscitiello, C.] European Inst Oncol, Dept Med, Div Med Oncol, Milan, Italy.
[Azim, H. A., Jr.; de Azambuja, E.; Piccart, M.] Univ Libre Brussels, Inst Jules Bordet, Dept Med, BrEAST Data Ctr, Brussels, Belgium.
[Agbor-tarh, D.; Bradbury, I.] Frontier Sci, Kincraig, Kingussie, Scotland.
[Baselga, J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Eidtmann, H.] Univ Hosp Kiel, Kiel, Germany.
[Di Cosimo, S.] Ist Nazl Tumori, Dept Med Oncol, I-20133 Milan, Italy.
[Rubio, I. T.] Univ Vall DHebron, Breast Surg Oncol Unit, Barcelona, Spain.
RP Azim, HA (reprint author), Inst Jules Bordet, BrEAST Data Ctr, Dept Med, Brussels, Belgium.
EM hatem.azim@bordet.be
RI Serena, Di Cosimo/E-9418-2017
OI Serena, Di Cosimo/0000-0002-4666-8052
FU European Society for Medical Oncology
FX CC acknowledges a TRANSBIG fellowship. HAA Jr acknowledges a fellowship
grant from the European Society for Medical Oncology (no grant numbers).
NR 29
TC 13
Z9 13
U1 1
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD AUG
PY 2013
VL 24
IS 8
BP 1980
EP 1985
DI 10.1093/annonc/mdt129
PG 6
WC Oncology
SC Oncology
GA 190KR
UT WOS:000322339300006
PM 23567146
ER
PT J
AU Weiner, M
Skoog, L
Fornander, T
Nordenskjold, B
Sgroi, DC
Stal, O
AF Weiner, M.
Skoog, L.
Fornander, T.
Nordenskjold, B.
Sgroi, D. C.
Stal, O.
TI Oestrogen receptor co-activator AIB1 is a marker of tamoxifen benefit in
postmenopausal breast cancer
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE AIB1; breast cancer; HER2; prognosis; SRC-3; treatment prediction
ID TRANSCRIPTIONAL COACTIVATOR; PROTEIN EXPRESSION; RESISTANCE;
COREGULATORS; ANTIESTROGEN; PREDICTS; GROWTH; SRC-3
AB The oestrogen receptor (ER) co-activator amplified in breast cancer 1 (AIB1) has been suggested as a treatment predictive and prognostic marker in breast cancer. Studies have however not been unanimous.
AIB1 protein expression was analysed by immunohistochemistry on tissue micro-arrays with tumour samples from 910 postmenopausal women randomised to tamoxifen treatment or no adjuvant treatment. Associations between AIB1 expression, clinical outcome in the two arms and other clinicopathological variables were examined.
In patients with ER-positive breast cancer expressing low tumour levels of AIB1 (< 75%), we found no significant difference in recurrence-free survival (RFS) or breast cancer-specific survival (BCS) between tamoxifen treated and untreated patients. In patients with high AIB1 expression (> 75%), there was a significant decrease in recurrence rate (HR 0.40, 95% CI 0.26-0.61, P < 0.001) and breast cancer mortality rate (HR 0.38, 95% CI 0.21-0.69, P = 0.0015) with tamoxifen treatment. In the untreated arm, we found high expression of AIB1 to be significantly associated with lower RFS (HR 1.74, 95% CI 1.20-2.53, P = 0.0038).
Our results suggest that high AIB1 is a predictive marker of good response to tamoxifen treatment in postmenopausal women and a prognostic marker of decreased RFS in systemically untreated patients.
C1 [Weiner, M.; Nordenskjold, B.; Stal, O.] Linkoping Univ, Fac Hlth Sci, Cty Council Ostergotland, Div Oncol,Dept Clin & Expt Med, Linkoping, Sweden.
[Weiner, M.] Linkoping Univ, Dept Med & Hlth, Div Drug Res, Linkoping, Sweden.
[Skoog, L.] Karolinska Inst, Karolinska Univ Hosp, Dept Pathol, Stockholm, Sweden.
[Fornander, T.] Karolinska Inst, Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
[Sgroi, D. C.] Massachusetts Gen Hosp, Mol Pathol Res Unit, Dept Pathol, Boston, MA 02114 USA.
RP Stal, O (reprint author), Linkoping Univ Hosp, Div Oncol, Dept Clin & Expt Med, SE-58185 Linkoping, Sweden.
EM olle.stal@liu.se
FU Swedish Cancer Society [110504]; Swedish Research Council [B0771901]
FX The work was supported by grants from the Swedish Cancer Society
(#110504) and the Swedish Research Council (#B0771901).
NR 24
TC 5
Z9 5
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD AUG
PY 2013
VL 24
IS 8
BP 1994
EP 1999
DI 10.1093/annonc/mdt159
PG 6
WC Oncology
SC Oncology
GA 190KR
UT WOS:000322339300008
PM 23670096
ER
PT J
AU Henry, NL
Xia, R
Banerjee, M
Gersch, C
McConnell, D
Giacherio, D
Schott, AF
Pearlman, M
Stearns, V
Partridge, AH
Hayes, DF
AF Henry, N. L.
Xia, R.
Banerjee, M.
Gersch, C.
McConnell, D.
Giacherio, D.
Schott, A. F.
Pearlman, M.
Stearns, V.
Partridge, A. H.
Hayes, D. F.
TI Predictors of recovery of ovarian function during aromatase inhibitor
therapy
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE aromatase inhibitor; breast cancer; chemotherapy-induced ovarian
failure; estradiol; ovarian function
ID MASS-SPECTROMETRY ASSAY; EARLY BREAST-CANCER; CHEMOTHERAPY; TAMOXIFEN;
ESTRADIOL; HORMONE; TRIALS; PLASMA
AB Aromatase inhibitors (AIs) may cause a rise in estrogen levels due to ovarian function recovery in women with clinical chemotherapy-induced ovarian failure (CIOF). We carried out a prospective registry trial to identify predictors of ovarian function recovery during AI therapy.
Women with hormone receptor (HR)-positive breast cancer who remained amenorrheic and had hormonal levels consistent with ovarian failure after adjuvant chemotherapy were enrolled in a multi-institutional clinical trial of anastrozole. Subjects underwent frequent assessment using an ultrasensitive estradiol assay. Multivariable analysis was used to evaluate clinical and biochemical predictors of ovarian function recovery within 48 weeks.
Recovery of ovarian function during AI therapy was observed in 13 of 45 (28.9%) assessable subjects after a median 2.1 months (range 0.6-11.9). Median age at chemotherapy initiation was statistically significantly different between those who regained ovarian function (43 years, range 40-51) and those who remained postmenopausal (49 years, range 44-52; P < 0.0001).
A significant proportion of women with CIOF recover ovarian function during AI therapy, including a woman over age 50 at initiation of chemotherapy. Tamoxifen remains the standard of care for women with CIOF. If an AI is used, patients should be monitored frequently with high-quality estradiol assays.
Clinicaltrials.gov: NCT00555477.
C1 [Henry, N. L.; Gersch, C.; Schott, A. F.; Hayes, D. F.] Univ Michigan, Ctr Comprehens Canc, Breast Oncol Program, Ann Arbor, MI 48109 USA.
[Xia, R.; Banerjee, M.] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA.
[McConnell, D.] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Giacherio, D.] Univ Michigan, Sch Med, Dept Pathol, Ann Arbor, MI 48109 USA.
[Pearlman, M.] Univ Michigan, Sch Med, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
[Stearns, V.] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Breast Canc Program, Baltimore, MD USA.
[Partridge, A. H.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Henry, NL (reprint author), Univ Michigan, Ctr Comprehens Canc, Breast Oncol Program, 1500 East Med Ctr Dr,Med Inn Bldg C450, Ann Arbor, MI 48109 USA.
EM norahh@med.umich.edu
FU National Cancer Institute at the National Institutes of Health
[5K07CA134747]; AstraZeneca; Fashion Footwear Association of New
York/QVC Presents Shoes on Sale(TM); University of Michigan
Comprehensive Cancer Center; Lilly Pharmaceuticals; sanofi aventis;
Novartis; Pfizer
FX This work was supported by the National Cancer Institute at the National
Institutes of Health [grant number 5K07CA134747] to NLH; AstraZeneca;
the Fashion Footwear Association of New York/QVC Presents Shoes on Sale
(TM) to DFH and the University of Michigan Comprehensive Cancer Center
to NLH. NLH received research funding from AstraZeneca, Lilly
Pharmaceuticals and sanofi aventis. DFH received research funding from
AstraZeneca. DFH and VS received research funding from Novartis and
Pfizer.
NR 12
TC 14
Z9 14
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD AUG
PY 2013
VL 24
IS 8
BP 2011
EP 2016
DI 10.1093/annonc/mdt149
PG 6
WC Oncology
SC Oncology
GA 190KR
UT WOS:000322339300011
PM 23613476
ER
PT J
AU Choueiri, TK
Je, Y
Sonpavde, G
Richards, CJ
Galsky, MD
Nguyen, PL
Schutz, F
Heng, DY
Kaymakcalan, MD
AF Choueiri, T. K.
Je, Y.
Sonpavde, G.
Richards, C. J.
Galsky, M. D.
Nguyen, P. L.
Schutz, F.
Heng, D. Y.
Kaymakcalan, M. D.
TI Incidence and risk of treatment-related mortality in cancer patients
treated with the mammalian target of rapamycin inhibitors
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE cancer; renal cell carcinoma; mTOR inhibitors; fatal adverse events;
meta-analysis
ID RENAL-CELL CARCINOMA; ADVERSE DRUG-REACTIONS; PHASE-III; NEUROENDOCRINE
TUMORS; INTERFERON-ALPHA; CLINICAL-TRIALS; EVEROLIMUS; TEMSIROLIMUS;
THERAPY; EVENTS
AB Inhibition of the mammalian target of rapamycin (mTOR) is an established treatment for multiple malignancies. We carried out an up-to-date meta-analysis to determine the risk of fatal adverse events (FAEs) in cancer patients treated with mTOR inhibitors.
PubMed, conferences and clinicaltrials.gov databases were searched for articles reported from January 1966 to June 2012. Eligible studies were limited to approved mTOR inhibitors (everolimus and temsirolimus) and reported on patients with cancer, randomized design and adequate safety profiles. Data extraction was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement.
In all, 3193 patients from eight randomized, controlled trials (RCTs) were included, 2236 from everolimus trials and 957 from temsirolimus trials. The relative risk (RR) of FAEs related to mTOR inhibitors use was 2.20 (95% CI, 1.25-3.90; P = 0.006) compared with control patients. On subgroup analysis, no difference in the rate of FAEs was found between everolimus and temsirolimus or between tumor types [renal cell carcinoma (RCC) versus non-RCC]. No evidence of publication bias was observed.
The use of mTOR inhibitors is associated with a small but higher risk of FAEs compared to control patients. In the appropriate clinical scenario, the use of these drugs remains justified in their approved indications.
C1 [Choueiri, T. K.; Nguyen, P. L.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Je, Y.] Kyung Hee Univ, Dept Food & Nutr, Seoul, South Korea.
[Sonpavde, G.] UAB, Ctr Comprehens Canc, Dept Med Oncol, Birmingham, AL USA.
[Richards, C. J.] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Galsky, M. D.] Mt Sinai Sch Med, Tisch Canc Inst, Dept Med Oncol, New York, NY USA.
[Nguyen, P. L.] Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02115 USA.
[Schutz, F.] Hosp Sao Paulo, Dept Med Oncol, Sao Paulo, Brazil.
[Heng, D. Y.] Univ Calgary, Dept Med Oncol, Calgary, AB, Canada.
[Kaymakcalan, M. D.] Dana Farber Canc Inst, Dept Pharm, Boston, MA 02115 USA.
RP Choueiri, TK (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM toni_choueiri@dfci.harvard.edu
FU Trust Family Research Fund for Kidney Cancer
FX Trust Family Research Fund for Kidney Cancer. The funding source had no
role in study design, analysis, interpretation or writing the
manuscript. No grant number applicable.
NR 32
TC 12
Z9 13
U1 1
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD AUG
PY 2013
VL 24
IS 8
BP 2092
EP 2097
DI 10.1093/annonc/mdt155
PG 6
WC Oncology
SC Oncology
GA 190KR
UT WOS:000322339300024
PM 23658373
ER
PT J
AU Shahian, DM
He, X
Jacobs, JP
Rankin, JS
Peterson, ED
Welke, KF
Filardo, G
Shewan, CM
O'Brien, SM
AF Shahian, David M.
He, Xia
Jacobs, Jeffrey P.
Rankin, J. Scott
Peterson, Eric D.
Welke, Karl F.
Filardo, Giovanni
Shewan, Cynthia M.
O'Brien, Sean M.
TI Issues in Quality Measurement: Target Population, Risk Adjustment, and
Ratings
SO ANNALS OF THORACIC SURGERY
LA English
DT Review
ID PROFILING HOSPITAL PERFORMANCE; SURGERY REPORT CARDS; HEALTH-CARE;
CLINICAL-OUTCOMES; MORTALITY-RATES; SURGICAL CARE; TASK-FORCE; DEATH
RATE; DECISIONS; MODELS
AB This review investigates three fundamental issues in health care performance measurement: selection of a homogeneous target population, risk adjustment, and assignment of quality rating categories. Many but not all organizations involved in quality measurement have adopted similar approaches to these important methodological issues. To illustrate the practical implications of different profiling strategies, we use The Society of Thoracic Surgeons' data to compare profiling results derived using prevailing analytical methodologies with those obtained from alternative approaches, exemplified by those of a well-known health care performance rating organization. We demonstrate the differences in provider classification that may result from these methodologic decisions. (C) 2013 by The Society of Thoracic Surgeons
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
Duke Clin Res Inst, Durham, NC USA.
Congenital Heart Inst Florida, St Petersburg, FL USA.
Vanderbilt Univ, Centennial Med Ctr, Nashville, TN 37235 USA.
Seattle Childrens Hosp, Div Cardiothorac Surg, Seattle, WA USA.
Univ Washington, Seattle, WA 98195 USA.
Baylor Hlth Care Syst, Inst Hlth Care Res & Improvement, Dallas, TX USA.
Soc Thorac Surg, Chicago, IL USA.
RP Shahian, DM (reprint author), Massachusetts Gen Hosp, Dept Surg, 55 Fruit St, Boston, MA 02114 USA.
EM dshahian@partners.org
NR 44
TC 12
Z9 12
U1 3
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD AUG
PY 2013
VL 96
IS 2
BP 718
EP 726
DI 10.1016/j.athoracsur.2013.03.029
PG 9
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 201YA
UT WOS:000323177800073
PM 23816415
ER
PT J
AU Gerrard, P
Goldstein, R
DiVita, MA
Ryan, CM
Mix, J
Niewczyk, P
Kazis, L
Kowalske, K
Zafonte, R
Schneider, JC
AF Gerrard, Paul
Goldstein, Richard
DiVita, Margaret A.
Ryan, Colleen M.
Mix, Jacqueline
Niewczyk, Paulette
Kazis, Lewis
Kowalske, Karen
Zafonte, Ross
Schneider, Jeffrey C.
TI Validity and Reliability of the FIM Instrument in the Inpatient Burn
Rehabilitation Population
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Burns; Factor analysis; Outcome measures; Psychometrics; Rehabilitation;
Validation
ID FUNCTIONAL INDEPENDENCE MEASURE; ITEM RESPONSE THEORY; MOKKEN SCALE
ANALYSIS; OUTCOMES; IRT; HEALTH
AB Objective: To provide evidence of construct validity for the FIM instrument in the inpatient rehabilitation burn population.
Design: Confirmatory factor analysis and item response theory were used to assess construct validity. Confirmatory factor analysis was performed on a 2-factor model of the FIM instrument and on a 6-subfactor model. Mokken scale analysis, a nonparametric item response theory, was performed on each of the FIM instrument's 2 major factors, motor and cognitive domains. Internal consistency using Cronbach alpha and Molenaar and Sijtsma's statistic was also examined.
Setting: Inpatient rehabilitation facilities.
Participants: Data from the Uniform Data System for Medical Rehabilitation for patients with an impairment code of burn injury from the years 2002 to 2011 were used for this analysis. A total of 7569 subjects were included in the study.
Interventions: Not applicable.
Main Outcome Measures: Comparative fit index results for the confirmatory factor analyses and adherence to assumptions of the Mokken scale model.
Results: Confirmatory factor analysis provided a comparative fit index of 862 for the 2-factor model of 862 for the 6-subfactor model. Mokken scale analysis showed scalability coefficients of.681 and.891 for the motor and cognitive domains, respectively. Measures of internal consistency statistic gave values of >.95 for each major domain of the FIM instrument.
Conclusions: The FIM instrument has evidence of validity and reliability as an outcome measure for patients with burn injuries in the inpatient rehabilitation setting. The 6-subfactor model provides a better fit than the 2-factor model by confirmatory factor analysis. There is evidence that the motor and cognitive domains each form valid unidimensional metrics based on nonparametric item response theory. Archives of Physical Medicine and Rehabilitation 2013;94:1521-26 (C) 2013 by the American Congress of Rehabilitation Medicine
C1 [Gerrard, Paul; Goldstein, Richard; Zafonte, Ross; Schneider, Jeffrey C.] Harvard Univ, Sch Med, Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, Boston, MA 02115 USA.
[DiVita, Margaret A.; Mix, Jacqueline; Niewczyk, Paulette] Uniform Data Syst Med Rehabil, Amherst, NY USA.
[Ryan, Colleen M.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Surg Serv,Sumner Redstone Burn Ctr, Boston, MA 02115 USA.
[Ryan, Colleen M.] Shriners Hosp Children, Boston, MA USA.
[Niewczyk, Paulette] Daemen Coll, Hlth Care Studies Dept, Amherst, NY USA.
[Kazis, Lewis] Boston Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02215 USA.
[Kowalske, Karen] Univ Texas SW Med Ctr Dallas, Dept Phys Med & Rehabil, Dallas, TX 75390 USA.
RP Gerrard, P (reprint author), Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, 125 Nashua St, Boston, MA 02114 USA.
EM pbgerrard@partners.org
OI Gerrard, Paul/0000-0003-0654-5354; Kazis, Lewis/0000-0003-1800-5849;
DiVita, Margaret/0000-0002-4878-2959
NR 30
TC 9
Z9 9
U1 1
U2 9
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0003-9993
J9 ARCH PHYS MED REHAB
JI Arch. Phys. Med. Rehabil.
PD AUG
PY 2013
VL 94
IS 8
BP 1521
EP 1526
DI 10.1016/j.apmr.2013.02.019
PG 6
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 196TZ
UT WOS:000322801600012
PM 23473701
ER
PT J
AU Woodbury, ML
Velozo, CA
Richards, LG
Duncan, PW
AF Woodbury, Michelle L.
Velozo, Craig A.
Richards, Lorie G.
Duncan, Pamela W.
TI Rasch Analysis Staging Methodology to Classify Upper Extremity Movement
Impairment After Stroke
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Rehabilitation; Stroke; Upper extremity
ID FUGL-MEYER ASSESSMENT; COMPUTERIZED ADAPTIVE TEST; UPPER-LIMB; CLINICAL
INTERPRETATION; OUTCOME MEASURES; MOTOR DEFICITS; HEMIPARESIS;
REHABILITATION; RECOVERY; VALIDITY
AB Objectives: To define Fugl-Meyer Assessment of the Upper Extremity (FMA-UE) cutoff scores that demarcate 1 level of upper extremity (UE) impairment from another, and describe motor behaviors for each category in terms of expected FMA-UE item performance.
Design: Analysis of existing FMA-UE data.
Setting: University research laboratory.
Participants: Persons (N=512) 0 to 145 days poststroke, 42 to 90 years of age.
Intervention: Not applicable.
Main Outcome Measures: An item response Rasch analysis staging method was used to calculate cutoff scores, which were defined as the RaschAndrich threshold values of 2 criterion FMA-UE items derived from an analysis of this sample. The analysis enabled conversion of cutoff scores, in logit units, to FMA-UE points assessed on 30 FMA-UE voluntary movement items (60 possible points).
Results: The boundary between severe and moderate impairment was defined as -1.59 +/-.27 logits or 19 +/- 2 points; and between moderate and mild impairment was defined as 2.44 +/-.27 logits or 47 +/- 2 points. A description of expected performance in each impairment level shows that patients with severe impairment exhibited some distal movements, and patients with mild impairment had difficulties with some proximal movements.
Conclusions: The cutoff scores, which link to a description of specific movements a patient can, can partially, and cannot perform, may enable formation of heterogeneous patient groups, advance efforts to identify specific movement therapy targets, and define treatment response in terms of specific movement that changed or did not change with therapy. Archives of Physical Medicine and Rehabilitation 2013;94:1527-33 (C) 2013 by the American Congress of Rehabilitation Medicine
C1 [Woodbury, Michelle L.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
[Woodbury, Michelle L.] Med Univ S Carolina, Dept Hlth Sci & Res, Charleston, SC 29425 USA.
[Velozo, Craig A.] Malcom Randall VA Med Ctr, Gainesville, FL USA.
[Velozo, Craig A.] Univ Florida, Dept Occupat Therapy, Gainesville, FL USA.
[Richards, Lorie G.] Univ Utah, Dept Occupat Therapy, Salt Lake City, UT USA.
[Duncan, Pamela W.] Wake Forest Baptist Hlth, Dept Neurol, Winston Salem, NC USA.
RP Woodbury, ML (reprint author), Med Univ S Carolina, Coll Hlth Profess, 77 President St, Charleston, SC 29425 USA.
EM WoodbuML@musc.edu
FU Ralph H. Johnson Veterans Affairs Medical Center; Office of Research and
Development, Rehabilitation Research and Development, Department of
Veterans Affairs, Career Development-2 Award [B-6332W]; National
Institute on Aging, Claude D. Pepper Center [5P60AG14635]
FX Supported by the Ralph H. Johnson Veterans Affairs Medical Center and
the Office of Research and Development, Rehabilitation Research and
Development, Department of Veterans Affairs, Career Development-2 Award
(grant no. B-6332W); and the National Institute on Aging, Claude D.
Pepper Center (grant no. 5P60AG14635).
NR 51
TC 13
Z9 13
U1 0
U2 12
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0003-9993
J9 ARCH PHYS MED REHAB
JI Arch. Phys. Med. Rehabil.
PD AUG
PY 2013
VL 94
IS 8
BP 1527
EP 1533
DI 10.1016/j.apmr.2013.03.007
PG 7
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 196TZ
UT WOS:000322801600013
PM 23529144
ER
PT J
AU Cameron, MH
Asano, M
Bourdette, D
Finlayson, ML
AF Cameron, Michelle H.
Asano, Miho
Bourdette, Dennis
Finlayson, Marcia L.
TI People With Multiple Sclerosis Use Many Fall Prevention Strategies but
Still Fall Frequently
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Accidental falls; Activities of daily living; Multiple sclerosis;
Rehabilitation; Self care
ID OLDER-PEOPLE; RISK-FACTORS; ADULTS; METAANALYSIS; COMMUNITY; PROGRAM;
BALANCE; TRIAL; DRUGS; WOMEN
AB Objective: To compare the use of fall prevention strategies by people with multiple sclerosis (MS) who do or do not fall.
Design: Prospective cohort. All assessments were completed between January 2011 and December 2011. Data used in this analysis were collected as part of an observational study that included baseline assessment followed by prospective counting of falls using fall calendars.
Setting: Veterans Affairs and university medical centers.
Participants: People with MS (N=58) of any subtype, aged 18 to 50 years, with Expanded Disability Status Scale score <6.0, recruited from MS clinics at the Portland VA Medical Center and Oregon Health and Science University and from the surrounding areas.
Interventions: Not applicable.
Main Outcome Measures: Measures included the occurrence of falls over 3 months and scores on the Fall Prevention Strategy Survey (FPSS) and the relations between fall prevention strategy use reported on the FPSS and falls.
Results: A total of 52 subjects completed the study. Of these, 33 (63%) subjects fell at least once in the 3-month period, and 19 (36%) subjects did not fall. The mean total FPSS score for the fallers was significantly higher than the nonfallers (mean +/- SD, 8.1 +/- 6.4 vs 4.0 +/- 4.1; range, 0-20 vs 0-15; P=.007), and FPSS scores correlated with monthly fall rates (rho=.49, P=.01). A higher proportion of fallers than nonfallers used the strategies of turning on lights at home, asking others for help, and talking to a health care professional about fall prevention. However, both groups rarely talked to a health care professional about fall prevention or asked a provider to check whether any medications might increase fall risk.
Conclusions: People with MS who fall use more fall prevention strategies than those who do not fall. Archives of Physical Medicine and Rehabilitation 2013;94:1562-6 (C) 2013 by the American Congress of Rehabilitation Medicine
C1 [Cameron, Michelle H.; Bourdette, Dennis] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97239 USA.
[Cameron, Michelle H.; Bourdette, Dennis] Portland VA Med Ctr, Portland, OR USA.
[Asano, Miho; Finlayson, Marcia L.] Queens Univ, Sch Rehabil Therapy, Kingston, ON, Canada.
RP Cameron, MH (reprint author), Oregon Hlth & Sci Univ, Dept Neurol, L226,3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM cameromi@ohsu.edu
RI Finlayson, Marcia /G-2654-2014
OI Finlayson, Marcia /0000-0002-1774-4810
FU Department of Veterans Affairs, Rehabilitation Research and Development
[E7244W]
FX Supported by the Department of Veterans Affairs, Rehabilitation Research
and Development (grant no. E7244W).
NR 26
TC 3
Z9 4
U1 1
U2 10
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0003-9993
J9 ARCH PHYS MED REHAB
JI Arch. Phys. Med. Rehabil.
PD AUG
PY 2013
VL 94
IS 8
BP 1562
EP 1566
DI 10.1016/j.apmr.2013.01.021
PG 5
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 196TZ
UT WOS:000322801600018
PM 23391522
ER
PT J
AU Urraca, N
Cleary, J
Brewer, V
Pivnick, EK
McVicar, K
Thibert, RL
Schanen, NC
Esmer, C
Lamport, D
Reiter, LT
AF Urraca, Nora
Cleary, Julie
Brewer, Victoria
Pivnick, Eniko K.
McVicar, Kathryn
Thibert, Ronald L.
Schanen, N. Carolyn
Esmer, Carmen
Lamport, Dustin
Reiter, Lawrence T.
TI The Interstitial Duplication 15q11.2-q13 Syndrome Includes Autism, Mild
Facial Anomalies and a Characteristic EEG Signature
SO AUTISM RESEARCH
LA English
DT Article
DE autism; 15q duplication; imprinting; copy number variation; UBE3A
ID DE-NOVO MUTATIONS; PERVASIVE DEVELOPMENTAL DISORDERS; SLEEP HABITS
QUESTIONNAIRE; PRADER-WILLI-SYNDROME; SPECTRUM DISORDERS;
ANGELMAN-SYNDROME; PROXIMAL 15Q; LINKAGE-DISEQUILIBRIUM; RECEPTOR
SUBTYPES; REGION
AB Chromosomal copy number variants (CNV) are the most common genetic lesion found in autism. Many autism-associated CNVs are duplications of chromosome 15q. Although most cases of interstitial (int) dup(15) that present clinically are de novo and maternally derived or inherited, both pathogenic and unaffected paternal duplications of 15q have been identified. We performed a phenotype/genotype analysis of individuals with interstitial 15q duplications to broaden our understanding of the 15q syndrome and investigate the contribution of 15q duplication to increased autism risk. All subjects were recruited solely on the basis of interstitial duplication 15q11.2-q13 status. Comparative array genome hybridization was used to determine the duplication size and boundaries while the methylation status of the maternally methylated small nuclear ribonucleoprotein polypeptide N gene was used to determine the parent of origin of the duplication. We determined the duplication size and parental origin for 14 int dup(15) subjects: 10 maternal and 4 paternal cases. The majority of int dup(15) cases recruited were maternal in origin, most likely due to our finding that maternal duplication was coincident with autism spectrum disorder. The size of the duplication did not correlate with the severity of the phenotype as established by Autism Diagnostic Observation Scale calibrated severity score. We identified phenotypes not comprehensively described before in this cohort including mild facial dysmorphism, sleep problems and an unusual electroencephalogram variant. Our results are consistent with the hypothesis that the maternally expressed ubiquitin protein ligase E3A gene is primarily responsible for the autism phenotype in int dup(15) since all maternal cases tested presented on the autism spectrum. (C) 2013 International Society for Autism Research, Wiley Periodicals, Inc.
C1 [Urraca, Nora; Reiter, Lawrence T.] Univ Tennessee, Ctr Hlth Sci, Dept Neurol, Memphis, TN 38163 USA.
[Brewer, Victoria; Pivnick, Eniko K.; McVicar, Kathryn; Reiter, Lawrence T.] Univ Tennessee, Ctr Hlth Sci, Dept Pediat, Memphis, TN 38163 USA.
[Cleary, Julie] Univ Memphis, Dept Speech & Language Pathol, Memphis, TN 38152 USA.
[Thibert, Ronald L.] Mass Gen Hosp, Dept Neurol, Boston, MA USA.
[Schanen, N. Carolyn] Nemours Biomed Res, Human Genet Res Lab, Wilmington, DE USA.
[Esmer, Carmen] Hosp Cent Dr Ignacio Morones Prieto, Dept Genet, San Luis Potosi, Mexico.
[Lamport, Dustin] Univ S Alabama, Dept Psychol, Mobile, AL 36688 USA.
[Pivnick, Eniko K.] Univ Tennessee, Ctr Hlth Sci, Dept Ophthalmol, Memphis, TN 38163 USA.
RP Reiter, LT (reprint author), Univ Tennessee, Ctr Hlth Sci, Dept Neurol, 855 Monroe Ave,Link 415, Memphis, TN 38163 USA.
EM lreiter@uthsc.edu
OI Reiter, Lawrence/0000-0002-4100-2630
FU Herbert and Mary Shainberg Neuroscience Fund; Le Bonheur Children's
Foundation
FX This work was funded by a grant from the Herbert and Mary Shainberg
Neuroscience Fund to L.T.R. and additional support from the Le Bonheur
Children's Foundation to N.U. The authors would like to thank Edwin Cook
for his insightful critical review of the manuscript as well as the
Dup15q Alliance and all of the families who participated in this study.
NR 57
TC 40
Z9 42
U1 0
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-3792
J9 AUTISM RES
JI Autism Res.
PD AUG
PY 2013
VL 6
IS 4
BP 268
EP 279
DI 10.1002/aur.1284
PG 12
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 200ZY
UT WOS:000323111700005
PM 23495136
ER
PT J
AU Pompili, M
Gonda, X
Serafini, G
Innamorati, M
Sher, L
Amore, M
Rihmer, Z
Girardi, P
AF Pompili, Maurizio
Gonda, Xenia
Serafini, Gianluca
Innamorati, Marco
Sher, Leo
Amore, Mario
Rihmer, Zoltan
Girardi, Paolo
TI Epidemiology of suicide in bipolar disorders: a systematic review of the
literature
SO BIPOLAR DISORDERS
LA English
DT Review
DE adults; bipolar disorder; completed suicides; risk factors; suicide
rates
ID MAJOR DEPRESSION; RISK-FACTORS; FOLLOW-UP; COMPLETED SUICIDE; ANXIETY
DISORDERS; MIXED-STATE; STEP-BD; LITHIUM; BEHAVIOR; PREVALENCE
AB Objective: Suicidal behavior is a major public health problem worldwide, and its prediction and prevention represent a challenge for everyone, including clinicians. The aim of the present paper is to provide a systematic review of the existing literature on the epidemiology of completed suicides in adult patients with bipolar disorder (BD).
Methods: We performed a Pubmed/Medline, Scopus, PsycLit, PsycInfo, and Cochrane database search to identify all relevant papers published between 1980 and 2011. A total of 34 articles meeting our inclusion criteria were included in the present review.
Results: Several prospective follow-up contributions, many retrospective analyses, and a few psychological autopsy studies and review articles investigated the epidemiology of completed suicides in patients with BD. The main finding of the present review was that the risk for suicide among BD patients was up to 20-30 times greater than that for the general population.
Conclusion: Special attention should be given to the characteristics of suicides in patients with BD. Better insight and understanding of suicide and suicidal risk in this very disabling illness should ultimately help clinicians to adequately detect, and thus prevent, suicidal acts in patients with BD.
C1 [Pompili, Maurizio; Serafini, Gianluca; Innamorati, Marco; Girardi, Paolo] Univ Roma La Sapienza, St Andrea Hosp, Dept Neurosci Mental Hlth & Sensory Organs, Suicide Prevent Ctr, I-00189 Rome, Italy.
[Gonda, Xenia; Rihmer, Zoltan] Semmelweis Univ, Dept Clin & Theoret Mental Hlth, Kutvolgyi Clin Ctr, H-1085 Budapest, Hungary.
[Sher, Leo] Mt Sinai Sch Med, New York, NY USA.
[Sher, Leo] James J Peters Vet Adm Med Ctr, New York, NY USA.
[Amore, Mario] Univ Genoa, Sect Psychiat, Dept Neurosci Rehabil Ophthalmol Genet Maternal &, Genoa, Italy.
[Girardi, Paolo] Villa Rosa Med Res Ctr, Viterbo, Italy.
RP Pompili, M (reprint author), Univ Roma La Sapienza, St Andrea Hosp, Dept Psychiat, 1035-1039 Via Grottarossa, I-00189 Rome, Italy.
EM maurizio.pompili@uniroma1.it
OI Innamorati, Marco/0000-0003-1389-2290; Pompili,
Maurizio/0000-0003-1886-4977
NR 73
TC 56
Z9 57
U1 11
U2 35
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD AUG
PY 2013
VL 15
IS 5
SI SI
BP 457
EP 490
DI 10.1111/bdi.12087
PG 34
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 196KV
UT WOS:000322774700002
PM 23755739
ER
PT J
AU Yerevanian, BI
Choi, YM
AF Yerevanian, Boghos I.
Choi, Young Mee
TI Impact of psychotropic drugs on suicide and suicidal behaviors
SO BIPOLAR DISORDERS
LA English
DT Review
DE anticonvulsants; antidepressants; antipsychotics; bipolar disorder;
lithium; mood disorder; psychotropic drugs; sedatives and hypnotics;
suicide
ID BIPOLAR-I DISORDER; PLACEBO-CONTROLLED TRIAL; LITHIUM MAINTENANCE
TREATMENT; TREATMENT ENHANCEMENT PROGRAM; TERM ANTIDEPRESSANT TREATMENT;
MAJOR AFFECTIVE-DISORDERS; CONTROLLED 18-MONTH TRIAL; STEP-BD;
DOUBLE-BLIND; ANTIEPILEPTIC DRUGS
AB Objective: To examine the impact of psychotropic drugs on suicide and suicidal behaviors in bipolar disorders.
Methods: A Medline search of articles published from January 1960 to January 2013 was performed using relevant keywords to identify studies examining the relationship of psychotropic drugs to suicidal behaviors. The publications were further reviewed for relevant references and information. Additionally, the US Food and Drug Administration Center for Drug Evaluation Research website was searched.
Results: The available studies used differing methodologies, making interpretation of the findings difficult. Studies suggest that antidepressants may increase suicidal risk in bipolar disorder, this possibly being related to the induction of broadly defined mixed states. There is no evidence that antiepileptic drugs as a class increase suicidal risk in patients with bipolar disorder. Only lithium provides convincing data that it reduces the risk of suicide over the long term. There is little known regarding the effects of antipsychotics, as well as anti-anxiety and hypnotic drugs, on suicidal behavior.
Conclusions: The available evidence for the impact of psychotropics on suicidal risk in patients with bipolar disorder is largely methodologically flawed and, except for a few instances, clinically not useful at this point. Adequately powered, prospective randomized controlled studies are needed to assess the impact of each class of psychotropic and each psychotropic as well as common combination therapies. Until such studies have been carried out, clinicians are urged to exercise caution in using these drugs and rely on the traditional means of carefully assessing and monitoring patients with bipolar disorder who are at high risk for suicide.
C1 [Yerevanian, Boghos I.; Choi, Young Mee] Greater Los Angeles VA Healthcare Syst, Dept Psychiat, Sepulveda Ambulatory Care Ctr, North Hills, CA 91343 USA.
[Yerevanian, Boghos I.; Choi, Young Mee] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
RP Yerevanian, BI (reprint author), Greater Los Angeles VA Healthcare Syst, Dept Psychiat, Sepulveda Ambulatory Care Ctr, 16111 Plummer St Bldg 10,MC 116A3, North Hills, CA 91343 USA.
EM byerevan@ucla.edu
NR 137
TC 18
Z9 20
U1 1
U2 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1398-5647
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD AUG
PY 2013
VL 15
IS 5
SI SI
BP 594
EP 621
DI 10.1111/bdi.12098
PG 28
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 196KV
UT WOS:000322774700011
PM 23869907
ER
PT J
AU Loren, AW
Brazauskas, R
Chow, EJ
Gilleece, M
Halter, J
Jacobsohn, DA
Joshi, S
Pidala, J
Quinn, GP
Wang, Z
Apperley, JF
Burns, LJ
Hale, GA
Hayes-Lattin, BM
Kamble, R
Lazarus, H
McCarthy, PL
Reddy, V
Warwick, AB
Bolwell, BJ
Duncan, C
Socie, G
Sorror, ML
Wingard, JR
Majhail, NS
AF Loren, A. W.
Brazauskas, R.
Chow, E. J.
Gilleece, M.
Halter, J.
Jacobsohn, D. A.
Joshi, S.
Pidala, J.
Quinn, G. P.
Wang, Z.
Apperley, J. F.
Burns, L. J.
Hale, G. A.
Hayes-Lattin, B. M.
Kamble, R.
Lazarus, H.
McCarthy, P. L.
Reddy, V.
Warwick, A. B.
Bolwell, B. J.
Duncan, C.
Socie, G.
Sorror, M. L.
Wingard, J. R.
Majhail, N. S.
TI Physician perceptions and practice patterns regarding fertility
preservation in hematopoietic cell transplant recipients
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE hematopoietic cell transplantation; autologous; allogeneic; fertility
preservation; infertility; pregnancy
ID BONE-MARROW-TRANSPLANTATION; PREGNANCY OUTCOMES; CANCER-PATIENTS;
RESPONSE RATES; ONCOLOGISTS; INFERTILITY; CHILDHOOD; SURVIVORS; IMPACT;
RISK
AB Physician practice variation may be a barrier to informing hematopoietic cell transplant (HCT) recipients about fertility preservation (FP) options. We surveyed HCT physicians in the United States to evaluate FP knowledge, practices, perceptions and barriers. Of the 1035 physicians invited, 185 completed a 29-item web-survey. Most respondents demonstrated knowledge of FP issues and discussed and felt comfortable discussing FP. However, only 55% referred patients to an infertility specialist. Most did not provide educational materials to patients and only 35% felt that available materials were relevant for HCT. Notable barriers to discussing FP included perception that patients were too ill to delay transplant (63%), patients were already infertile from prior therapy (92%) and time constraints (41%). Pediatric HCT physicians and physicians with access to an infertility specialist were more likely to discuss FP and to discuss FP even when prognosis was poor. On analyses that considered physician demographics, knowledge and perceptions as predictors of referral for FP, access to an infertility specialist and belief that patients were interested in FP were observed to be significant. We highlight variation in HCT physician perceptions and practices regarding FP. Physicians are generally interested in discussing fertility issues with their patients but lack educational materials.
C1 [Loren, A. W.] Univ Penn, Med Ctr, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Brazauskas, R.; Wang, Z.] Ctr Int Blood & Marrow Transplant Res, Milwaukee, WI USA.
[Chow, E. J.; Sorror, M. L.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Gilleece, M.] St James Univ Hosp, Leeds LS9 7TF, W Yorkshire, England.
[Halter, J.] Univ Basel Hosp, CH-4031 Basel, Switzerland.
[Jacobsohn, D. A.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Joshi, S.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Quinn, G. P.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Apperley, J. F.] Univ London Imperial Coll Sci Technol & Med, London, England.
[Burns, L. J.] Univ Minnesota, Med Ctr, Minneapolis, MN 55455 USA.
[Hale, G. A.] Childrens Hosp, St Petersburg, FL USA.
[Hayes-Lattin, B. M.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Kamble, R.] Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
[Lazarus, H.] Univ Hosp Cleveland, Case Med Ctr, Cleveland, OH 44106 USA.
[McCarthy, P. L.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Reddy, V.] Univ Cent Florida, Orlando, FL 32816 USA.
[Warwick, A. B.] Uniformed Serv Univ Hlth Sci, Bethesda, MD USA.
[Bolwell, B. J.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Duncan, C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Socie, G.] Hop St Louis, Paris, France.
[Wingard, J. R.] Shands HealthCare & Univ Florida, Gainesville, FL USA.
[Majhail, N. S.] Natl Marrow Donor Program, Minneapolis, MN USA.
RP Majhail, NS (reprint author), Natl Marrow Donor Program, Ctr Int Blood & Marrow Transplant Res, 3001 Broadway St NE,Suite 100, Minneapolis, MN 55413 USA.
