FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Jones, CK
Engers, DW
Thompson, AD
Field, JR
Blobaum, AL
Lindsley, SR
Zhou, Y
Gogliotti, RD
Jadhav, S
Zamorano, R
Bogenpohl, J
Smith, Y
Morrison, R
Daniels, JS
Weaver, CD
Conn, PJ
Lindsley, CW
Niswender, CM
Hopkins, CR
AF Jones, Carrie K.
Engers, Darren W.
Thompson, Analisa D.
Field, Julie R.
Blobaum, Anna L.
Lindsley, Stacey R.
Zhou, Ya
Gogliotti, Rocco D.
Jadhav, Satyawan
Zamorano, Rocio
Bogenpohl, Jim
Smith, Yoland
Morrison, Ryan
Daniels, J. Scott
Weaver, C. David
Conn, P. Jeffrey
Lindsley, Craig W.
Niswender, Colleen M.
Hopkins, Corey R.
TI Discovery, Synthesis, and Structure-Activity Relationship Development of
a Series of N-4-(2,5-Dioxopyrrolidin-1-yl)phenylpicolinamides
(VU0400195, ML182): Characterization of a Novel Positive Allosteric
Modulator of the Metabotropic Glutamate Receptor 4 (mGlu(4)) with Oral
Efficacy in an Antiparkinsonian Animal Model
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID PARKINSONS-DISEASE; MGLUR4; PHARMACOLOGY; DOPAMINE; LEVODOPA; PAMS
AB There is an increasing amount of literature data showing the positive effects on preclinical antiparkinsonian rodent models with selective positive allosteric modulators of metabotropic glutamate receptor 4 (mGlu(4)). However, most of the data generated utilize compounds that have not been optimized for druglike properties, and as a consequence, they exhibit poor pharmacokinetic properties and thus do not cross the blood-brain barrier. Herein, we report on a series of N-4-(2,5-dioxopyrrolidin-1-yl)phenylpicolinamides with improved PK properties with excellent potency and selectivity as well as improved brain exposure in rodents. Finally, ML182 was shown to be orally active in the haloperidol induced catalepsy model, a well-established antiparkinsonian model.
C1 [Jones, Carrie K.; Engers, Darren W.; Thompson, Analisa D.; Field, Julie R.; Blobaum, Anna L.; Lindsley, Stacey R.; Zhou, Ya; Gogliotti, Rocco D.; Jadhav, Satyawan; Zamorano, Rocio; Morrison, Ryan; Daniels, J. Scott; Weaver, C. David; Conn, P. Jeffrey; Lindsley, Craig W.; Niswender, Colleen M.; Hopkins, Corey R.] Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA.
[Jones, Carrie K.; Engers, Darren W.; Thompson, Analisa D.; Blobaum, Anna L.; Lindsley, Stacey R.; Zhou, Ya; Gogliotti, Rocco D.; Jadhav, Satyawan; Zamorano, Rocio; Morrison, Ryan; Daniels, J. Scott; Conn, P. Jeffrey; Lindsley, Craig W.; Niswender, Colleen M.; Hopkins, Corey R.] Vanderbilt Univ, Med Ctr, Vanderbilt Ctr Neurosci Drug Discovery, Nashville, TN 37232 USA.
[Jones, Carrie K.] US Dept Vet Affairs, Tennessee Valley Healthcare Syst, Nashville, TN 37212 USA.
[Lindsley, Craig W.; Hopkins, Corey R.] Vanderbilt Univ, Dept Chem, Nashville, TN 37232 USA.
[Weaver, C. David; Conn, P. Jeffrey; Lindsley, Craig W.] Vanderbilt Univ, Vanderbilt Inst Chem Biol, Nashville, TN 37232 USA.
[Engers, Darren W.; Conn, P. Jeffrey; Lindsley, Craig W.; Hopkins, Corey R.] Vanderbilt Specialized Chem Ctr Accelerated Probe, Nashville, TN 37232 USA.
[Bogenpohl, Jim; Smith, Yoland] Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30329 USA.
[Bogenpohl, Jim; Smith, Yoland] Emory Univ, Dept Neurol, Atlanta, GA 30329 USA.
RP Niswender, CM (reprint author), Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA.
EM colleen.niswender@vanderbilt.edu; corey.r.hopkins@vanderbilt.edu
RI Conn, Peter/D-7848-2012; Zhou, Ya/F-1220-2013
FU National Institute of Mental Health, National Institute of Neurological
Disorders and Stroke; Micheal J. Fox Foundation; Vanderbilt Department
of Pharmacology; Vanderbilt Institute of Chemical Biology; NIH/MLPCN
[5U54MH08465-02]
FX The authors warmly acknowledge Emily L. Days, Tasha Nalywajko, Cheryl A.
Austin, and Michael Baxter Williams for their critical contributions to
the HTS portion of the projects; Matt Mulder, Chris Denicola, Nathan
Kett, and Sichen Chang for the purification of compounds utilizing the
mass-directed HPLC system; and Katrina Brewer for technical assistance
with the PK assays. The dog cassette in vivo experiment was performed at
Calvert Labs, and the rhesus in vivo experiment was performed at the
Yerkes Primate Center at Emory University, GA. This work was supported
by the National Institute of Mental Health, National Institute of
Neurological Disorders and Stroke, the Micheal J. Fox Foundation, the
Vanderbilt Department of Pharmacology, and the Vanderbilt Institute of
Chemical Biology. In addition, the authors thank the NIH/MLPCN (Grant
5U54MH08465-02) for support of this research. Vanderbilt is a member of
the MLPCN and houses the Vanderbilt Specialized Chemistry Center for
Accelerated Probe Development.
NR 27
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U1 0
U2 6
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD NOV 10
PY 2011
VL 54
IS 21
BP 7639
EP 7647
DI 10.1021/jm200956q
PG 9
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 839ZN
UT WOS:000296408100018
PM 21966889
ER
PT J
AU Mizukawa, B
Wei, JP
Shrestha, M
Wunderlich, M
Chou, FS
Griesinger, A
Harris, CE
Kumar, AR
Zheng, Y
Williams, DA
Mulloy, JC
AF Mizukawa, Benjamin
Wei, Junping
Shrestha, Mahesh
Wunderlich, Mark
Chou, Fu-Sheng
Griesinger, Andrea
Harris, Chad E.
Kumar, Ashish R.
Zheng, Yi
Williams, David A.
Mulloy, James C.
TI Inhibition of Rac GTPase signaling and downstream prosurvival Bcl-2
proteins as combination targeted therapy in MLL-AF9 leukemia
SO BLOOD
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; GUANOSINE TRIPHOSPHATASES REPRESENT; ACUTE
MYELOGENOUS LEUKEMIA; TRANSCRIPTIONAL ELONGATION; FAMILY PROTEINS; RHO
GTPASES; DNA-DAMAGE; STEM-CELLS; MICE; FLT3
AB The Rac family of small Rho GTPases coordinates diverse cellular functions in hematopoietic cells including adhesion, migration, cytoskeleton rearrangements, gene transcription, proliferation, and survival. The integrity of Rac signaling has also been found to critically regulate cellular functions in the initiation and maintenance of hematopoietic malignancies. Using an in vivo gene targeting approach, we demonstrate that Rac2, but not Rac1, is critical to the initiation of acute myeloid leukemia in a retroviral expression model of MLL-AF9 leukemogenesis. However, loss of either Rac1 or Rac2 is sufficient to impair survival and growth of the transformed MLL-AF9 leukemia. Rac2 is known to positively regulate expression of Bcl-2 family proteins toward a prosurvival balance. We demonstrate that disruption of downstream survival signaling through antiapoptotic Bcl-2 proteins is implicated in mediating the effects of Rac2 deficiency in MLL-AF9 leukemia. Indeed, over-expression of Bcl-xL is able to rescue the effects of Rac2 deficiency and MLL-AF9 cells are exquisitely sensitive to direct inhibition of Bcl-2 family proteins by the BH3-mimetic, ABT-737. Furthermore, concurrent exposure to NSC23766, a small-molecule inhibitor of Rac activation, increases the apoptotic effect of ABT-737, indicating the Rac/Bcl-2 survival pathway may be targeted synergistically. (Blood. 2011;118(19):5235-5245)
C1 [Wei, Junping; Shrestha, Mahesh; Wunderlich, Mark; Chou, Fu-Sheng; Griesinger, Andrea; Zheng, Yi; Mulloy, James C.] Cincinnati Childrens Hosp Med Ctr, Canc & Blood Dis Inst, Div Expt Hematol & Canc Biol, Cincinnati, OH 45229 USA.
[Mizukawa, Benjamin] Cincinnati Childrens Hosp Med Ctr, Canc & Blood Dis Inst, Div Oncol, Cincinnati, OH 45229 USA.
[Harris, Chad E.; Williams, David A.] Harvard Univ, Div Hematol Oncol, Sch Med, Boston, MA 02115 USA.
[Harris, Chad E.; Williams, David A.] Harvard Univ, Harvard Stem Cell Inst, Sch Med, Childrens Hosp Boston, Boston, MA 02115 USA.
[Harris, Chad E.; Williams, David A.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kumar, Ashish R.] Cincinnati Childrens Hosp Med Ctr, Canc & Blood Dis Inst, Div Bone Marrow Transplantat & Immunodeficiency, Cincinnati, OH 45229 USA.
RP Mulloy, JC (reprint author), Cincinnati Childrens Hosp Med Ctr, Canc & Blood Dis Inst, Div Expt Hematol & Canc Biol, 3333 Burnet Ave, Cincinnati, OH 45229 USA.
EM james.mulloy@cchmc.org
RI Zheng, Yi/J-7235-2015
OI Zheng, Yi/0000-0001-7089-6074
FU National Institutes of Health/NICHD [K12-HD000850]; National Institutes
of Health [K08-CA12291, DK62757, CA140518]; United States Public Health
Service [MO1 RR 08 084]; National Center for Research Resources,
National Institutes of Health, a Center of Excellence in Molecular
Hematology [DK090971]; Gabrielle's Angel Foundation for Cancer Research
FX B.M. is a Fellow of the Pediatric Scientist Development Program (PSDP).
J.C.M. is a Leukemia & Lymphoma Society Scholar. This work was supported
by National Institutes of Health/NICHD grant K12-HD000850 (B.M.), a
Cancer Free Kids award (B.M.), ASH Scholar Award (J.W.), National
Institutes of Health grants K08-CA12291 (A.R.K.), DK62757 (D.A.W.), and
CA140518 (J.C.M.), United States Public Health Service grant MO1 RR 08
084, General Clinical Research Centers Program, National Center for
Research Resources, National Institutes of Health, a Center of
Excellence in Molecular Hematology P30 award (DK090971), and Gabrielle's
Angel Foundation for Cancer Research (J.C.M.).
NR 49
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U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 10
PY 2011
VL 118
IS 19
BP 5235
EP 5245
DI 10.1182/blood-2011-04-351817
PG 11
WC Hematology
SC Hematology
GA 845ZN
UT WOS:000296867100025
PM 21940819
ER
PT J
AU von Korff, M
Katon, WJ
Lin, EHB
Ciechanowski, P
Peterson, D
Ludman, EJ
Young, B
Rutter, CM
AF von Korff, Michael
Katon, Wayne J.
Lin, Elizabeth H. B.
Ciechanowski, Paul
Peterson, Do
Ludman, Evette J.
Young, Bessie
Rutter, Carolyn M.
TI Functional outcomes of multi-condition collaborative care and successful
ageing: results of randomised trial
SO BRITISH MEDICAL JOURNAL
LA English
DT Article
ID QUALITY-OF-LIFE; CORONARY-HEART-DISEASE; MAJOR DEPRESSION; HEALTH-CARE;
DISABILITY; MANAGEMENT; THERAPY; ANTIDEPRESSANT; COMPRESSION; VALIDATION
AB Objective To evaluate the effectiveness of integrated care for chronic physical diseases and depression in reducing disability and improving quality of life.
Design A randomised controlled trial of multi-condition collaborative care for depression and poorly controlled diabetes and/or risk factors for coronary heart disease compared with usual care among middle aged and elderly people
Setting Fourteen primary care clinics in Seattle, Washington.
Participants Patients with diabetes or coronary heart disease, or both, and blood pressure above 140/90 mm Hg, low density lipoprotein concentration >3.37 mmol/L, or glycated haemoglobin 8.5% or higher, and PHQ-9 depression scores of >= 10.
Intervention A 12 month intervention to improve depression, glycaemic control, blood pressure, and lipid control by integrating a "treat to target" programme for diabetes and risk factors for coronary heart disease with collaborative care for depression. The intervention combined self management support, monitoring of disease control, and pharmacotherapy to control depression, hyperglycaemia, hypertension, and hyperlipidaemia.
Main outcome measures Social role disability (Sheehan disability scale), global quality of life rating, and World Health Organization disability assessment schedule (WHODAS-2) scales to measure disabilities in activities of daily living (mobility, self care, household maintenance).
Results Of 214 patients enrolled (106 intervention and 108 usual care), disability and quality of life measures were obtained for 97 intervention patients at six months (92%) and 92 at 12 months (87%), and for 96 usual care patients at six months (89%) and 92 at 12 months (85%). Improvements from baseline on the Sheehan disability scale (-0.9, 95% confidence interval -1.5 to -0.2; P=0.006) and global quality of life rating (0.7, 0.2 to 1.2; P=0.005) were significantly greater at six and 12 months in patients in the intervention group. There was a trend toward greater improvement in disabilities in activities of daily living (-1.5, -3.3 to 0.4; P=0.10).
Conclusions Integrated care that covers chronic physical disease and comorbid depression can reduce social role disability and enhance global quality of life.
C1 [von Korff, Michael; Lin, Elizabeth H. B.; Peterson, Do; Ludman, Evette J.; Rutter, Carolyn M.] Grp Hlth Res Inst, Seattle, WA 98101 USA.
[Katon, Wayne J.; Ciechanowski, Paul] Univ Washington, Dept Psychiat & Behav Sci, Sch Med, Seattle, WA 98195 USA.
[Young, Bessie] Univ Washington, Vet Affairs Puget Sound Hlth Care Syst, Sch Med, Seattle, WA 98195 USA.
[Young, Bessie] Univ Washington, Div Nephrol, Sch Med, Dept Med, Seattle, WA 98195 USA.
[Rutter, Carolyn M.] Univ Washington, Dept Biostat, Sch Publ Hlth, Seattle, WA 98195 USA.
RP von Korff, M (reprint author), Grp Hlth Res Inst, 1730 Minor Ave, Seattle, WA 98101 USA.
EM vonkorff.m@ghc.org
FU Group Health; National Institute of Mental Health Services Division,
Bethesda, MD [MH041739, MH069741]
FX The TEAMcare study would not have been possible without the support and
participation of Group Health patients, primary care physicians,
consultants, and leaders. We also acknowledge efforts and expertise by
Tara Beatty, Malia Oliver, Sue Ruedebusch, Diana Griffith, and Sandy
Randles. We also thank Michelle Wong, R James Dudl, and Kaiser
Permanente Care Management Institute for providing the treat to target
diabetes guidelines that we adapted. The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the organisations that employ them.; This study was
supported by grants MH041739 and MH069741 from the National Institute of
Mental Health Services Division, Bethesda, MD (WJK) and by institutional
support from Group Health Cooperative. The sponsors of this research had
no influence over the conduct of the study, the analyses of study data,
or the content of this paper.
NR 41
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U2 13
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0959-535X
J9 BRIT MED J
JI Br. Med. J.
PD NOV 10
PY 2011
VL 343
AR d6612
DI 10.1136/bmj.d6612
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 848NT
UT WOS:000297059000003
PM 22074851
ER
PT J
AU Mroz, EA
Forastiere, AA
Rocco, JW
AF Mroz, Edmund A.
Forastiere, Arlene A.
Rocco, James W.
TI Implications of the Oropharyngeal Cancer Epidemic
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Editorial Material
ID SQUAMOUS-CELL CARCINOMA; HUMAN-PAPILLOMAVIRUS; NECK-CANCER; CONCURRENT
CHEMORADIATION; HEAD; SURVIVAL; HPV; P16; PROGNOSIS; THERAPY
C1 [Mroz, Edmund A.; Rocco, James W.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Forastiere, Arlene A.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Rocco, James W.] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
RP Mroz, EA (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
FU NIDCR NIH HHS [R01 DE022087]
NR 27
TC 11
Z9 11
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2011
VL 29
IS 32
BP 4222
EP 4223
DI 10.1200/JCO.2011.37.8893
PG 2
WC Oncology
SC Oncology
GA 845BJ
UT WOS:000296797500009
PM 21969506
ER
PT J
AU Domchek, SM
Mitchell, G
Lindeman, GJ
Tung, NM
Balmana, J
Isakoff, SJ
Schmutzler, R
Audeh, MW
Loman, N
Scott, C
Friedlander, M
Kaufman, B
Garber, JE
Tutt, A
Robson, ME
AF Domchek, Susan M.
Mitchell, Gillian
Lindeman, Geoffrey J.
Tung, Nadine M.
Balmana, Judith
Isakoff, Steven J.
Schmutzler, Rita
Audeh, M. William
Loman, Niklas
Scott, Clare
Friedlander, Michael
Kaufman, Bella
Garber, Judy E.
Tutt, Andrew
Robson, Mark E.
TI Challenges to the Development of New Agents for Molecularly Defined
Patient Subsets: Lessons From BRCA1/2-Associated Breast Cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Editorial Material
ID POLY(ADP-RIBOSE) POLYMERASE; MUTATION CARRIERS; INHIBITION; REPAIR;
TUMORS
C1 [Domchek, Susan M.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Mitchell, Gillian] Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
[Lindeman, Geoffrey J.; Scott, Clare] Walter & Eliza Hall Inst Med Res, Melbourne, Vic 3050, Australia.
[Lindeman, Geoffrey J.; Scott, Clare] Royal Melbourne Hosp, Melbourne, Vic, Australia.
[Tung, Nadine M.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Balmana, Judith] Vall dHebron Univ Hosp, Barcelona, Spain.
[Isakoff, Steven J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Schmutzler, Rita] Univ Cologne, Cologne, Germany.
[Audeh, M. William] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Loman, Niklas] Skane Univ Hosp, Malmo, Sweden.
[Friedlander, Michael] Prince Wales Canc Ctr, Sydney, NSW, Australia.
[Kaufman, Bella] Chaim Sheba Med Ctr, Tel Aviv, Israel.
[Garber, Judy E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Tutt, Andrew] Guys Hosp, Kings Hlth Partners Acad Hlth Sci Ctr, London SE1 9RT, England.
[Robson, Mark E.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RP Domchek, SM (reprint author), Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
RI friedlander, michael/G-3490-2013;
OI friedlander, michael/0000-0002-6488-0604; Robson,
Mark/0000-0002-3109-1692
NR 14
TC 10
Z9 10
U1 0
U2 5
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2011
VL 29
IS 32
BP 4224
EP 4226
DI 10.1200/JCO.2011.36.8134
PG 3
WC Oncology
SC Oncology
GA 845BJ
UT WOS:000296797500010
PM 21931031
ER
PT J
AU Richardson, PG
Wolf, J
Jakubowiak, A
Zonder, J
Lonial, S
Irwin, D
Densmore, J
Krishnan, A
Raje, N
Bar, M
Martin, T
Schlossman, R
Ghobrial, IM
Munshi, N
Laubach, J
Allerton, J
Hideshima, T
Colson, K
Poradosu, E
Gardner, L
Sportelli, P
Anderson, KC
AF Richardson, Paul G.
Wolf, Jeff
Jakubowiak, Andrzej
Zonder, Jeff
Lonial, Sagar
Irwin, David
Densmore, John
Krishnan, Amrita
Raje, Noopur
Bar, Michael
Martin, Tom
Schlossman, Robert
Ghobrial, Irene M.
Munshi, Nikhil
Laubach, Jacob
Allerton, Jeff
Hideshima, Teru
Colson, Kathleen
Poradosu, Enrique
Gardner, Lesa
Sportelli, Peter
Anderson, Kenneth C.
TI Perifosine Plus Bortezomib and Dexamethasone in Patients With
Relapsed/Refractory Multiple Myeloma Previously Treated With Bortezomib:
Results of a Multicenter Phase I/II Trial
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID EXTENDED FOLLOW-UP; APEX TRIAL; PERIPHERAL NEUROPATHY; CLINICAL BENEFIT;
COMBINATION; TANESPIMYCIN; VORINOSTAT; THERAPIES; SAFETY; REVERSIBILITY
AB Purpose
Novel agents have improved patient outcome in relapsed or relapsed/refractory multiple myeloma (MM). Preclinical data show that the novel signal transduction modulator, perifosine, enhances the cytotoxicity of dexamethasone and bortezomib. Clinical data suggest that perifosine in combination with dexamethasone has activity in relapsed or relapsed/refractory MM.
Patients and Methods
In a phase I/II study, perifosine in combination with bortezomib with or without dexamethasone was prospectively evaluated in 84 patients with relapsed or relapsed/refractory MM. All were heavily pretreated and bortezomib exposed; 73% were refractory to bortezomib, and 51% were refractory to bortezomib and dexamethasone. The dose selected for the phase II study was perifosine 50 mg/d plus bortezomib 1.3 mg/m(2), with the addition of low-dose dexamethasone at 20 mg if progression occurred on perifosine plus bortezomib alone.
Results
An overall response rate (ORR; defined as minimal response or better) of 41% was demonstrated with this combination in 73 evaluable patients, including an ORR of 65% in bortezomib-relapsed patients and 32% in bortezomib-refractory patients. Therapy was generally well tolerated; toxicities, including gastrointestinal adverse effects and fatigue, proved manageable. No treatment-related mortality was seen. Median progression-free survival was 6.4 months, with a median overall survival of 25 months (22.5 months in bortezomib-refractory patients).
Conclusion
Perifosine-bortezomib +/- dexamethasone demonstrated encouraging activity in heavily pretreated bortezomib-exposed patients with advanced MM. A phase III trial is underway comparing perifosine-bortezomib plus dexamethasone with bortezomib-dexamethasone in patients with relapsed/refractory MM previously treated with bortezomib. J Clin Oncol 29: 4243-4249. (C) 2011 by American Society of Clinical Oncology
C1 [Richardson, Paul G.; Schlossman, Robert; Ghobrial, Irene M.; Munshi, Nikhil; Laubach, Jacob; Hideshima, Teru; Colson, Kathleen; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Raje, Noopur] Massachusetts Gen Canc Ctr, Boston, MA USA.
[Wolf, Jeff; Martin, Tom] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Irwin, David] Alta Bates Canc Ctr, Berkeley, CA USA.
[Krishnan, Amrita] City Hope Natl Med Ctr, Duarte, CA USA.
[Jakubowiak, Andrzej] Univ Michigan, Ann Arbor, MI 48109 USA.
[Zonder, Jeff] Karmanos Canc Ctr, Detroit, MI USA.
[Lonial, Sagar] Winship Emory Canc Ctr, Atlanta, GA USA.
[Densmore, John] Univ Virginia, Charlottesville, VA USA.
[Bar, Michael] Bennett Canc Ctr, Stamford, CT USA.
[Allerton, Jeff] Guthrie Canc Clin, Sayre, PA USA.
[Poradosu, Enrique; Gardner, Lesa; Sportelli, Peter] Keryx Biopharmaceut, New York, NY USA.
RP Richardson, PG (reprint author), Dana Farber Canc Inst, 44 Binney St,Dana 1B02, Boston, MA 02115 USA.
EM paul_richardson@dfciharvard.edu
FU Millennium Pharmaceuticals; Kerys Biopharmaceuticals; AstraZeneca;
Acetylon Pharmaceuticals; Keryx Biopharmaceuticals, New York, NY
FX Jeff Zonder, Millennium Pharmaceuticals; John Densmore, Kerys
Biopharmaceuticals; Noopur Raje, AstraZeneca, Acetylon Pharmaceuticals;
Irene M. Ghobrial, Millennium Pharmaceuticals; Supported by Keryx
Biopharmaceuticals, New York, NY.
NR 42
TC 73
Z9 75
U1 0
U2 2
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2011
VL 29
IS 32
BP 4243
EP 4249
DI 10.1200/JCO.2010.33.9788
PG 7
WC Oncology
SC Oncology
GA 845BJ
UT WOS:000296797500013
PM 21990396
ER
PT J
AU Chen, AB
Schrag, D
AF Chen, Aileen B.
Schrag, Deborah
TI Computed Tomography-Based Simulation for Thoracic Radiation Therapy:
Technical Advance or Clinical Evidence? Reply
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
ID CELL LUNG-CANCER; VARIABLES; SURVIVAL; OUTCOMES
C1 [Chen, Aileen B.; Schrag, Deborah] Dana Farber Canc Inst, Ctr Outcomes & Policy Res, Boston, MA 02115 USA.
[Chen, Aileen B.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Chen, AB (reprint author), Dana Farber Canc Inst, Ctr Outcomes & Policy Res, Boston, MA 02115 USA.
NR 9
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2011
VL 29
IS 32
BP 4336
EP 4336
DI 10.1200/JCO.2011.38.2259
PG 1
WC Oncology
SC Oncology
GA 845BJ
UT WOS:000296797500027
ER
PT J
AU Jha, AK
Classen, DC
AF Jha, Ashish K.
Classen, David C.
TI Getting Moving on Patient Safety - Harnessing Electronic Data for Safer
Care
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
C1 [Jha, Ashish K.] Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA.
[Jha, Ashish K.] VA Boston Healthcare Syst, Boston, MA USA.
[Classen, David C.] Comp Sci Corp, Salt Lake City, UT USA.
[Classen, David C.] Univ Utah, Salt Lake City, UT USA.
RP Jha, AK (reprint author), Harvard Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02115 USA.
NR 5
TC 24
Z9 24
U1 0
U2 3
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 10
PY 2011
VL 365
IS 19
BP 1756
EP 1758
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 844QQ
UT WOS:000296762800002
PM 22070474
ER
PT J
AU Cash, SS
Larvie, M
Dalmau, J
AF Cash, Sydney S.
Larvie, Mykol
Dalmau, Josep
TI Case 34-2011: A 75-Year-Old Man with Memory Loss and Partial Seizures
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID TEMPORAL-LOBE EPILEPSY; POTASSIUM CHANNEL ANTIBODY; LIMBIC ENCEPHALITIS;
LGI1; MUTATIONS
C1 [Cash, Sydney S.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Larvie, Mykol] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Cash, Sydney S.] Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Larvie, Mykol] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Dalmau, Josep] Univ Penn, Dept Neurol, Div Neurooncol, Hosp Univ Penn, Philadelphia, PA 19104 USA.
RP Cash, SS (reprint author), Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
OI Dalmau, Josep/0000-0001-5856-2813
NR 19
TC 10
Z9 10
U1 1
U2 3
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 10
PY 2011
VL 365
IS 19
BP 1825
EP 1833
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 844QQ
UT WOS:000296762800013
PM 22070480
ER
PT J
AU Abrams, JL
Ecker, JL
Barth, WH
AF Abrams, Joshua L.
Ecker, Jeffrey L.
Barth, William H.
TI Case 23-2011-Legal Considerations
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Letter
C1 [Abrams, Joshua L.; Ecker, Jeffrey L.; Barth, William H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Abrams, JL (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 10
PY 2011
VL 365
IS 19
BP 1846
EP 1847
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 844QQ
UT WOS:000296762800029
PM 22070495
ER
PT J
AU Wu, YN
Johnson, SW
AF Wu, Y. -N.
Johnson, S. W.
TI DOPAMINE OXIDATION FACILITATES ROTENONE-DEPENDENT POTENTIATION OF
N-METHYL-D-ASPARTATE CURRENTS IN RAT SUBSTANTIA NIGRA DOPAMINE NEURONS
SO NEUROSCIENCE
LA English
DT Article
DE reactive oxygen species; rotenone; N-methyl-D-aspartate; monoamine
oxidase; pargyline; reserpine
ID PROTEIN-KINASE-C; MITOCHONDRIAL COMPLEX-I; PARKINSONS-DISEASE;
NMDA-RECEPTOR; TYROSINE KINASE; DEPRENYL PROTECTS; RAPID DEVELOPMENT;
TREATED RATS; PC12 CELLS; TOXICITY
AB Rotenone is a mitochondrial poison that causes dopamine cell death and is used as a model of Parkinson's disease in rodents. Recently, we showed that rotenone augments currents evoked by N-methyl-D-aspartate (NMDA) by relieving voltage-dependent Mg(2+) block in rat substantia nigra compacta (SNC) dopamine neurons. Because rotenone is well known to generate reactive oxygen species (ROS), we conducted the present experiments to evaluate the role of ROS in mediating the effect of rotenone on NMDA current augmentation. Using patch pipettes to record whole-cell currents from SNC neurons in slices of rat brain, we found that the ability of rotenone (100 nM) to increase NMDA (3-30 mu M) current was antagonized by the antioxidant agent N-acetylcysteine (1 mM). In contrast, mercaptosuccinate (1 mM), which blocks glutathione peroxidase and raises tissue levels of H(2)O(2), mimicked rotenone by augmenting inward currents evoked by NMDA. Because oxidation of dopamine can also generate ROS, we explored the role of dopamine on this action of rotenone. We prepared dopamine-depleted midbrain slices from rats that had been pretreated with reserpine (5 mg/kg ip) and alpha-methyl-para-tyrosine (AMPT, 250 mg/kg ip). Dopamine depletion blocked the ability of rotenone (100 nM) to increase inward current evoked by NMDA (30 mu M). Rotenone-dependent augmentation of NMDA current was also blocked by the monoamine oxidase inhibitor pargyline (100 mu M) in slices prepared from normal rats. In contrast, the dopamine precursor levodopa potentiated the action of rotenone on NMDA current. These results suggest that ROS and/or dopamine oxidation products mediate the ability of rotenone to potentiate NMDA currents. Because excessive NMDA receptor stimulation can produce excitotoxicity, our results suggest that oxidative metabolism of dopamine might facilitate the neurotoxicity of rotenone. Published by Elsevier Ltd on behalf of IBRO.
C1 [Wu, Y. -N.; Johnson, S. W.] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97239 USA.
[Johnson, S. W.] Portland VA Med Ctr, Portland, OR 97207 USA.
RP Johnson, SW (reprint author), Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97239 USA.
EM johnsost@ohsu.edu
FU Veterans Affairs Merit Review [0383]; Portland Veterans Affairs
Parkinson's Disease Research, Education, and Clinical Center
FX This research was supported by Veterans Affairs Merit Review grant 0383
and by the Portland Veterans Affairs Parkinson's Disease Research,
Education, and Clinical Center.
NR 53
TC 11
Z9 11
U1 0
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
J9 NEUROSCIENCE
JI Neuroscience
PD NOV 10
PY 2011
VL 195
BP 138
EP 144
DI 10.1016/j.neuroscience.2011.08.041
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 833EF
UT WOS:000295863900014
PM 21884756
ER
PT J
AU Hill-Burns, EM
Factor, SA
Zabetian, CP
Thomson, G
Payami, H
AF Hill-Burns, Erin M.
Factor, Stewart A.
Zabetian, Cyrus P.
Thomson, Glenys
Payami, Haydeh
TI Evidence for More than One Parkinson's Disease-Associated Variant within
the HLA Region
SO PLOS ONE
LA English
DT Article
ID POPULATION; METAANALYSIS; HAPLOTYPES; IMPUTATION; GENETICS; SNCA
AB Parkinson's disease (PD) was recently found to be associated with HLA in a genome-wide association study (GWAS). Followup GWAS's replicated the PD-HLA association but their top hits differ. Do the different hits tag the same locus or is there more than one PD-associated variant within HLA? We show that the top GWAS hits are not correlated with each other (0.00 <= r(2)<= 0.15). Using our GWAS (2000 cases, 1986 controls) we conducted step-wise conditional analysis on 107 SNPs with P, 10 23 for PD-association; 103 dropped-out, four remained significant. Each SNP, when conditioned on the other three, yielded P(SNP1) = 5610 24, P(SNP2) = 5610 24, P(SNP3) = 4610 23 and P(SNP4) = 0.025. The four SNPs were not correlated (0.01 <= r(2)<= 0.20). Haplotype analysis (excluding rare SNP2) revealed increasing PD risk with increasing risk alleles from OR = 1.27, P = 5610 23 for one risk allele to OR = 1.65, P = 4610 28 for three. Using additional 843 cases and 856 controls we replicated the independent effects of SNP1 (P(conditioned-on-SNP4) = 0.04) and SNP4 (P(conditioned-on-SNP1) = 0.04); SNP2 and SNP3 could not be replicated. In pooled GWAS and replication, SNP1 had OR(conditioned-on-SNP4) = 1.23, P(conditioned-on-SNP4) = 6610 27; SNP4 had OR(conditioned-on-SNP1) = 1.18, P(conditioned-on-SNP1) = 3610 23; and the haplotype with both risk alleles had OR = 1.48, P = 2x10(-12). Genotypic OR increased with the number of risk alleles an individual possessed up to OR = 1.94, P = 2610 211 for individuals who were homozygous for the risk allele at both SNP1 and SNP4. SNP1 is a variant in HLA-DRA and is associated with HLA-DRA, DRB5 and DQA2 gene expression. SNP4 is correlated (r(2) = 0.95) with variants that are associated with HLA-DQA2 expression, and with the top HLA SNP from the IPDGC GWAS (r(2) = 0.60). Our findings suggest more than one PD-HLA association; either different alleles of the same gene, or separate loci.
C1 [Hill-Burns, Erin M.; Payami, Haydeh] New York State Dept Hlth, Wadsworth Ctr, Albany, NY USA.
[Factor, Stewart A.] Emory Univ, Sch Med, Dept Neurol, Atlanta, GA 30322 USA.
[Zabetian, Cyrus P.] Univ Washington, Dept Neurol, Seattle, WA 98195 USA.
[Zabetian, Cyrus P.] Univ Washington, Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Thomson, Glenys] Univ Calif Berkeley, Dept Integrat Biol, Berkeley, CA 94720 USA.
RP Hill-Burns, EM (reprint author), New York State Dept Hlth, Wadsworth Ctr, Albany, NY USA.
EM hpayami@wadsworth.org
OI Zabetian, Cyrus/0000-0002-7739-4306
FU National Institute of Neurological Disorders And Stroke (NINDS) [R01
NS36960, R01 NS067469]; Edmond J. Safra Michael J. Fox Foundation Global
Genetic Consortium Initiative; Department of Veterans Affairs
[I01BX000531]; Close to a Cure Foundation: A Fund for Parkinson's
Research of Foundation for the Carolinas; National Institute of Allergy
and Infectious Disease [AI40076]
FX Study was supported by grants from the National Institute of
Neurological Disorders And Stroke (NINDS R01 NS36960 and R01 NS067469 to
HP), the Edmond J. Safra Michael J. Fox Foundation Global Genetic
Consortium Initiative (HP), the Department of Veterans Affairs
('I01BX000531 to CZ), The Close to a Cure Foundation: A Fund for
Parkinson's Research of Foundation for the Carolinas (SF), and the
National Institute of Allergy and Infectious Disease (AI40076, GT).
Funding support for the replication dataset was provided by the National
Institute of Neurological Disorders and Stroke (Foroud/Myers, PI). The
content is solely the responsibility of the authors and does not
necessarily represent the official views of the funding agencies. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 29
TC 20
Z9 20
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 9
PY 2011
VL 6
IS 11
AR e27109
DI 10.1371/journal.pone.0027109
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852II
UT WOS:000297350800027
PM 22096524
ER
PT J
AU Li, JF
Bush, J
Xiong, Y
Li, L
McCormack, M
AF Li, Jian-Feng
Bush, Jenifer
Xiong, Yan
Li, Lei
McCormack, Matthew
TI Large-Scale Protein-Protein Interaction Analysis in Arabidopsis
Mesophyll Protoplasts by Split Firefly Luciferase Complementation
SO PLOS ONE
LA English
DT Article
ID AUXIN RESPONSE FACTORS; FRAGMENT-ASSISTED COMPLEMENTATION; LATERAL ROOT
DEVELOPMENT; SIGNAL-TRANSDUCTION; INTERACTION NETWORK; REGULATED
PROTEIN; CIRCADIAN CLOCK; GENE-EXPRESSION; AUX/IAA PROTEIN; LIVING
SUBJECTS
AB Protein-protein interactions (PPIs) constitute the regulatory network that coordinates diverse cellular functions. There are growing needs in plant research for creating protein interaction maps behind complex cellular processes and at a systems biology level. However, only a few approaches have been successfully used for large-scale surveys of PPIs in plants, each having advantages and disadvantages. Here we present split firefly luciferase complementation (SFLC) as a highly sensitive and noninvasive technique for in planta PPI investigation. In this assay, the separate halves of a firefly luciferase can come into close proximity and transiently restore its catalytic activity only when their fusion partners, namely the two proteins of interest, interact with each other. This assay was conferred with quantitativeness and high throughput potential when the Arabidopsis mesophyll protoplast system and a microplate luminometer were employed for protein expression and luciferase measurement, respectively. Using the SFLC assay, we could monitor the dynamics of rapamycin-induced and ascomycin-disrupted interaction between Arabidopsis FRB and human FKBP proteins in a near real-time manner. As a proof of concept for large-scale PPI survey, we further applied the SFLC assay to testing 132 binary PPIs among 8 auxin response factors (ARFs) and 12 Aux/IAA proteins from Arabidopsis. Our results demonstrated that the SFLC assay is ideal for in vivo quantitative PPI analysis in plant cells and is particularly powerful for large-scale binary PPI screens.
C1 [Li, Jian-Feng; Xiong, Yan; Li, Lei; McCormack, Matthew] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Li, Jian-Feng; Bush, Jenifer; Xiong, Yan; Li, Lei; McCormack, Matthew] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
RP Li, JF (reprint author), Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
EM jli@molbio.mgh.harvard.edu
RI Li, Lei/F-9826-2015
FU Massachusetts General Hospital; National Institutes of Health [GM070567]
FX This work was supported by Massachusetts General Hospital postdoctoral
fellowship for medical discovery awarded to Dr. Li, and the National
Institutes of Health grant GM070567 to Dr. Sheen (Massachusetts General
Hospital, United States of America). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 50
TC 23
Z9 36
U1 1
U2 19
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 9
PY 2011
VL 6
IS 11
AR e27364
DI 10.1371/journal.pone.0027364
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852II
UT WOS:000297350800050
PM 22096563
ER
PT J
AU Fainzilber, M
Budnik, V
Segal, RA
Kreutz, MR
AF Fainzilber, Mike
Budnik, Vivian
Segal, Rosalind A.
Kreutz, Michael R.
TI From Synapse to Nucleus and Back Again-Communication over Distance
within Neurons
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID SURVIVAL RESPONSE; PROTEIN-SYNTHESIS; BCL-W; NERVE; PLASTICITY; IMPORT;
TRANSLOCATION; TRANSCRIPTION; TRANSLATION; TRANSPORT
AB How do neurons integrate intracellular communication from synapse to nucleus and back? Here we briefly summarize aspects of this topic covered by a symposium at Neuroscience 2011. A rich repertoire of signaling mechanisms link both dendritic terminals and axon tips with neuronal soma and nucleus, using motor-dependent transport machineries to traverse the long intracellular distances along neuronal processes. Activation mechanisms at terminals include localized translation of dendritic or axonal RNA, proteolytic cleavage of receptors or second messengers, and differential phosphorylation of signaling moieties. Signaling complexes may be transported in endosomes, or as non-endosomal complexes associated with importins and dynein. Anterograde transport of RNA granules from the soma to neuronal processes, coupled with retrograde transport of proteins translated locally at terminals or within processes, may fuel ongoing bidirectional communication between soma and synapse to modulate synaptic plasticity as well as neuronal growth and survival decisions.
C1 [Fainzilber, Mike] Weizmann Inst Sci, Dept Biol Chem, IL-76100 Rehovot, Israel.
[Budnik, Vivian] Univ Massachusetts, Sch Med, Dept Neurobiol, Worcester, MA 01605 USA.
[Segal, Rosalind A.] Dana Farber Canc Inst, Dept Pediat Oncol & Canc Biol, Boston, MA 02215 USA.
[Segal, Rosalind A.] Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02215 USA.
[Kreutz, Michael R.] Leibniz Inst Neurobiol, Neuroplast Grp, D-39118 Magdeburg, Germany.
RP Fainzilber, M (reprint author), Weizmann Inst Sci, Dept Biol Chem, IL-76100 Rehovot, Israel.
EM mike.fainzilber@weizmann.ac.il
OI Fainzilber, Mike/0000-0001-8173-8557
FU Israel Science Foundation; German-Israeli Foundation; Minerva
Foundation; International Foundation for Research in Paraplegia;
Christopher and Dana Reeve Foundation; Dr. Miriam and Sheldon G. Adelson
Medical Research Foundation; NIH [R01 NS063228, R01 MH091662, R01
NS050674]; Center for Brain and Behavior Sciences Magdeburg; Deutsche
Forschungsgemeinschaft; Bundesministerium fur Bildung und Forschung;
DZNE Magdeburg; Deutsche-Israelische Projektkooperation; Leibniz
Foundation (Pakt fur Forschung); Schram Foundation
FX We gratefully acknowledge grant support as follows: M.F.-from the Israel
Science Foundation, the German-Israeli Foundation, the Minerva
Foundation, the International Foundation for Research in Paraplegia, the
Christopher and Dana Reeve Foundation, and the Dr. Miriam and Sheldon G.
Adelson Medical Research Foundation; V.B.-NIH Grant R01 NS063228;
R.A.S.-NIH Grants R01 MH091662 and R01 NS050674; M.R.K.-Center for Brain
and Behavior Sciences Magdeburg, Deutsche Forschungsgemeinschaft,
Bundesministerium fur Bildung und Forschung, DZNE Magdeburg, the
Deutsche-Israelische Projektkooperation, Leibniz Foundation (Pakt fur
Forschung), and Schram Foundation.
NR 34
TC 13
Z9 13
U1 0
U2 6
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 9
PY 2011
VL 31
IS 45
BP 16045
EP 16048
DI 10.1523/JNEUROSCI.4006-11.2011
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA 845CE
UT WOS:000296799700001
PM 22072654
ER
PT J
AU Konno, T
Hata, S
Hamada, Y
Horikoshi-Sakuraba, Y
Nakaya, T
Saito, Y
Yamamoto, T
Yamamoto, T
Maeda, M
Ikeuchi, T
Gandy, S
Akatsu, H
Suzuki, T
AF Konno, Tomoko
Hata, Saori
Hamada, Yukiko
Horikoshi-Sakuraba, Yuko
Nakaya, Tadashi
Saito, Yuhki
Yamamoto, Tohru
Yamamoto, Takayuki
Maeda, Masahiro
Ikeuchi, Takeshi
Gandy, Sam
Akatsu, Hiroyasu
Suzuki, Toshiharu
CA Japanese Alzheimers Dis
TI Coordinated increase of gamma-secretase reaction products in the plasma
of some female Japanese sporadic Alzheimer's disease patients:
quantitative analysis of p3-Alc alpha with a new ELISA system
SO MOLECULAR NEURODEGENERATION
LA English
DT Article
ID TRAUMATIC BRAIN-INJURY; AMYLOID-BETA; APOLIPOPROTEIN-E; ASSOCIATION;
ESTROGEN; PEPTIDE; GENE; NEURODEGENERATION; DEGRADATION; METABOLISM
AB Background: Aggregatable amyloid beta-peptide (A beta) and non-aggregatable p3-Alc alpha are metabolic products of the gamma-secretase cleavage of amyloid beta-protein precursor (APP) and Alcadein alpha (Alc alpha), respectively. Familial AD (FAD)-linked mutations in the presenilin 1 or 2 (PS1 or PS2) component of gamma-secretase can cause alternative intramembranous processing of APP and Alc alpha, leading to a coordinated generation of variants of both A beta and p3-Alc alpha. Variant Alc alpha peptides have been observed in the cerebrospinal fluid (CSF) of patients with mild cognitive impairment and sporadic Alzheimer's disease (AD). Since, like APP, Alc alpha is largely expressed in brain, one might predict that alternative processing of Alca would be reflected in body fluids of some AD patients. These patients with misprocessing of multiple gamma-secretase substrates might define an endophenotype of p3-Alc alpha, in whom AD is due either to dysfunction of gamma-secretase or to a disorder of the clearance of hydrophobic peptides such as those derived from transmembrane domains.
Results: We developed a simple procedure for extraction of p3-Alc alpha from plasma and for analyzing this extract in a sensitive, p3-Alc alpha-specific sandwich enzyme-linked immunosorbent assay (ELISA) system. Plasma p3-Alca levels and A beta 40 levels were examined in sporadic AD subjects from two independent Japanese cohorts. In some of these patients, levels of plasma p3-Alc alpha were significantly higher, and were accompanied by parallel changes in A beta 40 levels. This AD-related difference was more marked in female subjects, but this phenomenon was not observed in subjects with frontotemporal lobar degeneration (FTLD).
Conclusion: Reagents and procedures have been established that enable extraction of p3-Alc alpha from plasma and for quantification of plasma p3-Alc alpha levels by ELISA. Some populations of AD subjects apparently show increased levels of both p3-Alc alpha and A beta 40. Quantification of p3-Alc alpha level may be useful as a readily accessible biomarker for a population of sporadic AD patients in which disease pathogenesis is associated with either dysfunction of gamma-secretase or with a disorder of the clearance of transmembrane domain-derived peptides.
C1 [Konno, Tomoko; Hata, Saori; Nakaya, Tadashi; Saito, Yuhki; Yamamoto, Tohru; Suzuki, Toshiharu] Hokkaido Univ, Grad Sch Pharmaceut Sci, Neurosci Lab, Sapporo, Hokkaido 0600812, Japan.
[Hamada, Yukiko; Horikoshi-Sakuraba, Yuko; Maeda, Masahiro] Immunobiol Labs Co Ltd IBL, Fujioka 3750005, Japan.
[Yamamoto, Takayuki; Akatsu, Hiroyasu] Fukushimura Hosp, Choju Med Inst, Toyohashi, Aichi 4418124, Japan.
[Ikeuchi, Takeshi] Niigata Univ, Brain Res Inst, Dept Mol Neurosci, Niigata 9518585, Japan.
[Gandy, Sam] Alzheimers Dis Res Ctr, Mt Sinai Sch Med, Dept Neurol, New York, NY 10029 USA.
[Gandy, Sam] Alzheimers Dis Res Ctr, Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
[Gandy, Sam] James J Peters Vet Adm Med Ctr, Bronx, NY 10468 USA.
RP Suzuki, T (reprint author), Hokkaido Univ, Grad Sch Pharmaceut Sci, Neurosci Lab, Sapporo, Hokkaido 0600812, Japan.
EM tsuzuki@pharm.hokudai.ac.jp
RI Hata, Saori /A-3829-2012; Yamamoto, Tohru/A-3801-2012; Suzuki,
Toshiharu/B-5342-2013
OI Yamamoto, Tohru/0000-0002-1652-0233;
FU Ministry of Education, Culture, Sports, Science and Technology (MEXT);
Ministry of Health, Labor and Welfare (MHLW); New Energy and Industrial
Technology Development Organization (NEDO) in Japan; NIA Alzheimer's
Disease Research Center [P50 05138]
FX This work was supported in part by Grants-in-aid for Scientific Research
from the Ministry of Education, Culture, Sports, Science and Technology
(MEXT), a grant from the Ministry of Health, Labor and Welfare (MHLW),
and a grant from the New Energy and Industrial Technology Development
Organization (NEDO) in Japan. S.G. was supported by the NIA Alzheimer's
Disease Research Center grant P50 05138 to Mary Sano.
NR 32
TC 5
Z9 5
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1750-1326
J9 MOL NEURODEGENER
JI Mol. Neurodegener.
PD NOV 8
PY 2011
VL 6
AR 76
DI 10.1186/1750-1326-6-76
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 864NT
UT WOS:000298247600001
PM 22067061
ER
PT J
AU Singh, T
Sharma, SD
Katiyar, SK
AF Singh, Tripti
Sharma, Som D.
Katiyar, Santosh K.
TI Grape Proanthocyanidins Induce Apoptosis by Loss of Mitochondrial
Membrane Potential of Human Non-Small Cell Lung Cancer Cells In Vitro
and In Vivo
SO PLOS ONE
LA English
DT Article
ID SKH-1 HAIRLESS MICE; DEPENDENT KINASES; ANTICANCER DRUGS;
CARCINOMA-CELLS; CYCLE CONTROL; BCL-2 FAMILY; DEATH; INHIBITORS;
PROTEIN; GROWTH
AB Lung cancer remains the leading cause of cancer-related deaths worldwide, and non-small cell lung cancer (NSCLC) represents approximately 80% of total lung cancer cases. The use of non-toxic dietary phytochemicals can be considered as a chemotherapeutic strategy for the management of the NSCLC. Here, we report that grape seed proanthocyanidins (GSPs) induce apoptosis of NSCLC cells, A549 and H1299, in vitro which is mediated through increased expression of pro-apoptotic protein Bax, decreased expression of anti-apoptotic proteins Bcl2 and Bcl-xl, disruption of mitochondrial membrane potential, and activation of caspases 9, 3 and poly (ADP-ribose) polymerase (PARP). Pre-treatment of A549 and H1299 cells with the caspase-3 inhibitor (z-DEVD-fmk) significantly blocked the GSPs-induced apoptosis of these cells confirmed that GSPs-induced apoptosis is mediated through activation of caspases-3. Treatments of A549 and H1299 cells with GSPs resulted in an increase in G1 arrest. G0/G1 phase of the cell cycle is known to be controlled by cyclin dependent kinases (Cdk), cyclin-dependent kinase inhibitors (Cdki) and cyclins. Our western blot analyses showed that GSPs-induced G1 cell cycle arrest was mediated through the increased expression of Cdki proteins (Cip1/p21 and Kip1/p27), and a simultaneous decrease in the levels of Cdk2, Cdk4, Cdk6 and cyclins. Further, administration of 50, 100 or 200 mg GSPs/kg body weight of mice by oral gavage (5 d/week) markedly inhibited the growth of s.c. A549 and H1299 lung tumor xenografts in athymic nude mice, which was associated with the induction of apoptotic cell death, increased expression of Bax, reduced expression of anti-apoptotic proteins and activation of caspase-3 in tumor xenograft cells. Based on the data obtained in animal study, human equivalent dose of GSPs was calculated, which seems affordable and attainable. Together, these results suggest that GSPs may represent a potential therapeutic agent for the non-small cell lung cancer.
C1 [Singh, Tripti; Sharma, Som D.; Katiyar, Santosh K.] Univ Alabama, Dept Dermatol, Birmingham, AL 35294 USA.
[Katiyar, Santosh K.] Birmingham Vet Affairs Med Ctr, Birmingham, AL USA.
[Katiyar, Santosh K.] Univ Alabama, Nutr Obes Res Ctr, Birmingham, AL USA.
[Katiyar, Santosh K.] Univ Alabama, Ctr Comprehens Canc, Birmingham, AL 35294 USA.
RP Singh, T (reprint author), Univ Alabama, Dept Dermatol, Birmingham, AL 35294 USA.
EM skatiyar@uab.edu
FU Veterans Administration Merit Review Award
FX This work was supported by funds from the Veterans Administration Merit
Review Award (SKK). The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 41
TC 34
Z9 37
U1 1
U2 12
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 8
PY 2011
VL 6
IS 11
AR e27444
DI 10.1371/journal.pone.0027444
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 852HZ
UT WOS:000297349700046
PM 22087318
ER
PT J
AU Azadani, A
Chitsaz, S
Tseng, E
Ge, L
AF Azadani, Ali
Chitsaz, Sam
Tseng, Elaine
Ge, Liang
TI Finite Element Analysis of Transcatheter Aortic Valve Implantation:
Impact of Oversizing on Stent and Leaflet Stresses
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Azadani, Ali; Chitsaz, Sam; Tseng, Elaine; Ge, Liang] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Azadani, Ali; Chitsaz, Sam; Tseng, Elaine; Ge, Liang] San Francisco VA Med Ctr, San Francisco, CA USA.
RI Chitsaz, Sam/C-4586-2008
NR 0
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 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B198
EP B198
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900736
ER
PT J
AU Chitsaz, S
Jaussaud, N
Meadows, A
Wintermark, M
Cambronero, N
Azadani, AN
Saloner, DA
Chuter, TA
Ge, L
Tseng, EE
AF Chitsaz, Sam
Jaussaud, Nicolas
Meadows, Alison
Wintermark, Max
Cambronero, Neil
Azadani, Ali N.
Saloner, David A.
Chuter, Timothy A.
Ge, Liang
Tseng, Elaine E.
TI Thoracic Endovascular Aortic Repair for Acute Type A Dissection: A
Computational and Anatomic Analysis of Technical Limitations for
Available Devices
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Chitsaz, Sam; Jaussaud, Nicolas; Wintermark, Max; Cambronero, Neil; Azadani, Ali N.; Chuter, Timothy A.; Ge, Liang; Tseng, Elaine E.] Univ Calif San Francisco, Dept Surg, San Francisco, CA USA.
[Chitsaz, Sam; Jaussaud, Nicolas; Azadani, Ali N.; Saloner, David A.; Ge, Liang; Tseng, Elaine E.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Meadows, Alison; Saloner, David A.] Univ Calif San Francisco, Dept Radiol, San Francisco, CA USA.
RI Chitsaz, Sam/C-4586-2008
NR 0
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B155
EP B155
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900575
ER
PT J
AU Dattilo, PB
Tsai, TT
Casserly, IP
AF Dattilo, Philip B.
Tsai, Thomas T.
Casserly, Ivan P.
TI Endovascular Therapy of Common Femoral Arterial Disease
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Dattilo, Philip B.; Tsai, Thomas T.; Casserly, Ivan P.] Univ Colorado, Sch Med, Aurora, CO USA.
[Tsai, Thomas T.; Casserly, Ivan P.] Denver VA Med Ctr, Denver, CO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B157
EP B157
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900582
ER
PT J
AU Fleming, CP
Tanaka, A
Gardecki, JA
Maurovich-Horvat, P
Winger, WC
Eckert, JE
Hoffmann, T
Bouma, BE
Tearney, GJ
AF Fleming, Christine P.
Tanaka, Atsushi
Gardecki, Joseph A.
Maurovich-Horvat, Pal
Winger, William C.
Eckert, Jocelyn E.
Hoffmann, Tido
Bouma, Bren E.
Tearney, Guillermo J.
TI Classification of Atherosclerotic Plaques using Depth Resolved Spectral
Analysis of Optical Frequency Domain Imaging Datasets
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Fleming, Christine P.; Tanaka, Atsushi; Gardecki, Joseph A.; Winger, William C.; Eckert, Jocelyn E.; Bouma, Bren E.; Tearney, Guillermo J.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Maurovich-Horvat, Pal] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Fleming, Christine P.; Tanaka, Atsushi; Gardecki, Joseph A.; Maurovich-Horvat, Pal; Winger, William C.; Hoffmann, Tido; Bouma, Bren E.; Tearney, Guillermo J.] Harvard Univ, Sch Med, Boston, MA USA.
RI Hendon, Christine/F-8261-2016
OI Hendon, Christine/0000-0001-7318-1517
NR 0
TC 0
Z9 0
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B174
EP B174
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900648
ER
PT J
AU Kim, JS
Afari, ME
Ha, J
Tellez, A
Milewski, K
Condin, G
Cheng, YP
Kaluza, GL
Granada, JF
AF Kim, Jung-Sun
Afari, Maxwell E.
Ha, Jinyoung
Tellez, Armando
Milewski, Krzysztof
Condin, Gerard
Cheng, Yanping
Kaluza, Greg L.
Granada, Juan F.
TI Optical Characteristics of Neointimal Formation Correlate with
Histological Markers of Stent Healing in a Porcine Model of Restenosis
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Kim, Jung-Sun; Afari, Maxwell E.; Tellez, Armando; Milewski, Krzysztof; Condin, Gerard; Cheng, Yanping; Kaluza, Greg L.; Granada, Juan F.] Skirball Ctr, Orangeburg, NY USA.
[Ha, Jinyoung] Harvard Univ, Sch Med, Boston, MA USA.
[Ha, Jinyoung] Massachusetts Gen Hosp, Wellman Ctr Photo Med, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B121
EP B121
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900446
ER
PT J
AU Maini, B
O'Neill, W
Dixon, S
Palacios, I
Schreiber, T
Gregory, DA
Scotti, DJ
AF Maini, Brijeshwar
O'Neill, William
Dixon, Simon
Palacios, Igor
Schreiber, Theodore
Gregory, David A.
Scotti, D. J.
TI Cost-effectiveness and Clinical Outcomes of Impella Hemodynamic Support
Compared with Intra-Aortic Balloon Pump in High Risk Patients Receiving
PCI: Results from the PROTECT II Trial
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Maini, Brijeshwar] PinnacleHlth Cardiovasc Inst, Wormleysburg, PA USA.
[O'Neill, William] Univ Miami, Miami, FL USA.
[Palacios, Igor] Beaumont Hosp, Royal Oak, MI USA.
[Dixon, Simon] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Schreiber, Theodore] Detroit Med Ctr, Detroit, MI USA.
[Gregory, David A.; Scotti, D. J.] Presscott Associates Ltd, Avon, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B131
EP B132
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900485
ER
PT J
AU McCabe, JM
Armstrong, EJ
Hoffmayer, KS
Bhave, P
Stein, JC
Kinlay, S
Ganz, P
AF McCabe, James M.
Armstrong, Ehrin J.
Hoffmayer, Kurt S.
Bhave, Prashant
Stein, John C.
Kinlay, Scott
Ganz, Peter
TI Factors Associated with Belays in Primary PCI and Cardiac
Catheterization Laboratory Activation for ST-Segment Elevation
Myocardial Infarctions; A report from the Activate-SF registry
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Stein, John C.] Univ Calif San Francisco, Dept Emergency Med, San Francisco, CA 94143 USA.
[Kinlay, Scott] Brigham & Womens Hosp, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Kinlay, Scott] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B21
EP B21
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900092
ER
PT J
AU Owens, CD
Gasper, WJ
Kim, JM
Rapp, J
Grenon, M
Seward, K
AF Owens, Christopher D.
Gasper, Warren J.
Kim, Ji Min
Rapp, Joseph
Grenon, Marlene
Seward, Kirk
TI Dexamethasone Infusion to the Adventitia to Enhance Clinical Efficacy
after Femoropopliteal Revascularization: A First in Man Study
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Owens, Christopher D.; Gasper, Warren J.; Kim, Ji Min; Rapp, Joseph; Grenon, Marlene] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Owens, Christopher D.; Gasper, Warren J.; Rapp, Joseph; Grenon, Marlene] San Francisco Vet Adm Med Ctr, San Francisco, CA USA.
[Seward, Kirk] Mercator MedSyst Inc, San Leandro, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B155
EP B155
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900574
ER
PT J
AU Xu, H
Nguyen, KT
Terada, LS
Fuh, E
Garcia, JA
Brilakis, ES
Bhatt, DL
Banerjee, S
AF Xu, Hao
Kytai T Nguyen
Terada, Lance S.
Fuh, Eric
Garcia, Joseph A.
Brilakis, Emmanouil S.
Bhatt, Deepak L.
Banerjee, Subhash
TI Response of Endothelial Progenitor Cells To Antiproliferative Drugs
Currently Used in Drug Eluting Stents
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Meeting Abstract
CT 23rd Annual Transcatheter Cardiovascular Therapeutics (TCT) Symposium
CY NOV 07-11, 2011
CL San Francisco, CA
C1 [Terada, Lance S.; Fuh, Eric; Garcia, Joseph A.; Brilakis, Emmanouil S.; Banerjee, Subhash] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Xu, Hao; Garcia, Joseph A.; Brilakis, Emmanouil S.; Banerjee, Subhash] VA N Texas Hlth Care Ctr, Dallas, TX USA.
[Kytai T Nguyen] Univ Texas Arlington, Arlington, TX 76019 USA.
[Bhatt, Deepak L.] VA Boston Healthcare Syst, Boston, MA USA.
[Bhatt, Deepak L.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0735-1097
J9 J AM COLL CARDIOL
JI J. Am. Coll. Cardiol.
PD NOV 8
PY 2011
VL 58
IS 20
SU B
BP B70
EP B71
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846IZ
UT WOS:000296891900267
ER
PT J
AU Kinlay, S
AF Kinlay, Scott
TI Changes in Stroke Epidemiology, Prevention, and Treatment
SO CIRCULATION
LA English
DT Review
DE stroke; epidemiology; risk factors; anticoagulation; atrial
fibrillation; thrombolysis; stents; revascularization; clinical trials
ID ATRIAL-FIBRILLATION; MYOCARDIAL-INFARCTION; ISCHEMIC-STROKE;
BLOOD-PRESSURE; HEART-DISEASE; RISK; ENDARTERECTOMY; WARFARIN;
METAANALYSIS; STENOSIS
C1 [Kinlay, Scott] Brigham & Womens Hosp, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Kinlay, Scott] Harvard Univ, Sch Med, Boston, MA USA.
RP Kinlay, S (reprint author), VA Boston Healthcare Syst, Cardiac Catheterizat Lab & Vasc Med, Cardiovasc Div, 1400 VFW Pkwy, W Roxbury, MA 02132 USA.
EM scott.kinlay@va.gov
FU CSRD Merit [1I01CX000440-01A1]
FX Dr Kinlay is supported by a CSR&D Merit 1I01CX000440-01A1.
NR 26
TC 26
Z9 28
U1 0
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 8
PY 2011
VL 124
IS 19
BP E494
EP E496
DI 10.1161/CIRCULATIONAHA.111.069633
PG 3
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 844SE
UT WOS:000296766800002
PM 22064961
ER
PT J
AU Santagata, S
Hu, R
Lin, NU
Mendillo, ML
Collins, LC
Hankinson, SE
Schnitt, SJ
Whitesell, L
Tamimi, RM
Lindquist, S
Ince, TA
AF Santagata, Sandro
Hu, Rong
Lin, Nancy U.
Mendillo, Marc L.
Collins, Laura C.
Hankinson, Susan E.
Schnitt, Stuart J.
Whitesell, Luke
Tamimi, Rulla M.
Lindquist, Susan
Ince, Tan A.
TI High levels of nuclear heat-shock factor 1 (HSF1) are associated with
poor prognosis in breast cancer
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE heat-shock protein 90; signature; pathology; heat-shock response;
immunohistochemistry
ID TRANSCRIPTION FACTOR HSF1; ESTROGEN-RECEPTOR-ALPHA; NON-ONCOGENE
ADDICTION; TANESPIMYCIN 17-AAG; PROTEIN 90; HSP90; GROWTH; PROGRESSION;
ADENOCARCINOMA; TRANSFORMATION
AB Heat-shock factor 1 (HSF1) is the master transcriptional regulator of the cellular response to heat and a wide variety of other stressors. We previously reported that HSF1 promotes the survival and proliferation of malignant cells. At this time, however, the clinical and prognostic significance of HSF1 in cancer is unknown. To address this issue breast cancer samples from 1,841 participants in the Nurses' Health Study were scored for levels of nuclear HSF1. Associations of HSF1 status with clinical parameters and survival outcomes were investigated by Kaplan-Meier analysis and Cox proportional hazard models. The associations were further delineated by Kaplan-Meier analysis using publicly available mRNA expression data. Our results show that nuclear HSF1 levels were elevated in similar to 80% of in situ and invasive breast carcinomas. In invasive carcinomas, HSF1 expression was associated with high histologic grade, larger tumor size, and nodal involvement at diagnosis (P < 0.0001). By using multivariate analysis to account for the effects of covariates, high HSF1 levels were found to be independently associated with increased mortality (hazards ratio: 1.62; 95% confidence interval: 1.21-2.17; P < 0.0013). This association was seen in the estrogen receptor (ER)-positive population (hazards ratio: 2.10; 95% confidence interval: 1.45-3.03; P < 0.0001). In public expression profiling data, high HSF1 mRNA levels were also associated with an increase in ER-positive breast cancer-specific mortality. We conclude that increased HSF1 is associated with reduced breast cancer survival. The findings indicate that HSF1 should be evaluated prospectively as an independent prognostic indicator in ER-positive breast cancer. HSF1 may ultimately be a useful therapeutic target in cancer.
C1 [Hu, Rong; Hankinson, Susan E.; Tamimi, Rulla M.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Santagata, Sandro; Hu, Rong; Collins, Laura C.; Hankinson, Susan E.; Schnitt, Stuart J.; Tamimi, Rulla M.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Santagata, Sandro; Mendillo, Marc L.; Whitesell, Luke; Lindquist, Susan] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA.
[Santagata, Sandro] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Hu, Rong; Hankinson, Susan E.; Tamimi, Rulla M.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Lin, Nancy U.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Collins, Laura C.; Schnitt, Stuart J.] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02115 USA.
[Lindquist, Susan] MIT, Howard Hughes Med Inst, Dept Biol, Cambridge, MA 02139 USA.
[Ince, Tan A.] Univ Miami, Sch Med, Interdisciplinary Stem Cell Inst, Miami, FL 33136 USA.
[Ince, Tan A.] Univ Miami, Sch Med, Braman Family Breast Canc Inst, Dept Pathol, Miami, FL 33136 USA.
RP Tamimi, RM (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, 665 Huntington Ave, Boston, MA 02115 USA.
EM nhrmt@channing.harvard.edu; lindquist_admin@wi.mit.edu;
tince@med.miami.edu
FU Breast Cancer Research Foundation (New York, NY); National Cancer
Institute [R01-CA146445-01, CA089393]; Department of Defense
[W81XWH-08-1-0282 BC-07456]; Public Health Service [CA087969];
Department of Health and Human Services; GlaxoSmithKline [WE234,
EPI40307]; Susan G. Komen Breast Cancer Foundation; Howard Hughes
Medical Institute; American Cancer Society New England Division
[PF-09-253-01-DMC]; National Institutes of Health [K08NS064168]; Marble
Foundation; V Foundation for Cancer Research
FX We thank the participants and staff of the NHS cohort for their valuable
contributions. We thank the following state cancer registries for their
help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME,
MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA,
WA, and WY. We thank Terri Woo for expert assistance with IHC. We
acknowledge grants from the Breast Cancer Research Foundation (New York,
NY), National Cancer Institute Grant R01-CA146445-01, and Department of
Defense Congressionally Directed Medical Research Program Breast Cancer
Research Program Grant W81XWH-08-1-0282 BC-07456 (to T.A.I.); Public
Health Service Grant CA087969 (to S.E.H.); National Cancer Institute
Specialized Program of Research Excellence (SPORE) in Breast Cancer
Grant CA089393 (to Dirk Iglehart, Dana-Farber Cancer Institute); funds
from the Department of Health and Human Services and GlaxoSmithKline
Grant WE234, EPI40307 (to R.M.T.); grants from the Susan G. Komen Breast
Cancer Foundation (to L.W. and N.U.L.); funding from the Howard Hughes
Medical Institute (to S.L.); American Cancer Society New England
Division-SpinOdyssey Postdoctoral Fellowship PF-09-253-01-DMC (to
M.L.M.); and National Institutes of Health Grant K08NS064168 and funds
from the Marble Foundation and the V Foundation for Cancer Research (to
S.S.).
NR 42
TC 94
Z9 96
U1 1
U2 12
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 8
PY 2011
VL 108
IS 45
BP 18378
EP 18383
DI 10.1073/pnas.1115031108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 843UT
UT WOS:000296700000047
PM 22042860
ER
PT J
AU Rustagi, T
Mashimo, H
AF Rustagi, Tarun
Mashimo, Hiroshi
TI Endoscopic management of chronic radiation proctitis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Chronic; Radiation proctitis; Endoscopic; Argon plasma coagulation;
Radiofrequency; Cryoablation
ID ARGON PLASMA COAGULATION; ND-YAG LASER; TERM-FOLLOW-UP; RADIOFREQUENCY
ABLATION; DOUBLE-BLIND; BIPOLAR ELECTROCOAGULATION; INDUCED
PROCTOSIGMOIDITIS; THERAPY; PROCTOPATHY; INJURY
AB Chronic radiation proctopathy occurs in 5%-20% of patients following pelvic radiotherapy. Although many cases resolve spontaneously, some lead to chronic symptoms including diarrhea, tenesmus, urgency and persistent rectal bleeding with iron deficiency anemia requiring blood transfusions. Treatments for chronic radiation proctitis remain unsatisfactory and the basis of evidence for various therapies is generally insufficient. There are very few controlled or prospective trials, and comparisons between therapies are limited because of different evaluation methods. Medical treatments, including formalin, topical sucralfate, 5-amino salicylic acid enemas, and short chain fatty acids have been used with limited success. Surgical management is associated with high morbidity and mortality. Endoscopic therapy using modalities such as the heater probe, neodymium: yttrium-aluminium-garnet laser, potassium titanyl phosphate laser and bipolar electrocoagulation has been reported to be of some benefit, but with frequent complications. Argon plasma coagulation is touted to be the preferred endoscopic therapy due to its efficacy and safety profile. Newer methods of endoscopic ablation such as radiofrequency ablation and cryotherapy have been recently described which may afford broader areas of treatment per application, with lower rate of complications. This review will focus on endoscopic ablation therapies, including such newer modalities, for chronic radiation proctitis. (C) 2011 Baishideng. All rights reserved.
C1 [Mashimo, Hiroshi] Harvard Univ, Sch Med, Brigham & Womens Hosp, VA Boston Healthcare Syst,Gastroenterol Sect 111, Boston, MA 02130 USA.
[Rustagi, Tarun] Univ Connecticut, Dept Internal Med, Farmington, CT 06030 USA.
RP Mashimo, H (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, VA Boston Healthcare Syst,Gastroenterol Sect 111, 150 S Huntington Ave, Boston, MA 02130 USA.
EM hmashimo@hms.harvard.edu
NR 85
TC 25
Z9 27
U1 0
U2 0
PU BAISHIDENG PUBL GRP CO LTD
PI BEIJING
PA RM 903, BLDG D, OCEAN INTERNATIONAL CTR, NO 62 DONGSIHUAN ZHONGLU,
BEIJING, CHAOYANG DISTRICT 100025, PEOPLES R CHINA
SN 1007-9327
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 7
PY 2011
VL 17
IS 41
BP 4554
EP 4562
DI 10.3748/wjg.v17.i41.4554
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 861ER
UT WOS:000298002500002
PM 22147960
ER
PT J
AU Rugge, M
Fassan, M
Pizzi, M
Farinati, F
Sturniolo, GC
Plebani, M
Graham, DY
AF Rugge, Massimo
Fassan, Matteo
Pizzi, Marco
Farinati, Fabio
Sturniolo, Giacomo Carlo
Plebani, Mario
Graham, David Y.
TI Operative link for gastritis assessment vs operative link on intestinal
metaplasia assessment
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Gastritis; Staging; Atrophic gastritis; Intestinal metaplasia; Operative
link for gastritis assessment; Operative link on intestinal metaplasia
assessment
ID LYMPH-NODE DISSECTION; ASSISTED DISTAL GASTRECTOMY; OPEN SUBTOTAL
GASTRECTOMY; BILLROTH-I GASTRECTOMY; QUALITY-OF-LIFE; CANCER; TRIAL
AB AIM: To compare the reliability of gastritis staging systems in ranking gastritis-associated cancer risk in a large series of consecutive patients.
METHODS: Gastric mucosal atrophy is the precancerous condition in which intestinal-type gastric cancer (GC) most frequently develops. The operative link for gastritis assessment (OLGA) staging system ranks the GC risk according to both the topography and the severity of gastric atrophy (as assessed histologically on the basis of the Sydney protocol for gastric mucosal biopsy). Both cross-sectional and long-term follow-up trials have consistently associated OLGA stages III-IV with a higher risk of GC. A recently-proposed modification of the OLGA staging system (OLGIM) basically incorporates the OLGA frame, but replaces the atrophy score with an assessment of intestinal metaplasia (IM) alone. A series of 4552 consecutive biopsy sets (2007-2009) was retrieved and reassessed according to both the OLGA and the OLGIM staging systems. A set of at least 5 biopsy samples was available for all the cases considered.
RESULTS: In 4460 of 4552 cases (98.0%), both the high-risk stages (III + IV) and the low-risk stages (0 + I + II) were assessed applying the OLGA and OLGIM criteria. Among the 243 OLGA high-risk stages, 14 (5.8%) were down-staged to a low risk using OLGIM. The 67 (1.5%) incidentally-found neoplastic lesions (intraepithelial or invasive) were consistently associated with high-risk stages, as assessed by both OLGA and OLGIM (P < 0.001 for both). Two of 34 intestinal-type GCs coexisting with a high-risk OLGA stage (stage III) were associated with a low-risk OLGIM stage (stage II).
CONCLUSION: Gastritis staging systems (both OLGA and OLGIM) convey prognostically important information on the gastritis-associated cancer risk. Because of its clinical impact, the stage of gastritis should be included as a conclusive message in the gastritis histology report. Since it focuses on IM alone, OLGIM staging is less sensitive than OLGA staging in the identification of patients at high risk of gastric cancer. (C) 2011 Baishideng. All rights reserved.
C1 [Rugge, Massimo] Univ Padua, Surg Pathol & Cytopathol Unit, Dept Med Diagnost Sci & Special Therapies, Ist Oncol Veneto IOV IRCCS, I-35100 Padua, Italy.
[Farinati, Fabio; Sturniolo, Giacomo Carlo] Univ Padua, Dept Gastroenterol & Surg Sci, Gastroenterol Unit, I-35100 Padua, Italy.
[Plebani, Mario] Univ Padua, Dept Diagnost Med Sci & Special Therapies, Clin Chem Unit, I-35100 Padua, Italy.
[Graham, David Y.] Vet Adm Hosp, Baylor Coll Med, Div Digest Dis, Houston, TX 77030 USA.
RP Rugge, M (reprint author), Univ Padua, Surg Pathol & Cytopathol Unit, Dept Med Diagnost Sci & Special Therapies, Ist Oncol Veneto IOV IRCCS, Via Aristide Gabelli 61, I-35100 Padua, Italy.
EM massimo.rugge@unipd.it
RI Fassan, Matteo/F-5152-2012; Rugge, Massimo/K-7525-2016
OI Fassan, Matteo/0000-0001-6515-5482;
FU AIRC from the Veneto Regional Authorities; "Guido Berlucchi" Foundation;
"Morgagni" Association for Oncological Research (Padova; PD)
FX Supported by An AIRC grant from the Veneto Regional Authorities, 2009;
the "Guido Berlucchi" Foundation; and the "Morgagni" Association for
Oncological Research (Padova; PD)
NR 18
TC 26
Z9 27
U1 0
U2 2
PU BAISHIDENG PUBL GRP CO LTD
PI BEIJING
PA RM 903, BLDG D, OCEAN INTERNATIONAL CTR, NO 62 DONGSIHUAN ZHONGLU,
BEIJING, CHAOYANG DISTRICT 100025, PEOPLES R CHINA
SN 1007-9327
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 7
PY 2011
VL 17
IS 41
BP 4596
EP 4606
DI 10.3748/wjg.v17.i41.4596
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 861ER
UT WOS:000298002500007
PM 22147965
ER
PT J
AU McQuaid, D
Bortfeld, T
AF McQuaid, D.
Bortfeld, T.
TI 4D planning over the full course of fractionation: assessment of the
benefit of tumor trailing
SO PHYSICS IN MEDICINE AND BIOLOGY
LA English
DT Article
ID TRACKING SYSTEM; MOTION; RADIOTHERAPY; ERRORS
AB Tumor trailing techniques have been proposed as a method of reducing the problem of intrafraction motion in radiotherapy. However the dosimetric assessment of trailing strategies is complicated by the requirement to study dose deposition over a full fraction delivery. Common 4D planning strategies allowing assessment of dosimetric motion effects study a single cycle acquired with 4DCT. In this paper, a methodology to assess dose deposited over an entire treatment course is advanced and used to assess the potential benefit of tumor trailing strategies for lung cancer patients. Two digital phantoms mimicking patient anatomy were each programmed to follow the tumor respiratory trajectory observed from 33 lung cancer patients. The two phantoms were designed to represent the cases of a small (volume = 13.6 cm(3)) and large (volume = 181.7 cm(3)) lung lesion. Motion margins required to obtain CTV coverage by 95% of the prescription dose to 90% of the available cases were computed for a standard treatment strategy and a trailing treatment strategy. The trailing strategy facilitated a margin reduction of over 30% relative to the conventional delivery. When the dose was computed across the entire delivery for the 33 cases, the trailing strategy was found to significantly reduce the underdosage to the outlier cases and the reduced trailing margin facilitated a 15% (small lesion) and 4% (large lesion) reduction for the mean lung dose and 7% (small lesion) and 10% (large lesion) for the mean esophagus dose. Finally, for comparison an ideal continuous tracking strategy was assessed and found to further reduce the mean lung and esophagus dose. However, this improvement comes at the price of increased delivery complexity and increased reliance on tumor localization accuracy.
C1 [McQuaid, D.; Bortfeld, T.] Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
RP McQuaid, D (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Boston, MA 02114 USA.
EM dualta.mcquaid@icr.ac.uk
FU National Cancer Institute [5R01CA118200-05]
FX This work has been supported by the National Cancer Institute under
grant number 5R01CA118200-05. The authors would like to thank Greg
Sharp, Alex Trofimov, Jan Unkelbach and David Craft for their useful
discussions and Hiroki Shirato and Greg Sharp for their work on the
patient data used in this study.
NR 16
TC 3
Z9 3
U1 0
U2 1
PU IOP PUBLISHING LTD
PI BRISTOL
PA TEMPLE CIRCUS, TEMPLE WAY, BRISTOL BS1 6BE, ENGLAND
SN 0031-9155
J9 PHYS MED BIOL
JI Phys. Med. Biol.
PD NOV 7
PY 2011
VL 56
IS 21
BP 6935
EP 6949
DI 10.1088/0031-9155/56/21/011
PG 15
WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging
SC Engineering; Radiology, Nuclear Medicine & Medical Imaging
GA 842NH
UT WOS:000296605700012
PM 22008696
ER
PT J
AU Sikorski, TW
Ficarro, SB
Holik, J
Kim, T
Rando, OJ
Marto, JA
Buratowski, S
AF Sikorski, Timothy W.
Ficarro, Scott B.
Holik, John
Kim, TaeSoo
Rando, Oliver J.
Marto, Jarrod A.
Buratowski, Stephen
TI Sub1 and RPA Associate with RNA Polymerase II at Different Stages of
Transcription
SO MOLECULAR CELL
LA English
DT Article
ID REPLICATION PROTEIN-A; PC4 COACTIVATOR FUNCTION; MESSENGER-RNA;
SACCHAROMYCES-CEREVISIAE; MULTIPLE FUNCTIONS; PREINITIATION COMPLEX;
GENE-TRANSCRIPTION; BINDING PROTEIN; TERMINAL DOMAIN; DYNAMIC-MODEL
AB Single-stranded DNA-binding proteins play many roles in nucleic acid metabolism, but their importance during transcription remains unclear. Quantitative proteomic analysis of RNA polymerase II (RNApII) preinitiation complexes (PICs) identified Sub1 and the replication protein A complex (RPA), both of which bind single-stranded DNA (ssDNA). Sub1, homolog of mammalian coactivator PC4, exhibits strong genetic interactions with factors necessary for promoter melting. Sub1 localizes near the transcription bubble in vitro and binds to promoters in vivo dependent upon PIC assembly. In contrast, RPA localizes to transcribed regions of active genes, strongly correlated with transcribing RNApII but independently of replication. RFA1 interacts genetically with transcription elongation factor genes. Interestingly, RPA levels increase at active promoters in cells carrying a Sub1 deletion or ssDNA-binding mutant, suggesting competition for a common binding site. We propose that Sub1 and RPA interact with the nontemplate strand of RNApII complexes during initiation and elongation, respectively.
C1 [Sikorski, Timothy W.; Ficarro, Scott B.; Kim, TaeSoo; Marto, Jarrod A.; Buratowski, Stephen] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Sikorski, Timothy W.; Ficarro, Scott B.; Marto, Jarrod A.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Ficarro, Scott B.; Marto, Jarrod A.] Dana Farber Canc Inst, Blais Prote Ctr, Boston, MA 02115 USA.
[Holik, John; Rando, Oliver J.] Univ Massachusetts, Sch Med, Dept Biochem & Mol Pharmacol, Worcester, MA USA.
RP Marto, JA (reprint author), Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
EM jarrod_marto@dfci.harvard.edu; steveb@hms.harvard.edu
FU NIH [GM46498]; Burroughs Wellcome Fund Career Award in the Biomedical
Sciences; NIGMS [GM079205]; DFCI/Blaise Proteomics Center; NDSEG
FX We thank Olga Calvo, Steve Hahn, Richard Kolodner, Michael Hampsey, and
Claire Moore for strains and plasmids; Steven Brill for the Rfa1
antibody; Manor Askenazi and Jignesh Parikh for help with mass
spectrometry and microarray data analysis; and Minkyu Kim, Sebastian
Marquardt, and Nihal Terzi for technical assistance. We also thank Steve
Hahn, Michael Meisterernst, Olga Ca Ivo, Alicia Martinez, Doug Koshland,
and members of the Buratowski and Marto labs for helpful discussions.
This work was supported by NIH grant GM46498 to S.B., a Burroughs
Wellcome Fund Career Award in the Biomedical Sciences and NIGMS grant
GM079205 to O.J.R., DFCI/Blaise Proteomics Center support to J.M., and a
NDSEG predoctoral fellowship to T.S.
NR 75
TC 35
Z9 36
U1 1
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
J9 MOL CELL
JI Mol. Cell
PD NOV 4
PY 2011
VL 44
IS 3
BP 397
EP 409
DI 10.1016/j.molcel.2011.09.013
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 844OE
UT WOS:000296756100008
PM 22055186
ER
PT J
AU Junqueira, JC
Fuchs, BB
Muhammed, M
Coleman, JJ
Suleiman, JMAH
Vilela, SFG
Costa, ACBP
Rasteiro, VMC
Jorge, AOC
Mylonakis, E
AF Junqueira, Juliana C.
Fuchs, Beth B.
Muhammed, Maged
Coleman, Jeffrey J.
Suleiman, Jamal M. A. H.
Vilela, Simone F. G.
Costa, Anna C. B. P.
Rasteiro, Vanessa M. C.
Jorge, Antonio O. C.
Mylonakis, Eleftherios
TI Oral Candida albicans isolates from HIV-positive individuals have
similar in vitro biofilm-forming ability and pathogenicity as invasive
Candida isolates
SO BMC MICROBIOLOGY
LA English
DT Article
ID GALLERIA-MELLONELLA LARVAE; FUNGAL PATHOGENESIS; MODEL HOST; INFECTION;
VIRULENCE; DUBLINIENSIS; COLONIZATION; SUSCEPTIBILITY; EXPRESSION;
RESISTANCE
AB Background: Candida can cause mucocutaneous and/or systemic infections in hospitalized and immunosuppressed patients. Most individuals are colonized by Candida spp. as part of the oral flora and the intestinal tract. We compared oral and systemic isolates for the capacity to form biofilm in an in vitro biofilm model and pathogenicity in the Galleria mellonella infection model. The oral Candida strains were isolated from the HIV patients and included species of C. albicans, C. glabrata, C. tropicalis, C. parapsilosis, C. krusei, C. norvegensis, and C. dubliniensis. The systemic strains were isolated from patients with invasive candidiasis and included species of C. albicans, C. glabrata, C. tropicalis, C. parapsilosis, C. lusitaniae, and C. kefyr. For each of the acquired strains, biofilm formation was evaluated on standardized samples of silicone pads and acrylic resin. We assessed the pathogenicity of the strains by infecting G. mellonella animals with Candida strains and observing survival.
Results: The biofilm formation and pathogenicity in Galleria was similar between oral and systemic isolates. The quantity of biofilm formed and the virulence in G. mellonella were different for each of the species studied. On silicone pads, C. albicans and C. dubliniensis produced more biofilm (1.12 to 6.61 mg) than the other species (0.25 to 3.66 mg). However, all Candida species produced a similar biofilm on acrylic resin, material used in dental prostheses. C. albicans, C. dubliniensis, C. tropicalis, and C. parapsilosis were the most virulent species in G. mellonella with 100% of mortality, followed by C. lusitaniae (87%), C. novergensis (37%), C. krusei (25%), C. glabrata (20%), and C. kefyr (12%).
Conclusions: We found that on silicone pads as well as in the Galleria model, biofilm formation and virulence depends on the Candida species. Importantly, for C. albicans the pathogenicity of oral Candida isolates was similar to systemic Candida isolates, suggesting that Candida isolates have similar biofilm-forming ability and virulence regardless of the infection site from which it was isolated.
C1 [Junqueira, Juliana C.; Vilela, Simone F. G.; Costa, Anna C. B. P.; Rasteiro, Vanessa M. C.; Jorge, Antonio O. C.] Univ Estadual Paulista UNESP, Dept Biosci & Oral Diag, BR-12245000 Sao Jose Dos Campos, SP, Brazil.
[Fuchs, Beth B.; Muhammed, Maged; Coleman, Jeffrey J.; Mylonakis, Eleftherios] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Suleiman, Jamal M. A. H.] Emilio Ribas Inst Infectol, BR-01246900 Sao Paulo, Brazil.
RP Junqueira, JC (reprint author), Univ Estadual Paulista UNESP, Dept Biosci & Oral Diag, 777 Av Eng Francisco Jose Longo, BR-12245000 Sao Jose Dos Campos, SP, Brazil.
EM juliana@fosjc.unesp.br
RI Junqueira, Juliana/F-7785-2012; vilela, simone/B-8728-2014; Coleman,
Jeffrey/E-2981-2015;
OI Coleman, Jeffrey/0000-0001-8579-1996
FU Sao Paulo Council of Research - FAPESP, Brazil [09/52283-0]; Univ
Estadual Paulista - PROPG/UNESP
FX This study was supported by the Sao Paulo Council of Research - FAPESP,
Brazil (Grant no 09/52283-0) and Univ Estadual Paulista -
PROPG/UNESP.
NR 43
TC 24
Z9 25
U1 0
U2 14
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2180
J9 BMC MICROBIOL
JI BMC Microbiol.
PD NOV 4
PY 2011
VL 11
AR 247
DI 10.1186/1471-2180-11-247
PG 9
WC Microbiology
SC Microbiology
GA 848MQ
UT WOS:000297056100001
PM 22053894
ER
PT J
AU Rapley, J
Oshiro, N
Ortiz-Vega, S
Avruch, J
AF Rapley, Joseph
Oshiro, Noriko
Ortiz-Vega, Sara
Avruch, Joseph
TI The Mechanism of Insulin-stimulated 4E-BP Protein Binding to Mammalian
Target of Rapamycin (mTOR) Complex 1 and Its Contribution to mTOR
Complex 1 Signaling
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RICH AKT SUBSTRATE; AMINO-ACID SUFFICIENCY; P70 S6 KINASE; 40 KDA
PRAS40; CELL-GROWTH; DISTINCT ROLES; RAG GTPASES; TOS MOTIF; IN-VITRO;
RAPTOR
AB Insulin activation of mTOR complex 1 is accompanied by enhanced binding of substrates. We examined the mechanism and contribution of this enhancement to insulin activation of mTORC1 signaling in 293E and HeLa cells. In 293E, insulin increased the amount of mTORC1 retrieved by the transiently expressed nonphosphorylatable 4E-BP[5A] to an extent that varied inversely with the amount of PRAS40 bound to mTORC1. RNAi depletion of PRAS40 enhanced 4E-BP[5A] binding to similar to 70% the extent of maximal insulin, and PRAS40 RNAi and insulin together did not increase 4E-BP[5A] binding beyond insulin alone, suggesting that removal of PRAS40 from mTORC1 is the predominant mechanism of an insulin-induced increase in substrate access. As regards the role of increased substrate access in mTORC1 signaling, RNAi depletion of PRAS40, although increasing 4E-BP[5A] binding, did not stimulate phosphorylation of endogenous mTORC1 substrates S6K1(Thr(389)) or 4E-BP (Thr(37)/Thr(46)), the latter already similar to 70% of maximal in amino acid replete, serum-deprived 293E cells. In HeLa cells, insulin and PRAS40 RNAi also both enhanced the binding of 4E-BP[5A] to raptor but only insulin stimulated S6K1 and 4E-BP phosphorylation. Furthermore, Rheb overexpression in 293E activated mTORC1 signaling completely without causing PRAS40 release. In the presence of Rheb and insulin, PRAS40 release is abolished by Akt inhibition without diminishing mTORC1 signaling. In conclusion, dissociation of PRAS40 from mTORC1 and enhanced mTORC1 substrate binding results from Akt and mTORC1 activation and makes little or no contribution to mTORC1 signaling, which rather is determined by Rheb activation of mTOR catalytic activity, through mechanisms that remain to be fully elucidated.
C1 [Avruch, Joseph] Massachusetts Gen Hosp, Diabet Res Lab, Dept Mol Biol, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Diabet Unit, Med Serv, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Dept Med, Boston, MA 02114 USA.
RP Avruch, J (reprint author), Massachusetts Gen Hosp, Diabet Res Lab, Dept Mol Biol, Simches Res Bldg 6408,185 Cambridge St, Boston, MA 02114 USA.
EM avruch@molbio.mgh.harvard.edu
FU National Institutes of Health [DK17776, CA73818]
FX This work was supported, in whole or in part, by National Institutes of
Health Grants DK17776 and CA73818.
NR 42
TC 19
Z9 20
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 4
PY 2011
VL 286
IS 44
BP 38043
EP 38053
DI 10.1074/jbc.M111.245449
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 842JD
UT WOS:000296594200016
PM 21914810
ER
PT J
AU Liu, Z
Turan, S
Wehbi, VL
Vilardaga, JP
Bastepe, M
AF Liu, Zun
Turan, Serap
Wehbi, Vanessa L.
Vilardaga, Jean-Pierre
Bastepe, Murat
TI Extra-long G alpha s Variant XL alpha s Protein Escapes
Activation-induced Subcellular Redistribution and Is Able to Provide
Sustained Signaling
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID STIMULATORY G-PROTEIN; MCCUNE-ALBRIGHT-SYNDROME; GNAS1 T393C
POLYMORPHISM; PARATHYROID-HORMONE RECEPTOR; COUPLED RECEPTORS;
ADENYLYL-CYCLASE; CELL CARCINOMA; FREE SURVIVAL; GENE VARIANT; SUBUNIT
AB Murine models indicate that G alpha s and its extra-long variant XL alpha s, both of which are derived from GNAS, markedly differ regarding their cellular actions, but these differences are unknown. Here we investigated activation-induced trafficking of G alpha s and XL alpha s, using immunofluorescence microscopy, cell fractionation, and total internal reflection fluorescence microscopy. In transfected cells, XL alpha s remained localized to the plasma membrane, whereas G alpha s redistributed to the cytosol after activation by GTPase-inhibiting mutations, cholera toxin treatment, or G protein-coupled receptor agonists (isoproterenol or parathyroid hormone (PTH)(1-34)). Cholera toxin treatment or agonist (isoproterenol or pituitary adenylate cyclase activating peptide-27) stimulation of PC12 cells expressing G alpha s and XL alpha s endogenously led to an increased abundance of G alpha s, but not XL alpha s, in the soluble fraction. Mutational analyses revealed two conserved cysteines and the highly charged domain as being critically involved in the plasma membrane anchoring of XL alpha s. The cAMP response induced by M-PTH(1-14), a parathyroid hormone analog, terminated quickly in HEK293 cells stably expressing the type 1 PTH/PTH-related peptide receptor, whereas the response remained maximal for at least 6 min in cells that co-expressed the PTH receptor and XL alpha s. Although isoproterenol-induced cAMP response was not prolonged by XL alpha s expression, a GTPase-deficient XL alpha s mutant found in certain tumors and patients with fibrous dysplasia of bone and McCune-Albright syndrome generated more basal cAMP accumulation in HEK293 cells and caused more severe impairment of osteoblastic differentiation of MC3T3-E1 cells than the cognate G alpha s mutant (gsp oncogene). Thus, activated XL alpha s and G alpha s traffic differently, and this may form the basis for the differences in their cellular actions.
C1 [Liu, Zun; Turan, Serap; Vilardaga, Jean-Pierre; Bastepe, Murat] Massachusetts Gen Hosp, Endocrine Unit, Dept Med, Boston, MA 02114 USA.
[Liu, Zun; Turan, Serap; Vilardaga, Jean-Pierre; Bastepe, Murat] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Turan, Serap] Marmara Univ, Sch Med Hosp, TR-34662 Istanbul, Turkey.
[Wehbi, Vanessa L.; Vilardaga, Jean-Pierre] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Lab Protein Coupled Receptor Biol G, Pittsburgh, PA 15213 USA.
RP Bastepe, M (reprint author), Massachusetts Gen Hosp, Endocrine Unit, Dept Med, 50 Blossom St Thier 10, Boston, MA 02114 USA.
EM bastepe@helix.mgh.harvard.edu
FU National Institutes of Health from NIDDK [R01DK073911, R01DK087688];
March of Dimes Foundation [6-FY10-336]; European Society for Paediatric
Endocrinology through Lilly, LLC.
FX This work was supported, in whole or in part, by National Institutes of
Health Grants R01DK073911 (to M. B.) and R01DK087688 (to J.-P. V.) from
NIDDK. This work was also supported in part by March of Dimes Foundation
Research Grant 6-FY10-336 (to M. B.).; Supported by a grant of the
Sabbatical Leave Programme from the European Society for Paediatric
Endocrinology through an educational grant from Lilly, LLC.
NR 69
TC 9
Z9 9
U1 0
U2 1
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 4
PY 2011
VL 286
IS 44
BP 38558
EP 38569
DI 10.1074/jbc.M111.240150
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 842JD
UT WOS:000296594200069
PM 21890629
ER
PT J
AU Lee, E
Kamlet, AS
Powers, DC
Neumann, CN
Boursalian, GB
Furuya, T
Choi, DC
Hooker, JM
Ritter, T
AF Lee, Eunsung
Kamlet, Adam S.
Powers, David C.
Neumann, Constanze N.
Boursalian, Gregory B.
Furuya, Takeru
Choi, Daniel C.
Hooker, Jacob M.
Ritter, Tobias
TI A Fluoride-Derived Electrophilic Late-Stage Fluorination Reagent for PET
Imaging
SO SCIENCE
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; REDUCTIVE ELIMINATION; RADIOSYNTHESIS;
F-18
AB The unnatural isotope fluorine-18 (F-18) is used as a positron emitter in molecular imaging. Currently, many potentially useful F-18-labeled probe molecules are inaccessible for imaging because no fluorination chemistry is available to make them. The 110-minute half-life of F-18 requires rapid syntheses for which [F-18]fluoride is the preferred source of fluorine because of its practical access and suitable isotope enrichment. However, conventional [F-18]fluoride chemistry has been limited to nucleophilic fluorination reactions. We report the development of a palladium-based electrophilic fluorination reagent derived from fluoride and its application to the synthesis of aromatic F-18-labeled molecules via late-stage fluorination. Late-stage fluorination enables the synthesis of conventionally unavailable positron emission tomography (PET) tracers for anticipated applications in pharmaceutical development as well as preclinical and clinical PET imaging.
C1 [Hooker, Jacob M.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Lee, Eunsung; Kamlet, Adam S.; Powers, David C.; Neumann, Constanze N.; Boursalian, Gregory B.; Furuya, Takeru; Choi, Daniel C.; Ritter, Tobias] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA.
[Hooker, Jacob M.] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Hooker, Jacob M.; Ritter, Tobias] Massachusetts Gen Hosp, Dept Radiol, Div Nucl Med & Mol Imaging, Boston, MA 02114 USA.
RP Hooker, JM (reprint author), Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
EM hooker@nmr.mgh.harvard.edu; ritter@chemistry.harvard.edu
RI Furuya, Takeru/A-6622-2012; Ritter, Tobias/A-6244-2013; Lee,
Eunsung/F-5308-2013; Powers, David/J-8203-2015; Boursalian,
Gregory/M-7729-2016;
OI Ritter, Tobias/0000-0002-5478-0036; Powers, David/0000-0003-3717-2001;
Boursalian, Gregory/0000-0002-6644-0987; Hooker,
Jacob/0000-0002-9394-7708
FU National Institute of General Medical Sciences [GM088237]; National
Institute of Biomedical Imaging and Bioengineering [EB013042]; National
Center for Research Resources [1S10RR017208-01A1]; National Institute on
Drug Abuse [5P30DA028800-02]; Richard and Susan Smith Family Foundation;
Massachusetts Life Science Center; Harvard Catalyst; NSF [DGE0644491];
Harvard Accelerator Fund; Sloan Research Fellowship; Eli Lilly and Co.;
AstraZeneca; Camille Dreyfus; Amgen
FX Supported by National Institute of General Medical Sciences grant
GM088237, National Institute of Biomedical Imaging and Bioengineering
grant EB013042, National Center for Research Resources grant
1S10RR017208-01A1, National Institute on Drug Abuse grant
5P30DA028800-02, the Richard and Susan Smith Family Foundation, the
Massachusetts Life Science Center, the Harvard Catalyst, NSF Graduate
Research Fellowship Program grant DGE0644491, and the Harvard
Accelerator Fund. T.R. was also supported by a Sloan Research
Fellowship, grants from Eli Lilly and Co. and AstraZeneca, a Camille
Dreyfus Teacher-Scholar Award, and an Amgen Young Investigators Award.
We thank S.-L. Zheng for x-ray crystallographic analysis. DFT
computation was performed using the computer facilities at the Odyssey
cluster at Harvard University. Metrical parameters for the crystal
structures of compounds 1, 2, 3, 8, and S10 are available free of charge
from the Cambridge Crystallographic Data Centre under reference nos.
CCDC 829427, 829428, 840744, 829429, and 839058, respectively. A patent
application has been filed through Harvard on methods and reagents
presented in this manuscript.
NR 29
TC 187
Z9 187
U1 10
U2 133
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 4
PY 2011
VL 334
IS 6056
BP 639
EP 642
DI 10.1126/science.1212625
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 841EG
UT WOS:000296494700046
PM 22053044
ER
PT J
AU Jacobson, CA
Ritz, J
AF Jacobson, Caron A.
Ritz, Jerome
TI Time to put the CAR-T before the horse
SO BLOOD
LA English
DT Editorial Material
ID DOMAINS
C1 [Jacobson, Caron A.; Ritz, Jerome] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Jacobson, CA (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA.
OI Ritz, Jerome/0000-0001-5526-4669
FU NCI NIH HHS [P01 CA142106, T32 CA009172]
NR 6
TC 2
Z9 2
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 3
PY 2011
VL 118
IS 18
BP 4761
EP 4762
PG 2
WC Hematology
SC Hematology
GA 843YS
UT WOS:000296714500001
PM 22053170
ER
PT J
AU Kawano, Y
Kim, HT
Matsuoka, K
Bascug, G
McDonough, S
Ho, VT
Cutler, C
Koreth, J
Alyea, EP
Antin, JH
Soiffer, RJ
Ritz, J
AF Kawano, Yutaka
Kim, Haesook T.
Matsuoka, Ken-ichi
Bascug, Gregory
McDonough, Sean
Ho, Vincent T.
Cutler, Corey
Koreth, John
Alyea, Edwin P.
Antin, Joseph H.
Soiffer, Robert J.
Ritz, Jerome
TI Low telomerase activity in CD4(+) regulatory T cells in patients with
severe chronic GVHD after hematopoietic stem cell transplantation
SO BLOOD
LA English
DT Article
ID VERSUS-HOST-DISEASE; CHROMOSOME INSTABILITY; INDUCED APOPTOSIS; GRAFT;
HTERT; ACTIVATION; CANCER; LENGTH; RISK; DYSFUNCTION
AB CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) play an important role in the control of chronic graft-versus-host disease (cGVHD). In this study, we examined telomere length and telomerase activity of Treg and conventional CD4(+) T cells (Tcon) in 61 patients who survived more than 2 years after allogeneic hematopoietic stem cell transplantation. Cell proliferation and expression of Bcl-2 were also measured in each subset. Treg telomere length was shorter and Treg telomerase activity was increased compared with Tcon (P < .0001). After transplantation, Treg were also more highly proliferative than Tcon (P < .0001). Treg number, telomerase activity, and expression of Bcl-2 were each inversely associated with severity of cGVHD. These data indicate that activation of telomerase is not sufficient to prevent telomere shortening in highly proliferative Treg. However, telomerase activation is associated with increased Bcl-2 expression and higher Treg numbers in patients with no or mild cGVHD. In contrast, patients with moderate or severe cGVHD have fewer Treg with lower levels of telomerase activity and Bcl-2 expression. These results suggest that failure to activate Treg telomerase may restrict proliferative capacity and increase apoptotic susceptibility, resulting in the loss of peripheral tolerance and the development of cGVHD. (Blood. 2011; 118(18):5021-5030)
C1 [Kawano, Yutaka; Matsuoka, Ken-ichi; Bascug, Gregory; McDonough, Sean; Ho, Vincent T.; Cutler, Corey; Koreth, John; Alyea, Edwin P.; Antin, Joseph H.; Soiffer, Robert J.; Ritz, Jerome] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
[Kawano, Yutaka; Matsuoka, Ken-ichi; Bascug, Gregory; McDonough, Sean; Ho, Vincent T.; Cutler, Corey; Koreth, John; Alyea, Edwin P.; Antin, Joseph H.; Soiffer, Robert J.; Ritz, Jerome] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA USA.
[Kawano, Yutaka; Matsuoka, Ken-ichi; Ho, Vincent T.; Cutler, Corey; Koreth, John; Alyea, Edwin P.; Antin, Joseph H.; Soiffer, Robert J.; Ritz, Jerome] Harvard Univ, Sch Med, Boston, MA USA.
[Kim, Haesook T.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA USA.
[Kim, Haesook T.; Ritz, Jerome] Dana Farber Canc Inst, Canc Vaccine Ctr, Boston, MA USA.
[Kim, Haesook T.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Ritz, Jerome] Harvard Stem Cell Inst, Boston, MA USA.
RP Ritz, J (reprint author), Dana Farber Canc Inst, Div Hematol Malignancies, 450 Brookline Ave, Boston, MA 02115 USA.
EM jerome_ritz@dfci.harvard.edu
OI Ritz, Jerome/0000-0001-5526-4669
FU National Institutes of Health [AI29530, CA142106]; Jock and Bunny Adams
Education and Research Endowment; Ted and Eileen Pasquarello Research
Fund
FX This work was supported by the National Institutes of Health (grants
AI29530 and CA142106), the Jock and Bunny Adams Education and Research
Endowment, and the Ted and Eileen Pasquarello Research Fund.
NR 43
TC 18
Z9 19
U1 0
U2 5
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 3
PY 2011
VL 118
IS 18
BP 5021
EP 5030
DI 10.1182/blood-2011-06-362137
PG 10
WC Hematology
SC Hematology
GA 843YS
UT WOS:000296714500033
PM 21900196
ER
PT J
AU Lee, AI
Koo, S
Vaidya, A
Katz, JT
Loscalzo, J
AF Lee, Alfred Ian
Koo, Sophia
Vaidya, Anand
Katz, Joel T.
Loscalzo, Joseph
TI A Bird's-Eye View of Fever
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID HISTOPLASMA-CAPSULATUM; ENDOPHTHALMITIS; MYCOSES; UPDATE; TISSUE
C1 [Lee, Alfred Ian; Koo, Sophia; Vaidya, Anand; Katz, Joel T.; Loscalzo, Joseph] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med, Boston, MA USA.
[Lee, Alfred Ian] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Katz, JT (reprint author), 75 Francis St, Boston, MA 02115 USA.
EM jkatz@partners.org
OI Koo, Sophia/0000-0002-4973-7439
NR 14
TC 0
Z9 0
U1 0
U2 2
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 3
PY 2011
VL 365
IS 18
BP 1727
EP 1732
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA 840FL
UT WOS:000296424200013
PM 22047564
ER
PT J
AU Yoon, TJ
Lee, H
Shao, HL
Hilderbrand, SA
Weissleder, R
AF Yoon, Tae-Jong
Lee, Hakho
Shao, Huilin
Hilderbrand, Scott A.
Weissleder, Ralph
TI Multicore Assemblies Potentiate Magnetic Properties of Biomagnetic
Nanoparticles
SO ADVANCED MATERIALS
LA English
DT Article
ID CORE-SHELL NANOPARTICLES; ULTRASENSITIVE DETECTION; DRUG-DELIVERY;
RESONANCE; SPHERES; CELLS; MRI; SEPARATION; THERAPY; CANCER
AB Highly potent magnetic nanomaterials are developed by encasing multiple magnetic cores inside a thin silica shell, in much the same way as the pomegranate fruit contains many seeds within a thin skin. This construct not only produces materials that are biocompatible but also ones that reach theoretically maximum transverse relaxivity.
C1 [Yoon, Tae-Jong; Lee, Hakho; Shao, Huilin; Hilderbrand, Scott A.; Weissleder, Ralph] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Yoon, Tae-Jong] CHA Univ, Dept Appl Biosci, Seoul 135081, South Korea.
[Weissleder, Ralph] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
RP Lee, H (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Syst Biol, 185 Cambridge St, Boston, MA 02114 USA.
EM hlee@mgh.harvard.edu; rweissleder@mgh.harvard.edu
FU National Institute of Health [R01-EB0044626, R01-EB010011, P50CA86355];
CCNE [U54CA151884]; TPEN [HHSN268201000044C]
FX T.J.Y. and H. L. contributed equally to this work. The authors thank: C.
Ross (MIT) for his generous support in performing magnetic measurements;
P. Waterman, J. Donahoe, G. Wojtkiewicz, J. Figueiredo, J. Chen, and M.
Nahrendorf for assistance in MRI and FMT; N. Sergeyev for synthesizing
CLIO; and Y. Fisher-Jeffes for reviewing the manuscript. This work was
supported in part by National Institute of Health Grants R01-EB0044626,
R01-EB010011, P50 grant P50CA86355, CCNE contract U54CA151884, and TPEN
contract HHSN268201000044C.
NR 35
TC 52
Z9 52
U1 5
U2 54
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0935-9648
J9 ADV MATER
JI Adv. Mater.
PD NOV 2
PY 2011
VL 23
IS 41
BP 4793
EP +
DI 10.1002/adma.201102948
PG 6
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary; Physics, Applied;
Physics, Condensed Matter
SC Chemistry; Science & Technology - Other Topics; Materials Science;
Physics
GA 848HD
UT WOS:000297041600007
PM 21953810
ER
PT J
AU Banks, AS
Kim-Muller, JY
Mastracci, TL
Kofler, NM
Qiang, L
Haeusler, RA
Jurczak, MJ
Laznik, D
Heinrich, G
Samuel, VT
Shulman, GI
Papaioannou, VE
Accili, D
AF Banks, Alexander S.
Kim-Muller, Ja Young
Mastracci, Teresa L.
Kofler, Natalie M.
Qiang, Li
Haeusler, Rebecca A.
Jurczak, Michael J.
Laznik, Dina
Heinrich, Garrett
Samuel, Varman T.
Shulman, Gerald I.
Papaioannou, Virginia E.
Accili, Domenico
TI Dissociation of the Glucose and Lipid Regulatory Functions of FoxO1 by
Targeted Knockin of Acetylation-Defective Alleles in Mice
SO CELL METABOLISM
LA English
DT Article
ID TRANSCRIPTION FACTOR FOXO1; HEPATIC INSULIN-RESISTANCE; ACTIVATED
RECEPTOR-GAMMA; FORKHEAD PROTEIN FOXO1; CAENORHABDITIS-ELEGANS;
DEPENDENT REGULATION; FOOD-INTAKE; GENE; DIFFERENTIATION; LIVER
AB FoxO1 integrates multiple metabolic pathways. Nutrient levels modulate FoxO1 acetylation, but the functional consequences of this posttranslational modification are unclear. To answer this question, we generated mice bearing alleles that encode constitutively acetylated and acetylation-defective FoxO1 proteins. Homozygosity for an allele mimicking constitutive acetylation (Foxo1(KQ/KQ)) results in embryonic lethality due to cardiac and angiogenesis defects. In contrast, mice homozygous for a constitutively deacetylated Foxo1 allele (Foxo1(KR/KR)) display a unique metabolic phenotype of impaired insulin action on hepatic glucose metabolism but decreased plasma lipid levels and low respiratory quotient that are consistent with a state of preferential lipid usage. Moreover, Foxo1KR/KR mice show a dissociation between weight gain and insulin resistance in predisposing conditions (high fat diet, diabetes, and insulin receptor mutations), possibly due to decreased cytokine production in adipose tissue. Thus, acetylation inactivates FoxO1 during nutrient excess whereas deacetylation selectively potentiates FoxO1 activity, protecting against excessive catabolism during nutrient deprivation.
C1 [Banks, Alexander S.; Kim-Muller, Ja Young; Kofler, Natalie M.; Qiang, Li; Haeusler, Rebecca A.; Heinrich, Garrett; Accili, Domenico] Columbia Univ, Dept Med, New York, NY 10032 USA.
[Mastracci, Teresa L.; Papaioannou, Virginia E.] Columbia Univ, Dept Genet & Dev, Coll Phys & Surg, New York, NY 10032 USA.
[Banks, Alexander S.; Laznik, Dina] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Laznik, Dina] Dana Farber Canc Inst, Dept Cell Biol, Boston, MA 02115 USA.
[Laznik, Dina] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Jurczak, Michael J.; Samuel, Varman T.; Shulman, Gerald I.] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06510 USA.
[Jurczak, Michael J.; Samuel, Varman T.; Shulman, Gerald I.] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA.
[Jurczak, Michael J.; Samuel, Varman T.; Shulman, Gerald I.] Yale Univ, Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06510 USA.
RP Accili, D (reprint author), Columbia Univ, Dept Med, New York, NY 10032 USA.
EM da230@columbia.edu
RI Qiang, Li/C-9560-2012; Banks, Alexander/B-4832-2012; Mastracci,
Teresa/C-4565-2013;
OI Banks, Alexander/0000-0003-1787-6925; Jurczak,
Michael/0000-0002-6335-6915
FU NIH [DK079496, DK057539, HL087123]; NIH, Columbia University Diabetes &
Endocrinology Research Center [DK63608]; NIH, Yale Mouse Metabolic
Phenotyping Center [DK059635]
FX Supported by NIH grants DK079496 (to A.S.B.), DK057539 and HL087123 (to
D.A.), DK63608 (Columbia University Diabetes & Endocrinology Research
Center) and DK059635 (Yale Mouse Metabolic Phenotyping Center). We thank
members of the Accili laboratory for helpful discussions of the data and
critical reading of the manuscript, Dr. Thomas Ludwig for the gift of
the DT-A plasmid, Dr. Lori Sussel for making her laboratory available
for embryo analysis, and Dr. Bruce Spiegelman for guidance and support.
NR 55
TC 32
Z9 33
U1 0
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
J9 CELL METAB
JI Cell Metab.
PD NOV 2
PY 2011
VL 14
IS 5
BP 587
EP 597
DI 10.1016/j.cmet.2011.09.012
PG 11
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 849RG
UT WOS:000297142200005
PM 22055502
ER
PT J
AU Kramer, MA
Eden, UT
Lepage, KQ
Kolaczyk, ED
Bianchi, MT
Cash, SS
AF Kramer, Mark A.
Eden, Uri T.
Lepage, Kyle Q.
Kolaczyk, Eric D.
Bianchi, Matt T.
Cash, Sydney S.
TI Emergence of Persistent Networks in Long-Term Intracranial EEG
Recordings
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID GRAPH-THEORETICAL ANALYSIS; COMPLEX BRAIN NETWORKS; STATE FUNCTIONAL
CONNECTIVITY; POSITRON-EMISSION-TOMOGRAPHY; SMALL-WORLD;
CEREBRAL-CORTEX; DEFAULT MODE; MEASURING SYNCHRONIZATION; GAMMA
OSCILLATIONS; CORTICAL NETWORKS
AB Over the past two decades, the increased ability to analyze network relationships among neural structures has provided novel insights into brain function. Most network approaches, however, focus on static representations of the brain's physical or statistical connectivity. Few studies have examined how brain functional networks evolve spontaneously over long epochs of continuous time. To address this, we examine functional connectivity networks deduced from continuous long-term electrocorticogram recordings. For a population of six human patients, we identify a persistent pattern of connections that form a frequency-band-dependent network template, and a set of core connections that appear frequently and together. These structures are robust, emerging from brief time intervals (similar to 100 s) regardless of cognitive state. These results suggest that a metastable, frequency-band-dependent scaffold of brain connectivity exists from which transient activity emerges and recedes.
C1 [Kramer, Mark A.; Eden, Uri T.; Lepage, Kyle Q.; Kolaczyk, Eric D.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Bianchi, Matt T.; Cash, Sydney S.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Bianchi, Matt T.; Cash, Sydney S.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
RP Kramer, MA (reprint author), Boston Univ, Dept Math & Stat, 111 Cummington St, Boston, MA 02215 USA.
EM mak@bu.edu
RI Kramer, Mark/A-1291-2014
FU Burroughs Wellcome Fund; National Science Foundation [IIS-0643995];
Office of Naval Research [N00014-06-1-0096]; National Institutes of
Health, National Institute of Neurological Disorders and Stroke
[NS062092]
FX M.A.K. holds a Career Award at the Scientific Interface from the
Burroughs Wellcome Fund. U.T.E. acknowledges support by the National
Science Foundation under Grant IIS-0643995. E.D.K. acknowledges support
by the Office of Naval Research Award N00014-06-1-0096. S.S.C. is
supported by a grant from the National Institutes of Health, National
Institute of Neurological Disorders and Stroke NS062092. We thank Emad
Eskandar for electrode placement and surgical management.
NR 83
TC 28
Z9 28
U1 0
U2 3
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 2
PY 2011
VL 31
IS 44
BP 15757
EP 15767
DI 10.1523/JNEUROSCI.2287-11.2011
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 844ES
UT WOS:000296731100014
PM 22049419
ER
PT J
AU Chang, HJ
Liang, MH
AF Chang, Huan J.
Liang, Matthew H.
TI The Quiet Epidemic
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
C1 [Liang, Matthew H.] Brigham & Womens Hosp, Rheumatol Sect, Boston VA Healthcare Syst, Rehabil Serv, Boston, MA 02115 USA.
[Liang, Matthew H.] Brigham & Womens Hosp, Rheumatol Sect, Boston VA Healthcare Syst, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA.
EM tina.chang@jama-archives.org
NR 1
TC 1
Z9 3
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 2
PY 2011
VL 306
IS 17
BP 1843
EP 1844
DI 10.1001/jama.2011.1587
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 839OD
UT WOS:000296376200001
PM 22045757
ER
PT J
AU Sorror, ML
Sandmaier, BM
Storer, BE
Franke, GN
Laport, GG
Chauncey, TR
Agura, E
Maziarz, RT
Langston, A
Hari, P
Pulsipher, MA
Bethge, W
Sahebi, F
Bruno, B
Maris, MB
Yeager, A
Petersen, FB
Vindelov, L
McSweeney, PA
Hubel, K
Mielcarek, M
Georges, GE
Niederwieser, D
Blume, KG
Maloney, DG
Storb, R
AF Sorror, Mohamed L.
Sandmaier, Brenda M.
Storer, Barry E.
Franke, Georg N.
Laport, Ginna G.
Chauncey, Thomas R.
Agura, Edward
Maziarz, Richard T.
Langston, Amelia
Hari, Parameswaran
Pulsipher, Michael A.
Bethge, Wolfgang
Sahebi, Firoozeh
Bruno, Benedetto
Maris, Michael B.
Yeager, Andrew
Petersen, Finn Bo
Vindelov, Lars
McSweeney, Peter A.
Huebel, Kai
Mielcarek, Marco
Georges, George E.
Niederwieser, Dietger
Blume, Karl G.
Maloney, David G.
Storb, Rainer
TI Long-term Outcomes Among Older Patients Following Nonmyeloablative
Conditioning and Allogeneic Hematopoietic Cell Transplantation for
Advanced Hematologic Malignancies
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; VERSUS-HOST-DISEASE; MINIMAL RESIDUAL DISEASE;
MARROW TRANSPLANTATION; MYELODYSPLASTIC SYNDROMES; COMORBIDITY INDEX;
RISK-ASSESSMENT; FLOW-CYTOMETRY; AGE; METHOTREXATE
AB Context A minimally toxic nonmyeloablative regimen was developed for allogeneic hematopoietic cell transplantation (HCT) to treat patients with advanced hematologic malignancies who are older or have comorbid conditions.
Objective To describe outcomes of patients 60 years or older after receiving minimally toxic nonmyeloablative allogeneic HCT.
Design, Setting, and Participants From 1998 to 2008, 372 patients aged 60 to 75 years were enrolled in prospective clinical HCT trials at 18 collaborating institutions using conditioning with low-dose total body irradiation alone or combined with fludarabine, 90 mg/m(2), before related (n=184) or unrelated (n=188) donor transplants. Postgrafting immunosuppression included mycophenolate mofetil and a calcineurin inhibitor.
Main Outcome Measures Overall and progression-free survival were estimated by Kaplan-Meier method. Cumulative incidence estimates were calculated for acute and chronic graft-vs-host disease, toxicities, achievement of full donor chimerism, complete remission, relapse, and nonrelapse mortality. Hazard ratios (HRs) were estimated from Cox regression models.
Results Overall, 5-year cumulative incidences of nonrelapse mortality and relapse were 27% (95% CI, 22%-32%) and 41% (95% CI, 36%-46%), respectively, leading to 5-year overall and progression-free survival of 35% (95% CI, 30%-40%) and 32% (95% CI, 27%-37%), respectively. These outcomes were not statistically significantly different when stratified by age groups. Furthermore, increasing age was not associated with increases in acute or chronic graft-vs-host disease or organ toxicities. In multivariate models, HCT-specific comorbidity index scores of 1 to 2 (HR, 1.58 [95% CI, 1.08-2.31]) and 3 or greater (HR, 1.97 [95% CI, 1.38-2.80]) were associated with worse survival compared with an HCT-specific comorbidity index score of 0 (P=.003 overall). Similarly, standard relapse risk (HR, 1.67 [95% CI, 1.10-2.54]) and high relapse risk (HR, 2.22 [95% CI, 1.43-3.43]) were associated with worse survival compared with low relapse risk (P<.001 overall).
Conclusion Among patients aged 60 to 75 years treated with nonmyeloablative allogeneic HCT, 5-year overall and progression-free survivals were 35% and 32%, respectively. JAMA. 2011; 306(17): 1874-1883
C1 [Sorror, Mohamed L.; Sandmaier, Brenda M.; Chauncey, Thomas R.; Mielcarek, Marco; Georges, George E.; Maloney, David G.; Storb, Rainer] Fred Hutchinson Canc Res Ctr, Div Clin Res, Transplantat Biol Program, Seattle, WA 98109 USA.
[Storer, Barry E.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Clin Stat Program, Seattle, WA 98109 USA.
[Sorror, Mohamed L.; Sandmaier, Brenda M.; Chauncey, Thomas R.; Mielcarek, Marco; Georges, George E.; Maloney, David G.; Storb, Rainer] Univ Washington, Sch Med, Dept Med, Div Med Oncol, Seattle, WA 98195 USA.
[Storer, Barry E.] Univ Washington, Sch Publ Hlth, Dept Biostat, Seattle, WA 98195 USA.
[Chauncey, Thomas R.] VA Puget Sound Hlth Care Syst, Marrow Transplant Unit, Seattle, WA USA.
[Franke, Georg N.; Niederwieser, Dietger] Univ Leipzig, Dept Med, Div Hematol Oncol & Hemostaseol, Leipzig, Germany.
[Laport, Ginna G.; Blume, Karl G.] Stanford Sch Med, Div Blood & Marrow Transplantat, Dept Med, Stanford, CA USA.
[Agura, Edward] Baylor Univ, Hematopoiet Stem Cell Program, Sch Med, Dallas, TX USA.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Sch Med, Hematopoiet Stem Cell Transplant Program, Portland, OR 97201 USA.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Sch Med, Ctr Hematol Malignancies, Knight Canc Inst, Portland, OR 97201 USA.
[Maziarz, Richard T.] Oregon Hlth & Sci Univ, Sch Med, Div Hematol & Med Oncol, Portland, OR 97201 USA.
[Langston, Amelia] Emory Univ, Sch Med, Div Hematol Oncol, Atlanta, GA USA.
[Langston, Amelia] Emory Univ, Bone Marrow & Stem Cell Transplant Ctr, Winship Canc Inst, Atlanta, GA 30322 USA.
[Hari, Parameswaran] Med Coll Wisconsin, Div Hematol & Oncol, Sch Med, Milwaukee, WI 53226 USA.
[Pulsipher, Michael A.] Univ Utah, Sch Med, Div Hematol Blood & Marrow Transplantat, Salt Lake City, UT USA.
[Pulsipher, Michael A.] Primary Childrens Med Ctr, Pediat Blood & Marrow Transplant Program, Huntsman Canc Inst, Salt Lake City, UT 84103 USA.
[Bethge, Wolfgang] Univ Tubingen, Sch Med, Tubingen, Germany.
[Sahebi, Firoozeh] City Hope Sch Med, Duarte, CA USA.
[Bruno, Benedetto] Univ Turin, Sch Med, Turin, Italy.
[Maris, Michael B.; McSweeney, Peter A.] Colorado Blood Canc Inst, Denver, CO USA.
[Yeager, Andrew] Univ Arizona, Sch Med, Dept Med & Pediat, Tucson, AZ USA.
[Petersen, Finn Bo] Intermt Hlth Care, Intermt Blood & Marrow Transplant Acute Leukemia, Salt Lake City, UT USA.
[Petersen, Finn Bo] Univ Aarhus, Sch Med, Aarhus, Denmark.
[Vindelov, Lars] Rigshosp, Hematopoiet Cell Transplantat Program, Dept Hematol, DK-2100 Copenhagen, Denmark.
[McSweeney, Peter A.] Univ Colorado, Sch Med, Boulder, CO 80309 USA.
[Huebel, Kai] Univ Cologne, Dept Internal Med, Sch Med, Stem Cell Transplant Program, Cologne, Germany.
RP Sorror, ML (reprint author), Fred Hutchinson Canc Res Ctr, Clin Res Div D1 100, 1100 Fairview Ave N, Seattle, WA 98109 USA.
EM msorror@fhcrc.org
OI Hari, Parameswaran/0000-0002-8800-297X
FU Japanese Heath Sciences; Athersys Inc; BMT/CTN; Medac GmbH; Fresenius
GmbH; Pfizer; Miltenyi Biotech GmbH; Millennium Pharmaceuticals; Danish
Cancer Society; Lundbeck Foundation; Research Council of Rigshospitalet;
Region of the Capital of Denmark; National Institutes of Health (NIH)
[P01HL036444, P01CA078902, P01CA018029, P30CA015704, R00HL088021];
Leukemia/Lymphoma Society [7008-08]
FX All authors have completed and submitted the ICMJE Form for Disclosure
of Potential Conflicts of Interest. Dr Sandmaier reported serving on the
board of ArevaMed. Dr Franke reported receiving
travel/accommodations/meeting expenses for the European Group of Blood
and Marrow Transplantation 2009 meeting. Dr Maziarz reported receiving
grants or grants pending (grant money to institution) from Japanese
Heath Sciences, Athersys Inc, and BMT/CTN; serving on the speakers
bureaus of Millennium Pharmaceuticals Inc and Genzyme Inc; receiving
royalties from Springer for publication of a book; and receiving
honoraria for lectures (groups change yearly; usually related to
community oncology educational efforts). Dr Bethge reported serving as a
consultant for Miltenyi Biotech GmbH; receiving grants or grants pending
from Medac GmbH, Fresenius GmbH, Pfizer, and Miltenyi Biotech GmbH;
receiving payment for lectures from Miltenyi Biotech GmbH; and receiving
travel/accommodations/meeting expenses from Medac GmbH. Dr Sahebi
reported receiving travel/accommodations/meeting expenses and a research
fund from Millennium Pharmaceuticals. Dr Vindelov reported receiving
research grants from the Danish Cancer Society, The Lundbeck Foundation,
and the Research Council of Rigshospitalet and receiving a travel and
research grant from the Region of the Capital of Denmark. No other
authors reported disclosures.; Research for this study has been
supported by grants from the National Institutes of Health (NIH)
(P01HL036444, P01CA078902, P01CA018029, P30CA015704, and R00HL088021)
and from the Leukemia/Lymphoma Society (7008-08).
NR 38
TC 101
Z9 101
U1 0
U2 5
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 2
PY 2011
VL 306
IS 17
BP 1874
EP 1883
DI 10.1001/jama.2011.1558
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 839OD
UT WOS:000296376200021
PM 22045765
ER
PT J
AU Chen, WY
Rosner, B
Hankinson, SE
Colditz, GA
Willett, WC
AF Chen, Wendy Y.
Rosner, Bernard
Hankinson, Susan E.
Colditz, Graham A.
Willett, Walter C.
TI Moderate Alcohol Consumption During Adult Life, Drinking Patterns, and
Breast Cancer Risk
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID PROGESTERONE-RECEPTOR STATUS; POSTMENOPAUSAL WOMEN; PROSPECTIVE COHORT;
ESTROGEN; DISEASE; HEALTH; AGE; PREMENOPAUSAL; ASSOCIATION; NUTRITION
AB Context Multiple studies have linked alcohol consumption to breast cancer risk, but the risk of lower levels of consumption has not been well quantified. In addition, the role of drinking patterns (ie, frequency of drinking and "binge" drinking) and consumption at different times of adult life are not well understood.
Objective To evaluate the association of breast cancer with alcohol consumption during adult life, including quantity, frequency, and age at consumption.
Design, Setting, and Participants Prospective observational study of 105 986 women enrolled in the Nurses' Health Study followed up from 1980 until 2008 with an early adult alcohol assessment and 8 updated alcohol assessments.
Main Outcome Measures Relative risks of developing invasive breast cancer.
Results During 2.4 million person-years of follow-up, 7690 cases of invasive breast cancer were diagnosed. Increasing alcohol consumption was associated with increased breast cancer risk that was statistically significant at levels as low as 5.0 to 9.9 g per day, equivalent to 3 to 6 drinks per week (relative risk, 1.15; 95% CI, 1.06-1.24; 333 cases/100 000 person-years). Binge drinking, but not frequency of drinking, was associated with breast cancer risk after controlling for cumulative alcohol intake. Alcohol intake both earlier and later in adult life was independently associated with risk.
Conclusions Low levels of alcohol consumption were associated with a small increase in breast cancer risk, with the most consistent measure being cumulative alcohol intake throughout adult life. Alcohol intake both earlier and later in adult life was independently associated with risk. JAMA. 2011; 306(17): 1884-1890
C1 [Chen, Wendy Y.; Rosner, Bernard; Hankinson, Susan E.; Willett, Walter C.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Chen, Wendy Y.; Rosner, Bernard; Hankinson, Susan E.; Willett, Walter C.] Harvard Univ, Sch Med, Boston, MA USA.
[Colditz, Graham A.] Washington Univ, Sch Med, Dept Surg, Alvin J Siteman Canc Ctr, St Louis, MO 63110 USA.
[Chen, Wendy Y.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Hankinson, Susan E.; Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Willett, Walter C.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Hankinson, Susan E.] Univ Massachusetts, Div Biostat & Epidemiol, Sch Publ Hlth & Hlth Sci, Amherst, MA 01003 USA.
RP Chen, WY (reprint author), Brigham & Womens Hosp, Dept Med, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.
EM wendy.chen@channing.harvard.edu
RI Colditz, Graham/A-3963-2009
OI Colditz, Graham/0000-0002-7307-0291
FU National Institutes of Health [P01 CA87969]
FX The work reported herein was supported by the National Institutes of
Health (grant P01 CA87969).
NR 44
TC 131
Z9 138
U1 3
U2 31
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 2
PY 2011
VL 306
IS 17
BP 1884
EP 1890
DI 10.1001/jama.2011.1590
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 839OD
UT WOS:000296376200022
PM 22045766
ER
PT J
AU Fiore, LD
D'Avolio, LW
AF Fiore, Louis D.
D'Avolio, Leonard William
TI Detours on the Road to Personalized Medicine Barriers to Biomarker
Validation and Implementation
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Editorial Material
C1 [Fiore, Louis D.; D'Avolio, Leonard William] VA Boston Healthcare Syst, Cooperat Studies Program Coordinating Ctr, Massachusetts Vet Epidemiol Res & Informat Ctr MA, Jamaica Plain, MA USA.
[Fiore, Louis D.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Fiore, Louis D.] Boston Univ, Sch Publ Hlth, Boston, MA 02118 USA.
[D'Avolio, Leonard William] Harvard Univ, Sch Med, Div Aging, Boston, MA 02115 USA.
[D'Avolio, Leonard William] Brigham & Womens Hosp, Ctr Surg & Publ Hlth, Boston, MA 02115 USA.
RP Fiore, LD (reprint author), Boston VA Healthcare Syst, MAVERIC, Jamaica Plain Campus,150 S Huntington Ave, Boston, MA 02130 USA.
EM louis.fiore@va.gov
NR 7
TC 10
Z9 10
U1 0
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 2
PY 2011
VL 306
IS 17
BP 1914
EP 1915
DI 10.1001/jama.2011.1605
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 839OD
UT WOS:000296376200027
PM 22045770
ER
PT J
AU Jawa, A
Shi, L
O'Brien, T
Wells, J
Higgins, L
Macy, J
Warner, JJP
AF Jawa, Andrew
Shi, Lewis
O'Brien, Travis
Wells, Jessica
Higgins, Laurence
Macy, John
Warner, Jon J. P.
TI Prosthesis of Antibiotic-Loaded Acrylic Cement (PROSTALAC) Use for the
Treatment of Infection After Shoulder Arthroplasty
SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME
LA English
DT Article
ID REPLACEMENT; MANAGEMENT
AB Background: There are limited data on Prosthesis of Antibiotic-Loaded Acrylic Cement (PROSTALAC) use for the treatment of infection following shoulder arthroplasty. We performed a retrospective review of our experience with the PROSTALAC in terms of infection eradication, complications, and outcomes.
Methods: Twenty-eight patients with an infection at the site of a. shoulder arthroplasty who were managed with the PROSTALAC were followed until eradication of the infection and maximum functional improvement. The average duration of follow-up was 27.6 months (range, twelve to sixty-nine months). In twenty-five of the twenty-eight patients, the PROSTALAC was created with antibiotic-impregnated cement, a standard humeral head mold, and a scaffold with either a one-third tubular plate or a 3.5-mm reconstruction plate. Three PROSTALAC implants had no scaffold.
Results: Although all patients benefited from the Use of the PROSTALAC, there were nine complications in eight patients (29%), with six additional unplanned surgical procedures being performed in this group. One patient had a dislocation, three had a fracture of the PROSTALAC, and five had recurrent infections requiring debridement and revision PROSTALAC placement. All fractures were associated with use of the semitubular plate. Twelve patients (43%), including two with revision PROSTALAC implants, were satisfied with pain relief and function and declined a second-stage procedure. With the exclusion of two patients who had a revision PROSTALAC implant, sixteen patients (57%) had a second-stage procedure; the procedures included ten reverse shoulder arthroplasties, three hemiarthroplasties, two total shoulder arthroplasties, and one resection arthroplasty. At the time of the latest follow-up, the average forward elevation of the shoulder was 77 degrees (range, 30 degrees to 130 degrees). Fifteen patients had no or mild pain, eight patients had moderate pain, and five had severe pain. Patients with reverse total shoulder arthroplasties did not have improved function compared with the other cohorts.
Conclusions: The use of the PROSTALAC for the treatment of infection following shoulder arthroplasty is beneficial. Infection was initially eradicated in twenty-three (82%) of twenty-eight patients, more than half of our patients had mild or no pain, and 43 of patients declined a second-stage procedure because of acceptable function and pain relief. Conversely, five of twenty-eight patients had severe pain and five patients had persistent infection requiring additional surgery. The use of the reverse total shoulder arthroplasty did not appear to improve outcomes.
Level of Evidence: Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.
C1 Massachusetts Gen Hosp, Boston, MA 02115 USA.
Brigham & Womens Hosp, Boston, MA 02115 USA.
Univ Vermont, Med Ctr, Burlington, VT 05401 USA.
RP Jawa, A (reprint author), Boston Univ, Med Ctr, Dept Orthopaed Surg, 850 Harrison Ave,Dowling Bldg,2 North, Boston, MA 02118 USA.
EM Andrew.Jawa@bmc.org
NR 11
TC 8
Z9 8
U1 0
U2 1
PU JOURNAL BONE JOINT SURGERY INC
PI NEEDHAM
PA 20 PICKERING ST, NEEDHAM, MA 02192 USA
SN 0021-9355
J9 J BONE JOINT SURG AM
JI J. Bone Joint Surg.-Am. Vol.
PD NOV 2
PY 2011
VL 93A
IS 21
BP 2001
EP 2009
DI 10.2106/JBJS.J.00833
PG 9
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 840ZZ
UT WOS:000296482800007
PM 22048095
ER
PT J
AU Guitton, TG
Ring, D
AF Guitton, Thierry G.
Ring, David
CA Sci Variation Grp
TI Interobserver Reliability of Radial Head Fracture Classification:
Two-Dimensional Compared with Three-Dimensional CT
SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME
LA English
DT Article
ID COMPUTED-TOMOGRAPHY; AGREEMENT
AB Background:, The Broberg and Morrey modification of the Mason classification of radial head fractures has substantial interobserver variation. This study used a large. web-based collaborative of experienced orthopaedic surgeons to test the. hypothesis that three-dimensional reconstructions of computed tomography (CT) scans improve the interobserver reliability of the classification of radial head fractures according to the Broberg and Morrey modification of the Mason classification.
Methods: Eighty-five orthopaedic surgeons evaluated twelve radial head fractures. They were randomly assigned to review either radiographs and two-dimensional CT scans or radiographs and three-dimensional CT images to determine the fracture Classification, fracture characteristics, and treatment recommendations. The kappa multirater measure (kappa) was calculated to estimate agreement between observers.
Results: Three-dimensional CT had moderate agreement and two-dimensional CT had fair agreement among observers for the Broberg and Morrey modification of the Mason classification, a difference that was significant. Observers assessed seven fracture characteristics, including fracture line, comminution, articular surface involvement, articular step or gap of >= 2 mm, central impaction, recognition of more than three fracture fragments, and fracture fragments too small to repair. There was a significant difference in kappa values between three-dimensional CT and two-dimensional CT for fracture fragments too small to repair, recognition of three fracture fragments, and central impaction. The difference between the other four fracture characteristics was not significant. Among treatment recommendations, there was fair agreement for both three-dimensional CT and two-dimensional CT.
Conclusions: Although three-dimensional CT led to some small but significant decreases in interobserver variation, there is still considerable disagreement regarding classification and characterization of radial head fractures. Three-dimensional CT may be insufficient to optimize interobserver agreement.
C1 [Guitton, Thierry G.] Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv, Yawkey Ctr, Boston, MA 02114 USA.
RP Guitton, TG (reprint author), Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv, Yawkey Ctr, Suite 2100,55 Fruit St, Boston, MA 02114 USA.
EM dring@partners.org
RI Page, Richard/K-6327-2015;
OI Page, Richard/0000-0002-2225-7144; van der Heide, Huub
JL/0000-0003-3910-5048; Frihagen, Frede/0000-0002-4811-669X; Ladd,
Amy/0000-0003-0948-1034; Guitton, Thierry/0000-0002-2599-1985; Soong,
Maximillian/0000-0003-0333-8181
NR 15
TC 26
Z9 29
U1 0
U2 0
PU JOURNAL BONE JOINT SURGERY INC
PI NEEDHAM
PA 20 PICKERING ST, NEEDHAM, MA 02192 USA
SN 0021-9355
J9 J BONE JOINT SURG AM
JI J. Bone Joint Surg.-Am. Vol.
PD NOV 2
PY 2011
VL 93A
IS 21
BP 2015
EP 2021
DI 10.2106/JBJS.J.00711
PG 7
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 840ZZ
UT WOS:000296482800009
PM 22048097
ER
PT J
AU Watkins, N
Irimia, D
Toner, M
Bashir, R
AF Watkins, Nicholas
Irimia, Daniel
Toner, Mehmet
Bashir, Rashid
TI On a Chip
SO IEEE PULSE
LA English
DT Article
ID CIRCULATING TUMOR-CELLS; ON-A-CHIP; GRADIENTS; CHEMOTAXIS; BIOSENSORS;
BLOOD
C1 [Watkins, Nicholas; Bashir, Rashid] Univ Illinois, Dept Elect & Comp Engn & Bioengn, Bioengn & Micro & Nanotechnol Lab, Urbana, IL USA.
[Irimia, Daniel; Toner, Mehmet] Massachusetts Gen Hosp, Surg Serv, Boston, MA 02114 USA.
[Irimia, Daniel; Toner, Mehmet] Massachusetts Gen Hosp, BioMEMS Resource Ctr, Boston, MA 02114 USA.
[Irimia, Daniel; Toner, Mehmet] Harvard Univ, Sch Med, Boston, MA USA.
RP Watkins, N (reprint author), Univ Illinois, Dept Elect & Comp Engn & Bioengn, Bioengn & Micro & Nanotechnol Lab, Urbana, IL USA.
EM watkins7@illinois.edu; rbashir@illinois.edu; dirimia@hms.harvard.edu;
mtoner@hms.harvard.edu
OI Irimia, Daniel/0000-0001-7347-2082
FU NCI NIH HHS [R01 CA120003, R25 CA154015]; NIBIB NIH HHS [P41 EB002503];
NIGMS NIH HHS [R01 GM092804]
NR 32
TC 6
Z9 6
U1 0
U2 15
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 2154-2287
J9 IEEE PULSE
JI IEEE Pulse
PD NOV-DEC
PY 2011
VL 2
IS 6
BP 19
EP 27
DI 10.1109/MPUL.2011.942762
PG 9
WC Engineering, Biomedical
SC Engineering
GA 992UF
UT WOS:000307804500008
PM 22147065
ER
PT J
AU Seker, E
Sung, JH
Shuler, ML
Yarmush, ML
AF Seker, Erkin
Sung, Jong Hwan
Shuler, Michael L.
Yarmush, Martin L.
TI Solving Medical Problems with BioMEMS
SO IEEE PULSE
LA English
DT Article
ID FLUID SHEAR-STRESS; LIVING CELL ARRAY; MICROFLUIDIC SYSTEMS; GRADIENTS;
CULTURE; CHIP; DIFFERENTIATION; STIMULATION; GENERATION; CHEMOTAXIS
C1 [Seker, Erkin] Harvard Univ, Sch Med, Ctr Engn Med, Boston, MA 02115 USA.
[Seker, Erkin] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Seker, Erkin] Univ Calif Davis, Dept Elect & Comp Engn, Davis, CA 95616 USA.
[Sung, Jong Hwan] Hongik Univ, Dept Chem Engn, Seoul, South Korea.
[Shuler, Michael L.] Cornell Univ, Dept Biomed Engn, Ithaca, NY USA.
[Yarmush, Martin L.] Rutgers State Univ, Dept Biomed Engn, Piscataway, NJ USA.
RP Seker, E (reprint author), Harvard Univ, Sch Med, Ctr Engn Med, Boston, MA 02115 USA.
EM eseker@ucdavis.edu; jhsung22@hongik.ac.kr; mls50@cornell.edu;
ireis@sbi.org
OI Seker, Erkin/0000-0003-2401-3562
FU National Institutes of Health [AI063795, EB002503]; Massachusetts
General Hospital Fund for Medical Discovery award [217035]; National
Research Foundation of Korea award [2011-0013862]; Hongik University new
faculty research support fund; Army Corps of Engineers (CERL) [W9132T-0]
FX Michael L. Shuler acknowledges support from the National Institutes of
Health awards AI063795 and EB002503, Erkin Seker from the Massachusetts
General Hospital Fund for Medical Discovery award 217035, Jong Hwan Sung
from the National Research Foundation of Korea award 2011-0013862 and
support from Hongik University new faculty research support fund, and
Michael L. Shuler acknowledges partial support from the Army Corps of
Engineers (CERL) W9132T-0. The first two authors, Erkin Seker and Jong
Hwan Sung, contributed equally to this work.
NR 54
TC 1
Z9 1
U1 0
U2 11
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 2154-2287
J9 IEEE PULSE
JI IEEE Pulse
PD NOV-DEC
PY 2011
VL 2
IS 6
BP 51
EP 59
DI 10.1109/MPUL.2011.942928
PG 9
WC Engineering, Biomedical
SC Engineering
GA 992UF
UT WOS:000307804500012
PM 22147069
ER
PT J
AU Patti, JA
AF Patti, John A.
TI The Challenges of Leadership in the New Era of Health Care
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Patti, JA (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,FND 202, Boston, MA 02114 USA.
EM jpatti@partners.org
NR 6
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1546-1440
J9 J AM COLL RADIOL
JI J. Am. Coll. Radiol.
PD NOV
PY 2011
VL 8
IS 11
BP 739
EP 740
DI 10.1016/j.jacr.2011.09.017
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 971KF
UT WOS:000306202100001
PM 22051451
ER
PT J
AU Rosen, MP
Ding, A
Blake, MA
Baker, ME
Cash, BD
Fidler, JL
Grant, TH
Greene, FL
Jones, B
Katz, DS
Lalani, T
Miller, FH
Small, WC
Spottswood, S
Sudakoff, GS
Tulchinsky, M
Warshauer, DM
Yee, J
Coley, BD
AF Rosen, Max P.
Ding, Alexander
Blake, Michael A.
Baker, Mark E.
Cash, Brooks D.
Fidler, Jeff L.
Grant, Thomas H.
Greene, Frederick L.
Jones, Bronwyn
Katz, Douglas S.
Lalani, Tasneem
Miller, Frank H.
Small, William C.
Spottswood, Stephanie
Sudakoff, Gary S.
Tulchinsky, Mark
Warshauer, David M.
Yee, Judy
Coley, Brian D.
TI ACR Appropriateness Criteria (R) Right Lower Quadrant Pain-Suspected
Appendicitis
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Article
DE Appropriateness criteria; CT; ultrasound; appendicitis; abdominal pain;
comparative studies
ID COMPUTED-TOMOGRAPHY SCAN; NEGATIVE APPENDECTOMY; PERFORATION RATES;
PREGNANT PATIENTS; HELICAL CT; DIAGNOSTIC PERFORMANCE; CONTRAST
MATERIAL; RECTAL CONTRAST; ABDOMINAL-PAIN; CHILDREN
AB The diagnostic imaging of patients presenting with right lower quadrant pain and suspected appendicitis may be organized according to age and gender and to the presence or absence of "classic" signs and symptoms of acute appendicitis. Among adult patients presenting with clinical signs of acute appendicitis, the sensitivity and specificity of CT are greater than those of ultrasound, with improved performance when CT is performed with intravenous contrast. The use of rectal contrast has been associated with decreased time in the emergency department. Computed tomography has also been shown to reduce cost and negative appendectomy rates. Both CT and ultrasound are also effective in the identification of causes of right lower quadrant pain unrelated to appendicitis. Among pediatric patients, the sensitivity and specificity of graded-compression ultrasound can approach those of CT, without the use of ionizing radiation. Performing MRI after inconclusive ultrasound in pregnant patients has been associated with sensitivity and specificity of 80% to 86% and 97% to 99%, respectively. The ACR Appropriateness Criteria (R) 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 in which evidence is lacking or not definitive, expert opinion may be used to recommend imaging or treatment.
C1 [Rosen, Max P.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Ding, Alexander; Blake, Michael A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Baker, Mark E.] Cleveland Clin, Cleveland, OH 44106 USA.
[Cash, Brooks D.] Natl Naval Med Ctr, Bethesda, MD USA.
[Cash, Brooks D.] Amer Gastroenterol Assoc, Bethesda, MD USA.
[Fidler, Jeff L.] Mayo Clin, Rochester, MN USA.
[Grant, Thomas H.] NW Med Fac, Chicago, IL USA.
[Greene, Frederick L.] Carolinas Med Ctr, Charlotte, NC 28203 USA.
[Greene, Frederick L.] Amer Coll Surg, Chicago, IL USA.
[Jones, Bronwyn] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Katz, Douglas S.] Winthrop Univ Hosp, Mineola, NY 11501 USA.
[Lalani, Tasneem] Inland Imaging Associates, Seattle, WA USA.
[Lalani, Tasneem] Univ Washington, Seattle, WA 98195 USA.
[Miller, Frank H.] Northwestern Univ, Feinberg Sch Med, NMH, Chicago, IL 60611 USA.
[Small, William C.] Emory Univ, Atlanta, GA 30322 USA.
[Spottswood, Stephanie] Vanderbilt Childrens Hosp, Nashville, TN USA.
[Spottswood, Stephanie; Tulchinsky, Mark] Soc Nucl Med, Reston, VA USA.
[Sudakoff, Gary S.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Tulchinsky, Mark] Milton S Hershey Med Ctr, Hershey, PA USA.
[Warshauer, David M.] Univ N Carolina, Sch Med, Chapel Hill, NC USA.
[Yee, Judy] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Coley, Brian D.] Nationwide Childrens Hosp, Columbus, OH USA.
RP Rosen, MP (reprint author), Amer Coll Radiol, 1891 Preston White Dr, Reston, VA 20191 USA.
EM mrosen2@bidmc.harvard.edu
NR 56
TC 64
Z9 65
U1 0
U2 2
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 NOV
PY 2011
VL 8
IS 11
BP 749
EP 755
DI 10.1016/j.jacr.2011.07.010
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 971KF
UT WOS:000306202100006
PM 22051456
ER
PT J
AU Hawkins, CM
Krishnaraj, A
AF Hawkins, C. Matthew
Krishnaraj, Arun
TI Resident and Fellow State Chapters: Providing Impact From the Local
Level
SO JOURNAL OF THE AMERICAN COLLEGE OF RADIOLOGY
LA English
DT Editorial Material
C1 [Krishnaraj, Arun] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol,Div Abdominal Imaging & Intervent, Boston, MA 02114 USA.
[Hawkins, C. Matthew] Univ Cincinnati, Coll Med, Dept Radiol, Cincinnati, OH 45221 USA.
RP Krishnaraj, A (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol,Div Abdominal Imaging & Intervent, 55 Fruit St, Boston, MA 02114 USA.
EM hawkcm@gmail.com; akrishnaraj@partners.org
NR 1
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1546-1440
J9 J AM COLL RADIOL
JI J. Am. Coll. Radiol.
PD NOV
PY 2011
VL 8
IS 11
BP 812
EP 813
DI 10.1016/j.jacr.2011.06.004
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 971KF
UT WOS:000306202100019
PM 22051469
ER
PT J
AU Hoang, T
Byers, AL
Barnes, D
Cawthon, PM
Yaffe, K
AF Hoang, T.
Byers, A. L.
Barnes, D.
Cawthon, P. M.
Yaffe, K.
TI ALCOHOL CONSUMPTION OVER THE LIFE COURSE AND COGNITIVE OUTCOMES IN OLDER
WOMEN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hoang, T.; Byers, A. L.; Barnes, D.; Yaffe, K.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Byers, A. L.; Barnes, D.; Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Cawthon, P. M.] Calif Pacific Med Ctr, Res Inst, San Francisco Coordinating Ctr, San Francisco, CA USA.
[Yaffe, K.] Univ Calif San Francisco, Dept Neurol, Dept Epidemiol & Biostat, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 20
EP 20
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000094
ER
PT J
AU Spira, AP
Covinsky, K
Rebok, G
Punjabi, N
Stone, KL
Hillier, TA
Ensrud, K
Yaffe, K
AF Spira, A. P.
Covinsky, K.
Rebok, G.
Punjabi, N.
Stone, K. L.
Hillier, T. A.
Ensrud, K.
Yaffe, K.
TI OBJECTIVELY MEASURED SLEEP AND FUNCTIONAL DECLINE IN OLDER WOMEN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Spira, A. P.; Rebok, G.; Punjabi, N.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Covinsky, K.; Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Covinsky, K.; Yaffe, K.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Punjabi, N.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Stone, K. L.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Hillier, T. A.] Kaiser Permanente, Ctr Hlth Res, Portland, OR USA.
[Ensrud, K.] Minneapolis VAMC, Minneapolis, MN USA.
[Ensrud, K.] Univ Minnesota, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 20
EP 20
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000093
ER
PT J
AU Brady, CB
Kaiser, AP
Spiro, A
AF Brady, C. B.
Kaiser, A. Pless
Spiro, A.
TI COMBAT-RELATED STRESS SYMPTOMS IN AGING VETERANS: DISTINCT SUBGROUPS OR
POINTS ON A CONTINUUM?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Brady, C. B.; Kaiser, A. Pless; Spiro, A.] VA Boston Healthcare Syst, Boston, MA USA.
[Brady, C. B.; Kaiser, A. Pless] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Spiro, A.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 21
EP 21
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000099
ER
PT J
AU Hilgeman, MM
Archambault, E
Billings, RL
Gosian, J
Karel, M
Moye, J
AF Hilgeman, M. M.
Archambault, E.
Billings, R. L.
Gosian, J.
Karel, M.
Moye, J.
TI FROM COMBAT TO CANCER: RISK AND RESILIENCY IN VETERAN CANCER SURVIVORS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hilgeman, M. M.] Tuscaloosa VA Med Ctr, Tuscaloosa, AL USA.
[Archambault, E.; Gosian, J.; Karel, M.; Moye, J.] VA Boston Healthcare Syst, Boston, MA USA.
[Archambault, E.; Karel, M.; Moye, J.] Harvard Univ, Sch Med, Boston, MA USA.
[Billings, R. L.] Northshore Psychol Associates LLC, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 21
EP 22
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000100
ER
PT J
AU Park, C
Kaiser, AP
King, D
King, L
Spiro, A
AF Park, C.
Kaiser, A. Pless
King, D.
King, L.
Spiro, A.
TI WAR-TIME CAPTIVITY: DOES RESILIENCE MODERATE ITS IMPACT ON WELL-BEING
ACROSS THE LIFE COURSE?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Park, C.] Univ Connecticut, Storrs, CT USA.
[Kaiser, A. Pless; King, D.; King, L.; Spiro, A.] VA Boston Healthcare Syst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 21
EP 21
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000098
ER
PT J
AU Sanders, J
Fitzpatrick, A
Boudreau, R
Arnold, A
Aviv, A
Fried, LF
Harris, TB
Newman, AB
AF Sanders, J.
Fitzpatrick, A.
Boudreau, R.
Arnold, A.
Aviv, A.
Fried, L. F.
Harris, T. B.
Newman, A. B.
TI LEUKOCYTE TELOMERE LENGTH IS ASSOCIATED WITH AGE-RELATED CHRONIC DISEASE
BURDEN IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Sanders, J.; Boudreau, R.; Newman, A. B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Fitzpatrick, A.; Arnold, A.] Univ Washington, Seattle, WA 98195 USA.
[Aviv, A.] Univ Med & Dent New Jersey, Newark, NJ 07103 USA.
[Fried, L. F.] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Harris, T. B.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 22
EP 23
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000105
ER
PT J
AU Hilgeman, MM
Snow, A
Mahaney-Price, AF
Kertesz, S
Davis, L
AF Hilgeman, M. M.
Snow, A.
Mahaney-Price, A. F.
Kertesz, S.
Davis, L.
TI EXAMINATION OF THE MONTREAL COGNITIVE ASSESSMENT (MOCA): FINDINGS FROM
THE ALABAMA VETERANS RURAL HEALTH INITIATIVE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hilgeman, M. M.; Snow, A.; Mahaney-Price, A. F.; Davis, L.] Tuscaloosa VA Med Ctr, Tuscaloosa, AL USA.
[Kertesz, S.] Birmingham VA Med Ctr, Birmingham, AL USA.
[Kertesz, S.] Univ Alabama Birmingham, Birmingham, AL USA.
[Davis, L.] Univ Alabama, Sch Med, Tuscaloosa, AL 35401 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 31
EP 32
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000149
ER
PT J
AU Bolkan, C
Bonner, L
Campbell, DG
Lanto, A
Rubenstein, L
Chaney, E
AF Bolkan, C.
Bonner, L.
Campbell, D. G.
Lanto, A.
Rubenstein, L.
Chaney, E.
TI THE COMPLEX RELATIONSHIP BETWEEN SOCIAL SUPPORT AND DEPRESSION: THE
SIGNIFICANCE OF PATIENT SATISFACTION AND MEDICATION ADHERENCE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Bolkan, C.] Washington State Univ, Vancouver, WA USA.
[Bonner, L.] VA Puget Sound Hlth Care Syst, Dept Vet Affairs, Hlth Serv Res & Dev Ctr Excellence, Seattle, WA USA.
[Campbell, D. G.] Univ Montana, Missoula, MT 59812 USA.
[Lanto, A.; Rubenstein, L.] VA Greater Angeles Healthcare Syst, Dept Vet Affairs, Hlth Serv Res & Dev Ctr Excellence, Los Angeles, CA USA.
[Rubenstein, L.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Rubenstein, L.] RAND Hlth Program, Santa Monica, CA USA.
[Chaney, E.] Univ Washington, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 34
EP 34
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000159
ER
PT J
AU Kresevic, DM
Burant, CJ
Denton, JE
Ibrahim, S
AF Kresevic, D. M.
Burant, C. J.
Denton, J. E.
Ibrahim, S.
TI OUTPATIENT ANTICOAGULATION EDUCATION AND OUTCOMES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Kresevic, D. M.; Burant, C. J.; Denton, J. E.] Louis Stokes Cleveland VA Med Ctr, Cleveland, OH USA.
[Kresevic, D. M.] Univ Hosp, Case Med Ctr, Cleveland, OH USA.
[Kresevic, D. M.; Burant, C. J.] Case Western Reserve Univ, Frances Payne Bolton Sch Nursing, Cleveland, OH 44106 USA.
[Ibrahim, S.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 74
EP 74
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000332
ER
PT J
AU Hughes, J
Martin, JL
AF Hughes, J.
Martin, J. L.
TI SLEEP: AN OVERLOOKED COMPONENT OF HEALTH AND QUALITY OF LIFE IN OLDER
ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hughes, J.; Martin, J. L.] VA Greater Los Angeles Healthcare Syst, Geriatr Res Educ & Clin Ctr, North Hills, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 78
EP 78
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000348
ER
PT J
AU Vitiello, MV
Baker, LD
Borson, S
Friedman, SD
Barsness, S
Merriam, GR
AF Vitiello, M. V.
Baker, L. D.
Borson, S.
Friedman, S. D.
Barsness, S.
Merriam, G. R.
TI TESAMORELIN, A HUMAN GROWTH HORMONE RELEASING HORMONE ANALOGUE, IMPROVES
COGNITIVE FUNCTION IN MCI AND HEALTHY AGING: RESULTS OF A RANDOMIZED
PLACEBO-CONTROLLED TRIAL
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Vitiello, M. V.; Baker, L. D.; Borson, S.; Barsness, S.; Merriam, G. R.] Univ Washington, Seattle, WA 98195 USA.
[Friedman, S. D.] Childrens Hosp, Seattle, WA USA.
[Merriam, G. R.] VA Puget Sound Hlth Care Syst, Tacoma, WA USA.
[Merriam, G. R.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 106
EP 106
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000481
ER
PT J
AU Wittich, AR
Williams, BR
Woodby, LL
Burgio, KL
AF Wittich, A. R.
Williams, B. R.
Woodby, L. L.
Burgio, K. L.
TI "THE WHOLE POWER OF ATTORNEY": UNDERSTANDING ADVANCE DIRECTIVES AMONG
NEXT-OF-KIN IN VA MEDICAL CENTERS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Wittich, A. R.; Williams, B. R.; Woodby, L. L.; Burgio, K. L.] Birmingham VAMC, Birmingham, AL USA.
[Williams, B. R.; Woodby, L. L.; Burgio, K. L.] Univ Alabama Birmingham, Birmingham, AL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 136
EP 137
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000623
ER
PT J
AU Mavandadi, S
Mamikonyan, E
Duda, JE
Weintraub, D
AF Mavandadi, S.
Mamikonyan, E.
Duda, J. E.
Weintraub, D.
TI INTERPERSONAL FUNCTIONING IN PARKINSON'S DISEASE: A DYADIC ANALYSIS OF
VETERANS AND CAREGIVERS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mavandadi, S.; Weintraub, D.] Philadelphia VA Med Ctr, Mental Illness Res Educ & Clin Ctr, Philadelphia, PA USA.
[Mavandadi, S.; Mamikonyan, E.; Weintraub, D.] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA.
[Duda, J. E.; Weintraub, D.] Philadelphia VA Med Ctr, Parkinsons Dis Res Educ & Clin Ctr, Philadelphia, PA USA.
[Duda, J. E.] Univ Penn, Dept Neurol, Penn Hosp, Parkinsons Dis & Movement Disorders Ctr, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 141
EP 141
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602000643
ER
PT J
AU Mills, WL
Regev, T
Kunik, ME
Wilson, NL
Moye, J
McCullough, LB
Naik, AD
AF Mills, W. L.
Regev, T.
Kunik, M. E.
Wilson, N. L.
Moye, J.
McCullough, L. B.
Naik, A. D.
TI A SCREENING TOOL FOR CAPACITY TO LIVE SAFELY AND INDEPENDENTLY IN THE
COMMUNITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mills, W. L.; Kunik, M. E.; Wilson, N. L.; Naik, A. D.] Michael E DeBakey VA Med Ctr, Houston Hlth Serv Res & Dev Ctr Excellence, Houston, TX USA.
[Mills, W. L.; Kunik, M. E.; Wilson, N. L.; McCullough, L. B.; Naik, A. D.] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Regev, T.] Harris Cty Hosp Dist, Quentin Mease Community Hosp, Houston, TX USA.
[Kunik, M. E.] Michael E DeBakey VA Med Ctr, Vet Affairs S Cent Mental Illness Res Educ & Clin, Houston, TX USA.
[Moye, J.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Moye, J.] VA Boston Healthcare Syst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 168
EP 168
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001076
ER
PT J
AU Tennstedt, SL
Volandes, A
Welch, L
AF Tennstedt, S. L.
Volandes, A.
Welch, L.
TI AN INTERACTIVE DECISION AID TO FACILITATE THE PROCESS OF ADVANCE CARE
PLANNING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Tennstedt, S. L.; Welch, L.] New England Res Inst, Watertown, MA 02172 USA.
[Volandes, A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 172
EP 173
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001096
ER
PT J
AU Mahaney-Price, AF
Hilgeman, MM
Kertesz, S
Davis, L
AF Mahaney-Price, A. F.
Hilgeman, M. M.
Kertesz, S.
Davis, L.
TI RURAL ALABAMA VETERAN ADVANCE DIRECTIVE BEHAVIOR AND DESIRE FOR HELP
COMPLETING AN ADVANCE DIRECTIVE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mahaney-Price, A. F.; Hilgeman, M. M.; Davis, L.] Tuscaloosa VA Med Ctr, Tuscaloosa, AL USA.
[Kertesz, S.] Birmingham VA Med Ctr, Birmingham, AL USA.
[Davis, L.] Univ Alabama, Sch Med, Tuscaloosa, AL 35401 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 174
EP 174
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001103
ER
PT J
AU Wolden-Hanson, T
AF Wolden-Hanson, T.
TI HYPOTHALAMIC CONTROL OF THE ANOREXIA OF AGING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Wolden-Hanson, T.] VA Puget Sound Healthcare Syst, Seattle, WA USA.
[Wolden-Hanson, T.] Univ Washington, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 188
EP 188
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001162
ER
PT J
AU Kramer, B
Barczi, S
Chernoff, R
Horvath, KJ
Howe, JL
Huh, J
Tumosa, N
Saunders, MJ
AF Kramer, B.
Barczi, S.
Chernoff, R.
Horvath, K. J.
Howe, J. L.
Huh, J.
Tumosa, N.
Saunders, M. J.
TI THE VA GERIATRIC SCHOLARS PROGRAM: ENHANCING SKILLS IN RURAL PRIMARY
CARE SETTINGS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Kramer, B.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Kramer, B.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Horvath, K. J.] Bedford GRECC, Boston, MA USA.
[Barczi, S.] Madison GRECC, Madison, WI USA.
[Huh, J.] Palo Alto GRECC, Palo Alto, CA USA.
[Saunders, M. J.] San Antonio GRECC, San Antonio, TX USA.
[Tumosa, N.] St Louis GRECC, St Louis, MO USA.
[Chernoff, R.] Birmingham GRECC, Birmingham, AL USA.
[Howe, J. L.] Bronx GRECC, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 204
EP 204
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001244
ER
PT J
AU Moye, J
Danhauer, SC
Chapman, J
Doherty, KM
White, C
AF Moye, J.
Danhauer, S. C.
Chapman, J.
Doherty, K. M.
White, C.
TI OBSTACLES AND INROADS TO YOGA FOR OLDER VETERAN CANCER SURVIVORS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Moye, J.; Doherty, K. M.] VA Boston Healthcare Syst, Mental Hlth, Brockton, MA USA.
[Danhauer, S. C.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Chapman, J.] Hands Hlth, San Francisco, CA USA.
[White, C.] Michael E Debakey VA VA Med Ctr, Houston, TX USA.
[Moye, J.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 223
EP 223
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001343
ER
PT J
AU Ramsey, J
Neupert, SD
Mroczek, D
Spiro, A
AF Ramsey, J.
Neupert, S. D.
Mroczek, D.
Spiro, A.
TI EMOTIONAL COMPLEXITY MODERATES AGE DIFFERENCES IN REACTIVITY TO DAILY
HEALTH STRESSORS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Ramsey, J.; Neupert, S. D.] N Carolina State Univ, Raleigh, NC 27695 USA.
[Mroczek, D.] Purdue Univ, W Lafayette, IN 47907 USA.
[Spiro, A.] VA Boston Healthcare Syst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 225
EP 225
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001353
ER
PT J
AU Anderson, R
AF Anderson, R.
TI IMPACT OF CALORIE RESTRICTION (CR) ON CELLULAR ASPECTS OF METABOLIC
DECLINE IN AGING RHESUS SKELETAL MUSCLE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Anderson, R.] Univ Wisconsin, Madison, WI USA.
[Anderson, R.] William S Middleton Mem Vet Adm Med Ctr, GRECC, Madison, WI USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 242
EP 242
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001441
ER
PT J
AU Forman, D
Allsup, K
Zavin, A
Lazzari, A
Lecker, S
Joseph, J
Arena, R
AF Forman, D.
Allsup, K.
Zavin, A.
Lazzari, A.
Lecker, S.
Joseph, J.
Arena, R.
TI HANDGRIP STRENGTH REFLECTS DECREASED LEAN TISSUE AND FUNCTION IN ELDERLY
HEART FAILURE PATIENTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Forman, D.; Allsup, K.; Zavin, A.; Lazzari, A.; Joseph, J.] VA Boston Healthcare Syst, Boston, MA USA.
[Forman, D.; Lecker, S.; Joseph, J.] Harvard Univ, Sch Med, Boston, MA USA.
[Lazzari, A.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Arena, R.] Univ New Mexico, Albuquerque, NM 87131 USA.
RI Arena, Ross/A-3141-2008
OI Arena, Ross/0000-0002-6675-1996
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 267
EP 267
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001575
ER
PT J
AU Kelly, B
Karel, M
Moye, J
Archambault, E
Noecker, TL
Kaiser, AP
AF Kelly, B.
Karel, M.
Moye, J.
Archambault, E.
Noecker, T. L.
Kaiser, A. Pless
TI MENTAL HEALTH SYMPTOMS AND PATIENT SATISFACTION IN A VA GERIATRIC MENTAL
HEALTH CLINIC
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Kelly, B.; Karel, M.; Moye, J.; Archambault, E.; Noecker, T. L.; Kaiser, A. Pless] VA Boston Healthcare Syst, Boston, MA USA.
[Karel, M.; Moye, J.; Noecker, T. L.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Noecker, T. L.; Kaiser, A. Pless] Boston Univ, Sch Med, Boston, MA 02118 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 270
EP 270
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001588
ER
PT J
AU Garcia, C
Espinoza, SE
Hazuda, HP
AF Garcia, C.
Espinoza, S. E.
Hazuda, H. P.
TI LEVELS OF HEALTH LITERACY AMONG HISPANIC ELDERLY PATIENTS AND THEIR
CAREGIVERS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Garcia, C.; Espinoza, S. E.; Hazuda, H. P.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Espinoza, S. E.; Hazuda, H. P.] S Texas Vet Healthcare Syst, San Antonio, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 283
EP 283
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001643
ER
PT J
AU Pasinetti, GM
AF Pasinetti, G. M.
TI THE ROLE OF NUTRI-EPIGENETICS AND PERSONALIZED MEDICINE IN DIETARY
LIFESTYLE CHOICES IN ALZHEIMER'S DISEASE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 Mt Sinai Sch Med, New York, NY USA.
James J Peters Vet Affairs Med Ctr, Bronx, NY USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 296
EP 296
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602001704
ER
PT J
AU Espinoza, SE
Hazuda, HP
AF Espinoza, S. E.
Hazuda, H. P.
TI ETHNIC DIFFERENCE IN PERFORMANCE-BASED MEASURES OF BASIC AND
INSTRUMENTAL ACTIVITIES OF DAILY LIVING
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Espinoza, S. E.; Hazuda, H. P.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Espinoza, S. E.; Hazuda, H. P.] S Texas Vet Healthcare Syst, San Antonio, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 308
EP 309
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002041
ER
PT J
AU Sullivan, JL
Shwartz, M
Gerena-Melia, M
Berlowitz, D
Burgess, J
AF Sullivan, J. L.
Shwartz, M.
Gerena-Melia, M.
Berlowitz, D.
Burgess, J.
TI EXAMINING THE RELATIONSHIP BETWEEN A MINIMUM DATA SET COMPOSITE QUALITY
INDICATOR AND THE ARTIFACTS OF CULTURE CHANGE TOOL
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Sullivan, J. L.; Shwartz, M.; Gerena-Melia, M.; Burgess, J.] VA Boston Healthcare Syst, Ctr Org Leadership & Management Res, Boston, MA USA.
[Berlowitz, D.] Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA USA.
[Sullivan, J. L.; Shwartz, M.; Berlowitz, D.; Burgess, J.] Boston Univ, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 327
EP 327
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002121
ER
PT J
AU Milberg, W
McGlinchey, R
Leritz, E
Salat, D
Zade, D
Rudolph, JL
AF Milberg, W.
McGlinchey, R.
Leritz, E.
Salat, D.
Zade, D.
Rudolph, J. L.
TI CEREBROVASCULAR RISK, DECISION MAKING, AND THE BRAIN: A CRITICAL
CONNECTION TO THE MAINTENANCE OF HEALTH IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Milberg, W.; McGlinchey, R.; Leritz, E.; Salat, D.; Zade, D.; Rudolph, J. L.] VA Boston Healthcare Syst, Geriatr Res Educ & Clin Ctr, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 347
EP 348
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002224
ER
PT J
AU Atri, A
Mitchell, M
AF Atri, A.
Mitchell, M.
TI COGNITIVE ACTIVITY AND REDUCED RISK FOR COGNITIVE DECLINE AND
ALZHEIMER'S DISEASE: TRUTH OR MYTH?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Atri, A.; Mitchell, M.] Bedford VA Med Ctr, GRECC, Bedford, MA USA.
[Atri, A.; Mitchell, M.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Atri, A.; Mitchell, M.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 348
EP 348
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002227
ER
PT J
AU Kowall, N
Dedeoglu, A
AF Kowall, N.
Dedeoglu, A.
TI DOES EXERCISE ENHANCE PHARMACOTHERAPY IN TRANSGENIC MOUSE MODELS OF
AGE-RELATED NEURODEGENERATION?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Kowall, N.; Dedeoglu, A.] VA Boston Healthcare, GRECC, Boston, MA USA.
[Kowall, N.; Dedeoglu, A.] Boston Univ, Sch Med, Boston, MA 02118 USA.
RI Kowall, Neil/G-6364-2012
OI Kowall, Neil/0000-0002-6624-0213
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 348
EP 348
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002226
ER
PT J
AU Rudolph, JL
Grande, LJ
McGlinchey, R
Chester, JG
Milberg, W
AF Rudolph, J. L.
Grande, L. J.
McGlinchey, R.
Chester, J. G.
Milberg, W.
TI COGNITIVE THEN FUNCTIONAL IMPAIRMENT OR VISA VERSA: THE CLOCK IN THE BOX
EXPERIENCE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Rudolph, J. L.; Grande, L. J.; McGlinchey, R.; Milberg, W.] VA Boston Healthcare Syst, Geriatr Res Educ & Clin Ctr, Boston, MA USA.
[Chester, J. G.] Albert Einstein Coll Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 348
EP 348
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002225
ER
PT J
AU Jones, LI
Kramer, J
Chernoff, R
Howe, JL
Francisco, F
AF Jones, L. I.
Kramer, J.
Chernoff, R.
Howe, J. L.
Francisco, F.
TI CREATING A LEARNING COMMUNITY AND WEBINAR SERIES FOR CLINICIANS WORKING
WITH OLDER VETERANS IN RURAL SETTINGS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Kramer, J.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Howe, J. L.; Francisco, F.] Mt Sinai Sch Med, Dept Geriatr & Palliat Med, New York, NY USA.
[Howe, J. L.; Francisco, F.] James J Peters VAMC, VISN GRECC 3, Bronx, NY USA.
[Chernoff, R.] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Chernoff, R.] Cent Arkansas Vet Healthcare Syst Little Rock GRE, Little Rock, AR USA.
[Jones, L. I.; Kramer, J.] VA Greater Los Angeles Healthcare Syst Greater Lo, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 374
EP 374
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002363
ER
PT J
AU Kramer, J
Harker, JO
Mitchell, M
Rubenstein, L
AF Kramer, J.
Harker, J. O.
Mitchell, M.
Rubenstein, L.
TI INSTEP: MAJOR RESEARCH QUESTIONS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Kramer, J.] Univ Calif Los Angeles, David Geffen Sch Med, GRECC, VA Greater Los Angeles Healthcare Syst, Sepulveda, CA USA.
[Mitchell, M.] Ctr Study Healthcare Provider Behav, Dept Vet Affairs, Sepulveda, CA USA.
[Rubenstein, L.] Univ Oklahoma, Reynolds Dept Geriatr Med, Oklahoma City, OK USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 377
EP 378
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002379
ER
PT J
AU Semla, T
Damron-Rodriguez, J
Berger, S
Goodwin, C
Beizer, J
AF Semla, T.
Damron-Rodriguez, J.
Berger, S.
Goodwin, C.
Beizer, J.
TI THE RATIONALE AND DEVELOPMENT PROCESS FOR THE PHA MULTIDISCIPLINARY
COMPETENCIES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Semla, T.] US Dept Vet Affairs, PBM, Evanston, IL USA.
[Semla, T.] Northwestern Univ, Chicago, IL 60611 USA.
[Damron-Rodriguez, J.] UCLA Sch Publ Affairs, Los Angeles, CA USA.
[Berger, S.] Boston Univ, Coll Hlth & Rehabil Sci, Boston, MA 02215 USA.
[Goodwin, C.] Amer Geriatr Soc, New York, NY USA.
[Beizer, J.] St Johns Coll Pharmcy, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 377
EP 377
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002375
ER
PT J
AU Garrido, MM
Penrod, JD
AF Garrido, M. M.
Penrod, J. D.
TI DEPRESSION AND ANXIETY ASSESSMENT AND TREATMENT IN VETERANS RECEIVING
PALLIATIVE CARE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Garrido, M. M.; Penrod, J. D.] James J Peters VA Med Ctr, Bronx, NY USA.
[Garrido, M. M.; Penrod, J. D.] Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 388
EP 388
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002436
ER
PT J
AU Spira, AP
Covinsky, K
Rebok, G
Stone, KL
Redline, S
Punjabi, N
Yaffe, K
AF Spira, A. P.
Covinsky, K.
Rebok, G.
Stone, K. L.
Redline, S.
Punjabi, N.
Yaffe, K.
TI OBJECTIVELY MEASURED SLEEP FRAGMENTATION AND NURSING HOME PLACEMENT IN
OLDER WOMEN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Spira, A. P.; Rebok, G.; Punjabi, N.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Covinsky, K.; Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Covinsky, K.; Yaffe, K.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Stone, K. L.] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Redline, S.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Punjabi, N.] Johns Hopkins Sch Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 398
EP 398
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002490
ER
PT J
AU Roberge, BJ
Feldmannova, M
Hesse, KA
AF Roberge, B. J.
Feldmannova, M.
Hesse, K. A.
TI CHARACTERIZING EMERGENCY DEPARTMENT UTILIZATION PATTERNS FROM A
GERIATRIC PRIMARY CARE PRACTICE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Roberge, B. J.; Feldmannova, M.; Hesse, K. A.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 431
EP 431
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002658
ER
PT J
AU Beverly, EA
Lee, Y
Brooks, KM
Hultgren, BA
Bishop, JS
Ganda, OP
Munshi, M
Weinger, K
AF Beverly, E. A.
Lee, Y.
Brooks, K. M.
Hultgren, B. A.
Bishop, J. S.
Ganda, O. P.
Munshi, M.
Weinger, K.
TI BENEFITS OF GROUP DIABETES EDUCATION FOR OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Beverly, E. A.; Lee, Y.; Brooks, K. M.; Hultgren, B. A.; Bishop, J. S.; Ganda, O. P.; Munshi, M.; Weinger, K.] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Beverly, E. A.; Ganda, O. P.; Munshi, M.; Weinger, K.] Harvard Univ, Sch Med, Boston, MA USA.
[Ganda, O. P.; Munshi, M.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 440
EP 440
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602002705
ER
PT J
AU Archambault, E
Randazzo, R
Wilson, NL
Kunik, ME
Bass, DM
Judge, K
Looman, WJ
Moye, J
AF Archambault, E.
Randazzo, R.
Wilson, N. L.
Kunik, M. E.
Bass, D. M.
Judge, K.
Looman, W. J.
Moye, J.
TI TRAINING FOR TELEPHONE ADMINISTERED DEMENTIA CARE COORDINATION: LESSONS
LEARNED
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Archambault, E.; Moye, J.] VA Boston Healthcare Syst, Geriatr Mental Hlth, Brockton, MA USA.
[Randazzo, R.] Massachusetts Alzheimers Assoc, Watertown, MA USA.
[Wilson, N. L.; Kunik, M. E.] MEDVAMC, Houston Ctr Excellence Hlth Serv Res, Houston, TX USA.
[Wilson, N. L.; Kunik, M. E.] Baylor Coll Med, Houston, TX 77030 USA.
[Bass, D. M.; Looman, W. J.] Benjamin Rose Res Inst, Cleveland, OH USA.
[Judge, K.] Cleveland State Univ, Dept Psychol, Cleveland, OH 44115 USA.
[Moye, J.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 447
EP 447
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003028
ER
PT J
AU Mulligan, EA
Schuster, J
Naik, AD
Gosian, J
Doherty, KM
Moye, J
AF Mulligan, E. A.
Schuster, J.
Naik, A. D.
Gosian, J.
Doherty, K. M.
Moye, J.
TI DO MILITARY VETERANS IDENTIFY CANCER AS A TRAUMATIC STRESSOR?
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mulligan, E. A.; Schuster, J.; Gosian, J.; Doherty, K. M.; Moye, J.] VA Boston Healthcare Syst, Boston, MA USA.
[Mulligan, E. A.; Moye, J.] Harvard Univ, Sch Med, Boston, MA USA.
[Mulligan, E. A.] Washington Univ, St Louis, MO USA.
[Schuster, J.] Natl Ctr PTSD Womens Hlth Sci Div, Boston, MA USA.
[Naik, A. D.] Michael E DeBakey VA Med Ctr, Houston, TX USA.
[Naik, A. D.] Baylor Coll Med, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 458
EP 459
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003076
ER
PT J
AU Karel, MJ
Moye, J
Norris, R
Archambault, E
Walder, A
Naik, A
AF Karel, M. J.
Moye, J.
Norris, R.
Archambault, E.
Walder, A.
Naik, A.
TI ADULT DEVELOPMENTAL PERSPECTIVES ON COPING WITH CANCER: LIFE ACTIVITIES,
SATISFACTION, AND DEPRESSION
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Karel, M. J.; Moye, J.; Norris, R.; Archambault, E.] VA Boston Healthcare Syst, Mental Hlth, Brockton, MA USA.
[Walder, A.; Naik, A.] Michael E DeBakey VAMC, Houston, TX USA.
[Karel, M. J.; Moye, J.] Harvard Univ, Sch Med, Boston, MA USA.
[Naik, A.] Baylor Med Sch, Houston, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 459
EP 460
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003080
ER
PT J
AU Mulligan, EA
AF Mulligan, E. A.
TI MEASURING PREDEATH GRIEF IN FAMILY CAREGIVERS OF PERSONS WITH DEMENTIA
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mulligan, E. A.] Washington Univ, St Louis, MO USA.
[Mulligan, E. A.] VA Boston Healthcare Syst, Boston, MA USA.
[Mulligan, E. A.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 461
EP 461
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003088
ER
PT J
AU Kostas, TR
Hurwitz, S
Bernacki, R
AF Kostas, T. R.
Hurwitz, S.
Bernacki, R.
TI A MULTIPRONGED APPROACH TO IMPROVING GERIATRIC COMPETENCY IN INTERNAL
MEDICINE RESIDENTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Kostas, T. R.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Hurwitz, S.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Hurwitz, S.] Harvard Univ, Sch Med, Boston, MA USA.
[Bernacki, R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bernacki, R.] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 469
EP 469
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003123
ER
PT J
AU Wang, J
Kaiser, AP
Seligowski, AV
Potter, C
Spiro, A
King, L
King, D
Brady, CB
AF Wang, J.
Kaiser, A. Pless
Seligowski, A. V.
Potter, C.
Spiro, A.
King, L.
King, D.
Brady, C. B.
TI LATE-ONSET STRESS SYMPTOMATOLOGY: DEVELOPMENT AND VALIDATION OF A
SHORT-FORM SCREENING INSTRUMENT
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Wang, J.; Kaiser, A. Pless; Seligowski, A. V.; Potter, C.; Spiro, A.; King, L.; King, D.; Brady, C. B.] VA Boston Healthcare Syst, Boston, MA USA.
[Kaiser, A. Pless; Spiro, A.; King, L.; King, D.; Brady, C. B.] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Spiro, A.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 475
EP 475
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003146
ER
PT J
AU Cotter, VT
Streim, JE
O'Donnell, DF
Forciea, M
Evans, LK
AF Cotter, V. T.
Streim, J. E.
O'Donnell, D. F.
Forciea, M.
Evans, L. K.
TI TRAINING INITIATIVES IN BEHAVIORAL TREATMENT PLANNING IN LONG-TERM CARE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Cotter, V. T.; Evans, L. K.] Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA.
[Streim, J. E.; Forciea, M.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Streim, J. E.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[O'Donnell, D. F.] Coatesville VA Med Ctr, Coatesville, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 479
EP 479
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003163
ER
PT J
AU Byers, AL
Vittinghoff, E
Lui, L
Covinsky, K
Cauley, JA
Ensrud, K
Hillier, TA
Yaffe, K
AF Byers, A. L.
Vittinghoff, E.
Lui, L.
Covinsky, K.
Cauley, J. A.
Ensrud, K.
Hillier, T. A.
Yaffe, K.
TI CHARACTERIZATION OF LONG-TERM DEPRESSIVE TRAJECTORIES AMONG ELDERLY
WOMEN
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Byers, A. L.; Vittinghoff, E.; Covinsky, K.; Yaffe, K.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Byers, A. L.; Covinsky, K.; Yaffe, K.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Lui, L.] Calif Pacific Med Ctr Res Inst, San Francisco, CA USA.
[Cauley, J. A.] Univ Pittsburgh, Pittsburgh, PA USA.
[Ensrud, K.] Univ Minnesota, Minneapolis, MN USA.
[Ensrud, K.] Minneapolis VA Med Ctr, Minneapolis, MN USA.
[Hillier, T. A.] Kaiser Permanente Ctr Hlth Res, Portland, OR USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 518
EP 518
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003331
ER
PT J
AU Turiano, NA
Hill, PL
Roberts, BW
Spiro, A
Mroczek, D
AF Turiano, N. A.
Hill, P. L.
Roberts, B. W.
Spiro, A.
Mroczek, D.
TI SMOKING MEDIATES THE ASSOCIATION BETWEEN CONSCIENTIOUSNESS AND MORTALITY
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Turiano, N. A.; Mroczek, D.] Purdue Univ, W Lafayette, IN 47907 USA.
[Turiano, N. A.; Mroczek, D.] Ctr Aging & Life Course, W Lafayette, IN USA.
[Hill, P. L.; Roberts, B. W.] Univ Illinois, Champaign, IL USA.
[Spiro, A.] VA Boston Healthcare Syst, Boston, MA USA.
[Spiro, A.] Boston Univ, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 519
EP 520
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003341
ER
PT J
AU Hung, WW
Morano, B
Boockvar, K
AF Hung, W. W.
Morano, B.
Boockvar, K.
TI FEASIBILITY OF INTEGRATING THE USE OF REGIONAL HEALTH INFORMATION
ORGANIZATION FOR A VA-BASED CARE TRANSITION INTERVENTION
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Hung, W. W.; Morano, B.; Boockvar, K.] James J Peters Vet Affairs Med Ctr, Hlth Serv Res & Dev Res Enhancement Award Program, Bronx, NY USA.
[Hung, W. W.; Morano, B.; Boockvar, K.] James J Peters Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Bronx, NY USA.
[Hung, W. W.; Morano, B.; Boockvar, K.] Mt Sinai Sch Med, Dept Geriatr & Palliat Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 526
EP 526
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003374
ER
PT J
AU Goldstein, RH
Miller, EA
AF Goldstein, R. H.
Miller, E. A.
TI THE ROLE OF THE MEDIA IN LONG-TERM CARE REBALANCING: A COMPARATIVE STATE
ANALYSIS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Goldstein, R. H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Miller, E. A.] Univ Massachusetts, McCormack Grad Sch Policy & Global Studies, Boston, MA 02125 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 548
EP 548
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003489
ER
PT J
AU Paquin, AM
Rudolph, JL
Quinlan, N
Salow, M
AF Paquin, A. M.
Rudolph, J. L.
Quinlan, N.
Salow, M.
TI PILL CLINIC: A POST-DISCHARGE MEDICATION SERVICE FOR OLDER VETERANS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Paquin, A. M.; Rudolph, J. L.; Quinlan, N.; Salow, M.] VA Boston Healthcare Syst, GRECC, Boston, MA USA.
[Paquin, A. M.; Salow, M.] VA Boston Healthcare Syst, Dept Pharm, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 557
EP 557
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003533
ER
PT J
AU Archambault, E
Hill, J
Lawrence, K
Kelly, B
Rudolph, JL
AF Archambault, E.
Hill, J.
Lawrence, K.
Kelly, B.
Rudolph, J. L.
TI COMING HOME FROM THE HOSPITAL: SUPPORT FOR VETERANS WITH COGNITIVE
IMPAIRMENT
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Archambault, E.; Hill, J.; Lawrence, K.; Kelly, B.; Rudolph, J. L.] VA Boston Healthcare Syst, Geriatr Res Educ & Clin Ctr, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 558
EP 558
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602003535
ER
PT J
AU Schulman-Green, DJ
Fennie, K
McCorkle, R
Bradley, E
Prigerson, H
Knobf, T
DiGiovanna, M
Dixon, J
AF Schulman-Green, D. J.
Fennie, K.
McCorkle, R.
Bradley, E.
Prigerson, H.
Knobf, T.
DiGiovanna, M.
Dixon, J.
TI VALIDATION OF AN INSTRUMENT TO MEASURE UNDERSTANDING OF CURATIVE,
PALLIATIVE AND HOSPICE CARE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Schulman-Green, D. J.; Fennie, K.; McCorkle, R.; Knobf, T.; Dixon, J.] Yale Univ, Sch Nursing, New Haven, CT 06536 USA.
[Prigerson, H.] Harvard Univ, Cambridge, MA 02138 USA.
[Prigerson, H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[DiGiovanna, M.] Yale Univ, Sch Med, New Haven, CT USA.
[McCorkle, R.; Bradley, E.] Yale Univ, Sch Publ Hlth, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 571
EP 571
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602004003
ER
PT J
AU Mlinac, M
Stamm, K
Lees, F
Saint, J
Mulligan, J
AF Mlinac, M.
