FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Yu, WH
Lauffenburger, D
Alter, G
AF Yu, Wen-Han
Lauffenburger, Doug
Alter, Galit
TI Molecular regulation of antigen-specific antibody glycosylation
following B cell activation
SO GLYCOBIOLOGY
LA English
DT Meeting Abstract
CT Joint Meeting of the Society-for-Glycobiology (SFG) and the
Japanese-Society-of-Carbohydrate-Research (JSCR)
CY NOV 16-19, 2014
CL Honolulu, HI
SP Society For Glycobiology, Japanese Soc Carbohydrate Res
C1 [Yu, Wen-Han] Ragon Inst Massachusetts Gen Hosp Massachusetts I, Dept Biol Engn, MIT, Cambridge, MA USA.
[Lauffenburger, Doug] MIT, Dept Biol Engn, Cambridge, MA 02139 USA.
[Alter, Galit] Ragon Inst Massachusetts Gen Hosp Massachusetts I, Cambridge, 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 0959-6658
EI 1460-2423
J9 GLYCOBIOLOGY
JI Glycobiology
PD NOV
PY 2014
VL 24
IS 11
MA 11
BP 1088
EP 1089
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AT1CI
UT WOS:000344670300019
ER
PT J
AU Okamoto, R
Mandal, K
Ling, M
Luster, A
Sawaya, M
Yeates, T
Kajihara, Y
Kent, S
AF Okamoto, Ryo
Mandal, Kalyanswer
Ling, Morris
Luster, Andrew
Sawaya, Michael
Yeates, Todd
Kajihara, Yasuhiro
Kent, Stephen
TI Biological activities of the homogeneous glycosylated chemokines CCL1
and Ser-CCL1 prepared by total chemical synthesis
SO GLYCOBIOLOGY
LA English
DT Meeting Abstract
CT Joint Meeting of the Society-for-Glycobiology (SFG) and the
Japanese-Society-of-Carbohydrate-Research (JSCR)
CY NOV 16-19, 2014
CL Honolulu, HI
SP Society For Glycobiology, Japanese Soc Carbohydrate Res
ID NONGLYCOSYLATED FORMS
C1 [Okamoto, Ryo; Kajihara, Yasuhiro; Kent, Stephen] Osaka Univ, Suita, Osaka 565, Japan.
[Mandal, Kalyanswer] Univ Chicago, Chicago, IL 60637 USA.
[Ling, Morris; Luster, Andrew] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cambridge, MA 02138 USA.
NR 2
TC 0
Z9 0
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0959-6658
EI 1460-2423
J9 GLYCOBIOLOGY
JI Glycobiology
PD NOV
PY 2014
VL 24
IS 11
MA 91
BP 1118
EP 1119
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AT1CI
UT WOS:000344670300099
ER
PT J
AU Xu, YX
Ashline, D
Liu, L
Tassa, C
Shaw, S
Ravid, K
Layne, M
Reinhold, V
Robbins, P
AF Xu, Yuxin
Ashline, David
Liu, Li
Tassa, Carlos
Shaw, Stanley
Ravid, Katya
Layne, Matthew
Reinhold, Vernon
Robbins, Phillips
TI The glycosylation-dependent interaction of perlecan core protein with
LDL: implications for atherosclerosis
SO GLYCOBIOLOGY
LA English
DT Meeting Abstract
CT Joint Meeting of the Society-for-Glycobiology (SFG) and the
Japanese-Society-of-Carbohydrate-Research (JSCR)
CY NOV 16-19, 2014
CL Honolulu, HI
SP Society For Glycobiology, Japanese Soc Carbohydrate Res
C1 [Xu, Yuxin] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Xu, Yuxin] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Ashline, David; Reinhold, Vernon] Univ New Hampshire, Glyc Ctr, Durham, NH 03824 USA.
[Liu, Li; Robbins, Phillips] Boston Univ, Dept Mol & Cell Biol, Henry M Goldman Sch Dent Med, Boston, MA 02215 USA.
[Tassa, Carlos; Shaw, Stanley] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Ravid, Katya] Boston Univ, Sch Med, Dept Med, Boston, MA 02215 USA.
[Layne, Matthew] Boston Univ, Sch Med, Dept Biochem, 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 0959-6658
EI 1460-2423
J9 GLYCOBIOLOGY
JI Glycobiology
PD NOV
PY 2014
VL 24
IS 11
MA 297
BP 1194
EP 1194
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AT1CI
UT WOS:000344670300303
ER
PT J
AU Elbatarny, M
Mollah, S
Grabell, J
Bae, S
Deforest, M
Tuttle, A
Hopman, W
Clark, DS
Mauer, AC
Bowman, M
Riddel, J
Christopherson, PA
Montgomery, RR
Rand, ML
Coller, B
James, PD
AF Elbatarny, M.
Mollah, S.
Grabell, J.
Bae, S.
Deforest, M.
Tuttle, A.
Hopman, W.
Clark, D. S.
Mauer, A. C.
Bowman, M.
Riddel, J.
Christopherson, P. A.
Montgomery, R. R.
Rand, M. L.
Coller, B.
James, P. D.
CA Zimmerman Program Investigators
TI Normal range of bleeding scores for the ISTH-BAT: adult and pediatric
data from the merging project
SO HAEMOPHILIA
LA English
DT Article
DE bleeding questionnaire; bleeding score; ISTH-BAT; normal range
ID VON-WILLEBRAND-DISEASE; QUESTIONNAIRE; MULTICENTER; SYMPTOMS; HISTORY
AB Bleeding Assessment Tools (BATs) have been developed to aid in the standardized evaluation of bleeding symptoms. The Vicenza Bleeding Questionnaire (BQ), published in 2005, established a common framework and scoring key that has undergone subsequent modification over the years, culminating in the publication of the ISTH-BAT in 2010. Understanding the normal range of bleeding scores is critical when assessing the utility of a BAT. Within the context of The Merging Project, a bioinformatics system was created to facilitate the merging of legacy data derived from four different (but all Vicenza-based) BATs; the MCMDM1-VWD BQ, the Condensed MCMDM-1VWD BQ, the Pediatric Bleeding Questionnaire and the ISTH-BAT. Data from 1040 normal adults and 328 children were included in the final analysis, which showed that the normal range is 0-3 for adult males, 0-5 for adult females and 0-2 in children for both males and females. Therefore, the cut-off for a positive or abnormal BS is 4 in adult males, 6 in adult females and 3 in children. This information can now be used to objectively assess bleeding symptoms as normal or abnormal in future studies.
C1 [Elbatarny, M.; Grabell, J.; James, P. D.] Queens Univ, Dept Med, Kingston, ON K7L 3N6, Canada.
[Mollah, S.; Mauer, A. C.; Coller, B.] Rockefeller Univ, Lab Blood & Vasc Biol, New York, NY 10021 USA.
[Bae, S.; Deforest, M.; Tuttle, A.; Bowman, M.; James, P. D.] Queens Univ, Dept Pathol & Mol Med, Kingston, ON K7L 3N6, Canada.
[Hopman, W.; James, P. D.] Queens Univ, Kingston, ON K7L 3N6, Canada.
[Clark, D. S.; Rand, M. L.] Hosp Sick Children, Div Haematol Oncol, Toronto, ON M5G 1X8, Canada.
[Mauer, A. C.] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA.
[Riddel, J.] Childrens Hosp Oakland, Div Hematol, Oakland, CA USA.
[Christopherson, P. A.; Montgomery, R. R.] Med Coll Wisconsin, Blood Res Inst, Blood Ctr Wisconsin, Milwaukee, WI 53226 USA.
[Christopherson, P. A.; Montgomery, R. R.; Zimmerman Program Investigators] Med Coll Wisconsin, Dept Pediat, Milwaukee, WI 53226 USA.
RP James, PD (reprint author), Queens Univ, Room 2025 Etherington Hall, Kingston, ON K7L 3N6, Canada.
EM jamesp@queensu.ca
RI Kerlin, Bryce/E-3369-2011
OI Kerlin, Bryce/0000-0002-1756-8271
FU Canadian Hemophilia Society; Zimmerman Program for the Molecular and
Clinical Biology of von Willebrand disease - National Institutes of
Health Program Project [HL081588]; National Center for Advancing
Translational Sciences (NCATS) [UL1 TR000043]; National Institutes of
Health and Translational Science Award (CTSA); C17 Research Network
FX This research was funded by a Canadian Hemophilia Society Research Grant
and Summer Studentship; the Zimmerman Program for the Molecular and
Clinical Biology of von Willebrand disease - National Institutes of
Health Program Project Grant HL081588; Grant UL1 TR000043 from the
National Center for Advancing Translational Sciences (NCATS), National
Institutes of Health and Translational Science Award (CTSA) and
C17 Research Network.
NR 7
TC 17
Z9 17
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1351-8216
EI 1365-2516
J9 HAEMOPHILIA
JI Haemophilia
PD NOV
PY 2014
VL 20
IS 6
BP 831
EP 835
DI 10.1111/hae.12503
PG 5
WC Hematology
SC Hematology
GA AS8WL
UT WOS:000344525800033
PM 25196510
ER
PT J
AU Friedman, DJ
Upadhyay, GA
Rajabali, A
Altman, RK
Orencole, M
Parks, KA
Moore, SA
Park, MY
Picard, MH
Ruskin, JN
Singh, JP
Heist, EK
AF Friedman, Daniel J.
Upadhyay, Gaurav A.
Rajabali, Alefiyah
Altman, Robert K.
Orencole, Mary
Parks, Kimberly A.
Moore, Stephanie A.
Park, Mi Young
Picard, Michael H.
Ruskin, Jeremy N.
Singh, Jagmeet P.
Heist, E. Kevin
TI Progressive ventricular dysfunction among non responders to cardiac
resynchronization therapy: Baseline predictors and associated clinical
outcomes
SO HEART RHYTHM
LA English
DT Article
DE Remodeling; Heart failure; Cardiac resynchronization therapy;
Cardiomyopathy; Biventricular pacing; Ventricular tachycardia;
Ventricular fibrillation
ID CHRONIC HEART-FAILURE; REVERSE; DEFIBRILLATOR; CARE
AB BACKGROUND Cardiac resynchronization therapy (CRT) nonresponders have poor outcomes. The significance of progressive ventricular dysfunction among nonresponders remains unclear.
OBJECTIVE We sought to define predictors of and clinical outcomes associated with progressive ventricular dysfunction despite CRT.
METHODS We conducted an analysis of 328 patients undergoing CRT with defibrillator for standard indications. On the basis of 6-month echocardiograms, we classified patients as responders (those with a >= 5% increase in ejection fraction) and progressors (those with a >= 5% decrease in ejection fraction), and all others were defined as nonprogressors. Coprimary end points were 3-year (1) heart failure, left ventricular assist device (LVAD), transplantation, or death and (2) ventricular tachycardia (VT) or ventricular fibrillation (VF).
RESULTS MuLtivariable predictors of progressive ventricular dysfunction were aldosterone antagonist use (hazard ratio [HR] 0.23; P = .008), prior valve surgery (HR 3.3; P = .005), and QRS duration (HR 0.98; P = .02). More favorable changes in ventricular function were associated with Lower incidences of heart failure, LVAD, transplantation, or death (70% vs 54% vs 330/e; P < .0001) and VT or VF (66% vs 38% vs 28%; P = .001) for progressors, nonprogressors, and responders, respectively. After multivariable adjustment, progressors remained at increased risk of heart failure, LVAD, transplantation, or death (HR 2.14; P = .0029) and VT or VF (HR 2.03; P = .046) as compared with nonprogressors. Responders were at decreased risk of heart failure, LVAD, transplantation, or death (HR 0.44; P < .0001) and VT or VF (0.51; P = .015) as compared with nonprogressors.
CONCLUSION Patients with progressive deterioration in ventricular function despite CRT represent a high-risk group of nonresponders at increased risk of worsened clinical outcomes.
C1 [Friedman, Daniel J.] Duke Univ Hosp, Div Cardiol, Durham, NC USA.
[Upadhyay, Gaurav A.; Rajabali, Alefiyah; Orencole, Mary; Ruskin, Jeremy N.; Singh, Jagmeet P.; Heist, E. Kevin] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Altman, Robert K.] Mt Sinai St Lukes Roosevelt Hosp, Al Sabah Arrhythmia Inst, New York, NY USA.
[Parks, Kimberly A.; Moore, Stephanie A.] Massachusetts Gen Hosp, Heart Failure & Cardiac Transplantat Unit, Boston, MA 02114 USA.
[Park, Mi Young] Hallym Univ, Dongtan Sacred Hosp, Dept Cardiol, Hwaseong, South Korea.
[Picard, Michael H.] Massachusetts Gen Hosp, Cardiac Ultrasound Lab, Boston, MA 02114 USA.
RP Heist, EK (reprint author), Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, 55 Fruit St, Boston, MA 02114 USA.
EM kheist@partners.org
OI Orencole, Mary/0000-0002-7862-2796; Picard, Michael/0000-0002-9264-3243;
Friedman, Daniel /0000-0001-5791-1954
FU National Cardiovascular Data Registry; Biotronik; Sorin; St Jude
Medical; Boston Scientific; Sarin
FX Dr Friedman has received research support from the National
Cardiovascular Data Registry. Dr Heist has received honoraria from
Biotronik, Boston Scientific, Sorin, and St Jude Medical; research
grants from Biotronik, Sorin, and St Jude Medical; and consulting fees
from Boston Scientific, Sarin, and St Jude Medical. Dr Ruskin has served
as an advisor or consultant for Astellas/Cardiorne, Biosense Webster,
CardioFocus, CardioInsight, CryoCath, Medtronic, Pfizer, Porto la, and
Third Rock Ventures; has received fellowship support from Biosense
Webster, Boston Scientific, Medronic, and St Jude Medical; has received
honoraria from Med-IQ; and owns equity in Porto la. Dr Parks has
received consultant fees from Thoratec and honoraria from Biotronik and
Sorin. Dr Singh has received research grants from St Jude Medical,
Medtronic, Boston Scientific, and Biotronik; consulting fees from Boston
Scientific, Biotronik, St Jude Medical, Medtronic, CardioInsight,
Thoratec, and Biosense Webster; and honoraria from Medtronic, Biotronik,
Guidant, St Jude Medical, and Sorin. Dr Upadhyay has received salary
support from the Max Schaldach Fellowship of the Heart Rhythm Society.
NR 17
TC 1
Z9 1
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1547-5271
EI 1556-3871
J9 HEART RHYTHM
JI Heart Rhythm
PD NOV
PY 2014
VL 11
IS 11
BP 1991
EP 1998
DI 10.1016/j.hrthm.2014.08.005
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AS8DI
UT WOS:000344480000022
PM 25106864
ER
PT J
AU Larson, ER
Porterfield, JE
Sagar, S
Marmol-Velez, J
Panday, M
Escobedo, D
Michalek, J
Ouyang, YJ
Valvano, JW
Pearce, JA
Feldman, MD
AF Larson, Erik R.
Porterfield, John E.
Sagar, Sandeep
Marmol-Velez, Juan
Panday, Manoj
Escobedo, Daniel
Michalek, Joel
Ouyang, Yongjian
Valvano, Jonathan W.
Pearce, John A.
Feldman, Marc D.
TI Admittance to detect alterations in left ventricular stroke volume
SO HEART RHYTHM
LA English
DT Article
DE Shock reduction; Biventricular pacing/defibrillation; Ventricular
tachycardia; Ventricular fibrillation; Inappropriate shocks
ID CARDIOVERTER-DEFIBRILLATOR SHOCKS; CONDUCTANCE CATHETER; INAPPROPRIATE;
THERAPY; MORTALITY; TRIAL
AB BACKGROUND Implantable cardioverter-defibrillators monitor intracardiac electrograms (EGMs) to discriminate between ventricular and supraventricular tachycardias. The incidence of inappropriate shocks remains high because of misclassification of the tachycardia in an otherwise hemodynamically stable individual. Coupling EGMs with an assessment of left ventricular (LV) stroke volume (SV) could help in gauging hemodynamics during an arrhythmia and reducing inappropriate shocks.
OBJECTIVE The purpose of this study was to use the admittance method to accurately derive LV SV.
METHODS Ultrasonic flow probe and LV endocardial crystals were used in canines (n = 12) as the standard for LV SV. Biventricular pacing leads were inserted to obtain admittance measurements. A tetrapolar, complex impedance measurement was made between the Bi-V leads. The real and imaginary components of impedance were used to discard the myocardial component from the blood component to derive instantaneous blood conductance (G(b)). Alterations in SV were measured during right ventricular pacing, dopamine infusion, and inferior vena cava occlusion.
RESULTS G(b) tracks steady-state changes in SV more accurately than traditional magnitude (ie. IYI, without removal of the muscle signal) during right ventricular pacing and dopamine infusion (P = .004). Instantaneous LV volume also was tracked more accurately by G(b) than vertical bar Y vertical bar in the subset of subjects that underwent inferior vena cava occlusions (n = 5, P = .025). Finite element modeling demonstrates that admittance shifts more sensitivity of the measurement to the LV blood chamber as the mechanism for improvement (see Online Appendix).
CONCLUSION Monitoring LV SV is possible using the admittance method with biventricular pacing leads. The technique could be piggybacked to complement EGMs to determine if arrhythmias are hemodynamically unstable.
C1 [Larson, Erik R.; Valvano, Jonathan W.; Pearce, John A.] Univ Texas Austin, Dept Elect Engn, Austin, TX 78712 USA.
[Porterfield, John E.; Feldman, Marc D.] Admittance Technol, Austin, TX USA.
[Sagar, Sandeep; Marmol-Velez, Juan; Panday, Manoj; Escobedo, Daniel; Feldman, Marc D.] Univ Texas Hlth Sci Ctr San Antonio, Div Cardiol, San Antonio, TX 78229 USA.
[Michalek, Joel; Ouyang, Yongjian] Univ Texas Hlth Sci Ctr San Antonio, Dept Epidemiol & Biostat, San Antonio, TX 78229 USA.
[Feldman, Marc D.] South Texas Vet Hlth Care Syst, Dept Vet Affairs, San Antonio, TX USA.
RP Feldman, MD (reprint author), Univ Texas Hlth Sci Ctr San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78248 USA.
EM feldmanm@uthscsa.edu
OI Marmol-Velez, Juan/0000-0002-7450-9817
FU Janey and Dolph Briscoe Center for Cardiovascular Research; CTSA
[UL1RR025767]
FX Support was provided by the Janey and Dolph Briscoe Center for
Cardiovascular Research and a CTSA grant (UL1RR025767). Supplies were
provided by Transonic Systems and St. Jude Medical.
NR 20
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 1547-5271
EI 1556-3871
J9 HEART RHYTHM
JI Heart Rhythm
PD NOV
PY 2014
VL 11
IS 11
BP 2075
EP 2083
DI 10.1016/j.hrthm.2014.06.034
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AS8DI
UT WOS:000344480000034
PM 24981870
ER
PT J
AU Gaskins, AJ
Afeiche, MC
Hauser, R
Williams, PL
Gillman, MW
Tanrikut, C
Petrozza, JC
Chavarro, JE
AF Gaskins, A. J.
Afeiche, M. C.
Hauser, R.
Williams, P. L.
Gillman, M. W.
Tanrikut, C.
Petrozza, J. C.
Chavarro, J. E.
TI Paternal physical and sedentary activities in relation to semen quality
and reproductive outcomes among couples from a fertility center
SO HUMAN REPRODUCTION
LA English
DT Article
DE physical activity; semen quality; male fertility; assisted reproduction
ID ACTIVE MEN; EXERCISE; HORMONE; PROFILE; INTENSITIES; INFERTILITY;
PARAMETERS; VOLUME
AB Is paternal physical activity associated with semen quality parameters and with outcomes of infertility treatment?
Among men presenting for infertility treatment, weightlifting and outdoor activities were associated with higher sperm concentrations but not with greater reproductive success.
Higher physical activity is related to better semen quality but no studies to date have investigated whether it predicts greater reproductive success.
The Environment and Reproductive Health (EARTH) Study is an on-going prospective cohort study which enrolls subfertile couples presenting at Massachusetts General Hospital (2005-2013). In total, 231 men provided 433 semen samples and 163 couples underwent 421 IVF or intrauterine insemination cycles.
Leisure time spent in physical and sedentary activities over the past year was self-reported using a validated questionnaire. We used mixed models to analyze the association of physical and sedentary activities with semen quality and with clinical pregnancy and live birth rates.
Men in this cohort engaged in a median of 3.2 h/week of moderate-to-vigorous activities. Men in the highest quartile of moderate-to-vigorous activity had 43% (95% confidence interval (CI) 9, 87%) higher sperm concentrations than men in the lowest quartile (P-trend = 0.04). Men in the highest category of outdoor activity (a parts per thousand yen1.5 h/week) and weightlifting (a parts per thousand yen2 h/week) had 42% (95% CI 10, 84%) and 25% (95% CI -10, 74%) higher sperm concentrations, respectively, compared with men in the lowest category (0 h/week) (P-trend = 0.04 and 0.02). Conversely, men who reported bicycling a parts per thousand yen1.5 h/week had 34% (95% CI 4, 55%) lower sperm concentrations compared with men who reported no bicycling (P-trend = 0.05). Paternal physical and sedentary activities were not related to clinical pregnancy or live birth rates following infertility treatment.
The generalizability of the findings on live birth rates to populations not undergoing infertility treatment is limited.
Certain types of physical activity, specifically weightlifting and outdoor activities, may improve semen quality but may not lead to improved success of infertility treatments. Further research is needed in other non-clinical populations.
The authors are supported by NIH grants R01-ES009718, ES000002, P30-DK046200, T32-DK007703-16 and ES022955 T32-HD060454. None of the authors has any conflicts of interest to declare.
C1 [Gaskins, A. J.; Afeiche, M. C.; Gillman, M. W.; Chavarro, J. E.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Gaskins, A. J.; Hauser, R.; Williams, P. L.; Chavarro, J. E.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Hauser, R.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Williams, P. L.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Gillman, M. W.] Harvard Univ, Sch Med, Dept Populat Med, Harvard Pilgrim Hlth Care Inst, Boston, MA 02115 USA.
[Tanrikut, C.] Massachusetts Gen Hosp, Dept Urol, Boston, MA 02114 USA.
[Hauser, R.; Tanrikut, C.; Petrozza, J. C.; Chavarro, J. E.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Hauser, R.; Petrozza, J. C.] Massachusetts Gen Hosp, Vincent Obstet & Gynecol, Boston, MA 02114 USA.
[Chavarro, J. E.] Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.
RP Gaskins, AJ (reprint author), Harvard Univ, Sch Publ Hlth, Bldg 2 3rd Floor,655 Huntington Ave, Boston, MA 02115 USA.
EM ajg219@mail.harvard.edu
FU NIH [R01-ES009718, R01-ES022955, ES000002, P30-DK046200,
T32-DK007703-16, T32-HD060454]
FX The authors are supported by NIH grants R01-ES009718, R01-ES022955,
ES000002, P30-DK046200, T32-DK007703-16 and T32-HD060454. The funding
sources had no influence on the study design, data analysis, writing of
the report or the decision to submit the findings of the present study
for publication.
NR 33
TC 7
Z9 7
U1 1
U2 11
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0268-1161
EI 1460-2350
J9 HUM REPROD
JI Hum. Reprod.
PD NOV
PY 2014
VL 29
IS 11
BP 2575
EP 2582
DI 10.1093/humrep/deu212
PG 8
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AT1EJ
UT WOS:000344675700028
PM 25164027
ER
PT J
AU Gockley, AA
Rauh-Hain, JA
del Carmen, MG
AF Gockley, Allison A.
Rauh-Hain, J. Alejandro
del Carmen, Marcela G.
TI Uterine Leiomyosarcoma A Review Article
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
LA English
DT Review
DE Leiomyosarcoma; Uterine tumor; Review
ID GYNECOLOGIC-ONCOLOGY-GROUP; GEMCITABINE PLUS DOCETAXEL;
PROGNOSTIC-FACTORS; SARCOMA; SURVIVAL; RADIOTHERAPY; PATTERNS; THERAPY;
IMPACT
AB Uterine leiomyosarcomas (LMSs) are rare aggressive tumors, with high recurrence rates, even when confined to the uterine corpus at the time of diagnosis. These tumors are large myometrial masses, which typically spread hematogenously. Patients present with vague symptoms similar to those of patients with leiomyomas. Most patients are diagnosed with LMS postoperatively. In the presence of metastatic disease, complete surgical cytoreduction should be attempted when feasible. Lymphadenectomy should be performed only in patients with nodes suspected of harboring metastatic disease and as part of a cytoreductive effort. There are conflicting data to support adjuvant chemotherapy or radiation therapy for early-stage disease. Patients with advanced-stage disease should receive gemcitabine and docetaxel adjuvant chemotherapy. Patients with recurrent disease are candidates for a wide variety of second-line treatments, of which many are investigational. Although prognosis remains dismal, ongoing studies are investigating the role of advanced imaging, multimodality treatment, prognostic nomograms, and unique biomedical pathways to increase understanding of LMS and improve therapeutic options for patients.
C1 [Gockley, Allison A.; Rauh-Hain, J. Alejandro; del Carmen, Marcela G.] Vincent Obstet & Gynecol, Div Gynecol Oncol, Boston, MA USA.
RP del Carmen, MG (reprint author), Massachusetts Gen Hosp, Vincent Obstet & Gynecol, Div Gynecol Oncol, 55 Fruit St,Yawkey 9 E, Boston, MA 02114 USA.
EM mdelcarmen@partners.org
NR 25
TC 7
Z9 8
U1 0
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1048-891X
EI 1525-1438
J9 INT J GYNECOL CANCER
JI Int. J. Gynecol. Cancer
PD NOV
PY 2014
VL 24
IS 9
BP 1538
EP 1542
DI 10.1097/IGC.0000000000000290
PG 5
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA AT0FE
UT WOS:000344611800005
PM 25304676
ER
PT J
AU Berek, JS
Edwards, RP
Parker, LP
DeMars, LR
Herzog, TJ
Lentz, SS
Morris, RT
Akerley, WL
Holloway, RW
Method, MW
Plaxe, SC
Walker, JL
Friccius-Quecke, H
Krasner, CN
AF Berek, Jonathan S.
Edwards, Robert P.
Parker, Lynn P.
DeMars, Leslie R.
Herzog, Thomas J.
Lentz, Samuel S.
Morris, Robert T.
Akerley, Wallace L.
Holloway, Robert W.
Method, Michael W.
Plaxe, Steven C.
Walker, Joan L.
Friccius-Quecke, Hilke
Krasner, Carolyn N.
TI Catumaxomab for the Treatment of Malignant Ascites in Patients With
Chemotherapy-Refractory Ovarian Cancer A Phase II Study
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
LA English
DT Article
DE Catumaxomab; Trifunctional antibody; Malignant ascites; Ovarian cancer
ID CELL ADHESION MOLECULE; TRIFUNCTIONAL ANTIBODY CATUMAXOMAB; EPCAM X
ANTI-CD3; BISPECIFIC ANTIBODY; ACCESSORY CELLS; EP-CAM; EXPRESSION;
OVEREXPRESSION; ACTIVATION; EFFUSIONS
AB Objective: The aim of this study was to investigate the efficacy and safety of intraperitoneal catumaxomab in heavily pretreated patients with chemotherapy-refractory ovarian cancer and recurrent symptomatic malignant ascites.
Methods: The study is a single-arm open-label multicenter US phase II study. Patients received 4 three-hour intraperitoneal catumaxomab infusions (10, 20, 50, and 150 Kg within 10 days). The primary end point was the percentage of patients with at least a 4-fold increase in the puncture-free interval (PuFI) relative to the pretreatment interval. The main secondary end points were puncture-free survival, overall survival, ascites symptoms, and safety. Time to first therapeutic puncture (TTPu) was analyzed post hoc.
Results: Forty patients were screened, and 32 patients (80%) were treated. Seven patients (23%) achieved the primary end point. The median PuFI was prolonged 2-fold from 12 to 27.5 days. The median TTPu was prolonged 4-fold from 12 to 52 days. The median puncture-free survival and overall survival were 29.5 and 111 days, respectively. Nineteen patients (59%) required puncture after catumaxomab treatment. Ascites symptoms improved in most of the 13 predefined categories. At study end, most symptoms were still improved compared with screening. The most frequent treatment-related adverse events were related to cytokine release (vomiting, nausea, pyrexia, fatigue, and chills) or intraperitoneal administration (abdominal pain). Transient increases in liver parameters and transient decreases in blood lymphocytes were regularly observed but were generally without clinical relevance.
Conclusions: Catumaxomab prolonged PuFI and TTPu had a beneficial effect on quality of life, as shown by the improvement in ascites symptoms, and had an acceptable safety profile, which is consistent with its mode of action.
C1 [Berek, Jonathan S.] Stanford Univ, Sch Med, Div Gynecol Oncol,Dept Obstet & Gynecol, Stanford Womens Canc Ctr,Stanford Canc Inst, Stanford, CA 94305 USA.
[Edwards, Robert P.] UPMC, Magee Womens Hosp, Pittsburgh, PA USA.
[Parker, Lynn P.] Univ Louisville, James Graham Brown Canc Ctr, Louisville, KY 40292 USA.
[DeMars, Leslie R.] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
[Herzog, Thomas J.] Columbia Univ, Ctr Canc, New York, NY USA.
[Lentz, Samuel S.] WFU Baptist Med Ctr, Winston Salem, NC USA.
[Morris, Robert T.] Wayne State Univ, Barbara Ann Karmanos Canc Ctr, Detroit, MI USA.
[Akerley, Wallace L.] Huntsman Canc Inst, Salt Lake City, UT USA.
[Holloway, Robert W.] Florida Hosp, Inst Canc, Orlando, FL USA.
[Method, Michael W.] Northern Indiana Canc Res Consortium, South Bend, IN USA.
[Plaxe, Steven C.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Walker, Joan L.] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA.
[Friccius-Quecke, Hilke] Neovii Biotech GmbH, Munich, Germany.
[Krasner, Carolyn N.] Massachusetts Gen Hosp, Dana Farber Harvard Canc Ctr, Boston, MA 02114 USA.
RP Berek, JS (reprint author), Stanford Univ, Sch Med, 300 Pasteur Dr,Room HG332, Stanford, CA 94305 USA.
EM jberek@stanford.edu
FU Neovii Biotech GmbH, Munich, Germany
FX This study (NCT00326885) was sponsored by Neovii (formerly Fresenius)
Biotech GmbH, Munich, Germany.
NR 30
TC 11
Z9 12
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1048-891X
EI 1525-1438
J9 INT J GYNECOL CANCER
JI Int. J. Gynecol. Cancer
PD NOV
PY 2014
VL 24
IS 9
BP 1583
EP 1589
DI 10.1097/IGC.0000000000000286
PG 7
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA AT0FE
UT WOS:000344611800011
PM 25254563
ER
PT J
AU Mangili, G
Lorusso, D
Brown, J
Pfisterer, J
Massuger, L
Vaughan, M
Ngan, HYS
Golfier, F
Sekharan, PK
Charry, RC
Poveda, A
Kim, JW
Xiang, Y
Berkowtiz, R
Seckl, MJ
AF Mangili, Giorgia
Lorusso, Domenica
Brown, Jubilee
Pfisterer, Jacobus
Massuger, Leon
Vaughan, Michelle
Ngan, Hextan Y. S.
Golfier, Francois
Sekharan, Paradan K.
Charry, Rafael Cortes
Poveda, Andres
Kim, Jae-Weon
Xiang, Yang
Berkowtiz, Ross
Seckl, Michael J.
TI Trophoblastic Disease Review for Diagnosis and Management A Joint Report
From the International Society for the Study of Trophoblastic Disease,
European Organisation for the Treatment of Trophoblastic Disease, and
the Gynecologic Cancer InterGroup
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
LA English
DT Review
DE Gestational trophoblastic disease; Management; Diagnosis; Review
ID SINGLE-AGENT METHOTREXATE; FACTOR SCORING SYSTEM; MOLAR PREGNANCY;
NEOPLASIA; CHEMOTHERAPY; TUMORS; RESISTANCE; ETOPOSIDE; LUNG; HCG
AB Objective: The objective of this study was to provide a consensus review on gestational trophoblastic disease diagnosis and management from the combined International Society for the Study of Trophoblastic Disease, European Organisation for the Treatment of Trophoblastic Disease, and the Gynecologic Cancer InterGroup.
Methods: A joint committee representing various groups reviewed the literature obtained from PubMed searches.
Results and Conclusions: Guidelines were constructed on the basis of literature review. After initial diagnosis in local centers, centralization of pathology review and ongoing care is recommended to achieve the best outcomes.
C1 [Mangili, Giorgia] IRCCS San Raffaele Hosp, Dept Gynecol & Obstet, Milan, Italy.
[Lorusso, Domenica] Univ Cattolica Sacro Cuore, Dept Gynecol Oncol, I-00168 Rome, Italy.
[Brown, Jubilee] Univ Texas MD Anderson Canc Ctr, Gynecol Oncol Grp, Houston, TX 77030 USA.
[Pfisterer, Jacobus] AGO Study Grp, Gynecol Oncol Ctr, Kiel, Germany.
[Massuger, Leon] Radboud Univ Nijmegen Med Ctr, Dept Obstet & Gynaecol, Nijmegen, Netherlands.
[Vaughan, Michelle] ANZGOG, Camperdown, NSW, Australia.
[Ngan, Hextan Y. S.] Univ Hong Kong, Queen Mary Hosp, Dept Obstet & Gynecol, Hong Kong, Hong Kong, Peoples R China.
[Golfier, Francois] Hosp Civils Lyon, Ctr Reference Malad Trophoblast, Lyon, France.
[Sekharan, Paradan K.] Coll Med, Inst Maternal & Child Hlth, Dept Obstet & Gynecol, Calicut, Kerala, India.
[Charry, Rafael Cortes] Cent Univ Venezuela, Univ Hosp Caracas, GTD Unit, Caracas, Venezuela.
[Poveda, Andres] Fdn Inst Valenciano Oncol, Spanish Ovarian Canc Res Grp GEICO, Valencia, Spain.
[Kim, Jae-Weon] Seoul Natl Univ Hosp, Korean Gynaecol Oncol Grp, Seoul 110744, South Korea.
[Xiang, Yang] Chinese Acad Med Sci, Dept Obstet & Gynecol, Peking Union Med Coll Hosp, Beijing 100730, Peoples R China.
[Xiang, Yang] Peking Union Med Coll, Beijing 100021, Peoples R China.
[Berkowtiz, Ross] Harvard Univ, Brigham & Womens Hosp, Div Gynecol Oncol, Dept Obstet & Gynecol,Dana Farber Canc Inst,Sch M, Boston, MA 02115 USA.
[Seckl, Michael J.] Charing Cross Campus Imperial Coll London, Charing Cross Trophoblast Dis Ctr, Dept Histopathol, London, England.
[Seckl, Michael J.] Charing Cross Campus Imperial Coll London, Charing Cross Trophoblast Dis Ctr, Dept Med Oncol, London, England.
RP Seckl, MJ (reprint author), Charing Cross Hosp, Dept Med Oncol, Charing Cross Trophoblast Dis Ctr, Campus Imperial Coll London,Fulham Palace Rd, London W6 8RF, England.
EM m.seckl@imperial.ac.uk
RI Massuger, Leon/H-8072-2014; Lorusso, Domenica/K-6523-2016
OI Lorusso, Domenica/0000-0003-0981-0598
FU NCI NIH HHS [P30 CA016672]
NR 30
TC 21
Z9 24
U1 5
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1048-891X
EI 1525-1438
J9 INT J GYNECOL CANCER
JI Int. J. Gynecol. Cancer
PD NOV
PY 2014
VL 24
IS 9
SU 3
BP S109
EP S116
DI 10.1097/IGC.0000000000000294
PG 8
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA AT0FS
UT WOS:000344613200021
PM 25341573
ER
PT J
AU Sagae, S
Susumu, N
Viswanathan, AN
Aoki, D
Backes, FJ
Provencher, DM
Vaughan, M
Creutzberg, CL
Kurzeder, C
Kristensen, G
Lee, C
Kurtz, JE
Glasspool, RM
Small, W
AF Sagae, Satoru
Susumu, Nobuyuki
Viswanathan, Akila N.
Aoki, Daisuke
Backes, Floor J.
Provencher, Diane M.
Vaughan, Michelle
Creutzberg, Carien L.
Kurzeder, Christian
Kristensen, Gunnar
Lee, Chulmin
Kurtz, Jean-Emmanuel
Glasspool, Rosalind M.
Small, William, Jr.
TI Gynecologic Cancer InterGroup (GCIG) Consensus Review for Uterine Serous
Carcinoma
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
LA English
DT Review
DE Uterine serous carcinoma; GCIG; Review
ID ADVANCED ENDOMETRIAL CARCINOMA; WHOLE-ABDOMINAL IRRADIATION; PHASE-III
TRIAL; STAGE-I; ONCOLOGY-GROUP; CLEAR-CELL; SURVIVAL OUTCOMES;
PAPILLARY; CHEMOTHERAPY; DOXORUBICIN
AB Objectives: Uterine serous carcinoma (USC) represents a rare and aggressive histologic subtype of endometrial cancer, associated with a poor prognosis. This article critically reviews the literature pertinent to the epidemiology, pathology, molecular biology, diagnosis, management, and perspectives of patients with USC.
Methods: As one of a series of The Gynecologic Cancer InterGroup (GCIG) Rare Tumor Working Group in London, November 2013, we discussed about USC many times with various experts among international GCIG groups.
Results: Both USC and approximately 25% of high-grade endometrioid tumors represent extensive copy number alterations, few DNA methylation changes, low estrogen and progesterone levels, and frequent P53mutations. Uterine serous carcinoma shares molecular characteristics with ovarian serous and basal-like breast carcinomas. In addition to optimal surgery, platinum-and taxane-based chemotherapy should be considered in the treatment of both early-and advanced-stage disease. The combination of radiation and chemotherapy appears to be associated with the highest survival rates. The role of radiation therapy in the management of this disease, with a high propensity for distant failures, remains elusive.
Conclusions: Uterine serous carcinoma is a unique and biologically aggressive subtype of endometrial cancer and should be studied as a distinct entity. Futures studies should identify the optimized chemotherapy and radiation regimens, sequence of therapy and schedule, and the role of targeted biologic therapy.
C1 [Sagae, Satoru] JR Sapporo Hosp, Dept Obstet & Gynecol, Sapporo, Hokkaido 0600033, Japan.
[Susumu, Nobuyuki; Aoki, Daisuke] Keio Univ, Sch Med, Dept Obstet & Gynecol, Tokyo 160, Japan.
[Viswanathan, Akila N.] Harvard Univ, Sch Med, Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Backes, Floor J.] Ohio State Univ, Coll Med, Dept Obstet & Gynecol, Columbus, OH 43210 USA.
[Provencher, Diane M.] Ctr Hosp Univ Montreal, Montreal, PQ, Canada.
[Vaughan, Michelle] Christchurch Hosp, Dept Oncol, Canterbury, New Zealand.
[Creutzberg, Carien L.] Leiden Univ, Dept Clin Oncol, Med Ctr, Leiden, Netherlands.
[Kurzeder, Christian] Kliniken Essen Mitte KEM AGO, Dept Gynecol & Gynecol Oncol, Essen, Germany.
[Kristensen, Gunnar] Norwegian Radium Hosp, Oslo, Norway.
[Lee, Chulmin] Inje Univ, Sanggye Paik Hosp, Dept Obstet & Gynecol, Seoul, South Korea.
[Kurtz, Jean-Emmanuel] Hop Univ Strasbourg, Dept Hematol & Oncol, Strasbourg, France.
[Glasspool, Rosalind M.] Beatson West Scotland Canc Ctr, Glasgow, Lanark, Scotland.
[Small, William, Jr.] Loyola Univ, Stritch Sch Med, Dept Radiat Oncol, Chicago, IL 60611 USA.
RP Sagae, S (reprint author), JR Sapporo Hosp, Dept Obstet & Gynecol, Chuou Ku, North 3 East 1, Sapporo, Hokkaido 0600033, Japan.
EM s-sagae@jrhokkaido.co.jp
RI Kurtz, Jean-Emmanuel/R-3286-2016;
OI Backes, Floor/0000-0002-9225-6913; Glasspool,
Rosalind/0000-0002-5000-1680
NR 30
TC 16
Z9 16
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1048-891X
EI 1525-1438
J9 INT J GYNECOL CANCER
JI Int. J. Gynecol. Cancer
PD NOV
PY 2014
VL 24
IS 9
SU 3
BP S83
EP S89
DI 10.1097/IGC.0000000000000264
PG 7
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA AT0FS
UT WOS:000344613200017
PM 25341586
ER
PT J
AU Xia, YM
Gupta, GK
Castano, AP
Mroz, P
Avci, P
Hamblin, MR
AF Xia, Yumin
Gupta, Gaurav K.
Castano, Ana P.
Mroz, Pawel
Avci, Pinar
Hamblin, Michael R.
TI CpG oligodeoxynucleotide as immune adjuvant enhances photodynamic
therapy response in murine metastatic breast cancer
SO JOURNAL OF BIOPHOTONICS
LA English
DT Article
DE breast cancer; CpG oligodeoxynucleotide; dendritic cells; photodynamic
therapy
ID NF-KAPPA-B; ANTITUMOR IMMUNITY; DENDRITIC CELLS; SUPPRESSOR-CELLS; TLR9
AGONISTS; TUMOR; IMMUNOTHERAPY; ACTIVATION; DISEASE; MODEL
AB Breast cancer is the most common cause of cancer death in women. The side effects and complications following current breast cancer therapy can be devastating. Moreover, the prognosis in late stages of the diseases is usually poor. Photodynamic therapy (PDT) is a promising cancer treatment modality that is capable of both local tumor destruction and immune stimulation. However, treatment with PDT alone is often non-curative due to tumor-induced immune cell dysfunction and immune suppression. This phenomenon has motivated a new approach by combining immunostimulants with PDT to enhance anti-tumor immunity. In the present study, we investigated PDT mediated by verteporfin and 690 nm light delivered 15 min later, in combination with an immunomodulation approach using CpG oligodeoxynucleotide for the treatment of 4T1 metastatic breast cancer in a BALB/c immunocompetent mouse model. In vitro, CpG primed immature dendritic cells (DC) via toll like receptor 9 to phagocytose PDT killed tumor cells leading to DC maturation and activation. Peritumoral injection of CpG after PDT in mice gave improved local tumor control and a survival advantage compared to either treatment alone (p < 0.05). CpG may be a valuable dendritic cell targeted immunoadjuvant to combine with PDT. ((c) 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)
C1 [Xia, Yumin; Gupta, Gaurav K.; Castano, Ana P.; Mroz, Pawel; Avci, Pinar; Hamblin, Michael R.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
[Xia, Yumin; Gupta, Gaurav K.; Castano, Ana P.; Mroz, Pawel; Avci, Pinar; Hamblin, Michael R.] Harvard Univ, Sch Med, Dept Dermatol, Boston, MA 02115 USA.
[Avci, Pinar] Semmelweis Univ, Sch Med, Dept Dermatol Dermatooncol & Venerol, H-1085 Budapest, Hungary.
[Hamblin, Michael R.] Harvard MIT Div Hlth Sci & Technol, Cambridge, MA USA.
RP Hamblin, MR (reprint author), Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
EM hamblin@helix.mgh.harvard.edu
OI Hamblin, Michael/0000-0001-6431-4605
FU NCI NIH HHS [R01 CA083882]; NIAID NIH HHS [R01 AI050875]
NR 51
TC 10
Z9 11
U1 3
U2 19
PU WILEY-V C H VERLAG GMBH
PI WEINHEIM
PA BOSCHSTRASSE 12, D-69469 WEINHEIM, GERMANY
SN 1864-063X
EI 1864-0648
J9 J BIOPHOTONICS
JI J. Biophotonics
PD NOV
PY 2014
VL 7
IS 11-12
BP 897
EP 905
DI 10.1002/jbio.201300072
PG 9
WC Biochemical Research Methods; Biophysics; Optics
SC Biochemistry & Molecular Biology; Biophysics; Optics
GA AT0WB
UT WOS:000344651800005
PM 23922221
ER
PT J
AU Bose, A
Upadhyay, GA
Kandala, J
Heist, EK
Mela, T
Parks, KA
Singh, JP
AF Bose, Abhishek
Upadhyay, Gaurav A.
Kandala, Jagdesh
Heist, Edwin K.
Mela, Theofanie
Parks, Kimberly A.
Singh, Jagmeet P.
TI Does Prior Valve Surgery Change Outcome in Patients Treated with Cardiac
Resynchronization Therapy?
SO JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY
LA English
DT Article
DE coronary artery bypass surgery; cardiac resynchronization therapy;
cardiac valve surgery; heart failure; heart transplant
ID PERMANENT PACEMAKER IMPLANTATION; VENTRICULAR SYSTOLIC FUNCTION;
HEART-FAILURE PATIENTS; ATRIAL-FIBRILLATION; RISK-FACTORS;
ATRIOVENTRICULAR-CONDUCTION; CARDIOPULMONARY BYPASS; AORTIC-STENOSIS;
FOLLOW-UP; REPLACEMENT
AB Impact of Prior Valve Surgery in CRT Patients
AimsCardiac valve surgery (CVS) has been implicated as a potential barrier to optimal response after cardiac resynchronization therapy (CRT) though prospective data regarding outcome remains limited. We sought to determine CRT response in patients with a prior history of CVS.
Methods and ResultsWe performed a retrospective analysis of a prospectively acquired cohort of CRT patients with history of CVS. Echocardiographic response was evaluated at baseline and 6 months. The coprimary endpoints were time to first heart failure (HF) hospitalization and a composite of all-cause mortality, transplantation and left ventricular assist device (LVAD) assessed over a 3-year follow-up period. The study group consisted of 569 patients undergoing CRT. Of these, 86 patients had a history of CVS (46.5% aortic, 37.2% mitral, 16.3% combined, and tricuspid), and were compared to 483 patients with no history of CVS. Baseline clinical and echocardiographic characteristics were not significantly different between the groups except for a higher incidence of atrial fibrillation (AF; 74.4% vs. 55.3%; P = 0.001), coronary artery bypass surgery (CABG; 58.1% vs. 38.7%; P = 0.001), and longer QRS duration (167.6 29.3 milliseconds vs. 159.4 +/- 27.5 milliseconds; P = 0.01) in those with prior CVS. Survival with respect to HF hospitalization and composite outcome was comparable in both groups. Echocardiographic response (improvement in left ventricular ejection fraction of 10%) was similar. No difference in clinical or echocardiographic outcome was found by type of valve surgery performed.
ConclusionDespite a higher incidence of AF, CABG, and longer QRS duration, history of CVS is not associated with worse clinical or echocardiographic outcome after CRT.
C1 [Bose, Abhishek; Upadhyay, Gaurav A.; Kandala, Jagdesh; Heist, Edwin K.; Mela, Theofanie; Singh, Jagmeet P.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Corrigan Minehan Inst, Ctr Heart, Boston, MA 02114 USA.
[Parks, Kimberly A.] Massachusetts Gen Hosp, Heart Failure & Cardiac Transplant Program, Corrigan Minehan Inst, Ctr Heart, Boston, MA 02114 USA.
RP Upadhyay, GA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Cardiac Arrhythmia Serv,Heart Ctr, Boston, MA 02114 USA.
EM gaupadhyay@partners.org
FU Max Schaldach Fellowship Award of the Heart Rhythm Society; Biotronik;
Sorin; St. Jude Medical; Boston Scientific; Thoratec Inc.; Medtronic
FX Dr. Upadhyay reports receiving salary support from the Max Schaldach
Fellowship Award of the Heart Rhythm Society. Dr. Heist reports
receiving honoraria from Biotronik, Boston Scientific, Sorin, and St.
Jude Medical; research grants from Biotronik, Sorin, and St. Jude
Medical; and consulting fees from Boston Scientific, Sorin, and St. Jude
Medical. Dr. Mela reports receiving honoraria from Medtronic Inc.,
Biotronik, and St. Jude Medical. Dr. Parks reports receiving consulting
fees from Thoratec Inc. and honoraria from Biotronik and Sorin. Dr.
Singh reports serving as an advisor or consultant for Biotronik, Boston
Scientific, Medtronic, Sorin, St. Jude Medical, Respicardia, and
CardioInsight; serving as a speaker or a member of a speakers bureau for
Biotronik, Boston Scientific, Sorin, and St. Jude Medical; and receiving
grants for clinical research from Biotronik, Boston Scientific,
Medtronic, and St. Jude Medical. Other authors: No disclosures.
NR 38
TC 1
Z9 2
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1045-3873
EI 1540-8167
J9 J CARDIOVASC ELECTR
JI J. Cardiovasc. Electrophysiol.
PD NOV
PY 2014
VL 25
IS 11
BP 1206
EP 1213
DI 10.1111/jce.12469
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AS7ZL
UT WOS:000344470300010
PM 24903306
ER
PT J
AU Lerman, J
Everett, L
Cote, CJ
AF Lerman, Jerrold
Everett, Lucy
Cote, Charles J.
TI Correspondence on "Clinical Characterization of Gastroenteritis-Related
Seizures in Children: Impact of Fever and Serum Sodium Levels" Response
SO JOURNAL OF CHILD NEUROLOGY
LA English
DT Letter
C1 [Lerman, Jerrold] SUNY Buffalo, Women & Childrens Hosp Buffalo, Buffalo, NY 14260 USA.
[Lerman, Jerrold] Univ Rochester, Rocester, NY USA.
[Everett, Lucy] Massachusetts Gen Hosp, MassGen Hosp Children, Dept Anesthesia & Crit Care, Boston, MA 02114 USA.
[Cote, Charles J.] Massachusetts Gen Hosp, MassGen Hosp Children, Dept Anesthesia & Crit Care, Div Pediat Anesthesia, Boston, MA 02114 USA.
RP Lerman, J (reprint author), SUNY Buffalo, Women & Childrens Hosp Buffalo, Buffalo, NY 14260 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0883-0738
EI 1708-8283
J9 J CHILD NEUROL
JI J. Child Neurol.
PD NOV
PY 2014
VL 29
IS 11
BP 1580
EP 1580
DI 10.1177/0883073813510604
PG 1
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA AT0XB
UT WOS:000344655400034
PM 24282182
ER
PT J
AU Pineiro, ML
Roberts, AM
Waxler, JL
Mullett, JE
Pober, BR
McDougle, CJ
AF Pineiro, Mildred Lopez
Roberts, Antoinette M.
Waxler, Jessica L.
Mullett, Jennifer E.
Pober, Barbara R.
McDougle, Christopher J.
TI N-Acetylcysteine for Neuropsychiatric Symptoms in a Woman With Williams
Syndrome
SO JOURNAL OF CHILD NEUROLOGY
LA English
DT Article
DE Williams syndrome; N-acetylcysteine; behavior; glutamate;
neuropsychiatric
ID DOUBLE-BLIND; 2 CHILDREN; METHYLPHENIDATE; DISORDER; INDIVIDUALS;
GLUTAMATE
AB Williams syndrome is a relatively rare genetic disorder caused by the hemizygous microdeletion of a region in chromosome 7q11.23. Individuals with Williams syndrome typically present with a highly social, overfriendly, and empathic personality. Comorbid medical and neuropsychiatric disorders are common. Reports of effective pharmacological treatment of associated neuropsychiatric disorders are limited. The authors describe the successful treatment of interfering anger, aggression, and hair-pulling with N-acetylcysteine in a 19-year-old woman with Williams syndrome. The neuropsychiatric symptoms emerged 1 week following an upper gastrointestinal endoscopy, for which fentanyl, midazolam, and propofol were used as anesthetics. The patient's treatment course and hypothesized mechanisms underlying the clinical presentation and symptom resolution are described.
C1 [Pineiro, Mildred Lopez] Geisel Sch Med Dartmouth, Lebanon, NH USA.
[Waxler, Jessica L.; Pober, Barbara R.; McDougle, Christopher J.] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
[Mullett, Jennifer E.; McDougle, Christopher J.] Massachusetts Gen Hosp, Lurie Ctr Autism, Lexington, MA USA.
[Pober, Barbara R.; McDougle, Christopher J.] Harvard Univ, Sch Med, Boston, MA USA.
[Pober, Barbara R.] Quinnipiac Univ, Netter Sch Med, Dept Med Sci, Middletown, CT USA.
[McDougle, Christopher J.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
RP McDougle, CJ (reprint author), Lurie Ctr Autism, One Maguire Rd, Lexington, MA 02421 USA.
EM cmcdougle@partners.org
NR 15
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 0883-0738
EI 1708-8283
J9 J CHILD NEUROL
JI J. Child Neurol.
PD NOV
PY 2014
VL 29
IS 11
BP NP135
EP NP138
DI 10.1177/0883073813512025
PG 4
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA AT0XB
UT WOS:000344655400002
PM 24396132
ER
PT J
AU Lourenco, TGB
Heller, D
Silva-Boghossian, CM
Cotton, SL
Paster, BJ
Colombo, APV
AF Baeta Lourenco, Talita Gomes
Heller, Debora
Silva-Boghossian, Carina Maciel
Cotton, Sean L.
Paster, Bruce J.
Vieira Colombo, Ana Paula
TI Microbial signature profiles of periodontally healthy and diseased
patients
SO JOURNAL OF CLINICAL PERIODONTOLOGY
LA English
DT Article
DE aggressive periodontitis; biofilm; chronic periodontitis; gingivitis;
microarray analysis; microbiota
ID AGGRESSIVE PERIODONTITIS; IDENTIFICATION MICROARRAY; REFRACTORY
PERIODONTITIS; SUBGINGIVAL MICROBIOTA; BACTERIAL DIVERSITY; ORAL
MICROFLORA; COMMUNITY; INDIVIDUALS; GINGIVITIS; BIOFILMS
AB AimTo determine microbial profiles that discriminate periodontal health from different forms of periodontal diseases.
MethodsSubgingival biofilm was obtained from patients with periodontal health (27), gingivitis (11), chronic periodontitis (35) and aggressive periodontitis (24), and analysed for the presence of >250 species/phylotypes using HOMIM. Microbial differences among groups were examined by Mann-Whitney U-test. Regression analyses were performed to determine microbial risk indicators of disease.
ResultsPutative and potential new periodontal pathogens were more prevalent in subjects with periodontal diseases than periodontal health. Detection of Porphyromonas endodontalis/Porphyromonas spp. (OR 9.5 [1.2-73.1]) and Tannerella forsythia (OR 38.2 [3.2-450.6]), and absence of Neisseria polysaccharea (OR 0.004 [0-0.15]) and Prevotella denticola (OR 0.014 [0-0.49], p<0.05) were risk indicators of periodontal disease. Presence of Aggregatibacter actinomycetemcomitans (OR 29.4 [3.4-176.5]), Cardiobacterium hominis (OR 14.9 [2.3-98.7]), Peptostreptococcaceae sp. (OR 35.9 [2.7-483.9]), P.alactolyticus (OR 31.3 [2.1-477.2]), and absence of Fretibacterium spp. (OR 0.024 [0.002-0.357]), Fusobacterium naviforme/Fusobacterium nucleatum ss vincentii (OR 0.015 [0.001-0.223]), Granulicatella adiacens/Granulicatella elegans (OR 0.013 [0.001-0.233], p<0.05) were associated with aggressive periodontitis.
ConclusionThere were specific microbial signatures of the subgingival biofilm that were able to distinguish between microbiomes of periodontal health and diseases. Such profiles may be used to establish risk of disease.
C1 [Baeta Lourenco, Talita Gomes; Heller, Debora; Silva-Boghossian, Carina Maciel; Vieira Colombo, Ana Paula] Univ Fed Rio de Janeiro, Inst Microbiol, BR-21941 Rio De Janeiro, Brazil.
[Heller, Debora; Silva-Boghossian, Carina Maciel] Univ Fed Rio de Janeiro, Div Grad Periodont, Dept Dent Clin, BR-21941 Rio De Janeiro, Brazil.
[Heller, Debora] Goldman Sch Med, Dept Oral Biol, Boston, MA USA.
[Cotton, Sean L.; Paster, Bruce J.] Forsyth Inst, Dept Microbiol, Cambridge, MA USA.
[Paster, Bruce J.] Harvard Univ, Sch Dent Med, Boston, MA 02115 USA.
RP Colombo, APV (reprint author), Univ Fed Rio de Janeiro, CCS, Inst Microbiol, Paulo de Goes Bloco 1,Lab I2-03, BR-21941902 Rio de Janeiro, RJ, Brazil.
EM apcolombo@micro.ufrj.br
RI Silva-Boghossian, Carina M./G-9440-2012
OI Silva-Boghossian, Carina M./0000-0002-4500-4350
FU National Council for Scientific and Technological Development CNPq;
Coordination of Improvement of Higher Education Personnel (CAPES),
Brasilia, Brazil; Foundation for Research Financial Support in the State
of Rio de Janeiro (FAPERJ), Rio de Janeiro, Brazil; National Institutes
of Health [DE021565]
FX The authors declare that they have no conflict of interests regarding
this study. This work was supported in part by National Council for
Scientific and Technological Development CNPq, and Coordination of
Improvement of Higher Education Personnel (CAPES), Brasilia, Brazil;
Foundation for Research Financial Support in the State of Rio de Janeiro
(FAPERJ), Rio de Janeiro, Brazil and a grant from The National
Institutes of Health, DE021565 (BP).
NR 40
TC 26
Z9 26
U1 1
U2 24
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0303-6979
EI 1600-051X
J9 J CLIN PERIODONTOL
JI J. Clin. Periodontol.
PD NOV
PY 2014
VL 41
IS 11
BP 1027
EP 1036
DI 10.1111/jcpe.12302
PG 10
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA AS8CH
UT WOS:000344477400001
PM 25139407
ER
PT J
AU Hooper, DC
Hirsch, MS
AF Hooper, David C.
Hirsch, Martin S.
TI Clarification Regarding Novel Clostridium botulinum Toxin Reply
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Letter
C1 [Hooper, David C.; Hirsch, Martin S.] Massachusetts Gen Hosp, Div Infect Dis, Cambridge, MA 02139 USA.
RP Hirsch, MS (reprint author), Massachusetts Gen Hosp, Div Infect Dis, 65 Landsdowne St,Rm 419, Cambridge, MA 02139 USA.
EM mshirsch@partners.org
NR 3
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 0022-1899
EI 1537-6613
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 1
PY 2014
VL 210
IS 9
BP 1517
EP 1518
DI 10.1093/infdis/jiu270
PG 2
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA AT0ER
UT WOS:000344610600023
PM 24808388
ER
PT J
AU Hillblom, D
Schueth, A
Robertson, SM
Topor, L
Low, G
AF Hillblom, Douglas
Schueth, Anthony
Robertson, Scott M.
Topor, Laura
Low, Greg
TI The Impact of Information Technology on Managed Care Pharmacy: Today and
Tomorrow
SO JOURNAL OF MANAGED CARE PHARMACY
LA English
DT Editorial Material
ID ELECTRONIC HEALTH RECORD
AB Understanding the use of health information technology (HIT) and its implications is crucial for the future of managed care pharmacy. Information is the cornerstone of providing and managing care, and the ability to exchange data is easier and more complicated than ever before. In this commentary, a subset of the Academy of Managed Care Pharmacy Healthcare Information Technology Advisory Council addresses how HIT supports managed care today and its anticipated evolution, with a focus on quality, patient safety, communication, and efficiency. Among the tools and functions reviewed are electronic health records, electronic prescribing, health information exchange, electronic prior authorization, pharmacists as care team members, formularies, prescription drug abuse, and policy levers to address these issues. Copyright (C) 2014, Academy of Managed Care Pharmacy. All rights reserved.
C1 [Hillblom, Douglas] OptumRx, Profess Practice & Pharm Policy, Sacramento, CA 95826 USA.
[Schueth, Anthony] Point Care Partners LLC, Coral Springs, FL USA.
[Robertson, Scott M.] Kaiser Permanente, Pasadena, CA USA.
[Topor, Laura] Granada Hlth, Minnetonka, MN USA.
[Low, Greg] Massachusetts Gen Hosp, MGPO Pharm, Boston, MA 02114 USA.
RP Hillblom, D (reprint author), OptumRx, Profess Practice & Pharm Policy, 8880 Cal Ctr Dr,Ste 300, Sacramento, CA 95826 USA.
EM douglas.hillblom@optum.com
NR 48
TC 1
Z9 1
U1 2
U2 5
PU ACAD MANAGED CARE PHARMACY
PI ALEXANDRIA
PA 100 N PITT ST, 400, ALEXANDRIA, VA 22314-3134 USA
SN 1083-4087
J9 J MANAGE CARE PHARM
JI J. Manag. Care Pharm.
PD NOV
PY 2014
VL 20
IS 11
BP 1073
EP 1079
PG 7
WC Health Care Sciences & Services; Pharmacology & Pharmacy
SC Health Care Sciences & Services; Pharmacology & Pharmacy
GA AS8RF
UT WOS:000344515200001
PM 25351968
ER
PT J
AU Haggerty, G
Forlenza, N
Poland, C
Ray, S
Zodan, J
Mehra, A
Goyal, A
Baity, MR
Siefert, CJ
Sobin, S
Leite, D
Sinclair, SJ
AF Haggerty, Greg
Forlenza, Nicholas
Poland, Charlotte
Ray, Sagarika
Zodan, Jennifer
Mehra, Ashwin
Goyal, Ajay
Baity, Matthew R.
Siefert, Caleb J.
Sobin, Sean
Leite, David
Sinclair, Samuel J.
TI Assessing Overall Functioning With Adolescent Inpatients
SO JOURNAL OF NERVOUS AND MENTAL DISEASE
LA English
DT Article
DE Overall functioning; GAF; SOS-10; SCORS-G; adolescent; inpatient;
assessment
ID SCHWARTZ OUTCOME SCALE-10; GLOBAL ASSESSMENT SCALE; LENGTH-OF-STAY;
MENTAL-HEALTH; INITIAL-VALIDATION; CONSTRUCT-VALIDITY; PREDICTING
LENGTH; AXIS-II; PERSONALITY; CHILDREN
AB The current study sought to evaluate the validity and reliability of a brief measure of overall functioning for adolescents. Clinicians were asked to complete the Overall Functioning Scale (OFS) for 72 adolescents consecutively admitted to the adolescent psychiatric inpatient service of a community safety net medical center. The results revealed that this new measure is related to the patients' length of stay, clinician-rated measures of social cognition and object relations, Global Assessment of Functioning (GAF) score at admission, as well as global rating of engagement in individual psychotherapy. The results also showed that the OFS was related to the patients' history of nonsuicidal self-harm as well as treatment outcome as assessed by measures of psychological health and well-being as well as symptoms. Hierarchical regressions reveal that the OFS shows incremental validity greater than the admission GAF score in predicting length of stay. The results also showed that the OFS demonstrates interrater reliability in the excellent range (intraclass correlation coefficient(1,2)) of 0.88. Clinical implications of the use of this tool and areas of future research are discussed.
C1 [Haggerty, Greg; Forlenza, Nicholas; Poland, Charlotte; Ray, Sagarika; Zodan, Jennifer; Mehra, Ashwin; Goyal, Ajay] Nassau Univ, Med Ctr, Von Tauber Inst Global Psychiat, Dept Psychiat & Behav Sci, E Meadow, NY 11554 USA.
[Baity, Matthew R.] Alliant Int Univ, Dept Psychol, Sacramento, CA USA.
[Siefert, Caleb J.] Univ Michigan Dearborn, Dept Psychol, Dearborn, MI USA.
[Sobin, Sean] Long Isl Univ, Dept Psychol, Brookville, NY USA.
[Leite, David] Liberty Univ, Dept Psychol, Lynchburg, VA USA.
[Sinclair, Samuel J.] Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp,Psychol Evalut & Res Lab, Boston, MA 02115 USA.
RP Haggerty, G (reprint author), Nassau Univ, Med Ctr, 2201 Hempstead Tpke,Box 48, E Meadow, NY 11554 USA.
EM ghag541@aol.com
FU American Psychoanalytic Association; NIMH [1R21MH097781-01A1]
FX This study was supported in part by a grant awarded to the first author
from the American Psychoanalytic Association and by NIMH Grant No.
1R21MH097781-01A1, received by the first author.
NR 44
TC 0
Z9 0
U1 2
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3018
EI 1539-736X
J9 J NERV MENT DIS
JI J. Nerv. Ment. Dis.
PD NOV
PY 2014
VL 202
IS 11
BP 822
EP 828
DI 10.1097/NMD.0000000000000200
PG 7
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA AT4XB
UT WOS:000344944300009
PM 25259948
ER
PT J
AU Shepard, JA
Vajda, K
Nyer, M
Clarke, W
Gonder-Frederick, L
AF Shepard, Jaclyn A.
Vajda, Karen
Nyer, Maren
Clarke, William
Gonder-Frederick, Linda
TI Understanding the Construct of Fear of Hypoglycemia in Pediatric Type 1
Diabetes
SO JOURNAL OF PEDIATRIC PSYCHOLOGY
LA English
DT Article
DE anxiety; diabetes; quality of life
ID SUBCUTANEOUS INSULIN INFUSION; POOR GLYCEMIC CONTROL; YOUNG-CHILDREN;
EMOTIONAL DISTRESS; FIT INDEXES; PARENTS; ADOLESCENTS; MELLITUS;
FATHERS; MOTHERS
AB ObjectiveaEuro integral Fear of hypoglycemia (FoH) can be a significant barrier to glycemic control in pediatric type 1 diabetes (T1D). This study aimed to explore underlying constructs of the Hypoglycemia Fear Survey (HFS) for parents (PHFS) and children (CHFS).aEuro integral MethodsaEuro integral Data were aggregated from five studies of 259 youth with T1D and 250 parents. Exploratory Factor Analysis was used to determine the underlying factors of the CHFS and PHFS.aEuro integral ResultsaEuro integral Similar four-factor solutions were found for the CHFS and PHFS. Both subscales consisted of two factors: Behavior Subscale (1) behaviors used to keep blood glucose (BG) high to prevent hypoglycemia (Maintain High BG) and (2) other actions to avoid hypoglycemia (Avoidance); Worry Subscale (1) concerns about helplessness (Helplessness) and (2) negative social consequences associated with hypoglycemia (Social Consequences).aEuro integral ConclusionsaEuro integral These constructs provide a more comprehensive understanding of pediatric FoH and have implications for interventions aimed at reducing FoH in this population.
C1 [Shepard, Jaclyn A.; Vajda, Karen; Gonder-Frederick, Linda] Univ Virginia, Dept Psychiat & Neurobehav Sci, Charlottesville, VA 22908 USA.
[Nyer, Maren] Harvard Univ, Depress Clin & Res Program, Massachusetts Gen Hosp, Dept Psychiat,Med Sch, Cambridge, MA 02138 USA.
[Clarke, William] Univ Virginia, Dept Pediat, Charlottesville, VA 22908 USA.
RP Gonder-Frederick, L (reprint author), Univ Virginia, Sch Med, Behav Med Ctr, Box 800223, Charlottesville, VA 22908 USA.
EM Lag3g@virginia.edu
FU NIDDK NIH HHS [R21DK080896]
NR 38
TC 7
Z9 7
U1 1
U2 10
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0146-8693
EI 1465-735X
J9 J PEDIATR PSYCHOL
JI J. Pediatr. Psychol.
PD NOV-DEC
PY 2014
VL 39
IS 10
BP 1115
EP 1125
DI 10.1093/jpepsy/jsu068
PG 11
WC Psychology, Developmental
SC Psychology
GA AT0IU
UT WOS:000344620900007
PM 25214644
ER
PT J
AU Pan, C
Zhou, Y
Dator, R
Ginghina, C
Zhao, YC
Movius, J
Peskind, E
Zabetian, CP
Quinn, J
Galasko, D
Stewart, T
Shi, M
Zhang, J
AF Pan, Catherine
Zhou, Yong
Dator, Romel
Ginghina, Carmen
Zhao, Yanchun
Movius, James
Peskind, Elaine
Zabetian, Cyrus P.
Quinn, Joseph
Galasko, Douglas
Stewart, Tessandra
Shi, Min
Zhang, Jing
TI Targeted Discovery and Validation of Plasma Biomarkers of Parkinson's
Disease
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE Parkinsons disease; targeted mass spectrometry; peripheral biomarkers;
selected reaction monitoring
ID BLOOD-BRAIN-BARRIER; ALPHA-SYNUCLEIN; PRION PROTEIN; NEURODEGENERATIVE
DISEASES; CEREBROSPINAL-FLUID; ALZHEIMERS-DISEASE; MASS-SPECTROMETRY;
GROWTH-FACTOR; GLYCOPROTEINS; PROTEOMICS
AB Despite extensive research, an unmet need remains for protein biomarkers of Parkinson's disease (PD) in peripheral body fluids, especially blood, which is easily accessible clinically. The discovery of such biomarkers is challenging, however, due to the enormous complexity and huge dynamic range of human blood proteins, which are derived from nearly all organ systems, with those originating specifically from the central nervous system (CNS) being exceptionally low in abundance. In this investigation of a relatively large cohort (similar to 300 subjects), selected reaction monitoring (SRM) assays (a targeted approach) were used to probe plasma peptides derived from glycoproteins previously found to be altered in the CNS based on PD diagnosis or severity. Next, the detected peptides were interrogated for their diagnostic sensitivity and specificity as well as the correlation with PD severity, as determined by the Unified Parkinson's Disease Rating Scale (UPDRS). The results revealed that 12 of the 50 candidate glycopeptides were reliably and consistently identified in plasma samples, with three of them displaying significant differences among diagnostic groups. A combination of four peptides (derived from PRNP, HSPG2, MEGF8, and NCAM1) provided an overall area under curve (AUC) of 0.753 (sensitivity: 90.4%; specificity: 50.0%). Additionally, combining two peptides (derived from MEGF8 and ICAM1) yielded significant correlation with PD severity, that is, UPDRS (r = 0.293, p = 0.004). The significance of these results is at least two-fold: (1) it is possible to use a targeted approach to identify otherwise very difficult to detect CNS related biomarkers in peripheral blood and (2) the novel biomarkers, if validated in independent cohorts, can be employed to assist with clinical diagnosis of PD as well as monitoring disease progression.
C1 [Pan, Catherine; Dator, Romel; Ginghina, Carmen; Zhao, Yanchun; Movius, James; Stewart, Tessandra; Shi, Min; Zhang, Jing] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98104 USA.
[Pan, Catherine] Inarian Neurodiagnost, Mercer Isl, WA 98040 USA.
[Zhou, Yong] Inst Syst Biol, Seattle, WA 98109 USA.
[Peskind, Elaine] Univ Washington, Sch Med, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Peskind, Elaine] Vet Affairs Puget Sound Hlth Care Syst, Mental Illness Res Educ & Clin Ctr, Seattle, WA 98108 USA.
[Zabetian, Cyrus P.] Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Seattle, WA 98108 USA.
[Zabetian, Cyrus P.] Univ Washington, Sch Med, Dept Neurol, Seattle, WA 98195 USA.
[Quinn, Joseph] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97239 USA.
[Galasko, Douglas] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA.
RP Zhang, J (reprint author), Univ Washington, Sch Med, Dept Pathol, 325 9th Ave,HMC 359635, Seattle, WA 98104 USA.
EM zhangj@uw.edu
RI Shi, Min/G-6165-2012;
OI Shi, Min/0000-0002-6901-2558; Zabetian, Cyrus/0000-0002-7739-4306
FU University of Washington's Proteomics Resource [UWPR95794];
[R43NS065553]; [AG033398]; [AG05131]; [ES004696-5897];
[ES007033-6364]; [ES016873]; [ES019277]; [NS057567]; [NS062684];
[NS060252]; [NS062684-6221]; [NS082137]
FX We deeply appreciate the generous participation and donation of samples
by the patients in this study. The project described was supported by
Award Number R43NS065553 (to C.P.) as well as Award Numbers AG033398,
AG05131, ES004696-5897, ES007033-6364, ES016873, ES019277, NS057567,
NS062684, NS060252, NS062684-6221, and NS082137 (to J.Z.). It was also
partially supported by the University of Washington's Proteomics
Resource (UWPR95794). The content is solely the responsibility of the
authors and does not necessarily represent the official views of any
funding agency.
NR 58
TC 9
Z9 9
U1 6
U2 20
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
EI 1535-3907
J9 J PROTEOME RES
JI J. Proteome Res.
PD NOV
PY 2014
VL 13
IS 11
BP 4535
EP 4545
DI 10.1021/pr500421v
PG 11
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA AT0PA
UT WOS:000344636500006
PM 24853996
ER
PT J
AU Gbormittah, FO
Lee, LY
Taylor, K
Hancock, WS
Iliopoulos, O
AF Gbormittah, Francisca O.
Lee, Ling Y.
Taylor, KyOnese
Hancock, William S.
Iliopoulos, Othon
TI Comparative Studies of the Proteome, Glycoproteome, and N-Glycome of
Clear Cell Renal Cell Carcinoma Plasma before and after Curative
Nephrectomy
SO JOURNAL OF PROTEOME RESEARCH
LA English
DT Article
DE Glycoproteomics; glycomics; N-glycans; lectins; multi-lectin affinity
chromatography
ID D-BINDING PROTEIN; BREAST-CANCER PATIENTS; CHROMATOGRAPHY M-LAC;
AFFINITY-CHROMATOGRAPHY; STRUCTURAL-ANALYSIS; MASS-SPECTROMETRY;
SIALIC-ACID; SERUM; GLYCOSYLATION; EXPRESSION
AB Clear cell renal cell carcinoma is the most prevalent of all reported kidney cancer cases, and currently there are no markers for early diagnosis. This has stimulated great research interest recently because early detection of the disease can significantly improve the low survival rate. Combining the proteome, glycoproteome, and N-glycome data from clear cell renal cell carcinoma plasma has the potential of identifying candidate markers for early diagnosis and prognosis and/or to monitor disease recurrence. Here, we report on the utilization of a multi-dimensional fractionation approach (12P-M-LAC) and LCMS/MS to comprehensively investigate clear cell renal cell carcinoma plasma collected before (disease) and after (non-disease) curative nephrectomy (n = 40). Proteins detected in the subproteomes were investigated via label-free quantification. Protein abundance analysis revealed a number of low-level proteins with significant differential expression levels in disease samples, including HSPG2, CD146, ECM1, SELL, SYNE1, and VCAM1. Importantly, we observed a strong correlation between differentially expressed proteins and clinical status of the patient. Investigation of the glycoproteome returned 13 candidate glycoproteins with significant differential M-LAC column binding. Qualitative analysis indicated that 62% of selected candidate glycoproteins showed higher levels (upregulation) in M-LAC bound fraction of disease samples. This observation was further confirmed by released N-glycans data in which 53% of identified N-glycans were present at different levels in plasma in the disease vs non-disease samples. This striking result demonstrates the potential for significant protein glycosylation alterations in clear cell renal cell carcinoma cancer plasma. With future validation in a larger cohort, information derived from this study may lead to the development of clear cell renal cell carcinoma candidate biomarkers.
C1 [Gbormittah, Francisca O.; Taylor, KyOnese; Hancock, William S.] Northeastern Univ, Barnett Inst, Boston, MA 02115 USA.
[Gbormittah, Francisca O.; Taylor, KyOnese; Hancock, William S.] Northeastern Univ, Dept Chem & Chem Biol, Boston, MA 02115 USA.
[Lee, Ling Y.] Macquarie Univ, Dept Chem, Sydney, NSW 2109, Australia.
[Lee, Ling Y.] Macquarie Univ, Dept Biomol Sci, Sydney, NSW 2109, Australia.
[Iliopoulos, Othon] Massachusetts Gen Hosp, Ctr Canc, Ctr Canc Res, Charlestown, MA 02129 USA.
[Iliopoulos, Othon] Massachusetts Gen Hosp, Dept Med, Div Hematol Oncol, Boston, MA 02114 USA.
RP Hancock, WS (reprint author), Northeastern Univ, Barnett Inst, 360 Huntington Ave, Boston, MA 02115 USA.
EM wi.hancock@neu.edu; oiliopoulos@partners.org
FU Early Detection Research Network from National Cancer Institute (NCI)
[1U01CA152653-01]
FX This work was supported by the Early Detection Research Network grant
no. 1U01CA152653-01 from the National Cancer Institute (NCI).
NR 56
TC 4
Z9 4
U1 3
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1535-3893
EI 1535-3907
J9 J PROTEOME RES
JI J. Proteome Res.
PD NOV
PY 2014
VL 13
IS 11
BP 4889
EP 4900
DI 10.1021/pr500591e
PG 12
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA AT0PA
UT WOS:000344636500036
PM 25184692
ER
PT J
AU Taneja, AK
Torriani, M
Simeone, FJ
AF Taneja, Atul K.
Torriani, Martin
Simeone, F. Joseph
TI Septic Arthritis and Osteomyelitis of the Hip by Candida albicans
SO JOURNAL OF RHEUMATOLOGY
LA English
DT Editorial Material
ID PATIENT
C1 [Taneja, Atul K.] Hosp Israelita Albert Einstein, Hosp Coracao & Teleimagem, Diagnost Ctr,Div Musculoskeletal Radiol, Div Musculoskeletal Imaging,Imaging Dept, Sao Paulo, Brazil.
[Torriani, Martin; Simeone, F. Joseph] Massachusetts Gen Hosp, Div Musculoskeletal Imaging & Intervent, Boston, MA 02114 USA.
[Torriani, Martin; Simeone, F. Joseph] Harvard Univ, Sch Med, Boston, MA USA.
RP Taneja, AK (reprint author), Hosp Israelita Albert Einstein, Dept Imagem, Av Albert Einstein 627, BR-05652900 Sao Paulo, Brazil.
EM taneja@einstein.br
RI Taneja, Atul/N-3133-2014
OI Taneja, Atul/0000-0002-4655-2033
NR 5
TC 1
Z9 2
U1 0
U2 0
PU J RHEUMATOL PUBL CO
PI TORONTO
PA 365 BLOOR ST E, STE 901, TORONTO, ONTARIO M4W 3L4, CANADA
SN 0315-162X
EI 1499-2752
J9 J RHEUMATOL
JI J. Rheumatol.
PD NOV
PY 2014
VL 41
IS 11
BP 2270
EP 2270
DI 10.3899/jrheum.140354
PG 1
WC Rheumatology
SC Rheumatology
GA AT0AI
UT WOS:000344598900026
PM 25362708
ER
PT J
AU Nabors, LB
Portnow, J
Ammirati, M
Brem, H
Brown, P
Butowski, N
Chamberlain, MC
DeAngelis, LM
Fenstermaker, RA
Friedman, A
Gilbert, MR
Hattangadi-Gluth, J
Hesser, D
Holdhoff, M
Junck, L
Lawson, R
Loeffler, JS
Moots, PL
Mrugala, MM
Newton, HB
Raizer, JJ
Recht, L
Shonka, N
Shrieve, DC
Sills, AK
Swinnen, LJ
Tran, D
Tran, N
Vrionis, FD
Wen, PY
McMillian, NR
Ho, M
AF Nabors, Louis Burt
Portnow, Jana
Ammirati, Mario
Brem, Henry
Brown, Paul
Butowski, Nicholas
Chamberlain, Marc C.
DeAngelis, Lisa M.
Fenstermaker, Robert A.
Friedman, Allan
Gilbert, Mark R.
Hattangadi-Gluth, Jona
Hesser, Deneen
Holdhoff, Matthias
Junck, Larry
Lawson, Ronald
Loeffler, Jay S.
Moots, Paul L.
Mrugala, Maciej M.
Newton, Herbert B.
Raizer, Jeffrey J.
Recht, Lawrence
Shonka, Nicole
Shrieve, Dennis C.
Sills, Allen K., Jr.
Swinnen, Lode J.
David Tran
Nam Tran
Vrionis, Frank D.
Wen, Patrick Yung
McMillian, Nicole R.
Ho, Maria
TI Central Nervous System Cancers, Version 2.2014 Featured Updates to the
NCCN Guidelines
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID WHOLE-BRAIN RADIOTHERAPY; STEREOTACTIC RADIOSURGERY; PROGNOSTIC-FACTORS;
INTRACRANIAL METASTASES; CEREBRAL METASTASES; SURGICAL RESECTION;
RADIATION-THERAPY; BREAST-CANCER; MANAGEMENT; CARCINOMA
AB The NCCN Guidelines for Central Nervous System Cancers provide multidisciplinary recommendations for the clinical management of patients with cancers of the central nervous system. These NCCN Guidelines Insights highlight recent updates regarding the management of metastatic brain tumors using radiation therapy. Use of stereotactic radiosurgery (SRS) is no longer limited to patients with 3 or fewer lesions, because data suggest that total disease burden, rather than number of lesions, is predictive of survival benefits associated with the technique. SRS is increasingly becoming an integral part of management of patients with controlled, low-volume brain metastases.
C1 [Nabors, Louis Burt] Univ Alabama Birmingham, Ctr Comprehens Canc, Birmingham, AL 35203 USA.
[Portnow, Jana] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Ammirati, Mario; Newton, Herbert B.] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Ammirati, Mario; Newton, Herbert B.] Ohio State Univ, Ctr Comprehens Canc, Solove Res Inst, Columbus, OH 43210 USA.
[Brem, Henry; Holdhoff, Matthias; Swinnen, Lode J.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Sidney, BC, Canada.
[Brown, Paul; Gilbert, Mark R.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Butowski, Nicholas] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
[Chamberlain, Marc C.; Mrugala, Maciej M.] Univ Washington, Seattle Canc Care Alliance, Seattle, WA 98195 USA.
[DeAngelis, Lisa M.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[Fenstermaker, Robert A.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Hattangadi-Gluth, Jona] UC San Diego Moores Canc Ctr, La Jolla, CA 92093 USA.
[Hesser, Deneen] Amer Brain Tumor Assoc, Chicago, IL USA.
[Junck, Larry] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Lawson, Ronald] Univ Tennessee, Hlth Sci Ctr, St Jude Childrens Res Hosp, Knoxville, TN 37996 USA.
[Loeffler, Jay S.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Moots, Paul L.; Sills, Allen K., Jr.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Raizer, Jeffrey J.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Recht, Lawrence] Stanford Comprehens Canc Ctr, Stanford, CA 94305 USA.
[Shonka, Nicole] Nebraska Med Ctr, Fred & Pamela Buffett Canc Ctr, Omaha, NE USA.
[Shrieve, Dennis C.] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[David Tran] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO 63110 USA.
[David Tran] Washington Univ, Sch Med, St Louis, MO 63130 USA.
[Nam Tran; Vrionis, Frank D.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Wen, Patrick Yung] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[McMillian, Nicole R.; Ho, Maria] Natl Comprehens Canc Network, Ft Washington, PA USA.
RP Nabors, LB (reprint author), Univ Alabama Birmingham, Ctr Comprehens Canc, Birmingham, AL 35203 USA.
RI Gilbert, Mark/J-7494-2016
OI Gilbert, Mark/0000-0003-2556-9722
FU Eisai, Inc.; Millennium: The Takeda Oncology Company; Teva
Pharmaceuticals; Bayer HealthCare Pharmaceuticals Inc.; Celgene
Corporation; Endo Pharmaceuticals and HealthTronics; Genentech; ARIAD
Pharmaceuticals, Inc.
FX Supported by educational grants from Eisai, Inc.; Millennium: The Takeda
Oncology Company; Teva Pharmaceuticals; Bayer HealthCare Pharmaceuticals
Inc.; Celgene Corporation; Endo Pharmaceuticals and HealthTronics;
Genentech; and ARIAD Pharmaceuticals, Inc.
NR 32
TC 17
Z9 18
U1 0
U2 6
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 2014
VL 12
IS 11
BP 1517
EP 1523
PG 7
WC Oncology
SC Oncology
GA AS8RP
UT WOS:000344516200005
PM 25361798
ER
PT J
AU Denlinger, CS
Ligibel, JA
Are, M
Baker, KS
Demark-Wahnefried, W
Dizon, D
Friedman, DL
Goldman, M
Jones, L
King, A
Ku, GH
Kvale, E
Langbaum, TS
Leonardi-Warren, K
McCabe, MS
Melisko, M
Montoya, JG
Mooney, K
Morgan, MA
Moslehi, JJ
O'Connor, T
Overholser, L
Paskett, ED
Peppercorn, J
Raza, M
Rodriguez, MA
Syrjala, KL
Urba, SG
Wakabayashi, MT
Zee, P
McMillian, NR
Freedman-Cass, DA
AF Denlinger, Crystal S.
Ligibel, Jennifer A.
Are, Madhuri
Baker, K. Scott
Demark-Wahnefried, Wendy
Dizon, Don
Friedman, Debra L.
Goldman, Mindy
Jones, Lee
King, Allison
Ku, Grace H.
Kvale, Elizabeth
Langbaum, Terry S.
Leonardi-Warren, Kristin
McCabe, Mary S.
Melisko, Michelle
Montoya, Jose G.
Mooney, Kathi
Morgan, Mary Ann
Moslehi, Javid J.
O'Connor, Tracey
Overholser, Linda
Paskett, Electra D.
Peppercorn, Jeffrey
Raza, Muhammad
Rodriguez, M. Alma
Syrjala, Karen L.
Urba, Susan G.
Wakabayashi, Mark T.
Zee, Phyllis
McMillian, Nicole R.
Freedman-Cass, Deborah A.
TI Survivorship: Screening for Cancer and Treatment Effects, Version 2.2014
Clinical Practice Guidelines in Oncology
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Review
ID QUALITY-OF-LIFE; SF
AB The NCCN Guidelines for Survivorship provide screening, evaluation, and treatment recommendations for common physical and psychosocia I consequences of cancer and cancer treatment. This portion of the guidelines describes recommendations regarding screening for the effects of cancer and its treatment. The panel created a sample screening tool, specifically for use in combination with the NCCN Guidelines for Survivorship, to guide providers to topics that require more in-depth assessment. Effective screening and assessment can help providers deliver necessary and comprehensive survivorship care.
C1 [Denlinger, Crystal S.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Ligibel, Jennifer A.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA 02215 USA.
[Are, Madhuri] Nebraska Med Ctr, Fred & Pamela Buffett Canc Ctr, Omaha, NE USA.
[Baker, K. Scott; Syrjala, Karen L.] Fred Hutchinson Canc Res Ctr, Seattle Canc Care Alliance, Seattle, WA USA.
[Demark-Wahnefried, Wendy; Kvale, Elizabeth] Univ Alabama Birmingham, Ctr Comprehens Canc, Birmingham, AL USA.
[Dizon, Don] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Friedman, Debra L.; Moslehi, Javid J.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Goldman, Mindy; Melisko, Michelle] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
[Jones, Lee; McCabe, Mary S.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[King, Allison] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO USA.
[King, Allison] Washington Univ, Sch Med, St Louis, MO 63130 USA.
[Ku, Grace H.] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA USA.
[Langbaum, Terry S.] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Sidney, BC, Canada.
[Leonardi-Warren, Kristin; Overholser, Linda] Univ Colorado, Ctr Canc, Boulder, CO 80309 USA.
[Montoya, Jose G.] Stanford Canc Inst, Stanford, CA USA.
[Mooney, Kathi] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[Morgan, Mary Ann] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[O'Connor, Tracey] Roswell Pk Canc Inst, Buffalo, NY USA.
[Paskett, Electra D.] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Paskett, Electra D.] Ohio State Univ, Ctr Comprehens Canc, Solove Res Inst, Columbus, OH 43210 USA.
[Peppercorn, Jeffrey] Duke Canc Inst, Durham, NC USA.
[Raza, Muhammad] Univ Tennessee, Hlth Sci Ctr, St Jude Childrens Res Hosp, Knoxville, TN 37996 USA.
[Rodriguez, M. Alma] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
[Urba, Susan G.] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Wakabayashi, Mark T.] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Zee, Phyllis] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
RP Denlinger, CS (reprint author), Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
FU National Cancer Institute; American Cancer Society; Harvest for Health
Gardening Project for Breast Cancer Survivors; Nutrigenomic Link between
Alpha-Linolenic Acid and Aggressive Prostate Cancer; Bayer HealthCare;
Genentech, Inc.; ImClone Systems Incorporated; MedImmune Inc.; OncoMed
Pharmaceuticals; Astex Pharmaceuticals; Merrimack Pharmaceuticals;
Pfizer Inc.; Celldex Therapeutics; Galena Biopharma; University of Utah;
Millennium Pharmaceuticals, Inc.; Accleron, Inc.; Merck Co., Inc.; Amgen
Inc.; Ortho Biotech Products, L.P.; Philips/Respironics
FX Wendy Demark-Wahnefried, PhD, RD National Cancer Institute; American
Cancer Society; Harvest for Health Gardening Project for Breast Cancer
Survivors; and Nutrigenomic Link between Alpha-Linolenic Acid and
Aggressive Prostate Cancer; Crystal S. Denlinger, MD Bayer HealthCare;
Genentech, Inc.; ImClone Systems Incorporated; MedImmune Inc.; OncoMed
Pharmaceuticals; Astex Pharmaceuticals; Merrimack Pharmaceuticals; and
Pfizer Inc.; Michelle Melisko, MD Genentech, Inc.; Celldex Therapeutics;
and Galena Biopharma; Kathi Mooney, RN, PhD University of Utah; Javid J.
Moslehi, MD Millennium Pharmaceuticals, Inc.; and Accleron, Inc.;
Electra D. Paskett, PhD Merck & Co., Inc.; M. Alma Rodriguez, MD Amgen
Inc.; and Ortho Biotech Products, L.P.; Phyllis Zee, MD
Philips/Respironics
NR 6
TC 2
Z9 2
U1 0
U2 3
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 2014
VL 12
IS 11
BP 1526
EP 1530
PG 5
WC Oncology
SC Oncology
GA AS8RP
UT WOS:000344516200006
PM 25361799
ER
PT J
AU O'Brien, S
Radich, JP
Abboud, CN
Akhtari, M
Altman, JK
Berman, E
Curtin, P
DeAngelo, DJ
Deininger, M
Devine, S
Fathi, AT
Gotlib, J
Jagasia, M
Kropf, P
Moore, JO
Pallera, A
Reddy, VVB
Shah, NP
Smith, BD
Snyder, DS
Wetzler, M
Gregory, K
Sundar, H
AF O'Brien, Susan
Radich, Jerald P.
Abboud, Camille N.
Akhtari, Mojtaba
Altman, Jessica K.
Berman, Ellin
Curtin, Peter
DeAngelo, Daniel J.
Deininger, Michael
Devine, Steven
Fathi, Amir T.
Gotlib, Jason
Jagasia, Madan
Kropf, Patricia
Moore, Joseph O.
Pallera, Arnel
Reddy, Vishnu V. B.
Shah, Neil P.
Smith, B. Douglas
Snyder, David S.
Wetzler, Meir
Gregory, Kristina
Sundar, Hema
TI Chronic Myelogenous Leukemia, Version 1.2015 Clinical Practice
Guidelines in Oncology
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Review
ID CHRONIC MYELOID-LEUKEMIA; STEM-CELL TRANSPLANTATION; DONOR LYMPHOCYTE
INFUSIONS; TYROSINE KINASE INHIBITORS; BONE-MARROW-TRANSPLANTATION;
POLYMERASE-CHAIN-REACTION; TERM-FOLLOW-UP; PULMONARY
ARTERIAL-HYPERTENSION; ACUTE LYMPHOBLASTIC-LEUKEMIA; CHROMOSOME-POSITIVE
LEUKEMIA
AB Chronic myelogenous leukemia (CML) is usually diagnosed in the chronic phase. Untreated chronic phase CML will eventually progress to advanced phase (accelerated or blast phase) CML. Tyrosine kinase inhibitors (TKIs) have been shown to induce favorable response rates in patients with accelerated and blast phase CML. The addition of TKIs to chemotherapy has also been associated with improved outcomes in patients with blast phase CML. Allogeneic hematopoietic stem cell transplant remains a potentially curative option for patients with advanced phase CML, although treatment with a course of TKIs will be beneficial as a bridge to transplant. This manuscript discusses the recommendations outlined in the NCCN Guidelines for the diagnosis and management of patients with advanced phase CML.
C1 [O'Brien, Susan] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Radich, Jerald P.] Fred Hutchinson Canc Res Ctr, Seattle Canc Care Alliance, Seattle, WA USA.
[Abboud, Camille N.] Barnes Jewish Hosp, Siteman Canc Ctr, St Louis, MO USA.
[Abboud, Camille N.] Univ Washington, Sch Med, Seattle, WA USA.
[Akhtari, Mojtaba] Nebraska Med Ctr, Fred & Pamela Buffett Canc Ctr, Omaha, NE USA.
[Altman, Jessica K.] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Berman, Ellin] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[Curtin, Peter] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA USA.
[DeAngelo, Daniel J.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Deininger, Michael] Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA.
[Devine, Steven] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
[Devine, Steven] Solove Res Inst, Columbus, OH USA.
[Fathi, Amir T.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
[Gotlib, Jason] Stanford Canc Inst, Stanford, CA 94305 USA.
[Jagasia, Madan] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Kropf, Patricia] Fox Chase Canc Ctr, Philadelphia, PA USA.
[Moore, Joseph O.] Duke Canc Inst, Durham, NC USA.
[Pallera, Arnel] Univ Tennessee, Hlth Sci Ctr, St Jude Childrens Res Hosp, Knoxville, TN 37996 USA.
[Reddy, Vishnu V. B.] Univ Alabama, Ctr Comprehens Canc, Tuscaloosa, AL 35487 USA.
[Shah, Neil P.] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
[Smith, B. Douglas] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Sidney, BC, Canada.
[Snyder, David S.] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Wetzler, Meir] Roswell Pk Canc Inst, Buffalo, NY USA.
RP O'Brien, S (reprint author), Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
OI Reddy, Vishnu/0000-0001-5474-3289
FU Eli Lilly and Company; Merck Co., Inc.; Novartis Pharmaceuticals
Corporation; Teva; ARIAD Pharmaceuticals, Inc.; Boehringer Ingelheim
GmbH; Bristol-Myers Squibb Company; Millennium Pharmaceuticals, Inc.;
Agios; Ambit; Astellas; Cyclacel; Epizyme; Lilly Pharmaceuticals; Talon;
Pfizer Inc.; Ariad Pharmaceuticals; Onconova; Celgene Corporation;
Gilead; Genzyme Corporation; Genentech, Inc.; Infinity; Morphosys;
CSL-Behring; NCI; MedPace; OSU; Prime Oncology
FX Camille N. Abboud, MD Eli Lilly and Company; Merck & Co., Inc.; Novartis
Pharmaceuticals Corporation; and Teva; Jessica K. Altman, MD ARIAD
Pharmaceuticals, Inc.; Boehringer Ingelheim GmbH; Bristol-Myers Squibb
Company; Millennium Pharmaceuticals, Inc.; Agios; Ambit; Astellas;
Cyclacel; Epizyme; Lilly Pharmaceuticals; Talon; and Pfizer Inc.; Ellin
Berman, MD ARIAD Pharmaceuticals, Inc.; Novartis Pharmaceuticals
Corporation; and Ariad Pharmaceuticals; Peter Curtin, MD Onconova;
Michael Deininger, MD, PhD ARIAD Pharmaceuticals, Inc.; Bristol-Myers
Squibb Company; Celgene Corporation; Novartis Pharmaceuticals
Corporation; and Gilead; Steven Devine, MD Genzyme Corporation; Joseph
O. Moore, MD ARIAD Pharmaceuticals, Inc.; Genentech, Inc.; and Novartis
Pharmaceuticals Corporation; Susan O'Brien, MD Ariad; Infinity; and
Morphosys; Jerald P. Radich, MD Novartis Pharmaceuticals Corporation;
Neil P. Shah, MD, PhD ARIAD Pharmaceuticals, Inc.; and Bristol-Myers
Squibb Company; B. Douglas Smith, MD Bristol-Myers Squibb Company; Merck
& Co., Inc.; CSL-Behring; and Pfizer Inc.; David S. Snyder, MD
Bristol-Myers Squibb Company; and Novartis Pharmaceuticals Corporation;
Meir Wetzler, MD Bristol-Myers Squibb Company; NCI; Cyclacel; MedPace;
OSU; and Prime Oncology
NR 158
TC 16
Z9 17
U1 1
U2 7
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 2014
VL 12
IS 11
BP 1590
EP 1609
PG 20
WC Oncology
SC Oncology
GA AS8RP
UT WOS:000344516200013
PM 25361806
ER
PT J
AU Venook, AP
Arcila, ME
Benson, AB
Berry, DA
Camidge, DR
Carlson, RW
Choueiri, TK
Guild, V
Kalemkerian, GP
Kurzrock, R
Lovly, CM
McKee, AE
Morgan, RJ
Olszanski, AJ
Redman, MW
Stearns, V
McClure, J
Birkeland, ML
AF Venook, Alan P.
Arcila, Maria E.
Benson, Al B., III
Berry, Donald A.
Camidge, David Ross
Carlson, Robert W.
Choueiri, Toni K.
Guild, Valerie
Kalemkerian, Gregory P.
Kurzrock, Razelle
Lovly, Christine M.
McKee, Amy E.
Morgan, Robert J.
Olszanski, Anthony J.
Redman, Mary W.
Stearns, Vered
McClure, Joan
Birkeland, Marian L.
TI NCCN Working Group Report: Designing Clinical Trials in the Era of
Multiple Biomarkers and Targeted Therapies
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID CELL LUNG-CANCER; HER2-POSITIVE BREAST-CANCER; FACTOR RECEPTOR
MUTATIONS; DOSE-ESCALATION TRIAL; PHASE-II TRIAL; C-KIT PROTEIN;
COLORECTAL-CANCER; OVARIAN-CANCER; MONOCLONAL-ANTIBODY; SOLID TUMORS
AB Defining treatment-susceptible or -resistant populations of patients with cancer through the use of genetically defined biomarkers has revolutionized cancer care in recent years for some disease/patient groups. Research continues to show that histologically defined diseases are diverse in their expression of unique mutations or other genetic alterations, however, which presents opportunities for the development of personalized cancer treatments, but increased difficulty in testing these therapies, because potential patient populations are divided into ever smaller numbers. To address some of the growing challenges in biomarker development and clinical trial design, NCCN assembled a group of experts across specialties and solid tumor disease types to begin to define the problems and to consider alternate ways of designing clinical trials in the era of multiple biomarkers and targeted therapies. Results from that discussion are presented, focusing on issues of clinical trial design from the perspective of statisticians, clinical researchers, regulators, pathologists, and information developers.
C1 [Venook, Alan P.] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
[Arcila, Maria E.] Mem Sloan Kettering Canc Ctr, New York, NY USA.
[Benson, Al B., III] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Evanston, IL 60208 USA.
[Berry, Donald A.] Univ Texas MD Anderson Canc Ctr, Houston, TX USA.
[Camidge, David Ross] Univ Colorado, Ctr Canc, Boulder, CO 80309 USA.
[Carlson, Robert W.] Stanford Canc Inst, Fox Chase Canc Ctr, Natl Comprehens Canc Network, Stanford, CA USA.
[Choueiri, Toni K.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Guild, Valerie] Aim Melanoma Fdn, Richmond, CA USA.
[Kalemkerian, Gregory P.] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Kurzrock, Razelle] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
[Lovly, Christine M.] Vanderbilt Ingram Canc Ctr, Nashville, TN 37232 USA.
[Morgan, Robert J.] City Hope Comprehens Canc Ctr, Duarte, CA USA.
[Olszanski, Anthony J.] Fox Chase Canc Ctr, Philadelphia, PA USA.
[Redman, Mary W.] Fred Hutchinson Canc Res Center, Seattle Canc Care Alliance, Seattle, WA USA.
[Stearns, Vered] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Sidney, BC, Canada.
RP Venook, AP (reprint author), Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
FU Boehringer Ingelheim Pharmaceuticals, Inc.; Celgene Corporation;
Dendreon; Helsinn; Novartis Oncology; Xcenda, an AmerisourceBergen
Consulting Services company; Astellas Pharma US, Inc.; Biodesix; Gilead
Sciences, Inc.; Incyte Corporation; Janssen; Medivation Inc.;
Millennium: The Takeda Oncology Company; TEVA Oncology; Onyx
Pharmaceuticals, Inc.; Abbott Molecular and ImmunoGen, Inc.
FX This NCCN Working Group Report was sponsored by Boehringer Ingelheim
Pharmaceuticals, Inc.; Celgene Corporation; Dendreon; Helsinn; Novartis
Oncology; and Xcenda, an AmerisourceBergen Consulting Services company.
It was also supported by Astellas Pharma US, Inc.; Biodesix; Gilead
Sciences, Inc.; Incyte Corporation; Janssen; Medivation Inc.;
Millennium: The Takeda Oncology Company; TEVA Oncology; and Onyx
Pharmaceuticals, Inc., an Amgen subsidiary; by grants from Abbott
Molecular and ImmunoGen, Inc.; and by an educational donation provided
by Amgen.
NR 118
TC 5
Z9 5
U1 1
U2 6
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 2014
VL 12
IS 11
BP 1629
EP 1649
PG 21
WC Oncology
SC Oncology
GA AS8RP
UT WOS:000344516200015
PM 25361808
ER
PT J
AU Ahmed, M
Solbiati, L
Brace, CL
Breen, DJ
Callstrom, MR
Charboneau, JW
Chen, MH
Choi, BI
de Baere, T
Dodd, GD
Gervais, DA
Gianfelice, D
Gillams, AR
Lee, FT
Leen, E
Lencioni, R
Littrup, PJ
Livraghi, T
Lu, DS
McGahan, JP
Meloni, MF
Nikolic, B
Pereira, PL
Liang, P
Rhim, H
Rose, SC
Salem, R
Sofocleous, CT
Solomon, SB
Soulen, MC
Tanaka, M
Vogl, TJ
Wood, BJ
Goldberg, SN
AF Ahmed, Muneeb
Solbiati, Luigi
Brace, Christopher L.
Breen, David J.
Callstrom, Matthew R.
Charboneau, J. William
Chen, Min-Hua
Choi, Byung Ihn
de Baere, Thierry
Dodd, Gerald D., III
Gervais, Debra A.
Gianfelice, David
Gillams, Alice R.
Lee, Fred T., Jr.
Leen, Edward
Lencioni, Riccardo
Littrup, Peter J.
Livraghi, Tito
Lu, David S.
McGahan, John P.
Meloni, Maria Franca
Nikolic, Boris
Pereira, Philippe L.
Liang, Ping
Rhim, Hyunchul
Rose, Steven C.
Salem, Riad
Sofocleous, Constantinos T.
Solomon, Stephen B.
Soulen, Michael C.
Tanaka, Masatoshi
Vogl, Thomas J.
Wood, Bradford J.
Goldberg, S. Nahum
CA Int Working Grp Image-Guided Tumor
TI Image-Guided Tumor Ablation: Standardization of Terminology and
Reporting Criteria-A 10-Year Update
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
ID PERCUTANEOUS RADIOFREQUENCY ABLATION; RENAL-CELL CARCINOMA; VIVO PORCINE
LIVER; TRANSCATHETER ARTERIAL CHEMOEMBOLIZATION; IRREVERSIBLE
ELECTROPORATION ABLATION; CONTRAST-ENHANCED ULTRASOUND; INTERNALLY
COOLED ELECTRODES; LONG-TERM SURVIVAL; QUALITY-OF-LIFE;
HEPATOCELLULAR-CARCINOMA
AB Image-guided tumor ablation has become a well-established hallmark of local cancer therapy. The breadth of options available in this growing field increases the need for standardization of terminology and reporting criteria to facilitate effective communication of ideas and appropriate comparison among treatments that use different technologies, such as chemical (eg, ethanol or acetic acid) ablation, thermal therapies (eg, radiofrequency, laser, microwave, focused ultrasound, and cryoablation) and newer ablative modalities such as irreversible electroporation. This updated consensus document provides a framework that will facilitate the clearest communication among investigators regarding ablative technologies. An appropriate vehicle is proposed for reporting the various aspects of image-guided ablation therapy including classification of therapies, procedure terms, descriptors of imaging guidance, and terminology for imaging and pathologic findings. Methods are addressed for standardizing reporting of technique, follow-up, complications, and clinical results. As noted in the original document from 2003, adherence to the recommendations will improve the precision of communications in this field, leading to more accurate comparison of technologies and results, and ultimately to improved patient outcomes.
C1 [Ahmed, Muneeb] Beth Israel Deaconess Med Ctr, Dept Radiol, Boston, MA 02215 USA.
[Solbiati, Luigi] Osped Generale, Dept Radiol, Busto Arsizio, Italy.
[Brace, Christopher L.] Univ Wisconsin, Dept Radiol, Sch Med & Publ Hlth, Madison, WI 53706 USA.
[Brace, Christopher L.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Biomed Engn, Madison, WI USA.
[Brace, Christopher L.] Univ Wisconsin, Dept Med Phys, Sch Med & Publ Hlth, Madison, WI 53706 USA.
[Breen, David J.] Southampton Univ Hosp, Dept Radiol, Southampton, Hants, England.
[Callstrom, Matthew R.; Charboneau, J. William] Mayo Clin, Dept Radiol, Rochester, MN USA.
[Chen, Min-Hua] Peking Univ, Sch Oncol, Dept Ultrasound, Beijing 100871, Peoples R China.
[Choi, Byung Ihn] Seoul Natl Univ Hosp, Dept Radiol, Seoul 110744, South Korea.
[de Baere, Thierry] Inst Cancerol Gustave Roussy, Dept Imaging, Villejuif, France.
[Dodd, Gerald D., III] Univ Colorado Anschutz Med Campus, Sch Med, Dept Radiol, Aurora, CO USA.
Rhode Isl Hosp, Dept Diagnost Fladiol, Providence, RI USA.
[Gervais, Debra A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA USA.
[Gianfelice, David] Univ Hlth Network, Laval, PQ, Canada.
[Gillams, Alice R.] London Clin, Dept Imaging, London, England.
[Lee, Fred T., Jr.] Univ Wisconsin Hosp & Clin, Dept Radiol, Madison, WI 53792 USA.
[Leen, Edward] Royal Infirm, Dept Radiol, Glasgow G31 2ER, Lanark, Scotland.
[Lencioni, Riccardo] Univ Pisa, Pisa Univ Hosp, Cisanello Hosp, Dept Diagnost Imaging & Intervent, Pisa, Italy.
[Lencioni, Riccardo] Univ Pisa, Sch Med, I-56100 Pisa, Italy.
[Littrup, Peter J.] Wayne State Univ, Karmonos Canc Inst, Dept Radiol, Detroit, MI USA.
[Lu, David S.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Radiol, Los Angeles, CA 90095 USA.
[McGahan, John P.] Univ Calif Davis, Med Ctr, Ctr Ambulatory Care, Dept Radiol, Sacramento, CA 95817 USA.
[Meloni, Maria Franca] Osped Valduce, Dept Radiol, Como, Italy.
[Nikolic, Boris] Albert Einstein Med Ctr, Dept Radiol, Philadelphia, PA 19141 USA.
[Pereira, Philippe L.] Heidelberg Univ, Acad Hosp, Clin Radiol Minimally Invas Therapies & Nucl Med, Heilbronn, Germany.
[Liang, Ping] Chinese Peoples Liberat Army Gen Hosp, Dept Intervent Ultrasound, Beijing, Peoples R China.
[Rhim, Hyunchul] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Diagnost Radiol, Seoul, South Korea.
[Rose, Steven C.] Univ Calif San Diego, Dept Radiol, San Diego, CA 92103 USA.
[Salem, Riad] Northwestern Univ, Dept Radiol, Chicago, IL USA.
[Sofocleous, Constantinos T.; Solomon, Stephen B.] Mem Sloan Kettering Canc Ctr, Dept Radiol, New York, NY 10021 USA.
[Soulen, Michael C.] Hosp Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
[Tanaka, Masatoshi] Yokokura Hosp, Dept Hepatol, Miyama, Japan.
[Vogl, Thomas J.] Goethe Univ Frankfurt, Univ Hosp Frankfurt, Inst Diagnost & Intervent Radiol, D-60054 Frankfurt, Germany.
[Wood, Bradford J.] NIH, Bethesda, MD 20892 USA.
[Goldberg, S. Nahum] Hadassah Hebrew Univ, Med Ctr, Dept Radiol ImageGuided Therapy, Jerusalem, Israel.
[Goldberg, S. Nahum] Hadassah Hebrew Univ, Med Ctr, Intervent Oncol Unit, Jerusalem, Israel.
RP Ahmed, M (reprint author), Beth Israel Deaconess Med Ctr, Dept Radiol, 1 Deaconess Rd,WCC-308B, Boston, MA 02215 USA.
EM mahmed@bidmc.harvard.edu
OI Dupuy, Damian/0000-0003-0524-5982
FU NeuWave Medical; University of Wisconsin; Galil Medical; Siemens
Medical; GE Medical; Thermedical; Samsung Electronics; Terumo;
HS-Medical; Boston-Scientific; BSD Medical; Covidien;
Covidien/Valleylab; Endocare; Ethicon Endo-Surgery; Philips; Celon
Olympus; Siemens Medical Solutions; GE Healthcare; AngioDyamics; Guerbet
LLC; BTG; Merit Medical; Sirtex; Cooperative Research and Development
Agreement (CRADA) Philips Healthcare; CRADA Biocompatibles BTG; CRADA
Perfint; CRADA Celsion; CRADA Invivo; AngioDynamics; Cosman Medical
FX M.A. No relevant conflicts of interest to disclose. L.S. No relevant
conflicts of interest to disclose. C.L.B. Financial activities related
to the present article: none to disclose. Financial activities not
related to the present article: received consultancy fees from NeuWave
Medical, author and institution received payment for patents (planned,
pending, or issued) from University of Wisconsin and NeuWave Medical,
received payment for stock/stock options from NeuWave Medical Other
relationships: none to disclose. D.J.B. Financial activities related to
the present article: paid for occasional proctoring by Galli Medical.
Financial activities not related to the present article: none to
disclose. Other relationships: none to disclose. M.R.C. Financial
activities related to the present article: none to disclose. Financial
activities not related to the present article. received grants from
Galil Medical, Siemens Medical, GE Medical, Thermedical. Other
relationships: none to disclose. J.W.C. No relevant conflicts of
interest to disclose. M.H.C. No relevant conflicts of interest to
disclose. B.I.C. Financial activities related to the present article:
none to disclose. Financial activities not related to the present
article: institution received a research grant from Samsung Electronics.
Other relationships: none to disclose. T.d.B. Financial activities
related to the present article: none to disclose. Financial activities
not related to the present article: received personal fees from Terumo,
a grant from HS-Medical, and payment for travel to a meeting from
Boston-Scientific. Other relationships: none to disclose. G.D.D. No
relevant conflicts of interest to disclose. D.E.D. Financial activities
related to the present article. none to disclose. Financial activities
not related to the present article: paid for board membership by BSD
Medical, received consultancy fees from BSD Medical and Covidien,
received grants or has grants pending from NeuWave Medical, received
payment for lectures including service on speakers bureaus from BSD
Medical, was paid royalties by Springer Verlag and UpToDate, received
stock or stock options from BSD Medical. Other relationships: none to
disclose. D.A.G. Financial activities related to the present article:
none to disclose. Financial activities not related to the present
article. received a research grant from Covidien/Valleylab. Other
relationships: none to disclose. D.G. No relevant conflicts of interest
to disclose. A.R.G. Financial activities related to the present article:
received consulting fee or honorarium from Covidien, received fees for
participatient in review activities such as data monitoring boards,
statistical analysis, end point committees, and the like from Covidien
Financial activities not related to the present article: was paid for
board membership, consultancy, and lectures including service on
speakers bureaus by Covidien Other relationships: none to disclose.
F.T.L. Financial activities related to the present article: received
payment from NeuWave Medical. Financial activities not related to the
present article: received royalties from Covidien, is a stockholder and
on the Board of Directors for NeuWave Medical, has a patent on the
Switching Controller with royalties paid from Covidien, has multiple
patents on heat-based thermal therapies for microwave ablation systems
licensed to NeuWave Medical. Other relationships: none to disclose. E.L.
No relevant conflicts of interest to disclose. R.L. No relevant
conflicts of interest to disclose. P.J.L.; No relevant conflicts of
interest to disclose T.L. No relevant conflicts of interest to disclose.
D.S.L. Financial activities related to the present article. none to
disclose. Financial activities not related to the present article:
institution received grants or has grants pending from Endocare and
Ethicon Endo-Surgery, received payment for lectures including service on
speakers bureaus from Philips. Other relationships: none to disclose.
J.P.M. No relevant conflicts of interest to disclose. M.F.M. No relevant
conflicts of interest to disclose. B.N. No relevant conflicts of
interest to disclose. P.L.P. Financial activities related to the present
article: none to disclose. Financial activities not related to the
present article: received a grant from Celon Olympus; fees for
conferences from Siemens Medical Solutions; consultant's honoraries from
Terumo Europe, Terumo Germany, and Microsulis; materials from
AngioDynamics. Other relationships: none to disclose. P.L. No relevant
conflicts of interest to disclose. H.R. No relevant conflicts of
interest to disclose. S.C.R. No relevant conflicts of interest to
disclose. R.S. No relevant conflicts of interest to disclose. C.T.S. No
relevant conflicts of interest to disclose. S.B.S. Financial activities
related to the present article: institution received a grant from GE
Healthcare, author received consulting fee or honorarium from
AngioDyamics, Covidien, and GE Healthcare. Financial activities not
related to the present article: none to disclose. Other relationships:
none to disclose. M.C.S. Financial activities related to the present
article: none to disclose. Financial activities not related to the
present article: author received consultancy fees from Guerbet LLC, BTG,
Merit Medical; institution received grants or has grants pending from
Guerbet LLC and BTG; author received payment for lectures including
service on speakers bureaus from Sirtex; author received royalties from
Cambridge University Press. Other relationships: none to disclose. M.T.
No relevant conflicts of interest to disclose. T.J.V. No relevant
conflicts of interest to disclose. B.J.W. Financial activities related
to the present article: none to disclose. Financial activities not
related to the present article: institution received grants or has
grants pending from Cooperative Research and Development Agreement
(CRADA) Philips Healthcare, CRADA Biocompatibles BTG, CRADA Perfint,
CRADA Celsion, CRADA Invivo; the National Institutes of Health has
intellectual property in the field. Other relationships: none to
disclose. S.N.G. Financial activities related to the present article.
institution received a grant for sponsored research from AngioDynamics;
author received consulting fee or honorarium from AngioDynamics.
Financial activities not related to the present article: author received
consultancy fees from Cosman Medical and institution received grants or
has grants pending from Cosman Medical. Other relationships: none to
disclose.
NR 99
TC 58
Z9 58
U1 5
U2 28
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
EI 1535-7732
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD NOV
PY 2014
VL 25
IS 11
BP 1691
EP 1705
DI 10.1016/j.jvir.2014.08.027
PG 15
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA AT1UZ
UT WOS:000344720500005
PM 25442132
ER
PT J
AU Conrad, MF
Michalczyk, MJ
Opalacz, A
Patel, VI
LaMuraglia, GM
Cambria, RP
AF Conrad, Mark F.
Michalczyk, Michael J.
Opalacz, Arissa
Patel, Virendra I.
LaMuraglia, Glenn M.
Cambria, Richard P.
TI The natural history of asymptomatic severe carotid artery stenosis
SO JOURNAL OF VASCULAR SURGERY
LA English
DT Article
ID JUXTALUMINAL HYPOECHOIC AREA; VASCULAR-SURGERY; INTRAPLAQUE HEMORRHAGE;
HEART-ASSOCIATION; ULTRASOUND IMAGES; PLAQUES PREDICTS; ISCHEMIC EVENTS;
STROKE RISK; PROGRESSION; ENDARTERECTOMY
AB Background: Although level 1 evidence supports carotid endarterectomy (CEA) for stroke prevention in patients with asymptomatic severe carotid artery stenosis (ASCAS; >70%), medical therapy alone has been promulgated by some as equally effective. The goal of this study was to determine the natural history of medically treated patients with ASCAS.
Methods: Patients with ASCAS from 2005 to 2006 were identified in a health network database. Patients were included if the initial therapeutic plan involved medical therapy alone (usually because of comorbidities or patient preference). Study end points included: ipsilateral neurologic symptoms (INS) of transient ischemic attack and/or stroke, death, and INS and/or death.
Results: There were 126 carotid arteries identified in 115 patients. Using standard duplex velocity criteria, 88 (70%) had severe (70%-89%) and 38 (30%) had very severe stenoses (VSS; 90%-99%). The average age was 73.5 years, demographic characteristics included: 66% hypertension, 64% coronary artery disease, 30% diabetes, 5% chronic kidney disease (CKD), and 86% were taking a statin drug (28% had a low-density lipoprotein level <100 mg/dL). There were 31 patients (24.6%) who developed INS during a mean follow-up of 27 months; most (23 of 31; 74%) occurred within 12 months of the initial duplex ultrasound examination; 14 (45%) were strokes. The 5-year actuarial freedom from INS was 70.1 +/- 5%. Multivariate predictors of INS included: VSS (hazard ratio [HR], 3.23; 95% confidence interval [CI], 1.56-6.76; P = .002), CKD (HR, 6.25; 95% CI, 2.05-19.2; P = . 001), and age (HR, 0.94; 95% CI, 0.91-0.98; P = . 001). There were 41 patients (33%) who underwent eventual carotid revascularization (32 CEA, nine stent); 23 of 41 (56%) were performed for INS and 18 (44%) for plaque progression. Overall 5-year actuarial survival was 69.8% +/- 4.1%. Multivariate predictors of death included: age (HR, 1.06; 95% CI, 1.03-1.1; P = .0001), chronic obstructive pulmonary disease (HR, 1.92; 95% CI, 1.08-3.41; P = . 03), and diabetes (HR, 5.08; 95% CI, 2.86-9.01; P < .0001). The 5-year actuarial freedom from INS and/or death was 54 +/- 4.4%. Multivariate predictors of INS and/or death were: VSS (HR, 1.98; 95% CI, 1.22-3.23; P = .006), CKD (HR, 5.46; 95% CI, 2.12-14.08; P = .0004), and diabetes (HR, 2.6; 95% CI, 1.59-4.24; P = .0001). Statin use was not protective against INS or death in this cohort.
Conclusions: Medically managed patients with ASCAS develop INS early, especially in patients with VSS. Medical therapy with aspirin and statins failed to control ASCAS, thus validating the role of CEA in these patients as promulgated in multiple current treatment guidelines.
C1 [Conrad, Mark F.] Massachusetts Gen Hosp, Dept Surg, Div Vasc & Endovasc Surg, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Conrad, MF (reprint author), Massachusetts Gen Hosp, Dept Surg, Div Vasc & Endovasc Surg, 15 Parkman St,WAC 440, Boston, MA 02114 USA.
EM mconrad@partners.org
NR 43
TC 14
Z9 14
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-5214
J9 J VASC SURG
JI J. Vasc. Surg.
PD NOV
PY 2014
VL 60
IS 5
BP 1218
EP 1225
DI 10.1016/j.jvs.2014.05.047
PG 8
WC Surgery; Peripheral Vascular Disease
SC Surgery; Cardiovascular System & Cardiology
GA AS8TO
UT WOS:000344521100016
PM 25041986
ER
PT J
AU Quick, ED
Leser, JS
Clarke, P
Tyler, KL
AF Quick, Eamon D.
Leser, J. Smith
Clarke, Penny
Tyler, Kenneth L.
TI Activation of Intrinsic Immune Responses and Microglial Phagocytosis in
an Ex Vivo Spinal Cord Slice Culture Model of West Nile Virus Infection
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID CENTRAL-NERVOUS-SYSTEM; CD8(+) T-CELLS; JAPANESE ENCEPHALITIS; IN-VITRO;
BRAIN; NEURONS; MINOCYCLINE; INNATE; PATHOGENESIS; REPLICATION
AB West Nile virus (WNV) is a neurotropic flavivirus that causes significant neuroinvasive disease involving the brain and/or spinal cord. Experimental mouse models of WNV infection have established the importance of innate and adaptive immune responses in controlling the extent and severity of central nervous system (CNS) disease. However, differentiating between immune responses that are intrinsic to the CNS and those that are dependent on infiltrating inflammatory cells has proven difficult. We used a murine ex vivo spinal cord slice culture (SCSC) model to determine the innate immune processes specific to the CNS during WNV infections. By 7 days after ex vivo infection of SCSCs, the majority of neurons and a substantial percentage of astrocytes were infected with WNV, resulting in apoptotic cell death and astrogliosis. Microglia, the resident immune cells of the CNS, were activated by WNV infection, as exemplified by their amoeboid morphology, the development of filopodia and lamellipodia, and phagocytosis of WNV-infected cells and debris. Microglial cell activation was concomitant with increased expression of pro-inflammatory cytokines and chemokines, including CXCL10, CXCL1, CCL5, CCL3, CCL2, tumor necrosis factor alpha (TNF-alpha), TNF-related apoptosis-inducing ligand (TRAIL), and interleukin-6 (IL-6). The application of minocycline, an inhibitor of neuro-inflammation, altered the WNV-induced proinflammatory cytokine/chemokine expression profile, with inhibited production of CCL5, CCL2, and IL-6. Our findings establish that CNS-resident cells have the capacity to initiate a robust innate immune response against WNV infection in the absence of infiltrating inflammatory cells and systemic immune responses.
IMPORTANCE
There are no specific treatments of proven efficacy available for WNV neuroinvasive disease. A better understanding of the pathogenesis of WNV CNS infection is crucial for the rational development of novel therapies. Development of a spinal cord slice culture (SCSC) model facilitates the study of WNV pathogenesis and allows investigation of the intrinsic immune responses of the CNS. Our studies demonstrate that robust CNS innate immune responses, including microglial activation and proinflammatory cytokine/chemokine production, develop independently of contributions from the peripheral immune system and CNS-infiltrating inflammatory cells.
C1 [Quick, Eamon D.; Tyler, Kenneth L.] Univ Colorado Denver, Neurosci Program, Aurora, CO USA.
[Leser, J. Smith; Clarke, Penny; Tyler, Kenneth L.] Univ Colorado Denver, Dept Neurol, Aurora, CO 80045 USA.
[Tyler, Kenneth L.] Univ Colorado Denver, Dept Immunol & Microbiol, Aurora, CO USA.
[Tyler, Kenneth L.] Univ Colorado Denver, Dept Infect Dis, Aurora, CO USA.
[Tyler, Kenneth L.] Univ Colorado Denver, Dept Med, Aurora, CO USA.
[Tyler, Kenneth L.] Denver VA Med Ctr, Denver, CO USA.
RP Clarke, P (reprint author), Univ Colorado Denver, Dept Neurol, Aurora, CO 80045 USA.
EM Penny.Clarke@ucdenver.edu
OI Tyler, Kenneth/0000-0003-3294-5888
FU NIH [R01 NS076512, R21/R33 AI101064]; VA merit grant
FX The study described in this publication was supported by NIH grants R01
NS076512 (to K.L.T.) and R21/R33 AI101064 (to K.L.T.) and by a VA merit
grant (to K.L.T.). K. L. Tyler is also supported by the Reuler-Lewin
Family Professorship.
NR 72
TC 8
Z9 8
U1 0
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD NOV
PY 2014
VL 88
IS 22
BP 13005
EP 13014
DI 10.1128/JVI.01994-14
PG 10
WC Virology
SC Virology
GA AT3CG
UT WOS:000344812500007
PM 25165111
ER
PT J
AU Cohen, K
Altfeld, M
Alter, G
Stamatatos, L
AF Cohen, Kristen
Altfeld, Marcus
Alter, Galit
Stamatatos, Leonidas
TI Early Preservation of CXCR5(+) PD-1(+) Helper T Cells and B Cell
Activation Predict the Breadth of Neutralizing Antibody Responses in
Chronic HIV-1 Infection
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID SIMIAN/HUMAN IMMUNODEFICIENCY VIRUS; CXC CHEMOKINE RECEPTOR-5;
FOLLICULAR HELPER; GERMINAL CENTER; MONOCLONAL-ANTIBODIES; IN-VITRO;
IMMUNE-RESPONSES; PASSIVE TRANSFER; ICOS DEFICIENCY; SHIV CHALLENGE
AB Much is known about the characteristics of broadly neutralizing antibodies (bNAbs) generated during HIV-1 infection, but little is known about immunological mechanisms responsible for their development in only a minority of those infected by HIV-1. By monitoring longitudinally a cohort of HIV-1-infected subjects, we observed that the preservation of CXCR5(+) CD4(+) T helper cell frequencies and activation status of B cells during the first year of infection correlates with the maximum breadth of plasma neutralizing antibody responses during chronic infection independently of viral load. Although, during the first year of infection, no differences were observed in the abilities of peripheral CXCR5(+) CD4(+) T helper cells to induce antibody secretion by autologous naive B cells, higher frequencies of class-switched antibodies were detected in cocultures of CXCR5(+) CD4(+) T and B cells from the subjects who later developed broadly neutralizing antibody responses than those who did not. Furthermore, B cells from the former subjects had higher expression of AICDA than B cells from the latter subjects, and transcript levels correlated with the frequency of CXCR5(+) CD4(+) T cells. Thus, the early preservation of CXCR5(+) CD4(+) T cells and B cell function are central to the development of bNAbs. Our study provides a possible explanation for their infrequent generation during HIV-1 infection.
IMPORTANCE
Broadly neutralizing antibodies are developed by HIV-1-infected subjects, but so far (and despite intensive efforts over the past 3 decades) they have not been elicited by immunization. Understanding how bNAbs are generated during natural HIV-1 infection and why only some HIV-1-infected subjects generate such antibodies will assist our efforts to elicit bNAbs by immunization. CXCR5(+) PD-1(+) CD4(+) T cells are critical for the development of high-affinity antigen-specific antibody responses. In our study, we found that the HIV-1-infected subjects who develop bNAbs have a higher frequency of peripheral CXCR5(+) PD-1(+) CD4(+) T cells in early infection and also that this frequency mirrored what was observed in uninfected subjects and correlated with the level of B cell activation across subjects. Our study highlights the critical role helper T cell function has in the elicitation of broadly neutralizing antibody responses in the context of HIV infection.