EM nmajhail@nmdp.org
FU Public Health Service from the National Cancer Institute, the National
Heart, Lung and Blood Institute [U24-CA76518]; National Institute of
Allergy and Infectious Diseases; NHLBI [5U01HL069294]; NCI; Health
Resources and Services Administration (HRSA/DHHS) [HHSH234200637015C];
Office of Naval Research [N00014-06-1-0704, N00014-08-1-0058]; Allos,
Inc.; Amgen, Inc.; Angioblast; Ariad; Be the Match Foundation; Blue
Cross and Blue Shield Association; Buchanan Family Foundation;
CaridianBCT; Celgene Corporation; CellGenix; GmbH; Children's Leukemia
Research Association; Fresenius-Biotech North America, Inc.; Gamida Cell
Teva Joint Venture Ltd.; Genentech, Inc.; Genzyme Corporation;
GlaxoSmithKline; HistoGenetics, Inc.; Kiadis Pharma; Leukemia and
Lymphoma Society; Medical College of Wisconsin; Merck Co, Inc.;
Millennium: The Takeda Oncology Co.; Milliman USA, Inc.; Miltenyi
Biotec, Inc.; National Marrow Donor Program; Optum Healthcare Solutions,
Inc.; Osiris Therapeutics, Inc.; Otsuka America Pharmaceutical, Inc.;
RemedyMD; Sanofi; Seattle Genetics; Sigma-Tau Pharmaceuticals;
Soligenix, Inc.; StemCyte, A Global Cord Blood Therapeutics Co; Stemsoft
Software, Inc.; Swedish Orphan Biovitrum; Tarix Pharmaceuticals; Teva
Neuroscience, Inc.; THERAKOS, Inc.; Wellpoint, Inc.
FX The Center for International Blood and Marrow Transplant Research is
supported by Public Health Service Grant/Cooperative Agreement
U24-CA76518 from the National Cancer Institute, the National Heart, Lung
and Blood Institute and the National Institute of Allergy and Infectious
Diseases; a Grant/Cooperative Agreement 5U01HL069294 from NHLBI and NCI;
a contract HHSH234200637015C with Health Resources and Services
Administration (HRSA/DHHS); two Grants N00014-06-1-0704 and
N00014-08-1-0058 from the Office of Naval Research; and grants from
Allos, Inc.; Amgen, Inc.; Angioblast; Anonymous donation to the Medical
College of Wisconsin; Ariad; Be the Match Foundation; Blue Cross and
Blue Shield Association; Buchanan Family Foundation; CaridianBCT;
Celgene Corporation; CellGenix, GmbH; Children's Leukemia Research
Association; Fresenius-Biotech North America, Inc.; Gamida Cell Teva
Joint Venture Ltd.; Genentech, Inc.; Genzyme Corporation;
GlaxoSmithKline; HistoGenetics, Inc.; Kiadis Pharma; The Leukemia and
Lymphoma Society; The Medical College of Wisconsin; Merck & Co, Inc.;
Millennium: The Takeda Oncology Co.; Milliman USA, Inc.; Miltenyi
Biotec, Inc.; National Marrow Donor Program; Optum Healthcare Solutions,
Inc.; Osiris Therapeutics, Inc.; Otsuka America Pharmaceutical, Inc.;
RemedyMD; Sanofi; Seattle Genetics; Sigma-Tau Pharmaceuticals;
Soligenix, Inc.; StemCyte, A Global Cord Blood Therapeutics Co; Stemsoft
Software, Inc.; Swedish Orphan Biovitrum; Tarix Pharmaceuticals; Teva
Neuroscience, Inc.; THERAKOS, Inc.; and Wellpoint, Inc. The views
expressed in this article do not reflect the official policy or position
of the National Institute of Health, the Department of the Navy, the
Department of Defense, or any other agency of the US Government.
NR 19
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U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD AUG
PY 2013
VL 48
IS 8
BP 1091
EP 1097
DI 10.1038/bmt.2013.13
PG 7
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 197AR
UT WOS:000322819900013
PM 23419436
ER
PT J
AU Treister, N
Chai, X
Kurland, B
Pavletic, S
Weisdorf, D
Pidala, J
Palmer, J
Martin, P
Inamoto, Y
Arora, M
Flowers, M
Jacobsohn, D
Jagasia, M
Arai, S
Lee, SJ
Cutler, C
AF Treister, N.
Chai, X.
Kurland, B.
Pavletic, S.
Weisdorf, D.
Pidala, J.
Palmer, J.
Martin, P.
Inamoto, Y.
Arora, M.
Flowers, M.
Jacobsohn, D.
Jagasia, M.
Arai, S.
Lee, S. J.
Cutler, C.
TI Measurement of oral chronic GVHD: results from the Chronic GVHD
Consortium
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
DE oral cavity; SCT; GVHD; quality of life
ID VERSUS-HOST-DISEASE; CONSENSUS DEVELOPMENT PROJECT; WORKING
GROUP-REPORT; CLINICAL-TRIALS; THERAPEUTIC RESPONSE; CRITERIA;
RELIABILITY; DESIGN
AB Oral chronic GVHD (cGVHD) is a serious complication of alloSCT. Scales and instruments to measure oral cGVHD activity and severity have not been prospectively validated. The objective of this study was to describe the characteristics of oral cGVHD and determine the measures most sensitive to change. Patients enrolled in the cGVHD Consortium with oral involvement were included. Clinicians scored oral changes according to the National Institutes of Health (NIH) criteria, and patients completed symptom and quality-of-life measures at each visit. Both rated change on an eight-point scale. Of the 458 participants, 72% (n = 331) had objective oral involvement at enrollment. Lichenoid change was the most common feature (n = 293; 89%). At visits where oral change could be assessed, 50% of clinicians and 56% of patients reported improvement, with worsening reported in 4-5% for both the groups (weighted kappa = 0.41). Multivariable regression modeling suggested that the measurement changes most predictive of perceived change by clinicians and patients were erythema and lichenoid, NIH severity and symptom scores. Oral cGVHD is common and associated with a range of signs and symptoms. Measurement of erythema and lichenoid changes and symptoms may adequately capture the activity of oral cGVHD in clinical trials but require prospective validation.
C1 [Treister, N.] Brigham & Womens Hosp, Div Oral Med & Dent, Boston, MA 02115 USA.
[Chai, X.; Kurland, B.; Martin, P.; Inamoto, Y.; Flowers, M.; Lee, S. J.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Pavletic, S.] NCI, Ctr Canc Res, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Weisdorf, D.; Arora, M.] Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA.
[Pidala, J.] H Lee Moffitt Canc Ctr & Res Inst, Dept Blood & Marrow Transplantat, Tampa, FL USA.
[Palmer, J.] Med Coll Wisconsin, Dept Hematol & Oncol, Milwaukee, WI 53226 USA.
[Jacobsohn, D.] Childrens Natl Med Ctr, Ctr Canc & Blood Disorders, Div Blood & Marrow Transplantat, Washington, DC 20010 USA.
[Jagasia, M.] Vanderbilt Ingram Canc Ctr, Div Hematol Stem Cell Transplantat, Nashville, TN USA.
[Arai, S.] Stanford Univ, Ctr Med, Div Blood & Marrow Transplantat, Stanford, CA 94305 USA.
[Cutler, C.] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
RP Treister, N (reprint author), Brigham & Womens Hosp, Div Oral Med & Dent, 1620 Tremont St,3rd Floor, Boston, MA 02115 USA.
EM ntreister@partners.org
OI Kurland, Brenda/0000-0002-5669-0595
FU [CA118953]; [CA163438]
FX This work was supported by Grants CA118953 and CA163438.
NR 27
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U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD AUG
PY 2013
VL 48
IS 8
BP 1123
EP 1128
DI 10.1038/bmt.2012.285
PG 6
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 197AR
UT WOS:000322819900018
PM 23353804
ER
PT J
AU Bullock-Rest, N
Cerny, A
Sweeney, C
Palumbo, C
Kurowski, K
Blumstein, SE
AF Bullock-Rest, Natasha
Cerny, Alissa
Sweeney, Carol
Palumbo, Carole
Kurowski, Kathleen
Blumstein, Sheila E.
TI Neural systems underlying the influence of sound shape properties of the
lexicon on spoken word production: Do fMRI findings predict effects of
lesions in aphasia?
SO BRAIN AND LANGUAGE
LA English
DT Article
DE Aphasia; Spoken word production; Lesions; Functional neuroimaging;
Voice-onset time
ID VOICE ONSET TIME; PHONOLOGICAL NEIGHBORHOOD DENSITY; EVENT-RELATED FMRI;
SPEECH PRODUCTION; PHONOTACTIC PROBABILITY; WERNICKES APHASIA;
PREFRONTAL CORTEX; ELDERLY ADULTS; COMPETITION; RETRIEVAL
AB Previous behavioral work has shown that the phonetic realization of words in spoken word production is influenced by sound shape properties of the lexicon. A recent fMRI study (Peramunage, Blumstein, Myers, Goldrick, & Baese-Berk, 2011) showed that this influence of lexical structure on phonetic implementation recruited a network of areas that included the supramarginal gyrus (SMG) extending into the posterior superior temporal gyrus (pSTG) and the inferior frontal gyrus (IFG). The current study examined whether lesions in these areas result in a concomitant functional deficit. Ten individuals with aphasia and 8 normal controls read words aloud in which half had a voiced stop consonant minimal pair (e.g. tame; dame), and the other half did not (e.g. tooth; *dooth). Voice onset time (VOT) analysis of the initial voiceless stop consonant revealed that aphasic participants with lesions including the IFG and/or the SMG behaved as did normals, showing VOT lengthening effects for minimal pair words compared to non-minimal pair words. The failure to show a functional deficit in the production of VOT as a function of the lexical properties of a word with damage in the IFG or SMG suggests that fMRI findings do not always predict effects of lesions on behavioral deficits in aphasia. Nonetheless, the pattern of production errors made by the aphasic participants did reflect properties of the lexicon, supporting the view that the SMG and IFG are part of a lexical network involved in spoken word production. (c) 2013 Elsevier Inc. All rights reserved.
C1 [Bullock-Rest, Natasha; Cerny, Alissa; Sweeney, Carol; Kurowski, Kathleen; Blumstein, Sheila E.] Brown Univ, Dept Cognit Linguist & Psychol Sci, Providence, RI 02912 USA.
[Palumbo, Carole; Blumstein, Sheila E.] Boston Univ, Sch Med, Harold Goodglass Aphasia Res Ctr, Boston, MA 02215 USA.
[Bullock-Rest, Natasha; Sweeney, Carol; Palumbo, Carole; Kurowski, Kathleen; Blumstein, Sheila E.] VA Boston Healthcare Syst, Res Serv, Boston, MA USA.
[Blumstein, Sheila E.] Brown Univ, Brown Inst Brain Sci, Providence, RI 02912 USA.
RP Blumstein, SE (reprint author), Brown Univ, Dept Cognit Linguist & Psychol Sci, Providence, RI 02912 USA.
EM Sheila_Blumstein@Brown.EDU
FU NIH [DC00314, DC05207]
FX Portions of this research were presented at the 49th Annual Meeting of
the Academy of Aphasia, Montreal, Quebec, Canada, October 16-18, 2011.
This research was supported in part by NIH grants DC00314 to Brown
University and DC05207 to the Boston University School of Medicine. This
material is the result of work supported with resources and the use of
facilities at the Department of Veterans Affairs Medical Centers in
Boston, MA and Providence, RI. The content is solely the responsibility
of the authors and does not necessarily represent the official views or
policy of the Department of Veterans Affairs, the National Institute on
Deafness and Other Communication Disorders, or the National Institutes
of Health. We thank John Mertus for his technical contributions to this
project.
NR 65
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Z9 1
U1 2
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0093-934X
J9 BRAIN LANG
JI Brain Lang.
PD AUG
PY 2013
VL 126
IS 2
BP 159
EP 168
DI 10.1016/j.bandl.2013.05.002
PG 10
WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences;
Psychology, Experimental
SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences &
Neurology; Psychology
GA 197KL
UT WOS:000322850000006
PM 23743183
ER
PT J
AU Jevtovic-Todorovic, V
Absalom, AR
Blomgren, K
Brambrink, A
Crosby, G
Culley, DJ
Fiskum, G
Giffard, RG
Herold, KF
Loepke, AW
Ma, D
Orser, BA
Planel, E
Slikker, W
Soriano, SG
Stratmann, G
Vutskits, L
Xie, Z
Hemmings, HC
AF Jevtovic-Todorovic, V.
Absalom, A. R.
Blomgren, K.
Brambrink, A.
Crosby, G.
Culley, D. J.
Fiskum, G.
Giffard, R. G.
Herold, K. F.
Loepke, A. W.
Ma, D.
Orser, B. A.
Planel, E.
Slikker, W., Jr.
Soriano, S. G.
Stratmann, G.
Vutskits, L.
Xie, Z.
Hemmings, H. C., Jr.
TI Anaesthetic neurotoxicity and neuroplasticity: an expert group report
and statement based on the BJA Salzburg Seminar
SO BRITISH JOURNAL OF ANAESTHESIA
LA English
DT Article
DE anaesthesia; general; anaesthetics; cognitive disorder; neurotoxicity
syndromes; postoperative complications
ID POSTOPERATIVE COGNITIVE DYSFUNCTION; DEVELOPING RAT-BRAIN;
KETAMINE-INDUCED NEUROAPOPTOSIS; MEDIAL PREFRONTAL CORTEX; NITROUS-OXIDE
ANESTHESIA; ARTERY-BYPASS-SURGERY; D-ASPARTATE RECEPTOR; NEURONAL
CELL-DEATH; NEURAL STEM-CELLS; ALZHEIMERS-DISEASE
AB Although previously considered entirely reversible, general anaesthesia is now being viewed as a potentially significant risk to cognitive performance at both extremes of age. A large body of preclinical as well as some retrospective clinical evidence suggest that exposure to general anaesthesia could be detrimental to cognitive development in young subjects, and might also contribute to accelerated cognitive decline in the elderly. A group of experts in anaesthetic neuropharmacology and neurotoxicity convened in Salzburg, Austria for the BJA Salzburg Seminar on Anaesthetic Neurotoxicity and Neuroplasticity. This focused workshop was sponsored by the British Journal of Anaesthesia to review and critically assess currently available evidence from animal and human studies, and to consider the direction of future research. It was concluded that mounting evidence from preclinical studies reveals general anaesthetics to be powerful modulators of neuronal development and function, which could contribute to detrimental behavioural outcomes. However, definitive clinical data remain elusive. Since general anaesthesia often cannot be avoided regardless of patient age, it is important to understand the complex mechanisms and effects involved in anaesthesia-induced neurotoxicity, and to develop strategies for avoiding or limiting potential brain injury through evidence-based approaches.
C1 [Jevtovic-Todorovic, V.] Univ Virginia, Dept Anesthesiol, Charlottesville, VA 22903 USA.
[Absalom, A. R.] Univ Groningen, Univ Med Ctr Groningen, Dept Anesthesiol, Groningen, Netherlands.
[Blomgren, K.] Karolinska Inst, Dept Womens & Childrens Hlth, Stockholm, Sweden.
[Brambrink, A.] Oregon Hlth & Sci Univ, Dept Anesthesiol & Perioperat Med, Portland, OR 97201 USA.
[Crosby, G.; Culley, D. J.] Brigham & Womens Hosp, Dept Anesthesia, Boston, MA 02115 USA.
[Crosby, G.; Culley, D. J.; Soriano, S. G.] Harvard Univ, Sch Med, Boston, MA USA.
[Fiskum, G.] Univ Maryland, Sch Med, Dept Anesthesiol, Baltimore, MD 21201 USA.
[Giffard, R. G.] Stanford Univ, Sch Med, Dept Anesthesia, Stanford, CA 94305 USA.
[Herold, K. F.; Hemmings, H. C., Jr.] Weill Cornell Med Coll, Dept Anesthesiol, New York, NY USA.
[Loepke, A. W.] Cincinnati Childrens Hosp Med Ctr, Dept Anesthesia, Cincinnati, OH USA.
[Loepke, A. W.] Cincinnati Childrens Hosp Med Ctr, Dept Pediat, Cincinnati, OH 45229 USA.
[Loepke, A. W.] Univ Cincinnati, Coll Med, Cincinnati, OH USA.
[Ma, D.] Univ London Imperial Coll Sci Technol & Med, Sect Anaesthet Pain Med & Intens Care, Dept Surg & Canc, London, England.
[Orser, B. A.] Univ Toronto, Sunnybrook Hlth Sci Ctr, Dept Anesthesia, Toronto, ON, Canada.
[Planel, E.] Univ Laval, Dept Psychiat & Neurosci, Quebec City, PQ, Canada.
[Slikker, W., Jr.] US FDA, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
[Soriano, S. G.] Boston Childrens Hosp, Dept Anesthesiol Perioperat & Pain Med, Boston, MA USA.
[Stratmann, G.] UCSF, Dept Anesthesia & Crit Care, San Francisco, CA USA.
[Stratmann, G.] Grp Anesthesia Serv, Los Gatos, CA USA.
[Vutskits, L.] Univ Hosp Geneva, Dept Anesthesiol Pharmacol & Intens Care, Geneva, Switzerland.
[Xie, Z.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Charlestown, MA USA.
[Xie, Z.] Harvard Univ, Sch Med, Charlestown, MA USA.
[Hemmings, H. C., Jr.] Weill Cornell Med Coll, Dept Pharmacol, New York, NY USA.
RP Jevtovic-Todorovic, V (reprint author), Univ Virginia, Dept Anesthesiol, Charlottesville, VA 22903 USA.
EM vj3w@hscmail.mcc.virginia.edu; hchemmi@med.cornell.edu
OI Absalom, Anthony/0000-0001-7563-9157; Blomgren, Klas/0000-0002-0476-7271
FU National Institute of Academic Anaesthesia; Dutch Association of
Anesthesiologists; Swedish Research Council; Swedish Childhood Cancer
Foundation; Swedish Cancer Foundation; StratNeuro Network at the
Karolinska Institute; Stockholm and Gothenburg Freemasons' Pediatric
Research; National Institutes of Health (Bethesda, MD, USA) [K08
GM077057, R01 GM088817, 2P01 1HD16596-26, GM49831, NS053898, GM58055,
NS56315]; US Air Force [FA8650-11-2-6D04]; US Army [W81XWH-13-1-0016,
W81XWH-09-2-0187]
FX A.R.A., National Institute of Academic Anaesthesia and Dutch Association
of Anesthesiologists; K.B., Swedish Research Council, the Swedish
Childhood Cancer Foundation, the Swedish Cancer Foundation, governmental
grants from Agreement Concerning Research and Education of Doctors
(ALF), the StratNeuro Network at the Karolinska Institute, the Stockholm
and Gothenburg Freemasons' Pediatric Research grants; D.C., William F.
Milton Fund, National Institutes of Health (Bethesda, MD, USA) K08
GM077057; G.C., National Institutes of Health R01 GM088817; G. F.,
National Institutes of Health 2P01 1HD16596-26, US Air Force
FA8650-11-2-6D04, US Army W81XWH-13-1-0016 and W81XWH-09-2-0187; R.G.G.,
National Institutes of Health GM49831 and NS053898; H.C.H., National
Institutes of Health GM58055 and NS56315; KFH HE4554/5-1 DFG (German
Research Foundation); V.J.-T., NIH/NICHD HD 44517 and American Recovery
and Reinvestment Act supplement HD 44517S, John E. Fogarty Award
TW007423-128322, March of Dimes National Award and Harold Carron
endowment. V.J.-T. was an Established Investigator of the American Heart
Association; D.M., Medical Research Council, Alzheimer's Society-Bupa
Foundation, BJA/RCoA, AAGBI, Westminster Medical School Research Trust,
Action Medical Research and SPARKS, UK and European Society of
Anesthesiology, Brussels; B.A.O., Canada Research Chair in Anesthesia,
and Canadian Institutes of Health Research; E. P., Canadian Institutes
for Health Research (MOP-106423, PCN-102993), Natural Sciences and
Engineering Research Council (354722), Canada Foundation for Innovation
(23905), and Research Scholar Career Awards (16205, 20048) from the
Fonds de la Recherche en Sante du Quebec; S.G.S., Boston Children's
Hospital Endowed Chair in Pediatric Neuroanesthesia; G.S., John
Severinghaus Research Award Department of Anesthesia and Perioperative
Care, UCSF; L.V., Swiss National Science Foundation; Z.X., National
Institutes of Health R21AG038994, R01 GM088801, and R01 AG041274,
Investigator-initiated research grant from Alzheimer's Association,
Chicago, IL, USA, and Cure Alzheimer's Fund, Wellesley, MA, USA.
NR 83
TC 74
Z9 80
U1 5
U2 26
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0007-0912
J9 BRIT J ANAESTH
JI Br. J. Anaesth.
PD AUG
PY 2013
VL 111
IS 2
BP 143
EP 151
DI 10.1093/bja/aet177
PG 9
WC Anesthesiology
SC Anesthesiology
GA 190KF
UT WOS:000322337900005
PM 23722106
ER
PT J
AU Evans, KC
Keil, B
McLaren, DG
Bianciardi, M
Song, TY
Triantafyllou, C
AF Evans, K. C.
Keil, B.
McLaren, D. G.
Bianciardi, M.
Song, T. -Y.
Triantafyllou, C.
TI Hypercapnia evokes amygdalo-thalamic and brainstem activity: a 7 T
functional magnetic resonance imaging study in healthy humans
SO BRITISH JOURNAL OF ANAESTHESIA
LA English
DT Meeting Abstract
CT Spring Meeting of the Anaesthetic-Research-Society
CY APR 11-12, 2013
CL Merton Coll, Oxford, ENGLAND
SP Anaesthet Res Soc
HO Merton Coll
C1 [Evans, K. C.; Song, T. -Y.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Keil, B.; Bianciardi, M.; Triantafyllou, C.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[McLaren, D. G.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Evans, K. C.; Keil, B.; McLaren, D. G.; Bianciardi, M.; Triantafyllou, C.] Harvard Univ, Sch Med, Boston, MA USA.
RI Keil, Boris/P-1411-2014
NR 5
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0007-0912
J9 BRIT J ANAESTH
JI Br. J. Anaesth.
PD AUG
PY 2013
VL 111
IS 2
BP 312P
EP 312P
PG 1
WC Anesthesiology
SC Anesthesiology
GA 190KF
UT WOS:000322337900036
ER
PT J
AU O'Donnell, E
Raje, NS
AF O'Donnell, Elizabeth
Raje, Noopur S.
TI Targeting BRAF in Multiple Myeloma
SO CANCER DISCOVERY
LA English
DT Editorial Material
ID PATHOGENESIS; VEMURAFENIB; INHIBITION; MELANOMA; CANCER
AB In multiple myeloma, it is believed that multiple mutations in different pathways deregulate the intrinsic biology of the plasma cell, resulting in a genetically complex heterogeneous disease. Mutations in the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway have been identified and represent potential targets for therapy in this disease. BRAF, a serine/threonine kinase, has received considerable attention given the success of targeted therapy in malignant melanoma. Andrulis and colleagues report, for the first time, successful treatment of multiple myeloma with vemurafenib, a BRAF inhibitor, in a patient with a BRAF mutation. (C) 2013 AACR.
C1 [O'Donnell, Elizabeth; Raje, Noopur S.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
RP Raje, NS (reprint author), Massachusetts Gen Hosp, Ctr Multiple Myeloma, Ctr Canc, 55 Fruit St, Boston, MA 02114 USA.
EM nraje@partners.org
RI Waha, Andreas/J-2950-2014
NR 11
TC 7
Z9 7
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
J9 CANCER DISCOV
JI Cancer Discov.
PD AUG
PY 2013
VL 3
IS 8
BP 840
EP 842
DI 10.1158/2159-8290.CD-13-0297
PG 3
WC Oncology
SC Oncology
GA 198XQ
UT WOS:000322957600016
PM 23928771
ER
PT J
AU Liu, Y
Marks, K
Cowley, GS
Carretero, J
Liu, QS
Nieland, TJF
Xu, CX
Cohoon, TJ
Gao, P
Zhang, Y
Chen, Z
Altabef, AB
Tchaicha, JH
Wang, XX
Choe, S
Driggers, EM
Zhang, JM
Bailey, ST
Sharpless, NE
Hayes, DN
Patel, NM
Janne, PA
Bardeesy, N
Engelman, JA
Manning, BD
Shaw, RJ
Asara, JM
Scully, R
Kimmelman, A
Byers, LA
Gibbons, DL
Wistuba, II
Heymach, JV
Kwiatkowski, DJ
Kim, WY
Kung, AL
Gray, NS
Root, DE
Cantley, LC
Wong, KK
AF Liu, Yan
Marks, Kevin
Cowley, Glenn S.
Carretero, Julian
Liu, Qingsong
Nieland, Thomas J. F.
Xu, Chunxiao
Cohoon, Travis J.
Gao, Peng
Zhang, Yong
Chen, Zhao
Altabef, Abigail B.
Tchaicha, Jeremy H.
Wang, Xiaoxu
Choe, Sung
Driggers, Edward M.
Zhang, Jianming
Bailey, Sean T.
Sharpless, Norman E.
Hayes, D. Neil
Patel, Nirali M.
Janne, Pasi A.
Bardeesy, Nabeel
Engelman, Jeffrey A.
Manning, Brendan D.
Shaw, Reuben J.
Asara, John M.
Scully, Ralph
Kimmelman, Alec
Byers, Lauren A.
Gibbons, Don L.
Wistuba, Ignacio I.
Heymach, John V.
Kwiatkowski, David J.
Kim, William Y.
Kung, Andrew L.
Gray, Nathanael S.
Root, David E.
Cantley, Lewis C.
Wong, Kwok-Kin
TI Metabolic and Functional Genomic Studies Identify Deoxythymidylate
Kinase as a Target in LKB1-Mutant Lung Cancer
SO CANCER DISCOVERY
LA English
DT Article
ID DNA-DAMAGE; THYMIDYLATE KINASE; THYMINELESS DEATH; MASS-SPECTROMETRY;
CELL POLARITY; LKB1; PATHWAY; GROWTH; IDENTIFICATION; INACTIVATION
AB The LKB1/STK11 tumor suppressor encodes a serine/threonine kinase, which coordinates cell growth, polarity, motility, and metabolism. In non-small cell lung carcinoma, LKB1 is somatically inactivated in 25% to 30% of cases, often concurrently with activating KRAS mutations. Here, we used an integrative approach to define novel therapeutic targets in KRAS-driven LKB1-mutant lung cancers. High-throughput RNA interference screens in lung cancer cell lines from genetically engineered mouse models driven by activated KRAS with or without coincident Lkb1 deletion led to the identification of Dtymk, encoding deoxythymidylate kinase (DTYMK), which catalyzes dTTP biosynthesis, as synthetically lethal with Lkb1 deficiency in mouse and human lung cancer lines. Global metabolite profiling showed that Lkb1-null cells had a striking decrease in multiple nucleotide metabolites as compared with the Lkb1-wild-type cells. Thus, LKB1-mutant lung cancers have deficits in nucleotide metabolism that confer hypersensitivity to DTYMK inhibition, suggesting that DTYMK is a potential therapeutic target in this aggressive subset of tumors. (C) 2013 AACR.
C1 [Liu, Yan; Xu, Chunxiao; Cohoon, Travis J.; Gao, Peng; Zhang, Yong; Chen, Zhao; Altabef, Abigail B.; Tchaicha, Jeremy H.; Wang, Xiaoxu; Janne, Pasi A.; Bardeesy, Nabeel; Engelman, Jeffrey A.; Kimmelman, Alec; Kwiatkowski, David J.; Cantley, Lewis C.; Wong, Kwok-Kin] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Med, Boston, MA 02215 USA.
[Liu, Qingsong; Zhang, Jianming; Gray, Nathanael S.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02215 USA.
[Wang, Xiaoxu; Kimmelman, Alec] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Radiat Oncol, Boston, MA 02215 USA.
[Liu, Yan; Xu, Chunxiao; Cohoon, Travis J.; Gao, Peng; Zhang, Yong; Chen, Zhao; Altabef, Abigail B.; Tchaicha, Jeremy H.; Janne, Pasi A.; Kwiatkowski, David J.; Wong, Kwok-Kin] Harvard Univ, Sch Publ Hlth, Dept Med Oncol, Boston, MA 02115 USA.
[Liu, Yan; Xu, Chunxiao; Cohoon, Travis J.; Gao, Peng; Chen, Zhao; Altabef, Abigail B.; Tchaicha, Jeremy H.; Janne, Pasi A.; Kwiatkowski, David J.; Wong, Kwok-Kin] Harvard Univ, Sch Publ Hlth, Lowe Ctr Thorac Oncol, Boston, MA 02115 USA.
[Liu, Yan; Xu, Chunxiao; Cohoon, Travis J.; Gao, Peng; Chen, Zhao; Altabef, Abigail B.; Tchaicha, Jeremy H.; Wong, Kwok-Kin] Harvard Univ, Sch Publ Hlth, Ludwig Ctr, Dana Farber Harvard Canc Ctr, Boston, MA 02115 USA.
[Bardeesy, Nabeel; Engelman, Jeffrey A.] Harvard Univ, Sch Publ Hlth, Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02115 USA.
[Manning, Brendan D.] Harvard Univ, Sch Publ Hlth, Dept Genet & Complex Dis, Boston, MA 02115 USA.
[Marks, Kevin; Choe, Sung; Driggers, Edward M.] Agios Pharmaceut, Cambridge, MA USA.
[Cowley, Glenn S.; Nieland, Thomas J. F.; Root, David E.] Broad Inst MIT & Harvard, Cambridge, MA USA.
[Bailey, Sean T.; Sharpless, Norman E.; Hayes, D. Neil; Patel, Nirali M.; Kim, William Y.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Bailey, Sean T.; Sharpless, Norman E.; Hayes, D. Neil; Patel, Nirali M.; Kim, William Y.] Univ N Carolina, Dept Med & Genet, Chapel Hill, NC 27599 USA.
[Shaw, Reuben J.; Scully, Ralph] Salk Inst Biol Studies, Mol & Cell Biol Lab, La Jolla, CA 92037 USA.
[Byers, Lauren A.; Gibbons, Don L.; Wistuba, Ignacio I.; Heymach, John V.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Kung, Andrew L.] Columbia Univ, Dept Pediat, Med Ctr, New York, NY 10027 USA.
[Carretero, Julian] Univ Valencia, Dept Physiol, E-46100 Burjassot, Spain.
RP Wong, KK (reprint author), Dana Farber Canc Inst, Dana Bldg 810B,450 Brookline Ave,HIM243, Boston, MA 02115 USA.
EM kwong1@partners.org
RI Scully, Ralph/F-5008-2013; Cantley, Lewis/D-1800-2014; Carretero,
Julian/N-5214-2014
OI liu, qing song/0000-0002-7829-2547; Cantley, Lewis/0000-0002-1298-7653;
Kung, Andrew/0000-0002-9091-488X; wong, kwok kin/0000-0001-6323-235X;
Carretero, Julian/0000-0001-7269-8506
FU NIH [CA122794, CA140594, CA163896, CA166480, CA154303, Lung SPORE
P50CA090578, CA142794]; United against Lung Cancer Foundation; American
Lung Association; Susan Spooner Research Fund; Damon Runyon Cancer
Research Foundation
FX This work is supported by the NIH (CA122794, CA140594, CA163896,
CA166480, CA154303, and Lung SPORE P50CA090578), United against Lung
Cancer Foundation, American Lung Association, and Susan Spooner Research
Fund (to K.-K. Wong); and by NIH CA142794 as well as the Damon Runyon
Cancer Research Foundation (to W.Y. Kim).
NR 36
TC 28
Z9 28
U1 1
U2 16
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
J9 CANCER DISCOV
JI Cancer Discov.
PD AUG
PY 2013
VL 3
IS 8
BP 870
EP 879
DI 10.1158/2159-8290.CD-13-0015
PG 10
WC Oncology
SC Oncology
GA 198XQ
UT WOS:000322957600021
PM 23715154
ER
PT J
AU Hollstein, PE
Cichowski, K
AF Hollstein, Pablo E.
Cichowski, Karen
TI Identifying the Ubiquitin Ligase Complex that Regulates the NF1 Tumor
Suppressor and Ras
SO CANCER DISCOVERY
LA English
DT Article
ID NEUROFIBROMATOSIS TYPE-1 GENE; DOMAIN PROTEINS; CANCER-THERAPY; E3
LIGASE; INHIBITOR; MUTATIONS; SCF; PATHWAYS; NEUROBLASTOMA; DEGRADATION
AB The NF1 tumor suppressor protein neurofibromin is a negative regulator of Ras. Neurofibromin is dynamically regulated by the proteasome, and its degradation and reexpression are essential for maintaining appropriate levels of Ras-GTP. Like p53, NF1/neurofibromin can be inactivated in cancer by both mutations and excessive proteasomal destruction; however, little is known about the mechanisms that underlie this latter process. Here, we show that a Cullin 3 (Cul3)/kelch repeat and BTB domain-containing 7 complex controls both the regulated proteasomal degradation of neurofibromin and the pathogenic destabilization of neurofibromin in glioblastomas. Importantly, RNAi-mediated Cul3 ablation and a dominant-negative Cul3 directly stabilize neurofibromin, suppress Ras and extracellular signal-regulated kinase, and inhibit proliferation in an NF1-dependent manner. Moreover, in glioblastomas where neurofibromin is chronically destabilized, Cul3 inhibition restabilizes the protein and suppresses tumor development. Collectively, these studies show a previously unrecognized role for Cul3 in regulating Ras and provide a molecular framework that can be exploited to develop potential cancer therapies. (C) 2013 AACR.
C1 [Hollstein, Pablo E.; Cichowski, Karen] Brigham & Womens Hosp, Div Genet, Dept Med, Boston, MA 02115 USA.
[Hollstein, Pablo E.; Cichowski, Karen] Harvard Univ, Sch Med, Boston, MA USA.
[Cichowski, Karen] Dana Farber Harvard Canc Ctr, Ludwig Ctr, Boston, MA USA.
RP Cichowski, K (reprint author), Brigham & Womens Hosp, 77 Ave Louis Pasteur,NRB 0458C, Boston, MA 02115 USA.
EM kcichowski@rics.bwh.harvard.edu
FU Department of Defense [W81XWH-08-1-0136]; NCI [R01 CA111754]
FX This work was supported by the Department of Defense (W81XWH-08-1-0136)
and the NCI (R01 CA111754).
NR 50
TC 13
Z9 16
U1 0
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
J9 CANCER DISCOV
JI Cancer Discov.
PD AUG
PY 2013
VL 3
IS 8
BP 880
EP 893
DI 10.1158/2159-8290.CD-13-0146
PG 14
WC Oncology
SC Oncology
GA 198XQ
UT WOS:000322957600022
PM 23661552
ER
PT J
AU Huo, YY
Cai, H
Teplova, I
Bowman-Colin, C
Chen, GH
Price, S
Barnard, N
Ganesan, S
Karantza, V
White, E
Xia, B
AF Huo, Yanying
Cai, Hong
Teplova, Irina
Bowman-Colin, Christian
Chen, Guanghua
Price, Sandy
Barnard, Nicola
Ganesan, Shridar
Karantza, Vassiliki
White, Eileen
Xia, Bing
TI Autophagy Opposes p53-Mediated Tumor Barrier to Facilitate Tumorigenesis
in a Model of PALB2-Associated Hereditary Breast Cancer
SO CANCER DISCOVERY
LA English
DT Article
ID HOMOLOGOUS RECOMBINATION; SUSCEPTIBILITY GENE; FANCONI-ANEMIA;
SUPPRESSES TUMORIGENESIS; BRCA2 DEFICIENCY; TP53 MUTATIONS; PALB2; MICE;
P53; INACTIVATION
AB Hereditary breast cancers stem from germline mutations in susceptibility genes such as BRCA1, BRCA2, and PALB2, whose products function in the DNA damage response and redox regulation. Autophagy is an intracellular waste disposal and stress mitigation mechanism important for alleviating oxidative stress and DNA damage response activation; it can either suppress or promote cancer, but its role in breast cancer is unknown. Here, we show that similar to Brca1 and Brca2, ablation of Palb2 in the mouse mammary gland resulted in tumor development with long latency, and the tumors harbored mutations in Trp53. Interestingly, impaired autophagy, due to monoallelic loss of the essential autophagy gene Becn1, reduced Palb2-associated mammary tumorigenesis in a Trp53-wild-type but not conditionally null background. These results indicate that, in the face of DNA damage and oxidative stress elicited by PALB2 loss, p53 is a barrier to cancer development, whereas autophagy facilitates cell survival and tumorigenesis. (C) 2013 AACR.
C1 [Huo, Yanying; Cai, Hong; Teplova, Irina; Chen, Guanghua; Price, Sandy; Ganesan, Shridar; Karantza, Vassiliki; White, Eileen; Xia, Bing] Rutgers Canc Inst New Jersey, New Brunswick, NJ 08903 USA.
[Huo, Yanying; Cai, Hong; Xia, Bing] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Radiat Oncol, New Brunswick, NJ USA.
[Barnard, Nicola] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pathol, New Brunswick, NJ 08903 USA.
[Ganesan, Shridar; Karantza, Vassiliki] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Med, New Brunswick, NJ 08903 USA.
[White, Eileen] Rutgers State Univ, Dept Mol Biol & Biochem, Piscataway, NJ 08855 USA.
[Bowman-Colin, Christian] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
RP Xia, B (reprint author), Rutgers Canc Inst New Jersey, Dept Radiat Oncol, 195 Little Albany St, New Brunswick, NJ 08903 USA.
EM xiabi@rutgers.edu
FU National Cancer Institute [R01CA138804]; American Cancer Society (RSG)
[TBG-119822]; Cancer Institute of New Jersey
FX This work was supported by the National Cancer Institute (R01CA138804;
to B. Xia), the American Cancer Society (RSG #TBG-119822; to B. Xia),
and The Cancer Institute of New Jersey (to B. Xia).
NR 48
TC 30
Z9 33
U1 0
U2 18
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
J9 CANCER DISCOV
JI Cancer Discov.
PD AUG
PY 2013
VL 3
IS 8
BP 894
EP 907
DI 10.1158/2159-8290.CD-13-0011
PG 14
WC Oncology
SC Oncology
GA 198XQ
UT WOS:000322957600023
PM 23650262
ER
PT J
AU Curry, NL
Mino-Kenudson, M
Oliver, TG
Yilmaz, OH
Yilmaz, VO
Moon, JY
Jacks, T
Sabatini, DM
Kalaany, NY
AF Curry, Natasha L.
Mino-Kenudson, Mari
Oliver, Trudy G.
Yilmaz, Oemer H.
Yilmaz, Vedat O.
Moon, Jade Y.
Jacks, Tyler
Sabatini, David M.
Kalaany, Nada Y.
TI Pten-Null Tumors Cohabiting the Same Lung Display Differential AKT
Activation and Sensitivity to Dietary Restriction
SO CANCER DISCOVERY
LA English
DT Article
ID ONCOGENIC K-RAS; MOUSE MODEL; BREAST-CANCER; INACTIVATION; PROGRESSION;
EXPRESSION; EVOLUTION; PATHWAY; GROWTH; GENE
AB PTEN loss is considered a biomarker for activated phosphoinositide 3-kinase (PI3K)/AKT, a pathway frequently mutated in cancer, and was recently shown to confer resistance to dietary restriction. Here, we show that Pten loss is not sufficient to drive AKT activation and resistance to dietary restriction in tumors with low growth factor receptor levels. We describe a murine Pten-null Kras-driven lung cancer model that harbors both dietary restriction-resistant, higher-grade, bronchiolar tumors with high AKT activity, and dietary restriction-sensitive, lower-grade, alveolar tumors with low AKT activity. We find that this phenotype is cell autonomous and that normal bronchiolar cells express higher levels of insulin-like growth factor-I receptor (IGF-IR) and of ectonucleoside triphosphate diphosphohydrolase 5 (ENTPD5), an endoplasmic reticulum enzyme known to modulate growth factor receptor levels. Suppression of ENTPD5 is sufficient to decrease IGF-IR levels and sensitize bronchiolar tumor cells to serum in vitro and to dietary restriction in vivo. Furthermore, we find that a significant percentage of human non-small cell lung carcinomas (NSCLC) have low AKT activity despite PTEN loss. (C) 2013 AACR.
C1 [Curry, Natasha L.; Yilmaz, Vedat O.; Moon, Jade Y.; Kalaany, Nada Y.] Boston Childrens Hosp, Div Endocrinol, Ctr Basic & Translat Obes Res, Boston, MA 02115 USA.
[Mino-Kenudson, Mari; Yilmaz, Oemer H.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Mino-Kenudson, Mari; Yilmaz, Oemer H.] Harvard Univ, Sch Med, Boston, MA USA.
[Kalaany, Nada Y.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Oliver, Trudy G.; Jacks, Tyler; Sabatini, David M.] Howard Hughes Med Inst, Cambridge, MA USA.
[Oliver, Trudy G.; Jacks, Tyler; Sabatini, David M.] MIT, Dept Biol, Cambridge, MA USA.
[Oliver, Trudy G.; Jacks, Tyler; Sabatini, David M.] MIT, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA.
[Sabatini, David M.] Broad Inst Harvard & MIT, Cambridge, MA USA.
[Yilmaz, Oemer H.; Sabatini, David M.] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA.
RP Kalaany, NY (reprint author), Boston Childrens Hosp, Div Endocrinol, Ctr Basic & Translat Obes Res, Boston, MA 02115 USA.
EM nada.kalaany@childrens.harvard.edu
FU Anna Fuller Fund fellowship; Boston Children's Hospital; Alexander and
Margaret Stewart Trust; David H. Koch Cancer Research Award; NIH [R01
AI047389, R01 CA129105, 2-P30-CA14051]
FX This research was supported by the Anna Fuller Fund fellowship (to N.Y.
Kalaany); Boston Children's Hospital (to N.Y. Kalaany, N.L. Curry, and
V.O. Yilmaz); the Alexander and Margaret Stewart Trust Award (to D.M.
Sabatini); the David H. Koch Cancer Research Award (to D.M. Sabatini);
and NIH grants R01 AI047389, R01 CA129105 (to D.M. Sabatini), and
2-P30-CA14051 (to D. M. Sabatini, T. Jacks, and T.G. Oliver). D.M.