Stamm, K.
Lees, F.
Saint, J.
Mulligan, J.
TI LONGITUDINAL PATTERNS OF GOAL MAINTENANCE AND RESILIENCE IN OLDER ADULTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Mlinac, M.] VA Boston Healthcare Syst, Boston, MA USA.
[Mlinac, M.] Harvard Univ, Sch Med, Boston, MA USA.
[Stamm, K.; Lees, F.; Saint, J.; Mulligan, J.] Univ Rhode Isl, Kingston, RI 02881 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 579
EP 579
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602004042
ER
PT J
AU Vuckovic, NH
Edes, T
Nichols, LO
AF Vuckovic, N. H.
Edes, T.
Nichols, L. O.
TI I COULDN'T MAKE IT WITHOUT THEM: PATIENT AND CAREGIVER PERSPECTIVE OF
HOME BASED PRIMARY CARE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Vuckovic, N. H.] Intel Corp, Hlth Res & Innovat, Beaverton, OR USA.
[Edes, T.] US Dept Vet Affairs, Washington, DC USA.
[Nichols, L. O.] Vet Affairs Med Ctr, Memphis, TN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 614
EP 614
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602004207
ER
PT J
AU Stephens, C
Covinsky, K
Blegen, MA
Lee, S
AF Stephens, C.
Covinsky, K.
Blegen, M. A.
Lee, S.
TI FALLS ARE A POWERFUL DETERMINANT OF ER USE BY NURSING HOME RESIDENTS
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Stephens, C.; Covinsky, K.; Blegen, M. A.; Lee, S.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Stephens, C.; Covinsky, K.; Lee, S.] San Francisco VA Med Ctr, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2011
VL 51
SU 2
BP 627
EP 627
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 936PH
UT WOS:000303602004268
ER
PT J
AU Gupta, P
Goyal, S
Tobias, JD
Prodhan, P
Purohit, P
Gossett, JM
Chow, V
Noviski, N
AF Gupta, Punkaj
Goyal, Sunali
Tobias, Joseph D.
Prodhan, Parthak
Purohit, Prashant
Gossett, Jeffrey M.
Chow, Vinca
Noviski, Natan
TI Risk factors associated with hospital admission among healthy children
with adenovirus infection
SO TURKISH JOURNAL OF PEDIATRICS
LA English
DT Article
DE adenovirus; hospital admission; respiratory distress; wheezing; acute
gastroenteritis
ID RESPIRATORY SYNCYTIAL VIRUS; BRONCHIOLITIS OBLITERANS;
CLINICAL-FEATURES; YOUNG-CHILDREN; TRACT INFECTION; INFANTS;
EPIDEMIOLOGY; PNEUMONIA
AB Gupta P, Goyal S, Tobias JD, Prodhan P, Purohit P, Gossett JM, Chow V, Noviski N. Risk factors associated with hospital admission among healthy children with adenovirus infection. Turk J Pediatr 2011; 53: 597-603.
Adenovirus infections mimic bacterial infections on initial presentation in healthy children, leading to higher likelihood of hospital admission. The objective of this study was to identify risk factors associated with hospital admission in previously healthy children with adenovirus infection. This is a retrospective study of 125 previously healthy children, who tested positive with direct immunofluorescence assay (DFA) for adenoviral infection at our center between January 2001 and October 2007. The primary outcome of the study was the need for hospital admission. The relationship between clinical variables at initial emergency room (ER) presentation and need for hospital admission were explored using univariate and multivariate logistic regression models. The model's predictive value was investigated by calculating the area under the receiver operating characteristic (ROC) curve and Hosmer-Lemeshow test.
On stepwise multivariate logistic regression analysis, the presence of respiratory distress (odds ratio [OR]: 5.6; p=0.014), acute gastroenteritis (OR: 3.8; p=0.019) and wheezes at initial presentation (OR: 6.5; p=0.003) at the time of initial presentation in the ER were associated with need for hospital admission. For this model, the area under the ROC curve was 0.79, and there was no evidence of lack of fit on Hosmer-Lemeshow goodness-of-fit test (p=0.56). Our study identifies three risk factors, namely, respiratory distress, wheezing and acute gastroenteritis, associated with hospital admission for healthy children with adenoviral infections.
C1 [Gupta, Punkaj; Prodhan, Parthak] Univ Arkansas Med Ctr, Sect Pediat Cardiol & Crit Care, Little Rock, AR USA.
[Gossett, Jeffrey M.] Univ Arkansas Med Ctr, Biostat Program, Dept Pediat, Little Rock, AR USA.
[Goyal, Sunali] Univ Arkansas Med Ctr, Dept Ophthalmol, Little Rock, AR USA.
[Gupta, Punkaj; Purohit, Prashant; Noviski, Natan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Pediat Crit Care, Boston, MA USA.
[Tobias, Joseph D.] Nationwide Childrens Hosp, Dept Anesthesiol, Columbus, OH USA.
[Tobias, Joseph D.] Nationwide Childrens Hosp, Dept Pediat, Columbus, OH USA.
[Tobias, Joseph D.] Ohio State Univ, Columbus, OH 43210 USA.
[Chow, Vinca] Stanford Univ Med Ctr, Dept Med Educ, Palo Alto, CA USA.
RP Gupta, P (reprint author), Univ Arkansas Med Ctr, Sect Pediat Cardiol & Crit Care, Little Rock, AR USA.
NR 27
TC 2
Z9 2
U1 0
U2 1
PU TURKISH J PEDIATRICS
PI ANKARA
PA P K 66 SAMANPAZARI, 06240 ANKARA, TURKEY
SN 0041-4301
J9 TURKISH J PEDIATR
JI Turk. J. Pediatr.
PD NOV-DEC
PY 2011
VL 53
IS 6
BP 597
EP 603
PG 7
WC Pediatrics
SC Pediatrics
GA 911BA
UT WOS:000301691100001
PM 22389981
ER
PT J
AU Jue, JJS
Metlay, JP
AF Jue, J. Jane S.
Metlay, Joshua P.
TI Web-Based Health Resources at US Colleges: Early Patterns and Missed
Opportunities in Preventive Health
SO PREVENTING CHRONIC DISEASE
LA English
DT Article
ID STUDENT POPULATION; CONTROLLED-TRIAL; UNITED-STATES; INTERNET USE;
INFORMATION; ADOLESCENTS; INTERVENTIONS; TECHNOLOGY; PREVALENCE;
BEHAVIOR
AB Introduction
Web-based health resources on college websites have the potential to reach a substantial number of college students. The objective of this study was to characterize how colleges use their websites to educate about and promote health.
Methods
This study was a cross-sectional analysis of websites from a nationally representative sample of 426 US colleges. Reviewers abstracted information about Web-based health resources from college websites, namely health information, Web links to outside health resources, and interactive Web-based health programs.
Results
Nearly 60% of US colleges provided health resources on their websites, 49% provided health information, 48% provided links to outside resources, and 28% provided interactive Web-based health programs. The most common topics of Web-based health resources were mental health and general health.
Conclusion
We found widespread presence of Web-based health resources available from various delivery modes and covering a range of health topics. Although further research in this new modality is warranted, Web-based health resources hold promise for reaching more US college students.
C1 [Jue, J. Jane S.] Philadelphia VA Med Ctr, Dept Vet Affairs, Philadelphia, PA USA.
[Jue, J. Jane S.] Univ Penn, Sch Med, Robert Wood Johnson Fdn Clin Scholars Program, Philadelphia, PA 19104 USA.
RP Jue, JJS (reprint author), ECRI Inst, 5200 Butler Pike, Plymouth Meeting, PA 19462 USA.
EM janejuemd@gmail.com
FU Robert Wood Johnson Foundation at the University of Pennsylvania;
Department of Veterans Affairs; University of Pennsylvania
[K24-AI073957]
FX During the course of this study, Dr Jue was funded by the Robert Wood
Johnson Foundation Clinical Scholars Program at the University of
Pennsylvania in partnership with the Department of Veterans Affairs. Dr
Metlay was funded by a Mid-Career Patient Oriented Investigator Award
(K24-AI073957) at the University of Pennsylvania. Neither funding
entities had a role in the design or conduct of the study; collection,
management, analysis, or interpretation of the data; nor preparation,
review, or approval of the manuscript.
NR 30
TC 1
Z9 1
U1 2
U2 5
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1545-1151
J9 PREV CHRONIC DIS
JI Prev. Chronic Dis.
PD NOV
PY 2011
VL 8
IS 6
AR A138
PG 14
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 896JZ
UT WOS:000300563000021
PM 22005631
ER
PT J
AU Peacock, JM
Keo, HH
Duval, S
Baumgartner, I
Oldenburg, NC
Jaff, MR
Henry, TD
Yu, XH
Hirsch, AT
AF Peacock, James M.
Keo, Hong H.
Duval, Sue
Baumgartner, Iris
Oldenburg, Niki C.
Jaff, Michael R.
Henry, Timothy D.
Yu, Xinhua
Hirsch, Alan T.
TI The Incidence and Health Economic Burden of Ischemic Amputation in
Minnesota, 2005-2008
SO PREVENTING CHRONIC DISEASE
LA English
DT Article
ID LOWER-EXTREMITY; VASCULAR-DISEASE; BYPASS-SURGERY; UNITED-STATES;
MANAGEMENT; ANGIOPLASTY; DISPARITIES; PREVALENCE; CARE
AB Introduction
Critical limb ischemia (CLI) is the most severe manifestation of peripheral artery disease (PAD), is associated with high rates of myocardial infarction, stroke, and amputation, and has a high health economic cost. The objective of this study was to estimate the incidence of lower limb amputation, the most serious consequence of CLI, and to create a surveillance methodology for the incidence of ischemic amputation in Minnesota.
Methods
We assessed the incidence of ischemic amputation using all inpatient hospital discharge claims in Minnesota from 2005 through 2008. We identified major and minor ischemic amputations via the International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) procedure codes for lower limb amputation not due to trauma or cancer and assessed geographic and demographic differences in the incidence of ischemic amputation.
Results
The age-adjusted annual incidence of lower limb ischemic amputation in Minnesota during the 4-year period was 20.0 per 100,000 (95% confidence interval, 19.4-20.6). Amputations increased significantly with age, were more common in men and in people with diabetes, and were slightly more common in rural residents. The number of amputation-related hospitalizations was steady over 4 years. The median total charge for each amputation was $32,129, and cumulative inpatient hospitalization charges were $56.5 million in 2008.
Conclusion
The incidence of ischemic amputation is high and results in major illness and health economic costs. These data represent the first population-based estimate of ischemic amputation at the state level and provide a national model for state-based surveillance.
C1 [Keo, Hong H.; Duval, Sue; Oldenburg, Niki C.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Keo, Hong H.; Duval, Sue; Henry, Timothy D.] Minneapolis Heart Inst Fdn, Minneapolis, MN USA.
[Keo, Hong H.; Baumgartner, Iris] Univ Hosp Bern, Div Angiol, Swiss Cardiovasc Ctr, CH-3010 Bern, Switzerland.
[Jaff, Michael R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Jaff, Michael R.] Harvard Univ, Sch Med, Boston, MA USA.
[Yu, Xinhua] Univ Memphis, Sch Publ Hlth, Dept Epidemiol & Biostat, Memphis, TN 38152 USA.
[Hirsch, Alan T.] Univ Minnesota, Sch Med, Cardiovasc Div, Minneapolis, MN 55455 USA.
[Hirsch, Alan T.] Univ Minnesota, Sch Med, Lillihei Heart Inst, Minneapolis, MN 55455 USA.
RP Peacock, JM (reprint author), Minnesota Dept Hlth, Ctr Hlth Promot, Hlth Promot & Chron Dis Div, POB 64882, St Paul, MN 55164 USA.
EM james.peacock@state.mn.us
FU Centers for Disease Control and Prevention [5U50DP000721-04]
FX This work was funded by grant no. 5U50DP000721-04 from the Centers for
Disease Control and Prevention.
NR 28
TC 16
Z9 16
U1 0
U2 3
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1545-1151
J9 PREV CHRONIC DIS
JI Prev. Chronic Dis.
PD NOV
PY 2011
VL 8
IS 6
AR A141
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 896JZ
UT WOS:000300563000024
PM 22005634
ER
PT J
AU Hamburger, M
Baraf, HSB
Adamson, TC
Basile, J
Bass, L
Cole, B
Doghramji, PP
Guadagnoli, GA
Hamburger, F
Harford, R
Lieberman, JA
Mandel, DR
Mandelbrot, DA
McClain, BP
Mizuno, E
Morton, AH
Mount, DB
Pope, RS
Rosenthal, KG
Setoodeh, K
Skosey, JL
Edwards, NL
AF Hamburger, Max
Baraf, Herbert S. B.
Adamson, Thomas C., III
Basile, Jan
Bass, Lewis
Cole, Brent
Doghramji, Paul P.
Guadagnoli, Germano A.
Hamburger, Frances
Harford, Regine
Lieberman, Joseph A., III
Mandel, David R.
Mandelbrot, Didier A.
McClain, Bonny P.
Mizuno, Eric
Morton, Allan H.
Mount, David B.
Pope, Richard S.
Rosenthal, Kenneth G.
Setoodeh, Katy
Skosey, John L.
Edwards, N. Lawrence
TI 2011 Recommendations for the Diagnosis and Management of Gout and
Hyperuricemia
SO PHYSICIAN AND SPORTSMEDICINE
LA English
DT Article
DE gout; hyperuricemia; guideline recommendations; rheumatology
ID SERUM URIC-ACID; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; INDEPENDENT
RISK-FACTOR; POPULATION-BASED COHORT; URATE-LOWERING THERAPY;
TREATMENT-FAILURE GOUT; CHRONIC-RENAL-FAILURE; METABOLIC SYNDROME;
DOUBLE-BLIND; LONG-TERM
AB Gout is a major health problem in the United States; it affects 8.3 million people, which is approximately 4% of the adult population. Gout is most often diagnosed and managed in primary care practices; thus, primary care physicians have a significant opportunity to improve patient outcomes. Following publication of the 2006 European League Against Rheumatism (EULAR) gout guidelines, significant new evidence has accumulated, and new treatments for patients with gout have become available. It is the objective of these 2011 recommendations to update the 2006 EULAR guidelines, paying special attention to the needs of primary care physicians. The revised 2011 recommendations are based on the Grading of Recommendations Assessment, Development, and Evaluation approach as an evidence-based strategy for rating quality of evidence and grading the strength of recommendation formulated for use in clinical practice. A total of 26 key recommendations, 10 for diagnosis and 16 for management, of patients with gout were evaluated, resulting in important updates for patient care. The presence of monosodium urate crystals and/or tophus and response to colchicine have the highest clinical diagnostic value. The key aspect of effective management of an acute gout attack is initiation of treatment within hours of symptom onset. Low-dose colchicine is better tolerated and is as effective as a high dose. When urate-lowering therapy (ULT) is indicated, the xanthine oxidase inhibitors allopurinol and febuxostat are the options of choice. Febuxostat can be prescribed at unchanged doses for patients with mild-to-moderate renal or hepatic impairment. The target of ULT should be a serum uric acid level that is 6 mg/dL. For patients with refractory and tophaceous gout, intravenous pegloticase is a new treatment option. This article is a summary of the 2011 clinical guidelines published in Postgraduate Medicine. This article provides a streamlined, accessible overview intended for quick review by primary care physicians, with the full guidelines being a resource for those seeking additional background information and expanded discussion.
C1 [Hamburger, Max] Rheumatol Associates Long Isl, Melville, NY 11747 USA.
[Hamburger, Max] SUNY Stony Brook, Stony Brook, NY USA.
[Hamburger, Max] Amer Soc Clin Rheumatologists, Melville, NY USA.
[Baraf, Herbert S. B.] George Washington Univ, Wheaton, IL USA.
[Adamson, Thomas C., III] Sharp Rees Stealy Med Grp, Div Rheumatol, San Diego, CA USA.
[Basile, Jan] Med Univ S Carolina, Ralph H Johnson VA Med Ctr, Seinsheimer Cardiovasc Hlth Program, Div Gen Internal Med, Charleston, SC 29425 USA.
[Bass, Lewis] NYCOM, Ridgewood, NY USA.
[Bass, Lewis] Touro Coll Osteopath Med TouroCOM, Ridgewood, NY USA.
[Doghramji, Paul P.] Ursinus Coll, Collegeville, PA USA.
[Guadagnoli, Germano A.] Bridgeport Hosp, Rheumatol Sect, Bridgeport, CT USA.
[Hamburger, Frances] Rheumatol Associates Long Isl, Psychol Serv, Dix Hills, NY USA.
[Lieberman, Joseph A., III] Jefferson Med Coll, Hockessin, DE USA.
[Mandelbrot, Didier A.; Mount, David B.] Harvard Univ, Sch Med, Boston, MA USA.
[McClain, Bonny P.] ASSESSmint Analyt & Outcomes, Greensboro, NC USA.
[Mizuno, Eric] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Morton, Allan H.] Michigan State Univ, Coll Osteopath Med, E Lansing, MI 48824 USA.
[Mount, David B.] Brigham & Womens Hosp, Div Renal, Boston, MA 02115 USA.
[Pope, Richard S.] Quinnipiac Univ, Dept PA Studies, Hamden, CT USA.
[Skosey, John L.] Univ Chicago, Chicago, IL 60637 USA.
[Edwards, N. Lawrence] Univ Florida, Dept Med, Gainesville, FL USA.
RP Hamburger, M (reprint author), Rheumatol Associates Long Isl, 1895 Walt Whitman Rd, Melville, NY 11747 USA.
EM mcapacious@aol.com
FU Regine Harford; MS; MSTPC; URL Pharma; American Society of Clinical
Rheumatologists; Mary Shah; MLS; medical library archivist and Caroline
Marshall; Danbury Hospital Library; Abbott; Amgen; Bristol-Myers Squibb;
Crescendo Bioscience; Genentech; Janssen Biotech; Takeda
Pharmaceuticals; North America, Inc; NHLBI (SPRINT); AstraZeneca; Biogen
Idec; Celegene; Merck Sharp and Dohme; Novartis; Pfizer; Roche; Stryker;
VQ OrthoCare; Nuon Therapeutics
FX The authors wish to gratefully acknowledge the invaluable editorial
support from Regine Harford, MS, MSTPC, and statistical support from
Bonny McClain, MS, DC of ASSESS-mint Analytics. Funding for the
preparation of the article was received from URL Pharma, and from the
American Society of Clinical Rheumatologists. The authors also wish to
acknowledge the invaluable support from Mary Shah, MLS, medical library
archivist and Caroline Marshall, MLS, health sciences librarian, both
from Danbury Hospital Library.; Max Hamburger, MD is a member of the
speakers' bureau for Abbott, Amgen, Bristol-Myers Squibb, Genentech,
GSK, HGSI, Novartis, and UCB; is a consultant for Bristol-Myers Squibb,
Genentech, and UCB; is in receipt of educational grants in support of
CME activities from Abbott, Amgen, Bristol-Myers Squibb, Crescendo
Bioscience, Genentech, Janssen Biotech, Takeda Pharmaceuticals, North
America, Inc, and URL Pharma. Herbert S. B. Baraf, MD is a member of the
speakers' bureau for Savient Pharmaceuticals and Takeda Pharmaceuticals,
North America, Inc; is a consultant for Ardea Biosciences and Savient
Pharmaceuticals; is an investigator for Ardea Biosciences, Metabolex,
Novartis, Regeneron, Savient Pharmaceuticals., and Takeda
Pharmaceuticals, North America, Inc; and is a member of the advisory
board for Takeda Pharmaceuticals, North America, Inc. Thomas C. Adamson
III, MD, FACP, CPE is a member of the speakers' bureau for
sanofi-aventis, Takeda Pharmaceuticals, North America, Inc, and Warner
Chilcott; and is a consultant for Sanofi-Aventis and Takeda
Pharmaceuticals, North America, Inc. Jan Basile, MD is a member of the
speakers' bureau for Boehringer Ingelheim, Daiichi-Sankyo, Forest
Laboratories, and Takeda Pharmaceuticals, North America, Inc; is a
consultant for Daiichi-Sankyo, Eli Lilly/Boehringer Ingelheim, Forest
Laboratories, and Takeda Pharmaceuticals, North America, Inc; and has
received grant/research support from the NHLBI (SPRINT). Lewis Bass, DO,
FACOFP discloses no conflicts of interest. Brent Cole, MD discloses no
conflicts of interest. Paul P. Doghramji, MD is a member of the
speakers' bureau and advisory board for URL Pharma. Germano A.
Guadagnoli, MD is a member of the speakers' bureau for Amgen/Pfizer,
Forest Laboratories, and Takeda Pharmaceuticals, North America, Inc.
Frances Hamburger, PhD is employed by Miller Professional Group. Regine
Harford, MS, MSTPC discloses no conflicts of interest. Joseph A.
Lieberman III, MD, MPH is a member of the advisory board for Takeda
Pharmaceuticals, North America, Inc and URL Pharma. David R. Mandel, MD
is a member of the speakers' bureau for Abbott, Amgen, Auxilium
Pharmaceuticals, Forest Laboratories, Forest Pharmaceuticals,
GlaxoSmithKline, Lilly, Novartis, Savient Pharmaceuticals, Sunovion
Pharmaceuticals, Takeda Pharmaceuticals, North America, Inc, and UCB; is
a member of the advisory board for Amgen, Auxilium Pharmaceuticals,
Crescendo Bioscience, Pfizer, and Savient Pharmaceuticals; is a
consultant for Amgen, Auxilium Pharmaceuticals; Crescendo Bioscience,
Pfizer, Savient Pharmaceuticals, and UCB; and has received research
support from Abbott, Amgen, AstraZeneca, Biogen Idec, Celegene, Janssen
Biotech, Crescendo Bioscience, Genentech, Merck Sharp and Dohme,
Novartis, Pfizer, Roche, Stryker, and VQ OrthoCare. Didier A.
Mandelbrot, MD discloses no conflicts of interest. Bonny P. McClain, MS,
DC discloses no conflicts of interest. Eric Mizuno, MD is an advisor for
Takeda Pharmaceuticals, North America, Inc. Allan H. Morton, DO is a
member of the speakers' bureau for Abbott, Amgen, Bristol-Myers Squibb,
Genentech, Pfizer, Takeda Pharmaceuticals, North America, Inc, Savient
Pharmaceuticals, UCB, URL Pharma, and Warner Chilcott; and is a
consultant for Amgen, Bristol-Myers Squibb, Novartis, Pfizer, Savient
Pharmaceuticals, UCB, and URL Pharma. David B.; Mount, MD has received
grant support from Nuon Therapeutics; is on the medical advisory board
and educational planning committees for Savient Pharmaceuticals; and
provides internal talks for Takeda Pharmaceuticals, North America, Inc;
nd has pending grants with Takeda Pharmaceuticals, North America, Inc
and URL Pharma. Richard S. Pope, MPAS, PA-C, DFAAPA is a member of the
speakers' bureau for AstraZeneca, Amgen, Takeda Pharmaceuticals, North
America, Inc, UCB, and URL Pharma. Kenneth G. Rosenthal, MD, PC
discloses no conflicts of interest. Katy Setoodeh, MD, FACR is a member
of the speakers' bureau for Amgen and Human Genome Sciences. John L.
Skosey, MD, PhD, FACR, FACP is an advisory board participant for
Cardinal Health; a director of Theratest Laboratories; and a stockholder
in Amgen. N. Lawrence Edwards, MD, FACP, FACR is a consultant for Ardea
Biosciences, Savient Pharmaceuticals, Novartis, and Takeda
Pharmaceuticals, North America, Inc.
NR 137
TC 20
Z9 26
U1 4
U2 20
PU JTE MULTIMEDIA
PI BERWYN
PA 1235 WESTLAKES DR, STE 220, BERWYN, PA 19312 USA
SN 0091-3847
J9 PHYSICIAN SPORTSMED
JI Physician Sportsmed.
PD NOV
PY 2011
VL 39
IS 4
BP 98
EP 123
DI 10.3810/psm.2011.11.1946
PG 26
WC Primary Health Care; Orthopedics; Sport Sciences
SC General & Internal Medicine; Orthopedics; Sport Sciences
GA 893VD
UT WOS:000300384200016
PM 22293773
ER
PT J
AU Brooks-Worrell, B
Tree, T
Mannering, SI
Durinovic-Bello, I
James, E
Gottlieb, P
Wong, S
Zhou, Z
Yang, L
Cilio, CM
Reichow, J
Menart, B
Rutter, R
Schreiner, R
Pham, M
de Marquesini, LP
Lou, O
Scotto, M
Mallone, R
Schloot, NC
AF Brooks-Worrell, B.
Tree, T.
Mannering, S. I.
Durinovic-Bello, I.
James, E.
Gottlieb, P.
Wong, S.
Zhou, Z.
Yang, L.
Cilio, C. M.
Reichow, J.
Menart, B.
Rutter, R.
Schreiner, R.
Pham, M.
de Marquesini, L. Petrich
Lou, O.
Scotto, M.
Mallone, R.
Schloot, N. C.
CA Immunology Diabet Soc
TI Comparison of cryopreservation methods on T-cell responses to islet and
control antigens from type 1 diabetic patients and controls
SO DIABETES-METABOLISM RESEARCH AND REVIEWS
LA English
DT Article; Proceedings Paper
CT 11th International Congress of the Immunology-of-Diabetes-Society (IDS)
CY OCT 31-NOV 03, 2010
CL Incheon, SOUTH KOREA
SP Immunol Diabet Soc (IDS)
DE T cells; proliferation; ELISPOT; tetramer; cryopreservation; CFSE; islet
antigens; type 1 diabetes
ID BLOOD MONONUCLEAR-CELLS; PROINSULIN; IMMUNOLOGY; PHENOTYPE; PROTEINS;
WORKSHOP; SUBSETS; SOCIETY; LYT-2+; L3T4+
AB Background Type 1 diabetes (T1D) is a cell-mediated autoimmune disease characterized by destruction of the pancreatic islet cells. The use of cryopreserved cells is preferable to the use of freshly isolated cells to monitor clinical trials to decrease assay and laboratory variability.
Methods The T-Cell Workshop Committee of the Immunology of Diabetes Society compared two widely accepted T-cell freezing protocols (warm and cold) to freshly isolated peripheral blood mononuclear cells from patients with T1D and controls in terms of recovery, viability, cell subset composition, and performance in functional assays currently in use in T1D-related research. Nine laboratories participated in the study with four different functional assays included.
Results The cold freezing method yielded higher recovery and viability compared with the warm freezing method. Irrespective of freezing protocol, B cells and CD8+ T cells were enriched, monocyte fraction decreased, and islet antigen-reactive responses were lower in frozen versus fresh cells. However, these results need to take in to account that the overall response to islet autoantigens was low in some assays.
Conclusions In the current study, none of the tested T-cell functional assays performed well using frozen samples. More research is required to identify a freezing method and a T-cell functional assay that will produce responses in patients with T1D comparable to responses using fresh peripheral blood mononuclear cells. Copyright (C) 2011 John Wiley & Sons, Ltd.
C1 [Brooks-Worrell, B.] Univ Washington, Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA 98108 USA.
[Tree, T.] Kings Coll London, Sch Med, London WC2R 2LS, England.
[Mannering, S. I.] Univ Melbourne, Dept Med, St Vincents Inst Med Res, Fitzroy, Vic 3065, Australia.
[Durinovic-Bello, I.; James, E.] Benaroya Res Inst, Seattle, WA USA.
[Gottlieb, P.] Univ Colorado, Sch Med, Barbara Davis Ctr Childhood Diabet, Dept Pediat & Med, Denver, CO USA.
[Wong, S.] Cardiff Univ, Ctr Endocrine & Diabet Sci, Dept Med, Sch Med, Cardiff, S Glam, Wales.
[Zhou, Z.; Yang, L.] Cent S Univ, Sch Med, Changsha, Hunan, Peoples R China.
[Cilio, C. M.] Lund Univ, Dept Sci, Cellular Autoimmun Unit, Malmo, Sweden.
[Reichow, J.] Seattle Inst Biomed & Clin Res, Seattle, WA USA.
[Menart, B.; Rutter, R.; Schreiner, R.; Pham, M.; Schloot, N. C.] Univ Dusseldorf, German Diabet Ctr, Inst Clin Diabetol, D-40225 Dusseldorf, Germany.
[de Marquesini, L. Petrich] Univ Bristol, Henry Wellcome Lab Integrat Neurosci & Endocrinol, Bristol, Avon, England.
[Lou, O.] JDRF Int, JDRF Canadian Clin Trial Network, Toronto, ON, Canada.
[Scotto, M.; Mallone, R.] Hop St Vincent de Paul, INSERM, U986, DeAR Lab Avenir, F-75674 Paris, France.
[Schloot, N. C.] Univ Dusseldorf, Clin Metab Dis, D-40225 Dusseldorf, Germany.
RP Brooks-Worrell, B (reprint author), Univ Washington, Vet Affairs Puget Sound Hlth Care Syst, 1660 S Columbian Way, Seattle, WA 98108 USA.
EM bbrooks@u.washington.edu
RI Mallone, Roberto/H-4430-2013;
OI James, Eddie/0000-0002-7217-5729
NR 25
TC 9
Z9 9
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1520-7552
J9 DIABETES-METAB RES
JI Diabetes-Metab. Res. Rev.
PD NOV
PY 2011
VL 27
IS 8
SI SI
BP 737
EP 745
DI 10.1002/dmrr.1245
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 889XD
UT WOS:000300108000004
PM 22069253
ER
PT J
AU Medarova, Z
Greiner, DL
Ifediba, M
Dai, GP
Bolotin, E
Castillo, G
Bogdanov, A
Kumar, M
Moore, A
AF Medarova, Zdravka
Greiner, Dale L.
Ifediba, Marytheresa
Dai, Guangping
Bolotin, Elijah
Castillo, Gerardo
Bogdanov, Alexei
Kumar, Mohanraja
Moore, Anna
TI Imaging the pancreatic vasculature in diabetes models
SO DIABETES-METABOLISM RESEARCH AND REVIEWS
LA English
DT Article; Proceedings Paper
CT 11th International Congress of the Immunology-of-Diabetes-Society (IDS)
CY OCT 31-NOV 03, 2010
CL Incheon, SOUTH KOREA
SP Immunol Diabet Soc (IDS)
DE imaging; inflammation; vasculature; diabetes; protected graft copolymer
ID MAGNETIC-RESONANCE MICROSCOPY; ISLET BLOOD PERFUSION; PERMEABILITY;
FLOW; RAT; MOUSE; STREPTOZOTOCIN; VOLUME; PHASE; GRAFT
AB Background Vascular parameters, such as vascular volume, flow, and permeability, are important disease biomarkers for both type 1 and type 2 diabetes. Therefore, it is essential to develop approaches to monitor the changes in pancreatic microvasculature non-invasively.
Methods Here, we describe the application of the long-circulating, paramagnetic T1 contrast agent, protected Graft Copolymer bearing covalently linked gadolinium diethylenetriaminepentaacetic acid residues and labelled with fluorescein (PGC-GdDTPA-F) for the non-invasive semi-quantitative evaluation of vascular changes in diabetic models using magnetic resonance imaging.
Results We observed a significantly higher accumulation of protected graft copolymer bearing covalently linked gadolinium diethylenetriaminepentaacetic acid residues and labelled with fluorescein in the pancreata of BBDR rats induced to develop diabetes, as compared to non-diabetic controls at 1 h post-injection. No differences were seen in the blood pool, kidney, or muscle, indicating that the effect is specific to the diabetic pancreas. Fluorescence microscopy revealed a marked increase in contrast agent availability in the pancreas with the development of the pathology. Similar changes were noted in the homozygous Lepr(db) mouse model of type 2 diabetes. This effect appeared to result both from the increase of vascular volume and permeability.
Conclusions High-molecular weight paramagnetic blood volume contrast agents are valuable for the in vivo definition of pancreatic microvasculature dynamics by magnetic resonance imaging. The increase in vascular volume and permeability, associated with diabetic inflammation, can be monitored non-invasively and semi-quantitatively by magnetic resonance imaging in diabetic BBDR rats. This imaging strategy represents a valuable research tool for better understanding of the pathologic process. Copyright (C) 2011 John Wiley & Sons, Ltd.
C1 [Medarova, Zdravka; Ifediba, Marytheresa; Dai, Guangping; Kumar, Mohanraja; Moore, Anna] Harvard Univ, Sch Med, Massachusetts Gen Hosp,Dept Radiol, Mol Imaging Lab,Athinoula A Martinos Ctr Biomed I, Charlestown, MA 02129 USA.
[Greiner, Dale L.] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA USA.
[Bolotin, Elijah; Castillo, Gerardo] PharmaIN Corp, Seattle, WA USA.
[Bogdanov, Alexei] Univ Massachusetts, Sch Med, Dept Radiol, Worcester, MA USA.
[Bogdanov, Alexei] Univ Massachusetts, Sch Med, Dept Cell Biol, Worcester, MA 01655 USA.
RP Moore, A (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp,Dept Radiol, Mol Imaging Lab,Athinoula A Martinos Ctr Biomed I, Bldg 75,13th St, Charlestown, MA 02129 USA.
EM amoore@helix.mgh.harvard.edu
FU NIDDK NIH HHS [R44 DK069727, DK080264, P30 DK032520, R43 DK069727, R24
DK080264, DK069727, U01 DK089572, DK32520, DK089572]
NR 26
TC 5
Z9 5
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1520-7552
J9 DIABETES-METAB RES
JI Diabetes-Metab. Res. Rev.
PD NOV
PY 2011
VL 27
IS 8
SI SI
BP 767
EP 772
DI 10.1002/dmrr.1249
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 889XD
UT WOS:000300108000008
PM 22069257
ER
PT J
AU Klupa, T
Solecka, I
Nowak, N
Szopa, M
Kiec-Wilk, B
Skupien, J
Trybul, I
Matejko, B
Mlynarski, W
Malecki, MT
AF Klupa, T.
Solecka, I.
Nowak, N.
Szopa, M.
Kiec-Wilk, B.
Skupien, J.
Trybul, I.
Matejko, B.
Mlynarski, W.
Malecki, M. T.
TI The Influence of Dietary Carbohydrate Content on Glycaemia in Patients
with Glucokinase Maturity-onset Diabetes of the Young
SO JOURNAL OF INTERNATIONAL MEDICAL RESEARCH
LA English
DT Article
DE MATURITY-ONSET DIABETES OF THE YOUNG (MODY); MONOGENIC DIABETES;
GLUCOKINASE (GCK); DIET; CARBOHYDRATE; GLYCAEMIC CONTROL
ID HIGH PREVALENCE; BLOOD-GLUCOSE; TYPE-2 MODY-2; MUTATIONS; MELLITUS;
DEFINITION; GENE
AB Mutations in the glucokinase (GCK) gene result in maturity-onset diabetes of the young (MODY). Pharmacotherapy is not effective in GCK MODY. Thus, nutritional intervention seems to be the only therapeutic option. This study evaluated the effect of the quantity of dietary carbohydrate on glucose levels in 10 GCK mutation carriers: seven with MODY and three with prediabetes. All patients were exposed to high-carbohydrate diets for 2 days and then switched to low-carbohydrate diets (60% versus 25% of the daily calorie intake) for another 2 days, after a 1-day washout. Glucose levels were assessed by continuous blood glucose monitoring. In patients with GCK MODY on high-carbohydrate diets, glucose levels were significantly higher, and more hyperglycaemic episodes occurred, compared with patients on low-carbohydrate diets. This short-term observational study suggested that diets with a modestly limited carbohydrate content may improve glycaemic control in patients with GCK MODY.
C1 [Klupa, T.; Nowak, N.; Szopa, M.; Kiec-Wilk, B.; Trybul, I.; Matejko, B.; Malecki, M. T.] Jagiellonian Univ, Coll Med, Dept Metab Dis, PL-31501 Krakow, Poland.
[Szopa, M.] Jagiellonian Univ, Coll Med, Dept Med Educ, PL-31501 Krakow, Poland.
[Klupa, T.; Solecka, I.; Szopa, M.; Kiec-Wilk, B.; Trybul, I.; Malecki, M. T.] Krakow Univ Hosp, Krakow, Poland.
[Skupien, J.] Joslin Diabet Ctr, Sect Genet & Epidemiol, Boston, MA 02215 USA.
[Mlynarski, W.] Med Univ Lodz, Dept Paediat, Lodz, Poland.
RP Malecki, MT (reprint author), Jagiellonian Univ, Coll Med, Dept Metab Dis, 15 Kopernika St, PL-31501 Krakow, Poland.
EM malecki_malecki@yahoo.com
FU EU [HEALTH-F2-2008-223211]; Jagiellonian University Medical College
[K/ZDS/002310]
FX This study was supported by the EU Framework 7 CEED3 grant
(HEALTH-F2-2008-223211) and by funds from the Jagiellonian University
Medical College (K/ZDS/002310). We are grateful to Ms Aleksandra Malecka
for her editorial help in the preparation of the manuscript.
NR 21
TC 4
Z9 4
U1 0
U2 1
PU FIELD HOUSE PUBLISHING LLP
PI WORTHING
PA 6 SOMPTING AVENUE, WORTHING, BN14 8HN, ENGLAND
SN 0300-0605
J9 J INT MED RES
JI J. Int. Med. Res.
PD NOV-DEC
PY 2011
VL 39
IS 6
BP 2296
EP 2301
PG 6
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 887HC
UT WOS:000299916500027
PM 22289546
ER
PT J
AU Finlayson, E
Maselli, J
Steinman, MA
Rothberg, MB
Lindenauer, PK
Auerbach, AD
AF Finlayson, Emily
Maselli, Judith
Steinman, Michael A.
Rothberg, Michael B.
Lindenauer, Peter K.
Auerbach, Andrew D.
TI Inappropriate Medication Use in Older Adults Undergoing Surgery: A
National Study
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE surgery; potentially inappropriate medications (PIMs); older adults
ID POTENTIALLY INAPPROPRIATE; ADMINISTRATIVE DATA; SURGICAL-PATIENTS;
MEPERIDINE USE; HIP FRACTURE; DELIRIUM; OUTCOMES; INDICATORS; CRITERIA;
IMPACT
AB OBJECTIVES: To determine the prevalence and factors associated with use of potentially inappropriate medications (PIMs) in older adults undergoing surgery.
DESIGN: Retrospective cohort study.
SETTING: Three hundred seventy-nine acute care hospitals participating in the nationally representative Perspective database (2006-2008).
PARTICIPANTS: Individuals aged 65 and older under going major inpatient gastrointestinal, gynecological, urological, and orthopedic surgery (N=272,351).
MEASUREMENTS: Medications were classified as PIMs using previously published criteria defining 33 medications deemed potentially inappropriate in people aged 65 and older. Information about participant and provider characteristics and administration of PIMs was obtained from hospital discharge file data. Logistic regression techniques were used to examine factors associated with use of PIMs in the perioperative period.
RESULTS: One-quarter of participants received at least one PIM during their surgical admission. Meperidine was the most frequently prescribed PIM (37,855, 14% of participants). In adjusted analysis, PIM use was less likely as age advanced (adjusted odds ratio (AOR) = 0.98 per year of age, 95% confidence interval (CI) = 0.97-0.98) and in men (AOR = 0.83, 95% CI = 0.81-0.85). PIMs were more likely to be prescribed to participants cared for by orthopedic surgeons than for those cared for by general surgeons (AOR = 1.22, 95% CI = 1.08-1.40). Participants undergoing surgery in the West (AOR = 1.79, 95% CI = 1.02-3.16) and South (AOR = 2.24, 95% CI = 1.38-3.64) were more likely to receive a PIM than those in the Northeast.
CONCLUSION: Receipt of PIMs in older adults undergoing surgery is common and varies widely between providers and geographic regions and according to participant characteristics. Interventions aimed at reducing the use of PIMs in the perioperative period should be considered in quality improvement efforts. J Am Geriatr Soc 59:2139-2144, 2011.
C1 [Finlayson, Emily] Univ Calif San Francisco, Philip R Lee Inst Hlth Policy Studies, San Francisco, CA 94118 USA.
[Finlayson, Emily] Univ Calif San Francisco, Dept Surg, San Francisco, CA 94118 USA.
[Maselli, Judith; Auerbach, Andrew D.] Univ Calif San Francisco, Div Hosp Med, San Francisco, CA 94118 USA.
[Steinman, Michael A.] Univ Calif San Francisco, Div Geriatr, Dept Med, San Francisco, CA 94118 USA.
[Steinman, Michael A.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Rothberg, Michael B.; Lindenauer, Peter K.] Baystate Med Ctr, Ctr Qual Care Res, Springfield, MA USA.
[Rothberg, Michael B.; Lindenauer, Peter K.] Tufts Univ, Sch Med, Dept Med, Boston, MA 02111 USA.
RP Finlayson, E (reprint author), Univ Calif San Francisco, Philip R Lee Inst Hlth Policy Studies, 3333 Calif St, San Francisco, CA 94118 USA.
EM emily.finlayson@ucsfmedctr.org
FU National Heart, Blood, Lund Institute [K24HL098372]; National Institute
on Aging [K08AG028965]; American Federation for Aging Research
[K23AG030999]
FX Work on this study was funded in part by National Heart, Blood, Lund
Institute Award K24HL098372 to Dr. Auerbach. Dr. Finlayson was supported
by National Institute on Aging/Paul B. Beeson Clinical Scientist
Development Award in Aging K08AG028965. Dr. Steinman was supported by
the National Institute on Aging and the American Federation for Aging
Research (K23AG030999).
NR 23
TC 8
Z9 8
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-8614
EI 1532-5415
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD NOV
PY 2011
VL 59
IS 11
BP 2139
EP 2144
DI 10.1111/j.1532-5415.2011.03567.x
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 853FG
UT WOS:000297411000020
PM 21883113
ER
PT J
AU Wong, CH
Landefeld, CS
AF Wong, Chek Hooi
Landefeld, C. Seth
TI Academic Geriatrics in Singapore
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE education; research; geriatrics
ID CARE; MEDICINE; POPULATION; EDUCATION
AB Singapore is one of the fastest-aging countries in the world. The proportion of adults aged 65 and older is projected to increase from 8.7% to 20% over the next 20 years. The country has developed various strategies to meet the needs of this increase in older adults. There is an acute shortage of geriatricians and a need to train more healthcare workers to care for older adults. Geriatric medicine is a relatively new specialty, and a small number of geriatricians have been tasked with providing an increasing load of clinical service, education, and research. Hence, there is a need to develop a cohesive structure of support for faculty development and retention, advanced specialty trainee recruitment, leadership in medical education, research, and clinical service to care for the rapidly aging population. In addition, geriatric medicine is primarily a hospital-based specialty in Singapore. There is still opportunity to collaborate and improve the academic and practice integration of geriatric medicine into primary care and intermediate and long-term care where it is most needed. J Am Geriatr Soc 59:2145-2150, 2011.
C1 [Wong, Chek Hooi] Khoo Teck Puat Hosp, Dept Geriatr Med, Singapore 768828, Singapore.
[Landefeld, C. Seth] Univ Calif San Francisco, Div Geriatr, San Francisco, CA 94143 USA.
[Landefeld, C. Seth] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Wong, CH (reprint author), Khoo Teck Puat Hosp, Dept Geriatr Med, 90 Yishun Cent, Singapore 768828, Singapore.
EM chekhooi@yahoo.com
FU U.S., Department of State, Bureau of Educational and Cultural Affairs
FX Chek Hooi Wong and C. Seth Landefeld both state no financial interest,
stock, or derived direct financial benefit. Chek Hooi Wong was funded by
a Fulbright Singapore Researcher Program, U.S., Department of State,
Bureau of Educational and Cultural Affairs.
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PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD NOV
PY 2011
VL 59
IS 11
BP 2145
EP 2150
DI 10.1111/j.1532-5415.2011.03630.x
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 853FG
UT WOS:000297411000021
PM 22091794
ER
PT J
AU Gray, AN
Henderson-Frost, JM
Boyd, D
Shirafi, S
Niki, H
Goldberg, MB
AF Gray, Andrew N.
Henderson-Frost, Josephine M.
Boyd, Dana
Shirafi, Shirin
Niki, Hironori
Goldberg, Marcia B.
TI Unbalanced Charge Distribution as a Determinant for Dependence of a
Subset of Escherichia coli Membrane Proteins on the Membrane Insertase
YidC
SO MBIO
LA English
DT Article
ID F1F0 ATP SYNTHASE; INNER MEMBRANE; SUBUNIT-C; CYTOPLASMIC MEMBRANE;
TOPOLOGY; BIOGENESIS; SEC; COMPLEXES; DEPLETION; PROTEOME
AB Membrane proteins are involved in numerous essential cell processes, including transport, gene regulation, motility, and metabolism. To function properly, they must be inserted into the membrane and folded correctly. YidC, an essential protein in Escherichia coli with homologues in other bacteria, Archaea, mitochondria, and chloroplasts, functions by incompletely understood mechanisms in the insertion and folding of certain membrane proteins. Using a genome-scale approach, we identified 69 E. coli membrane proteins that, in the absence of YidC, exhibited aberrant localization by microscopy. Further examination of a subset revealed biochemical defects in membrane insertion in the absence of YidC, indicating their dependence on YidC for proper membrane insertion or folding. Membrane proteins possessing an unfavorable distribution of positively charged residues were significantly more likely to depend on YidC for membrane insertion. Correcting the charge distribution of a charge-unbalanced YidC-dependent membrane protein abrogated its requirement for YidC, while perturbing the charge distribution of a charge-balanced YidC-independent membrane protein rendered it YidC dependent, demonstrating that charge distribution can be a necessary and sufficient determinant of YidC dependence. These findings provide insights into a mechanism by which YidC promotes proper membrane protein biogenesis and suggest a critical function of YidC in all organisms and organelles that express it.
IMPORTANCE Biological membranes are fundamental components of cells, providing barriers that enclose the cell and separate compartments. Proteins inserted into biological membranes serve critical functions in molecular transport, molecular partitioning, and other essential cell processes. The mechanisms involved in the insertion of proteins into membranes, however, are incompletely understood. The YidC protein is critical for the insertion of a subset of proteins into membranes across an evolutionarily wide group of organisms. Here we identify a large group of proteins that depend on YidC for membrane insertion in Escherichia coli, and we identify unfavorable distribution of charge as an important determinant of YidC dependence for proper membrane insertion.
C1 [Gray, Andrew N.; Boyd, Dana; Goldberg, Marcia B.] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA.
[Henderson-Frost, Josephine M.; Shirafi, Shirin; Goldberg, Marcia B.] Massachusetts Gen Hosp, Dept Med, Div Infect Dis, Cambridge, MA USA.
[Niki, Hironori] Natl Inst Genet, Ctr Genet Resource Informat, Mishima, Shizuoka 411, Japan.
RP Goldberg, MB (reprint author), Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA.
EM mgoldberg1@partners.org
FU NIH [AI035817]; Ministry of Education, Culture, Sports, Science, and
Technology of Japan
FX This work was supported by NIH grant AI035817 (to M.B.G.) and by a
Grant-in-Aid for Scientific Research on Priority Areas from the Ministry
of Education, Culture, Sports, Science, and Technology of Japan (to
H.N.).
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PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 2150-7511
J9 MBIO
JI mBio
PD NOV-DEC
PY 2011
VL 2
IS 6
AR e00238-11
DI 10.1128/mBio.00238-11
PG 10
WC Microbiology
SC Microbiology
GA 888GV
UT WOS:000299992700012
ER
PT J
AU Beeri, MS
Moshier, E
Schmeidler, J
Godbold, J
Uribarri, J
Reddy, S
Sano, M
Grossman, HT
Cai, WJ
Vlassara, H
Silverman, JM
AF Beeri, Michal Schnaider
Moshier, Erin
Schmeidler, James
Godbold, James
Uribarri, Jaime
Reddy, Sarah
Sano, Mary
Grossman, Hillel T.
Cai, Weijing
Vlassara, Helen
Silverman, Jeremy M.
TI Serum concentration of an inflammatory glycotoxin, methylglyoxal, is
associated with increased cognitive decline in elderly individuals
SO MECHANISMS OF AGEING AND DEVELOPMENT
LA English
DT Article
DE Methylglyoxal; Advanced glycation end products; Type 2 diabetes;
Cognitive decline; Alzheimer's disease
ID ADVANCED GLYCATION ENDPRODUCTS; ALZHEIMERS-DISEASE; CARBONYL SCAVENGERS;
CEREBROSPINAL-FLUID; PROTEIN GLYCATION; OXIDATIVE STRESS; OLDEST-OLD;
DEMENTIA; AGE; NEUROPATHOLOGY
AB Background: Advanced glycations end products increase oxidant stress, inflammation, and neurotoxicity. Serum levels are increased in diabetes and aging. We examined the relationship between serum methylglyoxal derivatives (sMG), and cognitive decline, in 267 non-demented elderly.
Methods: Tobit mixed regression models assessed the association of baseline sMG with cognitive decline in the Mini Mental State Exam (MMSE) over time, controlling for sociodemographic factors (age, sex, and years of education), cardiovascular risk factors (diabetes and presence of an ApoE4 allele), and kidney function. sMG was assessed by ELISA.
Results: The fully adjusted model showed an annual decline of 0.26 MMSE points per unit increase in baseline sMG (p = 0.03). Significance was unchanged as additional risk factors were added to the model. The interactions of sMG with diabetes, sex, age, kidney function, and ApoE4 genotype were not significant.
Conclusions: Higher levels of baseline sMG were associated with a faster rate of cognitive decline, after adjusting for several sociodemographic and clinical characteristics. This relationship did not differ by sex, ApoE4 genotype, or diabetes status suggesting its generality. Since subjects were cognitively normal at the beginning of the study, elevated sMG may be indicative of brain cell injury initiated before clinically evident cognitive compromise. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Beeri, Michal Schnaider; Schmeidler, James; Reddy, Sarah; Sano, Mary; Grossman, Hillel T.; Silverman, Jeremy M.] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
[Moshier, Erin; Godbold, James] Mt Sinai Sch Med, Dept Biostat, New York, NY 10029 USA.
[Uribarri, Jaime] Mt Sinai Sch Med, Dept Med, New York, NY 10029 USA.
[Cai, Weijing; Vlassara, Helen] Mt Sinai Sch Med, Dept Geriatr, New York, NY 10029 USA.
[Beeri, Michal Schnaider; Sano, Mary] James J Peters Vet Affairs Med Ctr, Bronx, NY USA.
RP Beeri, MS (reprint author), Mt Sinai Sch Med, Dept Psychiat, 1 Gustave Levy Pl,Box 1230, New York, NY 10029 USA.
EM michal.beeri@mssm.edu
FU NIA [K01 AG023515-01, R01 AG034087, P01 AG02219, P50 AG05138,
R37AG023188]; Irma T. Hirschl Award; Berkman Trust
FX Supported by NIA grants K01 AG023515-01 and R01 AG034087 to Dr. Beeri,
Project 4 in P01 AG02219 to Dr. Silverman, P50 AG05138 to Dr. Mary Sano,
and R37AG023188 (MERIT) to Dr. Vlassara, as well as by the Irma T.
Hirschl Award to Dr. Beeri and the Berkman Trust to Dr. Vahram
Haroutunian.
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U2 8
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0047-6374
J9 MECH AGEING DEV
JI Mech. Ageing Dev.
PD NOV-DEC
PY 2011
VL 132
IS 11-12
BP 583
EP 587
DI 10.1016/j.mad.2011.10.007
PG 5
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 888CG
UT WOS:000299980800007
PM 22079406
ER
PT J
AU Baraghis, E
Bolduc, V
Lefebvre, J
Srinivasan, VJ
Boudoux, C
Thorin, E
Lesage, F
AF Baraghis, E.
Bolduc, V.
Lefebvre, J.
Srinivasan, V. J.
Boudoux, C.
Thorin, E.
Lesage, F.
TI Measurement of cerebral microvascular compliance in a model of
atherosclerosis with optical coherence tomography
SO BIOMEDICAL OPTICS EXPRESS
LA English
DT Article
ID ALZHEIMERS-DISEASE; BLOOD-FLOW; ANGIOGRAPHY; BRAIN
AB Optical coherence tomography (OCT) has recently been used to produce 3D angiography of microvasculature and blood flow maps of large vessels in the rodent brain in-vivo. However, use of this optical method for the study of cerebrovascular disease has not been fully explored. Recent developments in neurodegenerative diseases has linked common cardiovascular risk factors to neurodegenerative risk factors hinting at a vascular hypothesis for the development of the latter. Tools for studying cerebral blood flow and the myogenic tone of cerebral vasculature have thus far been either highly invasive or required ex-vivo preparations therefore not preserving the delicate in-vivo conditions. We propose a novel technique for reconstructing the flow profile over a single cardiac cycle in order to evaluate flow pulsatility and vessel compliance. A vascular model is used to simulate changes in vascular compliance and interpret OCT results. Comparison between atherosclerotic and wild type mice show a trend towards increased compliance in the smaller arterioles of the brain (diameter < 80 mu m) in the disease model. These results are consistent with previously published ex-vivo work confirming the ability of OCT to investigate vascular dysfunction. (C) 2011 Optical Society of America
C1 [Baraghis, E.; Lefebvre, J.; Boudoux, C.; Lesage, F.] Ecole Polytech Montreal, Montreal, PQ H3C 3A7, Canada.
[Bolduc, V.; Thorin, E.; Lesage, F.] Montreal Heart Inst, Res Ctr, Montreal, PQ H3T 1J4, Canada.
[Srinivasan, V. J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp,Opt Div, MGH MIT HMS Athinoula A Martinos Ctr Biomed Imagi, Charlestown, MA 02129 USA.
RP Baraghis, E (reprint author), Ecole Polytech Montreal, 2500 Chemin Polytech, Montreal, PQ H3C 3A7, Canada.
EM frederic.lesage@polymtl.ca
RI Boudoux, Caroline/A-6399-2012
FU Fonds de la recherche en sante du Quebec; Natural Sciences and
Engineering Research Council of Canada (NSERC); National Institutes of
Health [K99NS067050]; American Heart Association [11IRG5440002]
FX E. Baraghis was supported by scholarships from the "Fonds de la
recherche en sante du Quebec" and the Natural Sciences and Engineering
Research Council of Canada (NSERC). F. Lesage, C. Boudoux were supported
NSERC Discovery grants. V. J. Srinivasan was supported by the National
Institutes of Health (K99NS067050) and the American Heart Association
(11IRG5440002)
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PU OPTICAL SOC AMER
PI WASHINGTON
PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 USA
SN 2156-7085
J9 BIOMED OPT EXPRESS
JI Biomed. Opt. Express
PD NOV 1
PY 2011
VL 2
IS 11
BP 3079
EP 3093
PG 15
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
Medical Imaging
GA 886WB
UT WOS:000299883500014
PM 22076269
ER
PT J
AU Xu, ZP
Dong, YL
Wu, X
Zhang, J
McAuliffe, S
Pan, CX
Zhang, YY
Ichinose, F
Yue, Y
Xie, ZC
AF Xu, Zhipeng
Dong, Yuanlin
Wu, Xu
Zhang, Jun
McAuliffe, Sayre
Pan, Chuxiong
Zhang, Yiying
Ichinose, Fumito
Yue, Yun
Xie, Zhongcong
TI The Potential Dual Effects of Anesthetic Isoflurane on A beta-Induced
Apoptosis
SO CURRENT ALZHEIMER RESEARCH
LA English
DT Article
DE Anesthesia; Alzheimer's disease; isoflurane; apoptosis; beta-Amyloid
protein; dual effects; cytosolic calcium
ID AMYLOID PRECURSOR PROTEIN; INDUCED NEURONAL APOPTOSIS;
ALZHEIMERS-DISEASE; ENDOPLASMIC-RETICULUM; HIPPOCAMPAL-NEURONS;
INTRACELLULAR CA2+; CELL-DEATH; CASPASE-3 ACTIVATION; GLUCOSE
DEPRIVATION; PROAPOPTOTIC BAX
AB beta-amyloid protein (A beta)-induced neurotoxicity is the main component of Alzheimer's disease (AD) neuropathogenesis. Inhalation anesthetics have long been considered to protect against neurotoxicity. However, recent research studies have suggested that the inhalation anesthetic isoflurane may promote neurotoxicity by inducing apoptosis and increasing A beta levels. We therefore set out to determine whether isoflurane can induce dose-and time-dependent dual effects on A beta-induced apoptosis: protection versus promotion. H4 human neuroglioma cells, primary neurons from nave mice, and nave mice were treated with A beta and/or isoflurane, and levels of caspase-3 cleavage (activation), apoptosis, Bcl-2, Bax, and cytosolic calcium were determined. Here we show for the first time that the treatment with 2% isoflurane for six hours or 30 minutes potentiated, whereas the treatment with 0.5% isoflurane for six hours or 30 minutes attenuated, the A beta-induced caspase-3 activation and apoptosis in vitro. Moreover, anesthesia with 1.4% isoflurane for two hours potentiated, whereas the anesthesia with 0.7% isoflurane for 30 minutes attenuated, the A beta-induced caspase-3 activation in vivo. The high concentration isoflurane potentiated the A beta-induced reduction in Bcl-2/Bax ratio and caused a robust elevation of cytosolic calcium levels. The low concentration isoflurane attenuated the A beta-induced reduction in Bcl-2/Bax ratio and caused only a mild elevation of cytosolic calcium levels. These results suggest that isoflurane may have dual effects (protection or promotion) on A beta-induced toxicity, which potentially act through the Bcl-2 family proteins and cytosolic calcium. These findings would lead to more systematic studies to determine the potential dual effects of anesthetics on AD-associated neurotoxicity.
C1 [Xu, Zhipeng; Dong, Yuanlin; Wu, Xu; Zhang, Jun; McAuliffe, Sayre; Pan, Chuxiong; Zhang, Yiying; Xie, Zhongcong] Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Dept Anesthesia Crit Care & Pain Med,Dept Neurol, Geriatr Anesthesia Res Unit,Genet & Aging Res Uni, Charlestown, MA 02129 USA.
[Xu, Zhipeng; Dong, Yuanlin; Wu, Xu; Zhang, Jun; McAuliffe, Sayre; Pan, Chuxiong; Zhang, Yiying; Ichinose, Fumito; Xie, Zhongcong] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Wu, Xu] China Med Univ, Fac Forens Med, Dept Forens Pathol, Shenyang 110001, Peoples R China.
[Zhang, Jun] Fudan Univ, Dept Anesthesiol, Huashan Hosp, Shanghai 200041, Peoples R China.
[Pan, Chuxiong] Capital Med Univ, Beijing Tongren Hosp, Dept Anesthesia, Beijing 100050, Peoples R China.
[Yue, Yun] Capital Med Univ, Beijing Chaoyang Hosp, Dept Anesthesia, Beijing 100020, Peoples R China.
RP Xie, ZC (reprint author), Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Dept Anesthesia Crit Care & Pain Med,Dept Neurol, Geriatr Anesthesia Res Unit,Genet & Aging Res Uni, 149 13th St,4310, Charlestown, MA 02129 USA.
EM zxie@partners.org
FU National Institutes of Health [K08NS048140, R21AG029856, R01 GM088801,
R01GM079360]; American Geriatrics Society; Alzheimer's Association;
China National Science Foundation [NSF30928026]
FX This research was supported by K08NS048140, R21AG029856 and R01 GM088801
(National Institutes of Health), Jahnigen Career Development Award
(American Geriatrics Society), Investigator Initiated Research Grant
(Alzheimer's Association) (to Z. X.), R01GM079360 (National Institutes
of Health) (to FI), and China National Science Foundation Oversea young
scholar collaboration research award NSF30928026 (to Y.Y. and Z. X.).
NR 57
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PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1567-2050
J9 CURR ALZHEIMER RES
JI Curr. Alzheimer Res.
PD NOV
PY 2011
VL 8
IS 7
BP 741
EP 752
PG 12
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 882PI
UT WOS:000299575700004
PM 21244349
ER
PT J
AU Hirsch, AE
Yoo, AJ
Hirsch, JA
AF Hirsch, Ariel E.
Yoo, Albert J.
Hirsch, Joshua A.
TI In Response: Timing of EBRT Did Not Affect Outcome
SO PAIN PHYSICIAN
LA English
DT Letter
C1 [Hirsch, Ariel E.] Boston Univ, Med Ctr, Dept Radiat Oncol, Massachusetts Gen Hosp, Boston, MA 02118 USA.
[Yoo, Albert J.; Hirsch, Joshua A.] Massachusetts Gen Hosp, Dept Radiol, Div Intervent Neuroradiol, Boston, MA 02114 USA.
RP Hirsch, AE (reprint author), Boston Univ, Med Ctr, Dept Radiat Oncol, Massachusetts Gen Hosp, 830 Harrison Ave,Moakley Bldg LL, Boston, MA 02118 USA.
EM Ariel.hirsch@bmc.org; jahirsch@partners.org
NR 0
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PU AM SOC INTERVENTIONAL PAIN PHYSICIANS
PI PADUCAH
PA 81 LAKEVIEW DR, PADUCAH, KY 42001 USA
SN 1533-3159
J9 PAIN PHYSICIAN
JI Pain Physician
PD NOV-DEC
PY 2011
VL 14
IS 6
BP 570
EP 570
PG 1
WC Anesthesiology; Clinical Neurology
SC Anesthesiology; Neurosciences & Neurology
GA 885NC
UT WOS:000299784700011
ER
PT J
AU Basu, A
Jena, AB
Philipson, TJ
AF Basu, A.
Jena, A. B.
Philipson, T. J.
TI THE IMPACT OF COMPARATIVE EFFECTIVENESS RESEARCH ON HEALTH AND HEALTH
CARE SPENDING
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Basu, A.] Univ Washington, Seattle, WA 98195 USA.
[Jena, A. B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Philipson, T. J.] Univ Chicago, Chicago, IL 60637 USA.
NR 0
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U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD NOV
PY 2011
VL 14
IS 7
BP A301
EP A301
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 876KT
UT WOS:000299107100356
ER
PT J
AU Chan, K
Lai, MN
Groessl, EJ
Hanchate, A
Hernandez, L
Wong, JB
Clark, JA
Asch, S
Gifford, AL
Ho, S
AF Chan, K.
Lai, M. N.
Groessl, E. J.
Hanchate, A.
Hernandez, L.
Wong, J. B.
Clark, J. A.
Asch, S.
Gifford, A. L.
Ho, S.
TI POTENTIAL COSTS ASSOCIATED WITH NEW DIRECT ACTING ANTIVIRAL (DAAS)
THERAPY FOR UNTREATED CHRONIC HEPATITIS C GENOTYPE 1 INFECTION IN THE
VETERANS HEALTH ADMINISTRATION
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Chan, K.; Hanchate, A.; Hernandez, L.; Clark, J. A.] Boston Univ, Boston, MA 02215 USA.
[Lai, M. N.; Ho, S.] Vet Affairs San Diego Healthcare Syst, San Diego, CA USA.
[Groessl, E. J.] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Wong, J. B.] Tufts Univ, Boston, MA 02111 USA.
[Asch, S.] VA Greater Los Angeles Healthcare Syst GLA, Los Angeles, CA USA.
[Gifford, A. L.] Edith Nourse Rogers Mem Vet Adm Hosp, Bedford, MA 01730 USA.
NR 0
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U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD NOV
PY 2011
VL 14
IS 7
BP A269
EP A270
PG 2
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 876KT
UT WOS:000299107100193
ER
PT J
AU Jena, AB
Philipson, TJ
AF Jena, A. B.
Philipson, T. J.
TI ENDOGENOUS COST-EFFECTIVENESS ANALYSIS IN HEALTH CARE TECHNOLOGY
ADOPTION
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Jena, A. B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Philipson, T. J.] Univ Chicago, Chicago, IL 60637 USA.
NR 0
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U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD NOV
PY 2011
VL 14
IS 7
BP A363
EP A364
PG 2
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 876KT
UT WOS:000299107100688
ER
PT J
AU Negrier, S
Bushmakin, AG
Cappelleri, JC
Charbonneau, C
Sandin, R
Michaelson, MD
Figlin, RA
Motzer, RJ
AF Negrier, S.
Bushmakin, A. G.
Cappelleri, J. C.
Charbonneau, C.
Sandin, R.
Michaelson, M. D.
Figlin, R. A.
Motzer, R. J.
TI USING A WEIBULL PARAMETRIC MODEL FOR FAILURE-TIME DATA TO ASSESS
PROGRESSION-FREE SURVIVAL AS A SURROGATE ENDPOINT FOR OVERALL SURVIVAL
IN A TRIAL OF PATIENTS WITH METASTATIC RENAL CELL CARCINOMA
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Negrier, S.] Ctr Leon Berard, F-69373 Lyon, France.
[Bushmakin, A. G.; Cappelleri, J. C.] Pfizer Inc, Groton, CT 06340 USA.
[Charbonneau, C.] Pfizer Oncol, Global Outcomes Res, New York, NY USA.
[Sandin, R.] Pfizer Oncol, Global Hlth Econ & Outcomes Res, Stockholm, Sweden.
[Michaelson, M. D.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
[Figlin, R. A.] Cedars Sinai Med Ctr, Samuel Oschin Comprehens Canc Inst, Los Angeles, CA 90048 USA.
[Motzer, R. J.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
NR 0
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U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
J9 VALUE HEALTH
JI Value Health
PD NOV
PY 2011
VL 14
IS 7
BP A471
EP A471
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 876KT
UT WOS:000299107101372
ER
PT J
AU Denis, TGS
Dai, TH
Izikson, L
Astrakas, C
Anderson, RR
Hamblin, MR
Tegos, GP
AF Denis, Tyler G. St.
Dai, Tianhong
Izikson, Leonid
Astrakas, Christos
Anderson, Richard Rox
Hamblin, Michael R.
Tegos, George P.
TI All you need is light Antimicrobial photoinactivation as an evolving and
emerging discovery strategy against infectious disease
SO VIRULENCE
LA English
DT Review
DE photodynamic inactivation and therapy; photosensitizer; reactive oxygen
species; permeability barrier; multidrug efflux systems; biofilms; drug
delivery; nanomedicine; antimicrobial resistance; clinical applications
ID STAPHYLOCOCCUS-EPIDERMIDIS BIOFILMS; GRAM-NEGATIVE BACTERIA;
TOLUIDINE-BLUE-O; MEDIATED PHOTODYNAMIC INACTIVATION; RESISTANT
ACINETOBACTER-BAUMANNII; MYCOBACTERIUM-BOVIS BCG; N-METHYL-PYRIDYL;
PSEUDOMONAS-AERUGINOSA; IN-VITRO; MULTIDRUG-RESISTANCE
AB The story of prevention and control of infectious diseases remains open and a series of highly virulent pathogens are emerging both in and beyond the hospital setting. Antibiotics were an absolute success story for a previous era. The academic and industrial biomedical communities have now come together to formulate consensus beliefs regarding the pursuit of novel and effective alternative anti-infective countermeasures. Photodynamic therapy was established and remains a successful modality for malignancies but photodynamic inactivation has been transformed recently to an antimicrobial discovery and development platform. The concept of photodynamic inactivation is quite straightforward and requires microbial exposure to light energy, typically wavelengths in the visible region, that causes the excitation of photosensitizer molecules (either exogenous or endogenous), which results in the production of singlet oxygen and other reactive oxygen species that react with intracellular components, and consequently produce cell inactivation. It is an area of increasing interest, as research is advancing (1) to identify the photochemical and photophysical mechanisms involved in inactivation, (2) to develop potent and clinically compatible photosensitizer, (3) to understand how photoinactivation is affected by key microbial phenotypic elements (multidrug resistance and efflux, virulence and pathogenesis determinants, biofilms), (4) to explore novel delivery platforms inspired by current trends in pharmacology and nanotechnology and (5) to identify photoinactivation applications beyond the clinical setting such as environmental disinfectants.
C1 [Denis, Tyler G. St.; Dai, Tianhong; Izikson, Leonid; Anderson, Richard Rox; Hamblin, Michael R.; Tegos, George P.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Denis, Tyler G. St.] Columbia Univ, New York, NY USA.
[Dai, Tianhong; Izikson, Leonid; Anderson, Richard Rox; Hamblin, Michael R.; Tegos, George P.] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Astrakas, Christos] Democritus Univ, Thrace Med Sch, Div Internal Med, Alexandroupolis, Greece.
[Anderson, Richard Rox; Hamblin, Michael R.] MIT, Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Tegos, George P.] Univ New Mexico, Sch Med, Ctr Mol Discovery, Albuquerque, NM 87131 USA.
[Tegos, George P.] Univ New Mexico, Sch Med, Dept Pathol, Albuquerque, NM 87131 USA.
RP Tegos, GP (reprint author), Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
EM gtegos@salud.unm.edu
OI Hamblin, Michael/0000-0001-6431-4605
FU Columbia University; NIH [5U54MH084690-02, RO1 AI050875]; US Air Force
MFEL [FA9550-04-1-0079]; Bullock-Wellman Fellowship Award; Airlift
Research Foundation [109421]
FX Research conducted by Tyler G. St. Denis was supported by the Columbia
University I. I. Rabi Fellows Program. George P. Tegos is supported by
the NIH (grant 5U54MH084690-02). Research conducted in the Hamblin
Laboratory was supported by NIH (RO1 AI050875 to M. R. H.) and US Air
Force MFEL Program (FA9550-04-1-0079). T. D. was partially supported by
a Bullock-Wellman Fellowship Award and an Airlift Research Foundation
Extremity Trauma Research Grant (grant 109421).
NR 158
TC 16
Z9 19
U1 1
U2 41
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2150-5594
J9 VIRULENCE
JI Virulence
PD NOV-DEC
PY 2011
VL 2
IS 6
BP 509
EP 520
DI 10.4161/viru.2.6.17889
PG 12
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 878MP
UT WOS:000299261500005
ER
PT J
AU Chand, NS
Hung, DT
AF Chand, Nikhilesh S.
Hung, Deborah T.
TI The two-component sensor kinase KinB acts as a non-canonical switch
between acute and chronic infection
SO VIRULENCE
LA English
DT Article
DE Pseudomonas aeruginosa; two-component systems; regulation; KinB
ID PSEUDOMONAS-AERUGINOSA INFECTION; SIGNAL-TRANSDUCTION; REGULATORY
SYSTEMS; VIRULENCE FACTORS; HISTIDINE KINASES; MODEL; PATHOGENESIS;
PHOSPHORYLATION; IDENTIFICATION; RESISTANCE
C1 [Chand, Nikhilesh S.; Hung, Deborah T.] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Chand, Nikhilesh S.; Hung, Deborah T.] Massachusetts Gen Hosp, Ctr Computat & Integrat Biol, Boston, MA 02114 USA.
[Chand, Nikhilesh S.] Harvard Univ, Dept Mol & Cellular Biol, Cambridge, MA 02138 USA.
[Chand, Nikhilesh S.; Hung, Deborah T.] MIT & Harvard, Broad Inst, Cambridge, MA USA.
[Hung, Deborah T.] Harvard Univ, Sch Med, Dept Microbiol & Immunol, Boston, MA USA.
RP Hung, DT (reprint author), Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
EM hung@molbio.mgh.harvard.edu
NR 38
TC 2
Z9 2
U1 0
U2 1
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 2150-5594
J9 VIRULENCE
JI Virulence
PD NOV-DEC
PY 2011
VL 2
IS 6
BP 553
EP 558
DI 10.4161/viru.2.6.17987
PG 6
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 878MP
UT WOS:000299261500011
PM 21971182
ER
PT J
AU Yu, LY
Hales, CA
AF Yu, Lunyin
Hales, Charles A.
TI Silencing of Sodium-Hydrogen Exchanger 1 Attenuates the Proliferation,
Hypertrophy, and Migration of Pulmonary Artery Smooth Muscle Cells via
E2F1
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
DE sodium-hydrogen exchanger 1; E2F1; PASMC proliferation; hypertrophy;
hypoxia
ID CARDIAC MYOCYTE HYPERTROPHY; NA+/H+-EXCHANGER; ENDOTHELIAL-CELLS;
INTRACELLULAR PH; GENE-EXPRESSION; HEART-FAILURE; HYPOXIA; HYPERTENSION;
INHIBITION; HEPARIN
AB We previously found that deficiency of the sodium-hydrogen exchanger 1 (NHE1) gene prevented hypoxia-induced pulmonary hypertension and vascular remodeling in mice, which were accompanied by a significantly reduced proliferation of pulmonary artery smooth muscle cells(PASMCs), and which decreased the medial-wall thickness of pulmonary arteries. That finding indicated the involvement of NHE1 in the proliferation and hypertrophy of PASMCs, but the underlying mechanism was not fully understood. To define the mechanism by which the inhibition of NHE1 decreases hypoxic pulmonary hypertension and vascular remodeling, we investigated the role of E2F1, a nuclear transcription factor, in silencing the NHE1 gene-induced inhibition of the proliferation, hypertrophy, and migration of human PASMCs. We found that: (1) silencing of NHE1 by short, interfering RNA (siRNA) significantly inhibited PASMC proliferation and cell cycle progression, decreased hypoxia-induced hypertrophy (in terms of cell size and protein/DNA ratio) and migration (in terms of the wound-healing and migration chamber assays); (2) hypoxia induced the expression of E2F1, which was reversed by NHE1 siRNA; and (3) the overexpression of E2F1 blocked the inhibitory effect of NHE1 siRNA on the proliferation, hypertrophy, and migration of PASMCs. The present study determined that silencing the NHE1 gene significantly inhibited the hypoxia-induced proliferation, hypertrophy, and migration of human PASMCs via repression of the nuclear transcription factor E2F1. This study revealed a novel mechanism underlying the regulation of hypoxic pulmonary hypertension and vascular remodeling via NHE1.
C1 [Yu, Lunyin; Hales, Charles A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Pulm & Crit Care Unit,Dept Med, Boston, MA 02114 USA.
RP Yu, LY (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Pulm & Crit Care Unit,Dept Med, 55 Fruit St,Bulfinch 148, Boston, MA 02114 USA.
EM lyu3@partners.org
FU American Thoracic Society [PH-08-010]; National Institutes of Health
[HL39150]; Susannah Wood Foundation
FX This work was supported by American Thoracic Society/Pulmonary
Hypertension Research Grant PH-08-010 (L.Y.), by National Institutes of
Health grant HL39150 (C. A. H.), and by the Susannah Wood Foundation.
NR 49
TC 25
Z9 25
U1 2
U2 5
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1044-1549
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD NOV
PY 2011
VL 45
IS 5
BP 923
EP 930
DI 10.1165/rcmb.2011-0032OC
PG 8
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA 884CF
UT WOS:000299681800004
PM 21454803
ER
PT J
AU Hang, JQ
Lee, MS
Zhang, FY
Zheng, BY
Su, L
Yang, Z
Dai, HL
Zhang, HX
Christiani, DC
AF Hang, J-Q
Lee, M-S
Zhang, F-Y
Zheng, B-Y
Su, L.
Yang, Z.
Dai, H-L
Zhang, H-X
Christiani, David C.
TI HOUSEHOLD SOLID FUEL USE, BODY MASS INDEX, AND LUNG FUNCTION
SO RESPIROLOGY
LA English
DT Meeting Abstract
C1 [Lee, M-S; Su, L.; Zhang, H-X; Christiani, David C.] Harvard Univ, Sch Publ Hlth, Environm & Occupat Med & Epidemiol Program, Dept Environm Hlth, Boston, MA 02115 USA.
[Hang, J-Q; Zhang, F-Y; Zheng, B-Y; Dai, H-L] Shanghai Putuo Dist Peoples Hosp, Shanghai, Peoples R China.
[Christiani, David C.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Christiani, David C.] Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1323-7799
J9 RESPIROLOGY
JI Respirology
PD NOV
PY 2011
VL 16
SU 2
SI SI
BP 42
EP 42
PG 1
WC Respiratory System
SC Respiratory System
GA 868SZ
UT WOS:000298547100137
ER
PT J
AU Enzler, T
Sano, Y
Choo, MK
Cottam, HB
Karin, M
Tsao, H
Park, JM
AF Enzler, Thomas
Sano, Yasuyo
Choo, Min-Kyung
Cottam, Howard B.
Karin, Michael
Tsao, Hensin
Park, Jin Mo
TI Cell-Selective Inhibition of NF-kappa B Signaling Improves Therapeutic
Index in a Melanoma Chemotherapy Model
SO CANCER DISCOVERY
LA English
DT Article
ID METASTATIC MALIGNANT-MELANOMA; IKK-BETA; MOUSE MODEL; LIPOSOMAL
DOXORUBICIN; MACROPHAGE APOPTOSIS; PHASE-II; KINASE; CANCER;
INFLAMMATION; ACTIVATION
AB The transcription factor NF-kappa B promotes the survival of cancer cells exposed to doxorubicin and other chemotherapeutic agents. I kappa B kinase is essential for chemotherapy-induced NF-kappa B activation and considered a prime target for anticancer treatment. An I kappa B kinase inhibitor sensitized human melanoma xenografts in mice to killing by doxorubicin yet also exacerbated treatment toxicity in the host animals. By using mouse models that simulate cell-selective targeting, we found that impaired NF-kappa B activation in melanoma and host myeloid cells accounts for therapeutic and adverse effects, respectively. Ablation of tumor-intrinsic NF-kappa B activity resulted in apoptosis-driven tumor regression after treatment with doxorubicin. By contrast, chemotherapy in mice with myeloid-specific loss of NF-kappa B activation led to a massive intratumoral recruitment of interleukin-1 beta-producing neutrophils and necrotic tumor lesions, a condition associated with increased host mortality but not accompanied by tumor regression. Therefore, a molecular target-based therapy may be steered toward different clinical outcomes depending on the drug's cell-specific effects.
SIGNIFICANCE: Our findings show that the I kappa B kinase-NF-kappa B signaling pathway is important for both promoting treatment resistance and preventing host toxicity in cancer chemotherapy; however, the two functions are exerted by distinct cell type-specific mechanisms and can therefore be selectively targeted to achieve an improved therapeutic outcome. Cancer Discovery; 1(6); 496-507. (C) 2011 AACR.
C1 [Enzler, Thomas; Sano, Yasuyo; Choo, Min-Kyung; Park, Jin Mo] Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, Charlestown, MA 02129 USA.
[Enzler, Thomas; Sano, Yasuyo; Choo, Min-Kyung; Park, Jin Mo] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Tsao, Hensin] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Tsao, Hensin] Massachusetts Gen Hosp, MGH Canc Ctr, Boston, MA 02114 USA.
[Tsao, Hensin; Park, Jin Mo] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Tsao, Hensin; Park, Jin Mo] Harvard Univ, Sch Med, Boston, MA USA.
[Enzler, Thomas] Univ Med Goettingen, Dept Hematol & Oncol, Gottingen, Germany.
[Enzler, Thomas; Karin, Michael] Univ Calif San Diego, Sch Med, Dept Pharmacol, La Jolla, CA 92093 USA.
[Cottam, Howard B.] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
RP Park, JM (reprint author), Massachusetts Gen Hosp, Cutaneous Biol Res Ctr, 149 13th St, Charlestown, MA 02129 USA.
EM jmpark@cbrc2.mgh.harvard.edu
FU Cutaneous Biology Research Center-Wellman Center for Photomedicine
FX This work was supported by the Cutaneous Biology Research Center-Wellman
Center for Photomedicine Collaborative Project (J.M. Park).
NR 48
TC 17
Z9 17
U1 0
U2 4
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 NOV
PY 2011
VL 1
IS 6
BP 496
EP 507
DI 10.1158/2159-8290.CD-11-0143
PG 12
WC Oncology
SC Oncology
GA 880MR
UT WOS:000299411700029
PM 22389871
ER
PT J
AU Tanaka, K
Babic, I
Nathanson, D
Akhavan, D
Guo, DL
Gini, B
Dang, J
Zhu, SJ
Yang, HJ
De Jesus, J
Amzajerdi, AN
Zhang, YN
Dibble, CC
Dan, HC
Rinkenbaugh, A
Yong, WH
Vinters, HV
Gera, JF
Cavenee, WK
Cloughesy, TF
Manning, BD
Baldwin, AS
Mischel, PS
AF Tanaka, Kazuhiro
Babic, Ivan
Nathanson, David
Akhavan, David
Guo, Deliang
Gini, Beatrice
Dang, Julie
Zhu, Shaojun
Yang, Huijun
De Jesus, Jason
Amzajerdi, Ali Nael
Zhang, Yinan
Dibble, Christian C.
Dan, Hancai
Rinkenbaugh, Amanda
Yong, William H.
Vinters, Harry V.
Gera, Joseph F.
Cavenee, Webster K.
Cloughesy, Timothy F.
Manning, Brendan D.
Baldwin, Albert S.
Mischel, Paul S.
TI Oncogenic EGFR Signaling Activates an mTORC2-NF-kappa B Pathway That
Promotes Chemotherapy Resistance
SO CANCER DISCOVERY
LA English
DT Article
ID NF-KAPPA-B; GROWTH-FACTOR RECEPTOR; MTOR COMPLEX 2; MAMMALIAN TARGET;
MOTIF PHOSPHORYLATION; GLIOBLASTOMA PATIENTS; KINASE INHIBITORS;
CANCER-THERAPY; AKT; RICTOR
AB Although it is known that mTOR complex 2 (mTORC2) functions upstream of Akt, the role of this protein kinase complex in cancer is not well understood. Through an integrated analysis of cell lines, in vivo models, and clinical samples, we demonstrate that mTORC2 is frequently activated in glioblastoma (GBM), the most common malignant primary brain tumor of adults. We show that the common activating epidermal growth factor receptor (EGFR) mutation (EGFRvIII) stimulates mTORC2 kinase activity, which is partially suppressed by PTEN. mTORC2 signaling promotes GBM growth and survival and activates NF-kappa B. Importantly, this mTORC2-NF-kappa B pathway renders GBM cells and tumors resistant to chemotherapy in a manner independent of Akt. These results highlight the critical role of mTORC2 in the pathogenesis of GBM, including through the activation of NF-kappa B downstream of mutant EGFR, leading to a previously unrecognized function in cancer chemotherapy resistance. These findings suggest that therapeutic strategies targeting mTORC2, alone or in combination with chemotherapy, will be effective in the treatment of cancer. SIGNIFICANCE: This study demonstrates that EGFRvIII-activated mTORC2 signaling promotes GBM proliferation, survival, and chemotherapy resistance through Akt-independent activation of NF-kappa B. These results highlight the role of mTORC2 as an integrator of two canonical signaling networks that are commonly altered in cancer, EGFR/phosphoinositide-3 kinase (PI3K) and NF-kappa B. These results also validate the importance of mTORC2 as a cancer target and provide new insights into its role in mediating chemotherapy resistance, suggesting new treatment strategies. Cancer Discovery; 1(6); 524-38. (C) 2011 AACR.
C1 [Mischel, Paul S.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Ctr Hlth Sci, Los Angeles, CA 90095 USA.
[Mischel, Paul S.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Mol & Med Pharmacol, Los Angeles, CA 90095 USA.
[Yong, William H.; Cloughesy, Timothy F.; Mischel, Paul S.] Univ Calif Los Angeles, David Geffen Sch Med, Henry Singleton Brain Tumor Program, Los Angeles, CA 90095 USA.
[Yong, William H.; Cloughesy, Timothy F.; Mischel, Paul S.] Univ Calif Los Angeles, David Geffen Sch Med, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA.
[Vinters, Harry V.; Cloughesy, Timothy F.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
[Gera, Joseph F.] Greater Los Angeles Vet Affairs Healthcare Syst, Dept Res & Dev, Sepulveda, CA USA.
[Guo, Deliang] Ohio State Univ, Sch Med, Dept Radiat Oncol, Arthur G James Comprehens Canc Ctr, Columbus, OH 43210 USA.
[Cavenee, Webster K.] Univ Calif San Diego, Ludwig Inst Canc Res, La Jolla, CA 92093 USA.
[Zhang, Yinan; Dibble, Christian C.; Manning, Brendan D.] Harvard Univ, Sch Publ Hlth, Dept Genet & Complex Dis, Boston, MA 02115 USA.
[Dan, Hancai; Rinkenbaugh, Amanda; Baldwin, Albert S.] Univ N Carolina, Sch Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA.
RP Mischel, PS (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Ctr Hlth Sci, 10833 Le Conte Ave,Room 13-321, Los Angeles, CA 90095 USA.
EM pmischel@mednet.ucla.edu
RI Guo, Deliang/I-3735-2014; Zhang, Yinan/N-6432-2014;
OI Guo, Deliang/0000-0002-8359-390X; Zhang, Yinan/0000-0002-3471-6598;
Nael, Ali/0000-0002-9671-5531
FU NIH [CA119347, NS73831, P01-CA95616, CA122617, CA75080, CA73756];
Accelerate Brain Cancer Cure; STOP Cancer; Fred Miller Family; John W.
Carson Foundation; Lya and Harrison Latter endowed Chair; Ziering Family
Foundation in memory of Sigi Ziering; Ben and Catherine Ivy Foundation;
Art of the Brain Fund; Henry Singleton Brain Cancer Fund; Samuel Waxman
Cancer Research Foundation; Uehara Memorial Foundation
FX This work was supported by NIH grants CA119347 and NS73831 (P.S.
Mischel), Accelerate Brain Cancer Cure (P.S. Mischel), STOP Cancer (P.S.
Mischel), The Fred Miller Family (P.S. Mischel), The John W. Carson
Foundation (P.S. Mischel), The Lya and Harrison Latter endowed Chair
(P.S. Mischel), Ziering Family Foundation in memory of Sigi Ziering
(T.F. Cloughesy and P.S. Mischel), The Ben and Catherine Ivy Foundation
Fund (W.H. Yong and T.F. Cloughesy), Art of the Brain Fund (W.H. Yong
and T.F. Cloughesy), Henry Singleton Brain Cancer Fund (W.H. Yong and
T.F. Cloughesy), NIH grant P01-CA95616 (W.K. Cavenee), NIH grant
CA122617 (B.D. Manning), NIH grants CA75080 and CA73756 (A.S. Baldwin),
Samuel Waxman Cancer Research Foundation (A.S. Baldwin), and Uehara
Memorial Foundation (K. Tanaka).
NR 54
TC 111
Z9 115
U1 1
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 NOV
PY 2011
VL 1
IS 6
BP 524
EP 538
DI 10.1158/2159-8290.CD-11-0124
PG 15
WC Oncology
SC Oncology
GA 880MR
UT WOS:000299411700031
PM 22145100
ER
PT J
AU Beaser, RS
Okeke, E
Neighbours, J
Brown, J
Ronk, K
Wolyniec, WW
AF Beaser, Richard S.
Okeke, Eyiuche
Neighbours, James
Brown, Julie
Ronk, Katie
Wolyniec, Walter W.
TI COORDINATED PRIMARY AND SPECIALTY CARE FOR TYPE 2 DIABETES MELLITUS,
GUIDELINES, AND SYSTEMS: AN EDUCATIONAL NEEDS ASSESSMENT
SO ENDOCRINE PRACTICE
LA English
DT Article
ID BLOOD-GLUCOSE CONTROL; COMPLICATIONS; MANAGEMENT; ASSOCIATION;
PROGRESSION; THERAPY; ADULTS; RISK
AB Objective: To determine knowledge, competence, and attitudinal issues among primary care providers (PCPs) and diabetes specialists regarding the use and application of evidence-based clinical guidelines and the coordination of care between PCPs and diabetes specialists specifically related to referral practices for patients with diabetes.
Methods: A survey tool was completed by 491 PCPs and 249 diabetes specialists. Data were collected from specialists online and from PCP attendees at live symposia across the United States.
Results were analyzed for frequency of response and evaluation of significant relationships among the variables. Results: Suboptimal practice patterns and interprofessional communication as well as gaps in diabetes-related knowledge and processes were identified. PCPs reported a lack of clarity about who, PCP or specialist, should assume clinical responsibility for the management of diabetes after a specialty referral. PCPs were most likely to refer patients to diabetes specialists for management issues relating to insulin therapy and use of advanced treatment strategies, such as insulin pens and continuous glucose monitoring. A minority of PCPs and even fewer specialists reported the routine use of clinical guidelines in practice.
Conclusion: This research-based assessment identified critical educational needs and gaps related to coordinated care for patients with diabetes as well as the need for quality- and performance-based educational interventions. (Endocr Pract. 2011;17:880-890)
C1 [Beaser, Richard S.; Okeke, Eyiuche; Neighbours, James; Brown, Julie] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Ronk, Katie] Forward Hlth Grp Inc, Madison, WI USA.
[Wolyniec, Walter W.] Confluent Healthcare Solut Inc, Ridgefield, CT USA.
RP Beaser, RS (reprint author), Joslin Diabet Ctr, 1 Joslin Pl, Boston, MA 02215 USA.
EM Richard.Beaser@joslin.harvard.edu
FU Pfizer Inc.
FX Funding for this research was provided in the form of an independent
educational grant from Pfizer Inc. This research was conducted in
collaboration with the American Association of Clinical
Endocrinologists.
NR 19
TC 9
Z9 9
U1 1
U2 2
PU AMER ASSOC CLINICAL ENDOCRINOLOGISTS
PI JACKSONVILLE
PA 245 RIVERSIDE AVENUE, STE 200, JACKSONVILLE, FL 32202 USA
SN 1530-891X
J9 ENDOCR PRACT
JI Endocr. Pract.
PD NOV-DEC
PY 2011
VL 17
IS 6
BP 880
EP 890
DI 10.4158/EP10398.OR
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 876YQ
UT WOS:000299144100006
PM 21550953
ER
PT J
AU Kelly, M
Conway, M
Wirth, K
Potter-Bynoe, G
Billett, AL
Sandora, TJ
AF Kelly, Matthew
Conway, Margaret
Wirth, Kathleen
Potter-Bynoe, Gail
Billett, Amy L.
Sandora, Thomas J.
TI Moving CLABSI Prevention beyond the Intensive Care Unit: Risk Factors in
Pediatric Oncology Patients
SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY
LA English
DT Article
ID BLOOD-STREAM INFECTIONS; CRITICALLY-ILL PATIENTS; VENOUS ACCESS DEVICES;
SURVEILLANCE; CHILDREN; TRANSFUSION; CANCER; METAANALYSIS; CATHETERS;
MORTALITY
AB BACKGROUND AND OBJECTIVE. Central line-associated bloodstream infections (CLABSIs) frequently complicate the use of central venous catheters (CVCs) among pediatric patients with cancer. Our objectives were to describe the microbiology and identify risk factors for hospital-onset CLABSI in this patient population.
DESIGN. Retrospective case-control study.
SETTING. Oncology and stem cell transplant units of a freestanding, 396-bed quaternary care pediatric hospital.
PARTICIPANTS. Case subjects (N = 54) were patients with a diagnosis of malignancy and/or stem cell transplant recipients with CLABSI occurring during admission. Controls (N = 108) were identified using risk set sampling of hospitalizations among patients with a CVC, matched on date of admission.
METHODS. Multivariate conditional logistic regression was used to identify independent predictors of CLABSI.
RESULTS. The majority of CLABSI isolates were gram-positive bacteria (58%). The most frequently isolated organism was Enterococcus faecium, and 6 of 9 isolates were resistant to vancomycin. In multivariate analyses, independent risk factors for CLABSI included platelet transfusion within the prior week (odds ratio [OR], 10.90 [95% confidence interval (CI), 3.02-39.38]; P <.001) and CVC placement within the previous month (< 1 week vs >= 1 month: OR, 11.71 [95% CI, 1.98-69.20]; P = .02; >= 1 week and < 1 month vs >= 1 month: OR, 7.37 [95% CI, 1.85-29.36]; Pp. 004).
CONCLUSIONS. Adjunctive measures to prevent CLABSI among pediatric oncology patients may be most beneficial in the month following CVC insertion and in patients requiring frequent platelet transfusions. Vancomycin-resistant enterococci may be an emerging cause of CLABSI in hospitalized pediatric oncology patients and are unlikely to be treated by typical empiric antimicrobial regimens. Infect Control Hosp Epidemiol 2011; 32(11): 1079-1085
C1 [Kelly, Matthew; Sandora, Thomas J.] Childrens Hosp, Dept Med, Boston, MA 02115 USA.
[Conway, Margaret] Childrens Hosp, Med Patient Serv, Boston, MA 02115 USA.
[Wirth, Kathleen] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Billett, Amy L.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Billett, Amy L.] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Sandora, Thomas J.] Childrens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Sandora, Thomas J.] Childrens Hosp, Dept Lab Med, Boston, MA 02115 USA.
RP Kelly, M (reprint author), Childrens Hosp Philadelphia, Dept Global Hlth, 3535 Market St,13th Floor,Suite 1315, Philadelphia, PA 19104 USA.
EM kellym8@email.chop.edu
FU US National Institutes of Health [AI 007433]
FX Financial support. K.W. received grant support from the US National
Institutes of Health (AI 007433).
NR 40
TC 17
Z9 17
U1 1
U2 2
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0899-823X
J9 INFECT CONT HOSP EP
JI Infect. Control Hosp. Epidemiol.
PD NOV
PY 2011
VL 32
IS 11
BP 1079
EP 1085
DI 10.1086/662376
PG 7
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 876CB
UT WOS:000299083500004
PM 22011534
ER
PT J
AU Venkatesh, AK
Pallin, DJ
Kayden, S
Schuur, JD
AF Venkatesh, Arjun K.
Pallin, Daniel J.
Kayden, Stephanie
Schuur, Jeremiah D.
TI Predictors of Hand Hygiene in the Emergency Department
SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY
LA English
DT Article
AB We conducted an observational study to identify predictors of hand hygiene (HH) in the emergency department. Compliance with HH was 89.7% over 5,865 opportunities. Observation unit, hallway or high-visibility location, glove use, and worker type predicted worse HH. Hallway location was the strongest predictor (relative risk, 88.9% [95% confidence interval, 85.9%-92.1%]). Infect Control Hosp Epidemiol 2011; 32(11): 1120-1123
C1 [Pallin, Daniel J.; Kayden, Stephanie; Schuur, Jeremiah D.] Brigham & Womens Hosp, Dept Emergency Med, Boston, MA 02115 USA.
[Venkatesh, Arjun K.] Massachusetts Gen Hosp, Brigham & Womens Hosp, Boston, MA 02114 USA.
[Pallin, Daniel J.] Harvard Univ, Childrens Hosp, Sch Med, Div Emergency Med, Boston, MA 02115 USA.
[Pallin, Daniel J.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
RP Schuur, JD (reprint author), Brigham & Womens Hosp, Dept Emergency Med, 75 Francis St,Neville House,2nd Floor, Boston, MA 02115 USA.
EM jschuur@partners.org
RI Pallin, Daniel/H-6382-2013
OI Pallin, Daniel/0000-0002-8517-9702
FU Department of Emergency Medicine at Brigham and Women's Hospital; Agency
for Healthcare Research and Quality
FX Financial support. This study was funded by the Department of Emergency
Medicine at Brigham and Women's Hospital.; Potential conflicts of
interest. A.K.V. is part holder of a provisional patent for a hand
hygiene delivery device that had no relation to this study. J.D.S.
received no direct support for this project; he receives grant funding
from the Agency for Healthcare Research and Quality to identify and
develop best practices to prevent healthcare-associated infections in
emergency departments. D.J.P. and S.R. report no conflicts of interest
relevant to this article.
NR 10
TC 8
Z9 8
U1 0
U2 4
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0899-823X
J9 INFECT CONT HOSP EP
JI Infect. Control Hosp. Epidemiol.
PD NOV
PY 2011
VL 32
IS 11
BP 1120
EP 1123
DI 10.1086/662374
PG 4
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 876CB
UT WOS:000299083500011
PM 22011541
ER
PT J
AU Bryant, AS
Cheng, YW
Caughey, AB
AF Bryant, Allison S.
Cheng, Yvonne W.
Caughey, Aaron B.
TI Equality in Obstetrical Care: Racial/Ethnic Variation in Group B
Streptococcus Screening
SO MATERNAL AND CHILD HEALTH JOURNAL
LA English
DT Article
DE GBS screening; Disparities; Quality of care
ID PRETERM BIRTH; UNITED-STATES; RISK-FACTORS; DISEASE; DISPARITIES;
PREVENTION; COHORT
AB The objective of this article is to determine whether racial/ethnic disparities exist in screening for group B streptococcus (GBS) colonization among pregnant women. A retrospective cohort study of deliveries at a single institution was conducted. The primary outcome was the availability of GBS culture data at the time of delivery; the primary predictor was maternal race/ethnicity. Analyses were stratified by the time periods before and after the CDC recommendations for universal screening for GBS. Among 16,333 deliveries, 60.4% of the population was screened for GBS but screening rates varied markedly by year of delivery. Black women had a lower odds of having available GBS data (AOR 0.81 [0.69, 0.95]) but this disparity was limited to the period of time before universal screening was recommended. Prior to the recommendation for universal screening for GBS, racial/ethnic disparities existed in rates of screening among pregnant women delivering at term. These differences were reduced after 2002, suggesting that uniform policies regarding obstetrical care may be effective in eliminating disparities in obstetrical care and outcomes.
C1 [Bryant, Allison S.] Massachusetts Gen Hosp, Dept Obstet & Gynecol, Boston, MA 02114 USA.
[Cheng, Yvonne W.] Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA USA.
[Caughey, Aaron B.] Oregon Hlth & Sci Univ, Dept Obstet & Gynecol, Portland, OR 97201 USA.
RP Bryant, AS (reprint author), Massachusetts Gen Hosp, Dept Obstet & Gynecol, 55 Fruit St, Boston, MA 02114 USA.
EM abryant@partners.org
FU NIHJNCRR/CD UCSF-CTSI [KL2 RR024130]; Amos Medical Faculty Development
Award of the Robert Wood Johnson Foundation [RWJF-63524]; Robert Wood
Johnson Foundation as a Physician Faculty Scholar [RWJF-61535]; Women's
Reproductive Health Research Scholar at the University of California,
San Francisco
FX This publication was supported by NIHJNCRR/CD UCSF-CTSI Grant No. KL2
RR024130 (Dr. Bryant). Its contents arc solely the responsibility of the
authors and do not necessarily represent the official views of the NIH.
Dr. Bryant is also supported by the Amos Medical Faculty Development
Award of the Robert Wood Johnson Foundation, Grant No. RWJF-63524. Dr.
Caughey is supported by the Robert Wood Johnson Foundation as a
Physician Faculty Scholar Grant No. RWJF-61535. Dr. Cheng is supported
as a Women's Reproductive Health Research Scholar at the University of
California, San Francisco.
NR 21
TC 3
Z9 3
U1 0
U2 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1092-7875
J9 MATERN CHILD HLTH J
JI Matern. Child Health J.
PD NOV
PY 2011
VL 15
IS 8
BP 1160
EP 1165
DI 10.1007/s10995-010-0682-8
PG 6
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 875AK
UT WOS:000299001000005
PM 20853139
ER
PT J
AU Kerry, VB
Ndung'u, T
Walensky, RP
Lee, PT
Kayanja, VFIB
Bangsberg, DR
AF Kerry, Vanessa B.
Ndung'u, Thumbi
Walensky, Rochelle P.
Lee, Patrick T.
Kayanja, V. Frederick I. B.
Bangsberg, David R.
TI Managing the Demand for Global Health Education
SO PLOS MEDICINE
LA English
DT Editorial Material
ID MEDICAL-EDUCATION; ACADEMIC-INSTITUTIONS; INTERNATIONAL HEALTH; TROPICAL
MEDICINE; OPPORTUNITIES; CORPS; PROFESSIONALS; PROGRAMS; STUDENTS;
SCHOOLS
C1 [Kerry, Vanessa B.; Bangsberg, David R.] Massachusetts Gen Hosp, Ctr Global Hlth, Boston, MA 02114 USA.
[Kerry, Vanessa B.; Walensky, Rochelle P.; Lee, Patrick T.; Bangsberg, David R.] Harvard Univ, Sch Med, Boston, MA USA.
[Kerry, Vanessa B.] Massachusetts Gen Hosp, Dept Med, Div Pulm & Crit Care, Boston, MA 02114 USA.
[Ndung'u, Thumbi] Univ KwaZulu Natal, Nelson R Mandela Sch Med, Doris Duke Med Res Inst, HIV Pathogenesis Programme, Durban, South Africa.
[Walensky, Rochelle P.; Lee, Patrick T.] Massachusetts Gen Hosp, Dept Med, Div Gen Med, Boston, MA 02114 USA.
[Walensky, Rochelle P.] Massachusetts Gen Hosp, Dept Med, Div Infect Dis, Boston, MA 02114 USA.
[Walensky, Rochelle P.] Brigham & Womens Hosp, Dept Med, Div Infect Dis, Boston, MA 02115 USA.
[Kayanja, V. Frederick I. B.; Bangsberg, David R.] Mbarara Univ Sci & Technol, Mbarara, Uganda.
RP Kerry, VB (reprint author), Massachusetts Gen Hosp, Ctr Global Hlth, Boston, MA 02114 USA.
EM vkerry@partners.org
RI yan, liu/A-1822-2015;
OI yan, liu/0000-0001-8517-1084; Walensky, Rochelle P./0000-0002-8795-379X;
Ndung'u, Thumbi/0000-0003-2962-3992
FU NIAID NIH HHS [P30 AI060354, R01 AI058736]; NIMH NIH HHS [K24 MH087227,
K24 MH87227]
NR 63
TC 24
Z9 24
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1549-1277
J9 PLOS MED
JI PLos Med.
PD NOV
PY 2011
VL 8
IS 11
AR e1001118
DI 10.1371/journal.pmed.1001118
PG 6
WC Medicine, General & Internal
SC General & Internal Medicine
GA 862ZR
UT WOS:000298133100004
PM 22087076
ER
PT J
AU Kilpelainen, TO
Qi, L
Brage, S
Sharp, SJ
Sonestedt, E
Demerath, E
Ahmad, T
Mora, S
Kaakinen, M
Sandholt, CH
Holzapfel, C
Autenrieth, CS
Hypponen, E
Cauchi, S
He, MA
Kutalik, Z
Kumari, M
Stancakova, A
Meidtner, K
Balkau, B
Tan, JT
Mangino, M
Timpson, NJ
Song, YQ
Zillikens, MC
Jablonski, KA
Garcia, ME
Johansson, S
Bragg-Gresham, JL
Wu, Y
van Vliet-Ostaptchouk, JV
Onland-Moret, NC
Zimmermann, E
Rivera, NV
Tanaka, T
Stringham, HM
Silbernagel, G
Kanoni, S
Feitosa, MF
Snitker, S
Ruiz, JR
Metter, J
Larrad, MTM
Atalay, M
Hakanen, M
Amin, N
Cavalcanti-Proenca, C
Grontved, A
Hallmans, G
Jansson, JO
Kuusisto, J
Kahonen, M
Lutsey, PL
Nolan, JJ
Palla, L
Pedersen, O
Perusse, L
Renstrom, F
Scott, RA
Shungin, D
Sovio, U
Tammelin, TH
Ronnemaa, T
Lakka, TA
Uusitupa, M
Rios, MS
Ferrucci, L
Bouchard, C
Meirhaeghe, A
Fu, M
Walker, M
Borecki, IB
Dedoussis, GV
Fritsche, A
Ohlsson, C
Boehnke, M
Bandinelli, S
van Duijn, CM
Ebrahim, S
Lawlor, DA
Gudnason, V
Harris, TB
Sorensen, TIA
Mohlke, KL
Hofman, A
Uitterlinden, AG
Tuomilehto, J
Lehtimaki, T
Raitakari, O
Isomaa, B
Njolstad, PR
Florez, JC
Liu, SM
Ness, A
Spector, TD
Tai, ES
Froguel, P
Boeing, H
Laakso, M
Marmot, M
Bergmann, S
Power, C
Khaw, KT
Chasman, D
Ridker, P
Hansen, T
Monda, KL
Illig, T
Jarvelin, MR
Wareham, NJ
Hu, FB
Groop, LC
Orho-Melander, M
Ekelund, U
Franks, PW
Loos, RJF
AF Kilpelaeinen, Tuomas O.
Qi, Lu
Brage, Soren
Sharp, Stephen J.
Sonestedt, Emily
Demerath, Ellen
Ahmad, Tariq
Mora, Samia
Kaakinen, Marika
Sandholt, Camilla Helene
Holzapfel, Christina
Autenrieth, Christine S.
Hyppoenen, Elina
Cauchi, Stephane
He, Meian
Kutalik, Zoltan
Kumari, Meena
Stancakova, Alena
Meidtner, Karina
Balkau, Beverley
Tan, Jonathan T.
Mangino, Massimo
Timpson, Nicholas J.
Song, Yiqing
Zillikens, M. Carola
Jablonski, Kathleen A.
Garcia, Melissa E.
Johansson, Stefan
Bragg-Gresham, Jennifer L.
Wu, Ying
van Vliet-Ostaptchouk, Jana V.
Onland-Moret, N. Charlotte
Zimmermann, Esther
Rivera, Natalia V.
Tanaka, Toshiko
Stringham, Heather M.
Silbernagel, Guenther
Kanoni, Stavroula
Feitosa, Mary F.
Snitker, Soren
Ruiz, Jonatan R.
Metter, Jeffery
Martinez Larrad, Maria Teresa
Atalay, Mustafa
Hakanen, Maarit
Amin, Najaf
Cavalcanti-Proenca, Christine
Grontved, Anders
Hallmans, Goran
Jansson, John-Olov
Kuusisto, Johanna
Kahonen, Mika
Lutsey, Pamela L.
Nolan, John J.
Palla, Luigi
Pedersen, Oluf
Perusse, Louis
Renstrom, Frida
Scott, Robert A.
Shungin, Dmitry
Sovio, Ulla
Tammelin, Tuija H.
Ronnemaa, Tapani
Lakka, Timo A.
Uusitupa, Matti
Serrano Rios, Manuel
Ferrucci, Luigi
Bouchard, Claude
Meirhaeghe, Aline
Fu, Mao
Walker, Mark
Borecki, Ingrid B.
Dedoussis, George V.
Fritsche, Andreas
Ohlsson, Claes
Boehnke, Michael
Bandinelli, Stefania
van Duijn, Cornelia M.
Ebrahim, Shah
Lawlor, Debbie A.
Gudnason, Vilmundur
Harris, Tamara B.
Sorensen, Thorkild I. A.
Mohlke, Karen L.
Hofman, Albert
Uitterlinden, Andre G.
Tuomilehto, Jaakko
Lehtimaki, Terho
Raitakari, Olli
Isomaa, Bo
Njolstad, Pal R.
Florez, Jose C.
Liu, Simin
Ness, Andy
Spector, Timothy D.
Tai, E. Shyong
Froguel, Philippe
Boeing, Heiner
Laakso, Markku
Marmot, Michael
Bergmann, Sven
Power, Chris
Khaw, Kay-Tee
Chasman, Daniel
Ridker, Paul
Hansen, Torben
Monda, Keri L.
Illig, Thomas
Jarvelin, Marjo-Riitta
Wareham, Nicholas J.
Hu, Frank B.
Groop, Leif C.
Orho-Melander, Marju
Ekelund, Ulf
Franks, Paul W.
Loos, Ruth J. F.
TI Physical Activity Attenuates the Influence of FTO Variants on Obesity
Risk: A Meta-Analysis of 218,166 Adults and 19,268 Children
SO PLOS MEDICINE
LA English
DT Article
ID BODY-MASS INDEX; UNITED-STATES; ENVIRONMENT INTERACTION; RS9939609
POLYMORPHISM; DIABETES PREVENTION; WAIST CIRCUMFERENCE;
GENETIC-VARIANTS; IDENTICAL-TWINS; COMMON VARIANT; WEIGHT-LOSS
AB Background: The FTO gene harbors the strongest known susceptibility locus for obesity. While many individual studies have suggested that physical activity (PA) may attenuate the effect of FTO on obesity risk, other studies have not been able to confirm this interaction. To confirm or refute unambiguously whether PA attenuates the association of FTO with obesity risk, we meta-analyzed data from 45 studies of adults (n=218,166) and nine studies of children and adolescents (n=19,268).
Methods and Findings: All studies identified to have data on the FTO rs9939609 variant (or any proxy [r(2)>0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25% of adults and 13% of children were categorized as inactive. Interaction analyses were performed within each study by including the FTOxPA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A-) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95% CI 1.20-1.26), but PA attenuated this effect (p(interaction) = 0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio = 1.22/allele, 95% CI 1.19-1.25) than in the inactive group (odds ratio = 1.30/allele, 95% CI 1.24-1.36). No such interaction was found in children and adolescents.
Conclusions: The association of the FTO risk allele with the odds of obesity is attenuated by 27% in physically active adults, highlighting the importance of PA in particular in those genetically predisposed to obesity.
C1 [Kilpelaeinen, Tuomas O.; Brage, Soren; Sharp, Stephen J.; Palla, Luigi; Scott, Robert A.; Wareham, Nicholas J.; Ekelund, Ulf; Loos, Ruth J. F.] Inst Metab Sci, Med Res Council Epidemiol Unit, Cambridge, England.
[Qi, Lu; Renstrom, Frida; Franks, Paul W.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Qi, Lu; Renstrom, Frida; Franks, Paul W.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Sonestedt, Emily; Renstrom, Frida; Shungin, Dmitry; Groop, Leif C.; Orho-Melander, Marju; Franks, Paul W.] Lund Univ, Skane Univ Hosp, Dept Clin Sci, Lund Univ Diabet Ctr, Malmo, Sweden.
[Demerath, Ellen; Lutsey, Pamela L.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Ahmad, Tariq] Duke Univ, Med Ctr, Dept Med, Div Cardiol, Durham, NC 27710 USA.
[Kaakinen, Marika; Jarvelin, Marjo-Riitta] Univ Oulu, Inst Hlth Sci, Oulu, Finland.
[Kaakinen, Marika; Jarvelin, Marjo-Riitta] Univ Oulu, Bioctr Oulu, Oulu, Finland.
[Sandholt, Camilla Helene; Pedersen, Oluf; Hansen, Torben] Hagedorn Res Inst, Gentofte, Denmark.
[Holzapfel, Christina; Illig, Thomas] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Unit Mol Epidemiol, Neuherberg, Germany.
[Holzapfel, Christina] Tech Univ Munich, Klinikum Rechts Isar, Univ Hosp, Else Kroener Fresenius Ctr Nutr Med, D-8000 Munich, Germany.
[Autenrieth, Christine S.] German Res Ctr Environm Hlth, Helmholtz Zentrum Munchen, Inst Epidemiol 2, Neuherberg, Germany.
[Hyppoenen, Elina; Power, Chris] UCL, Inst Child Hlth, Ctr Paediat Epidemiol & Biostat, London, England.
[Hyppoenen, Elina; Power, Chris] UCL, Inst Child Hlth, MRC, Ctr Epidemiol Child Hlth, London, England.
[Cauchi, Stephane; Cavalcanti-Proenca, Christine; Froguel, Philippe] Inst Biol Lille, Dept Genom & Mol Physiol Metab Dis, CNRS UMR 8090, Lille, France.
[Kutalik, Zoltan; Bergmann, Sven] Univ Lausanne, Dept Med Genet, Lausanne, Switzerland.
[Kumari, Meena] UCL, Dept Epidemiol, Genet Epidemiol Grp, London, England.
[Stancakova, Alena; Kuusisto, Johanna; Laakso, Markku] Univ Eastern Finland, Dept Med, Kuopio, Finland.
[Meidtner, Karina; Boeing, Heiner] German Inst Human Nutr Potsdam Rehbrucke, Dept Epidemiol, Nuthetal, Germany.
[Balkau, Beverley] INSERM, CESP Ctr Res Epidemiol & Populat Hlth, U1018, Villejuif, France.
[Balkau, Beverley] Univ Paris 11, UMRS 1018, Villejuif, France.
[Tan, Jonathan T.] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Epidemiol & Publ Hlth, Singapore 117595, Singapore.
[Mangino, Massimo; Spector, Timothy D.] Kings Coll London, London WC2R 2LS, England.
[Timpson, Nicholas J.; Lawlor, Debbie A.] Univ Bristol, Sch Social & Community Med, Ctr Causal Anal Translat Epidemiol, MRC, Bristol, Avon, England.
[Song, Yiqing] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Prevent Med, Boston, MA 02115 USA.
[Zillikens, M. Carola; Uitterlinden, Andre G.] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Zillikens, M. Carola; van Duijn, Cornelia M.; Hofman, Albert; Uitterlinden, Andre G.] Netherlands Consortium Hlth Aging, Netherlands Genom Initiat, Leiden, Netherlands.
[Jablonski, Kathleen A.] George Washington Univ, Ctr Biostat, Rockville, MD USA.
[Johansson, Stefan] Haukeland Hosp, Ctr Med Genet & Mol Med, N-5021 Bergen, Norway.
[Johansson, Stefan; Njolstad, Pal R.] Univ Bergen, Dept Clin Med, Bergen, Norway.
[Bragg-Gresham, Jennifer L.; Stringham, Heather M.; Boehnke, Michael] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Bragg-Gresham, Jennifer L.; Stringham, Heather M.; Boehnke, Michael] Univ Michigan, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Wu, Ying; Mohlke, Karen L.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[van Vliet-Ostaptchouk, Jana V.] Univ Med Ctr Groningen, Dept Pathol & Med Biol, Mol Genet Sect, NL-9713 AV Groningen, Netherlands.
[van Vliet-Ostaptchouk, Jana V.] Univ Groningen, Groningen, Netherlands.
[Onland-Moret, N. Charlotte] Univ Med Ctr Utrecht, Dept Med Genet, Complex Genet Sect, Utrecht, Netherlands.
[Onland-Moret, N. Charlotte] Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
[Zimmermann, Esther; Sorensen, Thorkild I. A.] Copenhagen Univ Hosp, Inst Prevent Med, Copenhagen, Denmark.
[Zimmermann, Esther; Pedersen, Oluf] Univ Copenhagen, Fac Hlth Sci, Inst Biomed Sci, Copenhagen, Denmark.
[Rivera, Natalia V.; Amin, Najaf; van Duijn, Cornelia M.; Hofman, Albert; Uitterlinden, Andre G.] Erasmus MC, Dept Epidemiol, Genet Epidemiol Unit, Rotterdam, Netherlands.
[Tanaka, Toshiko] Medstar Res Inst, Baltimore, MD USA.
[Tanaka, Toshiko; Metter, Jeffery; Ferrucci, Luigi] NIA, Longitudinal Study Sect, NIH, Baltimore, MD 21224 USA.
[Silbernagel, Guenther; Fritsche, Andreas] Univ Tubingen, Dept Internal Med, Div Endocrinol Diabetol Nephrol Vasc Dis & Clin C, D-7400 Tubingen, Germany.
[Kanoni, Stavroula; Dedoussis, George V.] Harokopio Univ Athens, Dept Nutr Dietet, Athens, Greece.
[Feitosa, Mary F.; Borecki, Ingrid B.] Washington Univ, Sch Med, Div Stat Genom, St Louis, MO USA.
[Snitker, Soren] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Ruiz, Jonatan R.] Karolinska Inst, Novum, Dept Biosci & Nutr, Unit Prevent Nutr, Huddinge, Sweden.
[Ruiz, Jonatan R.] Univ Granada, Sch Phys Act & Sport Sci, Dept Phys Educ & Sport, Granada, Spain.
[Martinez Larrad, Maria Teresa; Serrano Rios, Manuel] Hosp Clin San Carlos, Ctr Invest Biomed Red Diabet & Enfermedades Metab, Madrid, Spain.
[Atalay, Mustafa; Lakka, Timo A.] Univ Eastern Finland, Dept Physiol, Inst Biomed, Kuopio, Finland.
[Hakanen, Maarit; Raitakari, Olli] Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland.
[Grontved, Anders] Univ So Denmark, Inst Sport Sci & Clin Biomech, Odense, Denmark.
[Hallmans, Goran] Umea Univ, Dept Publ Hlth & Clin Med, Sect Nutr Res, Umea, Sweden.
[Jansson, John-Olov] Univ Gothenburg, Sahlgrenska Acad, Dept Physiol, Inst Neurosci & Physiol, Gothenburg, Sweden.
[Nolan, John J.] Steno Diabet Ctr, DK-2820 Gentofte, Denmark.
[Kahonen, Mika] Univ Tampere, Dept Clin Physiol, FIN-33101 Tampere, Finland.
[Kahonen, Mika; Lehtimaki, Terho] Tampere Univ Hosp, Tampere, Finland.
[Pedersen, Oluf] Univ Aarhus, Fac Hlth Sci, Aarhus, Denmark.
[Pedersen, Oluf; Hansen, Torben] Univ Copenhagen, Fac Hlth Sci, Marie Krogh Ctr Metab Res, Copenhagen, Denmark.
[Perusse, Louis] Univ Laval, Dept Social & Prevent Med, Div Kinesiol, Ste Foy, PQ, Canada.
[Renstrom, Frida; Shungin, Dmitry; Franks, Paul W.] Umea Univ Hosp, Med Sect, Dept Publ Hlth & Clin Med, Genet Epidemiol & Clin Res Grp, S-90185 Umea, Sweden.
[Shungin, Dmitry] Umea Univ, Dept Odontol, Umea, Sweden.
[Sovio, Ulla] London Sch Hyg & Trop Med, Dept Med Stat, London WC1, England.
[Tammelin, Tuija H.] Finnish Inst Occupat Hlth, Oulu, Finland.
[Tammelin, Tuija H.] LIKES Res Ctr Sport & Hlth Sci, Jyvaskyla, Finland.
[Ronnemaa, Tapani] Univ Turku, Dept Med, Turku, Finland.
[Uusitupa, Matti] Univ Eastern Finland, Inst Publ Hlth & Clin Nutr, Kuopio, Finland.
[Uusitupa, Matti] Kuopio Univ Hosp, Res Unit, SF-70210 Kuopio, Finland.
[Bouchard, Claude] Pennington Biomed Res Ctr, Human Genom Lab, Baton Rouge, LA USA.
[Meirhaeghe, Aline] Univ Lille 2, Univ Lille Nord France, Inst Pasteur Lille, INSERM,U744, Lille, France.
[Fu, Mao] Univ Maryland, Sch Med, Div Endocrinol Diabet & Nutr, Baltimore, MD 21201 USA.
[Walker, Mark] Newcastle Univ, Inst Cell & Mol Biosci, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Ohlsson, Claes] Univ Gothenburg, Sahlgrenska Acad, Inst Med, Ctr Bone & Arthrit Res,Dept Internal Med, Gothenburg, Sweden.
[Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Rehabil Unit, Florence, Italy.
[van Duijn, Cornelia M.] Netherlands Genom Initiat, Ctr Med Syst Biol, Leiden, Netherlands.
[Ebrahim, Shah] London Sch Hyg & Trop Med, Fac Epidemiol & Populat Hlth, London WC1, England.
[Gudnason, Vilmundur] Iceland Heart Assoc, Heart Prevent Clin, Kopavogur, Iceland.
[Gudnason, Vilmundur] Iceland Heart Assoc, Res Inst, Kopavogur, Iceland.
[Gudnason, Vilmundur] Univ Iceland, Reykjavik, Iceland.
[Harris, Tamara B.] NIA, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Tuomilehto, Jaakko] Univ Helsinki, Dept Publ Hlth, Hjelt Inst, Helsinki, Finland.
[Tuomilehto, Jaakko] S Ostrobothnia Cent Hosp, Seinajoki, Finland.
[Tuomilehto, Jaakko] Danube Univ Krems, Dept Clin & Prevent Med, Krems, Austria.
[Lehtimaki, Terho] Univ Tampere, Dept Clin Chem, FIN-33101 Tampere, Finland.
[Raitakari, Olli] Turku Univ Hosp, Dept Clin Physiol, FIN-20520 Turku, Finland.
[Isomaa, Bo] Folkhalsan Res Ctr, Helsinki, Finland.
[Isomaa, Bo] Dept Social Serv & Hlth Care, Pietarsaari, Finland.
[Njolstad, Pal R.] Haukeland Hosp, Dept Pediat, N-5021 Bergen, Norway.
[Florez, Jose C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Florez, Jose C.] Massachusetts Gen Hosp, Diabet Res Ctr, Boston, MA 02114 USA.
[Florez, Jose C.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Florez, Jose C.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Liu, Simin] Univ Calif Los Angeles, Sch Publ Hlth, Ctr Metab Dis Prevent, Los Angeles, CA 90024 USA.
[Liu, Simin] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Ness, Andy] Univ Bristol, Sch Oral & Dent Sci, Bristol, Avon, England.
[Tai, E. Shyong] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Med, Singapore 117595, Singapore.
[Froguel, Philippe] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Ctr Genom Med, London, England.
[Froguel, Philippe] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Dept Genom Med, London, England.
[Marmot, Michael] UCL, Dept Epidemiol & Publ Hlth, London, England.
[Khaw, Kay-Tee] Univ Cambridge, Inst Publ Hlth, Dept Publ Hlth & Primary Care, Cambridge, England.
[Hansen, Torben] Univ So Denmark, Fac Hlth Sci, Odense, Denmark.
[Monda, Keri L.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Jarvelin, Marjo-Riitta] Univ London Imperial Coll Sci Technol & Med, Dept Epidemiol & Biostat, London, England.
[Jarvelin, Marjo-Riitta] Natl Inst Hlth & Welf, Dept Life Course & Serv, Oulu, Finland.
RP Kilpelainen, TO (reprint author), Inst Metab Sci, Med Res Council Epidemiol Unit, Cambridge, England.
EM luqi@hsph.harvard.edu; paul.franks@med.lu.se;
ruth.loos@mrc-epid.cam.ac.uk
RI Sonestedt, Emily/I-3814-2016; Bouchard, Claude/A-7637-2009; mangino,
massimo/F-5134-2011; Fox, Laura /C-6249-2016; Palla, Luigi/Q-4950-2016;
Rivera, Natalia V/S-4231-2016; Feitosa, Mary/K-8044-2012; Onland-Moret,
N. Charlotte/G-9185-2011; Gudnason, Vilmundur/K-6885-2015; RUIZ,
JONATAN/M-1338-2015; Kilpelainen, Tuomas/F-8569-2012; Brage,
Soren/C-6415-2013; Perusse, Louis/A-3444-2012; Hypponen,
Elina/B-2596-2014; Liu, Simin/I-3689-2014; Berryman, Katie/J-4236-2014;
Meirhaeghe, Aline/E-4663-2015; Johansson, Stefan/C-4394-2011; Colaus,
PsyColaus/K-6607-2013
OI van Vliet-Ostaptchouk, Jana/0000-0002-7943-3153; Lakka,
Timo/0000-0002-9199-2871; Grontved, Anders/0000-0003-1584-679X; Kumari,
Meena/0000-0001-9716-1035; Jarvelin, Marjo-Riitta/0000-0002-2149-0630;
Marmot, Michael/0000-0002-2431-6419; Lawlor, Debbie
A/0000-0002-6793-2262; Tai, E Shyong/0000-0003-2929-8966; Sonestedt,
Emily/0000-0002-0747-4562; mangino, massimo/0000-0002-2167-7470; Palla,
Luigi/0000-0001-6944-1750; Rivera, Natalia V/0000-0002-1298-1243;
Feitosa, Mary/0000-0002-0933-2410; Zimmermann,
Esther/0000-0001-5854-0542; Kaakinen, Marika/0000-0002-9228-0462;
Shungin, Dmitry/0000-0001-7900-5856; Meidtner,
Karina/0000-0001-5810-4062; Gudnason, Vilmundur/0000-0001-5696-0084;
RUIZ, JONATAN/0000-0002-7548-7138; Brage, Soren/0000-0002-1265-7355;
Hypponen, Elina/0000-0003-3670-9399; Liu, Simin/0000-0003-2098-3844;
Johansson, Stefan/0000-0002-2298-7008;
FU British Heart Foundation [RG/07/008/23674]; Cancer Research UK [14136];
Department of Health [PHCS/C4/4/016]; Medical Research Council
[G9815508, G0000934, G0100222, G0401527, G0601653, G0701863, G0902037,
G1000143, G19/35, G8802774, MC_U106179471, MC_U106179473,
MC_U106188470]; NIDDK NIH HHS [P30 DK017047, P30 DK072488, P30 DK079637,
R01 DK072041, R01 DK072193, R01 DK078150, R01 DK091718]; Wellcome Trust
[092731]
NR 39
TC 168
Z9 173
U1 1
U2 76
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1549-1676
J9 PLOS MED
JI PLos Med.
PD NOV
PY 2011
VL 8
IS 11
AR e1001116
DI 10.1371/journal.pmed.1001116
PG 14
WC Medicine, General & Internal
SC General & Internal Medicine
GA 862ZR
UT WOS:000298133100003
PM 22069379
ER
PT J
AU Horwitz, R
AF Horwitz, Russell
TI Rising From the Rubble: Perspectives of an American Expatriate in Haiti
SO ACADEMIC PSYCHIATRY
LA English
DT Editorial Material
C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
RP Horwitz, R (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
EM rhorwitz@partners.org
NR 15
TC 0
Z9 0
U1 0
U2 0
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 1042-9670
J9 ACAD PSYCHIATR
JI Acad. Psych.
PD NOV-DEC
PY 2011
VL 35
IS 6
BP 397
EP 399
PG 3
WC Education & Educational Research; Psychiatry
SC Education & Educational Research; Psychiatry
GA 861ZT
UT WOS:000298060300015
PM 22193739
ER
PT J
AU Morse, MD
Raviola, G
Fricchione, G
Berger, E
AF Morse, Michael Dorian
Raviola, Giuseppe
Fricchione, Gregory
Berger, Elizabeth
TI Telesupervision for Medical Student Rotations in Global Health
Psychiatry
SO ACADEMIC PSYCHIATRY
LA English
DT Letter
C1 [Morse, Michael Dorian; Berger, Elizabeth] George Washington Univ, Dept Psychiat, Washington, DC 20052 USA.
[Raviola, Giuseppe] Childrens Hosp, Dept Psychiat, Boston, MA 02115 USA.
[Fricchione, Gregory] Mass Gen Hosp, Dept Psychiat, Boston, MA USA.
RP Morse, MD (reprint author), George Washington Univ, Dept Psychiat, Washington, DC 20052 USA.
EM michael_morse@hms.harvard.edu
NR 6
TC 4
Z9 4
U1 1
U2 3
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 1042-9670
J9 ACAD PSYCHIATR
JI Acad. Psych.
PD NOV-DEC
PY 2011
VL 35
IS 6
BP 415
EP 416
PG 2
WC Education & Educational Research; Psychiatry
SC Education & Educational Research; Psychiatry
GA 861ZT
UT WOS:000298060300020
PM 22193744
ER
PT J
AU Banerji, A
AF Banerji, Aleena
TI Hereditary angioedema: Classification, pathogenesis, and diagnosis
SO ALLERGY AND ASTHMA PROCEEDINGS
LA English
DT Article
ID INTERNATIONAL CONSENSUS ALGORITHM; C1 INHIBITOR DEFICIENCY;
ANGIONEUROTIC-EDEMA; LABORATORY DIAGNOSIS; HELICOBACTER-PYLORI;
FACTOR-XII; MANAGEMENT; THERAPY; PATHOPHYSIOLOGY; MUTATIONS
AB Hereditary angioedema (HAE) is a rare autosomal dominant genetic disorder associated with a deficiency in Cl inhibitor. More than 200 mutations in this gene, located on chromosome 11, have been identified. Although HAE is often inherited, 20-25% of cases are from new spontaneous mutations and they have no family history of swelling. Decreased Cl inhibitor activity leads to inappropriate activation of multiple pathways, including the complement and contact systems and the fibrinolysis and coagulation systems. Reduced Cl inhibitor activity results in increased activation of plasma kallikrein-kinin system proteases and increased bradykinin levels. Bradykinin is felt to be the main mediator of symptoms in HAE. Patients with HAE have recurrent episodes of swelling of the extremities, abdomen, face, and upper airway. Angioedema involving the gastrointestinal tract can lead to intestinal wall edema, which results in abdominal pain, nausea, vomiting, and diarrhea. Laryngeal swelling is life-threatening and may lead to asphyxia. Common triggers of an attack include trauma, stress, infection, menstruation, oral contraceptives, hormone replacement therapy, and angiotensin-converting enzyme inhibitors. Laboratory testing including C4, C1 inhibitor level, and function is needed to confirm or rule out the diagnosis of HAE. The treatment of HAE has improved significantly in recent years with the availability of several safe and effective therapies. Several consensus guidelines have been created to further assist in the management of HAE patients. This review will provide an update on the classification, pathophysiology, clinical presentation, and diagnosis of HAE. (Allergy Asthma Proc 32:403-407, 2011; doi: 10.2500/aap.2011.32.3492)
C1 [Banerji, Aleena] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Rheumatol Allergy & Immunol, Boston, MA USA.
RP Banerji, A (reprint author), Cox 201,55 Fruit St, Boston, MA 02114 USA.
EM abanerji@partners.org
FU Dyax; Shire; ViroPharma
FX Supported by an educational grant from Dyax, Shire and ViroPharma A
Banerji is a consultant and advisory board member for Oyax, and Shire
NR 39
TC 14
Z9 14
U1 1
U2 3
PU OCEAN SIDE PUBLICATIONS INC
PI PROVIDENCE
PA 95 PITMAN ST, PROVIDENCE, RI 02906 USA
SN 1088-5412
J9 ALLERGY ASTHMA PROC
JI Allergy Asthma Proc.
PD NOV-DEC
PY 2011
VL 32
IS 6
BP 403
EP 407
DI 10.2500/aap.2011.32.3492
PG 5
WC Allergy
SC Allergy
GA 874FR
UT WOS:000298941300001
PM 22221432
ER
PT J
AU Kofonow, JM
Bhuskute, A
Doghramji, L
Palmer, JN
Cohen, NA
Chiu, AG
AF Kofonow, Jennifer M.
Bhuskute, Aditi
Doghramji, Laurel
Palmer, James N.
Cohen, Noam A.
Chiu, Alexander G.
TI One-way valve bottle contamination rates in the immediate
post-functional endoscopic sinus surgery period
SO AMERICAN JOURNAL OF RHINOLOGY & ALLERGY
LA English
DT Article
ID RHINOSINUSITIS PATIENTS
AB Background: Sinonasal saline irrigation has become an accepted practice in the immediate postoperative management of functional endoscopic sinus surgery (FESS) patients. Recent studies have found that valveless delivery systems of sinonasal irrigation are colonized with bacteria. An alternative delivery system uses a one-way valve to reduce saline backflow and may limit bottle contamination. Our sole objective was to determine whether this system in post-FESS patients eliminates microbial bottle contamination.
Methods: Eight patients undergoing FESS were given one-way valve irrigation bottles to use immediately after surgery. Bottles were collected after 1 week of use and another set of bottles after an additional week. Endoscopic-directed cultures of the middle meatus were performed at the time of surgery. Returned used bottles were swabbed for bacteria and the valve system of the bottle was analyzed under scanning electron microscopy (SEM) for the presence of bacteria.
Results: All sinus swabs collected at the time of surgery grew bacteria with Staphylococcus sp. present in all samples. After the 1st week of use, 5/8 bottles grew bacterial cultures and showed bacterial presence on the valves by SEM. After the 2nd week, 4/5 bottles had positive culture results and also showed bacterial presence on the valves by SEM.
Conclusion: Despite commercial claims that the use of valves and limit of backflow into the bottle will eliminate contamination, our study showed that one-way valve delivery systems become contaminated with bacteria after 1 week of use. We also showed that the bottle valves themselves harbor bacteria after 1 week of use. (Am J Rhinol Allergy 25, 393-396, 2011; doi:10.2500/ajra.2011.25.3664)
C1 [Kofonow, Jennifer M.; Doghramji, Laurel; Palmer, James N.; Cohen, Noam A.] Univ Penn, Dept Otorhinolaryngol, Philadelphia, PA 19104 USA.
[Bhuskute, Aditi; Chiu, Alexander G.] Univ Arizona, Dept Surg, Tucson, AZ USA.
[Cohen, Noam A.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
RP Cohen, NA (reprint author), Univ Penn, Dept Otorhinolaryngol, Ravdin Bldg 5th Floor,3400 Spruce St, Philadelphia, PA 19104 USA.
EM Noam.Cohen@uphs.upenn.edu
RI Chiu, Alexander/J-1230-2014;
OI Chiu, Alexander/0000-0002-7592-6575; Cohen, Noam/0000-0002-9462-3932
FU NeilMed Pharmaceuticals, Inc.
FX J.N. Palmer, N.A. Cohen and A.G. Chiu have in the past received
royalties from NeilMed Pharmaceuticals, Inc. The remaining authors have
nothing to declare pertaining to this article
NR 11
TC 2
Z9 2
U1 0
U2 5
PU OCEAN SIDE PUBLICATIONS INC
PI PROVIDENCE
PA 95 PITMAN ST, PROVIDENCE, RI 02906 USA
SN 1945-8924
J9 AM J RHINOL ALLERGY
JI Am. J. Rhinol. Allergy
PD NOV-DEC
PY 2011
VL 25
IS 6
BP 393
EP 396
DI 10.2500/ajra.2011.25.3664
PG 4
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 868RT
UT WOS:000298543100019
PM 22185742
ER
PT J
AU Kastrinos, F
Syngal, S
AF Kastrinos, Fay
Syngal, Sapna
TI Inherited Colorectal Cancer Syndromes
SO CANCER JOURNAL
LA English
DT Review
DE Inherited colorectal cancer syndromes
ID FAMILIAL ADENOMATOUS POLYPOSIS; MSH6 GERMLINE MUTATIONS;
REPAIR-GENE-MUTATIONS; LYNCH-SYNDROME; COLON-CANCER; MICROSATELLITE
INSTABILITY; DUODENAL ADENOMATOSIS; CLINICAL-IMPLICATIONS; MYH
MUTATIONS; RISK
AB Colorectal cancer is the most common gastrointestinal malignancy and the second leading cause of cancer death in both men and women in the United States. Most colorectal cancer cases diagnosed annually are due to sporadic events, but up to 5% are attributed to known monogenic disorders including Lynch syndrome, familial adenomatous polyposis, MYH-associated polyposis, and the rare hamartomatous polyposis syndromes. These inherited colorectal cancer syndromes confer a markedly increased risk for the development of multiple cancers, and predictive genetic testing is available to identify mutation carriers and at-risk family members. Through personalized strategies for diagnosis and management, a substantial reduction in morbidity and mortality has been appreciated among patients at highest risk for the development of colorectal cancer.
C1 [Syngal, Sapna] Dana Farber Canc Inst, Div Populat Sci, Boston, MA 02115 USA.
[Kastrinos, Fay] Columbia Univ Med Ctr, Herbert Irving Comprehens Canc Ctr, New York, NY USA.
[Kastrinos, Fay] Columbia Univ Med Ctr, Div Digest & Liver Dis, New York, NY USA.
[Syngal, Sapna] Brigham & Womens Hosp, Div Gastroenterol, Boston, MA 02115 USA.
[Syngal, Sapna] Harvard Univ, Sch Med, Boston, MA USA.
RP Syngal, S (reprint author), Dana Farber Canc Inst, Div Populat Sci, 1 Jimmy Fund Way,SM 209, Boston, MA 02115 USA.
EM ssyngal@partners.org
FU National Cancer Institute [K24 113433, K07 151769]
FX K24 113433 to Dr Syngal and K07 151769 to Dr Kastrinos from the National
Cancer Institute.
NR 71
TC 21
Z9 24
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1528-9117
J9 CANCER J
JI Cancer J.
PD NOV-DEC
PY 2011
VL 17
IS 6
SI SI
BP 405
EP 415
DI 10.1097/PPO.0b013e318237e408
PG 11
WC Oncology
SC Oncology
GA 863HH
UT WOS:000298152900002
PM 22157284
ER
PT J
AU Pomerantz, MM
Freedman, ML
AF Pomerantz, Mark M.
Freedman, Matthew L.
TI The Genetics of Cancer Risk
SO CANCER JOURNAL
LA English
DT Review
DE Inherited cancer risk; genetics; cancer biology; prostate cancer;
patient management; genotype; phenotype; trait-associated alleles
ID GENOME-WIDE ASSOCIATION; HEREDITARY PROSTATE-CANCER; SINGLE-NUCLEOTIDE
POLYMORPHISM; LONG-RANGE INTERACTION; FAMILY-HISTORY; SUSCEPTIBILITY
LOCI; BREAST-CANCER; COLORECTAL-CANCER; CHROMOSOME 8Q24; BLADDER-CANCER
AB One hundred years ago, decades before the discovery of the structure of DNA, debate raged regarding how human traits were passed from one generation to the next. Phenotypes, including risk of disease, had long been recognized as having a familial component. Yet it was difficult to reconcile genetic segregation as described by Mendel with observations exhaustively documented by Karl Pearson and others regarding the normal distribution of human characteristics. In 1918, R. A. Fisher published his landmark article, "The Correlation Between Relatives on the Supposition of Mendelian Inheritance," bridging this divide and demonstrating that multiple alleles, all individually obeying Mendel's laws, account for the phenotypic variation observed in nature.
Since that time, geneticists have sought to identify the link between genotype and phenotype. Trait-associated alleles vary in their frequency and degree of penetrance. Some minor alleles may approach a frequency of 50% in the human population, whereas others are present within only a few individuals. The spectrum for penetrance is similarly wide. These characteristics jointly determine the segregation pattern of a given trait, which, in turn, determine the method used to map the trait. Until recently, identification of rare, highly penetrant alleles was most practical. Revolutionary studies in genomics reported over the past decade have made interrogation of most of the spectrum of genetic variation feasible.
The following article reviews recent discoveries in the genetic basis of inherited cancer risk and how these discoveries inform cancer biology and patient management. Although this article focuses on prostate cancer, the principles are generic for any cancer and, indeed, for any trait.
C1 [Pomerantz, Mark M.; Freedman, Matthew L.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
RP Freedman, ML (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM freedman@broadinstitute.org
FU NCI NIH HHS [R01 CA129435]
NR 115
TC 9
Z9 9
U1 2
U2 19
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1528-9117
J9 CANCER J
JI Cancer J.
PD NOV-DEC
PY 2011
VL 17
IS 6
SI SI
BP 416
EP 422
DI 10.1097/PPO.0b013e31823e5387
PG 7
WC Oncology
SC Oncology
GA 863HH
UT WOS:000298152900003
PM 22157285
ER
PT J
AU Martin, NE
Mucci, LA
Loda, M
DePinho, RA
AF Martin, Neil E.
Mucci, Lorelei A.
Loda, Massimo
DePinho, Ronald A.
TI Prognostic Determinants in Prostate Cancer
SO CANCER JOURNAL
LA English
DT Review
DE Prognosis; prostate; gene expression signatures; immunohistochemistry
ID CIRCULATING TUMOR-CELLS; TMPRSS2-ERG FUSION TRANSCRIPTS; HUMAN GLANDULAR
KALLIKREIN-2; BEAM RADIATION-THERAPY; FATTY-ACID SYNTHASE; RADICAL
PROSTATECTOMY; GLEASON SCORE; FREE SURVIVAL; DISEASE RECURRENCE; PROTEIN
EXPRESSION
AB Clinical outcomes in prostate cancer are heterogeneous, and given the high prevalence of the disease, there is a pressing need to identify clinically useful markers of prognosis. Many clinical, pathological, molecular, and genetic factors have been investigated in this capacity, although relatively few are routinely used. With a growing understanding of the molecular pathogenesis of prostate cancer, there is the potential that the next generation of makers will prove sufficiently robust to guide the optimal management of men with prostate cancer. Here, we review the various clinical and molecular prognostic determinants in prostate cancer.
C1 [DePinho, Ronald A.] Univ Texas MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA.
[Martin, Neil E.] Brigham & Womens Hosp, Dana Farber Canc Inst, Dept Radiat Oncol, Boston, MA 02115 USA.
[Mucci, Lorelei A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Loda, Massimo] Brigham & Womens Hosp, Dept Pathol, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP DePinho, RA (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Canc Biol, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM ron_depinho@dfci.harvard.edu
RI Martin, Neil/E-2193-2014
OI Martin, Neil/0000-0002-8164-8516
FU Metamark Genetics
FX Dr DePinho is the co-founder of Metamark Genetics, Dr Loda is a
scientific advisor for Metamark Genetics, and Drs Mucci and Martin
receive research support from Metamark Genetics.
NR 116
TC 20
Z9 21
U1 1
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1528-9117
J9 CANCER J
JI Cancer J.
PD NOV-DEC
PY 2011
VL 17
IS 6
SI SI
BP 429
EP 437
DI 10.1097/PPO.0b013e31823b042c
PG 9
WC Oncology
SC Oncology
GA 863HH
UT WOS:000298152900005
PM 22157287
ER
PT J
AU Flaherty, KT
AF Flaherty, Keith T.
TI BRAF Inhibitors and Melanoma
SO CANCER JOURNAL
LA English
DT Review
DE BRAF; melanoma; oncogene; vemurafenib; dabrafenib
ID B-RAF; MALIGNANT-MELANOMA; METASTATIC MELANOMA; ONCOGENIC BRAF(V600E);
CELL-LINES; MUTATIONS; RESISTANCE; PATHWAY; KINASE; GROWTH
AB Selective BRAF inhibitors have recently emerged as a new standard treatment for patients with metastatic melanoma harboring activating BRAF mutations. Inhibition of the MAP kinase pathway and initial evidence of antitumor effects are very reliably observed. However, many patients experience short-lived responses, whereas others are durable. An overall survival benefit has been established for them, BRAF in it, the agents that have advanced furthest in clinical development. Nonetheless, attention has immediately turned to understanding de novo and acquired resistance and effort to develop rational combination therapy that will further improve patient outcomes. Opportunities for combining BRAF inhibitors with other signal transduction inhibitors as well as targeted therapies with distinct mechanisms of action are discussed.
C1 [Flaherty, Keith T.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
RP Flaherty, KT (reprint author), 55 Fruit St,Yawkey 9E, Boston, MA 02114 USA.
EM kflaherty@partners.org
NR 69
TC 18
Z9 18
U1 1
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1528-9117
EI 1540-336X
J9 CANCER J
JI Cancer J.
PD NOV-DEC
PY 2011
VL 17
IS 6
SI SI
BP 505
EP 511
DI 10.1097/PPO.0b013e31823e5357
PG 7
WC Oncology
SC Oncology
GA 863HH
UT WOS:000298152900013
PM 22157295
ER
PT J
AU Peacock, ZS
Chapman, PH
Gupta, R
Kaban, LB
AF Peacock, Z. S.
Chapman, P. H.
Gupta, R.
Kaban, L. B.
TI Replication of ancient Egyptian osteotomies of the facial skeleton:
insights into the mummification process
SO INTERNATIONAL JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
DE Egyptian mummy; coronoidectomy; mandibular hypomobility; muscles of
mastication
ID ANKYLOSIS; FRACTURE; HEAD
AB A recent radiographic study of an Egyptian mummified head from the Middle Kingdom revealed methodical mutilations of the facial skeleton that were performed after death and prior to wrapping the corpse for burial. These mutilations consisted of removal of the coronoid processes of the mandible and portions of the zygomas presumably via an intraoral approach. They are unique in the archaeological record. The authors hypothesize that the procedures were carried out to facilitate jaw opening and may be related to a ritual known as the 'Opening of the Mouth' ceremony. The purpose of this study was to demonstrate the feasibility of performing these remarkable osteotomies on two human cadavers using instruments similar to those available to the ancient embalmer. Bilateral osteotomies of the zygomas and coronoid processes were carried out transorally and the bones removed. Pre- and postoperative maximal incisal opening measured 25 mm and 53 mm, respectively. Postoperative high-resolution computed tomographic (CT) scans were obtained. Comparison of the postoperative cadaver and mummy CT scans demonstrate remarkable similarity between the resections. Results of this study demonstrate that the ancient skeletal mutilations could have been performed transorally during the mummification process and would have enhanced jaw opening.
C1 [Peacock, Z. S.] Harvard Univ, Sch Dent Med, Dept Oral & Maxillofacial Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
Harvard Univ, Sch Dent Med, Dept Neurosurg & Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Peacock, ZS (reprint author), Harvard Univ, Sch Dent Med, Dept Oral & Maxillofacial Surg, Massachusetts Gen Hosp, Warren 1201,55 Fruit St, Boston, MA 02115 USA.
EM zpeacock@partners.org
FU Department of Oral and Maxillofacial Surgery, Massachusetts General
Hospital
FX Education and Research Fund, Department of Oral and Maxillofacial
Surgery, Massachusetts General Hospital.
NR 21
TC 3
Z9 3
U1 2
U2 9
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0901-5027
J9 INT J ORAL MAX SURG
JI Int. J. Oral Maxillofac. Surg.
PD NOV
PY 2011
VL 40
IS 11
BP 1301
EP 1306
DI 10.1016/j.ijom.2011.05.017
PG 6
WC Dentistry, Oral Surgery & Medicine; Surgery
SC Dentistry, Oral Surgery & Medicine; Surgery
GA 871GV
UT WOS:000298726800012
PM 21723092
ER
PT J
AU Teitelman, AM
Stringer, M
Nguyen, GT
Hanlon, AL
Averbuch, T
Stimpfel, AW
AF Teitelman, Anne M.
Stringer, Marilyn
Nguyen, Giang T.
Hanlon, Alexandra L.
Averbuch, Tali
Stimpfel, Amy Witkoski
TI Social Cognitive and Clinical Factors Associated with HPV Vaccine
Initiation Among Urban, Economically Disadvantaged Women
SO JOGNN-JOURNAL OF OBSTETRIC GYNECOLOGIC AND NEONATAL NURSING
LA English
DT Article
DE HPV vaccine; theory of planned behavior; sexual health; adolescent;
women's health; cervical cancer; prevention
ID HUMAN-PAPILLOMAVIRUS VACCINATION; PLANNED BEHAVIOR; REASONED ACTION;
UNITED-STATES; CERVICAL-CANCER; ACCEPTABILITY; ACCEPTANCE; INFECTION;
DAUGHTERS; KNOWLEDGE
AB Objective: To learn more about human papilloma virus (HPV) knowledge and vaccination among teens and young women age 13 to 26 years from an economically disadvantaged, urban community. Our aim was to identify common beliefs about HPV vaccine initiation and describe the relationship between attitudes, norms, perceived control, and intention to receive HPV vaccine, drawing from the theory of planned behavior (TPB).
Design: Mixed method, descriptive design. Guided by the TPB, HPV vaccine beliefs were assessed through focus groups. Intention to receive the vaccine, demographic and clinical factors, and theoretical predictor variables (attitudes, norms, and control) were assessed through questionnaires.
Setting: After recruitment, focus groups were held at a convenient date and time for our participants in a small university conference room.
Participants: Participants were economically disadvantaged young women, age 13 to 26 (N = 34).
Methods: Specific behavioral, normative, and control beliefs were elicited in focus groups and analyzed using content analysis. Simple and multivariate general linear modeling with adjustment for prognostic demographic and clinical factors was completed to assess the influence of the theoretical predictor variables on the outcome of HPV vaccine initiation.
Results: Influential beliefs toward vaccination were identified. Analysis indicated attitudes, norms, and perceived control toward HPV vaccine initiation were highly significant predictors of intent, as was tobacco use; all p's < .001.
Conclusion: Barriers to HPV vaccine initiation were identified, and strong preliminary evidence supports use of the TPB to guide programs to promote urban, economically disadvantaged young women's intent to begin the HPV vaccine. JOGNN, 40, 691-701; 2011. DOI: 10.1111/j.1552-6909.2011.01297.x
C1 [Teitelman, Anne M.] Univ Penn, Sch Nursing, Ctr Hlth Equ Res, Philadelphia, PA 19194 USA.
[Nguyen, Giang T.] Univ Penn, Sch Med, Dept Family Med & Community Hlth, Philadelphia, PA 19194 USA.
[Averbuch, Tali] Univ Penn, Sch Nursing, Womens Hlth Nurse Practitioner Program, Philadelphia, PA 19194 USA.
[Averbuch, Tali] Univ Penn, Sch Nursing, Nurse Midwifery Program, Philadelphia, PA 19194 USA.
RP Teitelman, AM (reprint author), Univ Penn, Sch Nursing, Ctr Hlth Equ Res, Fagin Hall 2L,Rm 244,418 Curie Blvd, Philadelphia, PA 19194 USA.
EM teitelm@nursing.upenn.edu
OI Nguyen, Giang/0000-0003-2031-9943
FU University of Pennsylvania School of Nursing; American Cancer Society
[CCCDA-05-161-01]
FX Supported by University of Pennsylvania School of Nursing Investing in
the Future Grant. Dr. Nguyen was supported by a Cancer Control Career
Development Award from the American Cancer Society (CCCDA-05-161-01) and
a Pfizer Fellowship in Health Literacy/Clear Health Communication.
NR 49
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Z9 9
U1 2
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0884-2175
J9 JOGNN-J OBST GYN NEO
JI JOGNN
PD NOV-DEC
PY 2011
VL 40
IS 6
BP 691
EP 701
DI 10.1111/j.1552-6909.2011.01297.x
PG 11
WC Nursing; Obstetrics & Gynecology
SC Nursing; Obstetrics & Gynecology
GA 855OY
UT WOS:000297575300005
PM 22092373
ER
PT J
AU Cappiello, J
Beal, MW
Gallogly-Hudson, K
AF Cappiello, Joyce
Beal, Margaret W.
Gallogly-Hudson, Kim
TI Applying Ethical Practice Competencies to the Prevention and Management
of Unintended Pregnancy
SO JOGNN-JOURNAL OF OBSTETRIC GYNECOLOGIC AND NEONATAL NURSING
LA English
DT Article
DE Unintended pregnancy; ethical competencies; professional right of
conscience; social justice
ID SOCIAL-JUSTICE; REPRODUCTIVE HEALTH; CHILDBEARING WOMEN; UNITED-STATES;
CARE; DISPARITIES; CONSCIENCE; OPTIONS; ISSUES; ACCESS
AB Using a case study that incorporates patient, nurse practitioner, and student perspectives, we address ethical principles of respect for autonomy, beneficence, and fairness; professionals' right of conscience; and a social justice model for the discussion of prevention and management of unintended pregnancy. Through an ongoing process of self-reflection and values clarification, nurses can prepare for the challenge of applying ethical principles to the reproductive health care of women. JOGNN, 40, 808-816; 2011. DOI: 10.1111/j.1552-6909.2011.01307.x
C1 [Cappiello, Joyce] Abort Access Project, Reprod Opt Educ Consortium, Cambridge, MA USA.
[Beal, Margaret W.] Massachusetts Gen Hosp, Inst Hlth Profess, Boston, MA 02114 USA.
[Gallogly-Hudson, Kim] N Georgia Coll & State Univ, Dept Nursing, Dahlonega, GA USA.
RP Cappiello, J (reprint author), Univ New Hampshire, Dept Nursing, Hewitt Hall,4 Lib Way, Durham, NH 03824 USA.
EM joycec@unh.edu
NR 45
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Z9 2
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0884-2175
J9 JOGNN-J OBST GYN NEO
JI JOGNN
PD NOV-DEC
PY 2011
VL 40
IS 6
BP 808
EP 816
DI 10.1111/j.1552-6909.2011.01307.x
PG 9
WC Nursing; Obstetrics & Gynecology
SC Nursing; Obstetrics & Gynecology
GA 855OY
UT WOS:000297575300017
PM 22273453
ER
PT J
AU Villiger, M
Soroka, A
Tearney, GJ
Bouma, BE
Vakoc, BJ
AF Villiger, Martin
Soroka, Andrew
Tearney, Guillermo J.
Bouma, Brett E.
Vakoc, Benjamin J.
TI Injury depth control from combined wavelength and power tuning in
scanned beam laser thermal therapy
SO JOURNAL OF BIOMEDICAL OPTICS
LA English
DT Article
DE laser thermal therapy; laser injury; tissue response; damage model;
injury depth control; Barrett's esophagus; thulium fiber laser
ID BARRETTS-ESOPHAGUS; RADIOFREQUENCY ABLATION; MICROSCOPY; TISSUE; SKIN;
COAGULATION; CELL
AB Laser thermal therapy represents a possible method to treat premalignant epithelial lesions of the esophagus. Dynamically conforming the thermal injury profile to a specific lesion boundary is expected to improve the efficacy of such a treatment and avoid complications. In this work, we investigated wavelength tuning as a mechanism to achieve this aimed control over injury depth by using the strong variation of water absorption close to 1900 nm. We developed a numerical model simulating in steps the photon propagation in the tissue, the diffusion of the absorbed heat, and the resulting tissue damage. The model was compared with experimental results on porcine esophageal specimens ex vivo and showed good agreement. Combined with power tuning, the wavelength agility in the range of 1860 to 1895 nm extends the injury range compared to a fixed wavelength source beyond 1 mm, while at the same time improving control over shallow depths and avoiding vaporization at the tissue surface. The combination of two or three discrete wavelengths combined at variable ratios provides similar control, and may provide an improved strategy for the treatment of endothelial lesions. (C) 2011 Society of Photo-Optical Instrumentation Engineers (SPIE). [DOI: 10.1117/1.3647581]
C1 [Villiger, Martin] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Villiger, Martin] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
RP Villiger, M (reprint author), Harvard Univ, Sch Med, 40 Blossom St,Bartlett Hall 704, Boston, MA 02114 USA.
EM mvilliger@partners.org
FU National Institutes of Health [R33CA125560, K25CA127465]
FX This work was supported by the National Institutes of Health (Grant Nos.
R33CA125560 and K25CA127465).
NR 29
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U1 1
U2 7
PU SPIE-SOC PHOTO-OPTICAL INSTRUMENTATION ENGINEERS
PI BELLINGHAM
PA 1000 20TH ST, PO BOX 10, BELLINGHAM, WA 98225 USA
SN 1083-3668
J9 J BIOMED OPT
JI J. Biomed. Opt.
PD NOV
PY 2011
VL 16
IS 11
AR 118001
DI 10.1117/1.3647581
PG 9
WC Biochemical Research Methods; Optics; Radiology, Nuclear Medicine &
Medical Imaging
SC Biochemistry & Molecular Biology; Optics; Radiology, Nuclear Medicine &
Medical Imaging
GA 868SU
UT WOS:000298546500041
PM 22112139
ER
PT J
AU Bloch, MJ
Basile, JN
AF Bloch, Michael J.
Basile, Jan N.
TI New British Guidelines Mandate Ambulatory Blood Pressure Monitoring to
Diagnose Hypertension in All Patients: Not Ready for Prime Time in the
United States
SO JOURNAL OF CLINICAL HYPERTENSION
LA English
DT Editorial Material
C1 [Bloch, Michael J.] St Marys Reg Med Ctr, Risk Reduct Ctr, Reno, NV USA.
[Basile, Jan N.] Med Univ S Carolina, Seinsheimer Cardiovasc Hlth Program, Div Gen Internal Med Geriatr, Charleston, SC 29425 USA.
[Bloch, Michael J.] Univ Nevada, Sch Med, Dept Internal Med, Reno, NV 89557 USA.
[Basile, Jan N.] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
RP Bloch, MJ (reprint author), St Marys Reg Med Ctr, Risk Reduct Ctr, 645 N Arlington St,Suite 460, Reno, NV USA.
EM mbloch@aol.com
NR 1
TC 12
Z9 12
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1524-6175
J9 J CLIN HYPERTENS
JI J. Clin. Hypertens.
PD NOV
PY 2011
VL 13
IS 11
BP 785
EP 786
DI 10.1111/j.1751-7176.2011.00532.x
PG 2
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 859DG
UT WOS:000297854300001
PM 22051420
ER
PT J
AU Lynch, CP
Strom, JL
Egede, LE
AF Lynch, Cheryl P.
Strom, Joni L.
Egede, Leonard E.
TI Disparities in diabetes self-management and quality of care in rural
versus urban veterans
SO JOURNAL OF DIABETES AND ITS COMPLICATIONS
LA English
DT Article
DE Veterans; Diabetes; Quality of care; Self-management; Rural health
ID GLYCEMIC CONTROL; HEALTH-CARE; ACCESS; TELEMEDICINE; EDUCATION; POLICY
AB Background: There are distinct geographic differences in diabetes-related morbidity and mortality; however, data regarding self-management and clinical outcomes are limited. This study examined diabetes care among veterans residing in rural versus urban areas.
Methods: A national data set was analyzed based on 10,570 veterans with type 2 diabetes. Residence was determined according to US census-based metropolitan statistical area. Primary outcomes were self-management behaviors (lifestyle and self-monitoring) and quality of care indicators (provider visits, laboratory monitoring and preventive measures). Multivariate analyses were done using STATA v10 to assess the independent effect of veteran residence on each outcome measure and to account for the complex survey design.
Results: Among veterans with diabetes, 21.4% were rural residents. Compared to urban veterans, rural veterans had significantly lower education, less annual income and less received diabetes education (P=.002). The final regression model showed that daily foot self-check was the only self-management behavior significantly higher among rural veterans (odds ratio 1.36, 95% confidence interval 1.10-1.70). Provider-based quality of care was not significantly different between groups.
Conclusions: Diabetes self-foot care was significantly better among rural veterans than their urban counterparts, but quality of care was equivalent. This suggests that clinical diabetes care among veterans is uniform; however, greater efforts for patient education and support in diabetes self-management are needed to improve outcomes. Published by Elsevier Inc.
C1 [Egede, Leonard E.] Med Univ S Carolina, Charleston VA REAP, Ctr Hlth Dispar Res, Dept Med, Charleston, SC 29425 USA.
[Lynch, Cheryl P.; Egede, Leonard E.] Ralph H Johnson Vet Affairs Med Ctr, Ctr Dis Prevent & Hlth Intervent Diverse Populat, Charleston, SC USA.
RP Egede, LE (reprint author), Med Univ S Carolina, Charleston VA REAP, Ctr Hlth Dispar Res, Dept Med, Charleston, SC 29425 USA.
EM egedel@musc.edu
FU NIDDK NIH HHS [K24 DK093699]
NR 30
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Z9 7
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1056-8727
J9 J DIABETES COMPLICAT
JI J. Diabetes Complications
PD NOV-DEC
PY 2011
VL 25
IS 6
BP 387
EP 392
DI 10.1016/j.jdiacomp.2011.08.003
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 865UA
UT WOS:000298335200007
PM 21983152
ER
PT J
AU Lew, HL
Pogoda, TK
Baker, E
Stolzmann, KL
Meterko, M
Cifu, DX
Amara, J
Hendricks, AM
AF Lew, Henry L.
Pogoda, Terri K.
Baker, Errol
Stolzmann, Kelly L.
Meterko, Mark
Cifu, David X.
Amara, Jomana
Hendricks, Ann M.
TI Prevalence of Dual Sensory Impairment and Its Association With Traumatic
Brain Injury and Blast Exposure in OEF/OIF Veterans
SO JOURNAL OF HEAD TRAUMA REHABILITATION
LA English
DT Article
DE blast injuries; hearing impairment; traumatic brain injury; vision
impairment
ID VISUAL FUNCTION; POLYTRAUMA; MILITARY; HEARING; IRAQI; WAR; DYSFUNCTION;
POPULATION; SOLDIERS; OUTCOMES
AB Objective: To describe the prevalence of self-reported rates of auditory, visual, and dual sensory impairment (DSI) in Afghanistan and Iraq war Veterans receiving traumatic brain injury (TBI) evaluations. Design: Retrospective medical chart review. Participants: Thirty-six thousand nine hundred nineteen Veterans who received a TBI evaluation between October 2007 and June 2009. Final sample included 12,521 subjects judged to have deployment-related TBI and a comparison group of 9106 participants with no evidence of TBI. Main Outcome Measure: Self-reported auditory and visual impairment. Results: Self-reported sensory impairment rates were: 34.6% for DSI, 31.3% for auditory impairment only, 9.9% for visual impairment only, and 24.2% for none/mild sensory impairment. Those with TBI and blast exposure had highest rate of DSI. Regression analyses showed that auditory impairment was the strongest predictor of visual impairment, and vice versa, suggesting these impairments may derive from a common source. Conclusions: Veterans who self-report clinically significant hearing or vision difficulty during routine TBI evaluation should be evaluated systematically and comprehensively to determine the extent of sensory impairment. Identifying DSI could allow clinicians to collaborate and maximize rehabilitation.
C1 [Pogoda, Terri K.; Stolzmann, Kelly L.; Meterko, Mark] Ctr Org Leadership & Management Res, VA Boston Healthcare Syst, Boston, MA 02130 USA.
[Lew, Henry L.] Virginia Commonwealth Univ, Def & Vet Brain Injury Ctr DVBIC, Richmond, VA USA.
[Lew, Henry L.; Cifu, David X.] Virginia Commonwealth Univ, Dept Phys Med & Rehabil, Sch Med, Richmond, VA USA.
[Pogoda, Terri K.; Meterko, Mark; Hendricks, Ann M.] Boston Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA USA.
[Cifu, David X.] Hunter Holmes McGuire VA Med Ctr, Phys Med & Rehabil Serv, Richmond, VA USA.
[Amara, Jomana] Naval Postgrad Sch, Def Resources Management Inst, Monterey, CA USA.
[Hendricks, Ann M.] VA Boston Healthcare Syst, Boston, MA USA.
RP Pogoda, TK (reprint author), Ctr Org Leadership & Management Res, VA Boston Healthcare Syst, 150 S Huntington Ave 152M, Boston, MA 02130 USA.
EM terri.pogoda@va.gov
FU Office of Research and Development, Health Services R&D Service,
Department of Veterans Affairs [SDR 08-405]
FX This article is based on work supported by the Office of Research and
Development, Health Services R&D Service, Department of Veterans
Affairs, through SDR 08-405. The study was reviewed and approved by the
Institutional Review Board of the VA Boston Healthcare System.
NR 33
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U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-9701
J9 J HEAD TRAUMA REHAB
JI J. Head Trauma Rehabil.
PD NOV-DEC
PY 2011
VL 26
IS 6
BP 489
EP 496
DI 10.1097/HTR.0b013e318204e54b
PG 8
WC Clinical Neurology; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA 859AC
UT WOS:000297845000005
PM 21386715
ER
PT J
AU Mumenthaler, SM
Foo, J
Leder, K
Choi, NC
Agus, DB
Pao, W
Mallick, P
Michor, F
AF Mumenthaler, Shannon M.
Foo, Jasmine
Leder, Kevin
Choi, Nathan C.
Agus, David B.
Pao, William
Mallick, Parag
Michor, Franziska
TI Evolutionary Modeling of Combination Treatment Strategies To Overcome
Resistance to Tyrosine Kinase Inhibitors in Non-Small Cell Lung Cancer
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE non-small cell lung cancer; evolutionary modeling; erlotinib;
paclitaxel; resistance; treatment strategies
ID PHASE-III TRIAL; DRUG-RESISTANCE; TARGETED THERAPY; EGFR MUTATIONS;
GEFITINIB; ERLOTINIB; PACLITAXEL; CARBOPLATIN; TUMORS; CISPLATIN
AB Many initially successful anticancer therapies lose effectiveness over time, and eventually, cancer cells acquire resistance to the therapy. Acquired resistance remains a major obstacle to improving remission rates and achieving prolonged disease-free survival. Consequently, novel approaches to overcome or prevent resistance are of significant clinical importance. There has been considerable interest in treating non-small cell lung cancer (NSCLC) with combinations of EGFR-targeted therapeutics (e.g., erlotinib) and cytotoxic therapeutic; (e.g., paclitaxel); however, acquired resistance to erlotinib, driven by a variety of mechanisms, remains an obstacle to treatment success. In about 50% of cases, resistance is due to a T790M point mutation in EGER, and T790M-containing cells ultimately dominate the tumor composition and lead to tumor regrowth. We employed a combined experimental and mathematical modeling-based approach to identify treatment strategies that impede the outgrowth of primary T790M-mediated resistance in NSCLC populations. Our mathematical model predicts the population dynamics of mixtures of sensitive and resistant cells, thereby describing how the tumor composition, initial fraction of resistant cells, and degree of selective pressure influence the time until progression of disease. Model development relied upon quantitative experimental measurements of cell proliferation and death using a novel microscopy approach. Using this approach, we systematically explored the space of combination treatment strategies and demonstrated that optimally timed sequential strategies yielded large improvements in survival outcome relative to monotherapies at the same concentrations. Our investigations revealed regions of the treatment space in which low-dose sequential combination strategies, after predinical validation, may lead to a tumor reduction and improved survival outcome for patients with T790M-mediated resistance.
C1 [Mallick, Parag] Stanford Univ, Dept Radiol, Canary Ctr Stanford Canc Early Detect, Palo Alto, CA 94304 USA.
[Mumenthaler, Shannon M.; Choi, Nathan C.; Agus, David B.; Mallick, Parag] Univ So Calif, Keck Sch Med, Ctr Appl Mol Med, Los Angeles, CA 90033 USA.
[Foo, Jasmine] Univ Minnesota, Sch Math, Minneapolis, MN 55455 USA.
[Leder, Kevin] Univ Minnesota, Program Ind & Syst Engn, Minneapolis, MN USA.
[Pao, William] Vanderbilt Ingram Canc Ctr, Dept Med, Nashville, TN USA.
[Michor, Franziska] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Michor, Franziska] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
RP Mallick, P (reprint author), Stanford Univ, Dept Radiol, Canary Ctr Stanford Canc Early Detect, 1501 S Calif Ave,Room 2212, Palo Alto, CA 94304 USA.
EM paragm@stanford.edu; michor@jimmy.harvard.edu
FU National Cancer Institute Cancer Center [P30CA014089]; USC Provost
Office; Dean's Development Funds; Keck School of Medicine; National
Cancer Institute [U54CA143798, U54CA143907]; CCNE-T [U54CA151459-01]
FX The authors would like to thank Thea Tlsty, Philippe Gascard, Luis
Estevez-Salmeron, David Liao, Joshua LaBaer, and Laura Gonzalez for
their discussion of this project and Mitch Gross for providing his
clinical perspective and advice on the manuscript. Cellomics array scan
measurements were performed at the USC Broad CIRM Center and Norris
Comprehensive Cancer Center Flow Cytometry Core Facility that is
supported in part by the National Cancer Institute Cancer Center Shared
Grant award P30CA014089 and the USC Provost Office, Dean's Development
Funds, Keck School of Medicine. The content is solely the responsibility
of the authors and does not necessarily represent the official views of
the National Cancer Institute or the National Institutes of Health. This
work was funded by National Cancer Institute Grants U54CA143798 and
U54CA143907 to establish Physical Sciences-Oncology Centers at the
Dana-Farber Cancer Institute and University of Southern California,
respectively. In addition, funding support was received from CCNE-T
Grant U54CA151459-01.
NR 42
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Z9 24
U1 1
U2 10
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD NOV-DEC
PY 2011
VL 8
IS 6
BP 2069
EP 2079
DI 10.1021/mp200270v
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 855BA
UT WOS:000297537300011
PM 21995722
ER
PT J
AU Kuil, J
Buckle, T
Oldenburg, J
Yuan, HS
Borowsky, AD
Josephson, L
van Leeuwen, FWB
AF Kuil, Joeri
Buckle, Tessa
Oldenburg, Joppe
Yuan, Hushan
Borowsky, Alexander D.
Josephson, Lee
van Leeuwen, Fijs W. B.
TI Hybrid Peptide Dendrimers for Imaging of Chemokine Receptor 4 (CXCR4)
Expression
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
DE CXCR4; peptides; dendrimers; multimodal hybrid imaging; fluorescence;
SPECT/CT
ID CARCINOMA IN-SITU; MOUSE MODEL; ANTAGONIST; CANCER; PROBES; CELLS;
CONJUGATION; THERAPY; LIGANDS; AMD3100
AB The chemokine receptor 4 (CXCR4), which is overexpressed in many types of cancer, is an emerging target in the field of molecular imaging and therapeutics. The CXCR4 binding of several peptides, including the cyclic Ac-TZ14011, has already been validated. In this study mono-, di- and tetrameric Ac-TZ14011-containing dendrimers were prepared and functionalized with a multimodal (hybrid) label, consisting of a Cy5.5-like fluorophore and a DTPA chelate. Confocal microscopy revealed that all three dendrimers were membrane bound at 4 degrees C, consistent with CXCR4 binding in vitro. The unlabeled dimer and tetrarner had a somewhat lower affinity for CXCR4 than the unlabeled monomer. However, when labeled with the multimodal label the CXCR4 affinity of the dimer and tetramer was considerably higher compared to that of the labeled monomer. On top of that, biodistribution studies revealed that the additional peptides in the dimer and tetramer reduced nonspecific muscle uptake. Thus, multimerization of the cyclic Ac-TZ14011 peptide reduces the negative influence of the multimodal label on the receptor affinity and the biodistribution.
C1 [Kuil, Joeri; Buckle, Tessa; van Leeuwen, Fijs W. B.] Leiden Univ, Med Ctr, Dept Radiol, NL-2300 RC Leiden, Netherlands.
[Kuil, Joeri; Buckle, Tessa; Oldenburg, Joppe; van Leeuwen, Fijs W. B.] Netherlands Canc Inst, Antoni van Leeuwenhoek Hosp, Div Diagnost Oncol, NL-1066 CX Amsterdam, Netherlands.
[Yuan, Hushan; Josephson, Lee] Massachusetts Gen Hosp, Ctr Translat Nucl Med & Mol Imaging, Charlestown, MA 02129 USA.
[Yuan, Hushan; Josephson, Lee] Harvard Univ, Sch Med, Boston, MA 02129 USA.
[Borowsky, Alexander D.] Univ Calif Davis, Ctr Comparat Med, Sch Med, Dept Pathol & Lab Med, Sacramento, CA 95817 USA.
RP van Leeuwen, FWB (reprint author), Leiden Univ, Med Ctr, Dept Radiol, Albinusdreef 2, NL-2300 RC Leiden, Netherlands.
EM f.w.b.van_leeuwen@lumc.nl
OI van leeuwen, Fijs/0000-0002-6844-4025; Buckle, Tessa/0000-0003-2980-6895
FU KWF [PGF 2009-4344]; CTMM, the Centre for Translational Molecular
Medicine [030-104]
FX This research is supported, in part, by a KWF-translational research
award (Grant No. PGF 2009-4344; F.W.B.v.L.), and within the framework of
CTMM, the Centre for Translational Molecular Medicine
(http://www.ctmm.nl), project Breast CARE (Grant 030-104; J.K.).
NR 52
TC 21
Z9 21
U1 0
U2 27
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1543-8384
J9 MOL PHARMACEUT
JI Mol. Pharm.
PD NOV-DEC
PY 2011
VL 8
IS 6
BP 2444
EP 2453
DI 10.1021/mp200401p
PG 10
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 855BA
UT WOS:000297537300047
PM 22085282
ER
PT J
AU Weissleder, R
Castro, C
AF Weissleder, Ralph
Castro, Cesar
TI Nanomedicine in oncology: miniaturized means to an enormous end
SO NANOMEDICINE
LA English
DT Editorial Material
C1 [Castro, Cesar] Massachusetts Gen Hosp, Div Oncol, Boston, MA 02114 USA.
[Weissleder, Ralph] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
RP Castro, C (reprint author), Massachusetts Gen Hosp, Div Oncol, 55 Fruit St,Yawkey 9E, Boston, MA 02114 USA.
EM rweissleder@mgh.harvard.edu; Castro.Cesar@mgh.harvard.edu
NR 0
TC 0
Z9 0
U1 0
U2 3
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1743-5889
J9 NANOMEDICINE-UK
JI Nanomedicine
PD NOV
PY 2011
VL 6
IS 9
BP 1495
EP 1498
DI 10.2217/NNM.11.138
PG 4
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
SC Biotechnology & Applied Microbiology; Science & Technology - Other
Topics
GA 860FD
UT WOS:000297933300010
PM 22077461
ER
PT J
AU Murrough, JW
Iacoviello, B
Neumeister, A
Charney, DS
Iosifescu, DV
AF Murrough, James W.
Iacoviello, Brian
Neumeister, Alexander
Charney, Dennis S.
Iosifescu, Dan V.
TI Cognitive dysfunction in depression: Neurocircuitry and new therapeutic
strategies
SO NEUROBIOLOGY OF LEARNING AND MEMORY
LA English
DT Review
DE Depression; Cognition; Neuropsychology; Emotion regulation;
Neuroimaging; Therapeutics; Cognitive dysfunction
ID OBSESSIVE-COMPULSIVE DISORDER; WHITE-MATTER HYPERINTENSITIES;
POSITRON-EMISSION-TOMOGRAPHY; SUBGENUAL PREFRONTAL CORTEX; UNIPOLAR
MAJOR DEPRESSION; HAPPY FACIAL EXPRESSIONS; BRAIN GLUCOSE-METABOLISM;
STAR-ASTERISK-D; ANTIDEPRESSANT-TREATMENT; EMOTION REGULATION
AB Major depressive disorder (MDD) is a disabling medical condition associated with significant morbidity, mortality and public health costs. However, neurocircuitry abnormalities underlying depression remain incompletely understood and consequently current treatment options are unfortunately limited in efficacy. Recent research has begun to focus specifically on cognitive aspects of depression and potential neurobiological correlates. Two fundamental types of cognitive dysfunction observed in MOD are cognitive biases, which include distorted information processing or attentional allocation toward negative stimuli, and cognitive deficits, which include impairments in attention, short-term memory and executive functioning. In this article, we present a selective review of current research findings in these domains and examine neuroimaging research that is beginning to characterize the neurocircuitry underlying these biases and deficits. We propose that deficient cognitive functioning, attention biases and the sustained negative affect characteristic of MOD can be understood as arising in part from dysfunctional prefrontal-subcortical circuitry and related disturbances in the cognitive control of emotion. Finally, we highlight potential new pharmacological and non-pharmacological therapeutic strategies for MDD based on an evolving mechanistic understanding of the disorder. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Murrough, James W.; Iacoviello, Brian; Neumeister, Alexander; Iosifescu, Dan V.] Mt Sinai Sch Med, Dept Psychiat, Mood & Anxiety Disorders Program, New York, NY 10029 USA.
[Iacoviello, Brian] James J Peters VA Med Ctr, MIRECC, Bronx, NY USA.
[Neumeister, Alexander] VA Connecticut Healthcare Syst, Mol Imaging Program, West Haven, CT USA.
[Charney, Dennis S.] Mt Sinai Sch Med, Dept Neurosci, New York, NY 10029 USA.
[Charney, Dennis S.] Mt Sinai Sch Med, Dept Syst Pharmacol & Therapeut, New York, NY 10029 USA.
[Charney, Dennis S.] Mt Sinai Sch Med, Off Dean, New York, NY 10029 USA.
RP Murrough, JW (reprint author), Mt Sinai Sch Med, Dept Psychiat, Mood & Anxiety Disorders Program, Box 1230, New York, NY 10029 USA.
EM james.murrough@mssm.edu
RI Murrough, James/J-7129-2013
OI Murrough, James/0000-0001-6286-1242
FU Mount Sinai School of Medicine
FX Dr. Charney has been named as an inventor on a use-patent of ketamine
for the treatment of depression. If ketamine were shown to be effective
in the treatment of depression and received approval from the Food and
Drug Administration for this indication, Dr. Chamey and the Mount Sinai
School of Medicine could benefit financially. All other authors report
no completing interests.
NR 175
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U1 17
U2 65
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1074-7427
J9 NEUROBIOL LEARN MEM
JI Neurobiol. Learn. Mem.
PD NOV
PY 2011
VL 96
IS 4
SI SI
BP 553
EP 563
DI 10.1016/j.nlm.2011.06.006
PG 11
WC Behavioral Sciences; Neurosciences; Psychology; Psychology,
Multidisciplinary
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 859UD
UT WOS:000297900400006
PM 21704176
ER
PT J
AU McCoy, JG
Strecker, RE
AF McCoy, John G.
Strecker, Robert E.
TI The cognitive cost of sleep lost
SO NEUROBIOLOGY OF LEARNING AND MEMORY
LA English
DT Review
DE Sleep loss; Learning; Memory; Cognition; Attention; Sleep deprivation;
Executive function
ID PSYCHOMOTOR VIGILANCE TASK; MORRIS WATER MAZE; DECLARATIVE MEMORY
CONSOLIDATION; EXPERIENCE-DEPENDENT CHANGES; LONG-TERM POTENTIATION;
ELEVATED PLUS-MAZE; EYE-MOVEMENT SLEEP; REACTION-TIME-TASK; REM-SLEEP;
PARADOXICAL SLEEP
AB A substantial body of literature supports the intuitive notion that a good night's sleep can facilitate human cognitive performance the next day. Deficits in attention, learning & memory, emotional reactivity, and higher-order cognitive processes, such as executive function and decision making, have all been documented following sleep disruption in humans. Thus, whilst numerous clinical and experimental studies link human sleep disturbance to cognitive deficits, attempts to develop valid and reliable rodent models of these phenomena are fewer, and relatively more recent. This review focuses primarily on the cognitive impairments produced by sleep disruption in rodent models of several human patterns of sleep loss/sleep disturbance. Though not an exclusive list, this review will focus on four specific types of sleep disturbance: total sleep deprivation, experimental sleep fragmentation, selective REM sleep deprivation, and chronic sleep restriction. The use of rodent models can provide greater opportunities to understand the neurobiological changes underlying sleep loss induced cognitive impairments. Thus, this review concludes with a description of recent neurobiological findings concerning the neuroplastic changes and putative brain mechanisms that may underlie the cognitive deficits produced by sleep disturbances. Published by Elsevier Inc.
C1 [McCoy, John G.] VA Boston Healthcare Syst, Res Serv, Brockton, MA 02301 USA.
Harvard Univ, Sch Med, Dept Psychiat, Brockton, MA 02301 USA.
Stonehill Coll, Dept Psychol, Easton, MA 02357 USA.
RP McCoy, JG (reprint author), VA Boston Healthcare Syst, Res Serv, 940 Belmont St,151C, Brockton, MA 02301 USA.
EM jmccoy1@stonehill.edu; robert_strecker@hm-s.harvard.edu
FU Department of Veterans Affairs Medical Research Service; National
Institutes of Health [MH039683, HL060292, HL095491]
FX We thank authors of the original work cited, and M. Ali & L Shifflett
for assistance with the figures and editorial advice. The writing of
this review was supported by the Department of Veterans Affairs Medical
Research Service Award, and by the following grants from the National
Institutes of Health: MH039683, HL060292, and HL095491.
NR 171
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U1 8
U2 76
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1074-7427
J9 NEUROBIOL LEARN MEM
JI Neurobiol. Learn. Mem.
PD NOV
PY 2011
VL 96
IS 4
SI SI
BP 564
EP 582
DI 10.1016/j.nlm.2011.07.004
PG 19
WC Behavioral Sciences; Neurosciences; Psychology; Psychology,
Multidisciplinary
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 859UD
UT WOS:000297900400007
PM 21875679
ER
PT J
AU Bowman, CC
Johnson, L
Cox, M
Rick, C
Dougherty, M
Alt-White, AC
Wyte, T
Needleman, J
Dobalian, A
AF Bowman, Candice C.
Johnson, Linda
Cox, Malcolm
Rick, Catherine
Dougherty, Mary
Alt-White, Anna C.
Wyte, Tamar
Needleman, Jack
Dobalian, Aram
TI The Department of Veterans Affairs Nursing Academy (VANA): Forging
strategic alliances with schools of nursing to address nursing's
workforce needs
SO NURSING OUTLOOK
LA English
DT Article
DE Partnerships; Clinical instruction; Veterans Affairs
ID INTERORGANIZATIONAL RELATIONSHIPS; EDUCATION
AB In 2007, the Department of Veterans Affairs (VA) established the VA Nursing Academy (VANA), a 5-year, $60-million pilot program funding 15 partnerships between schools of nursing and local VA health care facilities nationwide, to expand nursing faculty, enhance clinical faculty development, increase nursing student enrollment, and promote educational innovations. VA is an ideal setting for educating nursing students owing to a well-educated registered nurse staff, an array of traditional and nontraditional settings, a state-of-the-art computerized electronic health record system, and a unique patient population. Challenges related to the complex nature of VANA partnerships, conceptualized as strategic alliances created between disparate subunits, each embedded in a larger organization, require careful governance to ensure smooth implementation. To ensure the program's aims are met, a 6-year national evaluation has been funded to help identify which strategies best achieve VANA's goals. The speed of economic recovery and the resulting changes in the nursing workforce are important determinants of VANA's future.
C1 [Bowman, Candice C.; Wyte, Tamar; Dobalian, Aram] VA Greater Los Angeles Healthcare Syst, HSR&D Ctr Study Healthcare Provider Behav, Sepulveda, CA 91343 USA.
[Johnson, Linda; Cox, Malcolm; Rick, Catherine; Dougherty, Mary; Alt-White, Anna C.] Vet Affairs Nursing Acad, Off Acad Affiliat, Dept Vet Affairs, Washington, DC USA.
[Needleman, Jack; Dobalian, Aram] Univ Calif Los Angeles, Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA 90024 USA.
RP Bowman, CC (reprint author), VA Greater Los Angeles Healthcare Syst, HSR&D Ctr Study Healthcare Provider Behav, 16111 Plummer St 152, Sepulveda, CA 91343 USA.
EM candice.bowman@va.gov
RI Needleman, Jack/I-5461-2013
OI Needleman, Jack/0000-0002-2875-0589
FU Department of Veterans Affairs, Veterans Health Administration, Office
of Academic Affiliations; Department of Veterans Affairs, Veterans
Health Administration, Office of Nursing Service
FX This material is based upon work supported by the Department of Veterans
Affairs, Veterans Health Administration, Offices of Academic
Affiliations and Nursing Service.
NR 31
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Z9 9
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0029-6554
J9 NURS OUTLOOK
JI Nurs. Outlook
PD NOV-DEC
PY 2011
VL 59
IS 6
BP 299
EP 307
DI 10.1016/j.outlook.2011.04.006
PG 9
WC Nursing
SC Nursing
GA 854IS
UT WOS:000297488800003
PM 21684561
ER
PT J
AU Miller, KK
Meenaghan, E
Lawson, EA
Misra, M
Gleysteen, S
Schoenfeld, D
Herzog, D
Klibanski, A
AF Miller, Karen K.
Meenaghan, Erinne
Lawson, Elizabeth A.
Misra, Madhusmita
Gleysteen, Suzanne
Schoenfeld, David
Herzog, David
Klibanski, Anne
TI Effects of Risedronate and Low-Dose Transdermal Testosterone on Bone
Mineral Density in Women With Anorexia Nervosa: A Randomized,
Placebo-Controlled Study EDITORIAL COMMENT
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
C1 [Miller, Karen K.] Massachusetts Gen Hosp, Harris Ctr Eating Disorders, Dept Biostat, Neuroendocrine Unit, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
RP Miller, KK (reprint author), Massachusetts Gen Hosp, Harris Ctr Eating Disorders, Dept Biostat, Neuroendocrine Unit, Boston, MA 02114 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7828
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD NOV
PY 2011
VL 66
IS 11
BP 690
EP 691
DI 10.1097/OGX.0b013e318234010f
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 865DX
UT WOS:000298292100011
ER
PT J
AU Tache, Y
Stengel, A
Vaudry, H
AF Tache, Yvette
Stengel, Andreas
Vaudry, Hubert
TI Special Issue: Ghrelin
SO PEPTIDES
LA English
DT Editorial Material
ID METABOLISM; PEPTIDES; HORMONE
C1 [Tache, Yvette] Univ Calif Los Angeles, David Geffen Sch Med, Digest Dis Res Ctr Anim Care, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90073 USA.
[Stengel, Andreas] Obes Ctr Berlin, Div Psychosomat Med, D-10117 Berlin, Germany.
[Vaudry, Hubert] Univ Rouen, Inserm U982, Lab Neuronal & Neuroendocrine Differentiat & Comm, Int Associated Lab Samuel de Champlain,European I, F-76821 Mont St Aignan, France.
RP Tache, Y (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Digest Dis Res Ctr Anim Care, VA Greater Los Angeles Healthcare Syst, 11301 Wilshire Blvd,CURE Bldg 115, Los Angeles, CA 90073 USA.