C1 [Cohen, Kristen; Stamatatos, Leonidas] Seattle Biomed Res Inst, Seattle, WA 98109 USA.
[Cohen, Kristen; Stamatatos, Leonidas] Univ Washington, Dept Global Hlth, Seattle, WA 98195 USA.
[Altfeld, Marcus; Alter, Galit] Massachusetts Gen Hosp, MIT & Harvard, MGH, Ragon Inst, Boston, MA 02114 USA.
[Altfeld, Marcus] Heinrich Pette Inst, Hamburg, Germany.
RP Stamatatos, L (reprint author), Seattle Biomed Res Inst, 4 Nickerson St, Seattle, WA 98109 USA.
EM leo.stamatatos@seattlebiomed.org
FU NIAID [R01AI081625]
FX These studies were supported by NIAID R01AI081625.
NR 67
TC 19
Z9 20
U1 0
U2 7
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD NOV
PY 2014
VL 88
IS 22
BP 13310
EP 13321
DI 10.1128/JVI.02186-14
PG 12
WC Virology
SC Virology
GA AT3CG
UT WOS:000344812500032
PM 25210168
ER
PT J
AU Landes, SD
Ardelt, M
Vaillant, GE
Waldinger, RJ
AF Landes, Scott D.
Ardelt, Monika
Vaillant, George E.
Waldinger, Robert J.
TI Childhood Adversity, Midlife Generativity, and Later Life Well-Being
SO JOURNALS OF GERONTOLOGY SERIES B-PSYCHOLOGICAL SCIENCES AND SOCIAL
SCIENCES
LA English
DT Article
DE Adjustment to aging; Adversarial childhood; Generativity; Later life
health; Longitudinal study
ID STRESS-RELATED GROWTH; CUMULATIVE ADVANTAGE; POSTTRAUMATIC GROWTH;
EMPIRICAL-EVIDENCE; HUMAN RESILIENCE; ADULT HEALTH; TRAUMA;
DISADVANTAGE; PERSPECTIVES; PERSONALITY
AB Objectives. Prior studies confirm that after experiencing childhood adversity, resilient adults can recover and engage in generative growth. This study explored the long-term effects of childhood adversity (assessed as harsh parenting and/or childhood poverty) on successful aging for individuals who either achieved or failed to achieve Erikson's psychosocial developmental stage of generativity in midlife.
Method. The study utilized a sample of 636 men from the Harvard Sample and Inner City Cohort of the 73-year longitudinal Study of Adult Development. Nested ordinary least squares regression models were used to test the mediating and moderating effects of midlife generativity on later life health and adjustment to aging.
Results. Men who experienced childhood adversity were less likely than men with no childhood adversity to achieve generativity in midlife. Although achievement of generativity was associated with better later life health and adjustment to aging, it neither mediated nor moderated the negative relation between childhood poverty and later life health outcomes. However, for men who experienced an adversarial childhood, achievement of generativity mediated and moderated adjustment to aging.
Discussion. Results suggest that psychosocial growth in adulthood can compensate for the long-term negative effects of an adversarial childhood on adjustment to aging, but not for later life health.
C1 [Landes, Scott D.] Univ N Florida, Dept Sociol Anthropol & Social Work, Jacksonville, FL 32224 USA.
[Ardelt, Monika] Univ Florida, Dept Sociol & Criminol & Law, Gainesville, FL USA.
[Vaillant, George E.; Waldinger, Robert J.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Vaillant, George E.; Waldinger, Robert J.] Harvard Univ, Sch Med, Boston, MA USA.
RP Landes, SD (reprint author), Univ N Florida, Dept Sociol Anthropol & Social Work, 1 UNF Dr, Jacksonville, FL 32224 USA.
EM scott.landes@unf.edu
FU NIA NIH HHS [R01 AG045230]
NR 67
TC 4
Z9 5
U1 7
U2 30
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5014
EI 1758-5368
J9 J GERONTOL B-PSYCHOL
JI J. Gerontol. Ser. B-Psychol. Sci. Soc. Sci.
PD NOV
PY 2014
VL 69
IS 6
BP 942
EP 952
DI 10.1093/geronb/gbu055
PG 11
WC Geriatrics & Gerontology; Gerontology; Psychology; Psychology,
Multidisciplinary
SC Geriatrics & Gerontology; Psychology
GA AT1BE
UT WOS:000344667300014
PM 24870028
ER
PT J
AU Ramalingam, SS
Janne, PA
Mok, T
O'Byrne, K
Boyer, MJ
Von Pawel, J
Pluzanski, A
Shtivelband, M
Docampo, LI
Bennouna, J
Zhang, H
Liang, JQ
Doherty, JP
Taylor, I
Mather, CB
Goldberg, Z
O'Connell, J
Paz-Ares, L
AF Ramalingam, Suresh S.
Jaenne, Pasi A.
Mok, Tony
O'Byrne, Kenneth
Boyer, Michael J.
Von Pawel, Joachim
Pluzanski, Adam
Shtivelband, Mikhail
Iglesias Docampo, Lara
Bennouna, Jaafar
Zhang, Hui
Liang, Jane Q.
Doherty, Jim P.
Taylor, Ian
Mather, Cecile B.
Goldberg, Zelanna
O'Connell, Joseph
Paz-Ares, Luis
TI Dacomitinib versus erlotinib in patients with advanced-stage, previously
treated non-small-cell lung cancer (ARCHER 1009): a randomised,
double-blind, phase 3 trial
SO LANCET ONCOLOGY
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; GEFITINIB; EGFR; INHIBITOR; CHEMOTHERAPY;
PF-00299804; MUTATIONS; RESISTANCE
AB Background Dacomitinib is an irreversible pan-EGFR family tyrosine kinase inhibitor. Findings from a phase 2 study in non-small cell lung cancer showed favourable efficacy for dacomitinib compared with erlotinib. We aimed to compare dacomitinib with erlotinib in a phase 3 study.
Methods In a randomised, multicentre, double-blind phase 3 trial in 134 centres in 23 countries, we enrolled patients who had locally advanced or metastatic non-small-cell lung cancer, progression after one or two previous regimens of chemotherapy, Eastern Cooperative Oncology Group (ECOG) performance status of 0-2, and presence of measurable disease. We randomly assigned patients in a 1:1 ratio to dacomitinib (45 mg/day) or erlotinib (150 mg/day) with matching placebo. Treatment allocation was masked to the investigator, patient, and study funder. Randomisation was stratified by histology (adenocarcinoma vs non-adenocarcinoma), ethnic origin (Asian vs non-Asian and Indian sub-continent), performance status (0-1 vs 2), and smoking status (never-smoker vs ever-smoker). The coprimary endpoints were progression-free survival per independent review for all randomly assigned patients, and for all randomly assigned patients with KRAS wild-type tumours.
Findings Between June 22, 2011, and March 12, 2013, we enrolled 878 patients and randomly assigned 439 to dacomitinib (256 KRAS wild type) and 439 (263 KRAS wild type) to erlotinib. Median progression-free survival was 2.6 months (95% CI 1.9-2.8) in both the dacomitinib group and the erlotinib group (stratifi ed hazard ratio [HR] 0.941, 95% CI 0.802-1.104, one-sided log-rank p= 0.229). For patients with wild-type KRAS, median progression-free survival was 2.6 months for dacomitinib (95% CI 1.9-2.9) and erlotinib (95% CI 1.9-3.0; stratifi ed HR 1.022, 95% CI 0.834-1.253, one-sided p=0.587). In patients who received at least one dose of study drug, the most frequent grade 3-4 adverse events were diarrhoea (47 [11%] patients in the dacomitinib group vs ten [2%] patients in the erlotinib group), rash (29 [7%] vs 12 [3%]), and stomatitis (15 [3%] vs two [<1%]). Serious adverse events were reported in 52 (12%) patients receiving dacomitinib and 40 (9%) patients receiving erlotinib.
Interpretation Irreversible EGFR inhibition with dacomitinib was not superior to erlotinib in an unselected patient population with advanced non-small-cell lung cancer or in patients with KRAS wild-type tumours. Further study of irreversible EGFR inhibitors should be restricted to patients with activating EGFR mutations.
C1 [Ramalingam, Suresh S.] Emory Univ, Sch Med, Winship Canc Inst, Atlanta, GA 30322 USA.
[Jaenne, Pasi A.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Mok, Tony] Chinese Univ Hong Kong, Dept Clin Oncol, State Key Lab South China, Hong Kong Canc Inst, Shatin, Hong Kong, Peoples R China.
[O'Byrne, Kenneth] Princess Alexandra Hosp, Woolloongabba, Qld 4102, Australia.
[Boyer, Michael J.] Chris OBrien Lifehouse Royal Prince Alfred Hosp, Sydney, NSW, Australia.
[Von Pawel, Joachim] Asklepios Fachkliniken, Munich, Germany.
[Pluzanski, Adam] Sklodowska Curie Mem Canc Ctr, Warsaw, Poland.
[Pluzanski, Adam] Inst Oncol, Warsaw, Poland.
[Shtivelband, Mikhail] Ironwood Canc & Res Ctr, Chandler, AZ USA.
[Iglesias Docampo, Lara] Hosp Univ 12 Octubre, Dept Med Oncol, Madrid, Spain.
[Bennouna, Jaafar] Inst Cancerol Ouest, Nantes, France.
[Zhang, Hui] Pfizer China Res & Dev, Shanghai, Peoples R China.
[Liang, Jane Q.; Taylor, Ian; Mather, Cecile B.] Pfizer Oncol, Groton, CT USA.
[Doherty, Jim P.; O'Connell, Joseph] Pfizer Oncol, New York, NY USA.
[Goldberg, Zelanna] Pfizer Oncol, San Diego, CA USA.
[Paz-Ares, Luis] Univ Hosp Virgen del Rocio, Seville, Spain.
RP Ramalingam, SS (reprint author), Emory Univ, Sch Med, Winship Canc Inst, Atlanta, GA 30322 USA.
EM ssramal@emory.edu
RI bennouna, jaafar/K-9350-2015; IBIS, NUEVAS TERAPIA/P-3415-2015
FU NCI NIH HHS [U10 CA180864]
NR 16
TC 31
Z9 33
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD NOV
PY 2014
VL 15
IS 12
BP 1369
EP 1378
DI 10.1016/S1470-2045(14)70452-8
PG 10
WC Oncology
SC Oncology
GA AS9ER
UT WOS:000344546400048
PM 25439691
ER
PT J
AU Rajkumar, SV
Dimopoulos, MA
Palumbo, A
Blade, J
Merlini, G
Mateos, MV
Kumar, S
Hillengass, J
Kastritis, E
Richardson, P
Landgren, O
Paiva, B
Dispenzieri, A
Weiss, B
Leleu, X
Zweegman, S
Lonial, S
Rosinol, L
Zamagni, E
Jagannath, S
Sezer, O
Kristinsson, SY
Caers, J
Usmani, SZ
Lahuerta, JJ
Johnsen, HE
Beksac, M
Cavo, M
Goldschmidt, H
Terpos, E
Kyle, RA
Anderson, KC
Durie, BGM
San Miguel, JF
AF Rajkumar, S. Vincent
Dimopoulos, Meletios A.
Palumbo, Antonio
Blade, Joan
Merlini, Giampaolo
Mateos, Maria-Victoria
Kumar, Shaji
Hillengass, Jens
Kastritis, Efstathios
Richardson, Paul
Landgren, Ola
Paiva, Bruno
Dispenzieri, Angela
Weiss, Brendan
Leleu, Xavier
Zweegman, Sonja
Lonial, Sagar
Rosinol, Laura
Zamagni, Elena
Jagannath, Sundar
Sezer, Orhan
Kristinsson, Sigurdur Y.
Caers, Jo
Usmani, Saad Z.
Lahuerta, Juan Jose
Johnsen, Hans Erik
Beksac, Meral
Cavo, Michele
Goldschmidt, Hartmut
Terpos, Evangelos
Kyle, Robert A.
Anderson, Kenneth C.
Durie, Brian G. M.
San Miguel, Jesus F.
TI International Myeloma Working Group updated criteria for the diagnosis
of multiple myeloma
SO LANCET ONCOLOGY
LA English
DT Review
ID LIGHT-CHAIN RATIO; MULTIPARAMETER FLOW-CYTOMETRY; MARROW PLASMA-CELLS;
LENALIDOMIDE PLUS DEXAMETHASONE; UNDETERMINED SIGNIFICANCE MGUS;
POSITRON-EMISSION-TOMOGRAPHY; EARLY TREATMENT STRATEGIES; INDEPENDENT
RISK-FACTOR; MONOCLONAL GAMMOPATHY; IMAGING TECHNIQUES
AB This International Myeloma Working Group consensus updates the disease definition of multiple myeloma to include validated biomarkers in addition to existing requirements of attributable CRAB features (hypercalcaemia, renal failure, anaemia, and bone lesions). These changes are based on the identification of biomarkers associated with near inevitable development of CRAB features in patients who would otherwise be regarded as having smouldering multiple myeloma. A delay in application of the label of multiple myeloma and postponement of therapy could be detrimental to these patients. In addition to this change, we clarify and update the underlying laboratory and radiographic variables that fulfil the criteria for the presence of myeloma-defining CRAB features, and the histological and monoclonal protein requirements for the disease diagnosis. Finally, we provide specific metrics that new biomarkers should meet for inclusion in the disease definition. The International Myeloma Working Group recommends the implementation of these criteria in routine practice and in future clinical trials, and recommends that future studies analyse any differences in outcome that might occur as a result of the new disease definition.
C1 [Rajkumar, S. Vincent; Kumar, Shaji; Dispenzieri, Angela; Kyle, Robert A.] Mayo Clin, Div Hematol, Rochester, MN 55905 USA.
[Dimopoulos, Meletios A.; Kastritis, Efstathios; Terpos, Evangelos] Univ Athens, Sch Med, Dept Clin Therapeut, GR-11527 Athens, Greece.
[Palumbo, Antonio] Univ Turin, Azienda Osped Univ Citta Salute & Sci Torino, Div Hematol, Myeloma Unit, Turin, Italy.
[Blade, Joan; Rosinol, Laura] Hosp Clin Barcelona, Barcelona, Spain.
[Merlini, Giampaolo] Univ Hosp Policlin San Matteo, Amyloidosis Ctr, Pavia, Italy.
[Mateos, Maria-Victoria] Univ Hosp Salamanca, IBSAL, Salamanca, Spain.
[Hillengass, Jens; Goldschmidt, Hartmut] Heidelberg Univ, Dept Hematol Oncol & Rheumatol, Heidelberg, Germany.
[Richardson, Paul; Anderson, Kenneth C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Landgren, Ola] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Paiva, Bruno; San Miguel, Jesus F.] Univ Navarra Clin, Ctr Invest Med Aplicada, Pamplona, Spain.
[Weiss, Brendan] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Leleu, Xavier] Univ Hosp Lille, Lille, France.
[Zweegman, Sonja] Vrije Univ Amsterdam Med Ctr, Dept Hematol, Amsterdam, Netherlands.
[Lonial, Sagar] Emory Univ, Winship Canc Inst, Dept Hematol & Med Oncol, Atlanta, GA 30322 USA.
[Zamagni, Elena; Cavo, Michele] Univ Bologna, Seragnoli Inst Hematol, Sch Med, Bologna, Italy.
[Jagannath, Sundar] Mt Sinai Canc Inst, New York, NY USA.
[Sezer, Orhan] Mem Hosp, Istanbul, Turkey.
[Kristinsson, Sigurdur Y.] Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden.
[Caers, Jo] CHU Liege, Dept Hematol, Liege, Belgium.
[Usmani, Saad Z.] Carolinas HealthCare Syst, Levine Canc Inst, Charlotte, NC USA.
[Lahuerta, Juan Jose] Hosp Univ 12 Octubre, Serv Hematol, Madrid, Spain.
[Johnsen, Hans Erik] Aalborg Univ Hosp, Dept Haematol, Aalborg, Denmark.
[Beksac, Meral] Ankara Univ, Sch Med, TR-06100 Ankara, Turkey.
[Durie, Brian G. M.] Cedars Sinai Comprehens Canc Ctr, Los Angeles, CA USA.
RP Rajkumar, SV (reprint author), Mayo Clin, Div Hematol, 200 First St SW, Rochester, MN 55905 USA.
EM rajkumar.vincent@mayo.edu
RI Kumar, Shaji/A-9853-2008; Merlini, Giampaolo/A-3817-2008; Kristinsson,
Sigurdur /M-2910-2015;
OI Kumar, Shaji/0000-0001-5392-9284; Merlini,
Giampaolo/0000-0001-7680-3254; Kristinsson, Sigurdur
/0000-0002-4964-7476; CAVO, MICHELE/0000-0003-4514-3227; Dispenzieri,
Angela/0000-0001-8780-9512
FU Celgene; Ortho Biotech; Onyx; Amgen; Bristol-Myers Squibb; Genmab A/S;
Janssen-Cilag; Millennium Pharmaceuticals; Onyx Pharmaceuticals; Sanofi
Aventis; Array BioPharma; Janssen; Millennium Takeda; Millennium;
Novartis; Cephalon/Teva; Abbvie; Pfizer; Jannsen; Research and
Development; Sanofi; Jansen-Cilag
FX MAD reports personal fees from Celgene, Ortho Biotech, and Onyx. AP
reports personal fees from Amgen, Bristol-Myers Squibb, Genmab A/S,
Janssen-Cilag, Millennium Pharmaceuticals, Onyx Pharmaceuticals,
Celgene, Sanofi Aventis, and Array BioPharma. JB reports personal fees
from Celgene and Janssen. GM reports personal fees from Millennium
Takeda. SK reports grants from Celgene, Millennium, Novartis,
Cephalon/Teva, Abbvie, and Onyx. PR has been a member of advisory
committees for Millennium, Celgene, Johnson & Johnson, and Novartis. BP
has received honoraria from Millennium, Celgene, Janssen, and The
Binding Site Group Ltd. AD reports grants from Celgene, Millennium,
Pfizer, and Jannsen. BW reports grants and personal fees from Janssen
Research and Development, personal fees from Celgene and Onyx, and
grants from Millennium. SZ reports grants from Celgene, Janssen, and
Millennium. SL reports personal fees from Millennium, Celgene, Novartis,
Onyx, Sanofi, Janssen, and Bristol-Myers Squibb. LR has received
honoraria from Janssen and Celgene. EZ reports grants from Jansen-Cilag
and Celgene. SJ has been a consultant for Celgene, Sanofi, and
Bristol-Myers Squibb. OS reports personal fees from Celgene and Janssen.
MB is in the speakers bureau for Celgene, Janssen-Cilag and Amgen, and
serves on advisory boards for Janssen-Cilag, Bristol-Myers Squibb, and
Novartis. MC reports personal fees from Janssen, Celgene, Millennium,
Onyx, and Bristol-Myers Squibb. KCA reports personal fees from Celgene,
Millennium, Gilead, Sanofi Aventis, and Onyx. All other authors declare
no competing interests.
NR 100
TC 264
Z9 284
U1 20
U2 59
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD NOV
PY 2014
VL 15
IS 12
BP E538
EP E548
PG 11
WC Oncology
SC Oncology
GA AS9ER
UT WOS:000344546400022
PM 25439696
ER
PT J
AU Chong, CR
Wirth, LJ
Nishino, M
Chen, AB
Sholl, LM
Kulke, MH
McNamee, CJ
Janne, PA
Johnson, BE
AF Chong, Curtis R.
Wirth, Lori J.
Nishino, Mizuki
Chen, Aileen B.
Sholl, Lynette M.
Kulke, Matthew H.
McNamee, Ciaran J.
Jaenne, Pasi A.
Johnson, Bruce E.
TI Chemotherapy for locally advanced and metastatic pulmonary carcinoid
tumors
SO LUNG CANCER
LA English
DT Article
DE Typical carcinoid; Atypical carcinoid; DIPNECH
ID CELL LUNG-CANCER; NEUROENDOCRINE TUMORS; BRONCHIAL CARCINOIDS;
OCTREOTIDE; CISPLATIN; RADIANT-2; SURVIVAL; PHASE-3
AB Objectives: The optimal management of locally advanced and metastatic pulmonary carcinoid tumors remains to be determined.
Materials and methods: A retrospective review was conducted on patients with typical and atypical pulmonary carcinoid tumors treated at our institutions between 1990 and 2012.
Results: 300 patients were identified with pulmonary carcinoid, (80 patients with atypical carcinoid), of whom 29 presented with metastatic disease (16 atypical). Of evaluable patients, 26 (41%) with stages I-III atypical carcinoid tumors recurred at a median time of 3.7 years (range, 0.4-32), compared to 3 (1%) patients with typical carcinoid (range, 8-12.3). 39 patients were treated with chemotherapy, including 30 patients with metastatic disease (27 atypical), and 7 patients were treated with adjuvant platinum etoposide chemoradiation (6 atypical, 1 typical, 6 stage IIIA, 1 stage JIB). At a median follow-up of 2 years there were 2 recurrences in the 7 patients receiving adjuvant treatment. Median survival after diagnosis of metastatic disease for patients with atypical pulmonary carcinoid was 3.3 years with a 5-year survival of 24%. Treatment regimens showing efficacy in pulmonary carcinoid include 15 patients treated with octreotide-based therapies (10% response rate (RR), 70% disease control rate (DCR), 15 month median progression-free survival (PFS)), 13 patients treated with etoposide + platinum (23% RR, 69% DCR, 7 month median PFS), and 14 patients treated with temozolomide-based therapies (14% RR, 57% DCR, 10 month median PFS). 8 of 10 patients with octreotide-avid disease treated with an octreotide-based regimen experienced disease control (1 partial response, 7 stable disease) for a median of 18 months (range 6-72 months).
Conclusions: These results support our previous finding that a subset of pulmonary carcinoid tumors are responsive to chemotherapy. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Chong, Curtis R.; Jaenne, Pasi A.; Johnson, Bruce E.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
[Wirth, Lori J.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Nishino, Mizuki] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02215 USA.
[Nishino, Mizuki; Chen, Aileen B.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Chen, Aileen B.] Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02215 USA.
[Sholl, Lynette M.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02215 USA.
[Kulke, Matthew H.] Dana Farber Canc Inst, Ctr Gastrointestinal Oncol, Boston, MA 02215 USA.
[McNamee, Ciaran J.] Brigham & Womens Hosp, Div Thorac Surg, Boston, MA 02215 USA.
[Jaenne, Pasi A.] Dana Farber Canc Inst, Belfer Inst Appl Canc Sci, Boston, MA 02215 USA.
RP Johnson, BE (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM Bruce_Johnson@dfci.harvard.edu
FU Conquer Cancer Foundation of ASCO Young Investigator Award; American
Cancer Society [PF-14-020-01-CDD]; Uniting Against Lung Cancer; National
Cancer Institute [1K23CA157631]
FX This work was funded by a Conquer Cancer Foundation of ASCO Young
Investigator Award, a postdoctoral fellowship, PF-14-020-01-CDD from the
American Cancer Society, and a grant from Uniting Against Lung Cancer to
C.R.C. Any opinions, findings, and conclusions expressed in this
material are those of the author(s) and do not necessarily reflect those
of the American Society of Clinical Oncology or the Conquer Cancer
Foundation. M.N. was supported by 1K23CA157631 (National Cancer
Institute). The authors express appreciation for a gift supporting the
study to the Dana-Farber Cancer Institute from the Gallup Foundation.
NR 34
TC 14
Z9 14
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0169-5002
EI 1872-8332
J9 LUNG CANCER
JI Lung Cancer
PD NOV
PY 2014
VL 86
IS 2
BP 241
EP 246
DI 10.1016/j.lungcan.2014.08.012
PG 6
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AS7LU
UT WOS:000344438400023
PM 25218177
ER
PT J
AU Zhao, N
Wilkerson, MD
Shah, U
Yin, XY
Wang, AY
Hayward, MC
Roberts, P
Lee, CB
Parsons, AM
Thorne, LB
Haithcock, BE
Grilley-Olson, JE
Stinchcombe, TE
Funkhouser, WK
Wong, KK
Sharpless, NE
Hayes, DN
AF Zhao, Ni
Wilkerson, Matthew D.
Shah, Usman
Yin, Xiaoying
Wang, Anyou
Hayward, Michele C.
Roberts, Patrick
Lee, Carrie B.
Parsons, Alden M.
Thorne, Leigh B.
Haithcock, Benjamin E.
Grilley-Olson, Juneko E.
Stinchcombe, Thomas E.
Funkhouser, William K.
Wong, Kwok-Kin
Sharpless, Norman E.
Hayes, D. Neil
TI Alterations of LKB1 and KRAS and risk of brain metastasis: Comprehensive
characterization by mutation analysis, copy number, and gene expression
in non-small-cell lung carcinoma
SO LUNG CANCER
LA English
DT Article
DE NSCLC; Brain Metastasis; Prognostic model; LKB1; KRAS
ID PROPHYLACTIC CRANIAL IRRADIATION; FOLLOW-UP; SOMATIC MUTATIONS;
LKB1/STK11 GENE; BREAST-CANCER; INACTIVATION; ADENOCARCINOMA; TRIALS
AB Background: Brain metastases are one of the most malignant complications of lung cancer and constitute a significant cause of cancer related morbidity and mortality worldwide. Recent years of investigation suggested a role of LKB1 in NSCLC development and progression, in synergy with KRAS alteration. In this study, we systematically analyzed how LKB1 and KRAS alteration, measured by mutation, gene expression (GE) and copy number (CN), are associated with brain metastasis in NSCLC.
Materials and methods: Patients treated at University of North Carolina Hospital from 1990 to 2009 with NSCLC provided frozen, surgically extracted tumors for analysis. GE was measured using Agilent 44,000 custom-designed arrays, CN was assessed by Affymetrix GeneChip Human Mapping 250K Sty Array or the Genome-Wide Human SNP Array 6.0 and gene mutation was detected using ABI sequencing. Integrated analysis was conducted to assess the relationship between these genetic markers and brain metastasis. A model was proposed for brain metastasis prediction using these genetic measurements.
Results: 17 of the 174 patients developed brain metastasis. LKB1 wild type tumors had significantly higher LKB1 CN (p < 0.001) and GE (p = 0.002) than the LKB1 mutant group. KRAS wild type tumors had significantly lower KR/IS GE (p<0.001) and lower CN, although the latter failed to be significant (p = 0.295). Lower LKB1 CN (p = 0.039) and KRAS mutation (p = 0.007) were significantly associated with more brain metastasis. The predictive model based on nodal (N) stage, patient age, LKB1 CN and KRAS mutation had a good prediction accuracy, with area under the ROC curve of 0.832 (p < 0.001).
Conclusion: LKB1 CN in combination with KRAS mutation predicted brain metastasis in NSCLC. (C) 2014 The Authors. Published by Elsevier Ireland Ltd.
C1 [Zhao, Ni; Yin, Xiaoying; Wang, Anyou; Hayward, Michele C.; Roberts, Patrick; Lee, Carrie B.; Thorne, Leigh B.; Grilley-Olson, Juneko E.; Stinchcombe, Thomas E.; Funkhouser, William K.; Sharpless, Norman E.; Hayes, D. Neil] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Zhao, Ni] Univ N Carolina, Gilling Sch Global Publ Hlth, Dept Biostat, Chapel Hill, NC 27599 USA.
[Shah, Usman] Lehigh Valley Hlth Network, Div Hematol Oncol, Dept Med, Allentown, PA USA.
[Lee, Carrie B.; Grilley-Olson, Juneko E.; Stinchcombe, Thomas E.; Sharpless, Norman E.; Hayes, D. Neil] Univ N Carolina, Multidisciplinary Thorac Oncol Program, Div Hematol Oncol, Dept Internal Med, Chapel Hill, NC 27599 USA.
[Parsons, Alden M.; Haithcock, Benjamin E.] Univ N Carolina, Div Cardiothorac Surg, Dept Surg, Chapel Hill, NC 27599 USA.
[Thorne, Leigh B.; Funkhouser, William K.] Univ N Carolina, UNC Sch Med, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA.
[Wong, Kwok-Kin] Harvard Univ, Sch Med, Dept Med, Dana Farber Canc Inst, Cambridge, MA 02138 USA.
[Sharpless, Norman E.] Univ N Carolina, Sch Med, Dept Genet, Chapel Hill, NC 27599 USA.
[Wilkerson, Matthew D.] Univ N Carolina, Sch Med, Dept Genet, Chapel Hill, NC 27599 USA.
RP Hayes, DN (reprint author), Univ N Carolina, Sch Med, UNC Lineberger Comprehens Canc Ctr, CB 7295,450 West Dr, Chapel Hill, NC 27599 USA.
EM hayes@med.unc.edu
RI Zhao, Ni/P-9086-2014;
OI Zhao, Ni/0000-0002-7762-3949; Wang, Anyou/0000-0002-4981-3606
FU Thomas G. Labreque Foundation, through Joan's Legacy Foundation;
Clinical/Translational Award from the UNC Lineberger Comprehensive
Cancer Center
FX This study was supported by the Thomas G. Labreque Foundation, through
Joan's Legacy Foundation and by a Clinical/Translational Award from the
UNC Lineberger Comprehensive Cancer Center.
NR 35
TC 10
Z9 10
U1 0
U2 5
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0169-5002
EI 1872-8332
J9 LUNG CANCER
JI Lung Cancer
PD NOV
PY 2014
VL 86
IS 2
BP 255
EP 261
DI 10.1016/j.lungcan.2014.08.013
PG 7
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AS7LU
UT WOS:000344438400025
PM 25224251
ER
PT J
AU Kaneko-Tarui, T
Commandeur, AE
Patterson, AL
DeKuiper, JL
Petillo, D
Styer, AK
Teixeira, JM
AF Kaneko-Tarui, Tomoko
Commandeur, Arno E.
Patterson, Amanda L.
DeKuiper, Justin L.
Petillo, David
Styer, Aaron K.
Teixeira, Jose M.
TI Hyperplasia and fibrosis in mice with conditional loss of the TSC2 tumor
suppressor in Mullerian duct mesenchyme-derived myometria
SO MOLECULAR HUMAN REPRODUCTION
LA English
DT Article
DE uterine fibroid; mTOR; tumourigenesis; infertility; TSC2
ID TUBEROUS SCLEROSIS; UTERINE LEIOMYOMA; PROGESTERONE-RECEPTOR;
ENDOMETRIAL CANCER; BETA-CATENIN; FIBROIDS; DELETION; GENE; PREGNANCY;
PATHWAY
AB Uterine leiomyomata are the most common tumors found in the female reproductive tract. Despite the high prevalence and associated morbidities of these benign tumors, little is known about the molecular basis of uterine leiomyoma development and progression. Loss of the Tuberous Sclerosis 2 (TSC2) tumor suppressor has been proposed as a mechanism important for the etiology of uterine leiomyomata based on the Eker rat model. However, conflicting evidence showing increased TSC2 expression has been reported in human uterine leiomyomata, suggesting that TSC2 might not be involved in the pathogenesis of this disorder. We have produced mice with conditional deletion of the Tsc2 gene in the myometria to determine whether loss of TSC2 leads to leiomyoma development in murine uteri. Myometrial hyperplasia and increased collagen deposition was observed in Tsc2(cKO) mice compared with control mice, but no leiomyomata were detected by post-natal week 24. Increased signaling activity of mammalian target of rapamycin complex 1, which is normally repressed by TSC2, was also detected in the myometria of Tsc2(cKO) mice. Treatment of the mutant mice with rapamycin significantly inhibited myometrial expansion, but treatment with the progesterone receptor modulator, mifepristone, did not. The ovaries of the Tsc2(cKO) mice appeared normal, but half the mice were infertile and most of the other half became infertile after a single litter, which was likely due to oviductal blockage. Our study shows that although TSC2 loss alone does not lead to leiomyoma development, it does lead to myometrial hyperplasia and fibrosis.
C1 [Kaneko-Tarui, Tomoko; Commandeur, Arno E.; Styer, Aaron K.] Harvard Univ, Sch Med, Dept Obstet Gynecol & Reprod Biol, Vincent Ctr Reprod Biol,Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Patterson, Amanda L.; DeKuiper, Justin L.; Petillo, David; Teixeira, Jose M.] Michigan State Univ, Coll Human Med, Dept Obstet Gynecol & Reprod Biol, Grand Rapids, MI 49503 USA.
RP Teixeira, JM (reprint author), Michigan State Univ, 333 Bostwick Ave NE,4018A, Grand Rapids, MI 49503 USA.
EM jose.teixeira@hc.msu.edu
OI Teixeira, Jose/0000-0002-6438-5064
FU Bayer Grant4Targets Program; A. David Mazzone Research Awards Program;
National Institutes of Health [HD072489]
FX These studies were supported by the Bayer Grant4Targets Program to
J.M.T., the A. David Mazzone Research Awards Program to A. K. S. and
J.M.T., and by the National Institutes of Health (HD072489 to J.M.T.).
NR 42
TC 2
Z9 2
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1360-9947
EI 1460-2407
J9 MOL HUM REPROD
JI Mol. Hum. Reprod.
PD NOV
PY 2014
VL 20
IS 11
BP 1126
EP 1134
DI 10.1093/molehr/gau077
PG 9
WC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology
SC Developmental Biology; Obstetrics & Gynecology; Reproductive Biology
GA AT0HW
UT WOS:000344618500008
PM 25189766
ER
PT J
AU Rotstein, BH
Wey, HY
Shoup, TM
Wilson, AA
Liang, SH
Hooker, JM
Vasdev, N
AF Rotstein, Benjamin H.
Wey, Hsiao-Ying
Shoup, Timothy M.
Wilson, Alan A.
Liang, Steven H.
Hooker, Jacob M.
Vasdev, Neil
TI PET Imaging of Fatty Acid Amide Hydrolase with [F-18]DOPP in Nonhuman
Primates
SO MOLECULAR PHARMACEUTICS
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; IN-VIVO EVALUATION; NERVOUS-SYSTEM;
ANANDAMIDE; INHIBITOR; BRAIN; PF-04457845; FAAH; ENDOCANNABINOIDS;
SELECTIVITY
AB Fatty acid amide hydrolase (FAAH) regulates endocannabinoid signaling. [C-11]CURB, an irreversibly binding FAAH inhibitor, has been developed for clinical research imaging with PET. However, no fluorine-18 labeled radiotracer for FAAH has yet advanced to human studies. [18F]DOPP ([18F]3-(4,5-dihydrooxazol-2-yl)phenyl (5-fluoropentyl)carbamate) has been identified as a promising 18F-labeled analogue based on rodent studies. The goal of this work is to evaluate [18F]DOPP in nonhuman primates to support its clinical translation. High specific activity [18F]DOPP (56 Ci center dot?mol1) was administered intravenously (iv) to three baboons (2M/1F, 34 years old). The distribution and pharmacokinetics were quantified following a 2 h dynamic imaging session using a simultaneous PET/MR scanner. Pretreatment with the FAAH-selective inhibitor, URB597, was carried out at 200 or 300 ?g/kg iv, 10 min prior to [18F]DOPP administration. Rapid arterial blood sampling for the first 3 min was followed by interval sampling with metabolite analysis to provide a parent radiotracer plasma input function that indicated ?95% baseline metabolism at 60 min and a reduced rate of metabolism after pretreatment with URB597. Regional distribution data were analyzed with 1-, 2-, and 3-tissue compartment models (TCMs), with and without irreversible trapping since [18F]DOPP covalently links to the active site of FAAH. Consistent with previous findings for [11C]CURB, the 2TCM with irreversible binding was found to provide the best fit for modeling the data in all regions. The composite parameter ?k3 was therefore used to evaluate whole brain (WB) and regional binding of [18F]DOPP. Pretreatment studies showed inhibition of ?k3 across all brain regions (WB baseline: 0.112 mL/cm3/min; 300 ?g/kg URB597: 0.058 mL/cm3/min), suggesting that [18F]DOPP binding is specific for FAAH, consistent with previous rodent data.
C1 [Rotstein, Benjamin H.; Shoup, Timothy M.; Liang, Steven H.; Vasdev, Neil] Massachusetts Gen Hosp, Div Nucl Med & Mol Imaging, Boston, MA 02114 USA.
[Rotstein, Benjamin H.; Shoup, Timothy M.; Liang, Steven H.; Vasdev, Neil] Massachusetts Gen Hosp, Ctr Adv Med Imaging Sci, Boston, MA 02114 USA.
[Rotstein, Benjamin H.; Wey, Hsiao-Ying; Shoup, Timothy M.; Liang, Steven H.; Hooker, Jacob M.; Vasdev, Neil] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02114 USA.
[Wey, Hsiao-Ying; Hooker, Jacob M.] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA.
[Wilson, Alan A.] Univ Toronto, Ctr Addict & Mental Hlth, Res Imaging Ctr, Toronto, ON M5T 1R8, Canada.
[Wilson, Alan A.] Univ Toronto, Dept Psychiat, Toronto, ON M5T 1R8, Canada.
RP Hooker, JM (reprint author), Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02114 USA.
EM hooker@nmr.mgh.harvard.edu; vasdev.neil@mgh.harvard.edu
OI Rotstein, Benjamin/0000-0001-9707-9357
FU Natural Sciences and Engineering Research Council of Canada (NSERC);
Harvard/MGH Nuclear Medicine Training Program from the Department of
Energy [DE-SC0008430]; NIH [1R21M1-1094424, 1K01DA038000-01]
FX We thank David F. Lee, Jr., and Dr. Ronald Moore for assistance with
radioisotope production, Dr. Ronald Borra, Shirley Hsu, Grae Arabasz,
and Helen Deng for assistance with PET/MR imaging experiments, and Dr.
Ramesh Neelamegam for assistance with plasma protein binding
experiments. We thank Dr. Dustin Wooten for helpful discussions. B.H.R.
is a Natural Sciences and Engineering Research Council of Canada (NSERC)
Postdoctoral Fellow. H.-Y.W. is supported by the Harvard/MGH Nuclear
Medicine Training Program from the Department of Energy (DE-SC0008430).
This work was supported in part by NIH Grants: 1R21M1-1094424 (A.A.W.)
and 1K01DA038000-01 (S.H.L.).
NR 35
TC 6
Z9 6
U1 2
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
PY 2014
VL 11
IS 11
BP 3832
EP 3838
DI 10.1021/mp500316h
PG 7
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA AS5JP
UT WOS:000344307700007
PM 25004399
ER
PT J
AU Stroupe, KT
Weaver, FM
Cao, LS
Ippolito, D
Barton, BR
Burnett-Zeigler, IE
Holloway, RG
Vickrey, BG
Simuni, T
Follett, KA
AF Stroupe, Kevin T.
Weaver, Frances M.
Cao, Lishan
Ippolito, Dolores
Barton, Brandon R.
Burnett-Zeigler, Inger E.
Holloway, Robert G.
Vickrey, Barbara G.
Simuni, Tanya
Follett, Kenneth A.
TI Cost of Deep Brain Stimulation for the Treatment of Parkinson's Disease
by Surgical Stimulation Sites
SO MOVEMENT DISORDERS
LA English
DT Article
DE Parkinson's disease; cost; deep brain stimulation
ID RANDOMIZED CONTROLLED-TRIAL; SUBTHALAMIC NUCLEUS; MEDICAL THERAPY;
GLOBUS-PALLIDUS; UNCERTAINTY
AB ObjectiveTo assess costs and effectiveness of deep brain stimulation (DBS) of the internal globus pallidum (GPi) versus subthalamic nucleus (STN) from the provider and societal perspectives for Parkinson's disease (PD) patients in a multicenter randomized trial.
MethodsAll costs from randomization to 36 months were included. Costs were from Department of Veterans Affairs (VA) and Medicare databases and clinical trial data. Quality adjusted life years (QALYs) were from Quality of Well Being questionnaires.
ResultsProvider costs were similar for the 144 GPi and 130 STN patients (GPi: $138,044 vs. STN: $131,822; difference = $6,222, 95% confidence interval [CI]: -$42,125 to $45,343). Societal costs were also similar (GPi: $171,061 vs. STN: $167,706; difference = $3,356, 95% CI: -$57,371 to $60,294). The GPi patients had nonsignificantly more QALYs.
ConclusionsThe QALYs and costs were similar; the level of uncertainty given the sample size suggests that these factors should not direct treatment or resource allocation decisions in selecting or making available either procedure for eligible PD patients. (c) 2014 International Parkinson and Movement Disorder Society
C1 [Stroupe, Kevin T.; Weaver, Frances M.; Cao, Lishan; Ippolito, Dolores] Hines VA Hosp, Ctr Management Complex Chron Healthcare, Hines, IL USA.
[Stroupe, Kevin T.; Weaver, Frances M.] Loyola Univ Stritch Sch Med, Maywood, IL USA.
[Barton, Brandon R.] Rush Univ Med Ctr, Chicago, IL USA.
[Barton, Brandon R.] Jesse Brown VA Med Ctr, Chicago, IL USA.
[Burnett-Zeigler, Inger E.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Holloway, Robert G.] Univ Rochester Med Ctr, Rochester, NY USA.
[Vickrey, Barbara G.] VA Southwest PADRECC, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
[Vickrey, Barbara G.] UCLA Dept Neurol, Los Angeles, CA USA.
[Simuni, Tanya] Northwestern Univ, Parkinsons Dis & Movement Disorders Ctr, Chicago, IL 60611 USA.
[Follett, Kenneth A.] Univ Nebraska Sch Med, Omaha, NE USA.
RP Stroupe, KT (reprint author), Edward Hines Jr VA Hosp, Ctr Innovat Complex Chron Care, 5000 South 5th Ave 151H, Hines, IL 60141 USA.
EM Kevin.Stroupe@va.gov
FU Department of Veterans Affairs, Veterans Health Administration, Health
Services Research and Development Service [IIR 08-124-2]; VA Research
Career Scientist Award
FX This study was supported by the Department of Veterans Affairs, Veterans
Health Administration, Health Services Research and Development Service
(Project Number: IIR 08-124-2). Dr. Weaver was also supported by a VA
Research Career Scientist Award.
NR 25
TC 8
Z9 8
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0885-3185
EI 1531-8257
J9 MOVEMENT DISORD
JI Mov. Disord.
PD NOV
PY 2014
VL 29
IS 13
BP 1666
EP 1674
DI 10.1002/mds.26029
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA AT0TT
UT WOS:000344648400014
PM 25220042
ER
PT J
AU Li, N
Fassl, A
Chick, J
Inuzuka, H
Li, XY
Mansour, MR
Liu, LJ
Wang, HZ
King, B
Shaik, S
Gutierrez, A
Ordureau, A
Otto, T
Kreslavsky, T
Baitsch, L
Bury, L
Meyer, CA
Ke, N
Mulry, KA
Kluk, MJ
Roy, M
Kim, S
Zhang, XW
Geng, Y
Zagozdzon, A
Jenkinson, S
Gale, RE
Linch, DC
Zhao, JJ
Mullighan, CG
Harper, JW
Aster, JC
Aifantis, I
von Boehmer, H
Gygi, SP
Wei, WY
Look, AT
Sicinski, P
AF Li, Na
Fassl, Anne
Chick, Joel
Inuzuka, Hiroyuki
Li, Xiaoyu
Mansour, Marc R.
Liu, Lijun
Wang, Haizhen
King, Bryan
Shaik, Shavali
Gutierrez, Alejandro
Ordureau, Alban
Otto, Tobias
Kreslavsky, Taras
Baitsch, Lukas
Bury, Leah
Meyer, Clifford A.
Ke, Nan
Mulry, Kristin A.
Kluk, Michael J.
Roy, Moni
Kim, Sunkyu
Zhang, Xiaowu
Geng, Yan
Zagozdzon, Agnieszka
Jenkinson, Sarah
Gale, Rosemary E.
Linch, David C.
Zhao, Jean J.
Mullighan, Charles G.
Harper, J. Wade
Aster, Jon C.
Aifantis, Iannis
von Boehmer, Harald
Gygi, Steven P.
Wei, Wenyi
Look, A. Thomas
Sicinski, Piotr
TI Cyclin C is a haploinsufficient tumour suppressor
SO NATURE CELL BIOLOGY
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; RNA-POLYMERASE-II; SQUAMOUS-CELL
CARCINOMA; IN-SITU HYBRIDIZATION; UBIQUITIN LIGASE; TRANSCRIPTIONAL
ACTIVATION; GENE AMPLIFICATION; NOTCH-1 MUTATIONS; DEPENDENT KINASE;
ALLELIC LOSS
AB Cyclin C was cloned as a growth-promoting G(1) cyclin, and was also shown to regulate gene transcription. Here we report that in vivo cyclin C acts as a haploinsufficient tumour suppressor, by controlling Notch1 oncogene levels. Cyclin C activates an 'orphan' CDK19 kinase, as well as CDK8 and CDK3. These cyclin-C-CDK complexes phosphorylate the Notch1 intracellular domain (ICN1) and promote ICN1 degradation. Genetic ablation of cyclin C blocks ICN1 phosphorylation in vivo, thereby elevating ICN1 levels in cyclin-C-knockout mice. Cyclin C ablation or heterozygosity collaborates with other oncogenic lesions and accelerates development of T-cell acute lymphoblastic leukaemia (T-ALL). Furthermore, the cyclin C encoding gene CCNC is heterozygously deleted in a significant fraction of human T-ALLs, and these tumours express reduced cyclin C levels. We also describe point mutations in human T-ALL that render cyclin-C-CDK unable to phosphorylate ICN1. Hence, tumour cells may develop different strategies to evade inhibition by cyclin C.
C1 [Li, Na; Fassl, Anne; Liu, Lijun; Wang, Haizhen; Otto, Tobias; Baitsch, Lukas; Bury, Leah; Ke, Nan; Mulry, Kristin A.; Geng, Yan; Zagozdzon, Agnieszka; Zhao, Jean J.; Sicinski, Piotr] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
[Li, Na; Fassl, Anne; Liu, Lijun; Wang, Haizhen; Otto, Tobias; Bury, Leah; Ke, Nan; Mulry, Kristin A.; Geng, Yan; Zagozdzon, Agnieszka; Sicinski, Piotr] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Chick, Joel; Ordureau, Alban; Harper, J. Wade; Gygi, Steven P.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
[Inuzuka, Hiroyuki; Shaik, Shavali; Wei, Wenyi] Harvard Univ, Sch Med, Dept Pathol, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Li, Xiaoyu; Kreslavsky, Taras; von Boehmer, Harald] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02215 USA.
[Li, Xiaoyu; Kreslavsky, Taras; von Boehmer, Harald] Harvard Univ, Sch Med, Dept Microbiol & Immunobiol, Boston, MA 02115 USA.
[Mansour, Marc R.; Gutierrez, Alejandro; Look, A. Thomas] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02215 USA.
[Mansour, Marc R.; Gutierrez, Alejandro; Look, A. Thomas] Childrens Hosp, Div Hematol Oncol, Boston, MA 02115 USA.
[Mansour, Marc R.; Gutierrez, Alejandro; Look, A. Thomas] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Mansour, Marc R.; Jenkinson, Sarah; Gale, Rosemary E.; Linch, David C.] UCL, Dept Haematol, London WC1E 6BT, England.
[King, Bryan; Aifantis, Iannis] NYU, Sch Med, Howard Hughes Med Inst, New York, NY 10016 USA.
[King, Bryan; Aifantis, Iannis] NYU, Sch Med, Dept Pathol, New York, NY 10016 USA.
[Baitsch, Lukas; Zhao, Jean J.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Meyer, Clifford A.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02215 USA.
[Meyer, Clifford A.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Kluk, Michael J.; Roy, Moni; Aster, Jon C.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Kim, Sunkyu] Novartis Inst BioMed Res, Cambridge, MA 02139 USA.
[Zhang, Xiaowu] Cell Signaling Technol Inc, Danvers, MA 01923 USA.
[Mullighan, Charles G.] St Jude Res Hosp, Dept Pathol, Memphis, TN 38105 USA.
RP Sicinski, P (reprint author), Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
EM peter_sicinski@dfci.harvard.edu
RI Ordureau, Alban/C-7558-2012;
OI Ordureau, Alban/0000-0002-4924-8520; Mullighan,
Charles/0000-0002-1871-1850
FU American Syrian Lebanese Associated Charities of St. Jude Children's
Research Hospital [P01 CA109901, R01 CA083688, GM094777, R01 AG011085]
FX We thank S. Blacklow, T. Sanda, T. Roberts, E. Sicinska, I.
Kalaszczynska, S. Bukarac and D. Payne-Turner for help at different
stages of the project. This work was supported by grants P01 CA109901
(to P.S., H.v.B. and A.T.L.), R01 CA083688 (to P.S.), GM094777 (to
W.W.), American Syrian Lebanese Associated Charities of St. Jude
Children's Research Hospital (to C.G.M.), and R01 AG011085 (to J.W.H.).
C.G.M. is a St. Baldrick's Scholar and Pew Scholar
NR 71
TC 24
Z9 24
U1 5
U2 20
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1465-7392
EI 1476-4679
J9 NAT CELL BIOL
JI Nat. Cell Biol.
PD NOV
PY 2014
VL 16
IS 11
BP 1080
EP +
DI 10.1038/ncb3046
PG 25
WC Cell Biology
SC Cell Biology
GA AT2EF
UT WOS:000344744000007
PM 25344755
ER
PT J
AU Ke, YG
Ong, LL
Sun, W
Song, J
Dong, MD
Shih, WM
Yin, P
AF Ke, Yonggang
Ong, Luvena L.
Sun, Wei
Song, Jie
Dong, Mingdong
Shih, William M.
Yin, Peng
TI DNA brick crystals with prescribed depths
SO NATURE CHEMISTRY
LA English
DT Article
ID SINGLE-STRANDED-DNA; NANOSCALE SHAPES; GOLD NANOPARTICLES;
BLOCK-COPOLYMERS; FOLDING DNA; ARRAYS; NANOSTRUCTURES; JUNCTIONS;
DESIGN; ORIGAMI
AB The ability to assemble functional materials with precise spatial arrangements is important for applications ranging from protein crystallography to photovoltaics. Here, we describe a general framework for constructing two-dimensional crystals with prescribed depths and sophisticated three-dimensional features. The crystals are self-assembled from single-stranded DNA components called DNA bricks. We demonstrate the experimental construction of DNA brick crystals that can grow to micrometre size in their lateral dimensions with precisely controlled depths up to 80 nm. They can be designed to pack DNA helices at angles parallel or perpendicular to the plane of the crystal and to display user-specified sophisticated three-dimensional nanoscale features, such as continuous or discontinuous cavities and channels.
C1 [Ke, Yonggang; Ong, Luvena L.; Sun, Wei; Shih, William M.; Yin, Peng] Harvard Univ, Wyss Inst Biologically Inspired Engn, Boston, MA 02115 USA.
[Ke, Yonggang; Shih, William M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
[Ke, Yonggang; Shih, William M.] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
[Ong, Luvena L.] MIT, Harvard MIT Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Sun, Wei; Yin, Peng] Harvard Univ, Sch Med, Dept Syst Biol, Boston, MA 02115 USA.
[Song, Jie; Dong, Mingdong] Aarhus Univ, Ctr DNA Nanotechnol, Interdisciplinary Nanosci Ctr iNANO, DK-8000 Aarhus C, Denmark.
RP Ke, YG (reprint author), Georgia Inst Technol, Wallace H Coulter Dept Biomed Engn, Atlanta, GA 30322 USA.
EM yonggang.ke@emory.edu; py@hms.harvard.edu
RI Dong, Mingdong/B-3341-2010;
OI Dong, Mingdong/0000-0002-2025-2171; /0000-0001-5317-3018
FU ONR [N000141110914, N000141010827, N000141410610, N000141310593,
N000014091118, N000141010241]; ARO [W911NF1210238]; NSF CAREER Award
[CCF1054898]; NSF Expedition in Computing Award [CCF1317291]; NSF
[CCF1162459, CMMI1333215, CMMI1334109, CMMI1344915]; NIH Director's New
Innovator Award [1DP2OD007292, 1DP2OD004641]; Wyss Institute Faculty
Startup Fund; Wyss Institute Faculty Grant; ARO MURI grant
[W911NF1210420]; NSF Graduate Research Fellowship; AUFF from Aarhus
University; Niels Bohr Foundation from The Royal Danish Academy of
Science; National Research Foundation; Villum Foundation
FX This work is supported by ONR Young Investigator Program Award
N000141110914, ONR Grants N000141010827, N000141410610 and
N000141310593, ARO Grant W911NF1210238, NSF CAREER Award CCF1054898, NSF
Expedition in Computing Award CCF1317291, NSF Grants CCF1162459,
CMMI1333215, CMMI1334109 and CMMI1344915, NIH Director's New Innovator
Award 1DP2OD007292 and a Wyss Institute Faculty Startup Fund to P.Y.,
and by a Wyss Institute Faculty Grant, ARO MURI grant W911NF1210420, ONR
Grants N000014091118 and N000141010241 and NIH Director's New Innovator
Award 1DP2OD004641 to W.M.S. L.L.O. is supported by an NSF Graduate
Research Fellowship. J.S. acknowledges AUFF funding from Aarhus
University and the Niels Bohr Foundation from The Royal Danish Academy
of Science. M. D. acknowledges financial support from the Danish
National Research Foundation and the Villum Foundation.
NR 48
TC 42
Z9 42
U1 8
U2 82
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1755-4330
EI 1755-4349
J9 NAT CHEM
JI Nat. Chem.
PD NOV
PY 2014
VL 6
IS 11
BP 994
EP 1002
DI 10.1038/NCHEM.2083
PG 9
WC Chemistry, Multidisciplinary
SC Chemistry
GA AS8BS
UT WOS:000344476000013
PM 25343605
ER
PT J
AU Wong, IY
Javaid, S
Wong, EA
Perk, S
Haber, DA
Toner, M
Irimia, D
AF Wong, Ian Y.
Javaid, Sarah
Wong, Elisabeth A.
Perk, Sinem
Haber, Daniel A.
Toner, Mehmet
Irimia, Daniel
TI Collective and individual migration following the epithelial-mesenchymal
transition
SO NATURE MATERIALS
LA English
DT Article
ID CANCER-CELL INVASION; EXPRESSION; MODEL; CYTOSKELETON; CONFINEMENT;
METASTASIS; ADHESION; BEHAVIOR; SNAIL; EMT
AB During cancer progression, malignant cells in the tumour invade surrounding tissues. This transformation of adherent cells to a motile phenotype has been associated with the epithelial-mesenchymal transition (EMT). Here, we show that EMT-activated cells migrate through micropillar arrays as a collectively advancing front that scatters individual cells. Individual cells with few neighbours dispersed with fast, straight trajectories, whereas cells that encountered many neighbours migrated collectively with epithelial biomarkers. We modelled these emergent dynamics using a physical analogy to phase transitions during binary-mixture solidification, and validated it using drug perturbations, which revealed that individually migrating cells exhibit diminished chemosensitivity. Our measurements also indicate a degree of phenotypic plasticity as cells interconvert between individual and collective migration. The study of multicellular behaviours with single-cell resolution should enable further quantitative insights into heterogeneous tumour invasion.
C1 [Wong, Ian Y.; Wong, Elisabeth A.; Perk, Sinem; Toner, Mehmet; Irimia, Daniel] Harvard Univ, Sch Med, Massachusetts Gen Hosp, BioMEMS Resource Ctr,Dept Surg, Charlestown, MA 02129 USA.
[Javaid, Sarah; Haber, Daniel A.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02129 USA.
[Haber, Daniel A.] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA.
RP Irimia, D (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, BioMEMS Resource Ctr,Dept Surg, Charlestown, MA 02129 USA.
EM dirimia@hms.harvard.edu
OI Irimia, Daniel/0000-0001-7347-2082; Wong, Ian Y/0000-0002-9439-2548
FU Merck Fellowship of the Damon Runyon Cancer Research Foundation
[DRG-2065-10]; Howard Hughes Medical Institute; National Institutes of
Health [CA129933, EB002503, CA135601, GM092804]
FX We thank J. Taunton for the gift of FMK-MEA, A. Besser and G. Danuser
for assistance with cell tracking, and O. Hurtado for assistance with
fabrication. This work was supported by the Merck Fellowship of the
Damon Runyon Cancer Research Foundation (DRG-2065-10) to I.Y.W., the
Howard Hughes Medical Institute to D. A. H., as well as the National
Institutes of Health under CA129933 to D. A. H., EB002503 (BioMEMS
Resource Center) to M. T., and CA135601 and GM092804 to D.I.
NR 48
TC 29
Z9 30
U1 5
U2 38
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1476-1122
EI 1476-4660
J9 NAT MATER
JI Nat. Mater.
PD NOV
PY 2014
VL 13
IS 11
BP 1063
EP 1071
DI 10.1038/NMAT4062
PG 9
WC Chemistry, Physical; Materials Science, Multidisciplinary; Physics,
Applied; Physics, Condensed Matter
SC Chemistry; Materials Science; Physics
GA AS8AC
UT WOS:000344471900015
PM 25129619
ER
PT J
AU Moverare-Skrtic, S
Henning, P
Liu, XW
Nagano, K
Saito, H
Borjesson, AE
Sjogren, K
Windahl, SH
Farman, H
Kindlund, B
Engdahl, C
Koskela, A
Zhang, FP
Eriksson, EE
Zaman, F
Hammarstedt, A
Isaksson, H
Bally, M
Kassem, A
Lindholm, C
Sandberg, O
Aspenberg, P
Savendahl, L
Feng, JQ
Tuckermann, J
Tuukkanen, J
Poutanen, M
Baron, R
Lerner, UH
Gori, F
Ohlsson, C
AF Moverare-Skrtic, Sofia
Henning, Petra
Liu, Xianwen
Nagano, Kenichi
Saito, Hiroaki
Borjesson, Anna E.
Sjogren, Klara
Windahl, Sara H.
Farman, Helen
Kindlund, Bert
Engdahl, Cecilia
Koskela, Antti
Zhang, Fu-Ping
Eriksson, Emma E.
Zaman, Farasat
Hammarstedt, Ann
Isaksson, Hanna
Bally, Marta
Kassem, Ali
Lindholm, Catharina
Sandberg, Olof
Aspenberg, Per
Savendahl, Lars
Feng, Jian Q.
Tuckermann, Jan
Tuukkanen, Juha
Poutanen, Matti
Baron, Roland
Lerner, Ulf H.
Gori, Francesca
Ohlsson, Claes
TI Osteoblast-derived WNT16 represses osteoclastogenesis and prevents
cortical bone fragility fractures
SO NATURE MEDICINE
LA English
DT Article
ID RECEPTOR-RELATED PROTEIN-5; BETA-CATENIN; TYROSINE KINASE; MINERAL
DENSITY; GENOME-WIDE; SOST GENE; DIFFERENTIATION; MASS; ACTIVATION;
CELLS
AB The WNT16 locus is a major determinant of cortical bone thickness and nonvertebral fracture risk in humans. The disability, mortality and costs caused by osteoporosis-induced nonvertebral fractures are enormous. We demonstrate here that Wnt16-deficient mice develop spontaneous fractures as a result of low cortical thickness and high cortical porosity. In contrast, trabecular bone volume is not altered in these mice. Mechanistic studies revealed that WNT16 is osteoblast derived and inhibits human and mouse osteoclastogenesis both directly by acting on osteoclast progenitors and indirectly by increasing expression of osteoprotegerin (Opg) in osteoblasts. The signaling pathway activated by WNT16 in osteoclast progenitors is noncanonical, whereas the pathway activated in osteoblasts is both canonical and noncanonical. Conditional Wnt16 inactivation revealed that osteoblast-lineage cells are the principal source of WNT16, and its targeted deletion in osteoblasts increases fracture susceptibility. Thus, osteoblast-derived WNT16 is a previously unreported key regulator of osteoclastogenesis and fracture susceptibility. These findings open new avenues for the specific prevention or treatment of nonvertebral fractures, a substantial unmet medical need.
C1 [Moverare-Skrtic, Sofia; Henning, Petra; Borjesson, Anna E.; Sjogren, Klara; Windahl, Sara H.; Farman, Helen; Kindlund, Bert; Engdahl, Cecilia; Lindholm, Catharina; Poutanen, Matti; Lerner, Ulf H.; Ohlsson, Claes] Univ Gothenburg, Sahlgrenska Acad, Ctr Bone & Arthrit Res, Inst Med, Gothenburg, Sweden.
[Liu, Xianwen; Nagano, Kenichi; Saito, Hiroaki; Baron, Roland; Gori, Francesca] Harvard Univ, Sch Dent Med, Dept Oral Med Infect & Immun, Boston, MA 02115 USA.
[Liu, Xianwen] Sichuan Univ, West China Hosp Stomatol, State Key Lab Oral Dis, Sichuan, Peoples R China.
[Liu, Xianwen] Sichuan Univ, West China Hosp Stomatol, Dept Oral & Maxillofacial Surg, Sichuan, Peoples R China.
[Koskela, Antti; Tuukkanen, Juha] Univ Oulu, Med Res Ctr, Dept Anat & Cell Biol, Oulu, Finland.
[Zhang, Fu-Ping; Poutanen, Matti] Univ Turku, Inst Biomed, Dept Physiol, Turku Ctr Dis Modeling, Turku, Finland.
[Eriksson, Emma E.; Zaman, Farasat; Savendahl, Lars] Karolinska Inst, Pediat Endocrinol Unit, Dept Womens & Childrens Hlth, Stockholm, Sweden.
[Zaman, Farasat] Univ Toronto, Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Hammarstedt, Ann] Univ Gothenburg, Sahlgrenska Acad, Lundberg Lab Diabet Res, Dept Mol & Clin Med, Gothenburg, Sweden.
[Isaksson, Hanna] Lund Univ, Dept Biomed Engn, Lund, Sweden.
[Isaksson, Hanna] Lund Univ, Dept Orthoped, Lund, Sweden.
[Bally, Marta] Chalmers, Dept Appl Phys, Div Biol Phys, S-41296 Gothenburg, Sweden.
[Kassem, Ali] Umea Univ, Umea, Sweden.
[Sandberg, Olof; Aspenberg, Per] Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden.
[Feng, Jian Q.] Texas A&M Hlth Sci Ctr, Baylor Coll Dent, Dept Biomed Sci, Dallas, TX USA.
[Tuckermann, Jan] Univ Ulm, Inst Gen Zool & Endocrinol, D-89069 Ulm, Germany.
[Baron, Roland; Gori, Francesca] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Endocrine Unit, Boston, MA USA.
RP Ohlsson, C (reprint author), Univ Gothenburg, Sahlgrenska Acad, Ctr Bone & Arthrit Res, Inst Med, Gothenburg, Sweden.
EM roland_baron@hsdm.harvard.edu; ulf.lerner@odont.umu.se;
francesca_gori@hsdm.harvard.edu; claes.ohlsson@medic.gu.se
RI Isaksson, Hanna/L-1340-2015; Bally, Marta/G-8744-2011;
OI Isaksson, Hanna/0000-0002-9690-8907; Kassem, Ali/0000-0002-1820-8518;
Bally, Marta/0000-0002-5865-8302; Engdahl, Cecilia/0000-0002-8914-0178
FU Swedish Research Council; Swedish Foundation for Strategic Research,
COMBINE; Avtal om Lakarutbildning och Forskning/Lakarutbildningsavtalet
(ALF/LUA) research grant in Gothenburg, Linkoping University, Swedish
National Graduate School in Odontological Sciences; Lundberg Foundation;
Torsten and Ragnar Soderberg's Foundation; Swedish Rheumatism
Association; Royal 80 Year Fund of King Gustav V; Novo Nordisk
Foundation; German Research Foundation [SPP 1468 Tu220/6]; University of
Turku and Biocenter Finland; US National Institutes of Health
[R01AR064724]
FX We are grateful to C. Uggla, M. Petersson, A. Hansevi, A. Lie, I.
Lundgren, B. Aleksic and the staff at the Turku Center for Disease
Modeling (TCDM) for technical assistance. We thank M. Johansson at
Bergman Labora for help with photographing the embryos. We thank R.
Brommage (Lexicon Pharmaceuticals Inc.) for providing the
Wnt164-/-,exon 1-3 mice. This study was supported
by the Swedish Research Council, the Swedish Foundation for Strategic
Research, COMBINE, the Avtal om Lakarutbildning och
Forskning/Lakarutbildningsavtalet (ALF/LUA) research grant in
Gothenburg, Linkoping University, Swedish National Graduate School in
Odontological Sciences, the Lundberg Foundation, the Torsten and Ragnar
Soderberg's Foundation, the Swedish Rheumatism Association, the Royal 80
Year Fund of King Gustav V, the Novo Nordisk Foundation and the German
Research Foundation (SPP 1468 Tu220/6, Immunobone). The work at TCDM was
supported by funding provided by University of Turku and Biocenter
Finland. This work was supported in part by a grant to R.B. from the US
National Institutes of Health (R01AR064724). The HSDM micro-CT core
facility performed the micro-CT analyses of the Wnt16-/-,exon
1-3 mice.
NR 48
TC 37
Z9 38
U1 6
U2 28
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD NOV
PY 2014
VL 20
IS 11
BP 1279
EP 1288
DI 10.1038/nm.3654
PG 10
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA AT1XM
UT WOS:000344724300017
PM 25306233
ER
PT J
AU Sistigu, A
Yamazaki, T
Vacchelli, E
Chaba, K
Enot, DP
Adam, J
Vitale, I
Goubar, A
Baracco, EE
Remedios, C
Fend, L
Hannani, D
Aymeric, L
Ma, Y
Niso-Santano, M
Kepp, O
Schultze, JL
Tuting, T
Belardelli, F
Bracci, L
La Sorsa, V
Ziccheddu, G
Sestili, P
Urbani, F
Delorenzi, M
Lacroix-Triki, M
Quidville, V
Conforti, R
Spano, JP
Pusztai, L
Poirier-Colame, V
Delaloge, S
Penault-Llorca, F
Ladoire, S
Arnould, L
Cyrta, J
Dessoliers, MC
Eggermont, A
Bianchi, ME
Pittet, M
Engblom, C
Pfirschke, C
Preville, X
Uze, G
Schreiber, RD
Chow, MT
Smyth, MJ
Proietti, E
Andre, F
Kroemer, G
Zitvogel, L
AF Sistigu, Antonella
Yamazaki, Takahiro
Vacchelli, Erika
Chaba, Kariman
Enot, David P.
Adam, Julien
Vitale, Ilio
Goubar, Aicha
Baracco, Elisa E.
Remedios, Catarina
Fend, Laetitia
Hannani, Dalil
Aymeric, Laetitia
Ma, Yuting
Niso-Santano, Mireia
Kepp, Oliver
Schultze, Joachim L.
Tueting, Thomas
Belardelli, Filippo
Bracci, Laura
La Sorsa, Valentina
Ziccheddu, Giovanna
Sestili, Paola
Urbani, Francesca
Delorenzi, Mauro
Lacroix-Triki, Magali
Quidville, Virginie
Conforti, Rosa
Spano, Jean-Philippe
Pusztai, Lajos
Poirier-Colame, Vichnou
Delaloge, Suzette
Penault-Llorca, Frederique
Ladoire, Sylvain
Arnould, Laurent
Cyrta, Joanna
Dessoliers, Marie-Charlotte
Eggermont, Alexander
Bianchi, Marco E.
Pittet, Mikael
Engblom, Camilla
Pfirschke, Christina
Preville, Xavier
Uze, Gilles
Schreiber, Robert D.
Chow, Melvyn T.
Smyth, Mark J.
Proietti, Enrico
Andre, Fabrice
Kroemer, Guido
Zitvogel, Laurence
TI Cancer cell-autonomous contribution of type I interferon signaling to
the efficacy of chemotherapy
SO NATURE MEDICINE
LA English
DT Article
ID TOLL-LIKE RECEPTOR-3; DOUBLE-STRANDED-RNA; BREAST-CANCER;
IMMUNE-RESPONSES; ANTICANCER CHEMOTHERAPY; DENDRITIC CELLS; RIG-I;
INNATE; TUMORS; GENE
AB Some of the anti-neoplastic effects of anthracyclines in mice originate from the induction of innate and T cell-mediated anticancer immune responses. Here we demonstrate that anthracyclines stimulate the rapid production of type I interferons (IFNs) by malignant cells after activation of the endosomal pattern recognition receptor Toll-like receptor 3 (TLR3). By binding to IFN-alpha and IFN-beta receptors (IFNARs) on neoplastic cells, type I IFNs trigger autocrine and paracrine circuitries that result in the release of chemokine (C-X-C motif) ligand 10 (CXCL10). Tumors lacking TIr3 or Ifnar failed to respond to chemotherapy unless type I IFN or Cxcl10, respectively, was artificially supplied. Moreover, a type I IFN-related signature predicted clinical responses to anthracycline-based chemotherapy in several independent cohorts of patients with breast carcinoma characterized by poor prognosis. Our data suggest that anthracycline-mediated immune responses mimic those induced by viral pathogens. We surmise that such 'viral mimicry' constitutes a hallmark of successful chemotherapy.
C1 [Sistigu, Antonella; Yamazaki, Takahiro; Vacchelli, Erika; Adam, Julien; Goubar, Aicha; Baracco, Elisa E.; Remedios, Catarina; Fend, Laetitia; Hannani, Dalil; Aymeric, Laetitia; Ma, Yuting; Niso-Santano, Mireia; Kepp, Oliver; Quidville, Virginie; Conforti, Rosa; Poirier-Colame, Vichnou; Delaloge, Suzette; Cyrta, Joanna; Dessoliers, Marie-Charlotte; Andre, Fabrice; Kroemer, Guido; Zitvogel, Laurence] Gustave Roussy Canc Campus, Villejuif, France.
[Sistigu, Antonella; Yamazaki, Takahiro; Remedios, Catarina; Fend, Laetitia; Hannani, Dalil; Aymeric, Laetitia; Conforti, Rosa; Poirier-Colame, Vichnou; Zitvogel, Laurence] INSERM, U1015, Villejuif, France.
[Sistigu, Antonella; Yamazaki, Takahiro; Vacchelli, Erika; Baracco, Elisa E.; Remedios, Catarina; Hannani, Dalil; Aymeric, Laetitia; Ma, Yuting; Niso-Santano, Mireia; Kepp, Oliver; Eggermont, Alexander; Andre, Fabrice; Zitvogel, Laurence] Univ Paris Saclay, Fac Med, Le Kremlin Bicetre, France.
[Sistigu, Antonella; Belardelli, Filippo; Bracci, Laura; La Sorsa, Valentina; Ziccheddu, Giovanna; Sestili, Paola; Urbani, Francesca] Ist Super Sanita, Dept Hematol Oncol & Mol Med, I-00161 Rome, Italy.
[Vacchelli, Erika; Chaba, Kariman; Enot, David P.; Baracco, Elisa E.; Ma, Yuting; Niso-Santano, Mireia; Kepp, Oliver; Kroemer, Guido] INSERM, U848, Villejuif, France.
[Chaba, Kariman; Enot, David P.; Kroemer, Guido] Ctr Rech Cordeliers, Equipe Labellisee Ligue Nationale Canc 11, Paris, France.
[Chaba, Kariman; Enot, David P.; Kroemer, Guido] Univ Paris 05, Sorbonne Paris Cite, Paris, France.
[Adam, Julien; Delaloge, Suzette; Andre, Fabrice] Gustave Roussy Canc Campus, Dept Biol & Pathol, Villejuif, France.
[Adam, Julien; Andre, Fabrice] Gustave Roussy Canc Campus, Dept Med Oncol, Villejuif, France.
[Vitale, Ilio] Regina Elena Inst Canc Res, Rome, Italy.
[Goubar, Aicha; Dessoliers, Marie-Charlotte; Andre, Fabrice] INSERM, U981, Villejuif, France.
[Fend, Laetitia; Preville, Xavier] Transgene SA, Illkirch Graffenstaden, France.
[Schultze, Joachim L.] Univ Bonn, Lab Genom & Immunoregulat Life & Med Sci LIMES, Bonn, Germany.
[Tueting, Thomas] Univ Hosp Bonn, Dept Dermatol, Lab Expt Dermatol, Bonn, Germany.
[Delorenzi, Mauro] SIB, Lausanne, Switzerland.
[Delorenzi, Mauro] Ecole Polytech Fed Lausanne, Sch Life Sci, ISREC, Natl Ctr Competence Res NCCR Mol Oncol, Lausanne, Switzerland.
[Delorenzi, Mauro] CHU Vaudois, Dept Format & Rech, Lausanne, Switzerland.
[Lacroix-Triki, Magali] Ctr Claudius Regaud, Dept Pathol, Toulouse, France.
[Conforti, Rosa; Poirier-Colame, Vichnou] Ctr Clin Invest Biotherapies Canc CICBT 507, Villejuif, France.
[Conforti, Rosa; Spano, Jean-Philippe] Hop La Pitie Salpetriere, Dept Med Oncol, Paris, France.
[Pusztai, Lajos] Yale Univ, Sch Med, New Haven, CT USA.
[Penault-Llorca, Frederique] Univ Auvergne, EA ERTICa 4677, Dept Pathol, Jean Perrin Ctr, Clermont Ferrand, France.
[Ladoire, Sylvain; Arnould, Laurent] Ctr Georges Francois Leclerc, Dept Med Oncol, Dijon, France.
[Ladoire, Sylvain; Arnould, Laurent] INSERM, Fac Med CRI 866, Dijon, France.
[Ladoire, Sylvain; Arnould, Laurent] Univ Burgundy, Dijon, France.
[Bianchi, Marco E.] San Raffaele Univ & Sci Inst, Milan, Italy.
[Pittet, Mikael; Engblom, Camilla; Pfirschke, Christina] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Pittet, Mikael; Engblom, Camilla; Pfirschke, Christina] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Uze, Gilles] Univ Montpellier 2, CNRS, UMR5235, Montpellier, France.
[Schreiber, Robert D.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA.
[Chow, Melvyn T.; Smyth, Mark J.] Queensland Inst Med Res, Herston, Qld 4006, Australia.
[Smyth, Mark J.] Univ Queensland, Sch Med, Herston, Qld, Australia.
[Sistigu, Antonella; Yamazaki, Takahiro; Vacchelli, Erika; Kroemer, Guido] Gustave Roussy Canc Campus, Metabol Platform, Villejuif, France.
[Kroemer, Guido] Hop Europeen Georges, AP HP, Paris, France.
RP Zitvogel, L (reprint author), Univ Paris Saclay, Fac Med, Le Kremlin Bicetre, France.
EM kroemer@orange.fr; laurence.zitvogel@gustaveroussy.fr
RI LACROIX-TRIKI, Magali/P-7184-2014; Smyth, Mark/H-8709-2014; Schultze,
Joachim/D-7794-2011; BRACCI, LAURA/J-8777-2016;
OI LACROIX-TRIKI, Magali/0000-0002-7157-3960; Smyth,
Mark/0000-0001-7098-7240; Schultze, Joachim/0000-0003-2812-9853; BRACCI,
LAURA/0000-0002-2535-4353; PROIETTI, ENRICO/0000-0001-9023-2072; VITALE,
ILIO/0000-0002-5918-1841; Niso-Santano, Mireia/0000-0002-6506-422X;
Sistigu, Antonella/0000-0002-2528-1238
FU Ligue Nationale contre le Cancer (Equipes labellisees); Site de
Recherche Integree sur le Cancer (IRIC) Socrates; ISREC Foundation;
Agence Nationale pour la Recherche (ANR AUTOPH, ANR Emergence); European
Commission (ArtForce); European Research Council Advanced Investigator
Grant; Fondation pour la Recherche Medicale (FRM); Institut National du
Cancer (INCa); Fondation de France; Canceropole Ile-de-France; Fondation
Bettencourt-Schueller; LabEx Immuno-Oncology and the Paris Alliance of
Cancer Research Institutes; Ligue Nationale contre le Cancer; Fondation
Association-pour-la-Recherche curie Cancer; National Health and Medical
Research Council (NH&MRC) Australia Fellowship; Victorian Cancer Agency;
Associazione Italiana Ricerca contro II Cancro (AIRC) [MFAG_13058];
Deutsche Forschungsgemeinschaft (DFG) [PF809/1-1]; Boerhinger Ingelheim;
Association Vie et Cancer; Institut national du Cancer et la Direction
Generale de l'Offre de Soins-INSERM [6043]
FX We acknowledge L. Galluzzi for help with preparation of the manuscript.
We thank P. Rameau, Y. Lecluse and M. Sanchez for assistance with FAGS
experiments, G. Schiavoni and G. D'Agostino (Istituto Superiore di
Sanita) for recombinant Ifn-alpha 1, our colleagues from the Gustave
Roussy Cancer Center and the Istituto Superiore di Sanita animal
facilities, P. Gonin, M. Macchia and E. Cardarelli. We acknowledge P.
Vielh for his help with immunohistochemical analyses and G. Stoll for
his support in statistical analyses. G.K. and L.Z. are supported by the
Ligue Nationale contre le Cancer (Equipes labellisees), Site de
Recherche Integree sur le Cancer (IRIC) Socrates, the ISREC Foundation,
Agence Nationale pour la Recherche (ANR AUTOPH, ANR Emergence), the
European Commission (ArtForce), a European Research Council Advanced
Investigator Grant (to G.K.), the Fondation pour la Recherche Medicale
(FRM), the Institut National du Cancer (INCa), the Fondation de France,
Canceropole Ile-de-France, the Fondation Bettencourt-Schueller, the
LabEx Immuno-Oncology and the Paris Alliance of Cancer Research
Institutes. A.S. is supported by Ligue Nationale contre le Cancer: D.H.
was supported-by Fondation Association-pour-la-Recherche curie Cancer.
M.J.S. was supported by a National Health and Medical Research Council
(NH&MRC) Australia Fellowship and Program Grant and a grant from the
Victorian Cancer Agency. E.P. and L.B. were supported by Associazione
Italiana Ricerca contro II Cancro (AIRC) (MFAG_13058). C.P. was
supported by the Deutsche Forschungsgemeinschaft (DFG) PF809/1-1. C.E.
was supported by Boerhinger Ingelheim. F.A. was supported by Association
Vie et Cancer. J.A. was supported by Institut national du Cancer et la
Direction Generale de l'Offre de Soins-INSERM 6043.
NR 60
TC 129
Z9 134
U1 5
U2 44
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD NOV
PY 2014
VL 20
IS 11
BP 1301
EP 1309
DI 10.1038/nm.3708
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA AT1XM
UT WOS:000344724300019
PM 25344738
ER
PT J
AU Tichauer, KM
Samkoe, KS
Gunn, JR
Kanick, SC
Hoopes, PJ
Barth, RJ
Kaufman, PA
Hasan, T
Pogue, BW
AF Tichauer, Kenneth M.
Samkoe, Kimberley S.
Gunn, Jason R.
Kanick, Stephen C.
Hoopes, P. Jack
Barth, Richard J.
Kaufman, Peter A.
Hasan, Tayyaba
Pogue, Brian W.
TI Microscopic lymph node tumor burden quantified by macroscopic
dual-tracer molecular imaging
SO NATURE MEDICINE
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; BREAST-CANCER; IN-VIVO; CORRESPONDING
METASTASES; HER3 EXPRESSION; EGFR; DIFFERENTIATION; TISSUES
AB Lymph node biopsy is employed in many cancer surgeries to identify metastatic disease and to determine cancer stage, yet morbidity and diagnostic delays associated with lymph node biopsy could be avoided if noninvasive imaging of nodal involvement were reliable. Molecular imaging has potential in this regard; however, variable delivery and nonspecific uptake of imaging tracers have made conventional approaches ineffective clinically. Here we present a method of correcting for nonspecific uptake with injection of a second untargeted tracer that allows for quantification of tumor burden in lymph nodes. We confirmed the approach in an athymic mouse model of metastatic human breast cancer by targeting epidermal growth factor receptor, a cell surface receptor overexpressed by many cancers. We observed a significant correlation between in vivo (dual-tracer) and ex vivo measures of tumor burden (r = 0.97, P < 0.01), with an ultimate sensitivity of approximately 200 cells (potentially more sensitive than conventional lymph node biopsy).
C1 [Tichauer, Kenneth M.] IIT, Dept Biomed Engn, Chicago, IL 60616 USA.
[Samkoe, Kimberley S.; Hoopes, P. Jack; Barth, Richard J.; Pogue, Brian W.] Geisel Sch Med, Dept Surg, Hanover, NH USA.
[Gunn, Jason R.; Kanick, Stephen C.; Hoopes, P. Jack; Pogue, Brian W.] Dartmouth Coll, Thayer Sch Engn, Hanover, NH 03755 USA.
[Kaufman, Peter A.] Geisel Sch Med, Dept Med, Lebanon, NH USA.
[Hasan, Tayyaba; Pogue, Brian W.] Massachusetts Gen Hosp, Wellman Ctr Photomed, Boston, MA 02114 USA.
RP Tichauer, KM (reprint author), IIT, Dept Biomed Engn, Chicago, IL 60616 USA.
EM ktichaue@iit.edu; brian.w.pogue@dartmouth.edu
FU US National Institutes of Health [R01 CA109558, R01 CA156177, U54
CA151662]; Canadian Institutes of Health Research postdoctoral
fellowship
FX This work was sponsored by US National Institutes of Health research
grants R01 CA109558, R01 CA156177, and U54 CA151662 as well as a the
Canadian Institutes of Health Research postdoctoral fellowship for
K.M.T.
NR 34
TC 21
Z9 21
U1 4
U2 17
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD NOV
PY 2014
VL 20
IS 11
BP 1348
EP 1353
DI 10.1038/nm.3732
PG 6
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA AT1XM
UT WOS:000344724300026
PM 25344739
ER
PT J
AU Bar-Nur, O
Brumbaugh, J
Verheul, C
Apostolou, E
Pruteanu-Malinici, I
Walsh, RM
Ramaswamy, S
Hochedlinger, K
AF Bar-Nur, Ori
Brumbaugh, Justin
Verheul, Cassandra
Apostolou, Effie
Pruteanu-Malinici, Iulian
Walsh, Ryan M.
Ramaswamy, Sridhar
Hochedlinger, Konrad
TI Small molecules facilitate rapid and synchronous iPSC generation
SO NATURE METHODS
LA English
DT Article
ID PLURIPOTENT STEM-CELLS; SOMATIC-CELLS; HUMAN FIBROBLASTS; DEFINED
FACTORS; VITAMIN-C; MOUSE; DIFFERENTIATION; MECHANISMS; CONVERSION;
INDUCTION
AB The reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) upon overexpression of OCT4, KLF4, SOX2 and c-MYC (OKSM) provides a powerful system to interrogate basic mechanisms of cell fate change. However, iPSC formation with standard methods is typically protracted and inefficient, resulting in heterogeneous cell populations. We show that exposure of OKSM-expressing cells to both ascorbic acid and a GSK3-beta inhibitor (AGi) facilitates more synchronous and rapid iPSC formation from several mouse cell types. AGi treatment restored the ability of refractory cell populations to yield iPSC colonies, and it attenuated the activation of developmental regulators commonly observed during the reprogramming process. Moreover, AGi supplementation gave rise to chimera-competent iPSCs after as little as 48 h of OKSM expression. Our results offer a simple modification to the reprogramming protocol, facilitating iPSC induction at unparalleled efficiencies and enabling dissection of the underlying mechanisms in more homogeneous cell populations.
C1 [Bar-Nur, Ori; Brumbaugh, Justin; Verheul, Cassandra; Apostolou, Effie; Pruteanu-Malinici, Iulian; Walsh, Ryan M.; Ramaswamy, Sridhar; Hochedlinger, Konrad] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
[Bar-Nur, Ori; Brumbaugh, Justin; Verheul, Cassandra; Apostolou, Effie; Walsh, Ryan M.; Ramaswamy, Sridhar; Hochedlinger, Konrad] Harvard Stem Cell Inst, Cambridge, MA USA.
[Bar-Nur, Ori; Brumbaugh, Justin; Verheul, Cassandra; Apostolou, Effie; Walsh, Ryan M.; Hochedlinger, Konrad] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Bar-Nur, Ori; Brumbaugh, Justin; Verheul, Cassandra; Apostolou, Effie; Walsh, Ryan M.; Hochedlinger, Konrad] Dept Stem Cell & Regenerat Biol, Cambridge, MA USA.
[Pruteanu-Malinici, Iulian; Ramaswamy, Sridhar; Hochedlinger, Konrad] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Pruteanu-Malinici, Iulian; Ramaswamy, Sridhar] Broad Inst MIT & Harvard, Cambridge, MA USA.
RP Hochedlinger, K (reprint author), Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
EM khochedlinger@mgh.harvard.edu
FU Gruss-Lipper postdoctoral fellowship; US National Institutes of Health
(NIH) [R01HD058013]; Howard Hughes Medical Institute; MGH Executive
Committee on Research; NIH [1F32HD078029-01A1]
FX We thank members of the Hochedlinger lab for helpful suggestions and
critical reading of the manuscript. We thank M. Borkent for providing
study material and to A. Foudi and D. Kramer for scientific discussion.
We thank L. Prickett, M. Weglarz and K. Folz-Donahue at the
Massachusetts General Hospital/Harvard Stem Cell Institute flow
cytometry core. O.B.-N. was supported by a Gruss-Lipper postdoctoral
fellowship. Support to K.H. was from the US National Institutes of
Health (NIH; R01HD058013) and the Howard Hughes Medical Institute. J.B.
is grateful for support from the Tosteson Fund for Medical Discovery
Post-doctoral Fellowship by the MGH Executive Committee on Research and
NIH (1F32HD078029-01A1).
NR 41
TC 28
Z9 29
U1 1
U2 27
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
EI 1548-7105
J9 NAT METHODS
JI Nat. Methods
PD NOV
PY 2014
VL 11
IS 11
BP 1170
EP 1176
DI 10.1038/NMETH.3142
PG 7
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA AS9SA
UT WOS:000344580600025
PM 25262205
ER
PT J
AU Sachdev, PS
Blacker, D
Blazer, DG
Ganguli, M
Jeste, DV
Paulsen, JS
Petersen, RC
AF Sachdev, Perminder S.
Blacker, Deborah
Blazer, Dan G.
Ganguli, Mary
Jeste, Dilip V.
Paulsen, Jane S.
Petersen, Ronald C.
TI Classifying neurocognitive disorders: the DSM-5 approach
SO NATURE REVIEWS NEUROLOGY
LA English
DT Review
ID MILD COGNITIVE IMPAIRMENT; ALZHEIMERS ASSOCIATION WORKGROUPS;
DIAGNOSTIC-CRITERIA; FRONTOTEMPORAL DEMENTIA; NATIONAL INSTITUTE;
VASCULAR DEMENTIA; DISEASE; RECOMMENDATIONS; GUIDELINES
AB Neurocognitive disorders-including delirium, mild cognitive impairment and dementia-are characterized by decline from a previously attained level of cognitive functioning. These disorders have diverse clinical characteristics and aetiologies, with Alzheimer disease, cerebrovascular disease, Lewy body disease, frontotemporal degeneration, traumatic brain injury, infections, and alcohol abuse representing common causes. This diversity is reflected by the variety of approaches to classifying these disorders, with separate groups determining criteria for each disorder on the basis of aetiology. As a result, there is now an array of terms to describe cognitive syndromes, various definitions for the same syndrome, and often multiple criteria to determine a specific aetiology. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) provides a common framework for the diagnosis of neurocognitive disorders, first by describing the main cognitive syndromes, and then defining criteria to delineate specific aetiological subtypes of mild and major neurocognitive disorders. The DSM-5 approach builds on the expectation that clinicians and research groups will welcome a common language to deal with the neurocognitive disorders. As the use of these criteria becomes more widespread, a common international classification for these disorders could emerge for the first time, thus promoting efficient communication among clinicians and researchers.
C1 [Sachdev, Perminder S.] Univ New S Wales, Prince Wales Hosp, Ctr Hlth Brain Ageing, Sch Psychiat, Randwick, NSW 2031, Australia.
[Blacker, Deborah] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Psychiat, Boston, MA 02215 USA.
[Blazer, Dan G.] Duke Univ, Duke Inst Brain Sci, Durham, NC 27710 USA.
[Ganguli, Mary] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15213 USA.
[Jeste, Dilip V.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Paulsen, Jane S.] Univ Iowa, Carver Coll Med, Iowa City, IA 52242 USA.
[Petersen, Ronald C.] Mayo Clin, Rochester, MN 55905 USA.
RP Sachdev, PS (reprint author), Univ New S Wales, Prince Wales Hosp, Ctr Hlth Brain Ageing, Sch Psychiat, Barker St, Randwick, NSW 2031, Australia.
EM p.sachdev@unsw.edu.au
RI MORAN, CATHERINE/C-9539-2015;
OI Sachdev, Perminder/0000-0002-9595-3220
FU National Institute on Aging, the National Institutes of Health;
Department of Health and Human Services, USA [K07 AG044395]; National
Institute of Mental Health, USA [R01 MH099987]; Sam and Rose Stein
Institute for Research on Aging; National Health and Medical Research
Council of Australia [568969]
FX The authors would like to thank Prof. Igor Grant, the members of the
DSM-5 Task Force and the other Work Groups, as well as many external
advisers and consultants who provided invaluable input to the
development of the classification. M.G. was supported in part by the
National Institute on Aging, the National Institutes of Health, and the
Department of Health and Human Services, USA (grant K07 AG044395).
D.V.J. was supported in part by the National Institute of Mental Health,
USA (grant R01 MH099987), and by the Sam and Rose Stein Institute for
Research on Aging. P.S. was supported in part by the National Health and
Medical Research Council of Australia (grant 568969).
NR 34
TC 26
Z9 27
U1 1
U2 35
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4758
EI 1759-4766
J9 NAT REV NEUROL
JI Nat. Rev. Neurol.
PD NOV
PY 2014
VL 10
IS 11
BP 634
EP 642
DI 10.1038/nrneurol.2014.181
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA AT2LU
UT WOS:000344767200006
PM 25266297
ER
PT J
AU Hsu, JJ
Katz, R
Ix, JH
de Boer, IH
Kestenbaum, B
Shlipak, MG
AF Hsu, Jeffrey J.
Katz, Ronit
Ix, Joachim H.
de Boer, Ian H.
Kestenbaum, Bryan
Shlipak, Michael G.
TI Association of fibroblast growth factor-23 with arterial stiffness in
the Multi-Ethnic Study of Atherosclerosis
SO NEPHROLOGY DIALYSIS TRANSPLANTATION
LA English
DT Article
DE ABI; arterial elasticity; arterial stiffness; FGF-23; pulse pressure
ID CHRONIC KIDNEY-DISEASE; ANKLE-BRACHIAL INDEX; CARDIOVASCULAR EVENTS;
PULSE PRESSURE; ALL-CAUSE; MORTALITY; CALCIFICATION; HEART; RISK;
COMMUNITY
AB Serum fibroblast growth factor-23 (FGF-23) is associated with cardiovascular disease (CVD), yet the mechanisms remain uncertain. Our objective was to determine whether higher FGF-23 concentrations are associated with arterial stiffness.
In this cross-sectional study, serum FGF-23 concentrations were measured in 5977 participants without known CVD in the Multi-Ethnic Study of Atherosclerosis. The primary outcomes of interest were large (LAE) and small artery elasticity (SAE), pulse pressure and ankle-brachial index (ABI) > 1.30. LAE and SAE were measured by pulse contour analysis of the radial artery. Pulse pressure was measured with an automated sphygmomanometer using the average of two resting blood pressure measurements. ABI was calculated as the ratio of the ankle and brachial systolic blood pressures.
Serum FGF-23 concentrations were not significantly associated with LAE [relative difference (RD) per doubling: 0%; 95% confidence interval (CI): -2-1%], SAE (RD per doubling: 0%; 95% CI: -3-2%), pulse pressure (beta per doubling: 0.44; 95% CI: -0.31-1.19), or a high ABI (odds ratio per doubling: 1.14; 95% CI: 0.84-1.55). Findings were similar irrespective of chronic kidney disease status.
Higher serum FGF-23 concentrations are not associated with arterial stiffness, as measured by pulse pressure, LAE, SAE or high ABI, in a community-based population without CVD.
C1 [Hsu, Jeffrey J.; Shlipak, Michael G.] Univ Calif San Francisco, San Francisco VA Med Ctr, Div Gen Internal Med, San Francisco, CA 94143 USA.
[Ix, Joachim H.] Univ Calif San Diego, Dept Med, Div Nephrol, La Jolla, CA 92093 USA.
[Katz, Ronit] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[de Boer, Ian H.; Kestenbaum, Bryan] Univ Washington, Dept Med, Div Nephrol, Seattle, WA 98195 USA.
RP Shlipak, MG (reprint author), Univ Calif San Francisco, San Francisco VA Med Ctr, Div Gen Internal Med, San Francisco, CA 94143 USA.
EM michael.shlipak@ucsf.edu
FU National Institute on Aging (NIA) [5R01-AG-027002-06]; National Heart,
Lung and Blood Institute [5R01-AG-027002-06]; UCSF Department of
Medicine
FX The authors thank the other investigators, the staff and the
participants of MESA for their valuable contributions. A full list of
participating MESA investigators and institutions can be found at
http://www.mesa-nhlbi.org. This research was supported by grants
5R01-AG-027002-06 from the National Institute on Aging (NIA) and
R01-HL-096875 from the National Heart, Lung and Blood Institute, and the
UCSF Department of Medicine.
NR 33
TC 9
Z9 12
U1 0
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0931-0509
EI 1460-2385
J9 NEPHROL DIAL TRANSPL
JI Nephrol. Dial. Transplant.
PD NOV
PY 2014
VL 29
IS 11
BP 2099
EP 2105
DI 10.1093/ndt/gfu101
PG 7
WC Transplantation; Urology & Nephrology
SC Transplantation; Urology & Nephrology
GA AT0KP
UT WOS:000344625400019
PM 24782533
ER
PT J
AU Reardon, DA
Freeman, G
Wu, C
Chiocca, EA
Wucherpfennig, KW
Wen, PY
Fritsch, EF
Curry, WT
Sampson, JH
Dranoff, G
AF Reardon, David A.
Freeman, Gordon
Wu, Catherine
Chiocca, E. Antonio
Wucherpfennig, Kai W.
Wen, Patrick Y.
Fritsch, Edward F.
Curry, William T., Jr.
Sampson, John H.
Dranoff, Glenn
TI Immunotherapy advances for glioblastoma
SO NEURO-ONCOLOGY
LA English
DT Review
DE glioblastoma; immune checkpoint; immunosuppression; immunotherapy;
vaccine
ID GROWTH-FACTOR RECEPTOR; CENTRAL-NERVOUS-SYSTEM; REGULATORY T-CELLS;
NEWLY-DIAGNOSED GLIOBLASTOMA; CHIMERIC-ANTIGEN-RECEPTOR; ANTITUMOR
IMMUNE-RESPONSES; RESISTANT PROSTATE-CANCER; COLONY-STIMULATING FACTOR;
RELAPSED MALIGNANT GLIOMA; DOSE-ESCALATION TRIAL
AB Survival for patients with glioblastoma, the most common high-grade primary CNS tumor, remains poor despite multiple therapeutic interventions including intensifying cytotoxic therapy, targeting dysregulated cell signaling pathways, and blocking angiogenesis. Exciting, durable clinical benefits have recently been demonstrated for a number of other challenging cancers using a variety of immunotherapeutic approaches. Much modern research confirms that the CNS is immunoactive rather than immunoprivileged. Preliminary results of clinical studies demonstrate that varied vaccine strategies have achieved encouraging evidence of clinical benefit for glioblastoma patients, although multiple variables will likely require systematic investigation before optimal outcomes are realized. Initial preclinical studies have also revealed promising results with other immunotherapies including cell-based approaches and immune checkpoint blockade. Clinical studies to evaluate a wide array of immune therapies for malignant glioma patients are being rapidly developed. Important considerations going forward include optimizing response assessment and identifiying correlative biomarkers for predict therapeutic benefit. Finally, the potential of complementary combinatorial immunotherapeutic regimens is highly exciting and warrants expedited investigation.
C1 [Reardon, David A.; Wen, Patrick Y.] Dana Farber Brigham & Womens Canc Ctr, Ctr Neurooncol, Boston, MA USA.
[Freeman, Gordon; Wu, Catherine; Wucherpfennig, Kai W.] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02215 USA.
[Reardon, David A.; Wu, Catherine] Dana Farber Brigham & Womens Canc Ctr, Dept Med Oncol, Boston, MA USA.
[Chiocca, E. Antonio] Brigham & Womens Hosp, Dept Neurosurg, Boston, MA 02115 USA.
[Wen, Patrick Y.] Brigham & Womens Hosp, Div Neurooncol, Dept Neurol, Boston, MA 02115 USA.
[Sampson, John H.] Duke Univ, Med Ctr, Div Neurosurg, Dept Surg, Durham, NC 27710 USA.
[Curry, William T., Jr.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
[Wu, Catherine; Fritsch, Edward F.; Dranoff, Glenn] Dana Farber Brigham & Womens Canc Ctr, Dept Med Oncol, Boston, MA USA.
[Wu, Catherine; Fritsch, Edward F.; Dranoff, Glenn] Dana Farber Brigham & Womens Canc Ctr, Canc Vaccine Ctr, Boston, MA USA.
[Dranoff, Glenn] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
RP Reardon, DA (reprint author), Dana Farber Canc Inst, Ctr Neurooncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM david_reardon@dfci.harvard.edu
FU Celldex Therapeutics; Bristol-= 60 y, codeleted), class IV (age 43-59 y, not codeleted, not frontal lobe tumor or age 60-69 y, not codeleted), and class V (age >= 70 y, not codeleted). Survival differences were highly significant (P<.0001), with medians ranging from 9.3 years (95% CI: 8.4-16.0) for class I to 0.6 years (95% CI: 0.5-0.9) for class V.
Conclusions. These 5 distinct classification groups were defined using prognostic factors typically obtained during routine management of patients with anaplastic oligodendroglial tumors. Validation in a prospective clinical trial may better differentiate patients with respect to treatment outcome.
C1 [Iwamoto, Fabio M.; Abrey, Lauren E.; DeAngelis, Lisa M.; Lassman, Andrew B.] Mem Sloan Kettering Canc Ctr, Dept Neurol, New York, NY 10021 USA.
[Jhanwar, Suresh C.; Rosenblum, Marc K.] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Panageas, Katherine S.; Reiner, Anne S.] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
Mem Sloan Kettering Canc Ctr, Brain Tumor 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, Dept Pathol, Houston, TX 77030 USA.
[Eichler, April F.; Louis, David N.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Eichler, April F.; Louis, David N.] Harvard Univ, Sch Med, Boston, MA USA.
[Paleologos, Nina A.] Univ Chicago, Pritzker Sch Med, NorthShore Univ Hlth Syst, 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. Gregory; Urgoiti, Gloria B. Roldan] Univ Calgary, Calgary, AB, Canada.
[Wen, Patrick Y.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Wen, Patrick Y.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ligon, Keith L.] Brigham & Womens Hosp, Ctr Mol Oncol Pathol, Dana Farber Canc Inst, Childrens Hosp Boston, Boston, MA 02115 USA.
[Schiff, David] Univ Virginia Hlth Syst, Charlottesville, VA USA.
[Robins, H. Ian; Rocque, Brandon G.] Univ Wisconsin, Madison, WI USA.
[Chamberlain, Marc C.] Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
[Chamberlain, Marc C.] Univ Washington, Seattle Canc Care Alliance, Seattle, WA 98195 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.
[Kamar, Francois G.] Univ St Esprit de Kaslik, Byblos, Lebanon.
RP Lassman, AB (reprint author), Columbia Univ, Med Ctr, 710 W 168th St, New York, NY 10032 USA.
EM ABL7@cumc.columbia.edu
OI Reiner, Anne/0000-0002-1258-6112; kamar , francois/0000-0001-8470-5515
FU [P30 CA008748]; [P30 CA013696-40]
FX Funding for development of the initial dataset was described previously.
In addition, K. S. P. and A. S. R. were supported in part by P30
CA008748 and A. B. L. in part by P30 CA013696-40. Funding sources had no
access to patient data and no role in conceiving or designing the study
or in data collection, analysis, or interpretation of results.
NR 38
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
EI 1523-5866
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2014
VL 16
IS 11
BP 1541
EP 1546
DI 10.1093/neuonc/nou083
PG 6
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA AT0MX
UT WOS:000344631200013
PM 24997140
ER
PT J
AU Aizer, AA
Arvold, ND
Catalano, P
Claus, EB
Golby, AJ
Johnson, MD
Al-Mefty, O
Wen, PY
Reardon, DA
Lee, EQ
Nayak, L
Rinne, ML
Beroukhim, R
Weiss, SE
Ramkissoon, SH
Abedalthagafi, M
Santagata, S
Dunn, IF
Alexander, BM
AF Aizer, Ayal A.
Arvold, Nils D.
Catalano, Paul
Claus, Elizabeth B.
Golby, Alexandra J.
Johnson, Mark D.
Al-Mefty, Ossama
Wen, Patrick Y.
Reardon, David A.
Lee, Eudocia Q.
Nayak, Lakshmi
Rinne, Mikael L.
Beroukhim, Rameen
Weiss, Stephanie E.
Ramkissoon, Shakti H.
Abedalthagafi, Malak
Santagata, Sandro
Dunn, Ian F.
Alexander, Brian M.
TI Adjuvant radiation therapy, local recurrence, and the need for salvage
therapy in atypical meningioma
SO NEURO-ONCOLOGY
LA English
DT Article
DE atypical meningioma; radiation; recurrence; salvage
ID FRACTIONATED STEREOTACTIC RADIOTHERAPY; GROSS-TOTAL RESECTION;
ANAPLASTIC MENINGIOMAS; CLINICAL ARTICLE; INTRACRANIAL MENINGIOMAS;
NONBENIGN MENINGIOMAS; RADIOSURGERY; OUTCOMES
AB Background. The impact of adjuvant radiation in patients with atypical meningioma remains poorly defined. We sought to determine the impact of adjuvant radiation therapy in this population.
Methods. We identified 91 patients with World Health Organization grade II (atypical) meningioma managed at Dana-Farber/Brigham and Women's Cancer Center between 1997 and 2011. A propensity score model incorporating age at diagnosis, gender, Karnofsky performance status, tumor location, tumor size, reason for diagnosis, and era of treatment was constructed using logistic regression for the outcome of receipt versus nonreceipt of radiation therapy. Propensity scores were then used as continuous covariates in a Cox proportional hazards model to determine the adjusted impact of adjuvant radiation therapy on both local recurrence and the combined endpoint of use of salvage therapy and death due to progressive meningioma.
Results. The median follow-up in patients without recurrent disease was 4.9 years. After adjustment for pertinent confounding variables, radiation therapy was associated with decreased local recurrence in those undergoing gross total resection (hazard ratio, 0.25; 95% CI, 0.07-0.96; P=.04). No differences in overall survival were seen in patients who did and did not receive radiation therapy.
Conclusion. Patients who have had a gross total resection of an atypical meningioma should be considered for adjuvant radiation therapy given the improvement in local control. Multicenter, prospective trials are required to definitively evaluate the potential impact of radiation therapy on survival in patients with atypical meningioma.
C1 [Aizer, Ayal A.] Brigham & Womens Hosp, Harvard Radiat Oncol Program, Boston, MA 02115 USA.
[Arvold, Nils D.; Alexander, Brian M.] Dana Farber Brigham & Womens Canc Ctr, Boston, MA 02215 USA.
[Catalano, Paul] Dana Farber Canc Inst, Dept Biostat, Boston, MA 02115 USA.
[Claus, Elizabeth B.; Golby, Alexandra J.; Johnson, Mark D.; Al-Mefty, Ossama; Dunn, Ian F.] Brigham & Womens Hosp, Dept Neurosurg, Boston, MA 02115 USA.
[Wen, Patrick Y.; Reardon, David A.; Lee, Eudocia Q.; Nayak, Lakshmi; Rinne, Mikael L.; Beroukhim, Rameen] Dana Farber Brigham & Womens Canc Ctr, Ctr Neurooncol, Boston, MA 02215 USA.
[Weiss, Stephanie E.] Fox Chase Canc Ctr, Dept Radiat Oncol, Philadelphia, PA 19111 USA.
[Ramkissoon, Shakti H.; Santagata, Sandro] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
RP Alexander, BM (reprint author), Dana Farber Brigham & Womens Canc Ctr, Dept Radiat Oncol, 450 Brookline Ave, Boston, MA 02215 USA.
EM bmalexander@lroc.harvard.edu
NR 22
TC 13
Z9 13
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
EI 1523-5866
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD NOV
PY 2014
VL 16
IS 11
BP 1547
EP 1553
DI 10.1093/neuonc/nou098
PG 7
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA AT0MX
UT WOS:000344631200014
PM 24891451
ER
PT J
AU Chen, TC
Chen, PP
Francis, BA
Junk, AK
Smith, SD
Singh, K
Lin, SC
AF Chen, Teresa C.
Chen, Philip P.
Francis, Brian A.
Junk, Anna K.
Smith, Scott D.
Singh, Kuldev
Lin, Shan C.
TI Pediatric Glaucoma Surgery A Report by the American Academy of
Ophthalmology
SO OPHTHALMOLOGY
LA English
DT Article
ID PRIMARY CONGENITAL GLAUCOMA; DIODE-LASER CYCLOPHOTOCOAGULATION; CHRONIC
CHILDHOOD UVEITIS; AHMED VALVE IMPLANTATION; TERM-FOLLOW-UP; 1ST 2
YEARS; MITOMYCIN-C; 360-DEGREES TRABECULOTOMY; PRIMARY TRABECULECTOMY;
SURGICAL TECHNIQUE
AB Objective: To review the current published literature to evaluate the success rates and long-term problems associated with surgery for pediatric glaucoma.
Methods: Literature searches of the PubMed and Cochrane Library databases were last conducted in May 2012. The search yielded 838 potentially relevant citations, of which 273 were in non-English languages. The titles and abstracts of these articles were reviewed by the authors, and 364 were selected for possible further review. Members of the Ophthalmic Technology Assessment Committee Glaucoma Panel reviewed the full text of these articles and used the 36 that met inclusion and exclusion criteria for this Ophthalmic Technology Assessment. There were no studies on the topic that provided level I evidence. The assessment included only level II and level III studies.
Results: Surgeons treat pediatric glaucoma most commonly with goniotomy, trabeculotomy, trabeculectomy, combined trabeculotomy and trabeculectomy, tube shunt surgery, cyclodestruction, and deep sclerectomy. Certain surgical options seem better for specific diagnoses, such as primary congenital glaucoma, aphakic glaucoma, and glaucomas associated with other ocular or systemic anomalies.
Conclusions: There are many surgical options for the treatment of the pediatric glaucomas. The relative efficacy of these various procedures for particular diagnoses and clinical situations should be weighed against the specific risks associated with the procedures for individual patients. (C) 2014 by the American Academy of Ophthalmology.
C1 [Chen, Teresa C.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Dept Ophthalmol,Glaucoma Serv, Boston, MA USA.
[Chen, Philip P.] Univ Washington, Dept Ophthalmol, Seattle, WA 98195 USA.
[Francis, Brian A.] Univ Calif Los Angeles, David Geffen Sch Med, Doheny Eye Inst, Dept Ophthalmol, Los Angeles, CA 90095 USA.
[Junk, Anna K.] Univ Miami, Miller Sch Med, Bascom Palmer Eye Inst, Miami, FL 33136 USA.
[Smith, Scott D.] Cleveland Clin Abu Dhabi, Abu Dhabi, U Arab Emirates.
[Singh, Kuldev] Stanford Univ, Sch Med, Stanford, CA USA.
[Lin, Shan C.] Univ Calif San Francisco, Dept Ophthalmol, San Francisco, CA USA.
RP Chen, TC (reprint author), Amer Acad Ophthalmol, Qual Care & Knowledge Base Dev, POB 7424, San Francisco, CA 94120 USA.
FU American Academy of Ophthalmology
FX Funded without commercial support by the American Academy of
Ophthalmology.
NR 51
TC 12
Z9 12
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0161-6420
EI 1549-4713
J9 OPHTHALMOLOGY
JI Ophthalmology
PD NOV
PY 2014
VL 121
IS 11
BP 2107
EP 2115
DI 10.1016/j.ophtha.2014.05.010
PG 9
WC Ophthalmology
SC Ophthalmology
GA AS8DM
UT WOS:000344480400014
PM 25066765
ER
PT J
AU Fernandes, J
Austen, WG
AF Fernandes, Justin
Austen, William G., Jr.
TI Reply: Prevention of Capsular Contracture with Photochemical Tissue
Passivation
SO PLASTIC AND RECONSTRUCTIVE SURGERY
LA English
DT Letter
C1 [Fernandes, Justin; Austen, William G., Jr.] Massachusetts Gen Hosp, Div Plast & Reconstruct Surg, Boston, MA 02114 USA.
RP Austen, WG (reprint author), Massachusetts Gen Hosp, Div Plast & Reconstruct Surg, 15 Parkman St,WAC 435, Boston, MA 02114 USA.
EM wausten@partners.org
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 0032-1052
EI 1529-4242
J9 PLAST RECONSTR SURG
JI Plast. Reconstr. Surg.
PD NOV
PY 2014
VL 134
IS 5
BP 849E
EP 850E
DI 10.1097/PRS.0000000000000628
PG 2
WC Surgery
SC Surgery
GA AS9EN
UT WOS:000344546000026
PM 25347665
ER
PT J
AU Goldstein, JM
Cherkerzian, S
Seidman, LJ
Donatelli, JAL
Remington, AG
Tsuang, MT
Hornig, M
Buka, SL
AF Goldstein, J. M.
Cherkerzian, S.
Seidman, L. J.
Donatelli, J. -A. L.
Remington, A. G.
Tsuang, M. T.
Hornig, M.
Buka, S. L.
TI Prenatal maternal immune disruption and sex-dependent risk for psychoses
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Fetal programming; inflammation; psychoses; schizophrenia; sex
differences
ID PITUITARY-ADRENAL AXIS; NEW-ENGLAND FAMILY; BRAIN-DEVELOPMENT;
ANIMAL-MODELS; PROINFLAMMATORY CYTOKINES; INFLAMMATORY RESPONSE; ADULT
SCHIZOPHRENIA; STEROID-HORMONES; NERVOUS-SYSTEM; FETAL-BRAIN
AB Background. Previous studies suggest that abnormalities in maternal immune activity during pregnancy alter the offspring's brain development and are associated with increased risk for schizophrenia (SCZ) dependent on sex.
Method. Using a nested case-control design and prospectively collected prenatal maternal sera from which interleukin (IL)-1 beta, IL-8, IL-6, tumor necrosis factor (TNF)-alpha and IL-10 were assayed, we investigated sex-dependent associations between these cytokines and 88 psychotic cases [SCZ=44; affective psychoses (AP)=44] and 100 healthy controls from a pregnancy cohort followed for >40 years. Analyses included sex-stratified non-parametric tests adjusted for multiple comparisons to screen cytokines associated with SCZ risk, followed by deviant subgroup analyses using generalized estimating equation (GEE) models.
Results. There were higher prenatal IL-6 levels among male SCZ than male controls, and lower TNF-alpha levels among female SCZ than female controls. The results were supported by deviant subgroup analyses with significantly more SCZ males with high IL-6 levels (>highest quartile) compared with controls [odd ratio (OR)(75)=3.33, 95% confidence interval (CI) 1.13-9.82], and greater prevalence of low TNF-alpha levels (2.5, >4.0, and >6.5 ng/mL).
METHODS We conducted a cross-sectional study of 323,426 men aged >= 65 years who had a screening PSA test in 2003 at a Veterans Affairs facility. The primary predictor was the use of statin medications at the time of index screening PSA test. The main outcome was the screening PSA value. Poisson regressions were performed to calculate adjusted relative risks for having an abnormal screening PSA result according to statin usage.
RESULTS Percentages of men with PSA results exceeding commonly used thresholds of >2.5, >4.0, and >6.5 ng/mL were 21.0%, 7.6%, and 1.6%, respectively. These percentages decreased with statin use, increasing statin dose, duration of statin use, and potency of the statin. For example, after adjusting for age, the percentage of men having a PSA level >4.0 ng/mL ranged from 8.2% in non-statin users to 6.2% in men prescribed with >40 mg of simvastatin dose. Adjusted relative risks of having a PSA level >4.0 ng/mL were 0.89 (95% confidence interval [CI], 0.86-0.93), 0.87 (95% CI, 0.84-0.91), and 0.83 (95% CI, 0.80-0.87), respectively for men on simvastatin dose of 5-20, >20-40, and >40 mg vs non-statin users.
CONCLUSION Statin use is associated with a reduction in the probability that an older man will have an abnormal screening PSA result, regardless of the PSA threshold. This reduction is more pronounced with higher statin dose, longer statin duration, and higher statin potency. (C) 2014 Elsevier Inc.
C1 Univ Calif San Francisco, Div Geriatr, San Francisco, CA 94121 USA.
Univ Calif San Francisco, San Francisco VA Med Ctr, San Francisco, CA 94121 USA.
Duke Univ, Durham VA Med Ctr, Durham, NC USA.
Duke Univ, Duke Prostate Ctr, Durham, NC USA.
Univ New Mexico, New Mexico VA Hlth Care Syst, Albuquerque, NM 87131 USA.
Univ New Mexico, Dept Med, Albuquerque, NM 87131 USA.
RP Shi, Y (reprint author), Univ Calif San Francisco, VA Med Ctr, Div Geriatr, 181G,4150 Clement St, San Francisco, CA 94121 USA.
EM Ying.Shi2@va.gov
FU National Cancer Institute at the National Institutes of Health [R01
CA134425]; National Institute on Aging at the National Institutes of
Health [K24AG041180, K24CA160653]; New Mexico Veterans Affairs Health
Care System
FX This work was supported by grant R01 CA134425 from the National Cancer
Institute at the National Institutes of Health (Louise C. Walter,
Stephen J. Freedland, and Richard M. Hoffman), by grant K24AG041180 from
the National Institute on Aging at the National Institutes of Health
(Louise C. Walter), by grant K24CA160653 from the National Cancer
Institute at the National Institutes of Health (Stephen J. Freedland),
and by the New Mexico Veterans Affairs Health Care System (Richard M.
Hoffman).
NR 29
TC 3
Z9 3
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0090-4295
EI 1527-9995
J9 UROLOGY
JI Urology
PD NOV
PY 2014
VL 84
IS 5
BP 1058
EP 1064
DI 10.1016/j.urology.2014.06.069
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA AS8CU
UT WOS:000344478700024
PM 25443902
ER
PT J
AU Shi, Y
Boscardin, WJ
Walter, LC
AF Shi, Ying
Boscardin, W. John
Walter, Louise C.
TI Statin Medications Are Associated With a Lower Probability of Having an
Abnormal Screening Prostate-specific Antigen Result REPLY
SO UROLOGY
LA English
DT Editorial Material
C1 [Shi, Ying] San Francisco VA Med Ctr, Div Geriatr, San Francisco, CA 94121 USA.
Univ Calif San Francisco, San Francisco, CA 94143 USA.
RP Shi, Y (reprint author), San Francisco VA Med Ctr, Div Geriatr, San Francisco, CA 94121 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0090-4295
EI 1527-9995
J9 UROLOGY
JI Urology
PD NOV
PY 2014
VL 84
IS 5
BP 1065
EP 1065
DI 10.1016/j.urology.2014.06.072
PG 1
WC Urology & Nephrology
SC Urology & Nephrology
GA AS8CU
UT WOS:000344478700026
PM 25443904
ER
PT J
AU Zhang, Q
Siroky, M
Yang, JH
Zhao, ZH
Azadzoi, K
AF Zhang, Qi
Siroky, Mike
Yang, Jing-Hua
Zhao, Zuohui
Azadzoi, Kazem
TI Effects of Ischemia and Oxidative Stress on Bladder Purinoceptors
Expression
SO UROLOGY
LA English
DT Article
ID PURINERGIC RECEPTOR EXPRESSION; URINARY-TRACT SYMPTOMS; P2X RECEPTORS;
DETRUSOR OVERACTIVITY; ATROPINE-RESISTANT; RAT; CONTRACTIONS; PRESSURE;
CULTURES; RELEASE
AB OBJECTIVE To study the effects of chronic ischemia on bladder purinoceptors. A close correlation between bladder ischemia and lower urinary tract symptoms has been reported. Purinoceptors contribute to important aspects of bladder function including sensation, neural signaling, and voiding contraction. Our goal was to examine purinoceptors expression in the ischemic overactive bladder.
MATERIALS AND METHODS Moderate bladder ischemia was produced in rabbits by creating bilateral iliac artery atherosclerosis. After 8 weeks, bladder blood flow was measured, and cystometrograms were obtained. Bladder tissues from 8-week ischemic and age-matched control bladders were processed for the analysis of oxidative stress markers, P2X and P2Y purinoceptors expression, and transmission electron microscopy.
RESULTS Arterial atherosclerosis significantly decreased bladder blood flow. Markers of oxidative stress characterized by increased levels of advanced oxidation protein products and malondialdehyde were evident in the ischemic bladder tissues. Chronic ischemia and oxidative stress decreased the bladder capacity and increased spontaneous bladder contractions. Bladder pressure at micturition and intravesical pressure rise during contractions tended to be greater in the ischemic bladder but did not reach significance. Transmission electron microscopy showed smooth muscle cell and microvasculature structural damage and diffuse fibrosis. These changes in the ischemic bladder were associated with significant increases in purinoceptors P2X1, P2X2, P2X3, P2X4, P2X5, and P2X7 expression. The P2Y isoforms were not expressed in the rabbit bladder.
CONCLUSION Structural and functional changes in the chronically ischemic bladder were associated with upregulation of P2X receptor isoforms. Increased P2X expression may play a role in ischemia-induced bladder overactivity and noncompliance.
C1 [Zhang, Qi; Siroky, Mike; Yang, Jing-Hua; Zhao, Zuohui; Azadzoi, Kazem] Boston Univ, Sch Med, VA Boston Healthcare Syst, Dept Urol, Boston, MA 02130 USA.
RP Azadzoi, K (reprint author), Boston Univ, VA Boston Healthcare Syst, Sch Med, Bldg 1A,Room 315 151,150 South Huntington Ave, Boston, MA 02130 USA.
EM kazadzoi@bu.edu
FU grant BLR&D MERIT from U.S. Department of Veterans Affairs
[1I01BX001428-01A1]
FX This study was supported by grant BLR&D MERIT 1I01BX001428-01A1 from the
U.S. Department of Veterans Affairs.
NR 30
TC 1
Z9 1
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0090-4295
EI 1527-9995
J9 UROLOGY
JI Urology
PD NOV
PY 2014
VL 84
IS 5
AR 1249.e1
DI 10.1016/j.urology.2014.07.023
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA AS8CU
UT WOS:000344478700077
PM 25219364
ER
PT J
AU Pang, J
Borjeson, TM
Muthupalani, S
Ducore, RM
Carr, CA
Feng, Y
Sullivan, MP
Cristofaro, V
Luo, J
Lindstrom, JM
Fox, JG
AF Pang, J.
Borjeson, T. M.
Muthupalani, S.
Ducore, R. M.
Carr, C. A.
Feng, Y.
Sullivan, M. P.
Cristofaro, V.
Luo, J.
Lindstrom, J. M.
Fox, J. G.
TI Megaesophagus in a Line of Transgenic Rats: A Model of Achalasia
SO VETERINARY PATHOLOGY
LA English
DT Article
DE achalasia; esophagus; imaging; immunohistochemistry; megaesophagus;
muscle studies; Pvrl3; ultrastructure; rat
ID LOWER ESOPHAGEAL SPHINCTER; ACQUIRED MYASTHENIA-GRAVIS; MYENTERIC
GANGLIAL CELLS; NITRIC-OXIDE SYNTHASE; RIGHT AORTIC-ARCH; CONGENITAL
ACHALASIA; OUTFLOW OBSTRUCTION; RISK-FACTORS; MUTANT MICE; DOGS
AB Megaesophagus is defined as the abnormal enlargement or dilatation of the esophagus, characterized by a lack of normal contraction of the esophageal walls. This is called achalasia when associated with reduced or no relaxation of the lower esophageal sphincter (LES). To date, there are few naturally occurring models for this disease. A colony of transgenic (Pvrl3-Cre) rats presented with megaesophagus at 3 to 4 months of age; further breeding studies revealed a prevalence of 90% of transgene-positive animals having megaesophagus. Affected rats could be maintained on a total liquid diet long term and were shown to display the classic features of dilated esophagus, closed lower esophageal sphincter, and abnormal contractions on contrast radiography and fluoroscopy. Histologically, the findings of muscle degeneration, inflammation, and a reduced number of myenteric ganglia in the esophagus combined with ultrastructural lesions of muscle fiber disarray and mitochondrial changes in the striated muscle of these animals closely mimic that seen in the human condition. Muscle contractile studies looking at the response of the lower esophageal sphincter and fundus to electrical field stimulation, sodium nitroprusside, and L-nitro-L-arginine methyl ester also demonstrate the similarity between megaesophagus in the transgenic rats and patients with achalasia. No primary cause for megaesophagus was found, but the close parallel to the human form of the disease, as well as ease of care and manipulation of these rats, makes this a suitable model to better understand the etiology of achalasia as well as study new management and treatment options for this incurable condition.
C1 [Pang, J.; Borjeson, T. M.; Muthupalani, S.; Ducore, R. M.; Feng, Y.; Fox, J. G.] MIT, Div Comparat Med, Cambridge, MA 02139 USA.
[Carr, C. A.] MIT, Picower Inst Learning & Memory, RIKEN MIT Ctr Neural Circuit Genet, Cambridge, MA 02139 USA.
[Sullivan, M. P.; Cristofaro, V.] Harvard Univ, Sch Med, VA Boston Healthcare Syst, West Roxbury, MA USA.
[Luo, J.; Lindstrom, J. M.] Univ Penn, Sch Med, Dept Neurosci, Philadelphia, PA 19104 USA.
RP Fox, JG (reprint author), MIT, Div Comparat Med, 77 Massachusetts Ave,16-825, Cambridge, MA 02139 USA.
EM jgfox@mit.edu
OI Ducore, Rebecca/0000-0001-5223-2266
FU National Institutes of Health [T32OD011141, P30ES002109]
FX The author(s) disclosed receipt of the following financial support for
the research, authorship, and/or publication of this article: This study
was supported by the National Institutes of Health (grant numbers
T32OD011141 and P30ES002109).
NR 90
TC 1
Z9 1
U1 1
U2 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0300-9858
EI 1544-2217
J9 VET PATHOL
JI Vet. Pathol.
PD NOV
PY 2014
VL 51
IS 6
BP 1187
EP 1200
DI 10.1177/0300985813519136
PG 14
WC Pathology; Veterinary Sciences
SC Pathology; Veterinary Sciences
GA AT1GQ
UT WOS:000344681800018
PM 24457157
ER
PT J
AU Shi, M
Liu, CQ
Cook, TJ
Bullock, KM
Zhao, YC
Ginghina, C
Li, YF
Aro, P
Dator, R
He, CM
Hipp, MJ
Zabetian, CP
Peskind, E
Hu, SC
Quinn, JF
Galasko, DR
Banks, WA
Zhang, J
AF Shi, Min
Liu, Changqin
Cook, Travis J.
Bullock, Kristin M.
Zhao, Yanchun
Ginghina, Carmen
Li, Yanfei
Aro, Patrick
Dator, Romel
He, Chunmei
Hipp, Michael J.
Zabetian, Cyrus P.
Peskind, Elaine R.
Hu, Shu-Ching
Quinn, Joseph F.
Galasko, Douglas R.
Banks, William A.
Zhang, Jing
TI Plasma exosomal alpha-synuclein is likely CNS-derived and increased in
Parkinson's disease
SO ACTA NEUROPATHOLOGICA
LA English
DT Article
DE Parkinson's disease; Exosome; alpha-synuclein; Biomarker; Plasma
ID BLOOD-BRAIN-BARRIER; CEREBROSPINAL-FLUID; ALZHEIMERS-DISEASE; LEWY
BODIES; NERVOUS-SYSTEM; AMYLOID-BETA; BIOMARKER; DJ-1; MICROVESICLES;
REABSORPTION
AB Extracellular alpha-synuclein is important in the pathogenesis of Parkinson's disease (PD) and also as a potential biomarker when tested in the cerebrospinal fluid (CSF). The performance of blood plasma or serum alpha-synuclein as a biomarker has been found to be inconsistent and generally ineffective, largely due to the contribution of peripherally derived alpha-synuclein. In this study, we discovered, via an intracerebroventricular injection of radiolabeled alpha-synuclein into mouse brain, that CSF alpha-synuclein was readily transported to blood, with a small portion being contained in exosomes that are relatively specific to the central nervous system (CNS). Consequently, we developed a technique to evaluate the levels of alpha-synuclein in these exosomes in individual plasma samples. When applied to a large cohort of clinical samples (267 PD, 215 controls), we found that in contrast to CSF alpha-synuclein concentrations, which are consistently reported to be lower in PD patients compared to controls, the levels of plasma exosomal alpha-synuclein were substantially higher in PD patients, suggesting an increased efflux of the protein to the peripheral blood of these patients. Furthermore, although no association was observed between plasma exosomal and CSF alpha-synuclein, a significant correlation between plasma exosomal alpha-synuclein and disease severity (r = 0.176, p = 0.004) was observed, and the diagnostic sensitivity and specificity achieved by plasma exosomal alpha-synuclein were comparable to those determined by CSF alpha-synuclein. Further studies are clearly needed to elucidate the mechanism involved in the transport of CNS alpha-synuclein to the periphery, which may lead to a more convenient and robust assessment of PD clinically.
C1 [Shi, Min; Zhao, Yanchun; Ginghina, Carmen; Aro, Patrick; Dator, Romel; Hipp, Michael J.; Zhang, Jing] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA.
[Liu, Changqin] Xiamen Univ, Affiliated Hosp 1, Dept Endocrinol & Diabet, Xiamen 361003, Fujian, Peoples R China.
[Cook, Travis J.; Li, Yanfei] Univ Washington, Dept Environm & Occupat Hlth Sci, Sch Publ Hlth, Seattle, WA 98195 USA.
[Bullock, Kristin M.; Zabetian, Cyrus P.; Hu, Shu-Ching; Banks, William A.] Vet Affairs Puget Sound Hlth Care Syst, Geriatr Res Educ & Clin Ctr, Seattle, WA 98108 USA.