Sabatini is an investigator of the Howard Hughes Medical Institute.
NR 30
TC 13
Z9 15
U1 0
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
J9 CANCER DISCOV
JI Cancer Discov.
PD AUG
PY 2013
VL 3
IS 8
BP 908
EP 921
DI 10.1158/2159-8290.CD-12-0507
PG 14
WC Oncology
SC Oncology
GA 198XQ
UT WOS:000322957600024
PM 23719831
ER
PT J
AU Castano, Z
Marsh, T
Tadipatri, R
Kuznetsov, HS
Al-Shahrour, F
Paktinat, M
Greene-Colozzi, A
Nilsson, B
Richardson, AL
McAllister, SS
AF Castano, Zafira
Marsh, Timothy
Tadipatri, Ramya
Kuznetsov, Hanna S.
Al-Shahrour, Fatima
Paktinat, Mahnaz
Greene-Colozzi, April
Nilsson, Bjorn
Richardson, Andrea L.
McAllister, Sandra S.
TI Stromal EGF and IGF-I Together Modulate Plasticity of Disseminated
Triple-Negative Breast Tumors
SO CANCER DISCOVERY
LA English
DT Article
ID EPITHELIAL-MESENCHYMAL TRANSITION; CANCER CELLS; STEM-CELLS;
ACQUIRED-RESISTANCE; GROWTH; INSULIN; RECEPTOR; MYC; PROGRESSION;
MACROENVIRONMENT
AB The causes for malignant progression of disseminated tumors and the reasons recurrence rates differ in women with different breast cancer subtypes are unknown. Here, we report novel mechanisms of tumor plasticity that are mandated by microenvironmental factors and show that recurrence rates are not strictly due to cell-intrinsic properties. Specifically, outgrowth of the same population of incipient tumors is accelerated in mice with triple-negative breast cancer (TNBC) relative to those with luminal breast cancer. Systemic signals provided by overt TNBCs cause the formation of a tumor-supportive microenvironment enriched for EGF and insulin-like growth factor-I (IGF-I) at distant indolent tumor sites. Bioavailability of EGF and IGF-I enhances the expression of transcription factors associated with pluripotency, proliferation, and epithelial-mesenchymal transition. Combinatorial therapy with EGF receptor and IGF-I receptor inhibitors prevents malignant progression. These results suggest that plasticity and recurrence rates can be dictated by host systemic factors and offer novel therapeutic potential for patients with TNBC. (C) 2013 AACR.
C1 [Castano, Zafira; Marsh, Timothy; Tadipatri, Ramya; Kuznetsov, Hanna S.; Al-Shahrour, Fatima; Paktinat, Mahnaz; McAllister, Sandra S.] Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA.
[Richardson, Andrea L.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Castano, Zafira; McAllister, Sandra S.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Greene-Colozzi, April; Richardson, Andrea L.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Al-Shahrour, Fatima; Nilsson, Bjorn; McAllister, Sandra S.] Broad Inst Harvard & MIT, Cambridge, MA USA.
[McAllister, Sandra S.] Harvard Stem Cell Inst, Cambridge, MA USA.
[Nilsson, Bjorn] Lund Univ, Dept Lab Med, Div Hematol & Transfus Med, Lund, Sweden.
RP McAllister, SS (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, 1 Blackfan Circle,Karp 5-214, Boston, MA 02115 USA.
EM smcallister1@partners.org
RI McAllister, Sandra/J-7373-2012
FU Harvard Stem Cell Institute; American Cancer Society; NIH [RO1
CA166284-01]; Dana-Farber/Harvard SPORE in Breast Cancer [2 P50
CA89393-06]
FX This work was supported by funds from the Harvard Stem Cell Institute,
the American Cancer Society, and NIH RO1 CA166284-01 (to S.S.
McAllister), and partially supported by the Dana-Farber/Harvard SPORE in
Breast Cancer (N.C.I., 2 P50 CA89393-06; to A.L. Richardson).
NR 49
TC 17
Z9 17
U1 2
U2 11
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
J9 CANCER DISCOV
JI Cancer Discov.
PD AUG
PY 2013
VL 3
IS 8
BP 922
EP 935
DI 10.1158/2159-8290.CD-13-0041
PG 14
WC Oncology
SC Oncology
GA 198XQ
UT WOS:000322957600025
PM 23689072
ER
PT J
AU Janzen, DM
Rosales, MA
Paik, DY
Lee, DS
Smith, DA
Witte, ON
Iruela-Arispe, ML
Memarzadeh, S
AF Janzen, Deanna M.
Rosales, Miguel A.
Paik, Daniel Y.
Lee, Daniel S.
Smith, Daniel A.
Witte, Owen N.
Iruela-Arispe, M. Luisa
Memarzadeh, Sanaz
TI Progesterone Receptor Signaling in the Microenvironment of Endometrial
Cancer Influences Its Response to Hormonal Therapy
SO CANCER RESEARCH
LA English
DT Article
ID UTERINE EPITHELIUM; ANDROGEN RECEPTOR; PROSTATE-CANCER; BREAST-CANCER;
ESTROGEN; CARCINOMA; HYPERPLASIA; EXPRESSION; MOUSE; ADENOCARCINOMA
AB Progesterone, an agonist for the progesterone receptor (PR), can be an efficacious and well-tolerated treatment in endometrial cancer. The clinical use of progesterone is limited because of the lack of biomarkers that predict hormone sensitivity. Despite its efficacy in cancer therapy, mechanisms and site of action for progesterone remain unknown. Using an in vivo endometrial cancer mouse model driven by clinically relevant genetic changes but dichotomous responses to hormonal therapy, we show that signaling through stromal PR is necessary and sufficient for progesterone antitumor effects. Endometrial cancers resulting from epithelial loss of PTEN (PTENKO) were hormone sensitive and had abundant expression of stromal PR. Stromal deletion of PR as a single genetic change in these tumors induced progesterone resistance indicating that paracrine signaling through the stroma is essential for the progesterone therapeutic effects. A hormone-refractory endometrial tumor with low levels of stromal PR developed when activation of KRAS was coupled with PTEN-loss (PTENKO/Kras). The innate progesterone resistance in PTENKO/Kras tumors stemmed from methylation of PR in the tumor microenvironment. Add-back of stromal PR expressed from a constitutively active promoter sensitized these tumors to progesterone therapy. Results show that signaling through stromal PR is sufficient for inducing hormone responsiveness. Our findings suggest that epigenetic derepression of stromal PR could be a potential therapeutic target for sensitizing hormone-refractory endometrial tumors to progesterone therapy. On the basis of these results, stromal expression of PR may emerge as a reliable biomarker in predicting response to hormonal therapy. (C)2013 AACR.
C1 [Janzen, Deanna M.; Rosales, Miguel A.; Paik, Daniel Y.; Lee, Daniel S.; Memarzadeh, Sanaz] Univ Calif Los Angeles, David Geffen Sch Med, Dept Obstet & Gynecol, Los Angeles, CA 90095 USA.
[Witte, Owen N.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Mol & Med Pharmacol, Los Angeles, CA 90095 USA.
[Iruela-Arispe, M. Luisa] Univ Calif Los Angeles, David Geffen Sch Med, Dept Mol Cell & Dev Biol, Los Angeles, CA 90095 USA.
[Smith, Daniel A.; Witte, Owen N.; Iruela-Arispe, M. Luisa] Univ Calif Los Angeles, Inst Mol Biol, Los Angeles, CA 90095 USA.
[Witte, Owen N.] Univ Calif Los Angeles, Howard Hughes Med Inst, Los Angeles, CA 90095 USA.
[Witte, Owen N.; Memarzadeh, Sanaz] Univ Calif Los Angeles, Eli & Edythe Broad Ctr Regenerat Med & Stem Cell, Los Angeles, CA 90095 USA.
[Smith, Daniel A.; Witte, Owen N.] Univ Calif Los Angeles, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA 90095 USA.
[Memarzadeh, Sanaz] VA Greater Los Angeles Hlth Care Syst, Los Angeles, CA USA.
RP Memarzadeh, S (reprint author), Univ Calif Los Angeles, 555 Westwood Plaza,Level B,Box 957243,1015 Terasa, Los Angeles, CA 90095 USA.
EM smemarzadeh@mednet.ucla.edu
FU VA CDA-2 Award; Scholars in Translational Medicine Program; Mary Kay
Award; CDU/UCLA NIH/NCI [U54-CA-143931]; Sidney Kimmel Foundation; UCLA
Cancer Research Coordinating Committee; Concern foundation
FX S. Memarzadeh is supported by a VA CDA-2 Award, Scholars in
Translational Medicine Program, Mary Kay Award, the CDU/UCLA NIH/NCI
Grant #U54-CA-143931 award, a Sidney Kimmel Foundation award, the UCLA
Cancer Research Coordinating Committee grant, and the Concern
foundation.
NR 49
TC 12
Z9 15
U1 1
U2 8
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 2013
VL 73
IS 15
BP 4697
EP 4710
DI 10.1158/0008-5472.CAN-13-0930
PG 14
WC Oncology
SC Oncology
GA 194HC
UT WOS:000322620800012
PM 23744837
ER
PT J
AU Tworoger, SS
Eliassen, AH
Zhang, XH
Qian, J
Sluss, PM
Rosner, BA
Hankinson, SE
AF Tworoger, Shelley S.
Eliassen, A. Heather
Zhang, Xuehong
Qian, Jing
Sluss, Patrick M.
Rosner, Bernard A.
Hankinson, Susan E.
TI A 20-Year Prospective Study of Plasma Prolactin as a Risk Marker of
Breast Cancer Development
SO CANCER RESEARCH
LA English
DT Article
ID POSTMENOPAUSAL WOMEN; PREMENOPAUSAL WOMEN; ESTROGEN-RECEPTOR;
STEROID-HORMONES; CELLS; GROWTH; BLOOD; REPRODUCIBILITY; ANGIOGENESIS;
ACTIVATION
AB Understanding how the timing of exposure to endogenous hormones influences cancer development is critical to elucidating disease etiology. Prolactin increases proliferation and cell motility, processes important in later stage tumor development, suggesting that levels proximate (versus distant) to diagnosis may better predict risk. Thus, we calculated relative risks (RR) and 95% confidence intervals (CI) for prolactin levels on samples collected <10 (proximate) versus >= 10 (distant) years before diagnosis in the Nurses' Health Study (NHS) and NHSII with breast cancer risk, including in a subset of NHS women providing two samples 10 years apart. We measured prolactin via immunoassay in cases diagnosed from 1990 to 2010 (NHS) and 1999 to 2009 (NHSII) and matched controls. Overall, 2,468 cases and 4,021 controls had prolactin measured <10 years and 953 cases and 1,339 controls >10 years before diagnosis/reference date. There was an increased risk for higher proximate prolactin levels [RR, >15.7 vs. <= 8.1 ng/mL (i.e., top vs. bottom quartiles) = 1.20; 95% CI, 1.03-1.40; P-trend = 0.005], but not for distant levels (RR = 0.97; P-trend = 0.94); results were similar among women with two blood samples (P-interaction, proximate vs. distant = 0.07). The positive association was stronger for ER+ disease (RR = 1.28; P-trend = 0.003) and postmenopausal women (RR = 1.37; P-trend = 0.0002). Among postmenopausal women, the association was strongest for ER+ disease (RR = 1.52) and lymph node-positive cases (RR = 1.63). Our data suggest that prolactin levels measured <10 years before diagnosis are most strongly associated with postmenopausal breast cancer risk, especially for ER+ tumors and metastatic disease. This corresponds with biologic data that prolactin is etiologically important in tumor promotion. (C)2013 AACR.
C1 [Tworoger, Shelley S.; Eliassen, A. Heather; Zhang, Xuehong; Rosner, Bernard A.; Hankinson, Susan E.] Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.
[Tworoger, Shelley S.; Eliassen, A. Heather; Zhang, Xuehong; Rosner, Bernard A.; Hankinson, Susan E.] Harvard Univ, Sch Med, Boston, MA USA.
[Tworoger, Shelley S.; Eliassen, A. Heather; Zhang, Xuehong; Hankinson, Susan E.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Sluss, Patrick M.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Qian, Jing; Hankinson, Susan E.] Univ Massachusetts, Sch Publ Hlth & Hlth Sci, Div Biostat & Epidemiol, Boston, MA 02125 USA.
[Rosner, Bernard A.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
RP Tworoger, SS (reprint author), Brigham & Womens Hosp, 181 Longwood Ave,3rd Fl, Boston, MA 02115 USA.
EM nhsst@channing.harvard.edu
OI Tworoger, Shelley/0000-0002-6986-7046
FU NIH [R01 CA138580, R01 CA49449, R01 CA67262, R01 CA50385, P01 CA87969]
FX This work was financially supported by the NIH (grant nos. R01 CA138580,
R01 CA49449, R01 CA67262, R01 CA50385, P01 CA87969).
NR 38
TC 50
Z9 51
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD AUG 1
PY 2013
VL 73
IS 15
BP 4810
EP 4819
DI 10.1158/0008-5472.CAN-13-0665
PG 10
WC Oncology
SC Oncology
GA 194HC
UT WOS:000322620800022
PM 23783576
ER
PT J
AU Antony, R
Emery, CM
Sawyer, AM
Garraway, LA
AF Antony, Rajee
Emery, Caroline M.
Sawyer, Allison M.
Garraway, Levi A.
TI C-RAF Mutations Confer Resistance to RAF Inhibitors
SO CANCER RESEARCH
LA English
DT Article
ID B-RAF; WILD-TYPE; METASTATIC MELANOMA; ACQUIRED-RESISTANCE;
KINASE-ACTIVITY; HUMAN CANCER; BRAF; ACTIVATION; PATHWAY; CRAF
AB Melanomas that contain B-RAF(V600E) mutations respond transiently to RAF and MEK inhibitors; however, resistance to these agents remains a formidable challenge. Although B- or C-RAF dysregulation represents prominent resistance mechanisms, resistance-associated point mutations in RAF oncoproteins are surprisingly rare. To gain insights herein, we conducted random mutagenesis screens to identify B- or C-RAF mutations that confer resistance to RAF inhibitors. Whereas bona fide B-RAF(V600E) resistance alleles were rarely observed, we identified multiple C-RAF mutations that produced biochemical and pharmacologic resistance. Potent C-RAF resistance alleles localized to a 14-3-3 consensus binding site or a separate site within the P loop. These mutations elicited paradoxical upregulation of RAF kinase activity in a dimerization-dependent manner following exposure to RAF inhibitors. Knowledge of resistance-associated C-RAF mutations may enhance biochemical understanding of RAF-dependent signaling, anticipate clinical resistance to novel RAF inhibitors, and guide the design of "next-generation" inhibitors for deployment in RAF- or RAS-driven malignancies. (C)2013 AACR.
C1 [Antony, Rajee; Emery, Caroline M.; Sawyer, Allison M.; Garraway, Levi A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Antony, Rajee; Emery, Caroline M.; Sawyer, Allison M.; Garraway, Levi A.] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Garraway, Levi A.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA.
[Garraway, Levi A.] Broad Inst Harvard & MIT, Cambridge, MA USA.
RP Garraway, LA (reprint author), Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM levi_garraway@dfci.harvard.edu
FU Novartis Institute for BioMedical Research
FX This study is supported by a grant from Novartis Institute for
BioMedical Research.
NR 46
TC 15
Z9 15
U1 6
U2 15
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 2013
VL 73
IS 15
BP 4840
EP 4851
DI 10.1158/0008-5472.CAN-12-4089
PG 12
WC Oncology
SC Oncology
GA 194HC
UT WOS:000322620800025
PM 23737487
ER
PT J
AU Yonetsu, T
Bouma, BE
Kato, K
Fujimoto, JG
Jang, IK
AF Yonetsu, Taishi
Bouma, Brett E.
Kato, Koji
Fujimoto, James G.
Jang, Ik-Kyung
TI Optical Coherence Tomography - 15 Years in Cardiology
SO CIRCULATION JOURNAL
LA English
DT Review
DE Coronary artery disease; Optical coherence tomography; Percutaneous
coronary intervention
ID ACUTE CORONARY SYNDROME; ELUTING STENT IMPLANTATION; ACUTE
MYOCARDIAL-INFARCTION; FIBROUS CAP THICKNESS; BARE-METAL STENTS;
INTRAVASCULAR ULTRASOUND; ATHEROSCLEROTIC PLAQUES; NEOINTIMAL COVERAGE;
PULMONARY-HYPERTENSION; ARTERY-DISEASE
AB Since its invention in the late 1990s, intravascular optical coherence tomography (OCT) has been rapidly adopted in clinical research and, more recently, in clinical practice. Given its unprecedented resolution and high image contrast, OCT has been used to visualize plaque characteristics and to evaluate the vascular response to percutaneous coronary intervention. In particular, OCT is becoming the standard modality to evaluate in vivo plaque vulnerability, including the presence of lipid content, thin fibrous cap, or macrophage accumulation. Furthermore, OCT findings after stent implantation, such as strut apposition, neointimal hyperplasia, strut coverage, and neoatherosclerosis, are used as surrogate markers of the vascular response. New applications for OCT are being explored, such as transplant vasculopathy or non-coronary vascular imaging. Although OCT has contributed to cardiovascular research by providing a better understanding of the pathophysiology of coronary artery disease, data linking the images and clinical outcomes are lacking. Prospective data are needed to prove that the use of OCT improves patient outcomes, which is the ultimate goal of any clinical diagnostic tool.
C1 [Yonetsu, Taishi; Kato, Koji; Jang, Ik-Kyung] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Bouma, Brett E.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Fujimoto, James G.] MIT, Dept Elect Engn & Comp Sci, Cambridge, MA 02139 USA.
[Fujimoto, James G.] MIT, Elect Res Lab, Cambridge, MA 02139 USA.
RP Jang, IK (reprint author), Massachusetts Gen Hosp, Div Cardiol, GRB 800,55 Fruit St, Boston, MA 02114 USA.
EM ijang@partners.org
FU LightLab Imaging/St. Jude Medical
FX Dr IK Jang received a research grant and consulting fee from LightLab
Imaging/St. Jude Medical.
NR 82
TC 28
Z9 29
U1 2
U2 14
PU JAPANESE CIRCULATION SOC
PI TOYKO
PA 18TH FLOOR IMPERIAL HOTEL TOWER, 1-1-1 UCHISAIWAI-CHO CHIYODA-KU, TOYKO,
100-0011, JAPAN
SN 1346-9843
J9 CIRC J
JI Circ. J.
PD AUG
PY 2013
VL 77
IS 8
BP 1933
EP 1940
DI 10.1253/circj.CJ-13-0643.1
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 196CW
UT WOS:000322752000002
PM 23856651
ER
PT J
AU Lopez-Cuenca, A
Manzano-Fernandez, S
Marin, F
Parra-Pallares, S
Navarro-Penalver, M
Montalban-Larrea, S
Andreu-Cayuelas, JM
Romero-Aniorte, AI
Aviles-Plaza, F
Valdes-Chavarri, M
Januzzi, JL
AF Lopez-Cuenca, Angel
Manzano-Fernandez, Sergio
Marin, Francisco
Parra-Pallares, Soledad
Navarro-Penalver, Marina
Montalban-Larrea, Salvador
Andreu-Cayuelas, Jose M.
Romero-Aniorte, Ana I.
Aviles-Plaza, Francisco
Valdes-Chavarri, Mariano
Januzzi, James L., Jr.
TI Beta-Trace Protein and Cystatin C as Predictors of Major Bleeding in
Non-ST-Segment Elevation Acute Coronary Syndrome
SO CIRCULATION JOURNAL
LA English
DT Article
DE Acute coronary syndrome; Beta-trace protein; Hemorrhage
ID GLOMERULAR-FILTRATION-RATE; MYOCARDIAL-INFARCTION; SERUM CREATININE;
OUTCOMES; EVENTS; RISK; MORTALITY; EQUATION; FAILURE; ANGINA
AB Background: Beta-trace protein (BTP) and cystatin C (CysC) are novel biomarkers of renal function. We assessed the ability of both to predict major bleeding (MB) in patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACS), compared to other renal function parameters and clinical risk scores.
Methods and Results: We included 273 patients. Blood samples were obtained within 24h of admission. The end-point was MB. During a follow-up of 760 days (411-1,098 days), 25 patients (9.2%) had MB. Patients with MB had higher concentrations of BTP (0.98 mg/L; 0.71-1.16 mg/L vs. 0.72 mg/L, 0.60-0.91 mg/L, P=0.002), CysC (1.05 mg/L; 0.91-1.30 mg/L vs. 0.90 mg/L, 0.75-1.08 mg/L, P=0.003), higher CRUSADE score (39 +/- 16 points vs. 29 +/- 15 points, P=0.002) and lower estimated glomerular filtration rate (eGFR; 66 +/- 27 vs. 80 +/- 30 ml .min(-1). 1.73 m(-2), P=0.02) than patients without MB; there was no difference in creatinine level between the groups (P=0.14). After multivariable adjustment, both were predictors of MB, while eGFR and creatinine did not achieve statistical significance. Among subjects with eGFR >60 ml .min(-1). 1.73 m(-2), those with elevated concentrations of both biomarkers had a significantly higher risk for MB. Net reclassification indexes from the addition of BTP and CysC to CRUSADE risk score were 38% and 21% respectively, while the relative integrated discrimination indexes were 12.5% and 3.8%.
Conclusions: Among NSTE-ACS patients, BTP and CysC were superior to conventional renal parameters for predicting MB, and improved clinical stratification for hemorrhagic risk.
C1 [Lopez-Cuenca, Angel; Manzano-Fernandez, Sergio; Marin, Francisco; Navarro-Penalver, Marina; Montalban-Larrea, Salvador; Andreu-Cayuelas, Jose M.; Romero-Aniorte, Ana I.; Valdes-Chavarri, Mariano] Univ Hosp Virgen Arrixaca, Div Cardiol, Murcia, Spain.
[Manzano-Fernandez, Sergio; Marin, Francisco; Valdes-Chavarri, Mariano] Univ Murcia, Murcia, Spain.
[Parra-Pallares, Soledad; Aviles-Plaza, Francisco] Univ Hosp Virgen Arrixaca, Dept Biochem, Murcia, Spain.
[Januzzi, James L., Jr.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
RP Januzzi, JL (reprint author), Massachusetts Gen Hosp, Div Cardiol, Yawkey 5984,32 Fruit St, Boston, MA 02114 USA.
EM jjanuzzi@partners.org
NR 24
TC 4
Z9 5
U1 0
U2 4
PU JAPANESE CIRCULATION SOC
PI TOYKO
PA 18TH FLOOR IMPERIAL HOTEL TOWER, 1-1-1 UCHISAIWAI-CHO CHIYODA-KU, TOYKO,
100-0011, JAPAN
SN 1346-9843
J9 CIRC J
JI Circ. J.
PD AUG
PY 2013
VL 77
IS 8
BP 2088
EP 2096
DI 10.1253/circj.CJ-13-0106
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 196CW
UT WOS:000322752000027
PM 23698027
ER
PT J
AU Ananthakrishnan, AN
Long, MD
Martin, CF
Sandler, RS
Kappelman, MD
AF Ananthakrishnan, Ashwin N.
Long, Millie D.
Martin, Christopher F.
Sandler, Robert S.
Kappelman, Michael D.
TI Sleep Disturbance and Risk of Active Disease in Patients With Crohn's
Disease and Ulcerative Colitis
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Intestinal Inflammation; Environment; PROMIS; Prospective Cohort Study
ID INFLAMMATORY-BOWEL-DISEASE; QUALITY-OF-LIFE; RHEUMATOID-ARTHRITIS;
METABOLIC SYNDROME; ACTIVITY INDEX; FATIGUE; INTERLEUKIN-6;
EPIDEMIOLOGY; DISABILITY; DEPRESSION
AB BACKGROUND & AIMS: Impairment of sleep quality is common in patients with inflammatory bowel diseases (IBDs) (eg, Crohn's disease [CD] and ulcerative colitis [UC]), even during clinical remission. Sleep impairment can activate inflammatory pathways. Few prospective studies have examined the role of sleep disturbance on risk of relapse in IBD.
METHODS: We analyzed data from 3173 patients with IBD (1798 in clinical remission at baseline) participating in the Crohn's and Colitis Foundation of America Partners study, a longitudinal, Internet-based cohort. Sleep disturbance was measured using a subset of questions from the Patient Reported Outcomes Measurement Information Systems sleep disturbance questionnaire. Disease activity was assessed using the short Crohn's Disease Activity Index and the simple clinical colitis activity index for CD and UC, respectively. Logistic regression was used to identify predictors of sleep quality and examine the effect of sleep quality at baseline among patients in remission on risk of active disease at 6 months.
RESULTS: Disease activity, depression, female sex, smoking, and use of corticosteroids or narcotics were associated with sleep disturbance at enrollment. Among 1291 patients whose CD was in remission at baseline, those with impaired sleep had a 2-fold increase in risk of active disease at 6 months (adjusted odds ratio, 2.00; 95% confidence interval, 1.45-2.76); however, no effect was observed in patients with UC (odds ratio, 1.14; 95% confidence interval, 0.75-1.74). These findings persisted in a number of sensitivity analyses.
CONCLUSIONS: Sleep disturbance was associated with an increased risk of disease flares in CD but not UC. These findings indicate that the evaluation and treatment of sleep disturbance in patients with CD might improve outcomes.
C1 [Ananthakrishnan, Ashwin N.] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Ananthakrishnan, Ashwin N.] Harvard Univ, Sch Med, Boston, MA USA.
[Long, Millie D.; Martin, Christopher F.; Sandler, Robert S.] Univ N Carolina, Dept Med, Div Gastroenterol & Hepatol, Chapel Hill, NC USA.
[Kappelman, Michael D.] Univ N Carolina, Dept Pediat, Div Gastroenterol, Chapel Hill, NC USA.
RP Ananthakrishnan, AN (reprint author), Massachusetts Gen Hosp, Crohns & Colitis Ctr, 165 Cambridge St,9th Floor, Boston, MA 02114 USA.
EM aananthakrishnan@partners.org
FU National Institutes of Health [K23 DK097142, P30 DK34987]; Crohn's and
Colitis Foundation of America
FX Supported in part by a grant from the National Institutes of Health (K23
DK097142 to A.N.A.), and the Crohn's and Colitis Foundation of America
Partners cohort is supported by grants from the Crohn's and Colitis
Foundation of America and the National Institutes of Health (P30
DK34987).
NR 41
TC 37
Z9 38
U1 6
U2 17
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 2013
VL 11
IS 8
BP 965
EP 971
DI 10.1016/j.cgh.2013.01.021
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 195MP
UT WOS:000322707100017
PM 23376797
ER
PT J
AU Kaufman, JL
Fabre, C
Lonial, S
Richardson, PG
AF Kaufman, Jonathan L.
Fabre, Claire
Lonial, Sagar
Richardson, Paul G.
TI Histone Deacetylase Inhibitors in Multiple Myeloma: Rationale and
Evidence for Their Use in Combination Therapy
SO CLINICAL LYMPHOMA MYELOMA & LEUKEMIA
LA English
DT Review
DE Hematologic malignancy; Histone modification; Immunomodulatory agent;
Proteasome inhibitor
ID UNFOLDED PROTEIN RESPONSE; PHASE-I TRIAL; PROTEASOME INHIBITION;
PANOBINOSTAT LBH589; ORAL VORINOSTAT; HDAC INHIBITORS; CANCER-THERAPY;
BORTEZOMIB; CELLS; APOPTOSIS
AB Multiple myeloma (MM) arises from abnormal proliferation and survival (ie, a high proliferative index and a low apoptotic index) of mature immunoglobulin-producing plasma cells in the bone marrow. Development of novel therapeutic options, such as proteasome inhibitors and immunomodulatory agents (IMiDs), has improved treatment outcomes. However, patients often develop relapsed and refractory MM, thus requiring alternative treatment approaches. Histone acetyltransferases and histone deacetylases (HDACs) control the acetylation status of proteins and affect a broad array of physiologic processes (eg, cell cycle, apoptosis, and protein folding) involved in cell growth and survival. The discovery that HDACs might have a role in various hematologic malignancies, including MM, has led to the development of HDAC inhibitors as potential antitumor agents. Preclinical evidence from studies of HDAC inhibitors in combination with proteasome inhibitors (eg, bortezomib and carfilzomib), other antimyeloma agents, including IMiDs (eg, lenalidomide), and cytotoxic agents (eg, melphalan, pegylated liposomal doxorubicin), provides a strong scientific rationale for the evaluation of these regimens. Results from early stage clinical trials further support the use of HDAC inhibitors as a therapeutic option for MM, in combination with current and emerging antimyeloma agents. In this review, we examine the role of protein acetylation that underlies the antimyeloma effects of HDAC inhibitors, discuss the preclinical rationale for the use of HDAC inhibitors in combination with other antimyeloma agents, and provide an overview of the current clinical evidence supporting the use of HDAC inhibitors as a therapeutic option in MM. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Kaufman, Jonathan L.; Lonial, Sagar] Emory Univ, Sch Med, Atlanta, GA 30322 USA.
[Fabre, Claire; Richardson, Paul G.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Kaufman, JL (reprint author), Emory Univ, Winship Canc Ctr, Dept Hematol & Med Oncol, 1365-C Clifton Rd NE, Atlanta, GA 30322 USA.
EM jlkaufm@emory.edu
FU Merck Sharp & Dohme Corp, a subsidiary of Merck Co, Inc.
FX Editorial assistance was provided by Joseph J. Abrajano, PhD, and
Georgia Gleason, PhD, of Integrus Scientific, a division of Medicus
International New York. This assistance was funded by Merck Sharp &
Dohme Corp, a subsidiary of Merck & Co, Inc.
NR 78
TC 23
Z9 24
U1 0
U2 16
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 2152-2650
EI 2152-2669
J9 CL LYMPH MYELOM LEUK
JI Clin. Lymphoma Myeloma Leuk.
PD AUG
PY 2013
VL 13
IS 4
BP 370
EP 376
DI 10.1016/j.clml.2013.03.016
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA 200QW
UT WOS:000323085000003
PM 23787122
ER
PT J
AU Trummer, M
Eustacchio, S
Barth, M
Klassen, PD
Stein, S
AF Trummer, Martin
Eustacchio, Sandro
Barth, Martin
Klassen, Peter Douglas
Stein, Shlomit
TI Protecting facet joints post-lumbar discectomy: Barricaid annular
closure device reduces risk of facet degeneration
SO CLINICAL NEUROLOGY AND NEUROSURGERY
LA English
DT Article
DE Lumbar; Discectomy; Facet joint; Facet degeneration; Facet arthrosis;
Annulus fibrosis; Disc herniation; Annular closure device
ID LUMBAR DISKECTOMY; DISC HERNIATION; BACK-PAIN; OSTEOARTHRITIS;
REPLACEMENT; RADICULOPATHY; PREVALENCE; ARTHROSIS; SURGERY; LEVEL
AB Lumbar discectomy is an effective treatment for lumbar disc herniation (LDH). Although the majority of patients experience successful outcomes, a significant fraction will experience a recurrence of their back pain due to facet joint degeneration. Facet joint degeneration after discectomy may be the result of excessive nuclear removal, disc space narrowing, and annular injury. This study investigated whether implantation with the Barricaid annular closure device (ACD) during discectomy reduced the rate of facet degeneration. Inclusion criteria were primary lumbar disc herniation failing conservative treatment, Visual Analog Scale (VAS) Leg >= 40/100, Oswestry Disability Index (ODI) >= 40/100 and defects that were <= 60 mm(2) (Barricaid arm only), and patient age 18-75. CT interpretations were collected preoperatively and 12 months post-discectomy. Patients implanted with Barricaid had significantly reduced rates and grades of facet degeneration than patients without Barricaid. Reinforcing the annulus fibrosus with Barricaid during lumbar discectomy may slow the progression of facet joint degeneration. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Trummer, Martin; Eustacchio, Sandro] Med Univ, Graz, Austria.
[Barth, Martin] Univ Med Mannheim, Dept Neurosurg, Mannheim, Germany.
[Klassen, Peter Douglas] St Bonifatius Hosp, Dept Neurosurg, Lingen, Germany.
[Stein, Shlomit] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Trummer, M (reprint author), LKH Graz, Auenbrugger Pl 1, A-8036 Graz, Austria.
EM martin.trummer@klinikum-graz.at
RI Barth, Martin/E-8265-2014
FU Intrinsic Therapeutics, Inc.
FX Funding for this research was provided in part by Intrinsic
Therapeutics, Inc.
NR 29
TC 7
Z9 8
U1 5
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0303-8467
J9 CLIN NEUROL NEUROSUR
JI Clin. Neurol. Neurosurg.
PD AUG
PY 2013
VL 115
IS 8
BP 1440
EP 1445
DI 10.1016/j.clineuro.2013.01.007
PG 6
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 198NJ
UT WOS:000322929300045
PM 23473658
ER
PT J
AU Pulsipher, DT
Stricker, NH
Sadek, JR
Haaland, KY
AF Pulsipher, Dalin T.
Stricker, Nikki H.
Sadek, Joseph R.
Haaland, Kathleen Y.
TI Clinical Utility of the Neuropsychological Assessment Battery (NAB)
after Unilateral Stroke
SO CLINICAL NEUROPSYCHOLOGIST
LA English
DT Article
DE Unilateral stroke; NAB; Clinical utility; Lateralized
ID MILD COGNITIVE IMPAIRMENT; TRAUMATIC BRAIN-INJURY; ATTENTION DEFICITS;
SCREENING MODULE; LEFT-HEMISPHERE; DISCONNEXION SYNDROMES; FUNCTIONAL
RECOVERY; NATURAL-HISTORY; ISCHEMIC-STROKE; TEMPORAL-LOBE
AB The NAB is a comprehensive battery assessing five cognitive domains (Attention, Language, Memory, Spatial, Executive Function). Despite the advantage of co-normative domain data, its clinical utility is not well established because few studies have reported full-battery findings. The aim of this study was to determine if the NAB was sensitive to well documented hemispheric differences in language and spatial skills after unilateral stroke. We compared demographically matched control participants (n = 52) and individuals after left (LHD, n = 36) or right (RHD, n = 33) hemisphere damage due to stroke on the NAB, parts of the Western Aphasia Battery, and traditional visuospatial tasks. Both stroke groups showed impaired NAB Attention, Spatial, and Executive Functions relative to controls, while the LHD group was more impaired than control and RHD groups on Language and Memory modules. LHD patients with aphasia on traditional measures performed worse than control and non-aphasic LHD patients on all NAB domains. RHD patients with spatial impairment on traditional measures performed worse than controls, but not RHD patients without spatial impairment, on the NAB Spatial domain. Findings suggest the NAB is generally comparable to traditional language and visuospatial measures, and it sufficiently detects attention and executive deficits.
C1 [Pulsipher, Dalin T.; Sadek, Joseph R.; Haaland, Kathleen Y.] New Mexico VA Hlth Care Syst, Behav Hlth Care Line 116, Albuquerque, NM USA.
[Stricker, Nikki H.] VA Boston Healthcare Syst, Boston, MA USA.
[Stricker, Nikki H.] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA.
[Sadek, Joseph R.; Haaland, Kathleen Y.] Univ New Mexico, Sch Med, Dept Psychiat, Albuquerque, NM 87131 USA.
[Haaland, Kathleen Y.] New Mexico VA Hlth Care Syst, Res Serv, Albuquerque, NM USA.
[Haaland, Kathleen Y.] Univ New Mexico, Sch Med, Dept Neurol, Albuquerque, NM 87131 USA.
RP Haaland, KY (reprint author), VA Med Ctr, Psychol Serv, 116B, Albuquerque, NM 87108 USA.
EM dpulsipher@chmca.org; khaaland@unm.edu
FU Department of Veterans Affairs; Office of Research and Development,
Clinical Sciences Research and Development; Rehabilitation Research and
Development Merit grant
FX This material is based upon work supported in part by the Department of
Veterans Affairs, Office of Research and Development, Clinical Sciences
Research and Development Merit grant and Career Scientist Award (to KYH)
and Rehabilitation Research and Development Merit grant (to KYH).
NR 84
TC 4
Z9 4
U1 1
U2 13
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA
SN 1385-4046
J9 CLIN NEUROPSYCHOL
JI Clin. Neuropsychol.
PD AUG 1
PY 2013
VL 27
IS 6
BP 924
EP 945
DI 10.1080/13854046.2013.799714
PG 22
WC Psychology, Clinical; Clinical Neurology; Psychology
SC Psychology; Neurosciences & Neurology
GA 197RA
UT WOS:000322867100003
PM 23682731
ER
PT J
AU Maw, TT
Fried, L
AF Maw, Thin Thin
Fried, Linda
TI Chronic Kidney Disease in the Elderly
SO CLINICS IN GERIATRIC MEDICINE
LA English
DT Article
DE Elderly; Geriatric; Chronic kidney disease; Renal function; Dialysis
ID GLOMERULAR-FILTRATION-RATE; CHRONIC RENAL-INSUFFICIENCY; BONE-MINERAL
DENSITY; BLOOD-PRESSURE; CYSTATIN-C; CARDIOVASCULAR OUTCOMES; SERUM
CREATININE; UNITED-STATES; OLDER INDIVIDUALS; GLUCOSE CONTROL
AB Chronic kidney disease (CKD) is increasingly being recognized as a disease of elderly individuals. In recent years the definition and categorization of kidney disease has been standardized. There are concerns that this standardization has led to an increase in the number of older individuals labeled as having CKD. This article addresses the definitions of CKD, recently published revised CKD stages with risk stratifications, and limitations of using formulas to assess renal function in the elderly. Also discussed are management of common risk factors of progression CKD, nonrenal-related outcomes, prognosis of CKD in older individuals, and criteria for referral to nephrology.
C1 [Maw, Thin Thin; Fried, Linda] Univ Pittsburgh, Sch Med, Renal Electrolyte Div, Pittsburgh, PA 15261 USA.
[Fried, Linda] VA Pittsburgh Healthcare Syst, Renal Sect, Pittsburgh, PA 15240 USA.
RP Fried, L (reprint author), Univ Pittsburgh, Sch Med, Renal Electrolyte Div, 3550 Terrace St, Pittsburgh, PA 15261 USA.
EM linda.fried@va.gov
NR 57
TC 6
Z9 6
U1 0
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0749-0690
J9 CLIN GERIATR MED
JI Clin. Geriatr. Med.
PD AUG
PY 2013
VL 29
IS 3
BP 611
EP +
DI 10.1016/j.cger.2013.05.003
PG 15
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 198MY
UT WOS:000322928200006
PM 23849011
ER
PT J
AU Kim, SJ
Lee, H
Cho, JM
Park, CB
Kim, W
Kato, K
Yonetsu, T
Kim, CJ
Jang, IK
AF Kim, Soo-Joong
Lee, Hang
Cho, Jin-Man
Park, Chang-Bum
Kim, Weon
Kato, Koji
Yonetsu, Taishi
Kim, Chong-Jin
Jang, Ik-Kyung
TI Comparison of zotarolimus-eluting stent and everolimus-eluting stent for
vascular healing response: serial 3-month and 12-month optical coherence
tomography study
SO CORONARY ARTERY DISEASE
LA English
DT Article
DE everolimus-eluting stent; malapposition; neointimal coverage; optical
coherence tomography; zotarolimus-eluting stent
ID POLYESTER ARTERIAL PROSTHESES; FOLLOW-UP; NEOINTIMAL COVERAGE; CORONARY
STENTS; RANDOMIZED-TRIALS; BARE-METAL; IMPLANTATION; THROMBOSIS;
FLUOROPASSIVATION; METAANALYSIS
AB Background Everolimus-eluting stents (EES) have shown favorable clinical outcomes. However, there have been no studies evaluating early vascular response after EES implantation. We designed a prospective study to compare the neointimal response between zotarolimus-eluting stents (ZES) and EES at 3 and 12 months using serial optical coherence tomography examinations.Methods and results Sixty patients who underwent 3-month and 12-month follow-up optical coherence tomography (36 EES, 24 ZES) were included. Neointimal coverage and malapposition were evaluated using a strut-based analysis at both 3 and 12 months. Neointimal hyperplasia area and thrombus were assessed. ZES showed a higher incidence of covered struts (81.5 vs. 77.1%, P<0.0001) and lower incidence of malapposed struts (1.4 vs. 2.3%, P=0.001) than EES at 3 months. However, at 12 months, EES showed a slightly higher incidence of covered struts (96.4 vs. 93.6%, P<0.0001) and a lower incidence of malapposed struts (0.9 vs. 1.1%, P=0.03) than ZES. Neointimal hyperplasia area was greater in the ZES group than in the EES group at both 3 and 12 months (0.77 vs. 0.49 mm(2), P=0.03 and 1.50 vs. 0.97 mm(2), P=0.01, respectively). No significant difference in the incidence of thrombus was observed at both 3 and 12 months.Conclusion ZES showed rapid neointimal healing compared with EES at 3 months. However, at 12 months, EES had a slightly better vascular healing profile than ZES.
C1 [Kim, Soo-Joong; Kato, Koji; Yonetsu, Taishi; Jang, Ik-Kyung] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Cardiol Div, Boston, MA USA.
[Lee, Hang] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Biostat Ctr, Boston, MA USA.
[Kim, Soo-Joong; Cho, Jin-Man; Park, Chang-Bum; Kim, Weon; Kim, Chong-Jin] Kyung Hee Univ, Dept Internal Med, Div Cardiol, Coll Med, Seoul, South Korea.
RP Jang, IK (reprint author), Massachusetts Gen Hosp, Dept Med, Div Cardiol, GRB 800,55 Fruit St, Boston, MA 02114 USA.
EM ijang@partners.org
FU Medtronic Inc., Santa Rosa, CA, USA
FX This study was supported by Medtronic Inc., Santa Rosa, CA, USA.