EM ytache@mednet.ucla.edu; hubert.vaudry@univ-rouen.fr
NR 12
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0196-9781
J9 PEPTIDES
JI Peptides
PD NOV
PY 2011
VL 32
IS 11
SI SI
BP 2151
EP 2152
DI 10.1016/j.peptides.2011.10.015
PG 2
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
GA 863XO
UT WOS:000298201800001
PM 22024141
ER
PT J
AU Stengel, A
Wang, LX
Tache, Y
AF Stengel, Andreas
Wang, Lixin
Tache, Yvette
TI Stress-related alterations of acyl and desacyl ghrelin circulating
levels: Mechanisms and functional implications
SO PEPTIDES
LA English
DT Review
DE Abdominal surgery; Food intake; Ghrelin-O-acyltransferase (GOAT);
Motility; Somatostatin 2 receptor
ID GROWTH-HORMONE SECRETAGOGUE; POSTOPERATIVE GASTRIC ILEUS; GENE-RELATED
PEPTIDE; O-ACYLTRANSFERASE GOAT; FASTED PLASMA GHRELIN; ACUTE LUNG
INJURY; RAT STOMACH; FOOD-INTAKE; MESSENGER-RNA; RECEPTOR EXPRESSION
AB Ghrelin is the only known peripherally produced and centrally acting peptide hormone that stimulates food intake and digestive functions. Ghrelin circulates as acylated and desacylated forms and recently the acylating enzyme, ghrelin-O-acyltransferase (GOAT) and the de-acylating enzyme, thioesterase 1/lysophospholipase 1 have been identified adding new layers of complexity to the regulation of ghrelin. Stress is known to alter gastrointestinal motility and food intake and was recently shown to modify circulating ghrelin and GOAT levels with differential responses related to the type of stressors including a reduction induced by physical stressors (abdominal surgery and immunological/endotoxin injection, exercise) and elevation by metabolic (cold exposure, acute fasting and caloric restriction) and psychological stressors. However, the pathways underlying the alterations of ghrelin under these various stress conditions are still largely to be defined and may relate to stress-associated autonomic changes. There is evidence that alterations of circulating ghrelin may contribute to the neuroendocrine and behavioral responses along with sustaining the energetic requirement needed upon repeated exposure to stressors. A better understanding of these mechanisms will allow targeting components of ghrelin signaling that may improve food intake and gastric motility alterations induced by stress. Published by Elsevier Inc.
C1 [Tache, Yvette] VA Greater Los Angeles Healthcare Syst, CURE Digest Dis Res Ctr, Los Angeles, CA 90073 USA.
[Stengel, Andreas; Wang, Lixin; Tache, Yvette] Univ Calif Los Angeles, David Geffen Sch Med, CURE Digest Dis Res Ctr, Los Angeles, CA 90095 USA.
[Stengel, Andreas; Wang, Lixin; Tache, Yvette] Univ Calif Los Angeles, David Geffen Sch Med, Ctr Neurobiol Stress & Womens Hlth, Div Digest Dis, Los Angeles, CA 90095 USA.
[Stengel, Andreas] Univ Med, Charite, Dept Med, Div Psychosomat Med & Psychotherapy, Berlin, Germany.
RP Tache, Y (reprint author), VA Greater Los Angeles Healthcare Syst, CURE Digest Dis Res Ctr, Bldg 115,Room 117,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM andreas.stengel@charite.de; ytache@mednet.ucla.edu
FU VA; NIH [DK-33061, DK-57238]
FX Y.T. is recipient of VA Research Career Scientist Award and NIH
R01grants DK-33061, DK-57238 and VA Merit Award. We thank Ms. Eugenia Hu
for careful reading of the manuscript.
NR 141
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U1 1
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0196-9781
EI 1873-5169
J9 PEPTIDES
JI Peptides
PD NOV
PY 2011
VL 32
IS 11
SI SI
BP 2208
EP 2217
DI 10.1016/j.peptides.2011.07.002
PG 10
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
GA 863XO
UT WOS:000298201800007
PM 21782868
ER
PT J
AU Vu, JP
Wang, HS
Germano, PM
Pisegna, JR
AF Vu, John P.
Wang, Hank S.
Germano, Patrizia M.
Pisegna, Joseph R.
TI Ghrelin in neuroendocrine tumors
SO PEPTIDES
LA English
DT Review
DE Ghrelin; Metastatic neuroendocrine tumors; Endogenous; Orexigenic;
Cancer cachexia
ID GROWTH-HORMONE SECRETAGOGUE; DES-ACYL GHRELIN; AGOUTI-RELATED PROTEIN;
CARCINOID-TUMORS; MESSENGER-RNA; GASTROINTESTINAL-TRACT; ENDOCRINE
TUMORS; CHROMOGRANIN-A; SOMATOSTATIN ANALOGS; HELICOBACTER-PYLORI
AB Ghrelin is a 28 amino acid peptide, primarily produced by the oxyntic mucosa X/A like neuroendocrine cells in the stomach. It is also found in the small intestine, hypothalamus, pituitary gland, pancreas, heart, adipose tissue, and immune system. In gastrointestinal neuroendocrine tumors (NETs) ghrelin release has been well documented. Ghrelin is a brain-gut circuit peptide with an important role in the physiological regulation of appetite, response to hunger and starvation, metabolic and endocrine functions as energy expenditure, gastric motility and acid secretion, insulin secretion and glucose homeostasis, as well as in the potential connection to the central nervous system. Recently, there has been a significant interest in the biological effects of ghrelin in NETs. In this article, we present a comprehensive review of ghrelin's expression and a brief summary of ghrelin's physiological role in NETs patients with carcinoids, type A chronic atrophic gastritis (CAG), with or without MEN-1, and with and without liver metastases. We hope, with the research reviewed here, to offer compelling evidence of the potential significance of ghrelin in NETs, as well as to provide a useful guide to the future work in this area. Published by Elsevier Inc.
C1 [Vu, John P.; Wang, Hank S.; Germano, Patrizia M.; Pisegna, Joseph R.] Vet Adm GIAHS, Dept Gastroenterol & Hepatol, Los Angeles, CA 90073 USA.
[Vu, John P.; Wang, Hank S.; Germano, Patrizia M.; Pisegna, Joseph R.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
RP Pisegna, JR (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Div Gastroenterol & Hepatol, VA Greater Los Angeles Healthcare Syst, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM jpisegna@ucla.edu
NR 73
TC 7
Z9 7
U1 1
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0196-9781
J9 PEPTIDES
JI Peptides
PD NOV
PY 2011
VL 32
IS 11
SI SI
BP 2340
EP 2347
DI 10.1016/j.peptides.2011.10.006
PG 8
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism;
Pharmacology & Pharmacy
GA 863XO
UT WOS:000298201800025
PM 22041110
ER
PT J
AU Maxwell, CA
Benitez, J
Gomez-Baldo, L
Osorio, A
Bonifaci, N
Fernandez-Ramires, R
Costes, SV
Guino, E
Chen, H
Evans, GJR
Mohan, P
Catala, I
Petit, A
Aguilar, H
Villanueva, A
Aytes, A
Serra-Musach, J
Rennert, G
Lejbkowicz, F
Peterlongo, P
Manoukian, S
Peissel, B
Ripamonti, CB
Bonanni, B
Viel, A
Allavena, A
Bernard, L
Radice, P
Friedman, E
Kaufman, B
Laitman, Y
Dubrovsky, M
Milgrom, R
Jakubowska, A
Cybulski, C
Gorski, B
Jaworska, K
Durda, K
Sukiennicki, G
Lubinski, J
Shugart, YY
Domchek, SM
Letrero, R
Weber, BL
Hogervorst, FBL
Rookus, MA
Collee, JM
Devilee, P
Ligtenberg, MJ
van der Luijt, RB
Aalfs, CM
Waisfisz, Q
Wijnen, J
van Roozendaal, CEP
Easton, DF
Peock, S
Cook, M
Oliver, C
Frost, D
Harrington, P
Evans, DG
Lalloo, F
Eeles, R
Izatt, L
Chu, C
Eccles, D
Douglas, F
Brewer, C
Nevanlinna, H
Heikkinen, T
Couch, FJ
Lindor, NM
Wang, XS
Godwin, AK
Caligo, MA
Lombardi, G
Loman, N
Karlsson, P
Ehrencrona, H
von Wachenfeldt, A
Barkardottir, RB
Hamann, U
Rashid, MU
Lasa, A
Caldes, T
Andres, R
Schmitt, M
Assmann, V
Stevens, K
Offit, K
Curado, J
Tilgner, H
Guigo, R
Aiza, G
Brunet, J
Castellsague, J
Martrat, G
Urruticoechea, A
Blanco, I
Tihomirova, L
Goldgar, DE
Buys, S
John, EM
Miron, A
Southey, M
Daly, MB
Schmutzler, RK
Wappenschmidt, B
Meindl, A
Arnold, N
Deissler, H
Varon-Mateeva, R
Sutter, C
Niederacher, D
Imyamitov, E
Sinilnikova, OM
Stoppa-Lyonne, D
Mazoyer, S
Verny-Pierre, C
Castera, L
de Pauw, A
Bignon, YJ
Uhrhammer, N
Peyrat, JP
Vennin, P
Ferrer, SF
Collonge-Rame, MA
Mortemousque, I
Spurdle, AB
Beesley, J
Chen, XQ
Healey, S
Barcellos-Hoff, MH
Vidal, M
Gruber, SB
Lazaro, C
Capella, G
McGuffog, L
Nathanson, KL
Antoniou, AC
Chenevix-Trench, G
Fleisch, MC
Moreno, V
Pujana, MA
AF Maxwell, Christopher A.
Benitez, Javier
Gomez-Baldo, Laia
Osorio, Ana
Bonifaci, Nuria
Fernandez-Ramires, Ricardo
Costes, Sylvain V.
Guino, Elisabet
Chen, Helen
Evans, Gareth J. R.
Mohan, Pooja
Catala, Isabel
Petit, Anna
Aguilar, Helena
Villanueva, Alberto
Aytes, Alvaro
Serra-Musach, Jordi
Rennert, Gad
Lejbkowicz, Flavio
Peterlongo, Paolo
Manoukian, Siranoush
Peissel, Bernard
Ripamonti, Carla B.
Bonanni, Bernardo
Viel, Alessandra
Allavena, Anna
Bernard, Loris
Radice, Paolo
Friedman, Eitan
Kaufman, Bella
Laitman, Yael
Dubrovsky, Maya
Milgrom, Roni
Jakubowska, Anna
Cybulski, Cezary
Gorski, Bohdan
Jaworska, Katarzyna
Durda, Katarzyna
Sukiennicki, Grzegorz
Lubinski, Jan
Shugart, Yin Yao
Domchek, Susan M.
Letrero, Richard
Weber, Barbara L.
Hogervorst, Frans B. L.
Rookus, Matti A.
Collee, J. Margriet
Devilee, Peter
Ligtenberg, Marjolijn J.
van der Luijt, Rob B.
Aalfs, Cora M.
Waisfisz, Quinten
Wijnen, Juul
van Roozendaal, Cornelis E. P.
Easton, Douglas F.
Peock, Susan
Cook, Margaret
Oliver, Clare
Frost, Debra
Harrington, Patricia
Evans, D. Gareth
Lalloo, Fiona
Eeles, Rosalind
Izatt, Louise
Chu, Carol
Eccles, Diana
Douglas, Fiona
Brewer, Carole
Nevanlinna, Heli
Heikkinen, Tuomas
Couch, Fergus J.
Lindor, Noralane M.
Wang, Xianshu
Godwin, Andrew K.
Caligo, Maria A.
Lombardi, Grazia
Loman, Niklas
Karlsson, Per
Ehrencrona, Hans
von Wachenfeldt, Anna
Barkardottir, Rosa Bjork
Hamann, Ute
Rashid, Muhammad U.
Lasa, Adriana
Caldes, Trinidad
Andres, Raquel
Schmitt, Michael
Assmann, Volker
Stevens, Kristen
Offit, Kenneth
Curado, Joao
Tilgner, Hagen
Guigo, Roderic
Aiza, Gemma
Brunet, Joan
Castellsague, Joan
Martrat, Griselda
Urruticoechea, Ander
Blanco, Ignacio
Tihomirova, Laima
Goldgar, David E.
Buys, Saundra
John, Esther M.
Miron, Alexander
Southey, Melissa
Daly, Mary B.
Schmutzler, Rita K.
Wappenschmidt, Barbara
Meindl, Alfons
Arnold, Norbert
Deissler, Helmut
Varon-Mateeva, Raymonda
Sutter, Christian
Niederacher, Dieter
Imyamitov, Evgeny
Sinilnikova, Olga M.
Stoppa-Lyonne, Dominique
Mazoyer, Sylvie
Verny-Pierre, Carole
Castera, Laurent
de Pauw, Antoine
Bignon, Yves-Jean
Uhrhammer, Nancy
Peyrat, Jean-Philippe
Vennin, Philippe
Ferrer, Sandra Fert
Collonge-Rame, Marie-Agnes
Mortemousque, Isabelle
Spurdle, Amanda B.
Beesley, Jonathan
Chen, Xiaoqing
Healey, Sue
Barcellos-Hoff, Mary Helen
Vidal, Marc
Gruber, Stephen B.
Lazaro, Conxi
Capella, Gabriel
McGuffog, Lesley
Nathanson, Katherine L.
Antoniou, Antonis C.
Chenevix-Trench, Georgia
Fleisch, Markus C.
Moreno, Victor
Angel Pujana, Miguel
CA HEBON
EMBRACE
SWE-BRCA
BCFR
GEMO Study Collaborators
kConFab
TI Interplay between BRCA1 and RHAMM Regulates Epithelial Apicobasal
Polarization and May Influence Risk of Breast Cancer
SO PLOS BIOLOGY
LA English
DT Article
ID CENTROSOMAL MICROTUBULE NUCLEATION; PROGENITOR-CELL FATE; MUTATION
CARRIERS; MAMMARY-GLAND; MITOTIC SPINDLE; STEM-CELLS; MULTIPLE-MYELOMA;
BRCA1-DEPENDENT UBIQUITINATION; ADHERENS JUNCTIONS; MISSENSE MUTATIONS
AB Differentiated mammary epithelium shows apicobasal polarity, and loss of tissue organization is an early hallmark of breast carcinogenesis. In BRCA1 mutation carriers, accumulation of stem and progenitor cells in normal breast tissue and increased risk of developing tumors of basal-like type suggest that BRCA1 regulates stem/progenitor cell proliferation and differentiation. However, the function of BRCA1 in this process and its link to carcinogenesis remain unknown. Here we depict a molecular mechanism involving BRCA1 and RHAMM that regulates apicobasal polarity and, when perturbed, may increase risk of breast cancer. Starting from complementary genetic analyses across families and populations, we identified common genetic variation at the low-penetrance susceptibility HMMR locus (encoding for RHAMM) that modifies breast cancer risk among BRCA1, but probably not BRCA2, mutation carriers: n = 7,584, weighted hazard ratio ((w)HR) = 1.09 (95% CI 1.02-1.16), p(trend) = 0.017; and n = 3,965, (w)HR = 1.04 (95% CI 0.94-1.16), p(trend) = 0.43; respectively. Subsequently, studies of MCF10A apicobasal polarization revealed a central role for BRCA1 and RHAMM, together with AURKA and TPX2, in essential reorganization of microtubules. Mechanistically, reorganization is facilitated by BRCA1 and impaired by AURKA, which is regulated by negative feedback involving RHAMM and TPX2. Taken together, our data provide fundamental insight into apicobasal polarization through BRCA1 function, which may explain the expanded cell subsets and characteristic tumor type accompanying BRCA1 mutation, while also linking this process to sporadic breast cancer through perturbation of HMMR/RHAMM.
C1 [Maxwell, Christopher A.; Gomez-Baldo, Laia; Bonifaci, Nuria; Aguilar, Helena; Villanueva, Alberto; Aytes, Alvaro; Serra-Musach, Jordi; Aiza, Gemma; Martrat, Griselda; Urruticoechea, Ander; Angel Pujana, Miguel] Bellvitge Biomed Res Inst IDIBELL, Catalan Inst Oncol, Translat Res Lab, Lhospitalet De Llobregat, Catalonia, Spain.
[Benitez, Javier; Osorio, Ana; Fernandez-Ramires, Ricardo] Spanish Natl Canc Res Ctr, Human Canc Genet Programme, Madrid, Spain.
[Bonifaci, Nuria; Guino, Elisabet; Serra-Musach, Jordi; Moreno, Victor; Angel Pujana, Miguel] IDIBELL, Catalan Inst Oncol, Biomarkers & Susceptibil Unit, Lhospitalet De Llobregat, Catalonia, Spain.
[Costes, Sylvain V.; Barcellos-Hoff, Mary Helen] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Div Life Sci, Berkeley, CA 94720 USA.
[Catala, Isabel; Petit, Anna] Univ Hosp Bellvitge, IDIBELL, Dept Pathol, Lhospitalet De Llobregat, Catalonia, Spain.
[Rennert, Gad; Lejbkowicz, Flavio] Technion Israel Inst Technol, Carmel Med Ctr, Dept Community Med & Epidemiol, CHS Natl Canc Control Ctr, Haifa, Israel.
[Rennert, Gad; Lejbkowicz, Flavio] Technion Israel Inst Technol, B Rappaport Fac Med, Haifa, Israel.
[Peterlongo, Paolo; Ripamonti, Carla B.; Radice, Paolo] Fdn IRCCS, Dept Prevent & Predict Med, Unit Mol Bases Genet Risk & Genet Testing, Ist Nazl Tumori, Milan, Italy.
[Peterlongo, Paolo; Ripamonti, Carla B.; Radice, Paolo] IFOM Fdn, Ist FIRC Oncol Mol, Milan, Italy.
[Manoukian, Siranoush; Peissel, Bernard; Ripamonti, Carla B.] Fdn IRCCS, Ist Nazl Tumori, Dept Prevent & Predict Med, Unit Med Genet, Milan, Italy.
[Bonanni, Bernardo] Ist Europeo Oncol, Div Canc Prevent & Genet, Milan, Italy.
[Viel, Alessandra] IRCCS, Ctr Riferimento Oncol, Div Expt Oncol 1, Aviano, Italy.
[Allavena, Anna] Univ Turin, Dept Genet Biol & Biochem, Turin, Italy.
[Bernard, Loris] Ist Europeo Oncol, Dept Expt Oncol, Milan, Italy.
[Bernard, Loris] Consortium Genom Technol Cogentech, Milan, Italy.
[Friedman, Eitan; Kaufman, Bella; Laitman, Yael; Dubrovsky, Maya; Milgrom, Roni] Chaim Sheba Med Ctr, Inst Human Genet, Susanne Levy Gertner Oncogenet Unit, Ramat Gan, Israel.
[Friedman, Eitan] Tel Aviv Univ, Sackler Fac Med, Ramat Aviv, Israel.
[Jakubowska, Anna; Cybulski, Cezary; Gorski, Bohdan; Jaworska, Katarzyna; Durda, Katarzyna; Sukiennicki, Grzegorz; Lubinski, Jan] Pomeranian Med Univ, Dept Genet & Pathol, Int Hereditary Canc Ctr, Szczecin, Poland.
[Shugart, Yin Yao] NIMH, Unit Stat Genet, Div Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Domchek, Susan M.; Letrero, Richard; Weber, Barbara L.; Nathanson, Katherine L.] Univ Penn, Sch Med, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Hogervorst, Frans B. L.] Netherlands Canc Inst, Dept Pathol, Family Canc Clin, NL-1066 CX Amsterdam, Netherlands.
[Rookus, Matti A.] Netherlands Canc Inst, Dept Epidemiol, Amsterdam, Netherlands.
[Collee, J. Margriet] Erasmus Univ, Dept Clin Genet, Med Ctr, Rotterdam Family Canc Clin, NL-3000 DR Rotterdam, Netherlands.
[Devilee, Peter] Leiden Univ, Dept Genet Epidemiol, Med Ctr, Leiden, Netherlands.
[Ligtenberg, Marjolijn J.] Radboud Univ Nijmegen, Dept Human Genet, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[van der Luijt, Rob B.] Univ Utrecht, Med Ctr, Dept Clin Mol Genet, Utrecht, Netherlands.
[Aalfs, Cora M.] Univ Amsterdam, Acad Med Ctr, Dept Clin Genet, NL-1105 AZ Amsterdam, Netherlands.
[Waisfisz, Quinten] Vrije Univ Amsterdam, Med Ctr, Dept Clin Genet, Amsterdam, Netherlands.
[Wijnen, Juul] Leiden Univ, Med Ctr, Ctr Human & Clin Genet, Leiden, Netherlands.
[van Roozendaal, Cornelis E. P.] Univ Med Ctr, Dept Clin Genet, Maastricht, Netherlands.
[Easton, Douglas F.; Peock, Susan; Cook, Margaret; Oliver, Clare; Frost, Debra; McGuffog, Lesley; Antoniou, Antonis C.; EMBRACE] Univ Cambridge, Dept Publ Hlth & Primary Care, Ctr Canc Genet Epidemiol, Cambridge, England.
[Harrington, Patricia] Univ Cambridge, Dept Oncol, Cambridge, England.
[Evans, D. Gareth; Lalloo, Fiona] Cent Manchester Univ Hosp NHS Fdn Trust, Manchester Acad Hlth Sci Ctr, Manchester, Lancs, England.
[Eeles, Rosalind] Royal Marsden NHS Fdn Trust, Sutton, Surrey, England.
[Izatt, Louise] Guys & St Thomas NHS Fdn Trust, London, England.
[Chu, Carol] St James Hosp, Yorkshire Reg Genet Serv, Leeds, W Yorkshire, England.
[Eccles, Diana] Princess Anne Hosp, Wessex Clin Genet Serv, Southampton, Hants, England.
[Douglas, Fiona] Newcastle Upon Tyne Hosp NHS Trust, Ctr Life, Inst Human Genet, Newcastle Upon Tyne, Tyne & Wear, England.
[Brewer, Carole] Royal Devon & Exeter Hosp, Dept Clin Genet, Exeter EX2 5DW, Devon, England.
[Nevanlinna, Heli; Heikkinen, Tuomas] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, FIN-00290 Helsinki, Finland.
[Couch, Fergus J.; Wang, Xianshu] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
[Lindor, Noralane M.] Mayo Clin, Dept Med Genet, Rochester, MN USA.
[Godwin, Andrew K.] Univ Kansas, Med Ctr, Dept Pathol & Lab Med, Kansas City, KS 66103 USA.
[Caligo, Maria A.; Lombardi, Grazia] Univ Pisa, Sect Genet Oncol, Dept Oncol, Pisa, Italy.
[Caligo, Maria A.; Lombardi, Grazia] Univ Hosp Pisa, Dept Lab Med, Pisa, Italy.
[Loman, Niklas] Univ Lund Hosp, Dept Oncol, S-22185 Lund, Sweden.
[Karlsson, Per] Sahlgrens Univ Hosp, Dept Oncol, Gothenburg, Sweden.
[Ehrencrona, Hans] Uppsala Univ, Rudbeck Lab, Dept Genet & Pathol, Uppsala, Sweden.
[von Wachenfeldt, Anna] Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
[Barkardottir, Rosa Bjork] Landspitali Univ Hosp, Dept Pathol, Reykjavik, Iceland.
[Hamann, Ute; Rashid, Muhammad U.] Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany.
[Rashid, Muhammad U.] Shaukat Khanum Mem Canc Hosp & Res Ctr, Dept Basic Sci, Lahore, Pakistan.
[Lasa, Adriana] Hosp Santa Creu & Sant Pau, Genet Serv, Barcelona, Catalonia, Spain.
[Caldes, Trinidad] Hosp Clin San Carlos, Mol Oncol Lab, Madrid, Spain.
[Andres, Raquel] Hosp Clin Zaragoza, Div Med Oncol, Zaragoza, Spain.
[Schmitt, Michael] Univ Rostock, Dept Internal Med 3, Rostock, Germany.
[Assmann, Volker] Univ Hosp Hamburg Eppendorf, Inst Tumor Biol, Ctr Med Expt, Hamburg, Germany.
[Stevens, Kristen] Univ Michigan, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Offit, Kenneth] Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, New York, NY 10021 USA.
[Curado, Joao; Tilgner, Hagen; Guigo, Roderic] Biomed Res Pk Barcelona PRBB, Ctr Genom Regulat CRG, Bioinformat & Genom Grp, Barcelona, Catalonia, Spain.
[Brunet, Joan; Castellsague, Joan; Blanco, Ignacio; Lazaro, Conxi; Capella, Gabriel] Girona Biomed Res Inst IdIBGi, Catalonia, Spain.
[Brunet, Joan; Castellsague, Joan; Blanco, Ignacio; Lazaro, Conxi; Capella, Gabriel] IDIBELL, Catalan Inst Oncol, Genet Counseling & Hereditary Canc Programme, Catalonia, Spain.
[Tihomirova, Laima] Latvian Biomed Res & Study Ctr, Riga, Latvia.
[Goldgar, David E.] Univ Utah, Sch Med, Dept Dermatol, Salt Lake City, UT USA.
[Buys, Saundra] Huntsman Canc Inst, Dept Internal Med, Salt Lake City, UT USA.
[John, Esther M.] Canc Prevent Inst Calif, Fremont, CA USA.
[Miron, Alexander] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Miron, Alexander] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Southey, Melissa] Univ Melbourne, Melbourne Sch Populat Hlth, Ctr Mol Environm Genet & Analyt MEGA Epidemiol, Melbourne, Vic 3010, Australia.
[Daly, Mary B.] Fox Chase Canc Ctr, Div Populat Sci, Philadelphia, PA 19111 USA.
[Schmutzler, Rita K.; Wappenschmidt, Barbara] Univ Cologne, Ctr Familial Breast & Ovarian Canc, D-50931 Cologne, Germany.
[Schmutzler, Rita K.; Wappenschmidt, Barbara] Univ Cologne, Ctr Integrated Oncol, D-50931 Cologne, Germany.
[Meindl, Alfons] Tech Univ Munich, Klinikum Rechts Isar, Dept Obstet & Gynaecol, D-8000 Munich, Germany.
[Arnold, Norbert] Univ Hosp Schleswig Holstein, Dept Obstet & Gynaecol, Div Oncol, Kiel, Germany.
[Deissler, Helmut] Univ Ulm, Dept Obstet & Gynecol, Ulm, Germany.
[Varon-Mateeva, Raymonda] Charite, Inst Humangenet, D-13353 Berlin, Germany.
[Sutter, Christian] Univ Heidelberg, Inst Human Genet, Heidelberg, Germany.
[Niederacher, Dieter] Univ Dusseldorf, Ctr Clin, Dept Obstet & Gynaecol, Div Mol Genet, D-40225 Dusseldorf, Germany.
[Imyamitov, Evgeny] NN Petrov Inst Oncol, St Petersburg, Russia.
[Sinilnikova, Olga M.] CHU Lyon, Ctr Leon Berard, Unite Mixte Genet Constitut Canc Frequents, Lyon, France.
[Sinilnikova, Olga M.; Mazoyer, Sylvie; Verny-Pierre, Carole] Univ Lyon, Ctr Leon Berard, CNRS UMR5201, Equipe Labellisee LIGUE 2008, Lyon, France.
[Stoppa-Lyonne, Dominique; Castera, Laurent; de Pauw, Antoine] Univ Paris 05, Serv Genet Oncol, INSERM, Inst Curie,U509, Paris, France.
[Bignon, Yves-Jean; Uhrhammer, Nancy] Univ Clermont Ferrand, Ctr Jean Perrin, Dept Oncogenet, Clermont Ferrand, France.
[Peyrat, Jean-Philippe] Ctr Oscar Lambret, Lab Oncol Mol Humaine, F-59020 Lille, France.
[Ferrer, Sandra Fert] Hotel Dieu Ctr Hosp, Lab Genet Chromosom, Chambery, France.
[Collonge-Rame, Marie-Agnes] CHU Besancon, Serv Genet Histol Biol Dev & Reprod, F-25030 Besancon, France.
[Mortemousque, Isabelle] CHU Bretonneau, Serv Genet, F-37044 Tours, France.
[Spurdle, Amanda B.; Beesley, Jonathan; Chen, Xiaoqing; Healey, Sue; Chenevix-Trench, Georgia] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
Peter MacCallum Canc Inst, Kathleen Cuningham Fdn, Consortium Res Familial Breast Canc, Melbourne, Australia.
[Vidal, Marc] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Vidal, Marc] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
[Vidal, Marc] Harvard Univ, Sch Med, Ctr Canc Syst Biol CCSB, Boston, MA USA.
[Gruber, Stephen B.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Fleisch, Markus C.] Univ Dusseldorf, Dept Obstet & Gynaecol, D-40225 Dusseldorf, Germany.
RP Maxwell, CA (reprint author), Child & Family Res Inst, Dept Pediat, Vancouver, BC, Canada.
EM cmaxwell@cfri.ubc.ca; mapujana@ico.scs.es
RI Spurdle, Amanda/A-4978-2011; Jakubowska, Anna/O-8050-2014; Guigo,
Roderic/D-1303-2010; Ligtenberg, Marjolijn/N-9666-2013;
Fernandez-Ramires, Ricardo/H-3707-2014; Ripamonti, Carla
Barbara/D-2247-2017; manoukian, siranoush/E-7132-2017; Peissel,
Bernard/E-8187-2017; Ehrencrona, Hans/M-5619-2014; pujana, Miguel
Angel/N-3127-2014; Arnold, Norbert/E-3012-2010; Maxwell,
Christopher/B-3044-2011; Costes, Sylvain/D-2522-2013; Radice,
Paolo/O-3119-2013; Aytes, Alvaro/B-5803-2014; Blanco,
Ignacio/D-2565-2013; Fleisch, Markus/E-4134-2014; Osorio,
Ana/I-4324-2014; Bernard, Loris/K-5953-2014; Aytes, Alvaro/M-1360-2014
OI Evans, Gareth/0000-0002-8482-5784; Spurdle, Amanda/0000-0003-1337-7897;
Brunet, Joan/0000-0003-1945-3512; Nevanlinna, Heli/0000-0002-0916-2976;
Moreno, Victor/0000-0002-2818-5487; Guigo, Roderic/0000-0002-5738-4477;
Ligtenberg, Marjolijn/0000-0003-1290-1474; Ripamonti, Carla
Barbara/0000-0002-2892-8164; manoukian, siranoush/0000-0002-6034-7562;
Peissel, Bernard/0000-0001-9233-3571; Eeles,
Rosalind/0000-0002-3698-6241; Nathanson, Katherine/0000-0002-6740-0901;
Ehrencrona, Hans/0000-0002-5589-3622; pujana, Miguel
Angel/0000-0003-3222-4044; Arnold, Norbert/0000-0003-4523-8808; Maxwell,
Christopher/0000-0002-0860-4031; Costes, Sylvain/0000-0002-8542-2389;
Aytes, Alvaro/0000-0003-0725-5340; Blanco, Ignacio/0000-0002-7414-7481;
Fleisch, Markus/0000-0002-8966-4721; Osorio, Ana/0000-0001-8124-3984;
Aytes, Alvaro/0000-0003-0725-5340
FU Spanish Ministries of Health, and Science ane Innovation [CB07/02/2005];
FIS [08/1120, 08/1359, 08/1635, 09/02483]; RTICCC [RD06/0020/1060,
RD06/0020/0028]; Transversal Action Against Cancer; Spanish Biomedical
Research Centre Networks for Epidemiology and Public Health, and Rare
Diseases; "Ramon y Cajal" Young Investigator Program; Spanish National
Society of Medical Oncology; Spanish Association Against Cancer [AECC
2010]; AGAUR Catalan Government Agency [2009SGR1489, 2009SGR293];
Beatriu Pinos Postdoctoral Program; Ramon Areces Foundation; "Roses
Contra el Cancer" Foundation; Michael Cuccione Foundation for Childhood
Cancer Research, Cancer Research-UK [C490/A10119, C1287/A8874,
C1287/A10118, C5047/A8385, C8197/A10123]; National Institute for Health
Research (UK); Association for International Cancer Research
[AICR-07-0454]; Ligue National Contre le Cancer (France); Association
"Le cancer du sein, parlons-en!"; Dutch Cancer Society [NKI 1998-1854,
2004-3088, 2007-3756]; Fondazione Italiana per la Ricerca sul Cancro
("Hereditary Tumors"); Associazione Italiana per la Ricerca sul Cancro
[4017]; Italian Ministero della Salute [RFPS-2006-3-340203]; Italian
Ministero dell'Universita e Ricerca [RBLAO3-BETH]; Fondazione IRCCS
Istituto Nazionale Tumori [INT "5x1000"]; Fondazione Cassa di Risparmio
di Pisa (Istituto Toscano Tumori); National Breast Cancer Foundation
(Australia); Australian National Health and Medical Research Council
[145684, 288704, 454508]; Queensland Cancer Fund; Cancer Councils of New
South Wales, Victoria, Tasmania, and South Australia; Cancer Foundation
of Western Australia; German Cancer Aid [107054]; Center for Molecular
Medicine Cologne [TV93]; National Cancer Institute (USA) [CA128978,
CA122340]; National Institutes of Health [RFA-CA-06-503, BCFR U01
CA69398, CA69417, CA69446, CA69467, CA69631, CA69638]; Research Triangle
Institute Informatics Support Center [RFP N02PC45022-46]; Specialized
Program of Research Excellence (SPORE) [P50 CA83638, CA113916];
Department of Defense [05/0612]; Eileen Stein Jacoby Fund; Breast Cancer
Research Foundation; Marianne and Robert MacDonald Foundation; Komen
Foundation; Helsinki University Central Hospital; Academy of Finland
[110663]; Finnish Cancer Society; Sigrid Juselius Foundation; EU
[223175, HEALTH-F2-2009-223175]
FX This work was funded by the Spanish Ministries of Health, and Science
ane Innovation (CB07/02/2005; FIS 08/1120, 08/1359, 08/1635, and
09/02483; RTICCC RD06/0020/1060 and RD06/0020/0028; Transversal Action
Against Cancer; the Spanish Biomedical Research Centre Networks for
Epidemiology and Public Health, and Rare Diseases; and the "Ramon y
Cajal" Young Investigator Program), the Spanish National Society of
Medical Oncology (2010), the Spanish Association Against Cancer (AECC
2010), the AGAUR Catalan Government Agency (2009SGR1489 and 2009SGR293;
and the Beatriu Pinos Postdoctoral Program), the Ramon Areces Foundation
(XV), the "Roses Contra el Cancer" Foundation, the Michael Cuccione
Foundation for Childhood Cancer Research, Cancer Research-UK
(C490/A10119, C1287/A8874, C1287/A10118, C5047/A8385, and C8197/A10123),
the National Institute for Health Research (UK), the Association for
International Cancer Research (AICR-07-0454), the Ligue National Contre
le Cancer (France), the Association "Le cancer du sein, parlons-en!",
the Dutch Cancer Society (NKI 1998-1854, 2004-3088, and 2007-3756), the
Fondazione Italiana per la Ricerca sul Cancro ("Hereditary Tumors"), the
Associazione Italiana per la Ricerca sul Cancro (4017), the Italian
Ministero della Salute (RFPS-2006-3-340203 and "Progetto Tumori
Femminili"), the Italian Ministero dell'Universita e Ricerca
(RBLAO3-BETH), the Fondazione IRCCS Istituto Nazionale Tumori (INT
"5x1000"), the Fondazione Cassa di Risparmio di Pisa (Istituto Toscano
Tumori), the National Breast Cancer Foundation (Australia), the
Australian National Health and Medical Research Council (145684, 288704,
and 454508), the Queensland Cancer Fund, the Cancer Councils of New
South Wales, Victoria, Tasmania, and South Australia, the Cancer
Foundation of Western Australia, the German Cancer Aid (107054), the
Center for Molecular Medicine Cologne (TV93), the National Cancer
Institute (USA; CA128978 and CA122340), National Institutes of Health
(RFA-CA-06-503, BCFR U01 CA69398, CA69417, CA69446, CA69467, CA69631,
and CA69638), the Research Triangle Institute Informatics Support Center
(RFP N02PC45022-46), the Specialized Program of Research Excellence
(SPORE P50 CA83638 and CA113916), the Department of Defense Breast
Cancer Research Program (05/0612), the Eileen Stein Jacoby Fund, the
Breast Cancer Research Foundation, the Marianne and Robert MacDonald
Foundation, the Komen Foundation, the Helsinki University Central
Hospital Research Fund, the Academy of Finland (110663), the Finnish
Cancer Society, the Sigrid Juselius Foundation, and the EU FP7 (223175,
HEALTH-F2-2009-223175). The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 68
TC 28
Z9 28
U1 1
U2 19
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1544-9173
J9 PLOS BIOL
JI PLoS. Biol.
PD NOV
PY 2011
VL 9
IS 11
AR e1001199
DI 10.1371/journal.pbio.1001199
PG 18
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics
GA 863HE
UT WOS:000298152600012
PM 22110403
ER
PT J
AU Peng, RR
Wang, AL
Li, J
Tucker, JD
Yin, YP
Chen, XS
AF Peng, Rui-Rui
Wang, Alberta L.
Li, Jing
Tucker, Joseph D.
Yin, Yue-Ping
Chen, Xiang-Sheng
TI Molecular Typing of Treponema pallidum: A Systematic Review and
Meta-Analysis
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Review
ID MACROLIDE RESISTANCE; SECONDARY SYPHILIS; TREATMENT FAILURE;
AZITHROMYCIN RESISTANCE; SUBSP PALLIDUM; SAN-FRANCISCO; SOUTH-AFRICA;
STRAINS; CHINA; BLOOD
AB Background: Syphilis is resurgent in many regions of the world. Molecular typing is a robust tool for investigating strain diversity and epidemiology. This study aimed to review original research on molecular typing of Treponema pallidum (T. pallidum) with three objectives: (1) to determine specimen types most suitable for molecular typing; (2) to determine T. pallidum subtype distribution across geographic areas; and (3) to summarize available information on subtypes associated with neurosyphilis and macrolide resistance.
Methodology/Principal Findings: Two researchers independently searched five databases from 1998 through 2010, assessed for eligibility and study quality, and extracted data. Search terms included "Treponema pallidum," or "syphilis," combined with the subject headings "molecular," "subtyping," "typing," "genotype," and "epidemiology." Sixteen eligible studies were included. Publication bias was not statistically significant by the Begg rank correlation test. Medians, inter-quartile ranges, and 95% confidence intervals were determined for DNA extraction and full typing efficiency. A random-effects model was used to perform subgroup analyses to reduce obvious between-study heterogeneity. Primary and secondary lesions and ear lobe blood specimens had an average higher yield of T. pallidum DNA (83.0% vs. 28.2%, chi(2) = 247.6, p<0.001) and an average higher efficiency of full molecular typing (80.9% vs. 43.1%, chi(2) = 102.3, p<0.001) compared to plasma, whole blood, and cerebrospinal fluid. A pooled analysis of subtype distribution based on country location showed that 14d was the most common subtype, and subtype distribution varied across geographic areas. Subtype data associated with macrolide resistance and neurosyphilis were limited.
Conclusions/Significance: Primary lesion was a better specimen for obtaining T. pallidum DNA than blood. There was wide geographic variation in T. pallidum subtypes. More research is needed on the relationship between clinical presentation and subtype, and further validation of ear lobe blood for obtaining T. pallidum DNA would be useful for future molecular studies of syphilis.
C1 [Peng, Rui-Rui; Wang, Alberta L.; Li, Jing; Yin, Yue-Ping; Chen, Xiang-Sheng] Chinese Acad Med Sci, Natl Ctr STD Control, Nanjing, Peoples R China.
[Peng, Rui-Rui; Wang, Alberta L.; Li, Jing; Yin, Yue-Ping; Chen, Xiang-Sheng] Peking Union Med Coll, Inst Dermatol, Nanjing, Peoples R China.
[Wang, Alberta L.] Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
[Tucker, Joseph D.] Massachusetts Gen Hosp, Infect Dis Unit, Boston, MA 02114 USA.
RP Peng, RR (reprint author), Chinese Acad Med Sci, Natl Ctr STD Control, Nanjing, Peoples R China.
EM chenxs@ncstdlc.org
FU Mega Project of the China National Science Research for the 11th
Five-Year Plan [2008ZX10001-005]; NIAID/UNC STI/TM Cooperative Research
Center [5U19 AI031496-18]
FX This study was supported by grants from the Mega Project of the China
National Science Research for the 11th Five-Year Plan (2008ZX10001-005)
and the NIAID/UNC STI/TM Cooperative Research Center (5U19 AI031496-18).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 47
TC 16
Z9 19
U1 0
U2 11
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 NOV
PY 2011
VL 5
IS 11
AR e1273
DI 10.1371/journal.pntd.0001273
PG 8
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 863AA
UT WOS:000298134000002
PM 22087340
ER
PT J
AU Maestas, KL
Benge, JF
Pastorek, NJ
LeMaire, A
Darrow, R
AF Maestas, Kacey Little
Benge, Jared F.
Pastorek, Nicholas J.
LeMaire, Ashley
Darrow, Rachel
TI Factor Structure of Posttraumatic Stress Disorder Symptoms in OEF/OIF
Veterans Presenting to a Polytrauma Clinic
SO REHABILITATION PSYCHOLOGY
LA English
DT Article
DE factor analysis; posttraumatic stress; veterans; mild traumatic brain
injury
ID TRAUMATIC BRAIN-INJURY; CONFIRMATORY FACTOR-ANALYSIS; PERSISTENT
POSTCONCUSSIVE SYMPTOMS; MEASUREMENT INVARIANCE; WAR VETERANS; CHRONIC
PAIN; CHECKLIST; COMBAT; IRAQ; AFGHANISTAN
AB Objective: A significant number of Operation Iraqi Freedom/Operation Enduring Freedom (OEF/OIF) veterans are returning from deployment and presenting to Veterans Health Administration (VHA) polytrauma clinics with elevated rates of posttraumatic stress disorder (PTSD) and mild traumatic brain injury (mTBI). Inherent to the accurate assessment and treatment of this diagnostically complex group of veterans is the assumption that the construct of PTSD is the same in this population as in other trauma groups. To our knowledge, no previous study has examined the structure of PTSD in this relevant and fast-growing population of treatment-seeking OEF/OIF veterans. Evidence suggests that the latent structure of PTSD symptoms is best represented by a four-factor model, rather than the three-factor model found in the current DSM-IV-TR. Thus, we examined the three and four-factor models using the PTSD Check List-Civilian (PCL-C) in a sample of treatment-seeking OEF/OIF veterans seen through a VHA polytrauma clinic. Method: A chart review was conducted for OEF/OIF veterans (N = 361) seen through a VHA outpatient polytrauma clinic from September 2007 through August 2008. Participants completed the PCL-C as part of a comprehensive polytrauma evaluation. Results: Confirmatory factor analyses showed that the DSM-IV-TR three-factor model did not fit the data well. A direct comparison showed that the four-factor model provided a superior fit relative to the three-factor model. Conclusion: Results extend the generalizability of the four-factor model to OEF/OIF veterans presenting to Veterans Health Administration (VHA) polytrauma clinics.
C1 [Maestas, Kacey Little] Michael E DeBakey VA Med Ctr, Houston, TX 77030 USA.
[Maestas, Kacey Little; Pastorek, Nicholas J.] Baylor Coll Med, Dept Phys Med & Rehabil, Houston, TX 77030 USA.
[Benge, Jared F.; Pastorek, Nicholas J.] Jack C Montgomery VA Med Ctr, Rehabil Care Line, Muskogee, OK USA.
[LeMaire, Ashley] Mem Hosp Gulfport, Dept Neurosci & Rehabil, Gulfport, MS USA.
[Darrow, Rachel] Ralph H Johnson VA Med Ctr, Mental Hlth Care Line, Charleston, SC USA.
RP Pastorek, NJ (reprint author), Michael E DeBakey VA Med Ctr, 2002 Holcombe Blvd,RCL 117, Houston, TX 77030 USA.
EM nicholas.pastorek@va.gov
RI Schueter, nicos/A-3625-2014
NR 51
TC 7
Z9 7
U1 2
U2 6
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 NOV
PY 2011
VL 56
IS 4
BP 366
EP 373
DI 10.1037/a0025447
PG 8
WC Psychology, Clinical; Rehabilitation
SC Psychology; Rehabilitation
GA 862AQ
UT WOS:000298062600010
PM 21928917
ER
PT J
AU Scalapino, KJ
Thomas, CR
AF Scalapino, Kenneth J.
Thomas, Charles R., Jr.
TI Preface Paraneoplastic and Cancer Treatment-Related Rheumatic Disorders
SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA
LA English
DT Editorial Material
C1 [Scalapino, Kenneth J.] Portland VA Med Ctr, Rheumatol Sect, Portland, OR 97239 USA.
[Thomas, Charles R., Jr.] Oregon Hlth & Sci Univ, Knight Canc Inst, Dept Radiat Med, Portland, OR 97239 USA.
RP Scalapino, KJ (reprint author), Portland VA Med Ctr, Rheumatol Sect, 3710 SW US Verterans Hosp Rd, Portland, OR 97239 USA.
EM Kenneth.Scalapino@va.gov; thomasch@ohsu.edu
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-857X
J9 RHEUM DIS CLIN N AM
JI Rheum. Dis. Clin. North Am.
PD NOV
PY 2011
VL 37
IS 4
BP IX
EP X
DI 10.1016/j.rdc.2011.09.005
PG 2
WC Rheumatology
SC Rheumatology
GA 865KU
UT WOS:000298310600001
PM 22075202
ER
PT J
AU Ashouri, JF
Daikh, DI
AF Ashouri, Judith F.
Daikh, David I.
TI Rheumatic Manifestations of Cancer
SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA
LA English
DT Article
DE Malignancy; Paraneoplastic manifestation; Rheumatic disease; Fasciitis;
POEMS; Inflammatory myopathy
ID SERONEGATIVE SYMMETRICAL SYNOVITIS; ENDOTHELIAL GROWTH-FACTOR;
POPULATION-BASED COHORT; HENOCH-SCHONLEIN PURPURA; GIANT-CELL ARTERITIS;
PRIMARY HYPERTROPHIC OSTEOARTHROPATHY; ASPARTATE RECEPTOR ENCEPHALITIS;
FASCIITIS-PANNICULITIS SYNDROME; DERMATOMYOSITIS SINE MYOSITIS; PITTING
EDEMA SYNDROME
AB The wide range of rheumatic and musculoskeletal conditions that can appear in association with cancer emphasizes that rheumatic disease is a major component of the spectrum of paraneoplastic manifestations. Although the pathogenetic mechanisms by which neoplasia causes these manifestations are only partially understood in select cases, many are because of immune-mediated effects stimulated by tumor antigens of endocrine factors produced by tumors. The broad overlap in signs and symptoms of occult malignancy and systemic rheumatic disease emphasizes the importance of considering and investigating the possibility of occult malignancy in the evaluation of patients with these symptoms.
C1 [Ashouri, Judith F.; Daikh, David I.] Univ Calif San Francisco, Dept Med, Div Rheumatol, San Francisco, CA 94143 USA.
[Ashouri, Judith F.; Daikh, David I.] San Francisco VA Med Ctr, Dept Med, San Francisco, CA USA.
RP Daikh, DI (reprint author), Univ Calif San Francisco, Dept Med, Div Rheumatol, 400 Parnassus, San Francisco, CA 94143 USA.
EM david.daikh@ucsf.edu
NR 156
TC 2
Z9 2
U1 1
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 0889-857X
J9 RHEUM DIS CLIN N AM
JI Rheum. Dis. Clin. North Am.
PD NOV
PY 2011
VL 37
IS 4
BP 489
EP +
DI 10.1016/j.rdc.2011.09.001
PG 18
WC Rheumatology
SC Rheumatology
GA 865KU
UT WOS:000298310600002
PM 22075194
ER
PT J
AU Lipton, S
Schwab, P
AF Lipton, Sarah
Schwab, Pascale
TI Neoplasm Mimics of Rheumatologic Presentations: Sialadenitis, Ocular
Masquerade Syndromes, Retroperitoneal Fibrosis, and Regional Pain
Syndromes
SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA
LA English
DT Article
DE Cancer; Sialadenitis; IgG4-related syndrome; Ocular masquerade syndrome;
Retroperitoneal fibrosis; Complex regional pain syndrome; Amyloidosis
ID REFLEX SYMPATHETIC DYSTROPHY; DIFFUSE INFILTRATING RETINOBLASTOMA;
IGG4-RELATED SCLEROSING DISEASE; PRIMARY INTRAOCULAR LYMPHOMA; PRIMARY
SYSTEMIC AMYLOIDOSIS; SALIVARY-GLAND TUMORS; SJOGRENS-SYNDROME;
CLINICAL-FEATURES; MIKULICZS-DISEASE; LONG-TERM
AB This article reviews a group of miscellaneous malignant conditions that may mimic rheumatologic diseases. Primary salivary gland cancer as well as lymphoproliferative conditions such as lymphoma and IgG4 related syndromes should be considered when evaluating a patient with sialadenosis. Primary intraocular lymphoma and melanoma in adults as well as leukemia and retinoblastoma in children may present as idiopathic ocular inflammation and require a high index of suspicion. Retroperitoneal fibrosis may mimic lymphoma or a solid malignancy and poses diagnostic challenges. Regional pain syndromes, such as complex regional pain and carpal tunnel syndromes, may be a manifestation of cancer and amyloidosis respectively. Awareness of these rare mimics may serve in guiding diagnostic investigations.
C1 [Lipton, Sarah; Schwab, Pascale] Oregon Hlth & Sci Univ, Portland Vet Affairs Med Ctr, Div Arthrit & Rheumat Dis, Portland, OR 97239 USA.
RP Schwab, P (reprint author), Oregon Hlth & Sci Univ, Portland Vet Affairs Med Ctr, Div Arthrit & Rheumat Dis, 3181 SW Sam Jackson Pk Rd,OP09, Portland, OR 97239 USA.
EM schwabp@ohsu.edu
NR 100
TC 1
Z9 1
U1 1
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-857X
EI 1558-3163
J9 RHEUM DIS CLIN N AM
JI Rheum. Dis. Clin. North Am.
PD NOV
PY 2011
VL 37
IS 4
BP 623
EP +
DI 10.1016/j.rdc.2011.09.004
PG 17
WC Rheumatology
SC Rheumatology
GA 865KU
UT WOS:000298310600009
PM 22075201
ER
PT J
AU Schaefer, EAK
Chung, RT
AF Schaefer, Esperance A. K.
Chung, Raymond T.
TI The Impact of Human Gene Polymorphisms on HCV Infection and Disease
Outcome
SO SEMINARS IN LIVER DISEASE
LA English
DT Review
DE Hepatitis C; IL28B; IFN lambda; PNPLA3; ITPA
ID CHRONIC HEPATITIS-C; VIRUS-COINFECTED PATIENTS; FATTY LIVER-DISEASE;
ALPHA-2A PLUS RIBAVIRIN; GENOTYPE 1 INFECTION; JAK-STAT PATHWAY;
SPONTANEOUS CLEARANCE; PEGYLATED INTERFERON; INTERLEUKIN 28B; IL28B
GENOTYPE
AB In recent years, some genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) associated with hepatitis C viral containment, treatment response, and disease progression. IL28B is a gene on chromosome 19, coding for interferon-lambda 3, and two polymorphisms upstream of this the gene have been strongly associated with clinical outcomes after treatment for the hepatitis C virus (HCV). The IL28B polymorphisms have additionally been associated with spontaneous clearance. The mechanism has yet to be clearly defined, but appears to involve differential responsiveness to interferon signaling between the favorable and unfavorable genotypes. ITPA is a gene on chromosome 20, coding for inosine triphosphatase, and polymorphisms on this gene have been associated with ribavirin-induced hemolytic anemia. Functional variants of ITPA have been identified that have decreased enzymatic activity, which appear to protect against anemia. Finally, PNPLA3 polymorphisms were initially described as predictors of non-alcoholic fatty liver disease, but have recently been associated with disease progression in HCV.
C1 [Schaefer, Esperance A. K.; Chung, Raymond T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, GI Unit, Boston, MA 02114 USA.
RP Schaefer, EAK (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, GI Unit, 55 Fruit St, Boston, MA 02114 USA.
EM eschaefer@partners.org
NR 92
TC 12
Z9 12
U1 0
U2 2
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0272-8087
J9 SEMIN LIVER DIS
JI Semin. Liver Dis.
PD NOV
PY 2011
VL 31
IS 4
BP 375
EP 386
DI 10.1055/s-0031-1297926
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 866QS
UT WOS:000298396900006
PM 22189977
ER
PT J
AU Nelson, CC
Sapp, A
Berkman, LF
Li, Y
Sorensen, G
AF Nelson, Candace C.
Sapp, Amy
Berkman, Lisa F.
Li, Yi
Sorensen, Glorian
TI Allocation of household responsibilities influences change in dietary
behavior
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Article
DE Nutrition; Food choice; Dietary behavior; Work-family; USA; Family
roles; Household labor; Households; Gender
ID FACTOR SURVEILLANCE SYSTEM; WORK-FAMILY SPILLOVER; FOOD CHOICE;
VEGETABLE CONSUMPTION; HEALTHY DIRECTIONS; UNITED-STATES; LOW-INCOME;
FRUIT; ADULTS; RISK
AB This study was undertaken to understand dietary behavior as situated within the household, an important social context that serves to either inhibit or promote a healthy diet. Data were collected as part of a worksite-based health behavior intervention trial that took place between 1999 and 2003 in small manufacturing businesses in New England, USA. The subjects were a cohort of 790 male and female workers who participated in the intervention trial and responded to both the baseline and the 18-month follow-up surveys. Regression models were built to determine whether proportion of household responsibility predicted daily fruit and vegetable consumption and weekly red meat consumption at 18-months. The results indicate that participants who were responsible for earning most or all of the money to support the household ate more servings of fruits and vegetables per day at 18-month follow-up than those without this responsibility. Further, those responsible for earning about half ate fewer servings of red meat than those responsible for earning most or all of the money to support the household. The results for red meat consumption differed by sex, such that responsibility for more than half or less than half of the money to support the household had different effects for men and women. The results of this study demonstrate that the distribution of household responsibilities can be an important factor in determining the effectiveness of a worksite-based health behavior intervention and that these effects can be different for women versus men. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Nelson, Candace C.; Sapp, Amy] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Sorensen, Glorian] Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA USA.
[Li, Yi] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Berkman, Lisa F.] Harvard Ctr Populat & Dev Studies, Cambridge, MA USA.
RP Nelson, CC (reprint author), Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, 677 Huntington Ave, Boston, MA 02115 USA.
EM candace_nelson@post.harvard.edu
FU National Cancer Institute [5 P01 CA 75308-03]
FX This work was supported by a grant from the National Cancer Institute
(grant 5 P01 CA 75308-03). The authors wish to express their gratitude
to the small businesses who participated in this study. We also thank
the anonymous reviewers for their comments on earlier versions of the
article.
NR 32
TC 1
Z9 1
U1 4
U2 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD NOV
PY 2011
VL 73
IS 10
BP 1517
EP 1524
DI 10.1016/j.socscimed.2011.08.030
PG 8
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 859WI
UT WOS:000297906100010
PM 21975026
ER
PT J
AU Gordon, CR
Abouhassan, W
Avery, RK
AF Gordon, C. R.
Abouhassan, W.
Avery, R. K.
TI What Is The True Significance of Donor-Related Cytomegalovirus
Transmission in the Setting of Facial Composite Tissue
Allotransplantation?
SO TRANSPLANTATION PROCEEDINGS
LA English
DT Article; Proceedings Paper
CT 10th International Congress of the
Hand-and-Composite-Tissue-Allotransplantation-Society (IHCTAS)
CY APR 07-09, 2011
CL Atlanta, GA
SP Hand & Composite Tissue Allotransplantat Soc (IHCTAS)
ID ORGAN-TRANSPLANT RECIPIENTS; CMV INFECTION; VALGANCICLOVIR PROPHYLAXIS;
FACE TRANSPLANTATION; HAND TRANSPLANTATION; PREEMPTIVE THERAPY; DISEASE;
STRATEGIES; EFFICACY; GANCICLOVIR
AB Face transplantation (FT) is fraught with complications parallel to solid organ transplantation (SOT). As such, donor-related cytomegalovirus (CMV) transmission remains one of the most commonly feared viruses associated with FT. With this in mind, a review of the literature seemed justified, knowing that two of the first four face transplant recipients acquired CMV donor-related viral infection. Although the risk of CMV transmission is acceptable in the setting of SOT, the scenario for those composite tissue allotransplantation (CTA) patients, who are often young and healthy, may be different. Experiences from France and Cleveland have both confirmed suboptimal events related to CMV transmission following transplantation. Therefore, using the information provided here, it is imperative that all FT teams remain aware of these potential risks. Furthermore, all patients pursuing facial CTA should be fully informed as to the risks of donor-related CMV transmission, understand the importance of prophylaxis, and be aware of alternative therapies required to prevent symptomatic disease.
C1 [Gordon, C. R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Plast & Reconstruct Surg,Dept Surg, Boston, MA 02114 USA.
[Gordon, C. R.; Abouhassan, W.] Cleveland Clin, Dept Plast Surg, Inst Dermatol & Plast Surg, Cleveland, OH 44106 USA.
[Avery, R. K.] Cleveland Clin, Dept Infect Dis, Inst Med, Cleveland, OH 44106 USA.
RP Gordon, CR (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Plast & Reconstruct Surg,Dept Surg, 15 Parkman St,WACC 435, Boston, MA 02114 USA.
EM cgordon5@partners.org
NR 49
TC 6
Z9 6
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0041-1345
EI 1873-2623
J9 TRANSPL P
JI Transplant. Proc.
PD NOV
PY 2011
VL 43
IS 9
BP 3516
EP 3520
DI 10.1016/j.transproceed.2011.08.043
PG 5
WC Immunology; Surgery; Transplantation
SC Immunology; Surgery; Transplantation
GA 854HL
UT WOS:000297485500090
PM 22099832
ER
PT J
AU Miyazono, S
Isayama, T
Delori, FC
Makino, CL
AF Miyazono, Sadaharu
Isayama, Tomoki
Delori, Francois C.
Makino, Clint L.
TI Vitamin A activates rhodopsin and sensitizes it to ultraviolet light
SO VISUAL NEUROSCIENCE
LA English
DT Article
DE Retinol; Retinal photoreceptors; GPCR; Allosteric regulation;
Electrophysiology
ID RETINOL-BINDING-PROTEIN; GATED ION CHANNELS; ROD PHOTORECEPTORS;
VISUAL-PIGMENT; CONE PHOTORECEPTORS; DARK-ADAPTATION; KNOCKOUT MICE;
TIGER SALAMANDER; OPSIN; MEMBRANE
AB The visual pigment, rhodopsin, consists of opsin protein with 11-cis retinal chromophore, covalently bound. Light activates rhodopsin by isomerizing the chromophore to the all-trans conformation. The activated rhodopsin sets in motion a biochemical cascade that evokes an electrical response by the photoreceptor. All-trans retinal is eventually released from the opsin and reduced to vitamin A. Rod and cone photoreceptors contain vast amounts of rhodopsin, so after exposure to bright light, the concentration of vitamin A can reach relatively high levels within their outer segments. Since a retinal analog, b-ionone, is capable of activating some types of visual pigments, we tested whether vitamin A might produce a similar effect. In single-cell recordings from isolated dark-adapted salamander green-sensitive rods, exogenously applied vitamin A decreased circulating current and flash sensitivity and accelerated flash response kinetics. These changes resembled those produced by exposure of rods to steady light. Microspectrophotometric measurements showed that vitamin A accumulated in the outer segments and binding of vitamin A to rhodopsin was confirmed in in vitro assays. In addition, vitamin A improved the sensitivity of photoreceptors to ultraviolet ( UV) light. Apparently, the energy of a UV photon absorbed by vitamin A transferred by a radiationless process to the 11-cis retinal chromophore of rhodopsin, which subsequently isomerized. Therefore, our results suggest that vitamin A binds to rhodopsin at an allosteric binding site distinct from the chromophore binding pocket for 11-cis retinal to activate the rhodopsin, and that it serves as a sensitizing chromophore for UV light.
C1 [Miyazono, Sadaharu; Isayama, Tomoki; Makino, Clint L.] Harvard Univ, Dept Ophthalmol, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
[Delori, Francois C.] Harvard Univ, Dept Ophthalmol, Sch Med, Schepens Eye Res Inst, Boston, MA 02114 USA.
RP Miyazono, S (reprint author), Harvard Univ, Dept Ophthalmol, Sch Med, Massachusetts Eye & Ear Infirm, 243 Charles St, Boston, MA 02114 USA.
EM miyazono@asahikawa-med.ac.jp
OI Makino, Clint/0000-0002-6005-9069
FU National Eye Institute [EY011358, EY014104]; Lions of Massachusetts
FX We thank Dr. E. R. Makino for helpful advice regarding the in vitro
assays, Drs. X.-H. Wen and T. R. Middendorf for insightful discussions,
and Dr. A. L. Zimmerman for comments on the manuscript. This research
was supported by Award Numbers EY011358 and EY014104 from the National
Eye Institute and the Lions of Massachusetts. The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Eye Institute or the National Institutes
of Health.
NR 71
TC 1
Z9 1
U1 0
U2 11
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0952-5238
J9 VISUAL NEUROSCI
JI Visual Neurosci.
PD NOV
PY 2011
VL 28
IS 6
BP 485
EP 497
DI 10.1017/S0952523811000423
PG 13
WC Neurosciences; Ophthalmology
SC Neurosciences & Neurology; Ophthalmology
GA 873AN
UT WOS:000298853000003
PM 22192505
ER
PT J
AU Choi, AI
Karter, AJ
Liu, JY
Young, BA
Go, AS
Schillinger, D
AF Choi, Andy I.
Karter, Andrew J.
Liu, Jennifer Y.
Young, Bessie A.
Go, Alan S.
Schillinger, Dean
TI Ethnic Differences in the Development of Albuminuria: The DISTANCE Study
SO AMERICAN JOURNAL OF MANAGED CARE
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; GLOMERULAR-FILTRATION-RATE;
CARDIOVASCULAR-DISEASE; GLYCEMIC CONTROL; POPULATION; ATHEROSCLEROSIS;
DISPARITIES; HEALTH; PREVALENCE; MORTALITY
AB Objectives: To determine whether ethnic differences in the incidence of albuminuria are present in patients with diabetes, and to identify social, behavioral, and provider factors that explain ethnic differences.
Study Design: Survey follow-up design with a race-stratified baseline survey (2005-2006) in diabetic patients from a nonprofit, fully integrated healthcare system in Northern California. We followed the 10,596 respondents (30% whites, 20% blacks, 23% Hispanics, 14% Asians, and 13% Filipinos) without evidence of prevalent albuminuria at baseline.
Methods: Incident albuminuria was defined by positive dipstick urinalysis (>= 1) or urine albumin to creatinine level (>= 30 mg/g), and confirmed with repeat testing at least 3 months later.
Results: The 27,292 person-years of observation yielded 981 incident albuminuria events. Age-standardized rates of albuminuria (per 1000 person-years) ranged from 13.6 (95% confidence interval [CI] 10.5-17.0) in whites to 27.8 (Cl 18.2-38.3) in blacks. In fully adjusted Cox models, the hazard ratio for blacks (1.22, 95% Cl 1.09-1.38), Asians (1.35, 95% Cl 1.13-1.61), and Filipinos (1.93, 95% Cl 1.61-2.32), but not Hispanics, was significantly greater than it was for whites. In some cases, point estimates changed markedly from the base model when fully adjusted for potential confounders. Moreover, adjustment for an array of potentially mediating factors explained only a small proportion of the observed ethnic disparities.
Conclusions: Despite uniform medical care coverage, Filipinos, blacks, and Asians with diabetes developed albuminuria at higher rates than white and Hispanic adults. (Am J Manag Care. 2071;17(11):737-745)
C1 [Karter, Andrew J.; Liu, Jennifer Y.] Kaiser Permanente, Div Res, Oakland, CA 94612 USA.
[Choi, Andy I.; Schillinger, Dean] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Choi, Andy I.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Karter, Andrew J.; Go, Alan S.] Univ Washington, Dept Hlth Serv Res, Seattle, WA 98195 USA.
VA Puget Sound Healthcare Syst, Seattle Epidemiol Res & Informat Ctr, Seattle, WA USA.
[Young, Bessie A.] Univ Washington, Dept Med, Seattle, WA USA.
[Schillinger, Dean] Univ Calif San Francisco, San Francisco Gen Hosp, Ctr Vulnerable Populat, San Francisco, CA USA.
RP Karter, AJ (reprint author), Kaiser Permanente, Div Res, 2000 Broadway, Oakland, CA 94612 USA.
EM andy.j.karter@kp.org
FU National Institute of Diabetes, Digestive and Kidney Diseases
[R01DK081796, RC1 DK086178, R01 DK080726, R01DK65664]; National
Institutes of Health [P60 DK20595]
FX This work was supported by the National Institute of Diabetes, Digestive
and Kidney Diseases (grants R01DK081796, RC1 DK086178, R01 DK080726, and
R01DK65664). The Diabetes Research and Training Center was also
supported by the National Institutes of Health (grant P60 DK20595).
NR 28
TC 2
Z9 2
U1 0
U2 1
PU MANAGED CARE & HEALTHCARE COMMUNICATIONS LLC
PI PLAINSBORO
PA 666 PLAINSBORO RD, STE 300, PLAINSBORO, NJ 08536 USA
SN 1088-0224
J9 AM J MANAG CARE
JI Am. J. Manag. Care
PD NOV
PY 2011
VL 17
IS 11
BP 737
EP 745
PG 9
WC Health Care Sciences & Services; Health Policy & Services; Medicine,
General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 854XO
UT WOS:000297528300002
PM 22084893
ER
PT J
AU Adler-Milstein, J
DesRoches, CM
Jha, AK
AF Adler-Milstein, Julia
DesRoches, Catherine M.
Jha, Ashish K.
TI Health Information Exchange Among US Hospitals
SO AMERICAN JOURNAL OF MANAGED CARE
LA English
DT Article
ID MEANINGFUL USE; ORGANIZATIONS; PROGRESS; RECORDS
AB Objectives: To determine the proportion of US hospitals engaged in health information exchange (HIE) with unaffiliated providers and to identify key hospital-level and market-level factors associated with participating in exchange.
Study Design: Using the 2009 American Hospital Association Information Technology survey, supplemented by Dartmouth Atlas, Area Resource File, and other national data, we examined which hospitals participated in regional efforts to electronically exchange clinical data.
Methods: We used logistic regression models to determine hospital-level characteristics and market-level characteristics associated with hospitals' likelihood of participating in HIE.
Results: We found that 10.7% of US hospitals engaged in HIE with unaffiliated providers. In communities where exchange occurred, for-profit hospitals and those with a small market share were far less likely to engage in HIE than non-profit hospitals or those with a larger market share. Hospitals in more concentrated markets were more likely to exchange and hospitals in markets with higher Medicare spending were less likely to exchange.
Conclusions: At the start of implementation of the Health Information Technology for Economic and Clinical Health (HITECH) Act, only a small minority of US hospitals electronically exchange clinical data with unaffiliated providers. Health information exchange is a key part of reforming the healthcare system, and factors related to competitiveness may be holding some providers back. (Am J Manag Care. 2010;17(11):761-768)
C1 [Adler-Milstein, Julia] Univ Michigan, Sch Informat, Ann Arbor, MI 48109 USA.
[Adler-Milstein, Julia] Univ Michigan, Sch Publ Hlth, Ann Arbor, MI 48109 USA.
[DesRoches, Catherine M.] Massachusetts Gen Hosp, Mongan Inst Hlth Policy, Boston, MA 02114 USA.
[Jha, Ashish K.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
RP Jha, AK (reprint author), Harvard Univ, Sch Publ Hlth, Harvard Med Sch, Boston Vet Affairs Hosp, 677 Huntington Ave, Boston, MA 02115 USA.
EM ajha@hsph.harvard.edu
FU Office of the National Coordinator at the Department of Health and Human
Services
FX Dr Jha reports consultancies or paid advisory boards from Humedica
Scientific Board and has also received grants from the Office of the
National Coordinator at the Department of Health and Human Services,
which has funded similar work. The other authors (JA-M, CMD) report no
relationship or financial interest with any entity that would pose a
conflict of interest with the subject matter of this article.
NR 14
TC 34
Z9 34
U1 5
U2 24
PU MANAGED CARE & HEALTHCARE COMMUNICATIONS LLC
PI PLAINSBORO
PA 666 PLAINSBORO RD, STE 300, PLAINSBORO, NJ 08536 USA
SN 1088-0224
J9 AM J MANAG CARE
JI Am. J. Manag. Care
PD NOV
PY 2011
VL 17
IS 11
BP 761
EP 768
PG 8
WC Health Care Sciences & Services; Health Policy & Services; Medicine,
General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 854XO
UT WOS:000297528300005
PM 22084896
ER
PT J
AU Kim, H
Helmer, DA
Zhao, ZL
Boockvar, K
AF Kim, Hongsoo
Helmer, Drew A.
Zhao, Zhonglin
Boockvar, Kenneth
TI Potentially Preventable Hospitalizations Among Older Adults With
Diabetes
SO AMERICAN JOURNAL OF MANAGED CARE
LA English
DT Article
ID MULTIPLE CHRONIC CONDITIONS; CARE-SENSITIVE CONDITIONS; AVOIDABLE
HOSPITALIZATIONS; DISPARITIES; MELLITUS; QUALITY; READMISSIONS;
POPULATION; PREVALENCE; INSURANCE
AB Objectives: To examine prevalence of and factors associated with different types of potentially preventable hospitalizations (PPHs) among older adults with diabetes.
Study Design: Population-based secondary analysis.
Methods: We analyzed the California State Inpatient Databases, 2005 to 2006. PPHs for 3 acute and 5 chronic ambulatory care-sensitive conditions relevant for older adults were defined by applying the Prevention Quality Indicator algorithm developed by the Agency for Health Research and Quality. Prevalence and costs of PPHs for acute conditions (acute PPHs) and chronic conditions (chronic PPHs) were examined. Associations of sociodemographic and health-related factors as well as hospitalization history with both types of PPH were estimated.
Results: One-fifth of 555,538 hospitalizations of adults 65 years and older with diabetes were PPHs. Of these, 43.7% were acute PPHs and 56.3% were chronic PPHs. The total hospital cost associated with these PPHs was more than $1.1 billion. Having Medi-Cal as the primary payer and hospitalization through the emergency department were positively associated with both types of PPH. Acute PPH rates were lower, but chronic PPH rates were higher, among blacks, patients with multiple chronic conditions, and those with previous admission(s) in the same year.
Conclusions: PPHs for common medical conditions are costly and prevalent among older patients with diabetes, suggesting a need for more comprehensive primary care, beyond glycemic control. The groups at risk for acute and chronic PPHs may differ, which suggests that more targeted and tailored approaches are necessary to reduce the rates of each type of PPH. (Am J Manag Care. 2011;17(11):e419-e426)
C1 [Kim, Hongsoo] Seoul Natl Univ, Grad Sch Publ Hlth, Seoul 151742, South Korea.
[Kim, Hongsoo] Seoul Natl Univ, Inst Hlth & Environm, Seoul 151742, South Korea.
[Helmer, Drew A.] Michael E DeBakey VA Med Ctr, Houston, TX USA.
[Helmer, Drew A.] Baylor Coll Med, Houston, TX 77030 USA.
[Zhao, Zhonglin] NYU, Coll Dent, New York, NY USA.
[Boockvar, Kenneth] James J Peters VA Med Ctr, Bronx, NY USA.
[Boockvar, Kenneth] Mt Sinai Sch Med, New York, NY USA.
[Boockvar, Kenneth] Jewish Home Lifecare, New York, NY USA.
RP Kim, H (reprint author), Seoul Natl Univ, Grad Sch Publ Hlth, Seoul 151742, South Korea.
EM hk65@snu.ac.kr
FU Greenwall Foundation
FX Dr Boockvar was supported by the Greenwall Foundation. The authors thank
the anonymous reviewers for their insightful comments.
NR 25
TC 10
Z9 10
U1 0
U2 9
PU MANAGED CARE & HEALTHCARE COMMUNICATIONS LLC
PI PLAINSBORO
PA 666 PLAINSBORO RD, STE 300, PLAINSBORO, NJ 08536 USA
SN 1088-0224
J9 AM J MANAG CARE
JI Am. J. Manag. Care
PD NOV
PY 2011
VL 17
IS 11
BP E419
EP E426
PG 8
WC Health Care Sciences & Services; Health Policy & Services; Medicine,
General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 854XO
UT WOS:000297528300006
PM 22200058
ER
PT J
AU Stein, MB
Siefert, CJ
Stewart, RV
Hilsenroth, MJ
AF Stein, Michelle B.
Siefert, Caleb J.
Stewart, Rosemarie Vala
Hilsenroth, Mark J.
TI Relationship between the Social Cognition and Object Relations Scale
(SCORS) and attachment style in a clinical sample
SO CLINICAL PSYCHOLOGY & PSYCHOTHERAPY
LA English
DT Article
DE SCORS; Attachment; Object Relations; RQ; ECR-R; Social Cognition
ID ADULT ATTACHMENT; RELATIONSHIP SATISFACTION; PERSONALITY-DEVELOPMENT;
CLIENT ATTACHMENT; SELF-DISCLOSURE; WORKING MODELS; PSYCHOTHERAPY;
PSYCHOPATHOLOGY; THERAPIST; RORSCHACH
AB This present study examined the relationship between the Social Cognition and Object Relations Scale (SCORS) and two measures of adult attachment: the Relationship Questionnaire (RQ) and the Experiences in Close Relationships Questionnaire-Revised (ECR-R). Forty-five patients (76% female) at a university-based outpatient treatment clinic participated in this study. We hypothesized that higher levels of attachment security would be associated with higher, more adaptive ratings on the SCORS variables. Results indicated that the SCORS Self-Esteem (SE) variable was significantly positively related to the RQ's Secure Attachment ratings and negatively related with the ECR-R's Anxious Attachment scale. Additionally, negative trends were noted between SE and the RQ's Fearful and Preoccupied Attachment scores. The SCORS Emotional Investments in Relationships and Affective Quality of Representations variables were associated with higher Secure scores and lower, more maladaptive Preoccupied scores on the RQ. It was also associated with greater attachment anxiety as measured by the ECR-R. Using both clinician (SCORS) and participant-rated measures (ECR-R and RQ), this study provides further understanding on how object representations and attachment style relate within a clinical sample. Results are discussed in light of prior research examining relationships between object relations and adult attachments, and clinical implications are also reviewed. Copyright (C) 2010 John Wiley & Sons, Ltd.
C1 [Stein, Michelle B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Stein, Michelle B.] Harvard Univ, Sch Med, Psychol Assessment Ctr, Boston, MA 02114 USA.
[Siefert, Caleb J.] Univ Michigan, Dearborn, MI 48128 USA.
[Stewart, Rosemarie Vala; Hilsenroth, Mark J.] Adelphi Univ, Derner Inst Adv Psychol Studies, Garden City, NY 11530 USA.
RP Stein, MB (reprint author), Massachusetts Gen Hosp, 1 Bowdoin Sq,Suite 701,7th Floor, Boston, MA 02114 USA.
EM mstein3@partners.org
NR 76
TC 5
Z9 5
U1 2
U2 20
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1063-3995
J9 CLIN PSYCHOL PSYCHOT
JI Clin. Psychol. Psychother.
PD NOV-DEC
PY 2011
VL 18
IS 6
BP 512
EP 523
DI 10.1002/cpp.721
PG 12
WC Psychology, Clinical
SC Psychology
GA 855GU
UT WOS:000297552700007
PM 20806423
ER
PT J
AU Carpenter, DJ
Fong, R
Kraus, JE
Davies, JT
Moore, C
Thase, ME
AF Carpenter, David J.
Fong, Regan
Kraus, John E.
Davies, John T.
Moore, Christine
Thase, Michael E.
TI Meta-Analysis of Efficacy and Treatment-Emergent Suicidality in Adults
by Psychiatric Indication and Age Subgroup Following Initiation of
Paroxetine Therapy: A Complete Set of Randomized Placebo-Controlled
Trials
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Review
ID SEROTONIN REUPTAKE INHIBITORS; NEW-YORK-CITY; ANTIDEPRESSANT TREATMENT;
CLINICAL-TRIALS; MAJOR DEPRESSION; RISK; RATES; ADOLESCENTS;
ASSOCIATION; PREVENTION
AB Objective: This meta-analysis of placebo-controlled paroxetine trials examines suicidality incidence in adults, focusing on disorder and age as potential risk factors. The findings are put in context with an efficacy meta-analysis of the same trial datasets.
Data Sources: GlaxoSmithKline paroxetine clinical trial database(s).
Study Selection: All double-blind, randomized, placebo-controlled, parallel-group studies of paroxetine therapy in adults enrolling at least 30 patients total were included in the analysis. The dataset comprised 14,911 patients from 61 trials.
Data Extraction: Possible cases of suicidality were identified and blindly categorized by an expert panel, using methodology previously used by the US Food and Drug Administration. Incidences of suicidal behavior (preparatory act, suicide attempt, or completed suicide) and any suicidality (suicidal behavior or ideation) were compared between paroxetine and placebo. Efficacy assessments were based on standard depression rating scales (eg, Hamilton Depression Rating Scale or Montgomery-Asberg Depression Rating Scale) and Clinical Global Impressions Improvement scale (CGI-I) scores.
Results: In the primary dataset, ie, all disorders combined, there were no significant differences between paroxetine and placebo for overall suicidality (suicidal behavior or ideation: n/n = 83/8,958 [0.93%] vs n/n = 65/5,953 [1.09%], respectively; OR = 0.9 [95% CI, 0.7-1.3]; P = .649) or for suicidal behavior specifically (n/n = 50/8,958 [0.56%] vs n/n = 40/5,953 [0.67%], respectively; OR = 1.2 [95% CI, 0.8-1.9]; P = .483). However, in patients with major depressive disorder (MDD), a greater incidence of suicidal behavior occurred in paroxetine-treated patients than in placebo-treated patients (n/n = 11/3,455 [0.32%] vs n/n = 1/1,978 [0.05%], respectively; OR = 6.7 [95% CI, 1.1-149.4]; P = .058). Across all indications, a higher incidence of suicidal behavior occurred in paroxetine-treated versus placebo-treated adults aged 18 to 24 years (n/n = 17/776 [2.19%] vs n/n = 5/542 [0.92%], respectively; OR = 2.4 [95% CI, 0.9-7.3]). In older age groups, no increase in suicidality was observed. Efficacy was demonstrated in all disorders evaluated, including MDD.
Conclusions: Across all disorders, overall suicidality incidence was similar between paroxetine and placebo. However, a higher frequency of suicidal behavior occurred with paroxetine in MDD, which was largely explained by the higher incidence in young adults. These data support the efficacy of paroxetine therapy; however, they also highlight the need for careful monitoring of suicidality during antidepressant therapy, particularly in younger adults.
C1 [Fong, Regan] GlaxoSmithKline Inc, Discovery Med, King Of Prussia, PA 19406 USA.
[Kraus, John E.] GlaxoSmithKline Inc, Res Triangle Pk, NC USA.
[Davies, John T.] GlaxoSmithKline Inc, Harlow, Essex, England.
[Moore, Christine] I3 Res, Cary, NC USA.
[Thase, Michael E.] Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
[Thase, Michael E.] Philadelphia Vet Affairs Med Ctr, Dept Psychiat, Philadelphia, PA USA.
[Thase, Michael E.] Univ Pittsburgh, Med Ctr, Dept Psychiat, Pittsburgh, PA 15260 USA.
RP Fong, R (reprint author), GlaxoSmithKline Inc, Discovery Med, 2301 Renaissance Blvd, King Of Prussia, PA 19406 USA.
EM Regan.2.fong@GSK.com
FU GlaxoSmithKline; Eli Lilly; National Institute of Mental Health;
Sepracor; American Psychiatric Publishing; Guilford Publications; Herald
House; W. W. Norton Company
FX Drs Carpenter, Fong, and Kraus and Mr Davies are employees of and
shareholders in GlaxoSmithKline. Dr Moore is an employee of i3 Research;
funding for her contribution to this article was provided by
GlaxoSmithKline. Dr Thase has been an advisor or consultant to
AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Forest, GlaxoSmithKline,
MedAvante, Neuronetics, Novartis, Otsuka, Ortho-McNeil, Pfizer,
Schering-Plough, Shire, Supernus, Takeda, and Transcept; has received
grant support from Eli Lilly, GlaxoSmithKline, National Institute of
Mental Health, and Sepracor; has served on speakers bureaus for
AstraZeneca, Bristol-Myers Squibb, Eli Lilly, and Pfizer; has equity
holdings in MedAvante; and has received royalties from American
Psychiatric Publishing, Guilford Publications, Herald House, and W. W.
Norton & Company. Dr Thase's spouse is an employee of Advogent.
NR 75
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U1 4
U2 10
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 240008, MEMPHIS, TN 38124 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD NOV
PY 2011
VL 72
IS 11
BP 1503
EP 1514
DI 10.4088/JCP.08m04927blu
PG 12
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 855ME
UT WOS:000297567700009
PM 21367354
ER
PT J
AU Lawson, EA
Donoho, DA
Blum, JI
Meenaghan, EM
Misra, M
Herzog, DB
Sluss, PM
Miller, KK
Klibanski, A
AF Lawson, Elizabeth A.
Donoho, Daniel A.
Blum, Justine I.
Meenaghan, Erinne M.
Misra, Madhusmita
Herzog, David B.
Sluss, Patrick M.
Miller, Karen K.
Klibanski, Anne
TI Decreased Nocturnal Oxytocin Levels in Anorexia Nervosa Are Associated
With Low Bone Mineral Density and Fat Mass
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Article
ID PARAVENTRICULAR NUCLEUS; BULIMIA-NERVOSA; DEFICIENT MICE; CSF OXYTOCIN;
WEIGHT-GAIN; FOOD-INTAKE; PEPTIDE-YY; ESTROGEN; RATS; RECEPTOR
AB Objective: Anorexia nervosa is characterized by self-induced starvation and associated with severe bone and fat loss. Oxytocin is a peptide hormone involved in appetite and energy homeostasis. Recent data show that oxytocin has an anabolic effect on bone and stimulates osteoblast function. There is limited information about oxytocin levels or their relationship to decreased bone mineral density in anorexia nervosa. Our objective was to investigate the relationship between oxytocin levels, bone mineral density, and body composition in women with anorexia nervosa.
Method: We studied 36 women, mean +/- SEM age 27.6 +/- 1.3 years: 17 with DSM-IV anorexia nervosa and 19 healthy controls in a cross-sectional study. Oxytocin levels were determined from pooled serum samples obtained every 20 minutes from 8 PM to RAM during an inpatient overnight visit. Fasting leptin levels were measured. Bone mineral density at the anterior-posterior and lateral spine and hip and body composition were assessed by dual energy x-ray absorptiometry. The study was conducted from September 2004 to June 2008.
Results: Subjects with anorexia nervosa versus healthy controls had lower mean SEM oxytocin levels (14.3 +/- 1.5 vs 31.8 +/- 5.1 pg/mL, P = .003), leptin levels (2.7 +/- 0.5 vs 11.4 +/- 1.1 ng/mL, P < .0001), bone mineral density (anterior-posterior spine: 0.83 +/- 0.02 vs 1.04 +/- 0.03; lateral spine: 0.63 +/- 0.02 vs 0.81 +/- 0.02; total hip: 0.79 +/- 0.03 vs 0.97 +/- 0.03 g/cm(2), P < .0001), and fat mass (8.8 +/- 0.6 vs 19.7 +/- 0.9 kg, P < .0001). Oxytocin levels were associated with bone mineral density at the anterior-posterior (r = 0.40, P = .02) and lateral (r = 0.36, P = .04) spine, fat mass (r = 0.42, P = .01), and leptin levels (r = 0.55, P = .001).
Conclusions: Overnight secretion of oxytocin in women with anorexia nervosa is decreased compared with healthy women. Low oxytocin levels are associated with decreased bone mineral density and body fat and may contribute to anorexia nervosa induced bone loss.
C1 [Lawson, Elizabeth A.; Donoho, Daniel A.; Blum, Justine I.; Meenaghan, Erinne M.; Misra, Madhusmita; Miller, Karen K.; Klibanski, Anne] Massachusetts Gen Hosp, Neuroendocrine Unit, Boston, MA 02114 USA.
[Herzog, David B.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Sluss, Patrick M.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Lawson, EA (reprint author), Massachusetts Gen Hosp, Neuroendocrine Unit, Bulfinch 457B, Boston, MA 02114 USA.
EM ealawson@partners.org
FU Bioenvision; National Institutes of Health [M01 RR01066, UL1 RR025758,
R01-DK052625]; Harvard/MIT Health Sciences and Technology-Beth Israel
Deaconess Medical Center; Pfizer; Merck
FX This work was supported in part by an investigator-initiated grant from
Bioenvision; National Institutes of Health grants M01 RR01066, UL1
RR025758, and R01-DK052625; and the Clinical Investigator Training
Program: Harvard/MIT Health Sciences and Technology-Beth Israel
Deaconess Medical Center, in collaboration with Pfizer and Merck.
NR 35
TC 37
Z9 38
U1 0
U2 10
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 240008, MEMPHIS, TN 38124 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD NOV
PY 2011
VL 72
IS 11
BP 1546
EP 1551
DI 10.4088/JCP.10m06617
PG 6
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 855ME
UT WOS:000297567700015
PM 21903023
ER
PT J
AU Carpenter, DJ
Fong, R
Kraus, JE
Davies, JT
Moore, C
Thase, ME
AF Carpenter, David J.
Fong, Regan
Kraus, John E.
Davies, John T.
Moore, Christine
Thase, Michael E.
TI Odd Odds Reply
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Letter
C1 [Carpenter, David J.; Fong, Regan] GlaxoSmithKline Inc, King Of Prussia, PA USA.
[Moore, Christine] I3 Res, Cary, NC USA.
[Thase, Michael E.] Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
[Thase, Michael E.] Philadelphia Vet Affairs Med Ctr, Dept Psychiat, Philadelphia, PA USA.
[Thase, Michael E.] Univ Pittsburgh, Med Ctr, Dept Psychiat, Pittsburgh, PA 15260 USA.
RP Carpenter, DJ (reprint author), GlaxoSmithKline Inc, King Of Prussia, PA USA.
EM Regan.2.Fong@gsk.com
NR 1
TC 0
Z9 0
U1 0
U2 0
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 240008, MEMPHIS, TN 38124 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD NOV
PY 2011
VL 72
IS 11
BP 1559
EP 1559
DI 10.4088/JCP.11lr07373a
PG 1
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 855ME
UT WOS:000297567700020
ER
PT J
AU Finn, KM
Heffner, R
Chang, YC
Bazari, H
Hunt, D
Pickell, K
Berube, R
Raju, S
Farrell, E
Iyasere, C
Thompson, R
O'Malley, T
O'Donnell, W
Karson, A
AF Finn, Kathleen M.
Heffner, Rebecca
Chang, Yuchiao
Bazari, Hasan
Hunt, Daniel
Pickell, Karen
Berube, Rhodes
Raju, Shveta
Farrell, Elizabeth
Iyasere, Christiana
Thompson, Ryan
O'Malley, Terrence
O'Donnell, Walter
Karson, Andrew
TI Improving the discharge process by embedding a discharge facilitator in
a resident team
SO JOURNAL OF HOSPITAL MEDICINE
LA English
DT Article
ID CARE TRANSITIONS INTERVENTION; HOSPITAL DISCHARGE; PROSPECTIVE PAYMENT;
CONTROLLED-TRIAL; PATIENT SAFETY; HEART-FAILURE; CASE MANAGER;
FOLLOW-UP; PHYSICIANS; READMISSIONS
AB BACKGROUND: Hospital discharges are vulnerable periods for patient safety, especially in teaching hospitals where discharges are done by residents with competing demands. We sought to assess whether embedding a nurse practitioner on a medical team to help physicians with the discharge process would improve communication, patient follow-up, and hospital reutilization.
METHODS: A 5-month randomized controlled trial was conducted on the medical service at an academic tertiarycare hospital. A nurse practitioner was randomly assigned to 1 resident team to complete discharge paperwork, arrange follow-up appointments and prescriptions, communicate discharge plans with nursing and primary care physicians, and answer questions from discharged patients.
RESULTS: Intervention patients had more discharge summaries completed within 24 hours (67% vs 47%, P < 0.001). Similarly, they had more follow-up appointments scheduled by the time of discharge (62% vs 36%, P < 0.0001) and attended those appointments more often within 2 weeks (36% vs 23%, P < 0.0002). Intervention patients knew whom to call with questions (95% vs 85%, P = 0.003) and were more satisfied with the discharge process (97% vs 76%, P < 0.0001). Attending rounds on the intervention team finished on time (45% vs 31%, P = 0.058), and residents signed out on average 46 minutes earlier each day. There was no significant difference between the groups in 30-day emergency department visits or readmissions.
CONCLUSIONS: Helping resident physicians with the discharge process improves many aspects of discharge communication and patient follow-up, and saves residents' time, but had no effect on hospital reutilization for a general medicine population. Journal of Hospital Medicine 2011; 6: 494-500. (C) 2011 Society of Hospital Medicine
C1 [Finn, Kathleen M.] Massachusetts Gen Hosp, MGH DOM Clin Educ Program, Dept Med, Boston, MA 02114 USA.
[Heffner, Rebecca] Univ Penn, Wharton Sch Business, Philadelphia, PA 19104 USA.
[Farrell, Elizabeth] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA USA.
RP Finn, KM (reprint author), Massachusetts Gen Hosp, MGH DOM Clin Educ Program, Dept Med, 50 Staniford St,Suite 503B, Boston, MA 02114 USA.
EM Kfinn@partners.org
FU Internal Partners Healthcare Physician Education/Care Delivery
Reengineering Innovation Grant
FX Funding: Internal Partners Healthcare Physician Education/Care Delivery
Reengineering Innovation Grant. The funding source had no role in the
design, collection of data, management, analysis, and interpretation of
the data; or preparation, review, or approval of the manuscript.
NR 30
TC 16
Z9 16
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1553-5592
J9 J HOSP MED
JI J. Hosp. Med.
PD NOV-DEC
PY 2011
VL 6
IS 9
BP 494
EP 500
DI 10.1002/jhm.924
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA 861JM
UT WOS:000298015200004
PM 22042739
ER
PT J
AU Greka, A
Mundel, P
AF Greka, Anna
Mundel, Peter
TI Balancing Calcium Signals through TRPC5 and TRPC6 in Podocytes
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID FOCAL SEGMENTAL GLOMERULOSCLEROSIS; RECEPTOR POTENTIAL CHANNELS;
SMOOTH-MUSCLE-CELLS; ANGIOTENSIN-II; NEPHROTIC SYNDROME; CATION CHANNEL;
SLIT DIAPHRAGM; ACTIN CYTOSKELETON; KIDNEY PODOCYTES; GLOMERULAR
PODOCYTES
AB Calcium (Ca(2+)) ions are important mediators of cellular homeostasis owing to their ability to elicit a dynamic, transient, and tightly regulated range of biochemical responses. More than a decade ago, a nonselective, Ca(2+)-permeable, cationic conductance was identified in podocytes downstream of angiotensin II (Ang II) signaling, but its molecular structure remained elusive. Six years ago, transient receptor potential canonical 6 (TRPC6) mutations were found in families with hereditary FSGS, and TRPC5 and TRPC6 channels are now known as the Ca(2+) influx pathways for this previously described, nonselective, cationic current in podocytes. Ang II activation engages this Ca(2+) influx to modulate the actin cytoskeleton in podocytes. These discoveries dovetail with previously described regulation of actin dynamics by the Ca(2+)-activated phosphatase, calcineurin, and the emergence of Rho GTPases as critical regulators of podocyte function in health and disease. Understanding the interconnected signaling regulated by Ca(2+) currents offers potential new therapeutic targets and highlights the notion that synergistic therapies targeting multiple levels of biochemistry may be useful in treating proteinuric kidney disease.
C1 Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Greka, A (reprint author), Massachusetts Gen Hosp, Div Nephrol, Dept Med, 149 13th St, Charlestown, MA 02129 USA.
EM greka.anna@mgh.harvard.edu; mundel.peter@mgh.harvard.edu
FU Nephcure Young Investigator Grant; NIH [DK083511, DK57683, DK062472]
FX We apologize to our colleagues whose work we were not able to cite in
this review because of space limitations. Reviews were often quoted at
the expense of original work. We thank D. Corey, W. Kriz, M. Winn, and
M.A. Arnaout for helpful discussions. A.G. is funded by a Nephcure Young
Investigator Grant and NIH Grant DK083511 and P.M. by NIH Grants DK57683
and DK062472.
NR 111
TC 44
Z9 46
U1 0
U2 10
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD NOV
PY 2011
VL 22
IS 11
BP 1969
EP 1980
DI 10.1681/ASN.2011040370
PG 12
WC Urology & Nephrology
SC Urology & Nephrology
GA 862ES
UT WOS:000298073200005
PM 21980113
ER
PT J
AU Kanji, Z
Powe, CE
Wenger, JB
Huang, CM
Ankers, E
Sullivan, DA
Collerone, G
Powe, NR
Tonelli, M
Bhan, I
Bernhardy, AJ
DiBartolo, S
Friedman, D
Genovese, G
Pollak, MR
Thadhani, R
AF Kanji, Zahra
Powe, Camille E.
Wenger, Julia B.
Huang, Chunmei
Ankers, Elizabeth
Sullivan, Dorothy A.
Collerone, Gina
Powe, Neil R.
Tonelli, Marcello
Bhan, Ishir
Bernhardy, Andrea J.
DiBartolo, Salvatore
Friedman, David
Genovese, Giulio
Pollak, Martin R.
Thadhani, Ravi
TI Genetic Variation in APOL1 Associates with Younger Age at Hemodialysis
Initiation
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID STAGE RENAL-DISEASE; CHRONIC KIDNEY-DISEASE; AFRICAN-AMERICANS;
RACIAL-DIFFERENCES; UNITED-STATES; RISK; MORTALITY; MYH9
AB African Americans have a markedly higher incidence of ESRD compared with other racial groups. Two variants in the APOL1 gene, to date observed only among individuals of recent African ancestry, associate with increased risk for renal disease among African Americans. Here, we investigated whether these risk alleles also associate with age at initiation of chronic hemodialysis. We performed a cross-sectional study of 407 nondiabetic African Americans with ESRD who participated in the Accelerated Mortality on Renal Replacement (ArMORR) study, a prospective cohort of incident chronic hemodialysis patients. African Americans carrying two copies of the G1 risk allele initiated chronic hemodialysis at a mean age of 49.0 +/- 14.9 years, which was significantly younger than both subjects with one copy of the G1 allele (55.9 +/- 16.7 years; P = 0.014) and subjects without either risk allele (61.8 +/- 17.1 years; P = 6.2 x 10(-7)). The association between the presence of the G1 allele and age at initiation of hemodialysis remained statistically significant after adjusting for sociodemographic and other potential confounders. We did not detect an association between the G2 risk allele and age at initiation of hemodialysis, but the sample size was limited. In conclusion, genetic variations in APOL1 identify African Americans that initiate chronic hemodialysis at a younger age. Early interventions to prevent progression of kidney disease may benefit this high-risk population.
C1 [Kanji, Zahra; Powe, Camille E.; Wenger, Julia B.; Huang, Chunmei; Ankers, Elizabeth; Sullivan, Dorothy A.; Collerone, Gina; Bhan, Ishir; Thadhani, Ravi] Massachusetts Gen Hosp, Div Nephrol, Dept Med, Boston, MA 02114 USA.
[Powe, Neil R.] Univ Calif San Francisco, Dept Med, San Francisco Gen Hosp, San Francisco, CA 94143 USA.
[Tonelli, Marcello] Univ Alberta, Dept Med, Edmonton, AB, Canada.
[Bernhardy, Andrea J.; DiBartolo, Salvatore; Friedman, David; Genovese, Giulio; Pollak, Martin R.] Beth Israel Deaconess Med Ctr, Dept Med, Div Nephrol, Boston, MA 02215 USA.
[Bernhardy, Andrea J.; DiBartolo, Salvatore; Friedman, David; Genovese, Giulio; Pollak, Martin R.] Harvard Univ, Sch Med, Boston, MA USA.
[Pollak, Martin R.] Broad Inst Harvard, Cambridge, MA USA.
[Pollak, Martin R.] MIT, Cambridge, MA 02139 USA.
RP Thadhani, R (reprint author), Massachusetts Gen Hosp, Div Nephrol, Dept Med, Bullfinch 127, Boston, MA 02114 USA.
EM thadhani.ravi@mgh.harvard.edu
RI Tonelli, Marcello/B-3028-2009
FU National Institutes of Health [NIH DK54931, NIH DK84974]; Abbott
FX M.R.P. was supported by National Institutes of Health grant NIH DK54931.
R.T. was supported by National Institutes of Health grant NIH DK84974.;
R.T. has a research grant from Abbott, and is a consultant to Fresenius
Medical Care North America and Shire Human Genetics.
NR 17
TC 43
Z9 43
U1 2
U2 6
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD NOV
PY 2011
VL 22
IS 11
BP 2091
EP 2097
DI 10.1681/ASN.2010121234
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 862ES
UT WOS:000298073200017
PM 21997398
ER
PT J
AU Kimbrel, NA
Steffen, LE
Meyer, EC
Kruse, MI
Knight, JA
Zimering, RT
Gulliver, SB
AF Kimbrel, Nathan A.
Steffen, Laurie E.
Meyer, Eric C.
Kruse, Marc I.
Knight, Jeffrey A.
Zimering, Rose T.
Gulliver, Suzy B.
TI A Revised Measure of Occupational Stress for Firefighters: Psychometric
Properties and Relationship to Posttraumatic Stress Disorder,
Depression, and Substance Abuse
SO PSYCHOLOGICAL SERVICES
LA English
DT Article
DE firefighters; PTSD; depression; substance abuse
ID URBAN FIREFIGHTERS; SCREENING-TEST; PREDICTORS; PARAMEDICS; INVENTORY;
SYMPTOMS
AB The Sources of Occupational Stress scale (SOOS; Beaton & Murphy, 1993) is a 57-item self-report measure designed to assess the different sources of occupational stress faced by firefighters. The objective of the present research was to develop and evaluate an abbreviated version of the SOOS in order to reduce respondent burden. The revised 14-item version of the SOOS was evaluated in 2 independent samples of firefighters (N = 408) along with measures of job outcomes, posttraumatic stress disorder, depression, and substance abuse. The SOOS-14 exhibited good internal consistency, good factor structure, and good validity coefficients across samples. Although additional studies are needed to replicate and expand on these results, the findings from the present research indicate that the SOOS-14 is a practical, reliable, and valid measure of occupational stress for firefighters.
C1 [Kimbrel, Nathan A.; Steffen, Laurie E.; Meyer, Eric C.; Kruse, Marc I.; Gulliver, Suzy B.] Texas A&M Hlth Sci Ctr, Dept Psychiat & Behav Sci, Houston, TX USA.
[Knight, Jeffrey A.; Zimering, Rose T.] VA Boston Healthcare Syst, Dept Psychol, Boston, MA USA.
[Knight, Jeffrey A.; Zimering, Rose T.] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02215 USA.
RP Kimbrel, NA (reprint author), VA VISN 17 Ctr Excellence Res Returning War Vet, 4800 Mem Dr 151C, Waco, TX 76711 USA.
EM nathan.kimbrel@va.gov
RI Kimbrel, Nathan/P-3109-2016
OI Kimbrel, Nathan/0000-0001-7218-1005
NR 32
TC 7
Z9 7
U1 0
U2 8
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 NOV
PY 2011
VL 8
IS 4
BP 294
EP 306
DI 10.1037/a0025845
PG 13
WC Psychology, Clinical
SC Psychology
GA 854XX
UT WOS:000297529200003
ER
PT J
AU MacMahon, PJ
Shelly, MJ
Scholz, D
Eustace, SJ
Kavanagh, EC
AF MacMahon, P. J.
Shelly, M. J.
Scholz, D.
Eustace, S. J.
Kavanagh, E. C.
TI Injectable Corticosteroid Preparations: An Embolic Risk Assessment by
Static and Dynamic Microscopic Analysis
SO AMERICAN JOURNAL OF NEURORADIOLOGY
LA English
DT Article
ID CERVICAL TRANSFORAMINAL INJECTION; EPIDURAL STEROID INJECTION; SPINAL
ARTERY SYNDROME; BENZYL ALCOHOL; VERTEBRAL ARTERY; IN-VITRO; ROOT;
RADICULOPATHY; AGGREGATION; PARAPLEGIA
AB BACKGROUND AND PURPOSE: Transforaminal CS injections have been associated with severe adverse CNS events, including brain and spinal cord infarction. Our purpose was to describe the static and dynamic microscopic appearances of CS preparations, with an emphasis on their potential to cause adverse central nervous system events by embolic mechanisms during transforaminal injection.
MATERIALS AND METHODS: Pharmaceutical preparations of nondilute injectable CSs were used after appropriate mixing: MPA (40 mg/mL), TA (40 mg/mL), and DSP (8 mg/2 mL). For dynamic imaging, a novel methodology was devised to replicate the flow of crystals within spinal cord arterioles. In addition, CS preparations were mixed with plasma to assess for changes in crystal size, morphology, and tendency to aggregate.
RESULTS: The CS preparations MPA and TA are composed of crystals of varying sizes. MPA crystal size range was 0.4-26 mu m (mean, 6.94 mu m), TA crystal size range 0.5-110 mu m (mean, 17.4 mu m), and DSP did not contain any significant crystals or particles. There was no change in the crystal morphology or propensity to aggregate after mixing with local anesthetic. After mixing with plasma, the crystals also were unchanged; however, there was a significant reduction in the size of aggregates. On dynamic imaging, these aggregates were proved to maintain their integrity and to act as potential embolization agents.
CONCLUSIONS: MPA and TA have a substantial risk of causing infarction by embolization if inadvertently injected intra-arterially at the time of TFESI. DSP is completely soluble and microscopically has no potential to obstruct arterioles. When performing cervical TFESI procedures, the administration of insoluble CSs should be avoided.
C1 [MacMahon, P. J.; Shelly, M. J.; Eustace, S. J.; Kavanagh, E. C.] Mater Misericordiae Univ Hosp, Dept Radiol, Dublin, Ireland.
[Scholz, D.] Univ Coll, Conway Inst, Dublin, Ireland.
RP MacMahon, PJ (reprint author), Massachusetts Gen Hosp, Dept Musculoskeletal Imaging & Intervent, YAW 6030, Boston, MA 02114 USA.
EM petermacmahon@yahoo.com
NR 37
TC 9
Z9 9
U1 0
U2 2
PU AMER SOC NEURORADIOLOGY
PI DENVILLE
PA PO BOX 3000, DENVILLE, NJ 07834-9349 USA
SN 0195-6108
EI 1936-959X
J9 AM J NEURORADIOL
JI Am. J. Neuroradiol.
PD NOV
PY 2011
VL 32
IS 10
BP 1830
EP 1835
DI 10.3174/ajnr.A2656
PG 6
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 859PM
UT WOS:000297888300013
PM 21940803
ER
PT J
AU Berkhout, B
Jeang, KT
AF Berkhout, B.
Jeang, K. -T.
TI MicroRNAs in viral gene regulation Preface
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS
LA English
DT Editorial Material
C1 [Berkhout, B.] Harvard Univ, Dana Farber Canc Inst, Sch Med, Cambridge, MA 02138 USA.
[Berkhout, B.] Univ Amsterdam, NL-1012 WX Amsterdam, Netherlands.
[Jeang, K. -T.] NIAID, NIH, Bethesda, MD 20892 USA.
[Jeang, K. -T.] MIT, Boston, MA USA.
RP Berkhout, B (reprint author), Harvard Univ, Dana Farber Canc Inst, Sch Med, Cambridge, MA 02138 USA.
RI Jeang, Kuan-Teh/A-2424-2008
NR 0
TC 5
Z9 5
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-9399
J9 BBA-GENE REGUL MECH
JI Biochim. Biophys. Acta-Gene Regul. Mech.
PD NOV-DEC
PY 2011
VL 1809
IS 11-12
SI SI
BP 587
EP 587
DI 10.1016/j.bbagrm.2011.10.009
PG 1
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 858WP
UT WOS:000297834200001
PM 22055652
ER
PT J
AU Girard, SL
Piche, M
Chen, HX
Schinn, GW
Oh, WY
Bouma, BE
AF Girard, Simon Lambert
Piche, Michel
Chen, Hongxin
Schinn, Gregory W.
Oh, Wang-Yuhl
Bouma, Brett E.
TI SOA Fiber Ring Lasers: Single-Versus Multiple-Mode Oscillation
SO IEEE JOURNAL OF SELECTED TOPICS IN QUANTUM ELECTRONICS
LA English
DT Article
DE Fiber laser; nonlinear optical device; optical tuning; semiconductor
device noise; semiconductor optical amplifiers
ID SEMICONDUCTOR-LASER; LINEWIDTH; AMPLIFIERS
AB Earlier investigations have demonstrated that a narrow bandwidth intracavity filter in a semiconductor optical amplifier (SOA) fiber ring laser results in an output spectrum comprising multiple longitudinal modes, whereas a large bandwidth filter generally leads to quasi-single-mode oscillation. In this paper, we report on a numerical model simulating the SOA fiber ring laser dynamics and compare its predictions with experimental results obtained with two different SOAs. We demonstrate that the observed experimental behavior results from the interplay between the complex transfer function of the intracavity optical filter, fast gain saturation and four-wave mixing (FWM) due to the linewidth enhancement factor. The dispersion introduced by the complex transfer function of the filter can lead to modulation instability, which plays a key role in the laser dynamics that can evolve into a single-longitudinal mode (SLM) operation. We also simulate the behavior of the laser emission when the wavelength of the optical filter is finely tuned.
C1 [Girard, Simon Lambert; Piche, Michel] Univ Laval, Ctr Opt Photon & Laser, Quebec City, PQ G1V 0A6, Canada.
[Chen, Hongxin; Schinn, Gregory W.] EXFO Inc, Quebec City, PQ G1M 2K2, Canada.
[Oh, Wang-Yuhl; Bouma, Brett E.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Oh, Wang-Yuhl; Bouma, Brett E.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Girard, SL (reprint author), Univ Laval, Ctr Opt Photon & Laser, Quebec City, PQ G1V 0A6, Canada.
EM simon.lambert-girard.1@ulaval.ca
FU Canadian Institute for Photonic Innovations (CIPI); Natural Sciences and
Engineering Research Council of Canada (NSERC); EXFO Inc.
FX This work was supported by the Canadian Institute for Photonic
Innovations (CIPI), the Natural Sciences and Engineering Research
Council of Canada (NSERC), and EXFO Inc.
NR 18
TC 10
Z9 10
U1 1
U2 7
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 1077-260X
J9 IEEE J SEL TOP QUANT
JI IEEE J. Sel. Top. Quantum Electron.
PD NOV-DEC
PY 2011
VL 17
IS 6
BP 1513
EP 1520
DI 10.1109/JSTQE.2011.2119294
PG 8
WC Engineering, Electrical & Electronic; Optics; Physics, Applied
SC Engineering; Optics; Physics
GA 859FA
UT WOS:000297861000006
ER
PT J
AU Tian, YJ
Rich, BE
Vena, N
Craig, JM
MacConaill, LE
Rajaram, V
Goldman, S
Taha, H
Mahmoud, M
Ozek, M
Sav, A
Longtine, JA
Lindeman, NI
Garraway, LA
Ligon, AH
Stiles, CD
Santagata, S
Chan, JA
Kieran, MW
Ligon, KL
AF Tian, Yongji
Rich, Benjamin E.
Vena, Natalie
Craig, Justin M.
MacConaill, Laura E.
Rajaram, Veena
Goldman, Stewart
Taha, Hala
Mahmoud, Madeha
Ozek, Memet
Sav, Aydin
Longtine, Janina A.
Lindeman, Neal I.
Garraway, Levi A.
Ligon, Azra H.
Stiles, Charles D.
Santagata, Sandra
Chan, Jennifer A.
Kieran, Mark W.
Ligon, Keith L.
TI Detection of KIAA1549-BRAF Fusion Transcripts in Formalin-Fixed
Paraffin-Embedded Pediatric Low-Grade Gliomas
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Article
ID MAPK PATHWAY ACTIVATION; PILOCYTIC ASTROCYTOMAS; BRAF MUTATION; GENE;
DUPLICATION; CANCER
AB Alterations of BRAF are the most common known genetic aberrations in pediatric gliomas. They frequently are found in pilocytic astrocytomas, where genomic duplications involving BRAF and the poorly characterized gene KIAA1549 create fusion proteins with constitutive B-Raf kinase activity. BRAF V600E point mutations are less common and generally occur in nonpilocytic tumors. The development of BRAF inhibitors as drugs has created an urgent need for robust clinical assays to identify activating lesions in BRAF. KIAA1549-BRAF fusion transcripts have been detected in frozen tissue, however, methods for FFPE tissue have not been reported. We developed a panel of FFPE-compatible quantitative RT-PCR assays for the most common KIAA1549-BRAF fusion transcripts. Application of these assays to a collection of 51 low-grade pediatric gliomas showed 97% sensitivity and 91% specificity compared with fluorescence in situ hybridization or array comparative genomic hybridization. In parallel, we assayed samples for the presence of the BRAF V600E mutation by PCR pyrosequencing. The data further support previous observations that these two alterations of the BRAF, KIAA1549 fusions and V600E point mutations, are associated primarily with pilocytic astrocytomas and nonpilocytic gliomas, respectively. These results show that fusion transcripts and mutations can be detected reliably in standard FFPE specimens and may be useful for incorporation into future studies of pediatric gliomas in basic science or clinical trials. (J Mal Diagn 2011, 13:669-677; DOI: 10.1016/j.jmoldx.2011.07.002)
C1 [Tian, Yongji; Rich, Benjamin E.; Vena, Natalie; Craig, Justin M.; MacConaill, Laura E.; Garraway, Levi A.; Ligon, Azra H.; Ligon, Keith L.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Stiles, Charles D.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
[Kieran, Mark W.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02215 USA.
[Vena, Natalie; Ligon, Azra H.; Ligon, Keith L.] Dana Farber Canc Inst, Ctr Mol Oncol Pathol, Boston, MA 02215 USA.
[MacConaill, Laura E.; Garraway, Levi A.] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02215 USA.
[Rajaram, Veena] Childrens Mem Hosp, Dept Pathol & Lab Med, Chicago, IL 60614 USA.
[Goldman, Stewart] Childrens Mem Hosp, Div NeuroOncol, Chicago, IL 60614 USA.
[Taha, Hala; Mahmoud, Madeha] Childrens Canc Hosp, Dept Pediat Oncol & Pathol, Cairo, Egypt.
[Ozek, Memet] Acibadem Univ, Med Ctr, Div Pediat Neurosurg, Istanbul, Turkey.
[Sav, Aydin] Acibadem Univ, Med Ctr, Dept Pathol, Istanbul, Turkey.
[Longtine, Janina A.; Lindeman, Neal I.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Santagata, Sandra; Chan, Jennifer A.; Ligon, Keith L.] Brigham & Womens Hosp, Div Neuropathol, Boston, MA 02115 USA.
[Santagata, Sandra; Ligon, Keith L.] Childrens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Kieran, Mark W.] Childrens Hosp, Dept Pediat, Boston, MA 02115 USA.
RP Ligon, KL (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM keith_ligon@dfci.harvard.edu
OI Ligon, Keith/0000-0002-7733-600X; Kieran, Mark/0000-0003-2184-7692; sav,
aydin/0000-0002-7326-7801
FU Pediatric Low Grade Astrocytoma Foundation
FX Supported by the Pediatric Low Grade Astrocytoma Foundation.
NR 23
TC 30
Z9 30
U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1525-1578
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2011
VL 13
IS 6
BP 669
EP 677
DI 10.1016/j.jmoldx.2011.07.002
PG 9
WC Pathology
SC Pathology
GA 856RZ
UT WOS:000297662400010
PM 21884820
ER
PT J
AU Lebrun, AH
Moll-Khosrawi, P
Pohl, S
Makrypidi, G
Storch, S
Kilian, D
Streichert, T
Otto, B
Mole, SE
Ullrich, K
Cotman, S
Kohlschutter, A
Braulke, T
Schulz, A
AF Lebrun, Anne-Helene
Moll-Khosrawi, Parisa
Pohl, Sandra
Makrypidi, Georgia
Storch, Stephan
Kilian, Dirk
Streichert, Thomas
Otto, Benjamin
Mole, Sara E.
Ullrich, Kurt
Cotman, Susan
Kohlschuetter, Alfried
Braulke, Thomas
Schulz, Angela
TI Analysis of Potential Biomarkers and Modifier Genes Affecting the
Clinical Course of CLN3 Disease
SO MOLECULAR MEDICINE
LA English
DT Article
ID NEURONAL CEROID-LIPOFUSCINOSES; BATTEN-DISEASE; LYSOSOMAL DISORDERS;
MOUSE MODEL; EXPRESSION; SPECIFICITY; PHOSPHATASE; PROTEINS; C3G;
MITOCHONDRIAL
AB Mutations in the CLN3 gene lead to juvenile neuronal ceroid lipofuscinosis, a pediatric neurodegenerative disorder characterized by visual loss, epilepsy and psychomotor deterioration, Although most CLN3 patients carry the same 1-kb deletion in the CLN3 gene, their disease phenotype can be variable. The aims of this study were to (i) study the clinical phenotype in CLN3 patients with identical genotype, (ii) identify genes that are dysregulated in CLN3 disease regardless of the clinical course that could be useful as biomarkers, and (iii) find modifier genes that affect the progression rate of the disease. A total of 25 CLN3 patients homozygous for the 1-kb deletion were classified into groups with rapid, average or slow disease progression using an established clinical scoring system. Genome-wide expression profiling was performed in eight CLN3 patients with different disease progression and matched controls. The study showed high phenotype variability in CLN3 patients. Five genes were dysregulated in all CLN3 patients and present candidate biomarkers of the disease. Of those, dual specificity phosphatase 2 (DUSP2) was also validated in acutely CLN3-depleted cell models and in CbCln3(Delta ex7/8) cerebellar precursor cells. A total of 13 genes were upregulated in patients with rapid disease progression and downregulated in patients with slow disease progression; one gene showed dysregulation in the opposite way. Among these potential modifier genes, guanine nucleotide exchange factor 1 for small GTPases of the Ras family (RAPGEF1) and transcription factor Spi-B (SPIB) were validated in an acutely CLN3-depleted cell model. These findings indicate that differential perturbations of distinct signaling pathways might alter disease progression and provide insight into the molecular alterations underlying neuronal dysfunction in CLN3 disease and neurodegeneration in general. (C) 2011 The Feinstein Institute for Medical Research, www.feinsteininstitute.org Online address: http://www.molmed.org doi: 10.2119/molmed.2010.00241
C1 [Lebrun, Anne-Helene; Moll-Khosrawi, Parisa; Pohl, Sandra; Makrypidi, Georgia; Storch, Stephan; Kilian, Dirk; Ullrich, Kurt; Kohlschuetter, Alfried; Braulke, Thomas; Schulz, Angela] Univ Med Ctr Hamburg Eppendorf, Childrens Hosp, D-20246 Hamburg, Germany.
[Streichert, Thomas; Otto, Benjamin] Univ Med Ctr Hamburg Eppendorf, Array Serv Ctr, D-20246 Hamburg, Germany.
[Mole, Sara E.] UCL, Med Res Council Lab Mol Cell Biol, Mol Med Unit, UCL Inst Child Hlth, London, England.
[Mole, Sara E.] UCL, Dept Genet Evolut & Environm, London, England.
[Cotman, Susan] Massachusetts Gen Hosp, Ctr Human Genet, Boston, MA 02114 USA.
RP Schulz, A (reprint author), Univ Med Ctr Hamburg Eppendorf, Childrens Hosp, Martinistr 52, D-20246 Hamburg, Germany.
EM an.schulz@uke.de
OI Mole, Sara/0000-0003-4385-4957
FU Deutsche Forschungsgemeinschaft [SCHU1597/2-1]; Nachstenliebe e.V.;
NCL-Gruppe Deutschland e.V.
FX We thank the affected and control families for participating in this
study and Johannes Brand for technical assistance. This work was
supported by the Deutsche Forschungsgemeinschaft (grant SCHU1597/2-1)
and the parent organizations Nachstenliebe e.V. and NCL-Gruppe
Deutschland e.V.
NR 35
TC 15
Z9 15
U1 0
U2 4
PU FEINSTEIN INST MED RES
PI MANHASSET
PA 350 COMMUNITY DR, MANHASSET, NY 11030 USA
SN 1076-1551
J9 MOL MED
JI Mol. Med.
PD NOV-DEC
PY 2011
VL 17
IS 11-12
BP 1253
EP 1261
DI 10.2119/molmed.2010.00241
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 860OY
UT WOS:000297958800016
PM 21863212
ER
PT J
AU Odierna, DH
Afable-Munsuz, A
Ikediobi, O
Beattie, M
Knight, S
Ko, M
Wilson, A
Ponce, NA
AF Odierna, Donna H.
Afable-Munsuz, Aimee
Ikediobi, Ogechi
Beattie, Mary
Knight, Sara
Ko, Michelle
Wilson, Adrienne
Ponce, Ninez A.
TI Early developments in gene-expression profiling of breast tumors:
potential for increasing black-white patient disparities in breast
cancer outcomes?
SO PERSONALIZED MEDICINE
LA English
DT Article
DE African-American women; breast cancer mortality; gene-expression
profiling; personalized medicine; racial disparities; social
determinants of health
ID POLYMERASE-CHAIN-REACTION; CORE BIOPSY-TISSUE; SOCIOECONOMIC-STATUS;
AFRICAN-AMERICAN; PROGNOSTIC ROLE; UNITED-STATES; ONCOTYPE DX; SURVIVAL;
WOMEN; STAGE
AB New prognostic tests, such as gene-expression profiling (GEP) of breast tumors, are expected to prolong survival and improve the quality of life for many breast cancer patients. In this article, we argue that GEP has not been adequately validated in minority populations, and that both biological and social factors might affect the broad utility of these tests in diverse populations. We suggest that the widespread use of this technology could potentially lead to suboptimal treatment for black women, resulting in a further increase in black-white patient disparities in treatment response, morbidity and mortality rates. We argue for the need to build a large and diverse evidence base for GEP and other emerging technologies in personalized medicine.
C1 [Odierna, Donna H.; Afable-Munsuz, Aimee] SUNY Downstate Sch Publ Hlth, Dept Community Hlth Sci, Brooklyn, NY 11203 USA.
[Odierna, Donna H.] Univ Calif San Francisco, Dept Clin Pharm, San Francisco Branch, UC Cochrane Ctr, San Francisco, CA 94118 USA.
[Beattie, Mary; Wilson, Adrienne] Univ Calif San Francisco, Div Gen Internal Med, UCSF Canc Risk Program, San Francisco, CA 94143 USA.
[Knight, Sara] Univ Calif San Francisco, Hlth Serv Res & Dev Serv, San Francisco Vet Affairs Med Ctr, Dept Psychiat, San Francisco, CA 94143 USA.
[Knight, Sara] Univ Calif San Francisco, Hlth Serv Res & Dev Serv, San Francisco Vet Affairs Med Ctr, Dept Urol, San Francisco, CA 94143 USA.
[Ko, Michelle; Ponce, Ninez A.] UCLA Sch Publ Hlth, Dept Hlth Serv, Los Angeles, CA 90095 USA.
RP Odierna, DH (reprint author), Univ Calif San Francisco, Dept Clin Pharm, San Francisco Branch, UC Cochrane Ctr, 3333 Calif St,Box 0613, San Francisco, CA 94118 USA.
EM Donna.Odierna@ucsf.edu
OI Odierna, Donna H/0000-0003-4156-1456; Ponce, Ninez/0000-0001-5151-6718
FU UCSF Center for Translational and Policy Research on Personalized
Medicine (TRANSPERS), National Cancer Institute (NCI) [P01
CA130818-02A1, P01 CA 130818]; UCSF Clinical and Translational Science
Institute, NIH/NCRR UCSF-CTSI [UL-1 RR024131]; Health Services Research
and Development, Interdisciplinary Program [IIR 09-135]; UCSF [NCI 2P50
058207]; Avon Foundation; CSF Center for Clinical and Translational
Research; Flight Attendant Medical Research Foundation
FX The study was supported by the UCSF Center for Translational and Policy
Research on Personalized Medicine (TRANSPERS P01 CA130818-02A1) National
Cancer Institute (NCI) P01 CA 130818 (principal investigator: K
Phillips). The study was also supported by the UCSF Clinical and
Translational Science Institute, NIH/NCRR UCSF-CTSI Grant Number UL-1
RR024131. Health Services Research and Development, Interdisciplinary
Program to Improve Health Care for Veterans with Complex Comorbid
Conditions and Health Services Research and Development Investigator
Initiated Award (IIR 09-135). Mary Beattie is also funded by the UCSF
Breast Specialized Program of Research Excellence (SPORE NCI 2P50
058207) and the Avon Foundation. Adrienne Wilson is funded by the Avon
Foundation. Donna H Odierna is funded by the UCSF Center for Clinical
and Translational Research and the Flight Attendant Medical Research
Foundation. Sara Knight is employed by the Health Services Research and
Development Service San Francisco Veterans Affairs Medical Center. This
paper is the responsibility of the authors and the perspectives
expressed within do not necessarily reflect the views of the Department
of Veterans Affairs. 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 84
TC 2
Z9 2
U1 0
U2 1
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1741-0541
J9 PERS MED
JI Pers. Med.
PD NOV
PY 2011
VL 8
IS 6
BP 669
EP 679
DI 10.2217/PME.11.67
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 853ZI
UT WOS:000297463800016
PM 22190978
ER
PT J
AU Greene, ER
Huang, S
Serhan, CN
Panigrahy, D
AF Greene, Emily R.
Huang, Sui
Serhan, Charles N.
Panigrahy, Dipak
TI Regulation of inflammation in cancer by eicosanoids
SO PROSTAGLANDINS & OTHER LIPID MEDIATORS
LA English
DT Review
DE Eicosanoids; Inflammation; Cancer; Metastasis; Tumor microenvironment
ID SOLUBLE EPOXIDE HYDROLASE; NONSTEROIDAL ANTIINFLAMMATORY DRUGS;
15-HYDROXYPROSTAGLANDIN DEHYDROGENASE EXPRESSION; SUPPRESSES
TUMOR-GROWTH; HUMAN COLORECTAL-CANCER; ARACHIDONIC-ACID;
CELL-PROLIFERATION; BREAST-CANCER; COLON-CANCER; EPOXYEICOSATRIENOIC
ACIDS
AB Inflammation in the tumor microenvironment is now recognized as one of the hallmarks of cancer. Endogenously produced lipid autacoids, locally acting small molecule lipid mediators, play a central role in inflammation and tissue homeostasis, and have recently been implicated in cancer. A well-studied group of autacoid mediators that are the products of arachidonic acid metabolism include: the prostaglandins, leukotrienes, lipoxins and cytochrome P450 (CYP) derived bioactive products. These lipid mediators are collectively referred to as eicosanoids and are generated by distinct enzymatic systems initiated by cyclooxygenases (COX 1 and 2), lipoxygenases (5-LOX, 12-LOX, 15-LOXa, 15-LOXb), and cytochrome P450s, respectively. These pathways are the target of approved drugs for the treatment of inflammation, pain, asthma, allergies, and cardiovascular disorders. Beyond their potent anti-inflammatory and anti-cancer effects, non-steroidal anti-inflammatory drugs (NSAIDs) and COX-2 specific inhibitors have been evaluated in both preclinical tumor models and clinical trials. Eicosanoid biosynthesis and actions can also be directly influenced by nutrients in the diet, as evidenced by the emerging role of omega-3 fatty acids in cancer prevention and treatment. Most research dedicated to using eicosanoids to inhibit tumor-associated inflammation has focused on the COX and LOX pathways. Novel experimental approaches that demonstrate the anti-tumor effects of inhibiting cancer-associated inflammation currently include: eicosanoid receptor antagonism, overexpression of eicosanoid metabolizing enzymes, and the use of endogenous anti-inflammatory lipid mediators. Here we review the actions of eicosanoids on inflammation in the context of tumorigenesis. Eicosanoids may represent a missing link between inflammation and cancer and thus could serve as therapeutic target(s) for inhibiting tumor growth. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Greene, Emily R.; Panigrahy, Dipak] Harvard Univ, Sch Med, Childrens Hosp Boston, Vasc Biol Program, Boston, MA 02115 USA.
[Greene, Emily R.; Panigrahy, Dipak] Harvard Univ, Sch Med, Dana Farber Canc Inst, Div Pediat Oncol, Boston, MA 02115 USA.
[Huang, Sui] Univ Calgary, Inst Biocomplex & Informat, Calgary, AB, Canada.
[Serhan, Charles N.] Brigham & Womens Hosp, Dept Anesthesiol Perioperat & Pain Med, Ctr Expt Therapeut & Reperfus Injury, Boston, MA 02115 USA.
RP Panigrahy, D (reprint author), Harvard Univ, Sch Med, Childrens Hosp Boston, Vasc Biol Program, Boston, MA 02115 USA.
EM emily.greene@childrens.harvard.edu; sui.huang@ucalgary.ca;
cnserhan@zeus.bwh.harvard.edu; dipak.panigrahy@childrens.harvard.edu
FU National Cancer Institute [RO1CA148633-01A1]
FX We thank Aria Kaipainen and Gabrielle Fredman for suggestions in
preparing the manuscript; Danielle Stanton for preparation of the
figure. This work was supported by National Cancer Institute grant
RO1CA148633-O1A1 (DP).
NR 183
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Z9 91
U1 2
U2 41
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-8823
J9 PROSTAG OTH LIPID M
JI Prostaglandins Other Lipid Mediat.
PD NOV
PY 2011
VL 96
IS 1-4
SI SI
BP 27
EP 36
DI 10.1016/j.prostaglandins.2011.08.004
PG 10
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 860RC
UT WOS:000297964400006
PM 21864702
ER
PT J
AU Garzon, B
Emblem, KE
Mouridsen, K
Nedregaard, B
Due-Tonnessen, P
Nome, T
Hald, JK
Bjornerud, A
Haberg, AK
Kvinnsland, Y
AF Garzon, Benjamin
Emblem, Kyrre E.
Mouridsen, Kim
Nedregaard, Beard
Due-Tonnessen, Pauline
Nome, Terje
Hald, John K.
Bjornerud, Atle
Haberg, Asta K.
Kvinnsland, Yngve
TI Multiparametric analysis of magnetic resonance images for glioma grading
and patient survival time prediction
SO ACTA RADIOLOGICA
LA English
DT Article
DE MR imaging; perfusion; brain; primary neoplasms
ID CEREBRAL BLOOD-VOLUME; HISTOGRAM ANALYSIS; TUMOR GRADE; MR;
OLIGODENDROGLIOMAS; PROGRESSION; MANAGEMENT; MAPS
AB Background: A systematic comparison of magnetic resonance imaging (MRI) options for glioma diagnosis is lacking.
Purpose: To investigate multiple MR-derived image features with respect to diagnostic accuracy in tumor grading and survival prediction in glioma patients.
Material and Methods: T1 pre- and post-contrast, T2 and dynamic susceptibility contrast scans of 74 glioma patients with histologically confirmed grade were acquired. For each patient, a set of statistical features was obtained from the parametric maps derived from the original images, in a region-of-interest encompassing the tumor volume. A forward stepwise selection procedure was used to find the best combinations of features for grade prediction with a cross-validated logistic model and survival time prediction with a cox proportional-hazards regression.
Results: Presence/absence of enhancement paired with kurtosis of the FM (first moment of the first-pass curve) was the feature combination that best predicted tumor grade (grade II vs. grade III-IV; median AUC = 0.96), with the main contribution being due to the first of the features. A lower predictive value (median AUC = 0.82) was obtained when grade IV tumors were excluded. Presence/absence of enhancement alone was the best predictor for survival time, and the regression was significant (P < 0.0001).
Conclusion: Presence/absence of enhancement, reflecting transendothelial leakage, was the feature with highest predictive value for grade and survival time in glioma patients.
C1 [Garzon, Benjamin; Haberg, Asta K.] NTNU, Dept Circulat & Med Imaging, Trondheim, Norway.
[Emblem, Kyrre E.; Bjornerud, Atle] Oslo Univ Hosp, Rikshosp, Intervent Ctr, Oslo, Norway.
[Emblem, Kyrre E.] Massachusetts Gen Hosp, Dept Radiol, MGH HST AA Martinos Ctr Biomed Imaging, Boston, MA 02114 USA.
[Emblem, Kyrre E.] Harvard Univ, Sch Med, Boston, MA USA.
[Mouridsen, Kim] Aarhus Univ, Ctr Functionally Integrat Neurosci, Aarhus, Denmark.
[Nedregaard, Beard; Due-Tonnessen, Pauline; Nome, Terje; Hald, John K.] Oslo Univ Hosp, Rikshosp, Dept Radiol & Nucl Med, Oslo, Norway.
[Haberg, Asta K.] St Olavs Hosp, Dept Med Imaging, Trondheim, Norway.
[Kvinnsland, Yngve] NordicImagingLab, Bergen, Norway.
RP Garzon, B (reprint author), NTNU, Dept Circulat & Med Imaging, Trondheim, Norway.
EM benjamin.garzon@ntnu.no
RI Emblem, Kyrre/H-6691-2012;
OI Emblem, Kyrre/0000-0002-6580-9519; Garzon, Benjamin/0000-0002-4647-7280
FU Rikshospitalet, Oslo University Hospital (Oslo, Norway)
FX We thank David Scheie, from Rikshospitalet, Oslo University Hospital
(Oslo, Norway), for contributions to this work.
NR 34
TC 7
Z9 8
U1 0
U2 11
PU ROYAL SOC MEDICINE PRESS LTD
PI LONDON
PA 1 WIMPOLE STREET, LONDON W1G 0AE, ENGLAND
SN 0284-1851
J9 ACTA RADIOL
JI Acta Radiol.
PD NOV
PY 2011
VL 52
IS 9
BP 1052
EP 1060
DI 10.1258/ar.2011.100510
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 854IW
UT WOS:000297489200020
PM 21969702
ER
PT J
AU Healy, JM
Patel, T
Lee, S
Sanchez-Reilly, S
AF Healy, Jennifer M.
Patel, Taral
Lee, Shuko
Sanchez-Reilly, Sandra
TI Do Symptoms Matter When Considering Patients for Phase I Clinical
Trials? A Pilot Study of Older Adults With Advanced Cancer
SO AMERICAN JOURNAL OF HOSPICE & PALLIATIVE MEDICINE
LA English
DT Article
DE phase I; palliative care; symptoms; quality of life; older adults
ID COOPERATIVE-ONCOLOGY-GROUP; PROGNOSTIC-FACTORS; BREAST-CANCER;
CHEMOTHERAPY; TOXICITY; SURVIVAL; BENEFITS; CRITERIA; AGE
AB Older adults (OA) with advanced cancer (AC) undergoing phase 1 clinical trials (PICT) have poor prognosis. There are no studies which describe symptoms experienced by OA. Methods: Retrospective chart review of PICT participants > 60 years. OA were compared by age (> 65 vs 60-65) and by number of symptoms (> 3 vs <= 3). Results: N = 56. Mean age = 67.09; 48.21% female. Median life-expectancy = 5 months (interquartile range = 2-9 months); 80.36% had pain; of those 64% without pain scale. Most did not have interdisciplinary professionals or hospice referrals. Older adults with > 3 symptoms had more admissions (37.5% vs 14.29%; P = .0335), complications (46.43% vs 16.07%; P = .0026), and greater decline in functional status (24 participants > 3 symptoms vs 8; P = .0173). There were no significant differences comparing OA by age. Conclusions: Older adults enrolled in PICT with more symptoms may sacrifice QOL for experimental treatment.
C1 [Healy, Jennifer M.; Sanchez-Reilly, Sandra] Univ Texas Hlth Sci Ctr San Antonio, Dept Med, Div Geriatr Gerontol & Palliat Care, San Antonio, TX 78229 USA.
[Patel, Taral; Lee, Shuko; Sanchez-Reilly, Sandra] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
RP Healy, JM (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Med, Div Geriatr Gerontol & Palliat Care, 7703 Floyd Curl Dr,MC 7875, San Antonio, TX 78229 USA.
EM Healyj@uthscsa.edu
NR 18
TC 0
Z9 0
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1049-9091
J9 AM J HOSP PALLIAT ME
JI Am. J. Hosp. Palliat. Med.
PD NOV
PY 2011
VL 28
IS 7
BP 463
EP 466
DI 10.1177/1049909111400723
PG 4
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 854IA
UT WOS:000297487000002
PM 21398266
ER
PT J
AU Zimmerman, K
Rudolph, J
Salow, M
Skarf, LM
AF Zimmerman, Kristin
Rudolph, James
Salow, Marci
Skarf, L. Michal
TI Delirium in Palliative Care Patients: Focus on Pharmacotherapy
SO AMERICAN JOURNAL OF HOSPICE & PALLIATIVE MEDICINE
LA English
DT Review
DE delirium; palliative care; assessment; pharmacotherapy; symptom
management; anticholinergic
ID SERUM ANTICHOLINERGIC ACTIVITY; ILL CANCER-PATIENTS; ELDERLY-PATIENTS;
ASSESSMENT SCALE; TERMINAL CANCER; PREDICTION RULE; COMPLICATIONS;
MEDICATIONS; HYDRATION; ASSOCIATION
AB Patients receiving palliative care often possess multiple risk factors and predisposing conditions for delirium. The impact of delirium on patient care in this population may also be far-reaching: affecting not only quality of remaining life but the dying process experienced by patients, caregivers, and the medical team as well. As palliative care focuses on comfort and symptom management, the approach to assessment and subsequent treatment of delirium in palliative care patients may prove difficult for providers to navigate. This article summarizes the multifactorial nature, numerous predisposing medical risk factors, neuropsychiatric adverse effects of palliative medications, pharmacokinetic changes, and challenges complicating delirium assessment and provides a systematic framework for assessment. The benefits, risks, and patient-specific considerations for treatment selection are also discussed.
C1 [Zimmerman, Kristin; Rudolph, James; Salow, Marci; Skarf, L. Michal] VA Boston Healthcare Syst, Dept Pharm, Boston, MA USA.
[Zimmerman, Kristin; Rudolph, James; Salow, Marci; Skarf, L. Michal] VA Boston Healthcare Syst, Geriatr Res Educ & Clin Ctr, Boston, MA USA.
[Zimmerman, Kristin; Rudolph, James; Salow, Marci; Skarf, L. Michal] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
RP Zimmerman, K (reprint author), VA Boston Healthcare Syst, Dept Pharm, 940 Belmont St,119, Brockton, MA 02301 USA.
EM Zimmerman.Kristin@gmail.com
NR 74
TC 5
Z9 5
U1 0
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1049-9091
J9 AM J HOSP PALLIAT ME
JI Am. J. Hosp. Palliat. Med.
PD NOV
PY 2011
VL 28
IS 7
BP 501
EP 510
DI 10.1177/1049909111403732
PG 10
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 854IA
UT WOS:000297487000008
PM 21454319
ER
PT J
AU Tranah, GJ
Blackwell, T
Stone, KL
Ancoli-Israel, S
Paudel, ML
Ensrud, KE
Cauley, JA
Redline, S
Hillier, TA
Cummings, SR
Yaffe, K
AF Tranah, Gregory J.
Blackwell, Terri
Stone, Katie L.
Ancoli-Israel, Sonia
Paudel, Misti L.
Ensrud, Kristine E.
Cauley, Jane A.
Redline, Susan
Hillier, Teresa A.
Cummings, Steven R.
Yaffe, Kristine
CA SOF Res Grp
TI Circadian activity rhythms and risk of incident dementia and mild
cognitive impairment in older women
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID NURSING-HOME PATIENTS; SLEEP-WAKE PATTERNS; AGE-RELATED-CHANGES;
CONSTANT DIM LIGHT; ALZHEIMERS-DISEASE; SUPRACHIASMATIC NUCLEUS;
OSTEOPOROTIC FRACTURES; LOCUS-COERULEUS; WRIST ACTIVITY; OREXIN
AB Objective: Previous cross-sectional studies have observed alterations in activity rhythms in dementia patients but the direction of causation is unclear. We determined whether circadian activity rhythms measured in community-dwelling older women are prospectively associated with incident dementia or mild cognitive impairment (MCI).
C1 [Tranah, Gregory J.] UCSF, San Francisco Coordinating Ctr, Calif Pacific Med Ctr Res Inst, San Francisco, CA 94107 USA.
[Ancoli-Israel, Sonia] Univ Calif San Diego, Dept Psychiat, San Diego, CA 92103 USA.
[Paudel, Misti L.; Ensrud, Kristine E.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN 55455 USA.
[Ensrud, Kristine E.] Minneapolis VA Med Ctr, Ctr Chron Dis Outcomes Res, Minneapolis, MN USA.
[Ensrud, Kristine E.] Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA.
[Cauley, Jane A.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Redline, Susan] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Redline, Susan] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
[Hillier, Teresa A.] Kaiser Permanente Ctr Hlth Res NW Hawaii, Portland, OR USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94107 USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94107 USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94107 USA.
San Francisco VA Med Ctr, San Francisco, CA USA.
RP Tranah, GJ (reprint author), UCSF, San Francisco Coordinating Ctr, Calif Pacific Med Ctr Res Inst, 185 Berry St,Lobby 4,Suite 5700, San Francisco, CA 94107 USA.
EM gtranah@sfcc-cpmc.net
OI Cauley, Jane A/0000-0003-0752-4408
FU National Institutes of Health [AG05407/NIA, AR35582/NIAMS, AG05394/NIA,
AR35583/NIAMS, AG005 407/NIA, AG027576-22/NIA, AG00539422A1,
AG08415/NIA, AG030474/NIA, AG027574-22A1/NIA, AG026 720/NIA]; National
Institute of Aging [K24 AG031155/NIA]; Novartis Pharmaceuticals; NIA;
NIH; Alzheimer Association; DOD; AHAF; California Pacific Medical
Center; Roche Molecular Systems; Sepracor and Litbebook, Inc.; NIAMSD
FX The Study of Osteoporotic Fractures (SOF) and SOF-WISE is supported by
the National Institutes of Health funding (AG05407/NIA/S.R.C.,
AR35582/NIAMS/J.A.C., AG05394/NIA/K.E.E., AR35583/NIAMS/S.A-I., AG005
407/NIA/S.R.C., AG027576-22/NIA/J.A.C., AG00539422A1/NIA/K.E.E.,
AG08415/NIA/S.A-I., AG030474/NIA/G.J.T., AG027574-22A1/NIA/J.A.C., and
AG026 720/NIA/K.L.S.). Dr Kristine Yaffe is supported in part by the
National Institute of Aging grant K24 AG031155/NIA/K.Y. and an
Independent Investigator Award from the Alzheimer's Association.; J.A.C.
receives research funding and consulting fees from Novartis
Pharmaceuticals. K.Y. has received a grant from the NIA; has been a
board member at Pfizer, Medivation, NIMH, and Beeson Scientific
Advisory; has grants/grants pending from the NIH, Alzheimer Association,
DOD, and AHAF; has received travel/accommodations/meeting expenses from
the Alzheimer Association, NIH, Beeson, Japan Geriatrics Society, Wake
Forest University, and State of California DHS. K.E.E. has received a
grant from the NIA; is a federal employee of the Veterans Affairs
Medical Center in Minneapolis, MN; and has received research support
from California Pacific Medical Center, which receives funding from
Roche Molecular Systems. S.R.C., K.L.S., T.B., and G.J.T. are employees
of the California Pacific Medical Center and receive research support
from Roche Molecular Systems. T.B., J.A.C., G.J.T., and K.L.S. have
received a grant from the NIH. S.A.-I. has received a grant from the
NIH; has received grants from Sepracor and Litbebook, Inc.; has served
as an advisor or consultant to Ferring Pharmaceuticals, Inc.,
GlaxoSmithKline, Merck, NeuroVigil, Inc., Neurocrine Biosciences,
Pfizer, Philips Respironics, sanofi-aventis, Sepracor, Inc.,
Schering-Plough, and Purdue Pharma LP. T.H. has received grants from the
NIH (from the NIAMSD and the NIA). S.R. has been under subcontract from
the NIH via California Pacific and is also a recipient of an endowed
professorship at Harvard Medical School, donated by Dr. Peter C.
Farrell, the CEO of RosMed, Inc.
NR 94
TC 99
Z9 100
U1 7
U2 22
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD NOV
PY 2011
VL 70
IS 5
BP 722
EP 732
DI 10.1002/ana.22468
PG 11
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 857TB
UT WOS:000297741600009
PM 22162057
ER
PT J
AU Mainero, C
Boshyan, J
Hadjikhani, N
AF Mainero, Caterina
Boshyan, Jasmine
Hadjikhani, Nouchine
TI Altered functional magnetic resonance imaging resting-state connectivity
in periaqueductal gray networks in migraine
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID VOXEL-BASED MORPHOMETRY; BRAIN-STEM ACTIVATION; GREY-MATTER CHANGES;
CUTANEOUS ALLODYNIA; CORTICAL HYPEREXCITABILITY; HEADACHE; PAIN; CORTEX;
STIMULATION; ABNORMALITIES
AB Objective: The periaqueductal gray matter (PAG), a known modulator of somatic pain transmission, shows evidence of interictal functional and structural abnormalities in migraineurs, which may contribute to hyperexcitability along spinal and trigeminal nociceptive pathways, and lead to the migraine attack. The aim of this study was to examine functional connectivity of the PAG in migraine.
C1 [Mainero, Caterina; Boshyan, Jasmine; Hadjikhani, Nouchine] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA USA.
[Hadjikhani, Nouchine] Swiss Fed Inst Technol, Brain Mind Inst, CH-1015 Lausanne, Switzerland.
RP Hadjikhani, N (reprint author), Martinos Ctr Biomed Imaging, Bldg149,13th St,Room 2301, Charlestown, MA 02129 USA.
EM nouchine@nmr.mgh.harvard.edu
RI Hadjikhani, Nouchine/C-2018-2008
OI Hadjikhani, Nouchine/0000-0003-4075-3106
FU NIH, National Institute of Neurological Disorders and Stroke (NINDS)
[5P01 NS 35611-09]
FX This work was supported by NIH, National Institute of Neurological
Disorders and Stroke (NINDS) grant 5P01 NS 35611-09.
NR 42
TC 103
Z9 115
U1 1
U2 14
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD NOV
PY 2011
VL 70
IS 5
BP 838
EP 845
DI 10.1002/ana.22537
PG 8
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 857TB
UT WOS:000297741600018
PM 22162064
ER
PT J
AU Foster, MC
Yang, Q
Hwang, SJ
Hoffmann, U
Fox, CS
AF Foster, Meredith C.
Yang, Qiong
Hwang, Shih-Jen
Hoffmann, Udo
Fox, Caroline S.
TI Heritability and genome-wide association analysis of renal sinus fat
accumulation in the Framingham Heart Study
SO BMC MEDICAL GENETICS
LA English
DT Article
ID BODY-MASS INDEX; CHRONIC KIDNEY-DISEASE; METABOLIC SYNDROME; RISK; CKD;
CIRCUMFERENCE; LIPODYSTROPHY; LINKAGE; OBESITY; VARIANT
AB Background: Ectopic fat accumulation in the renal sinus is associated with chronic kidney disease and hypertension. The genetic contributions to renal sinus fat accumulation in humans have not been well characterized.
Methods: The present analysis consists of participants from the Framingham Offspring and Third Generation who underwent computed tomography; renal sinus fat and visceral adipose tissue (VAT) were quantified. Renal sinus fat was natural log transformed and sex- and cohort-specific residuals were created, adjusted for (1) age, (2) age and body mass index (BMI), and (3) age and VAT. Residuals were pooled and used to calculate heritability using variance-components analysis in SOLAR. A genome-wide association study (GWAS) for renal sinus fat was performed using an additive model with approximately 2.5 million imputed single nucleotide polymorphisms (SNPs). Finally, we identified the associations of renal sinus fat in our GWAS results with validated SNPs for renal function (n = 16), BMI (n = 32), and waist-to-hip ratio (WHR, n = 14), and applied a multi-SNP genetic risk score method to determine if the SNPs for each renal and obesity trait were in aggregate associated with renal sinus fat.
Results: The heritability of renal sinus fat was 39% (p < 0.0001); results were not materially different after adjustment for BMI (39%) or VAT (40%). No SNPs reached genome-wide significance in our GWAS. In our candidate gene analysis, we observed nominal, direction consistent associations with renal sinus fat for one SNP associated with renal function (p = 0.01), two associated with BMI (p < 0.03), and two associated with WHR (p < 0.03); however, none remained significant after accounting for multiple testing. Finally, we observed that in aggregate, the 32 SNPs associated with BMI were nominally associated with renal sinus fat (multi-SNP genetic risk score p = 0.03).
Conclusions: Renal sinus fat is a heritable trait, even after accounting for generalized and abdominal adiposity. This provides support for further research into the genetic determinants of renal sinus fat. While our study was underpowered to detect genome-wide significant loci, our candidate gene BMI risk score results suggest that variability in renal sinus fat may be associated with SNPs previously known to be associated with generalized adiposity.
C1 [Foster, Meredith C.; Hwang, Shih-Jen; Fox, Caroline S.] Natl Heart Lung & Blood Inst Framingham Heart Stu, Framingham, MA 01702 USA.
[Foster, Meredith C.; Hwang, Shih-Jen; Fox, Caroline S.] NHLBI, Ctr Populat Studies, NIH, Bethesda, MD 20892 USA.
[Foster, Meredith C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Yang, Qiong] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02118 USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Fox, Caroline S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Endocrinol & Metab, Boston, MA 02115 USA.
RP Fox, CS (reprint author), Natl Heart Lung & Blood Inst Framingham Heart Stu, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM foxca@nhlbi.nih.gov
RI Yang, Qiong/G-5438-2014
FU National Heart, Lung and Blood Institute [N01-HC-25195]
FX We would like to acknowledge and thank Toby Johnson for sharing his
method for creating the multi-SNP genetic risk score test statistic. The
Framingham Heart Study is supported by the National Heart, Lung and
Blood Institute (N01-HC-25195). The funding body did not play a role in
the study design, collection, analysis, and interpretation of data, in
the writing of the manuscript, or the decision to submit the manuscript
for publication.
NR 33
TC 3
Z9 3
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2350
J9 BMC MED GENET
JI BMC Med. Genet.
PD NOV 1
PY 2011
VL 12
AR 148
DI 10.1186/1471-2350-12-148
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 856UT
UT WOS:000297669900001
PM 22044751
ER
PT J
AU Mintzer, J
O'Neill, C
AF Mintzer, Jacobo
O'Neill, Courtney
TI Depression in Alzheimer's disease: consequence or contributing factor?
SO EXPERT REVIEW OF NEUROTHERAPEUTICS
LA English
DT Editorial Material
DE Alzheimer's disease; cognitive impairment; dementia; depression
ID SERTRALINE; CRITERIA
C1 [Mintzer, Jacobo] Ralph H Johnson VA Med Ctr, Charleston, SC USA.
[O'Neill, Courtney] Med Univ S Carolina, Dept Neurosci, Charleston, SC 29425 USA.
RP Mintzer, J (reprint author), Ralph H Johnson VA Med Ctr, Charleston, SC USA.
EM mintzerj@musc.edu
FU NIMH NIH HHS [U01MH066136]
NR 10
TC 1
Z9 1
U1 0
U2 2
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1473-7175
EI 1744-8360
J9 EXPERT REV NEUROTHER
JI Expert Rev. Neurother.
PD NOV
PY 2011
VL 11
IS 11
BP 1501
EP 1503
DI 10.1586/ERN.11.145
PG 3
WC Clinical Neurology; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 856HP
UT WOS:000297629900001
PM 22014127
ER
PT J
AU Jiang, BN
Struthers, A
Sun, Z
Feng, Z
Zhao, XQ
Zhao, KY
Dai, WZ
Zhou, XB
Berens, ME
Zhang, L
AF Jiang, Beini
Struthers, Allan
Sun, Zhe
Feng, Zhuo
Zhao, Xuqian
Zhao, Kaiyong
Dai, Weizhong
Zhou, Xiaobo
Berens, Michael E.
Zhang, Le
TI Employing graphics processing unit technology, alternating direction
implicit method and domain decomposition to speed up the numerical
diffusion solver for the biomedical engineering research
SO INTERNATIONAL JOURNAL FOR NUMERICAL METHODS IN BIOMEDICAL ENGINEERING
LA English
DT Article
DE graphics processing unit (GPU); alternating direction implicit method
(ADI); parallel computing; domain decomposition
ID CYLINDRICAL SKIN-STRUCTURE; BRAIN-TUMORS; PRECONDITIONED RICHARDSON;
MULTICELLULAR PATTERNS; MULTISCALE; MODEL; PHENOTYPES; GLIOMAS; GROWTH;
CANCER
AB Diffusion of biological compounds, including nutrients, oxygen, and chemoattractants, is a common component of biomedical engineering models. Conventional numerical schemes, such as alternating direction implicit (ADI) for diffusion, are frequently the computational bottleneck. Our study employs graphics processing unit (GPU) technology to accelerate the diffusion model simulation. We tailor, implement, analyze, and test several parallel ADI algorithms on the highly parallel computational and data architecture of the GPU. Our study confirms that the proposed algorithms provide fast, high-quality simulation results suitable for inclusion in numerous bioengineering simulations. Copyright (C) 2011 John Wiley & Sons, Ltd.
C1 [Jiang, Beini; Struthers, Allan; Zhang, Le] Michigan Tech Univ, Dept Math Sci, Houghton, MI 49931 USA.
[Sun, Zhe] Massachusetts Gen Hosp, Harvard MIT HST Athinoula A Martinos Ctr Biomed I, Charlestown, MA USA.
[Feng, Zhuo; Zhao, Xuqian] Michigan Tech Univ, Dept Elect & Comp Engn, Houghton, MI 49931 USA.
[Zhao, Kaiyong] Hong Kong Baptist Univ, Dept Comp Sci, Hong Kong, Hong Kong, Peoples R China.
[Dai, Weizhong] Louisiana Tech Univ, Coll Engn & Sci, Ruston, LA 71270 USA.
[Zhou, Xiaobo] Methodist Hosp, Dept Pathol, Res Inst, Houston, TX 77030 USA.
[Zhou, Xiaobo] Methodist Hosp, Res Inst, Ctr Bioinformat, Houston, TX 77030 USA.
[Zhou, Xiaobo] Weill Cornell Med Coll, Houston, TX USA.
[Berens, Michael E.] TGen, Translat Genom Res Inst, Canc & Cell Biol Div, Phoenix, AZ 85005 USA.
RP Zhang, L (reprint author), Michigan Tech Univ, Dept Math Sci, Fisher Hall 216, Houghton, MI 49931 USA.
EM mberens@tgen.org; zhangle@mtu.edu
FU Mathematical Department Michigan Tech University; Harvard-MIT (HST)
Athinoula A. Martinos Center for Biomedical Imaging; Department of
Radiology at Massachusetts General Hospital and Translational Genomic
Research Institute
FX This work has been supported by startup funding of Mathematical
Department Michigan Tech University, the Harvard-MIT (HST) Athinoula A.
Martinos Center for Biomedical Imaging and the Department of Radiology
at Massachusetts General Hospital and Translational Genomic Research
Institute.
NR 58
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2040-7939
J9 INT J NUMER METH BIO
JI Int. J. Numer. Meth. Biomed.
PD NOV
PY 2011
VL 27
IS 11
BP 1829
EP 1849
DI 10.1002/cnm.1444
PG 21
WC Engineering, Biomedical; Mathematical & Computational Biology;
Mathematics, Interdisciplinary Applications
SC Engineering; Mathematical & Computational Biology; Mathematics
GA 853YG
UT WOS:000297461000008
ER
PT J
AU Potsidis, E
Berson, EL
Sandberg, MA
AF Potsidis, Emorfily
Berson, Eliot L.
Sandberg, Michael A.
TI Disease Course of Patients with Unilateral Pigmentary Retinopathy
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID RETINITIS-PIGMENTOSA; MUTATIONS; RATES; GENE
AB PURPOSE. To evaluate the change in ocular function by eye in patients with unilateral pigmentary retinopathy.
METHODS. Longitudinal regression was used to estimate mean exponential rates of change in Goldmann visual field area (V4e white test light) and in full-field electroretinogram (ERG) amplitudes to 0.5- and 30-Hz white flashes in 15 patients with unilateral pigmentary retinopathy. Snellen visual acuity was assessed case by case.
RESULTS. Mean annual rates of change for the affected eyes were -4.9% for visual field area, -4.7% for ERG amplitude to 0.5-Hz flashes, and -4.6% for ERG amplitude to 30-Hz flashes. All three rates were faster than the corresponding age-related rates of change for the fellow normal eyes (P = 0.0006, P = 0.003, P = 0.03, respectively). An initial cone ERG implicit time to 30-Hz flashes in affected eyes >= 40 ms predicted a faster mean rate of decline of visual field area and of ERG amplitude to 0.5- and 30-Hz flashes (P < 0.0001 for all three measures). The visual acuity of affected eyes was more likely to decrease in patients presenting at >35 years of age than in patients presenting at a younger age (P = 0.0004).
CONCLUSIONS. The affected eye in unilateral pigmentary retinopathy shows a progressive loss of peripheral retinal function that cannot be attributed to aging alone and that is faster in eyes with a more prolonged initial cone ERG implicit time. Patients presenting at >35 years of age are at greater risk for losing visual acuity. (Invest Ophthalmol Vis Sci. 2011;52:9244-9249) DOI: 10.1167/iovs.11-7892
C1 [Potsidis, Emorfily; Berson, Eliot L.; Sandberg, Michael A.] Harvard Univ, Massachusetts Eye & Ear Infirm, Berman Gund Lab, Study Retinal Degenerat,Med Sch, Boston, MA 02114 USA.
RP Sandberg, MA (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Berman Gund Lab, Study Retinal Degenerat,Med Sch, 243 Charles St, Boston, MA 02114 USA.
EM michael_sandberg@meei.harvard.edu
FU National Eye Institute [EY00169, EY019767]; The Foundation Fighting
Blindness (Columbia, MD)
FX Supported in part by National Eye Institute Grants EY00169 and EY019767
and The Foundation Fighting Blindness (Columbia, MD).
NR 17
TC 2
Z9 2
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 NOV
PY 2011
VL 52
IS 12
BP 9244
EP 9249
DI 10.1167/iovs.11-7892
PG 6
WC Ophthalmology
SC Ophthalmology
GA 856IB
UT WOS:000297631400060
PM 21989720
ER
PT J
AU Sels, JWEM
Tonino, PAL
Siebert, U
Fearon, WF
Van't Veer, M
De Bruyne, B
Pijls, NHJ
AF Sels, Jan-Willem E. M.
Tonino, Pim A. L.
Siebert, Uwe
Fearon, William F.
Van't Veer, Marcel
De Bruyne, Bernard
Pijls, Nico H. J.
TI Fractional Flow Reserve in Unstable Angina and Non-ST-Segment Elevation
Myocardial Infarction Experience From the FAME (Fractional flow reserve
versus Angiography for Multivessel Evaluation) Study
SO JACC-CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE FAME study; FFR; multivessel disease; NSTEMI; PCI; unstable angina
ID PERCUTANEOUS CORONARY INTERVENTION; ARTERY-DISEASE; LESIONS;
ANGIOPLASTY; REVASCULARIZATION; SEVERITY; PECTORIS
AB Objectives The aim of this study was to study whether there is a difference in benefit of fractional flow reserve (FFR) guidance for percutaneous coronary intervention (PCI) in multivessel coronary disease in patients with unstable angina (UA) or non-ST-segment elevation myocardial infarction (NSTEMI), compared with stable angina (SA).
Background The use of FFR to guide PCI has been well established for patients with SA. Its use in patients with UA or NSTEMI has not been investigated prospectively. Methods In the FAME (Fractional flow reserve versus Angiography for Multivessel Evaluation) study 1,005 patients with multivessel disease amenable to PCI were included and randomized to either angiography-guided PCI of all lesions >= 50% or FFR-guided PCI of lesions with an FFR >= 0.80. Patients admitted for UA or NSTEMI with positive troponin but total creatine kinase < 1,000 U/I were eligible for inclusion. We determined 2-year major adverse cardiac event rates of these patients and compared it with stable patients.
Results Of 1,005 patients, 328 had UA or NSTEMI. There was no evidence for heterogeneity among the subgroups for any of the outcome variables (all p values > 0.05). Using FFR to guide PCI resulted in similar risk reductions of major adverse cardiac events and its components in patients with UA or NSTEMI, compared with patients with SA (absolute risk reduction of 5.1% vs. 3.7%, respectively, p = 0.92). In patients with UA or NSTEMI, the number of stents was reduced without increase in hospital stay or procedure time and with less contrast use, in similarity to stable patients.
Conclusions The benefit of using FFR to guide PCI in multivessel disease does not differ between patients with UA or NSTEMI, compared with patients with SA. (J Am Coll Cardiol Intv 2011;4: 1133-9) (C) 2011 by the American College of Cardiology Foundation
C1 [Pijls, Nico H. J.] Univ Technol, Catharina Hosp, Dept Cardiol, NL-5602 ZA Eindhoven, Netherlands.
[Siebert, Uwe] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Siebert, Uwe] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Fearon, William F.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[De Bruyne, Bernard] Cardiovasc Ctr Aalst, Aalst, Belgium.
RP Pijls, NHJ (reprint author), Univ Technol, Catharina Hosp, Dept Cardiol, Michelangelolaan 2,POB 1350, NL-5602 ZA Eindhoven, Netherlands.
EM carias@cze.nl
FU Radi Medical Systems, Uppsala, Sweden; Stichting Vrienden van het Hart
Zuidoost Brabant, the Netherlands; St. Jude Medical
FX The FAME study was supported by unrestricted research grants from Radi
Medical Systems, Uppsala, Sweden and Stichting Vrienden van het Hart
Zuidoost Brabant, the Netherlands. Dr. Tonino has received lecture fees
from St. Jude Medical. Drs. Fearon and De Bruyne report institutional
research grants from St. Jude Medical. Dr. Pip received an educational
grant for the Catharina Hospital from St. Jude Medical. All other
authors have reported that they have no relationships relevant to the
contents of this paper to disclose.
NR 24
TC 54
Z9 57
U1 2
U2 4
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 NOV
PY 2011
VL 4
IS 11
BP 1183
EP 1189
DI 10.1016/j.jcin.2011.08.008
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 856RW
UT WOS:000297662100004
PM 22115657
ER
PT J
AU Don, CW
House, J
White, C
Kiernan, T
Weideman, M
Ruggiero, N
McCann, A
Rosenfield, K
AF Don, Creighton W.
House, John
White, Christopher
Kiernan, Thomas
Weideman, Mary
Ruggiero, Nicholas
McCann, Andrew
Rosenfield, Kenneth
TI Carotid Revascularization immediately Before Urgent Cardiac Surgery
Practice Patterns Associated With the Choice of Carotid Artery Stenting
or Endarterectomy: A Report From the CARE (Carotid Artery
Revascularization and Endarterectomy) Registry
SO JACC-CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE carotid artery stenting; carotid endarterectomy; carotid
revascularization
ID SINGLE-CENTER EXPERIENCE; CORONARY-BYPASS; HIGH-RISK; STENOSIS;
OUTCOMES; ANGIOPLASTY; DISEASE
AB Objectives We describe characteristics associated with use of endarterectomy (CEA) versus stenting (CAS) in patients before urgent cardiac surgery.
Background The optimal modality of carotid revascularization preceding cardiac surgery is unknown.
Methods Retrospective evaluation of the CARE (Carotid Artery Revascularization and Endarterectomy) registry from January 2005 to April 2010 was performed on patients undergoing CEA or CAS preceding urgent cardiac surgery within 30 days. Baseline characteristics were compared, and multivariate adjustment was performed.
Results Of 451 patients who met study criteria, 255 underwent CAS and 196 underwent CEA. Both procedures increased over time to a similar degree (p = 0.18). Patients undergoing CAS had more frequent history of peripheral artery disease (38.2% vs. 26.5%, p < 0.01), neck surgery (5.5% vs. 1.0%, p = 0.01), neck radiation (4.3% vs. 1.0%, p = 0.04), left-main coronary disease (34.8% vs. 23.5%, p < 0.01), neurological events (45.8% vs. 31.3%, p < 0.01), carotid intervention (20.8% vs. 7.6%, p < 0.01), and higher baseline creatinine (1.3 vs. 1.1 mg/dl, p = 0.02). The target carotid arteries of CAS patients were more likely to be symptomatic in the 6 months before revascularization and have restenosis from prior CEA. Patients undergoing CAS had a lower American Society of Anesthesiology grade. Midwest hospitals were less likely to perform CAS than CEA, whereas in the other regions CAS was more common (p < 0.01). Non-Caucasian race, a history of heart failure, previous carotid procedures, prior stroke, left main coronary artery stenosis, lower American Society of Anesthesiology grade, and teaching hospital were independent predictors of patients who would receive CAS.
Conclusions Carotid artery stenting and CEA have increased among patients undergoing urgent cardiac surgery. Patients who underwent CAS had more vascular disease but lower acute pre-surgical risk. Significant regional variation in procedure selection exists. (J Am Coll Cardiol Intv 2011;4: 1200-8) (C) 2011 by the American College of Cardiology Foundation
C1 [Don, Creighton W.] Univ Washington, Med Ctr, Div Cardiol, Seattle, WA 98195 USA.
[House, John] St Lukes Mid Amer Heart & Vasc Inst, Kansas City, MO USA.
[White, Christopher] Ochsner Heart & Vasc Clin, New Orleans, LA USA.
[Weideman, Mary] Amer Coll Cardiol, Washington, DC USA.
[Kiernan, Thomas] Natl Univ Ireland Univ Coll Cork, Sch Med, Cork Univ Hosp, Cork, Ireland.
[Ruggiero, Nicholas] Thomas Jefferson Univ Hosp, Philadelphia, PA 19107 USA.
[McCann, Andrew] Princess Alexandra Hosp, Brisbane, Qld 4102, Australia.
[Rosenfield, Kenneth] Massachusetts Gen Hosp, Cardiac & Vasc Invas Serv, Boston, MA 02114 USA.
RP Don, CW (reprint author), Univ Washington, Med Ctr, Med Div Cardiol, 1959 NE Pacific St, Seattle, WA 98195 USA.
EM cwdon@u.washington.edu
RI White, Christopher/J-6686-2012
OI White, Christopher/0000-0001-8618-7539
FU NCRR [5 KL2 RR025015]; Abbott Vascular; Lutonix; Atrium; IDEV
FX This study was funded under NCRR Grant 5 KL2 RR025015. Dr. Rosenfield is
a consultant for Abbott Vascular; has received royalty for Angioguard
from Cordis; and has received research support from Abbott Vascular,
Lutonix, Atrium, and IDEV. All other authors have reported that they
have no relationships relevant to the contents of this paper to
disclose. George W. Vetrovec, MD, has served as Guest Editor for this
paper.
NR 21
TC 6
Z9 6
U1 0
U2 1
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 NOV
PY 2011
VL 4
IS 11
BP 1200
EP 1208
DI 10.1016/j.jcin.2011.09.010
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 856RW
UT WOS:000297662100007
PM 22115660
ER
PT J
AU Wood, MJ
AF Wood, Malissa J.
TI NADPH oxidase: short-term foe, long-term friend
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Editorial Material
ID MYOCARDIAL INJURY; BOSTON-MARATHON; OXYGEN RADICALS; EXERCISE;
CARDIOPROTECTION; INCREASES
C1 Massachusetts Gen Hosp, MGH Heart Ctr, Corrigan Womens Heart Hlth Program, Boston, MA 02114 USA.
RP Wood, MJ (reprint author), Massachusetts Gen Hosp, MGH Heart Ctr, Corrigan Womens Heart Hlth Program, 55 Fruit St Blake 256, Boston, MA 02114 USA.
EM mjwood@partners.org
NR 9
TC 0
Z9 0
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD NOV
PY 2011
VL 111
IS 5
BP 1231
EP 1232
DI 10.1152/japplphysiol.01060.2011
PG 2
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 856ZX
UT WOS:000297684500002
PM 21885801
ER
PT J
AU de Prost, N
Costa, EL
Wellman, T
Musch, G
Winkler, T
Tucci, MR
Harris, RS
Venegas, JG
Melo, MFV
AF de Prost, Nicolas
Costa, Eduardo L.
Wellman, Tyler
Musch, Guido
Winkler, Tilo
Tucci, Mauro R.
Harris, R. Scott
Venegas, Jose G.
Melo, Marcos F. Vidal
TI Effects of surfactant depletion on regional pulmonary metabolic activity
during mechanical ventilation
SO JOURNAL OF APPLIED PHYSIOLOGY
LA English
DT Article
DE fluorodeoxyglucose F18; positron emission tomography; pulmonary edema;
pulmonary surfactant; respiratory distress syndrome; adult;
ventilator-induced lung injury
ID ACUTE LUNG INJURY; RESPIRATORY-DISTRESS-SYNDROME;
POSITRON-EMISSION-TOMOGRAPHY; END-EXPIRATORY PRESSURE; REPETITIVE
COLLAPSE; EXPERIMENTAL-MODEL; F-18-FDG UPTAKE; TIDAL VOLUMES;
ANIMAL-MODELS; SHEEP LUNGS
AB de Prost N, Costa EL, Wellman T, Musch G, Winkler T, Tucci MR, Harris RS, Venegas JG, Vidal Melo MF. Effects of surfactant depletion on regional pulmonary metabolic activity during mechanical ventilation. J Appl Physiol 111: 1249-1258, 2011. First published July 28, 2011; doi:10.1152/japplphysiol.00311.2011.-Inflammation during mechanical ventilation is thought to depend on regional mechanical stress. This can be produced by concentration of stresses and cyclic recruitment in low-aeration dependent lung. Positron emission tomography (PET) with (18)F-fluorodeoxyglucose ((18)F-FDG) allows for noninvasive assessment of regional metabolic activity, an index of neutrophilic inflammation. We tested the hypothesis that, during mechanical ventilation, surfactant-depleted low-aeration lung regions present increased regional (18)F-FDG uptake suggestive of in vivo increased regional metabolic activity and inflammation. Sheep underwent unilateral saline lung lavage and were ventilated supine for 4 h (positive end-expiratory pressure = 10 cmH(2)O, tidal volume adjusted to plateau pressure = 30 cmH(2)O). We used PET scans of injected (13)N-nitrogen to compute regional perfusion and ventilation and injected (18)F-FDG to calculate (18)F-FDG uptake rate. Regional aeration was quantified with transmission scans. Whole lung (18)F-FDG uptake was approximately two times higher in lavaged than in nonlavaged lungs (2.9 +/- 0.6 vs. 1.5 +/- 0.3 10(-3)/min; P < 0.05). The increased (18)F-FDG uptake was topographically heterogeneous and highest in dependent low-aeration regions (gas fraction 10-50%, P < 0.001), even after correction for lung density and wet-to-dry lung ratios. (18)F-FDG uptake in low-aeration regions of lavaged lungs was higher than that in low-aeration regions of nonlavaged lungs (P < 0.05). This occurred despite lower perfusion and ventilation to dependent regions in lavaged than nonlavaged lungs (P < 0.001). In contrast, (18)F-FDG uptake in normally aerated regions was low and similar between lungs. Surfactant depletion produces increased and heterogeneously distributed pulmonary (18)F-FDG uptake after 4 h of supine mechanical ventilation. Metabolic activity is highest in poorly aerated dependent regions, suggesting local increased inflammation.
C1 [de Prost, Nicolas; Costa, Eduardo L.; Wellman, Tyler; Musch, Guido; Winkler, Tilo; Tucci, Mauro R.; Venegas, Jose G.; Melo, Marcos F. Vidal] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Harris, R. Scott] Massachusetts Gen Hosp, Dept Med, Pulm & Crit Care Unit, Boston, MA 02114 USA.
[Harris, R. Scott] Harvard Univ, Sch Med, Boston, MA USA.
[Costa, Eduardo L.; Tucci, Mauro R.] Univ Sao Paulo, Sch Med, Resp Intens Care Unit, Sao Paulo, Brazil.
[Wellman, Tyler] Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA.
RP Melo, MFV (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, 55 Fruit St, Boston, MA 02114 USA.
EM mvidalmelo@partners.org
RI Winkler, Tilo/B-5337-2009;
OI Winkler, Tilo/0000-0002-7276-5550; de Prost, Nicolas/0000-0002-4833-4320
FU National Heart, Lung, and Blood Institute [HL-5R01HL086827]; Fondation
Recherche Medicale (FRM); College des Enseignants de Pneumologie (CEP);
AstraZeneca; CAPES (Brazilian Ministry of Education); [5K08HL076464]
FX This study was supported by National Heart, Lung, and Blood Institute
Grant HL-5R01HL086827. G. Musch received salary support from
5K08HL076464, N. de Prost received a scholarship from the Fondation
Recherche Medicale (FRM) and from the College des Enseignants de
Pneumologie (CEP) with the support of AstraZeneca, and M. R. Tucci
received a scholarship from CAPES (Brazilian Ministry of Education).
NR 69
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Z9 23
U1 0
U2 3
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 8750-7587
J9 J APPL PHYSIOL
JI J. Appl. Physiol.
PD NOV
PY 2011
VL 111
IS 5
BP 1249
EP 1258
DI 10.1152/japplphysiol.00311.2011
PG 10
WC Physiology; Sport Sciences
SC Physiology; Sport Sciences
GA 856ZX
UT WOS:000297684500006
PM 21799132
ER
PT J
AU Beinart, R
Abbara, S
Blum, A
Ferencik, M
Heist, K
Ruskin, J
Mansour, M
AF Beinart, Roy
Abbara, Suhny
Blum, Andrew
Ferencik, Maros
Heist, Kevin
Ruskin, Jeremy
Mansour, Moussa
TI Left Atrial Wall Thickness Variability Measured by CT Scans ?in Patients
Undergoing Pulmonary Vein Isolation
SO JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY
LA English
DT Article
DE atrial fibrillation; catheter ablation; CT scan; left atrium; pulmonary
vein isolation
ID RADIOFREQUENCY CATHETER ABLATION; FIBRILLATION ABLATION; FISTULA;
ANATOMY; HEART; PREVENTION; ESOPHAGUS; VOLUME; MODEL; TRIAL
AB Left Atrial Wall Thickness Variability Measured by CT Scans. Introduction: Successful catheter ablation of atrial fibrillation (AF) requires the creation of transmural lesions in the left atrium (LA). In addition, cardiac perforation is more likely to occur in areas of thin walls. The LA wall thickness is thus relevant both for procedural efficacy and safety. This study sought to evaluate the regional LA wall thickness in patients with AF.
Methods: The LA muscular wall thickness (excluding fat) was measured by 64 slice cardiac computed tomography (CT) in 60 patients with persistent AF prior to catheter ablation procedures. Measurements were performed in all patients at 12 distinct LA locations, including 3 at the roof (right, middle left), 3 at the floor (right, middle, left), 4 at the posterior wall (right, middle, middle-superior, left), 1 at the left lateral ridge (LLR), and 1 at the mitral isthmus.
Results: There was a large range of LA wall thickness (average thickness 1.89 +/- 0.48 mm, range 0.53.5 mm). In addition, there were significant regional differences in LA wall thickness. In particular, the LA roof was significantly thicker than the posterior wall and floor (P < 0.001), the LLR was significantly thicker than most regions (P < 0.04), and themitral isthmus was also significantly thicker than the posterior wall (P < 0.001) and floor (P < 0.001).
Conclusions: In patients with persistent AF, there is inter-and intra-patient variability in the thickness of the LA muscular wall. In most patients, however, the roof, mitral isthmus, and the ridge between the pulmonary veins and appendage are thicker compared to the posterior wall and floor. (J Cardiovasc Electrophysiol, Vol. 22, pp. 1232-1236, November 2011)
C1 [Beinart, Roy; Abbara, Suhny; Blum, Andrew; Ferencik, Maros; Heist, Kevin; Ruskin, Jeremy; Mansour, Moussa] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Ctr Heart, Boston, MA 02114 USA.
RP Mansour, M (reprint author), Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Ctr Heart, Gray 109,55 Fruit St, Boston, MA 02114 USA.
EM mmansour@partners.org
FU Deane Institute for Integrative Research in Stroke and Atrial
Fibrillation
FX This work has been partially supported by the Deane Institute for
Integrative Research in Stroke and Atrial Fibrillation.
NR 37
TC 24
Z9 24
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1045-3873
J9 J CARDIOVASC ELECTR
JI J. Cardiovasc. Electrophysiol.
PD NOV
PY 2011
VL 22
IS 11
BP 1232
EP 1236
DI 10.1111/j.1540-8167.2011.02100.x
PG 5
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 858XQ
UT WOS:000297837000008
PM 21615817
ER
PT J
AU Sharma, AK
Chander, R
Singh, JP
AF Sharma, Ajay K.
Chander, Ravi
Singh, Jagmeet P.
TI AV Nodal Ablation-Induced Gerbode Defect (LV-RA Shunt)
SO JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY
LA English
DT Article
DE AV nodal ablation; Gerbode defect; LV-RA shunt
ID RIGHT ATRIAL SHUNT
AB Ventriculoatrial Shunt After Nodal Ablation. A Gerbode defect that comprises a left ventricular to right atrial shunt is usually a congenital cardiac condition. Rarely, acquired Gerbode defects secondary to aortic or tricuspid valve endocarditis have been reported. We present a case of a Gerbode defect caused by catheter ablation of the AV node in a patient with a severely dilated cardiomyopathy and refractory atrial fibrillation. (J Cardiovasc Electrophysiol, Vol. 22, pp. 1288-1289, November 2011)
C1 [Singh, Jagmeet P.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Sharma, Ajay K.] Charlton Mem Hosp, Dept Internal Med, Fall River, MA USA.
[Chander, Ravi] Charlton Mem Hosp, Dept Cardiol, Fall River, MA USA.
[Singh, Jagmeet P.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Singh, JP (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, 55 Fruit St, Boston, MA 02114 USA.
EM jsingh@partners.org
FU Boston Scientific, Biotronik, Medtronic, St. Jude Medical
FX Dr. Singh reports participation on research grants supported by Boston
Scientific, Biotronik, Medtronic, St. Jude Medical, and Sorin Group.
Other authors: no disclosures.
NR 6
TC 7
Z9 7
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1045-3873
J9 J CARDIOVASC ELECTR
JI J. Cardiovasc. Electrophysiol.
PD NOV
PY 2011
VL 22
IS 11
BP 1288
EP 1289
DI 10.1111/j.1540-8167.2011.02111.x
PG 2
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 858XQ
UT WOS:000297837000019
PM 21649778
ER
PT J
AU Peacock, ZS
Resnick, CM
Faquin, WC
Kaban, LB
AF Peacock, Zachary S.
Resnick, Cory M.
Faquin, William C.
Kaban, Leonard B.
TI Accessory Mandibular Condyle at the Coronoid Process
SO JOURNAL OF CRANIOFACIAL SURGERY
LA English
DT Article
DE Mandibular condyle; Jacob disease; accessory condyle; coronoid
hyperplasia; mandibular hypomobility
ID PROCESS JACOBS-DISEASE; CRANIAL NEURAL CREST; OF-THE-LITERATURE; BIFID
CONDYLE; DUPLICATION; OSTEOCHONDROMA; HYPERPLASIA; NEUROCRISTOPATHY;
MAXILLARY; GROWTH
AB Coronoid process hyperplasia is a rare cause of mandibular hypomobility. It can result from temporalis muscle hyperactivity, trauma, and neoplasia, but often is idiopathic. Enlargement of the coronoid process leading to pseudojoint formation with the zygomatic arch is known as Jacob's disease. It results most commonly from an osteochondroma of the coronoid process. This is the first reported case of a non-neoplastic accessory mandibular condyle located at the coronoid process articulating with the zygoma.
C1 [Peacock, Zachary S.] Harvard Univ, Sch Dent Med, Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Boston, MA 02114 USA.
Harvard Univ, Sch Dent Med, Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Peacock, ZS (reprint author), Harvard Univ, Sch Dent Med, Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Warren 1201,55 Fruit St, Boston, MA 02114 USA.
EM zpeacock@partners.org
OI Resnick, Cory/0000-0002-6391-9618
NR 38
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1049-2275
J9 J CRANIOFAC SURG
JI J. Craniofac. Surg.
PD NOV
PY 2011
VL 22
IS 6
BP 2168
EP 2171
DI 10.1097/SCS.0b013e3182323fed
PG 4
WC Surgery
SC Surgery
GA 857TE
UT WOS:000297741900065
PM 22075815
ER
PT J
AU Beinart, R
Kabra, R
Heist, KE
Blendea, D
Barrett, CD
Danik, SB
Collins, R
Ruskin, JN
Mansour, M
AF Beinart, Roy
Kabra, Rajesh
Heist, Kevin E.
Blendea, Dan
Barrett, Conor D.
Danik, Stephan B.
Collins, Ryan
Ruskin, Jeremy N.
Mansour, Moussa
TI Respiratory compensation improves the accuracy of electroanatomic
mapping of the left atrium and pulmonary veins during atrial
fibrillation ablation
SO JOURNAL OF INTERVENTIONAL CARDIAC ELECTROPHYSIOLOGY
LA English
DT Article
DE Atrial fibrillation; Catheter ablation; Cardiac mapping
ID CATHETER ABLATION; COMPUTED-TOMOGRAPHY; IMAGE INTEGRATION; VENOUS
ANATOMY; HEART RHYTHM; IMPACT
AB Background The creation of accurate electroanatomic maps (EAM) of the left atrium and pulmonary veins is important for atrial fibrillation (AF) ablation to guide ablative lesions and improve the safety and efficacy of the procedure. Respiratory motion of the heart and the pulmonary veins affects the accuracy of these maps.
Purpose This study aims to assess changes in the left atrial and pulmonary venous anatomy due to respiration and to evaluate their implication for EAM acquisition.
Methods Two separate EAM were created using the CARTO 3 mapping system in 22 consecutive patients (63% males; mean age, 63 +/- 8 years) undergoing AF ablation at our center: a non-respiratory compensation (RC) map in which endocardial points were collected irrespective of respiratory phase and an RC map in which the points were collected during end expiration only. These maps were compared to pre-procedural cardiac CT/MRI images.
Results Non-RC mapping required 3.2 +/- 1.0 min versus 7.8 +/- 2.1 min for the maps with RC. In comparison to the pre-procedural CT/MRI images, maps without RC significantly overestimated the dimensions of the pulmonary veins' ostia compared to maps with RC in both long and short axes. Distances between the pulmonary veins were not significantly different when comparing non-RC to RC mapping at the left atrial roof or floor.
Conclusions Respiratory compensation at the time of EAM acquisition during AF ablation more accurately represents the true anatomical dimensions of the pulmonary vein ostia. The resulting more accurate maps may improve the safety and efficacy of atrial fibrillation ablation.
C1 [Mansour, Moussa] Massachusetts Gen Hosp, Cardiac Arrhythmia Unit, Boston, MA 02114 USA.
[Beinart, Roy; Kabra, Rajesh; Heist, Kevin E.; Blendea, Dan; Barrett, Conor D.; Danik, Stephan B.; Ruskin, Jeremy N.; Mansour, Moussa] Massachusetts Gen Hosp, Ctr Heart, Boston, MA 02114 USA.
[Collins, Ryan] Biosense Webster Incorp, Diamond Bar, CA USA.
RP Mansour, M (reprint author), Massachusetts Gen Hosp, Cardiac Arrhythmia Unit, Gray 109,55 Fruit St, Boston, MA 02114 USA.
EM mmansour@partners.org
FU MGH Deane Institute for Integrative Research in Stroke and Atrial
Fibrillation
FX This work was supported in part by the MGH Deane Institute for
Integrative Research in Stroke and Atrial Fibrillation.
NR 15
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U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1383-875X
J9 J INTERV CARD ELECTR
JI J. Interv. Card. Electrophysiol.
PD NOV
PY 2011
VL 32
IS 2
BP 105
EP 110
DI 10.1007/s10840-011-9583-z
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 855II
UT WOS:000297556800005
PM 21607726
ER
PT J
AU Buckner, RL
Krienen, FM
Castellanos, A
Diaz, JC
Yeo, BTT
AF Buckner, Randy L.
Krienen, Fenna M.
Castellanos, Angela
Diaz, Julio C.
Yeo, B. T. Thomas
TI The organization of the human cerebellum estimated by intrinsic
functional connectivity
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
DE somatotopy; motor control; prefrontal; functional magnetic resonance
imaging; default network; connectome
ID HUMAN CEREBRAL-CORTEX; BRAINS DEFAULT NETWORK; SURFACE-BASED ANALYSIS;
DEMENTED OLDER-ADULTS; OPEN ACCESS SERIES; RHESUS-MONKEY; CORTICAL
SURFACE; MOTOR CORTEX; CORTICOPONTINE PROJECTION; GEOMETRICALLY ACCURATE
AB Buckner RL, Krienen FM, Castellanos A, Diaz JC, Yeo BT. The organization of the human cerebellum estimated by intrinsic functional connectivity. J Neurophysiol 106: 2322-2345, 2011. First published July 27, 2011; doi:10.1152/jn.00339.2011.-The cerebral cortex communicates with the cerebellum via polysynaptic circuits. Separate regions of the cerebellum are connected to distinct cerebral areas, forming a complex topography. In this study we explored the organization of cerebrocerebellar circuits in the human using resting-state functional connectivity MRI (fcMRI). Data from 1,000 subjects were registered using nonlinear deformation of the cerebellum in combination with surface-based alignment of the cerebral cortex. The foot, hand, and tongue representations were localized in subjects performing movements. fcMRI maps derived from seed regions placed in different parts of the motor body representation yielded the expected inverted map of somatomotor topography in the anterior lobe and the upright map in the posterior lobe. Next, we mapped the complete topography of the cerebellum by estimating the principal cerebral target for each point in the cerebellum in a discovery sample of 500 subjects and replicated the topography in 500 independent subjects. The majority of the human cerebellum maps to association areas. Quantitative analysis of 17 distinct cerebral networks revealed that the extent of the cerebellum dedicated to each network is proportional to the network's extent in the cerebrum with a few exceptions, including primary visual cortex, which is not represented in the cerebellum. Like somatomotor representations, cerebellar regions linked to association cortex have separate anterior and posterior representations that are oriented as mirror images of one another. The orderly topography of the representations suggests that the cerebellum possesses at least two large, homotopic maps of the full cerebrum and possibly a smaller third map.
C1 [Buckner, Randy L.; Krienen, Fenna M.; Castellanos, Angela; Yeo, B. T. Thomas] Harvard Univ, Ctr Brain Sci, Dept Psychol, Cambridge, MA 02138 USA.
[Buckner, Randy L.; Castellanos, Angela; Diaz, Julio C.] Howard Hughes Med Inst, Cambridge, England.
[Buckner, Randy L.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Buckner, Randy L.; Krienen, Fenna M.; Yeo, B. T. Thomas] Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA USA.
[Diaz, Julio C.] Univ Miami, Dept Biol, Miami, FL USA.
RP Buckner, RL (reprint author), Harvard Univ, Ctr Brain Sci, Dept Psychol, 52 Oxford St,Northwest Bldg 280-06, Cambridge, MA 02138 USA.
EM randy_buckner@harvard.edu
OI Yeo, B.T. Thomas/0000-0002-0119-3276
FU Department of Defense; Ashford Graduate Fellowship in the Sciences;
Sackler Scholars Program in Psychobiology; Howard Hughes Medical
Institute; National Institutes of Health [AG021910, P41 RR14074, K08
MH067966]; Massachusetts General Hospital-University of California
[U54MH091665]; Simons Foundation
FX We thank Jeremy Schmahmann for discussion, the Harvard Center for Brain
Science Neuroimaging Core and the Athinoula A. Martinos Center for
imaging support, the Harvard FAS Research Computing Group (in particular
James Cuff, Jerry Lotto, and Jeff Chang), and the Neuroinformatics
Research Group (Gabriele Fariello, Timothy O'Keefe, and Victor Petrov).
We thank Haderer & Muller Biomedical Art for assistance with Fig. 5. F.