[Bullock, Kristin M.; Banks, William A.] Univ Washington, Sch Med, Dept Med, Div Gerontol & Geriatr Med, Seattle, WA 98195 USA.
[He, Chunmei] Xiamen Univ, Affiliated Hosp 1, Dept Endocrinol & Diabet, Xiamen Diabet Inst, Xiamen 361003, Fujian, Peoples R China.
[Zabetian, Cyrus P.; Hu, Shu-Ching] Vet Affairs Puget Sound Hlth Care Syst, Parkinsons Dis Res Educ & Clin Ctr, Seattle, WA 98108 USA.
[Zabetian, Cyrus P.; Hu, Shu-Ching] Univ Washington, Dept Neurol, Sch Med, Seattle, WA 98195 USA.
[Peskind, Elaine R.] Univ Washington, Dept Psychiat & Behav Sci, Sch Med, Seattle, WA 98195 USA.
[Peskind, Elaine R.] Vet Affairs Puget Sound Hlth Care Syst, Mental Illness Res Educ & Clin Ctr, Seattle, WA 98108 USA.
[Quinn, Joseph F.] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97239 USA.
[Galasko, Douglas R.] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA.
RP Zhang, J (reprint author), Univ Washington, Sch Med, Dept Pathol, 325 9th Ave,HMC Box 359635, Seattle, WA 98195 USA.
EM mshi70@u.washington.edu; zhangj@u.washington.edu
RI Shi, Min/G-6165-2012
OI Shi, Min/0000-0002-6901-2558
FU National Institutes of Health (NIH) [U01 NS082137, P42 ES004696-5897,
P30 ES007033-6364, R01 AG033398, R01 ES016873, R01 ES019277, R01
NS057567, P50 NS062684-6221, R01 NS065070, P50 AG005131]; NIH [P50
AG003156-30]; National Institute of Neurological Disorders and
Stroke/NIH [R21 NS085425]; University of Washington's Proteomics
Resource [UWPR95794]
FX We thank Drs. Honglian Li and Sangwoo Jung for their kind help on EM
method development, and Dr. Ane Korff for her assistance in Western blot
confirmation. We also deeply appreciate the patients and participants
for their generous participation and donation of samples. This study was
supported by generous grants from the National Institutes of Health
(NIH) (U01 NS082137, P42 ES004696-5897, P30 ES007033-6364, R01 AG033398,
R01 ES016873, R01 ES019277, R01 NS057567, and P50 NS062684-6221 to JZ,
R01 NS065070 to CPZ, and P50 AG005131 to DRG), and partially by a pilot
study award from the NIH-sponsored ADRC at the UW (P50 AG003156-30) and
a National Institute of Neurological Disorders and Stroke/NIH award R21
NS085425 to MS. It was also supported in part by the University of
Washington's Proteomics Resource (UWPR95794). The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the NIH.
NR 73
TC 43
Z9 44
U1 4
U2 26
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-6322
EI 1432-0533
J9 ACTA NEUROPATHOL
JI Acta Neuropathol.
PD NOV
PY 2014
VL 128
IS 5
BP 639
EP 650
DI 10.1007/s00401-014-1314-y
PG 12
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA AS1RL
UT WOS:000344058200003
PM 24997849
ER
PT J
AU Bechet, D
Gielen, GGH
Korshunov, A
Pfister, SM
Rousso, C
Faury, D
Fiset, PO
Benlimane, N
Lewis, PW
Lu, C
Allis, CD
Kieran, MW
Ligon, KL
Pietsch, T
Ellezam, B
Albrecht, S
Jabado, N
AF Bechet, Denise
Gielen, Gerrit G. H.
Korshunov, Andrey
Pfister, Stefan M.
Rousso, Caterina
Faury, Damien
Fiset, Pierre-Olivier
Benlimane, Naciba
Lewis, Peter W.
Lu, Chao
Allis, C. David
Kieran, Mark W.
Ligon, Keith L.
Pietsch, Torsten
Ellezam, Benjamin
Albrecht, Steffen
Jabado, Nada
TI Specific detection of methionine 27 mutation in histone 3 variants
(H3K27M) in fixed tissue from high-grade astrocytomas
SO ACTA NEUROPATHOLOGICA
LA English
DT Article
DE K27M; Histone 3 variants; IHC; K27 trimethylation; High-grade
astrocytomas
ID INTRINSIC PONTINE GLIOMA; ACTIVATING ACVR1 MUTATIONS; PEDIATRIC
GLIOBLASTOMA; DISTINCT SUBGROUPS; SOMATIC MUTATIONS; K27M MUTATION;
MEDULLOBLASTOMA; H3F3A; TUMORS; EXPRESSION
AB Studies in pediatric high-grade astrocytomas (HGA) by our group and others have uncovered recurrent somatic mutations affecting highly conserved residues in histone 3 (H3) variants. One of these mutations leads to analogous p.Lys27Met (K27M) mutations in both H3.3 and H3.1 variants, is associated with rapid fatal outcome, and occurs specifically in HGA of the midline in children and young adults. This includes diffuse intrinsic pontine gliomas (80 %) and thalamic or spinal HGA (> 90 %), which are surgically challenging locations with often limited tumor material available and critical need for specific histopathological markers. Here, we analyzed formalin-fixed paraffin-embedded tissues from 143 pediatric HGA and 297 other primary brain tumors or normal brain. Immunohistochemical staining for H3K27M was compared to tumor genotype, and also compared to H3 tri-methylated lysine 27 (H3K27me3) staining, previously shown to be drastically decreased in samples carrying this mutation. There was a 100 % concordance between genotype and immunohistochemical analysis of H3K27M in tumor samples. Mutant H3K27M was expressed in the majority of tumor cells, indicating limited intra-tumor heterogeneity for this specific mutation within the limits of our dataset. Both H3.1 and H3.3K27M mutants were recognized by this antibody while non-neoplastic elements, such as endothelial and vascular smooth muscle cells or lymphocytes, did not stain. H3K27me3 immunoreactivity was largely mutually exclusive with H3K27M positivity. These results demonstrate that mutant H3K27M can be specifically identified with high specificity and sensitivity using an H3K27M antibody and immunohistochemistry. Use of this antibody in the clinical setting will prove very useful for diagnosis, especially in the context of small biopsies in challenging midline tumors and will help orient care in the context of the extremely poor prognosis associated with this mutation.
C1 [Bechet, Denise; Jabado, Nada] McGill Univ, Dept Expt Med, Montreal, PQ H3Z 2Z3, Canada.
[Bechet, Denise; Jabado, Nada] McGill Univ, Dept Human Genet, Montreal, PQ H3Z 2Z3, Canada.
[Gielen, Gerrit G. H.; Pietsch, Torsten] Univ Bonn, Med Ctr, Inst Neuropathol, D-53127 Bonn, Germany.
[Korshunov, Andrey] German Canc Res Ctr, Clin Cooperat Unit Neuropathol, Heidelberg, Germany.
[Pfister, Stefan M.] German Canc Res Ctr, Div Pediat Neurooncol, Heidelberg, Germany.
[Rousso, Caterina; Faury, Damien; Jabado, Nada] McGill Univ, Dept Pediat, Ctr Hlth, Montreal Childrens Hosp, Montreal, PQ H3Z 2Z3, Canada.
[Fiset, Pierre-Olivier; Albrecht, Steffen] McGill Univ, Montreal Childrens Hosp, Ctr Hlth, Dept Pathol, Montreal, PQ H3Z 2Z3, Canada.
[Lewis, Peter W.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Biomol Chem, Madison, WI USA.
[Lu, Chao; Allis, C. David] Rockefeller Univ, Lab Chromatin Biol & Epigenet, New York, NY 10021 USA.
[Kieran, Mark W.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Div Pediat Hematol Oncol,Dept Pediat Oncol,Boston, Boston, MA 02115 USA.
[Ligon, Keith L.] Harvard Univ, Dana Farber Canc Inst, Ctr Mol Oncol Pathol, Boston, MA 02115 USA.
[Ellezam, Benjamin] Univ Montreal, Dept Pathol, CHU Ste Justine, Montreal, PQ H3C 3J7, Canada.
[Ellezam, Benjamin] Hop Ste Justine, Montreal, PQ, Canada.
[Albrecht, Steffen] Montreal Childrens Hosp, Montreal, PQ H3H 1P3, Canada.
RP Jabado, N (reprint author), McGill Univ, Dept Expt Med, 4060 Ste Catherine West,PT239, Montreal, PQ H3Z 2Z3, Canada.
EM Benjamin.ellezam@umontreal.ca; steffen.albrecht@hotmail.com;
nada.jabado@mcgill.ca
RI Gielen, Gerrit /B-4244-2015; Pfister, Stefan/F-6860-2013;
OI Pfister, Stefan/0000-0002-5447-5322; Lewis, Peter/0000-0002-9816-7823;
Kieran, Mark/0000-0003-2184-7692
FU Genome Canada; Genome Quebec; Institute for Cancer Research of the
Canadian Institutes for Health Research (CIHR) McGill University;
Montreal Children's Hospital Foundation; Chercheur Clinicien Senior
Award; T.D. Trust/Montreal Children's Hospital Foundation
FX This work was performed within the context of the I-CHANGE consortium
(International Childhood Astrocytoma iNntegrated Genomics and
Epigenomics consortium) and supported by funding from Genome Canada,
Genome Quebec, The Institute for Cancer Research of the Canadian
Institutes for Health Research (CIHR) McGill University and the Montreal
Children's Hospital Foundation. N. Jabado is a member of the Penny Cole
lab and the recipient of a Chercheur Clinicien Senior Award. D. B. is
supported by a studentship from the T.D. Trust/Montreal Children's
Hospital Foundation. The authors would like to thank Leonie Michael for
critical reading of the manuscript.
NR 26
TC 23
Z9 25
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-6322
EI 1432-0533
J9 ACTA NEUROPATHOL
JI Acta Neuropathol.
PD NOV
PY 2014
VL 128
IS 5
BP 733
EP 741
DI 10.1007/s00401-014-1337-4
PG 9
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA AS1RL
UT WOS:000344058200010
PM 25200321
ER
PT J
AU Behlau, I
Martin, KV
Martin, JN
Naumova, EN
Cadorette, JJ
Sforza, JT
Pineda, R
Dohlman, CH
AF Behlau, Irmgard
Martin, Kathryn V.
Martin, Jacqueline N.
Naumova, Elena N.
Cadorette, James J.
Sforza, J. Tammy
Pineda, Roberto, II
Dohlman, Claes H.
TI Infectious endophthalmitis in Boston keratoprosthesis: incidence and
prevention
SO ACTA OPHTHALMOLOGICA
LA English
DT Article
DE Boston keratoprosthesis; endophthalmitis; ocular infections; ocular
prophylaxis
ID COAGULASE-NEGATIVE STAPHYLOCOCCI; UNIVERSITY-OF-CALIFORNIA;
STEVENS-JOHNSON-SYNDROME; I KERATOPROSTHESIS; TYPE-1 KERATOPROSTHESIS;
PERMANENT KERATOPROSTHESIS; CORNEAL TRANSPLANTATION; CATARACT-SURGERY;
GLAUCOMA; OUTCOMES
AB PurposeTo determine the cumulative worldwide incidence of infectious endophthalmitis and associated vision loss after Boston keratoprosthesis (B-KPro) Type I/II implantation and to propose both safe and inexpensive prophylactic antibiotic regimens.
MethodsTwo retrospective methods were used to determine the incidence, visual outcomes and aetiologies of infectious endophthalmitis associated with the B-KPro divided per decade: (i) systematic review of the literature from 1990 through January 2013 and (ii) a surveillance survey sent to all surgeons who implanted B-KPros through 2010 with 1-year minimum follow-up. In addition, a single-Boston surgeon 20-year experience was examined.
ResultsFrom 1990 through 2010, there were 4729 B-KPros implanted worldwide by 209 U.S. surgeons and 159 international surgeons. The endophthalmitis cumulative mean incidence declined from 12% during its first decade of use to about 3% during its second decade in the Unites States and about 5% internationally during the second decade. There remains a large incidence range both in the United States (1-12.5%) and internationally (up to 17%). Poor compliance with daily topical antibiotics is an important risk factor. While Gram-positive organisms remained dominant, fungal infections emerged during the second decade.
ConclusionsDaily prophylactic topical antibiotics have dramatically reduced the endophthalmitis incidence. Although Gram-positive organisms are the most common aetiology, antimicrobials must be inclusive of Gram-negative organisms. Selection of prophylactic regimens should be tailored to local antibiotic susceptibility patterns, be cost-effective, and should not promote the emergence of antimicrobial resistance. An example of a broad-spectrum, low-cost prophylactic option for non-autoimmune patients includes trimethoprim/polymyxinB once daily.
C1 [Behlau, Irmgard; Martin, Kathryn V.; Martin, Jacqueline N.; Pineda, Roberto, II; Dohlman, Claes H.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Schepens Eye Res Inst, Boston, MA USA.
[Behlau, Irmgard] Tufts Univ, Sch Med, Tufts Sackler Grad Sch Biomed Sci, Boston, MA 02111 USA.
[Behlau, Irmgard] Harvard Univ, Sch Med, Mt Auburn Hosp, Div Infect Dis,Dept Med, Cambridge, MA 02138 USA.
[Behlau, Irmgard] Tufts Univ, Sch Med, Newton Wellesley Hosp, Div Infect Dis,Dept Med, Newton, MA USA.
[Naumova, Elena N.] Tufts Univ, Sch Engn, Tufts Initiat Forecasting & Modeling Infect Dis I, Medford, MA 02155 USA.
[Cadorette, James J.] Massachusetts Eye & Ear Infirm, Henry Whittier Porter Bacteriol Lab, Boston, MA 02114 USA.
[Sforza, J. Tammy] Massachusetts Eye & Ear Infirm, Dept Pharm, Boston, MA 02114 USA.
RP Behlau, I (reprint author), Tufts Univ, Sch Med, Dept Mol Biol & Microbiol & Ophthalmol, Tufts Sackler Grad Sch Biomed Sci, M&V 429,136 Harrison Ave, Boston, MA 02111 USA.
EM irmgard.behlau@tufts.edu
FU Fight for Sight; MEEI B-KPro Fund
FX This work was made possible by the generous support of Fight for Sight
Grant-In-Aid (IB) and MEEI B-KPro Fund.
NR 79
TC 13
Z9 13
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1755-375X
EI 1755-3768
J9 ACTA OPHTHALMOL
JI Acta Ophthalmol.
PD NOV
PY 2014
VL 92
IS 7
BP e546
EP e555
DI 10.1111/aos.12309
PG 10
WC Ophthalmology
SC Ophthalmology
GA AS3FN
UT WOS:000344162700007
PM 24460594
ER
PT J
AU Sahin, I
Azab, F
Mishima, Y
Moschetta, M
Tsang, B
Glavey, SV
Manier, S
Zhang, Y
Sacco, A
Roccaro, AM
Azab, AK
Ghobrial, IM
AF Sahin, Ilyas
Azab, Feda
Mishima, Yuji
Moschetta, Michele
Tsang, Brian
Glavey, Siobhan V.
Manier, Salomon
Zhang, Yu
Sacco, Antonio
Roccaro, Aldo M.
Azab, Abdel Kareem
Ghobrial, Irene M.
TI Targeting survival and cell trafficking in multiple myeloma and
Waldenstrom macroglobulinemia using pan-class I PI3K inhibitor,
buparlisib
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; MTOR INHIBITOR; PHOSPHOINOSITIDE
3-KINASES; SYNERGISTIC ACTIVITY; MAMMALIAN TARGET; AKT PATHWAY;
NVP-BKM120; IDELALISIB; RAPAMYCIN; COMBINATION
AB The phosphatidylinositol-3 kinase (PI3K) pathway is activated in multiple myeloma (MM) and Waldenstrom Macroglobulenima (WM), and plays a crucial role in tumor progression and drug resistance. In this study, we characterized the role of pan-class I PI3K inhibition on cell trafficking and survival of MM and WM cells. We tested the effect of pan-class I PI3K inhibition by siRNA silencing or pharmacologic inhibition with buparlisib on MM cell survival, apoptosis and cell cycle in vitro and tumor growth and mobilization of MM cells in vivo. We then evaluated buparlisib-dependent mechanisms of induced MM cell mobilization. Moreover, the effect of buparlisib on cell survival, apoptosis, and adhesion of WM cells to bone marrow stromal cells (BMSCs) has been evaluated. We showed that buparlisib induced toxicity in MM cells, supported by induction of apoptosis and cell cycle arrest. Buparlisib was also found to reduce tumor progression in vivo. Importantly, buparlisib enhanced MM cell mobilization in vivo which was driven by decreased adhesion of MM cells to BMSCs and increased chemotaxis via up-regulation of CXCR4 expression. Similar to its effects on MM cells, buparlisib also induced cell survival and apoptosis, and decreased adhesion in WM cells. These data highlight the critical contribution of class I PI3K signaling to the regulation of survival and cell dissemination in B-cell malignancies. Am. J. Hematol. 89:1030-1036, 2014. (c) 2014 Wiley Periodicals, Inc.
C1 [Sahin, Ilyas; Azab, Feda; Mishima, Yuji; Moschetta, Michele; Tsang, Brian; Glavey, Siobhan V.; Manier, Salomon; Zhang, Yu; Sacco, Antonio; Roccaro, Aldo M.; Azab, Abdel Kareem; Ghobrial, Irene M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Azab, Feda; Azab, Abdel Kareem] Washington Univ St Louis, Sch Med, Div Canc Biol, Dept Radiat Oncol, St Louis, MO USA.
RP Ghobrial, IM (reprint author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02115 USA.
EM irene_ghobrial@dfci.harvard.edu
RI Sacco, Antonio/K-4681-2016;
OI Sacco, Antonio/0000-0003-2945-9416; Roccaro, Aldo/0000-0002-1872-5128
FU International Waldenstrom Macroglobulinemia Foundation, Kirsch Lab; Heje
Fellowship [R01CA154648, 1R01F0003743]
FX Contract grant sponsor: International Waldenstrom Macroglobulinemia
Foundation, Kirsch Lab (to W. M.), and Heje Fellowship (to W. M.);
Contract grant numbers: R01CA154648; 1R01F0003743.
NR 49
TC 6
Z9 6
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
EI 1096-8652
J9 AM J HEMATOL
JI Am. J. Hematol.
PD NOV
PY 2014
VL 89
IS 11
BP 1030
EP 1036
DI 10.1002/ajh.23814
PG 7
WC Hematology
SC Hematology
GA AS1BA
UT WOS:000344010100008
PM 25060991
ER
PT J
AU Hasserjian, RP
Campigotto, F
Klepeis, V
Fu, B
Wang, SA
Bueso-Ramos, C
Cascio, MJ
Rogers, HJ
Hsi, ED
Soderquist, C
Bagg, A
Yan, J
Ochs, R
Orazi, A
Moore, F
Mahmoud, A
George, TI
Foucar, K
Odem, J
Booth, C
Morice, W
DeAngelo, DJ
Steensma, D
Stone, RM
Neuberg, D
Arber, DA
AF Hasserjian, Robert Paul
Campigotto, Federico
Klepeis, Veronica
Fu, Bin
Wang, Sa A.
Bueso-Ramos, Carlos
Cascio, Michael Joseph
Rogers, Heesun Joyce
Hsi, Eric Darryl
Soderquist, Craig
Bagg, Adam
Yan, Jiong
Ochs, Rachel
Orazi, Attilio
Moore, Frank
Mahmoud, Amer
George, Tracy Irene
Foucar, Kathryn
Odem, Jamie
Booth, Cassie
Morice, William
DeAngelo, Daniel J.
Steensma, David
Stone, Richard Maury
Neuberg, Donna
Arber, Daniel Alan
TI De novo acute myeloid leukemia with 20-29% blasts is less aggressive
than acute myeloid leukemia with >= 30% blasts in older adults: a Bone
Marrow Pathology Group study
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID CONVENTIONAL CARE REGIMENS; AML-TYPE CHEMOTHERAPY; MYELODYSPLASTIC
SYNDROMES; REFRACTORY-ANEMIA; SCORING SYSTEM; INTENSIVE CHEMOTHERAPY;
ELDERLY-PATIENTS; OPEN-LABEL; PHASE-III; SURVIVAL
AB It is controversial whether acute myeloid leukemia (AML) patients with 20-29% bone marrow (BM) blasts, formerly referred to as refractory anemia with excess blasts in transformation (RAEBT), should be considered AML or myelodysplastic syndrome (MDS) for the purposes of treatment and prognostication. We retrospectively studied 571 de novo AML in patients aged > 50 years, including 142 RAEBT and 429 with 30% blasts (AML30), as well as 151 patients with 10-19% BM blasts (RAEB2). RAEBT patients were older and had lower white blood count, but higher hemoglobin, platelet count, and karyotype risk scores compared to AML30, while these features were similar to RAEB2. FLT3 and NPM1 mutations and monocytic morphology occurred more commonly in AML30 than in RAEBT. RAEBT patients were treated less often with induction therapy than AML30, whereas allogeneic stem cell transplant frequency was similar. The median and 4-year OS of RAEBT patients were longer than those of AML30 patients (20.5 vs 12.0 months and 28.6% vs 20.4%, respectively, P=0.003); this difference in OS was manifested in patients in the intermediate UKMRC karyotype risk group, whereas OS of RAEBT patients and AML30 patients in the adverse karyotype risk group were not significantly different. Multivariable analysis showed that RAEBT (P<0.0001), hemoglobin (P=0.005), UKMRC karyotype risk group (P=0.002), normal BM karyotype (P=0.004), treatment with induction therapy (P<0.0001), and stem cell transplant (P<0.0001) were associated with longer OS. Our findings favor considering de novo RAEBT as a favorable prognostic subgroup of AML. Am. J. Hematol. 89:E193-E199, 2014. (c) 2014 Wiley Periodicals, Inc.
C1 [Hasserjian, Robert Paul; Klepeis, Veronica] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Campigotto, Federico; Neuberg, Donna] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Fu, Bin; Wang, Sa A.; Bueso-Ramos, Carlos] Univ Texas MD Anderson Canc Ctr, Dept Hematopathol, Houston, TX 77030 USA.
[Cascio, Michael Joseph; Arber, Daniel Alan] Stanford Univ, Dept Pathol, Stanford, CA 94305 USA.
[Rogers, Heesun Joyce; Hsi, Eric Darryl] Cleveland Clin, Dept Pathol, Cleveland, OH 44106 USA.
[Soderquist, Craig; Bagg, Adam] Univ Penn, Dept Pathol, Philadelphia, PA 19104 USA.
[Yan, Jiong; Ochs, Rachel; Orazi, Attilio] Weill Cornell Med Coll, Dept Pathol, New York, NY USA.
[Moore, Frank; Mahmoud, Amer; George, Tracy Irene; Foucar, Kathryn] Univ New Mexico, Hlth Sci Ctr, Dept Pathol, Albuquerque, NM 87131 USA.
[Odem, Jamie; Booth, Cassie; Morice, William] Mayo Clin, Dept Pathol, Rochester, MN USA.
[DeAngelo, Daniel J.; Steensma, David; Stone, Richard Maury] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
RP Hasserjian, RP (reprint author), Massachusetts Gen Hosp, Dept Pathol, WRN244,55 Fruit St, Boston, MA 02114 USA.
EM rhasserjian@partners.org
OI Cascio, Michael/0000-0002-5537-7740
NR 29
TC 8
Z9 9
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0361-8609
EI 1096-8652
J9 AM J HEMATOL
JI Am. J. Hematol.
PD NOV
PY 2014
VL 89
IS 11
BP E193
EP E199
DI 10.1002/ajh.23808
PG 7
WC Hematology
SC Hematology
GA AS1BA
UT WOS:000344010100001
PM 25042343
ER
PT J
AU Batal, I
Schlossman, RL
Safa, K
Rennke, HG
Campenot, ES
AF Batal, Ibrahim
Schlossman, Robert L.
Safa, Kassem
Rennke, Helmut G.
Campenot, Eric S.
TI Anemia, Fatigue, and Late-Failing Kidney Transplant
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Editorial Material
C1 [Batal, Ibrahim; Rennke, Helmut G.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Batal, Ibrahim; Schlossman, Robert L.; Safa, Kassem; Rennke, Helmut G.] Harvard Univ, Sch Med, Boston, MA USA.
[Schlossman, Robert L.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Safa, Kassem] Brigham & Womens Hosp, Div Renal, Boston, MA 02115 USA.
[Campenot, Eric S.] Columbia Univ, Dept Pathol & Cell Biol, Med Ctr, New York, NY 10032 USA.
[Campenot, Eric S.] New York Presbyterian Hosp, New York, NY USA.
RP Batal, I (reprint author), Columbia Univ, Dept Pathol & Cellular Biol, 630 W 168th St, New York, NY 10032 USA.
EM ib2349@columbia.edu
NR 4
TC 1
Z9 1
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 0272-6386
EI 1523-6838
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD NOV
PY 2014
VL 64
IS 5
BP XVI
EP XIX
DI 10.1053/j.ajkd.2014.06.032
PG 4
WC Urology & Nephrology
SC Urology & Nephrology
GA AS4IM
UT WOS:000344237900002
PM 25344006
ER
PT J
AU Kalim, S
Karumanchi, SA
Thadhani, RI
Berg, AH
AF Kalim, Sahir
Karumanchi, S. Ananth
Thadhani, Ravi I.
Berg, Anders H.
TI Protein Carbamylation in Kidney Disease: Pathogenesis and Clinical
Implications
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Carbamylation; uremia; posttranslational protein modification (PTM);
pathophysiology; chronic kidney disease (CKD); end-stage renal disease
(ESRD); cyanate; urea; inflammation; carbamoylation
ID LOW-DENSITY-LIPOPROTEIN; CHRONIC-RENAL-FAILURE; SICKLE-CELL DISEASE;
HEMOGLOBIN A(1C) LEVELS; ENDOTHELIAL-CELLS; UREMIC PATIENTS; SODIUM
CYANATE; PLASMA-PROTEIN; AMINO-ACID; GLUTAMATE DEHYDROGENASE
AB Carbamylation describes a nonenzymatic posttranslational protein modification mediated by cyanate, a dissociation product of urea. When kidney function declines and urea accumulates, the burden of carbamylation naturally increases. Free amino acids may protect proteins from carbamylation, and protein carbamylation has been shown to increase in uremic patients with amino acid deficiencies. Carbamylation reactions are capable of altering the structure and functional properties of certain proteins and have been implicated directly in the underlying mechanisms of various disease conditions. A broad range of studies has demonstrated how the irreversible binding of urea-derived cyanate to proteins in the human body causes inappropriate cellular responses leading to adverse outcomes such as accelerated atherosclerosis and inflammation. Given carbamylation's relationship to urea and the evidence that it contributes to disease pathogenesis, measurements of carbamylated proteins may serve as useful quantitative biomarkers of time-averaged urea concentrations while also offering risk assessment in patients with kidney disease. Moreover, the link between carbamylated proteins and disease pathophysiology creates an enticing therapeutic target for reducing the rate of carbamylation. This article reviews the biochemistry of the carbamylation reaction, its role in specific diseases, and the potential diagnostic and therapeutic implications of these findings based on recent advances. (C) 2014 by the National Kidney Foundation, Inc.
C1 [Kalim, Sahir; Thadhani, Ravi I.] Massachusetts Gen Hosp, Div Nephrol, Dept Med, Boston, MA USA.
[Kalim, Sahir; Karumanchi, S. Ananth; Thadhani, Ravi I.; Berg, Anders H.] Harvard Univ, Sch Med, Boston, 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.
[Berg, Anders H.] Beth Israel Deaconess Med Ctr, Dept Pathol, Div Clin Chem, Boston, MA 02215 USA.
RP Berg, AH (reprint author), Beth Israel Deaconess Med Ctr, Dept Pathol, 330 Brookline Ave,Dana 576, Boston, MA 02215 USA.
EM ahberg@bidmc.harvard.edu
FU National Kidney Foundation Young Investigator award; National Institutes
of Health [K24 DK094872]; Howard Hughes Medical Institute; American
Diabetes Association Junior Faculty Award [1-11-JF22]
FX Dr Kalim has received support from the National Kidney Foundation Young
Investigator award; Dr Thadhani receives support from National
Institutes of Health award K24 DK094872; Dr Karumanchi receives support
from the Howard Hughes Medical Institute; and Dr Berg received support
from the American Diabetes Association Junior Faculty Award (1-11-JF22).
NR 130
TC 19
Z9 20
U1 2
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 0272-6386
EI 1523-6838
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD NOV
PY 2014
VL 64
IS 5
BP 793
EP 803
DI 10.1053/j.ajkd.2014.04.034
PG 11
WC Urology & Nephrology
SC Urology & Nephrology
GA AS4IM
UT WOS:000344237900021
PM 25037561
ER
PT J
AU Pennock, S
Haddock, LJ
Mukai, S
Kazlauskas, A
AF Pennock, Steven
Haddock, Luis J.
Mukai, Shizuo
Kazlauskas, Andrius
TI Vascular Endothelial Growth Factor Acts Primarily via Platelet-Derived
Growth Factor Receptor alpha to Promote Proliferative Vitreoretinopathy
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID INTACT CAT EYE; RETINAL-DETACHMENT; PDGF RECEPTOR; RISK-FACTORS;
IN-VIVO; VEGF-E; CELLS; P53; KINASES; ELECTRORETINOGRAM
AB Proliferative vitreoretinopathy (PVR) is a nonneovascular blinding disease and the leading cause for failure in surgical repair of rhegmatogenous retinal detachments. Once formed, PVR is difficult to treat. Hence, there is an acute interest in developing approaches to prevent PVR. Of the many growth factors and cytokines that accumulate in vitreous as PVR develops, neutralizing vascular endothelial growth factor (VEGF) A has recently been found to prevent PVR in at least one animal model. The goal of this study was to test if Food and Drug Administration approved agents could protect the eye from PVR in multiple animal models and to further investigate the underlying mechanisms. Neutralizing VEGF with aflibercept (VEGF Trap-Eye) safely and effectively protected rabbits from PVR in multiple models of disease. Furthermore, aflibercept reduced the bioactivity of both experimental and clinical PVR vitreous. Finally, although VEGF could promote some PVR-associated cellular responses via VEGF receptors expressed on the retinal pigment epithelial cells that drive this disease, VEGF's major contribution to vitreal bioactivity occurred via platelet-derived growth factor receptor a. Thus, VEGF promotes PVR by a noncanonical ability to engage platelet-derived growth factor receptor a. These findings indicate that VEGF contributes to nonangiogenic diseases and that anti VEGF-based therapies may be effective on a wider spectrum of diseases than previously appreciated.
C1 [Kazlauskas, Andrius] Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Schepens Eye Res Inst, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA 02114 USA.
RP Kazlauskas, A (reprint author), Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Schepens Eye Res Inst, 20 Stamford St, Boston, MA 02114 USA.
EM andrius_kazlauskas@meei.harvard.edu
FU NIH [EY022970]; Mukai Fund of the Massachusetts Eye and Ear Infirmary
(Boston)
FX Supported by NIH grant EY022970 (A.K.) and the Mukai Fund of the
Massachusetts Eye and Ear Infirmary (Boston) (S.M.).
NR 59
TC 6
Z9 6
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
EI 1525-2191
J9 AM J PATHOL
JI Am. J. Pathol.
PD NOV
PY 2014
VL 184
IS 11
BP 3052
EP 3068
DI 10.1016/j.ajpath.2014.07.026
PG 17
WC Pathology
SC Pathology
GA AS0LS
UT WOS:000343969200018
PM 25261788
ER
PT J
AU Balamurugan, AN
Naziruddin, B
Lockridge, A
Tiwari, M
Loganathan, G
Takita, M
Matsumoto, S
Papas, K
Trieger, M
Rainis, H
Kin, T
Kay, TW
Wease, S
Messinger, S
Ricordi, C
Alejandro, R
Markmann, J
Kerr-Conti, J
Rickels, MR
Liu, C
Zhang, X
Witkowski, P
Posselt, A
Maffi, P
Secchi, A
Berney, T
O'Connell, PJ
Hering, BJ
Barton, FB
AF Balamurugan, A. N.
Naziruddin, B.
Lockridge, A.
Tiwari, M.
Loganathan, G.
Takita, M.
Matsumoto, S.
Papas, K.
Trieger, M.
Rainis, H.
Kin, T.
Kay, T. W.
Wease, S.
Messinger, S.
Ricordi, C.
Alejandro, R.
Markmann, J.
Kerr-Conti, J.
Rickels, M. R.
Liu, C.
Zhang, X.
Witkowski, P.
Posselt, A.
Maffi, P.
Secchi, A.
Berney, T.
O'Connell, P. J.
Hering, B. J.
Barton, F. B.
TI Islet Product Characteristics and Factors Related to Successful Human
Islet Transplantation From the Collaborative Islet Transplant Registry
(CITR) 1999-2010
SO AMERICAN JOURNAL OF TRANSPLANTATION
LA English
DT Article
DE Clinical research; practice; diabetes: type 1; endocrinology;
diabetology; health services and outcomes research; islet isolation;
islet transplantation; Organ Procurement and Transplantation Network
(OPTN); pancreas; simultaneous pancreas-kidney transplantation;
registry; registry analysis
ID HISTIDINE-TRYPTOPHAN-KETOGLUTARATE; OF-WISCONSIN SOLUTION;
ISOLATION-RELATED VARIABLES; PANCREAS PRESERVATION; ISOLATION OUTCOMES;
2-LAYER METHOD; CLINICAL TRANSPLANTATION; COLLAGENASE NB1;
GRAFT-SURVIVAL; CULTURE
AB The Collaborative Islet Transplant Registry (CITR) collects data on clinical islet isolations and transplants. This retrospective report analyzed 1017 islet isolation procedures performed for 537 recipients of allogeneic clinical islet transplantation in 1999-2010. This study describes changes in donor and islet isolation variables by era and factors associated with quantity and quality of final islet products. Donor body weight and BMI increased significantly over the period (p<0.001). Islet yield measures have improved with time including islet equivalent (IEQ)/particle ratio and IEQs infused. The average dose of islets infused significantly increased in the era of 2007-2010 when compared to 1999-2002 (445.4156.8 vs. 421.3 +/- 155.4x10(3) IEQ; p<0.05). Islet purity and total number of cells significantly improved over the study period (p<0.01 and <0.05, respectively). Otherwise, the quality of clinical islets has remained consistently very high through this period, and differs substantially from nonclinical islets. In multivariate analysis of all recipient, donor and islet factors, and medical management factors, the only islet product characteristic that correlated with clinical outcomes was total IEQs infused. This analysis shows improvements in both quantity and some quality criteria of clinical islets produced over 1999-2010, and these parallel improvements in clinical outcomes over the same period.
Product criteria from clinical grade allogeneic human islets exhibit consistently superior-quality characteristics and significantly increasing islet equivalent yield, paralleling improving success rates of islet transplantation for type I diabetes.
C1 [Balamurugan, A. N.; Lockridge, A.; Tiwari, M.; Loganathan, G.; Hering, B. J.] Univ Minnesota, Dept Surg, Schulze Diabet Inst, Minneapolis, MN 55455 USA.
[Naziruddin, B.; Takita, M.] Baylor Annette C & Harold C Simmons Transplant In, Dallas, TX USA.
[Matsumoto, S.] Otsuka Pharmaceut Factory Inc, Ctr Res & Dev, Tokushima, Japan.
[Papas, K.] Univ Arizona, Inst Cellular Transplantat, Tucson, AZ USA.
[Trieger, M.; Rainis, H.; Wease, S.; Barton, F. B.] EMMES Corp, Rockville, MD USA.
[Kin, T.] Univ Alberta, Clin Islet Lab, Edmonton, AB, Canada.
[Kay, T. W.] St Vincents Hosp, Melbourne, Vic, Australia.
[Messinger, S.] Univ Miami, Dept Publ Hlth Serv, Miami, FL USA.
[Ricordi, C.; Alejandro, R.] Univ Miami, Diabet Res Inst, Miami, FL USA.
[Markmann, J.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Kerr-Conti, J.] Lille Univ Hosp, Lille, France.
[Rickels, M. R.] Univ Penn, Dept Med, Philadelphia, PA 19104 USA.
[Liu, C.] Univ Penn, Dept Surg, Philadelphia, PA 19104 USA.
[Zhang, X.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Witkowski, P.] Univ Chicago, Dept Surg, Chicago, IL 60637 USA.
[Posselt, A.] Univ Calif San Francisco, Dept Surg, San Francisco, CA USA.
[Maffi, P.; Secchi, A.] San Raffaele Univ, Vita Salute, Milan, Italy.
[Berney, T.] Univ Hosp Geneva, Dept Surg, Geneva, Switzerland.
[O'Connell, P. J.] Univ Sydney, Westmead Hosp, Natl Pancreas Transplant Unit, Sydney, NSW 2006, Australia.
RP Balamurugan, AN (reprint author), Univ Louisville, Dept Surg, Cardiovasc Innovat Inst, Islet Cell Lab, Louisville, KY 40292 USA.
EM isletologist@hotmail.com; fbarton@emmes.com
RI Loganathan, Gopalakrishnan/D-8762-2014;
OI Ricordi, Camillo/0000-0001-8092-7153
FU NIDDK; National Institutes of Health; JDRF International
FX The CITR is funded by the NIDDK, National Institutes of Health and by a
supplemental grant from the JDRF International. Additional data were
made available through cooperative agreements with the U. S. United
Network for Organ Sharing (UNOS), Alexandria, Virginia, the
Administrative and Bioinformatics Coordinating Center of the City of
Hope, Duarte, California (1999-2009) and the NIDDK-sponsored CIT
(www.citisletstudy.org), coordinated by the University of Iowa Clinical
Trials and Data Management Center (2008-present).
NR 58
TC 25
Z9 25
U1 3
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1600-6135
EI 1600-6143
J9 AM J TRANSPLANT
JI Am. J. Transplant.
PD NOV
PY 2014
VL 14
IS 11
BP 2595
EP 2606
DI 10.1111/ajt.12872
PG 12
WC Surgery; Transplantation
SC Surgery; Transplantation
GA AS3LH
UT WOS:000344178800020
PM 25278159
ER
PT J
AU Rathmell, JP
AF Rathmell, James P.
TI The Proper Role for Epidural Injection of Corticosteroids
SO ANESTHESIOLOGY
LA English
DT Editorial Material
ID PAIN
C1 [Rathmell, James P.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Div Pain Med, Boston, MA 02114 USA.
[Rathmell, James P.] Harvard Univ, Sch Med, Boston, MA USA.
RP Rathmell, JP (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Div Pain Med, Boston, MA 02114 USA.
EM rathmell.james@mgh.harvard.edu
NR 9
TC 2
Z9 2
U1 2
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
EI 1528-1175
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2014
VL 121
IS 5
BP 919
EP 921
DI 10.1097/ALN.0000000000000439
PG 3
WC Anesthesiology
SC Anesthesiology
GA AS6JA
UT WOS:000344368700005
PM 25335170
ER
PT J
AU Sasaki, N
Meyer, MJ
Malviya, SA
Stanislaus, AB
MacDonald, T
Doran, ME
Igumenshcheva, A
Hoang, AH
Eikermann, M
AF Sasaki, Nobuo
Meyer, Matthew J.
Malviya, Sanjana A.
Stanislaus, Anne B.
MacDonald, Teresa
Doran, Mary E.
Igumenshcheva, Arina
Hoang, Alan H.
Eikermann, Matthias
TI Effects of Neostigmine Reversal of Nondepolarizing Neuromuscular
Blocking Agents on Postoperative Respiratory Outcomes A Prospective
Study
SO ANESTHESIOLOGY
LA English
DT Article
ID NEGATIVE PHARYNGEAL PRESSURE; GENIOGLOSSUS MUSCLE-ACTIVITY; PARTIALLY
PARALYZED HUMANS; POSTANESTHESIA CARE-UNIT; ACETYLCHOLINE-RECEPTOR;
AIRWAY COLLAPSIBILITY; BLOCKADE; COMPLICATIONS; EDROPHONIUM; ATRACURIUM
AB Background: We tested the hypothesis that neostigmine reversal of neuromuscular blockade reduced the incidence of signs and symptoms of postoperative respiratory failure.
Methods: We enrolled 3,000 patients in this prospective, observer-blinded, observational study. We documented the intraoperative use of neuromuscular blocking agents and neostigmine. At postanesthesia care unit admission, we measured train-of-four ratio and documented the ratio of peripheral oxygen saturation to fraction of inspired oxygen (S/F). The primary outcome was oxygenation at postanesthesia care unit admission (S/F). Secondary outcomes included the incidence of postoperative atelectasis and postoperative hospital length of stay. Post hoc, we defined high-dose neostigmine as more than 60 g/kg and unwarranted use of neostigmine as neostigmine administration in the absence of appropriate neuromuscular transmission monitoring.
Results: Neostigmine reversal did not improve S/F at postanesthesia care unit admission (164 [95% CI, 162 to 164] vs. 164 [161 to 164]) and was associated with an increased incidence of atelectasis (8.8% vs. 4.5%; odds ratio, 1.67 [1.07 to 2.59]). High-dose neostigmine was associated with longer time to postanesthesia care unit discharge readiness (176 min [165 to 188] vs. 157 min [153 to 160]) and longer postoperative hospital length of stay (2.9 days [2.7 to 3.2] vs. 2.8 days [2.8 to 2.9]). Unwarranted use of neostigmine (n = 492) was an independent predictor of pulmonary edema (odds ratio, 1.91 [1.21 to 3.00]) and reintubation (odds ratio, 3.68 [1.10 to 12.4]).
Conclusions: Neostigmine reversal did not affect oxygenation but was associated with increased atelectasis. High-dose neostigmine or unwarranted use of neostigmine may translate to increased postoperative respiratory morbidity.
C1 [Sasaki, Nobuo] Showa Gen Hosp, Dept Emergency & Crit Care Med, Tokyo, Japan.
[Meyer, Matthew J.; Eikermann, Matthias] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, Boston, MA USA.
[Malviya, Sanjana A.; Stanislaus, Anne B.; Igumenshcheva, Arina; Hoang, Alan H.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02115 USA.
[Igumenshcheva, Arina] Massachusetts Gen Hosp, MGH Anesthesia Res Grants, BWH Dept Prevent Med, Boston, MA 02115 USA.
[MacDonald, Teresa; Doran, Mary E.] Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Eikermann, Matthias] Univ Klinikum Essen, Klin Anaesthesie & Intens Med, Essen, Germany.
RP Meyer, MJ (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, 55 Fruit St, Boston, MA 02115 USA.
EM mjmeyer@mgh.harvard.edu
FU Schering-Plough Research Institute, Kenilworth, New Jersey, a Division
of Schering Corporation [39442]
FX An investigator-initiated grant (IISP# 39442) was provided by
Schering-Plough Research Institute, Kenilworth, New Jersey, a Division
of Schering Corporation, to the Massachusetts General Hospital.
NR 41
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Z9 32
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
EI 1528-1175
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2014
VL 121
IS 5
BP 959
EP 968
DI 10.1097/ALN.0000000000000440
PG 10
WC Anesthesiology
SC Anesthesiology
GA AS6JA
UT WOS:000344368700011
PM 25225821
ER
PT J
AU Akeju, O
Pavone, KJ
Westover, MB
Vazquez, R
Prerau, MJ
Harrell, PG
Hartnack, KE
Rhee, J
Sampson, AL
Habeeb, K
Lei, G
Pierce, ET
Walsh, JL
Brown, EN
Purdon, PL
AF Akeju, Oluwaseun
Pavone, Kara J.
Westover, M. Brandon
Vazquez, Rafael
Prerau, Michael J.
Harrell, Priscilla G.
Hartnack, Katharine E.
Rhee, James
Sampson, Aaron L.
Habeeb, Kathleen
Lei, Gao
Pierce, Eric T.
Walsh, John L.
Brown, Emery N.
Purdon, Patrick L.
TI A Comparison of Propofol- and Dexmedetomidine-induced
Electroencephalogram Dynamics Using Spectral and Coherence Analysis
SO ANESTHESIOLOGY
LA English
DT Article
ID GENERAL-ANESTHESIA; THALAMOCORTICAL MECHANISMS; INDUCED UNCONSCIOUSNESS;
BEHAVIORAL-EXPERIMENTS; BISPECTRAL INDEX; SLEEP; CONSCIOUSNESS; EEG;
SEDATION; AROUSAL
AB Background: Electroencephalogram patterns observed during sedation with dexmedetomidine appear similar to those observed during general anesthesia with propofol. This is evident with the occurrence of slow (0.1 to 1 Hz), delta (1 to 4 Hz), propofol-induced alpha (8 to 12 Hz), and dexmedetomidine-induced spindle (12 to 16 Hz) oscillations. However, these drugs have different molecular mechanisms and behavioral properties and are likely accompanied by distinguishing neural circuit dynamics.
Methods: The authors measured 64-channel electroencephalogram under dexmedetomidine (n = 9) and propofol (n = 8) in healthy volunteers, 18 to 36 yr of age. The authors administered dexmedetomidine with a 1-mu g/kg loading bolus over 10 min, followed by a 0.7 mu g kg(-1) h(-1) infusion. For propofol, the authors used a computer-controlled infusion to target the effect-site concentration gradually from 0 to 5 g/ml. Volunteers listened to auditory stimuli and responded by button press to determine unconsciousness. The authors analyzed the electroencephalogram using multitaper spectral and coherence analysis.
Results: Dexmedetomidine was characterized by spindles with maximum power and coherence at approximately 13 Hz (mean SD; power, -10.8 +/- 3.6 dB; coherence, 0.8 +/- 0.08), whereas propofol was characterized with frontal alpha oscillations with peak frequency at approximately 11 Hz (power, 1.1 +/- 4.5 dB; coherence, 0.9 +/- 0.05). Notably, slow oscillation power during a general anesthetic state under propofol (power, 13.2 +/- 2.4 dB) was much larger than during sedative states under both propofol (power, -2.5 +/- 3.5 dB) and dexmedetomidine (power, -0.4 +/- 3.1 dB).
Conclusion: The results indicate that dexmedetomidine and propofol place patients into different brain states and suggest that propofol enables a deeper state of unconsciousness by inducing large-amplitude slow oscillations that produce prolonged states of neuronal silence.
C1 [Akeju, Oluwaseun; Pavone, Kara J.; Vazquez, Rafael; Prerau, Michael J.; Harrell, Priscilla G.; Hartnack, Katharine E.; Rhee, James; Sampson, Aaron L.; Lei, Gao; Pierce, Eric T.; Walsh, John L.; Brown, Emery N.; Purdon, Patrick L.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Westover, M. Brandon] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Habeeb, Kathleen] Massachusetts Gen Hosp, Clin Res Ctr, Boston, MA 02114 USA.
[Akeju, Oluwaseun; Westover, M. Brandon; Vazquez, Rafael; Prerau, Michael J.; Harrell, Priscilla G.; Rhee, James; Lei, Gao; Pierce, Eric T.; Walsh, John L.; Brown, Emery N.; Purdon, Patrick L.] Harvard Univ, Sch Med, Boston, MA USA.
[Brown, Emery N.; Purdon, Patrick L.] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
[Brown, Emery N.] MIT, Harvard Massachusetts Inst Technol Div Hlth Sci &, Cambridge, MA 02139 USA.
[Brown, Emery N.] MIT, Inst Med Engn & Sci, Cambridge, MA 02139 USA.
RP Purdon, PL (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, 149 13th St,Rm 4005, Charlestown, MA 02129 USA.
EM patrickp@nmr.mgh.harvard.edu
OI Gao, Lei/0000-0003-1476-1460
FU National Institutes of Health, Bethesda, Maryland [DP2-OD006454,
DP1-OD003646, TR01-GM104948, T32GM007592]; Foundation of Anesthesia
Education and Research, Rochester, Minnesota; Massachusetts General
Hospital Faculty Development Award, Boston, Massachusetts; Department of
Anesthesia, Critical Care, and Pain Medicine, Massachusetts General
Hospital, Boston, Massachusetts
FX Supported by grant numbers DP2-OD006454 (to Dr. Purdon), DP1-OD003646
and TR01-GM104948 (to Dr. Brown), and T32GM007592 (to Drs. Akeju and
Rhee) from the National Institutes of Health, Bethesda, Maryland;
Foundation of Anesthesia Education and Research, Rochester, Minnesota
(to Dr. Akeju); Massachusetts General Hospital Faculty Development
Award, Boston, Massachusetts (to Dr. Akeju); and funds from the
Department of Anesthesia, Critical Care, and Pain Medicine,
Massachusetts General Hospital, Boston, Massachusetts.
NR 37
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U1 1
U2 14
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
EI 1528-1175
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2014
VL 121
IS 5
BP 978
EP 989
DI 10.1097/ALN.0000000000000419
PG 12
WC Anesthesiology
SC Anesthesiology
GA AS6JA
UT WOS:000344368700013
PM 25187999
ER
PT J
AU Akeju, O
Westover, MB
Pavone, KJ
Sampson, AL
Hartnack, KE
Brown, EN
Purdon, PL
AF Akeju, Oluwaseun
Westover, M. Brandon
Pavone, Kara J.
Sampson, Aaron L.
Hartnack, Katharine E.
Brown, Emery N.
Purdon, Patrick L.
TI Effects of Sevoflurane and Propofol on Frontal Electroencephalogram
Power and Coherence
SO ANESTHESIOLOGY
LA English
DT Article
ID INDUCED ALPHA-RHYTHM; GENERAL-ANESTHESIA; INDUCED UNCONSCIOUSNESS;
INHALED ANESTHETICS; CALCIUM CURRENTS; CONSCIOUSNESS; MECHANISMS;
ISOFLURANE; NEURONS; SLEEP
AB Background: The neural mechanisms of anesthetic vapors have not been studied in depth. However, modeling and experimental studies on the intravenous anesthetic propofol indicate that potentiation of -aminobutyric acid receptors leads to a state of thalamocortical synchrony, observed as coherent frontal alpha oscillations, associated with unconsciousness. Sevoflurane, an ether derivative, also potentiates -aminobutyric acid receptors. However, in humans, sevoflurane-induced coherent frontal alpha oscillations have not been well detailed.
Methods: To study the electroencephalogram dynamics induced by sevoflurane, the authors identified age- and sex-matched patients in which sevoflurane (n = 30) or propofol (n = 30) was used as the sole agent for maintenance of general anesthesia during routine surgery. The authors compared the electroencephalogram signatures of sevoflurane with that of propofol using time-varying spectral and coherence methods.
Results: Sevoflurane general anesthesia is characterized by alpha oscillations with maximum power and coherence at approximately 10 Hz, (mean SD; peak power, 4.3 +/- 3.5 dB; peak coherence, 0.73 +/- 0.1). These alpha oscillations are similar to those observed during propofol general anesthesia, which also has maximum power and coherence at approximately 10 Hz (peak power, 2.1 +/- 4.3 dB; peak coherence, 0.71 +/- 0.1). However, sevoflurane also exhibited a distinct theta coherence signature (peak frequency, 4.9 +/- 0.6 Hz; peak coherence, 0.58 +/- 0.1). Slow oscillations were observed in both cases, with no significant difference in power or coherence.
Conclusions: The study results indicate that sevoflurane, like propofol, induces coherent frontal alpha oscillations and slow oscillations in humans to sustain the anesthesia-induced unconscious state. These results suggest a shared molecular and systems-level mechanism for the unconscious state induced by these drugs.
C1 [Akeju, Oluwaseun; Pavone, Kara J.; Sampson, Aaron L.; Hartnack, Katharine E.; Brown, Emery N.; Purdon, Patrick L.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[Westover, M. Brandon] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Akeju, Oluwaseun; Brown, Emery N.; Purdon, Patrick L.] Harvard Univ, Sch Med, Boston, MA USA.
[Westover, M. Brandon; Brown, Emery N.; Purdon, Patrick L.] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
[Brown, Emery N.] MIT, Harvard Massachusetts Inst Technol Div Hlth Sci &, Cambridge, MA 02139 USA.
[Brown, Emery N.] MIT, Inst Med Engn & Sci, Cambridge, MA 02139 USA.
RP Purdon, PL (reprint author), Massachusetts Gen Hosp, 149 13th St,Rm 4005, Charlestown, MA 02129 USA.
EM patrickp@nmr.mgh.harvard.edu
FU National Institutes of Health, Bethesda, Maryland [DP2-OD006454,
DP1-OD003646, TR01-GM104948, T32GM007592]; Foundation of Anesthesia
Education and Research, Rochester, Minnesota; Massachusetts General
Hospital Faculty Development Award, Boston, Massachusetts; Department of
Anesthesia, Critical Care, and Pain Medicine, Massachusetts General
Hospital, Boston, Massachusetts
FX Supported by grant numbers DP2-OD006454 (to Dr. Purdon), DP1-OD003646
and TR01-GM104948 (to Dr. Brown), and T32GM007592 (to Dr. Akeju) from
the National Institutes of Health, Bethesda, Maryland; Foundation of
Anesthesia Education and Research, Rochester, Minnesota (to Dr. Akeju);
Massachusetts General Hospital Faculty Development Award, Boston,
Massachusetts (to Dr. Akeju); and funds from the Department of
Anesthesia, Critical Care, and Pain Medicine, Massachusetts General
Hospital, Boston, Massachusetts.
NR 32
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Z9 21
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
EI 1528-1175
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2014
VL 121
IS 5
BP 990
EP 998
DI 10.1097/ALN.0000000000000436
PG 9
WC Anesthesiology
SC Anesthesiology
GA AS6JA
UT WOS:000344368700014
PM 25233374
ER
PT J
AU Cohen, SP
Hayek, S
Semenov, Y
Pasquina, PF
White, RL
Veizi, E
Huang, JHY
Kurihara, C
Zhao, ZR
Guthmiller, KB
Griffith, SR
Verdun, AV
Giampetro, DM
Vorobeychik, Y
AF Cohen, Steven P.
Hayek, Salim
Semenov, Yevgeny
Pasquina, Paul F.
White, Ronald L.
Veizi, Elias
Huang, Julie H. Y.
Kurihara, Connie
Zhao, Zirong
Guthmiller, Kevin B.
Griffith, Scott R.
Verdun, Aubrey V.
Giampetro, David M.
Vorobeychik, Yakov
TI Epidural Steroid Injections, Conservative Treatment, or Combination
Treatment for Cervical Radicular Pain A Multicenter, Randomized,
Comparative-effectiveness Study
SO ANESTHESIOLOGY
LA English
DT Article
ID LOW-BACK-PAIN; LUMBAR SPINAL STENOSIS; NEUROPATHIC PAIN; TRANSFORAMINAL
INJECTION; CONTROLLED-TRIAL; DOUBLE-BLIND; CORTICOSTEROID INJECTIONS;
CHRONIC RADICULOPATHY; DISK HERNIATION; ACUTE SCIATICA
AB Background: Cervical radicular pain is a major cause of disability. No studies have been published comparing different types of nonsurgical therapy.
Methods: A comparative-effectiveness study was performed in 169 patients with cervical radicular pain less than 4 yr in duration. Participants received nortriptyline and/or gabapentin plus physical therapies, up to three cervical epidural steroid injections (ESI) or combination treatment over 6 months. The primary outcome measure was average arm pain on a 0 to 10 scale at 1 month.
Results: One-month arm pain scores were 3.5 (95% CI, 2.8 to 4.2) in the combination group, 4.2 (CI, 2.8 to 4.2) in ESI patients, and 4.3 (CI, 2.8 to 4.2) in individuals treated conservatively (P = 0.26). Combination group patients experienced a mean reduction of -3.1 (95% CI, -3.8 to -2.3) in average arm pain at 1 month versus -1.8 (CI, -2.5 to -1.2) in the conservative group and -2.0 (CI, -2.7 to -1.3) in ESI patients (P = 0.035). For neck pain, a mean reduction of -2.2 (95% CI, -3.0 to -1.5) was noted in combination patients versus -1.2 (CI, -1.9 to -0.5) in conservative group patients and -1.1 (CI, -1.8 to -0.4) in those who received ESI; P = 0.064). Three-month posttreatment, 56.9% of patients treated with combination therapy experienced a positive outcome versus 26.8% in the conservative group and 36.7% in ESI patients (P = 0.006).
Conclusions: For the primary outcome measure, no significant differences were found between treatments, although combination therapy provided better improvement than stand-alone treatment on some measures. Whereas these results suggest an interdisciplinary approach to neck pain may improve outcomes, confirmatory studies are needed.
C1 [Cohen, Steven P.] Johns Hopkins Sch Med, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21029 USA.
[Cohen, Steven P.] Johns Hopkins Sch Med, Dept Phys Med & Rehabil, Baltimore, MD 21029 USA.
[Cohen, Steven P.] Uniformed Serv Univ Hlth Sci, Dept Anesthesiol, Bethesda, MD 20814 USA.
[Hayek, Salim] Univ Hosp Cleveland, Dept Anesthesiol, Case Western Reserve Sch Med, Cleveland, OH 44106 USA.
[Semenov, Yevgeny] Harvard Univ, Sch Med, Dept Anesthesia, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Pasquina, Paul F.] Uniformed Serv Univ Hlth Sci, Dept Phys Med & Rehabil, Bethesda, MD 20814 USA.
[White, Ronald L.] Reg Med Ctr, Dept Surg, Pain Treatment Ctr, Landstuhl, Germany.
[Veizi, Elias] Case Western Reserve Univ, Dept Anesthesiol, Louis Stokes Cleveland VA Med Ctr, Cleveland, OH 44106 USA.
[Huang, Julie H. Y.] Weill Cornell Med Univ, Mem Sloan Kettering Canc Ctr, Dept Anesthesiol, New York, NY USA.
[Kurihara, Connie; Griffith, Scott R.; Verdun, Aubrey V.] Walter Reed Natl Mil Med Ctr, Dept Surg, Anesthesia Serv, Bethesda, MD USA.
[Zhao, Zirong] Dist Columbia VA Hosp, Dept Internal Med, Washington, DC USA.
[Zhao, Zirong] Dist Columbia VA Hosp, Dept Neurol, Washington, DC USA.
[Guthmiller, Kevin B.] San Antonio Mil Med Ctr, Dept Anesthesiol, Pain Treatment Ctr, San Antonio, TX USA.
[Griffith, Scott R.; Verdun, Aubrey V.] Uniformed Serv Univ Hlth Sci, Dept Anesthesiol, Bethesda, MD 20814 USA.
[Giampetro, David M.; Vorobeychik, Yakov] Penn State Hershey Med Ctr, Dept Anesthesiol, Hershey, PA USA.
[Giampetro, David M.; Vorobeychik, Yakov] Penn State Hershey Med Ctr, Dept Neurol, Hershey, PA USA.
RP Cohen, SP (reprint author), Johns Hopkins Sch Med, 550 North Broadway,Suite 301, Baltimore, MD 21029 USA.
EM scohen40@jhmi.edu
FU Congressional Grant from the Center for Rehabilitation Sciences
Research, Uniformed Services University of the Health Sciences,
Bethesda, Maryland, SAP Grant [111726]
FX Funded in part by a Congressional Grant from the Center for
Rehabilitation Sciences Research, Uniformed Services University of the
Health Sciences, Bethesda, Maryland, SAP Grant No. 111726. The role of
the funding source was only provisions to pay research personnel.
NR 64
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U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
EI 1528-1175
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2014
VL 121
IS 5
BP 1045
EP 1055
DI 10.1097/ALN.0000000000000409
PG 11
WC Anesthesiology
SC Anesthesiology
GA AS6JA
UT WOS:000344368700020
PM 25335172
ER
PT J
AU Baer, L
Ball, S
Sparks, JD
Raskin, J
Dube, S
Ferguson, M
Fava, M
AF Baer, Lee
Ball, Susan
Sparks, Jon David
Raskin, Joel
Dube, Sanjay
Ferguson, Margaret
Fava, Maurizio
TI Further evidence for the reliability and validity of the Massachusetts
General Hospital Cognitive and Physical Functioning Questionnaire (CPFQ)
SO ANNALS OF CLINICAL PSYCHIATRY
LA English
DT Article
ID MAJOR DEPRESSIVE DISORDER; REUPTAKE INHIBITOR TREATMENT; RATING-SCALE;
DOUBLE-BLIND; RESIDUAL SYMPTOMS; ANXIETY DISORDER; PLACEBO; OUTCOMES;
FATIGUE; AUGMENTATION
AB BACKGROUND: The Massachusetts General Hospital Cognitive and Physical Functioning Questionnaire (CPFQ) was developed to assess clinically relevant cognitive and physical symptoms associated with depression that are not adequately assessed by traditional measures. Although the CPFQ has been shown previously to be a reliable and valid measure, the purpose of the present study was to provide additional evidence using larger samples from 4 independent clinical trials that were designed to test the efficacy and safety of different antidepressants.
METHODS: The psychometric analyses were based on data from 4 independent clinical trials that were designed to test the safety and efficacy of different antidepressants. Reliability of the items and of the overall questionnaire was evaluated with principal components analysis, whereas validity was assessed by associations of the questionnaire scores with convergent and divergent external criteria.
RESULTS: Overall, the results have replicated previous findings that the CPFQ has good internal reliability. Validation also is strengthened by the demonstration of predictive differences among known groups as well as a sensitivity to change with antidepressant treatment.
CONCLUSIONS: Results support the use of the CPFQ as a valuable instrument for the detection of clinically relevant symptoms that are not captured by typical measures of depression used for the assessment of treatment outcomes.
C1 [Baer, Lee; Fava, Maurizio] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Ball, Susan; Sparks, Jon David; Raskin, Joel; Dube, Sanjay; Ferguson, Margaret] Eli Lilly & Co, Indianapolis, IN 46285 USA.
[Ball, Susan] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[Dube, Sanjay] Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Pittsburgh, PA USA.
[Dube, Sanjay] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
RP Baer, L (reprint author), Massachusetts Gen Hosp, Dept Psychiat, Wang Ambulatory Care Ctr, Room 812 15 Parkman St, Boston, MA 02114 USA.
EM baer.lee@mgh.harvard.edu
FU Eli Lilly and Company
FX We thank Dr. Rodney Moore (inVentiv Health Clinical, funded by Eli Lilly
and Company) for his assistance in drafting the manuscript.
NR 36
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U1 1
U2 2
PU QUADRANT HEALTHCOM INC
PI PARSIPPANY
PA 7 CENTURY DRIVE, STE 302, PARSIPPANY, NJ 07054-4603 USA
SN 1040-1237
EI 1547-3325
J9 ANN CLIN PSYCHIATRY
JI Ann. Clin. Psychiatry
PD NOV
PY 2014
VL 26
IS 4
BP 270
EP 280
PG 11
WC Psychiatry
SC Psychiatry
GA AS8QT
UT WOS:000344514100005
PM 25401714
ER
PT J
AU Caceres, SM
Malcolm, KC
Taylor-Cousar, JL
Nichols, DP
Saavedra, MT
Bratton, DL
Moskowitz, SM
Burns, JL
Nick, JA
AF Caceres, Silvia M.
Malcolm, Kenneth C.
Taylor-Cousar, Jennifer L.
Nichols, David P.
Saavedra, Milene T.
Bratton, Donna L.
Moskowitz, Samuel M.
Burns, Jane L.
Nick, Jerry A.
TI Enhanced In Vitro Formation and Antibiotic Resistance of Nonattached
Pseudomonas aeruginosa Aggregates through Incorporation of Neutrophil
Products
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID CYSTIC-FIBROSIS PATIENTS; BACTERIAL BIOFILMS; INHALED TOBRAMYCIN;
GENE-EXPRESSION; F-ACTIN; SPUTUM; INFECTION; DNA; INFLAMMATION;
AZITHROMYCIN
AB Pseudomonas aeruginosa is a major pathogen in cystic fibrosis (CF) lung disease. Children with CF are routinely exposed to P. aeruginosa from the natural environment, and by adulthood, 80% of patients are chronically infected. P. aeruginosa in the CF airway exhibits a unique biofilm-like structure, where it grows in small clusters or aggregates of bacteria in association with abundant polymers of neutrophil-derived components F-actin and DNA, among other components. These aggregates differ substantially in size and appearance compared to surface-attached in vitro biofilm models classically utilized for studies but are believed to share properties of surface-attached biofilms, including antibiotic resistance. However, little is known about the formation and function of surface-independent modes of biofilm growth, how they might be eradicated, and quorum sensing communication. To address these issues, we developed a novel in vitro model of P. aeruginosa aggregates incorporating human neutrophil-derived products. Aggregates grown in vitro and those found in CF patients' sputum samples were morphologically similar; viable bacteria were distributed in small pockets throughout the aggregate. The lasA quorum sensing gene was differentially expressed in the presence of neutrophil products. Importantly, aggregates formed in the presence of neutrophils acquired resistance to tobramycin, which was lost when the aggregates were dispersed with DNase, and antagonism of tobramycin and azithromycin was observed. This novel yet simple in vitro system advances our ability to model infection of the CF airway and will be an important tool to study virulence and test alternative eradication strategies against P. aeruginosa.
C1 [Caceres, Silvia M.; Malcolm, Kenneth C.; Taylor-Cousar, Jennifer L.; Nichols, David P.; Saavedra, Milene T.; Nick, Jerry A.] Natl Jewish Hlth, Dept Med, Denver, CO 80206 USA.
[Nichols, David P.; Bratton, Donna L.] Natl Jewish Hlth, Dept Pediat, Denver, CO USA.
[Malcolm, Kenneth C.; Taylor-Cousar, Jennifer L.; Nichols, David P.; Saavedra, Milene T.; Nick, Jerry A.] Univ Colorado, Dept Med, Aurora, CO USA.
[Moskowitz, Samuel M.] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
[Moskowitz, Samuel M.] Harvard Univ, Sch Med, Boston, MA USA.
[Burns, Jane L.] Univ Washington, Sch Med, Dept Pediat, Div Pediat Infect Dis,Seattle Childrens Hosp, Seattle, WA 98195 USA.
RP Malcolm, KC (reprint author), Natl Jewish Hlth, Dept Med, Denver, CO 80206 USA.
EM malcolmk@njhealth.org
FU Investigator Support Trial grant from Genentech; Rebecca Runyon Bryan
Chair for Cystic Fibrosis; NIH [HL34303]
FX Support for this work was provided by an Investigator Support Trial
grant from Genentech and the Rebecca Runyon Bryan Chair for Cystic
Fibrosis (J.A.N.) and NIH HL34303 (D. L. B.).
NR 61
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Z9 6
U1 7
U2 14
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
EI 1098-6596
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD NOV
PY 2014
VL 58
IS 11
BP 6851
EP 6860
DI 10.1128/AAC.03514-14
PG 10
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA AS3EF
UT WOS:000344158600061
PM 25182651
ER
PT J
AU Fan, KH
Jiang, JB
Wang, ZR
Fan, RC
Yin, W
Sun, YG
Li, HQ
AF Fan, Kuohai
Jiang, Junbing
Wang, Zhirui
Fan, Ruicheng
Yin, Wei
Sun, Yaogui
Li, Hongquan
TI Expression and Purification of Soluble Porcine Cystatin 11 in Pichia
pastoris
SO APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY
LA English
DT Article
DE Antimicrobial activity; Pichia pastoris; Expression; Purification;
Porcine CST11
ID ANTIMICROBIAL PEPTIDES
AB Cystatin 11 (CST11) belongs to the cystatin type 2 family of cysteine protease inhibitors and exhibits antimicrobial activity in vitro. In this study, we describe the expression and purification of recombinant porcine CST11 in the Pichia pastoris system. We then assess its antimicrobial activity against Escherichia coli, Staphylococcus aureus, Staphylococcus epidermidis, and Bacillus subtilis by liquid growth inhibition assay. Kinetic studies indicate that the recombinant porcine CST11 has high potency against E. coli and S. aureus. Scanning electronic microscope analysis showed that CST11 might be targeting the bacterial membrane and, thus, could potentially be developed as a therapeutic agent for inhibiting microbe infection without the risk of antibiotic resistance.
C1 [Fan, Kuohai; Jiang, Junbing; Fan, Ruicheng; Yin, Wei; Sun, Yaogui; Li, Hongquan] Shanxi Agr Univ, Coll Anim Sci & Vet Med, Taigu 030801, Shanxi, Peoples R China.
[Wang, Zhirui] Massachusetts Gen Hosp, Transplantat Biol Res Ctr, Boston, MA 02114 USA.
[Wang, Zhirui] Harvard Univ, Sch Med, Boston, MA USA.
[Wang, Zhirui] MGH DF HCC Recombinant Prot Express & Purificat C, Boston, MA USA.
RP Li, HQ (reprint author), Shanxi Agr Univ, Coll Anim Sci & Vet Med, Taigu 030801, Shanxi, Peoples R China.
EM livets@163.com
FU Key Scientific and Technological Project of Shanxi Province
[20100312016]
FX This research was sponsored by the Key Scientific and Technological
Project of Shanxi Province (Grant No. 20100312016). These experiments
comply with the current laws of China.
NR 13
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U1 1
U2 11
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0273-2289
EI 1559-0291
J9 APPL BIOCHEM BIOTECH
JI Appl. Biochem. Biotechnol.
PD NOV
PY 2014
VL 174
IS 5
BP 1959
EP 1968
DI 10.1007/s12010-014-1148-z
PG 10
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA AS5XK
UT WOS:000344339700021
PM 25161037
ER
PT J
AU Tsao, CW
Pencina, KM
Massaro, JM
Benjamin, EJ
Levy, D
Vasan, RS
Hoffmann, U
O'Donnell, CJ
Mitchell, GF
AF Tsao, Connie W.
Pencina, Karol M.
Massaro, Joseph M.
Benjamin, Emelia J.
Levy, Daniel
Vasan, Ramachandran S.
Hoffmann, Udo
O'Donnell, Christopher J.
Mitchell, Gary F.
TI Cross-Sectional Relations of Arterial Stiffness, Pressure Pulsatility,
Wave Reflection, and Arterial Calcification
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE hemodynamics; vascular calcification; vascular stiffness
ID ISOLATED SYSTOLIC HYPERTENSION; CORONARY-HEART-DISEASE; AORTIC
STIFFNESS; CARDIOVASCULAR EVENTS; OLDER-ADULTS; ATHEROSCLEROSIS;
ROTTERDAM; CALCIUM; AGE; ASSOCIATION
AB Objective Arterial hemodynamics and vascular calcification are associated with increased risk for cardiovascular disease, but their inter-relations remain unclear. We sought to examine the associations of arterial stiffness, pressure pulsatility, and wave reflection with arterial calcification in individuals free of prevalent cardiovascular disease.
Approach and Results Framingham Heart Study Third Generation and Offspring Cohort participants free of cardiovascular disease underwent applanation tonometry to measure arterial stiffness, pressure pulsatility, and wave reflection, including carotid-femoral pulse wave velocity, central pulse pressure, forward wave amplitude, and augmentation index. Participants in each cohort (n=1905, 456 years and n=1015, 65 +/- 9 years, respectively) underwent multidetector computed tomography to assess the presence and quantity of thoracic aortic calcification, abdominal aortic calcification, and coronary artery calcification. In multivariable-adjusted models, both higher carotid-femoral pulse wave velocity and central pulse pressure were associated with greater thoracic aortic calcification and abdominal aortic calcification, whereas higher augmentation index was associated with abdominal aortic calcification. Among the tonometry measures, carotid-femoral pulse wave velocity was the strongest correlate of all calcification measures in multivariable-adjusted models (odds ratio per SD for thoracic aortic calcification, 2.69 [95% confidence interval, 2.17-3.35]; abdominal aortic calcification, 1.47 [95% confidence interval, 1.26-1.73]; and coronary artery calcification, 1.48 [95% confidence interval, 1.28-1.72]; all P<0.001, respectively). We observed stronger relations of carotid-femoral pulse wave velocity, central pulse pressure, and forward wave amplitude with nearly all continuous calcification measures in the younger Third Generation Cohort as compared with the Offspring Cohort.
Conclusions In community-dwelling individuals without prevalent cardiovascular disease, abnormal central arterial hemodynamics were positively associated with vascular calcification and were observed at younger ages than previously recognized. The mechanisms of these associations may be bidirectional and deserve further study.
C1 [Tsao, Connie W.] Beth Israel Deaconess Med Ctr, Div Cardiovasc, Dept Med, Boston, MA 02215 USA.
[Pencina, Karol M.; Massaro, Joseph M.] Boston Univ, Sch Med, Dept Biostat, Sch Publ Hlth, Boston, MA 02215 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Epidemiol, Sch Publ Hlth, Boston, MA 02215 USA.
[Benjamin, Emelia J.; Vasan, Ramachandran S.] Boston Univ, Sch Med, Dept Med, Sect Cardiol & Preventat Med, Boston, MA 02215 USA.
[Levy, Daniel] NHLBI, Bethesda, MD 20892 USA.
[Tsao, Connie W.; Benjamin, Emelia J.; Levy, Daniel; Vasan, Ramachandran S.; O'Donnell, Christopher J.] Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Tsao, Connie W.; O'Donnell, Christopher J.] NHLBI, Div Intramural Res, Bethesda, MD 20892 USA.
[O'Donnell, Christopher J.] Massachusetts Gen Hosp, Dept Med, Div Cardiol, Boston, MA 02114 USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Mitchell, Gary F.] Cardiovasc Engn Inc, Norwood, MA USA.
RP Tsao, CW (reprint author), Beth Israel Deaconess Med Ctr, Div Cardiovasc, 330 Brookline Ave,RW-453, Boston, MA 02215 USA.
EM ctsao1@bidmc.harvard.edu
OI Ramachandran, Vasan/0000-0001-7357-5970; Benjamin,
Emelia/0000-0003-4076-2336
FU National Heart, Lung, and Blood Institute [N01-HC-25195, HL076784,
AG028321, HL070100, HL060040, HL080124, HL071039, HL077447, HL107385];
National Institutes of Health [K23 HL118529]; American Heart Association
[13SDG14250015]; Harvard Medical School Fellowship
FX The Framingham Heart Study is supported by the National Heart, Lung, and
Blood Institute (N01-HC-25195, HL076784, AG028321, HL070100, HL060040,
HL080124, HL071039, HL077447, and HL107385). Dr Tsao is supported by
National Institutes of Health K23 HL118529, the American Heart
Association (13SDG14250015), and the Harvard Medical School Fellowship.
NR 29
TC 17
Z9 18
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1079-5642
EI 1524-4636
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD NOV
PY 2014
VL 34
IS 11
BP 2495
EP 2500
DI 10.1161/ATVBAHA.114.303916
PG 6
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA AS1QX
UT WOS:000344056400018
PM 25169933
ER
PT J
AU Baker, JF
Von Feldt, J
Mostoufi-Moab, S
Noaiseh, G
Taratuta, E
Kim, W
Leonard, MB
AF Baker, Joshua F.
Von Feldt, Joan
Mostoufi-Moab, Sogol
Noaiseh, Ghaith
Taratuta, Elena
Kim, Woojin
Leonard, Mary B.
TI Deficits in Muscle Mass, Muscle Density, and Modified Associations With
Fat in Rheumatoid Arthritis
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID CHRONIC KIDNEY-DISEASE; METABOLIC RISK-FACTORS; BODY-COMPOSITION;
BONE-STRUCTURE; ADIPOSITY; CACHEXIA; ADIPONECTIN; CHILDREN; OBESITY;
PATHOPHYSIOLOGY
AB Objective. To quantify muscle outcomes, independent of fat mass, in rheumatoid arthritis (RA) patients compared to healthy controls.
Methods. Quantitative computed tomography scans measured calf muscle and fat cross-sectional area (CSA) and muscle density (an index of intramuscular adipose tissue), and isometric dynamometry was used to measure ankle muscle strength in 50 participants with RA ages 18-70 years and 500 healthy controls. Multivariable linear regression models assessed muscle deficits in RA after adjusting for group differences in adiposity and assessing for an altered muscle-fat association. Associations between RA disease characteristics and fat-adjusted muscle outcomes were also assessed.
Results. Compared to controls, RA subjects had significantly greater body mass index (BMI) and fat area, and lower muscle area, muscle density, and muscle strength (P < 0.001 for all). Strength deficits were eliminated with adjustment for the smaller muscle area. The magnitude of muscle deficits, relative to controls, was significantly greater (P < 0.03 for interaction) in participants with lower fat area and BMI. Among those in the lower tertiles of adiposity, RA subjects demonstrated more significant deficits compared to controls with similar adiposity. In contrast, among those in the highest tertile for adiposity, RA was not associated with muscle deficits. Among RA, greater Sharp/van der Heijde scores were associated with lower muscle CSA and muscle density. Greater disease activity and disability were associated with low muscle density.
Conclusion. Deficits in muscle area and muscle density are present in RA patients compared to controls and are most pronounced in subjects with low fat mass. Greater joint destruction is associated with greater muscle deficits.
C1 [Baker, Joshua F.; Von Feldt, Joan] Univ Penn, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
[Baker, Joshua F.; Von Feldt, Joan; Mostoufi-Moab, Sogol; Taratuta, Elena; Kim, Woojin; Leonard, Mary B.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Mostoufi-Moab, Sogol; Leonard, Mary B.] Univ Penn, Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Noaiseh, Ghaith] Univ Pittsburgh, Pittsburgh, PA USA.
RP Baker, JF (reprint author), Hosp Univ Penn, Dept Med, Div Rheumatol, 8 Penn Tower Bldg,34th & Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM bakerjo@uphs.upenn.edu
FU University of Pennsylvania Clinical and Translational Research Center
[UL1-RR024134]
FX Supported by the University of Pennsylvania Clinical and Translational
Research Center (UL1-RR024134).
NR 35
TC 11
Z9 11
U1 1
U2 6
PU WILEY-BLACKWELL
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 2014
VL 66
IS 11
BP 1612
EP 1618
DI 10.1002/acr.22328
PG 7
WC Rheumatology
SC Rheumatology
GA AS5UF
UT WOS:000344334200003
PM 24664868
ER
PT J
AU Kerr, G
Aujero, M
Richards, J
Sayles, H
Davis, L
Cannon, G
Caplan, L
Michaud, K
Mikuls, T
AF Kerr, Gail
Aujero, Mireille
Richards, John
Sayles, Harlan
Davis, Lisa
Cannon, Grant
Caplan, Liron
Michaud, Kaleb
Mikuls, Ted
TI Associations of Hydroxychloroquine Use With Lipid Profiles in Rheumatoid
Arthritis: Pharmacologic Implications
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID DENSITY-LIPOPROTEIN CHOLESTEROL; MODIFYING ANTIRHEUMATIC DRUGS;
RISK-FACTORS; CARDIOVASCULAR RISK; DISEASE-ACTIVITY; VETERANS;
ATHEROSCLEROSIS; METHOTREXATE; MANAGEMENT; THERAPY
AB Objective. To evaluate the association of hydroxychloroquine (HCQ) use with lipid profiles in a Veterans Affairs Rheumatoid Arthritis (VARA) cohort.
Methods. Lipid profiles in HCQ users were compared with HCQ nonusers, adjusting for potential confounders (age, sex, race, disease activity, prednisone, disease-modifying antirheumatic drugs, diabetes mellitus, and statin use). Applying current National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) guidelines for reduction of cardiovascular disease (CVD) events risk, the frequency of target lipid profiles with HCQ status was evaluated. Varied periods of HCQ exposure were compared to ascertain pharmacologic associations with lipid values. CVDs were compared between HCQ users and nonusers.
Results. In an elderly, predominantly male VARA cohort, 1,011 patients had lipid profiles; 787 patients (77.8%) were white. Statin use was recorded in 11.6% of patients, diabetes mellitus in 33.5%, and CVD in 31.2%. HCQ users (n = 150) were older, had longer rheumatoid arthritis (RA) disease duration, and had lower disease activity. Optimum lipid profiles, including total cholesterol: high-density lipoprotein (HDL) and HDL: low-density lipoprotein ratios (P <= 0.001), were more frequent in HCQ users, with the exception of HDL (P = 0.165), and persisted in multivariate analyses. Similarly, more HCQ users had NCEP-ATP III target levels. Varied periods of HCQ exposure suggested lipid changes to occur early, but lost within a year of drug discontinuation. HCQ users had less prevalent CVD.
Conclusion. In RA patients, HCQ use of at least 3 months' duration was associated with better lipid profiles irrespective of disease activity or statin use. Given the increased CVD risks in RA and the relative low cost and toxicity of HCQ, continued use, regardless of treatment regimen, should be considered.
C1 [Kerr, Gail] Georgetown Univ, Washington DC Vet Affairs Med Ctr, Washington, DC USA.
[Kerr, Gail] Howard Univ Hosp, Washington, DC USA.
[Aujero, Mireille; Richards, John] Washington DC Vet Affairs Med Ctr, Washington, DC USA.
[Richards, John] Georgetown Univ, Washington, DC USA.
[Sayles, Harlan; Michaud, Kaleb; Mikuls, Ted] Univ Nebraska Med Ctr, Nebraska Arthrit Outcomes Res Ctr, Omaha, NE USA.
[Davis, Lisa; Caplan, Liron] Denver Vet Affairs Med Ctr, Denver, CO USA.
[Davis, Lisa; Caplan, Liron] Univ Colorado, Denver, CO 80202 USA.
[Cannon, Grant] George Whalen Vet Affairs Med Ctr, Salt Lake City, UT USA.
[Mikuls, Ted] Univ Nebraska Med Ctr, Omaha Vet Affairs Med Ctr, Omaha, NE USA.
RP Kerr, G (reprint author), Vet Affairs Med Ctr, Rheumatol Sect 151K, 50 Irving St NW, Washington, DC 20422 USA.
EM gail.kerr@va.gov
FU Nebraska Arthritis Outcomes Research Center at the University of
Nebraska Medical Center; Veterans Affairs Health Services Research and
Development Program of the Veterans Health Administration; Abbott
Laboratories; Amgen; Bristol-Myers Squibb; Veterans Health
Administration (Veterans Affairs Merit award); Veterans Affairs Health
Services Research and Development Program Career Development Award [CDA
07-221]
FX The Veterans Affairs Rheumatoid Arthritis Registry was supported by the
Nebraska Arthritis Outcomes Research Center at the University of
Nebraska Medical Center, the Veterans Affairs Health Services Research
and Development Program of the Veterans Health Administration, and
unrestricted grants from Abbott Laboratories, Amgen, and Bristol-Myers
Squibb. Dr. Mikuls' work was supported by the Veterans Health
Administration (Veterans Affairs Merit award) and a Veterans Affairs
Health Services Research and Development Program Career Development
Award (CDA 07-221).
NR 45
TC 13
Z9 13
U1 0
U2 0
PU WILEY-BLACKWELL
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 2014
VL 66
IS 11
BP 1619
EP 1626
DI 10.1002/acr.22341
PG 8
WC Rheumatology
SC Rheumatology
GA AS5UF
UT WOS:000344334200004
PM 24692402
ER
PT J
AU Nagaraja, V
Hays, RD
Khanna, PP
Spiegel, BMR
Chang, L
Melmed, GY
Bolus, R
Khanna, D
AF Nagaraja, Vivek
Hays, Ron D.
Khanna, Puja P.
Spiegel, Brennan M. R.
Chang, Lin
Melmed, Gil Y.
Bolus, Roger
Khanna, Dinesh
TI Construct Validity of the Patient-Reported Outcomes Measurement
Information System Gastrointestinal Symptom Scales in Systemic Sclerosis
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID QUALITY-OF-LIFE; TRACT INSTRUMENT; GASTROESOPHAGEAL-REFLUX; PHYSICAL
FUNCTION; SCLERODERMA; PROMIS; VALIDATION; MANIFESTATIONS; INVOLVEMENT;
MOTILITY
AB Objective. Gastrointestinal (GI) involvement is common in patients with systemic sclerosis (SSc; scleroderma). The Patient-Reported Outcomes Measurement Information System (PROMIS) GI symptom item bank captures upper and lower GI symptoms (reflux, disrupted swallowing, nausea/vomiting, belly pain, gas/bloating/flatulence, diarrhea, constipation, and fecal incontinence). The objective of this study was to evaluate the construct validity of the PROMIS GI bank in SSc.
Methods. A total of 167 patients with SSc were administered the PROMIS GI bank and the University of California, Los Angeles, Scleroderma Clinical Trials Consortium Gastrointestinal Scale (GIT 2.0) instrument. GIT 2.0 is a multi-item instrument that measures SSc-associated GI symptoms. Product-moment correlations and a multitrait-multimethod analysis of the PROMIS GI scales with the GIT 2.0 symptom scales were used to evaluate convergent and discriminant validity.
Results. Patients with SSc GI involvement had PROMIS GI scale scores 0.2-0.7 SD worse than the US general population. Correlations among scales measuring the same domains for the PROMIS GI and GIT 2.0 measures were large, ranging from 0.61 to 0.87 (average r = 0.77). The average correlation between different symptom scales was 0.22, supporting discriminant validity.
Conclusion. This study provides support for the construct validity of the PROMIS GI scales in SSc. Future research is needed to assess the responsiveness to change of these scales in patients with SSc.
C1 [Nagaraja, Vivek; Khanna, Puja P.; Khanna, Dinesh] Univ Michigan, Ann Arbor, MI 48109 USA.
[Hays, Ron D.] RAND Corp, Santa Monica, CA USA.
[Hays, Ron D.; Bolus, Roger] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Spiegel, Brennan M. R.] Univ Calif Los Angeles, David Geffen Sch Med, VA Greater Los Angeles Healthcare Syst, Los Angeles, CA 90095 USA.
[Spiegel, Brennan M. R.; Bolus, Roger] VA Ctr Outcomes Res & Educ, Los Angeles, CA USA.
[Chang, Lin] Univ Calif Los Angeles, David Geffen Sch Med, Gail & Gerald Oppenheimer Family Ctr Neurobiol St, Los Angeles, CA 90095 USA.
[Melmed, Gil Y.] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
RP Khanna, D (reprint author), Univ Michigan Scleroderma Program, Div Rheumatol, Dept Internal Med, 300 North Ingalls St,Suite 7C27,SPC 5422, Ann Arbor, MI 48109 USA.
EM khannad@med.umich.edu
FU NIH Common Fund Initiative (Northwestern University) [U54-AR-057951,
U01-AR-052177, U54-AR057943]; American Institutes for Research
[U54-AR-057926]; State University of New York, Stony Brook
[U01-AR-057948, U01-AR-052170]; University of Washington, Seattle
[U01-AR-057954, U01-AR-052171]; University of North Carolina, Chapel
Hill [U01-AR-052181]; Children's Hospital of Philadelphia
[U01-AR-057956]; Stanford University [U01-AR-052158]; Boston University
[U01-AR-057929]; University of California, Los Angeles [U01-AR-057936];
University of Pittsburgh [U01-AR-052155]; Georgetown University
[U01-AR-057971]; Children's Hospital Medical Center, Cincinnati
[U01-AR-057940]; University of Maryland, Baltimore [U01-AR-057967]; Duke
University [U01-AR-052186]; NIH/National Institute on Aging
[P30-AG-028748, P30-AG-021684]; National Center on Minority Health and
Health Disparities [2P20-MD-000182]; NIH/National Institute for
Arthritis and Musculoskeletal and Skin Disease [K24-AR-063120-02]
FX PROMIS was funded with cooperative agreements from the NIH Common Fund
Initiative (Northwestern University, grants U54-AR-057951,
U01-AR-052177, and U54-AR057943; American Institutes for Research, grant
U54-AR-057926; State University of New York, Stony Brook, grants
U01-AR-057948 and U01-AR-052170; University of Washington, Seattle,
grants U01-AR-057954 and U01-AR-052171; University of North Carolina,
Chapel Hill, grant U01-AR-052181; Children's Hospital of Philadelphia,
grant U01-AR-057956; Stanford University, grant U01-AR-052158; Boston
University, grant U01-AR-057929; University of California, Los Angeles,
grant U01-AR-057936; University of Pittsburgh, grant U01-AR-052155;
Georgetown University, grant U01-AR-057971; Children's Hospital Medical
Center, Cincinnati, grant U01-AR-057940; University of Maryland,
Baltimore, grant U01-AR-057967; and Duke University, grant
U01-AR-052186). See Appendix A for principal investigators and NIH
science officers.; Dr. Hays's work was supported by the NIH/National
Institute on Aging (grants P30-AG-028748 and P30-AG-021684) and the
National Center on Minority Health and Health Disparities (grant
2P20-MD-000182). Dr. Dinesh Khanna's work was supported by the
NIH/National Institute for Arthritis and Musculoskeletal and Skin
Disease (grant K24-AR-063120-02).
NR 31
TC 6
Z9 6
U1 13
U2 16
PU WILEY-BLACKWELL
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 2014
VL 66
IS 11
BP 1725
EP 1730
DI 10.1002/acr.22337
PG 6
WC Rheumatology
SC Rheumatology
GA AS5UF
UT WOS:000344334200017
PM 24692332
ER
PT J
AU Miloslavsky, EM
Specks, U
Merkel, PA
Seo, P
Spiera, R
Langford, CA
Hoffman, GS
Kallenberg, CGM
Clair, EWS
Tchao, NK
Viviano, L
Ding, L
Ikle, D
Villarreal, M
Jepson, B
Brunetta, P
Allen, NB
Fervenza, FC
Geetha, D
Keogh, K
Kissin, EY
Monach, PA
Peikert, T
Stegeman, C
Ytterberg, SR
Stone, JH
AF Miloslavsky, E. M.
Specks, U.
Merkel, P. A.
Seo, P.
Spiera, R.
Langford, C. A.
Hoffman, G. S.
Kallenberg, C. G. M.
Clair, E. W. St.
Tchao, N. K.
Viviano, L.
Ding, L.
Ikle, D.
Villarreal, M.
Jepson, B.
Brunetta, P.
Allen, N. B.
Fervenza, F. C.
Geetha, D.
Keogh, K.
Kissin, E. Y.
Monach, P. A.
Peikert, T.
Stegeman, C.
Ytterberg, S. R.
Stone, J. H.
CA Rituximab ANCA-Associated Vasculit
TI Rituximab for the Treatment of Relapses in Antineutrophil Cytoplasmic
Antibody-Associated Vasculitis
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; ACTIVE RHEUMATOID-ARTHRITIS;
ANCA-ASSOCIATED VASCULITIS; REMISSION-INDUCTION;
WEGENERS-GRANULOMATOSIS; MAINTENANCE THERAPY; RANDOMIZED-TRIAL;
RISK-FACTORS; CYCLOPHOSPHAMIDE; EFFICACY
AB Objective. Disease relapses are frequent in anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV). This study was undertaken to evaluate outcomes in patients with AAV who are re-treated with rituximab (RTX) and prednisone for severe disease relapses.
Methods. The Rituximab in AAV trial was a randomized, double-blind, placebo-controlled trial comparing the rates of remission induction among patients treated with RTX (n = 99) and patients treated with cyclophosphamide (CYC) followed by azathioprine (AZA) (n = 98). Prednisone was tapered to discontinuation after 5.5 months. After remission was achieved, patients who experienced a severe disease relapse between months 6 and 18 were eligible to receive RTX and prednisone on an open-label basis according to a pre-specified protocol. Investigators remained blinded with regard to the original treatment assignment.
Results. Twenty-six patients received RTX for disease relapse after remission had initially been achieved with their originally assigned treatment. Fifteen of these patients were initially randomized to receive RTX and 11 to receive CYC/AZA. Thirteen (87%) of the patients originally assigned to receive RTX and 10 (91%) originally assigned to receive CYC/AZA achieved remission again with open-label RTX (an overall percentage of 88%). In half of the patients treated with open-label RTX, prednisone could be discontinued entirely. Patients in this cohort experienced fewer adverse events compared to the overall study population (4.7 adverse events per patient-year versus 11.8 adverse events per patient-year).
Conclusion. Re-treatment of AAV relapses with RTX and glucocorticoids appears to be a safe and effective strategy, regardless of previous treatment.
C1 [Miloslavsky, E. M.; Stone, J. H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Specks, U.; Fervenza, F. C.; Keogh, K.; Peikert, T.; Ytterberg, S. R.] Mayo Clin, Rochester, MN USA.
[Merkel, P. A.] Univ Penn, Philadelphia, PA 19104 USA.
[Seo, P.; Geetha, D.] Johns Hopkins Univ, Baltimore, MD USA.
[Spiera, R.] Hosp Special Surg, New York, NY 10021 USA.
[Langford, C. A.; Hoffman, G. S.] Cleveland Clin, Cleveland, OH 44106 USA.
[Kallenberg, C. G. M.; Stegeman, C.] Univ Groningen, Univ Med Ctr Groningen, Groningen, Netherlands.
[Kallenberg, C. G. M.; Stegeman, C.] Univ Groningen, Univ Med Ctr Groningen, NL-9713 AV Groningen, Netherlands.
[Clair, E. W. St.; Allen, N. B.] Duke Univ, Med Ctr, Durham, NC USA.
[Tchao, N. K.] Immune Tolerance Network, San Francisco, CA USA.
[Ding, L.] NIAID, NIH, Bethesda, MD 20892 USA.
[Ikle, D.; Villarreal, M.; Jepson, B.] Rho, Chapel Hill, NC USA.
[Brunetta, P.] Genentech Inc, San Francisco, CA 94080 USA.
[Kissin, E. Y.; Monach, P. A.] Boston Univ, Sch Med, Boston, MA 02118 USA.
RP Stone, JH (reprint author), Massachusetts Gen Hosp, Rheumatol Unit, Yawkey 2C,55 Fruit St, Boston, MA 02114 USA.
EM jhstone@mgh.harvard.edu
FU NIH [N01-AI-15416, 1 UL1-RR-024150-01, UL1-RR-025005, K23-AR-052820,
K24-AR-049185, UL1-RR-025771, M01-RR-00533, K24-AR-02224]; National
Institute of Allergy and Infectious Diseases, NIH; Juvenile Diabetes
Research Foundation; Genentech (Clinical Immunology Fellowship);
Arthritis Foundation
FX The Rituximab in ANCA-Associated Vasculitis (RAVE) trial was performed
with the support of the Immune Tolerance Network (NIH contract
N01-AI-15416, protocol number ITN021AI), an international clinical
research consortium headquartered at the University of California San
Francisco and supported by the National Institute of Allergy and
Infectious Diseases, NIH and the Juvenile Diabetes Research Foundation.
Genentech and Biogen Idec provided the study medication and partial
funding for the RAVE trial. At the Mayo Clinic, Johns Hopkins
University, and Boston University School of Medicine, the RAVE trial was
supported by the NIH (Mayo Clinic: National Center for Research
Resources Clinical and Translational Science award 1 UL1-RR-024150-01;
Johns Hopkins University: National Center for Research Resources
Clinical and Translational Science award UL1-RR-025005 and career
development awards K23-AR-052820 to Dr. Seo and K24-AR-049185 to Dr.
Stone; Boston University: National Center for Research Resources
Clinical and Translational Science award UL1-RR-025771, grant
M01-RR-00533, and career development award K24-AR-02224 to Dr. Merkel).
Dr. Miloslavsky's work was supported by Genentech (Clinical Immunology
Fellowship 2012-2013). Dr. Monach's work was supported by the Arthritis
Foundation (Arthritis Investigator Award).
NR 24
TC 22
Z9 22
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2326-5191
EI 2326-5205
J9 ARTHRITIS RHEUMATOL
JI Arthritis Rheumatol.
PD NOV
PY 2014
VL 66
IS 11
BP 3151
EP 3159
DI 10.1002/art.38788
PG 9
WC Rheumatology
SC Rheumatology
GA AS6BI
UT WOS:000344349500025
PM 25047592
ER
PT J
AU Baker, JF
Smolen, JS
Aletaha, D
Shults, J
Conaghan, PG
Emery, P
Baker, DG
Ostergaard, M
AF Baker, Joshua F.
Smolen, Josef S.
Aletaha, Daniel
Shults, Justine
Conaghan, Philip G.
Emery, Paul
Baker, Daniel G.
Ostergaard, Mikkel
TI Is the modified Disease Activity Score superior to the Disease Activity
Score in early arthritis and rheumatoid arthritis? Comment on the
article by Baker et al Reply
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Letter
ID JOINT DAMAGE
C1 [Baker, Joshua F.] Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
[Baker, Joshua F.; Shults, Justine] Univ Penn, Philadelphia, PA 19104 USA.
[Smolen, Josef S.; Aletaha, Daniel] Med Univ Vienna, Vienna, Austria.
[Conaghan, Philip G.; Emery, Paul] Univ Leeds, Leeds Inst Rheumat & Musculoskeletal Med, Leeds, W Yorkshire, England.
[Conaghan, Philip G.; Emery, Paul] NIHR Leeds Musculoskeletal Biomed Res Unit, Leeds, W Yorkshire, England.
[Baker, Daniel G.] Janssen Res & Dev LLC, Spring House, PA USA.
[Ostergaard, Mikkel] Glostrup Cty Hosp, Copenhagen, Denmark.
[Ostergaard, Mikkel] Univ Copenhagen, Copenhagen, Denmark.
RP Baker, JF (reprint author), Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
NR 3
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2326-5191
EI 2326-5205
J9 ARTHRITIS RHEUMATOL
JI Arthritis Rheumatol.
PD NOV
PY 2014
VL 66
IS 11
BP 3245
EP 3246
DI 10.1002/art.38810
PG 3
WC Rheumatology
SC Rheumatology
GA AS6BI
UT WOS:000344349500037
PM 25132673
ER
PT J
AU Khosroshahi, A
Cheryk, LA
Bloch, DB
Stone, JH
AF Khosroshahi, Arezou
Cheryk, Lynn A.
Bloch, Donald B.
Stone, John H.
TI The prozone effect in serum assays for IgG4: comment on the article by
Khosroshahi et al Reply
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Letter
C1 [Khosroshahi, Arezou] Emory Univ, Sch Med, Atlanta, GA 30322 USA.
[Cheryk, Lynn A.] Mayo Clin Labs, Andover, MA USA.
[Bloch, Donald B.; Stone, John H.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Khosroshahi, A (reprint author), Emory Univ, Sch Med, Atlanta, GA 30322 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2326-5191
EI 2326-5205
J9 ARTHRITIS RHEUMATOL
JI Arthritis Rheumatol.
PD NOV
PY 2014
VL 66
IS 11
BP 3247
EP 3248
DI 10.1002/art.38751
PG 3
WC Rheumatology
SC Rheumatology
GA AS6BI
UT WOS:000344349500039
PM 24965491
ER
PT J
AU Zhao, SD
Parmigiani, G
Huttenhower, C
Waldron, L
AF Zhao, Sihai Dave
Parmigiani, Giovanni
Huttenhower, Curtis
Waldron, Levi
TI Mas-o-menos: a simple sign averaging method for discrimination in
genomic data analysis
SO BIOINFORMATICS
LA English
DT Article
ID GENE-EXPRESSION PROFILE; NEGATIVE BREAST-CANCER; OVARIAN-CANCER;
BLADDER-CANCER; MOLECULAR SUBTYPES; LINEAR-MODELS; ESTIMATING
COEFFICIENTS; UROTHELIAL CARCINOMA; PROGNOSTIC SIGNATURE; NO NEVERMIND
AB Motivation: The successful translation of genomic signatures into clinical settings relies on good discrimination between patient sub-groups. Many sophisticated algorithms have been proposed in the statistics and machine learning literature, but in practice simpler algorithms are often used. However, few simple algorithms have been formally described or systematically investigated.
Results: We give a precise definition of a popular simple method we refer to as mas-o-menos, which calculates prognostic scores for discrimination by summing standardized predictors, weighted by the signs of their marginal associations with the outcome. We study its behavior theoretically, in simulations and in an extensive analysis of 27 independent gene expression studies of bladder, breast and ovarian cancer, altogether totaling 3833 patients with survival outcomes. We find that despite its simplicity, mas-o-menos can achieve good discrimination performance. It performs no worse, and sometimes better, than popular and much more CPU-intensive methods for discrimination, including lasso and ridge regression.
C1 [Zhao, Sihai Dave] Univ Illinois, Dept Stat, Champaign, IL 61820 USA.
[Parmigiani, Giovanni; Huttenhower, Curtis] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Parmigiani, Giovanni] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
[Waldron, Levi] CUNY Hunter Coll, Sch Publ Hlth, New York, NY 10035 USA.
RP Zhao, SD (reprint author), Univ Illinois, Dept Stat, Champaign, IL 61820 USA.
OI Waldron, Levi/0000-0003-2725-0694
FU National Cancer Institute at the National Institutes of Health
[1RC4CA156551-01, 5P30 CA006516-46]; National Science Foundation [CAREER
DBI-1053486]
FX This work was funded by the National Cancer Institute at the National
Institutes of Health (1RC4CA156551-01 and 5P30 CA006516-46 to G.P.) and
by the National Science Foundation (CAREER DBI-1053486 to C.H.).
NR 65
TC 2
Z9 2
U1 0
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
EI 1460-2059
J9 BIOINFORMATICS
JI Bioinformatics
PD NOV 1
PY 2014
VL 30
IS 21
BP 3062
EP 3069
DI 10.1093/bioinformatics/btu488
PG 8
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA AT0SG
UT WOS:000344644600010
PM 25061068
ER
PT J
AU Lindqvist, D
Wolkowitz, OM
Mellon, S
Yehuda, R
Flory, JD
Henn-Haase, C
Bierer, LM
Abu-Amara, D
Coy, M
Neylan, TC
Makotkine, L
Reus, VI
Yan, X
Taylor, NM
Marmar, CR
Dhabhar, FS
AF Lindqvist, Daniel
Wolkowitz, Owen M.
Mellon, Synthia
Yehuda, Rachel
Flory, Janine D.
Henn-Haase, Clare
Bierer, Linda M.
Abu-Amara, Duna
Coy, Michelle
Neylan, Thomas C.
Makotkine, Louri
Reus, Victor I.
Yan, Xiaodan
Taylor, Nicole M.
Marmar, Charles R.
Dhabhar, Firdaus S.
TI Proinflammatory milieu in combat-related PTSD is independent of
depression and early life stress
SO BRAIN BEHAVIOR AND IMMUNITY
LA English
DT Article
DE Post-traumatic stress disorder (PTSD); Inflammation; Cytokines;
Depression; Early life trauma; Combat
ID C-REACTIVE PROTEIN; MAJOR DEPRESSION; GLUCOCORTICOID SENSITIVITY;
MYOCARDIAL-INFARCTION; SERUM INTERLEUKIN-6; DISORDER; IMMUNE;
INFLAMMATION; RISK; SYMPTOMS
AB Background: Chronic inflammation may be involved in combat-related post-traumatic stress disorder (PTSD) and may help explain comorbid physical diseases. However, the extent to which combat exposure per se, depression, or early life trauma, all of which are associated with combat PTSD, may confound the relationship between PTSD and inflammation is unclear.
Methods: We quantified interleukin (IL)-6, IL-1 beta, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and C-reactive protein (CRP) in 51 combat-exposed males with PTSD and 51 combat-exposed males without PTSD, and assessed PTSD and depression severity as well as history of early life trauma. To decrease the possibility of Type I errors, we summed standardized scores of IL-1 beta, IL-6, TNF alpha, IFN gamma and CRP into a total "pro-inflammatory score". PTSD symptom severity was assessed with the Clinician Administered PTSD Scale (CAPS) rating scale.
Results: Subjects with PTSD had significantly higher pro-inflammatory scores compared to combat-exposed subjects without PTSD (p = 0.006), and even after controlling for early life trauma, depression diagnosis and severity, body mass index, ethnicity, education, asthma/allergies, time since combat and the use of possibly confounding medications (p = 0.002). Within the PTSD group, the pro-inflammatory score was not significantly correlated with depressive symptom severity, CAPS total score, or with the number of early life traumas.
Conclusions: Combat-related PTSD in males is associated with higher levels of pro-inflammatory cytokines, even after accounting for depression and early life trauma. These results, from one of the largest studies of inflammatory cytokines in PTSD to date, suggest that immune activation may be a core element of PTSD pathophysiology more so than a signature of combat exposure alone. (C) 2014 Published by Elsevier Inc.
C1 [Lindqvist, Daniel; Wolkowitz, Owen M.; Coy, Michelle; Neylan, Thomas C.; Reus, Victor I.] Univ Calif San Francisco, Dept Psychiat, Sch Med, San Francisco, CA 94143 USA.
[Lindqvist, Daniel] Lund Univ, Dept Clin Sci, Sect Psychiat, Lund, Sweden.
[Mellon, Synthia] Univ Calif San Francisco, Sch Med, Dept OB GYN & Reprod Sci, San Francisco, CA 94143 USA.
[Yehuda, Rachel; Flory, Janine D.; Bierer, Linda M.; Makotkine, Louri] James J Peters Vet Adm Med Ctr, MSSM, Dept Psychiat, New York, NY USA.
[Henn-Haase, Clare; Abu-Amara, Duna; Yan, Xiaodan; Marmar, Charles R.] NYU, Dept Psychiat, Steven & Alexandra Cohen Vet Ctr Posttraumat Stre, New York, NY 10003 USA.
[Taylor, Nicole M.; Dhabhar, Firdaus S.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
RP Wolkowitz, OM (reprint author), Univ Calif San Francisco, Dept Psychiat, Sch Med, 401 Parnassus Ave, San Francisco, CA 94143 USA.
EM Owen.Wolkowitz@ucsf.edu; Charles.Marmar@nyumc.org
RI reus, victor/I-7923-2015
OI reus, victor/0000-0002-8193-5697
FU U.S. Department of Defense [W81XWH-11-2-0223, W81XWH-10-1-0021]; Mental
Illness Research, Education and Clinical Center (MIRECC); Swedish
Society of Medicine; Sjobring Foundation; OM Persson Foundation;
province of Scania (Sweden)
FX This study was supported by the following grants: U.S. Department of
Defense, W81XWH-11-2-0223 (PI: Charles Marmar); U.S. Department of
Defense, W81XWH-10-1-0021 (PI: Owen M. Wolkowitz); The Mental Illness
Research, Education and Clinical Center (MIRECC). Daniel Lindqvist
received postdoc grants from the Swedish Society of Medicine; the
Sjobring Foundation; the OM Persson Foundation and the province of
Scania (Sweden) state grants (ALF). The authors declare no conflict of
interest.
NR 71
TC 32
Z9 32
U1 9
U2 21
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0889-1591
EI 1090-2139
J9 BRAIN BEHAV IMMUN
JI Brain Behav. Immun.
PD NOV
PY 2014
VL 42
BP 81
EP 88
DI 10.1016/j.bbi.2014.06.003
PG 8
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA AS7IK
UT WOS:000344429900012
PM 24929195
ER
PT J
AU Narla, A
Payne, EM
Abayasekara, N
Hurst, SN
Raiser, DM
Look, AT
Berliner, N
Ebert, BL
Khanna-Gupta, A
AF Narla, Anupama
Payne, Elspeth M.
Abayasekara, Nirmalee
Hurst, Slater N.
Raiser, David M.
Look, A. Thomas
Berliner, Nancy
Ebert, Benjamin L.
Khanna-Gupta, Arati
TI L-Leucine improves the anaemia in models of Diamond Blackfan anaemia and
the 5q-syndrome in a TP53-independent way
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE diamond-blackfan anaemia; leucine; haematopoiesis; TP53
ID MTOR PATHWAY; ZEBRAFISH; RIBOSOMOPATHIES
AB Haploinsufficiency of ribosomal proteins (RPs) and upregulation of the tumour suppressor TP53 have been shown to be the common basis for the anaemia observed in Diamond Blackfan anaemia and 5q- myelodysplastic syndrome. We previously demonstrated that treatment with L-Leucine resulted in a marked improvement in anaemia in disease models. To determine if the L-Leucine effect was Tp53-dependent, we used antisense MOs to rps19 and rps14 in zebrafish; expression of tp53 and its downstream target cdkn1a remained elevated following L-leucine treatment. We confirmed this observation in human CD34+ cells. L-Leucine thus alleviates anaemia in RP-deficient cells in a TP53-independent manner.
C1 [Narla, Anupama] Stanford Univ, Sch Med, Lucile Packard Childrens Hosp, Div Pediat Hematol Oncol, Stanford, CA 94305 USA.
[Narla, Anupama; Abayasekara, Nirmalee; Hurst, Slater N.; Raiser, David M.; Berliner, Nancy; Ebert, Benjamin L.; Khanna-Gupta, Arati] Harvard Univ, Brigham & Womens Hosp, Div Hematol, Sch Med, Boston, MA 02115 USA.
[Payne, Elspeth M.] UCL, London, England.
[Payne, Elspeth M.] Univ Coll London Hosp, Natl Inst Hlth Res, Biomed Res Ctr, London, England.
[Look, A. Thomas] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Khanna-Gupta, A (reprint author), Brigham & Womens Hosp, Div Hematol, Karp Res Bldg,5th Floor,Room 5117, Boston, MA 02115 USA.
EM akhanna-gupta@partners.org
RI Zebrafish, UCL/A-3125-2009
FU National Institutes of Health [K08 DK090145-01A1]; American Society of
Hematology; Leukaemia and Lymphoma Research UK (GSK); Tomasso Family
Hematology Fund
FX The authors would like to thank Marie McConkey and Hong Sun for
technical assistance. This work was funded by the National Institutes of
Health (K08 DK090145-01A1) and the American Society of Hematology
(Scholar Award) to A.N, Leukaemia and Lymphoma Research UK (GSK Greg
Harper fellowship) to E. M. P, and by the Tomasso Family Hematology Fund
to AK-G.
NR 15
TC 11
Z9 11
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2014
VL 167
IS 4
BP 524
EP 528
DI 10.1111/bjh.13069
PG 5
WC Hematology
SC Hematology
GA AS6CA
UT WOS:000344351200011
PM 25098371
ER
PT J
AU Recklitis, CJ
Zhou, ES
Zwemer, EK
Hu, JC
Kantoff, PW
AF Recklitis, Christopher J.
Zhou, Eric S.
Zwemer, Eric K.
Hu, Jim C.
Kantoff, Philip W.
TI Suicidal Ideation in Prostate Cancer Survivors: Understanding the Role
of Physical and Psychological Health Outcomes
SO CANCER
LA English
DT Article
DE suicide ideation; prostate cancer; physical well-being; emotional
well-being; depression
ID REPLICATION NCS-R; QUALITY-OF-LIFE; RADICAL PROSTATECTOMY;
CHILDHOOD-CANCER; ADULT SURVIVORS; RISK-FACTORS; POPULATION; DEPRESSION;
THOUGHTS; VALIDATION
AB BACKGROUNDEpidemiological studies have shown prostate cancer (PC) survivors are at an increased risk of suicide compared with the general population, but to the authors' knowledge very little is known regarding what factors are associated with this increased risk. The current study examined the prevalence of suicidal ideation (SI) and its association with cancer treatment and posttreatment physical and emotional health in a cohort of long-term PC survivors.
METHODSA total of 693 PC survivors (3-8 years after diagnosis) completed a mailed survey on physical and psychological functioning, including cancer treatments, the Short Form-12 (SF-12), the Expanded Prostate Cancer Index Composite Instrument (EPIC-26), a depression rating scale, and 8 items regarding recent suicidal thoughts and behaviors.
RESULTSA total of 86 PC survivors (12.4%) endorsed SI, with 10 individuals (1.4%) reporting serious SI. Serious SI was more common in this sample compared with age-adjusted and sex-adjusted normative data. SI was not associated with most demographic variables, or with PC stage or treatments. However, SI was found to be significantly associated with employment status, poor physical and emotional functioning, greater symptom burden on the EPIC-26, higher frequency of significant pain, and clinically significant depression (P<.01). In an adjusted logistic model, poor physical and emotional function, including disability status and pain, were found to be associated with SI (P<.05), even after adjusting for depression.
CONCLUSIONSA significant percentage of PC survivors report recent SI, which is associated with both physical and psychological dysfunction, but not PC treatments. The results of the current study help to explain the increased risk of suicide previously reported in PC survivors and have important implications for identifying and treating those survivors at greatest risk of suicidality. Cancer 2014;120:3393-3400. (c) 2014 American Cancer Society.
C1 [Recklitis, Christopher J.; Zhou, Eric S.; Kantoff, Philip W.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Perini Family Survivors Ctr, Boston, MA 02115 USA.
[Zwemer, Eric K.] Boston Childrens Hosp, Dept Med, Boston, MA USA.
[Hu, Jim C.] Univ Calif Los Angeles, Dept Urol, Los Angeles, CA USA.
RP Recklitis, CJ (reprint author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM christopher_recklitis@dfci.harvard.edu
FU American Foundation for Suicide Prevention [PRG-1-10-156]
FX Supported by the American Foundation for Suicide Prevention
(PRG-1-10-156).
NR 47
TC 10
Z9 10
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 1
PY 2014
VL 120
IS 21
BP 3393
EP 3400
DI 10.1002/cncr.28880
PG 8
WC Oncology
SC Oncology
GA AS3FZ
UT WOS:000344164100020
PM 24962506
ER
PT J
AU Gareen, IF
Duan, FH
Greco, EM
Snyder, BS
Boiselle, PM
Park, ER
Fryback, D
Gatsonis, C
AF Gareen, Ilana F.
Duan, Fenghai
Greco, Erin M.
Snyder, Bradley S.
Boiselle, Phillip M.
Park, Elyse R.
Fryback, Dennis
Gatsonis, Constantine
TI Impact of Lung Cancer Screening Results on Participant Health-Related
Quality of Life and State Anxiety in the National Lung Screening Trial
SO CANCER
LA English
DT Article
DE quality of life; anxiety; lung cancer; screening; clinical trials
ID RISK PERCEPTIONS; SOCIOECONOMIC-STATUS; PROSTATE-CANCER; GUIDELINES;
MANAGEMENT; SOCIETY; SF-36; AGE
AB BACKGROUNDLow-dose computed tomography (LDCT) lung screening has been associated with a 20% reduction in lung cancer mortality. A major barrier to the adoption of lung screening is the potential negative psychological impact of a false-positive (FP) screen, occurring in 20% to 50% of those screened. The objective of this study was to assess the impact of abnormal findings on health-related quality of life (HRQoL) and anxiety in the American College of Radiology (ACRIN)/National Lung Screening Trial (NLST).
METHODSThe NLST was a randomized screening trial comparing LDCT with chest X-ray screening (CXR). This study was part of the original protocol. A total of 2812 participants at 16 of 23 ACRIN sites who had baseline HRQoL assessments were asked to complete the Short Form-36 and the State Trait Anxiety Inventory (form Y-1) questionnaires to assess short-term (1 month) and long-term (6 months) effects of screening. FP were lung cancer-free at 1 year, and true-positives (TP) were not.
RESULTSOf the total participants, 1024 (36.4%) participants were FP, 63 (2.2%) were TP, 344 (12.2%) had significant incidental findings (SIFs), and 1381 (49.1%) had negative screens. Participants had been randomized to LDCT (n=1947) and CXR (n=865). Short-term and long-term HRQoL and state anxiety did not differ across participants with FP, SIF, or negative screens. Short-term and long-term HRQoL were lower and anxiety was higher for TP participants compared to participants with FP, SIF, and negative screens.
CONCLUSIONSIn a large multicenter lung screening trial, participants receiving a false-positive or SIF screen result experienced no significant difference in HRQoL or state anxiety at 1 or at 6 months after screening relative to those receiving a negative result. Cancer 2014;120:3401-3409. (c) 2014 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-No Derivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
C1 [Gareen, Ilana F.; Duan, Fenghai; Greco, Erin M.; Snyder, Bradley S.; Gatsonis, Constantine] Brown Univ, Ctr Stat Sci, Sch Publ Hlth, Providence, RI 02912 USA.
[Gareen, Ilana F.] Brown Univ, Dept Epidemiol, Sch Publ Hlth, Providence, RI 02912 USA.
[Duan, Fenghai; Gatsonis, Constantine] Brown Univ, Sch Publ Hlth, Dept Biostat, Providence, RI 02912 USA.
[Boiselle, Phillip M.] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Boiselle, Phillip M.] Harvard Univ, Sch Med, Boston, MA USA.
[Park, Elyse R.] Harvard Univ, Sch Med, Mongan Inst Hlth Policy, Boston, MA USA.
[Park, Elyse R.] Harvard Univ, Sch Med, Dept Med, Tobacco Res & Treatment Ctr,Massachusetts Gen Hos, Boston, MA USA.
[Park, Elyse R.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Fryback, Dennis] Univ Wisconsin Madison, Madison, WI USA.
RP Gareen, IF (reprint author), Brown Univ, Ctr Stat Sci, Box G-S121-7, Providence, RI 02912 USA.
EM igareen@stat.brown.edu
RI Gareen, Ilana/I-2816-2014
OI Gareen, Ilana/0000-0002-0457-5595
FU Cancer Imaging Program [U01-CA-80098, CA 79778]
FX This study was supported through grants U01-CA-80098 and CA 79778 under
a cooperative agreement with the Cancer Imaging Program.
NR 35
TC 28
Z9 28
U1 3
U2 28
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 1
PY 2014
VL 120
IS 21
BP 3401
EP 3409
DI 10.1002/cncr.28833
PG 9
WC Oncology
SC Oncology
GA AS3FZ
UT WOS:000344164100021
PM 25065710
ER
PT J
AU Beumer, JH
Owzar, K
Lewis, LD
Jiang, C
Holleran, JL
Christner, SM
Blum, W
Devine, S
Kolitz, JE
Linker, C
Vij, R
Alyea, EP
Larson, RA
Ratain, MJ
Egorin, MJ
AF Beumer, Jan H.
Owzar, Kouros
Lewis, Lionel D.
Jiang, Chen
Holleran, Julianne L.
Christner, Susan M.
Blum, William
Devine, Steven
Kolitz, Jonathan E.
Linker, Charles
Vij, Ravi
Alyea, Edwin P.
Larson, Richard A.
Ratain, Mark J.
Egorin, Merrill J.
TI Effect of age on the pharmacokinetics of busulfan in patients undergoing
hematopoietic cell transplantation; an alliance study (CALGB 10503,
19808, and 100103)
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Busulfan; Bone marrow transplant; Elderly; Pharmacokinetics
ID BONE-MARROW-TRANSPLANTATION; HIGH-DOSE BUSULFAN; DAILY IV BUSULFAN;
INTRAVENOUS BUSULFAN; BODY-WEIGHT; VENOOCCLUSIVE DISEASE; CONDITIONING
THERAPY; SYSTEMIC EXPOSURE; OLDER PATIENTS; CHILDREN
AB Older patients with acute myeloid leukemia (AML) and myelodysplastic syndrome have often been excluded from myeloablative-conditioning regimens containing busulfan because of non-disease-related morbidity and mortality. We hypothesized that busulfan clearance (BuCL) in older patients (> 60 years) would be reduced compared to that in younger patients, potentially explaining observed differences in busulfan tolerability.
AML patients in three CALGB hematopoietic cell transplantation studies were treated with a conditioning regimen using IV busulfan, dosed at 0.8 mg/kg. Plasma busulfan concentrations were determined by LC-MS and analyzed by non-compartmental methods. BuCL was normalized to actual (ABW), ideal (IBW), or corrected (CBW) body weight (kg). Differences in BuCL between age groups were examined using the Wilcoxon rank sum test.
One hundred and eighty-five patients were accrued; 174 provided useable pharmacokinetic data. Twenty-nine patients a parts per thousand yen60 years old (median 66; range 60-74) had a significantly higher BuCL versus those < 60 years old (median 50; range 18-60): BuCL 236 versus 168 mL/min, p = 0.0002; BuCL/ABW 3.0 versus 2.1 mL/min/kg, p = 0.0001; BuCL/IBW 3.8 versus 2.6 mL/min/kg, p = 0.0035; BuCL/CBW 3.4 versus 2.6 mL/min/kg, p = 0.0005. Inter-patient variability in clearance (CV %) was up to 48 % in both age groups. Phenytoin administration, a potential confounder, did not affect BuCL, regardless of weight normalization (p > 0.34).
Contrary to our hypothesis, BuCL was significantly higher in older patients compared to younger patients in these studies and does not explain the previously reported increase in busulfan toxicity observed in older patients.
C1 [Beumer, Jan H.] Univ Pittsburgh, Dept Pharmaceut Sci, Sch Pharm, Pittsburgh, PA 15213 USA.
[Beumer, Jan H.; Holleran, Julianne L.; Christner, Susan M.; Egorin, Merrill J.] Univ Pittsburgh, Canc Therapeut Program, Inst Canc, Pittsburgh, PA 15213 USA.
[Beumer, Jan H.] Univ Pittsburgh, Inst Canc, Melanoma Program, Pittsburgh, PA 15213 USA.
[Beumer, Jan H.] Univ Pittsburgh, Ctr Canc, Pittsburgh, PA 15213 USA.
[Owzar, Kouros; Jiang, Chen] Duke Univ, Med Ctr, Alliance Stat & Data Ctr, Durham, NC USA.
[Lewis, Lionel D.] Geisel Sch Med Dartmouth, Dartmouth Hitchcock Med Ctr, Norris Cotton Canc Ctr, Hanover, NH 03756 USA.
[Blum, William; Devine, Steven] Ohio State Univ, James Canc Hosp, Div Hematol, Columbus, OH 43210 USA.
[Kolitz, Jonathan E.] Hofstra North Shore LIJ Sch Med, Lake Success, NY 11042 USA.
[Linker, Charles] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Vij, Ravi] St Louis Univ, Sch Med, St Louis, MO 63110 USA.
[Alyea, Edwin P.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Alyea, Edwin P.] Brigham & Womens Hosp, Dept Med, Boston, MA 02215 USA.
[Alyea, Edwin P.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02215 USA.
[Larson, Richard A.; Ratain, Mark J.] Univ Chicago, Chicago, IL 60637 USA.
[Egorin, Merrill J.] Univ Pittsburgh, Dept Pharmacol & Chem Biol, Sch Med, Pittsburgh, PA 15213 USA.
[Egorin, Merrill J.] Univ Pittsburgh, Div Hematol Oncol, Sch Med, Dept Med, Pittsburgh, PA 15213 USA.
RP Beumer, JH (reprint author), Univ Pittsburgh, Ctr Canc, Hillman Res Pavilion,Room G27E,5117 Ctr Ave, Pittsburgh, PA 15213 USA.
EM beumerj@gmail.com; kouros.owzar@duke.edu; Lionel.D.Lewis@dartmouth.edu;
chen.jiang@duke.edu; HollJL@UPMC.EDU; christners@upmc.edu;
William.Blum@osumc.edu; Steven.Devine@osumc.edu; kolitz@nshs.edu;
chas.linker@gmail.com; rvij@dom.wustl.edu; Edwin_Alyea@dfci.harvard.edu;
rlarson@medicine.bsd.uchicago.edu; mratain@medicine.bsd.uchicago.edu
OI Larson, Richard/0000-0001-9168-3203; Beumer, Jan/0000-0002-8978-9401
FU National Cancer Institute [CA31946, CA33601]; Christiana Care Health
Services, Inc. CCOP, Wilmington, DE [CA45418]; Dana-Farber Cancer
Institute, Boston, MA [CA32291]; Monter Cancer Center of North Shore-LIJ
Health Systems, Lake Success, NY [CA35279]; Massachusetts General
Hospital, Boston, MA [CA32291]; Mount Sinai Medical Center, Miami, FL
[CA45564]; The Ohio State University Medical Center, Columbus, OH
[CA77658]; Rhode Island Hospital, Providence, RI [CA08025]; Roswell Park
Cancer Institute, Buffalo, NY [CA59518]; University of California at San
Francisco, San Francisco, CA [CA60138]; University of Chicago, Chicago,
IL [CA41287]; University of Maryland Greenebaum Cancer Center,
Baltimore, MD [CA31983]; University of Massachusetts Medical School,
Worcester, MA [CA37135]; University of Minnesota, Minneapolis, MN
[CA16450]; University of Nebraska Medical Center, Omaha, NE [CA77298];
University of North Carolina at Chapel Hill, Chapel Hill, NC [CA47559];
University of Vermont, Burlington, VT [CA77406]; Wake Forest University
School of Medicine, Winston-Salem, NC [CA03927]; Washington University
School of Medicine, St. Louis, MO [CA77440]; Weill Medical College of
Cornell University, New York, NY [CA07968]; Western Pennsylvania Cancer
Institute, Pittsburgh, PA [CA31946]; Dartmouth Medical School-Norris
Cotton Cancer Center, Lebanon, NH [CA04326]; Walter Reed Army Medical
Center, Washington, DC [CA26806]; [P30CA047904]
FX We thank the University of Pittsburgh Cancer Institute
Hematology/Oncology Writing Group for constructive suggestions regarding
the manuscript. This project used the UPCI Clinical Pharmacology
Analytical Facility (CPAF) and was supported in part by award
P30CA047904 (Jan H. Beumer). (Alliance) was supported, in part, by
grants from the National Cancer Institute (CA31946) to the Alliance for
Clinical Trials in Oncology (Monica M. Bertagnolli, M. D., Chair) and to
the Alliance Statistics and Data Center (Daniel J. Sargent, Ph.D.,
CA33601). The content of this manuscript is solely the responsibility of
the authors and does not necessarily represent the official views of the
National Cancer Institute. The following institutions participated in
this study: Christiana Care Health Services, Inc. CCOP, Wilmington, DE,
Stephen Grubbs, M.D., supported by CA45418; Dana-Farber Cancer
Institute, Boston, MA, Harold J. Burstein, M. D., Ph.D., supported by
CA32291; Monter Cancer Center of North Shore-LIJ Health Systems, Lake
Success, NY, Daniel Budman, MD, supported by CA35279; Massachusetts
General Hospital, Boston, MA, Jeffrey W. Clark, M. D., supported by
CA32291; Mount Sinai Medical Center, Miami, FL, Michael A. Schwartz, M.
D., supported by CA45564; The Ohio State University Medical Center,
Columbus, OH, Clara D. Bloomfield, M. D., supported by CA77658; Rhode
Island Hospital, Providence, RI, William Sikov, M. D., supported by
CA08025; Roswell Park Cancer Institute, Buffalo, NY, Ellis Levine, M.