NR 34
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U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0954-6928
J9 CORONARY ARTERY DIS
JI Coronary Artery Dis.
PD AUG
PY 2013
VL 24
IS 5
BP 431
EP 439
DI 10.1097/MCA.0b013e328362b2e7
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 202NZ
UT WOS:000323225700015
PM 23722649
ER
PT J
AU Nguyen, HM
Graber, CJ
AF Nguyen, Hien M.
Graber, Christopher J.
TI Cephalothin susceptibility testing as class representative for oral
cephalosporins: is it time to move on?
SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE
LA English
DT Article
DE Cephalothin; Antibiotics; Susceptibility; MIC; Urinary tract infection
ID ESCHERICHIA-COLI; KLEBSIELLA-PNEUMONIAE; CEPHALEXIN; CEFADROXIL;
CEFPODOXIME; MECHANISMS; CEFAZOLIN; CEFACLOR
AB Based on current epidemiologic and resistance trends, we propose reconsideration of the use of cephalothin susceptibility to predict susceptibility to oral narrow-spectrum cephalosporins among Enterobacteriaceae, particularly in predicting cephalexin susceptibility for urinary tract isolates. (c) 2013 Elsevier Inc. All rights reserved.
C1 [Nguyen, Hien M.] Dept Infect Dis, Portland, OR USA.
[Graber, Christopher J.] Univ Calif Los Angeles, David Geffen Sch Med, VA Greater Angeles Healthcare Syst, Infect Dis Sect, Los Angeles, CA 90095 USA.
RP Nguyen, HM (reprint author), Dept Infect Dis, Portland, OR USA.
EM hien.m.nguyen@kp.org
NR 18
TC 4
Z9 4
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0732-8893
J9 DIAGN MICR INFEC DIS
JI Diagn. Microbiol. Infect. Dis.
PD AUG
PY 2013
VL 76
IS 4
BP 483
EP 485
DI 10.1016/j.diagmicrobio.2013.03.022
PG 3
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA 195FK
UT WOS:000322687500015
PM 23680238
ER
PT J
AU Sutfin, EL
McCoy, TP
Morrell, HER
Hoeppner, BB
Wolfson, M
AF Sutfin, Erin L.
McCoy, Thomas P.
Morrell, Holly E. R.
Hoeppner, Bettina B.
Wolfson, Mark
TI Electronic cigarette use by college students
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE Electronic cigarettes; Young adults; College students; Nicotine;
Smoking; Tobacco; Cigarettes
ID SENSATION SEEKING; NICOTINE DELIVERY; NONRESPONSE BIAS; YOUNG-ADULTS;
ALCOHOL-USE; TOBACCO USE; SMOKING; TRAJECTORIES; ADOLESCENCE; PREVALENCE
AB Background: Electronic cigarettes, or e-cigarettes, are battery operated devices that deliver nicotine via inhaled vapor. There is considerable controversy about the disease risk and toxicity of e-cigarettes and empirical evidence on short- and long-term health effects is minimal. Limited data on e-cigarette use and correlates exist, and to our knowledge, no prevalence rates among U.S. college students have been reported. This study aimed to estimate the prevalence of e-cigarette use and identify correlates of use among a large, multi-institution, random sample of college students.
Methods: 4444 students from 8 colleges in North Carolina completed a Web-based survey in fall 2009.
Results: Ever use of e-cigarettes was reported by 4.9% of students, with 1.5% reporting past month use. Correlates of ever use included male gender, Hispanic or "Other race" (compared to non-Hispanic Whites), Greek affiliation, conventional cigarette smoking and e-cigarette harm perceptions. Although e-cigarette use was more common among conventional cigarette smokers, 12% of ever e-cigarette users had never smoked a conventional cigarette. Among current cigarette smokers, e-cigarette use was negatively associated with lack of knowledge about e-cigarette harm, but was not associated with intentions to quit.
Conclusions: Although e-cigarette use was more common among conventional cigarette smokers, it was not exclusive to them. E-cigarette use was not associated with intentions to quit smoking among a sub-sample of conventional cigarette smokers. Unlike older, more established cigarette smokers, e-cigarette use by college students does not appear to be motivated by the desire to quit cigarette smoking. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
C1 [Sutfin, Erin L.; Wolfson, Mark] Wake Forest Sch Med, Dept Social Sci & Hlth Policy, Winston Salem, NC 27157 USA.
[McCoy, Thomas P.] Univ N Carolina, Ctr Hlth Vulnerable Populat, Sch Nursing, Greensboro, NC 27402 USA.
[McCoy, Thomas P.] Univ N Carolina, Dept Educ Res Methodol, Greensboro, NC 27402 USA.
[Morrell, Holly E. R.] Loma Linda Univ, Dept Psychol, Loma Linda, CA 92350 USA.
[Hoeppner, Bettina B.] Harvard Univ, Dept Psychiat, Sch Med, Boston, MA 02114 USA.
[Hoeppner, Bettina B.] Massachusetts Gen Hosp, Ctr Addict Med, Boston, MA 02114 USA.
RP Sutfin, EL (reprint author), Wake Forest Sch Med, Dept Social Sci & Hlth Policy, Div Publ Hlth Sci, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM ESutfin@wakehealth.edu
FU National Institutes of Health [R01AA14007, F32CA141933, K01DA027097]
FX This work was supported by grants from the National Institutes of Health
(Grant Number R01AA14007 to Dr. Wolfson, Grant Number F32CA141933 to Dr.
Morrell, and Grant Number K01DA027097 to Dr. Hoeppner). The content is
solely the responsibility of the authors and does not necessarily
represent the official views of the National Institute of Alcohol Abuse
and Alcoholism or the National Institutes of Health.
NR 54
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U1 2
U2 77
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 2013
VL 131
IS 3
BP 214
EP 221
DI 10.1016/j.drugalcdep.2013.05.001
PG 8
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 197MP
UT WOS:000322855600005
PM 23746429
ER
PT J
AU Saxon, AJ
AF Saxon, Andrew J.
TI Donald A. Calsyn, Ph.D.: 1949-2013
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Biographical-Item
C1 VA Puget Sound Hlth Care Syst, Ctr Excellence Subst Abuse Treatment & Educ, Seattle, WA 98108 USA.
[Saxon, Andrew J.] Univ Washington, Seattle, WA 98195 USA.
RP Saxon, AJ (reprint author), VA Puget Sound Hlth Care Syst, Ctr Excellence Subst Abuse Treatment & Educ, Seattle, WA 98108 USA.
EM Andrew.Saxon@va.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
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 2013
VL 131
IS 3
BP 324
EP 324
DI 10.1016/j.drugalcdep.2013.04.011
PG 1
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 197MP
UT WOS:000322855600020
ER
PT J
AU Lindquist, KA
Gendron, M
Oosterwijk, S
Barrett, LF
AF Lindquist, Kristen A.
Gendron, Maria
Oosterwijk, Suzanne
Barrett, Lisa Feldman
TI Do People Essentialize Emotions? Individual Differences in Emotion
Essentialism and Emotional Experience
SO EMOTION
LA English
DT Article
DE psychological essentialism; emotional complexity; beliefs
ID BASIC EMOTIONS; PSYCHOLOGICAL CONSTRUCTION; SELF-REPORTS; PERCEPTION;
CATEGORIES; LANGUAGE; BELIEFS; BRAIN; DIFFERENTIATION; DIMENSIONS
AB Many scientific models of emotion assume that emotion categories are natural kinds that carve nature at its joints. These beliefs remain strong, despite the fact that the empirical record on the issue has remained equivocal for over a century. In this research, the authors examined one reason for this situation: People essentialize emotion categories by assuming that members of the same category (e.g., fear) have a shared metaphysical essence (i.e., a common causal mechanism). In Study 1, the authors found that lay people essentialize emotions by assuming that instances of the same emotion category have a shared essence that defines them, even when their surface features differ. Study 2 extended these findings, demonstrating that lay people tend to essentialize categories the more a category is of the body (vs. the mind). In Study 3, we examined the links between emotion essentialism and the complexity of actual emotional experiences. In particular, we predicted and found that individuals who hold essentialist beliefs about emotions describe themselves as experiencing highly differentiated emotional experiences but do not show evidence of stronger emotional differentiation in their momentary ratings of experience in everyday life. Implications for the science of emotion are discussed.
C1 [Lindquist, Kristen A.] Univ N Carolina, Dept Psychol, Chapel Hill, NC 27599 USA.
[Gendron, Maria] Boston Coll, Dept Psychol, Chestnut Hill, MA 02167 USA.
[Gendron, Maria; Oosterwijk, Suzanne; Barrett, Lisa Feldman] Northeastern Univ, Dept Psychol, Boston, MA USA.
[Oosterwijk, Suzanne] Univ Amsterdam, Dept Psychol, Amsterdam, Netherlands.
[Barrett, Lisa Feldman] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cambridge, MA 02138 USA.
RP Lindquist, KA (reprint author), Univ N Carolina, Dept Psychol, Davie Hall 321, Chapel Hill, NC 27599 USA.
EM kristen.lindquist@unc.edu
NR 81
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U1 4
U2 20
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 2013
VL 13
IS 4
BP 629
EP 644
DI 10.1037/a0032283
PG 16
WC Psychology, Experimental
SC Psychology
GA 195FM
UT WOS:000322687700006
PM 23668818
ER
PT J
AU Gaspard, N
Foreman, B
Judd, LM
Brenton, JN
Nathan, BR
McCoy, BM
Al-Otaibi, A
Kilbride, R
Fernandez, IS
Mendoza, L
Samuel, S
Zakaria, A
Kalamangalam, GP
Legros, B
Szaflarski, JP
Loddenkemper, T
Hahn, CD
Goodkin, HP
Claassen, J
Hirsch, LJ
LaRoche, SM
AF Gaspard, Nicolas
Foreman, Brandon
Judd, Lilith M.
Brenton, James N.
Nathan, Barnett R.
McCoy, Blathnaid M.
Al-Otaibi, Ali
Kilbride, Ronan
Fernandez, Ivan Sanchez
Mendoza, Lucy
Samuel, Sophie
Zakaria, Asma
Kalamangalam, Giridhar P.
Legros, Benjamin
Szaflarski, Jerzy P.
Loddenkemper, Tobias
Hahn, Cecil D.
Goodkin, Howard P.
Claassen, Jan
Hirsch, Lawrence J.
LaRoche, Suzette M.
CA Critical Care EEG Monitoring Res
TI Intravenous ketamine for the treatment of refractory status epilepticus:
A retrospective multicenter study
SO EPILEPSIA
LA English
DT Article
DE Ketamine; Treatment; Refractory status epilepticus; Anesthetics;
Antiepileptic drugs
ID NEUROTOXICITY; ISOFLURANE; MIDAZOLAM; ACIDOSIS; IMPACT
AB Purpose To examine patterns of use, efficacy, and safety of intravenous ketamine for the treatment of refractory status epilepticus (RSE).
Methods Multicenter retrospective review of medical records and electroencephalography (EEG) reports in 10 academic medical centers in North America and Europe, including 58 subjects, representing 60 episodes of RSE that were identified between 1999 and 2012. Seven episodes occurred after anoxic brain injury.
Key Findings Permanent control of RSE was achieved in 57% (34 of 60) of episodes. Ketamine was felt to have contributed to permanent control (possible or likely responses) in 32% (19 of 60) including seven (12%) in which ketamine was the last drug added (likely responses). Four of the seven likely responses, but none of the 12 possible ones, occurred in patients with postanoxic brain injury. No likely responses were observed when infusion rates were lower than 0.9mg/kg/h, when ketamine was introduced at least 8days after SE onset, or after failure of seven or more drugs. Ketamine was discontinued due to possible adverse events in five patients. Complications were mostly attributed to concurrent drugs, especially other anesthetics. Mortality rate was 43% (26 of 60), but was lower when SE was controlled within 24h of ketamine initiation (16% vs. 56%, p=0.0047).
Significance Ketamine appears to be a relatively effective and safe drug for the treatment of RSE. This retrospective series provides preliminary data on effective dose and appropriate time of intervention to aid in the design of a prospective trial to further define the role of ketamine in the treatment of RSE.
C1 [Gaspard, Nicolas; Hirsch, Lawrence J.] Yale Univ, Yale New Haven Hosp, Sch Med, Comprehens Epilepsy Ctr,Dept Neurol, New Haven, CT 06520 USA.
[Foreman, Brandon; Claassen, Jan] Columbia Univ Coll Phys & Surg, Div Crit Care Neurol, New York, NY 10032 USA.
[Foreman, Brandon; Claassen, Jan] Med Ctr, New York, NY USA.
[Judd, Lilith M.; LaRoche, Suzette M.] Emory Univ, Sch Med, Dept Neurol, Atlanta, GA 30322 USA.
[Brenton, James N.; Nathan, Barnett R.; Goodkin, Howard P.] Univ Virginia, Dept Neurol, Charlottesville, VA USA.
[McCoy, Blathnaid M.; Al-Otaibi, Ali; Hahn, Cecil D.] Hosp Sick Children, Div Neurol, Toronto, ON M5G 1X8, Canada.
[Kilbride, Ronan] Massachusetts Gen Hosp, Dept Neurol, Epilepsy Serv, Boston, MA 02114 USA.
[Kilbride, Ronan] Massachusetts Gen Hosp, Dept Neurol, Clin Neurophysiol Serv, Boston, MA 02114 USA.
[Fernandez, Ivan Sanchez; Loddenkemper, Tobias] Boston Childrens Hosp, Div Epilepsy & Clin Neurophysiol, Boston, MA USA.
[Mendoza, Lucy; Szaflarski, Jerzy P.] Univ Cincinnati, Acad Hlth Ctr, Dept Neurol, Cincinnati, OH USA.
[Samuel, Sophie; Zakaria, Asma; Kalamangalam, Giridhar P.] Univ Texas Hlth Sci Ctr Houston, Dept Neurol, Houston, TX 77030 USA.
[Legros, Benjamin] ULB Hop Erasme, Dept Neurol, Reference Ctr Treatment Refractory Epilepsy, Brussels, Belgium.
RP Gaspard, N (reprint author), Yale Univ, Comprehens Epilepsy Ctr, 15 York St,LLCI 714, New Haven, CT 06520 USA.
EM nicolas.gaspard@yale.edu
RI Hahn, Cecil/J-3372-2016;
OI Hahn, Cecil/0000-0002-0887-8761; Loddenkemper,
Tobias/0000-0003-2074-0674; Brenton, James/0000-0001-9432-1347
FU Belgian American Education Foundation; Commission for Educational
Exchange between the United States and Belgium; Belgian Neurological
Society; Pfizer's Medical and Academic Partnerships Program; Fundacion
Alfonso Martin Escudero; UCB Pharma; American Academy of Neurology;
David-Phinney Foundation/Sunflower Revolution; NIH/NINDS; University of
Cincinnati Research Council; National Institutes of Health/NINDS;
Harvard Medical School; Boston Children's Hospital; Program for Quality
and Safety at Boston Children's Hospital; Payer Provider Quality
Initiative; Epilepsy Foundation of America; Center for Integration of
Medicine and Innovative Technology; Epilepsy Therapy Project; American
Epilepsy Society; Cure; Lundbeck; Eisai; Canadian Institutes of Health
Research; PSI Foundation; SickKids Foundation; UCB-Pharma; Upsher-Smith;
GlaxoSmithKline; National Institutes of Health/SBIR
FX N.G. was the recipient of a Postdoctoral Research Fellowship from the
Belgian American Education Foundation, and received research grant from
the Commission for Educational Exchange between the United States and
Belgium and the Belgian Neurological Society. B. F. received funding
from Pfizer's Medical and Academic Partnerships Program.; I.S.F. was
funded by a grant for the study of Epileptic Encephalopathies from
'Fundacion Alfonso Martin Escudero.' B. L. has received funding for
research from UCB Pharma; serves on the advisory board of UCB Pharma,
GlaxoSmithKline (GSK), and Pfizer; and received speaker honoraria from
UCB Pharma and GSK. J.P.S. has served on an advisory board for UCB
Pharma. He serves on the editorial board of Epilepsy and Behavior,
Epileptologia, and Restorative Neurology and Neuroscience. He has
received honoraria from American Epilepsy Society and UCB Pharma, and he
is on speakers' bureaus for UCB Pharma. He has received funding for
research from the American Academy of Neurology, David-Phinney
Foundation/Sunflower Revolution, UCB Pharma, NIH/NINDS, and the
University of Cincinnati Research Council. He has served as an expert
witness in legal proceedings for the government.; T.L. serves on the
Laboratory Accreditation Board for Long Term (Epilepsy and Intensive
Care Unit) Monitoring, on the Council of the American Clinical
Neurophysiology Society, on the American Board of Clinical
Neurophysiology, as an Associate Editor for Seizure, and performs
video-electroencephalography long-term monitoring,
electroencephalography, and other electrophysiologic studies at Boston
Children's Hospital and bills for these procedures. T. L. receives
research support from the National Institutes of Health/NINDS, a Career
Development Fellowship Award from Harvard Medical School and Boston
Children's Hospital, the Program for Quality and Safety at Boston
Children's Hospital, the Payer Provider Quality Initiative, The Epilepsy
Foundation of America, the Center for Integration of Medicine and
Innovative Technology, the Epilepsy Therapy Project, the American
Epilepsy Society, Cure, and from investigator initiated research grants
from Lundbeck and Eisai.; C.D.H. is supported by research grants from
the Canadian Institutes of Health Research, PSI Foundation and SickKids
Foundation. L.J.H. has received research support for
investigator-initiated studies from UCB-Pharma, Upsher-Smith, and
Lundbeck; consultation fees for advising from Lundbeck, Upsher-Smith,
UCB-Pharma, and GlaxoSmithKline; and royalties for authoring chapters
for UpToDate-Neurology, and for co-authoring the book "Atlas of EEG in
Critical Care," by Hirsch and Brenner (2010). S. M. L. has received
research support from the National Institutes of Health/SBIR, and for
investigator-initiated studies from UCB Pharma. We confirm that we have
read the Journal's position on issues involved in ethical publication
and affirm that this report is consistent with those guidelines.
NR 27
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U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0013-9580
J9 EPILEPSIA
JI Epilepsia
PD AUG
PY 2013
VL 54
IS 8
BP 1498
EP 1503
DI 10.1111/epi.12247
PG 6
WC Clinical Neurology
SC Neurosciences & Neurology
GA 199KA
UT WOS:000322992200024
PM 23758557
ER
PT J
AU Zhou, T
Hasty, P
Walter, CA
Bishop, AJR
Scott, LM
Rebel, VI
AF Zhou, Ting
Hasty, Paul
Walter, Christi A.
Bishop, Alexander J. R.
Scott, Linda M.
Rebel, Vivienne I.
TI Myelodysplastic syndrome: An inability to appropriately respond to
damaged DNA?
SO EXPERIMENTAL HEMATOLOGY
LA English
DT Review
ID HEMATOPOIETIC STEM-CELLS; BASE EXCISION-REPAIR; ROTHMUND-THOMSON
SYNDROME; FLUDARABINE COMBINATION CHEMOTHERAPY; BONE-MARROW FAILURE;
FANCONI-ANEMIA; MYELOID-LEUKEMIA; MISMATCH REPAIR; MOUSE MODEL;
CHROMOSOMAL INSTABILITY
AB Myelodysplastic syndrome (MDS) is considered a hematopoietic stem cell disease that is characterized by abnormal hematopoietic differentiation and a high propensity to develop acute myeloid leukemia. It is mostly associated with advanced age, but also with prior cancer therapy and inherited syndromes related to abnormalities in DNA repair. Recent technologic advances have led to the identification of a myriad of frequently occurring genomic perturbations associated with MDS. These observations suggest that MDS and its progression to acute myeloid leukemia is a genomic instability disorder, resulting from a stepwise accumulation of genetic abnormalities. The notion is now emerging that the underlying mechanism of this disease could be a defect in one or more pathways that are involved in responding to or repairing damaged DNA. In this review, we discuss these pathways in relationship to a large number of studies performed with MDS patient samples and MDS mouse models. Moreover, in view of our current understanding of how DNA damage response and repair pathways are affected by age in hematopoietic stem cells, we also explore how this might relate to MDS development. (c) 2013 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc.
C1 [Zhou, Ting; Bishop, Alexander J. R.; Rebel, Vivienne I.] Univ Texas Hlth Sci Ctr San Antonio, Greehey Childrens Canc Res Inst, San Antonio, TX 78229 USA.
[Zhou, Ting; Walter, Christi A.; Bishop, Alexander J. R.; Rebel, Vivienne I.] Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA.
[Hasty, Paul] Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78229 USA.
[Hasty, Paul; Walter, Christi A.; Bishop, Alexander J. R.; Rebel, Vivienne I.] Univ Texas Hlth Sci Ctr San Antonio, Canc Therapy Res Ctr, San Antonio, TX 78229 USA.
[Hasty, Paul; Walter, Christi A.; Bishop, Alexander J. R.; Rebel, Vivienne I.] Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst Longev & Aging Studies, San Antonio, TX 78229 USA.
[Walter, Christi A.] South Texas Vet Hlth Care Syst, Audie Murphy Hosp, San Antonio, TX USA.
[Scott, Linda M.] Univ Queensland, Fac Hlth Sci, Diamantina Inst, Brisbane, Qld, Australia.
[Scott, Linda M.] Univ Queensland, Fac Hlth Sci, Sch Med, Brisbane, Qld, Australia.
RP Rebel, VI (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Greehey Childrens Canc Res Inst, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA.
EM rebel@uthscsa.edu
RI Scott, Linda/D-9777-2012
OI Scott, Linda/0000-0003-0334-1479
FU National Institute of Aging [5R21AG033339]; National Institute of
Environmental Health Sciences [1RO1ES022054]; Hyundai Hope on Wheels
FX This work was supported by the National Institute of Aging (grant
5R21AG033339 to V.I.R. and C.A.W.), the National Institute of
Environmental Health Sciences (grant 1RO1ES022054 to P.E.H. and V.I.R.),
and Hyundai Hope on Wheels (to A.J.R.B. and V.I.R.).
NR 108
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Z9 13
U1 0
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0301-472X
J9 EXP HEMATOL
JI Exp. Hematol.
PD AUG
PY 2013
VL 41
IS 8
BP 665
EP 674
DI 10.1016/j.exphem.2013.04.008
PG 10
WC Hematology; Medicine, Research & Experimental
SC Hematology; Research & Experimental Medicine
GA 199VX
UT WOS:000323024700001
PM 23643835
ER
PT J
AU Lynch, JA
Khoury, MJ
Borzecki, A
Cromwell, J
Hayman, LL
Ponte, PR
Miller, GA
Lathan, CS
AF Lynch, Julie A.
Khoury, Muin J.
Borzecki, Ann
Cromwell, Jerry
Hayman, Laura L.
Ponte, Pat Reid
Miller, Glenn A.
Lathan, Christopher S.
TI Utilization of epidermal growth factor receptor (EGFR) testing in the
United States: a case study of T3 translational research
SO GENETICS IN MEDICINE
LA English
DT Article
DE dissemination and implementation; EGFR assay; equity in access; lung
cancer genomics; T3 translation
ID CELL LUNG-CANCER; AFRICAN-AMERICANS; MUTATIONS; GEFITINIB; GENOMICS;
FREQUENCY; MEDICINE; SURGERY; RISK; CARE
AB Purpose: We examined hospital use of the epidermal growth factor receptor assay in patients with lung cancer in the United States. Our goal was to inform the development of a model to predict phase 3 translation of guideline-directed molecular diagnostic tests.
Methods: This was a retrospective observational study. Using logistic regression, we analyzed the association between hospitals' institutional and regional characteristics and the likelihood that an epidermal growth factor receptor assay would be ordered.
Results: Significant institutional predictors included affiliation with an academic medical center (odds ratio, 1.48; 95% confidence interval, 1.20-1.83), participation in a National Cancer Institute clinical research cooperative group (odds ratio, 2.06, 1.66-2.55), and availability of positron emission tomography scan (odds ratio, 1.44, 1.07-1.94) and cardiothoracic surgery (odds ratio, 1.90, 1.52-2.37) services. Significant regional predictors included metropolitan county (odds ratio, 2.08, 1.48-2.91), population with above-average education (odds ratio, 1.46, 1.09-1.96), and population with above-average income (odds ratio, 1.46, 1.04-2.05). Distance from a National Cancer Institute cancer center was a negative predictor (odds ratio, 0.996, 0.995-0.998), with a 34% decrease in likelihood for every 100 miles.
Conclusion: In 2010, only 12% of US acute-care hospitals ordered the epidermal growth factor receptor assay, suggesting that most patients with lung cancer did not have access to this test. This case study illustrated the need for: (i) increased dissemination and implementation research, and (ii) interventions to improve adoption of guideline-directed molecular diagnostic tests by community hospitals.
C1 [Lynch, Julie A.] Univ Massachusetts, Vet Hlth Adm, Boston, MA 02125 USA.
[Lynch, Julie A.; Ponte, Pat Reid; Lathan, Christopher S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Khoury, Muin J.] NCI, Off Publ Hlth Genom, CDC, Epidemiol & Genom Res Program, Bethesda, MD 20892 USA.
[Lynch, Julie A.; Borzecki, Ann] Vet Hlth Adm, Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA USA.
[Cromwell, Jerry; Hayman, Laura L.] Univ Massachusetts, Boston, MA 02125 USA.
[Cromwell, Jerry] Res Triangle Inst, Boston, MA USA.
[Miller, Glenn A.] Genzyme Genet, Santa Fe, NM USA.
RP Lynch, JA (reprint author), Univ Massachusetts, Vet Hlth Adm, Harbor Campusol, Boston, MA 02125 USA.
EM Julie.Lynch@va.gov
FU Center for Health Quality, Outcomes and Economic Research, a Veterans
Administration Health Services Research and Development Center of
Excellence; Department of Education GAANN [P200A060243]; National
Institute of Health [DFCI/UMB U54 CA156734-01]; Susan G. Komen
Foundation; Lynch Foundation
FX J.A.L. has received funding from the Center for Health Quality, Outcomes
and Economic Research, a Veterans Administration Health Services
Research and Development Center of Excellence; Department of Education
GAANN #P200A060243; National Institute of Health DFCI/UMB U54
CA156734-01, Susan G. Komen Foundation, and the Lynch Foundation.
Methodology and preliminary results were previously presented as a
poster at the 10th International Congress on Targeted Anticancer
Therapies, Amsterdam, 8-10 March 2012
NR 39
TC 13
Z9 13
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
J9 GENET MED
JI Genet. Med.
PD AUG
PY 2013
VL 15
IS 8
BP 630
EP 638
DI 10.1038/gim.2013.5
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 195NM
UT WOS:000322709800006
PM 23448725
ER
PT J
AU Maesta, I
Growdon, WB
Goldstein, DP
Bernstein, MR
Horowitz, NS
Rudge, MVC
Berkowitz, RS
AF Maesta, Izildinha
Growdon, Whitfield B.
Goldstein, Donald P.
Bernstein, Marilyn R.
Horowitz, Neil S.
Cunha Rudge, Marilza Vieira
Berkowitz, Ross S.
TI Prognostic factors associated with time to hCG remission in patients
with low-risk postmolar gestational trophoblastic neoplasia
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE Low-risk gestational trophoblastic neoplasia; hCG remission; Prognostic
factors; Chemotherapy
ID WEEKLY INTRAMUSCULAR METHOTREXATE; FOLINIC ACID; RETROSPECTIVE COHORT;
TREATMENT OUTCOMES; MOLAR PREGNANCY; PRIMARY THERAPY; ACTINOMYCIN-D;
DISEASE; MANAGEMENT; CHEMOTHERAPY
AB Objective. The purpose of this study was to identify the clinical factors associated with time to hCG remission among women with low-risk postmolar GTN.
Methods. This study included a non-concurrent cohort of 328 patients diagnosed with low-risk postmolar GTN according to FIGO 2002 criteria. Associations of time to hCG remission with history of prior mole, molar histology, time to persistence, use of D&C at persistence, presence of metastatic disease, FIGO score, hCG values at persistence, type of first line therapy and use of multiagent chemotherapy were investigated with both univariate and multivariate analyses.
Results. Overall median time to remission was 46 days. Ten percent of the patients required multi-agent chemotherapy to achieve hCG remission. Multivariate analysis incorporating the variables significant on univariate analysis confirmed that complete molar histology (HR 1.45), metastatic disease (HR 1.66), use of multi-agent therapy (HR 2.00) and FIGO score (HR 1.82) were associated with longer time to remission. There was a linear relationship between FIGO score and time to hCG remission. Each 1-point increment in FIGO score was associated with an average 17-day increase in hCG remission time (95% CI: 12.5-21.6).
Conclusions. Complete mole histology prior to GTN, presence of metastatic disease, use of multi-agent therapy and higher FIGO score were independent factors associated with longer time to hCG remission in low-risk GTN. Identifying the prognostic factors associated with time to remission and effective counseling may help improve treatment planning and reduce anxiety in patients and their families. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Maesta, Izildinha; Cunha Rudge, Marilza Vieira] Sao Paulo State Univ, UNESP, Botucatu Med Sch, Dept Gynecol & Obstet, Botucatu, SP, Brazil.
[Growdon, Whitfield B.] Massachusetts Gen Hosp, Div Gynecol Oncol, Dept Obstet & Gynaecol, Boston, MA 02114 USA.
[Goldstein, Donald P.; Bernstein, Marilyn R.; Horowitz, Neil S.; Berkowitz, Ross S.] Brigham & Womens Hosp, Div Gynecol Oncol, Dept Obstet & Gynaecol, Boston, MA 02115 USA.
[Goldstein, Donald P.; Bernstein, Marilyn R.; Horowitz, Neil S.; Berkowitz, Ross S.] Donald P Goldstein MD Tumor Registry, New England Trophoblast Dis Ctr, Boston, MA USA.
[Maesta, Izildinha; Cunha Rudge, Marilza Vieira] Sao Paulo State Univ, UNESP, Trophoblast Dis Ctr, Botucatu Med Sch, Botucatu, SP, Brazil.
[Growdon, Whitfield B.; Goldstein, Donald P.; Bernstein, Marilyn R.; Horowitz, Neil S.; Berkowitz, Ross S.] Harvard Canc Ctr, Dana Farber Canc Inst, Boston, MA USA.
[Growdon, Whitfield B.; Goldstein, Donald P.; Bernstein, Marilyn R.; Horowitz, Neil S.; Berkowitz, Ross S.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Berkowitz, RS (reprint author), ASBI, Brigham & Womens Hosp, Dept OBGYN, Div Gynecol Oncol, 75 Francis St, Boston, MA 02115 USA.
EM rberkowitz@partners.org
RI Rudge, Marilza /C-8338-2012
OI Rudge, Marilza /0000-0002-9227-832X
NR 33
TC 4
Z9 5
U1 1
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0090-8258
J9 GYNECOL ONCOL
JI Gynecol. Oncol.
PD AUG
PY 2013
VL 130
IS 2
BP 312
EP 316
DI 10.1016/j.ygyno.2013.05.017
PG 5
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 191KD
UT WOS:000322410900012
PM 23707672
ER
PT J
AU Hanna, J
Reimann, JDR
Haddad, RI
Krane, JF
AF Hanna, John
Reimann, Julie D. R.
Haddad, Robert I.
Krane, Jeffrey F.
TI Human papillomavirus-associated adenocarcinoma of the base of the tongue
SO HUMAN PATHOLOGY
LA English
DT Article
DE Human papillomavirus; Adenocarcinoma; Oropharynx; p16
ID SQUAMOUS-CELL CARCINOMA; OROPHARYNX; HEAD; CANCER; ENTITY
AB Human papillomavirus (HPV) is a major cause of oropharyngeal squamous cell carcinoma with characteristic clinical and pathologic features relative to their non-HPV-associated counterparts. Here we describe 2 cases of HPV-associated adenocarcinoma of the oropharynx. Both cases arose at the base of the tongue, and neither had the histologic or immunohistochemical features of a primary salivary gland tumor or metastasis from another location. One patient had metastases to neck lymph nodes and the lungs and died of disease 37 months after diagnosis. Evidence for an HPV association consisted of strong diffuse expression of p16, polyrnerase chain reaction-based detection of HPV16 DNA sequences, and localization of HPV by in situ hybridization within tumor cells of both primary and metastatic lesions. These results further expand the spectrum of HPV-associated head and neck malignancy. This rare entity should be distinguished from primary salivary gland adenocarcinoma and may be a candidate for HPV-specific targeted therapies. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Hanna, John; Reimann, Julie D. R.; Krane, Jeffrey F.] Harvard Univ, Sch Med, Dept Pathol, Brigham & Womens Hosp, Boston, MA 02115 USA.
[Haddad, Robert I.] Harvard Univ, Sch Med, Dept Med, Brigham & Womens Hosp, Boston, MA 02115 USA.
[Haddad, Robert I.] Harvard Univ, Sch Med, Dept Med Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Krane, JF (reprint author), Harvard Univ, Sch Med, Dept Pathol, Brigham & Womens Hosp, Boston, MA 02115 USA.
EM jkrane@partners.org
NR 12
TC 4
Z9 4
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 0046-8177
J9 HUM PATHOL
JI Hum. Pathol.
PD AUG
PY 2013
VL 44
IS 8
BP 1516
EP 1523
DI 10.1016/j.humpath.2012.12.004
PG 8
WC Pathology
SC Pathology
GA 191KX
UT WOS:000322413000009
PM 23465278
ER
PT J
AU Stirman, SW
Shields, N
Deloriea, J
Landy, MSH
Belus, JM
Maslej, MM
Monson, CM
AF Stirman, Shannon Wiltsey
Shields, Norman
Deloriea, Josh
Landy, Meredith S. H.
Belus, Jennifer M.
Maslej, Marta M.
Monson, Candice M.
TI A randomized controlled dismantling trial of post-workshop consultation
strategies to increase effectiveness and fidelity to an evidence-based
psychotherapy for Posttraumatic stress disorder
SO IMPLEMENTATION SCIENCE
LA English
DT Article
DE Training; Implementation; Consultation; Psychotherapy; PTSD; Cognitive
processing therapy
ID COGNITIVE-PROCESSING THERAPY; NATIONAL COMORBIDITY SURVEY;
MENTAL-HEALTH-SERVICES; VIETNAM VETERANS; PSYCHOLOGICAL TREATMENTS;
PSYCHOMETRIC PROPERTIES; BEHAVIOR PROBLEMS; PERCEIVED HEALTH;
DISSEMINATION; DEPRESSION
AB Background: Posttraumatic Stress Disorder (PTSD) is a serious mental health condition with substantial costs to individuals and society. Among military veterans, the lifetime prevalence of PTSD has been estimated to be as high as 20%. Numerous research studies have demonstrated that short-term cognitive-behavioral psychotherapies, such as Cognitive Processing Therapy (CPT), lead to substantial and sustained improvements in PTSD symptoms. Despite known benefits, only a minority of clinicians provide these therapies. Transferring this research knowledge into clinical settings remains one of the largest hurdles to improving the health of veterans with PTSD. Attending a workshop alone is insufficient to promote adequate knowledge transfer and sustained skill; however, relatively little research has been conducted to identify effective post-training support strategies.
Methods: The current study investigates whether clinicians receiving post-workshop support (six-month duration) will deliver CPT with greater fidelity (i.e., psychotherapy adherence and competence) and have improved patient outcomes compared with clinicians receiving no formal post-workshop support. The study conditions are: technology-enhanced group tele-consultation; standard group tele-consultation; and fidelity assessment with no consultation. The primary outcome is independent assessment (via audio-recordings) of the clinicians' adherence and competence in delivering CPT. The secondary outcome is observed changes in patient symptoms during and following treatment as a function of clinician fidelity. Post-consultation interviews with clinicians will help identify facilitators and barriers to psychotherapy skill acquisition. The study results will inform how best to implement and transfer evidence-based psychotherapy (e. g., CPT) to clinical settings to attain comparable outcomes to those observed in research settings.
Discussion: Findings will deepen our understanding of how much and what type of support is needed following a workshop to help clinicians become proficient in delivering a new protocol. Several influences on clinician learning and patient outcomes will be discussed. An evidence-based model of clinical consultation will be developed, with the ultimate goal of informing policy and influencing best practice in clinical consultation.
C1 [Stirman, Shannon Wiltsey] Boston Univ, VA Boston Healthcare Syst, Womens Hlth Sci Div, Natl Ctr PTSD, Boston, MA 02130 USA.
[Shields, Norman] Vet Affairs Canada, OSINN, Ste Anne De Bellevue, PQ H9X 1Y9, Canada.
[Deloriea, Josh; Landy, Meredith S. H.; Maslej, Marta M.; Monson, Candice M.] Ryerson Univ, Dept Psychol, Toronto, ON M5B 2K3, Canada.
[Belus, Jennifer M.] Univ N Carolina, Dept Psychol, Chapel Hill, NC 27599 USA.
RP Monson, CM (reprint author), Ryerson Univ, Dept Psychol, 350 Victoria St, Toronto, ON M5B 2K3, Canada.
EM candice.monson@psych.ryerson.ca
OI Wiltsey Stirman, Shannon/0000-0001-9917-5078
NR 71
TC 2
Z9 2
U1 3
U2 20
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1748-5908
J9 IMPLEMENT SCI
JI Implement. Sci.
PD AUG 1
PY 2013
VL 8
AR 82
DI 10.1186/1748-5908-8-82
PG 8
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 198ZW
UT WOS:000322964300001
ER
PT J
AU Psaltis, AJ
Schlosser, RJ
Yawn, JR
Henriquez, O
Mulligan, JK
AF Psaltis, Alkis J.
Schlosser, Rodney J.
Yawn, James R.
Henriquez, Oswaldo
Mulligan, Jennifer K.
TI Characterization of B-cell subpopulations in patients with chronic
rhinosinusitis
SO INTERNATIONAL FORUM OF ALLERGY & RHINOLOGY
LA English
DT Article
DE Chronic rhino sinusitis; B lymphocytes; B cells; plasma cells; Nasal
polyps; chronic inflammation; sinusitis
ID NASAL POLYPS
AB Background: Recent research suggest that B and plasma cells may play an important role in the pathogenesis of chronic rhinosinusitis with nasal polyposis (CRSwNP). The purpose of this study was to subcharacterize the B cell response in the sinus mucosa of control and CRS patients.
Methods: Representative tissue samples and peripheral blood samples were obtained from controls, CRS without nasal polyps (CRSsNP) and CRSwNP. Using single-cell suspension flow cytometry these samples were analyzed for overall and stage-specific B and plasma cell percentages.
Results: Both atopic and nonatopic CRSwNP patients showed an increase in local numbers of naive, active, and memory B cells compared to controls. CRSsNP patients only showed local elevations of naive B cells. Plasma cells were only significantly elevated in the sinus tissue of atopic CRSwNP patients. These local tissue increases did not correlate with increased numbers of circulating B cells.
Conclusion: This study provides further evidence of an important role of B cells in CRSwNP patients. The local increase appears to be independent of a systemic response. (C) 2013 ARS-AAOA, LLC.
C1 [Psaltis, Alkis J.; Schlosser, Rodney J.; Yawn, James R.; Henriquez, Oswaldo; Mulligan, Jennifer K.] Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, Charleston, SC 29425 USA.
[Schlosser, Rodney J.; Mulligan, Jennifer K.] Ralph H Johnson VA Med Ctr, Charleston, SC 29425 USA.
[Mulligan, Jennifer K.] Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA.
RP Psaltis, AJ (reprint author), Stanford Univ, Stanford Sch Med, Dept Otolaryngol Head & Neck Surg, 801 Welch Rd, Palo Alto, CA 94303 USA.
EM alkispsaltis@gmail.com
FU American Academy of Otolaryngic Allergy; Garnett Passe and Rodney
Williams Memorial Foundation; Department of Veterans Affairs; Flight
Attendant Medical Research Institutes
FX Funding sources for the study: American Academy of Otolaryngic Allergy
(to A.J.P.); Garnett Passe and Rodney Williams Memorial Foundation (to
A.J.P.); Department of Veterans Affairs (to R.J.S.); Flight Attendant
Medical Research Institutes (to J.K.M. and R.J.S.).
NR 23
TC 9
Z9 9
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2042-6976
J9 INT FORUM ALLERGY RH
JI Int. Forum Allergy Rhinol.
PD AUG
PY 2013
VL 3
IS 8
BP 621
EP 629
DI 10.1002/alr.21173
PG 9
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 201WE
UT WOS:000323172900004
PM 23640795
ER
PT J
AU Feldman, RE
Lam, AC
Sadow, PM
Bleier, BS
AF Feldman, Rachel E.
Lam, Allen C.
Sadow, Peter M.
Bleier, Benjamin S.
TI P-glycoprotein is a marker of tissue eosinophilia and radiographic
inflammation in chronic rhinosinusitis without nasal polyps
SO INTERNATIONAL FORUM OF ALLERGY & RHINOLOGY
LA English
DT Article
DE chronic sinusitis; nasal polyposis; P-glycoprotein; active efflux pumps;
inflammation; Th1; Th2; eosinophilia; eosinophilic chronic
rhinosinusitis; Lund-Mackay score
ID EPITHELIAL-CELLS
AB Background: P-glycoprotein (P-gp) is a membrane-bound efflux pump that is upregulated in chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) and participates in epithelial cytokine secretion. Eosinophilic CRS (ECRS) shares a similar cytokine profile with CRSwNP and is associated with significant inflammation and poor surgical outcomes. The goal of this study is to determine if P-gp expression is associated with degree of eosinophilia and severity of radiographic inflammation in patients with CRS without polyps (CRSsNP).