M. Krienen was supported by fellowships from the Department of Defense,
an Ashford Graduate Fellowship in the Sciences, and the Sackler Scholars
Program in Psychobiology. A. Castellanos and J. C. Diaz were supported
by the Howard Hughes Medical Institute Exceptional Research
Opportunities Program.; This work was supported by National Institutes
of Health Grants AG021910, P41 RR14074, and K08 MH067966, the
Massachusetts General Hospital-University of California, Los Angeles
Human Connectome Project (U54MH091665), the Howard Hughes Medical
Institute, and the Simons Foundation.
NR 111
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U1 6
U2 58
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD NOV
PY 2011
VL 106
IS 5
BP 2322
EP 2345
DI 10.1152/jn.00339.2011
PG 24
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 857CA
UT WOS:000297690500019
PM 21795627
ER
PT J
AU Cokol, M
Chua, HN
Tasan, M
Mutlu, B
Weinstein, ZB
Suzuki, Y
Nergiz, ME
Costanzo, M
Baryshnikova, A
Giaever, G
Nislow, C
Myers, CL
Andrews, BJ
Boone, C
Roth, FP
AF Cokol, Murat
Chua, Hon Nian
Tasan, Murat
Mutlu, Beste
Weinstein, Zohar B.
Suzuki, Yo
Nergiz, Mehmet E.
Costanzo, Michael
Baryshnikova, Anastasia
Giaever, Guri
Nislow, Corey
Myers, Chad L.
Andrews, Brenda J.
Boone, Charles
Roth, Frederick P.
TI Systematic exploration of synergistic drug pairs
SO MOLECULAR SYSTEMS BIOLOGY
LA English
DT Article
DE chemical genetics; drug combinations; drug discovery; genetic
interactions
ID GENETIC INTERACTION; COMBINATIONS; YEAST; NETWORK; THERAPEUTICS;
ANTIBIOTICS; INFECTIONS; DISCOVERY; RELEVANT
AB Drug synergy allows a therapeutic effect to be achieved with lower doses of component drugs. Drug synergy can result when drugs target the products of genes that act in parallel pathways ('specific synergy'). Such cases of drug synergy should tend to correspond to synergistic genetic interaction between the corresponding target genes. Alternatively, 'promiscuous synergy' can arise when one drug non-specifically increases the effects of many other drugs, for example, by increased bioavailability. To assess the relative abundance of these drug synergy types, we examined 200 pairs of antifungal drugs in S. cerevisiae. We found 38 antifungal synergies, 37 of which were novel. While 14 cases of drug synergy corresponded to genetic interaction, 92% of the synergies we discovered involved only six frequently synergistic drugs. Although promiscuity of four drugs can be explained under the bioavailability model, the promiscuity of Tacrolimus and Pentamidine was completely unexpected. While many drug synergies correspond to genetic interactions, the majority of drug synergies appear to result from non-specific promiscuous synergy. Molecular Systems Biology 7: 544; published online 8 November 2011; doi:10.1038/msb.2011.71
C1 [Cokol, Murat; Mutlu, Beste; Weinstein, Zohar B.] Sabanci Univ, Biol Sci & Bioengn Program, Fac Engn & Nat Sci, TR-34956 Istanbul, Turkey.
[Cokol, Murat; Chua, Hon Nian; Tasan, Murat; Suzuki, Yo; Roth, Frederick P.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Chua, Hon Nian; Tasan, Murat; Costanzo, Michael; Baryshnikova, Anastasia; Giaever, Guri; Nislow, Corey; Andrews, Brenda J.; Boone, Charles; Roth, Frederick P.] Univ Toronto, Donnelly Ctr Cellular & Biomol Res, Toronto, ON M5S 3E1, Canada.
[Suzuki, Yo] J Craig Venter Inst, Dept Synthet Biol & Bioenergy, San Diego, CA USA.
[Nergiz, Mehmet E.] Zirve Univ, Dept Comp Engn, Fac Engn, Gaziantep, Turkey.
[Giaever, Guri; Nislow, Corey; Andrews, Brenda J.; Boone, Charles; Roth, Frederick P.] Univ Toronto, Dept Mol Genet, Toronto, ON M5S 3E1, Canada.
[Giaever, Guri] Univ Toronto, Dept Pharmaceut Sci, Toronto, ON M5S 3E1, Canada.
[Myers, Chad L.] Univ Minnesota Twin Cities, Dept Comp Sci & Engn, Minneapolis, MN USA.
[Roth, Frederick P.] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
[Roth, Frederick P.] Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA.
RP Cokol, M (reprint author), Sabanci Univ, Biol Sci & Bioengn Program, Fac Engn & Nat Sci, TR-34956 Istanbul, Turkey.
EM cokol@sabanciuniv.edu; fritz.roth@utoronto.edu
RI Giaever, Guri/D-3930-2009; Roth, Frederick/H-6308-2011;
OI Baryshnikova, Anastasia/0000-0002-0123-2052; Roth,
Frederick/0000-0002-6628-649X
FU NIH [GM086115, HG004098, HG005853-01, HG003224, HG004756, CA130266,
MH087394, HG004233]; FP7 Marie Curie IRG Grant [268440]; Scientific and
Technological Research Council of Turkey [110S209]; Agency of Science,
Technology and Research, Singapore; Canadian Institutes of Health
[MOP-81340, MOP-84305]; Canadian Institute for Advanced Research; Canada
Excellence Research Chair
FX We are indebted to the anonymous reviewers, whose initial comments
substantially changed the direction of this study. We thank F Ozbay, C
Cenik, I Iossifov, M Yildirim, E Demir, J Mellor, R Deo, and Y Bulut for
their valuable comments, and to S Buratowski, N Gray, and C Shamu for
providing reagents. M Cokol (MC1) and MT were supported by NIH
Fellowships (GM086115 and HG004098, respectively). MC1 was supported by
a FP7 Marie Curie IRG Grant (268440) and Scientific and Technological
Research Council of Turkey (110S209). HNC was supported by the Agency of
Science, Technology and Research, Singapore. CN and GG were supported by
the Canadian Institutes of Health (MOP-81340 and MOP-84305). M Costanzo
(MC2), AB, CLM, BJA, and CB were supported by a grant from the National
Institutes of Health (HG005853-01). FPR was supported by NIH grants
(HG003224, HG004756, CA130266, MH087394 and HG004233), a Canadian
Institute for Advanced Research Fellowship and a Canada Excellence
Research Chair.
NR 32
TC 80
Z9 80
U1 1
U2 25
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1744-4292
J9 MOL SYST BIOL
JI Mol. Syst. Biol.
PD NOV
PY 2011
VL 7
AR 544
DI 10.1038/msb.2011.71
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 857AK
UT WOS:000297685900001
PM 22068327
ER
PT J
AU Hirschberg, R
Giacino, JT
AF Hirschberg, Ron
Giacino, Joseph T.
TI The Vegetative and Minimally Conscious States: Diagnosis, Prognosis and
Treatment
SO NEUROLOGIC CLINICS
LA English
DT Article
DE Consciousness; Vegetative state; Traumatic brain injury; Neuroimaging;
Outcomes
ID TRAUMATIC BRAIN-INJURY; FOLLOW-UP; DISORDERS; ZOLPIDEM; RECOVERY; SCALE;
COMA; RECOMMENDATIONS; REHABILITATION; AMANTADINE
AB Severe acquired brain injury has profound impact on alertness, cognition, and behavior. Among those who survive the initial injury, a significant minority fail to fully recover self and environmental awareness, and go on to experience prolonged disorders of consciousness (DOC) that can last a lifetime. Although there are no standards of care to guide clinical management, a growing body of empirical evidence is beginning to accrue to inform clinical decision making. In this article, we review the state of the science as it pertains to diagnosis, prognosis, and treatment of patients with DOC.
C1 [Hirschberg, Ron; Giacino, Joseph T.] Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, Boston, MA 02114 USA.
[Hirschberg, Ron; Giacino, Joseph T.] Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Boston, MA 02115 USA.
[Hirschberg, Ron] Massachusetts Gen Hosp, Dept Phys Med & Rehabil, Boston, MA 02114 USA.
[Giacino, Joseph T.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
RP Giacino, JT (reprint author), Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, 125 Nashua St, Boston, MA 02114 USA.
EM jgiacino@partners.org
NR 51
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U1 0
U2 22
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 NOV
PY 2011
VL 29
IS 4
BP 773
EP +
DI 10.1016/j.ncl.2011.07.009
PG 15
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 853BN
UT WOS:000297401300006
PM 22032660
ER
PT J
AU Wilson, MR
Roos, KL
AF Wilson, Michael R.
Roos, Karen L.
TI Infectious Diseases and Impaired Consciousness
SO NEUROLOGIC CLINICS
LA English
DT Article
DE Neuroinfectious diseases; Infectious disease; Disorders of
consciousness; Impaired consciousness
ID RECONSTITUTION INFLAMMATORY SYNDROME; NERVOUS-SYSTEM INFECTIONS; STATUS
EPILEPTICUS; PNEUMOCOCCAL MENINGITIS; CEREBROSPINAL-FLUID;
UNITED-STATES; SEVERE SEPSIS; ENCEPHALITIS; EPIDEMIOLOGY; INFLUENZA
AB Any of a number of neuroinfectious diseases can cause a disorder of consciousness. The priority in the care of the patient is to identify an infectious disease that is treatable. This article examines disorders of consciousness that may be caused by a septic encephalopathy, bacterial meningoencephalitis, viral encephalitis, tick-borne bacterial disease, fungal meningitis, tuberculous meningitis, a focal infectious mass lesion, such as a brain abscess, or an autoimmune-mediated disorder as a complication of infection.
C1 [Roos, Karen L.] Indiana Univ Sch Med, Dept Neurol, Indianapolis, IN 46202 USA.
[Wilson, Michael R.] Brigham & Womens Hosp, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Roos, KL (reprint author), Indiana Univ Sch Med, Dept Neurol, Suite 1711,550 N Univ Blvd, Indianapolis, IN 46202 USA.
EM kroos@iupui.edu
RI Wilson, Michael/E-8095-2013
NR 42
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U1 0
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0733-8619
J9 NEUROL CLIN
JI Neurol. Clin.
PD NOV
PY 2011
VL 29
IS 4
BP 927
EP +
DI 10.1016/j.ncl.2011.07.013
PG 17
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 853BN
UT WOS:000297401300013
PM 22032667
ER
PT J
AU Rubin, EB
Bernat, JL
AF Rubin, Emily B.
Bernat, James L.
TI Ethical Aspects of Disordered States of Consciousness
SO NEUROLOGIC CLINICS
LA English
DT Article
DE Disordered consciousness; Coma; Minimally conscious state; Vegetative
state; Traumatic brain injury; Ethics; Surrogate decision making;
End-of-life care
ID PERSISTENT VEGETATIVE STATE; LIFE-SUSTAINING TREATMENT; ARTIFICIAL
NUTRITION; MEDICAL FUTILITY; DECISION-MAKING; CRITICAL-CARE;
BRAIN-INJURY; SUPPORT; PATIENT; LAWS
AB The medical care of patients in disordered states of consciousness, including vegetative and minimally conscious states, raises some of the most intricate ethical questions in medicine. There is inherent ambiguity and uncertainty involved in diagnosing such patients and evaluating their level of awareness and prognosis for recovery. The care of these patients requires the weighing of competing ethical values, including respect for personal autonomy, protection of vulnerable patients, nonmaleficence, and the just use of limited medical resources. We highlight some of the major ethical issues in caring for patients with severe brain injury.
C1 [Rubin, Emily B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bernat, James L.] Dartmouth Med Sch, Hanover, NH 03755 USA.
[Bernat, James L.] Dartmouth Hitchcock Med Ctr, Dept Neurol, Lebanon, NH 03756 USA.
RP Rubin, EB (reprint author), 29 Lawrence St,Apartment B, Cambridge, MA 02139 USA.
EM erubin3@partners.org
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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 0733-8619
J9 NEUROL CLIN
JI Neurol. Clin.
PD NOV
PY 2011
VL 29
IS 4
BP 1055
EP +
DI 10.1016/j.ncl.2011.07.007
PG 18
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 853BN
UT WOS:000297401300019
PM 22032673
ER
PT J
AU Gladd, DK
Saunders, GH
AF Gladd, Dana K.
Saunders, Gabrielle H.
TI Ambient noise levels in the chemotherapy clinic
SO NOISE & HEALTH
LA English
DT Article
DE Chemotherapy; cisplatin; noise disturbance; noise
ID OFFICE NOISE; STRESS; OTOTOXICITY; CISPLATIN; EXPOSURE
AB Many of the drugs used for chemotherapy treatments are known to be ototoxic, and can result in permanent hearing threshold shifts. The degree of ototoxic damage can be influenced by many factors including dosage, duration of exposure, genetics, and coadministration with other ototoxic agents. Cisplatin is known for its ototoxic effects on hearing thresholds, particularly in the high frequencies. Recent studies have indicated a synergistic relationship between Cisplatin administration and moderate to high noise level exposure starting between 70-85 dB SPL. This study measured the noise levels in the Portland Veterans Affairs Medical Centers outpatient chemotherapy clinic. Average (LAeq) and peak (LCpeak) noise measures were recorded every minute from 7 am until 6 pm on the two busiest clinic days. Patients, visitors, and staff members filled out anonymous surveys regarding their reactions to noise levels. Cumulative noise levels were not at levels known to interact with Cisplatin for a significant period of time. Noise measurement analysis indicated that levels were at or above 70 dB SPL for less than ten minutes during the 11-hour recording window. The patient and visitor surveys indicated that both groups were unbothered by noise in the clinic. However, most staff members were bothered by or concerned about noise levels, and many felt that it caused stress and difficulty communicating on the phone.
C1 [Gladd, Dana K.; Saunders, Gabrielle H.] Portland VA Med Ctr, Natl Ctr Rehabil Auditory Res, Portland, OR USA.
RP Gladd, DK (reprint author), 3710 SW US Vet Hosp Rd NCRAR, Portland, OR 97239 USA.
EM dana.koltenuk@gmail.com
FU NIH [T35 DC008764]; VA RR and D Grant [C4844C]
FX Support for this work was provided by NIH Predoctoral Training Grant T35
DC008764 and VA RR and D Grant # C4844C. We thank Patricia Pulliam,
A.N.P., and other staff and patients of the Portland VA Medical Center
Chemotherapy outpatient clinic for their participation, Roger Ellingson
for his assistance with the equipment and Sarah Weidman for her
assistance with data collection.
NR 19
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Z9 4
U1 0
U2 2
PU MEDKNOW PUBLICATIONS
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
INDIA
SN 1463-1741
J9 NOISE HEALTH
JI Noise Health
PD NOV-DEC
PY 2011
VL 13
IS 55
BP 444
EP 451
DI 10.4103/1463-1741.90322
PG 8
WC Audiology & Speech-Language Pathology; Public, Environmental &
Occupational Health
SC Audiology & Speech-Language Pathology; Public, Environmental &
Occupational Health
GA 855WE
UT WOS:000297596000010
PM 22122961
ER
PT J
AU Tang, PA
Heng, DYC
Choueiri, TK
AF Tang, Patricia A.
Heng, Daniel Y. C.
Choueiri, Toni K.
TI Impact of Body Composition on Clinical Outcomes in Metastatic Renal Cell
Cancer
SO ONCOLOGIST
LA English
DT Editorial Material
ID MASS INDEX; CARCINOMA; OBESITY; SORAFENIB; TRIALS; TUMORS; RISK
C1 [Tang, Patricia A.; Heng, Daniel Y. C.] Univ Calgary, Tom Baker Canc Ctr, Dept Oncol, Calgary, AB T2N 4N2, Canada.
[Choueiri, Toni K.] Brigham & Womens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Choueiri, Toni K.] Harvard Univ, Sch Med, Boston, MA USA.
RP Tang, PA (reprint author), Univ Calgary, Tom Baker Canc Ctr, Dept Oncol, 1331 29 St NW, Calgary, AB T2N 4N2, Canada.
EM patricia.tang@albertahealthservices.ca
RI Inov Farmaceutica, Inct/K-2313-2013
NR 26
TC 6
Z9 6
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 NOV
PY 2011
VL 16
IS 11
BP 1484
EP 1486
DI 10.1634/theoncologist.2011-0337
PG 3
WC Oncology
SC Oncology
GA 859EZ
UT WOS:000297860900002
PM 22020214
ER
PT J
AU Kwak, E
AF Kwak, Eunice
TI The Role of Irreversible HER Family Inhibition in the Treatment of
Patients with Non-Small Cell Lung Cancer
SO ONCOLOGIST
LA English
DT Article
DE Irreversible EGFR/HER-2 tyrosine kinase inhibitors; Non-small cell lung
cancer; Resistance; Afatinib (BIBW 2992); PF00299804
ID EPIDERMAL-GROWTH-FACTOR; RECEPTOR TYROSINE KINASE; PHASE-III TRIAL;
PREVIOUSLY TREATED PATIENTS; ADVANCED SOLID TUMORS; BIBW 2992;
RESISTANCE MUTATION; ACQUIRED-RESISTANCE; 1ST-LINE GEFITINIB;
RANDOMIZED-TRIAL
AB Small-molecule tyrosine kinase inhibitors (TKIs) of the human epidermal growth factor receptor (HER) include the reversible epidermal growth factor receptor (EGFR/HER-1) inhibitors gefitinib and erlotinib. EGFR TKIs have demonstrated activity in the treatment of patients with non-small cell lung cancer (NSCLC) harboring activating EGFR mutations; however, multiple mechanisms of resistance limit the benefit of these drugs. Although resistance to EGFR TKIs can be intrinsic and correlated with molecular lesions such as in Kirsten rat sarcoma viral oncogene homolog (KRAS; generally observed in a wild-type EGFR background), acquired resistance to EGFR TKIs can evolve in the setting of activating EGFR mutations, such as in the case of EGFR T790M mutations. Several irreversible inhibitors that target multiple members of the HER family simultaneously are currently in clinical development for NSCLC and may have a role in the treatment of TKI-sensitive and TKI-resistant disease. These include PF00299804, an inhibitor of EGFR/HER-1, HER-2, and HER-4, and afatinib (BIBW 2992), an inhibitor of EGFR/HER-1, HER-2, and HER-4. Results of large, randomized trials of these agents may help to determine their potential for the treatment of NSCLC. The Oncologist 2011; 16: 1498-1507
C1 Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
RP Kwak, E (reprint author), Massachusetts Gen Hosp, Ctr Canc, 55 Fruit St,YAW 7, Boston, MA 02114 USA.
EM ekwak@partners.org
RI Inov Farmaceutica, Inct/K-2313-2013; Mendez, Pedro /J-8955-2016
OI Mendez, Pedro /0000-0001-6713-7907
FU Boehringer Ingelheim Pharmaceuticals, Inc (BIPI)
FX This work was supported by Boehringer Ingelheim Pharmaceuticals, Inc
(BIPI). The author received no compensation related to the development
of the manuscript.
NR 87
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Z9 29
U1 0
U2 7
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
EI 1549-490X
J9 ONCOLOGIST
JI Oncologist
PD NOV
PY 2011
VL 16
IS 11
BP 1498
EP 1507
DI 10.1634/theoncologist.2011-0087
PG 10
WC Oncology
SC Oncology
GA 859EZ
UT WOS:000297860900004
PM 22016476
ER
PT J
AU Chan, CC
Rubenstein, JL
Coupland, SE
Davis, JL
Harbour, JW
Johnston, PB
Cassoux, N
Touitou, V
Smith, JR
Batchelor, TT
Pulido, JS
AF Chan, Chi-Chao
Rubenstein, James L.
Coupland, Sarah E.
Davis, Janet L.
Harbour, J. William
Johnston, Patrick B.
Cassoux, Nathalie
Touitou, Valerie
Smith, Justine R.
Batchelor, Tracy T.
Pulido, Jose S.
TI Primary Vitreoretinal Lymphoma: A Report from an International Primary
Central Nervous System Lymphoma Collaborative Group Symposium
SO ONCOLOGIST
LA English
DT Article
ID PRIMARY INTRAOCULAR LYMPHOMA; PRIMARY CNS LYMPHOMA; B-CELL LYMPHOMA;
ATTRACTING CHEMOKINE-1 CXCL13; POLYMERASE-CHAIN-REACTION;
NON-HODGKINS-LYMPHOMA; INTRAVITREAL METHOTREXATE; MALIGNANT-LYMPHOMA;
GENE-EXPRESSION; RITUXIMAB INJECTIONS
AB Primary vitreoretinal lymphoma (PVRL), also known as primary intraocular lymphoma, is a rare malignancy typically classified as a diffuse large B-cell lymphoma and most frequently develops in elderly populations. PVRL commonly masquerades as posterior uveitis and has a unique tropism for the retina and central nervous system (CNS). Over 15% of primary CNS lymphoma patients develop intraocular lymphoma, usually occurring in the retina and/or vitreous. Conversely, 65%-90% of PVRL patients develop CNS lymphoma. Consequently, PVRL is often fatal because of ultimate CNS association. Current PVRL animal models are limited and require further development. Typical clinical findings include vitreous cellu-lar infiltration (lymphoma and inflammatory cells) and subretinal tumor infiltration as determined using dilated fundoscopy, fluorescent angiography, and optical coherent tomography. Currently, PVRL is most often diagnosed using both histology to identify lymphoma cells in the vitreous or retina and immunohistochemistry to indicate monoclonality. Additional adjuncts in diagnosing PVRL exist, including elevation of interleukin-10 levels in ocular fluids and detection of Ig H or T-cell receptor gene rearrangements in malignant cells. The optimal therapy for PVRL is not defined and requires the combined effort of oncologists and ophthalmologists. PVRL is sensitive to radiation therapy and exhibits high responsiveness to intravitreal methotrexate or rituximab. Although systemic chemotherapy alone can result in high response rates in patients with PVRL, there is a high relapse rate. Because of the disease rarity, international, multicenter, collaborative efforts are required to better understand the biology and pathogenesis of PVRL as well as to define both diagnostic markers and optimal therapies. The Oncologist 2011;16:1589-1599
C1 [Chan, Chi-Chao] NEI, Immunopathol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Rubenstein, James L.] Univ Calif San Francisco, Sch Med, Div Hematol & Oncol, San Francisco, CA USA.
[Coupland, Sarah E.] Royal Liverpool Hosp, Dept Cell & Mol Pathol, Liverpool L7 8XP, Merseyside, England.
[Davis, Janet L.] Univ Miami, Miller Sch Med, Bascom Palmer Eye Inst, Dept Ophthalmol, Miami, FL 33136 USA.
[Johnston, Patrick B.] Mayo Clin, Dept Hematol & Internal Med, Rochester, MN USA.
[Pulido, Jose S.] Mayo Clin, Dept Ophthalmol, Rochester, MN USA.
[Harbour, J. William] Washington Univ, Sch Med, Barnes Retina Inst, Ocular Oncol Serv, St Louis, MO USA.
[Cassoux, Nathalie; Touitou, Valerie] Hop La Pitie Salpetriere, Dept Ophthalmol, Paris, France.
[Cassoux, Nathalie] Inst Curie, Dept Ophthalmol, Paris, France.
[Smith, Justine R.] Oregon Hlth & Sci Univ, Dept Ophthalmol, Portland, OR 97201 USA.
[Batchelor, Tracy T.] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Batchelor, Tracy T.] Harvard Univ, Sch Med, Dept Radiat Oncol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Chan, CC (reprint author), NEI, Immunopathol Sect, Immunol Lab, NIH, 10 Ctr Dr,10-10N103, Bethesda, MD 20892 USA.
EM chanc@nei.nih.gov
RI Inov Farmaceutica, Inct/K-2313-2013
FU Novartis; Genentech; NIH; Pfizer; Millennium; AstraZeneca; Wyeth;
National Cancer Institute [1R13CA124293-01]; National Eye Institute
FX Disclosures: Chi-Chao Chan: None; James L. Rubenstein: None; Sarah E.
Coupland: None; Janet L. Davis: Centocor (C/A), Novartis (C/A, RF); J.
William Harbour: None; Patrick B. Johnston: Daiichi Sankyo, Spectrum
Pharmaceutical (C/A); Nathalie Cassoux: None; Valerie Touitou: None;
Justine R. Smith: Genentech (RF); Tracy T. Batchelor: Merck,
Roche/Genentech, Imedex, Educational Concepts (H); NIH, Pfizer,
Millennium, AstraZeneca, Wyeth (RF); Jose S. Pulido: None.; This work
was partially supported by a grant from the National Cancer Institute
(1R13CA124293-01) and the National Eye Institute intramural research
program.
NR 94
TC 80
Z9 87
U1 2
U2 8
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
J9 ONCOLOGIST
JI Oncologist
PD NOV
PY 2011
VL 16
IS 11
BP 1589
EP 1599
DI 10.1634/theoncologist.2011-0210
PG 11
WC Oncology
SC Oncology
GA 859EZ
UT WOS:000297860900015
PM 22045784
ER
PT J
AU Niederman, R
Richards, D
AF Niederman, Richard
Richards, Derek
TI What is Evidence-Based Dentistry, and Do Oral Infections Increase
Systemic Morbidity or Mortality?
SO ORAL AND MAXILLOFACIAL SURGERY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Evidence-based dentistry; Oral infections; Molecular medicine;
Inflammation
ID LOW-BIRTH-WEIGHT; DISEASE; THERAPY; HEALTH; TEETH; RISK
AB From Celsus' first reports of rubor, calor, dolor, tumor, and functio laesa, has come an understanding of inflammation's manifestations at the organ, tissue, vascular, cellular, genetic, and molecular levels. Molecular medicine now raises the opposite question: can local oral infections and their inflammatory mediators increase systemic morbidity or mortality? From these perspectives we examine the clinical evidence relating caries, periodontal disease, and pericoronitis to systemic disease. Widespread affirmation of an oral-systemic linkage remains elusive, raising sobering cautions.
C1 [Niederman, Richard] Forsyth Inst, Ctr Evidence Based Dent, Cambridge, MA 02142 USA.
[Richards, Derek] Univ Oxford, Ctr Evidence Based Dent, Oxford OX1 2JA, England.
RP Niederman, R (reprint author), Forsyth Inst, Ctr Evidence Based Dent, 245 1st St, Cambridge, MA 02142 USA.
EM rniederman1@gmail.com
OI niederman, richard/0000-0001-6674-1774
NR 29
TC 1
Z9 1
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 1042-3699
J9 ORAL MAXIL SURG CLIN
JI Oral Maxillofac. Surg. Clin. N. Am.
PD NOV
PY 2011
VL 23
IS 4
BP 491
EP +
DI 10.1016/j.coms.2011.07.001
PG 7
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 856DJ
UT WOS:000297616900002
PM 21982600
ER
PT J
AU Susarla, SM
Sharaf, B
Dodson, TB
AF Susarla, Srinivas M.
Sharaf, Basel
Dodson, Thomas B.
TI Do Antibiotics Reduce the Frequency of Surgical Site Infections After
Impacted Mandibular Third Molar Surgery?
SO ORAL AND MAXILLOFACIAL SURGERY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Third molars; Antibiotics; Surgical site infection; Impacted teeth
ID CONTROLLED CLINICAL-TRIAL; INFLAMMATORY COMPLICATIONS; PROPHYLACTIC
ANTIBIOTICS; PREVENTION; REMOVAL; METRONIDAZOLE; CLINDAMYCIN;
TINIDAZOLE; NECESSITY; OPINION
AB Surgical removal of impacted third molars remains the most common procedure performed by oral and maxillofacial surgeons. Given the abundance of host bacteria within the operative sites, surgical site infections are among the most common complications of third molar removal, with an estimated frequency of 1% to 30%. In this setting, significant controversy has surrounded the use of prophylactic antibiotics in the surgical management of impacted third molars. This article provides a comprehensive review of the available data on antibiotic prophylaxis in impacted third molar surgery and offers specific recommendations on antibiotic use.
C1 [Susarla, Srinivas M.; Dodson, Thomas B.] Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Ctr Appl Clin Investigat, Boston, MA 02114 USA.
[Sharaf, Basel] SUNY Buffalo, Buffalo Gen Hosp, Sch Med & Biomed Sci, Dept Surg, Buffalo, NY 14203 USA.
RP Susarla, SM (reprint author), Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Ctr Appl Clin Investigat, 55 Fruit St,WACC230, Boston, MA 02114 USA.
EM smsusarla@gmail.com
OI Susarla, Srinivas/0000-0003-0155-8260
NR 29
TC 10
Z9 10
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 1042-3699
J9 ORAL MAXIL SURG CLIN
JI Oral Maxillofac. Surg. Clin. N. Am.
PD NOV
PY 2011
VL 23
IS 4
BP 541
EP +
DI 10.1016/j.coms.2011.07.007
PG 7
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 856DJ
UT WOS:000297616900008
PM 21982606
ER
PT J
AU Sharaf, B
Dodson, TB
AF Sharaf, Basel
Dodson, Thomas B.
TI Does the Use of Prophylactic Antibiotics Decrease Implant Failure?
SO ORAL AND MAXILLOFACIAL SURGERY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Prophylactic antibiotics; Implant dentistry; Implant failure; Dental
implants
ID RANDOMIZED CLINICAL-TRIAL; DENTAL IMPLANTS; PERIOPERATIVE ANTIBIOTICS;
ORAL IMPLANTS; SURGERY; PLACEMENT
AB The use of prophylactic antibiotics in implant dentistry is controversial. Given the known risks of antibiotic treatment and lack of consensus on using antibiotics at the time of implant insertion, the purpose of this article was to review available studies on use of perioperative prophylactic antibiotics at the time of implant placement and to provide evidence-based recommendations for antibiotic use. The reviewed studies suggest that a single preoperative dose of 2 g amoxicillin 1 hour before implant placement or 1 g amoxicillin 1 hour preoperatively and 500 mg 4 times daily 2 days postoperatively can reduce the rate of implant failure.
C1 [Sharaf, Basel] SUNY Buffalo, Buffalo Gen Hosp, Dept Surg, Sch Med & Biomed Sci, Buffalo, NY 14203 USA.
[Dodson, Thomas B.] Harvard Univ, Sch Dent Med, Ctr Appl Clin Investigat, Dept Oral & Maxillofacial Surg, Boston, MA 02114 USA.
[Dodson, Thomas B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Sharaf, B (reprint author), SUNY Buffalo, Buffalo Gen Hosp, Dept Surg, Sch Med & Biomed Sci, 100 High St,Room C381, Buffalo, NY 14203 USA.
EM sharafddsmd@gmail.com
NR 12
TC 2
Z9 4
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 1042-3699
J9 ORAL MAXIL SURG CLIN
JI Oral Maxillofac. Surg. Clin. N. Am.
PD NOV
PY 2011
VL 23
IS 4
BP 547
EP +
DI 10.1016/j.coms.2011.07.008
PG 5
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 856DJ
UT WOS:000297616900009
PM 21982607
ER
PT J
AU Palmason, S
Marty, FM
Treister, NS
AF Palmason, Stefan
Marty, Francisco M.
Treister, Nathaniel S.
TI How Do We Manage Oral Infections in Allogeneic Stem Cell Transplantation
and Other Severely Immunocompromised Patients?
SO ORAL AND MAXILLOFACIAL SURGERY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Immunocompromise; Neutropenia; Infection; Odontogenic; Oral
ID HERPES-SIMPLEX-VIRUS; BONE-MARROW-TRANSPLANTATION; EPSTEIN-BARR-VIRUS;
VARICELLA-ZOSTER-VIRUS; POSTTRANSPLANTATION LYMPHOPROLIFERATIVE
DISORDER; INVASIVE FUNGAL-INFECTIONS; LIPOSOMAL AMPHOTERICIN-B;
PLACEBO-CONTROLLED TRIAL; BLOOD-STREAM INFECTIONS; RANDOMIZED
DOUBLE-BLIND
AB The oral cavity is among the sites in the body most susceptible to infections. In the immunocompetent population these are most frequently localized odontogenic infections caused by bacteria. In severely immunocompromised patients, such as those undergoing allogeneic stem cell transplantation, fungal and viral infections become especially prominent. Infections in this population can present in an unusual fashion, can spread rapidly to other organs in the body, and are more frequently resistant to therapies. This article discusses the current knowledge of the most frequent presentations of infections in this patient population and reviews contemporary approaches to prevention, diagnosis, and management.
C1 [Palmason, Stefan; Treister, Nathaniel S.] Brigham & Womens Hosp, Div Oral Med & Dent, Boston, MA 02120 USA.
[Palmason, Stefan; Treister, Nathaniel S.] Harvard Univ, Sch Dent Med, Dept Oral Med Infect & Immun, Boston, MA 02115 USA.
[Marty, Francisco M.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Infect Dis,Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Palmason, S (reprint author), Brigham & Womens Hosp, Div Oral Med & Dent, 1620 Tremont St, Boston, MA 02120 USA.
EM spalmason@partners.org
NR 204
TC 3
Z9 3
U1 0
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1042-3699
J9 ORAL MAXIL SURG CLIN
JI Oral Maxillofac. Surg. Clin. N. Am.
PD NOV
PY 2011
VL 23
IS 4
BP 579
EP +
DI 10.1016/j.coms.2011.07.012
PG 22
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 856DJ
UT WOS:000297616900013
PM 21982611
ER
PT J
AU Khan, S
Lefevre, J
Ammari, H
Baillet, S
AF Khan, Sheraz
Lefevre, Julien
Ammari, Habib
Baillet, Sylvain
TI Feature detection and tracking in optical flow on non-flat manifolds
SO PATTERN RECOGNITION LETTERS
LA English
DT Article
DE Optical flow; Helmholtz-Hodge decomposition; Feature detection; Image
processing; Riemannian formalism; Vector fields
ID HODGE-HELMHOLTZ DECOMPOSITION; FIELD DECOMPOSITION; MOTION FIELDS
AB Optical flow is a classical approach to estimating the velocity vector fields associated to illuminated objects traveling onto manifolds. The extraction of rotational (vortices) or curl-free (sources or sinks) features of interest from these vector fields can be obtained from their Helmholtz-Hodge decomposition (HHD). However, the applications of existing HHD techniques are limited to flat, 2D domains. Here we demonstrate the extension of the HHD to vector fields defined over arbitrary surface manifolds. We propose a Riemannian variational formalism, and illustrate the proposed methodology with synthetic and empirical examples of optical-flow vector field decompositions obtained on a variety of surface objects. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Khan, Sheraz; Baillet, Sylvain] Med Coll Wisconsin, Dept Neurol, Milwaukee, WI 53226 USA.
[Lefevre, Julien] Aix Marseille Univ, Dept Informat Luminy CNRS, LSIS, UMR 6168, F-13397 Marseille, France.
[Khan, Sheraz; Ammari, Habib] Ecole Polytech, Ctr Appl Math, F-91128 Palaiseau, France.
[Khan, Sheraz] MGH Harvard Med Sch, Dept Neurol, Boston, MA USA.
[Baillet, Sylvain] McGill Univ, Montreal Neurol Inst, Montreal, PQ, Canada.
RP Khan, S (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02129 USA.
EM sheraz@nmr.mgh.harvard.edu
RI Lefevre, Julien/G-1789-2013;
OI Khan, Sheraz/0000-0002-6792-3577
NR 16
TC 3
Z9 3
U1 1
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8655
J9 PATTERN RECOGN LETT
JI Pattern Recognit. Lett.
PD NOV 1
PY 2011
VL 32
IS 15
BP 2047
EP 2052
DI 10.1016/j.patrec.2011.09.017
PG 6
WC Computer Science, Artificial Intelligence
SC Computer Science
GA 859OO
UT WOS:000297885900013
ER
PT J
AU New, AS
AF New, Antonia S.
TI Partial Success?
SO PERSONALITY AND MENTAL HEALTH
LA English
DT Editorial Material
ID PERSONALITY-DISORDER; DSM-IV
C1 [New, Antonia S.] Mt Sinai Sch Med, New York, NY USA.
[New, Antonia S.] James J Peters VAMC, Mental Illness Res Educ & Clin Care Ctr, Bronx, NY USA.
RP New, AS (reprint author), Mt Sinai Sch Med, New York, NY USA.
EM antonia.new@mssm.edu
NR 4
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1932-8621
J9 PERSONAL MENT HEALTH
JI Personal. Ment. Health
PD NOV
PY 2011
VL 5
IS 4
SI SI
BP 301
EP 303
DI 10.1002/pmh.188
PG 3
WC Psychiatry; Psychology, Social
SC Psychiatry; Psychology
GA 854OS
UT WOS:000297504700010
ER
PT J
AU Zhang, F
Wang, SP
Gan, L
Vosler, PS
Gao, YQ
Zigmond, MJ
Chen, J
AF Zhang, Feng
Wang, Suping
Gan, Li
Vosler, Peter S.
Gao, Yanqin
Zigmond, Michael J.
Chen, Jun
TI Protective effects and mechanisms of sirtuins in the nervous system
SO PROGRESS IN NEUROBIOLOGY
LA English
DT Review
DE SIRT1; Deacetylation; Cell death; Cerebral ischemia; Neurodegenerative
disease; Neuroprotection
ID NF-KAPPA-B; GLOBAL CEREBRAL-ISCHEMIA; OXYGEN-GLUCOSE DEPRIVATION;
ACTIVATED RECEPTOR-ALPHA; NITRIC-OXIDE SYNTHASE; BASE-EXCISION-REPAIR;
FATTY-ACID OXIDATION; SIR2 HISTONE/PROTEIN DEACETYLASES;
AMYOTROPHIC-LATERAL-SCLEROSIS; STRESS-RESPONSIVE DEACETYLASE
AB Silent information regulator two proteins (sirtuins or SIRTs) are a group of histone deacetylases whose activities are dependent on and regulated by nicotinamide adenine dinucleotide (NAD(+)). They suppress genome-wide transcription, yet upregulate a select set of proteins related to energy metabolism and pro-survival mechanisms, and therefore play a key role in the longevity effects elicited by calorie restriction. Recently, a neuroprotective effect of sirtuins has been reported for both acute and chronic neurological diseases. The focus of this review is to summarize the latest progress regarding the protective effects of sirtuins, with a focus on SIRT1. We first introduce the distribution of sirtuins in the brain and how their expression and activity are regulated. We then highlight their protective effects against common neurological disorders, such as cerebral ischemia, axonal injury, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. Finally, we analyze the mechanisms underlying sirtuin-mediated neuroprotection, centering on their non-histone substrates such as DNA repair enzymes, protein kinases, transcription factors, and coactivators. Collectively, the information compiled here will serve as a comprehensive reference for the actions of sirtuins in the nervous system to date, and will hopefully help to design further experimental research and expand sirtuins as therapeutic targets in the future. Published by Elsevier Ltd.
C1 [Zhang, Feng; Wang, Suping; Vosler, Peter S.; Gao, Yanqin; Zigmond, Michael J.; Chen, Jun] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15213 USA.
[Zhang, Feng; Wang, Suping; Gao, Yanqin; Zigmond, Michael J.; Chen, Jun] Fudan Univ, State Key Lab Med Neurobiol, Shanghai 200032, Peoples R China.
[Zhang, Feng; Wang, Suping; Gao, Yanqin; Zigmond, Michael J.; Chen, Jun] Fudan Univ, Inst Brain Sci, Shanghai 200032, Peoples R China.
[Gan, Li] Univ Calif San Francisco, Gladstone Inst Neurol Dis, Dept Neurol, San Francisco, CA 94158 USA.
[Zhang, Feng; Wang, Suping; Vosler, Peter S.; Gao, Yanqin; Zigmond, Michael J.; Chen, Jun] Univ Pittsburgh, Sch Med, Ctr Cerebrovasc Dis Res, Pittsburgh, PA 15213 USA.
[Chen, Jun] Vet Affairs Pittsburgh Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Pittsburgh, PA 15261 USA.
RP Chen, J (reprint author), Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15213 USA.
EM zhanfx2@upmc.edu; chenj2@upmc.edu
RI Gao, Yanqin/I-6790-2016
OI Gao, Yanqin/0000-0002-4915-9819
FU Chinese Ministry of Science Technology; National Institutes of Health
[NS36736, NS43802, NS45048, NS62157]; American Heart Association
[10SDG2560122]
FX This work was supported by Special Research Funds from Chinese Ministry
of Science & Technology to State Key laboratories (Y. G., M. Z., and
J.C.), grants from the National Institutes of Health (NS36736, NS43802,
NS45048 and NS62157 to J.C.), and the American Heart Association
(10SDG2560122 to F.Z.). We thank Pat Strickler for secretarial support
and Carol Culver for editorial assistance.
NR 327
TC 69
Z9 74
U1 2
U2 31
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0301-0082
J9 PROG NEUROBIOL
JI Prog. Neurobiol.
PD NOV
PY 2011
VL 95
IS 3
BP 373
EP 395
DI 10.1016/j.pneurobio.2011.09.001
PG 23
WC Neurosciences
SC Neurosciences & Neurology
GA 856CJ
UT WOS:000297614000005
PM 21930182
ER
PT J
AU Kacmarek, RM
AF Kacmarek, Robert M.
TI Ventilator Software Version Markedly Affects Time to Trigger and Time
Delay respond
SO RESPIRATORY CARE
LA English
DT Letter
C1 Massachusetts Gen Hosp, Resp Care Dept, Boston, MA 02114 USA.
RP Kacmarek, RM (reprint author), Massachusetts Gen Hosp, Resp Care Dept, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU DAEDALUS ENTERPRISES INC
PI IRVING
PA 9425 N MAC ARTHUR BLVD, STE 100, IRVING, TX 75063-4706 USA
SN 0020-1324
J9 RESP CARE
JI Respir. Care
PD NOV
PY 2011
VL 56
IS 11
BP 1867
EP 1867
PG 1
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 859TQ
UT WOS:000297899100024
ER
PT J
AU Nigwekar, SU
Waikar, SS
AF Nigwekar, Sagar U.
Waikar, Sushrut S.
TI Diuretics in Acute Kidney Injury
SO SEMINARS IN NEPHROLOGY
LA English
DT Review
DE Acute kidney injury; diuretics; fenoldopam; natriuretic peptides
ID ACUTE-RENAL-FAILURE; CRITICALLY-ILL PATIENTS;
ATRIAL-NATRIURETIC-PEPTIDE; ACUTE TUBULAR-NECROSIS; INTENSIVE-CARE-UNIT;
HIGH-DOSE FRUSEMIDE; LOOP DIURETICS; DOUBLE-BLIND; CARDIAC-SURGERY;
REPLACEMENT THERAPY
AB Acute kidney injury (AKI) is common in hospitalized patients and is associated with significant morbidity and mortality. The incidence of AKI is increasing and despite clinical advances there has been little change in the outcomes associated with AKI. A variety of interventions, including loop diuretics, have been tested for the prevention and treatment of AKI; however, none to date have shown convincing benefits in clinical studies, and the management of AKI remains largely supportive. In this article, we review the pharmacology and experimental and clinical evidence for loop diuretics in the management of AKI. In addition, we also review evidence for other agents with diuretic and/or natriuretic properties such as thiazide diuretics, mannitol, fenoldopam, and natriuretic peptides in both the prevention and treatment of AKI. Implications for current clinical practice are outlined to guide clinical decisions in this field. Semin Nephrol 31:523-534 (C) 2011 Elsevier Inc. All rights reserved.
C1 [Nigwekar, Sagar U.] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
[Waikar, Sushrut S.] Harvard Univ, Sch Med, Scholars Clin Sci Program, Boston, MA USA.
RP Nigwekar, SU (reprint author), Massachusetts Gen Hosp, Div Nephrol, 55 Fruit St,Bulfinch 127, Boston, MA 02114 USA.
EM sagarnigs@gmail.com
NR 129
TC 6
Z9 8
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 0270-9295
J9 SEMIN NEPHROL
JI Semin. Nephrol.
PD NOV
PY 2011
VL 31
IS 6
BP 523
EP 534
DI 10.1016/j.semnephrol.2011.09.007
PG 12
WC Urology & Nephrology
SC Urology & Nephrology
GA 858FI
UT WOS:000297780900007
PM 22099509
ER
PT J
AU Lebl, DR
Bono, CM
Metkar, US
Grottkau, BE
Wood, KB
AF Lebl, Darren R.
Bono, Christopher M.
Metkar, Umesh S.
Grottkau, Brian E.
Wood, Kirkham B.
TI Bioabsorbable anterior cervical plate fixation for single-level
degenerative disorders: early clinical and radiographic experience
SO SPINE JOURNAL
LA English
DT Article
DE Bioabsorbable; Cervical; Fusion; Spinal instrumentation
ID BIOMECHANICAL EVALUATION; INTERBODY FUSION; SPINE; DISKECTOMY;
COMPLICATIONS; STABILIZATION; ALLOGRAFT; OUTCOMES; IMPLANT; SCREW
AB BACKGROUND CONTEXT: Increased fusion rates have been reported with the addition of an anterior cervical plate (ACP) to anterior cervical discectomy and fusion (ACDF). Bioabsorbable implants have become increasingly used in orthopedic and spine surgical procedures. There are limited data regarding the outcomes of bioabsorbable ACP (bACP) with ACDF.
PURPOSE: To compare the clinical and radiographic outcomes of patients undergoing ACDF for single-level degenerative disorders with a bACP versus a conventional metal ACP (mACP).
STUDY DESIGN: Retrospective comparative cohort study.
PATIENT SAMPLE: Thirty-one patients undergoing ACDF for a single-level degenerative disorder (ie, disc herniation or spondylotic neural compression).
OUTCOME MEASURES: Incidence of early (within 2 weeks) complications, postoperative sagittal alignment, Odom's criteria, and pseudarthrosis rate.
METHODS: The authors retrospectively reviewed the results of a consecutive series of patients undergoing ACDF for symptomatic single-level disc herniation or spondylotic neural compression with either a bACP or an mACP over a 3-year period. Operative notes, clinical charts, and radiographs were analyzed. Radiographic outcomes were assessed for intersegmental alignment, graft subsidence, fusion rate, prevertebral soft-tissue shadow, and graft containment. Clinical outcome was evaluated by Odom's criteria.
RESULTS: Fourteen patients underwent ACDF with a bACP and 15 with an mACP. Radiographic outcomes at the most recent follow-up demonstrated pseudarthrosis in 4 of 14 patients (29%) in the bACP group and 0 of 15 patients in the mACP group. Graft extrusion and anterior displacement was present in three of four pseudarthroses (75%). Comparing preoperative and final radiographs, cervical lordosis was maintained at the operative segment in only 3 of 14 bACP patients (21%) compared with 8 of 15 patients (53%) in the mACP group. The mean Cobb angle was 2.4 degrees +/- 1.9 degrees lordosis in the mACP group and -2.7 degrees +/- 2.5 degrees kyphosis in the bACP group (p=.12). In the mACP group, 14 of 15 patients had good or excellent results. In the bACP group, only 7 of 14 patients had good or excellent results.
CONCLUSIONS: Bioabsorbable ACP fixation was associated with a high rate of graft extrusion and early loss of intersegmental cervical alignment. Inferior clinical outcomes were observed in patients in the bACP group compared with the mACP group. Based on these findings, continued use of the bACP used in this study cannot be recommended. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Metkar, Umesh S.; Grottkau, Brian E.; Wood, Kirkham B.] Massachusetts Gen Hosp, Dept Orthopaed Surg, Yawkey Ctr Outpatient Care, Boston, MA 02114 USA.
[Lebl, Darren R.] Hosp Special Surg, New York, NY 10021 USA.
[Bono, Christopher M.] Brigham & Womens Hosp, Dept Orthopaed Surg, Boston, MA 02115 USA.
RP Wood, KB (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, Yawkey Ctr Outpatient Care, 32 Fruit St, Boston, MA 02114 USA.
EM kbwood@partners.org
NR 29
TC 4
Z9 5
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1529-9430
J9 SPINE J
JI Spine Journal
PD NOV
PY 2011
VL 11
IS 11
BP 1002
EP 1008
DI 10.1016/j.spinee.2011.09.010
PG 7
WC Clinical Neurology; Orthopedics
SC Neurosciences & Neurology; Orthopedics
GA 859GG
UT WOS:000297864300003
PM 22000725
ER
PT J
AU Elfiky, AA
Cho, DC
McDermott, DF
Rosenberg, JE
Fortner, B
Antras, L
Chen, K
Duh, MS
Jayawant, SS
Oh, WK
Atkins, MB
Choueiri, TK
AF Elfiky, Aymen A.
Cho, Daniel C.
McDermott, David F.
Rosenberg, Jonathan E.
Fortner, Barry
Antras, Lucia
Chen, Kristina
Duh, Mei Sheng
Jayawant, Sujata S.
Oh, William K.
Atkins, Michael B.
Choueiri, Toni K.
TI Predictors of response to sequential sunitinib and the impact of prior
VEGF-targeted drug washout in patients with metastatic clear-cell renal
cell carcinoma
SO UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS
LA English
DT Article
DE Sunitinib; Sorafenib; Bevacizumab; Angiogenesis inhibitors; Sequential
therapy
ID ENDOTHELIAL GROWTH-FACTOR; PHASE-III TRIAL; PROGNOSTIC-FACTORS;
ANTITUMOR-ACTIVITY; SORAFENIB; THERAPY; ANGIOGENESIS; PROGRESSION;
RECEPTOR
AB Objective: To identify factors that can be used to identify metastatic clear cell RCC patients more likely to benefit from sequential sunitinib.
Patients and methods: We identified patients who failed sorafenib or bevacizumab and subsequently received sunitinib. We looked at objective response rates (ORR), progression-free survival (PFS), and overall survival (OS) to sunitinib in relation to baseline clinical variables.
Results: Seventy-one patients received sunitinib sequential therapy. Median duration of follow-up after starting sunitinib was 9.3 months. Median PFS was 5.8 months; median OS was not reached. Significantly higher ORR was seen in patients with normal hemoglobin (25.6%) [defined as >12 gm/dl for female; >13 gm/dl for male]. In addition, a shorter PFS for patients with low hemoglobin, and patients with time from diagnosis to first treatment <= 1 year was found. There was a shorter OS for patients >= 60 years old, with brain metastasis, low hemoglobin, and time from diagnosis to treatment <= 1 year. There was no difference in ORR, PFS, or OS in patients who started sunitinib after or within a 30-day period.
Conclusions: Metastatic clear-cell RCC patients with anemia have less clinical benefit from sequential sunitinib after failure of bevacizumab or sorafenib. Other factors associated with poor outcome include brain metastases, older age, and <1 year between diagnosis and first treatment. Importantly, no difference in outcomes was observed if sequential therapy was initiated within or after 30 days. External validation and prospective evaluation are needed to confirm these findings. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Elfiky, Aymen A.; Cho, Daniel C.; McDermott, David F.; Rosenberg, Jonathan E.; Oh, William K.; Atkins, Michael B.; Choueiri, Toni K.] Harvard Univ, Sch Med, Dana Farber Harvard Canc Ctr, Boston, MA 02115 USA.
[Fortner, Barry] P4 Healthcare, Lakeland, TN 38002 USA.
[Antras, Lucia; Chen, Kristina; Duh, Mei Sheng; Jayawant, Sujata S.] Anal Grp Inc, Boston, MA 02115 USA.
RP Choueiri, TK (reprint author), Harvard Univ, Sch Med, Dana Farber Harvard Canc Ctr, Boston, MA 02115 USA.
EM Toni_Choueiri@dfci.harvard.edu
FU DF/HCC Kidney Cancer SPORE
FX This research was supported in part by the DF/HCC Kidney Cancer SPORE.
NR 18
TC 5
Z9 5
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1078-1439
J9 UROL ONCOL-SEMIN ORI
JI Urol. Oncol.-Semin. Orig. Investig.
PD NOV-DEC
PY 2011
VL 29
IS 6
BP 756
EP 763
DI 10.1016/j.urolonc.2010.01.008
PG 8
WC Oncology; Urology & Nephrology
SC Oncology; Urology & Nephrology
GA 853RL
UT WOS:000297443300025
PM 20451414
ER
PT J
AU Schutzer, WE
Xue, H
Reed, J
Oyama, T
Beard, DR
Anderson, S
Mader, SL
AF Schutzer, William E.
Xue, Hong
Reed, John
Oyama, Terry
Beard, Douglas R.
Anderson, Sharon
Mader, Scott L.
TI Age-related beta-adrenergic receptor-mediated vasorelaxation is changed
by altering G protein receptor kinase 2 expression
SO VASCULAR PHARMACOLOGY
LA English
DT Article
DE Adenovirus; Adrenergic-beta; Aging; Fischer 344; Vasorelaxation; G
protein receptor kinase (GRK)
ID VASCULAR SMOOTH-MUSCLE; RAT AORTA; BETA(2)-ADRENERGIC RECEPTOR;
BLOOD-PRESSURE; PLASMA-MEMBRANE; GENE-TRANSFER; DESENSITIZATION;
MECHANISMS; RELAXATION; PHOSPHORYLATION
AB Beta-adrenergic receptor- (beta-AR) mediated vasorelaxation declines with age. This change is likely related to receptor desensitization, rather than down regulation. One kinase responsible for desensitization is G protein receptor kinase 2 (GRK2). We have shown that GRK expression and activity increases with age in Fischer 344 rat aorta. In this study we validated that carotid arteries have similar age-related changes in the beta-AR signaling axis as aorta. This finding allowed use of in vivo infection and delivery of two adenovirus vectors to carotid arteries of 2-month-old (2 M) and 12-month-old (12 M) male Fischer 344 rats. Adeno-GRK2 was used to overexpress GRK2, and adeno-beta-ARK-ct was used to inhibit GRK2 function. Following a five-day infection, vessels were collected and ex vivo tissue bath was used to evaluate vasoreactivity. We used KCl contracted segments, and determined that overexpression of GRK2 significantly impaired isoproterenol (ISO)-mediated vasorelaxation in both age groups. Maximum relaxation (MA)() to ISO in vessels from 2 M decreased from 44% to 21%. MAX to ISO in vessels from 12 M decreased from 12% to 6%. Sensitivity (ED50) in vessels from 2 M and 12 M was also impaired 57%, and 30% respectively. We also determined that expression of adeno-beta-ARK-ct significantly improved ISO-mediated vasorelaxation in both age groups. MAX in vessels from 2 M increased from 44% to 58%. MAX in vessels from 12 M increased from 15% to 69%. ED50 in vessels from 2 M and 12 M was also improved 46%, and 50% respectively. These findings further implicate age-related increases in GRK2 expression as an important regulator of the age-related decline in beta-AR-mediated vasorelaxation. Published by Elsevier Inc.
C1 [Schutzer, William E.; Xue, Hong; Reed, John; Oyama, Terry; Beard, Douglas R.; Anderson, Sharon; Mader, Scott L.] Portland VA Med Ctr, Res Serv, Portland, OR 97239 USA.
[Schutzer, William E.; Anderson, Sharon; Mader, Scott L.] Oregon Hlth & Sci Univ, Sch Med, Portland, OR 97239 USA.
RP Mader, SL (reprint author), Portland VA Med Ctr, Res Serv, RD26,3710 SW US Vet Hosp Rd, Portland, OR 97239 USA.
EM scott.mader@va.gov
FU Research Service, Department of Veterans Affairs
FX This work was supported by the Research Service, Department of Veterans
Affairs. We thank Mohammed Gaballa, PhD, Banner Sun Health Research
Institute, Sun City, AZ for his guidance with the adenovirus delivery
surgical procedures.
NR 53
TC 5
Z9 5
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1537-1891
EI 1879-3649
J9 VASC PHARMACOL
JI Vasc. Pharmacol.
PD NOV-DEC
PY 2011
VL 55
IS 5-6
BP 178
EP 188
DI 10.1016/j.vph.2011.09.001
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 858EF
UT WOS:000297778000010
PM 21951806
ER
PT J
AU Weston, A
Barton, C
Lesselyong, J
Yaffe, K
AF Weston, Andrea
Barton, Cynthia
Lesselyong, Julia
Yaffe, Kristine
TI Functional deficits among patients with mild cognitive impairment
SO ALZHEIMERS & DEMENTIA
LA English
DT Article
DE Mild cognitive impairment; Dementia; Functional impairment; Instrumental
activities of daily living; Activities of daily living
ID DEMENTIA
AB Background: Diagnostic criteria for mild cognitive impairment (MCI) include no significant functional decline, but recent studies have suggested that subtle deficits often exist. It is not known whether these differ by MCI type. We investigated the level and type of functional impairment among patients with MCI.
Methods: We studied 498 patients, evaluated at the Alzheimer's Disease Research Centers of California between 2006 and 2009, who had multidisciplinary evaluations by experts, including neurologic examination and neuropsychological testing. Patients were diagnosed with MCI and subtype was determined using cognitive domain scores. In a cross-sectional descriptive study, we examined whether functional impairment differed by MCI subtype, using the Blessed Roth Dementia Rating Scale (range: 0-17, higher scores indicating more impairment).
Results: Among the participants, the mean age was 75.4 years, 50.7% were women, and 81.7% were white. Patients with amnestic- (n = 392, 78.7%) and nonamnestic-type (n = 106, 21.3%) MCI had similar total Blessed Roth Dementia Rating Scale (1.6 and 1.5, respectively; P = .84) and MiniMental State Examination (26.5 and 26.7, respectively; P = .60) scores. Patients with amnestic MCI were more likely to have difficulty in remembering lists and recalling recent events (P < .05 for both) and less likely to have difficulty in eating and with continence (P = .01 for both), as compared with those with nonamnestic MCI.
Conclusions: Despite the MCI diagnostic criteria suggesting no functional impairment, our results indicate that patients with MCI experience mild functional deficits that vary according to the type of MCI. (C) 2011 The Alzheimer's Association. All rights reserved.
C1 [Weston, Andrea; Yaffe, Kristine] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
[Weston, Andrea; Barton, Cynthia; Lesselyong, Julia; Yaffe, Kristine] San Francisco VA Med Ctr, San Francisco, CA USA.
[Barton, Cynthia; Yaffe, Kristine] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Lesselyong, Julia] No Calif Inst Res & Educ, San Francisco, CA USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
RP Weston, A (reprint author), Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
EM andrea.weston@ucsf.edu
FU National Institute of Aging [K24AG031155]; Mental Illness Research,
Educational, and Clinical Cente; Sierra Pacific Veterans Integrated
Service Network (VISN) Veteran's Administration
FX Dr. Yaffe is supported in part by a Grant from the National Institute of
Aging (K24AG031155) and by a Mental Illness Research, Educational, and
Clinical Center Grant from the Sierra Pacific Veterans Integrated
Service Network (VISN) Veteran's Administration.
NR 15
TC 4
Z9 5
U1 0
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1552-5260
J9 ALZHEIMERS DEMENT
JI Alzheimers. Dement.
PD NOV
PY 2011
VL 7
IS 6
BP 611
EP 614
DI 10.1016/j.jalz.2010.12.011
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA 852WD
UT WOS:000297387300008
PM 22055977
ER
PT J
AU Chou, SW
Marousek, G
Auerochs, S
Stamminger, T
Milbradt, J
Marschall, M
AF Chou, Sunwen
Marousek, Gail
Auerochs, Sabrina
Stamminger, Thomas
Milbradt, Jens
Marschall, Manfred
TI The unique antiviral activity of artesunate is broadly effective against
human cytomegaloviruses including therapy-resistant mutants
SO ANTIVIRAL RESEARCH
LA English
DT Article
DE Human cytomegalovirus; Antiviral activity of artesunate;
Artesunate-related drugs; Therapy-resistant virus mutants; Synergistic
effect
ID STEM-CELL TRANSPLANTATION; DRUG-RESISTANCE; MARIBAVIR; RECOMBINANT;
REPLICATION; INFECTIONS; RECIPIENTS; MUTATIONS; POTENT
AB Current therapy options to treat infections with human cytomegalovirus face severe limitations leading to a continued search for novel drug candidates. Here, we describe novel characteristics of the strong antiviral potency of the drug artesunate. In vitro virus replication systems were applied to analyze a number of laboratory and clinically relevant strains of human cytomegalovirus. An inhibitory block at a very early stage of infection was demonstrated. Time-of-addition experiments indicated that the antiviral efficacy could be optimized when artesunate was applied as fractional doses consecutively added post-infection. Artesunate showed a clearly higher anti-cytomegaloviral activity than its parental drug artemisinin (approximately 10-fold) or other artesunate-related compounds. Mean IC(50) values of artesunate for a variety of standard therapy-resistant virus mutants were within a 2-fold range compared to wild-type virus. Furthermore, a synergistic effect was identified when artesunate was combined with the mechanistically distinct antiviral compound maribavir. These findings point to unique antiviral properties of artesunate which may offer an advantage over standard antiviral therapy particularly in cases of drug resistance. (C) 2011 Published by Elsevier B.V.
C1 [Auerochs, Sabrina; Stamminger, Thomas; Milbradt, Jens; Marschall, Manfred] Univ Erlangen Nurnberg, Inst Clin & Mol Virol, D-91054 Erlangen, Germany.
[Chou, Sunwen] Oregon Hlth & Sci Univ, Div Infect Dis, Portland, OR 97201 USA.
[Chou, Sunwen; Marousek, Gail] US Dept Vet Affairs, Med Ctr, Portland, OR USA.
RP Marschall, M (reprint author), Univ Erlangen Nurnberg, Inst Clin & Mol Virol, Schlossgarten 4, D-91054 Erlangen, Germany.
EM manfred.marschall@viro.med.uni-erlangen.de
FU Department of Veterans Affairs (USA); Deutsche Forschungsgemeinschaft
[MA 1289/7-1, SFB 796 C3/B3]; HHV-6 Foundation (Santa Barbara, CA, USA
[M.M. 2009]; Bayerische Forschungsstiftung [4SC-2010]
FX We like to thank Herwig Jansen (Dafra Pharma, Turhout, Belgium) and
Duong Ngoc Ha (Saokim Pharma, Hanoi, Vietnam) for kindly providing ART,
ART-related drugs and product information. We appreciate the
cooperations with Thomas Efferth (Inst. Pharmacy and Biochem., Univ.
Mainz, Germany) and Dana Wolf (Clin. Virol. Unit, Dept. Clin. Microbiol.
Inf. Diseases, Hadassah Univ. Jerusalem, Israel) in the molecular and
clinical evaluation of ART, respectively. This work was supported by the
Department of Veterans Affairs (USA), Deutsche Forschungsgemeinschaft
(Grant MA 1289/7-1 and SFB 796 C3/B3), HHV-6 Foundation (Santa Barbara,
CA, USA, Grant M.M. 2009) and Bayerische Forschungsstiftung (Grant
4SC-2010).
NR 26
TC 19
Z9 20
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
J9 ANTIVIR RES
JI Antiviral Res.
PD NOV
PY 2011
VL 92
IS 2
BP 364
EP 368
DI 10.1016/j.antiviral.2011.07.018
PG 5
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA 853LG
UT WOS:000297427200027
PM 21843554
ER
PT J
AU Rehman, M
Jenkins, KJ
Juraszek, AL
Connor, JA
Gauvreau, K
Muneeb, M
Sena, LM
Colan, SD
Saia, T
Kieran, MW
AF Rehman, Maliha
Jenkins, Kathy J.
Juraszek, Amy L.
Connor, Jean A.
Gauvreau, Kimberlee
Muneeb, Muhammad
Sena, Laureen M.
Colan, Steven D.
Saia, Terry
Kieran, Mark W.
TI A Prospective Phase II Trial of Vinblastine and Methotrexate in
Multivessel Intraluminal Pulmonary Vein Stenosis in Infants and Children
SO CONGENITAL HEART DISEASE
LA English
DT Article
DE Chemotherapy; PVS; Myofibroblasts
ID LOW-DOSE CHEMOTHERAPY; DESMOID TUMOR; CONGENITAL STENOSIS;
MYOFIBROMATOSIS; FIBROMATOSIS; CHILDHOOD; RECURRENT; REPAIR; BONE
AB Objective. To determine the safety and efficacy of the chemotherapeutic agents vinblastine and methotrexate in the treatment of children with progressive multivessel intraluminal pulmonary vein stenosis (PVS).
Methods. Children received weekly vinblastine and methotrexate for a period of 1 year. Outcomes (for patients receiving >= 1 month of chemotherapy) were classified separately for patients with isolated PVS and PVS with congenital heart disease (CHD). Primary efficacy outcome was "response to treatment" categorized by echocardiographic criteria of response. Survival to 1 year was also evaluated. All adverse events were classified according to Cancer Therapy Evaluation Program, Common Terminology Criteria version 3.0. Events were further classified as related to chemotherapy, cardiac, or other causes.
Results. Among 29 patients enrolled, 28 received at least one dose of chemotherapy and were evaluable for toxicity, while 23 were evaluable for response (21 CHD, 2 isolated). Both patients in the isolated group had progressive disease and died. Overall, 33% (7/21) of patients with PVS and CHD had stable disease; 1-year survival of 38%; and four patients continue in remission (93, 96, 124, and 125 months after treatment initiation). While both cardiac-related (19%) and chemotherapy-related (53%) toxicities were common, most were asymptomatic laboratory changes. Grade 3 (13%) and grade 4 (4%) toxicities were reversible, and no treatment-related grade 5 toxicities were observed.
Conclusion. We report on the first prospective trial of chemotherapy for infants and children targeting the presence of myofibroblastic cells within the lesions of PVS based on myofibroblastic proliferation associated with desmoid tumors of infancy. The toxicity profile resulted in numerous treatment delays and interruptions that, combined with limited information on the natural history of PVS in this patient population, hampered our ability to determine the true efficacy of this approach. These results will be important as a baseline for clinical trials in this patient population.
C1 [Kieran, Mark W.] Dana Farber Canc Inst, Div Hematol Oncol, Boston, MA 02215 USA.
[Rehman, Maliha; Jenkins, Kathy J.; Connor, Jean A.; Gauvreau, Kimberlee; Muneeb, Muhammad; Colan, Steven D.; Saia, Terry] Childrens Hosp, Dept Cardiol, Boston, MA 02215 USA.
[Sena, Laureen M.] Childrens Hosp, Dept Radiol, Boston, MA 02215 USA.
[Juraszek, Amy L.] UT SW Med Ctr, Dept Pediat, Dallas, TX USA.
[Juraszek, Amy L.] UT SW Med Ctr, Dept Pathol, Dallas, TX USA.
RP Kieran, MW (reprint author), Dana Farber Canc Inst, Div Hematol Oncol, 450 Brookline Ave,Room SW331, Boston, MA 02215 USA.
EM Mark_Kieran@dfci.harvard.edu
OI Kieran, Mark/0000-0003-2184-7692
NR 34
TC 10
Z9 10
U1 0
U2 0
PU WILEY PERIODICALS, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN STREET, MALDEN, MA 02148-529 USA
SN 1747-079X
J9 CONGENIT HEART DIS
JI Congenit. Heart Dis.
PD NOV-DEC
PY 2011
VL 6
IS 6
BP 608
EP 623
DI 10.1111/j.1747-0803.2011.00574.x
PG 16
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 853GF
UT WOS:000297413500008
PM 22073909
ER
PT J
AU Haase, A
Rigosi, E
Frasnelli, E
Trona, F
Tessarolo, F
Vinegoni, C
Anfora, G
Vallortigara, G
Antolini, R
AF Haase, Albrecht
Rigosi, Elisa
Frasnelli, Elisa
Trona, Federica
Tessarolo, Francesco
Vinegoni, Claudio
Anfora, Gianfranco
Vallortigara, Giorgio
Antolini, Renzo
TI A multimodal approach for tracing lateralisation along the olfactory
pathway in the honeybee through electrophysiological recordings,
morpho-functional imaging, and behavioural studies
SO EUROPEAN BIOPHYSICS JOURNAL WITH BIOPHYSICS LETTERS
LA English
DT Article
DE Apis mellifera; Antennal lobe; Olfactory learning; Brain asymmetry; PER;
SEM; EAG; Two-photon microscopy
ID APIS-MELLIFERA; ANTENNAL LOBES; INSECT BRAIN; ODOR REPRESENTATION;
NERVOUS-SYSTEM; NEURONS; MEMORY; BEE; MICROSCOPY; ADVANTAGES
AB Recent studies have revealed asymmetries between the left and right sides of the brain in invertebrate species. Here we present a review of a series of recent studies from our laboratories, aimed at tracing asymmetries at different stages along the honeybee's (Apis mellifera) olfactory pathway. These include estimates of the number of sensilla present on the two antennae, obtained by scanning electron microscopy, as well as electroantennography recordings of the left and right antennal responses to odorants. We describe investigative studies of the antennal lobes, where multi-photon microscopy was used to search for possible morphological asymmetries between the two brain sides. Moreover, we report on recently published results obtained by two-photon calcium imaging for functional mapping of the antennal lobe aimed at comparing patterns of activity evoked by different odours. Finally, possible links to the results of behavioural tests, measuring asymmetries in single-sided olfactory memory recall, are discussed.
C1 [Haase, Albrecht; Tessarolo, Francesco; Antolini, Renzo] Univ Trent, Dept Phys, I-38050 Povo, TN, Italy.
[Haase, Albrecht; Tessarolo, Francesco; Antolini, Renzo] Univ Trent, Biotech Res Ctr, I-38050 Povo, TN, Italy.
[Rigosi, Elisa; Vallortigara, Giorgio] Univ Trent, CIMeC, Ctr Mind Brain Sci, I-38068 Rovereto, Italy.
[Rigosi, Elisa; Trona, Federica; Anfora, Gianfranco] Fdn Edmund Mach, Sustainable Agroecosyst & Bioresources Dept, IASMA Res & Innovat Ctr, I-38010 San Michele All Adige, TN, Italy.
[Frasnelli, Elisa] Konrad Lorenz Inst Evolut & Cognit Res, A-3422 Altenberg, Austria.
[Vinegoni, Claudio] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Syst Biol, Boston, MA 02114 USA.
[Vinegoni, Claudio] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Boston, MA 02114 USA.
RP Haase, A (reprint author), Univ Trent, Dept Phys, Via Sommarive 14, I-38050 Povo, TN, Italy.
EM albrecht.haase@unitn.it
RI Haase, Albrecht/H-4248-2012;
OI Haase, Albrecht/0000-0002-8324-0047; ANFORA,
Gianfranco/0000-0003-2545-1409
FU NIBIB NIH HHS [R01 EB006432, R01EB006432]
NR 60
TC 7
Z9 8
U1 4
U2 22
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0175-7571
J9 EUR BIOPHYS J BIOPHY
JI Eur. Biophys. J. Biophys. Lett.
PD NOV
PY 2011
VL 40
IS 11
BP 1247
EP 1258
DI 10.1007/s00249-011-0748-6
PG 12
WC Biophysics
SC Biophysics
GA 852PX
UT WOS:000297371000006
PM 21956452
ER
PT J
AU Toney, JH
Stover, E
AF Toney, Jeffrey H.
Stover, Eric
TI Retrospective: Richard Pierre Claude (1934-2011)
SO HUMAN RIGHTS QUARTERLY
LA English
DT Biographical-Item
C1 [Toney, Jeffrey H.] Kean Univ, Coll Nat Appl & Hlth Sci, Union, NJ 07083 USA.
[Stover, Eric] Human Rights Ctr, Berkeley, CA USA.
[Stover, Eric] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Stover, Eric] Amer Assoc Advancement Sci, Sci & Human Rights Program, Washington, DC USA.
[Toney, Jeffrey H.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Cambridge, MA 02138 USA.
[Toney, Jeffrey H.] MIT, Cambridge, MA 02139 USA.
[Toney, Jeffrey H.] Montclair State Univ, Montclair, NJ 07043 USA.
RP Toney, JH (reprint author), Kean Univ, Coll Nat Appl & Hlth Sci, Union, NJ 07083 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
21218-4363 USA
SN 0275-0392
J9 HUM RIGHTS QUART
JI Hum. Rights Q.
PD NOV
PY 2011
VL 33
IS 4
BP 1195
EP 1197
PG 3
WC Political Science; Social Issues
SC Government & Law; Social Issues
GA 846YQ
UT WOS:000296939500020
ER
PT J
AU Stange, JP
Eisner, LR
Holzel, BK
Peckham, AD
Dougherty, DD
Rauch, SL
Nierenberg, AA
Lazar, S
Deckersbach, T
AF Stange, Jonathan P.
Eisner, Lori R.
Hoelzel, Britta K.
Peckham, Andrew D.
Dougherty, Darin D.
Rauch, Scott L.
Nierenberg, Andrew A.
Lazar, Sara
Deckersbach, Thilo
TI Mindfulness-Based Cognitive Therapy for Bipolar Disorder: Effects on
Cognitive Functioning
SO JOURNAL OF PSYCHIATRIC PRACTICE
LA English
DT Article
DE bipolar disorder; executive functioning; cognitive functioning;
mindfulness; mindfulness-based cognitive therapy (MBCT); psychosocial
treatment
ID RANDOMIZED CONTROLLED-TRIAL; SHORT-TERM MEDITATION; INTERNATIONAL
NEUROPSYCHIATRIC INTERVIEW; TREATMENT ENHANCEMENT PROGRAM;
FAMILY-FOCUSED TREATMENT; SOCIAL RHYTHM THERAPY; ANTERIOR CINGULATE;
NEUROCOGNITIVE FUNCTION; RELAPSE PREVENTION; CORTICAL THICKNESS
AB Bipolar disorder is associated with impairments in cognition, including difficulties in executive functioning, even when patients are euthymic (neither depressed nor manic). The purpose of this study was to assess changes in self-reported cognitive functioning in patients with bipolar disorder who participated in an open pilot trial of mindfulness-based cognitive therapy (MBCT). Following MBCT, patients reported significant improvements in executive functioning, memory, and ability to initiate and complete tasks, as measured by the Behavior Rating Inventory of Executive Function (BRIEF) and the Frontal Systems Behavior Scale (FrSBe). Changes in cognitive functioning were correlated with increases in mindful, nonjudgmental observance and awareness of thoughts, feelings, and sensations, and were not associated with decreases in depression. Improvements tended to diminish after termination of treatment, but some improvements, particularly those in executive functioning, persisted after 3 months. These results provide preliminary evidence that MBCT may be a treatment option that can be used as an adjunct to medication to improve cognitive functioning in bipolar disorder. (Journal of Psychiatric Practice 2011; 17: 410-419)
C1 [Deckersbach, Thilo] Massachusetts Gen Hosp, Dept Psychiat, Bipolar Clin & Res Program, Boston, MA 02114 USA.
[Stange, Jonathan P.] Temple Univ, Dept Psychol, Philadelphia, PA 19122 USA.
[Eisner, Lori R.; Dougherty, Darin D.; Nierenberg, Andrew A.; Lazar, Sara; Deckersbach, Thilo] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Hoelzel, Britta K.; Peckham, Andrew D.; Rauch, Scott L.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Cambridge, MA 02138 USA.
[Hoelzel, Britta K.] Univ Giessen, D-35390 Giessen, Germany.
[Peckham, Andrew D.; Rauch, Scott L.] McLean Hosp, Belmont, MA USA.
RP Deckersbach, T (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Bipolar Clin & Res Program, 50 Staniford St,5th Floor, Boston, MA 02114 USA.
EM tdeckersbach@partners.org
RI Lazar, Sara/G-3809-2012
OI Lazar, Sara/0000-0003-1126-8363
FU NIMH [1K23MH074895-01A2]; European Community
FX This work was supported by a K-23 NIMH Career Award 1K23MH074895-01A2 to
Thilo Deckersbach. Part of this research was presented at the
Association for Behavioral and Cognitive Therapies, San Francisco, 2010,
and at the Ninth International Conference on Bipolar Disorder,
Pittsburgh, 2011. Britta K. Holzel was supported by a Marie Curie
International Outgoing Fellowship within the 7th European Community
Framework Programme.
NR 77
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Z9 26
U1 11
U2 48
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1527-4160
J9 J PSYCHIATR PRACT
JI J. Psychiatr. Pract.
PD NOV
PY 2011
VL 17
IS 6
BP 410
EP 419
DI 10.1097/01.pra.0000407964.34604.03
PG 10
WC Psychiatry
SC Psychiatry
GA 853DM
UT WOS:000297406400005
PM 22108398
ER
PT J
AU Rudolph, JL
Harrington, MB
Lucatorto, MA
Chester, JG
Francis, J
Shay, KJ
AF Rudolph, James L.
Harrington, Mary Beth
Lucatorto, Michelle A.
Chester, Jennifer G.
Francis, Joseph
Shay, Kenneth J.
CA Vet Affairs Delirium Working Grp
TI Validation of a Medical Record-Based Delirium Risk Assessment
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE delirium; risk; hospitalization; quality measurement
ID CONFUSION ASSESSMENT METHOD; ELDER-LIFE-PROGRAM; MINI-MENTAL-STATE; HIP
FRACTURE; PREDICTION RULE; CARE; SURGERY; POPULATION; OUTCOMES; SYSTEM
AB OBJECTIVES: To improve identification of patients at high risk for delirium, this study developed a chart abstraction tool for delirium risk and validated the tool against clinical expert diagnosis of delirium.
DESIGN: Prospective cohort study.
SETTING: Tertiary Veterans Affairs hospital in New England.
PARTICIPANTS: One hundred veterans admitted to the medical service.
MEASUREMENTS: While admitted, each participant underwent serial assessments for delirium by a clinical expert. Using the four criteria of a validated delirium prediction rule (cognitive impairment, sensory deficit, severe illness, and dehydration), chart review terms were selected for each criterion, and delirium risk was the sum of criteria present (range: 0-4; 4 = worst). After discharge, a nurse blinded to the expert's diagnosis completed the chart tool.
RESULTS: The participants were mostly male (94%) and older (mean age 81 +/- 7), and 23% developed overall delirium (14% incident). The rate of overall delirium was 11% in participants with zero risk factors, 18% in those with one or two, and 50% in those with three or four (P = .01; c-statistic 0.65, 95% confidence interval (CI) = 0.54-0.76). For incident delirium, the rates were 11%, 13%, and 25%, respectively (P = .53; c-statistic 0.56, 95% CI = 0.42-0.74). Discharge to a rehabilitation center or nursing home increased with increasing delirium risk (0%, 18%, 60%, P = .02).
CONCLUSION: A chart abstraction tool was effective at identifying overall delirium risk but not incident delirium risk. Although the tool cannot replace clinical assessment and diagnosis of delirium, the use of this tool as an educational, clinical, or quality measurement aid warrants additional study. J Am Geriatr Soc 59:S289-S294, 2011.
C1 [Rudolph, James L.; Harrington, Mary Beth] VA Boston Healthcare Syst, Geriatr Res Educ & Clin Ctr, Boston, MA 02130 USA.
[Rudolph, James L.] Brigham & Womens Hosp, Div Aging, Boston, MA 02115 USA.
[Lucatorto, Michelle A.; Francis, Joseph] Vet Hlth Adm, Off Qual & Performance, Washington, DC USA.
[Shay, Kenneth J.] Vet Hlth Adm, Off Geriatr Programs, Washington, DC USA.
[Chester, Jennifer G.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
RP Rudolph, JL (reprint author), VA Boston Healthcare Syst, Geriatr Res Educ & Clin Ctr, 150 S Huntington Ave, Boston, MA 02130 USA.
EM jrudolph@partners.org
FU VA Rehabilitation Research Career Development Award; Einstein Research
Fellowship; National Institutes of Health [AG026781-05, AG038027]; John
A. Hartford Foundation
FX Dr. Rudolph is supported by a VA Rehabilitation Research Career
Development Award. Ms. Chester was funded by an Einstein Research
Fellowship. Additional support was provided by the American Federation
for Aging Research, the Boston Medical Student Training in Aging
Research Program, and National Institutes of Health Grants AG026781-05
and AG038027. Drs. Rudolph, Harrington, Lucatorto, Shay, and Francis and
the VADWG are VA employees. Publication was supported by the John A.
Hartford Foundation. The authors maintained independence in the
development, execution, and reporting of this study. The views and
opinions expressed in this article are those of the authors and do not
reflect or represent the official positions or policies of the U.S.
Department of Veterans Affairs.
NR 28
TC 14
Z9 14
U1 0
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0002-8614
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD NOV
PY 2011
VL 59
SU 2
SI SI
BP S289
EP S294
DI 10.1111/j.1532-5415.2011.03677.x
PG 6
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 853FH
UT WOS:000297411100012
PM 22091575
ER
PT J
AU Psaila, B
Bussel, JB
Frelinger, AL
Babula, B
Linden, MD
Li, Y
Barnard, MR
Tate, C
Feldman, EJ
Michelson, AD
AF Psaila, B.
Bussel, J. B.
Frelinger, A. L.
Babula, B.
Linden, M. D.
Li, Y.
Barnard, M. R.
Tate, C.
Feldman, E. J.
Michelson, A. D.
TI Differences in platelet function in patients with acute myeloid leukemia
and myelodysplasia compared to equally thrombocytopenic patients with
immune thrombocytopenia
SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS
LA English
DT Article
DE autoimmunity; bleeding; flow cytometry; hemorrhage; thrombocytopenia;
thrombopoiesis
ID IB-IX COMPLEX; GLYCOPROTEIN IB; PURPURA ITP; IN-VITRO; AUTOANTIBODIES;
REDISTRIBUTION; HETEROGENEITY; TRANSFUSIONS; HEMORRHAGE; PREDICTION
AB Background: Severe thrombocytopenia is a major risk factor for hemorrhage, but platelet function and bleeding risk at low platelet counts are poorly understood, because of the limitations of platelet function testing at very low platelet counts. Objectives: To examine and compare platelet function in severely thrombocytopenic patients with acute myeloid leukemia(AML) ormyelodysplasia (MDS) with that in patients with immune thrombocytopenia (ITP). Methods: Whole blood flow cytometric measurement of platelet activation and platelet reactivity to agonists was correlated with the immature platelet fraction (IPF) and bleeding symptoms. Results: Patients with AML/MDS had smaller platelets, lower IPF and substantially lower platelet surface expression of activated glycoprotein (GP) IIb-IIIa and GPIb, both with and without addition of ex vivo ADP or thrombin receptor-activating peptide, than patients with ITP. In both ITP and AML/MDS patients, increased platelet surface GPIb on circulating platelets and expression of activated GPIIb-IIIa and GPIb on ex vivo activated platelets correlated with a higher IPF. Whereas platelet reactivity was higher for AML/MDS patients with bleeding than for those with no bleeding, platelet reactivity was lower for ITP patients with bleeding than for those with no bleeding. Conclusions: AML/MDS patients have lower in vivo platelet activation and ex vivo platelet reactivity than patients with ITP. The proportion of newly produced platelets correlates with the expression of platelet surface markers of activation. These differences might contribute to differences in bleeding tendency between AML/MDS and ITP patients. This study is the first to define differences in platelet function between AML/MDS patients and ITP patients with equivalent degrees of thrombocytopenia.
C1 [Bussel, J. B.] Weill Cornell Med Coll, Dept Pediat, Platelet Disorders Ctr, Div Pediat Hematol Oncol, New York, NY 10021 USA.
[Psaila, B.] Imperial Coll Sch Med, Dept Haematol, London, England.
[Frelinger, A. L.; Linden, M. D.; Li, Y.; Barnard, M. R.; Michelson, A. D.] Univ Massachusetts, Sch Med, Dept Pediat, Ctr Platelet Funct Studies, Worcester, MA USA.
[Frelinger, A. L.; Barnard, M. R.; Michelson, A. D.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Ctr Platelet Res Studies,Div Hematol Oncol,Childr, Boston, MA 02115 USA.
[Feldman, E. J.] Weill Cornell Med Coll, Div Hematol & Med Oncol, New York, NY 10021 USA.
RP Bussel, JB (reprint author), Weill Cornell Med Coll, Dept Pediat, Platelet Disorders Ctr, Div Pediat Hematol Oncol, 525 E 68th St,P-695, New York, NY 10021 USA.
EM jbussel@med.cornell.edu
RI Linden, Matthew/G-9644-2012;
OI Linden, Matthew/0000-0002-9126-2166; Psaila, Beth/0000-0001-8198-9663
FU GSK; Sysmex America Incorporated; Amgen; Cangene; GlaxoSmithKline;
Genzyme; IgG of America; Immunomedics; Ligand; Eisai, Inc.; Shionogi;
Sysmex
FX This study was supported in part by research funding from GSK and Sysmex
America Incorporated. Bussel currently receives clinical research
support from the following companies: Amgen, Cangene, GlaxoSmithKline,
Genzyme, IgG of America, Immunomedics, Ligand, Eisai, Inc., Shionogi,
and Sysmex. J. B. Bussel's family owns stock in Amgen and
GlaxoSmithKline, and he has participated in Advisory Boards and/or
consults for Amgen, GlaxoSmithKline, Ligand, Shionogi, Eisai, and
Portola. The services of M. Lesser and M. Fine were funded in part by
GlaxoSmithKline.
NR 29
TC 26
Z9 32
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1538-7933
J9 J THROMB HAEMOST
JI J. Thromb. Haemost.
PD NOV
PY 2011
VL 9
IS 11
BP 2302
EP 2310
DI 10.1111/j.1538-7836.2011.04506.x
PG 9
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 851SS
UT WOS:000297291800021
PM 21920014
ER
PT J
AU Stepp, CE
Heaton, JT
Stadelman-Cohen, TK
Braden, MN
Jette, ME
Hillman, RE
AF Stepp, Cara E.
Heaton, James T.
Stadelman-Cohen, Tara K.
Braden, Maia N.
Jette, Marie E.
Hillman, Robert E.
TI Characteristics of Phonatory Function in Singers and Nonsingers With
Vocal Fold Nodules
SO JOURNAL OF VOICE
LA English
DT Article
DE Vocal hyperfunction; Vocal nodules; Neck surface electromyography
ID LARYNGEAL MUSCLE-ACTIVITY; TENSION DYSPHONIA; VOICE ONSET; FREQUENCY;
ELECTROMYOGRAPHY; DIAGNOSIS; PRESSURE; SPEAKERS; POLYPS
AB Purpose. The goals of this study were to determine if there were significant differences between singers and nonsingers in the morphology of vocal nodules and the associated impact on vocal function.
Method. Participants were 10 professionally trained singers with nodules, eight nonsingers with nodules, and 10 individuals with healthy normal voice (controls). Surface electromyography (sEMG) from three anterior neck locations and acoustic rise times for vowels /a/ and /i/ were measured in all the participants. In individuals with nodules, dB SPL/cm H2O, glottal airflow, and nodule location and size were also measured.
Results. There were no significant differences between singers and nonsingers with nodules in terms of airflow, dB SPL/cm H2O, nodule size, or nodule location. In nonsingers with nodules, airflow and nodule size were significantly correlated, but were not significantly correlated in singers. Vowel rise times and sEMG during vocal tasks did not differentiate among nodule and control groups. Sternocleidomastoid sEMG during initiation of the vowel /a/ was statistically significantly stronger in nonsingers with nodules relative to singers with nodules and controls.
Conclusions. Nodule morphology did not differ between singers and nonsingers, although some behavioral aspects of phonation differed between the groups.
C1 [Stepp, Cara E.; Hillman, Robert E.] Harvard MIT Div Hlth Sci & Technol, Cambridge, MA USA.
[Stepp, Cara E.; Heaton, James T.; Stadelman-Cohen, Tara K.; Braden, Maia N.; Jette, Marie E.; Hillman, Robert E.] Massachusetts Gen Hosp, Ctr Laryngeal Surg & Voice Rehabil, Boston, MA 02114 USA.
[Heaton, James T.; Hillman, Robert E.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Heaton, James T.; Stadelman-Cohen, Tara K.; Hillman, Robert E.] MGH Inst Hlth Profess, Sch Hlth & Rehabil Sci, Boston, MA USA.
RP Stepp, CE (reprint author), Univ Washington, Box 352350, Seattle, WA 98195 USA.
EM cstepp@alum.mit.edu
OI Jette, Marie/0000-0003-4705-1289
FU NIDCD NIH HHS [T32 DC000038-20, T32 DC000038]
NR 34
TC 3
Z9 4
U1 1
U2 9
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0892-1997
J9 J VOICE
JI J. Voice
PD NOV
PY 2011
VL 25
IS 6
BP 714
EP 724
DI 10.1016/j.jvoice.2010.06.003
PG 11
WC Otorhinolaryngology
SC Otorhinolaryngology
GA 851NZ
UT WOS:000297279100011
PM 21216129
ER
PT J
AU Fischer, SEJ
Montgomery, TA
Zhang, C
Fahlgren, N
Breen, PC
Hwang, A
Sullivan, CM
Carrington, JC
Ruvkun, G
AF Fischer, Sylvia E. J.
Montgomery, Taiowa A.
Zhang, Chi
Fahlgren, Noah
Breen, Peter C.
Hwang, Alexia
Sullivan, Christopher M.
Carrington, James C.
Ruvkun, Gary
TI The ERI-6/7 Helicase Acts at the First Stage of an siRNA Amplification
Pathway That Targets Recent Gene Duplications
SO PLOS GENETICS
LA English
DT Article
ID CAENORHABDITIS-ELEGANS GENOME; PASSENGER-STRAND CLEAVAGE; C-ELEGANS;
ENDOGENOUS SIRNAS; RNA INTERFERENCE; CHROMOSOME SEGREGATION; MOUSE
OOCYTES; DROSOPHILA; EXPRESSION; REVEALS
AB Endogenous small interfering RNAs (siRNAs) are a class of naturally occuring regulatory RNAs found in fungi, plants, and animals. Some endogenous siRNAs are required to silence transposons or function in chromosome segregation; however, the specific roles of most endogenous siRNAs are unclear. The helicase gene eri-6/7 was identified in the nematode Caenorhabditis elegans by the enhanced response to exogenous double-stranded RNAs (dsRNAs) of the null mutant. eri-6/7 encodes a helicase homologous to small RNA factors Armitage in Drosophila, SDE3 in Arabidopsis, and Mov10 in humans. Here we show that eri-6/7 mutations cause the loss of 26-nucleotide (nt) endogenous siRNAs derived from genes and pseudogenes in oocytes and embryos, as well as deficiencies in somatic 22-nucleotide secondary siRNAs corresponding to the same loci. About 80 genes are eri-6/7 targets that generate the embryonic endogenous siRNAs that silence the corresponding mRNAs. These 80 genes share extensive nucleotide sequence homology and are poorly conserved, suggesting a role for these endogenous siRNAs in silencing of and thereby directing the fate of recently acquired, duplicated genes. Unlike most endogenous siRNAs in C. elegans, eri-6/7-dependent siRNAs require Dicer. We identify that the eri-6/7-dependent siRNAs have a passenger strand that is similar to 19 nt and is inset by similar to 3-4 nts from both ends of the 26 nt guide siRNA, suggesting non-canonical Dicer processing. Mutations in the Argonaute ERGO-1, which associates with eri-6/7-dependent 26 nt siRNAs, cause passenger strand stabilization, indicating that ERGO-1 is required to separate the siRNA duplex, presumably through endonucleolytic cleavage of the passenger strand. Thus, like several other siRNA-associated Argonautes with a conserved RNaseH motif, ERGO-1 appears to be required for siRNA maturation.
C1 [Fischer, Sylvia E. J.; Montgomery, Taiowa A.; Zhang, Chi; Breen, Peter C.; Hwang, Alexia; Ruvkun, Gary] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Mol Biol,Dept Genet, Boston, MA 02115 USA.
[Fahlgren, Noah; Sullivan, Christopher M.; Carrington, James C.] Oregon State Univ, Ctr Genome Res & Biocomp, Corvallis, OR 97331 USA.
RP Fischer, SEJ (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Mol Biol,Dept Genet, Boston, MA 02115 USA.
EM ruvkun@molbio.mgh.harvard.edu
RI Carrington, James/A-4656-2012; Fahlgren, Noah/D-4404-2011;
OI Carrington, James/0000-0003-3572-129X; Fahlgren,
Noah/0000-0002-5597-4537; Montgomery, Taiowa/0000-0001-7857-3253
FU National Institutes of Health [GM44619]; Massachusetts General Hospital
Executive Committee; Damon Runyon Cancer Research Foundation
[DRG-2029-09]
FX This work was supported by National Institutes of Health Grant GM44619
(to GR) and Massachusetts General Hospital Executive Committee of
Research Fund for Medical Discovery fellowship awards (to CZ and SEJF).
TAM is supported by Damon Runyon Cancer Research Foundation Grant
DRG-2029-09. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 51
TC 28
Z9 31
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7390
J9 PLOS GENET
JI PLoS Genet.
PD NOV
PY 2011
VL 7
IS 11
AR e1002369
DI 10.1371/journal.pgen.1002369
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 851JM
UT WOS:000297264500023
PM 22102828
ER
PT J
AU Lal, A
Thomas, MP
Altschuler, G
Navarro, F
O'Day, E
Li, XL
Concepcion, C
Han, YC
Thiery, J
Rajani, DK
Deutsch, A
Hofmann, O
Ventura, A
Hide, W
Lieberman, J
AF Lal, Ashish
Thomas, Marshall P.
Altschuler, Gabriel
Navarro, Francisco
O'Day, Elizabeth
Li, Xiao Ling
Concepcion, Carla
Han, Yoon-Chi
Thiery, Jerome
Rajani, Danielle K.
Deutsch, Aaron
Hofmann, Oliver
Ventura, Andrea
Hide, Winston
Lieberman, Judy
TI Capture of MicroRNA-Bound mRNAs Identifies the Tumor Suppressor miR-34a
as a Regulator of Growth Factor Signaling
SO PLOS GENETICS
LA English
DT Article
ID DOWN-REGULATION; CELL-CYCLE; HEPATOCELLULAR-CARCINOMA; TARGET
RECOGNITION; CANCER; GENES; EXPRESSION; APOPTOSIS; PROTEIN; P53
AB A simple biochemical method to isolate mRNAs pulled down with a transfected, biotinylated microRNA was used to identify direct target genes of miR-34a, a tumor suppressor gene. The method reidentified most of the known miR-34a regulated genes expressed in K562 and HCT116 cancer cell lines. Transcripts for 982 genes were enriched in the pull-down with miR-34a in both cell lines. Despite this large number, validation experiments suggested that similar to 90% of the genes identified in both cell lines can be directly regulated by miR-34a. Thus miR-34a is capable of regulating hundreds of genes. The transcripts pulled down with miR-34a were highly enriched for their roles in growth factor signaling and cell cycle progression. These genes form a dense network of interacting gene products that regulate multiple signal transduction pathways that orchestrate the proliferative response to external growth stimuli. Multiple candidate miR-34a-regulated genes participate in RAS-RAF-MAPK signaling. Ectopic miR-34a expression reduced basal ERK and AKT phosphorylation and enhanced sensitivity to serum growth factor withdrawal, while cells genetically deficient in miR-34a were less sensitive. Fourteen new direct targets of miR-34a were experimentally validated, including genes that participate in growth factor signaling (ARAF and PIK3R2) as well as genes that regulate cell cycle progression at various phases of the cell cycle (cyclins D3 and G2, MCM2 and MCM5, PLK1 and SMAD4). Thus miR-34a tempers the proliferative and pro-survival effect of growth factor stimulation by interfering with growth factor signal transduction and downstream pathways required for cell division.
C1 [Lal, Ashish; Thomas, Marshall P.; Navarro, Francisco; O'Day, Elizabeth; Thiery, Jerome; Rajani, Danielle K.; Deutsch, Aaron; Lieberman, Judy] Childrens Hosp Boston, Program Cellular & Mol Med, Immune Dis Inst, Boston, MA 02115 USA.
[Lal, Ashish; Thomas, Marshall P.; Navarro, Francisco; O'Day, Elizabeth; Thiery, Jerome; Rajani, Danielle K.; Deutsch, Aaron; Lieberman, Judy] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Lal, Ashish; Li, Xiao Ling] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Altschuler, Gabriel; Hofmann, Oliver; Hide, Winston] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Concepcion, Carla; Han, Yoon-Chi; Ventura, Andrea] Mem Sloan Kettering Canc Ctr, Dept Canc Biol & Genet, New York, NY 10021 USA.
RP Lal, A (reprint author), Childrens Hosp Boston, Program Cellular & Mol Med, Immune Dis Inst, Boston, MA 02115 USA.
EM lalas@mail.nih.gov; lieberman@idi.harvard.edu
RI Hofmann, Oliver/F-1800-2013; Hide, Winston Hide/C-7217-2009; Lieberman,
Judy/A-2717-2015;
OI Hofmann, Oliver/0000-0002-7738-1513; Hide, Winston
Hide/0000-0002-8621-3271; Deutsch, Aaron/0000-0001-6750-5335; Ventura,
Andrea/0000-0003-4320-9907
FU GSK-IDI Alliance; NSF
FX This work was supported by a research grant (JL) and fellowship (FN)
from the GSK-IDI Alliance and by NSF predoctoral fellowships (MPT, DKR).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 58
TC 91
Z9 92
U1 0
U2 11
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 NOV
PY 2011
VL 7
IS 11
AR e1002363
DI 10.1371/journal.pgen.1002363
PG 17
WC Genetics & Heredity
SC Genetics & Heredity
GA 851JM
UT WOS:000297264500018
PM 22102825
ER
PT J
AU Huang, AJ
Kattapuram, SV
AF Huang, Ambrose J.
Kattapuram, Susan V.
TI Musculoskeletal Neoplasms: Biopsy and Intervention
SO RADIOLOGIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Biopsy; Intervention; Tumor; Infection; Spondylodiscitis; Sarcoma;
Metastasis
ID PERCUTANEOUS RADIOFREQUENCY ABLATION; CORE-NEEDLE-BIOPSY; EXTREMITY
COMPARTMENTAL ANATOMY; METASTASES INVOLVING BONE; CT-GUIDED BIOPSY;
OSTEOID OSTEOMA; INTRALESIONAL INJECTION; ETHIBLOC INJECTION;
CLINICAL-RELEVANCE; FOLLOW-UP
AB Percutaneous core needle biopsy and fine-needle aspiration are safe and cost-effective methods and can be important steps in the workup of a bone or soft tissue lesion. These procedures should be performed in collaboration with the orthopedic oncologist who performs the definitive surgery. In the extremities, attention to compartmental anatomy is paramount. With frozen section evaluation at the time of biopsy, the chances of a nondiagnostic specimen necessitating rebiopsy are minimized. The principles underlying the percutaneous approach to various lesions are valuable and can be applied to minimally invasive percutaneous therapy for bone and soft tissue lesions.
C1 [Huang, Ambrose J.; Kattapuram, Susan V.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Kattapuram, SV (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,Yawkey 6E, Boston, MA 02114 USA.
EM skattapuram@partners.org
NR 52
TC 17
Z9 20
U1 1
U2 2
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0033-8389
J9 RADIOL CLIN N AM
JI Radiol. Clin. N. Am.
PD NOV
PY 2011
VL 49
IS 6
BP 1287
EP +
DI 10.1016/j.rcl.2011.07.010
PG 20
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 853OT
UT WOS:000297436300012
PM 22024299
ER
PT J
AU Wen, LS
Noble, JA
AF Wen, Leana S.
Noble, Jeanne A.
TI A Case of a Young Girl With Fever and Seizure
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Editorial Material
ID PULMONARY TUBERCULOSIS; EMERGENCY; CHILDREN
C1 [Wen, Leana S.] Massachusetts Gen Hosp, Div Emergency Med, Brigham & Womens Hosp, Boston, MA 02114 USA.
[Noble, Jeanne A.] Univ Calif San Francisco, Dept Emergency Med, San Francisco, CA 94143 USA.
RP Wen, LS (reprint author), Massachusetts Gen Hosp, Div Emergency Med, Brigham & Womens Hosp, Boston, MA 02114 USA.
EM wen.leana@gmail.com
OI Wen, Leana/0000-0003-0259-0537
NR 13
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1069-6563
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD NOV
PY 2011
VL 18
IS 11
BP e86
EP e92
DI 10.1111/j.1553-2712.2011.01193.x
PG 7
WC Emergency Medicine
SC Emergency Medicine
GA 849EG
UT WOS:000297107800001
PM 22092908
ER
PT J
AU Kontos, N
Querques, J
Freudenreich, O
AF Kontos, Nicholas
Querques, John
Freudenreich, Oliver
TI Two's Company, Three Hundred Million's a Crowd: Balancing Clinical
Integrity and Population Consciousness in Medical Education
SO ACADEMIC MEDICINE
LA English
DT Editorial Material
C1 [Kontos, Nicholas; Querques, John] Massachusetts Gen Hosp, Psychosomat Med Consultat Psychiat Fellowship Pro, Boston, MA 02114 USA.
[Kontos, Nicholas; Querques, John; Freudenreich, Oliver] Harvard Univ, Sch Med, Boston, MA USA.
[Freudenreich, Oliver] Massachusetts Gen Hosp, Episode & Early Psychosis Program 1, Boston, MA 02114 USA.
RP Kontos, N (reprint author), Massachusetts Gen Hosp, Psychosomat Med Consultat Psychiat Fellowship Pro, 55 Fruit St,Warren 605, Boston, MA 02114 USA.
EM nkontos@partners.org
RI liu, jing/D-9482-2012
NR 3
TC 3
Z9 3
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
J9 ACAD MED
JI Acad. Med.
PD NOV
PY 2011
VL 86
IS 11
BP 1341
EP 1341
DI 10.1097/ACM.0b013e3182308cea
PG 1
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA 842UB
UT WOS:000296624900030
PM 22030640
ER
PT J
AU Melloni, C
James, SK
White, JA
Giugliano, RP
Harrington, RA
Huber, K
Tricoci, P
Armstrong, PW
Van de Werf, F
Montalescot, G
Califf, RM
Newby, LK
AF Melloni, Chiara
James, Stefan K.
White, Jennifer A.
Giugliano, Robert P.
Harrington, Robert A.
Huber, Kurt
Tricoci, Pierluigi
Armstrong, Paul W.
Van de Werf, Frans
Montalescot, Gilles
Califf, Robert M.
Newby, L. Kristin
CA EARLY ACS Investigators
TI Safety and efficacy of adjusted-dose eptifibatide in patients with acute
coronary syndromes and reduced renal function
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID GLYCOPROTEIN IIB/IIIA INHIBITORS; RAPID RISK STRATIFICATION; SUPPRESS
ADVERSE OUTCOMES; PLACEBO-CONTROLLED TRIAL; UNSTABLE ANGINA;
MYOCARDIAL-INFARCTION; EARLY IMPLEMENTATION; INTERVENTION;
PHARMACOKINETICS; PHARMACODYNAMICS
AB Background Dose adjustment of renally excreted antithrombotic drugs is recommended for patients with reduced renal function. We examined the influence of dose modification on bleeding and efficacy.
Methods Based on initial study drug infusion rate, Early GP IIb/IIIa Inhibition in non-ST-segment elevation acute coronary syndromes (EARLY ACS) patients were categorized into groups: standard dose (2 mu g/kg/min; estimated creatinine clearance [eCrCl] >= 50 ml/min), adjusted dose (1 mu g/kg/min; eCrCl <50 ml/min, per protocol), excess dose (2 mu g/kg/min; eCrCl <50 ml/min). We explored relationships among initial dosing, randomized treatment assignment, and bleeding and ischemic end points (96-h composite of death, myocardial infarction [MI], recurrent ischemia requiring urgent revascularization or thrombotic bailout, and 30-d death or MI).
Results Of 8,708 patients with eCrCl and dosing data, 19% had eCrCl <50 ml/min. Of these, 13% received adjusted dose eptifibatide and 6% received an excess dose. Across all dosing groups, no significant reductions were found in ischemic end points between early versus delayed provisional eptifibatide (OR 1.14, 95% CI 0.80-1.65; OR 1.13, 95% CI 0.81-1.56, respectively, for 96-h and 30-d composite end points). Bleeding risk was not significantly increased in the early versus delayed provisional treatment group in either the adjusted (OR 1.50, 95% CI 0.95-2.39) or excess dose group (OR 1.67, 95% CI 0.85-3.39). There were no significant interactions between dose group and treatment strategy on bleeding or efficacy.
Conclusion Similar to observations in practice, despite guidelines recommendations and protocol guidance, 34% of EARLY ACS patients with reduced renal function failed to receive an appropriately adjusted study drug infusion. Use of an appropriately adjusted eptifibatide infusion was not associated with expected reductions in bleeding among patients with renal insufficiency. (Am Heart J 2011;162:884-892.e1.)
C1 [Melloni, Chiara; White, Jennifer A.; Harrington, Robert A.; Tricoci, Pierluigi; Newby, L. Kristin] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC 27705 USA.
[Melloni, Chiara; White, Jennifer A.; Harrington, Robert A.; Tricoci, Pierluigi; Newby, L. Kristin] Duke Univ, Med Ctr, Div Cardiol, Durham, NC 27705 USA.
[James, Stefan K.] Uppsala Univ, Uppsala Clin Res Ctr, Dept Med Sci, Uppsala, Sweden.
[Giugliano, Robert P.] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
[Huber, Kurt] Wilhelminenspital Stadt Wien, Dept Med, Vienna, Austria.
[Armstrong, Paul W.] Univ Alberta, Edmonton, AB, Canada.
[Van de Werf, Frans] Univ Hosp Gasthuisberg, B-3000 Louvain, Belgium.
[Van de Werf, Frans] Leuven Coordinating Ctr, Louvain, Belgium.
[Montalescot, Gilles] Hop La Pitie Salpetriere, Inst Cardiol, Paris, France.
[Califf, Robert M.] Duke Univ, Med Ctr, Duke Translat Med Inst, Durham, NC USA.
RP Melloni, C (reprint author), Duke Univ, Med Ctr, Duke Clin Res Inst, POB 17969, Durham, NC 27705 USA.
EM mello004@mc.duke.edu
OI Van de Werf, Frans/0000-0001-9479-7767
FU AstraZeneca; Sanofi-Aventis; BMS; Eli Lilly; Schering-Plough; Merck;
Bristol-Myers Squibb; Medtronic; Bayer; Boehringer-Ingelheim; Daiichi
Sankyo; Fibrex; Portola; Medicines Company; Boston Scientific;
Cordis/Johnson Johnson; GlaxoSmithKline; Pfizer; Schering-Plough
Research Institute; Portola Pharmaceutical; Roche; Merck through the
Duke Clinical Research Institute
FX Stefan K. James: Research grants and speaker fees received from
AstraZeneca, Sanofi-Aventis, BMS, Eli Lilly, and Schering-Plough.;
Robert A. Harrington: Research funding and consulting with
Schering-Plough, now Merck. A complete listing of Dr. Harrington's
relationships with industry is available at
http://www.dcri.duke.edu/research/coi.jsp.; Kurt Huber: Research grants
from Bristol-Myers Squibb, Eli Lilly, Medtronic, Sanofi-Aventis;
consulting fees from AstraZeneca, Bayer, Boehringer-Ingelheim,
Bristol-Myers Squibb, Daiichi Sankyo, Fibrex, Eli Lilly, Portola,
Sanofi-Aventis, Schering-Plough, and The Medicines Company; lecture fees
from AstraZeneca, Boehringer-Ingelheim, Boston Scientific, Bristol-Myers
Squibb, Cordis/Johnson & Johnson, Daiichi Sankyo, Eli Lilly,
GlaxoSmithKline, Pfizer, and Sanofi-Aventis.; Paul W. Armstrong:
Research grant or contract from Schering-Plough Research Institute,
Portola Pharmaceutical, AstraZeneca, and Merck, which partially supports
his university salary and/or research projects. A complete listing of
Dr. Armstrong's relationships with industry is available at
http://www.vigour.ualberta.ca.; Frans Van de Werf: Research grants from
Schering-Plough (now Merck) and Roche; advisory board and speakers fee
from Schering- Plough, Merck, and Roche.; L. Kristin Newby: Research
grant from Schering-Plough and Merck through the Duke Clinical Research
Institute; consulting honoraria from Schering-Plough. A complete listing
of Dr. Newby's relationships with industry is available at
www.dcri.duke.edu/research/coi.jsp.
NR 27
TC 2
Z9 3
U1 1
U2 8
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD NOV
PY 2011
VL 162
IS 5
DI 10.1016/j.ahj.2011.08.020
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 851DE
UT WOS:000297247800014
PM 22093205
ER
PT J
AU Peacock, WF
Nagurney, J
Birkhahn, R
Singer, A
Shapiro, N
Hollander, J
Glynn, T
Nowak, R
Safdar, B
Miller, C
Peberdy, M
Counselman, F
Chandra, A
Kosowsky, J
Neuenschwander, J
Schrock, J
Plantholt, S
Lewandrowski, E
Wong, V
Kupfer, K
Diercks, D
AF Peacock, W. Frank
Nagurney, John
Birkhahn, Robert
Singer, Adam
Shapiro, Nathan
Hollander, Judd
Glynn, Ted
Nowak, Richard
Safdar, Basmah
Miller, Chadwick
Peberdy, Mary
Counselman, Francis
Chandra, Abhinav
Kosowsky, Joshua
Neuenschwander, James
Schrock, Jon
Plantholt, Stephen
Lewandrowski, Elizabeth
Wong, Vance
Kupfer, Ken
Diercks, Deborah
TI Myeloperoxidase in the diagnosis of acute coronary syndromes: The
importance of spectrum
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID ACUTE MYOCARDIAL-INFARCTION; UNSTABLE ANGINA-PECTORIS; CHEST-PAIN;
EMERGENCY-DEPARTMENT; NEUTROPHIL; PHYSICIANS; OXIDATION; RISK
AB Background Myeloperoxidase (MPO) is proposed for risk stratification in patients with suspected acute coronary syndromes (ACSs). We determined if MPO has diagnostic value in patients being evaluated for ACS.
Method MIDAS was an 18-center prospective study enrolling suspected ACS emergency department patients who presented <8 hours after symptom onset and in whom serial cardiac markers and objective cardiac perfusion testing were planned. Blinded MPO (Biosite, Inc, San Diego, CA) and troponin I (Triage Cardio 3; Biosite, Inc) were drawn at arrival, and Troponin I (TnI) was measured at 90, 180, and 360 minutes. Final diagnoses were adjudicated by the local investigator blinded to study assay.
Results Of 1,018 patients, 54% were male, 26% black, with a mean age of 58 +/- 13 years. Diagnoses were ACS in 288 (23%) and noncardiac chest pain (NCCP) in 788 (77%). Of patients with ACS, 94 (9.2%) had a myocardial infarction (MI) at presentation (69 non-ST-elevation MI, 25 ST-elevation MI), and 136 had unstable angina. Using a cutpoint of 210 ng/mL to provide 90% specificity, MPO had a sensitivity of 0.18; negative predictive value, 0.69; positive predictive value, 0.47; negative likelihood ratio, 0.91; and a positive likelihood ratio of 1.83 to differentiate ACS and NCCP. Because of the large overlap of quartiles, MPO was not clinically useful to predict serial TnI changes. The C statistics +/- 95% CI for MPO differentiating ACS from NCCP and for AMI versus NCCP were 0.629 +/- 0.04 and 0.666 +/- 0.06, respectively.
Conclusions Myeloperoxidase has insufficient accuracy for decision making in patients with suspected ACS. (Am Heart J 2011;162:893-9.)
C1 [Peacock, W. Frank] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Nagurney, John; Lewandrowski, Elizabeth] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Birkhahn, Robert] New York Methodist Hosp, Brooklyn, NY USA.
[Singer, Adam] SUNY Stony Brook, Stony Brook, NY 11794 USA.
[Shapiro, Nathan] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Hollander, Judd] Univ Penn, Philadelphia, PA 19104 USA.
[Glynn, Ted] Ingham Reg Med Ctr, Lansing, MI USA.
[Nowak, Richard] Henry Ford Hlth Syst, Detroit, MI USA.
[Safdar, Basmah] Yale Univ, New Haven, CT USA.
[Miller, Chadwick] Wake Forrest Baptist Hosp, Winston Salem, NC USA.
[Peberdy, Mary] Virginia Commonwealth Univ, Richmond, VA USA.
[Counselman, Francis] Eastern Virginia Med Sch, Norfolk, VA 23501 USA.
[Chandra, Abhinav] Duke Univ, Durham, NC USA.
[Kosowsky, Joshua] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Neuenschwander, James] Ohio State Univ, Med Ctr, Columbus, OH 43210 USA.
[Schrock, Jon] Metrohlth Med Ctr, Cleveland, OH USA.
[Plantholt, Stephen] St Agnes Hosp, Baltimore, MD USA.
[Wong, Vance; Kupfer, Ken] Alere Inc, San Diego, CA USA.
[Diercks, Deborah] Univ Calif, Sacramento, CA USA.
RP Peacock, WF (reprint author), Cleveland Clin Fdn, 9500 Euclid Ave, Cleveland, OH 44195 USA.
EM meltonc@ccf.org
RI Shapiro, Nathan/F-1718-2016;
OI Hollander, Judd/0000-0002-1318-2785
NR 27
TC 15
Z9 16
U1 0
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD NOV
PY 2011
VL 162
IS 5
DI 10.1016/j.ahj.2011.08.017
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 851DE
UT WOS:000297247800015
PM 22093206
ER
PT J
AU Scirica, BM
Bhatt, DL
Braunwald, E
Steg, PG
Davidson, J
Hirshberg, B
Ohman, P
Price, DL
Chen, R
Udell, J
Raz, I
AF Scirica, Benjamin M.
Bhatt, Deepak L.
Braunwald, Eugene
Steg, Ph. Gabriel
Davidson, Jaime
Hirshberg, Boaz
Ohman, Peter
Price, Deborah L.
Chen, Roland
Udell, Jacob
Raz, Itamar
CA SAVOR-TIMI53 Steering Comm Investi
TI The design and rationale of the Saxagliptin Assessment of Vascular
Outcomes Recorded in patients with diabetes mellitus-Thrombolysis in
Myocardial Infarction (SAVOR-TIMI) 53 Study
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; IMPROVES GLYCEMIC CONTROL; BLOOD-GLUCOSE
CONTROL; CARDIOVASCULAR OUTCOMES; SECONDARY PREVENTION; THERAPY;
METFORMIN; DISEASE; ASPIRIN; PIOGLITAZONE
AB Objectives Saxagliptin, a dipeptidyl peptidase 4 inhibitor, improves glycemic control in patients with type 2 diabetes mellitus (T2DM) by increasing endogenous active, intact glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide in response to food, which augments insulin secretion and decreases glucagon release.
Research Design and Methods SAVOR-TIMI 53 is a phase 4, randomized, double-blind, placebo-controlled trial conducted in 25 countries that is designed to evaluate the safety and efficacy of saxagliptin during long-term treatment of approximately 16,500 patients with T2DM. Eligible patients who are either treatment naive or on any background antidiabetic treatment (except incretin therapy) with history of established cardiovascular (CV) disease or multiple risk factors are randomized 1: 1 to saxagliptin 5 mg QD (2.5 mg in subjects with moderate/severe renal impairment) or matching placebo, stratified by qualifying disease state. The primary end point is the composite of CV death, nonfatal myocardial infarction, or nonfatal ischemic stroke. The trial will continue until approximately 1,040 primary end points accrue, providing 85% power to identify a 17% relative reduction of the primary end point with saxagliptin versus placebo and 98% power to test for noninferiority of saxagliptin versus placebo (reject the upper limit of 95% CI for a hazard ratio <1.3 at a 1-sided alpha of .025).
Conclusion SAVOR-TIMI 53 is testing the hypothesis that treatment with saxagliptin is safe and reduces CV events in high-risk patients with T2DM. (Am Heart J 2011;162:818-825.e6.)
C1 [Scirica, Benjamin M.; Bhatt, Deepak L.; Braunwald, Eugene; Udell, Jacob] Brigham & Womens Hosp, TIMI Study Grp, Div Cardiovasc, Boston, MA 02115 USA.
[Scirica, Benjamin M.; Bhatt, Deepak L.; Braunwald, Eugene; Udell, Jacob] Harvard Univ, Sch Med, Boston, MA USA.
[Bhatt, Deepak L.] VA Boston Healthcare Syst, Boston, MA USA.
[Steg, Ph. Gabriel] Univ Paris 07, INSERM, U698, Paris, France.
[Steg, Ph. Gabriel] Hop Bichat Claude Bernard, AP HP, F-75877 Paris, France.
[Davidson, Jaime] Univ Texas SW Med Ctr Dallas, Div Endocrinol, Dept Internal Med, Dallas, TX 75390 USA.
[Hirshberg, Boaz; Ohman, Peter; Price, Deborah L.] AstraZeneca Res & Dev, Wilmington, DE USA.
[Chen, Roland] Bristol Myers Squibb Co, Princeton, NJ USA.
[Raz, Itamar] Hadassah Univ Hosp, Dept Med, Diabet Unit, IL-91240 Jerusalem, Israel.
RP Scirica, BM (reprint author), Brigham & Womens Hosp, TIMI Study Grp, Div Cardiovasc, 75 Francis St, Boston, MA 02115 USA.
EM bscirica@partners.org
FU AstraZeneca; Bristol-Myers Squibb; Merck; Johnson Johnson; Bayer
Healthcare; Gilead Sciences; Lexicon; Arena Pharmaceuticals; Eisai;
Sanofi Aventis; Medicines Company
FX Dr Scirica reports research grants from AstraZeneca, Bristol-Myers
Squibb, Merck, Johnson & Johnson, Bayer Healthcare, and Gilead Sciences
and consultancy fees from Gilead Sciences, Lexicon, and Arena
Pharmaceuticals. Dr Bhatt reports research grants from AstraZeneca,
Bristol-Myers Squibb, Eisai, Sanofi Aventis, and The Medicines Company.
Dr Braunwald reports research grants from AstraZeneca and Bristol-Myers
Squibb. Dr Steg reports research grants from Servier. Dr Davidson
reports serving on advisory panels for AstraZeneca, Bristol-Myers
Squibb, Merck, Johnson & Johnson, Boehringer Ingelheim, Eli Lilly,
Generex Biotechnology, Novo Nordisk A/S, Roche Diagnostics, and Takeda
Pharmaceutical Company and on the speaker's bureau of Eli Lilly and
Takeda Pharmaceutical Company. Drs Hirshberg and Ohman and Ms Price are
employees of and hold stock in AstraZeneca. Dr Chen is an employee of
and holds stock in Bristol-Myers Squibb. Dr Udell reports no conflicts.
Dr Raz has received honoraria/expenses for advisory board participation
from AstraZeneca, Bristol-Myers Squibb, Novo Nordisk, Merck Sharp &
Dohme, and Eli Lilly; served as a consultant for Andromeda, AstraZeneca,
Bristol-Myers Squibb, Eli Lilly, Johnson & Johnson, HealOr, Insuline,
Teva, and TransPharma; and participated in speakers bureaus for
AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Novo Nordisk, Johnson &
Johnson, and Roche. The authors are solely responsible for the design
and conduct of this study, all study analyses, and the drafting and
editing of the manuscript and its final contents.
NR 32
TC 50
Z9 54
U1 1
U2 13
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD NOV
PY 2011
VL 162
IS 5
DI 10.1016/j.ahj.2011.08.006
PG 14
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 851DE
UT WOS:000297247800005
PM 22093196
ER
PT J
AU Soleimani, M
Khazalpour, M
Cheng, GM
Zhang, ZH
Acevedo-Bolton, G
Saloner, DA
Mishra, R
Wallace, AW
Guccione, JM
Ge, L
Ratcliffe, MB
AF Soleimani, Mehrdad
Khazalpour, Michael
Cheng, Guangming
Zhang, Zhihong
Acevedo-Bolton, Gabriel
Saloner, David A.
Mishra, Rakesh
Wallace, Arthur W.
Guccione, Julius M.
Ge, Liang
Ratcliffe, Mark B.
TI Moderate Mitral Regurgitation Accelerates Left Ventricular Remodeling
After Posterolateral Myocardial Infarction
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID MAGNETIC-RESONANCE; 3-DIMENSIONAL ECHOCARDIOGRAPHY; REPAIR;
REVASCULARIZATION; QUANTIFICATION; METAANALYSIS; SEVERITY; MYOCYTES;
VOLUMES; STRESS
AB Background. Chronic ischemic mitral regurgitation (MR) is associated with poor outcome. However, the effect of chronic ischemic MR on left ventricular (LV) remodeling after posterolateral myocardial infarction (MI) remains controversial. We tested the hypothesis that moderate MR accelerates LV remodeling after posterolateral MI.
Methods. Posterolateral MI was created in 10 sheep. Cardiac magnetic resonance imaging was performed 2 weeks before and 2, 8, and 16 weeks after MI. Left ventricular and right ventricular volumes were measured, and regurgitant volume was calculated as the difference between LV and right ventricle stroke volumes.
Results. Multivariate mixed effects regression showed that LV volumes at end diastole and end systole and LV sphericity were strongly correlated with both regurgitant volume (p < 0.0001, p = 0.0086, and p = 0.0007, respectively) and percent infarct area (p = 0.0156, p = 0.0307, and p < 0.0001, respectively). Conversely, whereas LV hypertrophy (LV wall volume) increased from 2 weeks to 16 weeks after MI, there was no effect of either regurgitant volume or percent infarct.
Conclusions. Moderate MR accelerates LV remodeling after posterolateral MI. Further studies are needed to determine whether mitral valve repair is able to slow or reverse MI remodeling after posterolateral MI. (Ann Thorac Surg 2011;92:1614-20) (C) 2011 by The Society of Thoracic Surgeons
C1 Univ Calif San Francisco, Dept Surg, San Francisco, CA USA.
Univ Calif San Francisco, Dept Anesthesia, San Francisco, CA 94143 USA.
Univ Calif San Francisco, Dept Bioengn, San Francisco, CA 94143 USA.
Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
Univ Calif San Francisco, Dept Radiol, San Francisco, CA USA.
Vet Affairs Med Ctr, San Francisco, CA 94121 USA.
RP Ratcliffe, MB (reprint author), San Francisco VA Med Ctr, Div Surg Serv 112, 4150 Clement St, San Francisco, CA 94121 USA.
EM mark.ratcliffe@va.gov
FU National Institutes of Health [R01-HL-084431, R01-HL-077921]
FX This study was supported by National Institutes of Health grants
R01-HL-084431 (Dr Ratcliffe) and R01-HL-077921 (Dr Guccione).
NR 33
TC 10
Z9 10
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD NOV
PY 2011
VL 92
IS 5
BP 1614
EP 1620
DI 10.1016/j.athoracsur.2011.05.117
PG 7
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 846TF
UT WOS:000296925400020
PM 21945222
ER
PT J
AU Shah, DK
Li, Z
Park, SJ
Daly, RC
Dearani, JA
Schaff, HV
Sundt, TM
AF Shah, Dipesh K.
Li, Zhuo
Park, Soon J.
Daly, Richard C.
Dearani, Joseph A.
Schaff, Hartzell V.
Sundt, Thoralf M., III
TI Replacement of the Infected Composite Aortic Root Prosthesis
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID VALVE ENDOCARDITIS; ASCENDING AORTA; EXPERIENCE; REOPERATIONS;
ALLOGRAFT; SURGERY; RISK
AB Background. We sought to evaluate freedom from reinfection after surgery for infected aortic root replacement (ARR) and the impact of use of synthetic material at reoperation.
Methods. Adult patients (aged more than 18 years) undergoing surgery for infected composite aortic root prosthesis at our institution were identified and their perioperative outcomes and late survival evaluated.
Results. Between January 1, 1993, and December 31, 2009, 15 patients (male, 87%; mean [SD] age, 57 [16] years) underwent surgery. All but 1 patient (6.7%) underwent reconstruction with a homograft. Eight patients (53.3%) required synthetic material to complete the repair, including 4 patients who underwent hemiarch reconstruction. Ten patients (66.7%) had circulatory arrest (mean [SD] time, 23.3 [11.0] minutes) and 3 (20.0%) underwent concomitant coronary artery bypass grafting. The 30-day mortality rate was 13.3% (n = 2). Three patients (20.0%)-2 of whom had positive blood cultures in hospital after redo ARR-had reinfection, for which 2 underwent re-replacement of the aortic root. Survival was 86.7%, 65.0%, and 50.6%, and freedom from reinfection was 90.9%, 79.5%, and 79.5% at 3, 6, and 12 months, respectively. Freedom from reinfection was less for the patients who had positive blood cultures within 2 weeks of redo ARR (p < 0.03) and for patients who had multiple previous sternotomies (p = 0.006). Use of synthetic graft material had no adverse impact.
Conclusions. Infected ARR prostheses can be replaced with a homograft with favorable outcomes. Use of synthetic material to complete the repair does not adversely impact outcome. (Ann Thorac Surg 2011; 92: 1651-6) (C) 2011 by The Society of Thoracic Surgeons
C1 [Sundt, Thoralf M., III] Massachusetts Gen Hosp, Div Cardiac Surg, Boston, MA 02114 USA.
Mayo Clin, Div Cardiovasc Surg, Rochester, MN USA.
Mayo Clin, Div Biomed Stat & Informat, Rochester, MN USA.
RP Sundt, TM (reprint author), Massachusetts Gen Hosp, Div Cardiac Surg, 55 Fruit St, Boston, MA 02114 USA.
EM tsundt@partners.org
OI Schaff, Hartzell/0000-0003-0994-027X
NR 16
TC 3
Z9 5
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD NOV
PY 2011
VL 92
IS 5
BP 1651
EP 1656
DI 10.1016/j.athoracsur.2011.05.115
PG 6
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 846TF
UT WOS:000296925400028
PM 21937018
ER
PT J
AU Kim, S
Ott, HC
Wright, CD
Wain, JC
Morse, C
Gaissert, HA
Donahue, DM
Mathisen, DJ
Lanuti, M
AF Kim, Samuel
Ott, Harald C.
Wright, Cameron D.
Wain, John C.
Morse, Christopher
Gaissert, Henning A.
Donahue, Dean M.
Mathisen, Douglas J.
Lanuti, Michael
TI Pulmonary Resection of Metastatic Sarcoma: Prognostic Factors Associated
With Improved Outcomes
SO ANNALS OF THORACIC SURGERY
LA English
DT Article; Proceedings Paper
CT 47th Annual Meeting of the Society-of-Thoracic-Surgeons
CY JAN 31-FEB 02, 2011
CL San Diego, CA
SP Soc Thorac Surg
ID SOFT-TISSUE SARCOMA; SURVIVAL; METASTASECTOMY; MANAGEMENT; NUMBER
AB Background. There are few data to predict the benefit of pulmonary metastasectomy in patients with extrathoracic sarcoma. This study analyzes prognostic factors associated with improved outcomes.
Methods. Between June 2002 and December 2008, 97 patients underwent pulmonary resection for metastatic sarcoma at Massachusetts General Hospital. Eight patients were excluded because of lack of follow-up data. Analysis was performed using Kaplan-Meier estimates of survival, log-rank test, and multivariate Cox model.
Results. Overall 5-year survival for the cohort was 50.1%. Patients who had multiple operations for recurrent pulmonary metastases had better 5-year survival compared with patients who had a single operation (69 versus 41%; p = 0.017). Median disease-free survival (DFS) for the reoperation group was 12.9 months compared with 9.1 months for the single-operation group (p < 0.028). Patients with a disease-free interval (DFI) greater than 12 months from detection of primary sarcoma to pulmonary metastasectomy had improved survival compared with those whose DFI was less than 12 months (p < 0.0001). Patients with bilateral metastasectomy had lower 5-year survival compared with metastasectomy for unilateral disease (22% versus 68%; p < 0.0001). Two or more metastases were associated with poorer outcome compared with a single metastasis (p = 0.0007). A positive resection margin portended worse survival compared with a negative resection margin (p = 0.004). Patients with lesions larger than 3 cm had decreased survival compared with patients with lesions smaller than 3 cm (p = 0.017) with no difference in median DFS. Histologic type, grade of tumor, and use of chemotherapy had no effect on survival. Multivariate analysis showed that patients with a DFI greater than 12 months (p = 0.001), single-sided metastasis (p = 0.001), negative margins (p = 0.002), and multiple operations (p = 0.018) had better survival.
Conclusions. Pulmonary metastasectomy for sarcoma can be associated with prolonged survival. Tumor resectability, DFI, number of metastases, and laterality are important factors in determining patient selection for curative surgical intervention. Repeated pulmonary metastasectomy in select patients may improve survival despite recurrent disease. (Ann Thorac Surg 2011; 92: 1780-7) (C) 2011 by The Society of Thoracic Surgeons
C1 [Kim, Samuel; Ott, Harald C.; Wright, Cameron D.; Wain, John C.; Morse, Christopher; Gaissert, Henning A.; Donahue, Dean M.; Mathisen, Douglas J.; Lanuti, Michael] Harvard Univ, Div Thorac Surg, Sch Med, Massachusetts Gen Hosp, Boston, MA 01478 USA.
RP Lanuti, M (reprint author), Harvard Univ, Div Thorac Surg, Sch Med, Massachusetts Gen Hosp, 55 Fruit St,Blake 1570, Boston, MA 01478 USA.
EM mlanuti@partners.org
NR 21
TC 36
Z9 39
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD NOV
PY 2011
VL 92
IS 5
BP 1780
EP 1786
DI 10.1016/j.athoracsur.2011.05.081
PG 7
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 846TF
UT WOS:000296925400050
PM 22051274
ER
PT J
AU Raz, DJ
Lanuti, M
Gaissert, HC
Wright, CD
Mathisen, DJ
Wain, JC
AF Raz, Dan J.
Lanuti, Michael
Gaissert, Henning C.
Wright, Cameron D.
Mathisen, Douglas J.
Wain, John C.
TI Outcomes of Patients With Isolated Adrenal Metastasis From Non-Small
Cell Lung Carcinoma
SO ANNALS OF THORACIC SURGERY
LA English
DT Article; Proceedings Paper
CT 47th Annual Meeting of the Society-of-Thoracic-Surgeons
CY JAN 31-FEB 02, 2011
CL San Diego, CA
SP Soc Thorac Surg
ID LAPAROSCOPIC ADRENALECTOMY; CANCER
AB Background. Long-term survival of patients who undergo surgical resection of isolated adrenal metastasis from non-small cell lung cancer (NSCLC) has been reported. The aim of this study was to compare survival of patients who underwent adrenalectomy with those treated nonoperatively, and to analyze clinical characteristics associated with long-term survival.
Methods. Between January 1994 and July 2010, 37 patients with isolated adrenal metastasis from NSCLC were identified. Twenty patients underwent adrenalectomy. Patients did not undergo adrenalectomy owing to suspicion of N2 disease, medical comorbidities, or patient preference. Seven patients (35%) treated surgically had tumors that were ipsilateral to their primary tumor, and 8 (40%) had metachronous metastases.
Results. Five-year overall survival was 34% for patients treated operatively and 0% for patients treated nonoperatively (p = 0.002). Among patients treated with adrenalectomy, patients with ipsilateral metastases had a 5-year survival of 83% compared with 0% for patients with contralateral metastases (p = 0.003). Patients without mediastinal nodal disease had a 5-year survival of 52% compared with 0% for patients with mediastinal nodal disease (p = 0.008). Survival of patients who underwent adrenalectomy for synchronous and metachronous adrenal metastases was not significantly different (p = 0.81).
Conclusions. Surgical resection of isolated adrenal metastasis from lung cancer provides a survival benefit in well-selected patients compared with nonoperative management. No patient with contralateral adrenal metastases or mediastinal nodal disease survived long term after adrenalectomy. The time interval between treatment of the primary lung cancer and adrenal metastasis was not significantly associated with survival, but the cohort size was small. (Ann Thorac Surg 2011; 92: 1788 -93) (C) 2011 by The Society of Thoracic Surgeons
C1 [Raz, Dan J.; Lanuti, Michael; Gaissert, Henning C.; Wright, Cameron D.; Mathisen, Douglas J.; Wain, John C.] Massachusetts Gen Hosp, Div Thorac Surg, Boston, MA 02114 USA.
RP Raz, DJ (reprint author), Massachusetts Gen Hosp, Div Thorac Surg, 55 Fruit St,Blake 1570, Boston, MA 02114 USA.
EM draz@partners.org
NR 10
TC 27
Z9 30
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD NOV
PY 2011
VL 92
IS 5
BP 1788
EP 1792
DI 10.1016/j.athoracsur.2011.05.116
PG 5
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 846TF
UT WOS:000296925400052
PM 21944257
ER
PT J
AU Rajbanshi, BG
Rodrigues, E
Lynch, JJ
Gulati, R
Sundt, TM
AF Rajbanshi, Bijoy G.
Rodrigues, Eduardo
Lynch, James J.
Gulati, Rajiv
Sundt, Thoralf M., III
TI Coronary Artery Spasm After Cryo Maze III Procedure
SO ANNALS OF THORACIC SURGERY
LA English
DT Editorial Material
ID ATRIAL-FIBRILLATION; CATHETER ABLATION
AB The Cox Maze III procedure has been simplified with the availability of tissue ablation devices; however, complications related to their use are recognized. We report a case of 45-year-old woman who underwent mitral valve repair and concomitant Cryo-Maze procedure. She had reversible right coronary artery spasm develop after the procedure demonstrated by ST-segment elevation changes and coronary angiography, which was reversed with intracoronary nitroglycerin. The region of spasm suggested it as a consequence of proximity of the right coronary artery to the right atrial ablation lines. (Ann Thorac Surg 2011; 92: 1884-7) (C) 2011 by The Society of Thoracic Surgeons
C1 [Sundt, Thoralf M., III] Massachusetts Gen Hosp, Div Cardiac Surg, Boston, MA 02117 USA.
Mayo Clin & Mayo Fdn, Div Cardiovasc Surg, Dept Anesthesiol, Rochester, MN USA.
Mayo Clin & Mayo Fdn, Div Cardiovasc Dis, Rochester, MN USA.
RP Sundt, TM (reprint author), Massachusetts Gen Hosp, Div Cardiac Surg, 55 Fruit St,POB 652, Boston, MA 02117 USA.
EM tsundt@partners.org
NR 8
TC 1
Z9 3
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD NOV
PY 2011
VL 92
IS 5
BP 1884
EP 1887
DI 10.1016/j.athoracsur.2011.04.113
PG 4
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 846TF
UT WOS:000296925400075
PM 22051287
ER
PT J
AU Chang, AY
Piette, EW
Foering, KP
Tenhave, TR
Okawa, J
Werth, VP
AF Chang, Aileen Y.
Piette, Evan W.
Foering, Kristen P.
Tenhave, Thomas R.
Okawa, Joyce
Werth, Victoria P.
TI Response to Antimalarial Agents in Cutaneous Lupus Erythematosus
SO ARCHIVES OF DERMATOLOGY
LA English
DT Article
ID SEVERITY INDEX; DISEASE AREA; QUINACRINE; RESISTANT; HYDROXYCHLOROQUINE;
CHLOROQUINE; DERMATOLOGY; CLASSIFICATION; ASSOCIATION; THERAPY
AB Objective: To demonstrate response to antimalarial agents in patients with cutaneous lupus erythematosus (CLE) using activity scores from the Cutaneous Lupus Erythematosus Disease Area and Severity Index, a validated outcome measure.
Design: Prospective, longitudinal cohort study.
Setting: University cutaneous autoimmune disease clinic.
Participants: A total of 128 patients with CLE who presented from January 2007 to July 2010 and had at least 2 visits with activity scores.
Intervention: Administration of antimalarial agents.
Main Outcome Measures: Response was defined by a 4-point or 20% decrease in activity score. Response to initiation was determined by the difference between the scores before treatment and at the first visit at least 2 months after treatment. Response to continuation was determined by the difference between the scores at the first visit and the most recent visit while undergoing treatment.
Results: Of 11 patients who initiated treatment with hydroxychloroquine, 55% were responders (n = 6), showing a decrease in median (interquartile range [IQR]) activity score from 8.0 (3.5-13.0) to 3.0 (1.8-7.3) (P = .03). Of 15 patients for whom hydroxychloroquine failed, 67% were responders to initiation of hydroxychloroquine-quinacrine therapy (n = 10), showing a decrease in median (IQR) activity score from 6.0 (4.8-8.3) to 3.0 (0.75-5.0) (P = .004). Nine of 21 patients who continued hydroxychloroquine treatment (43%), and 9 of 21 patients who continued hydroxychloroquine-quinacrine (43%) were responders, showing a decrease in median (IQR) activity score from 6.0 (1.5-9.5) to 1.0 (0.0-4.5) (P = .01) and 8.5 (4.25-17.5) to 5.0 (0.5-11.5) (P = .01), respectively.
Conclusions: The use of quinacrine with hydroxychloroquine is associated with response in patients for whom hydroxychloroquine monotherapy fails. Further reduction in disease activity can be associated with continuation of treatment with antimalarial agents.
C1 [Chang, Aileen Y.; Piette, Evan W.; Foering, Kristen P.; Okawa, Joyce; Werth, Victoria P.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
[Chang, Aileen Y.; Piette, Evan W.; Foering, Kristen P.; Okawa, Joyce; Werth, Victoria P.] Univ Penn, Dept Dermatol, Philadelphia, PA 19104 USA.
[Foering, Kristen P.] Univ Penn, Inst Translat Med & Therapeut, Philadelphia, PA 19104 USA.
[Tenhave, Thomas R.] Univ Penn, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
RP Werth, VP (reprint author), Perelman Ctr Adv Med, Dept Dermatol, 3400 Civ Ctr Blvd,Ste 1-330A, Philadelphia, PA 19104 USA.
EM werth@mail.med.upenn.edu
FU National Institutes of Health [NIH K24-AR 18 02207]; Doris Duke
Charitable Foundation
FX This work was supported by National Institutes of Health grant NIH
K24-AR 18 02207 (Dr Werth) and a grant from the Doris Duke Charitable
Foundation to the Perelman School of Medicine at the University of
Pennsylvania to fund Clinical Research Fellow Ms Chang.
NR 30
TC 30
Z9 32
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-987X
J9 ARCH DERMATOL
JI Arch. Dermatol.
PD NOV
PY 2011
VL 147
IS 11
BP 1261
EP 1267
DI 10.1001/archdermatol.2011.191
PG 7
WC Dermatology
SC Dermatology
GA 850UW
UT WOS:000297226000003
PM 21768444
ER
PT J
AU Wan, J
Abuabara, K
Kurd, SK
Musiek, A
Steinemann, JM
Vittorio, CC
Gelfand, JM
AF Wan, Joy
Abuabara, Katrina
Kurd, Shanu K.
Musiek, Amy
Steinemann, Jane M.
Vittorio, Carmela C.
Gelfand, Joel M.
TI Reliability and Validity of a Photographic Method for Measuring Facial
Hair Density in Men
SO ARCHIVES OF DERMATOLOGY
LA English
DT Letter
C1 [Wan, Joy; Abuabara, Katrina; Kurd, Shanu K.; Musiek, Amy; Steinemann, Jane M.; Vittorio, Carmela C.; Gelfand, Joel M.] Univ Penn, Dept Dermatol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Abuabara, Katrina; Kurd, Shanu K.] Univ Penn, Dept Internal Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Gelfand, Joel M.] Univ Penn, Ctr Clin Epidemiol & Biostat, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Musiek, Amy] Philadelphia VA Med Ctr, Philadelphia, PA USA.
RP Gelfand, JM (reprint author), 1471 Penn Tower,1 Convent Ave, Philadelphia, PA 19104 USA.
EM Joel.Gelfand@uphs.upenn.edu
FU NIAMS NIH HHS [T32-AR07465, T32 AR007465]
NR 5
TC 1
Z9 1
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-987X
J9 ARCH DERMATOL
JI Arch. Dermatol.
PD NOV
PY 2011
VL 147
IS 11
BP 1328
EP 1329
PG 2
WC Dermatology
SC Dermatology
GA 850UW
UT WOS:000297226000020
PM 22106126
ER
PT J
AU Rosenbaum, JT
Davey, MP
AF Rosenbaum, James T.
Davey, Michael P.
TI Time for a Gut Check: Evidence for the Hypothesis That HLA-B27
Predisposes to Ankylosing Spondylitis by Altering the Microbiome
SO ARTHRITIS AND RHEUMATISM
LA English
DT Editorial Material
ID ACUTE ANTERIOR UVEITIS; HUMAN MONOCYTIC CELLS; IMMUNE-RESPONSE;
TRANSGENIC RATS; T-CELLS; DISEASE; KLEBSIELLA; BACTERIA; ARTHRITIS;
PEPTIDES
C1 [Rosenbaum, James T.] Oregon Hlth & Sci Univ, Portland, OR 97239 USA.
[Davey, Michael P.] Portland VA Med Ctr, Portland, OR USA.
RP Rosenbaum, JT (reprint author), Oregon Hlth & Sci Univ, 3181 SW Sam Jackson Pk Rd,L467Ad, Portland, OR 97239 USA.
EM rosenbaj@ohsu.edu
FU NEI NIH HHS [R01 EY019604, R01 EY019604-01, R01-EY-019604]
NR 44
TC 24
Z9 26
U1 1
U2 17
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD NOV
PY 2011
VL 63
IS 11
BP 3195
EP 3198
DI 10.1002/art.30558
PG 4
WC Rheumatology
SC Rheumatology
GA 850TC
UT WOS:000297221100002
PM 21792826
ER
PT J
AU Shahouri, SH
Michaud, K
Mikuls, TR
Caplan, L
Shaver, TS
Anderson, JD
Weidensaul, DN
Busch, RE
Wang, S
Wolfe, F
AF Shahouri, Shadi H.
Michaud, Kaleb
Mikuls, Ted R.
Caplan, Liron
Shaver, Timothy S.
Anderson, James D.
Weidensaul, David N.
Busch, Ruth E.
Wang, Shirley
Wolfe, Frederick
TI Remission of Rheumatoid Arthritis in Clinical Practice Application of
the American College of Rheumatology/European League Against Rheumatism
2011 Remission Criteria
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID HEALTH-ASSESSMENT QUESTIONNAIRE; MULTILEVEL LOGISTIC-REGRESSION;
DISEASE-ACTIVITY SCORE; TRIALS; DEFINITION; AGREEMENT; INDEX; CARE
AB Objective. To describe use of the American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) rheumatoid arthritis (RA) remission criteria in clinical practice.
Methods. Remission was examined using data on 1,341 patients with RA (91% men) from the US Department of Veterans Affairs RA (VARA) registry (total of 9,700 visits) and 1,153 patients with RA (25.8% men) in a community rheumatology practice (Arthritis and Rheumatology Clinics of Kansas [ARCK]) (total of 6,362 visits). Cross-sectional and cumulative probabilities were studied, and agreement between the various remission criteria was assessed. Aspects of reliability of the criteria were determined using Boolean-based definitions, as well as the Clinical Disease Activity Index (CDAI) and Simplified Disease Activity Index (SDAI) scoring methods proposed by the ACR/EULAR joint committee.
Results. When the 3-variable ACR/EULAR definition of remission recommended for use in community practice (swollen and tender joint counts <= 1, and visual analog scale score for patient's global assessment of disease activity <= 1) was applied, cross-sectional remission was 7.5% (95% confidence interval [95% CI] 6.4, 8.7%) for ARCK and 8.9% (95% CI 7.9, 9.9%) for VARA, and cumulative remission (remission at any observation) was 18.0% (for ARCK) and 24.4% (for VARA), over a mean followup of similar to 2.2 years. Addition of the erythrocyte sedimentation rate or C-reactive protein level to the criteria set reduced remission to 5.0-6.2%, and use of the CDAI/SDAI increased the proportions to 6.9-10.1%. Moreover, 1.8-4.6% of the patients met remission criteria at >= 2 visits. Agreement between criteria definitions was good, as assessed by kappa statistics and Jaccard coefficients. Among patients in remission, the probability of a remission lasting 2 years was 6.0-14.1%. Among all patients, the probability of a remission lasting 2 years was <3%. Remission status and examination results for each patient varied substantially among physicians, as determined by multilevel analyses.
Conclusion. Cross-sectional remission occurred in 5.0-10.1% of the patients in these cohorts, with cumulative remission being 2-3 times greater; however, long-term remission was rare. Problems with reliability and agreement limit the usefulness of these criteria in the individual patient. However, the criteria can be an effective method for measuring clinical status and treatment effect in groups of patients in the community.
C1 [Michaud, Kaleb; Wolfe, Frederick] Natl Data Bank Rheumat Dis, Wichita, KS 67214 USA.
[Shahouri, Shadi H.; Shaver, Timothy S.; Anderson, James D.; Weidensaul, David N.; Busch, Ruth E.; Wang, Shirley] Arthrit Clin Kansas, Wichita, KS USA.
[Shahouri, Shadi H.; Shaver, Timothy S.; Anderson, James D.; Weidensaul, David N.; Busch, Ruth E.; Wang, Shirley] Rheumatol Clin Kansas, Wichita, KS USA.
[Shahouri, Shadi H.; Shaver, Timothy S.; Anderson, James D.; Weidensaul, David N.; Wang, Shirley; Wolfe, Frederick] Univ Kansas, Sch Med, Wichita, KS 67214 USA.
[Michaud, Kaleb] Univ Nebraska Med Ctr, Omaha, NE USA.
[Mikuls, Ted R.] Omaha VA Med Ctr, Omaha, NE USA.
[Mikuls, Ted R.] Univ Nebraska, Omaha, NE 68182 USA.
[Caplan, Liron] Denver VA Med Ctr, Denver, CO USA.
[Caplan, Liron] Univ Colorado, Denver, CO 80202 USA.
[Busch, Ruth E.] Wichita State Univ, Wichita, KS USA.
RP Wolfe, F (reprint author), Natl Data Bank Rheumat Dis, 1035 N Emporia,Suite 288, Wichita, KS 67214 USA.
EM fwolfe@arthritis-research.org
FU VA Health Services Research & Development Service; Arthritis Foundation;
NIH [1RC1AR058601-01]; VA Merit grant; VA Career Development Award [CDA
07-221]
FX The US VA Rheumatoid Arthritis registry is supported by the VA Health
Services Research & Development Service. Dr. Michaud's work was
supported in part by an Arthritis Foundation New Investigator Award and
a grant from the NIH (American Recovery & Reinvestment Act grant
1RC1AR058601-01). Dr. Mikuls' work was supported by a VA Merit grant.
Dr. Caplan's work was supported by a VA Career Development Award (CDA
07-221).
NR 29
TC 42
Z9 43
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD NOV
PY 2011
VL 63
IS 11
BP 3204
EP 3215
DI 10.1002/art.30524
PG 12
WC Rheumatology
SC Rheumatology
GA 850TC
UT WOS:000297221100004
PM 21739423
ER
PT J
AU Bartels, CM
Everett, C
McBride, P
Smith, M
Kind, AJH
Mell, M
AF Bartels, Christie M.
Everett, Christine
McBride, Patrick
Smith, Maureen
Kind, Amy J. H.
Mell, Matthew
TI Is the "lipid paradox" in rheumatoid arthritis really a paradox? Comment
on the article by Bartels et al Reply
SO ARTHRITIS AND RHEUMATISM
LA English
DT Letter
ID MORTALITY
C1 [Bartels, Christie M.; Everett, Christine; McBride, Patrick; Smith, Maureen; Kind, Amy J. H.] Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI 53706 USA.
[Kind, Amy J. H.] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
[Mell, Matthew] Stanford Univ, Palo Alto, CA 94304 USA.
RP Bartels, CM (reprint author), Univ Wisconsin, Sch Med & Publ Hlth, Madison, WI 53706 USA.
NR 6
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD NOV
PY 2011
VL 63
IS 11
BP 3645
EP 3646
DI 10.1002/art.30587
PG 2
WC Rheumatology
SC Rheumatology
GA 850TC
UT WOS:000297221100061
ER
PT J
AU Anderson, JK
Zimmerman, L
Caplan, L
Michaud, K
AF Anderson, Jaclyn K.
Zimmerman, Lani
Caplan, Liron
Michaud, Kaleb
TI Measures of Rheumatoid Arthritis Disease Activity Patient (PtGA) and
Provider (PrGA) Global Assessment of Disease Activity, Disease Activity
Score (DAS) and Disease Activity Score With 28-Joint Counts (DAS28),
Simplified Disease Activity Index (SDAI), Clinical Disease Activity
Index (CDAI), Patient Activity Score (PAS) and Patient Activity Score-II
(PASII), Routine Assessment of Patient Index Data (RAPID), Rheumatoid
Arthritis Disease Activity Index (RADAI) and Rheumatoid Arthritis
Disease Activity Index-5 (RADAI-5), Chronic Arthritis Systemic Index
(CASI), Patient-Based Disease Activity Score With ESR (PDAS1) and
Patient-Based Disease Activity Score Without ESR (PDAS2), and Mean
Overall Index for Rheumatoid Arthritis (MOI-RA)
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID HEALTH-ASSESSMENT QUESTIONNAIRE; COLLEGE-OF-RHEUMATOLOGY; VISUAL ANALOG
SCALES; RANDOMIZED CONTROLLED-TRIALS; ACUTE-PHASE REACTANTS; FORMAL
JOINT COUNTS; CORE SET MEASURES; RESPONSE CRITERIA; FUNCTIONAL-CAPACITY;
IMPROVEMENT CRITERIA
C1 [Anderson, Jaclyn K.; Zimmerman, Lani; Michaud, Kaleb] Univ Nebraska Med Ctr, Omaha, NE USA.
[Anderson, Jaclyn K.] Abbott Labs, Abbott Pk, IL USA.
[Caplan, Liron] Denver Vet Affairs Med Ctr, Denver, CO USA.
[Caplan, Liron] Univ Colorado, Sch Med, Aurora, CO USA.
[Michaud, Kaleb] Natl Data Bank Rheumat Dis, Wichita, KS USA.
RP Anderson, JK (reprint author), 200 Abbott Pk Rd,Dept R4NE,Bldg AP34-1, Abbott Pk, IL 60064 USA.
EM Jaclyn.Anderson@abbott.com
OI Anderson, Jaclyn/0000-0002-0893-3900
FU American College of Rheumatology
FX Supported in part by the American College of Rheumatology.
NR 121
TC 41
Z9 44
U1 0
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 2151-464X
J9 ARTHRIT CARE RES
JI Arthritis Care Res.
PD NOV
PY 2011
VL 63
SU 11
BP S14
EP S36
DI 10.1002/acr.20621
PG 23
WC Rheumatology
SC Rheumatology
GA 850SR
UT WOS:000297219500003
PM 22588741
ER
PT J
AU Rider, LG
Werth, VP
Huber, AM
Alexanderson, H
Rao, AP
Ruperto, N
Herbelin, L
Barohn, R
Isenberg, D
Miller, FW
AF Rider, Lisa G.
Werth, Victoria P.
Huber, Adam M.
Alexanderson, Helene
Rao, Anand Prahalad
Ruperto, Nicolino
Herbelin, Laura
Barohn, Richard
Isenberg, David
Miller, Frederick W.
TI Measures of Adult and Juvenile Dermatomyositis, Polymyositis, and
Inclusion Body Myositis Physician and Patient/Parent Global Activity,
Manual Muscle Testing (MMT), Health Assessment Questionnaire
(HAQ)/Childhood Health Assessment Questionnaire (C-HAQ), Childhood
Myositis Assessment Scale (CMAS), Myositis Disease Activity Assessment
Tool (MDAAT), Disease Activity Score (DAS), Short Form 36 (SF-36), Child
Health Questionnaire (CHQ), Physician Global Damage, Myositis Damage
Index (MDI), Quantitative Muscle Testing (QMT), Myositis Functional
Index-2 (FI-2), Myositis Activities Profile (MAP), Inclusion Body
Myositis Functional Rating Scale (IBMFRS), Cutaneous Dermatomyositis
Disease Area and Severity Index (CDASI), Cutaneous Assessment Tool
(CAT), Dermatomyositis Skin Severity Index (DSSI), Skindex, and
Dermatology Life Quality Index (DLQI)
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID IDIOPATHIC INFLAMMATORY MYOPATHIES; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
MUSCULAR-DYSTROPHY FSHD; RANDOMIZED PILOT TRIAL; HOME EXERCISE PROGRAM;
OF-LIFE; PEDIATRIC RHEUMATOLOGY; NATURAL-HISTORY; PROGNOSTIC-FACTORS;
INTERNATIONAL CONSENSUS
C1 [Rider, Lisa G.] NIEHS, Environm Autoimmun Grp, Program Clin Res, NIH, Bethesda, MD 20892 USA.
[Werth, Victoria P.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[Werth, Victoria P.] Univ Penn, Philadelphia, PA 19104 USA.
[Huber, Adam M.] Dalhousie Univ, Halifax, NS, Canada.
[Huber, Adam M.] IWK Hlth Ctr, Halifax, NS, Canada.
[Alexanderson, Helene] Karolinska Inst, Stockholm, Sweden.
[Alexanderson, Helene] Karolinska Univ Hosp, Stockholm, Sweden.
[Rao, Anand Prahalad; Ruperto, Nicolino] IRCCS G Gaslini, Paediat Rheumatol Int Trials Org, Genoa, Italy.
[Herbelin, Laura; Barohn, Richard] Univ Kansas, Med Ctr, Kansas City, KS 66103 USA.
[Isenberg, David] UCL, London, England.
RP Rider, LG (reprint author), NIEHS, Environm Autoimmun Grp, Program Clin Res, NIH, CRC 4-2352,MSC 1301,10 Ctr Dr, Bethesda, MD 20892 USA.
EM rider1@mail.nih.gov
OI Rider, Lisa/0000-0002-6912-2458
FU NIH National Institute of Environmental Health Sciences
FX Supported in part by the Intramural Research Program of the NIH National
Institute of Environmental Health Sciences.
NR 112
TC 51
Z9 54
U1 2
U2 10
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2151-464X
EI 2151-4658
J9 ARTHRIT CARE RES
JI Arthritis Care Res.
PD NOV
PY 2011
VL 63
SU 11
BP S118
EP S157
DI 10.1002/acr.20532
PG 40
WC Rheumatology
SC Rheumatology
GA 850SR
UT WOS:000297219500011
PM 22588740
ER
PT J
AU Huang, SN
Chen, HH
Yuan, HS
Dai, GP
Schuhle, DT
Mekkaoui, C
Ngoy, S
Liao, RL
Caravan, P
Josephson, L
Sosnovik, DE
AF Huang, Shuning
Chen, Howard H.
Yuan, Hushan
Dai, Guangping
Schuhle, Daniel T.
Mekkaoui, Choukri
Ngoy, Soeun
Liao, Ronglih
Caravan, Peter
Josephson, Lee
Sosnovik, David E.
TI Molecular MRI of Acute Necrosis With a Novel DNA-Binding Gadolinium
Chelate Kinetics of Cell Death and Clearance in Infarcted Myocardium
SO CIRCULATION-CARDIOVASCULAR IMAGING
LA English
DT Article
DE molecular imaging; MRI; necrosis; myocardium; infarction
ID ENHANCED MAGNETIC-RESONANCE; NECROTIC CELLS; CONTRAST AGENTS;
MECHANISMS; APOPTOSIS; DISEASE; HEART; RATS; TC-99M-ANNEXIN-V;
REPERFUSION
AB Background-Current techniques to image cell death in the myocardium are largely nonspecific. We report the use of a novel DNA-binding gadolinium chelate (Gd-TO) to specifically detect the exposed DNA in acutely necrotic (ruptured) cells in vivo.
Methods and Results-In vivo MRI was performed in 20 mice with myocardial infarction (MI). The mice were injected with Gd-TO or Gd-DTPA at varying time points after MI. MRI was performed 2 hours after probe injection, to avoid nonspecific signal from the late gadolinium enhancement effect. Cell rupture (Gd-TO uptake) was present within 2 hours of infarction but peaked 9 to 18 hours after the onset of injury. A significant increase in the longitudinal relaxation rate (R(1)) in the infarct was seen in mice injected with Gd-TO within 48 hours of MI, but not in those injected more than 72 hours after MI (R(1)=1.24 +/- 0.08 and 0.92 +/- 0.03 s(-1), respectively, P<0.001). Gd-DTPA, unlike Gd-TO, washed completely out of acute infarcts within 2 hours of injection (P<0.001). The binding of Gd-TO to exposed DNA in acute infarcts was confirmed with fluorescence microscopy.
Conclusions-Gd-TO specifically binds to acutely necrotic cells and can be used to image the mechanism and chronicity of cell death in injured myocardium. Cell rupture in acute MI begins early but peaks many hours after the onset of injury. The ruptured cells are efficiently cleared by the immune system and are no longer present in the myocardium 72 hours after injury. (Circ Cardiovasc Imaging. 2011;4:729-737.)
C1 [Huang, Shuning; Chen, Howard H.; Dai, Guangping; Schuhle, Daniel T.; Mekkaoui, Choukri; Caravan, Peter; Josephson, Lee; Sosnovik, David E.] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp,Martinos Ctr Biomed Imagin, Boston, MA 02115 USA.
[Chen, Howard H.; Sosnovik, David E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Mol Imaging Res, Boston, MA USA.
[Yuan, Hushan; Josephson, Lee] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Translat Nucl Med & Mol Imaging, Boston, MA USA.
[Ngoy, Soeun; Liao, Ronglih] Harvard Univ, Sch Med, Brigham & Womans Hosp, Div Cardiol, Boston, MA USA.
[Sosnovik, David E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
RP Sosnovik, DE (reprint author), 149 13th St, Charlestown, MA 02129 USA.
EM sosnovik@nmr.mgh.harvard.edu
FU National Institutes of Health [R01 HL093038, R01 EB011996, S10RR025563,
P41RR14075]
FX This study was funded by the following National Institutes of Health
grants: R01 HL093038 (Dr Sosnovik), R01 EB011996 (Dr Josephson),
S10RR025563 (Dr Dai), and P41RR14075 (Martinos Center).
NR 36
TC 24
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U1 1
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-9651
J9 CIRC-CARDIOVASC IMAG
JI Circ.-Cardiovasc. Imaging
PD NOV
PY 2011
VL 4
IS 6
BP 729
EP U186
DI 10.1161/CIRCIMAGING.111.966374
PG 10
WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical
Imaging
SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine &
Medical Imaging
GA 850AZ
UT WOS:000297168100019
PM 21836081
ER
PT J
AU Yeh, RW
Mauri, L
AF Yeh, Robert W.
Mauri, Laura
TI Choosing Methods to Minimize Confounding in Observational Studies Do the
Ends Justify the Means?
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Editorial Material
DE Editorials; comparative effectiveness; confounding; bias; stents;
instrumental variables; propensity scores
ID ACUTE MYOCARDIAL-INFARCTION; CORONARY-ARTERY DISEASE; BARE-METAL STENTS;
INSTRUMENTAL VARIABLES; RANDOMIZED-TRIALS; OUTCOMES RESEARCH; MEDICAL
THERAPY; SAFETY; ANGIOPLASTY; EFFICACY
C1 [Yeh, Robert W.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiol Div,Dept Med, Boston, MA USA.
[Mauri, Laura] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc Med,Dept Med, Boston, MA 02115 USA.
RP Mauri, L (reprint author), 75 Francis St, Boston, MA 02115 USA.
EM lmauri1@partners.org
NR 15
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7713
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD NOV
PY 2011
VL 4
IS 6
BP 581
EP 583
DI 10.1161/CIRCOUTCOMES.111.963538
PG 3
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 850BC
UT WOS:000297168400002
PM 22085982
ER
PT J
AU Melloni, C
Roe, MT
Chen, AY
Wang, TY
Wiviott, SD
Ho, PM
Peterson, ED
Alexander, KP
AF Melloni, Chiara
Roe, Matthew T.
Chen, Anita Y.
Wang, Tracy Y.
Wiviott, Stephen D.
Ho, P. Michael
Peterson, Eric D.
Alexander, Karen P.
TI Use of Early Clopidogrel by Reperfusion Strategy Among Patients
Presenting With ST-Segment Elevation Myocardial Infarction
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE clopidogrel; guideline adherence; fibrinolysis; reperfusion
ID PERCUTANEOUS CORONARY INTERVENTION; PLACEBO-CONTROLLED TRIAL;
FIBRINOLYTIC THERAPY; ASPIRIN; PRETREATMENT; OUTCOMES; RISK
AB Background-The 2007 update of the ACC/AHA guidelines for STEMI patients recommended addition of clopidogrel to aspirin regardless of reperfusion strategy, with a bolus dose in patients <75 years of age.
Methods and Results-We evaluated use and dose of early clopidogrel among 52,140 STEMI patients enrolled in 368 hospitals participating in NCDR's ACTION Registry (R)-Get with the Guidelines (GWTG (TM)) from January 2007-September 2009. Patients were stratified by reperfusion strategy: primary percutaneous coronary intervention (PCI, n = 37,108), fibrinolysis (n = 5805), or no-reperfusion (n = 9227), and by age (<75 or >= 75 years). Adjusted odds for in-hospital outcomes are reported by clopidogrel use across reperfusion strategies. Clopidogrel was administered early to 97% of primary PCI, 18% of fibrinolytic, and 6% of non-reperfused patients. Among patients receiving clopidogrel, a loading dose (>= 300 mg) was often used in primary PCI (91%) but less frequently among fibrinolysis-treated (83%) and non-reperfused patients (74%). A positive time trend from Q1 2007-Q3 2009 in overall clopidogrel use was observed only in fibrinolytic patients (15-20%) Use of clopidogrel was associated with a significant increase in major bleeding only among older patients in the no-reperfusion group (21.9% vs. 13.2%; OR 2.19; 95% CI 1.47-3.27). A significantly lower risk of in-hospital death was associated with clopidogrel use across all reperfusion strategies (OR [95% CI], primary PCI: 0.15 [0.13-0.19]; fibrinolysis: 0.26 [0.12-0.57]; no reperfusion: 0.42 [0.27-0.65]).
Conclusion-Early clopidogrel use has not yet extended to the routine care of STEMI patients treated with fibrinolysis or those not receiving reperfusion as recommended in the guideline update. (Circ Cardiovasc Qual Outcomes. 2011;4:603-609.)
C1 [Melloni, Chiara; Roe, Matthew T.; Chen, Anita Y.; Wang, Tracy Y.; Peterson, Eric D.; Alexander, Karen P.] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC 27705 USA.
[Melloni, Chiara; Roe, Matthew T.; Chen, Anita Y.; Wang, Tracy Y.; Peterson, Eric D.; Alexander, Karen P.] Duke Univ, Med Ctr, Div Cardiol, Durham, NC 27705 USA.
[Wiviott, Stephen D.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Ho, P. Michael] Denver VA Med Ctr, Cardiol Sect, Denver, CO USA.
Univ Colorado Denver, Denver, CO USA.
RP Melloni, C (reprint author), Duke Univ, Med Ctr, Duke Clin Res Inst, 2400 Pratt St, Durham, NC 27705 USA.
EM mello004@mc.duke.edu
FU Bristol-Myers Squibb (BMS)/Sanofi Pharmaceuticals Partnership;
Schering-Plough Corporation; BMS/Sanofi-Aventis; BMS/Sanofi Partnership;
Merck/Schering-Plough; AstraZeneca; BMS; Ortho; McNeil; Pfizer;
Sanofi-Aventis; Daiichi Sankyo; Eli Lilly; Schering-Plough; VA Research
& Development Career Development Award [05-026-2]
FX The Bristol-Myers Squibb (BMS)/Sanofi Pharmaceuticals Partnership and
Schering-Plough Corporation are founding sponsors of the ACTION
Registry-GWTG. Dr Roe receives research grants from BMS/Sanofi-Aventis
and Merck/Schering-Plough, is on the speaker's bureau for
BMS/Sanofi-Aventis and Merck/Schering-Plough, and consults for
Merck/Schering-Plough; Dr Wang receives research grants from BMS/Sanofi
Partnership and Merck/Schering-Plough; Dr Wiviott receives honoraria for
educational presentations from BMS, Daiichi Sankyo, Eli Lilly,
Schering-Plough, Merck, and The Medicine's Company, receives consulting
fees from AstraZeneca, BMS, Ortho McNeil, Pfizer, and Sanofi-Aventis,
and research grants from Daiichi Sankyo, Eli Lilly, and Schering-Plough;
Dr Ho receives research support from a VA Research & Development Career
Development Award (05-026-2) and is also a consultant for Wellpoint,
Inc; and Dr Peterson receives research grants from BMS.
NR 17
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U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7713
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD NOV
PY 2011
VL 4
IS 6
BP 603
EP 609
DI 10.1161/CIRCOUTCOMES.111.961045
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 850BC
UT WOS:000297168400006
PM 21988922
ER
PT J
AU Eapen, ZJ
Fonarow, GC
Dai, D
O'Brien, SM
Schwamm, LH
Cannon, CP
Heidenreich, PA
Bhatt, DL
Peterson, ED
Hernandez, AF
AF Eapen, Zubin J.
Fonarow, Gregg C.
Dai, David
O'Brien, Sean M.
Schwamm, Lee H.
Cannon, Christopher P.
Heidenreich, Paul A.
Bhatt, Deepak L.
Peterson, Eric D.
Hernandez, Adrian F.
CA Get Guidelines Steering Comm Hosp
TI Comparison of Composite Measure Methodologies for Rewarding Quality of
Care An Analysis From the American Heart Association's Get With The
Guidelines Program
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE composite performance measure; coronary artery disease; outcomes
research
ID ACUTE MYOCARDIAL-INFARCTION; ACUTE CORONARY SYNDROMES;
PERFORMANCE-MEASURES; CLINICAL-OUTCOMES; HOSPITAL QUALITY; MORTALITY;
CARDIOLOGY; SURGERY; TRENDS
AB Background-Composite indices of health care performance are an aggregation of underlying individual performance measures and are increasingly being used to rank hospitals. We sought to conduct an observational analysis to determine the influence of the opportunity-based and all-or-none composite performance measures on hospital rankings.
Methods and Results-We examined 194 245 patients hospitalized with acute myocardial infarction between July 2006 and June 2009 from 334 hospitals participating in the Get With The Guidelines-Coronary Artery Disease (GWTG-CAD) quality improvement program. We analyzed hospital opportunity-based and all-or-none composite scores and 30-day risk-standardized all-cause mortality and readmission rates. We found that the median calculated opportunity-based score for these hospitals was 95.5 (interquartile range, 90.4, 98.0). The median all-or-none score was 88.9 (interquartile range, 79.7, 94.4). The 2 scoring methods were significantly correlated with one another (r=0.98, P<0.001). Rankings generated by the two methods were significantly correlated (r=0.93, P<0.001). The two methods had a modest correlation with the 30-day risk-standardized mortality rate (opportunity-based score: r=-0.25, P<0.001; all-or-none score: r=-0.24, P<0.001). Neither composite measure correlated with the 30-day risk-standardized readmission rate. Over time, the number of hospitals new to the top and bottom quintiles of hospital rankings diminished similarly for both composite measures. When including additional performance measures into the composite score, the two methods produced similar changes in hospital rankings.
Conclusions-The opportunity-based and all-or-none coronary artery disease composite indices are highly correlated and yield similar ranking of the top and bottom quintiles of hospitals. The two methods provide similarly modest correlations with 30-day mortality, but not readmission. (Circ Cardiovasc Qual Outcomes. 2011;4:610-618.)
C1 [Eapen, Zubin J.; Dai, David; O'Brien, Sean M.; Peterson, Eric D.; Hernandez, Adrian F.] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC 27715 USA.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Div Cardiol, Los Angeles, CA USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Cannon, Christopher P.; Bhatt, Deepak L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Heidenreich, Paul A.] Vet Affairs Palo Alto Healthcare Syst, Div Cardiol, Palo Alto, CA USA.
[Bhatt, Deepak L.] Vet Affairs Boston Healthcare Syst, Boston, MA USA.
RP Hernandez, AF (reprint author), Duke Univ, Med Ctr, Duke Clin Res Inst, POB 17969, Durham, NC 27715 USA.
EM adrian.hernandez@duke.edu
RI O'Brien, Sean/H-6268-2013; Hernandez, Adrian F./A-7818-2016
OI Heidenreich, Paul/0000-0001-7730-8490; Schwamm, Lee/0000-0003-0592-9145;
Hernandez, Adrian F./0000-0003-3387-9616
FU Merck/Schering-Plough Partnership; American Heart
Association-Pharmaceutical Roundtable [0875142N]; David and Stevie
Spina; Agency for Healthcare Research and Quality (AHRQ) [U18HS016964];
National Heart, Lung, and Blood Institute; Accumetrics; AstraZeneca;
GlaxoSmithKline; InteKrin Therapeutics; Merck; Takeda; Medtronic; Astra
Zeneca; Bristol-Myers Squibb; Eisai; Sanofi Aventis; Johnson Johnson;
Amylin
FX Get With the Guidelines-Coronary Artery Disease is a program of the
American Heart Association and is supported in part by an unrestricted
educational grant from Merck/Schering-Plough Partnership, which did not
participate in the design or analysis of the study or in manuscript
preparation. This work was supported by an award from the American Heart
Association-Pharmaceutical Roundtable and David and Stevie Spina. Dr
Eapen received funding from an American Heart Association-Pharmaceutical
Roundtable outcomes training grant (0875142N). This project received
infrastructure support from the Agency for Healthcare Research and
Quality (AHRQ), under grant No. U18HS016964. The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the AHRQ. The funding source had no role in the design
or implementation of the study or in the decision to seek publication.;
Dr Fonarow reports receiving research support from the National Heart,
Lung, and Blood Institute (significant) and the Agency for Healthcare
Research and Quality (significant). Dr Fonarow reports receiving
consulting support from Medtronic (modest) and Novartis (significant).
Dr Schwamm reports serving as Chair of the Get With The Guidelines
National Steering Committee (unpaid). Dr Schwamm reports receiving
consulting support from Stroke Systems, Massachusetts Department of
Public Health. Dr Cannon reports receiving research support from
Accumetrics, AstraZeneca, GlaxoSmithKline, InteKrin Therapeutics, Merck,
and Takeda. Dr Cannon serves on the advisory board of Alnylam,
Bristol-Myers Squibb/Sanofi Partnership, Novartis. Dr Cannon serves as a
clinical advisor for and has equity in Automedics Medical Systems. Dr
Heidenreich reports receiving research support from Medtronic. Dr Bhatt
reports receiving research support from Astra Zeneca, Bristol-Myers
Squibb, Eisai, Sanofi Aventis, and The Medicines Company. Dr Peterson
serves as the principal investigator for the American Heart Association
for GWTG data analysis. Dr Hernandez reports receiving research support
from Johnson & Johnson and Amylin.
NR 22
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U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7713
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD NOV
PY 2011
VL 4
IS 6
BP 610
EP 618
DI 10.1161/CIRCOUTCOMES.111.961391
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 850BC
UT WOS:000297168400007
PM 22010200
ER
PT J
AU Kim, YY
Gauvreau, K
Bacha, EA
Landzberg, MJ
Benavidez, OJ
AF Kim, Yuli Y.
Gauvreau, Kimberlee
Bacha, Emile A.
Landzberg, Michael J.
Benavidez, Oscar J.
TI Resource Use Among Adult Congenital Heart Surgery Admissions in
Pediatric Hospitals Risk Factors for High Resource Utilization and
Association With Inpatient Death
SO CIRCULATION-CARDIOVASCULAR QUALITY AND OUTCOMES
LA English
DT Article
DE heart defects; congenital; surgery; risk factors; resource utilization
ID ARTERY-BYPASS-SURGERY; SURGICAL CASE VOLUMES; CARDIAC-SURGERY;
MORTALITY-RATES; HEALTH-CARE; GRAFT-SURGERY; DISEASE; DEPRESSION;
ANXIETY; COMORBIDITY
AB Background-Pediatric hospitals frequently perform congenital heart surgery in adults with congenital heart disease. The impact of these admissions on pediatric hospital resources is unknown. Our goals were to examine resource use by adults undergoing congenital heart surgery in pediatric hospitals, explore the association between high resource use (HRU) and inpatient death, and identify HRU risk factors.
Methods and Results-We obtained inpatient data from 42 pediatric hospitals from 2000 to 2008 and selected adult congenital heart (ACH) surgery admissions. We defined HRU admissions as those exceeding the 90th percentile for total hospital charges. We performed multivariable analyses using generalized estimating equations to identify risk factors for HRU. Of 97 563 congenital heart surgery admissions to pediatric hospitals, 3061 (3.1%) were adults, accounting for 2.2% of total hospital charges. The threshold for HRU was total hospital charges >=$213 803. Although HRU admissions comprised 10% of admissions, they accounted for 34% of charges for all ACH surgery admissions. Mortality rate was 16% for HRU admissions and 0.7% for others (P<0.001). Multivariable analysis demonstrated higher case complexity: risk category 2 (adjusted odds ratio [AOR], 3.6; P=0.02), risk category 3 (AOR, 13.7; P<0.001), and risk category 4 + (AOR, 30.7; P<0.001) as compared with risk category 1; DiGeorge syndrome (AOR, 4.2; P=0.006); depression (AOR, 3.1; P<0.001); weekend admission (AOR, 2.6; P<0.001); and government insurance (AOR, 2.0; P<0.001) as risk factors for HRU.
Conclusions-High resource use ACH surgery admissions are associated with significantly greater mortality rates. ACH admissions with greater surgical complexity, government insurance, DiGeorge syndrome, weekend admission, and depression were more likely to result in HRU. (Circ Cardiovasc Qual Outcomes. 2011;4:634-639.)
C1 [Gauvreau, Kimberlee; Landzberg, Michael J.; Benavidez, Oscar J.] Harvard Univ, Sch Med, Childrens Hosp Boston, Dept Cardiol, Boston, MA 02115 USA.
[Kim, Yuli Y.] Univ Penn, Sch Med, Hosp Univ Penn, Div Cardiol, Philadelphia, PA 19104 USA.
[Kim, Yuli Y.] Univ Penn, Childrens Hosp Philadelphia, Sch Med, Philadelphia, PA 19104 USA.
[Landzberg, Michael J.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Cardiol, Boston, MA 02115 USA.
[Benavidez, Oscar J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Pediat Congenital Cardiol, Boston, MA 02115 USA.
[Bacha, Emile A.] Columbia Univ, Coll Phys & Surg, Morgan Stanley Childrens Hosp New York, Dept Surg, New York, NY USA.
RP Benavidez, OJ (reprint author), Harvard Univ, Sch Med, Childrens Hosp Boston, Dept Cardiol, 300 Longwood Ave, Boston, MA 02115 USA.
EM Oscar.Benavidez@cardio.chboston.org
FU Dunlevie Family Endowed Fund; Robert Wood Johnson, Harold Amos Medical
Faculty; Children's Hospital Boston Department of Cardiology
FX This study was supported in part by the Dunlevie Family Endowed Fund for
Adult Congenital Heart Disease, Boston, MA. Dr Benavidez was supported
by the Robert Wood Johnson, Harold Amos Medical Faculty Program and the
Children's Hospital Boston Department of Cardiology.
NR 40
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U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-7713
J9 CIRC-CARDIOVASC QUAL
JI Circ.-Cardiovasc. Qual. Outcomes
PD NOV
PY 2011
VL 4
IS 6
BP 634
EP 639
DI 10.1161/CIRCOUTCOMES.111.963223
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 850BC
UT WOS:000297168400010
PM 22010202
ER
PT J
AU McDonald, WM
Durkalski, V
Ball, ER
Holtzheimer, PE
Pavlicova, M
Lisanby, SH
Avery, D
Anderson, BS
Nahas, Z
Zarkowski, P
Sackeim, HA
George, MS
AF McDonald, William M.
Durkalski, Valerie
Ball, Edward R., III
Holtzheimer, Paul E., III
Pavlicova, Martina
Lisanby, Sarah H.
Avery, David
Anderson, Berry S.
Nahas, Ziad
Zarkowski, Paul
Sackeim, Harold A.
George, Mark S.
TI IMPROVING THE ANTIDEPRESSANT EFFICACY OF TRANSCRANIAL MAGNETIC
STIMULATION: MAXIMIZING THE NUMBER OF STIMULATIONS AND TREATMENT
LOCATION IN TREATMENT-RESISTANT DEPRESSION
SO DEPRESSION AND ANXIETY
LA English
DT Article
DE transcranial magnetic stimulation; rTMS; high frequency rTMS; low
frequency rTMS; treatment-resistant depression
ID ASTERISK-D REPORT; MAJOR DEPRESSION; CONTROLLED-TRIAL; DISORDER;
OUTPATIENTS; THERAPY
AB Objective: To assess the efficacy of increasing the number of fast left repetitive transcranial magnetic stimulations (rTMS) (10 Hz @ 120% of motor threshold (MT) over the left dorsolateral prefrontal cortex (DLPFC)) needed to achieve remission in treatment-resistant depression (TRD). And, to determine if patients who do not remit to fast left will remit using slow right rTMS (1 Hz @ 120% MTover the right DLPFC). Method: Patients were part of a multicenter sham-controlled trial investigating the efficacy of fast left rTMS. Patients who failed to meet minimal response criteria in the sham-controlled study could enroll in this open fast left rTMS study for an additional 3-6 weeks. Patients who failed to remit to fast left could switch to slow right rTMS for up to 4 additional weeks. The final outcome measure was remission, defined as a HAM-D score of < 3 or 2 consecutive HAM-D scores less than 10. Results: Forty-three of 141 (30.5%) patients who enrolled in the open phase study eventually met criteria for remission. Patients who remitted during fast left treatment received a mean of 26 active treatments (90,000 pulses). Twenty-six percent of patients who failed fast left remitted during slow right treatment. Conclusion: The total number of rTMS stimulations needed to achieve remission in TRD may be higher than is used in most studies. TRD patients who do not respond to fast left rTMS may remit to slow right rTMS or additional rTMS stimulations. Depression and Anxiety 28: 973-980, 2011. (C) 2011 Wiley Periodicals, Inc.
C1 [McDonald, William M.] Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA 30329 USA.
[Durkalski, Valerie; Ball, Edward R., III] Med Univ S Carolina, Div Biostat & Epidemiol, Charleston, SC 29425 USA.
[Pavlicova, Martina] Columbia Univ Coll Phys & Surg, Dept Biostat, New York, NY 10032 USA.
[Lisanby, Sarah H.] Duke Univ, Dept Psychiat, Durham, NC 27706 USA.
[Avery, David; Zarkowski, Paul] Univ Washington, Dept Psychiat, Seattle, WA 98195 USA.
[Anderson, Berry S.; Nahas, Ziad; George, Mark S.] Med Univ S Carolina, Dept Psychiat, Charleston, SC 29425 USA.
[Sackeim, Harold A.] Columbia Univ Coll Phys & Surg, Dept Psychiat, New York, NY 10032 USA.
[George, Mark S.] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
RP McDonald, WM (reprint author), Emory Univ, Sch Med, Dept Psychiat & Behav Sci, 1841 Clifton Rd NE, Atlanta, GA 30329 USA.
EM wmcdona@emory.edu
RI Holtzheimer, Paul/B-6212-2015
OI Holtzheimer, Paul/0000-0002-3552-3296
FU National Institute of Mental Health (NIMH) [5R01MH069929, 5R01MH069887,
5R01MH069896, 5R01MH069895, 5R01MH069886]; St. Jude Medical
Neuromodulation; AvaCat Consulting; Tetragenex; Neuronetics; Advanced
Neuromodulatory Systems; Brainsway; Cyberonics; Takeda; MECTA
Corporation; Medtronic; PureTech Ventures; NeoStim and NeoSync;
Brainsonix; Cephos
FX This study was supported by the National Institute of Mental Health
(NIMH) as the Optimization of TMS for the Treatment of Depression Study
(OPT-TMS) involving grants 5R01MH069929 (Dr. Avery), 5R01MH069887 (Dr.
George), 5R01MH069896 (Dr. George), 5R01MH069895 (Dr. Lisanby), and
5R01MH069886 (Dr. McDonald).; The authors disclose the following
financial relationships within the past 3 years: Following a competitive
bid and request involving all TMS manufacturers at the time of trial
initiation, Neuronetics Inc. was selected and loaned the TMS devices,
head holders, and coils for the trial and allowed use of the safety
Investigational Device Exemption for their device. Neuronetics did not
provide any financial support for the study which was funded by the
NIMH. Potential conflicts are reported over the past 3 years. Dr.
McDonald is presently an unpaid consultant to NeoStim. Dr. Holtzheimer
reports consulting fees from St. Jude Medical Neuromodulation, AvaCat
Consulting, and Tetragenex, and is an unpaid consultant to NeoStim. Drs.
McDonald and Holtzheimer are faculty at Emory University which holds a
patent on TMS technology. Neither received royalties or is involved in
the development or promotion of this patent. Dr. Lisanby reports
research grants, speaking fees, or advisory board work with Neuronetics,
Advanced Neuromodulatory Systems, Brainsway, and Cyberonics. Dr. Lisanby
has a patent application with Columbia University on neuromodulation
technology for which she receives no royalties or compensation. Dr.
Avery has received research support from Neuronetics and Takeda, has
been a consultant for Neuronetics and has been on the speaker's bureau
for Eli Lilly, Takeda and Forest Pharmaceuticals. Dr. Nahas reports past
and current research grants, speaking fees or consulting work with
Cyberonics, Neuronetics, MECTA Corporation, and Medtronic. Dr. Nahas has
acted as an unpaid consultant for Neuropace. Dr. Sackeim received
consultant fees from MECTA Corporation and Cyberonics. Dr. George
received consultant fees from PureTech Ventures and reports research
grants, speaking fees, or advisory work with Brainsway, Mecta
Corporation, Neuronetics, Cephos, NeoStim and NeoSync, Brainsonix,
Cyberonics, and Cephos. Dr. George is faculty at MUSC which has two
patent applications in Dr. George's name combining MRI and TMS.
NR 16
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U1 0
U2 12
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1091-4269
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PD NOV
PY 2011
VL 28
IS 11
BP 973
EP 980
DI 10.1002/da.20885
PG 8
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 850TH
UT WOS:000297221800005
PM 21898711
ER
PT J
AU Deckersbach, T
Moshier, SJ
Tuschen-Caffier, B
Otto, MW
AF Deckersbach, Thilo
Moshier, Samantha J.
Tuschen-Caffier, Brunna
Otto, Michael W.
TI MEMORY DYSFUNCTION IN PANIC DISORDER: AN INVESTIGATION OF THE ROLE OF
CHRONIC BENZODIAZEPINE USE
SO DEPRESSION AND ANXIETY
LA English
DT Article
DE anxiety disorders; anxiolytic; benzodiazepine; tests;
neuropsychological; psychopharmacology; memory; short term; memory; long
term
ID OBSESSIVE-COMPULSIVE DISORDER; ANXIETY DISORDERS; NEUROPSYCHOLOGICAL
PERFORMANCE; COGNITIVE IMPAIRMENT; FRONTAL LOBES; DEFICITS; DEPRESSION;
WITHDRAWAL; AMPHETAMINE; METABOLISM
AB Background: Studies of the neurocognitive effects of long-term benzodiazepine use have been confounded by the presence of neurocognitive deficits characterizing the clinical conditions for which these medications are taken. Similarly, studies of the neurocognitive effects of anxiety disorders have been confounded by the inclusion of chronically benzodiazepine-medicated patients. This study was designed to tease apart the potentially confounding effects of long-term benzodiazepine use and panic disorder (PD) on memory and visuoconstructive abilities. Methods: Twenty chronically benzodiazepine-medicated and 20 benzodiazepine-free patients with PD with agoraphobia were compared with a group of 20 normal control participants, group-matched for age, education, and gender on a battery of neuropsychological tests assessing short-term, episodic long-term, and semantic memory, as well as visuoconstructive abilities. Results: Results indicated that benzodiazepine-free panic patients were relatively impaired in nonverbal short-term and nonverbal episodic long-term memory and visuoconstructive abilities, whereas verbal short-term and verbal episodic memory and semantic memory were preserved. Only limited evidence was found for more pronounced impairments in chronically benzodiazepine-medicated PD patients. Conclusions: This study provides evidence that patients with PD are characterized by relative impairments in nonverbal memory and visuoconstructive abilities, independent of benzodiazepine use. Nonetheless, we found evidence that chronic treatment with benzodiazepines is associated with intensification of select relative impairments in this realm. Documentation of these deficits raises questions about the broader etiology of neurocognitive impairment in PD as well as its impact on daily functioning. Depression and Anxiety 28: 999-1007, 2011. (C) 2011 Wiley Periodicals, Inc.
C1 [Deckersbach, Thilo] Massachusetts Gen Hosp, Bipolar Clin, Dept Psychiat, Boston, MA 02114 USA.
[Moshier, Samantha J.; Otto, Michael W.] Boston Univ, Ctr Anxiety & Related Disorders, Boston, MA 02215 USA.
[Tuschen-Caffier, Brunna] Univ Freiburg, Freiburg, Germany.
RP Deckersbach, T (reprint author), Massachusetts Gen Hosp, Bipolar Clin, Dept Psychiat, 50 Staniford St,Suite 580, Boston, MA 02114 USA.