D., supported by CA59518; University of California at San Francisco, San
Francisco, CA, Charles J. Ryan, M. D., supported by CA60138; University
of Chicago, Chicago, IL, Hedy L. Kindler, M. D., supported by CA41287;
University of Maryland Greenebaum Cancer Center, Baltimore, MD, Martin
Edelman, M. D., supported by CA31983; University of Massachusetts
Medical School, Worcester, MA, William V. Walsh, M. D., supported by
CA37135; University of Minnesota, Minneapolis, MN, Bruce A. Peterson, M.
D., supported by CA16450; University of Nebraska Medical Center, Omaha,
NE, Apar Ganti, M. D., supported by CA77298; University of North
Carolina at Chapel Hill, Chapel Hill, NC, Thomas C. Shea, M. D.,
supported by CA47559; University of Vermont, Burlington, VT, Steven M.
Grunberg, M. D., supported by CA77406; Wake Forest University School of
Medicine, Winston-Salem, NC, David D. Hurd, M. D., supported by CA03927;
Washington University School of Medicine, St. Louis, MO, Nancy Bartlett,
M. D., supported by CA77440; Weill Medical College of Cornell
University, New York, NY, John Leonard, M. D., supported by CA07968;
Western Pennsylvania Cancer Institute, Pittsburgh, PA, John Lister, M.
D., supported by CA31946; Dartmouth Medical School-Norris Cotton Cancer
Center, Lebanon, NH, Konstantin Dragnev, M. D., supported by CA04326;
Walter Reed Army Medical Center, Washington, DC, David C. Van Echo, M.
D., supported by CA26806.
NR 61
TC 4
Z9 4
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD NOV
PY 2014
VL 74
IS 5
BP 927
EP 938
DI 10.1007/s00280-014-2571-0
PG 12
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA AS5QF
UT WOS:000344324200005
PM 25163570
ER
PT J
AU Yonetsu, T
Suh, W
Abtahian, F
Kato, K
Vergallo, R
Kim, SJ
Jia, HB
McNulty, I
Lee, H
Jang, IK
AF Yonetsu, Taishi
Suh, William
Abtahian, Farhad
Kato, Koji
Vergallo, Rocco
Kim, Soo-Joong
Jia, Haibo
McNulty, Iris
Lee, Hang
Jang, Ik-Kyung
TI Comparison of Near-Infrared Spectroscopy and Optical Coherence
Tomography for Detection of Lipid
SO CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
LA English
DT Article
DE optical coherence tomography; spectroscopy; atherosclerosis; plaque
ID CORONARY PLAQUES; INTRAVASCULAR ULTRASOUND; ATHEROSCLEROTIC PLAQUES;
FIBROUS CAP; MORPHOLOGY; THERAPY; IMPACT; IVUS
AB ObjectivesTo compare intracoronary near-infrared spectroscopy (NIRS) and optical coherence tomography (OCT) for the detection of lipid, to identify NIRS signals to differentiate superficial lipid, and to characterize the plaque with yellow block (YB) chemograms on NIRS.
BackgroundIntracoronary NIRS has been developed to detect lipid core plaque (LCP).
MethodsWe investigated a total of 17 patients who underwent both OCT and NIRS. NIRS analysis included plaque lipid core burden index (LCBI), LCP length, and the presence of YB on the block chemogram. OCT analysis included maximum lipid arc (LA), the length of lipid (LL), lipid index, and the thinnest fibrous cap thickness (FCT).
ResultsTwenty-five plaques with >40% plaque burden were analyzed. LCP, showing LCBI>0, was observed in 20 plaques (80%) and YB was detected in seven plaques (28%). Plaque LCBI showed modest correlations with maximum LA and lipid index by OCT (r(2)=0.319, P=0.003 and r(2)=0. 404, P=0.001, respectively). Lipid length showed a significant correlation between NIRS and OCT measurements (r(2)=0.581, P<0.001). There was no significant difference in NIRS parameters between superficial and deep lipid. Plaques with YB compared with those without YB showed a larger LA, longer LL, and thinner FCT (18529 degrees vs. 105 +/- 76 degrees, P=0.014; 8.5 +/- 3.3 mm vs. 3.3 +/- 2.7 mm, P=0.001; 112 +/- 42 vs. 166 +/- 61 mu m, P=0.033).
ConclusionsNIRS and OCT parameters showed modest linear correlations in the measurement of lipid. The accurate depth of lipid in the vessel wall could not be identified by quantitative NIRS parameters. YB chemograms represented more vulnerable features on OCT. (c) 2013 Wiley Periodicals, Inc.
C1 [Yonetsu, Taishi; Abtahian, Farhad; Kato, Koji; Vergallo, Rocco; Kim, Soo-Joong; Jia, Haibo; McNulty, Iris; Jang, Ik-Kyung] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[Suh, William] Ronald Reagan UCLA Med Ctr, Los Angeles, CA USA.
[Kim, Soo-Joong] Kyung Hee Univ, Coll Med, Div Cardiol, Seoul, South Korea.
[Jia, Haibo] Harbin Med Univ, Affiliated Hosp 2, Dept Cardiol, Harbin, Peoples R China.
[Lee, Hang] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Biostat, Boston, MA USA.
RP Jang, IK (reprint author), Brigham & Womens Hosp, Div Cardiol, GRB 800,55 Fruit St, Boston, MA 02115 USA.
EM ijang@partners.org
FU LightLab Imaging/St. Jude Medical; "Enrico ed Enrica Sovena" Foundation;
InfraReDex
FX Grant sponsor: LightLab Imaging/St. Jude Medical (to I.K.J.), The
"Enrico ed Enrica Sovena" Foundation (to R.V.), and InfraReDex.
NR 16
TC 7
Z9 7
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1522-1946
EI 1522-726X
J9 CATHETER CARDIO INTE
JI Catheter. Cardiovasc. Interv.
PD NOV 1
PY 2014
VL 84
IS 5
BP 710
EP 717
DI 10.1002/ccd.25084
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AS0MS
UT WOS:000343971700005
PM 23785015
ER
PT J
AU Papakostas, TD
Jakobiec, FA
Mantagos, J
Rashid, A
Fay, A
Vavvas, DG
AF Papakostas, Thanos D.
Jakobiec, Frederick A.
Mantagos, Jason
Rashid, Alia
Fay, Aaron
Vavvas, Demetrios G.
TI Idiopathic dacryoadenitis mimicking a primary intraocular tumour in a
young girl
SO CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY
LA English
DT Letter
ID INFLAMMATORY ORBITAL PSEUDOTUMOR; LACRIMAL GLAND; CHILDHOOD
C1 [Papakostas, Thanos D.; Vavvas, Demetrios G.] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Retina Serv, Boston, MA 02115 USA.
[Fay, Aaron] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Oculoplast Serv,Dept Ophthalmol, Boston, MA USA.
[Jakobiec, Frederick A.; Rashid, Alia] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, David G Cogan Lab Ophthalm Pathol, Boston, MA USA.
[Mantagos, Jason] Harvard Univ, Childrens Hosp, Sch Med, Dept Ophthalmol, Boston, MA 02115 USA.
RP Papakostas, TD (reprint author), Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Retina Serv, Boston, MA 02115 USA.
OI Vavvas, Demetrios/0000-0002-8622-6478
NR 6
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1442-6404
EI 1442-9071
J9 CLIN EXP OPHTHALMOL
JI Clin. Exp. Ophthalmol.
PD NOV
PY 2014
VL 42
IS 8
BP 785
EP 788
PG 4
WC Ophthalmology
SC Ophthalmology
GA AS6MB
UT WOS:000344376500011
PM 24533840
ER
PT J
AU Shores, MM
Arnold, AM
Biggs, ML
Longstreth, WT
Smith, NL
Kizer, JR
Cappola, AR
Hirsch, CH
Marck, BT
Matsumoto, AM
AF Shores, Molly M.
Arnold, Alice M.
Biggs, Mary L.
Longstreth, W. T., Jr.
Smith, Nicholas L.
Kizer, Jorge R.
Cappola, Anne R.
Hirsch, Calvin H.
Marck, Brett T.
Matsumoto, Alvin M.
TI Testosterone and dihydrotestosterone and incident ischaemic stroke in
men in the Cardiovascular Health Study
SO CLINICAL ENDOCRINOLOGY
LA English
DT Article
ID HORMONE-BINDING GLOBULIN; SYMPTOMATIC ANDROGEN DEFICIENCY; OLDER MEN;
ELDERLY-MEN; SERUM TESTOSTERONE; METABOLIC SYNDROME; ARTERIAL STIFFNESS;
MASS-SPECTROMETRY; ESTRADIOL LEVELS; ALL-CAUSE
AB ObjectiveIschaemic stroke is a major cause of morbidity and mortality in elderly men. Our main objective was to examine whether testosterone (T) or dihydrotestosterone (DHT) was associated with incident ischaemic stroke in elderly men.
DesignCohort study.
ParticipantsElderly men in the Cardiovascular Health Study who had no history of stroke, heart disease or prostate cancer as of 1994 and were followed until December 2010.
MeasurementsAdjudicated ischaemic stroke.
ResultsAmong 1032 men (mean age 76, range 66-97), followed for a median of 10years, 114 had an incident ischaemic stroke. Total T and free T were not significantly associated with stroke risk, while DHT had a nonlinear association with incident stroke (P=0006) in analyses adjusted for stroke risk factors. The lowest risk of stroke was at DHT levels of 50-75ng/dl, with greater risk of stroke at DHT levels above 75ng/dl or below 50ng/dl. Results were unchanged when SHBG was added to the model. Calculated free DHT had an inverse linear association with incident ischaemic stroke with HR 077 (95% CI, 061, 098) per standard deviation in analyses adjusted for stroke risk factors.
ConclusionsDihydrotestosterone had a nonlinear association with stroke risk in which there was an optimal DHT level associated with the lowest stroke risk. Further studies are needed to confirm these results and to clarify whether there is an optimal androgen range associated with the least risk of adverse outcomes in elderly men.
C1 [Shores, Molly M.; Smith, Nicholas L.; Marck, Brett T.; Matsumoto, Alvin M.] VA Puget Sound Hlth Care Syst, Seattle, WA 98108 USA.
[Shores, Molly M.] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Arnold, Alice M.; Biggs, Mary L.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Longstreth, W. T., Jr.] Univ Washington, Dept Neurol, Seattle, WA 98195 USA.
[Longstreth, W. T., Jr.; Smith, Nicholas L.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Smith, Nicholas L.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
[Kizer, Jorge R.] Montefiore Med Ctr, Albert Einstein Coll Med, Dept Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Cappola, Anne R.] Univ Penn, Dept Internal Med, Div Endocrinol Diabet & Metab, Philadelphia, PA 19104 USA.
[Hirsch, Calvin H.] Univ Calif Davis, Dept Internal Med, Davis, CA 95616 USA.
[Marck, Brett T.; Matsumoto, Alvin M.] VA Puget Sound Hlth Care Syst, GRECC, Seattle, WA 98108 USA.
[Matsumoto, Alvin M.] Univ Washington, Dept Med, Div Gerontol & Geriatr Med, Seattle, WA USA.
RP Shores, MM (reprint author), VA Puget Sound Hlth Care Syst, 1660 S Columbian Way,S-116A, Seattle, WA 98108 USA.
EM molly.shores@va.gov
FU VA Research Service; VA Epidemiology Research and Information Center
(ERIC); VA Geriatric Research and Information Center (GRECC); National
Heart, Lung, and Blood Institute (NHLBI) [HHSN268201200036C,
N01-HC-85239, N01 HC-55222, N01-HC-85079, N01-HC-85080, N01-HC-85081,
N01-HC-85082, N01-HC-85083, N01-HC-85086, HL080295]; National Institute
on Aging (NIA) [AG-023629]; [1R01HL091952]
FX This project was supported by the VA Research Service, the VA
Epidemiology Research and Information Center (ERIC), and the VA
Geriatric Research and Information Center (GRECC) and by 1R01HL091952.
This research was supported by contracts HHSN268201200036C,
N01-HC-85239, N01 HC-55222, N01-HC-85079, N01-HC-85080, N01-HC-85081,
N01-HC-85082, N01-HC-85083, N01-HC-85086 and Grant HL080295 from the
National Heart, Lung, and Blood Institute (NHLBI), with additional
contribution from the National Institute of Neurological Disorders and
Stroke (NINDS). Additional support was provided by AG-023629 from the
National Institute on Aging (NIA). A full list of principal CHS
investigators and institutions can be found at http://www.chs-nhlbi.org.
NR 47
TC 12
Z9 12
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-0664
EI 1365-2265
J9 CLIN ENDOCRINOL
JI Clin. Endocrinol.
PD NOV
PY 2014
VL 81
IS 5
BP 746
EP 753
DI 10.1111/cen.12452
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AS3KR
UT WOS:000344176900015
PM 24645738
ER
PT J
AU Weisbord, SD
AF Weisbord, Steven D.
TI AKI and Medical Care after Coronary Angiography: Renalism Revisited
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Editorial Material
ID CHRONIC KIDNEY-DISEASE; MYOCARDIAL-INFARCTION; MORTALITY; INTERVENTION;
DECLINE; RISK
C1 [Weisbord, Steven D.] Vet Affairs Pittsburgh Healthcare Syst, Ctr Hlth Equity Res & Promot, Med Serv Line, Renal Sect, Pittsburgh, PA 15240 USA.
[Weisbord, Steven D.] Univ Pittsburgh, Sch Med, Dept Med, Renal Electrolyte Div, Pittsburgh, PA 15213 USA.
RP Weisbord, SD (reprint author), Vet Affairs Pittsburgh Healthcare Syst, Ctr Hlth Equity Res & Promot, Med Serv Line, Renal Sect, 7E 111F U,Room 120, Pittsburgh, PA 15240 USA.
EM weisbordsd@upmc.edu
NR 12
TC 1
Z9 1
U1 0
U2 2
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
EI 1555-905X
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD NOV
PY 2014
VL 9
IS 11
BP 1823
EP 1825
DI 10.2215/CJN.09430914
PG 3
WC Urology & Nephrology
SC Urology & Nephrology
GA AS7OY
UT WOS:000344446200001
PM 25318756
ER
PT J
AU Pendergraft, WF
Herlitz, LC
Thornley-Brown, D
Rosner, M
Niles, JL
AF Pendergraft, William F., III
Herlitz, Leal C.
Thornley-Brown, Denyse
Rosner, Mitchell
Niles, John L.
TI Nephrotoxic Effects of Common and Emerging Drugs of Abuse
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Review
ID ANDROGENIC STEROID USE; FOCAL SEGMENTAL GLOMERULOSCLEROSIS; COCAINE USE;
3,4-METHYLENEDIOXYMETHAMPHETAMINE MDMA; CANNABINOID RECEPTORS;
RENAL-DISEASE; GLOBAL BURDEN; ECSTASY MDMA; CASE SERIES; KIDNEY
AB The kidneys can be injured in diverse ways by many drugs, both legal and illegal. Novel associations and descriptions of nephrotoxic effects of common and emerging drugs of abuse have appeared over the past several years. Anabolic androgenic steroids, illicitly used by athletes and others for decades to increase muscle mass and decrease body fat, are emerging as podocyte toxins given recent descriptions of severe forms of FSGS in long-term abusers. Synthetic cannabinoids, a new group of compounds with marijuana-like effects, recently became popular as recreational drugs and have been associated with an atypical form of AKI. 3,4-Methylenedioxymethamphetamine, commonly known as ecstasy, is a widely used synthetic recreational drug with mood-enhancing properties and a constellation of toxicities that can result in death. These toxic effects include hyperthermia, hypotonic hyponatremia due to its arginine vasopressin secretagogue like effects, rhabdomyolysis, and cardiovascular collapse. Cocaine, a serotonin-norepinephrine-dopamine reuptake inhibitor that serves as an illegal stimulant, appetite suppressant, and anesthetic, also causes vasoconstriction and rhabdomyolysis. Recent adulteration of much of the world's supply of cocaine with levamisole, an antihelminthic agent with attributes similar to but distinct from those of cocaine, appears to have spawned a new type of ANCA-associated systemic vasculitis. This review discusses the nephrotoxic effects of these common and emerging drugs of abuse, of which both community and health care providers should become aware given their widespread abuse. Future investigation into pathogenetic mechanisms associated with these drugs is critical and may provide a window into ways to lessen and even prevent the nephrotoxic effects of these drugs of abuse and perhaps allow a deeper understanding of the nephrotoxicities themselves.
C1 [Pendergraft, William F., III] Univ N Carolina, Dept Med, Div Nephrol & Hypertens, UNC Kidney Ctr, Chapel Hill, NC USA.
[Pendergraft, William F., III; Niles, John L.] Massachusetts Gen Hosp, Dept Med, Div Nephrol, Boston, MA 02114 USA.
[Pendergraft, William F., III; Niles, John L.] Massachusetts Gen Hosp, Div Nephrol, Vasculitis & Glomerulonephritis Clin, Boston, MA 02114 USA.
[Herlitz, Leal C.] Columbia Univ, Ctr Med, Dept Pathol & Cell Biol, Div Renal Pathol, New York, NY USA.
[Thornley-Brown, Denyse] Univ Alabama Birmingham, Dept Internal Med, Div Nephrol, Birmingham, AL USA.
[Rosner, Mitchell] Univ Virginia Hlth Syst, Dept Med, Div Nephrol, Charlottesville, VA USA.
RP Niles, JL (reprint author), Massachusetts Gen Hosp, Dept Med, Div Nephrol, 151 Merrimac St,Floor 3, Boston, MA 02114 USA.
EM jlniles@partners.org
FU National Institute of Diabetes and Digestive and Kidney Diseases
[1-F32-DK097891-02]
FX W.F.P. is supported in part by National Institute of Diabetes and
Digestive and Kidney Diseases grant no. 1-F32-DK097891-02.
NR 92
TC 12
Z9 12
U1 3
U2 15
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 2014
VL 9
IS 11
BP 1996
EP 2005
DI 10.2215/CJN.00360114
PG 10
WC Urology & Nephrology
SC Urology & Nephrology
GA AS7OY
UT WOS:000344446200026
PM 25035273
ER
PT J
AU Fay, AP
Elfiky, A
Telo, GH
Mckay, RR
Kaymakcalan, M
Nguyen, PL
Vaidya, A
Ruan, DT
Bellmunt, J
Choueiri, TK
AF Fay, Andre P.
Elfiky, Aymen
Telo, Gabriela H.
Mckay, Rana R.
Kaymakcalan, Marina
Nguyen, Paul L.
Vaidya, Anand
Ruan, Daniel T.
Bellmunt, Joaquim
Choueiri, Toni K.
TI Adrenocortical carcinoma: The management of metastatic disease
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Adrenocortical carcinoma; Therapeutics; Targeted therapies; Metastatic
disease
ID ADRENAL-CORTICAL CARCINOMA; LONG-TERM SURVIVAL; ERLOTINIB PLUS
GEMCITABINE; PHASE-II; RADIATION-THERAPY; ADJUVANT MITOTANE;
RADIOFREQUENCY ABLATION; SURGICAL RESECTION; SIGNALING PATHWAY; MTOR
INHIBITORS
AB Adrenocortical cancer is a rare malignancy. While surgery is the cornerstone of the management of localized disease, metastatic disease is hard to treat. Cytotoxic chemotherapy and mitotane have been utilized with a variable degree of benefit and few long-term responses. A growing understanding of the molecular pathogenesis of this malignancy as well as multidisciplinary and multi-institutional collaborative efforts will result in better defined targets and subsequently, effective novel therapies. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Fay, Andre P.; Elfiky, Aymen; Mckay, Rana R.; Kaymakcalan, Marina; Nguyen, Paul L.; Ruan, Daniel T.; Bellmunt, Joaquim; Choueiri, Toni K.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Elfiky, Aymen; Nguyen, Paul L.; Vaidya, Anand; Ruan, Daniel T.; Bellmunt, Joaquim; Choueiri, Toni K.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Elfiky, Aymen; Nguyen, Paul L.; Vaidya, Anand; Ruan, Daniel T.; Bellmunt, Joaquim; Choueiri, Toni K.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Telo, Gabriela H.] Joslin Diabet Ctr, Boston, MA 02215 USA.
RP Choueiri, TK (reprint author), Dana Farber Canc Inst, 450 Brookline Ave DANA 1230, Boston, MA 02215 USA.
EM Andre_Fay@dfci.harvard.edu; toni_choueiri@dfci.harvard.edu
FU CAPES-CNPq - Brazil
FX Andre P. Fay receives a scholarship from CAPES-CNPq - Brazil.
NR 97
TC 8
Z9 8
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD NOV
PY 2014
VL 92
IS 2
BP 123
EP 132
DI 10.1016/j.critrevonc.2014.05.009
PG 10
WC Oncology; Hematology
SC Oncology; Hematology
GA AS8QW
UT WOS:000344514300005
PM 24958272
ER
PT J
AU Sabbatino, F
Fusciello, C
Somma, D
Pacelli, R
Poudel, R
Pepin, D
Leonardi, A
Carlomagno, C
Scarpati, GD
Ferrone, S
Pepe, S
AF Sabbatino, Francesco
Fusciello, Celeste
Somma, Domenico
Pacelli, Roberto
Poudel, Ravin
Pepin, David
Leonardi, Antonio
Carlomagno, Chiara
Scarpati, Giuseppina Della Vittoria
Ferrone, Soldano
Pepe, Stefano
TI Effect of p53 Activity on the Sensitivity of Human Glioblastoma Cells to
PARP-1 Inhibitor in Combination with Topoisomerase I Inhibitor or
Radiation
SO CYTOMETRY PART A
LA English
DT Article
DE p53; glioblastoma; PARP inhibitor; radiotherapy; topotecan;
combinatorial strategy
ID PHOSPHORYLATED HISTONE H2AX; ADP-RIBOSE POLYMERASE; DOUBLE-STRAND
BREAKS; POLY(ADP-RIBOSE) POLYMERASE; CANCER-THERAPY; PHASE-II;
MULTIFORME; TOPOTECAN; EXPRESSION; APOPTOSIS
AB Poly (ADP-Ribose) polymerase-1 (PARP-1) is involved in the DNA repairing system by sensing and signaling the presence of DNA damage. Inhibition of PARP-1 is tested in combination with DNA damaging agents such as topoisomerase I inhibitors or ionizing radiations (RT) for the treatment of glioblastoma (GBM). Disruption of p53, widely prevalent in GBMs, plays a major role in DNA repairing system. The current study investigates whether p53 activity has an effect on the sensitivity of human GBM cells to PARP-1 inhibitors in combination with topoisomerase I inhibitor topotecan (TPT) and/or RT. Human GBM cell lines carrying a different functional status of p53 were treated with PARP-1 inhibitor NU1025, in combination with TPT and/or RT. Cytotoxic effects were examined by analyzing the antiproliferative activity, the cell cycle perturbations, and the DNA damage induced by combined treatments. PARP inhibition enhanced the antiproliferative activity, the cell cycle perturbations and the DNA damage induced by both TPT or RT in GBM cells. These effects were influenced by the p53 activity: cells carrying an active p53 were more sensitive to the combination of PARP inhibitor and RT, while cells carrying an inactive p53 displayed a higher sensitivity to the combination of PARP inhibitor and TPT. Our study suggests that p53 activity influences the differential sensitivity of GBM cells to combined treatments of TPT, RT, and PARP inhibitors. (c) 2014 International Society for Advancement of Cytometry
C1 [Sabbatino, Francesco; Fusciello, Celeste; Carlomagno, Chiara] Univ Naples Federico II, Dept Clin Med & Surg, I-80131 Naples, Italy.
[Sabbatino, Francesco; Poudel, Ravin; Pepin, David; Ferrone, Soldano] Harvard Univ, Massachusetts Gen Hosp, Dept Surg, Sch Med, Boston, MA 02114 USA.
[Somma, Domenico; Leonardi, Antonio] Univ Naples Federico II, Dept Mol Med Med Biotechnol, I-80131 Naples, Italy.
[Pacelli, Roberto] Univ Naples Federico II, Dept Biomed Adv Sci, I-80131 Naples, Italy.
[Pacelli, Roberto] Inst Biostruct & Bioimaging CNR, I-80131 Naples, Italy.
[Scarpati, Giuseppina Della Vittoria] Univ Naples Federico II, Dept Diagnost Imaging & Radiat Oncol, I-80131 Naples, Italy.
[Pepe, Stefano] Univ Salerno, Fac Pharm & Med, Dept Med, I-84131 Salerno, Italy.
RP Sabbatino, F (reprint author), Massachusetts Gen Hosp, Dept Surg, 55 Fruit St, Boston, MA 02114 USA.
EM fsabbatino@partners.org
RI Sabbatino, Francesco/F-4992-2014;
OI LEONARDI, Antonio/0000-0001-8636-9623; Sabbatino,
Francesco/0000-0001-6431-8278; Poudel, Ravin/0000-0003-2622-3889
FU F.A.R.O. (Finanziamenti per l'avvio di ricerche originali); Polo delle
Scienze e delle Tecnologie per la Vita [0086257]; National Cancer
Institute PHS grants [RO1CA138188]; Fondazione Umberto Veronesi Post
Doctoral Fellowship
FX Grant sponsor: F.A.R.O. (Finanziamenti per l'avvio di ricerche
originali); Grant sponsor: Polo delle Scienze e delle Tecnologie per la
Vita, Grant number: 0086257; Grant sponsor: National Cancer Institute
PHS grants, Grant number: RO1CA138188; Grant sponsor: Fondazione Umberto
Veronesi Post Doctoral Fellowship
NR 44
TC 5
Z9 5
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4922
EI 1552-4930
J9 CYTOM PART A
JI Cytom. Part A
PD NOV
PY 2014
VL 85A
IS 11
BP 953
EP 961
DI 10.1002/cyto.a.22563
PG 9
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AS3GT
UT WOS:000344166300008
PM 25182801
ER
PT J
AU Choi, JH
Choi, SS
Kim, ES
Jedrychowski, MP
Yang, YR
Jang, HJ
Suh, PG
Banks, AS
Gygi, SP
Spiegelman, BM
AF Choi, Jang Hyun
Choi, Sun-Sil
Kim, Eun Sun
Jedrychowski, Mark P.
Yang, Yong Ryoul
Jang, Hyun-Jun
Suh, Pann-Ghill
Banks, Alexander S.
Gygi, Steven P.
Spiegelman, Bruce M.
TI Thrap3 docks on phosphoserine 273 of PPAR gamma and controls diabetic
gene programming
SO GENES & DEVELOPMENT
LA English
DT Article
DE PPAR gamma; phosphorylation; Thrap3 interaction; gene reprogramming;
energy homeostasis
ID ACTIVATED RECEPTOR-GAMMA; INSULIN-RESISTANCE; THYROID-HORMONE;
ADIPOSE-TISSUE; NUCLEAR RECEPTORS; COACTIVATOR COMPLEX; RETINOIC ACID;
CO-REPRESSOR; OBESITY; LIGAND
AB Phosphorylation of peroxisome proliferator-activated receptor gamma (PPAR gamma) at Ser273 by cyclin-dependent kinase 5 (CDK5) in adipose tissue stimulates insulin resistance, but the underlying molecular mechanisms are unclear. We show here that Thrap3 (thyroid hormone receptor-associated protein 3) can directly interact with PPAR gamma when it is phosphorylated at Ser273, and this interaction controls the diabetic gene programming mediated by the phosphorylation of PPAR gamma. Knockdown of Thrap3 restores most of the genes dysregulated by CDK5 action on PPAR gamma in cultured adipocytes. Importantly, reduced expression of Thrap3 in fat tissue by antisense oligonucleotides (ASOs) regulates a specific set of genes, including the key adipokines adiponectin and adipsin, and effectively improves hyperglycemia and insulin resistance in high-fat-fed mice without affecting body weight. These data indicate that Thrap3 plays a crucial role in controlling diabetic gene programming and may provide opportunities for the development of new therapeutics for obesity and type 2 diabetes.
C1 [Choi, Jang Hyun; Choi, Sun-Sil; Kim, Eun Sun; Yang, Yong Ryoul; Jang, Hyun-Jun; Suh, Pann-Ghill] Ulsan Natl Inst Sci & Technol, Dept Biol Sci, Ulsan 689798, South Korea.
[Jedrychowski, Mark P.; Gygi, Steven P.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
[Banks, Alexander S.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA.
[Spiegelman, Bruce M.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA.
RP Spiegelman, BM (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, 44 Binney St, Boston, MA 02115 USA.
EM janghchoi@unist.ac.kr; bruce_spiegelman@dfci.harvard.edu
RI Choi, Jang Hyun/B-3055-2012; Banks, Alexander/B-4832-2012
OI Banks, Alexander/0000-0003-1787-6925
FU National Research Foundation of Korea (NRF) - Ministry of Education,
Science, and Technology [NRF-2012R1A1A1015407]; NRF - Korean government
(Ministry of Science, ICT [Information and Communications Technology],
and Future Planning [MSIP]) [2010-0028684]; National Institutes of
Health (NIH) [K01DK093638]; NIH [DK031405]
FX We are grateful for technical assistance from the In Vivo Research
Center at Ulsan National Institute of Science and Technology. This work
was supported by the Basic Science Research Program through the National
Research Foundation of Korea (NRF) funded by Ministry of Education,
Science, and Technology grant NRF-2012R1A1A1015407 (to J.H.C., S.-S.C.,
and E.S.K.). Y.R.Y., H.-J.J, and P.-G.S. were supported by the NRF grant
funded by the Korean government (Ministry of Science, ICT [Information
and Communications Technology], and Future Planning [MSIP]) (no.
2010-0028684). A.S.B. is supported by National Institutes of Health
(NIH) K01DK093638, and B.M.S. is supported by NIH DK031405.
NR 48
TC 12
Z9 12
U1 0
U2 7
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 0890-9369
EI 1549-5477
J9 GENE DEV
JI Genes Dev.
PD NOV 1
PY 2014
VL 28
IS 21
BP 2361
EP 2369
DI 10.1101/gad.249367.114
PG 9
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA AS7OZ
UT WOS:000344446300003
PM 25316675
ER
PT J
AU Willems, T
Gymrek, M
Highnam, G
Mittelman, D
Erlich, Y
AF Willems, Thomas
Gymrek, Melissa
Highnam, Gareth
Mittelman, David
Erlich, Yaniv
CA 1000 Genomes Project Consortium
TI The landscape of human STR variation
SO GENOME RESEARCH
LA English
DT Article
ID MULTILOCUS GENOTYPE DATA; DINUCLEOTIDE REPEAT; TANDEM REPEATS; HUMAN
GENOME; MICROSATELLITE VARIABILITY; LINKAGE DISEQUILIBRIUM; ALLELE
FREQUENCIES; FUNCTIONAL IMPACT; PERSONAL GENOMES; MUTATION-RATES
AB Short tandem repeats are among the most polymorphic loci in the human genome. These loci play a role in the etiology of a range of genetic diseases and have been frequently utilized in forensics, population genetics, and genetic genealogy. Despite this plethora of applications, little is known about the variation of most STRs in the human population. Here, we report the largest-scale analysis of human STR variation to date. We collected information for nearly 700,000 STR loci across more than 1000 individuals in Phase 1 of the 1000 Genomes Project. Extensive quality controls show that reliable allelic spectra can be obtained for close to 90% of the STR loci in the genome. We utilize this call set to analyze determinants of STR variation, assess the human reference genome's representation of STR alleles, find STR loci with common loss-of-function alleles, and obtain initial estimates of the linkage disequilibrium between STRs and common SNPs. Overall, these analyses further elucidate the scale of genetic variation beyond classical point mutations.
C1 [Willems, Thomas; Gymrek, Melissa; 1000 Genomes Project Consortium] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA.
[Willems, Thomas] MIT, Computat & Syst Biol Program, Cambridge, MA 02139 USA.
[Gymrek, Melissa] MIT, Harvard MIT Div Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Gymrek, Melissa] Broad Inst & Harvard, Program Med & Populat Genet, Cambridge, MA 02142 USA.
[Gymrek, Melissa] Massachusetts Gen Hosp, Dept Mol Biol & Diabet Unit, Boston, MA 02114 USA.
[Highnam, Gareth; Mittelman, David] Virginia Tech, Virginia Bioinformat Inst, Blacksburg, VA 24061 USA.
[Highnam, Gareth; Mittelman, David] Virginia Tech, Dept Biol Sci, Blacksburg, VA 24061 USA.
[Mittelman, David] Gene Gene Ltd, Houston, TX 77008 USA.
RP Erlich, Y (reprint author), Whitehead Inst Biomed Res, 9 Cambridge Ctr, Cambridge, MA 02142 USA.
EM yaniv@wi.mit.edu
OI /0000-0002-6086-3903
FU National Defense Science and Engineering Graduate Fellowship; Burroughs
Wellcome Fund; AWS Education Grant award
FX M.G. is supported by a National Defense Science and Engineering Graduate
Fellowship. Y.E. is an Andria and Paul Heafy Family Fellow and holds a
Career Award at the Scientific Interface from the Burroughs Wellcome
Fund. This study was funded by a gift from Cathy and Jim Stone and an
AWS Education Grant award. We thank Chris Tyler-Smith, Wei Wei, Qasim
Ayub, and Yali Xue for providing the results of the Y-STR panel for the
1000 Genomes Project individuals and the 1000 Genomes Project Consortium
members for useful discussions. Y.E. dedicates this manuscript to Lia
Erlich, who was born during the last revision of this work.
NR 69
TC 20
Z9 21
U1 4
U2 25
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
EI 1549-5469
J9 GENOME RES
JI Genome Res.
PD NOV
PY 2014
VL 24
IS 11
BP 1894
EP 1904
DI 10.1101/gr.177774.114
PG 11
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA AS7NG
UT WOS:000344442000016
PM 25135957
ER
PT J
AU Caska, CM
Smith, TW
Renshaw, KD
Allen, SN
Uchino, BN
Birmingham, W
Carlisle, M
AF Caska, Catherine M.
Smith, Timothy W.
Renshaw, Keith D.
Allen, Steven N.
Uchino, Bert N.
Birmingham, Wendy
Carlisle, McKenzie
TI Posttraumatic stress disorder and responses to couple conflict:
Implications for cardiovascular risk
SO HEALTH PSYCHOLOGY
LA English
DT Article
DE medically unexplained symptoms; parental divorce; parental death;
adolescence
ID CORONARY-HEART-DISEASE; ANGER; VETERANS; PTSD; QUESTIONNAIRE;
METAANALYSIS; REACTIVITY; HOSTILITY; DIAGNOSES; QUALITY
AB Objective: Functional somatic symptoms (FSSs) are physical symptoms that cannot be (fully) explained by organic pathology. FSSs are very common among children and adolescents, yet their etiology is largely unknown. We hypothesize that (a) the experience of family disruption due to parental divorce or parental death increases FSSs in adolescents; (b) symptoms of depression and anxiety contribute to the relationship between family disruption and FSSs; (c) girls are more vulnerable to these effects than boys. Method: Data were obtained from the prospective population cohort of Dutch adolescents of the Tracking Adolescents' Individual Lives Survey (N = 2,230), aged 10 to 12 years at baseline. FSSs were assessed using the Somatic Complaints subscale of the Youth Self-Report. Parental divorce and parental death were assessed with self-reports. Both outcome and predictors were assessed during 3 assessment waves over the course of 5 years. Linear mixed models were used to investigate associations between both types of family disruption and FSSs. Results: An interaction with age was found for parental divorce (B = 0.01, p =.02) and parental death (B = 0.03, p =.04), indicating that the influence of family disruption on FSSs increases during adolescence. This relationship seems to be partly explained by symptoms of depression and anxiety. No gender differences were found with regard to the effects of family disruption on FSSs. Conclusions: Family disruption is associated with an increased level of FSSs in late adolescence in both genders. This relationship is partly explained by symptoms of depression and/or anxiety.
C1 [Caska, Catherine M.; Smith, Timothy W.; Uchino, Bert N.; Birmingham, Wendy; Carlisle, McKenzie] Univ Utah, Dept Psychol, Salt Lake City, UT 84112 USA.
[Renshaw, Keith D.] George Mason Univ, Dept Psychol, Fairfax, VA 22030 USA.
[Allen, Steven N.] VA Salt Lake City Hlth Care Team, PTSD Clin Team, Salt Lake City, UT USA.
RP Caska, CM (reprint author), VA Puget Sound Hlth Care Syst, Seattle Div, 1660 S Columbian Way 116MHC, Seattle, WA 98108 USA.
EM cmcaska@gmail.com
FU National Institute of Mental Health [1F31MH091915-01A1]
FX The research reported in this article was supported in part by National
Institute of Mental Health Grant 1F31MH091915-01A1 and is based on the
doctoral dissertation of Catherine M. Caska. We thank everyone who
assisted in this investigation, especially Courtney Smith, the Utah
National Guard, and the Salt Lake City VA's PTSD Clinical Team.
NR 42
TC 7
Z9 7
U1 5
U2 16
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0278-6133
EI 1930-7810
J9 HEALTH PSYCHOL
JI Health Psychol.
PD NOV
PY 2014
VL 33
IS 11
BP 1273
EP 1280
DI 10.1037/hea0000133
PG 8
WC Psychology, Clinical; Psychology
SC Psychology
GA AS1BC
UT WOS:000344010300001
PM 25110851
ER
PT J
AU Nillni, YI
Gradus, JL
Gutner, CA
Luciano, MT
Shipherd, JC
Street, AE
AF Nillni, Yael I.
Gradus, Jaimie L.
Gutner, Cassidy A.
Luciano, Matthew T.
Shipherd, Jillian C.
Street, Amy E.
TI Deployment Stressors and Physical Health Among OEF/OIF Veterans: The
Role of PTSD
SO HEALTH PSYCHOLOGY
LA English
DT Article
DE harassment; trauma; posttraumatic stress disorder; physical health;
veteran
ID SEXUAL-HARASSMENT; PERCEIVED HEALTH; MILITARY SERVICE; SOMATIC SYMPTOMS;
WAR VETERANS; CHRONIC PAIN; DISORDER; EXPOSURE; ASSAULT; TRAUMA
AB Objective: There is a large body of literature documenting the relationship between traumatic stress and deleterious physical health outcomes. Although posttraumatic stress disorder (PTSD) symptoms have been proposed to explain this relationship, previous research has produced inconsistent results when moderating variables such as gender or type of traumatic stressor are considered. Within a large sample of Operation Enduring Freedom and Operation Iraqi Freedom (OEF/OIF) Veterans, the current study examined if deployment stressors (i. e., combat stress, harassment stress) contributed unique variance to the prediction of physical health symptoms (i.e., pain, nonpain) beyond the effects of PTSD symptoms. Methods: A total of 2,332 OEF/OIF Veterans, with equal representation of women and men, completed a series of self-report measures assessing deployment stressors, PTSD symptoms, and physical health symptoms. Results: Results revealed that harassment, but not combat stress, added unique variance in the prediction of pain and nonpain symptoms after accounting for PTSD symptoms. Conclusions: This study extends the existing literature by demonstrating the unique influence of harassment stress on physical health outcomes. Specifically, the relationship between combat stress and physical health symptoms appears to be explained mainly by an individual's experience of PTSD symptoms, whereas the relationship between harassment stress and physical health symptoms is not fully explained by PTSD symptoms, suggesting that other variables may be involved in the pathway from harassment stress to physical health symptoms.
C1 [Nillni, Yael I.; Gradus, Jaimie L.; Gutner, Cassidy A.; Luciano, Matthew T.; Shipherd, Jillian C.; Street, Amy E.] Vet Affairs Boston Healthcare Syst, Natl Ctr PTSD, Womens Hlth Sci Div, Boston, MA 02130 USA.
[Nillni, Yael I.; Gradus, Jaimie L.; Gutner, Cassidy A.; Shipherd, Jillian C.; Street, Amy E.] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02215 USA.
RP Nillni, YI (reprint author), Vet Affairs Boston Healthcare Syst, Natl Ctr PTSD, Womens Hlth Sci Div, 150 South Huntington Ave,116B-3, Boston, MA 02130 USA.
EM yael.nillni@va.gov
OI Gradus, Jaimie/0000-0003-1459-5327
NR 38
TC 2
Z9 2
U1 2
U2 12
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0278-6133
EI 1930-7810
J9 HEALTH PSYCHOL
JI Health Psychol.
PD NOV
PY 2014
VL 33
IS 11
BP 1281
EP 1287
DI 10.1037/hea0000084
PG 7
WC Psychology, Clinical; Psychology
SC Psychology
GA AS1BC
UT WOS:000344010300002
PM 25020154
ER
PT J
AU El-Serag, HB
Kanwal, F
AF El-Serag, Hashem B.
Kanwal, Fasiha
TI Epidemiology of Hepatocellular Carcinoma in the United States: Where Are
We? Where Do We Go?
SO HEPATOLOGY
LA English
DT Review
ID CHRONIC HEPATITIS-B; C VIRUS-INFECTION; ADVANCED LIVER-DISEASE;
RISK-FACTORS; ANTIVIRAL THERAPY; REDUCES RISK; METAANALYSIS; CANCER;
CIRRHOSIS; PROGRESSION
C1 [El-Serag, Hashem B.; Kanwal, Fasiha] Baylor Coll Med, Michael E DeBakey Vet Affairs Med Ctr, Sect Gastroenterol & Hepatol, Houston, TX 77030 USA.
[El-Serag, Hashem B.; Kanwal, Fasiha] Houston VA HSR&D Ctr Excellence Houston, Houston, TX USA.
RP El-Serag, HB (reprint author), Michael E DeBakey VA Med Ctr, 2002 Holcombe Blvd 152, Houston, TX 77030 USA.
EM hasheme@bcm.edu
FU Houston VA HSR&D Center of Excellence [HFP90-020]; Texas Digestive
Disease Center NIH [DK58338]; National Institute of Diabetes and
Digestive and Kidney Diseases [K24-04-107]
FX This work is funded, in part, by the Houston VA HSR&D Center of
Excellence (HFP90-020) and the Texas Digestive Disease Center NIH
DK58338. Dr. El-Serag is also supported by the National Institute of
Diabetes and Digestive and Kidney Diseases (K24-04-107).
NR 58
TC 79
Z9 81
U1 3
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD NOV
PY 2014
VL 60
IS 5
BP 1767
EP 1775
DI 10.1002/hep.27222
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6CM
UT WOS:000344352400033
PM 24839253
ER
PT J
AU Hato, T
Goyal, L
Greten, TF
Duda, DG
Zhu, AX
AF Hato, Tai
Goyal, Lipika
Greten, Tim F.
Duda, Dan G.
Zhu, Andrew X.
TI Immune Checkpoint Blockade in Hepatocellular Carcinoma: Current Progress
and Future Directions
SO HEPATOLOGY
LA English
DT Review
ID REGULATORY T-CELLS; PERCUTANEOUS ETHANOL INJECTION; SUPPRESSOR-CELLS;
POSTOPERATIVE RECURRENCE; CTLA-4 BLOCKADE; LIVER; RESPONSES; PD-1;
RECEPTOR; MOLECULES
AB Immune checkpoint blockade has recently emerged as a promising therapeutic approach for various malignancies including hepatocellular carcinoma (HCC). Preclinical and clinical studies have shown the potential benefit of modulating the immunogenicity of HCC. In addition, recent advances in tumor immunology have broadened our understanding of the complex mechanism of immune evasion. In this review we summarize the current knowledge on HCC immunology and discuss the potential of immune checkpoint blockade as a novel HCC therapy from the basic, translational, and clinical perspectives.
C1 [Hato, Tai; Duda, Dan G.] Massachusetts Gen Hosp, Dept Radiat Oncol, Edwin L Steele Lab, Boston, MA 02114 USA.
[Goyal, Lipika; Zhu, Andrew X.] Massachusetts Gen Hosp, Ctr Canc, Dept Med, Boston, MA 02114 USA.
[Greten, Tim F.] NCI, Gastrointestinal Malignancy Sect, Thorac & Gastrointestinal Oncol Branch, Bethesda, MD 20892 USA.
RP Duda, DG (reprint author), Massachusetts Gen Hosp, Dept Radiat Oncol, Edwin L Steele Lab, Boston, MA 02114 USA.
EM GDUDA@PARTNERS.ORG; AZHU@PARTNERS.ORG
RI Greten, Tim/B-3127-2015
OI Greten, Tim/0000-0002-0806-2535
FU National Institutes of Health [P01-CA080124, R01-CA159258,
R21-CA139168]; National Cancer Institute/Proton Beam Federal Share
Program award; American Cancer Society [120733-RSG-11-073-01-TBG];
Astellas Foundation for Research on Metabolic Disorders, Japan
FX Supported by National Institutes of Health grants P01-CA080124,
R01-CA159258, and R21-CA139168, a National Cancer Institute/Proton Beam
Federal Share Program award, and the American Cancer Society grant
120733-RSG-11-073-01-TBG (to D. G. D.); and a Postdoctoral Fellowship
from Astellas Foundation for Research on Metabolic Disorders, Japan (to
T.H.).
NR 62
TC 23
Z9 26
U1 3
U2 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0270-9139
EI 1527-3350
J9 HEPATOLOGY
JI Hepatology
PD NOV
PY 2014
VL 60
IS 5
BP 1776
EP 1782
DI 10.1002/hep.27246
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6CM
UT WOS:000344352400034
PM 24912948
ER
PT J
AU Dutta, P
Nahrendorf, M
AF Dutta, Partha
Nahrendorf, Matthias
TI Regulation and consequences of monocytosis
SO IMMUNOLOGICAL REVIEWS
LA English
DT Review
DE monocytes; macrophages; stem cells; spleen
ID HEMATOPOIETIC STEM-CELLS; ACUTE MYOCARDIAL-INFARCTION; BINDING CASSETTE
TRANSPORTERS; PROGENITOR CELLS; DENDRITIC CELLS; ATHEROSCLEROTIC
LESIONS; INSULIN-RESISTANCE; ADIPOSE-TISSUE; IN-VIVO; ACCELERATES
ATHEROSCLEROSIS
AB Monocytes are part of the vertebrate innate immune system. Blood monocytes are produced by bone marrow and splenic progenitors that derive from hematopoietic stem cells (HSCs). In cardiovascular disease, such as atherosclerosis and myocardial infarction, HSCs proliferate at higher levels that in turn increase production of hematopoietic cells, including monocytes. Once produced in hematopoietic niches, monocytes intravasate blood vessels, circulate, and migrate to sites of inflammation. Monocyte recruitment to atherosclerotic plaque and the ischemic heart depends on various chemokines, such as CCL2, CX(3)CL1, and CCL5. Once in tissue, monocytes can differentiate into macrophages and dendritic cells. Macrophages are end effector cells that regulate the steady state and tissue healing, but they can also promote disease. At sites of inflammation, monocytes and macrophages produce inflammatory cytokines, which can exacerbate disease progression. Macrophages can also phagocytose tissue debris and produce pro-healing cytokines. Additionally, macrophages are antigen-presenting cells and can prime T cells. The tissue environment, including cytokines and types of inflammation, instructs macrophage specialization. Understanding monocytosis and its consequences in disease will reveal new therapeutic opportunities without compromising steady state functions.
C1 [Dutta, Partha; Nahrendorf, Matthias] Massachusetts Gen Hosp, Ctr Syst Biol, Boston, MA 02114 USA.
[Dutta, Partha; Nahrendorf, Matthias] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Dutta, P (reprint author), Massachusetts Gen Hosp, Ctr Syst Biol, Simches Res Bldg,185 Cambridge St, Boston, MA 02114 USA.
EM pdutta1@partners.org
FU National Institute of Health [R01-HL096576, R01HL117829, R01HL114477,
K99-HL121076]
FX This work was funded in part by grants from the National Institute of
Health R01-HL096576, R01HL117829, R01HL114477 (M. N.); K99-HL121076 (P.
D.). The authors have no conflicts of interest to declare.
NR 114
TC 7
Z9 8
U1 2
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0105-2896
EI 1600-065X
J9 IMMUNOL REV
JI Immunol. Rev.
PD NOV
PY 2014
VL 262
IS 1
SI SI
BP 167
EP 178
DI 10.1111/imr.12219
PG 12
WC Immunology
SC Immunology
GA AS0WX
UT WOS:000343997600012
PM 25319334
ER
PT J
AU Low, D
Mino-Kenudson, M
Mizoguchi, E
AF Low, Daren
Mino-Kenudson, Mari
Mizoguchi, Emiko
TI Recent Advancement in Understanding Colitis-associated Tumorigenesis
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE inflammatory bowel disease; epithelial dysplasia; guts microbiome
ID INFLAMMATORY-BOWEL-DISEASE; DEXTRAN SULFATE SODIUM; INTESTINAL
EPITHELIAL-CELLS; BETA-CATENIN ACTIVATION; ULCERATIVE-COLITIS;
COLORECTAL-CANCER; SUPPRESSOR-CELLS; OXIDATIVE STRESS; TUMOR-GROWTH;
COLON-CANCER
AB Chronic inflammation predisposes patients with inflammatory bowel disease to the risk of developing colitis-associated cancer (CAC). Growing evidence strongly suggests that CAC development is multifactorial and is attributed to concurrent, dynamic dysregulations in host immunity, enteric microbiota, and epithelial restitution during the course of chronic inflammation. This article discusses the recent advances in understanding the different forms of CAC that may develop in patients with inflammatory bowel disease and animal models, as well as molecular alterations and other processes that orchestrate the development of CAC.
C1 [Low, Daren; Mizoguchi, Emiko] Massachusetts Gen Hosp, Dept Med, Gastrointestinal Unit, Boston, MA 02114 USA.
[Mino-Kenudson, Mari] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Mizoguchi, Emiko] Massachusetts Gen Hosp, Ctr Study Inflammatory Bowel Dis, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Mizoguchi, E (reprint author), Massachusetts Gen Hosp, GRJ 825D,55 Fruit St, Boston, MA 02114 USA.
EM emizoguchi@mgh.harvard.edu
FU National Institutes of Health [DK 80070, DK74454, DK64289]; Eli and
Edythe L. Broad Medical Foundation; American Gastroenterological
Association Foundation; Singapore A*STAR International Fellowship;
National Cancer Institute [P50 CA127003, R01 CA169086]
FX Supported by National Institutes of Health (DK 80070, DK74454, and
DK64289) and grants from the Eli and Edythe L. Broad Medical Foundation
and American Gastroenterological Association Foundation to E. Mizoguchi.
D. Low was awarded the Singapore A*STAR International Fellowship. M.
Mino-Kenudson was supported by National Cancer Institute grants P50
CA127003 and R01 CA169086.
NR 82
TC 4
Z9 5
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1078-0998
EI 1536-4844
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD NOV
PY 2014
VL 20
IS 11
BP 2115
EP 2123
DI 10.1097/MIB.0000000000000094
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS5YI
UT WOS:000344342000027
PM 25337866
ER
PT J
AU Zhang, Z
Adappa, ND
Doghramji, LJ
Chiu, AG
Lautenbach, E
Cohen, NA
Palmer, JN
AF Zhang, Zi
Adappa, Nithin D.
Doghramji, Laurel J.
Chiu, Alexander G.
Lautenbach, Ebbing
Cohen, Noam A.
Palmer, James N.
TI Quality of life improvement from sinus surgery in chronic rhinosinusitis
patients with asthma and nasal polyps
SO INTERNATIONAL FORUM OF ALLERGY & RHINOLOGY
LA English
DT Article
DE chronic rhinosinusitis; quality of life; asthma; nasal polyps;
functional endoscopic sinus surgery
ID EUROPEAN POSITION PAPER; OUTCOMES; BACTERIA; ALLERGY; LONG; CARE
AB BackgroundIt is unclear whether chronic rhinosinusitis (CRS) patients with both nasal polyps and asthma have different quality of life (QOL) improvement after functional endoscopic sinus surgery (FESS). We aimed to determine whether CRS patients with asthma and nasal polyps had a greater QOL improvement after FESS compared to patients without asthma or polyps.
MethodsThis retrospective analysis included adult CRS patients who underwent FESS between 2007 and 2011. QOL was measured using the 22-item Sino-Nasal Outcome Test (SNOT-22). Variables collected included baseline demographics, clinical factors, SNOT-22 scores before FESS, and 1 month, 3 months, and 6 months post-FESS. Groups tested were asthma alone, polyps alone, asthma and polyps, and no asthma or polyps. Linear mixed-effects regression model was performed to calculate -coefficients, which represent the adjusted mean QOL differences.
ResultsAmong the 376 patients included, 40.16% had both asthma and polyps (n = 151), 14.36% had asthma alone (n = 54), 19.45% had polyps alone (n = 75), and 25.53% had no asthma or polyps (n = 96). After adjusting for all factors, there were significantly more QOL improvements in patients with both asthma and nasal polyps from baseline to 1-month (-coefficient = -10.05; 95% CI, -15.86 to -4.23; p = 0.001) and 3-month follow-up (-coefficient = -8.27; 95% CI, -14.98 to -1.56; p = 0.016), and patients with asthma alone from baseline to 6-month follow-up (-coefficient = -8.78; 95% CI, -17.45 to -0.11; p = 0.047), when compared to patients without asthma or nasal polyps.
ConclusionCRS patients with both asthma and nasal polyps or asthma alone experience a larger QOL benefit from FESS immediately after FESS compared to CRS patients without asthma or polyps.
C1 [Zhang, Zi; Lautenbach, Ebbing] Univ Penn, Ctr Clin Epidemiol & Biostat, Dept Biostat & Epidemiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Adappa, Nithin D.; Doghramji, Laurel J.; Cohen, Noam A.; Palmer, James N.] Univ Penn, Dept Otorhinolaryngol Head & Neck Surg, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Chiu, Alexander G.] Univ Arizona, Dept Surg, Tucson, AZ USA.
[Lautenbach, Ebbing] Univ Penn, Perelman Sch Med, Dept Med, Div Infect Dis, Philadelphia, PA 19104 USA.
[Cohen, Noam A.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA USA.
RP Zhang, Z (reprint author), 8th Floor,Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM zizhang@mail.med.upenn.edu
OI Cohen, Noam/0000-0002-9462-3932
FU National Institute of Allergy and Infectious Diseases (NIAID), National
Institutes of Health [K24 AI080942/AI/NIAID NIH HHS/United States]
FX National Institute of Allergy and Infectious Diseases (NIAID), National
Institutes of Health (K24 AI080942/AI/NIAID NIH HHS/United States to E.
L.).
NR 27
TC 13
Z9 13
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2042-6976
EI 2042-6984
J9 INT FORUM ALLERGY RH
JI Int. Forum Allergy Rhinol.
PD NOV
PY 2014
VL 4
IS 11
BP 885
EP 892
DI 10.1002/alr.21406
PG 8
WC Otorhinolaryngology
SC Otorhinolaryngology
GA AS6GE
UT WOS:000344361600005
PM 25256422
ER
PT J
AU Gerbasi, ME
Richards, LK
Thomas, JJ
Agnew-Blais, JC
Thompson-Brenner, H
Gilman, SE
Becker, AE
AF Gerbasi, Margaret E.
Richards, Lauren K.
Thomas, Jennifer J.
Agnew-Blais, Jessica C.
Thompson-Brenner, Heather
Gilman, Stephen E.
Becker, Anne E.
TI Globalization and Eating Disorder Risk: Peer Influence, Perceived Social
Norms, and Adolescent Disordered Eating in Fiji
SO INTERNATIONAL JOURNAL OF EATING DISORDERS
LA English
DT Article
DE peer influence; social norms; adolescent; cultural; Fiji; globalization
ID WEIGHT-CONTROL BEHAVIORS; GLOBAL MENTAL-HEALTH; QUESTIONNAIRE EDE-Q;
BODY-IMAGE CONCERNS; SOCIOCULTURAL INFLUENCES; BULIMIC SYMPTOMS; FIELD
EXPERIMENT; GIRLS; MEDIA; WOMEN
AB Objective: The increasing global health burden imposed by eating disorders warrants close examination of social exposures associated with globalization that potentially elevate risk during the critical developmental period of adolescence in low-and middle-income countries (LMICs). The study aim was to investigate the association of peer influence and perceived social norms with adolescent eating pathology in Fiji, a LMIC undergoing rapid social change.
Method: We measured peer influence on eating concerns (with the Inventory of Peer Influence on Eating Concerns; IPIEC), perceived peer norms associated with disordered eating and body concerns, perceived community cultural norms, and individual cultural orientations in a representative sample of school-going ethnic Fijian adolescent girls (n = 523). We then developed a multivariable linear regression model to examine their relation to eating pathology (measured by the Eating Disorder Examination-Questionnaire; EDE-Q).
Results: We found independent and statistically significant associations between both IPIEC scores and our proxy for perceived social norms specific to disordered eating (both p < .001) and EDEQ global scores in a fully adjusted linear regression model.
Discussion: Study findings support the possibility that peer influence as well as perceived social norms relevant to disordered eating may elevate risk for disordered eating in Fiji, during the critical developmental period of adolescence. Replication and extension of these research findings in other populations undergoing rapid social transition-and where globalization is also influencing local social norms-may enrich etiologic models and inform strategies to mitigate risk. (C) 2014 Wiley Periodicals, Inc.
C1 [Gerbasi, Margaret E.; Becker, Anne E.] Harvard Univ, Sch Med, Dept Global Hlth & Social Med, Boston, MA 02115 USA.
[Richards, Lauren K.; Thompson-Brenner, Heather] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
[Thomas, Jennifer J.; Becker, Anne E.] Massachusetts Gen Hosp, Eating Disorders Clin & Res Program, Boston, MA 02114 USA.
[Thomas, Jennifer J.; Becker, Anne E.] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Gilman, Stephen E.] Harvard Univ, Sch Publ Hlth, Dept Social & Behav Sci, Boston, MA 02115 USA.
[Agnew-Blais, Jessica C.; Gilman, Stephen E.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Gilman, Stephen E.; Becker, Anne E.] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
RP Becker, AE (reprint author), Harvard Univ, Sch Med, Dept Global Hlth & Social Med, 641 Huntington Ave, Boston, MA 02115 USA.
EM anne_becker@hms.harvard.edu
RI Agnew-Blais, Jessica/L-9236-2015; Gilman, Stephen/E-7632-2010;
OI Agnew-Blais, Jessica/0000-0002-0755-6867; Gilman,
Stephen/0000-0002-8331-6419; Gerbasi, Margaret/0000-0003-1786-6962
FU Harvard University; [K23 MH068575]; [K23 MH071641]; [R36MH095395]
FX Supported by K23 MH068575 (to A. E. B.), K23 MH071641 (to H. T. B.), and
R36MH095395 (to L. R.) and by Harvard University Research Enabling Grant
(to A. E. B.).
NR 54
TC 1
Z9 1
U1 2
U2 28
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0276-3478
EI 1098-108X
J9 INT J EAT DISORDER
JI Int. J. Eating Disord.
PD NOV
PY 2014
VL 47
IS 7
SI SI
BP 727
EP 737
DI 10.1002/eat.22349
PG 11
WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology
SC Psychology; Nutrition & Dietetics; Psychiatry
GA AS6CO
UT WOS:000344352600008
PM 25139374
ER
PT J
AU Swanson, SA
Horton, NJ
Crosby, RD
Micali, N
Sonneville, KR
Eddy, K
Field, AE
AF Swanson, Sonja A.
Horton, Nicholas J.
Crosby, Ross D.
Micali, Nadia
Sonneville, Kendrin R.
Eddy, Kamryn
Field, Alison E.
TI A Latent Class Analysis to Empirically Describe Eating Disorders Through
Developmental Stages
SO INTERNATIONAL JOURNAL OF EATING DISORDERS
LA English
DT Article
DE eating disorder; latent class analysis; eating disorder not otherwise
specified; purging disorder; binge eating disorder; classification
ID COMORBIDITY-SURVEY-REPLICATION; ADOLESCENT GIRLS; PURGING DISORDER;
LONGITUDINAL ASSOCIATIONS; DIAGNOSTIC INTERVIEW; ADVERSE OUTCOMES; RISK
BEHAVIOR; UNITED-STATES; DRUG-USE; PREVALENCE
AB Objectives: The current standards for classifying eating disorders were primarily informed by adult, clinical study populations, while it is unknown whether an empirically based classification system can be supported across preadolescence through young adulthood. Using latent class analyses, we sought to empirically classify disordered eating in females from preadolescence to young adulthood, and assess the association between classes and adverse outcomes.
Method: Latent class models were fit using observations from the 9,039 girls participating in the growing up today study, an on-going cohort following participants annually or biennially since 1996 when they were ages 9-14 years. Associations between classes and drug use, binge drinking, and depressive symptoms were assessed using generalized estimating equations.
Results: Across age groups, there was evidence of six classes: a large asymptomatic class, a class characterized by shape/weight concerns, a class characterized by overeating without loss of control, and three resembling full and subthreshold binge eating disorder, purging disorder, and bulimia nervosa. Relative prevalences of classes varied across developmental stages, with symptomatic classes increasing in prevalence with increasing age. Symptomatic classes were associated with concurrent and incident drug use, binge drinking, and high depressive symptoms.
Discussion: A classification system resembling broader definitions of DSM-5 diagnoses along with two further subclinical symptomatic classes may be a useful framework for studying disordered eating among adolescent and young adult females. (C) 2014 Wiley Periodicals, Inc. Int
C1 [Swanson, Sonja A.; Field, Alison E.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Horton, Nicholas J.] Amherst Coll, Dept Math & Stat, Amherst, MA 01002 USA.
[Crosby, Ross D.] Univ N Dakota, Sch Med & Hlth Sci, Neuropsychiat Res Inst, Fargo, ND USA.
[Crosby, Ross D.] Univ N Dakota, Sch Med & Hlth Sci, Dept Clin Neurosci, Fargo, ND USA.
[Micali, Nadia] UCL, Behav & Brain Sci Unit, Inst Child Hlth, London, England.
[Sonneville, Kendrin R.; Field, Alison E.] Boston Childrens Hosp, Dept Med, Div Adolescent Med, Boston, MA USA.
[Sonneville, Kendrin R.; Eddy, Kamryn; Field, Alison E.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Eddy, Kamryn] Massachusetts Gen Hosp, Dept Psychiat, Harris Ctr Educ & Advocacy Eating Disorders, Boston, MA 02114 USA.
[Field, Alison E.] Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.
RP Swanson, SA (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, 677 Huntington Ave,Kresge 9th Floor, Boston, MA 02115 USA.
EM sswanson@hsph.harvard.edu
OI Crosby, Ross/0000-0001-9131-1629
FU National Institutes of Health [MH087786, DK59570, DK46200, HL68041,
HD049889]
FX Supported by: MH087786, DK59570, DK46200, HL68041, and HD049889 from
National Institutes of Health and by National Institutes of Health.
NR 31
TC 5
Z9 5
U1 5
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0276-3478
EI 1098-108X
J9 INT J EAT DISORDER
JI Int. J. Eating Disord.
PD NOV
PY 2014
VL 47
IS 7
SI SI
BP 762
EP 772
DI 10.1002/eat.22308
PG 11
WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology
SC Psychology; Nutrition & Dietetics; Psychiatry
GA AS6CO
UT WOS:000344352600012
PM 24909947
ER
PT J
AU Slane, JD
Klump, KL
McGue, M
Iacono, WG
AF Slane, Jennifer D.
Klump, Kelly L.
McGue, Matthew
Iacono, William G.
TI Developmental Trajectories of Disordered Eating from Early Adolescence
to Young Adulthood: A Longitudinal Study
SO INTERNATIONAL JOURNAL OF EATING DISORDERS
LA English
DT Article
DE disordered eating; longitudinal; developmental; growth curve
ID RISK-FACTORS; ADVERSE OUTCOMES; NATURAL-HISTORY; BODY-WEIGHT; GIRLS;
BEHAVIORS; ATTITUDES; WOMEN; PREADOLESCENT; SYMPTOMS
AB Objective: Research examining changes in eating disorder symptoms across adolescence suggests an increase in disordered eating from early to late adolescence. However, relevant studies have largely been cross-sectional in nature and most have not examined the changes in the attitudinal symptoms of eating disorders (e. g., weight concerns). This longitudinal study aimed to address gaps in the available data by examining the developmental trajectories of disordered eating in females from preadolescence into young adulthood.
Method: Participants were 745 same-sex female twins from the Minnesota Twin Family Study. Disordered eating was assessed using the Total Score, Body Dissatisfaction subscale, Weight Preoccupation subscale, and a combined Binge Eating and Compensatory Behavior subscale from the Minnesota Eating Behavior Survey assessed at the ages of 11, 14, 18, 21, and 25. Several latent growth models were fit to the data to identify the trajectory that most accurately captures the changes in disordered eating symptoms from 11 to 25 years.
Results: The best-fitting models for overall levels of disordered eating, body dissatisfaction, and weight preoccupation showed an increase in from 11 through 25 years. In contrast, bulimic behaviors increased to age of 18 and then stabilized to age of 25.
Discussion: The findings expanded upon extant research by investigating longitudinal, symptom specific, within person changes and showing an increase in cognitive symptoms into young adulthood and the stability of disordered eating behaviors past late adolescence. (C) 2014 Wiley Periodicals, Inc.
C1 [Slane, Jennifer D.] VA Pittsburgh Healthcare Syst, VISN Mental Illness Res Educ & Clin Ctr MIRECC 4, Pittsburgh, PA USA.
[Slane, Jennifer D.] Univ Pittsburgh, Dept Psychiat, Med Ctr, Pittsburgh, PA USA.
[Klump, Kelly L.] Michigan State Univ, Dept Psychol, E Lansing, MI 48824 USA.
[McGue, Matthew; Iacono, William G.] Univ Minnesota, Dept Psychol, Minneapolis, MN 55455 USA.
RP Slane, JD (reprint author), VA Pittsburgh Healthcare Syst, VISN Mental Illness Res Educ & Clin Ctr 4, Univ Dr, Pittsburgh, PA 15261 USA.
EM slane@msu.edu
FU National Institute on Alcohol Abuse and Alcoholism [R01 AA009367]
FX Supported by R01 AA009367 from National Institute on Alcohol Abuse and
Alcoholism.
NR 42
TC 3
Z9 4
U1 6
U2 21
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0276-3478
EI 1098-108X
J9 INT J EAT DISORDER
JI Int. J. Eating Disord.
PD NOV
PY 2014
VL 47
IS 7
SI SI
BP 793
EP 801
DI 10.1002/eat.22329
PG 9
WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology
SC Psychology; Nutrition & Dietetics; Psychiatry
GA AS6CO
UT WOS:000344352600015
PM 24995824
ER
PT J
AU Wu, RI
Schorge, JO
Cin, PD
Young, RH
Oliva, E
AF Wu, Roseann I.
Schorge, John O.
Cin, Paola D.
Young, Robert H.
Oliva, Esther
TI Mullerian Adenosarcoma of the Uterus With Low-grade Sarcomatous
Overgrowth Characterized by Prominent Hydropic Change Resulting in
Mimicry of a Smooth Muscle Tumor
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY
LA English
DT Article
DE Mullerian adenosarcoma; Low-grade sarcomatous overgrowth; Hydropic
change; Sex cord-like; Smooth muscle differentiation
ID SEX-CORD TUMORS; ENDOMETRIAL STROMAL TUMORS; CLINICOPATHOLOGIC ANALYSIS;
DIFFERENTIATION; UPDATE
AB A 28-y-old woman was found to have a large subserosal uterine mass that was excised and interpreted as a "clear cell leiomyoma." Five years later, the tumor recurred as serosal-based ileal and uterine masses; they were treated by partial ileal resection and hysterectomy. All 3 masses were predominantly characterized by conspicuous edema separating bland cells growing in cords and clusters, with scant to moderately conspicuous clear cytoplasm. The edema was indistinguishable from the hydropic change commonly seen in benign smooth muscle tumors and the cords similar to those often present in them. However, the mass from the hysterectomy specimen had a small, grossly recognizable cystic region, which on microscopic examination was a typical low-grade mullerian adenosarcoma. The stroma of the latter ranged from cellular endometrial-type to edematous and hypocellular similar to that dominating the other specimens. The cellular and edematous regions focally had cords and tubules of sex cord-like type confirmed by inhibin and calretinin positivity. Smooth muscle differentiation was also seen as a "starburst" pattern. This case of adenosarcoma is unusual due to its (1) serosal location, (2) overgrowth of stroma, which differed from typical adenosarcoma with sarcomatous overgrowth by its low-grade nature, (3) hydropic change associated with cords and nests of cells with clear cytoplasm, which prompted the initial specimen to be considered an epithelioid leiomyoma, and (4) prominent smooth muscle metaplasia mostly with a "starburst" morphology. All these features have only rarely been documented in prior mullerian adenosarcomas.
C1 [Wu, Roseann I.; Young, Robert H.; Oliva, Esther] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Cin, Paola D.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Schorge, John O.] Harvard Univ, Dept Obstet & Gynecol, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
RP Oliva, E (reprint author), Massachusetts Gen Hosp, Dept Pathol, 55 Fruit St,Warren 219, Boston, MA 02114 USA.
EM eoliva@partners.org
NR 18
TC 4
Z9 4
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-1691
EI 1538-7151
J9 INT J GYNECOL PATHOL
JI Int. J. Gynecol. Pathol.
PD NOV
PY 2014
VL 33
IS 6
BP 573
EP 580
DI 10.1097/PGP.0000000000000100
PG 8
WC Obstetrics & Gynecology; Pathology
SC Obstetrics & Gynecology; Pathology
GA AS2QC
UT WOS:000344123500005
PM 25272296
ER
PT J
AU Clark, RM
Lynch, MP
Kolp, R
Zukerberg, LR
Growdon, WB
Rueda, BR
AF Clark, Rachel M.
Lynch, Maureen P.
Kolp, Rebecca
Zukerberg, Lawrence R.
Growdon, Whitfield B.
Rueda, Bo R.
TI The N-methyl-D-aspartate Receptor, a Precursor to N-methyl-D-aspartate
Receptor Encephalitis, is Found in the Squamous Tissue of Ovarian
Teratomas
SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY
LA English
DT Article
DE Ovarian teratoma; NMDA receptor encephalitis; Squamous tissue
ID ANTI-NMDAR ENCEPHALITIS; GLUTAMATE-RECEPTOR; ANTIBODIES; SYMPTOMS
AB Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is the most common antibody-mediated limbic encephalitis and is associated with underlying ovarian teratoma. Previous studies suggest that expression of NMDAR on teratoma neural tissue initiates an autoimmune response to NMDAR in the brain. As some teratomas of patients with anti-NMDAR encephalitis lack neuronal tissue, we questioned if there could be an alternate mechanism of the disease. We performed immunohistochemical analyses for NMDAR and correlated its expression with histology on 10 control teratomas and 5 teratomas associated with anti-NMDAR encephalitis. Both control and case teratomas expressed NMDAR-bearing neural tissue. All 15 teratomas contained large amounts of NMDAR bearing squamous epithelium; in 2 cases this was the only tissue expressing NMDAR. NMDAR-bearing neural tissue is not the sole source of encephalitis in all patients. Furthermore, we speculate that NMDAR expression by squamous epithelium may contribute to the disease development in some patients.
C1 [Clark, Rachel M.; Lynch, Maureen P.; Growdon, Whitfield B.; Rueda, Bo R.] Massachusetts Gen Hosp, Vincent Ctr Reprod Biol, Vincent Dept Obstet & Gynecol, Boston, MA 02114 USA.
[Clark, Rachel M.; Growdon, Whitfield B.; Rueda, Bo R.] Massachusetts Gen Hosp, Div Gynecol Oncol, Vincent Dept Obstet & Gynecol, Boston, MA 02114 USA.
[Zukerberg, Lawrence R.] Harvard Univ, Sch Med, Dept Pathol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Zukerberg, Lawrence R.] Harvard Univ, Sch Med, Dept Obstet Gynecol & Reprod Biol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Clark, Rachel M.; Lynch, Maureen P.; Kolp, Rebecca; Growdon, Whitfield B.; Rueda, Bo R.] Harvard Univ, Sch Med, Dept Obstet Gynecol & Reprod Biol, Boston, MA 02115 USA.
RP Rueda, BR (reprint author), Massachusetts Gen Hosp, Vincent Ctr Reprod Biol, Vincent Dept Obstet & Gynecol, 55 Fruit St, Boston, MA 02114 USA.
EM brueda@partners.org
FU Vincent Memorial Research Funds; Advanced Medical Research Foundation
FX Supported by the Vincent Memorial Research Funds and The Advanced
Medical Research Foundation.
NR 15
TC 2
Z9 2
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-1691
EI 1538-7151
J9 INT J GYNECOL PATHOL
JI Int. J. Gynecol. Pathol.
PD NOV
PY 2014
VL 33
IS 6
BP 598
EP 606
DI 10.1097/PGP.0000000000000104
PG 9
WC Obstetrics & Gynecology; Pathology
SC Obstetrics & Gynecology; Pathology
GA AS2QC
UT WOS:000344123500008
PM 25272299
ER
PT J
AU Kopacz, MS
AF Kopacz, Marek S.
TI Moral injury - A war trauma affecting current and former military
personnel
SO INTERNATIONAL JOURNAL OF SOCIAL PSYCHIATRY
LA English
DT Letter
ID EVENTS; COMBAT
C1 US Dept Vet Affairs, VISN Ctr Excellence Suicide Prevent 2, Canandaigua, NY 14424 USA.
RP Kopacz, MS (reprint author), US Dept Vet Affairs, VISN Ctr Excellence Suicide Prevent 2, 400 Ft Hill Ave, Canandaigua, NY 14424 USA.
EM marek.kopacz@va.gov
NR 12
TC 1
Z9 1
U1 0
U2 5
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0020-7640
EI 1741-2854
J9 INT J SOC PSYCHIATR
JI Int. J. Soc. Psychiatr.
PD NOV
PY 2014
VL 60
IS 7
BP 722
EP 723
DI 10.1177/0020764014547063
PG 2
WC Psychiatry
SC Psychiatry
GA AS4LD
UT WOS:000344246500014
PM 25336198
ER
PT J
AU Cohen, GM
Drain, PK
Noubary, F
Cloete, C
Bassett, IV
AF Cohen, Gabriel M.
Drain, Paul K.
Noubary, Farzad
Cloete, Christie
Bassett, Ingrid V.
TI Diagnostic Delays and Clinical Decision Making With Centralized Xpert
MTB/RIF Testing in Durban, South Africa
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE tuberculosis; HIV; AIDS; Xpert MTB; RIF assay; diagnostic testing; South
Africa
ID UNDERMINES POTENTIAL IMPACT; LOW-INCOME COUNTRIES; OF-CARE DIAGNOSIS;
PULMONARY TUBERCULOSIS; ANTIRETROVIRAL THERAPY; RIFAMPIN RESISTANCE;
MDR-TB; IMPLEMENTATION; SETTINGS; ACCURACY
AB Setting:We conducted a retrospective study among HIV-infected adult suspects (18 years) with pulmonary tuberculosis (TB), who underwent Xpert MTB/RIF (Xpert) testing at McCord Hospital and its adjoining HIV clinic in Durban, South Africa.Objective:To determine if Xpert testing performed at a centralized laboratory accelerated time to TB diagnosis.Design:We obtained data on sputum smear microscopy [acid-fast bacilli (AFB)], Xpert, and the rationale for treatment initiation from medical records. The primary outcome was total diagnostic time, defined as time from sputum collection to clinicians' receipt of results. A linear mixed-effect model compared the duration of steps in the diagnostic pathway across testing modalities.Results:Among 403 participants, the median total diagnostic time for AFB and Xpert was 3.3 and 6.4 days, respectively (P < 0.001). When compared with AFB, the median delay for Xpert laboratory processing was 1.4 days (P < 0.001) and result transfer to clinic was 1.7 days (P < 0.001). Among 86 Xpert-positive participants who initiated treatment, 49 (57%) started treatment based on clinical suspicion or AFB-positive results, whereas only 32 (37%) started treatment based on Xpert-positive results.Conclusions:In our setting, Xpert results took twice as long as AFB results to reach clinicians. Replacing AFB with centralized Xpert may delay TB diagnoses in some settings.
C1 [Cohen, Gabriel M.] Harvard Univ, Beth Israel Deaconess Med Ctr, Dept Med, Sch Med, Boston, MA 02215 USA.
[Drain, Paul K.; Bassett, Ingrid V.] Massachusetts Gen Hosp, Dept Med, Div Infect Dis, Boston, MA 02114 USA.
[Drain, Paul K.] Brigham & Womens Hosp, Dept Med, Div Infect Dis, Boston, MA 02115 USA.
[Drain, Paul K.; Bassett, Ingrid V.] Massachusetts Gen Hosp, Med Practice Evaluat Ctr, Boston, MA 02114 USA.
[Noubary, Farzad] Tufts Med Ctr, Inst Clin Res & Hlth Policy Studies, Boston, MA USA.
[Noubary, Farzad] Tufts Univ, Tufts Clin & Translat Sci Inst, Boston, MA 02111 USA.
[Cloete, Christie] McCord Hosp, Durban, Kwazulu Natal, South Africa.
[Bassett, Ingrid V.] Harvard Univ, Sch Med, Ctr AIDS Res, Boston, MA 02215 USA.
RP Cohen, GM (reprint author), Harvard Univ, Beth Israel Deaconess Med Ctr, Dept Med, Sch Med, 330 Brookline Ave, Boston, MA 02215 USA.
EM gcohen1@bidmc.harvard.edu
FU Fogarty International Clinical Research Scholars and Fellows Program at
Vanderbilt University [R24 TW007988]; Harvard Global Health Institute;
The Program for AIDS Clinical Research Training [T32 AI007433]; National
Institute of Mental Health [R01 MH090326]; NCATS/NIH [UL1TR000011]
FX G.C. and P. K. D. were supported by the Fogarty International Clinical
Research Scholars and Fellows Program at Vanderbilt University (R24
TW007988). The Centre for the AIDS Programme of Research in South Africa
(CAPRISA) in Durban, South Africa, served as the site for G.C.'s
clinical research training year. P. K. D. was also supported by the
Harvard Global Health Institute and The Program for AIDS Clinical
Research Training (T32 AI007433). I. V. B. was supported by the National
Institute of Mental Health (R01 MH090326). Access to REDCap was made
available through the Vanderbilt Institute for Clinical and
Translational Research grant support (UL1TR000011 from NCATS/NIH).
NR 35
TC 8
Z9 8
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
EI 1077-9450
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD NOV 1
PY 2014
VL 67
IS 3
BP E88
EP E93
DI 10.1097/QAI.0000000000000309
PG 6
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AS6GC
UT WOS:000344361400001
PM 25314255
ER
PT J
AU Gellad, WF
Stein, BD
Ruder, T
Henderson, R
Frazee, SG
Mehrotra, A
Donohue, JM
AF Gellad, Walid F.
Stein, Bradley D.
Ruder, Teague
Henderson, Rochelle
Frazee, Sharon G.
Mehrotra, Ateev
Donohue, Julie M.
TI Geographic Variation in Receipt of Psychotherapy in Children Receiving
Attention-Deficit/Hyperactivity Disorder Medications
SO JAMA PEDIATRICS
LA English
DT Letter
ID ADHD
C1 [Gellad, Walid F.] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Gellad, Walid F.; Stein, Bradley D.; Ruder, Teague; Mehrotra, Ateev] RAND Corp, Pittsburgh, PA 15213 USA.
[Gellad, Walid F.] Univ Pittsburgh, Div Gen Med, Pittsburgh, PA USA.
[Gellad, Walid F.] Univ Pittsburgh, Ctr Pharmaceut Policy & Prescribing, Pittsburgh, PA USA.
[Stein, Bradley D.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA.
[Henderson, Rochelle; Frazee, Sharon G.] Express Scripts, St Louis, MO USA.
[Mehrotra, Ateev] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Donohue, Julie M.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Hlth Policy & Management, Pittsburgh, PA USA.
RP Gellad, WF (reprint author), RAND Corp, 4570 Fifth Ave,Ste 600, Pittsburgh, PA 15213 USA.
EM wgellad@rand.org
OI Donohue, Julie/0000-0003-2418-6017
NR 6
TC 5
Z9 5
U1 1
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6203
EI 2168-6211
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD NOV
PY 2014
VL 168
IS 11
BP 1074
EP 1076
DI 10.1001/jamapediatrics.2014.1647
PG 4
WC Pediatrics
SC Pediatrics
GA AT1NS
UT WOS:000344701500024
PM 25243391
ER
PT J
AU Kwon, YM
Fehring, TK
Lombardi, AV
Barnes, CL
Cabanela, ME
Jacobs, JJ
AF Kwon, Young-Min
Fehring, Thomas K.
Lombardi, Adolph V.
Barnes, C. Lowry
Cabanela, Miguel E.
Jacobs, Joshua J.
TI Risk Stratification Algorithm for Management of Patients with Dual
Modular Taper Total Hip Arthroplasty: Consensus Statement of the
American Association of Hip and Knee Surgeons, the American Academy of
Orthopaedic Surgeons and the Hip Society
SO JOURNAL OF ARTHROPLASTY
LA English
DT Article
DE dual taper; taper corrosion; risk stratification
ID TISSUE-REACTIONS; CORROSION; NECK; JUNCTION; PROSTHESES; INFECTION;
FAILURE; STEM
AB Although 'dual taper' modular stems with interchangeable modular necks have the potential to optimize hip biomechanical parameters, there is increasing concern regarding the occurrence of adverse local tissue reactions from mechanically assisted crevice corrosion at the neck-stem taper junction. A systematic treatment approach (risk stratification algorithm) based on the currently available data is recommended to optimize patient management. While specialized tests such as metal ion analysis and MARS MRI are useful modalities in evaluating for adverse tissue reactions, over-reliance on any single investigative tool in the clinical decision-making process should be avoided. There should be a low threshold to perform a systematic evaluation of patients with dual taper stem total hip arthroplasty as early recognition and diagnosis will facilitate the initiation of appropriate treatment. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Kwon, Young-Min] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA.
[Fehring, Thomas K.] Ortho Carolina Hip & Knee Ctr, Charlotte, NC USA.
[Lombardi, Adolph V.] Ohio State Univ, Joint Implant Surg Inc, New Albany, OH USA.
[Barnes, C. Lowry] Univ Arkansas Med Sci, Arkansas Special Orthopaed, Little Rock, AR 72205 USA.
[Cabanela, Miguel E.] Mayo Clin, Dept Orthopaed Surg, Rochester, MN USA.
[Jacobs, Joshua J.] Rush Univ, Med Ctr, Dept Orthopaed Surg, Chicago, IL 60612 USA.
RP Kwon, YM (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA.
OI Jacobs, Joshua/0000-0003-3902-7334
NR 18
TC 20
Z9 20
U1 0
U2 3
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 0883-5403
EI 1532-8406
J9 J ARTHROPLASTY
JI J. Arthroplast.
PD NOV
PY 2014
VL 29
IS 11
BP 2060
EP 2064
DI 10.1016/j.arth.2014.07.029
PG 5
WC Orthopedics
SC Orthopedics
GA AS4FG
UT WOS:000344228000002
PM 25189673
ER
PT J
AU Gromov, K
Greene, ME
Sillesen, NH
Troelsen, A
Malchau, H
Huddleston, JI
Emerson, R
Garcia-Cimbrelo, E
Gebuhr, P
AF Gromov, Kirill
Greene, Meridith E.
Sillesen, Nanna H.
Troelsen, Anders
Malchau, Henrik
Huddleston, James I.
Emerson, Roger
Garcia-Cimbrelo, Eduardo
Gebuhr, Peter
CA Multictr Writing Comm
TI Regional Differences Between US and Europe in Radiological
Osteoarthritis and Self Assessed Quality of Life in Patients Undergoing
Total Hip Arthroplasty Surgery
SO JOURNAL OF ARTHROPLASTY
LA English
DT Article
DE hip arthroplasty; osteoarthritis; regional differences; patient-reported
outcome; quality of life
ID KNEE REPLACEMENT SURGERY; JOINT REPLACEMENT; SELECTION; PRIORITY;
CRITERIA
AB Precise indications for THA remain unclear and regional differences might exist in selecting patients for surgery. In this study we investigate radiological OA grade and self-reported quality of life in 909 patients undergoing THA in 16 centers across US and Europe. Patients in US were younger and had higher BMI. More patients with mild Tonnis OA grade underwent surgery in the US compared to Europe. Patients in the US had significantly higher pain VAS and significantly lower SF-36 Physical, while having significantly higher EQ-VAS scores preoperatively. Patient demographics and disease severity according to radiological OA grade and self-reported survey scores vary between the United States and Europe. This knowledge can be used in the interpretation of US and European based studies on outcome following THA. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Huddleston, James I.] Stanford Univ, Med Ctr, Dept Orthopaed Surg, Stanford, CA 94305 USA.
[Emerson, Roger] Texas Ctr Joint Replacement, Plano, TX USA.
[Garcia-Cimbrelo, Eduardo] Hosp La Paz, Dept Orthopaed, Madrid, Spain.
[Gebuhr, Peter] Copenhagen Univ Hosp, Dept Orthoped, Copenhagen, Denmark.
[Gromov, Kirill; Greene, Meridith E.; Sillesen, Nanna H.; Malchau, Henrik] Massachusetts Gen Hosp, Harris Orthopaed Lab, Boston, MA 02114 USA.
[Gromov, Kirill; Sillesen, Nanna H.; Troelsen, Anders] Copenhagen Univ Hosp, Dept Orthopaed Surg, Copenhagen, Denmark.
RP Gromov, K (reprint author), Copenhagen Univ Hosp, Dept Orthoped, Copenhagen, Denmark.
RI Garcia-Alonso, Maria Cristina/K-3779-2014
OI Garcia-Alonso, Maria Cristina/0000-0003-0275-4626
NR 32
TC 2
Z9 2
U1 0
U2 6
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 0883-5403
EI 1532-8406
J9 J ARTHROPLASTY
JI J. Arthroplast.
PD NOV
PY 2014
VL 29
IS 11
BP 2078
EP 2083
DI 10.1016/j.arth.2014.07.006
PG 6
WC Orthopedics
SC Orthopedics
GA AS4FG
UT WOS:000344228000005
PM 25129452
ER
PT J
AU Stoesz, M
Wood, K
Clark, W
Kwon, YM
Freiberg, AA
AF Stoesz, Michael
Wood, Kristin
Clark, Wesley
Kwon, Young-Min
Freiberg, Andrew A.
TI Utility of Noninvasive Transcutaneous Measurement of Postoperative
Hemoglobin in Total Joint Arthroplasty Patients
SO JOURNAL OF ARTHROPLASTY
LA English
DT Article
DE transcutaneous hemoglobin measurement; postoperative venipuncture; total
joint arthroplasty; anemia; cost-effective
ID PULSE CO-OXIMETRY; SPINE SURGERY; ACCURACY
AB This study prospectively evaluated the clinical utility of a noninvasive transcutaneous device for postoperative hemoglobin measurement in 100 total hip and knee arthroplasty patients. A protocol to measure hemoglobin noninvasively, prior to venipuncture, successfully avoided venipuncture in 73% of patients. In the remaining 27 patients, there were a total of 48 venipunctures performed during the postoperative hospitalization period due to reasons including transcutaneous hemoglobin measurement less than or equal to 9 g/dL (19), inability to obtain a transcutaneous hemoglobin measurement (8), clinical signs of anemia (3), and noncompliance with the study protocol (18). Such screening protocols may provide a convenient and cost-effective alternative to routine venipuncture for identifying patients at risk for blood transfusion after elective joint arthroplasty. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Stoesz, Michael; Wood, Kristin; Clark, Wesley; Kwon, Young-Min; Freiberg, Andrew A.] Massachusetts Gen Hosp, Dept Orthopaed Surg, Boston, MA 02114 USA.
RP Freiberg, AA (reprint author), Massachusetts Gen Hosp, Dept Orthopaed Surg, 55 Fruit St, Boston, MA 02114 USA.
NR 16
TC 2
Z9 2
U1 0
U2 0
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 0883-5403
EI 1532-8406
J9 J ARTHROPLASTY
JI J. Arthroplast.
PD NOV
PY 2014
VL 29
IS 11
BP 2084
EP 2086
DI 10.1016/j.arth.2014.06.029
PG 3
WC Orthopedics
SC Orthopedics
GA AS4FG
UT WOS:000344228000006
PM 25087726
ER
PT J
AU Sinha, P
Aarnisalo, P
Chubb, R
Ono, N
Fulzele, K
Selig, M
Saeed, H
Chen, M
Weinstein, LS
Pajevic, PD
Kronenberg, HM
Wu, JY
AF Sinha, Partha
Aarnisalo, Piia
Chubb, Rhiannon
Ono, Noriaki
Fulzele, Keertik
Selig, Martin
Saeed, Hamid
Chen, Min
Weinstein, Lee S.
Pajevic, Paola Divieti
Kronenberg, Henry M.
Wu, Joy Y.
TI Loss of G(s)alpha Early in the Osteoblast Lineage Favors Adipogenic
Differentiation of Mesenchymal Progenitors and Committed Osteoblast
Precursors
SO JOURNAL OF BONE AND MINERAL RESEARCH
LA English
DT Article
DE OSTEOBLASTS; G(S)A; MESENCHYMAL PROGENITORS; ADIPOCYTES
ID HEMATOPOIETIC STEM-CELLS; RECEPTOR-RELATED PROTEIN-5; BONE-MARROW FAT;
PARATHYROID-HORMONE; ADIPOCYTE DIFFERENTIATION; PPAR-GAMMA; TARGETED
DISRUPTION; ANOREXIA-NERVOSA; TRABECULAR BONE; LEAN PHENOTYPE
AB In humans, aging and glucocorticoid treatment are associated with reduced bone mass and increased marrow adiposity, suggesting that the differentiation of osteoblasts and adipocytes may be coordinately regulated. Within the bone marrow, both osteoblasts and adipocytes are derived from mesenchymal progenitor cells, but the mechanisms guiding the commitment of mesenchymal progenitors into osteoblast versus adipocyte lineages are not fully defined. The heterotrimeric G protein subunit G(s) activates protein kinase A signaling downstream of several G protein-coupled receptors including the parathyroid hormone receptor, and plays a crucial role in regulating bone mass. Here, we show that targeted ablation of G(s) in early osteoblast precursors, but not in differentiated osteocytes, results in a dramatic increase in bone marrow adipocytes. Mutant mice have reduced numbers of mesenchymal progenitors overall, with an increase in the proportion of progenitors committed to the adipocyte lineage. Furthermore, cells committed to the osteoblast lineage retain adipogenic potential both in vitro and in vivo. These findings have clinical implications for developing therapeutic approaches to direct the commitment of mesenchymal progenitors into the osteoblast lineage. (c) 2014 American Society for Bone and Mineral Research
C1 [Sinha, Partha; Aarnisalo, Piia; Chubb, Rhiannon; Ono, Noriaki; Fulzele, Keertik; Pajevic, Paola Divieti; Kronenberg, Henry M.; Wu, Joy Y.] Massachusetts Gen Hosp, Endocrine Unit, Boston, MA 02114 USA.
[Aarnisalo, Piia] Univ Helsinki, Dept Clin Chem, SF-00100 Helsinki, Finland.
[Aarnisalo, Piia] Univ Helsinki, Cent Hosp, Hosp Dist Helsinki & Uusimaa, Lab Serv HUSLAB, Helsinki, Finland.
[Selig, Martin] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Saeed, Hamid; Wu, Joy Y.] Stanford Univ, Sch Med, Div Endocrinol, Stanford, CA 94305 USA.
[Chen, Min; Weinstein, Lee S.] NIDDK, Metabol Dis Branch, Bethesda, MD USA.
RP Wu, JY (reprint author), Stanford Univ, Sch Med, 300 Pasteur Dr,Room S-025, Stanford, CA 94305 USA.
EM jywu1@stanford.edu
FU MGH Executive Committee on Research; Harvard Stem Cell Institute;
National Institutes of Health [AR054741, AR059942]; Ruth Kirschstein
NRSA [DK11794, AR060211]; National Institute of Diabetes and Digestive
and Kidney Diseases Intramural Research Program
FX This work was supported by the MGH Executive Committee on Research
(JYW), the Harvard Stem Cell Institute (JYW), and National Institutes of
Health grants AR054741 and AR059942 to JYW; Ruth Kirschstein NRSA to PS;
DK11794 to HMK; AR060211 to PDP; and by the National Institute of
Diabetes and Digestive and Kidney Diseases Intramural Research Program
(MC and LSW).
NR 86
TC 8
Z9 8
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0884-0431
EI 1523-4681
J9 J BONE MINER RES
JI J. Bone Miner. Res.
PD NOV
PY 2014
VL 29
IS 11
BP 2414
EP 2426
DI 10.1002/jbmr.2270
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AS4DF
UT WOS:000344222800011
PM 24806274
ER
PT J
AU Wu, CJ
AF Wu, Catherine J.
TI Shifting ecologies of malignant and nonmalignant cells following BRAF
inhibition
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Editorial Material
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; CANCER; MUTATIONS; EVOLUTION
AB Clinical vignette: A 49-year-old-man with stage IV BRAF(V600E)-driven melanoma was initiated on twice-daily 960 mg of vemurafenib for treatment of progressive and recurrent subcutaneous metastatic disease of the left lower extremity. The patient's melanoma responded well to targeted BRAF inhibition. At treatment onset, hematologic parameters were all within normal limits; however, within three months of initiating therapy, wbc were found to be elevated (to 20 K) with sustained lymphocytosis of mature phenotype. lmmunophenotypic analysis was consistent with chronic lymphocytic leukemia (CLL), and FISH results revealed presence of the CLL-associated deletion in chromosome 13q14 as well as in 2p33. Vemurafenib was withdrawn after approximately one year of therapy, and subsequently, his peripheral lymphocytosis resolved and CLL regressed. Nevertheless, a monoclonal B cell population persisted even 732 days after discontinuation of vemurafenib.
C1 [Wu, Catherine J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Canc Vaccine Ctr, Boston, MA 02115 USA.
[Wu, Catherine J.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Wu, Catherine J.] Broad Inst, Cambridge, MA USA.
RP Wu, CJ (reprint author), Dana Farber Canc Inst, Rm 540B,44 Binney St, Boston, MA 02115 USA.
EM cwu@partners.org
FU Blavatnik Family Foundation; American Association for Cancer Research
(AACR); Leukemia and Lymphoma Society; National Cancer Institute (NCI)
[1R01CA182461-01, 1R01CA184922-01]
FX C.J. Wu acknowledges support from the Blavatnik Family Foundation,
American Association for Cancer Research (AACR) (SU2C Innovative
Research Grant), the Leukemia and Lymphoma Society (Scholar Award, Quest
for Cures Award), and the National Cancer Institute (NCI)
(1R01CA182461-01, 1R01CA184922-01).
NR 15
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD NOV
PY 2014
VL 124
IS 11
BP 4681
EP 4683
DI 10.1172/JCI78783
PG 3
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AS3UK
UT WOS:000344203300004
PM 25329690
ER
PT J
AU Yuen, M
Sandaradura, SA
Dowling, JJ
Kostyukova, AS
Moroz, N
Quinlan, KG
Lehtokari, VL
Ravenscroft, G
Todd, EJ
Ceyhan-Birsoy, O
Gokhin, DS
Maluenda, J
Lek, M
Nolent, F
Pappas, CT
Novak, SM
D'Amico, A
Malfatti, E
Thomas, BP
Gabriel, SB
Gupta, N
Daly, MJ
Ilkovski, B
Houweling, PJ
Davidson, AE
Swanson, LC
Brownstein, CA
Gupta, VA
Medne, L
Shannon, P
Martin, N
Bick, DP
Flisberg, A
Holmberg, E
Van den Bergh, P
Lapunzina, P
Waddell, LB
Sioboda, DD
Bertini, E
Chitayat, D
Telfer, WR
Laquerriere, A
Gregorio, CC
Ottenheijm, CAC
Bonnemann, CG
Pelin, K
Beggs, AH
Hayashi, YK
Romero, NB
Laing, NG
Nishino, I
Wallgren-Pettersson, C
Melki, J
Fowler, VM
MacArthur, DG
North, KN
Clarke, NF
AF Yuen, Michaele
Sandaradura, Sarah A.
Dowling, James J.
Kostyukova, Alla S.
Moroz, Natalia
Quinlan, Kate G.
Lehtokari, Vilma-Lotta
Ravenscroft, Gianina
Todd, Emily J.
Ceyhan-Birsoy, Ozge
Gokhin, David S.
Maluenda, Jerome
Lek, Monkol
Nolent, Flora
Pappas, Christopher T.
Novak, Stefanie M.
D'Amico, Adele
Malfatti, Edoardo
Thomas, Brett P.
Gabriel, Stacey B.
Gupta, Namrata
Daly, Mark J.
Ilkovski, Biljana
Houweling, Peter J.
Davidson, Ann E.
Swanson, Lindsay C.
Brownstein, Catherine A.
Gupta, Vandana A.
Medne, Livija
Shannon, Patrick
Martin, Nicole
Bick, David P.
Flisberg, Anders
Holmberg, Eva
Van den Bergh, Peter
Lapunzina, Pablo
Waddell, Leigh B.
Sioboda, Darcee D.
Bertini, Enrico
Chitayat, David
Telfer, William R.
Laquerriere, Annie
Gregorio, Carol C.
Ottenheijm, Coen A. C.
Boennemann, Carsten G.
Pelin, Katarina
Beggs, Alan H.
Hayashi, Yukiko K.
Romero, Norma B.
Laing, Nigel G.
Nishino, Ichizo
Wallgren-Pettersson, Carina
Melki, Judith
Fowler, Velia M.
MacArthur, Daniel G.
North, Kathryn N.
Clarke, Nigel F.
TI Leiomodin-3 dysfunction results in thin filament disorganization and
nemaline myopathy
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID MUSCLE ALPHA-TROPOMYOSIN; SKELETAL-MUSCLE; POINTED-END; N-TERMINUS;
ACTIN; TROPOMODULIN; MUTATIONS; LENGTH; POLYMERIZATION; DEFICIENCY
AB Nemaline myopathy (NM) is a genetic muscle disorder characterized by muscle dysfunction and electron-dense protein accumulations (nemaline bodies) in myofibers. Pathogenic mutations have been described in 9 genes to date, but the genetic basis remains unknown in many cases. Here, using an approach that combined whole-exome sequencing (WES) and Sanger sequencing, we identified homozygous or compound heterozygous variants in LMOD3 in 21 patients from 14 families with severe, usually lethal, NM. LMOD3 encodes leiomodin-3 (LMOD3), a 65-kDa protein expressed in skeletal and cardiac muscle. LMOD3 was expressed from early stages of muscle differentiation; localized to actin thin filaments, with enrichment near the pointed ends; and had strong actin filament-nucleating activity. Loss of LMOD3 in patient muscle resulted in shortening and disorganization of thin filaments. Knockdown of Imod3 in zebrafish replicated NM-associated functional and pathological phenotypes. Together, these findings indicate that mutations in the gene encoding LMOD3 underlie congenital myopathy and demonstrate that LMOD3 is essential for the organization of sarcomeric thin filaments in skeletal muscle.
C1 [Yuen, Michaele; Sandaradura, Sarah A.; Quinlan, Kate G.; Ilkovski, Biljana; Houweling, Peter J.; Waddell, Leigh B.; North, Kathryn N.; Clarke, Nigel F.] Childrens Hosp Westmead, Inst Neurosci & Muscle Res, Sydney, NSW, Australia.
[Yuen, Michaele; Sandaradura, Sarah A.; Quinlan, Kate G.; Houweling, Peter J.; Waddell, Leigh B.; Clarke, Nigel F.] Univ Sydney, Discipline Paediat & Child Hlth, Sydney, NSW 2006, Australia.
[Dowling, James J.; Davidson, Ann E.; Telfer, William R.] Univ Michigan, Med Ctr, Dept Pediat, Ann Arbor, MI 48109 USA.
[Dowling, James J.; Davidson, Ann E.; Telfer, William R.] Univ Michigan, Med Ctr, Dept Neurol, Ann Arbor, MI 48109 USA.
[Dowling, James J.; Davidson, Ann E.] Hosp Sick Children, Div Neurol, Toronto, ON M5G 1X8, Canada.
[Dowling, James J.; Davidson, Ann E.] Hosp Sick Children, Program Genet & Genome Biol, Toronto, ON M5G 1X8, Canada.
[Kostyukova, Alla S.; Moroz, Natalia] Washington State Univ, Gene & Linda Voiland Sch Chem Engn & Bioengn, Pullman, WA 99164 USA.
[Lehtokari, Vilma-Lotta; Wallgren-Pettersson, Carina] Univ Helsinki, Folkhalsan Inst Genet, Haartman Inst, Helsinki, Finland.
[Lehtokari, Vilma-Lotta; Wallgren-Pettersson, Carina] Univ Helsinki, Haartman Inst, Dept Med Genet, Helsinki, Finland.
[Ravenscroft, Gianina; Todd, Emily J.; Laing, Nigel G.] Univ Western Australia, Western Australia Inst Med Res, Nedlands, WA 6009, Australia.
[Ravenscroft, Gianina; Todd, Emily J.; Laing, Nigel G.] Univ Western Australia, Med Res Ctr, Nedlands, WA 6009, Australia.
[Ceyhan-Birsoy, Ozge; Swanson, Lindsay C.; Brownstein, Catherine A.; Gupta, Vandana A.; Beggs, Alan H.] Harvard Univ, Boston Childrens Hosp, Sch Med, Div Genet & Genom,Manton Ctr Orphan Dis Res, Boston, MA USA.
[Gokhin, David S.; Fowler, Velia M.] Scripps Res Inst, Dept Cell & Mol Biol, La Jolla, CA 92037 USA.
[Maluenda, Jerome; Nolent, Flora; Melki, Judith] INSERM, Unite Mixte Rech 788, F-94275 Le Kremlin Bicetre, France.
[Maluenda, Jerome; Nolent, Flora; Melki, Judith] Univ Paris, Le Kremlin Bicetre, France.
[Lek, Monkol; Thomas, Brett P.; Daly, Mark J.; MacArthur, Daniel G.] Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
[Lek, Monkol; Thomas, Brett P.; Gabriel, Stacey B.; Gupta, Namrata; Daly, Mark J.; MacArthur, Daniel G.] Broad Inst Harvard & Massachusetts Inst Technol, Cambridge, MA USA.
[Pappas, Christopher T.; Novak, Stefanie M.; Gregorio, Carol C.] Univ Arizona, Dept Cellular & Mol Med, Tucson, AZ USA.
[D'Amico, Adele; Bertini, Enrico] Bambino Gesu Pediat Hosp, Lab Mol Med Neuromuscular & Neurodegenerat Dis, Rome, Italy.
[Malfatti, Edoardo; Romero, Norma B.] Grp Hosp Univ La Pitie Salpetriere, Inst Myol, Neuromuscular Morphol Unit, Paris, France.
[Houweling, Peter J.; North, Kathryn N.] Royal Childrens Hosp, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia.
[Medne, Livija] Childrens Hosp Philadelphia, Div Human Genet & Neurol, Philadelphia, PA 19104 USA.
[Shannon, Patrick] Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON M5G 1X5, Canada.
[Martin, Nicole; Chitayat, David] Univ Toronto, Mt Sinai Hosp, Dept Obstet & Gynaecol, Prenatal Diag & Med Genet Program, Toronto, ON M5G 1X5, Canada.
[Bick, David P.] Med Coll Wisconsin, Dept Pediat, Genet Sect, Milwaukee, WI 53226 USA.
[Bick, David P.] Med Coll Wisconsin, Ctr Mol Genet, Milwaukee, WI 53226 USA.
[Flisberg, Anders] Sahlgrens Univ Hosp, Dept Neonatol, Gothenburg, Sweden.
[Holmberg, Eva] Sahlgrens Univ Hosp, Dept Clin Genet, Gothenburg, Sweden.
[Van den Bergh, Peter] St Luc Univ Hosp, Neuromuscular Reference Ctr, Brussels, Belgium.
[Lapunzina, Pablo] Hosp Univ La Paz, Inst Invest Sanitaria, Inst Genet Med & Mol, Madrid, Spain.
[Lapunzina, Pablo] Univ Autonoma Madrid, Madrid, Spain.
[Lapunzina, Pablo] Inst Salud Carlos III, Ctr Invest Biomed Red Enfermedades Raras, Madrid, Spain.
[Sioboda, Darcee D.] Univ Michigan, Dept Biomed Engn, Ann Arbor, MI 48109 USA.
[Chitayat, David] Univ Toronto, Hosp Sick Children, Dept Paediat, Div Clin & Med Genet, Toronto, ON M5G 1X8, Canada.
[Laquerriere, Annie] Univ Rouen, Pathol Lab, Rouen, France.
[Laquerriere, Annie] Univ Rouen, NeoVasc Reg INSERM Team ERI28, Rouen, France.
[Ottenheijm, Coen A. C.] Vrije Univ Amsterdam, Med Ctr, Inst Cardiovasc Res, Dept Physiol, Amsterdam, Netherlands.
[Boennemann, Carsten G.] NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, NIH, Bethesda, MD 20892 USA.
[Pelin, Katarina] Univ Helsinki, Dept Biosci, Helsinki, Finland.
[Hayashi, Yukiko K.] Tokyo Med Univ, Dept Neurophysiol, Tokyo 1608402, Japan.
[Hayashi, Yukiko K.; Nishino, Ichizo] Natl Ctr Neurol & Psychiat, Natl Inst Neurosci, Dept Neuromuscular Res, Tokyo, Japan.
[Melki, Judith] Ctr Hosp Sud Francilien, Unite Genet Med, Corbel Essonnes, France.
[North, Kathryn N.] Univ Melbourne, Dept Paediat, Melbourne, Vic 3010, Australia.
RP North, KN (reprint author), Royal Childrens Hosp, Murdoch Childrens Res Inst, Flemington Rd, Parkville, Vic 3052, Australia.
EM kathryn.north@mcri.edu.au
RI North, Kathryn/K-6476-2012; Houweling, Peter/B-4157-2016; d'amico,
adele/J-9203-2016
OI North, Kathryn/0000-0003-0841-8009; Houweling,
Peter/0000-0001-6132-2554; Pelin, Katarina/0000-0002-7040-7266; d'amico,
adele/0000-0003-2438-2624
FU National Health and Medical Research Council of Australia [1022707,
1031893, 1035828, 1035955, 0511981, 1002147, 1075451]; Association
Francaise contre les Myopathies [15734, DAJ1891]; National Hospital
Clinical Research Program [A0M10181]; National Institute of Child Health
and Development of the NIH [R01 HD 075802]; Muscular Dystrophy
Association (USA) [MDA201302]; AUism Charitable Foundation; National
Institute on Aging [AG000114]; University of Sydney Australian
Postgraduate Award; International Postgraduate Research Scholarship;
University of Western Australia Postgraduate Award; Dubai-Harvard
Foundation for Medical Research postdoctoral fellowship; Schlumberger
Foundation Faculty; Italian Ministry of Health Ricerca finalizzata
[GR-2010-2310981]; NIH [GM081688, K01 AR062601]; Muscular Dystrophy
Association (USA); National Human Genome Research Institute of the NIH
[U54 HG003067]
FX This work was funded by the National Health and Medical Research Council
of Australia (1022707 and 1031893 to N.F. Clarke, K.N. North, and N.G.
Laing; 1035828 to N.F. Clarke; 1035955 to G. Ravenscroft; 0511981 to
K.G. Quinlan; 1002147 to N.G. Laing; and 1075451 to S.A. Sandaradura),
the Association Francaise contre les Myopathies (15734 to G. Ravenscroft
and N.G. Laing; DAJ1891 to J. Melki), the National Hospital Clinical
Research Program (A0M10181 to J. Melki), the National Institute of Child
Health and Development of the NIH (R01 HD 075802 to A.H. Beggs), the
Muscular Dystrophy Association (USA) (MDA201302 to A.H. Beggs), the
AUism Charitable Foundation (to A.H. Beggs), and the National Institute
on Aging (AG000114 to D.D. Sloboda). M. Kreissl is supported by a
University of Sydney Australian Postgraduate Award and an International
Postgraduate Research Scholarship. E.J. Todd is supported by a
University of Western Australia Postgraduate Award. O. Ceyhan-Birsoy is
supported by a Dubai-Harvard Foundation for Medical Research
postdoctoral fellowship and Schlumberger Foundation Faculty for the
Future grant. A. D'Amico and E. Bertini are supported by the Italian
Ministry of Health Ricerca finalizzata (GR-2010-2310981). A.S.
Kostyukova is supported by NIH grant GM081688, and V.A. Gupta is
supported by NIH grant K01 AR062601. D.S. Gokhin is supported by a
Development Grant from the Muscular Dystrophy Association (USA). Exome
sequencing was supported by grants from the National Human Genome
Research Institute of the NIH (Medical Sequencing Program grant U54
HG003067 to the Broad Institute principal investigator, Lander) and by
the Gene Partnership Project of Boston Children's Hospital. The authors
would like to thank the study patients and their families, without whose
participation this work would not have been possible. We thank F.
Muntoni (Dubowitz Neuromuscular Centre, UCL Institute of Child Health
and Great Ormond Street Hospital for Children), C. Lacroix, (Service de
Neuropathologie, CHU Bicetre), V. Zupan-Simunek (Service de
Neonatologie, Hopital Antoine Beclere), A. Kan and N. Graf (The
Children's Hospital at Westmead), and F. Fattori (Bambino Gesu
Children's Hospital) for contribution and/or analysis of patient
samples; S. Brammah(Concord Hospital) for provision of EM control
images; T. Peduto (The Children's Hospital at Westmead) for assistance
with analysis of muscle MRI; D.M. Margulies (Boston Children's Hospital)
for support of WES through The Gene Partnership; and T. Yu and P. Park
(Boston Children's Hospital) for WES pipeline development. We thank S.V.
Brooks (University of Michigan) for assistance with experimental work
and R. Dominguez (University of Pennsylvania) for providing reagents.
NR 37
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U1 1
U2 8
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PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD NOV
PY 2014
VL 124
IS 11
BP 4693
EP 4708
DI 10.1172/JCI75199
PG 16
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AS3UK
UT WOS:000344203300008
PM 25250574
ER
PT J
AU McCormick, JA
Yang, CL
Zhang, C
Davidge, B
Blankenstein, KI
Terker, AS
Yarbrough, B
Meermeier, NP
Park, HJ
McCully, B
West, M
Borschewski, A
Himmerkus, N
Bleich, M
Bachmann, S
Mutig, K
Argaiz, ER
Gamba, G
Singer, JD
Ellison, DH
AF McCormick, James A.
Yang, Chao-Ling
Zhang, Chong
Davidge, Brittney
Blankenstein, Katharina I.
Terker, Andrew S.
Yarbrough, Bethzaida
Meermeier, Nicholas P.
Park, Hae J.
McCully, Belinda
West, Mark
Borschewski, Aljona
Himmerkus, Nina
Bleich, Markus
Bachmann, Sebastian
Mutig, Kerim
Argaiz, Eduardo R.
Gamba, Gerardo
Singer, Jeffrey D.
Ellison, David H.
TI Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by
degrading KLHL3
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID NA-CL COTRANSPORTER; PSEUDOHYPOALDOSTERONISM TYPE-II; SODIUM-CHLORIDE
COTRANSPORTER; DISEASE-CAUSING MUTATIONS; BLOOD-PRESSURE; CYCLIN-E;
DISTAL NEPHRON; UBIQUITINATION; DEGRADATION; EXPRESSION
AB Familial hyperkalemic hypertension (FHHt) is a monogenic disease resulting from mutations in genes encoding WNK kinases, the ubiquitin scaffold protein cullin 3 (CUL3), or the substrate adaptor kelch-like 3 (KLHL3). Disease-associated CUL3 mutations abrogate WNK kinase degradation in cells, but it is not clear how mutant forms of CUL3 promote WNK stability. Here, we demonstrated that an FHHt-causing CUL3 mutant (CUL3 Delta 403-459) not only retains the ability to bind and ubiquitylate WNK kinases and KLHL3 in cells, but is also more heavily neddylated and activated than WT CUL3. In cells, activated CUL3 Delta 403-459 depleted KLHL3, preventing WNK degradation, despite increased CUL3-mediated WNK ubiquitylation; therefore, CUL3 loss in kidney should phenocopy FHHt in murine models. As predicted, nephron-specific deletion of Cul3 in mice did increase WNK kinase levels and the abundance of phosphorylated Na-Cl cotransporter (NCC). Over time, however, Cul3 deletion caused renal dysfunction, including hypochloremic alkalosis, diabetes insipidus, and salt-sensitive hypotension, with depletion of sodium potassium chloride cotransporter 2 and aquaporin 2. Moreover, these animals exhibited renal inflammation, fibrosis, and increased cyclin E. These results indicate that FHHt-associated CUL3 Delta 403-459 targets KLHL3 for degradation, thereby preventing WNK degradation, whereas general loss of CUL3 activity - while also impairing WNK degradation - has widespread toxic effects in the kidney.
C1 [McCormick, James A.; Yang, Chao-Ling; Zhang, Chong; Terker, Andrew S.; Yarbrough, Bethzaida; Meermeier, Nicholas P.; Park, Hae J.; Ellison, David H.] Oregon Hlth & Sci Univ, Div Nephrol & Hypertens, Dept Med, Portland, OR 97239 USA.
[Zhang, Chong] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Nephrol, Shanghai 200030, Peoples R China.
[Davidge, Brittney; West, Mark; Singer, Jeffrey D.] Portland State Univ, Dept Biol, Portland, OR 97207 USA.
[Blankenstein, Katharina I.; Borschewski, Aljona; Bachmann, Sebastian; Mutig, Kerim; Ellison, David H.] Charite, Inst Vegetat Anat, Campus Charite Mitte, D-13353 Berlin, Germany.
[McCully, Belinda] Oregon Hlth & Sci Univ, Dept Surg, Div Trauma Crit Care & Acute Care Surg, Portland, OR 97239 USA.
[Himmerkus, Nina; Bleich, Markus] Univ Kiel, Inst Physiol, Kiel, Germany.
[Argaiz, Eduardo R.; Gamba, Gerardo] Univ Nacl Autonoma Mexico, Mol Physiol Unit, Inst Invest Biomed, Mexico City 04510, DF, Mexico.
[Argaiz, Eduardo R.; Gamba, Gerardo] Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Mexico City, DF, Mexico.
[Ellison, David H.] Portland VA Med Ctr, Portland, OR USA.
RP Ellison, DH (reprint author), Oregon Hlth & Sci Univ, Div Nephrol & Hypertens, CH12R,3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM jsinger@pdx.edu; ellisond@ohsu.edu
OI Terker, Andrew/0000-0003-1498-9043; Bleich, Markus/0000-0002-1745-2295
FU NIH [R01 DK5149 6, K01 DK076617, R01 DK098141, R01 GM082940]; Department
of Veterans Affairs [1I01BX002228-01A1]; Shanghai Municipal Education
Commission; Shanghai Jiao Tong University K.C. Wong Medical Fellowship
Fund; Conacyt; Europeans Union; American Heart Association
[13PRE14090030]
FX This work was supported by NIH grants R01 DK5149 6 (to D.H. Ellison),
K01 DK076617 and R01 DK098141 (to J.A. McCormick), and R01 GM082940 (to
J.D. Singer) as well as by Merit Review grant 1I01BX002228-01A1 from the
Department of Veterans Affairs (to D.H. Ellison). C. Zhang was supported
by the Shanghai Municipal Education Commission and a Shanghai Jiao Tong
University K.C. Wong Medical Fellowship Fund. E.R. Argaiz was supported
by a scholarship from Conacyt and is a graduate student in the
biomedical science PhD program of Universidad Nacional Autonoma de
Mexico. D.H. Ellison received a Marie Curie Fellowship from the
Europeans Union during part of these studies. A.S. Terker is supported
by a Predoctoral Fellowship from the American Heart Association
(13PRE14090030). The authors appreciate the interpretation of the renal
morphology and advice provided by Megan Troxell, and the helpful
discussions with Juliette Hadchouel.
NR 40
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PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD NOV
PY 2014
VL 124
IS 11
BP 4723
EP 4736
DI 10.1172/JCI76126
PG 14
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AS3UK
UT WOS:000344203300010
PM 25250572
ER
PT J
AU Dubovsky, JA
Flynn, R
Du, J
Harrington, BK
Zhong, YM
Kaffenberger, B
Yang, C
Towns, WH
Lehman, A
Johnson, AJ
Muthusamy, N
Devine, SM
Jaglowski, S
Serody, JS
Murphy, WJ
Munn, DH
Luznik, L
Hill, GR
Wong, HK
MacDonald, KKP
Maillard, I
Koreth, J
Elias, L
Cutler, C
Soiffer, RJ
Antin, JH
Ritz, J
Panoskaltsis-Mortari, A
Byrd, JC
Blazar, BR
AF Dubovsky, Jason A.
Flynn, Ryan
Du, Jing
Harrington, Bonnie K.
Zhong, Yiming
Kaffenberger, Benjamin
Yang, Carrie
Towns, William H.
Lehman, Amy
Johnson, Amy J.
Muthusamy, Natarajan
Devine, Steven M.
Jaglowski, Samantha
Serody, Jonathan S.
Murphy, William J.
Munn, David H.
Luznik, Leo
Hill, Geoffrey R.
Wong, Henry K.
MacDonald, Kelli K. P.
Maillard, Ivan
Koreth, John
Elias, Laurence
Cutler, Corey
Soiffer, Robert J.
Antin, Joseph H.
Ritz, Jerome
Panoskaltsis-Mortari, Angela
Byrd, John C.
Blazar, Bruce R.
TI Ibrutinib treatment ameliorates murine chronic graft-versus-host disease
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID CD4(+) T-CELLS; CHRONIC LYMPHOCYTIC-LEUKEMIA; BRUTONS TYROSINE KINASE;
BRONCHIOLITIS OBLITERANS; BONE-MARROW; EXTRACORPOREAL PHOTOPHERESIS;
THERAPEUTIC TARGET; MICE LACKING; CHRONIC GVHD; ITK
AB Chronic graft-versus-host disease (cGVHD) is a life-threatening impediment to allogeneic hematopoietic stem cell transplantation, and current therapies do not completely prevent and/or treat cGVHD. CD4(+) T cells and B cells mediate cGVHD; therefore, targeting these populations may inhibit cGVHD pathogenesis. Ibrutinib is an FDA-approved irreversible inhibitor of Bruton's tyrosine kinase (BTK) and IL-2 inducible T cell kinase (ITK) that targets Th2 cells and B cells and produces durable remissions in B cell malignancies with minimal toxicity. Here, we evaluated whether ibrutinib could reverse established cGVHD in 2 complementary murine models, a model interrogating T cell-driven sclerodermatous cGVHD and an alloantibody-driven multiorgan system cGVHD model that induces bronchiolar obliterans (BO). In the T cell-mediated sclerodermatous cGVHD model, ibrutinib treatment delayed progression, improved survival, and ameliorated clinical and pathological manifestations. In the alloantibody-driven cGVHD model, ibrutinib treatment restored pulmonary function and reduced germinal center reactions and tissue immunoglobulin deposition. Animals lacking BTK and ITK did not develop cGVHD, indicating that these molecules are critical to cGVHD development. Furthermore, ibrutinib treatment reduced activation of T and B cells from patients with active cGVHD. Our data demonstrate that B cells and T cells drive cGVHD and suggest that ibrutinib has potential as a therapeutic agent, warranting consideration for cGVHD clinical trials.
C1 [Dubovsky, Jason A.; Zhong, Yiming; Kaffenberger, Benjamin; Yang, Carrie; Towns, William H.; Lehman, Amy; Johnson, Amy J.; Muthusamy, Natarajan; Devine, Steven M.; Jaglowski, Samantha; Wong, Henry K.; Byrd, John C.] Ohio State Univ, Dept Internal Med, Div Hematol, Columbus, OH 43210 USA.
[Flynn, Ryan; Du, Jing; Panoskaltsis-Mortari, Angela; Blazar, Bruce R.] Univ Minnesota, Mason Canc Ctr, Minneapolis, MN 55455 USA.
[Flynn, Ryan; Du, Jing; Panoskaltsis-Mortari, Angela; Blazar, Bruce R.] Univ Minnesota, Dept Pediat, Div Blood & Marrow Transplantat, Minneapolis, MN 55455 USA.
[Harrington, Bonnie K.] Ohio State Univ, Coll Vet Med Vet & Comparat Med, Columbus, OH 43210 USA.
[Serody, Jonathan S.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Sch Med, Chapel Hill, NC 27599 USA.
[Murphy, William J.] Univ Calif Davis, Ctr Canc, Dept Dermatol, Sacramento, CA 95817 USA.
[Murphy, William J.] Sch Med, Sacramento, CA 95816 USA.
[Munn, David H.] Med Coll Georgia, Sch Med, Dept Pediat, Augusta, GA 30912 USA.
[Luznik, Leo] Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Luznik, Leo] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA.
[Hill, Geoffrey R.; MacDonald, Kelli K. P.] Med Res Berghofer Med Res Inst, Queensland Inst, Brisbane, Qld, Australia.
[Maillard, Ivan] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
[Koreth, John; Cutler, Corey; Soiffer, Robert J.; Antin, Joseph H.; Ritz, Jerome] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Elias, Laurence] Pharmacyclics Inc, Sunnyvale, CA USA.
RP Blazar, BR (reprint author), Univ Minnesota, MMC 109, Minneapolis, MN 55455 USA.
EM blaza001@umn.edu
RI Hill, Geoffrey/O-2630-2016; MacDonald, Kelli/O-2722-2016; Jaglowski,
Samantha/E-3304-2011;
OI Ritz, Jerome/0000-0001-5526-4669; Hill, Geoffrey/0000-0003-2994-0429;
MacDonald, Kelli/0000-0003-3451-4221; Serody,
Jonathan/0000-0003-4568-1092; Harrington, Bonnie/0000-0003-2658-6188
FU NIH [P01 AI056299, P01 CA142106, R01 HL56067, R01 AI34495, T32
AI1007313]; National Cancer Institute [P01 CA095426, K12 CA133250-05,
P50 CA140158, T32 CA009338-33-03]; American Cancer Society
[125039-PF-13-246-01-LIB]; Leukemia & Lymphoma Society; American Society
of Hematology; Harry Mangurian Foundation; D. Warren Brown Family
Foundation; Jock and Bunny Adams Research and Education Endowment
FX The authors gratefully acknowledge Leslie J. Berg for providing critical
reagents as well as Jessica MacMurray for experimental assistance. This
work was supported by grants from the NIH (P01 AI056299, P01 CA142106,
R01 HL56067, and R01 AI34495 to B.R. Blazar; T32 AI1007313 to R. Flynn).
In addition, support was provided by National Cancer Institute grants
(P01 CA095426, K12 CA133250-05, and P50 CA140158 to J.C. Byrd; T32
CA009338-33-03 to J.A. Dubovsky), as well as grants from the American
Cancer Society (125039-PF-13-246-01-LIB to J.A. Dubovsky), the Leukemia
& Lymphoma Society, the American Society of Hematology, Mr. and Mrs.
Michael Thomas, the Harry Mangurian Foundation, the D. Warren Brown
Family Foundation, and the Jock and Bunny Adams Research and Education
Endowment (to J.H. Antin).
NR 61
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U2 14
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD NOV
PY 2014
VL 124
IS 11
BP 4867
EP 4876
DI 10.1172/JCI75328
PG 10
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AS3UK
UT WOS:000344203300022
PM 25271622
ER
PT J
AU Wegiel, B
Larsen, R
Gallo, D
Chin, BY
Harris, C
Mannam, P
Kaczmarek, E
Lee, PJ
Zuckerbraun, BS
Flavell, R
Soares, MP
Otterbein, LE
AF Wegiel, Barbara
Larsen, Rasmus
Gallo, David
Chin, Beek Yoke
Harris, Clair
Mannam, Praveen
Kaczmarek, Elzbieta
Lee, Patty J.
Zuckerbraun, Brian S.
Flavell, Richard
Soares, Miguel P.
Otterbein, Leo E.
TI Macrophages sense and kill bacteria through carbon monoxide-dependent
inflammasome activation
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID INNATE IMMUNE RECOGNITION; HEME OXYGENASE-1; NALP3 INFLAMMASOME; NLRP3
INFLAMMASOME; ESCHERICHIA-COLI; CELL-DEATH; EXPRESSION; RECEPTOR;
IL-1-BETA; CASPASE-1
AB Microbial clearance by eukaryotes relies on complex and coordinated processes that remain poorly understood. The gasotransmitter carbon monoxide (CO) is generated by the stress-responsive enzyme heme oxygenase-1 (HO-1, encoded by Hmox1), which is highly induced in macrophages in response to bacterial infection. HO-1 deficiency results in inadequate pathogen clearance, exaggerated tissue damage, and increased mortality. Here, we determined that macrophage-generated CO promotes ATP production and release by bacteria, which then activates the Nacht, LRR, and PYD domains-containing protein 3 (NALP3) inflammasome, intensifying bacterial killing. Bacterial killing defects in HO-1-deficient murine macrophages were restored by administration of CO. Moreover, increased CO levels enhanced the bacterial clearance capacity of human macrophages and WT murine macrophages. CO-dependent bacterial clearance required the NALP3 inflammasome, as CO did not increase bacterial killing in macrophages isolated from NALP3-deficient or caspase-1-deficient mice. IL-1 beta cleavage and secretion were impaired in HO-1-deficient macrophages, and CO-dependent processing of IL-1 beta required the presence of bacteria-derived ATR We found that bacteria remained viable to generate and release ATP in response to CO. The ATP then bound to macrophage nucleotide P2 receptors, resulting in activation of the NALP3/IL-1 beta inflammasome to amplify bacterial phagocytosis by macrophages. Taken together, our results indicate that macrophage-derived CO permits efficient and coordinated regulation of the host innate response to invading microbes.
C1 [Wegiel, Barbara; Gallo, David; Chin, Beek Yoke; Harris, Clair; Otterbein, Leo E.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Transplant Inst,Dept Surg, Boston, MA 02215 USA.
[Larsen, Rasmus; Soares, Miguel P.] Inst Gulbenkian Ciencias, Oeiras, Portugal.
[Mannam, Praveen; Lee, Patty J.; Flavell, Richard] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT USA.
[Kaczmarek, Elzbieta] Harvard Univ, Sch Med, BIDMC, Ctr Vasc Biol,Dept Surg, Boston, MA 02215 USA.
[Zuckerbraun, Brian S.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
[Flavell, Richard] Howard Hughes Med Inst, New Haven, CT 06510 USA.