Methods: An institutional review board (IRB)-approved study using sinus tissue in 39 steroid-naive patients with CRS. P-gp expression was calculated using quantitative fluorescent immunohistochemistry (Q-FIHC) to generate an epithelial to background staining ratio. Patients were stratified into low and high epithelial expression groups (<3 and >= 3, respectively). Average eosinophils per high powered field (hpf) and Lund-Mackay scores were calculated and compared with P-gp staining ratios using a 2-tailed Student t test.
Results: Among the 39 patients, 7 (17.95%) had high P-gp expression ratios (mean +/- SD, 4.86 +/- 1.33) while 32 (82.05%) had low expression ratios (1.91 +/- 0.45). The number of eosinophils/hpf were significantly greater in the high P-gp expression group as compared to the low expression group (62.38 +/- 83.69 vs 5.11 +/- 10.12, p = 0.0003). The Lund-Mackay scores were significantly greater in the high P-gp expression group as compared to the low expression group (11.86 +/- 2.79 vs 6.84 +/- 4.19, p = 0.005).
Conclusion: P-gp is known to be overexpressed in CRSwNP. This study suggests that among patients with CRSsNP, P-gp is similarly overexpressed in those with high tissue eosinophilia and correlates with severity of radiographic inflammation. (C) 2013 The Authors. International Forum of Allergy & Rhinology, published by Wiley Periodicals, Inc., on behalf of ARS-AAOA, LLC.
C1 [Feldman, Rachel E.; Lam, Allen C.; Bleier, Benjamin S.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otol & Laryngol, Boston, MA 02114 USA.
[Sadow, Peter M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA 02114 USA.
RP Bleier, BS (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Otol & Laryngol, 243 Charles St, Boston, MA 02114 USA.
EM bleierb@gmail.com
NR 15
TC 12
Z9 13
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2042-6976
J9 INT FORUM ALLERGY RH
JI Int. Forum Allergy Rhinol.
PD AUG
PY 2013
VL 3
IS 8
BP 684
EP 687
DI 10.1002/alr.21176
PG 4
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 201WE
UT WOS:000323172900014
PM 23677641
ER
PT J
AU Lochhead, P
Kuchiba, A
Imamura, Y
Liao, XY
Yamauchi, M
Nishihara, R
Qian, ZR
Morikawa, T
Shen, JN
Meyerhardt, JA
Fuchs, CS
Ogino, S
AF Lochhead, Paul
Kuchiba, Aya
Imamura, Yu
Liao, Xiaoyun
Yamauchi, Mai
Nishihara, Reiko
Qian, Zhi Rong
Morikawa, Teppei
Shen, Jeanne
Meyerhardt, Jeffrey A.
Fuchs, Charles S.
Ogino, Shuji
TI Microsatellite Instability and BRAF Mutation Testing in Colorectal
Cancer Prognostication
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID ISLAND METHYLATOR PHENOTYPE; III COLON-CANCER; MOLECULAR PATHOLOGICAL
EPIDEMIOLOGY; DEFECTIVE MISMATCH REPAIR; FATTY-ACID SYNTHASE; BODY-MASS
INDEX; STAGE-II; ADJUVANT THERAPY; KRAS MUTATION; PERSONALIZED MEDICINE
AB BRAF mutation in colorectal cancer is associated with microsatellite instability (MSI) through its relationship with high-level CpG island methylator phenotype (CIMP) and MLH1 promoter methylation. MSI and BRAF mutation analyses are routinely used for familial cancer risk assessment. To clarify clinical outcome associations of combined MSI/BRAF subgroups, we investigated survival in 1253 rectal and colon cancer patients within the Nurses Health Study and Health Professionals Follow-up Study with available data on clinical and other molecular features, including CIMP, LINE-1 hypomethylation, and KRAS and PIK3CA mutations. Compared with the majority subtype of microsatellite stable (MSS)/BRAFwild-type, MSS/BRAF-mutant, MSI-high/BRAF-mutant, and MSI-high/BRAFwild-type subtypes showed multivariable colorectal cancer-specific mortality hazard ratios of 1.60 (95% confidence interval [CI] 1.12 to 2.28; P .009), 0.48 (95% CI 0.27 to 0.87; P .02), and 0.25 (95% CI 0.12 to 0.52; P < .001), respectively. No evidence existed for a differential prognostic role of BRAF mutation by MSI status (P-interaction > .50). Combined BRAF/MSI status in colorectal cancer is a tumor molecular biomarker for prognosic risk stratification.
C1 [Lochhead, Paul; Kuchiba, Aya; Imamura, Yu; Liao, Xiaoyun; Yamauchi, Mai; Nishihara, Reiko; Qian, Zhi Rong; Morikawa, Teppei; Meyerhardt, Jeffrey A.; Fuchs, Charles S.; Ogino, Shuji] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Lochhead, Paul; Kuchiba, Aya; Imamura, Yu; Liao, Xiaoyun; Yamauchi, Mai; Nishihara, Reiko; Qian, Zhi Rong; Morikawa, Teppei; Meyerhardt, Jeffrey A.; Fuchs, Charles S.; Ogino, Shuji] Harvard Univ, Sch Med, Boston, MA 02215 USA.
[Lochhead, Paul] Univ Aberdeen, Inst Med Sci, Aberdeen, Scotland.
[Shen, Jeanne; Ogino, Shuji] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Fuchs, Charles S.] Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.
[Ogino, Shuji] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02215 USA.
RP Ogino, S (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave,Rm M422, Boston, MA 02215 USA.
EM shuji_ogino@dfci.harvard.edu
OI Qian, Zhi rong/0000-0003-1633-4120
FU US National Institutes of Health [P01 CA87969, P01 CA55075, UM1
CA167552, P50 CA127003, R01 CA151993]; Bennett Family Fund;
Entertainment Industry Foundation through the National Colorectal Cancer
Research Alliance; Frank Knox Memorial Fellowship at Harvard University;
Chief Scientist Office of the Scottish Government; Japan Society for
Promotion of Science
FX This work was supported by the US National Institutes of Health (P01
CA87969 to S. E. Hankinson; P01 CA55075 and UM1 CA167552 to W. C.
Willett; P50 CA127003 to CSF; and R01 CA151993 to SO); by the Bennett
Family Fund and the Entertainment Industry Foundation through the
National Colorectal Cancer Research Alliance; by the Frank Knox Memorial
Fellowship at Harvard University (to PL); by a fellowship from the Chief
Scientist Office of the Scottish Government (to PL); and by a fellowship
from the Japan Society for Promotion of Science (to TM).
NR 79
TC 133
Z9 133
U1 1
U2 25
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD AUG
PY 2013
VL 105
IS 15
BP 1151
EP 1156
DI 10.1093/jnci/djt173
PG 6
WC Oncology
SC Oncology
GA 199DZ
UT WOS:000322976000013
PM 23878352
ER
PT J
AU Bodenlos, JS
Noonan, M
Wells, SY
AF Bodenlos, Jamie S.
Noonan, Marleah
Wells, Stephanie Y.
TI Mindfulness and Alcohol Problems in College Students: The Mediating
Effects of Stress
SO JOURNAL OF AMERICAN COLLEGE HEALTH
LA English
DT Article
DE alcohol; college; mental health; mindfulness; stress
ID SUBSTANCE USE DISORDERS; PERCEIVED STRESS; RELAPSE PREVENTION; ACADEMIC
STRESS; REDUCTION MBSR; 1ST YEAR; MEDITATION; SYMPTOMS; DRINKING;
DISTRESS
AB Objective: To examine the relationship between mindfulness and alcohol problems in college students, as well as the role of stress as a mediator in this relationship. Participants: Participants were 310 students from a small, private college in the Northeast. Methods: Students completed self-report measures, including the Perceived Stress Scale, the Five Facet Mindfulness Questionnaire, and the Rutgers Alcohol Problems Index. Results: Mindfulness was negatively correlated with alcohol problems and stress, whereas stress positively correlated with alcohol problems. Results implicated stress as fully mediating the relationship between mindfulness and alcohol problems. Alcohol problems were negatively correlated with the Acting With Awareness and Describing Experience facets of mindfulness. Conclusion: Mindfulness-based stress reduction or other mindfulness programs may be useful in decreasing alcohol problems on college campuses via the effects on stress.
C1 [Bodenlos, Jamie S.] Hobart & William Smith Coll, Dept Psychol, Geneva, NY 14456 USA.
[Noonan, Marleah] Boston Coll, Counseling Dev & Educ Psychol Dept, Lynch Sch Educ, Boston, MA USA.
[Wells, Stephanie Y.] Natl Ctr PTSD, Womens Hlth Sci Div, Boston, MA USA.
RP Bodenlos, JS (reprint author), Hobart & William Smith Coll, Dept Psychol, 217 Gulick Hall, Geneva, NY 14456 USA.
EM bodenlos@hws.edu
NR 62
TC 9
Z9 10
U1 4
U2 52
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 0744-8481
J9 J AM COLL HEALTH
JI J. Am. Coll. Health
PD AUG 1
PY 2013
VL 61
IS 6
BP 371
EP 378
DI 10.1080/07448481.2013.805714
PG 8
WC Education & Educational Research; Public, Environmental & Occupational
Health
SC Education & Educational Research; Public, Environmental & Occupational
Health
GA 197PR
UT WOS:000322863600006
PM 23930751
ER
PT J
AU Jibodh, SR
Schwarzkopf, R
Anthony, SG
Malchau, H
Dempsey, KE
Estok, DM
AF Jibodh, Stefan R.
Schwarzkopf, Ran
Anthony, Shawn G.
Malchau, Henrik
Dempsey, Kyle E.
Estok, Daniel M., II
TI Revision Hip Arthroplasty with A Modular Cementless Stem: Mid-Term
Follow Up
SO JOURNAL OF ARTHROPLASTY
LA English
DT Article
DE revision hip arthroplasty; modular femoral stems; cementless femoral
stems; fully coated femoral stems
ID EXTENDED TROCHANTERIC OSTEOTOMY; POROUS-COATED STEMS; PROXIMAL BONE
LOSS; FEMORAL COMPONENT; UNITED-STATES; RADIOGRAPHIC ANALYSIS; KNEE
ARTHROPLASTY; FIXATION; REPLACEMENT; DISLOCATION
AB Despite the increasing volume of revision total hip arthroplasty (THA) being performed in the United States, there are few studies reporting mid-term clinical and radiographic outcomes of modular fully porous-coated femoral stems. We retrospectively studied a consecutive series of patients who underwent revision THA with a modular extensively porous-coated femoral component at a single institution and by a single surgeon. The final study group included 54 hips (52 patients) followed for an average of 84months. Ten-year survival rates with revision for any reason and revision for femoral loosening as endpoints were 94% and 100%, respectively. No complications regarding the modular junction were encountered. Of the 50 hips with adequate radiographs, all showed proximal ingrowth and 42 (84%) had both proximal and distal ingrowth. The modular, fully porous-coated femoral stem studied demonstrated excellent survivorship and bone ingrowth at mid-term follow up. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Jibodh, Stefan R.] Kaiser Permanente Walnut Creek, Dept Orthopaed Surg, Walnut Creek, CA USA.
[Schwarzkopf, Ran; Dempsey, Kyle E.; Estok, Daniel M., II] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Orthopaed Surg, Boston, MA 02115 USA.
[Anthony, Shawn G.; Malchau, Henrik] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Orthopaed Surg,Harris Orthopaed Biomech & Bi, Boston, MA USA.
RP Jibodh, SR (reprint author), 1425 South Main St, Walnut Creek, CA 94596 USA.
OI Malchau, Henrik/0000-0002-4291-2441
NR 51
TC 9
Z9 10
U1 1
U2 3
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 2013
VL 28
IS 7
BP 1167
EP 1172
DI 10.1016/j.arth.2012.07.031
PG 6
WC Orthopedics
SC Orthopedics
GA 198LN
UT WOS:000322924500023
PM 23114191
ER
PT J
AU CorveraTindel, T
Doering, LV
AF CorveraTindel, Teresita
Doering, Lynn V.
TI Social Connections and Depressive Symptoms in Heart Failure
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 17th Annual Scientific Meeting of the Heart-Failure-Society-of-America
(HFSA)
CY SEP 22-25, 2013
CL Orlando, FL
SP Heart Failure Soc Amer (HFSA)
C1 [CorveraTindel, Teresita] VA Greater Los Angeles Hlth Care Syst, Los Angeles, CA USA.
[Doering, Lynn V.] Univ Calif Los Angeles, Los Angeles, CA 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 2013
VL 19
IS 8
SU 1
MA 014
BP S6
EP S6
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 201LG
UT WOS:000323142500015
ER
PT J
AU Kashyap, A
Dezellem, S
Vardeny, O
AF Kashyap, Anita
Dezellem, Sheryl
Vardeny, Orly
TI A Retrospective Evaluation of Spironolactone Versus Eplerenone on
Potassium Homeostasis and Renal Function
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 17th Annual Scientific Meeting of the Heart-Failure-Society-of-America
(HFSA)
CY SEP 22-25, 2013
CL Orlando, FL
SP Heart Failure Soc Amer (HFSA)
C1 [Kashyap, Anita; Dezellem, Sheryl] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
[Vardeny, Orly] Univ Wisconsin, Madison, WI USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
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 2013
VL 19
IS 8
SU 1
MA 077
BP S28
EP S28
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 201LG
UT WOS:000323142500077
ER
PT J
AU Niehaus, ED
Malhotra, R
Cocca-Spofford, D
Lewis, GD
AF Niehaus, Emily D.
Malhotra, Rajeev
Cocca-Spofford, Diane
Lewis, Gregory D.
TI Repletion of Iron Stores in Patients with Systolic Heart Failure Using
Oral Iron Supplementation
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Meeting Abstract
CT 17th Annual Scientific Meeting of the Heart-Failure-Society-of-America
(HFSA)
CY SEP 22-25, 2013
CL Orlando, FL
SP Heart Failure Soc Amer (HFSA)
C1 [Niehaus, Emily D.; Malhotra, Rajeev; Cocca-Spofford, Diane; Lewis, Gregory D.] Massachusetts Gen Hosp, Boston, MA 02114 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 2013
VL 19
IS 8
SU 1
MA 239
BP S83
EP S83
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 201LG
UT WOS:000323142500241
ER
PT J
AU Vigersky, RA
Bhasin, S
Martin, KA
AF Vigersky, Robert A.
Bhasin, Shalender
Martin, Kathryn A.
TI The Endocrine Society Clinical Practice Guidelines: A Self-Assessment
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Editorial Material
ID TYPE-2 DIABETES-MELLITUS; RECOMMENDATIONS; DEFICIENCY; DIAGNOSIS;
STRENGTH; PREVENTION; QUALITY
C1 [Vigersky, Robert A.] Walter Reed Natl Mil Med Ctr, Bethesda, MD 20889 USA.
[Bhasin, Shalender] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Martin, Kathryn A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Vigersky, RA (reprint author), Walter Reed Natl Mil Med Ctr, Endocrinol & Diabet Serv, 8901 Wisconsin Ave, Bethesda, MD 20889 USA.
EM robert.vigersky@us.army.mil
NR 20
TC 0
Z9 0
U1 0
U2 0
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD AUG
PY 2013
VL 98
IS 8
BP 3174
EP 3177
DI 10.1210/jc.2013-2300
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 196NC
UT WOS:000322781300032
PM 23801367
ER
PT J
AU Gupta, A
Ly, S
Castroneves, LA
Frates, MC
Benson, CB
Feldman, HA
Wassner, AJ
Smith, JR
Marqusee, E
Alexander, EK
Barletta, J
Doubilet, PM
Peters, HE
Webb, S
Modi, BP
Paltiel, HJ
Kozakewich, H
Cibas, ES
Moore, FD
Shamberger, RC
Larsen, PR
Huang, SA
AF Gupta, Anjuli
Ly, Samantha
Castroneves, Luciana A.
Frates, Mary C.
Benson, Carol B.
Feldman, Henry A.
Wassner, Ari J.
Smith, Jessica R.
Marqusee, Ellen
Alexander, Erik K.
Barletta, Justine
Doubilet, Peter M.
Peters, Hope E.
Webb, Susan
Modi, Biren P.
Paltiel, Harriet J.
Kozakewich, Harry
Cibas, Edmund S.
Moore, Francis D., Jr.
Shamberger, Robert C.
Larsen, P. Reed
Huang, Stephen A.
TI A Standardized Assessment of Thyroid Nodules in Children Confirms Higher
Cancer Prevalence Than in Adults
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID FINE-NEEDLE-ASPIRATION; 4 CM; MANAGEMENT; ADOLESCENTS; CYTOLOGY;
SURGERY; BIOPSY; EXPERIENCE; CHILDHOOD; DIAGNOSIS
AB Context: Thyroid cancer is the most common endocrine malignancy, but due to its rare occurrence in the pediatric population, the cancer risk of childhood thyroid nodules is incompletely defined, and optimal management of children with suspected nodules is debated.
Objective: The aim was to study the presenting features and cancer risk of sporadic childhood thyroid nodules using a standardized clinical assessment and management plan.
Design and Setting: Boston Children's Hospital and Brigham and Women's Hospital collaborated to create a multidisciplinary pediatric thyroid nodule clinic and implement a standardized assessment plan. Upon referral for a suspected nodule, serum TSH was measured and hypothyrotropinemic patients underwent I-123 scintigraphy. All others underwent thyroid ultrasonography, and if this confirmed nodule(s) >= 1 cm, ultrasound-guided fine-needle aspiration was performed. Medical records were retrospectively reviewed and compared to a control population of 2582 adults evaluated by identical methods.
Patients and Results: Of 300 consecutive children referred for the initial evaluation of suspected thyroid nodules from 1997 to 2011, 17 were diagnosed with autonomous nodules by scintigraphy. Neck ultrasonography performed in the remainder revealed that biopsy was unnecessary in over half, either by documenting only sub-centimeter nodules or showing that no nodule was present. A total of 125 children met criteria for thyroid biopsy, which was performed without complication. Their rate of cancer was 22%, significantly higher than the adult rate of 14% (P = .02).
Conclusions: Neck ultrasonography and biopsy were key to the evaluation of children with suspected thyroid nodules. Although the relative cancer prevalence of sonographically confirmed nodules >= 1 cm is higher in pediatric patients than adults, most children referred for suspected nodules have benign conditions, and efforts to avoid unnecessary surgery in this majority are warranted.
C1 [Gupta, Anjuli; Ly, Samantha; Castroneves, Luciana A.; Feldman, Henry A.; Wassner, Ari J.; Smith, Jessica R.; Webb, Susan; Huang, Stephen A.] Boston Childrens Hosp, Thyroid Program, Div Endocrinol, Boston, MA 02115 USA.
[Feldman, Henry A.] Boston Childrens Hosp, Clin Res Ctr, Boston, MA 02115 USA.
[Paltiel, Harriet J.] Boston Childrens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Kozakewich, Harry] Boston Childrens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Modi, Biren P.; Shamberger, Robert C.] Boston Childrens Hosp, Dept Surg, Boston, MA 02115 USA.
[Wassner, Ari J.; Smith, Jessica R.; Marqusee, Ellen; Alexander, Erik K.; Larsen, P. Reed; Huang, Stephen A.] Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Thyroid Sect, Boston, MA 02115 USA.
[Frates, Mary C.; Benson, Carol B.; Doubilet, Peter M.; Peters, Hope E.] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Barletta, Justine; Cibas, Edmund S.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Moore, Francis D., Jr.] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Marqusee, Ellen; Alexander, Erik K.; Larsen, P. Reed; Huang, Stephen A.] Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Huang, SA (reprint author), Boston Childrens Hosp, 300 Longwood Ave, Boston, MA 02115 USA.
EM stephen.huang@childrens.harvard.edu
OI Wassner, Ari/0000-0003-0894-9301
FU Murray Family; National Institutes of Health [DK076099, DK007699,
DK007529]
FX This work was supported by a donation from the Murray Family and by
grants DK076099, DK007699 and DK007529 from the National Institutes of
Health.
NR 35
TC 43
Z9 44
U1 1
U2 9
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 2013
VL 98
IS 8
BP 3238
EP 3245
DI 10.1210/jc.2013-1796
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 196NC
UT WOS:000322781300040
PM 23737541
ER
PT J
AU Jovanovich, A
Buzkova, P
Chonchol, M
Robbins, J
Fink, HA
de Boer, IH
Kestenbaum, B
Katz, R
Carbone, L
Lee, J
Laughlin, GA
Mukamal, KJ
Fried, LF
Shlipak, MG
Ix, JH
AF Jovanovich, Anna
Buzkova, Petra
Chonchol, Michel
Robbins, John
Fink, Howard A.
de Boer, Ian H.
Kestenbaum, Bryan
Katz, Ronit
Carbone, Laura
Lee, Jennifer
Laughlin, Gail A.
Mukamal, Kenneth J.
Fried, Linda F.
Shlipak, Michael G.
Ix, Joachim H.
TI Fibroblast Growth Factor 23, Bone Mineral Density, and Risk of Hip
Fracture Among Older Adults: The Cardiovascular Health Study
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; PHOSPHATE HOMEOSTASIS; CYSTATIN-C; FGF-23;
FIBROBLAST-GROWTH-FACTOR-23; OSTEOMALACIA; OSTEOPOROSIS; HEMODIALYSIS;
ASSOCIATION; MORTALITY
AB Context: Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone that also inhibits calcitriol synthesis.
Objective: Our objective was to evaluate the relationships of plasma FGF23 concentrations with bone mineral density (BMD) and hip fracture in community-dwelling older adults.
Design and Setting: Linear regression and Cox proportional hazard models were used to examine the associations of plasma FGF23 concentrations with BMD and incident hip fracture, respectively. Analyses were also stratified by chronic kidney disease.
Participants: Participants included 2008 women and 1329 men >= 65 years from the 1996 to 1997 Cardiovascular Health Study visit.
Main Outcome Measures: Dual x-ray absorptiometry measured total hip (TH) and lumbar spine (LS) BMD in 1291 participants. Hip fracture incidence was assessed prospectively through June 30, 2008 by hospitalization records in all participants.
Results: Women had higher plasma FGF23 concentrations than men (75 [56-107] vs 66 [interquartile range = 52-92] relative units/mL; P < .001). After adjustment, higher FGF23 concentrations were associated with greater total hip and lumbar spine BMD in men only (beta per doubling of FGF23 = 0.02, with 95% confidence interval [CI] = 0.001-0.04 g/cm(2), and 0.03 with 95% CI = 0.01-0.06 g/cm(2)). During 9.6 +/- 5.1-11.0 years of follow-up, 328 hip fractures occurred. Higher FGF23 concentrations were not associated with hip fracture risk in women or men(adjusted hazard ratio = 0.95, with 95% CI = 0.78-1.15, and 1.09 with 95% CI = 0.82-1.46 per doubling of FGF23). Results did not differ by chronic kidney disease status (P > .4 for interactions).
Conclusions: In this large prospective cohort of community-dwelling older adults, higher FGF23 concentrations were weakly associated with greater lumbar spine and total hip BMD but not with hip fracture risk.
C1 [Jovanovich, Anna; Chonchol, Michel] Univ Colorado, Sch Med, Div Renal Dis & Hypertens, Aurora, CO 80045 USA.
[Buzkova, Petra; Katz, Ronit] Univ Washington, Collaborat Hlth Studies Coordinating Ctr, Seattle, WA 98105 USA.
[de Boer, Ian H.; Kestenbaum, Bryan] Univ Washington, Div Nephrol, Seattle, WA 98105 USA.
[de Boer, Ian H.; Kestenbaum, Bryan] Univ Washington, Kidney Res Inst, Seattle, WA 98105 USA.
[Robbins, John] Univ Calif Davis, Sacramento, CA 95817 USA.
[Fink, Howard A.] Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Minneapolis, MN 55417 USA.
[Carbone, Laura] Dept Vet Affairs Med Ctr, Memphis, TN 38104 USA.
[Lee, Jennifer] Calif Pacific Med Ctr, San Francisco Coordinating Ctr, Res Inst, San Francisco, CA 94115 USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Fried, Linda F.] Univ Pittsburgh, Sch Med, Vet Affairs Pittsburgh Healthcare Syst, Pittsburgh, PA 15261 USA.
[Shlipak, Michael G.] Univ Calif San Francisco, Vet Adm Med Ctr, Gen Internal Med Sect, San Francisco, CA 94121 USA.
[Ix, Joachim H.] Vet Affairs San Diego Healthcare Syst, Nephrol Sect, San Diego, CA 92161 USA.
[Laughlin, Gail A.] Univ Calif San Diego, Div Epidemiol, Dept Family & Prevent Med, San Diego, CA 92093 USA.
[Ix, Joachim H.] Univ Calif San Diego, Div Nephrol & Hypertens, Dept Med, San Diego, CA 92093 USA.
[Ix, Joachim H.] Univ Calif San Diego, Div Prevent, Dept Family & Prevent Med, San Diego, CA 92093 USA.
[Ix, Joachim H.] Univ Calif San Diego, Div Prevent, Dept Med, San Diego, CA 92093 USA.
RP Ix, JH (reprint author), Univ Calif San Diego, Div Nephrol & Hypertens, Dept Med, 3350 La Jolla Village Dr,Mail Code 111-H, San Diego, CA 92161 USA.
EM joeix@ucsd.edu
FU National Heart, Lung, and Blood Institute (NHLBI) [R01HL096851];
American Heart Association [0575021N]; NHLBI [U01 HL080295];
[HHSN268201200036C]; [N01 HC-85079]; [N01HC-85086]; [N01-HC-35129];
[N01 HC-15103]; [N01 HC-55222]; [N01 HC-75150]; [N01 HC-54133];
[N01-HC-80007]
FX This work was supported by grants from the National Heart, Lung, and
Blood Institute (NHLBI) (R01HL096851) and American Heart Association
(0575021N) to J.H.I. Additionally, this paper was supported in part with
resources of the Veterans Affairs San Diego Healthcare System. The
Cardiovascular Health Study was supported by contract numbers
HHSN268201200036C, N01 HC-85079 through N01HC-85086, N01-HC-35129, N01
HC-15103, N01 HC-55222, N01 HC-75150, N01 HC-54133, and N01-HC-80007 and
Grant U01 HL080295 from the NHLBI, with additional contributions from
the National Institute of Neurological Disorders and Stroke.
NR 31
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U1 2
U2 24
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 2013
VL 98
IS 8
BP 3323
EP 3331
DI 10.1210/jc.2013-1152
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 196NC
UT WOS:000322781300050
PM 23771921
ER
PT J
AU Rogg, J
Hoffmann, U
Truong, Q
Brown, DFM
Parry, B
Nagurney, JT
AF Rogg, Jonathan
Hoffmann, Udo
Quynh Truong
Brown, David F. M.
Parry, Blair
Nagurney, John T.
TI EVALUATION OF RENAL FUNCTION TESTS BY AGE AND SEX TO DETERMINE EMERGENCY
DEPARTMENT PATIENTS' ELIGIBILITY FOR CARDIAC COMPUTED TOMOGRAPHY
SO JOURNAL OF EMERGENCY MEDICINE
LA English
DT Article
DE cardiology; cardiac CT; CCTA; contrast-induced nephropathy; ACS; chest
pain
ID CONTRAST-INDUCED NEPHROPATHY; PERCUTANEOUS CORONARY INTERVENTION;
GLOMERULAR-FILTRATION-RATE; SERUM CREATININE; KIDNEY-FUNCTION;
RISK-FACTORS; ENHANCED CT; INSUFFICIENCY; NEPHROTOXICITY; ANGIOGRAPHY
AB Background: Coronary computed tomography angiography (CCTA) can be used for low-risk chest pain patients, but presents a risk of contrast-induced nephropathy. Objective: We compared, by age and sex, the percent of patients who would become ineligible for CCTA based on serum creatinine (SCr) and glomerular filtration rate (GFR) cutoff points. Methods: All adult patients who presented to the Emergency Department (ED) with chest pain were screened using their first ED SCr as part of the ROMICAT (Rule Out Myocardial Infarction Using Computer Assisted Tomography) study. This was a secondary analysis of the screening logs of that study. The Modification of Diet in Renal Disease formula was applied to calculate estimated GFR and the percent of patients, by age and sex, meeting commonly applied exclusion criteria using selected SCr and GFR cutoff values. This was our primary outcome. Results: Of 2398 patients screened, 384 (16%) were excluded for high-risk features or technical limitations of CCTA, leaving 2014 patients who were studied; 56% were male. For all cutoff points of SCr (>= 1.3 mg/dL, >= 1.5 mg/dL, >= 1.8 mg/dL), the percent of males excluded significantly exceeded that of females (p < 0.0001 [28.6% males to 18.5% females]; p < 0.0001 [17.4% males to 11.2% females]; p = 0.0004 [10.1% males to 5.8% females], respectively). Conversely, for two of the three cutoff points of GFR (<= 60 mL/min/1.73 m(2) and <= 45 mL/min/1.73 m(2)), the percent of females excluded significantly exceeded that of males (p < 0.0001 [33.6% females to 25.4% males] and p = 0.0015 [17.6% males to 12.5% females], respectively). Conclusions: The choice of SCr or GFR to screen patients for CCTA selectively excludes either males or females, respectively. Therefore, individual physicians and institutions must understand the impact of both renal function tests and cutoff points when identifying patients who may be eligible for CCTA. (C) 2013 Elsevier Inc.
C1 [Rogg, Jonathan] Brigham & Womens Hosp, Massachusetts Gen Hosp, Harvard Affiliated Emergency Med Residency, Boston, MA 02115 USA.
[Hoffmann, Udo; Quynh Truong] Massachusetts Gen Hosp, Dept Radiol, Div Cardiac Imaging, Boston, MA 02114 USA.
[Brown, David F. M.; Parry, Blair; Nagurney, John T.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
RP Nagurney, JT (reprint author), Massachusetts Gen Hosp, Emergency Serv 3B, Zero Emerson Pl, Boston, MA 02114 USA.
NR 28
TC 1
Z9 1
U1 0
U2 9
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 2013
VL 45
IS 2
BP 220
EP 226
DI 10.1016/j.jemermed.2013.03.026
PG 7
WC Emergency Medicine
SC Emergency Medicine
GA 201UL
UT WOS:000323168400020
PM 23735846
ER
PT J
AU Maldonado, NG
Nadel, ES
Brown, DFM
AF Maldonado, Nicholas G.
Nadel, Eric S.
Brown, David F. M.
TI LEFT LOWER EXTREMITY PAIN AND SWELLING
SO JOURNAL OF EMERGENCY MEDICINE
LA English
DT Article
ID PHLEGMASIA-CERULEA-DOLENS; ILIAC VEIN COMPRESSION; MAY-THURNER-SYNDROME;
DEEP VENOUS THROMBOSIS; DIAGNOSIS; (MAY-THURNER)-SYNDROME; VENOGRAPHY;
PATIENT
C1 [Maldonado, Nicholas G.; Nadel, Eric S.; Brown, David F. M.] Harvard Univ, Sch Med, Div Emergency Med, Boston, MA USA.
[Nadel, Eric S.; Brown, David F. M.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Nadel, Eric S.] Brigham & Womens Hosp, Dept Emergency Med, Boston, MA 02115 USA.
RP Brown, DFM (reprint author), Massachusetts Gen Hosp, Dept Emergency Med, 55 Fruit St,Founders 114, Boston, MA 02114 USA.
NR 31
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0736-4679
J9 J EMERG MED
JI J. Emerg. Med.
PD AUG
PY 2013
VL 45
IS 2
BP 244
EP 251
PG 8
WC Emergency Medicine
SC Emergency Medicine
GA 201UL
UT WOS:000323168400025
PM 23786778
ER
PT J
AU Nowak, R
Farrar, JR
Brenner, BE
Lewis, L
Silverman, RA
Emerman, C
Hays, DP
Russell, WS
Schmitz, N
Miller, J
Singer, E
Camargo, CA
Wood, J
AF Nowak, Richard
Farrar, Judith Rosen
Brenner, Barry E.
Lewis, Lawrence
Silverman, Robert A.
Emerman, Charles
Hays, Daniel P.
Russell, W. Scott
Schmitz, Natalie
Miller, Judi
Singer, Ethan
Camargo, Carlos A., Jr.
Wood, Joseph
TI CUSTOMIZING ANAPHYLAXIS GUIDELINES FOR EMERGENCY MEDICINE
SO JOURNAL OF EMERGENCY MEDICINE
LA English
DT Review
DE anaphylaxis; guidelines; epinephrine (adrenaline); allergic reaction;
life-threatening reaction
ID SELF-INJECTABLE EPINEPHRINE; WORLD ALLERGY ORGANIZATION; DEPARTMENT
PATIENTS; NATIONAL INSTITUTE; MANAGEMENT; EPIDEMIOLOGY; DEFINITION;
CHILDREN; VISITS; MULTICENTER
AB Background: Most episodes of anaphylaxis are managed in emergency medical settings, where the cardinal signs and symptoms often differ from those observed in the allergy clinic. Data suggest that low recognition of anaphylaxis in the emergency setting may relate to inaccurate coding and lack of a standard, practical definition. Objective: Develop a simple, consistent definition of anaphylaxis for emergency medicine providers, supported by clinically relevant consensus statements. Discussion: Definitions of anaphylaxis and criteria for diagnosis from current anaphylaxis guidelines were reviewed with regard to their utilization in emergency medical settings. The agreed-upon working definition is: Anaphylaxis is a serious reaction causing a combination of characteristic findings, and which is rapid in onset and may cause death. It is usually due to an allergic reaction but can be non-allergic. The definition is supported by Consensus Statements, each with referenced discussion. For a positive outcome, quick diagnosis and treatment of anaphylaxis are critical. However, even in the emergency setting, the patient may not present with life-threatening symptoms. Because mild initial symptoms can quickly progress to a severe, even fatal, reaction, the first-line treatment for any anaphylaxis episode-regardless of severity-is intramuscular injection of epinephrine into the anterolateral thigh; delaying its administration increases the potential for morbidity and mortality. When a reaction appears as "possible anaphylaxis," it is generally better to err on the side of caution and administer epinephrine. Conclusion: We believe that this working definition and the supporting Consensus Statements are a first step to better management of anaphylaxis in the emergency medical setting. (C) 2013 Elsevier Inc.
C1 [Nowak, Richard] Univ Michigan, Sch Med, Wayne State Univ, Detroit, MI USA.
[Farrar, Judith Rosen] Life Sci Press, Canandaigua, NY USA.
[Brenner, Barry E.] Case Western Reserve Sch Med, Cleveland, OH USA.
[Lewis, Lawrence] Washington Univ, Sch Med, St Louis, MO USA.
[Silverman, Robert A.] North Shore Long Isl Jewish Hosp Syst, New Hyde Pk, NY USA.
[Emerman, Charles] Cleveland Clin, Cleveland, OH 44106 USA.
[Hays, Daniel P.] Univ Arizona, Med Ctr, Tucson, AZ USA.
[Russell, W. Scott] Med Univ S Carolina, Charleston, SC 29425 USA.
[Schmitz, Natalie] DeKalb Med Ctr, Atlanta, GA USA.
[Miller, Judi] SRxA, Washington, DC USA.
[Singer, Ethan] Catskill Reg Med Ctr, Callicoon, NY USA.
[Camargo, Carlos A., Jr.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Wood, Joseph] Mayo Clin Arizona, Scottsdale, AZ USA.
RP Nowak, R (reprint author), Henry Ford Hosp, Dept Emergency Med, 2799 W Grand Blvd, Detroit, MI 48202 USA.
FU Mylan Pharmaceuticals
FX This manuscript was supported in part by an unrestricted educational
grant from Mylan Pharmaceuticals. The company had no involvement in the
development, writing, or review of the manuscript. All authors
participated in the original Roundtable meeting, Anaphylaxis in
Emergency Medicine, convened in Chicago, IL in July 2011, and agreed at
that time that there exists a need for a standard definition of
anaphylaxis that is appropriate for emergency medicine health
professionals. Richard Nowak, MD, chaired the Roundtable meeting and the
subsequent meeting of the authors (March 2012) to discuss the definition
and consensus statements. Judith Farrar, PHD, drafted the discussion
summary on which the manuscript was based; and the authors then used the
summary to develop/write the consensus statements and the supporting
discussion for each. The authors also all contributed substantially to
revising drafts of the full manuscript, and all have agreed to this
final version of the paper.
NR 34
TC 7
Z9 7
U1 0
U2 8
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 2013
VL 45
IS 2
BP 299
EP 305
DI 10.1016/j.jemermed.2013.01.018
PG 7
WC Emergency Medicine
SC Emergency Medicine
GA 201UL
UT WOS:000323168400036
PM 23643240
ER
PT J
AU Duckworth, AD
Jenkins, PJ
Roddam, P
Watts, AC
Ring, D
McEachan, JE
AF Duckworth, Andrew D.
Jenkins, Paul J.
Roddam, Philip
Watts, Adam C.
Ring, David
McEachan, Jane E.
TI Pain and Carpal Tunnel Syndrome
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Article
DE Carpal tunnel syndrome; pain; diagnosis; nerve conduction studies;
outcome
ID IDIOPATHIC ARM PAIN; SOCIOECONOMIC DEPRIVATION; DIABETES-MELLITUS;
SMOKING; QUESTIONNAIRE; PREDICTORS; DIAGNOSIS; RELEASE; NICOTINE;
OBESITY
AB Purpose Pain is not a classical symptom of carpal tunnel syndrome (CTS), with the exception of numbness that is so intense that it is described by patients as painful The primary aim of our study was to determine which factors correlated with pain for patients diagnosed with CTS.
Methods We prospectively assessed all patients diagnosed with CTS in our unit over a 1-year period. We recorded demographic details for all patients, including past medical history, body mass index, smoking, and occupation. The diagnosis and severity of carpal tunnel syndrome were established through a combination of history, clinical assessment, and nerve conduction studies. Of 275 patients diagnosed and treated for CTS, 183 were women (67%), the mean age was 55 years (range, 22-87 y), and 166 cases were bilateral (60%). The mean body mass index was 29.5 kg/m(2) (range, 17-48 kg/m(2)), and 81 patients smoked (30%). Patients completed a Short Form-McGill pain questionnaire (SF-MPQ) as a measure of pain at initial presentation. We assessed outcome 1 year after intervention using the Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH) score.
Results We found no association between pain according to the SF-MPQ and the positive clinical signs of CTS or positive nerve conduction studies. Multivariate analysis demonstrated that smoking and bilateral disease independently correlated with the overall SF-MPQ, with similar findings on subanalysis. Independent factors associated with an increased improvement in the QuickDASH at 1 year were the presentation QuickDASH score, positive nerve conduction studies, and smoking.
Conclusions The only independent factors that correlated with pain at presentation of CTS were smoking and bilateral disease. Pain according to the SF-MPQ was not associated with classical clinical findings of the disease or with positive findings on nerve conduction testing. (Copyright (C) 2013 by the American Society for Surgery of the Hand. All rights reserved.)
C1 [Duckworth, Andrew D.] Queen Margaret Hosp, Dept Orthopaed Surg, Dunfermline KY12 0SU, Fife, Scotland.
Wrightington Hosp, Upper Limb Unit, Wigan, Lancs, England.
Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv, Boston, MA 02114 USA.
RP Duckworth, AD (reprint author), Queen Margaret Hosp, Dept Orthopaed Surg, Whitefield Rd, Dunfermline KY12 0SU, Fife, Scotland.
EM andrew.duckworth@yahoo.co.uk
NR 45
TC 4
Z9 4
U1 0
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0363-5023
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD AUG
PY 2013
VL 38A
IS 8
BP 1540
EP 1546
DI 10.1016/j.jhsa.2013.05.027
PG 7
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 198LZ
UT WOS:000322925700012
PM 23890497
ER
PT J
AU Cross, DJ
Anzai, Y
Petrie, EC
Martin, N
Richards, TL
Maravilla, KR
Peskind, ER
Minoshima, S
AF Cross, Donna J.
Anzai, Yoshimi
Petrie, Eric C.
Martin, Nathalie
Richards, Todd L.
Maravilla, Kenneth R.
Peskind, Elaine R.
Minoshima, Satoshi
TI Loss of Olfactory Tract Integrity Affects Cortical Metabolism in the
Brain and Olfactory Regions in Aging and Mild Cognitive Impairment
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE olfactory tract; Alzheimer's disease; fiber tract integrity; glucose
metabolism; F-18-FDG PET; DTI
ID TRAUMATIC AXONAL INJURY; ALZHEIMERS-DISEASE; TAU PATHOLOGY; IN-VIVO;
DYSFUNCTION; MRI; EPSILON-4; BULB; PET
AB Olfactory dysfunction is an early feature of Alzheimer disease. This study used multimodal imaging of PET and F-18-FDG combined with diffusion tensor imaging (DTI) to investigate the association of fiber tract integrity in the olfactory tract with cortical glucose metabolism in subjects with mild cognitive impairment (MCI) and normal controls. We hypothesized that MCI subjects would show loss of olfactory tract integrity and may have altered associations with glucose metabolism. Methods: Subjects diagnosed with amnestic MCI (n = 12) and normal controls (n = 23) received standard brain F-18-FDG PET and DTI with 32 gradient directions on a 3-T MR imaging scanner. Fractional anisotropy (FA) maps were generated. Voxelwise correlation analysis of olfactory tract FA values with F-18-FDG PET images was performed. Results: Integrated analysis over all subjects indicated a positive correlation between white matter integrity in the olfactory tract and metabolic activity in olfactory processing structures, including the rostral prefrontal cortex, dorsomedial thalamus, hypothalamus, orbitofrontal cortex, and uncus, and in the superior temporal gyrus, insula, and anterior cingulate cortex. Subjects with MCI, compared with normal controls, showed differential associations of olfactory tract integrity with medial temporal lobe and posterior cortical structures. Conclusion: These findings indicate that impairment of axonal integrity or neuronal loss may be linked to functional metabolic changes and that disease-specific neurodegeneration may affect this relationship. Multimodal imaging using F-18-FDG PET and DTI may provide better insights into aging and neurodegenerative processes.