EM tdeckersbach@partners.org
FU DAAD (German Academic Exchange Service); NIMH [MH081116]; NARSAD; TSA;
OCF; Organon (Merck); Medacorp; MGH Psychiatry Academy; BrainCells Inc.;
Systems Research and Applications Corporation; Boston University;
Catalan Agency for Health Technology Assessment and Research; National
Association of Social Workers Massachusetts; Massachusetts Medical
Society; Oxford University Press; NIH; NIA; Janssen Pharmaceuticals;
Forest Research Institute; Shire Development Inc.; Medtronic;
Cyberonics; Northstar; Pfizer
FX Dr. Deckersbach was funded by a DAAD (German Academic Exchange Service)
dissertation fellowship. Dr. Otto's effort on this project was supported
in part by MH081116.; The authors disclose the following financial
relationships within the past 3 years: Contract grant sponsor: NIMH;
Contract grant number: MH081116; Contract grant sponsors: NIMH; NARSAD;
TSA; OCF.; Disclosures: In the last 3 years, Dr. Otto has served as a
consultant for Organon (Merck), has received royalties for use of the
SIGH-A from Lilly, and received research support from Organon (Merck).
Dr. Deckersbach has received honoraria, consultation fees and/or
royalties from Medacorp, MGH Psychiatry Academy, BrainCells Inc.,
Systems Research and Applications Corporation, Boston University, the
Catalan Agency for Health Technology Assessment and Research, the
National Association of Social Workers Massachusetts, the Massachusetts
Medical Society, and Oxford University Press. He has also participated
in research funded by NIH, NIA, Janssen Pharmaceuticals, The Forest
Research Institute, Shire Development Inc., Medtronic, Cyberonics, and
Northstar. Dr. Tuschen-Caffier has received research support and
honoraria from Pfizer. Samantha J. Moshier and Brunna Tuschen-Caffier
have reported no conflict of interest.
NR 67
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U1 1
U2 13
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1091-4269
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PD NOV
PY 2011
VL 28
IS 11
BP 999
EP 1007
DI 10.1002/da.20891
PG 9
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 850TH
UT WOS:000297221800008
PM 22065537
ER
PT J
AU Gros, DF
Antony, MM
McCabe, RE
Lydiard, RB
AF Gros, Daniel F.
Antony, Martin M.
McCabe, Randi E.
Lydiard, R. Bruce
TI A PRELIMINARY INVESTIGATION OF THE EFFECTS OF COGNITIVE BEHAVIORAL
THERAPY FOR PANIC DISORDER ON GASTROINTESTINAL DISTRESS IN PATIENTS WITH
COMORBID PANIC DISORDER AND IRRITABLE BOWEL SYNDROME
SO DEPRESSION AND ANXIETY
LA English
DT Article
DE cognitive behavioral therapy; comorbidity; panic disorder; irritable
bowel syndrome
ID RANDOMIZED CONTROLLED-TRIAL; ANXIETY STRESS SCALES; DEPRESSION;
SYMPTOMS; DYSREGULATION; FIBROMYALGIA; CYTOKINES; AXIS; INFLAMMATION;
RELIABILITY
AB Background: High comorbidity between panic disorder with/without agoraphobia (PD/A) and irritable bowel syndrome (IBS) has been identified in the literature. These findings have resulted in the recent development of neurobiological models to explain their overlapping symptoms and related origins. This study was a preliminary investigation of the influence of cognitive behavioral therapy (CBT) for PD/A on PD/A patients with and without comorbid IBS. Methods: All patients completed a thorough intake assessment, brief waitlist period, and a 12-week CBT group for PD/A. Results: The results demonstrated significant reductions in the symptoms of anxiety, depression, and overall impairment in both patient groups (ts > 2.3; Ps <.05). In addition, PD/A patients with comorbid IBS also experienced reductions in the disability and distress associated with their gastrointestinal symptoms of IBS (ts > 1.9; Ps <.07). Conclusions: Although additional research still is needed, these preliminary findings suggest that CBT for PD/A can be used to simultaneously treat comorbid symptoms of PD/A and IBS. Implications for the neurobiological models for these comorbid conditions were discussed. Depression and Anxiety 28: 1027-1033, 2011. (C) 2011 Wiley Periodicals, Inc.
C1 [Gros, Daniel F.; Lydiard, R. Bruce] Ralph H Johnson VAMC, Mental Hlth Serv, Charleston, SC USA.
[Gros, Daniel F.; Lydiard, R. Bruce] Med Univ S Carolina, Dept Psychiat & Behav Sci, Charleston, SC 29425 USA.
[Antony, Martin M.] Ryerson Univ, Dept Psychol, Toronto, ON, Canada.
[Antony, Martin M.; McCabe, Randi E.] St Josephs Healthcare, Anxiety Treatment & Res Ctr, Hamilton, ON, Canada.
[McCabe, Randi E.] McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada.
RP Gros, DF (reprint author), Ralph H Johnson VAMC, Mental Hlth Serv 116, 109 Bee St, Charleston, SC 29401 USA.
EM grosd@musc.edu
RI Antony, Martin/K-1991-2012
OI Antony, Martin/0000-0002-3508-377X
FU Ralph H. Johnson VAMC
FX This material is the result of work supported with resources and the use
of facilities at the Ralph H. Johnson VAMC. 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.
NR 45
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U1 3
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1091-4269
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PD NOV
PY 2011
VL 28
IS 11
BP 1027
EP 1033
DI 10.1002/da.20863
PG 7
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 850TH
UT WOS:000297221800011
PM 21770001
ER
PT J
AU Patwardhan, V
Paul, S
Corey, KE
Mazhar, SM
Richter, JM
Thiim, M
Chung, RT
AF Patwardhan, Vilas
Paul, Sonali
Corey, Kathleen E.
Mazhar, Sameer M.
Richter, James M.
Thiim, Michael
Chung, Raymond T.
TI Hepatocellular Carcinoma Screening Rates Vary by Etiology of Cirrhosis
and Involvement of Gastrointestinal Sub-specialists
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Cirrhosis; Hepatocellular carcinoma; Screening; Non-alcoholic
steatohepatitis
ID UNITED-STATES; BARIATRIC SURGERY; LIVER-DISEASE; RISK-FACTORS;
HEPATITIS-C; CANCER; SURVEILLANCE; MANAGEMENT; SURVIVAL; OUTCOMES
AB Background Regular screening of cirrhotic patients for hepatocellular carcinoma (HCC) has been suboptimal, but there is little data regarding specific risk factors for reduced screening.
Methods From 1996 to 2010, patients with cirrhosis were retrospectively identified from outpatient gastroenterology and primary care practices. Data was obtained from the diagnosis of cirrhosis until the time of elevated alpha-fetoprotein (AFP) or lesion suspicious for HCC, death, liver transplantation, or end of the data collection period. Recommended screening was defined as abdominal imaging (ultrasound, contrast-enhanced CT, or MRI) with or without serum alpha-fetoprotein (AFP) at least once every 12 months based on professional guidelines.
Results One hundred fifty-six patients with cirrhosis were identified. The etiologies of cirrhosis were viral hepatitis (n = 65), alcohol (n = 40), non-alcoholic steatohepatitis (NASH) (n = 27), and non-viral, non-alcoholic, non-NASH cirrhosis (n = 24). Of the 156 patients, 51% received recommended screening for HCC. Patients with NASH cirrhosis received recommended screening significantly less (p = 0.016) than cirrhotics with viral hepatitis, alcoholic cirrhosis, or non-viral, non-alcoholic, non-NASH cirrhosis and were less likely to receive gastroenterology referral (p < 0.001). Additionally, 20 patients were diagnosed with cirrhosis incidentally during a surgical procedure. These patients were significantly less likely to receive recommended HCC screening than those diagnosed non-surgically (10.0 vs. 56.6%; p < 0.001). Screening was significantly more likely to occur in patients seen regularly by a gastrointestinal subspecialist (66.7 vs. 22.8%; p < 0.001).
Conclusions Patients with NASH cirrhosis and incidentally discovered cirrhosis have low rates of HCC screening and are referred less often to gastroenterologists. These data suggest a need for increased education about NASH cirrhosis and better systems of communication among general practitioners, surgeons, and gastroenterologists.
C1 [Patwardhan, Vilas; Paul, Sonali; Corey, Kathleen E.; Mazhar, Sameer M.; Richter, James M.; Thiim, Michael; Chung, Raymond T.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Corey, Kathleen E.; Mazhar, Sameer M.; Richter, James M.; Thiim, Michael; Chung, Raymond T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
RP Chung, RT (reprint author), Massachusetts Gen Hosp, Dept Med, Warren 1007,55 Fruit St, Boston, MA 02114 USA.
EM vpatwardhan@partners.org; spaul1@partners.org; kcorey@partners.org;
smazhar@partners.org; jrichter@partners.org; mthiim@partners.org;
rtchung@partners.org
FU NIH [DK078772]
FX We thank Dr. Kathleen Finn and Dr. Daniel Hunt for their critical
reading of this manuscript and their suggestions. Part of this work was
presented at a poster session at the 61st Annual Meeting of the American
Association for the Study of Liver Diseases; 2010 November 2; Boston,
MA. Raymond T. Chung was supported by NIH DK078772.
NR 26
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U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD NOV
PY 2011
VL 56
IS 11
BP 3316
EP 3322
DI 10.1007/s10620-011-1836-2
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 843AE
UT WOS:000296643400029
PM 21805170
ER
PT J
AU Kesari, S
Advani, SJ
Lawson, JD
Kahle, KT
Ng, K
Carter, B
Chen, CC
AF Kesari, Santosh
Advani, Sunil J.
Lawson, Joshua D.
Kahle, Kristopher T.
Ng, Kimberly
Carter, Bob
Chen, Clark C.
TI DNA damage response and repair: insights into strategies for radiation
sensitization of gliomas
SO FUTURE ONCOLOGY
LA English
DT Review
DE chemotherapy; DNA damage response; DNA double strand break repair;
glioblastoma; radiosensitization; radiotherapy
ID DOUBLE-STRAND BREAK; DIAGNOSED GLIOBLASTOMA-MULTIFORME; IN-VIVO
RADIOSENSITIZATION; SUSCEPTIBILITY GENE BRCA2; DEPENDENT PROTEIN-KINASE;
END-JOINING PATHWAYS; MAMMALIAN-CELLS; CANCER-CELLS; HOMOLOGOUS
RECOMBINATION; ADJUVANT TEMOZOLOMIDE
AB The incorporation of radiotherapy into multimodality treatment plans has led to significant improvements in glioma patient survival. However, local recurrence from glioma resistance to ionizing radiation remains a therapeutic challenge. The tumoricidal effect of radiation therapy is largely attributed to the induction of dsDNA breaks (DSBs). In the past decade, there have been tremendous strides in understanding the molecular mechanisms underlying DSB repair. The identification of gene products required for DSB repair has provided novel therapeutic targets. Recent studies revealed that many US FDA-approved cancer agents inhibit DSB repair by interacting with repair proteins. This article will aim to provide discussion of DSB repair mechanisms to provide molecular targets for radiation sensitization of gliomas and a discussion of FDA-approved cancer therapies that modulate DSB repair to highlight opportunities for combination therapy with radiotherapy for glioma therapy.
C1 [Chen, Clark C.] Univ Calif San Diego, Div Neurosurg, Moores Canc Ctr, Ctr Theoret & Appl Neurooncol, La Jolla, CA 92093 USA.
[Kesari, Santosh] Univ Calif San Diego, Moores UCSD Canc Ctr, Dept Neurosci, La Jolla, CA 92093 USA.
[Advani, Sunil J.; Lawson, Joshua D.] Univ Calif San Diego, Moores Canc Ctr, Dept Radiat Oncol, La Jolla, CA 92093 USA.
[Kahle, Kristopher T.] Harvard Univ, Sch Med, Boston, MA USA.
[Kahle, Kristopher T.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Ng, Kimberly; Chen, Clark C.] Dana Farber Canc Inst, Div Genom Stabil & DNA Repair, Dept Radiat Oncol, Boston, MA 02115 USA.
RP Chen, CC (reprint author), Univ Calif San Diego, Div Neurosurg, Moores Canc Ctr, Ctr Theoret & Appl Neurooncol, 3855 Hlth Sci Dr 0987, La Jolla, CA 92093 USA.
EM clarkchen@ucsd.edu
RI Kesari, Santosh/E-8461-2013
FU Doris Duke Charitable Foundation; Sontag Foundation; Burroughs Wellcome
Fund Career Awards for Medical Sciences; Kimmel Scholar award; American
Brain Tumor Association; National Cancer Institute; NIH [K08CA124804,
ARRA 3P30CA023100-25S8]; James S McDonnell Foundation
FX CC Chen is supported by the Doris Duke Charitable Foundation Clinical
Scientist Development Award, the Sontag Foundation Distinguished
Scientist Award, the Burroughs Wellcome Fund Career Awards for Medical
Sciences, the Kimmel Scholar award, a Discovery Grant from the American
Brain Tumor Association, and a National Cancer Institute K12 award. This
work was supported in part by grants from NIH K08CA124804, ARRA
3P30CA023100-25S8 and a James S McDonnell Foundation award to S Kesari.
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 104
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U1 1
U2 7
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1479-6694
J9 FUTURE ONCOL
JI Future Oncol.
PD NOV
PY 2011
VL 7
IS 11
BP 1335
EP 1346
DI 10.2217/FON.11.111
PG 12
WC Oncology
SC Oncology
GA 850SQ
UT WOS:000297219300014
PM 22044206
ER
PT J
AU Huang, ES
Karsan, S
Kanwal, F
Singh, I
Makhani, M
Spiegel, BM
AF Huang, Edward S.
Karsan, Sundip
Kanwal, Fasiha
Singh, Inder
Makhani, Marc
Spiegel, Brennan M.
TI Impact of nasogastric lavage on outcomes in acute GI bleeding
SO GASTROINTESTINAL ENDOSCOPY
LA English
DT Article
ID UPPER GASTROINTESTINAL HEMORRHAGE; RANDOMIZED CONTROLLED-TRIAL; NATIONAL
ASGE SURVEY; LENGTH-OF-STAY; CONSENSUS RECOMMENDATIONS; TRACT
HEMORRHAGE; EARLY ENDOSCOPY; MANAGEMENT; PREDICTORS; GUIDELINE
AB Background: Nasogastric lavage (NGL) is often performed early in the management of GI bleeding. This practice assumes that NGL results can assist with timely risk stratification and management.
Objective: We performed a retrospective analysis to test whether NGL is associated with improved process measures and outcomes in GI bleeding.
Design: Propensity-matched retrospective analysis.
Setting: University-based Veterans Affairs medical center.
Patients: A total of 632 patients admitted with GI bleeding.
Main Outcome Measurements: Thirty-day mortality rate, length of hospital stay, transfusion requirements, surgery, and time to endoscopy.
Results: Patients receiving NGL were more likely to take nonsteroidal anti-inflammatory drugs and be admitted to intensive care, but less likely to have metastatic disease or tachycardia, be taking warfarin, or present on weekdays. After propensity matching, NGL did not affect mortality (odds ratio [OR] 0.84; 95% confidence interval [CI], 0.37-1.92), length of hospital stay (7.3 vs 8.1 days, P = .57), surgery (OR 1.51; 95% CI, 0.42-5.43), or transfusions (3.2 vs 3.0 units, P = .94). However, NGL was associated with earlier time to endoscopy (hazard ratio 1.49; 95% CI, 1.09-2.04), and bloody aspirates were associated high-risk lesions (OR 2.69; 95% CI, 1.08-6.73).
Limitations: Retrospective design.
Conclusions: Performing NGL is associated with the earlier performance of endoscopy, but does not affect clinical outcomes. Performing NGL at initial triage may promote more timely process of care, but further studies will be needed to confirm these findings. (Gastrointest Endosc 2011; 74: 971-80.)
C1 [Huang, Edward S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit, Boston, MA USA.
[Karsan, Sundip; Makhani, Marc] Cedars Sinai Med Ctr, Dept Med, Los Angeles, CA 90048 USA.
[Karsan, Sundip; Makhani, Marc] Vet Affairs Greater Los Angeles Healthcare Syst, Dept Med, Los Angeles, CA USA.
[Spiegel, Brennan M.] Vet Affairs Greater Los Angeles Healthcare Syst, Div Gastroenterol & Hepatol, Los Angeles, CA USA.
[Kanwal, Fasiha] St Louis Univ, Sch Med, Div Gastroenterol & Hepatol, St Louis, MO USA.
[Singh, Inder; Spiegel, Brennan M.] Univ Calif Los Angeles, David Geffen Sch Med, Div Digest Dis, Los Angeles, CA 90095 USA.
[Kanwal, Fasiha; Spiegel, Brennan M.] UCLA VA Ctr Outcomes Res & Educ, Los Angeles, CA USA.
RP Spiegel, BM (reprint author), 11301 Wilshire Blvd,Bldg 115,Room 215, Los Angeles, CA 90073 USA.
EM bspiegel@mednet.ucla.edu
FU American Gastroenterological Association
FX The authors disclosed no financial relationships relevant to this
publication. Dr. Huang is supported by American Gastroenterological
Association Fellowship to Faculty Transition Award. There was no
external funding for this study. The opinions and assertions contained
herein are the sole views of the authors and are not to be construed as
official or as reflecting the views of the Department of Veteran
Affairs.
NR 31
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U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0016-5107
J9 GASTROINTEST ENDOSC
JI Gastrointest. Endosc.
PD NOV
PY 2011
VL 74
IS 5
BP 971
EP 980
DI 10.1016/j.gie.2011.04.045
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 845ZP
UT WOS:000296867300006
PM 21737077
ER
PT J
AU Yoo, H
Kang, D
Katz, AJ
Lauwers, GY
Nishioka, NS
Yagi, Y
Tanpowpong, P
Namati, J
Bouma, BE
Tearney, GJ
AF Yoo, Hongki
Kang, DongKyun
Katz, Aubrey J.
Lauwers, Gregory Y.
Nishioka, Norman S.
Yagi, Yukako
Tanpowpong, Pornthep
Namati, Jacqueline
Bouma, Brett E.
Tearney, Guillermo J.
TI Reflectance confocal microscopy for the diagnosis of eosinophilic
esophagitis: a pilot study conducted on biopsy specimens
SO GASTROINTESTINAL ENDOSCOPY
LA English
DT Article
ID ORAL VISCOUS BUDESONIDE; LIGHT-SCATTERING; BARRETTS-ESOPHAGUS;
FLUTICASONE PROPIONATE; LASER ENDOMICROSCOPY; CERVICAL CELLS;
ACETIC-ACID; CHILDREN; ADULTS; ENDOSCOPY
AB Background: Diagnosis of eosinophilic esophagitis (EoE) currently requires endoscopic biopsy and histopathologic analysis of the biopsy specimens to count intraepithelial eosinophils. Reflectance confocal microscopy (RCM) is an endomicroscopy technology that is capable of obtaining high-resolution, optically sectioned images of esophageal mucosa without the administration of exogenous contrast.
Objective: In this study, we investigated the capability of a high-speed form of RCM, termed spectrally encoded confocal microscopy (SECM), to count intraepithelial esophageal eosinophils and characterize other microscopic findings of EoE.
Design: A total of 43 biopsy samples from 35 pediatric patients and 8 biopsy samples from 8 adult patients undergoing EGD for EoE were imaged by SECM immediately after their removal and then processed for routine histopathology. Two SECM readers, trained on adult cases, prospectively counted intraepithelial eosinophils and detected the presence of abscess, degranulation, and basal cell hyperplasia on SECM images from the pediatric patients. A pathologist blinded to the SECM data analyzed the same from corresponding slides.
Setting: The Gastrointestinal Unit, Massachusetts General Hospital.
Results: Eosinophils by SECM demonstrated a higher reflectance than the surrounding cells and other inflammatory cells. There was good correlation between SECM and histology maximum eosinophil counts/high-power field (R = 0.76, P < .0001). Intra-and interobserver correlations for SECM counts were very good (R = 0.93 and R = 0.92, respectively; P < .0001). For the commonly used eosinophil count cutoff of 15 per high-power field, the sensitivity and specificity of SECM for EoE were 100%. The sensitivity and specificity for abscess, degranulation, and basal cell hyperplasia were 100% and 82%, 91% and 60%, and 94% and 80%, respectively. Intra-and interobserver agreements for these microscopic features of EoE were very good (kappa = 0.9/0.9, 0.84/1.0, 0.91/0.81, respectively).
Limitation: Ex vivo study.
Conclusions: This study demonstrates that RCM can be used to accurately count intraepithelial eosinophils and identify other microscopic abnormalities associated with EoE on freshly excised biopsy samples. These findings suggest that RCM may be developed into a tool for assessing eosinophilic infiltration in the esophagus in vivo. (Gastrointest Endosc 2011;74:992-1000.)
C1 [Yoo, Hongki; Kang, DongKyun; Namati, Jacqueline; Bouma, Brett E.; Tearney, Guillermo J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Yoo, Hongki; Kang, DongKyun; Namati, Jacqueline; Tearney, Guillermo J.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
[Lauwers, Gregory Y.; Yagi, Yukako] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Katz, Aubrey J.; Nishioka, Norman S.; Tanpowpong, Pornthep] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Katz, Aubrey J.; Tanpowpong, Pornthep] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Food Allergy Ctr, Boston, MA 02114 USA.
[Bouma, Brett E.; Tearney, Guillermo J.] Harvard MIT Hlth Sci & Technol, Cambridge, MA USA.
RP Tearney, GJ (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Wellman Ctr Photomed, 40 Parkman St,RSH 160A, Boston, MA 02114 USA.
RI Yoo, Hongki/B-6421-2013; Kang, Dongkyun/C-1085-2013
OI Yoo, Hongki/0000-0001-9819-3135; Kang, Dongkyun/0000-0001-5063-5387
FU Ninepoint Medical Inc.; National Institutes of Health [R21CA122161,
R01DK091923]
FX The following authors disclosed a financial relationship relevant to
this publication: Drs Tearney and Bouma consult for and receive
nonclinical sponsored research from Ninepoint Medical Inc. Ninepoint
Medical Inc. has a technology-licensing agreement with Massachusetts
General Hospital. Some authors (G.J.T., B.E.B., H.Y., D.K.) have rights
to receive royalties as a result of this licensing arrangement. Dr.
Namati works as a consultant for and has equity interest in Ninepoint
Medical Inc. The other authors disclosed no financial relationships
relevant to this publication. This research was supported in part by
National Institutes of Health (grant numbers R21CA122161 and
R01DK091923).
NR 59
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U1 0
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0016-5107
J9 GASTROINTEST ENDOSC
JI Gastrointest. Endosc.
PD NOV
PY 2011
VL 74
IS 5
BP 992
EP 1000
DI 10.1016/j.gie.2011.07.020
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 845ZP
UT WOS:000296867300009
PM 21944314
ER
PT J
AU van Duin, M
Broyl, A
de Knegt, Y
Goldschmidt, H
Richardson, PG
Hop, WCJ
van der Holt, B
Joseph-Pietras, D
Mulligan, G
Neuwirth, R
Sahota, SS
Sonneveld, P
AF van Duin, Mark
Broyl, Annemiek
de Knegt, Yvonne
Goldschmidt, Hartmut
Richardson, Paul G.
Hop, Wim C. J.
van der Holt, Bronno
Joseph-Pietras, Debora
Mulligan, George
Neuwirth, Rachel
Sahota, Surinder S.
Sonneveld, Pieter
TI Cancer testis antigens in newly diagnosed and relapse multiple myeloma:
prognostic markers and potential targets for immunotherapy
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Article
DE multiple myeloma; relapse; testis antigen expression; prognosis;
immunotherapy
ID KINASE-INTERACTING PROTEIN; GENE-EXPRESSION; MOLECULAR CLASSIFICATION;
STRUCTURAL HOMOLOGY; DNA VACCINES; STEM-CELLS; T-CELLS; BORTEZOMIB;
PROLIFERATION; MAGE-C1/CT7
AB Background
In multiple myeloma, expression of cancer testis antigens may provide prognostic markers and potential targets for immunotherapy. Expression at relapse has not yet been evaluated for a large panel of cancer testis antigens which can be classified by varying expression in normal tissue: restricted to testis, expressed in testis and brain and not restricted but selectively expressed in testis.
Design and Methods
Evaluation of cancer testis antigen expression was made in newly diagnosed multiple myeloma cases (HOVON-65/GMMG-HD4 trial; n=320) and in relapse cases (APEX, SUMMIT, CREST trials; n=264). Presence of expression using Affymetrix GeneChips was determined for 123 cancer testis antigens. Of these 87 had a frequency of more than 5% in the newly diagnosed and relapsed patients, and were evaluated in detail.
Results
Tissue restriction was known for 58 out of 87 cancer testis antigens. A significantly lower frequency of presence calls in the relapsed compared to newly diagnosed cases was found for 3 out of 13 testis restricted genes, 2 out of 7 testis/brain restricted genes, and 17 out of 38 testis selective genes. MAGEC1, MAGEB2 and SSX1 were the most frequent testis-restricted cancer testis antigens in both data sets. Multivariate analysis demonstrated that presence of MAGEA6 and CDCA1 were clearly associated with shorter progression free survival, and presence of MAGEA9 with shorter overall survival in the set of newly diagnosed cases. In the set of relapse cases, presence of CTAG2 was associated with shorter progression free survival and presence of SSX1 with shorter overall survival.
Conclusions
Relapsed multiple myeloma reveals extensive cancer testis antigen expression. Cancer testis antigens are confirmed as useful prognostic markers in newly diagnosed multiple myeloma patients and in relapsed multiple myeloma patients.
C1 [van Duin, Mark; Broyl, Annemiek; de Knegt, Yvonne; Sonneveld, Pieter] Erasmus MC, Dept Hematol, Rotterdam, Netherlands.
[Goldschmidt, Hartmut] Univ Heidelberg, Dept Internal Med, Div Hematol Oncol, Sect Multiple Myeloma, D-6900 Heidelberg, Germany.
[Richardson, Paul G.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[van Duin, Mark; Hop, Wim C. J.] Erasmus MC, Dept Biostat, NL-3015 GE Rotterdam, Netherlands.
[van der Holt, Bronno] Erasmus MC Daniel den Hoed, HOVON Data Ctr, Rotterdam, Netherlands.
[Joseph-Pietras, Debora; Sahota, Surinder S.] Univ Southampton, Sch Med, Canc Sci Div, Southampton SO9 5NH, Hants, England.
[Mulligan, George; Neuwirth, Rachel] Millennium Pharmaceut Inc, Cambridge, MA USA.
RP van Duin, M (reprint author), Erasmus MC, Dept Biostat, Ee1391B,Dr Molewaterpl 50, NL-3015 GE Rotterdam, Netherlands.
EM m.vanduin@erasmusmc.nl
FU Leukemia Research Foundation (UK); Myeloma Stem Cell Network (MSCNET)
FX this study was funded by Leukemia Research Foundation (UK) and the
Myeloma Stem Cell Network (MSCNET/FP6).
NR 51
TC 27
Z9 27
U1 0
U2 4
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOL-HEMATOL J
JI Haematol-Hematol. J.
PD NOV
PY 2011
VL 96
IS 11
BP 1662
EP 1669
DI 10.3324/haematol.2010.037978
PG 8
WC Hematology
SC Hematology
GA 851BR
UT WOS:000297243800016
PM 21791470
ER
PT J
AU Jalovec, K
Swick, S
Becker, C
Reifsnyder, R
AF Jalovec, Kathryn
Swick, Susan
Becker, Corky
Reifsnyder, Robert
TI When the Lightning Rod Leaves Home: A Family Therapy Case Characterized
by Successive Generations of Familial Conflict During a Transition into
Young Adulthood
SO HARVARD REVIEW OF PSYCHIATRY
LA English
DT Article
DE eating disorder; family therapy; young adulthood
ID ANOREXIA-NERVOSA; PARENTAL CANCER; BULIMIA-NERVOSA; ADOLESCENTS;
CHILDREN; IMPACT
C1 [Jalovec, Kathryn; Swick, Susan; Reifsnyder, Robert] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Jalovec, Kathryn; Swick, Susan; Reifsnyder, Robert] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Becker, Corky] Cambridge Hosp, Cambridge, MA 02139 USA.
RP Jalovec, K (reprint author), 4535 Harding Rd,Suite 102, Nashville, TN 37205 USA.
EM kathryncody@gmail.com
NR 22
TC 0
Z9 0
U1 0
U2 2
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1067-3229
J9 HARVARD REV PSYCHIAT
JI Harv. Rev. Psychiatr.
PD NOV-DEC
PY 2011
VL 19
IS 6
BP 302
EP 312
DI 10.3109/10673229.2011.632600
PG 11
WC Psychiatry
SC Psychiatry
GA 850BT
UT WOS:000297170100003
PM 22098326
ER
PT J
AU Chang, MC
DeCaro, JJ
Zheng, M
Gearing, M
Shubeck, L
Sherman, SL
Welt, CK
AF Chang, Martin C.
DeCaro, John J.
Zheng, Mei
Gearing, Marla
Shubeck, Lisa
Sherman, Stephanie L.
Welt, Corrine K.
TI Ovarian histopathological and ubiquitin-immunophenotypic features in
fragile X-associated primary ovarian insufficiency: a study of five
cases and selected controls
SO HISTOPATHOLOGY
LA English
DT Letter
ID PREMUTATION CARRIERS; CGG REPEAT; EXPANSION; RNA
C1 [Chang, Martin C.] Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON M5G 1X5, Canada.
[DeCaro, John J.; Sherman, Stephanie L.] Emory Univ, Dept Human Genet, Atlanta, GA 30322 USA.
[Zheng, Mei] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Gearing, Marla; Shubeck, Lisa] Emory Univ, Dept Pathol & Lab Med, Atlanta, GA 30322 USA.
[Welt, Corrine K.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Chang, MC (reprint author), Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON M5G 1X5, Canada.
RI Chang, Martin/J-2329-2016;
OI Welt, Corrine/0000-0002-8219-5504
FU NICHD NIH HHS [R01 HD029909-14, R01 HD029909, R01 HD29909]
NR 11
TC 3
Z9 4
U1 1
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0309-0167
J9 HISTOPATHOLOGY
JI Histopathology
PD NOV
PY 2011
VL 59
IS 5
BP 1018
EP 1023
DI 10.1111/j.1365-2559.2011.03959.x
PG 6
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA 851CC
UT WOS:000297244900029
PM 22007616
ER
PT J
AU Pal, J
Sanal, MG
Gopal, GJ
AF Pal, Jagannath
Sanal, Madhusudana Girija
Gopal, Gopal Jee
TI Vitamin-C as anti-Helicobacter pylori agent: More prophylactic than
curative- Critical review
SO INDIAN JOURNAL OF PHARMACOLOGY
LA English
DT Review
DE Helicobacter pylori; prophylactic; supplementation; urease; vitamin C
ID PROTON PUMP INHIBITORS; ASCORBIC-ACID; GASTRIC-JUICE; ERADICATION RATE;
TRIPLE THERAPY; HUMAN STOMACH; INFECTION; UREASE; SUPPLEMENTATION;
NITROIMIDAZOLES
AB Potential of nonantibiotic therapies for treatment of Helicobacter pylori-related acid peptic disease remains underexplored. Several clinical studies have shown that higher prevalence of H. pylori infection is associated with low Vitamin C (Vit C) level in serum and gastric juice. However, there is no consensus regarding the usefulness of Vit C supplementation in the management of H. pylori infection. Surveying the existing literature we conclude that high concentration of Vit C in gastric juice might inactivate H. pylori urease, the key enzyme for the pathogen's survival and colonization into acidic stomach. Once infection established, urease is not very important for its survival. The role of Vit-C as anti-H. pylori agent in peptic ulcer diseases appears to be preventive rather than curative. Rather than supplementing high dose of Vit C along with conventional triple therapy, it is preferable to complete the conventional therapy and thereafter start Vit C supplementation for extended period which would prevent reinfection in susceptible individuals, provided the patients are not achlorhydric. Further studies are required to prove the role of Vit C in susceptible population.
C1 [Pal, Jagannath] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Sanal, Madhusudana Girija] Inst Liver & Biliary Sci, Dept Res, New Delhi 110070, India.
[Gopal, Gopal Jee] Jawaharlal Nehru Univ, Special Ctr Mol Med, New Delhi 110067, India.
RP Pal, J (reprint author), Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
EM jagannath_pal@dfci.harvard.edu
NR 45
TC 3
Z9 3
U1 1
U2 4
PU MEDKNOW PUBLICATIONS
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
INDIA
SN 0019-5472
J9 INDIAN J PHARMACOL
JI Indian J. Pharmacol.
PD NOV-DEC
PY 2011
VL 43
IS 6
BP 624
EP 627
DI 10.4103/0253-7613.89814
PG 4
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 850UL
UT WOS:000297224900002
PM 22144762
ER
PT J
AU Rosenblatt, LE
Gorantla, S
Torres, JA
Yarmush, RS
Rao, S
Park, ER
Denninger, JW
Benson, H
Fricchione, GL
Bernstein, B
Levine, JB
AF Rosenblatt, Lucy E.
Gorantla, Sasikanth
Torres, Jodi A.
Yarmush, Rubin S.
Rao, Surita
Park, Elyse R.
Denninger, John W.
Benson, Herbert
Fricchione, Gregory L.
Bernstein, Bruce
Levine, John B.
TI Relaxation Response-Based Yoga Improves Functioning in Young Children
with Autism: A Pilot Study
SO JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE
LA English
DT Article
ID ABERRANT BEHAVIOR CHECKLIST; PERVASIVE DEVELOPMENTAL DISORDERS; BRAIN
GABA LEVELS; SPECTRUM DISORDERS; ATYPICAL ANTIPSYCHOTICS; ASSESSMENT
SYSTEM; ADOLESCENTS; VALIDITY; COMPLEMENTARY; INTERVENTION
AB Objectives: The study objectives were to develop and objectively assess the therapeutic effect of a novel movement-based complementary and alternative medicine approach for children with an autism-spectrum disorder (ASD).
Design: A within-subject analysis comparing pre- to post-treatment scores on two standard measures of childhood behavioral problems was used.
Settings and location: The intervention and data analysis occurred at a tertiary care, medical school teaching hospital.
Subjects: Twenty-four (24) children aged 3-16 years with a diagnosis of an ASD comprised the study group.
Intervention: The efficacy of an 8-week multimodal yoga, dance, and music therapy program based on the relaxation response (RR) was developed and examined.
Outcome measures: The study outcome was measured using The Behavioral Assessment System for Children, Second Edition (BASC-2) and the Aberrant Behavioral Checklist (ABC).
Results: Robust changes were found on the BASC-2, primarily for 5-12-year-old children. Unexpectedly, the post-treatment scores on the Atypicality scale of the BASC-2, which measures some of the core features of autism, changed significantly (p = 0.003).
Conclusions: A movement-based, modified RR program, involving yoga and dance, showed efficacy in treating behavioral and some core features of autism, particularly for latency-age children.
C1 [Yarmush, Rubin S.; Denninger, John W.; Benson, Herbert; Fricchione, Gregory L.; Levine, John B.] Massachusetts Gen Hosp, Benson Henry Inst Mind Body Med, Boston, MA 02114 USA.
[Rosenblatt, Lucy E.; Gorantla, Sasikanth; Torres, Jodi A.; Yarmush, Rubin S.; Rao, Surita; Bernstein, Bruce; Levine, John B.] St Francis Hosp & Med Ctr, Dept Psychiat, Hartford, CT USA.
[Gorantla, Sasikanth; Park, Elyse R.] Univ Hartford, Dept Psychiat, Hartford, CT USA.
[Rao, Surita; Bernstein, Bruce] Univ Connecticut, Dept Psychiat, Farmington, CT 06107 USA.
[Park, Elyse R.; Denninger, John W.; Benson, Herbert; Fricchione, Gregory L.; Levine, John B.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
RP Levine, JB (reprint author), Massachusetts Gen Hosp, Benson Henry Inst Mind Body Med, 151 Merrimac St,4th Floor, Boston, MA 02114 USA.
EM jblevine@partners.org
RI Levine, John/G-6221-2015
FU Centers for Disease Control and Prevention [5R01DP000339]; Department of
Innovation and Quality Integration, Saint Francis Hospital and Medical
Center
FX This investigation was supported by funds from the Centers for Disease
Control and Prevention, Grant number 5R01DP000339, and a grant from the
Department of Innovation and Quality Integration, Saint Francis Hospital
and Medical Center.
NR 39
TC 13
Z9 15
U1 4
U2 47
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1075-5535
J9 J ALTERN COMPLEM MED
JI J. Altern. Complement Med.
PD NOV
PY 2011
VL 17
IS 11
BP 1029
EP 1035
DI 10.1089/acm.2010.0834
PG 7
WC Integrative & Complementary Medicine
SC Integrative & Complementary Medicine
GA 850SA
UT WOS:000297217000010
PM 21992466
ER
PT J
AU Sidhu, MS
Venkatesh, V
Hoffmann, U
Ghoshhajra, BB
AF Sidhu, Manavjot S.
Venkatesh, Vikram
Hoffmann, Udo
Ghoshhajra, Brian B.
TI Advanced Adaptive Axial-Sequential Prospectively
Electrocardiogram-Triggered Dual-Source Coronary Computed Tomographic
Angiography in a Patient With Atrial Fibrillation
SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY
LA English
DT Article
DE atrial fibrillation; dual-source coronary CT angiography
ID ARTERY-DISEASE
AB Atrial fibrillation is considered a relative contraindication to coronary computed tomographic angiography (CCTA) because image quality and radiation dose-saving measures largely depend on low and stable heart rates. Most published experiences with CCTA during atrial fibrillation have relied on retrospective gating to mitigate artifacts via electrocardiogram editing. However, a large number of patients arrive at the CT suite with irregular heart rates. We present a case in which we used a prospectively electrocardiogram-triggered axial-sequential scan mode with a novel arrhythmia protection algorithm to obtain motion-free, high-quality CCTA images at a low radiation dose.
C1 [Sidhu, Manavjot S.] Massachusetts Gen Hosp, Dept Radiol, Cardiac MR PET CT Program, Dept Cardiovasc Imaging, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Sidhu, Manavjot S.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Sidhu, MS (reprint author), Massachusetts Gen Hosp, Dept Radiol, Cardiac MR PET CT Program, Dept Cardiovasc Imaging, 165 Cambridge St,Suite 400, Boston, MA 02114 USA.
EM msidhu1@partners.org
NR 4
TC 5
Z9 8
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0363-8715
J9 J COMPUT ASSIST TOMO
JI J. Comput. Assist. Tomogr.
PD NOV-DEC
PY 2011
VL 35
IS 6
BP 747
EP 748
DI 10.1097/RCT.0b013e3182355960
PG 2
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 849GJ
UT WOS:000297113300015
PM 22082547
ER
PT J
AU Smart, RJ
Marsh, S
Rosenberg, M
AF Smart, Ryan J.
Marsh, Shawn
Rosenberg, Morton
TI Intraosseous Access in Oral and Maxillofacial Surgical Practice
SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
ID CARDIOPULMONARY-RESUSCITATION; INFUSION DEVICES; HUMERUS; ADULTS
C1 [Smart, Ryan J.] Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Boston, MA 02114 USA.
[Marsh, Shawn; Rosenberg, Morton] Tufts Univ, Sch Dent Med, Dept Oral & Maxillofacial Surg, Boston, MA 02111 USA.
[Rosenberg, Morton] Tufts Univ, Sch Dent Med, Div Anesthesia & Pain Control, Boston, MA 02111 USA.
[Rosenberg, Morton] Tufts Univ, Sch Med, Boston, MA 02111 USA.
RP Smart, RJ (reprint author), Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Warren 1201,55 Fruit St, Boston, MA 02114 USA.
EM rjsmart@partners.org
NR 23
TC 0
Z9 0
U1 1
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0278-2391
J9 J ORAL MAXIL SURG
JI J. Oral Maxillofac. Surg.
PD NOV
PY 2011
VL 69
IS 11
BP 2708
EP 2713
DI 10.1016/j.joms.2011.02.101
PG 6
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 849PQ
UT WOS:000297138000007
PM 21757277
ER
PT J
AU Susarla, SM
Abramson, ZR
Dodson, TB
Kaban, LB
AF Susarla, Srinivas M.
Abramson, Zachary R.
Dodson, Thomas B.
Kaban, Leonard B.
TI Upper Airway Length Decreases After Maxillomandibular Advancement in
Patients With Obstructive Sleep Apnea
SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY
LA English
DT Article
ID COMPUTED TOMOGRAPHIC ANALYSIS; SURGERY; ANATOMY
AB Purpose: Most reports on airway anatomy after maxillomandibular advancement (MMA) for obstructive sleep apnea (OSA) have focused on changes in airway diameter, ie, posterior airway space (PAS), rather than airway length. The purpose of this study was to evaluate changes in cephalometrically measured upper airway length (UAL) after MMA.
Materials and Methods: This was a retrospective cohort study. The sample was composed of subjects who underwent MMA for OSA. The primary outcome measurement was change in UAL measured on lateral cephalograms. Predictor variables included patient demographic and cephalometric characteristics. Secondary outcome measurements were changes in sleep disturbance. Descriptive, bivariate, and regression statistics were computed. For all analyses, P <= .05 was considered statistically significant.
Results: The sample included 23 adult subjects (mean age, 39.3 +/- 12.1 years; 6 women). Subjects had average maxillary and mandibular advancements of 9.8 +/- 2.0 and 10.8 +/- 2.2 mm, respectively. Mean pre- and postoperative UALs were 75.8 +/- 7.0 and 67.0 +/- 5.7 mm, respectively (P <.001). Mean pre- and postoperative respiratory disturbance indexes were 53.2 +/- 22.4 and 19.0 +/- 12.0 events/hour, respectively (P = .003). All patients had improvement in OSA symptoms, but 3 (13%) required continuous positive airway pressure.
Conclusion: The results of this study suggest that UAL decreases as a result of MMA. In addition, these results support the observation that MMA is associated with objective and subjective improvements in patients with OSA. (C) 2011 American Association of Oral and Maxillofacial Surgeons j Oral Maxi llofac Surg 69:2872-2878, 2011
C1 [Susarla, Srinivas M.; Abramson, Zachary R.; Kaban, Leonard B.] Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, Boston, MA 02114 USA.
[Dodson, Thomas B.] Massachusetts Gen Hosp, Ctr Appl Clin Invest, Boston, MA 02114 USA.
[Dodson, Thomas B.; Kaban, Leonard B.] Harvard Univ, Sch Dent Med, Boston, MA 02115 USA.
RP Susarla, SM (reprint author), Massachusetts Gen Hosp, Dept Oral & Maxillofacial Surg, WACC230, Boston, MA 02114 USA.
EM ssusarla1@partners.org
OI Susarla, Srinivas/0000-0003-0155-8260
FU Oral and Maxillofacial Surgery Foundation; AO/Synthes Research
Fellowship in Pediatric Maxillofacial Surgery; Massachusetts General
Hospital Department of Oral and Maxillofacial Surgery Education and
Research; Center for Applied Clinical Investigation; Massachusetts
General Physicians Organization
FX This study was completed with support from the Oral and Maxillofacial
Surgery Foundation Fellowship in Clinical Investigation (S.M.S.), the
AO/Synthes Research Fellowship in Pediatric Maxillofacial Surgery
(Z.R.A.), the Massachusetts General Hospital Department of Oral and
Maxillofacial Surgery Education and Research Fund (S.M.S., Z.R.A.) and
the Center for Applied Clinical Investigation (T.B.D., S.M.S.), and the
Massachusetts General Physicians Organization (T.B.D.,
NR 15
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Z9 17
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 0278-2391
J9 J ORAL MAXIL SURG
JI J. Oral Maxillofac. Surg.
PD NOV
PY 2011
VL 69
IS 11
BP 2872
EP 2878
DI 10.1016/j.joms.2011.01.005
PG 7
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 849PQ
UT WOS:000297138000034
PM 21507540
ER
PT J
AU Shin, JM
Inatomi, N
Munson, K
Strugatsky, D
Tokhtaeva, E
Vagin, O
Sachs, G
AF Shin, Jai Moo
Inatomi, Nobuhiro
Munson, Keith
Strugatsky, David
Tokhtaeva, Elmira
Vagin, Olga
Sachs, George
TI Characterization of a Novel Potassium-Competitive Acid Blocker of the
Gastric H,K-ATPase,
1-[5-(2-Fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl]-N-methylm
ethanamine Monofumarate (TAK-438)
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID GASTROESOPHAGEAL-REFLUX DISEASE; PROTON PUMP INHIBITOR; BINDING-SITES;
ESOMEPRAZOLE; H+,K+-ATPASE; ATPASE; LANSOPRAZOLE; SECRETION; MEMBRANES;
VESICLES
AB Inhibition of the gastric H, K-ATPase by the potassium-competitive acid blocker (P-CAB) 1-[5-(2-fluorophenyl)-1-(pyridin-3-ylsulfonyl)-1H-pyrrol-3-yl]-N-methylmethanamine (TAK-438), is strictly K(+)-competitive with a K(i) of 10 nM at pH 7. In contrast to previous P-CABs, this structure has a point positive charge (pK(a) 9.06) allowing for greater accumulation in parietal cells compared with previous P-CABs [e.g., (8-benzyloxy-2-methyl-imidazo(1,2-a)pyridin-3-yl)acetonitrile (SCH28080), pK(a) 5.6]. The dissociation rate of the compound from the isolated ATPase is slower than other P-CABs, with the t(1/2) being 7.5 h in 20 mM KCl at pH 7. The stoichiometry of binding of TAK-438 to the H,K-ATPase is 2.2 nmol/mg in the presence of Mg-ATP, vanadate, or MgP(i). However, TAK-438 also binds enzyme at 1.3 nmol/mg in the absence of Mg(2+). Modeling of the H, K-ATPase to the homologous Na,K-ATPase predicts a close approach and hydrogen bonding between the positively charged N-methylamino group and the negatively charged Glu795 in the K(+)-binding site in contrast to the planar diffuse positive charge of previous P-CABs. This probably accounts for the slow dissociation and high affinity. The model also predicts hydrogen bonding between the hydroxyl of Tyr799 and the oxygens of the sulfonyl group of TAK-438. A Tyr799Phe mutation resulted in a 3-fold increase of the dissociation rate, showing that this hydrogen bonding also contributes to the slow dissociation rate. Hence, this K(+)-competitive inhibitor of the gastric H,K-ATPase should provide longer-lasting inhibition of gastric acid secretion compared with previous drugs of this class.
C1 [Shin, Jai Moo] VA Greater Los Angeles Healthcare Syst, Membrane Biol Lab, Los Angeles, CA 90073 USA.
[Shin, Jai Moo; Munson, Keith; Strugatsky, David; Tokhtaeva, Elmira; Vagin, Olga; Sachs, George] Univ Calif Los Angeles, David Geffen Sch Med, Dept Physiol & Med, Los Angeles, CA 90024 USA.
[Inatomi, Nobuhiro] Takeda Pharmaceut Co Ltd, Div Pharmaceut Res, Osaka, Japan.
RP Shin, JM (reprint author), VA Greater Los Angeles Healthcare Syst, Membrane Biol Lab, 11301 Wilshire Blvd,Bldg 113,Rm 324, Los Angeles, CA 90073 USA.
EM jaishin@ucla.edu
FU Takeda Pharmaceutical Company Limited; National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases
[DK053642, DK058333, DK077149]; U.S. VA Merit Grant Award
[I01BX001006-01]
FX This work was supported by Takeda Pharmaceutical Company Limited; the
National Institutes of Health National Institute of Diabetes and
Digestive and Kidney Diseases [Grants DK053642, DK058333, DK077149]; and
a U.S. VA Merit Grant Award [I01BX001006-01].
NR 30
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Z9 42
U1 0
U2 10
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD NOV
PY 2011
VL 339
IS 2
BP 412
EP 420
DI 10.1124/jpet.111.185314
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 840TS
UT WOS:000296464800011
PM 21828261
ER
PT J
AU Wang, JH
Inoue, T
Higashiyama, M
Guth, PH
Engel, E
Kaunitz, JD
Akiba, Y
AF Wang, Joon-Ho
Inoue, Takuya
Higashiyama, Masaaki
Guth, Paul H.
Engel, Eli
Kaunitz, Jonathan D.
Akiba, Yasutada
TI Umami Receptor Activation Increases Duodenal Bicarbonate Secretion via
Glucagon-Like Peptide-2 Release in Rats
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID VASOACTIVE INTESTINAL POLYPEPTIDE; PIG SMALL-INTESTINE; ENTEROENDOCRINE
CELLS; TASTE RECEPTORS; GLP-2 RECEPTOR; GUT; ACID; STIMULATION;
MECHANISMS; TRANSPORT
AB Luminal nutrient chemosensing during meal ingestion is mediated by intestinal endocrine cells, which regulate secretion and motility via the release of gut hormones. We have reported that luminal coperfusion of L-Glu and IMP, common condiments providing the umami or proteinaceous taste, synergistically increases duodenal bicarbonate secretion (DBS) possibly via taste receptor heterodimers, taste receptor type 1, member 1 (T1R1)/R3. We hypothesized that glucose-dependent insulinotropic peptide (GIP) or glucagon-like peptide (GLP) is released by duodenal perfusion with L-Glu/IMP. We measured DBS with pH and CO(2) electrodes through a perfused rat duodenal loop in vivo. GIP, exendin (Ex)-4 (GLP-1 receptor agonist), or GLP-2 was intravenously infused (0.01-1 nmol/kg/h). L-Glu (10 mM) and IMP (0.1 mM) were luminally perfused with or without bolus intravenous injection (3 or 30 nmol/kg) of the receptor antagonists Pro(3)GIP, Ex-3(9-39), or GLP-2(3-33). GIP or GLP-2 infusion dose-dependently increased DBS, whereas Ex-4 infusion gradually decreased DBS. Luminal perfusion of L-Glu/IMP increased DBS, with no effect of Pro(3)GIP or Ex-3(9-39), whereas GLP-2(3-33) inhibited L-Glu/IMP-induced DBS. Vasoactive intestinal peptide (VIP)(6-28) intravenously or N(G)-nitro-L-arginine methyl ester coperfusion inhibited the effect of L-Glu/IMP. Perfusion of L-Glu/IMP increased portal venous concentrations of GLP-2, followed by a delayed increase of GLP-1, with no effect on GIP release. GLP-1/2 and T1R1/R3 were expressed in duodenal endocrine-like cells. These results suggest that luminal L-Glu/IMP-induced DBS is mediated via GLP-2 release and receptor activation followed by VIP and nitric oxide release. Because GLP-1 is insulinotropic and GLP-2 is intestinotrophic, umami receptor activation may have additional benefits in glucose metabolism and duodenal mucosal protection and regeneration.
C1 [Wang, Joon-Ho; Inoue, Takuya; Higashiyama, Masaaki; Kaunitz, Jonathan D.; Akiba, Yasutada] Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90024 USA.
[Engel, Eli] Univ Calif Los Angeles, Dept Biomath, Los Angeles, CA USA.
Greater Los Angeles Vet Affairs Healthcare Syst, Los Angeles, CA USA.
[Kaunitz, Jonathan D.; Akiba, Yasutada] Brentwood Biomed Res Inst, Los Angeles, CA USA.
RP Akiba, Y (reprint author), W Los Angeles VA Med Ctr, 11301 Wilshire Blvd,Bldg 114,Suite 217, Los Angeles, CA 90073 USA.
EM yakiba@mednet.ucla.edu
FU Ajinomoto, Inc. (Tokyo, Japan); Department of Veterans Affairs Merit
Review Award; National Institutes of Health National Institute of
Diabetes and Digestive and Kidney Diseases [R01-DK54221, P30-DK0413]
FX This work was supported by a research grant from Ajinomoto, Inc. (Tokyo,
Japan) (to Y.A.); a Department of Veterans Affairs Merit Review Award
(to J.D.K.); the National Institutes of Health National Institute of
Diabetes and Digestive and Kidney Diseases [Grant R01-DK54221] (to
J.D.K.); and the Animal Core of the National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases [Grant
P30-DK0413] (to J. E. Rozengurt).
NR 42
TC 38
Z9 39
U1 1
U2 5
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD NOV
PY 2011
VL 339
IS 2
BP 464
EP 473
DI 10.1124/jpet.111.184788
PG 10
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 840TS
UT WOS:000296464800016
PM 21846840
ER
PT J
AU Deyo, RA
Smith, DHM
Johnson, ES
Donovan, M
Tillotson, CJ
Yang, XH
Petrik, AF
Dobscha, SK
AF Deyo, Richard A.
Smith, David H. M.
Johnson, Eric S.
Donovan, Marilee
Tillotson, Carrie J.
Yang, Xiuhai
Petrik, Amanda F.
Dobscha, Steven K.
TI Opioids for Back Pain Patients: Primary Care Prescribing Patterns and
Use of Services
SO JOURNAL OF THE AMERICAN BOARD OF FAMILY MEDICINE
LA English
DT Article
DE Analgesics; Back Pain; Pain Control; Quality of Health Care
ID CHRONIC NONCANCER PAIN; UNITED-STATES; MENTAL-HEALTH; TRENDS;
PRESCRIPTIONS; ASSOCIATION; INDIVIDUALS; DISORDERS; WORKERS; ABUSE
AB Background: Opioid prescribing for noncancer pain has increased dramatically. We examined whether the prevalence of unhealthy lifestyles, psychologic distress, health care utilization, and co-prescribing of sedative-hypnotics increased with increasing duration of prescription opioid use.
Methods: We analyzed electronic data for 6 months before and after an index visit for back pain in a managed care plan. Use of opioids was characterized as "none," "acute" (<= 90 days), " episodic," or "long term." Associations with lifestyle factors, psychologic distress, and utilization were adjusted for demographics and comorbidity.
Results: There were 26,014 eligible patients. Of these, 61% received a course of opioids, and 19% were long-term users. Psychologic distress, unhealthy lifestyles, and utilization were associated incrementally with duration of opioid prescription, not just with chronic use. Among long-term opioid users, 59% received only short-acting drugs; 39% received both long-and short-acting drugs; and 44% received a sedative-hypnotic. Of those with any opioid use, 36% had an emergency visit.
Conclusions: Prescription of opioids was common among patients with back pain. The prevalence of psychologic distress, unhealthy lifestyles, and health care utilization increased incrementally with duration of use. Coprescribing sedative-hypnotics was common. These data may help in predicting long-term opioid use and improving the safety of opioid prescribing. (J Am Board Fam Med 2011;24:717-727.)
C1 [Deyo, Richard A.] Oregon Hlth & Sci Univ, Dept Family Med, Portland, OR 97239 USA.
[Deyo, Richard A.] Oregon Hlth & Sci Univ, Dept Med, Portland, OR USA.
[Dobscha, Steven K.] Oregon Hlth & Sci Univ, Dept Psychiat, Portland, OR USA.
[Deyo, Richard A.; Tillotson, Carrie J.] Oregon Hlth & Sci Univ, Oregon Clin & Translat Res Inst, Portland, OR USA.
[Deyo, Richard A.] Oregon Hlth & Sci Univ, Ctr Res Occupat & Environm Toxicol, Portland, OR USA.
[Deyo, Richard A.; Smith, David H. M.; Johnson, Eric S.; Donovan, Marilee; Yang, Xiuhai; Petrik, Amanda F.] Kaiser Permanente Ctr Hlth Res, Portland, OR USA.
[Dobscha, Steven K.] Portland VA Med Ctr, Ctr Study Comorbid Mental & Phys Disorders, Portland, OR USA.
RP Deyo, RA (reprint author), Oregon Hlth & Sci Univ, Dept Family Med, Mail Code FM,3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM deyor@ohsu.edu
FU Oregon Clinical and Translational Research Institute [UL1 RR024140];
National Center for Research Resources, National Institutes of Health;
National Institutes of Health Roadmap for Medical Research
FX This study was made possible with support from the Oregon Clinical and
Translational Research Institute grant no. UL1 RR024140; from the
National Center for Research Resources, a component of the National
Institutes of Health; and the National Institutes of Health Roadmap for
Medical Research.
NR 31
TC 48
Z9 49
U1 1
U2 6
PU AMER BOARD FAMILY MEDICINE
PI LEXINGTON
PA 2228 YOUNG DR, LEXINGTON, KY 40505 USA
SN 1557-2625
J9 J AM BOARD FAM MED
JI J. Am. Board Fam. Med.
PD NOV-DEC
PY 2011
VL 24
IS 6
BP 717
EP 727
DI 10.3122/jabfm.2011.06.100232
PG 11
WC Primary Health Care; Medicine, General & Internal
SC General & Internal Medicine
GA 849UI
UT WOS:000297150400016
PM 22086815
ER
PT J
AU Nace, DA
Perera, S
Handler, SM
Muder, R
Hoffman, EL
AF Nace, David A.
Perera, Subashan
Handler, Steven M.
Muder, Robert
Hoffman, Erika L.
TI Increasing Influenza and Pneumococcal Immunization Rates in a Nursing
Home Network
SO JOURNAL OF THE AMERICAN MEDICAL DIRECTORS ASSOCIATION
LA English
DT Article
DE Nursing homes; immunizations; influenza; health care workers;
pneumococcal vaccine
ID LONG-TERM-CARE; RANDOMIZED CONTROLLED-TRIAL; QUALITY IMPROVEMENT;
UNITED-STATES; VACCINATION RATES; WORKERS; STAFF; HOSPITALIZATIONS;
PERFORMANCE; MORTALITY
AB Introduction and Rationale: Influenza and pneumonia remain serious health concerns for long-term care (LTC) residents. Vaccination of LTC residents and health care workers are reasonable preventive strategies, although most facilities fall short of Healthy People 2010 goals. Improving immunization rates across multiple LTC facilities remains an elusive challenge. This quality improvement study sought to improve immunization rates across 6 LTC facilities and identify persistent barriers to better performance.
Methods: In 2002, 6 facilities associated with the University of Pittsburgh Institute on Aging established a quality improvement network addressing immunization rates. The facilities were provided with a written educational toolkit and shared information through an e-mail distribution list. To help determine optimal program structure in future years, 3 of the facilities participated in a single half-day collaborative training session. Change in immunization rates from baseline to year 2 were compared between those participating in the collaborative training and those not participating. Barriers to improved performance were sought from all groups through focus group analysis.
Results: Facilities participating in the single collaborative training program improved immunization rates modestly, whereas facilities not participating in the collaborative training saw decreases in immunization rates. Staff turnover was cited as a significant barrier to improved performance.
Discussion: It may be possible to improve immunization rates in LTC facilities, at least modestly, using a collaborative training process. Staff turnover may be an important barrier to improved LTC immunization rates. (J Am Med Dir Assoc 2011; 12: 678-684)
C1 [Nace, David A.; Perera, Subashan; Handler, Steven M.] Univ Pittsburgh, Dept Med, Div Geriatr Med, Sch Med, Pittsburgh, PA 15213 USA.
[Perera, Subashan] Univ Pittsburgh, Dept Biostat, Grad Sch Publ Hlth, Pittsburgh, PA 15213 USA.
[Handler, Steven M.; Muder, Robert; Hoffman, Erika L.] Vet Affairs Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
RP Nace, DA (reprint author), Univ Pittsburgh, Dept Med, Div Geriatr Med, Sch Med, 3471 5th Ave,Suite 500, Pittsburgh, PA 15213 USA.
EM naceda@upmc.edu
RI Nace, David/D-2638-2014; Perera, Subashan/D-7603-2014;
OI Handler, Steven/0000-0002-3940-3224
FU American Medical Directors Association Foundation/Pfizer
FX This project was funded by the 2002 American Medical Directors
Association Foundation/Pfizer Quality Improvement Awards.
NR 41
TC 3
Z9 3
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1525-8610
J9 J AM MED DIR ASSOC
JI J. Am. Med. Dir. Assoc.
PD NOV
PY 2011
VL 12
IS 9
BP 678
EP 684
DI 10.1016/j.jamda.2010.05.002
PG 7
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 850ZT
UT WOS:000297238800012
PM 21450182
ER
PT J
AU Leuschner, F
Dutta, P
Gorbatov, R
Novobrantseva, TI
Donahoe, JS
Courties, G
Lee, KM
Kim, JI
Markmann, JF
Marinelli, B
Panizzi, P
Lee, WW
Iwamoto, Y
Milstein, S
Epstein-Barash, H
Cantley, W
Wong, J
Cortez-Retamozo, V
Newton, A
Love, K
Libby, P
Pittet, MJ
Swirski, FK
Koteliansky, V
Langer, R
Weissleder, R
Anderson, DG
Nahrendorf, M
AF Leuschner, Florian
Dutta, Partha
Gorbatov, Rostic
Novobrantseva, Tatiana I.
Donahoe, Jessica S.
Courties, Gabriel
Lee, Kang Mi
Kim, James I.
Markmann, James F.
Marinelli, Brett
Panizzi, Peter
Lee, Won Woo
Iwamoto, Yoshiko
Milstein, Stuart
Epstein-Barash, Hila
Cantley, William
Wong, Jamie
Cortez-Retamozo, Virna
Newton, Andita
Love, Kevin
Libby, Peter
Pittet, Mikael J.
Swirski, Filip K.
Koteliansky, Victor
Langer, Robert
Weissleder, Ralph
Anderson, Daniel G.
Nahrendorf, Matthias
TI Therapeutic siRNA silencing in inflammatory monocytes in mice
SO NATURE BIOTECHNOLOGY
LA English
DT Article
ID LIPID-LIKE MATERIALS; MYOCARDIAL-INFARCTION; SPLENIC RESERVOIR; IN-VIVO;
MACROPHAGES; CCR2; DELIVERY; CANCER; ATHEROSCLEROSIS; PROGRESSION
AB Excessive and prolonged activity of inflammatory monocytes is a hallmark of many diseases with an inflammatory component. In such conditions, precise targeting of these cells could be therapeutically beneficial while sparing many essential functions of the innate immune system, thus limiting unwanted effects. Inflammatory monocytes-but not the noninflammatory subset-depend on the chemokine receptor CCR2 for localization to injured tissue. Here we present an optimized lipid nanoparticle and a CCR2-silencing short interfering RNA that, when administered systemically in mice, show rapid blood clearance, accumulate in spleen and bone marrow, and localize to monocytes. Efficient degradation of CCR2 mRNA in monocytes prevents their accumulation in sites of inflammation. Specifically, the treatment attenuates their number in atherosclerotic plaques, reduces infarct size after coronary artery occlusion, prolongs normoglycemia in diabetic mice after pancreatic islet transplantation, and results in reduced tumor volumes and lower numbers of tumor-associated macrophages.
C1 [Leuschner, Florian; Dutta, Partha; Gorbatov, Rostic; Donahoe, Jessica S.; Courties, Gabriel; Marinelli, Brett; Iwamoto, Yoshiko; Cortez-Retamozo, Virna; Newton, Andita; Pittet, Mikael J.; Swirski, Filip K.; Weissleder, Ralph; Nahrendorf, Matthias] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Leuschner, Florian; Dutta, Partha; Gorbatov, Rostic; Donahoe, Jessica S.; Courties, Gabriel; Marinelli, Brett; Iwamoto, Yoshiko; Cortez-Retamozo, Virna; Newton, Andita; Pittet, Mikael J.; Swirski, Filip K.; Weissleder, Ralph; Nahrendorf, Matthias] Harvard Univ, Sch Med, Boston, MA USA.
[Novobrantseva, Tatiana I.; Milstein, Stuart; Epstein-Barash, Hila; Cantley, William; Wong, Jamie; Koteliansky, Victor] Alnylam Pharmaceut, Cambridge, MA USA.
[Lee, Kang Mi; Kim, James I.; Markmann, James F.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Panizzi, Peter] Auburn Univ, Harrison Sch Pharm, Dept Pharmacal Sci, Auburn, AL 36849 USA.
[Lee, Won Woo] Seoul Natl Univ, Bundang Hosp, Dept Nucl Med, Seoul, South Korea.
[Love, Kevin; Langer, Robert; Anderson, Daniel G.] MIT, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA.
[Libby, Peter] Brigham & Womens Hosp, Dept Med, Div Cardiovasc, Boston, MA 02115 USA.
[Langer, Robert; Anderson, Daniel G.] MIT, Dept Chem Engn, Cambridge, MA 02139 USA.
[Langer, Robert; Anderson, Daniel G.] MIT, Div Hlth Sci Technol, Cambridge, MA 02139 USA.
[Weissleder, Ralph] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA USA.
RP Nahrendorf, M (reprint author), Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
EM rweissleder@mgh.harvard.edu; mnahrendorf@mgh.harvard.edu
RI Lee, Won Woo/J-5589-2012;
OI Panizzi, Peter/0000-0003-0141-8807
FU US National Institutes of Health [R01-HL096576, R01-HL095629,
R01-EB006432, T32-CA79443, U24-CA92782, P50-CA86355, HHSN268201000044C,
R01-CA132091, R01-CA115527, R37-EB000244]; Deutsche Herzstiftung; SNUBH
Research Fund [02-2007-013]
FX The authors thank M. Waring, A. Chicoine and the Ragon Institute (MGH)
for cell sorting, the CSB Mouse Imaging Program (P. Waterman, B. Sena)
and B. Bettencourt for designing initial sets of siRNA. We acknowledge
the small, medium and large scale RNA synthesis groups at Alnylam as
well as analytical, duplex annealing and QC groups for synthesizing and
characterizing RNAs. This work was funded in part by grants from the US
National Institutes of Health R01-HL096576, R01-HL095629 (M.N.);
R01-EB006432, T32-CA79443, U24-CA92782, P50-CA86355, HHSN268201000044C
(R.W.); R01-CA132091, R01-CA115527, R37-EB000244 (R.L.); Deutsche
Herzstiftung (F.L.); and the SNUBH Research Fund 02-2007-013 (W.W.L.).
NR 43
TC 270
Z9 275
U1 4
U2 102
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 NOV
PY 2011
VL 29
IS 11
BP 1005
EP U73
DI 10.1038/nbt.1989
PG 9
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 845CT
UT WOS:000296801300021
PM 21983520
ER
PT J
AU Short, EB
Borckardt, JJ
Anderson, BS
Frohman, H
Beam, W
Reeves, ST
George, MS
AF Short, E. Baron
Borckardt, Jeffrey J.
Anderson, Berry S.
Frohman, Heather
Beam, William
Reeves, Scott T.
George, Mark S.
TI Ten sessions of adjunctive left prefrontal rTMS significantly reduces
fibromyalgia pain: A randomized, controlled pilot study
SO PAIN
LA English
DT Article
DE Depression; Fibromyalgia; Pain; Tender points; Transcranial magnetic
stimulation
ID TRANSCRANIAL MAGNETIC STIMULATION; MAJOR DEPRESSIVE DISORDER;
PLACEBO-CONTROLLED TRIAL; CHRONIC WIDESPREAD PAIN; DOUBLE-BLIND;
CLINICAL-TRIAL; MULTICENTER; EFFICACY; CORTEX; MILNACIPRAN
AB Transcranial magnetic stimulation (TMS) of the prefrontal cortex can cause changes in acute pain perception. Several weeks of daily left prefrontal TMS has been shown to treat depression. We recruited 20 patients with fibromyalgia, defined by American College of Rheumatology criteria, and randomized them to receive 4000 pulses at 10 Hz TMS (n = 10), or sham TMS (n = 10) treatment for 10 sessions over 2 weeks along with their standard medications, which were fixed and stable for at least 4 weeks before starting sessions. Subjects recorded daily pain, mood, and activity. Blinded raters assessed pain, mood, functional status, and tender points weekly with the Brief Pain Inventory, Hamilton Depression Rating Scale, and Fibromyalgia Impact Questionnaire. No statistically significant differences between groups were observed. Patients who received active TMS had a mean 29% (statistically significant) reduction in pain symptoms in comparison to their baseline pain. Sham TMS participants had a 4% nonsignificant change in daily pain from their baseline pain. At 2 weeks after treatment, there was a significant improvement in depression symptoms in the active group compared to baseline. Pain reduction preceded antidepressant effects. TMS was well tolerated, with few side effects. Further studies that address study limitations are needed to determine whether daily prefrontal TMS may be an effective, durable, and clinically useful treatment for fibromyalgia symptoms. (C) 2011 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
C1 [Short, E. Baron; Borckardt, Jeffrey J.; Frohman, Heather; Beam, William; George, Mark S.] Med Univ S Carolina, Dept Psychiat & Behav Sci, Brain Stimulat Lab, Charleston, SC 29425 USA.
[Borckardt, Jeffrey J.; Reeves, Scott T.] Med Univ S Carolina, Dept Anesthesia & Perioperat Med, Charleston, SC 29425 USA.
[Anderson, Berry S.] Med Univ S Carolina, Coll Nursing, Charleston, SC 29425 USA.
[George, Mark S.] Ralph H Johnson VA Med Ctr, Charleston, SC 29401 USA.
RP Short, EB (reprint author), Med Univ S Carolina, Dept Psychiat & Behav Sci, Brain Stimulat Lab, 67 President St,POB 250861, Charleston, SC 29425 USA.
EM shorteb@musc.edu
FU Office of the Provost and Vice President for Research [P60 AR049459]
FX Funding for this pilot project, under Multidisciplinary Clinical
Research Center Grant P60 AR049459, was generously provided by the
Office of the Provost and Vice President for Research.
ClinicalTrials.gov identifier NCT00523302.
NR 51
TC 34
Z9 37
U1 0
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
J9 PAIN
JI Pain
PD NOV
PY 2011
VL 152
IS 11
BP 2477
EP 2484
DI 10.1016/j.pain.2011.05.033
PG 8
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 842AB
UT WOS:000296556200009
PM 21764215
ER
PT J
AU Obara, I
Tochiki, KK
Geranton, SM
Carr, FB
Lumb, BM
Liu, QS
Hunt, SP
AF Obara, Ilona
Tochiki, Keri K.
Geranton, Sandrine M.
Carr, Fiona B.
Lumb, Bridget M.
Liu, Qingsong
Hunt, Stephen P.
TI Systemic inhibition of the mammalian target of rapamycin (mTOR) pathway
reduces neuropathic pain in mice
SO PAIN
LA English
DT Article
DE Inflammatory pain; Local translation; mTOR; Neuropathic pain;
Temsirolimus (CCI-779); Torin1
ID INDUCED THERMAL HYPERALGESIA; SPARED NERVE INJURY;
3-KINASE-AKT-MAMMALIAN TARGET; SYNAPTIC PLASTICITY; SIGNALING PATHWAY;
LOCAL TRANSLATION; PROTEIN-SYNTHESIS; ANALOG CCI-779; GROWTH-FACTOR;
MOUSE MODELS
AB The management of neuropathic pain is unsatisfactory, and new treatments are required. Because the sensitivity of a subset of fast-conducting primary afferent nociceptors is thought to be regulated by the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway, selectively targeting mTORC1 represents a new strategy for the control of chronic pain. Here we show that activated mTOR was expressed largely in myelinated sensory fibers in mouse and that inhibiting the mTORC1 pathway systemically alleviated mechanical hypersensitivity in mouse models of inflammatory and neuropathic pain. Specifically, systemic administration of mTORC1 inhibitor temsirolimus (CCI-779), both acutely (25 mg/kg i.p.) and chronically (4 daily 25 mg/kg i.p.), inhibited the mTORC1 pathway in sensory axons and the spinal dorsal horn and reduced mechanical and cold hypersensitivity induced by nerve injury. Moreover, systemic treatment with CCI-779 also reduced mechanical but not heat hypersensitivity in an inflammatory pain state. This treatment did not influence nociceptive thresholds in naive or sham-treated control animals. Also, there was no evidence for neuronal toxicity after repeated systemic treatment with CCI-779. Additionally, we show that acute and chronic i.p. administration of Torin1 (20 mg/kg), a novel ATP-competitive inhibitor targeting both mTORC1 and mTORC2 pathways, reduced the response to mechanical and cold stimuli in neuropathic mice. Our findings emphasize the importance of the mTORC1 pathway as a regulator of nociceptor sensitivity and therefore as a potential target for therapeutic intervention, particularly in chronic pain. (C) 2011 International Association for the Study of Pain. Published by Elsevier B. V. All rights reserved.
C1 [Obara, Ilona; Tochiki, Keri K.; Geranton, Sandrine M.; Carr, Fiona B.; Hunt, Stephen P.] UCL, Dept Cell & Dev Biol, London WC1E 6BT, England.
[Obara, Ilona] Polish Acad Sci, Inst Pharmacol, Dept Pain Pharmacol, PL-31343 Krakow, Poland.
[Lumb, Bridget M.] Univ Bristol, Dept Physiol, Bristol BS8 1TD, Avon, England.
[Liu, Qingsong] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Liu, Qingsong] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
RP Obara, I (reprint author), UCL, Dept Cell & Dev Biol, Mortimer St, London WC1E 6BT, England.
EM i.obara@ucl.ac.uk; hunt@ucl.ac.uk
OI liu, qing song/0000-0002-7829-2547
FU Medical Research Council [G0801381]
FX This research was supported by Grant G0801381 from the Medical Research
Council.
NR 63
TC 33
Z9 37
U1 1
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
J9 PAIN
JI Pain
PD NOV
PY 2011
VL 152
IS 11
BP 2582
EP 2595
DI 10.1016/j.pain.2011.07.025
PG 14
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 842AB
UT WOS:000296556200021
PM 21917376
ER
PT J
AU Hamel, LP
Benchabane, M
Nicole, MC
Major, IT
Morency, MJ
Pelletier, G
Beaudoin, N
Sheen, J
Seguin, A
AF Hamel, Louis-Philippe
Benchabane, Meriem
Nicole, Marie-Claude
Major, Ian T.
Morency, Marie-Josee
Pelletier, Gervais
Beaudoin, Nathalie
Sheen, Jen
Seguin, Armand
TI Stress-Responsive Mitogen-Activated Protein Kinases Interact with the
EAR Motif of a Poplar Zinc Finger Protein and Mediate Its Degradation
through the 26S Proteasome
SO PLANT PHYSIOLOGY
LA English
DT Article
ID LIGHT SIGNALING NETWORKS; MAP KINASE; ARABIDOPSIS-THALIANA;
TRANSCRIPTION FACTOR; GENE-EXPRESSION; HYBRID POPLAR; PATHOGEN
INTERACTIONS; MALACOSOMA-DISSTRIA; DISEASE RESISTANCE; AUX/IAA PROTEINS
AB Mitogen-activated protein kinases (MAPKs) contribute to the establishment of plant disease resistance by regulating downstream signaling components, including transcription factors. In this study, we identified MAPK-interacting proteins, and among the newly discovered candidates was a Cys-2/His-2-type zinc finger protein named PtiZFP1. This putative transcription factor belongs to a family of transcriptional repressors that rely on an ERF-associated amphiphilic repression (EAR) motif for their repression activity. Amino acids located within this repression motif were also found to be essential for MAPK binding. Close examination of the primary protein sequence revealed a functional bipartite MAPK docking site that partially overlaps with the EAR motif. Transient expression assays in Arabidopsis (Arabidopsis thaliana) protoplasts suggest that MAPKs promote PtiZFP1 degradation through the 26S proteasome. Since features of the MAPK docking site are conserved among other EAR repressors, our study suggests a novel mode of defense mechanism regulation involving stress-responsive MAPKs and EAR repressors.
C1 [Hamel, Louis-Philippe; Benchabane, Meriem; Nicole, Marie-Claude; Major, Ian T.; Morency, Marie-Josee; Pelletier, Gervais; Seguin, Armand] Nat Resources Canada, Canadian Forest Serv, Laurentian Forestry Ctr, Quebec City, PQ G1V 4C7, Canada.
[Hamel, Louis-Philippe; Sheen, Jen] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA.
[Beaudoin, Nathalie] Univ Sherbrooke, Dept Biol, Sherbrooke, PQ J1K 2R1, Canada.
RP Seguin, A (reprint author), Nat Resources Canada, Canadian Forest Serv, Laurentian Forestry Ctr, Quebec City, PQ G1V 4C7, Canada.
EM armand.seguin@nrcan-rncan.gc.ca
OI Beaudoin, Nathalie/0000-0001-7835-4077
FU Genomics R&D Initiative of Canada; Natural Sciences and Engineering
Research Council of Canada; Fonds Quebecois de la Recherche sur la
Nature et les Technologies scholarships
FX This work was supported by a grant from the Genomics R&D Initiative of
Canada and the Natural Sciences and Engineering Research Council of
Canada to A.S. and by Natural Sciences and Engineering Research Council
of Canada and Fonds Quebecois de la Recherche sur la Nature et les
Technologies scholarships to L.-P.H.
NR 79
TC 13
Z9 14
U1 1
U2 18
PU AMER SOC PLANT BIOLOGISTS
PI ROCKVILLE
PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 USA
SN 0032-0889
J9 PLANT PHYSIOL
JI Plant Physiol.
PD NOV
PY 2011
VL 157
IS 3
BP 1379
EP 1393
DI 10.1104/pp.111.178343
PG 15
WC Plant Sciences
SC Plant Sciences
GA 844BL
UT WOS:000296722300031
PM 21873571
ER
PT J
AU Herschhorn, A
Finzi, A
Jones, DM
Courter, JR
Sugawara, A
Smith, AB
Sodroski, JG
AF Herschhorn, Alon
Finzi, Andres
Jones, David M.
Courter, Joel R.
Sugawara, Akihiro
Smith, Amos B., III
Sodroski, Joseph G.
TI An Inducible Cell-Cell Fusion System with Integrated Ability to Measure
the Efficiency and Specificity of HIV-1 Entry Inhibitors
SO PLOS ONE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; SMALL-MOLECULE INHIBITOR; CHEMOKINE
RECEPTOR CCR5; HTLV-III/LAV ENVELOPE; CONFORMATIONAL-CHANGES;
REVERSE-TRANSCRIPTASE; CXCR4 CORECEPTOR; POTENT INHIBITOR; AIDS
PATIENTS; ASSAY SYSTEM
AB HIV-1 envelope glycoproteins (Envs) mediate virus entry by fusing the viral and target cell membranes, a multi-step process that represents an attractive target for inhibition. Entry inhibitors with broad-range activity against diverse isolates of HIV-1 may be extremely useful as lead compounds for the development of therapies or prophylactic microbicides. To facilitate the identification of such inhibitors, we have constructed a cell-cell fusion system capable of simultaneously monitoring inhibition efficiency and specificity. In this system, effector cells stably express a tetracycline-controlled transactivator (tTA) that enables tightly inducible expression of both HIV-1 Env and the Renilla luciferase (R-Luc) reporter protein. Target cells express the HIV-1 receptors, CD4 and CCR5, and carry the firefly luciferase (F-Luc) reporter gene under the control of a tTA-responsive promoter. Thus, Env-mediated fusion of these two cell types allows the tTA to diffuse to the target cell and activate the expression of the F-Luc protein. The efficiency with which an inhibitor blocks cell-cell fusion is measured by a decrease in the F-Luc activity, while the specificity of the inhibitor is evaluated by its effect on the R-Luc activity. The system exhibited a high dynamic range and high Z'-factor values. The assay was validated with a reference panel of inhibitors that target different steps in HIV-1 entry, yielding inhibitory concentrations comparable to published virus inhibition data. Our system is suitable for large-scale screening of chemical libraries and can also be used for detailed characterization of inhibitory and cytotoxic properties of known entry inhibitors.
C1 [Herschhorn, Alon; Finzi, Andres; Sodroski, Joseph G.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Immunol Canc & AIDS, Boston, MA 02115 USA.
[Herschhorn, Alon; Finzi, Andres; Sodroski, Joseph G.] Harvard Univ, Sch Med, Dept Microbiol & Immunobiol, Boston, MA 02115 USA.
[Jones, David M.; Courter, Joel R.; Sugawara, Akihiro; Smith, Amos B., III] Univ Penn, Dept Chem, Philadelphia, PA 19104 USA.
[Sodroski, Joseph G.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
RP Herschhorn, A (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Immunol Canc & AIDS, 44 Binney St, Boston, MA 02115 USA.
EM joseph_sodroski@dfci.harvard.edu
OI Sugawara, Akihiro/0000-0003-1266-7497
FU American Foundation for AIDS Research [107431-45-RFRL]; Japan Society
for the Promotion of Science (JSPS); National Institutes of Health
[GM56550, AI24755, AI67854, AI60354]; International AIDS Vaccine
Initiative
FX A.F. was supported by an American Foundation for AIDS Research Mathilde
Krim Fellowship in Basic Biomedical Research # 107431-45-RFRL. A.S. was
supported by a Japan Society for the Promotion of Science (JSPS)
research fellowship. The study was supported by the National Institutes
of Health (grants GM56550, AI24755, AI67854 and AI60354), the
International AIDS Vaccine Initiative, and the late William F.
McCarty-Cooper. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
NR 72
TC 5
Z9 5
U1 0
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 1
PY 2011
VL 6
IS 11
AR e26731
DI 10.1371/journal.pone.0026731
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849UN
UT WOS:000297150900028
PM 22069466
ER
PT J
AU Liao, YH
Tang, JS
Deng, QJ
Deng, YW
Luo, T
Wang, XY
Chen, HX
Liu, TQ
Chen, XG
Brody, AL
Hao, W
AF Liao, Yanhui
Tang, Jinsong
Deng, Qijian
Deng, Yongwen
Luo, Tao
Wang, Xuyi
Chen, Hongxian
Liu, Tieqiao
Chen, Xiaogang
Brody, Arthur L.
Hao, Wei
TI Bilateral Fronto-Parietal Integrity in Young Chronic Cigarette Smokers:
A Diffusion Tensor Imaging Study
SO PLOS ONE
LA English
DT Article
ID WHITE-MATTER ABNORMALITIES; SPINAL-CORD NEURONS; ANISOTROPIC WATER
DIFFUSION; MAGNETIC-RESONANCE; MICROSTRUCTURAL INTEGRITY;
HUNTINGTONS-DISEASE; TOBACCO CONTROL; NICOTINE; BRAIN; SMOKING
AB Background: Cigarette smoking continues to be the leading cause of preventable morbidity and mortality in China and other countries. Previous studies have demonstrated gray matter loss in chronic smokers. However, only a few studies assessed the changes of white matter integrity in this group. Based on those previous reports of alterations in white matter integrity in smokers, the aim of this study was to examine the alteration of white matter integrity in a large, well-matched sample of chronic smokers and non-smokers.
Methodology/Principal Findings: Using in vivo diffusion tensor imaging (DTI) to measure the differences of whole-brain white matter integrity between 44 chronic smoking subjects (mean age, 28.0 +/- 5.6 years) and 44 healthy age- and sex-matched comparison non-smoking volunteers (mean age, 26.3 +/- 5.8 years). DTI was performed on a 3-Tesla Siemens scanner (Allegra; Siemens Medical System). The data revealed that smokers had higher fractional anisotropy (FA) than healthy non-smokers in almost symmetrically bilateral fronto-parietal tracts consisting of a major white matter pathway, the superior longitudinal fasciculus (SLF).
Conclusion/Significance: We found the almost symmetrically bilateral fronto-parietal whiter matter changes in a relatively large sample of chronic smokers. These findings support the hypothesis that chronic cigarette smoking involves alterations of bilateral fronto-parietal connectivity.
C1 [Liao, Yanhui; Tang, Jinsong; Deng, Qijian; Luo, Tao; Wang, Xuyi; Chen, Hongxian; Liu, Tieqiao; Chen, Xiaogang; Hao, Wei] Cent S Univ, Xiangya Hosp 2, Mental Hlth Inst, Changsha, Hunan, Peoples R China.
[Deng, Yongwen] Peoples Hosp Hunan Prov, Dept Neurosurg, Changsha, Hunan, Peoples R China.
[Brody, Arthur L.] Univ Calif Los Angeles, Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA.
[Brody, Arthur L.] Greater Los Angeles VA Healthcare Syst, Dept Psychiat, Los Angeles, CA USA.
[Brody, Arthur L.] Greater Los Angeles VA Healthcare Syst, Dept Res, Los Angeles, CA USA.
RP Liao, YH (reprint author), Cent S Univ, Xiangya Hosp 2, Mental Hlth Inst, Changsha, Hunan, Peoples R China.
EM abrody@ucla.edu; weihaochangsha@gmail.com
RI Liao, Yanhui/L-1590-2016
OI Liao, Yanhui/0000-0003-4735-3252
FU Central Colleges basic scientific research operating expenses; National
Key Technology R&D Program in the 11th Five-Year Plan of China
[2011QNZT170, 2007BAI07B01]; Natural Science Foundation of China
[81100996, 30971050, 30900486, 81130020]; National Key Basic Research
and Development Program(NKBRDP) (973) [2009CB522000]; Hunan Provincial
Natural Science Foundation of China [10JJ5038]; Tobacco-Related Disease
Research Program [19XT-0135]; National Institute on Drug Abuse [R01
DA20872]; China Scholarship Council; University of Cambridge;
Behavioural and Clinical Neuroscience Institute; Veterans Affairs Type I
Merit Review Award; Richard Metzner Chair in Clinical Neuropharmacology
FX This work was supported by grants from the Central Colleges basic
scientific research operating expenses. 2011QNZT170, National Key
Technology R&D Program in the 11th Five-Year Plan of China
(2007BAI07B01), Natural Science Foundation of China (81100996, 30971050,
30900486, 81130020), National Key Basic Research and Development
Program(NKBRDP) (973, 2009CB522000) and from Hunan Provincial Natural
Science Foundation of China (10JJ5038). Tobacco-Related Disease Research
Program (19XT-0135), the National Institute on Drug Abuse (R01 DA20872),
a Veterans Affairs Type I Merit Review Award, and an endowment from the
Richard Metzner Chair in Clinical Neuropharmacology. Yanhui Liao is
supported by a fellowship from the China Scholarship Council to study at
University of Cambridge, Behavioural and Clinical Neuroscience
Institute. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 61
TC 20
Z9 21
U1 1
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 1
PY 2011
VL 6
IS 11
AR e26460
DI 10.1371/journal.pone.0026460
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849UN
UT WOS:000297150900014
PM 22069452
ER
PT J
AU Zhang, YY
Zhen, Y
Dong, YL
Xu, ZP
Yue, Y
Golde, TE
Tanzi, RE
Moir, RD
Xie, ZC
AF Zhang, Yiying
Zhen, Yu
Dong, Yuanlin
Xu, Zhipeng
Yue, Yun
Golde, Todd E.
Tanzi, Rudolph E.
Moir, Robert D.
Xie, Zhongcong
TI Anesthetic Propofol Attenuates the Isoflurane-Induced Caspase-3
Activation and A beta Oligomerization
SO PLOS ONE
LA English
DT Article
ID NITROUS OXIDE ANESTHESIA; ALZHEIMERS-DISEASE; SPATIAL MEMORY;
CEREBRAL-ISCHEMIA; INDUCED APOPTOSIS; DNA-DAMAGE; AGED RATS; IN-VITRO;
BRAIN; NEUROPROTECTION
AB Accumulation and deposition of beta-amyloid protein (A beta) are the hallmark features of Alzheimer's disease. The inhalation anesthetic isoflurane has been shown to induce caspase activation and increase A beta accumulation. In addition, recent studies suggest that isoflurane may directly promote the formation of cytotoxic soluble A beta oligomers, which are thought to be the key pathological species in AD. In contrast, propofol, the most commonly used intravenous anesthetic, has been reported to have neuroprotective effects. We therefore set out to compare the effects of isoflurane and propofol alone and in combination on caspase-3 activation and A beta oligomerization in vitro and in vivo. Naive and stably-transfected H4 human neuroglioma cells that express human amyloid precursor protein, the precursor for A beta; neonatal mice; and conditioned cell culture media containing secreted human A beta 40 or A beta 42 were treated with isoflurane and/or propofol. Here we show for the first time that propofol can attenuate isoflurane-induced caspase-3 activation in cultured cells and in the brain tissues of neonatal mice. Furthermore, propofol-mediated caspase inhibition occurred when there were elevated levels of A beta. Finally, isoflurane alone induces A beta 42, but not A beta 40, oligomerization, and propofol can inhibit the isoflurane-mediated oligomerization of A beta 42. These data suggest that propofol may mitigate the caspase-3 activation by attenuating the isoflurane-induced A beta 42 oligomerization. Our findings provide novel insights into the possible mechanisms of isoflurane-induced neurotoxicity that may aid in the development of strategies to minimize potential adverse effects associated with the administration of anesthetics to patients.
C1 [Zhang, Yiying; Zhen, Yu; Dong, Yuanlin; Xu, Zhipeng; Xie, Zhongcong] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Geriatr Anesthesia Res Unit, Charlestown, MA USA.
[Zhang, Yiying; Zhen, Yu; Dong, Yuanlin; Xu, Zhipeng; Tanzi, Rudolph E.; Moir, Robert D.; Xie, Zhongcong] Harvard Univ, Sch Med, Charlestown, MA USA.
[Zhang, Yiying; Zhen, Yu; Dong, Yuanlin; Xu, Zhipeng; Tanzi, Rudolph E.; Moir, Robert D.; Xie, Zhongcong] Massachusetts Gen Hosp, Genet & Aging Res Unit, MassGen Inst Neurodegenerat Dis, Dept Neurol, Charlestown, MA USA.
[Zhen, Yu] Capital Med Univ, Dept Anesthesia, Beijing Friendship Hosp, Beijing, Peoples R China.
[Yue, Yun] Capital Med Univ, Dept Anesthesia, Beijing Chaoyang Hosp, Beijing, Peoples R China.
[Golde, Todd E.] Univ Florida, Dept Neurosci, Ctr Translat Res Neurodegenerat Dis, Gainesville, FL 32610 USA.
RP Zhang, YY (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Geriatr Anesthesia Res Unit, Charlestown, MA USA.
EM zxie@partners.org
FU National Institutes of Health (Bethesda, Maryland) [K08 NS048140, R21
AG029856, R01 GM088801]; American Geriatrics Society (New York, New
York); Alzheimer's Association (Chicago, Illinois); National Natural
Science Foundation of China [30928026, 81000474/H0902]
FX This study was supported by National Institutes of Health grants
(Bethesda, Maryland) (K08 NS048140, R21 AG029856 and R01 GM088801);
American Geriatrics Society Jahnigen Award (New York, New York);
Investigator-Initiated Research Grant from Alzheimer's Association
(Chicago, Illinois) to ZX; National Natural Science Foundation of China
(30928026) to ZX and YY, and National Natural Science Foundation of
China (81000474/H0902) to Y. Zhen. The Department of Anesthesia,
Critical Care and Pain Medicine, Massachusetts General Hospital and
Harvard Medical School provided the cost of anesthetic isoflurane. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 48
TC 31
Z9 33
U1 0
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 NOV 1
PY 2011
VL 6
IS 11
AR e27019
DI 10.1371/journal.pone.0027019
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849UN
UT WOS:000297150900043
PM 22069482
ER
PT J
AU Zhu, XX
Liu, Q
Wang, MM
Liang, MR
Yang, X
Xu, X
Zou, HJ
Qiu, JH
AF Zhu, Xiaoxia
Liu, Qiong
Wang, Meimei
Liang, Minrui
Yang, Xue
Xu, Xue
Zou, Hejian
Qiu, Jianhua
TI Activation of Sirt1 by Resveratrol Inhibits TNF-alpha Induced
Inflammation in Fibroblasts
SO PLOS ONE
LA English
DT Article
ID NF-KAPPA-B; OBSTRUCTIVE PULMONARY-DISEASE; SMOOTH-MUSCLE-CELLS;
RHEUMATOID-ARTHRITIS; MEDIATED INFLAMMATION; PROTEIN TRANSLATION;
TRANS-RESVERATROL; RELA ACETYLATION; IN-VITRO; APOPTOSIS
AB Inflammation is one of main mechanisms of autoimmune disorders and a common feature of most diseases. Appropriate suppression of inflammation is a key resolution to treat the diseases. Sirtuin1 (Sirt1) has been shown to play a role in regulation of inflammation. Resveratrol, a potent Sirt1 activator, has anti-inflammation property. However, the detailed mechanism is not fully understood. In this study, we investigated the anti-inflammation role of Sirt1 in NIH/3T3 fibroblast cell line. Upregulation of matrix metalloproteinases 9 (MMP-9), interleukin-1beta (IL-1 beta), IL-6 and inducible nitric oxide synthase (iNOS) were induced by tumor necrosis factor alpha (TNF-alpha) in 3T3 cells and resveratrol suppressed overexpression of these pro-inflammatory molecules in a dose-dependent manner. Knockdown of Sirt1 by RNA interference caused 3T3 cells susceptible to TNF-alpha stimulation and diminished anti-inflammatory effect of resveratrol. We also explored potential anti-inflammatory mechanisms of resveratrol. Resveratrol reduced NF-kappa B subunit RelA/p65 acetylation, which is notably Sirt1 dependent. Resveratrol also attenuated phosphorylation of mammalian target of rapamycin (mTOR) and S6 ribosomal protein (S6RP) while ameliorating inflammation. Our data demonstrate that resveratrol inhibits TNF-alpha-induced inflammation via Sirt1. It suggests that Sirt1 is an efficient target for regulation of inflammation. This study provides insight on treatment of inflammation-related diseases.
C1 [Zhu, Xiaoxia; Liang, Minrui; Yang, Xue; Xu, Xue; Zou, Hejian] Fudan Univ, Shanghai Med Coll, Huashan Hosp, Div Rheumatol, Shanghai, Peoples R China.
[Zhu, Xiaoxia; Liu, Qiong; Liang, Minrui; Yang, Xue; Xu, Xue; Zou, Hejian] Fudan Univ, Inst Rheumatol Immunol & Allergy, Huashan Hosp, Shanghai Med Coll, Shanghai, Peoples R China.
[Liu, Qiong] Fudan Univ, Shanghai Med Coll, Dept Human Anat Histol & Embryol, Shanghai, Peoples R China.
[Wang, Meimei] Dongnan Univ, Zhongda Hosp, Div Rheumatol, Nanjing, Peoples R China.
[Qiu, Jianhua] Harvard Univ, Dept Neurol & Radiol, Sch Med, Massachusetts Gen Hosp, Charlestown, MA USA.
RP Zhu, XX (reprint author), Fudan Univ, Shanghai Med Coll, Huashan Hosp, Div Rheumatol, Shanghai, Peoples R China.
EM hjzou@fudan.edu.cn; jqiu@partners.org
FU Program of Shanghai Subject Chief Scientist [11XD1401100]; National
Natural Science Foundation of China [81072463]
FX This work was supported by Program of Shanghai Subject Chief Scientist
(NO. 11XD1401100) and National Natural Science Foundation of China (No.
81072463). The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 77
TC 16
Z9 22
U1 2
U2 21
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 NOV 1
PY 2011
VL 6
IS 11
AR e27081
DI 10.1371/journal.pone.0027081
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 849UN
UT WOS:000297150900049
PM 22069489
ER
PT J
AU Kuna, ST
AF Kuna, Samuel T.
TI Back to the Future or Forward to the Past?
SO SLEEP
LA English
DT Editorial Material
ID OBSTRUCTIVE SLEEP-APNEA; NERVE-STIMULATION; HYPOGLOSSAL NERVE; UPPER
AIRWAY
C1 [Kuna, Samuel T.] Philadelphia VA Med Ctr, Pulm Crit Care & Sleep Sect, Philadelphia, PA 19104 USA.
[Kuna, Samuel T.] Univ Penn, Philadelphia, PA 19104 USA.
RP Kuna, ST (reprint author), Philadelphia VA Med Ctr, Pulm Crit Care & Sleep Sect, 111P,3900 Woodland Av, Philadelphia, PA 19104 USA.
EM skuna@mail.med.upenn.edu
NR 14
TC 1
Z9 1
U1 0
U2 1
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PD NOV 1
PY 2011
VL 34
IS 11
BP 1455
EP 1456
DI 10.5665/sleep.1370
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 844DF
UT WOS:000296727200003
PM 22043113
ER
PT J
AU Luckey, CJ
Lu, Y
Marto, JA
AF Luckey, C. John
Lu, Yu
Marto, Jarrod A.
TI Understanding the first steps in embryonic stem cell exit from the
pluripotent state
SO TRANSFUSION
LA English
DT Article
ID SELF-RENEWAL; PHOSPHOPROTEOMICS; DIFFERENTIATION; ACTIVATION
AB BACKGROUND: We are interested in understanding how a given cell type, in response to external cues from its environment, makes the decision to differentiate. In the case of mouse embryonic stem cells (mESCs), the key external factor that maintains their undifferentiated state is the cytokine leukemia inhibitory factor (LIF). LIF removal causes mESCs to exit their pluripotent state and differentiate into more restricted precursors. Although LIF is known to activate multiple different phosphorylation cascades, the mechanisms by which its removal leads to mESC differentiation are not well understood.
STUDY DESIGN AND METHODS: In order to identify the molecular events that occur upon LIF removal, we developed a set of novel experimental approaches that allowed identification and quantification of global phosphorylation changes that occur when mESCs are deprived of LIF. These included growth of mESCs on permeable membranes and development of a robust and sensitive phospho-proteomics platform to quantify early signaling events.
RESULTS: In addition to the well-characterized tyrosine 705 phosphorylation of STAT3, LIF removal results in the rapid phosphorylation of multiple other proteins known to regulate the mESC self-renewal on both tyrosine, serine, and threonine residues. We hypothesize that these unique posttranslational modifications help drive the exit of mESCs from the pluripotent state.
CONCLUSIONS: Our data set the stage for future studies investigating the functional role of these phosphorylation events in mESCs. These studies were greatly facilitated by the National Blood Foundation, whose support in the crucial initiation phase of these studies was invaluable.
C1 [Luckey, C. John] Brigham & Womens Hosp, Dept Pathol, Joint Program Transfus Med, Dept Canc Biol,Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Luckey, CJ (reprint author), Brigham & Womens Hosp, Dept Pathol, Joint Program Transfus Med, Dept Canc Biol,Dana Farber Canc Inst, NRB Rm 652D,77 Ave Louis Pasteur, Boston, MA 02115 USA.
EM cluckey@partners.org
FU NHLBI NIH HHS [RC2 HL102815, R21 HL111866, RC2 HL102815-01]; NIAID NIH
HHS [K08 AI063386, K08 AI063386-04, K08 AI063386-03]
NR 24
TC 2
Z9 2
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0041-1132
EI 1537-2995
J9 TRANSFUSION
JI Transfusion
PD NOV
PY 2011
VL 51
SU 4
SI SI
BP 118S
EP 124S
DI 10.1111/j.1537-2995.2011.03374.x
PG 7
WC Hematology
SC Hematology
GA 851SH
UT WOS:000297290700007
PM 22074622
ER
PT J
AU Chung, HJ
Reiner, T
Budin, G
Min, C
Liong, M
Issadore, D
Lee, H
Weissleder, R
AF Chung, Hyun Jung
Reiner, Thomas
Budin, Ghyslain
Min, Changwook
Liong, Monty
Issadore, David
Lee, Hakho
Weissleder, Ralph
TI Ubiquitous Detection of Gram-Positive Bacteria with Bioorthogonal
Magnetofluorescent Nanoparticles
SO ACS NANO
LA English
DT Article
DE nanoparticles; bacteria; infection
ID SELF-ASSEMBLED MONOLAYERS; MAGNETIC NANOPARTICLES; CANCER-CELLS;
VANCOMYCIN; DAPTOMYCIN; INFECTIONS; BINDING; ANTIBIOTICS; ENTEROCOCCI
AB The ability to rapidly diagnose gram-positive pathogenic bacteria would have far reaching biomedical and technological applications. Here we describe the bloorthogonal modification of small molecule antibiotics (vancomycin and daptomycin), which bind to the cell wall of gram-positive bacteria. The bound antibiotics conjugates can be reacted orthogonally with tetrazine-modified nanoparticles, via an almost Instantaneous cycloaddition, which subsequently renders the bacteria detectable by optical or magnetic sensing. We show that this approach is specific, selective, fast and biocompatible. Furthermore, it can be adapted to the detection of intracellular pathogens. Importantly, this strategy enables detection of entire classes of bacteria, a feat that is difficult to achieve using current antibody approaches. Compared to covalent nanoparticle conjugates, our bioorthogonal method demonstrated 1-2 orders of magnitude greater sensitivity. This bioorthogonal labeling method could ultimately be applied to a variety of other small molecules with specificity for infectious pathogens, enabling their detection and diagnosis.
C1 [Chung, Hyun Jung; Reiner, Thomas; Budin, Ghyslain; Min, Changwook; Liong, Monty; Issadore, David; Lee, Hakho; Weissleder, Ralph] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Weissleder, Ralph] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
RP Lee, H (reprint author), Massachusetts Gen Hosp, Ctr Syst Biol, 185 Cambridge St,CPZN 5206, Boston, MA 02114 USA.
EM hlee@mgh.harvard.edu; rweissleder@mgh.harvard.edu
RI Chung, Hyun Jung/J-3205-2014; Issadore, David/L-8451-2014;
OI Reiner, Thomas/0000-0002-7819-5480
FU NHLBI [HHSN268201000044C]; NIBIB [R01-EB010011, R01-EB00462605A1];
German Academy of Sciences Leopoldina [LPDS 2009-24]
FX We acknowledge S. Hilderbrand and M. Karver for their help with the
synthesis of tetrazine, N. Sergeyev for the synthesis of cross-linked
dextran iron oxide nanoparticles, I. Bagayev for help in confocal
microscopy, J. Carlson for the helpful suggestions, and Y. Fisher-Jeffes
for review of the manuscript. This work was funded in part by NHLBI
Contract HHSN268201000044C and NIBIB Grants R01-EB010011 and
R01-EB00462605A1. T.R. was supported by a grant from the German Academy
of Sciences Leopoldina (LPDS 2009-24).
NR 27
TC 58
Z9 58
U1 5
U2 59
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1936-0851
J9 ACS NANO
JI ACS Nano
PD NOV
PY 2011
VL 5
IS 11
BP 8834
EP 8841
DI 10.1021/nn2029692
PG 8
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA 849RR
UT WOS:000297143300043
PM 21967150
ER
PT J
AU Ullal, AV
Reiner, T
Yang, KS
Gorbatov, R
Min, C
Issadore, D
Lee, H
Weissleder, R
AF Ullal, Adeeti V.
Reiner, Thomas
Yang, Katherine S.
Gorbatov, Rostic
Min, Changwook
Issadore, David
Lee, Hakho
Weissleder, Ralph
TI Nanoparticle-Mediated Measurement of Target-Drug Binding in Cancer Cells
SO ACS NANO
LA English
DT Article
DE nanoparticles; targeting; NMR; DMR; cancer; drugs; PARP
ID DIPHOSPHATE-RIBOSE) POLYMERASE EXPRESSION; POLY(ADP-RIBOSE)
POLYMERASE-1; PARP-1; INHIBITORS; PROTEINS; COMPLEX
AB Responses to molecularly targeted therapies can be highly variable and depend on mutations, fluctuations in target protein levels In individual cells, and drug delivery. The ability to rapidly quantitate drug response in cells harvested from patients in a point-of-care setting would have far reaching Implications. Capitalizing on recent developments with miniaturized NMR technologies, we have developed a magnetic nanoparticle-based approach to directly measure both target expression and drug binding In scant human cells. The method involves covalent conjugation of the small-molecule drug to a magnetic nanoparticle that Is then used as a read-out for target expression and drug-binding affinity. Using poly(ADP-ribose) polymerase (PARP) inhibition as a model system, we developed an approach to distinguish differential expression of PARP in scant cells with excellent correlation to gold standards, the ability to mimic drug pharmacodynamics ex vivo through competitive target drug binding, and the potential to perform such measurements In clinical samples.
C1 [Ullal, Adeeti V.; Reiner, Thomas; Yang, Katherine S.; Gorbatov, Rostic; Min, Changwook; Issadore, David; Lee, Hakho; Weissleder, Ralph] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Ullal, Adeeti V.] MIT, Harvard MIT Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Weissleder, Ralph] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
RP Weissleder, R (reprint author), Massachusetts Gen Hosp, Ctr Syst Biol, 185 Cambridge St,CPZN 5206, Boston, MA 02114 USA.
EM rweissleder@mgh.harvard.edu
RI Issadore, David/L-8451-2014;
OI Reiner, Thomas/0000-0002-7819-5480
FU NSF; German National Academy of Sciences Leopoldina [LPDS 2009-24];
National Institutes of Health [R01-EB0044626, R01-EB010011, P50CA86355,
U54CA151884]; TPEN [HHSN268201000044C]
FX The authors thank N. Sergeyev for synthesizing the CLIO, B. Marinelli
and K. Snyder for assisting with DMR measurements, J. Dunham with
imaging, M. Etzrodt and V. Cortez-Retamozo for assistance with flow
cytometry experiments, and C. Tassa and M. Liong for guidance on
nanoparticle conjugations. We especially thank G. Thurber and J. Haun
for many helpful discussions. A.V.U. was supported in part by an NSF
fellowship. T.R. was supported by a grant from the German National
Academy of Sciences Leopoldina (LPDS 2009-24). This work was supported
in part by National Institutes of Health Grants R01-EB0044626,
R01-EB010011, P50 grant P50CA86355, U54CA151884, and TPEN contract
HHSN268201000044C.
NR 39
TC 12
Z9 13
U1 1
U2 28
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1936-0851
J9 ACS NANO
JI ACS Nano
PD NOV
PY 2011
VL 5
IS 11
BP 9216
EP 9224
DI 10.1021/nn203450p
PG 9
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA 849RR
UT WOS:000297143300085
PM 21962084
ER
PT J
AU Fradley, MG
Larson, MG
Cheng, S
McCabe, E
Coglianese, E
Shah, RV
Levy, D
Vasan, RS
Wang, TJ
AF Fradley, Michael G.
Larson, Martin G.
Cheng, Susan
McCabe, Elizabeth
Coglianese, Erin
Shah, Ravi V.
Levy, Daniel
Vasan, Rarnachandran S.
Wang, Thomas J.
TI Reference Limits for N-Terminal-pro-B-Type Natriuretic Peptide in
Healthy Individuals (from the Framingham Heart Study)
SO AMERICAN JOURNAL OF CARDIOLOGY
LA English
DT Article
ID BIOLOGICAL VARIATION; AGE; FAILURE; BNP; DYSFUNCTION; GENDER; ADULTS;
IMPACT; SEX
AB N-terminal pro B-type natriuretic peptide (NT-pro-BNP) is a commonly measured cardiovascular biomarker in ambulatory and hospital settings. Nonetheless, there are limited data regarding "normal" ranges for NT-pro-BNP in healthy subjects, despite the importance of such information for interpreting natriuretic peptide measurements. In this study, a healthy reference sample free of cardiovascular disease from the Framingham Heart Study Generation 3 cohort was examined; there were 2,285 subjects (mean age 38 years, 56% women). Plasma NT-pro-BNP levels were measured using the Roche Diagnostics Elecsys 2010 assay, and reference values (2.5th, 50th, and 97.5th quantiles) were determined using empiric and quantile regression methods. Gender, age, blood pressure, and body mass index accounted for approximately 33% of the interindividual variability in NT-pro-BNP in the reference sample. NT-pro-BNP values were substantially higher in women compared to men at every age, and levels increased with increasing age for both genders. Using quantile regression, the upper reference values (97.5th quantile) for NT proBNP were 42.5 to 106.4 pg/ml in men (depending on age) and 111.0 to 215.9 pg/ml in women. Intraindividual variability was assessed in an additional 12 healthy subjects, who had serial NT-pro-BNP measurements over 1 month. Intraclass correlation was 0.85, indicating that most of the variability in NT-pro-BNP concentrations was among rather than within subjects. However, the reference change value was 100%, suggesting that small proportional differences in NT-pro-BNP could be attributable to analytic variability. In conclusion, the reference limits obtained from this large, healthy, community-based sample may aid in the evaluation of NT-pro-BNP concentrations measured for clinical and research purposes. (C) 2011 Elsevier Inc. All rights reserved. (Am J Cardiol 2011;108:1341-1345)
C1 [Fradley, Michael G.; McCabe, Elizabeth; Coglianese, Erin; Shah, Ravi V.; Wang, Thomas J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA 02215 USA.
[Larson, Martin G.; Cheng, Susan; Levy, Daniel; Vasan, Rarnachandran S.; Wang, Thomas J.] Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Cheng, Susan] Harvard Univ, Sch Med, Div Cardiovasc Med, Brigham & Womens Hosp, Boston, MA USA.
[Levy, Daniel] NHLBI, Ctr Populat Studies, Bethesda, MD 20892 USA.
[Levy, Daniel; Vasan, Rarnachandran S.] Boston Univ, Sch Med, Prevent Med & Cardiol Sect, Boston, MA 02118 USA.
RP Wang, TJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA 02215 USA.
EM tjwang@partners.org
OI Larson, Martin/0000-0002-9631-1254; Ramachandran,
Vasan/0000-0001-7357-5970
FU National Heart, Lung and Blood Institute's Framingham Heart Study
[NO1-HC-25195]; Siemens Healthcare Diagnostics, Deerfield, Illinois;
Brahms AG, Hennigsdorf, Germany; [R01-HL086875]
FX This work was supported by the National Heart, Lung and Blood
Institute's Framingham Heart Study (NO1-HC-25195) and grant
R01-HL086875.; Dr. Wang has been a coinvestigator on studies that have
received assay support from Siemens Healthcare Diagnostics, Deerfield,
Illinois, and Brahms AG, Hennigsdorf, Germany.
NR 20
TC 34
Z9 36
U1 0
U2 5
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9149
J9 AM J CARDIOL
JI Am. J. Cardiol.
PD NOV 1
PY 2011
VL 108
IS 9
BP 1341
EP 1345
DI 10.1016/j.amjcard.2011.06.057
PG 5
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 846YM
UT WOS:000296939100023
PM 21864812
ER
PT J
AU Quraishi, SA
Blosser, SA
Cherry, RA
AF Quraishi, Sadeq A.
Blosser, Sandralee A.
Cherry, Robert A.
TI BISPECTRAL INDEX MONITORING IN THE MANAGEMENT OF SEDATION IN AN
INTENSIVE CARE UNIT PATIENT WITH LOCKED-IN SYNDROME
SO AMERICAN JOURNAL OF CRITICAL CARE
LA English
DT Article
ID CRITICALLY-ILL PATIENTS; ICU PATIENTS; LEVEL
AB Locked-in syndrome is an extremely rare neurological state caused by injury of the ventral pons. The syndrome is characterized by quadriplegia and anarthria with concomitant preservation of cortical function. When a reversible underlying pathological abnormality is identified and managed aggressively, meaningful recovery is possible. Because patients retain consciousness through out their illness, a dependable method for titrating sedation may improve their quality of life. The case presented suggests that bispectral index monitoring may be a cost-effective and reliable method for managing sedation in patients with locked-in syndrome. (American Journal of Critical Care. 2011;20:491,487-490)
C1 [Quraishi, Sadeq A.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Quraishi, Sadeq A.] Harvard Univ, Sch Med, Boston, MA USA.
[Blosser, Sandralee A.] Penn State Univ, Dept Anesthesiol, Coll Med, Hershey, PA USA.
[Blosser, Sandralee A.; Cherry, Robert A.] Penn State Univ, Dept Surg, Coll Med, Hershey, PA USA.
[Blosser, Sandralee A.] Penn State Univ, Dept Med, Coll Med, Hershey, PA USA.
[Blosser, Sandralee A.] Penn State Milton S Hershey Med Ctr, Adult Crit Care Serv, Hershey, PA USA.
[Cherry, Robert A.] Penn State Univ, Coll Med, Dept Publ Hlth Sci, Hershey, PA USA.
[Cherry, Robert A.] Penn State Milton S Hershey Med Ctr, Ctr Shock Trauma, Hershey, PA USA.
RP Quraishi, SA (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, 55 Fruit St,GRJ 402, Boston, MA 02114 USA.
EM squraishi@partners.org
NR 18
TC 0
Z9 1
U1 1
U2 1
PU AMER ASSOC CRITICAL CARE NURSES
PI ALISO VIEJO
PA 101 COLUMBIA, ALISO VIEJO, CA 92656 USA
SN 1062-3264
J9 AM J CRIT CARE
JI Am. J. Crit. Care
PD NOV 1
PY 2011
VL 20
IS 6
BP 487
EP 491
DI 10.4037/ajcc2011674
PG 5
WC Critical Care Medicine; Nursing
SC General & Internal Medicine; Nursing
GA 843FK
UT WOS:000296657500020
PM 22045147
ER
PT J
AU Hazin, R
Coyer, M
Lum, F
Barazi, MK
AF Hazin, Ribhi
Coyer, Marcus
Lum, Flora
Barazi, Mohammed K.
TI Revisiting Diabetes 2000: Challenges in Establishing Nationwide Diabetic
Retinopathy Prevention Programs
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Editorial Material
ID NUTRITION EXAMINATION SURVEY; PREFERRED PRACTICE PATTERN; IMPAIRED
FASTING GLUCOSE; TREATING RETINOPATHY; US POPULATION; UNITED-STATES;
RISK-FACTORS; EYE DISEASE; FOLLOW-UP; MELLITUS
AB PURPOSE: To evaluate the impact of the Diabetes 2000 program, an initiative launched by the American Academy of Ophthalmology in 1990 to improve nationwide screening of diabetic retinopathy (DR) and to reduce the prevalence and severity of the condition.
DESIGN: Retrospective, observational case study of Diabetes 2000 program.
METHODS: This is a perspective piece with a review of literature and personal opinions.
RESULTS: Patients with diabetes are likely to see an increase in the disease burdens associated with DR unless effective programs for early detection and control of DR are implemented.
CONCLUSIONS: Despite recent efforts to educate both patients and physicians alike about the importance of routine DR screening, the lessons learned from the Diabetes 2000 program illustrate the need for new strategies capable of improving accessibility to high-quality eye care, increasing involvement of primary care physicians in DR screening and encouraging at-risk individuals to seek testing. (Am J Ophthalmol 2011; 152:723-729. (C) 2011 by Elsevier Inc. All rights reserved.)
C1 [Hazin, Ribhi] Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA 02138 USA.
[Coyer, Marcus; Barazi, Mohammed K.] Retina Grp Washington, Manassas, VA USA.
[Coyer, Marcus] Walter Reed Army Med Ctr, Ophthalmol Serv, Washington, DC 20307 USA.
[Lum, Flora] Amer Acad Ophthalmol, San Francisco, CA USA.
RP Hazin, R (reprint author), Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, 243 Charles St, Boston, MA 02138 USA.
EM rhazin@mail.harvard.edu
NR 49
TC 16
Z9 16
U1 1
U2 12
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
EI 1879-1891
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD NOV
PY 2011
VL 152
IS 5
BP 723
EP 729
DI 10.1016/j.ajo.2011.06.022
PG 7
WC Ophthalmology
SC Ophthalmology
GA 840BK
UT WOS:000296413100004
PM 21917235
ER
PT J
AU Robinson, TN
Wu, DS
Stiegmann, GV
Moss, M
AF Robinson, Thomas N.
Wu, Daniel S.
Stiegmann, Gregory V.
Moss, Marc
TI Frailty predicts increased hospital and six-month healthcare cost
following colorectal surgery in older adults
SO AMERICAN JOURNAL OF SURGERY
LA English
DT Article; Proceedings Paper
CT 35th Annual Meeting of the Association of VA Surgeons
CY APR 10-12, 2011
CL Irvine, CA
SP Assoc VA Surg
DE Geriatric; Surgery; Financial; Frailty; Healthcare resources
AB BACKGROUND: The purpose of this study was to determine the relationship of frailty and 6-month postoperative costs.
METHODS: Subjects aged >= 65 years undergoing elective colorectal operations were enrolled in a prospective observational study. Frailty was assessed by a validated measure of function, cognition, nutrition, comorbidity burden, and geriatric syndromes. Frailty was quantified by summing the number of positive characteristics in each subject.
RESULTS: Sixty subjects (mean age, 75 +/- 8 years) were studied. Inpatient mortality was 2% (n = 1). Overall, 40% of subjects (n = 24) were considered nonfrail, 22% (n = 13) were prefrail, and 38% (n = 22) were frail. With advancing frailty, hospital costs increased (P < .001) and costs from discharge to 6-months increased (P < .001). Higher degrees of frailty were related to increased rates of discharge institutionalization (P < .001) and 30-day readmission (P = .044).
CONCLUSIONS: A simple, brief preoperative frailty assessment accurately forecasts increased surgical hospital costs and postdischarge to 6-month healthcare costs after colorectal operations in older adults. Published by Elsevier Inc.
C1 [Robinson, Thomas N.; Wu, Daniel S.; Stiegmann, Gregory V.] Denver Vet Affairs Med Ctr, Dept Surg, Denver, CO USA.
[Robinson, Thomas N.; Wu, Daniel S.; Stiegmann, Gregory V.] Univ Colorado Denver, Hlth Sci Ctr, Dept Surg, Aurora, CO USA.
[Moss, Marc] Univ Colorado Denver, Hlth Sci Ctr, Dept Med, Aurora, CO USA.
RP Robinson, TN (reprint author), Denver Vet Affairs Med Ctr, Dept Surg, Denver, CO USA.
EM thomas.robinson@ucdenver.edu
FU NHLBI NIH HHS [K24 HL089223-04, K24 HL089223, K24 HL089223-05,
K24-HL-089223]; NIA NIH HHS [K23 AG034632, K23 AG034632-01A1, K23
AG034632-02, K23AG034632]
NR 11
TC 70
Z9 71
U1 1
U2 7
PU EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
PI BRIDGEWATER
PA 685 ROUTE 202-206 STE 3, BRIDGEWATER, NJ 08807 USA
SN 0002-9610
J9 AM J SURG
JI Am. J. Surg.
PD NOV
PY 2011
VL 202
IS 5
BP 511
EP 514
DI 10.1016/j.amjsurg.2011.06.017
PG 4
WC Surgery
SC Surgery
GA 848CJ
UT WOS:000297025700005
PM 21890098
ER
PT J
AU Shepardson, NE
Shankar, GM
Selkoe, DJ
AF Shepardson, Nina E.
Shankar, Ganesh M.
Selkoe, Dennis J.
TI Cholesterol Level and Statin Use in Alzheimer Disease II. Review of
Human Trials and Recommendations
SO ARCHIVES OF NEUROLOGY
LA English
DT Review
ID COA REDUCTASE INHIBITORS; BLOOD-BRAIN-BARRIER; RANDOMIZED
CONTROLLED-TRIAL; LIPID-LOWERING AGENTS; COGNITIVE FUNCTION; INCIDENT
DEMENTIA; BETA-PEPTIDE; IN-VIVO; RISK; LOVASTATIN
AB Substantial evidence has accumulated in support of the hypothesis that elevated cholesterol levels increase the risk of developing Alzheimer disease (AD). As a result, much work has investigated the potential use of lipid-lowering agents, particularly statins, as preventive or therapeutic agents for AD. Although epidemiology and preclinical statin research (described in part I of this review) have generally supported an adverse role of high cholesterol levels regarding AD, human studies of statins (reviewed herein) show highly variable outcomes, making it difficult to draw firm conclusions. We identify several confounding factors among the human studies, including differing blood-brain barrier permeabilities among statins, the stage in AD at which statins were administered, and the drugs' pleiotropic metabolic effects, all of which contribute to the substantial variability observed to date. We recommend that future human studies of this important therapeutic topic (1) take the blood-brain barrier permeabilities of statins into account when analyzing results, (2) include specific analyses of the effects on low- and high-density lipoprotein cholesterol, and, most important, (3) conduct statin treatment trials solely in patients with mild AD, who have the best chance for disease modification. Arch Neurol. 2011; 68(11): 1385-1392
C1 [Shepardson, Nina E.; Shankar, Ganesh M.; Selkoe, Dennis J.] Brigham & Womens Hosp, Ctr Neurol Dis, Dept Neurol, Boston, MA 02115 USA.
[Shepardson, Nina E.; Shankar, Ganesh M.; Selkoe, Dennis J.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Shankar, Ganesh M.] Massachusetts Gen Hosp, Dept Neurol Surg, Boston, MA 02114 USA.
RP Selkoe, DJ (reprint author), Brigham & Womens Hosp, Ctr Neurol Dis, Dept Neurol, HIM Room 730,77 Ave Louis Pasteur, Boston, MA 02115 USA.
EM dselkoe@rics.bwh.harvard.edu
FU National Institutes of Health [AG06173]
FX This study was supported by grant AG06173 from the National Institutes
of Health (Dr Selkoe).
NR 36
TC 74
Z9 75
U1 0
U2 10
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD NOV
PY 2011
VL 68
IS 11
BP 1385
EP 1392
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 847ZI
UT WOS:000297014900003
PM 22084122
ER
PT J
AU Khot, S
Billings, M
Owens, D
Longstreth, WT
AF Khot, Sandeep
Billings, Martha
Owens, Darrell
Longstreth, W. T., Jr.
TI Coping With Death and Dying on a Neurology Inpatient Service Death
Rounds as an Educational Initiative for Residents
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID CARE; PATIENT
AB Background: Residents in neurology may feel unprepared to care for dying patients. We developed Death Rounds to provide emotional support and end-of-life care teaching for residents caring for dying patients on the inpatient neurology service. Death Rounds are monthly 1-hour clinical case discussions where residents identify issues through shared experiences.
Objective: To survey neurology residents' perceptions of Death Rounds with respect to end-of-life care teaching and emotional support.
Design, Setting, and Participants: We conducted an electronic survey of all (n = 26) neurology residents and recent residency graduates at the University of Washington 2 years after instituting monthly Death Rounds.
Main Outcome Measure: The survey consisted of 10 questions examining residents' perceptions of the extent to which Death Rounds provided emotional support and end-of-life care teaching. We dichotomized responses to statements about Death Rounds as agree or disagree.
Results: All 26 residents responded to the survey and attended at least 1 Death Rounds session. More than half of residents attended more than 3 sessions. Residents agreed that Death Rounds helped them cope with dying patients (17 residents [65%]), delivered closure for the team (16 residents [61%]), and provided emotional support, more for the team (18 residents [69%]) than the individual (10 residents [38%]). Most residents felt that Death Rounds provided useful teaching about end-of-life care (18 residents [69%]), and they were satisfied overall with Death Rounds (16 residents [61%]).
Conclusions: Death Rounds afford an opportunity for physicians-in-training to process as a group their feelings, intense emotions, and insecurities while learning from the dying process. In our inpatient neurology service, most residents found it a rewarding and valuable experience.
C1 [Khot, Sandeep; Longstreth, W. T., Jr.] Univ Washington, Dept Neurol, Seattle, WA 98104 USA.
[Billings, Martha] Vet Affairs Puget Sound Hlth Care Syst, Hlth Serv Res & Dev, Div Pulm & Crit Care Med, Seattle, WA USA.
[Owens, Darrell] Univ Washington, Harborview Med Ctr, Palliat Care Serv, Seattle, WA 98104 USA.
RP Khot, S (reprint author), Univ Washington, Dept Neurol, 325 9th Ave,Box 359775, Seattle, WA 98104 USA.
EM skhot@uw.edu
NR 8
TC 10
Z9 10
U1 0
U2 4
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD NOV
PY 2011
VL 68
IS 11
BP 1395
EP 1397
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 847ZI
UT WOS:000297014900004
PM 22084123
ER
PT J
AU Fleisher, AS
Chen, KW
Liu, XF
Roontiva, A
Thiyyagura, P
Ayutyanont, N
Joshi, AD
Clark, CM
Mintun, MA
Pontecorvo, MJ
Doraiswamy, PM
Johnson, KA
Skovronsky, DM
Reiman, EM
AF Fleisher, Adam S.
Chen, Kewei
Liu, Xiaofen
Roontiva, Auttawut
Thiyyagura, Pradeep
Ayutyanont, Napatkamon
Joshi, Abhinay D.
Clark, Christopher M.
Mintun, Mark A.
Pontecorvo, Michael J.
Doraiswamy, P. Murali
Johnson, Keith A.
Skovronsky, Daniel M.
Reiman, Eric M.
TI Using Positron Emission Tomography and Florbetapir F 18 to Image
Cortical Amyloid in Patients With Mild Cognitive Impairment or Dementia
Due to Alzheimer Disease
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID EPSILON-4 ALLELE; BRAIN; PET; DEPOSITION; DIAGNOSIS; APOE; AGENTS;
INDIVIDUALS; POPULATION; STILBENES
AB Objectives: To characterize quantitative florbetapir F 18 (hereafter referred to as simply florbetapir) positron emission tomographic (PET) measurements of fibrillar beta-amyloid (A beta) burden in a large clinical cohort of participants with probable Alzheimer disease (AD) or mild cognitive impairment (MCI) and older healthy controls (OHCs).
Design: Cerebral-to-whole-cerebellar florbetapir standard uptake value ratios (SUVRs) were computed. Mean cortical SUVRs were compared. A threshold of SUVRs greater than or equal to 1.17 was used to reflect pathological levels of amyloid associated with AD based on separate antemortem PET and postmortem neuropathology data from 19 end-of-life patients. Similarly, a threshold of SUVRs greater than 1.08 was used to signify the presence of any identifiable A beta because this was the upper limit from a separate set of 46 individuals 18 to 40 years of age who did not carry apolipoprotein E (APOE) epsilon 4.
Setting: Multiple research imaging centers.
Participants: A total of 68 participants with probable AD, 60 participants with MCI, and 82 OHCs who were 55 years of age or older.
Main Outcome Measure: Florbetapir-PET activity.
Results: All of the participants (ie, those with probable AD or MCI and those who were OHCs) differed significantly in mean (SD) cortical florbetapir SUVRs (1.39 [0.24], 1.17 [0.27], and 1.05 [0.16], respectively; P < 1.0 X 10(-7)), in percentage meeting levels of amyloid associated with AD by SUVR criteria (80.9%, 40.0%, and 20.7%, respectively; P < 1.0 X 10(-7)), and in percentage meeting SUVR criteria for the presence of any identifiable A beta (85.3%, 46.6%, and 28.1%, respectively; P < 1.0 X 10(-7)). Among OHCs, the percentage of florbetapir positivity increased linearly by age decile (P =. 05). For the 54 OHCs with available APOE genotypes, APOE e4 carriers had a higher mean (SD) cortical SUVR than did noncarriers (1.14 [0.2] vs 1.03 [0.16]; P =. 048).
Conclusions: The findings of our analysis confirm the ability of florbetapir-PET SUVRs to characterize amyloid levels in clinically probable AD, MCI, and OHC groups using continuous and binary measures of fibrillar A beta burden. It introduces criteria to determine whether an image is associated with an intermediate-to-high likelihood of pathologic AD or with having any identifiable cortical amyloid level above that seen in low-risk young controls.
C1 [Fleisher, Adam S.; Chen, Kewei; Liu, Xiaofen; Roontiva, Auttawut; Thiyyagura, Pradeep; Ayutyanont, Napatkamon; Reiman, Eric M.] Univ Arizona, Banner Alzheimers Inst, Coll Med, Phoenix, AZ 85006 USA.
[Fleisher, Adam S.; Chen, Kewei; Reiman, Eric M.] Univ Arizona, Arizona Alzheimers Consortium, Coll Med, Phoenix, AZ 85006 USA.
[Reiman, Eric M.] Univ Arizona, Dept Psychiat, Coll Med, Phoenix, AZ 85006 USA.
[Reiman, Eric M.] Translat Genom Res Inst, Neurogen Div, Phoenix, AZ USA.
[Chen, Kewei] Arizona State Univ, Dept Math, Tempe, AZ 85287 USA.
[Fleisher, Adam S.] Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA.
[Clark, Christopher M.; Skovronsky, Daniel M.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Mintun, Mark A.] Washington Univ, Sch Med, St Louis, MO USA.
[Johnson, Keith A.] Harvard Univ, Sch Med, Dept Neurol, Brigham & Womens Hosp, Boston, MA 02115 USA.
[Johnson, Keith A.] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Johnson, Keith A.] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Doraiswamy, P. Murali] Duke Univ, Med Ctr, Dept Psychiat, Durham, NC 27710 USA.
RP Fleisher, AS (reprint author), Univ Arizona, Banner Alzheimers Inst, Coll Med, 901 E Willetta St, Phoenix, AZ 85006 USA.
EM adam.fleisher@bannerhealth.com
RI Chen, kewei/P-6304-2015
OI Chen, kewei/0000-0001-8497-3069
FU Avid Radiopharmaceuticals; Eli Lilly; Avid; Lundbeck; Medivation; TauRx;
Bayer; GE Healthcare; BMS; Astra; Shering; Neuroptix; Neuronetrix;
Alzheimer's Foundation; Sonexa; Janssen Alzheimer Immunotherapy
FX Dr Fleisher has received research support for nonrelated projects from
Avid Radiopharmaceuticals and Eli Lilly and is a consultant for Eli
Lilly. Mr Joshi and Drs Clark, Mintun, Pontecorvo, and Skovronsky are
employees of Avid Radiopharmaceuticals, a wholly owned subsidiary of Eli
Lilly. Dr Doraiswamy has received research support or advisory fees from
Avid, Lundbeck, Medivation, TauRx, Bayer, GE Healthcare, BMS, Astra,
Shering, Neuroptix, Neuronetrix, Alzheimer's Foundation, and Sonexa and
owns stock in Sonexa. Dr Johnson has received research support or
advisory fees from GE Healthcare, Bayer, Janssen Alzheimer
Immunotherapy, and Avid Radiopharmaceuticals. Dr Reiman has received
research support for nonrelated projects from Avid Radiopharmaceuticals
and Eli Lilly.; This study was supported by funding from Avid
Radiopharmaceuticals, a wholly owned subsidiary of Eli Lilly.
NR 39
TC 129
Z9 133
U1 1
U2 17
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD NOV
PY 2011
VL 68
IS 11
BP 1404
EP 1411
DI 10.1001/archneurol.2011.150
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 847ZI
UT WOS:000297014900006
PM 21747008
ER
PT J
AU Jakobiec, FA
Kirzhner, M
Tollett, MM
Mancini, R
Hogan, RN
AF Jakobiec, Frederick A.
Kirzhner, Maria
Tollett, Marlene Morales
Mancini, Ronald
Hogan, R. Nick
TI Solitary Epithelioid Histiocytoma (Reticulohistiocytoma) of the Eyelid
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Letter
ID MULTICENTRIC RETICULOHISTIOCYTOSIS
C1 [Jakobiec, Frederick A.; Kirzhner, Maria] Massachusetts Eye & Ear Infirm, David G Cogan Lab Ophthalm Pathol, Dept Ophthalmol, Boston, MA 02114 USA.
[Jakobiec, Frederick A.; Kirzhner, Maria] Harvard Univ, Sch Med, Boston, MA USA.
[Tollett, Marlene Morales; Mancini, Ronald; Hogan, R. Nick] Univ Texas SW Med Ctr Dallas, Dept Ophthalmol, Dallas, TX 75390 USA.
[Hogan, R. Nick] Univ Texas SW Med Ctr Dallas, Dept Pathol, Dallas, TX 75390 USA.
RP Jakobiec, FA (reprint author), Massachusetts Eye & Ear Infirm, David G Cogan Lab Ophthalm Pathol, Dept Ophthalmol, 243 Charles St,Room 321, Boston, MA 02114 USA.
EM fred_jakobiec@meei.harvard.edu
NR 6
TC 4
Z9 4
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD NOV
PY 2011
VL 129
IS 11
BP 1502
EP 1504
PG 4
WC Ophthalmology
SC Ophthalmology
GA 848JK
UT WOS:000297047600022
PM 22084226
ER
PT J
AU Wecht, JM
Radulovic, M
Rosado-Rivera, D
Zhang, RL
LaFountaine, MF
Bauman, WA
AF Wecht, Jill M.
Radulovic, Miroslav
Rosado-Rivera, Dwindally
Zhang, Run-Lin
LaFountaine, Michael F.
Bauman, William A.
TI Orthostatic Effects of Midodrine Versus L-NAME on Cerebral Blood Flow
and the Renin-Angiotensin-Aldosterone System in Tetraplegia
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Blood pressure; Hypotension; orthostatic; Rehabilitation; Spinal cord
injuries
ID NITRIC-OXIDE SYNTHASE; SPINAL-CORD-INJURY; SIMULATED MICROGRAVITY;
TRANSCRANIAL DOPPLER; MYOCARDIAL-INFARCTION; HYPOTENSION; INHIBITION;
PRESSURE; RISK; HYDROCHLORIDE
AB Objective: To compare responses to head-up tilt (HUT) in individuals with chronic tetraplegia after midodrine hydrochloride (10mg) versus nitro-L-arginine methyl ester (L-NAME, 1mg/kg) administration.
Design: Prospective comparative drug trial.
Setting: Veterans Affairs medical center.
Participants: Participants (N=7) were studied during 3 laboratory visits: no drug, midodrine (administered orally 30min before HUT), and L-NAME (infused over a 60-min period).
Interventions: Anti-hypotensive agents, midodrine, and L-NAME.
Main Outcome Measures: Mean arterial pressure (MAP), cerebral blood flow (CBF), and markers of the renin-angiotensin-aldosterone system (RAAS, plasma renin and serum aldosterone) were measured in the supine position at baseline (BL) and during a 45 degrees HUT maneuver. Data were compared between BL and the average of 3 assessments collected during HUT. Results: Orthostatic MAP and CBF were increased with the midodrine and L-NAME groups compared with the no drug trial and the relationship between the change in MAP and CBF was significant (r=0.770; P<0.001). Both L-NAME and midodrine appeared to suppress the post-HUT RAAS response compared with no drug.
Conclusions: Increasing orthostatic blood pressure with L-NAME or midodrine appears to increase CBF and suppress the RAAS during HUT in persons with tetraplegia, although more data are needed to confirm these preliminary findings.
C1 [Wecht, Jill M.; Radulovic, Miroslav; Rosado-Rivera, Dwindally; Zhang, Run-Lin; LaFountaine, Michael F.; Bauman, William A.] James J Peters VA Med Ctr, Ctr Excellence, Bronx, NY 10468 USA.
[Wecht, Jill M.; Radulovic, Miroslav; Bauman, William A.] James J Peters VA Med Ctr, Med Serv, Bronx, NY 10468 USA.
[Wecht, Jill M.; Radulovic, Miroslav; LaFountaine, Michael F.; Bauman, William A.] Mt Sinai Sch Med, Dept Med, New York, NY USA.
[Wecht, Jill M.; Radulovic, Miroslav; Bauman, William A.] Mt Sinai Sch Med, Dept Rehabil Med, New York, NY USA.
RP Wecht, JM (reprint author), James J Peters VA Med Ctr, Ctr Excellence Med Consequences Spinal Cord Injur, Room 1E-02,130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM jm.wecht@va.gov
FU Veterans Affairs Rehabilitation Research and Development Service
[A6161W, B3203R, B4162C]
FX Supported by the Veterans Affairs Rehabilitation Research and
Development Service (grant nos. A6161W, B3203R, and B4162C).
NR 46
TC 7
Z9 7
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 0003-9993
J9 ARCH PHYS MED REHAB
JI Arch. Phys. Med. Rehabil.
PD NOV
PY 2011
VL 92
IS 11
BP 1789
EP 1795
DI 10.1016/j.apmr.2011.03.022
PG 7
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 846WT
UT WOS:000296934600008
PM 21762873
ER
PT J
AU Karver, MR
Weissleder, R
Hilderbrand, SA
AF Karver, Mark R.
Weissleder, Ralph
Hilderbrand, Scott A.
TI Synthesis and Evaluation of a Series of 1,2,4,5-Tetrazines for
Bioorthogonal Conjugation
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID INVERSE-ELECTRON-DEMAND; DIELS-ALDER REACTIONS; LIVING CELLS; CLICK
CHEMISTRY; CANCER-CELLS; COPPER-FREE; LIGATION; CYCLOADDITIONS;
REACTIVITY
AB 1,2,4,5-Tetrazines have been established as effective dienes for inverse electron demand [4 + 2] Diels-Alder cycloaddition reactions with strained alkenes for over 50 years. Recently, this reaction pair combination has been applied to bioorthogonal labeling and cell detection applications; however, to date, there has been no detailed examination and optimization of tetrazines for use in biological experiments. Here, we report the synthesis and characterization of 12 conjugatable tetrazines. The tetrazines were all synthesized in a similar fashion and were screened in parallel to identify candidates most ideally suited for biological studies. In depth follow-up studies revealed compounds with varying degrees of stability and reactivity that could each be useful in different bioorthogonal applications. One promising, highly stable, and water-soluble derivative was used in pretargeted cancer cell labeling studies, confirming its utility as a bioorthogonal moiety.
C1 [Hilderbrand, Scott A.] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Hilderbrand, SA (reprint author), Massachusetts Gen Hosp, Ctr Syst Biol, 185 Cambridge St Suite 5-210, Boston, MA 02114 USA.
EM scott_hilderbrand@hms.harvard.edu
FU NIH [RO1EB010011, P50CA86355]
FX The authors would like to thank Dr. Jack Szostak at MGH for the use of
the Stopped-Flow spectrophotometer. The authors would also like to thank
Alex Chudnovskiy and Elizabeth Tiglao of CSB for technical assistance
with cell culture and flow cytometry and Neal K. Devaraj for helpful
discussions. This research is supported in part by NIH grants
RO1EB010011 and P50CA86355.
NR 33
TC 123
Z9 124
U1 2
U2 61
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD NOV
PY 2011
VL 22
IS 11
BP 2263
EP 2270
DI 10.1021/bc200295y
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 847VY
UT WOS:000297001800009
PM 21950520
ER
PT J
AU Tannous, BA
Teng, J
AF Tannous, Bakhos A.
Teng, Jian
TI Secreted blood reporters: Insights and applications
SO BIOTECHNOLOGY ADVANCES
LA English
DT Review
DE Secreted reporter; Gaussia luciferase; SEAP; Soluble peptides; Imaging;
Blood assay
ID PLACENTAL ALKALINE-PHOSPHATASE; RENILLA-RENIFORMIS LUCIFERASE;
OVARIAN-CANCER XENOGRAFTS; TERM GENE-EXPRESSION; IN-VIVO; GAUSSIA
LUCIFERASE; MEASLES-VIRUS; FIREFLY LUCIFERASE; PROMOTER ACTIVITY;
MAMMALIAN-CELLS
AB Secreted reporters detected in body fluids (blood, serum or urine) have shown to be simple and useful tools for ex vivo real-time monitoring of in vivo biological processes. Here we explore the most commonly used secreted blood reporters in experimental animals: secreted alkaline phosphatase, soluble marker peptides derived from human carcinoembryonic antigen and human chorionic gonadotropin, as well as Gaussia luciferase. We also comment on other recently discovered secreted luciferases and their potential use as blood reporters for multiplexing applications. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Tannous, Bakhos A.; Teng, Jian] Massachusetts Gen Hosp, Ctr Neurosci, Dept Neurol, Expt Therapeut & Mol Imaging Lab, Boston, MA 02129 USA.
[Tannous, Bakhos A.] Massachusetts Gen Hosp, Ctr Mol Imaging Res, Boston, MA 02114 USA.
[Tannous, Bakhos A.; Teng, Jian] Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA.
RP Tannous, BA (reprint author), Massachusetts Gen Hosp, Expt Therapeut & Mol Imaging Lab, Ctr Neurosci, Bldg 149,13th St, Charlestown, MA 02129 USA.
EM btannous@hms.harvard.edu
FU National Institutes of Health; National Cancer Institute [4R00CA126839];
National Institute of Neurological Disorders and Stroke [NS045776,
1R01NS064983]
FX Dr. Tannous is supported by grants from the National Institutes of
Health, the National Cancer Institute (4R00CA126839) and the National
Institute of Neurological Disorders and Stroke (NS045776 and
1R01NS064983). The authors would like to thank Marco Barazas for
assistance in drawing Fig. 1.
NR 67
TC 20
Z9 20
U1 1
U2 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0734-9750
J9 BIOTECHNOL ADV
JI Biotechnol. Adv.
PD NOV-DEC
PY 2011
VL 29
IS 6
BP 997
EP 1003
DI 10.1016/j.biotechadv.2011.08.021
PG 7
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 845KP
UT WOS:000296821900041
PM 21920429
ER
PT J
AU MacDonald, SM
Harris, EER
Arthur, DW
Bailey, L
Bellon, JR
Carey, L
Goyal, S
Halyard, MY
Moran, MS
Horst, KC
Haffty, BG
AF MacDonald, Shannon M.
Harris, Eleanor E. R.
Arthur, Douglas W.
Bailey, Lisa
Bellon, Jennifer R.
Carey, Lisa
Goyal, Sharad
Halyard, Michele Y.
Moran, Meena S.
Horst, Kathleen C.
Haffty, Bruce G.
TI ACR Appropriateness Criteria (R) Locally Advanced Breast Cancer
SO BREAST JOURNAL
LA English
DT Article
DE appropriateness criteria; breast cancer; locally advanced; radiation
ID CONCURRENT RADIATION-THERAPY; COMBINED-MODALITY TREATMENT; NEOADJUVANT
CHEMOTHERAPY; STAGE-III; POSTOPERATIVE RADIOTHERAPY; PREOPERATIVE
CHEMOTHERAPY; POSTMASTECTOMY RADIATION; COMBINATION CHEMOTHERAPY;
ADJUVANT CHEMOTHERAPY; REGIONAL RECURRENCE
AB Locally advanced breast cancer (LABC) is a disease that is heterogeneous in its presentation, potentially curable, and generally necessitating multidisciplinary management. Radiation therapy (RT) plays an important role in the management of LABC. The integration of radiation with surgery, chemotherapy, and sometimes breast reconstruction can be complex. The American College of Radiology Appropriateness Criteria Breast Committee aims to provide guidance for the management of a variety of LABC cases. The American College of Radiology Appropriateness Criteria is 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 either lacking or not definitive, expert opinion may be used to recommend imaging or treatment.
C1 [MacDonald, Shannon M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Harris, Eleanor E. R.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Arthur, Douglas W.] Virginia Commonwealth Univ, Med Coll Virginia, Richmond, VA 23298 USA.
[Bailey, Lisa] Amer Coll Surg, Alta Bates Summit Med Ctr, Oakland, CA USA.
[Bellon, Jennifer R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Carey, Lisa] Univ N Carolina Hlth Care Syst, Amer Soc Clin Oncol, Chapel Hill, NC USA.
[Goyal, Sharad; Haffty, Bruce G.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, New Brunswick, NJ USA.
[Halyard, Michele Y.] Mayo Clin Scottsdale, Scottsdale, AZ USA.
[Horst, Kathleen C.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Moran, Meena S.] Yale Univ, Sch Med, New Haven, CT USA.
RP MacDonald, SM (reprint author), Amer Coll Radiol, 1891 Preston White Dr, Reston, VA 20191 USA.
EM smacdonald@partners.org
OI Harris, Eleanor/0000-0002-7529-7473
NR 70
TC 5
Z9 6
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1075-122X
J9 BREAST J
JI Breast J.
PD NOV-DEC
PY 2011
VL 17
IS 6
BP 579
EP 585
DI 10.1111/j.1524-4741.2011.01150.x
PG 7
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 849DE
UT WOS:000297104900003
PM 21906206
ER
PT J
AU Kopans, D
Gavenonis, S
Halpern, E
Moore, R
AF Kopans, Daniel
Gavenonis, Sara
Halpern, Elkan
Moore, Richard
TI Calcifications in the Breast and Digital Breast Tomosynthesis
SO BREAST JOURNAL
LA English
DT Article
DE breast; calcifications; digital breast tomosynthesis; mammography;
screening
ID CARCINOMA MORTALITY; MAMMOGRAPHY; NUMBER
AB Our study was to compare the clarity with which calcifications are seen on conventional mammography (CM) with the same calcifications on digital breast tomosynthesis (DBT). We define clarity as the sharpness, contrast, and diagnostic quality by which the calcifications were depicted. In a HIPPA compliant Institutional Review Board approved study, 3,000 women volunteered to have both a screening mammogram and a DBT study. A total of 119 sequential cases with relevant calcifications (not clearly benign) were reviewed. Two board certified, dedicated, breast imaging radiologists reviewed the CM and DBT images in an unblinded paired comparison. Only the mediolateral oblique (MLO) projection was available for the DBT studies. The MLO and craniocaudal projections were reviewed using the 2D images. Window and leveling, and electronic zoom were permitted. Unlimited time was allowed to provide a subjective assessment as too how well the calcifications were seen, from a diagnostic perspective, when the two studies were evaluated side-by-side. In 41.6% of the cases, the readers felt that calcifications were seen with superior clarity on DBT. In 50.4% of the cases, the visibility of calcifications was the same for DBT and CM, and in 8% of the cases, calcifications were seen with greater clarity on CM than DBT. In 92% of the cases, the clarity with which calcifications were seen on DBT was equal to or better than for CM and in almost half, the clarity on DBT was judged to be better than for CM. Our analysis shows that calcifications can be demonstrated with equal or greater clarity on DBT as on CM, thus allowing for comparable, and, perhaps, improved interpretive analysis of detected calcifications.
C1 [Kopans, Daniel; Gavenonis, Sara; Halpern, Elkan; Moore, Richard] Massachusetts Gen Hosp Radiol, Avon Comprehens Breast Ctr, Boston, MA 02114 USA.
RP Kopans, D (reprint author), Massachusetts Gen Hosp Radiol, Avon Comprehens Breast Ctr, Wang ACC 240 15 Parkman St, Boston, MA 02114 USA.
EM kopans.daniel@mgh.harvard.edu
NR 19
TC 55
Z9 57
U1 1
U2 8
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1075-122X
J9 BREAST J
JI Breast J.
PD NOV-DEC
PY 2011
VL 17
IS 6
BP 638
EP 644
DI 10.1111/j.1524-4741.2011.01152.x
PG 7
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 849DE
UT WOS:000297104900010
PM 21906207
ER
PT J
AU Abuabara, K
Lee, H
Kimball, AB
AF Abuabara, K.
Lee, H.
Kimball, A. B.
TI The effect of systemic psoriasis therapies on the incidence of
myocardial infarction: a cohort study
SO BRITISH JOURNAL OF DERMATOLOGY
LA English
DT Article
ID NECROSIS-FACTOR-ALPHA; POSITIVE PREDICTIVE-VALUE; RHEUMATOID-ARTHRITIS;
CARDIOVASCULAR-DISEASE; VASCULAR-DISEASES; RISK-FACTORS;
CORONARY-ARTERY; DOUBLE-BLIND; MORTALITY; INFLIXIMAB
AB Background Psoriasis confers an independent risk of cardiovascular disease that is likely to be related to systemic inflammation. Anti-inflammatory treatment could theoretically reduce the risk of cardiovascular disease, and initial data suggest that treatment may reduce the incidence of cardiovascular risk factors.
Objectives To determine the impact of anti-inflammatory therapy on the risk of acute myocardial infarction (MI) in patients with moderate-to-severe psoriasis.
Methods Cohort study using administrative and pharmacy claims data from a large U. S. insurer comparing patients with psoriasis aged >= 18 years receiving systemic immunomodulatory therapies (methotrexate, ciclosporin, alefacept, efalizumab, adalimumab, etancercept and infliximab) with a control group treated with ultraviolet B phototherapy that has limited systemic anti-inflammatory effects. The risk of acute MI was calculated using a proportional hazards model while controlling for sex, age, hypertension, hyperlipidaemia, diabetes and depression. Significant interaction terms were included in the final model.
Results The study group included 25 554 patients with psoriasis receiving systemic treatment or phototherapy. There was a trend towards an increased risk of MI in the systemic treatment group but not a significant difference in overall MI risk [hazard ratio (HR) 1.33, 95% confidence interval (CI) 0.90-1 96]. Additionally, there was a significant interaction with age: in patients under 50 years the HR for MI if receiving systemic therapy was 0.65 (95% CI 0.32-1.34), and in patients aged 50-70 years it was 1.37 (95% CI 0.79-2.38).
Conclusions Overall, there does not appear to be a reduced risk of MI in patients with psoriasis receiving systemic therapy compared with a group undergoing phototherapy. The risk of MI may vary by age.
C1 [Kimball, A. B.] Massachusetts Gen Hosp, Dept Dermatol, Clin Unit Res Trials Skin, Boston, MA 02114 USA.
[Abuabara, K.] Univ Penn, Dept Dermatol, Philadelphia, PA 19104 USA.
[Lee, H.] Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
RP Kimball, AB (reprint author), Massachusetts Gen Hosp, Dept Dermatol, Clin Unit Res Trials Skin, Boston, MA 02114 USA.
EM harvardskinstudies@partners.org
FU Abbott, Inc.; American Academy of Dermatology; Centocor
FX The investigators received a physician-initiated grant from Abbott, Inc.
to support this work and to gain access to the UnitedHealth data. The
design and conduct of the study, data management, analysis and
interpretation, and preparation and approval of the manuscript were all
performed independently by the investigators. This work was also funded
by the American Academy of Dermatology's Minority Student Mentorship
Program.; K.A. and H. L.: none declared. A. B. K.: Investigator and
Consultant for Abbott, Centocor and Amgen. She has an outcomes
fellowship supported by Centocor. Her department administers
phototherapy.
NR 49
TC 53
Z9 54
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-0963
J9 BRIT J DERMATOL
JI Br. J. Dermatol.
PD NOV
PY 2011
VL 165
IS 5
BP 1066
EP 1073
DI 10.1111/j.1365-2133.2011.10525.x
PG 8
WC Dermatology
SC Dermatology
GA 852BG
UT WOS:000297318700022
PM 21777216
ER
PT J
AU Zhang, DF
Kearney, CJ
Cheriyan, T
Schmid, TM
Spector, M
AF Zhang, Dafang
Kearney, Cathal J.
Cheriyan, Thomas
Schmid, Thomas M.
Spector, Myron
TI Extracorporeal shockwave-induced expression of lubricin in tendons and
septa
SO CELL AND TISSUE RESEARCH
LA English
DT Article
DE ESWT; Lubricin; Tendon; Septum; Rat
ID SUPERFICIAL ZONE PROTEIN; WAVE THERAPY; GENE-EXPRESSION;
ARTICULAR-CARTILAGE; FLEXOR TENDON; BONE; KNEE; PROTEOGLYCAN;
CHONDROCYTES; TENDINITIS
AB Lubricin, a lubricating glycoprotein that facilitates tendon gliding, is upregulated by mechanical as well as biochemical stimuli, prompting this study of its induction by extracorporeal shockwave therapy (ESWT). The objective of this study was to characterize and quantify the effect of ESWT on lubricin expression in tendons and septa in a rat model. Hindlimbs of six rats were treated with low-dose ESWT and those of another six with high-dose ESWT, using contralateral limbs as controls. After 4 days, resected samples were processed for immunolocalization of lubricin using a purified monoclonal antibody. ESWT was found to increase lubricin expression in both low-dose and high-dose ESWT-treated tendons and also in septa. Lubricin expression generally increased with increasing dose of ESWT. Increased lubricin expression may contribute to the beneficial effects of ESWT in providing pain and symptom relief in musculoskeletal disorders by decreasing erosive wear.
C1 [Zhang, Dafang; Kearney, Cathal J.; Cheriyan, Thomas; Spector, Myron] VA Boston Healthcare Syst, Boston, MA 02130 USA.
[Zhang, Dafang; Cheriyan, Thomas; Spector, Myron] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Zhang, Dafang; Kearney, Cathal J.; Spector, Myron] Harvard Mit Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Zhang, Dafang; Cheriyan, Thomas; Spector, Myron] Brigham & Womens Hosp, Dept Orthopaed Surg, Boston, MA 02115 USA.
[Schmid, Thomas M.] Rush Univ, Med Ctr, Dept Biochem, Chicago, IL 60612 USA.
RP Spector, M (reprint author), VA Boston Healthcare Syst, Mail Stop 151 Res,150 S Huntington Ave, Boston, MA 02130 USA.
EM mspector@rics.bwh.harvard.edu
OI Kearney, Cathal/0000-0002-9514-6517
FU Dept. of Veterans Affairs
FX This work was supported in part by the Dept. of Veterans Affairs.
NR 30
TC 3
Z9 3
U1 1
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0302-766X
J9 CELL TISSUE RES
JI Cell Tissue Res.
PD NOV
PY 2011
VL 346
IS 2
BP 255
EP 262
DI 10.1007/s00441-011-1258-7
PG 8
WC Cell Biology
SC Cell Biology
GA 849JU
UT WOS:000297122600011
PM 22009294
ER
PT J
AU Kullgren, JT
Werner, RM
AF Kullgren, Jeffrey T.
Werner, Rachel M.
TI Counterpoint: Will Pubic Reporting of Health-care Quality Measures
Inform and Educate Patients? No
SO CHEST
LA English
DT Editorial Material
ID OF-CARE; CONSUMERS; NETWORK
C1 [Kullgren, Jeffrey T.] Robert Wood Johnson Fdn Clin Scholars, Philadelphia, PA 19104 USA.
[Kullgren, Jeffrey T.; Werner, Rachel M.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
[Kullgren, Jeffrey T.; Werner, Rachel M.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Werner, Rachel M.] Univ Penn, Div Gen Internal Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
RP Kullgren, JT (reprint author), Robert Wood Johnson Fdn Clin Scholars, 1303B Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM kullgren@mail.med.upenn.edu
NR 20
TC 3
Z9 3
U1 2
U2 10
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD NOV
PY 2011
VL 140
IS 5
BP 1117
EP 1120
DI 10.1378/chest.11-2094
PG 4
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 846UK
UT WOS:000296928500006
PM 22045876
ER
PT J
AU Kullgren, JT
Werner, RM
AF Kullgren, Jeffrey T.
Werner, Rachel M.
TI Counterpoint: Will Pubic Reporting of Health-care Quality Measures
Inform and Educate Patients? No Reply
SO CHEST
LA English
DT Editorial Material
ID HOSPITALS
C1 [Kullgren, Jeffrey T.] Robert Wood Johnson Fdn Clin Scholars, Philadelphia, PA 19104 USA.
[Kullgren, Jeffrey T.; Werner, Rachel M.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
[Kullgren, Jeffrey T.; Werner, Rachel M.] Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA.
[Werner, Rachel M.] Univ Penn, Perelman Sch Med, Div Gen Internal Med, Philadelphia, PA 19104 USA.
RP Kullgren, JT (reprint author), Robert Wood Johnson Fdn Clin Scholars, 1303B Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM kullgren@mail.med.upenn.med
NR 7
TC 0
Z9 0
U1 1
U2 2
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD NOV
PY 2011
VL 140
IS 5
BP 1121
EP 1122
DI 10.1378/chest.11-2095
PG 2
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 846UK
UT WOS:000296928500008
ER
PT J
AU Krodel, DJ
Bittner, EA
Abdulnour, REE
Brown, RH
Eikermann, M
AF Krodel, David J.
Bittner, Edward A.
Abdulnour, Raja-Elie E.
Brown, Robert H.
Eikermann, Matthias
TI Negative Pressure Pulmonary Edema Following Bronchospasm
SO CHEST
LA English
DT Article
ID ASTHMA
AB Negative pressure pulmonary edema (NPPE) is an important cause of noncardiogenic pulmonary edema but is rarely reported in the setting of bronchospasm. A 43-year-old woman with severe reactive airway disease suffered an episode of severe bronchospasm after endotracheal extubation following an otherwise uneventful general anesthetic. Subsequently, she developed clinical and radiographic signs of pulmonary edema in the absence of other symptoms of acute left-sided heart failure, leading to the diagnosis of noncardiogenic pulmonary edema. She received noninvasive positive pressure ventilation for a few hours, after which her clinical and radiologic signs and symptoms of pulmonary edema were greatly improved. This clinical scenario strongly suggests NPPE. We submit that it is possible to create NPPE by generating highly negative intrathoracic pressures in the setting of severe bronchospasm. CHEST 2011; 140(5):1351-1354
C1 [Krodel, David J.; Bittner, Edward A.; Eikermann, Matthias] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Abdulnour, Raja-Elie E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Pulm & Crit Care Unit,Dept Med, Boston, MA 02114 USA.
[Brown, Robert H.] Johns Hopkins Univ, Dept Anesthesiol & Crit Care Med, Baltimore, MD USA.
[Brown, Robert H.] Johns Hopkins Univ, Dept Environm Hlth Sci, Div Physiol, Baltimore, MD 21205 USA.
[Brown, Robert H.] Johns Hopkins Univ, Dept Med, Div Pulm Med, Baltimore, MD USA.
[Brown, Robert H.] Johns Hopkins Univ, Dept Radiol, Baltimore, MD USA.
RP Krodel, DJ (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, 55 Fruit St, Boston, MA 02114 USA.
EM dkrodel@partners.org
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U1 1
U2 8
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD NOV
PY 2011
VL 140
IS 5
BP 1351
EP 1354
DI 10.1378/chest.11-0529
PG 4
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 846UK
UT WOS:000296928500038
PM 22045880
ER
PT J
AU O'Connor, CM
Fiuzat, M
Lombardi, C
Fujita, K
Jia, G
Davison, BA
Cleland, J
Bloomfield, D
Dittrich, HC
DeLucca, P
Givertz, MM
Mansoor, G
Ponikowski, P
Teerlink, JR
Voors, AA
Massie, BM
Cotter, G
Metra, M
AF O'Connor, Christopher M.
Fiuzat, Mona
Lombardi, Carlo
Fujita, Kenji
Jia, Gang
Davison, Beth A.
Cleland, John
Bloomfield, Daniel
Dittrich, Howard C.
DeLucca, Paul
Givertz, Michael M.
Mansoor, George
Ponikowski, Piotr
Teerlink, John R.
Voors, Adriaan A.
Massie, Barry M.
Cotter, Gad
Metra, Marco
TI Impact of Serial Troponin Release on Outcomes in Patients With Acute
Heart Failure Analysis From the PROTECT Pilot Study
SO CIRCULATION-HEART FAILURE
LA English
DT Article
DE cardiac troponin; acute heart failure; rolofylline
ID IN-HOSPITAL MORTALITY; LONG-TERM PROGNOSIS; CARDIAC TROPONIN; AMBULATORY
PATIENTS; ADENOSINE A(1); OPTIMIZE-HF; TASK-FORCE; ASSOCIATION;
DYSFUNCTION; GUIDELINES
AB Background-Cardiac troponin T (cTnT) elevation is common and is a predictor of outcomes in patients with acute heart failure (AHF). The degree and progression of cTnT release during hospitalization of patients with AHF is unclear. We evaluated the incidence of cTnT release during AHF hospitalization and the relationship of cTnT release with outcomes.
Methods and Results-The Placebo-controlled Randomized study of the selective A(1) adenosine receptor antagonist rolofylline for patients hospitalized with acute heart failure and volume Overload to assess Treatment Effect on Congestion and renal funcTion (PROTECT) pilot study was a multicenter, double-blind study of patients with AHF. Measurements of cTnT were collected at randomization and days 2, 3, 4, and 7. Patients were classified on the basis of their serum cTnT levels at baseline: positive (>0.03 ng/mL), detectable (>0.01 ng/mL), and negative (>= 0.01 ng/mL). A detectable cTnT level developed during the study (after baseline) was classified as cTnT conversion: 288 patients were included; 172 (60%) patients had detectable cTnT levels and 97 (34%) had positive values (>0.03 ng/mL) at baseline. Of the 116 patients with negative troponin at baseline, 24 (21%) had elevated cTnT levels by day 7. On multivariable analysis, positive cTnT at baseline was an independent predictor of the composite end point of cardiovascular/renal rehospitalization or death at 60 days (hazard ratio, 1.84; 95% confidence interval, 1.04-3.26; P=0.036). Kaplan-Meier curves showed similar worse outcomes in patients with troponin conversion and positive troponin at baseline.
Conclusions-There was a high prevalence of baseline cTnT elevation in this cohort; 21% of those negative at baseline converted to detectable levels by day 7. Positive troponin at baseline, and conversion to positive levels, were associated with worse outcomes at 60 days. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifiers: NCT00328692 and NCT00354458. (Circ Heart Fail. 2011;4:724-732.)
C1 [O'Connor, Christopher M.; Fiuzat, Mona] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC USA.
[Lombardi, Carlo; Metra, Marco] Univ Brescia, Dept Expt & Appl Med, Brescia, Italy.
[Fujita, Kenji; Jia, Gang; Bloomfield, Daniel; Dittrich, Howard C.; DeLucca, Paul; Mansoor, George] Merck Res Labs, Rahway, NJ USA.
[Davison, Beth A.; Cotter, Gad] Momentum Res, Durham, NC USA.
[Cleland, John] Univ Hull, Kingston Upon Hull HU6 7RX, N Humberside, England.
[Givertz, Michael M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Ponikowski, Piotr] Med Univ, Clin Mil Hosp, Wroclaw, Poland.
[Teerlink, John R.; Massie, Barry M.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Teerlink, John R.; Massie, Barry M.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Voors, Adriaan A.] Univ Groningen, Univ Med Ctr Groningen, Groningen, Netherlands.
RP O'Connor, CM (reprint author), DUMC Box 3356, Durham, NC 27705 USA.
EM oconn002@mc.duke.edu
RI Teerlink, John/D-2986-2012; lombardi, carlo /O-2130-2013; Ponikowski,
Piotr/O-6454-2015;
OI lombardi, carlo /0000-0002-7120-5877; Ponikowski,
Piotr/0000-0002-3391-7064; Davison, Beth/0000-0003-2374-6449; Cleland,
John/0000-0002-1471-7016; Metra, Marco/0000-0001-6691-8568
FU Merck
FX Drs O'Connor, Voors, Ponikowski, Dittrich, Metra, Teerlink, Massie,
Givertz, Cleland, Weatherley, and Cotter received research funding from
Merck. Drs Jia, Fujita, Mansoor, Bloomfield, and DeLucca are employees
of Merck.
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-3289
J9 CIRC-HEART FAIL
JI Circ.-Heart Fail.
PD NOV
PY 2011
VL 4
IS 6
BP 724
EP 732
DI 10.1161/CIRCHEARTFAILURE.111.961581
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 850AF
UT WOS:000297166100012
PM 21900185
ER
PT J
AU Ge, XW
Wu, L
Hu, WG
Fernandes, S
Wang, C
Li, X
Brown, JR
Qin, XB
AF Ge, Xiaowen
Wu, Lin
Hu, Weiguo
Fernandes, Stacey
Wang, Chun
Li, Xu
Brown, Jennifer R.
Qin, Xuebin
TI rILYd4, a Human CD59 Inhibitor, Enhances Complement-Dependent
Cytotoxicity of Ofatumumab against Rituximab-Resistant B-cell Lymphoma
Cells and Chronic Lymphocytic Leukemia
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID ANTI-CD20 MONOCLONAL-ANTIBODY; MEMBRANE ATTACK COMPLEX; NON-HODGKIN
LYMPHOMAS; REGULATORY PROTEINS; IN-VITRO; AUTOIMMUNE DISORDERS;
PROTECTIN CD59; CANCER-CELLS; HUMAN CD20; ACTIVATION
AB Purpose: Ofatumumab is an anti-CD20 antibody recently approved for treatment of fludarabine and alemtuzumab refractory chronic lymphocytic leukemia (CLL); it mediates much stronger complement-dependent cytotoxicity (CDC) than rituximab. Human CD59, a key membrane complement regulator that inhibits CDC, is highly expressed in B-cell malignancies and its upregulation is an important determinant of the sensitivity of B-cell malignancies to rituximab treatment. Previously, we have shown that the potent CD59 inhibitor rILYd4 sensitizes rituximab-resistant lymphoma cells to rituximab-mediated CDC. Here, we further investigated whether rILYd4 can sensitize B-cell malignancies to ofatumumab-mediated CDC and whether either ofatumumab-mediated CDC or rILYd4-enhanced ofatumumab-mediated CDC correlates with CD20 or CD59 expression, known biomarkers involved in rituximab activity.
Experimental Design: Rituximab-resistant cell lines and primary CLL cells were used to investigate the antitumor efficacy of the combination of rILYd4 with ofatumumab or rituximab. Propidium iodide staining or alamarBlue assay were used to evaluate the CDC effect. The levels of CD20 and CD59 on the cell membrane were analyzed by flow cytometry.
Results: rILYd4 enhanced CDC effects mediated by ofatumumab or rituximab on rituximab-resistant lymphoma cells and primary CLL cells in vitro. The sensitivity to CDC effects mediated by ofatumumab positively correlated with the ratio of CD20/CD59 and negatively correlated with CD59 levels on CLL cells. The degree to which rILYd4 enhanced CDC correlated positively with the CD59 levels on CLL cells.
Conclusions: These data suggest that rILYd4 may enhance the anticancer activity of ofatumumab and rituximab in B-cell malignancies that have relapsed after prior antibody-based therapies. Clin Cancer Res; 17(21); 6702-11. (C)2011 AACR.
C1 [Ge, Xiaowen; Wu, Lin; Hu, Weiguo; Qin, Xuebin] Harvard Univ, Sch Med, Lab Translat Res, Cambridge, MA 02139 USA.
[Ge, Xiaowen; Li, Xu] Xi An Jiao Tong Univ, Sch Med, Affiliated Hosp 1, Ctr Mol Med, Xian, Peoples R China.
[Hu, Weiguo; Brown, Jennifer R.; Qin, Xuebin] Harvard Univ, Sch Med, Dept Med, Brigham & Womens Hosp, Boston, MA USA.
[Fernandes, Stacey; Brown, Jennifer R.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Wu, Lin; Wang, Chun] Shanghai First Peoples Hosp, Dept Hematol, Shanghai, Peoples R China.
RP Qin, XB (reprint author), Harvard Univ, Sch Med, Lab Translat Res, 1 Kendall Sq,Bldg 600,3rd Floor, Cambridge, MA 02139 USA.
EM xuebin_qin@hms.harvard.edu
FU GSK; Harvard Technology Development Accelerator Fund; China Scholarship
Council [2009628090]; ASH; Leukemia and Lymphoma Society;
[NIHRO1AI061174]; [NIHR21CA141324]; [NIHK23CA115682]
FX J.R. Brown receives research funding from GSK. No potential conflicts of
interest were disclosed by the other authors.; This work was supported
by NIHRO1AI061174 (to X. B. Qin) and NIHR21CA141324 (to X. B. Qin),
Harvard Technology Development Accelerator Fund (to X. B. Qin), and
China Scholarship Council (2009628090; to X. Ge). J.R. Brown is
supported by NIHK23CA115682 as well as by an ASH Scholar award and the
Leukemia and Lymphoma Society Scholar in Clinical Research Award.
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U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 1
PY 2011
VL 17
IS 21
BP 6702
EP 6711
DI 10.1158/1078-0432.CCR-11-0647
PG 10
WC Oncology
SC Oncology
GA 842TS
UT WOS:000296624000014
PM 21918174
ER
PT J
AU Ouillette, P
Collins, R
Shakhan, S
Li, JH
Li, C
Shedden, K
Malek, SN
AF Ouillette, Peter
Collins, Roxane
Shakhan, Sajid
Li, Jinghui
Li, Cheng
Shedden, Kerby
Malek, Sami N.
TI The Prognostic Significance of Various 13q14 Deletions in Chronic
Lymphocytic Leukemia
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID ACUTE MYELOGENOUS LEUKEMIA; CHROMOSOME 13Q14; GENOMIC COMPLEXITY;
TRANSCRIPTION MAP; GENE; REGION; CLL; LOCUS; SEQUENCE; SURVIVAL
AB Purpose: To further our understanding of the biology and prognostic significance of various chromosomal 13q14 deletions in chronic lymphocytic leukemia (CLL).
Experimental Design: We analyzed data from SNP 6.0 arrays to define the anatomy of various 13q14 deletions in a cohort of 255 CLL patients and have correlated two subsets of 13q14 deletions (type I exclusive of RB1 and type II inclusive of RB1) with patient survival. Furthermore, we measured the expression of the 13q14-resident microRNAs by quantitative PCR (Q-PCR) in 242 CLL patients and subsequently assessed their prognostic significance. We sequenced all coding exons of RB1 in patients with monoallelic RB1 deletion and have sequenced the 13q14-resident miR locus in all patients.
Results: Large 13q14 (type II) deletions were detected in approximately 20% of all CLL patients and were associated with shortened survival. A strong association between 13q14 type II deletions and elevated genomic complexity, as measured through CLL-FISH or SNP 6.0 array profiling, was identified, suggesting that these lesions may contribute to CLL disease evolution through genomic destabilization. Sequence and copy number analysis of the RB1 gene identified a small CLL subset that is RB1 null. Finally, neither the expression levels of the 13q14-resident microRNAs nor the degree of 13q14 deletion, as measured through SNP 6.0 array-based copy number analysis, had significant prognostic importance.
Conclusions: Our data suggest that the clinical course of CLL is accelerated in patients with large (type II) 13q14 deletions that span the RB1 gene, therefore justifying routine identification of 13q14 subtypes in CLL management. Clin Cancer Res; 17(21); 6778-90. (C)2011 AACR.
C1 [Ouillette, Peter; Collins, Roxane; Shakhan, Sajid; Li, Jinghui; Malek, Sami N.] Univ Michigan, Dept Internal Med, Div Hematol & Oncol, Ann Arbor, MI 48109 USA.
[Shedden, Kerby] Univ Michigan, Dept Stat, Ann Arbor, MI 48109 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Li, Cheng] Harvard Univ, Sch Publ Hlth, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Li, Cheng] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Malek, SN (reprint author), Univ Michigan, Dept Internal Med, Div Hematol & Oncol, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM smalek@med.umich.edu
FU NIH [1R01 CA136537-01]; Leukemia and Lymphoma Society of America; NIH
through the University of Michigan [5 P30 CA46592]
FX This work was supported by the NIH through grant 1R01 CA136537-01 (to
S.N. Malek), the Translational Research Program of the Leukemia and
Lymphoma Society of America (to S.N. Malek), and a Scholar in Clinical
Research Award from the Leukemia and Lymphoma Society of America (to
S.N. Malek). This research is supported (in part) by the NIH through the
University of Michigan's Cancer Center Support grant (5 P30 CA46592).
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U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 1
PY 2011
VL 17
IS 21
BP 6778
EP 6790
DI 10.1158/1078-0432.CCR-11-0785
PG 13
WC Oncology
SC Oncology
GA 842TS
UT WOS:000296624000021
PM 21890456
ER
PT J
AU Mayer, EL
Baurain, JF
Sparano, J
Strauss, L
Campone, M
Fumoleau, P
Rugo, H
Awada, A
Sy, O
Llombart-Cussac, A
AF Mayer, Erica L.
Baurain, Jean-Francois
Sparano, Joseph
Strauss, Lewis
Campone, Mario
Fumoleau, Pierre
Rugo, Hope
Awada, Ahmad
Sy, Oumar
Llombart-Cussac, Antonio
TI A Phase 2 Trial of Dasatinib in Patients with Advanced HER2-Positive
and/or Hormone Receptor-Positive Breast Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID TYROSINE KINASE-ACTIVITY; C-SRC; SOLID TUMORS; INHIBITS GROWTH;
CELL-LINES; METASTASIS; EXPRESSION; SURVIVAL; TAMOXIFEN; BONE
AB Purpose: SRC-family kinases (SFK) are involved in numerous oncogenic signaling pathways. A phase 2 trial of dasatinib, a potent oral tyrosine kinase inhibitor of SFKs, was carried out in patients with human epidermal growth factor receptor 2-positive (HER2+) and/or hormone receptor-positive (HR+) advanced breast cancer.
Experimental Design: Patients with measurable tumors and progression after chemotherapy and HER2 and/or HR-targeted agents in adjuvant or metastatic settings (maximum of two prior metastatic setting regimens) received twice daily dasatinib. Primary endpoint was Response Evaluation Criteria in Solid Tumors-defined response rate. Secondary endpoints included toxicity and limited pharmacokinetics.
Results: Seventy patients (55 years median age) were treated, 83% of HER2+ patients had received prior HER2-directed therapy, and 61% of HR+ patients had received prior endocrine therapy in the advanced setting. Dasatinib starting dose was reduced from 100 to 70 mg twice daily to limit toxicity. Median therapy duration was 1.8 months in both dose groups and most discontinuations were due to progression. Of 69 evaluable patients, three had confirmed partial responses and six had stable disease for 16 weeks or more (disease control rate 13.0%); all nine of these tumors were HR+ (two were also HER2+). The most common drug-related toxicities were gastrointestinal complaints, headache, asthenia, and pleural effusion. Grade 3-4 toxicity occurred in 37% of patients and was comparable between doses; drug-related serious adverse events were less frequent with 70 mg twice daily than 100 mg twice daily.
Conclusion: Limited single-agent activity was observed with dasatinib in patients with advanced HR+ breast cancer. Clin Cancer Res; 17(21); 6897-904. (C)2011 AACR.
C1 [Mayer, Erica L.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Awada, Ahmad] Inst Jules Bordet, B-1000 Brussels, Belgium.
[Sparano, Joseph] Montefiore Einstein Canc Ctr, New York, NY USA.
[Strauss, Lewis; Sy, Oumar] Bristol Myers Squibb Co, Wallingford, CT 06492 USA.
[Campone, Mario] Ctr Lutte Canc Nantes Atlantique, St Herblain, France.
[Fumoleau, Pierre] Ctr Georges Francois Leclerc, Dijon, France.
[Rugo, Hope] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
[Llombart-Cussac, Antonio] Hosp Arnau Vilanova, Lleida, Spain.
RP Mayer, EL (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM Erica_Mayer@dfci.harvard.edu
RI Llombart-Cussac, Antonio/A-6706-2010
FU Bristol-Myers Squibb Oncology, Princeton, NJ; Bristol-Myers Squibb
FX This study was sponsored by Bristol-Myers Squibb Oncology, Princeton,
NJ.; This study was designed by employees of Bristol-Myers Squibb with
input from investigators. Patient data were collected at participating
institutes, analyzed using the data-management systems of the sponsor,
and interpreted by the statistical team of the sponsor in collaboration
with the authors. Study data were available to all authors. An initial
version of the manuscript was written by Erica Mayer, and further
developed with assistance from an independent company funded by
Bristol-Myers Squibb. All authors contributed to writing and reviewing
of the manuscript and agreed with the decision to submit for
publication.
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U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 1
PY 2011
VL 17
IS 21
BP 6897
EP 6904
DI 10.1158/1078-0432.CCR-11-0070
PG 8
WC Oncology
SC Oncology
GA 842TS
UT WOS:000296624000033
PM 21903773
ER
PT J
AU Stedman, MR
Gagnon, DR
Lew, RA
Jung, SH
Losina, E
Brookhart, MA
AF Stedman, Margaret R.
Gagnon, David R.
Lew, Robert A.
Jung, Sin-Ho
Losina, Elena
Brookhart, M. Alan
TI A SAS macro for a clustered logrank test
SO COMPUTER METHODS AND PROGRAMS IN BIOMEDICINE
LA English
DT Article
DE Logrank test; Cluster randomized trial; Clustered logrank test; SAS
macro
ID SURVIVAL-DATA; RANK-TESTS
AB The clustered logrank test is a nonparametric method of significance testing for correlated survival data. Examples of its application include cluster randomized trials where groups of patients rather than individuals are randomized to either a treatment or a control intervention. We describe a SAS macro that implements the 2-sample clustered logrank test for data where the entire cluster is randomized to the same treatment group. We discuss the theory and applications behind this test as well as details of the SAS code. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Stedman, Margaret R.; Losina, Elena] Brigham & Womens Hosp, Orthoped & Arthrit Ctr Outcomes Res, Dept Orthoped, Boston, MA 02115 USA.
[Gagnon, David R.; Lew, Robert A.; Losina, Elena] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Gagnon, David R.; Lew, Robert A.] Boston VA Healthcare Syst, MAVERIC, VA Cooperat Studies, Boston, MA USA.
[Stedman, Margaret R.; Losina, Elena] Harvard Univ, Sch Med, Boston, MA USA.
[Jung, Sin-Ho] Duke Univ, Sch Med, Dept Biostat & Bioinformat, Durham, NC USA.
[Brookhart, M. Alan] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
RP Stedman, MR (reprint author), Brigham & Womens Hosp, Orthoped & Arthrit Ctr Outcomes Res, Dept Orthoped, 75 Francis St, Boston, MA 02115 USA.
EM mstedman2@partners.org
OI Gagnon, David/0000-0002-6367-3179; Stedman, Margaret/0000-0001-9271-8332
FU National Institutes of Health [AG-027400]; [NRSA/T32 AR055885-03]
FX I would like to acknowledge Dr. Daniel H. Solomon at Harvard Medical
School and Brigham and Women's Hospital for his osteoporosis studies
which provided inspiration for this work. This research was supported by
the National Institutes of Health, Grant #AG-027400 awarded to M. Alan
Brookhart and NRSA/T32 AR055885-03 awarded to Margaret Stedman.
NR 8
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U1 0
U2 3
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0169-2607
J9 COMPUT METH PROG BIO
JI Comput. Meth. Programs Biomed.
PD NOV
PY 2011
VL 104
IS 2
BP 266
EP 270
DI 10.1016/j.cmpb.2011.02.001
PG 5
WC Computer Science, Interdisciplinary Applications; Computer Science,
Theory & Methods; Engineering, Biomedical; Medical Informatics
SC Computer Science; Engineering; Medical Informatics
GA 847AU
UT WOS:000296945100031
PM 21496938
ER
PT J
AU Hamrah, P
Alipour, F
Jiang, S
Sohn, JH
Foulks, GN
AF Hamrah, P.
Alipour, F.
Jiang, S.
Sohn, J-H
Foulks, G. N.
TI Optimizing evaluation of Lissamine Green parameters for ocular surface
staining
SO EYE
LA English
DT Article
DE Lissamine Green; corneal staining; dry eye; ocular surface; conjunctiva;
vital dye
ID EYE WORKSHOP 2007; DRY EYE; ROSE-BENGAL; IN-VITRO; SUBCOMMITTEE;
CORNEAL; DISEASE; TESTS
AB Purpose The recently published seminal dry eye workshop proceedings defined Lissamine Green (LG), an organic dye, as a gold standard for demonstrating ocular surface staining. The purpose of the current study was to determine the optimal parameters of 1% LG instillation for the ocular surface examination in dry eye patients.
Design Prospective and observational quality improvement study.
Methods A quality improvement study evaluated 16 eyes from eight dry eye patients with different levels of severity. LG (1%), in three volumes (5, 10, and 20 mu l) was instilled into the conjunctival cul-de-sac, and four masked observers with different levels of clinical expertise examined the patients with and without red filter. The staining pattern of the conjunctiva and cornea was documented with the Oxford scale within 4 min of LG instillation. Optimal volume and inter-observer reliability were assessed.
Results All dye volumes were tolerated well by all patients. Experienced observers preferred 10 mu l volume because of the ease of examination and accuracy. Although instillation of 20 mu l yielded similar scores as 10 mu l, it resulted in overflow of the lid and facial skin staining. The use of red filter significantly improved reading scores (P<0.01). Inter-observer reliability was higher for conjunctival scores than for corneal scores for all patients. The highest reliability was demonstrated with 10 mu l volume and increased with greater experience of the observer.
Conclusions Ocular surface examination with instillation of 10 mu l 1% LG has good inter-observer reliability and is well tolerated. Observation through a red filter facilitates the examination. Eye (2011) 25, 1429-1434; doi:10.1038/eye.2011.184; published online 12 August 2011
C1 [Hamrah, P.; Jiang, S.; Sohn, J-H; Foulks, G. N.] Univ Louisville, Dept Ophthalmol & Visual Sci, Louisville, KY 40292 USA.
[Hamrah, P.; Alipour, F.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Cornea & Refract Surg Serv,Dept Ophthalmol, Boston, MA USA.
RP Foulks, GN (reprint author), Univ Louisville, Dept Ophthalmol & Visual Sci, Louisville, KY 40292 USA.
EM gnfoul01@louisville.edu
FU NIH [K08-EY020575]; New England Corneal Transplant Research Fund; RPB
Department
FX Financial support was provided by NIH K08-EY020575 (PH), New England
Corneal Transplant Research Fund (PH) and RPB Department Grant (GF).
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PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-222X
J9 EYE
JI Eye
PD NOV
PY 2011
VL 25
IS 11
BP 1429
EP 1434
DI 10.1038/eye.2011.184
PG 6
WC Ophthalmology
SC Ophthalmology
GA 850PY
UT WOS:000297209400006
PM 21836630
ER
PT J
AU Jurkunas, UV
Jakobiec, FA
Shin, J
Zakka, FR
Michaud, N
Jethva, R
AF Jurkunas, U. V.
Jakobiec, F. A.
Shin, J.
Zakka, F. R.
Michaud, N.
Jethva, R.
TI Reversible corneal epitheliopathy caused by vitamin B12 and folate
deficiency in a vegan with a genetic mutation: a new disease
SO EYE
LA English
DT Letter
C1 [Jurkunas, U. V.; Jakobiec, F. A.; Shin, J.; Zakka, F. R.; Michaud, N.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA.
[Jurkunas, U. V.] Harvard Univ, Sch Med, Dept Ophthalmol, Schepens Eye Res Inst, Boston, MA USA.
Harvard Univ, Sch Med, Cogan Lab Ophthalm Pathol, Dept Ophthalmol, Boston, MA USA.
[Jethva, R.] Floating Hosp Children, Tufts Med Ctr, Boston, MA USA.
RP Jurkunas, UV (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA.
EM Ula_Jurkunas@meei.harvard.edu
FU NEI NIH HHS [R01 EY020581, R01EY020581]
NR 5
TC 1
Z9 1
U1 2
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-222X
J9 EYE
JI Eye
PD NOV
PY 2011
VL 25
IS 11
BP 1512
EP 1514
DI 10.1038/eye.2011.177
PG 3
WC Ophthalmology
SC Ophthalmology
GA 850PY
UT WOS:000297209400018
PM 21818128
ER
PT J
AU Bhattacharya, A
Jernigan, AL
Sabia, M
Zhang, YQ
Li, Y
Qi, WB
Van Remmen, H
AF Bhattacharya, Arunabh
Jernigan, Amanda L.
Sabia, Marian
Zhang, Yiqiang
Li, Yan
Qi, Wenbo
Van Remmen, Holly
TI Disruption of the 12/15-Lipoxygenase Gene (Alox15) Protects Against
Denervation-Induced Muscle Atrophy
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 18th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine
(SFRBM)
CY NOV 16-20, 2011
CL Atlanta, GA
SP Soc Free Rad Biol & Med (SFRBM)
C1 [Bhattacharya, Arunabh; Jernigan, Amanda L.; Sabia, Marian; Zhang, Yiqiang; Li, Yan; Qi, Wenbo; Van Remmen, Holly] Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst, San Antonio, TX 78229 USA.
[Van Remmen, Holly] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
NR 0
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 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD NOV 1
PY 2011
VL 51
SU 1
BP S76
EP S76
DI 10.1016/j.freeradbiomed.2011.10.420
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 848FS
UT WOS:000297036600186
ER
PT J
AU Kachadourian, R
Day, BJ
Pugazhenti, S
Franklin, CC
Mahaffey, G
Gauthier, C
Valdameri, G
Di Pietro, A
Boumendjel, A
AF Kachadourian, Remy
Day, Brian J.
Pugazhenti, Subbiah
Franklin, Christopher C.
Mahaffey, Gregory
Gauthier, Charlotte
Valdameri, Glaucio
Di Pietro, Attilio
Boumendjel, Ahcene
TI A New Synthetic Chalcone Derivative is a Potent Inducer of Glutathione
Synthesis
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 18th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine
(SFRBM)
CY NOV 16-20, 2011
CL Atlanta, GA
SP Soc Free Rad Biol & Med (SFRBM)
C1 [Kachadourian, Remy; Day, Brian J.; Pugazhenti, Subbiah; Franklin, Christopher C.] Univ Colorado Denver, Denver, CO USA.
[Pugazhenti, Subbiah; Mahaffey, Gregory] Denver VA Med Ctr, Denver, CO USA.
[Gauthier, Charlotte; Valdameri, Glaucio; Di Pietro, Attilio] CNRS, Inst Biol & Chim Prot, Lyon, France.
[Boumendjel, Ahcene] Univ Grenoble 1, Grenoble, France.