RP Otterbein, LE (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Transplant Inst,Ctr Life Sci, 3 Blackfan Circle, Boston, MA 02215 USA.
EM lotterbe@bidmc.harvard.edu
OI Soares, Miguel/0000-0002-9314-4833; Flavell, Richard/0000-0003-4461-0778
FU NIH [HL-071797, HL-076167, R21CA169904-01, HL-106227]; American Heart
Association [10SDG2640091]; Julie Henry Fund at the Transplant Center of
the BIDMC; Fundacao para a Ciencia e Tecnologia (Portugal)
[SFRH/BPD/25436/2005, PTDC/BI0/70815/2006, PTDC/BIA-B CM/101311/2008,
PTDC/SAU-FCF/100762/2008]; European Community [LSH-2005-1.2.5-1,
ERC-2011-AdG, 294709 - DAMAGECONTROL]
FX This work was largely supported by NIH grants HL-071797 and HL-076167
(to L.E. Otterbein) and American Heart Association grants 10SDG2640091
and NIH R21CA169904-01 (to B. Wegiel). We thank Bryan Davis (MIT/Harvard
Medical School) and Bernard Strauss (MIT) for providing mutant strains
from the Keio E. coli knockout library. We are grateful to D. Nakatsu
for providing QC-15. We thank the Julie Henry Fund at the Transplant
Center of the BIDMC for their support. L.E. Otterbein holds an honorary
visiting professorship at Aston University (Birmingham, United Kingdom).
This work was supported by Fundacao para a Ciencia e Tecnologia
(Portugal) grants SFRH/BPD/25436/2005 and PTDC/BI0/70815/2006 (to R.
Larsen) and PTDC/BIA-B CM/101311/2008 and PTDC/SAU-FCF/100762/2008 (to
M.P. Soares), the European Community, 6th Framework grant
LSH-2005-1.2.5-1 and ERC-2011-AdG, 294709 - DAMAGECONTROL (to M.P.
Soares), and in part by NIH grant HL-106227 (to E. Kaczmarek). R.
Flavell is an investigator of the Howard Hughes Medical Institute.
NR 72
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U1 5
U2 20
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD NOV
PY 2014
VL 124
IS 11
BP 4926
EP 4940
DI 10.1172/JCI72853
PG 15
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AS3UK
UT WOS:000344203300028
PM 25295542
ER
PT J
AU Freireich, EJ
Wiernik, PH
Steensma, DP
AF Freireich, Emil J.
Wiernik, Peter H.
Steensma, David P.
TI The Leukemias: A Half-Century of Discovery
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID ACUTE PROMYELOCYTIC LEUKEMIA; ACUTE MYELOID-LEUKEMIA; ACUTE
LYMPHOBLASTIC-LEUKEMIA; CHRONIC LYMPHOCYTIC-LEUKEMIA; TRANS-RETINOIC
ACID; NORTH-AMERICAN INTERGROUP; ABL TYROSINE KINASE; CHRONIC
MYELOGENOUS LEUKEMIA; MINIMAL RESIDUAL DISEASE; LOW-DOSE CYTARABINE
C1 [Freireich, Emil J.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Wiernik, Peter H.] Canc Res Fdn New York, New York, NY USA.
[Steensma, David P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
RP Freireich, EJ (reprint author), Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
FU NCI NIH HHS [P30 CA016672]
NR 105
TC 13
Z9 13
U1 1
U2 8
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 2014
VL 32
IS 31
BP 3463
EP +
DI 10.1200/JCO.2014.57.1034
PG 8
WC Oncology
SC Oncology
GA AS6MY
UT WOS:000344378700002
PM 25185093
ER
PT J
AU Bardia, A
Haber, DA
AF Bardia, Aditya
Haber, Daniel A.
TI Solidifying Liquid Biopsies: Can Circulating Tumor Cell Monitoring Guide
Treatment Selection in Breast Cancer?
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Editorial Material
ID PROSTATE-CANCER; PROGRESSION; SURVIVAL; MARKERS; TRIAL; BLOOD
C1 [Bardia, Aditya] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Bardia, A (reprint author), Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
FU NCI NIH HHS [R01 CA129933]
NR 19
TC 4
Z9 4
U1 0
U2 7
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 2014
VL 32
IS 31
BP 3470
EP +
DI 10.1200/JCO.2014.57.1505
PG 4
WC Oncology
SC Oncology
GA AS6MY
UT WOS:000344378700003
PM 25024075
ER
PT J
AU Smerage, JB
Barlow, WE
Hortobagyi, GN
Winer, EP
Leyland-Jones, B
Srkalovic, G
Tejwani, S
Schott, AF
O'Rourke, MA
Lew, DL
Doyle, GV
Gralow, JR
Livingston, RB
Hayes, DF
AF Smerage, Jeffrey B.
Barlow, William E.
Hortobagyi, Gabriel N.
Winer, Eric P.
Leyland-Jones, Brian
Srkalovic, Gordan
Tejwani, Sheela
Schott, Anne F.
O'Rourke, Mark A.
Lew, Danika L.
Doyle, Gerald V.
Gralow, Julie R.
Livingston, Robert B.
Hayes, Daniel F.
TI Circulating Tumor Cells and Response to Chemotherapy in Metastatic
Breast Cancer: SWOG S0500
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID SURVIVAL; SINGLE; BLOOD
AB Purpose
Increased circulating tumor cells (CTCs; five or more CTCs per 7.5 mL of whole blood) are associated with poor prognosis in metastatic breast cancer (MBC). A randomized trial of patients with persistent increase in CTCs tested whether changing chemotherapy after one cycle of first-line chemotherapy would improve the primary outcome of overall survival (OS).
Patients and Methods
Patients with MBC who did not have increased CTCs at baseline remained on initial therapy until progression (arm A). Patients with initially increased CTCs that decreased after 21 days of therapy remained on initial therapy (arm B). Patients with persistently increased CTCs after 21 days of therapy were randomly assigned to continue initial therapy (arm C1) or change to an alternative chemotherapy (arm C2).
Results
Of 595 eligible and evaluable patients, 276 (46%) did not have increased CTCs (arm A). Of those with initially increased CTCs, 31 (10%) were not retested, 165 were assigned to arm B, and 123 were randomly assigned to arm C1 or C2. No difference in median OS was observed between arm C1 and C2 (10.7 and 12.5 months, respectively; P = .98). CTCs were strongly prognostic. Median OS for arms A, B, and C (C1 and C2 combined) were 35 months, 23 months, and 13 months, respectively (P < .001).
Conclusion
This study confirms the prognostic significance of CTCs in patients with MBC receiving first-line chemotherapy. For patients with persistently increased CTCs after 21 days of first-line chemotherapy, early switching to an alternate cytotoxic therapy was not effective in prolonging OS. For this population, there is a need for more effective treatment than standard chemotherapy. (C) 2014 by American Society of Clinical Oncology
C1 [Smerage, Jeffrey B.; Schott, Anne F.; Hayes, Daniel F.] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Srkalovic, Gordan] Sparrow Reg Canc Ctr, Lansing, MI USA.
[Tejwani, Sheela] Henry Ford Hosp, Detroit, MI 48202 USA.
[Barlow, William E.; Lew, Danika L.] SWOG Stat Ctr, Seattle, WA USA.
[Gralow, Julie R.] Seattle Canc Care Alliance, Seattle, WA USA.
[Hortobagyi, Gabriel N.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Winer, Eric P.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Leyland-Jones, Brian] Avera Canc Inst, Sioux Falls, SD USA.
[O'Rourke, Mark A.] Greenville Hlth Syst, Inst Canc, Greenville Community Clin Oncol Program, Greenville, SC USA.
[Doyle, Gerald V.] Immunicon, Huntingdon Valley, PA USA.
[Livingston, Robert B.] Univ Arizona, Ctr Canc, Tucson, AZ USA.
RP Hayes, DF (reprint author), Univ Michigan, Ctr Comprehens Canc, 1500 E Med Ctr Dr,6312 CCC, Ann Arbor, MI 48109 USA.
EM hayesdf@umich.edu
FU Public Health Service Cooperative Agreement Grants from the National
Cancer Institute [CA32102, CA38926, CA 63848, CA27057, CA67663, CA58416,
CA22433, CA 95860, CA04919, CA16385, CA 63844, CA45808, CA20319,
CA58882, CA35192, CA14028, CA45807, CA74647, CA37981, CA46441, CA42777,
CA35178]; Department of Health and Human Services; Immunicon and
Veridex; [CA86780]; [CA58861]; [CA67575]; [CA45560]; [CA12644];
[CA45377]; [CA35281]; [CA35431]; [CA76447]; [CA46368]; [CA73590];
[CA105409]; [CA46113]; [CA48723]; [CA31946]; [CA21115]; [CA35103]
FX Supported in part by Public Health Service Cooperative Agreement Grants
No. CA32102, CA38926, CA 63848, CA27057, CA67663, CA58416, CA22433, CA
95860, CA04919, CA16385, CA 63844, CA45808, CA20319, CA58882, CA35192,
CA14028, CA45807, CA74647, CA37981, CA46441, CA42777, CA35178, CA86780,
CA58861, CA67575, CA45560, CA12644, CA45377, CA35281, CA35431, CA76447,
CA46368, CA73590, CA105409, CA46113, CA48723, CA31946, CA21115, and
CA35103 from the National Cancer Institute, Department of Health and
Human Services, and by Immunicon and Veridex. Circulating tumor cell
assays were performed by Janssen Diagnostics at no charge to the
clinical sponsor (SWOG).
NR 12
TC 133
Z9 140
U1 2
U2 16
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 2014
VL 32
IS 31
BP 3483
EP +
DI 10.1200/JCO.2014.56.2561
PG 8
WC Oncology
SC Oncology
GA AS6MY
UT WOS:000344378700007
PM 24888818
ER
PT J
AU Wright, AA
Hatfield, LA
Earle, CC
Keating, NL
AF Wright, Alexi A.
Hatfield, Laura A.
Earle, Craig C.
Keating, Nancy L.
TI End-of-Life Care for Older Patients With Ovarian Cancer Is Intensive
Despite High Rates of Hospice Use
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID MEDICARE BENEFICIARIES; MENTAL-HEALTH; QUALITY; DEATH; AGGRESSIVENESS;
SURVIVAL; TRENDS; ASSOCIATIONS; DISCUSSIONS; TRANSITIONS
AB Purpose
To date, few studies have examined end-of-life care for patients with ovarian cancer. One study documented increased hospice use among older patients with ovarian cancer from 2000 to 2005. We sought to determine whether increased hospice use was associated with less-intensive end-of-life medical care.
Patients and Methods
We identified 6,956 individuals age >= 66 years living in SEER areas who were enrolled in fee-for-service Medicare, diagnosed with epithelial ovarian cancer between 1997 and 2007, and died as a result of ovarian cancer by December 2007. We examined changes in medical care during patients' last month of life over time.
Results
Between 1997 and 2007, hospice use increased significantly, and terminal hospitalizations decreased (both P < .001). However, during this time, we also observed statistically significant increases in intensive care unit admissions, hospitalizations, repeated emergency department visits, and health care transitions (all P <= .01). In addition, the proportion of patients referred to hospice from inpatient settings rose over time (P = .001). Inpatients referred to hospice were more likely to enroll in hospice within 3 days of death than outpatients (adjusted odds ratio, 1.36; 95% CI, 1.12 to 1.66).
Conclusion
Older women with ovarian cancer were more likely to receive hospice services near death and less likely to die in a hospital in 2007 compared with earlier years. Despite this, use of hospital-based services increased over time, and patients underwent more transitions among health care settings near death, suggesting that the increasing use of hospice did not offset intensive end-of-life care. (C) 2014 by American Society of Clinical Oncology
C1 [Wright, Alexi A.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Wright, Alexi A.; Hatfield, Laura A.; Keating, Nancy L.] Harvard Univ, Sch Med, Boston, MA USA.
[Keating, Nancy L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Earle, Craig C.] Canc Care Ontario, Toronto, ON, Canada.
[Earle, Craig C.] Ontario Inst Canc Res, Toronto, ON, Canada.
RP Wright, AA (reprint author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA.
EM alexi_wright@dfci.harvard.edu
FU National Cancer Institute (NCI) [1K07 CA166210]; American Cancer
Society, a Conquer Cancer Foundation of the American Society for
Clinical Oncology Career Development Award [MRSG-13-013]; National
Palliative Care Research Center Junior Faculty Career Development Award;
Gloria Spivak Faculty Advancement Fund; NCI [1R01 CA164021]
FX Supported in part by Grant No. 1K07 CA166210 from the National Cancer
Institute (NCI), Grant No. MRSG-13-013 from the American Cancer Society,
a Conquer Cancer Foundation of the American Society for Clinical
Oncology Career Development Award, the National Palliative Care Research
Center Junior Faculty Career Development Award, and the Gloria Spivak
Faculty Advancement Fund (A.A.W.) and by Research Grant No. 1R01
CA164021 from the NCI (N.L.K.).
NR 36
TC 16
Z9 16
U1 4
U2 9
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 2014
VL 32
IS 31
BP 3534
EP +
DI 10.1200/JCO.2014.55.5383
PG 7
WC Oncology
SC Oncology
GA AS6MY
UT WOS:000344378700014
PM 25287831
ER
PT J
AU Ganz, PA
Petersen, L
Castellon, SA
Bower, JE
Silverman, DHS
Cole, SW
Irwin, MR
Belin, TR
AF Ganz, Patricia A.
Petersen, Laura
Castellon, Steven A.
Bower, Julienne E.
Silverman, Daniel H. S.
Cole, Steven W.
Irwin, Michael R.
Belin, Thomas R.
TI Cognitive Function After the Initiation of Adjuvant Endocrine Therapy in
Early-Stage Breast Cancer: An Observational Cohort Study
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID STANDARD-DOSE CHEMOTHERAPY; HEALTH SURVEY SF-36; HORMONAL-THERAPY;
WOMEN; MEMORY; TAMOXIFEN; ESTROGEN; DYSFUNCTION; IMPAIRMENT; BRAIN
AB Purpose
This report examines cognitive complaints and neuropsychological (NP) testing outcomes in patients with early-stage breast cancer after the initiation of endocrine therapy (ET) to determine whether this therapy plays any role in post-treatment cognitive complaints.
Patients and Methods
One hundred seventy-three participants from the Mind Body Study (MBS) observational cohort provided data from self-report questionnaires and NP testing obtained at enrollment (T1, before initiation of ET), and 6 months later (T2). Bivariate analyses compared demographic and treatment variables, cognitive complaints, depressive symptoms, quality of life, and NP functioning between those who received ET versus not. Multivariable linear regression models examined predictors of cognitive complaints at T2, including selected demographic variables, depressive symptoms, ET use, and other medical variables, along with NP domains that were identified in bivariate analyses.
Results
Seventy percent of the 173 MBS participants initiated ET, evenly distributed between tamoxifen or aromatase inhibitors. ET-treated participants reported significantly increased language and communication (LC) cognitive complaints at T2 (P = .003), but no significant differences in NP test performance. Multivariable regression on LC at T2 found higher LC complaints significantly associated with T1 LC score (P < .001), ET at T2 (P = .004), interaction between ET and past hormone therapy (HT) (P < .001), and diminished improvement in NP psychomotor function (P = .05). Depressive symptoms were not significant (P = .10).
Conclusion
Higher LC complaints are significantly associated with ET 6 months after starting treatment and reflect diminished improvements in some NP tests. Past HT is a significant predictor of higher LC complaints after initiation of ET. (C) 2014 by American Society of Clinical Oncology
C1 [Ganz, Patricia A.; Belin, Thomas R.] Univ Calif Los Angeles, Fielding Sch Publ Hlth, Los Angeles, CA 90095 USA.
[Ganz, Patricia A.; Petersen, Laura] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA.
[Ganz, Patricia A.; Silverman, Daniel H. S.; Cole, Steven W.; Irwin, Michael R.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Castellon, Steven A.] VA Greater Los Angeles Hlth Care Syst, Los Angeles, CA USA.
[Castellon, Steven A.; Bower, Julienne E.] Univ Calif Los Angeles, Los Angeles, CA 90095 USA.
[Bower, Julienne E.; Cole, Steven W.; Irwin, Michael R.] Univ Calif Los Angeles, Semel Inst, Cousins Ctr Psychoneuroimmunol, Los Angeles, CA 90095 USA.
RP Ganz, PA (reprint author), Univ Calif Los Angeles, Div Canc Prevent & Control Res, Jonsson Comprehens Canc Ctr, A2-125 CHS,Box 956900, Los Angeles, CA 90095 USA.
EM pganz@mednet.ucla.edu
RI Irwin, Michael/H-4870-2013
OI Irwin, Michael/0000-0002-1502-8431
FU National Cancer Institute [R01-CA109650]; Breast Cancer Research
Foundation [R01-AG034588, R01-AG026364, R01-CA119159, R01-HL079955,
R01-HL095799, P30-AG028748, UL RR 033176]; Cousins Center for
Psychoneuroimmunology
FX Supported by funding from the National Cancer Institute Grant No.
R01-CA109650 and the Breast Cancer Research Foundation (P.A.G.), Grants
No. R01-AG034588, R01-AG026364, R01-CA119159, R01-HL079955,
R01-HL095799, P30-AG028748, UL RR 033176 (M.R.I.), and the Cousins
Center for Psychoneuroimmunology (M.R.I.).
NR 48
TC 25
Z9 25
U1 1
U2 11
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 2014
VL 32
IS 31
BP 3559
EP +
DI 10.1200/JCO.2014.56.1662
PG 16
WC Oncology
SC Oncology
GA AS6MY
UT WOS:000344378700018
PM 25267747
ER
PT J
AU Ligibel, JA
Alfano, CM
Courneya, KS
Demark-Wahnefried, W
Burger, RA
Chlebowski, RT
Fabian, CJ
Gucalp, A
Hershman, DL
Hudson, MM
Jones, LW
Kakarala, M
Ness, KK
Merrill, JK
Wollins, DS
Hudis, CA
AF Ligibel, Jennifer A.
Alfano, Catherine M.
Courneya, Kerry S.
Demark-Wahnefried, Wendy
Burger, Robert A.
Chlebowski, Rowan T.
Fabian, Carol J.
Gucalp, Ayca
Hershman, Dawn L.
Hudson, Melissa M.
Jones, Lee W.
Kakarala, Madhuri
Ness, Kirsten K.
Merrill, Janette K.
Wollins, Dana S.
Hudis, Clifford A.
TI American Society of Clinical Oncology Position Statement on Obesity and
Cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID BODY-MASS INDEX; LONG-TERM EFFECTIVENESS; BREAST-CANCER; WEIGHT-LOSS;
PHYSICAL-ACTIVITY; HEALTH BEHAVIORS; LIFE-STYLE; POSTMENOPAUSAL WOMEN;
TEACHABLE MOMENT; RANDOMIZED-TRIAL
AB Rates of obesity have increased significantly over the last three decades in the United States and globally. In addition to contributing to heart disease and diabetes, obesity is a major unrecognized risk factor for cancer. Obesity is associated with worsened prognosis after cancer diagnosis and also negatively affects the delivery of systemic therapy, contributes to morbidity of cancer treatment, and may raise the risk of second malignancies and comorbidities. Research shows that the time after a cancer diagnosis can serve as a teachable moment to motivate individuals to adopt risk-reducing behaviors. For this reason, the oncology care team-the providers with whom a patient has the closest relationships in the critical period after a cancer diagnosis-is in a unique position to help patients lose weight and make other healthy lifestyle changes. The American Society of Clinical Oncology is committed to reducing the impact of obesity on cancer and has established a multipronged initiative to accomplish this goal by 1) increasing education and awareness of the evidence linking obesity and cancer; 2) providing tools and resources to help oncology providers address obesity with their patients; 3) building and fostering a robust research agenda to better understand the pathophysiology of energy balance alterations, evaluate the impact of behavior change on cancer outcomes, and determine the best methods to help cancer survivors make effective and useful changes in lifestyle behaviors; and 4) advocating for policy and systems change to address societal factors contributing to obesity and improve access to weight management services for patients with cancer. (C) 2014 by American Society of Clinical Oncology
C1 [Ligibel, Jennifer A.] Dana Farber Canc Inst, Boston, MA 02155 USA.
[Alfano, Catherine M.] NCI, Bethesda, MD 20892 USA.
[Courneya, Kerry S.] Univ Alberta, Edmonton, AB, Canada.
[Demark-Wahnefried, Wendy] Univ Alabama Birmingham, Birmingham, AL USA.
[Burger, Robert A.] Univ Penn, Philadelphia, PA 19104 USA.
[Chlebowski, Rowan T.] Harbor UCLA Med Ctr, Torrance, CA 90509 USA.
[Fabian, Carol J.] Univ Kansas, Med Ctr, Westwood, KS USA.
[Gucalp, Ayca; Jones, Lee W.; Hudis, Clifford A.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Hershman, Dawn L.] Columbia Univ, Med Ctr, New York, NY USA.
[Hudson, Melissa M.; Ness, Kirsten K.] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
[Kakarala, Madhuri] Van Andel Inst, Grand Rapids, MI USA.
[Merrill, Janette K.; Wollins, Dana S.] Amer Soc Clin Oncol, Alexandria, VA USA.
RP Ligibel, JA (reprint author), Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02155 USA.
EM jligibel@partners.org
NR 48
TC 79
Z9 79
U1 0
U2 10
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 2014
VL 32
IS 31
BP 3568
EP +
DI 10.1200/JCO.2014.58.4680
PG 8
WC Oncology
SC Oncology
GA AS6MY
UT WOS:000344378700019
PM 25273035
ER
PT J
AU Azzoli, CG
Engelman, J
Fidias, P
Gainor, JF
Heist, RS
Lamont, EB
Lennes, IT
Rosovsky, RP
Sequist, LV
Shaw, AT
Temel, JS
AF Azzoli, Christopher G.
Engelman, Jeffrey
Fidias, Panos
Gainor, Justin F.
Heist, Rebecca S.
Lamont, Elizabeth B.
Lennes, Inga T.
Rosovsky, Rachel P.
Sequist, Lecia V.
Shaw, Alice Tsang
Temel, Jennifer S.
TI Genotyping Lung Cancer Is an Investment in the Future
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
ID CRIZOTINIB; EGFR
C1 [Azzoli, Christopher G.; Engelman, Jeffrey; Fidias, Panos; Gainor, Justin F.; Heist, Rebecca S.; Lamont, Elizabeth B.; Lennes, Inga T.; Rosovsky, Rachel P.; Sequist, Lecia V.; Shaw, Alice Tsang; Temel, Jennifer S.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
RP Azzoli, CG (reprint author), Massachusetts Gen Hosp, Ctr Canc, Boston, MA 02114 USA.
NR 10
TC 2
Z9 2
U1 1
U2 3
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 1
PY 2014
VL 32
IS 31
BP 3576
EP +
DI 10.1200/JCO.2014.56.6430
PG 3
WC Oncology
SC Oncology
GA AS6MY
UT WOS:000344378700022
PM 25199750
ER
PT J
AU Beca, F
Andre, R
Martins, DS
Bilhim, T
Martins, D
Schmitt, F
AF Beca, Francisco
Andre, Rosario
Martins, Duarte Saraiva
Bilhim, Tiago
Martins, Diana
Schmitt, Fernando
TI p-mTOR expression is associated with better prognosis in luminal breast
carcinoma
SO JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
ID RENAL-CELL CARCINOMA; CANCER; THERAPY; RECOMMENDATIONS; ACTIVATION;
PATHWAY; GROWTH; PTEN
AB Aims Despite considerable interest in the PI3K/AKT/mTOR pathway in breast carcinomas (BC), published data reports contradictory results regarding the association of phosphorylated mammalian target of Rapamycin (p-mTOR) expression with clinico-pathological features and prognosis in BC. Here, we evaluate the main clinico-pathological associations with p-mTOR expression in BC, with focus on the different molecular subtypes.
Methods In this retrospective study, 331 BC patients were included in final analysis. Outcome measures included disease-free survival (DFS) and overall survival (OS) times. Baseline data and outcome measures were compared between immunohistochemical p-mTOR expressing and non-expressing BCs. Subgroup analysis was performed to assess the effect of p-mTOR expression in the outcome for each BC molecular subtype.
Results 43.8% of the tumours were positive for p-mTOR, with a significant correlation between p-mTOR expression with smaller (<2 cm) (p=0.021) and lower-grade tumours (p<0.001). Expression of p-mTOR was also associated with longer DFS (HR of 0.32, p<0.001) and OS (HR of 0.20, p<0.001). In a multivariable analysis, the HR remained significant with minimal change (HR=0.26, p=0.002 for OS; HR=0.40, p=0.002 for DFS). In subgroup analysis, luminal p-mTOR-expressing tumours demonstrated longer DFS and OS (HR 0.33, p=0.003; HR 0.20, p=0.003, respectively) independently of size, grade, lymph node status and Her-2 overexpression.
Conclusions p-mTOR expression is associated with smaller, lower-grade and with luminal BC. In multivariable analysis, p-mTOR expression was associated with longer DFS and OS, independently of the size, grade and lymph node status, especially in luminal BCs.
C1 [Beca, Francisco] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Beca, Francisco; Martins, Diana; Schmitt, Fernando] Univ Porto, IPATIMUP Inst Mol Pathol & Immunol, P-4100 Oporto, Portugal.
[Beca, Francisco] Univ Porto, Fac Med, Dept Pathol & Oncol, P-4100 Oporto, Portugal.
[Andre, Rosario] Champalimaud Fdn, Champalimaud Clin Ctr, Lisbon, Portugal.
[Andre, Rosario] Univ Nova Lisboa, Fac Ciencias Med, Dept Genet Oncol & Human Toxicol, P-1200 Lisbon, Portugal.
[Martins, Duarte Saraiva] Ctr Hosp Lisboa Ocidental, Hosp Santa Cruz, Dept Pediat Cardiol, Lisbon, Portugal.
[Bilhim, Tiago] Univ Nova Lisboa, Fac Ciencias Med, Dept Radiol, P-1200 Lisbon, Portugal.
[Bilhim, Tiago] Ctr Hosp Lisboa Cent, Hosp Sao Jose, Lisbon, Portugal.
[Schmitt, Fernando] Univ Toronto, Fac Med, Dept Lab Med & Pathobiol, Toronto, ON, Canada.
[Schmitt, Fernando] Univ Hlth Network, Dept Pathol, Toronto, ON, Canada.
RP Schmitt, F (reprint author), Univ Toronto, Toronto Gen Hosp, Univ Hlth Network, Fac Med,Dept Lab Med & Pathobiol, 200 Elizabeth St,11E-215B, Toronto, ON M5G 2C4, Canada.
EM fernando.schmitt@ipatimup.pt
RI Faculdade de Ciencias Medicas, Nova Medical School/K-6209-2013
OI Beca, Francisco/0000-0002-4409-012X;
FU Portuguese National Funds through Fundacao para a Ciencia e Tecnologia
(FCT) [FCT: HMSP-ICJ/0006/2012]; FCT
FX This work was partially supported by Portuguese National Funds through
Fundacao para a Ciencia e Tecnologia (FCT) regarding project's reference
FCT: HMSP-ICJ/0006/2012 in the framework of Harvard Medical
School-Portugal Program. IPATIMUP is an Associate Laboratory of the
Portuguese Ministry of Science, Technology and Higher Education and is
partially supported by FCT.
NR 26
TC 4
Z9 7
U1 1
U2 2
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0021-9746
EI 1472-4146
J9 J CLIN PATHOL
JI J. Clin. Pathol.
PD NOV
PY 2014
VL 67
IS 11
BP 961
EP 967
DI 10.1136/jclinpath-2014-202320
PG 7
WC Pathology
SC Pathology
GA AS1UP
UT WOS:000344067700006
PM 25053543
ER
PT J
AU Shimizu, T
Takebayashi, T
Sato, Y
Niizeki, H
Aoyama, Y
Kitajima, Y
Iwatsuki, K
Hashimoto, T
Yamagami, J
Werth, VP
Amagai, M
Tanikawa, A
AF Shimizu, Tomoko
Takebayashi, Toru
Sato, Yuji
Niizeki, Hironori
Aoyama, Yumi
Kitajima, Yasuo
Iwatsuki, Keiji
Hashimoto, Takashi
Yamagami, Jun
Werth, Victoria P.
Amagai, Masayuki
Tanikawa, Akiko
TI Grading criteria for disease severity by pemphigus disease area index
SO JOURNAL OF DERMATOLOGY
LA English
DT Article
DE clinical trial; Japanese pemphigus disease severity score; outcome
instrument; pemphigus; pemphigus disease area index; severity index
ID DISORDER INTENSITY SCORE
AB Pemphigus is a group of autoimmune blistering diseases that affect the skin and mucous membranes. A reliable and accurate disease severity tool to assess pemphigus severity is crucial for managing pemphigus and for clinical trials. The purpose of this study was to compare the pemphigus disease area index activity score (PDAI), the Japanese pemphigus disease severity score (JPDSS) and the physician's subjective impression, and also to find appropriate severity grading cut-offs for the PDAI. We also evaluated the correlation between PDAI activity score and the JPDSS. Thirty-seven pemphigus patients and 110 assessments were analyzed in this study. The optimal points of pemphigus disease severity score in PDAI were: mild (0-8), moderate (9-24) and severe (25). In mild or moderate cases, the JPDSS was well correlated with the PDAI, but in severe cases the JPDSS reached a plateau at a PDAI score of approximately 30. The PDAI evaluates disease severity more accurately than the JPDSS, particularly in severe cases. The PDAI is not only a useful tool to measure the extent of cutaneous lesions, but also an excellent scoring system for evaluating pemphigus disease severity.
C1 [Shimizu, Tomoko; Yamagami, Jun; Amagai, Masayuki; Tanikawa, Akiko] Keio Univ, Sch Med, Dept Dermatol, Tokyo 1608582, Japan.
[Takebayashi, Toru] Keio Univ, Sch Med, Dept Prevent Med & Publ Hlth, Tokyo 1608582, Japan.
[Sato, Yuji] Keio Univ, Sch Med, Clin Res Ctr, Tokyo 1608582, Japan.
[Niizeki, Hironori] Natl Ctr Child Hlth & Dev, Dept Dermatol, Tokyo, Japan.
[Niizeki, Hironori] Nara Med Univ, Sch Med, Nara, Japan.
[Aoyama, Yumi; Iwatsuki, Keiji] Okayama Univ Hosp, Okayama, Japan.
[Kitajima, Yasuo] Kizawa Mem Hosp, Gifu, Japan.
[Hashimoto, Takashi] Kurume Univ, Sch Med, Fukuoka, Japan.
[Werth, Victoria P.] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[Werth, Victoria P.] Univ Penn, Philadelphia, PA 19104 USA.
RP Tanikawa, A (reprint author), Keio Univ, Sch Med, Dept Dermatol, Shinjuku Ku, 35 Shinanomachi, Tokyo 1608582, Japan.
EM tanikawa@z3.keio.jp
RI Takebayashi, Toru/K-7526-2013; Amagai, Masayuki/K-5325-2013
OI Takebayashi, Toru/0000-0002-8268-8026; Amagai,
Masayuki/0000-0003-3314-7052
FU Ministry of Health, Labor and Welfare of Japan [H23-028]
FX This work was supported by the Research on Measures for Intractable
Diseases Project: matching fund subsidy (H23-028) from the Ministry of
Health, Labor and Welfare of Japan.
NR 10
TC 4
Z9 4
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0385-2407
EI 1346-8138
J9 J DERMATOL
JI J. Dermatol.
PD NOV
PY 2014
VL 41
IS 11
BP 969
EP 973
DI 10.1111/1346-8138.12649
PG 5
WC Dermatology
SC Dermatology
GA AS5XN
UT WOS:000344340000004
PM 25346300
ER
PT J
AU Hayashi, M
Tanemura, A
Matsuda, K
Hosokawa, K
Izumi, M
Ohara, K
Mihm, MC
Katayama, I
AF Hayashi, Misa
Tanemura, Atsushi
Matsuda, Ken
Hosokawa, Ko
Izumi, Miki
Ohara, Kuniaki
Mihm, Martin C.
Katayama, Ichiro
TI Pigmented epithelioid melanocytoma with lymph node metastasis in a
patient with uncontrolled atopic dermatitis
SO JOURNAL OF DERMATOLOGY
LA English
DT Letter
ID BLUE NEVUS; MELANOMA
C1 [Hayashi, Misa; Tanemura, Atsushi; Katayama, Ichiro] Osaka Univ, Grad Sch Med, Dept Dermatol Integrated Med, Suita, Osaka 5650871, Japan.
[Matsuda, Ken; Hosokawa, Ko] Osaka Univ, Grad Sch Med, Dept Plast Surg, Suita, Osaka 5650871, Japan.
[Izumi, Miki] Tokyo Med Univ, Dept Med Educ, Tokyo 1608402, Japan.
[Ohara, Kuniaki] Toranomon Gen Hosp, Dept Dermatol, Tokyo, Japan.
[Mihm, Martin C.] Massachusetts Gen Hosp, Div Dermatopathol, Boston, MA 02114 USA.
[Mihm, Martin C.] Harvard Univ, Sch Med, Boston, MA USA.
RP Tanemura, A (reprint author), Osaka Univ, Grad Sch Med, Dept Dermatol Integrated Med, 2-2 Yamadaoka, Suita, Osaka 5650871, Japan.
EM tanemura@derma.med.osaka-u.ac.jp
NR 5
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0385-2407
EI 1346-8138
J9 J DERMATOL
JI J. Dermatol.
PD NOV
PY 2014
VL 41
IS 11
BP 1023
EP 1025
DI 10.1111/1346-8138.12631
PG 3
WC Dermatology
SC Dermatology
GA AS5XN
UT WOS:000344340000021
PM 25294720
ER
PT J
AU Mackesy, DZ
Goalstone, ML
AF Mackesy, Daniel Z.
Goalstone, Marc L.
TI Extracellular signal-regulated kinase-5: Novel mediator of insulin and
tumor necrosis factor alpha-stimulated vascular cell adhesion molecule-1
expression in vascular cells
SO JOURNAL OF DIABETES
LA English
DT Article
DE extracellular signal-regulated kinase-5; hyperinsulinemia; tumor
necrosis factor alpha; type-2 diabetes mellitus; vascular cell adhesion
molecule-1
ID ENDOTHELIAL DYSFUNCTION; PROTEIN-KINASE; ERK5; ATHEROSCLEROSIS;
MECHANISM; PATHWAY; MIGRATION; SURVIVAL; GROWTH; TISSUE
AB Background: Atherosclerosis may be stimulated by the increased presence of insulin and tumor necrosis-factor-alpha (TNF alpha) with subsequent expression of vascular cell adhesion molecule-1 (VCAM-1). We hypothesized that extracellular signal-regulated kinase-5 (ERK5) plays an important role in insulin and TNF alpha-stimulated total and cell surface VCAM-1 expression.
Methods: Rat aorta vascular endothelial cells were first transfected with either no inhibitory RNA, inactive (scrambled) inhibitory ERK5 RNA (scERK5) or active inhibitory ERK5 RNA (siERK5) and then treated with either (i) no analog; (ii) insulin (1 nM), or TNF alpha (1 ng/mL) alone, or (iii) insulin plus TNFa for 6 h. Thereafter either total VCAM-1 protein or surface VCAM-1 protein was determined.
Results: Genetic inhibition of ERK5 decreased TNF alpha-stimulated total VCAM-1 expression by 57% and surface expression by 27%. In contrast, genetic inhibition of ERK5 did not significantly decrease insulin-stimulated total or surface VCAM-1 expression. Interestingly, genetic inhibition of ERK5 did not significantly decrease insulin plus TNFa-stimulated total VCAM-1 expression, but significantly (P < 0.05) decreased insulin plus TNFa-stimulated surface VCAM-1 expression 41%.
Conclusions: We report here that ERK5 plays a minor role in insulin-stimulation of VCAM-1, but plays a significant role in TNF alpha-stimulation of both total and cell surface VCAM-1 protein expression. Taken together, these results demonstrate that not only does ERK5 have differential mediation of insulin and TNF alpha-stimulated VCAM-1 expression, but also has differential regulation of insulin plus TNF alpha-stimulated total and surface VCAM-1 expression, suggesting that other intermediates of the insulin and TNF alpha intracellular pathways are contributing to atherogenesis.
C1 [Mackesy, Daniel Z.; Goalstone, Marc L.] Eastern Colorado Hlth Care Syst, Res Dept, Denver, CO USA.
[Goalstone, Marc L.] Univ Colorado, Sch Med, Dept Endocrinol, Denver, CO USA.
RP Goalstone, ML (reprint author), Denver VA Med Ctr, 1055 Clermont St,MS 151, Denver, CO 80220 USA.
EM marc.goalstone@va.gov
FU Research Service of the Department of Veterans Affairs; VA Career
Development Award
FX This work was supported by the Research Service of the Department of
Veterans Affairs (to M.L.G.), in which Dr Goalstone is a recipient of a
VA Career Development Award. We would also like to acknowledge the
assistance of Harsh Pratap (Flow Cytometry technician for the Mucosal
and Vaccine Research Colorado) of the Eastern Colorado Health Care
Service (Denver VAMC).
NR 30
TC 6
Z9 7
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1753-0393
EI 1753-0407
J9 J DIABETES
JI J. Diabetes
PD NOV
PY 2014
VL 6
IS 6
BP 595
EP 602
DI 10.1111/1753-0407.12132
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AS6BS
UT WOS:000344350500016
PM 24460840
ER
PT J
AU Richards, KA
Negron, E
Cohn, JA
Steinberg, Z
Eggener, SE
Shalhav, AL
AF Richards, Kyle A.
Negron, Edris
Cohn, Joshua A.
Steinberg, Zoe
Eggener, Scott E.
Shalhav, Arieh L.
TI The Impact of Body Mass Index on Renal Functional Outcomes Following
Minimally Invasive Partial Nephrectomy
SO JOURNAL OF ENDOUROLOGY
LA English
DT Article
ID LAPAROSCOPIC PARTIAL NEPHRECTOMY; CHRONIC KIDNEY-DISEASE; INTRAABDOMINAL
FAT; OBESITY; CANCER; PREDICTORS; EQUATION
AB Objective: To assess the impact of body mass index (BMI) on perioperative and renal functional outcomes in patients undergoing minimally invasive partial nephrectomy (MIPN).
Materials and Methods: In our IRB-approved, prospectively maintained clinical database, we identified 1206 patients who underwent kidney surgery from 2002 to 2013. Estimated glomerular filtration rate (eGFR) was obtained at baseline and each follow-up visit. From this group, patients who underwent MIPN with more than 12 months of follow-up were selected. Patients were separated into 4 cohorts based on BMI: normal weight (<25kg/m(2)), preobese (25-30kg/m(2)), obese class 1 (30-35kg/m(2)), and obese class >= 2 (>35kg/m(2)). Change in eGFR was compared across demographic and clinical variables through linear and logistic regression models.
Results: A total of 235 patients met inclusion criteria with median follow-up of 29 months (interquartile range [IQR] 19, 45). There were no differences in demographic, perioperative, or pathologic features between BMI groups. While controlling for gender, race, Charlson comorbidity score, tumor size, and ischemia time, obese class 1 (odds ratio [OR] 4.68, p=0.019), obese class >= 2 (OR 4.27, p=0.033), and age (OR 1.06, p=0.014) were associated with increased risk of CKD stage >= 3; however, higher baseline eGFR (OR 0.91, p<0.001) was associated with a reduced risk of CKD stage >= 3. While controlling for the same variables, increasing BMI was associated with a significant absolute reduction in eGFR at 1 year (0.38mL/minute/1.73m(2) reduction in GFR per 1kg/m(2) increase in BMI, p=0.009).
Conclusions: MIPN is technically feasible in obese patients with similar perioperative outcomes to nonobese patients. BMI is an independent risk factor for worsening kidney function following MIPN.
C1 [Richards, Kyle A.; Negron, Edris; Cohn, Joshua A.; Steinberg, Zoe; Eggener, Scott E.; Shalhav, Arieh L.] Univ Chicago, Med Ctr, Dept Surg, Urol Sect, Chicago, IL 60637 USA.
[Richards, Kyle A.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Urol, Madison, WI 53705 USA.
[Richards, Kyle A.] William S Middleton Mem Vet Adm Med Ctr, Dept Surg, Madison, WI USA.
RP Richards, KA (reprint author), Univ Wisconsin, Sch Med & Publ Hlth, Third Floor,1685 Highland Ave, Madison, WI 53705 USA.
EM richardsk@urology.wisc.edu
OI Richards, Kyle/0000-0001-8773-6413; Cohn, Joshua/0000-0002-4953-3321
FU NCATS NIH HHS [UL1 TR000430]
NR 26
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
EI 1557-900X
J9 J ENDOUROL
JI J. Endourol.
PD NOV 1
PY 2014
VL 28
IS 11
BP 1338
EP 1344
DI 10.1089/end.2014.0360
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA AS0PM
UT WOS:000343979900016
PM 24935823
ER
PT J
AU Perissinotto, CM
Covinsky, KE
AF Perissinotto, Carla M.
Covinsky, Kenneth E.
TI Living Alone, Socially Isolated or Lonely-What are We Measuring?
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Editorial Material
DE aging; loneliness; social isolation; geriatrics
ID OLDER-ADULTS; LONELINESS; HEALTH; INTERVENTIONS; VALIDITY; PEOPLE
C1 [Perissinotto, Carla M.; Covinsky, Kenneth E.] Univ Calif San Francisco, Div Geriatr, Dept Med, San Francisco, CA 94143 USA.
[Covinsky, Kenneth E.] San Francisco VA Med Ctr, San Francisco, CA USA.
RP Perissinotto, CM (reprint author), Univ Calif San Francisco, Div Geriatr, Dept Med, 3333 Calif St,Suite 380, San Francisco, CA 94143 USA.
EM carla.perissinotto@ucsf.edu
NR 13
TC 1
Z9 1
U1 2
U2 18
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD NOV
PY 2014
VL 29
IS 11
BP 1429
EP 1431
DI 10.1007/s11606-014-2977-8
PG 3
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA AS1ZC
UT WOS:000344077900003
PM 25092012
ER
PT J
AU Piller, LB
Simpson, LM
Baraniuk, S
Habib, GB
Rahman, M
Basile, JN
Dart, RA
Ellsworth, AJ
Fendley, H
Probstfield, JL
Whelton, PK
Davis, BR
AF Piller, Linda B.
Simpson, Lara M.
Baraniuk, Sarah
Habib, Gabriel B.
Rahman, Mahboob
Basile, Jan N.
Dart, Richard A.
Ellsworth, Allan J.
Fendley, Herbert
Probstfield, Jeffrey L.
Whelton, Paul K.
Davis, Barry R.
CA ALLHAT Collaborative Res Grp
TI Characteristics and Long-Term Follow-Up of Participants with Peripheral
Arterial Disease During ALLHAT
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE cardiovascular disease; hypertension; clinical trials
ID LIPID-LOWERING TREATMENT; HEART-ATTACK TRIAL; NUTRITION EXAMINATION
SURVEY; JOINT NATIONAL COMMITTEE; HIGH BLOOD-PRESSURE; INTERMITTENT
CLAUDICATION; LOWER-EXTREMITY; HYPERTENSION; MANAGEMENT; PREVALENCE
AB Hypertension is a major risk factor for peripheral artery disease (PAD). Little is known about relative efficacy of antihypertensive treatments for preventing PAD.
To compare, by randomized treatment groups, hospitalized or revascularized PAD rates and subsequent morbidity and mortality among participants in the Antihypertensive and Lipid-Lower Treatment to Prevent Heart Attack Trial (ALLHAT).
Randomized, double-blind, active-control trial in high-risk hypertensive participants.
Eight hundred thirty participants with specified secondary outcome of lower extremity PAD events during the randomized phase of ALLHAT.
In-trial PAD events were reported during ALLHAT (1994-2002). Post-trial mortality data through 2006 were obtained from administrative databases. Mean follow-up was 8.8 years.
Baseline characteristics and intermediate outcomes in three treatment groups, using the Kaplan-Meier method to calculate cumulative event rates and post-PAD mortality rates, Cox proportional hazards regression model for hazard ratios and 95 % confidence intervals, and multivariate Cox regression models to examine risk differences among treatment groups.
Following adjustment for baseline characteristics, neither participants assigned to the calcium-channel antagonist amlodipine nor to the ACE-inhibitor lisinopril showed a difference in risk of clinically advanced PAD compared with those in the chlorthalidone arm (HR, 0.86; 95 % CI, 0.72-1.03 and HR, 0.98; 95 % CI, 0.83-1.17, respectively). Of the 830 participants with in-trial PAD events, 63 % died compared to 34 % of those without PAD; there were no significant treatment group differences for subsequent nonfatal myocardial infarction, coronary revascularizations, strokes, heart failure, or mortality.
Neither amlodipine nor lisinopril showed superiority over chlorthalidone in reducing clinically advanced PAD risk. These findings reinforce the compelling need for comparative outcome trials examining treatment of PAD in high-risk hypertensive patients. Once PAD develops, cardiovascular event and mortality risk is high, regardless of type of antihypertensive treatment.
C1 [Piller, Linda B.; Simpson, Lara M.; Baraniuk, Sarah; Davis, Barry R.] Univ Texas Sch Publ Hlth, Houston, TX 77030 USA.
[Habib, Gabriel B.] Michael E DeBakey VA Med Ctr, Houston, TX USA.
[Rahman, Mahboob] Case Western Reserve Univ, Louis Stokes Cleveland VA Med Ctr, Univ Hosp Case Med Ctr, Cleveland, OH 44106 USA.
[Basile, Jan N.] Ralph H Johnson Vet Affairs Med Ctr, Charleston, SC USA.
[Dart, Richard A.] Marshfield Clin Res Fdn, Marshfield, WI USA.
[Ellsworth, Allan J.] Univ Washington, Seattle, WA 98195 USA.
[Fendley, Herbert] AHEC Family Practice Ctr, Pine Bluff, AR USA.
[Probstfield, Jeffrey L.] Univ Washington, Sch Med, Div Cardiol, Seattle, WA USA.
[Whelton, Paul K.] Tulane Univ, Sch Publ Hlth & Trop Med, New Orleans, LA USA.
RP Piller, LB (reprint author), Univ Texas Sch Publ Hlth, 1200 Herman Pressler St,W-906, Houston, TX 77030 USA.
EM Linda.b.piller@uth.tmc.edu
FU National Heart, Lung, and Blood Institute [NO1-HC-35130,
HHSN268201100036C]; Pfizer, Inc.
FX This research was supported by contracts NO1-HC-35130 and
HHSN268201100036C from the National Heart, Lung, and Blood Institute.
The ALLHAT investigators acknowledge contributions of study medications
supplied by Pfizer, Inc. (amlodipine and doxazosin), AstraZeneca
(atenolol and lisinopril), and Bristol-Myers Squibb (pravastatin) and
financial support provided by Pfizer, Inc.
NR 33
TC 4
Z9 5
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD NOV
PY 2014
VL 29
IS 11
BP 1475
EP 1483
DI 10.1007/s11606-014-2947-1
PG 9
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA AS1ZC
UT WOS:000344077900014
PM 25002161
ER
PT J
AU Richter, JM
AF Richter, James M.
TI Capsule Commentary on Tang et al., Evaluation of a Primary Care-Based
Post-Discharge Phone Call Program: Keeping the Primary Care Practice at
the Center of Post-Hospitalization Care Transition
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Editorial Material
C1 [Richter, James M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Richter, James M.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Richter, JM (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
EM jrichter@partners.org
NR 4
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD NOV
PY 2014
VL 29
IS 11
BP 1532
EP 1532
DI 10.1007/s11606-014-2957-z
PG 1
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA AS1ZC
UT WOS:000344077900027
PM 25183472
ER
PT J
AU Jena, AB
Stevens, W
McWilliams, JM
AF Jena, Anupam B.
Stevens, Warren
McWilliams, J. Michael
TI Turning Evidence into Practice Under Payment Reform: The New Frontier of
Translational Science
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE health care reform; health care quality; cost effectiveness
ID PHYSICIANS; CARE
AB Momentum is building to replace the current fee-for-service payment system with value-based reimbursement models that aim to deliver high quality care at lower costs. Although the goals of payment and delivery system reforms to improve quality and reduce costs are clear, the actual path by which provider groups can achieve these goals is not well understood, in large part because the role of identifying and discouraging the use of low-value, high-cost services and encouraging the use of high-value, low-cost services has traditionally fallen to health plans, not provider groups. The shifting focus towards provider accountability for costs and quality promises to expand the role of provider organizations from mainly delivering care to both delivering and prioritizing it based on costs and quality. We discuss how progress on two important but challenging fronts will be needed for provider groups to successfully translate evidence into value. First, robust evidence on the costs and benefits of treatments will need to be developed and made easily accessible to provider groups. Second, provider groups will need to translate that evidence into systems that support cost-effective clinical decisions.
C1 [Jena, Anupam B.; McWilliams, J. Michael] Harvard Univ, Sch Med, Dept Hlth Care Policy, Boston, MA 02115 USA.
[Jena, Anupam B.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Jena, Anupam B.] Natl Bur Econ Res, Cambridge, MA 02138 USA.
[Stevens, Warren] Precis Hlth Econ, Los Angeles, CA USA.
[McWilliams, J. Michael] Brigham & Womens Hosp, Div Gen Internal Med & Primary Care, Boston, MA 02115 USA.
RP Jena, AB (reprint author), Harvard Univ, Sch Med, Dept Hlth Care Policy, 180 Longwood Ave, Boston, MA 02115 USA.
EM jena@hcp.med.harvard.edu
FU Office of the Director, National Institutes of Health (NIH Early
Independence Award) [1DP5OD017897-01]; Doris Duke Charitable Foundation
(Clinical Scientist Development Award) [2010053]; Beeson Career
Development Award Program (National Institute on Aging) [K08 AG038354];
Beeson Career Development Award Program (American Federation for Aging
Research); National Institute on Aging [P01 AG032952]; Abbott
Laboratories
FX Dr. Jena reports receipt of an award from the Office of the Director,
National Institutes of Health (NIH Early Independence Award,
1DP5OD017897-01). Dr. McWilliams is supported by grants from the Doris
Duke Charitable Foundation (Clinical Scientist Development Award
#2010053), Beeson Career Development Award Program (National Institute
on Aging K08 AG038354 and the American Federation for Aging Research),
and National Institute on Aging (P01 AG032952). Support for this
research was provided by Abbott Laboratories.
NR 15
TC 0
Z9 0
U1 2
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
EI 1525-1497
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD NOV
PY 2014
VL 29
IS 11
BP 1542
EP 1545
DI 10.1007/s11606-014-2979-6
PG 4
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA AS1ZC
UT WOS:000344077900030
PM 25092013
ER
PT J
AU Doring, ACD
Hageman, MGJS
Mulder, FJ
Guitton, TG
Ring, D
AF Doering, Anne-Carolin D.
Hageman, Michiel G. J. S.
Mulder, Frans J.
Guitton, Thierry G.
Ring, David
CA Sci Variation Grp
TI Trigger Finger: Assessment of Surgeon and Patient Preferences and
Priorities for Decision Making
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Article
DE Shared decision making; assessment of needs; trigger finger; decision
aids
ID SUPPORT FRAMEWORK; AIDS; INSTRUMENTS; QUALITY; VIEWS
AB Purpose To test the null hypothesis that there are no differences in the priorities and preferences of patients with idiopathic trigger finger (TF) and hand surgeons.
Methods One hundred five hand surgeons of the Science of Variation Group and 84 patients with TF completed a survey about their priorities and preferences in decision making regarding the management of TF. The questionnaire was structured according the Ottawa Decision Support Framework for the development of a decision aid.
Results Patients desired orthotics more and surgery less than physicians. Patients and physicians disagreed on the main advantage of several treatment options for TFs and on disadvantages of the treatment options. Patients preferred to decide for themselves after receiving advice, whereas physicians preferred a shared decision. Patients preferred booklets, and physicians opted for Internet and video decision aids.
Conclusions Comparing patients and hand surgeons, there were some differences in treatment preferences and perceived advantages and disadvantages regarding idiopathic TF differences that might be addressed by a decision aid. Copyright (C) 2014 by the American Society for Surgery of the Hand. All rights reserved.
C1 [Doering, Anne-Carolin D.; Hageman, Michiel G. J. S.; Mulder, Frans J.; Guitton, Thierry G.; Ring, David; Sci Variation Grp] Massachusetts Gen Hosp, Orthopaed Hand & Upper Extrem Serv, Boston, MA 02114 USA.
RP Ring, D (reprint author), Massachusetts Gen Hosp, Yawkey Ctr, Orthopaed Hand Serv, Suite 2100,55 Fruit St, Boston, MA 02114 USA.
EM dring@partners.org
RI Fernandes, C/F-9839-2012;
OI Fernandes, C/0000-0003-0146-6091; Kennedy, Stephen/0000-0001-8177-4988;
Guitton, Thierry/0000-0002-2599-1985; Ring, David/0000-0002-6506-4879;
Bainbridge, Lionel/0000-0001-7987-2845
FU Marti-Keunig Eckhart Stichting; Anna Foundation
FX M.G.H. is supported by Dutch research grants from Marti-Keunig Eckhart
Stichting and Anna Foundation.
NR 23
TC 7
Z9 7
U1 2
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 0363-5023
EI 1531-6564
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD NOV
PY 2014
VL 39
IS 11
BP 2208
EP 2213
DI 10.1016/j.jhsa.2014.08.010
PG 6
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA AS5KU
UT WOS:000344310700010
PM 25283491
ER
PT J
AU Kitay, A
Mudgal, C
AF Kitay, Alison
Mudgal, Chaitanya
TI Volar Carpal Subluxation Following Lunate Facet Fracture
SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME
LA English
DT Editorial Material
ID DISTAL RADIUS FRACTURES; FIXATION
C1 [Kitay, Alison; Mudgal, Chaitanya] Massachusetts Gen Hosp, Dept Hand & Upper Extrem Surg, Boston, MA 02114 USA.
RP Kitay, A (reprint author), Brigham & Womens Hosp, Dept Hand & Upper Extrem Surg, 75 Francis St, Boston, MA 02115 USA.
EM Alison.kitay@gmail.com
NR 9
TC 2
Z9 2
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0363-5023
EI 1531-6564
J9 J HAND SURG-AM
JI J. Hand Surg.-Am. Vol.
PD NOV
PY 2014
VL 39
IS 11
BP 2335
EP 2341
DI 10.1016/j.jhsa.2014.04.027
PG 7
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA AS5KU
UT WOS:000344310700035
PM 24908555
ER
PT J
AU Ring, D
AF Ring, D.
TI The future of hand surgery
SO JOURNAL OF HAND SURGERY-EUROPEAN VOLUME
LA English
DT Editorial Material
ID TUNNEL-SYNDROME
C1 Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Ring, D (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
EM dring@mgh.harvard.edu
NR 13
TC 0
Z9 0
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1753-1934
EI 2043-6289
J9 J HAND SURG-EUR VOL
JI J. Hand Surg.-Eur. Vol.
PD NOV
PY 2014
VL 39
IS 9
BP 1016
EP 1017
DI 10.1177/1753193414535886
PG 2
WC Orthopedics; Surgery
SC Orthopedics; Surgery
GA AS4LM
UT WOS:000344247500022
PM 25336675
ER
PT J
AU Dinter, J
Gourdain, P
Lai, NY
Duong, E
Bracho-Sanchez, E
Rucevic, M
Liebesny, PH
Xu, Y
Shimada, M
Ghebremichael, M
Kavanagh, DG
Le Gall, S
AF Dinter, Jens
Gourdain, Pauline
Lai, Nicole Y.
Ellen Duong
Bracho-Sanchez, Edith
Rucevic, Marijana
Liebesny, Paul H.
Xu, Yang
Shimada, Mariko
Ghebremichael, Musie
Kavanagh, Daniel G.
Le Gall, Sylvie
TI Different Antigen-Processing Activities in Dendritic Cells, Macrophages,
and Monocytes Lead to Uneven Production of HIV Epitopes and Affect CTL
Recognition
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID MHC CLASS-I; CD8(+) T-CELLS; IMMUNODEFICIENCY-VIRUS TYPE-1;
CROSS-PRESENTATION; LEUCINE AMINOPEPTIDASE; IMMUNE ESCAPE; GAG PROTEIN;
ENDOPLASMIC-RETICULUM; THIMET OLIGOPEPTIDASE; PROTEASOME REGULATOR
AB Dendritic cells (DCs), macrophages (MPs), and monocytes are permissive to HIV. Whether they similarly process and present HIV epitopes to HIV-specific CD8 T cells is unknown despite the critical role of peptide processing and presentation for recognition and clearance of infected cells. Cytosolic peptidases degrade endogenous proteins originating from self or pathogens, exogenous Ags preprocessed in endolysosomes, thus shaping the peptidome available for endoplasmic reticulum translocation, trimming, and MHC-I presentation. In this study, we compared the capacity of DCs, MPs, and monocyte cytosolic extracts to produce epitope precursors and epitopes. We showed differences in the proteolytic activities and expression levels of cytosolic proteases between monocyte-derived DCs and MPs and upon maturation with LPS, R848, and CL097, with mature MPs having the highest activities. Using cytosol as a source of proteases to degrade epitope-containing HIV peptides, we showed by mass spectrometry that the degradation patterns of long peptides and the kinetics and amount of antigenic peptides produced differed among DCs, MPs, and monocytes. Additionally, variable intracellular stability of HIV peptides prior to loading onto MHC may accentuate the differences in epitope availability for presentation by MHC-I between these subsets. Differences in peptide degradation led to 2- to 25-fold differences in the CTL responses elicited by the degradation peptides generated in DCs, MPs, and monocytes. Differences in Ag-processing activities between these subsets might lead to variations in the timing and efficiency of recognition of HIV-infected cells by CTLs and contribute to the unequal capacity of HIV-specific CTLs to control viral load.
C1 [Le Gall, Sylvie] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ragon Inst MGH,MIT, Cambridge, MA 02139 USA.
Harvard Univ, Sch Med, Massachusetts Gen Hosp, Cambridge, MA 02139 USA.
RP Le Gall, S (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Ragon Inst MGH,MIT, 400 Technol Sq, Cambridge, MA 02139 USA.
EM sylvie_legall@hms.harvard.edu
FU National Institute of Allergy and Infectious Diseases [AI084753,
AI084106]; Ernst Schering Foundation
FX This work was supported by National Institute of Allergy and Infectious
Diseases Grants AI084753 and AI084106 (to S.L.G.). J.D. is supported in
part by a Ph.D. training fellowship from the Ernst Schering Foundation.
NR 81
TC 7
Z9 7
U1 0
U2 10
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD NOV 1
PY 2014
VL 193
IS 9
BP 4322
EP 4334
DI 10.4049/jimmunol.1400491
PG 13
WC Immunology
SC Immunology
GA AS1ZS
UT WOS:000344079500008
PM 25230751
ER
PT J
AU Collins, E
Gu, F
Qi, MS
Molano, I
Ruiz, P
Sun, LY
Gilkeson, GS
AF Collins, Erin
Gu, Fei
Qi, Maosong
Molano, Ivan
Ruiz, Phillip
Sun, Lingyun
Gilkeson, Gary S.
TI Differential Efficacy of Human Mesenchymal Stem Cells Based on Source of
Origin
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; STROMAL CELLS; MEDIATED IMMUNOSUPPRESSION;
INTERFERON-GAMMA; NITRIC-OXIDE; T-CELLS; TRANSPLANTATION; MICE;
NEPHRITIS; SUPPRESSION
AB Mesenchymal stem cells (MSCs) are useful in tissue repair but also possess immunomodulatory properties. Murine and uncontrolled human trials suggest efficacy of MSCs in treating lupus. Autologous cells are preferable; however, recent studies suggest that lupus-derived MSCs lack efficacy in treating disease. Thus, the optimum derivation of MSCs for use in lupus is unknown. It is also unknown which in vitro assays of MSC function predict in vivo efficacy. The objectives for this study were to provide insight into the optimum source of MSCs and to identify in vitro assays that predict in vivo efficacy. We derived MSCs from four umbilical cords, four healthy bone marrows (BMs), and four lupus BMs. In diseased MRL/lpr mice, MSCs from healthy BM and umbilical cords significantly decreased renal disease, whereas lupus BM MSCs only delayed disease. Current in vitro assays did not differentiate efficacy of the different MSCs. However, differences in MSC efficacy were observed in B cell proliferation assays. Our results suggest that autologous MSCs from lupus patients are not effective in treating disease. Furthermore, standard in vitro assays for MSC licensing are not predictive of in vivo efficacy, whereas inhibiting B cell proliferation appears to differentiate effective MSCs from ineffective MSCs.
C1 [Collins, Erin; Gu, Fei; Qi, Maosong; Molano, Ivan; Gilkeson, Gary S.] Med Univ S Carolina, Dept Med, Div Rheumatol & Immunol, Charleston, SC 29425 USA.
[Gu, Fei; Sun, Lingyun] Nanjing Univ, Affiliated Hosp, Sch Med, Dept Rheumatol & Immunol,Nanjing Drum Tower Hosp, Nanjing 210008, Jiangsu, Peoples R China.
[Ruiz, Phillip] Univ Miami, Sch Med, Dept Pathol, Miami, FL 33136 USA.
[Gilkeson, Gary S.] Ralph H Johnson Vet Affairs Med Ctr, Med Res Serv, Charleston, SC 29403 USA.
RP Collins, E (reprint author), Med Univ S Carolina, Dept Med, 96 Jonathan Lucas St,Suite 912, Charleston, SC 29425 USA.
EM collinel@musc.edu
FU Lupus Foundation; National Institutes of Health [National Center for
Research Resources] [UL1 RR029882]; National Institutes of Health
[National Center for Advancing Translational Sciences] [UL1 TR000062];
Medical Research Service, Ralph H. Johnson Veterans Affairs Medical
Center
FX This work was supported by grants from the Lupus Foundation; the
National Institutes of Health (UL1 RR029882 [National Center for
Research Resources] and UL1 TR000062 [National Center for Advancing
Translational Sciences]); and the Medical Research Service, Ralph H.
Johnson Veterans Affairs Medical Center.
NR 41
TC 6
Z9 8
U1 0
U2 9
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD NOV 1
PY 2014
VL 193
IS 9
BP 4381
EP 4390
DI 10.4049/jimmunol.1401636
PG 10
WC Immunology
SC Immunology
GA AS1ZS
UT WOS:000344079500013
PM 25274529
ER
PT J
AU Wen, ZM
Fan, LY
Li, YH
Zou, Z
Scott, MJ
Xiao, GZ
Li, S
Billiar, TR
Wilson, MA
Shi, XY
Fan, J
AF Wen, Zongmei
Fan, Liyan
Li, Yuehua
Zou, Zui
Scott, Melanie J.
Xiao, Guozhi
Li, Song
Billiar, Timothy R.
Wilson, Mark A.
Shi, Xueyin
Fan, Jie
TI Neutrophils Counteract Autophagy-Mediated Anti-Inflammatory Mechanisms
in Alveolar Macrophage: Role in Posthemorrhagic Shock Acute Lung
Inflammation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID NF-KAPPA-B; TLR2 UP-REGULATION; HEMORRHAGIC-SHOCK; NADPH OXIDASE; NLRP3
INFLAMMASOME; ENDOTHELIAL-CELLS; SIGNALING PATHWAYS; NAD(P)H OXIDASE;
FAMILY-MEMBER; ORGAN INJURY
AB Acute lung injury (ALI) is a major component of multiple organ dysfunction syndrome after hemorrhagic shock (HS) resulting from major surgery and trauma. The increased susceptibility in HS patients to the development of ALI suggests not yet fully elucidated mechanisms that enhance proinflammatory responses and/or suppress anti-inflammatory responses in the lung. Alveolar macrophages (AM phi) are at the center of the pathogenesis of ALI after HS. We have previously reported that HS-activated polymorphonuclear neutrophils (PMNs) interact with macrophages to influence inflammation progress. In this study, we explore a novel function of PMNs regulating AM phi anti-inflammatory mechanisms involving autophagy. Using a mouse "two-hit" model of HS/resuscitation followed by intratracheal injection of muramyl dipeptide, we demonstrate that HS initiates high mobility group box 1/TLR4 signaling, which upregulates NOD2 expression in AM phi and sensitizes them to subsequent NOD2 ligand muramyl dipeptide to augment lung inflammation. In addition, upregulated NOD2 signaling induces autophagy in AM phi, which negatively regulates lung inflammation through feedback suppression of NOD2-RIP2 signaling and inflammasome activation. Importantly, we further demonstrate that HS-activated PMNs that migrate in alveoli counteract the anti-inflammatory effect of autophagy in AM phi, possibly through NAD(P)H oxidase-mediated signaling to enhance I-kappa B kinase gamma phosphorylation, NF-kappa B activation, and nucleotide-binding oligomerization domain protein 3 inflammasome activation, and therefore augment post-HS lung inflammation. These findings explore a previously unidentified complexity in the mechanisms of ALI, which involves cell-cell interaction and receptor cross talk.
C1 [Wen, Zongmei; Zou, Zui; Shi, Xueyin] Second Mil Med Univ, Changzheng Hosp, Dept Anesthesiol, Shanghai 200003, Peoples R China.
[Wen, Zongmei] Tongji Univ, Sch Med, Dept Anesthesiol, Shanghai Pulm Hosp, Shanghai 200433, Peoples R China.
[Wen, Zongmei; Li, Yuehua; Scott, Melanie J.; Billiar, Timothy R.; Wilson, Mark A.; Fan, Jie] Univ Pittsburgh, Sch Med, Dept Surg, Pittsburgh, PA 15213 USA.
[Fan, Liyan] Univ Pittsburgh, Sch Arts & Sci, Dept Biol Sci, Pittsburgh, PA 15213 USA.
[Xiao, Guozhi] Rush Univ, Med Ctr, Dept Biochem, Chicago, IL 60612 USA.
[Li, Song] Univ Pittsburgh, Sch Pharm, Dept Pharmaceut Sci, Ctr Pharmacogenet, Pittsburgh, PA 15261 USA.
[Billiar, Timothy R.; Fan, Jie] Univ Pittsburgh, McGowan Inst Regenerat Med, Pittsburgh, PA 15219 USA.
[Wilson, Mark A.; Fan, Jie] Vet Affairs Pittsburgh Healthcare Syst, Pittsburgh, PA 15240 USA.
RP Fan, J (reprint author), Univ Pittsburgh, Sch Med, Dept Surg, 3500 Terrace St, Pittsburgh, PA 15213 USA.
EM shixueyin1128@163.com; jif7@pitt.edu
FU National Institutes of Health [R01-HL-079669, P50-GM-53789]; U.S.
Department Veterans' Affairs merit award; 12th Five-Year Plan of the
People's Liberation Army Key Project Grant [BWS12J027]; Natural Science
Foundation of China [81372013, 81400052]; Project of Shanghai Leading
Talent; Shanghai Pujiang Program [14PJD030]
FX This work was supported by National Institutes of Health Grants
R01-HL-079669 (to J.F. and M.A.W.) and P50-GM-53789 (to T.R.B. and
J.F.), a U.S. Department Veterans' Affairs merit award (to J.F.), 12th
Five-Year Plan of the People's Liberation Army Key Project Grant
BWS12J027 (to X.S.), Natural Science Foundation of China Grant 81372013
(to X.S.), the Project of Shanghai Leading Talent (to X.S.), Natural
Science Foundation of China Grant 81400052 (to Z.W.), and Shanghai
Pujiang Program 14PJD030 (to Z.W.).
NR 64
TC 10
Z9 10
U1 0
U2 10
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD NOV 1
PY 2014
VL 193
IS 9
BP 4623
EP 4633
DI 10.4049/jimmunol.1400899
PG 11
WC Immunology
SC Immunology
GA AS1ZS
UT WOS:000344079500036
PM 25267975
ER
PT J
AU Alkozei, A
McMahon, E
Lahav, A
AF Alkozei, Anna
McMahon, Erin
Lahav, Amir
TI Stress levels and depressive symptoms in NICU mothers in the early
postpartum period
SO JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
LA English
DT Article
DE Maternal stress; neonatal; preterm
ID INTENSIVE-CARE-UNIT; PRETERM BIRTH; PSYCHOLOGICAL DISTRESS;
POSTNATAL-DEPRESSION; PARENTAL STRESS; MATERNAL STRESS; RISK; INFANTS;
SCALE; DISCHARGE
AB Objective: This study examined whether particular maternal and infant factors can identify mothers at risk for increased stress upon admission to the neonatal intensive care unit (NICU).
Methods: Eighty-five mothers of preterm infants (25-34 weeks gestation) were assessed using the Parental Stressor Scale (PSS: NICU) and the Edinburgh Postnatal Depression Scale (EPDS) within 3.24 +/- 1.58 d postpartum. Hierarchical linear regression models were used to determine the extent to which maternal stress is influenced by individual factors.
Results: Fifty-two percent of mothers experienced increased stress (PSS: NICU score >= 3) and 38% had significant depressive symptoms (EPDS score >= 10). Stress related to alterations in parental role was the most significant source of stress among NICU mothers. Distance from the hospital and married marital status were significant predictors for stress related to alterations in parental role (p = 0.003) and NICU sights and sounds (p = 0.01), respectively. Higher stress levels were associated with higher depressive scores (p = 0.001). Maternal mental health factors, demographic factors, pregnancy factors and infant characteristics were not associated with increased stress.
Conclusion: Elevated stress levels and depressive symptoms are already present in mothers of preterm infants upon NICU admission. Being married or living long distance from the hospital is associated with higher stress. Future work is needed to develop effective interventions for alleviating stress in NICU mothers and preventing its potential development into postnatal depression.
C1 [Alkozei, Anna; McMahon, Erin; Lahav, Amir] Harvard Univ, Brigham & Womens Hosp, Dept Pediat & Newborn Med, Sch Med, Boston, MA 02115 USA.
[Lahav, Amir] MassGen Hosp Children, Dept Pediat, Boston, MA USA.
RP Lahav, A (reprint author), Brigham & Womens Hosp, Dept Pediat & Newborn Med, 75 Francis St, Boston, MA 02115 USA.
EM amir_lahav@hms.harvard.edu
FU Charles H. Hood Foundation; Peter and Elizabeth C. Tower Foundation;
Jackson L. Graves Foundation; Little Giraffe Foundation; Nexxspan
Healthcare
FX This work was supported, in part, by the Charles H. Hood Foundation,
Peter and Elizabeth C. Tower Foundation, Jackson L. Graves Foundation,
Little Giraffe Foundation and Nexxspan Healthcare.
NR 31
TC 8
Z9 8
U1 3
U2 17
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1476-7058
EI 1476-4954
J9 J MATERN-FETAL NEO M
JI J. Matern.-Fetal Neonatal Med.
PD NOV
PY 2014
VL 27
IS 17
BP 1738
EP 1743
DI 10.3109/14767058.2014.942626
PG 6
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA AS2AE
UT WOS:000344080600004
PM 25005861
ER
PT J
AU Rajakesari, S
Arvold, ND
Jimenez, RB
Christianson, LW
Horvath, MC
Claus, EB
Golby, AJ
Johnson, MD
Dunn, IF
Lee, EQ
Lin, NU
Friesen, S
Mannarino, EG
Wagar, M
Hacker, FL
Weiss, SE
Alexander, BM
AF Rajakesari, Selvan
Arvold, Nils D.
Jimenez, Rachel B.
Christianson, Laura W.
Horvath, Margaret C.
Claus, Elizabeth B.
Golby, Alexandra J.
Johnson, Mark D.
Dunn, Ian F.
Lee, Eudocia Q.
Lin, Nancy U.
Friesen, Scott
Mannarino, Edward G.
Wagar, Matthew
Hacker, Fred L.
Weiss, Stephanie E.
Alexander, Brian M.
TI Local control after fractionated stereotactic radiation therapy for
brain metastases
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Article; Proceedings Paper
CT 55th Annual Meeting of the American-Society-for-Radiation-Oncology
CY SEP 22-25, 2013
CL Atlanta, GA
SP Amer Soc Radiat Oncol
DE Brain metastases; Stereotactic radiosurgery; Stereotactic radiotherapy;
Hypofractionated
ID GAMMA-KNIFE RADIOSURGERY; STEM METASTASES; CEREBRAL METASTASES; SURGICAL
RESECTION; CLINICAL ARTICLE; RADIOTHERAPY; CANCER; TRIAL; TOXICITY;
IRRADIATION
AB Stereotactic radiosurgery (SRS) is frequently used in the management of brain metastases, but concerns over potential toxicity limit applications for larger lesions or those in eloquent areas. Fractionated stereotactic radiation therapy (SRT) is often substituted for SRS in these cases. We retrospectively analyzed the efficacy and toxicity outcomes of patients who received SRT at our institution. Seventy patients with brain metastases treated with SRT from 2006-2012 were analyzed. The rates of local and distant intracranial progression, overall survival, acute toxicity, and radionecrosis were determined. The SRT regimen was 25 Gy in 5 fractions among 87 % of patients. The most common tumor histologies were non-small cell lung cancer (37 %), breast cancer (20 %) and melanoma (20 %), and the median tumor diameter was 1.7 cm (range 0.4-6.4 cm). Median survival after SRT was 10.7 months. Median time to local progression was 17 months, with a local control rate of 68 % at 6 months and 56 % at 1 year. Acute toxicity was seen in 11 patients (16 %), mostly grade 1 or 2 with the most common symptom being mild headache. Symptomatic radiation-induced treatment change was seen on follow-up MRIs in three patients (4.3 %). SRT appears to be a safe and reasonably effective technique to treat brain metastases deemed less suitable for SRS, though dose intensification strategies may further improve local control.
C1 [Rajakesari, Selvan; Arvold, Nils D.; Christianson, Laura W.; Horvath, Margaret C.; Friesen, Scott; Mannarino, Edward G.; Wagar, Matthew; Hacker, Fred L.; Alexander, Brian M.] Harvard Univ, Sch Med, Dept Radiat Oncol, Dana Farber Brigham & Womens Canc Ctr, Boston, MA 02163 USA.
[Jimenez, Rachel B.] Harvard Radiat Oncol Program, Boston, MA USA.
[Claus, Elizabeth B.; Golby, Alexandra J.; Johnson, Mark D.; Dunn, Ian F.] Harvard Univ, Sch Med, Dept Neurosurg, Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Claus, Elizabeth B.] Yale Univ, Sch Publ Hlth, New Haven, CT USA.
[Lee, Eudocia Q.] Harvard Univ, Sch Med, Ctr Neurooncol, Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Lin, Nancy U.] Harvard Univ, Sch Med, Dept Med, Dana Farber Brigham & Womens Canc Ctr, Boston, MA USA.
[Weiss, Stephanie E.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
RP Alexander, BM (reprint author), Harvard Univ, Sch Med, Dept Radiat Oncol, Dana Farber Brigham & Womens Canc Ctr, Boston, MA 02163 USA.
EM bmalexander@lroc.harvard.edu
NR 42
TC 8
Z9 8
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
EI 1573-7373
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD NOV
PY 2014
VL 120
IS 2
BP 339
EP 346
DI 10.1007/s11060-014-1556-5
PG 8
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA AS3JD
UT WOS:000344172600013
PM 25059451
ER
PT J
AU D'Ambrosio, AL
Barker, FG
AF D'Ambrosio, Anthony L.
Barker, Fred G., II
TI AANS/CNS Section on Tumors (vol 119, pg 449, 2014)
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Correction
C1 [D'Ambrosio, Anthony L.] Neurosurg New Jersey, Ridgewood, NJ 07450 USA.
[Barker, Fred G., II] Massachusetts Gen Hosp, Neurosurg Serv, Boston, MA 02114 USA.
[Barker, Fred G., II] Harvard Univ, Sch Med, Dept Surg Neurosurg, Boston, MA USA.
RP D'Ambrosio, AL (reprint author), Neurosurg New Jersey, 1200 East Ridgewood Ave, Ridgewood, NJ 07450 USA.
EM dambrosio@neurosurgerynj.com; barker@helix.mgh.harvard.edu
NR 1
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
EI 1573-7373
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD NOV
PY 2014
VL 120
IS 2
BP 449
EP 449
DI 10.1007/s11060-014-1615-y
PG 1
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA AS3JD
UT WOS:000344172600026
ER
PT J
AU Donovan, WD
Leslie-Mazwi, TM
Silva, E
Woo, HH
Nicola, GN
Barr, RM
Bello, JA
Tu, R
Hirsch, JA
AF Donovan, William D.
Leslie-Mazwi, Thabele M.
Silva, Ezequiel, III
Woo, Henry H.
Nicola, Gregory N.
Barr, Robert M.
Bello, Jacqueline A.
Tu, Raymond
Hirsch, Joshua A.
TI Diagnostic carotid and cerebral angiography: a historical summary of the
evolving changes in coding and reimbursement in a complex procedure
family
SO JOURNAL OF NEUROINTERVENTIONAL SURGERY
LA English
DT Review
ID RUC
AB Carotid and cerebral angiography have been a mainstay of neurointerventional and neuroradiologic practice for years. Centers for Medicare and Medicaid Services (CMS) and Relative Value Scale Update Committee (RUC) initiatives have compelled the professional societies to bundle component codes under threat of unilateral CMS revision and revaluation. Code bundling usually results in a decrease in the professional Relative Value Unit (RVU) valuation, and thus the MD reimbursement. The year 2013 saw a dramatic revision to the Current Procedural Terminology (CPT) code set that defines carotid and cerebral procedures. This paper reviews the process that led to that code set being revised and estimates the impact on professional reimbursement. We show the current and previous carotid angiography CPT codes and use clinical examples to assess professional RVU valuation before and after code revision.
C1 [Donovan, William D.] William W Backus Hosp, Norwich, CT USA.
[Leslie-Mazwi, Thabele M.; Hirsch, Joshua A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neuroendovasc Program, Boston, MA 02114 USA.
[Silva, Ezequiel, III] Univ Texas Hlth Sci Ctr San Antonio, Dept Radiol, South Texas Radiol Grp, San Antonio, TX 78229 USA.
[Woo, Henry H.] SUNY Stony Brook, Med Ctr, Cerebrovasc Ctr, Dept Neurol Surg & Radiol, Stony Brook, NY 11794 USA.
[Nicola, Gregory N.] Hackensack Univ, Med Ctr, Dept Radiol, Hackensack, NJ USA.
[Barr, Robert M.] Mecklenburg Radiol Associates PA, Charlotte, NC USA.
[Bello, Jacqueline A.] Montefiore Med Ctr, Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Tu, Raymond] George Washington Univ, Dept Progress Radiol, Falls Church, VA USA.
RP Hirsch, JA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neuroendovasc Program, Boston, MA 02114 USA.
EM hirsch@snisonline.org
NR 6
TC 7
Z9 7
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1759-8478
EI 1759-8486
J9 J NEUROINTERV SURG
JI J. NeuroInterventional Surg.
PD NOV
PY 2014
VL 6
IS 9
BP 712
EP 717
DI 10.1136/neurintsurg-2014-011416
PG 6
WC Neuroimaging; Surgery
SC Neurosciences & Neurology; Surgery
GA AS2HJ
UT WOS:000344100200020
PM 25179635
ER
PT J
AU Hirsch, JA
Barr, RM
McGinty, G
Nicola, GN
Schaefer, PW
Silva, E
Manchikanti, L
AF Hirsch, Joshua A.
Barr, Robert M.
McGinty, Geraldine
Nicola, Gregory N.
Schaefer, Pamela W.
Silva, Ezequiel, III
Manchikanti, Laxmaiah
TI Affordable care 2014: a tale of two boards
SO JOURNAL OF NEUROINTERVENTIONAL SURGERY
LA English
DT Review
ID OUTCOMES RESEARCH-INSTITUTE; EVOLUTION; IMPACT; ACT
AB The Patient Protection and Affordable Care Act (ACA) became law on 23 March 2010. As part of the law, two independent boards were established. The Patient-Centered Outcomes Research Institute embodies national aspirations for employing comparative effectiveness research in healthcare decision-making, and the Independent Payment Advisory Board is focused on the need for a group of impartial experts to establish anticipatable growth rates for Medicare. Approximately 4 years after the bill was passed into law, these independent boards are at very different points in their life cycles. This article provides a status update.
C1 [Hirsch, Joshua A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neuroendovasc Program, Boston, MA 02114 USA.
[Barr, Robert M.] Mecklenburg Radiol Associates PA, Charlotte, NC USA.
[McGinty, Geraldine] Weill Cornell Med Coll, Dept Radiol, New York, NY USA.
[Nicola, Gregory N.] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
[Schaefer, Pamela W.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA.
[Silva, Ezequiel, III] Univ Texas Hlth Sci Ctr San Antonio, South Texas Radiol Grp, San Antonio, TX 78229 USA.
[Silva, Ezequiel, III] South Texas Radiol Grp, San Antonio, TX USA.
[Silva, Ezequiel, III] Univ Texas Hlth Sci Ctr San Antonio, Dept Radiol, San Antonio, TX 78229 USA.
[Manchikanti, Laxmaiah] Pain Management Ctr Paducah, Paducah, KY USA.
[Manchikanti, Laxmaiah] Univ Louisville, Dept Anesthesiol & Perioperat Med, Louisville, KY 40292 USA.
RP Hirsch, JA (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neuroendovasc Program, Boston, MA 02114 USA.
EM Hirsch@snisonline.org
OI McGinty, Geraldine/0000-0001-6111-2514
NR 12
TC 3
Z9 3
U1 0
U2 2
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1759-8478
EI 1759-8486
J9 J NEUROINTERV SURG
JI J. NeuroInterventional Surg.
PD NOV
PY 2014
VL 6
IS 9
BP 718
EP 720
DI 10.1136/neurintsurg-2014-011322
PG 3
WC Neuroimaging; Surgery
SC Neurosciences & Neurology; Surgery
GA AS2HJ
UT WOS:000344100200021
PM 24962452
ER
PT J
AU Izquierdo-Garcia, D
Hansen, AE
Forster, S
Benoit, D
Schachoff, S
Furst, S
Chen, KT
Chonde, DB
Catana, C
AF Izquierdo-Garcia, David
Hansen, Adam E.
Foerster, Stefan
Benoit, Didier
Schachoff, Sylvia
Fuerst, Sebastian
Chen, Kevin T.
Chonde, Daniel B.
Catana, Ciprian
TI An SPM8-Based Approach for Attenuation Correction Combining Segmentation
and Nonrigid Template Formation: Application to Simultaneous PET/MR
Brain Imaging
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE integrated PET/MRI; attenuation correction; segmentation; template
ID ULTRASHORT ECHO TIME; OF-FLIGHT PET; CT IMAGES; MR; REGISTRATION;
RECONSTRUCTION; SEQUENCES; EMISSION; SCANNER; ATLAS
AB We present an approach for head MR-based attenuation correction (AC) based on the Statistical Parametric Mapping 8 (SPM8) software, which combines segmentation- and atlas-based features to provide a robust technique to generate attenuation maps (mu maps) from MR data in integrated PET/MR scanners. Methods: Coregistered anatomic MR and CT images of 15 glioblastoma subjects were used to generate the templates. The MR images from these subjects were first segmented into 6 tissue classes (gray matter, white matter, cerebrospinal fluid, bone, soft tissue, and air), which were then nonrigidly coregistered using a diffeomorphic approach. A similar procedure was used to coregister the anatomic MR data for a new subject to the template. Finally, the CT-like images obtained by applying the inverse transformations were converted to linear attenuation coefficients to be used for AC of PET data. The method was validated on 16 new subjects with brain tumors (n = 12) or mild cognitive impairment (n = 4) who underwent CT and PET/MR scans. The p maps and corresponding reconstructed PET images were compared with those obtained using the gold standard CT-based approach and the Dixon-based method available on the Biograph mMR scanner. Relative change (RC) images were generated in each case, and voxel- and regionof-interest based analyses were performed. Results: The leave-one-out cross-validation analysis of the data from the 15 atlas-generation subjects showed small errors in brain linear attenuation coefficients (RC, 1.38% +/- 4.52%) compared with the gold standard. Similar results (RC, 1.86% +/- 4.06%) were obtained from the analysis of the atlas-validation datasets. The voxel- and region-of-interest based analysis of the corresponding reconstructed PET images revealed quantification errors of 3.87% +/- 5.0% and 2.74% +/- 2.28%, respectively. The Dixon-based method performed substantially worse (the mean RC values were 13.0% +/- 10.25% and 9.38% +/- 4.97%, respectively). Areas closer to the skull showed the largest improvement. Conclusion: We have presented an SPM8-based approach for deriving the head p map from MR data to be used for PET AC in integrated PET/MR scanners. Its implementation is straightforward and requires only the morphologic data acquired with a single MR sequence. The method is accurate and robust, combining the strengths of both segmentation- and atlas-based approaches while minimizing their drawbacks.
C1 [Izquierdo-Garcia, David; Chen, Kevin T.; Chonde, Daniel B.; Catana, Ciprian] Massachusetts Gen Hosp, Dept Radiol, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA USA.
[Izquierdo-Garcia, David; Chen, Kevin T.; Chonde, Daniel B.; Catana, Ciprian] Harvard Univ, Sch Med, Charlestown, MA USA.
[Hansen, Adam E.; Benoit, Didier] Copenhagen Univ Hosp, Dept Clin Physiol Nucl Med & PET, Rigshosp, Copenhagen, Denmark.
[Foerster, Stefan; Schachoff, Sylvia; Fuerst, Sebastian] Tech Univ Munich, Dept Nucl Med, D-80290 Munich, Germany.
[Chen, Kevin T.; Chonde, Daniel B.] MIT, Dept Hlth Sci & Technol, Cambridge, MA 02139 USA.
[Chonde, Daniel B.] Harvard Univ, Program Biophys, Cambridge, MA 02138 USA.
RP Catana, C (reprint author), Athinoula A Martinos Ctr Biomed Imaging, 149,13th St,Room 1116, Charlestown, MA 02129 USA.
EM ccatana@nmr.mgh.harvard.edu
RI Hansen, Adam/G-7735-2011
FU NIH [R01CA137254, 1R01EB014894]
FX The costs of publication of this article were defrayed in part by the
payment of page charges. Therefore, and solely to indicate this fact,
this article is hereby marked "advertisement" in accordance with 18 USC
section 1734. Funding for this work was provided by NIH grants
R01CA137254 and 1R01EB014894. No other potential conflict of interest
relevant to this article was reported.
NR 31
TC 36
Z9 36
U1 0
U2 14
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD NOV
PY 2014
VL 55
IS 11
BP 1825
EP 1830
DI 10.2967/jnumed.113.136341
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AS3XT
UT WOS:000344209200013
PM 25278515
ER
PT J
AU de Prost, N
Feng, Y
Wellman, T
Tucci, MR
Costa, EL
Musch, G
Winkler, T
Harris, RS
Venegas, JG
Chao, W
Melo, MFV
AF de Prost, Nicolas
Feng, Yan
Wellman, Tyler
Tucci, Mauro R.
Costa, Eduardo L.
Musch, Guido
Winkler, Tilo
Harris, R. Scott
Venegas, Jose G.
Chao, Wei
Melo, Marcos F. Vidal
TI F-18-FDG Kinetics Parameters Depend on the Mechanism of Injury in Early
Experimental Acute Respiratory Distress Syndrome
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE respiratory distress syndrome; adult; endotoxemia; pulmonary edema;
positron emission tomography; fluorodeoxyglucose F18
ID INDUCED LUNG INJURY; REGIONAL VENTILATION; METABOLIC-ACTIVITY; PET;
INFLAMMATION; ENDOTOXIN; SHEEP; RABBITS; MODEL
AB PET with F-18-FDG allows for noninvasive assessment of regional lung metabolism reflective of neutrophilic inflammation. This study aimed at determining during early acute lung injury whether local F-18-FDG phosphorylation rate and volume of distribution were sensitive to the initial regional inflammatory response and whether they depended on the mechanism of injury: endotoxemia and surfactant depletion. Methods: Twelve sheep underwent homogeneous unilateral surfactant depletion (alveolar lavage) and were mechanically ventilated for 4 h (positive end-expiratory pressure, 10 cm H2O; plateau pressure, 30 cm H2O) while receiving intravenous endotoxin (lipopolysaccharide-positive [LPS+] group; n = 6) or not (lipopolysaccharide-negative group; n = 6). F-18-FDG PET emission scans were then acquired. F-18-FDG phosphorylation rate and distribution volume were calculated with a 4-compartment model. Lung tissue expression of inflammatory cytokines was measured using real-time quantitative reverse transcription polymerase chain reaction. Results: F-18-FDG uptake increased in LPS+ (P = 0.012) and in surfactant-depleted sheep (P < 0.001). These increases were topographically heterogeneous, predominantly in dependent lung regions, and without interaction between alveolar lavage and LPS. The increase of F-18-FDG uptake in the LPS+ group was related both to increases in the F-18-FDG phosphorylation rate (P < 0.05) and to distribution volume (P < 0.01). F-18-FDG distribution volume increased with infiltrating neutrophils (P < 0.001) and phosphorylation rate with the regional expression of IL-1 beta (P = 0.026), IL-8 (P = 0.011), and IL-10 (P = 0.023). Conclusion: Noninvasive F-18-FDG PET-derived parameters represent histologic and gene expression markers of early lung injury. Pulmonary metabolism assessed with F-18-FDG PET depends on the mechanism of injury and appears to be additive for endotoxemia and surfactant depletion. F-18-FDG PET may be a valuable imaging biomarker of early lung injury.
C1 [de Prost, Nicolas; Feng, Yan; Wellman, Tyler; Tucci, Mauro R.; Costa, Eduardo L.; Musch, Guido; Winkler, Tilo; Venegas, Jose G.; Chao, Wei; Melo, Marcos F. Vidal] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia Crit Care & Pain Med, Boston, MA USA.
[de Prost, Nicolas] Hop Henri Mondor, AP HP, Med Intens Care Unit, F-94010 Creteil, France.
[Wellman, Tyler] Boston Univ, Dept Biomed Engn, Boston, MA 02215 USA.
[Tucci, Mauro R.; Costa, Eduardo L.] Univ Sao Paulo, Heart Inst Incor, Cardiopulm Dept, Div Pulm, Sao Paulo, Brazil.
[Harris, R. Scott] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Med,Pulm & Crit Care Unit, Boston, MA USA.
RP de Prost, N (reprint author), Hop Henri Mondor, AP HP, Serv Reanimat Med, F-94010 Creteil, France.
EM nicolas.de-prost@hmn.aphp.fr
RI Winkler, Tilo/B-5337-2009;
OI Winkler, Tilo/0000-0002-7276-5550; de Prost, Nicolas/0000-0002-4833-4320
FU NIH [HL 5R01HL086827, 1R01HL121228]; [5R01HL094639]
FX The costs of publication of this article were defrayed in part by the
payment of page charges. Therefore, and solely to indicate this fact,
this article is hereby marked "advertisement" in accordance with 18 USC
section 1734. This work was supported by NIH grant HL 5R01HL086827 and
1R01HL121228. GM was supported by 5R01HL094639. No other potential
conflict of interest relevant to this article was reported.
NR 28
TC 8
Z9 8
U1 1
U2 3
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD NOV
PY 2014
VL 55
IS 11
BP 1871
EP 1877
DI 10.2967/jnumed.114.140962
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AS3XT
UT WOS:000344209200019
PM 25286924
ER
PT J
AU Way, D
Smucker, WD
AF Way, Deborah
Smucker, William D.
TI A Reflection on "Death as Harm"
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Letter
ID CARE
C1 [Way, Deborah] Philadelphia Vet Affairs Med Ctr, Palliat Care Serv, Philadelphia, PA USA.
[Smucker, William D.] Summa Hlth Syst, Family Med Ctr Akron, Akron, OH 44304 USA.
RP Smucker, WD (reprint author), Summa Hlth Syst, Family Med Ctr Akron, Akron, OH 44304 USA.
EM Smuckerw@summahealth.org
NR 3
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 1096-6218
EI 1557-7740
J9 J PALLIAT MED
JI J. Palliat. Med.
PD NOV 1
PY 2014
VL 17
IS 11
BP 1196
EP 1196
DI 10.1089/jpm.2014.0289
PG 1
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA AS9XX
UT WOS:000344592800002
PM 25302418
ER
PT J
AU Moghanaki, D
Cheuk, AV
Fosmire, H
Anscher, MS
Lutz, ST
Hagan, MP
Dawson, GA
AF Moghanaki, Drew
Cheuk, Alice V.
Fosmire, Helen
Anscher, Mitchell S.
Lutz, Stephen T.
Hagan, Michael P.
Dawson, George A.
CA US Vet Healthcare Adm Natl
TI Availability of Single-Fraction Palliative Radiotherapy for Cancer
Patients Receiving End-of-Life Care within the Veterans Healthcare
Administration
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Article
ID BONE METASTASES; HOSPICE; DELIVERY; ONCOLOGY; SYSTEM
AB Background: Surveys demonstrate <20% of radiation oncologists in the United States offer single-fraction palliative radiotherapy (RT) even though it is an acceptable standard of care. A study was conducted to investigate whether this held true for those practicing within the Veterans Healthcare Administration (VHA).
Methods: All radiation oncologists currently practicing at VHA medical centers were surveyed. Comparisons and associations of responses were evaluated by Fisher's exact test.
Results: The response rate was 90%. Half were full-time employees of the VHA, and the majority (70%) had thoroughly read guidelines on palliative RT for bone metastases recently published by either the American College of Radiology (ACR, 2009, 2012) or the American Society of Radiation Oncology (ASTRO, 2011). Single-fraction palliative RT for bone metastases had been prescribed by 76% of respondents, and 93% had prescribed a short course of <= 6 fractions. Respondents were less likely to have prescribed a single fraction for patients who had survival estimates of either >6 months or >12 months (66% versus 37%, p<0.0001).Those not offering single-fraction palliative RT (24%) were more likely to be >10 years out of training (37% versus 10%, p=0.01), and to have worked in a private practice setting at some point in their career (36% versus 12%, p=0.03).
Conclusions: A majority of radiation oncologists within the VHA offer single-fraction therapy to their patients. These data ensure access to palliative RT is not limited within this health care system by a preference for prolonged treatment courses that may discourage patients and clinicians from seeking this care.
C1 [Moghanaki, Drew] Hunter Holmes McGuire Vet Affairs Med Ctr, Richmond, VA 23249 USA.
[Moghanaki, Drew; Anscher, Mitchell S.; Hagan, Michael P.] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA USA.
[Cheuk, Alice V.; Dawson, George A.] James J Peters Vet Affairs Med Ctr, New York, NY USA.
[Cheuk, Alice V.; Dawson, George A.] Icahn Sch Med Mt Sinai, New York, NY 10029 USA.
[Fosmire, Helen] Richard L Roudebush Vet Affairs Med Ctr, Indianapolis, IN 46202 USA.
[Lutz, Stephen T.] Blanchard Valley Reg Hlth Ctr, Findlay, OH USA.
[Hagan, Michael P.] US Dept Vet Affairs, Natl Radiat Oncol Program, Richmond, VA USA.
[Dawson, George A.] Vet Affairs New Jersey Healthcare Syst, E Orange, NJ USA.
RP Moghanaki, D (reprint author), Hunter Holmes McGuire Vet Affairs Med Ctr, Dept Radiat Oncol, 1201 Broad Rock Blvd, Richmond, VA 23249 USA.
EM drew.moghanaki@va.gov
OI Anscher, Mitchell/0000-0003-4480-111X
NR 22
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 1096-6218
EI 1557-7740
J9 J PALLIAT MED
JI J. Palliat. Med.
PD NOV 1
PY 2014
VL 17
IS 11
BP 1221
EP 1225
DI 10.1089/jpm.2014.0041
PG 5
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA AS9XX
UT WOS:000344592800008
PM 25188468
ER
PT J
AU Back, AL
Park, ER
Greer, JA
Jackson, VA
Jacobsen, JC
Gallagher, ER
Temel, JS
AF Back, Anthony L.
Park, Elyse R.
Greer, Joseph A.
Jackson, Vicki A.
Jacobsen, Juliet C.
Gallagher, Emily R.
Temel, Jennifer S.
TI Clinician Roles in Early Integrated Palliative Care for Patients with
Advanced Cancer: A Qualitative Study
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Article
ID CELL LUNG-CANCER; CONSULT SERVICE; ONCOLOGY; OUTCOMES
AB Background: Early palliative care provides better quality of life, increased prognostic awareness, and even improved survival for patients with advanced cancer but how the integrated care model achieves these outcomes has not been completely explained.
Methods: To better understand the clinical approach to early outpatient care from the clinicians' perspective, we conducted focus groups with the palliative care clinicians who had participated in a randomized trial of early palliative care for metastatic lung cancer.
Results: Clinicians described their role in providing early palliative care as having three distinct roles in the outpatient setting: (1) managing symptoms to improve functional status and as a bridge to other issues; (2) engaging patients in emotional work to facilitate coping, accepting, and planning; and (3) interpreting the oncologist for the patient and the patient for the oncologist.
Conclusions: These data lay the foundation for developing training programs for clinicians in early integrated palliative care.
C1 [Back, Anthony L.] Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
[Park, Elyse R.; Greer, Joseph A.; Jackson, Vicki A.; Jacobsen, Juliet C.; Gallagher, Emily R.; Temel, Jennifer S.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
RP Back, AL (reprint author), Seattle Canc Care Alliance, 825 Eastlake Ave E, Seattle, WA 98102 USA.
EM tonyback@uw.edu
FU National Institutes of Nursing Research [R01NR012735]
FX Funding received from the National Institutes of Nursing Research
R01NR012735.
NR 17
TC 12
Z9 12
U1 1
U2 11
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-6218
EI 1557-7740
J9 J PALLIAT MED
JI J. Palliat. Med.
PD NOV 1
PY 2014
VL 17
IS 11
BP 1244
EP 1248
DI 10.1089/jpm.2014.0146
PG 5
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA AS9XX
UT WOS:000344592800012
PM 25390467
ER
PT J
AU Potosek, J
Curry, M
Buss, M
Chittenden, E
AF Potosek, Jamie
Curry, Michael
Buss, Mary
Chittenden, Eva
TI Integration of Palliative Care in End-Stage Liver Disease and Liver
Transplantation
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Review
ID QUALITY-OF-LIFE; ADVANCED HEART-FAILURE; UNITED-STATES;
HEPATIC-ENCEPHALOPATHY; DOSAGE ADJUSTMENT; ADVANCED LUNG; WAITING-LIST;
CIRRHOSIS; HOSPICE; SURVIVAL
AB Background: Patients with end-stage liver disease (ESLD) have a life-limiting illness that causes multiple distressing symptoms and negatively affects quality of life (QOL). This population traditionally has not had much attention within the palliative care community.
Discussion: This article provides an evidence-based review of palliative care issues that patients with ESLD and those awaiting liver transplant face, including approaches to prognosis, symptom management, advance care planning, and end-of-life care.
Conclusion: Tremendous opportunity exists to integrate palliative medicine into the care of these patients.
C1 [Potosek, Jamie] Providence Reg Canc Ctr, Dept Hematol Oncol, Lacey, WA USA.
[Buss, Mary] Beth Israel Deaconess Med Ctr, Dept Hematol Oncol, Boston, MA 02215 USA.
[Curry, Michael] Beth Israel Deaconess Med Ctr, Dept Gastroenterol, Boston, MA 02215 USA.
[Chittenden, Eva] Massachusetts Gen Hosp, Dept Med, Div Palliat Care, Boston, MA 02114 USA.
RP Potosek, J (reprint author), Providence Reg Canc Ctr Syst Lacey, Dept Hematol Oncol, 4525 Third Ave SE,Suite 200, Lacey, WA 98503 USA.
EM jamie.potosek@providence.org
NR 72
TC 5
Z9 5
U1 0
U2 2
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-6218
EI 1557-7740
J9 J PALLIAT MED
JI J. Palliat. Med.
PD NOV 1
PY 2014
VL 17
IS 11
BP 1271
EP 1277
DI 10.1089/jpm.2013.0167
PG 7
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA AS9XX
UT WOS:000344592800017
PM 25390468
ER
PT J
AU Lakdawalla, DN
Mascarenhas, M
Jena, AB
Vanderpuye-Orgle, J
LaVallee, C
Linthicum, MT
Snider, JT
AF Lakdawalla, Darius N.
Mascarenhas, Maria
Jena, Anupam B.
Vanderpuye-Orgle, Jacqueline
LaVallee, Chris
Linthicum, Mark T.
Snider, Julia Thornton
TI Impact of Oral Nutrition Supplements on Hospital Outcomes in Pediatric
Patients
SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION
LA English
DT Article
DE pediatrics; life cycle; CAM; outcomes research; quality; nutrition
support practice
ID RANDOMIZED CONTROLLED-TRIAL; CONGENITAL HEART-DISEASE;
PLACEBO-CONTROLLED TRIAL; LENGTH-OF-STAY; INSTRUMENTAL VARIABLES;
CYSTIC-FIBROSIS; 3-MONTH INTERVENTION; PARENTERAL-NUTRITION; ACUTE
ILLNESS; MALNUTRITION
AB Background: Nutrition deficiency is common among hospitalized children. Although oral nutrition supplements (ONS) may improve malnutrition in this population, the benefits and healthcare costs associated with their use have not yet been fully explored. The objective of this study was to assess the effect of ONS use on inpatient length of stay (LOS) and episode cost in hospitalized children. Materials and Methods: Retrospective analysis of 557,348 hospitalizations of children aged 2-8 years in the Premier Research Database. The effect of ONS use on LOS and episode cost in a propensity score- matched sample was estimated in analyses with and without the use of instrumental variables (IVs) to reduce confounding from unobserved variables. Results: ONS were prescribed in 6066 of 557,348 inpatient episodes (1.09%). In IV analysis, using a matched sample of 11,031 episodes, hospitalizations with ONS use had 14.8% shorter LOS (6.4 vs 7.5 days; 1.1 days [95% CI, 0.2-2.4]). Hospitalizations with ONS use had 9.7% lower cost ($16,552 vs $18,320; $1768 [95% CI, $1924-$1612]). Conclusions: ONS use was associated with lower LOS and episode cost among pediatric inpatients. ONS use in hospitalized pediatric patients may provide a cost-effective, evidence-based approach to improving pediatric hospital care.
C1 [Lakdawalla, Darius N.] Univ So Calif, Schaeffer Ctr Hlth Policy & Econ, Los Angeles, CA 90089 USA.
[Mascarenhas, Maria] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Jena, Anupam B.] Harvard Univ, Sch Med, Boston, MA USA.
[Jena, Anupam B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Vanderpuye-Orgle, Jacqueline; LaVallee, Chris; Linthicum, Mark T.; Snider, Julia Thornton] Precis Hlth Econ, Los Angeles, CA USA.
RP Lakdawalla, DN (reprint author), Univ So Calif, Schaeffer Ctr Hlth Policy & Econ, 635 Downey Way,VPD 210-F, Los Angeles, CA 90089 USA.
EM dlakdawa@usc.edu
OI Lakdawalla, Darius/0000-0001-5934-8042
FU Abbott Nutrition
FX Financial disclosure: Financial support for the publication of the
supplement in which this article appears was provided by Abbott
Nutrition.
NR 62
TC 7
Z9 7
U1 3
U2 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0148-6071
EI 1941-2444
J9 JPEN-PARENTER ENTER
JI J. Parenter. Enter. Nutr.
PD NOV
PY 2014
VL 38
SU 2
BP 42S
EP 49S
DI 10.1177/0148607114549769
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AS5MF
UT WOS:000344314200004
PM 25233942
ER
PT J
AU Hamdy, O
Ernst, FR
Baumer, D
Mustad, V
Partridge, J
Hegazi, R
AF Hamdy, Osama
Ernst, Frank R.
Baumer, Dorothy
Mustad, Vikkie
Partridge, Jamie
Hegazi, Refaat
TI Differences in Resource Utilization Between Patients With Diabetes
Receiving Glycemia-Targeted Specialized Nutrition vs Standard Nutrition
Formulas in US Hospitals
SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION
LA English
DT Article
DE diabetes; nutrition; inpatient; length of stay; costs
ID CRITICALLY-ILL PATIENTS; PROPENSITY SCORE; ENTERAL FORMULA; BIAS
AB Objectives: The purpose of the study was to compare patient outcomes and costs for patients with diabetes mellitus (DM) receiving glycemia-targeted specialized nutrition (GTSN) with similar patients receiving standard nutrition (STDN) formulas during acute care hospitalizations. Research Design and Methods: The study was designed as a retrospective analysis over a 10-year period (2000-2009) of clinical and cost data from 125,000 hospital inpatient episodes in the Premier Research Database. Patients received either GTSN or STDN, by tube or orally, as a component of comprehensive care for hyperglycemia in patients with DM. To adjust for potential cohort imbalances, GTSN patients were matched with STDN patients on the basis of propensity scores, adjusting for many characteristics, including age, sex, race, All Patient Refined Diagnosis-Related Group (APR-DRG) illness severity, APR-DRG mortality risk, and comorbidities. Results: Tube-fed patients with DM who were provided GTSN had a 0.88-day (95% confidence interval [CI], 0.73-1.02) shorter length of hospital stay (LOS) on average compared with those patients provided STDN. Orally fed patients with DM who were provided GTSN had a 0.17-day (95% CI, 0.14-0.21) shorter LOS than did those patients provided STDN. The shorter LOS associated with GTSN contributed to a cost savings of $2586 for tube-fed patients and $1356 for orally fed patients. Conclusions: The use of GTSN feeding formulas for patients with DM in acute care hospital settings was associated with reduced LOS and inpatient hospital episode cost in comparison to STDN.
C1 [Hamdy, Osama] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Ernst, Frank R.; Baumer, Dorothy] Premier Healthcare Alliance, Charlotte, NC USA.
[Mustad, Vikkie; Partridge, Jamie; Hegazi, Refaat] Abbott Nutr, Res & Dev, Columbus, OH 43219 USA.
[Hegazi, Refaat] E Carolina Univ, Brody Sch Med, Dept Internal Med, Greenville, NC 27858 USA.
RP Hegazi, R (reprint author), Abbott Nutr, 3300 Stelzer Rd, Columbus, OH 43219 USA.
EM Refaat.Hegazi@abbott.com
FU Abbott Nutrition
FX Financial disclosure: Financial support for the publication of the
supplement in which this article appears was provided by Abbott
Nutrition.
NR 13
TC 6
Z9 6
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0148-6071
EI 1941-2444
J9 JPEN-PARENTER ENTER
JI J. Parenter. Enter. Nutr.
PD NOV
PY 2014
VL 38
SU 2
BP 86S
EP 91S
DI 10.1177/0148607114550315
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AS5MF
UT WOS:000344314200010
PM 25227669
ER
PT J
AU Ananthakrishnan, AN
AF Ananthakrishnan, Ashwin N.
TI Does Vitamin D Deficiency Inhibit Anti-Tumor Necrosis Factor Therapy in
Patients With Irritable Bowel Disease or Does It Simply Result From More
Severe Disease? Reply
SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION
LA English
DT Letter
ID CROHNS-DISEASE; REDUCED RISK
C1 [Ananthakrishnan, Ashwin N.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Ananthakrishnan, Ashwin N.] Harvard Univ, Sch Med, Boston, MA USA.
RP Ananthakrishnan, AN (reprint author), Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 4
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 0148-6071
EI 1941-2444
J9 JPEN-PARENTER ENTER
JI J. Parenter. Enter. Nutr.
PD NOV
PY 2014
VL 38
IS 8
BP 925
EP 925
DI 10.1177/0148607114533349
PG 1
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AS5MI
UT WOS:000344314500003
PM 25342587
ER
PT J
AU Legault, G
Kieran, MW
Scott, RM
Chordas, C
Milla, SS
Karajannis, MA
AF Legault, Genevieve
Kieran, Mark W.
Scott, Robert Michael
Chordas, Christine
Milla, Sarah S.
Karajannis, Matthias A.
TI Recurrent Ascites in a Patient With Low-grade Astrocytoma and
Ventriculo-Peritoneal Shunt Treated With the Multikinase Inhibitor
Sorafenib
SO JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY
LA English
DT Article
DE pediatric low-grade astrocytoma; ascites; sorafenib; toxicity
ID OVARIAN-CANCER; PHASE-II; TUMOR; HYDROCEPHALUS; CARCINOMA; GROWTH;
GLIOMA
AB This report describes a 6-year-old boy with disseminated low-grade astrocytoma and ventriculo-peritoneal shunt, who developed recurrent ascites while receiving sorafenib on a clinical trial. Laboratory analysis of the peritoneal fluid showed no elevation of protein content and no evidence of underlying infection or tumor dissemination. This report highlights ascites as a previously unrecognized adverse reaction to sorafenib in a patient with a ventriculo-peritoneal shunt. We conclude that such patients should be closely monitored for this complication when treated with sorafenib.
C1 [Legault, Genevieve; Karajannis, Matthias A.] NYU Langone Med Ctr, Dept Pediat, New York, NY USA.
[Milla, Sarah S.] NYU Langone Med Ctr, Dept Radiol, New York, NY USA.
[Kieran, Mark W.] Boston Childrens Hosp, Dept Pediat Oncol, Boston, MA USA.
[Scott, Robert Michael] Boston Childrens Hosp, Dept Neurosurg, Boston, MA USA.
[Kieran, Mark W.; Chordas, Christine] Dana Farber Canc Inst, Dept Pediat Neurooncol, Boston, MA 02115 USA.
RP Karajannis, MA (reprint author), Hassenfeld Childrens Ctr Canc & Blood Disorders, NYU Langone Med Ctr, 160 East 32nd St,2nd Floor, New York, NY 10016 USA.
EM matthias.karajannis@nyumc.org
FU Pediatric Low-Grade Astrocytoma Foundation; Making Headway Foundation;
Bayer HealthCare Pharmaceuticals
FX The phase II clinical trial with sorafenib for children and young adults
with recurrent or progressive low-grade astrocytomas (ClinicalTrials.gov
identifier NCT01338857) was supported by the Pediatric Low-Grade
Astrocytoma Foundation, Making Headway Foundation and Bayer HealthCare
Pharmaceuticals.
NR 19
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1077-4114
EI 1536-3678
J9 J PEDIAT HEMATOL ONC
JI J. Pediatr. Hematol. Oncol.
PD NOV
PY 2014
VL 36
IS 8
BP E533
EP E535
PG 3
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA AS4DX
UT WOS:000344224500013
PM 24351969
ER
PT J
AU Yager, PH
Clark, ME
Dapul, HR
Murphy, S
Zheng, H
Noviski, N
AF Yager, Phoebe H.
Clark, Maureen E.
Dapul, Heda R.
Murphy, Sarah
Zheng, Hui
Noviski, Natan
TI Reliability of Circulatory and Neurologic Examination by Telemedicine in
a Pediatric Intensive Care Unit
SO JOURNAL OF PEDIATRICS
LA English
DT Article
AB Objective To test the hypothesis that telemedicine can reliably be used for many aspects of circulatory and neurologic examinations of children admitted to a pediatric intensive care unit (PICU).
Study design A prospective, randomized study in a 14-bed PICU in a tertiary care, academic-affiliated institution. Eligible patients were >2 months or <19 years of age, not involved in a concurrent study, had parents/guardian able to sign an informed consent form, were not at end-of-life, and had an attending who not only deemed them medically stable, but also felt that the study would not interrupt their care. Other than the Principal Investigator, 6 pediatric intensivists and 7 pediatric critical care fellows were eligible study providers. Two physician providers were randomly assigned to perform circulatory and neurologic examinations according to the American Heart Association/Pediatric Advanced Life Support guidelines in-person and via telemedicine. Findings were recorded on a standardized data collection form and compared.
Results One hundred ten data collection forms were completed. For many aspects of the circulatory and neurologic examinations, outcomes showed substantial to perfect agreement between the in-person and telemedical care providers (kappa = 0.64-1.00). However, assessments of muscle tone had a kappa = 0.23, with a kappa = 0.37 for skin color.
Conclusions Telemedicine can reliably identify normal and abnormal findings of many aspects of circulatory and neurologic examinations in PICU patients. This finding opens the door to further studies on the use of telemedicine across other disciplines.
C1 [Yager, Phoebe H.; Clark, Maureen E.; Murphy, Sarah; Zheng, Hui; Noviski, Natan] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Dapul, Heda R.] Maimonides Hosp, Brooklyn, NY 11219 USA.
RP Noviski, N (reprint author), Massachusetts Gen Hosp, Dept Pediat, 175 Cambridge St, Boston, MA 02114 USA.
EM nnoviski@partners.org
NR 19
TC 0
Z9 0
U1 1
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
EI 1097-6833
J9 J PEDIATR-US
JI J. Pediatr.
PD NOV
PY 2014
VL 165
IS 5
BP 962
EP U403
DI 10.1016/j.jpeds.2014.07.002
PG 10
WC Pediatrics
SC Pediatrics
GA AS4HP
UT WOS:000344235000019
PM 25112695
ER
PT J
AU Langdon, KJ
Leventhal, AM
AF Langdon, Kirsten J.
Leventhal, Adam M.
TI Posttraumatic stress symptoms and tobacco abstinence effects in a
non-clinical sample: Evaluating the mediating role of negative affect
reduction smoking expectancies
SO JOURNAL OF PSYCHOPHARMACOLOGY
LA English
DT Article
DE Posttraumatic stress; cigarette smoking; nicotine withdrawal; negative
affect; abstinence
ID RECRUITED DAILY SMOKERS; LAPSE BEHAVIOR; NICOTINE DEPENDENCE; RESIST
SMOKING; DISORDER; PTSD; VETERANS; WITHDRAWAL; DEPRESSION; TRAUMA
AB The relation between posttraumatic stress symptoms and smoking is well documented but poorly understood. The present investigation sought to evaluate the impact of posttraumatic stress symptoms on subjective and behavioral tobacco abstinence effects both directly and indirectly through negative affect reduction smoking outcome expectancies. Participants included 275 (68.7% male; M-age=43.9, 10+ cig/day) adult non-treatment seeking smokers, who attended two counterbalanced laboratory sessions (16 h of smoking deprivation vs ad libitum smoking), during which they completed self-report measures of withdrawal symptoms and mood followed by a smoking lapse task in which they could earn money for delaying smoking and purchase cigarettes to smoke. Results supported a mediational pathway whereby higher baseline symptoms of posttraumatic stress predicted greater endorsement of expectancies that smoking will effectively reduce negative affect, which in turn predicted greater abstinence-provoked exacerbations in nicotine withdrawal symptoms and negative affect. Posttraumatic stress symptoms also predicted number of cigarettes purchased independent of negative affect reduction expectancies, but did not predict delaying smoking for money. Findings highlight tobacco abstinence effects as a putative mechanism underlying posttraumatic stress disorder (PTSD)-smoking comorbidity, indicate an important mediating role of beliefs for smoking-induced negative affect reduction, and shed light on integrated treatment approaches for these two conditions.
C1 [Langdon, Kirsten J.] VA Boston Healthcare Syst, Natl Ctr PTSD, Womens Hlth Sci Div, Boston, MA 02130 USA.
[Langdon, Kirsten J.] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA.
[Leventhal, Adam M.] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
RP Langdon, KJ (reprint author), VA Boston Healthcare Syst, Natl Ctr PTSD, Womens Hlth Sci Div, 150 South Huntington Ave 116B-3, Boston, MA 02130 USA.
EM kirsten.langdon@va.gov
FU National Research Service Award (NRSA) by National Institute on Drug
Abuse [F31DA026634]; National Institute of Health [R01DA026831,
K08DA025041]
FX This project was supported by a National Research Service Award (NRSA)
F31DA026634 awarded to KJ Langdon by the National Institute on Drug
Abuse. This work was also supported by grants R01DA026831 and
K08DA025041 awarded to AM Leventhal by the National Institute of Health.
NR 55
TC 1
Z9 1
U1 1
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0269-8811
EI 1461-7285
J9 J PSYCHOPHARMACOL
JI J. Psychopharmacol.
PD NOV
PY 2014
VL 28
IS 11
BP 1009
EP 1017
DI 10.1177/0269881114546708
PG 9
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA AS0OG
UT WOS:000343976600005
PM 25142407
ER
PT J
AU Tomar, R
Mudumana, SP
Pathak, N
Hukriede, NA
Drummond, IA
AF Tomar, Ritu
Mudumana, Sudha P.
Pathak, Narendra
Hukriede, Neil A.
Drummond, Iain A.
TI osr1 Is Required for Podocyte Development Downstream of wt1a
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID CONGENITAL NEPHROTIC SYNDROME; ZEBRAFISH PRONEPHROS; KIDNEY DEVELOPMENT;
INTERMEDIATE MESODERM; EXPRESSION ANALYSIS; HOMEOBOX GENE; NEPHRIN GENE;
MICE LACKING; CELL FATE; DIFFERENTIATION
AB Odd-skipped related 1 (Osr1) encodes a zinc finger transcription factor required for kidney development. Osr1 deficiency in mice results in metanephric kidney agenesis, whereas knockdown or mutation studies in zebrafish revealed that pronephric nephrons require osr1 for proximal tubule and podocyte development. osr1-deficient pronephric podocyte progenitors express the Wilms' tumor suppressor wt1a but do not undergo glomerular morphogenesis or express the foot process junctional markers nephrin and podocin. The function of osr1 in podocyte differentiation remains unclear, however. Here, we found by double fluorescence in situ hybridization that podocyte progenitors coexpress osr1 and wt1a. Knockdown of wt1a disrupted podocyte differentiation and prevented expression of osr1. Blocking retinoic acid signaling, which regulates wt1a, also prevented osr1 expression in podocyte progenitors. Furthermore, unlike the osr1-deficient proximal tubule phenotype, which can be rescued by manipulation of endoderm development, podocyte differentiation was not affected by altered endoderm development, as assessed by nephrin and podocin expression in double osr1/sox32-deficient embryos. These results suggest a different, possibly cell- autonomous requirement for osr1 in podocyte differentiation downstream of wt1a. Indeed, osr1-deficient embryos did not exhibit podocyte progenitor expression of the transcription factor Ihx1a, and forced expression of activated forms of the Ihx1a gene product rescued nephrin expression in osrl-deficient podocytes. Our results place osr1 in a framework of transcriptional regulators that control the expression of podocin and nephrin and thereby mediate podocyte differentiation.
C1 [Tomar, Ritu; Mudumana, Sudha P.; Pathak, Narendra; Drummond, Iain A.] Massachusetts Gen Hosp, Div Nephrol, Charlestown, MA 02129 USA.
[Hukriede, Neil A.] Univ Pittsburgh, Dept Dev Biol, Pittsburgh, PA USA.
[Drummond, Iain A.] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
RP Drummond, IA (reprint author), Massachusetts Gen Hosp, Div Nephrol, 149 13th St,Room 149-8000, Charlestown, MA 02129 USA.
EM idrummond@mgh.harvard.edu
FU National Institutes of Health [R01-DK071041, 2R01-DK069403,
K01-DK078741]; American Heart Association [0625923T]
FX The authors acknowledge the support of the Massachusetts General
Hospital fish facility staff and technical support from Ms. Yan Liu.
This work was supported by the National Institutes of Health grant
R01-DK071041 to I.A.D., 2R01-DK069403 to N.A.H., K01-DK078741 to N.P.,
and the American Heart Association postdoctoral fellowship 0625923T to
S.P.M.
NR 46
TC 3
Z9 3
U1 1
U2 3
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
EI 1533-3450
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD NOV
PY 2014
VL 25
IS 11
BP 2539
EP 2545
DI 10.1681/ASN.2013121327
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA AS1KO
UT WOS:000344040300017
PM 24722440
ER
PT J
AU Chan, KE
Thadhani, RI
Maddux, FW
AF Chan, Kevin E.
Thadhani, Ravi I.
Maddux, Franklin W.
TI Adherence Barriers to Chronic Dialysis in the United States
SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID STAGE RENAL-DISEASE; HEMODIALYSIS; DEPRESSION; MORTALITY;
HOSPITALIZATION; ASSOCIATIONS; NONADHERENCE; DOPPS; CARE
AB Hemodialysis patients often do not attend their scheduled treatment session. We investigated factors associated with missed appointments and whether such nonadherence poses significant harm to patients and increases overall health care utilization in an observational analysis of 44 million hemodialysis treatments for 182,536 patients with ESRD in the United States. We assessed the risk of hospitalization, emergency room visit, or intensive-coronary care unit (ICU-CCU) admission in the 2 days after a missed treatment relative to the risk for patients who received hemodialysis. Over the 5-year study period, the average missed treatment rate was 7.1 days per patient-year. In covariate adjusted logistic regression, the risk of hospitalization (odds ratio [OR], 3.98; 95% confidence interval [95% CI], 3.93 to 4.04), emergency room visit (OR, 2.00; 95% CI, 1.87 to 2.14), or ICU-CCU admission (OR, 3.89; 95% Cl, 3.81 to 3.96) increased significantly after a missed treatment. Overall, 0.9 missed treatment days per year associated with suboptimal transportation to dialysis, inclement weather, holidays, psychiatric illness, pain, and gastrointestinal upset. These barriers also associated with excess hospitalization (5.6 more events per patient-year), emergency room visits (1.1 more visits), and ICU-CCU admissions (0.8 more admissions). In conclusion, poor adherence to hemodialysis treatments may be a substantial roadblock to achieving better patient outcomes. Addressing systemic and patient barriers that impede access to hemodialysis care may decrease missed appointments and reduce patient morbidity.
C1 [Chan, Kevin E.; Maddux, Franklin W.] Fresenius Med Care North Amer, Div Clin Res, Waltham, MA 02451 USA.
[Chan, Kevin E.; Thadhani, Ravi I.] Massachusetts Gen Hosp, Div Nephrol, Boston, MA 02114 USA.
RP Chan, KE (reprint author), Fresenius Med Care North Amer, Div Clin Res, 920 Winter St, Waltham, MA 02451 USA.
EM kevin.chan@fmc-na.com
FU Fresenius Medical Care North America
FX K.E.C. and F.W.M. receive salary support from Fresenius Medical Care
North America. R.I.T. is a consultant to Fresenius Medical Care North
America. The Management Board of Fresenius Medical Care had no role in
the design and conduct of this study.
NR 14
TC 5
Z9 5
U1 1
U2 10
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1046-6673
EI 1533-3450
J9 J AM SOC NEPHROL
JI J. Am. Soc. Nephrol.
PD NOV
PY 2014
VL 25
IS 11
BP 2642
EP 2648
DI 10.1681/ASN.2013111160
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA AS1KO
UT WOS:000344040300027
PM 24762400
ER
PT J
AU Blackhall, F
Kim, DW
Besse, B
Nokihara, H
Han, JY
Wilner, KD
Reisman, A
Iyer, S
Hirsh, V
Shaw, AT
AF Blackhall, Fiona
Kim, Dong-Wan
Besse, Benjamin
Nokihara, Hiroshi
Han, Ji-Youn
Wilner, Keith D.
Reisman, Arlene
Iyer, Shrividya
Hirsh, Vera
Shaw, Alice T.
TI Patient-Reported Outcomes and Quality of Life in PROFILE 1007: A
Randomized Trial of Crizotinib Compared with Chemotherapy in Previously
Treated Patients with ALK-Positive Advanced Non-Small-Cell Lung Cancer
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
DE Patient-reported outcomes; Quality of life; Crizotinib; Non-small-cell
lung cancer
ID CLINICAL-TRIALS; PHASE-III; SYMPTOM; ERLOTINIB; ADENOCARCINOMA;
GEFITINIB; DISTRESS; AFATINIB; FATIGUE; QLQ-C30
AB Introduction: The main objective of the current post hoc analysis was to compare patient-reported outcomes between crizotinib (N = 172) and chemotherapy subgroups (pemetrexed [N = 99] and docetaxel [N = 72]) in previously treated patients with advanced ALK-positive non-small-cell lung cancer, in PROFILE 1007 study (Pfizer; NCT0093283).
Methods: Patient-reported outcomes were assessed at baseline, day 1 of each cycle, and end of treatment. General health status was measured using the EuroQol-5D visual analog scale and health utility index scores were assessed using the EuroQol-5D descriptive system. Functioning, lung cancer symptoms, and global quality of life (QOL) were assessed using European Organisation for Research and Treatment of Cancer QLQ-C30 and the QLQ-LC13 lung cancer module. Repeated measures mixed-effects analyses compared overall scores and change from baseline scores, controlling for baseline scores.
Results: The overall mean EQ-5D health utility index scores (95% CI) on treatment were significantly greater (p < 0.05) for crizotinib (0.82 [0.79-0.85]) than for chemotherapy (0.73 [0.70-0.77]; 0.74 [0.70-0.79] for pemetrexed and 0.66 [0.58-0.74] for docetaxel). A significantly greater improvement from baseline was observed with crizotinib versus pemetrexed and versus docetaxel treatment groups for general health status, physical functioning, global QOL, dyspnea, fatigue, and pain. Improvement rates for fatigue, cough, pain, dyspnea, and global QOL were significantly greater on crizotinib compared with pemetrexed and docetaxel, respectively. Worsening rates for diarrhea and constipation were higher with crizotinib.
Conclusion: The benefits of crizotinib in improving symptoms and QOL are demonstrated regardless of whether the comparator is pemetrexed or docetaxel.
C1 [Blackhall, Fiona] Univ Manchester, Inst Canc Sci, Dept Med Oncol, Manchester, Lancs, England.
[Blackhall, Fiona] Christie Hosp NHS Fdn Trust, Manchester M20 4BX, Lancs, England.
[Kim, Dong-Wan] Seoul Natl Univ Hosp, Dept Internal Med, Seoul 110744, South Korea.
[Besse, Benjamin] Inst Gustave Roussy, Dept Thorac Oncol, Villejuif, France.
[Nokihara, Hiroshi] Natl Canc Ctr, Tokyo, Japan.
[Han, Ji-Youn] Natl Canc Ctr, Ctr Lung Canc, Div Translat & Clin Res, Goyang, South Korea.
[Wilner, Keith D.] Pfizer Oncol, Clin Dev, La Jolla, CA USA.
[Reisman, Arlene] Pfizer Global Innovat Pharma Business, Biostat, New York, NY USA.