C1 [Cross, Donna J.; Anzai, Yoshimi; Petrie, Eric C.; Martin, Nathalie; Richards, Todd L.; Maravilla, Kenneth R.; Minoshima, Satoshi] Univ Washington, Dept Radiol, Seattle, WA 98195 USA.
[Petrie, Eric C.; Peskind, Elaine R.] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Petrie, Eric C.; Peskind, Elaine R.] MIRECC, VA Puget Sound, Seattle, WA USA.
RP Cross, DJ (reprint author), Univ Washington, Dept Radiol, 1959 NE Pacific St,Box 357115, Seattle, WA 98195 USA.
EM dcross@uw.edu
FU NIH [R01 NS045254]; NIA [P50AG005136]; VA Puget Sound Mental Illness
Research, Education and Clinical Center (MIRECC)
FX The costs of publication of this article were defrayed in part by the
payment of page charges. Therefore, and solely to indicate this fact,
this article is hereby marked "advertisement" in accordance with 18 USC
section 1734. This study was supported by NIH R01 NS045254, NIA grant
P50AG005136, and the VA Puget Sound Mental Illness Research, Education
and Clinical Center (MIRECC). No other potential conflict of interest
relevant to this article was reported.
NR 31
TC 13
Z9 14
U1 0
U2 4
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD AUG
PY 2013
VL 54
IS 8
BP 1278
EP 1284
DI 10.2967/jnumed.112.116558
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 195HH
UT WOS:000322692400035
PM 23804325
ER
PT J
AU Zeglis, BM
Sevak, KK
Reiner, T
Mohindra, P
Carlin, SD
Zanzonico, P
Weissleder, R
Lewis, JS
AF Zeglis, Brian M.
Sevak, Kuntal K.
Reiner, Thomas
Mohindra, Priya
Carlin, Sean D.
Zanzonico, Pat
Weissleder, Ralph
Lewis, Jason S.
TI A Pretargeted PET Imaging Strategy Based on Bioorthogonal Diels-Alder
Click Chemistry
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE positron emission tomography (PET); pretargeting; click chemistry;
antibody; colorectal cancer
ID RADIOIMMUNOTHERAPY; CANCER; ANTIBODIES; THERAPY; A33
AB The specificity of antibodies have made immunoconjugates promising vectors for the delivery of radioisotopes to cancer cells; however, their long pharmacologic half-lives necessitate the use of radioisotopes with long physical half-lives, a combination that leads to high radiation doses to patients. Therefore, the development of targeting modalities that harness the advantages of antibodies without their pharmacokinetic limitations is desirable. To this end, we report the development of a methodology for pretargeted PET imaging based on the bioorthogonal Diels-Alder click reaction between tetrazine and transcyclooctene. Methods: A proof-of-concept system based on the A33 antibody, SW1222 colorectal cancer cells, and Cu-64 was used. The huA33 antibody was covalently modified with transcyclooctene, and a NOTA-modified tetrazine was synthesized and radiolabeled with Cu-64. Pretargeted in vivo biodistribution and PET imaging experiments were performed with athymic nude mice bearing A33 antigen-expressing, SW1222 colorectal cancer xenografts. Results: The huA33 antibody was modified with transcyclooctene to produce a conjugate with high immunoreactivity, and the Cu-64-NOTA-labeled tetrazine ligand was synthesized with greater than 99% purity and a specific activity of 9-10 MBq/mu g. For in vivo experiments, mice bearing SW1222 xenografts were injected with transcyclooctene-modified A33; after allowing 24 h for accumulation of the antibody in the tumor, the mice were injected with Cu-64-NOTA-labeled tetrazine for PET imaging and biodistribution experiments. At 12 h after injection, the retention of uptake in the tumor (4.1 +/- 0.3 percent injected dose per gram), coupled with the fecal excretion of excess radioligand, produced images with high tumor-to-background ratios. PET imaging and biodistribution experiments performed using A33 directly labeled with either Cu-64 or Zr-89 revealed that although absolute tumor uptake was higher with the directly radiolabeled antibodies, the pretargeted system yielded comparable images and tumor-to-muscle ratios at 12 and 24 h after injection. Further, dosimetry calculations revealed that the Cu-64 pretargeting system resulted in only a fraction of the absorbed background dose of A33 directly labeled with Zr-89 (0.0124 mSv/MBq vs. 0.4162 mSv/MBq, respectively). Conclusion: The high quality of the images produced by this pretargeting approach, combined with the ability of the methodology to dramatically reduce nontarget radiation doses to patients, marks this system as a strong candidate for clinical translation.
C1 [Zeglis, Brian M.; Sevak, Kuntal K.; Reiner, Thomas; Mohindra, Priya; Carlin, Sean D.; Lewis, Jason S.] Mem Sloan Kettering Canc Ctr, Dept Radiol, New York, NY 10021 USA.
[Zanzonico, Pat] Mem Sloan Kettering Canc Ctr, Dept Med Phys, New York, NY 10021 USA.
[Weissleder, Ralph] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
RP Lewis, JS (reprint author), 1275 York Ave, New York, NY 10065 USA.
EM lewisj2@mskcc.org
OI Carlin, Sean/0000-0002-5401-0648; Reiner, Thomas/0000-0002-7819-5480
FU NIH [1F32CA1440138-01, R01EB010011, P50-CA86355, R24-CA83084,
P30-CA08748]; DOE [DE-SC0002184, DE-SC0002456]
FX The costs of publication of this article were defrayed in part by the
payment of page charges. Therefore, and solely to indicate this fact,
this article is hereby marked "advertisement" in accordance with 18 USC
section 1734. This work received financial support from the NIH
(1F32CA1440138-01, R01EB010011, and P50-CA86355) and the DOE
(DE-SC0002184 and DE-SC0002456). Services provided by the MSKCC
Small-Animal Imaging Core Facility were supported in part by NIH grants
R24-CA83084 and P30-CA08748. No other potential conflict of interest
relevant to this article was reported.
NR 25
TC 76
Z9 77
U1 12
U2 99
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD AUG
PY 2013
VL 54
IS 8
BP 1389
EP 1396
DI 10.2967/jnumed.112.115840
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 195HH
UT WOS:000322692400052
PM 23708196
ER
PT J
AU Dorbala, S
Di Carli, MF
Delbeke, D
Abbara, S
DePuey, EG
Dilsizian, V
Forrester, J
Janowitz, W
Kaufmann, PA
Mahmarian, J
Moore, SC
Stabin, MG
Shreve, P
AF Dorbala, Sharmila
Di Carli, Marcelo F.
Delbeke, Dominique
Abbara, Suhny
DePuey, E. Gordon
Dilsizian, Vasken
Forrester, Joey
Janowitz, Warren
Kaufmann, Philipp A.
Mahmarian, John
Moore, Stephen C.
Stabin, Michael G.
Shreve, Paul
TI SNMMI/ASNC/SCCT Guideline for Cardiac SPECT/CT and PET/CT 1.0
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
ID CORONARY-ARTERY-DISEASE; MYOCARDIAL-PERFUSION SPECT;
AMERICAN-HEART-ASSOCIATION; EMISSION COMPUTED-TOMOGRAPHY; 64-SLICE CT
ANGIOGRAPHY; LOW-DOSE CT; STATISTICAL ITERATIVE RECONSTRUCTION;
CARDIOVASCULAR MAGNETIC-RESONANCE; APPROPRIATE USE CRITERIA;
STRESS-INDUCED ISCHEMIA
C1 [Dorbala, Sharmila; Di Carli, Marcelo F.; Moore, Stephen C.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Delbeke, Dominique; Forrester, Joey; Stabin, Michael G.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Abbara, Suhny] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[DePuey, E. Gordon] St Lukes Roosevelt Hosp, New York, NY 10025 USA.
[Dilsizian, Vasken] Univ Maryland, Med Ctr, Baltimore, MD 21201 USA.
[Janowitz, Warren] Baptist Hosp Miami, Miami, FL USA.
[Kaufmann, Philipp A.] Univ Zurich Hosp, CH-8091 Zurich, Switzerland.
[Mahmarian, John] Methodist Hosp, Houston, TX 77030 USA.
[Shreve, Paul] Adv Radiol Serv, Grand Rapids, MI USA.
RP Dorbala, S (reprint author), Brigham & Womens Hosp, 70 Francis St, Boston, MA 02115 USA.
EM sdorbala@partners.org
NR 148
TC 36
Z9 36
U1 1
U2 4
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD AUG
PY 2013
VL 54
IS 8
BP 1485
EP 1507
DI 10.2967/jnumed.112.105155
PG 23
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 195HH
UT WOS:000322692400065
PM 23781013
ER
PT J
AU Burstein, HJ
AF Burstein, Harold J.
TI Lucky to Be an Oncologist
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 02115 USA.
[Burstein, Harold J.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Burstein, HJ (reprint author), Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
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 2013
VL 11
IS 8
BP 909
EP 910
PG 2
WC Oncology
SC Oncology
GA 201QE
UT WOS:000323156900001
PM 23946169
ER
PT J
AU Pfister, DG
Ang, KK
Brizel, DM
Burtness, BA
Busse, PM
Caudell, JJ
Cmelak, AJ
Colevas, AD
Dunphy, F
Eisele, DW
Gilbert, J
Gillison, ML
Haddad, RI
Haughey, BH
Hicks, WL
Hitchcock, YJ
Kies, MS
Lydiatt, WM
Maghami, E
Martins, R
McCaffrey, T
Mittal, BB
Pinto, HA
Ridge, JA
Samant, S
Schuller, DE
Shah, JP
Spencer, S
Weber, RS
Wolf, GT
Worden, F
Yom, SS
McMillian, NR
Hughes, M
AF Pfister, David G.
Ang, Kie-Kian
Brizel, David M.
Burtness, Barbara A.
Busse, Paul M.
Caudell, Jimmy J.
Cmelak, Anthony J.
Colevas, A. Dimitrios
Dunphy, Frank
Eisele, David W.
Gilbert, Jill
Gillison, Maura L.
Haddad, Robert I.
Haughey, Bruce H.
Hicks, Wesley L.
Hitchcock, Ying J.
Kies, Merrill S.
Lydiatt, William M.
Maghami, Ellie
Martins, Renato
McCaffrey, Thomas
Mittal, Bharat B.
Pinto, Harlan A.
Ridge, John A.
Samant, Sandeep
Schuller, David E.
Shah, Jatin P.
Spencer, Sharon
Weber, Randal S.
Wolf, Gregory T.
Worden, Frank
Yom, Sue S.
McMillian, Nicole R.
Hughes, Miranda
TI Head and Neck Cancers, Version 2.2013 Featured Updates to the NCCN
Guidelines
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID ENDOSCOPIC GASTROSTOMY TUBE; QUALITY-OF-LIFE; WEIGHT-LOSS; NASOGASTRIC
TUBE; PLACEMENT; RADIOTHERAPY; CHEMORADIOTHERAPY; PREDICTORS; CARCINOMA;
NUTRITION
AB These NCCN Guidelines Insights focus on nutrition and supportive care for patients with head and neck cancers. This topic was a recent addition to the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Head and Neck Cancers. The NCCN Guidelines Insights focus on major updates to the NCCN Guidelines and discuss the new updates in greater detail. The complete version of the NCCN Guidelines for Head and Neck Cancers is available on the NCCN Web site (NCCN.org). (JNCCN 2013; 11: 917-923)
C1 [Pfister, David G.; Shah, Jatin P.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Ang, Kie-Kian] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
[Burtness, Barbara A.; Ridge, John A.] Fox Chase Canc Ctr, Philadelphia, PA USA.
[Busse, Paul M.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Caudell, Jimmy J.; McCaffrey, Thomas] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Cmelak, Anthony J.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Colevas, A. Dimitrios] Stanford Canc Inst, Stanford, CA USA.
[Eisele, David W.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD USA.
[Gillison, Maura L.; Schuller, David E.] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Gillison, Maura L.; Schuller, David E.] Solove Res Inst, Columbus, OH USA.
[Haddad, Robert I.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Haughey, Bruce H.] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO USA.
[Haughey, Bruce H.] Washington Univ, Sch Med, St Louis, MO 63130 USA.
[Hicks, Wesley L.] Roswell Pk Canc Inst, Buffalo, NY USA.
[Hitchcock, Ying J.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[Lydiatt, William M.] Nebraska Med Ctr, UNMC Eppley Canc Ctr, Omaha, NE USA.
[Maghami, Ellie] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Martins, Renato] Univ Washington, Seattle Canc Care Alliance, Seattle, WA 98195 USA.
[Mittal, Bharat B.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Samant, Sandeep] Univ Tennessee, St Jude Childrens Res Hosp, Hlth Sci Ctr, Knoxville, TN 37996 USA.
[Spencer, Sharon] Univ Alabama, Birmingham Comprehens Canc Ctr, Tuscaloosa, AL 35487 USA.
[Wolf, Gregory T.; Worden, Frank] Univ Michigan, Comprehens Canc Ctr, Ann Arbor, MI 48109 USA.
[Yom, Sue S.] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
RP Pfister, DG (reprint author), Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
OI Shah, Jatin/0000-0002-6444-6592
FU Genentech, Inc.; Novartis Pharmaceuticals; Bayer HealthCare; Exelixis
Inc.; ActoGeniX NV; Boehringer Ingelheim GmbH; GlaxoSmithKline; Eisai,
Inc.; Millennium: The Takeda Oncology Company; Teva Pharmaceuticals;
Bayer HealthCare Pharmaceuticals Inc.; Celgene Corporation; Endo
Pharmaceuticals; HealthTronics; Genentech; ARIAD Pharmaceuticals, Inc.
FX Dr. Burtness: Advisor for Bristol-Myers Squibb Company. Research funding
from Genentech, Inc. and Novartis Pharmaceuticals; Dr. Colevas: Clinical
research support from Bayer HealthCare; Exelixis Inc.; Genentech, Inc.;
and ActoGeniX NV. Research funding from Boehringer Ingelheim GmbH and
GlaxoSmithKline. Serves on the Head and Neck Steering Subcommittee for
NCI. Site investigator for RTOG and ECOG. Committee member for ECOG.;
Dr. Martins: PI for Bayer HealthCare; Eisai Inc.; Genentech, Inc.;
Novartis Pharmaceuticals Corporation; and Pfizer Inc. Clinical research
support from Exelixis Inc.; Supported by educational grants from Eisai,
Inc.; Millennium: The Takeda Oncology Company; Teva Pharmaceuticals;
Bayer HealthCare Pharmaceuticals Inc.; Celgene Corporation; Endo
Pharmaceuticals and HealthTronics; Genentech; and ARIAD Pharmaceuticals,
Inc.
NR 32
TC 62
Z9 68
U1 3
U2 8
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 2013
VL 11
IS 8
BP 917
EP 923
PG 7
WC Oncology
SC Oncology
GA 201QE
UT WOS:000323156900003
PM 23946171
ER
PT J
AU Lloyd, S
Buscariollo, DL
Gross, CP
Makarov, DV
Yu, JB
AF Lloyd, Shane
Buscariollo, Daniela L.
Gross, Cary P.
Makarov, Danil V.
Yu, James B.
TI Determinants of Enrollment in Cancer Clinical Trials: The Relationship
Between the Current State of Knowledge, Societal Disease Burden, and
Randomized Clinical Trial Enrollment
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID RECOMMENDATIONS
AB Whether clinical cancer research currently focuses on gaps in the evidentiary basis for clinical guidelines and/or on cancers that impose greater societal burden is unclear. This study assessed the relationship between cancer research efforts in terms of planned randomized controlled trial (RCT) enrollment, objective measures of evidence quality, and a cancer's burden on society. The authors calculated the planned RCT enrollment listed on ClinicalTrials.gov for the 17 most prevalent solid cancers. Using cancer type as the unit of analysis, linear regression was used to examine the association between planned enrollment in RCTs and 1) evidence quality, as measured by the absolute number and percent of highest quality category (category 1 [C1]) recommendations in the NCCN Clinical Practice Guidelines in Oncology for each cancer, and 2) measures of burden on society, including prevalence, incidence, person-years of life lost (PYLL), and disability-adjusted life years (DALY). Non-normal distributions were log transformed when appropriate. Overall, 15% of the NCCN recommendations were based on the highest quality evidence. Results produced 1260 RCTs. Planned RCT enrollment ranged from 2270 (testis) to 492,876 (breast) and was correlated neither with absolute number nor percent of C1 recommendations for that cancer. Planned RCT enrollment was positively correlated with a cancer's prevalence (P=.01), incidence (P<.01), PYLL (P<.01), and DALY (P<0.01). In multivariate analysis, prevalence (P<.01) and PYLL (P<.01) had the strongest association with planned RCT enrollment. Findings showed, therefore, that planned cancer RCT enrollment is associated with higher societal disease burden, not the quality of a cancer's clinical guidelines.
C1 [Lloyd, Shane; Yu, James B.] Yale Univ, Sch Med, Dept Therapeut Radiol, New Haven, CT 06510 USA.
[Buscariollo, Daniela L.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Gross, Cary P.] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA.
[Makarov, Danil V.] NYU, Sch Med, Dept Urol, US Dept Vet Affairs, New York, NY 10003 USA.
[Makarov, Danil V.] NYU, Sch Med, US Dept Vet Affairs, Dept Populat Hlth & Canc, New York, NY 10003 USA.
RP Yu, JB (reprint author), Yale Univ, Sch Med, Dept Therapeut Radiol, LL 516 Smilow,POB 208040, New Haven, CT 06510 USA.
EM james.b.yu@yale.edu
FU Medtronic
FX Drs. Lloyd, Buscariollo, Makarov, and Yu have disclosed that they have
no financial interests, arrangements, affiliations, or commercial
interests with the manufacturers of any products discussed in this
article or their competitors. Dr. Gross has disclosed that he receives a
research grant from Medtronic and is on the advisory board for Fair
Health Inc.
NR 18
TC 0
Z9 0
U1 0
U2 0
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD AUG
PY 2013
VL 11
IS 8
BP 928
EP 936
PG 9
WC Oncology
SC Oncology
GA 201QE
UT WOS:000323156900004
PM 23946172
ER
PT J
AU Chen, RC
Shipley, WU
Efstathiou, JA
Zietman, AL
AF Chen, Ronald C.
Shipley, William U.
Efstathiou, Jason A.
Zietman, Anthony L.
TI Trimodality Bladder Preservation Therapy for Muscle-Invasive Bladder
Cancer
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID PHASE I-II; SELECTIVE ORGAN PRESERVATION; COMBINED-MODALITY THERAPY;
QUALITY-OF-LIFE; RADICAL CYSTECTOMY; NEOADJUVANT CHEMOTHERAPY; ADJUVANT
CHEMOTHERAPY; COMBINED RADIATION; PROSPECTIVE TRIAL; SPARING THERAPY
AB Potentially curative treatments for patients with muscle-invasive bladder cancer (MIBC) are underused, especially in the elderly. Trimodality bladder preservation therapy, which includes a maximally safe transurethral resection of the bladder tumor, followed by concurrent chemoradiation, fulfills this currently unmet need. In multiple prospective clinical trials and large institutional series, trimodality therapy has demonstrated excellent 5-year overall survival rates of 48% to 65%, comparable to those reported in cystectomy studies. Approximately 75% to 80% of long-term survivors maintain their native bladders, which tend to function well and allow patients to maintain excellent quality of life. Salvage cystectomy for patients who develop a local invasive recurrence can be performed with acceptable operative complication rates, and results in excellent long-term disease control and survival outcomes. For patients with MIBC who are noncystectomy candidates, or select patients who are motivated to keep their native bladders, trimodality bladder preservation therapy is recognized by the International Consultation on Urological Diseases-European Association of Urology and the NCCN Clinical Practice Guidelines in Oncology for Bladder Cancer as an effective alternative to radical cystectomy, and should be considered. In the future, biomarkers may allow improved selection of patients for whom trimodality bladder preservation therapy is most likely to succeed.
C1 [Chen, Ronald C.] Univ N Carolina, Dept Radiat Oncol, Chapel Hill, NC 27599 USA.
[Shipley, William U.; Efstathiou, Jason A.; Zietman, Anthony L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, Boston, MA USA.
RP Chen, RC (reprint author), Univ N Carolina, Dept Radiat Oncol, 101 Manning Dr,CB 7512, Chapel Hill, NC 27599 USA.
EM ronald_chen@med.unc.edu
NR 40
TC 17
Z9 18
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 2013
VL 11
IS 8
BP 952
EP 960
PG 9
WC Oncology
SC Oncology
GA 201QE
UT WOS:000323156900006
PM 23946174
ER
PT J
AU Swarm, RA
Abernethy, AP
Anghelescu, DL
Benedetti, C
Buga, S
Cleeland, C
DeLeon-Casasola, OA
Eilers, JG
Ferrell, B
Green, M
Janjan, NA
Kamdar, MM
Levy, MH
Lynch, M
McDowell, RM
Moryl, N
Nesbit, SA
Paice, JA
Rabow, MW
Syrjala, KL
Urba, SG
Weinstein, SM
Dwyer, M
Kumar, R
AF Swarm, Robert A.
Abernethy, Amy Pickar
Anghelescu, Doralina L.
Benedetti, Costantino
Buga, Sorin
Cleeland, Charles
DeLeon-Casasola, Oscar A.
Eilers, June G.
Ferrell, Betty
Green, Mark
Janjan, Nora A.
Kamdar, Mihir M.
Levy, Michael H.
Lynch, Maureen
McDowell, Rachel M.
Moryl, Natalie
Nesbit, Suzanne A.
Paice, Judith A.
Rabow, Michael W.
Syrjala, Karen L.
Urba, Susan G.
Weinstein, Sharon M.
Dwyer, Mary
Kumar, Rashmi
TI Adult Cancer Pain Clinical Practice Guidelines in Oncology
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID OPIOID-INDUCED CONSTIPATION; FENTANYL BUCCAL TABLET; CONTROLLED
PHASE-III; QUALITY-OF-LIFE; DIABETIC PERIPHERAL NEUROPATHY; OXYCODONE
CONTROLLED-RELEASE; TAPENTADOL EXTENDED-RELEASE; RANDOMIZED
CONTROLLED-TRIAL; METASTATIC BONE-DISEASE; CHRONIC NONCANCER PAIN
AB Pain is a common symptom associated with cancer and its treatment. Pain management is an important aspect of oncologic care, and unrelieved pain significantly comprises overall quality of life. These NCCN Guidelines list the principles of management and acknowledge the range of complex decisions faced in the management oncologic pain. In addition to pain assessment techniques, these guidelines provide principles of use, dosing, management of adverse effects, and safe handling procedures of pharmacologic therapies and discuss a multidisciplinary approach for the management of cancer pain.
C1 [Swarm, Robert A.] Washington Univ, Sch Med, St Louis, MO 63130 USA.
[Anghelescu, Doralina L.] Univ Tennessee, Hlth Sci Ctr, St Jude Childrens Res Hosp, Knoxville, TN 37996 USA.
[Benedetti, Costantino] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Cleeland, Charles; Janjan, Nora A.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[DeLeon-Casasola, Oscar A.] Roswell Pk Canc Inst, Buffalo, NY USA.
[Eilers, June G.] Nebraska Med Ctr, UNMC Eppley Canc Ctr, Omaha, NE USA.
[Kamdar, Mihir M.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Levy, Michael H.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[McDowell, Rachel M.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Moryl, Natalie] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Paice, Judith A.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Rabow, Michael W.] UCSF Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
[Syrjala, Karen L.] Seattle Canc Care Alliance, Fred Hutchinson Canc Res Ctr, Seattle, WA USA.
[Urba, Susan G.] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Weinstein, Sharon M.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
FU NCI NIH HHS [R01 CA160684]
NR 164
TC 20
Z9 26
U1 3
U2 17
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 2013
VL 11
IS 8
BP 992
EP 1022
PG 31
WC Oncology
SC Oncology
GA 201QE
UT WOS:000323156900009
PM 23946177
ER
PT J
AU Goodson, JT
Lefkowitz, CM
Helstrom, AW
Gawrysiak, MJ
AF Goodson, Jason T.
Lefkowitz, Carin M.
Helstrom, Amy W.
Gawrysiak, Michael J.
TI Outcomes of Prolonged Exposure Therapy for Veterans With Posttraumatic
Stress Disorder
SO JOURNAL OF TRAUMATIC STRESS
LA English
DT Article
ID PSYCHOLOGICAL TREATMENTS; COMPENSATION-SEEKING; PTSD; IRAQ; WAR;
PSYCHOTHERAPY; METAANALYSIS; TRIAL; MOOD; PAIN
AB Prolonged Exposure (PE) is an evidenced-based psychotherapy for posttraumatic stress disorder (PTSD) that is being disseminated nationally within the U.S. Department of Veterans Affairs (VA) with promising initial results. Empirical evidence, however, regarding the effectiveness of PE for treatment of PTSD in military veterans is limited. Building on previous treatment outcome research, the current study investigated the effectiveness of PE in a diverse veteran sample. One-hundred fifteen veterans were enrolled in PE at an urban VA medical center and its surrounding outpatient clinics. PTSD and depression symptoms as well as quality of life were measured before and after treatment. Several baseline patient characteristics were examined as predictors of treatment response. Eighty-four participants completed treatment. Participants experienced a 42% reduction in PTSD symptoms, a 31% reduction in depression symptoms, and an increase in quality of life following PE. Veterans not prescribed psychotropic medication reported greater PTSD symptom reduction than veterans prescribed such medication. The implications of these results for treatment programs targeting PTSD in veterans are discussed.
C1 [Goodson, Jason T.; Lefkowitz, Carin M.; Helstrom, Amy W.; Gawrysiak, Michael J.] Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
[Goodson, Jason T.; Lefkowitz, Carin M.; Helstrom, Amy W.; Gawrysiak, Michael J.] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA.
RP Goodson, JT (reprint author), Philadelphia VA Med Ctr, 3900 Woodland Ave, Philadelphia, PA 19104 USA.
EM Jason.Goodson@va.gov
NR 40
TC 20
Z9 20
U1 0
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0894-9867
J9 J TRAUMA STRESS
JI J. Trauma Stress
PD AUG
PY 2013
VL 26
IS 4
BP 419
EP 425
DI 10.1002/jts.21830
PG 7
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 198CD
UT WOS:000322898400001
PM 23934939
ER
PT J
AU Kearney, DJ
Malte, CA
McManus, C
Martinez, ME
Felleman, B
Simpson, TL
AF Kearney, David J.
Malte, Carol A.
McManus, Carolyn
Martinez, Michelle E.
Felleman, Ben
Simpson, Tracy L.
TI Loving-Kindness Meditation for Posttraumatic Stress Disorder: A Pilot
Study
SO JOURNAL OF TRAUMATIC STRESS
LA English
DT Article
ID ADMINISTERED PTSD SCALE; ALTERNATIVE MEDICINE; MILITARY VETERANS;
SELF-COMPASSION; MINDFULNESS; COMPLEMENTARY; CLINICIAN; SYMPTOMS;
THERAPY; PSYCHOTHERAPY
AB Loving-kindness meditation is a practice designed to enhance feelings of kindness and compassion for self and others. Loving-kindness meditation involves repetition of phrases of positive intention for self and others. We undertook an open pilot trial of loving-kindness meditation for veterans with posttraumatic stress disorder (PTSD). Measures of PTSD, depression, self-compassion, and mindfulness were obtained at baseline, after a 12-week loving-kindness meditation course, and 3 months later. Effect sizes were calculated from baseline to each follow-up point, and self-compassion was assessed as a mediator. Attendance was high; 74% attended 9-12 classes. Self-compassion increased with large effect sizes and mindfulness increased with medium to large effect sizes. A large effect size was found for PTSD symptoms at 3-month follow-up (d = -0.89), and a medium effect size was found for depression at 3-month follow-up (d = -0.49). There was evidence of mediation of reductions in PTSD symptoms and depression by enhanced self-compassion. Overall, loving-kindness meditation appeared safe and acceptable and was associated with reduced symptoms of PTSD and depression. Additional study of loving-kindness meditation for PTSD is warranted to determine whether the changes seen are due to the loving-kindness meditation intervention versus other influences, including concurrent receipt of other treatments.
C1 [Kearney, David J.] VA Puget Sound Hlth Care Syst, Dept Med, Seattle, WA USA.
[Kearney, David J.] Univ Washington, Sch Med, Dept Med, Seattle, WA 98195 USA.
[Malte, Carol A.; Simpson, Tracy L.] VA Puget Sound Hlth Care Syst, Ctr Excellence Subst Abuse Treatment & Educ, Seattle, WA USA.
[McManus, Carolyn] Swedish Med Ctr, Dept Phys Therapy, Seattle, WA USA.
[Martinez, Michelle E.; Felleman, Ben] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Simpson, Tracy L.] Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
RP Kearney, DJ (reprint author), Seattle VAMC 111GI,1660 S Columbian Way, Seattle, WA 98108 USA.
EM david.kearney@va.gov
NR 40
TC 33
Z9 33
U1 6
U2 52
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0894-9867
J9 J TRAUMA STRESS
JI J. Trauma Stress
PD AUG
PY 2013
VL 26
IS 4
BP 426
EP 434
DI 10.1002/jts.21832
PG 9
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 198CD
UT WOS:000322898400002
PM 23893519
ER
PT J
AU Franz, MR
Wolf, EJ
MacDonald, HZ
Marx, BP
Proctor, SP
Vasterling, JJ
AF Franz, Molly R.
Wolf, Erika J.
MacDonald, Helen Z.
Marx, Brian P.
Proctor, Susan P.
Vasterling, Jennifer J.
TI Relationships Among Predeployment Risk Factors, Warzone-Threat
Appraisal, and Postdeployment PTSD Symptoms
SO JOURNAL OF TRAUMATIC STRESS
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; NEUROCOGNITION DEPLOYMENT HEALTH;
MENTAL-HEALTH; PROSPECTIVE COHORT; VIETNAM VETERANS; MILITARY SERVICE;
FIT INDEXES; IRAQ; AFGHANISTAN; EXPERIENCES
AB Previous research indicates a relationship between perceived fear for one's safety (i.e., threat appraisal) and posttraumatic stress disorder (PTSD). This prospective study examined relationships among deployment- and predeployment-related variables, threat appraisal, and postdeployment PTSD symptom severity. Prior to Iraq deployment, 774 U.S. Army soldiers completed self-report measures assessing previous life stressors, deployment history, current (predeployment) PTSD symptoms, deployment preparedness, and unit cohesion. Following deployment, participants completed self-report measures assessing combat intensity, deployment threat appraisal, and current (postdeployment) PTSD symptoms. Structural equation modeling revealed that predeployment PTSD symptom severity, prior warzone deployment, unit cohesion, and preparedness were each independently associated with deployment threat appraisal, even after taking into account combat intensity. Deployment threat appraisal was associated with postdeployment PTSD severity. Results indicated that predeployment PTSD symptom severity, history of warzone deployment, and preparednessrisk factors previously thought to influence PTSD outcomes directlywere either partially or fully mediated by threat appraisal. The model explained 15% of the variance in deployment threat appraisal and 50% of the variance in postdeployment PTSD severity. Helping service members cope with exposure to extreme stress during deployment by modifying certain prewar risk factors may facilitate reduction of PTSD symptoms following deployment.
C1 [Franz, Molly R.; MacDonald, Helen Z.; Proctor, Susan P.] VA Boston Healthcare Syst, Res Serv, Boston, MA 02130 USA.
[Wolf, Erika J.; Marx, Brian P.; Vasterling, Jennifer J.] VA Boston Healthcare Syst, Natl Ctr PTSD, Boston, MA 02130 USA.
[Wolf, Erika J.; Marx, Brian P.; Vasterling, Jennifer J.] VA Boston Healthcare Syst, Psychol Serv, Boston, MA 02130 USA.
[Wolf, Erika J.; MacDonald, Helen Z.; Marx, Brian P.; Vasterling, Jennifer J.] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA.
[Proctor, Susan P.] US Army Res Inst Environm Med, Mil Performance Div, Natick, MA USA.
RP Vasterling, JJ (reprint author), VA Boston Healthcare Syst, 150 S Huntington Ave 116B, Boston, MA 02130 USA.
EM jennifer.vasterling@va.gov
OI Wolf, Erika/0000-0003-2666-2435
NR 35
TC 10
Z9 10
U1 2
U2 16
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0894-9867
J9 J TRAUMA STRESS
JI J. Trauma Stress
PD AUG
PY 2013
VL 26
IS 4
BP 498
EP 506
DI 10.1002/jts.21827
PG 9
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 198CD
UT WOS:000322898400011
PM 23893499
ER
PT J
AU Creech, SK
Benzer, JK
Liebsack, BK
Proctor, S
Taft, CT
AF Creech, Suzannah K.
Benzer, Justin K.
Liebsack, Brittany K.
Proctor, Susan
Taft, Casey T.
TI Impact of Coping Style and PTSD on Family Functioning After Deployment
in Operation Desert Shield/Storm Returnees
SO JOURNAL OF TRAUMATIC STRESS
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; GULF-WAR VETERANS; COUPLE ADJUSTMENT;
SYMPTOMS; VALIDITY
AB The relationship between military combat and postdeployment family functioning difficulties has been frequently investigated in the literature, as has the relationship between types of coping and posttraumatic stress disorder (PTSD). Few studies, however, have examined these variables together, and no studies of which we are aware have examined the effect of coping on family functioning after combat exposure. This study examined coping style measured immediately after return from deployment, and PTSD symptoms and family functioning 18-24 months after return from deployment in a sample of Operation Desert Shield/Storm veterans (N = 2,949). Structural equation models suggested that the relationships between distinct coping styles on family functioning were differentially mediated by postdeployment PTSD symptoms. Results are consistent with full mediation for avoidant coping ((direct) = -.09, p = .07; (indirect) = -.17, p < .001) and partial mediation for approach coping ((direct) = .16, p < .001; (indirect) = .09, p < .001). Results suggest that the strategies used to cope with a combat stress event may impact both PTSD and family functioning outcomes, and highlight the potential utility of pre- and postdeployment coping skills training.
C1 [Creech, Suzannah K.; Liebsack, Brittany K.; Taft, Casey T.] VA Boston Healthcare Syst, Natl Ctr PTSD, Behav Sci Div, Boston, MA USA.
[Creech, Suzannah K.] Providence VA Med Ctr, Vulnerable Vet Populat Res Grp, Providence, RI USA.
[Creech, Suzannah K.] Brown Univ, Warren Alpert Med Sch, Dept Psychiat, Providence, RI 02912 USA.
[Benzer, Justin K.] VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA USA.
[Benzer, Justin K.] Boston Univ, Dept Hlth Policy & Management, Boston, MA 02215 USA.
[Proctor, Susan] US Army Res Inst Environm Med, Mil Performance Div, Natick, MA USA.
[Proctor, Susan] VA Boston Healthcare Syst, Res Serv, Boston, MA USA.
[Proctor, Susan] Boston Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA USA.
[Taft, Casey T.] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA.
RP Creech, SK (reprint author), Providence VAMC, 830 Chalkstone Ave, Providence, RI 02908 USA.
EM Suzannah.Creech@va.gov
OI Benzer, Justin/0000-0001-5151-2127; Creech, Suzannah/0000-0002-6582-1673
NR 22
TC 4
Z9 4
U1 0
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0894-9867
J9 J TRAUMA STRESS
JI J. Trauma Stress
PD AUG
PY 2013
VL 26
IS 4
BP 507
EP 511
DI 10.1002/jts.21823
PG 5
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 198CD
UT WOS:000322898400012
PM 23893396
ER
PT J
AU Talbot, LS
Maguen, S
Epel, ES
Metzler, TJ
Neylan, TC
AF Talbot, Lisa S.
Maguen, Shira
Epel, Elissa S.
Metzler, Thomas J.
Neylan, Thomas C.
TI Posttraumatic Stress Disorder Is Associated With Emotional Eating
SO JOURNAL OF TRAUMATIC STRESS
LA English
DT Article
ID ADMINISTERED PTSD SCALE; ABDOMINAL OBESITY; FOOD; SYSTEM; WOMEN
AB The present study investigated the relationship between posttraumatic stress disorder (PTSD) and emotional eating in a sample of medically healthy and medication-free adults. Participants with PTSD (n= 44) and control participants free of lifetime psychiatric history (n= 49) completed a measure of emotional eating. Emotional eating is the tendency to eat or overeat in response to negative emotions. PTSD participants exhibited greater emotional eating than control participants ((2)= .20) and emotional eating increased with higher PTSD symptom severity (R-2= .11). Results supported the stress-eating-obesity model whereby emotional eating is a maladaptive response to stressors. Over time, this could lead to weight gain, particularly abdominal stores, and contribute to higher risk for comorbid medical disorders. Findings suggest the importance of future longitudinal research to understand whether emotional eating contributes to the high rates of obesity, diabetes, and heart disease in PTSD.
C1 [Talbot, Lisa S.; Maguen, Shira; Metzler, Thomas J.; Neylan, Thomas C.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Talbot, Lisa S.; Maguen, Shira; Epel, Elissa S.; Neylan, Thomas C.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
RP Talbot, LS (reprint author), San Francisco VA Med Ctr 116H, 4150 Clement St, San Francisco, CA 94121 USA.
EM lisa.talbot@gmail.com
FU NIMH NIH HHS [R01 MH073978, 5R01MH073978-04, 5R34MH077667-03, R34
MH077667]
NR 23
TC 19
Z9 19
U1 3
U2 17
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0894-9867
J9 J TRAUMA STRESS
JI J. Trauma Stress
PD AUG
PY 2013
VL 26
IS 4
BP 521
EP 525
DI 10.1002/jts.21824
PG 5
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 198CD
UT WOS:000322898400014
PM 23893425
ER
PT J
AU Dekel, S
Mandl, C
Solomon, Z
AF Dekel, Sharon
Mandl, Christine
Solomon, Zahava
TI Is the Holocaust Implicated in Posttraumatic Growth in Second-Generation
Holocaust Survivors? A Prospective Study
SO JOURNAL OF TRAUMATIC STRESS
LA English
DT Article
ID TRAUMA; LEGACY
AB With the growing interest in posttraumatic growth (PTG), and the ongoing debate on the implications of transgenerational transmission of trauma, this longitudinal study examined PTG among Holocaust survivor offspring following their own exposure to trauma. Using self-report questionnaires, we assessed PTG over time in middle aged (age: M = 53 years) Israeli male combat veterans of the 1973 Yom Kippur War whose parents were (n = 43) and were not (n = 156) second-generation survivors of the Nazi Holocaust at 2 time points: 30 and 35 years following the war (in 2003 and 2008). Posttraumatic stress disorder symptoms and trauma exposure were also assessed in 1991. We hypothesized that second-generation survivors would report more PTG than controls. However, repeated measures design revealed that the second-generation veterans reported less PTG than veterans who were not second generation, which was evident in the PTG domains of relations to others, personal strength, and appreciation of life. Our findings suggest that transmission of trauma from one generation to the next is possibly implicated in the offspring's propensity for growth following subsequent trauma. Future research is warranted to examine the link between transmission of trauma and positive outcomes following trauma.
C1 [Dekel, Sharon; Mandl, Christine; Solomon, Zahava] Tel Aviv Univ, Bob Shapell Sch Social Work, IL-69978 Tel Aviv, Israel.
RP Dekel, S (reprint author), Massachusetts Gen Hosp East, PTSD Res Lab, 120 2nd Ave, Charlestown, MA 02129 USA.
EM dekel.sharon@gmail.com
NR 18
TC 7
Z9 7
U1 2
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0894-9867
J9 J TRAUMA STRESS
JI J. Trauma Stress
PD AUG
PY 2013
VL 26
IS 4
BP 530
EP 533
DI 10.1002/jts.21836
PG 4
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 198CD
UT WOS:000322898400016
PM 23893570
ER
PT J
AU Gervais, DA
AF Gervais, Debra A.
TI Cryoablation versus Radiofrequency Ablation for Renal Tumor Ablation:
Time to Reassess?
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Editorial Material
ID RADIO-FREQUENCY ABLATION; CELL CARCINOMA; PERCUTANEOUS CRYOABLATION;
ONCOLOGIC OUTCOMES; METAANALYSIS; EXPERIENCE; CANCER
C1 Massachusetts Gen Hosp, Dept Radiol Abdominal Imaging & Intervent, Boston, MA 02114 USA.
RP Gervais, DA (reprint author), Massachusetts Gen Hosp, Dept Radiol Abdominal Imaging & Intervent, White 270,55 Fruit St, Boston, MA 02114 USA.
EM dgervais@partners.org
NR 19
TC 9
Z9 9
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD AUG
PY 2013
VL 24
IS 8
BP 1135
EP 1138
DI 10.1016/j.jvir.2013.05.030
PG 4
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 198LL
UT WOS:000322924300007
PM 23885912
ER
PT J
AU Sheth, RA
Hesketh, R
Kong, DS
Wicky, S
Oklu, R
AF Sheth, Rahul A.
Hesketh, Robin
Kong, David S.
Wicky, Stephan
Oklu, Rahmi
TI Barriers to Drug Delivery in Interventional Oncology
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Review
ID INTERSTITIAL FLUID PRESSURE; UNRESECTABLE HEPATOCELLULAR-CARCINOMA;
RANDOMIZED CONTROLLED TRIAL; RENAL-CELL CARCINOMA; SOLID TUMORS;
VASCULAR NORMALIZATION; LUNG-CANCER; CHEMOEMBOLIZATION; PENETRATION;
BEVACIZUMAB
AB Although much attention has been paid to mechanisms of anticancer drug resistance that focus. on intracellular processes that,. protect tumor cells, it has recently become increasingly evident that the unique features of the tumor microenvironment profoundly impact the efficacy of cancer therapies. The properties of this extracellular milieu, including increased interstitial pressure, decreased pH, hypoxia, and abnormal vascularity, result in limited drug efficacy; this finding is true not only for systemic chemotherapy but also for catheter-based therapies, including chemoembolization and radioembolization. The present review summarizes the bathers to drug delivery imposed by the tumor microenvironment and provides methods' to overcome these hurdles.