RI Valdameri, Glaucio/A-8909-2013
OI Valdameri, Glaucio/0000-0003-1882-1512
NR 2
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD NOV 1
PY 2011
VL 51
SU 1
BP S88
EP S89
DI 10.1016/j.freeradbiomed.2011.10.407
PG 2
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 848FS
UT WOS:000297036600221
ER
PT J
AU Mostoslavsky, R
AF Mostoslavsky, Raul
TI SIRT6, A MASTER REGULATOR OF GLUCOSE HOMEOSTASIS AND CANCER METABOLISM
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 18th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine
(SFRBM)
CY NOV 16-20, 2011
CL Atlanta, GA
SP Soc Free Rad Biol & Med (SFRBM)
C1 [Mostoslavsky, Raul] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, Cambridge, MA 02138 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD NOV 1
PY 2011
VL 51
SU 1
BP S8
EP S8
DI 10.1016/j.freeradbiomed.2011.10.017
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 848FS
UT WOS:000297036600014
ER
PT J
AU Shi, Y
Liu, YH
Li, Y
Hamilton, RT
Jernigan, AL
Jang, YC
Van Remmen, H
AF Shi, Yun
Liu, Yuhong
Li, Yan
Hamilton, Ryan T.
Jernigan, Amanda L.
Jang, Youngmok C.
Van Remmen, Holly
TI Age-related Changes in Neurotrophic Factors Expression in Skeletal
Muscle Undergoing Atrophy
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 18th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine
(SFRBM)
CY NOV 16-20, 2011
CL Atlanta, GA
SP Soc Free Rad Biol & Med (SFRBM)
C1 [Shi, Yun; Liu, Yuhong; Li, Yan; Hamilton, Ryan T.; Jernigan, Amanda L.; Van Remmen, Holly] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX USA.
[Jang, Youngmok C.] Harvard Univ, Cambridge, MA 02138 USA.
[Van Remmen, Holly] S Texas Vet Hlth Care Syst, San Antonio, TX USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD NOV 1
PY 2011
VL 51
SU 1
BP S79
EP S80
DI 10.1016/j.freeradbiomed.2011.10.431
PG 2
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 848FS
UT WOS:000297036600197
ER
PT J
AU Boudreaux, ED
Niro, K
Sullivan, A
Rosenbaum, CD
Allen, M
Camargo, CA
AF Boudreaux, Edwin D.
Niro, Kathryn
Sullivan, Ashley
Rosenbaum, Christopher D.
Allen, Michael
Camargo, Carlos A., Jr.
TI Current practices for mental health follow-up after psychiatric
emergency department/psychiatric emergency service visits: a national
survey of academic emergency departments
SO GENERAL HOSPITAL PSYCHIATRY
LA English
DT Article
DE Emergency; Psychiatry; Follow-up; Referral; Outpatient
ID USERS; TEAM; CARE
AB Objective: The objective was to describe continuity of care approaches for psychiatric emergencies in the emergency department.
Methods: A national survey of all 138 academic emergency departments in the United States was conducted.
Results: Most emergency physicians (81%) had no systematic method for identifying psychiatric emergency patients with high recidivism. In order to promote outpatient care, sites commonly reported using intensive interventions, including scheduling outpatient appointments prior to discharge (72%) and in-house case management (64%).
Conclusion: While systematic identification of repeat psychiatric emergency patients was uncommon, emergency departments reported using a variety of fairly intensive strategies to promote continuity of care with outpatient mental health services. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Boudreaux, Edwin D.; Rosenbaum, Christopher D.] Univ Massachusetts, Sch Med, Dept Emergency Med, Worcester, MA 01655 USA.
[Niro, Kathryn; Sullivan, Ashley; Camargo, Carlos A., Jr.] Massachusetts Gen Hosp, Dept Emergency Med, Emergency Med Network, Boston, MA 02114 USA.
[Allen, Michael] Univ Colorado, Depress Ctr, Aurora, CO 80045 USA.
RP Rosenbaum, CD (reprint author), Univ Massachusetts, Sch Med, Dept Emergency Med, Worcester, MA 01655 USA.
EM edwin.boudreaux@umassmed.edu; kniro@partners.org;
afsullivan@partners.org; Christopher.Rosenbaum@umassmemorial.org;
michael.allen@ucdenver.edu; ccamargo@partners.org
RI McCarthy, Jodie/B-5760-2012; Allen, Michael/A-8776-2011;
OI Boudreaux, Edwin/0000-0002-3223-6371
NR 25
TC 6
Z9 6
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0163-8343
J9 GEN HOSP PSYCHIAT
JI Gen. Hosp. Psych.
PD NOV-DEC
PY 2011
VL 33
IS 6
BP 631
EP 633
DI 10.1016/j.genhosppsych.2011.05.020
PG 3
WC Psychiatry
SC Psychiatry
GA 848EU
UT WOS:000297034000015
PM 21872940
ER
PT J
AU Dupuy, JM
Ostacher, MJ
Huffman, J
Perlis, RH
Nierenberg, AA
AF Dupuy, Jamie M.
Ostacher, Michael J.
Huffman, Jeffrey
Perlis, Roy H.
Nierenberg, Andrew A.
TI A critical review of pharmacotherapy for major depressive disorder
SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
LA English
DT Review
DE Antidepressant; major depressive disorder; outcomes; pharmacological
treatment
ID SEROTONIN REUPTAKE INHIBITORS; STAR-ASTERISK-D;
PLACEBO-CONTROLLED-TRIAL; ANTIDEPRESSANT PRESCRIPTION RATES; RESISTANT
UNIPOLAR DEPRESSION; DOUBLE-BLIND; 2ND-GENERATION ANTIDEPRESSANTS;
MODAFINIL AUGMENTATION; ADJUNCTIVE TREATMENT; RESIDUAL SYMPTOMS
AB Newer generation antidepressant drugs, with improvements in safety and tolerability, have replaced tricyclic antidepressants as first-line treatment of depressive illness. However, no single antidepressant drug from any class has distinguished itself as the obvious first-line treatment of major depression. The choice of therapy is driven primarily by patient choice, with informed consent for the risks of adverse effects. Cost has become an additional factor in this decision as several of the newer antidepressant drugs are now available in generic form. Several augmentation and drug-switching strategies have demonstrated benefit in refractory illness. While no single strategy distinguished itself as superior to the others, some have been more rigorously tested. Ongoing efforts at improving effectiveness, time to response, and tolerability have led to novel drug therapies. Efforts at characterizing predictors of treatment outcomes now include pharmacogenetic studies.
C1 [Dupuy, Jamie M.; Huffman, Jeffrey; Perlis, Roy H.; Nierenberg, Andrew A.] Massachusetts Gen Hosp, Bipolar Clin & Res Program, Dept Psychiat, Boston, MA 02114 USA.
[Dupuy, Jamie M.; Huffman, Jeffrey; Perlis, Roy H.; Nierenberg, Andrew A.] Harvard Univ, Sch Med, Boston, MA USA.
[Ostacher, Michael J.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA USA.
RP Dupuy, JM (reprint author), Massachusetts Gen Hosp, Bipolar Clin & Res Program, Dept Psychiat, 50 Staniford St,Suite 580, Boston, MA 02114 USA.
EM jdupuy@partners.org
OI Ostacher, Michael/0000-0003-0353-7535
FU National Institute on Alcoholism and Alcohol Abuse [K23AA016340-01A1];
Harvard Catalyst/The Harvard Clinical and Translational Science Center
[UL1 RR 025758]; Harvard University; Pfizer; AstraZeneca; Bristol-Myers
Squibb; Eli Lilly Company; GlaxoSmithKline; Janssen Pharmaceutica;
Massachusetts General Psychiatry Academy; Eli Lilly Co.; Proteus
Biomedical; Concordant Rater Systems; MGH from NIMH; PamLabs; Pfizer
Pharmaceuticals; Shire; Eli Lilly; Janssen Pharmaceuticals
FX Supported in part by the National Institute on Alcoholism and Alcohol
Abuse (Grant K23AA016340-01A1), and the Scholars in Clinical Science
Program of Harvard Catalyst/The Harvard Clinical and Translational
Science Center (Award #UL1 RR 025758 and financial contributions from
Harvard University and its affiliated academic health care centres) (Dr
Ostacher). 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 centres, the
National Center for Research Resources or the National Institutes of
Health.; Dr Ostacher has received research support from Pfizer, and has
served on the advisory/consulting boards of Pfizer, Schering-Plough, and
Concordant Rater Systems. He has received speaker's fees from
AstraZeneca, Bristol-Myers Squibb, Eli Lilly & Company, GlaxoSmithKline,
Janssen Pharmaceutica, Pfizer, and Massachusetts General Psychiatry
Academy.; Dr Perlis has received honoraria, consulting, or speaker's
fees from AstraZeneca, Bristol-Myers Squibb, Eli Lilly & Co.,
GlaxoSmithKline, Pfizer, Proteus Biomedical, and Concordant Rater
Systems. He holds patents and receives royalties with Concordant Rater
Systems.; Dr Nierenberg is a full-time employee of the Massachusetts
General Hospital (MGH). In the past 12 months (as of 3 March 2009), he
has served as a consultant to the American Psychiatric Association (only
travel expenses paid), Appliance Computing Inc. (Mindsite), Brandeis
University. Through the MGH Clinical Trials Network and Institute, he
has consulted for Brain Cells, Inc., Dianippon Sumitomo/Sepracor
Novartis, PGx Health, Shire, Schering-Plough, Targacept, and
Takeda/Lundbeck Pharmaceuticals. He received grant/research support
through MGH from NIMH, PamLabs, Pfizer Pharmaceuticals, and Shire. He
received honoraria from Belvior Publishing, University of Texas
Southwestern Dallas, Hillside Hospital, American Drug Utilization
Review, American Society for Clinical Psychopharmacology, Baystate
Medical Center, Columbia University, IMEDEX, MJ Consulting, New York
State, MBL Publishing, Physicians Postgraduate Press, SUNY Buffalo,
University of Wisconsin, and the University of Pisa. Dr Nierenberg is a
presenter for the Massachusetts General Hospital Psychiatry Academy
(MGHPA). The education programs conducted by the MGHPA were supported
through Independent Medical Education (IME) grants from the following
pharmaceutical companies in 2008: Astra Zeneca, Eli Lilly, and Janssen
Pharmaceuticals; in 2009 Astra Zeneca, Eli Lilly, and Bristol-Myers
Squibb. No speakers' bureaus or boards since 2003. He is on the advisory
boards of Appliance Computing, Inc., Brain Cells, Inc., Eli Lilly and
Company, and Takeda/Lundbeck and Targacept. Dr. Nierenberg owns stock
options in Appliance Computing, Inc. and Brain Cells, Inc. Through MGH,
he is named for copyrights to the Clinical Positive Affect Scale and the
MGH Structured Clinical Interview for the Montgomery-Asberg Depression
Scale exclusively licensed to the MGH Clinical Trials Network and
Institute (CTNI). Also, through MGH, Dr Nierenberg has a patent
extension application for the combination of buspirone, bupropion, and
melatonin for the treatment of depression.
NR 93
TC 10
Z9 12
U1 1
U2 12
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1461-1457
J9 INT J NEUROPSYCHOPH
JI Int. J. Neuropsychopharmacol.
PD NOV
PY 2011
VL 14
IS 10
BP 1417
EP 1431
DI 10.1017/S1461145711000083
PG 15
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 849DO
UT WOS:000297106000012
PM 21349226
ER
PT J
AU Vogt, D
Vaughn, R
Glickman, ME
Schultz, M
Drainoni, ML
Elwy, R
Eisen, S
AF Vogt, Dawne
Vaughn, Rachel
Glickman, Mark E.
Schultz, Mark
Drainoni, Mari-Lynn
Elwy, Rani
Eisen, Susan
TI Gender Differences in Combat-Related Stressors and Their Association
With Postdeployment Mental Health in a Nationally Representative Sample
of US OEF/OIF Veterans
SO JOURNAL OF ABNORMAL PSYCHOLOGY
LA English
DT Article
DE gender; veterans; military personnel; trauma exposure; mental health
ID ARMED-FORCES PERSONNEL; MALE VIETNAM VETERANS; WAR-ZONE STRESSORS;
RISK-FACTORS; SEX-DIFFERENCES; IRAQ WAR; RESILIENCE INVENTORY; MILITARY
PERSONNEL; DEPLOYMENT RISK; UK MILITARY
AB Though the broader literature suggests that women may be more vulnerable to the effects of trauma exposure, most available studies on combat trauma have relied on samples in which women's combat exposure is limited and analyses that do not directly address gender differences in associations between combat exposure and postdeployment mental health. Female service members' increased exposure to combat in Afghanistan and Iraq provides a unique opportunity to evaluate gender differences in different dimensions of combat-related stress and associated consequence for postdeployment mental health. The current study addressed these research questions in a representative sample of female and male U. S. veterans who had returned from deployment to Afghanistan or Iraq within the previous year. As expected, women reported slightly less exposure than men to most combat-related stressors, but higher exposure to other stressors (i.e., prior life stress, deployment sexual harassment). No gender differences were observed in reports of perceived threat in the war zone. Though it was hypothesized that combat-related stressors would demonstrate stronger negative associations with postdeployment mental health for women, only one of 16 stressor X gender interactions achieved statistical significance and an evaluation of the clinical significance of these interactions revealed that effects were trivial. Results suggest that female Operation Enduring Freedom/Operation Iraqi Freedom service members may be as resilient to combat-related stress as men. Future research is needed to evaluate gender differences in the longer-term effects of combat exposure.
C1 [Vogt, Dawne] Boston Univ, Sch Med, Natl Ctr PTSD, Div Psychiat, Boston, MA 02130 USA.
[Vogt, Dawne; Vaughn, Rachel] VA Boston Healthcare Syst, Womens Hlth Sci Div, Natl Ctr PTSD, Boston, MA USA.
[Glickman, Mark E.; Schultz, Mark; Drainoni, Mari-Lynn; Elwy, Rani; Eisen, Susan] Edith Nourse Rogers Mem Vet Hosp, Ctr Hlth Qual Outcomes & Econ Res, Bedford, MA USA.
[Glickman, Mark E.; Drainoni, Mari-Lynn; Elwy, Rani; Eisen, Susan] Boston Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA 02130 USA.
RP Vogt, D (reprint author), Boston Univ, Sch Med, Natl Ctr PTSD, Div Psychiat, 150 S Huntington Ave,116-3, Boston, MA 02130 USA.
EM Dawne.Vogt@va.gov
OI Glickman, Mark/0000-0003-3993-2801
NR 51
TC 79
Z9 79
U1 1
U2 12
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 NOV
PY 2011
VL 120
IS 4
BP 797
EP 806
DI 10.1037/a0023452
PG 10
WC Psychology, Clinical; Psychology, Multidisciplinary
SC Psychology
GA 847XT
UT WOS:000297009400003
PM 21639595
ER
PT J
AU Vogt, D
Smith, B
Elwy, R
Martin, J
Schultz, M
Drainoni, ML
Eisen, S
AF Vogt, Dawne
Smith, Brian
Elwy, Rani
Martin, James
Schultz, Mark
Drainoni, Mari-Lynn
Eisen, Susan
TI Predeployment, Deployment, and Postdeployment Risk Factors for
Posttraumatic Stress Symptomatology in Female and Male OEF/OIF Veterans
SO JOURNAL OF ABNORMAL PSYCHOLOGY
LA English
DT Article
DE trauma exposure; risk factors; posttraumatic stress disorder;
conservation of resources theory; Veterans
ID MALE VIETNAM VETERANS; WAR-ZONE STRESSORS; SOCIAL SUPPORT; LIFE EVENTS;
PSYCHOMETRIC PROPERTIES; RESILIENCE INVENTORY; NATIONAL SAMPLE; PTSD
CHECKLIST; FIT INDEXES; DISORDER
AB Prior research on risk factors for posttraumatic stress symptomatology (PTSS) in war-exposed Veterans has revealed both direct and indirect mechanisms of risk that span predeployment, deployment, and postdeployment timeframes. The aims of the present study were to identify the mechanisms through which previously documented risk factors contribute to PTSS in a national sample of 579 female and male Veterans deployed to Afghanistan for Operation Enduring Freedom (OEF) or to Iraq for Operation Iraqi Freedom (OIF), as well as to examine the extent to which results mirror associations observed among Vietnam Veterans (King, King, Foy, Keane, & Fairbank, 1999). Consistent with conservation of resources (COR) theory (Hobfoll, 1989, 2001), findings indicated that PTSS is accounted for by multiple chains of risk, many originating in predeployment experiences that place Veterans at risk for additional stress exposure, and foretell difficulty accessing resources in the face of subsequent stressors. Importantly, the majority of previously documented mechanisms were replicated in this study, suggesting key pathways through which risk factors may contribute to PTSS across different Veteran populations. Results also revealed a number of novel risk mechanisms for OEF/OIF female Veterans, particularly with respect to the role of deployment family relationships in risk for PTSS.
C1 [Vogt, Dawne; Smith, Brian] VA Boston Healthcare Syst, Natl Ctr PTSD, Womens Hlth Sci Div, Boston, MA 02130 USA.
[Vogt, Dawne; Smith, Brian] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA.
[Elwy, Rani; Schultz, Mark; Drainoni, Mari-Lynn; Eisen, Susan] Edith Nourse Rogers Mem Vet Hosp, CHQOER, Bedford, MA USA.
[Martin, James] Bryn Mawr Coll, Grad Sch Social Work & Social Res, Bryn Mawr, PA 19010 USA.
[Drainoni, Mari-Lynn] Boston Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA USA.
[Drainoni, Mari-Lynn] Boston Univ, Sch Med, Dept Med, Infect Dis Sect, Boston, MA 02118 USA.
RP Vogt, D (reprint author), VA Boston Healthcare Syst, Natl Ctr PTSD, Womens Hlth Sci Div, 116B-3,150 S Huntington Ave, Boston, MA 02130 USA.
EM Dawne.Vogt@va.gov
RI Schueter, nicos/A-3625-2014
NR 63
TC 50
Z9 50
U1 2
U2 9
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 NOV
PY 2011
VL 120
IS 4
BP 819
EP 831
DI 10.1037/a0024457
PG 13
WC Psychology, Clinical; Psychology, Multidisciplinary
SC Psychology
GA 847XT
UT WOS:000297009400005
PM 21707125
ER
PT J
AU Lo Celso, C
Scadden, DT
AF Lo Celso, Cristina
Scadden, David T.
TI The haematopoietic stem cell niche at a glance
SO JOURNAL OF CELL SCIENCE
LA English
DT Editorial Material
ID BONE-MARROW NICHE; PROGENITOR CELLS; IN-VIVO; SELF-RENEWAL;
ENDOTHELIAL-CELLS; OSTEOBLASTIC NICHE; ENDOSTEAL NICHE; BETA-CATENIN;
TGF-BETA; MICROENVIRONMENT
C1 [Lo Celso, Cristina] Univ London Imperial Coll Sci Technol & Med, Div Cell & Mol Biol, London SW7 2AZ, England.
[Scadden, David T.] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
[Scadden, David T.] Harvard Univ, Dept Stem Cells & Regenerat Biol, Cambridge, MA 02138 USA.
RP Lo Celso, C (reprint author), Univ London Imperial Coll Sci Technol & Med, Div Cell & Mol Biol, Sir Alexander Fleming Bldg,S Kensington Campus, London SW7 2AZ, England.
EM clocelso@imperial.ac.uk
OI Lo Celso, Cristina/0000-0002-1163-4207
FU Biotechnology and Biological Sciences Research Council [BB/I004033/1];
Cancer Research UK [CEA C36195/A11831]; NHLBI NIH HHS [HL044851,
HL097748, HL097794, HL100402, R01 HL044851, R01 HL097748, R01 HL097794,
U01 HL100402]
NR 92
TC 56
Z9 57
U1 0
U2 14
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD NOV 1
PY 2011
VL 124
IS 21
BP 3529
EP 3535
DI 10.1242/jcs.074112
PG 7
WC Cell Biology
SC Cell Biology
GA 847LV
UT WOS:000296975300002
PM 22083139
ER
PT J
AU Alston, TA
AF Alston, Theodore A.
TI Precipitation of sugammadex by protamine
SO JOURNAL OF CLINICAL ANESTHESIA
LA English
DT Letter
ID REVERSAL AGENT
C1 [Alston, Theodore A.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Alston, Theodore A.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Alston, TA (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
EM alstoncorbett@comcast.net
NR 2
TC 2
Z9 2
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0952-8180
J9 J CLIN ANESTH
JI J. Clin. Anesth.
PD NOV
PY 2011
VL 23
IS 7
BP 593
EP 593
DI 10.1016/j.jclinane.2011.04.004
PG 1
WC Anesthesiology
SC Anesthesiology
GA 848FJ
UT WOS:000297035600020
PM 22050813
ER
PT J
AU Goldwasser, J
Cohen, PY
Lin, WY
Kitsberg, D
Balaguer, P
Polyak, SJ
Chung, RT
Yarmush, ML
Nahmias, Y
AF Goldwasser, Jonathan
Cohen, Pazit Y.
Lin, Wenyu
Kitsberg, Danny
Balaguer, Patrick
Polyak, Stephen J.
Chung, Raymond T.
Yarmush, Martin L.
Nahmias, Yaakov
TI Naringenin inhibits the assembly and long-term production of infectious
hepatitis C virus particles through a PPAR-mediated mechanism
SO JOURNAL OF HEPATOLOGY
LA English
DT Article
DE HCV; Naringenin; Lipid metabolism; PPAR alpha
ID TRIGLYCERIDE TRANSFER PROTEIN; LOW-DENSITY; FLAVONOID NARINGENIN; CITRUS
FLAVONOIDS; RNA REPLICATION; CELL-LINES; IN-VITRO; SECRETION;
EXPRESSION; RESISTANCE
AB Background & Aims: Hepatitis C virus (HCV) infection affects 3% of the world population and is the leading cause of chronic liver disease worldwide. Current standard of care is effective in only 50% of the patients, poorly tolerated, and associated with significant side effects and viral resistance. Recently, our group and others demonstrated that the HCV lifecycle is critically dependent on host lipid metabolism and that its production is metabolically modulated.
Methods: The JFH1/Huh7.5.1 full lifecycle model of HCV was used to study the antiviral effects of naringenin on viral replication, assembly, and production. Activation of PPAR alpha was elucidated using GAL4-PPAR alpha fusion reporters, PPRE reporters, qRT-PCR, and metabolic studies. Metabolic results were confirmed in primary human hepatocytes.
Results: We demonstrate that the grapefruit flavonoid naringenin dose-dependently inhibits HCV production without affecting intracellular levels of the viral RNA or protein. We show that naringenin blocks the assembly of intracellular infectious viral particles, upstream of viral egress. This antiviral effect is mediated in part by the activation of PPARa, leading to a decrease in VLDL production without causing hepatic lipid accumulation in Huh7.5.1 cells and primary human hepatocytes. Long-term treatment with naringenin leads to a rapid 1.4 log reduction in HCV, similar to 1000 U of interferon. During the washout period, HCV levels returned to normal, consistent with our proposed mechanism of action.
Conclusions: The data demonstrates that naringenin is a nontoxic assembly inhibitor of HCV and that other PPARa agonists play a similar role in blocking viral production. The combination of naringenin with STAT-C agents could potentially bring a rapid reduction in HCV levels during the early treatment phase, an outcome associated with sustained virological response. (C) 2011 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
C1 [Cohen, Pazit Y.; Kitsberg, Danny; Nahmias, Yaakov] Hebrew Univ Jerusalem, Selim & Rachel Benin Sch Engn, Jerusalem, Israel.
[Goldwasser, Jonathan; Yarmush, Martin L.; Nahmias, Yaakov] Shriners Burns Hosp, Ctr Engn Med, Boston, MA USA.
[Goldwasser, Jonathan] Harvard MIT Div Hlth Sci & Technol, Cambridge, MA USA.
[Goldwasser, Jonathan; Lin, Wenyu; Chung, Raymond T.; Yarmush, Martin L.; Nahmias, Yaakov] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Balaguer, Patrick] Univ Montpellier 1, INSERM, Montpellier, France.
[Polyak, Stephen J.] Univ Washington, Seattle, WA 98195 USA.
RP Nahmias, Y (reprint author), Hebrew Univ Jerusalem, Selim & Rachel Benin Sch Engn, Jerusalem, Israel.
EM ynahmias@gmail.com
RI Nahmias, Yaakov/H-4725-2013; Balaguer, Patrick/I-2973-2016;
OI Nahmias, Yaakov/0000-0002-6051-616X
FU National Institute of Diabetes and Digestive and Kidney Diseases
[K01DK080241]; Harvard Clinical Nutrition Research Center
[P30-DK040561]; European Research Council [TMIHCV 242699]; BioMEMS
Resource Center [P41EB-002503]; Alexander Silberman Institute of Life
Sciences
FX This work was supported by the National Institute of Diabetes and
Digestive and Kidney Diseases (K01DK080241) and the Harvard Clinical
Nutrition Research Center (P30-DK040561). Resources were provided by
European Research Council Starting Grant (TMIHCV 242699), the BioMEMS
Resource Center (P41EB-002503), and the Alexander Silberman Institute of
Life Sciences.
NR 43
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U1 1
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD NOV
PY 2011
VL 55
IS 5
BP 963
EP 971
DI 10.1016/j.jhep.2011.02.011
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 846BN
UT WOS:000296872300005
PM 21354229
ER
PT J
AU Nadazdin, O
Boskovic, S
Wee, SL
Sogawa, H
Koyama, I
Colvin, RB
Smith, RN
Tocco, G
O'Connor, DH
Karl, JA
Madsen, JC
Sachs, DH
Kawai, T
Cosimi, AB
Benichou, G
AF Nadazdin, Ognjenka
Boskovic, Svjetlan
Wee, Siew-Lin
Sogawa, Hiroshi
Koyama, Ichiro
Colvin, Robert B.
Smith, R. Neal
Tocco, Georges
O'Connor, David H.
Karl, Julie A.
Madsen, Joren C.
Sachs, David H.
Kawai, Tatsuo
Cosimi, A. Benedict
Benichou, Gilles
TI Contributions of Direct and Indirect Alloresponses to Chronic Rejection
of Kidney Allografts in Nonhuman Primates
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID MEMORY T-CELLS; PERSISTENT ALLOPEPTIDE REACTIVITY; CLASS-II PEPTIDES;
INDIRECT RECOGNITION; INDIRECT ALLORECOGNITION; MHC PEPTIDES;
HOMEOSTATIC PROLIFERATION; TRANSPLANT RECIPIENTS; HETEROLOGOUS IMMUNITY;
REGULATORY TOLERANCE
AB The relative contribution of direct and indirect allorecognition pathways to chronic rejection of allogeneic organ transplants in primates remains unclear. In this study, we evaluated T and B cell alloresponses in cynomolgus monkeys that had received combined kidney/bone marrow allografts and myeloablative immunosuppressive treatments. We measured donor-specific direct and indirect T cell responses and alloantibody production in monkeys (n = 5) that did not reject their transplant acutely but developed chronic humoral rejection (CHR) and in tolerant recipients (n = 4) that never displayed signs of CHR. All CHR recipients exhibited high levels of anti-donor Abs and mounted potent direct T cell alloresponses in vitro. Such direct alloreactivity could be detected for more than 1 y after transplantation. In contrast, only two of five monkeys with CHR had a detectable indirect alloresponse. No indirect alloresponse by T cells and no alloantibody responses were found in any of the tolerant monkeys. Only one of four tolerant monkeys displayed a direct T cell alloresponse. These observations indicate that direct T cell alloresponses can be sustained for prolonged periods posttransplantation and result in alloantibody production and chronic rejection of kidney transplants, even in the absence of detectable indirect alloreactivity. The Journal of Immunology, 2011, 187: 4589-4597.
C1 [Benichou, Gilles] Massachusetts Gen Hosp, Dept Surg, Transplantat Unit, Transplant Ctr, Boston, MA 02114 USA.
[Nadazdin, Ognjenka; Boskovic, Svjetlan; Wee, Siew-Lin; Sogawa, Hiroshi; Koyama, Ichiro; Colvin, Robert B.; Smith, R. Neal; Tocco, Georges; Madsen, Joren C.; Sachs, David H.; Kawai, Tatsuo; Cosimi, A. Benedict; Benichou, Gilles] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Colvin, Robert B.; Smith, R. Neal] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[O'Connor, David H.; Karl, Julie A.] Univ Wisconsin, Dept Pathol & Lab Med, Wisconsin Natl Primate Res Ctr, Madison, WI 53711 USA.
RP Benichou, G (reprint author), Massachusetts Gen Hosp, Dept Surg, Transplantat Unit, Transplant Ctr, 55 Fruit St,Thier 807, Boston, MA 02114 USA.
EM gbenichou@partners.org
OI o'connor, david/0000-0003-2139-470X
FU Massachusetts General Hospital Executive Committee on Research; National
Institute of Allergy and Infectious Diseases [U19 AI066705, PO1HL18646,
RO1HL093131]; National Institutes of Health [19 DK080652, HL018446]
FX This work was supported by Massachusetts General Hospital Executive
Committee on Research, National Institute of Allergy and Infectious
Diseases Grants U19 AI066705 (to G. B.) and PO1HL18646 and RO1HL093131
(to J.C.M.), and National Institutes of Health Grants 19 DK080652 and
HL018446 (to A.B.C.).
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U1 2
U2 4
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 1
PY 2011
VL 187
IS 9
BP 4589
EP 4597
DI 10.4049/jimmunol.1003253
PG 9
WC Immunology
SC Immunology
GA 841ET
UT WOS:000296496000025
PM 21957140
ER
PT J
AU Xiang, M
Shi, XL
Li, YH
Xu, J
Yin, LH
Xiao, GZ
Scott, MJ
Billiar, TR
Wilson, MA
Fan, J
AF Xiang, Meng
Shi, Xiaolian
Li, Yuehua
Xu, Jia
Yin, Lianhua
Xiao, Guozhi
Scott, Melanie J.
Billiar, Timothy R.
Wilson, Mark A.
Fan, Jie
TI Hemorrhagic Shock Activation of NLRP3 Inflammasome in Lung Endothelial
Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID MOBILITY GROUP BOX-1; INTERLEUKIN-1 RECEPTOR ANTAGONIST;
RESPIRATORY-DISTRESS-SYNDROME; NEUTROPHIL NADPH OXIDASE; MULTIPLE ORGAN
FAILURE; SEVERE BLUNT TRAUMA; TLR2 UP-REGULATION; NAD(P)H OXIDASE;
ISCHEMIA/REPERFUSION INJURY; ALVEOLAR MACROPHAGES
AB Hemorrhagic shock (HS) due to major trauma and surgery predisposes the host to the development of systemic inflammatory response syndrome (SIRS), including acute lung injury (ALI), through activating and exaggerating the innate immune response. IL-1 beta is a crucial proinflammatory cytokine that contributes to the development of SIRS and ALI. Lung endothelial cells (EC) are one important source of IL-1 beta, and the production of active IL-1 beta is controlled by the inflammasome. In this study, we addressed the mechanism underlying HS activation of the inflammasome in lung EC. We show that high mobility group box 1 acting through TLR4, and a synergistic collaboration with TLR2 and receptor for advanced glycation end products signaling, mediates HS-induced activation of EC NAD(P) H oxidase. In turn, reactive oxygen species derived from NAD(P) H oxidase promote the association of thioredoxin-interacting protein with the nucleotide-binding oligomerization domain-like receptor protein NLRP3 and subsequently induce inflammasome activation and IL-1 beta secretion from the EC. We also show that neutrophil-derived reactive oxygen species play a role in enhancing EC NAD(P) H oxidase activation and therefore an amplified inflammasome activation in response to HS. The present study explores a novel mechanism underlying HS activation of EC inflammasome and thus presents a potential therapeutic target for SIRS and ALI induced after HS. The Journal of Immunology, 2011, 187: 4809-4817.
C1 [Fan, Jie] Vet Affairs Pittsburgh Healthcare Syst, Dept Surg, Res & Dev, Pittsburgh, PA 15240 USA.
[Xiang, Meng; Shi, Xiaolian; Li, Yuehua; Xu, Jia; Scott, Melanie J.; Billiar, Timothy R.; Wilson, Mark A.; Fan, Jie] Univ Pittsburgh, Sch Med, Dept Surg, Pittsburgh, PA 15213 USA.
[Xiang, Meng; Yin, Lianhua] Fudan Univ, Shanghai Med Coll, Dept Physiol & Pathophysiol, Shanghai 200032, Peoples R China.
[Shi, Xiaolian] Xi An Jiao Tong Univ, Coll Med, Dept Pharmacol, Xian 710061, Peoples R China.
[Xu, Jia] So Med Univ, Dept Pathophysiol, Guangzhou 510515, Guangdong, Peoples R China.
[Xiao, Guozhi] Univ Pittsburgh, Sch Med, Dept Med, Pittsburgh, PA 15213 USA.
RP Fan, J (reprint author), Vet Affairs Pittsburgh Healthcare Syst, Dept Surg, Res & Dev, Bldg 1,Room 2W109 151L-U,Univ Dr C, Pittsburgh, PA 15240 USA.
EM jif7@pitt.edu
FU National Institutes of Health [R01-HL-079669]; National Institutes of
Health Center [P50-GM-53789]; Veterans Administration
FX This work was supported by National Institutes of Health Grant
R01-HL-079669 (to J.F. and M.A.W.), National Institutes of Health Center
Grant P50-GM-53789 (to T.R.B. and J.F.), and a Veterans Administration
Merit Award (to J.F.).
NR 61
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U1 0
U2 6
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 1
PY 2011
VL 187
IS 9
BP 4809
EP 4817
DI 10.4049/jimmunol.1102093
PG 9
WC Immunology
SC Immunology
GA 841ET
UT WOS:000296496000046
PM 21940680
ER
PT J
AU Spires-Jones, TL
Kopeikina, KJ
Koffie, RM
de Calignon, A
Hyman, BT
AF Spires-Jones, Tara L.
Kopeikina, Katherine J.
Koffie, Robert M.
de Calignon, Alix
Hyman, Bradley T.
TI Are Tangles as Toxic as They Look?
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Article
DE Tau; Alzheimer; Neurofibrillary tangle; Neurodegeneration
ID ALZHEIMERS-DISEASE; NEUROFIBRILLARY TANGLES; HYPERPHOSPHORYLATED-TAU;
TRANSGENIC MICE; NEURONAL LOSS; ENDOPLASMIC-RETICULUM; CASPASE
ACTIVATION; AXONAL-TRANSPORT; ENDOGENOUS-TAU; REPEAT DOMAIN
AB Neurofibrillary tangles are intracellular accumulations of hyperphosphorylated and misfolded tau protein characteristic of Alzheimer's disease and other tauopathies. Classic cross-sectional studies of Alzheimer patient brains showed associations of tangle accumulation with neuronal loss, synapse loss, and dementia, which led to the supposition that tangles are toxic to neurons. More recent advances in imaging techniques and mouse models have allowed the direct exploration of the question of toxicity of aggregated versus soluble tau and have surprisingly challenged the view of tangles as toxic species in the brain. Here, we review these recent experiments on the nature of the toxicity of tau with particular emphasis on our experiments imaging tangles in the intact brain through a cranial window, which allows observation of tangle formation and longitudinal imaging of the fate of tangle-bearing neurons.
C1 [Spires-Jones, Tara L.; Kopeikina, Katherine J.; Koffie, Robert M.; Hyman, Bradley T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02129 USA.
[Kopeikina, Katherine J.] Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA.
[de Calignon, Alix] Univ Oxford, Dept Physiol Anat & Genet, Oxford OX1 3PT, England.
RP Spires-Jones, TL (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, 114 16th St, Boston, MA 02129 USA.
EM tspires@partners.org; bhyman@partners.org
OI Spires-Jones, Tara/0000-0003-2530-0598
FU National Institute of Health [AG08487, T32AG000278, AG026249,
K99AG33670]; Alzheimer's Association
FX This work was supported by National Institute of Health grants AG08487,
T32AG000278, AG026249, K99AG33670 and the Alzheimer's Association Zenith
Award.
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Z9 40
U1 2
U2 12
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2011
VL 45
IS 3
SI SI
BP 438
EP 444
DI 10.1007/s12031-011-9566-7
PG 7
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 841NL
UT WOS:000296518900020
PM 21638071
ER
PT J
AU Dickerson, BC
AF Dickerson, Bradford C.
TI Quantitating Severity and Progression in Primary Progressive Aphasia
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Article
DE Magnetic resonance imaging; Cerebral cortex; Primary progressive
aphasia; Frontotemporal dementia; Clinical trials; Biomarkers
ID FRONTOTEMPORAL LOBAR DEGENERATION; ALZHEIMERS-DISEASE; SEMANTIC
DEMENTIA; SYMPTOM SEVERITY; PICKS-DISEASE; 3 VARIANTS; PATHOLOGY;
DISORDERS; SIGNATURE; DIAGNOSIS
AB Primary progressive aphasia (PPA) is an insidiously progressive clinical syndrome that includes at its core an impairment in language. From a clinical perspective, there are a variety of diagnostic challenges; international consensus has only recently been reached on the nomenclature for specific clinical subtypes. There are at present no established treatments, and efforts to develop treatments have been hampered by the lack of standardized methods to monitor progression of the illness. This is further complicated by the multiplicity of underlying neuropathologies. Although measures developed from work with stroke aphasia and from work with disorders such as Alzheimer's disease and frontotemporal dementia have provided a valuable foundation for monitoring progression, PPA presents unique challenges to clinicians aiming to quantify impairments for the purposes of full characterization and monitoring, and ultimately with the goal of designing clinical trials of interventions to make a meaningful difference in patients' lives. In this review, I will summarize the main points made in my presentation at the 2010 International Conference on Frontotemporal Dementia, expand from there to summarize our current approach to monitoring progression of PPA, and finally will outline some ideas about goals for the development of better tools for this purpose.
C1 MGH Frontotemporal Dementia Unit, Charlestown, MA 02129 USA.
[Dickerson, Bradford C.] Massachusetts Gen Hosp, Dept Neurol,Frontotemporal Dementia Unit, Athinoula A Martinos Ctr Biomed Imaging, Massachusetts Alzheimers Dis Res Ctr, Boston, MA 02114 USA.
[Dickerson, Bradford C.] Massachusetts Gen Hosp, Dept Psychiat,Frontotemporal Dementia Unit, Athinoula A Martinos Ctr Biomed Imaging, Massachusetts Alzheimers Dis Res Ctr, Boston, MA 02114 USA.
[Dickerson, Bradford C.] Harvard Univ, Sch Med, Boston, MA USA.
RP Dickerson, BC (reprint author), MGH Frontotemporal Dementia Unit, 149 13th St,Suite 2691, Charlestown, MA 02129 USA.
EM bradd@nmr.mgh.harvard.edu
FU NIA [R01-AG29411, R21-AG29840, P50-AG005134]; Alzheimer's Association
FX This work was supported by grants from the NIA R01-AG29411, R21-AG29840,
P50-AG005134, and the Alzheimer's Association. We express special
appreciation to the participants in our program and their families for
their valuable contributions. The author thanks Daisy Sapolsky, MS,
CCC-SLP for her dedicated collaborative partnership in these efforts.
The author reports no disclosures.
NR 46
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U1 0
U2 3
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2011
VL 45
IS 3
SI SI
BP 618
EP 628
DI 10.1007/s12031-011-9534-2
PG 11
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 841NL
UT WOS:000296518900039
PM 21573887
ER
PT J
AU Penrod, JD
Luhrs, CA
Livote, EE
Cortez, TB
Kwak, J
AF Penrod, Joan D.
Luhrs, Carol A.
Livote, Elayne E.
Cortez, Therese B.
Kwak, Jennifer
TI Implementation and Evaluation of a Network-Based Pilot Program to
Improve Palliative Care in the Intensive Care Unit
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Palliative care; critical care; intensive care unit; ICU; quality
improvement
AB Background. Intensive care unit (ICU) care could be improved by implementation of time-triggered evidence-based interventions including identification of a patient/family medical decision maker, the patient's advance directive status, and cardiopulmonary resuscitation preferences by Day 1; offer of social work and spiritual support by Day 3; and a family meeting establishing goals of care by Day 5. We implemented a program to improve care for ICU patients in five Department of Veterans Affairs' ICUs.
Measures. We measured the percent of ICU patients with lengths of stay of five or more days that received the care processes by the appropriate day.
Intervention. Critical care and palliative care providers trained ICU nurse teams to improve care through auditing, performance feedback, improvement tools, education, and monthly team meetings.
Outcomes. Pre- and postintervention care were compared. Offering social work and spiritual support, identification of the medical decision maker, and documentation of family meetings significantly improved.
Conclusions/Lessons Learned. ICU nurse teams can be engaged to improve care under the aegis of a collaborative quality improvement project. J Pain Symptom Manage 2011;42:668-671. Published by Elsevier Inc. on behalf of U.S. Cancer Pain Relief Committee.
C1 [Penrod, Joan D.; Livote, Elayne E.; Kwak, Jennifer] James J Peters VA Med Ctr, Bronx, NY 10468 USA.
[Luhrs, Carol A.; Cortez, Therese B.] VA New York Harbor Healthcare Syst, Brooklyn, NY USA.
RP Penrod, JD (reprint author), James J Peters VA Med Ctr, 130 W Kingsbridge Rd, Bronx, NY 10468 USA.
EM joan.penrod@mssm.edu
FU Department of Veterans Affairs; Health Services Research; Development
Service
FX This work was supported in part by the Department of Veterans Affairs,
Health Services Research and Development Service. The authors declare no
conflicts of interest.
NR 5
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Z9 13
U1 0
U2 7
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 NOV
PY 2011
VL 42
IS 5
BP 668
EP 671
DI 10.1016/j.jpainsymman.2011.06.012
PG 4
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA 847YL
UT WOS:000297011800005
PM 22045370
ER
PT J
AU Villarreal, D
Restrepo, MI
Healy, J
Howard, B
Tidwell, J
Ross, J
Hartronft, S
Jawad, M
Sanchez-Reilly, S
Reed, K
Espinoza, SE
AF Villarreal, Deborah
Restrepo, Marcos I.
Healy, Jennifer
Howard, Bonita
Tidwell, Janet
Ross, Jeanette
Hartronft, Scotte
Jawad, Marriyam
Sanchez-Reilly, Sandra
Reed, Kristin
Espinoza, Sara E.
TI A Model for Increasing Palliative Care in the Intensive Care Unit:
Enhancing Interprofessional Consultation Rates and Communication
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Palliative care; critical care; end of life; quality improvement;
interprofessional
ID OUTCOMES; STATES
AB Background. Only a minority of patients who die in the medical intensive care unit (MICU) receive palliative care services. At the South Texas Veterans Health Care System Audie L. Murphy Hospital, only 5% of patients who died in the MICU from May to August 2010 received a palliative care consultation.
Measures. We measured the percentage of MICU patients for which there was a palliative care consultation during the intervention period.
Intervention. Starting October 1, 2010 and ending April 30, 2011, the palliative care and MICU teams participated in daily "pre-rounds'' to identify patients at risk for poor outcomes, who may benefit from a palliative care consultation.
Outcomes. Palliative care consultation increased significantly from 5% to 59% for patients who died in the MICU during the intervention period. Additionally, palliative care consultation increased from 5% to 21% for all patients admitted to the MICU during the intervention period.
Conclusions/Lessons Learned. Daily pre-rounds between the palliative care and MICU teams increased palliative care services for MICU patients at risk for poor outcomes, who may benefit from a palliative care consultation. J Pain Symptom Manage 2011;42:676-679. Published by Elsevier Inc. on behalf of U.S. Cancer Pain Relief Committee.
C1 [Villarreal, Deborah] Audie L Murphy Mem Vet Adm Med Ctr, S Texas Vet Hlth Care Syst, Div Geriatr Gerontol & Palliat Med, San Antonio, TX 78229 USA.
[Villarreal, Deborah; Healy, Jennifer; Ross, Jeanette; Jawad, Marriyam; Sanchez-Reilly, Sandra; Espinoza, Sara E.] Univ Texas Hlth Sci Ctr San Antonio, Div Geriatr Gerontol & Palliat Med, San Antonio, TX 78229 USA.
[Restrepo, Marcos I.] Univ Texas Hlth Sci Ctr San Antonio, Div Pulm & Crit Care, San Antonio, TX 78229 USA.
[Jawad, Marriyam] Univ Texas Hlth Sci Ctr San Antonio, Sch Med, San Antonio, TX 78229 USA.
RP Villarreal, D (reprint author), Audie L Murphy Mem Vet Adm Med Ctr, S Texas Vet Hlth Care Syst, Div Geriatr Gerontol & Palliat Med, 7400 Merton Minter, San Antonio, TX 78229 USA.
EM villarreald4@uthscsa.edu
RI Restrepo, Marcos/H-4442-2014
FU U.S. Department of Health and Human Services, Health Resources and
Services Administration, Bureau of Health Professions
FX Dr. Villareal is receiving career development support from the U.S.
Department of Health and Human Services, Health Resources and Services
Administration, Bureau of Health Professions, Geriatric Academic Career
Award.
NR 9
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U1 1
U2 5
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 NOV
PY 2011
VL 42
IS 5
BP 676
EP 679
DI 10.1016/j.jpainsymman.2011.07.004
PG 4
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA 847YL
UT WOS:000297011800007
PM 22045372
ER
PT J
AU Vig, EK
Sudore, RL
Berg, KM
Fromme, EK
Arnold, RM
AF Vig, Elizabeth K.
Sudore, Rebecca L.
Berg, Karina M.
Fromme, Erik K.
Arnold, Robert M.
TI Responding to Surrogate Requests That Seem Inconsistent With a Patient's
Living Will
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Surrogates; decision making; advance directives; substituted judgment
ID LIFE DECISION-MAKING; SUSTAINING TREATMENT; PREFERENCES; CHOICES;
INTERESTS; JUDGMENTS; STABILITY; DISAGREE; OTHERS; FAMILY
AB Clinicians may feel conflicted when a patient's legal decision maker is making decisions that seem inconsistent with a patient's living will. We provide evidence-based information to help clinicians consider whether a surrogate's inconsistent decisions are ethically appropriate. Surrogates are not flawless translators of their loved one's preferences; they are influenced by their own hopes and the current clinical context. Patients may be aware of this, are often concerned about burdening their loved ones, and often grant their surrogates leeway in interpreting their wishes. When appropriate, clinicians should respect surrogates' interpretations of patient values and take steps to decrease surrogate stress during the decision-making process. Finally, if clinicians are cognizant of their own values and preferences, they may recognize how these may affect their responses to certain clinical cases. J Pain Symptom Manage 2011;42:777-782. (C) 2011 U.S. Cancer Pain Relief Committee. Published by Elsevier Inc. All rights reserved.
C1 [Vig, Elizabeth K.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Vig, Elizabeth K.] Univ Washington, Seattle, WA 98195 USA.
[Sudore, Rebecca L.] San Francisco VA Med Ctr, San Francisco, CA USA.
[Sudore, Rebecca L.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Berg, Karina M.] Yale Univ, Sch Med, New Haven, CT USA.
[Fromme, Erik K.] Oregon Hlth & Sci Univ, Dept Med, Div Hematol & Med Oncol, Portland, OR 97201 USA.
[Arnold, Robert M.] Univ Pittsburgh, Sch Med, Div Gen Internal Med, Sect Palliat Care & Med Eth,Ctr Bioeth & Hlth Law, Pittsburgh, PA USA.
RP Vig, EK (reprint author), 1660 Columbian Way,S 182 Eth, Seattle, WA 98108 USA.
EM vigster@u.washington.edu
FU Pfizer Fellowship in Clear Communication
FX Dr. Sudore is supported in part by a Pfizer Fellowship in Clear
Communication. The other authors have no sponsorship related to this
manuscript. The authors have no financial conflicts of interest to
disclose.
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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 0885-3924
EI 1873-6513
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD NOV
PY 2011
VL 42
IS 5
BP 777
EP 782
DI 10.1016/j.jpainsymman.2011.08.003
PG 6
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA 847YL
UT WOS:000297011800017
PM 22045374
ER
PT J
AU Pierre, JF
Heneghan, AF
Tsao, FHC
Sano, Y
Jonker, MA
Omata, J
Lan, JG
Kudsk, KA
AF Pierre, Joseph F.
Heneghan, Aaron F.
Tsao, Francis H. C.
Sano, Yoshifumi
Jonker, Mark A.
Omata, Jiro
Lan, Jinggang
Kudsk, Kenneth A.
TI Route and Type of Nutrition and Surgical Stress Influence Secretory
Phospholipase A2 Secretion of the Murine Small Intestine
SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION
LA English
DT Article; Proceedings Paper
CT Meeting of the
American-Society-for-Parenteral-and-Enteral-Nutrition/Clinical Nutrition
Week
CY FEB 07, 2010
CL Las Vegas, NV
SP Amer Soc Parenteral & Enteral Nutr
DE secretory phospholipase A2; parenteral nutrition; surgical stress; small
intestine; defensins; enteral feeding; innate immunity
ID TOTAL PARENTERAL-NUTRITION; BACTERICIDAL PROPERTIES; INFLAMMATORY
MEDIATORS; STAPHYLOCOCCUS-AUREUS; ENTERAL NUTRITION; LYMPHOID-TISSUE;
CELL-WALL; GROUP-II; A(2); EXPRESSION
AB Background: The function of secretory phospholipase A2 (sPLA2) is site dependent. In tissue, sPLA2 regulates eicosanoid production; in circulation, sPLA2 primes neutrophils; and in the intestinal lumen, sPLA2 provides innate bactericidal immunity as a defensin-related protein. Since parenteral nutrition (PN) primes leukocytes while suppressing intraluminal mucosal immunity, the authors hypothesized that (1) PN would diminish luminal sPLA2 activity but increase activity in intestinal tissue and serum and (2) stress would accentuate these changes. Methods: Mice received chow, a complex enteral diet (CED), intragastric PN (IG-PN), or PN in experiment 1 and chow, chow+stress, PN, or PN+stress in experiment 2. Results: In experiment 1, luminal sPLA2 activity was greatest in chow and decreased in CED, IG-PN, and PN, with PN lower than CED and IG-PN. Compared to that after chow, serum sPLA2 activity dropped after CED, IG-PN, and PN. Serum sPLA2 was higher in portal than systemic serum. In experiment 2, PN lowered luminal sPLA2 activity vs chow. Stress lowered luminal sPLA2 activity in chow, without change in PN. Following stress, luminal immunoglobulin A increased in chow but not PN. Serum sPLA2 activity increased in PN. Conclusions: PN attenuates sPLA2 activity in intestinal fluid, consistent with suppressed innate mucosal defense. Stress suppresses luminal fluid sPLA2 activity in chow but not the immunoglobulin A response; PN impairs both. Stress significantly elevates serum sPLA2 in PN-fed mice, consistent with known increased neutrophil priming with PN. PN reduces innate bactericidal immunity of the gut but upregulates serum proinflammatory products poststress. (JPEN J Parenter Enteral Nutr. 2011;35:748-756)
C1 [Pierre, Joseph F.; Heneghan, Aaron F.; Sano, Yoshifumi; Jonker, Mark A.; Omata, Jiro; Lan, Jinggang; Kudsk, Kenneth A.] Univ Wisconsin, Dept Surg, Sch Med & Publ Hlth, Madison, WI USA.
[Pierre, Joseph F.] Univ Wisconsin, Dept Nutr Sci, Madison, WI 53706 USA.
[Heneghan, Aaron F.; Lan, Jinggang; Kudsk, Kenneth A.] William S Middleton Mem Vet Adm Med Ctr, Vet Adm Surg Serv, Madison, WI USA.
[Tsao, Francis H. C.] Univ Wisconsin, Dept Med, Div Allergy Pulm & Crit Care Med, Sch Med & Publ Hlth, Madison, WI USA.
RP Kudsk, KA (reprint author), 600 Highland Ave,H4-736 CSC, Madison, WI 53792 USA.
EM kudsk@sur-gery.wisc.edu
FU NIGMS NIH HHS [R01 GM53439, R01 GM053439]
NR 32
TC 13
Z9 13
U1 0
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0148-6071
J9 JPEN-PARENTER ENTER
JI J. Parenter. Enter. Nutr.
PD NOV
PY 2011
VL 35
IS 6
BP 748
EP 756
DI 10.1177/0148607111414025
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 839UL
UT WOS:000296394800011
PM 22042050
ER
PT J
AU Atesok, KI
Alman, BA
Schemitsch, EH
Peyser, A
Mankin, H
AF Atesok, Kivanc I.
Alman, Benjamin A.
Schemitsch, Emil H.
Peyser, Amos
Mankin, Henry
TI Osteoid Osteoma and Osteoblastoma
SO JOURNAL OF THE AMERICAN ACADEMY OF ORTHOPAEDIC SURGEONS
LA English
DT Review
ID PERCUTANEOUS RADIOFREQUENCY ABLATION; BONE-FORMING LESIONS;
DIAGNOSTIC-ACCURACY; OPERATIVE TREATMENT; IMAGING FEATURES; CHILDREN;
MANAGEMENT; RESECTION; SPINE; TUMOR
AB Osteoid osteoma and osteoblastoma are commonly seen benign osteogenic bone neoplasms. Both tumors are typically seen in the second decade of life, with a notable predilection in males. Histologically, these tumors resemble each other, with characteristically increased osteoid tissue formation surrounded by vascular fibrous stroma and perilesional sclerosis. However, osteoblastomas are larger than osteoid osteomas, and they exhibit greater osteoid production and vascularity. Clinically, osteoid osteoma most commonly occurs in the long bones (eg, femur, tibia). The lesions cause night pain that is relieved with nonsteroidal anti-inflammatory drugs (NSAIDs). Osteoblastoma is most frequently located in the axial skeleton, and the pain is usually not worse at night and is less likely to be relieved with NSAIDs. Osteoblastoma can be locally aggressive; osteoid osteoma lacks growth potential. Osteoid osteoma may be managed nonsurgically with NSAIDs. When surgery is required, minimally invasive methods (eg, CT-guided excision, radiofrequency ablation) are preferred. Osteoblastoma has a higher rate of recurrence than does osteoid osteoma, and patients must be treated surgically with intralesional curettage or en bloc resection.
C1 [Atesok, Kivanc I.] Univ Toronto, Inst Med Sci, Toronto, ON M5S 1A1, Canada.
[Alman, Benjamin A.] Hosp Sick Children, Div Orthopaed Surg, Toronto, ON M5G 1X8, Canada.
[Schemitsch, Emil H.] Univ Toronto, St Michaels Hosp, Div Orthopaed, Dept Surg, Toronto, ON M5S 1A1, Canada.
[Peyser, Amos] Shaare Zedek Med Ctr, Dept Orthoped, Jerusalem, Israel.
[Mankin, Henry] Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA.
RP Atesok, KI (reprint author), Univ Toronto, Inst Med Sci, Toronto, ON M5S 1A1, Canada.
NR 45
TC 31
Z9 37
U1 1
U2 10
PU AMER ACAD ORTHOPAEDIC SURGEONS
PI ROSEMENT
PA 6300 N RIVER ROAD, ROSEMENT, IL 60018-4262 USA
SN 1067-151X
J9 J AM ACAD ORTHOP SUR
JI J. Am. Acad. Orthop. Surg.
PD NOV
PY 2011
VL 19
IS 11
BP 678
EP 689
PG 12
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA 839WI
UT WOS:000296399800004
PM 22052644
ER
PT J
AU Dowsett, M
Nielsen, TO
A'Hern, R
Bartlett, J
Coombes, RC
Cuzick, J
Ellis, M
Henry, NL
Hugh, JC
Lively, T
McShane, L
Paik, S
Penault-Llorca, F
Prudkin, L
Regan, M
Salter, J
Sotiriou, C
Smith, IE
Viale, G
Zujewski, JA
Hayes, DF
AF Dowsett, Mitch
Nielsen, Torsten O.
A'Hern, Roger
Bartlett, John
Coombes, R. Charles
Cuzick, Jack
Ellis, Matthew
Henry, N. Lynn
Hugh, Judith C.
Lively, Tracy
McShane, Lisa
Paik, Soon
Penault-Llorca, Frederique
Prudkin, Ljudmila
Regan, Meredith
Salter, Janine
Sotiriou, Christos
Smith, Ian E.
Viale, Giuseppe
Zujewski, Jo Anne
Hayes, Daniel F.
TI Assessment of Ki67 in Breast Cancer: Recommendations from the
International Ki67 in Breast Cancer Working Group
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID PATHOLOGISTS GUIDELINE RECOMMENDATIONS; IMPROVED SURGICAL OUTCOMES;
PHASE-II TRIAL; POSTMENOPAUSAL WOMEN; CELL PROLIFERATION; AMERICAN
SOCIETY; PROGNOSTIC VALUE; CLINICAL ONCOLOGY/COLLEGE; NEOADJUVANT
CHEMOTHERAPY; PROGESTERONE-RECEPTORS
AB Uncontrolled proliferation is a hallmark of cancer. In breast cancer, immunohistochemical assessment of the proportion of cells staining for the nuclear antigen Ki67 has become the most widely used method for comparing proliferation between tumor samples. Potential uses include prognosis, prediction of relative responsiveness or resistance to chemotherapy or endocrine therapy, estimation of residual risk in patients on standard therapy and as a dynamic biomarker of treatment efficacy in samples taken before, during, and after neoadjuvant therapy, particularly neoadjuvant endocrine therapy. Increasingly, Ki67 is measured in these scenarios for clinical research, including as a primary efficacy endpoint for clinical trials, and sometimes for clinical management. At present, the enormous variation in analytical practice markedly limits the value of Ki67 in each of these contexts. On March 12, 2010, an international panel of investigators with substantial expertise in the assessment of Ki67 and in the development of biomarker guidelines was convened in London by the cochairs of the Breast International Group and North American Breast Cancer Group Biomarker Working Party to consider evidence for potential applications. Comprehensive recommendations on preanalytical and analytical assessment, and interpretation and scoring of Ki67 were formulated based on current evidence. These recommendations are geared toward achieving a harmonized methodology, create greater between-laboratory and between-study comparability, and allow earlier valid applications of this marker in clinical practice.
C1 [Dowsett, Mitch; Salter, Janine] Royal Marsden Hosp, Acad Dept Biochem, London SW3 6JJ, England.
[Dowsett, Mitch; Salter, Janine] Breakthrough Breast Canc Ctr, London, England.
[Nielsen, Torsten O.] Univ British Columbia, Vancouver Hosp, Vancouver, BC V5Z 1M9, Canada.
[A'Hern, Roger] Inst Canc Res, Canc Res UK Clin Trials & Stat Unit, Surrey, England.
[Bartlett, John] Univ Edinburgh, Western Gen Hosp, Edinburgh Canc Res Ctr, Edinburgh, Midlothian, Scotland.
[Coombes, R. Charles] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Div Canc, London, England.
[Cuzick, Jack] Univ London, Barts & London Sch Med & Dent, Wolfson Inst Prevent Med, London, England.
[Ellis, Matthew] Washington Univ, Sch Med, Siteman Canc Ctr, Breast Canc Program, St Louis, MO USA.
[Henry, N. Lynn; Hayes, Daniel F.] Univ Michigan, Ctr Comprehens Canc, Breast Oncol Program, Ann Arbor, MI 48109 USA.
[Hugh, Judith C.] Univ Alberta, Dept Lab Med & Pathol, Edmonton, AB, Canada.
[Lively, Tracy] NCI, Diagnost Evaluat Branch, Canc Diag Program, Rockville, MD USA.
[McShane, Lisa] NCI, Biometr Res Branch, DCTD, Bethesda, MD 20892 USA.
[Paik, Soon] NSABP Fdn, Div Pathol, Pittsburgh, PA USA.
[Penault-Llorca, Frederique] Univ Auvergne, Dept Biopathol, Clermont Ferrand, France.
[Prudkin, Ljudmila] Hosp Univ Vall Hebron, Lab Patol Mol, Barcelona, Spain.
[Regan, Meredith] Dana Farber Canc Inst, IBCSG Stat Ctr, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Regan, Meredith] Harvard Univ, Sch Med, Boston, MA USA.
[Sotiriou, Christos] Inst Jules Bordet, Dept Med Oncol, B-1000 Brussels, Belgium.
[Sotiriou, Christos] Breast Canc Translat Res Lab BCTL, Brussels, Belgium.
[Smith, Ian E.] Royal Marsden Hosp, Breast Unit, London SW3 6JJ, England.
[Viale, Giuseppe] Univ Milan, European Inst Oncol, Dept Pathol, Milan, Italy.
[Zujewski, Jo Anne] NCI, Canc Therapy Evaluat Program, Rockville, MD USA.
RP Dowsett, M (reprint author), Royal Marsden Hosp, Dept Biochem, Fulham Rd, London SW3 6JJ, England.
EM mitch.dowsett@icr.ac.uk
FU Cancer Research UK
NR 55
TC 500
Z9 525
U1 3
U2 36
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD NOV
PY 2011
VL 103
IS 22
BP 1656
EP 1664
DI 10.1093/jnci/djr393
PG 9
WC Oncology
SC Oncology
GA 850PV
UT WOS:000297209000007
PM 21960707
ER
PT J
AU Zafar, SN
Millham, FH
Chang, YC
Fikry, K
Alam, HB
King, DR
Velmahos, GC
de Moya, MA
AF Zafar, Syed Nabeel
Millham, Frederick H.
Chang, Yuchiao
Fikry, Karim
Alam, Hasan B.
King, David R.
Velmahos, George C.
de Moya, Marc A.
TI Presenting Blood Pressure in Traumatic Brain Injury: A Bimodal
Distribution of Death
SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE
LA English
DT Article
DE Traumatic brain injury; Mortality; Blood pressure
ID SEVERE HEAD-INJURY; 110 MM HG; PREHOSPITAL HYPOTENSION; TEAM ACTIVATION;
BLUNT TRAUMA; REDEFINING HYPOTENSION; PROGNOSTIC VALUE; VALID INDICATOR;
MORTALITY; IMPACT
AB Background: Recent research explores the relationship between vital signs on arrival to the emergency department and early outcomes. This work has not included traumatic brain injury (TBI). We aimed to evaluate the relationship of the initial emergency department systolic blood pressure (EDSBP) with outcome.
Methods: By using the National Trauma Data Bank (v7), we analyzed patients older than 16 years with isolated moderate to severe blunt TBI. TBI was defined by International Classification of Diseases-9th Rev diagnosis codes and Abbreviated Injury Scale scores. We determined mortality rates while controlling for age, gender, race, payment type, and injury severity using logistic regression. Survival analysis was performed to determine 3-day survival rates. Scores and rates were plotted against EDSBP.
Results: A total of 7,238 patients were included in the analysis. Plots of adverse outcomes versus EDSBP demonstrated bimodal distributions. The mortality curve had one inflection point at EDSBP 120 mm Hg, indicating higher mortality when blood pressures were lower than this threshold. Another inflection began at EDSBP 140 mm Hg. The mortality rate was 21% when EDSBP was <120 mm Hg, 9% when it was between 120 mm Hg and 140 mm Hg, and 19% when EDSBP was >= 140 mm Hg. Multivariate analysis demonstrated that patients presenting with an EDSBP of <120 mm Hg and >= 140 mm Hg were 2.7 (95% confidence interval = 2.13,3.48) and 1.6 (95% confidence interval = 1.32,1.96) times more likely to die, respectively, than those who presented with a EDSBP of 120 mm Hg to 140 mm Hg.
Conclusions: Mortality in moderate to severe TBI has a bimodal distribution. Like hypotension, hypertension at hospital admission seems to be associated with increased mortality in TBI, even after controlling for other factors.
C1 [Fikry, Karim; Alam, Hasan B.; King, David R.; Velmahos, George C.; de Moya, Marc A.] Massachusetts Gen Hosp, Div Trauma Emergency Surg & Surg Crit Care, Boston, MA 02114 USA.
[Zafar, Syed Nabeel] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Millham, Frederick H.] Newton Wellesley Hosp, Dept Surg, Newton, MA USA.
[Chang, Yuchiao] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
RP de Moya, MA (reprint author), Massachusetts Gen Hosp, Div Trauma Emergency Surg & Surg Crit Care, 165 Cambridge St,Suite 810, Boston, MA 02114 USA.
EM mdemoya@partners.org
OI King, David/0000-0003-1028-1478; Zafar, Syed Nabeel/0000-0003-3843-9687
NR 31
TC 13
Z9 13
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-5282
J9 J TRAUMA
JI J. Trauma-Injury Infect. Crit. Care
PD NOV
PY 2011
VL 71
IS 5
BP 1179
EP 1184
DI 10.1097/TA.0b013e3182140d38
PG 6
WC Critical Care Medicine; Surgery
SC General & Internal Medicine; Surgery
GA 849IG
UT WOS:000297118600021
PM 21502878
ER
PT J
AU Fang, Y
Xu, P
Gu, C
Wang, Y
Fu, XJ
Yu, WR
Yao, M
AF Fang, Yong
Xu, Peng
Gu, Chuan
Wang, Ying
Fu, Xiu-Jun
Yu, Wei-Rong
Yao, Min
TI Ulinastatin Improves Pulmonary Function in Severe Burn-Induced Acute
Lung Injury by Attenuating Inflammatory Response
SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE
LA English
DT Article
DE Ulinastatin; Thermal injury; Acute lung injury; Inflammatory response;
Permeability
ID URINARY TRYPSIN-INHIBITOR; RESPIRATORY-DISTRESS-SYNDROME; NEUTROPHIL
CHEMOTACTIC FACTOR; ENDOTHELIAL-CELLS; SYSTEMIC INFLAMMATION; INHALATION
INJURY; HEMORRHAGIC-SHOCK; GENE-EXPRESSION; TNF-ALPHA; ACTIVATION
AB Background: Acute systemic inflammatory response to severe skin burn injury mediates burn-induced acute lung injury. Ulinastatin is potentially an effective intervention, because it attenuates the systemic inflammatory response induced by endotoxin and improves myocardial function during ischemic shock and reperfusion.
Methods: Rats received full-thickness burn wounds to 30% total body surface area followed by delayed resuscitation. The treatment group received 50,000 U/kg of ulinastatin and the burn group was given vehicle only. A sham group was not burned but otherwise was treated identically. After killing, blood and lung samples were harvested for histology and measurement of inflammatory mediators.
Results: Administration of ulinastatin significantly decreased the mRNA and protein levels of tumor necrosis factor-alpha, interleukin-1 beta, -6, and -8 both locally and systemically in burn-injured rats. The secretion of neutrophil elastase and myeloperoxidase in the lung and the expression of intercellular adhesion molecule-1 on the surface of lung epithelium were inhibited by ulinastatin. Ulinastatin also reduced the increase in pulmonary microvascular permeability. Consistent with these findings, ulinastatin ameliorated the lung edema and pulmonary oxygenation in burn-injured rats.
Conclusions: These results indicate that the inhibitory effects of ulinastatin on inflammatory mediator production, neutrophil activation, and microvascular permeability are associated with the recovery of pulmonary functions in severe burn-induced acute lung injury and suggest that ulinastatin may serve as a potential therapeutic administration in critical burn care.
C1 [Fang, Yong; Xu, Peng; Gu, Chuan; Wang, Ying; Fu, Xiu-Jun; Yu, Wei-Rong; Yao, Min] Shanghai Jiao Tong Univ, Peoples Hosp 3, Dept Burns & Plast Surg, Shanghai 201900, Peoples R China.
Shanghai Jiao Tong Univ, Sch Med, Inst Traumat Med, Shanghai 201900, Peoples R China.
[Yao, Min] Harvard Univ, Sch Med, Dept Dermatol, Wellman Ctr Photomed,Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Yao, M (reprint author), Shanghai Jiao Tong Univ, Peoples Hosp 3, Dept Burns & Plast Surg, 280 Mohe Rd, Shanghai 201900, Peoples R China.
EM myao2@partners.org
FU Foundation of Nature and Science at the School of Medicine, Shanghai
Jiao Tong University [09XJ21073]
FX Supported by a grant from the Foundation of Nature and Science at the
School of Medicine, Shanghai Jiao Tong University (09XJ21073).
NR 25
TC 27
Z9 37
U1 1
U2 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-5282
J9 J TRAUMA
JI J. Trauma-Injury Infect. Crit. Care
PD NOV
PY 2011
VL 71
IS 5
BP 1297
EP 1304
DI 10.1097/TA.0b013e3182127d48
PG 8
WC Critical Care Medicine; Surgery
SC General & Internal Medicine; Surgery
GA 849IG
UT WOS:000297118600040
PM 21926648
ER
PT J
AU Liteplo, AS
Noble, VE
Attwood, BHC
AF Liteplo, Andrew S.
Noble, Vicki E.
Attwood, Ben H. C.
TI Real-time Video Streaming of Sonographic Clips Using Domestic Internet
Networks and Free Videoconferencing Software
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Article
DE image quality; sonography; telesonography; videoconferencing; wireless
ID PREHOSPITAL ULTRASOUND; TRAUMA
AB Objectives-As the use of point-of-care sonography spreads, so too does the need for remote expert over-reading via telesonogrpahy. We sought to assess the feasibility of using familiar, widespread, and cost-effective existent technology to allow remote over-reading of sonograms in real time and to compare 4 different methods of transmission and communication for both the feasibility of transmission and image quality.
Methods-Sonographic video clips were transmitted using 2 different connections (WiFi and 3G) and via 2 different videoconferencing modalities (iChat [Apple Inc, Cupertino, CA] and Skype [Skype Software Sarl, Luxembourg]), for a total of 4 different permutations. The clips were received at a remote location and recorded and then scored by expert reviewers for image quality, resolution, and detail.
Results-Wireless transmission of sonographic clips was feasible in all cases when WiFi was used and when Skype was used over a 3G connection. Images transmitted via a WiFi connection were statistically superior to those transmitted via 3G in all parameters of quality (average P = .031), and those sent by iChat were superior to those sent by Skype but not statistically so (average P = .057).
Conclusions-Wireless transmission of sonographic video clips using inexpensive hardware, free videoconferencing software, and domestic Internet networks is feasible with retention of image quality sufficient for interpretation. WiFi transmission results in greater image quality than transmission by a 3G network.
C1 [Liteplo, Andrew S.; Noble, Vicki E.] Massachusetts Gen Hosp, Div Emergency Ultrasound, Dept Emergency Med, Boston, MA 02114 USA.
[Attwood, Ben H. C.] Stoke Mandeville Hosp, Dept Anesthet & Intens Care, Aylesbury HP21 8AL, Bucks, England.
RP Liteplo, AS (reprint author), Massachusetts Gen Hosp, Div Emergency Ultrasound, Dept Emergency Med, 0 Emerson Pl,Suite 3B, Boston, MA 02114 USA.
EM aliteplo@partners.org
NR 16
TC 5
Z9 5
U1 0
U2 1
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
USA
SN 0278-4297
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD NOV
PY 2011
VL 30
IS 11
BP 1459
EP 1466
PG 8
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 846XN
UT WOS:000296936600002
PM 22039018
ER
PT J
AU Shipp, TD
Nguyen, HT
Bromley, B
Lyons, JG
Benacerraf, BR
AF Shipp, Thomas D.
Nguyen, Hiep T.
Bromley, Bryann
Lyons, Jennifer G.
Benacerraf, Beryl R.
TI Importance of Renal Abnormalities First Identified in the Third
Trimester After Normal Findings on a Detailed Second-Trimester
Structural Fetal Survey
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Article
DE Renal abnormalities; structural survey; third trimester
ID DILATATION; PREDICTOR
AB Objectives-The purpose of this study was to evaluate the importance of renal abnormalities first identified in the third trimester of pregnancy after normal findings on a detailed second-trimester structural fetal survey.
Methods-Between March 1, 2007, and August 1, 2009, all patients having a sonographic examination in the third trimester who previously had normal findings on a second-trimester detailed structural fetal survey were retrospectively identified. Fetal renal abnormalities first detected in the third trimester and not seen during the second-trimester survey were tabulated. Neonatal follow-up was obtained for those with sonographic abnormalities.
Results-Overall, 4170 patients had third-trimester scans after normal findings on a detailed second-trimester survey. A new renal abnormality was detected in 77 (1.8%) of these third-trimester scans. Detailed postnatal imaging follow-up was available in 49 of 77 (63.6%), of which 44 (89.8%) had prenatal hydronephosis. Of these, 9 of 44 (20.5%) had reflux; 14 of 44 (31.8%) had normal findings or had hydronephosis that resolved on follow-up sonography after birth; and the rest had hydronephosis (13 of 44 [29.5%]), ureterovesical junction obstruction (3 of 44 [6.8%]), or ureteropelvic junction obstruction (5 of 44 [11.4%]). The other 5 fetuses with nonhydronephrotic renal abnormalities had pelvic kidneys (3) and unilateral renal agenesis (2). Two of those with reflux (22.2%) required surgery, and 1 of those with ureterovesical junction obstruction (33.3%) required surgery.
Conclusions-Most renal abnormalities first identified in the third trimester after normal findings on a detailed second-trimester structural fetal survey were hydronephrosis, of which approximately one-third resolved after birth. Among the remaining neonates with persistent hydronephrosis, almost one-third had reflux that was not detected on the second-trimester anatomy scan.
C1 [Shipp, Thomas D.] Brigham & Womens Hosp, Dept Obstet & Gynecol, Div Maternal Fetal Med, Boston, MA 02115 USA.
[Shipp, Thomas D.; Bromley, Bryann; Benacerraf, Beryl R.] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Shipp, Thomas D.; Bromley, Bryann; Benacerraf, Beryl R.] Diagnost Ultrasound Associates PC, Boston, MA USA.
[Shipp, Thomas D.; Bromley, Bryann; Benacerraf, Beryl R.] Massachusetts Gen Hosp, Dept Obstet & Gynecol, Boston, MA 02114 USA.
[Benacerraf, Beryl R.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Nguyen, Hiep T.] Childrens Hosp, Dept Urol, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA USA.
[Lyons, Jennifer G.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
RP Shipp, TD (reprint author), Brigham & Womens Hosp, Dept Obstet & Gynecol, Div Maternal Fetal Med, CWN 3,75 Francis St, Boston, MA 02115 USA.
EM tshipp@partners.mg
NR 9
TC 3
Z9 3
U1 0
U2 1
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
USA
SN 0278-4297
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD NOV
PY 2011
VL 30
IS 11
BP 1567
EP 1572
PG 6
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA 846XN
UT WOS:000296936600014
PM 22039030
ER
PT J
AU Iezzoni, LI
AF Iezzoni, Lisa I.
TI Last Word: Barbara Starfield's Road Map
SO MEDICAL CARE
LA English
DT Editorial Material
ID CARE
C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Mongan Inst Hlth Policy, Boston, MA 02114 USA.
RP Iezzoni, LI (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Mongan Inst Hlth Policy, 50 Staniford St,Suite 901H, Boston, MA 02114 USA.
EM liezzoni@partners.org
NR 5
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD NOV
PY 2011
VL 49
IS 11
BP 976
EP 977
DI 10.1097/MLR.0b013e318233a906
PG 2
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 841UO
UT WOS:000296540400003
PM 22005604
ER
PT J
AU Edwardsen, EA
Dichter, ME
Walsh, P
Cerulli, C
AF Edwardsen, Elizabeth A.
Dichter, Melissa E.
Walsh, Patrick
Cerulli, Catherine
TI Instructional Curriculum Improves Medical Staff Knowledge and Efficacy
for Patients Experiencing Intimate Partner Violence
SO MILITARY MEDICINE
LA English
DT Article
ID DOMESTIC VIOLENCE; MENTAL-HEALTH; PRIMARY-CARE; WOMEN; PHYSICIANS;
VICTIMS
AB Objectives: This study assesses Veterans Affairs mental health providers' understanding of intimate partner violence (IPV) and the perception of patient benefit of routine inquiry and service referral. The impact of an instructional curriculum was also examined following an interactive training. Methods: An evidence-based curriculum was offered to Veterans Affairs mental health providers. The curriculum utilized didactic methods, case scenarios, and resources regarding referrals and statutes regarding crimes related to violence and abuse. The participants completed pre- and post-training surveys to assess their perceptions about IPV and to evaluate the training. Results: Seventy-three individuals completed the training. Fifty-four of the participants were female, and thirty-three were over the age of 45 years. Fifty-one individuals completed both surveys. There were no differences between participants' views of the seriousness of IPV in the community or their practices before or after the training. However, participants scored significantly higher on the knowledge and efficacy measures after the training (p < 0.001). Conclusion: Following an educational intervention, providers demonstrate more knowledge and efficacy regarding routine inquiry and referral for IPV. Barriers to universal implementation still warrant attention.
C1 [Edwardsen, Elizabeth A.] Univ Rochester, Sch Med & Dent, Dept Emergency Med, Rochester, NY 14642 USA.
[Dichter, Melissa E.] Philadelphia VA Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA 19104 USA.
[Walsh, Patrick] Univ Rochester, Sch Med & Dent, Ctr Excellence, Dept Psychiat, Rochester, NY 14642 USA.
[Cerulli, Catherine] Univ Rochester, Sch Med & Dent, Dept Psychiat, Lab Interpersonal Violence & Victimizat, Rochester, NY 14642 USA.
RP Edwardsen, EA (reprint author), Univ Rochester, Sch Med & Dent, Dept Emergency Med, 601 Elmwood Ave, Rochester, NY 14642 USA.
FU NIMH [K01MH75965-01]; Center of Excellence for Suicide Prevention,
Department of VA
FX Funding for this work is provided by NIMH K01MH75965-01 (C. Cerulli).
Additional funding is provided by the Center of Excellence for Suicide
Prevention, Department of VA.
NR 25
TC 3
Z9 4
U1 0
U2 5
PU ASSOC MILITARY SURG US
PI BETHESDA
PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 USA
SN 0026-4075
J9 MIL MED
JI Milit. Med.
PD NOV
PY 2011
VL 176
IS 11
BP 1260
EP 1264
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 845NR
UT WOS:000296830300009
PM 22165653
ER
PT J
AU Qin, Y
Ekmekcioglu, S
Liu, P
Duncan, LM
Lizee, G
Poindexter, N
Grimm, EA
AF Qin, Yong
Ekmekcioglu, Suhendan
Liu, Ping
Duncan, Lyn M.
Lizee, Gregory
Poindexter, Nancy
Grimm, Elizabeth A.
TI Constitutive Aberrant Endogenous Interleukin-1 Facilitates Inflammation
and Growth in Human Melanoma
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID FACTOR-KAPPA-B; SUPPRESSOR-CELLS; CANCER; EXPRESSION; REGULATORS;
APOPTOSIS; AUTOPHAGY; PATHWAY; METASTASIS; ACTIVATION
AB Interleukin (IL)-1-mediated inflammation is proposed to contribute to the development and progression of some cancers. IL-1 family member proteins are known to be expressed constitutively in many melanoma tumor cells, and we hypothesize that these support molecular pathways of inflammation and facilitate tumor growth. To investigate the expression of IL-1 alpha and IL-1 beta in melanoma patients, and their association with disease progression, immunohistochemical staining was carried out on tissues from 170 patients including benign nevi, primary melanomas, and metastatic melanomas. IL-1 beta levels were low (or zero) in benign nevi and higher in primary and metastatic melanomas (P < 0.0001). IL-1 alpha was expressed in about 73% of nevi and 55% of metastatic melanomas, with levels significantly higher in primary tumors (P < 0.0001); most (98%) primary melanoma samples were positive for IL-1 alpha. In vitro studies with seven human melanoma cell lines showed that five cell lines expressed IL-1 alpha and IL-1 beta proteins and mRNA. We identified for the first time several important downstream signaling pathways affected by endogenous IL-1, including reactive oxygen and nitrogen species, COX-2, and phosphorylated NF-kappa B inhibitor (I kappa B) and stress-activated protein kinase/c-jun-NH2-kinase; all of which were decreased by siRNA to IL-1s. Downregulation of IL-1 alpha, IL-1 beta, or MyD88 substantially increased p21 and p53 levels. Treatment with IL-1 receptor type I neutralizing antibody or IL-1 pathway-specific siRNAs led to growth arrest in IL-1-positive melanoma cells. Furthermore, blocking the IL-1 pathway increased autophagy in IL-1-positive melanoma cells. These results indicate that the endogenous IL-1 system is functional in most human melanoma and interrupting its signaling inhibits the growth of IL-1-positive melanoma cells. Mol Cancer Res; 9(11); 1537-50. (C) 2011 AACR.
C1 [Qin, Yong; Ekmekcioglu, Suhendan; Lizee, Gregory; Poindexter, Nancy; Grimm, Elizabeth A.] Univ Texas MD Anderson Canc Ctr, Dept Melanoma Med Oncol, Houston, TX 77030 USA.
[Liu, Ping] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
[Duncan, Lyn M.] Massachusetts Gen Hosp, Pathol Serv, Dept Dermatopathol Unit, Boston, MA 02114 USA.
RP Grimm, EA (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Melanoma Med Oncol, Box 362,1515 Holcombe Blvd, Houston, TX 77030 USA.
EM egrimm@mdanderson.org
FU National Cancer Institute [CA16672]; University of Texas, MD Anderson
Cancer Center [P50 CA093459]; Dr. Miriam and Sheldon G. Adelson Medical
Research Foundation
FX The authors thank Sandra Kinney (MD Anderson) for assistance in the IHC
studies and Wendy Schawa (MD Anderson) for assistance in flow cytometric
studies. The authors are grateful to Karen Muller for proofreading and
editing the manuscript and figures and also thank MDACC Characterized
Cell Line Core Facility for STR DNA fingerprinting of the melanoma cell
lines, the Flow Cytometry, and Cellular Imagine Facility at MD Anderson
(funded by National Cancer Institute CA16672) for AO staining analysis.;
This research was supported by the University of Texas, MD Anderson
Cancer Center SPORE in Melanoma (P50 CA093459) and Dr. Miriam and
Sheldon G. Adelson Medical Research Foundation.
NR 38
TC 32
Z9 33
U1 0
U2 5
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD NOV
PY 2011
VL 9
IS 11
BP 1537
EP 1550
DI 10.1158/1541-7786.MCR-11-0279
PG 14
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA 850QH
UT WOS:000297211100011
PM 21954434
ER
PT J
AU Gerstner, E
Jennings, D
Chi, AS
Plotkin, S
Kwon, SJ
Pinho, M
Polaskova, P
Batchelor, TT
Sorensen, AG
AF Gerstner, Elizabeth
Jennings, Dominique
Chi, Andrew S.
Plotkin, Scott
Kwon, Seon Joo
Pinho, Marco
Polaskova, Pavlina
Batchelor, Tracy T.
Sorensen, A. Gregory
TI COMPARISON OF CHANGES IN MRI CONTRAST ENHANCEMENT AND FLAIR
HYPERINTENSITY IN PATIENTS WITH NEWLY DIAGNOSED GLIOBLASTOMA DURING
CHEMORADIATION WITH AND WITHOUT AN ANTI-VEGF AGENT
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Gerstner, Elizabeth; Chi, Andrew S.; Plotkin, Scott; Batchelor, Tracy T.; Sorensen, A. Gregory] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Jennings, Dominique; Kwon, Seon Joo; Pinho, Marco; Polaskova, Pavlina] Martinos Ctr Biomed Imaging, Charlestown, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 7
EP 8
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600032
ER
PT J
AU Furnari, F
Fenton, T
Nathanson, D
de Alberquerque, CP
Kuga, D
Wanami, A
Dang, J
Yang, HJ
Tanaka, K
Gao, L
Oba-Shinjo, S
Uno, M
Inda, M
Bachoo, R
James, CD
DePinho, R
Vandenberg, S
Zhou, HL
Marie, S
Mischel, P
Cavenee, W
AF Furnari, Frank
Fenton, Timothy
Nathanson, David
de Alberquerque, Claudio Ponte
Kuga, Daisuke
Wanami, Akio
Dang, Julie
Yang, Huijun
Tanaka, Kazuhiro
Gao, Lu
Oba-Shinjo, Sueli
Uno, Miyuki
Inda, Maria-del-Mar
Bachoo, Robert
James, C. David
DePinho, Ronald
Vandenberg, Scott
Zhou, Huilin
Marie, Suely
Mischel, Paul
Cavenee, Webster
TI PTEN PHOSPHORYLATION BY FIBROBLAST GROWTH FACTOR RECEPTORS AND SRC
MEDIATES RESISTANCE TO EPIDERMAL GROWTH FACTOR RECEPTOR INHIBITORS IN
GLIOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Furnari, Frank; Fenton, Timothy; de Alberquerque, Claudio Ponte; Gao, Lu; Inda, Maria-del-Mar; Zhou, Huilin; Cavenee, Webster] Ludwig Inst UCSD, La Jolla, CA USA.
[Nathanson, David; Kuga, Daisuke; Wanami, Akio; Dang, Julie; Yang, Huijun; Tanaka, Kazuhiro; Mischel, Paul] Univ Calif Los Angeles, Los Angeles, CA USA.
[Oba-Shinjo, Sueli; Uno, Miyuki] Univ Sao Paulo, Sao Paulo, Brazil.
[Bachoo, Robert] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[James, C. David] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[DePinho, Ronald] Dana Farber Canc Inst, Boston, MA USA.
[Vandenberg, Scott] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Marie, Suely] Univ Sao Paulo, Sao Paulo, CA, Brazil.
RI James, Charles/E-2721-2012; Marie, Suely/D-1870-2012; Oba-Shinjo, Sueli
/C-4017-2012
OI James, Charles/0000-0002-1027-203X;
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 10
EP 10
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600039
ER
PT J
AU Kouri, FM
Chin, L
Stegh, AH
AF Kouri, Foteini M.
Chin, Lynda
Stegh, Alexander H.
TI MICRORNA-182 ACTS AS A CHEMOSENSITIZER IN GBM BY REPRESSING BCL2L12
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Kouri, Foteini M.; Stegh, Alexander H.] Northwestern Univ, Chicago, IL 60611 USA.
[Chin, Lynda] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 24
EP 24
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600101
ER
PT J
AU Terry, AR
Barker, FG
Leffert, LR
Bateman, B
Souter, I
Plotkin, SR
AF Terry, Anna R.
Barker, Fred G., II
Leffert, Lisa R.
Bateman, Brian
Souter, Irene
Plotkin, Scott R.
TI OUTCOMES OF HOSPITALIZATION AMONG PREGNANT WOMEN WITH CNS NEOPLASMS: A
POPULATION-BASED STUDY
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Terry, Anna R.; Barker, Fred G., II; Leffert, Lisa R.; Bateman, Brian; Souter, Irene; Plotkin, Scott R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 28
EP 28
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600119
ER
PT J
AU Kleijn, A
Kloezeman, J
Treffers-Westerlaken, E
Fulci, G
Leenstra, S
Dirven, C
Debets, R
Lamfers, M
AF Kleijn, Anne
Kloezeman, Jenneke
Treffers-Westerlaken, Elike
Fulci, Giulia
Leenstra, Sieger
Dirven, Clemens
Debets, Reno
Lamfers, Martine
TI CHARACTERIZATION OF THE IMMUNE RESPONSE TO ONCOLYTIC ADENOVIRUS THERAPY
FOR MALIGNANT GLIOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Kleijn, Anne; Kloezeman, Jenneke; Treffers-Westerlaken, Elike; Leenstra, Sieger; Dirven, Clemens; Debets, Reno; Lamfers, Martine] Erasmus MC, Rotterdam, Netherlands.
[Fulci, Giulia] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 32
EP 32
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600132
ER
PT J
AU Kong, S
Tyler, B
Zhou, JY
Carter, BS
Brem, H
Junghans, RP
Sampath, P
AF Kong, Seogkyoung
Tyler, Betty
Zhou, Jinyuan
Carter, Bob S.
Brem, Henry
Junghans, Richard P.
Sampath, Prakash
TI SUCCESSFUL SUPPRESSION OF A HUMAN GLIOMA XENOGRAFT USING
IL13RA2-SPECIFIC MONOMERIC CHIMERIC ANTIGEN RECEPTOR
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Kong, Seogkyoung; Sampath, Prakash] Boston Univ, Sch Med, Roger Williams Med Ctr, Dept Neurosurg, Providence, RI USA.
[Tyler, Betty; Brem, Henry] Johns Hopkins Univ, Sch Med, Dept Neurosurg, Hunterian Neurosurg Res Lab, Baltimore, MD 21205 USA.
[Zhou, Jinyuan] Johns Hopkins Univ, Sch Med, Dept Radiol, Baltimore, MD 21205 USA.
[Carter, Bob S.] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp,Neurosurg Serv, Boston, MA 02115 USA.
[Junghans, Richard P.] Boston Univ, Sch Med, Roger Williams Hosp, Dept Surg,Div Surg Res, Providence, RI USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 34
EP 34
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600138
ER
PT J
AU Cloughesy, T
Raizer, J
Drappatz, J
Gerena-Lewis, M
Rogerio, J
Yacoub, S
Desjardin, A
AF Cloughesy, Timothy
Raizer, J.
Drappatz, J.
Gerena-Lewis, M.
Rogerio, J.
Yacoub, S.
Desjardin, A.
TI A PHASE II TRIAL OF EVEROLIMUS IN PATIENTS WITH RECURRENT GLIOBLASTOMA
MULTIFORME
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Cloughesy, Timothy] Ronald Reagan UCLA Med Ctr, Los Angeles, CA USA.
[Raizer, J.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Drappatz, J.] Dana Farber Brigham & Womens Canc Ctr, Ctr Neurooncol, Boston, MA USA.
[Gerena-Lewis, M.] Summit Oncol Associates, Akron, OH USA.
[Rogerio, J.; Yacoub, S.] Novartis Pharmaceut, Florham Pk, NJ USA.
[Desjardin, A.] Duke Univ, Med Ctr, Durham, NC USA.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 42
EP 43
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600172
ER
PT J
AU Reiner, AS
Panageas, KS
Iwamoto, FM
Cloughesy, TF
Aldape, KD
Rivera, AL
Eichler, AF
Louis, DN
Paleologos, NA
Fisher, BJ
Ashby, LS
Cairncross, JG
Roldan, GB
Wen, PY
Ligon, KL
Shiff, D
Robins, HI
Rocque, BG
Chamberlain, MC
Mason, WP
Weaver, SA
Green, RM
Kamar, FG
Abrey, LE
DeAngelis, LM
Jhanwar, SC
Rosenblum, MK
Lassman, AB
AF Reiner, Anne S.
Panageas, Katherine S.
Iwamoto, Fabio M.
Cloughesy, Timothy F.
Aldape, Kenneth D.
Rivera, Andreana L.
Eichler, April F.
Louis, David N.
Paleologos, Nina A.
Fisher, Barbara J.
Ashby, Lynn S.
Cairncross, J. G.
Roldan, Gloria B.
Wen, Patrick Y.
Ligon, Keith L.
Shiff, David
Robins, H. I.
Rocque, Brandon G.
Chamberlain, Marc C.
Mason, Warren P.
Weaver, Susan A.
Green, Richard M.
Kamar, Francois G.
Abrey, Lauren E.
DeAngelis, Lisa M.
Jhanwar, Suresh C.
Rosenblum, Marc K.
Lassman, Andrew B.
TI RECURSIVE PARTITIONING ANALYSIS OF PROGNOSTIC VARIABLES IN NEWLY
DIAGNOSED ANAPLASTIC OLIGODENDROGLIAL TUMORS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Reiner, Anne S.; Panageas, Katherine S.; Iwamoto, Fabio M.; Abrey, Lauren E.; DeAngelis, Lisa M.; Jhanwar, Suresh C.; Rosenblum, Marc K.; Lassman, Andrew B.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Cloughesy, Timothy F.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Aldape, Kenneth D.; Rivera, Andreana L.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Eichler, April F.; Louis, David N.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Paleologos, Nina A.] NorthShore Univ Hlth Syst, Evanston Hosp Kellogg Canc, Pritzker Sch Med, Evanston, IL USA.
[Fisher, Barbara J.] London Reg Canc Program, London, ON, Canada.
[Ashby, Lynn S.] Barrow Neurol Inst, Phoenix, AZ 85013 USA.
[Cairncross, J. G.; Roldan, Gloria B.] Univ Calgary, Calgary, AB, Canada.
[Wen, Patrick Y.; Ligon, Keith L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Wen, Patrick Y.; Ligon, Keith L.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Shiff, David] Univ Virginia Hlth Syst, Charlottesville, VA USA.
[Robins, H. I.; Rocque, Brandon G.] Univ Wisconsin, Madison, WI USA.
[Chamberlain, Marc C.] Univ Washington, Seattle, WA 98195 USA.
[Chamberlain, Marc C.] Seattle Canc Care Alliance, Seattle, WA USA.
[Mason, Warren P.] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Green, Richard M.] Kaiser Permanente Angeles Med Ctr, Los Angeles, CA USA.
[Weaver, Susan A.] Albany Med Ctr, Albany, NY USA.
[Kamar, Francois G.] Clemenceau Med Ctr, Beirut, Lebanon.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 43
EP 44
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600176
ER
PT J
AU Sparagana, S
Belousova, E
Jozwiak, S
Korf, B
Frost, M
Kuperman, R
Kohrman, M
Witt, O
Wu, J
Flamini, R
Jansen, A
Curtalolo, P
Thiele, E
Whittemore, V
De Vries, P
Ford, J
Shah, G
Cauwel, H
Edrich, P
Sahmoud, T
Franz, D
AF Sparagana, Steven
Belousova, E.
Jozwiak, Sergiusz
Korf, Bruce
Frost, Michael
Kuperman, Rachel
Kohrman, Michael
Witt, Olaf
Wu, Joyce
Flamini, Robert
Jansen, Anna
Curtalolo, P.
Thiele, E.
Whittemore, V.
De Vries, Petrus
Ford, James
Shah, Gaurav
Cauwel, H.
Edrich, Pascal
Sahmoud, Tarek
Franz, David
TI EVEROLIMUS TREATMENT OF SUBEPENDYMAL GIANT CELL ASTROCYTOMAS (SEGAs)
ASSOCIATED WITH TUBEROUS SCLEROSIS COMPLEX (TSC): THE EXIST-1 TRIAL
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Sparagana, Steven] Texas Scottish Rite Hosp Children, Dallas, TX 75219 USA.
[Belousova, E.] Moscow Res Inst Pediat Pediat Surg, Moscow, Russia.
[Jozwiak, Sergiusz] Childrens Mem Hlth Inst Warsaw, Warsaw, Poland.
[Korf, Bruce] Univ Alabama, Birmingham, AL USA.
[Frost, Michael] Minnesota Epilepsy Grp, St Paul, MN USA.
[Kuperman, Rachel] Childrens Hosp & Res Ctr Oakland, Oakland, CA USA.
[Kohrman, Michael] Univ Chicago, Chicago, IL 60637 USA.
[Kohrman, Michael] Comer Childrens Hosp, Chicago, IL USA.
[Witt, Olaf] Univ Heidelberg, Med Ctr, Heidelberg, Germany.
[Witt, Olaf] German Canc Res Ctr, D-6900 Heidelberg, Germany.
[Wu, Joyce] Univ Calif Los Angeles, Mattel Childrens Hosp, Los Angeles, CA USA.
[Flamini, Robert] Childrens Healthcare Atlanta, Atlanta, GA USA.
[Jansen, Anna] UZ Brussel, Brussels, Belgium.
[Curtalolo, P.] Univ Rome Tor Vega, Rome, Italy.
[Thiele, E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Whittemore, V.] Tuberous Sclerosis Alliance, Silver Spring, MD USA.
[De Vries, Petrus] Univ Cambridge, Neurodev Serv, Cambridgeshire & Peterborough NHS Fdn Trust, Cambridge, England.
[De Vries, Petrus] Univ Cambridge, Dev Psychiat Sect, Cambridge, England.
[Ford, James; Shah, Gaurav; Cauwel, H.; Edrich, Pascal; Sahmoud, Tarek] Novartis Pharmaceut, Florham Pk, NJ USA.
[Franz, David] Cincinnati Childrens Hosp, Med Ctr, Cincinnati, OH USA.
RI Jansen, Anna/P-3121-2014
OI Jansen, Anna/0000-0002-3835-2824
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 50
EP 50
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600202
ER
PT J
AU Ram, Z
Wong, ET
Gutin, PH
AF Ram, Zvi
Wong, Eric T.
Gutin, Philip H.
TI COMPARING THE EFFECT OF NOVOTTF TO BEVACIZUMAB IN RECURRENT GBM: A
POST-HOC SUB-ANALYSIS OF THE PHASE III TRIAL DATA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Ram, Zvi] Tel Aviv Med Ctr & Sch Med, Dana Childrens Hosp, IL-64239 Tel Aviv, Israel.
[Wong, Eric T.] BIDMC, Boston, MA USA.
[Gutin, Philip H.] NYC, MSKCC, New York, NY USA.
NR 0
TC 1
Z9 1
U1 1
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 52
EP 52
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600211
ER
PT J
AU Nunes, FP
Merker, V
Jennings, D
Caruso, P
Muzikansky, A
Stemmer-Rachamimov, A
Plotkin, S
AF Nunes, Fabio P.
Merker, Vanessa
Jennings, Dominique
Caruso, Paul
Muzikansky, Alona
Stemmer-Rachamimov, Anat
Plotkin, Scott
TI MENINGIOMA RESPONSE TO BEVACIZUMAB: A RETROSPECTIVE ANALYSIS OF
TREATMENT RESULTS IN 14 NF2 PATIENTS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Nunes, Fabio P.; Merker, Vanessa; Jennings, Dominique; Caruso, Paul; Muzikansky, Alona; Stemmer-Rachamimov, Anat; Plotkin, Scott] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 59
EP 59
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600240
ER
PT J
AU Nayak, L
Iwamoto, FM
Rudnick, JD
Norden, AD
Omuro, A
Kaley, TJ
AF Nayak, Lakshmi
Iwamoto, Fabio M.
Rudnick, Jeremy D.
Norden, Andrew D.
Omuro, Antonio
Kaley, Thomas J.
TI BEVACIZUMAB IN MULTIPLY RECURRENT AGGRESSIVE MENINGIOMAS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Nayak, Lakshmi; Omuro, Antonio; Kaley, Thomas J.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Iwamoto, Fabio M.] NCI, NIH, Bethesda, MD 20892 USA.
[Rudnick, Jeremy D.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Norden, Andrew D.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 61
EP 61
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600248
ER
PT J
AU Panageas, KS
Iwamoto, FM
Cloughesy, TF
Aldape, KD
Rivera, AL
Eichler, AF
Louis, DN
Paleologos, NA
Fisher, BJ
Ashby, LS
Cairncross, JG
Roldan, GB
Wen, PY
Ligon, KL
Schiff, D
Robins, HI
Rocque, BG
Chamberlain, MC
Mason, WP
Weaver, SA
Green, RM
Kamar, FG
Abrey, LE
DeAngelis, LM
Jhanwar, SC
Rosenblum, MK
Lassman, AB
AF Panageas, Katherine S.
Iwamoto, Fabio M.
Cloughesy, Timothy F.
Aldape, Kenneth D.
Rivera, Andreana L.
Eichler, April F.
Louis, David N.
Paleologos, Nina A.
Fisher, Barbara J.
Ashby, Lynn S.
Cairncross, J. G.
Roldan, Gloria B.
Wen, Patrick Y.
Ligon, Keith L.
Schiff, David
Robins, H. I.
Rocque, Brandon G.
Chamberlain, Marc C.
Mason, Warren P.
Weaver, Susan A.
Green, Richard M.
Kamar, Francois G.
Abrey, Lauren E.
DeAngelis, Lisa M.
Jhanwar, Suresh C.
Rosenblum, Marc K.
Lassman, Andrew B.
TI TIME TRENDS IN TREATMENT OF ANAPLASTIC OLIGODENDROGLIAL TUMORS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Panageas, Katherine S.; Iwamoto, Fabio M.; Abrey, Lauren E.; DeAngelis, Lisa M.; Jhanwar, Suresh C.; Rosenblum, Marc K.; Lassman, Andrew B.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Cloughesy, Timothy F.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Aldape, Kenneth D.; Rivera, Andreana L.] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Eichler, April F.; Louis, David N.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Paleologos, Nina A.] NorthShore Univ HealthSyst, Evanston Hosp, Kellogg Canc Ctr, Evanston, IL USA.
[Fisher, Barbara J.] London Reg Canc Program, London, ON, Canada.
[Ashby, Lynn S.] Barrow Neurol Inst, Phoenix, AZ 85013 USA.
[Cairncross, J. G.; Roldan, Gloria B.] Univ Calgary, Calgary, AB, Canada.
[Wen, Patrick Y.; Ligon, Keith L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Wen, Patrick Y.; Ligon, Keith L.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Schiff, David] Univ Virginia Hlth Syst, Charlottesville, VA USA.
[Robins, H. I.; Rocque, Brandon G.] Univ Wisconsin, Madison, WI USA.
[Chamberlain, Marc C.] Univ Washington, Seattle, WA 98195 USA.
[Chamberlain, Marc C.] Seattle Canc Care Alliance, Seattle, WA USA.
[Mason, Warren P.] Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
[Weaver, Susan A.] Albany Med Ctr, Albany, NY USA.
[Green, Richard M.] Kaiser Permanente, Los Angeles Med Ctr, Los Angeles, CA USA.
[Kamar, Francois G.] Clemenceau Med Ctr, Beirut, Lebanon.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 62
EP 63
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600256
ER
PT J
AU Rangarajan, HG
Kieran, MW
Scott, RM
Lew, SM
Firat, SY
Segura, AD
Jogal, SA
AF Rangarajan, Hemalatha G.
Kieran, Mark W.
Scott, Robert M.
Lew, Sean M.
Firat, Selim Y.
Segura, Annette D.
Jogal, Sachin A.
TI RECURRENT PAPILLARY TUMOR OF THE PINEAL REGION (PTPR) IN A PEDIATRIC
PATIENT: A BRIEF REPORT
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Rangarajan, Hemalatha G.; Lew, Sean M.; Firat, Selim Y.; Segura, Annette D.; Jogal, Sachin A.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Kieran, Mark W.; Scott, Robert M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RI champier, jacques/B-4160-2012; Rangarajan, Hemalatha/E-2011-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 62
EP 62
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600252
ER
PT J
AU Plotkin, SR
Supko, JG
Curry, WT
Chi, AS
Gerstner, ER
Stemmer-Rachamimov, A
Batchelor, TT
AF Plotkin, Scott R.
Supko, Jeffrey G.
Curry, William T.
Chi, Andrew S.
Gerstner, Elizabeth R.
Stemmer-Rachamimov, Anat
Batchelor, Tracy T.
TI INTRATUMORAL CONCENTRATIONS OF SUNITINIB AFTER ORAL ADMINISTRATION IN
PATIENTS WITH HIGH GRADE GLIOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Plotkin, Scott R.; Supko, Jeffrey G.; Curry, William T.; Chi, Andrew S.; Gerstner, Elizabeth R.; Stemmer-Rachamimov, Anat; Batchelor, Tracy T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 66
EP 66
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600271
ER
PT J
AU Plotkin, SR
Halpin, C
Merker, V
Barker, FG
AF Plotkin, Scott R.
Halpin, Chris
Merker, Vanessa
Barker, Fred G., II
TI HEARING AND RADIOGRAPHIC RESPONSE OF NEUROFIBROMATOSIS 2-RELATED
VESTIBULAR SCHWANNOMA TO BEVACIZUMAB: A RETROSPECTIVE REVIEW OF 31
PATIENTS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Plotkin, Scott R.; Merker, Vanessa; Barker, Fred G., II] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Halpin, Chris] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 67
EP 67
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600277
ER
PT J
AU Guo, DL
Reinitz, F
Youssef, M
Hong, C
Nathanson, D
Akhavan, D
Kuga, D
Amzajerdi, AN
Soto, H
Zhu, SJ
Babic, I
Iwanami, A
Tanaka, K
Gini, B
DeJesus, J
Lisiero, DD
Huang, T
Prins, R
Wen, P
Robbins, HI
Prados, M
DeAngelis, L
Mellinghoff, I
Mehta, M
James, CD
Chakravarti, A
Cloughesy, T
Tontonoz, P
Mischel, P
AF Guo, Deliang
Reinitz, Felicia
Youssef, Mary
Hong, Cynthia
Nathanson, David
Akhavan, David
Kuga, Daisuke
Amzajerdi, Ali Nael
Soto, Horacio
Zhu, Shaojun
Babic, Ivan
Iwanami, Akio
Tanaka, Kazuhiro
Gini, Beatrice
DeJesus, Jason
Lisiero, Dominique D.
Huang, Tiffany
Prins, Robert
Wen, Patrick
Robbins, H. Ian
Prados, Michael
DeAngelis, Lisa
Mellinghoff, Ingo
Mehta, Minesh
James, C. David
Chakravarti, Arnab
Cloughesy, Timothy
Tontonoz, Peter
Mischel, Paul
TI TARGETING EGFR/PI3K/AKT REGULATED SREBP-1/LDLR MEDIATED CHOLESTEROL
METABOLISM TO TREAT GLIOBLASTOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Guo, Deliang; Chakravarti, Arnab] Ohio State Univ, James Comprehens Canc Ctr, Columbus, OH 43210 USA.
[Reinitz, Felicia; Youssef, Mary; Hong, Cynthia; Nathanson, David; Akhavan, David; Kuga, Daisuke; Amzajerdi, Ali Nael; Soto, Horacio; Zhu, Shaojun; Babic, Ivan; Iwanami, Akio; Tanaka, Kazuhiro; Gini, Beatrice; DeJesus, Jason; Lisiero, Dominique D.; Huang, Tiffany; Prins, Robert; Cloughesy, Timothy; Tontonoz, Peter; Mischel, Paul] Univ Calif Los Angeles, Los Angeles, CA USA.
[Wen, Patrick] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Robbins, H. Ian] Univ Wisconsin, Madison, WI USA.
[Prados, Michael; James, C. David] UCSF, San Francisco, CA USA.
[DeAngelis, Lisa; Mellinghoff, Ingo] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Mehta, Minesh] Northwestern Univ, Chicago, IL 60611 USA.
RI James, Charles/E-2721-2012; Guo, Deliang/I-3735-2014
OI James, Charles/0000-0002-1027-203X; Guo, Deliang/0000-0002-8359-390X
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 70
EP 71
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600290
ER
PT J
AU Zhang, W
Zhang, J
Hoadley, K
Carter, B
Li, SW
Kang, CS
You, YP
Jiang, CL
Song, SY
Jiang, T
Chen, C
AF Zhang, Wei
Zhang, Jing
Hoadley, Katherine
Carter, Bob
Li, Shouwei
Kang, Chunsheng
You, Yongping
Jiang, Chuanlu
Song, Sonya
Jiang, Tao
Chen, Clark
TI MIR-181D: A PREDICTIVE GLIOBLASTOMA BIOMARKER THAT DOWNREGULATES MGMT
EXPRESSION
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Zhang, Wei; Li, Shouwei; Jiang, Tao] Tiantan Hosp, Dept Neurosurg, Beijing, Peoples R China.
[Zhang, Jing] Beijing Inst Genom, Beijing, Peoples R China.
[Hoadley, Katherine] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Carter, Bob] Univ Calif San Diego, Div Neurosurg, San Diego, CA 92103 USA.
[Kang, Chunsheng] Tianjin Hosp, Lab Neurooncol, Tianjin, Peoples R China.
[You, Yongping] Jiangsu Prov Peoples Hosp, Dept Neurosurg, Nanjing, Peoples R China.
[Jiang, Chuanlu] Harbin Med Coll, Dept Neurosurg, Harbin, Peoples R China.
[Song, Sonya] Peking Univ, Sch Oncol, Beijing 100871, Peoples R China.
[Chen, Clark] Dana Farber Canc Inst, Boston, MA 02115 USA.
RI Jiang, Tao/N-8142-2014; Zhang, Jing/F-4707-2015
OI Zhang, Jing/0000-0001-5903-6487
NR 0
TC 0
Z9 0
U1 1
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 77
EP 77
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600312
ER
PT J
AU Sperduto, PW
Kased, N
Roberge, D
Xu, ZY
Shanley, R
Luo, XH
Sneed, PK
Chao, ST
Weil, RJ
Suh, J
Bhatt, A
Jensen, AW
Brown, PD
Shih, HA
Kirkpatrick, J
Gaspar, LE
Fiveash, JB
Chiang, V
Knisely, JP
Sperduto, CM
Lin, N
Mehta, MP
AF Sperduto, Paul W.
Kased, Norbert
Roberge, David
Xu, Zhiyuan
Shanley, Ryan
Luo, Xianghua
Sneed, Penny K.
Chao, Samuel T.
Weil, Robert J.
Suh, John
Bhatt, Amit
Jensen, Ashley W.
Brown, Paul D.
Shih, Helen A.
Kirkpatrick, John
Gaspar, Laurie E.
Fiveash, John B.
Chiang, Veronica
Knisely, Jonathan P.
Sperduto, Christina M.
Lin, Nancy
Mehta, Minesh P.
TI THE EFFECT OF TUMOR SUBTYPE ON SURVIVAL AND THE GRADED PROGNOSTIC
ASSESSMENT (GPA) FOR PATIENTS WITH BREAST CANCER AND BRAIN METASTASES
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Shanley, Ryan] Univ Minnesota, Mason Canc Ctr, Minneapolis, MN USA.
[Kased, Norbert; Sneed, Penny K.] Univ Calif San Francisco, Dept Radiat Oncol, San Francisco, CA USA.
[Roberge, David] McGill Univ, Dept Radiat Oncol, Ctr Hlth, Montreal, PQ H3A 2T5, Canada.
[Xu, Zhiyuan; Weil, Robert J.] Cleveland Clin, Dept Neurosurg, Cleveland, OH 44106 USA.
[Luo, Xianghua] Univ Minnesota, Sch Publ Hlth, Minneapolis, MN USA.
[Bhatt, Amit] Univ Wisconsin, Dept Human Oncol, Madison, WI USA.
[Shih, Helen A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiat Oncol, Boston, MA USA.
[Kirkpatrick, John] Duke Med Ctr, Dept Radiat Oncol, Durham, NC USA.
[Gaspar, Laurie E.] Univ Colorado, Sch Med, Dept Radiat Oncol, Aurora, CO USA.
[Fiveash, John B.] Univ Alabama, Dept Radiat Oncol, Birmingham, AL USA.
[Chiang, Veronica] Yale Univ, Sch Med, Dept Neurosurg, New Haven, CT USA.
[Knisely, Jonathan P.] Yale Univ, Sch Med, Dept Radiat Oncol, New Haven, CT USA.
[Sperduto, Christina M.] Dartmouth Coll, Hanover, NH 03755 USA.
[Lin, Nancy] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Mehta, Minesh P.] Northwestern Univ, Dept Radiat Oncol, Chicago, IL 60611 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 82
EP 82
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600333
ER
PT J
AU Lee, EQ
Batchelor, TT
Lassman, AB
Schiff, DS
Kaley, TJ
Wong, ET
Mikkelsen, T
Purow, BW
Drappatz, J
Norden, AD
Beroukhim, R
Weiss, S
Alexander, BM
Sceppa, C
Gerard, M
Hallisey, SD
Bochacki, CA
Smith, KH
Muzikansky, AM
Wen, PY
AF Lee, Eudocia Quant
Batchelor, Tracy T.
Lassman, Andrew B.
Schiff, David S.
Kaley, Thomas J.
Wong, Eric T.
Mikkelsen, Tom
Purow, Benjamin W.
Drappatz, Jan
Norden, Andrew D.
Beroukhim, Rameen
Weiss, Stephanie
Alexander, Brian M.
Sceppa, Christine
Gerard, Mary
Hallisey, Stephen D.
Bochacki, Caelainn A.
Smith, Katrina H.
Muzikansky, Alona M.
Wen, Patrick Y.
TI PRELIMINARY DATA FROM A MULTICENTER, PHASE II, RANDOMIZED,
NONCOMPARATIVE CLINICAL TRIAL OF RADIATION THERAPY AND TEMOZOLOMIDE WITH
OR WITHOUT VANDETANIB IN NEWLY-DIAGNOSED GLIOBLASTOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Lee, Eudocia Quant; Drappatz, Jan; Norden, Andrew D.; Beroukhim, Rameen; Wen, Patrick Y.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Batchelor, Tracy T.; Muzikansky, Alona M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Lassman, Andrew B.; Kaley, Thomas J.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Schiff, David S.; Purow, Benjamin W.] Univ Virginia, Charlottesville, VA USA.
[Wong, Eric T.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Mikkelsen, Tom] Henry Ford Hosp, Hermelin Brain Tumor Ctr, Detroit, MI 48202 USA.
[Weiss, Stephanie; Alexander, Brian M.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Hallisey, Stephen D.; Bochacki, Caelainn A.; Smith, Katrina H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 86
EP 86
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600349
ER
PT J
AU Peereboom, DM
Mikkelson, T
Sloan, AE
Rich, JN
Supko, JG
Ye, XB
Brewer, C
Lamborn, K
Prados, M
Grossman, SA
AF Peereboom, David M.
Mikkelson, Tom
Sloan, Andrew E.
Rich, Jeremy N.
Supko, Jeffrey G.
Ye, Xiaobu
Brewer, Cathy
Lamborn, Kathleen
Prados, Michael
Grossman, Stuart A.
TI A PHASE II AND PHARMACODYNAMIC TRIAL OF RO4929097 FOR PATIENTS WITH
RECURRENT/PROGRESSIVE GLIOBLASTOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Peereboom, David M.; Rich, Jeremy N.; Brewer, Cathy] Cleveland Clin, Cleveland, OH 44106 USA.
[Mikkelson, Tom] Henry Ford Hosp, Detroit, MI 48202 USA.
[Sloan, Andrew E.] Univ Hosp, Cleveland, OH USA.
[Supko, Jeffrey G.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Ye, Xiaobu; Grossman, Stuart A.] Johns Hopkins Univ, Baltimore, MD USA.
[Lamborn, Kathleen] Univ Calif San Francisco, San Francisco, CA 94143 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 86
EP 86
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600350
ER
PT J
AU Batchelor, T
Grossman, S
Brem, S
Lesser, G
Voloschin, A
Nabors, LB
Mikkelsen, T
Desideri, S
Supko, J
Peereboom, D
AF Batchelor, Tracy
Grossman, Stuart
Brem, Steve
Lesser, Glenn
Voloschin, Alfredo
Nabors, Louis B.
Mikkelsen, Tom
Desideri, Serena
Supko, Jeffrey
Peereboom, David
TI FEASIBILITY AND PHASE I/II TRIAL OF TANDUTINIB IN PATIENTS WITH
RECURRENT GLIOBLASTOMA
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Batchelor, Tracy; Supko, Jeffrey] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Grossman, Stuart; Desideri, Serena] Johns Hopkins Univ, Baltimore, MD USA.
[Brem, Steve] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Lesser, Glenn] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Voloschin, Alfredo] Emory Univ, Atlanta, GA 30322 USA.
[Nabors, Louis B.] Univ Alabama, Birmingham, AL USA.
[Mikkelsen, Tom] Henry Ford Hosp, Detroit, MI 48202 USA.
[Peereboom, David] Cleveland Clin, Cleveland, OH 44106 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 89
EP 89
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600360
ER
PT J
AU Lucas, MR
AF Lucas, Michele R.
TI HYPERAROUSAL/HYPERVIGILANCE IN PATIENTS WITH BRAIN CANCER CREATES A
CYCLE OF SLEEP DISTURBANCE AND DAYTIME SLEEPINESS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Lucas, Michele R.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 121
EP 121
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600476
ER
PT J
AU Gerard, ME
Drappatz, J
Muzikansky, A
Weiss, S
Kesari, S
Wong, E
Fadul, CE
Norden, AD
Quant, EC
Beroukhim, R
Alexander, B
Ruland, S
Ciampa, AS
LaFrankie, DC
Sceppa, C
Smith, KH
Hammond, SN
Wen, PY
AF Gerard, Mary E.
Drappatz, Jan
Muzikansky, Alona
Weiss, Stephanie
Kesari, Santosh
Wong, Eric
Fadul, Camilo E.
Norden, Andrew D.
Quant, Eudocia C.
Beroukhim, Rameen
Alexander, Brian
Ruland, Sandra
Ciampa, Abigail S.
LaFrankie, Debra C.
Sceppa, Christine
Smith, Katrina H.
Hammond, Samantha N.
Wen, Patrick Y.
TI INTERIM ANALYSIS OF A RANDOMIZED PLACEBO-CONTROLLED PILOT TRIAL OF
ARMODAFINIL FOR FATIGUE IN PATIENTS WITH MALIGNANT GLIOMAS UNDERGOING
RADIOTHERAPY WITH OR WITHOUT STANDARD CHEMOTHERAPY
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Gerard, Mary E.; Drappatz, Jan; Weiss, Stephanie; Norden, Andrew D.; Quant, Eudocia C.; Beroukhim, Rameen; Alexander, Brian; Ruland, Sandra; Ciampa, Abigail S.; LaFrankie, Debra C.; Sceppa, Christine; Smith, Katrina H.; Hammond, Samantha N.; Wen, Patrick Y.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Muzikansky, Alona] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Kesari, Santosh] Univ Calif San Diego, San Diego, CA 92103 USA.
[Wong, Eric] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Fadul, Camilo E.] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
RI Kesari, Santosh/E-8461-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 125
EP 125
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600493
ER
PT J
AU Mahajan, A
Grosshans, D
McAleer, MF
Brown, PD
Chintagumpala, M
Vats, T
Puduvalli, V
Yock, T
AF Mahajan, Anita
Grosshans, David
McAleer, Mary Francis
Brown, Paul D.
Chintagumpala, Murali
Vats, Tribhawan
Puduvalli, Vinay
Yock, Torunn
TI A MATCHED COMPARISON OF BLOOD COUNTS DURING WHOLE VERSUS PARTIAL
VERTEBRAL PROTON CRANIOSPINAL IRRADIATION
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Mahajan, Anita; Grosshans, David; McAleer, Mary Francis; Brown, Paul D.; Vats, Tribhawan; Puduvalli, Vinay] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Chintagumpala, Murali] Baylor Coll Med, Houston, TX 77030 USA.
[Yock, Torunn] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 128
EP 128
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600506
ER
PT J
AU Wang, CC
Floyd, S
Chang, CH
Warnke, P
Chio, CC
Kasper, E
Mahadevan, A
Wong, E
Jeyapalan, S
Chen, C
AF Wang, Che-Chuan
Floyd, Scott
Chang, Chin-Hong
Warnke, Peter
Chio, Chung-Ching
Kasper, Ekkehard
Mahadevan, Anand
Wong, Eric
Jeyapalan, Suriya
Chen, Clark
TI CYBERKNIFE HYPOFRACTIONATED STEREOTACTIC RADIOSURGERY (HSRS) OF
RESECTION CAVITY AFTER EXCISION OF LARGE CEREBRAL METASTASIS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Wang, Che-Chuan; Chang, Chin-Hong; Chio, Chung-Ching] Chi Mei Med Ctr, Tainan, Taiwan.
[Floyd, Scott; Kasper, Ekkehard; Mahadevan, Anand; Wong, Eric] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Warnke, Peter] Univ Chicago, Chicago, IL 60637 USA.
[Jeyapalan, Suriya] Rhode Isl Hosp, Providence, RI USA.
[Chen, Clark] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 128
EP 128
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600505
ER
PT J
AU Colen, RR
Mahajan, B
Jolesz, FA
Zinn, PO
AF Colen, Rivka R.
Mahajan, Bhanu
Jolesz, Ferenc A.
Zinn, Pascal O.
TI RADIOGENOMIC MAPPING IN GBM IN PATIENTS WITH HIGH VERSUS LOW EDEMA/TUMOR
INFILTRATION USING AN IMAGE-GENOMIC ANALYSIS OF 12,764 GENES AND 555
MICRORNAS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Colen, Rivka R.; Mahajan, Bhanu; Jolesz, Ferenc A.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Zinn, Pascal O.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 142
EP 143
PG 2
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600560
ER
PT J
AU Chen, C
Kasper, E
Warnke, P
AF Chen, Clark
Kasper, Ekkehard
Warnke, Peter
TI PALLIATIVE ENDOSCOPIC THIRD VENTRICULOSTOMY VERSUS VENTRICULOPERITONEAL
SHUNTING IN THE TREATMENT OF OBSTRUCTIVE HYDROCEPHALUS FROM CEREBRAL
METASTASIS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Chen, Clark] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Kasper, Ekkehard] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Warnke, Peter] Univ Chicago, Dept Neurosurg, Chicago, IL 60637 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 155
EP 155
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600610
ER
PT J
AU Sheth, SA
Snuderl, M
Kwon, CS
Wirth, D
Yaroslavsky, A
Curry, WT
AF Sheth, Sameer A.
Snuderl, Matija
Kwon, Churl-Su
Wirth, Dennis
Yaroslavsky, Anna
Curry, William T.
TI CONFOCAL MICROSCOPIC FLUORESCENCE IMAGING OF GLIOMAS
SO NEURO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Sheth, Sameer A.; Snuderl, Matija; Kwon, Churl-Su; Curry, William T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Wirth, Dennis; Yaroslavsky, Anna] Univ Massachusetts, Lowell, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
SU 3
BP 162
EP 162
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CP
UT WOS:000297026600638
ER
PT J
AU Badr, CE
Wurdinger, T
Nilsson, J
Niers, JM
Whalen, M
Degterev, A
Tannous, BA
AF Badr, Christian E.
Wurdinger, Thomas
Nilsson, Jonas
Niers, Johanna M.
Whalen, Michael
Degterev, Alexei
Tannous, Bakhos A.
TI Lanatoside C sensitizes glioblastoma cells to tumor necrosis
factor-related apoptosis-inducing ligand and induces an alternative cell
death pathway
SO NEURO-ONCOLOGY
LA English
DT Article
DE cardiac glycoside; glioblastoma; lanatoside C; non-apoptotic cell death;
TRAIL
ID TRAIL-INDUCED APOPTOSIS; CARDIAC-GLYCOSIDES; CYTOCHROME-C; CANCER-CELLS;
DOWN-REGULATION; CULTURED-CELLS; GLIOMA-CELLS; SODIUM-PUMP; IN-VIVO;
INHIBITORS
AB Human glioblastoma (GBM) cells are notorious for their resistance to apoptosis-inducing therapeutics. We have identified lanatoside C as a sensitizer of GBM cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cell death partly by upregulation of the death receptor 5. We show that lanatoside C sensitizes GBM cells to TRAIL-induced apoptosis in a GBM xenograft model in vivo. Lanatoside C on its own serves as a therapeutic agent against GBM by activating a caspase-independent cell death pathway. Cells treated with lanatoside C showed necrotic cell morphology with absence of caspase activation, low mitochondrial membrane potential, and early intracellular ATP depletion. In conclusion, lanatoside C sensitizes GBM cells to TRAIL-induced cell death and mitigates apoptosis resistance of glioblastoma cells by inducing an alternative cell death pathway. To our knowledge, this is one of the first examples of use of caspase-independent cell death inducers to trigger tumor regression in vivo. Activation of such mechanism may be a useful strategy to counter resistance of cancer cells to apoptosis.
C1 [Badr, Christian E.; Wurdinger, Thomas; Niers, Johanna M.; Whalen, Michael; Tannous, Bakhos A.] Massachusetts Gen Hosp, Ctr Neurosci, Charlestown, MA 02129 USA.
[Badr, Christian E.; Wurdinger, Thomas; Niers, Johanna M.; Whalen, Michael; Tannous, Bakhos A.] Massachusetts Gen Hosp, Dept Neurol, Mol Neurogenet Unit, Charlestown, MA 02129 USA.
[Wurdinger, Thomas; Tannous, Bakhos A.] Massachusetts Gen Hosp, Dept Radiol, Ctr Mol Imaging Res, Charlestown, MA 02129 USA.
Massachusetts Gen Hosp, Dept Pathol, Charlestown, MA 02129 USA.
[Badr, Christian E.; Wurdinger, Thomas; Niers, Johanna M.; Whalen, Michael; Tannous, Bakhos A.] Harvard Univ, Sch Med, Neurosci Program, Boston, MA 02115 USA.
[Badr, Christian E.; Wurdinger, Thomas; Nilsson, Jonas; Niers, Johanna M.] Vrije Univ Amsterdam Med Ctr, Dept Neurosurg, Neurooncol Res Grp, Amsterdam, Netherlands.
[Degterev, Alexei] Tufts Univ, Sch Med, Dept Biochem, Boston, MA 02111 USA.
RP Tannous, BA (reprint author), Massachusetts Gen Hosp, Ctr Neurosci, Bldg 149,13th St, Charlestown, MA 02129 USA.
EM btannous@hms.harvard.edu
FU National Institutes of Health (NIH)/National Cancer Institute
[4R00CA126839]; NIH/National Institute of Neurological Disorders
[1R21NS061051, P30 NS045776, 1R01NS064983]; Executive Committee on
Research at Massachusetts General Hospital; American Brain Tumor
Association
FX This work was supported by grants from the National Institutes of Health
(NIH)/National Cancer Institute 4R00CA126839, NIH/National Institute of
Neurological Disorders 1R21NS061051, P30 NS045776 and 1R01NS064983
(B.A.T.) as well as Executive Committee on Research at Massachusetts
General Hospital (C.B.) and the American Brain Tumor Association (T.W.).
NR 51
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U1 1
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2011
VL 13
IS 11
BP 1213
EP 1224
DI 10.1093/neuonc/nor067
PG 12
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 848CH
UT WOS:000297025500006
PM 21757445
ER
PT J
AU Biffi, A
Battey, TWK
Ayres, AM
Cortellini, L
Schwab, K
Gilson, AJ
Rost, NS
Viswanathan, A
Goldstein, JN
Greenberg, SM
Rosand, J
AF Biffi, A.
Battey, T. W. K.
Ayres, A. M.
Cortellini, L.
Schwab, K.
Gilson, A. J.
Rost, N. S.
Viswanathan, A.
Goldstein, J. N.
Greenberg, S. M.
Rosand, J.
TI Warfarin-related intraventricular hemorrhage Imaging and outcome
SO NEUROLOGY
LA English
DT Article
ID SPONTANEOUS INTRACEREBRAL HEMORRHAGE; HEMATOMA EXPANSION; THERAPY
AB Objective: Oral anticoagulation therapy (OAT) with warfarin increases mortality and disability after intracerebral hemorrhage (ICH), the result of increased ICH volume and risk of hematoma expansion. We investigated whether OAT also influences risk of development of intraventricular hemorrhage (IVH), the volume of IVH and IVH expansion, and whether IVH is a substantive mediator of the overall effect of OAT on ICH outcome.
Methods: We performed a retrospective analysis of a prospectively collected single-center cohort of 1,879 consecutive ICH cases (796 lobar, 865 deep, 153 cerebellar, 15 multiple location, 50 primary IVH) from 1999 to 2009. ICH and IVH volumes at presentation, as well as hematoma expansion (>33% or >6 mL increase) and IVH expansion (>2 mL increase), were determined using established semiautomated methods. Outcome was assessed at 90 days using either the modified Rankin Scale or Glasgow Outcome Scale.
Results: Warfarin use was associated with IVH risk, IVH volume at presentation, and IVH expansion in both lobar and deep ICH (all p < 0.05) in a dose-response relationship with international normalized ratio. Warfarin was associated with poor outcome in both lobar and deep ICH (p < 0.01), and > 95% of this effect was accounted for by baseline ICH and IVH volumes, as well as ICH and IVH expansion.
Conclusion: Warfarin increases IVH volume and risk of IVH expansion in lobar and deep ICH. These findings (along with effects on ICH volume and expansion) likely represent the mechanisms by which anticoagulation worsens ICH functional outcome. Neurology (R) 2011;77:1840-1846
C1 [Biffi, A.; Battey, T. W. K.; Cortellini, L.; Rost, N. S.; Rosand, J.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Biffi, A.; Battey, T. W. K.; Ayres, A. M.; Cortellini, L.; Schwab, K.; Gilson, A. J.; Rost, N. S.; Viswanathan, A.; Greenberg, S. M.; Rosand, J.] Massachusetts Gen Hosp, Hemorrhag Stroke Res Grp, Boston, MA 02114 USA.
[Biffi, A.; Battey, T. W. K.; Cortellini, L.; Rost, N. S.; Rosand, J.] Massachusetts Gen Hosp, Div Neurocrit Care & Emergency Neurol, Dept Neurol, Boston, MA 02114 USA.
[Goldstein, J. N.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 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
FU National Institute for Neurologic Disorders and Stroke [R01 NS063925,
R01 NS059727, P50 NS051343, K23 NS064052, K23 NS059774]; American Heart
Association/ Bugher Foundation Centers for Stroke Prevention Research
[0775011N, 0755984T]; American Heart Association Bugher Foundation; NIH;
NIH/NINDS; NIH (NINDS, NIA); National Stroke Association; American Heart
Association-Bugher Foundation; NIH/NIA; CSL Behring; Alzheimer's
Association; NIH (NINDS, NHLBI); MGH Deane Institute for Integrative
Research in Atrial Fibrillation and Stroke
FX Study funding: The authors' work on this study was supported by funding
from the National Institute for Neurologic Disorders and Stroke (R01
NS063925, R01 NS059727, P50 NS051343, K23 NS064052, K23 NS059774). Dr.
Biffi received support from the American Heart Association/ Bugher
Foundation Centers for Stroke Prevention Research (0775011N, 0755984T).
Funding entities had no involvement in study design, data collection,
analysis, and interpretation, writing of the report, and in the decision
to submit the paper for publication.; Dr. Biffi receives research
support from the American Heart Association Bugher Foundation. T. W. K.
Battey reports no disclosures. A. M. Ayres receives research support
from the NIH. L. Cortellini receives research support from the
NIH/NINDS. K. M. Schwab receives research support from the NIH (NINDS,
NIA). A.J. Gilson reports no disclosures. Dr. Rost serves as Associate
Editor for Frontiers in Hospitalist Neurology and Assistant Editor for
Stroke and receives research support from the NIH/NINDS, the National
Stroke Association, and the American Heart Association-Bugher
Foundation. Dr. Viswanathan has served as consultant for Athena
Diagnostics, Inc. and receives research support from the NIH/NIA. Dr.
Goldstein serves on a scientific advisory board for and received funding
for travel and consulting honoraria from CSL Behring; serves as an
Associate Editor for Academic Emergency Medicine and on the editorial
board of the International Journal of Emergency Medicine; and receives
research support from CSL Behring and the NIH/NINDS. Dr. Greenberg
serves on a data safety monitoring board for the NIH/NINDS; has received
speaker honoraria from Esteve, Medtronics, Inc., and Pfizer Inc; serves
on the editorial boards of Neurology (R), Stroke, Cerebrovascular
Disease, and the Journal of Alzheimer's Disease and Other Dementias; has
served as a consultant for Roche, Janssen Alzheimer Immunotherapy, and
Bristol-Myers Squibb; and has received/receives research support from
the NIH and the Alzheimer's Association. Dr. Rosand receives research
support from the NIH (NINDS, NHLBI), the American Heart
Association-Bugher Foundation, and the MGH Deane Institute for
Integrative Research in Atrial Fibrillation and Stroke.
NR 16
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U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD NOV
PY 2011
VL 77
IS 20
BP 1840
EP 1846
DI 10.1212/WNL.0b013e3182377e12
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 849WS
UT WOS:000297156700018
PM 22049204
ER
PT J
AU Perez, DL
Larvie, M
Acar, D
Daffner, K
AF Perez, D. L.
Larvie, M.
Acar, D.
Daffner, K.
TI Teaching NeuroImages: Apathetic variant of frontotemporal dementia
SO NEUROLOGY
LA English
DT Editorial Material
C1 [Perez, D. L.; Acar, D.; Daffner, K.] Brigham & Womens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Perez, D. L.] Brigham & Womens Hosp, Dept Psychiat, Boston, MA 02115 USA.
[Perez, D. L.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Larvie, M.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Perez, DL (reprint author), Brigham & Womens Hosp, Dept Neurol, 75 Francis St, Boston, MA 02115 USA.
EM david.lperez@gmail.com
NR 2
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD NOV
PY 2011
VL 77
IS 20
BP E117
EP E117
DI 10.1212/WNL.0b013e3182377e4c
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 849WS
UT WOS:000297156700001
PM 22084280
ER
PT J
AU Bley, AE
Giannikopoulos, OA
Hayden, D
Kubilus, K
Tifft, CJ
Eichler, FS
AF Bley, Annette E.
Giannikopoulos, Ourania A.
Hayden, Doug
Kubilus, Kim
Tifft, Cynthia J.
Eichler, Florian S.
TI Natural History of Infantile G(M2) Gangliosidosis
SO PEDIATRICS
LA English
DT Article
DE infantile G(M2) gangliosidosis; natural history; Tay Sachs; Sandhoff;
survival; lysosomal disorders; neurodegeneration
ID TAY-SACHS-DISEASE; HEXOSAMINIDASE ALPHA-GENE; SANDHOFF DISEASE; NEUTRAL
GLYCOSPHINGOLIPIDS; GM2 GANGLIOSIDOSIS; GENERALIZED ACCUMULATION;
FINE-STRUCTURE; BRAIN; STORAGE; MUTATION
AB OBJECTIVE: GM2 gangliosidoses are caused by an inherited deficiency of lysosomal beta-hexosaminidase and result in ganglioside accumulation in the brain. Onset during infancy leads to rapid neurodegeneration and death before 4 years of age. We set out to quantify the rate of functional decline in infantile GM2 gangliosidosis on the basis of patient surveys and a comprehensive review of existing literature.
METHODS: Patients with infantile GM2 gangliosidosis (N = 237) were surveyed via questionnaire by the National Tay Sachs & Allied Diseases Association (NTSAD). These data were supplemented by survival data from the NTSAD database and a literature survey. Detailed retrospective surveys from 97 patients were available. Five patients who had received hematopoietic stem cell transplantation were evaluated separately. The mortality rate of the remaining 92 patients was comparable to that of the 103 patients from the NTSAD database and 121 patients reported in the literature.
RESULTS: Common symptoms at onset were developmental arrest (83%), startling (65%), and hypotonia (60%). All 55 patients who had learned to sit without support lost that ability within 1 year. Individual functional measures correlated with each other but not with survival. Gastric tube placement was associated with prolonged survival. Tay Sachs and Sandhoff variants did not differ. Hematopoietic stem cell transplantation was not associated with prolonged survival.
CONCLUSIONS: We studied the timing of regression in 97 cases of infantile GM2 gangliosidosis and conclude that clinical disease progression does not correlate with survival, likely because of the impact of improved supportive care over time. However, functional measures are quantifiable and can inform power calculations and study design of future interventions. Pediatrics 2011; 128: e1233-e1241
C1 [Bley, Annette E.; Giannikopoulos, Ourania A.; Eichler, Florian S.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Hayden, Doug] Massachusetts Gen Hosp, Dept Biostat, Boston, MA 02114 USA.
[Kubilus, Kim] Natl Tay Sachs & Allied Dis Assoc, Boston, MA USA.
[Tifft, Cynthia J.] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Eichler, FS (reprint author), Massachusetts Gen Hosp, Dept Neurol, 55 Fruit St,ACC 708, Boston, MA 02114 USA.
EM feichler@partners.org
FU Harvard Catalyst/Harvard Clinical and Translational Science Center
(National Institutes of Health) [UL1 RR 025758]; Harvard University;
National Institutes of Health [K08NS52550]; National Institutes of
Health "Lysosomal Disease Network" [5U54NS065768]; NTSAD
FX This work was conducted with support from Harvard Catalyst/Harvard
Clinical and Translational Science Center (National Institutes of Health
award UL1 RR 025758 and financial contributions from Harvard University
and its affiliated academic health care centers), National Institutes of
Health training grant K08NS52550 (to Dr Eichler), and National
Institutes of Health "Lysosomal Disease Network" grant 5U54NS065768. Ms.
Giannikopoulos, Mrs. Kubilus, and Dr. Eichler were supported by the
NTSAD.
NR 76
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U1 1
U2 12
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD NOV
PY 2011
VL 128
IS 5
BP E1233
EP E1241
DI 10.1542/peds.2011-0078
PG 9
WC Pediatrics
SC Pediatrics
GA 843YO
UT WOS:000296714000024
PM 22025593
ER
PT J
AU Schinka, JA
Casey, RJ
Kasprow, W
Rosenheck, RA
AF Schinka, John A.
Casey, Roger J.
Kasprow, Wesley
Rosenheck, Robert A.
TI Requiring Sobriety at Program Entry: Impact on Outcomes in Supported
Transitional Housing for Homeless Veterans
SO PSYCHIATRIC SERVICES
LA English
DT Article
ID 1ST
AB Objective: An important distinction in models of housing for the homeless is whether programs that require abstinence prior to program admission produce better outcomes than unrestricted programs. Data from a large transitional housing program were used to compare client characteristics of and outcomes from programs requiring abstinence at admission and programs not requiring abstinence. Methods: The U.S. Department of Veterans Affairs (VA) Northeast Program Evaluation Center provided records of individuals who were admitted into, and discharged from, the VA Grant and Per Diem program in 2003-2005. Records contained information from intake interviews, program discharge information, and descriptions of provider characteristics. Analyses were based on 3,188 veteran records, 1,250 from programs requiring sobriety at admission and 1,938 from programs without a sobriety requirement. Group differences were examined with t tests and chi square analyses; predictors of program outcome were determined with logistic regression. Results: Individuals using drugs or alcohol at program admission had more problematic histories, as indicated by several general health and mental health variables, and shorter program stays. There were significant differences between groups in the frequency of program completion, recidivism for homelessness, and employment on program discharge, but effect sizes for these analyses were uniformly small and of questionable importance. Regression analyses did not find meaningful support for the importance of sobriety on program entry on any of the outcome measures. Conclusions: The results add evidence to the small body of literature supporting the position that sobriety on program entry is not a critical variable in determining outcomes for individuals in transitional housing programs. (Psychiatric Services 62:1325-1330, 2011)
C1 [Schinka, John A.; Casey, Roger J.] Natl Ctr Homelessness Vet, Tampa, FL 33612 USA.
[Kasprow, Wesley] US Dept Vet Affairs, NE Program Evaluat Ctr, West Haven, CT USA.
[Rosenheck, Robert A.] Yale Univ, Dept Psychiat, West Haven, CT USA.
RP Schinka, JA (reprint author), Natl Ctr Homelessness Vet, MHBS 116B,13000 BB Downs Blvd, Tampa, FL 33612 USA.
EM jschinka@health.usf.edu
RI McCarthy, Jodie/B-5760-2012
FU VA National Center on Homelessness Among Veterans
FX This research was supported by the VA National Center on Homelessness
Among Veterans.
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U1 0
U2 5
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 1075-2730
J9 PSYCHIAT SERV
JI Psychiatr. Serv.
PD NOV
PY 2011
VL 62
IS 11
BP 1325
EP 1330
PG 6
WC Health Policy & Services; Public, Environmental & Occupational Health;
Psychiatry
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Psychiatry
GA 843LT
UT WOS:000296674000012
PM 22211212
ER
PT J
AU Kim, HM
Pfeiffer, P
Ganoczy, D
Valenstein, M
AF Kim, Hyungjin Myra
Pfeiffer, Paul
Ganoczy, Dara
Valenstein, Marcia
TI Intensity of Outpatient Monitoring After Discharge and Psychiatric
Rehospitalization of Veterans With Depression
SO PSYCHIATRIC SERVICES
LA English
DT Article
ID SUBSTANCE USE DISORDERS; HOSPITALIZATION; PREDICTORS; SUICIDE; RISK;
CARE
AB Objective: This study assessed whether increased frequency of clinical monitoring during the high-risk period of 12 weeks after discharge from a psychiatric hospitalization reduced subsequent rehospitalization in a national cohort of Veterans Health Administration patients receiving depression treatment between 1999 and 2004. Methods: A case-control design was used. Patients who had at least two inpatient psychiatric hospitalizations were identified (case group, N=17,852) and then individually matched with up to two patients who also had been discharged from psychiatric inpatient settings but were not rehospitalized for the number of days between the case-group patient's discharge and subsequent rehospitalization (N=35,511). Results: Covariate-adjusted relative risk (RR) did not show an association between increased monitoring and subsequent psychiatric hospitalization, but there was a significant negative interaction between monitoring and a comorbid substance use disorder diagnosis (p<.001). Increased monitoring was positively associated with rehospitalization of patients without a substance use disorder, whereas increased monitoring was not associated with increased risk of rehospitalization of those with a comorbid substance use disorder. The RR of rehospitalization associated with a weekly monitoring visit (12 visits per 84 days) versus no monitoring visit was 1.14 for patients without a substance use disorder, whereas the RR was reduced to .94 for patients with a substance use disorder. Conclusions: Increased outpatient monitoring during the high-risk period after discharge appears to have a modest protective effect on rehospitalization among depressed patients with a comorbid substance use disorder. (Psychiatric Services 62:1346-1352, 2011)
C1 [Kim, Hyungjin Myra] Univ Michigan, Ctr Stat Consultat & Res, Ann Arbor, MI 48109 USA.
[Kim, Hyungjin Myra; Pfeiffer, Paul; Ganoczy, Dara; Valenstein, Marcia] US Dept Vet Affairs, Serious Mental Illness Treatment Resource & Evalu, Ann Arbor Ctr Excellence, Ann Arbor, MI USA.
[Pfeiffer, Paul; Valenstein, Marcia] Univ Michigan, Dept Psychianj, Ann Arbor, MI 48109 USA.
RP Kim, HM (reprint author), Univ Michigan, Ctr Stat Consultat & Res, 3550 Rackham,915 E Washington St, Ann Arbor, MI 48109 USA.
EM myrakim@umich.edu
FU U.S. Department of Veterans Affairs, Health Services Research and
Development Service [IIR 04-211-1, MRP 03-320]; National Institute of
Mental Health [R01-MH078698-01]
FX The funding sources for this work were grants IIR 04-211-1 and MRP
03-320 from the U.S. Department of Veterans Affairs, Health Services
Research and Development Service, and grant R01-MH078698-01 from the
National Institute of Mental Health. Resources were also contributed by
the Serious Mental Illness Treatment Resource and Evaluation Center, Ann
Arbor.
NR 19
TC 10
Z9 10
U1 2
U2 4
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 NOV
PY 2011
VL 62
IS 11
BP 1346
EP 1352
PG 7
WC Health Policy & Services; Public, Environmental & Occupational Health;
Psychiatry
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health; Psychiatry
GA 843LT
UT WOS:000296674000015
PM 22211215
ER
PT J
AU Nicolson, SE
Chabon, B
Larsen, KA
Kelly, SE
Potter, AW
Stern, TA
AF Nicolson, Stephen E.
Chabon, Brenda
Larsen, Kenneth A.
Kelly, Susan E.
Potter, Adam W.
Stern, Theodore A.
TI Primitive Reflexes Associated with Delirium: A Prospective Trial
SO PSYCHOSOMATICS
LA English
DT Article
ID POSTOPERATIVE DELIRIUM; VASCULAR DEMENTIA; OLDER-PEOPLE; DISEASE; SIGNS;
ADULTS; HEALTHY
AB Background: The presence of primitive reflexes (PRs) may have diagnostic or prognostic value in the evaluation of cognitive impairment. Objective: We hypothesized that the presence of preoperative PRs would predict the development of postoperative delirium and that the emergence of PRs postoperatively would be positively associated with the emergence of delirium. Methods: Patients participating in a larger study on the prophylaxis of postoperative delirium were evaluated for the presence of six PRs (grasp reflex [left and right], palmomental reflex [left and right], glabellar tap, and snout reflex), preoperatively and postoperatively The presence of PRs was then correlated with the development of delirium. Results: Of the 79 patients studied, 29% (n = 23) developed delirium during the postoperative period. The preoperative presence of one PR did not predict the development of delirium, but the only patient with > 1 PR preoperatively went on to develop delirium in the postoperative period. Similarly, having one frontal release sign in the postoperative period did not correlate with delirium, while the appearance of more than one PR was associated with a greater likelihood of delirium. Of the 11 patients who had two or more frontal release signs during one postoperative examination, six (55%) developed delirium. Of the five patients who showed three or more frontal release signs, 4 (80%) developed delirium. Conclusion: Our study is the first to investigate the relationship between the appearance of PRs and the development of delirium. We have provided some evidence that PRs are associated with acute CNS dysfunction. (Psychosomatics 2011; 52:507-512)
C1 [Nicolson, Stephen E.; Chabon, Brenda] Montefiore Med Ctr, Albert Einstein Coll Med, Dept Psychiat & Behav Sci, Bronx, NY 10467 USA.
[Larsen, Kenneth A.; Kelly, Susan E.; Potter, Adam W.] New England Baptist Hosp, Dept Med, Boston, MA USA.
[Kelly, Susan E.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Kelly, Susan E.] Tufts Med Ctr, Dept Med, Boston, MA USA.
[Stern, Theodore A.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
RP Nicolson, SE (reprint author), Montefiore Med Ctr, Dept Psychiat, 111 E 210 St, Bronx, NY 10467 USA.
EM snicolso@montefiore.org
RI Potter, Adam/D-9893-2014;
OI Potter, Adam/0000-0003-4980-8353
NR 33
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Z9 5
U1 0
U2 3
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0033-3182
J9 PSYCHOSOMATICS
JI Psychosomatics
PD NOV-DEC
PY 2011
VL 52
IS 6
BP 507
EP 512
PG 6
WC Psychiatry; Psychology
SC Psychiatry; Psychology
GA 849PJ
UT WOS:000297137300002
PM 22054619
ER
PT J
AU Chang, BH
Dusek, JA
Benson, H
AF Chang, Bei-Hung
Dusek, Jeffery A.
Benson, Herbert
TI Psychobiological Changes from Relaxation Response Elicitation: Long-Term
Practitioners vs. Novices
SO PSYCHOSOMATICS
LA English
DT Article
ID TRANSCENDENTAL-MEDITATION PROGRAM; QUALITY-OF-LIFE; STRESS REDUCTION;
PSYCHOSOCIAL STRESS; AFRICAN-AMERICANS; BREAST-CANCER; DEPRESSION;
CORTISOL; MODEL; METAANALYSIS
AB Objective: The relaxation response (RR) is a physiological state that is the counterpart to the stress response. We investigate the psychological and biological effects, as well as the correlation between these two effects that are associated with short-term vs. long-term practice of techniques that elicit the RR ("RR practice"). Methods: The study comprised both a cross sectional and an 8-week prospective design. The study sample included individuals with a long-term RR practice ("long-term practitioners" n = 28) and those with no prior RI? practice experience ("novices" n = 28). The novices received 8 weeks of RR-elicitation training ("RR training") for the prospective analysis (short-term practice). Results: Long-term practitioners reported lower levels of psychological distress than the novices before they received RR training. As a result of the 8-week RR training, novices significantly reduced their psychological distress to levels comparable to that of long-term practitioners. Long-term practitioners had greater immediate (after listening to a RR-eliciting CD) decreases in psychological distress level than the 8-week trained novices. Furthermore, the reduction in psychological distress levels for long-term practitioners correlated with a reduction in biological measures of stress, after controlling for baseline values. There was no reduction in biological measures and no correlation with psychological measures in the 8-week trained novices. Conclusions: While our data indicate that even a short-term 8-week RR-eliciting practice can decrease psychological distress levels, only after years of RR practice does psychological distress reduction coincide with biological change. (Psychosomatics 2011; 52:550-559)
C1 [Chang, Bei-Hung] Boston Univ, Sch Publ Hlth, Dept Hlth Policy & Management, Boston, MA USA.
[Chang, Bei-Hung] VA Boston Hlth Care Syst, Boston, MA USA.
[Dusek, Jeffery A.; Benson, Herbert] Massachusetts Gen Hosp, Benson Henry Inst Mind Body Med, Boston, MA 02114 USA.
[Dusek, Jeffery A.] Abbott NW Hosp, Penny George Inst Hlth & Healing, Minneapolis, MN 55407 USA.
RP Chang, BH (reprint author), 150 S Huntington Ave,152H,Bldg 9,4th Floor, Boston, MA 02130 USA.
EM bhchang@bu.edu
OI Dusek, Jeffery/0000-0001-9581-0564
FU Center for Disease Control and Prevention [5 R01 DP000339,
H75/CCH119124, H75/CCH123424]
FX The study was funded by the Center for Disease Control and Prevention:
grant numbers 5 R01 DP000339, H75/CCH119124, and H75/CCH123424. The
authors disclosed no proprietary or commercial interest in any product
mentioned or concept discussed in this article.
NR 39
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U1 3
U2 15
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0033-3182
J9 PSYCHOSOMATICS
JI Psychosomatics
PD NOV-DEC
PY 2011
VL 52
IS 6
BP 550
EP 559
PG 10
WC Psychiatry; Psychology
SC Psychiatry; Psychology
GA 849PJ
UT WOS:000297137300008
PM 22054625
ER
PT J
AU Beach, SR
Stern, TA
AF Beach, Scott R.
Stern, Theodore A.
TI "Playing Possum:" Differential Diagnosis, Work-Up, and Treatment of
Profound Interpersonal Withdrawal
SO PSYCHOSOMATICS
LA English
DT Article
AB Patients who exhibit profound interpersonal withdrawal 1 challenge clinicians in terms of diagnostic formulation, elucidation of the etiology or mechanism of disease, and treatment. Insufficient history provided directly by the patient leads to a greater reliance on the physical examination and a need for heightened recognition of consistencies and inconsistencies in presenting signs and symptoms. Strategies to establish the potential causes and to refine the appropriate work-up are crucial for clinicians who care for such complex patients.
We present two case vignettes to highlight the differential diagnosis, the mechanisms of disease, and the potential treatments of patients who appear to be "playing possum" (a term that refers to the instinctive defense mechanism exhibited by the Virginia opossum [involving inertia, rigidity, drooling, and release of anal gland fluid] in the face of threat).(1)
C1 [Beach, Scott R.; Stern, Theodore A.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Beach, Scott R.; Stern, Theodore A.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Beach, SR (reprint author), Massachusetts Gen Hosp, Dept Psychiat, 55 Fruit St,Warren 605, Boston, MA 02114 USA.
EM sbeach1@partners.org
NR 5
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 0033-3182
J9 PSYCHOSOMATICS
JI Psychosomatics
PD NOV-DEC
PY 2011
VL 52
IS 6
BP 560
EP 562
PG 3
WC Psychiatry; Psychology
SC Psychiatry; Psychology
GA 849PJ
UT WOS:000297137300009
PM 22054626
ER
PT J
AU Mendez, MF
Ramirez-Bermudez, J
AF Mendez, Mario F.
Ramirez-Bermudez, Jesus
TI Cotard Syndrome in Semantic Dementia
SO PSYCHOSOMATICS
LA English
DT Article
ID DELUSIONS; BRAIN
C1 [Mendez, Mario F.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
[Mendez, Mario F.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, Los Angeles, CA 90095 USA.
[Ramirez-Bermudez, Jesus] Natl Inst Neurol & Neurosurg Mexico, Dept Neuropsychiat, Mexico City, DF, Mexico.
RP Mendez, MF (reprint author), VA Greater Angeles, 11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM mmendez@UCLA.edu
FU [R01AG034499-03]
FX This work was funded and supported by #R01AG034499-03
NR 17
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Z9 8
U1 1
U2 4
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0033-3182
J9 PSYCHOSOMATICS
JI Psychosomatics
PD NOV-DEC
PY 2011
VL 52
IS 6
BP 571
EP 574
PG 4
WC Psychiatry; Psychology
SC Psychiatry; Psychology
GA 849PJ
UT WOS:000297137300012
PM 22054629
ER
PT J
AU Horan, WP
Kring, AM
Gur, RE
Reise, SP
Blanchard, JJ
AF Horan, William P.
Kring, Ann M.
Gur, Raquel E.
Reise, Steven P.
Blanchard, Jack J.
TI Development and psychometric validation of the Clinical Assessment
Interview for Negative Symptoms (CAINS)
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Schizophrenia; Rating scale; Expression; Experience; Negative symptoms;
Clinical trials
ID PSYCHIATRIC RATING-SCALE; SCHIZOPHRENIA; DEFICITS
AB Progress in the development of new pharmacological and psychosocial treatments for the negative symptoms of schizophrenia is impeded by limitations of available assessment instruments. The multi-site Collaboration to Advance Negative Symptom Assessment in Schizophrenia (CANSAS) was established to develop and validate a new clinical rating scale using a transparent, iterative, and data-driven process. The Clinical Assessment Interview for Negative Symptoms (CAINS) was designed to address limitations of existing measures and assess consensus-based sub-domains, including asociality, avolition, anhedonia, affective blunting, and alogia. The structure and psychometric properties of the CAINS were evaluated in a sample of 281 schizophrenia and schizoaffective outpatients at four sites. Converging structural analyses indicated that the scale was comprised of two moderately correlated factors one reflecting experiential impairments (diminished motivation and enjoyment of social, vocational, and recreational activities) and one reflecting expressive impairments (diminished non-verbal and verbal communication). Item-level analyses revealed generally good distributional properties, inter-rater agreement, discriminating anchor points, and preliminary convergent and discriminant validity. Results indicate that the CAINS is a promising new measure for quantifying negative symptoms in clinical neuroscience and treatment studies, Results guided item modification or deletion, and the reliability and validity of the revised, shorter version of the CAINS is in the final phase of development within the CANSAS project. Published by Elsevier B.V.
C1 [Horan, William P.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90095 USA.
[Kring, Ann M.] Univ Calif Berkeley, Berkeley, CA 94720 USA.
[Gur, Raquel E.] Univ Penn, Philadelphia, PA 19104 USA.
[Blanchard, Jack J.] Univ Maryland, College Pk, MD 20742 USA.
RP Horan, WP (reprint author), Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, VA Greater Los Angeles Healthcare Syst, 300 UCLA Med Plaza,Suite 2255, Los Angeles, CA 90095 USA.
EM horan@ucla.edu
FU National Institute of Mental Health [K02-MH079231, R01-MH082839,
RO1-MH082890, R01-MH082782, R01-MH82783]
FX This work was supported by the National Institute of Mental Health
(K02-MH079231 and R01-MH082839 to JJB: RO1-MH082890 to AMK: R01-MH082782
to WPH; and R01-MH82783 to REG). Funding sources had no role in study
design or in the collection, analysis and interpretation of data; or in
the writing of this report.
NR 32
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U1 4
U2 14
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD NOV
PY 2011
VL 132
IS 2-3
BP 140
EP 145
DI 10.1016/j.schres.2011.06.030
PG 6
WC Psychiatry
SC Psychiatry
GA 848ZB
UT WOS:000297092500008
PM 21798716
ER
PT J
AU Meszaros, ZS
Dimmock, JA
Ploutz-Snyder, R
Chauhan, SVS
Abdul-Malak, Y
Middleton, FA
Batki, SL
AF Meszaros, Zsuzsa Szombathyne
Dimmock, Jacqueline A.
Ploutz-Snyder, Robert
Chauhan, Sumerendra Vir Singh
Abdul-Malak, Ynesse
Middleton, Frank A.
Batki, Steven L.
TI Accuracy of self-reported medical problems in patients with alcohol
dependence and co-occurring schizophrenia or schizoaffective disorder
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Alcohol; Schizophrenia; Schizoaffective disorder; Medical illness;
Self-report
ID MENTAL-DISORDERS; UNITED-STATES; COMORBIDITY; CARE; MORBIDITY;
MORTALITY; ILLNESS; PEOPLE; HEALTH; SCALE
AB Background: Schizophrenia and alcohol dependence (AD) are both major risk factors for a variety of medical problems, yet little is known about the medical status of patients in whom both conditions coexist.
Objective: The objectives of this study are to assess accuracy of self-reported medical problems and to compare the accuracy reports in patients with schizophrenia or schizoaffective disorder and co-occurring AD compared to patients with AD only and to controls. Our hypothesis was that medical problems are under-reported in patients with co-occurring disorders, possibly due to the combination of alcohol use and symptoms of schizophrenia.
Methods: Self-reported medical diagnoses were recorded and compared to medical records obtained from all area hospitals in 42 patients with schizophrenia and AD, 44 patients with schizoaffective disorder and AD, 41 patients with AD only, and 15 control subjects. Patients underwent medical history, physical examination, and review of medical records. Results: Patients with schizophrenia or schizoaffective disorder and co-occurring AD underreported their medical problems significantly more than patients with AD only and controls. Accuracy of self report was significantly lower in patients with schizophrenia-spectrum disorders plus co-occurring alcohol dependence than in AD alone or in controls. The most commonly underreported diagnoses included coronary artery disease, chronic renal failure, seizure disorder, hyperlipidemia, asthma and hypertension.
Discussion: In order to detect potentially unreported medical conditions in patients with co-occurring schizophrenia/schizoaffective disorder and alcohol dependence, the use of targeted screening questionnaires is recommended in addition to physical examination and thorough review of medical records. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Meszaros, Zsuzsa Szombathyne; Dimmock, Jacqueline A.; Chauhan, Sumerendra Vir Singh; Abdul-Malak, Ynesse; Batki, Steven L.] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY 13210 USA.
[Ploutz-Snyder, Robert] NASA, Univ Space Res Assoc, Houston, TX USA.
[Middleton, Frank A.] SUNY Upstate Med Univ, Dept Neurosci Physiol, Syracuse, NY 13210 USA.
[Batki, Steven L.] UCSF, Dept Psychiat, San Francisco, CA USA.
[Batki, Steven L.] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Meszaros, ZS (reprint author), SUNY Upstate Med Univ, Dept Psychiat, 750 E Adams St, Syracuse, NY 13210 USA.
EM meszaroz@upstate.edu
FU NIH-NIAAA [RO1 AA01365501, RO1 AA01615103]
FX This research was supported by NIH-NIAAA grant RO1 AA01365501,
"Naltrexone Treatment of Alcohol Abuse in Schizophrenia" (PI: Batki) and
by NIH-NIAAA grant RO1 AA01615103 "Peripheral Pathophysiogenomic Markers
of Ethanol-induced Brain Damage" (PI: Middleton). The NIH had no further
role in study design; in the collection, analysis and interpretation of
data; in the writing of the report; and in the decision to submit this
paper for publication.
NR 32
TC 3
Z9 3
U1 1
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
EI 1573-2509
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD NOV
PY 2011
VL 132
IS 2-3
BP 190
EP 193
DI 10.1016/j.schres.2011.07.033
PG 4
WC Psychiatry
SC Psychiatry
GA 848ZB
UT WOS:000297092500016
PM 21852074
ER
PT J
AU Selim, M
Yeatts, S
Goldstein, JN
Gomes, J
Greenberg, S
Morgenstern, LB
Schlaug, G
Torbey, M
Waldman, B
Xi, GH
Palesch, Y
AF Selim, Magdy
Yeatts, Sharon
Goldstein, Joshua N.
Gomes, Joao
Greenberg, Steven
Morgenstern, Lewis B.
Schlaug, Gottfried
Torbey, Michel
Waldman, Bonnie
Xi, Guohua
Palesch, Yuko
CA The Deferoxamine Mesylate In Intra
TI Safety and Tolerability of Deferoxamine Mesylate in Patients With Acute
Intracerebral Hemorrhage
SO STROKE
LA English
DT Article
DE deferoxamine mesylate; iron; ICH
ID PERIHEMATOMAL EDEMA; BRAIN EDEMA; NATURAL-HISTORY; BLOOD-PRESSURE; AGED
RATS; IRON; HEMATOMA; INJURY; EXPRESSION; FERRITIN
AB Background and Purpose-Treatment with the iron chelator, deferoxamine mesylate (DFO), improves neurological recovery in animal models of intracerebral hemorrhage (ICH). We aimed to evaluate the feasibility, safety, and tolerability of varying dose-tiers of DFO in patients with spontaneous ICH, and to determine the maximum tolerated dose to be adopted in future efficacy studies.
Methods-This was a multicenter, phase-I, dose-finding study using the Continual Reassessment Method. DFO was administered by intravenous infusion for 3 consecutive days, starting within 18 hours of ICH onset. Subjects underwent repeated clinical assessments through 90 days, and computed tomography neuroimaging pre- and post-drug-administration.
Results-Twenty subjects were enrolled onto 5 dose tiers, starting with 7 mg/kg per day and ending with 62 mg/kg per day as the maximum tolerated dose. Median age was 68 years (range, 50-90); 60% were men; and median Glasgow Coma Scale and National Institutes of Health Stroke Scale scores on admission were 15 (5-15) and 9 (0-39), respectively. ICH location was lobar in 40%, deep in 50%, and brain stem in 10%; intraventricular hemorrhage was present in 15%. DFO was discontinued because of adverse events in 2 subjects (10%). Six subjects (30%) experienced 12 serious adverse events, none of which were drug-related. DFO infusions were associated with mild blood-pressure-lowering effects. Fifty percent of patients had modified Rankin scale scores <= 2, and 39% had modified Rankin scale scores of 4 to 6 on day 90; 15% died.
Conclusions-Consecutive daily infusions of DFO after ICH are feasible, well-tolerated, and not associated with excessive serious adverse events or mortality. Our findings lay the groundwork for future studies to evaluate the efficacy of DFO in ICH. (Stroke. 2011; 42:3067-3074.)
C1 [Selim, Magdy; Schlaug, Gottfried] Harvard Univ, Beth Israel Deaconess Med Ctr, Stroke Div, Dept Neurol,Med Sch, Boston, MA 02215 USA.
[Yeatts, Sharon; Waldman, Bonnie; Palesch, Yuko] Med Univ S Carolina, Dept Med, Div Biostat & Epidemiol, Charleston, SC 29425 USA.
[Goldstein, Joshua N.; Greenberg, Steven] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Goldstein, Joshua N.; Greenberg, Steven] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Morgenstern, Lewis B.; Xi, Guohua] Univ Michigan, Stroke Program, Ann Arbor, MI 48109 USA.
[Morgenstern, Lewis B.; Xi, Guohua] Univ Michigan, Dept Neurosurg, Ann Arbor, MI 48109 USA.
[Gomes, Joao] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Torbey, Michel] Med Coll Wisconsin, Dept Neurol, Milwaukee, WI 53226 USA.
[Torbey, Michel] Med Coll Wisconsin, Dept Neurosurg, Milwaukee, WI 53226 USA.
RP Selim, M (reprint author), Harvard Univ, Beth Israel Deaconess Med Ctr, Stroke Div, Dept Neurol,Med Sch, 330 Brookline Ave Palmer 127, Boston, MA 02215 USA.
EM mselim@bidmc.harvard.edu
RI Goldstein, Joshua/H-8953-2016
FU NIH/NINDS [1R01-NS 057127]; NINDS [1R01-NS 057127, U01 NS052510]
FX The study was sponsored by the NIH/NINDS (1R01-NS 057127). The content
is solely the responsibility of the authors and does not necessarily
represent the official views of the NIH.; All investigators received
modest support from the NINDS (1R01-NS 057127). Dr. Selim received
significant support as the Principal Investigator. L.B.M. and G.X.
received additional significant support from the NINDS (U01 NS052510).
NR 33
TC 48
Z9 51
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD NOV
PY 2011
VL 42
IS 11
BP 3067
EP U237
DI 10.1161/STROKEAHA.111.617589
PG 24
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 842EM
UT WOS:000296574500249
PM 21868742
ER
PT J
AU Carandang, RA
Barton, B
Rordorf, GA
Ogilvy, CS
Sims, JR
AF Carandang, Raphael A.
Barton, Bruce
Rordorf, Guy A.
Ogilvy, Christopher S.
Sims, John R.
TI Nicotine Replacement Therapy After Subarachnoid Hemorrhage Is Not
Associated With Increased Vasospasm
SO STROKE
LA English
DT Article
DE neurocritical care; nicotine; subarachnoid hemorrhage; vascular tone
regul; vasospasm
ID ALPHA(7)-NICOTINIC ACETYLCHOLINE-RECEPTORS; RATS IN-VIVO;
CIGARETTE-SMOKING; NEUROGENIC VASODILATION; TRANSDERMAL NICOTINE;
BASILAR ARTERY; RISK-FACTORS; MECHANISMS; NEUROPROTECTION; DEFINITION
AB Background and Purpose-A significant number of patients with aneurysmal subarachnoid hemorrhage are active smokers and at risk for acute nicotine withdrawal. There is conflicting literature regarding the vascular effects of nicotine and theoretical concern that it may worsen vasospasm. The literature on the safety of nicotine replacement therapy and its effects on vasospasm is limited.
Methods-A retrospective analysis was conducted of a prospectively collected database of aneurysmal subarachnoid hemorrhage patients admitted to the neurointensive care unit from 1994 to 2008. Paired control subjects matched for age, sex, Fisher score, aneurysm size and number, hypertension, and current medication were analyzed. The primary outcome was clinical and angiographic vasospasm and the secondary outcome was Glasgow Outcome Score on discharge. Conditional logistic models were used to investigate univariate and multivariate relationships between predictors and outcome.
Results-Two hundred fifty-eight active smoking patients were included of which 87 were treated with transdermal nicotine replacement therapy. Patients were well matched for age, sex, gender, Fisher score, aneurysm size and number, hypertension, and current medications, but patients who received nicotine replacement therapy had less severe Hunt-Hess scores and Glasgow coma scores. There was no difference in angiographic vasospasm, but patients who received nicotine replacement therapy were less likely to have clinical vasospasm (19.5 versus 32.8%; P=0.026) and a Glasgow Outcome Score <4 on discharge (62.6% versus 81.6%; P=0.005) on multivariate analysis.
Conclusions-Nicotine replacement therapy was not associated with increased angiographic vasospasm and was associated with less clinical vasospasm and better Glasgow Outcome Score scores on discharge. (Stroke. 2011;42:3080-3086.)
C1 [Carandang, Raphael A.] Univ Massachusetts, Sch Med, Dept Neurol, UMASS Mem Med Ctr, Worcester, MA USA.
[Barton, Bruce] Univ Massachusetts, Sch Med, Dept Quantitat Hlth Sci, UMASS Mem Med Ctr, Worcester, MA USA.
[Rordorf, Guy A.; Sims, John R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA USA.
[Rordorf, Guy A.; Ogilvy, Christopher S.; Sims, John R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurosurg, Boston, MA USA.
[Rordorf, Guy A.; Sims, John R.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA USA.
Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
RP Carandang, RA (reprint author), 55 Lake Ave N, Worcester, MA 01655 USA.
EM raphael.carandang@umassmemorial.org
OI Barton, Bruce/0000-0001-7878-8895
FU National Institutes of Health [K08NS049241]; Eli Lilly
FX J.R.S. is supported by National Institutes of Health K08NS049241.;
J.R.S. is currently employed by Eli Lilly and receives salary and stock
as compensation.
NR 29
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Z9 2
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD NOV
PY 2011
VL 42
IS 11
BP 3080
EP 3086
DI 10.1161/STROKEAHA.111.620955
PG 7
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 842EM
UT WOS:000296574500251
PM 21868740
ER
PT J
AU Smith, EE
Fonarow, GC
Reeves, MJ
Cox, M
Olson, DM
Hernandez, AF
Schwamm, LH
AF Smith, Eric E.
Fonarow, Gregg C.
Reeves, Mathew J.
Cox, Margueritte
Olson, DaiWai M.
Hernandez, Adrian F.
Schwamm, Lee H.
TI Outcomes in Mild or Rapidly Improving Stroke Not Treated With
Intravenous Recombinant Tissue-Type Plasminogen Activator Findings From
Get With The Guidelines-Stroke
SO STROKE
LA English
DT Article
DE acute stroke; thrombolysis; outcomes
ID TRANSIENT ISCHEMIC ATTACK; PERIPHERAL VASCULAR-DISEASE; CARDIOVASCULAR
RADIOLOGY; SCIENTIFIC STATEMENT; EARLY MANAGEMENT; ASSOCIATION; COUNCIL;
CARE; INTERVENTION; ELIGIBILITY
AB Background and Purpose-Mild or rapidly improving stroke is a frequently cited reason for not giving intravenous recombinant tissue-type plasminogen activator (rtPA), but some of these patients may have poor outcomes. We used data from a large nationwide study (Get With The Guidelines-Stroke) to determine risk factors for poor outcomes after mild or improving stroke at hospital discharge.
Methods-Between 2003 and 2009, there were 29 200 ischemic stroke patients (from 1092 hospitals) arriving within 2 hours after symptom onset with mild or rapidly improving stroke symptoms as the only contraindication to rtPA. Logistic regression was used to determine the independent predictors of discharge to home.
Results-Among 93 517 patients arriving within 2 hours, 31.2% (29 200) did not receive rtPA solely because of mild/improving stroke. Among the 29 200 mild/improving cases, 28.3% were not discharged to home, and 28.5% were unable to ambulate without assistance at hospital discharge. The likelihood of home discharge was strongly related to initial National Institutes of Health Stroke Scale score (P<0.001). In multivariable-adjusted analysis, patients not discharged to home were more likely to be older, female, and black; have a higher National Institutes of Health Stroke Scale score and vascular risk factors; and were less likely to be taking lipid-lowering medication before admission.
Conclusions-In this large, nationwide study, a sizeable minority of patients who did not receive intravenous rtPA solely because of mild/improving stroke had poor short-term outcomes, raising the possibility that stroke-related disability is relatively common, even in "mild" stroke. A controlled trial of reperfusion therapy in this population may be warranted. (Stroke. 2011;42:3110-3115.)
C1 [Smith, Eric E.] Univ Calgary, Dept Clin Neurosci, Hotchkiss Brain Inst, Calgary, AB, Canada.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Div Cardiol, Los Angeles, CA USA.
[Reeves, Mathew J.] Michigan State Univ, Dept Epidemiol, E Lansing, MI 48824 USA.
[Cox, Margueritte; Olson, DaiWai M.; Hernandez, Adrian F.] Duke Univ, Duke Clin Res Inst, Durham, NC USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
RP Smith, EE (reprint author), Foothills Med Ctr, Room C1212,1403 29 St NW, Calgary, AB T2N 2T9, Canada.
EM eesmith@ucalgary.ca
RI Hernandez, Adrian F./A-7818-2016;
OI Schwamm, Lee/0000-0003-0592-9145; Hernandez, Adrian
F./0000-0003-3387-9616; Smith, Eric/0000-0003-3956-1668
FU Bristol-Myers Squib/Sanofi Pharmaceutical; American Heart Association
Pharmaceutical Roundtable; Boehringer-Ingelheim; GWTG-Stroke
FX The GWTG-Stroke program is provided by the American Heart
Association/American Stroke Association. The GWTG-Stroke program is
currently supported in part by a charitable contribution from
Bristol-Myers Squib/Sanofi Pharmaceutical Partnership and the American
Heart Association Pharmaceutical Roundtable. GWTG-Stroke has been funded
in the past through support from Boehringer-Ingelheim and Merck.
NR 16
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Z9 90
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD NOV
PY 2011
VL 42
IS 11
BP 3110
EP U309
DI 10.1161/STROKEAHA.111.613208
PG 17
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 842EM
UT WOS:000296574500256
PM 21903949
ER
PT J
AU Paramsothy, P
Knopp, RH
Kahn, SE
Retzlaff, BM
Fish, B
Ma, LN
Ostlund, RE
AF Paramsothy, Pathmaja
Knopp, Robert H.
Kahn, Steven E.
Retzlaff, Barbara M.
Fish, Brian
Ma, Lina
Ostlund, Richard E., Jr.
TI Plasma sterol evidence for decreased absorption and increased synthesis
of cholesterol in insulin resistance and obesity
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID CARDIOVASCULAR-DISEASE; METABOLIC SYNDROME; DIETARY-CHOLESTEROL;
MASS-SPECTROMETRY; SENSITIVITY; RISK; FAT; QUANTIFICATION; DYSLIPIDEMIA;
LIPOPROTEINS
AB Background: The rise in LDL with egg feeding in lean insulin-sensitive (LIS) participants is 2- and 3-fold greater than in lean insulin-resistant (LIR) and obese insulin-resistant (OIR) participants, respectively.
Objective: We determined whether differences in cholesterol absorption, synthesis, or both could be responsible for these differences by measuring plasma sterols as indexes of cholesterol absorption and endogenous synthesis.
Design: Plasma sterols were measured by gas chromatography-mass spectrometry in a random subset of 34 LIS, 37 LIR, and 37 OIR participants defined by the insulin sensitivity index (SI) and by BMI criteria selected from a parent group of 197 participants. Cholestanol and plant sterols provide a measure of cholesterol absorption, and lathosterol provides a measure of cholesterol synthesis.
Results: The mean (+/-SD) ratio of plasma total absorption biomarker sterols to cholesterol was 4.48 +/- 1.74 in LIS, 3.25 +/- 1.06 in LIR, and 2.82 +/- 1.08 in OIR participants. After adjustment for age and sex, the relations of the absorption sterol-cholesterol ratios were as follows: LIS. OIR (P < 0.001), LIS. LIR (P < 0.001), and LIR. OIR (P = 0.11). Lathosterol-cholesterol ratios were 0.71 +/- 0.32 in the LIS participants, 0.95 +/- 0.47 in the LIR participants, and 1.29 +/- 0.55 in the OIR participants. After adjustment for age and sex, the relations of lathosterol-cholesterol ratios were as follows: LIS, OIR (P < 0.001), LIS, LIR (P = 0.03), and LIR, OIR (P = 0.002). Total sterol concentrations were positively associated with SI and negatively associated with obesity, whereas lathosterol correlations were the opposite.
Conclusions: Cholesterol absorption was highest in the LIS participants, whereas cholesterol synthesis was highest in the LIR and OIR participants. Therapeutic diets for hyperlipidemia should emphasize low-cholesterol diets in LIS persons and weight loss to improve SI and to decrease cholesterol overproduction in LIR and OIR persons. Am J Clin Nutr 2011;94:1182-8.
C1 [Paramsothy, Pathmaja] Univ Washington, Div Cardiol, Seattle, WA 98195 USA.
[Paramsothy, Pathmaja; Knopp, Robert H.; Retzlaff, Barbara M.; Fish, Brian] Univ Washington, NW Lipid Res Clin, Seattle, WA 98195 USA.
[Knopp, Robert H.; Kahn, Steven E.] Univ Washington, Div Metab Endocrinol & Nutr, Seattle, WA 98195 USA.
[Kahn, Steven E.] VA Puget Sound Hlth Care Syst, Dept Med, Seattle, WA USA.
[Ma, Lina; Ostlund, Richard E., Jr.] Washington Univ, Sch Med, Div Endocrinol Metab & Lipid Res, St Louis, MO USA.
RP Paramsothy, P (reprint author), 325 9th Ave,PSB 5064,UW Mailstop 359720, Seattle, WA 98104 USA.
EM nmbob@uw.edu
OI Kahn, Steven/0000-0001-7307-9002
FU Egg Nutrition Center; NIH [1KL2RR025015-01, RO1 50420, DK20579,
RR00954]; Clinical Nutrition Research Unit at the University of
Washington [DK 35816]; Diabetes and Endocrinology Research Center at the
University of Washington [DK 17047]; General Clinical Research Center
[RR 00037]; Department of Veterans Affairs
FX Supported by a grant in aid from the Egg Nutrition Center (administered
through the US Department of Agriculture), NIH 1KL2RR025015-01 (to PP);
the Clinical Nutrition Research Unit at the University of Washington (DK
35816), the Diabetes and Endocrinology Research Center at the University
of Washington (DK 17047), the General Clinical Research Center (RR
00037), the Department of Veterans Affairs (to SEK), and NIH grants RO1
50420, DK20579 and RR00954 (to REO).
NR 38
TC 17
Z9 18
U1 0
U2 5
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD NOV
PY 2011
VL 94
IS 5
BP 1182
EP 1188
DI 10.3945/ajcn.110.006668
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 837VV
UT WOS:000296236100005
PM 21940599
ER
PT J
AU Kurtz, B
Thibault, HB
Raher, MJ
Popovich, JR
Cawley, S
Atochin, DN
Hayton, S
Shakartzi, HR
Huang, PL
Bloch, KD
Buys, E
Scherrer-Crosbie, M
AF Kurtz, Baptiste
Thibault, Helene B.
Raher, Michael J.
Popovich, John R.
Cawley, Sharon
Atochin, Dmitriy N.
Hayton, Sarah
Shakartzi, Hannah R.
Huang, Paul L.
Bloch, Kenneth D.
Buys, Emmanuel
Scherrer-Crosbie, Marielle
TI Nitric oxide synthase 3 deficiency limits adverse ventricular remodeling
after pressure overload in insulin resistance
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE oxidative stress; cardiac dysfunction
ID HIGH-FAT DIET; CARDIAC-HYPERTROPHY; OXIDATIVE STRESS; HEART-FAILURE;
MITOCHONDRIAL DYSFUNCTION; LIVER-MITOCHONDRIA; KNOCKOUT MICE;
COMPLEX-III; HYPERTENSION; ACTIVATION
AB Kurtz B, Thibault HB, Raher MJ, Popovich JR, Cawley S, Atochin DN, Hayton S, Shakartzi HR, Huang PL, Bloch KD, Buys E, Scherrer-Crosbie M. Nitric oxide synthase 3 deficiency limits adverse ventricular remodeling after pressure overload in insulin resistance. Am J Physiol Heart Circ Physiol 301: H2093-H2101, 2011. First published August 19, 2011; doi:10.1152/ajpheart.00744.2010.-Insulin resistance (IR) and systemic hypertension are independently associated with heart failure. We reported previously that nitric oxide synthase 3 (NOS3) has a beneficial effect on left ventricular (LV) remodeling and function after pressure-overload in mice. The aim of our study was to investigate the interaction of IR and NOS3 in pressure-overload-induced LV remodeling and dysfunction. Wild-type (WT) and NOS3-deficient (NOS3(-/-)) mice were fed either a standard diet (SD) or a high-fat diet (HFD) to induce IR. After 9 days of diet, mice underwent transverse aortic constriction (TAC). LV structure and function were assessed serially using echocardiography. Cardiomyocytes were isolated, and levels of oxidative stress were evaluated using 2',7'-dichlorodihydrofluorescein diacetate. Cardiac mitochondria were isolated, and mitochondrial respiration and ATP production were measured. TAC induced LV remodeling and dysfunction in all mice. The TAC-induced decrease in LV function was greater in SD-fed NOS3(-/-) mice than in SD-fed WT mice. In contrast, HFD-fed NOS3(-/-) developed less LV remodeling and dysfunction and had better survival than did HFD-fed WT mice. Seven days after TAC, oxidative stress levels were lower in cardiomyocytes from HFD-fed NOS3(-/-) than in those from HFD-fed WT. N(omega)-nitro-L-arginine methyl ester and mitochondrial inhibitors (rotenone and 2-thenoyltrifluoroacetone) decreased oxidative stress levels in cardiomyocytes from HFD-fed WT mice. Mitochondrial respiration was altered in NOS3(-/-) mice but did not worsen after HFD and TAC. In contrast with its protective role in SD, NOS3 increases LV adverse remodeling after pressure overload in HFD-fed, insulin resistant mice. Interactions between NOS3 and mitochondria may be responsible for increased oxidative stress levels in HFD-fed WT mice hearts.
C1 [Kurtz, Baptiste; Thibault, Helene B.; Scherrer-Crosbie, Marielle] Massachusetts Gen Hosp, Cardiac Ultrasound Lab, Boston, MA 02114 USA.
[Kurtz, Baptiste; Thibault, Helene B.; Raher, Michael J.; Popovich, John R.; Cawley, Sharon; Atochin, Dmitriy N.; Hayton, Sarah; Shakartzi, Hannah R.; Huang, Paul L.; Bloch, Kenneth D.; Buys, Emmanuel; Scherrer-Crosbie, Marielle] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Div Cardiol, Dept Med, Boston, MA 02114 USA.
[Raher, Michael J.; Cawley, Sharon; Hayton, Sarah; Shakartzi, Hannah R.; Bloch, Kenneth D.; Buys, Emmanuel] Massachusetts Gen Hosp, Anesthesia Ctr Crit Care Res, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
RP Scherrer-Crosbie, M (reprint author), Massachusetts Gen Hosp, Cardiac Ultrasound Lab, 55 Fruit St, Boston, MA 02114 USA.
EM marielle@crosbie.com
RI Atochin, Dmitriy/Q-3150-2016
FU National Institutes of Health/National Heart, Lung, Blood Institute
[1S10RR022586-01A1]; Federation Francaise de Cardiologie; Milton Fund
FX This study was supported by a Shared Equipment Grant (National
Institutes of Health/National Heart, Lung, Blood Institute
1S10RR022586-01A1; to M. Scherrer-Crosbie) as well as by fellowship
grants from the Federation Francaise de Cardiologie (to B. Kurtz and H.
B. Thibault) and by the Milton Fund (to M. Scherrer-Crosbie).
NR 41
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U1 0
U2 4
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD NOV
PY 2011
VL 301
IS 5
BP H2093
EP H2101
DI 10.1152/ajpheart.00744.2010
PG 9
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 843ZN
UT WOS:000296716900036
PM 21856905
ER
PT J
AU Shelton, RC
McNeill, LH
Puleo, E
Wolin, KY
Emmons, KM
Bennett, GG
AF Shelton, Rachel C.
McNeill, Lorna H.
Puleo, Elaine
Wolin, Kathleen Y.
Emmons, Karen M.
Bennett, Gary G.
TI The Association Between Social Factors and Physical Activity Among
Low-Income Adults Living in Public Housing
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID UNITED-STATES; MINORITY WOMEN; CANCER PREVENTION; COLLEGE-STUDENTS;
HEALTH BEHAVIOR; WORKING-CLASS; ENVIRONMENT; LEISURE; WALKING; OLDER
AB Objectives. We sought to examine the association between structural, functional, and normative social factors and physical activity among urban, low-income, racially/ethnically diverse adults.
Methods. We conducted a baseline cross-sectional survey among residents of 12 low-income housing communities in metropolitan Boston, Massachusetts. Participants were also asked to wear a pedometer for 5 days. We analyzed complete data from 1112 residents (weighted n = 1635).
Results. Residents with smaller social networks were significantly less physically active than were residents with larger social networks (b = -1503.7; P = .01) and residents with conflicting demands were more active than were residents with none (b = 601.6; P = .01), when we controlled for employment status, gender, poverty level, current health status, age, and perceived safety. Social networks were most strongly associated with physical activity among Hispanics and younger residents (aged 18-35 years).
Conclusions. These findings indicate that social factors, including social networks and role-related conflicting demands, may be important drivers of physical activity among low-income populations. Researchers and practitioners should consider social factors in developing multilevel physical activity interventions for this population. (Am J Public Health. 2011;101:2102-2110. doi: 10.2105/AJPH.2010.196030)
C1 [Shelton, Rachel C.] Columbia Univ, Mailman Sch Publ Hlth, Dept Sociomed Sci, New York, NY 10032 USA.
[Shelton, Rachel C.] Mt Sinai Sch Med, Dept Oncol Sci, New York, NY USA.
[McNeill, Lorna H.] Univ Texas MD Anderson Canc Ctr, Dept Hlth Dispar Res, Houston, TX 77030 USA.
[Puleo, Elaine] Univ Massachusetts, Sch Publ Hlth & Hlth Sci, Amherst, MA 01003 USA.
[Wolin, Kathleen Y.] Washington Univ, Sch Med, St Louis, MO USA.
[Emmons, Karen M.] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Emmons, Karen M.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bennett, Gary G.] Duke Univ, Dept Psychol & Neurosci, Durham, NC USA.
RP Shelton, RC (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Dept Sociomed Sci, 722 W 168th St,Room 548, New York, NY 10032 USA.
EM rshelton@post.harvard.edu
RI Wolin, Kathleen/I-2154-2014
OI Wolin, Kathleen/0000-0001-7950-9042
FU National Cancer Institute [5R01CA098864-02, 1K22CA126992-01, K05
CA124415, 5R25-CA057711-14]; Liberty Mutual, National Grid, and the
Patterson Fellowship; Mount Sinai Program in Cancer Prevention and
Control: Multidisciplinary Training [5R25-CA081137]
FX This research was supported by the National Cancer Institute (grants
5R01CA098864-02, 1K22CA126992-01, and K05 CA124415) and by support to
the Dana-Farber Cancer Institute from Liberty Mutual, National Grid, and
the Patterson Fellowship. Funding for the lead author was also provided
through the National Cancer Institute by the Harvard Education Program
in Cancer Prevention and Control (grant 5R25-CA057711-14) and the Mount
Sinai Program in Cancer Prevention and Control: Multidisciplinary
Training (grant 5R25-CA081137).
NR 68
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Z9 22
U1 4
U2 25
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD NOV
PY 2011
VL 101
IS 11
BP 2102
EP 2110
DI 10.2105/AJPH.2010.196030
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 835NA
UT WOS:000296041900022
PM 21330588
ER
PT J
AU Lund, BC
Steinman, MA
Chrischilles, EA
Kaboli, PJ
AF Lund, Brian C.
Steinman, Michael A.
Chrischilles, Elizabeth A.
Kaboli, Peter J.