[Iyer, Shrividya] Pfizer Oncol, Global Outcomes & Evidence, New York, NY USA.
[Hirsh, Vera] McGill Univ, Ctr Hlth, Dept Oncol, Montreal, PQ, Canada.
[Shaw, Alice T.] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
RP Blackhall, F (reprint author), Christie Hosp NHS Fdn Trust, Dept Med Oncol, Wilmslow Rd, Manchester M20 4BX, Lancs, England.
EM Fiona.Blackhall@chris-tie.nhs.ukx
RI Blackhall, Fiona/N-2186-2015
OI Blackhall, Fiona/0000-0001-8716-3395
FU Pfizer, Inc.
FX Editorial support was provided by Roger Wild at ACUMED (Tytherington,
UK) with funding from Pfizer, Inc. Programming support was provided by
Pfizer, Inc.
NR 27
TC 8
Z9 8
U1 1
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2014
VL 9
IS 11
BP 1625
EP 1633
DI 10.1097/JTO.0000000000000318
PG 9
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AS6IT
UT WOS:000344368100010
PM 25436797
ER
PT J
AU Awad, MM
Lax, TP
Slawski, BR
Shaw, AT
AF Awad, Mark M.
Lax, Timothy P.
Slawski, Benjamin R.
Shaw, Alice T.
TI Successful Desensitization of Two Patients with ALK-Positive Lung Cancer
and Hypersensitivity to Crizotinib
SO JOURNAL OF THORACIC ONCOLOGY
LA English
DT Article
DE Anaplastic lymphoma kinase; Crizotinib; Hypersensitivity;
Desensitization
ID CHEMOTHERAPY; EML4-ALK; GENE
AB The tyrosine kinase inhibitor crizotinib is an effective therapy for patients with cancers harboring rearrangements of the anaplastic lymphoma kinase (ALK) gene. Here, we describe two patients with advanced ALK-positive lung cancer who developed hypersensitivity to crizotinib, requiring temporary discontinuation of the drug. Both patients were treated with a rapid oral desensitization protocol allowing them to resume crizotinib without further signs or symptoms of hypersensitivity.
C1 [Awad, Mark M.; Shaw, Alice T.] Massachusetts Gen Hosp, Dept Med, Div Med Oncol, Boston, MA 02114 USA.
[Lax, Timothy P.; Slawski, Benjamin R.] Massachusetts Gen Hosp, Dept Med, Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA.
RP Shaw, AT (reprint author), Massachusetts Gen Hosp, Dept Med, Div Med Oncol, Ctr Canc, Yawkey 7B,32 Fruit St, Boston, MA 02114 USA.
EM ashaw1@mgh.harvard.edu
FU Pfizer; Ariad; Chugai; Novartis; Genentech; Ignyta; Roche; Bristol-Myers
Squibb
FX Dr. Shaw has served as a paid consultant for Pfizer, Ariad, Chugai,
Novartis, Genentech, and Ignyta. Dr. Shaw has also received
institutional research funding from Pfizer, Ariad, Novartis, Roche, and
Bristol-Myers Squibb. All other authors declare no conflict of interest.
NR 11
TC 3
Z9 3
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1556-0864
EI 1556-1380
J9 J THORAC ONCOL
JI J. Thorac. Oncol.
PD NOV
PY 2014
VL 9
IS 11
BP 1726
EP 1728
DI 10.1097/JTO.0000000000000350
PG 3
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AS6IT
UT WOS:000344368100026
PM 25436807
ER
PT J
AU Herr, MW
Bonanno, A
Montalbano, LA
Deschler, DG
Emerick, KS
AF Herr, Marc W.
Bonanno, Andrea
Montalbano, Lisa A.
Deschler, Daniel G.
Emerick, Kevin S.
TI Shoulder Function Following Reconstruction With the Supraclavicular
Artery Island Flap
SO LARYNGOSCOPE
LA English
DT Article
DE Head and neck; reconstructive surgery; flaps
ID SELECTIVE NECK DISSECTION; MAJOR MYOCUTANEOUS FLAP; DONOR-SITE; HEAD;
COMPLICATIONS; NERVE; EXPERIENCE; MORBIDITY
AB Objectives/HypothesisThe supraclavicular artery island flap (SCAIF) is a pedicled fasciocutaneous flap used for head and neck reconstruction. In recent years, its use has significantly increased as a result of several advantageous characteristics, including pliability, an excellent color and texture match, ability to reconstruct a variety of skin and aerodigestive tract defects, and short harvest times. Clinical experience suggests that donor site complications are relatively infrequent and typically self-limiting, and there have been no documented cases of prolonged or permanent shoulder dysfunction. However, formal studies have not been performed to assess this outcome. The goal of this study was to evaluate the effects of SCAIF flap harvest on postoperative shoulder strength and flexibility.
Study DesignProspective cohort pilot study.
MethodsData was gathered prospectively during routine follow-up and surveillance. The Penn Shoulder Score and Constant Shoulder Scale were used to measure subjective and objective outcomes. Physical therapists performed testing for strength and flexibility.
ResultsTen patients were evaluated from January to July, 2013. Subjective self-reporting of shoulder function and satisfaction was good to excellent in most patients. The majority of patients demonstrated limitations in range of motion for one or more shoulder movements. Muscle strength was preserved postoperatively.
ConclusionHarvest of the SCAIF appears to have limited postoperative morbidity. Postoperative shoulder strength and function appears to be very good; however, some limitation of range of motion was observed.
Level of Evidence4 Laryngoscope, 124:2478-2483, 2014
C1 [Herr, Marc W.; Deschler, Daniel G.; Emerick, Kevin S.] Massachusetts Eye & Ear Infirm, Div Head & Neck Surg Oncol & Reconstruct, Boston, MA 02114 USA.
[Herr, Marc W.; Deschler, Daniel G.; Emerick, Kevin S.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02115 USA.
[Bonanno, Andrea; Montalbano, Lisa A.] Massachusetts Gen Hosp, Dept Phys Therapy, Boston, MA 02114 USA.
RP Herr, MW (reprint author), Massachusetts Eye & Ear Infirm, Boston, MA 02114 USA.
EM marc.w.herr@gmail.com
NR 38
TC 4
Z9 5
U1 2
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0023-852X
EI 1531-4995
J9 LARYNGOSCOPE
JI Laryngoscope
PD NOV
PY 2014
VL 124
IS 11
BP 2478
EP 2483
DI 10.1002/lary.24761
PG 6
WC Medicine, Research & Experimental; Otorhinolaryngology
SC Research & Experimental Medicine; Otorhinolaryngology
GA AS6OH
UT WOS:000344382100017
PM 24913956
ER
PT J
AU Chen, MH
Blackington, LH
Zhou, J
Chu, TF
Gauvreau, K
Marcus, KJ
Fisher, DC
Diller, LR
Ng, AK
AF Chen, Ming Hui
Blackington, Lauren H.
Zhou, Jing
Chu, Tammy F.
Gauvreau, Kimberlee
Marcus, Karen J.
Fisher, David C.
Diller, Lisa R.
Ng, Andrea K.
TI Blood pressure is associated with occult cardiovascular disease in
prospectively studied Hodgkin lymphoma survivors after chest radiation
SO LEUKEMIA & LYMPHOMA
LA English
DT Article
DE Blood pressure; radiation; Hodgkin lymphoma; cardiovascular risk
factors; hs-CRP
ID CHILDHOOD-CANCER SURVIVOR; CORONARY-ARTERY-DISEASE; MEDIASTINAL
IRRADIATION; CARDIAC MORBIDITY; 5-YEAR SURVIVORS; ADULT SURVIVORS; RISK;
MORTALITY; RECOMMENDATIONS; INFLAMMATION
AB The objectives of this study were to prospectively screen a cohort of asymptomatic long-term survivors of Hodgkin lymphoma (HL) treated with chest irradiation for occult cardiovascular disease (CVD), and correlate screen-detected disease with prospectively measured cardiovascular risk factors (CRFs). A total of 182 HL survivors treated with chest irradiation (median follow-up time 14.8 years) were enrolled and underwent prospective CRF measurement and resting and stress echocardiography to assess coronary artery disease (CAD)/valve disease and left ventricular systolic dysfunction (LVSD). Forty-seven (26%) patients had occult CAD/valve disease and/or LVSD. LVSD was not correlated with CRFs. Controlling for treatment factors, hypertension (odds ratio [OR] = 3.0) and elevated high-sensitivity C-reactive protein (hs-CRP) (OR = 2.7) increased the likelihood of occult CAD/valve disease. Risk of CAD/valve disease rose exponentially with increasing blood pressure (BP) values, even in the normal range. Our findings suggest that BP screening may be useful in determining those survivors at greatest risk for occult CVD.
C1 [Chen, Ming Hui; Blackington, Lauren H.; Zhou, Jing; Chu, Tammy F.; Gauvreau, Kimberlee] Boston Childrens Hosp, Dept Cardiol, Boston, MA 02115 USA.
[Chen, Ming Hui] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Ng, Andrea K.] Brigham & Womens Hosp, Dept Radiat Oncol, Boston, MA 02115 USA.
[Chen, Ming Hui; Gauvreau, Kimberlee; Marcus, Karen J.; Fisher, David C.; Diller, Lisa R.; Ng, Andrea K.] Harvard Univ, Sch Med, Boston, MA USA.
[Marcus, Karen J.; Diller, Lisa R.] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Fisher, David C.] Dana Farber Canc Inst, Dept Hematol Oncol, Boston, MA 02115 USA.
RP Chen, MH (reprint author), Boston Childrens Hosp, Dept Cardiol, 300 Longwood Ave, Boston, MA 02115 USA.
EM minghui.chen@cardio.chboston.org
FU Translational Fund for Research in Cardiology and Oncology, Department
of Cardiology, Boston Children's Hospital; Swim-Across-America
Foundation
FX We gratefully acknowledge the staff of the Perini Survivors Clinic and
Adult Survivorship Clinic at Dana-Farber Cancer Institute, in particular
Richard Boyajian, NP, for their assistance with patient recruitment.
Support from the Translational Fund for Research in Cardiology and
Oncology, Department of Cardiology, Boston Children's Hospital and the
Swim-Across-America Foundation helped to make this study possible. We
appreciate the invaluable contribution of our research assistants, Molly
Cook, Elizabeth Abernathey and Siri Kirin Khalsa, in data collection and
preparation of this manuscript. Furthermore, we are grateful to our
patients with HL whose participation and dedication inspired us.
Finally, we acknowledge Dr. Peter M.Mauch's valuable input in the
conduction of this study, and for all the patients with HL he has
treated and followed over the years that allow the study of late effects
in these long-term survivors.
NR 28
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U1 0
U2 2
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1042-8194
EI 1029-2403
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD NOV
PY 2014
VL 55
IS 11
BP 2477
EP 2483
DI 10.3109/10428194.2013.879716
PG 7
WC Oncology; Hematology
SC Oncology; Hematology
GA AS5XD
UT WOS:000344339000011
PM 24397615
ER
PT J
AU Garcia-Albeniz, X
Logan, RW
Schrag, D
Hernan, MA
AF Garcia-Albeniz, Xabier
Logan, Roger W.
Schrag, Deborah
Hernan, Miguel A.
TI Evaluation of the Duplication of Staging CT Scans for Localized Colon
Cancer in a Medicare Population
SO MEDICAL CARE
LA English
DT Article
DE colon cancer; CAT scan; SEER-Medicare; staging; prognosis
ID COMBINED ANTIRETROVIRAL THERAPY; HEALTH-CARE; FOLLOW-UP; DIAGNOSIS;
COUNTRIES; MORTALITY
AB Background: To quantify and characterize duplicated tests performed during the staging of localized colon cancer in the Medicare population.
Methods: We used the SEER-Medicare linked database to select patients diagnosed with localized colon cancer between the years 1996 and 2009. We considered a patient as adequately staged after having received a colonoscopy, an abdominal computed tomography (CT) scan, and a pelvic CT scan. Abdominal and pelvic CT scans performed between complete staging and first cancer-directed treatment, if not ordered due to an acute condition, were considered duplicates. We characterized the institutions providing the tests and evaluated the association with survival using a weighted pooled logistic regression adjusted by baseline and time-varying confounders.
Results: Of 36,291 patients with a complete staging, 2680 (7.4%) had at least 1 duplicated test. Patients receiving a duplicate had a higher comorbidity score, were more symptomatic, and had more visits to the emergency department and clinical evaluations. They also were treated with surgery less frequently and had worse survival (hazard ratio 1.22, 95% confidence interval, 1.16-1.28). The type of institution involved in the staging (nonprofit/government centers, proprietary centers, free-standing facilities) was not associated with receiving duplicated tests.
Conclusions: We found a low frequency of duplicated abdominal or pelvic CT scans in the staging of colon cancer in the Medicare population.
C1 [Garcia-Albeniz, Xabier; Logan, Roger W.; Hernan, Miguel A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Schrag, Deborah] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Hernan, Miguel A.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Hernan, Miguel A.] Harvard Mit Div Hlth Sci & Technol, Boston, MA USA.
RP Garcia-Albeniz, X (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, 677 Huntington Ave, Boston, MA 02115 USA.
EM xabi@post.harvard.edu
FU NIH [P01-CA134294]; ASISA Fellowship; National Cancer Institute's
Surveillance, Epidemiology and End Results Program [N01-PC-35136,
N01-PC-35139, N02-PC-15105]; Centers for Disease Control and
Prevention's National Program of Cancer Registries [U55/CCR921930-02]
FX Partly funded by NIH grant P01-CA134294. X.G.-A. is a recipient of an
"ASISA Fellowship." The collection of the California cancer incidence
data used in this study was supported by the California Department of
Public Health as part of the statewide cancer reporting program mandated
by California Health and Safety Code Section 103885; the National Cancer
Institute's Surveillance, Epidemiology and End Results Program under
contract N01-PC-35136 awarded to the Northern California Cancer Center,
contract N01-PC-35139 awarded to the University of Southern California,
and contract N02-PC-15105 awarded to the Public Health Institute; and
the Centers for Disease Control and Prevention's National Program of
Cancer Registries, under agreement #U55/CCR921930-02 awarded to the
Public Health Institute.
NR 22
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U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
EI 1537-1948
J9 MED CARE
JI Med. Care
PD NOV
PY 2014
VL 52
IS 11
BP 963
EP 968
PG 6
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA AR9XL
UT WOS:000343930300005
PM 25226545
ER
PT J
AU Quinones, AR
Ramsey, K
Newsom, JT
Dorr, DA
AF Quinones, Ana R.
Ramsey, Katrina
Newsom, Jason T.
Dorr, David A.
TI Racial and Ethnic Differences in Clinical Outcome Trajectories for Care
Managed Patients
SO MEDICAL CARE
LA English
DT Article
DE racial/ethnic differences; complex care patients; multimorbidity;
hemoglobin A1c; blood pressure; multilevel modeling
ID RANDOMIZED CONTROLLED-TRIAL; HEALTH-CARE; MEXICAN-AMERICANS;
MULTIMORBIDITY; QUALITY; HOSPITALIZATION; CONSEQUENCES; PREVALENCE;
DISEASES; SENIORS
AB Background: Care management has demonstrated improvements in quality of care for patients with complex care needs. The extent to which these interventions benefit race/ethnic minority populations is unclear.
Objectives: To characterize race/ethnic differences in the longitudinal control of clinical outcomes for patients with complex care needs enrolled in Care Management Plus, a health information technology-enabled care coordination intervention.
Research Design: Multilevel models of repeated observations from clinical encounters before and after program enrollment for 6 Oregon and California primary care clinics.
Subjects: A total of 18,675 clinic patients were examined. We estimated multilevel models for 1481 and 5320 care-managed individuals with repeated hemoglobin A1c and blood pressure measurements, respectively.
Measures: Primary outcomes were changes over time for 2 clinical markers of health status for complex care patients: (1) hemoglobin A1c for patients with diabetes; and (2) mid-blood pressure (BP) (average systolic and diastolic blood pressure).
Results: We found significant reductions in A1c for patients with previously uncontrolled A1c (preperiod slope, b = 1.03 [0.83, 1.24]; postperiod slope, b = -0.63 [-0.91, -0.35]). For mid-BP we found increasing unconditional preperiod trajectories (b = 3.52 [2.39, 4.64]) and decreasing postperiod trajectories (b= -5.21 [-5.70, -4.72]). We also found the trajectories of A1c and mid-BP were not statistically different for black, Latino, and white patients.
Conclusions: These analyses demonstrate some promising results for intermediate clinical outcomes for underrepresented patients with complex chronic care needs. It remains to be seen whether these health care system delivery redesigns yield long-term benefits for patients, such as improvements in function and quality of life.
C1 [Quinones, Ana R.; Ramsey, Katrina] Oregon Hlth & Sci Univ, Dept Publ Hlth & Prevent Med, Portland, OR 97239 USA.
[Quinones, Ana R.] Portland VA Med Ctr, Portland, OR USA.
[Newsom, Jason T.] Portland State Univ, Sch Community Hlth, Portland, OR 97207 USA.
[Newsom, Jason T.] Portland State Univ, Inst Aging, Portland, OR 97207 USA.
[Dorr, David A.] Oregon Hlth & Sci Univ, Portland, OR 97239 USA.
RP Quinones, AR (reprint author), Oregon Hlth & Sci Univ, Dept Publ Hlth & Prevent Med, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA.
EM quinones@ohsu.edu
FU Medical Research Foundation of Oregon [MRF-1217]; American Diabetes
Association [ADA 7-13-CD-08]; Programs to Increase Diversity among
Individuals Engaged in Health Related-Research [NIH/NHLBI R25HL105430]
FX Supported by the Medical Research Foundation of Oregon (MRF-1217,
Quinones PI) and the American Diabetes Association (ADA 7-13-CD-08,
Quinones PI). A.R.Q. was also supported by the Programs to Increase
Diversity among Individuals Engaged in Health Related-Research
(NIH/NHLBI R25HL105430). The views expressed in this article are those
of the authors and do not necessarily represent the views of the Medical
Research Foundation, the National Institutes of Health, or the American
Diabetes Association.
NR 33
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U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
EI 1537-1948
J9 MED CARE
JI Med. Care
PD NOV
PY 2014
VL 52
IS 11
BP 998
EP 1005
PG 8
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA AR9XL
UT WOS:000343930300010
PM 25304019
ER
PT J
AU Pozdnyakova, O
Wu, KD
Patki, A
Rodig, SJ
Thiele, J
Hasserjian, RP
AF Pozdnyakova, Olga
Wu, Kaida
Patki, Abhay
Rodig, Scott J.
Thiele, Juergen
Hasserjian, Robert P.
TI High concordance in grading reticulin fibrosis and cellularity in
patients with myeloproliferative neoplasms
SO MODERN PATHOLOGY
LA English
DT Article
DE anti-JAK2 therapy; bone marrow; collagen deposition; hematopoietic
cellularity; inter-rater agreement; reticulin fibrosis
ID CHRONIC IDIOPATHIC MYELOFIBROSIS; BONE-MARROW FIBROSIS; INTERNATIONAL
WORKING GROUP; REVISED RESPONSE CRITERIA; PLACEBO-CONTROLLED TRIAL;
ESSENTIAL THROMBOCYTHEMIA; POLYCYTHEMIA-VERA; EUROPEAN CONSENSUS;
FOLLOW-UP; IWG-MRT
AB The myeloproliferative neoplasms primary myelofibrosis, polycythemia vera, and, rarely, essential thrombocythemia are characterized by variable degrees of bone marrow fibrosis, either at presentation or upon progression. The increasing use of emerging therapies that may alter disease biology and morphology demands accurate and reproducible assessment of fibrosis grade. To assess concordance of hematopoietic cellularity and fibrosis grading, three hematopathologists independently evaluated a total of 728 bone marrow biopsies from 261 patients with myeloproliferative neoplasms on three clinical trials using fedratinib (SAR302503), a JAK2 inhibitor, including 249 taken at baseline and 479 on therapy. Concordance between the pathologists was evaluated by Pearson correlation coefficient (cellularity) and unweighted kappa statistic (fibrosis grade). There was high correlation of cellularity assessment (r = 0.92) and fibrosis grading (kappa = 0.83) between the three pathologists. Concordance with World Health Organization (WHO) grade 3 samples was higher compared with grades 0, 1, and 2. Concordance of fibrosis grading in pretreatment samples was superior to that of post-treatment samples (kappa = 0.83 and 0.79, respectively, P = 0.023). Our analysis suggests that the updated 2008 WHO reticulin fibrosis grading system is highly reproducible, even in patients undergoing JAK2 inhibitor therapy. This system is practically applicable to establish baseline fibrosis grade as well as changes in fibrosis in subsequent samples on therapy.
C1 [Pozdnyakova, Olga; Rodig, Scott J.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Wu, Kaida; Patki, Abhay] Sanofi Oncol, Cambridge, MA USA.
[Thiele, Juergen] Univ Cologne, D-50931 Cologne, Germany.
[Hasserjian, Robert P.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Hasserjian, RP (reprint author), Massachusetts Gen Hosp, Dept Pathol, WRN244,55 Fruit St, Boston, MA 02114 USA.
EM rhasserjian@partners.org
NR 51
TC 10
Z9 10
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
EI 1530-0285
J9 MODERN PATHOL
JI Mod. Pathol.
PD NOV
PY 2014
VL 27
IS 11
BP 1447
EP 1454
DI 10.1038/modpathol.2014.69
PG 8
WC Pathology
SC Pathology
GA AS7HW
UT WOS:000344428500003
PM 24762543
ER
PT J
AU Wood, AR
Esko, T
Yang, J
Vedantam, S
Pers, TH
Gustafsson, S
Chun, AY
Estrada, K
Luan, J
Kutalik, Z
Amin, N
Buchkovich, ML
Croteau-Chonka, DC
Day, FR
Duan, Y
Fall, T
Fehrmann, R
Ferreira, T
Jackson, AU
Karjalainen, J
Lo, KS
Locke, AE
Magi, R
Mihailov, E
Porcu, E
Randall, JC
Scherag, A
Vinkhuyzen, AAE
Westra, HJ
Winkler, TW
Workalemahu, T
Zhao, JH
Absher, D
Albrecht, E
Anderson, D
Baron, J
Beekman, M
Demirkan, A
Ehret, GB
Feenstra, B
Feitosa, MF
Fischer, K
Fraser, RM
Goel, A
Gong, J
Justice, AE
Kanoni, S
Kleber, ME
Kristiansson, K
Lim, U
Lotay, V
Lui, JC
Mangino, M
Leach, IM
Medina-Gomez, C
Nalls, MA
Nyholt, DR
Palmer, CD
Pasko, D
Pechlivanis, S
Prokopenko, I
Ried, JS
Ripke, S
Shungin, D
Stancakova, A
Strawbridge, RJ
Sung, YJ
Tanaka, T
Teumer, A
Trompet, S
van der Laan, SW
van Setten, J
Van Vliet-Ostaptchouk, JV
Wang, ZM
Yengo, L
Zhang, WH
Afzal, U
Arnlov, J
Arscott, GM
Bandinelli, S
Barrett, A
Bellis, C
Bennett, AJ
Berne, C
Bluher, M
Bolton, JL
Bottcher, Y
Boyd, HA
Bruinenberg, M
Buckley, BM
Buyske, S
Caspersen, IH
Chines, PS
Clarke, R
Claudi-Boehm, S
Cooper, M
Daw, EW
De Jong, PA
Deelen, J
Delgado, G
Denny, JC
Dhonukshe-Rutten, R
Dimitriou, M
Doney, ASF
Dorr, M
Eklund, N
Eury, E
Folkersen, L
Garcia, ME
Geller, F
Giedraitis, V
Go, AS
Grallert, H
Grammer, TB
Grassler, J
Gronberg, H
de Groot, LCPGM
Groves, CJ
Haessler, J
Hall, P
Haller, T
Hallmans, G
Hannemann, A
Hartman, CA
Hassinen, M
Hayward, C
Heard-Costa, NL
Helmer, Q
Hemani, G
Henders, AK
Hillege, HL
Hlatky, MA
Hoffmann, W
Hoffmann, P
Holmen, O
Houwing-Duistermaat, JJ
Illig, T
Isaacs, A
James, AL
Jeff, J
Johansen, B
Johansson, A
Jolley, J
Juliusdottir, T
Junttila, J
Kho, AN
Kinnunen, L
Klopp, N
Kocher, T
Kratzer, W
Lichtner, P
Lind, L
Lindstrom, J
Lobbens, S
Lorentzon, M
Lu, YC
Lyssenko, V
Magnusson, PKE
Mahajan, A
Maillard, M
McArdle, WL
McKenzie, CA
McLachlan, S
McLaren, PJ
Menni, C
Merger, S
Milani, L
Moayyeri, A
Monda, KL
Morken, MA
Muller, G
Muller-Nurasyid, M
Musk, AW
Narisu, N
Nauck, M
Nolte, IM
Nothen, MM
Oozageer, L
Pilz, S
Rayner, NW
Renstrom, F
Robertson, NR
Rose, LM
Roussel, R
Sanna, S
Scharnagl, H
Scholtens, S
Schumacher, FR
Schunkert, H
Scott, RA
Sehmi, J
Seufferlein, T
Shin, JX
Silventoinen, K
Smit, JH
Smith, AV
Smolonska, J
Stanton, AV
Stirrups, K
Stott, DJ
Stringham, HM
Sundstrom, J
Swertz, MA
Syvanen, AC
Tayo, BO
Thorleifsson, G
Tyrer, JP
van Dijk, S
van Schoor, NM
van der Velde, N
van Heemst, D
van Oort, FVA
Vermeulen, SH
Verweij, N
Vonk, JM
Waite, LL
Waldenberger, M
Wennauer, R
Wilkens, LR
Willenborg, C
Wilsgaard, T
Wojczynski, MK
Wong, A
Wright, AF
Zhang, QY
Arveiler, D
Bakker, SJL
Beilby, J
Bergman, RN
Bergmann, S
Biffar, R
Blangero, J
Boomsma, DI
Bornstein, SR
Bovet, P
Brambilla, P
Brown, MJ
Campbell, H
Caulfield, MJ
Chakravarti, A
Collins, R
Collins, FS
Crawford, DC
Cupples, LA
Danesh, J
de Faire, U
den Ruijter, HM
Erbel, R
Erdmann, J
Eriksson, JG
Farrall, M
Ferrannini, E
Ferrieres, J
Ford, I
Forouhi, NG
Forrester, T
Gansevoort, RT
Gejman, PV
Gieger, C
Golay, A
Gottesman, O
Gudnason, V
Gyllensten, U
Haas, DW
Hall, AS
Harris, TB
Hattersley, AT
Heath, AC
Hengstenberg, C
Hicks, AA
Hindorff, LA
Hingorani, AD
Hofman, A
Hovingh, GK
Humphries, SE
Hunt, SC
Hypponen, E
Jacobs, KB
Jarvelin, MR
Jousilahti, P
Jula, AM
Kaprio, J
Kastelein, JJP
Kayser, M
Kee, F
Keinanen-Kiukaanniemi, SM
Kiemeney, LA
Kooner, JS
Kooperberg, C
Koskinen, S
Kovacs, P
Kraja, AT
Kumari, M
Kuusisto, J
Lakka, TA
Langenberg, C
Le Marchand, L
Lehtimaki, T
Lupoli, S
Madden, PAF
Mannisto, S
Manunta, P
Marette, A
Matise, TC
McKnight, B
Meitinger, T
Moll, FL
Montgomery, GW
Morris, AD
Morris, AP
Murray, JC
Nelis, M
Ohlsson, C
Oldehinkel, AJ
Ong, KK
Ouwehand, WH
Pasterkamp, G
Peters, A
Pramstaller, PP
Price, JF
Qi, L
Raitakari, OT
Rankinen, T
Rao, DC
Rice, TK
Ritchie, M
Rudan, I
Salomaa, V
Samani, NJ
Saramies, J
Sarzynski, MA
Schwarz, PEH
Sebert, S
Sever, P
Shuldiner, AR
Sinisalo, J
Steinthorsdottir, V
Stolk, RP
Tardif, JC
Tonjes, A
Tremblay, A
Tremoli, E
Virtamo, J
Vohl, MC
Amouyel, P
Asselbergs, FW
Assimes, TL
Bochud, M
Boehm, BO
Boerwinkle, E
Bottinger, EP
Bouchard, C
Cauchi, S
Chambers, JC
Chanock, SJ
Cooper, RS
de Bakker, PIW
Dedoussis, G
Ferrucci, L
Franks, PW
Froguel, P
Groop, LC
Haiman, CA
Hamsten, A
Hayes, MG
Hui, J
Hunter, DJ
Hveem, K
Jukema, JW
Kaplan, RC
Kivimaki, M
Kuh, D
Laakso, M
Liu, YM
Martin, NG
Marz, W
Melbye, M
Moebus, S
Munroe, PB
Njolstad, I
Oostra, BA
Palmer, CNA
Pedersen, NL
Perola, M
Perusse, L
Peters, U
Powell, JE
Power, C
Quertermous, T
Rauramaa, R
Reinmaa, E
Ridker, PM
Rivadeneira, F
Rotter, JI
Saaristo, TE
Saleheen, D
Schlessinger, D
Slagboom, PE
Snieder, H
Spector, TD
Strauch, K
Stumvoll, M
Tuomilehto, J
Uusitupa, M
van der Harst, P
Volzke, H
Walker, M
Wareham, NJ
Watkins, H
Wichmann, HE
Wilson, JF
Zanen, P
Deloukas, P
Heid, IM
Lindgren, CM
Mohlke, KL
Speliotes, EK
Thorsteinsdottir, U
Barroso, I
Fox, CS
North, KE
Strachan, DP
Beckmann, JS
Berndt, SI
Boehnke, M
Borecki, IB
McCarthy, MI
Metspalu, A
Stefansson, K
Uitterlinden, AG
van Duijn, CM
Franke, L
Willer, CJ
Price, AL
Lettre, G
Loos, RJF
Weedon, MN
Ingelsson, E
O'Connell, JR
Abecasis, GR
Chasman, DI
Goddard, ME
Visscher, PM
Hirschhorn, JN
Frayling, TM
AF Wood, Andrew R.
Esko, Tonu
Yang, Jian
Vedantam, Sailaja
Pers, Tune H.
Gustafsson, Stefan
Chun, Audrey Y.
Estrada, Karol
Luan, Jian'an
Kutalik, Zoltan
Amin, Najaf
Buchkovich, Martin L.
Croteau-Chonka, Damien C.
Day, Felix R.
Duan, Yanan
Fall, Tove
Fehrmann, Rudolf
Ferreira, Teresa
Jackson, Anne U.
Karjalainen, Juha
Lo, Ken Sin
Locke, Adam E.
Maegi, Reedik
Mihailov, Evelin
Porcu, Eleonora
Randall, Joshua C.
Scherag, Andre
Vinkhuyzen, Anna A. E.
Westra, Harm-Jan
Winkler, Thomas W.
Workalemahu, Tsegaselassie
Zhao, Jing Hua
Absher, Devin
Albrecht, Eva
Anderson, Denise
Baron, Jeffrey
Beekman, Marian
Demirkan, Ayse
Ehret, Georg B.
Feenstra, Bjarke
Feitosa, Mary F.
Fischer, Krista
Fraser, Ross M.
Goel, Anuj
Gong, Jian
Justice, Anne E.
Kanoni, Stavroula
Kleber, Marcus E.
Kristiansson, Kati
Lim, Unhee
Lotay, Vaneet
Lui, Julian C.
Mangino, Massimo
Leach, Irene Mateo
Medina-Gomez, Carolina
Nalls, Michael A.
Nyholt, Dale R.
Palmer, Cameron D.
Pasko, Dorota
Pechlivanis, Sonali
Prokopenko, Inga
Ried, Janina S.
Ripke, Stephan
Shungin, Dmitry
Stancakova, Alena
Strawbridge, Rona J.
Sung, Yun Ju
Tanaka, Toshiko
Teumer, Alexander
Trompet, Stella
van der Laan, Sander W.
van Setten, Jessica
Van Vliet-Ostaptchouk, Jana V.
Wang, Zhaoming
Yengo, Loic
Zhang, Weihua
Afzal, Uzma
Arnloev, Johan
Arscott, Gillian M.
Bandinelli, Stefania
Barrett, Amy
Bellis, Claire
Bennett, Amanda J.
Berne, Christian
Blueher, Matthias
Bolton, Jennifer L.
Boettcher, Yvonne
Boyd, Heather A.
Bruinenberg, Marcel
Buckley, Brendan M.
Buyske, Steven
Caspersen, Ida H.
Chines, Peter S.
Clarke, Robert
Claudi-Boehm, Simone
Cooper, Matthew
Daw, E. Warwick
De Jong, Pim A.
Deelen, Joris
Delgado, Graciela
Denny, Josh C.
Dhonukshe-Rutten, Rosalie
Dimitriou, Maria
Doney, Alex S. F.
Doerr, Marcus
Eklund, Niina
Eury, Elodie
Folkersen, Lasse
Garcia, Melissa E.
Geller, Frank
Giedraitis, Vilmantas
Go, Alan S.
Grallert, Harald
Grammer, Tanja B.
Graessler, Juergen
Groenberg, Henrik
de Groot, Lisette C. P. G. M.
Groves, Christopher J.
Haessler, Jeffrey
Hall, Per
Haller, Toomas
Hallmans, Goran
Hannemann, Anke
Hartman, Catharina A.
Hassinen, Maija
Hayward, Caroline
Heard-Costa, Nancy L.
Helmer, Quinta
Hemani, Gibran
Henders, Anjali K.
Hillege, Hans L.
Hlatky, Mark A.
Hoffmann, Wolfgang
Hoffmann, Per
Holmen, Oddgeir
Houwing-Duistermaat, Jeanine J.
Illig, Thomas
Isaacs, Aaron
James, Alan L.
Jeff, Janina
Johansen, Bent
Johansson, Asa
Jolley, Jennifer
Juliusdottir, Thorhildur
Junttila, Juhani
Kho, Abel N.
Kinnunen, Leena
Klopp, Norman
Kocher, Thomas
Kratzer, Wolfgang
Lichtner, Peter
Lind, Lars
Lindstroem, Jaana
Lobbens, Stephane
Lorentzon, Mattias
Lu, Yingchang
Lyssenko, Valeriya
Magnusson, Patrik K. E.
Mahajan, Anubha
Maillard, Marc
McArdle, Wendy L.
McKenzie, Colin A.
McLachlan, Stela
McLaren, Paul J.
Menni, Cristina
Merger, Sigrun
Milani, Lili
Moayyeri, Alireza
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Morken, Mario A.
Mueller, Gabriele
Mueller-Nurasyid, Martina
Musk, Arthur W.
Narisu, Narisu
Nauck, Matthias
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Farrall, Martin
Ferrannini, Ele
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Forrester, Terrence
Gansevoort, Ron T.
Gejman, Pablo V.
Gieger, Christian
Golay, Alain
Gottesman, Omri
Gudnason, Vilmundur
Gyllensten, Ulf
Haas, David W.
Hall, Alistair S.
Harris, Tamara B.
Hattersley, Andrew T.
Heath, Andrew C.
Hengstenberg, Christian
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Hingorani, Aroon D.
Hofman, Albert
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Humphries, Steve E.
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Hypponen, Elina
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Jarvelin, Marjo-Riitta
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Kaprio, Jaakko
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Kayser, Manfred
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Keinanen-Kiukaanniemi, Sirkka M.
Kiemeney, Lambertus A.
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Kooperberg, Charles
Koskinen, Seppo
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Kivimaki, Mika
Kuh, Diana
Laakso, Markku
Liu, Yongmei
Martin, Nicholas G.
Maerz, Winfried
Melbye, Mads
Moebus, Susanne
Munroe, Patricia B.
Njolstad, Inger
Oostra, Ben A.
Palmer, Colin N. A.
Pedersen, Nancy L.
Perola, Markus
Perusse, Louis
Peters, Ulrike
Powell, Joseph E.
Power, Chris
Quertermous, Thomas
Rauramaa, Rainer
Reinmaa, Eva
Ridker, Paul M.
Rivadeneira, Fernando
Rotter, Jerome I.
Saaristo, Timo E.
Saleheen, Danish
Schlessinger, David
Slagboom, P. Eline
Snieder, Harold
Spector, Tim D.
Strauch, Konstantin
Stumvoll, Michael
Tuomilehto, Jaakko
Uusitupa, Matti
van der Harst, Pim
Voelzke, Henry
Walker, Mark
Wareham, Nicholas J.
Watkins, Hugh
Wichmann, H-Erich
Wilson, James F.
Zanen, Pieter
Deloukas, Panos
Heid, Iris M.
Lindgren, Cecilia M.
Mohlke, Karen L.
Speliotes, Elizabeth K.
Thorsteinsdottir, Unnur
Barroso, Ines
Fox, Caroline S.
North, Kari E.
Strachan, David P.
Beckmann, Jacques S.
Berndt, Sonja I.
Boehnke, Michael
Borecki, Ingrid B.
McCarthy, Mark I.
Metspalu, Andres
Stefansson, Kari
Uitterlinden, Andre G.
van Duijn, Cornelia M.
Franke, Lude
Willer, Cristen J.
Price, Alkes L.
Lettre, Guillaume
Loos, Ruth J. F.
Weedon, Michael N.
Ingelsson, Erik
O'Connell, Jeffrey R.
Abecasis, Goncalo R.
Chasman, Daniel I.
Goddard, Michael E.
Visscher, Peter M.
Hirschhorn, Joel N.
Frayling, Timothy M.
CA Elect Med Records & Genom eMERGE C
MIGen Consortium
PAGE Consortium
LifeLines Cohort Study
TI Defining the role of common variation in the genomic and biological
architecture of adult human height
SO NATURE GENETICS
LA English
DT Article
ID GENETIC-VARIATION; COMPLEX TRAITS; HERITABILITY; MUTATIONS; SNPS
AB Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated similar to 2,000, similar to 3,700 and similar to 9,500 SNPs explained similar to 21%, similar to 24% and similar to 29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/beta-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.
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[Doney, Alex S. F.; Morris, Andrew D.; Palmer, Colin N. A.] Univ Dundee, Ninewells Hosp, Med Res Inst, Dundee, Scotland.
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[Graessler, Juergen; Bornstein, Stefan R.; Schwarz, Peter E. H.] Tech Univ Dresden, Univ Hosp Carl Gustav Carus, Dept Med 3, D-01062 Dresden, Germany.
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[Bovet, Pascal; Bochud, Murielle] Univ Lausanne, Lausanne, Switzerland.
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[Brambilla, Paolo] Univ Milan, Hosp Desio, Dept Hlth Sci, Bicocca, Italy.
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[Jarvelin, Marjo-Riitta] Oulu Univ Hosp, Unit Primary Care, Oulu, Finland.
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[Kooner, Jaspal S.; Chambers, John C.] Imperial Coll Healthcare NHS Trust, London, England.
[Kooner, Jaspal S.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England.
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[Lupoli, Sara] Fdn Filarete, Milan, Italy.
[Manunta, Paolo] Ist Sci San Raffaele, Div Nephrol & Dialysis, I-20132 Milan, Italy.
[Manunta, Paolo] Univ Vita Salute San Raffaele, Milan, Italy.
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[Tremoli, Elena] IRCCS, Ctr Cardiol Monzmo, Milan, Italy.
[Vohl, Marie-Claude] Univ Laval, Dept Food Sci & Nutr, Quebec City, PQ, Canada.
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Univ London Imperial Coll Sci Technol & Med, Lee Kong Chian Sch Med, Singapore, Singapore.
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[Maerz, Winfried] Synlab Acad, Synlab Serv, Mannheim, Germany.
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[Saaristo, Timo E.] Finnish Diabet Assoc, Tampere, Finland.
[Saaristo, Timo E.] Pirkanmaa Hosp Dist, Tampere, Finland.
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[Wichmann, H-Erich] Univ Munich, Inst Med Informat Biometry & Epidemiol, Chair Epidemiol, Munich, Germany.
[Walker, Mark; Wichmann, H-Erich] Univ Munich, Klinikum Grosshadern, D-80539 Munich, Germany.
[Wichmann, H-Erich] Helmholtz Zentrum Munchen, German Res Ctr Environm Hlth, Inst Epidemiol 1, Neuherberg, Germany.
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[Strachan, David P.] Univ London, Div Populat Hlth Sci & Educ, London, England.
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[Goddard, Michael E.] Univ Melbourne, Dept Food & Agr Syst, Melbourne, Vic, Australia.
RP Visscher, PM (reprint author), Univ Queensland, Queensland Brain Inst, Brisbane, Qld 4072, Australia.
EM peter.visscher@uq.edu.au; joelh@broadinstitute.org;
t.m.frayling@exeter.ac.uk
RI Beckmann, Jacques S /A-9772-2008; Yengo, Loic/D-2692-2017; Feitosa,
Mary/K-8044-2012; Hicks, Andrew/E-9518-2017; Hypponen,
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Mark/A-9798-2014; Lui, Chun Kin Julian/E-2253-2012; Fehrmann,
Rudolf/E-2551-2011; Darbar, Dawood/C-9079-2015; Boehm,
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Thomas/O-1318-2015; Rivadeneira, Fernando/O-5385-2015; Prokopenko,
Inga/H-3241-2014; Erdmann, Jeanette/P-7513-2014; Sundstrom,
Johan/A-6286-2009; Peters, Annette/A-6117-2011; Vermeulen,
H.H.M./L-4716-2015; Bovet, Pascal/F-4477-2011; Bouchard,
Claude/A-7637-2009; Rudan, Igor/I-1467-2012; Smith, Albert/K-5150-2015;
Nato, Alejandro/J-3880-2016; Yang, Jian/A-5852-2010; kinnunen,
leena/B-7059-2012; Study, GoDARTS/K-9448-2016; Bochud,
Murielle/A-3981-2010; mangino, massimo/F-5134-2011; Schwarz,
Peter/B-5127-2013; Ramos , Rafel/D-9627-2016; Franke, Lude/P-7036-2016;
Ormel, Johan/C-6094-2013; Wijmenga, Cisca/D-2173-2009; Karjalainen,
Juha/P-8624-2016; Slagboom, P. Eline/R-4790-2016; Wong,
Andrew/M-8899-2016; Verweij, Niek/A-4499-2017; Magnusson,
Patrik/C-4458-2017
OI Beckmann, Jacques S /0000-0002-9741-1900; Yengo,
Loic/0000-0002-4272-9305; Feitosa, Mary/0000-0002-0933-2410; Hicks,
Andrew/0000-0001-6320-0411; Franks, Paul/0000-0002-0520-7604; Scherag,
Andre/0000-0002-9406-4704; Manunta, Paolo/0000-0003-3976-9696; Shungin,
Dmitry/0000-0001-7900-5856; Stanton, Alice/0000-0002-4961-165X; Day,
Felix/0000-0003-3789-7651; Magi, Reedik/0000-0002-2964-6011; van der
Velde, Nathalie/0000-0002-6477-6209; Moayyeri,
Alireza/0000-0002-9143-2161; Deelen, Joris/0000-0003-4483-3701; van
Vliet-Ostaptchouk, Jana/0000-0002-7943-3153; Cooper,
Matthew/0000-0003-1139-3682; Kristiansson, Kati/0000-0003-4688-107X;
Asselta, Rosanna/0000-0001-5351-0619; Bush, William/0000-0002-9729-6519;
Ramos , Rafel/0000-0001-7970-5537; Menni, Cristina/0000-0001-9790-0571;
Goddard, Michael/0000-0001-9917-7946; TREMOLI,
ELENA/0000-0002-0929-6106; Sinisalo, Juha/0000-0002-0169-5137; Kleber,
Marcus/0000-0003-0663-7275; Martin, Nicholas/0000-0003-4069-8020;
Hypponen, Elina/0000-0003-3670-9399; Kiemeney,
Lambertus/0000-0002-2368-1326; EHRET, Georg/0000-0002-5730-0675; Palmer,
Colin/0000-0002-6415-6560; Strawbridge, Rona/0000-0001-8506-3585; de
Bakker, Paul/0000-0001-7735-7858; Fehrmann, Rudolf/0000-0002-7516-315X;
Darbar, Dawood/0000-0002-4103-5977; de Jong, Pim/0000-0003-4840-6854;
Bakker, Stephan/0000-0003-3356-6791; Gudnason,
Vilmundur/0000-0001-5696-0084; Wilson, James F/0000-0001-5751-9178;
Montgomery, Grant/0000-0002-4140-8139; Deloukas,
Panos/0000-0001-9251-070X; Rivadeneira, Fernando/0000-0001-9435-9441;
Prokopenko, Inga/0000-0003-1624-7457; Medina-Gomez,
Carolina/0000-0001-7999-5538; Visscher, Peter/0000-0002-2143-8760;
Eriksson, Johan/0000-0002-2516-2060; Assimes,
Themistocles/0000-0003-2349-0009; Ouwehand, Willem/0000-0002-7744-1790;
Kaprio, Jaakko/0000-0002-3716-2455; Johansson, Asa/0000-0002-2915-4498;
Hattersley, Andrew/0000-0001-5620-473X; Bergmann,
Sven/0000-0002-6785-9034; Forouhi, Nita/0000-0002-5041-248X; Jarvelin,
Marjo-Riitta/0000-0002-2149-0630; Nothen, Markus/0000-0002-8770-2464;
Buyske, Steven/0000-0001-8539-5416; Watkins, Hugh/0000-0002-5287-9016;
Vinkhuyzen, Anna/0000-0003-3352-0603; Mannisto,
Satu/0000-0002-8668-3046; Lakka, Timo/0000-0002-9199-2871; Folkersen,
Lasse/0000-0003-0708-9530; van der Laan, Sander W./0000-0001-6888-1404;
Humphries, Stephen E/0000-0002-8221-6547; Gieger,
Christian/0000-0001-6986-9554; Kumari, Meena/0000-0001-9716-1035;
Verweij, Niek/0000-0002-4303-7685; Wolffenbuttel, Bruce
H.R./0000-0001-9262-6921; sanna, serena/0000-0002-3768-1749; Fraser,
Ross/0000-0003-0488-2592; Beekman, Marian/0000-0003-0585-6206; Esko,
Tonu/0000-0003-1982-6569; Locke, Adam/0000-0001-6227-198X; Erdmann,
Jeanette/0000-0002-4486-6231; Sundstrom, Johan/0000-0003-2247-8454;
Bovet, Pascal/0000-0002-0242-4259; Rudan, Igor/0000-0001-6993-6884;
Smith, Albert/0000-0003-1942-5845; Nato, Alejandro/0000-0002-8745-9046;
Yang, Jian/0000-0003-2001-2474; kinnunen, leena/0000-0001-8739-4812;
Bochud, Murielle/0000-0002-5727-0218; mangino,
massimo/0000-0002-2167-7470; Schwarz, Peter/0000-0001-6317-7880; Ramos ,
Rafel/0000-0001-8146-5288; Franke, Lude/0000-0002-5159-8802; Slagboom,
P. Eline/0000-0002-2875-4723; Wong, Andrew/0000-0003-2079-4779;
FU British Heart Foundation [FS/11/35/28871, FS/12/33/29561, FS/12/8/29377,
FS/14/12/30540, PG/07/085/23349, RG/08/008/25291, RG/08/014/24067,
RG/09/012/28096, RG/10/12/28456, SP/08/002/24118]; Chief Scientist
Office [CZB/4/672, CZB/4/710]; Department of Health [RP-PG-0310-1002];
European Research Council [323195]; Medical Research Council
[MC_UU_12015/2, G0500070, G0601463, G1002084, MC_PC_U127561128,
MC_U106179471, MC_U106179472, MC_UP_A100_1003, MC_UU_12015/1,
MC_UU_12015/5, MC_UU_12019/1, MR/K006584/1, MR/K013351/1, MR/L003120/1,
MR/L01629X/1]; NCATS NIH HHS [UL1 TR000124]; NCI NIH HHS [P30 CA015704,
P30 CA071789]; NHGRI NIH HHS [U01 HG007419]; NHLBI NIH HHS [R01
HL109946, R01 HL117626, T32 HL007055]; NICHD NIH HHS [P30 HD018655];
NIDDK NIH HHS [P30 DK063491, P30 DK072488, R01 DK072193, R01 DK075787,
R01 DK093757, U01 DK062370]; NIGMS NIH HHS [P01 GM099568, P30 GM103341,
R01 GM075091, T32 GM080178]; Wellcome Trust [085301, 090532, 098381,
098395]
NR 21
TC 296
Z9 299
U1 28
U2 179
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD NOV
PY 2014
VL 46
IS 11
BP 1173
EP 1186
DI 10.1038/ng.3097
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA AS2TI
UT WOS:000344131900008
PM 25282103
ER
PT J
AU Xu, P
Zhang, XF
Wang, XM
Li, JT
Liu, GM
Kuang, YY
Xu, J
Zheng, XH
Ren, LF
Wang, GL
Zhang, Y
Huo, LH
Zhao, ZX
Cao, DC
Lu, CY
Li, C
Zhou, Y
Liu, ZJ
Fan, ZH
Shan, GL
Li, XG
Wu, SX
Song, LP
Hou, GY
Jiang, YL
Jeney, Z
Yu, D
Wang, L
Shao, CJ
Song, L
Sun, J
Ji, PF
Wang, J
Li, Q
Xu, LM
Sun, FY
Feng, JX
Wang, CH
Wang, SL
Wang, BS
Li, Y
Zhu, YP
Xue, W
Zhao, L
Wang, JT
Gu, Y
Lv, WH
Wu, KJ
Xiao, JF
Wu, JY
Zhang, Z
Yu, J
Sun, XW
AF Xu, Peng
Zhang, Xiaofeng
Wang, Xumin
Li, Jiongtang
Liu, Guiming
Kuang, Youyi
Xu, Jian
Zheng, Xianhu
Ren, Lufeng
Wang, Guoliang
Zhang, Yan
Huo, Linhe
Zhao, Zixia
Cao, Dingchen
Lu, Cuiyun
Li, Chao
Zhou, Yi
Liu, Zhanjiang
Fan, Zhonghua
Shan, Guangle
Li, Xingang
Wu, Shuangxiu
Song, Lipu
Hou, Guangyuan
Jiang, Yanliang
Jeney, Zsigmond
Yu, Dan
Wang, Li
Shao, Changjun
Song, Lai
Sun, Jing
Ji, Peifeng
Wang, Jian
Li, Qiang
Xu, Liming
Sun, Fanyue
Feng, Jianxin
Wang, Chenghui
Wang, Shaolin
Wang, Baosen
Li, Yan
Zhu, Yaping
Xue, Wei
Zhao, Lan
Wang, Jintu
Gu, Ying
Lv, Weihua
Wu, Kejing
Xiao, Jingfa
Wu, Jiayan
Zhang, Zhang
Yu, Jun
Sun, Xiaowen
TI Genome sequence and genetic diversity of the common carp, Cyprinus
carpio
SO NATURE GENETICS
LA English
DT Article
ID LINKAGE MAP; MICROSATELLITE LOCI; TELEOST FISH; HOX CLUSTERS; EVOLUTION;
DUPLICATION; L.; DIVERSIFICATION; PIGMENTATION; ANNOTATION
AB The common carp, Cyprinus carpio, is one of the most important cyprinid species and globally accounts for 10% of freshwater aquaculture production. Here we present a draft genome of domesticated C. carpio (strain Songpu), whose current assembly contains 52,610 protein-coding genes and approximately 92.3% coverage of its paleotetraploidized genome (2n = 100). The latest round of whole-genome duplication has been estimated to have occurred approximately 8.2 million years ago. Genome resequencing of 33 representative individuals from worldwide populations demonstrates a single origin for C. carpio in 2 subspecies (C. carpio Haematopterus and C. carpio carpio). Integrative genomic and transcriptomic analyses were used to identify loci potentially associated with traits including scaling patterns and skin color. In combination with the high-resolution genetic map, the draft genome paves the way for better molecular studies and improved genome-assisted breeding of C. carpio and other closely related species.
C1 [Xu, Peng; Li, Jiongtang; Xu, Jian; Zhang, Yan; Zhao, Zixia; Liu, Zhanjiang; Hou, Guangyuan; Jiang, Yanliang; Ji, Peifeng; Wang, Jian; Li, Qiang; Xu, Liming; Wang, Baosen; Li, Yan; Zhu, Yaping; Xue, Wei; Zhao, Lan; Wang, Jintu; Sun, Xiaowen] Chinese Acad Fishery Sci, Ctr Appl Aquat Genom, Beijing, Peoples R China.
[Zhang, Xiaofeng; Kuang, Youyi; Zheng, Xianhu; Cao, Dingchen; Lu, Cuiyun; Li, Chao; Gu, Ying; Lv, Weihua; Sun, Xiaowen] Chinese Acad Fishery Sci, Heilongjiang River Fisheries Res Inst, Harbin, Peoples R China.
[Wang, Xumin; Liu, Guiming; Ren, Lufeng; Wang, Guoliang; Huo, Linhe; Fan, Zhonghua; Shan, Guangle; Li, Xingang; Wu, Shuangxiu; Song, Lipu; Yu, Dan; Wang, Li; Shao, Changjun; Song, Lai; Sun, Jing; Wu, Kejing; Xiao, Jingfa; Wu, Jiayan; Zhang, Zhang; Yu, Jun] Chinese Acad Sci, Key Lab Genome Sci & Informat, Beijing Inst Genom, Beijing, Peoples R China.
[Zhou, Yi] Harvard Univ, Sch Med, Stem Cell Program, Div Hematol & Oncol,Boston Childrens Hosp, Boston, MA USA.
[Zhou, Yi] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Liu, Zhanjiang; Sun, Fanyue] Auburn Univ, Dept Fisheries & Allied Aquacultures, Fish Mol Genet & Biotechnol Lab, Auburn, AL 36849 USA.
[Jeney, Zsigmond] Res Inst Fisheries Aquaculture & Irrigat, Szarvas, Hungary.
[Feng, Jianxin] Henan Acad Fishery Sci, Zhengzhou, Peoples R China.
[Wang, Chenghui] Shanghai Ocean Univ, Coll Fisheries & Life Sci, Shanghai, Peoples R China.
[Wang, Shaolin] Univ Virginia, Dept Psychiat & Neurobiol Sci, Charlottesville, VA USA.
RP Sun, XW (reprint author), Chinese Acad Fishery Sci, Ctr Appl Aquat Genom, Beijing, Peoples R China.
EM junyu@big.ac.cn; sunxw@cafs.ac.cn
RI Xu, Peng/J-4018-2012; Wang, Shaolin/M-2282-2013
OI Wang, Shaolin/0000-0003-0866-4584
FU National High-Technology Research and Development Program of China (863
program) [2011AA100401, 2011AA100402, 2009AA10Z105]; National Department
Public Benefit Research Foundation of China [200903045]; National Basic
Research Program of China (973 Program) [2010CB126305]; National Natural
Science Foundation of China [31302174, 31101893]; Special Scientific
Research Funds for Central Non-Profit Institutes of the Chinese Academy
of Fishery Sciences [2009B002, 2011C016]
FX We acknowledge Z. Zhu, N. Li, J. Gui, Z. Bao, G. Zhang, X.L. Zhang, J.
Li, Y. Liu, Q. Liu and S. Chen for their support on the common carp
genome project. We thank H. Hu, G.Z. Liu, J.H. Yu and C.J. Li for their
assistance in sample collection and Y. Wan, T. Sun, W. Liu, L. Jiang,
Shu Wang, Y. Zhu, X. Xing, P. Zhou and R. Cut for genotyping and
sequencing. We thank J. Postlethwait, G. Hulata, L. David, L. Orban and
F. Zhao for their helpful discussions. We acknowledge grant support from
the National High-Technology Research and Development Program of China
(863 program; 2011AA100401,2011AA100402 and 2009AA10Z105), the National
Department Public Benefit Research Foundation of China (200903045), the
National Basic Research Program of China (973 Program; 2010CB126305),
the National Natural Science Foundation of China (31302174 and 31101893)
and Special Scientific Research Funds for Central Non-Profit Institutes
of the Chinese Academy of Fishery Sciences (2009B002 and 2011C016).
NR 43
TC 80
Z9 88
U1 16
U2 92
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD NOV
PY 2014
VL 46
IS 11
BP 1212
EP 1219
DI 10.1038/ng.3098
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA AS2TI
UT WOS:000344131900012
PM 25240282
ER
PT J
AU Cox, AD
Fesik, SW
Kimmelman, AC
Luo, J
Der, CJ
AF Cox, Adrienne D.
Fesik, Stephen W.
Kimmelman, Alec C.
Luo, Ji
Der, Channing J.
TI Drugging the undruggable RAS: Mission Possible?
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Review
ID PANCREATIC TUMOR-GROWTH; ONCOGENIC K-RAS; INDUCED MYELOPROLIFERATIVE
DISEASE; SYNTHETIC LETHAL INTERACTIONS; MEDIATED NUCLEOTIDE EXCHANGE;
SMALL-MOLECULE INHIBITION; SQUAMOUS-CELL CARCINOMAS; INDUCED
LUNG-CANCER; IN-VIVO; FARNESYLTHIOSALICYLIC ACID
AB Despite more than three decades of intensive effort, no effective pharmacological inhibitors of the RAS oncoproteins have reached the clinic, prompting the widely held perception that RAS proteins are 'undruggable'. However, recent data from the laboratory and the clinic have renewed our hope for the development of RAS-inhibitory molecules. In this Review, we summarize the progress and the promise of five key approaches. Firstly, we focus on the prospects of using direct inhibitors of RAS. Secondly, we address the issue of whether blocking RAS membrane association is a viable approach. Thirdly, we assess the status of targeting RAS downstream effector signalling, which is arguably the most favourable current approach. Fourthly, we address whether the search for synthetic lethal interactors of mutant RAS still holds promise. Finally, RAS-mediated changes in cell metabolism have recently been described and we discuss whether these changes could be exploited for new therapeutic directions. We conclude with perspectives on how additional complexities, which are not yet fully understood, may affect each of these approaches.
C1 [Cox, Adrienne D.; Der, Channing J.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Fesik, Stephen W.] Vanderbilt Univ, Sch Med, Nashville, TN 37232 USA.
[Kimmelman, Alec C.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Luo, Ji] NCI, Bethesda, MD 20892 USA.
RP Der, CJ (reprint author), Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
EM cjder@med.unc.edu
FU US National Institutes of Health (NIH) [CA042978, CA179193, CA175747];
Lustgarten Foundation for Pancreatic Cancer Research, USA; Pancreatic
Cancer Action Network-American Association for Cancer Research; NIH [DPI
OD006933/DP1CA174419, P50A095103-12, RC2CA148375, R01 CA157490];
Lustgarten Foundation for Pancreatic Cancer Research; American Cancer
Society Research Scholar Grant [RSG-13-298-01-TBG]; Lustgarten
Foundation; US National Cancer Institute Intramural Program
FX The work of C.J.D. and A.D.C. is supported by US National Institutes of
Health (NIH) grants CA042978, CA179193 and CA175747, and by grants from
the Lustgarten Foundation for Pancreatic Cancer Research, USA, and the
Pancreatic Cancer Action Network-American Association for Cancer
Research. The work of S.W.F. is supported by NIH grants DPI
OD006933/DP1CA174419 (NIH Director's Pioneer Award; S.W F.),
P50A095103-12 (NCI SPORE in GI Cancer; R. J. Coffey), and RC2CA148375
(NIH ARRA Stimulus Grant; L. J. Marnett), and by the Lustgarten
Foundation for Pancreatic Cancer Research. The work of A.C.K. is
supported by NIH grant R01 CA157490, American Cancer Society Research
Scholar Grant RSG-13-298-01-TBG and by the Lustgarten Foundation. A.C.K.
is a consultant for Forma Therapeutics. The work of J.L. is supported by
the US National Cancer Institute Intramural Program.
NR 230
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U1 13
U2 92
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1776
EI 1474-1784
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD NOV
PY 2014
VL 13
IS 11
BP 828
EP 851
DI 10.1038/nrd4389
PG 24
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA AS4AR
UT WOS:000344216500027
PM 25323927
ER
PT J
AU Meyer, CA
Liu, XS
AF Meyer, Clifford A.
Liu, X. Shirley
TI Identifying and mitigating bias in next-generation sequencing methods
for chromatin biology
SO NATURE REVIEWS GENETICS
LA English
DT Review
ID CHIP-SEQ DATA; DIFFERENTIAL EXPRESSION ANALYSIS; ALLELE-SPECIFIC
EXPRESSION; DNA-BINDING PROTEINS; SHORT READ ALIGNMENT; HI-C DATA;
TRANSCRIPTION FACTORS; QUALITY-CONTROL; HUMAN GENOME; GENE-EXPRESSION
AB Next-generation sequencing (NGS) technologies have been used in diverse ways to investigate various aspects of chromatin biology by identifying genomic loci that are bound by transcription factors, occupied by nucleosomes or accessible to nuclease cleavage, or loci that physically interact with remote genomic loci. However, reaching sound biological conclusions from such NGS enrichment profiles requires many potential biases to be taken into account. In this Review, we discuss common ways in which biases may be introduced into NGS chromatin profiling data, approaches to diagnose these biases and analytical techniques to mitigate their effect.
C1 [Meyer, Clifford A.] Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
Dana Farber Canc Inst, Ctr Funct Canc Epigenet, Boston, MA 02215 USA.
RP Meyer, CA (reprint author), Dana Farber Canc Inst, Dept Biostat & Computat Biol, Boston, MA 02115 USA.
EM cliff@research.dfci.harvard.edu; xsliu@jimmy.harvard.edu
FU US National Institutes of Health [R01GM099409]
FX The authors thank members of X.S.L and M. Brown's laboratories for their
discussions. This work is supported by the US National Institutes of
Health grant R01GM099409.
NR 117
TC 43
Z9 43
U1 9
U2 57
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-0056
EI 1471-0064
J9 NAT REV GENET
JI Nat. Rev. Genet.
PD NOV
PY 2014
VL 15
IS 11
BP 709
EP 721
DI 10.1038/nrg3788
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA AS1CI
UT WOS:000344014300008
PM 25223782
ER
PT J
AU Kambayashi, T
Laufer, TM
AF Kambayashi, Taku
Laufer, Terri M.
TI Atypical MHC class II-expressing antigen-presenting cells: can anything
replace a dendritic cell?
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Review
ID CD4(+) T-CELLS; INNATE LYMPHOID-CELLS; INTESTINAL EPITHELIAL-CELLS;
ALLERGIC AIRWAY INFLAMMATION; HELPER TYPE-2 RESPONSE; HUMAN MAST-CELLS;
FC-EPSILON-RI; IN-VIVO; HUMAN EOSINOPHILS; IL-4 PRODUCTION
AB Dendritic cells, macrophages and B cells are regarded as the classical antigen-presenting cells of the immune system. However, in recent years, there has been a rapid increase in the number of cell types that are suggested to present antigens on MHC class II molecules to CD4(+) T cells. In this Review, we describe the key characteristics that define an antigen-presenting cell by examining the functions of dendritic cells. We then examine the functions of the haematopoietic cells and non-haematopoietic cells that can express MHC class II molecules and that have been suggested to represent 'atypical' antigen-presenting cells. We consider whether any of these cell populations can prime naive CD4(+) T cells and, if not, question the effects that they do have on the development of immune responses.
C1 [Kambayashi, Taku] Univ Penn, Dept Pathol & Lab Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Kambayashi, Taku] Univ Penn, Div Rheumatol, Perelman Sch Med, Dept Med, Philadelphia, PA 19104 USA.
[Laufer, Terri M.] Philadelphia Vet Affairs Med Ctr, Philadelphia, PA 19104 USA.
RP Laufer, TM (reprint author), Philadelphia Vet Affairs Med Ctr, Philadelphia, PA 19104 USA.
EM tlaufer@mail.med.upenn.edu
FU VA Merit Award; US National Institutes of Health; American Asthma
Foundation
FX Work in the laboratory of T.M.L. is supported by a VA Merit Award.
Research in the laboratory of T.K. is supported by funding from the US
National Institutes of Health and the American Asthma Foundation.
NR 159
TC 49
Z9 49
U1 5
U2 33
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1733
EI 1474-1741
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD NOV
PY 2014
VL 14
IS 11
BP 719
EP 730
DI 10.1038/nri3754
PG 12
WC Immunology
SC Immunology
GA AS8BQ
UT WOS:000344475800008
PM 25324123
ER
PT J
AU Fishman, JA
Grossi, PA
AF Fishman, Jay A.
Grossi, Paolo A.
TI Donor-derived infection-the challenge for transplant safety
SO NATURE REVIEWS NEPHROLOGY
LA English
DT Review
ID SOLID-ORGAN TRANSPLANTATION; WEST-NILE-VIRUS;
HUMAN-IMMUNODEFICIENCY-VIRUS; HEPATITIS-C VIRUS; COMMERCIAL
RENAL-TRANSPLANTATION; MUSCULOSKELETAL TISSUE DONORS; (KPC)-PRODUCING K.
PNEUMONIAE; TRANSMITTED VIRAL-INFECTIONS; GRAM-NEGATIVE BACTERIA;
UNITED-STATES
AB Organ transplantation, including of the heart, lung, kidney, liver, pancreas, and small bowel, is considered the therapy of choice for end-stage organ failure. Each year, over 70,000 organs are implanted worldwide. One donor may provide multiple organs, as well as corneas and other tissues, for multiple recipients. The degree of risk for transmission of infection carried with grafts, notably of viruses, is largely unknown and, for a specific organ, difficult to assess. The approach to microbiological screening of organ donors varies with national and regional regulations and with the availability and performance of microbiological assays used for potential donors. Transmission of both expected or common, and unexpected infections has been observed in organ transplants, generally recognized after development of clusters of infections among recipients of organs from a common donor. Other than for unusual or catastrophic events, few data exist that define the incidence and manifestations of donor-derived infections or the ideal assays to use in screening to prevent such transmissions. Absolute prevention of the transmission of donor-derived infections in organ transplantation is not possible. However, improvements in screening technologies will enhance the safety of transplantation in the future.
C1 [Fishman, Jay A.] Massachusetts Gen Hosp, Div Infect Dis, Transplant Infect Dis Program, Boston, MA 02114 USA.
[Fishman, Jay A.] Massachusetts Gen Hosp, MGH Transplantat Ctr, Boston, MA 02114 USA.
[Fishman, Jay A.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Grossi, Paolo A.] Univ Insubria, Natl Ctr Transplantat, Infect & Trop Dis Dept, I-21100 Varese, Italy.
RP Fishman, JA (reprint author), Massachusetts Gen Hosp, Div Infect Dis, Transplant Infect Dis Program, 55 Fruit St, Boston, MA 02114 USA.
EM jfishman@partners.org
NR 100
TC 4
Z9 5
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5061
EI 1759-507X
J9 NAT REV NEPHROL
JI Nat. Rev. Nephrol.
PD NOV
PY 2014
VL 10
IS 11
BP 663
EP 672
DI 10.1038/nrneph.2014.159
PG 10
WC Urology & Nephrology
SC Urology & Nephrology
GA AS0GH
UT WOS:000343955600010
PM 25178971
ER
PT J
AU Prabhakaran, S
Fonarow, GC
Smith, EE
Liang, L
Xian, Y
Neely, M
Peterson, ED
Schwamm, LH
AF Prabhakaran, Shyam
Fonarow, Gregg C.
Smith, Eric E.
Liang, Li
Xian, Ying
Neely, Megan
Peterson, Eric D.
Schwamm, Lee H.
TI Hospital Case Volume Is Associated With Mortality in Patients
Hospitalized With Subarachnoid Hemorrhage
SO NEUROSURGERY
LA English
DT Article
DE Comprehensive stroke centers; Referral bias; Quality of care
ID GUIDELINES-STROKE; UNITED-STATES; OUTCOME RELATIONSHIP; SURGEON VOLUME;
CARE; RECOMMENDATIONS; ADMISSIONS; MORBIDITY; ANEURYSMS; REGISTRY
AB BACKGROUND: Prior studies have suggested that hospital case volume may be associated with improved outcomes after subarachnoid hemorrhage (SAH), but contemporary national data are limited.
OBJECTIVE: To assess the association between hospital case volume for SAH and in-hospital mortality.
METHODS: Using the Get With The Guidelines-Stroke registry, we analyzed patients with a discharge diagnosis of SAH between April 2003 and March 2012. We assessed the association of annual SAH case volume with in-hospital mortality by using multivariable logistic regression adjusting for relevant patient, hospital, and geographic characteristics.
RESULTS: Among 31,973 patients with SAH from 685 hospitals, the median annual case volume per hospital was 8.5 (25th-75th percentile, 6.7-12.9) patients. Mean in-hospital mortality was 25.7%, but was lower with increasing annual SAH volume: 29.5% in quartile 1 (range, 4-6.6), 27.0% in quartile 2 (range, 6.7-8.5), 24.1% in quartile 3 (range, 8.5-12.7), and 22.1% in quartile 4 (range, 12.9-94.5). Adjusting for patient and hospital characteristics, hospital SAH volume was independently associated with in-hospital mortality (adjusted odds ratio 0.79 for quartile 4 vs 1, 95% confidence interval, 0.67-0.92). The quartile of SAH volume also was associated with length of stay but not with discharge home or independent ambulatory status.
CONCLUSION: In a large nationwide registry, we observed that patients treated at hospitals with higher volumes of SAH patients have lower in-hospital mortality, independent of patient and hospital characteristics. Our data suggest that experienced centers may provide more optimized care for SAH patients.
C1 [Prabhakaran, Shyam] Northwestern Univ, Dept Neurol, Chicago, IL 60611 USA.
[Fonarow, Gregg C.] Ahmanson UCLA Cardiomyopathy Ctr, Los Angeles, CA USA.
[Smith, Eric E.] Univ Calgary, Hotchkiss Brain Inst, Calgary, AB, Canada.
[Liang, Li; Xian, Ying; Neely, Megan; Peterson, Eric D.] Duke Clin Res Inst, Durham, NC USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Div Neurol, Boston, MA 02114 USA.
RP Prabhakaran, S (reprint author), Northwestern Univ, Dept Neurol, Feinberg Sch Med, 710 N Lake Shore Dr,Suite 1417, Chicago, IL 60611 USA.
EM sprabhak@nmff.org
OI Schwamm, Lee/0000-0003-0592-9145; Smith, Eric/0000-0003-3956-1668
NR 34
TC 7
Z9 7
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-396X
EI 1524-4040
J9 NEUROSURGERY
JI Neurosurgery
PD NOV
PY 2014
VL 75
IS 5
BP 500
EP 508
DI 10.1227/NEU.0000000000000475
PG 9
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA AS2PD
UT WOS:000344121100003
PM 24979097
ER
PT J
AU Sun, PZ
Wang, Y
Mandeville, E
Chan, ST
Lo, EH
Ji, XM
AF Sun, Phillip Zhe
Wang, Yu
Mandeville, Emiri
Chan, Suk-Tak
Lo, Eng H.
Ji, Xunming
TI Validation of fast diffusion kurtosis MRI for imaging acute ischemia in
a rodent model of stroke
SO NMR IN BIOMEDICINE
LA English
DT Article
DE acute stroke; diffusion-weighted imaging (DWI); diffusion kurtosis
imaging (DKI); mean diffusion (MD); mean kurtosis (MK)
ID EXPERIMENTAL CEREBRAL-ISCHEMIA; PERFUSION-WEIGHTED MRI; TISSUE;
VISUALIZATION; COEFFICIENT; PARAMETERS; INFARCTION; MISMATCH; LESIONS;
HUMANS
AB Diffusion-weighted imaging (DWI) captures ischemic tissue that is likely to infarct, and has become one of the most widely used acute stroke imaging techniques. Diffusion kurtosis imaging (DKI) has lately been postulated as a complementary MRI method to stratify the heterogeneously damaged DWI lesion. However, the conventional DKI acquisition time is relatively long, limiting its use in the acute stroke setting. Recently, a fast kurtosis mapping method has been demonstrated in fixed brains and control subjects. The fast DKI approach provides mean diffusion and kurtosis measurements under substantially reduced scan time, making it amenable to acute stroke imaging. Because it is not practical to obtain and compare different means of DKI to test whether the fast DKI method can reliably detect diffusion and kurtosis lesions in acute stroke patients, our study investigated its diagnostic value using an animal model of acute stroke, a critical step before fast DKI acquisition can be routinely applied in the acute stroke setting. We found significant correlation, per voxel, between the diffusion and kurtosis coefficients measured using the fast and conventional DKI protocols. In acute stroke rats, the two DKI methods yielded diffusion and kurtosis lesions that were in good agreement. Importantly, substantial kurtosis-diffusion lesion mismatch was observed using the conventional (26 +/- 13%, P<0.01) and fast DKI methods (23 +/- 8%, P<0.01). In addition, regression analysis showed that the kurtosis-diffusion lesion mismatches obtained using conventional and fast DKI methods were substantially correlated (R-2=0.57, P=0.02). Our results confirmed that the recently proposed fast DKI method is capable of capturing heterogeneous diffusion and kurtosis lesions in acute ischemic stroke, and thus is suitable for translational applications in the acute stroke clinical setting. Copyright (c) 2014 John Wiley & Sons, Ltd.
C1 [Sun, Phillip Zhe; Wang, Yu; Chan, Suk-Tak] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Dept Radiol, Charlestown, MA USA.
[Sun, Phillip Zhe; Wang, Yu; Mandeville, Emiri; Chan, Suk-Tak; Lo, Eng H.] Harvard Univ, Sch Med, Charlestown, MA USA.
[Wang, Yu; Ji, Xunming] Capital Med Univ, Xuanwu Hosp, Cerebrovasc Dis Res Inst, Beijing, Peoples R China.
[Mandeville, Emiri; Lo, Eng H.] Massachusetts Gen Hosp, Neuroprotect Res Lab, Dept Radiol & Neurol, Charlestown, MA USA.
RP Ji, XM (reprint author), Capital Med Univ, Xuanwu Hosp, Cerebrovasc Dis Res Inst, Beijing, Peoples R China.
EM jixm@ccmu.edu.cn
RI Chan, Suk-tak/G-5846-2015
FU NIH/NIBIB [1K01EB009771]; NIH/NINDS [1R21NS085574]; NBRPC
[2011CB-70780420]
FX This study was supported in part by grants from NIH/NIBIB 1K01EB009771,
NIH/NINDS 1R21NS085574 and NBRPC 2011CB-70780420.
NR 37
TC 12
Z9 14
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0952-3480
EI 1099-1492
J9 NMR BIOMED
JI NMR Biomed.
PD NOV
PY 2014
VL 27
IS 11
BP 1413
EP 1418
DI 10.1002/nbm.3188
PG 6
WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
GA AR9WR
UT WOS:000343927900017
PM 25208309
ER
PT J
AU Nieminen, HJ
Salmi, A
Karppinen, P
Haeggstrom, E
Hacking, SA
AF Nieminen, H. J.
Salmi, A.
Karppinen, P.
Haeggstrom, E.
Hacking, S. A.
TI The potential utility of high-intensity ultrasound to treat
osteoarthritis
SO OSTEOARTHRITIS AND CARTILAGE
LA English
DT Review
DE Ultrasound; Osteoarthritis; Cartilage; Bone; Drug delivery; Orthopedic
surgery
ID GUIDED FOCUSED ULTRASOUND; INTRAARTICULAR DRUG-DELIVERY; ACOUSTIC
RADIATION FORCE; TEMPERATURE-SENSITIVE LIPOSOMES; SHOCK-WAVE
LITHOTRIPSY; CHONDROCYTES IN-VITRO; ARTICULAR-CARTILAGE; POSTTRAUMATIC
OSTEOARTHRITIS; THERAPEUTIC ULTRASOUND; KNEE OSTEOARTHRITIS
AB Osteoarthritis (OA) is a widespread musculoskeletal disease that reduces quality of life and for which there is no cure. The treatment of OA is challenging since cartilage impedes the local and systemic delivery of therapeutic compounds (TCs). This review identifies high-intensity ultrasound (HIU) as a non-contact technique to modify articular cartilage and subchondral bone. HIU enables new approaches to overcome challenges associated with drug delivery to cartilage and new non-invasive approaches for the treatment of joint disease. Specifically, HIU has the potential to facilitate targeted drug delivery and release deep within cartilage, to repair soft tissue damage, and to physically alter tissue structures including cartilage and bone. The localized, non-invasive ultrasonic delivery of TCs to articular cartilage and subchondral bone appears to be a promising technique in the immediate future. (C) 2014 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
C1 [Nieminen, H. J.; Salmi, A.; Karppinen, P.; Haeggstrom, E.] Univ Helsinki, Dept Phys, FIN-00014 Helsinki, Finland.
[Hacking, S. A.] Massachusetts Gen Hosp, Dept Orthopaed, Boston, MA 02114 USA.
[Hacking, S. A.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
RP Hacking, SA (reprint author), Harvard Univ, Sch Med, Dept Orthopaed, Lab Musculoskeletal Res & Innovat, 55 Fruit St,Rm GRJ 1120, Boston, MA 02114 USA.
EM heikki.nieminen@helsinki.fi; ari.salmi@helsinki.fi;
pasi.karppinen@gmail.com; edward.haeggstrom@helsinki.fi;
ahacking@yahoo.com
RI Salmi, Ari/B-1317-2009
FU Academy of Finland [253579]
FX The authors are grateful for the insight, suggestions and constructive
criticisms provided by Prof A.J. Grodzinsky. Thank you. The work of H.J.
Nieminen is supported by the Academy of Finland (no. 253579).
NR 152
TC 3
Z9 3
U1 3
U2 21
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1063-4584
EI 1522-9653
J9 OSTEOARTHR CARTILAGE
JI Osteoarthritis Cartilage
PD NOV
PY 2014
VL 22
IS 11
BP 1784
EP 1799
DI 10.1016/j.joca.2014.07.025
PG 16
WC Orthopedics; Rheumatology
SC Orthopedics; Rheumatology
GA AS3NR
UT WOS:000344186000004
PM 25106678
ER
PT J
AU Tan, CO
Battaglino, RA
Doherty, AL
Gupta, R
Lazzari, AA
Garshick, E
Zafonte, R
Morse, LR
AF Tan, C. O.
Battaglino, R. A.
Doherty, A. L.
Gupta, R.
Lazzari, A. A.
Garshick, E.
Zafonte, R.
Morse, L. R.
TI Adiponectin is associated with bone strength and fracture history in
paralyzed men with spinal cord injury
SO OSTEOPOROSIS INTERNATIONAL
LA English
DT Article
DE Adiponectin; Biomarker; Finite element analysis; Fracture;
Rehabilitation medicine; Spinal cord injury
ID MAPK SIGNALING PATHWAY; LOWER-EXTREMITY BONE; MINERAL DENSITY; SERUM
ADIPONECTIN; POSTMENOPAUSAL WOMEN; CANDIDATE BIOMARKER; PLASMA
ADIPONECTIN; HUMAN OSTEOBLASTS; ELDERLY-MEN; FAT MASS
AB We explored the association between adiponectin levels and bone strength in paralyzed men with spinal cord injury. We found that bone strength was inversely associated with circulating adiponectin levels. Thus, strength estimates and adiponectin levels may improve fracture risk prediction and detection of response to osteogenic therapies following spinal cord injury.
Previous research has demonstrated an inverse relationship between circulating adiponectin and bone mineral density, suggesting that adiponectin may be used as a biomarker for bone health. However, this relationship may reflect indirect effects on bone metabolism via adipose-mediated mechanical pathways rather than the direct effects of adipokines on bone metabolism. Thus, we explored the association between circulating adiponectin levels and bone strength in 27 men with spinal cord injury.
Plasma adiponectin levels were quantified by ELISA assay. Axial stiffness and maximal load to fracture of the distal femur were quantified via finite element analysis using reconstructed 3D models of volumetric CT scans. We also collected information on timing, location, and cause of previous fractures.
Axial stiffness and maximal load were inversely associated with circulating adiponectin levels (R (2) = 0.44, p = 0.01; R (2) = 0.58, p = 0.05) after adjusting for injury duration and lower extremity lean mass. In individuals with post-SCI osteoporotic fractures, distal femur stiffness (p = 0.01) and maximal load (p = 0.005) were lower, and adiponectin was higher (p = 0.04) than those with no fracture history.
Based on these findings, strength estimates may improve fracture risk prediction and detection of response to osteogenic therapies following spinal cord injury. Furthermore, our findings suggest that circulating adiponectin may indeed be a feasible biomarker for bone health and osteoporotic fracture risk in paralyzed individuals with spinal cord injury.
C1 [Tan, C. O.; Doherty, A. L.; Zafonte, R.; Morse, L. R.] Spaulding Rehabil Hosp, Spaulding Harvard SCI Model Syst, Boston, MA USA.
[Tan, C. O.; Zafonte, R.; Morse, L. R.] Harvard Univ, Sch Med, Dept Phys Med & Rehabil, Boston, MA USA.
[Morse, L. R.] Forsyth Inst, Cambridge, MA 02115 USA.
[Battaglino, R. A.] Harvard Univ, Sch Dent Med, Dept Oral Med Infect & Immun, Boston, MA 02115 USA.
[Gupta, R.] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Lazzari, A. A.] Boston Univ Sch Med, Primary Care Sect, VA Boston Healthcare Syst, Boston, MA USA.
[Lazzari, A. A.] Boston Univ Sch Med, Rheumatol Sect, VA Boston Healthcare Syst, Boston, MA USA.
[Garshick, E.] VA Boston Healthcare Syst, Pulm & Crit Care Med Sect, Med Serv, Boston, MA USA.
[Garshick, E.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Div Network Med, Boston, MA 02115 USA.
RP Morse, LR (reprint author), Forsyth Inst, Cambridge, MA 02115 USA.
EM Leslie.morse@mgh.harvard.edu
RI battaglino, ricardo/D-2892-2015; Morse, Leslie/C-9442-2015; Tan, Can
Ozan/E-2598-2016
OI Morse, Leslie/0000-0002-7426-6341; Tan, Can Ozan/0000-0001-9673-9907
FU Department of Defense [W81XWH-10-1-1043]; National Institute of
Arthritis and Musculoskeletal and Skin Diseases [1R01AR059270-01];
Department of Education, National Institute on Disability and
Rehabilitation Research [H133N110010]
FX We thank Sam Davis, clinical research coordinator and technician, Boston
VA Healthcare System, for assisting with bone density scans; and Rachael
Burns and Kara Loo, research assistants, Boston VA Healthcare System,
for collection of anthropometric data. This study received support from
the Department of Defense (W81XWH-10-1-1043), the National Institute of
Arthritis and Musculoskeletal and Skin Diseases (1R01AR059270-01), and
the Department of Education, National Institute on Disability and
Rehabilitation Research (H133N110010).
NR 43
TC 3
Z9 3
U1 0
U2 10
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0937-941X
EI 1433-2965
J9 OSTEOPOROSIS INT
JI Osteoporosis Int.
PD NOV
PY 2014
VL 25
IS 11
BP 2599
EP 2607
DI 10.1007/s00198-014-2786-2
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AS3HE
UT WOS:000344167500010
PM 24980185
ER
PT J
AU Sethi, RKV
Kozin, ED
Fagenholz, PJ
Lee, DJ
Shrime, MG
Gray, ST
AF Sethi, Rosh K. V.
Kozin, Elliott D.
Fagenholz, Peter J.
Lee, Daniel J.
Shrime, Mark G.
Gray, Stacey T.
TI Epidemiological Survey of Head and Neck Injuries and Trauma in the
United States
SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY
LA English
DT Article
DE otolaryngology; head and neck; trauma; injury; emergency department
ID FACIAL FRACTURES; RISK-FACTORS; MANAGEMENT; OUTCOMES; PATTERNS; SURGERY;
COSTS
AB Objective. Head and neck trauma results in a range of injuries, spanning minor lacerations to life-threatening airway compromise. Few studies provide in-depth analysis of injuries to the head and neck (HN). We aim to (1) describe HN injury prevalence in the US and (2) investigate patient disposition and the outcome of mortality.
Study Design. Case series with chart review.
Setting. Nationwide emergency department (ED) sample.
Methods. The 2011 database was queried for encounters with a primary diagnosis of HN injury, as categorized by the Barell Injury Matrix. Weighted estimates for demographics, injury category, and mechanism were extracted. Predictors of mortality and admission were determined by multivariable regression.
Results. We identified 131 million ED encounters. A weighted total of 5,418,539 visits were related to primary HN injuries. Average age was 30 (SE = 0.4), and 56.8% were male. Sixty-four percent of injuries were attributed to fall or blunt trauma. Open wounds comprised 41.8% of injuries. The most common procedure was laceration repair (70%). The majority of patients (97%) were discharged home. Mortality rate was less than 1%. Predictors of admission and mortality (P < .05) included multiple trauma, vessel trauma, and burns. Other risk factors included foreign-body, older age, and male gender.
Conclusions. Primary HN injuries commonly present to emergency rooms in the US. The majority of HN injuries are non-life threatening and do not require admission to the hospital or result in death. These data have implications for HN injury surveillance and may be used to risk-stratify patients who present with injuries in the acute care setting.
C1 [Sethi, Rosh K. V.; Kozin, Elliott D.; Lee, Daniel J.; Shrime, Mark G.; Gray, Stacey T.] Harvard Univ, Sch Med, Dept Otol & Laryngol, Boston, MA 02114 USA.
[Sethi, Rosh K. V.; Kozin, Elliott D.; Lee, Daniel J.; Shrime, Mark G.; Gray, Stacey T.] Massachusetts Gen Hosp, Massachusetts Eye & Ear Infirm, Dept Otolaryngol Head & Neck Surg, Boston, MA 02114 USA.
[Fagenholz, Peter J.] Massachusetts Gen Hosp, Dept Surg, Div Trauma Emergency Surg & Surg Crit Care, Boston, MA 02114 USA.
[Shrime, Mark G.] Harvard Interfac Initiat Hlth Policy, Cambridge, MA USA.
RP Kozin, ED (reprint author), Harvard Univ, Sch Med, Massachusetts Eye & Ear Infirm, Dept Otol & Laryngol, 243 Charles St, Boston, MA 02114 USA.
EM Elliott_kozin@meei.harvard.edu
RI Kozin, Elliott/J-1225-2014
OI Kozin, Elliott/0000-0002-0305-0682
FU NIDCD NIH HHS [T32 DC000020]
NR 27
TC 5
Z9 5
U1 0
U2 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0194-5998
EI 1097-6817
J9 OTOLARYNG HEAD NECK
JI Otolaryngol. Head Neck Surg.
PD NOV
PY 2014
VL 151
IS 5
BP 776
EP 784
DI 10.1177/0194599814546112
PG 9
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA AS6FO
UT WOS:000344360100011
PM 25139950
ER
PT J
AU Steinberg, WM
Nauck, MA
Zinman, B
Daniels, GH
Bergenstal, RM
Mann, JFE
Ravn, LS
Moses, AC
Stockner, M
Baeres, FMM
Marso, SP
Buse, JB
AF Steinberg, William M.
Nauck, Michael A.
Zinman, Bernard
Daniels, Gilbert H.
Bergenstal, Richard M.
Mann, Johannes F. E.
Ravn, Lasse Steen
Moses, Alan C.
Stockner, Mette
Baeres, Florian M. M.
Marso, Steven P.
Buse, John B.
CA LEADER Trial Investigators
TI LEADER 3-Lipase and Amylase Activity in Subjects With Type 2 Diabetes
Baseline Data From Over 9000 Subjects in the LEADER Trial
SO PANCREAS
LA English
DT Article
DE pancreatitis; lipase; amylase; type 2 diabetes
ID ACUTE-PANCREATITIS; ALPHA-AMYLASE; LIPASE; EXENATIDE; LIRAGLUTIDE; RISK;
OBESITY; CANCER; COHORT; SERUM
AB Objectives: This report from the LEADER (Liraglutide Effect and Action in Diabetes: Evaluation of Cardiovascular Outcome Results) trial describes baseline lipase and amylase activity in type 2 diabetic subjects without acute pancreatitis symptoms before randomization to the glucagonlike peptide analog liraglutide or placebo.
Methods: The LEADER is an international randomized placebo-controlled trial evaluating the cardiovascular safety of liraglutide in 9340 type 2 diabetic patients at high cardiovascular risk. Fasting lipase and amylase activity was assessed at baseline, before receiving liraglutide or placebo, using a commercial assay (Roche) with upper limit of normal values of 63 U/L for lipase and 100 U/L for amylase.
Results: Either or both enzymes were above the upper limit of normal in 22.7% of subjects; 16.6%(n = 1540) had an elevated lipase level (including 1.2% >3-fold elevated), and 11.8% (n = 1094) had an elevated amylase level (including 0.2% >3-fold elevated). In multivariable regression models, severely reduced kidney function was associated with the largest effect on increasing activity of both. However, even among subjects with normal kidney function, 12.2% and 7.7% had elevated lipase and amylase levels.
Conclusions: In this large study of type 2 diabetic patients, nearly 25% had elevated lipase or amylase levels without symptoms of acute pancreatitis. The clinician must take these data into account when evaluating abdominal symptoms in type 2 diabetic patients.
C1 [Steinberg, William M.] George Washington Univ, Med Ctr, Dept Med, Rockville, MD 20854 USA.
[Nauck, Michael A.] Diabet Zentrum Bad Lauterberg, Dept Internal Med Diabetol, Bad Lauterberg Im Harz, Germany.
[Zinman, Bernard] Univ Toronto, Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Dept Med, Toronto, ON M5G 1X5, Canada.
[Daniels, Gilbert H.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Thyroid Unit, Boston, MA USA.
[Daniels, Gilbert H.] Harvard Univ, Sch Med, Dept Med, Massachusetts Gen Hosp, Boston, MA USA.
[Bergenstal, Richard M.] Pk Nicollet Inst Res & Educ, Int Diabet Ctr, Minneapolis, MN USA.
[Mann, Johannes F. E.] Univ Erlangen Nurnberg, Dept Med, D-91054 Erlangen, Germany.
[Ravn, Lasse Steen; Moses, Alan C.; Stockner, Mette; Baeres, Florian M. M.] Novo Nordisk AS, Bagsvaerd, Denmark.
[Marso, Steven P.] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Div Cardiol, Dallas, TX 75390 USA.
[Buse, John B.] Univ N Carolina, Sch Med, Dept Med, Div Endocrinol, Chapel Hill, NC USA.
RP Steinberg, WM (reprint author), George Washington Univ, Rockville Internal Med Grp, Dept Med, 1201 Seven Locks Rd, Rockville, MD 20854 USA.
EM wstein6905@aol.com
RI Zinman, Bernard/E-7266-2013; BALCI, Mustafa Kemal/C-2979-2016
OI BALCI, Mustafa Kemal/0000-0002-6494-3249
NR 43
TC 17
Z9 17
U1 1
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1223
EP 1231
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600015
PM 25275271
ER
PT J
AU Biczo, G
Vegh, ET
Shalbueva, N
French, SW
Elperin, J
Lotshaw, E
Mareninova, OA
Hegyi, P
Rakonczay, Z
Gukovskaya, AS
AF Biczo, G.
Vegh, E. T.
Shalbueva, N.
French, S. W.
Elperin, J.
Lotshaw, E.
Mareninova, O. A.
Hegyi, P.
Rakonczay, Z., Jr.
Gukovskaya, A. S.
TI Mitochondrial ATP Synthase Dysfunction Mediates L-arginine-Induced
Pancreatitis
SO PANCREAS
LA English
DT Meeting Abstract
C1 [Biczo, G.; Vegh, E. T.; Shalbueva, N.; Elperin, J.; Lotshaw, E.; Mareninova, O. A.; Gukovskaya, A. S.] VA Greater Los Angeles, Los Angeles, CA USA.
[Biczo, G.; Vegh, E. T.; Shalbueva, N.; Elperin, J.; Lotshaw, E.; Mareninova, O. A.; Gukovskaya, A. S.] Univ Calif Los Angeles, Los Angeles, CA 90024 USA.
[Biczo, G.; Vegh, E. T.; Hegyi, P.; Rakonczay, Z., Jr.] Univ Szeged, Szeged, Hungary.
[French, S. W.] Harbor UCLA Med Ctr, Torrance, CA 90509 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1344
EP 1345
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600055
ER
PT J
AU Das, KK
Marchegiani, G
Geng, X
Xiao, H
Huynh, T
Fernandez-del Castillo, C
Pitman, MB
Das, KM
Mino-Kenudson, M
AF Das, K. K.
Marchegiani, G.
Geng, X.
Xiao, H.
Huynh, T.
Fernandez-del Castillo, C.
Pitman, M. B.
Das, K. M.
Mino-Kenudson, M.
TI Comparison of the International Consensus Guidelines for Management of
Intraductal Papillary Mucinous Neoplasm (IPMN) With Analysis of
Pancreatic Cyst Fluid Aspirates for mAb Das-1 Reactivity in Identifying
High-risk and Malignant IPMN
SO PANCREAS
LA English
DT Meeting Abstract
C1 [Das, K. K.] Univ Penn, Div Gastroenterol, Philadelphia, PA 19104 USA.
[Marchegiani, G.; Fernandez-del Castillo, C.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Xiao, H.; Huynh, T.; Pitman, M. B.; Mino-Kenudson, M.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Geng, X.; Das, K. M.] Rutgers RWJMS, Div Gastroenterol, New Brunswick, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1352
EP 1352
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600085
ER
PT J
AU Maertin, S
Nitsche, CJ
Elperin, JM
Sendler, M
Grippo, PJ
Eibl, G
Mayerle, J
Lerch, MM
Gukovskaya, AS
AF Maertin, S.
Nitsche, C. J.
Elperin, J. M.
Sendler, M.
Grippo, P. J.
Eibl, G.
Mayerle, J.
Lerch, M. M.
Gukovskaya, A. S.
TI Prosurvival Effect of Autophagy in Pancreatic Cancer Cells is Determined
by Kras and p53 Mutational Status
SO PANCREAS
LA English
DT Meeting Abstract
C1 [Maertin, S.; Elperin, J. M.; Gukovskaya, A. S.] VA Greater Los Angeles, Los Angeles, CA USA.
[Maertin, S.; Eibl, G.; Gukovskaya, A. S.] Univ Calif Los Angeles, Los Angeles, CA 90024 USA.
[Maertin, S.; Nitsche, C. J.; Sendler, M.; Mayerle, J.; Lerch, M. M.] Ernst Moritz Arndt Univ Greifswald, Greifswald, Germany.
[Grippo, P. J.] Univ Illinois, Chicago, IL USA.
RI Lerch, Markus M./E-2206-2016
OI Lerch, Markus M./0000-0002-9643-8263
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1386
EP 1386
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600228
ER
PT J
AU Marchegiani, G
Paulo, JA
Sahora, K
Fernandez-del Castillo, C
AF Marchegiani, G.
Paulo, J. A.
Sahora, K.
Fernandez-del Castillo, C.
TI The Proteome of Surgical Pancreatic Juice
SO PANCREAS
LA English
DT Meeting Abstract
C1 [Marchegiani, G.; Sahora, K.; Fernandez-del Castillo, C.] Harvard Univ, Sch Med, Dept Surg, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Paulo, J. A.] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1388
EP 1388
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600236
ER
PT J
AU Marchegiani, G
Kenudson, MM
Ferrone, C
Warshaw, AL
Lillemoe, K
Fernandez-del Castillo, C
AF Marchegiani, G.
Kenudson, M. Mino
Ferrone, C.
Warshaw, A. L.
Lillemoe, K.
Fernandez-del Castillo, C.
TI Oncocytic Type IPMN: A Unique Malignant Subset With Good Long-Term
Prognosis
SO PANCREAS
LA English
DT Meeting Abstract
C1 [Marchegiani, G.; Ferrone, C.; Warshaw, A. L.; Lillemoe, K.; Fernandez-del Castillo, C.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Kenudson, M. Mino] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1388
EP 1388
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600235
ER
PT J
AU Nakagawa, A
Mino-Kenudson, M
Lillemoe, KD
Fernandez-del Castillo, C
Warshaw, AL
Thayer, SP
Liss, AS
AF Nakagawa, A.
Mino-Kenudson, M.
Lillemoe, K. D.
Fernandez-del Castillo, C.
Warshaw, A. L.
Thayer, S. P.
Liss, A. S.
TI Pancreatic Tuft Cells Principally Reside in the Ampulla and Proximal
Intrapancreatic Biliary Duct in Mouse and Exhibit Increased Expression
and Altered Localization in Response to Inflammatory Injury
SO PANCREAS
LA English
DT Meeting Abstract
C1 [Nakagawa, A.; Lillemoe, K. D.; Fernandez-del Castillo, C.; Warshaw, A. L.; Thayer, S. P.; Liss, A. S.] Massachusetts Gen Hosp, Warshaw Inst Pancreat Canc Res, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Mino-Kenudson, M.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1394
EP 1395
PG 2
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600263
ER
PT J
AU Pimienta, M
Lee, GE
Gukovskaya, AS
Gukovsky, I
Mareninova, OA
AF Pimienta, M.
Lee, G. E.
Gukovskaya, A. S.
Gukovsky, I.
Mareninova, O. A.
TI mTOR Mediates p62/SQSTM1 Synthesis in Pancreatic Acinar Cells
SO PANCREAS
LA English
DT Meeting Abstract
C1 Univ Calif Los Angeles, VA Greater Los Angeles, Los Angeles, CA USA.
Southern Calif Res Ctr ALPD & Cirrhosis, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1401
EP 1401
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600289
ER
PT J
AU Soll, AH
Keefer, LA
Streiner, DL
Lee, ML
Freedman, SD
Mahvi, D
Buxbaum, J
Pandol, S
Lo, S
AF Soll, A. H.
Keefer, L. A.
Streiner, D. L.
Lee, M. L.
Freedman, S. D.
Mahvi, D.
Buxbaum, J.
Pandol, S.
Lo, S.
TI A Comprehensive Biopsychosocial (BPS) Assessment of Patients With
Pancreatobiliary Disorders (PD) Illuminates Mechanisms Underlying
Symptoms and Alters Clinical Decision-Making
SO PANCREAS
LA English
DT Meeting Abstract
C1 Univ Calif Los Angeles, Los Angeles, CA USA.
Northwestern, Chicago, IL USA.
BIDMC, Boston, MA USA.
Cedars Sinai, Los Angeles, CA USA.
USC, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1409
EP 1409
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600324
ER
PT J
AU Wu, SV
Pham, H
Million, M
Chen, MC
Go, VLW
Jiang, M
AF Wu, S. V.
Pham, H.
Million, M.
Chen, M. C.
Go, V. L. W.
Jiang, M.
TI Expression and Functional Characterization of Bitter Taste Receptors in
Rat Pancreas
SO PANCREAS
LA English
DT Meeting Abstract
C1 [Wu, S. V.; Chen, M. C.; Go, V. L. W.] Univ Calif Los Angeles, Ctr Excellence Pancreat Dis, Los Angeles, CA USA.
[Pham, H.; Million, M.] Univ Calif Los Angeles, Dept Med, Div Digest Dis, Los Angeles, CA 90024 USA.
[Jiang, M.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pharmacol, Los Angeles, CA 90095 USA.
[Wu, S. V.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1422
EP 1422
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600381
ER
PT J
AU Wu, SV
Chen, MC
Tache, Y
Go, VLW
AF Wu, S. V.
Chen, M. C.
Tache, Y.
Go, V. L. W.
TI Characterization of Corticotropin-Releasing Hormone (CRH) Type I System
in Human Pancreatic Endocrine Tumors
SO PANCREAS
LA English
DT Meeting Abstract
C1 [Wu, S. V.; Chen, M. C.; Go, V. L. W.] Univ Calif Los Angeles, David Geffen Sch Med, Ctr Excellence Pancreat Dis, Los Angeles, CA 90095 USA.
[Wu, S. V.; Tache, Y.] VA Greater Los Angeles Healthcare Syst, Los Angeles, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD NOV
PY 2014
VL 43
IS 8
BP 1423
EP 1423
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AS6GO
UT WOS:000344362600384
ER
PT J
AU Powis, K
Lockman, S
Smeaton, L
Hughes, MD
Fawzi, W
Ogwu, A
Moyo, S
van Widenfelt, E
von Oettingen, J
Makhema, J
Essex, M
Shapiro, RL
AF Powis, Kathleen
Lockman, Shahin
Smeaton, Laura
Hughes, Michael D.
Fawzi, Wafaie
Ogwu, Anthony
Moyo, Sikhulile
van Widenfelt, Erik
von Oettingen, Julia
Makhema, Joseph
Essex, Max
Shapiro, Roger L.
TI Vitamin D Insufficiency in HIV-infected Pregnant Women Receiving
Antiretroviral Therapy is Not Associated With Morbidity, Mortality or
Growth Impairment in Their Uninfected Infants in Botswana
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE HIV-exposed uninfected infants; maternal vitamin D; morbidity;
mortality; growth
ID SUB-SAHARAN AFRICA; CHILD-MORTALITY; D DEFICIENCY; OUTCOMES; AGE;
UNDERNUTRITION; TRANSMISSION; PNEUMONIA; COUNTRIES; TANZANIA
AB Background: Low maternal 25(OH) D (vitamin D) values have been associated with higher mortality and impaired growth among HIV-exposed uninfected (HEU) infants of antiretroviral (ART)-naive women. These associations have not been studied among HEU infants of women receiving ART.
Methods: We performed a nested case-control study in the Botswana Mma Bana Study, a study providing ART to women during pregnancy and breast-feeding. Median maternal vitamin D values, and the proportion with maternal vitamin D insufficiency, were compared between women whose HEU infants experienced morbidity/mortality during 24 months of follow-up and women with nonhospitalized HEU infants. Growth faltering was assessed for never hospitalized infants attending the 24-month-of-life visit. Multivariate logistic regression models determined associations between maternal vitamin D insufficiency and infant morbidity/mortality and growth faltering.
Results: Delivery plasma was available and vitamin D levels assayable from 119 (86%) of 139 cases and 233 (84%) of 278 controls, and did not differ significantly between cases and controls [median: 36.7 ng/mL, interquartile range (IQR): 29.1-44.7 vs. 37.1 ng/mL, IQR: 30.0-47.2, P = 0.32]. Vitamin D insufficiency (<32 ng/mL) was recorded among 112 (31.8%) of 352 women at delivery and occurred most frequently among women delivering in winter. Multivariate logistic regression models adjusted for maternal HIV disease progression did not show associations between maternal vitamin D insufficiency at delivery and child morbidity/mortality, or 24-month-of-life growth faltering.
Conclusions: Vitamin D insufficiency was common among ART-treated pregnant women in Botswana, but was not associated with morbidity, mortality or growth impairment in their HIV-uninfected children.
C1 [Powis, Kathleen] Massachusetts Gen Hosp, Dept Internal Med, Boston, MA 02114 USA.
[Powis, Kathleen] Massachusetts Gen Hosp, Dept Pediat, Boston, MA 02114 USA.
[Powis, Kathleen; Lockman, Shahin; Essex, Max; Shapiro, Roger L.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Powis, Kathleen; Lockman, Shahin; Ogwu, Anthony; Moyo, Sikhulile; van Widenfelt, Erik; Makhema, Joseph; Essex, Max; Shapiro, Roger L.] Botswana Harvard AIDS Inst Partnership, Gaborone, Botswana.
[Lockman, Shahin] Brigham & Womens Hosp, Div Infect Dis, Boston, MA 02115 USA.
[Smeaton, Laura; Hughes, Michael D.] Harvard Univ, Sch Publ Hlth, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
[Fawzi, Wafaie] Harvard Univ, Sch Publ Hlth, Dept Global Hlth & Populat, Boston, MA 02115 USA.
[von Oettingen, Julia] Boston Childrens Hosp, Div Endocrinol, Boston, MA USA.
[Shapiro, Roger L.] Beth Israel Deaconess Med Ctr, Div Infect Dis, Boston, MA 02215 USA.
RP Powis, K (reprint author), 100 Cambridge St,15th Floor, Boston, MA 02114 USA.
EM kpowis@partners.org
RI Moyo, Sikhulile/E-1464-2015;
OI Moyo, Sikhulile/0000-0003-3821-4592; von Oettingen, Julia
Elisabeth/0000-0003-0631-1435
FU National Institute of Allergy and Infectious Diseases [U01-AI066454];
Brigham and Women's Global Women's Health Fellowship; Harvard University
Center for AIDS Research [P30 AI060354]; National Institute of Child
Health and Human Development Grant [1K23HD070774-01A1]; Fogarty AITRP
[D43 TW000004]
FX Mma Bana study was supported by a grant (U01-AI066454) from the National
Institute of Allergy and Infectious Diseases. Funding support from
Brigham and Women's Global Women's Health Fellowship supported K.P.'s
salary during the Mma Bana study. K. P. received salary support from a
Harvard University Center for AIDS Research grant (P30 AI060354) and a
National Institute of Child Health and Human Development Grant
(1K23HD070774-01A1) for this project. The Fogarty AITRP grant (D43
TW000004) provided funding for A.O. and S. M. Mma Bana study drugs were
provided by Abbott Pharmaceuticals, GlaxoSmithKline, and the government
of Botswana.
NR 38
TC 1
Z9 1
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
EI 1532-0987
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD NOV
PY 2014
VL 33
IS 11
BP 1141
EP 1147
DI 10.1097/INF.0000000000000428
PG 7
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA AS6DH
UT WOS:000344354400015
PM 25037041
ER
PT J
AU Tyson, ME
Bohl, DD
Blickman, JG
AF Tyson, Mary E.
Bohl, Daniel D.
Blickman, Johan G.
TI A randomized controlled trial: child life services in pediatric imaging
SO PEDIATRIC RADIOLOGY
LA English
DT Article
DE Randomized controlled trial; Child life specialists; Family-centered
care; Pediatric imaging sciences; Child distress; Parent satisfaction
ID HOSPITALIZED CHILDREN; PREPARING CHILDREN; PSYCHOLOGICAL INTERVENTIONS;
EMERGENCY-DEPARTMENT; LACERATION REPAIR; PAIN MANAGEMENT; MRI; DISTRESS;
SEDATION; THERAPY
AB Children undergoing procedures in pediatric health care facilities and their families have been shown to benefit from psychosocial services and interventions such as those provided by a Certified Child Life Specialist (CCLS). The comprehensive impact of a CCLS in a pediatric imaging department is well recognized anecdotally but has not been examined in a prospective or randomized controlled fashion.
We prospectively assessed the impact of a CCLS on parent satisfaction, staff satisfaction, child satisfaction, and parent and staff perceptions of child pain and distress in a pediatric imaging department.
Eligible children between 1 and 12 years of age (n = 137) presenting to the pediatric imaging department for an imaging procedure were randomly assigned to an intervention or control arm. Those assigned to the intervention received the comprehensive services of a CCLS. The control group received standard of care, which did not include any child life services. Quantitative measures of satisfaction and perception of child pain and distress were assessed by parents and staff using a written 5-point Likert scale questionnaire after the imaging procedure. Children 4 and older were asked to answer 3 questions on a 3-point scale.
Statistically significant differences between the intervention and control groups were found in 19 out of 24 measures. Parents in the intervention group indicated higher satisfaction and a lower perception of their child's pain and distress. Staff in the intervention group indicated greater child cooperation and a lower perception of the child's pain and distress. Children in the intervention group indicated a better overall experience and less fear than those in the control group.
Child life specialists have a quantifiably positive impact on the care of children in imaging departments. Measures of parent satisfaction, staff satisfaction, child satisfaction, child pain and child distress are shown to be positively impacted by the services of a CCLS. These results have significant implications for hospitals striving to increase satisfaction, decrease costs and improve quality of care. In a health care landscape that is changing quickly and increasingly focused on the cost of care, future research should assess whether the core tenants of the child life profession support and contribute quantifiably to high-quality, cost-effective practices in health care.
C1 [Tyson, Mary E.; Blickman, Johan G.] Univ Rochester, Med Ctr, Golisano Childrens Hosp, Rochester, NY 14642 USA.
[Tyson, Mary E.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Bohl, Daniel D.] Yale Univ, Sch Med, New Haven, CT USA.
RP Tyson, ME (reprint author), 601 Elwood Ave,Box 648, Rochester, NY 14642 USA.
EM Mary_Tyson@dfci.harvard.edu
NR 79
TC 7
Z9 7
U1 3
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0301-0449
EI 1432-1998
J9 PEDIATR RADIOL
JI Pediatr. Radiol.
PD NOV
PY 2014
VL 44
IS 11
BP 1426
EP 1432
DI 10.1007/s00247-014-3005-1
PG 7
WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging
SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging
GA AS3HF
UT WOS:000344167600015
PM 24801818
ER
PT J
AU Lemly, DC
Lawlor, K
Scherer, EA
Kelemen, S
Weitzman, ER
AF Lemly, Diana C.
Lawlor, Katherine
Scherer, Emily A.
Kelemen, Skyler
Weitzman, Elissa R.
TI College Health Service Capacity to Support Youth With Chronic Medical
Conditions
SO PEDIATRICS
LA English
DT Article
DE health care transition; young adults; college/university health; chronic
medical conditions/special health care needs
ID CARE NEEDS; YOUNG-ADULTS; INCREASING INCIDENCE; CHRONIC ILLNESS;
UNITED-STATES; ADOLESCENTS; CHILDREN; TYPE-1; TRANSITION; STUDENTS
AB BACKGROUND AND OBJECTIVE: Twenty percent of US youth have a chronic medical condition and many attend college. Guidelines for transition from pediatric to adult care do not address college health services, and little is known about their capacity to identify, support, and provide care for these youth. The objective of this study was to describe college health center policies, practices, and resources for youth with chronic medical conditions (YCMC).
METHODS: Survey of medical directors from health centers of a representative sample of 200 4-year US colleges with >= 400 enrolled undergraduate students. Patterns of identification, management, and support for youth with a general chronic medical condition and with asthma, diabetes, and depression, were investigated; chi(2) and Fisher exact tests were used to ascertain differences by institutional demographics.
RESULTS: Directors at 153 institutions completed the survey (76.5% response rate). Overall, 42% of schools had no system to identify YCMC. However, almost a third (31%) did identify and add to a registry of incoming YCMC on review of medical history, more likely in private (P < .001) and small (<5000 students, P = .002) colleges; 24% of health centers contacted YCMC to check-in/make initial appointments. Most institutions could manage asthma and depression (83% and 69%, respectively); 51% could manage diabetes on campus.
CONCLUSIONS: Relatively few US colleges have health systems to identify and contact YCMC, although many centers have capacity to provide primary care and management of some conditions. Guidelines for transition should address policy and practices for pediatricians and colleges to enhance comanagement of affected youth.
C1 [Lemly, Diana C.; Lawlor, Katherine; Scherer, Emily A.; Weitzman, Elissa R.] Boston Childrens Hosp, Div Adolescent Young Adult Med, Boston, MA USA.
[Kelemen, Skyler; Weitzman, Elissa R.] Boston Childrens Hosp, Dept Emergency Med, Boston, MA USA.
[Lemly, Diana C.; Scherer, Emily A.; Weitzman, Elissa R.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Scherer, Emily A.] Geisel Sch Med Dartmouth, Hanover, NH USA.
RP Lemly, DC (reprint author), Massachusetts Gen Hosp, Div Adolescent & Young Adult Med, 55 Fruit St, Boston, MA 02114 USA.
EM dlemly@partners.org
FU Leadership Education in Adolescent Health training grant from the
Maternal and Child Health Bureau, Health Resources and Services
Administration [T71MC00009]; Gallagher Grant, Adolescent Division Boston
Children's Hospital; Boston Children's Hospital Program for Patient
Safety and Quality; Center for Integration of Medicine and Innovative
Technology [220376]; National Institute on Alcohol Abuse and Alcoholism
[1R01AA021913-01]; Harvard Catalyst under parent National Institute of
Health [027343.386541.05230, 1U54RR025224-0]; National Institutes of
Health (NIH)
FX Funded in part by Leadership Education in Adolescent Health training
grant T71MC00009 from the Maternal and Child Health Bureau, Health
Resources and Services Administration (Dr Lemly, trainee); the Gallagher
Grant, Adolescent Division Boston Children's Hospital to Dr Lemly; and
to Dr Weitzman, an intramural research grant from the Boston Children's
Hospital Program for Patient Safety and Quality, award 220376 from the
Center for Integration of Medicine and Innovative Technology, award
1R01AA021913-01 from the National Institute on Alcohol Abuse and
Alcoholism and award 027343.386541.05230 from the Harvard Catalyst under
parent National Institute of Health award 1U54RR025224-0. Funded by the
National Institutes of Health (NIH).
NR 41
TC 6
Z9 6
U1 0
U2 3
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD NOV
PY 2014
VL 134
IS 5
BP 885
EP 891
DI 10.1542/peds.2014-1304
PG 7
WC Pediatrics
SC Pediatrics
GA AS6PU
UT WOS:000344385900036
PM 25349315
ER
PT J
AU Winickoff, JP
Nabi-Burza, E
Chang, YC
Regan, S
Drehmer, J
Finch, S
Wasserman, R
Ossip, D
Hipple, B
Woo, H
Klein, J
Rigotti, NA
AF Winickoff, Jonathan P.
Nabi-Burza, Emara
Chang, Yuchiao
Regan, Susan
Drehmer, Jeremy
Finch, Stacia
Wasserman, Richard
Ossip, Deborah
Hipple, Bethany
Woo, Heide
Klein, Jonathan
Rigotti, Nancy A.
TI Sustainability of a Parental Tobacco Control Intervention in Pediatric
Practice
SO PEDIATRICS
LA English
DT Article
DE parental smoking; smoking cessation; secondhand smoke
ID SMOKING-CESSATION; ADOLESCENT SMOKING; UNITED-STATES; CHILDREN;
EXPOSURE; HEALTH; SMOKERS; PROTECT; LEAD; CARE
AB OBJECTIVE: To determine whether an evidence-based pediatric outpatient intervention for parents who smoke persisted after initial implementation.
METHODS: A cluster randomized controlled trial of 20 pediatric practices in 16 states that received either Clinical and Community Effort Against Second- hand Smoke Exposure (CEASE) intervention or usual care. The intervention provided practices with training to provide evidence-based assistance to parents who smoke. The primary outcome, assessed by the 12-month follow-up telephone survey with parents, was provision of meaningful tobacco control assistance, defined as discussing various strategies to quit smoking, discussing smoking cessation medication, or recommending the use of the state quitline after initial enrollment visit. We also assessed parental quit rates at 12 months, determined by self-report and biochemical verification.
RESULTS: Practices' rates of providing any meaningful tobacco control assistance (55% vs 19%), discussing various strategies to quit smoking (25% vs 10%), discussing cessation medication (41% vs 11%), and recommending the use of the quitline (37% vs 9%) were all significantly higher in the intervention than in the control groups, respectively (P<.0001 for each), during the 12-month postintervention implementation. Receiving any assistance was associated with a cotinine-confirmed quitting adjusted odds ratio of 1.89 (95% confidence interval: 1.13-3.19). After controlling for demographic and behavioral factors, the adjusted odds ratio for cotinine-confirmed quitting in intervention versus control practices was 1.07 (95% confidence interval: 0.64-1.78).
CONCLUSIONS: Intervention practices had higher rates of delivering tobacco control assistance than usual care practices over the 1-year follow-up period. Parents who received any assistance were more likely to quit smoking; however, parents' likelihood of quitting smoking was not statistically different between the intervention and control groups. Maximizing parental quit rates will require more complete systems-level integration and adjunctive cessation strategies.
C1 [Winickoff, Jonathan P.; Nabi-Burza, Emara; Drehmer, Jeremy; Hipple, Bethany] Massachusetts Gen Hosp Children, Div Gen Acad Pediat, Ctr Child & Adolescent Hlth Res & Policy, Boston, MA 02114 USA.
[Winickoff, Jonathan P.; Klein, Jonathan] AAP Richmond Ctr Excellence, Elk Grove Village, IL USA.
[Finch, Stacia; Wasserman, Richard; Woo, Heide] Amer Acad Pediat, Elk Grove Village, IL USA.
[Winickoff, Jonathan P.; Nabi-Burza, Emara; Chang, Yuchiao; Regan, Susan; Drehmer, Jeremy; Hipple, Bethany; Rigotti, Nancy A.] Massachusetts Gen Hosp, Tobacco Res & Treatment Ctr, Boston, MA 02114 USA.
[Chang, Yuchiao; Regan, Susan; Rigotti, Nancy A.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Wasserman, Richard] Univ Vermont, Dept Pediat, Burlington, VT USA.
[Ossip, Deborah] Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
[Woo, Heide] Univ Calif Los Angeles, Los Angeles, CA USA.
RP Winickoff, JP (reprint author), Massachusetts Gen Hosp Children, Div Gen Acad Pediat, Ctr Child & Adolescent Hlth Res & Policy, 15th Floor,Suite 1542A,100 Cambridge St, Boston, MA 02114 USA.
EM jwinickoff@partners.org
RI Wasserman , Richard/G-3775-2015;
OI Drehmer, Jeremy/0000-0002-5022-5836
FU National Institutes of Health National Cancer Institute [R01-CA127127];
National Institute on Drug Abuse; Agency for Healthcare Research and
Quality; Flight Attendant Medical Research Institute; Pediatric Research
in Office Settings (PROS) Network; Health Resources and Services
Administration Maternal and Child Health Bureau [UA6MC15585]; American
Academy of Pediatrics; National Institutes of Health (NIH)
FX This study was supported by the National Institutes of Health National
Cancer Institute grant R01-CA127127 (to Dr Winickoff), the National
Institute on Drug Abuse, and the Agency for Healthcare Research and
Quality. This study was also partially supported by a grant from the
Flight Attendant Medical Research Institute to the AAP Julius B.
Richmond Center and the Pediatric Research in Office Settings (PROS)
Network, which receives core funding from the Health Resources and
Services Administration Maternal and Child Health Bureau (UA6MC15585)
and the American Academy of Pediatrics. Funded by the National
Institutes of Health (NIH).
NR 36
TC 9
Z9 9
U1 1
U2 7
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD NOV
PY 2014
VL 134
IS 5
BP 933
EP 941
DI 10.1542/peds.2014-0639
PG 9
WC Pediatrics
SC Pediatrics
GA AS6PU
UT WOS:000344385900042
PM 25332492
ER
PT J
AU Van Cleave, J
AF Van Cleave, Jeanne
TI Escalating Violence in PG-13 Movies
SO PEDIATRICS
LA English
DT Editorial Material
DE violence; movie
ID CHILDREN
C1 [Van Cleave, Jeanne] Boston Univ, Sch Med, Dept Pediat, Boston, MA 02118 USA.
[Van Cleave, Jeanne] MassGen Hosp Children, Div Gen Acad Pediat, Boston, MA USA.
RP Van Cleave, J (reprint author), 15th Floor C100,100 Cambridge St, Boston, MA 02144 USA.
EM jvancleave@partners.org
NR 7
TC 0
Z9 0
U1 1
U2 7
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD NOV
PY 2014
VL 134
IS 5
BP 1024
EP 1025
DI 10.1542/peds.2014-2803
PG 2
WC Pediatrics
SC Pediatrics
GA AS6PU
UT WOS:000344385900052
PM 25332493
ER
PT J
AU Sullivan, DR
Ganzini, L
Lopez-Chavez, A
Slatore, CG
AF Sullivan, Donald R.
Ganzini, Linda
Lopez-Chavez, Ariel
Slatore, Christopher G.
TI Association of patient characteristics with chemotherapy receipt among
depressed and non-depressed patients with non-small cell lung cancer
SO PSYCHO-ONCOLOGY
LA English
DT Article
DE Depression; Lung Cancer; Epidemiology; Treatment Receipt; Race
ID RACIAL-DIFFERENCES; DISPARITIES; TRENDS; COMORBIDITY; OUTCOMES; IMPACT;
AGE
C1 [Sullivan, Donald R.; Ganzini, Linda; Slatore, Christopher G.] Portland VA Med Ctr, Portland, OR USA.
[Sullivan, Donald R.; Slatore, Christopher G.] Oregon Hlth & Sci Univ, Dept Med, Div Pulm & Crit Care Med, Portland, OR 97201 USA.
[Ganzini, Linda] Oregon Hlth & Sci Univ, Dept Psychiat, Portland, OR 97201 USA.
[Lopez-Chavez, Ariel] Oregon Hlth & Sci Univ, Dept Med, Div Hematol & Med Oncol, Portland, OR 97201 USA.
[Slatore, Christopher G.] Portland VA Med Ctr, Sect Pulm & Crit Care Med, Portland, OR USA.
RP Sullivan, DR (reprint author), 3710 SW US Vet Hosp Rd,R&D 66, Portland, OR 97239 USA.
EM sullivad@ohsu.edu
OI Sullivan, Donald/0000-0003-3266-3389; Slatore,
Christopher/0000-0003-0958-8122
FU NCATS NIH HHS [UL1 TR000128, UL1TR000128]; NHLBI NIH HHS [5 T32
HL083808-05-32, T32 HL083808]
NR 18
TC 1
Z9 1
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1057-9249
EI 1099-1611
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD NOV
PY 2014
VL 23
IS 11
BP 1318
EP 1322
DI 10.1002/pon.3528
PG 5
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA AS4JX
UT WOS:000344242500016
PM 24771684
ER
PT J
AU Grant, P
Sakellis, C
Jacene, HA
AF Grant, Paul
Sakellis, Christopher
Jacene, Heather A.
TI Gynecologic Oncologic Imaging With PET/CT
SO SEMINARS IN NUCLEAR MEDICINE
LA English
DT Review
ID POSITRON-EMISSION-TOMOGRAPHY; RECURRENT OVARIAN-CANCER; ADVANCED
CERVICAL-CANCER; PARAAORTIC NODAL METASTASIS; POST-THERAPY SURVEILLANCE;
SQUAMOUS-CELL CARCINOMA; SECONDARY CYTOREDUCTIVE SURGERY;
GASTROINTESTINAL STROMAL TUMORS; CLINICAL-PRACTICE GUIDELINES;
STANDARDIZED UPTAKE VALUE
AB FDG-PET/CT has been evaluated in a variety of gynecologic malignancies in a variety of settings and is approved by the Centers for Medicare & Medicaid Services for the initial and subsequent treatment strategies of these malignancies. Cervical cancer is typically very FDG avid, and FDG-PET/CT appears to be most valuable for initial staging, radiation therapy planning, and detection of recurrent disease. For ovarian cancer, the most value of FDG-PET/ CT appears to be for detecting recurrent disease in the setting of rising CA-125 level and negative or equivocal anatomical imaging studies. Initial studies evaluating response to therapy are promising and further work in this area is needed. FDG uptake in both nonmalignant and physiological processes in the pelvis can make interpretation of FDG-PET/CT in this region challenging and knowledge of these entities and patterns can avoid misinterpretation. Some of the most common findings relate to the cyclic changes that occur as part of the menstrual cycle in premenopausal women. Mucinous tumors and low-volume or peritoneal carcinomatosis are causes of false-negative results on FDG-PET/CT studies. As new tracers are developed, comparisons with patient outcomes and standards of care (eg, FDG-PET/CD will be needed. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Grant, Paul; Sakellis, Christopher; Jacene, Heather A.] Dana Farber Canc Inst, Dept Imaging, Boston, MA 02115 USA.
[Grant, Paul; Sakellis, Christopher; Jacene, Heather A.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Radiol, Boston, MA USA.
RP Jacene, HA (reprint author), 450 Brookline Ave,DL203, Boston, MA 02215 USA.
EM hjacene@partners.org
NR 151
TC 6
Z9 6
U1 3
U2 17
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0001-2998
EI 1558-4623
J9 SEMIN NUCL MED
JI Semin. Nucl. Med.
PD NOV
PY 2014
VL 44
IS 6
BP 461
EP 478
DI 10.1053/j.semnuclmed.2014.06.005
PG 18
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AS3WQ
UT WOS:000344206400007
PM 25362236
ER
PT J
AU Tracy, M
Morgenstern, H
Zivin, K
Aiello, AE
Galea, S
AF Tracy, Melissa
Morgenstern, Hal
Zivin, Kara
Aiello, Allison E.
Galea, Sandro
TI Traumatic event exposure and depression severity over time: results from
a prospective cohort study in an urban area
SO SOCIAL PSYCHIATRY AND PSYCHIATRIC EPIDEMIOLOGY
LA English
DT Article
DE Depression; Traumatic events; Stressful events; Violence; Injuries
ID POSTTRAUMATIC-STRESS-DISORDER; NATIONAL COMORBIDITY SURVEY;
POPULATION-BASED COHORT; PRIMARY-CARE PATIENTS; LIFE EVENTS;
GENERAL-POPULATION; MAJOR DEPRESSION; MENTAL-HEALTH; RISK-FACTORS;
SOCIAL SUPPORT
AB Purpose A substantial proportion of adults experience traumatic events each year, yet little is known about the effects of different types of traumatic events on depression severity over time. We prospectively assessed the effects of traumatic event exposure during a 1-year period on changes in depression severity during that period among a representative sample of adults living in Detroit, Michigan in the United States.
Methods We used data from 1,054 participants in the first two waves of the Detroit Neighborhood Health Study (2008-2010). Depression severity was measured with the Patient Health Questionnaire-9 (PHQ-9). Negative binomial regression was used to estimate the effect of traumatic event exposure on depression severity at Wave 2, adjusting for Wave 1 PHQ-9 score and potential confounders.
Results The mean depression severity score at Wave 2 among those exposed to at least one traumatic event during follow-up was 1.71 times higher than among those with no traumatic event exposure [95 % confidence interval (CI) 1.27-2.29]. Also positively associated with depression severity at Wave 2 (vs. no traumatic events) were assaultive violence (mean ratio 2.49, 95 % CI 1.41-4.38), injuries and other directly experienced shocking events (mean ratio 2.59, 95 % CI 1.62-3.82), and three or more traumatic events (mean ratio 2.58, 95 % CI 1.62-4.09).
Conclusions Violence, injuries, and other directly experienced traumatic events increase depression severity and may be useful targets for interventions to alleviate the burden of depression in urban areas.
C1 [Tracy, Melissa; Galea, Sandro] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10032 USA.
[Tracy, Melissa; Morgenstern, Hal; Aiello, Allison E.] Univ Michigan, Sch Publ Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Morgenstern, Hal] Univ Michigan, Sch Publ Hlth, Dept Environm Hlth Sci, Ann Arbor, MI 48109 USA.