C1 [Sheth, Rahul A.; Wicky, Stephan; Oklu, Rahmi] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Imaging,Div Vasc Imaging & Intervent, Boston, MA USA.
[Kong, David S.] MIT, Lincoln Lab, Lexington, MA 02173 USA.
[Hesketh, Robin] Univ Cambridge, Dept Biochem, Cambridge CB2 1QW, England.
RP Oklu, R (reprint author), Massachusetts Gen Hosp, Dept Imaging, Div Vasc Imaging & Intervent, 55 Fruit St,Gray Bigelow 290, Boston, MA 02114 USA.
EM roklu@partners.org
FU Defense for Research and Engineering under Air Force Contract
[FA8721-05-C-0002]
FX This work was sponsored by the Assistant Secretary of Defense for
Research and Engineering under Air Force Contract FA8721-05-C-0002.
Opinions, interpretations, recommendations, and conclusions are those of
the authors and are not necessarily endorsed by the United States
Government. None of the authors have identified a conflict of interest.
NR 43
TC 12
Z9 12
U1 1
U2 17
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 2013
VL 24
IS 8
BP 1201
EP 1207
DI 10.1016/j.jvir.2013.03.034
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 198LL
UT WOS:000322924300016
PM 23735316
ER
PT J
AU Wardlaw, JM
Smith, EE
Biessels, GJ
Cordonnier, C
Fazekas, F
Frayne, R
Lindley, RI
O'Brien, JT
Barkhof, F
Benavente, OR
Black, SE
Brayne, C
Breteler, M
Chabriat, H
DeCarli, C
de Leeuw, FE
Doubal, F
Duering, M
Fox, NC
Greenberg, S
Hachinski, V
Kilimann, I
Mok, V
van Oostenbrugge, R
Pantoni, L
Speck, O
Stephan, BCM
Teipel, S
Viswanathan, A
Werring, D
Chen, C
Smith, C
van Buchem, M
Norrving, B
Gorelick, PB
Dichgans, M
AF Wardlaw, Joanna M.
Smith, Eric E.
Biessels, Geert J.
Cordonnier, Charlotte
Fazekas, Franz
Frayne, Richard
Lindley, Richard I.
O'Brien, John T.
Barkhof, Frederik
Benavente, Oscar R.
Black, Sandra E.
Brayne, Carol
Breteler, Monique
Chabriat, Hugues
DeCarli, Charles
de Leeuw, Frank-Erik
Doubal, Fergus
Duering, Marco
Fox, Nick C.
Greenberg, Steven
Hachinski, Vladimir
Kilimann, Ingo
Mok, Vincent
van Oostenbrugge, Robert
Pantoni, Leonardo
Speck, Oliver
Stephan, Blossom C. M.
Teipel, Stefan
Viswanathan, Anand
Werring, David
Chen, Christopher
Smith, Colin
van Buchem, Mark
Norrving, Bo
Gorelick, Philip B.
Dichgans, Martin
CA STand Reporting Vasc Changes
TI Neuroimaging standards for research into small vessel disease and its
contribution to ageing and neurodegeneration
SO LANCET NEUROLOGY
LA English
DT Review
ID VIRCHOW-ROBIN SPACES; WHITE-MATTER HYPERINTENSITIES; SPONTANEOUS
INTRACEREBRAL HEMORRHAGE; VASCULAR COGNITIVE IMPAIRMENT;
MAGNETIC-RESONANCE IMAGES; ASSOCIATION/AMERICAN-STROKE-ASSOCIATION;
SMALL SUBCORTICAL INFARCTIONS; ENLARGED PERIVASCULAR SPACES; CEREBRAL
AMYLOID ANGIOPATHY; SILENT BRAIN INFARCTS
AB Cerebral small vessel disease (SVD) is a common accompaniment of ageing. Features seen on neuroimaging include recent small subcortical infarcts, lacunes, white matter hyperintensities, perivascular spaces, microbleeds, and brain atrophy. SVD can present as a stroke or cognitive decline, or can have few or no symptoms. SVD frequently coexists with neurodegenerative disease, and can exacerbate cognitive deficits, physical disabilities, and other symptoms of neurodegeneration. Terminology and definitions for imaging the features of SVD vary widely, which is also true for protocols for image acquisition and image analysis. This lack of consistency hampers progress in identifying the contribution of SVD to the pathophysiology and clinical features of common neurodegenerative diseases. We are an international working group from the Centres of Excellence in Neurodegeneration. We completed a structured process to develop definitions and imaging standards for markers and consequences of SVD. We aimed to achieve the following: first, to provide a common advisory about terms and definitions for features visible on MRI; second, to suggest minimum standards for image acquisition and analysis; third, to agree on standards for scientific reporting of changes related to SVD on neuroimaging; and fourth, to review emerging imaging methods for detection and quantification of preclinical manifestations of SVD. Our findings and recommendations apply to research studies, and can be used in the clinical setting to standardise image interpretation, acquisition, and reporting. This Position Paper summarises the main outcomes of this international effort to provide the STandards for Reporting Vascular changes on nEuroimaging (STRIVE).
C1 [Wardlaw, Joanna M.] Univ Edinburgh, Edinburgh, Midlothian, Scotland.
[Wardlaw, Joanna M.; Smith, Colin] Univ Edinburgh, Ctr Clin Brain Sci, Edinburgh, Midlothian, Scotland.
[Wardlaw, Joanna M.] Univ Edinburgh, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh, Midlothian, Scotland.
[Doubal, Fergus] Univ Edinburgh, Brain Res Imaging Ctr, Edinburgh, Midlothian, Scotland.
[Smith, Eric E.] Univ Calgary, Dept Clin Neurosci & Radiol, Hotchkiss Brain Inst, Calgary, AB, Canada.
[Smith, Eric E.; Frayne, Richard] Univ Calgary, Seaman Family MR Res, Calgary, AB, Canada.
[Biessels, Geert J.] UMC, Rudolf Magnus Inst Neurosci, Dept Neurol, Utrecht, Netherlands.
[Cordonnier, Charlotte] Lille Univ Hosp, Dept Neurol, Lille, France.
[Fazekas, Franz] Graz Univ, Dept Med Neurol, Graz, Austria.
[Lindley, Richard I.] Univ Sydney, Westmead Hosp, Sydney, NSW 2006, Australia.
[O'Brien, John T.] Univ Cambridge, Dept Psychiat, Addenbrookes Hosp, Cambridge, England.
[Barkhof, Frederik] Vrije Univ Amsterdam Med Ctr, Dept Radiol & Nucl Med, Amsterdam, Netherlands.
[Benavente, Oscar R.] Univ British Columbia, Dept Med, Div Neurol, Brain Res Ctr, Vancouver, BC, Canada.
[Black, Sandra E.] Sunnybrook Hlth Sci Ctr, Toronto, ON M4N 3M5, Canada.
[Brayne, Carol] Cambridge Inst Publ Hlth, Sch Clin Med, Cambridge, England.
[Breteler, Monique] German Ctr Neurodegenerat Dis, Bonn, Germany.
[Chabriat, Hugues] Univ Paris 07, INSERM, Hop Lariboisiere, Serv Neurol, Paris, France.
[DeCarli, Charles] Univ Calif Davis, Dept Neurol, Sacramento, CA 95817 USA.
[de Leeuw, Frank-Erik] Radboud Univ Nijmegen, Med Ctr, Dept Neurol, Donders Inst Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
[Duering, Marco; Dichgans, Martin] Univ Munich, Inst Stroke & Dementia Res, Klinikum Univ Munchen, Munich, Germany.
[Werring, David] UCL, Inst Neurol, Dept Brain Repair & Rehabil, London, England.
[Greenberg, Steven; Viswanathan, Anand] Massachusetts Gen Hosp, Ctr Stroke Res, Boston, MA 02114 USA.
[Hachinski, Vladimir] Western Univ, Dept Clin Neurol Sci, London, ON, Canada.
[Kilimann, Ingo; Teipel, Stefan] German Ctr Neurodegenerat Dis DZNE Rostock Greifs, Rostock, Germany.
[Mok, Vincent] Chinese Univ Hong, Div Neurol, Dept Med andTherapeut, Prince Wales Hosp, Hong Kong, Hong Kong, Peoples R China.
[Mok, Vincent; van Oostenbrugge, Robert] Maastricht Univ Med Ctr, Dept Neurol, Sch Mental Hlth & Neurosci, Maastricht, Netherlands.
[van Oostenbrugge, Robert] Maastricht Univ Med Ctr, Cardiovasc Res Inst Maastricht, Maastricht, Netherlands.
[Pantoni, Leonardo] Univ Florence, Azienda Univ Osped Careggi, Dept Neurosci Pharmacol & Childs Hlth NEUROFA, Florence, Italy.
[Speck, Oliver] Univ Magdeburg, Inst Expt Phys, Fac Nat Sci, Dept Biomed Magnet Resonance, D-39106 Magdeburg, Germany.
[Stephan, Blossom C. M.] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Chen, Christopher] Natl Univ Singapore, Yong Loo Lin Sch Med, Singapore 117595, Singapore.
[van Buchem, Mark] Leiden Univ, Dept Radiol, Med Ctr, Leiden, Netherlands.
[Norrving, Bo] Skane Univ Hosp, Dept Clin Sci, Neurol Sect, Lund, Sweden.
[Gorelick, Philip B.] Hauenstein Neurosci Ctr, St Marys Hlth Care, Grand Rapids, MI USA.
[Dichgans, Martin] Munich Cluster Syst Neurol SyNergy, Munich, Germany.
RP Wardlaw, JM (reprint author), Univ Edinburgh, Western Gen Hosp, Div Neuroimaging Sci, Edinburgh EH4 2XU, Midlothian, Scotland.
EM joanna.wardiaw@ed.ac.uk
RI Chen, Christopher/E-7023-2013; Frayne, Richard/F-9347-2012; Fox,
Nick/B-1319-2009; Leeuw, H.F./L-4479-2015; Smith, Eric/C-5443-2012; Mok,
Vincent /N-6421-2015; Lindley, Richard/B-8148-2013; Chabriat,
Hugues/G-5699-2010; de Leeuw, Frank-Erik/E-4795-2012;
OI Stephan, Blossom/0000-0002-1235-360X; Norrving, Bo/0000-0002-8024-5096;
Frayne, Richard/0000-0003-0358-1210; Fox, Nick/0000-0002-6660-657X;
Smith, Eric/0000-0003-3956-1668; Lindley, Richard/0000-0002-0104-5679;
Chabriat, Hugues/0000-0001-8436-6074; Black, Sandra/0000-0001-7093-8289
FU Centre of Excellence in Neurodegeneration (COEN) concordat (UK Medical
Research Council) [COEN017]; Centre of Excellence in Neurodegeneration
(COEN) concordat (German Centre for Neurodegenerative Disease [DZNE])
[COEN017]; Centre of Excellence in Neurodegeneration (COEN) concordat
(Canadian Institutes of Health Research [CIHR]) [COEN017]; Royal Society
of Edinburgh; Scottish Imaging Network, a Platform for Scientific
Excellence (SINAPSE) Collaboration; UK Cross-Council Centre for
Cognitive Ageing and Cognitive Epidemiology, Edinburgh, UK; Carl
Friedrich von Siemens Foundation; Vascular Dementia Research Foundation;
NIHR Biomedical Research Unit in Dementia; FP6 ERA-NET NEURON grant [01
EW1207]; Canadian Stroke Network
FX The following institutions provided funding: the Centres of Excellence
in Neurodegeneration (COEN) concordat (UK Medical Research Council, the
German Centre for Neurodegenerative Disease [DZNE], and the Canadian
Institutes of Health Research [CIHR]) reference COEN017; Royal Society
of Edinburgh; Scottish Imaging Network, a Platform for Scientific
Excellence (SINAPSE) Collaboration; UK Cross-Council Centre for
Cognitive Ageing and Cognitive Epidemiology, Edinburgh, UK; Carl
Friedrich von Siemens Foundation; Vascular Dementia Research Foundation;
NIHR Biomedical Research Unit in Dementia awarded to Cambridge
University Hospitals NHS Trust and the University of Cambridge,
Cambridge, UK; NIHR Biomedical Research Unit in Dementia awarded to UCL
Hospitals NHS Trust and UCL, London UK; FP6 ERA-NET NEURON grant (01
EW1207); and the Canadian Stroke Network. We thank M Henderson, K
Shuler, L Thomas, I Wittko, and Anna Charlton for administrative
support.
NR 111
TC 502
Z9 516
U1 18
U2 134
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1474-4422
J9 LANCET NEUROL
JI Lancet Neurol.
PD AUG
PY 2013
VL 12
IS 8
BP 822
EP 838
PG 17
WC Clinical Neurology
SC Neurosciences & Neurology
GA 195GP
UT WOS:000322690600020
PM 23867200
ER
PT J
AU DeAngelo, DJ
Spencer, A
Bhalla, KN
Prince, HM
Fischer, T
Kindler, T
Giles, FJ
Scott, JW
Parker, K
Liu, A
Woo, M
Atadja, P
Mishra, KK
Ottmann, OG
AF DeAngelo, D. J.
Spencer, A.
Bhalla, K. N.
Prince, H. M.
Fischer, T.
Kindler, T.
Giles, F. J.
Scott, J. W.
Parker, K.
Liu, A.
Woo, M.
Atadja, P.
Mishra, K. K.
Ottmann, O. G.
TI Phase Ia/II, two-arm, open-label, dose-escalation study of oral
panobinostat administered via two dosing schedules in patients with
advanced hematologic malignancies
SO LEUKEMIA
LA English
DT Article
DE panobinostat; histone deacetylase; myelofibrosis; Hodgkin lymphoma;
myelodysplastic disorders; myeloma
ID HISTONE DEACETYLASE INHIBITORS; T-CELL LYMPHOMA; HYPOXIA-INDUCIBLE
FACTOR-1-ALPHA; REFRACTORY MULTIPLE-MYELOMA;
INTERNATIONAL-WORKING-GROUP; RESPONSE CRITERIA; HYDROXAMIC ACID; LBH589;
ACETYLATION; VORINOSTAT
AB Panobinostat is a potent oral pandeacetylase inhibitor that leads to acetylation of intracellular proteins, inhibits cellular proliferation and induces apoptosis in leukemic cell lines. A phase Ia/II study was designed to determine the maximum-tolerated dose (MTD) of daily panobinostat, administered on two schedules: three times a week every week or every other week on a 28-day treatment cycle in patients with advanced hematologic malignancies. The criteria for hematologic dose-limiting toxicities differed between patients with indications associated with severe cytopenias at baseline (leukemia and myeloid disorders) and those less commonly associated with baseline cytopenias (lymphoma and myeloma). In patients with leukemia and myeloid disorders, 60 mg was the MTD for weekly as well as biweekly panobinostat. In patients with lymphoma and myeloma, 40 mg was the recommended dose for phase II evaluation (formal MTD not determined) of weekly panobinostat, and 60 mg was the MTD for biweekly panobinostat. Overall, panobinostat-related grade 3-4 adverse events included thrombocytopenia (41.5%), fatigue (21%) and neutropenia (21%). Single-agent activity was observed in several indications, including Hodgkin lymphoma and myelofibrosis. This phase Ia/II study provided a broad analysis of the safety profile and efficacy of single-agent panobinostat in patients with hematologic malignancies.
C1 [DeAngelo, D. J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Spencer, A.] Alfred Hosp, Malignant Haematol & Stem Cell Transplantat Serv, Melbourne, Vic, Australia.
[Bhalla, K. N.] Univ Kansas, Ctr Canc, Kansas City, MO USA.
[Prince, H. M.] Peter MacCallum Canc Inst, Melbourne, Vic 3000, Australia.
[Prince, H. M.] Univ Melbourne, Melbourne, Vic, Australia.
[Fischer, T.] Univ Magdeburg, Med Ctr, Dept Hematol Oncol, D-39106 Magdeburg, Germany.
[Kindler, T.; Giles, F. J.] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Div Hematol Oncol Pneumol, Dept Med 3, D-55122 Mainz, Germany.
[Giles, F. J.] Natl Univ Ireland Univ Coll Galway, Galway, Ireland.
[Giles, F. J.] Trinity Coll, Galway, Ireland.
[Scott, J. W.; Parker, K.; Liu, A.; Woo, M.; Atadja, P.; Mishra, K. K.] Novartis Oncol, Florham Pk, NJ USA.
[Scott, J. W.; Parker, K.; Liu, A.; Woo, M.; Atadja, P.; Mishra, K. K.; Ottmann, O. G.] Goethe Univ, Dept Hematol & Oncol, Med Klin 2, Frankfurt, Germany.
RP DeAngelo, DJ (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM Daniel_Deangelo@dfci.harvard.edu
RI Kindler, Thomas/K-5995-2013; Ottmann, Oliver/D-5007-2016
OI Ottmann, Oliver/0000-0001-9559-1330
FU Novartis Pharmaceuticals
FX Oliver G Ottmann is an endowed professor of the German Jose Carreras
Leukemia Foundation. Financial support for this study was provided by
Novartis Pharmaceuticals. We thank William Fazzone, PhD, for medical
editorial assistance with this manuscript and Tracy Liu, Hannah Mosca
and Glen Laird for assistance with data collection and analysis.
NR 54
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U1 1
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
EI 1476-5551
J9 LEUKEMIA
JI Leukemia
PD AUG
PY 2013
VL 27
IS 8
BP 1628
EP 1636
DI 10.1038/leu.2013.38
PG 9
WC Oncology; Hematology
SC Oncology; Hematology
GA 197BP
UT WOS:000322823200003
PM 23385375
ER
PT J
AU Scullen, T
Santo, L
Vallet, S
Fulciniti, M
Eda, H
Cirstea, D
Patel, K
Nemani, N
Yee, A
Mahindra, A
Raje, N
AF Scullen, T.
Santo, L.
Vallet, S.
Fulciniti, M.
Eda, H.
Cirstea, D.
Patel, K.
Nemani, N.
Yee, A.
Mahindra, A.
Raje, N.
TI Lenalidomide in combination with an activin A-neutralizing antibody:
preclinical rationale for a novel anti-myeloma strategy
SO LEUKEMIA
LA English
DT Article
DE lenalidomide; activin A; myeloma
ID REFRACTORY MULTIPLE-MYELOMA; IMMUNOMODULATORY THALIDOMIDE ANALOGS;
DEPENDENT KINASE INHIBITOR; BONE-DISEASE; OSTEOBLAST DIFFERENTIATION;
THERAPEUTIC APPLICATIONS; PLUS DEXAMETHASONE; CELLS; DLX5;
OSTEOCLASTOGENESIS
AB Given the prevalence of osteolytic bone disease in multiple myeloma (MM), novel therapies targeting bone microenvironment are essential. Previous studies have identified activin A to be of critical importance in MM-induced osteolysis. Lenalidomide is a known and approved treatment strategy for relapsed MM. Our findings demonstrate that lenalidomide acts directly on bone marrow stromal cells via an Akt-mediated increase in Jun N-terminal kinase-dependent signaling resulting in activin A secretion, with consequent inhibition of osteoblastogenesis. Here, we attempted to augment the antitumor benefits of lenalidomide while overcoming its effects on osteoblastogenesis by combining it with a neutralizing antibody to activin A. Increased activin A secretion induced by lenalidomide was abrogated by the addition of activin A-neutralizing antibody, which effectively restored osteoblast function and inhibited MM-induced osteolysis without negating the cytotoxic effects of lenalidomide on malignant cells. This provides the rationale for an ongoing clinical trial (NCT01562405) combining lenalidomide with an anti-activin A strategy.
C1 [Scullen, T.; Santo, L.; Vallet, S.; Eda, H.; Cirstea, D.; Patel, K.; Nemani, N.; Yee, A.; Mahindra, A.; Raje, N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc,Div Hematol & Oncol, Boston, MA 02114 USA.
[Fulciniti, M.; Cirstea, D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Raje, N (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc,Div Hematol & Oncol, 55 Fruit St, Boston, MA 02114 USA.
EM nraje@partners.org
FU LLS; MMRF
FX NR is supported by LLS and MMRF.
NR 39
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U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD AUG
PY 2013
VL 27
IS 8
BP 1715
EP 1721
DI 10.1038/leu.2013.50
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA 197BP
UT WOS:000322823200012
PM 23417027
ER
PT J
AU Bueno, M
Paganetti, H
Duch, MA
Schuemann, J
AF Bueno, M.
Paganetti, H.
Duch, M. A.
Schuemann, J.
TI An algorithm to assess the need for clinical Monte Carlo dose
calculation for small proton therapy fields based on quantification of
tissue heterogeneity
SO MEDICAL PHYSICS
LA English
DT Article
DE Monte Carlo; proton therapy; heterogeneities; small fields;
heterogeneity index
ID PENCIL BEAM ALGORITHM; BRAGG PEAK; INHOMOGENEITIES; UNCERTAINTIES;
SIMULATIONS; SETTINGS; ACCURACY; TOOLKIT; CANCER; RANGE
AB Purpose: In proton therapy, complex density heterogeneities within the beam path constitute a challenge to dose calculation algorithms. This might question the reliability of dose distributions predicted by treatment planning systems based on analytical dose calculation. For cases in which substantial dose errors are expected, resorting to Monte Carlo dose calculations might be essential to ensure a successful treatment outcome and therefore the benefit is worth a presumably long computation time. The aim of this study was to define an indicator for the accuracy of dose delivery based on analytical dose calculations in treatment planning systems for small proton therapy fields to identify those patients for which Monte Carlo dose calculation is warranted.
Methods: Fourteen patients treated at our facility with small passively scattered proton beams (apertures diameters below 7 cm) were selected. Plans were generated in the XiO treatment planning system in combination with a pencil beam algorithm developed at the Massachusetts General Hospital and compared to Monte Carlo dose calculations. Differences in the dose to the 50% of the gross tumor volume (D50, GTV) were assessed in a field-by-field basis. A simple and fast methodology was developed to quantify the inhomogeneity of the tissue traversed by a single small proton beam using a heterogeneity index (HI)-a concept presented by Plugfelder et al. [Med. Phys. 34, 1506-1513 (2007)] for scanned proton beams. Finally, the potential correlation between the error made by the pencil beam based treatment planning algorithm for each field and the level of tissue heterogeneity traversed by the proton beam given by the HI was evaluated.
Results: Discrepancies up to 5.4% were found in D50 for single fields, although dose differences were within clinical tolerance levels (<3%) when combining all of the fields involved in the treatment. The discrepancies found for each field exhibited a strong correlation to their associated HI-values (Spearman's rho = 0.8, p < 0.0001); the higher the level of tissue inhomogeneities for a particular field, the larger the error by the analytical algorithm. With the established correlation a threshold for HI can be set by choosing a tolerance level of 2-3%-commonly accepted in radiotherapy.
Conclusions: The HI is a good indicator for the accuracy of proton field delivery in terms of GTV prescription dose coverage when small fields are delivered. Each HI-value was obtained from the CT image in less than 3 min on a computer with 2 GHz CPU allowing implementation of this methodology in clinical routine. For HI-values exceeding the threshold, either a change in beam direction (if feasible) or a recalculation of the dose with Monte Carlo would be highly recommended. (C) 2013 American Association of Physicists in Medicine.
C1 [Bueno, M.; Duch, M. A.] Univ Politecn Cataluna, Inst Tecn Energet, Dept Dosimetria & Fis Med, E-08028 Barcelona, Spain.
[Bueno, M.] Inst Bioengn Catalonia, Barcelona 08028, Spain.
[Paganetti, H.; Schuemann, J.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
[Paganetti, H.; Schuemann, J.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Bueno, M (reprint author), Univ Politecn Cataluna, Inst Tecn Energet, Dept Dosimetria & Fis Med, E-08028 Barcelona, Spain.
EM marta.bueno@upc.edu
RI Duch, Maria /F-8593-2016
OI Duch, Maria /0000-0002-1560-1576
FU Institute for Bioengineering of Catalonia; Institut de Tecniques
Energetiques
FX The authors would like to thank Hanne Kooy, Tom Madden, and Nicolas
Depauw for providing detailed information about our analytical dose
calculation algorithm and for helpful discussions on proton treatment
planning. The authors also thank Carles Goma for fruitful discussions on
the definition of the heterogeneity index. The authors gratefully
acknowledge the Monte Carlo group at MGH, especially Clemens
Grassberger, for helpful comments and support throughout the development
of this project. Treatment plans were made by Brian Winey. This work was
supported in part by the Institute for Bioengineering of Catalonia and
the Institut de Tecniques Energetiques.
NR 34
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U1 1
U2 9
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 2013
VL 40
IS 8
AR 081704
DI 10.1118/1.4812682
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 195XC
UT WOS:000322735900009
PM 23927301
ER
PT J
AU Li, XH
Zhang, D
Liu, B
AF Li, Xinhua
Zhang, Da
Liu, Bob
TI Calculations of two new dose metrics proposed by AAPM Task Group 111
using the measurements with standard CT dosimetry phantoms
SO MEDICAL PHYSICS
LA English
DT Article
DE computed tomography (CT); dose metric; equilibrium dose-pitch product;
midpoint dose; calculation
ID COMPUTED-TOMOGRAPHY; PRACTICAL APPROACH; FEASIBILITY; CTDI100; INDEX;
EXAMS; MDCT
AB Purpose: AAPM Task Group 111 proposed to measure the equilibrium dose-pitch product (D) over cap (eq) for scan modes involving table translation and the midpoint dose D-L(0) for stationary-table modes on the central and peripheral axes of sufficiently long (e.g., at least 40 cm) phantoms. This paper presents an alternative approach to calculate both metrics using the measurements of scanning the standard computed tomographic (CT) dosimetry phantoms on CT scanners.
Methods: (D) over cap (eq) was calculated from CTDI100 and epsilon(CTDI100) (CTDI100 efficiency), and D-L(0) was calculated from (D) over cap (eq) and the approach to equilibrium function H(L) = D-L(0)/D-eq, where D-eq was the equilibrium dose. CTDI100 may be directly obtained from several sources (such as medical physicist's CT scanner performance evaluation or the IMPACT CT patient dosimetry calculator), or be derived from CTDIVol using the central to peripheral CTDI100 ratio (R-100). The authors have provided the required epsilon(CTDI100) and H(L) data in two previous papers [X. Li, D. Zhang, and B. Liu, Med. Phys. 39, 901-905 (2012); 40, 031903 (10pp.) (2013)]. R-100 was assessed for a series of GE, Siemens, Philips, and Toshiba CT scanners with multiple settings of scan field of view, tube voltage, and bowtie filter.
Results: The calculated D-L(0) and D-L(0)/D-eq in PMMA and water cylinders were consistent with the measurements on two GE CT scanners (LightSpeed 16 and VCT) by Dixon and Ballard [Med. Phys. 34, 3399-3413 (2007)], the measurements on a Siemens CT scanner (SOMATOM Spirit Power) by Descamps et al. [J. Appl. Clin. Med. Phys. 13, 293-302 (2012)], and the Monte Carlo simulations by Boone [Med. Phys. 36, 4547-4554 (2009)].
Conclusions: (D) over cap (eq) and DL(0) can be calculated using the alternative approach. The authors have provided the required epsilon(CTDI100) and H(L) data in two previous papers. R-100 is presented for a majority of multidetector CT scanners currently on the market, and can be easily assessed for other CT scanners or operating conditions not covered in this study. The central to peripheral D-eq ratio is about 1.50 and 1.12 times of R-100 for the 32- and 16-cm diameter PMMA phantom, respectively. (C) 2013 American Association of Physicists in Medicine.
C1 [Liu, Bob] Massachusetts Gen Hosp, Div Diagnost Imaging Phys, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Dept Radiol, Webster Ctr Adv Res & Educ Radiat, Boston, MA 02114 USA.
RP Liu, B (reprint author), Massachusetts Gen Hosp, Div Diagnost Imaging Phys, Boston, MA 02114 USA.
EM bliu7@bics.bwh.harvard.edu
NR 17
TC 7
Z9 7
U1 0
U2 3
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 2013
VL 40
IS 8
AR 081914
DI 10.1118/1.4813899
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 195XC
UT WOS:000322735900036
PM 23927328
ER
PT J
AU Petrick, N
Sahiner, B
Armato, SG
Bert, A
Correale, L
Delsanto, S
Freedman, MT
Fryd, D
Gur, D
Hadjiiski, L
Huo, ZM
Jiang, YL
Morra, L
Paquerault, S
Raykar, V
Samuelson, F
Summers, RM
Tourassi, G
Yoshida, H
Zheng, B
Zhou, C
Chan, HP
AF Petrick, Nicholas
Sahiner, Berkman
Armato, Samuel G., III
Bert, Alberto
Correale, Loredana
Delsanto, Silvia
Freedman, Matthew T.
Fryd, David
Gur, David
Hadjiiski, Lubomir
Huo, Zhimin
Jiang, Yulei
Morra, Lia
Paquerault, Sophie
Raykar, Vikas
Samuelson, Frank
Summers, Ronald M.
Tourassi, Georgia
Yoshida, Hiroyuki
Zheng, Bin
Zhou, Chuan
Chan, Heang-Ping
TI Evaluation of computer-aided detection and diagnosis systems
SO MEDICAL PHYSICS
LA English
DT Article
DE computer-aided detection and diagnosis (CAD); computer-aided detection
(CADe); computer-aided diagnosis (CADx); performance assessment;
standalone performance; reader performance; clinical performance
ID OPERATING CHARACTERISTIC ANALYSIS; BREAST-CANCER DETECTION;
MAXIMUM-LIKELIHOOD-ESTIMATION; IMAGE DATABASE CONSORTIUM; SMALL
PULMONARY NODULES; MEMORIAL FUND LECTURE; CT COLONOGRAPHY; LUNG NODULES;
SCREENING MAMMOGRAPHY; OBSERVER-PERFORMANCE
AB Computer-aided detection and diagnosis (CAD) systems are increasingly being used as an aid by clinicians for detection and interpretation of diseases. Computer-aided detection systems mark regions of an image that may reveal specific abnormalities and are used to alert clinicians to these regions during image interpretation. Computer-aided diagnosis systems provide an assessment of a disease using image-based information alone or in combination with other relevant diagnostic data and are used by clinicians as a decision support in developing their diagnoses. While CAD systems are commercially available, standardized approaches for evaluating and reporting their performance have not yet been fully formalized in the literature or in a standardization effort. This deficiency has led to difficulty in the comparison of CAD devices and in understanding how the reported performance might translate into clinical practice. To address these important issues, the American Association of Physicists in Medicine (AAPM) formed the Computer Aided Detection in Diagnostic Imaging Subcommittee (CADSC), in part, to develop recommendations on approaches for assessing CAD system performance. The purpose of this paper is to convey the opinions of the AAPM CADSC members and to stimulate the development of consensus approaches and "best practices" for evaluating CAD systems. Both the assessment of a standalone CAD system and the evaluation of the impact of CAD on end-users are discussed. It is hoped that awareness of these important evaluation elements and the CADSC recommendations will lead to further development of structured guidelines for CAD performance assessment. Proper assessment of CAD system performance is expected to increase the understanding of a CAD system's effectiveness and limitations, which is expected to stimulate further research and development efforts on CAD technologies, reduce problems due to improper use, and eventually improve the utility and efficacy of CAD in clinical practice. (C) 2013 American Association of Physicists in Medicine.
C1 [Petrick, Nicholas; Sahiner, Berkman; Samuelson, Frank] US FDA, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
[Armato, Samuel G., III; Jiang, Yulei] Univ Chicago, Dept Radiol, Chicago, IL 60637 USA.
[Bert, Alberto; Correale, Loredana; Delsanto, Silvia; Morra, Lia] im3D SpA, I-10153 Turin, Italy.
[Freedman, Matthew T.] Georgetown Univ, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
[Fryd, David] Riverain Med, Miamisburg, OH 45342 USA.
[Gur, David] Univ Pittsburgh, Dept Radiol, Pittsburgh, PA 15213 USA.
[Hadjiiski, Lubomir; Zhou, Chuan; Chan, Heang-Ping] Univ Michigan, Dept Radiol, Ann Arbor, MI 48109 USA.
[Huo, Zhimin] Carestream Hlth Inc, Rochester, NY 14615 USA.
[Raykar, Vikas] IBM Res, Nagawara Bangalore 560045, India.
[Summers, Ronald M.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Tourassi, Georgia] Oak Ridge Natl Lab, Computat Sci & Engn Div, Oak Ridge, TN 37831 USA.
[Yoshida, Hiroyuki] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Yoshida, Hiroyuki] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Zheng, Bin] Univ Oklahoma, Sch Elect & Comp Engn, Norman, OK 73019 USA.
RP Chan, HP (reprint author), Univ Michigan, Dept Radiol, 1500 East Med Ctr Dr,MIB C479, Ann Arbor, MI 48109 USA.
EM chanhp@umich.edu
OI Bert, Alberto/0000-0001-8391-7508; Tourassi,
Georgia/0000-0002-9418-9638; Zheng, Bin/0000-0002-7682-6648
FU Intramural Research Program of the National Institutes of Health,
Clinical Center; University of Chicago; iCAD; Riverain Technologies
through Georgetown University Medical Center
FX The authors are grateful to the members and participants of the CADSC
who have contributed to the stimulating discussions during many meetings
and teleconferences. R. M. S. is supported in part by the Intramural
Research Program of the National Institutes of Health, Clinical Center;
the views expressed in this paper are the opinions of the authors and do
not necessarily represent the views of the National Institutes of Health
or the Department of Health and Human Services. S. G. A. and H.Y.
receive royalties and licensing fees through the University of Chicago
related to CAD. R. M. S. receives patent royalties and research support
related to CAD from iCAD. M. T. F. receives funding from Riverain
Technologies through Georgetown University Medical Center.
NR 139
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U1 4
U2 34
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 2013
VL 40
IS 8
AR 087001
DI 10.1118/1.4816310
PG 17
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 195XC
UT WOS:000322735900073
PM 23927365
ER
PT J
AU Zhang, D
Li, XH
Gao, YM
Xu, XG
Liu, B
AF Zhang, Da
Li, Xinhua
Gao, Yiming
Xu, X. George
Liu, Bob
TI A method to acquire CT organ dose map using OSL dosimeters and ATOM
anthropomorphic phantoms
SO MEDICAL PHYSICS
LA English
DT Article
DE CT; dose measurement; organ dose; OSL; ATOM phantom
ID COMPUTED-TOMOGRAPHY; MONTE-CARLO; PATIENT; DEPENDENCE; PROFILES; SCANNER
AB Purpose: To present the design and procedure of an experimental method for acquiring densely sampled organ dose map for CT applications, based on optically stimulated luminescence (OSL) dosimeters "nanoDots" and standard ATOM anthropomorphic phantoms; and to provide the results of applying the method-a dose data set with good statistics for the comparison with Monte Carlo simulation result in the future.
Methods: A standard ATOM phantom has densely located holes (in 3 x 3 cm or 1.5 x 1.5 cm grids), which are too small (5 mm in diameter) to host many types of dosimeters, including the nanoDots. The authors modified the conventional way in which nanoDots are used, by removing the OSL disks from the holders before inserting them inside a standard ATOM phantom for dose measurements. The authors solved three technical difficulties introduced by this modification: (1) energy dependent dose calibration for raw OSL readings; (2) influence of the brief background exposure of OSL disks to dimmed room light; (3) correct pairing between the dose readings and measurement locations. The authors acquired 100 dose measurements at various positions in the phantom, which was scanned using a clinical chest protocol with both angular and z-axis tube current modulations.
Results: Dose calibration was performed according to the beam qualities inside the phantom as determined from an established Monte Carlo model of the scanner. The influence of the brief exposure to dimmed room light was evaluated and deemed negligible. Pairing between the OSL readings and measurement locations was ensured by the experimental design. The organ doses measured for a routine adult chest scan protocol ranged from 9.4 to 18.8 mGy, depending on the composition, location, and surrounding anatomy of the organs. The dose distribution across different slices of the phantom strongly depended on the z-axis mA modulation. In the same slice, doses to the soft tissues other than the spinal cord demonstrated relatively small variations, with the maximum COV around 11.4%. This might be attributed to the angular mA modulation, the placement of the dosimeters, the chest cavity of the scanned region, and the size of the phantom. Doses to the spinal cord were consistently lower than those to other soft tissues.
Conclusions: The method is suited for acquiring densely sampled organ dose maps, and can be used for studying dose distributions relevant to subject size, organ location, and clinical CT protocols. (C) 2013 American Association of Physicists in Medicine.
C1 [Zhang, Da; Li, Xinhua; Liu, Bob] Massachusetts Gen Hosp, Div Diagnost Imaging Phys, Boston, MA 02114 USA.
[Zhang, Da; Li, Xinhua; Liu, Bob] Massachusetts Gen Hosp, Dept Radiol, Webster Ctr Adv Res & Educ Radiat, Boston, MA 02114 USA.
[Gao, Yiming; Xu, X. George] Rensselaer Polytech Inst, Nucl Engn Program, Troy, NY 12180 USA.
RP Liu, B (reprint author), Massachusetts Gen Hosp, Div Diagnost Imaging Phys, Boston, MA 02114 USA.
EM bliu7@bics.bwh.harvard.edu
FU National Institute of Biomedical Imaging and Bioengineering
[R01EB015478]
FX This research is sponsored in part by the National Institute of
Biomedical Imaging and Bioengineering (R01EB015478). The authors want to
acknowledge Dr. Dominic Crotty and Dr. Roy Nilsen of GE for providing
the tube current data at each projection. The authors also want to thank
Radcal Inc. for providing the thimble chamber.
NR 21
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Z9 7
U1 1
U2 6
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 2013
VL 40
IS 8
AR 081918
DI 10.1118/1.4816299
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 195XC
UT WOS:000322735900040
PM 23927332
ER
PT J
AU Anand, S
Hasan, T
Maytin, EV
AF Anand, Sanjay
Hasan, Tayyaba
Maytin, Edward V.
TI Mechanism of Differentiation-Enhanced Photodynamic Therapy for Cancer:
Upregulation of Coproporphyrinogen Oxidase by C/EBP Transcription
Factors
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID BINDING-PROTEIN-BETA; MAMMARY EPITHELIAL-CELLS; NF-KAPPA-B; DNA-BINDING;
PROTOPORPHYRIN-IX; IN-VITRO; ENDOGENOUS PROTOPORPHYRIN; AMINOLEVULINIC
ACID; GENE-TRANSCRIPTION; CARCINOMA-CELLS
AB The efficacy of photodynamic therapy (PDT) for epithelial cancers is increased when PDT is combined with calcitriol (Vit D), a form of differentiation therapy (DT). Here, we describe an underlying mechanism for this effect. Differentiation-promoting agents are known to upregulate CCAAT/enhancer-binding proteins (C/EBP), powerful regulators of cellular differentiation. In subcutaneous A431 tumors in mice, pretreatment with Vit D induced the expression of C/EBP beta isoforms, and of coproporphyrinogen oxidase (CPO), a heme pathway enzyme responsible for the conversion of 5-aminolevulinic acid (ALA) into protoporphyrin IX (PpIX), the principal light-absorbing molecule during PDT. To further investigate this apparent link between C/EBPs and CPO, two cell lines (MEL and LNCaP) were exposed to differentiating agents, and levels of PpIX, C/EBPs, and CPO were measured. Differentiating agents, or transfection of C/EBP expression vectors, increased C/EBP and CPO levels in parallel. Focusing on approximately 1,300 bp of upstream CPO gene promoter, we tested the ability of recombinant C/EBP alpha, C/EBP beta, C/EBP delta, and C/EBP zeta to bind to CPO gene sequences [electrophoretic mobility shift assay (EMSA) assays] and to affect transcriptional activity (luciferase assays). Multiple C/EBP consensus binding sites were identified (15 for mouse, 18 for human). Individual probes representing each site bound to C/EBPs with characteristic affinities (strong, moderate, or weak), but when sites were inactivated in the context of the native promoter, transcriptional activity was reduced nearly equally for strong or weak sites. Cooperative interactions between regularly spaced C/EBP sites seem critical for CPO transcriptional regulation by differentiation therapy. These results provide a mechanistic rationale for DT/PDT combination therapy for cancer. (C)2013 AACR.
C1 [Anand, Sanjay; Maytin, Edward V.] Cleveland Clin, Dept Biomed Engn, Lerner Res Inst, Cleveland, OH 44106 USA.
[Anand, Sanjay; Maytin, Edward V.] Cleveland Clin, Dept Dermatol, Cleveland, OH 44106 USA.
[Hasan, Tayyaba; Maytin, Edward V.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
RP Maytin, EV (reprint author), Cleveland Clin Fdn, Mailstop ND-20,9500 Euclid Ave, Cleveland, OH 44195 USA.
EM maytine@ccf.org
FU National Cancer Institute at the NIH [P01-CA84203]; Dermatology
Foundation
FX This work was supported by the National Cancer Institute at the NIH,
P01-CA84203 (to T. Hasan and E. V. Maytin), and a grant from the
Dermatology Foundation (to S. Anand).
NR 50
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U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD AUG
PY 2013
VL 12
IS 8
BP 1638
EP 1650
DI 10.1158/1535-7163.MCT-13-0047
PG 13
WC Oncology
SC Oncology
GA 198FU
UT WOS:000322908400024
PM 23686770
ER
PT J
AU Li, JF
Norville, JE
Aach, J
McCormack, M
Zhang, DD
Bush, J
Church, GM
Sheen, J
AF Li, Jian-Feng
Norville, Julie E.