TI Beers Criteria as a Proxy for Inappropriate Prescribing of Other
Medications Among Older Adults
SO ANNALS OF PHARMACOTHERAPY
LA English
DT Article
DE Beers criteria; health care; inappropriate drug use; older adult;
quality indicators
ID ADVERSE DRUG-REACTIONS; EXPLICIT CRITERIA; QUALITY; EVENTS; OUTPATIENTS;
OUTCOMES; PEOPLE
AB BACKGROUND: The Beers criteria are a compilation of medications deemed potentially inappropriate for older adults, widely used as a prescribing quality indicator.
OBJECTIVE: To determine whether Beers criteria serve as a proxy measure for other forms of inappropriate prescribing, as measured by comprehensive implicit review.
METHODS: Data for patients 65 years and older were obtained from the Veterans Affairs Enhanced Pharmacy Outpatient Clinic (EPOC) and the Iowa Medicaid Pharmaceutical Case Management (PCM) studies. Comprehensive measurement of prescribing quality was conducted using expert clinician review of medical records according to the Medication Appropriateness Index (MAI). MAI scores attributable to non-Beers medications were contrasted between patients who did and did not receive a Beers criteria medication.
RESULTS: Beers criteria medications accounted for 12.9% (EPOC) and 14.0% (PCM) of total MAI scores. Importantly, non-Beers MAI scores were significantly higher in patients receiving a Beers criteria medication in both studies (EPOC: 15.1 vs 12.4, p = 0.02; PCM: 11.1 vs 8.7, p = 0.04), after adjusting for important confounding factors.
CONCLUSIONS: Beers criteria utility extended beyond direct measurement of a limited set of inappropriate prescribing practices by serving as a clinically meaningful proxy for other inappropriate practices. Using prescribing quality indicators to guide interventions should thus identify patients for comprehensive medication review, rather than identifying specific medication targets for discontinuation. Future research should explore both the quality measurement and the intervention targeting applications of the Beers criteria, particularly when integrated with other indicators.
C1 [Lund, Brian C.] Vet Affairs Iowa City Hlth Care Syst, Ctr Comprehens Access & Delivery Res & Evaluat, Iowa City, IA USA.
[Steinman, Michael A.] San Francisco VA Med Ctr, Div Geriatr, San Francisco, CA USA.
[Steinman, Michael A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Chrischilles, Elizabeth A.] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA USA.
[Kaboli, Peter J.] Univ Iowa, Dept Internal Med, Div Gen Internal Med, Carver Coll Med, Iowa City, IA 52242 USA.
RP Lund, BC (reprint author), Vet Affairs Iowa City Hlth Care Syst, Ctr Comprehens Access & Delivery Res & Evaluat, Iowa City, IA USA.
EM Brian.Lund@va.gov
FU Health Services Research and Development Service, Department of Veterans
Affairs [SAF98-152]; Research Career Development award [RCD 01-013-1];
Center for Research in the Implementation of Innovative Strategies in
Practice at the Iowa City Veterans Affairs Medical Center [HFP 04-149];
State of Iowa General Assembly; Iowa Pharmacy Foundation, McKesson HBOC;
Institute for the Advancement of Community Pharmacy; Agency for
Healthcare Research and Quality (AHRQ) Centers for Education and
Research on Therapeutics [5 U18 HS016094]; National Institute on Aging;
American Federation for Aging Research [K23-AG030999]
FX The Enhanced Pharmacy Outpatient Clinic trial was supported by the
Health Services Research and Development Service, Department of Veterans
Affairs, through an investigator-initiated research award (SAF98-152);
Research Career Development award to Dr. Kaboli (RCD 01-013-1); and the
Center for Research in the Implementation of Innovative Strategies in
Practice (HFP 04-149) at the Iowa City Veterans Affairs Medical Center.
The Iowa Medicaid Pharmaceutical Case Management program evaluation was
funded by the State of Iowa General Assembly, the Iowa Pharmacy
Foundation, McKesson HBOC, and the Institute for the Advancement of
Community Pharmacy. This study was supported in part by an Agency for
Healthcare Research and Quality (AHRQ) Centers for Education and
Research on Therapeutics cooperative agreement #5 U18 HS016094. Dr.
Steinman was supported by an award from the National Institute on Aging
and the American Federation for Aging Research (K23-AG030999).
NR 26
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U1 1
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1060-0280
EI 1542-6270
J9 ANN PHARMACOTHER
JI Ann. Pharmacother.
PD NOV
PY 2011
VL 45
IS 11
BP 1363
EP 1370
DI 10.1345/aph.1Q361
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 845LK
UT WOS:000296824000005
PM 21972251
ER
PT J
AU Niess, H
Bao, Q
Conrad, C
Zischek, C
Notohamiprodjo, M
Schwab, F
Schwarz, B
Huss, R
Jauch, KW
Nelson, PJ
Bruns, CJ
AF Niess, Hanno
Bao, Qi
Conrad, Claudius
Zischek, Christoph
Notohamiprodjo, Mike
Schwab, Felix
Schwarz, Bettina
Huss, Ralf
Jauch, Karl-Walter
Nelson, Peter J.
Bruns, Christiane J.
TI Selective Targeting of Genetically Engineered Mesenchymal Stem Cells to
Tumor Stroma Microenvironments Using Tissue-Specific Suicide Gene
Expression Suppresses Growth of Hepatocellular Carcinoma
SO ANNALS OF SURGERY
LA English
DT Article
ID BONE-MARROW; PERIPHERAL-BLOOD; BREAST-CARCINOMA; CANCER; METASTASIS;
DELIVERY; ANGIOGENESIS; INVASION; THERAPY; PROLIFERATION
AB Background: The use of engineered mesenchymal stem cells (MSCs) as therapeutic vehicles for the treatment of experimental pancreatic and breast cancer has been previously demonstrated. The potential application of MSCs for the treatment of hepatocellular carcinoma (HCC) has been controversial. The general approach uses engineered MSCs to target different aspects of tumor biology, including angiogenesis or the fibroblast-like stromal compartment, through the use of tissue-specific expression of therapeutic transgenes. The aim of the present study was (1) to evaluate the effect of exogenously added MSCs on the growth of HCC and (2) the establishment of an MSC-based suicide gene therapy for experimental HCC.
Methods: Mesenchymal stem cells were isolated from bone marrow of C57/B16 p53(-/-) mice. The cells were injected into mice with HCC xenografts and the effect on tumor proliferation and angiogenesis was evaluated. The cells were then stably transfected with red fluorescent protein (RFP) or Herpes simplex virus thymidine kinase (HSV-Tk) gene under control of the Tie2 promoter/enhancer or the CCL5 promoter. Mesenchymal stem cells were injected intravenously into mice with orthotopically growing xenografts of HCC and treated with ganciclovir (GCV).
Results: Ex vivo examination of hepatic tumors revealed tumor-specific recruitment, enhanced tumor growth, and increased microvessel density after nontherapeutic MSC injections. After their homing to the hepatic xenografts, engineered MSCs demonstrated activation of the Tie2 or CCL5 promoter as shown by RFP expression. Application of CCL5/HSV-TK transfected MSCs in combination with GCV significantly reduced tumor growth by 56.4% as compared with the control group and by 71.6% as compared with nontherapeutic MSC injections. CCL5/HSV-TK+ transfected MSCs proved more potent in tumor inhibition as compared with Tie2/HSV-TK+ MSCs.
Conclusion: Exogenously added MSCs are recruited to growing HCC xenografts with concomitant activation of the CCL5 or Tie2 promoters within the MSCs. Stem cell-mediated introduction of suicide genes into the tumor followed by prodrug administration was effective for treatment of experimental HCC and thus may help fill the existing gap in bridging therapies for patients suffering from advanced HCCs.
C1 [Niess, Hanno; Bao, Qi; Zischek, Christoph; Schwarz, Bettina; Jauch, Karl-Walter; Bruns, Christiane J.] Univ Munich, Dept Surg, D-81371 Munich, Germany.
[Huss, Ralf] Univ Munich, Inst Pathol, D-8000 Munich, Germany.
[Conrad, Claudius] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Conrad, Claudius] Harvard Stem Cell Inst, Boston, MA USA.
[Schwab, Felix] Univ Hosp Munich, Josef Lissner Inst Biomed Imaging, Munich, Germany.
[Notohamiprodjo, Mike] Univ Hosp Munich, Dept Clin Radiol, Munich, Germany.
RP Bruns, CJ (reprint author), Univ Munich, Dept Surg, Marchioninistr 15, D-81371 Munich, Germany.
EM Christiane.bruns@med.uni-muenchen.de
FU Deutsche Forschungsgemeinschaft [SPP1190]; Wilhelm Sander-Stiftung;
medical faculty of the University of Munich
FX The work was supported by grants from the Deutsche
Forschungsgemeinschaft (SPP1190 to CB and PJN), the Wilhelm
Sander-Stiftung to PJN and the "Forderprogramm fur Forschung und Lehre"
of the medical faculty of the University of Munich to HN.
NR 44
TC 48
Z9 53
U1 0
U2 17
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-4932
J9 ANN SURG
JI Ann. Surg.
PD NOV
PY 2011
VL 254
IS 5
BP 767
EP 775
DI 10.1097/SLA.0b013e3182368c4f
PG 9
WC Surgery
SC Surgery
GA 844IK
UT WOS:000296740700013
PM 22042469
ER
PT J
AU Jacoby, GA
Griffin, CM
Hooper, DC
AF Jacoby, George A.
Griffin, Caitlin M.
Hooper, David C.
TI Citrobacter spp. as a Source of qnrB Alleles
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID MEDIATED QUINOLONE RESISTANCE; KLEBSIELLA-PNEUMONIAE; GENE;
IDENTIFICATION; DETERMINANTS; PREVALENCE; EXPRESSION; WERKMANII; AMPC
AB qnrB is the most common of the five qnr families and has the greatest number of allelic variants. Almost two-thirds of the qnrB alleles have been reported in Citrobacter spp., and several were shown to be located on the chromosome. In this study, PCR was used to investigate the prevalence of plasmid-mediated quinolone resistance genes in 71 clinical isolates belonging to the Citrobacter freundii complex. Thirty-seven percent contained qnrB alleles, including 7 (qnrB32 to qnrB38) that were novel and 1 pseudogene, while none contained qnrA, qnrC, qnrD, qnrS, or aac(6')-Ib-cr. When the strains were arrayed by related 16S rRNA sequence and further separated into subspecies by biochemical criteria, clustering of qnrB-positive strains was evident. In only two strains with qnrB2 and qnrB4 was quinolone resistance transferable by conjugation, and only these strains contained the ISCR1 sequence that is often associated with qnrB on plasmids. Five of 26 qnrB-positive strains contained integrase genes, but these included the strains with qnrB2 and qnrB4 as well as two strains with other transmissible plasmids. In a fully sequenced genome of Citrobacter youngae, a member of the C. freundii complex, another novel qnrB allele, qnrB39, occurs in a sequence of genes that is 90% identical to sequence surrounding integron-associated qnrB4 incorporated into plasmids. The chromosome of Citrobacter is the likely source of plasmid-mediated qnrB.
C1 [Jacoby, George A.; Griffin, Caitlin M.] Lahey Clin Fdn, Burlington, MA 01805 USA.
[Hooper, David C.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
RP Jacoby, GA (reprint author), Lahey Clin Fdn, 41 Mall Rd, Burlington, MA 01805 USA.
EM george.a.jacoby@lahey.org
FU National Institutes of Health, U.S. Public Health Service [R01 AI057576]
FX This work was supported by grant R01 AI057576 (to D. C. H. and G.A.J.)
from the National Institutes of Health, U.S. Public Health Service.
NR 24
TC 43
Z9 44
U1 0
U2 10
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD NOV
PY 2011
VL 55
IS 11
BP 4979
EP 4984
DI 10.1128/AAC.05187-11
PG 6
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 839NX
UT WOS:000296375600004
PM 21844311
ER
PT J
AU Hammond, SP
Baden, LR
Marty, FM
AF Hammond, Sarah P.
Baden, Lindsey R.
Marty, Francisco M.
TI Mortality in Hematologic Malignancy and Hematopoietic Stem Cell
Transplant Patients with Mucormycosis, 2001 to 2009
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID MYCOSES STUDY-GROUP; EUROPEAN-ORGANIZATION; FUNGAL-INFECTIONS; SALVAGE
THERAPY; ZYGOMYCOSIS; VORICONAZOLE; POSACONAZOLE; RECIPIENTS; DISEASES;
OUTCOMES
AB Mortality due to mucormycosis is high. We assessed clinical characteristics and mortality among stem cell transplant and hematologic malignancy patients diagnosed with mucormycosis from 2001 to 2009. Thirty patients were diagnosed with probable or proven mucormycosis during the study. Twenty-six were diagnosed premortem, and most were treated with liposomal amphotericin B single-agent antifungal therapy initially. While the initial antifungal and surgical treatment approach remained stable throughout the study period, 6-week mortality significantly declined over time (67% in 2001 to 2003 versus 45% in 2004 to 2006 versus 20% in 2007 to 2009 [P = 0.04]), as did 12-week mortality (78% in 2001 to 2003 versus 55% in 2004 to 2006 versus 20% in 2007 to 2009 [P = 0.01]).
C1 [Hammond, Sarah P.] Brigham & Womens Hosp, Div Infect Dis, Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Hammond, SP (reprint author), Brigham & Womens Hosp, Div Infect Dis, Dana Farber Canc Inst, 75 Francis St,PBB A4, Boston, MA 02115 USA.
EM shammond2@partners.org
FU Scott James Thaler Award
FX This work was supported in part by the Scott James Thaler Award. We
declare no competing financial interests.
NR 17
TC 16
Z9 16
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD NOV
PY 2011
VL 55
IS 11
BP 5018
EP 5021
DI 10.1128/AAC.00536-11
PG 4
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 839NX
UT WOS:000296375600010
PM 21876046
ER
PT J
AU Robinson, EB
Koenen, KC
McCormick, MC
Munir, K
Hallett, V
Happe, F
Plomin, R
Ronald, A
AF Robinson, Elise B.
Koenen, Karestan C.
McCormick, Marie C.
Munir, Kerim
Hallett, Victoria
Happe, Francesca
Plomin, Robert
Ronald, Angelica
TI Evidence That Autistic Traits Show the Same Etiology in the General
Population and at the Quantitative Extremes (5%, 2.5%, and 1%)
SO ARCHIVES OF GENERAL PSYCHIATRY
LA English
DT Article
ID MULTIPLE-REGRESSION ANALYSIS; RECIPROCAL SOCIAL-BEHAVIOR; CAST CHILDHOOD
ASPERGER; TWIN DATA; INDIVIDUAL-DIFFERENCES; GENETIC-RELATIONSHIP;
DISORDERS; SPECTRUM; HERITABILITY; CHILDREN
AB Context: Genetic factors play an important role in the etiology of both autism spectrum disorders and autistic traits. However, little is known about the etiologic consistency of autistic traits across levels of severity.
Objective: To compare the etiology of typical variation in autistic traits with extreme scoring groups (including top 1%) that mimicked the prevalence of diagnosed autism spectrum disorders in the largest twin study of autistic traits to date.
Design: Twin study using phenotypic analysis and genetic model-fitting in the total sample and extreme scoring groups (top 5%, 2.5%, and 1%).
Setting: A nationally representative twin sample from the general population of England.
Participants: The families of 5968 pairs aged 12 years old in the Twins' Early Development Study.
Main Outcome Measure: Autistic traits as assessed by the Childhood Autism Spectrum Test.
Results: Moderate to high heritability was found for autistic traits in the general population (53% for females and 72% for males). High heritability was found in extreme-scoring groups. There were no differences in heritability among extreme groups or between the extreme groups and the general population. A continuous liability shift toward autistic trait affectedness was seen in the cotwins of individuals scoring in the top 1%, suggesting shared etiology between extreme scores and normal variation.
Conclusion: This evidence of similar etiology across normal variation and the extremes has implications for molecular genetic models of autism spectrum disorders and for conceptualizing autism spectrum disorders as the quantitative extreme of a neurodevelopmental continuum.
C1 [Robinson, Elise B.] Massachusetts Gen Hosp, Ctr Human Genet Res, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA.
[Robinson, Elise B.; Koenen, Karestan C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Koenen, Karestan C.; McCormick, Marie C.] Harvard Univ, Sch Publ Hlth, Dept Soc Human Dev & Hlth, Boston, MA 02115 USA.
[Robinson, Elise B.; Munir, Kerim] Harvard Univ, Sch Med, Childrens Hosp Boston, Mental Hlth & Dev Disabil Program,Div Dev Med, Boston, MA USA.
[Munir, Kerim] Harvard Univ, Sch Med, Dept Psychiat, Childrens Hosp Boston, Boston, MA 02115 USA.
[Koenen, Karestan C.] Harvard Univ, Harvard Ctr Dev Child, Cambridge, MA 02138 USA.
[Hallett, Victoria; Happe, Francesca; Plomin, Robert; Ronald, Angelica] Kings Coll London, Inst Psychiat, Med Res Council Social Genet & Dev Psychiat Ctr, London WC2R 2LS, England.
[Ronald, Angelica] Univ London, Dept Psychol Sci, Ctr Brain & Cognit Dev, London, England.
RP Robinson, EB (reprint author), Massachusetts Gen Hosp, Ctr Human Genet Res, Psychiat & Neurodev Genet Unit, 185 Cambridge St,6th Floor, Boston, MA 02114 USA.
EM erobinso@hsph.harvard.edu
RI Happe, Francesca/D-5544-2012; Ronald, Angelica/C-7812-2009; Munir,
Kerim/D-6910-2015; Koenen, Karestan/K-5402-2014;
OI Ronald, Angelica/0000-0002-9576-2176; Munir, Kerim/0000-0002-2404-1806;
McCormmick, Marie/0000-0002-3938-1707; Koenen,
Karestan/0000-0003-3293-4281; Plomin, Robert/0000-0002-0756-3629
FU Medical Research Council [G0500079]; Harvard Medical School [MH71286];
Harvard School of Public Health [T32MH017119]; National Institute of
Mental Health/National Institutes of Health at The Children's Hospital
Boston
FX The Twins Early Development Study is funded by grant G0500079 from the
Medical Research Council. This study was supported by a National
Institute of Mental Health/National Institutes of Health Research
Fellowship at The Children's Hospital Boston, Harvard Medical School
(grant MH71286) and the Training Program in Psychiatric Genetics and
Translational Research at the Harvard School of Public Health (grant
T32MH017119).
NR 49
TC 93
Z9 95
U1 3
U2 23
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-990X
J9 ARCH GEN PSYCHIAT
JI Arch. Gen. Psychiatry
PD NOV
PY 2011
VL 68
IS 11
BP 1113
EP 1121
PG 9
WC Psychiatry
SC Psychiatry
GA 843CL
UT WOS:000296649800006
PM 22065527
ER
PT J
AU Lewandrowski, K
Gregory, K
Macmillan, D
AF Lewandrowski, Kent
Gregory, Kimberly
Macmillan, Donna
TI Assuring Quality in Point-of-Care Testing Evolution of Technologies,
Informatics, and Program Management
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID UNITED-STATES
AB Context.-Managing the quality of point-of-care testing (POCT) is a continuing challenge. Advances in testing technologies and the development of specialized informatics for POCT have greatly improved the ability of hospitals to manage their POCT program.
Objectives.-To present the evolving role of technology improvement, informatics, and program management as the key developments to ensure the quality of POCT.
Data Sources.-This presentation is based on a review of the literature and on our experiences with POCT at the Massachusetts General Hospital (Boston).
Conclusions.-Federal and state regulations, along with accreditation standards developed by the College of American Pathologists and The Joint Commission, have established guidelines for the performance of POCT and have provided a strong incentive to improve the quality of testing. Many instruments for POCT have incorporated advanced design features to prevent analytic and operator errors. This, along with the development of connectivity standards and specialized data management software, has enabled remote review of test data and electronic flow of information to hospital information systems. However, documentation of manually performed, visually read tests remains problematic and some POCT devices do not have adequate safeguards to prevent significant errors. In the past 2 decades the structure of a successful POCT management program has been defined, emphasizing the role of POCT managers working in conjunction with a pathology-based medical director. The critical skill set of POCT managers has also been identified. The POCT manager is now recognized as a true specialist in laboratory medicine. (Arch Pathol Lab Med. 2011;135:1405-1414; doi:10.5858/arpa.2011-0157-RA)
C1 [Lewandrowski, Kent; Gregory, Kimberly; Macmillan, Donna] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Lewandrowski, Kent] Harvard Univ, Sch Med, Boston, MA USA.
RP Lewandrowski, K (reprint author), Massachusetts Gen Hosp, Dept Pathol, Gray 5 Chem,55 Fruit St, Boston, MA 02114 USA.
EM klewandrowski@partners.org
NR 13
TC 20
Z9 22
U1 1
U2 9
PU COLLEGE AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD NOV
PY 2011
VL 135
IS 11
BP 1405
EP 1414
DI 10.5858/arpa.2011-0157-RA
PG 10
WC Medical Laboratory Technology; Medicine, Research & Experimental;
Pathology
SC Medical Laboratory Technology; Research & Experimental Medicine;
Pathology
GA 847KT
UT WOS:000296972500009
PM 22032566
ER
PT J
AU Maurovich-Horvat, P
Kallianos, K
Engel, LC
Szymonifka, J
Fox, CS
Hoffmann, U
Truong, QA
AF Maurovich-Horvat, Pal
Kallianos, Kimberly
Engel, Leif-Christopher
Szymonifka, Jackie
Fox, Caroline S.
Hoffmann, Udo
Truong, Quynh A.
TI Influence of pericoronary adipose tissue on local coronary
atherosclerosis as assessed by a novel MDCT volumetric method
SO ATHEROSCLEROSIS
LA English
DT Article
DE Coronary artery disease; Pericoronary fat; Epicardial fat; Adipose
tissue; Inflammation; Computed tomography
ID MULTIDETECTOR COMPUTED-TOMOGRAPHY; VISCERAL ABDOMINAL FAT; PUBLIC-HEALTH
PRACTICE; C-REACTIVE PROTEIN; CARDIOVASCULAR-DISEASE; PERICARDIAL FAT;
RISK-FACTORS; ASSOCIATION; ANGIOGRAPHY; INFLAMMATION
AB Objective: Pericoronary adipose tissue (PCAT) may create a pro-inflammatory state, contributing to the development of coronary artery disease (CAD). We sought to evaluate the feasibility of a novel volumetric PCAT quantification method using a novel threshold based computed tomography approach. In addition we determined the relation between PCAT volumes and CAD.
Methods: In 51 patients (49.5 +/- 5.1 years, 64.8% male) who underwent 64-slice MDCT, we measured threshold-based PCAT volumes using distance and anatomic-based methods. Using the most reproducible method, we performed the proximal 40-mm distance measurement in three groups as stratified by coronary plaque and high-sensitivity C-reactive protein (hs-CRP) levels: Group 1 (presence of coronary plaque, hs-CRP > 2.0 mg/L); an intermediate group (Group 2, no plaque, hs-CRP > 2.0 mg/L); and Group 3 (no plaque, hs-CRP < 1.0 mg/L). We compared PCAT volumes to the presence of coronary plaque on a patient (n = 51) and vessel (n = 153) basis. On a subsegment basis (n = 1224), we compared PCAT volume to the presence of plaque as well as plaque morphology.
Results: Distance-based PCAT volume measurements yielded excellent reproducibility with intra-observer intraclass correlation (ICC) of 0.997 and inter-observer ICC of 0.951. On a both a per-patient and per-vessel analysis, adjusted PCAT volume was greater in patients with plaque (Group 1) than without plaque (Groups 2 and 3, p < 0.001). No difference in PCAT volume was seen between high and low hs-CRP groups without plaque (p = 0.51). Adjusted PCAT volumes were higher in subsegments with plaque as compared without (p < 0.001). Additionally, adjusted PCAT volume was greatest in subsegments with mixed plaque followed by non-calcified plaque, calcified plaque, and the lowest volume in segments with no plaque (p < 0.001).
Conclusion: In this proof-of-concept study, threshold based PCAT volume assessment is feasible and highly reproducible. PCAT volume is increased in patients and vessels with coronary plaques. Surrounding vessel subsegments with coronary plaque, particularly mixed plaques, have greatest PCAT volume and highlight the effect of local PCAT in the development of coronary atherosclerosis. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Maurovich-Horvat, Pal; Kallianos, Kimberly; Engel, Leif-Christopher; Hoffmann, Udo; Truong, Quynh A.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac MR PET CT Program,Div Cardiol, Boston, MA 02114 USA.
[Maurovich-Horvat, Pal; Kallianos, Kimberly; Engel, Leif-Christopher; Hoffmann, Udo; Truong, Quynh A.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Maurovich-Horvat, Pal] Semmelweis Univ, Ctr Heart, Budapest, Hungary.
[Szymonifka, Jackie] Massachusetts Gen Hosp, Dept Biostat, Boston, MA 02114 USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
RP Truong, QA (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cardiac MR PET CT Program,Div Cardiol, 165 Cambridge St,Suite 400, Boston, MA 02114 USA.
EM qtruong@partners.org
OI Maurovich-Horvat, Pal/0000-0003-0885-736X
FU NIH [R01 HL080053, K23HL098370, L30HL093896]; Siemens Medical Solutions;
General Electrics Healthcare; [TAMOP-4.2.2-08/01/KMR-2008-2004]
FX Sources of funding: This work was supported by the NIH R01 HL080053, and
in part supported by Siemens Medical Solutions and General Electrics
Healthcare. Dr. Truong received support from NIH grant K23HL098370 and
L30HL093896. Dr. Maurovich-Horvat received support from
TAMOP-4.2.2-08/01/KMR-2008-2004.
NR 23
TC 12
Z9 13
U1 0
U2 5
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0021-9150
J9 ATHEROSCLEROSIS
JI Atherosclerosis
PD NOV
PY 2011
VL 219
IS 1
BP 151
EP 157
DI 10.1016/j.atherosclerosis.2011.06.049
PG 7
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 842HK
UT WOS:000296587200023
PM 21782176
ER
PT J
AU Podar, K
Zimmerhackl, A
Fulciniti, M
Tonon, G
Hainz, U
Tai, YT
Vallet, S
Halama, N
Jager, D
Olson, DL
Sattler, M
Chauhan, D
Anderson, KC
AF Podar, Klaus
Zimmerhackl, Alexander
Fulciniti, Mariateresa
Tonon, Giovanni
Hainz, Ursula
Tai, Yu-Tzu
Vallet, Sonia
Halama, Niels
Jaeger, Dirk
Olson, Dian L.
Sattler, Martin
Chauhan, Dharminder
Anderson, Kenneth C.
TI The selective adhesion molecule inhibitor Natalizumab decreases multiple
myeloma cell growth in the bone marrow microenvironment: therapeutic
implications
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE multiple myeloma; integrin-alpha 4; bone marrow microenvironment;
adhesion; cell adhesion-mediated drug resistance
ID MEDIATED DRUG-RESISTANCE; STROMAL CELLS; IN-VIVO; ANGIOGENESIS;
INTEGRIN; LINES; PROGRESSION; ACTIVATION; INTERLEUKIN-6; EXPRESSION
AB Recent advances regarding the introduction of anti-adhesion strategies as a novel therapeutic concept in oncology hold great promise. Here we evaluated the therapeutic potential of the new-in-class-molecule selective-adhesion-molecule (SAM) inhibitor Natalizumab, a recombinant humanized IgG4 monoclonal antibody, which binds integrin-alpha 4, in multiple myeloma (MM). Natalizumab, but not a control antibody, inhibited adhesion of MM cells to non-cellular and cellular components of the microenvironment as well as disrupted the binding of already adherent MM cells. Consequently, Natalizumab blocked both the proliferative effect of MM-bone marrow (BM) stromal cell interaction on tumour cells, and vascular endothelial growth factor (VEGF)-induced angiogenesis in the BM milieu. Moreover, Natalizumab also blocked VEGF-and insulin-like growth factor 1 (IGF-1)-induced signalling sequelae triggering MM cell migration. In agreement with our in vitro results, Natalizumab inhibited tumour growth, VEGF secretion, and angiogenesis in a human severe combined immunodeficiency murine model of human MM in the human BM microenvironment. Importantly, Natalizumab not only blocked tumour cell adhesion, but also chemosensitized MM cells to bortezomib, in an in vitro therapeutically representative human MM-stroma cell co-culture system model. Our data therefore provide the rationale for the clinical evaluation of Natalizumab, preferably in combination with novel agents (e. g. bortezomib) to enhance MM cytotoxicity and improve patient outcome.
C1 [Podar, Klaus] LeBow Inst Myeloma Therapeut, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Podar, Klaus; Halama, Niels; Jaeger, Dirk] Univ Heidelberg, Natl Ctr Tumour Dis NCT, Heidelberg, Germany.
[Halama, Niels; Jaeger, Dirk] German Canc Res Ctr, Heidelberg, Germany.
[Fulciniti, Mariateresa] VA Boston Healthcare Syst, Milan, Italy.
[Tonon, Giovanni] Ist Sci San Raffaele, I-20132 Milan, Italy.
[Vallet, Sonia] Massachusetts Gen Hosp, Ctr Multiple Myeloma, Boston, MA 02114 USA.
[Vallet, Sonia] Harvard Univ, Sch Med, Boston, MA USA.
[Olson, Dian L.] Mol Discovery Biogen Idec, Cambridge, MA USA.
RP Podar, K (reprint author), LeBow Inst Myeloma Therapeut, Jerome Lipper Multiple Myeloma Ctr, Dept Med Oncol, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA.
EM klaus_podar@dfci.harvard.edu
FU Multiple Myeloma Research Foundation (MMRF); Dunkin' Donuts Rising Star
Award; National Institutes of Health [IP50 CA 100707, RO-1 CA 50947,
PO-1 78378]; LeBow Fund; Biogen Idec; Elan; Millenium; Celgene; Novartis
FX This work was supported by a Multiple Myeloma Research Foundation (MMRF)
Senior Research Grant Award and the Dunkin' Donuts Rising Star Award (to
K. P.); National Institutes of Health Grants IP50 CA 100707, RO-1 CA
50947 and PO-1 78378, as well as the LeBow Fund to Myeloma (to K. C.
A.); K. P. received research support from Biogen Idec and Elan. K. C.
Anderson is a consultant for and received research support from
Millenium, Celgene and Novartis. D. L. O. is employee of Biogen Idec,
Cambridge, MA. The other authors declare no potential conflicts of
interest.
NR 37
TC 27
Z9 29
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2011
VL 155
IS 4
BP 438
EP 448
DI 10.1111/j.1365-2141.2011.08864.x
PG 11
WC Hematology
SC Hematology
GA 846LI
UT WOS:000296901500006
PM 21923653
ER
PT J
AU Kong, CY
Nattinger, KJ
Hayeck, TJ
Omer, ZB
Wang, YC
Spechler, SJ
McMahon, PM
Gazelle, GS
Hur, C
AF Kong, Chung Yin
Nattinger, Kevin J.
Hayeck, Tristan J.
Omer, Zehra B.
Wang, Y. Claire
Spechler, Stuart J.
McMahon, Pamela M.
Gazelle, G. Scott
Hur, Chin
TI The Impact of Obesity on the Rise in Esophageal Adenocarcinoma
Incidence: Estimates from a Disease Simulation Model
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GASTROESOPHAGEAL-REFLUX DISEASE; BODY-MASS INDEX; BARRETTS-ESOPHAGUS;
GASTRIC CARDIA; ABDOMINAL OBESITY; UNITED-STATES; CLINICAL SPECTRUM;
ACID REFLUX; POPULATION; PREVALENCE
AB Background: The United States has experienced an alarming and unexplained increase in the incidence of esophageal adenocarcinoma (EAC) since the 1970s. A concurrent increase in obesity has led some to suggest a relationship between the two trends. We explore the extent of this relationship.
Methods: Using a previously validated disease simulation model of white males in the United States, we estimated EAC incidence 1973 to 2005 given constant obesity prevalence and low population progression rates consistent with the early 1970s. Introducing only the observed, rising obesity prevalence, we calculated the incremental incidence caused by obesity. We compared these with EAC incidence data from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) registry to determine obesity's contribution to the rise therein. Incidences were converted to absolute numbers of cases using U. S. population data.
Results: Using constant obesity prevalence, we projected a total of 30,555 EAC cases cumulatively over 1973 to 2005 and 1,151 in 2005 alone. Incorporating the observed obesity trend resulted in 35,767 cumulative EACs and 1,608 in 2005. Estimates derived from SEER data showed 111,223 cumulative and 7,173 cases in 2005. We conclude that the rise in obesity accounted for 6.5% of the increase in EAC cases that occurred from 1973 to 2005 and 7.6% in the year 2005.
Conclusion: Using published OR for EAC among obese individuals, we found that only a small percentage of the rise in EAC incidence is attributable to secular trends in obesity.
Impact: Other factors, alone and in combination, should be explored as causes of the EAC epidemic. Cancer Epidemiol Biomarkers Prev; 20(11); 2450-6. (C) 2011 AACR.
C1 [Kong, Chung Yin; Nattinger, Kevin J.; Hayeck, Tristan J.; McMahon, Pamela M.; Gazelle, G. Scott; Hur, Chin] Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA.
[Nattinger, Kevin J.; Hayeck, Tristan J.; Omer, Zehra B.; Hur, Chin] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
[Kong, Chung Yin; McMahon, Pamela M.; Gazelle, G. Scott; Hur, Chin] Harvard Univ, Sch Med, Boston, MA USA.
[Gazelle, G. Scott] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Wang, Y. Claire] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
[Spechler, Stuart J.] VA N Texas Hlth Care Syst, Dallas, TX USA.
RP Hur, C (reprint author), 101 Merrimac St,10th Floor, Boston, MA 02114 USA.
EM chur@mgh-ita.org
OI Hur, Chin/0000-0002-2819-7576
FU AstraZeneca Pharmaceuticals; Ironwood Pharmaceuticals Inc.; Takeda
Pharmaceutical Company Ltd.; XenoPort, Inc.; Torax Medical, Inc.; BARRX
Medical, Inc.; GE Healthcare; National Cancer Institute at the NIH
[U01CA152926, R01CA140574, K25CA133141, R00CA126147]
FX S.Y. Spechler received grant/research support from AstraZeneca
Pharmaceuticals and Ironwood Pharmaceuticals Inc.; consulting fee from
Takeda Pharmaceutical Company Ltd.; grant/research support from
XenoPort, Inc.; consulting fee from both Torax Medical and BARRX
Medical, Inc. G. S. Gazelle received grant/research support and
consulting fee from GE Healthcare.; This work was supported by the
National Cancer Institute at the NIH (grant numbers U01CA152926 and
R01CA140574 to C. Hur, K25CA133141 to C.Y. Kong, and R00CA126147 to P.M.
McMahon).
NR 61
TC 14
Z9 14
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2011
VL 20
IS 11
BP 2450
EP 2456
DI 10.1158/1055-9965.EPI-11-0547
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 844RO
UT WOS:000296765200014
PM 21930957
ER
PT J
AU Marshall, JR
Tangen, CM
Sakr, WA
Wood, DP
Berry, DL
Klein, EA
Lippman, SM
Parnes, HL
Alberts, DS
Jarrard, DF
Lee, WR
Gaziano, JM
Crawford, ED
Ely, B
Ray, M
Davis, W
Minasian, LM
Thompson, IM
AF Marshall, James R.
Tangen, Catherine M.
Sakr, Wael A.
Wood, David P., Jr.
Berry, Donna L.
Klein, Eric A.
Lippman, Scott M.
Parnes, Howard L.
Alberts, David S.
Jarrard, David F.
Lee, W. Robert
Gaziano, J. Michael
Crawford, E. David
Ely, Benjamin
Ray, Michael
Davis, Warren
Minasian, Lori M.
Thompson, Ian M., Jr.
TI Phase III Trial of Selenium to Prevent Prostate Cancer in Men with
High-grade Prostatic Intraepithelial Neoplasia: SWOG S9917
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID VITAMIN-E; SUBSEQUENT RISK; SERUM SELENIUM; CLINICAL-TRIAL; REPEAT
BIOPSY; SELECT; SUPPLEMENTATION; CHEMOPREVENTION; ADENOCARCINOMA;
ASSOCIATION
AB The threat of prostate cancer and the significant and often negative impact of its treatment underscore the importance of prevention. High-grade prostatic intraepithelial neoplasia (HGPIN) has been identified as a potential premalignant lesion marking an increased risk of prostate cancer and substantial evidence suggests that men with HGPIN are in need of prostate cancer prevention. In vitro, in vivo, epidemiologic, and clinical trial evidence that selenium supplementation protects against prostate cancer motivated the study we report here: a double-blind, randomized, placebo-controlled trial of selenium 200 (mu g/d) as selenomethionine in men with HGPIN. The primary endpoint was progression of HGPIN to prostate cancer over a 3-year period. This National Cancer Institute Intergroup trial was coordinated by the Southwest Oncology Group (SWOG). Of 619 enrolled patients, 423 randomized men with HGPIN (212 selenium and 211 placebo) were eligible (by central pathology review) and included in the primary analysis. Three-year cancer rates were 36.6% (placebo) versus 35.6% (selenium; P = 0.73, adjusted). The majority of patients who developed cancer on trial (70.8%, selenium and 75.5%, placebo) had a Gleason score of 6 or less than 6; there were no differences in Gleason scores between the two arms. Subset analyses included the finding of a nonsignificantly reduced prostate cancer risk (relative risk = 0.82; 95% CI: 0.40-1.69) in selenium versus placebo patients in the lowest quartile of baseline plasma selenium level (<106 ng/mL). Overall, and in all other subsets defined by baseline blood selenium levels, selenium supplementation had no effect on prostate cancer risk. The 36% prostate cancer rate in men with HGPIN indicates the association of this lesion with an elevated prostate cancer risk. Future study in this setting should focus on selenium-deficient populations and selenium pharmacogenetics. Cancer Prev Res; 4(11); 1761-9. (C) 2011 AACR.
C1 [Marshall, James R.] Roswell Pk Canc Inst, Dept Canc Prevent & Populat Sci, Buffalo, NY 14263 USA.
[Tangen, Catherine M.; Ely, Benjamin] SW Oncol Grp Stat Ctr, Seattle, WA USA.
[Sakr, Wael A.] Wayne State Univ, Detroit, MI USA.
[Wood, David P., Jr.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Berry, Donna L.] Dana Farber Canc Inst, Boston, MA USA.
[Gaziano, J. Michael] Brigham & Womens Hosp, Canc & Leukemia Grp B, MAVERIC Cooperat Studies Program Coordinating Ctr, VA Boston Healthcare Syst, Boston, MA 02115 USA.
[Gaziano, J. Michael] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Klein, Eric A.] Cleveland Clin, Cleveland, OH 44106 USA.
[Lippman, Scott M.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Parnes, Howard L.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
[Alberts, David S.] Univ Arizona, Arizona Canc Ctr, Tucson, AZ USA.
[Jarrard, David F.] Univ Wisconsin, Madison, WI USA.
[Lee, W. Robert] Duke Univ, Sch Med, Eastern Cooperat Oncol Grp, Durham, NC USA.
[Crawford, E. David] Univ Colorado, Hlth Sci Ctr, Aurora, CO USA.
[Thompson, Ian M., Jr.] Univ Texas San Antonio, Hlth Sci Ctr, San Antonio, TX USA.
RP Marshall, JR (reprint author), Roswell Pk Canc Inst, Dept Canc Prevent & Populat Sci, Elm & Carlton St, Buffalo, NY 14263 USA.
EM james.marshall@roswellpark.org
FU National Cancer Institute, DHHS [CA11083, CA35261, CA46282, CA35119,
CA45377, CA35431, CA45450, CA27057, CA67663, CA128567, CA13612, CA74647,
CA45807, CA58348, CA67575, CA63844, CA58882, CA46368, CA45560, CA63850,
CA35262, CA16385, CA76132, CACA04919, CA76447, CA58416, CA46113,
CA68183, CA2106, CA21115, CA59518]
FX This investigation was supported in part by the following PHS
Cooperative Agreement grant numbers awarded by the National Cancer
Institute, DHHS: CA32102, CA38926, CA14028, CA35178, CA04919, CA35192,
CA105409, CA86780, CA20319, CA95860, CA42777, CA58686, CA11083, CA35261,
CA46282, CA35119, CA45377, CA35431, CA45450, CA27057, CA67663, CA128567,
CA13612, CA74647, CA45807, CA58348, CA67575, CA63844, CA58882, CA46368,
CA45560, CA63850, CA35262, CA16385, CA76132, CA68183, CACA04919,
CA76447, CA58686, CA27057, CA58416, CA46113, CA68183, CA2106, CA21115,
and CA59518.
NR 52
TC 49
Z9 49
U1 0
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD NOV
PY 2011
VL 4
IS 11
BP 1761
EP 1769
DI 10.1158/1940-6207.CAPR-10-0343
PG 9
WC Oncology
SC Oncology
GA 844NA
UT WOS:000296752800007
PM 21896650
ER
PT J
AU Lee, JE
Baba, Y
Ng, K
Giovannucci, E
Fuchs, CS
Ogino, S
Chan, AT
AF Lee, Jung Eun
Baba, Yoshifumi
Ng, Kimmie
Giovannucci, Edward
Fuchs, Charles S.
Ogino, Shuji
Chan, Andrew T.
TI Statin Use and Colorectal Cancer Risk According to Molecular Subtypes in
Two Large Prospective Cohort Studies
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID ISLAND METHYLATOR PHENOTYPE; POPULATION-BASED SAMPLE; MICROSATELLITE
INSTABILITY; COLON-CANCER; PATHOLOGICAL EPIDEMIOLOGY; INDUCED APOPTOSIS;
COMPETING RISKS; LOWERING DRUGS; BREAST-CANCER; ASPIRIN
AB Use of statins is hypothesized to reduce colorectal cancer risk but the evidence remains inconsistent. This may be partly explained by differential associations according to tumor location or molecular subtypes of colorectal cancer. We examined the association between statin use and colorectal cancer risk according to tumor location, KRAS mutation status, microsatellite instability (MSI) status, PTGS2 (COX-2) expression, or CpG island methylator phenotype (CIMP) status in two large prospective cohort studies, the Nurses' Health Study and Health Professionals Follow-up Study. We applied Cox regression to a competing risks analysis. We identified 1,818 colorectal cancers during 1990 to 2006. Compared with nonusers, current statin use was not associated with colorectal cancer [relative risk (RR) = 0.99, 95% CI = 0.86-1.14] or colon cancer (RR = 1.10, 95% CI = 0.94-1.29) but was inversely associated with rectal cancer (RR = 0.59, 95% CI = 0.41-0.84, P(heterogeneity) < 0.001). When we examined the association within strata of KRAS mutation status, we found no association with KRAS-mutated cancers (RR = 1.20, 95% CI = 0.87-1.67) but did observe a possible inverse association among KRAS wild-type cancers (RR = 0.80, 95% CI = 0.60-1.06, P(heterogeneity) = 0.06). The association did not substantially differ by PTGS2 expression, MSI status, or CIMP status. Current statin use was not associated with risk of overall colorectal cancer. The possibility that statin use may be associated with lower risk of rectal cancer or KRAS wild-type colorectal cancer requires further confirmation. Cancer Prev Res; 4(11); 1808-15. (C) 2011 AACR.
C1 [Lee, Jung Eun] Sookmyung Womens Univ, Dept Food & Nutr, Seoul, South Korea.
[Baba, Yoshifumi; Ng, Kimmie; Fuchs, Charles S.; Ogino, Shuji] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA USA.
[Giovannucci, Edward; Fuchs, Charles S.; Chan, Andrew T.] Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA.
[Ogino, Shuji] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Ogino, Shuji; Chan, Andrew T.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Nutr, Cambridge, MA 02138 USA.
[Giovannucci, Edward] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Cambridge, MA 02138 USA.
[Chan, Andrew T.] Massachusetts Gen Hosp, Gastrointestinal Unit, Boston, MA 02114 USA.
RP Chan, AT (reprint author), Massachusetts Gen Hosp, Gastrointestinal Unit, 55 Fruit St,GRJ 728A, Boston, MA 02114 USA.
EM achan@partners.org
FU NIH/National Cancer Institute [P01 CA87969, P01 CA55075, P50 CA127003,
K07 CA122826, R01 CA151993, R01 CA137178]
FX This work was supported by grants P01 CA87969, P01 CA55075, P50
CA127003, K07 CA122826, R01 CA151993, and R01 CA137178 from NIH/National
Cancer Institute.
NR 50
TC 27
Z9 28
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD NOV
PY 2011
VL 4
IS 11
BP 1808
EP 1815
DI 10.1158/1940-6207.CAPR-11-0113
PG 8
WC Oncology
SC Oncology
GA 844NA
UT WOS:000296752800012
PM 21680706
ER
PT J
AU Hanratty, R
Chonchol, M
Havranek, EP
Powers, JD
Dickinson, LM
Ho, PM
Magid, DJ
Steiner, JF
AF Hanratty, Rebecca
Chonchol, Michel
Havranek, Edward P.
Powers, J. David
Dickinson, L. Miriam
Ho, P. Michael
Magid, David J.
Steiner, John F.
TI Relationship between Blood Pressure and Incident Chronic Kidney Disease
in Hypertensive Patients
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID HEMODIALYSIS-PATIENTS; DIABETES-MELLITUS; RENAL-DISEASE; UNITED-STATES;
PROGRESSION; POPULATION; PREVALENCE; DECLINE; TRIAL; TIME
AB Background and objectives Hypertension is an important cause of chronic kidney disease (CKD). Identifying risk factors for progression to CKD in patients with normal kidney function and hypertension may help target therapies to slow or prevent decline of kidney function. Our objective was to identify risk factors for development of incident CKD and decline in estimated GFR (eGFR) in hypertensive patients.
Design, setting, participants, & measurements Cox proportional hazards models were used to assess the relationship between incident CKD (defined as eGFR <60 ml/min per 1.73 m(2)) and potential risk factors for CKD from a registry of hypertensive patients.
Results Of 43,305 patients meeting the inclusion criteria, 12.1% (5236 patients) developed incident CKD. Diabetes was the strongest predictor of incident CKD (hazard ratio, 1.96; 95% confidence interval, 1.84 to 2.09) and was associated with the greatest rate of decline in eGFR (-2.2 ml/min per 1.73 m(2) per year). Time-varying systolic BP was associated with incident CKD with risk increasing above 120 mmHg; each 10-mmHg increase in baseline and time-varying systolic BP was associated with a 6% increase in the risk of developing CKD (hazard ratio, 1.06; 95% confidence interval, 1.04 to 1.08 for both). Time-weighted systolic BP was associated with a more rapid decline in eGFR of an additional 0.2 ml/min per 1.73 m(2) per year decline for every 10-mmHg increase in systolic BP.
Conclusions We found that time-varying systolic BP was associated with incident CKD, with an increase in risk above a systolic BP of 120 mmHg among individuals with hypertension. Clin J Am Soc Nephrol 6: 2605-2611, 2011. doi: 10.2215/CJN.02240311
C1 [Hanratty, Rebecca] Denver Hlth, Med Ctr, Denver, CO 80204 USA.
[Chonchol, Michel] Univ Colorado, Div Renal Dis & Hypertens, Denver, CO 80202 USA.
[Powers, J. David; Ho, P. Michael; Magid, David J.; Steiner, John F.] Kaiser Permanente Colorado, Inst Hlth Res, Denver, CO USA.
[Dickinson, L. Miriam] Univ Colorado, Colorado Hlth Outcomes Program, Denver, CO USA.
[Ho, P. Michael] Denver Vet Affairs Med Ctr, Denver, CO USA.
RP Hanratty, R (reprint author), Denver Hlth, Med Ctr, 777 Bannock St,MC 3600, Denver, CO 80204 USA.
EM Rebecca.hanratty@dhha.org
FU National Heart Lung and Blood Institute [U19 HL91179-01]; Veterans
Affairs Health Services Research; Development Career Development Award
[05-026]
FX This study was conducted within the Cardiovascular Research Network, a
consortium of research organizations affiliated with the HMO Research
Network and sponsored by the National Heart Lung and Blood Institute
(U19 HL91179-01). The results presented in this paper have not been
published previously in whole or part, except in abstract form at the
43rd Annual American Society of Nephrology Conference.; Dr.
Ho is supported by a Veterans Affairs Health Services Research and
Development Career Development Award 05-026 and serves as a consultant
for Wellpoint, Inc.
NR 24
TC 14
Z9 16
U1 0
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD NOV
PY 2011
VL 6
IS 11
BP 2605
EP 2611
DI 10.2215/CJN.02240311
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 845KJ
UT WOS:000296821300010
PM 21921154
ER
PT J
AU Chan, KE
Maddux, FW
Tolkoff-Rubin, N
Karumanchi, SA
Thadhani, R
Hakim, RM
AF Chan, Kevin E.
Maddux, Frank W.
Tolkoff-Rubin, Nina
Karumanchi, S. Ananth
Thadhani, Ravi
Hakim, Raymond M.
TI Early Outcomes among Those Initiating Chronic Dialysis in the United
States
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID RENAL-DISEASE PROGRAM; HEMODIALYSIS-PATIENTS; EARLY INTERVENTION;
MORTALITY; HOSPITALIZATION; KIDNEY; RATES; DEATH
AB Background and objectives Approximately one million Americans initiated chronic dialysis over the past decade; the first-year mortality rate reported by the U.S. Renal Data System was 19.6% in 2007. This estimate has historically excluded the first 90 days of chronic dialysis.
Design, setting, participants, & measurements To characterize the mortality and hospitalization risks for patients starting chronic renal replacement therapy, we followed all patients initiating dialysis in 1733 facilities throughout the United States (n = 303,289). Mortality and hospitalizations within the first 90 days were compared with outcomes after this period, and the results were analyzed. Standard time-series analyses were used to depict the weekly risk estimates for each outcome.
Results Between 1997 and 2009, >300,000 patients initiated chronic dialysis and were followed for >35 million dialysis treatments; the highest risk for morbidity and mortality occurred in the first 2 weeks of treatment. The initial 2-week risk of death for a typical dialysis patient was 2.72-fold higher, and the risk of hospitalization was 1.95-fold higher when compared to a patient who survived the first year of chronic dialysis (week 53 after initiation). Similarly, over the first 90 days, the risk of mortality and hospitalization remained elevated. Thereafter, between days 91 and 365, these risks decreased considerably by more than half. Surviving these first weeks of dialysis was most associated with the type of vascular access. Initiating dialysis with a fistula was associated with a decreased early death risk by 61%, whereas peritoneal dialysis decreased the risk by 87%.
Conclusions The first 2 weeks of chronic dialysis are associated with heightened mortality and hospitalization risks, which remain elevated over the ensuing 90 days. Clin J Am Soc Nephrol 6: 2642-2649, 2011. doi: 10.2215/CJN.03680411
C1 [Chan, Kevin E.; Tolkoff-Rubin, Nina; Thadhani, Ravi] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
[Chan, Kevin E.; Maddux, Frank W.; Hakim, Raymond M.] Fresenius Med Care N Amer, Waltham, MA USA.
[Karumanchi, S. Ananth] Beth Israel Deaconess Med Ctr, Div Nephrol, Boston, MA 02215 USA.
[Karumanchi, S. Ananth] Howard Hughes Med Inst, Boston, MA 02115 USA.
RP Thadhani, R (reprint author), Massachusetts Gen Hosp, Div Nephrol, Bullfinch 127, Boston, MA 02114 USA.
EM thadhani.r@mgh.harvard.edu
FU Abbott Labs
FX Drs. Chan, Hakim, and Maddux are employees of Fresenius Medial Care
North America. Dr. Thadhani has received grants from Abbott Labs and is
a consultant to Shire Biopharmaceuticals and Fresenius Medial Care North
America.
NR 31
TC 32
Z9 32
U1 0
U2 2
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD NOV
PY 2011
VL 6
IS 11
BP 2642
EP 2649
DI 10.2215/CJN.03680411
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 845KJ
UT WOS:000296821300015
PM 21959599
ER
PT J
AU Chan, KE
Pflederer, TA
Steele, DJR
Lilly, MP
Ikizler, TA
Maddux, FW
Hakim, RM
AF Chan, Kevin E.
Pflederer, Timothy A.
Steele, David J. R.
Lilly, Michael P.
Ikizler, T. Alp
Maddux, Frank W.
Hakim, Raymond M.
TI Access Survival amongst Hemodialysis Patients Referred for Preventive
Angiography and Percutaneous Transluminal Angioplasty
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; CLINICAL-TRIALS; BLOOD-FLOW; VITAMIN-D;
SURVEILLANCE; SUBGROUPS; MORTALITY; STENOSIS; GRAFTS; RISK
AB Background and objectives Referring hemodialysis patients for elective access angiography and percutaneous transluminal angioplasty (PTA) is commonly done to prevent access failure, yet the effectiveness of this procedure remains unclear.
Design, setting, participants, & measures An observational matched cohort analysis among 40,132 Medicare beneficiaries receiving hemodialysis with a fistula or graft was performed. Cox regression was used to determine whether access intervention was associated with improved 1-year access survival.
Results Nonsurgical access intervention was found to be frequent at a rate of 20.9 procedures per 100 access years. In the 1-year period after intervention using angiography and PTA, the overall access failure rate was 53.7 per 100 access years in the intervention group and 49.6 in the nonintervention group (HR = 1.02; 95% CI, 0.96 to 1.08). Similar findings were also seen when the analysis was repeated in only fistulas (HR = 1.06; 95% CI, 0.98 to 1.15) and grafts (HR = 0.95; 95% CI, 0.86 to 1.05). In patients with a low intra-access flow rate (HR = 0.86; 95% CI, 0.75 to 0.99) or a new access (HR = 0.79; 95% CI, 0.71 to 0.89), angiography and PTA significantly increased access survival when compared with nonintervention (P for interaction was <0.0001). Angiography-PTA-related upper-extremity hematoma, vessel injury, or embolism-thrombosis occurred in 1.1% of all patients.
Conclusions Access characteristics significantly modify the survival benefits of angiography and PTA intervention where the benefits of these interventions are most seen in newer accesses or accesses with insufficient flow. Clin J Am Soc Nephrol 6: 2669-2680, 2011. doi: 10.2215/CJN.02860311
C1 [Chan, Kevin E.; Maddux, Frank W.; Hakim, Raymond M.] Fresenius Med Care N Amer, Div Clin Res, Waltham, MA 02451 USA.
[Chan, Kevin E.; Steele, David J. R.] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
[Pflederer, Timothy A.] Renal Care Associates, Morton, IL USA.
[Lilly, Michael P.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Ikizler, T. Alp] Vanderbilt Univ, Div Nephrol, Nashville, TN USA.
RP Chan, KE (reprint author), Fresenius Med Care N Amer, Div Clin Res, 920 Winter St, Waltham, MA 02451 USA.
EM kevin.chan@fmc-na.com
NR 28
TC 8
Z9 8
U1 0
U2 1
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD NOV
PY 2011
VL 6
IS 11
BP 2669
EP 2680
DI 10.2215/CJN.02860311
PG 12
WC Urology & Nephrology
SC Urology & Nephrology
GA 845KJ
UT WOS:000296821300019
PM 21959600
ER
PT J
AU Isakova, T
Xie, HL
Barchi-Chung, A
Vargas, G
Sowden, N
Houston, J
Wahl, P
Lundquist, A
Epstein, M
Smith, K
Contreras, G
Ortega, L
Lenz, O
Briones, P
Egbert, P
Ikizler, TA
Jueppner, H
Wolf, M
AF Isakova, Tamara
Xie, Huiliang
Barchi-Chung, Allison
Vargas, Gabriela
Sowden, Nicole
Houston, Jessica
Wahl, Patricia
Lundquist, Andrew
Epstein, Michael
Smith, Kelsey
Contreras, Gabriel
Ortega, Luis
Lenz, Oliver
Briones, Patricia
Egbert, Phyllis
Ikizler, T. Alp
Jueppner, Harald
Wolf, Myles
TI Fibroblast Growth Factor 23 in Patients Undergoing Peritoneal Dialysis
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; STAGE RENAL-DISEASE; MINERAL METABOLISM;
HEMODIALYSIS-PATIENTS; PARATHYROID-HORMONE; MORTALITY RISK; PHOSPHATE;
HYPERPHOSPHATEMIA; PROTEIN; VARIABILITY
AB Background and objectives Fibroblast growth factor 23 (FGF23) is an independent risk factor for mortality in patients with ESRD. Before FGF23 testing can be integrated into clinical practice of ESRD, further understanding of its determinants is needed.
Design, setting, participants, & measurements In a study of 67 adults undergoing peritoneal dialysis, we tested the hypothesis that longer dialysis vintage and lower residual renal function and renal phosphate clearance are associated with higher FGF23. We also compared the monthly variability of FGF23 versus parathyroid hormone (PTH) and serum phosphate.
Results In unadjusted analyses, FGF23 correlated with serum phosphate (r = 0.66, P < 0.001), residual renal function (r = -0.37, P = 0.002), dialysis vintage (r = 0.31, P = 0.01), and renal phosphate clearance (r = -0.38, P = 0.008). In adjusted analyses, absence of residual renal function and greater dialysis vintage associated with higher FGF23, independent of demographics, laboratory values, peritoneal dialysis modality and adequacy, and treatment with vitamin D analogs and phosphate binders. Urinary and dialysate FGF23 clearances were minimal. In three serial monthly measurements, within-subject variability accounted for only 10% of total FGF23 variability compared with 50% for PTH and 60% for serum phosphate.
Conclusions Increased serum phosphate, loss of residual renal function, longer dialysis vintage, and lower renal phosphate clearance are associated with elevated FGF23 levels in ESRD patients undergoing peritoneal dialysis. FGF23 may be a more stable marker of phosphate metabolism in ESRD than PTH or serum phosphate. Clin J Am Soc Nephrol 6: 2688-2695, 2011. doi: 10.2215/CJN.04290511
C1 [Isakova, Tamara; Xie, Huiliang; Barchi-Chung, Allison; Vargas, Gabriela; Sowden, Nicole; Houston, Jessica; Wahl, Patricia; Smith, Kelsey; Contreras, Gabriel; Ortega, Luis; Lenz, Oliver; Briones, Patricia; Wolf, Myles] Univ Miami, Miller Sch Med, Div Nephrol & Hypertens, Miami, FL 33136 USA.
[Lundquist, Andrew; Epstein, Michael] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
[Egbert, Phyllis; Ikizler, T. Alp] Vanderbilt Univ, Med Ctr, Div Nephrol, Nashville, TN USA.
[Jueppner, Harald] Massachusetts Gen Hosp, Div Pediat Nephrol, Boston, MA 02114 USA.
RP Wolf, M (reprint author), Univ Miami, Miller Sch Med, Div Nephrol & Hypertens, 1120 NW 14th St, Miami, FL 33136 USA.
EM mwolf2@med.miami.edu
RI Lenz, Oliver/M-4672-2016
OI Lenz, Oliver/0000-0003-2997-3976
FU National Center for Research Resources [1UL-1RR024975]; National
Institute of Diabetes and Digestive and Kidney Diseases [K24 DK 62849,
K23DK087858, R01DK076116, R01DK081374]; Center for D-Receptor Activation
Research
FX This study was supported in part by the Clinical Translational Science
Award 1UL-1RR024975 from the National Center for Research Resources
(T.A.I.), and by grants K24 DK 62849 (T.A.I.), K23DK087858 (T.I.),
R01DK076116 (M.W.), and R01DK081374 (M.W.) from the National Institute
of Diabetes and Digestive and Kidney Diseases and the Center for
D-Receptor Activation Research (T.A.I.).
NR 34
TC 38
Z9 45
U1 0
U2 14
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
EI 1555-905X
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD NOV
PY 2011
VL 6
IS 11
BP 2688
EP 2695
DI 10.2215/CJN.04290511
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 845KJ
UT WOS:000296821300021
PM 21903990
ER
PT J
AU Schutz, FAB
Je, YJ
Choueiri, TK
AF Schutz, Fabio A. B.
Je, Youjin
Choueiri, Toni K.
TI Hematologic toxicities in cancer patients treated with the
multi-tyrosine kinase sorafenib: A meta-analysis of clinical trials
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Vascular endothelial growth factor receptor; Targeted therapy; Tyrosine
kinase inhibitors; Sorafenib; Anemia; Neutropenia; Lymphopenia;
Thrombocytopenia; Bone marrow toxicities; Hematologic toxicities;
Meta-analysis
ID RENAL-CELL CARCINOMA; ACUTE MYELOID-LEUKEMIA; RANDOMIZED PHASE-II;
GROWTH-FACTOR VEGF; STEM-CELLS; HEMATOPOIETIC-CELLS; FLT3 LIGAND;
COMBINATION; BIAS; PROLIFERATION
AB Background: Sorafenib is a vascular endothelial growth factor receptor tyrosine-kinase inhibitor currently used in several malignancies. While not a traditional cytotoxic chemotherapeutic agent, hematological toxicities have been reported with this drug but the incidence and risk have not been formerly assessed. We performed a meta-analysis to determine the incidence and risk of hematologic toxicities associated with sorafenib use.
Methods: The databases of Medline were searched for articles from 1966 to May 2010. Abstracts presented at the American Society of Clinical Oncology meetings were also searched. Eligible studies include randomized trials with sorafenib, and adequate safety data profile reporting anemia, neutropenia, lymphopenia or thrombocytopenia. Statistical analyses were conducted to calculate the summary incidence, RR and 95% confidence intervals (CI).
Results: A total of 3221 patients were included. The incidences of sorafenib-associated all-grade anemia, neutropenia, thrombocytopenia and lymphopenia were 43.9%, 18.0%, 25.3% and 34.1%, respectively. The incidences of high-grade events were 2.0%, 5.1%, 4.0% and 13.1%, respectively. Sorafenib was associated with a decreased risk of high-grade anemia (RR = 0.62; 95% CI, 0.39-0.98), an increased risk of all-grade (RR = 1.69; 95% CI, 1.33-2.17) and high-grade (RR = 1.61; 95% CI, 1.02-2.57) neutropenia, all-grade (RR = 2.56; 95% CI, 1.37-4.80) and high-grade (RR = 3.63; 95% CI, 1.98-6.66) thrombocytopenia, and high-grade lymphopenia (RR = 1.84; 95% CI, 1.22-2.78). Stratified analysis by the presence or not of concomitant chemotherapy demonstrated similar risks.
Conclusions: Independent of cytotoxic chemotherapy, sorafenib has significant hematologic toxicities, with a decreased risk of anemia and increased risk of neutropenia, thrombocytopenia and lymphopenia. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
C1 [Schutz, Fabio A. B.; Choueiri, Toni K.] Harvard Univ, Sch Med, Kidney Canc Ctr, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Je, Youjin] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
RP Choueiri, TK (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Lank Ctr Genitourinary Oncol,Dana Farber Canc Ins, 44 Binney St,Dana 1230, Boston, MA 02115 USA.
EM Toni_Choueiri@dfci.harvard.edu
FU philanthropic Trust Family Research Fund for Kidney Cancer
FX This study was funded by the philanthropic Trust Family Research Fund
for Kidney Cancer. The funding source did not have any role in this
study. The authors had access to all raw data and had the final
responsibility for the decision to submit the manuscript for
publication.
NR 43
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U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1040-8428
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD NOV
PY 2011
VL 80
IS 2
BP 291
EP 300
DI 10.1016/j.critrevonc.2010.11.007
PG 10
WC Oncology; Hematology
SC Oncology; Hematology
GA 843PA
UT WOS:000296683200009
PM 21339073
ER
PT J
AU Habib, N
Saedi, N
Zachary, C
AF Habib, Nancy
Saedi, Nazanin
Zachary, Christopher
TI Cold-Induced Urticaria After Fractional Carbon Dioxide Laser Resurfacing
of the Face
SO DERMATOLOGIC SURGERY
LA English
DT Editorial Material
C1 [Saedi, Nazanin; Zachary, Christopher] Univ Calif Irvine, Dept Dermatol, Irvine, CA 92717 USA.
[Habib, Nancy] Massachusetts Gen Hosp, Dept Dermatol, Boston, MA 02114 USA.
RP Saedi, N (reprint author), Univ Calif Irvine, Dept Dermatol, Irvine, CA 92717 USA.
EM nsaedi@gmail.com
NR 0
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1076-0512
EI 1524-4725
J9 DERMATOL SURG
JI Dermatol. Surg.
PD NOV
PY 2011
VL 37
IS 11
BP 1700
EP 1703
DI 10.1111/j.1524-4725.2011.02121.x
PG 4
WC Dermatology; Surgery
SC Dermatology; Surgery
GA 847KO
UT WOS:000296972000023
PM 21883643
ER
PT J
AU Lee, CG
Boyko, EJ
Barrett-Connor, E
Miljkovic, I
Hoffman, AR
Everson-Rose, SA
Lewis, CE
Cawthon, PM
Strotmeyer, ES
Orwoll, ES
AF Lee, Christine G.
Boyko, Edward J.
Barrett-Connor, Elizabeth
Miljkovic, Iva
Hoffman, Andrew R.
Everson-Rose, Susan A.
Lewis, Cora E.
Cawthon, Peggy Mannen
Strotmeyer, Elsa S.
Orwoll, Eric S.
CA Osteoporotic Fractures Men MrOS
TI Insulin Sensitizers May Attenuate Lean Mass Loss in Older Men With
Diabetes
SO DIABETES CARE
LA English
DT Article
ID MUSCLE IN-VIVO; SKELETAL-MUSCLE; OSTEOPOROTIC FRACTURES; 1ST-DEGREE
RELATIVES; METFORMIN INCREASES; BODY-COMPOSITION; EXERCISE; PROTEIN;
PHOSPHORYLATION; TROGLITAZONE
AB OBJECTIVE-To examine longitudinal changes in total and appendicular lean body mass in older men with impaired fasting glucose (IFG) or diabetes and to determine whether these changes differ by diabetes treatment.
RESEARCH DESIGN AND METHODS-A total of 3,752 ambulatory men aged 65 years at baseline participated in a multicenter longitudinal cohort study. Baseline glycemic status was categorized as normoglycemia, IFG, undiagnosed/untreated diabetes, or treated diabetes. Insulin sensitizer medication use (metformin and/or thiazolidinediones) was assessed by prescription medication inventory. The change in total lean and appendicular lean mass was derived from dual X-ray absorptiometry scans taken at baseline and 3.5 +/- 0.7 years later.
RESULTS-This male cohort included 1,853 individuals with normoglycemia, 1,403 with IFG, 234 with untreated diabetes, 151 with diabetes treated with insulin sensitizers, and 111 with diabetes treated without insulin sensitizers. Men with untreated diabetes, diabetes treated without insulin sensitizers, or IFG had greater percentage loss in total or appendicular lean mass (P <= 0.05 in comparison to normoglycemic men). There remained a significantly greater percentage loss in appendicular lean mass for these groups even after adjustment for medical comorbidities or lifestyle factors. In contrast, the percentage loss in total or appendicular lean mass in men with diabetes treated with insulin sensitizers was significantly less than that in normoglycemic men in minimally and fully adjusted models.
CONCLUSIONS-Skeletal muscle loss was accelerated in men with IFG and diabetes, except when the latter was treated with insulin sensitizers. These findings suggest that insulin sensitizers may attenuate muscle loss
C1 [Lee, Christine G.; Orwoll, Eric S.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Boyko, Edward J.] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Barrett-Connor, Elizabeth] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Miljkovic, Iva; Strotmeyer, Elsa S.] Univ Pittsburgh, Pittsburgh, PA USA.
[Hoffman, Andrew R.] Stanford Univ, Sch Med, Palo Alto, CA 94304 USA.
[Everson-Rose, Susan A.] Univ Minnesota, Minneapolis, MN USA.
[Lewis, Cora E.] Univ Alabama, Birmingham, AL USA.
[Cawthon, Peggy Mannen] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
RP Lee, CG (reprint author), Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
EM leechr@ohsu.edu
RI Strotmeyer, Elsa/F-3015-2014;
OI Orwoll, Eric/0000-0002-8520-7355; Miljkovic, Iva/0000-0002-3155-9777;
Strotmeyer, Elsa/0000-0002-4093-6036
FU National Institutes of Health; National Institute of Arthritis and
Musculoskeletal and Skin Diseases (NIAMS); National Institute on Aging
(NIA); National Center for Research Resources (NCRR); National
Institutes of Health Roadmap for Medical Research [U01-AR45580,
U01-AR45614, U01-AR45632, U01-AR45647, U01-AR45654, U01-AR45583,
U01-AG18197, U01-AG027810, UL1-RR024140]; Building Interdisciplinary
Careers in Women's Health Program [K12-HD043488-09]; American Diabetes
Association [1-04-JF-46]; National Institute of Diabetes and Digestive
and Kidney Diseases [K01-DK083029]
FX The MrOS study was supported by funding from the National Institutes of
Health. The following institutes provided support: the National
Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS),
the National Institute on Aging (NIA), the National Center for Research
Resources (NCRR), and the National Institutes of Health Roadmap for
Medical Research under the following grant numbers: U01-AR45580,
U01-AR45614, U01-AR45632, U01-AR45647, U01-AR45654, U01-AR45583,
U01-AG18197, U01-AG027810, and UL1-RR024140. C.G.L. received additional
support from the Building Interdisciplinary Careers in Women's Health
Program (grant number K12-HD043488-09). Additional support was provided
by the American Diabetes Association (grant number 1-04-JF-46) to E.S.S.
I.M. was supported by the Mentored Research Scientist Development Award
from the National Institute of Diabetes and Digestive and Kidney
Diseases (K01-DK083029). VA Puget Sound Health Care System provided
support for participation of E.J.B. in this research.
NR 22
TC 33
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U1 1
U2 2
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD NOV
PY 2011
VL 34
IS 11
BP 2381
EP 2386
DI 10.2337/dc11-1032
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 847EQ
UT WOS:000296955100010
PM 21926282
ER
PT J
AU Chang, MH
Valdez, R
Ned, RM
Liu, TB
Yang, QH
Yesupriya, A
Dowling, NF
Meigs, JB
Bowen, MS
Khoury, MJ
AF Chang, Man-huei
Valdez, Rodolfo
Ned, Renee M.
Liu, Tiebin
Yang, Quanhe
Yesupriya, Ajay
Dowling, Nicole F.
Meigs, James B.
Bowen, Michael S.
Khoury, Muin J.
TI Influence of Familial Risk on Diabetes Risk-Reducing Behaviors Among US
Adults Without Diabetes
SO DIABETES CARE
LA English
DT Article
ID PUBLIC-HEALTH; IMPROVING HEALTH; PRIMARY-CARE; HISTORY; TOOL;
POPULATION; PREVALENCE; MEDICINE; ADVICE
AB OBJECTIVE-To test the association of family history of diabetes with the adoption of diabetes risk-reducing behaviors and whether this association is strengthened by physician advice or commonly known factors associated with diabetes risk.
RESEARCH DESIGN AND METHODS-We used cross-sectional data from the 20052008 National Health and Nutrition Examination Survey (NHANES) to examine the effects of family history of diabetes on the adoption of selected risk-reducing behaviors in 8,598 adults (aged >= 20 years) without diabetes. We used multiple logistic regression to model three risk reduction behaviors (controlling or losing weight, increasing physical activity, and reducing the amount of dietary fat or calories) with family history of diabetes.
RESULTS-Overall, 36.2% of U.S. adults without diabetes had a family history of diabetes. Among them, similar to 39.8% reported receiving advice from a physician during the past year regarding any of the three selected behaviors compared with 29.2% of participants with no family history (P < 0.01). In univariate analysis, adults with a family history of diabetes were more likely to perform these risk-reducing behaviors compared with adults without a family history. Physician advice was strongly associated with each of the behavioral changes (P < 0.01), and this did not differ by family history of diabetes.
CONCLUSIONS-Familial risk for diabetes and physician advice both independently influence the adoption of diabetes risk-reducing behaviors. However, fewer than half of participants with familial risk reported receiving physician advice for adopting these behaviors.
C1 [Chang, Man-huei; Valdez, Rodolfo; Ned, Renee M.; Liu, Tiebin; Yang, Quanhe; Yesupriya, Ajay; Dowling, Nicole F.; Bowen, Michael S.; Khoury, Muin J.] Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA 30333 USA.
[Meigs, James B.] Harvard Univ, Sch Med, Boston, MA USA.
[Meigs, James B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Chang, MH (reprint author), Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA 30333 USA.
EM mdc9@cdc.gov
FU Office of Public Health Genomics, CDC; National Institute of Diabetes
and Digestive and Kidney Diseases [K24-DK-080140]
FX Financial support for this work was provided by the Office of Public
Health Genomics, CDC. J.B.M. was supported by a grant from the National
Institute of Diabetes and Digestive and Kidney Diseases (K24-DK-080140).
NR 25
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U2 2
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD NOV
PY 2011
VL 34
IS 11
BP 2393
EP 2399
DI 10.2337/dc11-0876
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 847EQ
UT WOS:000296955100013
PM 21933907
ER
PT J
AU Sosenko, JM
Skyler, JS
Palmer, JP
Krischer, JP
Cuthbertson, D
Yu, LP
Schatz, DA
Orban, T
Eisenbarth, G
AF Sosenko, Jay M.
Skyler, Jay S.
Palmer, Jerry P.
Krischer, Jeffrey P.
Cuthbertson, David
Yu, Liping
Schatz, Desmond A.
Orban, Tihamer
Eisenbarth, George
CA Diabet Prevention Trial-Type 1
Type 1 Diabet TrialNet Study Grp
TI A Longitudinal Study of GAD65 and ICA512 Autoantibodies During the
Progression to Type 1 Diabetes in Diabetes Prevention Trial-Type 1
(DPT-1) Participants
SO DIABETES CARE
LA English
DT Article
ID INSULIN; MELLITUS; PREDICTION; ANTIBODIES; RISK
AB OBJECTIVE-We examined changes in GAD65 and ICA-512 autoantibodies (GADA and IA-2A) during progression to type I diabetes (T1D).
RESEARCH DESIGN AND METHODS-Diabetes Prevention Trial-Type 1 (OPT-1) participants were assessed for changes in positivity and titers of GADA and IA-2A during the progression to T1D.
RESULTS-Among 99 progressors to T1D with GADA and IA-2A measurements at baseline and diagnosis (mean interval = 3.3 +/- 1.5 years), GADA positivity changed little and GADA titers decreased (P < 0.01). In contrast, both IA-2A positivity and titers increased substantially (P < 0.001). Even among those positive at baseline, IA-2A titers increased from baseline to diagnosis (n = 57; P < 0.001), whereas GADA titers decreased (n = 80; P < 0.01). The same patterns of change were also evident among those positive for both autoantibodies (n = 48) at baseline.
CONCLUSIONS-IA-2A titers increase during the years before the diagnosis of T1D, even among those positive for IA-2A. In contrast, GADA titers tend to decline during those years.
C1 [Sosenko, Jay M.; Skyler, Jay S.] Univ Miami, Div Endocrinol, Miami, FL USA.
[Palmer, Jerry P.] Univ Washington, Div Endocrinol Metab & Nutr, VA Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Krischer, Jeffrey P.] Univ S Florida, Div Informat & Biostat, Tampa, FL USA.
[Cuthbertson, David] Univ S Florida, Pediat Epidemiol Ctr, Tampa, FL USA.
[Yu, Liping; Eisenbarth, George] Univ Colorado, HLA DNA Lab, Barbara Davis Ctr Childhood Diabet, Denver, CO 80202 USA.
[Schatz, Desmond A.] Univ Florida, Div Endocrinol, Gainesville, FL USA.
[Orban, Tihamer] Joslin Diabet Ctr, Boston, MA 02215 USA.
RP Sosenko, JM (reprint author), Univ Miami, Div Endocrinol, Miami, FL USA.
EM jsosenko@med.miami.edu
RI Skyler, Jay/F-4211-2016
FU Type 1 Diabetes Trial Net Study Group; National Institutes of Health
through the National Institute of Diabetes and Digestive and Kidney
Diseases; National Institute of Allergy and Infectious Diseases; Eunice
Kennedy Shriver National Institute of Child Health and Human Development
[U01 DK061010, U01 DK061016, U01 DK061034, U01 DK061036, U01 DK061040,
U01 DK061041, U01 DK061042, U01 DK061055, U01 DK061058, U01 DK084565,
U01 DK085453, U01 DK085461, U01 DK085463, U01 DK085466, U01 DK085499,
U01 DK085505, U01 DK085509, HHSN267200800019C]; National Center for
Research Resources [UL1 RR024131, UL1 RR024139, UL1 RR024153, UL1
RR024975, UL1 RR024982, UL1 RR025744, UL1 RR025761, UL1 RR025780, UL1
RR029890, UL1 RR031986]; General Clinical Research Center Award [M01
RR00400]; Juvenile Diabetes Research Foundation International; American
Diabetes Association
FX The sponsor of the study was the Type 1 Diabetes Trial Net Study Group.
Type 1 Diabetes Trial Net Study Group is a clinical trials network
funded by the National Institutes of Health through the National
Institute of Diabetes and Digestive and Kidney Diseases, the National
Institute of Allergy and Infectious Diseases, and the Eunice Kennedy
Shriver National Institute of Child Health and Human Development,
through the cooperative agreements U01 DK061010, U01 DK061016, U01
DK061034, U01 DK061036, U01 DK061040, U01 DK061041, U01 DK061042, U01
DK061055, U01 DK061058, U01 DK084565, U01 DK085453, U01 DK085461, U01
DK085463, U01 DK085466, U01 DK085499, U01 DK085505, U01 DK085509, and a
contract HHSN267200800019C; the National Center for Research Resources,
through Clinical Translational Science Awards UL1 RR024131, UL1
RR024139, UL1 RR024153, UL1 RR024975, UL1 RR024982, UL1 RR025744, UL1.
RR025761, UL1 RR025780, UL1 RR029890, UL1 RR031986, and General Clinical
Research Center Award M01 RR00400; the Juvenile Diabetes Research
Foundation International; and the American Diabetes Association.
NR 11
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U2 3
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 NOV
PY 2011
VL 34
IS 11
BP 2435
EP 2437
DI 10.2337/dc11-0981
PG 3
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 847EQ
UT WOS:000296955100022
PM 21911777
ER
PT J
AU Peters, A
Laffel, L
AF Peters, Anne
Laffel, Lori
CA Amer Diabet Assoc Transitions
TI Diabetes Care for Emerging Adults: Recommendations for Transition From
Pediatric to Adult Diabetes Care Systems
SO DIABETES CARE
LA English
DT Editorial Material
ID AMERICAN YOUTH PREVALENCE; DISEASE RISK-FACTORS; QUALITY-OF-LIFE;
YOUNG-ADULTS; GLYCEMIC CONTROL; CLINICAL CHARACTERISTICS; DEPRESSIVE
SYMPTOMS; INTENSIVE TREATMENT; ADOLESCENT FEMALES; EATING HABITS
C1 [Laffel, Lori] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
[Peters, Anne] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
RP Laffel, L (reprint author), Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02115 USA.
EM lori.laffel@joslin.harvard.edu
OI Peters, Anne/0000-0003-0520-0776
FU NIDDK NIH HHS [R01 DK095273]
NR 78
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U1 12
U2 29
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD NOV
PY 2011
VL 34
IS 11
BP 2477
EP 2485
DI 10.2337/dc11-1723
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 847EQ
UT WOS:000296955100031
PM 22025785
ER
PT J
AU Ritholz, MD
Beverly, EA
Abrahamson, MJ
Brooks, KM
Hultgren, BA
Weinger, K
AF Ritholz, Marilyn D.
Beverly, Elizabeth A.
Abrahamson, Martin J.
Brooks, Kelly M.
Hultgren, Brittney A.
Weinger, Katie
TI Physicians' Perceptions of the Type 2 Diabetes Multidisciplinary
Treatment Team A Qualitative Study
SO DIABETES EDUCATOR
LA English
DT Article
ID PRIMARY-CARE; MANAGEMENT; COMPLICATIONS; INSULIN; PART
AB Purpose
The purpose of this study was to explore physicians' perceptions of the multidisciplinary type 2 diabetes treatment team.
Methods
Nineteen physicians (74% endocrinologists; 26% primary care) participated in semistructured interviews. Audiorecorded data were transcribed, coded, and analyzed using thematic analysis and NVivo 8 software.
Results
Physicians considered the multidisciplinary team, including a physician and diabetes educator, as very important to diabetes treatment. Participants described how diabetes, with its many comorbidities and challenging lifestyle recommendations, is difficult for any single physician to treat. They further described how the team's diverse staff offers complementary skills and more contact time for assessment and treatment of patients, developing treatment relationships, and supporting patients in learning diabetes self-care. Physicians stressed the necessity of regular and ongoing communication among team members to ensure patients receive consistent information, and some reported that institutional factors interfere with intra-team communication. They also expressed concerns about the team approach in relation to individualized treatment and patients' reluctance to see multiple providers.
Conclusions
This study highlights physicians' positive perceptions of and concerns about the type 2 diabetes multidisciplinary team. Further study of diabetes educators' and patients' perceptions of the team approach is needed.
C1 [Ritholz, Marilyn D.; Beverly, Elizabeth A.; Abrahamson, Martin J.; Brooks, Kelly M.; Hultgren, Brittney A.; Weinger, Katie] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Ritholz, Marilyn D.; Beverly, Elizabeth A.; Abrahamson, Martin J.; Weinger, Katie] Harvard Univ, Sch Med, Boston, MA USA.
[Ritholz, Marilyn D.] Childrens Hosp, Boston, MA 02115 USA.
RP Weinger, K (reprint author), Joslin Diabet Ctr, 1 Joslin Pl, Boston, MA 02215 USA.
EM Katie.Weinger@joslin.harvard.edu
FU Kathleen P. Welsh Fund; NIDDK [RO1-060115]; Diabetes and Endocrinology
Research Core NIH [P30 DK36836]; NIH [T32 DK007260]
FX The authors thank the physicians who shared their experiences and
perceptions with us. This study was supported by grants from the
Kathleen P. Welsh Fund, NIDDK RO1-060115, the Diabetes and Endocrinology
Research Core NIH P30 DK36836, and the NIH Training Grant No. T32
DK007260.
NR 33
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U1 0
U2 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0145-7217
J9 DIABETES EDUCATOR
JI Diabetes Educ.
PD NOV-DEC
PY 2011
VL 37
IS 6
BP 794
EP 800
DI 10.1177/0145721711423320
PG 7
WC Endocrinology & Metabolism; Public, Environmental & Occupational Health
SC Endocrinology & Metabolism; Public, Environmental & Occupational Health
GA 845XZ
UT WOS:000296862200006
PM 22002972
ER
PT J
AU Zorick, T
Sugar, CA
Hellemann, G
Shoptaw, S
London, ED
AF Zorick, Todd
Sugar, Catherine A.
Hellemann, Gerhard
Shoptaw, Steve
London, Edythe D.
TI Poor response to sertraline in methamphetamine dependence is associated
with sustained craving for methamphetamine
SO DRUG AND ALCOHOL DEPENDENCE
LA English
DT Article
DE Antidepressants; Sertraline; Methamphetamine; Addiction; Craving;
Classification and regression trees
ID PLACEBO-CONTROLLED TRIAL; DRUG-USERS; DEPRESSION; WITHDRAWAL; SEVERITY;
PHARMACOTHERAPY; FLUOXETINE; MANAGEMENT; INVENTORY; OUTCOMES
AB Background: Depression is common among individuals with methamphetamine (MA) use disorders. As agents that enhance serotonergic function are frequently used to treat depression, one might predict that they would be useful medications for MA dependence. However, clinical trials of serotonergic agents for MA addiction have been unsuccessful.
Objective: To identify factors that distinguish MA-dependent research participants who increased MA self-administration while receiving treatment with the selective serotonin reuptake inhibitor (SSRI) sertraline from other groups of participants.
Method: Using a dataset from a 12-week randomized, placebo-controlled trial of sertraline (100 mg daily) for MA addiction, we identified participants who had completed at least 8 weeks of the trial (n = 61 sertraline, n = 68 placebo). We compared the proportions of MA-positive urine tests for weeks 8-12 of the trial for these subjects to their pre-randomization baseline, and identified those subjects who increased MA use during treatment. Using classification trees, we then assessed all data collected during the study to identify factors associated with increasing MA use during treatment with sertraline, compared to placebo.
Results: More subjects in the sertraline condition increased MA use during treatment (n = 13) than in the placebo condition (n = 5: p = 0.03). Classification trees identified multiple factors from both pre-treatment and in-treatment data that were associated with increased MA use during treatment. Only elevated in-treatment craving for MA specifically characterized subjects in the sertraline group who increased their MA use.
Conclusions: Some MA-abusing individuals treated with SSRIs have sustained craving with an increased propensity to relapse during treatment despite psychosocial treatment interventions. Published by Elsevier Ireland Ltd.
C1 [Zorick, Todd] Greater Los Angeles Vet Adm Healthcare Syst, Dept Psychiat, Los Angeles, CA 90073 USA.
[Zorick, Todd; Sugar, Catherine A.; Hellemann, Gerhard; London, Edythe D.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Sugar, Catherine A.] Univ Calif Los Angeles, Dept Biostat, Los Angeles, CA 90095 USA.
[Shoptaw, Steve] Univ Calif Los Angeles, Dept Family Med, Los Angeles, CA 90095 USA.
[London, Edythe D.] Univ Calif Los Angeles, Dept Mol & Med Pharmacol, Los Angeles, CA 90095 USA.
[London, Edythe D.] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA.
RP Zorick, T (reprint author), 11301 Wilshire Blvd,MC 116A, Los Angeles, CA 90073 USA.
EM todd.zorick@va.gov
FU NIH [R01 DA010923, P50 DA018185, P20 DA022539]
FX NIH Grants R01 DA010923 (SS), P50 DA018185 (SS, EDL), P20 DA022539
(EDL), endowments from the Katherine K. and Thomas P. Pike Chair in
Addiction Studies (EDL), and the Marjorie M. Greene Trust.
NR 34
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U1 0
U2 7
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 NOV 1
PY 2011
VL 118
IS 2-3
BP 500
EP 503
DI 10.1016/j.drugalcdep.2011.04.015
PG 4
WC Substance Abuse; Psychiatry
SC Substance Abuse; Psychiatry
GA 837EL
UT WOS:000296173800060
PM 21592681
ER
PT J
AU Johnson, JR
Menard, ME
Lauderdale, TL
Kosmidis, C
Gordon, D
Collignon, P
Maslow, JN
Andrasevic, AT
Kuskowski, MA
AF Johnson, James R.
Menard, Megan E.
Lauderdale, Tsai-Ling
Kosmidis, Chris
Gordon, David
Collignon, Peter
Maslow, Joel N.
Andrasevic, Arjana Tambic
Kuskowski, Michael A.
CA Trans-Global Initiative
TI Global Distribution and Epidemiologic Associations of Escherichia coli
Clonal Group A, 1998-2007
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID URINARY-TRACT-INFECTIONS; TRIMETHOPRIM-SULFAMETHOXAZOLE RESISTANCE;
EXTRAINTESTINAL INFECTIONS; UNCOMPLICATED CYSTITIS; MOLECULAR
EPIDEMIOLOGY; NEONATAL MENINGITIS; COMMUNITY; PYELONEPHRITIS;
O-18-K1-H7; PREVALENCE
AB Escherichia coli clonal group A (CGA) was first reported in 2001 as an emerging multidrug-resistant extraintestinal pathogen. Because CGA has considerable implications for public health, we examined the trends of its global distribution, clinical associations, and temporal prevalence for the years 1998-2007. We characterized 2,210 E. coli extraintestinal clinical isolates from 32 centers on 6 continents by CGA status for comparison with trimethoprim/sulfamethoxazole (TMP/SMZ) phenotype, specimen type, inpatient/outpatient source, and adult/child host; we adjusted for clustering by center. CGA prevalence varied greatly by center and continent, was strongly associated with TMP/SMZ resistance but not with other epidemiologic variables, and exhibited no temporal prevalence trend. Our findings indicate that CGA is a prominent, primarily TMP/SMZ-resistant extraintestinal pathogen concentrated within the Western world, with considerable pathogenic versatility. The stable prevalence of CGA over time suggests full emergence by the late 1990s, followed by variable endemicity worldwide as an antimicrobial drug resistant public health threat.
C1 [Johnson, James R.; Menard, Megan E.; Kuskowski, Michael A.] VA Med Ctr, Minneapolis, MN 55417 USA.
[Johnson, James R.] Univ Minnesota, Infect Dis Fellowship Program, Minneapolis, MN USA.
[Lauderdale, Tsai-Ling] Natl Hlth Res Inst, Zhunan, Taiwan.
[Kosmidis, Chris] Univ Athens, Sch Med, GR-11527 Athens, Greece.
[Gordon, David; Collignon, Peter] Australian Natl Univ, Canberra, ACT, Australia.
[Collignon, Peter] Canberra Hosp, Canberra, ACT, Australia.
[Maslow, Joel N.] Vet Affairs Med Ctr, Philadelphia, PA USA.
[Maslow, Joel N.] Univ Penn, Philadelphia, PA 19104 USA.
[Andrasevic, Arjana Tambic] Univ Hosp Infect Dis, Zagreb, Croatia.
RP Johnson, JR (reprint author), VA Med Ctr, 1 Vet Dr, Minneapolis, MN 55417 USA.
EM johns007@umn.edu
RI Lauderdale, Tsai-Ling/B-2660-2010; Toniolo, Antonio/B-4103-2015;
OI Toniolo, Antonio/0000-0003-3008-2126; Kosmidis,
Chris/0000-0003-0662-1265
FU Office of Research and Development, Medical Research Service, US
Department of Veterans Affairs; Merck, Inc.; Rochester Medical Group
FX This material is based on work supported by Office of Research and
Development, Medical Research Service, US Department of Veterans Affairs
(J.R.J.). J.R.J. has received research support (grant and contract) from
Merck, Inc., and Rochester Medical Group.
NR 25
TC 19
Z9 19
U1 1
U2 8
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
EI 1080-6059
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD NOV
PY 2011
VL 17
IS 11
BP 2001
EP 2009
DI 10.3201/eid1711.110488
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 843KI
UT WOS:000296670300002
PM 22099087
ER
PT J
AU Ryan, ET
AF Ryan, Edward T.
TI Haiti in the Context of the Current Global Cholera Pandemic
SO EMERGING INFECTIOUS DISEASES
LA English
DT Editorial Material
C1 [Ryan, Edward T.] Massachusetts Gen Hosp, Div Infect Dis, Boston, MA 02114 USA.
[Ryan, Edward T.] Harvard Univ, Sch Med, Boston, MA USA.
RP Ryan, ET (reprint author), Massachusetts Gen Hosp, Div Infect Dis, Jackson 504,55 Fruit St, Boston, MA 02114 USA.
EM etryan@partners.org
NR 0
TC 5
Z9 5
U1 0
U2 2
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD NOV
PY 2011
VL 17
IS 11
BP 2175
EP 2176
DI 10.3201/eid1711.110849
PG 2
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 843KI
UT WOS:000296670300045
PM 22204041
ER
PT J
AU Konstas, AA
Digumarthy, SR
Avery, LL
Wallace, KL
Lisovsky, M
Misdraji, J
Hahn, PF
AF Konstas, Angelos A.
Digumarthy, Subba R.
Avery, Laura L.
Wallace, Karen L.
Lisovsky, Mikhail
Misdraji, Joseph
Hahn, Peter F.
TI Congenital portosystemic shunts: Imaging findings and clinical
presentations in 11 patients
SO EUROPEAN JOURNAL OF RADIOLOGY
LA English
DT Article
DE Congenital posrtosystemic shunts; Abernethy malformation; Park
classification; Splenic artery aneurysms
ID SPLENIC ARTERY ANEURYSM; VENOUS SHUNT; PORTAL-VEIN;
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS; HEPATOPULMONARY SYNDROME;
LIVER-CIRRHOSIS; ABERNETHY MALFORMATION; PULMONARY-HYPERTENSION;
SPLENORENAL SHUNT; PORTACAVAL-SHUNT
AB Objective: To evaluate the clinical anatomy and presentations of congenital portosystemic shunts, and determine features that promote recognition on imaging.
Materials and methods: Institutional review board approval was obtained for this HIPAA-compliant study. The requirement for written informed consent was waived. Radiology reports were retrospectively reviewed from non-cirrhotic patients who underwent imaging studies from January 1999 through February 2009. Clinical sources reviewed included electronic medical records, archived images and histopathological material.
Results: Eleven patients with congenital portosystemic shunts were identified (six male and five female; age range 20 days to 84 years). Seven patients had extrahepatic and four patients had intrahepatic shunts. All 11 patients had absent or hypoplastic intrahepatic portal veins, a feature detected by CT and MRI, but not by US. Seven patients presented with shunt complications and four with presentations unrelated to shunt pathophysiology. Three adult patients had four splenic artery aneurysms. Prospective radiological evaluation of five adult patients with cross-sectional imaging had failed prospectively to recognize the presence of congenital portosystemic shunts on one or more imaging examinations.
Conclusions: Congenital portosystemic shunts are associated with splenic artery aneurysms, a previously unrecognized association. Portosystemic shunts were undetected during prospective radiologic evaluation in the majority of adult patients, highlighting the need to alert radiologists to this congenital anomaly. (C) 2010 Published by Elsevier Ireland Ltd.
C1 [Konstas, Angelos A.; Digumarthy, Subba R.; Avery, Laura L.; Hahn, Peter F.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Konstas, Angelos A.; Digumarthy, Subba R.; Avery, Laura L.; Lisovsky, Mikhail; Misdraji, Joseph; Hahn, Peter F.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Wallace, Karen L.] Mt Auburn Hosp, Dept Radiol, Cambridge, MA 02138 USA.
[Wallace, Karen L.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Lisovsky, Mikhail; Misdraji, Joseph] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Konstas, AA (reprint author), Massachusetts Gen Hosp, Dept Radiol, 55 Fruit St,FND 210, Boston, MA 02114 USA.
EM akonstas@partners.org
NR 34
TC 16
Z9 18
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0720-048X
J9 EUR J RADIOL
JI Eur. J. Radiol.
PD NOV
PY 2011
VL 80
IS 2
BP 175
EP 181
DI 10.1016/j.ejrad.2009.12.031
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 839JC
UT WOS:000296360500033
PM 20106622
ER
PT J
AU Roemer, FW
Kwoh, CK
Hannon, MJ
Crema, MD
Moore, CE
Jakicic, JM
Green, SM
Guermazi, A
AF Roemer, Frank W.
Kwoh, C. Kent
Hannon, Michael J.
Crema, Michel D.
Moore, Carolyn E.
Jakicic, John M.
Green, Stephanie M.
Guermazi, Ali
TI Semiquantitative assessment of focal cartilage damage at 3 T MRI: A
comparative study of dual echo at steady state (DESS) and
intermediate-weighted (IW) fat suppressed fast spin echo sequences
SO EUROPEAN JOURNAL OF RADIOLOGY
LA English
DT Article
DE MRI; Cartilage; Knee; Focal defect; Osteoarthritis
ID ARTICULAR-CARTILAGE; WATER-EXCITATION; NATURAL-HISTORY; KNEE; DEFECTS;
OSTEOARTHRITIS; PATHOLOGY; PROTOCOL; 3-TESLA; LESIONS
AB Purpose: The aim of the study was to compare semiquantitative assessment of focal cartilage damage using the dual echo at steady state (DESS)- and intermediate-weighted (IW) fat suppressed (fs) sequences at 3 T MRI.
Methods: Included were 201 subjects aged 35-65 with frequent knee pain. MRI was performed with the same sequence protocol as in the Osteoarthritis Initiative (OAI): sagittal IW fs, triplanar DESS and coronal IW sequences. Cartilage status was scored according to the WORMS system using all five sequences. A total of 243 focal defects were detected. In an additional consensus reading, the lesions were evaluated side-by-side using only the sagittal DESS and IW fs sequences. Lesion conspicuity was graded from 0 to 3, intrachondral signal changes adjacent to the defect were recorded and the sequence that depicted the lesion with larger diameter was noted. Wilcoxon signed-rank tests, controlled for clustering by person, were used to examine differences between the sequences.
Results: 37 (17.5%) of the scorable lesions were located in the medial tibio-femoral (TF), 48 (22.7%) in the lateral TF and 126 (59.7%) in the patello-femoral compartment. 82.5% were superficial and 17.5% full-thickness defects. Conspicuity was superior for the IW sequence (p < 0.001). The DESS sequence showed moreassociated intrachondral signal changes (p < 0.001). In 103 (48.8%) cases, the IW fs sequence depicted the lesions as being larger (p < 0.001).
Conclusions: The IW fs sequence detected more and larger focal cartilage defects than the DESS. More intrachondral signal changes were observed with the DESS. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
C1 [Roemer, Frank W.; Crema, Michel D.; Guermazi, Ali] Boston Univ, Dept Radiol, Med Ctr, Quantitat Imaging Ctr, Boston, MA 02118 USA.
[Roemer, Frank W.] Klinikum Augsburg, Dept Radiol, Augsburg, Germany.
[Kwoh, C. Kent; Hannon, Michael J.; Green, Stephanie M.] Univ Pittsburgh, Div Rheumatol & Clin Immunol, Sch Med, Pittsburgh, PA 15260 USA.
[Kwoh, C. Kent] VA Pittsburgh Healthcare Syst, Pittsburgh, PA USA.
[Moore, Carolyn E.] Texas Womans Univ, Dept Nutr & Food Sci, Denton, TX 76204 USA.
[Jakicic, John M.] Univ Pittsburgh, Dept Hlth & Phys Act, Pittsburgh, PA 15260 USA.
RP Roemer, FW (reprint author), Boston Univ, Dept Radiol, Med Ctr, Quantitat Imaging Ctr, FGH Bldg,3rd Floor,820 Harrison Ave, Boston, MA 02118 USA.
EM froemer@bu.edu
FU Beverage Institute for Health Wellness
FX The JOG study is funded by a grant from the Beverage Institute for
Health & Wellness.
NR 20
TC 32
Z9 32
U1 3
U2 4
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0720-048X
J9 EUR J RADIOL
JI Eur. J. Radiol.
PD NOV
PY 2011
VL 80
IS 2
BP E126
EP E131
DI 10.1016/j.ejrad.2010.07.025
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 839JC
UT WOS:000296360500020
PM 20833493
ER
PT J
AU Lin, XY
Cai, TX
Wu, MC
Zhou, Q
Liu, G
Christiani, DC
Lin, XH
AF Lin, Xinyi
Cai, Tianxi
Wu, Michael C.
Zhou, Qian
Liu, Geoffrey
Christiani, David C.
Lin, Xihong
TI Kernel Machine SNP-Set Analysis for Censored Survival Outcomes in
Genome-Wide Association Studies
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE Cox model; genetic studies; gene-based analysis; kernel machine;
multi-locus test; score test; single nucleotide polymorphism
ID LINKAGE DISEQUILIBRIUM; GENETIC PATHWAY; MIXED MODELS; REGRESSION;
TESTS; CANCER; HAPLOTYPES; SIMILARITY; POWER
AB In this article, we develop a powerful test for identifying single nucleotide polymorphism (SNP)-sets that are predictive of survival with data from genome-wide association studies. We first group typed SNPs into SNP-sets based on genomic features and then apply a score test to assess the overall effect of each SNP-set on the survival outcome through a kernel machine Cox regression framework. This approach uses genetic information from all SNPs in the SNP-set simultaneously and accounts for linkage disequilibrium (LD), leading to a powerful test with reduced degrees of freedom when the typed SNPs are in LD with each other. This type of test also has the advantage of capturing the potentially nonlinear effects of the SNPs, SNP-SNP interactions (epistasis), and the joint effects of multiple causal variants. By simulating SNP data based on the LD structure of real genes from the HapMap project, we demonstrate that our proposed test is more powerful than the standard single SNP minimum P-value-based test for association studies with censored survival outcomes. We illustrate the proposed test with a real data application. Genet. Epidemiol. 35:620-631, 2011. (C) 2011 Wiley Periodicals, Inc.
C1 [Lin, Xinyi; Cai, Tianxi; Zhou, Qian; Lin, Xihong] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Wu, Michael C.] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Liu, Geoffrey] Princess Margaret Hosp, Ontario Canc Inst, Toronto, ON M4X 1K9, Canada.
[Christiani, David C.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Christiani, David C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Christiani, David C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA USA.
RP Lin, XH (reprint author), Harvard Univ, Sch Publ Hlth, Dept Biostat, 655 Huntington Ave, Boston, MA 02115 USA.
EM xlin@hsph.harvard.edu
RI Liu, Geoffrey/N-4421-2016;
OI Wu, Michael C./0000-0002-3357-6570
FU National Institutes of Health [R37 CA076404, P01 CA134294, R01 CA092824,
R01 CA074386, P50 CA090578, P42 ES016454, P30 ES00002, R01 GM079330];
National Science Foundation [DMS 0854970]
FX This research is supported by National Institutes of Health grants R37
CA076404 (X.L.), P01 CA134294 (X.L.), R01 CA092824 (D.C.C), R01 CA074386
(D.C.C), P50 CA090578 (D.C.C), P42 ES016454 (X.L and D.C.C), P30 ES00002
(X.L and D.C.C), R01 GM079330 (T.C.) and National Science Foundation
grant DMS 0854970 (T.C.).
NR 30
TC 23
Z9 23
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0741-0395
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD NOV
PY 2011
VL 35
IS 7
BP 620
EP 631
DI 10.1002/gepi.20610
PG 12
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 845TT
UT WOS:000296846900005
PM 21818772
ER
PT J
AU Coticchia, CM
Curatolo, AS
Zurakowski, D
Yang, J
Daniels, KE
Matulonis, UA
Moses, MA
AF Coticchia, Christine M.
Curatolo, Adam S.
Zurakowski, David
Yang, Jiang
Daniels, Kathryn E.
Matulonis, Ursula A.
Moses, Marsha A.
TI Urinary MMP-2 and MMP-9 predict the presence of ovarian cancer in women
with normal CA125 levels
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE Ovarian cancer; Biomarkers; Matrix metalloproteinases; Neutrophil
gelatinase-associated lipocalin
ID CA-125 LEVELS; LIPOCALIN 2; THERAPY; METALLOPROTEINASES; PROGRESSION;
BIOMARKERS; MARKERS; ASSAY
AB Objective. To determine whether urinary matrix metalloproteinases (MMPs) predict the presence of ovarian cancer in patients with CA125 levels below the normal threshold of 35 U/mL, a critical group of patients for whom no ovarian cancer biomarker is currently available. To determine whether these noninvasive biomarkers provide clinically useful information in the general ovarian cancer patient population as well.
Methods. ELISA analyses and substrate gel electrophoresis detected the levels and activity of urinary MMP-2, MMP-9, MMP-9/neutrophil gelatinase-associated lipocalin (NGAL) complex, and MMP-9 dimer in all ovarian cancer patients (n = 97), those with CA125 <35 U/mL (n = 26) and controls (n = 81).
Results. In patients with CA125 <35 U/mL, receiver-operating characteristic (ROC) area under curve (AUC) analysis demonstrated that either urinary MMP-2 or MMP-9 or NGAL significantly discriminated between controls and ovarian cancer patients with normal CA125. Multivariate logistic regression revealed that the combination of urinary MMP-2 and MMP-9 provided the best diagnostic accuracy when multiplexed. When further multiplexed with age, the diagnostic accuracy of these biomarkers increased to a significant AUC of 0.820. These findings were consistent among the general ovarian cancer population studied as well, where the combination of urinary MMP-2 and MMP-9 multiplexed with age resulted in a highly significant AUC of 0.881. Pearson chi-square analysis revealed that higher urinary levels of either MMP-2 or MMP-9 were strongly associated with the increasing percentage of women with ovarian cancer independent of CA125 levels.
Conclusion. This study demonstrates the potential utility of urinary MMP-2 and MMP-9 to differentiate between ovarian cancer patients with normal CA125 levels and controls and suggests that urinary MMP-2 and MMP-9 may be a clinically useful aid in the diagnosis of advanced or recurrent ovarian cancer. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Coticchia, Christine M.; Curatolo, Adam S.; Yang, Jiang; Moses, Marsha A.] Childrens Hosp Boston, Program Vasc Biol, Boston, MA 02115 USA.
[Coticchia, Christine M.; Curatolo, Adam S.; Yang, Jiang; Moses, Marsha A.] Childrens Hosp Boston, Dept Surg, Boston, MA 02115 USA.
[Coticchia, Christine M.; Yang, Jiang; Moses, Marsha A.] Harvard Univ, Sch Med, Dept Surg, Boston, MA 02115 USA.
[Zurakowski, David] Childrens Hosp Boston, Dept Anesthesiol, Boston, MA 02115 USA.
[Daniels, Kathryn E.; Matulonis, Ursula A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Matulonis, Ursula A.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
RP Moses, MA (reprint author), Childrens Hosp Boston, Program Vasc Biol, Karp Family Res Bldg,Room 12129,300 Longwood Ave, Boston, MA 02115 USA.
EM marsha.moses@childrens.harvard.edu
FU Ovations for the Cure of Ovarian Cancer; Stuart Weitzman Foundation;
Advanced Medical Research Foundation; Lillian E. Tymkewicz Memorial Fund
FX The authors gratefully acknowledge the support of Ovations for the Cure
of Ovarian Cancer (UAM and MAM), the Stuart Weitzman Foundation,
Advanced Medical Research Foundation and the Lillian E. Tymkewicz
Memorial Fund.
NR 28
TC 17
Z9 21
U1 0
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0090-8258
J9 GYNECOL ONCOL
JI Gynecol. Oncol.
PD NOV
PY 2011
VL 123
IS 2
BP 295
EP 300
DI 10.1016/j.ygyno.2011.07.034
PG 6
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 839ZJ
UT WOS:000296407700022
PM 21889192
ER
PT J
AU Carroll, A
Thompson, MS
Co, C
Zaid, TM
Wong, KK
Yeung, TL
Schmandt, R
Birrer, MJ
Mok, SC
AF Carroll, A.
Thompson, M. S.
Co, C.
Zaid, T. M.
Wong, K. K.
Yeung, T. L.
Schmandt, R.
Birrer, M. J.
Mok, S. C.
TI Overexpression of stromal biglycan correlates with improved survival in
patients with high-grade serous ovarian cancer
SO GYNECOLOGIC ONCOLOGY
LA English
DT Meeting Abstract
C1 [Carroll, A.; Thompson, M. S.; Co, C.; Zaid, T. M.; Wong, K. K.; Yeung, T. L.; Schmandt, R.; Mok, S. C.] Univ Texas MD Anderson Canc Ctr, Dept Gynecol Oncol, Houston, TX 77030 USA.
[Birrer, M. J.; Mok, S. C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0090-8258
J9 GYNECOL ONCOL
JI Gynecol. Oncol.
PD NOV
PY 2011
VL 123
IS 2
BP 438
EP 438
DI 10.1016/j.ygyno.2011.07.060
PG 1
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 839ZJ
UT WOS:000296407700072
ER
PT J
AU Corey, KE
Chalasani, N
AF Corey, Kathleen E.
Chalasani, Naga
TI Should Combination Therapy Be the Paradigm for Future Nonalcoholic
Steatohepatitis Clinical Trials?
SO HEPATOLOGY
LA English
DT Editorial Material
ID FATTY LIVER-DISEASE; VITAMIN-E; ANTAGONIST; LOSARTAN; RATS; CCL4
C1 [Chalasani, Naga] Indiana Univ Sch Med, Div Gastroenterol & Hepatol, Indianapolis, IN 46202 USA.
[Corey, Kathleen E.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Div Gastroenterol & Hepatol, Cambridge, MA 02138 USA.
RP Chalasani, N (reprint author), Indiana Univ Sch Med, Div Gastroenterol & Hepatol, RG 4100,1050 Wishard Blvd, Indianapolis, IN 46202 USA.
EM nchalasa@iupui.edu
FU NIDDK NIH HHS [K24 DK069290]
NR 11
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD NOV
PY 2011
VL 54
IS 5
BP 1503
EP 1505
DI 10.1002/hep.24696
PG 3
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 840LX
UT WOS:000296443100004
PM 21953015
ER
PT J
AU Golden-Mason, L
Bambha, KM
Cheng, LL
Howell, CD
Taylor, MW
Clark, PJ
Afdhal, N
Rosen, HR
AF Golden-Mason, Lucy
Bambha, Kiran M.
Cheng, Linling
Howell, Charles D.
Taylor, Milton W.
Clark, Paul J.
Afdhal, Nezam
Rosen, Hugo R.
CA Virahep-C Study Grp
TI Natural Killer Inhibitory Receptor Expression Associated with Treatment
Failure and Interleukin-28B Genotype in Patients with Chronic Hepatitis
C
SO HEPATOLOGY
LA English
DT Article
ID VIRUS-INFECTION; TREATMENT RESPONSE; ANTIVIRAL THERAPY; GENE-EXPRESSION;
INTERFERON; IL28B; RIBAVIRIN; CELLS; PEGINTERFERON; PREDICTS
AB Natural killer (NK) cells constitute a first line of defense against viral infections; their function is governed by the integration of signals from multiple activating and inhibitory surface receptors. We hypothesized that because NKs become rapidly activated by cytokines, response to anti-hepatitis C virus (HCV) therapy would be predicted by the phenotype and function of NKs. We used a cohort of 101 patients (55 African, 46 Caucasian-American) who received pegylated-interferon (IFN) and ribavirin for 48 weeks. Multi-parameter FACS analysis was used to examine relative expression of 14 different inhibitory/activating receptors. Interleukin (IL)-28B genotyping (rs12979860) was also performed. Pretreatment levels of inhibitory receptors CD158a, CD158b, and CD158e were higher in patients who demonstrated poor viral decline within the first 28 days of therapy. Higher expression levels of inhibitory receptors NKG2A, CD158b, and CD158e were demonstrable in patients who failed to achieve sustained virologic response (SVR). Patients carrying the IL-28B T allele had higher NKG2A expression on effector NKs. We created a mathematical regression model incorporating race, viral level, and two inhibitory receptors. The area-under-the curve was 0.88, which is highly predictive of SVR. Moreover, the model performed complementarily with IL-28B across the CC, CT, and TT genotypes. Purified NKG2A neg NKs treated with pegylated-IFN-alpha for 4 hours demonstrated higher levels of IFN-c-inducible protein-10 (IP-10) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) compared with their NKG2A(pos) counterparts. Conclusions: These results provide novel insights into the associations of NK phenotype with IL-28B genotype and gene expression patterns, as well as the role of NKs in mediating IFN-induced viral clearance of chronic HCV infection. (HEPATOLOGY 2011;54:1559-1569)
C1 [Golden-Mason, Lucy; Bambha, Kiran M.; Cheng, Linling; Rosen, Hugo R.] Univ Colorado, Dept Med, Div Gastroenterol & Hepatol, Hepatitis Ctr C, Denver, CO USA.
[Golden-Mason, Lucy; Bambha, Kiran M.; Cheng, Linling; Rosen, Hugo R.] Natl Jewish Hosp, Denver, CO USA.
[Golden-Mason, Lucy] Univ Colorado, Integrated Program Immunol, Denver, CO 80202 USA.
[Howell, Charles D.] Univ Maryland, Baltimore Sch Med, Baltimore, MD 21201 USA.
[Taylor, Milton W.] Indiana Univ, Dept Biol, Bloomington, IN USA.
[Clark, Paul J.] Duke Univ, Med Ctr, Sch Med, Div Gastroenterol, Durham, NC 27710 USA.
[Clark, Paul J.] Duke Clin Res Inst, Durham, NC USA.
[Afdhal, Nezam] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Rosen, Hugo R.] Denver VA Med Ctr, Denver, CO USA.
RP Rosen, HR (reprint author), Div GI Hepatol B 158, Acad Off Bldg 1,12631 E 17th Ave,Rm 7614,POB 6511, Aurora, CO 80045 USA.
EM hugo.rosen@ucdenver.edu
RI Clark, Paul/A-1480-2012
OI Clark, Paul/0000-0002-1821-4969
FU NIDDK [1 K24 DK072036-01]; National Institute of Diabetes and Digestive
and Kidney Diseases (NIDDK); National Cancer Institute (NCI) with Roche
Laboratories, Inc.; National Health and Medical Research Council of
Australia; Duke Clinical Research Institute; Richard Boebel Family Fund;
National Centre in HIV Epidemiology and Clinical Research (now the Kirby
Institute for Infection and Immunity in Society), University of New
South Wales, Australia; [RO1 DK071560]; [U01 DK60329]; [U01 DK60340];
[U01 DK60324]; [U01 DK60344]; [U01 DK60327]; [U01 DK60335]; [U01
DK60352]; [U01 DK60342]; [U01 DK60345]; [U01 DK60309]; [U01 K60346];
[U01 DK60349]; [U01 DK60341]
FX Supported by RO1 DK071560 (to H. R. R.) and by NIDDK 1 K24 DK072036-01.
(to. C. D. H). This study was funded as a cooperative agreement by the
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
and the Intramural Research Program of the National Cancer Institute
(NCI) with further support under a Cooperative Research and Development
Agreement (CRADA) with Roche Laboratories, Inc. A complete listing of
participants in the Virahep-C study is given in Reference 5. Grant
numbers: U01 DK60329, U01 DK60340, U01 DK60324, U01 DK60344, U01
DK60327, U01 DK60335, U01 DK60352, U01 DK60342, U01 DK60345, U01
DK60309, U01 DK60346, U01 DK60349, U01 DK60341. Dr. Howell is supported
by NIDDK 1 K24 DK072036-01. Dr. Clark received funding support from the
National Health and Medical Research Council of Australia, the Duke
Clinical Research Institute, the Richard Boebel Family Fund, the
National Centre in HIV Epidemiology and Clinical Research (now the Kirby
Institute for Infection and Immunity in Society), University of New
South Wales, Australia.
NR 26
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U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD NOV
PY 2011
VL 54
IS 5
BP 1559
EP 1569
DI 10.1002/hep.24556
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 840LX
UT WOS:000296443100010
PM 21983945
ER
PT J
AU Foster, MC
Hwang, SJ
Porter, SA
Massaro, JM
Hoffmann, U
Fox, CS
AF Foster, Meredith C.
Hwang, Shih-Jen
Porter, Stacy A.
Massaro, Joseph M.
Hoffmann, Udo
Fox, Caroline S.
TI Fatty Kidney, Hypertension, and Chronic Kidney Disease The Framingham
Heart Study
SO HYPERTENSION
LA English
DT Article
DE renal sinus fat; hypertension; chronic kidney disease; blood pressure;
computed tomography; epidemiology
ID GLOMERULAR-FILTRATION-RATE; SERUM CYSTATIN-C; OBESITY-INDUCED
HYPERTENSION; RENAL-VEIN CONSTRICTION; METABOLIC SYNDROME;
ADIPOSE-TISSUE; BLOOD-PRESSURE; RISK-FACTORS; ASSOCIATION; CREATININE
AB Ectopic fat depots may mediate local and systemic disease. Animal models of diet-induced obesity demonstrate increased fat accumulation in the renal sinus. The association of renal sinus fat with hypertension, chronic kidney disease, and other metabolic disorders has not been studied in a large, community-based sample. Participants from the Framingham Heart Study (n = 2923; mean age: 54 years; 51% women) underwent quantification of renal sinus fat area using computed tomography. High renal sinus fat ("fatty kidney") was defined using sex-specific 90th percentiles in a healthy referent subsample. Multivariable linear and logistic regression was used to model metabolic risk factors as a function of fatty kidney and log-transformed renal sinus fat. Multivariable models were adjusted for age, sex, and outcome-specific covariates and then additionally adjusted for body mass index or abdominal visceral adipose tissue. The prevalence of fatty kidney was 30.1% (n = 879). Individuals with fatty kidney had a higher odds ratio (OR) of hypertension (OR: 2.12; P < 0.0001), which persisted after adjustment for body mass index (OR: 1.49; P < 0.0001) or visceral adipose tissue (OR: 1.24; P = 0.049). Fatty kidney was also associated with an increased OR for chronic kidney disease (OR: 2.30; P = 0.005), even after additionally adjusting for body mass index (OR: 1.86; P = 0.04) or visceral adipose tissue (OR: 1.86; P = 0.05). We observed no association between fatty kidney and diabetes mellitus after adjusting for visceral adipose tissue. In conclusion, fatty kidney is a common condition that is associated with an increased risk of hypertension and chronic kidney disease. Renal sinus fat may play a role in blood pressure regulation and chronic kidney disease. (Hypertension. 2011;58:784-790.). Online Data Supplement
C1 [Foster, Meredith C.; Hwang, Shih-Jen; Fox, Caroline S.] Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Foster, Meredith C.; Hwang, Shih-Jen; Fox, Caroline S.] NHLBI, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Foster, Meredith C.; Hwang, Shih-Jen; Fox, Caroline S.] NHLBI, Ctr Populat Studies, NIH, Bethesda, MD 20892 USA.
[Foster, Meredith C.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol & Metab, Boston, MA 02115 USA.
[Porter, Stacy A.] Harvard Univ, Sch Med, Boston, MA USA.
[Massaro, Joseph M.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
RP Fox, CS (reprint author), 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM foxca@nhlbi.nih.gov
OI Massaro, Joseph/0000-0002-2682-4812
FU National Heart, Lung, and Blood Institute [N01-HC-25195]
FX The Framingham Heart Study is supported by the National Heart, Lung, and
Blood Institute (N01-HC-25195).
NR 42
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U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0194-911X
J9 HYPERTENSION
JI Hypertension
PD NOV
PY 2011
VL 58
IS 5
BP 784
EP U266
DI 10.1161/HYPERTENSIONAHA.111.175315
PG 15
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 842HQ
UT WOS:000296588100644
PM 21931075
ER
PT J
AU Hill, CA
Litvak, A
Canapari, C
Cummings, B
Collins, C
Keamy, DG
Ferris, TG
Hartnick, CJ
AF Hill, Courtney A.
Litvak, Andrea
Canapari, Craig
Cummings, Brian
Collins, Corey
Keamy, Donald G.
Ferris, Timothy G.
Hartnick, Christopher J.
TI A pilot study to identify pre- and peri-operative risk factors for
airway complications following adenotonsillectomy for treatment of
severe pediatric OSA
SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY
LA English
DT Article
DE Pediatrics; Sleep apnea
ID OBSTRUCTIVE SLEEP-APNEA; CLINICAL-PRACTICE GUIDELINE; QUALITY-OF-LIFE;
RESPIRATORY COMPLICATIONS; CHILDREN; TONSILLECTOMY; BEHAVIOR
AB Objective: A pilot study to identify risk factors predicting post-operative complications in children with severe OSA undergoing adenotonsillectomy.
Methods: Retrospective review in a tertiary care academic institution. Two-stage least squares regression analysis and instrumental variable analysis to allow for modeling of pre- and peri-operative risk factors as having significance in predicting post-operative morbidity.
Results: Eighty-three children (mean age 4.88 +/- 3.09 years) with apnea-hypopnea index (AHI) >= 10 who were observed overnight following adenotonsillectomy were evaluated for rates of major (increased level of care, CPAP/BiPAP use, pulmonary edema and reintubation) and minor (oxygen saturation <90%) airway complications as well as total observation costs. Major and minor complications occurred in 4.8% and 19.3% of children, respectively. Age <2 years (p < 0.01), AHI > 24 (p < 0.05), intra-operative laryngospasm requiring treatment (p < 0.05). oxygen saturations <90% on room air in PACU (p < 0.05) and PACU stay >100 min (p < 0.01) independently predicted post-operative complications. Children with any one of these factors experienced a 38% complication rate versus 4% in all others.
Conclusions: This pilot study identified pre- and peri-operative risk factors that collectively can be investigated as predictors of post-operative airway complications in a prospective study. By identifying preliminary results comparing the complication rates between those children with and without these risk factors, we will be able to calculate the sample size for a future prospective validation study. Such a study is necessary to understand the safety and potential significant cost savings of observing children without risk factors on the pediatric floor and not in an ICU setting. A best practice algorithm can be created for children with severe OSA only after completing this prospective study. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Hill, Courtney A.; Keamy, Donald G.; Hartnick, Christopher J.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Cambridge, MA 02138 USA.
[Litvak, Andrea] Massachusetts Gen Hosp, Massachusetts Gen Phys Org, Boston, MA 02114 USA.
[Canapari, Craig; Cummings, Brian] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
[Collins, Corey] Harvard Univ, Sch Med, Dept Anesthesiol, Cambridge, MA 02138 USA.
[Ferris, Timothy G.] Harvard Univ, Sch Med, Dept Med, Cambridge, MA 02138 USA.
[Ferris, Timothy G.] Harvard Univ, Sch Med, Dept Pediat, Cambridge, MA 02138 USA.
RP Hartnick, CJ (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, 243 Charles St, Boston, MA 02114 USA.
EM Christopher_Hartnick@meei.harvard.edu
NR 30
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U1 0
U2 3
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0165-5876
J9 INT J PEDIATR OTORHI
JI Int. J. Pediatr. Otorhinolaryngol.
PD NOV
PY 2011
VL 75
IS 11
BP 1385
EP 1390
DI 10.1016/j.ijporl.2011.07.034
PG 6
WC Otorhinolaryngology; Pediatrics
SC Otorhinolaryngology; Pediatrics
GA 843PQ
UT WOS:000296684800008
PM 21871668
ER
PT J
AU Sachs, G
AF Sachs, Gary
TI Why Do Clinical Trials Fail? Learning from Computer Administered
Assessments
SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN CLINICAL PRACTICE
LA English
DT Meeting Abstract
C1 [Sachs, Gary] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Sachs, Gary] Bracket, Lexington, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1365-1501
J9 INT J PSYCHIAT CLIN
JI Int. J. Psychiat. Clin.
PD NOV
PY 2011
VL 15
SU 2
BP 12
EP 13
PG 2
WC Psychiatry
SC Psychiatry
GA 844WD
UT WOS:000296780400028
ER
PT J
AU Dastjerdi, MH
Sadrai, Z
Saban, DR
Zhang, Q
Dana, R
AF Dastjerdi, Mohammad H.
Sadrai, Zahra
Saban, Daniel R.
Zhang, Qiang
Dana, Reza
TI Corneal Penetration of Topical and Subconjunctival Bevacizumab
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID INTRAVITREAL BEVACIZUMAB; ANTIBODY FRAGMENTS; NEOVASCULARIZATION;
AVASTIN; INJECTION; INHIBITION; EYE; ANGIOGENESIS; OCCLUSION; DELIVERY
AB PURPOSE. To investigate the ability of bevacizumab to penetrate the cornea after topical application or subconjunctival injection.
METHODS. Bevacizumab 1% was topically applied three times a day to the corneas of mice (BALB/c) with intact corneas (n = 14), and with corneal neovascularization (n = 14). Animals were euthanized at 1, 6, 12, and 24 hours, and 2, 4, and 7 days for immunohistochemical analyses. Donkey anti-human IgG labeled with Cy3 was used for bevacizumab immunoreactivity detection. Additionally, one-time topical bevacizumab 1% was tested in corneas with denuded epithelium (n = 16). In another group (n = 16), a single dose of 0.5 mg bevacizumab was injected subconjunctivally. Animals were euthanized at 1, 6, and 24 hours, and 2, 4, 7, 14, and 21 days for immunohistochemical studies.
RESULTS. Bevacizumab was barely detected beyond the very superficial layer of the corneal epithelium in mice with intact corneas even after 7 days of topical administration. Application of bevacizumab in mice with corneal neovascularization; however, showed variable penetration into the corneal stroma. Experimentation with single application of topical bevacizumab in corneas with denuded epithelium or subconjunctivally injected bevacizumab showed intense staining for bevacizumab.
CONCLUSIONS. Topically applied bevacizumab has limited capacity to penetrate the corneas with intact epithelium. However, bevacizumab can penetrate the neovascularized cornea after topical application. This study demonstrates that subconjunctivally injected bevacizumab in eyes with an intact cornea penetrates well into the corneal stroma. (Invest Ophthalmol Vis Sci. 2011;52:8718-8723) DOI: 10.1167/iovs.11-7871
C1 [Dastjerdi, Mohammad H.; Sadrai, Zahra; Saban, Daniel R.; Zhang, Qiang; Dana, Reza] Schepens Eye Res Inst, Boston, MA 02114 USA.
[Dastjerdi, Mohammad H.; Sadrai, Zahra; Saban, Daniel R.; Zhang, Qiang; Dana, Reza] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA.
[Dastjerdi, Mohammad H.; Dana, Reza] Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
RP Dana, R (reprint author), Schepens Eye Res Inst, 20 Staniford St, Boston, MA 02114 USA.
EM reza.dana@schepens.harvard.edu
FU NIH [EY12963, EY19098]
FX Supported in part by NIH Grants EY12963 and EY19098.
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U2 7
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD NOV
PY 2011
VL 52
IS 12
BP 8718
EP 8723
DI 10.1167/iovs.11-7871
PG 6
WC Ophthalmology
SC Ophthalmology
GA 844PW
UT WOS:000296760700022
PM 22003112
ER
PT J
AU Aronis, KN
Vamvini, MT
Chamberland, JP
Mantzoros, CS
AF Aronis, Konstantinos N.
Vamvini, Maria T.
Chamberland, John P.
Mantzoros, Christos S.
TI Circulating Clusterin (Apolipoprotein J) Levels Do Not Have Any
Day/Night Variability and Are Positively Associated with Total and LDL
Cholesterol Levels in Young Healthy Individuals
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID TYPE-2 DIABETES-MELLITUS; CORONARY-HEART-DISEASE; LEPTIN; ADIPONECTIN;
NEUROENDOCRINE; PURIFICATION; CANCER; MEN; CLU
AB Context: Clusterin has been associated with several pathologies, including cardiovascular disease and neoplasias. However, little is known about its physiology and its association with metabolic and anthropometric parameters in humans.
Objective: The aim of the study was to examine whether circulating clusterin levels exhibit a day/night variation pattern and whether clusterin is associated with anthropometric and metabolic parameters.
Design: Study A was a frequent sampling study to evaluate potential periodicity in clusterin secretion. Study B was an observational study to evaluate the cross-sectional and prospective associations of clusterin with anthropometric and metabolic parameters.
Participants: Study A participants were healthy males (n = 6) and females (n = 6), aged 22.3 +/- 3.1 and 22.8 +/- 3.4 yr, respectively. Study B participants were 186 healthy males aged 18.4 +/- 0.14 yr. Ninety-one of the study B subjects were studied again 2 yr later and clusterin's associations with change of anthropometric and metabolic parameters were thus investigated prospectively.
Intervention: Samples in study A were collected every 15 min during an overnight admission, and subsequently pooled every hour. Samples in study B were collected during a screening visit.
Main Outcome Measure: Circulating clusterin levels were measured.
Results: In study A, spectral domain and cosinor regression analysis failed to reveal any day/night variation pattern. In study B, clusterin was positively correlated with total and low-density lipoprotein cholesterol (r = 0.23, P = 0.002; and r = 0.20, P = 0.005). Baseline clusterin did not predict change of any anthropometric, biochemical, or metabolic parameters prospectively.
Conclusions: We report for the first time that circulating clusterin does not have a day/night variation pattern in healthy young individuals. Clusterin levels are associated with total and low-density lipoprotein cholesterol cross-sectionally but do not predict short-term changes in metabolic parameters in healthy young males. (J Clin Endocrinol Metab 96: E1871-E1875, 2011)
C1 [Aronis, Konstantinos N.; Vamvini, Maria T.; Chamberland, John P.; Mantzoros, Christos S.] Harvard Univ, Div Endocrinol Diabet & Metab, Sch Med, Dept Internal Med,Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Mantzoros, Christos S.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Chamberland, John P.; Mantzoros, Christos S.] Harvard Univ, Endocrinol Sect, Sch Med, Dept Internal Med,VA Boston Healthcare Syst, Boston, MA 02130 USA.
RP Mantzoros, CS (reprint author), Harvard Univ, Div Endocrinol Diabet & Metab, Sch Med, Dept Internal Med,Beth Israel Deaconess Med Ctr, 330 Brookline Ave,Stoneman 816, Boston, MA 02215 USA.
EM cmantzor@bidmc.harvard.edu
RI Aronis, Konstantinos/F-3586-2012;
OI Aronis, Konstantinos/0000-0001-7189-8434; Chamberland,
John/0000-0002-7862-1371
FU National Center for Research Resources [M01-RR-01032-328840]; National
Institute of Diabetes and Digestive and Kidney Diseases [DK058785,
DK079929, DK081913]; National Institute on Aging [AG032030]; VA Merit
award
FX This work was supported by National Center for Research Resources Grant
M01-RR-01032-328840 (to the Harvard Clinical and Translational Science
Center). The content is solely the responsibility of the authors and
does not necessarily represent the official views of the National Center
for Research Resources or the National Institutes of Health. Funding was
also received from the National Institute of Diabetes and Digestive and
Kidney Diseases (Grants DK058785, DK079929, and DK081913), the National
Institute on Aging (Grant AG032030), and a VA Merit award.
NR 20
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U1 0
U2 2
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 NOV
PY 2011
VL 96
IS 11
BP E1871
EP E1875
DI 10.1210/jc.2011-1555
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 844MF
UT WOS:000296750600022
PM 21900379
ER
PT J
AU Chan, YM
Broder-Fingert, S
Paraschos, S
Lapatto, R
Au, M
Hughes, V
Bianco, SDC
Min, L
Plummer, L
Cerrato, F
De Guillebon, A
Wu, IH
Wahab, F
Dwyer, A
Kirsch, S
Quinton, R
Cheetham, T
Ozata, M
Ten, S
Chanoine, JP
Pitteloud, N
Martin, KA
Schiffmann, R
Van der Kamp, HJ
Nader, S
Hall, JE
Kaiser, UB
Seminara, SB
AF Chan, Yee-Ming
Broder-Fingert, Sarabeth
Paraschos, Sophia
Lapatto, Risto
Au, Margaret
Hughes, Virginia
Bianco, Suzy D. C.
Min, Le
Plummer, Lacey
Cerrato, Felecia
De Guillebon, Adelaide
Wu, I-Hsuan
Wahab, Fazal
Dwyer, Andrew
Kirsch, Susan
Quinton, Richard
Cheetham, Timothy
Ozata, Metin
Ten, Svetlana
Chanoine, Jean-Pierre
Pitteloud, Nelly
Martin, Kathryn A.
Schiffmann, Raphael
Van der Kamp, Hetty J.
Nader, Shahla
Hall, Janet E.
Kaiser, Ursula B.
Seminara, Stephanie B.
TI GnRH-Deficient Phenotypes in Humans and Mice with Heterozygous Variants
in KISS1/Kiss1
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID GONADOTROPIN-RELEASING-HORMONE; IDIOPATHIC HYPOGONADOTROPIC
HYPOGONADISM; CENTRAL PRECOCIOUS PUBERTY; KALLMANN-SYNDROME; RECEPTOR
GPR54; KISS1 GENE; MUTATIONS; PROTEIN; PROKINETICIN-2; POLYMORPHISMS
AB Context: KISS1 is a candidate gene for GnRH deficiency.
Objective: Our objective was to identify deleterious mutations in KISS1.
Patients and Methods: DNA sequencing and assessment of the effects of rare sequence variants (RSV) were conducted in 1025 probands with GnRH-deficient conditions.
Results: Fifteen probands harbored 10 heterozygous RSV in KISS1 seen in less than 1% of control subjects. Of the variants that reside within the mature kisspeptin peptide, p.F117L (but not p.S77I, p.Q82K, p.H90D, or p.P110T) reduces inositol phosphate generation. Of the variants that lie within the coding region but outside the mature peptide, p.G35S and p.C53R (but not p.A129V) are predicted in silico to be deleterious. Of the variants that lie outside the coding region, one (g.13659C -> T) impairs transcription in vitro, and another (c.1-7C -> T) lies within the consensus Kozak sequence. Of five probands tested, four had abnormal baseline LH pulse patterns. In mice, testosterone decreases with heterozygous loss of Kiss1 and Kiss1r alleles (wild-type, 274 +/- 99, to double heterozygotes, 69 +/- 16 ng/dl; r(2) = 0.13; P = 0.03). Kiss1/Kiss1r double-heterozygote males have shorter anogenital distances (13.0 +/- 0.2 vs. 15.6 +/- 0.2 mm at P34, P < 0.001), females have longer estrous cycles (7.4 +/- 0.2 vs. 5.6 +/- 0.2 d, P < 0.01), and mating pairs have decreased litter frequency (0.59 +/- 0.09 vs. 0.71 +/- 0.06 litters/month, P < 0.04) and size (3.5 +/- 0.2 vs. 5.4 +/- 0.3 pups/litter, P < 0.001) compared with wild-type mice.
Conclusions: Deleterious, heterozygous RSV in KISS1 exist at a low frequency in GnRH-deficient patients as well as in the general population in presumably normal individuals. As in Kiss1(+/-)/Kiss1r(+/-) mice, heterozygous KISS1 variants in humans may work with other genetic and/or environmental factors to cause abnormal reproductive function. (J Clin Endocrinol Metab 96: E1771-E1781, 2011)
C1 [Chan, Yee-Ming; Broder-Fingert, Sarabeth; Paraschos, Sophia; Lapatto, Risto; Au, Margaret; Hughes, Virginia; Plummer, Lacey; Cerrato, Felecia; De Guillebon, Adelaide; Wu, I-Hsuan; Wahab, Fazal; Dwyer, Andrew; Pitteloud, Nelly; Martin, Kathryn A.; Hall, Janet E.; Seminara, Stephanie B.] Massachusetts Gen Hosp, Reprod Endocrine Unit, Dept Med, Boston, MA 02114 USA.
[Chan, Yee-Ming; Broder-Fingert, Sarabeth; Paraschos, Sophia; Lapatto, Risto; Au, Margaret; Hughes, Virginia; Plummer, Lacey; Cerrato, Felecia; De Guillebon, Adelaide; Wu, I-Hsuan; Wahab, Fazal; Dwyer, Andrew; Pitteloud, Nelly; Martin, Kathryn A.; Hall, Janet E.; Seminara, Stephanie B.] Massachusetts Gen Hosp, Harvard Ctr Reprod Sci, Dept Med, Boston, MA 02114 USA.
[Chan, Yee-Ming] Childrens Hosp, Dept Med, Div Endocrinol, Boston, MA 02115 USA.
[Bianco, Suzy D. C.; Min, Le; Kaiser, Ursula B.] Brigham & Womens Hosp, Harvard Ctr Reprod Sci, Boston, MA 02115 USA.
[Bianco, Suzy D. C.; Min, Le; Kaiser, Ursula B.] Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Kirsch, Susan] Hosp Sick Children, Dept Endocrinol, Toronto, ON M5G 1X8, Canada.
[Quinton, Richard; Cheetham, Timothy] Newcastle Univ, Inst Human Genet, Endocrinol Res Grp, Newcastle Upon Tyne NE1 3BZ, Tyne & Wear, England.
[Ozata, Metin] Gulhane Mil Med Acad, Dept Endocrinol, TR-06018 Ankara, Turkey.
[Ten, Svetlana] Maimonides Infants & Childrens Hosp, Dept Pediat, Div Endocrinol, Brooklyn, NY 11219 USA.
[Chanoine, Jean-Pierre] Univ British Columbia, Dept Pediat, Endocrinol & Diabet Unit, Vancouver, BC V6H 3V4, Canada.
[Schiffmann, Raphael] Inst Metab Dis, Dallas, TX 75226 USA.
[Van der Kamp, Hetty J.] Leiden Univ, Med Ctr, Dept Pediat, Leiden, Netherlands.
[Nader, Shahla] Univ Texas Hlth Sci Ctr Houston, Dept Internal Med, Div Endocrinol, Houston, TX 77030 USA.
RP Seminara, SB (reprint author), Massachusetts Gen Hosp, Reprod Endocrine Unit, Dept Med, Bartlett Hall Extens 504,55 Fruit St, Boston, MA 02114 USA.
EM seminara.stephanie@mgh.harvard.edu
RI Dwyer, Andrew/D-8099-2012; PITTELOUD, Nelly/K-2709-2014; Wahab,
Fazal/G-2478-2012;
OI Dwyer, Andrew/0000-0002-7023-6794; Broder-Fingert,
Sarabeth/0000-0002-0932-4461
FU National Institutes of Health (NIH) [R01 HD015788]; Eunice Kennedy
Shriver National Institute of Child Health and Human Development, NICHD
[M01-RR-01066]; Harvard Clinical and Translational Science Center, from
the National Center for Research Resources [T32 DK007529]; National
Institute of Diabetes and Digestive and Kidney Disorders [U54HD028138];
Specialized Cooperative Center, NICHD [K12 HD051959]
FX This work was supported by National Institutes of Health (NIH) Grants
R01 HD015788 (Eunice Kennedy Shriver National Institute of Child Health
and Human Development, NICHD), M01-RR-01066 (Harvard Clinical and
Translational Science Center, from the National Center for Research
Resources), T32 DK007529 (National Institute of Diabetes and Digestive
and Kidney Disorders), U54HD028138(through cooperative agreement as part
of the Specialized Cooperative Centers Program in Reproduction and
Infertility Research, NICHD), and K12 HD051959 (as part of the Building
Interdisciplinary Research Careers in Women's Health program, National
Institute of Mental Health, National Institute of Allergy and Infectious
Diseases, HICHD, and Office of the Director).
NR 45
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U2 2
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 NOV
PY 2011
VL 96
IS 11
BP E1771
EP E1781
DI 10.1210/jc.2011-0518
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 844MF
UT WOS:000296750600007
PM 21880801
ER
PT J
AU Yu, EW
Kumbhani, R
Siwila-Sackman, E
Leder, BZ
AF Yu, Elaine W.
Kumbhani, Ruchit
Siwila-Sackman, Erica
Leder, Benjamin Z.
TI Acute Decline in Serum Sclerostin in Response to PTH Infusion in Healthy
Men
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID PARATHYROID-HORMONE; PRIMARY HYPERPARATHYROIDISM; POSTMENOPAUSAL WOMEN;
SKELETAL SENSITIVITY; BONE ENHANCER; ESTROGEN; SOST; OSTEOCYTES; DISEASE
AB Context: Animal models suggest that the osteoblast-stimulating actions of PTH are mediated by acute suppression of sclerostin, an inhibitor of the anabolic Wnt pathway. The immediate physiological changes in serum sclerostin in response to PTH infusion have not been reported in human studies.
Objective: We sought to determine the acute physiological effects of PTH infusion on serum sclerostin and bone turnover markers in healthy adult men.
Design, Setting, and Participants: Fifty-three healthy adult men underwent an 18-h iv infusion of human PTH(1-34) at a dose of 0.55 U/kg . h.
Outcomes: Serum levels of ionized calcium, sclerostin, and markers of bone formation (osteocalcin and amino-terminal propeptide of type I procollagen) and bone resorption (C-telopeptide and N-telopeptide) were obtained at 0, 6, 12, and 18 h.
Results: Serum ionized calcium, C-telopeptide, and N-telopeptide increased, and osteocalcin and amino-terminal propeptide of type I procollagen fell linearly throughout the PTH infusion (P < 0.001 for all). Average +/- SEM sclerostin levels declined from 936 +/- 65 to 813 +/- 63 pg/ml at 6 h (P < 0.001) and remained stably suppressed for the duration of the PTH infusion. There were no significant correlations between change in sclerostin and change in bone markers.
Conclusions: Serum sclerostin declined in response to acute PTH infusion within 6 h in healthy adult men. The early plateau in sclerostin suppression may indicate that maximal stimulation of the Wnt pathway is achieved quickly after exposure to PTH. Our findings support the hypothesis that PTH may mediate its anabolic effects in part via suppression of sclerostin. (J Clin Endocrinol Metab 96: E1848-E1851, 2011)
C1 [Yu, Elaine W.; Kumbhani, Ruchit; Siwila-Sackman, Erica; Leder, Benjamin Z.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
RP Yu, EW (reprint author), Massachusetts Gen Hosp, Endocrine Unit, 50 Blossom St,Thier 1051, Boston, MA 02114 USA.
EM ewyu@partners.org
FU National Institutes of Health [K23-RR16310]; Massachusetts General
Hospital Clinical Research Center [RR-1066]
FX This work was supported by National Institutes of Health Grants
K23-RR16310 and Massachusetts General Hospital Clinical Research Center
Grant RR-1066.
NR 19
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U1 0
U2 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD NOV
PY 2011
VL 96
IS 11
BP E1848
EP E1851
DI 10.1210/jc.2011-1534
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 844MF
UT WOS:000296750600017
PM 21865370
ER
PT J
AU Pellegrini, CN
Scheinman, MM
Badhwar, N
AF Pellegrini, Cara N.
Scheinman, Melvin M.
Badhwar, Nitish
TI Idiopathic epicardial ventricular tachycardia with origin remote from
vascular structures
SO JOURNAL OF ELECTROCARDIOLOGY
LA English
DT Article
DE Idiopathic ventricular tachycardia; Epicardial; Perivascular; Catheter
ablation
ID CATHETER ABLATION; OUTFLOW TRACT; IDENTIFY; VALSALVA; SINUS; SITE
AB We report a case of a patient with idiopathic left ventricular tachycardia (VT) successfully ablated from the epicardial aspect of the left ventricle, after a previous failed endocardial ablation. The VT appeared to be catecholamine sensitive. An excellent epicardial pacemap was found in the midlateral region of the left ventricle, remote from vascular structures. Following ablation, the patient discontinued antiarrhythmic drug use and has not experienced any recurrence of VT for more than 2 1/2 years. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Pellegrini, Cara N.] San Francisco VA Med Ctr, Dept Med, San Francisco, CA 94121 USA.
[Pellegrini, Cara N.; Scheinman, Melvin M.; Badhwar, Nitish] Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Pellegrini, CN (reprint author), San Francisco VA Med Ctr, Dept Med, 4150 Clement St,111C, San Francisco, CA 94121 USA.
EM pellegrinic@medicine.ucsf.edu
FU American Heart Association
FX Supported in part by a grant from the American Heart Association
NR 13
TC 1
Z9 1
U1 0
U2 0
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 0022-0736
J9 J ELECTROCARDIOL
JI J. Electrocardiol.
PD NOV-DEC
PY 2011
VL 44
IS 6
BP 792
EP 795
DI 10.1016/j.jelectrocard.2011.01.007
PG 4
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 843GO
UT WOS:000296660500031
PM 21419422
ER
PT J
AU Eswara, JR
Gervais, DA
Mueller, PR
Cantwell, CP
Uppot, RN
McGovern, FJ
AF Eswara, Jairam R.
Gervais, Debra A.
Mueller, Peter R.
Cantwell, Colin P.
Uppot, Raul N.
McGovern, Francis J.
TI OUTCOMES OF RENAL RADIOFREQUENCY ABLATION WITH PYELOPERFUSION
SO JOURNAL OF ENDOUROLOGY
LA English
DT Meeting Abstract
C1 [Eswara, Jairam R.; McGovern, Francis J.] Massachusetts Gen Hosp, Dept Urol, Boston, MA 02114 USA.
[Gervais, Debra A.; Mueller, Peter R.; Cantwell, Colin P.; Uppot, Raul N.] Massachusetts Gen Hosp, Div Abdominal Imaging & Intervent Radiol, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0892-7790
J9 J ENDOUROL
JI J. Endourol.
PD NOV
PY 2011
VL 25
SU 1
BP A134
EP A134
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA 844ZI
UT WOS:000296792200408
ER
PT J
AU Eswara, JR
Sharif-Tabrizi, A
Sacco, D
AF Eswara, Jairam R.
Sharif-Tabrizi, Ahmad
Sacco, Dianne
TI POSITIVE STONE CULTURE IS ASSOCIATED WITH UROSEPSIS AFTER ENDOUROLOGICAL
PROCEDURES - AN UPDATE
SO JOURNAL OF ENDOUROLOGY
LA English
DT Meeting Abstract
C1 [Eswara, Jairam R.; Sharif-Tabrizi, Ahmad; Sacco, Dianne] Massachusetts Gen Hosp, Dept Urol, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0892-7790
J9 J ENDOUROL
JI J. Endourol.
PD NOV
PY 2011
VL 25
SU 1
BP A45
EP A46
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA 844ZI
UT WOS:000296792200144
ER
PT J
AU Londono, DC
Wuerstle, M
Thomas, AA
Tsu, JW
Danial, T
Chien, G
AF Londono, Diana C.
Wuerstle, Melanie
Thomas, Anil A.
Tsu, Jin-Wen
Danial, Tarek
Chien, Gary
TI ACCURACY AND IMPLICATION OF PERCUTANEOUS RENAL BIOPSY IN THE MANAGEMENT
OF RENAL MASSES
SO JOURNAL OF ENDOUROLOGY
LA English
DT Meeting Abstract
C1 [Londono, Diana C.; Wuerstle, Melanie; Thomas, Anil A.; Danial, Tarek; Chien, Gary] W Los Angeles Vet Affairs Med Ctr, Dept Urol, Los Angeles, CA 90073 USA.
[Tsu, Jin-Wen] Kaiser Permanente So Calif, Dept Res & Evaluat, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0892-7790
J9 J ENDOUROL
JI J. Endourol.
PD NOV
PY 2011
VL 25
SU 1
BP A95
EP A95
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA 844ZI
UT WOS:000296792200292
ER
PT J
AU Siddiqui, M
Prien, EL
Dretler, SP
Sacco, DE
AF Siddiqui, Mohummad
Prien, Edwin L.
Dretler, Stephen P.
Sacco, Dianne E.
TI PROSPECTIVE INTERVENTIONAL TRIAL OF CALCIUM CARBONATE SUPPLEMENTS ON
HYPEROXALURIA IN STONE FORMERS
SO JOURNAL OF ENDOUROLOGY
LA English
DT Meeting Abstract
C1 [Siddiqui, Mohummad; Prien, Edwin L.; Dretler, Stephen P.; Sacco, Dianne E.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Urol, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0892-7790
J9 J ENDOUROL
JI J. Endourol.
PD NOV
PY 2011
VL 25
SU 1
BP A46
EP A46
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA 844ZI
UT WOS:000296792200146
ER
PT J
AU Siddiqui, MM
Alvi, K
Sharif-Tabrizi, A
Dretler, SP
Sacco, D
AF Siddiqui, Mohummad Minhaj
Alvi, Kashif
Sharif-Tabrizi, Ahmad
Dretler, Stephen P.
Sacco, Dianne
TI CHANGES IN STONE COMPOSITION IN REPEAT STONE FORMERS
SO JOURNAL OF ENDOUROLOGY
LA English
DT Meeting Abstract
C1 [Siddiqui, Mohummad Minhaj; Alvi, Kashif; Sharif-Tabrizi, Ahmad; Dretler, Stephen P.; Sacco, Dianne] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Urol, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0892-7790
J9 J ENDOUROL
JI J. Endourol.
PD NOV
PY 2011
VL 25
SU 1
BP A48
EP A48
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA 844ZI
UT WOS:000296792200151
ER
PT J
AU Yamamoto, H
Negro, CLA
Gomez-Sancha, F
Bachmann, A
Choi, BB
Tabatabaei, S
Malek, RS
Woo, H
Muir, G
AF Yamamoto, Hidekazu
Negro, C. L. A.
Gomez-Sancha, F.
Bachmann, A.
Choi, B. B.
Tabatabaei, S.
Malek, R. S.
Woo, H.
Muir, G.
TI GREENLIGHT HPS LASER PROSTATECTOMY IS SAFE AND GIVES EXCELLENT
FUNCTIONAL RESULTS AT MEDIUM-TERM FOLLOW-UP. A PROSPECTIVE INTERNATIONAL
MULTICENTRE STUDY
SO JOURNAL OF ENDOUROLOGY
LA English
DT Meeting Abstract
C1 [Yamamoto, Hidekazu; Negro, C. L. A.; Malek, R. S.; Woo, H.; Muir, G.] Kings Coll Hosp, London, England.
[Gomez-Sancha, F.] Inst Adv Urol Surg, Madrid, Spain.
[Bachmann, A.] Univ Basel Hosp, Dept Urol, CH-4031 Basel, Switzerland.
[Choi, B. B.] Weill Cornell Med Ctr, Dept Urol, New York, NY USA.
[Tabatabaei, S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Malek, R. S.] Westmead Hosp, Dept Urol, Sydney, NSW, Australia.
Mayo Clin, Dept Urol, Rochester, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0892-7790
J9 J ENDOUROL
JI J. Endourol.
PD NOV
PY 2011
VL 25
SU 1
BP A39
EP A39
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA 844ZI
UT WOS:000296792200123
ER
PT J
AU Harris, RS
Venegas, JG
Wongviriyawong, C
Winkler, T
Kone, M
Musch, G
Melo, MFV
de Prost, N
Hamilos, DL
Afshar, R
Cho, J
Luster, AD
Medoff, BD
AF Harris, R. Scott
Venegas, Jose G.
Wongviriyawong, Chanikarn
Winkler, Tilo
Kone, Mamary
Musch, Guido
Melo, Marcos F. Vidal
de Prost, Nicolas
Hamilos, Daniel L.
Afshar, Roshi
Cho, Josalyn
Luster, Andrew D.
Medoff, Benjamin D.
TI F-18-FDG Uptake Rate Is a Biomarker of Eosinophilic Inflammation and
Airway Response in Asthma
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE airway constriction; ventilation-perfusion ratio; pulmonary gas
exchange; fluorine isotopes; emission-computed tomography; nitrogen
isotopes
ID POSITRON-EMISSION-TOMOGRAPHY; BRAIN TRANSFER CONSTANTS; ACUTE LUNG
INJURY; TIME UPTAKE DATA; GRAPHICAL EVALUATION; VENTILATION DEFECTS;
ATOPIC ASTHMA; KINETICS; PET; MEPOLIZUMAB
AB In asthma, the relationship among airway inflammation, airway hyperresponsiveness, and lung function is poorly understood. Methods to noninvasively assess these relationships in human subjects are needed. We sought to determine whether F-18-FDG uptake rate (K-i, min(-1)) could serve as a biomarker of eosinophilic inflammation and local lung function. Methods: We used PET/CT to assess regional pulmonary perfusion ((Q) over dot), specific ventilation per unit volume (s(V) over dot(A)), fractional gas content (Fgas), airway wall thickness, and regional K-i 10 h after segmental allergen challenge to the right middle lobe in 6 asthmatic subjects with demonstrated atopy. (Q) over dot, s(V) over dot(A), and Fgas in the allergen-challenged lobe were compared with the right upper lobe, where diluent was applied as a control. The airway wall thickness aspect ratio (omega) of the allergen-challenged airway was compared with those of similarly sized airways from unaffected areas of the lung. Differences in K-i between allergen and diluent segments were compared with those in cell counts obtained 24 h after the allergen challenge by a bronchoalveolar lavage of the respective segments. Results: We found systematic reductions in regional (Q) over dot, s(V) over dot(A), and Fgas and increased v in all subjects. The ratio of eosinophil count (allergen to diluent) was linearly related (R-2 = 0.9917, P < 0.001) to the ratio of K-i. Conclusion: Regional K-i measured with PET is a noninvasive and highly predictive biomarker of eosinophilic airway inflammation and its functional effects. This method may serve to help in the understanding of allergic inflammation and test the therapeutic effectiveness of novel drugs or treatments.
C1 [Harris, R. Scott; Kone, Mamary; Hamilos, Daniel L.; Afshar, Roshi; Cho, Josalyn; Luster, Andrew D.; Medoff, Benjamin D.] Massachusetts Gen Hosp, Pulm & Crit Care Unit, Dept Med, Boston, MA 02114 USA.
[Harris, R. Scott; Kone, Mamary; Hamilos, Daniel L.; Afshar, Roshi; Cho, Josalyn; Luster, Andrew D.; Medoff, Benjamin D.] Massachusetts Gen Hosp, Allergy & Immunol Unit, Dept Med, Boston, MA 02114 USA.
[Harris, R. Scott; Venegas, Jose G.; Wongviriyawong, Chanikarn; Winkler, Tilo; Kone, Mamary; Musch, Guido; Melo, Marcos F. Vidal; de Prost, Nicolas; Hamilos, Daniel L.; Afshar, Roshi; Cho, Josalyn; Luster, Andrew D.; Medoff, Benjamin D.] Harvard Univ, Sch Med, Boston, MA USA.
[Venegas, Jose G.; Wongviriyawong, Chanikarn; Winkler, Tilo; Musch, Guido; Melo, Marcos F. Vidal; de Prost, Nicolas] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
RP Harris, RS (reprint author), Massachusetts Gen Hosp, Pulm & Crit Care Unit, Dept Med, Bulfinch 148,55 Fruit St, Boston, MA 02114 USA.
EM rsharris@mgh.harvard.edu
RI Winkler, Tilo/B-5337-2009;
OI Winkler, Tilo/0000-0002-7276-5550; de Prost, Nicolas/0000-0002-4833-4320
FU NIH [HL088297, HL07874, AI40618, HL68011, AI095261, HL-04501]
FX We thank Mary Loveless and Melissa Bruen for technical assistance with
image acquisition and processing; Carol Leary for help with the human
studies protocol; Allegra Bruce, Peter Rice, and Ronald Callahan for
radiation safety and quality assurance testing of the radioisotopes; and
John Correia, William Bucelewicz, and David Lee for preparation of the
radioisotopes. This work was supported by grants from the NIH: HL088297,
HL07874, AI40618, HL68011, AI095261, and HL-04501. No other potential
conflict of interest relevant to this article was reported.
NR 29
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Z9 23
U1 0
U2 2
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD NOV 1
PY 2011
VL 52
IS 11
BP 1713
EP 1720
DI 10.2967/jnumed.110.086355
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 844BJ
UT WOS:000296722000015
PM 21990575
ER
PT J
AU Bona, K
Bates, J
Wolfe, J
AF Bona, Kira
Bates, Jennifer
Wolfe, Joanne
TI Massachusetts' Pediatric Palliative Care Network: Successful
Implementation of a Novel State-Funded Pediatric Palliative Care Program
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Article
AB Background: U.S. children with life-limiting illness face barriers to accessing palliative care. In 2006, Massachusetts signed into law a statute providing for the creation and funding of the Pediatric Palliative Care Network (PPCN). This innovative, exclusively state-funded program provides comprehensive direct and consultative community-based pediatric palliative care services including: (1) pain and symptom management, (2) case management and assessment, (3) social services, counseling, and bereavement services, (4) volunteer support services, (5) respite services, and (6) complementary therapies. Provision of care is through a network of state-licensed hospice programs, and an array of professional and volunteer services.
Objective: To describe Massachusetts' experience in implementing a novel pediatric palliative care program.
Design: Enrollment and service trends were identified using Massachusetts Department of Public Health administrative data. Responses to a written family satisfaction survey provided to each family enrolled on PPCN are summarized.
Results: In fiscal year 2010, PPCN partnered with 11 hospice programs to provide services to 227 children with life-limiting illness. A total of $680,850 (86.7%) of state funding went to direct contract funds for hospices. Admitting diagnoses included cancer (30%), chromosomal abnormalities (17%), neurodegenerative disorders (15%), and other (38%). There were 11 deaths, 100% of which occurred in the family's requested location. Median length of stay on service prior to death was 233 days. Families most commonly implemented psychosocial and case management services, followed by complementary therapies, and volunteer services.
Conclusions: Successful implementation of a statewide pediatric palliative care program as modeled in Massachusetts is highly feasible at relatively low cost.
C1 [Wolfe, Joanne] Dana Farber Canc Inst, Dept Psychosocial Oncol & Palliat Care, Ctr Outcomes & Policy Res, Boston, MA 02215 USA.
[Bona, Kira; Wolfe, Joanne] Childrens Hosp, Dept Med, Boston, MA 02115 USA.
[Bona, Kira; Wolfe, Joanne] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02215 USA.
[Bates, Jennifer] Massachusetts Dept Publ Hlth, Pediat Palliat Care Network, Boston, MA USA.
RP Wolfe, J (reprint author), Dana Farber Canc Inst, Dept Psychosocial Oncol & Palliat Care, Ctr Outcomes & Policy Res, 450 Brookline Ave SM-206, Boston, MA 02215 USA.
EM joanne_wolfe@dfci.harvard.edu
NR 17
TC 14
Z9 14
U1 1
U2 6
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-6218
J9 J PALLIAT MED
JI J. Palliat. Med.
PD NOV
PY 2011
VL 14
IS 11
BP 1217
EP 1223
DI 10.1089/jpm.2011.0070
PG 7
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 843HV
UT WOS:000296663800008
PM 21823906
ER
PT J
AU Higgs, MH
Spain, WJ
AF Higgs, Matthew H.
Spain, William J.
TI Kv1 channels control spike threshold dynamics and spike timing in
cortical pyramidal neurones
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Article
ID AXON INITIAL SEGMENT; ACTION-POTENTIAL INITIATION; HIGH-FREQUENCY
OSCILLATIONS; AVIAN COCHLEAR NUCLEUS; COINCIDENCE DETECTION; FAST
RIPPLES; IN-VIVO; EPILEPTIC HIPPOCAMPUS; POTASSIUM CHANNELS; AUDITORY
NEURONS
AB Previous studies showed that cortical pyramidal neurones (PNs) have a dynamic spike threshold that functions as a high-pass filter, enhancing spike timing in response to high-frequency input. While it is commonly assumed that Na(+) channel inactivation is the primary mechanism of threshold accommodation, the possible role of K(+) channel activation in fast threshold changes has not been well characterized. The present study tested the hypothesis that low-voltage activated Kv1 channels affect threshold dynamics in layer 2-3 PNs, using alpha-dendrotoxin (DTX) or 4-aminopyridine (4-AP) to block these conductances. We found that Kv1 blockade reduced the dynamic changes of spike threshold in response to a variety of stimuli, including stimulus-evoked synaptic input, current steps and ramps of varied duration, and noise. Analysis of the responses to noise showed that Kv1 channels increased the coherence of spike output with high-frequency components of the stimulus. A simple model demonstrates that a dynamic spike threshold can account for this effect. Our results show that the Kv1 conductance is a major mechanism that contributes to the dynamic spike threshold and precise spike timing of cortical PNs.
C1 [Higgs, Matthew H.; Spain, William J.] Dept Vet Affairs Med Ctr, Neurol Sect, Seattle, WA USA.
[Higgs, Matthew H.; Spain, William J.] Univ Washington, Dept Physiol & Biophys, Seattle, WA 98195 USA.
[Spain, William J.] Univ Washington, Dept Neurol, Seattle, WA 98195 USA.
RP Higgs, MH (reprint author), Vet Affairs Puget Sound Hlth Care Syst, Neurol Mail Stop 127,1660 S Columbian Way, Seattle, WA 98108 USA.
EM higgsm@uw.edu
FU US Department of Veterans Affairs, Office of Research and Development,
Biomedical Laboratory; Veterans Affairs Merit Review; Veterans Affairs
Epilepsy Centre of Excellence
FX This material is based on work supported by the US Department of
Veterans Affairs, Office of Research and Development, Biomedical
Laboratory Research Program. Funding was provided by a Veterans Affairs
Merit Review to W.J.S. and a Veterans Affairs Epilepsy Centre of
Excellence. We thank Robert Foehring and Adrienne Fairhall for helpful
discussions, Steve Redman for helpful comments on the manuscript, and
Susan Usher for excellent technical assistance.
NR 60
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U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-3751
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD NOV
PY 2011
VL 589
IS 21
BP 5125
EP 5142
DI 10.1113/jphysiol.2011.216721
PG 18
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 839MA
UT WOS:000296369000012
PM 21911608
ER
PT J
AU Burstein, HJ
AF Burstein, Harold J.
TI The Continuity of Care Checklist: A Critical Frontier in Patient Safety
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Editorial Material
C1 [Burstein, Harold J.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Burstein, Harold J.] Dana Farber Canc Inst, Boston, MA USA.
[Burstein, Harold J.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Burstein, HJ (reprint author), Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
NR 2
TC 1
Z9 1
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 NOV
PY 2011
VL 9
IS 11
BP 1217
EP 1218
PG 2
WC Oncology
SC Oncology
GA 845VR
UT WOS:000296853400002
PM 22056653
ER
PT J
AU Benson, AB
Arnoletti, JP
Bekaii-Saab, T
Chan, E
Chen, YJ
Choti, MA
Cooper, HS
Dilawari, RA
Engstrom, PF
Enzinger, PC
Fleshman, JW
Fuchs, CS
Grem, JL
Knol, JA
Leong, LA
Lin, E
May, KS
Mulcahy, MF
Murphy, K
Rohren, E
Ryan, DP
Saltz, L
Sharma, S
Shibata, D
Skibber, JM
Small, W
Sofocleous, CT
Venook, AP
Willett, C
AF Benson, Al B., III
Arnoletti, J. Pablo
Bekaii-Saab, Tanios
Chan, Emily
Chen, Yi-Jen
Choti, Michael A.
Cooper, Harry S.
Dilawari, Raza A.
Engstrom, Paul F.
Enzinger, Peter C.
Fleshman, James W., Jr.
Fuchs, Charles S.
Grem, Jean L.
Knol, James A.
Leong, Lucille A.
Lin, Edward
May, Kilian Salerno
Mulcahy, Mary F.
Murphy, Kate
Rohren, Eric
Ryan, David P.
Saltz, Leonard
Sharma, Sunil
Shibata, David
Skibber, John M.
Small, William, Jr.
Sofocleous, Constantinos T.
Venook, Alan P.
Willett, Christopher
TI Clinical Practice Guidelines in Oncology
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Review
DE NCCN Clinical Practice Guidelines; NCCN Guidelines; colonic neoplasms;
colorectal surgery; adjuvant chemotherapy; 5-fluorouracil;
adenocarcinoma; neoplasm staging; neoplasm recurrence; irinotecan;
oxaliplatin; capecitabine; bevacizumab; cetuximab; panitumumab;
metastatic colorectal cancer; neoadjuvant therapy; liver resection
ID METASTATIC COLORECTAL-CANCER; III COLON-CANCER; CAPECITABINE PLUS
OXALIPLATIN; GROWTH-FACTOR RECEPTOR; RANDOMIZED PHASE-III; HIGH-DOSE
LEUCOVORIN; UNRESECTABLE LIVER METASTASES; SURGICAL ADJUVANT BREAST;
DISEASE-FREE SURVIVAL; LONG-TERM SURVIVAL
C1 [Benson, Al B., III; Mulcahy, Mary F.; Small, William, Jr.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Arnoletti, J. Pablo] Univ Alabama Birmingham, Ctr Comprehens Canc, Birmingham, AL 35294 USA.
[Bekaii-Saab, Tanios] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Chan, Emily] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Choti, Michael A.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Sidney, BC, Canada.
[Cooper, Harry S.; Engstrom, Paul F.] Fox Chase Canc Ctr, Philadelphia, PA USA.
[Dilawari, Raza A.] Univ Tennessee, St Jude Childrens Res Hosp, Inst Canc, Knoxville, TN 37996 USA.
[Fleshman, James W., Jr.] Washington Univ, Sch Med, St Louis, MO 63130 USA.
[Fleshman, James W., Jr.] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO USA.
[Grem, Jean L.] Nebraska Med Ctr, UNMC Eppley Canc Ctr, Omaha, NE USA.
[Knol, James A.] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Lin, Edward] Seattle Canc Care Alliance, Fred Hutchinson Canc Res Ctr, Seattle, WA USA.
[May, Kilian Salerno] Roswell Pk Canc Inst, Buffalo, NY USA.
[Rohren, Eric; Skibber, John M.] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
[Ryan, David P.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Saltz, Leonard; Sofocleous, Constantinos T.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[Sharma, Sunil] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[Shibata, David] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Venook, Alan P.] UCSF Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
RP Benson, AB (reprint author), Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
OI Saltz, Leonard/0000-0001-8353-4670
NR 397
TC 19
Z9 20
U1 2
U2 8
PU HARBORSIDE PRESS
PI COLD SPRING HARBOR
PA 37 MAIN ST, COLD SPRING HARBOR, NY 11724 USA
SN 1540-1405
EI 1540-1413
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD NOV
PY 2011
VL 9
IS 11
BP 1238
EP 1290
PG 53
WC Oncology
SC Oncology
GA 845VR
UT WOS:000296853400005
PM 22056656
ER
PT J
AU Wierwille, J
Andrews, PM
Onozato, ML
Jiang, J
Cable, A
Chen, Y
AF Wierwille, Jeremiah
Andrews, Peter M.
Onozato, Maristela L.
Jiang, James
Cable, Alex
Chen, Yu
TI In vivo, label-free, three-dimensional quantitative imaging of kidney
microcirculation using Doppler optical coherence tomography
SO LABORATORY INVESTIGATION
LA English
DT Article
DE doppler optical coherence tomography (DOCT); glomerular blood flow;
kidney microcirculation; optical coherence tomography (OCT)
ID RENAL BLOOD-FLOW; SCANNING CONFOCAL MICROSCOPY;
POSITRON-EMISSION-TOMOGRAPHY; MULTIPHOTON MICROSCOPY; ANGIOTENSIN-II;
DIABETIC-NEPHROPATHY; PERFUSION INDEX; HIGH-SPEED; HEMODYNAMICS;
CONTRAST
AB Doppler optical coherence tomography (DOCT) is a functional extension of optical coherence tomography (OCT) and is currently being employed in several clinical arenas to quantify blood flow in vivo. In this study, the objective was to investigate the feasibility of DOCT to image kidney microcirculation, specifically, glomerular blood flow. DOCT is able to capture three-dimensional (3D) data sets consisting of a series of cross-sectional images in real time, which enables label-free and non-destructive quantification of glomerular blood flow. The kidneys of adult, male Munich-Wistar rats were exposed through laparotomy procedure after being anesthetized. Following exposure of the kidney beneath the DOCT microscope, glomerular blood flow was observed. The effects of acute mannitol and angiotensin II infusion were also observed. Glomerular blood flow was quantified for the induced physiological states and compared with baseline measurements. Glomerular volume, cumulative Doppler volume, and Doppler flow range parameters were computed from 3D OCT/DOCT data sets. Glomerular size was determined from OCT, and DOCT readily revealed glomerular blood flow. After infusion of mannitol, a significant increase in blood flow was observed and quantified, and following infusion of angiontensin II, a significant decrease in blood flow was observed and quantified. Also, blood flow histograms were produced to illustrate differences in blood flow rate and blood volume among the induced physiological states. We demonstrated 3D DOCT imaging of rat kidney microcirculation in the glomerulus in vivo. Dynamic changes in blood flow were detected under altered physiological conditions demonstrating the real-time imaging capability of DOCT. This method holds promise to allow non-invasive imaging of kidney blood flow for transplant graft evaluation or monitoring of altered-renal hemodynamics related to disease progression. Laboratory Investigation (2011) 91, 1596-1604; doi: 10.1038/labinvest.2011.112; published online 1 August 2011
C1 [Wierwille, Jeremiah; Chen, Yu] Univ Maryland, Fischell Dept Bioengn, College Pk, MD 20742 USA.
[Andrews, Peter M.] Georgetown Univ, Dept Biochem, Washington, DC USA.
[Onozato, Maristela L.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA USA.
[Jiang, James; Cable, Alex] Thorlabs Inc, Newton, NJ USA.
RP Chen, Y (reprint author), Univ Maryland, Fischell Dept Bioengn, 2218 Jeong H Kim Bldg, College Pk, MD 20742 USA.
EM yuchen@umd.edu
FU State of Maryland; Minta Martin Foundation; Prevent Cancer Foundation;
UMB-UMCP SEED; A. Ward Ford Memorial Research Grant; NIH [R21-EB012215]
FX This work is supported in part by the Nanobiotechnology Award of the
State of Maryland, the Minta Martin Foundation, the Prevent Cancer
Foundation, the UMB-UMCP SEED Grant Program, the A. Ward Ford Memorial
Research Grant, and NIH R21-EB012215.
NR 74
TC 13
Z9 14
U1 1
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
EI 1530-0307
J9 LAB INVEST
JI Lab. Invest.
PD NOV
PY 2011
VL 91
IS 11
BP 1596
EP 1604
DI 10.1038/labinvest.2011.112
PG 9
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 842MK
UT WOS:000296603400005
PM 21808233
ER
PT J
AU Anttonen, M
Farkkila, A
Tauriala, H
Kauppinen, M
MacLaughlin, DT
Unkila-Kallio, L
Butzow, R
Heikinheimo, M
AF Anttonen, Mikko
Farkkila, Anniina
Tauriala, Hanna
Kauppinen, Marjut
MacLaughlin, David T.
Unkila-Kallio, Leila
Butzow, Ralf
Heikinheimo, Markku
TI Anti-Mullerian hormone inhibits growth of AMH type II receptor-positive
human ovarian granulosa cell tumor cells by activating apoptosis
SO LABORATORY INVESTIGATION
LA English
DT Article
DE ALK; cancer treatment; Mullerian inhibiting substance; ovarian cancer;
sex cord stromal tumor; Smad
ID CANCER IN-VIVO; PROGNOSTIC-FACTORS; ENHANCED PURIFICATION; INDEPENDENT
MECHANISM; SIGNAL-TRANSDUCTION; DUCT REGRESSION; TGF-BETA; SUBSTANCE;
EXPRESSION; FOXL2
AB Ovarian granulosa cell tumors (GCTs) are sex cord stromal tumors that constitute 3-5% of all ovarian cancers. GCTs usually present with an indolent course but there is a high risk of recurrence, which associates with increased mortality, and targeted treatments would be desirable. Anti-Mullerian hormone (AMH), a key factor regulating sexual differentiation of the reproductive organs, has been implicated as a growth inhibitor in ovarian cancer. GCTs and normal granulosa cells produce AMH, but its expression in large GCTs is usually downregulated. Further, as the lack of specific AMH-signaling pathway components leads to GCT development in mice, we hypothesized that AMH inhibits growth of GCTs. Utilizing a large panel of human GCT tissue samples, we found that AMH type I receptors (ALK2, ALK3 and ALK6) and type II receptor (AMHRII), as well as their downstream effectors Smad1/5, are expressed and active in GCTs. AMHRII expression was detected in the vast majority (96%) of GCTs and correlated with AMH mRNA and protein expression. AMH mRNA level was low in large GCTs, confirming previous findings on low-AMH protein expression in large human as well as mouse GCTs. To study the functional role of AMH in this peculiar ovarian cancer, we utilized a human GCT cell line (KGN) and 10 primary GCT cell cultures. We found that the AMH-Smad1/5-signaling pathway was active in these cells, and that exogenous AMH further activated Smad1/5 in KGN cells. Furthermore, AMH treatment reduced the number of KGN cells and primary GCT cells, with increasing amounts of AMH leading to augmented activation of caspase-3 and subsequent apoptosis. All in all, these data support the premise that AMH is a growth inhibitor of GCTs. Laboratory Investigation (2011) 91, 1605-1614; doi:10.1038/labinvest.2011.116; published online 1 August 2011
C1 [Anttonen, Mikko; Farkkila, Anniina; Unkila-Kallio, Leila; Butzow, Ralf] Univ Helsinki, Dept Obstet & Gynecol, Helsinki 00029, Finland.
[Anttonen, Mikko] Univ Helsinki, Cent Hosp, Biomedicum 2U, Helsinki 00029, Finland.
[Anttonen, Mikko; Farkkila, Anniina; Tauriala, Hanna; Kauppinen, Marjut; Heikinheimo, Markku] Univ Helsinki, Childrens Hosp, Pediat Res Ctr, Helsinki 00029, Finland.
[Anttonen, Mikko; Farkkila, Anniina; Unkila-Kallio, Leila; Butzow, Ralf; Heikinheimo, Markku] Univ Helsinki, Program Womens Hlth, Helsinki 00029, Finland.
[MacLaughlin, David T.] Harvard Univ, Sch Med, Boston, MA USA.
[MacLaughlin, David T.] Massachusetts Gen Hosp, Pediat Surg Res Labs, Boston, MA 02114 USA.
[Butzow, Ralf] Univ Helsinki, Dept Pathol, Helsinki 00029, Finland.
[Heikinheimo, Markku] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA.
RP Anttonen, M (reprint author), Univ Helsinki, Dept Obstet & Gynecol, POB 705, Helsinki 00029, Finland.
EM mikko.anttonen@helsinki.fi
FU Academy of Finland; National Clinical Graduate School; Helsinki
University Central Hospital; Sigrid Juselius Foundation; Finnish Cancer
Organizations
FX We thank all the gynecologists and operation room staff for supporting
the patient recruitment and tissue sample collection for the entire GCT
project. We also thank Taru Jokinen and Teija Karkkulainen for excellent
assistance, and Dr T Yanase and Dr I Navarro-Teulon for kindly providing
the KGN cell line and the AMHRII antibody, respectively. This study was
supported by grants from the Academy of Finland (to MA and MH), the
National Clinical Graduate School (to AF), Helsinki University Central
Hospital Research Funds (to MA, LU-K, RB, and MH), the Sigrid Juselius
Foundation (to MH), and Finnish Cancer Organizations (to MH).
NR 62
TC 9
Z9 13
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
EI 1530-0307
J9 LAB INVEST
JI Lab. Invest.
PD NOV
PY 2011
VL 91
IS 11
BP 1605
EP 1614
DI 10.1038/labinvest.2011.116
PG 10
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 842MK
UT WOS:000296603400006
PM 21808236
ER
PT J
AU Regan, MM
Neven, P
Giobbie-Hurder, A
Goldhirsch, A
Ejlertsen, B
Mauriac, L
Forbes, JF
Smith, I
Lang, I
Wardley, A
Rabaglio, M
Price, KN
Gelber, RD
Coates, AS
Thurlimann, B
AF Regan, Meredith M.
Neven, Patrick
Giobbie-Hurder, Anita
Goldhirsch, Aron
Ejlertsen, Bent
Mauriac, Louis
Forbes, John F.
Smith, Ian
Lang, Istvan
Wardley, Andrew
Rabaglio, Manuela
Price, Karen N.
Gelber, Richard D.
Coates, Alan S.
Thuerlimann, Beat
CA BIG 1-98 Collaborative Grp
IBCSG
TI Assessment of letrozole and tamoxifen alone and in sequence for
postmenopausal women with steroid hormone receptor-positive breast
cancer: the BIG 1-98 randomised clinical trial at 8.1 years median
follow-up
SO LANCET ONCOLOGY
LA English
DT Article
ID ADJUVANT ENDOCRINE THERAPY; COMPARING LETROZOLE; DOUBLE-BLIND; PHASE-III
AB Background Postmenopausal women with hormone receptor-positive early breast cancer have persistent, long-term risk of breast-cancer recurrence and death. Therefore, trials assessing endocrine therapies for this patient population need extended follow-up. We present an update of efficacy outcomes in the Breast International Group (BIG) 1-98 study at 8.1 years median follow-up.
Methods BIG 1-98 is a randomised, phase 3, double-blind trial of postmenopausal women with hormone receptor-positive early breast cancer that compares 5 years of tamoxifen or letrozole monotherapy, or sequential treatment with 2 years of one of these drugs followed by 3 years of the other. Randomisation was done with permuted blocks, and stratified according to the two-arm or four-arm randomisation option, participating institution, and chemotherapy use. Patients, investigators, data managers, and medical reviewers were masked. The primary efficacy endpoint was disease-free survival (events were invasive breast cancer relapse, second primaries [ contralateral breast and non-breast], or death without previous cancer event). Secondary endpoints were overall survival, distant recurrence-free interval (DRFI), and breast cancer-free interval (BCFI). The monotherapy comparison included patients randomly assigned to tamoxifen or letrozole for 5 years. In 2005, after a significant disease-free survival benefit was reported for letrozole as compared with tamoxifen, a protocol amendment facilitated the crossover to letrozole of patients who were still receiving tamoxifen alone; Cox models and Kaplan-Meier estimates with inverse probability of censoring weighting (IPCW) are used to account for selective crossover to letrozole of patients (n=619) in the tamoxifen arm. Comparison of sequential treatments to letrozole monotherapy included patients enrolled and randomly assigned to letrozole for 5 years, letrozole for 2 years followed by tamoxifen for 3 years, or tamoxifen for 2 years followed by letrozole for 3 years. Treatment has ended for all patients and detailed safety results for adverse events that occurred during the 5 years of treatment have been reported elsewhere. Follow-up is continuing for those enrolled in the four-arm option. BIG 1-98 is registered at clinicaltrials.gov NCT00004205.
Findings 8010 patients were included in the trial, with a median follow-up of 8.1 years (range 0-12.4). 2459 were randomly assigned to monotherapy with tamoxifen for 5 years and 2463 to monotherapy with letrozole for 5 years. In the four-arm option of the trial, 1546 were randomly assigned to letrozole for 5 years, 1548 to tamoxifen for 5 years, 1540 to letrozole for 2 years followed by tamoxifen for 3 years, and 1548 to tamoxifen for 2 years followed by letrozole for 3 years. At a median follow-up of 8.7 years from randomisation (range 0-12.4), letrozole monotherapy was significantly better than tamoxifen, whether by IPCW or intention-to-treat analysis (IPCW disease-free survival HR 0.82 [95% CI 0.74-0.92], overall survival HR 0.79 [ 0.69-0.90], DRFI HR 0.79 [ 0.68-0.92], BCFI HR 0.80 [ 0.70-0.92]; intention-to-treat disease-free survival HR 0.86 [ 0.78-0.96], overall survival HR 0.87 [ 0.77-0.999], DRFI HR 0.86 [ 0.74-0.998], BCFI HR 0.86 [ 0.76-0.98]). At a median follow-up of 8.0 years from randomisation (range 0-11.2) for the comparison of the sequential groups with letrozole monotherapy, there were no statistically significant differences in any of the four endpoints for either sequence. 8-year intention-to-treat estimates (each with SE <= 1.1%) for letrozole monotherapy, letrozole followed by tamoxifen, and tamoxifen followed by letrozole were 78.6%, 77.8%, 77.3% for disease-free survival; 87.5%, 87.7%, 85.9% for overall survival; 89.9%, 88.7%, 88.1% for DRFI; and 86.1%, 85.3%, 84.3% for BCFI.
Interpretation For postmenopausal women with endocrine-responsive early breast cancer, a reduction in breast cancer recurrence and mortality is obtained by letrozole monotherapy when compared with tamoxifen montherapy. Sequential treatments involving tamoxifen and letrozole do not improve outcome compared with letrozole monotherapy, but might be useful strategies when considering an individual patient's risk of recurrence and treatment tolerability.
C1 [Regan, Meredith M.; Giobbie-Hurder, Anita; Price, Karen N.; Gelber, Richard D.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Ctr Stat, IBCSG, Boston, MA 02215 USA.
[Regan, Meredith M.; Gelber, Richard D.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Neven, Patrick] Catholic Univ Louvain, Univ Hosp Gasthuisberg, Dept Med Oncol, B-3000 Louvain, Belgium.
[Goldhirsch, Aron] European Inst Oncol, Milan, Italy.
[Goldhirsch, Aron] St Anna Clin, Swiss Ctr Breast Hlth, Lugano, Switzerland.
[Ejlertsen, Bent] Rigshosp, Danish Breast Canc Cooperat Grp DBCG, DK-2100 Copenhagen, Denmark.
[Mauriac, Louis] Inst Bergonie, Federat Natl Ctr Lutte Canc, Bordeaux, France.
[Forbes, John F.] Univ Newcastle, Australian New Zealand Breast Canc Trials Grp, Newcastle, NSW 2300, Australia.
[Smith, Ian] Royal Marsden Hosp, London SW3 6JJ, England.
[Smith, Ian] Royal Marsden NHS Trust, Surrey, England.
[Lang, Istvan] Natl Inst Oncol, Budapest, Hungary.
[Wardley, Andrew] S Manchester Univ Hosp Trust, Christie Hosp NHS Trust, Manchester, Lancs, England.
[Rabaglio, Manuela] IBCSG Coordinating Ctr, Bern, Switzerland.
[Rabaglio, Manuela] Univ Bern, Inselspital, CH-3010 Bern, Switzerland.
[Price, Karen N.; Gelber, Richard D.] Frontier Sci & Technol Res Fdn Inc, Boston, MA USA.
[Coates, Alan S.] Int Breast Canc Study Grp, Sydney, NSW, Australia.
[Coates, Alan S.] Univ Sydney, Sydney, NSW 2006, Australia.
[Thuerlimann, Beat] Kantonsspital, Breast Ctr, St Gallen, Switzerland.
[Thuerlimann, Beat] Swiss Grp Clin Canc Res SAKK, Bern, Switzerland.
RP Regan, MM (reprint author), Dana Farber Canc Inst, Dept Biostat & Computat Biol, Ctr Stat, IBCSG, Mailstop CLS11007,450 Brookline Ave, Boston, MA 02215 USA.
EM mregan@jimmy.harvard.edu
RI Munzone, Elisabetta/G-8848-2011; friedlander, michael/G-3490-2013;
Cheuk, Robyn/H-1944-2013; GLADIEFF, Laurence/O-5129-2014; Wardley,
ANdrew/N-8135-2015; Gonzalez Larriba, Jose Luis/G-6177-2016; Petruzelka,
Lubos/A-2750-2017; Rimassa, Lorenza/N-4884-2016; Sedlackova,
Eva/B-9959-2017; Wyld, David/B-8893-2015; Procopio, Giuseppe/K-2072-2016
OI friedlander, michael/0000-0002-6488-0604; Cheuk,
Robyn/0000-0001-9516-5526; GLADIEFF, Laurence/0000-0002-6980-9719;
Wardley, ANdrew/0000-0002-9639-0888; Gonzalez Larriba, Jose
Luis/0000-0003-2631-0309; Petruzelka, Lubos/0000-0002-4397-0635;
Rimassa, Lorenza/0000-0001-9957-3615; Sedlackova,
Eva/0000-0002-0089-1611; Wyld, David/0000-0001-9523-4333; Procopio,
Giuseppe/0000-0002-2498-402X
FU Novartis; United States National Cancer Institute; International Breast
Cancer Study Group; Roche; Takeda; Swedish Cancer Society; Cancer
Council Australia; Australian New Zealand Breast Cancer Trials Group;
Frontier Science and Technology Research Foundation; Swiss Group for
Clinical Cancer Research (SAKK); United States National Cancer Institute
[CA-75362]; Cancer Research Switzerland/Oncosuisse; Foundation for
Clinical Cancer Research of Eastern Switzerland (OSKK)
FX Funding Novartis, United States National Cancer Institute, International
Breast Cancer Study Group.; AW had a consultant or advisory role for
Novartis and BE had a consultant or advisory role for Pfizer. BT own
stocks for Novartis. JFF has received honoraria from AstraZeneca; AW has
received honoraria from Novartis. AG has received honoraria from
Novartis and Pfizer. BT has received honoraria from AstraZeneca,
Novartis. RDG has received research funding from Novartis; BE has
received research funding from Novartis. AC has received travel grants
from Roche and Takeda. All other authors declared no conflicts of
interest.; The BIG 1-98 trial was financed by Novartis and coordinated
by International Breast Cancer Study Group (IBCSG). Other support for
the IBCSG was provided by: Swedish Cancer Society, The Cancer Council
Australia, Australian New Zealand Breast Cancer Trials Group, Frontier
Science and Technology Research Foundation, Swiss Group for Clinical
Cancer Research (SAKK), United States National Cancer Institute Grant
CA-75362, Cancer Research Switzerland/Oncosuisse, and the Foundation for
Clinical Cancer Research of Eastern Switzerland (OSKK).
NR 23
TC 137
Z9 143
U1 3
U2 34
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 NOV
PY 2011
VL 12
IS 12
BP 1101
EP 1108
DI 10.1016/S1470-2045(11)70270-4
PG 8
WC Oncology
SC Oncology
GA 842GC
UT WOS:000296581400019
PM 22018631
ER
PT J
AU Mar, BG
Amakye, D
Aifantis, I
Buonamici, S
AF Mar, B. G.
Amakye, D.
Aifantis, I.
Buonamici, S.