[Morgenstern, Hal] Univ Michigan, Sch Med, Dept Urol, Ann Arbor, MI 48109 USA.
[Zivin, Kara] Univ Michigan, Sch Med, Dept Psychiat, Ann Arbor, MI 48109 USA.
[Zivin, Kara] US Dept Vet Affairs, Ann Arbor, MI 48113 USA.
RP Tracy, M (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, 722 W 168th St,Room 515, New York, NY 10032 USA.
EM mt2682@columbia.edu
FU National Institutes of Health [DA022720, DA022720-S1, MH088283,
MH078152, MH082729]
FX This study was supported by the National Institutes of Health (Grants
DA022720, DA022720-S1, MH088283, MH078152, and MH082729).
NR 121
TC 3
Z9 3
U1 5
U2 14
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0933-7954
EI 1433-9285
J9 SOC PSYCH PSYCH EPID
JI Soc. Psychiatry Psychiatr. Epidemiol.
PD NOV
PY 2014
VL 49
IS 11
BP 1769
EP 1782
DI 10.1007/s00127-014-0884-2
PG 14
WC Psychiatry
SC Psychiatry
GA AS1UM
UT WOS:000344067300009
PM 24816599
ER
PT J
AU Foroud, T
Lai, DB
Koller, D
van't Hof, F
Kurki, MI
Anderson, CS
Brown, RD
Connolly, ES
Eriksson, JG
Flaherty, M
Fornage, M
von und zu Fraunberg, M
Gaal, EI
Laakso, A
Hernesniemi, J
Huston, J
Jaaskelainen, JE
Kiemeney, LA
Kivisaari, R
Kleindorfer, D
Ko, N
Lehto, H
Mackey, J
Meissner, I
Moomaw, CJ
Mosley, TH
Moskala, M
Niemela, M
Palotie, A
Pera, J
Rinkel, G
Ripke, S
Rouleau, G
Ruigrok, Y
Sauerbeck, L
Slowik, A
Vermeulen, SH
Woo, D
Worrall, BB
Broderick, J
AF Foroud, Tatiana
Lai, Dongbing
Koller, Daniel
van't Hof, Femke
Kurki, Mitja I.
Anderson, Craig S.
Brown, Robert D., Jr.
Connolly, Edward Sander
Eriksson, Johan G.
Flaherty, Matthew
Fornage, Myriam
von und zu Fraunberg, Mikael
Gaal, Emilia I.
Laakso, Aki
Hernesniemi, Juha
Huston, John
Jaaskelainen, Juha E.
Kiemeney, Lambertus A.
Kivisaari, Riku
Kleindorfer, Dawn
Ko, Nerissa
Lehto, Hanna
Mackey, Jason
Meissner, Irene
Moomaw, Charles J.
Mosley, Thomas H.
Moskala, Marek
Niemela, Mika
Palotie, Aarno
Pera, Joanna
Rinkel, Gabriel
Ripke, Stephan
Rouleau, Guy
Ruigrok, Ynte
Sauerbeck, Laura
Slowik, Agnieszka
Vermeulen, Sita H.
Woo, Daniel
Worrall, Bradford B.
Broderick, Joseph
CA Familial Intracranial
TI Genome-Wide Association Study of Intracranial Aneurysm Identifies a New
Association on Chromosome 7
SO STROKE
LA English
DT Article
DE chromosomes; human; pair 7; genome-wide association study; intracranial
aneurysm
ID GENETIC RISK-FACTORS; SUBARACHNOID HEMORRHAGE; CEREBRAL ANEURYSMS;
SEQUENCE VARIANT; ISCHEMIC-STROKE; FAMILY-HISTORY; METAANALYSIS; AGE;
REGION; SUSCEPTIBILITY
AB Background and Purpose Common variants have been identified using genome-wide association studies which contribute to intracranial aneurysms (IA) susceptibility. However, it is clear that the variants identified to date do not account for the estimated genetic contribution to disease risk.
Methods Initial analysis was performed in a discovery sample of 2617 IA cases and 2548 controls of white ancestry. Novel chromosomal regions meeting genome-wide significance were further tested for association in 2 independent replication samples: Dutch (717 cases; 3004 controls) and Finnish (799 cases; 2317 controls). A meta-analysis was performed to combine the results from the 3 studies for key chromosomal regions of interest.
Results Genome-wide evidence of association was detected in the discovery sample on chromosome 9 (CDKN2BAS; rs10733376: P<1.0x10(-11)), in a gene previously associated with IA. A novel region on chromosome 7, near HDAC9, was associated with IA (rs10230207; P=4.14x10(-8)). This association replicated in the Dutch sample (P=0.01) but failed to show association in the Finnish sample (P=0.25). Meta-analysis results of the 3 cohorts reached statistical significant (P=9.91x10(-10)).
Conclusions We detected a novel region associated with IA susceptibility that was replicated in an independent Dutch sample. This region on chromosome 7 has been previously associated with ischemic stroke and the large vessel stroke occlusive subtype (including HDAC9), suggesting a possible genetic link between this stroke subtype and IA.
C1 [Foroud, Tatiana; Lai, Dongbing; Koller, Daniel; Mackey, Jason] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[van't Hof, Femke; Ruigrok, Ynte] Univ Med Ctr Utrecht, Utrecht, Netherlands.
[Kurki, Mitja I.; von und zu Fraunberg, Mikael; Jaaskelainen, Juha E.] Kuopio Univ Hosp, SF-70210 Kuopio, Finland.
[Kurki, Mitja I.; von und zu Fraunberg, Mikael; Jaaskelainen, Juha E.] Univ Eastern Finland, Kuopio, Finland.
[Kurki, Mitja I.; Palotie, Aarno; Ripke, Stephan] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Kurki, Mitja I.; Palotie, Aarno; Ripke, Stephan] Harvard Univ, Sch Med, Boston, MA USA.
[Kurki, Mitja I.; Palotie, Aarno; Ripke, Stephan] Broad Inst Harvard & MIT, Cambridge, MA USA.
[Anderson, Craig S.] Univ Sydney, Sydney, NSW 2006, Australia.
[Anderson, Craig S.] Royal Prince Alfred Hosp, Sydney, NSW, Australia.
[Brown, Robert D., Jr.; Huston, John; Meissner, Irene] Mayo Clin, Rochester, MN USA.
[Connolly, Edward Sander] Columbia Univ, Sch Med, New York, NY USA.
[Eriksson, Johan G.; Gaal, Emilia I.] Univ Helsinki, Helsinki, Finland.
[Eriksson, Johan G.] Folkhalsan Res Ctr, Helsinki, Finland.
[Eriksson, Johan G.] Natl Inst Hlth & Welf, Helsinki, Finland.
[Eriksson, Johan G.] Vasa Cent Hosp, Vaasa, Finland.
[Eriksson, Johan G.; Gaal, Emilia I.; Laakso, Aki; Hernesniemi, Juha; Kivisaari, Riku; Lehto, Hanna; Niemela, Mika] Univ Helsinki, Cent Hosp, Helsinki, Finland.
[Flaherty, Matthew; Kleindorfer, Dawn; Moomaw, Charles J.; Sauerbeck, Laura; Woo, Daniel; Broderick, Joseph] Univ Cincinnati, Cincinnati, OH 45221 USA.
[Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Kiemeney, Lambertus A.; Vermeulen, Sita H.] Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Ko, Nerissa] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Mosley, Thomas H.] Univ Mississippi, Med Ctr, Jackson, MS USA.
[Moskala, Marek; Pera, Joanna; Slowik, Agnieszka] Jagiellonian Univ, Coll Med, Krakow, Poland.
[Palotie, Aarno] Wellcome Trust Sanger Inst, Cambridge, England.
[Rouleau, Guy] Univ Montreal, Montreal, PQ, Canada.
[Worrall, Bradford B.] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
RP Foroud, T (reprint author), Indiana Univ Sch Med, 410 W 10th St,HS 4021, Indianapolis, IN 46202 USA.
EM tforoud@iu.edu
RI Kiemeney, Lambertus/D-3357-2009; Niemela, Mika/F-2539-2015; Vermeulen,
H.H.M./L-4716-2015;
OI Kiemeney, Lambertus/0000-0002-2368-1326; Niemela,
Mika/0000-0003-1526-0684; Eriksson, Johan/0000-0002-2516-2060
FU National Institutes of Health (NIH) [UL1RR025005]; National Health and
Medical Research Council (NHMRC) of Australia [R01NS39512, R03NS083468];
Health Research Council of New Zealand; NHMRC Senior Principal Research
Fellowship; Veni grant by The Netherlands Organization for Scientific
Research (NOW) [91610016]; Dutch Heart Foundation [2008B004];
Jagiellonian University Medical College [K/ZDS/001456]; National Heart,
Lung, and Blood Institute [HHSN268201100005C, HHSN268201100006C,
HHSN268201100007C, HHSN268201100008C, HHSN268201100 009C,
HHSN268201100010C, HHSN268201100011C, HHSN 268201100012C, R01HL087641,
R01HL59367, R01HL086694]; National Human Genome Research Institute
[U01HG004402]; NIH [HHSN268200625226C]; [R01-HL70825]
FX Infrastructure was partly supported by grant number UL1RR025005, a
component of the National Institutes of Health (NIH) and NIH Roadmap for
Medical Research. This study was also supported by R01NS39512 (Dr
Broderick), R03NS083468 (Dr Foroud), the National Health and Medical
Research Council (NHMRC) of Australia, and the Health Research Council
of New Zealand. Additional funding was provided by an NHMRC Senior
Principal Research Fellowship (Dr Anderson), a Veni grant by The
Netherlands Organization for Scientific Research (NOW; project no.
91610016; Dr Ruigrok), a grant from the Dutch Heart Foundation (project
no. 2008B004; Dr van't Hof), and a grant from Jagiellonian University
Medical College K/ZDS/001456. Atherosclerosis Risk in Communities is
performed as a collaborative study supported by National Heart, Lung,
and Blood Institute contracts (HHSN268201100005C, HHSN268201100006C,
HHSN268201100007C, HHSN268201100008C, HHSN268201100 009C,
HHSN268201100010C, HHSN268201100011C, and HHSN 268201100012C),
R01HL087641, R01HL59367, and R01HL086694; National Human Genome Research
Institute contract U01HG004402; and NIH contract HHSN268200625226C.
Neurocognitive data were collected by U01 HL096812, HL096814, HL096899,
HL096902, and HL096917 with previous brain MRI examinations funded by
R01-HL70825.
NR 29
TC 6
Z9 7
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD NOV
PY 2014
VL 45
IS 11
BP 3194
EP 3199
DI 10.1161/STROKEAHA.114.006096
PG 6
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA AS6CD
UT WOS:000344351500021
PM 25256182
ER
PT J
AU Xian, Y
Holloway, RG
Smith, EE
Schwamm, LH
Reeves, MJ
Bhatt, DL
Schulte, PJ
Cox, M
Olson, DM
Hernandez, AF
Lytle, BL
Anstrom, KJ
Fonarow, GC
Peterson, ED
AF Xian, Ying
Holloway, Robert G.
Smith, Eric E.
Schwamm, Lee H.
Reeves, Mathew J.
Bhatt, Deepak L.
Schulte, Phillip J.
Cox, Margueritte
Olson, DaiWai M.
Hernandez, Adrian F.
Lytle, Barbara L.
Anstrom, Kevin J.
Fonarow, Gregg C.
Peterson, Eric D.
TI Racial/Ethnic Differences in Process of Care and Outcomes Among Patients
Hospitalized With Intracerebral Hemorrhage
SO STROKE
LA English
DT Article
DE cerebral hemorrhage; continental population groups; ethnology; outcomes
research; quality of health care
ID ASSOCIATION/AMERICAN STROKE ASSOCIATION; NOT-RESUSCITATE ORDERS; ACUTE
ISCHEMIC-STROKE; QUALITY-OF-CARE; AMERICAN-HEART-ASSOCIATION;
GUIDELINES-STROKE; MORTALITY; PROFESSIONALS; BLACKS; MODELS
AB Background and Purpose Although racial/ethnic differences in care are pervasive in many areas of medicine, little is known whether intracerebral hemorrhage (ICH) care processes or outcomes differ by race/ethnicity.
Methods We analyzed 123 623 patients with ICH (83 216 white, 22 147 black, 10 519 Hispanic, and 7741 Asian) hospitalized at 1199 Get With The Guidelines-Stroke hospitals between 2003 and 2012. Multivariable logistic regression with generalized estimating equation was used to evaluate the association among race, stroke performance measures, and in-hospital outcomes.
Results Relative to white patients, black, Hispanic, and Asian patients were significantly younger, but more frequently had more severe stroke (median National Institutes of Health Stroke Scale, 9, 10, 10, and 11, respectively; P<0.001). After adjustment for both patient and hospital-level characteristics, black patients were more likely to receive deep venous thrombosis prophylaxis, rehabilitation assessment, dysphagia screening, and stroke education, but less likely to have door to computed tomographic time 25 minutes and smoking cessation counseling than whites. Both Hispanic and Asian patients had higher odds of dysphagia screening but lower odds of smoking cessation counseling. In-hospital all-cause mortality was lower for blacks (23.0%), Hispanics (22.8%), and Asians (25.3%) than for white patients (27.6%). After risk adjustment, all minority groups had lower odds of death, of receiving comfort measures only or of being discharged to hospice. In contrast, they were more likely to exceed the median length of stay when compared with white patients.
Conclusions Although individual quality indicators in ICH varied by race/ethnicity, black, Hispanic, and Asian patients with ICH had lower risk-adjusted in-hospital mortality than white patients with ICH.
C1 [Xian, Ying; Schulte, Phillip J.; Cox, Margueritte; Hernandez, Adrian F.; Lytle, Barbara L.; Peterson, Eric D.] Duke Clin Res Inst, Durham, NC 27705 USA.
[Holloway, Robert G.] Univ Rochester, Med Ctr, Dept Neurol, Rochester, NY 14627 USA.
[Smith, Eric E.] Univ Calgary, Dept Clin Neurosci, Calgary, AB, Canada.
[Smith, Eric E.] Univ Calgary, Hotchkiss Brain Inst, Calgary, AB, Canada.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Reeves, Mathew J.] Michigan State Univ, Dept Epidemiol, E Lansing, MI 48824 USA.
[Bhatt, Deepak L.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Bhatt, Deepak L.] Harvard Univ, Sch Med, Boston, MA USA.
[Olson, DaiWai M.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Div Cardiol, Los Angeles, CA USA.
RP Xian, Y (reprint author), Duke Clin Res Inst, 2400 Pratt St, Durham, NC 27705 USA.
EM ying.xian@duke.edu
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 American Heart Association-Pharmaceutical Roundtable; David and Stevie
Spina; Boeringher-Ingelheim; Merck; Bristol-Myers Squib/Sanofi
Pharmaceutical Partnership; Janseen Pharmaceutical Companies of Johnson
Johnson; AHA Pharmaceutical Roundtable
FX This study received an award from the American Heart
Association-Pharmaceutical Roundtable and from David and Stevie Spina.
The Get With The Guidelines-Stroke (GWTG-Stroke) program is provided by
the American Heart Association/American Stroke Association (AHA/ASA).
The GWTG-Stroke has been funded in the past through support from
Boeringher-Ingelheim, Merck, Bristol-Myers Squib/Sanofi Pharmaceutical
Partnership, Janseen Pharmaceutical Companies of Johnson & Johnson and
the AHA Pharmaceutical Roundtable. The funding organizations had no role
in the design and conduct of the study; the collection, management,
analysis, and interpretation of the data; or the preparation of the
article. Representatives from the AHA reviewed and approved a draft of
the article. This study used the GWTG-Stroke database. The
interpretation and reporting of these data are the sole responsibility
of the authors and do not necessarily represent the official views of
the AHA.
NR 35
TC 5
Z9 5
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD NOV
PY 2014
VL 45
IS 11
BP 3243
EP 3250
DI 10.1161/STROKEAHA.114.005620
PG 8
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA AS6CD
UT WOS:000344351500029
PM 25213344
ER
PT J
AU Ciura, VA
Brouwers, HB
Pizzolato, R
Ortiz, CJ
Rosand, J
Goldstein, JN
Greenberg, SM
Pomerantz, SR
Gonzalez, RG
Romero, JM
AF Ciura, Viesha A.
Brouwers, H. Bart
Pizzolato, Raffaella
Ortiz, Claudia J.
Rosand, Jonathan
Goldstein, Joshua N.
Greenberg, Steven M.
Pomerantz, Stuart R.
Gonzalez, R. Gilberto
Romero, Javier M.
TI Spot Sign on 90-Second Delayed Computed Tomography Angiography Improves
Sensitivity for Hematoma Expansion and Mortality Prospective Study
SO STROKE
LA English
DT Article
DE cerebral hemorrhage; computed tomography angiography; mortality
ID PRIMARY INTRACEREBRAL HEMORRHAGE; CONTRAST EXTRAVASATION; IDENTIFIES
PATIENTS; POSTCONTRAST CT; HIGHEST RISK; SCORE; PREDICTOR; GROWTH;
VOLUME
AB Background and Purpose The computed tomography angiography (CTA) spot sign is a validated biomarker for poor outcome and hematoma expansion in intracerebral hemorrhage. The spot sign has proven to be a dynamic entity, with multimodal imaging proving to be of additional value. We investigated whether the addition of a 90-second delayed CTA acquisition would capture additional intracerebral hemorrhage patients with the spot sign and increase the sensitivity of the spot sign.
Methods We prospectively enrolled consecutive intracerebral hemorrhage patients undergoing first pass and 90-second delayed CTA for 18 months at a single academic center. Univariate and multivariate logistic regression were performed to assess clinical and neuroimaging covariates for relationship with hematoma expansion and mortality.
Results Sensitivity of the spot sign for hematoma expansion on first pass CTA was 55%, which increased to 64% if the spot sign was present on either CTA acquisition. In multivariate analysis the spot sign presence was associated with significant hematoma expansion: odds ratio, 17.7 (95% confidence interval, 3.7-84.2; P=0.0004), 8.3 (95% confidence interval, 2.0-33.4; P=0.004), and 12.0 (95% confidence interval, 2.9-50.5; P=0.0008) if present on first pass, delayed, or either CTA acquisition, respectively. Spot sign presence on either acquisitions was also significant for mortality.
Conclusions We demonstrate improved sensitivity for predicting hematoma expansion and poor outcome by adding a 90-second delayed CTA, which may enhance selection of patients who may benefit from hemostatic therapy.
C1 [Ciura, Viesha A.; Pizzolato, Raffaella; Ortiz, Claudia J.; Pomerantz, Stuart R.; Gonzalez, R. Gilberto; Romero, Javier M.] Harvard Univ, Sch Med, Dept Radiol, Div Neuroradiol,Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Brouwers, H. Bart; Rosand, Jonathan] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Human Genet Res, Boston, MA 02115 USA.
[Brouwers, H. Bart; Rosand, Jonathan; Goldstein, Joshua N.] Harvard Univ, Sch Med, Dept Neurol, Div Neurocrit Care & Emergency Neurol,Massachuset, Boston, MA 02115 USA.
[Brouwers, H. Bart; Rosand, Jonathan; Goldstein, Joshua N.; Greenberg, Steven M.] Harvard Univ, Sch Med, Dept Neurol, Hemorrhag Stroke Res Grp,Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Brouwers, H. Bart; Rosand, Jonathan; Goldstein, Joshua N.] Harvard Univ, Sch Med, Dept Neurol, J Philip Kistler Stroke Res Ctr,Massachusetts Gen, Boston, MA 02115 USA.
[Goldstein, Joshua N.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Emergency Med, Boston, MA 02115 USA.
[Brouwers, H. Bart] Univ Utrecht, Univ Med Ctr Utrecht, Brain Ctr Rudolf Magnus, Dept Neurosurg, Utrecht, Netherlands.
RP Romero, JM (reprint author), Massachusetts Gen Hosp, Div Neuroradiol, 55 Fruit St,Gray 2,Rm 273A, Boston, MA 02114 USA.
EM jmromero@mgh.harvard.edu
RI Goldstein, Joshua/H-8953-2016
FU National Institutes of Health-National Institute of Neurological
Disorders and Stroke Specialized Programs of Translational Research in
Acute Stroke (NIH-NINDS SPOTRIAS) [P50NS051343]
FX Dr Brouwers was supported by the National Institutes of Health-National
Institute of Neurological Disorders and Stroke Specialized Programs of
Translational Research in Acute Stroke (NIH-NINDS SPOTRIAS) fellowship
grant P50NS051343.
NR 31
TC 10
Z9 11
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD NOV
PY 2014
VL 45
IS 11
BP 3293
EP 3297
DI 10.1161/STROKEAHA.114.005570
PG 5
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA AS6CD
UT WOS:000344351500037
PM 25300974
ER
PT J
AU Saposnik, G
Fonarow, GC
Pan, WQ
Liang, L
Hernandez, AF
Schwamm, LH
Smith, EE
AF Saposnik, Gustavo
Fonarow, Gregg C.
Pan, Wenquin
Liang, Li
Hernandez, Adrian F.
Schwamm, Lee H.
Smith, Eric E.
CA AHA Get-With-The-Guidelines Stroke
TI Guideline-Directed Low-Density Lipoprotein Management in High-Risk
Patients With Ischemic Stroke Findings From Get With The
Guidelines-Stroke 2003 to 2012
SO STROKE
LA English
DT Article
DE cardiovascular diseases; cholesterol; diabetes mellitus; dyslipidemias;
LDL cholesterol; prevention & control; standards; stroke; therapeutics
ID HEALTH-CARE PROFESSIONALS; CARDIOVASCULAR-DISEASE; PERFORMANCE-MEASURES;
TASK-FORCE; PREVENTION; CHOLESTEROL; ATTACK; ASSOCIATION; OUTCOMES;
PROGRAM
AB Background and Purpose Limited information is available on stroke prevention in high-risk patients with preexisting cardiovascular disease. Our aim was to use admission low-density lipoprotein (LDL) values to evaluate differences in the attainment of National Cholesterol Education Program-Adult Treatment Panel III guidelines goals at the time of the index event in high-risk patients with stroke and preexisting cardio- or cerebrovascular disease.
Methods Observational study, using data from the Get-With-The-Guidelines-Stroke Registry including 913 436 patients with an acute ischemic stroke or transient ischemic attack from April 2003 to September 2012. Participants were classified as high risk if they had history of transient ischemic attack (TIA), stroke (cardiovascular disease), and coronary artery disease (CAD).
Results Of the 913 436 patients admitted with an acute stroke or TIA, 194 557 (21.3%) had previous stroke/TIA, 148 833 (16.3%) had previous CAD, and 88 605 (9.7%) had concomitant CAD and cardiovascular disease. Overall, only 68% of patients with stroke were at their preadmission National Cholesterol Education Program III guideline-recommended LDL target; 51.3% had LDL <100 mg/dL; and only 19.8% had LDL<70 mg/dL. Among those presenting with a recurrent stroke, >45% had LDL>100 mg/dL. When compared with patients with CAD, patients with previous TIA/stroke were less likely to have LDL<100 or <70 mg/dL. In multivariable analysis, older age, men, white race, lack of major vascular risk factors, previous use of cholesterol-lowering therapy, and care provided in larger hospitals were associated with meeting LDL targets on admission testing.
Conclusions Management of dyslipidemia in high-risk patients with preexistent CAD or stroke continues to be suboptimal. Only 1 in 5 patients with prior TIA/stroke had LDL levels <70 mg/dL.
C1 [Saposnik, Gustavo] Univ Toronto, St Michaels Hosp, Dept Med, Div Neurol,Stroke Outcomes Res Ctr, Toronto, ON M5B 1W8, Canada.
[Fonarow, Gregg C.] Univ Calif Los Angeles, Div Cardiol, Los Angeles, CA USA.
[Pan, Wenquin; Liang, Li; Hernandez, Adrian F.] Duke Clin Res Inst, Durham, NC USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Stroke Serv, Boston, MA 02114 USA.
[Schwamm, Lee H.] Massachusetts Gen Hosp, Inst Heart Vasc & Stroke Care, Boston, MA 02114 USA.
[Smith, Eric E.] Univ Calgary, Hotchkiss Brain Inst, Calgary Stroke Program, Calgary, AB, Canada.
RP Saposnik, G (reprint author), St Michaels Hosp, Stroke Outcomes Res Ctr, Div Neurol, 55 Queen St E,Room 93, Toronto, ON M5C 1R6, Canada.
EM saposnikg@smh.ca
RI Smith, Eric/C-5443-2012; Hernandez, Adrian F./A-7818-2016
OI Smith, Eric/0000-0003-3956-1668; Schwamm, Lee/0000-0003-0592-9145;
Hernandez, Adrian F./0000-0003-3387-9616
FU American Heart Association; American Stroke Association; Pfizer, Inc,
New York, NY; Merck-Schering Plough Partnership (North Wales, PA)
FX The Get-with-the-Guidelines is funded by the American Heart Association
and the American Stroke Association. The program is also supported in
part by unrestricted educational grants to the American Heart
Association by Pfizer, Inc, New York, NY, and the Merck-Schering Plough
Partnership (North Wales, PA), who did not participate in the design,
analysis, article preparation, or approval.
NR 33
TC 9
Z9 10
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD NOV
PY 2014
VL 45
IS 11
BP 3343
EP 3351
DI 10.1161/STROKEAHA.114.006736
PG 9
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA AS6CD
UT WOS:000344351500045
PM 25300975
ER
PT J
AU Hattori, Y
Okamoto, Y
Maki, T
Yamamoto, Y
Oishi, N
Yamahara, K
Nagatsuka, K
Takahashi, R
Kalaria, RN
Fukuyama, H
Kinoshita, M
Ihara, M
AF Hattori, Yorito
Okamoto, Yoko
Maki, Takakuni
Yamamoto, Yumi
Oishi, Naoya
Yamahara, Kenichi
Nagatsuka, Kazuyuki
Takahashi, Ryosuke
Kalaria, Raj N.
Fukuyama, Hidenao
Kinoshita, Makoto
Ihara, Masafumi
TI Silent Information Regulator 2 Homolog 1 Counters Cerebral Hypoperfusion
Injury by Deacetylating Endothelial Nitric Oxide Synthase
SO STROKE
LA English
DT Article
DE carotid artery stenosis; cerebral ischemia; dementia; endothelial nitric
oxide synthase; mouse; SIRT1
ID AMYOTROPHIC-LATERAL-SCLEROSIS; CELLULAR PRION PROTEIN; EXTENDS
LIFE-SPAN; ALZHEIMERS-DISEASE; MOUSE MODEL; NEURODEGENERATIVE DISEASE;
SACCHAROMYCES-CEREVISIAE; SIRT1 DEACETYLASE; ISCHEMIC DAMAGE; BRAIN
AB Background and Purpose Silent information regulator 2 homolog 1 (SIRT1) is a protein deacetylase that has been reported to suppress neurodegenerative and cardiovascular diseases in model organisms. We hypothesized that neurovascular protection is one of the diverse actions of SIRT1. This study was designed to determine whether SIRT1 protects against the consequences of cerebral hypoperfusion in vivo.
MethodsSirt1-overexpressing (Sirt1-Tg) mice driven by a prion promoter and their wild-type littermates were subjected to bilateral common carotid artery stenosis using external microcoils. Using Sirt1-Tg mice, we assessed the effect of SIRT1 on cerebral blood flow, cerebral angioarchitecture, histological and ultrastructural changes, and spatial working memory at several time points. We also evaluated the effects of preadministration of SIRT1 inhibitors or endothelial nitric oxide synthase inhibitors on cerebral blood flow after bilateral common carotid artery stenosis in Sirt1-Tg mice. Levels of acetylated and nonacetylated endothelial nitric oxide synthase were measured semiquantitatively with immunoblotting.
Results Cerebral hypoperfusion induced by bilateral common carotid artery stenosis caused memory impairment and histological changes in wild-type littermates. However, these phenotypes were rescued in Sirt1-Tg mice, where cerebral blood flow was maintained even poststenosis. Electron microscopic analyses showed irregularities in the vascular endothelia, such as tight junction openings in wild-type mice, which were absent in Sirt1-Tg littermates. Brain endothelial nitric oxide synthase was acetylated after cerebral hypoperfusion in wild-type littermates but remained unacetylated in Sirt1-Tg mice. Moreover, treatment with SIRT1 inhibitors and endothelial nitric oxide synthase inhibitors abolished the vasculoprotective effects of SIRT1.
Conclusions Our results indicate that neurovascular endothelial SIRT1 potentiation upregulates the nitric oxide system and counters cerebral hypoperfusion injury. This novel cerebral blood flow-preserving mechanism offers potential molecular targets for future therapeutic intervention.
C1 [Hattori, Yorito; Takahashi, Ryosuke] Kyoto Univ, Grad Sch Med, Dept Neurol, Kyoto, Japan.
[Oishi, Naoya; Fukuyama, Hidenao] Kyoto Univ, Grad Sch Med, Human Brain Res Ctr, Kyoto, Japan.
[Hattori, Yorito; Yamamoto, Yumi; Yamahara, Kenichi; Ihara, Masafumi] Natl Cerebral & Cardiovasc Ctr, Dept Regenerat Med & Tissue Engn, Osaka 5658565, Japan.
[Okamoto, Yoko] Natl Cerebral & Cardiovasc Ctr, Dept Pathol, Osaka 5658565, Japan.
[Nagatsuka, Kazuyuki; Ihara, Masafumi] Natl Cerebral & Cardiovasc Ctr, Dept Stroke & Cerebrovasc Dis, Osaka 5658565, Japan.
[Maki, Takakuni] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Maki, Takakuni] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Maki, Takakuni] Harvard Univ, Sch Med, Boston, MA USA.
[Takahashi, Ryosuke; Kinoshita, Makoto] Japan Sci Technol Corp, CREST, Saitama, Japan.
[Kalaria, Raj N.] Newcastle Univ, Inst Ageing & Hlth, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Kinoshita, Makoto] Nagoya Univ, Grad Sch Sci, Div Biol Sci, Nagoya, Aichi 4648601, Japan.
RP Ihara, M (reprint author), Natl Cerebral & Cardiovasc Ctr, Dept Stroke & Cerebrovasc Dis, Osaka 5658565, Japan.
EM ihara@ncvc.go.jp
OI Ihara, Masafumi/0000-0002-7102-4048; Yamamoto, Yumi/0000-0001-7188-9618
FU Ministry of Health, Labour, and Welfare [0605-1]; Ministry of Education,
Culture, Sports, Science, and Technology [23390233]; Takeda Science
Foundation; Japan Science Technology Corporation; Alzheimer's Research
UK; [2311531]; [25116514]; [25893301]
FX We gratefully acknowledge grant support from the Ministry of Health,
Labour, and Welfare (Dr Ihara, no. 0605-1), the Ministry of Education,
Culture, Sports, Science, and Technology (Dr Ihara, Grant-in-Aid for
Scientific Research (B), no. 23390233; Dr Hattori, Grant-in-Aid for
Research Activity Start-up, no. 25893301; Dr Kinoshita, Grant-in-Aid for
Scientific Research on Innovative Areas, no. 2311531 and 25116514), the
Takeda Science Foundation (Dr Ihara), Japan Science Technology
Corporation (Dr Takahashi), and Alzheimer's Research UK (Dr Kalaria).
NR 40
TC 9
Z9 9
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
EI 1524-4628
J9 STROKE
JI Stroke
PD NOV
PY 2014
VL 45
IS 11
BP 3403
EP 3411
DI 10.1161/STROKEAHA.114.006265
PG 9
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA AS6CD
UT WOS:000344351500053
PM 25213338
ER
PT J
AU Chellali, A
Schwaitzberg, SD
Jones, DB
Romanelli, J
Miller, A
Rattner, D
Roberts, KE
Cao, CGL
AF Chellali, Amine
Schwaitzberg, Steven D.
Jones, Daniel B.
Romanelli, John
Miller, Amie
Rattner, David
Roberts, Kurt E.
Cao, Caroline G. L.
TI Toward scar-free surgery: an analysis of the increasing complexity from
laparoscopic surgery to NOTES
SO SURGICAL ENDOSCOPY AND OTHER INTERVENTIONAL TECHNIQUES
LA English
DT Article
DE NOTES continuum; Laparoscopic surgery; Cholecystectomy; Hierarchical
task analysis; Timeline analysis; Cognitive task analysis
ID TRANSLUMENAL ENDOSCOPIC SURGERY; NOTES TRANSVAGINAL CHOLECYSTECTOMY;
HIERARCHICAL DECOMPOSITION; SERIES
AB NOTES is an emerging technique for performing surgical procedures, such as cholecystectomy. Debate about its real benefit over the traditional laparoscopic technique is on-going. There have been several clinical studies comparing NOTES to conventional laparoscopic surgery. However, no work has been done to compare these techniques from a Human Factors perspective. This study presents a systematic analysis describing and comparing different existing NOTES methods to laparoscopic cholecystectomy.
Videos of endoscopic/laparoscopic views from fifteen live cholecystectomies were analyzed to conduct a detailed task analysis of the NOTES technique. A hierarchical task analysis of laparoscopic cholecystectomy and several hybrid transvaginal NOTES cholecystectomies was performed and validated by expert surgeons. To identify similarities and differences between these techniques, their hierarchical decomposition trees were compared. Finally, a timeline analysis was conducted to compare the steps and substeps.
At least three variations of the NOTES technique were used for cholecystectomy. Differences between the observed techniques at the substep level of hierarchy and on the instruments being used were found. The timeline analysis showed an increase in time to perform some surgical steps and substeps in NOTES compared to laparoscopic cholecystectomy.
As pure NOTES is extremely difficult given the current state of development in instrumentation design, most surgeons utilize different hybrid methods-combination of endoscopic and laparoscopic instruments/optics. Results of our hierarchical task analysis yielded an identification of three different hybrid methods to perform cholecystectomy with significant variability among them. The varying degrees to which laparoscopic instruments are utilized to assist in NOTES methods appear to introduce different technical issues and additional tasks leading to an increase in the surgical time. The NOTES continuum of invasiveness is proposed here as a classification scheme for these methods, which was used to construct a clear roadmap for training and technology development.
C1 [Chellali, Amine; Schwaitzberg, Steven D.] Harvard Univ, Sch Med, Dept Surg, Cambridge Hlth Alliance, Cambridge, MA 02138 USA.
[Chellali, Amine] Univ Evry, Dept Comp Engn, Evry, France.
[Jones, Daniel B.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Dept Surg, Boston, MA 02215 USA.
[Romanelli, John] Tufts Univ, Sch Med, Dept Surg, Baystate Med Ctr, Springfield, MA 01199 USA.
[Miller, Amie] Wright State Univ, Dept Surg, Dayton, OH 45435 USA.
[Rattner, David] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Roberts, Kurt E.] Yale Univ, Sch Med, Dept Surg, New Haven, CT 06510 USA.
[Cao, Caroline G. L.] Wright State Univ, Dept Biomed Ind & Human Factors Engn, Russ Engn Ctr 207, Dayton, OH 45435 USA.
RP Cao, CGL (reprint author), Wright State Univ, Dept Biomed Ind & Human Factors Engn, Russ Engn Ctr 207, 3640 Colonel Glenn Hwy, Dayton, OH 45435 USA.
EM amine.chellali@issyl-lab.org; caroline.cao@wright.edu
FU NIH/NIBIB [R01EB009362]
FX The authors gratefully acknowledge the support of this study by
NIH/NIBIB (Grant No. R01EB009362).
NR 34
TC 1
Z9 1
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0930-2794
EI 1432-2218
J9 SURG ENDOSC
JI Surg. Endosc.
PD NOV
PY 2014
VL 28
IS 11
BP 3119
EP 3133
DI 10.1007/s00464-014-3565-z
PG 15
WC Surgery
SC Surgery
GA AS3HL
UT WOS:000344168200013
PM 24902811
ER
PT J
AU Jakobiec, FA
Rai, R
Rashid, A
Kanoff, J
Mukai, S
AF Jakobiec, Frederick A.
Rai, Ruju
Rashid, Alia
Kanoff, Justin
Mukai, Shizuo
TI Dystrophic hyaloid artery remnants and other abnormalities in a
buphthalmic eye with retinoblastoma
SO SURVEY OF OPHTHALMOLOGY
LA English
DT Review
DE hyaloid artery; dystrophic calcification; retinoblastoma; buphthalmos;
crystalline lens; cataract; deformation of lens; lens capsule; lens
epithelium
ID PERSISTENT FETAL VASCULATURE; EXUDATIVE VITREORETINOPATHY; CATARACTS;
MUTATION; GENE
AB Partial persistence of the hyaloid artery unaccompanied by hyperplastic primary vitreous has not been previously reported in association with retinoblastoma. We describe an 18-month-old child with such a finding who had a retinoblastoma that was undifferentiated, extensively necrotic, heavily calcified, and completely filled the eyeball. The enucleated globe harbored a nonperfused, fossilized remnant of the hyaloid artery due to DNA/calcium deposition in the vascular wall. This structure inserted into a lenticular, extracapsular, fibrous plaque corresponding to a Mittendorf dot. The tumor had induced a placoid cataractous lens, obliterated the anterior and posterior chambers, caused glaucoma leading to buphthalmos, and extended into the optic nerve and extraocularly to involve the orbit. We conclude that the retinoblastoma arose early in ocular morphogenesis, at around 4 months gestation, when the programmed involution of the hyaloid artery begins. This process would typically end at 7-8 months gestation, but was aborted by the tumor. The patient died 6 weeks after surgery without receiving further treatment because of the parents' resistance. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Jakobiec, Frederick A.; Rai, Ruju; Rashid, Alia] Massachusetts Eye & Ear Infirm, David G Cogan Lab Ophthalm Pathol, Dept Ophthalmol, Boston, MA 02114 USA.
[Jakobiec, Frederick A.; Rai, Ruju; Rashid, Alia; Kanoff, Justin; Mukai, Shizuo] Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA.
[Kanoff, Justin; Mukai, Shizuo] Massachusetts Eye & Ear Infirm, Retina Serv, Dept Ophthalmol, Boston, MA 02114 USA.
RP Jakobiec, FA (reprint author), Massachusetts Eye & Ear Infirm, David G Cogan Lab Ophthalm Pathol, 243 Charles St Suite 328, Boston, MA 02114 USA.
EM Fred_jakobiec@meei.harvard.edu
FU Mukai Fund of the Massachusetts Eye and Ear Infirmary
FX SM is supported in part by gifts to the Mukai Fund of the Massachusetts
Eye and Ear Infirmary. None of the authors reported a proprietary or
commercial interest in any product mentioned or concept discussed in
this article.
NR 26
TC 1
Z9 1
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-6257
EI 1879-3304
J9 SURV OPHTHALMOL
JI Surv. Ophthalmol.
PD NOV-DEC
PY 2014
VL 59
IS 6
BP 636
EP 642
DI 10.1016/j.survophthal.2014.05.002
PG 7
WC Ophthalmology
SC Ophthalmology
GA AS0LC
UT WOS:000343967600005
PM 25233827
ER
PT J
AU Pantanowitz, L
Dickinson, K
Evans, AJ
Hassell, LA
Henricks, WH
Lennerz, JK
Lowe, A
Parwani, AV
Riben, M
Smith, CD
Tuthill, JM
Weinstein, RS
Wilbur, DC
Krupinski, EA
Bernard, J
AF Pantanowitz, Liron
Dickinson, Kim
Evans, Andrew J.
Hassell, Lewis A.
Henricks, Walter H.
Lennerz, Jochen K.
Lowe, Amanda
Parwani, Anil V.
Riben, Michael
Smith, Daniel
Tuthill, J. Mark
Weinstein, Ronald S.
Wilbur, David C.
Krupinski, Elizabeth A.
Bernard, Jordana
TI ATA Clinical Guidelines for Telepathology
SO TELEMEDICINE AND E-HEALTH
LA English
DT Article
ID DIGITAL PATHOLOGY; FROZEN-SECTION; SURGICAL PATHOLOGY; PRIMARY
DIAGNOSIS; PATIENT-CARE; WHOLE; SYSTEM; CYTOPATHOLOGY; PROSPECTS; FUTURE
C1 [Pantanowitz, Liron; Parwani, Anil V.] Univ Pittsburgh, Dept Pathol, Med Ctr, Pittsburgh, PA USA.
[Dickinson, Kim] Digital Pathol Assoc, LabCorp, Irvine, CA USA.
[Evans, Andrew J.] Toronto Gen Hosp, Dept Pathol, Univ Hlth Network, Toronto, ON, Canada.
[Hassell, Lewis A.] Univ Oklahoma, Hlth Sci Ctr, Dept Pathol, Oklahoma City, OK USA.
[Henricks, Walter H.] Cleveland Clin, Dept Pathol, Cleveland, OH 44106 USA.
[Henricks, Walter H.] Cleveland Clin, Inst Lab Med, Cleveland, OH 44106 USA.
[Lennerz, Jochen K.] Univ Ulm, Inst Pathol, D-89069 Ulm, Germany.
[Lowe, Amanda] Visiopharm, Broomfield, CO USA.
[Riben, Michael] MD Anderson Hosp, Dept Pathol, Houston, TX USA.
[Smith, Daniel] Keesler Air Force Base, Dept Pathol, Biloxi, MS USA.
[Tuthill, J. Mark] Henry Ford Hlth Syst, Pathol Informat, Detroit, MI USA.
[Weinstein, Ronald S.] Univ Arizona, Dept Pathol, Tucson, AZ USA.
[Wilbur, David C.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA USA.
[Krupinski, Elizabeth A.] Univ Arizona, Dept Med Imaging, Tucson, AZ USA.
[Bernard, Jordana] Amer Telemed Assoc, Washington, DC USA.
RP Pantanowitz, L (reprint author), Univ Pittsburgh, UPMC Shadyside Hosp, Dept Pathol, 5150 Ctr Ave,Suite 201, Pittsburgh, PA 15232 USA.
EM pantanowitzl@upmc.edu
NR 65
TC 5
Z9 5
U1 0
U2 3
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1530-5627
EI 1556-3669
J9 TELEMED E-HEALTH
JI Telemed. e-Health
PD NOV 1
PY 2014
VL 20
IS 11
BP 1049
EP 1056
DI 10.1089/tmj.2014.9976
PG 8
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA AS8BZ
UT WOS:000344476600012
PM 25384254
ER
PT J
AU Haugen, B
McDermott, M
Carrothers, TC
Daniels, GH
Ross, DS
Klibanski, A
Crowley, WF
Bigos, ST
Wartofsky, L
Cooper, DS
Ladenson, PW
Hershman, JM
Brent, G
Shupnik, P
Samuels, MH
Nagataki, S
Pacini, F
Maciel, RMB
Singer, P
Donelson, CH
Ridgway, H
AF Haugen, Bryan
McDermott, Michael
Carrothers, Terri C.
Daniels, Gilbert H.
Ross, Douglas S.
Klibanski, Anne
Crowley, William F., Jr.
Bigos, S. Thomas
Wartofsky, Leonard
Cooper, David S.
Ladenson, Paul W.
Hershman, Jerome M.
Brent, Gregory
Shupnik, Peggy
Samuels, Mary H.
Nagataki, Shigenobu
Pacini, Furio
Maciel, Rui M. B.
Singer, Peter
Donelson, Carla Hamre
Ridgway, Hap
CA Colorado Grp
Massachusetts Gen Hosp Grp
TI E. Chester Ridgway, MD, MACP (1942-2014) IN MEMORIAM
SO THYROID
LA English
DT Biographical-Item
C1 [Haugen, Bryan; McDermott, Michael; Carrothers, Terri C.] Univ Colorado, Sch Med, Aurora, CO 80045 USA.
[Haugen, Bryan] Univ Colorado, Sch Med, Div Endocrinol Metab & Diabet, Aurora, CO USA.
[Daniels, Gilbert H.] Mass Gen Hosp, Boston, MA USA.
[Daniels, Gilbert H.; Ross, Douglas S.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Daniels, Gilbert H.; Ross, Douglas S.; Klibanski, Anne; Crowley, William F., Jr.] Harvard Univ, Sch Med, Boston, MA USA.
[Klibanski, Anne] Massachusetts Gen Hosp, Partners HealthCare, Boston, MA 02114 USA.
[Klibanski, Anne] Massachusetts Gen Hosp, Neuroendocrine Unit, Boston, MA 02114 USA.
[Crowley, William F., Jr.] Massachusetts Gen Hosp, Harvard Reprod Endocrine Unit, Boston, MA 02114 USA.
[Bigos, S. Thomas] Togus Vet Affairs Med Ctr, Endocrine Serv, Augusta, ME USA.
[Wartofsky, Leonard] MedStar Washington Hosp Ctr, Washington, DC USA.
[Wartofsky, Leonard] Georgetown Univ, Sch Med, Washington, DC USA.
[Cooper, David S.; Ladenson, Paul W.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Hershman, Jerome M.] Univ Calif Los Angeles, David Geffen Sch Med, Vet Affairs Greater Los Angeles Healthcare Syst, Los Angeles, CA 90095 USA.
[Brent, Gregory] Univ Calif Los Angeles, David Geffen Sch Med, Vet Affairs Greater Los Angeles Healthcare Syst, Dept Med, Los Angeles, CA 90095 USA.
[Shupnik, Peggy] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
[Samuels, Mary H.] Oregon Hlth & Sci Univ, Div Endocrinol Diabet & Clin Nutr, Portland, OR 97201 USA.
[Samuels, Mary H.] Oregon Hlth & Sci Univ, Clin & Translat Res Ctr, Portland, OR 97201 USA.
[Nagataki, Shigenobu] Nagasaki Univ, Tokyo, Japan.
[Nagataki, Shigenobu] AOTA, Tokyo, Japan.
[Nagataki, Shigenobu] Radiat Effects Assoc, Tokyo, Japan.
[Pacini, Furio] Univ Siena, European Thyroid Assoc, I-53100 Siena, Italy.
[Pacini, Furio] Univ Siena, Dept Endocrinol & Metab, I-53100 Siena, Italy.
[Maciel, Rui M. B.] Univ Fed Sao Paulo, Lab Mol & Translat Endocrinol, Div Endocrinol, Dept Med,Escola Paulista Med, Sao Paulo, Brazil.
[Singer, Peter] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
RP Haugen, B (reprint author), Univ Colorado, Sch Med, Aurora, CO 80045 USA.
EM Bryan.haugen@ucdenver.edu; Michael.mcdermott@ucdenver.edu;
Terri.carrothers@ucdenver.edu; gdaniels@partners.org;
dross@partners.org; aklibanski@partners.org; wcrowley@partners.org;
BIGOS_STHOMAS@comcast.net; Leonard.Wartofsky@Medstar.net;
DSCooper@jhmi.edu; ladenson@jhmi.edu; jhershmn@g.ucla.edu;
gbrent@ucla.edu; mas3x@virginia.edu; samuelsm@ohsu.edu;
shigenobu.nagataki@nifty.com; pacini8@unisi.it;
Rui.Maciel@grupofleury.com.br; psinger@med.usc.edu;
carladonelson@aol.com; rockinrrranch@wildblue.net
NR 1
TC 0
Z9 0
U1 0
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1050-7256
EI 1557-9077
J9 THYROID
JI Thyroid
PD NOV 1
PY 2014
VL 24
IS 11
BP 1555
EP 1565
DI 10.1089/thy.2014.2411
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AS9EZ
UT WOS:000344547100001
ER
PT J
AU Mann, JK
Chopera, D
Omarjee, S
Kuang, XMT
Le, AQ
Anmole, G
Danroth, R
Mwimanzi, P
Reddy, T
Carlson, J
Radebe, M
Goulder, PJR
Walker, BD
Karim, SA
Novitsky, V
Williamson, C
Brockman, MA
Brumme, ZL
Ndung'u, T
AF Mann, Jaclyn K.
Chopera, Denis
Omarjee, Saleha
Kuang, Xiaomei T.
Le, Anh Q.
Anmole, Gursev
Danroth, Ryan
Mwimanzi, Philip
Reddy, Tarylee
Carlson, Jonathan
Radebe, Mopo
Goulder, Philip J. R.
Walker, Bruce D.
Karim, Salim Abdool
Novitsky, Vladimir
Williamson, Carolyn
Brockman, Mark A.
Brumme, Zabrina L.
Ndung'u, Thumbi
TI Nef-mediated down-regulation of CD4 and HLA class I in HIV-1 subtype C
infection: Association with disease progression and influence of immune
pressure
SO VIROLOGY
LA English
DT Article
DE HIV-1 Nef; HIV-1 subtype C; CD4 down-regulation; HLA-I down-regulation;
HIV-1 disease progression; HLA-associated polymorphisms; Immune evasion
ID T-CELL RESPONSES; SIMIAN IMMUNODEFICIENCY VIRUS; COMPLEX CLASS-I; VIRAL
LOAD; TYPE-1 REPLICATION; GAG; TRANSMISSION; ESCAPE; MUTATIONS; EPITOPES
AB Nef plays a major role in HIV-1 pathogenicity. We studied HIV-1 subtype C infected individuals in acute/early (n=120) or chronic (n=207) infection to investigate the relationship between Nef-mediated CD4/HLA-I down-regulation activities and disease progression, and the influence of immune-driven sequence variation on these Nef functions. A single Nef sequence per individual was cloned into an expression plasmid, followed by transfection of a T cell line and measurement of CD4 and HLA-I expression. In early infection, a trend of higher CD4 down-regulation ability correlating with higher viral load set point was observed (r=0.19, p=0.05), and higher HLA-I down-regulation activity was significantly associated with faster rate of CD4 decline (p=0.02). HLA-I down-regulation function correlated inversely with the number HLA-associated polymorphisms previously associated with reversion in the absence of the selecting HLA allele (r=-0.21, p=0.0002). These data support consideration of certain Nef regions in HIV-1 vaccine strategies designed to attenuate the infection course. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Mann, Jaclyn K.; Chopera, Denis; Omarjee, Saleha; Radebe, Mopo; Ndung'u, Thumbi] Univ KwaZulu Natal, HIV Pathogenesis Programme, ZA-4001 Durban, South Africa.
[Mann, Jaclyn K.; Chopera, Denis; Omarjee, Saleha; Radebe, Mopo; Ndung'u, Thumbi] Univ KwaZulu Natal, KwaZulu Natal Res Inst TB & HIV, ZA-4001 Durban, South Africa.
[Chopera, Denis; Williamson, Carolyn] Univ Cape Town, Inst Infect Dis & Mol Med, ZA-7925 Cape Town, South Africa.
[Chopera, Denis; Williamson, Carolyn] Univ Cape Town, Div Med Virol, ZA-7925 Cape Town, South Africa.
[Chopera, Denis; Williamson, Carolyn] Natl Hlth Lab Serv, ZA-7925 Cape Town, South Africa.
[Kuang, Xiaomei T.; Anmole, Gursev; Brockman, Mark A.] Simon Fraser Univ, Burnaby, BC V5A 1S6, Canada.
[Le, Anh Q.; Danroth, Ryan; Mwimanzi, Philip; Brockman, Mark A.; Brumme, Zabrina L.] Simon Fraser Univ, Fac Hlth Sci, Burnaby, BC V5A 1S6, Canada.
[Reddy, Tarylee] MRC, Biostat Unit, ZA-4001 Durban, South Africa.
[Carlson, Jonathan] Microsoft Res, Los Angeles, CA 90024 USA.
[Goulder, Philip J. R.] Univ Oxford, Dept Paediat, Oxford OX1 3SY, England.
[Goulder, Philip J. R.; Walker, Bruce D.; Ndung'u, Thumbi] Ragon Inst MGH MIT & Harvard Univ, Cambridge, MA 02139 USA.
[Walker, Bruce D.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Walker, Bruce D.] Harvard Univ, Boston, MA 02114 USA.
[Walker, Bruce D.] Howard Hughes Med Res Inst, Chevy Chase, MD 20815 USA.
[Karim, Salim Abdool] Univ KwaZulu Natal, Ctr AIDS Programme Res South Africa, ZA-4001 Durban, South Africa.
[Novitsky, Vladimir] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Novitsky, Vladimir] Botswana Harvard Sch Publ Hlth, AIDS Initiat Partnership HIV Res & Educ, Gaborone, Botswana.
[Brockman, Mark A.; Brumme, Zabrina L.] British Columbia Ctr Excellence HIV AIDS, Vancouver, BC V6Z 1Y6, Canada.
[Ndung'u, Thumbi] Max Planck Inst Infect Biol, D-10117 Berlin, Germany.
RP Ndung'u, T (reprint author), Univ KwaZulu Natal, HIV Pathogenesis Programme, 719 Umbilo Rd, ZA-4013 Durban, South Africa.
EM ndungu@ukzn.ac.za
OI , Carolyn/0000-0003-0125-1226; Ndung'u, Thumbi/0000-0003-2962-3992;
Abdool Karim, Salim/0000-0002-4986-2133; Brockman,
Mark/0000-0001-6432-1426
FU NIH [R37AI067073, RO1-AI057027]; International AIDS Vaccine Initiative
[UKZNRSA1001]; Canada-Sub Saharan Africa (CANSSA) HIV/AIDS Network -
Global Health Research Initiative; Canadian Institutes of Health
Research (CIHR); Canadian International Development Agency;
International Development Research Centre [106355-001]; Canadian
Institutes for Health Research (CIHR); Sanofi-Aventis; Clinical
Infectious Diseases Research Initiative Fellowship; Claude Leon
Foundation, South Africa; CAHR/BMS Master's Scholarship in Basic
Science; CIHR Frederick Banting and Charles Best Masters Award;
Merck-Canada Training of Aboriginal Youth in Biomedical Labs program at
Simon Fraser University; Michael Smith Foundation for Health Research
(MSFHR; Canada); CIHR; MSFHR; Howard Hughes Medical Institute
FX This research was funded by the NIH (R37AI067073, RO1-AI057027) and the
International AIDS Vaccine Initiative (UKZNRSA1001). JKM received a
pilot grant from the Canada-Sub Saharan Africa (CANSSA) HIV/AIDS
Network, funded by the Global Health Research Initiative, a
collaborative partnership of the Canadian Institutes of Health Research
(CIHR), the Canadian International Development Agency, and the
International Development Research Centre (project 106355-001). DRC is a
recipient of the Canada-HOPE fellowship from the Canadian Institutes for
Health Research (CIHR) and Sanofi-Aventis, and fellowships from the
Clinical Infectious Diseases Research Initiative Fellowship and the
Claude Leon Foundation, South Africa. XTK is funded by a CAHR/BMS
Master's Scholarship in Basic Science. AQL is funded by a CIHR Frederick
Banting and Charles Best Masters Award. RD is supported by the
Merck-Canada Training of Aboriginal Youth in Biomedical Labs program at
Simon Fraser University. PM is the recipient of Postdoctoral fellowships
from the Michael Smith Foundation for Health Research (MSFHR; Canada)
and the CIHR. MAB holds a Canada Research Chair, Tier 2, in Viral
Pathogenesis and Immunity. ZLB is the recipient of a CIHR New
Investigator Award and a Scholar Award from the MSFHR. TN holds the
South African DST/NRF Research Chair in Systems Biology of HIV/AIDS, the
Victor Daitz Chair in HIV/TB Research and an International Early Career
Scientist Award from the Howard Hughes Medical Institute.
NR 56
TC 5
Z9 5
U1 1
U2 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD NOV
PY 2014
VL 468
BP 214
EP 225
DI 10.1016/j.virol.2014.08.009
PG 12
WC Virology
SC Virology
GA AS7KF
UT WOS:000344434400025
PM 25193656
ER
PT J
AU Smith, JA
Haberstroh, FS
White, EA
Livingston, DM
DeCaprio, JA
Howley, PM
AF Smith, Jennifer A.
Haberstroh, Friederike S.
White, Elizabeth A.
Livingston, David M.
DeCaprio, James A.
Howley, Peter M.
TI SMCX and components of the TIP60 complex contribute to E2 regulation of
the HPV E6/E7 promoter
SO VIROLOGY
LA English
DT Article
DE Papillomavirus; E2; LCR; Transcriptional repression; SMCX; Methylation;
Chromatin; H3K4; EP400; TIP60
ID PAPILLOMAVIRUS ONCOGENE EXPRESSION; HISTONE ACETYLASE COMPLEX;
CERVICAL-CARCINOMA CELLS; E2-MEDIATED REPRESSION; GROWTH-INHIBITION;
PROTEIN; DEMETHYLASE; DNA; REGION; BRD4
AB An important step in the malignant progression of HPV-associated lesions is the dysregulation of expression of the viral E6 and E7 oncogenes. This is often achieved through the loss of expression of E2, which represses the HPV LCR promoter and E6/E7 expression. Our previous studies confirmed a role for Brd4 in mediating the E2 transcriptional repression function, and identified JARID1C/SMCX and EP400 as contributors to E2-mediated repression. Here we show that TIP60, a component of the TIP60/TRRAP histone acetyltransferase complex, also contributes to the E2 repression function, and we extend our studies on SMCX. Di- and tri-methyl marks on histone H3K4 are reduced in the presence of E2 and SMCX, suggesting a mechanism by which SMCX contributes to E2-mediated repression of the HPV LCR. Together, these findings lead us to hypothesize that E2 recruits histone-modifying cellular proteins to the HPV LCR, resulting in transcriptional repression of E6 and E7. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Smith, Jennifer A.; Haberstroh, Friederike S.; White, Elizabeth A.; Howley, Peter M.] Harvard Univ, Sch Med, Dept Microbiol & Immunobiol, Boston, MA 02115 USA.
[Livingston, David M.] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA.
[Livingston, David M.; DeCaprio, James A.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Livingston, David M.; DeCaprio, James A.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[DeCaprio, James A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA.
RP Howley, PM (reprint author), Harvard Univ, Sch Med, Dept Microbiol & Immunobiol, 77 Ave Louis Pasteur, Boston, MA 02115 USA.
EM peter_howley@hms.harvard.edu
FU NIH [T32CA009361]; NRSA [F32A1080075, R01CA116720, P01CA050661]
FX We thank S. Iwase and Y. Shi (Harvard Medical School) for providing SMCX
expression constructs, D. Di Maio (Yale University) for the
HeLa/16E6/16E7 cells, B. Price (Dana Farber Cancer Institute) for TIP60
expression construct, and R. Roeder (Rockefeller University) for EP400
fragment expression constructs. We are grateful to members of the Howley
lab for helpful discussions and feedback on various aspects on this
project, in particular L. Zhao for constructing the mutant BPV1 E2
plasmids. This work was supported by the NIH Grants T32CA009361 to
J.A.S., individual NRSA F32A1080075 to E.A.W., R01CA116720 to P.M.H. and
P01CA050661 to D.M.L., J.A.D. and P.M.H.
NR 46
TC 7
Z9 7
U1 0
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0042-6822
J9 VIROLOGY
JI Virology
PD NOV
PY 2014
VL 468
BP 311
EP 321
DI 10.1016/j.virol.2014.08.022
PG 11
WC Virology
SC Virology
GA AS7KF
UT WOS:000344434400036
PM 25222147
ER
PT J
AU Dhaliwal, G
Sehgal, NL
AF Dhaliwal, Gurpreet
Sehgal, Niraj L.
TI Demystify Leadership in Order to Cultivate It
SO ACADEMIC MEDICINE
LA English
DT Editorial Material
C1 [Dhaliwal, Gurpreet; Sehgal, Niraj L.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Dhaliwal, Gurpreet] San Francisco VA Med Ctr, San Francisco, CA 94121 USA.
[Sehgal, Niraj L.] Univ Calif San Francisco, Ctr Hlth Profess, San Francisco, CA USA.
RP Dhaliwal, G (reprint author), San Francisco VA Med Ctr, 4150 Clement St 111, San Francisco, CA 94121 USA.
EM gurpreet.dhaliwal@ucsf.edu
NR 3
TC 4
Z9 4
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1040-2446
EI 1938-808X
J9 ACAD MED
JI Acad. Med.
PD NOV
PY 2014
VL 89
IS 11
BP 1441
EP 1441
DI 10.1097/ACM.0000000000000489
PG 1
WC Education, Scientific Disciplines; Health Care Sciences & Services
SC Education & Educational Research; Health Care Sciences & Services
GA AR9MC
UT WOS:000343897500012
PM 25350336
ER
PT J
AU McDonald, CC
Curry, AE
Kandadai, V
Sommers, MS
Winston, FK
AF McDonald, Catherine C.
Curry, Allison E.
Kandadai, Venk
Sommers, Marilyn S.
Winston, Flaura K.
TI Comparison of teen and adult driver crash scenarios in a nationally
representative sample of serious crashes
SO ACCIDENT ANALYSIS AND PREVENTION
LA English
DT Article
DE Teen drivers; Adult drivers; Crash-contributing factors; Crash
scenarios; Risk factors; Traffic safety
ID RISKY DRIVING BEHAVIOR; NOVICE DRIVERS; PASSENGERS
AB Motor vehicle crashes are the leading cause of death and acquired disability during the first four decades of life. While teen drivers have the highest crash risk, few studies examine the similarities and differences in teen and adult driver crashes. We aimed to: (1) identify and compare the most frequent crash scenarios integrated information on a vehicle's movement prior to crash, immediate pre-crash event, and crash configuration for teen and adult drivers involved in serious crashes, and (2) for the most frequent scenarios, explore whether the distribution of driver critical errors differed for teens and adult drivers. We analyzed data from the National Motor Vehicle Crash Causation Survey, a nationally representative study of serious crashes conducted by the U.S. National Highway Traffic Safety Administration from 2005 to 2007. Our sample included 642 16- to 19-year-old and 1167 35- to 54-year-old crash-involved drivers (weighted n = 296,482 and 439,356, respectively) who made a critical error that led to their crash's critical pre-crash event (i.e., event that made the crash inevitable). We estimated prevalence ratios (PR) and 95% confidence intervals (CI) to compare the relative frequency of crash scenarios and driver critical errors. The top five crash scenarios among teen drivers, accounting for 37.3% of their crashes, included: (1) going straight, other vehicle stopped, rear end; (2) stopped in traffic lane, turning left at intersection, turn into path of other vehicle; (3) negotiating curve, off right edge of road, right roadside departure; (4) going straight, off right edge of road, right roadside departure; and (5) stopped in lane, turning left at intersection, turn across path of other vehicle. The top five crash scenarios among adult drivers, accounting for 33.9% of their crashes, included the same scenarios as the teen drivers with the exception of scenario (3) and the addition of going straight, crossing over an intersection, and continuing on a straight path. For two scenarios ((1) and (3) above), teens were more likely than adults to make a critical decision error (e.g., traveling too fast for conditions). Our findings indicate that among those who make a driver critical error in a serious crash, there are few differences in the scenarios or critical driver errors for teen and adult drivers. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [McDonald, Catherine C.; Sommers, Marilyn S.] Univ Penn, Sch Nursing, Ctr Global Womens Hlth, Ctr Hlth Equ Res, Philadelphia, PA 19104 USA.
[McDonald, Catherine C.; Curry, Allison E.; Kandadai, Venk; Winston, Flaura K.] Childrens Hosp Philadelphia, Ctr Injury Res & Prevent, Philadelphia, PA 19104 USA.
[Curry, Allison E.] Univ Penn, Ctr Clin Epidemiol & Biostat, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Winston, Flaura K.] Univ Penn, Perelman Sch Med, Div Gen Pediat, Philadelphia, PA 19104 USA.
[Winston, Flaura K.] Childrens Hosp Philadelphia, Natl Sci Fdn Ctr Child Injury Prevent Studies, Philadelphia, PA 19104 USA.
RP McDonald, CC (reprint author), Univ Penn, Sch Nursing, Ctr Global Womens Hlth, Ctr Hlth Equ Res, Claire Fagin Hall,418 Curie Blvd, Philadelphia, PA 19104 USA.
EM mcdonalc@nursing.upenn.edu; currya@email.chop.edu;
kandadaiv@email.chop.edu; ssommer@nursing.upenn.edu;
flaura@mail.med.upenn.edu
NR 31
TC 7
Z9 7
U1 2
U2 9
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0001-4575
EI 1879-2057
J9 ACCIDENT ANAL PREV
JI Accid. Anal. Prev.
PD NOV
PY 2014
VL 72
BP 302
EP 308
DI 10.1016/j.aap.2014.07.016
PG 7
WC Ergonomics; Public, Environmental & Occupational Health; Social
Sciences, Interdisciplinary; Transportation
SC Engineering; Public, Environmental & Occupational Health; Social
Sciences - Other Topics; Transportation
GA AR8SC
UT WOS:000343843700030
PM 25103321
ER
PT J
AU Beidas, RS
Edmunds, J
Ditty, M
Watkins, J
Walsh, L
Marcus, S
Kendall, P
AF Beidas, Rinad S.
Edmunds, Julie
Ditty, Matthew
Watkins, Jessica
Walsh, Lucia
Marcus, Steven
Kendall, Philip
TI Are Inner Context Factors Related to Implementation Outcomes in
Cognitive-Behavioral Therapy for Youth Anxiety?
SO ADMINISTRATION AND POLICY IN MENTAL HEALTH AND MENTAL HEALTH SERVICES
RESEARCH
LA English
DT Article
DE Evidence-based practice; Inner context; Implementation outcomes
ID MENTAL-HEALTH; RANDOMIZED-TRIAL; ORGANIZATIONAL READINESS; DISSEMINATION
TRIAL; TREATMENT INTEGRITY; CHILDHOOD ANXIETY; CONSULTATION; CLINICIAN;
STRATEGIES; SERVICES
AB Among the challenges facing the mental health field are the dissemination and implementation of evidence-based practices. The present study investigated the relationships between inner context variables (i.e., adopter characteristics and individual perceptions of intra-organizational factors) and two implementation outcomes-independently rated therapist fidelity on a performance-based role-play (i.e., adherence and skill) and self-reported penetration of cognitive behavioral therapy for youth anxiety following training. A significant relationship was found between inner context variables and fidelity. Specifically, adopter characteristics were associated with adherence and skill; individual perceptions of intra-organizational factors were associated with adherence. Inner context variables were not associated with penetration. Future directions are discussed.
C1 [Beidas, Rinad S.; Walsh, Lucia] Univ Penn, Perelman Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
[Edmunds, Julie] Judge Baker Childrens Ctr, Ctr Effect Child Therapy, Boston, MA USA.
[Ditty, Matthew; Marcus, Steven] Univ Penn, Sch Social Policy & Practice, Philadelphia, PA 19104 USA.
[Watkins, Jessica] Bryn Mawr Coll, Bryn Mawr, PA 19010 USA.
[Marcus, Steven] Philadelphia Vet Affairs Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA.
[Kendall, Philip] Temple Univ, Dept Psychol, Philadelphia, PA 19122 USA.
RP Beidas, RS (reprint author), Univ Penn, Perelman Sch Med, Dept Psychiat, 3535 Market St,3015, Philadelphia, PA 19104 USA.
EM rbeidas@upenn.edu
FU NIMH NIH HHS [K23 MH099179, MH063747, MH086436, R01 MH063747, R25
MH080916, U01 MH063747, F31 MH083333, MH083333, MH099179]
NR 62
TC 8
Z9 8
U1 1
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0894-587X
EI 1573-3289
J9 ADM POLICY MENT HLTH
JI Adm. Policy. Ment. Health
PD NOV
PY 2014
VL 41
IS 6
BP 788
EP 799
DI 10.1007/s10488-013-0529-x
PG 12
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA AS0UW
UT WOS:000343994900009
PM 24202067
ER
PT J
AU Tsai, AC
Weiser, SD
AF Tsai, Alexander C.
Weiser, Sheri D.
TI Population-Based Study of Food Insecurity and HIV Transmission Risk
Behaviors and Symptoms of Sexually Transmitted Infections Among Linked
Couples in Nepal
SO AIDS AND BEHAVIOR
LA English
DT Article
DE Food insecurity; Nepal; HIV
ID SUB-SAHARAN AFRICA; FEMALE SEX WORKERS; INTRAHOUSEHOLD ALLOCATION;
TRANSACTIONAL SEX; WOMEN; HIV/AIDS; POVERTY; PREVALENCE; HEALTH; ISSUES
AB Food insecurity has recently emerged as an important risk factor for HIV acquisition among women worldwide. No previous studies have used linked data that would permit investigation of the extent to which food insecurity may have differential associations with HIV transmission risk behaviors or symptoms of sexually transmitted infections (STIs) among men and women in the same households. We used nationally representative data on linked couples from the Nepal 2011 Demographic and Health Survey. The primary explanatory variable of interest was food insecurity, measured with a modified version of the Household Food Insecurity Access Scale. In multivariable logistic regression models, women in food insecure households were less likely to report recent condom use and more likely to report symptoms consistent with STIs. These patterns were absent among men. Interventions targeting food insecurity may have beneficial implications for both HIV prevention and gender equity in Nepal.
C1 [Tsai, Alexander C.] Massachusetts Gen Hosp, Chester M Pierce MD Div Global Psychiat, Boston, MA 02114 USA.
[Tsai, Alexander C.] Massachusetts Gen Hosp, Ctr Global Hlth, Boston, MA 02114 USA.
[Tsai, Alexander C.] Harvard Univ, Sch Med, Boston, MA USA.
[Tsai, Alexander C.] Mbarara Univ Sci & Technol, Mbarara, Uganda.
[Weiser, Sheri D.] Univ Calif San Francisco, San Francisco Gen Hosp, Div HIV AIDS, San Francisco, CA USA.
RP Tsai, AC (reprint author), Massachusetts Gen Hosp, Chester M Pierce MD Div Global Psychiat, Room 1529-E3,100 Cambridge St,15th Floor, Boston, MA 02114 USA.
EM actsai@partners.org
RI Nguyen, Giang/D-9027-2016;
OI Tsai, Alexander/0000-0001-6397-7917
FU NIMH NIH HHS [K23 MH096620, K23MH096620]
NR 55
TC 4
Z9 4
U1 1
U2 5
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1090-7165
EI 1573-3254
J9 AIDS BEHAV
JI AIDS Behav.
PD NOV
PY 2014
VL 18
IS 11
BP 2187
EP 2197
DI 10.1007/s10461-014-0794-z
PG 11
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA AR8BY
UT WOS:000343801700014
PM 24833522
ER
PT J
AU Wang, S
Luo, XD
Barnes, D
Sano, M
Yaffe, K
AF Wang, Sophia
Luo, Xiaodong
Barnes, Deborah
Sano, Mary
Yaffe, Kristine
TI Physical Activity and Risk of Cognitive Impairment Among Oldest-Old
Women
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
DE Cognitive aging; cohort studies; dementia; physical activity; oldest-old
ID ALZHEIMERS-DISEASE; EXECUTIVE FUNCTION; DEMENTIA; PREVALENCE; AGE;
ASSOCIATION; EXERCISE; DECLINE; COHORT; ADULTS
AB Objectives: Physical activity may reduce the risk of cognitive decline in the elderly, but its effects among the oldest-old (i.e., those aged 85 years and older) are not well known. Our study assessed the association between very late-life physical activity and 5-year risk of mild cognitive impairment (MCI) or dementia and neuropsychological test performance among oldest-old women. Methods: This prospective study was conducted at three sites. Participants included 1,249 women (mean [standard deviation] age: 83.3 [2.8] years). Baseline physical activity was measured by self-reported blocks walked per week and analyzed according to tertile. Five years later, surviving participants who were 85 years and older (oldest-old) completed neuropsychological testing and underwent adjudication of clinical cognitive status (normal, MCI, or dementia). All analyses were adjusted for baseline age, education, cognition, depression, body mass index, hypertension, smoking, and coronary artery disease. Results: Compared with women in the lowest tertile, women in the highest tertile were less likely to develop dementia (13.0% versus 23.2%; multivariate adjusted odds ratio: 0.54 [95% confidence interval: 0.36-0.82]). However, risk of MCI was not associated with physical activity. Physical activity was also associated with higher performance 5 years later on tests of global cognition, category fluency, and executive function but not phonemic fluency, memory, or attention. Conclusions: Higher level of very late-life physical activity was associated with a lower risk of subsequent dementia in oldest-old women. These findings support future studies for late-life physical activity interventions for the prevention of dementia among oldest-old women.
C1 [Wang, Sophia; Barnes, Deborah; Yaffe, Kristine] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Wang, Sophia; Barnes, Deborah; Yaffe, Kristine] San Francisco VA Med Ctr, San Francisco, CA USA.
[Luo, Xiaodong; Sano, Mary] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Luo, Xiaodong; Sano, Mary] Vet Affairs Med Ctr, Bronx, NY USA.
[Barnes, Deborah; Yaffe, Kristine] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
RP Wang, S (reprint author), Langley Porter Neuropsychiat Inst, 401 Parnassus Ave,GPP 0984, San Francisco, CA 94103 USA.
EM sophia.wang@ucsf.edu
FU VA Neurosciences Research fellowship; Mount Sinai Alzheimer's Disease
Research Center award from National Institute of Aging (NIA)
[P50AG005138-27]; National Center for Research Resources' Clinical and
Translational Science Award [UL1RR029887]; NIA [K24 AG 031155];
Alzheimer's Association; APA/Lilly Resident Research Award; [AG05407];
[AR35582]; [AG05394]; [AR3354]; [AR35583]; [R01 AG005407]; [R01
AG027576-22]; [2 R01 AG005394-22A1]; [2R01 AG027574-22A1];
[5R01AG026720-04]
FX Data collection and sharing for SOF and SOF-WISE are supported by grants
AG05407, AR35582, AG05394, AR3354, AR35583, R01 AG005407, R01
AG027576-22, 2 R01 AG005394-22A1, 2R01 AG027574-22A1, and
5R01AG026720-04. The study was coordinated by the University of
California at San Francisco, and the SOF data are disseminated by the
University of California at San Francisco. This study was also supported
in part by a VA Neurosciences Research fellowship (S. W.), Mount Sinai
Alzheimer's Disease Research Center award P50AG005138-27 from the
National Institute of Aging (NIA) (X. L., M. S.), UL1RR029887 from the
National Center for Research Resources' Clinical and Translational
Science Award (M. S.), grant K24 AG 031155 from the NIA and an
Independent Investigator Award from the Alzheimer's Association (KY).
Dr. Wang also received the APA/Lilly Resident Research Award for this
work.
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PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1064-7481
EI 1545-7214
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD NOV
PY 2014
VL 22
IS 11
BP 1149
EP 1157
DI 10.1016/j.jagp.2013.03.002
PG 9
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA AR8YG
UT WOS:000343856600011
PM 23831179
ER
PT J
AU Donovan, NJ
Wadsworth, LP
Lorius, N
Locascio, JJ
Rentz, DM
Johnson, KA
Sperling, RA
Marshall, GA
AF Donovan, Nancy J.
Wadsworth, Lauren P.
Lorius, Natacha
Locascio, Joseph J.
Rentz, Dorene M.
Johnson, Keith A.
Sperling, Reisa A.
Marshall, Gad A.
CA Alzheimer Dis Neuroimaging
TI Regional Cortical Thinning Predicts Worsening Apathy and Hallucinations
Across the Alzheimer Disease Spectrum
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
DE Apathy; hallucinations; MRI; cortical thinning; CSF biomarkers;
Alzheimer disease
ID POSITRON-EMISSION-TOMOGRAPHY; MILD COGNITIVE IMPAIRMENT;
NEUROPSYCHIATRIC SYMPTOMS; CEREBROSPINAL-FLUID; FUNCTIONAL IMPAIRMENT;
VISUAL HALLUCINATIONS; PSYCHOSIS; SIGNATURE; PERFUSION; DEMENTIA
AB Objectives: To examine regions of cortical thinning and cerebrospinal fluid (CSF) Alzheimer disease (AD) biomarkers associated with apathy and hallucinations in a continuum of individuals including clinically normal elderly, mild cognitive impairment, and mild AD dementia. Design: Cross-sectional and longitudinal studies. Setting: Fifty-seven research sites across North America. Participants: Eight-hundred twelve community-dwelling volunteers; 413 participants in the CSF substudy. Measurements: Structural magnetic resonance imaging data and CSF concentrations of amyloid-beta 1-42, total tau, and phosphorylated tau derived from the Alzheimer Disease Neuroimaging Initiative database were analyzed. Apathy and hallucinations were measured at baseline and over 3 years using the Neuropsychiatric Inventory-Questionnaire. General linear models and mixed effects models were used to evaluate the relationships among baseline cortical thickness in seven regions, and baseline CSF biomarkers, apathy, and hallucinations at baseline and longitudinally. Covariates included diagnosis, sex, age, apolipoprotein E genotype, premorbid intelligence, memory performance, processing speed, antidepressant use, and AD duration. Results: Reduced baseline inferior temporal cortical thickness was predictive of increasing apathy over time, and reduced supramarginal cortical thickness was predictive of increasing hallucinations over time. There was no association with cortical thickness at baseline. CSF biomarkers were not related to severity of apathy or hallucinations in cross-sectional or longitudinal analyses. Conclusions: These results suggest that greater baseline temporal and parietal atrophy is associated with worsening apathy and hallucinations in a large AD spectrum cohort, while adjusting for multiple disease-related variables. Localized cortical neurodegeneration may contribute to the pathophysiology of apathy and hallucinations and their adverse consequences in AD.
C1 [Donovan, Nancy J.; Lorius, Natacha; Rentz, Dorene M.; Johnson, Keith A.; Sperling, Reisa A.; Marshall, Gad A.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Ctr Alzheimer Res & Treatment, Boston, MA 02115 USA.
[Donovan, Nancy J.; Rentz, Dorene M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Donovan, Nancy J.; Rentz, Dorene M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
[Wadsworth, Lauren P.; Lorius, Natacha; Locascio, Joseph J.; Rentz, Dorene M.; Sperling, Reisa A.; Marshall, Gad A.] Harvard Univ, Sch Med, Dept Neurol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Johnson, Keith A.] Harvard Univ, Sch Med, Dept Radiol, Massachusetts Gen Hosp, Boston, MA 02115 USA.
RP Donovan, NJ (reprint author), Brigham & Womens Hosp, Ctr Alzheimer Res & Treatment, 221 Longwood Ave,BL 104H, Boston, MA 02115 USA.
EM njdonovan@partners.org
FU National Institute on Aging, the National Institute of Biomedical
Imaging and Bioengineering [U01 AG024904]; Rosalinde and Arthur Gilbert
Foundation/AFAR New Investigator Awards in Alzheimer's disease;
Massachusetts Alzheimer's Disease Research Center [P50 AG005134];
Harvard Aging Brain Study [P01 AGO36694]; [R01 AG027435]; [K23
AG033634]; [K24 AG035007]; [D01 HP08794-04-00]
FX The Alzheimer's Disease Neuroimaging Initiative (ADNI) (NIH grant U01
AG024904) is funded by the National Institute on Aging, the National
Institute of Biomedical Imaging and Bioengineering, and through generous
contributions from the following: Abbott; AstraZeneca AB; Bayer Schering
Pharma AG; Bristol-Myers Squibb; Eisai Global Clinical Development; Elan
Corporation; Genentech; GE Healthcare; GlaxoSmithKline; Innogenetics;
Johnson and Johnson; Eli Lilly and Co.; Medpace, Inc.; Merck and Co.,
Inc.; Novartis AG; Pfizer, Inc.; F. Hoffman-La Roche; Schering-Plough;
Synarc, Inc.; as well as nonprofit partners the Alzheimer's Association
and Alzheimer's Drug Discovery Foundation, with participation from the
U.S. Food and Drug Administration. Private sector contributions to ADNI
are facilitated by the Foundation for the National Institutes of Health
(www.fnih.org). The grantee organization is the Northern California
Institute for Research and Education, and the study is coordinated by
the Alzheimer's Disease Cooperative Study at the University of
California, San Diego. ADNI data are disseminated by the Laboratory for
Neuro Imaging at the University of California, Los Angeles.; This study
was also supported by R01 AG027435, K23 AG033634, K24 AG035007, D01
HP08794-04-00, the Rosalinde and Arthur Gilbert Foundation/AFAR New
Investigator Awards in Alzheimer's disease, the Massachusetts
Alzheimer's Disease Research Center (P50 AG005134) and the Harvard Aging
Brain Study (P01 AGO36694).
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PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1064-7481
EI 1545-7214
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD NOV
PY 2014
VL 22
IS 11
BP 1168
EP 1179
DI 10.1016/j.jagp.2013.03.006
PG 12
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA AR8YG
UT WOS:000343856600013
PM 23890751
ER
PT J
AU Gurrera, RJ
Karel, MJ
Azar, AR
Moye, J
AF Gurrera, Ronald J.
Karel, Michele J.
Azar, Armin R.
Moye, Jennifer
TI Neuropsychological Performance Within-Person Variability Is Associated
with Reduced Treatment Consent Capacity
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
DE Decisional capacity; executive function; cognitive impairment
ID ALZHEIMERS-DISEASE; COGNITIVE IMPAIRMENT; COMPETENCE; DEMENTIA;
PREDICTORS; ADULTS; HEALTH; SPAN
AB Objective: The capacity of older adults to make healthcare decisions is often impaired in dementia and has been linked to performance on specific neuropsychological tasks. Within-person across-test neuropsychological performance variability has been shown to predict future dementia. This study examined the relationship of within-person across-test neuropsychological performance variability to a current construct of treatment decision (consent) capacity. Methods: Participants completed a neuropsychological test battery and a standardized capacity assessment. Standard scores were used to compute mean neuropsychological performance and within-person across-test variability. Assessments were performed in the participant's preferred location (e.g., outpatient clinic office, senior center, or home). Participants were recruited from the community with fliers and advertisements and consisted of men (N = 79) and women (N = 80) with (N = 83) or without (N = 76) significant cognitive impairment. Participants completed the MacArthur Competence Assessment Tool-Treatment and 11 neuropsychological tests commonly used in the cognitive assessment of older individuals. Results: Neuropsychological performance and within-person variability were independently associated with continuous and dichotomous measures of capacity, and within-person neuropsychological variability was significantly associated with within-person decisional ability variability. Prevalence of incapacity was greater than expected in participants with and without significant cognitive impairment when decisional abilities were considered separately. Conclusion: These findings are consistent with an emerging construct of consent capacity in which discrete decisional abilities are differentially associated with cognitive processes and indicate that the sensitivity and accuracy of consent capacity assessments can be improved by evaluating decisional abilities separately.
C1 [Gurrera, Ronald J.; Karel, Michele J.; Azar, Armin R.; Moye, Jennifer] VA Boston Healthcare Syst, Brockton, MA 02301 USA.
[Gurrera, Ronald J.; Karel, Michele J.; Azar, Armin R.; Moye, Jennifer] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
RP Gurrera, RJ (reprint author), VA Boston Healthcare Syst, 940 Belmont St 116A, Brockton, MA 02301 USA.
EM ronald_gurrera@hms.harvard.edu
RI Moye, Jennifer/F-2240-2017
OI Moye, Jennifer/0000-0002-3434-347X
FU NIMH [R29 MH57104]
FX Supported by a NIMH grant to Jennifer Moye (R29 MH57104) and with
resources and the use of facilities at the VA Boston Healthcare System.
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SN 1064-7481
EI 1545-7214
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD NOV
PY 2014
VL 22
IS 11
BP 1200
EP 1209
DI 10.1016/j.jagp.2013.03.010
PG 10
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA AR8YG
UT WOS:000343856600016
PM 23831178
ER
PT J
AU Bartels, SJ
Pratt, SI
Mueser, KT
Forester, BP
Wolfe, R
Cather, C
Xie, HY
McHugo, GJ
Bird, B
Aschbrenner, KA
Naslund, JA
Feldman, J
AF Bartels, Stephen J.
Pratt, Sarah I.
Mueser, Kim T.
Forester, Brent P.
Wolfe, Rosemarie
Cather, Corinne
Xie, Haiyi
McHugo, Gregory J.
Bird, Bruce
Aschbrenner, Kelly A.
Naslund, John A.
Feldman, James
TI Long-Term Outcomes of a Randomized Trial of Integrated Skills Training
and Preventive Healthcare for Older Adults with Serious Mental Illness
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
DE Older adults; serious mental illness; psychosocial skills training;
healthcare management; preventive healthcare; integrated care
ID PILOT PSYCHOSOCIAL INTERVENTION; CHRONIC PSYCHOTIC DISORDERS;
CHRONIC-SCHIZOPHRENIA; PEOPLE; RELIABILITY; INSTRUMENT; DEPRESSION;
CLINICIAN; CONSUMERS; OLMSTEAD
AB Objective: This report describes 1-, 2-, and 3-year outcomes of a combined psychosocial skills training and preventive healthcare intervention (Helping Older People Experience Success [HOPES]) for older persons with serious mental illness. Methods: A randomized controlled trial compared HOPES with treatment as usual (TAU) for 183 older adults (age >= 50 years [mean age: 60.2]) with serious mental illness (28% schizophrenia, 28% schizoaffective disorder, 20% bipolar disorder, 24% major depression) from two community mental health centers in Boston, Massachusetts, and one in Nashua, New Hampshire. HOPES comprised 12 months of weekly skills training classes, twice-monthly community practice trips, and monthly nurse preventive healthcare visits, followed by a 1-year maintenance phase of monthly sessions. Blinded evaluations of functioning, symptoms, and service use were conducted at baseline and at a 1-year (end of the intensive phase), 2-year (end of the maintenance phase), and 3-year (12 months after the intervention) follow-up. Results: HOPES compared with TAU was associated with improved community living skills and functioning, greater self-efficacy, lower overall psychiatric and negative symptoms, greater acquisition of preventive healthcare (more frequent eye exams, visual acuity, hearing tests, mammograms, and Pap smears), and nearly twice the rate of completed advance directives. No differences were found for medical severity, number of medical conditions, subjective health status, or acute service use at the 3-year follow-up. Conclusion: Skills training and nurse facilitated preventive healthcare for older adults with serious mental illness was associated with sustained long-term improvement in functioning, symptoms, self-efficacy, preventive healthcare screening, and advance care planning.
C1 [Bartels, Stephen J.; Pratt, Sarah I.; Mueser, Kim T.; Aschbrenner, Kelly A.] Geisel Sch Med Dartmouth, Dept Psychiat, Hanover, NH USA.
[Bartels, Stephen J.] Geisel Sch Med Dartmouth, Dept Community & Family Med, Hanover, NH USA.
[Bartels, Stephen J.; Pratt, Sarah I.; Naslund, John A.] Dartmouth Coll, Dartmouth Inst Hlth Policy & Clin Practice, Hanover, NH 03755 USA.
[Mueser, Kim T.; Wolfe, Rosemarie; Xie, Haiyi; McHugo, Gregory J.] Dartmouth Psychiat Res Ctr, Lebanon, NH USA.
[Mueser, Kim T.] Boston Univ, Ctr Psychiat Rehabil, Boston, MA 02215 USA.
[Forester, Brent P.] Harvard Univ, Dept Psychiat, Cambridge, MA 02138 USA.
[Forester, Brent P.] McLean Hosp, Geriatr Psychiat Res Program, Belmont, MA 02178 USA.
[Cather, Corinne] Massachusetts Gen Hosp, Schizophrenia Program, Boston, MA 02114 USA.
[Bird, Bruce] Vinfen, Cambridge, MA USA.
[Feldman, James] Massachusetts Mental Hlth Ctr, Boston, MA 02115 USA.
RP Bartels, SJ (reprint author), Ctr Hlth & Aging, 46 Centerra Pkwy,Ste 200, Lebanon, NH 03766 USA.
EM sbartels@dartmouth.edu
FU National Institute of Mental Health [R01 MH62324]
FX The study was supported by a grant from the National Institute of Mental
Health (R01 MH62324).
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PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1064-7481
EI 1545-7214
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD NOV
PY 2014
VL 22
IS 11
BP 1251
EP 1261
DI 10.1016/j.jagp.2013.04.013
PG 11
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA AR8YG
UT WOS:000343856600021
PM 23954039
ER
PT J
AU Sultzer, DL
Leskin, LP
Melrose, RJ
Harwood, DG
Narvaez, TA
Ando, TK
Mandelkern, MA
AF Sultzer, David L.
Leskin, Lorraine P.
Melrose, Rebecca J.
Harwood, Dylan G.
Narvaez, Theresa A.
Ando, Timothy K.
Mandelkern, Mark A.
TI Neurobiology of Delusions, Memory, and Insight in Alzheimer Disease
SO AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
LA English
DT Article
DE Alzheimer disease; delusions; insight; memory; FDG-PET; cerebral
metabolism
ID NEUROBEHAVIORAL RATING-SCALE; REGIONAL CORTICAL METABOLISM;
CEREBRAL-BLOOD-FLOW; BEHAVIORAL DISTURBANCES; PSYCHIATRIC-SYMPTOMS;
COGNITIVE DEFICITS; NATIONAL INSTITUTE; PSYCHOTIC SYMPTOMS; IMPAIRED
INSIGHT; WORKING-MEMORY
AB Objective: Delusional thoughts are common among patients with Alzheimer disease (AD) and may be conceptually linked to memory deficits (cannot recall accurate information, which leads to inaccurate beliefs) and poor insight (unable to appreciate the illogic of beliefs). This study's goals were to examine the clinical associations among delusions, memory deficits, and poor insight; explore neurobiologic correlates for these symptoms; and identify shared mechanisms. Methods: In a cross-sectional analysis, 88 outpatients with AD (mean Mini-Mental State Exam score: 19.3) were studied. Delusional thoughts were assessed with the Neuropsychiatric Inventory, level of inaccurate insight was assessed with the Neurobehavioral Rating Scale, and memory was assessed with the Mattis Dementia Rating Scale memory subscale. F-18-fluorodeoxyglucose positron emission tomography was used to measure regional cortical metabolism. Relationships between clinical ratings and regional cortical metabolic activity (voxel-based) were assessed using SPM2. Results: Patients with delusions had lower Dementia Rating Scale memory subscale scores. Neurobehavioral Rating Scale inaccurate insight scores were no different in those with and without delusions. Cortical metabolic activity was lower in the right lateral frontal cortex, orbitofrontal cortex, and bilateral temporal cortex in patients with delusions. Low cortical metabolic activity in the right lateral, inferior, and medial temporal cortex was associated with poorer memory. This region partially overlapped the region of hypometabolism associated with delusions. In contrast, low cortical metabolic activity in bilateral medial frontal cortex was associated with poor insight. Conclusion: Delusions in AD are associated with dysfunction in specific frontal and temporal cortical regions. Delusions are partially clinically and neurobiologically linked to memory deficits but not to poor insight.
C1 [Sultzer, David L.; Leskin, Lorraine P.; Melrose, Rebecca J.; Harwood, Dylan G.; Narvaez, Theresa A.; Ando, Timothy K.] VA Greater Los Angeles Healthcare Syst, Brain Behav & Aging Res Ctr, Los Angeles, CA 90073 USA.
[Mandelkern, Mark A.] VA Greater Los Angeles Healthcare Syst, Nucl Med Serv, Los Angeles, CA 90073 USA.
[Sultzer, David L.; Melrose, Rebecca J.; Harwood, Dylan G.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Mandelkern, Mark A.] Univ Calif Irvine, Dept Phys, Irvine, CA 92717 USA.
RP Sultzer, DL (reprint author), VA Greater Los Angeles Healthcare Syst, Brain Behav & Aging Res Ctr, 11301 Wilshire Blvd,116AE, Los Angeles, CA 90073 USA.
EM dsultzer@ucla.edu
FU Department of Veterans Affairs; National Institute of Mental Health
[R01MH56031]; Eli Lilly
FX Supported in part by the Department of Veterans Affairs (Merit Review
Award to DLS; Career Development Award to RJM) and the National
Institute of Mental Health (R01MH56031).; Dr. Sultzer has received
research support from Eli Lilly and has served as a consultant to Otsuka
Pharmaceutical and Eli Lilly.
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PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1064-7481
EI 1545-7214
J9 AM J GERIAT PSYCHIAT
JI Am. J. Geriatr. Psychiatr.
PD NOV
PY 2014
VL 22
IS 11
BP 1346
EP 1355
DI 10.1016/j.jagp.2013.06.005
PG 10
WC Geriatrics & Gerontology; Gerontology; Psychiatry
SC Geriatrics & Gerontology; Psychiatry
GA AR8YG
UT WOS:000343856600030
PM 24021220
ER
PT J
AU Leyva, B
Allen, JD
Tom, LS
Ospino, H
Torres, MI
Abraido-Lanza, AF
AF Leyva, Bryan
Allen, Jennifer D.
Tom, Laura S.
Ospino, Hosffman
Torres, Maria Idali
Abraido-Lanza, Ana F.
TI Religion, Fatalism, and Cancer Control: A Qualitative Study among
Hispanic Catholics
SO AMERICAN JOURNAL OF HEALTH BEHAVIOR
LA English
DT Article
DE fatalism; cancer fatalism; religion; Catholic; Latinos; Hispanics;
cancer; cancer screening
ID MEXICAN-AMERICAN WOMEN; BREAST-CANCER; CERVICAL-CANCER;
AFRICAN-AMERICAN; HEALTH BEHAVIORS; PROSTATE-CANCER; SCREENING
BEHAVIORS; EXPLANATORY MODELS; UNITED-STATES; BELIEFS
AB Objectives: To assess cancer perceptions among churchgoers and to examine the potential influence of fatalism and religious beliefs on the use of cancer screening tests. Methods: Eight semi-structured focus groups were conducted among 67 Hispanic Catholics in Massachusetts. Results: In this sample, there were few references to fatalistic beliefs about cancer and nearly universal endorsement of the utility of cancer screening for cancer early detection. Most participants reported that their religious beliefs encouraged them to use health services, including cancer-screening tests. Although participants agreed that God plays an active role in health, they also affirmed the importance of self-agency in determining cancer outcomes. Conclusions: Our findings challenge the assumption that fatalism is an overriding perspective among Hispanics. Catholic religious beliefs may contribute to positive health attitudes and behaviors.
C1 [Leyva, Bryan] NCI, NIH, Bethesda, MD 20892 USA.
[Allen, Jennifer D.] Tufts Univ, Boston, MA 02111 USA.
[Tom, Laura S.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ospino, Hosffman] Boston Coll, Sch Theol & Minist, Chestnut Hill, MA 02167 USA.
[Torres, Maria Idali] Univ Massachusetts, Dept Anthropol, Boston, MA 02125 USA.
[Abraido-Lanza, Ana F.] Columbias Mailman Sch Publ Hlth, New York, NY USA.
RP Leyva, B (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM leyvabryan@gmail.com
RI Allen, Jennifer/M-2113-2015
FU NCATS NIH HHS [UL1TR000040, UL1 TR000040]; NCCDPHP CDC HHS [U48DP001946,
U48 DP001946]; NCI NIH HHS [U54CA156732, U54 CA156732]; NIGMS NIH HHS
[R25 GM062454, R25GM062454]
NR 85
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PU PNG PUBLICATIONS
PI OAK RIDGE
PA 2205-K OAK RIDGE RD, #115, OAK RIDGE, NC 27310 USA
SN 1945-7359
J9 AM J HEALTH BEHAV
JI Am. J. Health Behav.
PD NOV
PY 2014
VL 38
IS 6
BP 839
EP 849
DI 10.5993/AJHB.38.6.6
PG 11
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AS1JE
UT WOS:000344036600006
PM 25207510
ER
PT J
AU Welsh, MM
Federinko, SP
Burnett, DG
Gackstetter, GD
Boyko, EJ
Seelig, AD
Wells, TS
Hooper, TI
AF Welsh, Marleen M.
Federinko, Susan P.
Burnett, Daniel G.
Gackstetter, Gary D.
Boyko, Edward J.
Seelig, Amber D.
Wells, Timothy S.
Hooper, Tomoko I.
TI Deployment-Related Depression Screening, 2001-2008 Comparing Clinical
Versus Research Surveys
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; MILITARY SERVICE MEMBERS; HEALTH-CARE
UTILIZATION; MILLENNIUM COHORT; US MILITARY; SMALLPOX VACCINATION;
COMBAT DEPLOYMENT; ENROLLMENT; IMPACT; AFGHANISTAN
AB Background: Potential adverse mental health effects of deployment, including depression, are an ongoing concern. Although a previous study assessed under-reporting of depression on post-deployment health assessments compared to anonymous surveys, those results were not examined at the individual level to identify demographic or military factors that may be associated with unwillingness to report depression symptoms.
Purpose: To compare self-reported depression symptoms on post-deployment health assessments with responses to the same depression questions on a research survey.
Methods: This cross-sectional study analyzed depression screening responses from 2001 to 2008 from participants of the Millennium Cohort Study, a longitudinal military cohort study, who completed a post-deployment health assessment within 30 days of a research survey. Kappa statistics and percent positive and negative agreement were calculated. Demographic and military characteristics associated with discordant screening results were examined. Initial analyses were performed in 2011, with additional analyses in 2013.
Results: Moderate agreement (kappa=0.464) was observed between paired survey responses. A higher proportion of active duty members, the unmarried, and new accessions into military service endorsed depression symptoms on the research survey but not the military-linked survey. In stratified analyses, agreement was higher in Reserve/National Guard members than active duty (kappa=0.561 vs 0.409). New active duty accessions showed lower agreement (kappa=0.388), as did unmarried active duty participants (kappa=0.304).
Conclusions: Deployment health surveys are important tools for identifying returning service members experiencing depression symptoms. However, these findings suggest that ongoing stigma and barriers to appropriate follow-up mental health care remain to be addressed in the military setting. (C) 2014 American Journal of Preventive Medicine. All rights reserved.
C1 [Welsh, Marleen M.; Federinko, Susan P.; Burnett, Daniel G.; Hooper, Tomoko I.] Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, Bethesda, MD 20814 USA.
[Gackstetter, Gary D.] Analyt Serv Inc, Falls Church, VA USA.
[Boyko, Edward J.] Vet Affairs Puget Sound Hlth Care Syst, Epidemiol Res & Informat Ctr, Seattle, WA USA.
[Seelig, Amber D.] Naval Hlth Res Ctr, Deployment Hlth Res Dept, San Diego, CA USA.
[Wells, Timothy S.] Optum, Ann Arbor, MI USA.
RP Welsh, MM (reprint author), Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, Room A1040H,4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM marleen.welsh.ctr@usuhs.edu
FU Management Information Division, U.S. Defense Manpower Data Center
(Seaside CA); Military Operational Medicine Research Program; U.S. Army
Medical Research and Materiel Command; Military Operational Medicine
Research Program, U.S. Army Medical Research and Materiel Command (Fort
Detrick MD)
FX We would like to thank the entire Millennium Cohort Study Team from the
Deployment Health Research Department, Naval Health Research Center, San
Diego CA, for their support, as well as the Millennium Cohort Study
co-investigators for their leadership. We are also indebted to the
Millennium Cohort Study participants, without whom these analyses would
not be possible. We appreciate the support from the Management
Information Division, U.S. Defense Manpower Data Center (Seaside CA),
Military Operational Medicine Research Program, and U.S. Army Medical
Research and Materiel Command.; The Millennium Cohort Study is funded
through the Military Operational Medicine Research Program, U.S. Army
Medical Research and Materiel Command (Fort Detrick MD). Resources from
the Veterans Affairs Puget Sound Health Care System supported Dr.
Boyko's involvement in this research.
NR 26
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 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD NOV
PY 2014
VL 47
IS 5
BP 531
EP 540
DI 10.1016/j.amepre.2014.07.036
PG 10
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA AR6DP
UT WOS:000343673800001
PM 25241198
ER
PT J
AU Lehavot, K
Browne, KC
Simpson, TL
AF Lehavot, Keren
Browne, Kendall C.
Simpson, Tracy L.
TI Examining Sexual Orientation Disparities in Alcohol Misuse Among Women
Veterans
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; SUBSTANCE USE; MENTAL-HEALTH; PHYSICAL
ABUSE; MINORITY VETERANS; TRAUMA EXPOSURE; FEMALE VETERANS; BINGE
DRINKING; UNITED-STATES; CHILD-ABUSE
AB Background: Alcohol misuse is a significant health concern among women veterans, especially among lesbian and bisexual veterans. Mediators that might explain alcohol disparities between heterosexual and sexual minority veterans have not yet been identified.
Purpose: To examine the role of civilian and military traumas and mental health symptoms (i.e., depression, post-traumatic stress disorder) in explaining sexual orientation disparities in alcohol misuse between sexual minority and heterosexual women veterans across the U.S.
Methods: Women veterans were recruited using Internet methods to participate in an online, anonymous, national survey (N=699, 37% lesbian or bisexual) from February to May 2013. Path analysis was used to examine a model wherein sexual orientation both directly and indirectly predicted alcohol misuse through trauma exposures and mental health symptoms. Data were analyzed in November 2013.
Results: Findings indicated significant disparities in alcohol misuse among women veterans by sexual orientation, with indirect effects via childhood trauma, physical victimization in adulthood both during the military and as a civilian, and depressive and post-traumatic stress disorder symptoms.
Conclusions: Lesbian and bisexual women veterans reported higher rates of some trauma exposures and mental health symptoms than their heterosexual counterparts, partly accounting for their higher rates of alcohol misuse. Interventions that attend to both victimization and drinking among this population are needed, as well as future research that addresses other factors influencing alcohol misuse. Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
C1 [Lehavot, Keren; Browne, Kendall C.; Simpson, Tracy L.] Univ Washington, Mental Illness Res Educ & Clin Ctr, Seattle, WA 98195 USA.
[Simpson, Tracy L.] Univ Washington, Ctr Excellence Substance Abuse Treatment & Educ, Seattle, WA 98195 USA.
[Lehavot, Keren; Browne, Kendall C.; Simpson, Tracy L.] Univ Washington, Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA 98195 USA.
[Lehavot, Keren; Browne, Kendall C.; Simpson, Tracy L.] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
RP Lehavot, K (reprint author), Vet Affairs Puget Sound Hlth Care Syst, 1660 S Columbian Way S-116-POC, Seattle, WA 98108 USA.
EM klehavot@uw.edu
FU VISN-20 Mental Illness Research, Education, and Clinical Center; VA
CSR&D Career Development Award [CX000867]; Advanced Fellowship Program
in Mental Illness Research and Treatment
FX This research was supported by a research grant to K. Lehavot and T.
Simpson from the VISN-20 Mental Illness Research, Education, and
Clinical Center. Dr. Lehavot's effort was supported by a VA CSR&D Career
Development Award (CX000867). This material is the result of work
supported by resources from the U.S. Department of Veterans Affairs
Office of Academic Affiliations, Advanced Fellowship Program in Mental
Illness Research and Treatment, and the Veterans Affairs Puget Sound
Health Care System, Seattle WA. The views expressed in this article are
those of the authors and do not represent the views of the Department of
Veterans Affairs or the U.S. government.
NR 55
TC 5
Z9 6
U1 3
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD NOV
PY 2014
VL 47
IS 5
BP 554
EP 562
DI 10.1016/j.amepre.2014.07.002
PG 9
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA AR6DP
UT WOS:000343673800003
PM 25241197
ER
PT J
AU Mahabee-Gittens, EM
Collins, BN
Murphy, S
Woo, H
Chang, Y
Dempsey, J
Weiley, V
Winickoff, JP
AF Mahabee-Gittens, E. Melinda
Collins, Bradley N.
Murphy, Sybil
Woo, Heide
Chang, Yuchiao
Dempsey, Janelle
Weiley, Victoria
Winickoff, Jonathan P.
TI The Parent-Child Dyad and Risk Perceptions Among Parents Who Quit
Smoking
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID RANDOMIZED CONTROLLED-TRIAL; TOBACCO CONTROL; INTERVENTION; EXPOSURE;
SECONDHAND; CESSATION; ASTHMA; METAANALYSIS; BEHAVIOR; DISEASE
AB Background: Most parental smokers are deeply invested in their child's health, but it is unknown what factors influence parent risk perceptions of the effects of smoking on their child's health and benefits to the child of cessation.
Purpose: To explore differences in former versus current smokers' beliefs about harm of continuing to smoke, benefits of quitting, and how much smoking interferes with their parenting.
Methods: As part of a cluster RCT to increase tobacco control in the pediatric setting, we analyzed data collected at the ten control arm practices for 24 months starting in May 2010; a cross-sectional secondary data analysis was conducted in 2013. Parents were asked about smoking status and perceived harm, benefit, and well-being related to smoking behaviors.
Results: Of the 981 enrolled smoking parents, 710 (72.4%) were contacted at 12 months. The odds of having successfully quit at 12 months was 4.12 times more likely (95% CI=1.57, 10.8) for parents who believed that quitting will benefit their children; 1.68 times more likely (95% CI=1.13, 2.51) for parents with more than a high school education; and 1.74 times greater (95% CI=1.13, 2.68) for parents with children under age 3 years. Another factor associated with having successfully quit was a prior quit attempt.
Conclusions: Providers' smoking-cessation advice and support should begin early and underscore how cessation will benefit the health and well-being of patients' children. Additionally, parents who have recently attempted to quit may be particularly primed for another attempt. (C) 2014 American Journal of Preventive Medicine
C1 [Mahabee-Gittens, E. Melinda] Univ Cincinnati, Sch Med, Cincinnati Childrens Hosp Med Ctr, Div Emergency Med, Cincinnati, OH USA.
[Collins, Bradley N.] Temple Univ, Hlth Behav Res Clin, Dept Publ Hlth, Philadelphia, PA 19122 USA.
[Collins, Bradley N.] Temple Univ, Hlth Behav Res Clin, Dept Pediat, Philadelphia, PA 19122 USA.
[Murphy, Sybil; Dempsey, Janelle; Winickoff, Jonathan P.] Massachusetts Gen Hosp, Tobacco Res & Treatment Ctr, Ctr Child & Adolescent Hlth Res & Policy, Boston, MA 02114 USA.
[Chang, Yuchiao] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Woo, Heide] Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90024 USA.
[Weiley, Victoria] Amer Acad Pediat, Pediat Res Off Settings, Elk Grove Village, IL USA.
[Winickoff, Jonathan P.] Amer Acad Pediat, Richmond Ctr Excellence, Elk Grove Village, IL USA.
RP Mahabee-Gittens, EM (reprint author), Cincinnati Childrens Hosp Med Ctr, 3333 Burnet Ave, Cincinnati, OH 45229 USA.
EM melinda.mahabee-gittens@cchmc.org
FU NIH National Cancer Institute [R01-CA127127]; National Institute on Drug
Abuse; Agency for Healthcare Research and Quality; Flight Attendant
Medical Research Institute; Health Resources and Services Administration
Maternal and Child Health Bureau [HRSA 5-UA6-10-001]; AAP
FX This study was funded by the NIH National Cancer Institute (grant No.
R01-CA127127 to Dr. Winickoff), National Institute on Drug Abuse, and
the Agency for Healthcare Research and Quality. This study was also
partially supported by a grant from the Flight Attendant Medical
Research Institute to the AAP Julius B. Richmond Center, and the PROS
Network, which receives core funding from the Health Resources and
Services Administration Maternal and Child Health Bureau (No. HRSA
5-UA6-10-001) and the AAP. Clinical trial registration: NCT00664261.
NR 26
TC 4
Z9 4
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
EI 1873-2607
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD NOV
PY 2014
VL 47
IS 5
BP 596
EP 603
DI 10.1016/j.amepre.2014.07.010
PG 8
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA AR6DP
UT WOS:000343673800007
PM 25201508
ER
PT J
AU Ushiku, T
Arnason, T
Fukayama, M
Lauwers, GY
AF Ushiku, Tetsuo
Arnason, Thomas
Fukayama, Masashi
Lauwers, Gregory Y.
TI Extra-ampullary Duodenal Adenocarcinoma
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE adenocarcinoma; Brunner gland hyperplasia; gastric metaplasia;
extra-ampullary duodenum; carcinogenesis
ID GASTRIC-FOVEOLAR METAPLASIA; SMALL-BOWEL ADENOCARCINOMA;
SMALL-INTESTINE; UNITED-STATES; CANCER; CARCINOMA; HYPERPLASIA;
EXPRESSION; CETUXIMAB; PATTERNS
AB Extra-ampullary duodenal adenocarcinomas are rare, and when studied, frequently have been grouped with jejunoileal adenocarcinomas. Nevertheless, anecdotal experiences suggest that these neoplasms may present 2 or more distinct phenotypes. To better characterize these neoplasms, we performed a retrospective review of 38 cases with a special focus on the morphologic and immunophenotypic characteristics and their clinicopathologic significance. Our cohort of extra-ampullary duodenal adenocarcinomas was classified on the basis of the morphologic features into gastric type (n = 19, 50%), intestinal type (n = 14, 37%), pancreaticobiliary type (n = 2, 5%), and others (n = 3, 8%). Most gastric-type adenocarcinomas (n = 18, 95%) developed in the proximal duodenum, whereas the other types were located equally in the proximal and distal duodenum. Intestinal-type dysplasia was present at the periphery of 8 (57%) intestinal-type adenocarcinomas, and 8 (42%) gastric-type adenocarcinoma were associated with gastric-type dysplasia. Gastric foveolar metaplasia (n = 12) and Brunner gland hyperplasia (n = 10) were exclusively recognized adjacent to gastric-type adenocarcinomas. Notably, intestinal-type histology and the absence of lymph node metastasis were significantly associated with favorable disease-free survival in univariate and multivariate analyses. In summary, this study demonstrated that 2 major subsets of extra-ampullary duodenal adenocarcinoma, intestinal type and gastric type, are associated with distinct histopathologic features and clinical behavior.
C1 [Ushiku, Tetsuo; Arnason, Thomas; Lauwers, Gregory Y.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Ushiku, Tetsuo; Fukayama, Masashi] Univ Tokyo, Dept Pathol, Tokyo 1130033, Japan.
[Arnason, Thomas] Queen Elizabeth 2 Hlth Sci Ctr, Div Anat Pathol, Halifax, NS, Canada.
RP Ushiku, T (reprint author), Univ Tokyo, Dept Pathol, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan.
EM usikut-tky@umin.ac.jp
NR 33
TC 7
Z9 7
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD NOV
PY 2014
VL 38
IS 11
BP 1484
EP 1493
PG 10
WC Pathology; Surgery
SC Pathology; Surgery
GA AR9GE
UT WOS:000343880200004
PM 25310836
ER
PT J
AU Wojcik, JB
Bellizzi, AM
Dal Cin, P
Bredella, MA
Fletcher, CDM
Hornicek, FJ
Deshpande, V
Hornick, JL
Nielsen, GP
AF Wojcik, John B.
Bellizzi, Andrew M.
Dal Cin, Paola
Bredella, Miriam A.
Fletcher, Christopher D. M.
Hornicek, Francis J.
Deshpande, Vikram
Hornick, Jason L.
Nielsen, G. Petur
TI Primary Sclerosing Epithelioid Fibrosarcoma of Bone Analysis of a Series
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE primary bone tumor; sarcoma; immunohistochemistry; MUC4; SATB2;
sclerosing epithelioid fibrosarcoma
ID GRADE-FIBROMYXOID-SARCOMA; MARKER; MUC4; DIFFERENTIATION;
REARRANGEMENTS; TUMORS
AB Sclerosing epithelioid fibrosarcoma (SEF) is a rare, aggressive malignant neoplasm characterized by small nests and linear arrays of epithelioid cells embedded in a dense collagenous matrix. Very few primary SEFs of bone have been reported. Recognition is critical, as the dense extracellular collagenous matrix can be interpreted as osteoid, leading to misdiagnosis as-osteosarcoma. MUC4 and SATB2 are 2 recently characterized immunohistochemical markers for SEF and osteosarcoma, respectively. In reports to date, osteosarcomas are positive for SATB2 and negative for MUC4, whereas soft tissue SEFs have shown the opposite immunohistochemical profile (SATB2 - /MUC4+). The purpose of this study was to characterize the clinicopathologic and immunohistochemical features of 8 primary SEFs of bone. The patients presented at a wide range of ages (25 to 73 y; median 52 y). Tumors mostly involved long bones of the extremities, with 3 cases involving the femur, 2 involving the ulna, and 1 involving the humerus. Other sites of involvement included the second rib (1) and the C6 vertebra (1). Follow-up information was available for 7 patients, 3 of whom developed metastases within 2 years of diagnosis. The other 4 patients were free of local recurrence or metastases at 1, 5, 12, and > 84 months of follow-up, respectively. Radiographically, the tumors were predominantly lytic and poorly marginated. Histologically, 6 tumors showed pure SEF morphology, and 2 showed hybrid SEF/low-grade fibromyxoid sarcoma morphology. Focal dystrophic mineralization was seen in 1 case but was limited to areas of necrosis. None of the tumors showed the lace-like pattern of mineralization typical of osteosarcoma. The majority (6/8) of the tumors strongly expressed MUC4. SATB2 was negative in all but 1 case, which showed variable weak to moderate staining in similar to 50% of nuclei. In general, the combination of morphology, MUC4 expression, and the absence of SATB2 expression was highly useful in arriving at the correct diagnosis.
C1 [Wojcik, John B.; Bredella, Miriam A.; Hornicek, Francis J.; Deshpande, Vikram; Nielsen, G. Petur] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Dal Cin, Paola; Fletcher, Christopher D. M.; Hornick, Jason L.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Bellizzi, Andrew M.] Univ Iowa, Dept Pathol, Iowa City, IA 52242 USA.
RP Wojcik, JB (reprint author), Massachusetts Gen Hosp, Dept Pathol, MGH Pathol Serv, Warren Bldg 225,55 Fruit St, Boston, MA 02114 USA.
EM jwojcik@partners.org
NR 23
TC 8
Z9 9
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD NOV
PY 2014
VL 38
IS 11
BP 1538
EP 1544
PG 7
WC Pathology; Surgery
SC Pathology; Surgery
GA AR9GE
UT WOS:000343880200011
PM 24921641
ER
PT J
AU Sakurai, U
Lauwers, GY
Vieth, M
Sawabe, M
Arai, T
Yoshida, T
Aida, J
Takubo, K
AF Sakurai, Urara
Lauwers, Gregory Y.
Vieth, Michael
Sawabe, Motoji
Arai, Tomio
Yoshida, Tatsuya
Aida, Junko
Takubo, Kaiyo
TI Gastric High-grade Dysplasia Can Be Associated With Submucosal Invasion
Evaluation of its Prevalence in a Series of 121 Endoscopically Resected
Specimens
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE gastric neoplasm; gastric dysplasia; intramucosal adenocarcinoma;
endoscopic resection
ID GASTROINTESTINAL EPITHELIAL NEOPLASIA; WESTERN PATHOLOGISTS; DIAGNOSIS;
BIOPSIES; JAPANESE
AB Gastric neoplasms classified as high-grade dysplasia (HGD) by Western pathologists are frequently diagnosed as tubular adenocarcinoma in Japan. Here, we evaluated the prevalence of submucosal and lymphovascular invasion in a series of 125 endoscopically resected gastric neoplasms. On the basis of Western criteria, the lesions were classified as poorly cohesive carcinomas (n = 4) (excluded from further analysis), low-grade dysplasia (n = 4), pure HGD (n = 78), HGD with tubular adenocarcinoma (n = 4), and pure tubular adenocarcinoma (n = 35). Submucosal invasion was found in 3.8% of the 78 HGDs, 75.0% of the 4 HGDs combined with adenocarcinoma, and 11.4% of the 35 adenocarcinomas. Venous invasion was detected in 1.3% of the 78 HGDs, 75% of the 4 HGDs combined with adenocarcinoma, and none of the 35 tubular adenocarcinomas. Lymphatic invasion was absent in HGD but noted in 25% of the HGDs combined with adenocarcinoma, and 2.9% of the tubular adenocarcinomas. Thus, we demonstrated that lesions characterized as HGD on the basis of Western criteria can be associated with submucosal and lymphovascular invasion. Endoscopic therapy has made it less crucial to differentiate between HGD and intramucosal adenocarcinoma in biopsy samples of small tubular neoplasms. However, it is important to recognize that the criteria for dysplasia currently used in the West may understate the degree of malignant potential. To limit any diagnostic discrepancy between biopsy, endoscopic resection, and surgical specimens, it is suggested that the features of HGD and adenocarcinoma be reevaluated, which may result in some lesions being classified as mucosal adenocarcinoma.
C1 [Sakurai, Urara; Vieth, Michael; Sawabe, Motoji] Tokyo Metropolitan Geriatr Hosp, Dept Pathol, Tokyo, Japan.
[Yoshida, Tatsuya] Kudanzaka Hosp, Dept Surg, Tokyo, Japan.
[Aida, Junko; Takubo, Kaiyo] Metropolitan Inst Gerontol, Res Team Geriatr Pathol, Itabashi Ku, Tokyo 1730015, Japan.
[Lauwers, Gregory Y.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Vieth, Michael] Klinikum Bayreuth, Inst Pathol, Bayreuth, Germany.
RP Takubo, K (reprint author), Metropolitan Inst Gerontol, Res Team Geriatr Pathol, Itabashi Ku, Sakae Cho 35-2, Tokyo 1730015, Japan.
EM uraras@musa-shino.jrc.or.jp; GLAUWERS@mgh.harvard.edu;
vieth.lkpathol@uni-bayreuth.de; takubo@tmig.or.jp
NR 14
TC 5
Z9 7
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD NOV
PY 2014
VL 38
IS 11
BP 1545
EP 1550
PG 6
WC Pathology; Surgery
SC Pathology; Surgery
GA AR9GE
UT WOS:000343880200012
PM 25310837
ER
PT J
AU Chung, JW
Ju, MH
Kinnier, CV
Haut, ER
Baker, DW
Bilimoria, KY
AF Chung, Jeanette W.
Ju, Mila H.
Kinnier, Christine V.
Haut, Elliott R.
Baker, David W.
Bilimoria, Karl Y.
TI Evaluation of hospital factors associated with hospital postoperative
venous thromboembolism imaging utilisation practices
SO BMJ QUALITY & SAFETY
LA English
DT Article
ID DEEP-VEIN THROMBOSIS; TRAUMA DATA-BANK; FACTORS-AN ANALYSIS; REPORTED
DVT RATES; QUALITY-OF-CARE; SURVEILLANCE BIAS; DEFENSIVE MEDICINE;
UNCERTAINTY; PHYSICIANS; OUTCOMES
AB Background Recent research suggests that hospital rates of postoperative venous thromboembolism (VTE) are subject to surveillance bias: the more hospitals 'look for' VTE, the more VTE they find. However, little is known about what drives variation in hospital VTE imaging rates. We conducted an observational study to examine hospital and market characteristics that were associated with hospital-level rates of postoperative VTE imaging, focusing on hospitals with particularly high rates.
Methods For Medicare beneficiaries undergoing 11 major operations (2009-2010) at 2820 hospitals, hospital-level postoperative VTE imaging use rates were calculated. Hospital characteristics associated with hospital VTE imaging use rates were examined including case severity, size, ownership, VTE process measure adherence, accreditations, staffing, malpractice environment, and county market factors. Associations between explanatory variables and VTE imaging rates were assessed using quantile regressions at the 25th, median, 75th and 90th quantiles.
Results Mean postoperative VTE imaging rates ranged from 85.26 (SD=67.38) per 1000 discharges in the lowest quartile of hospitals ranked by VTE imaging rates to 168.86 (SD=76.70) in the highest quartile. Drivers of high imaging rates at the 90th quantile were high resident-to-bed ratio (coefficient=51.35, p<0.01), Joint Commission accreditation (coefficient=19.05, p<0.01), presence of other hospitals in the same market with high imaging rates (coefficient=15.29, p<0.01), average case severity (coefficient=11.97, p<0.01), local malpractice costs (coefficient=11.29, p<0.01), and market competition (coefficient=11.03, p<0.01).
Conclusions Hospital teaching status, resident-to-bed ratio, malpractice environment and local market factors drive hospital postoperative VTE imaging use, suggesting that non-clinical forces predominantly drive hospital VTE imaging practices.
C1 [Chung, Jeanette W.; Ju, Mila H.; Kinnier, Christine V.; Bilimoria, Karl Y.] Northwestern Univ, Feinberg Sch Med, Dept Surg, SOQIC, Chicago, IL 60611 USA.
[Kinnier, Christine V.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Haut, Elliott R.] Johns Hopkins Univ, Sch Med, Dept Surg Anesthesiol & Crit Care Med, Baltimore, MD USA.
[Haut, Elliott R.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Baker, David W.] Northwestern Univ, Div Gen Internal Med & Geriatr, Chicago, IL 60611 USA.
RP Bilimoria, KY (reprint author), Northwestern Univ, Feinberg Sch Med, NW Mem Hosp, Surg Outcomes & Qual Improvement Ctr,Dept Surg, 676 St Clair St,Arkes Pavil Suite 6-650, Chicago, IL 60611 USA.
EM k-bilimoria@northwestern.edu
FU Northwestern Memorial Hospital
FX Northwestern Memorial Hospital.
NR 42
TC 3
Z9 3
U1 1
U2 2
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 2044-5415
EI 2044-5423
J9 BMJ QUAL SAF
JI BMJ Qual. Saf.
PD NOV
PY 2014
VL 23
IS 11
BP 947
EP 956
DI 10.1136/bmjqs-2014-003150
PG 10
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA AR9EZ
UT WOS:000343876600010
PM 25136140
ER
PT J
AU Golshan, M
Losk, K
Kadish, S
Lin, NU
Hirshfield-Bartek, J
Cutone, L
Sagara, Y
Aydogan, F
Camuso, K
Weingart, SN
Bunnell, C
AF Golshan, Mehra
Losk, Katya
Kadish, Sarah
Lin, Nancy U.
Hirshfield-Bartek, Judith
Cutone, Linda
Sagara, Yasuaki
Aydogan, Fatih
Camuso, Kristen
Weingart, Saul N.
Bunnell, Craig
TI Understanding process-of-care delays in surgical treatment of breast
cancer at a comprehensive cancer center
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Breast cancer; Surgery; Waits and delays
ID DIAGNOSIS; SURVIVAL; TIME
AB Few studies have examined care processes within providers' and institutions' control that expedite or delay care. The authors investigated the timeliness of breast cancer care at a comprehensive cancer center, focusing on factors influencing the time from initial consultation to first definitive surgery (FDS). The care of 1,461 women with breast cancer who underwent surgery at Dana-Farber/Brigham and Women's Cancer Center from 2011 to 2013 was studied. The interval between consultation and FDS was calculated to identify variation in timeliness of care based on procedure, provider, and patients' sociodemographic characteristics. Targets of 14 days for lumpectomy and mastectomy and 28 days from mastectomy with immediate reconstruction were set and used to define delay. Mean days between consultation and FDS was 21.6 (range 1-175, sd 15.8) for lumpectomy, 36.7 (5-230, 29.1) for mastectomy, and 37.5 (7-111, 16) for mastectomy with reconstruction. Patients under 40 were less likely to be delayed (OR = 0.56, 95 % CI = 0.33-0.94, p = 0.03). Patients undergoing mastectomy alone (OR = 2.64, 95 % CI = 1.80-3.89, p < 0.0001) and mastectomy with immediate reconstruction (OR = 1.34 95 % CI = 1.00-1.79, p = 0.05) were more likely to be delayed when compared to lumpectomy. Substantial variation in surgical timeliness was identified. This study provides insight into targets for improvement including better coordination with plastic surgery and streamlining pre-operative testing. Cancer centers may consider investing in efforts to measure and improve the timeliness of cancer care.
C1 [Golshan, Mehra] Dana Farber Canc Inst, Dept Surg, Boston, MA 02215 USA.
[Golshan, Mehra; Cutone, Linda; Sagara, Yasuaki; Aydogan, Fatih] Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA.
[Losk, Katya; Kadish, Sarah; Lin, Nancy U.; Hirshfield-Bartek, Judith; Camuso, Kristen; Weingart, Saul N.; Bunnell, Craig] Dana Farber Canc Inst, Boston, MA 02215 USA.
RP Golshan, M (reprint author), Dana Farber Canc Inst, Dept Surg, 450 Brookline Ave, Boston, MA 02215 USA.
EM mgloshan@partners.org
FU National Comprehensive Cancer Network (NCCN) Opportunities for
Improvement Grant
FX This initiative was supported in part by the National Comprehensive
Cancer Network (NCCN) Opportunities for Improvement Grant
NR 15
TC 6
Z9 7
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
EI 1573-7217
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD NOV
PY 2014
VL 148
IS 1
BP 125
EP 133
DI 10.1007/s10549-014-3124-2
PG 9
WC Oncology
SC Oncology
GA AR8DT
UT WOS:000343806400013
PM 25270121
ER
PT J
AU Iyer, SP
Beck, JT
Stewart, AK
Shah, J
Kelly, KR
Isaacs, R
Bilic, S
Sen, S
Munshi, NC
AF Iyer, Swaminathan P.
Beck, Joseph Taddeus
Stewart, A. Keith
Shah, Jatin
Kelly, Kevin R.
Isaacs, Randi
Bilic, Sanela
Sen, Suman
Munshi, Nikhil C.
TI A Phase IB multicentre dose-determination study of BHQ880 in combination
with anti-myeloma therapy and zoledronic acid in patients with relapsed
or refractory multiple myeloma and prior skeletal-related events
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE BHQ880; multiple myeloma; skeletal-related event; Phase I
ID RECEPTOR-RELATED PROTEIN-5; STEM-CELL TRANSPLANTATION; BONE-DISEASE;
SERUM CONCENTRATIONS; DOUBLE-BLIND; IN-VITRO; DKK1; DICKKOPF-1;
OSTEOBLASTS; GROWTH
AB Dickkopf-1 (DKK1), expressed by myeloma cells, suppresses osteoblast function and plays a key role in bone disease in multiple myeloma. BHQ880, a human neutralizing IgG1 anti-DKK1 monoclonal antibody, is being investigated for its impact on multiple myeloma-related bone disease and as an agent with potential anti-myeloma activity. The primary objectives of this Phase IB study were to determine the maximum tolerated dose (MTD) of BHQ880 and to characterize the dose-limiting toxicity (DLT) of escalating doses in combination with anti-myeloma therapy and zoledronic acid. Twenty-eight patients were enrolled and received BHQ880 at doses of 3-40mg/kg. No DLTs were reported, therefore, the MTD was not determined. The recommended Phase II dose was declared as 10mg/kg, based mainly on saturation data. There was a general trend towards increased bone mineral density (BMD) observed over time; specific increases in spine BMD from Cycle 12 onwards irrespective of new skeletal-related events on study were observed, and increases in bone strength at the spine and hip were also demonstrated in some patients. BHQ880 in combination with zoledronic acid and anti-myeloma therapy was well tolerated and demonstrated potential clinical activity in patients with relapsed or refractory multiple myeloma.