Aach, John
McCormack, Matthew
Zhang, Dandan
Bush, Jenifer
Church, George M.
Sheen, Jen
TI Multiplex and homologous recombination-mediated genome editing in
Arabidopsis and Nicotiana benthamiana using guide RNA and Cas9
SO NATURE BIOTECHNOLOGY
LA English
DT Letter
ID GENE-EXPRESSION; CRISPR; SYSTEMS; NUCLEASES; TALEN
C1 [Li, Jian-Feng; McCormack, Matthew; Zhang, Dandan; Bush, Jenifer; Sheen, Jen] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Li, Jian-Feng; McCormack, Matthew; Zhang, Dandan; Bush, Jenifer; Sheen, Jen] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
[Li, Jian-Feng; Norville, Julie E.; Aach, John; McCormack, Matthew; Zhang, Dandan; Bush, Jenifer; Church, George M.; Sheen, Jen] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
[Norville, Julie E.; Aach, John; Church, George M.] Harvard Univ, Wyss Inst Biol Inspired Engn, Cambridge, MA 02138 USA.
RP Li, JF (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
EM sheen@molbio.mgh.harvard.edu
FU NIGMS NIH HHS [R01 GM060493, R01 GM60493, R01 GM070567, R01 GM70567]
NR 14
TC 290
Z9 332
U1 30
U2 308
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 2013
VL 31
IS 8
BP 688
EP 691
DI 10.1038/nbt.2654
PG 5
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 198GS
UT WOS:000322911000011
PM 23929339
ER
PT J
AU Barzel, B
Barabasi, AL
AF Barzel, Baruch
Barabasi, Albert-Laszlo
TI Network link prediction by global silencing of indirect correlations
SO NATURE BIOTECHNOLOGY
LA English
DT Article
ID GENE REGULATORY NETWORKS; PROTEIN INTERACTIONS; EXPRESSION PATTERNS;
COMPLEX NETWORKS; DISEASE; MAP; LANDSCAPE; BIOLOGY; CELL
AB Predictions of physical and functional links between cellular components are often based on correlations between experimental measurements, such as gene expression. However, correlations are affected by both direct and indirect paths, confounding our ability to identify true pairwise interactions. Here we exploit the fundamental properties of dynamical correlations in networks to develop a method to silence indirect effects. The method receives as input the observed correlations between node pairs and uses a matrix transformation to turn the correlation matrix into a highly discriminative silenced matrix, which enhances only the terms associated with direct causal links. Against empirical data for Escherichia coli regulatory interactions, the method enhanced the discriminative power of the correlations by twofold, yielding >50% predictive improvement over traditional correlation measures and 6% over mutual information. Overall this silencing method will help translate the abundant correlation data into insights about a system's interactions, with applications ranging from link prediction to inferring the dynamical mechanisms governing biological networks.
C1 [Barzel, Baruch; Barabasi, Albert-Laszlo] Northeastern Univ, Ctr Complex Network Res, Boston, MA 02115 USA.
[Barzel, Baruch; Barabasi, Albert-Laszlo] Northeastern Univ, Dept Phys, Boston, MA 02115 USA.
[Barzel, Baruch; Barabasi, Albert-Laszlo] Northeastern Univ, Dept Comp Sci, Boston, MA 02115 USA.
[Barzel, Baruch; Barabasi, Albert-Laszlo] Northeastern Univ, Dept Biol, Boston, MA 02115 USA.
[Barzel, Baruch] Harvard Univ, Sch Med, Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA.
[Barabasi, Albert-Laszlo] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA.
RP Barabasi, AL (reprint author), Northeastern Univ, Ctr Complex Network Res, Boston, MA 02115 USA.
EM barabasi@gmail.com
FU US National Institutes of Health (NIH), Center of Excellence of Genomic
Science (CEGS) [NIH CEGS 1P50HG4233]; NIH [1U01HL108630-01]; DARPA
[11645021]; DARPA Social Media in Strategic Communications project
[W911NF-12-C-0028]; Network Science Collaborative Technology Alliance;
US Army Research Laboratory [NS-CTA W911NF-09-02-0053]; Office of Naval
Research [N000141010968]; Defense Threat Reduction Agency [WMD
BRBAA07-J-2-0035, BRBAA08-Per4-C-2-0033]
FX We thank B. Alipanahi and B. Frey for their valuable insights, A.
Sharma, F. Simini, J. Menche, S. Rabello, G. Ghoshal, Y.-Y. Liu, T. Jia,
M. Posfai, C. Song, Y.-Y. Ahn, N. Blumm, D. Wang, Z. Qu, M. Schich, D.
Ghiassian, S. Gil, P. Hovel, J. Gao, M. Kitsak, M. Martino, R. Sinatra,
G. Tsekenis, L. Chi, B. Gabriel, Q. Jin and Y. Li for discussions, and
S. S. Aleva, S. Morrison, J. De Nicolo and A. Pawling for their support.
This work was supported by the US National Institutes of Health (NIH),
Center of Excellence of Genomic Science (CEGS), Grant number NIH CEGS
1P50HG4233; and the NIH, award number 1U01HL108630-01; DARPA Grant
Number 11645021; DARPA Social Media in Strategic Communications project
under agreement number W911NF-12-C-0028; the Network Science
Collaborative Technology Alliance sponsored by the US Army Research
Laboratory under agreement number NS-CTA W911NF-09-02-0053; the Office
of Naval Research under agreement number N000141010968; and the Defense
Threat Reduction Agency awards WMD BRBAA07-J-2-0035 and
BRBAA08-Per4-C-2-0033.
NR 41
TC 64
Z9 66
U1 1
U2 31
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 2013
VL 31
IS 8
BP 720
EP 725
DI 10.1038/nbt.2601
PG 6
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 198GS
UT WOS:000322911000021
PM 23851447
ER
PT J
AU Su, XL
Arellano-Santoyo, H
Portran, D
Gaillard, J
Vantard, M
Thery, M
Pellman, D
AF Su, Xiaolei
Arellano-Santoyo, Hugo
Portran, Didier
Gaillard, Jeremie
Vantard, Marylin
Thery, Manuel
Pellman, David
TI Microtubule-sliding activity of a kinesin-8 promotes spindle assembly
and spindle-length control
SO NATURE CELL BIOLOGY
LA English
DT Article
ID MITOTIC SPINDLE; SACCHAROMYCES-CEREVISIAE; METAPHASE SPINDLE; ANAPHASE
SPINDLE; YEAST KINESIN-8; BINDING PROTEIN; CROSS-LINKS; KIF18A; MITOSIS;
MOTORS
AB Molecular motors play critical roles in the formation of mitotic spindles, either through controlling the stability of individual microtubules, or by crosslinking and sliding microtubule arrays. Kinesin-8 motors are best known for their regulatory roles in controlling microtubule dynamics. They contain microtubule-destabilizing activities, and restrict spindle length in a wide variety of cell types and organisms. Here, we report an antiparallel microtubule-sliding activity of the budding yeast kinesin-8, Kip3. The in vivo importance of this sliding activity was established through the identification of complementary Kip3 mutants that separate the sliding activity and microtubule-destabilizing activity. In conjunction with Cin8, a kinesin-5 family member, the sliding activity of Kip3 promotes bipolar spindle assembly and the maintenance of genome stability. We propose a slide disassemble model where the sliding and destabilizing activity of Kip3 balance during pre-anaphase. This facilitates normal spindle assembly. However, the destabilizing activity of Kip3 dominates in late anaphase, inhibiting spindle elongation and ultimately promoting spindle disassembly.
C1 [Su, Xiaolei; Arellano-Santoyo, Hugo; Pellman, David] Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA.
[Su, Xiaolei; Arellano-Santoyo, Hugo; Pellman, David] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Su, Xiaolei; Arellano-Santoyo, Hugo; Pellman, David] Harvard Univ, Sch Med, Childrens Hosp, Boston, MA 02115 USA.
[Su, Xiaolei; Arellano-Santoyo, Hugo; Pellman, David] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
[Portran, Didier; Gaillard, Jeremie; Vantard, Marylin; Thery, Manuel] Univ Grenoble 1, Lab Physiol Cellulaire & Vegetale, Inst Rech Technol & Sci Vivant, CNRS,CEA,INRA,UMR5168, F-38054 Grenoble, France.
RP Pellman, D (reprint author), Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA.
EM David_Pellman@dfci.harvard.edu
FU Howard Hughes Medical Institute; National Institute of Health [GM61345];
Human Frontier Scientific Program [RGY0088/201]
FX We are grateful to the Reck-Peterson Laboratory at Harvard Medical
School for sharing the usage of their TIRE microscope. We appreciate H.
Li's help with FAGS analysis. We thank M. Gupta and R. Ohi for
suggestions and comments on the manuscript. D. Penman is supported by
Howard Hughes Medical Institute and a National Institute of Health grant
(GM61345). M. Thery is supported by the Human Frontier Scientific
Program (RGY0088/201). H. Arellano-Santoyo is an international fellow of
the Howard Hughes Medical Institute.
NR 47
TC 25
Z9 26
U1 0
U2 26
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD AUG
PY 2013
VL 15
IS 8
BP 948
EP U400
DI 10.1038/ncb2801
PG 20
WC Cell Biology
SC Cell Biology
GA 193OX
UT WOS:000322570900011
PM 23851487
ER
PT J
AU Sadasivam, S
DeCaprio, JA
AF Sadasivam, Subhashini
DeCaprio, James A.
TI The DREAM complex: master coordinator of cell cycle-dependent gene
expression
SO NATURE REVIEWS CANCER
LA English
DT Review
ID MYB-MUVB/DREAM COMPLEX; TRANSCRIPTION FACTOR TRIDENT; E2F FAMILY-MEMBER;
ELEGANS VULVAR INDUCTION; N-TERMINAL DOMAIN; HUMAN B-MYB;
CAENORHABDITIS-ELEGANS; DROSOPHILA-MYB; S-PHASE; DNA-BINDING
AB The dimerization partner, RB-like, E2F and multi-vulval class B (DREAM) complex provides a previously unsuspected unifying role in the cell cycle by directly linking p130, p107, E2F, BMYB and forkhead box protein M1. DREAM mediates gene repression during the G0 phase and coordinates periodic gene expression with peaks during the G1/S and G2/M phases. Perturbations in DREAM complex regulation shift the balance from quiescence towards proliferation and contribute to the increased mitotic gene expression levels that are frequently observed in cancers with a poor prognosis.
C1 [Sadasivam, Subhashini] Natl Ctr Biol Sci TIFR, Inst Stem Cell Biol & Regenerat Med, Bangalore 560065, Karnataka, India.
[DeCaprio, James A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[DeCaprio, James A.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[DeCaprio, James A.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
RP DeCaprio, JA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM james_decaprio@dfci.harvard.edu
FU US Public Health Service [P01CA050661, R01CA63113]
FX The authors gratefully acknowledge the many helpful discussions about
DREAM with L. Litovchick, N. Dyson, M. Botchan and K. Engeland. This
work was supported in part by US Public Health Service grants
P01CA050661 and R01CA63113 to J.A.D.
NR 141
TC 73
Z9 73
U1 2
U2 49
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-175X
J9 NAT REV CANCER
JI Nat. Rev. Cancer
PD AUG
PY 2013
VL 13
IS 8
BP 585
EP 595
DI 10.1038/nrc3556
PG 11
WC Oncology
SC Oncology
GA 187YS
UT WOS:000322158200012
PM 23842645
ER
PT J
AU Pfeffer, G
Horvath, R
Klopstock, T
Mootha, VK
Suomalainen, A
Koene, S
Hirano, M
Zeviani, M
Bindoff, LA
Yu-Wai-Man, P
Hanna, M
Carelli, V
McFarland, R
Majamaa, K
Turnbull, DM
Smeitink, J
Chinnery, PF
AF Pfeffer, Gerald
Horvath, Rita
Klopstock, Thomas
Mootha, Vamsi K.
Suomalainen, Anu
Koene, Saskia
Hirano, Michio
Zeviani, Massimo
Bindoff, Laurence A.
Yu-Wai-Man, Patrick
Hanna, Michael
Carelli, Valerio
McFarland, Robert
Majamaa, Kari
Turnbull, Douglas M.
Smeitink, Jan
Chinnery, Patrick F.
TI New treatments for mitochondrial disease-no time to drop our standards
SO NATURE REVIEWS NEUROLOGY
LA English
DT Article
ID HEREDITARY OPTIC NEUROPATHY; PLACEBO-CONTROLLED TRIAL; CONGENITAL
LACTIC-ACIDOSIS; CONTROLLED CLINICAL-TRIAL; COENZYME Q(10) TREATMENT;
COMPLEX-I DEFICIENCY; SKELETAL-MUSCLE; DOUBLE-BLIND; MELAS SYNDROME;
DICHLOROACETATE TREATMENT
AB Mitochondrial dysfunction is a common cause of inherited multisystem disease that often involves the nervous system. Despite major advances in our understanding of the pathophysiology of mitochondrial diseases, clinical management of these conditions remains largely supportive. Using a systematic approach, we identified 1,039 publications on treatments for mitochondrial diseases, only 35 of which included observations on more than five patients. Reports of a positive outcome on the basis of a biomarker of unproven clinical significance were more common in nonrandomized and nonblinded studies, suggesting a publication bias toward positive but poorly executed studies. Although trial design is improving, there is a critical need to develop new biomarkers of mitochondrial disease. In this Perspectives article, we make recommendations for the design of future treatment trials in mitochondrial diseases. Patients and physicians should no longer rely on potentially biased data, with the associated costs and risks.
C1 [Pfeffer, Gerald; Yu-Wai-Man, Patrick; McFarland, Robert; Turnbull, Douglas M.; Chinnery, Patrick F.] Newcastle Univ, Wellcome Trust Ctr Mitochondrial Res, Inst Genet Med Ageing & Hlth, Newcastle Upon Tyne NE1 3BZ, Tyne & Wear, England.
[Klopstock, Thomas] Univ Munich, Dept Neurol, Friedrich Baur Inst, D-80539 Munich, Germany.
[Mootha, Vamsi K.] Massachusetts Gen Hosp, Dept Mol Biol, Ctr Human Genet Res, Boston, MA 02114 USA.
[Suomalainen, Anu] Univ Helsinki, Dept Neurol, Cent Hosp, Helsinki, Finland.
[Koene, Saskia; Smeitink, Jan] Radboud Univ Nijmegen, Med Ctr, Nijmegen Ctr Mitochondrial Disorders, NL-6525 ED Nijmegen, Netherlands.
[Hirano, Michio] Columbia Univ, Med Ctr, Dept Neurol, New York, NY 10027 USA.
[Zeviani, Massimo] Fdn Carlo Besta Inst Neurol IRCCS, Unit Mol Neurogenet, Milan, Italy.
[Bindoff, Laurence A.] Univ Bergen, IKM, Bergen, Norway.
[Bindoff, Laurence A.] Haukeland Hosp, Dept Neurol, N-5021 Bergen, Norway.
[Hanna, Michael] UCL Inst Neurol, London, England.
[Carelli, Valerio] IRCCS Ist Sci Neurol, Bologna, Italy.
[Majamaa, Kari] Univ Oulu, Dept Neurol, Inst Clin Med, SF-90100 Oulu, Finland.
RP Chinnery, PF (reprint author), Newcastle Univ, Wellcome Trust Ctr Mitochondrial Res, Inst Genet Med Ageing & Hlth, Newcastle Upon Tyne NE1 3BZ, Tyne & Wear, England.
EM patrick.chinnery@ncl.ac.uk
RI Zeviani, Massimo/K-2891-2014; Koene, Saskia/G-9321-2015; Smeitink,
Jan/C-1351-2013;
OI Koene, Saskia/0000-0002-9876-744X; CARELLI, VALERIO/0000-0003-4923-6404;
Bindoff, Laurence/0000-0003-0988-276X
FU Canadian Institutes of Health Research; Sigrid Juselius Foundation; Jane
and Atos Erkko Foundation; DoH/HEFCE; Eurostars Programme [ESTAR 11205];
ZonMW PM Rare; Dutch Science Organisation (NWO) CSBR Program
[853.00.130]; Wellcome Trust Centre for Mitochondrial Research
[096919Z/11/Z]; Medical Research Council (UK) Centre for Translational
Research in Neuromuscular Diseases; EU FP7 TIRCON; NIHR Newcastle
Biomedical Research Centre based at Newcastle upon Tyne Hospital NHS
Foundation Trust; NIHR Newcastle Biomedical Research Centre based at
Newcastle upon Tyne Hospital Newcastle University; Marriott Foundation;
Telethon Italy [GPP10005]; German Federal Ministry of Education and
Research (BMBF) [01GM1113A]; BMBF (German Centre for Vertigo and Balance
Disorders) [01E00901]; European Commission Seventh Framework Programme
(FP7, HEALTH-F2-2011) [277984]
FX G. Pfeffer is the recipient of a Bisby Fellowship from the Canadian
Institutes of Health Research.; A. Suomalainen is supported by the
Sigrid Juselius Foundation and the Jane and Atos Erkko Foundation. R.
McFarland is an honorary consultant paediatric neurologist at Newcastle
upon Tyne Foundation Hospitals NHS Trust and a DoH/HEFCE-funded Clinical
Senior Lecturer. J. Smeitink receives additional support from the
Eurostars Programme (ESTAR 11205), ZonMW PM Rare and the Dutch Science
Organisation (NWO) CSBR Program (853.00.130). P. F. Chinnery is an
Honorary Consultant Neurologist at Newcastle upon Tyne Foundation
Hospitals NHS Trust, is a Wellcome Trust Senior Fellow in Clinical
Science (084980/Z/08/Z), and a UK National Institute for Health Research
(NIHR) Senior Investigator. P. F. Chinnery receives additional support
from the Wellcome Trust Centre for Mitochondrial Research
(096919Z/11/Z), the Medical Research Council (UK) Centre for
Translational Research in Neuromuscular Diseases, EU FP7 TIRCON, and the
NIHR Newcastle Biomedical Research Centre based at Newcastle upon Tyne
Hospitals NHS Foundation Trust and Newcastle University. The support of
the Marriott Foundation is gratefully acknowledged. The views expressed
are those of the authors and not necessarily those of the NHS, MF,
ZonMW, NOW, the NIHR or the Department of Health. M. Zeviani (GPP10005)
and V. Carelli are supported by Telethon Italy. For this study, T.
Klopstock acknowledges funding from the German Federal Ministry of
Education and Research (BMBF, grant number 01GM1113A) for the German
Network for Mitochondrial Disorders (mitoNET). T. Klopstock receives
additional support from the BMBF (German Centre for Vertigo and Balance
Disorders, grant number 01E00901) and from the European Commission
Seventh Framework Programme (FP7/2007-2013, HEALTH-F2-2011, grant
agreement No. 277984, TIRCON).
NR 69
TC 63
Z9 65
U1 1
U2 17
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4758
J9 NAT REV NEUROL
JI Nat. Rev. Neurol.
PD AUG
PY 2013
VL 9
IS 8
BP 474
EP 481
DI 10.1038/nrneurol.2013.129
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 196LE
UT WOS:000322775900010
PM 23817350
ER
PT J
AU Kaiser, NC
Lee, GJ
Lu, PH
Mather, MJ
Shapira, J
Jimenez, E
Thompson, PM
Mendez, MF
AF Kaiser, Natalie C.
Lee, Grace J.
Lu, Po H.
Mather, Michelle J.
Shapira, Jill
Jimenez, Elvira
Thompson, Paul M.
Mendez, Mario F.
TI What dementia reveals about proverb interpretation and its
neuroanatomical correlates
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE Frontotemporal dementia; Alzheimer's disease; MRI; Tensor based
morphometry; Proverbs; Executive functioning
ID ONSET ALZHEIMERS-DISEASE; FRONTOTEMPORAL DEMENTIA; BEHAVIORAL VARIANT;
COGNITIVE DEFICITS; CLINICAL-DIAGNOSIS; RIGHT-HEMISPHERE; FRONTAL
VARIANT; LANGUAGE; BRAIN; COMPREHENSION
AB Objective: Neuropsychologists frequently include proverb interpretation as a measure of executive abilities. A concrete interpretation of proverbs, however, may reflect semantic impairments from anterior temporal lobes, rather than executive dysfunction from frontal lobes. The investigation of proverb interpretation among patients with different dementias with varying degrees of temporal and frontal dysfunction may clarify the underlying brain-behavior mechanisms for abstraction from proverbs. We propose that patients with behavioral variant frontotemporal dementia (bvFTD), who are characteristically more impaired on proverb interpretation than those with Alzheimer's disease (AD), are disproportionately impaired because of anterior temporal-mediated semantic deficits.
Methods: Eleven patients with bvFTD and 10 with AD completed the Delis-Kaplan Executive Function System (D-KEFS) Proverbs Test and a series of neuropsychological measures of executive and semantic functions. The analysis included both raw and age-adjusted normed data for multiple choice responses on the D-KEFS Proverbs Test using independent samples t-tests. Tensor-based morphometry (TBM) applied to 3D T1-weighted MRI scans mapped the association between regional brain volume and proverb performance. Computations of mean Jacobian values within select regions of interest provided a numeric summary of regional volume, and voxel-wise regression yielded 3D statistical maps of the association between tissue volume and proverb scores.
Results: The patients with bvFTD were significantly worse than those with AD in proverb interpretation. The worse performance of the bvFTD patients involved a greater number of concrete responses to common, familiar proverbs, but not to uncommon, unfamiliar ones. These concrete responses to common proverbs correlated with semantic measures, whereas concrete responses to uncommon proverbs correlated with executive functions. After controlling for dementia diagnosis, TBM analyses indicated significant correlations between impaired proverb interpretation and the anterior temporal lobe region (left > right).
Conclusions: Among two dementia groups, those with bvFTD, demonstrated a greater number of concrete responses to common proverbs compared to those with AD, and this performance correlated with semantic deficits and the volume of the left anterior lobe, the hub of semantic knowledge. The findings of this study suggest that common proverb interpretation is greatly influenced by semantic dysfunction and that the use of proverbs for testing executive functions needs to include the interpretation of unfamiliar proverbs. Published by Elsevier Ltd.
C1 [Kaiser, Natalie C.; Mather, Michelle J.; Shapira, Jill; Jimenez, Elvira; Mendez, Mario F.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Lee, Grace J.; Lu, Po H.; Shapira, Jill; Jimenez, Elvira; Thompson, Paul M.; Mendez, Mario F.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
RP Kaiser, NC (reprint author), VA Greater Los Angeles Healthcare Syst, 11301 Wilshire Blvd,Bldg 401 Room A235, Los Angeles, CA USA.
EM Natalie.Kaiser@va.gov
FU National Institute of Health [R01AG034499-3]; GRECC Advanced Geriatric
Fellowship Award
FX Research supported by National Institute of Health Grant #R01AG034499-3
(M. Mendez PI); GRECC Advanced Geriatric Fellowship Award to N. Kaiser
NR 56
TC 6
Z9 6
U1 1
U2 9
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 2013
VL 51
IS 9
BP 1726
EP 1733
DI 10.1016/j.neuropsychologia.2013.05.021
PG 8
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 199TM
UT WOS:000323018400008
PM 23747602
ER
PT J
AU Specks, U
Merkel, PA
Seo, P
Spiera, R
Langford, CA
Hoffman, GS
Kallenberg, CGM
Clair, EWS
Fessler, BJ
Ding, L
Viviano, L
Tchao, NK
Phippard, DJ
Asare, AL
Lim, N
Ikle, D
Jepson, B
Brunetta, P
Allen, NB
Fervenza, FC
Geetha, D
Keogh, K
Kissin, EY
Monach, PA
Peikert, T
Stegeman, C
Ytterberg, SR
Mueller, M
Sejismundo, LP
Mieras, K
Stone, JH
AF Specks, Ulrich
Merkel, Peter A.
Seo, Philip
Spiera, Robert
Langford, Carol A.
Hoffman, Gary S.
Kallenberg, Cees G. M.
Clair, E. William St.
Fessler, Barri J.
Ding, Linna
Viviano, Lisa
Tchao, Nadia K.
Phippard, Deborah J.
Asare, Adam L.
Lim, Noha
Ikle, David
Jepson, Brett
Brunetta, Paul
Allen, Nancy B.
Fervenza, Fernando C.
Geetha, Duvuru
Keogh, Karina
Kissin, Eugene Y.
Monach, Paul A.
Peikert, Tobias
Stegeman, Coen
Ytterberg, Steven R.
Mueller, Mark
Sejismundo, Lourdes P.
Mieras, Kathleen
Stone, John H.
CA RAVE-ITN Res Grp
TI Efficacy of Remission-Induction Regimens for ANCA-Associated Vasculitis
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID ANTIBODY-ASSOCIATED VASCULITIS; ANTINEUTROPHIL CYTOPLASMIC
AUTOANTIBODIES; WEGENERS-GRANULOMATOSIS; RANDOMIZED-TRIAL; SYSTEMIC
VASCULITIDES; RENAL VASCULITIS; CELL-ACTIVATION; CYCLOPHOSPHAMIDE;
MAINTENANCE; RITUXIMAB
AB Background
The 18-month efficacy of a single course of rituximab as compared with conventional immunosuppression with cyclophosphamide followed by azathioprine in patients with severe (organ-threatening) antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is unknown.
Methods
In a multicenter, randomized, double-blind, double-dummy, noninferiority trial, we compared rituximab (375 mg per square meter of body-surface area administered once a week for 4 weeks) followed by placebo with cyclophosphamide administered for 3 to 6 months followed by azathioprine for 12 to 15 months. The primary outcome measure was complete remission of disease by 6 months, with the remission maintained through 18 months.
Results
A total of 197 patients were enrolled. As reported previously, 64% of the patients in the rituximab group, as compared with 53% of the patients in the cyclophosphamide-azathioprine group, had a complete remission by 6 months. At 12 and 18 months, 48% and 39%, respectively, of the patients in the rituximab group had maintained the complete remissions, as compared with 39% and 33%, respectively, in the comparison group. Rituximab met the prespecified criteria for noninferiority (P<0.001, with a noninferiority margin of 20%). There was no significant difference between the groups in any efficacy measure, including the duration of complete remission and the frequency or severity of relapses. Among the 101 patients who had relapsing disease at baseline, rituximab was superior to conventional immunosuppression at 6 months (P=0.01) and at 12 months (P=0.009) but not at 18 months (P=0.06), at which time most patients in the rituximab group had reconstituted B cells. There was no significant between-group difference in adverse events.
Conclusions
In patients with severe ANCA-associated vasculitis, a single course of rituximab was as effective as continuous conventional immunosuppressive therapy for the induction and maintenance of remissions over the course of 18 months. (Funded by the National Institute of Allergy and Infectious Diseases and others; RAVE ClinicalTrials.gov number, .)
C1 [Specks, Ulrich; Fervenza, Fernando C.; Keogh, Karina; Peikert, Tobias; Ytterberg, Steven R.; Mieras, Kathleen] Mayo Clin Fdn, Rochester, MN USA.
[Merkel, Peter A.; Kissin, Eugene Y.; Monach, Paul A.] Boston Univ, Med Ctr, Boston, MA USA.
[Stone, John H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Seo, Philip; Geetha, Duvuru; Sejismundo, Lourdes P.] Johns Hopkins Univ, Baltimore, MD USA.
[Ding, Linna; Viviano, Lisa; Mueller, Mark] NIAID, Bethesda, MD 20892 USA.
[Tchao, Nadia K.; Phippard, Deborah J.; Asare, Adam L.; Lim, Noha] Immune Tolerance Network, Bethesda, MD USA.
[Spiera, Robert] Hosp Special Surg, New York, NY 10021 USA.
[Langford, Carol A.; Hoffman, Gary S.] Cleveland Clin Fdn, Cleveland, OH USA.
[Kallenberg, Cees G. M.; Stegeman, Coen] Univ Groningen, Univ Med Ctr Groningen, Groningen, Netherlands.
[Clair, E. William St.; Allen, Nancy B.] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Ikle, David; Jepson, Brett] Rho, Chapel Hill, NC USA.
[Fessler, Barri J.] Univ Alabama Birmingham, Birmingham, AL USA.
[Brunetta, Paul] Genentech Inc, San Francisco, CA USA.
RP Stone, JH (reprint author), Massachusetts Gen Hosp, Rheumatol Unit, 55 Fruit St, Boston, MA 02114 USA.
EM jhstone@partners.org
OI Carey, John/0000-0001-7292-2328; molloy, Eleanor/0000-0001-6798-2158
FU NIH [N01-AI-15416, ITN021AI]; National Institute of Allergy and
Infectious Diseases; Juvenile Diabetes Research Foundation; Genentech;
Biogen Idec; National Center for Research Resources (NCRR) [UL1
RR024150-01, UL1 RR025005, UL1 RR025771, NIH M01 RR00533]; National
Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
[K24 AR049185, K23 AR052820, K24 AR02224]; Arthritis Foundation
Investigator Award
FX This research was performed as a project of the Immune Tolerance Network
(NIH contract N01-AI-15416; protocol number ITN021AI), an international
clinical research consortium head-quartered at the University of
California, San Francisco.; Supported by the National Institute of
Allergy and Infectious Diseases, the Juvenile Diabetes Research
Foundation, Genentech, and Biogen Idec. At the Mayo Clinic, the trial
was supported by a Clinical and Translational Science Award (CTSA) grant
(UL1 RR024150-01) from the National Center for Research Resources
(NCRR). At Johns Hopkins, the trial was supported by a CTSA grant (UL1
RR025005) from the NCRR and by grants (K24 AR049185, to Dr. Stone; and
K23 AR052820, to Dr. Seo) from the National Institute of Arthritis and
Musculoskeletal and Skin Diseases (NIAMS). At Boston University, the
trial was supported by CTSA grants (UL1 RR025771 and NIH M01 RR00533)
from the NCRR and a grant (K24 AR02224) from the NIAMS (all to Dr.
Merkel) and an Arthritis Foundation Investigator Award (to Dr. Monach).
NR 33
TC 180
Z9 190
U1 0
U2 11
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD AUG 1
PY 2013
VL 369
IS 5
BP 417
EP 427
DI 10.1056/NEJMoa1213277
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 193GQ
UT WOS:000322547400008
PM 23902481
ER
PT J
AU Conwell, WD
Josephson, SA
Li, H
Saint, S
Janssen, WJ
AF Conwell, Walter D.
Josephson, S. Andrew
Li, Howard
Saint, Sanjay
Janssen, William J.
TI Weak in the Knees
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID EATON MYASTHENIC SYNDROME
AB A 61-year-old woman presented to her primary care physician with a 4-week history of progressive leg weakness, bilateral leg pain, and difficulty walking. The weakness was symmetric and did not fluctuate during the course of the day. Foreword In this Journal feature, information about a real patient is presented in stages (boldface type) to an expert clinician, who responds to the information, sharing his or her reasoning with the reader (regular type). The authors' commentary follows. Stage A 61-year-old woman presented to her primary care physician with a 4-week history of progressive bilateral leg weakness, bilateral leg pain, and difficulty walking. The weakness was symmetric, without exacerbating or ameliorating factors, and did not fluctuate during the course of the day. The patient also reported depression, anxiety, memory problems, and intermittent headaches that had begun several months earlier. She had a dry mouth but no difficulty swallowing. Previously very active, she had become homebound over a period of several months because of the leg weakness. ResponseWeakness is a common symptom and can result from dysfunction of either the central nervous system (brain or spinal cord) or the peripheral nervous system (anterior horn cell, nerve, neuromuscular junction, or muscle). Bilateral symmetric weakness of the legs can also result from problems with either the central ...
C1 [Conwell, Walter D.; Li, Howard; Janssen, William J.] Univ Colorado, Dept Med, Div Pulm Sci & Crit Care Med, Denver, CO USA.
[Li, Howard] Denver Vet Affairs Med Ctr, Dept Med, Denver, CO USA.
[Janssen, William J.] Natl Jewish Hlth, Dept Med, Div Pulm Med, Denver, CO 80206 USA.
[Josephson, S. Andrew] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Saint, Sanjay] Univ Michigan, Dept Vet Affairs, Hlth Serv Res & Dev Ctr Excellence, Ann Arbor, MI 48109 USA.
[Saint, Sanjay] Univ Michigan, Dept Med, Ann Arbor, MI 48109 USA.
RP Janssen, WJ (reprint author), Natl Jewish Hlth, 1400 Jackson St, Denver, CO 80206 USA.
EM janssenw@njhealth.org
NR 10
TC 0
Z9 0
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
EI 1533-4406
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD AUG 1
PY 2013
VL 369
IS 5
BP 459
EP 464
DI 10.1056/NEJMcps1210293
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA 193GQ
UT WOS:000322547400013
PM 23902486
ER
PT J
AU Schumacher, HR
Pullman-Mooar, S
Gupta, SR
Dinnella, JE
Kim, R
McHugh, MP
AF Schumacher, H. R.
Pullman-Mooar, S.
Gupta, S. R.
Dinnella, J. E.
Kim, R.
McHugh, M. P.
TI Randomized double-blind crossover study of the efficacy of a tart cherry
juice blend in treatment of osteoarthritis (OA) of the knee
SO OSTEOARTHRITIS AND CARTILAGE
LA English
DT Article
DE WOMAC; C-reactive protein; Inflammation; Placebo
ID CONTROLLED-TRIAL; CLINICAL-TRIAL; PLACEBO; PAIN; ANTHOCYANINS;
INFLAMMATION; CONSUMPTION; HIP; METHYLSULFONYLMETHANE; GLUCOSAMINE
AB Objective: To assess the efficacy of tart cherry juice in treating pain and other features of knee osteoarthritis (OA).
Methods: 58 non-diabetic patients with Kellgren grade 2-3 OA were randomized to begin treatment with cherry juice or placebo. Two 8 oz bottles of tart cherry juice or placebo were consumed daily for 6 weeks with a 1 week washout period before switching treatments (crossover design). Western Ontario McMaster Osteoarthritis Index (WOMAC) scores and walking times were recorded prior to and after each treatment period. Additionally, plasma urate, creatinine and high sensitivity C-reactive protein (hsCRP) were recorded at baseline, after the first treatment period and after the second treatment period. Acetaminophen was allowed as a rescue drug and self reported after each treatment period. Treatment effect was examined with repeated measures analysis of variance (ANOVA) using an intention-to-treat (ITT) analysis.
Results: There were five withdrawals during the cherry juice treatment (four adverse events (AEs)) and seven withdrawals during the placebo treatment (three AEs). WOMAC scores decreased significantly (P < 0.01) after the cherry juice treatment but not after the placebo treatment (P = 0.46); differences between treatments were not significant (P = 0.16). hsCRP declined during the cherry juice treatment vs placebo (P < 0.01). The decline in hsCRP was associated with WOMAC improvement (P < 0.01). Walking time, acetaminophen use, plasma urate and creatinine were unaffected by treatments.
Conclusions: Tart cherry juice provided symptom relief for patients with mild to moderate knee OA, but this effect was not significantly greater than placebo. Tart cherry juice lowered hsCRP levels and this effect was associated with improved WOMAC scores. (C) 2013 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
C1 [Schumacher, H. R.; Pullman-Mooar, S.; Gupta, S. R.; Dinnella, J. E.; Kim, R.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Schumacher, H. R.; Pullman-Mooar, S.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[Kim, R.] Childrens Hosp Philadelphia, Philadelphia, PA USA.
[McHugh, M. P.] Lenox Hill Hosp, Nicholas Inst Sports Med & Athlet Trauma, New York, NY 10075 USA.
RP McHugh, MP (reprint author), Lenox Hill Hosp, Nicholas Inst Sports Med & Athlet Trauma, 100 E 77 ST, New York, NY 10075 USA.
EM schumacr@mail.med.upenn.edu; sally.pullman-mooar@va.gov;
Smita.Gupta@uphs.upenn.edu; jdinnell@mail.med.upenn.edu;
rosakim330@gmail.com; mchugh@nismat.org
FU CherryPharm, Inc., Geneva, NY
FX Funding and cherry juice were provided by CherryPharm, Inc., Geneva, NY.
NR 38
TC 9
Z9 9
U1 1
U2 11
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1063-4584
J9 OSTEOARTHR CARTILAGE
JI Osteoarthritis Cartilage
PD AUG
PY 2013
VL 21
IS 8
BP 1035
EP 1041
DI 10.1016/j.joca.2013.05.009
PG 7
WC Orthopedics; Rheumatology
SC Orthopedics; Rheumatology
GA 196VU
UT WOS:000322806300003
PM 23727631
ER
PT J
AU Blagoev, KB
Shukla, K
Levine, H
AF Blagoev, Krastan B.
Shukla, Kamal
Levine, Herbert
TI We need theoretical physics approaches to study living systems
SO PHYSICAL BIOLOGY
LA English
DT Editorial Material
C1 [Blagoev, Krastan B.; Shukla, Kamal] Natl Sci Fdn, Arlington, VA 22230 USA.
[Blagoev, Krastan B.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Charlestown, MA 02129 USA.
[Blagoev, Krastan B.] Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Levine, Herbert] Rice Univ, Dept Bioengn, Houston, TX 77030 USA.
RP Blagoev, KB (reprint author), Natl Sci Fdn, 4201 Wilson Blvd, Arlington, VA 22230 USA.
EM herbert.levine@rice.edu
RI Levine, Herbert/C-1704-2008
OI Levine, Herbert/0000-0002-8819-9055
NR 2
TC 0
Z9 0
U1 0
U2 24
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 1478-3967
J9 PHYS BIOL
JI Phys. Biol.
PD AUG
PY 2013
VL 10
IS 4
AR 040201
DI 10.1088/1478-3975/10/4/040201
PG 2
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 195KM
UT WOS:000322701100001
PM 23883648
ER
PT J
AU Goodman, JD
McKay, JR
DePhilippis, D
AF Goodman, Jessica D.
McKay, James R.
DePhilippis, Dominick
TI Progress Monitoring in Mental Health and Addiction Treatment: A Means of
Improving Care
SO PROFESSIONAL PSYCHOLOGY-RESEARCH AND PRACTICE
LA English
DT Article
DE psychotherapy outcome; progress monitoring; outcome monitoring;
substance abuse services; research synthesis
ID TREATMENT OUTCOME PACKAGE; CLINICAL SUPPORT TOOLS; PSYCHOMETRIC
PROPERTIES; CLIENT FEEDBACK; CONTINUING CARE; COCAINE DEPENDENCE;
24-MONTH OUTCOMES; BRIEF INSTRUMENT; STEPPED-CARE; CORE-OM
AB Although monitoring of treatment response is standard practice for many medical conditions, practitioners in mental health treatments, and substance abuse treatment in particular, have been slow to adopt these practices. Progress monitoring (PM), consisting of measurement and feedback, has the potential to significantly improve treatment outcomes. This paper reviews the existing literature on the effects of PM in mental health and substance use disorder (SUD) treatment. Whereas previous reviews have examined aspects of PM in mental health treatment, this is the first such review to cover monitoring efforts in substance abuse treatment, conceptualized here as diverse forms of measurement-based care. To address drug use, monitoring in SUD treatment has typically relied on treatment attendance and urine screens as indicators of treatment progress. However, some research has shown that other means of PM can significantly improve SUD treatment effectiveness. Previous meta-analyses show that PM significantly improves outcomes in mental health treatment. More extensive research on three particular measures, demonstrate the effectiveness of PM in mental health treatment. With the growing focus on quality improvement in medical care, there is need for further research and adoption of progress monitoring methods in mental health and SUD treatment.
C1 [Goodman, Jessica D.; McKay, James R.; DePhilippis, Dominick] Philadelphia Vet Affairs Med Ctr, CESATE, Philadelphia, PA USA.
[DePhilippis, Dominick] Univ Penn, Perelman Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
RP McKay, JR (reprint author), Univ Penn, Ctr Continuum Care, 3440 Market St,Suite 370, Philadelphia, PA 19104 USA.
EM jimrache@mail.med.upenn.edu
NR 78
TC 11
Z9 11
U1 4
U2 22
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0735-7028
J9 PROF PSYCHOL-RES PR
JI Prof. Psychol.-Res. Pract.
PD AUG
PY 2013
VL 44
IS 4
BP 231
EP 246
DI 10.1037/a0032605
PG 16
WC Psychology, Multidisciplinary
SC Psychology
GA 198GI
UT WOS:000322909900006
ER
PT J
AU Kessler, RC
Calabrese, JR
Farley, PA
Gruber, MJ
Jewell, MA
Katon, W
Keck, PE
Nierenberg, AA
Sampson, NA
Shear, MK
Shillington, AC
Stein, MB
Thase, ME
Wittchen, HU
AF Kessler, R. C.
Calabrese, J. R.
Farley, P. A.
Gruber, M. J.
Jewell, M. A.
Katon, W.
Keck, P. E., Jr.
Nierenberg, A. A.
Sampson, N. A.
Shear, M. K.
Shillington, A. C.
Stein, M. B.
Thase, M. E.
Wittchen, H. -U.
TI Composite International Diagnostic Interview screening scales for DSM-IV
anxiety and mood disorders
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Bipolar disorder; Composite International Diagnostic Interview (CIDI);
generalized anxiety disorder; major depression; panic disorder;
screening scales; validity
ID PATIENT HEALTH QUESTIONNAIRE; COMMON MENTAL-DISORDERS; COMORBIDITY
SURVEY REPLICATION; PRIMARY-CARE PATIENTS; GENERALIZED ANXIETY; BIPOLAR
DISORDER; PANIC DISORDER; DEPRESSION SCALE; HOSPITAL ANXIETY; CES-D
AB Background. Lack of coordination between screening studies for common mental disorders in primary care and c