TI The controversial role of the Hedgehog pathway in normal and malignant
hematopoiesis
SO LEUKEMIA
LA English
DT Review
DE Hedgehog pathway; hematopoietic stem cells; Smoothened inhibitors;
chronic myeloid leukemia
ID CHRONIC MYELOID-LEUKEMIA; BASAL-CELL CARCINOMA; CHRONIC MYELOGENOUS
LEUKEMIA; CHRONIC MYELOCYTIC-LEUKEMIA; PATIENTS RECEIVING IMATINIB;
CANCER STEM-CELLS; MURINE YOLK-SAC; SONIC HEDGEHOG; BCR-ABL; SIGNALING
PATHWAY
AB Hedgehog (Hh) is a developmental signaling pathway in which Hh ligands bind Patched (Ptch), which relieves its inhibition of Smoothened (Smo), allowing the Gli family of transcription factors to translocate to the nucleus and activate Hh target genes. The role of Hh signaling in hematopoiesis is controversial and ill defined. Although some groups observed self-renewal defects with decreased replating and reduced efficiency of secondary murine transplants, other groups reported no hematopoietic phenotypes, which may be related to the timing of Hh abrogation. In malignant hematopoiesis, most attention has been focused on the role of Hh signaling in chronic myeloid leukemia (CML), considered by many to be a stem cell disorder that bears the constitutively active BCR-ABL tyrosine kinase. Despite the elimination of most leukemia cells through BCR-ABL inhibition, most patients remain PCR positive, suggesting that the putative CML stem cell may be resistant to kinase antagonism. Groups are now exploring the Hh pathway as an alternate pathway supporting CML stem cell survival. Knockdown or inhibition of Smo abrogates or delays the appearance of CML in several in vitro and in vivo models. These data have lead to clinical trials using BCR-ABL kinase and novel Smo inhibitors in combination. Leukemia (2011) 25, 1665-1673; doi:10.1038/leu.2011.143; published online 10 June 2011
C1 [Amakye, D.; Buonamici, S.] Novartis Inst Biomed Res, Dept Oncol, Cambridge, MA 02139 USA.
[Mar, B. G.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Aifantis, I.] NYU, Sch Med, Howard Hughes Med Inst, New York, NY USA.
[Aifantis, I.] NYU, Sch Med, Dept Pathol, New York, NY USA.
[Aifantis, I.] NYU, Sch Med, Helen & Martin S Kimmel Stem Cell Ctr, New York, NY USA.
RP Buonamici, S (reprint author), Novartis Inst Biomed Res, Dept Oncol, 250 Massachusetts Ave, Cambridge, MA 02139 USA.
EM silvia.buonamici@novartis.com
OI Mar, Brenton/0000-0002-3857-9324
FU National Institutes of Health [RO1CA133379, RO1CA105129, R21CA141399,
RO1CA149655]; Leukemia & Lymphoma Society; American Cancer Society
[RSG0806801]
FX We thank the Smoothened team and Yao Yung-mae at Novartis for
stimulating discussions and critical reading of the manuscript. IA is
supported by the National Institutes of Health (RO1CA133379,
RO1CA105129, R21CA141399 and RO1CA149655 to IA), the Leukemia & Lymphoma
Society and the American Cancer Society (RSG0806801 to IA). IA is a
Howard Hughes Medical Institute Early Career Scientist.
NR 96
TC 33
Z9 33
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD NOV
PY 2011
VL 25
IS 11
BP 1665
EP 1673
DI 10.1038/leu.2011.143
PG 9
WC Oncology; Hematology
SC Oncology; Hematology
GA 846RY
UT WOS:000296922100001
PM 21660044
ER
PT J
AU Tranah, GJ
Manini, TM
Lohman, KK
Nalls, MA
Kritchevsky, S
Newman, AB
Harris, TB
Miljkovic, I
Biffi, A
Cummings, SR
Liu, YM
AF Tranah, Gregory J.
Manini, Todd M.
Lohman, Kurt K.
Nalls, Michael A.
Kritchevsky, Stephen
Newman, Anne B.
Harris, Tamara B.
Miljkovic, Iva
Biffi, Alessandro
Cummings, Steven R.
Liu, Yongmei
TI Mitochondrial DNA variation in human metabolic rate and energy
expenditure
SO MITOCHONDRION
LA English
DT Article
DE Metabolic rate; Energetics; Mitochondria; Mitochondrial haplogroups;
mtDNA; Oxidative phosphorylation
ID DOUBLY-LABELED WATER; CYTOCHROME-C-OXIDASE; PHYSICAL-ACTIVITY;
DROSOPHILA-MELANOGASTER; ADAPTIVE SELECTION; HUMAN MTDNA; SPERM
MOTILITY; LONGEVITY; EPISTASIS; EVOLUTION
AB The role of climate in driving selection of mtDNA as Homo sapiens migrated out of Africa into Eurasia remains controversial. We evaluated the role of mtDNA variation in resting metabolic rate (RMR) and total energy expenditure (TEE) among 294 older, community-dwelling African and European American adults from the Health, Aging and Body Composition Study. Common African haplogroups L0, L2 and L3 had significantly lower RMRs than European haplogroups H, JT and UK with haplogroup L1 RMR being intermediate to these groups. This study links mitochondrial haplogroups with ancestry-associated differences in metabolic rate and energy expenditure. (C) 2011 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
C1 [Tranah, Gregory J.] UCSF, Calif Pacific Med Ctr Res Inst, San Francisco Coordinating Ctr, San Francisco, CA 94107 USA.
[Manini, Todd M.] Univ Florida, Dept Aging & Geriatr Res, Gainesville, FL 32601 USA.
[Lohman, Kurt K.] Wake Forest Univ, Bowman Gray Sch Med, Dept Biostat Sci, Winston Salem, NC 27157 USA.
[Nalls, Michael A.] NIA, Neurogenet Lab, Intramural Res Program, Bethesda, MD 20892 USA.
[Kritchevsky, Stephen; Liu, Yongmei] Wake Forest Univ, Bowman Gray Sch Med, Sticht Ctr Aging, Winston Salem, NC 27157 USA.
[Newman, Anne B.; Miljkovic, Iva] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15213 USA.
[Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Biffi, Alessandro] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Biffi, Alessandro] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Biffi, Alessandro] Broad Inst, Program Med & Populat Genet, Cambridge, MA 02142 USA.
RP Tranah, GJ (reprint author), UCSF, Calif Pacific Med Ctr Res Inst, San Francisco Coordinating Ctr, 185 Berry St,Lobby 4,Suite 5700, San Francisco, CA 94107 USA.
EM gtranah@sfcc-cpmc.edu
RI Newman, Anne/C-6408-2013;
OI Newman, Anne/0000-0002-0106-1150; Miljkovic, Iva/0000-0002-3155-9777;
Kritchevsky, Stephen/0000-0003-3336-6781
FU NIH, National Institute on Aging; NIA [N01AG62101, N01AG62103,
N01AG62106, 1R03AG032498-01, 1R01AG032098-01A1]; National Institutes of
Health [HHSN268200782096C]
FX This research is supported in part by the Intramural Research Program of
the NIH, National Institute on Aging. This research was supported by NIA
contracts N01AG62101, N01AG62103, N01AG62106 and NIA grant
1R03AG032498-01. The genome-wide association study was funded by NIA
grant 1R01AG032098-01A1 to Wake Forest University Health Sciences and
genotyping services were provided by the Center for Inherited Disease
Research (CIDR). CIDR is fully funded through a federal contract from
the National Institutes of Health to The Johns Hopkins University,
contract number HHSN268200782096C.
NR 66
TC 13
Z9 13
U1 1
U2 12
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1567-7249
J9 MITOCHONDRION
JI Mitochondrion
PD NOV
PY 2011
VL 11
IS 6
BP 855
EP 861
DI 10.1016/j.mito.2011.04.005
PG 7
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 846ZI
UT WOS:000296941300003
PM 21586348
ER
PT J
AU Hideshima, T
Richardson, PG
Anderson, KC
AF Hideshima, Teru
Richardson, Paul G.
Anderson, Kenneth C.
TI Mechanism of Action of Proteasome Inhibitors and Deacetylase Inhibitors
and the Biological Basis of Synergy in Multiple Myeloma
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Review
ID NF-KAPPA-B; UNFOLDED PROTEIN RESPONSE; ENDOTHELIAL GROWTH-FACTOR;
PANOBINOSTAT LBH589; PLUS DEXAMETHASONE; MOLECULAR SEQUELAE; MURINE
MODEL; CELL-GROWTH; PHASE-I; BORTEZOMIB
AB Novel agents, including the proteasome inhibitor bortezomib, have significantly improved the response and survival of patients with multiple myeloma over the last decade. Despite these advances, many patients relapse or do not benefit from the currently available therapies; thus, multiple myeloma remains an incurable disease. Deacetylase inhibitors (DACi), including panobinostat and vorinostat, have recently emerged as novel agents being evaluated in the treatment of multiple myeloma. Deacetylases are a group of enzymes with effects on various intracellular proteins, including histones, transcription factors, and molecular chaperones. Although DACi inhibit cell growth and induce apoptosis in multiple myeloma cells as a single agent, synergistic activity has been observed when they were used in combination with bortezomib. The mechanistic basis of synergy is multifactorial and includes disruption of protein degradation and inhibition of the interaction of multiple myeloma cells with the tumor microenvironment. This review summarizes recent advancements in the understanding of the mechanism of action of proteasome inhibitors and DACi in multiple myeloma and examines the biological basis of their synergistic effects. Data from the studies summarized here have been used as the rationale for the implementation of phase II and III clinical trials of DACi, alone and combined with bortezomib, in relapsed and refractory multiple myeloma. Mol Cancer Ther; 10(11); 2034-42. (C) 2011 AACR.
C1 [Hideshima, Teru] Dana Farber Canc Inst, Jerome Lipper Myeloma Ctr, Dept Med Oncol, Boston, MA 02115 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Hideshima, T (reprint author), Dana Farber Canc Inst, Jerome Lipper Myeloma Ctr, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM teru_hideshima@dfci.harvard.edu
FU NIH SPORE [IP50 CA-10070, PO-1 78378, RO-1 CA-50947]; LeBow Family Fund
to Cure Myeloma; American Cancer Society
FX This study is supported by NIH SPORE IP50 CA-10070, PO-1 78378, and RO-1
CA-50947 grants; the LeBow Family Fund to Cure Myeloma (K.C. Anderson);
and American Cancer Society Clinical Reward Professorship (K.C.
Anderson). Financial support for editorial assistance was provided by
Novartis.
NR 52
TC 106
Z9 109
U1 0
U2 14
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
EI 1538-8514
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD NOV
PY 2011
VL 10
IS 11
BP 2034
EP 2042
DI 10.1158/1535-7163.MCT-11-0433
PG 9
WC Oncology
SC Oncology
GA 844ZA
UT WOS:000296791300018
PM 22072815
ER
PT J
AU Underhill, ML
Dickerson, SS
AF Underhill, Meghan L.
Dickerson, Suzanne S.
TI Engaging in Medical Vigilance: Understanding the Personal Meaning of
Breast Surveillance
SO ONCOLOGY NURSING FORUM
LA English
DT Article
ID FAMILY-HISTORY; PSYCHOLOGICAL IMPACT; YOUNGER WOMEN; HIGH-RISK; GENETIC
PREDISPOSITION; HEREDITARY BREAST; SCREENING-PROGRAM; OVARIAN-CANCER;
MRI; MAMMOGRAPHY
AB Purpose/Objectives: To explore how women with a hereditary risk of breast cancer experience living with and managing that risk through surveillance.
Research Approach: Hermeneutic phenomenology guided the qualitative research design.
Setting: The Facing Our Risk of Cancer Empowered online organization.
Participants: 9 women undergoing breast surveillance for hereditary breast cancer risk recruited through purposive sampling.
Methodologic Approach: Data were collected through semistructured interviews lasting about an hour. A team approach guided data analysis of transcribed interview text based on a modified Diekelman, Allen, and Tanner method.
Main Research Variables: Lived experience and personal meaning of hereditary breast cancer risk and surveillance.
Findings: Hereditary risk of breast cancer involves a change in one's view of life and necessitates engaging in medical vigilance, often making these women feel ill when they are otherwise healthy. Most have personal family experiences of cancer and value surveillance, although they live with the "what if" of a cancer diagnosis when waiting for surveillance results. All women discussed a need for accurate information, support, and guidance from healthcare providers.
Conclusions: Women became their own experts at living with and managing hereditary breast cancer risk. Experiences and interactions within the healthcare system influenced the meaning of breast surveillance.
Interpretation: Nurses should be aware of the high level of knowledge among women living with hereditary risk and respect their knowledge by providing accurate and informed care. That can occur only through proper education of nurses and all healthcare professionals working with women at risk for hereditary breast cancer so that they understand current standards of care and how hereditary breast cancer risk-is defined and managed.
C1 [Underhill, Meghan L.] Dana Farber Canc Inst, Phyllis F Cantor Ctr Res Nursing & Patient Care S, Boston, MA 02115 USA.
[Underhill, Meghan L.] Univ Massachusetts, Sch Nursing, Boston, MA 02125 USA.
[Dickerson, Suzanne S.] SUNY Buffalo, Sch Nursing, Buffalo, NY 14260 USA.
RP Underhill, ML (reprint author), Dana Farber Canc Inst, Phyllis F Cantor Ctr Res Nursing & Patient Care S, Boston, MA 02115 USA.
EM meghanl_underhill@dfci.harvard.edu
NR 33
TC 4
Z9 4
U1 0
U2 5
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 0190-535X
J9 ONCOL NURS FORUM
JI Oncol. Nurs. Forum
PD NOV
PY 2011
VL 38
IS 6
BP 686
EP 694
DI 10.1188/11.ONF.686-694
PG 9
WC Oncology; Nursing
SC Oncology; Nursing
GA 846WE
UT WOS:000296933100010
PM 22037331
ER
PT J
AU Koyfman, A
Brem, E
Chiang, VW
AF Koyfman, Alex
Brem, Elizabeth
Chiang, Vincent W.
TI Thrombotic Thrombocytopenic Purpura
SO PEDIATRIC EMERGENCY CARE
LA English
DT Review
DE thrombotic thrombocytopenic purpura; fever; anemia; thrombocytopenia;
renal abnormalities; neurologic abnormalities
ID HEMOLYTIC-UREMIC SYNDROME; VON-WILLEBRAND-FACTOR; FACTOR-CLEAVING
PROTEASE; PLASMA-EXCHANGE; CLINICAL-OUTCOMES; ADAMTS13 ACTIVITY;
CYCLOSPORINE; RITUXIMAB; ADOLESCENTS; CHILDHOOD
AB In 1924, Dr Eli Moschcowitz described a 16-year-old adolescent girl with abrupt onset of petechiae, hemolytic anemia, followed by paralysis, coma, and death. Autopsy showed widespread hyaline thrombi in the terminal arterioles and capillaries of various organs. The syndrome described by Moschowitz is now known as thrombotic thrombocytopenic purpura.
C1 [Koyfman, Alex] Brigham & Womens Hosp, Dept Emergency Med, Boston, MA 02115 USA.
[Koyfman, Alex] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Brem, Elizabeth] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Chiang, Vincent W.] Childrens Hosp, Div Emergency Med, Boston, MA 02115 USA.
RP Koyfman, A (reprint author), Brigham & Womens Hosp, Dept Emergency Med, 75 Francis St,Neville House, Boston, MA 02115 USA.
EM akoyfman@partners.org
NR 27
TC 1
Z9 3
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0749-5161
J9 PEDIATR EMERG CARE
JI Pediatr. Emerg. Care
PD NOV
PY 2011
VL 27
IS 11
BP 1085
EP 1091
DI 10.1097/PEC.0b013e318236068c
PG 7
WC Emergency Medicine; Pediatrics
SC Emergency Medicine; Pediatrics
GA 844RB
UT WOS:000296763900020
PM 22068077
ER
PT J
AU Johnson, CV
Mimiaga, MJ
Reisner, SL
VanDerwarker, R
Mayer, KH
AF Johnson, Carey V.
Mimiaga, Matthew J.
Reisner, Sari L.
VanDerwarker, Rodney
Mayer, Kenneth H.
TI Barriers and Facilitators to Routine HIV Testing: Perceptions from
Massachusetts Community Health Center Personnel
SO AIDS PATIENT CARE AND STDS
LA English
DT Article
ID FOR-DISEASE-CONTROL; UNITED-STATES; REVISED RECOMMENDATIONS; CARE
SETTINGS; PREVALENCE; WOMEN; ADOLESCENTS; KNOWLEDGE; ADULTS
AB Since 2006, the Centers for Disease Control and Prevention (CDC) has recommended routine, voluntary HIV testing for persons aged 13-64 in all health care settings, including the elimination of separate informed consent, which remains in effect in five states including Massachusetts. Community health centers (CHCs) represent an important HIV testing site for at-risk populations. From April to December 2008 a qualitative interview was administered to one senior personnel from each of 30 CHCs in Massachusetts, to identify barriers and facilitators to implementing CDC recommendations and to elucidate strategies to improve routine HIV testing. The following themes emerged as routine HIV testing barriers: (1) provider time constraints, including time to administer counseling and separate informed consent; (2) lack of funding, staff, and space; (3) provider, patient, and community discomfort; (4) inconsistent levels of awareness regarding CDC recommendations; and (5) perceived incompatibility with Massachusetts HIV testing policy. Facilitators included designation of personnel to serve as organizational "champions" for routine testing and use of clinical reminders within electronic medical records to prompt HIV testing. Strategies identified to improve routine HIV testing rates among Massachusetts CHCs included more explicit state-level guidelines; organizational buy-in; collaborative analysis to integrate testing within existing activities; and provider, patient and community education.
C1 [Johnson, Carey V.; Mimiaga, Matthew J.; Reisner, Sari L.; VanDerwarker, Rodney; Mayer, Kenneth H.] Fenway Hlth, Fenway Inst, Boston, MA USA.
[Mimiaga, Matthew J.] Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Mimiaga, Matthew J.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Reisner, Sari L.] Harvard Univ, Sch Med, Dept Soc Human Dev & Hlth, Boston, MA USA.
[Mayer, Kenneth H.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
RP Mimiaga, MJ (reprint author), MGH Harvard Behav Med, 1 Bowdoin Sq,7th Floor, Boston, MA 02114 USA.
EM mmimiaga@partners.org
FU Gilead Science, Inc. [2691]
FX This project was supported by a Testing and Linkage to Care grant
(#2691) from Gilead Science, Inc. awarded to Drs. Mayer and Mimiaga, who
exercised full control over the project. The content is solely the
responsibility of the authors and does not necessarily represent the
official view of Gilead Science, Inc.
NR 35
TC 10
Z9 10
U1 1
U2 5
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1087-2914
J9 AIDS PATIENT CARE ST
JI Aids Patient Care STDS
PD NOV
PY 2011
VL 25
IS 11
BP 647
EP 655
DI 10.1089/apc.2011.0180
PG 9
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 842FD
UT WOS:000296577100004
PM 22023315
ER
PT J
AU Schacht, JP
Randall, PK
Waid, LR
Baros, AM
Latham, PK
Wright, TM
Myrick, H
Anton, RF
AF Schacht, Joseph P.
Randall, Patrick K.
Waid, L. R.
Baros, Alicia M.
Latham, Patricia K.
Wright, Tara M.
Myrick, Hugh
Anton, Raymond F.
TI Neurocognitive Performance, Alcohol Withdrawal, and Effects of a
Combination of Flumazenil and Gabapentin in Alcohol Dependence
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcoholism; Anticonvulsant; gamma-Aminobutyric Acid; Neurocognitive;
Withdrawal
ID ETHANOL WITHDRAWAL; GABA(A) RECEPTORS; SUBSTANCE-ABUSE; MULTIPLE
DETOXIFICATIONS; COGNITIVE IMPAIRMENT; HEALTHY-VOLUNTEERS;
GENE-EXPRESSION; OUTCOMES; CARBAMAZEPINE; INTERFERENCE
AB Background: Among some alcohol-dependent individuals, early alcohol abstinence is marked by alcohol withdrawal (AW), a phenomenon mediated by GABA and glutamate signaling. We previously reported that a combination of 2 medications that affect GABA and glutamate tone, gabapentin and flumazenil, more effectively reduced drinking among individuals with higher pretreatment AW (Anton et al., 2009). This study evaluated whether this finding is related to changes in neurocognitive performance, which is also affected by cortical GABA and glutamate tone.
Methods: Neurocognitive performance was assessed at baseline and twice during the first week of treatment among 60 alcohol-dependent participants in the previously published clinical trial.
Results: AW was associated with poorer baseline performance on 4 of 8 measures, and individuals with higher baseline AW who received the gabapentin and flumazenil combination demonstrated greater improvement on a measure of response inhibition than those with lower AW or those who received a combination of placebos. Improvement in response inhibition during the first week and medication group interacted in their effect on subsequent drinking, such that improvement predicted greater abstinence only among individuals who received gabapentin and flumazenil. Improvement on other neurocognitive measures was neither differentially impacted by medication or baseline AW nor related to subsequent drinking.
Conclusions: Taken together, these data suggest that acute AW accounts for a small proportion of variance in neurocognitive performance, that gabapentin and flumazenil slightly improve response inhibition during early abstinence, and that such improvement may somewhat reduce later drinking. However, these medications may not affect other neurocognitive domains.
C1 [Schacht, Joseph P.; Randall, Patrick K.; Waid, L. R.; Baros, Alicia M.; Latham, Patricia K.; Wright, Tara M.; Myrick, Hugh; Anton, Raymond F.] Med Univ S Carolina, Ctr Drug & Alcohol Programs, Charleston, SC 29425 USA.
[Wright, Tara M.; Myrick, Hugh] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
RP Schacht, JP (reprint author), Med Univ S Carolina, Ctr Drug & Alcohol Programs, 67 President St,MSC 861, Charleston, SC 29425 USA.
EM schacht@musc.edu
FU Hythiam, Inc.; National Institute on Alcohol Abuse and Alcoholism [T32
AA007474, K05 AA017435]
FX This work was conducted under an unrestricted grant from Hythiam, Inc.
JPS was supported by an institutional training grant (T32 AA007474) and
RFA by a senior scientist research and mentorship award (K05 AA017435)
from the National Institute on Alcohol Abuse and Alcoholism.
NR 68
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Z9 5
U1 6
U2 11
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD NOV
PY 2011
VL 35
IS 11
BP 2030
EP 2038
DI 10.1111/j.1530-0277.2011.01554.x
PG 9
WC Substance Abuse
SC Substance Abuse
GA 841SG
UT WOS:000296532800014
PM 21631542
ER
PT J
AU Schlansky, B
Sonnenberg, A
AF Schlansky, Barry
Sonnenberg, Amnon
TI Epidemiology of Noncardia Gastric Adenocarcinoma in the United States
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID HELICOBACTER-PYLORI INFECTION; STOMACH-CANCER MORTALITY; US ADULTS;
CARDIA; TRENDS; ESOPHAGEAL; PREVENTION; BURDEN; RISK
AB OBJECTIVES: Adenocarcinomas of the cardia (International Classification of Diseases (ICD)-9 code 151.0) and stomach (ICD-9 codes 151.1-151.9) are frequently grouped together in epidemiologic statistics, but are clearly distinct diseases. The objective of this study was to describe the current epidemiology of noncardia gastric cancer (noncardia gastric adenocarcinoma (NCGA)) in the United States.
METHODS: Rates of NCGA in the United States from 1997 to 2008 were analyzed in three national databases: the Surveillance, Epidemiology, and End Results registry was used for incidence, the Healthcare Costs and Utilization Project for hospitalizations, and the Compressed Mortality File for mortality. Population-based rates were calculated and age-adjusted to the US 2000 population using direct standardization. Odds ratios (ORs) and their 95% confidence intervals (CIs) were calculated and adjusted for confounders with the Mantel-Haenszel method.
RESULTS: Annually, NCGA was associated with 18,873 incident cases, 17,284 hospitalizations for principal discharge diagnoses, 31,354 hospitalizations for all-listed diagnoses, and 11,562 deaths. Incidence was greater in men (OR = 1.56, CI = 1.53-1.59) and non-White races (OR = 2.38, 2.33-2.43). Hospitalization was more common in men (1.82, 1.81-1.83) and non-White races (2.13, 2.10-2.15). Mortality was more common in men (1.83, 1.81-1.86) and non-White races (2.23, 2.20-2.26). NCGA rates showed a marked age-dependent rise (P < 0.001). Hospitalization and mortality were greatest in the Northeast region of the United States (P < 0.001).
CONCLUSIONS: Epidemiologic patterns of NCGA were congruent in three national databases. Older age, male gender, non-White race, and residence in the Northeast region were associated with increased risk. These patterns may reflect the underlying variations in Helicobacter pylori, lifestyle, and environmental exposures.
C1 [Sonnenberg, Amnon] Portland VA Med Ctr, Portland, OR 97239 USA.
[Schlansky, Barry; Sonnenberg, Amnon] Oregon Hlth & Sci Univ, Dept Med, Div Gastroenterol & Hepatol, Portland, OR 97201 USA.
RP Sonnenberg, A (reprint author), Portland VA Med Ctr, P3-GI,3710 SW US,Vet Hosp Rd, Portland, OR 97239 USA.
EM sonnenbe@ohsu.edu
NR 39
TC 28
Z9 30
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD NOV
PY 2011
VL 106
IS 11
BP 1978
EP 1985
DI 10.1038/ajg.2011.213
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 844ZD
UT WOS:000296791700014
PM 22008896
ER
PT J
AU Ananthakrishnan, AN
Hur, C
Juillerat, P
Korzenik, JR
AF Ananthakrishnan, Ashwin N.
Hur, Chin
Juillerat, Pascal
Korzenik, Joshua R.
TI Strategies for the Prevention of Postoperative Recurrence in Crohn's
Disease: Results of a Decision Analysis
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID SCHEDULED MAINTENANCE TREATMENT; COST-EFFECTIVENESS; CONTROLLED-TRIAL;
ILEAL RESECTION; MARKOV MODEL; RISK-FACTORS; DOUBLE-BLIND; INFLIXIMAB;
SURGERY; AZATHIOPRINE
AB OBJECTIVES: Nearly 70% of patients with Crohn's disease (CD) undergo surgical resection, with one-quarter subsequently developing clinical recurrence within 12 months. Several options exist for the prevention of postoperative recurrence in CD, but the comparative cost effectiveness of these competing strategies has not been previously analyzed.
METHODS: We developed a decision analytic model comprising five strategies-No Treatment, azathioprine (AZA), antibiotics(ABX), upfront infliximab(IFX), and tailored IFX that consisted of no upfront therapy with initiation of IFX in patients with severe endoscopic recurrence at 6 months. The base-case 1-year clinical recurrence rate was 24% with reduction in recurrence by 41%, 77%, and 99% for AZA, ABX, and IFX, respectively. A 1-year time horizon was used and sensitivity analyses were performed.
RESULTS: At the base-case analysis, the ABX (0.82 quality-adjusted life years (QALYs)) and AZA (0.81 QALYs) arms were more effective and less expensive than the No Treatment strategy (0.80 QALYs). The most effective strategy was upfront IFX (0.83 QALYs); however, this was also the most expensive and resulted in a high incremental cost-effectiveness ratio (ICER) ($777,732/QALY) compared with no treatment. The tailored IFX arm was less effective than upfront use but had a more acceptable ICER. On increasing the recurrence rate to 78% (high-risk patients), upfront IFX resulted in 0.07 QALYs (ICER $130,580/QALY) gained compared with No Treatment, whereas ABX, AZA, and tailored IFX arms dominated No Treatment.
CONCLUSION: Antibiotics are the most cost-effective option for preventing postoperative recurrence, but they have been associated with high rates of intolerance precluding widespread use. Upfront IFX is the most efficacious strategy but is not cost effective even in high-risk patients. Reserving IFX use for high-risk patients with early endoscopic recurrence is more cost effective than upfront use in all patients.
C1 [Ananthakrishnan, Ashwin N.] Massachusetts Gen Hosp, Crohns & Colitis Ctr, Gastrointestinal Unit, Boston, MA 02114 USA.
[Ananthakrishnan, Ashwin N.; Hur, Chin; Korzenik, Joshua R.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Hur, Chin] Massachusetts Gen Hosp, Inst Technol Assessment, Boston, MA 02114 USA.
RP Ananthakrishnan, AN (reprint author), Massachusetts Gen Hosp, Crohns & Colitis Ctr, Gastrointestinal Unit, 165 Cambridge St,9th Floor, Boston, MA 02114 USA.
EM aananthakrishnan@partners.org
OI Hur, Chin/0000-0002-2819-7576
FU Procter and Gamble; Warner Chilcott
FX Dr Korzenik has been a consultant for Procter and Gamble, Shire
Pharmaceuticals, and CytokinePharma, and receives research support from
Procter and Gamble and Warner Chilcott. Drs Ananthakrishnan, Hur, and
Juillerat have no financial disclosures.
NR 35
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Z9 19
U1 1
U2 8
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD NOV
PY 2011
VL 106
IS 11
BP 2009
EP 2017
DI 10.1038/ajg.2011.237
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 844ZD
UT WOS:000296791700018
PM 21788991
ER
PT J
AU Leung, AA
Wright, A
Pazo, V
Karson, A
Bates, DW
AF Leung, Alexander A.
Wright, Adam
Pazo, Valeria
Karson, Andrew
Bates, David W.
TI Risk of Thiazide-induced Hyponatremia in Patients with Hypertension
SO AMERICAN JOURNAL OF MEDICINE
LA English
DT Article
DE Hypertension; Hyponatremia; Incidence; Thiazide diuretics
ID CALCIUM-CHANNEL BLOCKER; PROSPECTIVELY-DESIGNED OVERVIEWS; MAJOR
CARDIOVASCULAR EVENTS; BLOOD-PRESSURE; RANDOMIZED-TRIALS;
HOSPITALIZED-PATIENTS; LOWERING TREATMENT; MILD HYPONATREMIA; DIURETICS;
OUTCOMES
AB BACKGROUND: Although hyponatremia is a well-recognized complication of treatment with thiazide diuretics, the risk of thiazide-induced hyponatremia remains uncertain in routine care.
METHODS: We conducted a retrospective cohort study using a multicenter clinical research registry to identify 2613 adult outpatients that were newly treated for hypertension between January 1, 2000 and December 31, 2005 at 2 teaching hospitals in Boston, Massachusetts, and followed them for up to 10 years.
RESULTS: Two hundred twenty patients exposed to ongoing thiazide therapy were compared with 2393 patients who were not exposed. In the exposed group, 66 (30%) developed hyponatremia (sodium <= 130 mmol/L). The adjusted incidence rate of hyponatremia was 140 cases per 1000 person-years for patients treated with thiazides, compared with 87 cases per 1000 person-years in those without thiazides. Patients exposed to thiazides were more likely to develop hyponatremia (adjusted incidence rate ratio, 1.61; 95% confidence interval [CI], 1.15-2.25). There was no significant difference in the risk of hospitalizations associated with hyponatremia (adjusted rate ratio, 1.04; 95% CI, 0.46-2.32) or mortality (adjusted rate ratio, 0.41; 95% CI, 0.12-1.42). The number needed to harm (to result in one excess case of incident hyponatremia in 5 years) was 15.02 (95% CI, 7.88-160.30).
CONCLUSIONS: Approximately 3 in 10 patients exposed to thiazides who continue to take them develop hyponatremia. (C) 2011 Elsevier Inc. All rights reserved. . The American Journal of Medicine (2011) 124, 1064-1072
C1 [Leung, Alexander A.; Wright, Adam; Pazo, Valeria; Bates, David W.] Brigham & Womens Hosp, Div Gen Internal Med & Primary Care, Boston, MA 02120 USA.
[Karson, Andrew] Massachusetts Gen Hosp, Div Gen Internal Med, Boston, MA 02114 USA.
RP Bates, DW (reprint author), Brigham & Womens Hosp, Div Gen Internal Med & Primary Care, 1620 Tremont St,3rd Floor, Boston, MA 02120 USA.
EM dbates@partners.org
NR 43
TC 28
Z9 30
U1 0
U2 4
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 NOV
PY 2011
VL 124
IS 11
BP 1064
EP 1072
DI 10.1016/j.amjmed.2011.06.031
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 842EW
UT WOS:000296576200024
PM 22017784
ER
PT J
AU Gerlock, AA
Grimesey, JL
Pisciotta, AK
Harel, O
AF Gerlock, April A.
Grimesey, Jackie L.
Pisciotta, Alisa K.
Harel, Ofer
TI Documentation of Screening for Perpetration of Intimate Partner Violence
in Male Veterans with PTSD
SO AMERICAN JOURNAL OF NURSING
LA English
DT Article
DE documentation; intimate partner violence; partner abuse; perpetrators;
posttraumatic stress disorder; screening; veterans
ID DOMESTIC VIOLENCE; ABUSED WOMEN; HEALTH; FAMILY; CARE; SETTINGS;
GUIDELINES; BEHAVIORS; SUICIDE; SYSTEM
AB Background: Men seeking care for posttraumatic stress disorder (PTSD) are believed to have high rates of relationship conflict and intimate partner violence (IPV). But little is known about screening for IPV perpetration in this population.
Objective: In phase one of a two-phase study of male veterans treated for PTSD, the primary objective was to determine how many veterans' records showed documentation that they'd been screened for IPV perpetration. The secondary objective was to count the total number of screenings and to determine whether an initial screening affected future screenings.
Methods: For this retrospective cohort study, a stratified random sample of 10% (N = 507) of all male veterans receiving treatment for PTSD at a U.S. Department of Veterans Affairs health care facility in a five-year period (November 2002 to November 2007) was selected and more than 70,000 progress notes were reviewed. The presence or absence of a documented screening for IPV perpetration in each record was noted and a Spearman rank correlation test to determine the relationship between the documentation of a first screening and future screenings was performed.
Results: Of the 507 records examined, 120 (24%) showed documentation of screening for IPV perpetration. Of those, 73 (61%) showed positive results for IPV perpetration, and 61 (51%) showed more than one screening. Documentation of screening was most likely to have occurred at the veteran's initial appointment (71%) and in an outpatient mental health setting (72%); IPV perpetration was determined most often as the result of a provider's inquiry (45%). There was a total of 415 screenings, including 356 in records in which there was more than one screening. The documentation of a single screening for IPV perpetration was significantly correlated with the documentation of subsequent screenings and with IPV perpetration determination (Spearman rank correlation = 0.611, P < 0.001). Also, veterans with documented IPV perpetration and high rates of relationship conflict accessed the health care system twice as often as those without such documentation.
Conclusions: In the sample analyzed, fewer than a quarter of male veterans with PTSD had a documented screening for IPV perpetration. Also, because those identified as IPV perpetrators accessed the health care system at a higher rate than those not so identified and repeated screenings were associated with a higher rate of IPV perpetrator determinations, health care providers should be made more aware of opportunities for screening for IPV in this population.
C1 [Gerlock, April A.] Univ Washington, Sch Nursing, Seattle, WA 98195 USA.
[Grimesey, Jackie L.] VA Puget Sound Hlth Care Syst, Hlth Serv Res & Dev Ctr Excellence, Tacoma, WA USA.
[Harel, Ofer] Univ Connecticut, Dept Stat, Storrs, CT 06269 USA.
RP Gerlock, AA (reprint author), Univ Washington, Sch Nursing, Seattle, WA 98195 USA.
EM april.gerlock@va.gov
RI Schueter, nicos/A-3625-2014
FU Office of Research and Development, Nursing Research Initiative,
Department of Veterans Affairs [NRI 04-040]; University of Connecticut
FX This material is based upon the work supported by the Office of Research
and Development, Nursing Research Initiative (NRI 04-040), Department of
Veterans Affairs, and by the University of Connecticut. The authors
acknowledge Anne Ganley, Jeff Edleson, and Patricia Betrus for their
assistance in project design and manuscript development; they received a
consultation fee from the grant.
NR 37
TC 4
Z9 4
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0002-936X
J9 AM J NURS
JI Am. J. Nurs.
PD NOV
PY 2011
VL 111
IS 11
BP 26
EP 32
DI 10.1097/01.NAJ.0000407296.10524.d7
PG 7
WC Nursing
SC Nursing
GA 842HG
UT WOS:000296586500017
PM 22005050
ER
PT J
AU Gerlock, AA
Grimesey, JL
Pisciotta, AK
Harel, O
AF Gerlock, April A.
Grimesey, Jackie L.
Pisciotta, Alisa K.
Harel, Ofer
TI Ask a Few More Questions
SO AMERICAN JOURNAL OF NURSING
LA English
DT Editorial Material
ID INTIMATE PARTNER VIOLENCE; NURSES; SCREEN; WOMEN
C1 [Gerlock, April A.] Univ Washington, Sch Nursing, Seattle, WA 98195 USA.
[Grimesey, Jackie L.] VA Puget Sound Hlth Care Syst, Hlth Serv Res & Dev Ctr Excellence, Tacoma, WA USA.
[Harel, Ofer] Univ Connecticut, Dept Stat, Storrs, CT 06269 USA.
RP Gerlock, AA (reprint author), Univ Washington, Sch Nursing, Seattle, WA 98195 USA.
EM april.gerlock@va.gov
FU NIMH NIH HHS [K01 MH087219]
NR 18
TC 4
Z9 4
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0002-936X
J9 AM J NURS
JI Am. J. Nurs.
PD NOV
PY 2011
VL 111
IS 11
BP 35
EP 39
DI 10.1097/01.NAJ.0000407299.00222.ac
PG 5
WC Nursing
SC Nursing
GA 842HG
UT WOS:000296586500018
PM 22030925
ER
PT J
AU Winter, C
Kampik, NB
Vedovelli, L
Rothenberger, F
Paunescu, TG
Stehberger, PA
Brown, D
John, H
Wagner, CA
AF Winter, Christian
Kampik, Nicole B.
Vedovelli, Luca
Rothenberger, Florina
Paunescu, Teodor G.
Stehberger, Paul A.
Brown, Dennis
John, Hubert
Wagner, Carsten A.
TI Aldosterone stimulates vacuolar H+-ATPase activity in renal
acid-secretory intercalated cells mainly via a protein kinase
C-dependent pathway
SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
LA English
DT Article
DE collecting duct; kidney; receptor; signaling cascade
ID MEDULLARY COLLECTING DUCT; THICK ASCENDING LIMB; NEM-SENSITIVE ATPASE;
SMOOTH-MUSCLE-CELLS; MINERALOCORTICOID-RECEPTOR; STEROID-HORMONES;
NONGENOMIC ACTIONS; NA+/H+-EXCHANGE; PROTON CONDUCTANCE; NEPHRON
SEGMENTS
AB Winter C, Kampik NB, Vedovelli L, Rothenberger F, Paunescu TG, Stehberger PA, Brown D, John H, Wagner CA. Aldosterone stimulates vacuolar H+-ATPase activity in renal acid-secretory intercalated cells mainly via a protein kinase C-dependent pathway. Am J Physiol Cell Physiol 301: C1251-C1261, 2011. First published August 10, 2011; doi: 10.1152/ajpcell.00076.2011.-Urinary acidification in the collecting duct is mediated by the activity of H+-ATPases and is stimulated by various factors including angiotensin II and aldosterone. Classically, aldosterone effects are mediated via the mineralocorticoid receptor. Recently, we demonstrated a nongenomic stimulatory effect of aldosterone on H+-ATPase activity in acid-secretory intercalated cells of isolated mouse outer medullary collecting ducts (OMCD). Here we investigated the intracellular signaling cascade mediating this stimulatory effect. Aldosterone stimulated H+-ATPase activity in isolated mouse and human OMCDs. This effect was blocked by suramin, a general G protein inhibitor, and GP-2A, a specific G(alpha q) inhibitor, whereas pertussis toxin was without effect. Inhibition of phospholipase C with U-73122, chelation of intracellular Ca2+ with BAPTA, and blockade of protein kinase C prevented the stimulation of H+-ATPases. Stimulation of PKC by DOG mimicked the effect of aldosterone on H+-ATPase activity. Similarly, aldosterone and DOG induced a rapid translocation of H+-ATPases to the luminal side of OMCD cells in vivo. In addition, PD098059, an inhibitor of ERK1/2 activation, blocked the aldosterone and DOG effects. Inhibition of PKA with H89 or KT2750 prevented and incubation with 8-bromoadenosine-cAMP mildly increased H+-ATPase activity. Thus, the nongenomic modulation of H+-ATPase activity in OMCD-intercalated cells by aldosterone involves several intracellular pathways and may be mediated by a G(alpha q) protein-coupled receptor and PKC. PKA and cAMP appear to have a modulatory effect. The rapid nongenomic action of aldosterone may participate in the regulation of H+-ATPase activity and contribute to final urinary acidification.
C1 [Winter, Christian; Kampik, Nicole B.; Rothenberger, Florina; Stehberger, Paul A.; Wagner, Carsten A.] Univ Zurich, Inst Physiol, Ctr Integrat Human Physiol, CH-8057 Zurich, Switzerland.
[Winter, Christian] Univ Hosp Dusseldorf, Urol Clin, Dusseldorf, Germany.
[Vedovelli, Luca; Paunescu, Teodor G.; Brown, Dennis] Massachusetts Gen Hosp, MGH Ctr Syst Biol, Program Membrane Biol, Boston, MA 02114 USA.
[Vedovelli, Luca; Paunescu, Teodor G.; Brown, Dennis] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
[Paunescu, Teodor G.; Brown, Dennis] Harvard Univ, Sch Med, Boston, MA USA.
[Vedovelli, Luca] Univ Padua, Dept Pharmacol & Anesthesiol, Padua, Italy.
[John, Hubert] Kantonsspital, Urol Clin, Winterthur, Switzerland.
RP Wagner, CA (reprint author), Univ Zurich, Inst Physiol, Ctr Integrat Human Physiol, Winterthurerstr 190, CH-8057 Zurich, Switzerland.
EM wagnerca@access.uzh.ch
OI Vedovelli, Luca/0000-0003-4847-2333
FU Swiss National Research Foundation [31-068318, 31-109677/1]; National
Institutes of Health (NIH) [DK-73266, DK-42956]; Boston Area Diabetes
and Endocrinology Research Center [NIH DK-57521]; Center for the Study
of Inflammatory Bowel Disease [NIH DK-43351]
FX This study was supported by Swiss National Research Foundation Grants
31-068318 and 31-109677/1 (to C. A. Wagner). This work was also
supported by National Institutes of Health (NIH) Grants DK-73266 (to T.
G. Paunescu) and DK-42956 (to D. Brown). The Microscopy Core Facility of
the Program in Membrane Biology received additional support from the
Boston Area Diabetes and Endocrinology Research Center (NIH DK-57521)
and from the Center for the Study of Inflammatory Bowel Disease (NIH
DK-43351).
NR 77
TC 22
Z9 22
U1 0
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6143
J9 AM J PHYSIOL-CELL PH
JI Am. J. Physiol.-Cell Physiol.
PD NOV
PY 2011
VL 301
IS 5
BP C1251
EP C1261
DI 10.1152/ajpcell.00076.2011
PG 11
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA 842GO
UT WOS:000296583400029
PM 21832245
ER
PT J
AU Eddy, KT
Rauch, SL
AF Eddy, Kamryn T.
Rauch, Scott L.
TI Neuroimaging in Eating Disorders: Coming of Age
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Editorial Material
ID BULIMIA-NERVOSA
C1 [Eddy, Kamryn T.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
McLean Hosp, Belmont, MA USA.
RP Eddy, KT (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
EM kamryn@gmail.com
NR 6
TC 4
Z9 4
U1 0
U2 3
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD NOV
PY 2011
VL 168
IS 11
BP 1139
EP 1141
DI 10.1176/appi.ajp.2011.11071125
PG 3
WC Psychiatry
SC Psychiatry
GA 843FS
UT WOS:000296658300004
PM 22193598
ER
PT J
AU Viguera, AC
Tondo, L
Koukopoulos, AE
Reginaldi, D
Lepri, B
Baldessarini, RJ
AF Viguera, Adele C.
Tondo, Leonardo
Koukopoulos, Alexia E.
Reginaldi, Daniela
Lepri, Beatrice
Baldessarini, Ross J.
TI Episodes of Mood Disorders in 2,252 Pregnancies and Postpartum Periods
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID BIPOLAR DISORDER; RISK-FACTORS; ANTIDEPRESSANT TREATMENT;
MENTAL-DISORDERS; WOMEN; DEPRESSION; DISCONTINUATION; CHILDBEARING;
RECURRENCE; PSYCHOSES
AB Objective: The risks of major affective episodes during pregnancy and during the postpartum period have rarely been compared in large samples across diagnoses. The authors hypothesized that perinatal episodes would mainly be depressive, would occur more in the postpartum than the prenatal period, and would be more prevalent with bipolar than unipolar depressive disorders.
Method: The authors pooled clinical information on 2,252 pregnancies of 1,162 women with clinically treated DSM-IV bipolar I disorder (479 pregnancies/283 women), bipolar II disorder (641/338), or recurrent major depressive disorder (1,132/541) to compare rates of affective episode types by diagnosis during pregnancy and the postpartum period and to identify risk factors.
Results: Among women with bipolar disorder, 23% had illness episodes during pregnancy and 52% during the postpartum period. Among women with unipolar depression, 4.6% had illness episodes during pregnancy and 30% during the postpartum period. Based on exposure-adjusted risk per pregnancy, episodes were 3.5 times more prevalent during the postpartum period than during pregnancy, and the risk was consistently higher with bipolar disorder. Depression was the most frequent morbidity during and following pregnancy. In multivariate modeling, factors associated with affective episodes in pregnancy, in descending order, were younger age at onset, previous postpartum episodes, fewer years of illness, bipolar disorder, fewer children, and not being married. Postpartum episodes were associated with younger age at onset, illness during pregnancy, bipolar disorder, fewer children, and more education. Moreover, pregnancy was less likely and perinatal episodes more likely if diagnosis preceded a first pregnancy. First lifetime episodes occurred in the perinatal period in 7.6% of cases.
Conclusions: Among women with major affective disorders, illness risk was much greater during the postpartum period than during pregnancy. Illness mainly involved depression and was strongly associated with younger age at illness onset, bipolar disorder, and high lifetime occurrence rates. The relative risk during pregnancy compared with nonpregnant periods remains uncertain.
C1 [Baldessarini, Ross J.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
McLean Hosp, Int Consortium Bipolar Disorder Res, Boston, MA USA.
Cleveland Clin, Dept Psychiat, Neurol Inst, Cleveland, OH USA.
Massachusetts Gen Hosp, Perinatal Unit, Boston, MA 02114 USA.
Lucio Bini Mood Disorders Ctr, Cagliari, Sardinia, Italy.
Lucio Bini Mood Disorders Ctr, Rome, Italy.
RP Baldessarini, RJ (reprint author), Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
EM rbaldessarini@mclean.harvard.edu
FU NIMH; Epilepsy Foundation; AstraZeneca; Bristol-Myers Squibb;
Ortho-McNeil-Janssen Pharmaceuticals; Pfizer; Sunovion; NIH [MH-011609,
MH-071762]; Lucio Bini Private Donors Mood Disorders Research Fund;
McLean Private Donors Mood Disorders Research Fund; Bruce J. Anderson
Foundation
FX Dr. Viguera has received research support from NIMH, the Epilepsy
Foundation, AstraZeneca, Bristol-Myers Squibb, Ortho-McNeil-Janssen
Pharmaceuticals, Pfizer, and Sunovion and has served on the advisory
board of Medco Health. The other authors report no financial
relationships with commercial interests.; Supported in part by NIH
grants MH-011609 and MH-071762 (to Dr. Viguera), the Lucio Bini Private
Donors Mood Disorders Research Fund (to Dr. Tondo), a grant from the
Bruce J. Anderson Foundation (to Dr. Baldessarini), and the McLean
Private Donors Mood Disorders Research Fund (to Dr. Baldessarini).
NR 40
TC 56
Z9 56
U1 0
U2 11
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD NOV
PY 2011
VL 168
IS 11
BP 1179
EP 1185
DI 10.1176/appi.ajp.2011.11010148
PG 7
WC Psychiatry
SC Psychiatry
GA 843FS
UT WOS:000296658300012
PM 21799064
ER
PT J
AU Malandraki, GA
Hind, JA
Gangnon, R
Logemann, JA
Robbins, J
AF Malandraki, Georgia A.
Hind, Jacqueline A.
Gangnon, Ronald
Logemann, Jeri A.
Robbins, JoAnne
TI The Utility of Pitch Elevation in the Evaluation of Oropharyngeal
Dysphagia: Preliminary Findings
SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY
LA English
DT Article
DE swallowing; voice; cricothyroid muscle; aspiration; pitch elevation
ID PENETRATION-ASPIRATION SCALE; SUPERIOR LARYNGEAL NERVE; MULTIPLE
IMPUTATION; VOICE; DISPLACEMENT; CLINICIAN; ANATOMY; STROKE; REFLEX;
ADULTS
AB Purpose: To evaluate the utility of a pitch elevation task in the assessment of oropharyngeal dysphagia.
Method: This study was a pilot prospective cohort study including 40 consecutive patients (16 male and 24 female) who were referred by their physician for a swallowing evaluation. Patients were evaluated with a noninstrumental clinical examination and a videofluoroscopic swallow study, and participated in a pitch elevation task during videofluoroscopic image acquisition. Relationships between pitch elevation measurements (acoustic and perceptual) and swallow parameters (penetration/aspiration and residue) were investigated.
Results: Results of this pilot study revealed that both maximum fundamental frequency (F(o)) and perceptual evaluation of pitch elevation independently significantly predicted Penetration-Aspiration Scale scores for thin liquid swallows (p = .01 and .03, respectively). Vocal range (average pitch to falsetto) was not sensitive in predicting likelihood of oropharyngeal dysphagia.
Conclusions: Findings indicate that reduced pitch elevation can be indicative of reduced airway protection and swallowing impairment in some dysphagia patients and may be a useful supplement to dysphagia screening and diagnosis. Further investigation is warranted to determine the optimal utility of this procedure for different diagnostic categories of patients.
C1 [Malandraki, Georgia A.; Hind, Jacqueline A.; Robbins, JoAnne] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
[Malandraki, Georgia A.; Hind, Jacqueline A.; Gangnon, Ronald; Robbins, JoAnne] Univ Wisconsin, Madison, WI 53706 USA.
[Malandraki, Georgia A.] Columbia Univ, Teachers Coll, New York, NY 10027 USA.
[Logemann, Jeri A.] Northwestern Univ, Evanston, IL USA.
RP Malandraki, GA (reprint author), William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
EM malandraki@tc.columbia.edu
NR 38
TC 4
Z9 5
U1 0
U2 1
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 1058-0360
J9 AM J SPEECH-LANG PAT
JI Am. J. Speech-Lang. Pathol.
PD NOV 1
PY 2011
VL 20
IS 4
BP 262
EP 268
DI 10.1044/1058-0360(2011/10-0097)
PG 7
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 844CE
UT WOS:000296724500002
PM 21813823
ER
PT J
AU Sohani, AR
Jaffe, ES
Harris, NL
Ferry, JA
Pittaluga, S
Hasserjian, RP
AF Sohani, Aliyah R.
Jaffe, Elaine S.
Harris, Nancy Lee
Ferry, Judith A.
Pittaluga, Stefania
Hasserjian, Robert P.
TI Nodular Lymphocyte-Predominant Hodgkin Lymphoma With Atypical T Cells: A
Morphologic Variant Mimicking Peripheral T-Cell Lymphoma
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE nodular lymphocyte-predominant Hodgkin lymphoma; LP cells; atypical T
cells; peripheral T-cell lymphoma; IgD
ID LARGE B-CELLS; DIFFERENTIAL-DIAGNOSIS; H-CELLS; DISEASE; EXPRESSION;
IMMUNOGLOBULIN; CLASSIFICATION; TRANSFORMATION; PROLIFERATION;
TRANSCRIPTION
AB Nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL) is a distinct Hodgkin lymphoma subtype composed of few neoplastic lymphocyte-predominant (LP) cells in a background of reactive small B and T cells. We have seen occasional NLPHL cases that contain background T cells with prominent cytologic atypia, raising the differential diagnosis of peripheral T-cell lymphoma not otherwise specified (PTCL-NOS) or a composite lymphoma. We sought to characterize the clinicopathologic features of such cases. Eleven NLPHL cases with atypical T cells diagnosed from 1977 to 2010 were identified at 2 institutions and compared with 24 control NLPHL cases lacking atypical T cells. All 9 male patients and 2 female patients presented with localized peripheral lymphadenopathy. In comparison with control patients, they were younger (median age, 13.8 vs. 36.1 y; P = 0.015), with more frequent cervical lymph node involvement (54.5% vs. 8.3%, P = 0.015). In all 11 cases, areas of NLPHL with typical B-cell-rich nodules containing LP cells were present. Nine cases contained sheets of atypical T cells surrounding primary and secondary follicles in a pattern mimicking the T-zone pattern of PTCL-NOS; the remaining 2 cases contained atypical T cells presented as large clusters at the periphery of B-cell-rich nodules. In all cases, the atypical T-cell-rich areas contained rare scattered LP cells, which were IgD(+) in 5 of 7 cases (71.4%). The atypical T cells showed no pan-T-cell antigen loss or aberrant T-cell antigen expression in any case, and polymerase chain reaction or Southern blot analysis showed no evidence of T-cell clonality in 6 cases tested. The atypical T cells exhibited a variable immunophenotype with respect to germinal center, follicular T-helper, T-regulatory, and cytotoxic T-cell markers. Among 8 patients with clinical follow-up (median follow-up: 6.4 y), 5 patients had recurrent NLPHL at 6 months to 12 years after diagnosis and 6 patients are alive without disease at 9 months to 18 years after diagnosis. In comparison with control patients, NLPHL patients with atypical T cells were more likely to develop recurrent NLPHL (71.4% vs. 13.6%, P = 0.008) and to have a shorter time to relapse (P = 0.04). Our findings suggest that some cases of NLPHL, occurring predominantly in younger patients, contain prominent populations of morphologically atypical T cells that may raise the possibility of concurrent nodal involvement by PTCL-NOS, a rare diagnosis in children. The clinical behavior of these cases appears similar to that of NLPHL with T-cell-rich diffuse areas, with a higher risk of disease recurrence and no difference in overall survival; however, this finding warrants confirmation in studies of larger numbers of patients.
C1 [Sohani, Aliyah R.] Massachusetts Gen Hosp, Dept Pathol, James Homer Wright Pathol Labs, Boston, MA 02114 USA.
[Sohani, Aliyah R.; Harris, Nancy Lee; Ferry, Judith A.; Hasserjian, Robert P.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Jaffe, Elaine S.; Pittaluga, Stefania] NCI, Hematopathol Sect, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Sohani, AR (reprint author), Massachusetts Gen Hosp, Dept Pathol, James Homer Wright Pathol Labs, 55 Fruit St,WRN 219, Boston, MA 02114 USA.
EM arsohani@partners.org
OI Jaffe, Elaine/0000-0003-4632-0301
NR 48
TC 17
Z9 19
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD NOV
PY 2011
VL 35
IS 11
BP 1666
EP 1678
DI 10.1097/PAS.0b013e31822832de
PG 13
WC Pathology; Surgery
SC Pathology; Surgery
GA 842DJ
UT WOS:000296569500007
PM 21997687
ER
PT J
AU Lincoln, R
Rosenthal, CF
Malte, CA
Simpson, T
AF Lincoln, Randi
Rosenthal, Christina F.
Malte, Carol A.
Simpson, Tracy
TI A Pilot Study of Memory Impairment Associated with Discrepancies between
Retrospective and Daily Recall of Alcohol Consumption
SO AMERICAN JOURNAL ON ADDICTIONS
LA English
DT Article
ID INTERACTIVE VOICE RESPONSE; AUTOBIOGRAPHICAL MEMORY; MEASURE DRINKING;
TECHNOLOGY
AB Prior studies have found discrepancies between daily report and retrospective recall of alcohol use. One possible explanation is that there may be an association between memory impairment and alcohol consumption recall errors. Should this possibility be substantiated it could have implications for the types of assessments conducted in alcohol treatment trials. The current study evaluated the degree to which memory impairment, as measured by the California Verbal Learning Test-II, predicted day-to-day discrepancies between daily Interactive Voice Response monitoring and retrospective recall of alcohol use assessed with a 42-day version of the Form-90. Significant differences were detected in absolute difference in days drinking across the two measurement methods between participants scoring above and below population means on two measures of immediate memory ability. Correlations between the absolute difference in days drinking and immediate memory ability and long-delay memory indices approached significance. There were no significant associations between memory indices and discrepancies in reports of standard drink units. These preliminary results suggest that verbal memory difficulties common in this population may result in inaccurate reports of days drinking for some individuals. (Am J Addict 2011;20:568-574)
C1 [Lincoln, Randi] VA Puget Sound Hlth Care Syst, Spinal Cord Injury Ctr Excellence, Seattle, WA 98108 USA.
[Rosenthal, Christina F.; Simpson, Tracy] Seattle Inst Biomed & Clin Res, Seattle, WA USA.
[Malte, Carol A.; Simpson, Tracy] Ctr Excellence Subst Abuse Treatment & Educ, Seattle, WA USA.
[Simpson, Tracy] VISN 20 Mental Illness Res Educ & Clin Ctr, Seattle, WA USA.
[Simpson, Tracy] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
RP Simpson, T (reprint author), VA Puget Sound Hlth Care Syst, Spinal Cord Injury Ctr Excellence, 1660 S Columbian Way ATC 116-S, Seattle, WA 98108 USA.
EM Tracy.Simpson@va.gov
NR 20
TC 5
Z9 5
U1 1
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1055-0496
J9 AM J ADDICTION
JI Am. J. Addict.
PD NOV-DEC
PY 2011
VL 20
IS 6
BP 568
EP 574
DI 10.1111/j.1521-0391.2011.00178.x
PG 7
WC Substance Abuse
SC Substance Abuse
GA 840EB
UT WOS:000296420000011
PM 21999504
ER
PT J
AU Mhyre, JM
Bateman, BT
Leffert, LR
AF Mhyre, Jill M.
Bateman, Brian T.
Leffert, Lisa R.
TI Influence of Patient Comorbidities on the Risk of Near-miss Maternal
Morbidity or Mortality
SO ANESTHESIOLOGY
LA English
DT Article
ID PREGNANCY-RELATED MORTALITY; SEVERE OBSTETRIC MORBIDITY; UNITED-STATES;
INTENSIVE-CARE; MULTIFETAL PREGNANCIES; HYPERTENSIVE DISORDERS; ADVERSE
OUTCOMES; ASTHMATIC WOMEN; POPULATION; DELIVERIES
AB Background: Maternal morbidity and mortality are increased in the United States compared with that of other developed countries. The objective of this investigation is to determine the extent to which it is possible to predict which patients will experience near-miss morbidity or mortality.
Methods: The authors defined near-miss morbidity as end-organ injury associated with length of stay greater than the 99(th) percentile or discharge to a second medical facility, and identified all cases of near-miss morbidity or death from admissions for delivery in the 2003-2006 Nationwide Inpatient Sample. Logistic regression was used to examine the effect of maternal characteristics on rates of near-miss morbidity/mortality.
Results: Approximately 1.3 per 1,000 hospitalizations for delivery was complicated by near-miss morbidity/mortality as defined in this study (95% CI 1.3-1.4). Most of these events (58.3%) occurred in 11.8% of the delivering population-in those women with important medical comorbidities or obstetric complications identified before admission for delivery. The highest rates were noted among women with pulmonary hypertension (98.0 cases per 1,000 deliveries), malignancy (23.4 per 1,000), and systemic lupus erythematosus (21.1 per 1,000).
Conclusions: Risk for near-miss morbidity or mortality is substantially increased among an identifiable subset of pregnant women. To the extent that antepartum multidisciplinary coordination and high-quality intrapartum care improve delivery outcomes for women with significant antepartum medical and obstetric disease, then public health investments to reduce the national burden of delivery-related near-miss morbidity and mortality will have the greatest effect by focusing resources on identifying and serving these high-risk groups.
C1 [Mhyre, Jill M.] Univ Michigan Hlth Syst, Dept Anesthesiol, Div Obstetr Anesthesia, Ann Arbor, MI 48105 USA.
Harvard Univ, Sch Med, Dept Anesthesiol Crit Care & Pain Med, Massachusetts Gen Hosp, Boston, MA USA.
RP Mhyre, JM (reprint author), Univ Michigan Hlth Syst, Dept Anesthesiol, Div Obstetr Anesthesia, Womens Hosp SPC 5278,Room L3622,1500 E Med Ctr Dr, Ann Arbor, MI 48105 USA.
EM jmmhyre@umich.edu
NR 66
TC 33
Z9 35
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2011
VL 115
IS 5
BP 963
EP 972
DI 10.1097/ALN.0b013e318233042d
PG 10
WC Anesthesiology
SC Anesthesiology
GA 842AR
UT WOS:000296558400012
PM 21934482
ER
PT J
AU Francis, RC
Vaporidi, K
Bloch, KD
Ichinose, F
Zapol, WM
AF Francis, Roland C.
Vaporidi, Katerina
Bloch, Kenneth D.
Ichinose, Fumito
Zapol, Warren M.
TI Protective and Detrimental Effects of Sodium Sulfide and Hydrogen
Sulfide in Murine Ventilator-induced Lung Injury
SO ANESTHESIOLOGY
LA English
DT Article
ID RESPIRATORY-DISTRESS-SYNDROME; OXIDATIVE STRESS; NITRIC-OXIDE; RATS;
MICE; PATHOGENESIS; INFLAMMATION; CONTRIBUTES; MECHANISMS
AB Background: The antiinflammatory effects of hydrogen sulfide (H2S) and sodium sulfide (Na2S) treatment may prevent acute lung injury induced by high tidal volume (HVT) ventilation. However, lung protection may be limited by direct pulmonary toxicity associated with H2S inhalation. Therefore, the authors tested whether the inhalation of H2S or intravascular Na2S treatment can protect against ventilator-induced lung injury in mice.
Methods: Anesthetized mice continuously inhaled 0, 1, 5, or 60 ppm H2S or received a single bolus infusion of Na2S (0.55 mg/kg) or vehicle and were then subjected to HVT (40 ml/kg) ventilation lasting 4 h (n = 4-8 per group).
Results: HVT ventilation increased the concentrations of protein and interleukin-6 in bronchoalveolar lavage fluid, contributing to reduced respiratory compliance and impaired arterial oxygenation, and caused death from lung injury and pulmonary edema. Inhalation of 1 or 5 ppm H2S during HVT ventilation did not alter lung injury, but inhalation of 60 ppm H2S accelerated the development of ventilator-induced lung injury and enhanced the pulmonary expression of the chemoattractant CXCL-2 and the leukocyte adhesion molecules CD11b and L-selectin. In contrast, pretreatment with Na2S attenuated the expression of CXCL-2 and CD11b during HVT ventilation and reduced pulmonary edema. Moreover, Na2S enhanced the pulmonary expression of Nrf2-dependent antioxidant genes (NQO1, GPX2, and GST-A4) and prevented oxidative stress-induced depletion of glutathione in lung tissue.
Conclusions: The data suggest that systemic intravascular treatment with Na2S represents a novel therapeutic strategy to prevent both ventilator-induced lung injury and pulmonary glutathione depletion by activating Nrf2-dependent antioxidant gene transcription.
C1 [Zapol, Warren M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med,Anesthesia C, Boston, MA 02114 USA.
[Francis, Roland C.; Vaporidi, Katerina; Zapol, Warren M.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Zapol, WM (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med,Anesthesia C, 55 Fruit St, Boston, MA 02114 USA.
EM wzapol@partners.org
FU German Research Foundation (Deutsche Forschungsgemeinschaft, Bonn,
Germany) [FR 2555/3-1]; United States Public Health Service, Washington,
D.C. [HL074352, HL101930]
FX Supported by fellowship grant FR 2555/3-1 (to Dr. Francis) from the
German Research Foundation (Deutsche Forschungsgemeinschaft, Bonn,
Germany); royalties from Ikaria Inc., Hampton, New Jersey, and Linde
Corp, Murray Hill, New Jersey (to Dr. Zapol); and grants HL074352 (to
Dr. Bloch) and HL101930 (to Dr. Ichinose) from the United States Public
Health Service, Washington, D.C.
NR 29
TC 25
Z9 29
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2011
VL 115
IS 5
BP 1012
EP 1021
DI 10.1097/ALN.0b013e31823306cf
PG 10
WC Anesthesiology
SC Anesthesiology
GA 842AR
UT WOS:000296558400017
PM 21912243
ER
PT J
AU Wallace, AW
Au, S
Cason, BA
AF Wallace, Arthur W.
Au, Selwyn
Cason, Brian A.
TI How Often Should Atenolol Be Dosed for Perioperative beta-Blockade?
Reply
SO ANESTHESIOLOGY
LA English
DT Letter
ID MORTALITY
C1 [Wallace, Arthur W.] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Wallace, AW (reprint author), San Francisco VA Med Ctr, San Francisco, CA USA.
EM awallace@cardiacengineering.com
NR 4
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2011
VL 115
IS 5
BP 1140
EP 1141
DI 10.1097/ALN.0b013e3182334092
PG 4
WC Anesthesiology
SC Anesthesiology
GA 842AR
UT WOS:000296558400040
ER
PT J
AU Ebaugh, JL
Gupta, N
Raffetto, JD
AF Ebaugh, James L.
Gupta, Naren
Raffetto, Joseph D.
TI Single-Incision External Iliac Artery Endarterectomy and Patch
Angioplasty
SO ANNALS OF VASCULAR SURGERY
LA English
DT Article
ID AORTOILIAC OCCLUSIVE DISEASE; BALLOON ANGIOPLASTY; BYPASS
AB An isolated external iliac artery chronic total occlusion is currently treated either with subintimal percutaneous transluminal angioplasty and stent or with a bypass. This article describes a new application of an old technique, endarterectomy and patch angioplasty, performed on the external iliac artery through a single flank incision. This novel approach can provide lasting patency with a low risk of complications. We present four cases and a review of the literature on the other available treatment options. This minimally invasive technique may provide a viable alternative that can be used alone or in combination with other open or endovascular techniques and can be applied in cases of groin sepsis.
C1 [Ebaugh, James L.; Gupta, Naren; Raffetto, Joseph D.] VA Boston Healthcare Syst, Surg Serv, W Roxbury, MA 02132 USA.
[Ebaugh, James L.; Gupta, Naren; Raffetto, Joseph D.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Vasc & Endovasc Surg, Boston, MA 02115 USA.
RP Ebaugh, JL (reprint author), VA Boston Healthcare Syst, Surg Serv 112, 1400 VFW Pkwy, W Roxbury, MA 02132 USA.
EM james.ebaugh2@med.va.gov
NR 20
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0890-5096
J9 ANN VASC SURG
JI Ann. Vasc. Surg.
PD NOV
PY 2011
VL 25
IS 8
BP 1165
EP 1169
DI 10.1016/j.avsg.2011.05.032
PG 5
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 841ZG
UT WOS:000296553100040
PM 22023946
ER
PT J
AU Hynes, B
Goodenough, RD
Slovut, DP
AF Hynes, Brian
Goodenough, Richard D.
Slovut, David P.
TI Carotid Artery Stenting After Carotid Endarterectomy
SO ANNALS OF VASCULAR SURGERY
LA English
DT Article
ID MANDIBULAR SUBLUXATION; PROTECTION DEVICES; INTRAOPERATIVE USE;
END-POINTS; SHORT-TERM; STENOSIS; PREVENTION; MANAGEMENT; EXPOSURE;
STROKES
AB Atherosclerotic carotid artery disease remains an important cause of cerebrovascular ischemic disease. We present a patient with residual stenosis of the distal internal carotid artery following carotid endarterectomy that was treated with stenting. The case highlights the potential complimentary benefits of carotid endarterectomy and carotid stenting.
C1 [Hynes, Brian] Massachusetts Gen Hosp, Dept Cardiol, Sect Vasc Med & Peripheral Intervent, Boston, MA 02114 USA.
[Goodenough, Richard D.] N Shore Med Ctr, Vasc Surg Sect, Salem, MA USA.
[Slovut, David P.] Montefiore Med Ctr, Div Cardiol, Bronx, NY 10467 USA.
[Slovut, David P.] Montefiore Med Ctr, Div Vasc Surg, Bronx, NY 10467 USA.
RP Hynes, B (reprint author), Massachusetts Gen Hosp, Div Cardiol, Sect Vasc Med & Intervent, 55 Fruit St, Boston, MA 02114 USA.
EM bhynes@hotmail.com
NR 25
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0890-5096
J9 ANN VASC SURG
JI Ann. Vasc. Surg.
PD NOV
PY 2011
VL 25
IS 8
AR 1143.e1
DI 10.1016/j.avsg.2011.08.006
PG 5
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA 841ZG
UT WOS:000296553100036
PM 22023956
ER
PT J
AU Bassett, EK
Hoganson, DM
Lo, JH
Penson, EJN
Vacanti, JP
AF Bassett, Erik K.
Hoganson, David M.
Lo, Justin H.
Penson, Elliot J. N.
Vacanti, Joseph P.
TI Influence of Vascular Network Design on Gas Transfer in Lung Assist
Device Technology
SO ASAIO JOURNAL
LA English
DT Article
ID CARBON-DIOXIDE REMOVAL; MICROCHANNEL TECHNOLOGIES; MEMBRANE-OXYGENATOR;
MATHEMATICAL-MODEL; ARTIFICIAL LUNGS; RECTANGULAR CHANNELS; BLOOD;
TRANSPLANTATION; POLY(DIMETHYLSILOXANE); CAPILLARIES
AB Blood oxygenators are vital for the critically ill, but their use is limited to the hospital setting. A portable blood oxygenator or a lung assist device for ambulatory or long-term use would greatly benefit patients with chronic lung disease. In this work, a biomimetic blood oxygenator system was developed which consisted of a microfluidic vascular network covered by a gas permeable silicone membrane. This system was used to determine the influence of key microfluidic parameters-channel size, oxygen exposure length, and blood shear rate-on blood oxygenation and carbon dioxide removal. Total gas transfer increased linearly with flow rate, independent of channel size and oxygen exposure length. On average, CO(2) transfer was 4.3 times higher than oxygen transfer. Blood oxygen saturation was also found to depend on the flow rate per channel but in an inverse manner; oxygenation decreased and approached an asymptote as the flow rate per channel increased. These relationships can be used to optimize future biomimetic vascular networks for specific lung applications: gas transfer for carbon dioxide removal in patients with chronic obstructive pulmonary disease or oxygenation for premature infants requiring complete lung replacement therapy. ASAIO Journal 2011; 57:533-538.
C1 [Bassett, Erik K.; Hoganson, David M.; Lo, Justin H.; Penson, Elliot J. N.; Vacanti, Joseph P.] Massachusetts Gen Hosp, Dept Surg, Ctr Regenerat Med, Boston, MA 02114 USA.
[Bassett, Erik K.; Hoganson, David M.; Lo, Justin H.; Penson, Elliot J. N.; Vacanti, Joseph P.] MassGen Hosp Children, Boston, MA USA.
[Lo, Justin H.; Vacanti, Joseph P.] Harvard Univ, Sch Med, Boston, MA USA.
RP Vacanti, JP (reprint author), Dept Pediat Surg, 55 Fruit St,Warren 1151, Boston, MA 02114 USA.
EM jvacanti@partners.org
OI Hoganson, David/0000-0002-8141-7793
FU NIH [F32 DK076349-01]; Health Resources and Services Administration
[234-2005-37011C]
FX This work was supported by the NIH (F32 DK076349-01, to D. M. H.) and in
part by Health Resources and Services Administration contract
234-2005-37011C.
NR 32
TC 4
Z9 4
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1058-2916
J9 ASAIO J
JI Asaio J.
PD NOV-DEC
PY 2011
VL 57
IS 6
BP 533
EP 538
DI 10.1097/MAT.0b013e318234a3ac
PG 6
WC Engineering, Biomedical; Transplantation
SC Engineering; Transplantation
GA 842IE
UT WOS:000296590100010
PM 22036722
ER
PT J
AU Kurusu, S
Sapirstein, A
Sawada, H
Kawaminami, M
Bonventre, JV
AF Kurusu, Shiro
Sapirstein, Adam
Sawada, Harumi
Kawaminami, Mitsumori
Bonventre, Joseph V.
TI Group IVA phospholipase A(2) regulates testosterone biosynthesis by
murine Leydig cells and is required for timely sexual maturation
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE arachidonic acid; Group IVA phospholipase A(2) (PLA(2)G4A); Leydig cell;
sexual maturation; testosterone
ID MALE REPRODUCTIVE-ORGANS; GROUP-II PHOSPHOLIPASE-A2; SPERM ACROSOME
REACTION; ARACHIDONIC-ACID; CYTOSOLIC PHOSPHOLIPASE-A(2)ALPHA;
STIMULATED STEROIDOGENESIS; RECOMBINANT EXPRESSION; REDUCED FERTILITY;
GENE-EXPRESSION; FATTY-ACIDS
AB In the present paper, we report that PLA(2)G4A (Group IVA phospholipase A(2)) is important in the development and function of rodent testes. Interstitial cells of rat testes had high PLA(2) (phospholipase A(2)) activity that was very sensitive to the PLA(2)G4A-preferential inhibitor AACOCF(3) (arachidonyl trifluoromethyl ketone). PLA(2)G4A protein was expressed primarily in the interstitial cells of wild-type mouse testes throughout maturation. Although Pla2g4a knockout (Pla2g4a(-/-)) male mice are fertile, their sexual maturation was delayed, as indicated by cauda epididymal sperm count and seminal vesicle development. Delayed function of Pla2g4a(-/-) mice testes was associated with histological abnormalities including disorganized architecture, swollen appearance and fewer interstitial cells. Basal secretion of testosterone was attenuated significantly and steroidogenic response to hCG (human chorionic gonadotropin) treatment was reduced in Pla2g4a(-/-) mice compared with their Pla2g4a(+/+) littermates during the sexual maturation period. Chemical inhibition of PLA(2)G4A activity by AACOCF(3) or pyrrophenone significantly reduced hCG-stimulated testosterone production in cultured rat interstitial cells. AACOCF(3) inhibited forskolin- and cAMP analogue-stimulated testosterone production. These results provide the first evidence that PLA(2)G4A plays a role in male testes physiology and development. These results may have implications for the potential clinical use of PLA(2)G4A inhibitors.
C1 [Kurusu, Shiro; Bonventre, Joseph V.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Kurusu, Shiro; Sawada, Harumi; Kawaminami, Mitsumori] Kitasato Univ, Sch Vet Med, Vet Physiol Lab, Aomori 0348628, Japan.
[Sapirstein, Adam] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
[Bonventre, Joseph V.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02115 USA.
[Bonventre, Joseph V.] Holyoke Ctr, Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
RP Bonventre, JV (reprint author), Massachusetts Gen Hosp, Dept Med, 55 Fruit St, Boston, MA 02114 USA.
EM jbonventre@partners.org
FU National Institutes of Health National Institute of Diabetes and
Digestive and Kidney Diseases [DK39773, DK54741]; Nakayama Foundation
for Human Science
FX The work done in the laboratory of J.V.B. was supported by the National
Institutes of Health National Institute of Diabetes and Digestive and
Kidney Diseases [grant numbers DK39773 and DK54741]. S.K. received a
fellowship for studies abroad from the Nakayama Foundation for Human
Science.
NR 58
TC 3
Z9 3
U1 0
U2 2
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD NOV 1
PY 2011
VL 439
BP 403
EP 411
DI 10.1042/BJ20102167
PN 3
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 841XK
UT WOS:000296548300005
PM 21762109
ER
PT J
AU Tanrikut, C
Goldstein, M
Rosoff, JS
Lee, RK
Nelson, CJ
Mulhall, JP
AF Tanrikut, Cigdem
Goldstein, Marc
Rosoff, James S.
Lee, Richard K.
Nelson, Christian J.
Mulhall, John P.
TI Varicocele as a risk factor for androgen deficiency and effect of repair
SO BJU INTERNATIONAL
LA English
DT Article
DE varicocele; testosterone; hypogonadism; androgen deficiency
ID INFERTILE MEN; TESTICULAR TEMPERATURE; TESTOSTERONE LEVELS; OLDER MEN;
PLASMA; AGE; POPULATION; PREVALENCE; FERTILITY; PITUITARY
AB OBJECTIVE
To determine whether men with varicoceles have lower testosterone levels than those without and to ascertain if testosterone levels increase after varicocelectomy.
PATIENTS AND METHODS
We measured preoperative testosterone levels in 325 men with palpable varicoceles and in 510 men with vasectomy reversal without varicoceles who served as a comparison group.
The testosterone levels between groups were compared by age. Of the men with varicoceles, 200 had data on both pre- and postoperative testosterone levels, which were compared to assess postoperative changes.
RESULTS
Men with varicocele had significantly lower testosterone levels than the comparison group, with mean (SD) levels of 416 (156) vs 469 (192) ng/dL (P < 0.001). This difference persisted when analysed by age.
The testosterone levels significantly increased after repair from 358 (126) to 454 (168) ng/dL (P < 0.001).
Of the 70% of patients with postoperative improvement in testosterone levels, the mean (SD) increase in testosterone was 178 (142) ng/dL. The percentage change in testosterone levels was: 30% had no increase, 41% increased by <= 50%, 19% increased between by 51-100%, and 10% increased by >100%.
There was no association between change in testosterone level and age, laterality of varicocele, or varicocele grade.
CONCLUSIONS
Men with varicoceles had significantly lower testosterone levels than the comparison group of men with vasectomy reversal.
Microsurgical varicocele ligation resulted in a significant increase in serum testosterone levels in more than two-thirds of men.
These findings suggest that varicocele is a significant risk factor for androgen deficiency and that repair may increase testosterone levels in men with varicocele and low testosterone levels.
C1 [Tanrikut, Cigdem] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Tanrikut, Cigdem; Goldstein, Marc; Rosoff, James S.; Lee, Richard K.; Mulhall, John P.] Cornell Univ, Weill Cornell Med Coll, Boston, MA USA.
[Tanrikut, Cigdem] Harvard Univ, Sch Med, New York, NY USA.
[Goldstein, Marc; Rosoff, James S.; Lee, Richard K.] New York Presbyterian Hosp, New York, NY USA.
[Goldstein, Marc] Populat Council, Ctr Biomed Res, New York, NY 10021 USA.
[Nelson, Christian J.; Mulhall, John P.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RP Tanrikut, C (reprint author), Massachusetts Gen Hosp, 55 Fruit St,YAW 10A, Boston, MA 02114 USA.
EM ctanrikut@partners.org
FU New York Community Trust
FX The authors thank Joshua Bloomberg, Judy Choi, and Sam Finkelberg, RN
for data accumulation and data entry. This study was supported by the
Frederick J. and Theresa Dow Wallace Fund of the New York Community
Trust.
NR 32
TC 47
Z9 52
U1 0
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1464-4096
J9 BJU INT
JI BJU Int.
PD NOV
PY 2011
VL 108
IS 9
BP 1480
EP 1484
DI 10.1111/j.1464-410X.2010.10030.x
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 846MA
UT WOS:000296905800021
PM 21435152
ER
PT J
AU Wu, WW
Johnson, R
Schepp, KG
Berry, DL
AF Wu, Wei-Wen
Johnson, Rebecca
Schepp, Karen G.
Berry, Donna L.
TI Electronic Self-report Symptom and Quality of Life for Adolescent
Patients With Cancer A Feasibility Study
SO CANCER NURSING
LA English
DT Article
DE Acceptability; Adolescent; Cancer; Cancer symptom; Computerized
assessment; Computerized questionnaire; Feasibility; Quality of life;
Web-based technology
ID CLINICAL-TRIALS; CHILDHOOD-CANCER; YOUNG-ADULTS; HEALTH; CHILDREN;
PROGRAM; CARE; WEB; QUESTIONNAIRES; ACCEPTABILITY
AB Background: Computerized symptom and quality of life (QoL) assessment has been tested and found feasible and acceptable in outpatient settings for adult patients with cancer, but has not been used often in pediatric oncology settings in the United States. Objective: The purpose of this pilot study was to evaluate the feasibility of an innovative, computerized symptom, and QoL assessment for adolescent patients who were being treated for cancer. Methods: A convenience sample of 40 adolescent patients with cancer, who were between 13 and 20 years old and able to communicate in English, agreed to participate. Each participant answered the Web-based Electronic Self-report Assessment-Cancer Adolescent Form on a wireless touch-screen computer just prior to a treatment visit in an ambulatory clinic setting. Descriptive frequencies and central tendency were used to describe sample characteristics and feasibility outcomes. Results: The computerized assessment was found to be feasible with regard to data completeness rates (>99%), acceptability (high), time to complete (30 minutes), and assistance required to complete (minimal). Conclusion: The Electronic Self-report Assessment-Cancer Adolescent Form is a feasible approach for obtaining adolescent patients' self-report of cancer symptoms and QoL in an ambulatory setting. Implications for Practice: Screening for symptoms and QoL may be integrated during check-in procedures as routine assessment for adolescent cancer patients in ambulatory settings.
C1 [Berry, Donna L.] Harvard Univ, Dana Farber Canc Inst, Sch Med, Phyllis F Cantor Ctr Res Nursing & Patient Care S, Boston, MA 02115 USA.
[Wu, Wei-Wen] Natl Taipei Univ, Nursing & Hlth Sci Sch Nursing, Dept Nursing, Taipei, Taiwan.
[Johnson, Rebecca] Childrens Hosp, Seattle, WA USA.
[Schepp, Karen G.] Univ Washington, Sch Nursing, Seattle, WA 98195 USA.
RP Berry, DL (reprint author), Harvard Univ, Dana Farber Canc Inst, Sch Med, Phyllis F Cantor Ctr Res Nursing & Patient Care S, 405 Brookline Ave,CP 305, Boston, MA 02115 USA.
EM donna_berry@dfci.harvard.edu
OI Wu, Wei-Wen/0000-0002-6439-5369
FU School of Nursing, University of Washington; Sigma Theta Tau
PSI-at-Large Chapter; Hematology/Oncology and Orthopedics clinics at
Seattle Children
FX Funding was received from Hester McLaws Fund, School of Nursing,
University of Washington, and the Sigma Theta Tau PSI-at-Large Chapter.;
The authors thank all participants and their parents for their time and
effort in sharing their experiences. Many thanks to the
Hematology/Oncology and Orthopedics clinics at Seattle Children's for
supporting this study, particularly Dr Ernest Conrad, Elizabeth
Scholzen, and Sarah Young.
NR 55
TC 5
Z9 5
U1 4
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0162-220X
EI 1538-9804
J9 CANCER NURS
JI Cancer Nurs.
PD NOV-DEC
PY 2011
VL 34
IS 6
BP 479
EP 486
DI 10.1097/NCC.0b013e31820a5bdd
PG 8
WC Oncology; Nursing
SC Oncology; Nursing
GA 842RA
UT WOS:000296615800011
PM 21372703
ER
PT J
AU Zhang, CP
Wang, LG
Wu, DY
Chen, HY
Chen, Z
Thomas-Ahner, JM
Zynger, DL
Eeckhoute, J
Yu, JD
Luo, J
Brown, M
Clinton, SK
Nephew, KP
Huang, THM
Li, W
Wang, QB
AF Zhang, Chunpeng
Wang, Liguo
Wu, Dayong
Chen, Hongyan
Chen, Zhong
Thomas-Ahner, Jennifer M.
Zynger, Debra L.
Eeckhoute, Jerome
Yu, Jindan
Luo, Jun
Brown, Myles
Clinton, Steven K.
Nephew, Kenneth P.
Huang, Tim H. -M.
Li, Wei
Wang, Qianben
TI Definition of a FoxA1 Cistrome That Is Crucial for G(1) to S-Phase
Cell-Cycle Transit in Castration-Resistant Prostate Cancer
SO CANCER RESEARCH
LA English
DT Article
ID TRANSCRIPTION FACTOR; ANDROGEN RECEPTOR; REGULATORY ELEMENTS; IN-VITRO;
CHROMATIN; BINDING; EXPRESSION; PROGRESSION; NUCLEOSOME; SIGNATURES
AB The enhancer pioneer transcription factor FoxA1 is a global mediator of steroid receptor (SR) action in hormone-dependent cancers. In castration-resistant prostate cancer (CRPC), FoxA1 acts as an androgen receptor cofactor to drive G(2) to M-phase cell-cycle transit. Here, we describe a mechanistically distinct SR-independent role for FoxA1 in driving G(1) to S-phase cell-cycle transit in CRPC. By comparing FoxA1 binding sites in prostate cancer cell genomes, we defined a codependent set of FoxA1-MYBL2 and FoxA1-CREB1 binding sites within the regulatory regions of the Cyclin E2 and E2F1 genes that are critical for CRPC growth. Binding at these sites upregulate the Cyclin E2 and Cyclin A2 genes in CRPC but not in earlier stage androgen-dependent prostate cancer, establishing a stage-specific role for this pathway in CRPC growth. Mechanistic investigations indicated that FoxA1, MYBL2, or CREB1 induction of histone H3 acetylation facilitated nucleosome disruption as the basis for codependent transcriptional activation and G(1) to S-phase cell-cycle transit. Our findings establish FoxA1 as a pivotal driver of the cell-cycle in CRPC which promotes G(1) to S-phase transit as well as G(2) to M-phase transit through two distinct mechanisms. Cancer Res; 71(21); 6738-48. (C)2011 AACR.
C1 [Zhang, Chunpeng; Wu, Dayong; Chen, Hongyan; Chen, Zhong; Wang, Qianben] Ohio State Univ, Coll Med, Dept Mol & Cellular Biochem, Columbus, OH 43210 USA.
[Zhang, Chunpeng; Wu, Dayong; Chen, Hongyan; Chen, Zhong; Thomas-Ahner, Jennifer M.; Clinton, Steven K.; Wang, Qianben] Ohio State Univ, Coll Med, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Thomas-Ahner, Jennifer M.; Clinton, Steven K.] Ohio State Univ, Coll Med, Div Med Oncol, Dept Internal Med, Columbus, OH 43210 USA.
[Zynger, Debra L.] Ohio State Univ, Coll Med, Dept Pathol, Columbus, OH 43210 USA.
[Huang, Tim H. -M.] Ohio State Univ, Human Canc Genet Program, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
[Wang, Liguo; Li, Wei] Baylor Coll Med, Div Biostat, Dan L Duncan Canc Ctr, Houston, TX 77030 USA.
[Wang, Liguo; Li, Wei] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA.
[Eeckhoute, Jerome] Univ Lille Nord France, Fac Med Lille Pole Rech, INSERM UMR Batiment J&K 1011, Lille, France.
[Yu, Jindan] Northwestern Univ, Dept Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Yu, Jindan] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Feinberg Sch Med, Chicago, IL 60611 USA.
[Luo, Jun] Johns Hopkins Univ, Sch Med, Dept Urol, Baltimore, MD 21205 USA.
[Brown, Myles] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Brown, Myles] Harvard Univ, Sch Med, Boston, MA USA.
[Nephew, Kenneth P.] Indiana Univ, Sch Med, Med Sci Program, Dept Cellular & Integrat Physiol, Bloomington, IN 47405 USA.
RP Wang, QB (reprint author), Ohio State Univ, Coll Med, Dept Mol & Cellular Biochem, 888 Biomed Res Tower,460 W 12th Ave, Columbus, OH 43210 USA.
EM WL1@bcm.edu; qianben.wang@osumc.edu
RI Wang, Qianben/E-4267-2011; Thomas-Ahner, Jennifer/I-7598-2013;
Thomas-Ahner, Jennifer/M-3955-2015;
OI Thomas-Ahner, Jennifer/0000-0001-5264-7592; Brown,
Myles/0000-0002-8213-1658; Eeckhoute, Jerome/0000-0002-7222-9264
FU NIH [R00 CA126160, U54 CA113001]; DOD [PC094421]; Ohio State University
Comprehensive Cancer Center
FX This work was supported by NIH grants R00 CA126160 (to Q. Wang and W.
Li) and U54 CA113001 (to Q.Wang, K.P. Nephew, and T.H.M. Huang), DOD
grant PC094421 (to W. Li), and the Ohio State University Comprehensive
Cancer Center (to Q. Wang and T.H.M. Huang).
NR 46
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Z9 43
U1 0
U2 7
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2011
VL 71
IS 21
BP 6738
EP 6748
DI 10.1158/0008-5472.CAN-11-1882
PG 11
WC Oncology
SC Oncology
GA 842ML
UT WOS:000296603500020
PM 21900400
ER
PT J
AU Bhalla, K
Hwang, BJ
Dewi, RE
Ou, LH
Twaddel, W
Fang, HB
Vafai, SB
Vazquez, F
Puigserver, P
Boros, L
Girnun, GD
AF Bhalla, Kavita
Hwang, Bor Jang
Dewi, Ruby E.
Ou, Lihui
Twaddel, William
Fang, Hong-Bin
Vafai, Scott B.
Vazquez, Francesca
Puigserver, Pere
Boros, Laszlo
Girnun, Geoffrey D.
TI PGC1 alpha Promotes Tumor Growth by Inducing Gene Expression Programs
Supporting Lipogenesis
SO CANCER RESEARCH
LA English
DT Article
ID ESTROGEN-RELATED RECEPTOR; FATTY-ACID SYNTHESIS;
OXIDATIVE-PHOSPHORYLATION; BREAST-CANCER; PPAR-GAMMA; ENERGY-METABOLISM;
NUCLEAR RECEPTORS; CELL-GROWTH; ERR-ALPHA; PGC-1
AB Despite the role of aerobic glycolysis in cancer, recent studies highlight the importance of the mitochondria and biosynthetic pathways as well. PPAR gamma coactivator 1 alpha (PGC1 alpha) is a key transcriptional regulator of several metabolic pathways including oxidative metabolism and lipogenesis. Initial studies suggested that PGC1 alpha expression is reduced in tumors compared with adjacent normal tissue. Paradoxically, other studies show that PGC1 alpha is associated with cancer cell proliferation. Therefore, the role of PGC1 alpha in cancer and especially carcinogenesis is unclear. Using Pgc1 alpha(-/-) and Pgc1 alpha(+/+) mice, we show that loss of PGC1 alpha protects mice from azoxymethane-induced colon carcinogenesis. Similarly, diethylnitrosamine-induced liver carcinogenesis is reduced in Pgc1 alpha(-/-) mice as compared with Pgc1 alpha(+/+) mice. Xenograft studies using gain and loss of PGC1 alpha expression showed that PGC1 alpha also promotes tumor growth. Interestingly, while PGC1 alpha induced oxidative phosphorylation and tricarboxylic acid cycle gene expression, we also observed an increase in the expression of two genes required for de novo fatty acid synthesis, ACC and FASN. In addition, SLC25A1 and ACLY, which are required for the conversion of glucose into acetyl-CoA for fatty acid synthesis, were also increased by PGC1 alpha, thus linking the oxidative and lipogenic functions of PGC1 alpha. Indeed, using stable C-13 isotope tracer analysis, we show that PGC1 alpha increased de novo lipogenesis. Importantly, inhibition of fatty acid synthesis blunted these progrowth effects of PGC1 alpha. In conclusion, these studies show for the first time that loss of PGC1 alpha protects against carcinogenesis and that PGC1 alpha coordinately regulates mitochondrial and fatty acid metabolism to promote tumor growth. Cancer Res; 71(21); 6888-98. (C) 2011 AACR.
C1 [Bhalla, Kavita; Hwang, Bor Jang; Dewi, Ruby E.; Ou, Lihui; Fang, Hong-Bin; Girnun, Geoffrey D.] Univ Maryland, Sch Med, Marlene & Stewart Greenebaum Canc Ctr, Dept Biochem & Mol Biol, Baltimore, MD 21201 USA.
[Twaddel, William] Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA.
[Vafai, Scott B.; Vazquez, Francesca; Puigserver, Pere] Harvard Univ, Sch Med, Boston, MA USA.
[Vazquez, Francesca; Puigserver, Pere] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Boros, Laszlo] Univ Calif Los Angeles, UCLA Sch Med, Los Angeles, CA USA.
[Boros, Laszlo] SiDMAP LLC, Los Angeles, CA USA.
RP Girnun, GD (reprint author), Univ Maryland, Sch Med, Marlene & Stewart Greenebaum Canc Ctr, Dept Biochem & Mol Biol, 655 W Baltimore St,BRB Room 10-039, Baltimore, MD 21201 USA.
EM ggirnun@som.umaryland.edu
FU University of Maryland Greenebaum Cancer Center CRF; Susan G. Komen
Breast Cancer Foundation [KG081400]; NIDDK [DK064685]
FX This work was supported by the University of Maryland Greenebaum Cancer
Center CRF, Susan G. Komen Breast Cancer Foundation (KG081400), and
NIDDK (DK064685) to Geoffrey D. Girnun.
NR 50
TC 55
Z9 57
U1 0
U2 16
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2011
VL 71
IS 21
BP 6888
EP 6898
DI 10.1158/0008-5472.CAN-11-1011
PG 11
WC Oncology
SC Oncology
GA 842ML
UT WOS:000296603500035
PM 21914785
ER
PT J
AU Rocha-Singh, KJ
Novack, V
Pencina, M
D'Agostino, R
Ansel, G
Rosenfield, K
Jaff, MR
AF Rocha-Singh, Krishna J.
Novack, Victor
Pencina, Michael
D'Agostino, Ralph
Ansel, Gary
Rosenfield, Kenneth
Jaff, Michael R.
TI Objective Performance Goals of Safety and Blood Pressure Efficacy For
Clinical Trials of Renal Artery Bare Metal Stents in Hypertensive
Patients with Atherosclerotic Renal Artery Stenosis
SO CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE renal artery stenosis; bare metal stents; resistant hypertension
ID ANGIOPLASTY; REVASCULARIZATION; INTERVENTIONS; PREVENTION; GUIDELINES;
MANAGEMENT; COMMITTEE; GRADIENT; DISEASE
AB Objective: To provide safety and performance goals for prospective single-arm trials of bare metal renal artery stenting in patients with resistant hypertension associated with high grade atherosclerotic renal artery stenosis. Background: To date, there have been no US Pre-Market Approval (PMA) bare metal renal stent device trials which have focused on improvement of blood pressure control as a primary effectiveness endpoint. Methods: Analysis of subject-level data from three large industry sponsored pre-market approval (PMA) trials was performed. Hypertensive patients (>= 155 mmHg) with a >= 50% atherosclerotic renal artery stenosis were included. Thirty day and 9-month systolic and diastolic blood pressure measurements, renal function and 9-month duplex ultrasound assessment of renal artery patency were analyzed. Results: Initial data analysis of 600 patients from the 3 PMA trials identified 286 patients who met inclusion criteria. The mean baseline systolic blood pressure was 177.8 +/- 19.3 mmHg with a mean 68.1% diameter renal artery stenosis. Nine months after successful stenting, the mean SBP was 156.7 +/- 24.1 mmHg; the 9 month restenosis rate was 14.4%. Conclusion: Based on the statistical modeling of these data and a priori established performance criteria, the co-primary endpoints of 9 month reduction in blood pressure and in-stent restenosis are proposed. The reduction in blood pressure will be analyzed as a continuous variable and will be compared to this performance goal. (C) 2011 Wiley Periodicals, Inc.
C1 [Rocha-Singh, Krishna J.] Prairie Educ & Res Cooperat, Springfield, IL 62794 USA.
[Novack, Victor; Pencina, Michael; D'Agostino, Ralph] Harvard Clin Res Inst, Boston, MA 02115 USA.
[Ansel, Gary] Riverside Hosp, Dept Cardiol, Columbus, OH USA.
[Rosenfield, Kenneth] Massachusetts Gen Hosp, Dept Cardiol, Boston, MA 02114 USA.
[Jaff, Michael R.] Massachusetts Gen Hosp, Dept Vasc Med, Boston, MA 02114 USA.
RP Rocha-Singh, KJ (reprint author), Prairie Educ & Res Cooperat, POB 19420, Springfield, IL 62794 USA.
EM ksingh@prairieheart.com
FU Abbott Vascular; Bard; Boston Scientific Corporation; Baxter; Atrium
Medical, Inc; Invatec
FX Dr. Krishna Rocha-Singh is a paid consultant for Medtronic, ev3 and
Minnow Medical and is salaried as the Medical Director of Prairie
Education and Research Cooperative and as a Board Member of VIVA
Physicians. Dr. Michal Jaff is a non-compensated consultant for Abbott
Vascular Devices, Boston Scientific Corporation., Covidien and
Medtronic, a compensated consultant for Harvard Clinical Research
Institute and Nexeon Medical Systems, and is a salaried Board Member of
VIVA Physicians. Dr. Gary Ansel is a paid consultant for Cordis
Corporation, Atrium Medical, Inc., Boston Scientific Corporation, Cook,
Inc. and Abbott Vascular Devices, and is a salaried Board Member of VIVA
Physicians. Dr. Kenneth Rosen-field is a paid consultant and Scientific
Advisory Board Member for Abbott Vascular Devices, Harvard Clinical
Research Institute, Lumen and Complete Conference Management, has
received research or fellowship support from Abbott Vascular, Bard,
Boston Scientific Corporation, Baxter, Atrium Medical, Inc. and Invatec,
has equity in Lumen Biomedical, Medical Simulation Corporation and
Primacea, and is a salaried Board Member of Viva Physicians. Drs. Victor
Novack, Michael Pencina and Ralph D'Agostino have nothing to disclose.
NR 28
TC 7
Z9 7
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1522-1946
J9 CATHETER CARDIO INTE
JI Catheter. Cardiovasc. Interv.
PD NOV 1
PY 2011
VL 78
IS 5
BP 779
EP 789
DI 10.1002/ccd.23055
PG 11
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 840BI
UT WOS:000296412800022
PM 21648052
ER
PT J
AU Forster, N
Ellisen, LW
AF Forster, Nicole
Ellisen, Leif W.
TI Notch signaling mediates p63-induced quiescence: A new facet of
p63/Notch crosstalk
SO CELL CYCLE
LA English
DT News Item
ID P63; CELLS; ROLES; LIMB
C1 [Forster, Nicole] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Forster, N (reprint author), Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
EM ellisen@helix.mgh.harvard.edu
FU NIDCR NIH HHS [R01 DE015945]
NR 9
TC 4
Z9 5
U1 0
U2 0
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD NOV 1
PY 2011
VL 10
IS 21
BP 3632
EP 3633
DI 10.4161/cc.10.21.18182
PG 2
WC Cell Biology
SC Cell Biology
GA 842DZ
UT WOS:000296572100014
PM 22041817
ER
PT J
AU Ferretti, R
Sbroggio, M
Di Savino, A
Fusella, F
Bertero, A
Michowski, W
Tarone, G
Brancaccio, M
AF Ferretti, Roberta
Sbroggio, Mauro
Di Savino, Augusta
Fusella, Federica
Bertero, Alessandro
Michowski, Wojciech
Tarone, Guido
Brancaccio, Mara
TI Morgana and Melusin Two fairies chaperoning signal transduction
SO CELL CYCLE
LA English
DT Article
DE Morgana; Melusin; ROCK; ERK1/2; genomic stability; centrosome
duplication; heart hypertrophy
ID HSP90 MOLECULAR CHAPERONE; CENTROSOME DUPLICATION; DISEASE RESISTANCE;
PRESSURE-OVERLOAD; ESSENTIAL COMPONENT; CONTAINING PROTEIN; ROCK-II;
SGT1; IQGAP1; RAR1
AB Chaperones and scaffold proteins are key elements involved in controlling the assembly of molecular complexes required for coordinated signal transduction. Here we describe morgana and melusin, two phylogenetically conserved chaperones that cooperate with Hsp90 and regulate signal transduction in important physiopathological processes. While morgana is ubiquitously expressed, melusin expression is restricted to striated muscles. Despite high sequence homology, the two chaperones have distinct functions. Morgana controls genomic stability by regulating the centrosome cycle via ROCKII kinase. Melusin, on the other hand, organizes ERK signal transduction in cardiomyocytes and regulates cardiac compensatory hypertrophy in response to different stress stimuli.
C1 [Ferretti, Roberta; Sbroggio, Mauro; Di Savino, Augusta; Fusella, Federica; Bertero, Alessandro; Tarone, Guido; Brancaccio, Mara] Univ Turin, Ctr Mol Biotechnol, Dipartimento Genet Biol & Biochim, Turin, Italy.
[Michowski, Wojciech] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
RP Brancaccio, M (reprint author), Univ Turin, Ctr Mol Biotechnol, Dipartimento Genet Biol & Biochim, Turin, Italy.
EM mara.brancaccio@unito.it
OI Tarone, Guido/0000-0003-4805-086X
FU EUGeneHeart [LSHM-CT-2005-018833]; Regione Piemonte POR F.E.S.R.;
Associazione Italiana per la Ricerca sul Cancro
FX We wish to thank R. Srinivasan for critical comments on the manuscript.
This work was supported by grants from EUGeneHeart (LSHM-CT-2005-018833
to G T.), Regione Piemonte POR F.E.S.R. 2007/2013 "DRUIDI: Piattaforme
Innovative per le Scienze della Vita" to G.T. and M.B. Regione Piemonte
CIPE 2006 to M.B., Fondazione Veronesi to G.T., AIRC 2008 to M.B. and
Foundation for Polish Science to W.M.
NR 41
TC 12
Z9 12
U1 0
U2 3
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD NOV 1
PY 2011
VL 10
IS 21
BP 3678
EP 3683
PG 6
WC Cell Biology
SC Cell Biology
GA 842DZ
UT WOS:000296572100021
PM 22037254
ER
PT J
AU Harris, KM
Strauss, CE
Eagle, KA
Hirsch, AT
Isselbacher, EM
Tsai, TT
Shiran, H
Fattori, R
Evangelista, A
Cooper, JV
Montgomery, DG
Froehlich, JB
Nienaber, CA
AF Harris, Kevin M.
Strauss, Craig E.
Eagle, Kim A.
Hirsch, Alan T.
Isselbacher, Eric M.
Tsai, Thomas T.
Shiran, Hadas
Fattori, Rossella
Evangelista, Arturo
Cooper, Jeanna V.
Montgomery, Daniel G.
Froehlich, James B.
Nienaber, Christoph A.
CA Int Registry Acute Aortic
TI Correlates of Delayed Recognition and Treatment of Acute Type A Aortic
Dissection The International Registry of Acute Aortic Dissection (IRAD)
SO CIRCULATION
LA English
DT Article
DE aorta; aortic; aneurysm; thoracic; diagnosis; imaging; surgery
ID TRANSESOPHAGEAL ECHOCARDIOGRAPHY; INTRAMURAL HEMATOMA;
COMPUTED-TOMOGRAPHY; FREQUENCY; ANEURYSM; OUTCOMES; EXPERIENCE;
DIAGNOSIS; DISEASE
AB Background-In acute aortic dissection, delays exist between presentation and diagnosis and, once diagnosed, definitive treatment. This study aimed to define the variables associated with these delays.
Methods and Results-Acute aortic dissection patients enrolled in the International Registry of Acute Aortic Dissection (IRAD) between 1996 and January 2007 were evaluated for factors contributing to delays in presentation to diagnosis and in diagnosis to surgery. Multiple linear regression was performed to determine relative delay time ratios (DTRs) for individual correlates. The median time from arrival at the emergency department to diagnosis was 4.3 hours (quartile 1-3, 1.5-24 hours; n = 894 patients) and from diagnosis to surgery was 4.3 hours (quartile 1-3, 2.4-24 hours; n = 751). Delays in acute aortic dissection diagnosis occurred in female patients; those with atypical symptoms that were not abrupt or did not include chest, back, or any pain; patients with an absence of pulse deficit or hypotension; or those who initially presented to a nontertiary care hospital (all P < 0.05). The largest relative DTRs were for fever (DTR = 5.11; P < 0.001) and transfer from nontertiary hospital (DTR = 3.34; P < 0.001). Delay in time from diagnosis to surgery was associated with a history of previous cardiac surgery, presentation without abrupt or any pain, and initial presentation to a nontertiary care hospital (all P < 0.001). The strongest factors associated with operative delay were prolonged time from presentation to diagnosis (DTR = 1.35; P < 0.001), race other than white (DTR = 2.25; P < 0.001), and history of coronary artery bypass surgery (DTR = 2.81; P < 0.001).
Conclusions-Improved physician awareness of atypical presentations and prompt transport of acute aortic dissection patients could reduce crucial time variables. (Circulation. 2011; 124: 1911-1918.)
C1 [Harris, Kevin M.; Strauss, Craig E.] Abbott NW Hosp, Minneapolis Heart Inst Fdn, Minneapolis, MN 55407 USA.
[Strauss, Craig E.; Hirsch, Alan T.] Univ Minnesota, Div Cardiovasc, Minneapolis, MN 55455 USA.
[Hirsch, Alan T.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Eagle, Kim A.; Shiran, Hadas; Cooper, Jeanna V.; Montgomery, Daniel G.; Froehlich, James B.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Isselbacher, Eric M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Tsai, Thomas T.] Univ Colorado, Denver, CO 80202 USA.
[Fattori, Rossella] Univ Hosp S Orsola, Bologna, Italy.
[Evangelista, Arturo] Hosp Gen Univ Vall dHebron, Barcelona, Spain.
[Nienaber, Christoph A.] Univ Rostock, Rostock, Germany.
RP Harris, KM (reprint author), Abbott NW Hosp, Minneapolis Heart Inst Fdn, 920 E 28th St,Ste 300, Minneapolis, MN 55407 USA.
EM kharris@mplsheart.com
FU University of Michigan Health System; Varbedian Fund for Aortic
Research; Hewlett Foundation; Mardigian Foundation; GORE, Inc.; Bristol
Myers Squibb; Blue Cross/Blue Shield of Michigan; GORE; Pfizer;
SanofiAventis; Varbedian Fund; National Institutes of Health National
Heart, Lung, and Blood Institute; Robert Wood Johnson Foundation
FX IRAD is supported by grants from the University of Michigan Health
System, Varbedian Fund for Aortic Research, Hewlett Foundation,
Mardigian Foundation, and GORE, Inc.; Dr Eagle has received
grant/research support from Bristol Myers Squibb, Blue Cross/Blue Shield
of Michigan, GORE, Hewlett Foundation, Mardigian Foundation, Pfizer,
SanofiAventis, and Varbedian Fund and consultant fees from the National
Institutes of Health National Heart, Lung, and Blood Institute, Pfizer,
SanofiAventis, and Robert Wood Johnson Foundation. Dr Froehlich has
consulted with Pfizer and Sanofi-aventis; served on the speakers' bureau
for Pfizer, Sanofi-aventis, and Merck; and has contracted research with
Blue Cross/Blue Shield of Michigan, Mardigian Foundation, and
Fibromuscular Disease Society of America. Dr Nienaber has received
grant/research support from Varbedian Fund, Hewlett Foundation,
Mardigian Foundation, and GORE, Inc. The sponsors had no role in the
design and conduct of the study; the collection, management, analysis,
or interpretation of the data; or the preparation, review, or approval
of the manuscript.
NR 25
TC 46
Z9 49
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 1
PY 2011
VL 124
IS 18
BP 1911
EP U82
DI 10.1161/CIRCULATIONAHA.110.006320
PG 10
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 842JB
UT WOS:000296593800013
PM 21969019
ER
PT J
AU Reynolds, MR
Magnuson, EA
Lei, Y
Leon, MB
Smith, CR
Svensson, LG
Webb, JG
Babaliaros, VC
Bowers, BS
Fearon, WF
Herrmann, HC
Kapadia, S
Kodali, SK
Makkar, RR
Pichard, AD
Cohen, DJ
AF Reynolds, Matthew R.
Magnuson, Elizabeth A.
Lei, Yang
Leon, Martin B.
Smith, Craig R.
Svensson, Lars G.
Webb, John G.
Babaliaros, Vasilis C.
Bowers, Bruce S.
Fearon, William F.
Herrmann, Howard C.
Kapadia, Samir
Kodali, Susheel K.
Makkar, Raj R.
Pichard, Augusto D.
Cohen, David J.
CA Placement Aortic Transcatheter
TI Health-Related Quality of Life After Transcatheter Aortic Valve
Replacement in Inoperable Patients With Severe Aortic Stenosis
SO CIRCULATION
LA English
DT Article
DE aortic valve stenosis; heart valves; quality of life
ID ACUTE MYOCARDIAL-INFARCTION; HEART-FAILURE; GREATER-THAN-80 YEARS;
ELDERLY-PATIENTS; IMPLANTATION; SURVIVAL; OUTCOMES; SURGERY; RISK;
EFFICACY
AB Background-Transcatheter aortic valve replacement (TAVR) has been shown to improve survival compared with standard therapy in patients with severe aortic stenosis who cannot have surgery. The effects of TAVR on health-related quality of life have not been reported from a controlled study.
Methods and Results-The Placement of Aortic Transcatheter Valves (PARTNER) trial randomized patients with symptomatic, severe aortic stenosis who were not candidates for surgical valve replacement to TAVR (n = 179) or standard therapy (n = 179). Health-related quality of life was assessed at baseline and at 1, 6, and 12 months with the Kansas City Cardiomyopathy Questionnaire (KCCQ) and the 12-item Short Form-12 General Health Survey (SF-12). The primary end point was the KCCQ overall summary score (range, 0-100; higher = better). At baseline, mean KCCQ summary scores (35 +/- 20) and SF-12 physical summary scores (28 +/- 7) were markedly depressed. Although the KCCQ summary score improved from baseline in both groups, the extent of improvement was greater after TAVR compared with control at 1 month (mean between-group difference, 13 points; 95% confidence interval, 8-19; P < 0.001) with larger benefits at 6 months (mean difference, 21 points; 95% confidence interval, 15-27; P < 0.001) and 12 months (mean difference, 26 points; 95% confidence interval, 19-33; P < 0.001). At 12 months, TAVR patients also reported higher SF-12 physical and mental health scores with mean differences compared with standard care of 5.7 and 6.4 points, respectively (P < 0.001 for both comparisons).
Conclusions-Among inoperable patients with severe aortic stenosis, compared with standard care, TAVR resulted in significant improvements in health-related quality of life that were maintained for at least 1 year.
C1 [Cohen, David J.] Univ Missouri Kansas City, Sch Med, St Lukes Mid Amer Heart Inst, Kansas City, MO 64111 USA.
[Reynolds, Matthew R.] Boston VA Healthcare Syst, Harvard Clin Res Inst, Boston, MA USA.
[Leon, Martin B.; Smith, Craig R.; Kodali, Susheel K.] Columbia Presbyterian Med Ctr, New York, NY USA.
[Svensson, Lars G.; Kapadia, Samir] Cleveland Clin, Cleveland, OH 44106 USA.
[Webb, John G.] St Pauls Hosp, Vancouver, BC V6Z 1Y6, Canada.
[Babaliaros, Vasilis C.] Emory Univ Hosp, Atlanta, GA 30322 USA.
[Bowers, Bruce S.] Med City Dallas, Dallas, TX USA.
[Fearon, William F.] Stanford Univ, Stanford, CA 94305 USA.
[Herrmann, Howard C.] Univ Penn, Philadelphia, PA 19104 USA.
[Makkar, Raj R.] Cedars Sinai Heart Inst, Los Angeles, CA USA.
[Pichard, Augusto D.] Washington Hosp Ctr, Washington, DC 20010 USA.
[Magnuson, Elizabeth A.; Lei, Yang; Cohen, David J.] Univ Missouri Kansas City, St Lukes Mid Amer Heart & Vasc Inst, Kansas City, MO 64111 USA.
RP Cohen, DJ (reprint author), Univ Missouri Kansas City, Sch Med, St Lukes Mid Amer Heart Inst, 4401 Wornall Rd, Kansas City, MO 64111 USA.
EM dcohen@saint-lukes.org
FU Edwards Lifesciences, Inc.; Edwards Lifesciences; Biosense Webster;
Sanofi-aventis; St. Jude Medical; Eli Lilly; Daiichi Sankyo;
Bristol-Myers Squibb; Medtronic; Embrella Cardiovascular; Guided
Delivery Systems; Siemens; Philips; Valtech Cardio; Cordis; Lilly
Pharmaceuticals; Daiichi-Sanyo Pharmaceuticals; Abbott Vascular; Access
Closure; National Institutes of Health; Tryton Medical; Gore; Johnson
Johnson; Boston Scientific; Merck; Astra-Zeneca; theHeart.org.; Lilly;
MedRad; Merck/Schering-Plough; Eli Lilly-Daiichi Sankyo
FX This work was supported by Edwards Lifesciences, Inc.
(http://www.clinicaltrials.gov; unique identifier: NCT00530894).; Dr
Reynolds has received research support from Edwards Lifesciences,
Biosense Webster, and Sanofi-aventis and consulting income from Biosense
Webster, Sanofi-aventis, and St. Jude Medical. Dr Magnuson has received
grant support from Eli Lilly, Daiichi Sankyo, Sanofi-aventis, and
Bristol-Myers Squibb. Dr Leon has received consulting fees from
Medtronic and has stock options in Sadra Medical. Dr Webb has received
research support from Edwards Lifesciences, Embrella Cardiovascular,
Guided Delivery Systems, and Siemens and consulting income from Edwards
Lifesciences, Embrella Cardiovascular, Guided Delivery Systems, Philips,
St. Jude Medical, Siemens, and Valtech Cardio. Dr Babaliaros has been a
consultant for Symetis and Direct Flow Medical. Dr Bowers has received
consulting fees or speaking honoraria from Cordis, St. Jude Medical,
Lilly Pharmaceuticals, Daiichi-Sanyo Pharmaceuticals, Abbott Vascular,
Medtronic, and Access Closure. Dr Fearon has received research support
from the National Institutes of Health and St. Jude Medical and
consulting fees from Tryton Medical. Dr Herrmann has received research
support from Edwards Lifesciences, Abbott, St. Jude Medical, Gore,
Johnson & Johnson, Boston Scientific, and Medtronic; speaking honoraria
from Edwards Lifesciences and Schering Plough; and consulting fees from
Gore, Merck, Astra-Zeneca; Dr Herrmann also has equity in Endovalve,
Inc. Dr Kodali has received consulting income from Edwards Lifesciences,
Medtronic, and theHeart.org. Dr Makkar has received consulting fees,
grant support, and lectures fees from Abbott, Medtronic, and Lilly;
consulting fees and grant support from Johnson & Johnson and Daiichi
Sankyo; and grant support from St. Jude Medical and Edwards
Lifesciences. Dr Pichard has received consulting income from Edwards
Lifesciences and speaking honoraria from St. Jude Medical. Dr Cohen has
received research support from Edwards Lifesciences, Medtronic, Boston
Scientific, Abbott Vascular, MedRad, Merck/Schering-Plough, and Eli
Lilly-Daiichi Sankyo; consulting income from Schering-Plough, Eli Lilly,
Medtronic, and Cordis; and speaking honoraria from Eli Lilly, The
Medicines Company, and St. Jude Medical. The other authors report no
conflicts.
NR 33
TC 147
Z9 154
U1 2
U2 12
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 1
PY 2011
VL 124
IS 18
BP 1964
EP 1972
DI 10.1161/CIRCULATIONAHA.111.040022
PG 9
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 842JB
UT WOS:000296593800019
PM 21969017
ER
PT J
AU Magnani, JW
Rienstra, M
Lin, H
Sinner, MF
Lubitz, SA
McManus, DD
Dupuis, J
Ellinor, PT
Benjamin, EJ
AF Magnani, Jared W.
Rienstra, Michiel
Lin, Honghuang
Sinner, Moritz F.
Lubitz, Steven A.
McManus, David D.
Dupuis, Josee
Ellinor, Patrick T.
Benjamin, Emelia J.
TI Atrial Fibrillation Current Knowledge and Future Directions in
Epidemiology and Genomics
SO CIRCULATION
LA English
DT Article
DE atrial fibrillation; arrhythmias, cardiac; epidemiology; genetics;
genomics; review; risk factors
ID OF-FUNCTION MUTATION; CA2+-ACTIVATED K+ CHANNEL;
CONGESTIVE-HEART-FAILURE; COMMUNITY-BASED COHORT; RISK-FACTORS;
ATHEROSCLEROSIS RISK; FUNCTIONAL MODULES; AFRICAN-AMERICANS;
SMALL-CONDUCTANCE; ISCHEMIC-STROKE
C1 [Magnani, Jared W.] Boston Univ, Sch Med, Sect Cardiovasc Med, Dept Med, Boston, MA 02118 USA.
[Magnani, Jared W.; Sinner, Moritz F.; Dupuis, Josee; Benjamin, Emelia J.] Natl Heart Lung & Blood Inst Framingham Heart Stu, Framingham, MA USA.
[Rienstra, Michiel] Univ Groningen, Dept Cardiol, Univ Med Ctr Groningen, Groningen, Netherlands.
[Sinner, Moritz F.; Lubitz, Steven A.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Lubitz, Steven A.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Sinner, Moritz F.] Univ Munich, Dept Med 1, Univ Hosp Grosshadern, Munich, Germany.
[McManus, David D.] Univ Massachusetts, Sch Med, Dept Med, Div Cardiovasc Med, Worcester, MA USA.
[Dupuis, Josee] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Prevent Med Sect, Boston, MA 02118 USA.
RP Magnani, JW (reprint author), Boston Univ, Sch Med, Sect Cardiovasc Med, Dept Med, 88 E Newton St, Boston, MA 02118 USA.
EM jmagnani@bu.edu
OI Lin, Honghuang/0000-0003-3043-3942; Dupuis, Josee/0000-0003-2871-3603;
Benjamin, Emelia/0000-0003-4076-2336; Rienstra,
Michiel/0000-0002-2581-070X
FU American Heart Association [09FTF 2190028]; Netherlands Organization for
Scientific Research [825.09.020]; German Heart Foundation; National
Institutes of Health (NIH) [R37HL69874-08, U01HL105268, HL092577,
RO1AG028321, RC1-HL01056, 1R01HL102214, 5R21DA027021, 1RO1HL104156,
1K24HL105780]; [6R01-NS17950]; [N01-HC25195]
FX Dr Magnani is supported by American Heart Association Award 09FTF
2190028. Dr Rienstra is supported by a grant from the Netherlands
Organization for Scientific Research (Rubicon grant 825.09.020). Dr
Sinner is supported by the German Heart Foundation. Dr McManus is
supported by grants from the National Institutes of Health (NIH;
R37HL69874-08, U01HL105268). This work was supported by grants from the
NIH to Drs Benjamin and Ellinor (HL092577), Dr Benjamin (RO1AG028321,
RC1-HL01056, 1R01HL102214), and Dr Ellinor (5R21DA027021, 1RO1HL104156,
1K24HL105780) and by 6R01-NS17950 and N01-HC25195.
NR 147
TC 102
Z9 106
U1 1
U2 17
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 1
PY 2011
VL 124
IS 18
BP 1982
EP U170
DI 10.1161/CIRCULATIONAHA.111.039677
PG 16
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 842JB
UT WOS:000296593800021
PM 22042927
ER
PT J
AU Lee, BY
Song, Y
McGlone, SM
Bailey, RR
Feura, JM
Tai, JHY
Lewis, GJ
Wiringa, AE
Smith, KJ
Muder, RR
Harrison, LH
Piraino, B
AF Lee, B. Y.
Song, Y.
McGlone, S. M.
Bailey, R. R.
Feura, J. M.
Tai, J. H. Y.
Lewis, G. J.
Wiringa, A. E.
Smith, K. J.
Muder, R. R.
Harrison, L. H.
Piraino, B.
TI The economic value of screening haemodialysis patients for
methicillin-resistant Staphylococcus aureus in the USA
SO CLINICAL MICROBIOLOGY AND INFECTION
LA English
DT Article
DE Cost-effectiveness; economics; haemodialysis; methicillin-resistant
Staphylococcus aureus; surveillance
ID HEALTH-CARE WORKERS; DIALYSIS PATIENTS; SURGERY PATIENTS; UNITED-STATES;
MUPIROCIN; COLONIZATION; INFECTIONS; PREVALENCE; CARRIAGE; CALCIUM
AB Methicillin-resistant Staphylococcus aureus (MRSA) can cause severe infections in patients undergoing haemodialysis. Routine periodic testing of haemodialysis patients and attempting to decolonize those who test positive may be a strategy to prevent MRSA infections. The economic value of such a strategy has not yet been estimated. We constructed a Markov computer simulation model to evaluate the economic value of employing routine testing (agar-based or PCR) at different MRSA prevalence, spontaneous clearance, costs of decolonization and decolonization success rates, performed every 3, 6 or 12 months. The model showed periodic MRSA surveillance with either test to be cost-effective (incremental cost-effectiveness ratio <=$50 000/quality-adjusted life-year) for all conditions tested. Agar surveillance was dominant (i.e. less costly and more effective) at an MRSA prevalence >= 10% and a decolonization success rate >= 25% for all decolonization treatment costs tested with no spontaneous clearance. PCR surveillance was dominant when the MRSA prevalence was >= 20% and decolonization success rate was >= 75% with no spontaneous clearance. Routine periodic testing and decolonization of haemodialysis patients for MRSA may be a cost-effective strategy over a wide range of MRSA prevalences, decolonization success rates, and testing intervals.
C1 [Lee, B. Y.; Song, Y.; McGlone, S. M.; Bailey, R. R.; Feura, J. M.; Tai, J. H. Y.; Lewis, G. J.; Wiringa, A. E.] Univ Pittsburgh, Publ Hlth Computat & Operat Res PHICOR, Pittsburgh, PA 15213 USA.
[Lee, B. Y.; Song, Y.; McGlone, S. M.; Bailey, R. R.; Feura, J. M.; Tai, J. H. Y.; Lewis, G. J.; Wiringa, A. E.] Univ Pittsburgh, Sch Med, Dept Biomed Informat, Pittsburgh, PA 15213 USA.
[Lee, B. Y.; Song, Y.; McGlone, S. M.; Bailey, R. R.; Feura, J. M.; Tai, J. H. Y.; Lewis, G. J.; Wiringa, A. E.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15213 USA.
[Smith, K. J.] Univ Pittsburgh, Sect Decis Sci & Clin Syst Modeling, Pittsburgh, PA 15213 USA.
[Muder, R. R.] Univ Pittsburgh, VA Pittsburgh Hlth Care Syst, Div Infect Dis, Pittsburgh, PA 15213 USA.
[Harrison, L. H.] Univ Pittsburgh, Sch Med, Infect Dis Epidemiol Res Unit, Pittsburgh, PA 15213 USA.
[Piraino, B.] Univ Pittsburgh, Div Nephrol, Pittsburgh, PA 15213 USA.
RP Lee, BY (reprint author), Univ Pittsburgh, Publ Hlth Computat & Operat Res PHICOR, 200 Meyran Ave,Suite 200, Pittsburgh, PA 15213 USA.
EM byl1@pitt.edu
OI Piraino, Beth/0000-0001-5061-0841; Slayton, Rachel/0000-0003-4699-8040
FU National Institute of General Medical Sciences Models of Infectious
Disease Agent Study (MIDAS) [5U54GM088491-02]; Pennsylvania Department
of Health (DOH) [4100047864]
FX This work was supported by the National Institute of General Medical
Sciences Models of Infectious Disease Agent Study (MIDAS) grant
5U54GM088491-02 and the Pennsylvania Department of Health (DOH) grant
4100047864. The funders had no role in the design and conduct of the
study, collection, management, analysis and interpretation of the data,
or preparation, review or approval of the manuscript.
NR 21
TC 11
Z9 11
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1198-743X
J9 CLIN MICROBIOL INFEC
JI Clin. Microbiol. Infect.
PD NOV
PY 2011
VL 17
IS 11
BP 1717
EP 1726
DI 10.1111/j.1469-0691.2011.03525.x
PG 10
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA 846PS
UT WOS:000296916300026
PM 21595796
ER
PT J
AU Cheng, CE
Kroshinsky, D
AF Cheng, Carol E.
Kroshinsky, Daniela
TI Iatrogenic skin injury in hospitalized patients
SO CLINICS IN DERMATOLOGY
LA English
DT Article
ID TOXIC EPIDERMAL NECROLYSIS; ALLERGIC CONTACT-DERMATITIS; GENERALIZED
EXANTHEMATOUS PUSTULOSIS; STEVENS-JOHNSON-SYNDROME; INDUCED
HYPERSENSITIVITY SYNDROME; LINEAR IGA DERMATOSIS; PYODERMA-GANGRENOSUM;
SYSTEMIC SYMPTOMS; PRESSURE ULCERS; POVIDONE-IODINE
AB Iatrogenic skin injuries in hospitalized patients range from drug-related complications to those related to procedures. Common drug complications include drug reaction with eosinophilia and systemic symptoms (DRESS), linear immunoglobulin (Ig) A bullous dermatosis, Stevens-Johnson syndrome/toxic epidermal necrolysis, and acute generalized exanthematous pustulosis. Contact dermatitis can result from surgical preparations of chlorhexidine and povidone-iodine, medical adhesives, topical postsurgical ointments, most commonly neomycin and bacitracin, and internal prostheses, including coronary stents, pacemakers, and metal joints. Complications arising from procedures include thrombosis caused by placement of peripherally inserted central catheters, pyoderma gangrenosum from sites of dermal trauma, and anetoderma of prematurity from cutaneous monitoring devices in neonates. Calcinosis cutis and decubitus ulcers are also hospital problems. (C) 2011 Published by Elsevier Inc.
C1 [Kroshinsky, Daniela] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol, Boston, MA 02114 USA.
RP Kroshinsky, D (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Dermatol, 50 Stanford St,Ste 200, Boston, MA 02114 USA.
EM dkroshinsky@partners.org
NR 77
TC 10
Z9 11
U1 0
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0738-081X
J9 CLIN DERMATOL
JI Clin. Dermatol.
PD NOV-DEC
PY 2011
VL 29
IS 6
BP 622
EP 632
DI 10.1016/j.clindermatol.2011.08.006
PG 11
WC Dermatology
SC Dermatology
GA 842MB
UT WOS:000296602500005
PM 22014984
ER
PT J
AU Adler, LA
Shaw, DM
Spencer, TJ
Newcorn, JH
Sitt, DJ
Morrill, M
Davidow, JV
Glatt, SJ
Faraone, SV
AF Adler, Lenard A.
Shaw, David M.
Spencer, Thomas J.
Newcorn, Jeffrey H.
Sitt, David J.
Morrill, Melinda
Davidow, Jennifer V.
Glatt, Stephen J.
Faraone, Stephen V.
TI Reliability and validity of the Time-Sensitive ADHD Symptom Scale in
adults
SO COMPREHENSIVE PSYCHIATRY
LA English
DT Article
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DOUBLE-BLIND;
EXTENDED-RELEASE; EFFICACY; SAFETY; TRIAL; VALIDATION
AB Objectives: The objective of this study was to examine the psychometric properties of the Time-Sensitive A DHD Symptom Scale (TASS) to evaluate change of attention-deficit/hyperactivity disorder (ADHD) symptoms over the course of a day in adults.
Methods: Eighty adults with ADHD participated in 1 or 2 visits, 1 to 9 weeks apart. At each visit, participants completed the TASS followed by raters administering the ADHD Rating Scale (ADHD-RS). Additional TASS and ADHD-RS ratings were completed 2 to 6 hours after each visit via telephone. Internal consistency of TASS items was assessed by Cronbach's alpha. Convergent validity of TASS and ADHD-RS total mean item scores was assessed using Pearson's correlation coefficients. kappa correlations were calculated to assess item-by-item reliability between TASS and ADHD-RS items.
Results: Internal consistency of TASS items was high, with an overall Cronbach's alpha coefficient of .93. The Pearson's correlation coefficient between the TASS and ADHD-RS was significant for all visits (r = 0.70, P < .0001). There was moderate agreement between individual items on the TASS and ADHD-RS, with significant kappa coefficients for almost all items (P < .05).
Discussion: The TASS showed high internal consistency and concurrent validity with the clinician-administered ADHD-RS and is a valid and reliable scale for measuring change in ADHD symptoms over the course of a day in adults. Published by Elsevier Inc.
C1 [Adler, Lenard A.; Shaw, David M.] NYU, Sch Med, Dept Psychiat, New York, NY 10010 USA.
[Adler, Lenard A.] NYU, Sch Med, Dept Child & Adolescent Psychiat, New York, NY 10010 USA.
[Adler, Lenard A.] VA NY Harbor Healthcare Syst, Psychiat Serv, New York, NY 10016 USA.
[Spencer, Thomas J.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA USA.
[Spencer, Thomas J.] Massachusetts Gen Hosp, Clin & Res Program Pediat Psychopharmacol, Boston, MA USA.
[Newcorn, Jeffrey H.; Davidow, Jennifer V.] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
[Sitt, David J.] Baruch Coll, Dept Psychol, New York, NY 10010 USA.
[Morrill, Melinda] Clark Univ, Dept Psychol, Worcester, MA 01610 USA.
[Glatt, Stephen J.; Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY 13210 USA.
[Glatt, Stephen J.; Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY 13210 USA.
RP Adler, LA (reprint author), NYU, Sch Med, New York, NY 10016 USA.
EM lenard.adler@nyumc.org
OI Glatt, Stephen/0000-0002-0360-7567; Newcorn, Jeffrey
/0000-0001-8993-9337; Adler, Len/0000-0002-9812-8234; Faraone,
Stephen/0000-0002-9217-3982
FU Shire Development, Inc.
FX This study was supported in part by an investigator-initiated research
grant from Shire Development, Inc.
NR 30
TC 6
Z9 6
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 0010-440X
J9 COMPR PSYCHIAT
JI Compr. Psychiat.
PD NOV-DEC
PY 2011
VL 52
IS 6
BP 769
EP 773
DI 10.1016/j.comppsych.2010.12.002
PG 5
WC Psychiatry
SC Psychiatry
GA 840WF
UT WOS:000296471800028
PM 21306705
ER
PT J
AU Miles, WO
Dyson, NJ
Walker, JA
AF Miles, Wayne O.
Dyson, Nicholas J.
Walker, James A.
TI Modeling tumor invasion and metastasis in Drosophila
SO DISEASE MODELS & MECHANISMS
LA English
DT Article
ID SRC FAMILY KINASES; CELL POLARITY; TRANSCRIPTIONAL REPRESSOR;
MOLECULAR-CLONING; ONCOGENIC RAS; HUMAN CANCER; GROWTH; MELANOGASTER;
PROTEIN; SUPPRESSOR
AB Conservation of major signaling pathways between humans and flies has made Drosophila a useful model organism for cancer research. Our understanding of the mechanisms regulating cell growth, differentiation and development has been considerably advanced by studies in Drosophila. Several recent high profile studies have examined the processes constraining the metastatic growth of tumor cells in fruit fly models. Cell invasion can be studied in the context of an in vivo setting in flies, enabling the genetic requirements of the microenvironment of tumor cells undergoing metastasis to be analyzed. This Perspective discusses the strengths and limitations of Drosophila models of cancer invasion and the unique tools that have enabled these studies. It also highlights several recent reports that together make a strong case for Drosophila as a system with the potential for both testing novel concepts in tumor progression and cell invasion, and for uncovering players in metastasis.
C1 [Miles, Wayne O.; Dyson, Nicholas J.; Walker, James A.] Massachusetts Gen Hosp, Ctr Canc Res, Charlestown, MA 02129 USA.
[Miles, Wayne O.; Dyson, Nicholas J.; Walker, James A.] Harvard Univ, Sch Med, Charlestown, MA 02129 USA.
[Walker, James A.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
RP Walker, JA (reprint author), Massachusetts Gen Hosp, Ctr Canc Res, 149 13th St, Charlestown, MA 02129 USA.
EM jwalker@helix.mgh.harvard.edu
FU National Institutes of Health (NIH) [R01GM53202]; Department of Defense
(DOD) [W81XWH-09-1-0487]
FX Work in the authors' laboratories is supported by the National
Institutes of Health (NIH) [R01GM53202] to N.J.D.; and the Department of
Defense (DOD) [W81XWH-09-1-0487] to J.A.W.
NR 68
TC 31
Z9 32
U1 0
U2 20
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 1754-8403
J9 DIS MODEL MECH
JI Dis. Model. Mech.
PD NOV
PY 2011
VL 4
IS 6
BP 753
EP 761
DI 10.1242/dmm.006908
PG 9
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA 844QD
UT WOS:000296761500008
PM 21979943
ER
PT J
AU Fredericks, WJ
McGarvey, T
Wang, HY
Lal, P
Puthiyaveettil, R
Tomaszewski, J
Sepulveda, J
Labelle, E
Weiss, JS
Nickerson, ML
Kruth, HS
Brandt, W
Wessjohann, LA
Malkowicz, SB
AF Fredericks, William J.
McGarvey, Terry
Wang, Huiyi
Lal, Priti
Puthiyaveettil, Raghunath
Tomaszewski, John
Sepulveda, Jorge
Labelle, Ed
Weiss, Jayne S.
Nickerson, Michael L.
Kruth, Howard S.
Brandt, Wolfgang
Wessjohann, Ludger A.
Malkowicz, S. Bruce
TI The Bladder Tumor Suppressor Protein TERE1 (UBIAD1) Modulates Cell
Cholesterol: Implications for Tumor Progression
SO DNA AND CELL BIOLOGY
LA English
DT Article
ID PROSTATE-CANCER CELLS; VITAMIN-K; APOLIPOPROTEIN-E; CARCINOMA-CELLS;
CORNEAL-DYSTROPHY; OXIDATIVE STRESS; MITOCHONDRIAL CHOLESTEROL;
HEPATOCELLULAR-CARCINOMA; XENOBIOTIC RECEPTOR; MACROPHAGE ABCA1
AB Convergent evidence implicates the TERE1 protein in human bladder tumor progression and lipid metabolism. Previously, reduced TERE1 expression was found in invasive urologic cancers and inhibited cell growth upon re-expression. A role in lipid metabolism was suggested by TERE1 binding to APOE, a cholesterol carrier, and to TBL2, a candidate protein in triglyceride disorders. Natural TERE1 mutations associate with Schnyder's corneal dystrophy, characterized by lipid accumulation. TERE1 catalyzes menaquinone synthesis, known to affect cholesterol homeostasis. To explore this relationship, we altered TERE1 and TBL2 dosage via ectopic expression and interfering RNA and measured cholesterol by Amplex red. Protein interactions of wild-type and mutant TERE1 with GST-APOE were evaluated by binding assays and molecular modeling. We conducted a bladder tumor microarray TERE1 expression analysis and assayed tumorigenicity of J82 cells ectopically expressing TERE1. TERE1 expression was reduced in a third of invasive specimens. Ectopic TERE1 expression in J82 bladder cancer cells dramatically inhibited nude mouse tumorigenesis. TERE1 and TBL2 proteins inversely modulated cellular cholesterol in HEK293 and bladder cancer cells from 20% to 50%. TERE1 point mutations affected APOE interactions, and resulted in cholesterol levels that differed from wild type. Elevated tumor cell cholesterol is known to affect apoptosis and growth signaling; thus, loss of TERE1 in invasive bladder cancer may represent a defect in menaquinone-mediated cholesterol homeostasis that contributes to progression.
C1 [Fredericks, William J.] Univ Penn, Dept Surg, Div Urol, VAMC Philadelphia, Philadelphia, PA 19104 USA.
[McGarvey, Terry] Kirksville Osteopath Med Sch, Dept Anat, Kirksville, MO USA.
[Lal, Priti; Puthiyaveettil, Raghunath; Tomaszewski, John; Sepulveda, Jorge] Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
[Malkowicz, S. Bruce] Vet Affairs Med Ctr, Dept Surg Urol & Pathol, Philadelphia, PA USA.
[Sepulveda, Jorge] Vet Affairs Med Ctr, Pathol Serv, Philadelphia, PA USA.
[Labelle, Ed] Gloucester Cty Coll, Sewell, NJ USA.
[Weiss, Jayne S.] Louisiana State Univ, Dept Ophthalmol, New Orleans, LA USA.
[Weiss, Jayne S.] Louisiana State Univ, Ctr Eye, New Orleans, LA 70112 USA.
[Nickerson, Michael L.] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Kruth, Howard S.] NHLBI, Sect Expt Atherosclerosis, NIH, Bethesda, MD 20892 USA.
[Brandt, Wolfgang; Wessjohann, Ludger A.] Leibniz Inst Plant Biochem, Halle, Germany.
RP Fredericks, WJ (reprint author), Univ Penn, Dept Surg, Div Urol, VAMC Philadelphia, Univ & Woodland Ave,Room A418, Philadelphia, PA 19104 USA.
EM william.fredericks@uphs.upenn.edu
FU Veterans Affairs Merit Review; Veterans Affairs Medical Center
Philadelphia
FX We thank the Veterans Affairs Merit Review and the Veterans Affairs
Medical Center Philadelphia for the grant support to S.B. Malkowicz. We
thank the Innisfree Foundation of Bryn Mawr, PA, and The Castleman
Family Fund for their generous support to S.B. Malkowicz and W.J.
Fredericks.
NR 92
TC 21
Z9 21
U1 1
U2 6
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1044-5498
J9 DNA CELL BIOL
JI DNA Cell Biol.
PD NOV
PY 2011
VL 30
IS 11
BP 851
EP 864
DI 10.1089/dna.2011.1315
PG 14
WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity
GA 843GW
UT WOS:000296661300001
PM 21740188
ER
PT J
AU Stengel, A
Tache, Y
AF Stengel, Andreas
Tache, Yvette
TI Minireview: Nesfatin-1-An Emerging New Player in the Brain-Gut,
Endocrine, and Metabolic Axis
SO ENDOCRINOLOGY
LA English
DT Review
ID SATIETY MOLECULE NESFATIN-1; PITUITARY-ADRENAL AXIS;
CENTRAL-NERVOUS-SYSTEM; FOOD-INTAKE; PARAVENTRICULAR NUCLEUS; ARCUATE
NUCLEUS; RAT-BRAIN; NEURONS; IMMUNOREACTIVITY; HYPOTHALAMUS
AB Nesfatin-1 is a recently identified 82-amino-acid peptide derived from the precursor protein, nucleobindin2 (NUCB2). The brain distribution of NUCB2/nesfatin-1 at the mRNA and protein level along with functional studies in rodents support a role for NUCB2/nesfatin-1 as a novel satiety molecule acting through leptin-independent mechanisms. In addition, nesfatin-1 induces a wide spectrum of central actions to stimulate the pituitary-adrenal axis and sympathetic nervous system and influences visceral functions and emotion. These central actions combined with the activation of NUCB2/nesfatin-1 neurons in the brain by various stressors are indicative of a role in the adaptive response under stressful conditions. In the periphery, evidence is mounting that nesfatin-1 exerts a direct glucose-dependent insulinotropic action on beta-cells of the pancreatic islets. However, the cellular mechanisms of nesfatin-1's action remain poorly understood, partly because the receptor through which nesfatin-1 exerts its pleiotropic actions is yet to be identified. (Endocrinology 152: 4033-4038, 2011)
C1 [Tache, Yvette] Vet Affairs Greater Los Angeles Healthcare Syst, Ctr Neurobiol Stress, Los Angeles, CA 90073 USA.
[Stengel, Andreas; Tache, Yvette] Univ Calif Los Angeles, Dept Med, CURE Digest Dis Res Ctr, Ctr Neurobiol Stress,Digest Dis Div, Los Angeles, CA 90024 USA.
[Stengel, Andreas] Univ Med Berlin, Charite, Div Psychosomat Med & Psychotherapy, Dept Med, D-10117 Berlin, Germany.
RP Tache, Y (reprint author), Vet Affairs Greater Los Angeles Healthcare Syst, Ctr Neurobiol Stress, CURE Bldg 115,Room 117,11301 Wilshire Blvd, Los Angeles, CA 90073 USA.
EM ytache@mednet.ucla.edu
FU National Institutes of Health (NIH) [R01 DK-33061]; NIH Center [DK-41301
(Animal Core)]; Veterans Affairs Research Career Scientist grant
FX This work was supported by National Institutes of Health (NIH) R01
DK-33061, NIH Center Grant DK-41301 (Animal Core), and a Veterans
Affairs Research Career Scientist grant (to Y.T.).
NR 58
TC 41
Z9 43
U1 2
U2 12
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD NOV
PY 2011
VL 152
IS 11
BP 4033
EP 4038
DI 10.1210/en.2011-1500
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 842GR
UT WOS:000296583900007
PM 21862618
ER
PT J
AU Ahmed, AA
Pineda, R
AF Ahmed, Abdalla Awadalla
Pineda, Roberto
TI Alcaligenes xylosoxidans Contact Lens-Related Keratitis-A Case Report
and Literature Review
SO EYE & CONTACT LENS-SCIENCE AND CLINICAL PRACTICE
LA English
DT Review
DE Alcaligenes xylosoxidans; Infectious keratitis; Contact lens
ID ACHROMOBACTER-XYLOSOXIDANS; CORNEAL ULCER; ENDOPHTHALMITIS
AB Background: Alcaligenes xylosoxidans can result in opportunistic infections in patients who are immunocompromised. Alcaligenes xylosoxidans keratitis is a rare infection, almost always occurring in a compromised cornea. Few reported cases have occurred as contact lens-induced keratitis. The purposes of this report are to report a case of A. xylosoxidans keratitis in an immunocompetent contact lens wearer (2-week disposable) and to review the related literature.
Methods: A 30-year-old man developed acute keratitis in the right eye. He was a 2-week disposable contact lens wearer. He did not report any ocular or systemic illness. Corneal scraping, contact lens, and conjunctiva cultures were performed.
Results: 0.5% moxifloxacin eye drops were started hourly with quick recovery and healing of the ulcer and epithelial defect noted within a few days. Culture of the contact lens was positive for A. xylosoxidans. The organism was sensitive to penicillins, third-generation cephalosporins, and fluoroquinolones but resistant to aminoglycosides.
Conclusions: Alcaligenes xylosoxidans is a potential pathogen in compromised corneas. It has high susceptibility to extended-spectrum penicillins and current generations of fluoroquinolones but rarely responds to aminoglycosides. Alcaligenes xylosoxidans should be considered in the differential diagnosis of contact lens-induced keratitis.
C1 [Pineda, Roberto] Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Boston, MA USA.
[Ahmed, Abdalla Awadalla] Makkah Eye Complex, Khartoum, Sudan.
RP Ahmed, AA (reprint author), Makkah Eye Complex, POB 12368, Khartoum, Sudan.
EM Abdu1974@hotmail.com
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 1542-2321
J9 EYE CONTACT LENS
JI Eye Contact Lens-Sci. Clin. Pra.
PD NOV
PY 2011
VL 37
IS 6
BP 386
EP 389
DI 10.1097/ICL.0b013e318235893a
PG 4
WC Ophthalmology
SC Ophthalmology
GA 841QS
UT WOS:000296528100013
PM 21993586
ER
PT J
AU Kakarala, K
Faquin, WC
Deschler, DG
AF Kakarala, Kiran
Faquin, William C.
Deschler, Daniel G.
TI EFFECT OF GLOSSECTOMY TECHNIQUE ON HISTOPATHOLOGIC ASSESSMENT IN A RAT
MODEL
SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND
NECK
LA English
DT Article; Proceedings Paper
CT Combined Section Meeting of the Triological-Society
CY FEB 04-07, 2010
CL Orlando, FL
SP Triol Soc
DE head and neck; glossectomy; histopathology; margin; ultrasonic
ID ULTRASONIC SCALPEL; SQUAMOUS CARCINOMA; SURGICAL-TREATMENT; ORAL-MUCOSA;
TONGUE; ELECTROSURGERY; MONOPOLAR; CO2-LASER; CANCER; NECK
AB Background. The purpose of this study was to compare the tissue effects of 3 surgical methods of glossectomy with respect to histopathologic assessment by a pathologist.
Methods. The anterior tongue of 30 Sprague-Dawley rats was excised using either a steel scalpel, monopolar electrosurgery, or ultrasonic scalpel (3 groups of 10). Specimens were examined by a pathologist blinded to the surgical procedure, using a previously described grading system for margin artifact assessment.
Results. Minimal tissue disruption at the surgical margin was produced by the steel scalpel, in contrast to monopolar electrosurgery and ultrasonic scalpel, which both produced varying levels of tissue distortion. Margin fragmentation was significantly greater with monopolar electrosurgery when compared to an ultrasonic scalpel.
Conclusion. Ultrasonic scalpel creates less tissue distortion at the surgical margin than monopolar electrosurgery. Further study is required to determine the clinical relevance of these findings. (C) 2010 Wiley Periodicals, Inc. Head Neck 33: 1576-1580, 2011
C1 [Kakarala, Kiran; Deschler, Daniel G.] Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Div Head & Neck Surg, Boston, MA 02114 USA.
[Faquin, William C.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Kakarala, Kiran; Deschler, Daniel G.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
RP Deschler, DG (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Div Head & Neck Surg, 243 Charles St, Boston, MA 02114 USA.
EM daniel_deschler@meei.harvard.edu
OI Kakarala, Kiran/0000-0002-1003-8024
NR 13
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1043-3074
J9 HEAD NECK-J SCI SPEC
JI Head Neck-J. Sci. Spec. Head Neck
PD NOV
PY 2011
VL 33
IS 11
BP 1576
EP 1580
DI 10.1002/hed.21632
PG 5
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 840GH
UT WOS:000296426700006
PM 21990222
ER
PT J
AU Silver, AL
Farkash, EA
Pitman, MB
Rocco, JW
AF Silver, Amanda L.
Farkash, Evan A.
Pitman, Martha B.
Rocco, James W.
TI ROSAI-DORFMAN DISEASE PRESENTING IN THE OROPHARYNX
SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND
NECK
LA English
DT Article
ID SINUS HISTIOCYTOSIS; SPECTRUM; HEAD; NECK
AB Background. We report a case of Rosai-Dorfman disease (RDD) presenting as an oropharyngeal mass, and we provide a detailed discussion of this rare clinical entity.
Methods. An initial biopsy, described as being consistent with lymphoma, was reviewed at a second outside institution and was thought to be reactive lymphoid hyperplasia. The patient then presented to our institution for a second opinion. Direct laryngoscopy revealed a firm 1- to 2-cm lesion involving the left soft palate and superior tonsillar pillar.
Results. The diagnosis of RDD was confirmed with immunohistochemical staining on both cytology and histology. The patient elected conservative management and has remained asymptomatic for over 15 months.
Conclusion. The diagnosis of RDD may be challenging in cases presenting initially with extranodal disease. Close follow-up and repeat biopsies may be necessary. Identification of Rosai-Dorfman cells with emperipolesis and confirmation with appropriate immunohistochemical staining on both cytology and histology is diagnostic of RDD. Conservative treatment is appropriate in select cases. (C) 2010 Wiley Periodicals, Inc. Head Neck 33: 1660-1663, 2011
C1 [Silver, Amanda L.; Rocco, James W.] Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Div Head & Neck Surg, Boston, MA 02114 USA.
[Farkash, Evan A.; Pitman, Martha B.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Rocco, James W.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
[Rocco, James W.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
RP Rocco, JW (reprint author), Massachusetts Eye & Ear Infirm, Dept Otolaryngol, Div Head & Neck Surg, 243 Charles St, Boston, MA 02114 USA.
EM jrocco@partners.org
NR 10
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1043-3074
J9 HEAD NECK-J SCI SPEC
JI Head Neck-J. Sci. Spec. Head Neck
PD NOV
PY 2011
VL 33
IS 11
BP 1660
EP 1663
DI 10.1002/hed.21446
PG 4
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA 840GH
UT WOS:000296426700017
PM 20544818
ER
PT J
AU Rothers, J
Wright, AL
Stern, DA
Halonen, M
Camargo, CA
AF Rothers, Janet
Wright, Anne L.
Stern, Debra A.
Halonen, Marilyn
Camargo, Carlos A., Jr.
TI Cord blood 25-hydroxyvitamin D levels are associated with aeroallergen
sensitization in children from Tucson, Arizona
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Vitamin D; IgE; aeroallergen; allergic rhinitis; asthma; children
ID VITAMIN-D INTAKE; CHILDHOOD ASTHMA; ALLERGIC RHINITIS; D
SUPPLEMENTATION; PREGNANCY; DISEASES; RISK; IGE; DEFICIENCY; INFANTS
AB Background: The association between vitamin D status at birth and childhood allergic outcomes is uncertain. The desert climate of Tucson offers a unique setting for studying the health effects of higher exposure to vitamin D.
Objective: To assess the relationship between cord blood 25-hydroxyvitamin D (25[OH]D) levels and allergic outcomes through age 5 years.
Methods: Cord blood 25(OH)D levels were measured in 219 participants in the Tucson Infant Immune Study, a population-based birth cohort. Plasma total IgE and specific IgE levels to 6 aeroallergens were measured at 1, 2, 3, and 5 years. Skin prick test (SPT) positivity (wheal diameter >= 3 mm) and physician-diagnosed active allergic rhinitis and asthma were assessed at age 5 years. Longitudinal models were used to assess the relationship between 25(OH)D and IgE levels. Logistic regression models were used to assess the relationship of 25(OH)D level with SPT positivity, allergic rhinitis, and asthma.
Results: The median cord blood 25(OH)D level was 64 nmol/L (interquartile range, 49-81 nmol/L). Relative to the reference group (50-74.9 nmol/L), both low (<50 nmol/L) and high (>= 100 nmol/L) levels were associated with increased total IgE (coefficient = 0.27, P = .006 and coefficient = 0.27, P = .04, respectively) and detectable inhalant allergen-specific IgE (odds ratio = 2.4, P = .03 and odds ratio = 4.0, P = .01, respectively) through age 5 years. High 25(OH)D levels were also associated with increased SPT positivity (odds ratio = 4.0, P = .02). By contrast, the 25(OH)D level was not significantly associated with allergic rhinitis or asthma.
Conclusion: Both low and high levels of cord blood 25(OH)D were associated with increased aeroallergen sensitization. The association between vitamin D status and actual allergic diseases merits further study. (J Allergy Clin Immunol 2011;128:1093-9.)
C1 [Wright, Anne L.] Univ Arizona, Arizona Hlth Sci Ctr, Arizona Resp Ctr, Tucson, AZ 85724 USA.
[Rothers, Janet] Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Tucson, AZ 85724 USA.
[Wright, Anne L.] Univ Arizona, Dept Pediat, Tucson, AZ 85724 USA.
[Halonen, Marilyn] Univ Arizona, Dept Pharmacol, Tucson, AZ 85724 USA.
[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 Wright, AL (reprint author), Univ Arizona, Arizona Hlth Sci Ctr, Arizona Resp Ctr, 1501 N Campbell Ave, Tucson, AZ 85724 USA.
EM awright@arc.arizona.edu
FU National Institutes of Health [AI 42268, AI 61811]
FX This study was funded by National Institutes of Health grants AI 42268
and AI 61811 and the Massachusetts General Hospital Center for
D-receptor Activation Research.; Disclosure of potential conflict of
interest: J. Rothers, A.L. Wright, and M. Halonen receive research
support from the National Institutes of Health. The rest of the authors
have declared that they have no conflict of interest.
NR 33
TC 77
Z9 77
U1 0
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD NOV
PY 2011
VL 128
IS 5
BP 1093
EP U275
DI 10.1016/j.jaci.2011.07.015
PG 12
WC Allergy; Immunology
SC Allergy; Immunology
GA 842FJ
UT WOS:000296578200024
PM 21855975
ER
PT J
AU Truong-Bolduc, QC
Dunman, PM
Eidem, T
Hooper, DC
AF Truong-Bolduc, Q. C.
Dunman, P. M.
Eidem, T.
Hooper, D. C.
TI Transcriptional Profiling Analysis of the Global Regulator NorG, a
GntR-Like Protein of Staphylococcus aureus
SO JOURNAL OF BACTERIOLOGY
LA English
DT Article
ID ESCHERICHIA-COLI; GENE-EXPRESSION; EFFLUX PUMPS; SARA; MGRA; AGR;
VIRULENCE; RESISTANCE; AUTOLYSIS; SYSTEM
AB The GntR-like protein NorG has been shown to affect Staphylococcus aureus genes involved in resistance to quinolones and beta-lactams, such as those encoding the NorB and AbcA transporters. To identify the target genes regulated by NorG, we carried out transcriptional-profiling assays using S. aureus RN6390 and its isogenic norG::cat mutant. Our data showed that NorG positively affected the transcription of global regulators mgrA, arlS, and sarZ. The three putative drug efflux pump genes most positively affected by NorG were the NorB efflux pump (5.1-fold), the MmpL-like protein SACOL2566 (5.2-fold), and the BcrA-like drug transporter SACOL2525 (5.7-fold) genes. The S. aureus predicted MmpL protein showed 53% homology with the MmpL lipid transporter of Mycobacterium tuberculosis, and the putative SACOL2525 protein showed 87% homology with the bacitracin drug transporter BcrA of Staphylococcus hominis. Two pump genes most negatively affected by NorG were the NorC (4-fold) and AbcA (6-fold) genes. Other categories of genes, such as those participating in amino acid, inorganic ion, or nucleotide transporters and metabolism, were also affected by NorG. Real-time reverse transcription (RT)-PCR assays for mgrA, arlS, sarZ, norB, norC, abcA, mmpL, and bcrA-like were carried out to verify microarray data and showed the same level of up-or downregulation by NorG. The norG mutant showed a 2-fold increase in resistance to norfloxacin and rhodamine, both substrates of the NorC transporter, which is consistent with the resistance phenotype conferred by overexpression of norC on a plasmid. These data indicate that NorG has broad regulatory function in S. aureus.
C1 [Truong-Bolduc, Q. C.; Hooper, D. C.] Harvard Univ, Div Infect Dis, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA.
[Dunman, P. M.; Eidem, T.] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA.
[Dunman, P. M.] Univ Rochester, Sch Med & Dent, Dept Microbiol & Immunol, Rochester, NY 14642 USA.
[Truong-Bolduc, Q. C.; Hooper, D. C.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Med Serv, Boston, MA 02114 USA.
RP Hooper, DC (reprint author), Harvard Univ, Div Infect Dis, Massachusetts Gen Hosp, Sch Med, 55 Fruit St, Boston, MA 02114 USA.
EM dhooper@partners.org
FU U.S. Public Health Service, National Institutes of Health
[R37-AI023988]; National Institutes of Health [R01AI073780]
FX This work was supported in part by a grant from the U.S. Public Health
Service, National Institutes of Health (R37-AI023988 to D.C.H.). Work in
the Dunman laboratory was supported in part by National Institutes of
Health grant R01AI073780.
NR 45
TC 14
Z9 14
U1 0
U2 10
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0021-9193
J9 J BACTERIOL
JI J. Bacteriol.
PD NOV
PY 2011
VL 193
IS 22
BP 6207
EP 6214
DI 10.1128/JB.05847-11
PG 8
WC Microbiology
SC Microbiology
GA 843XF
UT WOS:000296709600011
PM 21908673
ER
PT J
AU Cantor, H
AF Cantor, Harvey
TI A tribute to Baruj Benacerraf
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Biographical-Item
C1 Harvard Univ, Sch Med, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Cantor, H (reprint author), Harvard Univ, Sch Med, Dept Canc Immunol & AIDS, Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM Harvey_Cantor@dfci.harvard.edu
NR 1
TC 0
Z9 0
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 NOV
PY 2011
VL 121
IS 11
BP 4206
EP 4206
PG 1
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 840ZY
UT WOS:000296482700001
ER
PT J
AU Ebi, H
Corcoran, RB
Singh, A
Chen, Z
Song, Y
Lifshits, E
Ryan, DP
Meyerhardt, JA
Benes, C
Settleman, J
Wong, KK
Cantley, LC
Engelman, JA
AF Ebi, Hiromichi
Corcoran, Ryan B.
Singh, Anurag
Chen, Zhao
Song, Youngchul
Lifshits, Eugene
Ryan, David P.
Meyerhardt, Jeffrey A.
Benes, Cyril
Settleman, Jeffrey
Wong, Kwok-Kin
Cantley, Lewis C.
Engelman, Jeffrey A.
TI Receptor tyrosine kinases exert dominant control over PI3K signaling in
human KRAS mutant colorectal cancers
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; ANAPLASTIC LYMPHOMA KINASE;
PHOSPHATIDYLINOSITOL 3-KINASE; ONCOGENIC ACTIVATION;
ACQUIRED-RESISTANCE; MUTATION STATUS; BREAST-CANCER; CYCLIN D1; RAS
AB Therapies inhibiting receptor tyrosine kinases (RTKs) are effective against some human cancers when they lead to simultaneous downregulation of PI3K/AKT and MEK/ERK signaling. However, mutant KRAS has the capacity to directly activate ERK and PI3K signaling, and this is thought to underlie the resistance of KRAS mutant cancers to RTK inhibitors. Here, we have elucidated the molecular regulation of both the PI3K/AKT and MEK/ERK signaling pathways in KRAS mutant colorectal cancer cells and identified combination therapies that lead to robust cancer cell apoptosis. KRAS knockdown using shRNA suppressed ERK signaling in all of the human KRAS mutant colorectal cancer cell lines examined. However, no decrease, and actually a modest increase, in AKT phosphorylation was often seen. By performing PI3K immunoprecipitations, we determined that RTKs, often IGF-IR, regulated PI3K signaling in the KRAS mutant cell lines. This conclusion was also supported by the observation that specific RTK inhibition led to marked suppression of PI3K signaling and biochemical assessment of patient specimens. Interestingly, combination of RTK and MEK inhibitors led to concomitant inhibition of PI3K and MEK signaling, marked growth suppression, and robust apoptosis of human KRAS mutant colorectal cancer cell lines in vitro and upon xenografting in mice. These findings provide a framework for utilizing RTK inhibitors in the treatment of KRAS mutant colorectal cancers.
C1 [Ebi, Hiromichi; Corcoran, Ryan B.; Singh, Anurag; Song, Youngchul; Lifshits, Eugene; Ryan, David P.; Benes, Cyril; Settleman, Jeffrey; Engelman, Jeffrey A.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02129 USA.
[Ebi, Hiromichi; Corcoran, Ryan B.; Singh, Anurag; Chen, Zhao; Ryan, David P.; Meyerhardt, Jeffrey A.; Benes, Cyril; Settleman, Jeffrey; Wong, Kwok-Kin; Cantley, Lewis C.; Engelman, Jeffrey A.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Chen, Zhao; Meyerhardt, Jeffrey A.; Wong, Kwok-Kin] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Cantley, Lewis C.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
RP Engelman, JA (reprint author), Massachusetts Gen Hosp, Ctr Canc, Bldg 149,13th St, Boston, MA 02129 USA.
EM jengelman@partners.org
RI Singh, Anurag/C-7347-2014; Cantley, Lewis/D-1800-2014;
OI Singh, Anurag/0000-0003-4705-8683; Cantley, Lewis/0000-0002-1298-7653;
Ebi, Hiromichi/0000-0003-3155-7576; wong, kwok kin/0000-0001-6323-235X
FU NIH Gastrointestinal Cancer SPORE [P50 CA127003, CA120060-01,
R01CA140594, 1U01CA141457-01, R01CA122794, R01CA137181, 1RC2CA147940,
R01GM41890]; National Cancer Institute Lung SPORE [P50CA090578];
American Association for Cancer Research; V Foundation; American Cancer
Society [RSG-06-102-01-CCE]; Ellison Foundation; American Lung Cancer
Association; Uniting Against Lung Cancer Foundation; Susan Spooner
Research Fund; Kanae Foundation for the Promotion of Medical Science
FX This study is supported by grants from the NIH Gastrointestinal Cancer
SPORE P50 CA127003 (to J.A. Engelman, J.A. Meyerhardt, and L.C.
Cantley), K08 grant CA120060-01 (to J.A. Engelman), R01CA137008-01 (to
J.A. Engelman), R01CA140594 (to J.A. Engelman and K.-K. Wong),
1U01CA141457-01 (to J.A. Engelman), R01CA122794 (to K.-K. Wong),
R01CA137181 (to K.-K. Wong), 1RC2CA147940 (to K.-K. Wong), R01GM41890
(to L.C. Cantley), National Cancer Institute Lung SPORE P50CA090578 (to
J.A. Engelman and K.-K. Wong), the American Association for Cancer
Research (to J.A. Engelman), the V Foundation (to J.A. Engelman),
American Cancer Society RSG-06-102-01-CCE (to J.A. Engelman), the
Ellison Foundation Scholar Award (to J.A. Engelman), the American Lung
Cancer Association Lung Cancer Discover Award (to J.A. Engelman),
Uniting Against Lung Cancer Foundation (to K.-K. Wong), and the Susan
Spooner Research Fund (to K.-K. Wong). H. Ebi was supported by a
fellowship from the Kanae Foundation for the Promotion of Medical
Science. We also thank Mike Waring and Andrew Cosgrove (Massachusetts
General Hospital) for FACS analysis and Anna Kreshock for assistance
with IHC. We thank the GI tumor bank at Brigham and Women's Hospital for
assistance in obtaining samples for analyses.
NR 55
TC 81
Z9 82
U1 1
U2 10
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 NOV
PY 2011
VL 121
IS 11
BP 4311
EP 4321
DI 10.1172/JCI57909
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 840ZY
UT WOS:000296482700015
PM 21985784
ER
PT J
AU Ma, CHE
Omura, T
Cobos, EJ
Latremoliere, A
Ghasemlou, N
Brenner, GJ
van Veen, E
Barrett, L
Sawada, T
Gao, FY
Coppola, G
Gertler, F
Costigan, M
Geschwind, D
Woolf, CJ
AF Ma, Chi Him Eddie
Omura, Takao
Cobos, Enrique J.
Latremoliere, Alban
Ghasemlou, Nader
Brenner, Gary J.
van Veen, Ed
Barrett, Lee
Sawada, Tomokazu
Gao, Fuying
Coppola, Giovanni
Gertler, Frank
Costigan, Michael
Geschwind, Dan
Woolf, Clifford J.
TI Accelerating axonal growth promotes motor recovery after peripheral
nerve injury in mice
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID TERMINAL SCHWANN-CELLS; CONTRALATERAL C7 TRANSFER; BRACHIAL-PLEXUS
INJURIES; POOR FUNCTIONAL RECOVERY; PRIMARY SENSORY NEURONS; DORSAL-ROOT
GANGLION; SMOOTH-MUSCLE-CELLS; SPINAL-CORD-INJURY; MYOSIN-II ACTIVITY;
SHOCK-PROTEIN 27
AB Although peripheral nerves can regenerate after injury, proximal nerve injury in humans results in minimal restoration of motor function. One possible explanation for this is that injury-induced axonal growth is too slow. Heat shock protein 27 (Hsp27) is a regeneration-associated protein that accelerates axonal growth in vitro. Here, we have shown that it can also do this in mice after peripheral nerve injury. While rapid motor and sensory recovery occurred in mice after a sciatic nerve crush injury, there was little return of motor function after sciatic nerve transection, because of the delay in motor axons reaching their target. This was not due to a failure of axonal growth, because injured motor axons eventually fully re-extended into muscles and sensory function returned; rather, it resulted from a lack of motor end plate reinnervation. Tg mice expressing high levels of Hsp27 demonstrated enhanced restoration of motor function after nerve transection/resuture by enabling motor synapse reinnervation, but only within 5 weeks of injury. In humans with peripheral nerve injuries, shorter wait times to decompression surgery led to improved functional recovery, and, while a return of sensation occurred in all patients, motor recovery was limited. Thus, absence of motor recovery after nerve damage may result from a failure of synapse reformation after prolonged denervation rather than a failure of axonal growth.
C1 [Ma, Chi Him Eddie; Omura, Takao; Cobos, Enrique J.; Latremoliere, Alban; Ghasemlou, Nader; Barrett, Lee; Costigan, Michael; Woolf, Clifford J.] Harvard Univ, Childrens Hosp Boston, Sch Med, Program Neurobiol, Boston, MA 02115 USA.
[Ma, Chi Him Eddie; Omura, Takao; Cobos, Enrique J.; Latremoliere, Alban; Ghasemlou, Nader; Barrett, Lee; Costigan, Michael; Woolf, Clifford J.] Harvard Univ, Childrens Hosp Boston, Sch Med, FM Kirby Neurobiol Ctr, Boston, MA 02115 USA.
[Ma, Chi Him Eddie; Omura, Takao; Cobos, Enrique J.; Latremoliere, Alban; Ghasemlou, Nader; Barrett, Lee; Costigan, Michael; Woolf, Clifford J.] Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA.
[Brenner, Gary J.; Gertler, Frank] Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
[van Veen, Ed] MIT, Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA.
[Sawada, Tomokazu] Hamamatsu Univ Sch Med, Dept Orthopaed Surg, Shizuoka, Japan.
[Gao, Fuying; Coppola, Giovanni; Geschwind, Dan] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Program Neurogenet, Los Angeles, CA 90095 USA.
[Geschwind, Dan] Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90095 USA.
RP Woolf, CJ (reprint author), Harvard Univ, Childrens Hosp Boston, Sch Med, Program Neurobiol, 300 Longwood Ave,CLS 12258, Boston, MA 02115 USA.
EM eddiema@cityu.edu.hk; clifford.woolf@childrens.harvard.edu
RI Cobos, Enrique/E-9077-2016;
OI MA, Chi Him Eddie/0000-0003-2054-0445; Ghasemlou,
Nader/0000-0002-1696-7342
FU NIH [NS038253, FBG 068678]; Miriam and Sheldon G. Adelson Medical
Research Foundation; Hong Kong Croucher Foundation; IRP-IFP Switzerland;
MICINN/Fulbright program; Fonds de la recherche en sante du Quebec;
Massachusetts General Hospital Neuroscience Center Vector Development
and Production Core (NIH) [P30NS045776]
FX We thank the NIH (to C.J. Woolf; NS038253, FBG 068678), Miriam and
Sheldon G. Adelson Medical Research Foundation (to C.J. Woolf, D.
Geschwind, and G. Coppola), Hong Kong Croucher Foundation Fellowship
(CHEM), IRP-IFP Switzerland (to M. Costigan and G. Coppola), the
MICINN/Fulbright program (to E.J. Cobos), and the Fonds de la recherche
en sante du Quebec (to N. Ghasemlou) for financial support. We also
thank the Massachusetts General Hospital Neuroscience Center Vector
Development and Production Core (NIH grant P30NS045776) for production
of lentivirus vectors.
NR 72
TC 56
Z9 58
U1 1
U2 12
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 NOV
PY 2011
VL 121
IS 11
BP 4332
EP 4347
DI 10.1172/JCI58675
PG 16
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 840ZY
UT WOS:000296482700017
PM 21965333
ER
PT J
AU Faul, C
Amaral, AP
Oskouei, B
Hu, MC
Sloan, A
Isakova, T
Gutierrez, OM
Aguillon-Prada, R
Lincoln, J
Hare, JM
Mundel, P
Morales, A
Scialla, J
Fischer, M
Soliman, EZ
Chen, J
Go, AS
Rosas, SE
Nessel, L
Townsend, RR
Feldman, HI
Sutton, MS
Ojo, A
Gadegbeku, C
Di Marco, GS
Reuter, S
Kentrup, D
Tiemann, K
Brand, M
Hill, JA
Moe, OW
Kuro-o, M
Kusek, JW
Keane, MG
Wolf, M
AF Faul, Christian
Amaral, Ansel P.
Oskouei, Behzad
Hu, Ming-Chang
Sloan, Alexis
Isakova, Tamara
Gutierrez, Orlando M.
Aguillon-Prada, Robier
Lincoln, Joy
Hare, Joshua M.
Mundel, Peter
Morales, Azorides
Scialla, Julia
Fischer, Michael
Soliman, Elsayed Z.
Chen, Jing
Go, Alan S.
Rosas, Sylvia E.
Nessel, Lisa
Townsend, Raymond R.
Feldman, Harold I.
Sutton, Martin St. John
Ojo, Akinlolu
Gadegbeku, Crystal
Di Marco, Giovana Seno
Reuter, Stefan
Kentrup, Dominik
Tiemann, Klaus
Brand, Marcus
Hill, Joseph A.
Moe, Orson W.
Kuro-o, Makoto
Kusek, John W.
Keane, Martin G.
Wolf, Myles
TI FGF23 induces left ventricular hypertrophy
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; GROWTH-FACTOR 23; MYOSIN HEAVY-CHAIN; STAGE
RENAL-DISEASE; X-LINKED HYPOPHOSPHATEMIA; RECEPTOR TYROSINE KINASES; RAT
CARDIAC MYOCYTES; GENE-EXPRESSION; MYOCARDIAL PERFORMANCE; SIGNALING
PATHWAYS
AB Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease in individuals with CKD. Elevated levels of FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether these risks represent causal effects of FGF23 is unknown. Here, we report that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort. FGF23 caused pathological hypertrophy of isolated rat cardiomyocytes via FGF receptor-dependent activation of the calcineurin-NFAT signaling pathway, but this effect was independent of klotho, the coreceptor for FGF23 in the kidney and parathyroid glands. Intrarnyocardial or intravenous injection of FGF23 in wild-type mice resulted in LVH, and klotho-deficient mice demonstrated elevated FGF23 levels and LVH. In an established animal model of CKD, treatment with an FGF-receptor blocker attenuated LVH, although no change in blood pressure was observed. These results unveil a klotho-independent, causal role for FGF23 in the pathogenesis of LVH and suggest that chronically elevated FGF23 levels contribute directly to high rates of LVH and mortality in individuals with CKD.
C1 [Faul, Christian; Amaral, Ansel P.; Sloan, Alexis; Isakova, Tamara; Aguillon-Prada, Robier; Scialla, Julia; Wolf, Myles] Univ Miami, Miller Sch Med, Dept Med, Div Nephrol & Hypertens, Miami, FL 33136 USA.
[Faul, Christian; Amaral, Ansel P.; Sloan, Alexis] Univ Miami, Miller Sch Med, Dept Cell Biol & Anat, Miami, FL 33136 USA.
[Oskouei, Behzad; Hare, Joshua M.] Univ Miami, Miller Sch Med, Interdisciplinary Stem Cell Inst, Miami, FL 33136 USA.
[Hu, Ming-Chang; Hill, Joseph A.; Moe, Orson W.] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA.
[Hu, Ming-Chang] Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA.
[Hu, Ming-Chang; Kuro-o, Makoto] Univ Texas SW Med Ctr Dallas, Charles & Jane Pak Ctr Mineral Metab & Clin Res, Dallas, TX 75390 USA.
[Gutierrez, Orlando M.] Univ Alabama, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA.
[Gutierrez, Orlando M.] Univ Alabama, Sch Med, Dept Med, Div Nephrol, Birmingham, AL USA.
[Lincoln, Joy] Univ Miami, Miller Sch Med, Dept Mol & Cellular Pharmacol, Miami, FL 33136 USA.
[Lincoln, Joy] Univ Miami, Miller Sch Med, Dept Med, Miami, FL 33136 USA.
[Mundel, Peter] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Renal Unit, Boston, MA USA.
[Morales, Azorides] Univ Miami, Miller Sch Med, Dept Pathol, Miami, FL 33136 USA.
[Fischer, Michael] Jesse Brown VA Med Ctr, Dept Med, Chicago, IL USA.
[Fischer, Michael] Univ Illinois, Med Ctr, Chicago, IL USA.
[Fischer, Michael] Edward Hines Jr VA Hosp, Ctr Management Complex Chron Care, Hines, IL USA.
[Soliman, Elsayed Z.] Wake Forest Univ, Bowman Gray Sch Med, Dept Epidemiol & Prevent, Epidemiol Cardiol Res Ctr, Winston Salem, NC USA.
[Chen, Jing] Tulane Sch Med, Dept Med, New Orleans, LA USA.
[Go, Alan S.] Kaiser Permanente No Calif, Div Res, San Francisco, CA USA.
[Go, Alan S.] UCSF, Dept Epidemiol, San Francisco, CA USA.
[Go, Alan S.] UCSF, Dept Biostat, San Francisco, CA USA.
[Go, Alan S.] UCSF, Dept Med, San Francisco, CA USA.
[Rosas, Sylvia E.; Townsend, Raymond R.; Feldman, Harold I.] Univ Penn, Sch Med, Dept Med, Renal Electrolyte & Hypertens Div, Philadelphia, PA 19104 USA.
[Nessel, Lisa; Feldman, Harold I.] Univ Penn, Sch Med, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Sutton, Martin St. John; Keane, Martin G.] Univ Penn, Sch Med, Dept Med, Div Cardiol, Philadelphia, PA 19104 USA.
[Gadegbeku, Crystal] Temple Univ, Schostl Med, Dept Internal Med, Sect Nephrol & Kidney Transplantat, Philadelphia, PA 19122 USA.
[Ojo, Akinlolu] Univ Michigan Hlth Syst, Dept Internal Med, Ann Arbor, MI USA.
[Di Marco, Giovana Seno; Reuter, Stefan; Kentrup, Dominik; Brand, Marcus] Univ Munster, Dept Internal Med D, D-4400 Munster, Germany.
[Tiemann, Klaus] Univ Munster, Dept Cardiol & Angiol, Munster, Germany.
[Hill, Joseph A.] Univ Texas SW Med Ctr Dallas, Dept Mol Biol, Dallas, TX 75390 USA.
[Moe, Orson W.] Univ Texas SW Med Ctr Dallas, Dept Physiol, Dallas, TX 75390 USA.
[Kuro-o, Makoto] Univ Texas SW Med Ctr Dallas, Dept Pathol, Dallas, TX 75390 USA.
[Kusek, John W.] NIDDK, Bethesda, MD USA.
RP Wolf, M (reprint author), 1120 NW 14th St,Suite 819, Miami, FL 33136 USA.
EM cfaul@med.miami.edu; mwolf2@med.miami.edu
RI Rosas, Sylvia/D-1106-2009;
OI Seno Di Marco, Giovana/0000-0002-1877-638X
FU NephCure Foundation; American Heart Association; Charles and Jane Pak
Center for Mineral Metabolism and Clinical Research, University of Texas
Southwestern Medical Center; George M. O'Brien Kidney Research Core
Center/UT Southwestern Medical Center at Dallas [NIH P30DK-07938];
Stifterverband fur die Deutsche Wissenschaft and Simon-Claussen-Stiftung
[H 1405409999915626]; Inter-disciplinary Research Initiative of the
University of Miami Miller School of Medicine; Department of Veterans
Affairs; National Institutes of Health [F30DK091057, K23DK087858,
K23DK081673, R01DK091392, R01AG019712, R01DK076116, R01DK081374];
National Institute of Diabetes and Digestive and Kidney Diseases
[5U01DK060990, 5U01DK060984, 5U01DK06102, 5U01DK061021, 5U01DK061028,
5U01DK60980, 5U01DK060963, 5U01DK060902]; institutional Clinical
Translational Science Awards; NIH; University of Pennsylvania [UL1
RR024134]; Johns Hopkins University [UL1 RR025005]; University of
Maryland [GCRC M01 RR16500]; Case Western Reserve University Clinical
and Translational Science Collaborative (University Hospitals of
Cleveland, Cleveland Clinic Foundation, and MetroHealth) [UL1 RR024989];
University of Michigan [GCRC M01 RR-000042, UL1 RR024986]; University of
Illinois at Chicago [UL1 RR029879]; Tulane/LSU/Charity Hospital General
Clinical Research Center [RR05096]; Kaiser-UCSF-CTSI [RR024131]; Abbott
Laboratories; Ardelyx; Genzyme
FX This study was supported by grants from the NephCure Foundation (to C.
Faul), the American Heart Association (to C. Faul and M.C. Hu), the
Charles and Jane Pak Center for Mineral Metabolism and Clinical
Research, University of Texas Southwestern Medical Center (to M.C. Hu),
the George M. O'Brien Kidney Research Core Center/UT Southwestern
Medical Center at Dallas (NIH P30DK-07938 to O.W. Moe), the
Stifterverband fur die Deutsche Wissenschaft and Simon-Claussen-Stiftung
(H 1405409999915626 to M. Brand), the Inter-disciplinary Research
Initiative of the University of Miami Miller School of Medicine (to C.
Faul, J.M. Hare, and M. Wolf), a Health Services Research and
Development Service Career Development Award from the Department of
Veterans Affairs (to M.J. Fischer), and grants F30DK091057 (to A.P.
Amaral), K23DK087858 (to T. Isakova), K23DK081673 (to O.M. Gutierrez),
R01DK091392 (to M.C. Hu, M. Kuro-o, and O.W. Moe), R01AG019712 (to M.
Kuro-o), R01DK076116 (to M. Wolf), and R01DK081374 (to M. Wolf) from the
National Institutes of Health. Funding for the CRIC study was obtained
under a cooperative agreement from National Institute of Diabetes and
Digestive and Kidney Diseases (grant no. 5U01DK060990, 5U01DK060984,
5U01DK06102, 5U01DK061021, 5U01DK061028, 5U01DK60980, 5U01DK060963, and
5U01DK060902). In addition, this work was supported in part by the
following institutional Clinical Translational Science Awards and other
NIH grants: University of Pennsylvania, UL1 RR024134; Johns Hopkins
University, UL1 RR025005; University of Maryland, GCRC M01 RR16500; Case
Western Reserve University Clinical and Translational Science
Collaborative (University Hospitals of Cleveland, Cleveland Clinic
Foundation, and MetroHealth), UL1 RR024989; University of Michigan, GCRC
M01 RR-000042 and UL1 RR024986; University of Illinois at Chicago, UL1
RR029879; Tulane/LSU/Charity Hospital General Clinical Research Center,
RR05096; and Kaiser-UCSF-CTSI, RR024131.; Tamara Isakova has served as a
consultant and received honoraria from Shire. Orlando M. Gutierrez has
received honoraria from Genzyme. Sylvia E. Rosas has received research
support from Abbott Laboratories. Makoto Kuro-o has received research
support from Ardelyx and Genzyme and honoraria from Amgen and Genzyme.
Myles Wolf has served as a consultant or received honoraria from Abbott
Laboratories, Amgen, Ardelyx, Baxter, Cytochroma, Genzyme, Luitpold
Pharmaceuticals Inc., Novartis, Mitsubishi, and Shire.
NR 89
TC 615
Z9 645
U1 5
U2 31
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 NOV
PY 2011
VL 121
IS 11
BP 4393
EP 4408
DI 10.1172/JCI46122
PG 16
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 840ZY
UT WOS:000296482700022
PM 21985788
ER
PT J
AU Loehrer, PJ
Feng, Y
Cardenes, H
Wagner, L
Brell, JM
Cella, D
Flynn, P
Ramanathan, RK
Crane, CH
Alberts, SR
Benson, A
AF Loehrer, Patrick J., Sr.
Feng, Yang
Cardenes, Higinia
Wagner, Lynne
Brell, Joanna M.
Cella, David
Flynn, Patrick
Ramanathan, Ramesh K.
Crane, Christopher H.
Alberts, Steven R.
Benson, Al B., III
TI Gemcitabine Alone Versus Gemcitabine Plus Radiotherapy in Patients With
Locally Advanced Pancreatic Cancer: An Eastern Cooperative Oncology
Group Trial
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID PHASE-I TRIAL; RADIATION-DOSE ESCALATION; CONCURRENT RADIOTHERAPY; III
TRIAL; CISPLATIN; THERAPY; CHEMORADIOTHERAPY; ADENOCARCINOMA; INFUSION;
RADIOCHEMOTHERAPY
AB Purpose
The purpose of this trial was to evaluate the role of radiation therapy with concurrent gemcitabine (GEM) compared with GEM alone in patients with localized unresectable pancreatic cancer.
Patients and Methods
Patients with localized unresectable adenocarcinoma of the pancreas were randomly assigned to receive GEM alone (at 1,000 mg/m(2)/wk for weeks 1 to 6, followed by 1 week rest, then for 3 of 4 weeks) or GEM (600 mg/m2/wk for weeks 1 to 5, then 4 weeks later 1,000 mg/m(2) for 3 of 4 weeks) plus radiotherapy (starting on day 1, 1.8 Gy/Fx for total of 50.4 Gy). Measurement of quality of life using the Functional Assessment of Cancer Therapy-Hepatobiliary questionnaire was also performed.
Results
Of 74 patients entered on trial and randomly assigned to receive GEM alone (arm A; n = 37) or GEM plus radiation (arm B; n = 34), patients in arm B had greater incidence of grades 4 and 5 toxicities (41% v 9%), but grades 3 and 4 toxicities combined were similar (77% in A v 79% in B). No statistical differences were seen in quality of life measurements at 6, 15 to 16, and 36 weeks. The primary end point was survival, which was 9.2 months (95% CI, 7.9 to 11.4 months) and 11.1 months (95% CI, 7.6 to 15.5 months) for arms A and B, respectively (one-sided P = .017 by stratified log-rank test).
Conclusion
This trial demonstrates improved overall survival with the addition of radiation therapy to GEM in patients with localized unresectable pancreatic cancer, with acceptable toxicity. J Clin Oncol 29: 4105-4112. (C) 2011 by American Society of Clinical Oncology
C1 [Loehrer, Patrick J., Sr.; Cardenes, Higinia] Indiana Univ, Melvin & Bren Simon Canc Ctr, Indianapolis, IN 46202 USA.
[Feng, Yang] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Wagner, Lynne; Cella, David; Benson, Al B., III] Northwestern Univ, Sch Med, Chicago, IL USA.
[Brell, Joanna M.] Case Western Reserve Univ, Ireland Canc Ctr, Cleveland, OH 44106 USA.
[Flynn, Patrick] Minneapolis Hematol Oncol, Minneapolis, MN USA.
[Alberts, Steven R.] Mayo Clin, Rochester, MN USA.
[Ramanathan, Ramesh K.] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
[Crane, Christopher H.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Loehrer, PJ (reprint author), Indiana Univ, Melvin & Bren Simon Canc Ctr, 980 W Walnut St,Suite C528, Indianapolis, IN 46202 USA.
EM ploehrer@iupui.edu
FU Eli Lilly
FX Research Funding: Patrick J. Loehrer Sr, Eli Lilly
NR 38
TC 230
Z9 232
U1 1
U2 12
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 1
PY 2011
VL 29
IS 31
BP 4105
EP 4112
DI 10.1200/JCO.2011.34.8904
PG 8
WC Oncology
SC Oncology
GA 842NB
UT WOS:000296605100013
PM 21969502
ER
PT J
AU Saboo, SS
Jagannathan, JP
Krajewski, KM
O'Regan, K
Hornick, JL
Fisher, DC
Ramaiya, N
AF Saboo, Sachin S.
Jagannathan, Jyothi P.
Krajewski, Katherine M.
O'Regan, Kevin
Hornick, Jason L.
Fisher, David C.
Ramaiya, Nikhil
TI Symptomatic Extranodal Rosai-Dorfman Disease Treated With Steroids,
Radiation, and Surgery
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Editorial Material
ID ASSOCIATION
C1 [Saboo, Sachin S.; Jagannathan, Jyothi P.; Krajewski, Katherine M.; O'Regan, Kevin; Fisher, David C.; Ramaiya, Nikhil] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hornick, Jason L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Saboo, SS (reprint author), Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 10
TC 6
Z9 7
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 1
PY 2011
VL 29
IS 31
BP E772
EP E775
DI 10.1200/JCO.2011.36.9967
PG 4
WC Oncology
SC Oncology
GA 842NB
UT WOS:000296605100002
PM 21931038
ER
PT J
AU Schirmer, P
Winters, M
Holodniy, M
AF Schirmer, P.
Winters, M.
Holodniy, M.
TI HIV-HBV vaccine escape mutant infection with loss of HBV surface
antibody and persistent HBV viremia on tenofovir/emtricitabine without
antiviral resistance
SO JOURNAL OF CLINICAL VIROLOGY
LA English
DT Article
DE HIV; HBV; Vaccine escape; Tenofovir; Emtricitabine
ID HEPATITIS-B; COINFECTION; ANTIGEN; CARRIER
AB We report a case of acute hepatitis B virus genotype A vaccine escape mutant infection with loss of HBV vaccine-induced seropositivity in a HIV-1 infected patient. His HBV is unresponsive to tenofovir/emtricitabine treatment demonstrated by persistent viremia despite lacking known resistance mutations and while having an undetectable HIV-1 viral load. Published by Elsevier B. V.
C1 [Schirmer, P.; Holodniy, M.] US Dept Vet Affairs, Off Publ Hlth, Palo Alto, CA 94304 USA.
[Winters, M.; Holodniy, M.] Stanford Univ, Palo Alto, CA 94304 USA.
RP Schirmer, P (reprint author), US Dept Vet Affairs, Off Publ Hlth Surveillance & Res, 3801 Miranda Ave,132, Palo Alto, CA 94304 USA.
EM patricia.schirmer@va.gov
FU Department of Veterans Affairs [HOM0055]
FX This work was supported by a Department of Veterans Affairs grant
[HOM0055] to Mark Holodniy.
NR 14
TC 8
Z9 8
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1386-6532
J9 J CLIN VIROL
JI J. Clin. Virol.
PD NOV
PY 2011
VL 52
IS 3
BP 261
EP 264
DI 10.1016/j.jcv.2011.07.014
PG 4
WC Virology
SC Virology
GA 842AF
UT WOS:000296556800021
PM 21840252
ER
EF