C1 [Iyer, Swaminathan P.] Weill Cornell Med Coll, Houston Methodist Canc Ctr, Houston, TX 77030 USA.
[Beck, Joseph Taddeus] Highlands Oncol Grp PA, Fayetteville, AR USA.
[Stewart, A. Keith] Mayo Clin, Coll Med, Div Hematol Oncol, Scottsdale, AZ USA.
[Shah, Jatin] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Kelly, Kevin R.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Isaacs, Randi; Bilic, Sanela; Sen, Suman] Novartis Pharmaceut, E Hanover, NJ USA.
[Munshi, Nikhil C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Munshi, Nikhil C.] Harvard Univ, Sch Med, Boston VA Healthcare Syst, Boston, MA USA.
RP Iyer, SP (reprint author), Weill Cornell Med Coll, Houston Methodist Canc Ctr, 6445 Main St,Floor 21, Houston, TX 77030 USA.
EM spiyer@houstonmethodist.org
FU Novartis Pharmaceuticals
FX Financial support for medical editorial assistance was provided by
Novartis Pharmaceuticals. We thank Kate Gaffey, PhD for her medical
editorial assistance with this manuscript.
NR 35
TC 26
Z9 29
U1 2
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2014
VL 167
IS 3
BP 366
EP 375
DI 10.1111/bjh.13056
PG 10
WC Hematology
SC Hematology
GA AS0MB
UT WOS:000343970000009
PM 25139740
ER
PT J
AU Goldman, S
Smith, L
Galardy, P
Perkins, SL
Frazer, JK
Sanger, W
Anderson, JR
Gross, TG
Weinstein, H
Harrison, L
Shiramizu, B
Barth, M
Cairo, MS
AF Goldman, Stanton
Smith, Lynette
Galardy, Paul
Perkins, Sherrie L.
Frazer, John Kimble
Sanger, Warren
Anderson, James R.
Gross, Thomas G.
Weinstein, Howard
Harrison, Lauren
Shiramizu, Bruce
Barth, Matthew
Cairo, Mitchell S.
TI Rituximab with chemotherapy in children and adolescents with central
nervous system and/or bone marrow-positive Burkitt lymphoma/leukaemia: a
Children's Oncology Group Report
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE children; Burkitt lymphoma; Burkitt leukaemia; chemotherapy; rituximab
ID NON-HODGKINS-LYMPHOMA; B-CELL LYMPHOMA; ACUTE-LYMPHOBLASTIC-LEUKEMIA;
PLUS RITUXIMAB; ADULT BURKITT; CODOX-M/IVAC; PHASE-II; RISK;
INTERMEDIATE; THERAPY
AB Children and adolescents with Burkitt Lymphoma (BL) and combined central nervous system (CNS) and bone marrow involvement still have a poor prognosis with chemotherapy alone. We therefore investigated in children and adolescents with bone marrow (25% blasts) and/or CNS-positive Burkitt lymphoma the chemoimmunotherapy combination of rituximab (375mg/m(2)) and the standard chemotherapy arm of our previously reported French-American-British (FAB) Lymphome Malins de Burkitt (LMB) 96 trial. Central pathological and cytogenetic characterization was also performed. There were 40 evaluable patients with Burkitt histology (25 with leukaemia and 15 with CNS disease +/- leukaemia). The chemoimmunotherapy regimen was well tolerated. The incidence of grade III/IV mucositis during induction cycles with combined chemotherapy and rituximab was 31% and 26%, respectively. The 3-year event-free survival (EFS)/overall survival (OS) was 90% (95% confidence interval [CI], 76-96%) in the entire cohort and 93% (95% CI, 61-99%) in patients with CNS disease. Based on the results of this trial, an international randomized study of FAB/LMB 96 chemotherapy +/- rituximab for high-risk patients is currently under investigation.
C1 [Goldman, Stanton] Med City Childrens Hosp, Div Pediat Hematol Oncol, Dallas, TX USA.
[Smith, Lynette; Anderson, James R.] Univ Nebraska, Coll Publ Hlth, Dept Biostat, Omaha, NE 68182 USA.
[Galardy, Paul] Mayo Clin, Dept Pediat Hematol Oncol, Rochester, MN USA.
[Perkins, Sherrie L.] Univ Utah, Dept Pathol, Salt Lake City, UT USA.
[Frazer, John Kimble] Univ Oklahoma, Hlth Sci Ctr, Sect Pediat Hematol Oncol, Oklahoma City, OK USA.
[Sanger, Warren] Univ Nebraska, Ctr Human Genet, Omaha, NE 68182 USA.
[Gross, Thomas G.] NCI, Ctr Global Hlth, NIH, Rockville, MD USA.
[Weinstein, Howard] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Pediat Hematol Oncol, Boston, MA USA.
[Harrison, Lauren; Cairo, Mitchell S.] New York Med Coll, Dept Pediat, Valhalla, NY 10595 USA.
[Shiramizu, Bruce] Univ Hawaii, Div Pediat Hematol Oncol, Honolulu, HI 96822 USA.
[Barth, Matthew] Roswell Pk Canc Inst, Dept Pediat, Buffalo, NY 14263 USA.
[Cairo, Mitchell S.] New York Med Coll, Dept Med, Valhalla, NY 10595 USA.
[Cairo, Mitchell S.] New York Med Coll, Dept Pathol, Valhalla, NY 10595 USA.
[Cairo, Mitchell S.] New York Med Coll, Dept Microbiol & Immunol, Valhalla, NY 10595 USA.
[Cairo, Mitchell S.] New York Med Coll, Dept Cell Biol & Anat, Valhalla, NY 10595 USA.
RP Cairo, MS (reprint author), New York Med Coll, Div Pediat Hematol Oncol & Stem Cell Transplantat, 40 Sunshine Cottage Rd,Skyline IN D12, Valhalla, NY 10595 USA.
EM Mitchell_cairo@nymc.edu
OI Frazer, John Kimble/0000-0003-2936-2817
FU Division of Cancer Treatment, National Cancer Institute (NCI); National
Institutes of Health, Department of Health and Human Services (COG)
[CA98413-09]; Pediatric Cancer Research Foundation; National Institutes
of Health, Department of Health and Human Services (COG) (jn)
FX Supported by the Division of Cancer Treatment, National Cancer Institute
(NCI), and National Institutes of Health, Department of Health and Human
Services (COG) (jn and CA98413-09) and the Pediatric Cancer Research
Foundation. NCI provided support for data collection and analysis but no
role in data interpretation, writing of the manuscript or the decision
on journal submission.
NR 22
TC 19
Z9 19
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
EI 1365-2141
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2014
VL 167
IS 3
BP 394
EP 401
DI 10.1111/bjh.13040
PG 8
WC Hematology
SC Hematology
GA AS0MB
UT WOS:000343970000012
PM 25066629
ER
PT J
AU De Pascale, G
Bittner, EA
AF De Pascale, Gennaro
Bittner, Edward A.
TI Influenza-Associated Critical Illness: Estimating the Burden and the
Burden of Estimation
SO CRITICAL CARE MEDICINE
LA English
DT Editorial Material
DE burden of disease; critical illness; influenza
ID UNITED-STATES
C1 [De Pascale, Gennaro; Bittner, Edward A.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
[De Pascale, Gennaro] Univ Cattolica Sacro Cuore, Agostino Gemelli Hosp, Dept Intens Care & Anesthesiol, I-00168 Rome, Italy.
RP De Pascale, G (reprint author), Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
NR 11
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
EI 1530-0293
J9 CRIT CARE MED
JI Crit. Care Med.
PD NOV
PY 2014
VL 42
IS 11
BP 2441
EP 2442
DI 10.1097/CCM.0000000000000589
PG 2
WC Critical Care Medicine
SC General & Internal Medicine
GA AR9JC
UT WOS:000343889000028
PM 25319905
ER
PT J
AU Aizer, J
Bolster, MB
AF Aizer, Juliet
Bolster, Marcy B.
TI Fracture Liaison Services: Promoting Enhanced Bone Health Care
SO CURRENT RHEUMATOLOGY REPORTS
LA English
DT Article
DE Fracture liaison service; FLS; Osteoporosis management; Osteoporosis
treatment; Secondary fracture prevention; Fracture prevention; Quality
of care; Bone health
ID RANDOMIZED CONTROLLED-TRIAL; QUALITY-OF-LIFE; HIP FRACTURE;
COST-EFFECTIVENESS; OSTEOPOROSIS TREATMENT; ZOLEDRONIC ACID; TRAUMA
FRACTURE; UNITED-KINGDOM; OLDER WOMEN; MORTALITY
AB The high prevalence of osteoporotic fractures and their major effect on morbidity and mortality emphasizes the critical need to optimize bone health care. Patients presenting with fragility fractures are at high risk of subsequent fracture, but treatment rates have remained low for these patients. Recently developed fracture liaison services have successfully increased osteoporosis treatment, with improved patient outcomes. We review factors contributing to the treatment gap in osteoporosis, the function of fracture liaison services in reducing this gap, and lessons learned from the literature on effective formats, key elements, and suggestions for managing challenges in implementation of a fracture liaison service.
C1 [Aizer, Juliet] Weill Cornell Med Coll, Hosp Special Surg, Div Rheumatol, New York, NY 10021 USA.
[Bolster, Marcy B.] Harvard Univ, Div Rheumatol, Sch Med, Massachusetts Gen Hosp, Boston, MA 02114 USA.
RP Aizer, J (reprint author), Weill Cornell Med Coll, Hosp Special Surg, Div Rheumatol, 535 E 70th St, New York, NY 10021 USA.
EM AizerJ@HSS.edu; Mbolster@MGH.Harvard.edu
FU Rheumatology Research Foundation Clinician Scholar Educator Award; Eli
Lilly
FX Juliet Aizer reports that she has no conflict of interest. Dr. Aizer
received funding in part from the Rheumatology Research Foundation
Clinician Scholar Educator Award. Marcy B. Bolster reports the receipt
of a research grant from Eli Lilly, outside the submitted work.
NR 49
TC 6
Z9 6
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3774
EI 1534-6307
J9 CURR RHEUMATOL REP
JI Curr. Rheumatol. Rep.
PD NOV
PY 2014
VL 16
IS 11
AR 455
DI 10.1007/s11926-014-0455-2
PG 8
WC Rheumatology
SC Rheumatology
GA AR9KZ
UT WOS:000343893800003
PM 25240684
ER
PT J
AU Fisher, MC
Pillinger, MH
Keenan, RT
AF Fisher, Mark C.
Pillinger, Michael H.
Keenan, Robert T.
TI Inpatient Gout: A Review
SO CURRENT RHEUMATOLOGY REPORTS
LA English
DT Review
DE Gout, Inpatient; Hospitalization; Healthcare Burden
ID HEALTH-CARE UTILIZATION; SERUM URIC-ACID; HOSPITALIZED-PATIENTS;
POSTSURGICAL GOUT; ARTHRITIS; MANAGEMENT; ATTACKS; COMORBIDITIES;
POPULATION; PREVALENCE
C1 [Fisher, Mark C.] Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol, Boston, MA 02114 USA.
[Pillinger, Michael H.] NYU, Sch Med, Dept Med, New York, NY USA.
[Keenan, Robert T.] Duke Univ, Div Rheumatol & Immunol, Sch Med, Durham, NC 27706 USA.
RP Fisher, MC (reprint author), Massachusetts Gen Hosp, Div Rheumatol Allergy & Immunol, 2100 Yawkey 55 Fruit St, Boston, MA 02114 USA.
EM MFISHER6@mgh.harvard.edu
OI Pillinger, Michael/0000-0003-3168-1542
FU Takeda; Savient
FX Michael H. Pillinger reports that he has served as a consultant for
Savient, and for Crealta. He is the recipient of investigator-initiated
grants from Takeda and Savient, and currently serves as a site
investigator for a clinical study by Takeda, outside the submitted work.
NR 31
TC 0
Z9 0
U1 0
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1523-3774
EI 1534-6307
J9 CURR RHEUMATOL REP
JI Curr. Rheumatol. Rep.
PD NOV
PY 2014
VL 16
IS 11
AR 458
DI 10.1007/s11926-014-0458-z
PG 5
WC Rheumatology
SC Rheumatology
GA AR9KZ
UT WOS:000343893800005
PM 25304216
ER
PT J
AU Beca, F
Pinheiro, J
Rios, E
Pontes, P
Amendoeira, I
AF Beca, Francisco
Pinheiro, Jorge
Rios, Elisabete
Pontes, Patricia
Amendoeira, Isabel
TI Genotypes and Prevalence of HPV Single and Multiple Concurrent
Infections in Women with HSIL
SO DIAGNOSTIC CYTOPATHOLOGY
LA English
DT Article
DE Gynaecological cytology; genotyping; HPV
ID NUTRITION EXAMINATION SURVEY; HUMAN-PAPILLOMAVIRUS; UNITED-STATES;
NATIONAL-HEALTH; CERVICAL-CANCER; FEMALES; VACCINE
AB The contribution of human papillomavirus (HPV) types to the carcinogenesis of cervical cancer has been established for a long time. However, the role of phylogenetically related and rare variants remains uncertain, as well as the influence of concurrent multiple HPV genotypes infection. We aimed at studying the prevalence of several HPV genotypes infecting women with single versus concurrent multiple HPV genotypes infection with a HSIL diagnosis in a cervical cytology. We conducted a cross-sectional study using Thin-Prep((R)) liquid-based cervical cytology specimens with the diagnosis of high-grade squamous intraepithelial lesion (HSIL), in which HPV genotype was sequentially tested. Genotypes were determined with a PapilloCheck((R)) system, a DNA-Chip for the type-specific identification of 18 high-risk and six low-risk types of HPV. Of the total study population, 176 cases had a diagnosis of HSIL and positive HPV genotyping result, being HPV16 the most prevalent genotype (48.86%; 95%CI: 41.58-56.19) followed by HPV31 (14.20%; 95%CI: 9.75-20.18). Concurrent multiple HPV genotypes were detected in 36.93% (95%CI: 30.15-44.27) of the patients. The prevalence of the 10 most common HPV genotypes detected varied significantly according to the presence of single vs. concurrent multiple HPV genotypes (P=0.022). Moreover, women with concurrent multiple HPV genotypes were on average 3.53 (95%CI: 0.43-6.64) years younger than women with single genotype infection. Our results suggest that women with multiple genotype HPV infection differ in terms of age and distribution of the most prevalent HPV genotypes. Additionally, we provide further evidence of the predominance of HPV16 in HSIL lesions of the uterine cervix. Diagn. Cytopathol. 2014;42:919-923. (c) 2014 Wiley Periodicals, Inc.
C1 [Beca, Francisco; Rios, Elisabete; Amendoeira, Isabel] Univ Porto, IPATIMUP Inst Mol Pathol & Immunol, P-4100 Oporto, Portugal.
[Beca, Francisco; Pinheiro, Jorge; Rios, Elisabete] Univ Porto, Fac Med, Dept Pathol & Oncol, P-4100 Oporto, Portugal.
[Beca, Francisco; Pinheiro, Jorge; Rios, Elisabete; Pontes, Patricia; Amendoeira, Isabel] Ctr Hosp Sao Joao, Dept Pathol, Oporto, Portugal.
RP Beca, F (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, 450 Brookline Ave, Boston, MA 02115 USA.
EM francisco_debeca@dfci.harvard.edu
OI Beca, Francisco/0000-0002-4409-012X
FU Fundacao para a Ciencia e Tecnologia (FCT); FCT [HMSP-ICJ/0006/2012]
FX Contract grant sponsor: Fundacao para a Ciencia e Tecnologia (FCT).;
Contract grant sponsor: FCT (F.F.B.); contract grant number:
HMSP-ICJ/0006/2012.
NR 17
TC 6
Z9 6
U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 8755-1039
EI 1097-0339
J9 DIAGN CYTOPATHOL
JI Diagn. Cytopathol.
PD NOV
PY 2014
VL 42
IS 11
BP 919
EP 923
DI 10.1002/dc.23143
PG 5
WC Medical Laboratory Technology; Pathology
SC Medical Laboratory Technology; Pathology
GA AS0MA
UT WOS:000343969900001
PM 24623593
ER
PT J
AU Michot, C
Le Goff, C
Mahaut, C
Afenjar, A
Brooks, AS
Campeau, PM
Destree, A
Di Rocco, M
Donnai, D
Hennekam, R
Heron, D
Jacquemont, S
Kannu, P
Lin, AE
Manouvrier-Hanu, S
Mansour, S
Marlin, S
McGowan, R
Murphy, H
Raas-Rothschild, A
Rio, M
Simon, M
Stolte-Dijkstra, I
Stone, JR
Sznajer, Y
Tolmie, J
Touraine, R
van den Ende, J
Van der Aa, N
van Essen, T
Verloes, A
Munnich, A
Cormier-Daire, V
AF Michot, Caroline
Le Goff, Carine
Mahaut, Clementine
Afenjar, Alexandra
Brooks, Alice S.
Campeau, Philippe M.
Destree, Anne
Di Rocco, Maja
Donnai, Dian
Hennekam, Raoul
Heron, Delphine
Jacquemont, Sebastien
Kannu, Peter
Lin, Angela E.
Manouvrier-Hanu, Sylvie
Mansour, Sahar
Marlin, Sandrine
McGowan, Ruth
Murphy, Helen
Raas-Rothschild, Annick
Rio, Marlene
Simon, Marleen
Stolte-Dijkstra, Irene
Stone, James R.
Sznajer, Yves
Tolmie, John
Touraine, Renaud
van den Ende, Jenneke
Van der Aa, Nathalie
van Essen, Ton
Verloes, Alain
Munnich, Arnold
Cormier-Daire, Valerie
TI Myhre and LAPS syndromes: clinical and molecular review of 32 patients
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Review
DE Myhre syndrome; SMAD4; LAPS; long-term follow-up
ID TUMOR-SUPPRESSOR GENE; SHORT STATURE; MUTATIONS; FEMALE; SMAD4;
DELINEATION; DPC4
AB Myhre syndrome is characterized by short stature, brachydactyly, facial features, pseudomuscular hypertrophy, joint limitation and hearing loss. We identified SMAD4 mutations as the cause of Myhre syndrome. SMAD4 mutations have also been identified in laryngotracheal stenosis, arthropathy, prognathism and short stature syndrome (LAPS). This study aimed to review the features of Myhre and LAPS patients to define the clinical spectrum of SMAD4 mutations. We included 17 females and 15 males ranging in age from 8 to 48 years. Thirty were diagnosed with Myhre syndrome and two with LAPS. SMAD4 coding sequence was analyzed by Sanger sequencing. Clinical and radiological features were collected from a questionnaire completed by the referring physicians. All patients displayed a typical facial gestalt, thickened skin, joint limitation and muscular pseudohypertrophy. Growth retardation was common (68.7%) and was variable in severity (from -5.5 to -2 SD), as was mild-to-moderate intellectual deficiency (87.5%) with additional behavioral problems in 56.2% of the patients. Significant health concerns like obesity, arterial hypertension, bronchopulmonary insufficiency, laryngotracheal stenosis, pericarditis and early death occurred in four. Twenty-nine patients had a de novo heterozygous SMAD4 mutation, including both patients with LAPS. In 27 cases mutation affected Ile500 and in two cases Arg496. The three patients without SMAD4 mutations had typical findings of Myhre syndrome. Myhre-LAPS syndrome is a clinically homogenous condition with life threatening complications in the course of the disease. Our identification of SMAD4 mutations in 29/32 cases confirms that SMAD4 is the major gene responsible for Myhre syndrome.
C1 [Michot, Caroline; Le Goff, Carine; Mahaut, Clementine; Rio, Marlene; Munnich, Arnold; Cormier-Daire, Valerie] Paris Descartes Univ, Sorbonne Paris Cite, Necker Enfants Malad Hosp, Inst Imagine,Dept Genet,INSERM Unit U781, F-75015 Paris, France.
[Afenjar, Alexandra] Armand Trousseau CHU, Ctr Reference Malad Rares Anomalies Dev & Syndrom, Neuropediat Dept, Paris, France.
[Brooks, Alice S.; Simon, Marleen] Ersamus MC, Dept Clin Genet, Rotterdam, Netherlands.
[Campeau, Philippe M.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Destree, Anne] Inst Pathol & Genet, Dept Human Genet, Gosselies, Belgium.
[Di Rocco, Maja] Gaslini Inst, Dept Pediat, Unit Rare Dis, Genoa, Italy.
[Donnai, Dian; Murphy, Helen] Univ Manchester, St Marys Hosp, Manchester Acad Hlth Sci Ctr, Manchester M13 0JH, Lancs, England.
[Hennekam, Raoul] Univ Amsterdam, Acad Med Ctr, Dept Pediat, NL-1105 AZ Amsterdam, Netherlands.
[Heron, Delphine] CHU Pitie Salpetriere, UPMC, GRC, Genet & Cytogenet Dept, Paris, France.
[Jacquemont, Sebastien] CHUV, Dept Genet, Vaud, Switzerland.
[Kannu, Peter] Hosp Sick Children, Div Clin & Metab Genet, Toronto, ON M5G 1X8, Canada.
[Lin, Angela E.] Massachussets Gen Hosp Children, Boston, MA USA.
[Manouvrier-Hanu, Sylvie] Univ Hosp, Dept Clin Genet, Lille, France.
[Mansour, Sahar] St Georges Healthcare NHS Trust, Clin Genet, London, England.
[Marlin, Sandrine] Armand Trousseau CHU, Ctr Reference Surdites Genet, Genet & Med Embryol Unit, Paris, France.
[McGowan, Ruth; Tolmie, John] West Scotland Reg Genet Serv, Glasgow, Lanark, Scotland.
[Raas-Rothschild, Annick] Meir Med Ctr, Inst Human Genet, Kefar Sava, Israel.
[Stolte-Dijkstra, Irene; van Essen, Ton] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, Groningen, Netherlands.
[Stone, James R.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Sznajer, Yves] Clin Univ St Luc, Ctr Human Genet, B-1200 Brussels, Belgium.
[Touraine, Renaud] St Etienne CHU, Dept Clin Genet, St Etienne, France.
[van den Ende, Jenneke; Van der Aa, Nathalie] Dept Med Genet, Edegem, Belgium.
[van den Ende, Jenneke; Van der Aa, Nathalie] Univ Antwerp Hosp, Edegem, Belgium.
[Verloes, Alain] Robert Debre Hosp, AP HP, Dept Genet, INSERM U676, Paris, France.
RP Cormier-Daire, V (reprint author), Paris Descartes Univ, Sorbonne Paris Cite, Necker Enfants Malad Hosp, Dept Genet,INSERM Unit U781, 149 Rue Sevres, F-75015 Paris, France.
EM valerie.cormier-daire@inserm.fr
RI Campeau, Philippe/J-8614-2015
OI Campeau, Philippe/0000-0001-9713-7107
NR 28
TC 8
Z9 8
U1 3
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD NOV
PY 2014
VL 22
IS 11
BP 1272
EP 1277
DI 10.1038/ejhg.2013.288
PG 6
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AR8UR
UT WOS:000343850200007
PM 24424121
ER
PT J
AU Deelen, P
Menelaou, A
van Leeuwen, EM
Kanterakis, A
van Dijk, F
Medina-Gomez, C
Francioli, LC
Hottenga, JJ
Karssen, LC
Estrada, K
Kreiner-Moller, E
Rivadeneira, F
van Setten, J
Gutierrez-Achury, J
Westra, HJ
Franke, L
van Enckevort, D
Dijkstra, M
Byelas, H
van Duijn, CM
de Bakker, PIW
Wijmenga, C
Swertz, MA
AF Deelen, Patrick
Menelaou, Androniki
van Leeuwen, Elisabeth M.
Kanterakis, Alexandros
van Dijk, Freerk
Medina-Gomez, Carolina
Francioli, Laurent C.
Hottenga, Jouke Jan
Karssen, Lennart C.
Estrada, Karol
Kreiner-Moller, Eskil
Rivadeneira, Fernando
van Setten, Jessica
Gutierrez-Achury, Javier
Westra, Harm-Jan
Franke, Lude
van Enckevort, David
Dijkstra, Martijn
Byelas, Heorhiy
van Duijn, Cornelia M.
de Bakker, Paul I. W.
Wijmenga, Cisca
Swertz, Morris A.
CA Genome Netherlands Consortium
TI Improved imputation quality of low-frequency and rare variants in
European samples using the 'Genome of The Netherlands'
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE genotype imputation; GWAS; GoNL; rare variants; reference sets;
reference panel
ID GENOTYPE IMPUTATION; WIDE ASSOCIATION; DISEASE; COMMON; ARRAY; POWER;
LOCI
AB Although genome-wide association studies (GWAS) have identified many common variants associated with complex traits, low-frequency and rare variants have not been interrogated in a comprehensive manner. Imputation from dense reference panels, such as the 1000 Genomes Project (1000G), enables testing of ungenotyped variants for association. Here we present the results of imputation using a large, new population-specific panel: the Genome of The Netherlands (GoNL). We benchmarked the performance of the 1000G and GoNL reference sets by comparing imputation genotypes with 'true' genotypes typed on ImmunoChip in three European populations (Dutch, British, and Italian). GoNL showed significant improvement in the imputation quality for rare variants (MAF 0.05-0.5%) compared with 1000G. In Dutch samples, the mean observed Pearson correlation, r(2), increased from 0.61 to 0.71. We also saw improved imputation accuracy for other European populations (in the British samples, r(2) improved from 0.58 to 0.65, and in the Italians from 0.43 to 0.47). A combined reference set comprising 1000G and GoNL improved the imputation of rare variants even further. The Italian samples benefitted the most from this combined reference (the mean r(2) increased from 0.47 to 0.50). We conclude that the creation of a large population-specific reference is advantageous for imputing rare variants and that a combined reference panel across multiple populations yields the best imputation results.
C1 [Deelen, Patrick; Kanterakis, Alexandros; van Dijk, Freerk; Gutierrez-Achury, Javier; Westra, Harm-Jan; Franke, Lude; Dijkstra, Martijn; Byelas, Heorhiy; Wijmenga, Cisca; Swertz, Morris A.] Univ Groningen, Univ Med Ctr Groningen, Dept Genet, NL-9700 RB Groningen, Netherlands.
[Deelen, Patrick; Kanterakis, Alexandros; van Dijk, Freerk; van Enckevort, David; Dijkstra, Martijn; Byelas, Heorhiy; Swertz, Morris A.] Univ Groningen, Univ Med Ctr Groningen, Genom Coordinat Ctr, NL-9700 RB Groningen, Netherlands.
[Menelaou, Androniki; Francioli, Laurent C.; van Setten, Jessica; de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Dept Med Genet, NL-9700 RB Utrecht, Netherlands.
[van Leeuwen, Elisabeth M.; Karssen, Lennart C.] Erasmus MC, Dept Epidemiol, Genet Epidemiol Unit, Rotterdam, Netherlands.
[Kreiner-Moller, Eskil; Rivadeneira, Fernando] Erasmus MC, Dept Internal Med, Rotterdam, Netherlands.
[Medina-Gomez, Carolina; Estrada, Karol; Kreiner-Moller, Eskil; Rivadeneira, Fernando; van Duijn, Cornelia M.] Erasmus Univ, Med Ctr, Dept Epidemiol, Rotterdam, Netherlands.
[Medina-Gomez, Carolina; Rivadeneira, Fernando] Netherlands Consortium Hlth Aging, Netherlands Genom Initiat, Rotterdam, Netherlands.
[Hottenga, Jouke Jan] Vrije Univ Amsterdam, Dept Biol Psychol, Amsterdam, Netherlands.
[Estrada, Karol] Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Dept Med, Boston, MA 02114 USA.
[Estrada, Karol] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Kreiner-Moller, Eskil] COPSAC, Copenhagen, Denmark.
[Kreiner-Moller, Eskil] Copenhagen Prospect Studies Asthma Childhood, Copenhagen, Denmark.
[Kreiner-Moller, Eskil] Univ Copenhagen, Fac Hlth Sci, Copenhagen, Denmark.
[van Enckevort, David] Netherlands Bioinformat Ctr, NBIC BioAssist, Nijmegen, Netherlands.
[de Bakker, Paul I. W.] Univ Med Ctr Utrecht, Dept Epidemiol, Utrecht, Netherlands.
[de Bakker, Paul I. W.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Genet, Boston, MA 02115 USA.
[de Bakker, Paul I. W.] Broad Inst Harvard & MIT, Cambridge, MA USA.
RP Swertz, MA (reprint author), Univ Groningen, Univ Med Ctr Groningen, Genom Coordinat Ctr, NL-9700 RB Groningen, Netherlands.
EM m.a.swertz@gmail.com
RI Ye, Kai/B-3640-2012; de Bakker, Paul/B-8730-2009; Franke,
Lude/P-7036-2016; Wijmenga, Cisca/D-2173-2009; Slagboom, P.
Eline/R-4790-2016; Suchiman, H. Eka D./F-5024-2017;
OI Wolffenbuttel, Bruce H.R./0000-0001-9262-6921; Deelen,
Patrick/0000-0002-5654-3966; Medina-Gomez, Carolina/0000-0001-7999-5538;
Karssen, Lennart C./0000-0002-1959-342X; de Bakker,
Paul/0000-0001-7735-7858; van Schaik, Barbera/0000-0002-5568-8127;
Wijmenga, Cisca/0000-0002-5635-1614; Beekman,
Marian/0000-0003-0585-6206; Franke, Lude/0000-0002-5159-8802; Slagboom,
P. Eline/0000-0002-2875-4723; Suchiman, H. Eka D./0000-0002-7168-5516;
Rivadeneira, Fernando/0000-0001-9435-9441; Kreiner,
Eskil/0000-0003-1204-2438
FU BBMRI-NL; Netherlands Organization for Scientific Research (NWO)
[184.021.007]; Netherlands Organization for Scientific Research
[184021007]
FX This study was made possible by rainbow grant 2 from BBMRI-NL to MS, a
research infrastructure financed by the Netherlands Organization for
Scientific Research (NWO project 184.021.007). We thank the Target
project (http://www.rug.nl/target) for providing the compute
infrastructure, and the BigGrid/eBioGrid project
(http://www.ebiogrid.nl) for sponsoring the pipeline implementation. We
thank Jackie Senior for careful reading and editing the manuscript. This
study made use of data generated by the 'Genome of the Netherlands'
project, which is funded by the Netherlands Organization for Scientific
Research (grant no. 184021007). The data were made available as a
Rainbow Project of BBMRI-NL. Samples were contributed by LifeLines
(http://lifelines.nl/lifelines-research/general), the Leiden Longevity
Study (http://www.healthy-ageing.nl; http://www.langleven.net), the
Netherlands Twin Registry (NTR: http://www.tweelingenregister.org), the
Rotterdam studies, (http://www.erasmus-epidemiology.nl/rotterdamstudy),
and the Genetic Research in Isolated Populations program
(http://www.epib.nl/research/geneticepi/research.html#gip). The
sequencing was carried out in collaboration with BGI (Shenzhen, China).
NR 26
TC 27
Z9 27
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
EI 1476-5438
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD NOV
PY 2014
VL 22
IS 11
BP 1321
EP 1326
DI 10.1038/ejhg.2014.19
PG 6
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AR8UR
UT WOS:000343850200014
PM 24896149
ER
PT J
AU Sweeney, EM
Thakur, KT
Lyons, JL
Smith, BR
Willey, JZ
Cervantes-Arslanian, AM
Hickey, MK
Uchino, K
Haussen, DC
Koch, S
Schwamm, LH
Elkind, MSV
Shinohara, RT
Mateen, FJ
AF Sweeney, E. M.
Thakur, K. T.
Lyons, J. L.
Smith, B. R.
Willey, J. Z.
Cervantes-Arslanian, A. M.
Hickey, M. K.
Uchino, K.
Haussen, D. C.
Koch, S.
Schwamm, L. H.
Elkind, M. S. V.
Shinohara, R. T.
Mateen, F. J.
TI Outcomes of intravenous tissue plasminogen activator for acute ischaemic
stroke in HIV-infected adults
SO EUROPEAN JOURNAL OF NEUROLOGY
LA English
DT Article
DE cerebral infarction; cerebrovascular diseases and cerebral circulation;
HIV; infections; neurological disorders; stroke; thrombolysis
ID UNITED-STATES; RISK; EVENTS
AB Background and purposeTo our knowledge there are no studies reporting the use and short-term outcomes of intravenous tissue plasminogen activator (IV-TPA) for the treatment of acute ischaemic stroke (AIS) in people living with HIV.
MethodsThe US Nationwide Inpatient Sample (NIS) (2006-2010) was searched for HIV-infected AIS patients treated with IV-TPA.
ResultsIn the NIS, 2.2% (62/2877) of HIV-infected AIS cases were thrombolyzed with IV-TPA (median age 52years, range 27-78, 32% female, 22% Caucasian) vs. 2.1% (19335/937896) of HIV-uninfected cases (median age 72years, range 17-102years, 50% female, 74% Caucasian; P=0.77). There were more deaths in HIV-infected versus uninfected patients with stroke (220/2877, 7.6% vs. 49089/937547, 5.2%, P<0.001) but no difference in the proportion of deaths amongst IV-TPA-treated patients. The age- and sex-adjusted odds ratio for death following IV-TPA administration in HIV-infected versus uninfected patients was 2.26 (95% CI 1.12, 4.58), but the interaction on mortality between HIV and IV-TPA use was not statistically significant, indicating no difference in risk of in-hospital death by HIV serostatus with IV-TPA use. A higher number of HIV-infected patients remained in hospital versus died or were discharged at both 10 and 30days (P<0.01 at 10 and 30days). No difference in the proportion of intracerebral hemorrhage in the two groups was found (P=0.362).
ConclusionsThe in-hospital mortality is higher amongst HIV-infected AIS patients than HIV-uninfected patients. However, the risk of death amongst HIV-infected patients treated with IV-TPA is similar to HIV-uninfected groups.
C1 [Sweeney, E. M.] Johns Hopkins Univ, Dept Biostat, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
[Thakur, K. T.] Johns Hopkins Univ Hosp, Dept Neurol, Baltimore, MD 21287 USA.
[Lyons, J. L.] Brigham & Womens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Smith, B. R.] NINDS, Sect Infect Nervous Syst, NIH, Bethesda, MD 20892 USA.
[Willey, J. Z.; Elkind, M. S. V.] Columbia Univ, Dept Neurol, Coll Phys & Surg, New York, NY USA.
[Cervantes-Arslanian, A. M.] Boston Univ, Dept Neurol, Boston, MA 02215 USA.
[Hickey, M. K.; Schwamm, L. H.; Mateen, F. J.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
[Uchino, K.] Cleveland Clin, Cerebrovasc Ctr, Cleveland, OH 44106 USA.
[Haussen, D. C.; Koch, S.] Univ Miami, Dept Neurol, Miami, FL USA.
[Elkind, M. S. V.] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA.
[Shinohara, R. T.] Univ Penn, Perelman Sch Med, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
RP Mateen, FJ (reprint author), Massachusetts Gen Hosp, Dept Neurol, 55 Fruit St,AC-720, Boston, MA 02114 USA.
EM fmateen@partners.org
OI Schwamm, Lee/0000-0003-0592-9145
FU HIV/AIDS from Canadian Institute of Health Research (CIHR)
FX Dr Mateen received salary support from an HIV/AIDS priority grant from
the Canadian Institute of Health Research (CIHR).
NR 13
TC 3
Z9 4
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1351-5101
EI 1468-1331
J9 EUR J NEUROL
JI Eur. J. Neurol.
PD NOV
PY 2014
VL 21
IS 11
BP 1394
EP 1399
DI 10.1111/ene.12506
PG 6
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AR8EH
UT WOS:000343808000009
PM 25040336
ER
PT J
AU Agaku, IT
Odukoya, OO
Olufajo, O
Filippidis, FT
Vardavas, CI
AF Agaku, Israel T.
Odukoya, Oluwakemi O.
Olufajo, Olubode
Filippidis, Filippos T.
Vardavas, Constantine I.
TI Support for smoke-free cars when children are present: a secondary
analysis of 164,819 US adults in 2010/2011
SO EUROPEAN JOURNAL OF PEDIATRICS
LA English
DT Article
DE Secondhand smoke; Tobacco control; Cars; Children; Exposure
ID SECONDHAND SMOKE; UNITED-STATES; EXPOSURE; MIDDLE
AB Comprehensive smoke-free legislations prohibiting smoking in indoor areas of workplaces, bars, and restaurants have been adopted in most of the USA; however, limited efforts have focused on regulating secondhand smoke (SHS) exposure in the family car. The objective of this study was to identify the determinants and national/state-specific population support for smoke-free cars, in the presence of any occupant in general, but particularly when children are present. National data of US adults aged a parts per thousand yen18 years (n = 164,819) were obtained from the 2010/2011 Tobacco Use Supplement of the Current Population Survey. Among all US adults, a significantly greater proportion supported smoke-free cars when it was specified that the occupant was a child compared to when not specified (93.4 vs. 73.7 %, p < 0.05). Age, race/ethnicity, gender, current tobacco use, marital status, and the existence of household smoke-free regulations all mediated population support for smoke-free cars. Conclusion: While differences within the US population were noted, this study however showed overwhelming support for smoke-free car policies, particularly when children are present. Policies which prohibit smoking in indoor or confined areas such as cars may benefit public health by protecting nonsmoking children and adults from involuntary SHS exposure.
C1 [Agaku, Israel T.; Vardavas, Constantine I.] Harvard Univ, Sch Publ Hlth, Ctr Global Tobacco Control, Dept Social & Behav Sci, Boston, MA 02215 USA.
[Odukoya, Oluwakemi O.] Univ Lagos, Coll Med, Dept Community Hlth & Primary Care, Idi Araba, Lagos State, Nigeria.
[Olufajo, Olubode] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
[Filippidis, Filippos T.] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, London, England.
[Vardavas, Constantine I.] Univ Crete, Clin Social & Family Med, Iraklion, Greece.
RP Agaku, IT (reprint author), Harvard Univ, Sch Publ Hlth, Ctr Global Tobacco Control, Dept Social & Behav Sci, 401 Pk Dr Landmark Ctr 4th Floor West Wing 677, Boston, MA 02215 USA.
EM iagaku@post.harvard.edu; drolukemiodukoya@yahoo.com;
oao777@mail.harvard.edu; f.filippidis@mail.harvard.edu;
vardavas@hsph.harvard.edu
RI Vardavas, Constantine/O-4961-2016;
OI Filippidis, Filippos/0000-0002-2101-2559
NR 24
TC 3
Z9 3
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6199
EI 1432-1076
J9 EUR J PEDIATR
JI Eur. J. Pediatr.
PD NOV
PY 2014
VL 173
IS 11
BP 1459
EP 1466
DI 10.1007/s00431-014-2344-0
PG 8
WC Pediatrics
SC Pediatrics
GA AR8FQ
UT WOS:000343811600008
PM 24889334
ER
PT J
AU Thomadsen, B
Nath, R
Bateman, FB
Farr, J
Glisson, C
Islam, MK
LaFrance, T
Moore, ME
Xu, XG
Yudelev, M
AF Thomadsen, Bruce
Nath, Ravinder
Bateman, Fred B.
Farr, Jonathan
Glisson, Cal
Islam, Mohammad K.
LaFrance, Terry
Moore, Mary E.
Xu, X. George
Yudelev, Mark
TI POTENTIAL HAZARD DUE TO INDUCED RADIOACTIVITY SECONDARY TO RADIOTHERAPY:
THE REPORT OF TASK GROUP 136 OF THE AMERICAN ASSOCIATION OF PHYSICISTS
IN MEDICINE
SO HEALTH PHYSICS
LA English
DT Review
DE accelerators, medical; exposure, occupational; radiation risk; radiation
therapy
ID NEUTRON-THERAPY FACILITY; RADIATION PROTECTION ASPECTS; ENERGY
LINEAR-ACCELERATOR; ACTIVATION PRODUCTS; PROTON THERAPY; MULTILEAF
COLLIMATOR; STAFF PROTECTION; DOSE-EQUIVALENT; LAYER-STACKING; SAFETY
SURVEY
AB External-beam radiation therapy mostly uses high-energy photons (x-rays) produced by medical accelerators, but many facilities now use proton beams, and a few use fast-neutron beams. High-energy photons offer several advantages over lower-energy photons in terms of better dose distributions for deep-seated tumors, lower skin dose, less sensitivity to tissue heterogeneities, etc. However, for beams operating at or above 10 MV, some of the materials in the accelerator room and the radiotherapy patient become radioactive due primarily to photonuclear reactions and neutron capture, exposing therapy staff and patients to unwanted radiation dose. Some recent advances in radiotherapy technology require treatments using a higher number of monitor units and monitor-unit rates for the same delivered dose, and compared to the conventional treatment techniques and fractionation schemes, the activation dose to personnel can be substantially higher. Radiotherapy treatments with proton and neutron beams all result in activated materials in the treatment room. In this report, the authors review critically the published literature on radiation exposures from induced radioactivity in radiotherapy. They conclude that the additional exposure to the patient due to induced radioactivity is negligible compared to the overall radiation exposure as a part of the treatment. The additional exposure to the staff due to induced activity from photon beams is small at an estimated level of about 1 to 2 mSv y(-1). This is well below the allowed occupational exposure limits. Therefore, the potential hazard to staff from induced radioactivity in the use of high-energy x-rays is considered to be low, and no specific actions are considered necessary or mandatory. However, in the spirit of the "As Low as Reasonably Achievable (ALARA)" program, some reasonable steps are recommended that can be taken to reduce this small exposure to an even lower level. The dose reduction strategies suggested should be followed only if these actions are considered reasonable and practical in the individual clinics. Therapists working with proton beam and neutron beam units handle treatment devices that do become radioactive, and they should wear extremity monitors and make handling apertures and boluses their last task upon entering the room following treatment. Personnel doses from neutron-beam units can approach regulatory limits depending on the number of patients and beams, and strategies to reduce doses should be followed.
C1 [Thomadsen, Bruce] Univ Wisconsin, Dept Med Phys, Madison, WI 53706 USA.
[Nath, Ravinder] Yale Univ, Sch Med, Dept Therapeut Radiol, New Haven, CT 06520 USA.
[Bateman, Fred B.] NIST, Radiat Phys Div, Gaithersburg, MD 20899 USA.
[Farr, Jonathan] St Jude Childrens Res Hosp, Dept Radiol Sci, Div Radiat Oncol, Memphis, TN 38105 USA.
[Glisson, Cal] Loma Linda Univ, Off Radiat Safety, Loma Linda, CA 92354 USA.
[Islam, Mohammad K.] Princess Margaret Hosp, Dept Radiat Phys, Toronto, ON M5G 2M9, Canada.
[LaFrance, Terry] Baystate Hlth Syst Inc, Med Phys Radiat Safety Dept, Springfield, MA 01199 USA.
[Moore, Mary E.] Philadelphia VA Med Ctr, Radiat Safety Off, Philadelphia, PA 19104 USA.
[Xu, X. George] Rensselaer Polytech Inst, Program Nucl Engn & Engn Phys, Troy, NY 12180 USA.
[Yudelev, Mark] Ted B Wahby Canc Ctr, Mt Clemens, MI 48043 USA.
RP Thomadsen, B (reprint author), Univ Wisconsin, Dept Med Phys, Wisconsin Inst Med Res 1005, 1111 Highland Ave, Madison, WI 53705 USA.
EM brthomad@wisc.edu
NR 72
TC 3
Z9 3
U1 1
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0017-9078
EI 1538-5159
J9 HEALTH PHYS
JI Health Phys.
PD NOV
PY 2014
VL 107
IS 5
BP 442
EP 460
DI 10.1097/HP.0000000000000139
PG 19
WC Environmental Sciences; Public, Environmental & Occupational Health;
Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical
Imaging
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Nuclear Science & Technology; Radiology, Nuclear Medicine &
Medical Imaging
GA AR7QF
UT WOS:000343773700009
PM 25271934
ER
PT J
AU Augustinack, JC
van der Kouwe, AJW
Salat, DH
Benner, T
Stevens, AA
Annese, J
Fischl, B
Frosch, MP
Corkin, S
AF Augustinack, Jean C.
van der Kouwe, Andre J. W.
Salat, David H.
Benner, Thomas
Stevens, Allison A.
Annese, Jacopo
Fischl, Bruce
Frosch, Matthew P.
Corkin, Suzanne
TI HM's Contributions to Neuroscience: A Review and Autopsy Studies
SO HIPPOCAMPUS
LA English
DT Editorial Material
DE hippocampus; entorhinal cortex; perirhinal cortex; parahippocampal
cortex; amygdala
ID MEDIAL TEMPORAL-LOBE; AMNESIC PATIENT HM; WHITE-MATTER LESIONS; SEMANTIC
KNOWLEDGE; ALZHEIMERS-DISEASE; PERCEPTUAL IDENTIFICATION; PATHOLOGICAL
MARKERS; PERIRHINAL CORTEX; PROFOUND AMNESIA; CEREBRAL-CORTEX
AB H.M., Henry Molaison, was one of the world's most famous amnesic patients. His amnesia was caused by an experimental brain operation, bilateral medial temporal lobe resection, carried out in 1953 to relieve intractable epilepsy. He died on December 2, 2008, and that night we conducted a wide variety of in situ MRI scans in a 3 T scanner at the Massachusetts General Hospital (Mass General) Athinoula A. Martinos Center for Biomedical Imaging. For the in situ experiments, we acquired a full set of standard clinical scans, 1 mm isotropic anatomical scans, and multiple averages of 440 m isotropic anatomical scans. The next morning, H.M.'s body was transported to the Mass General Morgue for autopsy. The photographs taken at that time provided the first documentation of H.M.'s lesions in his physical brain. After tissue fixation, we obtained ex vivo structural data at ultra-high resolution using 3 T and 7 T magnets. For the ex vivo acquisitions, the highest resolution images were 210 m isotropic. Based on the MRI data, the anatomical areas removed during H.M.'s experimental operation were the medial temporopolar cortex, piriform cortex, virtually all of the entorhinal cortex, most of the perirhinal cortex and subiculum, the amygdala (except parts of the dorsal-most nucleicentral and medial), anterior half of the hippocampus, and the dentate gyrus (posterior head and body). The posterior parahippocampal gyrus and medial temporal stem were partially damaged. Spared medial temporal lobe tissue included the dorsal-most amygdala, the hippocampal-amygdalo-transition-area, approximate to 2 cm of the tail of the hippocampus, a small part of perirhinal cortex, a small portion of medial hippocampal tissue, and approximate to 2 cm of posterior parahippocampal gyrus. H.M.'s impact on the field of memory has been remarkable, and his contributions to neuroscience continue with a unique dataset that includes in vivo, in situ, and ex vivo high-resolution MRI. (c) 2014 Wiley Periodicals, Inc.
C1 [Augustinack, Jean C.; van der Kouwe, Andre J. W.; Salat, David H.; Benner, Thomas; Stevens, Allison A.; Fischl, Bruce; Corkin, Suzanne] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Dept Radiol, Charlestown, MA USA.
[Annese, Jacopo] Brain Observ, San Diego, CA 92101 USA.
[Annese, Jacopo] Univ Calif San Diego, Dept Radiol, San Diego, CA 92093 USA.
[Fischl, Bruce] MIT, CSAIL, Cambridge, MA 02139 USA.
[Frosch, Matthew P.] Massachusetts Gen Hosp, CS Kubik Lab Neuropathol, Boston, MA 02114 USA.
[Corkin, Suzanne] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA.
RP Augustinack, JC (reprint author), 149,13th St,Room 2301, Charlestown, MA 02129 USA.
EM jean@nmr.mgh.harvard.edu
FU NCRR NIH HHS [P41-RR14075, U24 RR021382]; NIA NIH HHS [5R01AG008122-22,
AG022381]; NIBIB NIH HHS [R01EB006758]; NIMH NIH HHS [5U01-MH093765]
NR 95
TC 15
Z9 15
U1 6
U2 53
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1050-9631
EI 1098-1063
J9 HIPPOCAMPUS
JI Hippocampus
PD NOV
PY 2014
VL 24
IS 11
BP 1267
EP 1286
DI 10.1002/hipo.22354
PG 20
WC Neurosciences
SC Neurosciences & Neurology
GA AR8NC
UT WOS:000343830700002
PM 25154857
ER
PT J
AU Rossaint, R
Lewandowski, K
Zapol, WM
AF Rossaint, R.
Lewandowski, K.
Zapol, W. M.
TI Our paper 20 years later: Inhaled nitric oxide for the acute respiratory
distress syndrome-discovery, current understanding, and focussed targets
of future applications
SO INTENSIVE CARE MEDICINE
LA English
DT Article
DE Nitric oxide; Acute respiratory distress syndrome; Pulmonary arterial
hypertension; Selective vasodilation; Arterial oxygenation
ID RANDOMIZED CONTROLLED-TRIAL; PERSISTENT PULMONARY-HYPERTENSION;
CONGENITAL HEART-DISEASE; ACUTE LUNG INJURY; PRETERM INFANTS;
PREMATURE-INFANTS; CARDIAC-SURGERY; AEROSOLIZED PROSTACYCLIN; MECHANICAL
VENTILATION; CEREBRAL MALARIA
AB More than 20 years have passed since we reported our results of treating patients with the acute respiratory distress syndrome (ARDS) with inhaled nitric oxide (iNO). The main finding was that iNO alleviated pulmonary hypertension (PH) by selective vasodilation of pulmonary vessels in ventilated lung areas. This, in turn, improved arterial oxygenation.
We now set out to review the time span between the discovery of NO in 1987 and today in order to identify and describe interesting areas of research and clinical practice surrounding the application of iNO.
Enhancement of ventilation-perfusion matching and alleviation of PH in ARDS, treatment of PH of the newborn, and treatment of perioperative PH in congenital heart disease serve as just a few exciting examples for the successful use of iNO. Breathing NO prevents PH induced by stored blood transfusions or sickle cell disease. Exploiting the anti-inflammatory properties of NO helps to treat malaria.
Regarding the use of iNO in ARDS, there remains the unresolved question of whether important outcome parameters can be positively influenced. At first glance, several randomized controlled trials and meta-analyses seem to send the clear message: "There is none!" Careful analyses, however, leave sufficient room for doubt that the ideal study to produce the unequivocal proof for the inability of iNO to positively impact on important outcome parameters has, as yet, not been conducted.
In summary, the discovery of and research on the many positive effects of iNO has improved care of critically ill patients worldwide. It is a noble effort to continue on this path.
C1 [Rossaint, R.] Univ Klinikum Aachen, Anasthesiol Klin, D-52074 Aachen, Germany.
[Lewandowski, K.] Elisabeth Krankenhaus Essen, Klin Anasthesiol Intens Med & Schmerztherapie, D-45138 Essen, Germany.
[Zapol, W. M.] Massachusetts Gen Hosp, Dept Anesthesia Crit Care & Pain Med, Boston, MA 02114 USA.
RP Rossaint, R (reprint author), Univ Klinikum Aachen, Anasthesiol Klin, Pauwelsstr 30, D-52074 Aachen, Germany.
EM rrossaint@ukaachen.de; k.lewandowski@contilia.de
NR 78
TC 8
Z9 9
U1 0
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0342-4642
EI 1432-1238
J9 INTENS CARE MED
JI Intensive Care Med.
PD NOV
PY 2014
VL 40
IS 11
BP 1649
EP 1658
DI 10.1007/s00134-014-3458-6
PG 10
WC Critical Care Medicine
SC General & Internal Medicine
GA AR9GF
UT WOS:000343880300004
PM 25201565
ER
PT J
AU Williams, DL
Mazefsky, CA
Walker, JD
Minshew, NJ
Goldstein, G
AF Williams, Diane L.
Mazefsky, Carla A.
Walker, Jon D.
Minshew, Nancy J.
Goldstein, Gerald
TI Associations Between Conceptual Reasoning, Problem Solving, and Adaptive
Ability in High-functioning Autism
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Conceptual reasoning; Problem solving; Adaptive behavior;
Cognitive
ID DIAGNOSTIC OBSERVATION SCHEDULE; SOCIAL-SKILLS INTERVENTIONS;
DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; IMPAIRED MEMORY;
YOUNG-ADULTS; CHILDREN; INDIVIDUALS; BEHAVIOR; DYSFUNCTION
AB The Abstract thinking is generally highly correlated with problem-solving ability which is predictive of better adaptive functioning. Measures of conceptual reasoning, an ecologically-valid laboratory measure of problem-solving, and a report measure of adaptive functioning in the natural environment, were administered to children and adults with and without autism. The individuals with autism had weaker conceptual reasoning ability than individuals with typical development of similar age and cognitive ability. For the autism group, their flexible thinking scores were significantly correlated with laboratory measures of strategy formation and rule shifting and with reported overall adaptive behavior but not socialization scores. Therefore, in autism, flexibility of thought is potentially more important for adaptive functioning in the natural environment than conceptual reasoning or problem-solving.
C1 [Williams, Diane L.] Duquesne Univ, Dept Speech Language Pathol, Pittsburgh, PA 15219 USA.
[Mazefsky, Carla A.; Minshew, Nancy J.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA.
[Walker, Jon D.; Goldstein, Gerald] VA Pittsburgh Healthcare Syst, Pittsburgh, PA 15240 USA.
[Minshew, Nancy J.] Univ Pittsburgh, Dept Neurol, Pittsburgh, PA 15260 USA.
RP Goldstein, G (reprint author), VA Pittsburgh Healthcare Syst, Univ Dr, Pittsburgh, PA 15240 USA.
EM Ggold@nb.net
RI Williams, Diane/B-4128-2017
FU NICHD NIH HHS [HD35469]; NIDCD NIH HHS [K23DC006691]
NR 56
TC 3
Z9 3
U1 4
U2 13
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2014
VL 44
IS 11
SI SI
BP 2908
EP 2920
DI 10.1007/s10803-014-2190-y
PG 13
WC Psychology, Developmental
SC Psychology
GA AR6XK
UT WOS:000343724000022
PM 25099486
ER
PT J
AU Proctor, SP
Maule, AL
Heaton, KJ
Adam, GE
AF Proctor, Susan P.
Maule, Alexis L.
Heaton, Kristin J.
Adam, Gina E.
TI Permethrin exposure from fabric-treated military uniforms under
different wear-time scenarios
SO JOURNAL OF EXPOSURE SCIENCE AND ENVIRONMENTAL EPIDEMIOLOGY
LA English
DT Article
DE permethrin; urinary biomarkers; absorbed dose; military; biomonitoring;
pesticides; epidemiology
ID PYRETHROID INSECTICIDES; IXODES-RICINUS; US POPULATION; METABOLITES;
IMPREGNATION; HEALTH; TICKS
AB The objective of the project was to ascertain whether urinary biomarkers of permethrin exposure are detected after wearing post-tailored, fabric-treated military uniforms under two different wear-time exposure scenarios. Study A occurred over 3.5 days and involved six participants wearing treated uniforms continuously for 30-32 h. Urine collection occurred at scheduled time points before, during, and after wearing the uniform. Study B, conducted over 19 days, included 11 participants wearing treated uniforms for 3 consecutive days, 8 h each day (with urine collection before, during, and after wear). Urinary biomarkers of permethrin (3-phenoxybenzoic acid (3PBA), cis- 2,2-(dichlorovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid (cDCCA), trans- 2,2(dichlorovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid (tDCCA)) were detected during and after wear. Biomarker detection generally occurred over the 10- to 12-h period after putting on the uniform and subsided 24 h following uniform removal (in both Study A and B scenarios). Those wearing permethrin-treated uniforms under the longer wear-time scenario (Study A) excreted significantly higher cumulative mean levels compared with those in Study B (3.29 times higher for 3PBA and 2.23 times higher for the sum of c/tDCCA (P <= 0.001)). Findings suggest that wearing permethrin-treated clothing does increase absorbed, internal dose levels of permethrin above population levels and is significantly related to wear-time duration.
C1 [Proctor, Susan P.; Maule, Alexis L.; Heaton, Kristin J.; Adam, Gina E.] US Army Res Inst Environm Med, Mil Performance Div, Natick, MA 01760 USA.
[Proctor, Susan P.; Maule, Alexis L.; Heaton, Kristin J.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Proctor, Susan P.] VA Boston Healthcare Syst, Boston, MA USA.
RP Proctor, SP (reprint author), US Army Res Inst Environm Med, Mil Performance Div, Kansas St Bldg 42, Natick, MA 01760 USA.
EM susan.p.proctor.civ@mail.mil
NR 20
TC 3
Z9 3
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1559-0631
EI 1559-064X
J9 J EXPO SCI ENV EPID
JI J. Expo. Sci. Environ. Epidemiol.
PD NOV-DEC
PY 2014
VL 24
IS 6
BP 572
EP 578
DI 10.1038/jes.2013.65
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA AS0IJ
UT WOS:000343960800004
PM 24104061
ER
PT J
AU Steele, SR
Bleier, J
Champagne, B
Hassan, I
Russ, A
Senagore, AJ
Sylla, P
Pigazzi, A
AF Steele, Scott R.
Bleier, Joshua
Champagne, Brad
Hassan, Imran
Russ, Andrew
Senagore, Anthony J.
Sylla, Patricia
Pigazzi, Alessio
TI Improving Outcomes and Cost-Effectiveness of Colorectal Surgery
SO JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Article
DE Enhanced recovery; Surgical site infection; Simulation; Outcomes;
Anastomotic leak; Ostomy; Colorectal surgery
ID RANDOMIZED-CLINICAL-TRIAL; SURGICAL SITE INFECTION; POSTOPERATIVE
INSULIN-RESISTANCE; LAPAROSCOPIC SIGMOID RESECTION; THORACIC EPIDURAL
ANALGESIA; ENHANCED RECOVERY PATHWAYS; RECTAL-CANCER SURGERY; SPECIMEN
EXTRACTION; DIVERTING ILEOSTOMY; ANASTOMOTIC LEAKAGE
C1 [Steele, Scott R.] Madigan Army Med Ctr, Ft Lewis, WA 98431 USA.
[Bleier, Joshua] Hosp Univ PA, Penn Hosp, Div Colon & Rectal Surg, Philadelphia, PA 19106 USA.
[Champagne, Brad; Russ, Andrew] Case Med Ctr, Univ Hosp, Div Colorectal Surg, Cleveland, OH USA.
[Hassan, Imran] Univ Iowa, Dept Surg, Iowa City, IA 52242 USA.
[Senagore, Anthony J.] Cent Michigan Univ, Coll Med, Saginaw, MI 48601 USA.
[Sylla, Patricia] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02142 USA.
[Pigazzi, Alessio] Univ Calif Irvine, Sch Med, Dept Surg, Orange, CA 92868 USA.
RP Steele, SR (reprint author), Madigan Army Med Ctr, Ft Lewis, WA 98431 USA.
EM harkersteele@mac.com; Joshua.bleier@uphs.upenn.edu;
brad.champagne@uhhospitals.org; ihassan1995@yahoo.com;
Andrew.Russ@UHhospitals.org; anthony.senagore@cmich.edu;
psylla@partners.org; apigazzi@uci.edu
NR 95
TC 4
Z9 4
U1 2
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1091-255X
EI 1873-4626
J9 J GASTROINTEST SURG
JI J. Gastrointest. Surg.
PD NOV
PY 2014
VL 18
IS 11
BP 1944
EP 1956
DI 10.1007/s11605-014-2643-9
PG 13
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA AR9TM
UT WOS:000343919700008
PM 25205538
ER
PT J
AU Fisichella, PM
Patti, MG
AF Fisichella, P. Marco
Patti, Marco G.
TI GERD Procedures: When and What?
SO JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Article
DE Gastroesophageal reflux disease; Esophageal manometry; Ambulatory pH
monitoring; Partial fundoplication; Total fundoplication; Morbid
obesity; Roux-en-Y gastric bypass
ID GASTROESOPHAGEAL-REFLUX DISEASE; LAPAROSCOPIC NISSEN FUNDOPLICATION;
ANTIREFLUX SURGERY; ESOPHAGEAL; OBESITY; PATHOPHYSIOLOGY; PERISTALSIS;
EXPERIENCE; TRIAL
AB Background The topic of "when and what" for gastroesophageal reflux disease (GERD) procedures centers on the correct indications for antireflux surgery gleaned from a thorough preoperative evaluation (the "when") and on the right antireflux operation to perform once the ideal candidate is identified (the "what").
Aims The goals of this evidence-based review are the following: (1) to identify the key indications for surgery and predictors of good outcomes in the initial evaluation of patients with symptoms of GERD; (2) to describe the operations for GERD in the armamentarium of the general surgeon and their indications, as well as the technical elements of the operation; and (3) to describe the optimal surgical treatment of GERD and obesity when the two diseases coexist.
C1 [Fisichella, P. Marco] Harvard Univ, Sch Med, Dept Surg, Boston VA Healthcare Syst, Boston, MA 02132 USA.
[Patti, Marco G.] Univ Chicago, Pritzker Sch Med, Ctr Esophageal Dis, Dept Surg, Chicago, IL 60637 USA.
RP Fisichella, PM (reprint author), Harvard Univ, Sch Med, Dept Surg, Boston VA Healthcare Syst, 1400 VFW Pkwy, Boston, MA 02132 USA.
EM piero.fisichella@va.gov
NR 28
TC 2
Z9 2
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1091-255X
EI 1873-4626
J9 J GASTROINTEST SURG
JI J. Gastrointest. Surg.
PD NOV
PY 2014
VL 18
IS 11
BP 2047
EP 2053
DI 10.1007/s11605-014-2558-5
PG 7
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA AR9TM
UT WOS:000343919700020
PM 24981658
ER
PT J
AU Kitchens, WH
Liu, C
Ryan, ET
Fernandez-del Castillo, C
AF Kitchens, William H.
Liu, Charles
Ryan, Edward T.
Fernandez-del Castillo, Carlos
TI Hepatic Hydatid Cyst: A Rare Cause of Recurrent Pancreatitis
SO JOURNAL OF GASTROINTESTINAL SURGERY
LA English
DT Article
DE Pancreatitis; Hydatid cysts; Echinococcus
ID INTRABILIARY RUPTURE
AB A case of pancreatitis secondary to a hepatic hydatid cyst is illustrated together with its preoperative imaging and intraoperative appearance. Cystobiliary communication is a common complication of large hydatid cysts, and episodes of recurrent pancreatitis resulting from passage of cyst contents down the biliary tract are rarely described. The clinical manifestations, diagnostic workup, and surgical management options of echinococcal-related pancreatitis are discussed, and a review of the literature is provided.
C1 [Kitchens, William H.; Fernandez-del Castillo, Carlos] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Kitchens, William H.] Emory Univ Hosp, Emory Transplant Ctr, Atlanta, GA 30322 USA.
[Liu, Charles] Harvard Univ, Sch Med, Boston, MA USA.
[Ryan, Edward T.] Massachusetts Gen Hosp, Dept Med, Div Infect Dis, Boston, MA 02114 USA.
RP Fernandez-del Castillo, C (reprint author), Massachusetts Gen Hosp, Dept Surg, ACC 366 15 Parkman St, Boston, MA 02114 USA.
EM cfernandez@mgh.harvard.edu
NR 11
TC 1
Z9 1
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1091-255X
EI 1873-4626
J9 J GASTROINTEST SURG
JI J. Gastrointest. Surg.
PD NOV
PY 2014
VL 18
IS 11
BP 2057
EP 2059
DI 10.1007/s11605-014-2630-1
PG 3
WC Gastroenterology & Hepatology; Surgery
SC Gastroenterology & Hepatology; Surgery
GA AR9TM
UT WOS:000343919700022
PM 25149853
ER
PT J
AU O'Leary, TJ
AF O'Leary, Timothy J.
TI Reflecting on My Time as Editor-in-Chief
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Editorial Material
C1 US Dept Vet Affairs, Washington, DC 20420 USA.
RP O'Leary, TJ (reprint author), US Dept Vet Affairs, Washington, DC 20420 USA.
NR 3
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 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
BP 593
EP 594
DI 10.1016/j.jmoldx.2014.09.001
PG 2
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200001
PM 25307753
ER
PT J
AU O'Leary, TJ
AF O'Leary, Timothy J.
TI Regulating Laboratory-Developed Tests
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Editorial Material
ID LOCALIZED PROSTATE-CANCER; RETRACTED ARTICLE. SEE; RADICAL
PROSTATECTOMY; INTERVENTION; PIVOT
C1 US Dept Vet Affairs, Washington, DC 20420 USA.
RP O'Leary, TJ (reprint author), US Dept Vet Affairs, Washington, DC 20420 USA.
NR 19
TC 0
Z9 1
U1 2
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
BP 595
EP 598
DI 10.1016/j.jmoldx.2014.09.002
PG 4
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200002
PM 25307754
ER
PT J
AU Mandelker, D
Amr, SS
Pugh, T
Gowrisankar, S
Shakhbatyan, R
Duffy, E
Bowser, M
Harrison, B
Lafferty, K
Mahanta, L
Rehm, HL
Funke, BH
AF Mandelker, Diana
Amr, Sami S.
Pugh, Trevor
Gowrisankar, Sivakumar
Shakhbatyan, Rimma
Duffy, Elizabeth
Bowser, Mark
Harrison, Bryan
Lafferty, Katherine
Mahanta, Lisa
Rehm, Heidi L.
Funke, Birgit H.
TI Comprehensive Diagnostic Testing for Stereocilin An Approach for
Analyzing Medically Important Genes with High Homology
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Article
ID POLYCYSTIC KIDNEY-DISEASE; HEARING-LOSS; GENOME; LOCUS; PSEUDOGENES;
DFNB16; DUPLICATIONS; MUTATIONS; DEAFNESS
AB Next-generation sequencing (NGS) technologies have revolutionized genetic testing by enabling simultaneous analysis of unprecedented numbers of genes. However, genes with high-sequence homology pose challenges to current NGS technologies. Because diagnostic sequencing is moving toward exome analysis, knowledge of these homologous genes is essential to avoid false positive and negative results. An example is the STRC gene, one of >70 genes known to contribute to the genetic basis of hearing loss. STRC is 99.6% identical to a pseudogene (pSTRC) and therefore inaccessible to standard NGS methodologies. The STRC locus is also known to be a common site for large deletions. Comprehensive diagnostic testing for inherited hearing loss therefore necessitates a combination of several approaches to avoid pseudogene interference. We have developed a clinical test that combines standard NGS and NGS-based copy number assessment supplemented with a long-range PCR-based Sanger or MiSeq assay to eliminate pseudogene contamination. By using this combination of assays we could identify biallelic STRC variants in 14% (95% CI, 8%-24%) of individuals with isolated nonsyndromic hearing loss who had previously tested negative on our 70-gene hearing loss panel, corresponding to a detection rate of 11.2% (95% CI, 6%-19%) for previously untested patients. This approach has broad applicability because medically significant genes for many disease areas include genes with high-sequence homology.
C1 [Mandelker, Diana] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[Amr, Sami S.; Pugh, Trevor; Gowrisankar, Sivakumar; Shakhbatyan, Rimma; Duffy, Elizabeth; Bowser, Mark; Harrison, Bryan; Lafferty, Katherine; Mahanta, Lisa; Rehm, Heidi L.; Funke, Birgit H.] Partners Healthcare Personalized Med, Mol Med Lab, Cambridge, MA USA.
[Funke, Birgit H.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Pathol, Boston, MA USA.
RP Funke, BH (reprint author), 65 Landsdowne St, Cambridge, MA 02139 USA.
EM bfunke@partners.org
OI Amr, Sami/0000-0003-0927-6057
FU Partners HealthCare Center for Personalized Genetic Medicine (PCPGM)
FX Supported by the Partners HealthCare Center for Personalized Genetic
Medicine (PCPGM).
NR 19
TC 5
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 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
BP 639
EP 647
DI 10.1016/j.jmoldx.2014.06.003
PG 9
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200008
PM 25157971
ER
PT J
AU MacConaill, LE
Garcia, E
Shivdasani, P
Ducar, M
Adusumilli, R
Breneiser, M
Byrne, M
Chung, L
Conneely, J
Crosby, L
Garraway, LA
Gong, X
Hahn, WC
Hatton, C
Kantoff, PW
Kluk, M
Kuo, F
Jia, YH
Joshi, R
Longtine, J
Manning, A
Palescandolo, E
Sharaf, N
Sholl, L
van Hummelen, P
Wade, J
Wollinson, BM
Zepf, D
Rollins, BJ
Lindeman, NI
AF MacConaill, Laura E.
Garcia, Elizabeth
Shivdasani, Priyanka
Ducar, Matthew
Adusumilli, Ravali
Breneiser, Marc
Byrne, Mark
Chung, Lawrence
Conneely, Jodie
Crosby, Lauren
Garraway, Levi A.
Gong, Xin
Hahn, William C.
Hatton, Charlie
Kantoff, Philip W.
Kluk, Michael
Kuo, Frank
Jia, Yonghui
Joshi, Ruchi
Longtine, Janina
Manning, Allison
Palescandolo, Emanuele
Sharaf, Nematullah
Sholl, Lynette
van Hummelen, Paul
Wade, Jacqueline
Wollinson, Bruce M.
Zepf, Dimity
Rollins, Barrett J.
Lindeman, Neal I.
TI Prospective Enterprise-Level Molecular Genotyping of a Cohort of Cancer
Patients
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Article
ID CELL LUNG-CANCER; METASTATIC COLORECTAL-CANCER; GASTROINTESTINAL STROMAL
TUMORS; BRAF MUTATIONS; GENE-MUTATIONS; SOMATIC MUTATIONS;
ADENOCARCINOMA; LEUKEMIA; THERAPY; GENOME
AB Ongoing cancer genome characterization studies continue to elucidate the spectrum of genomic abnormalities that drive many cancers, and in the clinical arena assessment of the driver genetic alterations in patients is playing an increasingly important diagnostic and/or prognostic rote for many cancer types. However, the landscape of genomic abnormalities is still unknown for less common cancers, and the influence of specific genotypes on clinical behavior is often still unclear. To address some of these deficiencies, we developed Profile, a prospective cohort study to obtain genomic information on all patients at a large tertiary care medical center for cancer-related care. We enrolled patients with any cancer diagnosis, and, for each patient (unselected for cancer site or type) we applied mass spectrometric genotyping (OncoMap) of 471 common recurrent mutations in 41 cancer-related genes. We report the results of the first 5000 patients, of which 26% exhibited potentially actionable somatic mutations. These observations indicate the utility of genotyping in advancing the field of precision oncology.
C1 [MacConaill, Laura E.; Garcia, Elizabeth; Shivdasani, Priyanka; Byrne, Mark; Chung, Lawrence; Conneely, Jodie; Crosby, Lauren; Gong, Xin; Kluk, Michael; Kuo, Frank; Jia, Yonghui; Joshi, Ruchi; Longtine, Janina; Manning, Allison; Sharaf, Nematullah; Sholl, Lynette; Wade, Jacqueline; Zepf, Dimity; Lindeman, Neal I.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[MacConaill, Laura E.; Ducar, Matthew; Adusumilli, Ravali; Breneiser, Marc; Garraway, Levi A.; Hahn, William C.; Hatton, Charlie; Palescandolo, Emanuele; van Hummelen, Paul; Wollinson, Bruce M.] Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA.
[Garraway, Levi A.; Hahn, William C.; Kantoff, Philip W.; Rollins, Barrett J.] Harvard Univ, Sch Med, Dept Med Oncol, Boston, MA USA.
RP Lindeman, NI (reprint author), Brigham & Womens Hosp, Dept Pathol, 75 Francis St,Shapiro 2020, Boston, MA 02115 USA.
EM laura_macconaill@dfci.harvard.edu; nlindeman@partners.org
FU Dana-Farber Cancer Institute; NITA [R33 CA 155554]; National Heart,
Lung, and Blood Institute Grand Opportunity (GO); Lung GO Sequencing
Project [HL-102923]; WHI Sequencing Project [HL-102924]; Broad GO
Sequencing Project [HL-102925]; Seattle GO Sequencing Project
[HL-102926]; Heart GO Sequencing Project [HL-103010]
FX Supported by the Dana-Farber Cancer Institute and NITA grant R33 CA
155554.; We thank the National Heart, Lung, and Blood Institute Grand
Opportunity (GO) Exome Sequencing Project and its ongoing studies, which
produced and provided exome variant calls for comparison: the Lung GO
Sequencing Project (HL-102923), the WHI Sequencing Project (HL-102924),
the Broad GO Sequencing Project (HL-102925), the Seattle GO Sequencing
Project (HL-102926), and the Heart GO Sequencing Project (HL-103010).
NR 62
TC 28
Z9 28
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
BP 660
EP 672
DI 10.1016/j.jmoldx.2014.06.004
PG 13
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200010
PM 25157968
ER
PT J
AU Lincoln, S
Kurian, A
Desmond, A
Gabree, M
Powers, M
Monzon, F
Ellisen, L
Ford, J
AF Lincoln, S.
Kurian, A.
Desmond, A.
Gabree, M.
Powers, M.
Monzon, F.
Ellisen, L.
Ford, J.
TI Traditional vs. Next-Generation Testing of Hereditary Breast and Ovarian
Cancer Genes in a Large Clinical Population
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Meeting Abstract
CT Annual Meeting of the Association-for-Molecular-Pathology (AMP)
CY NOV 12-15, 2014
CL National Harbor, MD
SP Assoc Mol Pathol
C1 [Lincoln, S.; Powers, M.; Monzon, F.] Invitae, San Francisco, CA USA.
[Kurian, A.; Ford, J.] Stanford Univ, Stanford, CA 94305 USA.
[Desmond, A.; Gabree, M.; Ellisen, L.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
MA G04
BP 699
EP 700
PG 2
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200018
ER
PT J
AU Church, A
Grimmett, L
Garcia, E
Kim, A
Glade-Bender, J
DuBois, SG
MacConaill, LE
Stegmaier, K
London, WB
Crompton, BD
Shusterman, S
Diller, L
Rodriguez-Galindo, C
Lindeman, NI
Janeway, KA
Harris, MH
AF Church, A.
Grimmett, L.
Garcia, E.
Kim, A.
Glade-Bender, J.
DuBois, S. G.
MacConaill, L. E.
Stegmaier, K.
London, W. B.
Crompton, B. D.
Shusterman, S.
Diller, L.
Rodriguez-Galindo, C.
Lindeman, N. I.
Janeway, K. A.
Harris, M. H.
TI Analysis of Somatic Copy Number Alterations in Pediatric Solid Tumors
Using Both Array Comparative Genomic Hybridization and High Throughput
Sequencing
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Meeting Abstract
CT Annual Meeting of the Association-for-Molecular-Pathology (AMP)
CY NOV 12-15, 2014
CL National Harbor, MD
SP Assoc Mol Pathol
C1 [Church, A.; Stegmaier, K.; London, W. B.; Crompton, B. D.; Shusterman, S.; Diller, L.; Rodriguez-Galindo, C.; Janeway, K. A.; Harris, M. H.] Boston Childrens Hosp, Boston, MA USA.
[Grimmett, L.] Claritas Genom, Cambridge, MA USA.
[Garcia, E.; Lindeman, N. I.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Kim, A.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Glade-Bender, J.] Columbia Univ, Med Ctr, New York, NY USA.
[DuBois, S. G.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[MacConaill, L. E.] Dana Farber Canc Inst, Boston, MA 02115 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 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
MA ST30
BP 752
EP 752
PG 1
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200246
ER
PT J
AU Stachler, MD
Carter, S
Taylor-Weiner, A
Peng, S
Getz, G
Bass, A
AF Stachler, M. D.
Carter, S.
Taylor-Weiner, A.
Peng, S.
Getz, G.
Bass, A.
TI Barrett's Esophagus Has a Mutation Frequency Comparable to Invasive
Cancers but Lacks Oncogene Activation
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Meeting Abstract
CT Annual Meeting of the Association-for-Molecular-Pathology (AMP)
CY NOV 12-15, 2014
CL National Harbor, MD
SP Assoc Mol Pathol
C1 [Stachler, M. D.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Carter, S.; Taylor-Weiner, A.; Getz, G.] Broad Inst, Cambridge, MA USA.
[Peng, S.; Bass, A.] Dana Farber Canc Inst, Boston, MA 02115 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 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
MA ST40
BP 754
EP 754
PG 1
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200256
ER
PT J
AU Ducar, M
Abo, R
Leslin, C
Shivdasani, P
Chung, L
Gong, X
Fendler, B
Davineni, P
Chin, G
Van Hummelen, P
Garcia, E
Rollins, B
Lindeman, N
Macconaill, L
AF Ducar, M.
Abo, R.
Leslin, C.
Shivdasani, P.
Chung, L.
Gong, X.
Fendler, B.
Davineni, P.
Chin, G.
Van Hummelen, P.
Garcia, E.
Rollins, B.
Lindeman, N.
Macconaill, L.
TI Building a Clinical-Grade Next-Generation Sequence Analysis Pipeline
from Research Tools
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Meeting Abstract
CT Annual Meeting of the Association-for-Molecular-Pathology (AMP)
CY NOV 12-15, 2014
CL National Harbor, MD
SP Assoc Mol Pathol
C1 [Ducar, M.; Abo, R.; Van Hummelen, P.; Rollins, B.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Leslin, C.; Shivdasani, P.; Chung, L.; Gong, X.; Fendler, B.; Davineni, P.; Chin, G.; Garcia, E.; Lindeman, N.; Macconaill, L.] Brigham & Womens Hosp, Boston, MA 02115 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 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
MA TT02
BP 772
EP 772
PG 1
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200332
ER
PT J
AU Castellanos-Rizaldos, E
Paweletz, C
Oxnard, GR
Mamon, H
Janne, PA
Makrigiorgos, MG
AF Castellanos-Rizaldos, E.
Paweletz, C.
Oxnard, G. R.
Mamon, H.
Jaenne, P. A.
Makrigiorgos, M. G.
TI Digital Mutation Scanning by Using an Enhanced Ratio of Signals
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Meeting Abstract
CT Annual Meeting of the Association-for-Molecular-Pathology (AMP)
CY NOV 12-15, 2014
CL National Harbor, MD
SP Assoc Mol Pathol
C1 [Castellanos-Rizaldos, E.; Paweletz, C.; Oxnard, G. R.; Mamon, H.; Jaenne, P. A.; Makrigiorgos, M. G.] Harvard Univ, Brigham & Womens Hosp, Dana Farber Canc Inst, Sch Med, Boston, MA 02115 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 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
MA TT07
BP 773
EP 773
PG 1
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200337
ER
PT J
AU Aziz, N
Zhao, Q
Durtschi, J
Bry, L
Driscoll, DK
Funke, BH
Gibson, JS
Grody, WW
Hedge, MR
Leonard, DG
Merker, JD
Nagarajan, R
Palicki, LA
Robetorye, RS
Santani, AB
Schrijver, I
Weck, KE
Voelkerding, KV
AF Aziz, N.
Zhao, Q.
Durtschi, J.
Bry, L.
Driscoll, D. K.
Funke, B. H.
Gibson, J. S.
Grody, W. W.
Hedge, M. R.
Leonard, D. G.
Merker, J. D.
Nagarajan, R.
Palicki, L. A.
Robetorye, R. S.
Santani, A. B.
Schrijver, I.
Weck, K. E.
Voelkerding, K. V.
TI A Pilot Methods-Based Proficiency Test for Next-Generation Sequencing
(NGS)
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Meeting Abstract
CT Annual Meeting of the Association-for-Molecular-Pathology (AMP)
CY NOV 12-15, 2014
CL National Harbor, MD
SP Assoc Mol Pathol
C1 [Aziz, N.] Phoenix Childrens Hosp, Phoenix, AZ USA.
[Aziz, N.; Zhao, Q.; Driscoll, D. K.; Palicki, L. A.] Coll Amer Pathologists, Northfield, IL USA.
[Durtschi, J.; Voelkerding, K. V.] ARUP Labs, Salt Lake City, UT USA.
[Bry, L.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Funke, B. H.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Gibson, J. S.] Univ Cent Florida, Coll Med, Orlando, FL 32816 USA.
[Grody, W. W.] Univ Calif Los Angeles, Ctr Hlth Sci, Los Angeles, CA 90024 USA.
[Hedge, M. R.] Emory Univ, Sch Med, Decatur, GA 30033 USA.
[Leonard, D. G.] Univ Vermont, Coll Med, Burlington, VT USA.
[Merker, J. D.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Nagarajan, R.] Washington Univ, St Louis, MO USA.
[Robetorye, R. S.] Mayo Clin, Phoenix, AZ USA.
[Santani, A. B.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Schrijver, I.] Stanford Univ, Stanford, CA 94305 USA.
[Weck, K. E.] Univ N Carolina, Chapel Hill, NC 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 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
MA TT13
BP 775
EP 775
PG 1
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200343
ER
PT J
AU MacConaill, LE
Garcia, E
Sholl, L
Ducar, M
Leslin, C
Jia, Y
Kuo, FC
Rollins, BJ
Lindeman, N
AF MacConaill, L. E.
Garcia, E.
Sholl, L.
Ducar, M.
Leslin, C.
Jia, Y.
Kuo, F. C.
Rollins, B. J.
Lindeman, N.
TI Profile Oncopanel: Clinical-grade Next-Generation Sequencing of 275
Cancer-Related Genes Applied to Specimens from 1800 Consecutive
Unselected Cancer Patients
SO JOURNAL OF MOLECULAR DIAGNOSTICS
LA English
DT Meeting Abstract
CT Annual Meeting of the Association-for-Molecular-Pathology (AMP)
CY NOV 12-15, 2014
CL National Harbor, MD
SP Assoc Mol Pathol
C1 [MacConaill, L. E.; Garcia, E.; Sholl, L.; Leslin, C.; Jia, Y.; Kuo, F. C.; Lindeman, N.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[MacConaill, L. E.; Garcia, E.; Ducar, M.; Rollins, B. J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1525-1578
EI 1943-7811
J9 J MOL DIAGN
JI J. Mol. Diagn.
PD NOV
PY 2014
VL 16
IS 6
MA TT44
BP 782
EP 782
PG 1
WC Pathology
SC Pathology
GA AR7YZ
UT WOS:000343794200374
ER
PT J
AU Liu, XH
Joshi, SK
Ravishankar, B
Laron, D
Kim, HT
Feeley, BT
AF Liu, Xuhui
Joshi, Sunil K.
Ravishankar, Bharat
Laron, Dominique
Kim, Hubert T.
Feeley, Brian T.
TI Upregulation of transforming growth factor-beta signaling in a rat model
of rotator cuff tears
SO JOURNAL OF SHOULDER AND ELBOW SURGERY
LA English
DT Article
DE Massive rotator cuff tear; transforming growth factor-beta; fibrosis
ID SUPRASCAPULAR NERVE INJURY; SKELETAL-MUSCLE; FATTY INFILTRATION;
MESENCHYMAL TRANSITION; ARTHROSCOPIC REPAIR; INTERVAL SLIDES; SCAR
FORMATION; ATROPHY; FIBROSIS; SMAD2
AB Background: Muscle atrophy, fatty infiltration, and fibrosis of the muscle have been described as important factors governing outcome after rotator cuff injury and repair. Muscle fibrosis is also thought to have a role in determining muscle compliance at the time of surgery. The transforming growth factor-beta (TGF-beta) pathways are highly conserved pathways that exert a potent level of control over muscle gene expression and are critical regulators of fibrosis in multiple organ systems. It has been shown that TGF-beta can regulate important pathways of muscle atrophy, including the Akt/mammalian target of rapamycin pathway. The purpose of this study was to evaluate the expression of TGF-beta and its downstream effectors of fibrosis after a massive rotator cuff tear (RCT) in a previously established rat model.
Methods: To simulate a massive RCT, infraspinatus and supraspinatus tenotomy and suprascapular nerve transection were performed on Sprague-Dawley rats with use of a validated model. Two and 6 weeks after surgery, supraspinatus muscles were harvested to study alterations in TGF-beta signaling by Western blotting, quantitative polymerase chain reaction, and histologic analysis.
Results: There was a significant increase in fibrosis in the rotator cuff muscle after RCT in our animal model. There was a concomitant increase in TGF-beta gene and protein expression at both 2 and 6 weeks after RCT. Evaluation of the TGF-beta signaling pathway revealed an increase in SMAD2 activation but not in SMAD3. There was an increase in profibrotic markers collagen I, collagen III, and alpha-smooth muscle actin.
Conclusions: TGF-beta signaling is significantly upregulated in rat supraspinatus muscles after RCTs. (C) 2014 Journal of Shoulder and Elbow Surgery Board of Trustees.
C1 [Liu, Xuhui; Joshi, Sunil K.; Ravishankar, Bharat; Kim, Hubert T.] San Francisco VA Med Ctr, Dept Vet Affairs, San Francisco, CA USA.
[Liu, Xuhui; Joshi, Sunil K.; Ravishankar, Bharat; Laron, Dominique; Kim, Hubert T.; Feeley, Brian T.] Univ Calif San Francisco, Dept Orthopaed Surg, San Francisco, CA 94158 USA.
RP Feeley, BT (reprint author), Univ Calif San Francisco, Dept Orthopaed Surg, 1500 Owens Ave,Box 3004, San Francisco, CA 94158 USA.
EM feeleyb@orthosurg.ucsf.edu
FU Orthopaedic Research and Education Foundation; National Institutes of
Health [NIH R03AR060871]
FX Funding was provided by a grant from the Orthopaedic Research and
Education Foundation (Young Investigator Grant) and the National
Institutes of Health (NIH R03AR060871).
NR 34
TC 3
Z9 3
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1058-2746
J9 J SHOULDER ELB SURG
JI J. Shoulder Elbow Surg.
PD NOV
PY 2014
VL 23
IS 11
BP 1709
EP 1716
DI 10.1016/j.jse.2014.02.029
PG 8
WC Orthopedics; Sport Sciences; Surgery
SC Orthopedics; Sport Sciences; Surgery
GA AR8DF
UT WOS:000343805000021
PM 24875732
ER
PT J
AU Sherman, KL
Kinnier, CV
Farina, DA
Wayne, JD
Laskin, WB
Agulnik, M
Attar, S
Hayes, JP
Peabody, T
Bilimoria, KY
AF Sherman, Karen L.
Kinnier, Christine V.
Farina, Domenico A.
Wayne, Jeffrey D.
Laskin, William B.
Agulnik, Mark
Attar, Samer
Hayes, John P.
Peabody, Terrance
Bilimoria, Karl Y.
TI Examination of National Lymph Node Evaluation Practices for Adult
Extremity Soft Tissue Sarcoma
SO JOURNAL OF SURGICAL ONCOLOGY
LA English
DT Article
DE neoplasms; lymph node excision; lymphatic metastasis; retrospective
studies
ID MM THICK MELANOMAS; PROGNOSTIC-FACTORS; BIOPSY; METASTASIS;
LYMPHADENECTOMY; POPULATION; DISSECTION; EFFICACY; YOUNGER; SPREAD
AB Background and ObjectivesLymph node evaluation recommendations for extremity soft tissue sarcoma (ESTS) are absent from national guidelines. Our objectives were (1) to assess rates and predictors of nodal evaluation, and (2) to assess rates and predictors of nodal metastases.
MethodsESTS patients from the National Cancer Data Base (2000-2009) were assessed, and regression models were used to identify factors associated with nodal evaluation and metastases.
ResultsOf 27,536 ESTS patients, 1,924 (7%) underwent nodal evaluation, and of these, 290 (15%) had nodal metastases. Nodal evaluation was most frequently performed for rhabdomyosarcoma (15.6%), angiosarcoma (10.0%), clear cell sarcoma (39.3%), epithelioid sarcoma (28.1%), and synovial sarcoma (9.3%). On multivariable analysis, factors associated with nodal evaluation included histologic subtype, tumor size, and grade. Nodal metastasis rates were highest among patients with rhabdomyosarcoma (32.1%), angiosarcoma (24.1%), clear cell sarcoma (27.7%), and epithelioid sarcoma (31.8%). On multivariable analysis, factors associated with nodal metastases included histologic subtype, tumor size, and grade.
ConclusionsNodal evaluation rates are highest among certain expected subtypes but are generally low. However, nodal metastasis rates for many histologic subtypes in patients selected for lymph node evaluation may be higher than previously reported. Multi-institutional studies should address nodal evaluation for ESTS. J. Surg. Oncol. 2014 110:682-688. (c) 2014 Wiley Periodicals, Inc.
C1 [Sherman, Karen L.; Kinnier, Christine V.; Farina, Domenico A.; Wayne, Jeffrey D.; Laskin, William B.; Agulnik, Mark; Attar, Samer; Hayes, John P.; Peabody, Terrance; Bilimoria, Karl Y.] Robert H Lurie Comprehens Canc Ctr, Northwestern Inst Comparat Effectiveness Res NICE, Chicago, IL USA.
[Sherman, Karen L.; Kinnier, Christine V.; Farina, Domenico A.; Wayne, Jeffrey D.; Bilimoria, Karl Y.] Northwestern Univ, Dept Surg, Feinberg Sch Med, Surg Oncol & Qual Improvement Ctr, Chicago, IL 60611 USA.
[Kinnier, Christine V.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
[Laskin, William B.] NW Mem Hosp, Dept Pathol, Chicago, IL 60611 USA.
[Agulnik, Mark] NW Mem Hosp, Dept Med, Div Hematol Oncol, Chicago, IL 60611 USA.
[Attar, Samer; Peabody, Terrance] NW Mem Hosp, Dept Orthoped Surg, Chicago, IL 60611 USA.
[Hayes, John P.] NW Mem Hosp, Dept Radiat Oncol, Chicago, IL 60611 USA.
RP Bilimoria, KY (reprint author), Northwestern Univ, Dept Surg, Surg Outcomes & Qual Improvement Ctr, 676N St Clair St,Suite 6-650, Chicago, IL 60611 USA.
EM k-bilimoria@northwestern.edu
FU American Cancer Society; De Boer Family Sarcoma Foundation
FX Grant sponsor: American Cancer Society; Grant sponsor: De Boer Family
Sarcoma Foundation.
NR 26
TC 6
Z9 6
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4790
EI 1096-9098
J9 J SURG ONCOL
JI J. Surg. Oncol.
PD NOV
PY 2014
VL 110
IS 6
BP 682
EP 688
DI 10.1002/jso.23687
PG 7
WC Oncology; Surgery
SC Oncology; Surgery
GA AR9FN
UT WOS:000343878300009
PM 24910401
ER
PT J
AU Walker, KL
Kirillova, O
Gillespie, SE
Hsiao, D
Pishchalenko, V
Pai, AK
Puro, JE
Plumley, R
Kudyakov, R
Hu, WM
Allisany, A
McBurnie, M
Kurtz, SE
Hazlehurst, BL
AF Walker, Kari L.
Kirillova, Olga
Gillespie, Suzanne E.
Hsiao, David
Pishchalenko, Valentyna
Pai, Akshatha Kalsanka
Puro, Jon E.
Plumley, Robert
Kudyakov, Rustam
Hu, Weiming
Allisany, Art
McBurnie, MaryAnn
Kurtz, Stephen E.
Hazlehurst, Brian L.
TI Using the CER Hub to ensure data quality in a multi-institution smoking
cessation study
SO JOURNAL OF THE AMERICAN MEDICAL INFORMATICS ASSOCIATION
LA English
DT Article
ID CLINICAL-RESEARCH; INFORMATICS; RECORDS
AB Comparative effectiveness research (CER) studies involving multiple institutions with diverse electronic health records (EHRs) depend on high quality data. To ensure uniformity of data derived from different EHR systems and implementations, the CER Hub informatics platform developed a quality assurance (QA) process using tools and data formats available through the CER Hub. The QA process, implemented here in a study of smoking cessation services in primary care, used the `emrAdapter' tool programmed with a set of quality checks to query large samples of primary care encounter records extracted in accord with the CER Hub common data framework. The tool, deployed to each study site, generated error reports indicating data problems to be fixed locally and aggregate data sharable with the central site for quality review. Across the CER Hub network of six health systems, data completeness and correctness issues were prevalent in the first iteration and were considerably improved after three iterations of the QA process. A common issue encountered was incomplete mapping of local EHR data values to those defined by the common data framework. A highly automated and distributed QA process helped to ensure the correctness and completeness of patient care data extracted from EHRs for a multi-institution CER study in smoking cessation.
C1 [Walker, Kari L.; Kirillova, Olga; Gillespie, Suzanne E.; Hu, Weiming; Allisany, Art; McBurnie, MaryAnn; Hazlehurst, Brian L.] Kaiser Permanente Northwest, Ctr Hlth Res, Portland, OR 97227 USA.
[Hsiao, David; Pishchalenko, Valentyna] Kaiser Permanente Hawaii, Ctr Hlth Res, Honolulu, HI USA.
[Pai, Akshatha Kalsanka] Emory Univ, Atlanta, GA 30322 USA.
[Puro, Jon E.] OCHIN Inc, Portland, OR USA.
[Plumley, Robert] VA Puget Sound Hlth Care Syst, Seattle, WA USA.
[Kudyakov, Rustam] Baylor Hlth Care Syst, Ctr Clin Innovat, Dallas, TX USA.
[Kurtz, Stephen E.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
RP Hazlehurst, BL (reprint author), Kaiser Permanente Northwest, Ctr Hlth Res, 3800 N Interstate Ave, Portland, OR 97227 USA.
EM Brian.hazlehurst@kpchr.org
FU Agency for Health Care Research and Quality (AHRQ), US Department of
Health and Human Services [R01HS019828]
FX This research, and the CER Hub project (http://www.cerhub.org), is
funded by grant R01HS019828 (Hazlehurst, PI) from the Agency for Health
Care Research and Quality (AHRQ), US Department of Health and Human
Services.
NR 21
TC 2
Z9 2
U1 3
U2 4
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1067-5027
EI 1527-974X
J9 J AM MED INFORM ASSN
JI J. Am. Med. Inf. Assoc.
PD NOV
PY 2014
VL 21
IS 6
BP 1129
EP 1135
DI 10.1136/amiajnl-2013-002629
PG 7
WC Computer Science, Information Systems; Computer Science,
Interdisciplinary Applications; Health Care Sciences & Services;
Information Science & Library Science; Medical Informatics
SC Computer Science; Health Care Sciences & Services; Information Science &
Library Science; Medical Informatics
GA AR7RJ
UT WOS:000343776700029
PM 24993545
ER
PT J
AU Groszmann, Y
Howitt, BE
Bromley, B
Feltmate, CM
Benacerraf, BR
AF Groszmann, Yvette
Howitt, Brooke E.
Bromley, Bryann
Feltmate, Colleen M.
Benacerraf, Beryl R.
TI Decidualized Endometrioma Masquerading as Ovarian Cancer in Pregnancy
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Article
DE decidualized endometrioma; gynecologic ultrasound; pregnancy; sonography
ID SONOGRAPHIC FEATURES; MIMICKING MALIGNANCY; ADNEXAL MASSES; MANAGEMENT;
DIAGNOSIS; TUMORS
AB Objectives To identify the sonographic features of decidualized endometriomas in patients treated at a single institution and to determine whether sonographic findings can distinguish these lesions from malignant ovarian tumors during pregnancy.
Methods We conducted a retrospective cohort study that included pregnant women with a histologic diagnosis of decidualized endometrioma between January 1, 2005, and December 1, 2012, and had an ovarian cyst or mass seen preoperatively on obstetrical sonography. Sonographic characteristics of these masses were retrospectively evaluated using the International Ovarian Tumor Analysis Group definitions for adnexal masses.
Results Seventeen patients with 22 adnexal masses were included in our study. Nine of 22 lesions (41%) were classified as unilocular solid, and 14 of 22 (64%) had solid components, of which 12 of 14(86%) had substantial blood flow. Septations were present in 8 of 22 masses (36%). Cyst sizes varied from 30 to 120 and 32 to 270 mm at the initial and follow-up scans, respectively. Eight patients had no follow-up scans and underwent surgery within 3 weeks of diagnosis. The other 9 patients (14 masses), had follow-up scans and underwent surgery from 3 to 34 weeks after their initial scans. Eight of these masses showed no notable change in size or appearance, and 1 became smaller.
Conclusions There were no characteristic sonographic features identified to distinguish decidualized endometrioma from ovarian malignancy. However, lesions showing no change in size over 4 weeks or lacking solid components and vascularity are more likely to be benign rather than malignant and may justify delaying surgery until delivery or postpartum.
C1 [Groszmann, Yvette; Bromley, Bryann; Benacerraf, Beryl R.] Diagnost Ultrasound Associates PC, Boston, MA USA.
[Groszmann, Yvette; Bromley, Bryann; Feltmate, Colleen M.; Benacerraf, Beryl R.] Brigham & Womens Hosp, Dept Obstet & Gynecol, Boston, MA 02115 USA.
[Howitt, Brooke E.] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA.
[Bromley, Bryann; Benacerraf, Beryl R.] Brigham & Womens Hosp, Dept Radiol, Boston, MA 02115 USA.
[Bromley, Bryann; Feltmate, Colleen M.; Benacerraf, Beryl R.] Dana Farber Canc Inst, Dept Obstet & Gynecol, Boston, MA 02115 USA.
[Bromley, Bryann; Benacerraf, Beryl R.] Massachusetts Gen Hosp, Dept Obstet & Gynecol, Boston, MA 02114 USA.
RP Groszmann, Y (reprint author), Diagnost Ultrasound Associates PC, 1 Brookline Pl,Suite 506, Brookline, MA 02445 USA.
EM bbsono@aol.com
NR 15
TC 1
Z9 1
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
EI 1550-9613
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD NOV
PY 2014
VL 33
IS 11
BP 1909
EP 1915
DI 10.7863/ultra.33.11.1909
PG 7
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA AR7ZB
UT WOS:000343794400004
PM 25336477
ER
PT J
AU Cudkowicz, ME
Titus, S
Kearney, M
Yu, H
Sherman, A
Schoenfeld, D
Hayden, D
Shui, A
Brooks, B
Conwit, R
Felsenstein, D
Greenblatt, DJ
Keroack, M
Kissel, JT
Miller, R
Rosenfeld, J
Rothstein, JD
Simpson, E
Tolkoff-Rubin, N
Zinman, L
Shefner, JM
AF Cudkowicz, Merit E.
Titus, Sarah
Kearney, Marianne
Yu, Hong
Sherman, Alexander
Schoenfeld, David
Hayden, Douglas
Shui, Amy
Brooks, Benjamin
Conwit, Robin
Felsenstein, Donna
Greenblatt, David J.
Keroack, Myles
Kissel, John T.
Miller, Robert
Rosenfeld, Jeffrey
Rothstein, Jeffrey D.
Simpson, Ericka
Tolkoff-Rubin, Nina
Zinman, Lorne
Shefner, Jeremy M.
CA Ceftriaxone Study Investigators
TI Safety and efficacy of ceftriaxone for amyotrophic lateral sclerosis: a
multi-stage, randomised, double-blind, placebo-controlled trial
SO LANCET NEUROLOGY
LA English
DT Article
ID CEREBROSPINAL-FLUID; NERVOUS-SYSTEM; ALS; GLUTAMATE; RILUZOLE;
INFECTIONS; EXPRESSION; SURVIVAL; MODELS; STROKE
AB Background Glutamate excitotoxicity might contribute to the pathophysiology of amyotrophic lateral sclerosis. In animal models, decreased excitatory aminoacid transporter 2 (EAAT2) overexpression delays disease onset and prolongs survival, and ceftriaxone increases EAAT2 activity We aimed to assess the safety and efficacy of ceftriaxone for amyotrophic lateral sclerosis in a combined phase 1, 2, and 3 clinical trial.
Methods This three-stage randomised, double-blind, placebo-controlled study was done at 59 clinical sites in the USA and Canada between Sept 4, 2006, and July 30, 2012. Eligible adult patients had amyotrophic lateral sclerosis, a vital capacity of more than 60% of that predicted for age and height, and symptom duration of less than 3 years. In stages 1 (pharmacokinetics) and 2 (safety), participants were randomly allocated (2:1) to ceftriaxone (2 g or 4 g per day) or placebo. In stage 3 (efficacy), participants assigned to ceftriaxone in stage 2 received 4 g ceftriaxone, participants assigned to placebo in stage 2 received placebo, and new participants were randomly assigned (2:1) to 4 g ceftriaxone or placebo. Participants, family members, and site staff were masked to treatment assignment. Randomisation was done by a computerised randomisation sequence with permuted blocks of 3. Participants received 2 g ceftriaxone or placebo twice daily through a central venous catheter administered at home by a trained caregiver. To minimise biliary side-effects, participants assigned to ceftriaxone also received 300 mg ursodeoxycholic acid twice daily and those assigned to placebo received matched placebo capsules. The coprimary efficacy outcomes were survival and functional decline, measured as the slope of Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) scores. Analyses were by intention to treat. This study is registered with ClinicalTrials.gov, number NCT00349622.
Findings Stage 3 included 66 participants from stages 1 and 2 and 448 new participants. In total, 340 participants were randomly allocated to ceftriaxone and 173 to placebo. During stages 1 and 2, mean ALSFRS-R declined more slowly in participants who received 4 g ceftriaxone than in those on placebo (difference 0.51 units per month, 95% CI 0.02 to 1. 00; P=0.0416), but in stage 3 functional decline between the treatment groups did not differ (0.09, 0-06 to 024; p=0.2370). No significant differences in survival between the groups were recorded in singe 3 (HR 0.90, 95% CI 0-71 to 1-15; p=0.4146). Gastrointestinal adverse events and hepatobiliary adverse events were more common in the ceftriaxone group than in the placebo group (gastrointestinal, 245 of 340 [72%] ceftriaxone vs 97 of 173 [56%] placebo, p=0. 0004; hepatobiliary, 211 [62%] vs 19 [11%], p<0.0001). Significantly more participants who received ceftriaxone had serious hepatobiliary serious adverse events (41 participants [12%]) than did those who received placebo (0 participants).
Interpretation Despite promising stage 2 data, stage 3 of this trial of ceftriaxone in amyotrophic lateral sclerosis did not show clinical efficacy. The adaptive design allowed for seamless transition from one phase to another, and central venous catheter use in the home setting was shown to be feasible.
C1 [Cudkowicz, Merit E.; Titus, Sarah; Kearney, Marianne; Yu, Hong; Sherman, Alexander; Schoenfeld, David; Hayden, Douglas; Shui, Amy; Felsenstein, Donna; Tolkoff-Rubin, Nina] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Brooks, Benjamin] Carolinas Med Ctr, Charlotte, NC 28203 USA.
[Conwit, Robin] NINDS, Bethesda, MD 20892 USA.
[Greenblatt, David J.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Keroack, Myles] Eliot Hlth Syst, Manchester, NH USA.
[Kissel, John T.] Ohio State Univ, Columbus, OH 43210 USA.
[Miller, Robert] Calif Pacific Med Ctr, San Francisco, CA USA.
[Rosenfeld, Jeffrey] Univ Calif San Francisco, Fresno, CA USA.
[Rothstein, Jeffrey D.] Johns Hopkins Univ, Baltimore, MD USA.
[Simpson, Ericka] Methodist Hosp, Houston, TX 77030 USA.
[Zinman, Lorne] Sunnybrook Hlth Sci Ctr, Toronto, ON M4N 3M5, Canada.
[Shefner, Jeremy M.] SUNY Upstate Med Univ, Syracuse, NY 13210 USA.
RP Cudkowicz, ME (reprint author), Neurol Clin Res Inst, 165 Cambridge St,Floor 6, Boston, MA 02114 USA.
EM mcudkowicz@partners.org
OI Caress, James/0000-0002-5814-6083
FU National Institute of Neurological Disorders and Stroke
FX National Institute of Neurological Disorders and Stroke.
NR 42
TC 22
Z9 22
U1 1
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1474-4422
EI 1474-4465
J9 LANCET NEUROL
JI Lancet Neurol.
PD NOV
PY 2014
VL 13
IS 11
BP 1083
EP 1091
DI 10.1016/S1474-4422(14)70222-4
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA AR7TZ
UT WOS:000343783900015
PM 25297012
ER
PT J
AU Bilgic, B
Fan, AP
Polimeni, JR
Cauley, SF
Bianciardi, M
Adalsteinsson, E
Wald, LL
Setsompop, K
AF Bilgic, Berkin
Fan, Audrey P.
Polimeni, Jonathan R.
Cauley, Stephen F.
Bianciardi, Marta
Adalsteinsson, Elfar
Wald, Lawrence L.
Setsompop, Kawin
TI Fast Quantitative Susceptibility Mapping with L1-Regularization and
Automatic Parameter Selection
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE Quantitative susceptibility mapping; Regularization; Total variation;
L-curve
ID ENABLED DIPOLE INVERSION; MAGNETIC-SUSCEPTIBILITY; BRAIN IRON;
HIGH-FIELD; IN-VIVO; MRI; PHASE; MULTIPLE; MAP; COSMOS
AB PurposeTo enable fast reconstruction of quantitative susceptibility maps with total variation penalty and automatic regularization parameter selection.
Methods(1)-Regularized susceptibility mapping is accelerated by variable splitting, which allows closed-form evaluation of each iteration of the algorithm by soft thresholding and fast Fourier transforms. This fast algorithm also renders automatic regularization parameter estimation practical. A weighting mask derived from the magnitude signal can be incorporated to allow edge-aware regularization.
ResultsCompared with the nonlinear conjugate gradient (CG) solver, the proposed method is 20 times faster. A complete pipeline including Laplacian phase unwrapping, background phase removal with SHARP filtering, and (1)-regularized dipole inversion at 0.6 mm isotropic resolution is completed in 1.2 min using MATLAB on a standard workstation compared with 22 min using the CG solver. This fast reconstruction allows estimation of regularization parameters with the L-curve method in 13 min, which would have taken 4 h with the CG algorithm. The proposed method also permits magnitude-weighted regularization, which prevents smoothing across edges identified on the magnitude signal. This more complicated optimization problem is solved 5 times faster than the nonlinear CG approach. Utility of the proposed method is also demonstrated in functional blood oxygen level-dependent susceptibility mapping, where processing of the massive time series dataset would otherwise be prohibitive with the CG solver.
ConclusionOnline reconstruction of regularized susceptibility maps may become feasible with the proposed dipole inversion. Magn Reson Med 72:1444-1459, 2014. (c) 2013 Wiley Periodicals, Inc.
C1 [Bilgic, Berkin; Fan, Audrey P.; Polimeni, Jonathan R.; Cauley, Stephen F.; Bianciardi, Marta; Adalsteinsson, Elfar; Wald, Lawrence L.; Setsompop, Kawin] Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA USA.
[Fan, Audrey P.; Adalsteinsson, Elfar] MIT, Dept Elect Engn & Comp Sci, Cambridge, MA 02139 USA.
[Polimeni, Jonathan R.; Bianciardi, Marta; Wald, Lawrence L.; Setsompop, Kawin] Harvard Univ, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Adalsteinsson, Elfar; Wald, Lawrence L.] Harvard MIT Hlth Sci & Technol, Cambridge, MA USA.
RP Bilgic, B (reprint author), Bldg 75,Room 2-102,13th St, Charlestown, MA 02129 USA.
EM berkin@nmr.mgh.harvard.edu
RI Polimeni, Jonathan/P-1395-2014; Cauley, Stephen/P-1386-2014; Setsompop,
Kawin/P-1464-2014; bilgic, berkin/P-1811-2014; Wald,
Lawrence/D-4151-2009
OI Polimeni, Jonathan/0000-0002-1348-1179; Setsompop,
Kawin/0000-0003-0455-7634;
FU NIH [R00EB012107]
FX Grant sponsor: NIH; Grant number: R00EB012107.
NR 40
TC 30
Z9 30
U1 1
U2 16
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0740-3194
EI 1522-2594
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD NOV
PY 2014
VL 72
IS 5
BP 1444
EP 1459
DI 10.1002/mrm.25029
PG 16
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AR9ED
UT WOS:000343873900026
PM 24259479
ER
PT J
AU Guerriero, RM
Pier, DB
de Gusmao, CM
Bernson-Leung, ME
Maski, KP
Urion, DK
Waugh, JL
AF Guerriero, Rejean M.
Pier, Danielle B.
de Gusmao, Claudio M.
Bernson-Leung, Miya E.
Maski, Kiran P.
Urion, David K.
Waugh, Jeff L.
TI Increased Pediatric Functional Neurological Symptom Disorders After the
Boston Marathon Bombings: A Case Series
SO PEDIATRIC NEUROLOGY
LA English
DT Article
DE functional neurological disorder; somatoform disorder; conversion
disorder; terrorism
ID HEALTH-CARE UTILIZATION; TERRORIST ATTACKS; CONVERSION DISORDER;
FOLLOW-UP; ADOLESCENTS; COMPLAINTS; DIAGNOSIS; CHILDREN; ILLNESS; TERM
AB BACKGROUND: Functional neurological symptom disorders are frequently the basis for acute neurological consultation. In children, they are often precipitated by high-frequency everyday stressors. The extent to which a severe traumatic experience may also precipitate functional neurological abnormalities is unknown. METHODS: For the 2-week period after the Boston Marathon bombings, we prospectively collected data on patients whose presentation suggested a functional neurological symptom disorder. We assessed clinical and demographic variables, duration of symptoms, extent of educational impact, and degree of connection to the Marathon bombing. We contacted all patients at 6 months after presentation to determine the outcome and accuracy of the diagnosis. RESULTS: In a parallel study, we reported a baseline of 2.6 functional neurological presentations per week in our emergency room. In the week after the Marathon bombings, this frequency tripled. Ninety-one percent of presentations were delayed by 1 week, with onset around the first school day after a city-wide lockdown. Seventy-three percent had a history of a prior psychiatric diagnosis. At the 6 months follow-up, no functional neurological symptom disorder diagnoses were overturned and no new organic diagnosis was made. CONCLUSIONS: Pediatric functional neurological symptom disorder may be precipitated by both casual and high-intensity stressors. The 3.4-fold increase in incidence after the Boston Marathon bombings and city-wide lockdown demonstrates the marked effect that a community-wide tragedy can have on the mental health of children. Care providers must be aware of functional neurological symptom disorders after stressful community events in vulnerable patient populations, particularly those with prior psychiatric diagnoses.
C1 [Guerriero, Rejean M.; Pier, Danielle B.; de Gusmao, Claudio M.; Bernson-Leung, Miya E.; Maski, Kiran P.; Urion, David K.; Waugh, Jeff L.] Boston Childrens Hosp, Dept Neurol, Boston, MA 02115 USA.
[Waugh, Jeff L.] Massachusetts Gen Hosp, Pediat Movement Disorders Clin, Boston, MA 02114 USA.
RP Waugh, JL (reprint author), Boston Childrens Hosp, Dept Neurol, 300 Longwood Ave,Fegan 11, Boston, MA 02115 USA.
EM jeff.waugh@childrens.harvard.edu
OI Pier, Danielle/0000-0001-8621-9131; Bernson-Leung,
Miya/0000-0002-7766-2323
NR 25
TC 2
Z9 3
U1 1
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0887-8994
EI 1873-5150
J9 PEDIATR NEUROL
JI Pediatr. Neurol.
PD NOV
PY 2014
VL 51
IS 5
BP 619
EP 623
DI 10.1016/j.pediatrneurol.2014.07.011
PG 5
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA AS0GF
UT WOS:000343955400006
PM 25152961
ER
PT J
AU Lin, LS
Jung, M
Mgcloud, RF
Viswanath, K
AF Lin, Leesa
Jung, Mins
Mgcloud, Rachel F.
Viswanath, Kasisomayajula
TI Media Use and Communication Inequalities in a Public Health Emergency: A
Case Study of 2009-2010 Pandemic Influenza A Virus Subtype H1N1
SO PUBLIC HEALTH REPORTS
LA English
DT Article
ID OF-THE-LITERATURE; NONPHARMACEUTICAL INTERVENTIONS;
BEHAVIORAL-RESPONSES; TELEPHONE SURVEYS; HONG-KONG; KNOWLEDGE;
TRANSMISSION; PREPAREDNESS; ASSOCIATIONS; PERCEPTIONS
AB Objectives. Studies have shown that differences among individuals and social groups in accessing and using information on health and specific threats have an impact on their knowledge and behaviors. These differences, characterized as communication inequalities, may hamper the strength of a society's response to a public health emergency. Such inequalities not only make vulnerable populations subject to a disproportionate burden of adversity, but also compromise the public health system's efforts to prevent and respond to pandemic influenza outbreaks. We investigated the effect of socioeconomic status (SES) and health communication behaviors (including barriers) on people's knowledge and misconceptions about pandemic influenza A(H1N1) (pH1N1) and adoption of prevention behaviors.
Methods. The data for this study came from a survey of 1,569 respondents drawn from a nationally representative sample of American adults during pH1N1. We conducted logistic regression analyses when appropriate.
Results. We found that (1) SES has a significant association with barriers to information access and processing, levels of pH1N1-related knowledge, and misconceptions; (2) levels of pH1N1-related knowledge are associated positively with the adoption of recommended prevention measures and negatively with the adoption of incorrect protective behaviors; and (3) people with higher SES, higher news exposure, and higher levels of pH1N1-related knowledge, as well as those who actively seek information, are less likely than their counterparts to adopt incorrect prevention behaviors.
Conclusion. Strategic public health communication efforts in public health preparedness and during emergencies should take into account potential communication inequalities and develop campaigns that reach across different social groups.
C1 [Lin, Leesa; Jung, Mins; Mgcloud, Rachel F.; Viswanath, Kasisomayajula] Dana Farber Canc Inst, Ctr Community Based Res, Boston, MA USA.
[Lin, Leesa; Mgcloud, Rachel F.; Viswanath, Kasisomayajula] Harvard Univ, Sch Publ Hlth, Dept Social & Behav Sci, Boston, MA 02115 USA.
[Lin, Leesa] Harvard Univ, Sch Publ Hlth, Div Policy Translat & Leadership Dev, Boston, MA 02115 USA.
[Jung, Mins] Dongduk Womens Univ, Dept Hlth Sci, Seoul, South Korea.
RP Lin, LS (reprint author), Harvard Univ, Sch Publ Hlth, Dept Social & Behav Sci, 677 Huntington Ave,Landmark Ctr,3rd Fl E, Boston, MA 02115 USA.
EM llin@hsph.harvard.edu
FU Centers for Disease Control and Prevention (CDC) [5PO1TP000307-05]
FX Institutional Review Board approval was obtained from the Harvard School
of Public Health. The authors acknowledge funding support from the
Centers for Disease Control and Prevention (CDC) grant #5PO1TP000307-05.
The content of this publication as well as the views expressed in this
article are solely those of the authors and do not necessarily represent
the views of CDC.
NR 55
TC 5
Z9 5
U1 0
U2 8
PU ASSOC SCHOOLS PUBLIC HEALTH
PI WASHINGTON
PA 1900 M ST NW, STE 710, WASHINGTON, DC 20036 USA
SN 0033-3549
J9 PUBLIC HEALTH REP
JI Public Health Rep.
PD NOV-DEC
PY 2014
VL 129
SU 4
BP 49
EP 60
PG 12
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AS3XD
UT WOS:000344207600008
PM 25355975
ER
PT J
AU Wander, PL
Fahrenbruch, CE
Rea, TD
AF Wander, P. L.
Fahrenbruch, C. E.
Rea, T. D.
TI The dispatcher assisted resuscitation trial: Indirect benefits of
emergency research
SO RESUSCITATION
LA English
DT Article
DE Cardiac arrest; Waiver of consent; Ethics; Hawthorne effect;
Epidemiology
ID HOSPITAL CARDIAC-ARREST; ASSOCIATION; SURVIVAL
AB Objective: Conduct of emergency research under waiver of consent produces special challenges. Moreover, the act of performing research may have unintended effects, potentially beneficial or detrimental. The Dispatcher-Assisted Randomized Trial (DART) was designed to compare 2 types of dispatcher cardiopulmonary (CPR) instruction, but not intended to affect the proportion of arrest victims that received bystander CPR. We sought to determine whether odds of receiving bystander CPR were higher during DART than during the periods before and after.
Methods: We conducted an observational cohort study of 8626 adults who suffered non-traumatic out-of-hospital cardiac arrest prior to emergency medical services (EMS) arrival in greater King County, Washington, between January 1, 1999, and December 31, 2011. Bystander CPR status was assessed through review of dispatch recordings and EMS reports to classify any bystander CPR (any B-CPR), and further categorized as bystander CPR with or without dispatcher assistance (DA-CPR and B-CPR, no DA). We used multivariable logistic regression to evaluate odds of B-CPR before, during, and after DART.
Results: The proportions receiving any B- CPR were 52% before DART (1817/3468), 59% during DART (2093/3527), and 54% after DART (885/1631). Compared to the period before DART, odds of receiving any B- CPR were higher during DART (OR = 1.35, 95% CI = 1.23-1.49), but no different after (OR = 1.10, 0.98-1.24). Compared to the before period, odds of DA-CPR were higher during DART (OR = 1.79, 1.59-2.02) but no different after (OR = 0.94, 0.80-1.10).
Conclusions: Odds of bystander CPR were higher during the trial, an increase related to higher likelihood of DA-CPR. The finding suggests a possible indirect community-wide benefit due to the interventional trial. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Wander, P. L.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Wander, P. L.; Rea, T. D.] Univ Washington, Dept Med, Seattle, WA 98195 USA.
[Fahrenbruch, C. E.; Rea, T. D.] Publ Hlth Seattle & King Cty, Emergency Med Serv Div, Seattle, WA USA.
[Wander, P. L.] VA Puget Sound Hlth Care Syst, Hosp & Specialty Med Serv, Seattle, WA 98108 USA.
RP Wander, PL (reprint author), Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
EM lwander@u.washington.edu
OI Wander, Pandora/0000-0003-3671-1464
FU NHLBI NIH HHS [T32 HL007902]
NR 16
TC 1
Z9 1
U1 2
U2 3
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0300-9572
J9 RESUSCITATION
JI Resuscitation
PD NOV
PY 2014
VL 85
IS 11
BP 1594
EP 1598
DI 10.1016/j.resuscitation.2014.08.026
PG 5
WC Critical Care Medicine; Emergency Medicine
SC General & Internal Medicine; Emergency Medicine
GA AR8LQ
UT WOS:000343827100035
PM 25195982
ER
PT J
AU Lee-Huang, S
Huang, PL
Huang, PL
AF Lee-Huang, Sylvia
Huang, Philip Lin
Huang, Paul Lee
TI Live-Cell Real-Time Imaging of Mitochondria in HIV-1-Infected Cells
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Editorial Material
C1 [Lee-Huang, Sylvia; Huang, Philip Lin] NYU, Sch Med, Dept Biochem & Mol Pharmacol, New York, NY 10016 USA.
[Huang, Paul Lee] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Huang, Paul Lee] Harvard Univ, Sch Med, Boston, MA USA.
RP Lee-Huang, S (reprint author), NYU, Sch Med, Dept Biochem & Mol Pharmacol, 550 1st St, New York, NY 10016 USA.
EM sylvia.leehuang@nyumc.org
OI Lee-Huang, Sylvia/0000-0003-3302-241X
FU NIAID NIH HHS [R01 AI031343]
NR 4
TC 1
Z9 1
U1 0
U2 4
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
EI 1931-8405
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV 1
PY 2014
VL 30
IS 11
BP 1025
EP 1026
DI 10.1089/aid.2014.0161
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA AR7OY
UT WOS:000343770300003
PM 25275699
ER
PT J
AU Torriani, M
Gill, CM
Daley, S
Oliveira, AL
Azevedo, DC
Bredella, MA
AF Torriani, Martin
Gill, Corey M.
Daley, Scott
Oliveira, Adriana L.
Azevedo, Debora C.
Bredella, Miriam A.
TI Compartmental neck fat accumulation and its relation to cardiovascular
risk and metabolic syndrome
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID SUBCUTANEOUS ADIPOSE-TISSUE; CARDIOMETABOLIC RISK; ABDOMINAL OBESITY;
CIRCUMFERENCE; ASSOCIATION; ADULTS; MEN
AB Background: Neck circumference is a predictor of cardiovascular disease (CVD) risk. However, detailed assessment of neck fat has not been explored, and the contribution from individual neck fat compartments to CVD risk is unknown.
Objective: The objective was to measure neck adipose tissue (NAT) compartments and examine relations with CVD risk markers, with the hypothesis that neck adipose tissue (NAT) accumulation preferentially involves specific compartments that contribute differently to metabolic risk.
Design: We retrospectively studied 303 subjects with successfully treated malignancies or benign etiologies [151 women, 152 men; mean (+/- SD) age: 55 +/- 17 y; mean body mass index (BMI; in kg/m(2)): 28 +/- 6] who underwent whole-body positron emission tomography/computed tomography. NAT was measured at the level of the C5 vertebral body, subdivided into posterior (NATpost), subcutaneous (NATsc), and perivertebral (NATperivert) compartments. Data on CVD risk factors (BMI, abdominal circumference, visceral and abdominal subcutaneous adipose tissue, blood pressure, serum lipids, and fasting plasma glucose) were collected. We compared NAT compartments across lean, overweight, and obese groups and performed multivariate regression models correlating NAT with CVD risk factors. Receiver operating characteristic curve and prevalence ratio analyses were performed to examine the association of NAT compartments with metabolic syndrome.
Results: NATpost and NATsc were more consistently associated with cardiometabolic risk, especially in women, correlating with visceral adipose tissue (P < 0.0001) and triglycerides (P < 0.001) and a nearly 1.5-fold increase in the prevalence ratio for metabolic syndrome after adjustment for age and BMI (P < 0.05). NATsc was most abundant in women, whereas intermuscular compartments (NATpost and NATperivert) were higher in men. In both sexes, NATpost and NATperivert showed the largest increment between lean and obese subjects.
Conclusions: Neck fat compartments expand differently with increasing adiposity, correlate with CVD risk factors, and are associated with metabolic syndrome, most notably NATpost and NATsc in women. Although neck circumference remains an important method to assess metabolic risk, cross-sectional NAT assessment provides further insight into fat accumulation in the neck.
C1 [Torriani, Martin] Massachusetts Gen Hosp, Dept Radiol, Div Musculoskeletal Imaging & Intervent, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA USA.
RP Torriani, M (reprint author), Massachusetts Gen Hosp, Dept Radiol, Div Musculoskeletal Imaging & Intervent, 55 Fruit St,YAW 6048, Boston, MA 02114 USA.
EM mtorriani@mgh.harvard.edu
FU NIH/National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK) Pilot and Feasibility Grant, Nutrition and Obesity Research
Center at Harvard [P30DK040561]
FX Supported in part by NIH/National Institute of Diabetes and Digestive
and Kidney Diseases (NIDDK) P30DK040561 Pilot and Feasibility Grant,
Nutrition and Obesity Research Center at Harvard.
NR 23
TC 7
Z9 7
U1 0
U2 5
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD NOV
PY 2014
VL 100
IS 5
BP 1244
EP 1251
DI 10.3945/ajcn.114.088450
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AR3ZT
UT WOS:000343528500005
PM 25332322
ER
PT J
AU Crocker, JB
Lee-Lewandrowski, E
Lewandrowski, N
Baron, J
Gregory, K
Lewandrowski, K
AF Crocker, J. Benjamin
Lee-Lewandrowski, Elizabeth
Lewandrowski, Nicole
Baron, Jason
Gregory, Kimberly
Lewandrowski, Kent
TI Implementation of Point-of-Care Testing in an Ambulatory Practice of an
Academic Medical Center
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE Point-of-care testing; Practice efficiency; Cost-effectiveness; Primary
care; Hemoglobin A,c; Lipid panel; Comprehensive metabolic panel
ID EMERGENCY-DEPARTMENT; CENTER IMPACT; STAY
AB Objectives: Point-of-care laboratory testing (POCT) offers reduced turnaround time and may promote improved operational efficiency. Few studies have been reported that document improvements from implementing POCT in primary care.
Methods: We measured metrics of practice efficiency in a primary care practice before and after implementation of POCT, including the total number of tests ordered, letters and phone calls to patients, and revisits due to abnormal test results. We performed a cost and revenue analysis.
Results: Following implementation of POCT, there was a 21% decrease in tests ordered per patient (P <.0001); a decrease in follow-up phone calls and letters by 89% and 85%, respectively (i) <.0001 and P <.0001); and a 61% decrease in patient revisits (13 =.0002). Estimated testing revenues exceeded expenses by $6.62 per patient, and potential cost savings from improved efficiency were $24.64 per patient.
Conclusions: POCT can significantly improve clinical operations with cost reductions through improved practice efficiency.
C1 [Crocker, J. Benjamin; Lewandrowski, Nicole] Massachusetts Gen Hosp, Dept Med, Boston, MA 02114 USA.
[Lee-Lewandrowski, Elizabeth; Baron, Jason; Gregory, Kimberly; Lewandrowski, Kent] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
[Crocker, J. Benjamin; Lee-Lewandrowski, Elizabeth; Baron, Jason; Lewandrowski, Kent] Harvard Univ, Sch Med, Boston, MA USA.
RP Lewandrowski, K (reprint author), Massachusetts Gen Hosp, 55 Fruit St,Gray 5 Chem, Boston, MA 02114 USA.
EM klewandrowski@partners.org
FU Siemens Point-of-Care; Abaxis
FX This study was funded or supported in part by Siemens Point-of-Care and
Abaxis. The authors have no other conflicts of interest to declare. All
authors had access to the study data and participated in the design and
implementation of the study and contributed to the preparation of the
manuscript. Siemens and Abaxis had no role in the design of the study or
in its implementation and had no role in developing the manuscript.
NR 14
TC 8
Z9 8
U1 0
U2 1
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0002-9173
EI 1943-7722
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD NOV
PY 2014
VL 142
IS 5
BP 640
EP 646
DI 10.1309/AJCPYK1KV2KBCDDL
PG 7
WC Pathology
SC Pathology
GA AR6IJ
UT WOS:000343687100011
PM 25319979
ER
PT J
AU Pace, M
Koury, K
Gulur, P
AF Pace, Meredith
Koury, Katharine
Gulur, Padma
TI Epidurals in Patients Receiving Thromboprophylaxis with Unfractionated
Heparin Three Times a Day: The Value of Activated Partial Thromboplastin
Time Testing
SO ANESTHESIA AND